PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset
2680682-0 1989 Up-regulation of embryonic NCAM in an EC cell line by retinoic acid. Tretinoin 54-67 neural cell adhesion molecule 1 Mus musculus 27-31
2694034-0 1989 Regulation of growth hormone gene expression by retinoic acid. Tretinoin 48-61 growth hormone 1 Homo sapiens 14-28
2519621-0 1989 Retinoic acid induces transforming growth factor-beta 2 in cultured keratinocytes and mouse epidermis. Tretinoin 0-13 transforming growth factor, beta 2 Mus musculus 22-55
2519621-2 1989 Treatment with retinoic acid increases expression of TGF-beta 2 in cultured keratinocytes in vitro, as well as in the epidermis in vivo. Tretinoin 15-28 transforming growth factor, beta 2 Mus musculus 53-63
2519621-4 1989 Specific antibodies to TGF-beta 2 partially reverse the ability of retinoic acid to inhibit DNA synthesis in cultured keratinocytes. Tretinoin 67-80 transforming growth factor, beta 2 Mus musculus 23-33
2519621-5 1989 The regulation of TGF-beta 2 expression by retinoic acid may have important physiological and pharmacological roles in the maintenance of epidermal homeostasis. Tretinoin 43-56 transforming growth factor, beta 2 Mus musculus 18-28
2573830-4 1989 An increase in the level of mdr1 mRNA was observed after retinoic acid treatment of four neuroblastoma cell lines, including the SK-N-SH cell line. Tretinoin 57-70 ATP binding cassette subfamily B member 1 Homo sapiens 28-32
2613750-0 1989 Modulation of transforming growth factor alpha-dependent expression of epidermal growth factor receptor gene by transforming growth factor beta, triiodothyronine, and retinoic acid. Tretinoin 167-180 tumor necrosis factor Homo sapiens 14-46
2613750-0 1989 Modulation of transforming growth factor alpha-dependent expression of epidermal growth factor receptor gene by transforming growth factor beta, triiodothyronine, and retinoic acid. Tretinoin 167-180 epidermal growth factor receptor Homo sapiens 71-103
2613750-6 1989 Similarly, retinoic acid treatment also enhanced in a time- and dose-dependent manner the TGF alpha-dependent response of EGF receptor mRNA and acted synergistically with TGF beta 1. Tretinoin 11-24 epidermal growth factor receptor Homo sapiens 122-134
2613750-6 1989 Similarly, retinoic acid treatment also enhanced in a time- and dose-dependent manner the TGF alpha-dependent response of EGF receptor mRNA and acted synergistically with TGF beta 1. Tretinoin 11-24 transforming growth factor beta 1 Homo sapiens 171-181
2550479-3 1989 Retinoic acid-induced cells showed a slow, sustained response to both FMLP and PMA. Tretinoin 0-13 formyl peptide receptor 1 Homo sapiens 70-74
2476509-0 1989 All-trans retinoic acid stimulates growth of adult human keratinocytes cultured in growth factor-deficient medium, inhibits production of thrombospondin and fibronectin, and reduces adhesion. Tretinoin 10-23 thrombospondin 1 Homo sapiens 138-152
2476509-0 1989 All-trans retinoic acid stimulates growth of adult human keratinocytes cultured in growth factor-deficient medium, inhibits production of thrombospondin and fibronectin, and reduces adhesion. Tretinoin 10-23 fibronectin 1 Homo sapiens 157-168
2476509-10 1989 In regard to extracellular matrix production, TSP production was inhibited by greater than 90% under all three conditions in the presence of all-trans retinoic acid. Tretinoin 151-164 thrombospondin 1 Homo sapiens 46-49
2573830-7 1989 To provide evidence that Pgp was localized on the cell surface, an immunotoxin conjugate directed against Pgp was added to cells before and after treatment with retinoic acid. Tretinoin 161-174 ATP binding cassette subfamily B member 1 Homo sapiens 25-28
2484657-7 1989 Treatment of P19 cells with retinoic acid resulted in a decrease in the expression of Thy-1 antigen which preceded changes in morphology of the cells. Tretinoin 28-41 thymus cell antigen 1, theta Mus musculus 86-99
2546746-10 1989 In contrast to inhibin secretion, for which FSH is the principal regulator, transferrin secretion by Sertoli cells is more evenly bidirectional (overall mean upper to lower chamber ratio of 1.5) and requires exposure to other stimuli (insulin, retinoic acid, and testosterone) in addition to FSH to achieve maximal secretion. Tretinoin 244-257 transferrin Rattus norvegicus 76-87
2546814-0 1989 Retinoic acid enhances VIP receptor expression and responsiveness in human neuroblastoma cell, SH-SY5Y. Tretinoin 0-13 vasoactive intestinal peptide Homo sapiens 23-26
2558941-6 1989 Furthermore, and again in contrast to murine embryonal carcinoma cells, treatment of the human embryonal carcinoma cells with retinoic acid causes a nearly complete loss of TGF-beta 1 binding sites. Tretinoin 126-139 transforming growth factor beta 1 Homo sapiens 173-183
2546814-4 1989 Pretreatment of SH-SY5Y cells with 10 microM RA over 6 days dramatically increased VIP receptor number from approximately 3,000 to approximately 70,000 sites per cell and enhanced threefold the cAMP accumulation after external VIP addition, while VIP immunoreactive content in the cells increased 2-3-fold. Tretinoin 45-47 vasoactive intestinal peptide Homo sapiens 83-86
2546814-4 1989 Pretreatment of SH-SY5Y cells with 10 microM RA over 6 days dramatically increased VIP receptor number from approximately 3,000 to approximately 70,000 sites per cell and enhanced threefold the cAMP accumulation after external VIP addition, while VIP immunoreactive content in the cells increased 2-3-fold. Tretinoin 45-47 vasoactive intestinal peptide Homo sapiens 227-230
2546814-4 1989 Pretreatment of SH-SY5Y cells with 10 microM RA over 6 days dramatically increased VIP receptor number from approximately 3,000 to approximately 70,000 sites per cell and enhanced threefold the cAMP accumulation after external VIP addition, while VIP immunoreactive content in the cells increased 2-3-fold. Tretinoin 45-47 vasoactive intestinal peptide Homo sapiens 227-230
2546814-5 1989 In the light of the recently proposed autocrine function of VIP in this cell lineage, the strong enhancement of the VIP system may contribute to the differentiation effects of RA. Tretinoin 176-178 vasoactive intestinal peptide Homo sapiens 116-119
2762980-1 1989 Cells from three patients showed maturation after incubation with retinoic acid (2 had M-3 AML and 1 had CML-B). Tretinoin 66-79 myoregulin Homo sapiens 87-100
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 89-102 alkaline phosphatase, placental Homo sapiens 18-21
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 89-102 tumor necrosis factor Homo sapiens 173-182
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 89-102 alkaline phosphatase, placental Homo sapiens 240-243
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 89-102 tumor necrosis factor Homo sapiens 275-284
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 200-213 alkaline phosphatase, placental Homo sapiens 18-21
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 200-213 tumor necrosis factor Homo sapiens 173-182
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 200-213 alkaline phosphatase, placental Homo sapiens 240-243
2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 200-213 tumor necrosis factor Homo sapiens 275-284
2742744-5 1989 The potentiation of retinoic acid-induced ALP activity was correlated with an increased amount of mRNA for ALP with the combined treatment. Tretinoin 20-33 alkaline phosphatase, placental Homo sapiens 42-45
2742744-5 1989 The potentiation of retinoic acid-induced ALP activity was correlated with an increased amount of mRNA for ALP with the combined treatment. Tretinoin 20-33 alkaline phosphatase, placental Homo sapiens 107-110
2742744-6 1989 By observing the rate of decay of mRNA for actin and ALP, we were able to demonstrate that the interaction between retinoic acid and recombinant TNF-alpha modulated the steady state of ALP mRNA. Tretinoin 115-128 alkaline phosphatase, placental Homo sapiens 53-56
2742744-6 1989 By observing the rate of decay of mRNA for actin and ALP, we were able to demonstrate that the interaction between retinoic acid and recombinant TNF-alpha modulated the steady state of ALP mRNA. Tretinoin 115-128 tumor necrosis factor Homo sapiens 145-154
2742744-6 1989 By observing the rate of decay of mRNA for actin and ALP, we were able to demonstrate that the interaction between retinoic acid and recombinant TNF-alpha modulated the steady state of ALP mRNA. Tretinoin 115-128 alkaline phosphatase, placental Homo sapiens 185-188
2568572-0 1989 Changes in expression of tyrosine hydroxylase immunoreactivity in human SMS-KCNR neuroblastoma following retinoic acid or phorbol ester-induced differentiation. Tretinoin 105-118 tyrosine hydroxylase Homo sapiens 25-45
2568572-2 1989 Tyrosine hydroxylase (TH) immunoreactivity was measured in this cell line following treatment with retinoic acid (1-10 microM), 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 16-160 nM), or combinations of these agents. Tretinoin 99-112 tyrosine hydroxylase Homo sapiens 0-20
2568572-2 1989 Tyrosine hydroxylase (TH) immunoreactivity was measured in this cell line following treatment with retinoic acid (1-10 microM), 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 16-160 nM), or combinations of these agents. Tretinoin 99-112 tyrosine hydroxylase Homo sapiens 22-24
2742744-0 1989 Retinoic acid and tumour necrosis factor-alpha act in concert to control the level of alkaline phosphatase mRNA. Tretinoin 0-13 alkaline phosphatase, placental Homo sapiens 86-106
2742744-2 1989 In the present work, evidence is provided to show that alkaline phosphatase (ALP) gene expression is mediated by retinoic acid in a model clonal cell line (UMR 201) derived from rat neonatal calvaria. Tretinoin 113-126 alkaline phosphatase, placental Homo sapiens 55-75
2742744-2 1989 In the present work, evidence is provided to show that alkaline phosphatase (ALP) gene expression is mediated by retinoic acid in a model clonal cell line (UMR 201) derived from rat neonatal calvaria. Tretinoin 113-126 alkaline phosphatase, placental Homo sapiens 77-80
2742744-3 1989 These cells have the characteristics of relatively undifferentiated mesenchymal cells with a very low basal ALP activity which is dramatically increased by retinoic acid. Tretinoin 156-169 alkaline phosphatase, placental Homo sapiens 108-111
2568572-3 1989 After 21 days of treatment with either TPA or retinoic acid (RA), TH immunoreactivity was measured in this using densitometric scans of Western blots, was doubled relative to untreated or serum-deprived SMS-KCNR cultures. Tretinoin 46-59 tyrosine hydroxylase Homo sapiens 66-68
2568572-3 1989 After 21 days of treatment with either TPA or retinoic acid (RA), TH immunoreactivity was measured in this using densitometric scans of Western blots, was doubled relative to untreated or serum-deprived SMS-KCNR cultures. Tretinoin 61-63 tyrosine hydroxylase Homo sapiens 66-68
2568572-5 1989 Treatment with RA for 3 days followed by phorbol esters for an additional 3 days resulted in a 3-fold increase in TH immunoreactivity at day 6; reversing the order of drug treatment did not have this effect. Tretinoin 15-17 tyrosine hydroxylase Homo sapiens 114-116
2542765-2 1989 Rev-ErbA alpha is an approximately 56-kilodalton protein most similar in structure to the thyroid hormone receptor (c-erbA) and the retinoic acid receptor, but it does not bind either thyroid hormone or retinoic acid. Tretinoin 132-145 nuclear receptor subfamily 1, group D, member 1 Rattus norvegicus 0-14
2497027-2 1989 In RA-treated cells, Ara-C transport was reduced and there was a concomitant increase of the ID50 values of Ara-C in comparison with the controls. Tretinoin 3-5 ATP binding cassette subfamily C member 6 Homo sapiens 21-24
2497027-2 1989 In RA-treated cells, Ara-C transport was reduced and there was a concomitant increase of the ID50 values of Ara-C in comparison with the controls. Tretinoin 3-5 ATP binding cassette subfamily C member 6 Homo sapiens 108-111
2472992-1 1989 The effect of retinoic acid (RA) on the level of interferon (IFN)-induced 2-5 oligoadenylate (2-5A) synthetase activity was examined in human histiocytic lymphoma U937 cells and WISH cells** in order to ascertain the role of this polymerase in interaction between IFNs and RA. Tretinoin 14-27 interferon alpha 1 Homo sapiens 61-64
2917804-4 1989 Decreased N-myc expression and increased c-src expression were observed during neuronal differentiation by retinoic acid, polyprenoic acid (E5166) and dibutyryl cyclic AMP, whereas the expression of N-myc and c-src genes was considerably reduced during schwannian differentiation by bromodeoxyuridine, demonstrating that the expression of N-myc and c-src genes was regulated independently in the bipolar differentiation processes of NB cells. Tretinoin 107-120 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 41-46
2912547-0 1989 Modulation of growth and epidermal growth factor receptor activity by retinoic acid in human glioma cells. Tretinoin 70-83 epidermal growth factor receptor Homo sapiens 25-57
2542014-6 1989 In addition, treatment of human hepatoma cells with RA leads to a rapid 10- to 50-fold increase in RAR beta mRNA levels, whereas RAR alpha mRNA expression is not affected. Tretinoin 52-54 retinoic acid receptor beta Homo sapiens 99-107
2575317-1 1989 The effects of 13-cis retinoic acid (RA) and dexamethasone on the levels of epidermal growth factor (EGF) receptor and fibroblast derived proteoglycan core protein (PG40) mRNAs were studied in human skin fibroblasts. Tretinoin 37-39 epidermal growth factor receptor Homo sapiens 76-114
2465548-4 1989 This induction of surface IL-1R can be blocked by the addition of retinoic acid and parallels induction of squamous differentiation markers. Tretinoin 66-79 interleukin 1 receptor type 1 Homo sapiens 26-31
2463259-8 1989 In normal epidermal cells, the suppressive effect of retinoic acid was much more evident with particulate transglutaminase than involucrin levels. Tretinoin 53-66 involucrin Homo sapiens 128-138
2640155-1 1989 The initial cell association and metabolic conversion of retinoic acid (RA) by HL-60 cells in serum-free, transferrin/insulin-supplemented, RPMI 1640 medium was greater than or equal to 10-fold greater than in RPMI 1640 medium containing 10% fetal bovine serum (FBS). Tretinoin 57-70 transferrin Homo sapiens 106-117
2640155-1 1989 The initial cell association and metabolic conversion of retinoic acid (RA) by HL-60 cells in serum-free, transferrin/insulin-supplemented, RPMI 1640 medium was greater than or equal to 10-fold greater than in RPMI 1640 medium containing 10% fetal bovine serum (FBS). Tretinoin 57-70 insulin Homo sapiens 118-125
2640155-1 1989 The initial cell association and metabolic conversion of retinoic acid (RA) by HL-60 cells in serum-free, transferrin/insulin-supplemented, RPMI 1640 medium was greater than or equal to 10-fold greater than in RPMI 1640 medium containing 10% fetal bovine serum (FBS). Tretinoin 72-74 transferrin Homo sapiens 106-117
2640155-1 1989 The initial cell association and metabolic conversion of retinoic acid (RA) by HL-60 cells in serum-free, transferrin/insulin-supplemented, RPMI 1640 medium was greater than or equal to 10-fold greater than in RPMI 1640 medium containing 10% fetal bovine serum (FBS). Tretinoin 72-74 insulin Homo sapiens 118-125
2610595-4 1989 Thus, while RA (0.1-50 microM) invariably suppressed the activity of IFN-alpha, it enhanced the action of IFN-beta at low dose (0.1-1.0 microM) but became suppressive at higher concentrations (greater than or equal to 10 microM). Tretinoin 12-14 interferon alpha 1 Homo sapiens 69-78
2610595-5 1989 Furthermore, higher antiviral activity was consistently obtained when RA (0.1-10 microM) was added prior to either IFN-alpha or IFN-beta comparing to cultures with IFN alone. Tretinoin 70-72 interferon alpha 1 Homo sapiens 115-124
2610595-5 1989 Furthermore, higher antiviral activity was consistently obtained when RA (0.1-10 microM) was added prior to either IFN-alpha or IFN-beta comparing to cultures with IFN alone. Tretinoin 70-72 interferon alpha 1 Homo sapiens 115-118
2492900-1 1989 Retinoic acid alone has no effect on the human breast cancer cell line BT-20 but can amplify the antiproliferative action of interferon-gamma (IFN-gamma). Tretinoin 0-13 interferon gamma Homo sapiens 125-141
2492900-1 1989 Retinoic acid alone has no effect on the human breast cancer cell line BT-20 but can amplify the antiproliferative action of interferon-gamma (IFN-gamma). Tretinoin 0-13 interferon gamma Homo sapiens 143-152
2521339-1 1989 The retinoic acid-induced differentiation of F-9 teratocarcinoma cells in monolayer culture is accompanied by the accumulation of fibrillar fibronectin deposits, the appearance of a highly structured actin cytoskeleton, and the redistribution of integrin to apparent sites of substrate contact. Tretinoin 4-17 fibronectin 1 Homo sapiens 140-151
3191488-5 1988 N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Tretinoin 26-39 transforming growth factor beta 1 Homo sapiens 184-192
2562438-5 1989 RAR-beta, transcribed and translated in vitro from the cloned cDNA coding region, sedimented at 4 S and this suggests that the 4-svedberg nuclear retinoic-acid-binding activity may represent the retinoic acid receptors. Tretinoin 146-159 retinoic acid receptor beta Homo sapiens 0-8
2562184-5 1989 We give particular attention to tamoxifen and retinoic acid, since it has been shown that these agents, which are of known efficacy for prevention of cancer, can markedly enhance the secretion of specific isotypes of TGF-beta by several types of cells. Tretinoin 46-59 transforming growth factor beta 1 Homo sapiens 217-225
2586142-0 1989 Studies on the relationship between protein kinase C and differentiation of human promyelocytic leukemia cells induced by retinoic acid. Tretinoin 122-135 proline rich transmembrane protein 2 Homo sapiens 36-52
2586142-6 1989 We presumed that the activity of PKC is closely related to the differentiation of human promyelocytic leukemia cells induced by all-trans-retinoic acid. Tretinoin 128-151 proline rich transmembrane protein 2 Homo sapiens 33-36
2849937-1 1988 Two cellular retinoic acid binding proteins, CRABP I and II, which behaved differently on a DEAE-cellulose column, were purified from 14-day chick embryos. Tretinoin 13-26 cellular retinoic acid binding protein 1 Gallus gallus 45-59
2849937-4 1988 CRABP II was a novel cellular retinoic acid binding protein, in which the amino acids at 6 positions of the NH2 terminal sequence are different from those in CRABP I. Tretinoin 30-43 cellular retinoic acid binding protein 1 Gallus gallus 0-7
3191488-5 1988 N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Tretinoin 26-39 transforming growth factor beta 1 Homo sapiens 268-276
2458288-1 1988 F9 teratocarcinoma cells secrete the serine protease, tissue plasminogen activator (t-PA), upon differentiation induced in vitro by retinoic acid (RA) or RA and dibutyryl cAMP (RA/dbcAMP). Tretinoin 132-145 coagulation factor II, thrombin Homo sapiens 37-52
2846157-3 1988 However, when the cells were induced to differentiate with dibutyryl cyclic AMP (dbcAMP) or retinoic acid, they acquired the ability to undergo actin polymerization on stimulation with FMLP or phorbol myristate acetate. Tretinoin 92-105 formyl peptide receptor 1 Homo sapiens 185-189
2846157-4 1988 Kinetic experiments revealed that in the first 48 h of retinoic acid treatment there was no increase in the chemotactic peptide receptors on HL-60 cells, but the cells were capable of undergoing actin polymerization on stimulation with FMLP. Tretinoin 55-68 formyl peptide receptor 1 Homo sapiens 236-240
3142527-9 1988 In contrast to IL-1, retinoic acid increased the detectable levels of only u-PA in the chondrocyte cell layers. Tretinoin 21-34 plasminogen activator, urokinase Homo sapiens 75-79
2458913-9 1988 Other agents that can also substitute for 1,25-(OH)2D, but not for cAMP, in facilitating C5a receptor expression include retinoic acid and ionomycin, but with less potency. Tretinoin 121-134 complement C5a receptor 1 Homo sapiens 89-101
2458288-1 1988 F9 teratocarcinoma cells secrete the serine protease, tissue plasminogen activator (t-PA), upon differentiation induced in vitro by retinoic acid (RA) or RA and dibutyryl cAMP (RA/dbcAMP). Tretinoin 132-145 plasminogen activator, tissue type Homo sapiens 54-88
3136932-0 1988 Retinoic acid upregulates interleukin-2 receptors on activated human thymocytes. Tretinoin 0-13 interleukin 2 Homo sapiens 26-39
3136932-3 1988 When RA was added to resting thymocyte cultures in the presence of recombinant interleukin-2 (rIL-2), blastogenesis was increased two- to fourfold. Tretinoin 5-7 interleukin 2 Homo sapiens 79-92
3136932-6 1988 Thus, RA enhancement of thymocyte responses appears to be mediated by an increase in IL-2-receptor expression on thymocyte blasts, resulting in augmented IL-2-dependent growth. Tretinoin 6-8 interleukin 2 Homo sapiens 85-89
2851384-6 1988 The rate of retinoic acid hydroxylation via the cytochrome P-450 system to 4-hydroxyretinoic acid plus the subsequent oxidation to 4-ketoretinoic acid was significantly elevated. Tretinoin 12-25 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 48-64
3136932-9 1988 Taken together, the results of this study suggest that RA can modulate IL-2-dependent immune responses, in part, by upregulating the expression of IL-2 receptors on proliferating T lymphoblasts generated from cells at restricted stages of development. Tretinoin 55-57 interleukin 2 Homo sapiens 71-75
3136932-9 1988 Taken together, the results of this study suggest that RA can modulate IL-2-dependent immune responses, in part, by upregulating the expression of IL-2 receptors on proliferating T lymphoblasts generated from cells at restricted stages of development. Tretinoin 55-57 interleukin 2 Homo sapiens 147-151
2842422-4 1988 RA, but not ROH, significantly enhanced ADA activity in a monocytic leukemia cell (THP-1) line. Tretinoin 0-2 GLI family zinc finger 2 Homo sapiens 83-88
2972558-2 1988 RA suppressed IgG-coated erythrocyte (EA) rosette formation of myelomonocytic cells blocked at relatively late stages of differentiation such as ML-1, U-937, THP-1-T, normal monocytes, and fresh cells of patients with acute myelomonocytic leukemia. Tretinoin 0-2 GLI family zinc finger 2 Homo sapiens 158-163
2972558-5 1988 A kinetic study using HL-60 and THP-1-T demonstrated that an increase required at least a 48-h exposure and that the maximum decrease required approximately 6 h. The RA effect on both cell lines was dose-dependent. Tretinoin 166-168 GLI family zinc finger 2 Homo sapiens 32-37
2972558-6 1988 The number of Fc gamma R of HL-60 and THP-1-T treated with RA became very close, although untreated THP-1 had almost 10 times as many as HL-60. Tretinoin 59-61 GLI family zinc finger 2 Homo sapiens 38-43
2842422-5 1988 Addition of RA or the tumor promoter, phorbol 12-myristic 13-acetate (PMA), to HPBM or THP-1 cells resulted in significant increases in 5NT activity with opposite effects on ADA activity. Tretinoin 12-14 GLI family zinc finger 2 Homo sapiens 87-92
3136776-0 1988 Modulation of urokinase-type plasminogen activator messenger RNA levels in human synovial fibroblasts by interleukin-1, retinoic acid, and a glucocorticoid. Tretinoin 120-133 plasminogen activator, urokinase Homo sapiens 14-50
3136776-1 1988 Previous studies have shown that mononuclear cell-conditioned medium (MCCM), interleukin-1 (IL-1), and all-trans-retinoic acid rapidly stimulate, while glucocorticoids lower, the urokinase-type plasminogen activator (u-PA) activity of human synovial fibroblast-like cells. Tretinoin 103-126 plasminogen activator, urokinase Homo sapiens 179-215
3136776-1 1988 Previous studies have shown that mononuclear cell-conditioned medium (MCCM), interleukin-1 (IL-1), and all-trans-retinoic acid rapidly stimulate, while glucocorticoids lower, the urokinase-type plasminogen activator (u-PA) activity of human synovial fibroblast-like cells. Tretinoin 103-126 plasminogen activator, urokinase Homo sapiens 217-221
2838167-4 1988 Moreover, the antitumor promoter retinoic acid (RA, 0.1 microM), when added simultaneously with TPA to the PYS cells, completely abolished the TPA effects on PK.A. Tretinoin 33-46 promotion susceptibility QTL 1 Mus musculus 96-99
3175950-0 1988 Interaction between the splotch mutation and retinoic acid in mouse neural tube defects in vitro. Tretinoin 45-58 paired box 3 Mus musculus 24-31
2838167-4 1988 Moreover, the antitumor promoter retinoic acid (RA, 0.1 microM), when added simultaneously with TPA to the PYS cells, completely abolished the TPA effects on PK.A. Tretinoin 33-46 promotion susceptibility QTL 1 Mus musculus 143-146
2838167-4 1988 Moreover, the antitumor promoter retinoic acid (RA, 0.1 microM), when added simultaneously with TPA to the PYS cells, completely abolished the TPA effects on PK.A. Tretinoin 48-50 promotion susceptibility QTL 1 Mus musculus 143-146
2838167-5 1988 When RA was added 25 min before TPA, the counteraction was not observed, indicating that RA was counteracting the TPA effect directly. Tretinoin 5-7 promotion susceptibility QTL 1 Mus musculus 114-117
2838167-5 1988 When RA was added 25 min before TPA, the counteraction was not observed, indicating that RA was counteracting the TPA effect directly. Tretinoin 89-91 promotion susceptibility QTL 1 Mus musculus 114-117
2838167-7 1988 This possible translocation of PK.A seems to be blocked by RA, suggesting that the early antagonistic effects of RA toward TPA-mediated events occur at the plasma membranes. Tretinoin 59-61 promotion susceptibility QTL 1 Mus musculus 123-126
2838167-7 1988 This possible translocation of PK.A seems to be blocked by RA, suggesting that the early antagonistic effects of RA toward TPA-mediated events occur at the plasma membranes. Tretinoin 113-115 promotion susceptibility QTL 1 Mus musculus 123-126
2841888-8 1988 The tritiated, heterocyclic retinoic acid analog, CD270, is thus proposed as an alternative ligand for cytosolic retinoic acid binding protein. Tretinoin 28-41 TNF receptor superfamily member 14 Homo sapiens 50-55
2841888-8 1988 The tritiated, heterocyclic retinoic acid analog, CD270, is thus proposed as an alternative ligand for cytosolic retinoic acid binding protein. Tretinoin 113-126 TNF receptor superfamily member 14 Homo sapiens 50-55
2841310-0 1988 Transformation with SV40 virus prevents retinoic acid inhibition of plasma membrane NADH diferric transferrin reductase in rat liver cells. Tretinoin 40-53 transferrin Rattus norvegicus 98-109
2841310-1 1988 Retinoic acid inhibits the reduction of diferric transferrin through the transplasma membrane electron transport system on fetal rat liver cells infected with a temperature-sensitive SV40 virus when the cells are in the nontransformed state cultured at 40 degrees C. When the cells are in the transformed state (grown at the permissive 33 degrees C temperature), retinoic acid does not inhibit the diferric transferrin reduction. Tretinoin 0-13 transferrin Rattus norvegicus 49-60
2897254-1 1988 Retinoic acid and retinyl acetate induce tissue transglutaminase to high levels in cultured SCC-4 keratinocytes, increasing the enzyme specific activity over 50-fold under optimal conditions. Tretinoin 0-13 transglutaminase 2 Homo sapiens 41-64
2897254-1 1988 Retinoic acid and retinyl acetate induce tissue transglutaminase to high levels in cultured SCC-4 keratinocytes, increasing the enzyme specific activity over 50-fold under optimal conditions. Tretinoin 0-13 MAU2 sister chromatid cohesion factor Homo sapiens 92-97
2841310-1 1988 Retinoic acid inhibits the reduction of diferric transferrin through the transplasma membrane electron transport system on fetal rat liver cells infected with a temperature-sensitive SV40 virus when the cells are in the nontransformed state cultured at 40 degrees C. When the cells are in the transformed state (grown at the permissive 33 degrees C temperature), retinoic acid does not inhibit the diferric transferrin reduction. Tretinoin 0-13 transferrin Rattus norvegicus 407-418
2841310-1 1988 Retinoic acid inhibits the reduction of diferric transferrin through the transplasma membrane electron transport system on fetal rat liver cells infected with a temperature-sensitive SV40 virus when the cells are in the nontransformed state cultured at 40 degrees C. When the cells are in the transformed state (grown at the permissive 33 degrees C temperature), retinoic acid does not inhibit the diferric transferrin reduction. Tretinoin 363-376 transferrin Rattus norvegicus 49-60
2835037-4 1988 Retinal and retinoic acid enhanced the effects of PMA and FMLP in HL-60 cells and of FMLP in HN up to 4.5-fold. Tretinoin 12-25 formyl peptide receptor 1 Homo sapiens 58-62
2841310-3 1988 Isolated rat liver plasma membrane NADH diferric transferrin reductase is also inhibited by retinoic acid. Tretinoin 92-105 transferrin Rattus norvegicus 49-60
3360803-7 1988 We also show that in human synovial fibroblast cultures human recombinant interleukin-1 beta rapidly induces high levels of MMP-3 mRNA and, conversely, that retinoic acid or dexamethasone can suppress the MMP-3 mRNA levels. Tretinoin 157-170 interleukin 1 beta Homo sapiens 74-92
3360803-7 1988 We also show that in human synovial fibroblast cultures human recombinant interleukin-1 beta rapidly induces high levels of MMP-3 mRNA and, conversely, that retinoic acid or dexamethasone can suppress the MMP-3 mRNA levels. Tretinoin 157-170 matrix metallopeptidase 3 Homo sapiens 124-129
3360803-7 1988 We also show that in human synovial fibroblast cultures human recombinant interleukin-1 beta rapidly induces high levels of MMP-3 mRNA and, conversely, that retinoic acid or dexamethasone can suppress the MMP-3 mRNA levels. Tretinoin 157-170 matrix metallopeptidase 3 Homo sapiens 205-210
2835037-4 1988 Retinal and retinoic acid enhanced the effects of PMA and FMLP in HL-60 cells and of FMLP in HN up to 4.5-fold. Tretinoin 12-25 formyl peptide receptor 1 Homo sapiens 85-89
2835037-6 1988 In the presence of cytochalasin B, retinal inhibited the effect of FMLP in HN, whereas retinoic acid inhibited NO activation by FMLP in both cell types. Tretinoin 87-100 formyl peptide receptor 1 Homo sapiens 128-132
2448754-3 1988 Modified AFP genes introduced stably into F9 embryonal carcinoma stem cells by DNA transfection were silent until activated by treatment with retinoic acid to form visceral endoderm. Tretinoin 142-155 alpha fetoprotein Homo sapiens 9-12
3280124-3 1988 We find that these retinoic acid-induced changes are accompanied by a marked decrease in the levels of p53 and p53 mRNA. Tretinoin 19-32 tumor protein p53 Homo sapiens 103-106
3280124-3 1988 We find that these retinoic acid-induced changes are accompanied by a marked decrease in the levels of p53 and p53 mRNA. Tretinoin 19-32 tumor protein p53 Homo sapiens 111-114
3355557-1 1988 By the differential hybridization technique, we isolated a cDNA clone, MK1, whose RNA level increased in early stages of retinoic acid-induced differentiation of embryonal carcinoma cells. Tretinoin 121-134 potassium voltage-gated channel, shaker-related subfamily, member 1 Mus musculus 71-74
2451772-2 1988 The phosphorylation of 22 kD, pI 6.0 and 5.8 proteins (pp22) in HL-60 cells or myeloid leukemic cells from patients, was enhanced by treatment with granuloid inducers such as retinoic acid, dimethyl sulfoxide or G-CSF, in common with prostaglandin E2 and theophylline, or dibutyryl c-AMP, which increased intracellular c-AMP. Tretinoin 175-188 cathelicidin antimicrobial peptide Homo sapiens 282-287
3365571-7 1988 Retinoic acid did not induce CEA production in clone D or MIP-101 cells, but did enhance the production of CEA in DLD-2 cells. Tretinoin 0-13 CEA cell adhesion molecule 3 Homo sapiens 107-110
3365571-8 1988 When both retinoic acid and sodium butyrate were added together, CEA production was either additive (DLD-2) or was inhibited (clone D and MIP-101). Tretinoin 10-23 CEA cell adhesion molecule 3 Homo sapiens 65-68
2451772-2 1988 The phosphorylation of 22 kD, pI 6.0 and 5.8 proteins (pp22) in HL-60 cells or myeloid leukemic cells from patients, was enhanced by treatment with granuloid inducers such as retinoic acid, dimethyl sulfoxide or G-CSF, in common with prostaglandin E2 and theophylline, or dibutyryl c-AMP, which increased intracellular c-AMP. Tretinoin 175-188 cathelicidin antimicrobial peptide Homo sapiens 319-324
2823943-3 1987 With the promyelocytic HL-60 cells, TNF alpha (greater than or equal to 2.5 U/mL) in combination with RA synergistically inhibited clonal growth; TNF alpha at lower concentrations (less than or equal to 1 U/mL) plus RA (10(-9) mol/L) were antagonistic in their inhibition of growth. Tretinoin 216-218 tumor necrosis factor Homo sapiens 36-45
2856164-0 1988 Cytochrome-P-450-dependent metabolism of retinoic acid in rat skin microsomes: inhibition by ketoconazole. Tretinoin 41-54 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 0-16
2856164-8 1988 The RA metabolism in rat epidermal microsomes shows the typical characteristics of a cytochrome-P-450 (P450)-dependent enzyme system, i.e. a requirement for NADPH and oxygen and inhibition by CO and SKF-525A. Tretinoin 4-6 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 85-101
2826339-1 1987 The combination of retinoic acid or tumor necrosis factor alpha (TNF-alpha) with interferon gamma (IFN-gamma) resulted in a synergistic amplification of the anti-proliferative effect of IFN-gamma on cultured breast cancer cells. Tretinoin 19-32 interferon gamma Homo sapiens 81-108
2826339-1 1987 The combination of retinoic acid or tumor necrosis factor alpha (TNF-alpha) with interferon gamma (IFN-gamma) resulted in a synergistic amplification of the anti-proliferative effect of IFN-gamma on cultured breast cancer cells. Tretinoin 19-32 interferon gamma Homo sapiens 99-108
2826339-5 1987 On the other hand, only TNF-alpha and not retinoic acid was able to increase the IFN-gamma induced expression of HLA-DR on the cell surface. Tretinoin 42-55 interferon gamma Homo sapiens 81-90
2826339-7 1987 The combinations of retinoic acid with IFN-gamma increased the down-regulation of specific binding sites for 125I-IFN-gamma. Tretinoin 20-33 interferon gamma Homo sapiens 39-48
2826339-7 1987 The combinations of retinoic acid with IFN-gamma increased the down-regulation of specific binding sites for 125I-IFN-gamma. Tretinoin 20-33 interferon gamma Homo sapiens 114-123
2826339-9 1987 Data obtained in this study demonstrate a different pattern of action between retinoic acid and TNF-alpha regarding their synergism in combination with IFN-gamma. Tretinoin 78-91 interferon gamma Homo sapiens 152-161
2823943-5 1987 In addition, RA (10(-9) to 10(-7) mol/L) increased the number of TNF alpha receptors on HL-60 cells 1.3- to 1.7-fold without changing the affinity for the TNF alpha receptor. Tretinoin 13-15 tumor necrosis factor Homo sapiens 65-74
2823943-6 1987 With the more immature KG-1 myeloblasts, concentrations of TNF alpha greater than 10 U/mL synergistically interacted with RA to inhibit clonal growth; at lower concentrations of TNF alpha (less than 10 U/mL), RA appeared to inhibit the expected effect of TNF alpha. Tretinoin 122-124 tumor necrosis factor Homo sapiens 59-68
2823943-6 1987 With the more immature KG-1 myeloblasts, concentrations of TNF alpha greater than 10 U/mL synergistically interacted with RA to inhibit clonal growth; at lower concentrations of TNF alpha (less than 10 U/mL), RA appeared to inhibit the expected effect of TNF alpha. Tretinoin 209-211 tumor necrosis factor Homo sapiens 59-68
3484302-3 1987 Triamcinolone acetate concentrations of 10(-8) and 10(-9) M or 10(-6) M retinoic acid were effective in enhancing the 1,25-dihydroxyvitamin D3 stimulation of BGP secretion. Tretinoin 72-85 bone gamma-carboxyglutamate protein Rattus norvegicus 158-161
3484302-10 1987 We conclude that, although both triamcinolone acetate and retinoic acid increase the 1,25-dihydroxyvitamin D3 stimulation of BGP secretion by ROS 17/2 cells, they have different effects on the regulation of collagen production. Tretinoin 58-71 bone gamma-carboxyglutamate protein Rattus norvegicus 125-128
2822142-8 1987 (4) Inhibition of protein kinase C activity by drugs reported to inhibit the enzyme (retinoic acid, quercetin) abolishes the stimulation of brain isozyme of creatine kinase activity and of DNA synthesis by PTH. Tretinoin 85-98 parathyroid hormone Homo sapiens 206-209
3424222-0 1987 Retinoic acid-induced selective mortality of splotch-delayed mouse neural tube defect mutants. Tretinoin 0-13 paired box 3 Mus musculus 45-52
2444456-4 1987 On the other hand retinoic acid 10(-5) M, N methyl-formamide 1% and N,N hexamethylene bisacetamide 2.5 mM decreased CEA 2-, 4- and 3-fold respectively. Tretinoin 18-31 CEA cell adhesion molecule 3 Homo sapiens 116-119
2444242-0 1987 Modulation of placental alkaline phosphatase activity and cytokeratins in human HN-1 cells by butyrate, retinoic acid, catecholamines and histamine. Tretinoin 104-117 alkaline phosphatase, placental Homo sapiens 14-44
2886219-4 1987 Treatment of both EC cell lines with retinoic acid leads to the appearance of irreversibly differentiated cells that begin to exhibit receptors for TGF-beta by 48 h. After an additional 3-5 days, the differentiated cells express approximately 6000 high affinity receptors for TGF-beta, with an apparent dissociation constant of 45 PM. Tretinoin 37-50 transforming growth factor beta 1 Homo sapiens 148-156
2886219-4 1987 Treatment of both EC cell lines with retinoic acid leads to the appearance of irreversibly differentiated cells that begin to exhibit receptors for TGF-beta by 48 h. After an additional 3-5 days, the differentiated cells express approximately 6000 high affinity receptors for TGF-beta, with an apparent dissociation constant of 45 PM. Tretinoin 37-50 transforming growth factor beta 1 Homo sapiens 276-284
3619945-0 1987 Retinoic acid inhibition of transplasmalemma diferric transferrin reductase. Tretinoin 0-13 transferrin Homo sapiens 54-65
3619945-1 1987 All trans retinoic acid inhibited diferric transferrin reduction by HeLa cells. Tretinoin 4-23 transferrin Homo sapiens 43-54
3619945-2 1987 The NADH diferric transferrin reductase activity of isolated liver plasma membranes was also inhibited by retinoic acid. Tretinoin 106-119 transferrin Homo sapiens 18-29
3619945-5 1987 Since the transmembrane electron transport has been shown to stimulate cell growth, the growth inhibition by retinoic acid thus may be based on inhibition of the NADH diferric transferrin reductase. Tretinoin 109-122 transferrin Homo sapiens 176-187
2444242-9 1987 PLAP activity could be modulated by a concerted action of either butyrate plus retinoic acid or butyrate plus catecholamines or histamine, indicating a possible role for PLAP in tumour cell proliferation. Tretinoin 79-92 alkaline phosphatase, placental Homo sapiens 0-4
2444242-4 1987 However, retinoic acid inhibited the efficacy of butyrate to induce PLAP activity. Tretinoin 9-22 alkaline phosphatase, placental Homo sapiens 68-72
3582730-8 1987 Under these conditions, retinol and retinoic acid both stimulated transferrin mRNA levels but did not affect SGP-2 mRNA levels. Tretinoin 36-49 transferrin Rattus norvegicus 66-77
3607514-6 1987 Furthermore, TPA- and RA-treated cells showed a significant increase in acetylcholinesterase activity compared with non-treated cells. Tretinoin 22-24 acetylcholinesterase (Cartwright blood group) Homo sapiens 72-92
3607514-8 1987 These findings demonstrate that TPA and RA can regulate both the number of muscarinic receptors and the acetylcholinesterase activity in human SH-SY5Y neuroblastoma cells. Tretinoin 40-42 acetylcholinesterase (Cartwright blood group) Homo sapiens 104-124
3113420-5 1987 Furthermore, the RNA expression of the poly(ADP-ribose) polymerase gene was shown to decrease during the granulocytic differentiation of HL-60 cells upon induction by retinoic acid. Tretinoin 167-180 poly(ADP-ribose) polymerase 1 Homo sapiens 39-66
3308117-3 1987 The concentration of beta S-100 was markedly increased in the cells after treatment with retinoic acid, whereas the concentration of alpha S-100 was undetectably low, indicating that the S-100b (beta beta) protein was induced by retinoic acid. Tretinoin 229-242 S100 calcium binding protein B Homo sapiens 187-193
3476218-0 1987 Effects of retinoic acid on the differentiation of THP-1 cell lines containing aneuploid or diploid chromosomes. Tretinoin 11-24 GLI family zinc finger 2 Homo sapiens 51-56
3029143-1 1987 [3H]Retinoic acid (RA) and [3H]retinol bind in an unsaturable manner to isolated nuclei from Nulli-SCC1 and PCC4.aza1R embryonal carcinoma (EC) cells. Tretinoin 4-17 protein tyrosine phosphatase, receptor type, J Mus musculus 99-103
3032574-5 1987 Exposure to PTH and, to a lesser extent, 1,25-dihydroxyvitamin D3, prostaglandin E2, retinoic acid, and epidermal growth factor stimulated the release of collagenase, an effect not seen with interleukin-1 or heparin. Tretinoin 85-98 parathyroid hormone Rattus norvegicus 12-15
3030944-6 1987 Retinoic acid treatment had no significant effect on MHC antigens, but it decreased expression of 5A7 and Leu7 antigens, and markedly increased the expression of the melanoma-associated antigen Me14-D12. Tretinoin 0-13 beta-1,3-glucuronyltransferase 1 Homo sapiens 106-110
3103717-1 1987 In this study, we analyzed the effect of tumor necrosis factor (TNF) on retinoic acid (RA)-induced myeloid differentiation of the promyelocytic HL-60 leukemia cell line. Tretinoin 72-85 tumor necrosis factor Homo sapiens 41-62
3103717-1 1987 In this study, we analyzed the effect of tumor necrosis factor (TNF) on retinoic acid (RA)-induced myeloid differentiation of the promyelocytic HL-60 leukemia cell line. Tretinoin 72-85 tumor necrosis factor Homo sapiens 64-67
3471521-0 1987 Recombinant human interferon alpha enhancement of retinoic-acid-induced differentiation of HL-60 cells. Tretinoin 50-63 interferon alpha 1 Homo sapiens 18-28
3471521-5 1987 The addition of 1000 IU/ml of IFN and 10(-7) M RA at the initiation of culture reduced the number of viable cells to 28% of that observed for cells treated with RA alone. Tretinoin 161-163 interferon alpha 1 Homo sapiens 30-33
3471521-7 1987 IFN-RA-treated cells differentiated more rapidly than cells treated with RA alone. Tretinoin 4-6 interferon alpha 1 Homo sapiens 0-3
3471521-8 1987 In addition, the final percentage of mature cells was increased at day 7 in IFN-RA-treated cultures, as compared with RA-treated cells. Tretinoin 80-82 interferon alpha 1 Homo sapiens 76-79
3468509-1 1987 Apolipoprotein E (apoE) expression was studied in F9 embryonal carcinoma cells that differentiate in response to retinoic acid into cells resembling either parietal endoderm or visceral endoderm of the parietal or visceral yolk sac. Tretinoin 113-126 apolipoprotein E Mus musculus 0-16
3470744-9 1987 Radiolabeled probes prepared by nicktranslation of p lambda 1E were used to monitor the steady-state levels of entactin mRNA in F9 embryonal carcinoma cells that were induced to differentiate by exposure to retinoic acid and dibutyryl cyclic AMP. Tretinoin 207-220 nidogen 1 Rattus norvegicus 111-119
3026615-5 1987 Also, IFN-gamma neither induced differentiation of NTERA-2 cl.D1 cells, which are pluripotent human stem cells, nor influenced their differentiation induced by retinoic acid. Tretinoin 160-173 interferon gamma Homo sapiens 6-15
3468509-1 1987 Apolipoprotein E (apoE) expression was studied in F9 embryonal carcinoma cells that differentiate in response to retinoic acid into cells resembling either parietal endoderm or visceral endoderm of the parietal or visceral yolk sac. Tretinoin 113-126 apolipoprotein E Mus musculus 18-22
3468509-6 1987 The apoE phenotype reflected the differentiated state of the F9 cell since either the up-regulated or down-regulated pattern was stable to the removal of the retinoic acid inducer. Tretinoin 158-171 apolipoprotein E Mus musculus 4-8
3549002-3 1987 The addition of insulin enhanced the AIG of the cells in both groups even in the presence of RA. Tretinoin 93-95 insulin Cricetulus griseus 16-23
2892751-5 1987 Treatment of the stem cells with a chemical inducer like retinoic acid (RA), and also hexamethylenebisacetamide (HMBA), or 5-bromo-2"-deoxyuridine (BUdR), simultaneously accelerates differentiation and stimulates accumulation of Hox2.3 mRNA to high levels. Tretinoin 57-70 homeobox B7 Mus musculus 229-235
3030555-0 1987 Effect of retinoic acid on nerve growth factor receptors. Tretinoin 10-23 nerve growth factor Homo sapiens 27-46
3030555-1 1987 Retinoic acid (RA), a naturally occurring metabolite of vitamin A, increased the number of receptors for nerve growth factor (NGF) in cultured human neuroblastoma cells (LA-N-1), as indicated by an immunofluorescence assay of cell surface receptors and by specific binding of 125I-NGF to solubilized receptors. Tretinoin 0-13 nerve growth factor Homo sapiens 105-124
3030555-1 1987 Retinoic acid (RA), a naturally occurring metabolite of vitamin A, increased the number of receptors for nerve growth factor (NGF) in cultured human neuroblastoma cells (LA-N-1), as indicated by an immunofluorescence assay of cell surface receptors and by specific binding of 125I-NGF to solubilized receptors. Tretinoin 0-13 nerve growth factor Homo sapiens 126-129
3030555-1 1987 Retinoic acid (RA), a naturally occurring metabolite of vitamin A, increased the number of receptors for nerve growth factor (NGF) in cultured human neuroblastoma cells (LA-N-1), as indicated by an immunofluorescence assay of cell surface receptors and by specific binding of 125I-NGF to solubilized receptors. Tretinoin 0-13 nerve growth factor Homo sapiens 281-284
3030555-1 1987 Retinoic acid (RA), a naturally occurring metabolite of vitamin A, increased the number of receptors for nerve growth factor (NGF) in cultured human neuroblastoma cells (LA-N-1), as indicated by an immunofluorescence assay of cell surface receptors and by specific binding of 125I-NGF to solubilized receptors. Tretinoin 15-17 nerve growth factor Homo sapiens 105-124
3030555-1 1987 Retinoic acid (RA), a naturally occurring metabolite of vitamin A, increased the number of receptors for nerve growth factor (NGF) in cultured human neuroblastoma cells (LA-N-1), as indicated by an immunofluorescence assay of cell surface receptors and by specific binding of 125I-NGF to solubilized receptors. Tretinoin 15-17 nerve growth factor Homo sapiens 126-129
3030555-1 1987 Retinoic acid (RA), a naturally occurring metabolite of vitamin A, increased the number of receptors for nerve growth factor (NGF) in cultured human neuroblastoma cells (LA-N-1), as indicated by an immunofluorescence assay of cell surface receptors and by specific binding of 125I-NGF to solubilized receptors. Tretinoin 15-17 nerve growth factor Homo sapiens 281-284
3030555-2 1987 Analysis of 125I-NGF binding showed that RA increased the number of both high affinity and low affinity receptors for NGF without affecting the equilibrium dissociation constants. Tretinoin 41-43 nerve growth factor Homo sapiens 17-20
3030555-2 1987 Analysis of 125I-NGF binding showed that RA increased the number of both high affinity and low affinity receptors for NGF without affecting the equilibrium dissociation constants. Tretinoin 41-43 nerve growth factor Homo sapiens 118-121
3030555-4 1987 Whether morphological changes following RA treatment are directly related to the increase in NGF receptors is unknown. Tretinoin 40-42 nerve growth factor Homo sapiens 93-96
3030555-5 1987 Data presented here are consistent with literature reports that RA modifies cell surface glycoproteins, including those that act as cell surface receptors for epidermal growth factor and insulin. Tretinoin 64-66 insulin Homo sapiens 187-194
2892751-14 1987 We have shown that addition of RA to primary cultures of cells from rat embryo mesencephalon leads to strong accumulation of Hox2.3 mRNA. Tretinoin 31-33 homeobox B7 Mus musculus 125-131
2892751-15 1987 A possible interpretation is that RA mimics one or more spatially restricted effectors, accounting for the local accumulation of Hox2.3 transcripts in the embryonic central nervous system. Tretinoin 34-36 homeobox B7 Mus musculus 129-135
3666278-4 1987 The addition of varying concentrations of retinoic acid (RA) to varying concentrations of tamoxifen (TMX) resulted in an additive effect on the inhibition of proliferation of the ER-positive human carcinoma cell lines (MCF-7). Tretinoin 42-55 estrogen receptor 1 Homo sapiens 179-181
2871126-1 1986 Retinoic acid has been shown to induce large accumulations of tissue transglutaminase in cultured myeloid cells. Tretinoin 0-13 transglutaminase 2 Homo sapiens 62-85
3095923-1 1986 The expression of the cellular src gene product pp60c-src was examined in an embryonal carcinoma cell line that differentiates in vitro into neuronlike cells after being treated with retinoic acid. Tretinoin 183-196 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 31-34
3095923-1 1986 The expression of the cellular src gene product pp60c-src was examined in an embryonal carcinoma cell line that differentiates in vitro into neuronlike cells after being treated with retinoic acid. Tretinoin 183-196 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 54-57
3095923-6 1986 These results indicate that expression of pp60c-src induced by retinoic acid in these embryonal carcinoma cells mimics the expression of c-src in developing neurons. Tretinoin 63-76 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 48-51
3095923-6 1986 These results indicate that expression of pp60c-src induced by retinoic acid in these embryonal carcinoma cells mimics the expression of c-src in developing neurons. Tretinoin 63-76 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 46-51
3015560-1 1986 Based on the finding that retinoic acid (RA) increases 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptor number in ROS 17/2 cells, we investigated the effects of RA on the ability of 1,25-(OH)2D3 to regulate alkaline phosphatase activity and PTH-responsive adenylate cyclase in these cells. Tretinoin 41-43 parathyroid hormone Homo sapiens 241-244
3015560-2 1986 A maximally effective dose of 1,25-(OH)2D3 (10(-8) M) caused a 75-80% increase in alkaline phosphatase activity and an approximately 70-75% attenuation of the cAMP response to PTH, while RA (10(-6) M) decreased alkaline phosphatase activity by 30-45% and decreased PTH-stimulated cAMP levels by approximately 20%. Tretinoin 187-189 parathyroid hormone Homo sapiens 176-179
2940106-3 1986 The dependence of retinoic acid (RA)-induced terminal myeloid differentiation of HL-60 promyelocytic leukemia cells on calmodulin levels and calcium ion flux was ascertained. Tretinoin 18-31 calmodulin 1 Homo sapiens 119-129
2940106-3 1986 The dependence of retinoic acid (RA)-induced terminal myeloid differentiation of HL-60 promyelocytic leukemia cells on calmodulin levels and calcium ion flux was ascertained. Tretinoin 33-35 calmodulin 1 Homo sapiens 119-129
3088310-0 1986 Variants of a human monocytic leukemia cell line (THP-1): induction of differentiation by retinoic acid, interferon-gamma, and T-lymphocyte-derived differentiation-inducing activity. Tretinoin 90-103 GLI family zinc finger 2 Homo sapiens 50-55
3088310-1 1986 Induction of terminal differentiation of two variant sublines derived from the human monocytic leukemia cell line THP-1 by all-trans-beta-retinoic acid (RA) was studied. Tretinoin 123-151 GLI family zinc finger 2 Homo sapiens 114-119
3088310-1 1986 Induction of terminal differentiation of two variant sublines derived from the human monocytic leukemia cell line THP-1 by all-trans-beta-retinoic acid (RA) was studied. Tretinoin 153-155 GLI family zinc finger 2 Homo sapiens 114-119
3088310-2 1986 One of the variants was approximately 10 times more resistant to RA and the other, approximately 10 times more sensitive than the parent THP-1. Tretinoin 65-67 GLI family zinc finger 2 Homo sapiens 137-142
3088310-3 1986 Differentiation of the RA-resistant variant could be induced by immune interferon (IFN-gamma) and a T-lymphocyte-derived lymphokine of a differentiation-inducing activity (DIA), alone or in combination with 10 nM RA. Tretinoin 23-25 interferon gamma Homo sapiens 83-92
3021829-5 1986 Many studies have indicated that retinoic acid can markedly increase the number of cellular receptors for epidermal growth factor, which is partially encoded by another oncogene, erb-B. Tretinoin 33-46 epidermal growth factor receptor Homo sapiens 179-184
2871126-3 1986 Retinoic acid also increased tissue transglutaminase mRNA levels in human promyelocytic leukemia (HL-60) cells. Tretinoin 0-13 transglutaminase 2 Homo sapiens 29-52
3099098-5 1986 Protein kinase C (PK-C) activity was increased 35-40% in cells treated for 1 h with TPA alone or after subsequent exposure to RA. Tretinoin 126-128 proline rich transmembrane protein 2 Homo sapiens 0-16
3512256-5 1986 Retinoic acid alone had no significant effect on the synthesis of casein, but suppressed alpha-lactalbumin activity dose dependently. Tretinoin 0-13 lactalbumin, alpha Mus musculus 89-106
3512256-6 1986 Concomitant addition of retinoic acid with EGF had no significant effect on EGF-induced inhibition of casein synthesis, but enhanced EGF-induced inhibition of alpha-lactalbumin activity dose dependently. Tretinoin 24-37 lactalbumin, alpha Mus musculus 159-176
2867824-1 1986 Retinoic acid (RA) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) induced differentiation of a human monocytic leukemia cell line, THP-1. Tretinoin 0-13 GLI family zinc finger 2 Homo sapiens 132-137
2867824-1 1986 Retinoic acid (RA) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) induced differentiation of a human monocytic leukemia cell line, THP-1. Tretinoin 15-17 GLI family zinc finger 2 Homo sapiens 132-137
2867824-6 1986 Dibutyryl cyclic AMP potentiated the RA-induced expression of tissue transglutaminase. Tretinoin 37-39 transglutaminase 2 Homo sapiens 62-85
3099098-7 1986 The changes in PK-C activity in TPA + RA-treated cells were accompanied by Ca2+/phospholipid(PL)-dependent phosphorylation in vitro of pp38 which is characteristic of treatment with RA alone, as well as the Ca2+/PL-independent phosphorylation in vitro of pp82 and pp130 (vinculin) which is prevalent in cells treated continuously with TPA alone and is absent in RA-treated cells. Tretinoin 182-184 proline rich transmembrane protein 2 Homo sapiens 15-19
3781745-1 1986 The temporal effects of retinoic acid supplementation on hepatic cytochrome P-450-dependent enzymes were studied on the rat. Tretinoin 24-37 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 65-81
3099098-5 1986 Protein kinase C (PK-C) activity was increased 35-40% in cells treated for 1 h with TPA alone or after subsequent exposure to RA. Tretinoin 126-128 proline rich transmembrane protein 2 Homo sapiens 18-22
3099098-6 1986 Cells treated for 48 h with RA exhibited a 2-fold increase in PK-C activity while cells exposed to TPA for 48 h lost all PK-C activity. Tretinoin 28-30 proline rich transmembrane protein 2 Homo sapiens 62-66
2431266-1 1986 Three cDNA clones coding for the 3" region of the intracisternal A-particle (IAP), a mouse endogenous retrovirus, were isolated during screening of a library for genes whose expression was modulated during the retinoic acid-induced differentiation of the embryonal carcinoma cell line F9 into parietal endoderm-like (PE-like) cells. Tretinoin 210-223 intracisternal A particle, Eya1 linked Mus musculus 50-75
3099098-6 1986 Cells treated for 48 h with RA exhibited a 2-fold increase in PK-C activity while cells exposed to TPA for 48 h lost all PK-C activity. Tretinoin 28-30 proline rich transmembrane protein 2 Homo sapiens 121-125
2431266-1 1986 Three cDNA clones coding for the 3" region of the intracisternal A-particle (IAP), a mouse endogenous retrovirus, were isolated during screening of a library for genes whose expression was modulated during the retinoic acid-induced differentiation of the embryonal carcinoma cell line F9 into parietal endoderm-like (PE-like) cells. Tretinoin 210-223 intracisternal A particle, Eya1 linked Mus musculus 77-80
2431266-3 1986 Instead, IAP transcripts as well as IAPs were abundant in the PE-like cells PYS-2 and F9AcCl 9 and in retinoic acid-induced F9 cells but not in the other differentiated cell types of teratocarcinoma origin which were examined. Tretinoin 102-115 intracisternal A particle, Eya1 linked Mus musculus 9-12
3099098-7 1986 The changes in PK-C activity in TPA + RA-treated cells were accompanied by Ca2+/phospholipid(PL)-dependent phosphorylation in vitro of pp38 which is characteristic of treatment with RA alone, as well as the Ca2+/PL-independent phosphorylation in vitro of pp82 and pp130 (vinculin) which is prevalent in cells treated continuously with TPA alone and is absent in RA-treated cells. Tretinoin 38-40 proline rich transmembrane protein 2 Homo sapiens 15-19
4044595-1 1985 F9 embryonal carcinoma cells treated with 5 X 10(-8) M retinoic acid and cultured in suspension for 8 days form aggregates consisting of an outer epithelial layer of alpha-fetoprotein-producing visceral endoderm cells. Tretinoin 55-68 alpha fetoprotein Homo sapiens 166-183
2988768-1 1985 After ethyl methane sulfonate mutagenesis of the mammary carcinoma cell line, MCF-7, we have isolated three clones, U-2, U-3, and U-9, resistant to retinoic acid. Tretinoin 148-161 RNA, U2 small nuclear 4, pseudogene Homo sapiens 116-133
3931632-0 1985 Stimulation of interleukin 1 and 3 production by retinoic acid in vitro. Tretinoin 49-62 interleukin 3 Mus musculus 15-34
3931632-3 1985 Hence we have studied the effect of retinoic acid on the production of interleukins (ILs) 1 and 3 in vitro. Tretinoin 36-49 interleukin 3 Mus musculus 71-97
3931632-6 1985 IL 3 release by WEHI-3 cells was also stimulated by retinoic acid in a dose-related fashion. Tretinoin 52-65 interleukin 3 Mus musculus 0-4
3898457-0 1985 Reduction in the frequency of neural tube defects in splotch mice by retinoic acid. Tretinoin 69-82 paired box 3 Mus musculus 53-60
3866800-3 1985 Within 2 days after the addition of DMSO or retinoic acid to growing HL-60 cells, the binding of IFN-alpha A to treated cells increases significantly relative to its binding to untreated cells. Tretinoin 44-57 interferon alpha 1 Homo sapiens 97-106
2411582-2 1985 At least an additive differentiation-inducing effect was found between IFN-gamma and 1-100 nM retinoic acid (RA). Tretinoin 94-107 interferon gamma Homo sapiens 71-86
2411582-2 1985 At least an additive differentiation-inducing effect was found between IFN-gamma and 1-100 nM retinoic acid (RA). Tretinoin 109-111 interferon gamma Homo sapiens 71-86
3861180-2 1985 When IFN-alpha A is combined with agents capable of inducing differentiation in HL-60 cells, such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA), cis or trans retinoic acid (RA) or dimethylsulfoxide (DMSO), growth suppression and induction of differentiation are dramatically increased. Tretinoin 159-172 interferon alpha 1 Homo sapiens 5-14
3986782-5 1985 For further testing of this hypothesis, the retinoic acid analogue of the mouse skin irritant and initiation-promoter TPA, i.e., RPA, was designed (7). Tretinoin 44-57 promotion susceptibility QTL 1 Mus musculus 118-121
2987698-3 1985 Colony formation induced by the combined action of PDGF and TGF-beta is 100-fold more sensitive to inhibition by retinoic acid than is colony formation induced by treatment of the myc-transfected cells with EGF. Tretinoin 113-126 transforming growth factor, beta 1 Rattus norvegicus 60-68
2987698-4 1985 Moreover, retinoic acid (10(-8) M) is inhibitory for colony growth whenever TGF-beta is present, regardless of whether the effects of TGF-beta are stimulatory, as occurs in the presence of PDGF, or inhibitory, as found in the presence of EGF. Tretinoin 10-23 transforming growth factor, beta 1 Rattus norvegicus 76-84
2989063-0 1985 Induction of functional differentiation of a human monocytic leukemia cell line (THP-1) by retinoic acid and cholera toxin. Tretinoin 91-104 GLI family zinc finger 2 Homo sapiens 81-86
2987306-1 1985 Inhibition of collagen production by retinoic acid accompanied by reduced type I procollagen messenger ribonucleic acid levels in human skin fibroblast cultures. Tretinoin 37-50 collagen type I alpha 2 chain Homo sapiens 74-92
2987306-7 1985 The reduction in procollagen production by all-trans-retinoic acid was accompanied by a similar reduction in pro alpha 2(I) of type I procollagen specific messenger RNA (mRNA), as detected by dot blot and Northern blot hybridizations. Tretinoin 43-66 collagen type I alpha 2 chain Homo sapiens 127-145
2989063-1 1985 The human monocytic leukemia cell line, THP-1, is induced to differentiate into more functionally mature monocyte (macrophage)-like cells by incubation with retinoic acid at concentrations of 10nM or higher. Tretinoin 157-170 GLI family zinc finger 2 Homo sapiens 40-45
2989063-4 1985 Prostaglandin E2, dibutyryl cyclic adenosine 3":5"-monophosphate, or T-lymphocyte-derived differentiation-inducing activity, all inactive or less active alone, increase the extent of differentiation of THP-1 in combination with 10nM retinoic acid. Tretinoin 233-246 GLI family zinc finger 2 Homo sapiens 202-207
2989063-8 1985 THP-1 thus joins the list of leukemic myelomonocytic cell lines (e.g., the promyelocytic HL-60 and the monoblast-like U-937) that are blocked at a relatively late stage of maturation and which differentiate in response to retinoic acid. Tretinoin 222-235 GLI family zinc finger 2 Homo sapiens 0-5
6386496-0 1984 Regulation of acetylcholinesterase activity by retinoic acid in a human neuroblastoma cell line. Tretinoin 47-60 acetylcholinesterase (Cartwright blood group) Homo sapiens 14-34
2982650-0 1985 Effects of retinoic acid on ascites cells of the TA3 mouse mammary carcinoma. Tretinoin 11-24 RIKEN cDNA 2700049A03 gene Mus musculus 49-52
3972179-1 1985 The electrophysiological properties of differentiated cells which were derived from teratocarcinoma OTT6050 in culture showed two different types of spike generation: (1) In the differentiated cells treated by retinoic acid, the action potential of cells involved Ca2+; (2) in the differentiated cells treated by both retinoic acid and nerve growth factor (NGF), the action potential of cells involved Na+ and CA2+. Tretinoin 210-223 nerve growth factor Homo sapiens 336-355
3972179-1 1985 The electrophysiological properties of differentiated cells which were derived from teratocarcinoma OTT6050 in culture showed two different types of spike generation: (1) In the differentiated cells treated by retinoic acid, the action potential of cells involved Ca2+; (2) in the differentiated cells treated by both retinoic acid and nerve growth factor (NGF), the action potential of cells involved Na+ and CA2+. Tretinoin 210-223 nerve growth factor Homo sapiens 357-360
2859286-0 1985 Retinoic acid-induced expression of tissue transglutaminase in human promyelocytic leukemia (HL-60) cells. Tretinoin 0-13 transglutaminase 2 Homo sapiens 36-59
2859286-3 1985 Retinoic acid-induced expression of tissue transglutaminase is potentiated by analogues of cyclic AMP. Tretinoin 0-13 transglutaminase 2 Homo sapiens 36-59
2984029-4 1985 Their actions on insulin receptors were the opposite, however; 1 alpha,25-dihydroxyvitamin D3 increased the binding of the hormone, while RA plus db-cAMP decreased the binding. Tretinoin 138-140 insulin Homo sapiens 17-24
2981174-0 1985 Lack of correlation between loss of anchorage-independent growth and levels of transformation-specific p53 protein in retinoic acid-treated F9 embryonal carcinoma cells. Tretinoin 118-131 tumor protein p53 Homo sapiens 103-106
6435868-3 1984 Like IFN, RA induced 2-5A synthetase activity in a time- and dose-dependent manner. Tretinoin 10-12 interferon alpha 1 Homo sapiens 5-8
6435868-6 1984 In WISH cells, the growth of encephalomyocarditis virus was inhibited by RA treatment, which is consistent with the hypothesis that 2-5A synthetase plays an important role in the antiviral action of IFN, at least in encephalomyocarditis virus replication. Tretinoin 73-75 interferon alpha 1 Homo sapiens 199-202
6386496-1 1984 The ability of retinoic acid (RA) to modulate acetylcholinesterase (AChE) activity in a human neuroblastoma cell line (LN-N-5) was examined. Tretinoin 15-28 acetylcholinesterase (Cartwright blood group) Homo sapiens 46-66
6386496-1 1984 The ability of retinoic acid (RA) to modulate acetylcholinesterase (AChE) activity in a human neuroblastoma cell line (LN-N-5) was examined. Tretinoin 15-28 acetylcholinesterase (Cartwright blood group) Homo sapiens 68-72
6386496-1 1984 The ability of retinoic acid (RA) to modulate acetylcholinesterase (AChE) activity in a human neuroblastoma cell line (LN-N-5) was examined. Tretinoin 30-32 acetylcholinesterase (Cartwright blood group) Homo sapiens 46-66
6386496-1 1984 The ability of retinoic acid (RA) to modulate acetylcholinesterase (AChE) activity in a human neuroblastoma cell line (LN-N-5) was examined. Tretinoin 30-32 acetylcholinesterase (Cartwright blood group) Homo sapiens 68-72
6386496-2 1984 The specific activity of AChE was significantly increased 3 days after exposure of LA-N-5 to RA and reached its maximum values after 9 or more days of culturing. Tretinoin 93-95 acetylcholinesterase (Cartwright blood group) Homo sapiens 25-29
6386496-3 1984 Dose-response experiments demonstrated that large increases of AChE occurred at RA concentrations between 10(-7) and 10(-6) M with maximum AChE values detected at 10(-6)-10(-5) M. Increased AChE activity paralleled neurite outgrowth in LA-N-5 cultures. Tretinoin 80-82 acetylcholinesterase (Cartwright blood group) Homo sapiens 63-67
6386496-3 1984 Dose-response experiments demonstrated that large increases of AChE occurred at RA concentrations between 10(-7) and 10(-6) M with maximum AChE values detected at 10(-6)-10(-5) M. Increased AChE activity paralleled neurite outgrowth in LA-N-5 cultures. Tretinoin 80-82 acetylcholinesterase (Cartwright blood group) Homo sapiens 139-143
6386496-3 1984 Dose-response experiments demonstrated that large increases of AChE occurred at RA concentrations between 10(-7) and 10(-6) M with maximum AChE values detected at 10(-6)-10(-5) M. Increased AChE activity paralleled neurite outgrowth in LA-N-5 cultures. Tretinoin 80-82 acetylcholinesterase (Cartwright blood group) Homo sapiens 139-143
6386496-4 1984 These findings demonstrate that RA can regulate specific AChE activity in human neuroblastoma cells in a manner consistent with neuronal maturation. Tretinoin 32-34 acetylcholinesterase (Cartwright blood group) Homo sapiens 57-61
6486823-0 1984 Retinoic acid metabolism by a system reconstituted with cytochrome P-450. Tretinoin 0-13 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 56-72
6733848-10 1984 We conclude that phorbol ester action and RA counteraction on the release of FN takes place on a cell-surface target; that FN which is released into the medium by TPA is derived from pre-existing FN; that RA specifically antagonizes TPA action. Tretinoin 42-44 fibronectin 1 Homo sapiens 77-79
6095043-11 1984 In vitro transcription experiments demonstrate that the retinoic acid-mediated decrease in pST 6-135- and pST 1-68-specific RNA occurs at the transcriptional level and that dibutyryl cyclic AMP acts posttranscriptionally to further depress the levels of these RNAs. Tretinoin 56-69 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 Mus musculus 91-94
6095043-11 1984 In vitro transcription experiments demonstrate that the retinoic acid-mediated decrease in pST 6-135- and pST 1-68-specific RNA occurs at the transcriptional level and that dibutyryl cyclic AMP acts posttranscriptionally to further depress the levels of these RNAs. Tretinoin 56-69 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 Mus musculus 106-111
6611208-4 1984 In this study, we explored the mechanism(s) of this effect by determining the phenotype of cells that show augmented responses to PHA and by analyzing RA effects on regulatory events mediated by interleukin-2 (IL-2). Tretinoin 151-153 interleukin 2 Homo sapiens 195-208
6611208-4 1984 In this study, we explored the mechanism(s) of this effect by determining the phenotype of cells that show augmented responses to PHA and by analyzing RA effects on regulatory events mediated by interleukin-2 (IL-2). Tretinoin 151-153 interleukin 2 Homo sapiens 210-214
6611208-6 1984 In the presence of saturating concentrations of exogeneous IL-2, RA caused further enhancement of both unfractionated and T3+ thymocyte proliferation, but could not induce immature T3- cells to become PHA responsive. Tretinoin 65-67 interleukin 2 Homo sapiens 59-63
6733848-0 1984 Kinetics of fibronectin release from fibroblasts in response to 12-O-tetradecanoylphorbol-13-acetate and retinoic acid. Tretinoin 105-118 fibronectin 1 Homo sapiens 12-23
6733848-1 1984 We have studied the effects of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and its in vivo and in vitro antagonist retinoic acid (RA) on the synthesis and release of a major extracellular glycoprotein, fibronectin (FN), in human lung fibroblasts (HLF). Tretinoin 148-150 fibronectin 1 Homo sapiens 220-231
6733848-1 1984 We have studied the effects of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and its in vivo and in vitro antagonist retinoic acid (RA) on the synthesis and release of a major extracellular glycoprotein, fibronectin (FN), in human lung fibroblasts (HLF). Tretinoin 148-150 fibronectin 1 Homo sapiens 233-235
6733848-5 1984 RA, given simultaneously with TPA, prevented the increased release and resulted in a normal FN accumulation in the medium. Tretinoin 0-2 fibronectin 1 Homo sapiens 92-94
6733848-10 1984 We conclude that phorbol ester action and RA counteraction on the release of FN takes place on a cell-surface target; that FN which is released into the medium by TPA is derived from pre-existing FN; that RA specifically antagonizes TPA action. Tretinoin 205-207 fibronectin 1 Homo sapiens 77-79
6561070-4 1984 Inhibition of IFN action in vitro by retinoic acid (vitamin A acid) was found to be reversed by beta-carotene (pro-vitamin A). Tretinoin 37-50 interferon alpha 1 Homo sapiens 14-17
6322983-2 1984 Retinoic acid by itself has no effect on colony formation; but at concentrations of 10(-9) M or greater, it can greatly enhance the response of the cells to EGF and TGF-beta, as measured by colony growth in soft agar and expression of a transformed morphology in monolayer culture. Tretinoin 0-13 transforming growth factor, beta 1 Rattus norvegicus 165-173
6322983-9 1984 It can be concluded that the abilities of retinoic acid and dexamethasone to alter expression of the transformed phenotype induced by treatment of normal rat kidney cells with TGF-beta and EGF are mediated at least in part through their effects on the EGF receptor. Tretinoin 42-55 transforming growth factor, beta 1 Rattus norvegicus 176-184
6321491-1 1984 When human myeloid leukemia HL-60 cells were induced to differentiate into mature cells by dimethyl sulfoxide or retinoic acid, the amount of myeloperoxidase activity per cell decreased to 20 to 30% of that of uninduced cells, and the rate of myeloperoxidase biosynthesis decreased to an undetectable level in 19 h after induction of differentiation. Tretinoin 113-126 myeloperoxidase Homo sapiens 142-157
6321491-1 1984 When human myeloid leukemia HL-60 cells were induced to differentiate into mature cells by dimethyl sulfoxide or retinoic acid, the amount of myeloperoxidase activity per cell decreased to 20 to 30% of that of uninduced cells, and the rate of myeloperoxidase biosynthesis decreased to an undetectable level in 19 h after induction of differentiation. Tretinoin 113-126 myeloperoxidase Homo sapiens 243-258
6715343-0 1984 Retinoic acid alters the proportion of high mannose to complex type oligosaccharides on fibronectin secreted by cultured chondrocytes. Tretinoin 0-13 fibronectin 1 Homo sapiens 88-99
6715343-1 1984 Fibronectin synthesized by retinoic acid-treated chondrocytes exhibits a higher apparent subunit molecular weight in sodium dodecyl sulfate-polyacrylamide gels than fibronectin from untreated cultures. Tretinoin 27-40 fibronectin 1 Homo sapiens 0-11
6715343-1 1984 Fibronectin synthesized by retinoic acid-treated chondrocytes exhibits a higher apparent subunit molecular weight in sodium dodecyl sulfate-polyacrylamide gels than fibronectin from untreated cultures. Tretinoin 27-40 fibronectin 1 Homo sapiens 165-176
6607753-6 1984 An activity, co-chromatographing with DIF, acts synergistically with retinoic acid to induce maturation not only of HL-60, but also of the monoblast-like cell line U-937 (measured as percentage of cells reducing NBT). Tretinoin 69-82 tumor necrosis factor Homo sapiens 38-41
6582309-10 1984 Analyses of conditioned media of cells labeled with [35S]methionine or [14C]proline demonstrated that RA decreased the secretion of procollagen chains and fibronectin. Tretinoin 102-104 fibronectin 1 Homo sapiens 155-166
6582309-11 1984 Immunofluorescence revealed that RA alters the distribution of cell-associated fibronectin. Tretinoin 33-35 fibronectin 1 Homo sapiens 79-90
6561070-4 1984 Inhibition of IFN action in vitro by retinoic acid (vitamin A acid) was found to be reversed by beta-carotene (pro-vitamin A). Tretinoin 52-66 interferon alpha 1 Homo sapiens 14-17
6573952-5 1983 The kinetics of disappearance of one major labeled cell surface protein (Mr 95,000) within two days during treatment with retinoic acid correlated with the loss of cellular transferrin binding. Tretinoin 122-135 transferrin Homo sapiens 173-184
6083892-1 1984 Analysis of two-dimensional gel electrophoretic patterns of proteins labeled with [35S]methionine was undertaken to investigate changes in gene expression in embryonal carcinoma cell line Nulli-SCC1 during the induction of differentiation in vitro by retinoic acid. Tretinoin 251-264 protein tyrosine phosphatase, receptor type, J Mus musculus 194-198
6090250-7 1984 The expression of EGF receptors increases about two fold while that of transferrin increases up to 40 fold after treating F9 aggregates with retinoic acid. Tretinoin 141-154 transferrin Homo sapiens 71-82
6665745-0 1983 Early morphological abnormalities in splotch mouse embryos and predisposition to gene- and retinoic acid-induced neural tube defects. Tretinoin 91-104 paired box 3 Mus musculus 37-44
7076843-4 1982 Maximal stimulation occurred at 30 nM retinoic acid, which increased the number of BFU-E by a mean of 225 +/- 25% (+/- SE) over plates containing erythropoietin alone. Tretinoin 38-51 erythropoietin Homo sapiens 146-160
6297484-0 1982 Induction by retinoic acid of NAD+-glycohydrolase activity of myelomonocytic cell lines HL-60, THP-1 and U-937, and fresh human acute promyelocytic leukemia cells in primary culture. Tretinoin 13-26 GLI family zinc finger 2 Homo sapiens 95-100
6181013-0 1982 Retinoic acid suppression of human leukocyte interferon production. Tretinoin 0-13 interferon alpha 1 Homo sapiens 45-55
6181013-1 1982 Retinoic acid (RA) suppressed the production of interferon (IFN) alpha and IFN gamma of human peripheral blood leukocytes in response to stimulation with lectin mitogens, bacterial products, synthetic polynucleotides, viruses, and tumor cell lines in vitro. Tretinoin 0-13 interferon alpha 1 Homo sapiens 48-70
6176589-5 1982 In addition to stimulating PS beta G production, retinoic acid increased the production of hCG and its alpha-subunit (hCG alpha) by choriocarcinoma cells. Tretinoin 49-62 chromogranin A Homo sapiens 118-127
6176589-7 1982 Passage of choriocarcinoma cells in medium containing retinoic acid induced a stable altered phenotype characterized by elevated levels of PS beta G, hCG, and hCG alpha. Tretinoin 54-67 chromogranin A Homo sapiens 159-168
6188873-3 1983 Thus retinoic acid (and retinol) inhibited the stimulatory action of interferon (IFN) on monocyte membrane function, and this inhibition was reversed by beta-carotene; beta-carotene alone modestly potentiated IFN in this system. Tretinoin 5-18 interferon alpha 1 Homo sapiens 69-85
6188873-3 1983 Thus retinoic acid (and retinol) inhibited the stimulatory action of interferon (IFN) on monocyte membrane function, and this inhibition was reversed by beta-carotene; beta-carotene alone modestly potentiated IFN in this system. Tretinoin 5-18 interferon alpha 1 Homo sapiens 81-84
6188873-4 1983 Remarkably, for the inhibitory action of IFN on lymphoblastoid cell division, the converse was true: beta-Carotene inhibited the cytostatic action of IFN, and this inhibition was reversed by retinoic acid; retinoic acid alone modestly potentiated IFN in this system. Tretinoin 191-204 interferon alpha 1 Homo sapiens 41-44
6188873-4 1983 Remarkably, for the inhibitory action of IFN on lymphoblastoid cell division, the converse was true: beta-Carotene inhibited the cytostatic action of IFN, and this inhibition was reversed by retinoic acid; retinoic acid alone modestly potentiated IFN in this system. Tretinoin 191-204 interferon alpha 1 Homo sapiens 150-153
6188873-4 1983 Remarkably, for the inhibitory action of IFN on lymphoblastoid cell division, the converse was true: beta-Carotene inhibited the cytostatic action of IFN, and this inhibition was reversed by retinoic acid; retinoic acid alone modestly potentiated IFN in this system. Tretinoin 191-204 interferon alpha 1 Homo sapiens 150-153
6188873-4 1983 Remarkably, for the inhibitory action of IFN on lymphoblastoid cell division, the converse was true: beta-Carotene inhibited the cytostatic action of IFN, and this inhibition was reversed by retinoic acid; retinoic acid alone modestly potentiated IFN in this system. Tretinoin 206-219 interferon alpha 1 Homo sapiens 41-44
6188873-4 1983 Remarkably, for the inhibitory action of IFN on lymphoblastoid cell division, the converse was true: beta-Carotene inhibited the cytostatic action of IFN, and this inhibition was reversed by retinoic acid; retinoic acid alone modestly potentiated IFN in this system. Tretinoin 206-219 interferon alpha 1 Homo sapiens 150-153
6188873-4 1983 Remarkably, for the inhibitory action of IFN on lymphoblastoid cell division, the converse was true: beta-Carotene inhibited the cytostatic action of IFN, and this inhibition was reversed by retinoic acid; retinoic acid alone modestly potentiated IFN in this system. Tretinoin 206-219 interferon alpha 1 Homo sapiens 150-153
6181013-1 1982 Retinoic acid (RA) suppressed the production of interferon (IFN) alpha and IFN gamma of human peripheral blood leukocytes in response to stimulation with lectin mitogens, bacterial products, synthetic polynucleotides, viruses, and tumor cell lines in vitro. Tretinoin 0-13 interferon gamma Homo sapiens 75-84
6181013-1 1982 Retinoic acid (RA) suppressed the production of interferon (IFN) alpha and IFN gamma of human peripheral blood leukocytes in response to stimulation with lectin mitogens, bacterial products, synthetic polynucleotides, viruses, and tumor cell lines in vitro. Tretinoin 15-17 interferon alpha 1 Homo sapiens 48-70
6181013-1 1982 Retinoic acid (RA) suppressed the production of interferon (IFN) alpha and IFN gamma of human peripheral blood leukocytes in response to stimulation with lectin mitogens, bacterial products, synthetic polynucleotides, viruses, and tumor cell lines in vitro. Tretinoin 15-17 interferon gamma Homo sapiens 75-84
6181013-3 1982 RA-mediated suppression was dose-dependent and required the near-concurrent addition of RA and inducers to human leukocyte cultures, thus suggesting that RA affects an early cellular function in the generation of IFN. Tretinoin 0-2 interferon alpha 1 Homo sapiens 213-216
6181013-3 1982 RA-mediated suppression was dose-dependent and required the near-concurrent addition of RA and inducers to human leukocyte cultures, thus suggesting that RA affects an early cellular function in the generation of IFN. Tretinoin 88-90 interferon alpha 1 Homo sapiens 213-216
6181013-3 1982 RA-mediated suppression was dose-dependent and required the near-concurrent addition of RA and inducers to human leukocyte cultures, thus suggesting that RA affects an early cellular function in the generation of IFN. Tretinoin 88-90 interferon alpha 1 Homo sapiens 213-216
984876-5 1976 In human skin homogenates, LDH-, GAPDH-, and G-6-PDH-activities were inhibited by retinoic acid whereas GOT-, LAP-, and ALD-activites remained practically unchanged following an incubation with retinoic acid in concentrations between 1 and 100 mug/ml for 60 min.--The data collected in this study were briefly discussed with regard to the use of retinoic acid and its derivatives in psoriasis. Tretinoin 82-95 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 33-38
6249683-0 1980 Induction of neural-like cells and acetylcholinesterase activity in cultures of F9 teratocarcinoma treated with retinoic acid and dibutyryl cyclic adenosine monophosphate. Tretinoin 112-125 acetylcholinesterase (Cartwright blood group) Homo sapiens 35-55
6119810-10 1980 Retinoic acid (vitamin A acid; 100 mg/kg), administered to pregnant female mice on day 10, produced severe forelimb defects and resulted in a significant reduction in day 14 forelimb HP and RNA content, without altering CPK, DNA, or protein; thus, the HP:CPK ratio was decreased. Tretinoin 0-13 cystin 1 Mus musculus 255-258
6119810-10 1980 Retinoic acid (vitamin A acid; 100 mg/kg), administered to pregnant female mice on day 10, produced severe forelimb defects and resulted in a significant reduction in day 14 forelimb HP and RNA content, without altering CPK, DNA, or protein; thus, the HP:CPK ratio was decreased. Tretinoin 15-29 cystin 1 Mus musculus 255-258
6119810-11 1980 These results indicated that 1) 6-AN nonspecifically retards growth and cyto-differentiation in limbs; 2) retinoic acid inhibits synthesis of collagen and RNA; 3) retinoic acid has a differential effect upon chondrogenic and myogenic tissues of the limb, and 4) the comparison of HP content and CPK activity in tissue homogenates is an acceptable method of evaluating teratogenic compounds for selective effects. Tretinoin 106-119 cystin 1 Mus musculus 295-298
6119810-11 1980 These results indicated that 1) 6-AN nonspecifically retards growth and cyto-differentiation in limbs; 2) retinoic acid inhibits synthesis of collagen and RNA; 3) retinoic acid has a differential effect upon chondrogenic and myogenic tissues of the limb, and 4) the comparison of HP content and CPK activity in tissue homogenates is an acceptable method of evaluating teratogenic compounds for selective effects. Tretinoin 163-176 cystin 1 Mus musculus 295-298
7004463-2 1980 Dimethyl sulfoxide (DMSO) and retinoic acid myeloid induced differentiation in HHL 60 cells was accompanied by a marked decrease of insulin receptors. Tretinoin 30-43 insulin Homo sapiens 132-139
7188772-5 1980 Retinoic acid is more potent than retinol in this regard: 50% growth inhibition is achieved by 6 nM retinoic acid in ZR-75-B and by 700 nM in MCF-7 and Hs578T, whereas 5-8 muM retinol is required in all three cell lines. Tretinoin 0-13 latexin Homo sapiens 172-175
33757404-0 2021 Retinoic acid abrogates LPS-induced inflammatory response via negative regulation of NF-kappa B/miR-21 signaling. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 85-95
33986873-7 2021 Finally, the induction through to terminal differentiation of the keratinocyte by all-trans retinoic acid on parental ESCC cell lines led to the upregulation of the terminal differentiation marker Involucrin and a decrease in cell viability similar to that observed in ZNF750-overexpressing ESCC cells. Tretinoin 92-105 zinc finger protein 750 Mus musculus 269-275
33866277-7 2021 Typical CYP3A7 substrates such as zonisamide and retinoic acids took their placements without occupying a left side region of Template for their metabolisms. Tretinoin 49-63 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 8-14
127554-1 1975 A 1 per cent Vitamin A-acid solution was applied externally for 2 weeks on normal epidermis. Tretinoin 13-27 BCL2 related protein A1 Homo sapiens 0-3
33616807-5 2021 We aimed at studying the influence of STZ treatment on insulin signaling in SH-SY5Y cells differentiated by retinoic acid (RA). Tretinoin 108-121 insulin Homo sapiens 55-62
33423323-7 2021 Kyoto Encyclopedia of Genes and Genomes pathway results indicated that most DEGs caused by SCRV infection were identified in the immune system (retinoic acid-inducible gene-I-like receptor/Toll-like receptor/nucleotide-binding oligomerization domain-like receptor/C-type lectin receptor signalling pathway), cellular processes, cell growth and death (p53 signalling pathway, cellular senescence, apoptosis and phagosome), and metabolism. Tretinoin 144-157 tumor protein p53 Homo sapiens 351-354
33616807-5 2021 We aimed at studying the influence of STZ treatment on insulin signaling in SH-SY5Y cells differentiated by retinoic acid (RA). Tretinoin 123-125 insulin Homo sapiens 55-62
34050114-0 2021 All-trans retinoic acid reduces mammalian target of rapamycin via a Sirtuin1-dependent mechanism in neurons. Tretinoin 0-23 mechanistic target of rapamycin kinase Homo sapiens 32-61
34058077-10 2021 Therefore, hnRNP K/SET and ERK are potential therapeutic targets for both anti-neoplastic leukemia therapy and relapsed APL patients with ATRA resistance. Tretinoin 138-142 mitogen-activated protein kinase 1 Homo sapiens 27-30
34058203-0 2021 A novel all-trans retinoic acid derivative regulates cell cycle and differentiation of myelodysplastic syndrome cells by USO1. Tretinoin 18-31 USO1 vesicle transport factor Homo sapiens 121-125
34047175-0 2021 A Pin1/PML/P53 axis activated by retinoic acid in NPM-1c-acute myeloid leukemia. Tretinoin 33-46 tumor protein p53 Homo sapiens 11-14
34047175-2 2021 We reported that ex vivo, RA triggers NPM-1c degradation, P53 activation and growth arrest. Tretinoin 26-28 tumor protein p53 Homo sapiens 58-61
34042183-7 2022 Retinoic acid and leucine were upregulated in the SF group and were respectively responsible for the intestinal immune network for IgA production and the mammalian target of rapamycin signaling pathway in the enriched pathways according to the Kyoto Encyclopedia of Genes and Genomes Database classification. Tretinoin 0-13 CD79a molecule Homo sapiens 131-134
34042183-7 2022 Retinoic acid and leucine were upregulated in the SF group and were respectively responsible for the intestinal immune network for IgA production and the mammalian target of rapamycin signaling pathway in the enriched pathways according to the Kyoto Encyclopedia of Genes and Genomes Database classification. Tretinoin 0-13 mechanistic target of rapamycin kinase Homo sapiens 154-183
34050114-4 2021 Previous studies have suggested that all-trans retinoic acid (atRA) and rapamycin (RAPA), an mTOR inhibitor, protect lipopolysaccharide (LPS)-induced neuronal inflammation through inhibiting nuclear import of NFkappaB. Tretinoin 37-60 mechanistic target of rapamycin kinase Homo sapiens 93-97
34050114-4 2021 Previous studies have suggested that all-trans retinoic acid (atRA) and rapamycin (RAPA), an mTOR inhibitor, protect lipopolysaccharide (LPS)-induced neuronal inflammation through inhibiting nuclear import of NFkappaB. Tretinoin 37-60 nuclear factor kappa B subunit 1 Homo sapiens 209-217
34050114-4 2021 Previous studies have suggested that all-trans retinoic acid (atRA) and rapamycin (RAPA), an mTOR inhibitor, protect lipopolysaccharide (LPS)-induced neuronal inflammation through inhibiting nuclear import of NFkappaB. Tretinoin 62-66 mechanistic target of rapamycin kinase Homo sapiens 93-97
34050114-4 2021 Previous studies have suggested that all-trans retinoic acid (atRA) and rapamycin (RAPA), an mTOR inhibitor, protect lipopolysaccharide (LPS)-induced neuronal inflammation through inhibiting nuclear import of NFkappaB. Tretinoin 62-66 nuclear factor kappa B subunit 1 Homo sapiens 209-217
34050114-5 2021 The aim of this study was to test the effects of atRA on mTOR expression. Tretinoin 49-53 mechanistic target of rapamycin kinase Homo sapiens 57-61
34050114-6 2021 Here we discovered that mTOR and p-mTOR expression are elevated in LPS-treated mice or primary rat neurons, while atRA blocks the mTOR gene upregulation via a SIRT1-dependent mechanism. Tretinoin 114-118 sirtuin 1 Rattus norvegicus 159-164
34031932-2 2021 Retinoic acid-inducible gene (RIG)-I-like receptors (RLR), including melanoma differentiation-associated protein 5 (MDA5) and RIG-I, recognize the double-strand (ds) virus RNA and induce the production of Type I interferon (Type I IFN) as well as pro-inflammatory cytokines like Interleukin (IL)-6. Tretinoin 0-13 interleukin 6 Homo sapiens 279-297
34051632-5 2021 RESULTS: In CLP model, ATRA was found to reduce frequency of MDSCs in spleen of mice and inhibit activity of MDSCs by regulating the generation and activity of arginase-1 and iNOS, and the secretion of immune-supressive cytokines. Tretinoin 23-27 nitric oxide synthase 2, inducible Mus musculus 175-179
34024029-0 2021 Downregulation of fibronectin 1 attenuates ATRA-induced inhibition of cell migration and invasion in neuroblastoma cells. Tretinoin 43-47 fibronectin 1 Homo sapiens 18-31
34035369-6 2021 Of interest, retinoic acid and forskolin had anti-fibrosis effects by decreasing expression of alpha-SMA and F-actin in LX2 cells and HUVEC cells. Tretinoin 13-26 actin alpha 1, skeletal muscle Homo sapiens 95-104
34024029-6 2021 Cancer-related pathway enrichment and subsequent protein-protein interaction (PPI) network analysis identified fibronectin 1 (FN1) as one of the central molecules in the network, which was significantly upregulated during ATRA treatment. Tretinoin 222-226 fibronectin 1 Homo sapiens 111-124
34024029-6 2021 Cancer-related pathway enrichment and subsequent protein-protein interaction (PPI) network analysis identified fibronectin 1 (FN1) as one of the central molecules in the network, which was significantly upregulated during ATRA treatment. Tretinoin 222-226 fibronectin 1 Homo sapiens 126-129
33721419-8 2021 Indeed, retinoic acid levels were reduced owing to increased degradation following the elevation of Cyp26b1 in Sox30-null testes. Tretinoin 8-21 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 100-107
34024029-7 2021 In addition, we found that although downregulation of FN1 had no significant effects on either cell proliferation or cell cycle distributions in the presence or absence of ATRA, it increased cell migration and invasion in NB cells and partially blocked ATRA-induced inhibition of cell migration and invasion in SY5Y NB cells. Tretinoin 253-257 fibronectin 1 Homo sapiens 54-57
34024029-9 2021 Taken together, our data suggest that FN1 is a potential target for effective ATRA treatment on NB patients, likely by facilitating ATRA-induced inhibition of cell migration and invasion. Tretinoin 78-82 fibronectin 1 Homo sapiens 38-41
34024029-9 2021 Taken together, our data suggest that FN1 is a potential target for effective ATRA treatment on NB patients, likely by facilitating ATRA-induced inhibition of cell migration and invasion. Tretinoin 132-136 fibronectin 1 Homo sapiens 38-41
34057078-3 2021 Here, we show that the expression and localization of amyloid-beta protein precursor (AbetaPP), one of the key molecules involved in AD pathogenesis, is dramatically altered in SH-SY5Y cells fully differentiated by combined treatment with retinoic acid and BDNF. Tretinoin 239-252 amyloid beta precursor protein Homo sapiens 54-66
34057078-3 2021 Here, we show that the expression and localization of amyloid-beta protein precursor (AbetaPP), one of the key molecules involved in AD pathogenesis, is dramatically altered in SH-SY5Y cells fully differentiated by combined treatment with retinoic acid and BDNF. Tretinoin 239-252 amyloid beta precursor protein Homo sapiens 86-93
34023410-20 2021 This study showed that retinoic acid regulates bcl-2 family proteins and caspase proteins in focal cerebral ischemia. Tretinoin 23-36 BCL2, apoptosis regulator Rattus norvegicus 47-52
34023410-20 2021 This study showed that retinoic acid regulates bcl-2 family proteins and caspase proteins in focal cerebral ischemia. Tretinoin 23-36 caspase 9 Rattus norvegicus 73-80
34001245-5 2021 METHODS: Bone morphogenetic protein 9 (BMP9)-transfected mesenchymal stem cells (MSCs) were used as an in vitro osteogenic model to deduce the relationship between ATRA and dexamethasone (DEX). Tretinoin 164-168 growth differentiation factor 2 Homo sapiens 39-43
34001245-12 2021 RESULTS: ATRA enhanced BMP9-induced ALP, RUNX2 expressions, ALP activities, and matrix mineralization in mouse embryonic fibroblasts as well as C3H10T1/2 and C2C12 cells, while a high concentration of DEX attenuated these markers. Tretinoin 9-13 alkaline phosphatase, placental Homo sapiens 36-39
34001245-12 2021 RESULTS: ATRA enhanced BMP9-induced ALP, RUNX2 expressions, ALP activities, and matrix mineralization in mouse embryonic fibroblasts as well as C3H10T1/2 and C2C12 cells, while a high concentration of DEX attenuated these markers. Tretinoin 9-13 alkaline phosphatase, placental Homo sapiens 60-63
34001245-13 2021 When DEX was combined with ATRA, the latter reversed DEX-inhibited ALP activities and osteogenic markers. Tretinoin 27-31 alkaline phosphatase, placental Homo sapiens 67-70
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 nuclear mitotic apparatus protein 1 Homo sapiens 28-32
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 interferon regulatory factor 2 binding protein 2 Homo sapiens 52-59
34015278-11 2021 Treatment with free ATRA and the selected formulations led to a significant amelioration of DN by reducing of creatinine, urea, TNF-alpha, ICAM-1, GM-CSF, VEGF levels as well as elevating AMPK and LKB1 levels. Tretinoin 20-24 tumor necrosis factor Rattus norvegicus 128-137
34015278-11 2021 Treatment with free ATRA and the selected formulations led to a significant amelioration of DN by reducing of creatinine, urea, TNF-alpha, ICAM-1, GM-CSF, VEGF levels as well as elevating AMPK and LKB1 levels. Tretinoin 20-24 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 188-192
33556379-4 2021 RA-differentiation induced an upregulation of ace2 and tmprss2 gene expression while inducing downregulation of ctsb and ctsl. Tretinoin 0-2 transmembrane serine protease 2 Homo sapiens 55-62
33556379-4 2021 RA-differentiation induced an upregulation of ace2 and tmprss2 gene expression while inducing downregulation of ctsb and ctsl. Tretinoin 0-2 cathepsin L Homo sapiens 121-125
33493612-5 2021 Smad signaling was also suppressed by atRA treatment in these cells, and RNA immunoprecipitation analyses revealed that Smad2 can directly interact with Meg3 in MEPM cells following atRA treatment. Tretinoin 38-42 SMAD family member 2 Mus musculus 120-125
33878891-9 2021 Conclusion: The authors propose that HDAC7 controls the uptake of all-trans-retinoic acid, thus influencing RXRA activity and IGF1 signaling. Tretinoin 66-89 insulin like growth factor 1 Homo sapiens 126-130
33662750-11 2021 Thus ATRA is ionized in a wide range of pHs but protonated in anionic vesicles. Tretinoin 5-9 pterin-4 alpha-carbinolamine dehydratase 1 Homo sapiens 40-43
33493612-5 2021 Smad signaling was also suppressed by atRA treatment in these cells, and RNA immunoprecipitation analyses revealed that Smad2 can directly interact with Meg3 in MEPM cells following atRA treatment. Tretinoin 182-186 SMAD family member 2 Mus musculus 120-125
33909480-3 2021 In this study, we tried to investigate the effects of tretinoin-loaded solid lipid core nanocapsules (TTN-SLN) added to freezing/thawing and handling media (in three experimental groups) on sperm motility (total/progressive), viability, DNA fragmentation, and extracellular reactive oxygen species (ROS) levels. Tretinoin 54-63 titin Mus musculus 102-105
33933435-2 2021 Here, a series of amphiphilic retinoyl-bPEI conjugates (RP-1, RP-2 and RP-3) has been synthesized by allowing the reaction between bPEI (1.8 kDa) and a bioactive and hydrophobic vitamin A metabolite, all-trans-retinoic acid (ATRA), in varying amounts. Tretinoin 200-223 RP2 activator of ARL3 GTPase Homo sapiens 62-66
33933435-2 2021 Here, a series of amphiphilic retinoyl-bPEI conjugates (RP-1, RP-2 and RP-3) has been synthesized by allowing the reaction between bPEI (1.8 kDa) and a bioactive and hydrophobic vitamin A metabolite, all-trans-retinoic acid (ATRA), in varying amounts. Tretinoin 225-229 RP2 activator of ARL3 GTPase Homo sapiens 62-66
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 phosphatase and tensin homolog Mus musculus 122-126
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 Rho GTPase activating protein 5 Mus musculus 132-139
33995625-1 2021 Retinoic acid receptor beta is a nuclear receptor protein that binds to retinoic acid (RA) to mediate cellular signalling in embryogenic morphogenesis, cell growth, and differentiation. Tretinoin 72-85 retinoic acid receptor beta Homo sapiens 0-27
33987177-0 2021 Bhlhe40/Sirt1 Axis-Regulated Mitophagy Is Implicated in All-Trans Retinoic Acid-Induced Spina Bifida Aperta. Tretinoin 66-79 sirtuin 1 Rattus norvegicus 8-13
33987177-10 2021 Collectively, our results for the first time demonstrate that Bhlhe40/Sirt1 axis regulated mitophagy is implicated in ATRA-induced SBA. Tretinoin 118-122 sirtuin 1 Rattus norvegicus 70-75
33901013-7 2021 Moreover, silencing of C/EBPalpha attenuated ATRA-induced NEAT1 upregulation and APL cell differentiation. Tretinoin 45-49 CCAAT enhancer binding protein alpha Homo sapiens 23-33
33901013-8 2021 Finally, simultaneous knockdown of C/EBPalpha and C/EBPbeta reduces ATRA-induced upregulation of C/EBPepsilon and dramatically impaired NEAT1 activation and APL cell differentiation. Tretinoin 68-72 CCAAT enhancer binding protein alpha Homo sapiens 35-45
33901013-8 2021 Finally, simultaneous knockdown of C/EBPalpha and C/EBPbeta reduces ATRA-induced upregulation of C/EBPepsilon and dramatically impaired NEAT1 activation and APL cell differentiation. Tretinoin 68-72 CCAAT enhancer binding protein alpha Homo sapiens 50-59
33724958-5 2021 Specifically, high expression of the ATRA-catabolizing enzyme, CYP26A1, in human IDCM could dampen prospects for an ATRA-based therapy. Tretinoin 37-41 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 63-70
33724958-5 2021 Specifically, high expression of the ATRA-catabolizing enzyme, CYP26A1, in human IDCM could dampen prospects for an ATRA-based therapy. Tretinoin 116-120 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 63-70
33995625-1 2021 Retinoic acid receptor beta is a nuclear receptor protein that binds to retinoic acid (RA) to mediate cellular signalling in embryogenic morphogenesis, cell growth, and differentiation. Tretinoin 87-89 retinoic acid receptor beta Homo sapiens 0-27
33854358-8 2021 To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated LPS toxicity with a higher oxidative and inflammatory cytokine level. Tretinoin 69-92 NFE2 like bZIP transcription factor 2 Rattus norvegicus 35-39
33895500-4 2021 ATRA can promote the transcriptional activation of differentiation-related genes and regulate autophagy by inhibiting mTOR, which results in anti-APL effects. Tretinoin 0-4 mechanistic target of rapamycin kinase Homo sapiens 118-122
33853830-6 2021 Depletion of G-MDSCs with antibody or functional inhibition via all-trans-retinoic acid (ATRA) led to enhanced anti-tumor T cell responses and sensitized LKB1-deficent murine tumors to PD-1 blockade. Tretinoin 89-93 serine/threonine kinase 11 Mus musculus 154-158
33854358-8 2021 To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated LPS toxicity with a higher oxidative and inflammatory cytokine level. Tretinoin 69-92 NFE2 like bZIP transcription factor 2 Rattus norvegicus 57-61
33854358-8 2021 To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated LPS toxicity with a higher oxidative and inflammatory cytokine level. Tretinoin 94-98 NFE2 like bZIP transcription factor 2 Rattus norvegicus 35-39
33854358-8 2021 To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated LPS toxicity with a higher oxidative and inflammatory cytokine level. Tretinoin 94-98 NFE2 like bZIP transcription factor 2 Rattus norvegicus 57-61
33694304-3 2021 The schedule dosage involves repeated intravitreal injections of anti-VEGF agents to achieve and maintain effective concentrations in retina and choroids, which are administrated as solutions form. Tretinoin 134-140 vascular endothelial growth factor A Homo sapiens 70-74
33889575-5 2021 Furthermore, retinoic acid inhibits NF-kappaB signaling, decreases chemokine expression, and suppresses the tumor-promoting function of transformed TA-MSCs by prohibiting the recruitment of macrophages/monocytes and MDSCs in the tumor microenvironment. Tretinoin 13-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 36-45
33532870-5 2021 In the Kyoto Encyclopedia of Genes and Genomes pathway analysis, pathogen recognition receptor (PRR) signaling pathways such as the retinoic-acid-inducible gene-I-like receptor signaling pathway and the Toll-like receptor signaling pathway were identified at all time points. Tretinoin 132-145 nuclear receptor subfamily 1 group I member 2 Homo sapiens 96-99
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin D1 Bos taurus 162-167
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin D3 Bos taurus 176-181
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 164-177 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 229-236
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 179-181 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 229-236
33726556-8 2022 NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells. Tretinoin 81-85 vascular endothelial growth factor A Homo sapiens 44-50
33607186-3 2021 Results from the present study also point to a role for the murine AHR in the control of circulating REOH and ATRA concentrations. Tretinoin 110-114 aryl-hydrocarbon receptor Mus musculus 67-70
33165749-0 2021 Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA). Tretinoin 112-135 insulin Homo sapiens 77-84
33165749-0 2021 Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA). Tretinoin 137-141 insulin Homo sapiens 77-84
33165749-1 2021 All-trans retinoic acid (ATRA) promotes the development and the function of insulin producing cells and induces partial differentiation of pancreatic tumor cells. Tretinoin 0-23 insulin Homo sapiens 76-83
33165749-1 2021 All-trans retinoic acid (ATRA) promotes the development and the function of insulin producing cells and induces partial differentiation of pancreatic tumor cells. Tretinoin 25-29 insulin Homo sapiens 76-83
33165749-6 2021 Using pancreatic ductal adenocarcinoma (PDAC)-derived cells, we also revealed that the ATRA induced up-modulation of Vav1 is essential for the retinoid-induced trans-differentiation of neoplastic cells into insulin producing cells. Tretinoin 87-91 insulin Homo sapiens 207-214
33165749-7 2021 The results of this study identify Vav1 as crucial molecule in ATRA induced maturation of insulin producing cells and suggest this protein as a marker for new strategies ended to restore functional beta-cells. Tretinoin 63-67 insulin Homo sapiens 90-97
33726556-8 2022 NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells. Tretinoin 81-85 DNA damage inducible transcript 3 Homo sapiens 52-56
33726556-8 2022 NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells. Tretinoin 81-85 caspase 3 Homo sapiens 61-70
33600562-4 2021 The neuronal-like cell line SK-N-SH is a useful model in the study of the cellular and molecular effects of apoE as it can be differentiated with retinoic acid to express and secrete high levels of apoE and it also shows the same apoE fragmentation patterns observed in the human brain. Tretinoin 146-159 apolipoprotein E Homo sapiens 108-112
33355213-11 2021 The results suggest that in the case of ALDH1A dysfunction or excess vitamin A, AOX may play an important role in regulating hepatic vitamin A homeostasis and that inhibition of AOX may alter atRA biosynthesis and signaling. Tretinoin 192-196 aldehyde oxidase 1 Homo sapiens 178-181
33355213-12 2021 Significance Statement This study provides direct evidence to show that human AOX converts retinaldehyde to atRA and contributes to hepatic atRA biosynthesis. Tretinoin 108-112 aldehyde oxidase 1 Homo sapiens 78-81
33355213-12 2021 Significance Statement This study provides direct evidence to show that human AOX converts retinaldehyde to atRA and contributes to hepatic atRA biosynthesis. Tretinoin 140-144 aldehyde oxidase 1 Homo sapiens 78-81
33355213-13 2021 The finding that AOX may be responsible for 20-50% of overall hepatic atRA formation suggests that alterations in AOX activity via drug-drug interactions, genetic polymorphisms or disease states may impact hepatic atRA concentrations, signaling and alter vitamin A homeostasis. Tretinoin 70-74 aldehyde oxidase 1 Homo sapiens 17-20
33355213-13 2021 The finding that AOX may be responsible for 20-50% of overall hepatic atRA formation suggests that alterations in AOX activity via drug-drug interactions, genetic polymorphisms or disease states may impact hepatic atRA concentrations, signaling and alter vitamin A homeostasis. Tretinoin 70-74 aldehyde oxidase 1 Homo sapiens 114-117
33355213-13 2021 The finding that AOX may be responsible for 20-50% of overall hepatic atRA formation suggests that alterations in AOX activity via drug-drug interactions, genetic polymorphisms or disease states may impact hepatic atRA concentrations, signaling and alter vitamin A homeostasis. Tretinoin 214-218 aldehyde oxidase 1 Homo sapiens 17-20
33355213-13 2021 The finding that AOX may be responsible for 20-50% of overall hepatic atRA formation suggests that alterations in AOX activity via drug-drug interactions, genetic polymorphisms or disease states may impact hepatic atRA concentrations, signaling and alter vitamin A homeostasis. Tretinoin 214-218 aldehyde oxidase 1 Homo sapiens 114-117
33723318-7 2021 Here we demonstrate that a classical PKC inhibitor potentiates ATRA antitumor effects also targeting cancer stem cells growth, self-renewal and frequency. Tretinoin 63-67 protein kinase C alpha Homo sapiens 37-40
33713676-0 2021 Pontin Functions as A Transcriptional Co-activator for Retinoic Acid-induced HOX Gene Expression. Tretinoin 55-68 RuvB like AAA ATPase 1 Homo sapiens 0-6
33713676-5 2021 Using an in vivo biotin tagging technology, we mapped the genome-wide binding pattern of Pontin before and after RA-induced differentiation in the pluripotent embryo carcinoma cell line NTEAR-2. Tretinoin 113-115 RuvB like AAA ATPase 1 Homo sapiens 89-95
33713676-6 2021 Biotin ChIP-seq revealed significant changes in genome-wide Pontin binding sites upon RA stimulation. Tretinoin 86-88 RuvB like AAA ATPase 1 Homo sapiens 60-66
33713676-8 2021 Pontin knockdown experiments showed that its chromatin binding at the HOX gene clusters is required for RA-induced HOX gene expression. Tretinoin 104-106 RuvB like AAA ATPase 1 Homo sapiens 0-6
33713676-11 2021 Altogether, we have demonstrated that Pontin is a critical transcriptional co-activator for RA-induced HOX gene activation. Tretinoin 92-94 RuvB like AAA ATPase 1 Homo sapiens 38-44
33355213-0 2021 Aldehyde Oxidase Contributes to all-trans-Retinoic Acid Biosynthesis in Human Liver. Tretinoin 32-55 aldehyde oxidase 1 Homo sapiens 0-16
33355213-2 2021 atRA is predominantly synthesized from retinaldehyde by aldehyde dehydrogenase 1A1 (ALDH1A1) but aldehyde oxidase (AOX) may also contribute to atRA biosynthesis. Tretinoin 143-147 aldehyde oxidase 1 Homo sapiens 97-113
33355213-2 2021 atRA is predominantly synthesized from retinaldehyde by aldehyde dehydrogenase 1A1 (ALDH1A1) but aldehyde oxidase (AOX) may also contribute to atRA biosynthesis. Tretinoin 143-147 aldehyde oxidase 1 Homo sapiens 115-118
33355213-3 2021 The goal of this study was to test the hypothesis that AOX contributes significantly to atRA formation in human liver. Tretinoin 88-92 aldehyde oxidase 1 Homo sapiens 55-58
33355213-4 2021 Human recombinant AOX formed atRA from retinaldehyde (Km~1.5{plus minus}0.4 microM; kcat ~3.6{plus minus}2.0 min-1). Tretinoin 29-33 aldehyde oxidase 1 Homo sapiens 18-21
33355213-5 2021 In human liver S9 fractions (HLS9) atRA formation was observed in the absence of NAD+, suggesting AOX contribution to atRA formation. Tretinoin 118-122 aldehyde oxidase 1 Homo sapiens 98-101
33355213-7 2021 The two enzymes were identified as AOX and ALDH1A1 based on inhibition of atRA formation by AOX inhibitor hydralazine (20-50% inhibition) and ALDH1A1 inhibitor WIN18,446 (50-80% inhibition). Tretinoin 74-78 aldehyde oxidase 1 Homo sapiens 35-38
33355213-7 2021 The two enzymes were identified as AOX and ALDH1A1 based on inhibition of atRA formation by AOX inhibitor hydralazine (20-50% inhibition) and ALDH1A1 inhibitor WIN18,446 (50-80% inhibition). Tretinoin 74-78 aldehyde oxidase 1 Homo sapiens 92-95
33355213-9 2021 The formation velocity of atRA in the presence of NAD+ correlated significantly with the expression of ALDH1A1 and AOX protein. Tretinoin 26-30 aldehyde oxidase 1 Homo sapiens 115-118
33355213-10 2021 Taken together the data show that both AOX and ALDH1A1 contribute to atRA biosynthesis in the human liver with ALDH1A1 being the high affinity low capacity enzyme and AOX the low affinity high capacity enzyme. Tretinoin 69-73 aldehyde oxidase 1 Homo sapiens 39-42
33355213-10 2021 Taken together the data show that both AOX and ALDH1A1 contribute to atRA biosynthesis in the human liver with ALDH1A1 being the high affinity low capacity enzyme and AOX the low affinity high capacity enzyme. Tretinoin 69-73 aldehyde oxidase 1 Homo sapiens 167-170
33530513-6 2021 Interestingly, the beneficial effects of quercetin on diquat-induced oxidative damage were abolished by all-trans-retinoic acid (Atra), a specific inhibitor of Nrf2, indicating a Nrf2-dependent regulation manner. Tretinoin 104-127 nuclear factor, erythroid derived 2, like 2 Mus musculus 160-164
33668324-0 2021 FOXC1 Downregulates Nanog Expression by Recruiting HDAC2 to Its Promoter in F9 Cells Treated by Retinoic Acid. Tretinoin 96-109 histone deacetylase 2 Homo sapiens 51-56
33594180-0 2021 Retinoic acid regulates erythropoietin production cooperatively with hypoxia-inducible factors in human iPSC-derived erythropoietin-producing cells. Tretinoin 0-13 erythropoietin Homo sapiens 24-38
33594180-0 2021 Retinoic acid regulates erythropoietin production cooperatively with hypoxia-inducible factors in human iPSC-derived erythropoietin-producing cells. Tretinoin 0-13 erythropoietin Homo sapiens 117-131
33594180-4 2021 In this study, we aimed to examine the roles of retinoic acid (RA) in EPO production using EPO-producing cells derived from human induced pluripotent stem cells (hiPSC-EPO cells) that we previously established. Tretinoin 48-61 erythropoietin Homo sapiens 70-73
33594180-4 2021 In this study, we aimed to examine the roles of retinoic acid (RA) in EPO production using EPO-producing cells derived from human induced pluripotent stem cells (hiPSC-EPO cells) that we previously established. Tretinoin 63-65 erythropoietin Homo sapiens 70-73
33594180-5 2021 RA augmented EPO production by hiPSC-EPO cells under hypoxia or by treatment with prolyl hydroxylase domain-containing protein (PHD) inhibitors that upregulate HIF signals. Tretinoin 0-2 erythropoietin Homo sapiens 13-16
33594180-5 2021 RA augmented EPO production by hiPSC-EPO cells under hypoxia or by treatment with prolyl hydroxylase domain-containing protein (PHD) inhibitors that upregulate HIF signals. Tretinoin 0-2 erythropoietin Homo sapiens 37-40
33541392-13 2021 Furthermore, our CD10-mediated screening analysis identified dexamethasone and retinoic acid as stimulator and inhibitor of adipogenesis, respectively, indicating CD10 as a useful biomarker for pro-adipogenic drug screening. Tretinoin 79-92 membrane metalloendopeptidase Homo sapiens 17-21
33541392-13 2021 Furthermore, our CD10-mediated screening analysis identified dexamethasone and retinoic acid as stimulator and inhibitor of adipogenesis, respectively, indicating CD10 as a useful biomarker for pro-adipogenic drug screening. Tretinoin 79-92 membrane metalloendopeptidase Homo sapiens 163-167
33044585-13 2021 KLF5-induced inducible nitric oxide synthase (iNOS) expression activation could be significantly inhibited by ATRA. Tretinoin 110-114 nitric oxide synthase 2 Homo sapiens 13-44
33044585-13 2021 KLF5-induced inducible nitric oxide synthase (iNOS) expression activation could be significantly inhibited by ATRA. Tretinoin 110-114 nitric oxide synthase 2 Homo sapiens 46-50
33597885-6 2020 Furthermore, an inhibitor of Nrf2, called all-trans retinoic acid (ATRA), was used, which exaggerated APAP toxicity, in addition to abrogating the protective effects of carveol; this effect was accompanied by overexpression of inflammatory mediators and liver = 2ltoxicity biomarkers. Tretinoin 42-65 nuclear factor, erythroid derived 2, like 2 Mus musculus 29-33
33597885-6 2020 Furthermore, an inhibitor of Nrf2, called all-trans retinoic acid (ATRA), was used, which exaggerated APAP toxicity, in addition to abrogating the protective effects of carveol; this effect was accompanied by overexpression of inflammatory mediators and liver = 2ltoxicity biomarkers. Tretinoin 67-71 nuclear factor, erythroid derived 2, like 2 Mus musculus 29-33
33627760-0 2021 All-trans-retinoic acid ameliorates atherosclerosis, promotes perivascular adipose tissue browning, and increases adiponectin production in Apo-E mice. Tretinoin 0-23 apolipoprotein E Mus musculus 140-145
33627760-6 2021 Long-term atRA treatment in Apo-E mice did not affect insulin resistance. Tretinoin 10-14 apolipoprotein E Mus musculus 28-33
33627760-7 2021 AtRa administration ameliorated atherosclerosis, induced PVAT browning, and increased adiponectin production in PVAT in Apo-E mice. Tretinoin 0-4 apolipoprotein E Mus musculus 120-125
33627760-11 2021 Besides, atRA increased the synthesis of adiponectin in PVAT and augmented NO level in the aorta in ApoE mice. Tretinoin 9-13 apolipoprotein E Mus musculus 100-104
33747646-2 2021 Hypercalcemia is a rare yet important side-effect of ATRA, especially when it is used concomitantly with a medication that impedes its metabolism by inhibiting cytochrome P-450 in the liver and thus increasing the duration of exposure to ATRA. Tretinoin 53-57 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 160-176
33747646-4 2021 These medications inhibit two vital enzymes of cytochrome P-450, CYP2C9 and CYP3A4, potentiating the effects of ATRA on calcium metabolism. Tretinoin 112-116 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 47-63
33747646-4 2021 These medications inhibit two vital enzymes of cytochrome P-450, CYP2C9 and CYP3A4, potentiating the effects of ATRA on calcium metabolism. Tretinoin 112-116 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82
33576062-10 2021 Additionally, FSK and ATRA ameliorated oxidative stress and inflammation, reduced TGF-beta1 levels and reversed the effect of BLM on the mRNA expression of Ptch-1, Smo and Gli-2. Tretinoin 22-26 transforming growth factor, beta 1 Rattus norvegicus 82-91
33576062-10 2021 Additionally, FSK and ATRA ameliorated oxidative stress and inflammation, reduced TGF-beta1 levels and reversed the effect of BLM on the mRNA expression of Ptch-1, Smo and Gli-2. Tretinoin 22-26 smoothened, frizzled class receptor Rattus norvegicus 164-167
33643304-5 2020 Different Toll-like receptors (TLRs), Nod-like receptors (NLRs) and absent in melanoma-2 (AIM-2)-like receptors (ALRs) forming inflammasomes in the cytosol, RIG (retinoic acid-inducible gene)-1-like receptors (RLRs), and C-type lectin receptors (CLRs) are some of the PRRs. Tretinoin 162-175 absent in melanoma 2 Homo sapiens 68-88
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 0-13 lecithin retinol acyltransferase a Danio rerio 33-38
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 0-13 diacylglycerol O-acyltransferase 1a Danio rerio 234-240
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 151-164 lecithin retinol acyltransferase a Danio rerio 33-38
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 151-164 diacylglycerol O-acyltransferase 1a Danio rerio 234-240
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 187-200 lecithin retinol acyltransferase a Danio rerio 33-38
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 187-200 diacylglycerol O-acyltransferase 1a Danio rerio 234-240
33074481-5 2021 Moreover, combining ATRA and SIK inhibition synergistically activated the Akt signaling pathway but not the MAPK pathway. Tretinoin 20-24 AKT serine/threonine kinase 1 Homo sapiens 74-77
33585479-7 2021 Importantly, a miR-4680-3p-specific inhibitor normalized cell proliferation and altered expression of ERBB2 and JADE1 in cells treated with atRA. Tretinoin 140-144 microRNA 4680 Homo sapiens 15-23
33585479-7 2021 Importantly, a miR-4680-3p-specific inhibitor normalized cell proliferation and altered expression of ERBB2 and JADE1 in cells treated with atRA. Tretinoin 140-144 erb-b2 receptor tyrosine kinase 2 Homo sapiens 102-107
33585479-8 2021 Taken together, our results suggest that upregulation of miR-4680-3p induced by atRA may cause cleft palate through suppression of ERBB2 and JADE1. Tretinoin 80-84 erb-b2 receptor tyrosine kinase 2 Homo sapiens 131-136
33495566-0 2021 PRMT3 interacts with ALDH1A1 and regulates gene-expression by inhibiting retinoic acid signaling. Tretinoin 73-86 protein arginine methyltransferase 3 Homo sapiens 0-5
33495566-6 2021 PRMT3 inhibits the enzymatic activity of ALDH1A1 and negatively regulates the expression of retinoic acid responsive genes in a methyltransferase activity independent manner. Tretinoin 92-105 protein arginine methyltransferase 3 Homo sapiens 0-5
33530513-6 2021 Interestingly, the beneficial effects of quercetin on diquat-induced oxidative damage were abolished by all-trans-retinoic acid (Atra), a specific inhibitor of Nrf2, indicating a Nrf2-dependent regulation manner. Tretinoin 104-127 nuclear factor, erythroid derived 2, like 2 Mus musculus 179-183
33530513-6 2021 Interestingly, the beneficial effects of quercetin on diquat-induced oxidative damage were abolished by all-trans-retinoic acid (Atra), a specific inhibitor of Nrf2, indicating a Nrf2-dependent regulation manner. Tretinoin 129-133 nuclear factor, erythroid derived 2, like 2 Mus musculus 160-164
33530513-6 2021 Interestingly, the beneficial effects of quercetin on diquat-induced oxidative damage were abolished by all-trans-retinoic acid (Atra), a specific inhibitor of Nrf2, indicating a Nrf2-dependent regulation manner. Tretinoin 129-133 nuclear factor, erythroid derived 2, like 2 Mus musculus 179-183
33537305-6 2020 Exogenous RA treatments act as a stress factor inhibiting germ cell differentiation probably by activation of dmrt1a and amh. Tretinoin 10-12 doublesex- and mab-3-related transcription factor 1Y Oryzias latipes 110-116
33495541-0 2021 Intracellular alpha-fetoprotein interferes with all-trans retinoic acid induced ATG7 expression and autophagy in hepatocellular carcinoma cells. Tretinoin 58-71 alpha fetoprotein Homo sapiens 14-31
33495541-11 2021 Knockdown of AFP in PLC/PRF/5 cells augmented the up-regulation of ATG7 by ATRA while overexpression of AFP in HLE cells attenuated ATRA induced ATG7 expression and autophagy. Tretinoin 75-79 alpha fetoprotein Homo sapiens 13-16
33495541-11 2021 Knockdown of AFP in PLC/PRF/5 cells augmented the up-regulation of ATG7 by ATRA while overexpression of AFP in HLE cells attenuated ATRA induced ATG7 expression and autophagy. Tretinoin 132-136 alpha fetoprotein Homo sapiens 13-16
33495541-11 2021 Knockdown of AFP in PLC/PRF/5 cells augmented the up-regulation of ATG7 by ATRA while overexpression of AFP in HLE cells attenuated ATRA induced ATG7 expression and autophagy. Tretinoin 132-136 alpha fetoprotein Homo sapiens 104-107
33537305-7 2020 Disruption of the RA degrading enzyme gene cyp26a1 induced precocious meiosis and oogenesis in embryos/hatchlings of female and even some males. Tretinoin 18-20 cytochrome P450, family 26, subfamily A, polypeptide 1 Oryzias latipes 43-50
33215509-9 2020 Insulin-induced phosphorylation of Akt Thr308 was further enhanced by RA treatment through the activation of retinoic acid receptor. Tretinoin 70-72 AKT serine/threonine kinase 1 Rattus norvegicus 35-38
33840258-2 2021 Retinoic acid induced 14 (RAI14) acts as an oncogene in human cancers, but the underlying mechanisms by which RAI14 is regulated by circRNA/miRNA axis remain elusive. Tretinoin 0-13 retinoic acid induced 14 Homo sapiens 26-31
33840258-2 2021 Retinoic acid induced 14 (RAI14) acts as an oncogene in human cancers, but the underlying mechanisms by which RAI14 is regulated by circRNA/miRNA axis remain elusive. Tretinoin 0-13 retinoic acid induced 14 Homo sapiens 110-115
32032154-7 2021 After adding 5 muM all-trans retinoic acid, the viability of cells decreased significantly (P < 0.01), the proportion of cells in S phase decreased significantly (P < 0.05). Tretinoin 29-42 latexin Homo sapiens 15-18
33301441-0 2020 Retinoic acid improves baseline barrier function and attenuates TNF-alpha-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o. Tretinoin 0-13 tumor necrosis factor Homo sapiens 64-73
33301441-2 2020 This paper thus sought to determine whether RA could improve baseline barrier function and attenuate TNF-alpha-induced barrier leak in the human bronchial epithelial cell culture model, 16HBE14o- (16HBE). Tretinoin 44-46 tumor necrosis factor Homo sapiens 101-110
33301441-4 2020 A simultaneous, RA-induced 70% increase in claudin-4 attests to RA affecting the tight junctional (TJ) complex itself. Tretinoin 16-18 claudin 4 Homo sapiens 43-52
33301441-4 2020 A simultaneous, RA-induced 70% increase in claudin-4 attests to RA affecting the tight junctional (TJ) complex itself. Tretinoin 64-66 claudin 4 Homo sapiens 43-52
32771670-12 2020 Treatment with ox-LDL significantly inhibited Akt phosphorylation (P < 0.05) and CREB phosphorylation induced by ATRA, EGF, and basic FGF (P < 0.05). Tretinoin 113-117 cAMP responsive element binding protein 1 Mus musculus 81-85
33422029-12 2021 CONCLUSIONS: AA genotype of the TGM2 SNP (rs4811528) may be a risk factor for development of DS in patients with APL following the use of ATRA/ATO. Tretinoin 138-142 transglutaminase 2 Homo sapiens 32-36
33069641-11 2021 Effects of HDACi, DXM and ATRA were seen on the expression of Connexins and E-Cadherin in both the cell lines. Tretinoin 26-30 cadherin 1 Homo sapiens 76-86
32469071-0 2021 Retinoic Acid Is Elevated in the Mucosa of Patients With Active Ulcerative Colitis and Displays a Proinflammatory Role by Augmenting IL-17 and IFNgamma Production. Tretinoin 0-13 interferon gamma Homo sapiens 143-151
32469071-2 2021 Our previous research highlighted that in the face of inflammatory conditions, RA plays a contrary role where it aggravates intestinal inflammation by promoting interferon (IFN) gamma and interleukin (IL)-17 differentiation in vitro. Tretinoin 79-81 interferon gamma Homo sapiens 161-183
32469071-6 2021 Moreover, the raised RA levels in patients with active disease showed a positive correlation with proinflammatory cytokines (IL-17, IFNgamma) and a negative correlation with IL-10. Tretinoin 21-23 interferon gamma Homo sapiens 132-140
32505549-3 2021 Substrate-based inhibitor DX314 has enhanced selectivity for RA-metabolizing enzyme CYP26B1 and may offer an improved treatment option for keratinization disorders such as congenital ichthyosis and Darier disease. Tretinoin 61-63 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 84-91
33254967-5 2021 The capability of Ln5-P4/NGF-RA-ASLNs to induce neuronal differentiation was much higher than that of free NGF-ASLNs and RA-ASLNs, as visualized using immunochemical staining. Tretinoin 29-31 nerve growth factor Homo sapiens 25-28
33254967-6 2021 Flow cytometry analysis indicated that Ln5-P4 on NGF-RA-ASLNs promoted the uptake of NGF and RA by iPSCs and accelerated neuronal production. Tretinoin 53-55 nerve growth factor Homo sapiens 49-52
33254967-6 2021 Flow cytometry analysis indicated that Ln5-P4 on NGF-RA-ASLNs promoted the uptake of NGF and RA by iPSCs and accelerated neuronal production. Tretinoin 53-55 nerve growth factor Homo sapiens 85-88
33254967-6 2021 Flow cytometry analysis indicated that Ln5-P4 on NGF-RA-ASLNs promoted the uptake of NGF and RA by iPSCs and accelerated neuronal production. Tretinoin 93-95 nerve growth factor Homo sapiens 49-52
33112288-7 2021 Network modelling identified tumour necrosis factor (TNF) and all-trans retinoic acid (RA) as upstream regulators of the mating-induced transcriptional response, which was confirmed by intraoviductal injection of TNF or RA in unmated rats. Tretinoin 220-222 tumor necrosis factor Rattus norvegicus 29-51
33112288-7 2021 Network modelling identified tumour necrosis factor (TNF) and all-trans retinoic acid (RA) as upstream regulators of the mating-induced transcriptional response, which was confirmed by intraoviductal injection of TNF or RA in unmated rats. Tretinoin 220-222 tumor necrosis factor Rattus norvegicus 53-56
33601383-8 2021 13-cis-retinoic acid and all-trans-retinoic acid regulated IL-6 release. Tretinoin 25-48 interleukin 6 Homo sapiens 59-63
33351133-4 2020 Here, we identified insulin-like growth factor binding protein 7 (IGFBP7) as part of ATRA-induced responses in APL cells. Tretinoin 85-89 insulin like growth factor binding protein 7 Homo sapiens 20-64
33351133-4 2020 Here, we identified insulin-like growth factor binding protein 7 (IGFBP7) as part of ATRA-induced responses in APL cells. Tretinoin 85-89 insulin like growth factor binding protein 7 Homo sapiens 66-72
33351133-5 2020 Most importantly, we observed that addition of recombinant human IGFBP7 (rhIGFBP7) increased ATRA-driven responses in a subset of non-APL AML samples: those with high RARA expression. Tretinoin 93-97 insulin like growth factor binding protein 7 Homo sapiens 65-71
33301441-5 2020 RA was also effective in alleviating TNF-alpha-induced 16HBE barrier leak, attenuating 60% of the TNF-alpha-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Tretinoin 0-2 tumor necrosis factor Homo sapiens 37-46
33301441-5 2020 RA was also effective in alleviating TNF-alpha-induced 16HBE barrier leak, attenuating 60% of the TNF-alpha-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Tretinoin 0-2 tumor necrosis factor Homo sapiens 98-107
33301441-6 2020 Interleukin-6-induced barrier leak was also reduced by RA. Tretinoin 55-57 interleukin 6 Homo sapiens 0-13
33301441-8 2020 The presence of RA partially reversed TNF-alpha"s effects on these select TJ proteins. Tretinoin 16-18 tumor necrosis factor Homo sapiens 38-47
33301441-9 2020 Lastly, RA completely abrogated the TNF-alpha-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. Tretinoin 8-10 tumor necrosis factor Homo sapiens 36-45
33301441-9 2020 Lastly, RA completely abrogated the TNF-alpha-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. Tretinoin 8-10 mitogen-activated protein kinase 3 Homo sapiens 66-73
33301441-9 2020 Lastly, RA completely abrogated the TNF-alpha-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. Tretinoin 8-10 tumor necrosis factor Homo sapiens 36-39
33241756-4 2021 Chromatin immunoprecipitation (ChIP) assays indicated that C/EBPbeta upregulated HOTAIR during ATRA induced differentiation in HL-60 cells. Tretinoin 95-99 CCAAT enhancer binding protein alpha Homo sapiens 59-68
33276438-5 2020 These genes were enriched in schizophrenia-associated signalling pathways, including PI3K/Akt, axon guidance, and signalling by retinoic acid. Tretinoin 128-141 AKT serine/threonine kinase 1 Homo sapiens 90-93
33126128-8 2020 Tretinoin bound within the lumen of the channel formed by E protein, which is lined by hydrophobic residues like Phe, Val and Ala, indicating its potential for blocking the channel and inhibiting the viroporin functionality of E. Tretinoin 0-9 envelope protein Severe acute respiratory syndrome coronavirus 2 58-59
33126128-8 2020 Tretinoin bound within the lumen of the channel formed by E protein, which is lined by hydrophobic residues like Phe, Val and Ala, indicating its potential for blocking the channel and inhibiting the viroporin functionality of E. Tretinoin 0-9 envelope protein Severe acute respiratory syndrome coronavirus 2 227-228
33126128-10 2020 This work thus highlights the possibility of exploring Tretinoin as a potential SARS-CoV-2 E protein ion channel blocker and virus assembly inhibitor, which could be an important therapeutic strategy in the treatment for coronaviruses. Tretinoin 55-64 envelope protein Severe acute respiratory syndrome coronavirus 2 91-92
33022719-0 2020 In Vitro Anticancer Effects of All-trans Retinoic Acid in Combination with Dacarbazine against CD117+ Melanoma Cells. Tretinoin 31-54 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 95-100
33022719-4 2020 Here, we aim to improve response to dacarbazine therapy by pretreatment with all-trans retinoic acid (ATRA) in CD117+ melanoma cells. Tretinoin 77-100 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 111-116
33022719-4 2020 Here, we aim to improve response to dacarbazine therapy by pretreatment with all-trans retinoic acid (ATRA) in CD117+ melanoma cells. Tretinoin 102-106 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 111-116
33022719-9 2020 RESULTS: Here, the CD117+ melanoma cells were incubated with various concentrations of ATRA, dacarbazine, and their combination to determine IC50 values. Tretinoin 87-91 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 19-24
33022719-13 2020 CONCLUSION: Collectively, combined treatment with ATRA and dacarbazine induced more apoptosis and enhanced the cell cycle arrest of CD117+ melanoma cells. Tretinoin 50-54 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 132-137
32424865-10 2020 Mechanistically, RA could activate the AKT/GSK3beta/beta-catenin pathway during the process of iPSCs osteogenesis. Tretinoin 17-19 AKT serine/threonine kinase 1 Homo sapiens 39-42
32865619-2 2020 All-trans retinoic acid (ATRA), the main active metabolite of vitamin A, exerts non-genomic interactions with different members of the protein kinase C (PKC) family, recognized modulators of different tumor progression pathways. Tretinoin 0-23 protein kinase C alpha Homo sapiens 153-156
33105029-3 2020 In adult rodents, inhibition of Cyp26a1 and Cyp26b1 increases atRA concentrations and signaling. Tretinoin 62-66 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 44-51
33105029-11 2020 Postnatal knockout of Cyp26b1 resulted in increased atRA concentrations in the skin while the postnatal knockout of both Cyp26a1 and Cyp26b1 resulted in increased atRA concentrations in the liver, serum, skin, spleen, and intestines. Tretinoin 52-56 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 22-29
33105029-11 2020 Postnatal knockout of Cyp26b1 resulted in increased atRA concentrations in the skin while the postnatal knockout of both Cyp26a1 and Cyp26b1 resulted in increased atRA concentrations in the liver, serum, skin, spleen, and intestines. Tretinoin 163-167 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 133-140
32865619-2 2020 All-trans retinoic acid (ATRA), the main active metabolite of vitamin A, exerts non-genomic interactions with different members of the protein kinase C (PKC) family, recognized modulators of different tumor progression pathways. Tretinoin 25-29 protein kinase C alpha Homo sapiens 153-156
32865619-3 2020 To determine whether a group of patients could become benefited employing a retinoid therapy, in this study we have evaluated whether PKCalpha expression (a poor prognosis marker in breast cancer) could sensitizes mammary cells to ATRA treatment. Tretinoin 231-235 protein kinase C alpha Homo sapiens 134-142
32594050-7 2020 From days 1 to 21 after DEACMP, the intraperitoneal injection of retinoic acid (10 mg/kg), which can inhibit LINGO-1 expression, was able to improve the above changes observed in the DEACMP model. Tretinoin 65-78 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 109-116
32865619-9 2020 RESULTS: Our findings suggest that high PKCalpha levels improve the differentiation response to ATRA in a RAR signaling-dependent manner. Tretinoin 96-100 protein kinase C alpha Homo sapiens 40-48
33090723-5 2020 Our data indicated that AFP could significantly promote the proliferation and weaken ATRA-induced apoptosis of hepatoma cells. Tretinoin 85-89 alpha fetoprotein Homo sapiens 24-27
33196459-7 2020 In retinoic acid-differentiated ATXN3/Q75-GFP SH-SY5Y cells inflamed with IFN-gamma-primed HMC3 conditioned medium, treatment with the tested compounds mitigated the increased caspase 1 activity and lactate dehydrogenase release, reduced polyQ aggregation and ROS and/or promoted neurite outgrowth. Tretinoin 3-16 interferon gamma Homo sapiens 74-83
33196459-7 2020 In retinoic acid-differentiated ATXN3/Q75-GFP SH-SY5Y cells inflamed with IFN-gamma-primed HMC3 conditioned medium, treatment with the tested compounds mitigated the increased caspase 1 activity and lactate dehydrogenase release, reduced polyQ aggregation and ROS and/or promoted neurite outgrowth. Tretinoin 3-16 caspase 1 Homo sapiens 176-185
32372724-9 2020 Furthermore, co-immunoprecipitation revealed an RA-induced interaction between PIWIL4 and the H3K27me3 demethylase UTX. Tretinoin 48-50 lysine demethylase 6A Homo sapiens 115-118
32964418-7 2020 ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO). Tretinoin 0-4 translocator protein Mus musculus 149-153
32964418-7 2020 ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO). Tretinoin 0-4 translocator protein Mus musculus 250-254
32964418-8 2020 CONCLUSION AND IMPLICATIONS: Our results demonstrate brain protective effects of posttraumatic ATRA administration including long-term protection of hippocampal GCL integrity in experimental TBI. Tretinoin 95-99 germ cell-less, spermatogenesis associated 1 Mus musculus 161-164
32799009-1 2020 Midkine (MK) is a low molecular-weight protein that was first identified as the product of a retinoic acid-responsive gene involved in embryonic development. Tretinoin 93-106 midkine Homo sapiens 0-7
32799009-1 2020 Midkine (MK) is a low molecular-weight protein that was first identified as the product of a retinoic acid-responsive gene involved in embryonic development. Tretinoin 93-106 midkine Homo sapiens 9-11
32536235-0 2020 Arsenic trioxide and all-trans retinoic acid suppress the expression of FLT3-ITD. Tretinoin 31-44 fms related receptor tyrosine kinase 3 Homo sapiens 72-76
32536235-2 2020 Arsenic trioxide (ATO) and all-trans retinoic acid (ATRA) can down-regulate FLT3-ITD level and selectively kill leukemia cells carrying the FLT3-ITD mutation. Tretinoin 27-50 fms related receptor tyrosine kinase 3 Homo sapiens 76-80
32536235-2 2020 Arsenic trioxide (ATO) and all-trans retinoic acid (ATRA) can down-regulate FLT3-ITD level and selectively kill leukemia cells carrying the FLT3-ITD mutation. Tretinoin 27-50 fms related receptor tyrosine kinase 3 Homo sapiens 140-144
32536235-2 2020 Arsenic trioxide (ATO) and all-trans retinoic acid (ATRA) can down-regulate FLT3-ITD level and selectively kill leukemia cells carrying the FLT3-ITD mutation. Tretinoin 52-56 fms related receptor tyrosine kinase 3 Homo sapiens 76-80
32536235-2 2020 Arsenic trioxide (ATO) and all-trans retinoic acid (ATRA) can down-regulate FLT3-ITD level and selectively kill leukemia cells carrying the FLT3-ITD mutation. Tretinoin 52-56 fms related receptor tyrosine kinase 3 Homo sapiens 140-144
32536235-6 2020 Further studies revealed that ATO/ATRA may suppress the Expression of FLT3-ITD by promoting the UBE2L6-mediated ubiquitination pathway and decreasing the expression of C-MYC. Tretinoin 34-38 fms related receptor tyrosine kinase 3 Homo sapiens 70-74
33148658-5 2020 Mechanistically, LSD1 tightly controls retinoic acid signaling through regulation of Aldh1a2 expression level. Tretinoin 39-52 lysine (K)-specific demethylase 1A Mus musculus 17-21
33148658-6 2020 The increased retinoic acid signaling in LSD1-deficient mice suppressed SOX9 expression and impeded the cartilaginous callus formation during fracture repair. Tretinoin 14-27 lysine (K)-specific demethylase 1A Mus musculus 41-45
32865844-9 2020 The expression of T-bet and IFN-gamma genes in the splenocytes of ATRA, calcitriol and combination- treated mice were significantly reduced compared to vehicle group (p < 0.05). Tretinoin 66-70 interferon gamma Mus musculus 28-37
33218406-1 2020 OBJECTIVE: The main goal of the present study is to investigate the effects of retinoic acid and fibroblast growth factor-2 on serum levels of FSH and LH, histology, and apoptosis in the mouse model of Poly Cystic Ovary Syndrome (PCOS). Tretinoin 79-92 follicle stimulating hormone beta Mus musculus 143-146
33194073-10 2020 Additionally, we confirmed that Bcl-2 is associated with the induction of ATRA-induced autophagy instead of the PI3K/Akt/mTOR pathway. Tretinoin 74-78 BCL2 apoptosis regulator Homo sapiens 32-37
33194073-11 2020 These findings suggest that ATRA induces autophagy and autophagic cell death through the Bcl-2/Beclin1 pathway. Tretinoin 28-32 BCL2 apoptosis regulator Homo sapiens 89-94
33081033-0 2020 Retinoic Acid Sensitivity of Triple-Negative Breast Cancer Cells Characterized by Constitutive Activation of the notch1 Pathway: The Role of Rarbeta. Tretinoin 0-13 notch receptor 1 Homo sapiens 113-119
33081033-3 2020 The only three cell lines (HCC-1599, MB-157 and MDA-MB-157) endowed with ATRA-sensitivity are characterized by genetic aberrations of the NOTCH1-gene, causing constitutive activation of the NOTCH1 gamma-secretase product, N1ICD. Tretinoin 73-77 notch receptor 1 Homo sapiens 138-144
33081033-3 2020 The only three cell lines (HCC-1599, MB-157 and MDA-MB-157) endowed with ATRA-sensitivity are characterized by genetic aberrations of the NOTCH1-gene, causing constitutive activation of the NOTCH1 gamma-secretase product, N1ICD. Tretinoin 73-77 notch receptor 1 Homo sapiens 190-196
33081033-6 2020 RNA-sequencing studies of HCC-1599 and MB-157 cells exposed to ATRA and DAPT and ATRA+DAPT demonstrate that the two compounds act on common gene sets, some of which belong to the NOTCH1 pathway. Tretinoin 63-67 notch receptor 1 Homo sapiens 179-185
33081033-6 2020 RNA-sequencing studies of HCC-1599 and MB-157 cells exposed to ATRA and DAPT and ATRA+DAPT demonstrate that the two compounds act on common gene sets, some of which belong to the NOTCH1 pathway. Tretinoin 81-85 notch receptor 1 Homo sapiens 179-185
33081033-9 2020 In conclusion, we demonstrate that ATRA exerts a significant anti-tumor action only in TNBC cells showing constitutive NOTCH1 activation. Tretinoin 35-39 notch receptor 1 Homo sapiens 119-125
32765864-0 2020 Combined effect of (-)-epigallocatechin-3-gallate and all-trans retinoic acid in FLT3-mutated cell lines. Tretinoin 54-77 fms related receptor tyrosine kinase 3 Homo sapiens 81-85
33190441-0 2020 [Effect of endoplasmic reticulum stress induced by all-trans retinoic acid on apoptosis of FLT3-ITD mutated leukemia cells by activating autophagy in FLT3-ITD mutated protein]. Tretinoin 51-74 fms related receptor tyrosine kinase 3 Homo sapiens 91-95
33190441-0 2020 [Effect of endoplasmic reticulum stress induced by all-trans retinoic acid on apoptosis of FLT3-ITD mutated leukemia cells by activating autophagy in FLT3-ITD mutated protein]. Tretinoin 51-74 fms related receptor tyrosine kinase 3 Homo sapiens 150-154
33190441-1 2020 Objective: Endoplasmic reticulum stress(ERS)was used as the research emphasis to further investigate the mechanisms of apoptosis of FLT3-ITD-mutated leukemia cells and decreased expression of FLT3-ITD mutated protein induced by all-trans retinoic acid(ATRA). Tretinoin 228-251 fms related receptor tyrosine kinase 3 Homo sapiens 192-196
33190441-1 2020 Objective: Endoplasmic reticulum stress(ERS)was used as the research emphasis to further investigate the mechanisms of apoptosis of FLT3-ITD-mutated leukemia cells and decreased expression of FLT3-ITD mutated protein induced by all-trans retinoic acid(ATRA). Tretinoin 252-256 fms related receptor tyrosine kinase 3 Homo sapiens 192-196
33190441-2 2020 Methods: FLT3-ITD-mutated leukemia cell lines(MV4-11 and MOLM13)were treated with ATRA. Tretinoin 82-86 fms related receptor tyrosine kinase 3 Homo sapiens 9-13
33190441-5 2020 Results: A low-dose ATRA further increased FLT3-ITD cells and ERS levels. Tretinoin 20-24 fms related receptor tyrosine kinase 3 Homo sapiens 43-47
33190441-6 2020 ATRA acted on the ERS-related PERK/eif2alpha signaling pathway and continued to increase the ERS of FLT3-ITD cells, resulting in an upregulation of apoptotic gene CHOP expression. Tretinoin 0-4 fms related receptor tyrosine kinase 3 Homo sapiens 100-104
33190441-6 2020 ATRA acted on the ERS-related PERK/eif2alpha signaling pathway and continued to increase the ERS of FLT3-ITD cells, resulting in an upregulation of apoptotic gene CHOP expression. Tretinoin 0-4 DNA damage inducible transcript 3 Homo sapiens 163-167
33190441-7 2020 After the treatment with ATRA, FLT3-ITD protein in FLT3-ITD cells was decreased. Tretinoin 25-29 fms related receptor tyrosine kinase 3 Homo sapiens 31-35
33190441-7 2020 After the treatment with ATRA, FLT3-ITD protein in FLT3-ITD cells was decreased. Tretinoin 25-29 fms related receptor tyrosine kinase 3 Homo sapiens 51-55
33190441-9 2020 Conclusions: ATRA further raises the ERS level of FLT3-ITD cells continuously by activating the ERS-related PERK/eif2alpha signal pathway and induces FLT3-ITD protein autophagy degradation through ERAA pathway, which induces apoptosis of FLT3-ITD-mutated leukemia cells. Tretinoin 13-17 fms related receptor tyrosine kinase 3 Homo sapiens 50-54
33190441-9 2020 Conclusions: ATRA further raises the ERS level of FLT3-ITD cells continuously by activating the ERS-related PERK/eif2alpha signal pathway and induces FLT3-ITD protein autophagy degradation through ERAA pathway, which induces apoptosis of FLT3-ITD-mutated leukemia cells. Tretinoin 13-17 fms related receptor tyrosine kinase 3 Homo sapiens 150-154
33190441-9 2020 Conclusions: ATRA further raises the ERS level of FLT3-ITD cells continuously by activating the ERS-related PERK/eif2alpha signal pathway and induces FLT3-ITD protein autophagy degradation through ERAA pathway, which induces apoptosis of FLT3-ITD-mutated leukemia cells. Tretinoin 13-17 fms related receptor tyrosine kinase 3 Homo sapiens 150-154
33190441-10 2020 These results provide preliminary evidence on the use of ATRA in the treatment of refractory leukemia with FLT3-ITD. Tretinoin 57-61 fms related receptor tyrosine kinase 3 Homo sapiens 107-111
32765864-6 2020 In the present study, an in vitro evaluation of the effects of the combination of EGCG and ATRA on FLT3-mutated cell lines was performed using the isobologram method. Tretinoin 91-95 fms related receptor tyrosine kinase 3 Homo sapiens 99-103
32738032-11 2020 Moreover, ZYG11B expression regulates a cartilage master regulator, SOX6, and is regulated by Retinoic Acid, a known developmental toxic molecule leading to clinical features of OAVS. Tretinoin 94-107 zyg-11 family member, cell cycle regulator Danio rerio 10-16
32638255-0 2020 All-trans retinoic acid increases NF-kappaB activity in PMA-stimulated THP-1 cells upon unmethylated CpG challenge by enhancing cell surface TLR9 expression. Tretinoin 0-23 nuclear factor kappa B subunit 1 Homo sapiens 34-43
32638255-2 2020 This study investigates the possible immune potentiating effect of ATRA on NF-kappaB activity in human monocytic THP-1 cells after exposure to unmethylated CpG DNA ODN2006. Tretinoin 67-71 nuclear factor kappa B subunit 1 Homo sapiens 75-84
32638255-4 2020 ATRA synergistically enhanced NF-kappaB activity of cells, in a concentration- and time-dependent manner. Tretinoin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 30-39
32638255-9 2020 To determine whether the ATRA-enhanced NF-kappaB activity is due to the enhanced cell surface TLR9 expression, we examined NF-kappaB activity after treatment with anti-TLR9 blocking antibody. Tretinoin 25-29 nuclear factor kappa B subunit 1 Homo sapiens 39-48
32638255-9 2020 To determine whether the ATRA-enhanced NF-kappaB activity is due to the enhanced cell surface TLR9 expression, we examined NF-kappaB activity after treatment with anti-TLR9 blocking antibody. Tretinoin 25-29 nuclear factor kappa B subunit 1 Homo sapiens 123-132
32998330-0 2020 Evi1 Counteracts Anti-Leukemic and Stem Cell Inhibitory Effects of All-Trans Retinoic Acid on Flt3-ITD/Npm1c-Driven Acute Myeloid Leukemia Cells. Tretinoin 67-90 fms related receptor tyrosine kinase 3 Homo sapiens 94-98
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 86-90 nuclear factor kappa B subunit 1 Homo sapiens 100-109
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 86-90 nuclear factor kappa B subunit 1 Homo sapiens 150-159
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 136-140 nuclear factor kappa B subunit 1 Homo sapiens 100-109
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 136-140 nuclear factor kappa B subunit 1 Homo sapiens 150-159
32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 MLLT3 super elongation complex subunit Homo sapiens 30-33
32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 fms related receptor tyrosine kinase 3 Homo sapiens 104-108
32953569-7 2020 Western blot and qRT-PCR revealed that levels of CHOP and BIP were elevated in a concentration-dependent pattern after the cells were incubated with ATRA (2.5-20 micromol/L). Tretinoin 149-153 DNA damage inducible transcript 3 Homo sapiens 49-53
32953569-7 2020 Western blot and qRT-PCR revealed that levels of CHOP and BIP were elevated in a concentration-dependent pattern after the cells were incubated with ATRA (2.5-20 micromol/L). Tretinoin 149-153 heat shock protein family A (Hsp70) member 5 Homo sapiens 58-61
32953569-8 2020 The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro. Tretinoin 47-51 vascular endothelial growth factor A Homo sapiens 20-26
32953569-8 2020 The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro. Tretinoin 47-51 DNA damage inducible transcript 3 Homo sapiens 31-35
32932813-9 2020 In addition, flow cytometry analysis revealed that RA improved estimates of various viral reservoir assays by eliciting broad CD4 T-cell activation as demonstrated by elevated CD25 and CD38 but reduced CD69 and PD-1 expressing cells. Tretinoin 51-53 CD38 molecule Sus scrofa 185-189
32957082-2 2020 Although retinoic acid induced 14 (RAI14) is involved in various cancer processes, the relationship between EC and RAI14 has not been elucidated. Tretinoin 9-22 retinoic acid induced 14 Homo sapiens 35-40
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 239-252 mitogen-activated protein kinase 1 Homo sapiens 100-138
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 239-252 mitogen-activated protein kinase 1 Homo sapiens 140-143
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 254-256 mitogen-activated protein kinase 1 Homo sapiens 100-138
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 254-256 mitogen-activated protein kinase 1 Homo sapiens 140-143
32741018-0 2020 Novel evidence for retinoic acid-induced G (Rig-G) as a tumor suppressor by activating p53 signaling pathway in lung cancer. Tretinoin 19-32 tumor protein p53 Homo sapiens 87-90
32664002-10 2020 Moreover, long-term potentiation was decreased in both the excitatory postsynaptic potential and the population spike in RA-treated rats, presumably a consequence of the reduced glur1 transcript level. Tretinoin 121-123 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 178-183
32882760-5 2020 RESULTS: Combined treatment with AG-221 and ATRA inhibited 2-HG production and resulted in synergistic effects on differentiation among IDH2-mutant AML cells and primary AML cells expressing IDH2 mutation. Tretinoin 44-48 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 136-140
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 93-120
32882760-0 2020 All-Trans Retinoic Acid Synergizes with Enasidenib to Induce Differentiation of IDH2-Mutant Acute Myeloid Leukemia Cells. Tretinoin 0-23 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 80-84
32705280-0 2020 Retinoic acid induces differentiation in neuroblastoma via ROR1 by modulating retinoic acid response elements. Tretinoin 0-13 receptor tyrosine kinase like orphan receptor 1 Homo sapiens 59-63
32705280-0 2020 Retinoic acid induces differentiation in neuroblastoma via ROR1 by modulating retinoic acid response elements. Tretinoin 78-91 receptor tyrosine kinase like orphan receptor 1 Homo sapiens 59-63
32882760-5 2020 RESULTS: Combined treatment with AG-221 and ATRA inhibited 2-HG production and resulted in synergistic effects on differentiation among IDH2-mutant AML cells and primary AML cells expressing IDH2 mutation. Tretinoin 44-48 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 191-195
32882760-7 2020 AG-221 and ATRA treatment-induced differentiation of IDH2-mutant AML cells was associated with autophagy induction, without suppressing autophagy flux at maturation and degradation stages. Tretinoin 11-15 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 53-57
32882760-8 2020 A RAF-1/MEK/ERK pathway was founded to be associated with AG-221 and ATRA-induced differentiation in IDH2-mutant AML cells. Tretinoin 69-73 mitogen-activated protein kinase kinase 7 Homo sapiens 8-11
32882760-8 2020 A RAF-1/MEK/ERK pathway was founded to be associated with AG-221 and ATRA-induced differentiation in IDH2-mutant AML cells. Tretinoin 69-73 mitogen-activated protein kinase 1 Homo sapiens 12-15
32882760-8 2020 A RAF-1/MEK/ERK pathway was founded to be associated with AG-221 and ATRA-induced differentiation in IDH2-mutant AML cells. Tretinoin 69-73 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 101-105
32882760-10 2020 CONCLUSION: Our preliminary evidence indicates that the addition of ATRA to treatments with IDH2 inhibitor may lead to further improvements or increases in response rates in IDH2-mutant AML patients who do not appear to benefit from treatments with IDH2 inhibitor alone. Tretinoin 68-72 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 92-96
32882760-10 2020 CONCLUSION: Our preliminary evidence indicates that the addition of ATRA to treatments with IDH2 inhibitor may lead to further improvements or increases in response rates in IDH2-mutant AML patients who do not appear to benefit from treatments with IDH2 inhibitor alone. Tretinoin 68-72 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 174-178
32882760-10 2020 CONCLUSION: Our preliminary evidence indicates that the addition of ATRA to treatments with IDH2 inhibitor may lead to further improvements or increases in response rates in IDH2-mutant AML patients who do not appear to benefit from treatments with IDH2 inhibitor alone. Tretinoin 68-72 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 174-178
32492473-4 2020 IgA secretion was induced from IgD+ B cells in vitro by stimulus with lipopolysaccharide in the presence of only retinoic acid (RA) and low doses of TGF-beta1. Tretinoin 113-126 immunoglobulin heavy constant delta Mus musculus 31-34
32859169-6 2020 RESULTS: In non-DS patients, IL-8 plasma levels were significantly reduced in the seventh day of ATRA treatment (34.16; 6.99 to 147.11 pg mL- 1 in D0 vs. 10.9; 0 to 26.81 pg mL- 1 in D7; p = 0.02) whereas their levels did not discriminate between DS and non-DS development during the entire induction period (all p > 0.05 in D0, D3, and D7). Tretinoin 97-101 C-X-C motif chemokine ligand 8 Homo sapiens 29-33
32929351-9 2020 Although arsenic/ATRA therapy degraded PML-RARalpha and restored PPARgamma expression, it exacerbated dyslipidemia in APL patients. Tretinoin 17-21 peroxisome proliferator activated receptor gamma Homo sapiens 65-74
32929351-10 2020 The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy. Tretinoin 53-57 peroxisome proliferator activated receptor gamma Homo sapiens 77-86
32929351-10 2020 The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy. Tretinoin 53-57 peroxisome proliferator activated receptor gamma Homo sapiens 114-123
32929351-12 2020 Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment. Tretinoin 189-193 peroxisome proliferator activated receptor gamma Homo sapiens 67-76
32751185-0 2020 Impaired CPT1A Gene Expression Response to Retinoic Acid Treatment in Human PBMC as Predictor of Metabolic Risk. Tretinoin 43-56 carnitine palmitoyltransferase 1A Homo sapiens 9-14
32548665-0 2020 All-Trans Retinoic Acid Exerts Neuroprotective Effects in Amyotrophic Lateral Sclerosis-Like Tg (SOD1*G93A)1Gur Mice. Tretinoin 0-23 superoxide dismutase 1, soluble Mus musculus 97-101
32863954-9 2020 Results: We found that RA treatment at the lateral mesoderm stage (days 2-4) significantly improved cardiomyocyte differentiation, as evidenced by the upregulation of TNNT2, NKX2.5 and MYH6 on day 10 of differentiation. Tretinoin 23-25 troponin T2, cardiac type Homo sapiens 167-172
32863954-9 2020 Results: We found that RA treatment at the lateral mesoderm stage (days 2-4) significantly improved cardiomyocyte differentiation, as evidenced by the upregulation of TNNT2, NKX2.5 and MYH6 on day 10 of differentiation. Tretinoin 23-25 NK2 homeobox 5 Homo sapiens 174-180
32863954-9 2020 Results: We found that RA treatment at the lateral mesoderm stage (days 2-4) significantly improved cardiomyocyte differentiation, as evidenced by the upregulation of TNNT2, NKX2.5 and MYH6 on day 10 of differentiation. Tretinoin 23-25 myosin heavy chain 6 Homo sapiens 185-189
32751185-6 2020 Particularly, the response to ATRA of CPT1A, previously reported as a sensitive metabolic risk predictive biomarker, was dependent on HDL levels and not on BMI, being impaired in those individuals with lower HDL levels, specifically in OW-OB. Tretinoin 30-34 carnitine palmitoyltransferase 1A Homo sapiens 38-43
32615991-0 2020 All-trans retinoic acid attenuates the progression of Ang II-induced abdominal aortic aneurysms in ApoE-/-mice. Tretinoin 0-23 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 54-60
32707918-9 2020 The increased expression of ATG5 affects the differentiation of HL-60 cells with ATRA, ROS production and phagocytosis. Tretinoin 81-85 autophagy related 5 Homo sapiens 28-32
32193285-8 2020 Together our study reveals that Pin1 inhibition with widely used ATRA acts as an effective HR disrupter that sensitizes BRCA1-proficient tumors to PARP inhibition. Tretinoin 65-69 poly(ADP-ribose) polymerase 1 Homo sapiens 147-151
32339486-2 2020 Later, Lotan"s laboratory found the same gene product in response to retinoic acid analogues, naming it with the symbol RAIG1. Tretinoin 69-82 G protein-coupled receptor class C group 5 member A Homo sapiens 120-125
32615991-0 2020 All-trans retinoic acid attenuates the progression of Ang II-induced abdominal aortic aneurysms in ApoE-/-mice. Tretinoin 0-23 apolipoprotein E Mus musculus 99-103
32615991-1 2020 BACKGROUND: To determine whether all-trans retinoic acid (ATRA) can influence the development of Angiotensin II (Ang II) induced experimental abdominal aortic aneurysms (AAAs). Tretinoin 33-56 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 97-111
32615991-1 2020 BACKGROUND: To determine whether all-trans retinoic acid (ATRA) can influence the development of Angiotensin II (Ang II) induced experimental abdominal aortic aneurysms (AAAs). Tretinoin 33-56 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 113-119
32615991-1 2020 BACKGROUND: To determine whether all-trans retinoic acid (ATRA) can influence the development of Angiotensin II (Ang II) induced experimental abdominal aortic aneurysms (AAAs). Tretinoin 58-62 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 97-111
32615991-1 2020 BACKGROUND: To determine whether all-trans retinoic acid (ATRA) can influence the development of Angiotensin II (Ang II) induced experimental abdominal aortic aneurysms (AAAs). Tretinoin 58-62 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 113-119
32615991-9 2020 Western blot analysis indicated that protein levels of retinoic acid receptor alpha (RARalpha), MMP2, MMP9, and AT1 were dramatically affected by ATRA treatment. Tretinoin 146-150 angiotensin II receptor, type 1a Mus musculus 112-115
32615991-10 2020 CONCLUSIONS: In conclusion, ATRA attenuates the progression of Ang II-induced AAAs, possibly by downregulating MMP2, MMP9, and AT-1 expression. Tretinoin 28-32 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 63-69
32615991-10 2020 CONCLUSIONS: In conclusion, ATRA attenuates the progression of Ang II-induced AAAs, possibly by downregulating MMP2, MMP9, and AT-1 expression. Tretinoin 28-32 angiotensin II receptor, type 1a Mus musculus 127-131
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 mitogen-activated protein kinase kinase 7 Homo sapiens 106-109
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 137-140
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 145-148
32032659-9 2020 The Lyn-knockdown cells expressed slightly higher Raf, pS259-Raf, pS289/296/301-Raf, and Slp-76 than wt-parental cells, and this was associated with enhanced ATRA-induced upregulation of Fgr and cell differentiation, consistent with heightened signaling, suggesting that enhanced Fgr may have compensated for loss of Lyn to enhance differentiation in the Lyn-knockdown cells. Tretinoin 158-162 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 187-190
32032659-4 2020 Roscovitine enhanced ATRA-induced c-Raf interaction with Lyn, Vav, and c-Cbl. Tretinoin 21-25 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 57-60
32032659-9 2020 The Lyn-knockdown cells expressed slightly higher Raf, pS259-Raf, pS289/296/301-Raf, and Slp-76 than wt-parental cells, and this was associated with enhanced ATRA-induced upregulation of Fgr and cell differentiation, consistent with heightened signaling, suggesting that enhanced Fgr may have compensated for loss of Lyn to enhance differentiation in the Lyn-knockdown cells. Tretinoin 158-162 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 280-283
32032659-9 2020 The Lyn-knockdown cells expressed slightly higher Raf, pS259-Raf, pS289/296/301-Raf, and Slp-76 than wt-parental cells, and this was associated with enhanced ATRA-induced upregulation of Fgr and cell differentiation, consistent with heightened signaling, suggesting that enhanced Fgr may have compensated for loss of Lyn to enhance differentiation in the Lyn-knockdown cells. Tretinoin 158-162 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 317-320
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3
32032659-9 2020 The Lyn-knockdown cells expressed slightly higher Raf, pS259-Raf, pS289/296/301-Raf, and Slp-76 than wt-parental cells, and this was associated with enhanced ATRA-induced upregulation of Fgr and cell differentiation, consistent with heightened signaling, suggesting that enhanced Fgr may have compensated for loss of Lyn to enhance differentiation in the Lyn-knockdown cells. Tretinoin 158-162 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 317-320
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 138-141
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 12-16 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 147-150
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 134-138 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 147-150
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 134-138 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 147-150
32032659-9 2020 The Lyn-knockdown cells expressed slightly higher Raf, pS259-Raf, pS289/296/301-Raf, and Slp-76 than wt-parental cells, and this was associated with enhanced ATRA-induced upregulation of Fgr and cell differentiation, consistent with heightened signaling, suggesting that enhanced Fgr may have compensated for loss of Lyn to enhance differentiation in the Lyn-knockdown cells. Tretinoin 158-162 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 4-7
32361568-9 2020 DMSO-HL and ATRA-HL cells both produced TNF-alpha and IL-8 after lipopolysaccharide (LPS) or PM treatment, whereas non-differentiated HL-60 cells did not. Tretinoin 12-16 C-X-C motif chemokine ligand 8 Homo sapiens 54-58
32630207-7 2020 ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK. Tretinoin 0-4 interleukin 1 beta Homo sapiens 86-98
32630207-7 2020 ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK. Tretinoin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 156-165
32630207-7 2020 ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK. Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 167-170
32630207-7 2020 ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK. Tretinoin 0-4 mitogen-activated protein kinase 1 Homo sapiens 176-179
32630207-8 2020 We show that ATRA alleviates the negative feedback loop effect of IL-10 anti-inflammatory cytokine on NLRP3 inflammasome function by inhibiting the Akt-mTOR-STAT3 signaling axis. Tretinoin 13-17 NLR family pyrin domain containing 3 Homo sapiens 102-107
32630207-8 2020 We show that ATRA alleviates the negative feedback loop effect of IL-10 anti-inflammatory cytokine on NLRP3 inflammasome function by inhibiting the Akt-mTOR-STAT3 signaling axis. Tretinoin 13-17 AKT serine/threonine kinase 1 Homo sapiens 148-151
32630207-8 2020 We show that ATRA alleviates the negative feedback loop effect of IL-10 anti-inflammatory cytokine on NLRP3 inflammasome function by inhibiting the Akt-mTOR-STAT3 signaling axis. Tretinoin 13-17 mechanistic target of rapamycin kinase Homo sapiens 152-156
32630207-8 2020 We show that ATRA alleviates the negative feedback loop effect of IL-10 anti-inflammatory cytokine on NLRP3 inflammasome function by inhibiting the Akt-mTOR-STAT3 signaling axis. Tretinoin 13-17 signal transducer and activator of transcription 3 Homo sapiens 157-162
32630207-9 2020 We also provide evidence that ATRA enhances hexokinase 2 expression, and shifts the metabolism of LPS-activated macrophages toward glycolysis, leading to the activation of NLRP3 inflammasome. Tretinoin 30-34 NLR family pyrin domain containing 3 Homo sapiens 172-177
32630207-0 2020 All-Trans Retinoic Acid Enhances both the Signaling for Priming and the Glycolysis for Activation of NLRP3 Inflammasome in Human Macrophage. Tretinoin 10-23 NLR family pyrin domain containing 3 Homo sapiens 101-106
32630207-5 2020 Here, we showed that ATRA prolongs the expression of IL-6 and IL-1beta following a 2-, 6-, 12-, and 24-h LPS (100ng/mL) activation in human monocyte-derived macrophages. Tretinoin 21-25 interleukin 6 Homo sapiens 53-57
32630207-6 2020 We describe for the first time that ATRA modulates both priming and activation signals required for NLRP3 inflammasome function. Tretinoin 36-40 NLR family pyrin domain containing 3 Homo sapiens 100-105
32630207-7 2020 ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK. Tretinoin 0-4 NLR family pyrin domain containing 3 Homo sapiens 19-24
32630207-7 2020 ATRA alone induces NLRP3 expression, and enhances LPS-induced expression of NLRP3 and pro-IL-1beta via the regulation of signal transduction pathways, like NF-kappaB, p38, and ERK. Tretinoin 0-4 NLR family pyrin domain containing 3 Homo sapiens 76-81
32247021-7 2020 RESULTS: A combination of retinoic acid and lymphotoxin induced differentiation of glycoprotein 2-positive human M cells, which lack apical microvilli structure. Tretinoin 26-39 glycoprotein 2 Homo sapiens 83-97
32361568-7 2020 The MEK inhibitor also inhibited the differentiation of ATRA-HL cells to neutrophils. Tretinoin 56-60 mitogen-activated protein kinase kinase 7 Homo sapiens 4-7
32361568-9 2020 DMSO-HL and ATRA-HL cells both produced TNF-alpha and IL-8 after lipopolysaccharide (LPS) or PM treatment, whereas non-differentiated HL-60 cells did not. Tretinoin 12-16 tumor necrosis factor Homo sapiens 40-49
31903789-4 2020 Retinoic acid metabolism blocking agents (RAMBAs), which inhibit CYP26 enzymes, can improve retinoic acid (RA) pharmacokinetics in pre-clinical neuroblastoma models. Tretinoin 0-13 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 65-70
32663289-0 2020 Retinoic Acid Potentiates Orbital Tissues for Inflammation Through NF-kappaB and MCP-1. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 67-76
31903789-4 2020 Retinoic acid metabolism blocking agents (RAMBAs), which inhibit CYP26 enzymes, can improve retinoic acid (RA) pharmacokinetics in pre-clinical neuroblastoma models. Tretinoin 92-105 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 65-70
31903789-4 2020 Retinoic acid metabolism blocking agents (RAMBAs), which inhibit CYP26 enzymes, can improve retinoic acid (RA) pharmacokinetics in pre-clinical neuroblastoma models. Tretinoin 42-44 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 65-70
32676119-9 2020 Activation of RA signal in vitro inhibited ALP activities and mineralization of human DPSCs and decreased the mRNA expression of ALP, osteocalcin, osteopontin, and a transcription factor, osterix. Tretinoin 14-16 alkaline phosphatase, placental Homo sapiens 43-46
32676119-9 2020 Activation of RA signal in vitro inhibited ALP activities and mineralization of human DPSCs and decreased the mRNA expression of ALP, osteocalcin, osteopontin, and a transcription factor, osterix. Tretinoin 14-16 alkaline phosphatase, placental Homo sapiens 129-132
32676119-9 2020 Activation of RA signal in vitro inhibited ALP activities and mineralization of human DPSCs and decreased the mRNA expression of ALP, osteocalcin, osteopontin, and a transcription factor, osterix. Tretinoin 14-16 bone gamma-carboxyglutamate protein Homo sapiens 134-145
32714135-9 2020 Further, to determine the possible involvement of Nrf2 in carveol mediated neuroprotection, we antagonized Nrf2 by all-trans retinoic acid (ATRA), and such treatment abrogated the protective effects of carveol accompanied with exaggerated neuronal toxicity as demonstrated by higher infarction area. Tretinoin 115-138 NFE2 like bZIP transcription factor 2 Rattus norvegicus 50-54
32714135-9 2020 Further, to determine the possible involvement of Nrf2 in carveol mediated neuroprotection, we antagonized Nrf2 by all-trans retinoic acid (ATRA), and such treatment abrogated the protective effects of carveol accompanied with exaggerated neuronal toxicity as demonstrated by higher infarction area. Tretinoin 115-138 NFE2 like bZIP transcription factor 2 Rattus norvegicus 107-111
32714135-9 2020 Further, to determine the possible involvement of Nrf2 in carveol mediated neuroprotection, we antagonized Nrf2 by all-trans retinoic acid (ATRA), and such treatment abrogated the protective effects of carveol accompanied with exaggerated neuronal toxicity as demonstrated by higher infarction area. Tretinoin 140-144 NFE2 like bZIP transcription factor 2 Rattus norvegicus 50-54
32714135-9 2020 Further, to determine the possible involvement of Nrf2 in carveol mediated neuroprotection, we antagonized Nrf2 by all-trans retinoic acid (ATRA), and such treatment abrogated the protective effects of carveol accompanied with exaggerated neuronal toxicity as demonstrated by higher infarction area. Tretinoin 140-144 NFE2 like bZIP transcription factor 2 Rattus norvegicus 107-111
32467243-4 2020 In this study, we demonstrate that the disruption of RA signaling within the NEUROG3-expressing endocrine progenitor population impairs mouse beta cell differentiation and induces ectopic expression of crucial delta cell genes, including somatostatin. Tretinoin 53-55 neurogenin 3 Mus musculus 77-84
32467243-4 2020 In this study, we demonstrate that the disruption of RA signaling within the NEUROG3-expressing endocrine progenitor population impairs mouse beta cell differentiation and induces ectopic expression of crucial delta cell genes, including somatostatin. Tretinoin 53-55 somatostatin Mus musculus 238-250
32467243-5 2020 In addition, the inhibition of the RA pathway in hESC-derived pancreatic progenitors downstream of NEUROG3 induction impairs insulin expression. Tretinoin 35-37 neurogenin 3 Mus musculus 99-106
32467243-5 2020 In addition, the inhibition of the RA pathway in hESC-derived pancreatic progenitors downstream of NEUROG3 induction impairs insulin expression. Tretinoin 35-37 insulin Homo sapiens 125-132
32445470-3 2020 From previous results of high throughput transcriptome sequencing, we selected transcription factor Nkx2.1 as a candidate to investigate its role on brain abnormalities induced by excessive retinoic acid. Tretinoin 190-203 NK2 homeobox 1 Homo sapiens 100-106
32124141-2 2020 The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 32-45 tumor protein p53 Homo sapiens 300-303
32295917-2 2020 Both cellular and viral RNA cleavage products of RNase L bind pattern recognition receptors (PRR) like Retinoic acid-inducible I (Rig-I) and or melanoma differentiation-associated protein 5 (MDA5) to further amplify interferon (IFN) production and antiviral response. Tretinoin 103-116 interferon alpha 1 Homo sapiens 228-231
32374610-2 2020 This system, based on the cellular retinoic acid binding protein, is structurally different from natural rhodopsin systems; but exhibits a similar isomerization upon light irradiation. Tretinoin 35-48 rhodopsin Homo sapiens 105-114
31480153-8 2020 Conclusion: ATRA promotes the synthesis of casein by regulating JAK2/STAT5 pathway and downstream mTOR signaling pathway, and it improves the fatty acid composition of MAC-T cells by regulating SREBP1-related genes. Tretinoin 12-16 mechanistic target of rapamycin kinase Homo sapiens 98-102
31480153-8 2020 Conclusion: ATRA promotes the synthesis of casein by regulating JAK2/STAT5 pathway and downstream mTOR signaling pathway, and it improves the fatty acid composition of MAC-T cells by regulating SREBP1-related genes. Tretinoin 12-16 sterol regulatory element binding transcription factor 1 Bos taurus 194-200
32124141-7 2020 CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 77-90 tumor protein p53 Homo sapiens 232-235
32124141-7 2020 CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 77-90 lactate dehydrogenase A Homo sapiens 244-248
32124141-2 2020 The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 32-45 lactate dehydrogenase A Homo sapiens 312-316
32448273-9 2020 In vivo studies suggested the topical application of TRA and BT dual-loaded liposomal gel had the best ability to reduce the thickness of epidermal and the level of cytokines (TNF-alpha and IL-6), largely alleviating the symptoms of psoriasis. Tretinoin 53-56 tumor necrosis factor Homo sapiens 176-185
32251704-2 2020 The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects. Tretinoin 63-76 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 41-46
32251704-2 2020 The proposed MIE for azole fungicides is CYP26 inhibition with retinoic acid (RA) local increase, triggering key events leading to craniofacial defects. Tretinoin 78-80 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 41-46
32251704-10 2020 Unexpectedly, VPA showed also a weak, but not marginal, capability to enter the CYP 26A1 and CYP 26C1 catalytic sites, suggesting a possible role of VPA in decreasing RA catabolism, acting as an additional MIE. Tretinoin 167-169 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 80-88
32466476-7 2020 We employed ATRA to antagonize Nrf2, which abrogated the neuroprotective effects of A3 to further assess the possible involvement of the Nrf2 pathway, as demonstrated by increased infarction and hyperexpression of inflammatory markers. Tretinoin 12-16 nuclear factor, erythroid 2 Homo sapiens 31-35
32173553-5 2020 The ERRgamma agonist GSK4716 increased DAT and TH expression, and the ERRgamma inverse agonist GSK5182 attenuated the retinoic acid-induced upregulation of DAT and TH in differentiated SH-SY5Y cells. Tretinoin 118-131 tyrosine hydroxylase Homo sapiens 164-166
32448273-9 2020 In vivo studies suggested the topical application of TRA and BT dual-loaded liposomal gel had the best ability to reduce the thickness of epidermal and the level of cytokines (TNF-alpha and IL-6), largely alleviating the symptoms of psoriasis. Tretinoin 53-56 interleukin 6 Homo sapiens 190-194
32617521-1 2020 The known collaboration between all-transretinoic acid and interferon motivates this study of the dependence of RA-induced leukemic cell differentiation on interferon regulatory factor-1 (IRF-1), a transcription factor that is the main mediator of interferon effects. Tretinoin 32-54 interferon regulatory factor 1 Homo sapiens 156-186
32617521-1 2020 The known collaboration between all-transretinoic acid and interferon motivates this study of the dependence of RA-induced leukemic cell differentiation on interferon regulatory factor-1 (IRF-1), a transcription factor that is the main mediator of interferon effects. Tretinoin 32-54 interferon regulatory factor 1 Homo sapiens 188-193
32385093-3 2020 Here we analyze male and female mice and show that HBCs also are activated with increasing age as well as non-cell-autonomously by increased expression of the retinoic acid-degrading enzyme CYP26B1. Tretinoin 159-172 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 190-197
32385093-5 2020 Odor/air stimulates CYP26B1 expression in olfactory sensory neurons mainly located in the dorsomedial OE, which is spatially inverse to ventrolateral constitutive expression of the retinoic acid-synthesizing enzyme (RALDH1) in supporting cells. Tretinoin 181-194 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 20-27
31659279-0 2020 Caspase-8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3 regulate retinoic acid-induced cell differentiation and necroptosis. Tretinoin 77-90 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 11-48
32478755-2 2020 The E14 mouse embryonic stem cells were used to form embryoid bodies through the hanging drop method, and then induced to differentiate into neural progenitor cells by retinoic acid, and finally differentiated into neurons. Tretinoin 168-181 skull morphology 21 Mus musculus 4-7
32508820-11 2020 Several stress proteins, like mouse UL-16-binding protein-like transcript 1 (Mult-1), histocompatibility 60 (H60) and retinoic acid early inducible-1 (Rae-1) alpha-epsilon family in mice and major histocompatibility complex (MHC) class I-chain-related A (MICA) in humans, are upregulated on allergen-exposed KC. Tretinoin 118-131 inhibitor of carbonic anhydrase Mus musculus 255-259
32499767-15 2020 In conclusion, we demonstrate that memory CD4+ T-cell splitting for optimal density in culture and ATRA supplementation significantly improved the efficacy of HIV outgrowth in a simplified ATRA-based QVOA performed in the absence of feeder/target cells or indicator cell lines. Tretinoin 189-193 CD4 molecule Homo sapiens 42-45
32384653-6 2020 ATRA induces a non-canonical type of viral mimicry, which results in increased expression of the IRF1 (Interferon Responsive Factor 1) transcription factor and the DTX3L (Deltex-E3-Ubiquitin-Ligase-3L) downstream effector. Tretinoin 0-4 interferon regulatory factor 1 Homo sapiens 97-101
32384653-6 2020 ATRA induces a non-canonical type of viral mimicry, which results in increased expression of the IRF1 (Interferon Responsive Factor 1) transcription factor and the DTX3L (Deltex-E3-Ubiquitin-Ligase-3L) downstream effector. Tretinoin 0-4 interferon regulatory factor 1 Homo sapiens 103-133
32384653-7 2020 Functional knockdown studies indicate that IRF1 and DTX3L are part of a negative feedback loop controlling ATRA-dependent growth inhibition of breast cancer cells. Tretinoin 107-111 interferon regulatory factor 1 Homo sapiens 43-47
32431691-0 2020 Potentiation of IL-4 Signaling by Retinoic Acid in Intestinal Epithelial Cells and Macrophages-Mechanisms and Targets. Tretinoin 34-47 interleukin 4 Homo sapiens 16-20
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 141-160 chloride channel accessory 1 Sus scrofa 43-48
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 162-166 chloride channel accessory 1 Sus scrofa 43-48
32431691-2 2020 We also demonstrated that in vitro ATRA induced a state of partial alternative activation in porcine macrophages (Mphis) and amplified certain aspects of M2a activation induced by IL-4. Tretinoin 35-39 interleukin 4 Homo sapiens 180-184
32431691-3 2020 Given these results, we tested the effect of ATRA on IL-4 responses in two porcine intestinal epithelial cell lines, IPEC1 and IPEC-J2 and observed that ATRA increased mRNA for the IL-4 receptor alpha chain. Tretinoin 45-49 interleukin 4 Homo sapiens 53-57
32431691-3 2020 Given these results, we tested the effect of ATRA on IL-4 responses in two porcine intestinal epithelial cell lines, IPEC1 and IPEC-J2 and observed that ATRA increased mRNA for the IL-4 receptor alpha chain. Tretinoin 153-157 interleukin 4 Homo sapiens 53-57
32431691-4 2020 ATRA also increased IL-4 induced phosphorylation of signal transducer and activator of transcription 6 (STAT6) and mRNA expression of the chloride channel, calcium activated, family member 1 (CLCA1), important for mucus formation, and chemokine (C-C motif) ligand 26 (CCL26), a potent eosinophil chemoattractant. Tretinoin 0-4 interleukin 4 Homo sapiens 20-24
32431691-4 2020 ATRA also increased IL-4 induced phosphorylation of signal transducer and activator of transcription 6 (STAT6) and mRNA expression of the chloride channel, calcium activated, family member 1 (CLCA1), important for mucus formation, and chemokine (C-C motif) ligand 26 (CCL26), a potent eosinophil chemoattractant. Tretinoin 0-4 chloride channel accessory 1 Sus scrofa 192-197
32431691-5 2020 We extended these findings to human Mphi THP-1 cells and showed that ATRA synergistically increased IL-4-induced CCL2, CCL13, and CCL26 mRNA and protein levels. Tretinoin 69-73 interleukin 4 Homo sapiens 100-104
32431691-6 2020 Transglutaminase 2 mRNA, protein, and enzyme activity were synergistically induced in THP-1 cells pretreated with ATRA and then treated with IL-4, thus, ATRA increased signaling in response to IL-4 in porcine epithelial cells and porcine and human Mphis. Tretinoin 114-118 transglutaminase 2 Homo sapiens 0-18
32431691-6 2020 Transglutaminase 2 mRNA, protein, and enzyme activity were synergistically induced in THP-1 cells pretreated with ATRA and then treated with IL-4, thus, ATRA increased signaling in response to IL-4 in porcine epithelial cells and porcine and human Mphis. Tretinoin 114-118 interleukin 4 Homo sapiens 193-197
32431691-6 2020 Transglutaminase 2 mRNA, protein, and enzyme activity were synergistically induced in THP-1 cells pretreated with ATRA and then treated with IL-4, thus, ATRA increased signaling in response to IL-4 in porcine epithelial cells and porcine and human Mphis. Tretinoin 153-157 transglutaminase 2 Homo sapiens 0-18
32431691-6 2020 Transglutaminase 2 mRNA, protein, and enzyme activity were synergistically induced in THP-1 cells pretreated with ATRA and then treated with IL-4, thus, ATRA increased signaling in response to IL-4 in porcine epithelial cells and porcine and human Mphis. Tretinoin 153-157 interleukin 4 Homo sapiens 141-145
32431691-6 2020 Transglutaminase 2 mRNA, protein, and enzyme activity were synergistically induced in THP-1 cells pretreated with ATRA and then treated with IL-4, thus, ATRA increased signaling in response to IL-4 in porcine epithelial cells and porcine and human Mphis. Tretinoin 153-157 interleukin 4 Homo sapiens 193-197
31659279-0 2020 Caspase-8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3 regulate retinoic acid-induced cell differentiation and necroptosis. Tretinoin 77-90 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 50-55
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 112-125 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 208-213
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 127-129 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 208-213
31659279-5 2020 RA treatment obviously enhanced the expression of RA-specific target genes having the retinoic acid response element (RARE) in their promoter regions to induce cell differentiation, and induced marked expression of RIPK1, RIPK3, and MLKL to stimulate necroptosis. Tretinoin 0-2 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 215-220
31659279-8 2020 Thus, Caspase-8, RIPK1, and RIPK3 regulate RA-induced cell differentiation and necroptosis both in vitro and in vivo. Tretinoin 43-45 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 17-22
32104972-0 2020 All-trans retinoic acid regulates TGF-beta1-induced extracellular matrix production via p38, JNK, and NF-kappaB-signaling pathways in nasal polyp-derived fibroblasts. Tretinoin 10-23 transforming growth factor beta 1 Homo sapiens 34-43
32104972-0 2020 All-trans retinoic acid regulates TGF-beta1-induced extracellular matrix production via p38, JNK, and NF-kappaB-signaling pathways in nasal polyp-derived fibroblasts. Tretinoin 10-23 mitogen-activated protein kinase 14 Homo sapiens 88-91
32104972-0 2020 All-trans retinoic acid regulates TGF-beta1-induced extracellular matrix production via p38, JNK, and NF-kappaB-signaling pathways in nasal polyp-derived fibroblasts. Tretinoin 10-23 mitogen-activated protein kinase 8 Homo sapiens 93-96
32104972-0 2020 All-trans retinoic acid regulates TGF-beta1-induced extracellular matrix production via p38, JNK, and NF-kappaB-signaling pathways in nasal polyp-derived fibroblasts. Tretinoin 10-23 nuclear factor kappa B subunit 1 Homo sapiens 102-111
32104972-6 2020 TGF-beta1-induced fibroblasts were pretreated with ATRA. Tretinoin 51-55 transforming growth factor beta 1 Homo sapiens 0-9
32104972-12 2020 TGF-beta1-induced cell migration and collagen gel contraction were significantly inhibited by ATRA pretreatment. Tretinoin 94-98 transforming growth factor beta 1 Homo sapiens 0-9
32104972-13 2020 ATRA also significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), p38, and p50 in TGF-beta1-induced NPDFs, but did not inhibit phosphorylation of extracellular signal-related kinase (ERK). Tretinoin 0-4 mitogen-activated protein kinase 8 Homo sapiens 53-76
32104972-13 2020 ATRA also significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), p38, and p50 in TGF-beta1-induced NPDFs, but did not inhibit phosphorylation of extracellular signal-related kinase (ERK). Tretinoin 0-4 mitogen-activated protein kinase 8 Homo sapiens 78-81
32104972-13 2020 ATRA also significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), p38, and p50 in TGF-beta1-induced NPDFs, but did not inhibit phosphorylation of extracellular signal-related kinase (ERK). Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 84-87
32104972-13 2020 ATRA also significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), p38, and p50 in TGF-beta1-induced NPDFs, but did not inhibit phosphorylation of extracellular signal-related kinase (ERK). Tretinoin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 93-96
32104972-13 2020 ATRA also significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), p38, and p50 in TGF-beta1-induced NPDFs, but did not inhibit phosphorylation of extracellular signal-related kinase (ERK). Tretinoin 0-4 transforming growth factor beta 1 Homo sapiens 100-109
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 18-20 tumor necrosis factor receptor superfamily, member 9 Mus musculus 36-41
32037722-8 2020 At the time of chromatoblast differentiation on the ocular-side, cyp26b1, which inactivates RA, was upregulated on the blind-side skin compared with the ocular-side. Tretinoin 92-94 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 65-72
32037722-9 2020 Therefore, we surmise that ocular-side-specific pigmentation is regulated by the inhibition of RA-signaling by cyp26b1 on the blind-side. Tretinoin 95-97 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 111-118
32323852-5 2020 In addition, through transient expression assays in breast cancer cells, it was revealed that a transcriptional mechanism dependent on protein kinase A and susceptible to retinoic acid in ER-positive cells induces GPR30 expression through a cis-regulatory element for E26 transformation-specific transcription factors, located between -631 and -625 bp from the GPR30 translation start codon. Tretinoin 171-184 estrogen receptor 1 Homo sapiens 188-190
32350257-0 2020 LSD1-mediated enhancer silencing attenuates retinoic acid signalling during pancreatic endocrine cell development. Tretinoin 44-57 lysine (K)-specific demethylase 1A Mus musculus 0-4
32350257-4 2020 Examination of enhancer and transcriptome landscapes revealed that LSD1 silences transiently active retinoic acid (RA)-induced enhancers and their target genes. Tretinoin 100-113 lysine (K)-specific demethylase 1A Mus musculus 67-71
32350257-4 2020 Examination of enhancer and transcriptome landscapes revealed that LSD1 silences transiently active retinoic acid (RA)-induced enhancers and their target genes. Tretinoin 115-117 lysine (K)-specific demethylase 1A Mus musculus 67-71
32350257-5 2020 Furthermore, prolonged RA exposure phenocopies LSD1 inhibition, suggesting that LSD1 regulates endocrine cell differentiation by limiting the duration of RA signalling. Tretinoin 23-25 lysine (K)-specific demethylase 1A Mus musculus 80-84
32350257-5 2020 Furthermore, prolonged RA exposure phenocopies LSD1 inhibition, suggesting that LSD1 regulates endocrine cell differentiation by limiting the duration of RA signalling. Tretinoin 154-156 lysine (K)-specific demethylase 1A Mus musculus 80-84
32284990-0 2020 Targeting the scaffolding role of LSD1 (KDM1A) poises acute myeloid leukemia cells for retinoic acid-induced differentiation. Tretinoin 87-100 lysine (K)-specific demethylase 1A Mus musculus 34-38
32284990-0 2020 Targeting the scaffolding role of LSD1 (KDM1A) poises acute myeloid leukemia cells for retinoic acid-induced differentiation. Tretinoin 87-100 lysine (K)-specific demethylase 1A Mus musculus 40-45
32284990-3 2020 APL cells are resistant to LSD1 inhibition or knockout, but targeting LSD1 sensitizes them to physiological doses of RA without altering of PML-RAR levels, and extends survival of leukemic mice upon RA treatment. Tretinoin 117-119 lysine (K)-specific demethylase 1A Mus musculus 70-74
32284990-3 2020 APL cells are resistant to LSD1 inhibition or knockout, but targeting LSD1 sensitizes them to physiological doses of RA without altering of PML-RAR levels, and extends survival of leukemic mice upon RA treatment. Tretinoin 144-146 lysine (K)-specific demethylase 1A Mus musculus 70-74
32255397-4 2020 Moreover, in C3H tumor-bearing mice, ATRA-PLGA-PEG-PD-L1 nanoparticles more specifically targeted tumor cells, enhanced anticancer activity and reduced side effects when compared with free ATRA. Tretinoin 37-41 CD274 antigen Mus musculus 51-56
31953222-9 2020 Reduced retinoic acid receptor (RXRalpha) signaling also increases conjunctival monocyte infiltration, IFN-gamma expression and goblet cell loss. Tretinoin 8-21 interferon gamma Mus musculus 103-112
31904486-0 2020 All-trans retinoic acid exerts selective anti-FLT3-ITD acute myeloid leukemia efficacy through downregulating Chk1 kinase. Tretinoin 0-23 fms related receptor tyrosine kinase 3 Homo sapiens 46-50
31904486-0 2020 All-trans retinoic acid exerts selective anti-FLT3-ITD acute myeloid leukemia efficacy through downregulating Chk1 kinase. Tretinoin 0-23 checkpoint kinase 1 Homo sapiens 110-114
31904486-2 2020 In this work, we report that ATRA causes fatal mitotic catastrophe in FLT3-ITD AML cells by degrading Chk1 kinase, and therefore preventing DNA damage repair. Tretinoin 29-33 fms related receptor tyrosine kinase 3 Homo sapiens 70-74
31904486-2 2020 In this work, we report that ATRA causes fatal mitotic catastrophe in FLT3-ITD AML cells by degrading Chk1 kinase, and therefore preventing DNA damage repair. Tretinoin 29-33 checkpoint kinase 1 Homo sapiens 102-106
31904486-6 2020 Taken together, our results indicate that ATRA down-regulates Chk1 in FLT3-ITD AML cells, and the combination of ATRA and SN38 significantly improves the anti-tumor effect of either ATRA or SN38 when used alone. Tretinoin 42-46 checkpoint kinase 1 Homo sapiens 62-66
32251364-11 2020 MYT1 is, therefore, a promising therapeutic target for enhancing the neurite-inducing effect of retinoic acid and for inhibiting the growth of neuroblastoma. Tretinoin 96-109 myelin transcription factor 1 Homo sapiens 0-4
32272634-6 2020 Importantly, these protective effects of NAS were abrogated by Atra, an inhibitor of Nrf2, indicating a dependence on Nrf2 signaling. Tretinoin 63-67 NFE2 like bZIP transcription factor 2 Homo sapiens 85-89
32272634-6 2020 Importantly, these protective effects of NAS were abrogated by Atra, an inhibitor of Nrf2, indicating a dependence on Nrf2 signaling. Tretinoin 63-67 NFE2 like bZIP transcription factor 2 Homo sapiens 118-122
31731254-4 2020 The results showed that 10 nM ATRA sufficiently inhibited cell proliferation, which might be through downregulation of cyclin D1 (P < 0.05) and cyclin-dependent kinase 4 (P < 0.05) and proliferating cell nuclear antigen protein (P < 0.05) abundance. Tretinoin 30-34 cyclin-dependent kinase 4 Ovis aries 147-172
32236320-11 2020 CONCLUSION: ATRA has a protective effect on renal ischemia-reperfusion injury in diabetic rats, maybe relating to DJ/Nrf2 pathway. Tretinoin 12-16 NFE2 like bZIP transcription factor 2 Rattus norvegicus 117-121
31980418-1 2020 BACKGROUND: T helper 17 (Th17) cells are a subset of CD4-positive T cells, which secrete interleukin 17 and specifically express the retinoic acid receptor-related orphan receptors gammat gene. Tretinoin 133-146 CD4 molecule Homo sapiens 53-56
32256976-8 2020 Roscovitine also enhanced the ATRA-induced nuclear enrichment of other signaling molecules traditionally perceived as cytoplasmic promoters of proliferation, but now known to promote differentiation; in particular: SFKs, Lyn, Fgr; adaptor proteins, c-Cbl, SLP-76; a guanine exchange factor, Vav1; and a transcription factor, IRF-1. Tretinoin 30-34 interferon regulatory factor 1 Homo sapiens 325-330
32256976-10 2020 Lyn-pS608RB association was greatly diminished by ATRA and essentially lost in ATRA plus roscovitine treated cells. Tretinoin 50-54 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3
32256976-11 2020 Interestingly Lyn-KD enhanced such ATRA-induced nuclear signaling and differentiation and made roscovitine more effective. Tretinoin 35-39 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 14-17
32266229-8 2020 atRA release from scaffolds led to an increase in mucociliary gene expression at high scaffold loading doses, with augmented MUC5AC and FOXJ1 detected by RT-PCR. Tretinoin 0-4 forkhead box J1 Homo sapiens 136-141
32258025-1 2020 Organogenesis, including renal development, requires an appropriate retinoic acid concentration, which is established by differential expression of aldehyde dehydrogenase 1 family member A2 (ALDH1A2) and cytochrome P450 family 26 subfamily A/B/C member 1 (CYP26A1/B1/C1). Tretinoin 68-81 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 256-263
32151018-0 2020 Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes. Tretinoin 11-24 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 91-96
32151018-1 2020 This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration. Tretinoin 76-89 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 39-67
32151018-1 2020 This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration. Tretinoin 76-89 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 69-74
32151018-1 2020 This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration. Tretinoin 91-93 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 39-67
32151018-1 2020 This review focuses on the role of the Cytochrome p450 subfamily 26 (CYP26) retinoic acid (RA) degrading enzymes during development and regeneration. Tretinoin 91-93 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 69-74
32151018-2 2020 Cyp26 enzymes, along with retinoic acid synthesising enzymes, are absolutely required for RA homeostasis in these processes by regulating availability of RA for receptor binding and signalling. Tretinoin 26-39 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
32151018-2 2020 Cyp26 enzymes, along with retinoic acid synthesising enzymes, are absolutely required for RA homeostasis in these processes by regulating availability of RA for receptor binding and signalling. Tretinoin 90-92 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
32151018-2 2020 Cyp26 enzymes, along with retinoic acid synthesising enzymes, are absolutely required for RA homeostasis in these processes by regulating availability of RA for receptor binding and signalling. Tretinoin 154-156 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
32151018-3 2020 Cyp26 enzymes are necessary to generate RA gradients and to protect specific tissues from RA signalling. Tretinoin 40-42 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
32151018-3 2020 Cyp26 enzymes are necessary to generate RA gradients and to protect specific tissues from RA signalling. Tretinoin 90-92 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
32151018-5 2020 Here, the function of CYP26 enzymes is discussed in the context of the RA signalling pathway, enzymatic structure and biochemistry, human genetic disease, and function in development and regeneration as elucidated from animal model studies. Tretinoin 71-73 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 22-27
32256976-8 2020 Roscovitine also enhanced the ATRA-induced nuclear enrichment of other signaling molecules traditionally perceived as cytoplasmic promoters of proliferation, but now known to promote differentiation; in particular: SFKs, Lyn, Fgr; adaptor proteins, c-Cbl, SLP-76; a guanine exchange factor, Vav1; and a transcription factor, IRF-1. Tretinoin 30-34 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 221-224
32256976-8 2020 Roscovitine also enhanced the ATRA-induced nuclear enrichment of other signaling molecules traditionally perceived as cytoplasmic promoters of proliferation, but now known to promote differentiation; in particular: SFKs, Lyn, Fgr; adaptor proteins, c-Cbl, SLP-76; a guanine exchange factor, Vav1; and a transcription factor, IRF-1. Tretinoin 30-34 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 226-229
32168763-5 2020 The amount of secreted TNF-alpha in the supernatant of NB4 TG2 knockout cells was close to 50 times lower than in ATRA-treated differentiated wild-type NB4 cells. Tretinoin 114-118 tumor necrosis factor Homo sapiens 23-32
32168763-6 2020 The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1beta and TNF-alpha 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. Tretinoin 216-220 transglutaminase 2 Homo sapiens 30-33
32168763-6 2020 The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1beta and TNF-alpha 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. Tretinoin 216-220 tumor necrosis factor Homo sapiens 156-165
31634391-2 2020 All-trans retinoic acid (ATRA), a key vitamin A metabolite, was earlier shown by us to stimulate DRA expression in intestinal epithelial cells. Tretinoin 0-23 solute carrier family 26 member 3 Homo sapiens 97-100
31634391-2 2020 All-trans retinoic acid (ATRA), a key vitamin A metabolite, was earlier shown by us to stimulate DRA expression in intestinal epithelial cells. Tretinoin 25-29 solute carrier family 26 member 3 Homo sapiens 97-100
31634391-4 2020 AIMS: Our aim was to analyze the efficacy of ATRA in counteracting inflammation-induced decrease in DRA in vitro and in vivo. Tretinoin 45-49 solute carrier family 26 member 3 Homo sapiens 100-103
31634391-6 2020 The effect of ATRA on IFN-gamma-mediated inhibition of DRA function, expression, and promoter activity were elucidated. Tretinoin 14-18 interferon gamma Homo sapiens 22-31
31634391-6 2020 The effect of ATRA on IFN-gamma-mediated inhibition of DRA function, expression, and promoter activity were elucidated. Tretinoin 14-18 solute carrier family 26 member 3 Homo sapiens 55-58
31634391-8 2020 RESULTS: All-trans retinoic acid (10 muM, 24 h) abrogated IFN-gamma (30 ng/mL, 24 h)-induced decrease in DRA function, expression, and promoter activity in Caco-2 cells. Tretinoin 9-32 interferon gamma Homo sapiens 58-67
31634391-8 2020 RESULTS: All-trans retinoic acid (10 muM, 24 h) abrogated IFN-gamma (30 ng/mL, 24 h)-induced decrease in DRA function, expression, and promoter activity in Caco-2 cells. Tretinoin 9-32 solute carrier family 26 member 3 Homo sapiens 105-108
31634391-9 2020 All-trans retinoic acid altered IFN-gamma signaling via blocking IFN-gamma-induced tyrosine phosphorylation of STAT-1. Tretinoin 0-23 interferon gamma Homo sapiens 32-41
31634391-9 2020 All-trans retinoic acid altered IFN-gamma signaling via blocking IFN-gamma-induced tyrosine phosphorylation of STAT-1. Tretinoin 0-23 interferon gamma Homo sapiens 65-74
32016357-0 2020 All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b). Tretinoin 10-23 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 125-130
32194732-11 2020 Furthermore, ADH7 and CYP26B1 were enriched in the retinoic acid metabolic process and the retinol metabolism pathway. Tretinoin 51-64 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 22-29
31957262-11 2020 Co-administration of ATRA and Hst1 was associated with significantly higher metabolic activity, DNA content and ALP activity than either ATRA or Hst1 alone. Tretinoin 21-25 alkaline phosphatase, placental Homo sapiens 112-115
31801970-1 2020 Midkine is a heparin-binding growth factor, originally reported as the product of a retinoic acid-responsive gene during embryogenesis, but currently viewed as a multifaceted factor contributing to both normal tissue homeostasis and disease development. Tretinoin 84-97 midkine Homo sapiens 0-7
32016357-3 2020 In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. Tretinoin 61-84 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 149-154
32016357-3 2020 In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. Tretinoin 86-90 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 149-154
32016357-4 2020 In VAD rats, the intestinal Pi uptake activity and the expression of Npt2b were increased, but were reduced by the administration of ATRA. Tretinoin 133-137 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 69-74
32016357-9 2020 Together, these results suggest that ATRA may reduce the intestinal Pi uptake by preventing C/EBP activation of the intestinal Npt2b gene. Tretinoin 37-41 solute carrier family 34 (sodium phosphate), member 2 Mus musculus 127-132
32001436-4 2020 Here, we investigate the role of the RA catabolizing protein Cyp26b1 in the lung. Tretinoin 37-39 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 61-68
32007421-9 2020 Cardioprotective potential of rosuvastatin and retinoic acid could be attributed to their influence on the redox pathways, immunomodulation, membrane stability, Nrf2 preservation, iNOS and Bax expression levels. Tretinoin 47-60 NFE2 like bZIP transcription factor 2 Rattus norvegicus 161-165
32007421-9 2020 Cardioprotective potential of rosuvastatin and retinoic acid could be attributed to their influence on the redox pathways, immunomodulation, membrane stability, Nrf2 preservation, iNOS and Bax expression levels. Tretinoin 47-60 nitric oxide synthase 2 Rattus norvegicus 180-184
32190725-5 2020 Data analysis revealed that the expression of OCC-1 was reduced by about 69% after 4-day treatment with RA, when significant down-regulation of key pluripotency factors, including OCT4 and Nanog was observed [1]. Tretinoin 104-106 Nanog homeobox Mus musculus 189-194
32001436-9 2020 These data suggest that defects observed in Cyp26b1-/- lungs are caused by both RA-dependent and RA-independent mechanisms. Tretinoin 80-82 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 44-51
32001436-9 2020 These data suggest that defects observed in Cyp26b1-/- lungs are caused by both RA-dependent and RA-independent mechanisms. Tretinoin 97-99 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 44-51
31801802-11 2020 In conclusion, these results have demonstrated the therapeutic potential of retinoic acid on RA FLS provided TNF could be counterbalanced, either with high ATRA doses or with TNF inhibitors. Tretinoin 76-89 tumor necrosis factor Homo sapiens 109-112
32027669-6 2020 Use in situ hybridization to resolve effects on mRNA distributions of Aldh1a2 and Cyp26a1 (RA homeostasis); Hoxb1 and Pax6 (RA targets). Tretinoin 124-126 paired box 6 Mus musculus 118-122
31913463-3 2020 We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1.Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. Tretinoin 291-304 paired like homeodomain factor 1 Mus musculus 135-140
31913463-3 2020 We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1.Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. Tretinoin 291-304 paired like homeodomain factor 1 Mus musculus 141-146
31955210-12 2020 Moreover, the budding rates, buddings number per organoid, and Chromogranin A and Muc2 expression of piglet intestinal organoids were significantly reduced (P < 0.05) by VA and its metabolites (retinoic acid). Tretinoin 194-207 chromogranin A Homo sapiens 63-77
31959382-10 2020 Importantly, RALDH1/ALDH1A1 enzyme oxidizing retinaldehyde to retinoic acid, an inducer of Tregs, was preferentially expressed by CD11b-CD103- DCs and its expression levels were elevated in bleomycin-injected skin lesions, to a greater extent in Cd103-/- mice than in wild-type mice. Tretinoin 62-75 integrin alpha M Mus musculus 130-135
31959382-10 2020 Importantly, RALDH1/ALDH1A1 enzyme oxidizing retinaldehyde to retinoic acid, an inducer of Tregs, was preferentially expressed by CD11b-CD103- DCs and its expression levels were elevated in bleomycin-injected skin lesions, to a greater extent in Cd103-/- mice than in wild-type mice. Tretinoin 62-75 integrin alpha E, epithelial-associated Mus musculus 136-141
31959382-10 2020 Importantly, RALDH1/ALDH1A1 enzyme oxidizing retinaldehyde to retinoic acid, an inducer of Tregs, was preferentially expressed by CD11b-CD103- DCs and its expression levels were elevated in bleomycin-injected skin lesions, to a greater extent in Cd103-/- mice than in wild-type mice. Tretinoin 62-75 integrin alpha E, epithelial-associated Mus musculus 246-251
32030959-17 2020 qRT-PCR test showed that the combined use of ATRA and Ad-VEGF also increased the relative mRNA expressions of early-stage osteogenesis-related markers ALP, OPN, and collagen type I ( P<0.05); the relative mRNA expressions of angiogenesis-related markers VEGF, EMCN, and ANGPT1 increased at 7 days ( P<0.05). Tretinoin 45-49 endomucin Mus musculus 263-267
32030959-17 2020 qRT-PCR test showed that the combined use of ATRA and Ad-VEGF also increased the relative mRNA expressions of early-stage osteogenesis-related markers ALP, OPN, and collagen type I ( P<0.05); the relative mRNA expressions of angiogenesis-related markers VEGF, EMCN, and ANGPT1 increased at 7 days ( P<0.05). Tretinoin 45-49 angiopoietin 1 Mus musculus 273-279
31837824-0 2020 Retinoic acid-loaded NFL-lipid nanocapsules promote oligodendrogenesis in focal white matter lesion. Tretinoin 0-13 neurofilament light chain Rattus norvegicus 21-24
31837824-5 2020 The aim of this work was to induce endogenous NSC differentiation by specifically delivering retinoic acid (RA) to SVZ-NSC via NFL-LNC. Tretinoin 93-106 neurofilament light chain Rattus norvegicus 127-130
31837824-5 2020 The aim of this work was to induce endogenous NSC differentiation by specifically delivering retinoic acid (RA) to SVZ-NSC via NFL-LNC. Tretinoin 108-110 neurofilament light chain Rattus norvegicus 127-130
31837824-6 2020 RA was successfully encapsulated into NFL-LNC and RA-NFL-LNC were incubated with primary rat SVZ-NSC. Tretinoin 0-2 neurofilament light chain Rattus norvegicus 38-41
31837824-6 2020 RA was successfully encapsulated into NFL-LNC and RA-NFL-LNC were incubated with primary rat SVZ-NSC. Tretinoin 50-52 neurofilament light chain Rattus norvegicus 53-56
31837824-7 2020 In vitro, RA-NFL-LNC decreased the number of nestin+ (NSC marker) cells and neurospheres compared to controls and increased the number of GalC+ (oligodendrocytic marker) cells. Tretinoin 10-12 neurofilament light chain Rattus norvegicus 13-16
31837824-8 2020 Then, RA-NFL-LNC were injected in the right lateral ventricle of a lysolecithin-induced rat focal white matter lesion model to evaluate their impact on oligodendrocyte repopulation and remyelination. Tretinoin 6-8 neurofilament light chain Rattus norvegicus 9-12
31837824-9 2020 RA-NFL-LNC significantly increased the percentage of mature oligodendrocytes, stimulating oligodendrogenesis, nearly to the pre-lesion levels. Tretinoin 0-2 neurofilament light chain Rattus norvegicus 3-6
31837824-10 2020 Thus, RA-NFL-LNC represent a promising nanomedicine to be further investigated in the treatment of demyelinating diseases. Tretinoin 6-8 neurofilament light chain Rattus norvegicus 9-12
31913463-0 2020 PROP1-Dependent Retinoic Acid Signaling Regulates Developmental Pituitary Morphogenesis and Hormone Expression. Tretinoin 16-29 paired like homeodomain factor 1 Mus musculus 0-5
31913463-3 2020 We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1.Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. Tretinoin 18-31 paired like homeodomain factor 1 Mus musculus 135-140
31913463-3 2020 We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1.Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. Tretinoin 18-31 paired like homeodomain factor 1 Mus musculus 141-146
31633442-5 2020 Knockdown of the pattern recognition receptors, retinoic acid-inducible gene I and melanoma differentiation-associated protein 5 or their intermediary signaling protein mitochondrial antiviral-signaling protein (MAVS) blocked IFN production. Tretinoin 48-61 interferon alpha 1 Homo sapiens 226-229
31801802-11 2020 In conclusion, these results have demonstrated the therapeutic potential of retinoic acid on RA FLS provided TNF could be counterbalanced, either with high ATRA doses or with TNF inhibitors. Tretinoin 76-89 tumor necrosis factor Homo sapiens 175-178
31936807-5 2020 Retinoic acid induced differentiation of ES cells, decreased the short form of NFYA (NFYAs), increased phosphorylation of STAT3, and decreased B3GALT5-LTR expression. Tretinoin 0-13 signal transducer and activator of transcription 3 Homo sapiens 122-127
31899223-9 2020 At the same time, All-trans retinoic acid (ATRA), which has the properties of pro-differentiation and inhibition of invasion and metastasis, upregulated the expression of PD-L1 and E-cadherin. Tretinoin 18-41 cadherin 1 Homo sapiens 181-191
31899223-9 2020 At the same time, All-trans retinoic acid (ATRA), which has the properties of pro-differentiation and inhibition of invasion and metastasis, upregulated the expression of PD-L1 and E-cadherin. Tretinoin 43-47 cadherin 1 Homo sapiens 181-191
32476372-0 2020 [The role of ZFP580 in the regulation of rat VSMCs migration by ATRA and its mechanism]. Tretinoin 64-68 zinc finger protein 580 Rattus norvegicus 13-19
32476372-1 2020 OBJECTIVE: To investigate the probable roles of the novel C2H2 zinc finger transcription factor ZFP580 on all-transretinoic acid (ATRA)-regulated VSMCs migration and underlying mechanisms. Tretinoin 106-128 zinc finger protein 580 Rattus norvegicus 96-102
32476372-1 2020 OBJECTIVE: To investigate the probable roles of the novel C2H2 zinc finger transcription factor ZFP580 on all-transretinoic acid (ATRA)-regulated VSMCs migration and underlying mechanisms. Tretinoin 130-134 zinc finger protein 580 Rattus norvegicus 96-102
32476372-6 2020 ZFP580 protein expression in VSMCs was detected under ATRA stimulation when ERK inhibitor PD98059 was used to inhibit the protein expression of ERK. Tretinoin 54-58 zinc finger protein 580 Rattus norvegicus 0-6
32476372-6 2020 ZFP580 protein expression in VSMCs was detected under ATRA stimulation when ERK inhibitor PD98059 was used to inhibit the protein expression of ERK. Tretinoin 54-58 Eph receptor B1 Rattus norvegicus 76-79
32476372-10 2020 Compared with the control group, VSMCs treated by 20 mumol/L ATRA reduced the cell migration by 49%, 36% and 22% at 24, 48 and 72 h. The mRNA and protein expression levels of ZFP580 were increased with the increase of ATRA stimulation solubility and the extension of stimulation time. Tretinoin 61-65 zinc finger protein 580 Rattus norvegicus 175-181
32476372-10 2020 Compared with the control group, VSMCs treated by 20 mumol/L ATRA reduced the cell migration by 49%, 36% and 22% at 24, 48 and 72 h. The mRNA and protein expression levels of ZFP580 were increased with the increase of ATRA stimulation solubility and the extension of stimulation time. Tretinoin 218-222 zinc finger protein 580 Rattus norvegicus 175-181
32476372-11 2020 ERK was increased significantly after 15 min of ATRA stimulation. Tretinoin 48-52 Eph receptor B1 Rattus norvegicus 0-3
32476372-12 2020 Pretreatment with ERK inhibitor PD98059 (20 mumol/L) inhibited the expression of ERK protein and reduced the expression of ATRA-induced ZFP580 protein. Tretinoin 123-127 Eph receptor B1 Rattus norvegicus 18-21
32476372-12 2020 Pretreatment with ERK inhibitor PD98059 (20 mumol/L) inhibited the expression of ERK protein and reduced the expression of ATRA-induced ZFP580 protein. Tretinoin 123-127 zinc finger protein 580 Rattus norvegicus 136-142
32476372-14 2020 CONCLUSION: ATRA increased the expression of ZFP580 through the ERK signaling pathway, while ZFP580 was involved in ATRA"s inhibition of VSMCs migration by affecting the expression of downstream MMP-2 and MMP-9. Tretinoin 12-16 zinc finger protein 580 Rattus norvegicus 45-51
32476372-14 2020 CONCLUSION: ATRA increased the expression of ZFP580 through the ERK signaling pathway, while ZFP580 was involved in ATRA"s inhibition of VSMCs migration by affecting the expression of downstream MMP-2 and MMP-9. Tretinoin 12-16 Eph receptor B1 Rattus norvegicus 64-67
32476372-14 2020 CONCLUSION: ATRA increased the expression of ZFP580 through the ERK signaling pathway, while ZFP580 was involved in ATRA"s inhibition of VSMCs migration by affecting the expression of downstream MMP-2 and MMP-9. Tretinoin 116-120 zinc finger protein 580 Rattus norvegicus 93-99
32158187-8 2020 Dose-dependent assays show ER-50891 could also rescue ATRA inhibited OCN expression and mineralization with or without the induction of BMP. Tretinoin 54-58 bone gamma-carboxyglutamate protein Homo sapiens 69-72
32158187-9 2020 ER-50891 also suppressed the ALP activity that was synergistically enhanced by BMP and ATRA. Tretinoin 87-91 alkaline phosphatase, placental Homo sapiens 29-32
31936807-8 2020 Retinoic acid decreased the binding of NFYA to B3GALT5-LTR promoter and increased phospho-STAT3 binding. Tretinoin 0-13 signal transducer and activator of transcription 3 Homo sapiens 90-95
31936807-11 2020 Repression of SSEA3 and sialyl Lewis a synthesis mediated by retinoic acid was partially reversed by lamin A short interfering RNA (siRNA) and a STAT3 inhibitor. Tretinoin 61-74 signal transducer and activator of transcription 3 Homo sapiens 145-150
31629555-0 2020 Corrigendum to "Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP" [Gene 551 (2014) 230-235]. Tretinoin 36-40 interleukin 6 Homo sapiens 49-53
31629555-0 2020 Corrigendum to "Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP" [Gene 551 (2014) 230-235]. Tretinoin 36-40 DNA damage inducible transcript 3 Homo sapiens 119-123
31896743-2 2020 We found that formation of striolar/central zones during embryogenesis requires Cytochrome P450 26b1 (Cyp26b1)-mediated degradation of retinoic acid (RA). Tretinoin 135-148 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 80-100
31896743-2 2020 We found that formation of striolar/central zones during embryogenesis requires Cytochrome P450 26b1 (Cyp26b1)-mediated degradation of retinoic acid (RA). Tretinoin 135-148 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 102-109
31896743-2 2020 We found that formation of striolar/central zones during embryogenesis requires Cytochrome P450 26b1 (Cyp26b1)-mediated degradation of retinoic acid (RA). Tretinoin 150-152 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 80-100
31896743-2 2020 We found that formation of striolar/central zones during embryogenesis requires Cytochrome P450 26b1 (Cyp26b1)-mediated degradation of retinoic acid (RA). Tretinoin 150-152 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 102-109
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 mitogen-activated protein kinase 1 Mus musculus 109-147
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 mitogen-activated protein kinase 1 Mus musculus 149-152
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 mitogen-activated protein kinase 1 Mus musculus 109-147
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 thymoma viral proto-oncogene 1 Mus musculus 176-183
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 mitogen-activated protein kinase 1 Mus musculus 149-152
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 thymoma viral proto-oncogene 1 Mus musculus 176-183
33268713-2 2020 We previously reported that the combined therapy of oral immune therapy (OIT) and kakkonto downregulates the mRNA expression of Cyp26b1, a major retinoic acid (RA)-degrading enzyme, in the colon of food allergy mice and thereby ameliorates allergic symptoms. Tretinoin 145-158 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 128-135
33268713-2 2020 We previously reported that the combined therapy of oral immune therapy (OIT) and kakkonto downregulates the mRNA expression of Cyp26b1, a major retinoic acid (RA)-degrading enzyme, in the colon of food allergy mice and thereby ameliorates allergic symptoms. Tretinoin 160-162 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 128-135
32568176-10 2020 Moreover, miR-638, which is specifically downregulated in APL cell lines, was upregulated after all-trans retinoic acid (ATRA)-induced myeloid differentiation. Tretinoin 106-119 microRNA 638 Homo sapiens 10-17
32568176-10 2020 Moreover, miR-638, which is specifically downregulated in APL cell lines, was upregulated after all-trans retinoic acid (ATRA)-induced myeloid differentiation. Tretinoin 121-125 microRNA 638 Homo sapiens 10-17
32640966-8 2020 TH, dopamine -hydroxylase and vesicular monoamine transporter-2 were also significantly upregulated in ST-differentiated cells compared to both undifferentiated and retinoic acid (RA)-differentiated cells. Tretinoin 166-179 tyrosine hydroxylase Homo sapiens 0-2
32640966-8 2020 TH, dopamine -hydroxylase and vesicular monoamine transporter-2 were also significantly upregulated in ST-differentiated cells compared to both undifferentiated and retinoic acid (RA)-differentiated cells. Tretinoin 181-183 tyrosine hydroxylase Homo sapiens 0-2
32640966-9 2020 RA induced the highest number of CHT1-immunoreactive cells while ST- and BDNF-differentiation reduced CHT1-immunoreactive cells, indicating a decrease in the cholinergic phenotype. Tretinoin 0-2 solute carrier family 5 member 7 Homo sapiens 33-37
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 interleukin 6 Rattus norvegicus 57-61
33583383-7 2020 RESULTS: We observed significantly higher morphological resilience against Amyloid Beta toxicity in cells which were differentiated by both Retinoic Acid and Brain Derived Neurotrophic Factor compared to Retinoic Acid only. Tretinoin 140-153 amyloid beta precursor protein Homo sapiens 75-87
33583383-7 2020 RESULTS: We observed significantly higher morphological resilience against Amyloid Beta toxicity in cells which were differentiated by both Retinoic Acid and Brain Derived Neurotrophic Factor compared to Retinoic Acid only. Tretinoin 204-217 amyloid beta precursor protein Homo sapiens 75-87
33583383-8 2020 However, the electrophysiological properties of the Retinoic Acid + Brain-Derived Neurotrophic Factor differentiated cells were significantly altered after Amyloid Beta treatment. Tretinoin 52-65 amyloid beta precursor protein Homo sapiens 156-168
31518508-5 2020 The protective effect of RA on GDM cardiomyopathy was related to the decreased MDA content and ROS generation, the increased GSH-Px and SOD content as well as the reduced TNF-alpha and IL-1beta content and inhibition of NF-kappaB signaling. Tretinoin 25-27 tumor necrosis factor Mus musculus 171-180
31518508-5 2020 The protective effect of RA on GDM cardiomyopathy was related to the decreased MDA content and ROS generation, the increased GSH-Px and SOD content as well as the reduced TNF-alpha and IL-1beta content and inhibition of NF-kappaB signaling. Tretinoin 25-27 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 220-229
31518508-7 2020 In conclusion, RA treatment could increase the activity of the antioxidant enzyme and suppress the oxidative stress, inflammation response, and activation of NF-kappaB signaling, thereby improving blood glucose level and cardiac injury of GDM mice before and after delivery. Tretinoin 15-17 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 158-167
32863302-0 2020 Effects of All-Trans Retinoic Acid on the Optimization of Synovial Explant Induced by Tumor Necrosis Factor Alpha. Tretinoin 11-34 tumor necrosis factor Rattus norvegicus 86-113
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 7-11 interleukin 6 Rattus norvegicus 57-61
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 interleukin 6 Rattus norvegicus 57-61
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 BCL2, apoptosis regulator Rattus norvegicus 106-111
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 BCL2, apoptosis regulator Rattus norvegicus 106-111
32863302-9 2020 In short, ATRA inhibited TNF-alpha induced synovitis by the regulation of inflammatory cytokines and inhibiting NF-kappaB signal transduction and potentially promoting autophagy, apoptosis and angiogenesis, displaying its role in alleviating synovial inflammation in patients with RA. Tretinoin 10-14 tumor necrosis factor Homo sapiens 25-34
32863302-9 2020 In short, ATRA inhibited TNF-alpha induced synovitis by the regulation of inflammatory cytokines and inhibiting NF-kappaB signal transduction and potentially promoting autophagy, apoptosis and angiogenesis, displaying its role in alleviating synovial inflammation in patients with RA. Tretinoin 10-14 nuclear factor kappa B subunit 1 Homo sapiens 112-121
32521127-1 2020 CYP26B1 is a member of the cytochrome P450 family and is responsible for the break-down of retinoic acid for which appropriate levels are important for normal development of the cardiovascular and lymphatic systems. Tretinoin 91-104 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-7
32175266-9 2020 It was found that the use of retinoic acid led to the highest expression of C-kit, SSEA4, VASA genes and lower expression of Oct4. Tretinoin 29-42 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 76-81
32521127-6 2020 Balanced levels of retinoic acid maintained by CYP26B1 are crucial for the lymphatic system. Tretinoin 19-32 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 47-54
31744925-0 2020 Correction to "Induction of CYP26A1 by Metabolites of Retinoic Acid: Evidence That CYP26A1 Is an Important Enzyme in the Elimination of Active Retinoids". Tretinoin 54-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 28-35
31619506-7 2020 Pathway analysis implicated the MAPK13/p38delta and retinoic acid regulatory nodes, which were confirmed to display divergent responses in different HER2+ cancer lines. Tretinoin 52-65 erb-b2 receptor tyrosine kinase 2 Homo sapiens 149-153
31744925-0 2020 Correction to "Induction of CYP26A1 by Metabolites of Retinoic Acid: Evidence That CYP26A1 Is an Important Enzyme in the Elimination of Active Retinoids". Tretinoin 54-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 83-90
31755607-2 2020 CYP26B1 degrades retinoic acid in the testis during prenatal development preventing meiosis initiation. Tretinoin 17-30 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
31950055-8 2019 Anti-CD14 antibody treatment prior to ATRA and flagellin treatments completely abolished ATRA-enhanced TNF-alpha and IL-1beta production. Tretinoin 89-93 tumor necrosis factor Homo sapiens 103-112
31501521-0 2020 Targeting the TR4 nuclear receptor-mediated lncTASR/AXL signaling with tretinoin increases the sunitinib sensitivity to better suppress the RCC progression. Tretinoin 71-80 nuclear receptor subfamily 2 group C member 2 Homo sapiens 14-17
31501521-6 2020 Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression. Tretinoin 238-247 nuclear receptor subfamily 2 group C member 2 Homo sapiens 183-186
31501521-6 2020 Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression. Tretinoin 238-247 nuclear receptor subfamily 2 group C member 2 Homo sapiens 183-186
31501521-6 2020 Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression. Tretinoin 432-441 nuclear receptor subfamily 2 group C member 2 Homo sapiens 183-186
31501521-6 2020 Human clinical surveys also linked the expression of TR4, lncTASR, and AXL to the RCC survival, and results from multiple RCC cell lines revealed that targeting this newly identified TR4-mediated signaling with small molecules, including tretinoin, metformin, or TR4-shRNAs, all led to increase the sunitinib sensitivity to better suppress the RCC progression, and our preclinical study using the in vivo mouse model further proved tretinoin had a better synergistic effect to increase sunitinib sensitivity to suppress RCC progression. Tretinoin 432-441 nuclear receptor subfamily 2 group C member 2 Homo sapiens 183-186
31950055-0 2019 All-Trans Retinoic Acid Enhances Bacterial Flagellin-Stimulated Proinflammatory Responses in Human Monocyte THP-1 Cells by Upregulating CD14. Tretinoin 0-23 GLI family zinc finger 2 Homo sapiens 108-113
31950055-2 2019 In this study, we examined the immune potentiating effect of ATRA on bacterial flagellin-induced NF-kappaB activation and proinflammatory cytokine production in human monocytic cell line THP-1. Tretinoin 61-65 GLI family zinc finger 2 Homo sapiens 187-192
31950055-3 2019 ATRA treatment significantly enhanced the flagellin-induced NF-kappaB/AP-1 activity in THP-1 via the RAR/RXR pathway. Tretinoin 0-4 GLI family zinc finger 2 Homo sapiens 87-92
31950055-8 2019 Anti-CD14 antibody treatment prior to ATRA and flagellin treatments completely abolished ATRA-enhanced TNF-alpha and IL-1beta production. Tretinoin 89-93 interleukin 1 beta Homo sapiens 117-125
31950055-4 2019 Similarly, ATRA enhanced the expression and production of TNF-alpha and IL-1beta in THP-1 cells upon flagellin challenge. Tretinoin 11-15 tumor necrosis factor Homo sapiens 58-67
31950055-4 2019 Similarly, ATRA enhanced the expression and production of TNF-alpha and IL-1beta in THP-1 cells upon flagellin challenge. Tretinoin 11-15 interleukin 1 beta Homo sapiens 72-80
31950055-9 2019 Our results suggest that ATRA enhances flagellin-stimulated proinflammatory responses in human monocyte THP-1 cells by upregulating CD14 in a RAR/RXR-dependent manner. Tretinoin 25-29 GLI family zinc finger 2 Homo sapiens 104-109
31950055-4 2019 Similarly, ATRA enhanced the expression and production of TNF-alpha and IL-1beta in THP-1 cells upon flagellin challenge. Tretinoin 11-15 GLI family zinc finger 2 Homo sapiens 84-89
31950055-6 2019 To determine the mechanisms underlying the ATRA-enhanced immune response against bacterial flagellin despite the reduced cell surface expression of TLR5 in ATRA-treated THP-1, we examined the cell surface expression of CD14, which has been proposed to be a TLR co-receptor that enhances the response to microbial components. Tretinoin 156-160 GLI family zinc finger 2 Homo sapiens 169-174
31596288-7 2019 Luciferase report showed RA binding to RARalpha regulated stimulated by RA 8 (Stra8) promoter activity during SSC formation, while mutations in RAR binding sites inhibited the Stra8 expression and SSC formation. Tretinoin 25-27 stimulated by retinoic acid 8 Gallus gallus 58-76
31834935-0 2019 Retinoic acid synergizes with the unfolded protein response and oxidative stress to induce cell death in FLT3-ITD+ AML. Tretinoin 0-13 fms related receptor tyrosine kinase 3 Homo sapiens 105-109
31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tretinoin 71-84 fms related receptor tyrosine kinase 3 Homo sapiens 336-340
31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tretinoin 86-88 fms related receptor tyrosine kinase 3 Homo sapiens 336-340
31834935-6 2019 Our data provide a proof of concept that low amounts of drugs that generate ER and oxidative stresses combined with RA could be an effective targeted therapy to hit AML cells characterized by MLL fusion proteins and FLT3-ITD mutation. Tretinoin 116-118 fms related receptor tyrosine kinase 3 Homo sapiens 216-220
31810919-6 2019 Importantly, PLX4032, when used in combination with ATRA, an inhibitor of PIN1, reduced EGFR expression, and consequently reduced cell viability and anchorage-independent growth of A375R cells compared to PLX4032 alone. Tretinoin 52-56 epidermal growth factor receptor Homo sapiens 88-92
31810919-7 2019 Furthermore, co-treatment with ATRA and PLX4032 increased cleaved PARP and DNA fragmentation in A375R cells. Tretinoin 31-35 poly(ADP-ribose) polymerase 1 Homo sapiens 66-70
31749343-4 2019 Moreover, we found that mRNA expression of retinoic acid-specific hydroxylase CYP26b1 was dose-dependently up-regulated by atRal exposure in RPE cells, indicating that atRA inactivation may be also initiated in atRal-accumulated RPE cells. Tretinoin 43-56 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 78-85
31752312-8 2019 By analyzing whole-genome transcriptome alterations of the Rybp-/- embryonic stem (ES) cells and correlating this data with experimentally identified binding sites of ncPRC1.6 subunits and retinoic acid receptors in ES cells, we propose a model how germ-cell-specific transcription can be governed by an RYBP centered regulatory network, underlining the possible role of RYBP in germ cell differentiation and tumorigenesis. Tretinoin 189-202 RING1 and YY1 binding protein Homo sapiens 59-63
31586630-5 2019 In Peyer"s patches (PP), ATRA/TGF-beta MPs up-regulated tolerogenic dendritic cells (tolDCs) (CD11c+CD11b-CD103+), while the proportion of mature dendritic cells was not altered. Tretinoin 25-29 integrin alpha M Mus musculus 100-105
31586630-9 2019 Moreover, ATRA/TGF-beta MPs treatment resulted in increased Treg proliferation and frequency of CTLA-4+PD1+ and CD39+IL-10+ Tregs, suggestive of their higher suppressive capacity. Tretinoin 10-14 interleukin 10 Mus musculus 117-122
31586630-11 2019 In conclusion, oral application of ATRA/TGF-beta MPs ameliorated T1D through potentiation of tolDCs and Tregs, inhibition of Th1 response and prevention of the immune cell entrance into the islets. Tretinoin 35-39 negative elongation factor complex member C/D, Th1l Mus musculus 125-128
31372995-5 2019 In mesenteric lymph nodes, retinoic acid (RA) released by CD103+ dendritic cells downregulated lamin A/C in CD4+ T-cells, enhancing Treg differentiation. Tretinoin 27-40 integrin alpha E, epithelial-associated Mus musculus 58-63
31372995-5 2019 In mesenteric lymph nodes, retinoic acid (RA) released by CD103+ dendritic cells downregulated lamin A/C in CD4+ T-cells, enhancing Treg differentiation. Tretinoin 42-44 integrin alpha E, epithelial-associated Mus musculus 58-63
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 99-118 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 10-15
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 99-118 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 32-39
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 99-118 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 41-48
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 120-124 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 10-15
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 120-124 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 32-39
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 120-124 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 41-48
31419517-4 2019 All three CYP26 enzymes are inducible by treatment with atRA in various prenatal and postnatal tissues and cell types. Tretinoin 56-60 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 10-15
31419517-6 2019 In humans and in animal models the expression patterns of CYP26 enzymes have been shown to be tissue and cell type specific, and the expression of the CYP26 enzymes is believed to regulate the formation of critical atRA concentration gradients in various tissue types. Tretinoin 215-219 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 58-63
31419517-6 2019 In humans and in animal models the expression patterns of CYP26 enzymes have been shown to be tissue and cell type specific, and the expression of the CYP26 enzymes is believed to regulate the formation of critical atRA concentration gradients in various tissue types. Tretinoin 215-219 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 151-156
31849602-8 2019 RA treatment of Neuro-2a cells increased by three-fold the amount of active ABHD6. Tretinoin 0-2 abhydrolase domain containing 6 Mus musculus 76-81
31682623-3 2019 In this study, using a germ cell culture system, we investigated (1) whether RA treatment activates any mitogen-activated protein kinase (MAPK) pathways in fetal germ cells at the time of sex differentiation, and (2) if this is the case, whether the corresponding RA-stimulated signaling pathway regulates Stra8 expression in fetal germ cells and their entry into meiosis. Tretinoin 77-79 mitogen-activated protein kinase 1 Mus musculus 138-142
31596288-7 2019 Luciferase report showed RA binding to RARalpha regulated stimulated by RA 8 (Stra8) promoter activity during SSC formation, while mutations in RAR binding sites inhibited the Stra8 expression and SSC formation. Tretinoin 25-27 stimulated by retinoic acid 8 Gallus gallus 78-83
31479736-11 2019 Simultaneously, RA significantly reduced the expression of the WNT genes cMyc, Lef1, Lrp5, Lrp6 and Wnt11 compared to the controls (p < 0.05). Tretinoin 16-18 wingless-type MMTV integration site family, member 11 Mus musculus 63-66
31479736-0 2019 Retinoic acid disrupts osteogenesis in pre-osteoblasts by down-regulating WNT signaling. Tretinoin 0-13 wingless-type MMTV integration site family, member 11 Mus musculus 74-77
31479736-11 2019 Simultaneously, RA significantly reduced the expression of the WNT genes cMyc, Lef1, Lrp5, Lrp6 and Wnt11 compared to the controls (p < 0.05). Tretinoin 16-18 wingless-type MMTV integration site family, member 11 Mus musculus 100-105
31479736-12 2019 In contrast, RA increased the expression of the WNT inhibitors Dkk1 at day 21 and Dkk2 at days 14 and 21 (p < 0.01). Tretinoin 13-15 wingless-type MMTV integration site family, member 11 Mus musculus 48-51
31479736-12 2019 In contrast, RA increased the expression of the WNT inhibitors Dkk1 at day 21 and Dkk2 at days 14 and 21 (p < 0.01). Tretinoin 13-15 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 63-67
31479736-13 2019 Our data indicate that RA disrupts osteogenic differentiation and mineralization by inhibiting WNT signaling. Tretinoin 23-25 wingless-type MMTV integration site family, member 11 Mus musculus 95-98
31580014-3 2019 To clarify the mechanism of meiotic initiation in chicken germ cells, we investigated the role of Cyp26b1, a retinoic acid-degrading enzyme. Tretinoin 109-122 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 98-105
31613407-2 2019 Our previous work has shown that depletion of RA using the vitamin A deficiency (VAD) model in Wistar rats leads to spatial memory deficits in relation to elevated intrahippocampal basal corticosterone (CORT) levels and increased hippocampal 11beta-Hydroxysteroid Dehydrogenase type 1 (11beta-HSD1) activity. Tretinoin 46-48 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 5 Rattus norvegicus 242-297
31755049-0 2019 The Effect of Arsenic Trioxide on All-trans Retinoic Acid Binding to Human Serum Albumin. Tretinoin 34-57 albumin Homo sapiens 75-88
31755049-3 2019 In this study, the effect of ATO on ATRA binding to human serum albumin (HSA) was investigated. Tretinoin 36-40 albumin Homo sapiens 58-71
31591086-9 2019 More specifically, the expression of Shh and its downstream genes Ptch1 and Gli1 was spatiotemporally downregulated in the developing face of RA-treated embryos. Tretinoin 142-144 patched 1 Homo sapiens 66-71
31685995-4 2019 Upon virus infection, ZNFX1 immediately recognizes viral RNA through its Armadillo-type fold and P-loop domain and then interacts with mitochondrial antiviral signalling protein to initiate the type I IFN response without depending on retinoic acid-inducible gene I-like receptors (RLRs). Tretinoin 235-248 zinc finger NFX1-type containing 1 Homo sapiens 22-27
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 tumor protein p53 Homo sapiens 117-120
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 tumor protein p53 Homo sapiens 117-120
31235507-0 2019 TRIB3 Stabilizes High TWIST1 Expression to Promote Rapid APL Progression and ATRA Resistance. Tretinoin 77-81 twist family bHLH transcription factor 1 Homo sapiens 22-28
31235507-8 2019 TRIB3 depletion promoting TWIST1 degradation reverses resistance to induction therapy and improves sensitivity to ATRA. Tretinoin 114-118 twist family bHLH transcription factor 1 Homo sapiens 26-32
31728810-8 2019 In addition, signaling of growth factors including VEGF, PDGF, and IGF1, and retinoic acid signaling were activated in the SATB2 and NRG1 lines, respectively. Tretinoin 77-90 SATB homeobox 2 Homo sapiens 123-128
31606046-8 2019 H1d knockdown primed ATRA-mediated differentiation of OCI-AML3 and U937 AML cell lines, as assessed on CD11b/CD11c markers, morphological and gene expression analyses. Tretinoin 21-25 H1.3 linker histone, cluster member Homo sapiens 0-3
29592769-0 2019 All trans retinoic acid modulates TNF-alpha and CYP2E1 pathways and enhances regression of ethanol-induced fibrosis markers in hepatocytes and HSCs in abstaining rodent model. Tretinoin 10-23 tumor necrosis factor Rattus norvegicus 34-43
29592769-0 2019 All trans retinoic acid modulates TNF-alpha and CYP2E1 pathways and enhances regression of ethanol-induced fibrosis markers in hepatocytes and HSCs in abstaining rodent model. Tretinoin 10-23 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 48-54
31288066-4 2019 One of the pathways that RA is able to modulate is the activity of NRF2 transcription factor, which is highly associated with tumour progression and resistance. Tretinoin 25-27 NFE2 like bZIP transcription factor 2 Homo sapiens 67-71
31288066-5 2019 Therefore, the aim of this work was to investigate molecular mechanism of RA and cisplatin co-treatment in A549 cells, focusing in NRF2 pathway. Tretinoin 74-76 NFE2 like bZIP transcription factor 2 Homo sapiens 131-135
31288066-7 2019 RA demonstrated to have an inhibitory effect over NRF2 activation, which regulates the expression of thiol antioxidants enzymes. Tretinoin 0-2 NFE2 like bZIP transcription factor 2 Homo sapiens 50-54
31370073-2 2019 ATRA also regulates protein kinase C (PKC) activity. Tretinoin 0-4 protein kinase C alpha Homo sapiens 38-41
31394504-8 2019 The enhanced inhibitory interaction between RA and BMP-4 pathways occurs also in another relevant corticotroph gene promoter, the Corticotropin-releasing hormone receptor 1 (CRH-R1). Tretinoin 44-46 bone morphogenetic protein 4 Mus musculus 51-56
31389093-9 2019 In addition to its role in the inflammatory phase of wound healing, retinoic acid has been demonstrated to enhance production of extracellular matrix components such as collagen type I and fibronectin, increase proliferation of keratinocytes and fibroblasts, and decrease levels of degrading matrix metalloproteinases. Tretinoin 68-81 fibronectin 1 Homo sapiens 189-200
31370073-8 2019 ATRA-treated platelets demonstrated reduced spreading on immobilized fibrinogen or collagen and reduced thrombin-induced clot retraction together with reduced phosphorylation of Syk and PLCgamma2. Tretinoin 0-4 fibrinogen beta chain Homo sapiens 69-79
31370073-8 2019 ATRA-treated platelets demonstrated reduced spreading on immobilized fibrinogen or collagen and reduced thrombin-induced clot retraction together with reduced phosphorylation of Syk and PLCgamma2. Tretinoin 0-4 coagulation factor II, thrombin Homo sapiens 104-112
31419710-0 2019 Retinoic acid modulates IL-4, IL-10 and MCP-1 pathways in immune mediated hepatitis and interrupts CD4+ T cells infiltration. Tretinoin 0-13 interleukin 10 Mus musculus 30-35
31419710-0 2019 Retinoic acid modulates IL-4, IL-10 and MCP-1 pathways in immune mediated hepatitis and interrupts CD4+ T cells infiltration. Tretinoin 0-13 mast cell protease 1 Mus musculus 40-45
31419710-9 2019 Hepatic injury, necrosis and expression of NF-kappab were significantly decreased by RA when injected before ConA challenge. Tretinoin 85-87 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 43-52
31419710-10 2019 A significant decrease in the measured cytokines TNF-alpha and IL-4 was observed in ConA + RA group in addition to a decrease in MCP-1 level. Tretinoin 91-93 tumor necrosis factor Mus musculus 49-58
31419710-10 2019 A significant decrease in the measured cytokines TNF-alpha and IL-4 was observed in ConA + RA group in addition to a decrease in MCP-1 level. Tretinoin 91-93 mast cell protease 1 Mus musculus 129-134
31419710-12 2019 SIGNIFICANCE: RA can protect against ConA-induced hepatitis through: interrupting early inflammatory response as neutrophils, monocytes and CD4+ T cells infiltration, modulating IL-4 level and subsequent production of TNF-alpha and NF-kappab activation, mitigating second inflammatory responses through increasing IL-10 liver production. Tretinoin 14-16 tumor necrosis factor Mus musculus 218-227
31419710-12 2019 SIGNIFICANCE: RA can protect against ConA-induced hepatitis through: interrupting early inflammatory response as neutrophils, monocytes and CD4+ T cells infiltration, modulating IL-4 level and subsequent production of TNF-alpha and NF-kappab activation, mitigating second inflammatory responses through increasing IL-10 liver production. Tretinoin 14-16 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 232-241
31419710-12 2019 SIGNIFICANCE: RA can protect against ConA-induced hepatitis through: interrupting early inflammatory response as neutrophils, monocytes and CD4+ T cells infiltration, modulating IL-4 level and subsequent production of TNF-alpha and NF-kappab activation, mitigating second inflammatory responses through increasing IL-10 liver production. Tretinoin 14-16 interleukin 10 Mus musculus 314-319
31323146-0 2019 All-trans retinoic acid induces anti-tumor effects via STAT3 signaling inhibition in oral squamous cell carcinoma and oral dysplasia. Tretinoin 10-23 signal transducer and activator of transcription 3 Homo sapiens 55-60
31323146-8 2019 ATRA led to inhibition of p-STAT3, p-JAK2, increased the level of p-ERK, and significantly decreased the PD-L1 expression. Tretinoin 0-4 signal transducer and activator of transcription 3 Homo sapiens 28-33
31323146-10 2019 The effect of ATRA on cell growth inhibition, apoptosis induction, and PD-L1 expression decrease was significantly (P < .05) enhanced after the STAT3 signaling blockade. Tretinoin 14-18 signal transducer and activator of transcription 3 Homo sapiens 147-152
31323146-11 2019 CONCLUSION: These findings suggested that ATRA-induced anti-tumor effects and downregulated PD-L1 expression via STAT3 signaling inhibition in both OSCC and oral dysplasia. Tretinoin 42-46 signal transducer and activator of transcription 3 Homo sapiens 113-118
31300983-4 2019 The qPCR results also showed significant (p <= 0.05) difference in both TIG3 and PPAR (RQ values of TIG3, lipo-ATRA 23.85 +- 1.29; free ATRA 10.43 +- 1.81 and for PPARgamma, lipo-ATRA 4.707 +- 1.21; free ATRA 15.78 +- 2.34). Tretinoin 139-143 peroxisome proliferator activated receptor alpha Mus musculus 84-88
31485618-4 2019 The present study investigates, to the best of our knowledge, for the first time, the influence of CIF in combination with RSV or ATRA on the expression of relevant modifiers of DNA methylation machinery, including DNA Methyltransferase 1 (DNMT1) and Cyclin dependent kinase inhibitor 1A (CDKN1A) in CML cells. Tretinoin 130-134 cyclin dependent kinase inhibitor 1A Homo sapiens 251-287
31485618-4 2019 The present study investigates, to the best of our knowledge, for the first time, the influence of CIF in combination with RSV or ATRA on the expression of relevant modifiers of DNA methylation machinery, including DNA Methyltransferase 1 (DNMT1) and Cyclin dependent kinase inhibitor 1A (CDKN1A) in CML cells. Tretinoin 130-134 cyclin dependent kinase inhibitor 1A Homo sapiens 289-295
31370073-10 2019 Further, in platelets stimulated with either collagen-related peptide or thrombin, ATRA selectively inhibited phosphorylation of PKCssI (Ser661) and PKCdelta (Thr505), but not PKCalpha or PKCssII phosphorylation (Thr638/641). Tretinoin 83-87 coagulation factor II, thrombin Homo sapiens 73-81
31370073-10 2019 Further, in platelets stimulated with either collagen-related peptide or thrombin, ATRA selectively inhibited phosphorylation of PKCssI (Ser661) and PKCdelta (Thr505), but not PKCalpha or PKCssII phosphorylation (Thr638/641). Tretinoin 83-87 protein kinase C alpha Homo sapiens 176-184
31370073-7 2019 ATRA inhibited platelet aggregation and adenosine triphosphate release induced by collagen (5 mug/mL) or thrombin (0.05 U/mL) in a dose-dependent manner without affecting P-selectin expression or surface levels of glycoprotein (GP) Ibalpha, GPVI, or alphaIIbbeta3. Tretinoin 0-4 coagulation factor II, thrombin Homo sapiens 105-113
31570689-0 2019 The ATRA-21 gene-expression model predicts retinoid sensitivity in CEBPA double mutant, t(8;21) and inv(16) AML patients. Tretinoin 4-8 CCAAT enhancer binding protein alpha Homo sapiens 67-72
31445893-2 2019 CYP3A7 has been demonstrated to metabolize two endogenous compounds that are known to be important in the growth and development of the fetus and neonate, namely dehydroepiandrosterone sulfate (DHEA-S) and all-trans retinoic acid (atRA). Tretinoin 206-229 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 0-6
31445893-2 2019 CYP3A7 has been demonstrated to metabolize two endogenous compounds that are known to be important in the growth and development of the fetus and neonate, namely dehydroepiandrosterone sulfate (DHEA-S) and all-trans retinoic acid (atRA). Tretinoin 231-235 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 0-6
31561560-3 2019 In fetal testes, the RA-degrading enzyme CYP26B1 prevents meiosis initiation. Tretinoin 21-23 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 41-48
31880511-4 2019 Our results indicate that ATRA can augment the expression of RARalpha and PHB proteins and reduce the expression of TGF-beta1, FN and Col-IV proteins. Tretinoin 26-30 transforming growth factor beta 1 Homo sapiens 116-125
31561560-11 2019 Collectively, our data reveal that CYP26B1 has other activities apart from metabolizing RA in fetal gonads and suggest a role of endogenous RA in amplifying Stra8, rather than being the initial inducer of Stra8. Tretinoin 88-90 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 35-42
31561560-11 2019 Collectively, our data reveal that CYP26B1 has other activities apart from metabolizing RA in fetal gonads and suggest a role of endogenous RA in amplifying Stra8, rather than being the initial inducer of Stra8. Tretinoin 140-142 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 35-42
31440819-2 2019 Several variant isoforms and non-coding RNAs are present in cancer and this report explored the expression of these transcripts of the TGM2 gene in cancer cell lines after induction with all-trans retinoic acid. Tretinoin 197-210 transglutaminase 2 Homo sapiens 135-139
31557800-0 2019 All-Trans Retinoic Acid Attenuates Fibrotic Processes by Downregulating TGF-beta1/Smad3 in Early Diabetic Nephropathy. Tretinoin 0-23 transforming growth factor, beta 1 Rattus norvegicus 72-81
31557800-0 2019 All-Trans Retinoic Acid Attenuates Fibrotic Processes by Downregulating TGF-beta1/Smad3 in Early Diabetic Nephropathy. Tretinoin 0-23 SMAD family member 3 Rattus norvegicus 82-87
31557800-8 2019 Remarkably, ATRA treatment ameliorated these alterations and attenuated expression and nuclear translocation of Smad3, with increment of glomerular and tubular Smad7. Tretinoin 12-16 SMAD family member 3 Rattus norvegicus 112-117
31557800-8 2019 Remarkably, ATRA treatment ameliorated these alterations and attenuated expression and nuclear translocation of Smad3, with increment of glomerular and tubular Smad7. Tretinoin 12-16 SMAD family member 7 Rattus norvegicus 160-165
31557800-11 2019 ATRA prevented fibrogenesis through down-regulation of TGF-beta1/Smad3 signaling. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 55-64
31557800-11 2019 ATRA prevented fibrogenesis through down-regulation of TGF-beta1/Smad3 signaling. Tretinoin 0-4 SMAD family member 3 Rattus norvegicus 65-70
31547462-4 2019 Cells were also treated with retinoic acid in combination with a poly(ADP-ribosyl) polymerase (PARP) inhibitor because PARP1 is a known chromatin modulator and can influence the process of differentiation. Tretinoin 29-42 poly(ADP-ribose) polymerase 1 Homo sapiens 119-124
31500289-6 2019 Here, we demonstrated that inhibition of Cdc42 or Rac not only prevented growth cone turning toward retinoic acid but could also induce a switch in growth cone responsiveness to chemorepulsion or growth cone collapse. Tretinoin 100-113 AKT serine/threonine kinase 1 Homo sapiens 50-53
31500289-9 2019 These data strongly suggest that Cdc42 and Rac are downstream effectors of retinoic acid during growth cone guidance. Tretinoin 75-88 AKT serine/threonine kinase 1 Homo sapiens 43-46
32648650-6 2019 Results indicate beta-catenin translocalization and activation of TCF/LEF responsive transcription in response to MNP and magnetic fields, which result in dopaminergic marker expression when synergistically combined with differentiation factors retinoic acid and the phorbol ester phorbol 12-myristate 13-acetate. Tretinoin 245-258 hepatocyte nuclear factor 4 alpha Homo sapiens 66-73
31006867-10 2019 CONCLUSIONS: ATRA-induced dermatitis could be achieved by activating mast cells via MRGPRX2/MrgprB2, which may provide a potential therapy target to reduce the side-effect. Tretinoin 13-17 MAS related GPR family member X2 Homo sapiens 84-91
31328782-7 2019 RT-PCR analysis indicated that RA stimulated the expression of Stra8 but reduced the expression of NANOS2 in spermatogonia. Tretinoin 31-33 nanos C2HC-type zinc finger 2 Sus scrofa 99-105
30974109-1 2019 We previously demonstrated that the most bioactive vitamin A metabolite, all-trans retinoic acid (ATRA), increased T helper 2-associated responses induced in pigs by infection with the parasitic nematode Ascaris suum We also showed that ATRA potentiated the mRNA expression of several IL-4 induced chemokines (chemokine (CC motif) ligand 11 [(CCL11), CCL17, CCL22 and CCL26] associated with alternative activation (M2a) in porcine macrophages in vitro. Tretinoin 73-96 interleukin 4 Homo sapiens 285-289
30974109-1 2019 We previously demonstrated that the most bioactive vitamin A metabolite, all-trans retinoic acid (ATRA), increased T helper 2-associated responses induced in pigs by infection with the parasitic nematode Ascaris suum We also showed that ATRA potentiated the mRNA expression of several IL-4 induced chemokines (chemokine (CC motif) ligand 11 [(CCL11), CCL17, CCL22 and CCL26] associated with alternative activation (M2a) in porcine macrophages in vitro. Tretinoin 98-102 interleukin 4 Homo sapiens 285-289
30974109-4 2019 ATRA synergistically enhanced IL-4 up-regulation of Hepatitis A virus cellular receptor 2 (HAVCR2) and transglutaminase 2 (TGM2) and further repressed IL-4 down-regulated CD163 and Cytochrome b-245, beta polypeptide (CYBB) mRNA. Tretinoin 0-4 interleukin 4 Homo sapiens 30-34
30974109-4 2019 ATRA synergistically enhanced IL-4 up-regulation of Hepatitis A virus cellular receptor 2 (HAVCR2) and transglutaminase 2 (TGM2) and further repressed IL-4 down-regulated CD163 and Cytochrome b-245, beta polypeptide (CYBB) mRNA. Tretinoin 0-4 transglutaminase 2 Homo sapiens 123-127
30974109-4 2019 ATRA synergistically enhanced IL-4 up-regulation of Hepatitis A virus cellular receptor 2 (HAVCR2) and transglutaminase 2 (TGM2) and further repressed IL-4 down-regulated CD163 and Cytochrome b-245, beta polypeptide (CYBB) mRNA. Tretinoin 0-4 interleukin 4 Homo sapiens 151-155
30974109-7 2019 These data indicate that ATRA induces a state of partial alternative activation in porcine macrophages, and amplifies certain aspects of M2a activation induced by IL-4. Tretinoin 25-29 interleukin 4 Homo sapiens 163-167
31322186-9 2019 Notably, overexpression of Hrd1 abolished the protective effect of ATRA on the UV-induced decrease of Nrf2 expression, the production of reactive oxygen species (ROS) and the decrease of cell viability. Tretinoin 67-71 NFE2 like bZIP transcription factor 2 Homo sapiens 102-106
31328782-8 2019 Genes involved in post-meiotic development, transition protein 1 (Tnp1) and protamine 1 (Prm1) were upregulated in the presence of RA. Tretinoin 131-133 transition protein 1 Sus scrofa 44-64
31200068-6 2019 In addition, the capabilities of a retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) system to activate IFN promoter were decreased during the overexpression of FGFR3. Tretinoin 35-48 interferon alpha 1 Homo sapiens 113-116
31056772-4 2019 The expression of Adh1 and Aldh1a2 (alcohol dehydrogenase), two enzymes that convert retinol to retinoic acid in this pathway, were decreased at both the gene and protein levels. Tretinoin 96-109 aldo-keto reductase family 1 member A1 Rattus norvegicus 36-57
31322252-0 2019 All-trans-retinoic acid modulates TGF-beta-induced apoptosis, proliferation, migration and extracellular matrix synthesis of conjunctival fibroblasts by inhibiting PI3K/AKT signaling. Tretinoin 0-23 AKT serine/threonine kinase 1 Homo sapiens 169-172
31322252-8 2019 ATRA treatment resulted in an increased level of HConF apoptosis, reduced proliferation and migration, decreased collagen I and fibronectin expression, and decreased phosphorylation of PI3K and AKT. Tretinoin 0-4 fibronectin 1 Homo sapiens 128-139
31322252-8 2019 ATRA treatment resulted in an increased level of HConF apoptosis, reduced proliferation and migration, decreased collagen I and fibronectin expression, and decreased phosphorylation of PI3K and AKT. Tretinoin 0-4 AKT serine/threonine kinase 1 Homo sapiens 194-197
31322252-9 2019 Thus, the present study showed a role for ATRA in inhibiting HConF migration, proliferation and ECM synthesis, and in promoting HConF apoptosis through the inhibition of the PI3K/AKT signaling pathway. Tretinoin 42-46 AKT serine/threonine kinase 1 Homo sapiens 179-182
31328782-7 2019 RT-PCR analysis indicated that RA stimulated the expression of Stra8 but reduced the expression of NANOS2 in spermatogonia. Tretinoin 31-33 stimulated by retinoic acid 8 Sus scrofa 63-68
31328782-8 2019 Genes involved in post-meiotic development, transition protein 1 (Tnp1) and protamine 1 (Prm1) were upregulated in the presence of RA. Tretinoin 131-133 transition protein 1 Sus scrofa 66-70
31406210-4 2019 Stimulation of myeloid blasts" maturation by all-trans retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (vitamin D) increased the CD11b+ fraction that expressed PD-1 ligands in response to IFN-gamma. Tretinoin 45-68 interferon gamma Homo sapiens 194-203
31406210-4 2019 Stimulation of myeloid blasts" maturation by all-trans retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (vitamin D) increased the CD11b+ fraction that expressed PD-1 ligands in response to IFN-gamma. Tretinoin 70-74 interferon gamma Homo sapiens 194-203
31268160-0 2019 [Corrigendum] All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway. Tretinoin 18-37 growth differentiation factor 2 Homo sapiens 73-77
30679324-0 2019 All-trans retinoic acid protects mesenchymal stem cells from immune thrombocytopenia by regulating the complement-interleukin-1beta loop. Tretinoin 10-23 interleukin 1 beta Homo sapiens 114-131
30679324-6 2019 In vitro treatment with all-trans retinoic acid increased the number and improved the function of the complement-positive bone marrow mesenchymal stem cells by upregulating DNA hypermethylation of the interleukin-1beta promoter. Tretinoin 34-47 interleukin 1 beta Homo sapiens 201-218
31263060-3 2019 TNF-alpha treatment has been investigated as part of a combined therapy for acute myeloid leukemia due to its modifying effects on all-trans retinoic acid (ATRA) mediated differentiation into granulocytes. Tretinoin 141-154 tumor necrosis factor Homo sapiens 0-9
31263060-3 2019 TNF-alpha treatment has been investigated as part of a combined therapy for acute myeloid leukemia due to its modifying effects on all-trans retinoic acid (ATRA) mediated differentiation into granulocytes. Tretinoin 156-160 tumor necrosis factor Homo sapiens 0-9
30222904-9 2019 Consistent with this, the LY367385-induced increase in surface GluA1 was blocked by anisomycin (translation inhibitor) or 4-(diethylamino)-benzaldehyde (RA synthesis inhibitor). Tretinoin 153-155 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 63-68
31268160-0 2019 [Corrigendum] All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway. Tretinoin 18-37 mitogen-activated protein kinase 14 Homo sapiens 106-109
31399314-5 2019 As a result, RA increased the gene expression of a drug-metabolizing enzyme CYP3A4, as a functional molecule of intestinal mature development, in iPSC-derived intestinal organoids. Tretinoin 13-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 76-82
30859584-3 2019 Moreover, flow cytometry results revealed that the proliferation promoting effect of RA was attenuated by U0126, a specific inhibitor of extracellular signal-regulated kinase (ERK). Tretinoin 85-87 mitogen-activated protein kinase 1 Homo sapiens 137-174
30859584-3 2019 Moreover, flow cytometry results revealed that the proliferation promoting effect of RA was attenuated by U0126, a specific inhibitor of extracellular signal-regulated kinase (ERK). Tretinoin 85-87 mitogen-activated protein kinase 1 Homo sapiens 176-179
30859584-4 2019 Western blot analysis showed the protein level of ERK, phosphorylated ERK, cyclin D1 (CCND1), and cyclin-dependent kinase 2 (CDK2) increased after stimulation with RA, and this effect could also be abolished by U0126. Tretinoin 164-166 mitogen-activated protein kinase 1 Homo sapiens 50-53
30859584-4 2019 Western blot analysis showed the protein level of ERK, phosphorylated ERK, cyclin D1 (CCND1), and cyclin-dependent kinase 2 (CDK2) increased after stimulation with RA, and this effect could also be abolished by U0126. Tretinoin 164-166 mitogen-activated protein kinase 1 Homo sapiens 70-73
31399314-7 2019 Finally, RA increased the expression of ZO-1, a marker of tight junctions, which are essential for intestinal epithelial barrier function. Tretinoin 9-11 tight junction protein 1 Homo sapiens 40-44
31399314-8 2019 Taken together, these results indicate that RA promotes barrier functions of iPSC-derived intestinal epithelial monolayers by increasing ZO-1 expression. Tretinoin 44-46 tight junction protein 1 Homo sapiens 137-141
31231034-5 2019 Retinoic acid-dependent and -independent hallmark genes of GATA6+ macrophages were induced by mesothelial and fibroblastic stromal cells that express the transcription factor Wilms" Tumor 1 (WT1), which drives the expression of two rate-limiting enzymes in retinol metabolism. Tretinoin 0-13 WT1 transcription factor Homo sapiens 175-189
31251021-6 2019 Furthermore, the interactions between two model proteins, Erv1C (C-terminal domain of flavine adenine dinucleotide-dependent mitochondrial cytochrome c reductase Erv1) and AFP (alpha-fetoprotein), and their ligands Cyt c (cytochrome c) and ATRA (all-trans-retinoic acid) are examined, respectively. Tretinoin 240-244 alpha fetoprotein Homo sapiens 172-175
31251021-6 2019 Furthermore, the interactions between two model proteins, Erv1C (C-terminal domain of flavine adenine dinucleotide-dependent mitochondrial cytochrome c reductase Erv1) and AFP (alpha-fetoprotein), and their ligands Cyt c (cytochrome c) and ATRA (all-trans-retinoic acid) are examined, respectively. Tretinoin 246-269 alpha fetoprotein Homo sapiens 172-175
31358819-3 2019 We recently reported that all-trans retinoic acid (atRA) rapidly (within minutes) activates Erk1/2 to modulate cell cycle progression in stem cells, which is mediated by cellular retinoic acid binding protein 1 (Crabp1). Tretinoin 26-49 mitogen-activated protein kinase 3 Homo sapiens 92-98
31358819-3 2019 We recently reported that all-trans retinoic acid (atRA) rapidly (within minutes) activates Erk1/2 to modulate cell cycle progression in stem cells, which is mediated by cellular retinoic acid binding protein 1 (Crabp1). Tretinoin 51-55 mitogen-activated protein kinase 3 Homo sapiens 92-98
31231034-5 2019 Retinoic acid-dependent and -independent hallmark genes of GATA6+ macrophages were induced by mesothelial and fibroblastic stromal cells that express the transcription factor Wilms" Tumor 1 (WT1), which drives the expression of two rate-limiting enzymes in retinol metabolism. Tretinoin 0-13 WT1 transcription factor Homo sapiens 191-194
30681285-2 2019 All-trans-retinoic acid (atRA) downregulates cytochrome P450 (CYP)2D6 in several model systems. Tretinoin 0-23 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 45-69
31039331-1 2019 Of numerous genes regulated by retinoic acid (RA), CYP26A1 is the most inducible gene by RA. Tretinoin 31-44 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 51-58
30681285-2 2019 All-trans-retinoic acid (atRA) downregulates cytochrome P450 (CYP)2D6 in several model systems. Tretinoin 25-29 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 45-69
30681285-4 2019 The retinoids atRA, 13cisRA, and 4-oxo-13cisRA all decreased CYP2D6 mRNA in human hepatocytes in a concentration-dependent manner. Tretinoin 14-18 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 61-67
30826380-5 2019 Our experiments revealed that ATRA alone, but also a cocktail of mediators consisting of IL2, TGFbeta and ATRA, upregulate expression of FOXP3 gene in normal and leukemic myeloid cells. Tretinoin 30-34 interleukin 2 Homo sapiens 89-92
30826380-5 2019 Our experiments revealed that ATRA alone, but also a cocktail of mediators consisting of IL2, TGFbeta and ATRA, upregulate expression of FOXP3 gene in normal and leukemic myeloid cells. Tretinoin 30-34 transforming growth factor beta 1 Homo sapiens 94-101
30991836-1 2019 Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) regulates the concentration of all-trans retinoic acid (RA) and plays a key role in germ cell differentiation by controlling local distribution of RA. Tretinoin 98-111 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-46
30991836-1 2019 Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) regulates the concentration of all-trans retinoic acid (RA) and plays a key role in germ cell differentiation by controlling local distribution of RA. Tretinoin 98-111 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 48-55
30991836-1 2019 Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) regulates the concentration of all-trans retinoic acid (RA) and plays a key role in germ cell differentiation by controlling local distribution of RA. Tretinoin 113-115 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-46
30991836-1 2019 Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) regulates the concentration of all-trans retinoic acid (RA) and plays a key role in germ cell differentiation by controlling local distribution of RA. Tretinoin 113-115 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 48-55
30991836-1 2019 Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) regulates the concentration of all-trans retinoic acid (RA) and plays a key role in germ cell differentiation by controlling local distribution of RA. Tretinoin 204-206 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-46
30991836-1 2019 Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) regulates the concentration of all-trans retinoic acid (RA) and plays a key role in germ cell differentiation by controlling local distribution of RA. Tretinoin 204-206 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 48-55
30760649-5 2019 Retinoic acid significantly reduced the mRNA transcript levels of apoptosis-related genes, including BAX and P53, and reduced the BAX/BCL2 ratio. Tretinoin 0-13 LOW QUALITY PROTEIN: apoptosis regulator Bcl-2 Camelus dromedarius 134-138
31215681-4 2019 Treatment with ATRA during the early and late stage of adipogenesis resulted in an increase in the expression level of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12, respectively, whereas expression of Pgc-1alpha, another gene expressed during brown adipogenesis, was unaffected by ATRA. Tretinoin 15-19 PPARG coactivator 1 alpha Homo sapiens 236-246
31241704-3 2019 This study aimed to explore the relationship and potential mechanism between TBX22 exon 5 methylation and palatal shelf fusion induced by all-trans retinoic acid (ATRA). Tretinoin 138-161 T-box 22 Mus musculus 77-82
31241704-3 2019 This study aimed to explore the relationship and potential mechanism between TBX22 exon 5 methylation and palatal shelf fusion induced by all-trans retinoic acid (ATRA). Tretinoin 163-167 T-box 22 Mus musculus 77-82
31241704-5 2019 TBX22 exon 5 was hyper-methylated at the CpG site at E13.5 (P=0.025, log2FC=1.5) and E14.5 (P=0.011, log2FC:1.5) in ATRA-treated, whereas methylation TBX22 exon 5 at the CpG site was not significantly different at E16.5 (P=0.808, log2FC=-0.2) between control and ATRA-treated. Tretinoin 116-120 T-box 22 Mus musculus 0-5
31241704-5 2019 TBX22 exon 5 was hyper-methylated at the CpG site at E13.5 (P=0.025, log2FC=1.5) and E14.5 (P=0.011, log2FC:1.5) in ATRA-treated, whereas methylation TBX22 exon 5 at the CpG site was not significantly different at E16.5 (P=0.808, log2FC=-0.2) between control and ATRA-treated. Tretinoin 263-267 T-box 22 Mus musculus 0-5
31063220-0 2019 Chemerin partly mediates tumor-inhibitory effect of all-trans retinoic acid via CMKLR1-dependent natural killer cell recruitment. Tretinoin 62-75 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 0-8
31063220-2 2019 All-trans retinoic acid (atRA) is a potent inducer of chemerin, and we previously reported that atRA inhibited murine melanoma growth through enhancement of anti-tumor T-cell immunity. Tretinoin 0-23 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 54-62
31063220-2 2019 All-trans retinoic acid (atRA) is a potent inducer of chemerin, and we previously reported that atRA inhibited murine melanoma growth through enhancement of anti-tumor T-cell immunity. Tretinoin 25-29 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 54-62
31063220-2 2019 All-trans retinoic acid (atRA) is a potent inducer of chemerin, and we previously reported that atRA inhibited murine melanoma growth through enhancement of anti-tumor T-cell immunity. Tretinoin 96-100 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 54-62
31063220-3 2019 Here, we aimed to investigate whether loss of endogenous chemerin accelerated melanoma growth and whether chemerin was involved in the melanoma-inhibitory effect of atRA. Tretinoin 165-169 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 106-114
31063220-6 2019 Topical treatment with atRA up-regulated skin chemerin expression, which was primarily derived from dermal cells. Tretinoin 23-27 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 46-54
31063220-7 2019 Moreover, atRA treatment significantly enhanced tumor-infiltrating NK cells, which was completely abrogated in Rarres2-/- mice and Cmklr1-/- mice, suggesting a dependency of NK cell recruitment on the chemerin-CMKLR1 axis in melanoma. Tretinoin 10-14 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 201-209
31063220-10 2019 Collectively, our study suggests that down-regulation of chemerin could be a strategy used by cancers such as melanoma to impair anti-tumor NK cell immunity and identifies a new anti-tumor mechanism of atRA by up-regulating chemerin to enhance CMKLR1-dependent NK cell recruitment. Tretinoin 202-206 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 57-65
31063220-10 2019 Collectively, our study suggests that down-regulation of chemerin could be a strategy used by cancers such as melanoma to impair anti-tumor NK cell immunity and identifies a new anti-tumor mechanism of atRA by up-regulating chemerin to enhance CMKLR1-dependent NK cell recruitment. Tretinoin 202-206 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 224-232
30576481-9 2019 RA treatment elicited activation of the MEK-ERK pathway and induced rapid and transient activation of the extracellular signal-regulated kinase 1/2 (ERK-1/2). Tretinoin 0-2 mitogen-activated protein kinase kinase 7 Homo sapiens 40-43
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 7 Homo sapiens 121-125
30576481-9 2019 RA treatment elicited activation of the MEK-ERK pathway and induced rapid and transient activation of the extracellular signal-regulated kinase 1/2 (ERK-1/2). Tretinoin 0-2 mitogen-activated protein kinase 1 Homo sapiens 44-47
30576481-9 2019 RA treatment elicited activation of the MEK-ERK pathway and induced rapid and transient activation of the extracellular signal-regulated kinase 1/2 (ERK-1/2). Tretinoin 0-2 mitogen-activated protein kinase 3 Homo sapiens 106-147
30576481-9 2019 RA treatment elicited activation of the MEK-ERK pathway and induced rapid and transient activation of the extracellular signal-regulated kinase 1/2 (ERK-1/2). Tretinoin 0-2 mitogen-activated protein kinase 3 Homo sapiens 149-156
30576481-12 2019 Our study shows that PPM1D plays an important role in maintaining the undifferentiation state and a new function in RA-induced ERK regulation and cell differentiation. Tretinoin 116-118 mitogen-activated protein kinase 1 Homo sapiens 127-130
31218101-5 2019 Therefore, RAF-1-independent MEK/ERK signaling was required for enz-ATRA treatment-induced differentiation via modulation of the protein levels of C/EBPbeta and/or PU.1. Tretinoin 68-72 mitogen-activated protein kinase kinase 7 Homo sapiens 29-32
31109864-9 2019 A large number of oral cDCs with the CD103-CD11b+ phenotype exert retinoic acid-producing activity and convert naive CD4+ T cells into Foxp3+ Treg cells in vitro in a transforming growth factor-beta-dependent and retinoic acid-dependent manner. Tretinoin 66-79 integrin alpha E, epithelial-associated Mus musculus 37-42
31109864-9 2019 A large number of oral cDCs with the CD103-CD11b+ phenotype exert retinoic acid-producing activity and convert naive CD4+ T cells into Foxp3+ Treg cells in vitro in a transforming growth factor-beta-dependent and retinoic acid-dependent manner. Tretinoin 66-79 integrin alpha M Mus musculus 43-48
31091225-8 2019 Our study highlights that transcriptional repression via the epigenetic regulator Hdac1 facilitates OFT development through directly preventing expression of the RA-responsive gene ripply3 within SHF progenitors. Tretinoin 162-164 ripply transcriptional repressor 3 Danio rerio 181-188
31143119-6 2019 Our results also demonstrated that ATRA altered the expression of proliferation-related proteins, including CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 in VSMC. Tretinoin 35-39 cyclin-dependent kinase 4 Mus musculus 144-148
31218101-5 2019 Therefore, RAF-1-independent MEK/ERK signaling was required for enz-ATRA treatment-induced differentiation via modulation of the protein levels of C/EBPbeta and/or PU.1. Tretinoin 68-72 mitogen-activated protein kinase 1 Homo sapiens 33-36
30779601-3 2019 Here, we have investigated the physical interactome of EZH2, the enzymatic core of PRC2, during retinoic acid-mediated differentiation of neuroepithelial, pluripotent NT2 cells and the dedifferentiation of neuroretinal epithelial ARPE19 cells in response to TGF-beta. Tretinoin 96-109 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 55-59
30674471-8 2019 Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication. Tretinoin 31-35 promyelocytic leukemia Mus musculus 133-136
30339851-7 2019 Ubiquitin protein ligase E3 component N-recognin 5 (Ubr5) and nuclear receptor subfamily 2 group F member 6 (Nr2f6) expression levels decreased in RhoH-deficient T cells, resulting in increased protein levels and DNA binding activity of retinoic acid-related orphan receptor gammat. Tretinoin 237-250 ubiquitin protein ligase E3 component n-recognin 5 Mus musculus 0-50
31035455-2 2019 In F9 embryonic carcinoma cells, RA can induce differentiation towards somatic lineages via the Ras-extracellular signal-regulated kinase (Ras/Erk) pathway, but the mechanism through which it induces the Erk1/2 phosphorylation is unclear. Tretinoin 33-35 mitogen-activated protein kinase 1 Mus musculus 143-146
30938528-4 2019 In contrast, the mRNA expression of peroxisome-proliferator-activated receptor gamma (PPARG) was strongly induced by ATRA alone but decreased by CLA isomers from 1.00 (ATRA alone) to 0.80 +- 0.06 (200 muM c9t11-CLA, P < 0.05) and 0.86 +- 0.06 (200 muM t10c12-CLA, P < 0.05). Tretinoin 117-121 peroxisome proliferator activated receptor gamma Homo sapiens 36-84
30938528-4 2019 In contrast, the mRNA expression of peroxisome-proliferator-activated receptor gamma (PPARG) was strongly induced by ATRA alone but decreased by CLA isomers from 1.00 (ATRA alone) to 0.80 +- 0.06 (200 muM c9t11-CLA, P < 0.05) and 0.86 +- 0.06 (200 muM t10c12-CLA, P < 0.05). Tretinoin 117-121 peroxisome proliferator activated receptor gamma Homo sapiens 86-91
30938528-5 2019 Overexpression of PPARgamma in MCF-7 cells increased basal NIS-promoter activity, and treatment with the PPARgamma ligand troglitazone stimulated ATRA-induced NIS-promoter activity. Tretinoin 146-150 peroxisome proliferator activated receptor gamma Homo sapiens 18-27
30938528-5 2019 Overexpression of PPARgamma in MCF-7 cells increased basal NIS-promoter activity, and treatment with the PPARgamma ligand troglitazone stimulated ATRA-induced NIS-promoter activity. Tretinoin 146-150 peroxisome proliferator activated receptor gamma Homo sapiens 105-114
30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 interleukin 4 Homo sapiens 52-55
30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 interleukin 6 Homo sapiens 57-60
30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 tumor necrosis factor Homo sapiens 65-73
30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 tumor necrosis factor Homo sapiens 118-126
30992691-14 2019 Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed. Tretinoin 35-39 general transcription factor IIi Homo sapiens 49-54
30992691-14 2019 Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed. Tretinoin 35-39 general transcription factor IIi Homo sapiens 104-109
30885956-1 2019 Recent studies have underscored the critical role of retinoic acid (RA) in the development of lineage-committed CD4 and CD8 T cells in vivo. Tretinoin 53-66 CD4 molecule Homo sapiens 112-115
30885956-1 2019 Recent studies have underscored the critical role of retinoic acid (RA) in the development of lineage-committed CD4 and CD8 T cells in vivo. Tretinoin 68-70 CD4 molecule Homo sapiens 112-115
30885956-4 2019 In this study, we demonstrate that enhancing RA degradation in the host and to a lesser extent donor hematopoietic cells by overexpressing the RA-catabolizing enzyme CYP26A1 reduced GVHD. Tretinoin 45-47 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 166-173
30885956-4 2019 In this study, we demonstrate that enhancing RA degradation in the host and to a lesser extent donor hematopoietic cells by overexpressing the RA-catabolizing enzyme CYP26A1 reduced GVHD. Tretinoin 143-145 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 166-173
31049420-0 2019 Inhibition of thrombin, an unexplored function of retinoic acid. Tretinoin 50-63 coagulation factor II, thrombin Homo sapiens 14-22
31049420-4 2019 Retinoic acid, retinaldehyde and retinol exhibited potent inhibition of thrombin, with IC50 values of 67mug/ml, 74mug/ml and 152mug/ml, respectively for the inhibition of thrombin (Sigma); and 49mug/ml, 74mug/ml and 178mug/ml, respectively for the inhibition of thrombin (plasma). Tretinoin 0-13 coagulation factor II, thrombin Homo sapiens 72-80
31049420-4 2019 Retinoic acid, retinaldehyde and retinol exhibited potent inhibition of thrombin, with IC50 values of 67mug/ml, 74mug/ml and 152mug/ml, respectively for the inhibition of thrombin (Sigma); and 49mug/ml, 74mug/ml and 178mug/ml, respectively for the inhibition of thrombin (plasma). Tretinoin 0-13 coagulation factor II, thrombin Homo sapiens 171-179
31049420-4 2019 Retinoic acid, retinaldehyde and retinol exhibited potent inhibition of thrombin, with IC50 values of 67mug/ml, 74mug/ml and 152mug/ml, respectively for the inhibition of thrombin (Sigma); and 49mug/ml, 74mug/ml and 178mug/ml, respectively for the inhibition of thrombin (plasma). Tretinoin 0-13 coagulation factor II, thrombin Homo sapiens 171-179
31049420-5 2019 Amongst vitamin A and its derivatives, retinoic acid showed the highest inhibition of both the forms of thrombin. Tretinoin 39-52 coagulation factor II, thrombin Homo sapiens 104-112
31285641-6 2019 The possible role of Wnt-Fzd interactions in developmental toxicity due to selected teratogens were also investigated using molecular docking studies which showed that Retinoic Acid possessed the maximum binding affinity with binding energy of for hWnt5b-hFzd8 complex while VPA was observed to have lowest binding affinity towards all the studied hWnt5b-hFzd complexes. Tretinoin 168-181 frizzled class receptor 8 Homo sapiens 255-260
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 forkhead box O1 Homo sapiens 56-61
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 forkhead box O3 Homo sapiens 63-69
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 161-197
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 199-204
30978209-5 2019 Also, RA and/or bexarotene influenced the recruitment of FOXO3A and FOXM1 to target genes. Tretinoin 6-8 forkhead box O3 Homo sapiens 57-63
30978209-8 2019 This research suggests novel influences of the drugs RA and bexarotene on the expression of FOXM1 and FOXO3A in transcriptional regulatory pathways of human OSCC. Tretinoin 53-55 forkhead box O3 Homo sapiens 102-108
30737277-5 2019 We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum. Tretinoin 148-150 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 71-117
30737277-5 2019 We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum. Tretinoin 148-150 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 119-126
30992691-0 2019 RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance. Tretinoin 24-28 general transcription factor IIi Homo sapiens 85-90
30992691-7 2019 Flow cytometry and Wright-Giemsa staining were used to study the effect of MG132 and ATRA on the GTF2I-RARA-transfected HL60 cell model. Tretinoin 85-89 general transcription factor IIi Homo sapiens 97-102
30992691-8 2019 Result: We confirmed resistance of GTF2I-RARA to ATRA. Tretinoin 49-53 general transcription factor IIi Homo sapiens 35-45
30992691-9 2019 Compared with PML-RARA, GTF2I-RARA has a higher affinity to HDAC3 under ATRA treatment. Tretinoin 72-76 general transcription factor IIi Homo sapiens 24-34
30944806-7 2019 The mRNA expression levels of both RAR-beta and RXR-beta were found to be increased in co-treatment (band density of 0.75 and 0.806, respectively) when compared with 9cisRA treatment (0.25 and 0.112) and ATRA treatment (0.01 and 0.081). Tretinoin 204-208 retinoic acid receptor beta Homo sapiens 35-43
30944806-9 2019 We thus conclude that the co-treatment had increased the availability of ATRA, by isomerization of the 9cisRA which then resulted in an increased expression of both RAR-beta and RXR-beta receptors and the target protein RAR-beta which in turn inhibited lung cancer cell growth. Tretinoin 73-77 retinoic acid receptor beta Homo sapiens 165-173
30944806-9 2019 We thus conclude that the co-treatment had increased the availability of ATRA, by isomerization of the 9cisRA which then resulted in an increased expression of both RAR-beta and RXR-beta receptors and the target protein RAR-beta which in turn inhibited lung cancer cell growth. Tretinoin 73-77 retinoic acid receptor beta Homo sapiens 220-228
30816426-11 2019 By contrast, Claudin-4 was upregulated in HaCaT cells and the mouse epidermis following treatment with ATRA. Tretinoin 103-107 claudin 4 Homo sapiens 13-22
30816426-12 2019 In conclusion, ATRA exerts a dual effect on epidermal barrier genes: It downregulates the expression of Claudin-1 and upregulates the expression of Claudin-4. Tretinoin 15-19 claudin 4 Mus musculus 148-157
30709899-0 2019 Repression of hepatocyte nuclear factor 4 alpha by AP-1 underlies dyslipidemia associated with retinoic acid. Tretinoin 95-108 hepatocyte nuclear factor 4 alpha Homo sapiens 14-47
30709899-4 2019 We investigated CYP7A1 expression in the presence of atRA in human hepatocytes and hepatic cell lines. Tretinoin 53-57 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 16-22
30709899-5 2019 In HepaRG cells, atRA increased cholesterol levels dose-dependently alongside dramatic decreases in CYP7A1 expression. Tretinoin 17-21 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 100-106
30709899-6 2019 Lentiviral-mediated CYP7A1 overexpression reversed atRA-induced cholesterol accumulation, suggesting that CYP7A1 repression mediated cholesterol accumulation. Tretinoin 51-55 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 20-26
30709899-6 2019 Lentiviral-mediated CYP7A1 overexpression reversed atRA-induced cholesterol accumulation, suggesting that CYP7A1 repression mediated cholesterol accumulation. Tretinoin 51-55 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 106-112
30709899-7 2019 In CYP7A1 promoter reporter assays and gene-knockdown studies, altered binding of hepatocyte nuclear factor 4 alpha (HNF4alpha) to the proximal promoter was essential for atRA-mediated CYP7A1 repression. Tretinoin 171-175 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 3-9
30709899-7 2019 In CYP7A1 promoter reporter assays and gene-knockdown studies, altered binding of hepatocyte nuclear factor 4 alpha (HNF4alpha) to the proximal promoter was essential for atRA-mediated CYP7A1 repression. Tretinoin 171-175 hepatocyte nuclear factor 4 alpha Homo sapiens 82-115
30709899-7 2019 In CYP7A1 promoter reporter assays and gene-knockdown studies, altered binding of hepatocyte nuclear factor 4 alpha (HNF4alpha) to the proximal promoter was essential for atRA-mediated CYP7A1 repression. Tretinoin 171-175 hepatocyte nuclear factor 4 alpha Homo sapiens 117-126
30709899-7 2019 In CYP7A1 promoter reporter assays and gene-knockdown studies, altered binding of hepatocyte nuclear factor 4 alpha (HNF4alpha) to the proximal promoter was essential for atRA-mediated CYP7A1 repression. Tretinoin 171-175 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 185-191
30709899-8 2019 Pharmacologic inhibition of c-Jun N-terminal kinase (JNK) and ERK pathways attenuated atRA-mediated CYP7A1 repression and cholesterol accumulation. Tretinoin 86-90 mitogen-activated protein kinase 8 Homo sapiens 28-51
30709899-8 2019 Pharmacologic inhibition of c-Jun N-terminal kinase (JNK) and ERK pathways attenuated atRA-mediated CYP7A1 repression and cholesterol accumulation. Tretinoin 86-90 mitogen-activated protein kinase 8 Homo sapiens 53-56
30709899-8 2019 Pharmacologic inhibition of c-Jun N-terminal kinase (JNK) and ERK pathways attenuated atRA-mediated CYP7A1 repression and cholesterol accumulation. Tretinoin 86-90 mitogen-activated protein kinase 1 Homo sapiens 62-65
30709899-8 2019 Pharmacologic inhibition of c-Jun N-terminal kinase (JNK) and ERK pathways attenuated atRA-mediated CYP7A1 repression and cholesterol accumulation. Tretinoin 86-90 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 100-106
30709899-11 2019 Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4alpha transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia. Tretinoin 42-46 mitogen-activated protein kinase 8 Homo sapiens 57-60
30709899-11 2019 Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4alpha transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia. Tretinoin 42-46 mitogen-activated protein kinase 1 Homo sapiens 65-68
30709899-11 2019 Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4alpha transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia. Tretinoin 42-46 hepatocyte nuclear factor 4 alpha Homo sapiens 119-128
30709899-11 2019 Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4alpha transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia. Tretinoin 42-46 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 152-158
28291070-5 2019 As a result of the fluorescein angiography findings, we believe ATRA-mediated upregulation of vascular endothelial growth factor may be the etiology of the NVD. Tretinoin 64-68 vascular endothelial growth factor A Homo sapiens 94-128
28291070-6 2019 Literature review shows some in vitro studies, which describe ATRA-induced upregulation of vascular endothelial growth factor in ocular tissues. Tretinoin 62-66 vascular endothelial growth factor A Homo sapiens 91-125
28291070-8 2019 CONCLUSION: Acute promyelocytic leukemia treated with ATRA may result in upregulation of vascular endothelial growth factor in retinal tissues. Tretinoin 54-58 vascular endothelial growth factor A Homo sapiens 89-123
30674471-3 2019 APL is a model for oncogene-targeted therapies: all-trans retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor alpha (PML/RARA) driver. Tretinoin 58-71 promyelocytic leukemia Mus musculus 172-175
30674471-3 2019 APL is a model for oncogene-targeted therapies: all-trans retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor alpha (PML/RARA) driver. Tretinoin 73-77 promyelocytic leukemia Mus musculus 172-175
30674471-7 2019 Remarkably, although the transcriptional output of initial ATRA response is unaffected, ATRA-induced PML/RARA degradation is blunted, as is PML nuclear body reformation and activation of P53 signaling. Tretinoin 88-92 promyelocytic leukemia Mus musculus 101-104
30674471-8 2019 Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication. Tretinoin 31-35 promyelocytic leukemia Mus musculus 111-114
30674471-10 2019 These unexpected results explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic combination. Tretinoin 175-179 promyelocytic leukemia Mus musculus 130-133
30601699-0 2019 All-trans retinoic acid suppresses bone morphogenetic protein 4 in mouse diabetic nephropathy through a unique retinoic acid response element. Tretinoin 0-23 bone morphogenetic protein 4 Mus musculus 35-63
30868103-3 2019 Here we show that the retinoic acid (RA)-degrading enzyme CYP26B1 (cytochrome P450 family 26, subfamily B, member 1) is transiently expressed in the mouse frontal cortex during postnatal development, and that medial ganglionic eminence (MGE)-derived interneurons, particularly in parvalbumin (PV)-expressing neurons, are the main cell type that has active RA signaling during this period. Tretinoin 22-35 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 58-65
30868103-3 2019 Here we show that the retinoic acid (RA)-degrading enzyme CYP26B1 (cytochrome P450 family 26, subfamily B, member 1) is transiently expressed in the mouse frontal cortex during postnatal development, and that medial ganglionic eminence (MGE)-derived interneurons, particularly in parvalbumin (PV)-expressing neurons, are the main cell type that has active RA signaling during this period. Tretinoin 22-35 parvalbumin Mus musculus 280-291
30868103-3 2019 Here we show that the retinoic acid (RA)-degrading enzyme CYP26B1 (cytochrome P450 family 26, subfamily B, member 1) is transiently expressed in the mouse frontal cortex during postnatal development, and that medial ganglionic eminence (MGE)-derived interneurons, particularly in parvalbumin (PV)-expressing neurons, are the main cell type that has active RA signaling during this period. Tretinoin 37-39 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 58-65
30868103-3 2019 Here we show that the retinoic acid (RA)-degrading enzyme CYP26B1 (cytochrome P450 family 26, subfamily B, member 1) is transiently expressed in the mouse frontal cortex during postnatal development, and that medial ganglionic eminence (MGE)-derived interneurons, particularly in parvalbumin (PV)-expressing neurons, are the main cell type that has active RA signaling during this period. Tretinoin 37-39 parvalbumin Mus musculus 280-291
30868103-3 2019 Here we show that the retinoic acid (RA)-degrading enzyme CYP26B1 (cytochrome P450 family 26, subfamily B, member 1) is transiently expressed in the mouse frontal cortex during postnatal development, and that medial ganglionic eminence (MGE)-derived interneurons, particularly in parvalbumin (PV)-expressing neurons, are the main cell type that has active RA signaling during this period. Tretinoin 356-358 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 58-65
30868103-4 2019 We found that frontal cortex-specific Cyp26b1 knock-out mice had an increased density of PV-expressing, but not somatostatin-expressing, interneurons in medial PFC, indicating a novel role of RA signaling in controlling PV neuron development. Tretinoin 192-194 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 38-45
30914656-5 2019 LXN protein is both cytosolic and secreted by prostate cells and expression is directly and potently upregulated by all-trans retinoic acid (atRA). Tretinoin 126-139 latexin Homo sapiens 0-3
30914656-5 2019 LXN protein is both cytosolic and secreted by prostate cells and expression is directly and potently upregulated by all-trans retinoic acid (atRA). Tretinoin 141-145 latexin Homo sapiens 0-3
30874620-6 2019 However, based on inhibition studies, metabolite profiles and correlation of atRA metabolism with testosterone hydroxylation, clearance of atRA in the fetal livers was mediated by CYP3A7. Tretinoin 139-143 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 180-186
30601699-0 2019 All-trans retinoic acid suppresses bone morphogenetic protein 4 in mouse diabetic nephropathy through a unique retinoic acid response element. Tretinoin 10-23 bone morphogenetic protein 4 Mus musculus 35-63
30601699-7 2019 In cultured mouse mesangial cells, treatment with ATRA or a retinoic acid receptor-alpha (RARalpha) agonist significantly decreased BMP4 and COL4 expression. Tretinoin 50-54 bone morphogenetic protein 4 Mus musculus 132-136
30601699-8 2019 Genomic analysis suggested two putative retinoic acid response elements (RAREs) for the mouse Bmp4 gene. Tretinoin 40-53 bone morphogenetic protein 4 Mus musculus 94-98
30601699-9 2019 Chromatin immunoprecipitation analysis and reporter assays indicated a putative RARE of the Bmp4 gene, located 11,488-11,501 bp upstream of exon 1A and bound to RARalpha and retinoid X receptor (RXR), which suppressed BMP4 expression after ATRA addition. Tretinoin 240-244 bone morphogenetic protein 4 Mus musculus 92-96
30601699-10 2019 ATRA suppressed BMP4 via binding of a RARalpha/RXR heterodimer to a unique RARE, alleviating glomerular matrix expansion in diabetic mice. Tretinoin 0-4 bone morphogenetic protein 4 Mus musculus 16-20
30529222-2 2019 The nuclear RXR receptors are one of the main mediators of RA cellular effects, classically by joining the direct receptors of RA, the nuclear RAR receptors, in RAR/RXR dimers which act as transcription factors. Tretinoin 59-61 RAB40B, member RAS oncogene family Homo sapiens 143-146
30159645-7 2019 Compared with the model group, UA-M and UA-H significantly reversed the RA-induced changes in S-P, U-Ca, U-P, ALP, OCN and urine DPD ratio and markedly enhanced the BMD of right femur, 4th lumbar vertebra and tibia (Plt;0.05 or Plt;0.01). Tretinoin 72-74 bone gamma-carboxyglutamate protein Rattus norvegicus 115-118
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 76-89 AKT serine/threonine kinase 1 Homo sapiens 142-145
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 91-95 AKT serine/threonine kinase 1 Homo sapiens 142-145
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 93-97 AKT serine/threonine kinase 1 Homo sapiens 122-125
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 93-97 AKT serine/threonine kinase 1 Homo sapiens 189-192
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 174-178 AKT serine/threonine kinase 1 Homo sapiens 122-125
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 174-178 AKT serine/threonine kinase 1 Homo sapiens 189-192
30529222-2 2019 The nuclear RXR receptors are one of the main mediators of RA cellular effects, classically by joining the direct receptors of RA, the nuclear RAR receptors, in RAR/RXR dimers which act as transcription factors. Tretinoin 59-61 RAB40B, member RAS oncogene family Homo sapiens 161-164
30237268-0 2019 Transglutaminase 2 programs differentiating acute promyelocytic leukemia cells in all-trans retinoic acid treatment to inflammatory stage through NF-kappaB activation. Tretinoin 92-105 transglutaminase 2 Homo sapiens 0-18
30632787-0 2019 Gen1 Modulates Metanephric Morphology Through Retinoic Acid Signaling. Tretinoin 46-59 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 0-4
30632787-4 2019 The expression of Raldh2, which encodes the key enzyme in RA synthesis, was reduced in Gen1 mutant metanephros through RNA sequencing. Tretinoin 58-60 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 87-91
30632787-6 2019 Further studies showed that all-trans retinoic acid (ATRA) rescued solitary kidney phenotype and improved ureteric branching; ATRA should be administered after ureteric budding to avoid increasing the incidence of ectopic budding in Gen1 mutants. Tretinoin 126-130 GEN1 Holliday junction 5' flap endonuclease Homo sapiens 233-237
30237268-2 2019 Administration of all-trans retinoic acid leads to significant changes in gene expression, among the most induced of which is transglutaminase 2, which is not normally expressed in neutrophil granulocytes. Tretinoin 28-41 transglutaminase 2 Homo sapiens 126-144
30237268-7 2019 This study demonstrates that transglutaminase 2 expression induced by all-trans retinoic acid treatment reprograms inflammatory signaling networks governed by nuclear factor kappa-light-chain-enhancer of activated B-cell activation, resulting in overexpression of TNF-alpha and IL-1beta in differentiating APL cells, suggesting that atypically expressed transglutaminase 2 is a promising target for leukemia treatment. Tretinoin 80-93 transglutaminase 2 Homo sapiens 29-47
30237268-7 2019 This study demonstrates that transglutaminase 2 expression induced by all-trans retinoic acid treatment reprograms inflammatory signaling networks governed by nuclear factor kappa-light-chain-enhancer of activated B-cell activation, resulting in overexpression of TNF-alpha and IL-1beta in differentiating APL cells, suggesting that atypically expressed transglutaminase 2 is a promising target for leukemia treatment. Tretinoin 80-93 tumor necrosis factor Homo sapiens 264-273
30237268-7 2019 This study demonstrates that transglutaminase 2 expression induced by all-trans retinoic acid treatment reprograms inflammatory signaling networks governed by nuclear factor kappa-light-chain-enhancer of activated B-cell activation, resulting in overexpression of TNF-alpha and IL-1beta in differentiating APL cells, suggesting that atypically expressed transglutaminase 2 is a promising target for leukemia treatment. Tretinoin 80-93 interleukin 1 beta Homo sapiens 278-286
30237268-7 2019 This study demonstrates that transglutaminase 2 expression induced by all-trans retinoic acid treatment reprograms inflammatory signaling networks governed by nuclear factor kappa-light-chain-enhancer of activated B-cell activation, resulting in overexpression of TNF-alpha and IL-1beta in differentiating APL cells, suggesting that atypically expressed transglutaminase 2 is a promising target for leukemia treatment. Tretinoin 80-93 transglutaminase 2 Homo sapiens 354-372
30864551-0 2019 All-trans Retinoic Acid Regulates the Balance of Treg-Th17 Cells through ERK and P38 Signaling Pathway. Tretinoin 10-23 mitogen-activated protein kinase 1 Mus musculus 73-76
30864551-3 2019 OBJECTIVE: To investigates the effect of ATRA on the regulation of Th17-Treg balance through ERK and p38 signaling pathway. Tretinoin 41-45 mitogen-activated protein kinase 1 Mus musculus 93-96
30864551-5 2019 The effect of ATRA on the phosphorylation of ERK and P38 was evaluated. Tretinoin 14-18 mitogen-activated protein kinase 1 Mus musculus 45-48
30609263-5 2019 The mRNA expression of HOXB4 was found to significantly increase in the retinoic acid-treated group. Tretinoin 72-85 HOXB4 Sus scrofa 23-28
30252536-2 2019 Our data revealed for the first time that retinoic acid (RA) and histone deacetylase (HDAC) inhibitors, including short-chain fatty acids and suberanilohydroxamic acid (SAHA), could individually or in combination induce miR-22. Tretinoin 42-55 microRNA 22 Homo sapiens 220-226
30810639-9 2019 RESULTS: RA promoted the highest ALP activity at days 7, 14, 21, and 28, in comparison to BMP-2 and BMP-2+RA. Tretinoin 9-11 alkaline phosphatase, placental Homo sapiens 33-36
30820351-8 2019 Finally, we prospectively validated the drug combination for BRAF-mutant melanoma that was top ranked by our approach, vemurafenib (BRAF inhibitor) + tretinoin (retinoic acid receptor agonist), using both in vitro and in vivo models of BRAF-mutant melanoma and RNA-sequencing analysis of drug-treated melanoma cells to validate the predicted mechanisms. Tretinoin 150-159 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 61-65
29992578-1 2019 GPRC5A, a retinoic acid induced gene, is preferentially expressed in lung tissue. Tretinoin 10-23 G protein-coupled receptor class C group 5 member A Homo sapiens 0-6
30761406-5 2019 RESULTS: SLNs provided significant encapsulation of atRA and also sustained its release over 72 h. A549 cells were viable following the addition of atRA SLNs and showed a reduction in IL-6 and IL-8 levels. Tretinoin 148-152 C-X-C motif chemokine ligand 8 Homo sapiens 193-197
30252536-2 2019 Our data revealed for the first time that retinoic acid (RA) and histone deacetylase (HDAC) inhibitors, including short-chain fatty acids and suberanilohydroxamic acid (SAHA), could individually or in combination induce miR-22. Tretinoin 57-59 microRNA 22 Homo sapiens 220-226
30252536-6 2019 Thus, HDAC inhibitors and RA-induced miR-22 resulted in simultaneous induction of cytoplasmic RARbeta and NUR77, leading to apoptosis of colon cancer cells. Tretinoin 26-28 microRNA 22 Homo sapiens 37-43
30252536-6 2019 Thus, HDAC inhibitors and RA-induced miR-22 resulted in simultaneous induction of cytoplasmic RARbeta and NUR77, leading to apoptosis of colon cancer cells. Tretinoin 26-28 retinoic acid receptor beta Homo sapiens 94-101
30252536-6 2019 Thus, HDAC inhibitors and RA-induced miR-22 resulted in simultaneous induction of cytoplasmic RARbeta and NUR77, leading to apoptosis of colon cancer cells. Tretinoin 26-28 nuclear receptor subfamily 4 group A member 1 Homo sapiens 106-111
30709378-0 2019 Correction to: Stemness marker ALDH1A1 promotes tumor angiogenesis via retinoic acid/HIF-1alpha/VEGF signalling in MCF-7 breast cancer cells. Tretinoin 71-84 hypoxia inducible factor 1 subunit alpha Homo sapiens 85-95
30709378-0 2019 Correction to: Stemness marker ALDH1A1 promotes tumor angiogenesis via retinoic acid/HIF-1alpha/VEGF signalling in MCF-7 breast cancer cells. Tretinoin 71-84 vascular endothelial growth factor A Homo sapiens 96-100
30250298-5 2019 Moreover, we demonstrated that pharmacological inhibition of 15-PGDH enhanced CYP26A1 expression, leading to depletion of all-trans retinoic acid (ATRA) and expansion of the ALDH1-positive subset in both human PDAC cells and tumor cells of KrasLSL-G12D/+; Ptf1aCre/+ (KC) mice. Tretinoin 132-145 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 78-85
30250298-5 2019 Moreover, we demonstrated that pharmacological inhibition of 15-PGDH enhanced CYP26A1 expression, leading to depletion of all-trans retinoic acid (ATRA) and expansion of the ALDH1-positive subset in both human PDAC cells and tumor cells of KrasLSL-G12D/+; Ptf1aCre/+ (KC) mice. Tretinoin 147-151 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 78-85
30535439-7 2019 Furthermore, the intranasal EPO-exerted neuroprotection was almost abolished when the specific Nrf2 antagonist ATRA was administered intraperitoneally prior to intranasal EPO treatment. Tretinoin 111-115 nuclear factor, erythroid derived 2, like 2 Mus musculus 95-99
30431066-12 2019 In addition, ethinyl targeted to TNF, whereas TNF and ERBB2 were targeted by cyclosporine, and tretinoin was a targeted chemical of ERBB2. Tretinoin 95-104 erb-b2 receptor tyrosine kinase 2 Homo sapiens 132-137
30329139-7 2019 Real-time RT-PCR analysis confirmed that ATRA enhanced the expression of the key ovarian development gene Wnt4 and the antitestis gene Nr0b1 in a concentration-dependent manner. Tretinoin 41-45 Wnt family member 4 Rattus norvegicus 106-110
30329139-8 2019 After 3 days of culture, ATRA-treated testes contained both immunohistochemically DMRT1-positive and FOXL2-positive somatic cells, providing evidence of disrupted testicular cell fate maintenance following ATRA exposure. Tretinoin 25-29 doublesex and mab-3 related transcription factor 1 Rattus norvegicus 82-87
30310934-3 2019 We established a chemically defined protocol by application of Activin A, BMP4, and Retinoic acid followed by GDNF, which steered hPSCs to the renal lineage and resulted in populations of SIX2+/CITED1+ metanephric mesenchyme- (MM) and of HOXB7+/GRHL2+ ureteric bud (UB)-like cells already by 6 days. Tretinoin 84-97 homeobox B7 Homo sapiens 238-243
30016600-4 2019 Microarray analysis of mouse articular cartilage cells indicated that retinoic acid, a destructive stimulus in articular cartilage, up-regulated expression of sex-determining region Y-box (Sox)4, a SoxC family transcription factor, together with increases in Adamts4 and Adamts5, both of which are aggrecanases of articular cartilages. Tretinoin 70-83 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 4 Mus musculus 259-266
30621740-3 2019 The aim of this study was to investigate the potential utility of all-trans retinoid acid (ATRA), an inhibitor of the annexin A2-S100A10 signalling pathway, as a new therapeutic against serous ovarian cancer. Tretinoin 91-95 S100 calcium binding protein A10 Homo sapiens 129-136
30621740-4 2019 METHODS: In this study we determined the effects of ATRA treatment (1-5 muM) on annexin A2 and S100A10 expression, plasmin activation, and the ability of ATRA to inhibit serous ovarian cancer cell survival, motility and invasion in vitro. Tretinoin 52-56 latexin Homo sapiens 72-75
30621740-4 2019 METHODS: In this study we determined the effects of ATRA treatment (1-5 muM) on annexin A2 and S100A10 expression, plasmin activation, and the ability of ATRA to inhibit serous ovarian cancer cell survival, motility and invasion in vitro. Tretinoin 52-56 S100 calcium binding protein A10 Homo sapiens 95-102
30621740-8 2019 RESULTS: Survival of serous ovarian cancer cells (OVCAR-3, OV-90, & OAW28) was significantly decreased by ATRA treatment (1-5 muM). Tretinoin 110-114 latexin Homo sapiens 130-133
30621740-10 2019 In OAW28 cells, reduced cell survival following ATRA treatment was associated with a reduction of S100A10 mRNA and protein levels, S100A10 and annexin A2 membrane localization, plasmin generation, motility and invasion. Tretinoin 48-52 S100 calcium binding protein A10 Homo sapiens 98-105
30621740-10 2019 In OAW28 cells, reduced cell survival following ATRA treatment was associated with a reduction of S100A10 mRNA and protein levels, S100A10 and annexin A2 membrane localization, plasmin generation, motility and invasion. Tretinoin 48-52 S100 calcium binding protein A10 Homo sapiens 131-138
30621740-12 2019 CONCLUSIONS: These findings suggest that ATRA inhibits serous ovarian cancer proliferation and invasion via both S100A10 dependant and S100A10 independent mechanisms. Tretinoin 41-45 S100 calcium binding protein A10 Homo sapiens 113-120
30621740-12 2019 CONCLUSIONS: These findings suggest that ATRA inhibits serous ovarian cancer proliferation and invasion via both S100A10 dependant and S100A10 independent mechanisms. Tretinoin 41-45 S100 calcium binding protein A10 Homo sapiens 135-142
32195202-8 2019 RA upregulated Stra8 and Piwil2, and downregulated Nanog and Oct-4. Tretinoin 0-2 piwi-like RNA-mediated gene silencing 2 Mus musculus 25-31
32195202-8 2019 RA upregulated Stra8 and Piwil2, and downregulated Nanog and Oct-4. Tretinoin 0-2 Nanog homeobox Mus musculus 51-56
29543550-9 2019 CONCLUSION: It is indicated that the combination region of Vitamin A acid and fractional laser may lead to low expression of miR-29a, thus the inhibition of downstream Akt activation is loss, Akt activation is enhanced, enhancement of the expression of TGF-beta is induced, leading to proliferation of fibroblasts, and promotion of the collagen proteins" synthesis in skin. Tretinoin 59-73 AKT serine/threonine kinase 1 Rattus norvegicus 168-171
29543550-9 2019 CONCLUSION: It is indicated that the combination region of Vitamin A acid and fractional laser may lead to low expression of miR-29a, thus the inhibition of downstream Akt activation is loss, Akt activation is enhanced, enhancement of the expression of TGF-beta is induced, leading to proliferation of fibroblasts, and promotion of the collagen proteins" synthesis in skin. Tretinoin 59-73 AKT serine/threonine kinase 1 Rattus norvegicus 192-195
29543550-9 2019 CONCLUSION: It is indicated that the combination region of Vitamin A acid and fractional laser may lead to low expression of miR-29a, thus the inhibition of downstream Akt activation is loss, Akt activation is enhanced, enhancement of the expression of TGF-beta is induced, leading to proliferation of fibroblasts, and promotion of the collagen proteins" synthesis in skin. Tretinoin 59-73 transforming growth factor, beta 1 Rattus norvegicus 253-261
29543550-10 2019 Therefore miR-29a/Akt/TGF-beta signal pathway may participate in the skin rejuvenation mechanism of action Vitamin A acid and fractional laser. Tretinoin 107-121 AKT serine/threonine kinase 1 Rattus norvegicus 18-21
29543550-10 2019 Therefore miR-29a/Akt/TGF-beta signal pathway may participate in the skin rejuvenation mechanism of action Vitamin A acid and fractional laser. Tretinoin 107-121 transforming growth factor, beta 1 Rattus norvegicus 22-30
30806286-3 2019 ATRA treatment causes ~12-fold increase in the number of acidic vesicular organelles and induces marked up-regulation of LC3-II, autophagy-related 5 (ATG5), and Beclin-1. Tretinoin 0-4 autophagy related 5 Homo sapiens 150-154
30806286-8 2019 ATRA inhibits Bcl-2, up-regulates Beclin-1 expression, and reduces induction of mTOR activation/phosphorylation in NB4 cells. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 14-19
30806286-8 2019 ATRA inhibits Bcl-2, up-regulates Beclin-1 expression, and reduces induction of mTOR activation/phosphorylation in NB4 cells. Tretinoin 0-4 mechanistic target of rapamycin kinase Homo sapiens 80-84
30814416-11 2019 In the ATRA-experiment, ATRA suppressed the expression of IL-6, TNF-alpha, NO, a disintegrin and metalloprotease with thrombospondin motifs-4 (ADAMTS-4), MMP-3, and MMP-9. Tretinoin 7-11 interleukin 6 Rattus norvegicus 58-62
30295852-9 2019 The effect of CREG1 on Ucp1 promoter activity was also stimulated by retinoic acid. Tretinoin 69-82 cellular repressor of E1A-stimulated genes 1 Mus musculus 14-19
30472251-6 2019 On the molecular level, ATRA signalling causes induction of TXNIP, a potent inhibitor of the physiological antioxidant thioredoxin (TRX1) and sensitizes cells to necrotic cell death upon hypoxia. Tretinoin 24-28 thioredoxin 1 Rattus norvegicus 119-130
30472251-7 2019 5ML-mediated prevention of ATRA effects were shown to be based on the inhibition of cellular ATRA uptake by interference with the cholesterol (and retinol) binding motif of the transmembrane protein STRA6. Tretinoin 27-31 signaling receptor and transporter of retinol STRA6 Rattus norvegicus 199-204
28125332-4 2019 We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in Syx-/- cells facilitated noggin secretion; and we report unpublished results showing that pharmacological inhibition of RhoA accelerates the neuronal differentiation of human embryonic stem cells. Tretinoin 115-128 ras homolog family member A Homo sapiens 51-55
28125332-4 2019 We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in Syx-/- cells facilitated noggin secretion; and we report unpublished results showing that pharmacological inhibition of RhoA accelerates the neuronal differentiation of human embryonic stem cells. Tretinoin 115-128 pleckstrin homology and RhoGEF domain containing G5 Homo sapiens 280-283
28125332-4 2019 We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in Syx-/- cells facilitated noggin secretion; and we report unpublished results showing that pharmacological inhibition of RhoA accelerates the neuronal differentiation of human embryonic stem cells. Tretinoin 115-128 ras homolog family member A Homo sapiens 202-206
31359396-1 2019 Dysregulation of retinoic acid signaling is implicated in several human cancer types, including melanoma where the gene encoding retinoic acid receptor beta (RARbeta) is frequently silenced by promoter hypermethylation. Tretinoin 17-30 retinoic acid receptor beta Homo sapiens 129-156
31359396-1 2019 Dysregulation of retinoic acid signaling is implicated in several human cancer types, including melanoma where the gene encoding retinoic acid receptor beta (RARbeta) is frequently silenced by promoter hypermethylation. Tretinoin 17-30 retinoic acid receptor beta Homo sapiens 158-165
31359396-4 2019 The levels of RARbeta signaling can be modulated using RARbeta agonists (e.g., all-trans retinoic acid) and antagonists (e.g., LE135). Tretinoin 79-102 retinoic acid receptor beta Homo sapiens 14-21
31359396-4 2019 The levels of RARbeta signaling can be modulated using RARbeta agonists (e.g., all-trans retinoic acid) and antagonists (e.g., LE135). Tretinoin 79-102 retinoic acid receptor beta Homo sapiens 55-62
28125332-4 2019 We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in Syx-/- cells facilitated noggin secretion; and we report unpublished results showing that pharmacological inhibition of RhoA accelerates the neuronal differentiation of human embryonic stem cells. Tretinoin 115-128 ras homolog family member A Homo sapiens 202-206
30641601-6 2019 Furthermore, CYP2E1 induction results in an enhanced activation of various procarcinogens and an increased degradation of retinol and retinoic acid (RA), a compound responsible for cell differentiation and proliferation. Tretinoin 134-147 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 13-19
29926545-0 2019 The Effects of Retinoic Acid and MAPK Inhibitors on Phosphorylation of Smad2/3 Induced by Transforming Growth Factor beta1. Tretinoin 15-28 SMAD family member 2 Mus musculus 71-78
29926545-2 2019 We investigated the effect of RA and the role of these signaling molecules on the phosphorylation of Smad2/3 (p-Smad2/3) induced by TGF-beta1. Tretinoin 30-32 SMAD family member 2 Mus musculus 101-108
29926545-2 2019 We investigated the effect of RA and the role of these signaling molecules on the phosphorylation of Smad2/3 (p-Smad2/3) induced by TGF-beta1. Tretinoin 30-32 SMAD family member 2 Mus musculus 101-106
30641601-6 2019 Furthermore, CYP2E1 induction results in an enhanced activation of various procarcinogens and an increased degradation of retinol and retinoic acid (RA), a compound responsible for cell differentiation and proliferation. Tretinoin 149-151 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 13-19
30575756-5 2018 In exploring how emx1 influences nephron patterning, we found that retinoic acid (RA), a morphogen that induces proximal and represses distal segments, negatively regulates emx1 expression. Tretinoin 67-80 empty spiracles homeobox 1 Danio rerio 17-21
30622531-10 2018 In MoDCs generated in the presence of retinoic acid, which express increased CD103, intracellular CD103 significantly redistributed toward the E-cadherin-coated glass surface. Tretinoin 38-51 cadherin 1 Homo sapiens 143-153
30575756-5 2018 In exploring how emx1 influences nephron patterning, we found that retinoic acid (RA), a morphogen that induces proximal and represses distal segments, negatively regulates emx1 expression. Tretinoin 67-80 empty spiracles homeobox 1 Danio rerio 173-177
30566883-5 2018 Deletion of Rdh7 in IECs diminished RA signaling in immune cells, reduced the IL-22-dependent antimicrobial response, and enhanced resistance to colonization by Salmonella Typhimurium. Tretinoin 36-38 retinol dehydrogenase 7 Mus musculus 12-16
30446224-0 2018 Retinoic acid modulates iron metabolism imbalance in anemia of inflammation induced by LPS via reversely regulating hepcidin and ferroportin expression. Tretinoin 0-13 toll-like receptor 4 Mus musculus 87-90
30723587-2 2019 The LXR ligands/oxysterols and the RXR ligand 9-cis Retinoic Acid (9-cis RA) were shown to dampen DC migration to lymphoid organs through the inhibition of CCR7 expression. Tretinoin 52-65 chemokine (C-C motif) receptor 7 Mus musculus 156-160
30566883-3 2018 Here we found that commensal bacteria belonging to class Clostridia modulate RA concentration in the gut by suppressing the expression of retinol dehydrogenase 7 (Rdh7) in IECs. Tretinoin 77-79 retinol dehydrogenase 7 Mus musculus 138-161
30566883-3 2018 Here we found that commensal bacteria belonging to class Clostridia modulate RA concentration in the gut by suppressing the expression of retinol dehydrogenase 7 (Rdh7) in IECs. Tretinoin 77-79 retinol dehydrogenase 7 Mus musculus 163-167
30446224-1 2018 The present study was designed to investigate the effect of retinoic acid (RA) on anemia of inflammation (AI) induced by lipopolysaccharide (LPS) and explore the potential mechanisms. Tretinoin 60-73 toll-like receptor 4 Mus musculus 141-144
30446224-1 2018 The present study was designed to investigate the effect of retinoic acid (RA) on anemia of inflammation (AI) induced by lipopolysaccharide (LPS) and explore the potential mechanisms. Tretinoin 75-77 toll-like receptor 4 Mus musculus 141-144
30446224-7 2018 Furthermore, RA down-regulated the protein expression of hepcidin, toll-like receptor 4 (TLR4) and p-p65 in liver tissue, while up-regulated that of ferroportin. Tretinoin 13-15 toll-like receptor 4 Mus musculus 67-87
30446224-7 2018 Furthermore, RA down-regulated the protein expression of hepcidin, toll-like receptor 4 (TLR4) and p-p65 in liver tissue, while up-regulated that of ferroportin. Tretinoin 13-15 toll-like receptor 4 Mus musculus 89-93
30446224-8 2018 RA modulates iron metabolism imbalance in AI induced by LPS via reversely regulating hepcidin and ferroportin expression, which might be mediated by TLT-4/NFkappaB signaling pathway. Tretinoin 0-2 toll-like receptor 4 Mus musculus 56-59
30446224-8 2018 RA modulates iron metabolism imbalance in AI induced by LPS via reversely regulating hepcidin and ferroportin expression, which might be mediated by TLT-4/NFkappaB signaling pathway. Tretinoin 0-2 triggering receptor expressed on myeloid cells-like 4 Mus musculus 149-154
29943815-7 2018 ATRA induced the superoxide dismutase (SOD) and glutathione transferase activities, while it reduced the malondialdehyde and reactive oxygen species (ROS) production both in healthy and varicocele sperm. Tretinoin 0-4 superoxide dismutase 1 Homo sapiens 39-42
30415163-0 2018 A novel all-trans retinoic acid derivative inhibits proliferation and induces apoptosis of myelodysplastic syndromes cell line SKM-1 cells via up-regulating p53. Tretinoin 18-31 tumor protein p53 Homo sapiens 157-160
30355624-13 2018 Importantly, this form of synaptic plasticity is absent when fragile X mental retardation protein is selectively deleted in parvalbumin-expressing interneurons, suggesting a functional connection between RARalpha and fragile X mental retardation protein signaling pathways in vivo Thus, dysfunction of RA-dependent homeostatic plasticity may contribute to cortical circuit abnormalities in fragile X syndrome. Tretinoin 204-206 parvalbumin Mus musculus 124-135
30372846-4 2018 OBJECTIVE: To investigate the therapeutic potential effect of ATRA via the amelioration of the ERK/JAK-STAT pathways in the lungs of emphysematous rats. Tretinoin 62-66 Eph receptor B1 Rattus norvegicus 95-98
30372846-8 2018 RESULTS AND DISCUSSION: In silico docking, analysis confirms that ATRA interferes with the normal binding of ligands (TNF-alpha, IL6ST) and receptors (TNFR1, IL6) of ERK/JAK-STAT pathways respectively. Tretinoin 66-70 tumor necrosis factor Rattus norvegicus 118-127
30372846-8 2018 RESULTS AND DISCUSSION: In silico docking, analysis confirms that ATRA interferes with the normal binding of ligands (TNF-alpha, IL6ST) and receptors (TNFR1, IL6) of ERK/JAK-STAT pathways respectively. Tretinoin 66-70 interleukin 6 Rattus norvegicus 129-132
30372846-8 2018 RESULTS AND DISCUSSION: In silico docking, analysis confirms that ATRA interferes with the normal binding of ligands (TNF-alpha, IL6ST) and receptors (TNFR1, IL6) of ERK/JAK-STAT pathways respectively. Tretinoin 66-70 Eph receptor B1 Rattus norvegicus 166-169
30372846-9 2018 ATRA restored the histology, proteases/antiproteases balance, levels of inflammatory markers, antioxidants, expression of candidate genes of ERK and JAK-STAT pathways in the therapy group. Tretinoin 0-4 Eph receptor B1 Rattus norvegicus 141-144
29569971-0 2018 Src family kinase inhibitor bosutinib enhances retinoic acid-induced differentiation of HL-60 leukemia cells. Tretinoin 47-60 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3
30155966-2 2018 This study aimed to explore the relationship and potential mechanism between enhancer DNA methylation and mRNA expression of histone deacetylase 4 (HDAC4) during palatal fusion induced by maternal exposure to all-trans retinoic acid (ATRA). Tretinoin 219-232 histone deacetylase 4 Mus musculus 125-146
30155966-2 2018 This study aimed to explore the relationship and potential mechanism between enhancer DNA methylation and mRNA expression of histone deacetylase 4 (HDAC4) during palatal fusion induced by maternal exposure to all-trans retinoic acid (ATRA). Tretinoin 219-232 histone deacetylase 4 Mus musculus 148-153
30155966-2 2018 This study aimed to explore the relationship and potential mechanism between enhancer DNA methylation and mRNA expression of histone deacetylase 4 (HDAC4) during palatal fusion induced by maternal exposure to all-trans retinoic acid (ATRA). Tretinoin 234-238 histone deacetylase 4 Mus musculus 148-153
30062698-11 2018 Over-expression of VRK2 in human neuroblastoma (SH-SY5Y) cells reduced neurite outgrowth induced by retinoic acid. Tretinoin 100-113 VRK serine/threonine kinase 2 Homo sapiens 19-23
30155966-2 2018 This study aimed to explore the relationship and potential mechanism between enhancer DNA methylation and mRNA expression of histone deacetylase 4 (HDAC4) during palatal fusion induced by maternal exposure to all-trans retinoic acid (ATRA). Tretinoin 234-238 histone deacetylase 4 Mus musculus 125-146
30059166-8 2018 ATRA inhibited physiologically induced (RANKL) osteoclast formation of human peripheral blood monocytes and mouse BMM as well as human monocytes stimulated with the pro-inflammatory compounds, TNF-alpha and LPS. Tretinoin 0-4 tumor necrosis factor Homo sapiens 193-202
30397350-4 2018 CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. Tretinoin 29-48 killer cell lectin like receptor B1 Homo sapiens 0-5
30397350-4 2018 CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. Tretinoin 50-54 killer cell lectin like receptor B1 Homo sapiens 0-5
30209176-3 2018 During viral infection, LUBAC is reported to inhibit the induction of interferon (IFN) by the cytosolic RNA sensor retinoic acid-inducible gene I (RIG-I). Tretinoin 115-128 interferon alpha 1 Homo sapiens 82-85
30397350-4 2018 CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. Tretinoin 132-136 killer cell lectin like receptor B1 Homo sapiens 0-5
30397350-4 2018 CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. Tretinoin 132-136 killer cell lectin like receptor B1 Homo sapiens 86-91
30397350-4 2018 CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. Tretinoin 132-136 killer cell lectin like receptor B1 Homo sapiens 86-91
30366671-0 2018 Adenylate cyclase 7 regulated by miR-192 promotes ATRA-induced differentiation of acute promyelocytic leukemia cells. Tretinoin 50-54 microRNA 192 Homo sapiens 33-40
30267739-0 2018 Inhibition of NRF2 signaling and increased reactive oxygen species during embryogenesis in a rat model of retinoic acid-induced neural tube defects. Tretinoin 106-119 NFE2 like bZIP transcription factor 2 Rattus norvegicus 14-18
30267739-9 2018 These data demonstrate substantial oxidative stress and NRF2 signaling pathway disruption in a model of NTDs induced by atRA. Tretinoin 120-124 NFE2 like bZIP transcription factor 2 Rattus norvegicus 56-60
30267739-10 2018 The inhibitory effects of atRA on NRF2 signaling may lower cellular defenses against RA-induced oxidative stress and could play important roles in NTD occurrence during embryonic development. Tretinoin 26-30 NFE2 like bZIP transcription factor 2 Rattus norvegicus 34-38
30267739-10 2018 The inhibitory effects of atRA on NRF2 signaling may lower cellular defenses against RA-induced oxidative stress and could play important roles in NTD occurrence during embryonic development. Tretinoin 28-30 NFE2 like bZIP transcription factor 2 Rattus norvegicus 34-38
30222957-5 2018 Furthermore, exposure to all-trans Retinoic acid at E10.0 can mimic the Ezh2 mutant calvarial phenotype, and administration of the pan retinoic acid receptor (RAR) antagonist, BMS-453, to Ezh2 mutants partially restores the commitment to the calvarial bone lineage and PM-derived bone development in vivo. Tretinoin 35-48 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 72-76
30322383-2 2018 In addition to nuclear receptors, there are other intracellular RA binding proteins such as cellular retinoic acid binding proteins (CRABP1 and CRABP2) and cytochrome P450 (CYP) enzymes, whose contributions to the RA signaling pathway have not been fully understood. Tretinoin 64-66 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 156-171
29920752-9 2018 In addition, treatment with pilocarpine significantly suppressed ATRA-induced phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB). Tretinoin 65-69 cAMP responsive element binding protein 1 Mus musculus 169-173
29920752-10 2018 These findings suggest that the stimulation of m2 - or m4 -AchR suppresses ATRA-induced differentiation of mouse iPS cells into NPCs by inhibiting the cAMP/protein kinase A pathway and CREB activation. Tretinoin 75-79 cAMP responsive element binding protein 1 Mus musculus 185-189
29520716-0 2018 Rhythmic Diurnal Synthesis and Signaling of Retinoic Acid in the Rat Pineal Gland and Its Action to Rapidly Downregulate ERK Phosphorylation. Tretinoin 44-57 Eph receptor B1 Rattus norvegicus 121-124
30420837-11 2018 ADH1 could increase retinoic acid (RA) synthesis, then RA facilitates Leydig cell differentiation by activating the steroidogenic factor 1 gene (Nr5a1) promoter activity, which consequently promotes Leydig cell specific gene expression, resulting in progenitor Leydig cells differentiation into functional Leydig cells. Tretinoin 20-33 alcohol dehydrogenase 1 (class I) Mus musculus 0-4
30420837-11 2018 ADH1 could increase retinoic acid (RA) synthesis, then RA facilitates Leydig cell differentiation by activating the steroidogenic factor 1 gene (Nr5a1) promoter activity, which consequently promotes Leydig cell specific gene expression, resulting in progenitor Leydig cells differentiation into functional Leydig cells. Tretinoin 35-37 alcohol dehydrogenase 1 (class I) Mus musculus 0-4
30420837-11 2018 ADH1 could increase retinoic acid (RA) synthesis, then RA facilitates Leydig cell differentiation by activating the steroidogenic factor 1 gene (Nr5a1) promoter activity, which consequently promotes Leydig cell specific gene expression, resulting in progenitor Leydig cells differentiation into functional Leydig cells. Tretinoin 55-57 alcohol dehydrogenase 1 (class I) Mus musculus 0-4
30425691-9 2018 Consistent with this finding, knocking out IRF3 or IRF7, two key downstream regulatory factors in most nucleic acid sensing pathways, resulted in a significant decrease in the adjuvant effect of ATRA/NAFL. Tretinoin 195-199 interferon regulatory factor 7 Homo sapiens 51-55
30359286-11 2018 This effect of UCHL1 was associated with positively regulating RA-induced AKT and ERK1/2 signaling activation. Tretinoin 63-65 AKT serine/threonine kinase 1 Homo sapiens 74-77
30359286-11 2018 This effect of UCHL1 was associated with positively regulating RA-induced AKT and ERK1/2 signaling activation. Tretinoin 63-65 mitogen-activated protein kinase 3 Homo sapiens 82-88
30322383-2 2018 In addition to nuclear receptors, there are other intracellular RA binding proteins such as cellular retinoic acid binding proteins (CRABP1 and CRABP2) and cytochrome P450 (CYP) enzymes, whose contributions to the RA signaling pathway have not been fully understood. Tretinoin 64-66 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 173-176
30322383-2 2018 In addition to nuclear receptors, there are other intracellular RA binding proteins such as cellular retinoic acid binding proteins (CRABP1 and CRABP2) and cytochrome P450 (CYP) enzymes, whose contributions to the RA signaling pathway have not been fully understood. Tretinoin 134-136 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 173-176
30322383-9 2018 The cellular levels of CRABP1 are more important than that of CRABP2 in controlling RA metabolite formation at pharmacological conditions (RA = 0.1-1 muM). Tretinoin 24-26 latexin Homo sapiens 150-153
30349195-3 2018 Our previous studies demonstrated that heterodimeric bone morphogenetic protein 2/7 (BMP2/7) was a more potent BMP than homodimeric BMP2 or BMP7, and could antagonize the inhibitive effect of ATRA to rescue osteoblastogenesis. Tretinoin 192-196 bone morphogenetic protein 2 Mus musculus 53-83
30349195-7 2018 When cells were treated by ATRA, BMP2/7 was superior only in rescuing cell viability and ALP activity, compared to BMP2 or BMP7. Tretinoin 27-31 bone morphogenetic protein 2 Mus musculus 33-39
30349195-7 2018 When cells were treated by ATRA, BMP2/7 was superior only in rescuing cell viability and ALP activity, compared to BMP2 or BMP7. Tretinoin 27-31 bone morphogenetic protein 2 Mus musculus 33-37
30349195-3 2018 Our previous studies demonstrated that heterodimeric bone morphogenetic protein 2/7 (BMP2/7) was a more potent BMP than homodimeric BMP2 or BMP7, and could antagonize the inhibitive effect of ATRA to rescue osteoblastogenesis. Tretinoin 192-196 bone morphogenetic protein 2 Mus musculus 85-91
30349195-3 2018 Our previous studies demonstrated that heterodimeric bone morphogenetic protein 2/7 (BMP2/7) was a more potent BMP than homodimeric BMP2 or BMP7, and could antagonize the inhibitive effect of ATRA to rescue osteoblastogenesis. Tretinoin 192-196 bone morphogenetic protein 2 Mus musculus 85-89
30349195-4 2018 Materials and methods: In this study, we compared the effectiveness of BMP2/7, BMP2 and BMP7 in restoring osteoblastogenesis of murine preosteoblasts upon inhibition with 1 microM ATRA, and we further analyzed the potential mechanisms. Tretinoin 180-184 bone morphogenetic protein 2 Mus musculus 71-77
29964319-8 2018 However, the changes in Nrf2 target-genes, as well as ameliorative liver histology induced by Rg1 were abrogated by Nrf2 antagonist all-transretinoic acid in vivo and Nrf2 siRNA in vitro. Tretinoin 136-154 nuclear factor, erythroid derived 2, like 2 Mus musculus 24-28
29964319-8 2018 However, the changes in Nrf2 target-genes, as well as ameliorative liver histology induced by Rg1 were abrogated by Nrf2 antagonist all-transretinoic acid in vivo and Nrf2 siRNA in vitro. Tretinoin 136-154 nuclear factor, erythroid derived 2, like 2 Mus musculus 116-120
29964319-8 2018 However, the changes in Nrf2 target-genes, as well as ameliorative liver histology induced by Rg1 were abrogated by Nrf2 antagonist all-transretinoic acid in vivo and Nrf2 siRNA in vitro. Tretinoin 136-154 nuclear factor, erythroid derived 2, like 2 Mus musculus 116-120
30193155-0 2018 All-trans retinoic acid ameliorates inflammatory response mediated by TLR4/NF-kappaB during initiation of diabetic nephropathy. Tretinoin 10-23 toll-like receptor 4 Rattus norvegicus 70-74
30193155-9 2018 To further explore the mechanisms through which ATRA decreased inflammatory response, the NF-kappaB/p65 signaling mediated by TLR4 was studied. Tretinoin 48-52 synaptotagmin 1 Rattus norvegicus 100-103
30193155-9 2018 To further explore the mechanisms through which ATRA decreased inflammatory response, the NF-kappaB/p65 signaling mediated by TLR4 was studied. Tretinoin 48-52 toll-like receptor 4 Rattus norvegicus 126-130
30193155-10 2018 We found that ATRA administration attenuates the TLR4/NF-kappaB inflammatory signaling and prevents NF-kappaB nuclear translocation in glomeruli and proximal tubules. Tretinoin 14-18 toll-like receptor 4 Rattus norvegicus 49-53
30249243-8 2018 Using all-trans retinoic acid (tRA)-induced gene as a model, we show that the dynamic deposition of H2A.Z and H3.3 coordinately regulates the PRC2-dependent H3K27 methylation by modulating local chromatin structure at the promoter region during the process of turning genes off. Tretinoin 16-29 H2A.Z variant histone 1 Mus musculus 100-105
30217263-11 2018 Interestingly, rhein potentiated all-trans retinoic acid (ATRA)-induced macrophage differentiation in NB4 cells by inducing changes in morphology, expression of the differentiation markers CD11b and CD14, ROS production, phagocytic activity, and expression of CCR1 and CCR2. Tretinoin 58-62 C-C motif chemokine receptor 2 Homo sapiens 269-273
30288053-0 2018 All-trans retinoic acid-encapsulated, CD20 antibody-conjugated poly(lactic-co-glycolic acid) nanoparticles effectively target and eliminate melanoma-initiating cells in vitro. Tretinoin 10-23 keratin 20 Homo sapiens 38-42
30288053-5 2018 In this study, we examined the activity of ATRA against melanoma-initiating cells and developed ATRA-encapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles, which were conjugated with a CD20 antibody (ATRA-PNP-CD20) for targeted delivery of ATRA to CD20+ melanoma-initiating cells. Tretinoin 96-100 keratin 20 Homo sapiens 195-199
30288053-5 2018 In this study, we examined the activity of ATRA against melanoma-initiating cells and developed ATRA-encapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles, which were conjugated with a CD20 antibody (ATRA-PNP-CD20) for targeted delivery of ATRA to CD20+ melanoma-initiating cells. Tretinoin 96-100 keratin 20 Homo sapiens 219-223
30030101-9 2018 However, the changes in transporters and enzymes, as well as ameliorative liver histology induced by Rg1 were abrogated by Nrf2 antagonist all-transretinoic acid in vivo and Nrf2 siRNA in vitro. Tretinoin 139-161 nuclear factor, erythroid derived 2, like 2 Mus musculus 123-127
30010888-0 2018 Goblet cell-produced retinoic acid suppresses CD86 expression and IL-12 production in bone marrow-derived cells. Tretinoin 21-34 CD86 antigen Mus musculus 46-50
30010888-2 2018 This study tested the hypothesis that mouse conjunctival goblet cells produce biologically active retinoic acid (RA) that suppresses CD86 expression and IL-12 production by myeloid cells. Tretinoin 98-111 CD86 antigen Mus musculus 133-137
30010888-2 2018 This study tested the hypothesis that mouse conjunctival goblet cells produce biologically active retinoic acid (RA) that suppresses CD86 expression and IL-12 production by myeloid cells. Tretinoin 113-115 CD86 antigen Mus musculus 133-137
30288053-5 2018 In this study, we examined the activity of ATRA against melanoma-initiating cells and developed ATRA-encapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles, which were conjugated with a CD20 antibody (ATRA-PNP-CD20) for targeted delivery of ATRA to CD20+ melanoma-initiating cells. Tretinoin 96-100 keratin 20 Homo sapiens 195-199
30288053-5 2018 In this study, we examined the activity of ATRA against melanoma-initiating cells and developed ATRA-encapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles, which were conjugated with a CD20 antibody (ATRA-PNP-CD20) for targeted delivery of ATRA to CD20+ melanoma-initiating cells. Tretinoin 96-100 keratin 20 Homo sapiens 219-223
30288053-5 2018 In this study, we examined the activity of ATRA against melanoma-initiating cells and developed ATRA-encapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles, which were conjugated with a CD20 antibody (ATRA-PNP-CD20) for targeted delivery of ATRA to CD20+ melanoma-initiating cells. Tretinoin 96-100 keratin 20 Homo sapiens 219-223
30249243-8 2018 Using all-trans retinoic acid (tRA)-induced gene as a model, we show that the dynamic deposition of H2A.Z and H3.3 coordinately regulates the PRC2-dependent H3K27 methylation by modulating local chromatin structure at the promoter region during the process of turning genes off. Tretinoin 31-34 H2A.Z variant histone 1 Mus musculus 100-105
30288053-5 2018 In this study, we examined the activity of ATRA against melanoma-initiating cells and developed ATRA-encapsulated poly(lactic-co-glycolic acid) (PLGA) nanoparticles, which were conjugated with a CD20 antibody (ATRA-PNP-CD20) for targeted delivery of ATRA to CD20+ melanoma-initiating cells. Tretinoin 96-100 keratin 20 Homo sapiens 219-223
30248940-6 2018 Combined treatment with melatonin and retinoic acid decreased the expression of the Bcl-2. Tretinoin 38-51 BCL2 apoptosis regulator Homo sapiens 84-89
30111657-5 2018 Despite overlapping expression patterns of the genes encoding the RA-synthesizing enzyme Aldh1a2 and the RA-degrading enzyme Cyp26a1, RARgamma1 functions as a transcriptional activator in early mesoderm development, suggesting that RA ligand is available to the embryo earlier than previously appreciated. Tretinoin 66-68 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 89-96
30195874-16 2018 Allicin combination with ATRA increased the mRNA level of RARbeta in CD117+ cells. Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 58-65
30288053-8 2018 The drug-loading capacity of ATRA-PNP-CD20 was 8.7%, and ATRA-PNP-CD20 displayed a sustained release of ATRA for 144 hours. Tretinoin 29-33 keratin 20 Homo sapiens 38-42
30288053-8 2018 The drug-loading capacity of ATRA-PNP-CD20 was 8.7%, and ATRA-PNP-CD20 displayed a sustained release of ATRA for 144 hours. Tretinoin 29-33 keratin 20 Homo sapiens 66-70
30288053-9 2018 The results showed that ATRA-PNP-CD20 could effectively and specifically deliver ATRA to CD20+ melanoma-initiating cells, achieving superior inhibitory effects against CD20+ melanoma-initiating cells compared with those of free ATRA and nontargeted nanoparticles. Tretinoin 24-28 keratin 20 Homo sapiens 33-37
30288053-9 2018 The results showed that ATRA-PNP-CD20 could effectively and specifically deliver ATRA to CD20+ melanoma-initiating cells, achieving superior inhibitory effects against CD20+ melanoma-initiating cells compared with those of free ATRA and nontargeted nanoparticles. Tretinoin 24-28 keratin 20 Homo sapiens 89-93
30288053-9 2018 The results showed that ATRA-PNP-CD20 could effectively and specifically deliver ATRA to CD20+ melanoma-initiating cells, achieving superior inhibitory effects against CD20+ melanoma-initiating cells compared with those of free ATRA and nontargeted nanoparticles. Tretinoin 24-28 keratin 20 Homo sapiens 89-93
30288053-9 2018 The results showed that ATRA-PNP-CD20 could effectively and specifically deliver ATRA to CD20+ melanoma-initiating cells, achieving superior inhibitory effects against CD20+ melanoma-initiating cells compared with those of free ATRA and nontargeted nanoparticles. Tretinoin 81-85 keratin 20 Homo sapiens 33-37
30288053-9 2018 The results showed that ATRA-PNP-CD20 could effectively and specifically deliver ATRA to CD20+ melanoma-initiating cells, achieving superior inhibitory effects against CD20+ melanoma-initiating cells compared with those of free ATRA and nontargeted nanoparticles. Tretinoin 81-85 keratin 20 Homo sapiens 89-93
30288053-9 2018 The results showed that ATRA-PNP-CD20 could effectively and specifically deliver ATRA to CD20+ melanoma-initiating cells, achieving superior inhibitory effects against CD20+ melanoma-initiating cells compared with those of free ATRA and nontargeted nanoparticles. Tretinoin 81-85 keratin 20 Homo sapiens 89-93
30288053-10 2018 To the best of our knowledge, we report for the first time a potent activity of ATRA against CD20+ melanoma-initiating cells, targeted drug delivery of ATRA via nanoparticles to melanoma-initiating cells, and the achievement of a superior inhibitory effect against melanoma-initiating cells by using a CD20 antibody. Tretinoin 80-84 keratin 20 Homo sapiens 93-97
30288053-10 2018 To the best of our knowledge, we report for the first time a potent activity of ATRA against CD20+ melanoma-initiating cells, targeted drug delivery of ATRA via nanoparticles to melanoma-initiating cells, and the achievement of a superior inhibitory effect against melanoma-initiating cells by using a CD20 antibody. Tretinoin 80-84 keratin 20 Homo sapiens 302-306
30288053-10 2018 To the best of our knowledge, we report for the first time a potent activity of ATRA against CD20+ melanoma-initiating cells, targeted drug delivery of ATRA via nanoparticles to melanoma-initiating cells, and the achievement of a superior inhibitory effect against melanoma-initiating cells by using a CD20 antibody. Tretinoin 152-156 keratin 20 Homo sapiens 302-306
30241502-4 2018 RESULTS: As hypothesized, minocycline exposure resulted in a substantial increase of RA levels in the human monocytic cell line THP-1. Tretinoin 85-87 GLI family zinc finger 2 Homo sapiens 128-133
30248940-12 2018 The changes in the activation of proliferation in HL-60 cells, the mitotic index, and Bcl-2 expression under combined effect of retinoic acid (10 nM) with melatonin (1 mM) are similar to changes that are induced by 1 muM retinoic acid. Tretinoin 128-141 BCL2 apoptosis regulator Homo sapiens 86-91
30206209-0 2018 Regulation of cell surface protease receptor S100A10 by retinoic acid therapy in acute promyelocytic leukemia (APL) . Tretinoin 56-69 S100 calcium binding protein A10 Homo sapiens 45-52
30206209-4 2018 Furthermore, treatment of the APL cell line, NB4 with all-trans retinoic acid (ATRA) causes the rapid loss of p36 and p11 protein. Tretinoin 54-77 S100 calcium binding protein A10 Homo sapiens 118-121
30206209-7 2018 ATRA treatment of MCF-7 breast cancer cells reduced p11 but not p36 transcript and protein levels, thus indicating that ATRA can regulate p11 levels independently of PML/RARalpha and p36. Tretinoin 0-4 S100 calcium binding protein A10 Homo sapiens 52-55
30206209-4 2018 Furthermore, treatment of the APL cell line, NB4 with all-trans retinoic acid (ATRA) causes the rapid loss of p36 and p11 protein. Tretinoin 79-83 S100 calcium binding protein A10 Homo sapiens 118-121
30206209-7 2018 ATRA treatment of MCF-7 breast cancer cells reduced p11 but not p36 transcript and protein levels, thus indicating that ATRA can regulate p11 levels independently of PML/RARalpha and p36. Tretinoin 0-4 S100 calcium binding protein A10 Homo sapiens 138-141
30206209-6 2018 Here, we show that the proteasomal inhibitor, lactacystin reversed the ATRA-dependent loss of p11, but did not cause an accumulation of ubiquitylated forms of p11, suggesting that ATRA promotes the proteasomal degradation of p11 in an ubiquitin-independent manner. Tretinoin 71-75 S100 calcium binding protein A10 Homo sapiens 94-97
30206209-7 2018 ATRA treatment of MCF-7 breast cancer cells reduced p11 but not p36 transcript and protein levels, thus indicating that ATRA can regulate p11 levels independently of PML/RARalpha and p36. Tretinoin 120-124 S100 calcium binding protein A10 Homo sapiens 138-141
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 lipoprotein lipase Rattus norvegicus 77-80
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 retinaldehyde binding protein 1 Rattus norvegicus 115-120
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 14-27 retinoic acid receptor beta Homo sapiens 72-76
28536942-0 2018 LRRC25 plays a key role in all-trans retinoic acid-induced granulocytic differentiation as a novel potential leukocyte differentiation antigen. Tretinoin 37-50 leucine rich repeat containing 25 Homo sapiens 0-6
28536942-8 2018 Therefore, LRRC25, a potential leukocyte differentiation antigen, is a key regulator of ATRA-induced granulocytic differentiation. Tretinoin 88-92 leucine rich repeat containing 25 Homo sapiens 11-17
29350080-0 2018 IRF2BP2-RARA t(1;17)(q42.3;q21.2) APL blasts differentiate in response to all-trans retinoic acid. Tretinoin 84-97 interferon regulatory factor 2 binding protein 2 Homo sapiens 0-7
30022380-0 2018 All Trans Retinoic Acid Attenuates Markers of Neuroinflammation in Rat Brain by Modulation of SIRT1 and NFkappaB. Tretinoin 10-23 sirtuin 1 Rattus norvegicus 94-99
30022380-8 2018 Ethanol exposure increased markers of oxidative stress, inflammation and the activities of alcohol and acetaldehyde dehydrogenases and reduced the expression of SIRT1 in the whole brain.The ethanol induced altered expressions of NFkappaB and SIRT1 were modulated by supplementation of ATRA. Tretinoin 285-289 sirtuin 1 Rattus norvegicus 242-247
30022380-10 2018 Our results seemed to suggest that ATRA regressed the mediators of ethanol induced neuroinflammation by reducing oxidative stress and by regulating the expression of NFkappaB and SIRT1. Tretinoin 35-39 sirtuin 1 Rattus norvegicus 179-184
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 72-76
30225259-10 2018 Our results suggest that ATRA enhances MMP-2 expression and secretion in human myeloid leukemia THP-1 cells in a calcium ion dependent manner through RAR/RXR signaling pathways, and this enhanced expression and secretion may be associated with the possible mechanisms of RAS. Tretinoin 25-29 GLI family zinc finger 2 Homo sapiens 96-101
30166520-0 2018 High NRF2 level mediates cancer stem cell-like properties of aldehyde dehydrogenase (ALDH)-high ovarian cancer cells: inhibitory role of all-trans retinoic acid in ALDH/NRF2 signaling. Tretinoin 137-160 NFE2 like bZIP transcription factor 2 Homo sapiens 5-9
30166520-11 2018 Second, all-trans retinoic acid (ATRA) suppressed ALDH1 expression, inhibiting NRF2 activation, which led to the attenuation of CSC-like properties in ALDH-H cells but not in ALDH-L cells. Tretinoin 8-31 NFE2 like bZIP transcription factor 2 Homo sapiens 79-83
30166520-11 2018 Second, all-trans retinoic acid (ATRA) suppressed ALDH1 expression, inhibiting NRF2 activation, which led to the attenuation of CSC-like properties in ALDH-H cells but not in ALDH-L cells. Tretinoin 33-37 NFE2 like bZIP transcription factor 2 Homo sapiens 79-83
30225259-0 2018 All-Trans Retinoic Acid Enhances Matrix Metalloproteinase 2 Expression and Secretion in Human Myeloid Leukemia THP-1 Cells. Tretinoin 10-23 GLI family zinc finger 2 Homo sapiens 111-116
30225259-4 2018 In this study, we examined the possible modulatory effects of ATRA on MMP-2 expression and secretion in human myeloid leukemia cell line THP-1. Tretinoin 62-66 GLI family zinc finger 2 Homo sapiens 137-142
29940355-4 2018 RA treatment up-regulated the expression of SETD1A (SET1), a dedicated H3K4 methyltransferase, and augmented SETD1A occupancies on the THBD promoter. Tretinoin 0-2 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 44-50
30142172-0 2018 Retinoic acid promotes in vitro follicle activation in the cat ovary by regulating expression of matrix metalloproteinase 9. Tretinoin 0-13 matrix metallopeptidase 9 Felis catus 97-123
30093655-5 2018 ATRA increases cellular ATO uptake through upregulating aquaporin-9. Tretinoin 0-4 aquaporin 9 Homo sapiens 56-67
29945210-5 2018 When being added after 18-24 h of RA-induced F9 cell differentiation, SC1 transitorily activated Nanog and Oct4. Tretinoin 34-36 Nanog homeobox Mus musculus 97-102
29772445-7 2018 Furthermore, the association between MAPK/ERK pathway and ATRA or miR-3666/E2F7 was explored. Tretinoin 58-62 mitogen-activated protein kinase 1 Homo sapiens 37-41
29772445-7 2018 Furthermore, the association between MAPK/ERK pathway and ATRA or miR-3666/E2F7 was explored. Tretinoin 58-62 mitogen-activated protein kinase 1 Homo sapiens 42-45
29772445-12 2018 Besides, ATRA inhibited the activation of MAPK/ERK signaling pathway, which was reversed by inhibition of miR-3666. Tretinoin 9-13 mitogen-activated protein kinase 1 Homo sapiens 42-46
29772445-12 2018 Besides, ATRA inhibited the activation of MAPK/ERK signaling pathway, which was reversed by inhibition of miR-3666. Tretinoin 9-13 mitogen-activated protein kinase 1 Homo sapiens 47-50
29772445-14 2018 MiR-3666/E2F7 may play a key role in regulating the inhibitory effects of ATRA on HCT116 cells via suppressing the activation of MAPK/ERK signaling pathway. Tretinoin 74-78 mitogen-activated protein kinase 1 Homo sapiens 129-133
29772445-14 2018 MiR-3666/E2F7 may play a key role in regulating the inhibitory effects of ATRA on HCT116 cells via suppressing the activation of MAPK/ERK signaling pathway. Tretinoin 74-78 mitogen-activated protein kinase 1 Homo sapiens 134-137
30159139-0 2018 All-trans retinoic-acid inhibits heterodimeric bone morphogenetic protein 2/7-stimulated osteoclastogenesis, and resorption activity. Tretinoin 10-23 bone morphogenetic protein 2 Mus musculus 47-75
30159139-9 2018 ATRA strongly inhibited Rank and Nfatc1 expression. Tretinoin 0-4 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1 Mus musculus 33-39
30159139-10 2018 Conclusions: All-trans retinoic acid inhibits BMP2/7-induced osteoclastogenesis, and resorption activity possibly via RANKL-RANK pathway. Tretinoin 23-36 bone morphogenetic protein 2 Mus musculus 46-50
29940355-7 2018 In summary, our data illustrate a previously unrecognized pathway in which SETD1A contributes to RA-induced TM expression in vascular endothelial cells by modulating the activity and expression of KLF4. Tretinoin 97-99 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 75-81
29940355-4 2018 RA treatment up-regulated the expression of SETD1A (SET1), a dedicated H3K4 methyltransferase, and augmented SETD1A occupancies on the THBD promoter. Tretinoin 0-2 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 52-56
29940355-4 2018 RA treatment up-regulated the expression of SETD1A (SET1), a dedicated H3K4 methyltransferase, and augmented SETD1A occupancies on the THBD promoter. Tretinoin 0-2 SET domain containing 1A, histone lysine methyltransferase Homo sapiens 109-115
30111392-1 2018 OBJECTIVE: To investigate the effect of all transretinoicacid(ATRA) combined with decitabine (5-Aza-2"-deoxycytidine;DAC) on DNA methylation and gene expression of p16INK4a (p16) and retinoic acid receptor beta (RARbeta), and to explore their combined anti neoplastic effect on U937 cells and newly diagnose delder acute myeloid leukemia(AML) patients. Tretinoin 44-61 cyclin dependent kinase inhibitor 2A Homo sapiens 164-172
30067986-2 2018 Here, we investigated whether removal of the signaling molecule retinoic acid (RA) by the degradative enzyme CYP26B1 is necessary for proper development of somatic cells of the testes. Tretinoin 64-77 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 109-116
29901102-4 2018 In the present study, the role of USP48 in ATRA-induced differentiation of APL cells was studied. Tretinoin 43-47 ubiquitin specific peptidase 48 Homo sapiens 34-39
29901102-5 2018 The expression of USP48 decreased following ATRA treatment. Tretinoin 44-48 ubiquitin specific peptidase 48 Homo sapiens 18-23
29901102-8 2018 Furthermore, the expression of USP48 was increased in the nucleus upon ATRA exposure for <=24 h, suggesting that USP48 was translocated into the nucleus. Tretinoin 71-75 ubiquitin specific peptidase 48 Homo sapiens 31-36
29901102-8 2018 Furthermore, the expression of USP48 was increased in the nucleus upon ATRA exposure for <=24 h, suggesting that USP48 was translocated into the nucleus. Tretinoin 71-75 ubiquitin specific peptidase 48 Homo sapiens 116-121
29901102-11 2018 In conclusion, the present study highlights the function of USP48 in the ATRA-induced granulocytic differentiation of APL cells and provides a theoretical basis for identifying novel targets for differentiation therapy of APL. Tretinoin 73-77 ubiquitin specific peptidase 48 Homo sapiens 60-65
30068571-5 2018 FMR1 inactivation impaired homeostatic plasticity by blocking retinoic acid-mediated regulation of synaptic strength. Tretinoin 62-75 fragile X messenger ribonucleoprotein 1 Homo sapiens 0-4
30068571-6 2018 Repairing the genetic mutation in the FMR1 gene in an FXS patient cell line restored fragile X mental retardation protein (FMRP) expression and fully rescued synaptic retinoic acid signaling. Tretinoin 167-180 fragile X messenger ribonucleoprotein 1 Homo sapiens 38-42
30111392-1 2018 OBJECTIVE: To investigate the effect of all transretinoicacid(ATRA) combined with decitabine (5-Aza-2"-deoxycytidine;DAC) on DNA methylation and gene expression of p16INK4a (p16) and retinoic acid receptor beta (RARbeta), and to explore their combined anti neoplastic effect on U937 cells and newly diagnose delder acute myeloid leukemia(AML) patients. Tretinoin 44-61 cyclin dependent kinase inhibitor 2A Homo sapiens 164-167
30111392-1 2018 OBJECTIVE: To investigate the effect of all transretinoicacid(ATRA) combined with decitabine (5-Aza-2"-deoxycytidine;DAC) on DNA methylation and gene expression of p16INK4a (p16) and retinoic acid receptor beta (RARbeta), and to explore their combined anti neoplastic effect on U937 cells and newly diagnose delder acute myeloid leukemia(AML) patients. Tretinoin 44-61 retinoic acid receptor beta Homo sapiens 183-210
30111392-1 2018 OBJECTIVE: To investigate the effect of all transretinoicacid(ATRA) combined with decitabine (5-Aza-2"-deoxycytidine;DAC) on DNA methylation and gene expression of p16INK4a (p16) and retinoic acid receptor beta (RARbeta), and to explore their combined anti neoplastic effect on U937 cells and newly diagnose delder acute myeloid leukemia(AML) patients. Tretinoin 44-61 retinoic acid receptor beta Homo sapiens 212-219
30111392-1 2018 OBJECTIVE: To investigate the effect of all transretinoicacid(ATRA) combined with decitabine (5-Aza-2"-deoxycytidine;DAC) on DNA methylation and gene expression of p16INK4a (p16) and retinoic acid receptor beta (RARbeta), and to explore their combined anti neoplastic effect on U937 cells and newly diagnose delder acute myeloid leukemia(AML) patients. Tretinoin 62-66 cyclin dependent kinase inhibitor 2A Homo sapiens 164-172
30111392-1 2018 OBJECTIVE: To investigate the effect of all transretinoicacid(ATRA) combined with decitabine (5-Aza-2"-deoxycytidine;DAC) on DNA methylation and gene expression of p16INK4a (p16) and retinoic acid receptor beta (RARbeta), and to explore their combined anti neoplastic effect on U937 cells and newly diagnose delder acute myeloid leukemia(AML) patients. Tretinoin 62-66 cyclin dependent kinase inhibitor 2A Homo sapiens 164-167
30111392-6 2018 Combination treatment of ATRA and DAC induced DNA hypomethylation as well as gene expression of p16 and RARbeta, which contributed to the growth inhibition, differentiation, apoptosis and cell cycle arrest of U937 cells. Tretinoin 25-29 cyclin dependent kinase inhibitor 2A Homo sapiens 96-99
30111392-6 2018 Combination treatment of ATRA and DAC induced DNA hypomethylation as well as gene expression of p16 and RARbeta, which contributed to the growth inhibition, differentiation, apoptosis and cell cycle arrest of U937 cells. Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 104-111
30111392-7 2018 In addition for elder AML patients intolerable to standard chemotherapy, the combination regimen of ATRA and DAC showed antineoplastic activity accompamied by up-regulation of p16 and RARbeta expression and decrease of bone marrow blast, moreover the parients showed good tolerence to the reginen. Tretinoin 100-104 cyclin dependent kinase inhibitor 2A Homo sapiens 176-179
30111392-7 2018 In addition for elder AML patients intolerable to standard chemotherapy, the combination regimen of ATRA and DAC showed antineoplastic activity accompamied by up-regulation of p16 and RARbeta expression and decrease of bone marrow blast, moreover the parients showed good tolerence to the reginen. Tretinoin 100-104 retinoic acid receptor beta Homo sapiens 184-191
29731343-3 2018 We show that switching occurs during normal development and is mediated by feedback between segment identity and the retinoic acid degrading enzymes, cyp26b1 and cyp26c1. Tretinoin 117-130 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 150-157
29945667-1 2018 BACKGROUND: Previous work aimed at understanding the gene regulatory networks (GRNs) governing caudal hindbrain formation identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Tretinoin 152-165 homeobox B1a Danio rerio 255-261
29945667-1 2018 BACKGROUND: Previous work aimed at understanding the gene regulatory networks (GRNs) governing caudal hindbrain formation identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Tretinoin 167-169 homeobox B1a Danio rerio 255-261
30003121-8 2018 This study supports the notion that the skeletal phenotype in CYP26B1 deficient human bone is caused by excess RA. Tretinoin 111-113 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 62-69
29731429-4 2018 We report a mechanism by which RA generates an atrial-like electrophysiologic signature through the downstream regulation of calcium channel gene expression by COUP-TFII and modulation of calcium handling. Tretinoin 31-33 nuclear receptor subfamily 2 group F member 2 Homo sapiens 160-169
29899874-0 2018 Synergistic antitumor activity by combining trastuzumab with retinoic acid in HER2 positive human breast cancer cells. Tretinoin 61-74 erb-b2 receptor tyrosine kinase 2 Homo sapiens 78-82
29522756-9 2018 Activation of Hoxd4 mRNA using transretinoic acid (RA) resulted in 18-fold increase of UII mRNA expression in CNSS and high locomotor activity in medaka, confirming that Hoxd4 is also involved in UII gene transcriptional regulation. Tretinoin 31-49 hoxd4 Oryzias latipes 14-19
29522756-9 2018 Activation of Hoxd4 mRNA using transretinoic acid (RA) resulted in 18-fold increase of UII mRNA expression in CNSS and high locomotor activity in medaka, confirming that Hoxd4 is also involved in UII gene transcriptional regulation. Tretinoin 31-49 hoxd4 Oryzias latipes 170-175
29688244-0 2018 Retinoic acid and CTCF play key roles in inducing the collinear expression of the Hoxa cluster. Tretinoin 0-13 homeobox A cluster Mus musculus 82-86
29688244-7 2018 Here, we examine the relationship between RA and CTCF during the RA-induced expression of the Hoxa cluster genes, using F9 murine embryonic teratocarcinoma cells as a model system. Tretinoin 42-44 homeobox A cluster Mus musculus 94-98
29688244-7 2018 Here, we examine the relationship between RA and CTCF during the RA-induced expression of the Hoxa cluster genes, using F9 murine embryonic teratocarcinoma cells as a model system. Tretinoin 65-67 homeobox A cluster Mus musculus 94-98
29972129-13 2018 Compared with the ATRA group, the OM-85BV+ATRA group had significantly increased levels of IL-10 and IL-17 in BALF (P<0.05). Tretinoin 42-46 interleukin 10 Mus musculus 91-96
29899874-10 2018 Tz+RA strongly reduced FAK and HER2 expression and induced nuclear FAK translocation. Tretinoin 3-5 erb-b2 receptor tyrosine kinase 2 Homo sapiens 31-35
29881371-12 2018 The orphan nuclear receptor COUP-TFI is expressed in normal corticotroph cells, but not in corticotroph tumoral cells, and inhibits RA pathways. Tretinoin 132-134 nuclear receptor subfamily 2 group F member 1 Homo sapiens 28-36
29757260-6 2018 TFPI2 was vital in the ATRA-mediated suppression of HuH7 cell invasion. Tretinoin 23-27 tissue factor pathway inhibitor 2 Homo sapiens 0-5
29891447-8 2018 ATRA treatment resulted in significantly increased the expressions of autophagy-related markers LC3-II, Beclin-1, RAB7 and P62 and also an increased ratio of LC3-II/LC3-I(P<0.05). Tretinoin 0-4 RAB7, member RAS oncogene family Mus musculus 114-118
29601728-8 2018 Treatment of human articular chondrocytes in vitro reveals that CccS BMS493 demonstrates a marked improvement in efficacy in reducing the mRNA levels of matrix metalloproteinase-13 (MMP-13), one of the main proteases responsible for the degradation of the extracellular cartilage matrix compared to BMS493 alone in the presence of ATRA, interleukin-1 beta (IL-1beta), or IL-1 beta together with ATRA. Tretinoin 331-335 matrix metallopeptidase 13 Homo sapiens 153-180
29601728-8 2018 Treatment of human articular chondrocytes in vitro reveals that CccS BMS493 demonstrates a marked improvement in efficacy in reducing the mRNA levels of matrix metalloproteinase-13 (MMP-13), one of the main proteases responsible for the degradation of the extracellular cartilage matrix compared to BMS493 alone in the presence of ATRA, interleukin-1 beta (IL-1beta), or IL-1 beta together with ATRA. Tretinoin 331-335 matrix metallopeptidase 13 Homo sapiens 182-188
29601728-8 2018 Treatment of human articular chondrocytes in vitro reveals that CccS BMS493 demonstrates a marked improvement in efficacy in reducing the mRNA levels of matrix metalloproteinase-13 (MMP-13), one of the main proteases responsible for the degradation of the extracellular cartilage matrix compared to BMS493 alone in the presence of ATRA, interleukin-1 beta (IL-1beta), or IL-1 beta together with ATRA. Tretinoin 395-399 matrix metallopeptidase 13 Homo sapiens 153-180
29601728-8 2018 Treatment of human articular chondrocytes in vitro reveals that CccS BMS493 demonstrates a marked improvement in efficacy in reducing the mRNA levels of matrix metalloproteinase-13 (MMP-13), one of the main proteases responsible for the degradation of the extracellular cartilage matrix compared to BMS493 alone in the presence of ATRA, interleukin-1 beta (IL-1beta), or IL-1 beta together with ATRA. Tretinoin 395-399 matrix metallopeptidase 13 Homo sapiens 182-188
29757260-8 2018 The knockdown of RARα or MAFB counteracted the ATRA-mediated suppression of HuH7 cell invasion while the knockdown of MAFF inhibited the invasion. Tretinoin 57-61 MAF bZIP transcription factor B Homo sapiens 35-39
29579175-6 2018 When either T or RA in the presence or absence of FSH was added to granulosa cell cultures, the combined treatment with FSH and RA induced demethylation of Lhcgr-promoter region and Lhcgr expression. Tretinoin 17-19 follicle stimulating hormone beta Mus musculus 120-123
29774040-9 2018 TBL1 forms a transcriptional repression complex with the histone deacetylase (HDAC) HDAC3 and either nuclear receptor co-repressor (N-CoR) or silencing mediator for retinoic acid and thyroid receptor (SMRT). Tretinoin 165-178 trichome birefringence-like protein (DUF828) Arabidopsis thaliana 0-4
29728589-0 2018 All-trans-retinoic acid activates the pro-invasive Src-YAP-Interleukin 6 axis in triple-negative MDA-MB-231 breast cancer cells while cerivastatin reverses this action. Tretinoin 0-23 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 51-54
29728589-0 2018 All-trans-retinoic acid activates the pro-invasive Src-YAP-Interleukin 6 axis in triple-negative MDA-MB-231 breast cancer cells while cerivastatin reverses this action. Tretinoin 0-23 interleukin 6 Homo sapiens 59-72
29728589-4 2018 We show here that RA activates the pro-invasive axis Src-YAP-Interleukin 6 (Src-YAP-IL6) in triple negative MDA-MB-231 breast cancer cells, yielding to increased invasion of these cells. Tretinoin 18-20 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 53-56
29728589-4 2018 We show here that RA activates the pro-invasive axis Src-YAP-Interleukin 6 (Src-YAP-IL6) in triple negative MDA-MB-231 breast cancer cells, yielding to increased invasion of these cells. Tretinoin 18-20 interleukin 6 Homo sapiens 61-74
29728589-4 2018 We show here that RA activates the pro-invasive axis Src-YAP-Interleukin 6 (Src-YAP-IL6) in triple negative MDA-MB-231 breast cancer cells, yielding to increased invasion of these cells. Tretinoin 18-20 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 76-79
29728589-5 2018 On the contrary, RA inhibits the Src-YAP-IL6 axis of triple-negative MDA-MB-468 cells, which results in decreased invasion phenotype. Tretinoin 17-19 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 33-36
29728589-9 2018 These results altogether suggest that RA induces pro-invasive or anti-invasive actions in two triple-negative breast cancer cell lines due to its ability to activate or inhibit the Src-YAP-IL6 axis in different cancer cells. Tretinoin 38-40 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 181-184
29579175-6 2018 When either T or RA in the presence or absence of FSH was added to granulosa cell cultures, the combined treatment with FSH and RA induced demethylation of Lhcgr-promoter region and Lhcgr expression. Tretinoin 17-19 luteinizing hormone/choriogonadotropin receptor Mus musculus 156-161
29579175-6 2018 When either T or RA in the presence or absence of FSH was added to granulosa cell cultures, the combined treatment with FSH and RA induced demethylation of Lhcgr-promoter region and Lhcgr expression. Tretinoin 17-19 luteinizing hormone/choriogonadotropin receptor Mus musculus 182-187
29579175-6 2018 When either T or RA in the presence or absence of FSH was added to granulosa cell cultures, the combined treatment with FSH and RA induced demethylation of Lhcgr-promoter region and Lhcgr expression. Tretinoin 128-130 follicle stimulating hormone beta Mus musculus 50-53
29579175-6 2018 When either T or RA in the presence or absence of FSH was added to granulosa cell cultures, the combined treatment with FSH and RA induced demethylation of Lhcgr-promoter region and Lhcgr expression. Tretinoin 128-130 luteinizing hormone/choriogonadotropin receptor Mus musculus 156-161
29579175-6 2018 When either T or RA in the presence or absence of FSH was added to granulosa cell cultures, the combined treatment with FSH and RA induced demethylation of Lhcgr-promoter region and Lhcgr expression. Tretinoin 128-130 luteinizing hormone/choriogonadotropin receptor Mus musculus 182-187
29579175-7 2018 FSH-dependent RA synthesis was negatively regulated by coculture of granulosa cells with denuded oocytes, suggesting that oocyte-secreted factors downregulate RA production in cumulus cells where Lhcgr expression was not induced. Tretinoin 14-16 follicle stimulating hormone beta Mus musculus 0-3
29579175-7 2018 FSH-dependent RA synthesis was negatively regulated by coculture of granulosa cells with denuded oocytes, suggesting that oocyte-secreted factors downregulate RA production in cumulus cells where Lhcgr expression was not induced. Tretinoin 159-161 follicle stimulating hormone beta Mus musculus 0-3
29579175-9 2018 These results indicate the demethylation of the Lhcgr-promoter region is mediated, at least in part, by RA synthesis and is a key mechanism regulating the cell type-specific differentiation during follicular development. Tretinoin 104-106 luteinizing hormone/choriogonadotropin receptor Mus musculus 48-53
29854846-0 2018 All-Trans Retinoic Acid Induces CD4+CD25+FOXP3+ Regulatory T Cells by Increasing FOXP3 Demethylation in Systemic Sclerosis CD4+ T Cells. Tretinoin 10-23 CD4 molecule Homo sapiens 32-35
29488619-11 2018 Western blot analysis and immunohistochemical analysis identified an increase in occludin expression after treatment with ATRA, in contrast to CAV-1 expression under the same conditions. Tretinoin 122-126 occludin Oryctolagus cuniculus 81-89
29854846-0 2018 All-Trans Retinoic Acid Induces CD4+CD25+FOXP3+ Regulatory T Cells by Increasing FOXP3 Demethylation in Systemic Sclerosis CD4+ T Cells. Tretinoin 10-23 CD4 molecule Homo sapiens 123-126
29854846-5 2018 The addition of all-trans retinoic acid (ATRA) to human naive CD4+ cells could promote the maturation of Tregs and increase the stable expression of Foxp3. Tretinoin 16-39 CD4 molecule Homo sapiens 62-65
29854846-5 2018 The addition of all-trans retinoic acid (ATRA) to human naive CD4+ cells could promote the maturation of Tregs and increase the stable expression of Foxp3. Tretinoin 41-45 CD4 molecule Homo sapiens 62-65
29854846-11 2018 Results: The expression of Tregs and FOXP3 in CD4+ T cells from patients with SSc increased in response to ATRA. Tretinoin 107-111 CD4 molecule Homo sapiens 46-49
29854846-13 2018 Further studies revealed that stimulation with ATRA increased the expression of FOXP3 in SSc CD4+ T cells by downregulating FOXP3 promoter methylation levels. Tretinoin 47-51 CD4 molecule Homo sapiens 93-96
29854846-14 2018 Conclusions: ATRA acts as an inducer of Treg response in SSc CD4+ T cells via demethylation of the FOXP3 promoter and activation of FOXP3 expression. Tretinoin 13-17 CD4 molecule Homo sapiens 61-64
29650946-7 2018 The patient completed a course of daunorubicin, cytarabine, and AII trans-retinoic acid (ATRA) with complete remission. Tretinoin 89-93 NLR family pyrin domain containing 3 Homo sapiens 64-67
29523306-6 2018 Such suppression is in response to a retinoic acid-RARalpha binding initiated pathway and results in the upregulation of gut-homing chemokine receptor CCR9 and downregulation of lymphoid tissue-homing receptor CCR7, which can then guide ILC3 cells to intestine. Tretinoin 37-50 C-C motif chemokine receptor 7 Homo sapiens 210-214
29326073-0 2018 Retinoic acid promotes stem cell differentiation and embryonic development by transcriptionally activating CFTR. Tretinoin 0-13 CF transmembrane conductance regulator Homo sapiens 107-111
29326073-4 2018 Loss of CFTR by siRNA-mediated knockdown blunts the RA-induced spermatogonial differentiation. Tretinoin 52-54 CF transmembrane conductance regulator Homo sapiens 8-12
29326073-7 2018 Together, our study discovers an essential role of CFTR in mediating the RA-dependent signaling for stem cell differentiation and embryonic development. Tretinoin 73-75 CF transmembrane conductance regulator Homo sapiens 51-55
29417442-12 2018 The combination of DAPT and ATRA effectively increased the proportion of apoptotic cells and the level of caspase 3/7 activities compared to single treatment. Tretinoin 28-32 caspase 3 Homo sapiens 106-115
29417442-13 2018 Moreover, augmented caspase-3 up-regulation and bcl-2 down-regulation were found following combined application of DAPT and ATRA. Tretinoin 124-128 caspase 3 Homo sapiens 20-29
29417442-13 2018 Moreover, augmented caspase-3 up-regulation and bcl-2 down-regulation were found following combined application of DAPT and ATRA. Tretinoin 124-128 BCL2 apoptosis regulator Homo sapiens 48-53
29297599-7 2018 Unexpectedly, the majority of missense variants in NTD cases were found in CYP26B1, which encodes a RA degradation enzyme, whereas no missense variants in this gene were found in controls. Tretinoin 100-102 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 75-82
29297599-8 2018 Functional analysis indicated that the CYP26B1 NTD variants were inefficient in the degradation of RA using assays of RA-induced transcription and RA-initiated neuronal differentiation. Tretinoin 99-101 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 39-46
29297599-8 2018 Functional analysis indicated that the CYP26B1 NTD variants were inefficient in the degradation of RA using assays of RA-induced transcription and RA-initiated neuronal differentiation. Tretinoin 118-120 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 39-46
29297599-8 2018 Functional analysis indicated that the CYP26B1 NTD variants were inefficient in the degradation of RA using assays of RA-induced transcription and RA-initiated neuronal differentiation. Tretinoin 118-120 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 39-46
29447503-4 2018 The aim of this study was to evaluate the effects of AtRA on ERalpha-mediated signaling in the ERalpha positive cell lines MCF7/BUS and U2OS-ERalpha-Luc to investigate some of the possible underlying modes of action. Tretinoin 53-57 estrogen receptor 1 Homo sapiens 61-68
29447503-4 2018 The aim of this study was to evaluate the effects of AtRA on ERalpha-mediated signaling in the ERalpha positive cell lines MCF7/BUS and U2OS-ERalpha-Luc to investigate some of the possible underlying modes of action. Tretinoin 53-57 estrogen receptor 1 Homo sapiens 95-102
29447503-4 2018 The aim of this study was to evaluate the effects of AtRA on ERalpha-mediated signaling in the ERalpha positive cell lines MCF7/BUS and U2OS-ERalpha-Luc to investigate some of the possible underlying modes of action. Tretinoin 53-57 estrogen receptor 1 Homo sapiens 95-102
29447503-5 2018 To do so, this study assessed the effects of AtRA on different ERalpha-related events such as ERalpha-mediated cell proliferation and gene expression, ERalpha-coregulator binding and ERalpha subcellular localization. Tretinoin 45-49 estrogen receptor 1 Homo sapiens 63-70
29447503-8 2018 Interestingly, in the absence of E2, ERalpha-mediated gene expression, ERalpha-coregulator binding and ERalpha subcellular mobilization were increased upon exposure to micromolar concentrations of AtRA found to inhibit cell proliferation after long-term exposure. Tretinoin 197-201 estrogen receptor 1 Homo sapiens 37-44
29447503-8 2018 Interestingly, in the absence of E2, ERalpha-mediated gene expression, ERalpha-coregulator binding and ERalpha subcellular mobilization were increased upon exposure to micromolar concentrations of AtRA found to inhibit cell proliferation after long-term exposure. Tretinoin 197-201 estrogen receptor 1 Homo sapiens 71-110
29447503-9 2018 Nevertheless, experiments using purified ERalpha showed that direct binding of AtRA to ERalpha does not occur. Tretinoin 79-83 estrogen receptor 1 Homo sapiens 87-94
29633731-4 2018 IL-6 seems to play an important role in the pathogenesis of the thrombocytosis induced by ATRA. Tretinoin 90-94 interleukin 6 Homo sapiens 0-4
28944567-6 2018 The expression of Bax gene (an apoptotic marker) was significantly observed in high dosage of retinoic acid (RA). Tretinoin 94-107 BCL2 associated X, apoptosis regulator Homo sapiens 18-21
28944567-6 2018 The expression of Bax gene (an apoptotic marker) was significantly observed in high dosage of retinoic acid (RA). Tretinoin 109-111 BCL2 associated X, apoptosis regulator Homo sapiens 18-21
29620445-6 2018 RA induction led to slender spindles and tadpole-like changes of cell morphology, and the expression of germ cell-specific markers (Oct4, Piwil2, Itgb1, SSEA-1, and Stra8) presented significant upregulation in the RA treatment group according to the polymerase chain reaction and immunofluorescence results. Tretinoin 0-2 fucosyltransferase 4 Homo sapiens 153-159
29321172-0 2018 Modest Decreases in Endogenous All-trans-Retinoic Acid Produced by a Mouse Rdh10 Heterozygote Provoke Major Abnormalities in Adipogenesis and Lipid Metabolism. Tretinoin 31-54 retinol dehydrogenase 10 (all-trans) Mus musculus 75-80
29321172-3 2018 This study examined postnatal contributions of Rdh10 to atRA biosynthesis and physiological functions of endogenous atRA. Tretinoin 56-60 retinol dehydrogenase 10 (all-trans) Mus musculus 47-52
29321172-4 2018 Embryonic fibroblasts from Rdh10 heterozygote hypomorphs or with a total Rdh10 knockout exhibit decreased atRA biosynthesis and escalated adipogenesis. Tretinoin 106-110 retinol dehydrogenase 10 (all-trans) Mus musculus 27-32
29321172-4 2018 Embryonic fibroblasts from Rdh10 heterozygote hypomorphs or with a total Rdh10 knockout exhibit decreased atRA biosynthesis and escalated adipogenesis. Tretinoin 106-110 retinol dehydrogenase 10 (all-trans) Mus musculus 73-78
29414786-4 2018 ApoE fragments were detectable in culture supernatants after 3 days, and their levels were increased for up to 9 days in the presence of ATRA. Tretinoin 137-141 apolipoprotein E Homo sapiens 0-4
29337257-5 2018 Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51. Tretinoin 57-70 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 330-337
29337257-5 2018 Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51. Tretinoin 57-70 cytochrome P450 family 51 subfamily A member 1 Homo sapiens 342-347
28920418-9 2018 CONCLUSION: Retinoic acid was found to produce smaller preadipocytes which have been assumed to have insulin sensitization and hence retinoic acid could be used as a potential agent to sensitize tissues to insulin in combination with TZD"s to treat diabetic conditions in humans and animals in future. Tretinoin 12-25 insulin Homo sapiens 101-108
29398485-7 2018 Rescue experiments indicate that FOXD3-AS1 harbors tumor-suppressive properties by inhibiting the oncogenic roles of PARP1 or CTCF and plays crucial roles in all-trans-retinoic-acid-mediated therapeutic effects on NB. Tretinoin 168-181 forkhead box D3 Homo sapiens 33-38
28920418-9 2018 CONCLUSION: Retinoic acid was found to produce smaller preadipocytes which have been assumed to have insulin sensitization and hence retinoic acid could be used as a potential agent to sensitize tissues to insulin in combination with TZD"s to treat diabetic conditions in humans and animals in future. Tretinoin 12-25 insulin Homo sapiens 206-213
28920418-9 2018 CONCLUSION: Retinoic acid was found to produce smaller preadipocytes which have been assumed to have insulin sensitization and hence retinoic acid could be used as a potential agent to sensitize tissues to insulin in combination with TZD"s to treat diabetic conditions in humans and animals in future. Tretinoin 133-146 insulin Homo sapiens 206-213
29490681-9 2018 At the protein level RA treatment was found to increase the expression of the gap junction protein CX43 and the pluripotency marker OCT4. Tretinoin 21-23 gap junction protein, alpha 1 Mus musculus 99-103
29266770-10 2018 In vitro, atRA increases the Ca2+ excitability of neurons, which might further promote the release of OXT. Tretinoin 10-14 oxytocin/neurophysin I prepropeptide Rattus norvegicus 102-105
29257130-3 2018 We found that Celsr1, a cadherin of the adhesion G protein coupled receptor family, controls branching of aNPC basal processes abutting the meninges and thereby regulates retinoic acid (RA)-dependent neurogenesis. Tretinoin 171-184 cadherin, EGF LAG seven-pass G-type receptor 1 Mus musculus 14-20
29266770-12 2018 Furthermore, atRA enhances the binding of RARbeta to the proximal promoter of CD38, indicating a potential upregulation of CD38 transcriptional activity by RARbeta. Tretinoin 13-17 retinoic acid receptor, beta Rattus norvegicus 42-49
29257130-3 2018 We found that Celsr1, a cadherin of the adhesion G protein coupled receptor family, controls branching of aNPC basal processes abutting the meninges and thereby regulates retinoic acid (RA)-dependent neurogenesis. Tretinoin 186-188 cadherin, EGF LAG seven-pass G-type receptor 1 Mus musculus 14-20
29257130-4 2018 Loss-of-function of Celsr1 results in a decreased number of endfeet, modifies RA-dependent transcriptional activity and biases aNPC commitment toward self-renewal at the expense of basal progenitor and neuron production. Tretinoin 78-80 cadherin, EGF LAG seven-pass G-type receptor 1 Mus musculus 20-26
29266770-12 2018 Furthermore, atRA enhances the binding of RARbeta to the proximal promoter of CD38, indicating a potential upregulation of CD38 transcriptional activity by RARbeta. Tretinoin 13-17 CD38 molecule Rattus norvegicus 78-82
29266770-12 2018 Furthermore, atRA enhances the binding of RARbeta to the proximal promoter of CD38, indicating a potential upregulation of CD38 transcriptional activity by RARbeta. Tretinoin 13-17 CD38 molecule Rattus norvegicus 123-127
29266770-12 2018 Furthermore, atRA enhances the binding of RARbeta to the proximal promoter of CD38, indicating a potential upregulation of CD38 transcriptional activity by RARbeta. Tretinoin 13-17 retinoic acid receptor, beta Rattus norvegicus 156-163
29467333-0 2018 CHD7 represses the retinoic acid synthesis enzyme ALDH1A3 during inner ear development. Tretinoin 19-32 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 50-57
29274429-0 2018 Retinoic acid synthesis by NG2 expressing cells promotes a permissive environment for axonal outgrowth. Tretinoin 0-13 chondroitin sulfate proteoglycan 4 Homo sapiens 27-30
29274429-1 2018 Stimulation of retinoic acid (RA) mediated signalling pathways following neural injury leads to regeneration in the adult nervous system and numerous studies have shown that the specific activation of the retinoic acid receptor beta (RARbeta) is required for this process. Tretinoin 15-28 retinoic acid receptor beta Homo sapiens 205-232
29274429-1 2018 Stimulation of retinoic acid (RA) mediated signalling pathways following neural injury leads to regeneration in the adult nervous system and numerous studies have shown that the specific activation of the retinoic acid receptor beta (RARbeta) is required for this process. Tretinoin 15-28 retinoic acid receptor beta Homo sapiens 234-241
29274429-1 2018 Stimulation of retinoic acid (RA) mediated signalling pathways following neural injury leads to regeneration in the adult nervous system and numerous studies have shown that the specific activation of the retinoic acid receptor beta (RARbeta) is required for this process. Tretinoin 30-32 retinoic acid receptor beta Homo sapiens 205-232
29274429-1 2018 Stimulation of retinoic acid (RA) mediated signalling pathways following neural injury leads to regeneration in the adult nervous system and numerous studies have shown that the specific activation of the retinoic acid receptor beta (RARbeta) is required for this process. Tretinoin 30-32 retinoic acid receptor beta Homo sapiens 234-241
29274429-3 2018 Using an established rodent model of RARbeta induced axonal regeneration, we show that neuronal RARbeta activation upregulates the enzymes involved in RA synthesis in a cell specific manner; alcohol dehydrogenase7 (ADH7) in neurons and aldehyde dehydrogenase 2 (Raldh2) in NG2 expressing cells (NG2+ cells). Tretinoin 37-39 retinoic acid receptor beta Homo sapiens 96-103
29440484-0 2018 Synergistic and additive effect of retinoic acid in circumventing resistance to p53 restoration. Tretinoin 35-48 tumor protein p53 Homo sapiens 80-83
29235036-6 2018 Differentiation of SH-SY5Y cells with retinoic acid resulted in increased neurite outgrowth and Alox15 mRNA expression, while co-treatment with the p300 HAT inhibitor C646 and retinoic acid modulated the increases, indicating a role of p300 HAT in differentiation-associated Alox15 upregulation. Tretinoin 38-51 arachidonate 15-lipoxygenase Homo sapiens 96-102
29235036-6 2018 Differentiation of SH-SY5Y cells with retinoic acid resulted in increased neurite outgrowth and Alox15 mRNA expression, while co-treatment with the p300 HAT inhibitor C646 and retinoic acid modulated the increases, indicating a role of p300 HAT in differentiation-associated Alox15 upregulation. Tretinoin 38-51 arachidonate 15-lipoxygenase Homo sapiens 275-281
29337120-5 2018 Two developmentally relevant factors, retinoic acid in combination with bone morphogenetic protein 4, can be used to generate three classes of sensory INs: the proprioceptive dI1s, the dI2s, and mechanosensory dI3s. Tretinoin 38-51 l(1)16Fa Drosophila melanogaster 175-178
28960887-5 2018 Here the authors identified that RA application to iPSC-derived BMECs at days 6-8 of differentiation led to a substantial elevation in transendothelial electrical resistance and induction of VE-cadherin expression. Tretinoin 33-35 cadherin 5 Homo sapiens 191-202
28960887-7 2018 Moreover, RAR/RXRalpha costimulation elevated VE-cadherin expression and improved barrier fidelity to levels that recapitulated the effects of RA. Tretinoin 10-12 cadherin 5 Homo sapiens 46-57
29301505-9 2018 RESULTS: Treatment of IMR32 and BE2C cells in vitro with 10 muM ATRA resulted in a change in cell morphology, a 65% decrease in cell proliferation, upregulation of STMN4 and ROBO2 and downregulation of KLF4. Tretinoin 64-68 latexin Homo sapiens 60-63
29233047-2 2018 Our previous study demonstrated that the gene expression of glucose-regulated protein-78 (Grp78) was downregulation in the all-trans retinoic acid-induced mouse models of cleft palate (CP) during embryogenesis. Tretinoin 133-146 heat shock protein 5 Mus musculus 60-88
29233047-2 2018 Our previous study demonstrated that the gene expression of glucose-regulated protein-78 (Grp78) was downregulation in the all-trans retinoic acid-induced mouse models of cleft palate (CP) during embryogenesis. Tretinoin 133-146 heat shock protein 5 Mus musculus 90-95
29434845-0 2018 All-trans retinoic acid inhibits the proliferation of SGC7901 cells by regulating caveolin-1 localization via the ERK/MAPK signaling pathway. Tretinoin 10-23 caveolin 1 Homo sapiens 82-92
29434845-0 2018 All-trans retinoic acid inhibits the proliferation of SGC7901 cells by regulating caveolin-1 localization via the ERK/MAPK signaling pathway. Tretinoin 10-23 mitogen-activated protein kinase 1 Homo sapiens 114-117
29434845-0 2018 All-trans retinoic acid inhibits the proliferation of SGC7901 cells by regulating caveolin-1 localization via the ERK/MAPK signaling pathway. Tretinoin 10-23 mitogen-activated protein kinase 1 Homo sapiens 118-122
29434845-5 2018 The markedly increased membrane localization of caveolin-1 was observed in the cells that were treated with 10 micromol/l ATRA for > 48 h. In addition, it was observed that treatment with ATRA was able to regulate the level of phosphorylation of extracellular signal-regulated kinase (ERK). Tretinoin 122-126 caveolin 1 Homo sapiens 48-58
29434845-5 2018 The markedly increased membrane localization of caveolin-1 was observed in the cells that were treated with 10 micromol/l ATRA for > 48 h. In addition, it was observed that treatment with ATRA was able to regulate the level of phosphorylation of extracellular signal-regulated kinase (ERK). Tretinoin 122-126 mitogen-activated protein kinase 1 Homo sapiens 249-286
29434845-5 2018 The markedly increased membrane localization of caveolin-1 was observed in the cells that were treated with 10 micromol/l ATRA for > 48 h. In addition, it was observed that treatment with ATRA was able to regulate the level of phosphorylation of extracellular signal-regulated kinase (ERK). Tretinoin 122-126 mitogen-activated protein kinase 1 Homo sapiens 288-291
29434845-5 2018 The markedly increased membrane localization of caveolin-1 was observed in the cells that were treated with 10 micromol/l ATRA for > 48 h. In addition, it was observed that treatment with ATRA was able to regulate the level of phosphorylation of extracellular signal-regulated kinase (ERK). Tretinoin 191-195 caveolin 1 Homo sapiens 48-58
29434845-5 2018 The markedly increased membrane localization of caveolin-1 was observed in the cells that were treated with 10 micromol/l ATRA for > 48 h. In addition, it was observed that treatment with ATRA was able to regulate the level of phosphorylation of extracellular signal-regulated kinase (ERK). Tretinoin 191-195 mitogen-activated protein kinase 1 Homo sapiens 249-286
29434845-5 2018 The markedly increased membrane localization of caveolin-1 was observed in the cells that were treated with 10 micromol/l ATRA for > 48 h. In addition, it was observed that treatment with ATRA was able to regulate the level of phosphorylation of extracellular signal-regulated kinase (ERK). Tretinoin 191-195 mitogen-activated protein kinase 1 Homo sapiens 288-291
29434845-7 2018 The results of the present study demonstrated that ATRA-induced increase in membrane localization of caveolin-1 was reversed by treatment with a specific agonist of ERK/MAPK. Tretinoin 51-55 caveolin 1 Homo sapiens 101-111
29434845-7 2018 The results of the present study demonstrated that ATRA-induced increase in membrane localization of caveolin-1 was reversed by treatment with a specific agonist of ERK/MAPK. Tretinoin 51-55 mitogen-activated protein kinase 1 Homo sapiens 165-168
29434845-7 2018 The results of the present study demonstrated that ATRA-induced increase in membrane localization of caveolin-1 was reversed by treatment with a specific agonist of ERK/MAPK. Tretinoin 51-55 mitogen-activated protein kinase 1 Homo sapiens 169-173
29170140-10 2018 Moreover ATRA-PLLA microparticles significantly enhanced the efficacy of ATRA against HCC tumor growth in mice through reducing Pin1, with a better potency than the slow-releasing ATRA formulation, consistent with its improved pharmacokinetic profiles. Tretinoin 9-13 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 128-132
29170140-10 2018 Moreover ATRA-PLLA microparticles significantly enhanced the efficacy of ATRA against HCC tumor growth in mice through reducing Pin1, with a better potency than the slow-releasing ATRA formulation, consistent with its improved pharmacokinetic profiles. Tretinoin 73-77 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 128-132
29301505-12 2018 40 muM ATRA treatment at E11 and E13 reduced proliferation by 37% (p < 0.05) and also changed cell morphology within the tumour. Tretinoin 7-11 latexin Homo sapiens 3-6
29330906-4 2018 The developing embryo contains regions that produce RA, and specific intracellular concentrations of RA are created through local degradation mediated by Cyp26 enzymes. Tretinoin 101-103 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 154-159
28436029-2 2018 Here we showed that ATRA could stimulate the proliferation of antler chondrocytes and expression of COL X and MMP13 which were two well-known markers for hypertrophic chondrocytes. Tretinoin 20-24 matrix metallopeptidase 13 Homo sapiens 110-115
29232592-4 2018 Since induction therapy with RIF and ATRA, the median levels of Fbg, PT and platelets were recovered to the normal range within 4days, 10days and 28days, respectively. Tretinoin 37-41 fibrinogen beta chain Homo sapiens 64-67
29434845-10 2018 These effects of ATRA may be mediated by inhibiting the activation of ERK/MAPK signaling pathway. Tretinoin 17-21 mitogen-activated protein kinase 1 Homo sapiens 70-73
29434845-10 2018 These effects of ATRA may be mediated by inhibiting the activation of ERK/MAPK signaling pathway. Tretinoin 17-21 mitogen-activated protein kinase 1 Homo sapiens 74-78
29390039-6 2018 Finally, BMDC lacking SAA3 demonstrate an impaired endotoxin tolerance response and inhibited responses to retinoic acid. Tretinoin 107-120 serum amyloid A 3 Mus musculus 22-26
29177441-7 2018 These variants altered the expression of CYP26A1, a direct CDX2 target encoding the major retinoic acid (RA)-degrading enzyme. Tretinoin 90-103 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 41-48
29177441-7 2018 These variants altered the expression of CYP26A1, a direct CDX2 target encoding the major retinoic acid (RA)-degrading enzyme. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 41-48
29305588-5 2018 Our findings show that RA inhibits the Wnt canonical pathway and positively modulates the Akt/mTOR signaling, explaining why such perturbations, under our experimental conditions, do not lead to hiPSCs differentiation. Tretinoin 23-25 AKT serine/threonine kinase 1 Homo sapiens 90-93
29305588-5 2018 Our findings show that RA inhibits the Wnt canonical pathway and positively modulates the Akt/mTOR signaling, explaining why such perturbations, under our experimental conditions, do not lead to hiPSCs differentiation. Tretinoin 23-25 mechanistic target of rapamycin kinase Homo sapiens 94-98
30064139-12 2018 All-trans-retinoic acid (ATRA), an inhibitor of Nrf2, abolished zedoarondiol-mediated anti-oxidative effect. Tretinoin 0-23 NFE2 like bZIP transcription factor 2 Homo sapiens 48-52
29487709-3 2018 Retinoic acid (RA)-induced binucleation of H9c2 cells was associated with increased SIRT1 expression. Tretinoin 0-13 sirtuin 1 Rattus norvegicus 84-89
29487709-3 2018 Retinoic acid (RA)-induced binucleation of H9c2 cells was associated with increased SIRT1 expression. Tretinoin 15-17 sirtuin 1 Rattus norvegicus 84-89
29487709-4 2018 Inhibition of SIRT1 activity or expression significantly decreased RA-induced binucleation. Tretinoin 67-69 sirtuin 1 Rattus norvegicus 14-19
30064139-12 2018 All-trans-retinoic acid (ATRA), an inhibitor of Nrf2, abolished zedoarondiol-mediated anti-oxidative effect. Tretinoin 25-29 NFE2 like bZIP transcription factor 2 Homo sapiens 48-52
29108781-6 2018 Moreover, ectopic expression of the transcription factor meis3 and/or the receptor ret, partially rescues enteric neuron colonization after RA attenuation. Tretinoin 140-142 ret proto-oncogene receptor tyrosine kinase Danio rerio 83-86
30114691-4 2018 RESULTS: The protein and messenger RNA expression of KCa3.1 substantially diminished as NSC-34 cells were differentiated with low serum (1%) and 1 microM RA. Tretinoin 154-156 potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4 Mus musculus 53-59
30423583-0 2018 Novel Zinc Finger Transcription Factor ZFP580 Facilitates All-Trans Retinoic Acid -Induced Vascular Smooth Muscle Cells Differentiation by Raralpha-Mediated PI3K/Akt and ERK Signaling. Tretinoin 68-81 zinc finger protein 580 Rattus norvegicus 39-45
30423583-0 2018 Novel Zinc Finger Transcription Factor ZFP580 Facilitates All-Trans Retinoic Acid -Induced Vascular Smooth Muscle Cells Differentiation by Raralpha-Mediated PI3K/Akt and ERK Signaling. Tretinoin 68-81 AKT serine/threonine kinase 1 Rattus norvegicus 162-165
30423583-0 2018 Novel Zinc Finger Transcription Factor ZFP580 Facilitates All-Trans Retinoic Acid -Induced Vascular Smooth Muscle Cells Differentiation by Raralpha-Mediated PI3K/Akt and ERK Signaling. Tretinoin 68-81 Eph receptor B1 Rattus norvegicus 170-173
30423583-4 2018 Here, we have investigated the probable roles and underlying mechanisms of the novel C2H2 zinc finger transcription factor ZFP580 on ATRA-induced VSMC differentiation. Tretinoin 133-137 zinc finger protein 580 Rattus norvegicus 123-129
30423583-12 2018 In contrast, silencing of the RARalpha gene or inhibiting RARalpha with its antagonist Ro41-5253 abrogated the ATRA-induced ZFP580 expression. Tretinoin 111-115 zinc finger protein 580 Rattus norvegicus 124-130
30423583-13 2018 Furthermore, ATRA binding to RARalpha induced ZFP580 expression via the PI3K/Akt and ERK pathways. Tretinoin 13-17 zinc finger protein 580 Rattus norvegicus 46-52
30423583-13 2018 Furthermore, ATRA binding to RARalpha induced ZFP580 expression via the PI3K/Akt and ERK pathways. Tretinoin 13-17 AKT serine/threonine kinase 1 Rattus norvegicus 77-80
30423583-13 2018 Furthermore, ATRA binding to RARalpha induced ZFP580 expression via the PI3K/Akt and ERK pathways. Tretinoin 13-17 Eph receptor B1 Rattus norvegicus 85-88
30423583-17 2018 CONCLUSION: The novel zinc finger transcription factor ZFP580 facilitates ATRA-induced VSMC differentiation by the RARalpha-mediated PI3K/Akt and ERK signaling pathways. Tretinoin 74-78 zinc finger protein 580 Rattus norvegicus 55-61
30423583-17 2018 CONCLUSION: The novel zinc finger transcription factor ZFP580 facilitates ATRA-induced VSMC differentiation by the RARalpha-mediated PI3K/Akt and ERK signaling pathways. Tretinoin 74-78 AKT serine/threonine kinase 1 Rattus norvegicus 138-141
30423583-17 2018 CONCLUSION: The novel zinc finger transcription factor ZFP580 facilitates ATRA-induced VSMC differentiation by the RARalpha-mediated PI3K/Akt and ERK signaling pathways. Tretinoin 74-78 Eph receptor B1 Rattus norvegicus 146-149
29108781-7 2018 Collectively, our findings suggest that retinoic acid plays a critical temporal role in promoting enteric neural crest chain migration and neuronal survival upstream of Meis3 and RET in vivo. Tretinoin 40-53 ret proto-oncogene receptor tyrosine kinase Danio rerio 179-182
29376871-0 2018 Retinoic Acid Enhances Apolipoprotein E Synthesis in Human Macrophages. Tretinoin 0-13 apolipoprotein E Homo sapiens 23-39
30216786-2 2018 With retinoic acid (RA) induction, a high percentage of cells were found to be arrested at the G0/G1 phase, with decreased levels of cyclinD1, CDK4, phosphorylation status of pRb and E2F1, in addition to an elevated level of p27. Tretinoin 5-18 dynactin subunit 6 Homo sapiens 225-228
29984664-5 2018 METHODS: Real-time RT-PCR was used to examine the expression of genes families involved in xenobiotic metabolism, such as CYP1 (CYP1A1, CYP1B1), CYP2 (CYP2E1, CYP2D6), CYP3 (CYP3A4); and of a family involved in the catabolism of the all-trans-retinoic acid (ATRA), CYP26 (CYP26A1, CYP26B1). Tretinoin 233-256 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 145-149
29984664-5 2018 METHODS: Real-time RT-PCR was used to examine the expression of genes families involved in xenobiotic metabolism, such as CYP1 (CYP1A1, CYP1B1), CYP2 (CYP2E1, CYP2D6), CYP3 (CYP3A4); and of a family involved in the catabolism of the all-trans-retinoic acid (ATRA), CYP26 (CYP26A1, CYP26B1). Tretinoin 258-262 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 145-149
29376871-1 2018 Apolipoprotein E (ApoE) represents a pivotal target in Alzheimer"s disease (AD) and is modulated through retinoic acid (RA), an endogenous neuroprotective and anti-inflammatory compound. Tretinoin 105-118 apolipoprotein E Homo sapiens 0-16
29376871-1 2018 Apolipoprotein E (ApoE) represents a pivotal target in Alzheimer"s disease (AD) and is modulated through retinoic acid (RA), an endogenous neuroprotective and anti-inflammatory compound. Tretinoin 105-118 apolipoprotein E Homo sapiens 18-22
28322443-0 2018 All-trans retinoic acid ameliorates hepatic stellate cell activation via suppression of thioredoxin interacting protein expression. Tretinoin 0-23 thioredoxin interacting protein Homo sapiens 88-119
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 138-157 thioredoxin interacting protein Homo sapiens 14-45
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 138-157 thioredoxin interacting protein Homo sapiens 47-52
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 159-163 thioredoxin interacting protein Homo sapiens 14-45
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 159-163 thioredoxin interacting protein Homo sapiens 47-52
28322443-5 2018 In the present study, we demonstrate that ATRA ameliorates activation of HSCs through TXNIP suppression. Tretinoin 42-46 thioredoxin interacting protein Homo sapiens 86-91
29380316-4 2018 In the described method, the SH-SY5Y neuroblastoma cell line is differentiated to neuronal cell which expresses NSE, neuronal marker, and dopamine transporter (DAT) by treatment with all-trans-retinoic acid. Tretinoin 186-206 enolase 2 Homo sapiens 112-115
28857442-3 2018 Here, we show that Yes-associated protein (YAP) is a direct target induced by CREB upon retinoic acid (RA)-induced neurite outgrowth stimuli in N2a cells. Tretinoin 88-101 cAMP responsive element binding protein 1 Mus musculus 78-82
28857442-3 2018 Here, we show that Yes-associated protein (YAP) is a direct target induced by CREB upon retinoic acid (RA)-induced neurite outgrowth stimuli in N2a cells. Tretinoin 103-105 cAMP responsive element binding protein 1 Mus musculus 78-82
27685949-7 2018 Supplementing the differentiation medium with combinations of fibroblast growth factor-2, transforming growth factor-beta3 and retinoic acid maintained viability, restored expression of CD34, aldehyde dehydrogenase 3A1 and keratocan, and facilitated production of abundant extracellular matrix as shown by immunofluorescent staining for collagen-I and lumican, alongside quantitative assays for collagen and glycosaminoglycan production. Tretinoin 127-140 CD34 molecule Homo sapiens 186-190
29039475-5 2017 The effect was more pronounced after pretreatment of the animals with all-trans retinoic acid or brusatol, potent inhibitors of Nrf2. Tretinoin 70-93 nuclear factor, erythroid derived 2, like 2 Mus musculus 128-132
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 63-70
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 retinoic acid receptor beta Homo sapiens 130-137
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 fibroblast growth factor 10 Homo sapiens 213-218
29017757-2 2017 We hypothesize that retinoic acid regulates Pitx2 expression in EOM myogenic precursor cells and that its effects would differ in leg muscle. Tretinoin 20-33 paired like homeodomain 2 Homo sapiens 44-49
29017757-7 2017 Both EOM and LEG-derived EECD34 cells exposed to retinoic acid showed a higher percentage of cells expressing Pitx2 compared to vehicle, supporting the hypothesis that retinoic acid plays a role in maintaining Pitx2 expression. Tretinoin 49-62 paired like homeodomain 2 Homo sapiens 110-115
29017757-7 2017 Both EOM and LEG-derived EECD34 cells exposed to retinoic acid showed a higher percentage of cells expressing Pitx2 compared to vehicle, supporting the hypothesis that retinoic acid plays a role in maintaining Pitx2 expression. Tretinoin 49-62 paired like homeodomain 2 Homo sapiens 210-215
29017757-7 2017 Both EOM and LEG-derived EECD34 cells exposed to retinoic acid showed a higher percentage of cells expressing Pitx2 compared to vehicle, supporting the hypothesis that retinoic acid plays a role in maintaining Pitx2 expression. Tretinoin 168-181 paired like homeodomain 2 Homo sapiens 110-115
29017757-7 2017 Both EOM and LEG-derived EECD34 cells exposed to retinoic acid showed a higher percentage of cells expressing Pitx2 compared to vehicle, supporting the hypothesis that retinoic acid plays a role in maintaining Pitx2 expression. Tretinoin 168-181 paired like homeodomain 2 Homo sapiens 210-215
29258184-6 2017 We recently observed that cPA negatively regulates PPARgamma function by stabilizing the binding of the co-repressor protein, a silencing mediator of retinoic acid, and the thyroid hormone receptor. Tretinoin 150-163 peroxisome proliferator activated receptor gamma Homo sapiens 51-60
29321784-10 2017 Inhibition of TGM2 activity by cystamine (CTM) in Sj-infected mice or in HSCs induced with all-trans-retinoic acid (ATRA) stimulation led to a lowered activation of TLR4 signaling and a reduced alpha-SMA expression. Tretinoin 91-114 toll-like receptor 4 Mus musculus 165-169
29321784-10 2017 Inhibition of TGM2 activity by cystamine (CTM) in Sj-infected mice or in HSCs induced with all-trans-retinoic acid (ATRA) stimulation led to a lowered activation of TLR4 signaling and a reduced alpha-SMA expression. Tretinoin 91-114 actin alpha 2, smooth muscle, aorta Mus musculus 194-203
29321784-10 2017 Inhibition of TGM2 activity by cystamine (CTM) in Sj-infected mice or in HSCs induced with all-trans-retinoic acid (ATRA) stimulation led to a lowered activation of TLR4 signaling and a reduced alpha-SMA expression. Tretinoin 116-120 toll-like receptor 4 Mus musculus 165-169
29321784-10 2017 Inhibition of TGM2 activity by cystamine (CTM) in Sj-infected mice or in HSCs induced with all-trans-retinoic acid (ATRA) stimulation led to a lowered activation of TLR4 signaling and a reduced alpha-SMA expression. Tretinoin 116-120 actin alpha 2, smooth muscle, aorta Mus musculus 194-203
29321952-8 2018 The analysis of gene expression showed that only in the presence of retinoic acid did FEZ1 induce hoxb4 gene expression. Tretinoin 68-81 fasciculation and elongation protein zeta 1 Homo sapiens 86-90
29344218-14 2017 ATRA treatment decreased the expression of phosphorylated (p-)beta-catenin, p-GSK-3beta, vimentin, and fibronectin, and increased the expression of NIS and E-cadherin, compared with the control. Tretinoin 0-4 fibronectin 1 Homo sapiens 103-114
28436114-0 2017 All-Trans-Retinoic Acid Stimulates Overexpression of Tumor Protein D52 (TPD52, Isoform 3) and Neuronal Differentiation of IMR-32 Cells. Tretinoin 0-23 tumor protein D52 Homo sapiens 53-70
28436114-0 2017 All-Trans-Retinoic Acid Stimulates Overexpression of Tumor Protein D52 (TPD52, Isoform 3) and Neuronal Differentiation of IMR-32 Cells. Tretinoin 0-23 tumor protein D52 Homo sapiens 72-77
28436114-2 2017 In the present study we found that the treatment of IMR-32 neuroblastoma (NB) cells with retinoic acid (RA) stimulates an increase in expression of TPD52. Tretinoin 89-102 tumor protein D52 Homo sapiens 148-153
29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 tumor necrosis factor Homo sapiens 133-160
29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 tumor necrosis factor Homo sapiens 162-171
29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 mitogen-activated protein kinase 14 Homo sapiens 222-225
29055789-7 2017 Importantly, addition of rTM to this co-culture system inhibited the RA-induced phosphorylation of p38 and VE-cadherin and decreased ICAM1 and vascular permeability in EA.hy926 cells, without a decrease inthe levels of TNF-alpha. Tretinoin 69-71 mitogen-activated protein kinase 14 Homo sapiens 99-102
29055789-7 2017 Importantly, addition of rTM to this co-culture system inhibited the RA-induced phosphorylation of p38 and VE-cadherin and decreased ICAM1 and vascular permeability in EA.hy926 cells, without a decrease inthe levels of TNF-alpha. Tretinoin 69-71 cadherin 5 Homo sapiens 107-118
29055789-7 2017 Importantly, addition of rTM to this co-culture system inhibited the RA-induced phosphorylation of p38 and VE-cadherin and decreased ICAM1 and vascular permeability in EA.hy926 cells, without a decrease inthe levels of TNF-alpha. Tretinoin 69-71 tumor necrosis factor Homo sapiens 219-228
28981191-12 2017 When platelets were treated with atRA, binding interactions between RARalpha protein and mRNA for MAP1LC3B2, SLAIN2 and ANGPT1 were significantly decreased. Tretinoin 33-37 SLAIN motif family member 2 Homo sapiens 109-115
29344218-14 2017 ATRA treatment decreased the expression of phosphorylated (p-)beta-catenin, p-GSK-3beta, vimentin, and fibronectin, and increased the expression of NIS and E-cadherin, compared with the control. Tretinoin 0-4 cadherin 1 Homo sapiens 156-166
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 10-23 notch receptor 2 Homo sapiens 140-146
29192143-8 2017 Manipulation of the IRF1 transcription factor demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). Tretinoin 83-87 interferon regulatory factor 1 Homo sapiens 20-24
29184163-0 2017 All-trans retinoic acid enhances cytotoxicity of CIK cells against human lung adenocarcinoma by upregulating MICA and IL-2 secretion. Tretinoin 10-23 interleukin 2 Homo sapiens 118-122
29184163-4 2017 Furthermore, analysis of apoptosis markers Bcl-2, Bax, Survivin and cleaved Caspase-3 showed that Bcl-2 and Survivin mRNA levels significantly decreased, and that Bax mRNA significantly increased, in the CIK + ATRA-treated cells, with corresponding effects on their respective proteins. Tretinoin 210-214 BCL2 associated X, apoptosis regulator Homo sapiens 163-166
29166590-4 2017 IL-33 promoted beta cell function through islet-resident group 2 innate lymphoid cells (ILC2s) that elicited retinoic acid (RA)-producing capacities in macrophages and dendritic cells via the secretion of IL-13 and colony-stimulating factor 2. Tretinoin 124-126 interleukin 13 Mus musculus 205-242
28943101-5 2017 Through a combination of Western blotting, enzymatic activity assays, flow cytometry and fluorescence microscopy we provide evidence that TG2 is inhibited during initiation of apoptosis by cisplatin, an observation that was reversed by increasing the expression of TG2, by treating cells with retinoic acid. Tretinoin 293-306 transglutaminase 2 Homo sapiens 138-141
29169400-10 2017 Stimulation with 5-aza-2"-deoxycytidine significantly induced RARRES1 expression, which then could be further increased with Am580, Tazarotene and all-trans retinoic acid. Tretinoin 157-170 retinoic acid receptor responder 1 Homo sapiens 62-69
28946811-13 2017 Pretreatment with all-trans retinoic acid (ATRA) was found to partially restore the capacity of MSCs in both ITP patients and healthy controls in inducing CD34+-derived regDCs. Tretinoin 18-41 CD34 molecule Homo sapiens 155-159
28946811-13 2017 Pretreatment with all-trans retinoic acid (ATRA) was found to partially restore the capacity of MSCs in both ITP patients and healthy controls in inducing CD34+-derived regDCs. Tretinoin 43-47 CD34 molecule Homo sapiens 155-159
29131833-0 2017 MEK inhibitors enhance therapeutic response towards ATRA in NF1 associated malignant peripheral nerve sheath tumors (MPNST) in-vitro. Tretinoin 52-56 mitogen-activated protein kinase kinase 7 Homo sapiens 0-3
29131833-0 2017 MEK inhibitors enhance therapeutic response towards ATRA in NF1 associated malignant peripheral nerve sheath tumors (MPNST) in-vitro. Tretinoin 52-56 neurofibromin 1 Homo sapiens 60-63
29131833-3 2017 In this study, we investigated whether human tumor Schwann cells derived from NF1 associated MPNST respond to all-trans retinoic acid (ATRA). Tretinoin 110-133 neurofibromin 1 Homo sapiens 78-81
29131833-3 2017 In this study, we investigated whether human tumor Schwann cells derived from NF1 associated MPNST respond to all-trans retinoic acid (ATRA). Tretinoin 135-139 neurofibromin 1 Homo sapiens 78-81
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 25-29 notch receptor 2 Homo sapiens 140-146
28886987-7 2017 We determined that derivatives of retinoic acid led to significantly reduced level of proteins belonging to metabolic pathway (e.g. glyceraldehyde-3-phosphate dehydrogenase or pyruvate kinase 2) or to other cellular processes as apoptosis, regulation of transcription process or epithelial-mesenchymal transition (e.g. annexins, nucleoside diphosphate kinase B, vimentin). Tretinoin 34-47 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 132-172
29972949-8 2017 Moreover, atRA decreased the levels of p-Smad2 and Smad4 in embryonic palate mesenchymal cells, whereas the expression of Smad7 was significantly increased at GD14 and GD15. Tretinoin 10-14 SMAD family member 2 Mus musculus 41-46
28327618-5 2017 HIC1 expression is regulated by the Vitamin A metabolite retinoic acid, as mice raised on a Vitamin A-deficient diet lack HIC1-positive cells in the intestine. Tretinoin 57-70 hypermethylated in cancer 1 Mus musculus 0-4
29183042-9 2017 In HMGECs serum-induced differentiation and application of all-trans retinoic acid significantly increased HRNR gene expression. Tretinoin 69-82 hornerin Homo sapiens 107-111
29068287-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes. Tretinoin 0-23 tumor protein p53 Homo sapiens 162-165
29068287-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes. Tretinoin 25-29 tumor protein p53 Homo sapiens 162-165
29068287-2 2017 In this study, we found that the oncogenic hepatitis B virus (HBV) X protein (HBx) of HBV, derived from both overexpression and 1.2-mer replicon systems, suppresses ATRA-induced apoptosis in p53-positive human hepatocytes. Tretinoin 165-169 tumor protein p53 Homo sapiens 191-194
29068287-4 2017 As a result, HBx was able to impair the potential of ATRA to activate apoptosis-related molecules, including Bax, p53-upregulated modulator of apoptosis, caspase-9, caspase-3 and poly (ADP-ribose) polymerase. Tretinoin 53-57 BCL2 associated X, apoptosis regulator Homo sapiens 109-112
29068287-4 2017 As a result, HBx was able to impair the potential of ATRA to activate apoptosis-related molecules, including Bax, p53-upregulated modulator of apoptosis, caspase-9, caspase-3 and poly (ADP-ribose) polymerase. Tretinoin 53-57 tumor protein p53 Homo sapiens 114-117
29068287-5 2017 In conclusion, the present study provides a new oncogenic action mechanism of HBx, namely by suppressing the anticancer potential of ATRA to induce p53-dependent apoptosis in HBV-infected hepatocytes. Tretinoin 133-137 tumor protein p53 Homo sapiens 148-151
27771902-4 2017 We found that RA treatment for 7 days reduced the cell number and proliferative capacity and induced the expression of adult catecholaminergic/neuronal markers such as tyrosine hydroxylase (TH), beta-III tubulin, and enolase-2. Tretinoin 14-16 enolase 2 Homo sapiens 217-226
27771902-9 2017 Importantly, Trolox co-treatment inhibited the appearance of morphological characteristics such as neurite extension and branching, and decreased the expression of TH, beta-III tubulin, and enolase-2 after a seven-day differentiation with RA, indicating that RS production is a necessary step in this process. Tretinoin 240-242 enolase 2 Homo sapiens 191-200
28327618-5 2017 HIC1 expression is regulated by the Vitamin A metabolite retinoic acid, as mice raised on a Vitamin A-deficient diet lack HIC1-positive cells in the intestine. Tretinoin 57-70 hypermethylated in cancer 1 Mus musculus 122-126
28651670-0 2017 Alterations in vitamin A/retinoic acid homeostasis in diet-induced obesity and insulin resistance. Tretinoin 25-38 insulin Homo sapiens 79-86
29166739-7 2017 (4)p-ERK decreased obviously after ATRA exposure in NPM1 mutated leukemic cells. Tretinoin 35-39 mitogen-activated protein kinase 1 Homo sapiens 5-8
28667519-5 2017 The mechanism studies indicated that RA indeed increased the expression of hepatic Sirt1 and superoxide dismutase 2 (Sod2), and inhibited the expression of sterol regulatory element binding protein 1c (Srebp-1c) in WT mice in vivo and in vitro. Tretinoin 37-39 superoxide dismutase 2, mitochondrial Mus musculus 93-115
28667519-5 2017 The mechanism studies indicated that RA indeed increased the expression of hepatic Sirt1 and superoxide dismutase 2 (Sod2), and inhibited the expression of sterol regulatory element binding protein 1c (Srebp-1c) in WT mice in vivo and in vitro. Tretinoin 37-39 superoxide dismutase 2, mitochondrial Mus musculus 117-121
29166739-9 2017 Conclusions: ATRA could inhibit cell proliferation and colony formation, blocked the cell cycle in the G(0)/G(1) stage accompanied by the significant reduction of p-ERK in U937 leukemic cells with NPM1 mutation. Tretinoin 13-17 mitogen-activated protein kinase 1 Homo sapiens 165-168
28687611-3 2017 A screening campaign revealed retinol (vitamin A alcohol) and all-trans retinoic acid (vitamin A acid) (RA) as hits that time-dependently (>=24 h) deplete phosphatidylcholine-bound polyunsaturated fatty acids (PUFA-PCs) from NIH-3T3 mouse fibroblasts while inducing Akt activation (EC50 0.1-1 microM). Tretinoin 72-85 thymoma viral proto-oncogene 1 Mus musculus 269-272
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 synaptonemal complex protein 3 Bubalus bubalis 187-192
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 synaptonemal complex protein 3 Bubalus bubalis 187-192
28754309-7 2017 Induction of stromal CYP26 by either one of these pathways limits retinoic acid concentration in the stem cell niche, with profound effects on tissue homeostasis and drug resistance. Tretinoin 66-79 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 21-26
29021914-4 2017 RA triggered angiogenesis and elicited de novo generation of platelet-derived growth factor receptor alpha positive (PDGFRalpha+) adipose precursor cells via VEGFA/VEGFR2 signaling. Tretinoin 0-2 platelet derived growth factor receptor, alpha polypeptide Mus musculus 61-106
28919262-5 2017 We also converted PDGFRA-deficient embryonic stem cell lines into XEN cell lines chemically by transient culturing with retinoic acid and Activin A. Tretinoin 120-133 platelet derived growth factor receptor, alpha polypeptide Mus musculus 18-24
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 synaptonemal complex protein 3 Bubalus bubalis 187-192
28687611-3 2017 A screening campaign revealed retinol (vitamin A alcohol) and all-trans retinoic acid (vitamin A acid) (RA) as hits that time-dependently (>=24 h) deplete phosphatidylcholine-bound polyunsaturated fatty acids (PUFA-PCs) from NIH-3T3 mouse fibroblasts while inducing Akt activation (EC50 0.1-1 microM). Tretinoin 87-101 thymoma viral proto-oncogene 1 Mus musculus 269-272
28276286-0 2017 Arsenic trioxide and all-trans-retinoic acid selectively exert synergistic cytotoxicity against FLT3-ITD AML cells via co-inhibition of FLT3 signaling pathways. Tretinoin 21-44 fms related receptor tyrosine kinase 3 Homo sapiens 96-100
28938749-20 2017 Expression of the gene encoding STRA8 (stimulated by retinoic acid 8), a protein generally considered to mark activation of retinoic acid signaling, was below our limit of detection. Tretinoin 53-66 stimulated by retinoic acid 8 Macaca mulatta 32-37
28556970-7 2017 Interestingly, atRA did not affect tumoral CD4+ T-cell response, and even inhibited the differentiation of interferon-gamma-expressing T helper type 1 cells in DLN. Tretinoin 15-19 interferon gamma Mus musculus 107-123
28276286-0 2017 Arsenic trioxide and all-trans-retinoic acid selectively exert synergistic cytotoxicity against FLT3-ITD AML cells via co-inhibition of FLT3 signaling pathways. Tretinoin 21-44 fms related receptor tyrosine kinase 3 Homo sapiens 136-140
28276286-4 2017 Here, we demonstrate that an ATO/ATRA combination selectively exerts synergistic cytotoxicity against FLT3-ITD AML cell lines (MV4;11/MOLM-13). Tretinoin 33-37 fms related receptor tyrosine kinase 3 Homo sapiens 102-106
28276286-3 2017 Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Tretinoin 50-73 fms related receptor tyrosine kinase 3 Homo sapiens 161-165
28276286-3 2017 Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Tretinoin 50-73 fms related receptor tyrosine kinase 3 Homo sapiens 215-219
28276286-3 2017 Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Tretinoin 50-73 fms related receptor tyrosine kinase 3 Homo sapiens 215-219
28276286-3 2017 Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Tretinoin 75-79 fms related receptor tyrosine kinase 3 Homo sapiens 161-165
28276286-3 2017 Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Tretinoin 75-79 fms related receptor tyrosine kinase 3 Homo sapiens 215-219
28276286-3 2017 Reports have shown that an arsenic trioxide (ATO)/all-trans-retinoic acid (ATRA) combination improves prognosis in acute promyelocytic leukemia, especially with FLT3-ITD, and ATO or ATRA alone enhances apoptosis in FLT3-ITD AML cells treated with FLT3 inhibitors, providing a rationale to investigate the role of ATO/ATRA in FLT3-ITD AML. Tretinoin 75-79 fms related receptor tyrosine kinase 3 Homo sapiens 215-219
29018329-12 2017 Our findings indicate that IMR32 differentiation induced by CDDO in combination with ATRA enhances, differentiation followed by cell death via cAMP-response-element binding protein (CREB) independent and PPARgamma dependent signaling mechanisms. Tretinoin 85-89 peroxisome proliferator activated receptor gamma Homo sapiens 204-213
28959017-5 2017 We demonstrate that Wdr5, Hdac1, and Hdac2 are required for RA signaling in vitro and in vivo. Tretinoin 60-62 histone deacetylase 2 Mus musculus 37-42
29047260-3 2017 Embryoid bodies were treated with retinoic acid (10 muM) to induce neural differentiation in the presence or absence of GSK-J4. Tretinoin 34-47 latexin Homo sapiens 52-55
28928446-4 2017 Upon treating APL with all-trans retinoic acid and achieving complete remission, the levels of PGD2, NKp30, ILC2s, IL-13 and M-MDSCs are restored. Tretinoin 33-46 prostaglandin D2 synthase Homo sapiens 95-99
28743499-7 2017 However, administration of ATRA attenuated the upregulation of EphA2-EphrinA1 and PI3K-Akt after bleomycin instillation, and decreased pulmonary fibrosis. Tretinoin 27-31 thymoma viral proto-oncogene 1 Mus musculus 87-90
28743499-8 2017 In addition, ATRA suppressed IL-6 and TNF-alpha production induced by bleomycin-induced injury. Tretinoin 13-17 interleukin 6 Mus musculus 29-33
28743499-8 2017 In addition, ATRA suppressed IL-6 and TNF-alpha production induced by bleomycin-induced injury. Tretinoin 13-17 tumor necrosis factor Mus musculus 38-47
28743499-9 2017 Collectively, these data suggest that ATRA attenuates bleomycin-induced pulmonary fibrosis by regulating EphA2-EphrinA1 and PI3K-Akt signaling. Tretinoin 38-42 thymoma viral proto-oncogene 1 Mus musculus 129-132
28927457-2 2017 All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tretinoin 0-23 tumor protein p53 Homo sapiens 79-82
28927457-2 2017 All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tretinoin 25-29 tumor protein p53 Homo sapiens 79-82
28928446-4 2017 Upon treating APL with all-trans retinoic acid and achieving complete remission, the levels of PGD2, NKp30, ILC2s, IL-13 and M-MDSCs are restored. Tretinoin 33-46 interleukin 13 Homo sapiens 115-120
28704716-12 2017 Retinoic acid treatment led to modest XPA-dependent activation of some genes with transcription-related functions. Tretinoin 0-13 XPA, DNA damage recognition and repair factor Homo sapiens 38-41
28625776-1 2017 The enzyme beta-carotene oxygenase 1 (BCO1) catalyzes the breakdown of provitamin A, including beta-carotene (BC), into retinal, prior to its oxidation into retinoic acid (RA). Tretinoin 157-170 beta-carotene oxygenase 1 Gallus gallus 11-36
28625776-1 2017 The enzyme beta-carotene oxygenase 1 (BCO1) catalyzes the breakdown of provitamin A, including beta-carotene (BC), into retinal, prior to its oxidation into retinoic acid (RA). Tretinoin 157-170 beta-carotene oxygenase 1 Gallus gallus 38-42
28625776-1 2017 The enzyme beta-carotene oxygenase 1 (BCO1) catalyzes the breakdown of provitamin A, including beta-carotene (BC), into retinal, prior to its oxidation into retinoic acid (RA). Tretinoin 172-174 beta-carotene oxygenase 1 Gallus gallus 11-36
28663132-6 2017 Mass spectrometry analysis of the neurospheres proteome revealed a reduced expression of Rbp1, a regulator of retinoic acid synthesis, when Nosip was absent. Tretinoin 110-123 retinol binding protein 1 L homeolog Xenopus laevis 89-93
28681415-6 2017 Retinoic acid represses many anteriorly expressed genes, including Bmp4, Lhx9, Msx2, and Alx4. Tretinoin 0-13 msh homeobox 2 Gallus gallus 79-83
28681415-7 2017 We provide evidence that retinoic acid influences transcription via induction of dHAND and inhibition of Gli3 to establish a new anteroposterior pre-pattern. Tretinoin 25-38 GLI family zinc finger 3 Gallus gallus 105-109
28625776-1 2017 The enzyme beta-carotene oxygenase 1 (BCO1) catalyzes the breakdown of provitamin A, including beta-carotene (BC), into retinal, prior to its oxidation into retinoic acid (RA). Tretinoin 172-174 beta-carotene oxygenase 1 Gallus gallus 38-42
28542882-5 2017 The results showed that RA-induced DCs (RA-DCs) showed mucosal DC properties, including expression of CD103 and gut homing receptor alpha4 beta7 , low proinflammatory cytokine secretion and low priming capability to antigen-specific CD4+ T cells. Tretinoin 24-26 CD4 molecule Homo sapiens 233-236
28542882-5 2017 The results showed that RA-induced DCs (RA-DCs) showed mucosal DC properties, including expression of CD103 and gut homing receptor alpha4 beta7 , low proinflammatory cytokine secretion and low priming capability to antigen-specific CD4+ T cells. Tretinoin 40-42 CD4 molecule Homo sapiens 233-236
28612832-2 2017 Recently, MYT1, encoding the myelin transcription factor 1, was reported as the first gene involved in OAVS, within the retinoic acid (RA) pathway. Tretinoin 120-133 myelin transcription factor 1 Homo sapiens 10-14
28612832-2 2017 Recently, MYT1, encoding the myelin transcription factor 1, was reported as the first gene involved in OAVS, within the retinoic acid (RA) pathway. Tretinoin 135-137 myelin transcription factor 1 Homo sapiens 10-14
28612832-2 2017 Recently, MYT1, encoding the myelin transcription factor 1, was reported as the first gene involved in OAVS, within the retinoic acid (RA) pathway. Tretinoin 120-133 myelin transcription factor 1 Homo sapiens 29-58
28612832-2 2017 Recently, MYT1, encoding the myelin transcription factor 1, was reported as the first gene involved in OAVS, within the retinoic acid (RA) pathway. Tretinoin 135-137 myelin transcription factor 1 Homo sapiens 29-58
28687976-8 2017 Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Tretinoin 66-89 S100 calcium binding protein A10 Homo sapiens 142-149
28612832-7 2017 Furthermore, we confirmed MYT1 connection to RA signaling pathway. Tretinoin 45-47 myelin transcription factor 1 Homo sapiens 26-30
28687976-8 2017 Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Tretinoin 91-95 S100 calcium binding protein A10 Homo sapiens 142-149
28643469-5 2017 In antler chondrocytes, CYP26A1 and CYP26B1 weakened the sensitivity of ATRA to COL9A1. Tretinoin 72-76 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 24-31
28677722-0 2017 Regulation of retinoic acid synthetic enzymes by WT1 and HDAC inhibitors in 293 cells. Tretinoin 14-27 WT1 transcription factor Homo sapiens 49-52
28677722-4 2017 In this study, we provide in vitro evidence to demonstrate that Wilms" tumor 1 (WT1) negatively regulates the expression of the atRA synthetic enzymes, ALDH1A1, ALDH1A2 and ALDH1A3, in the 293 cell line, leading to significant blockage of atRA production. Tretinoin 128-132 WT1 transcription factor Homo sapiens 64-78
28677722-4 2017 In this study, we provide in vitro evidence to demonstrate that Wilms" tumor 1 (WT1) negatively regulates the expression of the atRA synthetic enzymes, ALDH1A1, ALDH1A2 and ALDH1A3, in the 293 cell line, leading to significant blockage of atRA production. Tretinoin 128-132 WT1 transcription factor Homo sapiens 80-83
28677722-6 2017 Taken together, we provide evidence to indicate that WT1 and HDACs are strong regulators of endogenous retinoic acid synthetic enzymes in 293 cells, indicating that they may be involved in the regulation of atRA synthesis. Tretinoin 103-116 WT1 transcription factor Homo sapiens 53-56
28677722-6 2017 Taken together, we provide evidence to indicate that WT1 and HDACs are strong regulators of endogenous retinoic acid synthetic enzymes in 293 cells, indicating that they may be involved in the regulation of atRA synthesis. Tretinoin 207-211 WT1 transcription factor Homo sapiens 53-56
28643469-5 2017 In antler chondrocytes, CYP26A1 and CYP26B1 weakened the sensitivity of ATRA to COL9A1. Tretinoin 72-76 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 36-43
28811909-13 2017 We also show that 4-oxygenated ATRA metabolites have the potential to activate cyp26a1, the metabolic enzyme of ATRA. Tretinoin 31-35 cytochrome P450, family 26, subfamily A, polypeptide 1 Oryzias latipes 79-86
28656276-7 2017 Further investigations indicated that with ATRA-induced expression of RIG-I, levels of phosphorylated (p)AKT-Thr308 and pForkhead Box (FOX) O3A-Thr32 were decreased, the expression levels of cell cycle arrest protein p27 and the apoptotic protein, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), directly transcribed by FOXO3A were increased. Tretinoin 43-47 AKT serine/threonine kinase 1 Homo sapiens 105-108
28656276-7 2017 Further investigations indicated that with ATRA-induced expression of RIG-I, levels of phosphorylated (p)AKT-Thr308 and pForkhead Box (FOX) O3A-Thr32 were decreased, the expression levels of cell cycle arrest protein p27 and the apoptotic protein, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), directly transcribed by FOXO3A were increased. Tretinoin 43-47 TNF superfamily member 10 Homo sapiens 248-303
28656276-7 2017 Further investigations indicated that with ATRA-induced expression of RIG-I, levels of phosphorylated (p)AKT-Thr308 and pForkhead Box (FOX) O3A-Thr32 were decreased, the expression levels of cell cycle arrest protein p27 and the apoptotic protein, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), directly transcribed by FOXO3A were increased. Tretinoin 43-47 TNF superfamily member 10 Homo sapiens 305-310
28656276-7 2017 Further investigations indicated that with ATRA-induced expression of RIG-I, levels of phosphorylated (p)AKT-Thr308 and pForkhead Box (FOX) O3A-Thr32 were decreased, the expression levels of cell cycle arrest protein p27 and the apoptotic protein, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), directly transcribed by FOXO3A were increased. Tretinoin 43-47 forkhead box O3 Homo sapiens 337-343
28656276-8 2017 By contrast, following the knockdown of ATRA-induced expression of RIG-I, the levels of pAKT-Thr308 and pFOXO3A-Thr32 were increased, and the protein expression levels of p27 and TRAIL were decreased. Tretinoin 40-44 TNF superfamily member 10 Homo sapiens 179-184
28656276-9 2017 Taken together, these results showed that the knockdown of RIG-I reduced the inhibition of cell proliferation, cell cycle arrest and apoptosis in the ATRA-induced NB4 cells via the AKT-FOXO3A signaling pathway. Tretinoin 150-154 AKT serine/threonine kinase 1 Homo sapiens 181-184
28656276-9 2017 Taken together, these results showed that the knockdown of RIG-I reduced the inhibition of cell proliferation, cell cycle arrest and apoptosis in the ATRA-induced NB4 cells via the AKT-FOXO3A signaling pathway. Tretinoin 150-154 forkhead box O3 Homo sapiens 185-191
28927033-0 2017 All-trans retinoic acid enhances temozolomide-induced autophagy in human glioma cells U251 via targeting Keap1/Nrf2/ARE signaling pathway. Tretinoin 10-23 kelch like ECH associated protein 1 Homo sapiens 105-110
28927033-0 2017 All-trans retinoic acid enhances temozolomide-induced autophagy in human glioma cells U251 via targeting Keap1/Nrf2/ARE signaling pathway. Tretinoin 10-23 NFE2 like bZIP transcription factor 2 Homo sapiens 111-115
28927033-7 2017 Moreover, Keap1/Nrf2/ARE expression was downregulated significantly, indicating the involvement in the mechanisms that RA treatment could enhance the TMZ effects on U251 cells. Tretinoin 119-121 kelch like ECH associated protein 1 Homo sapiens 10-15
28927033-7 2017 Moreover, Keap1/Nrf2/ARE expression was downregulated significantly, indicating the involvement in the mechanisms that RA treatment could enhance the TMZ effects on U251 cells. Tretinoin 119-121 NFE2 like bZIP transcription factor 2 Homo sapiens 16-20
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 synaptonemal complex protein 3 Bubalus bubalis 187-192
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 synaptonemal complex protein 3 Bubalus bubalis 187-192
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 synaptonemal complex protein 3 Bubalus bubalis 187-192
28713967-7 2017 It was demonstrated that Notch2 silencing partially reversed the atRA-induced inhibition of ERK phosphorylation in MEPM cells. Tretinoin 65-69 mitogen-activated protein kinase 1 Mus musculus 92-95
28713967-10 2017 The present findings suggested that during embryonic development, atRA may enhance the expression of Notch2, which may inhibit cellular proliferation, possibly through ERK signaling. Tretinoin 66-70 mitogen-activated protein kinase 1 Mus musculus 168-171
28587808-10 2017 Importantly, co-treatment with RA prevented all of the effects of ethanol including survivability, body length, M-cell morphology, AMPA mEPSC frequency and escape response movements. Tretinoin 31-33 glutamate receptor, ionotropic, AMPA 3b Danio rerio 131-135
29137417-3 2017 Here, we show that in primary human melanocytes, all-trans retinoic acid (a RARbeta agonist) induced growth inhibition accompanied by a decrease in both glycolytic and oxidative metabolism, whereas selective inhibition of RARbeta led to an increase in the basal glycolytic rate and increased sensitivity to inhibition of glycolysis. Tretinoin 59-72 retinoic acid receptor beta Homo sapiens 76-83
29137417-3 2017 Here, we show that in primary human melanocytes, all-trans retinoic acid (a RARbeta agonist) induced growth inhibition accompanied by a decrease in both glycolytic and oxidative metabolism, whereas selective inhibition of RARbeta led to an increase in the basal glycolytic rate and increased sensitivity to inhibition of glycolysis. Tretinoin 59-72 retinoic acid receptor beta Homo sapiens 222-229
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 0-23 tumor protein p53 Homo sapiens 174-177
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 0-23 tumor protein p53 Homo sapiens 220-223
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 25-29 tumor protein p53 Homo sapiens 174-177
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 25-29 tumor protein p53 Homo sapiens 220-223
29156743-2 2017 In the present study, we found that hepatitis C virus (HCV) Core derived from ectopic expression or HCV infection overcomes ATRA-induced apoptosis in p53-positive hepatoma cells. Tretinoin 124-128 tumor protein p53 Homo sapiens 150-153
29156743-6 2017 Based on these observations, we conclude that HCV Core executes its oncogenic potential by suppressing the p53-dependent apoptosis induced by ATRA in human hepatoma cells. Tretinoin 142-146 tumor protein p53 Homo sapiens 107-110
28811909-13 2017 We also show that 4-oxygenated ATRA metabolites have the potential to activate cyp26a1, the metabolic enzyme of ATRA. Tretinoin 112-116 cytochrome P450, family 26, subfamily A, polypeptide 1 Oryzias latipes 79-86
29044428-3 2017 In developing mouse testes, cytochrome P450 family 26, subfamily b, polypeptide 1 (CYP26B1) produced by the Sertoli cells degrades retinoic acid, preventing Stimulated by Retinoic Acid Gene 8 (Stra8), expression and inhibiting meiosis. Tretinoin 131-144 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 83-90
28768913-6 2017 Of note, mTOR expression/phosphorylation was distinctively induced by RA in CCR6+ T cells. Tretinoin 70-72 mechanistic target of rapamycin kinase Homo sapiens 9-13
28768913-7 2017 Consistently, mTOR inhibitors counteracted the effect of RA on HIV replication in vitro and viral reactivation in CD4+ T cells from HIV+ART individuals via postentry mechanisms independent of CCR5. Tretinoin 57-59 mechanistic target of rapamycin kinase Homo sapiens 14-18
28568315-11 2017 The retinoate biosynthesis pathway was also enriched due to the differential expression of the genes AKR1C3, ALDH8A1, RDH8, RDH13 and SDR9C7. Tretinoin 4-13 retinol dehydrogenase 8 Bos taurus 118-122
28601022-6 2017 Nrf2 overexpression, in contrast to Nrf2 deficiency, induced the accumulation of lipid droplets via decreasing the expression of lipolytic gene peroxisome proliferator-activated receptor alpha (PPARalpha) and increasing the expression of genes involved in lipogenesis and retinoic acid responsiveness, including CCAAT/enhancer-binding protein alpha, PPARgamma, retinoid X receptor alpha, and retinoic acid receptor beta. Tretinoin 272-285 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4
27655446-8 2017 The precise function of retinoic acid and its alterations in HSCs has yet to be elucidated, and nonetheless in various cell types retinoic acid and its receptors (RAR and RXR) are known to act synergistically with peroxisome proliferator-activated receptor gamma (PPAR-gamma) signaling through the activity of transcriptional heterodimers. Tretinoin 24-37 peroxisome proliferator activated receptor gamma Homo sapiens 214-262
28810607-10 2017 Intriguingly, 1% ethanol intake remarkably elevated (10-fold, P<0.05) mRNA of brain alcohol dehydrogenase 1 (Adh1), which metabolizes lipid-peroxidation products and is involved in the synthesis of retinoic acid, a neuroprotective factor. Tretinoin 201-214 alcohol dehydrogenase 1 (class I) Mus musculus 87-110
28810607-10 2017 Intriguingly, 1% ethanol intake remarkably elevated (10-fold, P<0.05) mRNA of brain alcohol dehydrogenase 1 (Adh1), which metabolizes lipid-peroxidation products and is involved in the synthesis of retinoic acid, a neuroprotective factor. Tretinoin 201-214 alcohol dehydrogenase 1 (class I) Mus musculus 112-116
28684780-0 2017 Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 102-106
33429696-7 2017 Immunofluorescence studies and RT-PCR revealed that the atRA-loaded biomaterials increased the expression of two epithelial markers of mucociliary differentiation, MUC5AC and beta-tubulin IV, via upregulation of MUC5AC and FOXJ1 genes, both in epithelial monoculture and in a 3D scaffold coculture system with lung fibroblasts. Tretinoin 56-60 forkhead box J1 Homo sapiens 223-228
28746369-7 2017 Culturing naive human T cells with IL-2/TGFbeta1 resulted in the generation of 54.2% of Treg cells (CD4+CD25+FOXP3+) whereas the addition of 100 nM atRA increased the yield of Treg cells to 66% (p = 0.0088). Tretinoin 148-152 interleukin 2 Homo sapiens 35-39
28684780-5 2017 In addition, our results demonstrate that RA inhibits EGFR and Wnt signaling activation, two pathways involved in NSCLC progression. Tretinoin 42-44 epidermal growth factor receptor Homo sapiens 54-58
28684780-6 2017 Furthermore, we uncovered a novel mechanism in NSCLC that shows how RA exerts its function; we found that RA-mediated GATA6 activation is necessary for EGFR and Wnt inhibition, thus leading to 1) increased differentiation and 2) loss of proliferation. Tretinoin 68-70 epidermal growth factor receptor Homo sapiens 152-156
28684780-6 2017 Furthermore, we uncovered a novel mechanism in NSCLC that shows how RA exerts its function; we found that RA-mediated GATA6 activation is necessary for EGFR and Wnt inhibition, thus leading to 1) increased differentiation and 2) loss of proliferation. Tretinoin 106-108 epidermal growth factor receptor Homo sapiens 152-156
28446509-0 2017 Inhibition of the all-trans Retinoic Acid (atRA) Hydroxylases CYP26A1 and CYP26B1 Results in Dynamic, Tissue-Specific Changes in Endogenous atRA Signaling. Tretinoin 43-47 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 74-81
28515123-4 2017 ATRA suppressed IL13- or IL4-induced M2-type macrophages, and then inhibited migration of osteosarcoma cells as promoted by M2-type macrophages in vitro ATRA reduced the number of pulmonary metastatic nodes of osteosarcoma and decreased expression of M2-type macrophages in metastatic nodes both in intravenous injection and orthotopic transplantation models. Tretinoin 0-4 interleukin 13 Mus musculus 16-20
28515123-6 2017 Quantitative genomic and functional analyses revealed that MMP12, a macrophage-secreted elastase, was elevated in IL13-skewed TAM polarization, whereas ATRA treatment downregulated IL13-induced secretion of MMP12. Tretinoin 152-156 interleukin 13 Mus musculus 181-185
28409399-3 2017 RA, co-administered with the dsRNA mimic polyinosinic-polycytidylic acid (poly(I:C)), synergizes to induce a TRAIL (Tumor-Necrosis-Factor Related Apoptosis-Inducing Ligand)- dependent apoptotic program in breast cancer cells. Tretinoin 0-2 TNF superfamily member 10 Homo sapiens 109-114
28409399-3 2017 RA, co-administered with the dsRNA mimic polyinosinic-polycytidylic acid (poly(I:C)), synergizes to induce a TRAIL (Tumor-Necrosis-Factor Related Apoptosis-Inducing Ligand)- dependent apoptotic program in breast cancer cells. Tretinoin 0-2 TNF superfamily member 10 Homo sapiens 116-171
28446509-10 2017 The increased atRA concentrations in serum without a change in liver suggest that CYP26B1 in extrahepatic sites plays a key role in regulating systemic atRA exposure. Tretinoin 14-18 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 82-89
28446509-10 2017 The increased atRA concentrations in serum without a change in liver suggest that CYP26B1 in extrahepatic sites plays a key role in regulating systemic atRA exposure. Tretinoin 152-156 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 82-89
28051090-0 2017 Retinoic acid takes effector T cells to the gallows: P2X7, the molecular hangman. Tretinoin 0-13 purinergic receptor P2X 7 Homo sapiens 53-57
28584011-5 2017 All-trans retinoic acid also increased regulatory T cells and prevented the hypertension, endothelial dysfunction, and glomerular injury in genetically modified mice that phenocopy calcineurin inhibitor-treated mice (FKBP12-Tie2 knockout). Tretinoin 10-23 calcineurin binding protein 1 Mus musculus 181-202
28584011-5 2017 All-trans retinoic acid also increased regulatory T cells and prevented the hypertension, endothelial dysfunction, and glomerular injury in genetically modified mice that phenocopy calcineurin inhibitor-treated mice (FKBP12-Tie2 knockout). Tretinoin 10-23 TEK receptor tyrosine kinase Mus musculus 224-228
27966552-4 2017 We found that P2X7 upregulation on CD4+ effector T cells is induced by retinoic acid through retinoic acid receptor alpha binding to an intragenic enhancer region of the P2rx7 gene. Tretinoin 71-84 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 14-18
27966552-4 2017 We found that P2X7 upregulation on CD4+ effector T cells is induced by retinoic acid through retinoic acid receptor alpha binding to an intragenic enhancer region of the P2rx7 gene. Tretinoin 71-84 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 170-175
27966552-9 2017 We conclude that retinoic acid controls intestinal effector T-cell populations by inducing P2X7 expression. Tretinoin 17-30 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 91-95
28051090-2 2017 In this issue of Mucosal Immunology, Hashimoto-Hill et al.1 show that retinoic acid (RA) transcriptionally upregulates P2X7 primarily in effector T cells of the intestine sensitizing them to NAD-induced cell death (NICD); thus, demonstrating a previously unrecognized role of RA in effector T-cell contraction. Tretinoin 70-83 purinergic receptor P2X 7 Homo sapiens 119-123
28665981-4 2017 In this study, we demonstrate that ATRA induces multi-drug-resistant subpopulations of HL60 cells with a putative stem-like signature by up-regulating the expression of the new gene segment HA117. Tretinoin 35-39 regulator of G protein signaling 6 Homo sapiens 190-195
28592877-2 2017 In this study, we found that combination of omega-3 free fatty acids (omega-3 FFAs) and ATRA exhibited synergistic inhibition of cell growth in three subtypes (ER+ MCF7, HER2+ SK-BR-3, Triple negative HCC1806 and MDA-MB-231 cells) of human breast cancer cell lines. Tretinoin 88-92 erb-b2 receptor tyrosine kinase 2 Homo sapiens 170-174
28620241-0 2017 TGF-beta/atRA-induced Tregs express a selected set of microRNAs involved in the repression of transcripts related to Th17 differentiation. Tretinoin 9-13 transforming growth factor beta 1 Homo sapiens 0-8
28595619-8 2017 RESULTS: IFN-gamma and a multiple cytokine cocktail (MC) consisting of IFN-gamma, TGFbeta and retinoic acid upregulated the expression of immunomodulatory factor PD-L1 and IDO activity. Tretinoin 94-107 CD274 antigen Mus musculus 162-167
28637487-7 2017 CONCLUSION: As neurofibromin activity is a key to regulating the RAS/MAPK pathway, NF1 mutations are important in the acquisition of drug resistance, to BRAF, EGFR inhibitors, tamoxifen and retinoic acid in melanoma, lung and breast cancers and neuroblastoma. Tretinoin 190-203 neurofibromin 1 Homo sapiens 15-28
28637487-7 2017 CONCLUSION: As neurofibromin activity is a key to regulating the RAS/MAPK pathway, NF1 mutations are important in the acquisition of drug resistance, to BRAF, EGFR inhibitors, tamoxifen and retinoic acid in melanoma, lung and breast cancers and neuroblastoma. Tretinoin 190-203 neurofibromin 1 Homo sapiens 83-86
28488421-6 2017 Transfection of SREBP-1 siRNA suppressed RA-induced enhancement of lipid accumulation and FAS expression in the cells cultured with HG. Tretinoin 41-43 fatty acid synthase Mus musculus 90-93
28589680-5 2017 Furthermore, we showed that ATRA promoted CNTF expression through CREB binding to its promoter region. Tretinoin 28-32 cAMP responsive element binding protein 1 Mus musculus 66-70
28488421-7 2017 Transfection of the nuclear form of SREBP-1a cDNA into the cells cultured with NG inhibited RA-induced suppression of lipid accumulation and FAS expression. Tretinoin 92-94 fatty acid synthase Mus musculus 141-144
28488421-8 2017 Moreover, RA- and HG-induced SREBP-1a expression occurred at the early phase of adipogenesis and was dependent on glucocorticoid to induce liver X receptor (LXR) beta, peroxisomal proliferator-activated receptor (PPAR) gamma and retinoid X receptor (RXR), the key nuclear factors influencing the SREBP-1a gene expression. Tretinoin 10-12 peroxisome proliferator activated receptor alpha Mus musculus 168-211
28488421-8 2017 Moreover, RA- and HG-induced SREBP-1a expression occurred at the early phase of adipogenesis and was dependent on glucocorticoid to induce liver X receptor (LXR) beta, peroxisomal proliferator-activated receptor (PPAR) gamma and retinoid X receptor (RXR), the key nuclear factors influencing the SREBP-1a gene expression. Tretinoin 10-12 peroxisome proliferator activated receptor alpha Mus musculus 213-217
28087752-6 2017 Localisation of RA synthetic (RALDH-1) and degrading (cytochrome P450 subfamily 26 A1 (CYP26A1)) enzymes in human lung was determined by immunofluorescence. Tretinoin 16-18 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 54-85
28087752-6 2017 Localisation of RA synthetic (RALDH-1) and degrading (cytochrome P450 subfamily 26 A1 (CYP26A1)) enzymes in human lung was determined by immunofluorescence. Tretinoin 16-18 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 87-94
28087752-13 2017 CONCLUSIONS: RA regulates lung microvascular angiogenesis; the endothelium produces CYP26A1 which is increased in emphysema, possibly leading to reduced RA availability. Tretinoin 153-155 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 84-91
28087752-9 2017 RA induced mRNA expression of vascular endothelial growth factor A (VEGFA) and VEGFR2. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 30-66
28087752-9 2017 RA induced mRNA expression of vascular endothelial growth factor A (VEGFA) and VEGFR2. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 68-73
28396148-0 2017 DOK1/PPARgamma pathway mediates anti-tumor ability of all-trans retinoic acid in breast cancer MCF-7 cells. Tretinoin 64-77 peroxisome proliferator activated receptor gamma Homo sapiens 5-14
28396148-6 2017 Taken together, these results indicate that ATRA-enhanced expression of DOK1 activates PPARgamma leading to inhibition of cell proliferation and enhancement of cell apoptosis in MCF-7 cell. Tretinoin 44-48 peroxisome proliferator activated receptor gamma Homo sapiens 87-96
28396148-5 2017 Moreover, inactivation of PPARgamma by its specific inhibitor GW9662 reversed the impacts of ATRA on cell proliferation and apoptosis. Tretinoin 93-97 peroxisome proliferator activated receptor gamma Homo sapiens 26-35
28560318-7 2017 We found that BBB function and junctional protein expression was unaffected in mouse mutants that have a reduced capacity to synthesize RA (Rdh10 mutants). Tretinoin 136-138 retinol dehydrogenase 10 (all-trans) Mus musculus 140-145
28526071-1 2017 BACKGROUND: We previously reported that Wnt5a/CaMKIIdelta (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Tretinoin 186-199 Wnt family member 5A Homo sapiens 40-111
28560318-10 2017 Like other studies, we found that pharmacological concentrations of RA induce BBB genes in cultured murine brain endothelial cells, and this may involve activation of the LXR/RXR signaling pathway. Tretinoin 68-70 nuclear receptor subfamily 1, group H, member 3 Mus musculus 171-174
28542170-10 2017 Finally, the introduction of the INTS8 deletion mutation in P19 cells using genome editing alters gene expression throughout the course of retinoic acid-induced neural differentiation. Tretinoin 139-152 integrator complex subunit 8 Homo sapiens 33-38
28526071-1 2017 BACKGROUND: We previously reported that Wnt5a/CaMKIIdelta (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Tretinoin 201-203 Wnt family member 5A Homo sapiens 40-111
28526071-3 2017 Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKIIdelta pathway through miR-31-5p in embryonic tongue. Tretinoin 38-40 Wnt family member 5A Homo sapiens 51-56
28363907-3 2017 RA can promote gammadelta T cells to produce mTORC1-dependent IL-22 in the liver, but inhibits IFN-gamma and IL-17. Tretinoin 0-2 interferon gamma Mus musculus 95-104
28025671-6 2017 Retinoic acid inhibits the expression of early and late muscle differentiation markers and enhances the expression of myogenic specification genes, such as PAX7 and PAX3. Tretinoin 0-13 paired box 3 Homo sapiens 165-169
28320523-10 2017 Consistent with these data, the mRNA expression levels of synaptopodin, podocin, WT-1 and ZO-1 were synergistically increased by FSS and RA treatment. Tretinoin 137-139 NPHS2 stomatin family member, podocin Homo sapiens 72-79
28320523-10 2017 Consistent with these data, the mRNA expression levels of synaptopodin, podocin, WT-1 and ZO-1 were synergistically increased by FSS and RA treatment. Tretinoin 137-139 WT1 transcription factor Homo sapiens 81-94
28404959-10 2017 Moreover, ATRA also synergistically enhanced the ability of sorafenib to reduce Pin1 and inhibit tumor growth of HCC in mouse xenograft models. Tretinoin 10-14 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 80-84
28341635-8 2017 Furthermore, we found that depletion of sept7b diminished the expression of retinaldehyde dehydrogenase 2, which catalyzes the synthesis of retinoic acid necessary for heart morphogenesis. Tretinoin 140-153 septin 7b Danio rerio 40-46
28375930-2 2017 The effects of RA are mediated by the RA receptor (RAR), and RARalpha/RARbeta especially acts as a tumor suppressor. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 70-77
28375930-8 2017 RARalpha and RARbeta knockdown dose dependently reduced the inhibition of migration by ATRA, but the effect was more pronounced with RARbeta knockdown than with RARalpha knockdown. Tretinoin 87-91 retinoic acid receptor beta Homo sapiens 13-20
28375930-8 2017 RARalpha and RARbeta knockdown dose dependently reduced the inhibition of migration by ATRA, but the effect was more pronounced with RARbeta knockdown than with RARalpha knockdown. Tretinoin 87-91 retinoic acid receptor beta Homo sapiens 133-140
27998933-3 2017 Here, we report that miR-202 is highly expressed in mouse spermatogonial stem cells (SSCs), and is oppositely regulated by Glial cell-Derived Neurotrophic Factor (GDNF) and retinoic acid (RA), two key factors for SSC self-renewal and differentiation. Tretinoin 173-186 microRNA 202 Mus musculus 21-28
26953980-4 2017 In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced. Tretinoin 105-124 caspase 3 Homo sapiens 77-86
26953980-4 2017 In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced. Tretinoin 126-130 caspase 3 Homo sapiens 77-86
27981737-3 2017 METHODS AND RESULTS: 9-cis RA and all-trans RA treatment of human and murine AT explants, as well as adipocytes (3T3-F442A cell line) induces PDK4 expression both at the mRNA and the protein level, via a transcriptional mechanism. Tretinoin 27-29 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 142-146
27981737-3 2017 METHODS AND RESULTS: 9-cis RA and all-trans RA treatment of human and murine AT explants, as well as adipocytes (3T3-F442A cell line) induces PDK4 expression both at the mRNA and the protein level, via a transcriptional mechanism. Tretinoin 44-46 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 142-146
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 deleted in azoospermia-like Mus musculus 212-216
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 stem cell proliferation 1 Mus musculus 234-238
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 deleted in azoospermia-like Mus musculus 212-216
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 stem cell proliferation 1 Mus musculus 234-238
28275201-9 2017 The population-based PBPK model of atRA disposition incorporated saturable metabolic clearance of atRA, induction of CYP26A1 by atRA, and the absorption and distribution kinetics of atRA. Tretinoin 35-39 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 117-124
28404891-3 2017 HMGB1 and the pro-inflammatory cytokines IL-1beta and TNF-alpha were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO. Tretinoin 126-130 interleukin 1 beta Homo sapiens 41-49
28404891-3 2017 HMGB1 and the pro-inflammatory cytokines IL-1beta and TNF-alpha were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO. Tretinoin 126-130 tumor necrosis factor Homo sapiens 54-63
28404891-8 2017 Treatment with a HMGB1-neutralizing antibody reduced secretion of TNF-alpha and IL-1beta, arrested the elevation of ICAM-1 and blunted the activation of ERK1/2 in ATRA-induced NB4 cells. Tretinoin 163-167 mitogen-activated protein kinase 3 Homo sapiens 153-159
28232094-6 2017 We show here that ATRA causes dynamic changes in recruitment of transcription factor YY1 in concert with HDAC1 at ZMYND8 promoter. Tretinoin 18-22 YY1 transcription factor Mus musculus 85-88
28369068-11 2017 Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Tretinoin 13-17 vascular endothelial growth factor A Homo sapiens 102-106
28369068-11 2017 Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Tretinoin 13-17 vascular endothelial growth factor A Homo sapiens 112-116
28177772-7 2017 Dkk1, encoding a WNT antagonist, was examined and results showed that its expression increased in F9 cells treated with retinoic acid (RA) or overexpressing Wnt6. Tretinoin 120-133 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 0-4
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 23-25 AKT serine/threonine kinase 1 Homo sapiens 82-85
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 23-25 mechanistic target of rapamycin kinase Homo sapiens 86-115
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 23-25 mechanistic target of rapamycin kinase Homo sapiens 117-121
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 313-315 mechanistic target of rapamycin kinase Homo sapiens 117-121
28189972-0 2017 Novel lineage- and stage-selective effects of retinoic acid on mouse granulopoiesis: Blockade by dexamethasone or inducible NO synthase inactivation. Tretinoin 46-59 nitric oxide synthase 2, inducible Mus musculus 114-135
28087565-5 2017 Embryonic tissues expressing Cyp26a1 show reduced efficiency of RA clearance. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 29-36
28408241-4 2017 Furthermore, RA-induced beige adipogenesis was blocked following vascular endothelial growth factor receptor (VEGFR) 2 knock out in PDGFRalpha+ cells, suggesting its mediatory role. Tretinoin 13-15 platelet derived growth factor receptor alpha Homo sapiens 132-142
28091942-11 2017 Whereas, RA treatment prevented the induction of fibrosis and restored the levels of cytokines and RAGE expression. Tretinoin 9-11 advanced glycosylation end product-specific receptor Rattus norvegicus 99-103
28211306-0 2017 Ex vivo all-trans retinoic acid modulates NO production and regulates IL-6 effect during rheumatoid arthritis: a study in Algerian patients. Tretinoin 18-31 interleukin 6 Homo sapiens 70-74
28211306-5 2017 Then, we assessed the possible regulatory effect of ATRA on NO production induced by IL-6. Tretinoin 52-56 interleukin 6 Homo sapiens 85-89
28211306-12 2017 Interestingly, it seems that NO production mediated by IL-6 on PBMCs of RA patients is downregulated by ATRA. Tretinoin 104-108 interleukin 6 Homo sapiens 55-59
28211306-13 2017 Taken together, our results highlight the immunomodulatory effect of ATRA on NO pathway in RA patients and its possible role in regulating IL-6-mediated NO production. Tretinoin 69-73 interleukin 6 Homo sapiens 139-143
28418498-7 2017 Results: Interleukin-1beta-induced collagen degradation by corneal fibroblasts was inhibited by ATRA, Am580, and R667 in a concentration-dependent manner but was unaffected by AC55649, with the inhibitory effects of ATRA and R667 being markedly greater than that of Am580. Tretinoin 96-100 interleukin-1 beta Oryctolagus cuniculus 9-26
28350136-0 2017 All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway. Tretinoin 10-23 growth differentiation factor 2 Homo sapiens 59-63
28350136-0 2017 All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway. Tretinoin 10-23 mitogen-activated protein kinase 14 Homo sapiens 92-95
28350136-3 2017 All-trans retinoic acid (ATRA) can induce osteogenic differentiation of OS cells and potentiate BMP9-induced osteogenesis in preadipocytes. Tretinoin 0-23 growth differentiation factor 2 Homo sapiens 96-100
28350136-3 2017 All-trans retinoic acid (ATRA) can induce osteogenic differentiation of OS cells and potentiate BMP9-induced osteogenesis in preadipocytes. Tretinoin 25-29 growth differentiation factor 2 Homo sapiens 96-100
28350136-6 2017 ATRA inhibited proliferation and induced osteogenesis in 143B cells; these effects could be enhanced by BMP9 overexpression (p<0.05). Tretinoin 0-4 growth differentiation factor 2 Homo sapiens 104-108
28350136-9 2017 Both the osteogenic differentiation and the anti-proliferative activity of BMP9 in the presence of ATRA decreased upon treatment with a specific inhibitor of p38 MAPK (SB203580) (p<0.01). Tretinoin 99-103 mitogen-activated protein kinase 14 Homo sapiens 158-161
28350136-10 2017 This study indicates that the osteogenic differentiation ability of BMP9 in 143B cells can be restored by ATRA, and the combination of BMP9 and ATRA generated a stronger anti-proliferative effect on 143B cells than ATRA alone. Tretinoin 106-110 growth differentiation factor 2 Homo sapiens 68-72
28350136-10 2017 This study indicates that the osteogenic differentiation ability of BMP9 in 143B cells can be restored by ATRA, and the combination of BMP9 and ATRA generated a stronger anti-proliferative effect on 143B cells than ATRA alone. Tretinoin 144-148 growth differentiation factor 2 Homo sapiens 68-72
28350136-7 2017 ATRA could significantly increase the level of phosphorylated p38 MAPK (p-p38) in 143B cells, while BMP9 did not have any significant effect. Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 62-65
28418498-7 2017 Results: Interleukin-1beta-induced collagen degradation by corneal fibroblasts was inhibited by ATRA, Am580, and R667 in a concentration-dependent manner but was unaffected by AC55649, with the inhibitory effects of ATRA and R667 being markedly greater than that of Am580. Tretinoin 216-220 interleukin-1 beta Oryctolagus cuniculus 9-26
28350136-7 2017 ATRA could significantly increase the level of phosphorylated p38 MAPK (p-p38) in 143B cells, while BMP9 did not have any significant effect. Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 74-77
28350136-9 2017 Both the osteogenic differentiation and the anti-proliferative activity of BMP9 in the presence of ATRA decreased upon treatment with a specific inhibitor of p38 MAPK (SB203580) (p<0.01). Tretinoin 99-103 growth differentiation factor 2 Homo sapiens 75-79
28039033-4 2017 In this work, we identified an IRF-1 splicing transcript (IRF-1-s) in all-trans retinoic acid (ATRA)-treated acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 80-93 interferon regulatory factor 1 Homo sapiens 31-36
28350049-7 2017 Co-treatment of the cells with curcumin and RA results in increased apoptosis as demonstrated by elevated cleavage of poly(ADP-ribose) polymerase and cleaved caspase-9. Tretinoin 44-46 poly(ADP-ribose) polymerase 1 Homo sapiens 118-145
27990704-5 2017 Later the SSEA-1+ stem cells were induced to differentiate along male germ cell lineage with retinoic acid. Tretinoin 93-106 fucosyltransferase 4 Mus musculus 10-16
27927069-5 2017 Furthermore, we describe a convenient chemically defined, immunogen-free, small molecule-based method for generating TBX18+/WT1+ epicardial-like cell populations with 80% homogeneity from human pluripotent stem cells by modulation of the WNT and retinoic acid signaling pathways. Tretinoin 246-259 T-box transcription factor 18 Homo sapiens 117-122
28039033-5 2017 It lost the exon 8 and 9 of the full length IRF-1, expressed in numerous cell types and could be induced to expression by ATRA in NB4 cells. Tretinoin 122-126 interferon regulatory factor 1 Homo sapiens 44-49
28039033-4 2017 In this work, we identified an IRF-1 splicing transcript (IRF-1-s) in all-trans retinoic acid (ATRA)-treated acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 80-93 interferon regulatory factor 1 Homo sapiens 58-63
28039033-4 2017 In this work, we identified an IRF-1 splicing transcript (IRF-1-s) in all-trans retinoic acid (ATRA)-treated acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 95-99 interferon regulatory factor 1 Homo sapiens 31-36
28039033-4 2017 In this work, we identified an IRF-1 splicing transcript (IRF-1-s) in all-trans retinoic acid (ATRA)-treated acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 95-99 interferon regulatory factor 1 Homo sapiens 58-63
27940088-9 2017 Conversely, when LETs, but not MACs, were exposed to RA, there was an increase in transcripts for RARbeta, an RA receptor with known inhibitory effects on cell metabolism. Tretinoin 53-55 retinoic acid receptor beta Homo sapiens 98-105
28192098-9 2017 In addition, our study has shown that Belinostat and DZNep together with RA caused a depletion in HDAC1 and HDAC2 protein levels, HDAC2 gene expression and increased hyperacetylation of histone H4 in both leukemia cell lines. Tretinoin 73-75 histone deacetylase 1 Homo sapiens 98-103
28192098-9 2017 In addition, our study has shown that Belinostat and DZNep together with RA caused a depletion in HDAC1 and HDAC2 protein levels, HDAC2 gene expression and increased hyperacetylation of histone H4 in both leukemia cell lines. Tretinoin 73-75 histone deacetylase 2 Homo sapiens 108-113
28192098-9 2017 In addition, our study has shown that Belinostat and DZNep together with RA caused a depletion in HDAC1 and HDAC2 protein levels, HDAC2 gene expression and increased hyperacetylation of histone H4 in both leukemia cell lines. Tretinoin 73-75 histone deacetylase 2 Homo sapiens 130-135
28262728-4 2017 However, it was challenging to evaluate the significance of targeting Pin1 in cancer treatment until the recent identification of all-trans retinoic acid (ATRA) as a Pin1 inhibitor. Tretinoin 130-153 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 166-170
28262728-4 2017 However, it was challenging to evaluate the significance of targeting Pin1 in cancer treatment until the recent identification of all-trans retinoic acid (ATRA) as a Pin1 inhibitor. Tretinoin 155-159 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 166-170
28262728-7 2017 ATRA-induced Pin1 degradation inhibited the growth of HCC cells, although at a higher IC50 as compared with breast cancer cells, likely due to more active ATRA metabolism in liver cells. Tretinoin 0-4 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 13-17
28262728-7 2017 ATRA-induced Pin1 degradation inhibited the growth of HCC cells, although at a higher IC50 as compared with breast cancer cells, likely due to more active ATRA metabolism in liver cells. Tretinoin 155-159 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 13-17
28361034-10 2017 Two genes comprising OGS (CYP26A1 and RDH10) are strongly associated with ALDH1A2 in the retinoic acid (RA) pathways, suggesting a major role of RA signaling in early PCa progression. Tretinoin 89-102 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-33
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 5-18 killer cell lectin like receptor B1 Homo sapiens 34-39
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 5-18 killer cell lectin like receptor B1 Homo sapiens 116-121
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 20-22 killer cell lectin like receptor B1 Homo sapiens 34-39
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 20-22 killer cell lectin like receptor B1 Homo sapiens 116-121
28321213-7 2017 CD161+ T cells from the site of autoimmune arthritis showed a diminished gut-homing phenotype and blunted response to RA suggesting prior imprinting by RA in the gut or at peripheral sites rather than during synovial inflammation. Tretinoin 118-120 killer cell lectin like receptor B1 Homo sapiens 0-5
28321213-7 2017 CD161+ T cells from the site of autoimmune arthritis showed a diminished gut-homing phenotype and blunted response to RA suggesting prior imprinting by RA in the gut or at peripheral sites rather than during synovial inflammation. Tretinoin 152-154 killer cell lectin like receptor B1 Homo sapiens 0-5
27677346-0 2017 Curcumin synergistically increases effects of beta-interferon and retinoic acid on breast cancer cells in vitro and in vivo by up-regulation of GRIM-19 through STAT3-dependent and STAT3-independent pathways. Tretinoin 66-79 signal transducer and activator of transcription 3 Homo sapiens 160-165
27677346-0 2017 Curcumin synergistically increases effects of beta-interferon and retinoic acid on breast cancer cells in vitro and in vivo by up-regulation of GRIM-19 through STAT3-dependent and STAT3-independent pathways. Tretinoin 66-79 signal transducer and activator of transcription 3 Homo sapiens 180-185
27677346-8 2017 In addition, curcumin and IFN-beta/RA combination inhibited the expression of COX-2 and up-regulated GADD153. Tretinoin 35-37 mitochondrially encoded cytochrome c oxidase II Homo sapiens 78-83
27677346-8 2017 In addition, curcumin and IFN-beta/RA combination inhibited the expression of COX-2 and up-regulated GADD153. Tretinoin 35-37 DNA damage inducible transcript 3 Homo sapiens 101-108
27862498-8 2017 RESULTS: In ATRA-treated MSCs, expressions of COX-2, HIF-1, CXCR4, CCR2, VEGF, Ang-2 and Ang-4 increased compared to control groups. Tretinoin 12-16 C-C motif chemokine receptor 2 Rattus norvegicus 67-71
28264498-10 2017 Intriguingly, RA fostered allergic MC degranulation, in a way completely uncoupled from FcepsilonRI expression, but it simultaneously restricted MRGPRX2-triggered histamine release in agreement with the reduced receptor expression. Tretinoin 14-16 MAS related GPR family member X2 Homo sapiens 145-152
28187790-11 2017 Co-targeting of the retinoic acid and TGF-beta pathways, through RA and kartogenin (KGN; a TGF-beta signalling activating small molecule) combination treatment, induced the loss of viability of MYCN-amplified retinoid-resistant neuroblastoma cells. Tretinoin 20-33 transforming growth factor beta 1 Homo sapiens 91-99
27740626-5 2017 We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. Tretinoin 80-93 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 47-55
27740626-5 2017 We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. Tretinoin 95-99 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 47-55
28442062-0 2017 Retinoic acid triggers c-kit gene expression in spermatogonial stem cells through an enhanceosome constituted between transcription factor binding sites for retinoic acid response element (RARE), spleen focus forming virus proviral integration oncogene (SPFI1) (PU.1) and E26 transformation-specific (ETS). Tretinoin 0-13 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 23-28
28442062-0 2017 Retinoic acid triggers c-kit gene expression in spermatogonial stem cells through an enhanceosome constituted between transcription factor binding sites for retinoic acid response element (RARE), spleen focus forming virus proviral integration oncogene (SPFI1) (PU.1) and E26 transformation-specific (ETS). Tretinoin 157-170 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 23-28
28442062-1 2017 Restricted availability of retinoic acid (RA) in the testicular milieu regulates transcriptional activity of c-kit (KIT, CD117), which aids in the determination of spermatogonial stem-cell differentiation. Tretinoin 27-40 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 109-114
28442062-1 2017 Restricted availability of retinoic acid (RA) in the testicular milieu regulates transcriptional activity of c-kit (KIT, CD117), which aids in the determination of spermatogonial stem-cell differentiation. Tretinoin 27-40 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 116-119
28442062-1 2017 Restricted availability of retinoic acid (RA) in the testicular milieu regulates transcriptional activity of c-kit (KIT, CD117), which aids in the determination of spermatogonial stem-cell differentiation. Tretinoin 27-40 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 121-126
28442062-1 2017 Restricted availability of retinoic acid (RA) in the testicular milieu regulates transcriptional activity of c-kit (KIT, CD117), which aids in the determination of spermatogonial stem-cell differentiation. Tretinoin 42-44 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 109-114
28442062-1 2017 Restricted availability of retinoic acid (RA) in the testicular milieu regulates transcriptional activity of c-kit (KIT, CD117), which aids in the determination of spermatogonial stem-cell differentiation. Tretinoin 42-44 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 116-119
28442062-1 2017 Restricted availability of retinoic acid (RA) in the testicular milieu regulates transcriptional activity of c-kit (KIT, CD117), which aids in the determination of spermatogonial stem-cell differentiation. Tretinoin 42-44 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 121-126
28442062-2 2017 The effect of RA on c-kit has been reported previously, but its mode of genomic action remains unresolved. Tretinoin 14-16 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 20-25
28442062-3 2017 We studied the molecular machinery guiding RA responsiveness to the c-kit gene using spermatogonial stem-cell line C18-4 and primary spermatogonial cells. Tretinoin 43-45 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 68-73
28442062-5 2017 RA treatment influenced c-kit promoter activity, along with endogenous c-kit expression in C18-4 cells. Tretinoin 0-2 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 24-29
28442062-9 2017 We propose that for RA response, an enhanceosome is orchestrated through scaffolding of a CREB-binding protein (CBP)/p300 molecule between RARE and elements in the proximal promoter region, controlling germ-line expression of the c-kit gene. Tretinoin 20-22 CREB binding protein Homo sapiens 90-110
28442062-9 2017 We propose that for RA response, an enhanceosome is orchestrated through scaffolding of a CREB-binding protein (CBP)/p300 molecule between RARE and elements in the proximal promoter region, controlling germ-line expression of the c-kit gene. Tretinoin 20-22 CREB binding protein Homo sapiens 112-115
28442062-9 2017 We propose that for RA response, an enhanceosome is orchestrated through scaffolding of a CREB-binding protein (CBP)/p300 molecule between RARE and elements in the proximal promoter region, controlling germ-line expression of the c-kit gene. Tretinoin 20-22 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 230-235
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 128-148 microRNA 27a Homo sapiens 0-6
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 150-154 microRNA 27a Homo sapiens 0-6
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 microRNA 27a Homo sapiens 18-25
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 microRNA 27a Homo sapiens 82-89
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 microRNA 27a Homo sapiens 82-89
28219352-0 2017 Retinoic acid promotes expression of germline-specific genes in chicken blastoderm cells by stimulating Smad1/5 phosphorylation in a feeder-free culture system. Tretinoin 0-13 SMAD family member 1 Gallus gallus 104-111
28219352-6 2017 Using western blot, we determined that RA stimulated Smad1/5 phosphorylation. Tretinoin 39-41 SMAD family member 1 Gallus gallus 53-60
28153738-0 2017 Myocilin expression is regulated by retinoic acid in the trabecular meshwork-derived cellular environment. Tretinoin 36-49 myocilin Homo sapiens 0-8
27884045-6 2017 Moreover, we demonstrate that inhibition of RA signaling represses cell proliferation and expression of FGF10 signaling targets, and upregulates expression of basal epithelial keratins Krt5 and Krt14. Tretinoin 44-46 fibroblast growth factor 10 Homo sapiens 104-109
28153738-6 2017 This study demonstrates that the global retinoids signaling machinery is present in immortalized TM cells and that Myocilin (MYOC) expression is upregulated by retinoic acid alone or combined with a glucocorticoid co-treatment. Tretinoin 160-173 myocilin Homo sapiens 115-123
28153738-6 2017 This study demonstrates that the global retinoids signaling machinery is present in immortalized TM cells and that Myocilin (MYOC) expression is upregulated by retinoic acid alone or combined with a glucocorticoid co-treatment. Tretinoin 160-173 myocilin Homo sapiens 125-129
28153738-7 2017 This regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha/RXRalpha heterodimer. Tretinoin 19-32 myocilin Homo sapiens 50-54
28153738-7 2017 This regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha/RXRalpha heterodimer. Tretinoin 106-119 myocilin Homo sapiens 50-54
27428727-8 2017 The addition of ATRA to UDCA reduced the median serum ALP levels (277+-211 to 243+-225 U/L, P=0.09) although this, the primary endpoint, did not reach significance. Tretinoin 16-20 alkaline phosphatase, placental Homo sapiens 54-57
28065603-5 2017 Retinoic acid-induced the hypersegmentation of human neutrophils via retinoic acid receptors and mTOR pathways. Tretinoin 0-13 mechanistic target of rapamycin kinase Homo sapiens 97-101
28065603-6 2017 Retinoic acid-induced hypersegmented neutrophils enhanced neutrophil extracellular traps (NETs) formation in response to phorbol-12-myristate 13-acetate (PMA) and fMLP (N-Formylmethionine-leucyl-phenylalanine) stimulation, and increased cytotoxicity against various tumor cells. Tretinoin 0-13 formyl peptide receptor 1 Homo sapiens 163-167
28065603-6 2017 Retinoic acid-induced hypersegmented neutrophils enhanced neutrophil extracellular traps (NETs) formation in response to phorbol-12-myristate 13-acetate (PMA) and fMLP (N-Formylmethionine-leucyl-phenylalanine) stimulation, and increased cytotoxicity against various tumor cells. Tretinoin 0-13 formyl peptide receptor 1 Homo sapiens 169-208
27889377-6 2017 MiR-27b-3p mimics recapitulated the RA repression on DTNA expression, C2C12 proliferation and differentiation, while the miR-27b-3p inhibitor circumvented these defects resulting from excess RA. Tretinoin 36-38 dystrobrevin alpha Mus musculus 53-57
27889377-8 2017 Therefore, these findings indicated that excess RA inhibited the myoblast proliferation and differentiation by up-regulating miR-27b-3p to target DTNA, which implied a new mechanism in myogenic hypoplasia. Tretinoin 48-50 dystrobrevin alpha Mus musculus 146-150
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 49-51 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 106-113
28111553-3 2016 Robust expression of RA-degrading enzymes Cyp26b1 and Cyp26c1 in developing murine teeth suggested RA excess would reduce tooth hard tissue mineralization, adversely affecting enamel. Tretinoin 21-23 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 42-49
28111553-3 2016 Robust expression of RA-degrading enzymes Cyp26b1 and Cyp26c1 in developing murine teeth suggested RA excess would reduce tooth hard tissue mineralization, adversely affecting enamel. Tretinoin 99-101 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 42-49
27889102-10 2017 Using berberine or retinoic acid (which can regulate the activities of Hnf4a and Foxd3, respectively), we demonstrated suppression of C2H9orf152 by the chemicals in chicken primary hepatocytes. Tretinoin 19-32 hepatocyte nuclear factor 4 alpha Gallus gallus 71-76
29160747-6 2017 Additionally, LPS-induced autophagy further reduced retinoic acid (RA) signaling, as demonstrated by a decrease in the intracellular RA level and Rar target genes, resulting in the downregulation of Bambi and promoting the sensitization of the HSC"s fibrosis response to TGFB. Tretinoin 52-65 BMP and activin membrane bound inhibitor Homo sapiens 199-204
28715808-0 2017 Retinoic Acid Facilitates Toll-Like Receptor 4 Expression to Improve Intestinal Barrier Function through Retinoic Acid Receptor Beta. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 105-132
28715808-10 2017 RESULTS: In the present study, ATRA treatment not only increased the TER of the Caco-2 monolayer but also up-regulated the expression levels of RARbeta, TLR4 and ZO-2 in Caco-2 cells. Tretinoin 31-35 retinoic acid receptor beta Homo sapiens 144-151
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 retinoic acid receptor, beta Rattus norvegicus 40-47
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 retinoid X receptor beta Rattus norvegicus 49-56
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 peroxisome proliferator-activated receptor delta Rattus norvegicus 62-71
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 retinoic acid receptor, beta Rattus norvegicus 118-125
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 retinoid X receptor beta Rattus norvegicus 131-138
28680330-6 2017 CONCLUSIONS: We showed that although ATRA did not increase the frequency of Treg in culture, it significantly increased expression of rarbeta and rxrbeta only in lymphocytes taken from diseased animals and foxp3 expression only in healthy animals. Tretinoin 37-41 retinoic acid receptor, beta Rattus norvegicus 134-141
28680330-6 2017 CONCLUSIONS: We showed that although ATRA did not increase the frequency of Treg in culture, it significantly increased expression of rarbeta and rxrbeta only in lymphocytes taken from diseased animals and foxp3 expression only in healthy animals. Tretinoin 37-41 retinoid X receptor beta Rattus norvegicus 146-153
28980226-6 2017 Retinoic acid controls meiotic entry in developing chicken gonads through the expressions of retinaldehyde dehydrogenase 2, a major retinoic acid synthesizing enzyme, and cytochrome P450 family 26, subfamily B member 1, a major retinoic acid-degrading enzyme. Tretinoin 0-13 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 171-218
28980226-6 2017 Retinoic acid controls meiotic entry in developing chicken gonads through the expressions of retinaldehyde dehydrogenase 2, a major retinoic acid synthesizing enzyme, and cytochrome P450 family 26, subfamily B member 1, a major retinoic acid-degrading enzyme. Tretinoin 228-241 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 171-218
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 49-51 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 149-155
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 197-199 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 106-113
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 197-199 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 149-155
27834666-8 2016 Immunocytochemistry/PCR results showed higher expression of Mvh, the PGC-specific marker, in 3 muM RA concentrations on the top of the STO feeder layer. Tretinoin 100-102 progastricsin (pepsinogen C) Mus musculus 69-72
28408791-0 2017 All-Trans Retinoic Acid Modulates TLR4/NF-kappaB Signaling Pathway Targeting TNF-alpha and Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer. Tretinoin 10-23 nuclear factor kappa B subunit 1 Homo sapiens 39-48
28408791-0 2017 All-Trans Retinoic Acid Modulates TLR4/NF-kappaB Signaling Pathway Targeting TNF-alpha and Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer. Tretinoin 10-23 tumor necrosis factor Homo sapiens 77-86
28408791-0 2017 All-Trans Retinoic Acid Modulates TLR4/NF-kappaB Signaling Pathway Targeting TNF-alpha and Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer. Tretinoin 10-23 nitric oxide synthase 2 Homo sapiens 91-114
28408791-9 2017 Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF-kappaB signaling pathway targeting NOS2 and TNF-alpha expression. Tretinoin 39-43 nuclear factor kappa B subunit 1 Homo sapiens 71-80
28408791-9 2017 Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF-kappaB signaling pathway targeting NOS2 and TNF-alpha expression. Tretinoin 39-43 nitric oxide synthase 2 Homo sapiens 109-113
28408791-9 2017 Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF-kappaB signaling pathway targeting NOS2 and TNF-alpha expression. Tretinoin 39-43 tumor necrosis factor Homo sapiens 118-127
28798778-5 2017 However, the expression levels of Activin A and BMP4 increased more sharply in the EC cells during retinoic acid-induced differentiation. Tretinoin 99-112 bone morphogenetic protein 4 Mus musculus 48-52
27924485-4 2017 Here, we describe these two methodologies that we recently used to select a specific compound able to interfere with the AGO2 functional activity and able to improve the retinoic acid-dependent myeloid differentiation of leukemic cells. Tretinoin 170-183 argonaute RISC catalytic component 2 Homo sapiens 121-125
29199257-0 2017 [Retinoic Acid Prevents Dendritic Cells from Inducing Novel Inflammatory T Cells That Produce Abundant Interleukin-13]. Tretinoin 1-14 interleukin 13 Mus musculus 103-117
29199257-9 2017 These results suggest that MLN-DCs possess the latent ability to induce IL-13-producing inflammatory Th2 cells and that RA prevents them from inducing IL-13-dependent allergic or inflammatory responses to orally administered antigens. Tretinoin 120-122 interleukin 13 Mus musculus 151-156
27546728-2 2016 Retinoic acid (RA) signalling initiates germ cell meiosis by activating Stra8 (stimulated by RA gene 8). Tretinoin 0-13 stimulated by retinoic acid 8 Gallus gallus 72-77
27911779-4 2016 Retinol dehydrogenase 10 (RDH10) and aldehyde dehydrogenase family 1 subfamily A2 (ALDH1A2) mRNAs and proteins and transactivation activity of endogenous RA were found in the stroma of proximal Mullerian ducts and gradually decreased from the proximal to caudal regions in fetal mice. Tretinoin 154-156 retinol dehydrogenase 10 (all-trans) Mus musculus 0-24
27911779-4 2016 Retinol dehydrogenase 10 (RDH10) and aldehyde dehydrogenase family 1 subfamily A2 (ALDH1A2) mRNAs and proteins and transactivation activity of endogenous RA were found in the stroma of proximal Mullerian ducts and gradually decreased from the proximal to caudal regions in fetal mice. Tretinoin 154-156 retinol dehydrogenase 10 (all-trans) Mus musculus 26-31
27546728-2 2016 Retinoic acid (RA) signalling initiates germ cell meiosis by activating Stra8 (stimulated by RA gene 8). Tretinoin 0-13 stimulated by retinoic acid 8 Gallus gallus 79-102
27740873-0 2016 Retinol Dehydrogenase-10 Regulates Pancreas Organogenesis and Endocrine Cell Differentiation via Paracrine Retinoic Acid Signaling. Tretinoin 107-120 retinol dehydrogenase 10 (all-trans) Mus musculus 0-24
27720952-0 2016 Retinoylation (covalent modification by retinoic acid) of Rho-GDIbeta in the human myeloid leukemia cell line HL60 and its functional significance. Tretinoin 40-53 Rho GDP dissociation inhibitor beta Homo sapiens 58-69
27720952-8 2016 RA covalently bound to the Thr2 residue in Rho-GDIbeta (5kDa), which is the second product resulting from the cleavage of Rho-GDIbeta (28kDa) by caspase-3. Tretinoin 0-2 Rho GDP dissociation inhibitor beta Homo sapiens 43-54
27720952-8 2016 RA covalently bound to the Thr2 residue in Rho-GDIbeta (5kDa), which is the second product resulting from the cleavage of Rho-GDIbeta (28kDa) by caspase-3. Tretinoin 0-2 Rho GDP dissociation inhibitor beta Homo sapiens 122-133
27720952-8 2016 RA covalently bound to the Thr2 residue in Rho-GDIbeta (5kDa), which is the second product resulting from the cleavage of Rho-GDIbeta (28kDa) by caspase-3. Tretinoin 0-2 caspase 3 Homo sapiens 145-154
27720952-9 2016 RA treatment increased the level of Rho-GDIbeta (28kDa) and decreased the level of Rho-GDIbeta (23kDa). Tretinoin 0-2 Rho GDP dissociation inhibitor beta Homo sapiens 36-47
27720952-9 2016 RA treatment increased the level of Rho-GDIbeta (28kDa) and decreased the level of Rho-GDIbeta (23kDa). Tretinoin 0-2 Rho GDP dissociation inhibitor beta Homo sapiens 83-94
27671872-0 2016 Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF-A pathways downstream of retinoic acid from the meninges. Tretinoin 103-116 vascular endothelial growth factor A Homo sapiens 73-79
27671872-7 2016 We provide data that suggests that meninges-derived RA ensures adequate growth of the neocortical vasculature via regulating expression of WNT pathway proteins and neural progenitor derived-VEGF-A. Tretinoin 52-54 vascular endothelial growth factor A Homo sapiens 190-196
27740873-11 2016 We further propose a model in which the Rdh10-expressing exocrine tissue acts as an essential source of RA signals in the second wave of endocrine cell differentiation. Tretinoin 104-106 retinol dehydrogenase 10 (all-trans) Mus musculus 40-45
27888400-5 2016 Furthermore, all-trans retinoic acid treatment induced CDKN2C expression by releasing the PML/RARalpha binding on chromatin in NB4 cells. Tretinoin 23-36 cyclin dependent kinase inhibitor 2C Homo sapiens 55-61
27919568-4 2016 Cell attachment on FN activated PI3K/Akt and MAPK cascades, whereas ATRA pretreatment blunted the early phosphorylation of Akt and MAPK signaling mediators including p38 MAPK, JNK1/2, and ERK1/2. Tretinoin 68-72 AKT serine/threonine kinase 1 Homo sapiens 123-126
27647308-0 2016 A Novel Combination of Docosahexaenoic Acid, All-Trans Retinoic Acid, and 1, 25-Dihydroxyvitamin D3 Reduces T-Bet Gene Expression, Serum Interferon Gamma, and Clinical Scores but Promotes PPARgamma Gene Expression in Experimental Autoimmune Encephalomyelitis. Tretinoin 45-68 interferon gamma Mus musculus 137-153
27647308-9 2016 These findings highlighted that ATRA, D3, and DHA combination modulated PPARgamma and T-bet gene expression and resulted in decrease in Th1 response and lymphocyte invasion into the central nervous system (CNS) and resultant inflammation. Tretinoin 32-36 negative elongation factor complex member C/D, Th1l Mus musculus 136-139
26615761-8 2016 The results revealed that the culture of OEPs on laminin with the conditioned medium from chicken utricle stromal cells supplemented with EGF and all-trans retinoic acid (RA) could promote the organization of cells into epithelial clusters displaying hair-cell-like cells with stereociliary bundles. Tretinoin 156-169 laminin, beta 2 (laminin S) Gallus gallus 49-56
27775549-3 2016 We previously showed that expression of CYP26 in BM stromal cells maintains a retinoic acid-low (RA-low) microenvironment that prevents the differentiation of normal and malignant hematopoietic cells. Tretinoin 78-91 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-45
27919568-4 2016 Cell attachment on FN activated PI3K/Akt and MAPK cascades, whereas ATRA pretreatment blunted the early phosphorylation of Akt and MAPK signaling mediators including p38 MAPK, JNK1/2, and ERK1/2. Tretinoin 68-72 mitogen-activated protein kinase 1 Homo sapiens 166-169
27919568-4 2016 Cell attachment on FN activated PI3K/Akt and MAPK cascades, whereas ATRA pretreatment blunted the early phosphorylation of Akt and MAPK signaling mediators including p38 MAPK, JNK1/2, and ERK1/2. Tretinoin 68-72 mitogen-activated protein kinase 8 Homo sapiens 176-182
27919568-4 2016 Cell attachment on FN activated PI3K/Akt and MAPK cascades, whereas ATRA pretreatment blunted the early phosphorylation of Akt and MAPK signaling mediators including p38 MAPK, JNK1/2, and ERK1/2. Tretinoin 68-72 mitogen-activated protein kinase 3 Homo sapiens 188-194
27751853-5 2016 Treatment with BC or retinoic acid (RA) upregulated RARbeta mRNA expression in two NB cell lines. Tretinoin 21-34 retinoic acid receptor beta Homo sapiens 52-59
27989102-9 2016 Furthermore, silencing of either TIG1 or TMEM192 led to alleviation of the upregulation of autophagy induced by all-trans retinoic acid. Tretinoin 122-135 retinoic acid receptor responder 1 Homo sapiens 33-37
27989102-11 2016 Our study also suggests that TIG1 and TMEM192 play an important role in the all-trans retinoic acid-mediated upregulation of autophagic activity. Tretinoin 86-99 retinoic acid receptor responder 1 Homo sapiens 29-33
27893754-3 2016 Molecularly, excess RA signaling negatively regulates fibroblast growth factor 8a (fgf8a) expression and positively regulates matrix metalloproteinase 9 (mmp9) expression. Tretinoin 20-22 fibroblast growth factor 8a Danio rerio 54-81
27893754-3 2016 Molecularly, excess RA signaling negatively regulates fibroblast growth factor 8a (fgf8a) expression and positively regulates matrix metalloproteinase 9 (mmp9) expression. Tretinoin 20-22 fibroblast growth factor 8a Danio rerio 83-88
27569851-4 2016 The objective was to elucidate gene expression of these RA-metabolizing enzymes (ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1 and CYP26C1) and their protein presence in testes of young, peripubertal and adult dogs. Tretinoin 56-58 cytochrome P450 family 26 subfamily A member 1 Canis lupus familiaris 108-115
27569851-4 2016 The objective was to elucidate gene expression of these RA-metabolizing enzymes (ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1 and CYP26C1) and their protein presence in testes of young, peripubertal and adult dogs. Tretinoin 56-58 cytochrome P450 26C1 Canis lupus familiaris 129-136
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 15-17 cytochrome P450 family 26 subfamily A member 1 Canis lupus familiaris 97-104
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 15-17 cytochrome P450 26C1 Canis lupus familiaris 118-125
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 73-75 cytochrome P450 family 26 subfamily A member 1 Canis lupus familiaris 97-104
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 73-75 cytochrome P450 26C1 Canis lupus familiaris 118-125
30460049-11 2017 We also found atRA inhibited phosphorylation of Smad2 compared with untreated group (P < .05). Tretinoin 14-18 SMAD family member 2 Mus musculus 48-53
27751853-5 2016 Treatment with BC or retinoic acid (RA) upregulated RARbeta mRNA expression in two NB cell lines. Tretinoin 36-38 retinoic acid receptor beta Homo sapiens 52-59
27778276-4 2016 Foxp3 expression is increased by the activation of several transcription factors including nuclear factor-kappa B (NF-kappaB), nuclear factor of activated T cells (NFAT), and Smad3 in response to various signals such as TGFbeta, retinoic acid, and rapamycin. Tretinoin 229-242 nuclear factor kappa B subunit 1 Homo sapiens 91-113
27778276-4 2016 Foxp3 expression is increased by the activation of several transcription factors including nuclear factor-kappa B (NF-kappaB), nuclear factor of activated T cells (NFAT), and Smad3 in response to various signals such as TGFbeta, retinoic acid, and rapamycin. Tretinoin 229-242 nuclear factor kappa B subunit 1 Homo sapiens 115-124
27242163-3 2016 Immunocytochemistry was used to localize different components of RA signaling within sections of the retina and optic tectum, namely, the synthetic enzyme retinaldehyde dehydrogenase (RALDH), the RA binding proteins CRABPI and II, the retinoic acid receptors RARalpha, beta and gamma, and finally the catabolic enzyme CYP26A1. Tretinoin 65-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 318-325
27589347-2 2016 Similarly, homozygous loss-of-function mutations in CYP26B1, one of the major RA-metabolizing enzymes, cause advanced bone age, premature epiphyseal fusion, and craniosynostosis. Tretinoin 78-80 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 52-59
27589347-7 2016 The 79 deleted genes included CYP26A1 and C1, both major RA-metabolizing enzymes. Tretinoin 57-59 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 30-37
27589347-11 2016 CYP26A1 and C1 haploinsufficiency may contribute to the elevated retinoic acid concentrations and clinical findings of the patient, although this phenotype has not been reported in other patients with similar deletions, suggesting that other unknown genetic or environmental factors may also contribute. Tretinoin 65-78 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
27665842-0 2016 Staurosporine enhances ATRA-induced granulocytic differentiation in human leukemia U937 cells via the MEK/ERK signaling pathway. Tretinoin 23-27 mitogen-activated protein kinase kinase 7 Homo sapiens 102-105
27614840-5 2016 As a mammary epithelial cell model, the human MCF-7 cell line, a breast adenocarcinoma cell line, which shows inducible expression of NIS by all-trans retinoic acid (ATRA), and unlike bovine mammary epithelial cells, is widely used to investigate the regulation of mammary gland NIS and NIS-specific iodide uptake, was used. Tretinoin 151-164 solute carrier family 5 member 5 Homo sapiens 134-137
27614840-6 2016 Inhibition of SREBP maturation by treatment with 25-hydroxycholesterol (5 microM) for 48h reduced ATRA (1 microM)-induced mRNA concentration of NIS and iodide uptake in MCF-7 cells by approximately 20%. Tretinoin 98-102 solute carrier family 5 member 5 Homo sapiens 144-147
26541884-0 2016 NRF2 Mediates Neuroblastoma Proliferation and Resistance to Retinoic Acid Cytotoxicity in a Model of In Vitro Neuronal Differentiation. Tretinoin 60-73 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4
26541884-5 2016 Simultaneously, NAC pre-incubation attenuated nuclear factor erythroid 2-like factor 2 (NRF2) activation by RA. Tretinoin 108-110 NFE2 like bZIP transcription factor 2 Homo sapiens 46-86
26541884-5 2016 Simultaneously, NAC pre-incubation attenuated nuclear factor erythroid 2-like factor 2 (NRF2) activation by RA. Tretinoin 108-110 NFE2 like bZIP transcription factor 2 Homo sapiens 88-92
26541884-7 2016 NRF2 knockdown increased cell sensibility to RA after 96 h of treatment and diminished neuroblastoma proliferation rate. Tretinoin 45-47 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4
26541884-9 2016 In addition, a rapid and non-genomic activation of the ERK 1/2 and PI3K/AKT pathways revealed to be equally required to promote NRF2 activation and necessary for RA-induced differentiation. Tretinoin 162-164 mitogen-activated protein kinase 3 Homo sapiens 55-62
26541884-9 2016 In addition, a rapid and non-genomic activation of the ERK 1/2 and PI3K/AKT pathways revealed to be equally required to promote NRF2 activation and necessary for RA-induced differentiation. Tretinoin 162-164 AKT serine/threonine kinase 1 Homo sapiens 72-75
26541884-10 2016 Together, we provide data correlating NRF2 activity with neuroblastoma proliferation and resistance to RA treatments; thus, this pathway could be a potential target to optimize neuroblastoma chemotherapeutic response as well as in vitro neuronal differentiation protocols. Tretinoin 103-105 NFE2 like bZIP transcription factor 2 Homo sapiens 38-42
27358179-11 2016 Treatment with all-trans retinoic acid (RA), a known teratogenic agent causing OAVS, led to an upregulation of cellular endogenous MYT1 expression. Tretinoin 15-38 myelin transcription factor 1 Homo sapiens 131-135
27358179-11 2016 Treatment with all-trans retinoic acid (RA), a known teratogenic agent causing OAVS, led to an upregulation of cellular endogenous MYT1 expression. Tretinoin 40-42 myelin transcription factor 1 Homo sapiens 131-135
27665842-0 2016 Staurosporine enhances ATRA-induced granulocytic differentiation in human leukemia U937 cells via the MEK/ERK signaling pathway. Tretinoin 23-27 mitogen-activated protein kinase 1 Homo sapiens 106-109
27665842-10 2016 Taken together, we concluded that staurosporine enhanced ATRA-induced granulocytic differentiation in U937 cells via MEK/ERK-mediated modulation of the protein level of C/EBPs. Tretinoin 57-61 mitogen-activated protein kinase kinase 7 Homo sapiens 117-120
27665842-10 2016 Taken together, we concluded that staurosporine enhanced ATRA-induced granulocytic differentiation in U937 cells via MEK/ERK-mediated modulation of the protein level of C/EBPs. Tretinoin 57-61 mitogen-activated protein kinase 1 Homo sapiens 121-124
27894404-6 2016 As with the result of RA treatment, STZ administration increased MAP2-positive cells. Tretinoin 22-24 microtubule-associated protein 2 Mus musculus 65-69
27486269-1 2016 We previously described a novel germ cell-specific X-linked reproductive homeobox gene (Rhox13) that is upregulated at the level of translation in response to retinoic acid (RA) in differentiating spermatogonia and preleptotene spermatocytes. Tretinoin 159-172 reproductive homeobox 13 Mus musculus 88-94
27486269-1 2016 We previously described a novel germ cell-specific X-linked reproductive homeobox gene (Rhox13) that is upregulated at the level of translation in response to retinoic acid (RA) in differentiating spermatogonia and preleptotene spermatocytes. Tretinoin 174-176 reproductive homeobox 13 Mus musculus 88-94
27410456-3 2016 The disorder is caused by biallelic missense mutations in CYP26B1, which encodes for a cytochrome P450 enzyme responsible for the catabolism of retinoic acid in a temporally and spatially restricted fashion during embryonic development. Tretinoin 144-157 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 58-65
27980750-1 2016 Based upon the clinical behavior of three patients, we suggest that the combination of low-dose Ara-C and all-trans retinoic acid may potentially be effective in some elderly patients, unfit for intensive chemotherapy, affected with NPM1-mutated acute myeloid leukemia without FLT3 mutations, warranting perspective clinical studies in these selected patients. Tretinoin 116-129 fms related receptor tyrosine kinase 3 Homo sapiens 277-281
27501050-6 2016 Consistently, the beneficial effects of IPo were abolished by ATRA and Brusatol, potent inhibitors of Nrf2. Tretinoin 62-66 nuclear factor, erythroid derived 2, like 2 Mus musculus 102-106
27480083-0 2016 A network including PU.1, Vav1 and miR-142-3p sustains ATRA-induced differentiation of acute promyelocytic leukemia cells - a short report. Tretinoin 55-59 microRNA 142 Homo sapiens 35-42
27480083-2 2016 In APL-derived cells, miR-142-3p expression can be restored by all-trans retinoic acid (ATRA), which induces the completion of their maturation program. Tretinoin 73-86 microRNA 142 Homo sapiens 22-29
27480083-2 2016 In APL-derived cells, miR-142-3p expression can be restored by all-trans retinoic acid (ATRA), which induces the completion of their maturation program. Tretinoin 88-92 microRNA 142 Homo sapiens 22-29
27480083-4 2016 METHODS: ATRA-induced increases in PU.1 and Vav1 expression in APL-derived NB4 cells were counteracted with specific siRNAs, and the expression of miR-142-3p was measured by quantitative real-time PCR (qRT-PCR). Tretinoin 9-13 microRNA 142 Homo sapiens 147-154
27480083-9 2016 CONCLUSIONS: Our results suggest the existence of a Vav1/PU.1/miR-142-3p network that supports ATRA-induced differentiation in APL-derived cells. Tretinoin 95-99 microRNA 142 Homo sapiens 62-69
27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 44-67 BCL2 apoptosis regulator Homo sapiens 190-212
27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 44-67 BCL2 apoptosis regulator Homo sapiens 214-218
27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 69-73 BCL2 apoptosis regulator Homo sapiens 190-212
27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 69-73 BCL2 apoptosis regulator Homo sapiens 214-218
27354299-11 2016 CONCLUSIONS: ATRA treatment on PI3K pathway suppression significantly affected growth, signaling pattern and interactions among PI3K/Bcl2/retinol proteins involved in the growth, survival and apoptosis of leiomyomas. Tretinoin 13-17 BCL2 apoptosis regulator Homo sapiens 133-137
26883918-8 2016 The retinoic acid induced bovine mGSCs were positive for Stra8, SCP3, DZAL, EMA1 and VASA, and resembled spermatid cells morphologically. Tretinoin 4-17 stimulated by retinoic acid 8 Bos taurus 57-62
27133819-0 2016 PML-RARalpha kinetics and impact of FLT3-ITD mutations in newly diagnosed acute promyelocytic leukaemia treated with ATRA and ATO or ATRA and chemotherapy. Tretinoin 117-121 fms related receptor tyrosine kinase 3 Homo sapiens 36-40
27684493-6 2016 RA is a potent activating ligand for the RAR/RXR nuclear receptors. Tretinoin 0-2 RAB40B, member RAS oncogene family Homo sapiens 41-44
27564600-4 2016 ATRA inhibited the expression and activation of myosin light chain kinase (MLCK) in RKO cells, while the expression level of MLC phosphatase (MLCP) had no change in RKO cells treated with or without ATRA. Tretinoin 0-4 modulator of VRAC current 1 Homo sapiens 75-78
27564600-5 2016 The expression and activity of MLC was also inhibited in RKO cells exposed to ATRA. Tretinoin 78-82 modulator of VRAC current 1 Homo sapiens 31-34
27564600-7 2016 However, ATRA did not change the expression of zonula occludens 1 (ZO-1), but increased the accumulation of ZO-1 on RKO cells membrane. Tretinoin 9-13 tight junction protein 1 Homo sapiens 108-112
27564600-13 2016 In conclusion, ATRA inhibits RKO migration by reducing MLCK expression via extracellular signal-regulated kinase 1/Mitogen-activated protein kinase (ERK1/MAPK) signaling pathway. Tretinoin 15-19 mitogen-activated protein kinase 3 Homo sapiens 75-147
27564600-13 2016 In conclusion, ATRA inhibits RKO migration by reducing MLCK expression via extracellular signal-regulated kinase 1/Mitogen-activated protein kinase (ERK1/MAPK) signaling pathway. Tretinoin 15-19 mitogen-activated protein kinase 3 Homo sapiens 149-153
27166374-4 2016 This involves feed forward regulation of Raldh2, a rate-limiting enzyme for RA biosynthesis, and requires Med25 to coordinate RAR, STAT6 and chromatin remodeler, Brg1 to remodel the +1 nucleosome of Arg1 for transcription initiation. Tretinoin 76-78 RAB40B, member RAS oncogene family Homo sapiens 126-129
27590114-6 2016 Consistent with these findings, increased colonic expression of the atRA-catabolizing enzyme, CYP26A1, correlated with reduced frequencies of tumoral cytotoxic CD8(+) T cells and with worse disease prognosis in human CRC. Tretinoin 68-72 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 94-101
27166374-6 2016 This study uncovers synergistic activation of Arg1 by RA and IL-4 in M2 macrophages that involves feed forward regulation of RA synthesis and dual functions of Med25 in nucleosome remodeling and transcription initiation-elongation coupling that underlies robust modulatory activity of RA in innate immunity. Tretinoin 125-127 interleukin 4 Homo sapiens 61-65
27166374-6 2016 This study uncovers synergistic activation of Arg1 by RA and IL-4 in M2 macrophages that involves feed forward regulation of RA synthesis and dual functions of Med25 in nucleosome remodeling and transcription initiation-elongation coupling that underlies robust modulatory activity of RA in innate immunity. Tretinoin 125-127 interleukin 4 Homo sapiens 61-65
27600527-3 2016 Here we report that ATRA, an active metabolite of vitamin A, restores mechanical quiescence in PSCs via a mechanism involving a retinoic acid receptor beta (RAR-beta)-dependent downregulation of actomyosin (MLC-2) contractility. Tretinoin 20-24 retinoic acid receptor beta Homo sapiens 128-155
27600527-3 2016 Here we report that ATRA, an active metabolite of vitamin A, restores mechanical quiescence in PSCs via a mechanism involving a retinoic acid receptor beta (RAR-beta)-dependent downregulation of actomyosin (MLC-2) contractility. Tretinoin 20-24 retinoic acid receptor beta Homo sapiens 157-165
27600527-5 2016 Our findings implicate a RAR-beta/MLC-2 pathway in peritumoural stromal remodelling and mechanosensory-driven activation of PSCs, and further suggest that mechanical reprogramming of PSCs with retinoic acid derivatives might be a viable alternative to stromal ablation strategies for the treatment of PDAC. Tretinoin 193-206 retinoic acid receptor beta Homo sapiens 25-33
27402828-7 2016 Expression of apolipoprotein A-I mRNA and protein synthesis were markedly up-regulated in choroids of chick eyes during the recovery from induced myopia, and apolipoprotein A-I mRNA was significantly increased in choroids following retinoic acid treatment. Tretinoin 232-245 apolipoprotein AI Gallus gallus 14-32
27608010-7 2016 Similarly, in F9 embryonal carcinoma cells, a mouse TGCT cell line with embryonic stem cell properties, there is a significant decrease in TSPO expression during RA-induced differentiation. Tretinoin 162-164 translocator protein Mus musculus 139-143
27402828-7 2016 Expression of apolipoprotein A-I mRNA and protein synthesis were markedly up-regulated in choroids of chick eyes during the recovery from induced myopia, and apolipoprotein A-I mRNA was significantly increased in choroids following retinoic acid treatment. Tretinoin 232-245 apolipoprotein AI Gallus gallus 158-176
27402828-8 2016 Together, these data suggest that apolipoprotein A-I may participate in a regulatory feedback mechanism with retinoic acid to control the action of retinoic acid on ocular targets during postnatal ocular growth. Tretinoin 109-122 apolipoprotein AI Gallus gallus 34-52
27402828-8 2016 Together, these data suggest that apolipoprotein A-I may participate in a regulatory feedback mechanism with retinoic acid to control the action of retinoic acid on ocular targets during postnatal ocular growth. Tretinoin 148-161 apolipoprotein AI Gallus gallus 34-52
27089940-1 2016 Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. Tretinoin 0-13 negative elongation factor complex member C/D, Th1l Mus musculus 128-131
27488031-2 2016 We have identified retinoic acid (RA) and the RA-degrading enzyme CYP26B1 as regulators of ovarian follicle development and showed that RA and a CYP26 inhibitor stimulated ovarian granulosa cell proliferation. Tretinoin 46-48 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 66-73
27488031-2 2016 We have identified retinoic acid (RA) and the RA-degrading enzyme CYP26B1 as regulators of ovarian follicle development and showed that RA and a CYP26 inhibitor stimulated ovarian granulosa cell proliferation. Tretinoin 46-48 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 66-73
26883953-9 2016 Both the acetylation and SUMOylation status of the PXR protein is affected by its ability to associate with the lysine de-acetylating enzyme histone de-acetylase (HDAC)3 in a complex with silencing mediator of retinoic acid and thyroid hormone receptor (SMRT). Tretinoin 210-223 nuclear receptor subfamily 1 group I member 2 Homo sapiens 51-54
27089940-1 2016 Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. Tretinoin 0-13 negative elongation factor complex member C/D, Th1l Mus musculus 136-139
27089940-1 2016 Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. Tretinoin 15-17 negative elongation factor complex member C/D, Th1l Mus musculus 128-131
27089940-1 2016 Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. Tretinoin 15-17 negative elongation factor complex member C/D, Th1l Mus musculus 136-139
27089940-4 2016 We found that RA had a dramatic suppressive effect on IL-17A and IL-17F production by gammadelta T cells stimulated with IL-1beta and IL-23. Tretinoin 14-16 interleukin 1 beta Mus musculus 121-129
27089940-10 2016 Our findings demonstrate that the anti-inflammatory properties of RA are mediated in part by suppressing STAT3-mediated activation of cytokine production and cytokine receptor expression in gammadelta T cells, which suppresses their ability to activate Th17 cells. Tretinoin 66-68 signal transducer and activator of transcription 3 Mus musculus 105-110
27366899-2 2016 Cytochrome P450 oxidoreductase (POR) is the only obligate electron donor for all of the microsomal cytochrome P450 enzymes including CYP26A1 which is highly specific for ATRA metabolism and efficacy in human myeloid leukaemia cells. Tretinoin 170-174 cytochrome p450 oxidoreductase Homo sapiens 32-35
27443528-11 2016 ATRA treatment led to downregulation of the ALDH1A1, P-gp and BCRP proteins. Tretinoin 0-4 ATP binding cassette subfamily B member 1 Homo sapiens 53-57
27443528-11 2016 ATRA treatment led to downregulation of the ALDH1A1, P-gp and BCRP proteins. Tretinoin 0-4 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 62-66
27366899-6 2016 The potential roles of POR on ATRA efficacy in HL-60 cells were explored by cell viability assay, cell cycle distribution, cellular differentiation and apoptosis analysis. Tretinoin 30-34 cytochrome p450 oxidoreductase Homo sapiens 23-26
27421841-6 2016 RNA-seq analysis indicated an upregulation of genes important for neuronal development, such as Ntng2, Enah, Gas1, Slit2, and Dscam, in response to the RA treatment in control Neuro2a cells transfected with GFP or wild-type KDM5C. Tretinoin 152-154 ENAH actin regulator Mus musculus 103-107
27421841-6 2016 RNA-seq analysis indicated an upregulation of genes important for neuronal development, such as Ntng2, Enah, Gas1, Slit2, and Dscam, in response to the RA treatment in control Neuro2a cells transfected with GFP or wild-type KDM5C. Tretinoin 152-154 growth arrest specific 1 Mus musculus 109-113
27421841-6 2016 RNA-seq analysis indicated an upregulation of genes important for neuronal development, such as Ntng2, Enah, Gas1, Slit2, and Dscam, in response to the RA treatment in control Neuro2a cells transfected with GFP or wild-type KDM5C. Tretinoin 152-154 slit guidance ligand 2 Mus musculus 115-120
27366899-7 2016 KEY FINDINGS: All-trans-retinoic acid treatment caused the expression of POR upregulation and CYP26A1 downregulation in dose- and time-dependent manners. Tretinoin 14-37 cytochrome p450 oxidoreductase Homo sapiens 73-76
27366899-2 2016 Cytochrome P450 oxidoreductase (POR) is the only obligate electron donor for all of the microsomal cytochrome P450 enzymes including CYP26A1 which is highly specific for ATRA metabolism and efficacy in human myeloid leukaemia cells. Tretinoin 170-174 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 133-140
27366899-7 2016 KEY FINDINGS: All-trans-retinoic acid treatment caused the expression of POR upregulation and CYP26A1 downregulation in dose- and time-dependent manners. Tretinoin 14-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 94-101
27366899-10 2016 In addition, POR overexpression in HL-60 cells significantly compromised ATRA-induced cell proliferation inhibition, cell cycle arrest, differentiation and apoptosis, whereas downregulation of POR significantly potentiated ATRA effects. Tretinoin 73-77 cytochrome p450 oxidoreductase Homo sapiens 13-16
27307294-9 2016 All-trans retinoic acid increased CD38 levels and decreased CD55 and CD59 expression on MM cells from patients who developed daratumumab resistance, to approximately pretreatment values. Tretinoin 10-23 CD59 molecule (CD59 blood group) Homo sapiens 69-73
27402843-3 2016 beta-Carotene can also be cleaved by beta-carotene 9",10"-oxygenase (BCO2) to form beta-apo-10"-carotenal, a precursor of retinoic acid and a transcriptional regulator per se The mammalian embryo obtains beta-carotene from the maternal circulation. Tretinoin 122-135 beta-carotene oxygenase 2 Homo sapiens 37-67
27402843-3 2016 beta-Carotene can also be cleaved by beta-carotene 9",10"-oxygenase (BCO2) to form beta-apo-10"-carotenal, a precursor of retinoic acid and a transcriptional regulator per se The mammalian embryo obtains beta-carotene from the maternal circulation. Tretinoin 122-135 beta-carotene oxygenase 2 Homo sapiens 69-73
27416800-3 2016 atRA bound to CRABPs (holo-CRABP) was efficiently metabolized by CYP26B1. Tretinoin 0-4 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 65-72
29541688-5 2016 Our results demonstrated that atRA enhanced progesterone production by upregulating the levels of steroidogenic acute regulatory protein (StAR) and cytochrome P450scc (Cyp11a1) mRNAs, but not 3beta-hydroxysteroid dehydrogenase mRNA in immature rat GCs. Tretinoin 30-34 steroidogenic acute regulatory protein Rattus norvegicus 98-136
29541688-5 2016 Our results demonstrated that atRA enhanced progesterone production by upregulating the levels of steroidogenic acute regulatory protein (StAR) and cytochrome P450scc (Cyp11a1) mRNAs, but not 3beta-hydroxysteroid dehydrogenase mRNA in immature rat GCs. Tretinoin 30-34 steroidogenic acute regulatory protein Rattus norvegicus 138-142
27595139-5 2016 In the mouse model of allergic eye disease (AED), classical CD11b+ DCs in the ocular mucosa showed increased activity of aldehyde dehydrogenase (ALDH), the enzyme required for retinoic acid synthesis. Tretinoin 176-189 integrin alpha M Mus musculus 60-65
27060579-4 2016 When NHKs were exposed to disruptive stimuli such as Staphylococcus aureus, ultraviolet irradiation and retinoic acid, the secretion of S100A7 into the culture medium increased and the expression of epidermal differentiation markers decreased. Tretinoin 104-117 S100 calcium binding protein A7 Homo sapiens 136-142
26836442-6 2016 RESULTS: All-trans retinoic acid inhibited interleukin-1beta-induced collagen degradation by corneal fibroblasts in a concentration- and time-dependent manner. Tretinoin 19-32 interleukin-1 beta Oryctolagus cuniculus 43-60
26836442-9 2016 CONCLUSIONS: All-trans retinoic acid inhibited collagen degradation mediated by corneal fibroblasts exposed to interleukin-1beta, with this effect being accompanied by suppression of nuclear factor-kappaB signalling as well as of matrix metalloproteinase release and activation in these cells. Tretinoin 23-36 interleukin-1 beta Oryctolagus cuniculus 111-128
27416800-4 2016 Isotope dilution experiments showed that delivery of atRA to CYP26B1 in solution was similar with or without CRABP. Tretinoin 53-57 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 61-68
27460990-3 2016 We found that disruption of Syx, a gene encoding a RhoA-specific guanine nucleotide exchange factor, accelerated retinoic acid-induced neural differentiation in murine embryonic stem cells aggregated into embryoid bodies. Tretinoin 113-126 pleckstrin homology domain containing, family G (with RhoGef domain) member 5 Mus musculus 28-31
26660958-11 2016 Taken together, ATRA can reverse the suppressive effect of MED28 on HBP1 and E-cadherin and inactivate the Wnt/beta-catenin pathway in colorectal cancer, suggesting a protective effect of ATRA against colorectal cancer. Tretinoin 16-20 cadherin 1 Homo sapiens 77-87
27281783-8 2016 Retinoic acid induced AIRE expression in GC1-spg cells. Tretinoin 0-13 guanylate cyclase 2e Mus musculus 41-44
27374082-9 2016 However, further depletion of Cdh1 in APL significantly reduced viability of leukemia cells upon ATRA-induced differentiation. Tretinoin 97-101 cadherin 1 Homo sapiens 30-34
27445154-4 2016 Our analysis of globally RA-deficient embryos (Rdh10 mutants) points to an important, non-cell-autonomous function for RA in the development of the vasculature in the neocortex. Tretinoin 25-27 retinol dehydrogenase 10 (all-trans) Mus musculus 47-52
27435798-0 2016 Corrigendum: All trans-retinoic acid analogs promote cancer cell apoptosis through non-genomic Crabp1 mediating ERK1/2 phosphorylation. Tretinoin 17-36 mitogen-activated protein kinase 3 Homo sapiens 112-118
27130522-0 2016 Retinoic acid induces nuclear FAK translocation and reduces breast cancer cell adhesion through Moesin, FAK, and Paxillin. Tretinoin 0-13 moesin Homo sapiens 96-102
27422020-0 2016 Col1a1+ perivascular cells in the brain are a source of retinoic acid following stroke. Tretinoin 56-69 collagen, type I, alpha 1 Mus musculus 0-6
27499693-0 2016 NLS-RARalpha Inhibits the Effects of All-trans Retinoic Acid on NB4 Cells by Interacting with P38alpha MAPK. Tretinoin 47-60 mitogen-activated protein kinase 14 Homo sapiens 94-102
27499693-4 2016 We found that all-trans retinoic acid(ATRA) could promote differentiation while inhibit proliferation of APL NB4 cells via upregulating the expression of phosphorylated p38alpha mitogen-activated protein kinase(p-p38alpha MAPK). Tretinoin 14-37 mitogen-activated protein kinase 14 Homo sapiens 169-177
27499693-4 2016 We found that all-trans retinoic acid(ATRA) could promote differentiation while inhibit proliferation of APL NB4 cells via upregulating the expression of phosphorylated p38alpha mitogen-activated protein kinase(p-p38alpha MAPK). Tretinoin 14-37 mitogen-activated protein kinase 14 Homo sapiens 213-221
27499693-4 2016 We found that all-trans retinoic acid(ATRA) could promote differentiation while inhibit proliferation of APL NB4 cells via upregulating the expression of phosphorylated p38alpha mitogen-activated protein kinase(p-p38alpha MAPK). Tretinoin 38-42 mitogen-activated protein kinase 14 Homo sapiens 169-177
27499693-4 2016 We found that all-trans retinoic acid(ATRA) could promote differentiation while inhibit proliferation of APL NB4 cells via upregulating the expression of phosphorylated p38alpha mitogen-activated protein kinase(p-p38alpha MAPK). Tretinoin 38-42 mitogen-activated protein kinase 14 Homo sapiens 213-221
27499693-5 2016 We also found that NLS-RARalpha could inhibit differentiation while accelerate proliferation of NB4 cells via downregulating the expression of p-p38alpha protein in the presence of ATRA. Tretinoin 181-185 mitogen-activated protein kinase 14 Homo sapiens 145-153
27499693-7 2016 Finally, application of PD169316, an inhibitor of p38alpha protein, suggested that recruitment p38alpha-combinded NLS-RARalpha by ATRA eventually caused activation of p38alpha protein. Tretinoin 130-134 mitogen-activated protein kinase 14 Homo sapiens 50-58
27499693-7 2016 Finally, application of PD169316, an inhibitor of p38alpha protein, suggested that recruitment p38alpha-combinded NLS-RARalpha by ATRA eventually caused activation of p38alpha protein. Tretinoin 130-134 mitogen-activated protein kinase 14 Homo sapiens 95-103
27499693-7 2016 Finally, application of PD169316, an inhibitor of p38alpha protein, suggested that recruitment p38alpha-combinded NLS-RARalpha by ATRA eventually caused activation of p38alpha protein. Tretinoin 130-134 mitogen-activated protein kinase 14 Homo sapiens 95-103
27499693-8 2016 In summary, our study demonstrated that ATRA cound promote differentiation while inhibit proliferation of APL NB4 cells via activating p38alpha protein after recruiting p38alpha-combinded NLS-RARalpha, while NLS-RARalpha could inhibit the effects of ATRA in the process. Tretinoin 40-44 mitogen-activated protein kinase 14 Homo sapiens 135-143
27499693-8 2016 In summary, our study demonstrated that ATRA cound promote differentiation while inhibit proliferation of APL NB4 cells via activating p38alpha protein after recruiting p38alpha-combinded NLS-RARalpha, while NLS-RARalpha could inhibit the effects of ATRA in the process. Tretinoin 40-44 mitogen-activated protein kinase 14 Homo sapiens 169-177
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 44-57 moesin Homo sapiens 244-250
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 44-57 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 252-257
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 59-61 moesin Homo sapiens 244-250
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 59-61 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 252-257
27130522-4 2016 Here we identify that the administration of 10(-6) M RA (10-20 min) induces the activation of the migration-related proteins Moesin, FAK, and Paxillin in T-47D breast cancer cells. Tretinoin 53-55 moesin Homo sapiens 125-131
27130522-5 2016 The phosphorylation exerted by the selective agonists for RARalpha and RARbeta, on Moesin, FAK, and Paxillin was comparable to the activation exerted by RA. Tretinoin 58-60 moesin Homo sapiens 83-89
27251091-7 2016 Further, retinoic acid downregulated the expression of Cnnm1 in GC1-spg cells. Tretinoin 9-22 guanylate cyclase 2e Mus musculus 64-67
27286452-8 2016 Additionally, expression of the cancer stem cell marker, aldehyde dehydrogenase 1A3, which provides the required ligand (retinoic acid) for RARRES1 transcription, is also specific to the basal-like subtype. Tretinoin 121-134 retinoic acid receptor responder 1 Homo sapiens 140-147
27286452-9 2016 We functionally demonstrate that the combination of promoter methylation and retinoic acid signaling dictates expression of tumor suppressor RARRES1 in a subtype-specific manner. Tretinoin 77-90 retinoic acid receptor responder 1 Homo sapiens 141-148
27375161-0 2016 ATRA modulates mechanical activation of TGF-beta by pancreatic stellate cells. Tretinoin 0-4 transforming growth factor beta 1 Homo sapiens 40-48
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 151-170 transforming growth factor beta 1 Homo sapiens 43-51
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 151-170 transforming growth factor beta 1 Homo sapiens 289-297
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 172-176 transforming growth factor beta 1 Homo sapiens 43-51
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 172-176 transforming growth factor beta 1 Homo sapiens 289-297
27375161-5 2016 Therefore, ATRA inhibits the ability of PSCs to mechanically release active TGF-beta, which might otherwise act in an autocrine manner to sustain PSCs in an active state and a tumour-favouring stiff microenvironment. Tretinoin 11-15 transforming growth factor beta 1 Homo sapiens 76-84
28591946-9 2016 The serum levels of TNF-alpha, IFN-gamma and IL-17A were decreased in both ATRA groups; ATRA also can increase the serum level of IL-4. Tretinoin 75-79 tumor necrosis factor Rattus norvegicus 20-29
26374207-0 2016 Expression of the retinoic acid catabolic enzyme CYP26B1 in the human brain to maintain signaling homeostasis. Tretinoin 18-31 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 49-56
26374207-3 2016 The catabolic enzymes Cyp26a1 and Cyp26b1 have been studied in detail in the embryo, where they limit gradients of RA that form patterns of gene expression, crucial for morphogenesis. Tretinoin 115-117 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 22-29
26374207-3 2016 The catabolic enzymes Cyp26a1 and Cyp26b1 have been studied in detail in the embryo, where they limit gradients of RA that form patterns of gene expression, crucial for morphogenesis. Tretinoin 115-117 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 34-41
26374207-7 2016 In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone. Tretinoin 152-154 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 49-54
26374207-7 2016 In vivo use of a new and potent inhibitor of the Cyp26 enzymes, ser 2-7, demonstrated a function for endogenous Cyp26 in the brain and that hippocampal RA levels can be raised by ser 2-7, altering the effect of RA on differential patterning of cell proliferation in the hippocampal region of neurogenesis, the subgranular zone. Tretinoin 211-213 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 49-54
27214556-8 2016 Finally, spleen growth was impaired in mice lacking either cytochrome P450 26B1 (Cyp26b1), which results in excess RA, or retinol dehydrogenase 10 (Rdh10), which results in RA deficiency. Tretinoin 115-117 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 59-79
27214556-8 2016 Finally, spleen growth was impaired in mice lacking either cytochrome P450 26B1 (Cyp26b1), which results in excess RA, or retinol dehydrogenase 10 (Rdh10), which results in RA deficiency. Tretinoin 115-117 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 81-88
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 60-79 somatostatin receptor 5 Rattus norvegicus 195-201
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 81-85 somatostatin receptor 5 Rattus norvegicus 195-201
27320915-5 2016 Finally, RA regulates the competence of the endoderm to activate the Nkx2-1+ respiratory program in response to these mesodermal WNT and BMP signals. Tretinoin 9-11 NK2 homeobox 1 Homo sapiens 69-75
27156125-9 2016 According to the previous results, ATRA causes a decline in Th17 populations; increase in CD4+ induced regulatory T cells (iTregs), stabilization of nTregs, and promotion of suppressive B cells, which are critical in the improvement of pemphigus. Tretinoin 35-39 CD4 molecule Homo sapiens 90-93
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 26-39 interferon gamma Homo sapiens 233-242
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 72-85 interferon gamma Homo sapiens 233-242
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 72-85 interferon gamma Homo sapiens 233-242
26980802-7 2016 Experiments with naive CD4(+) T cells, activated in the presence of Th1/Th17 conditions and absence of DCs, indicated that retinoic acid inhibited IFN-gamma and IL-17 expression on T cells. Tretinoin 123-136 interferon gamma Homo sapiens 147-156
27177208-0 2016 A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP. Tretinoin 18-31 tumor protein p53 Homo sapiens 228-231
27177208-0 2016 A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP. Tretinoin 18-31 protein phosphatase 1 regulatory subunit 13B Homo sapiens 236-241
27177208-0 2016 A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP. Tretinoin 18-31 protein phosphatase 1 regulatory subunit 13 like Homo sapiens 264-269
27177208-14 2016 Moreover, the fluorescent density of p53 was higher in the nuclei after exposure to ATPR than that in the ATRA group. Tretinoin 106-110 tumor protein p53 Homo sapiens 37-40
27363269-7 2016 The expressions of p-JAK2 and p-STAT3 were down-regulated while the expressions of GRIM-19 and Bax were up-regulated after treated with IFN-beta or ATRA on HepG2 cells, especially the combination of IFN-beta and ATRA. Tretinoin 148-152 signal transducer and activator of transcription 3 Homo sapiens 32-37
27363269-7 2016 The expressions of p-JAK2 and p-STAT3 were down-regulated while the expressions of GRIM-19 and Bax were up-regulated after treated with IFN-beta or ATRA on HepG2 cells, especially the combination of IFN-beta and ATRA. Tretinoin 148-152 BCL2 associated X, apoptosis regulator Homo sapiens 95-98
27334688-8 2016 Induction of neural differentiation with retinoic acid resulted in downregulation of Sox2 and VRK1 that inversely correlated with the expression of differentiation markers such as N-cadherin, Pax6, mH2A1.2 and mH2A2. Tretinoin 41-54 VRK serine/threonine kinase 1 Homo sapiens 94-98
27103744-0 2016 All-trans retinoic acid synergizes with FLT3 inhibition to eliminate FLT3/ITD+ leukemia stem cells in vitro and in vivo. Tretinoin 10-23 fms related receptor tyrosine kinase 3 Homo sapiens 69-73
27314326-0 2016 All-Trans Retinoic Acid Modulates DNA Damage Response and the Expression of the VEGF-A and MKI67 Genes in ARPE-19 Cells Subjected to Oxidative Stress. Tretinoin 10-23 vascular endothelial growth factor A Homo sapiens 80-86
27314326-0 2016 All-Trans Retinoic Acid Modulates DNA Damage Response and the Expression of the VEGF-A and MKI67 Genes in ARPE-19 Cells Subjected to Oxidative Stress. Tretinoin 10-23 marker of proliferation Ki-67 Homo sapiens 91-96
27314326-10 2016 ATRA induced over-expression of proliferation marker MKI67 and neovascularization marker VEGF-A. Tretinoin 0-4 marker of proliferation Ki-67 Homo sapiens 53-58
27314326-10 2016 ATRA induced over-expression of proliferation marker MKI67 and neovascularization marker VEGF-A. Tretinoin 0-4 vascular endothelial growth factor A Homo sapiens 89-95
27285327-2 2016 Among dietary factors, high dextrose, low protein, methionine restriction, short-chain fatty acids (butyric acid and lipoic acid), and all-trans-retinoic acid were repeatedly shown to induce FGF21 expression and circulating levels. Tretinoin 135-158 fibroblast growth factor 21 Homo sapiens 191-196
27103744-6 2016 Colony-forming unit assays further demonstrate decreased clonogenicity of FLT3/ITD(+) cells upon treatment with ATRA and TKI. Tretinoin 112-116 fms related receptor tyrosine kinase 3 Homo sapiens 74-78
27103744-8 2016 Furthermore, engraftment of primary FLT3/ITD(+) patient samples is reduced in mice following treatment with FLT3 TKI and ATRA in combination, with evidence of cellular differentiation occurring in vivo. Tretinoin 121-125 fms related receptor tyrosine kinase 3 Homo sapiens 36-40
27103744-10 2016 However, cotreatment with ATRA reduces Bcl6 expression to baseline levels through suppression of interleukin-6 receptor signaling. Tretinoin 26-30 interleukin 6 receptor Homo sapiens 97-119
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 58-71 cyclin dependent kinase inhibitor 2A Homo sapiens 238-241
27151945-11 2016 In enteroids, the stimulation of RA production by SCFA was mimicked by inhibitors of histone deacetylase 3 (HDAC3) but not by HDAC1/2 inhibitors nor by agonists of butyrate receptors G-protein-coupled receptor (GPR)43 or GPR109A, indicating that butyrate stimulates RA production via HDAC3 inhibition. Tretinoin 33-35 free fatty acid receptor 2 Homo sapiens 211-217
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 58-71 retinoic acid receptor beta Homo sapiens 316-324
27151945-11 2016 In enteroids, the stimulation of RA production by SCFA was mimicked by inhibitors of histone deacetylase 3 (HDAC3) but not by HDAC1/2 inhibitors nor by agonists of butyrate receptors G-protein-coupled receptor (GPR)43 or GPR109A, indicating that butyrate stimulates RA production via HDAC3 inhibition. Tretinoin 33-35 hydroxycarboxylic acid receptor 2 Homo sapiens 221-228
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 58-71 cyclin dependent kinase inhibitor 2A Homo sapiens 337-340
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 58-71 retinoic acid receptor beta Homo sapiens 345-353
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 73-77 cyclin dependent kinase inhibitor 2A Homo sapiens 238-241
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 73-77 retinoic acid receptor beta Homo sapiens 316-324
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 73-77 cyclin dependent kinase inhibitor 2A Homo sapiens 337-340
27116384-1 2016 In our previous in vitro trials, decitabine and all-trans retinoic acid (ATRA) demonstrated synergistic effects on growth inhibition, differentiation, and apoptosis in SHI-1 cells; in K562 cells, ATRA enhanced the effect of decitabine on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression (p16 and RAR-beta are two tumor suppressor genes). Tretinoin 73-77 retinoic acid receptor beta Homo sapiens 345-353
26729628-2 2016 Studies show that this regulation is executed by a single protein, the nuclear isoform of FGFR1 (nFGFR1), which integrates signals from development-initiating factors, such as retinoic acid (RA), and operates at the interface of genomic and epigenomic information. Tretinoin 176-189 fibroblast growth factor receptor 1 Homo sapiens 90-95
26638120-10 2016 Moreover, RA augments ISG induction in response to viral infection or exposure to IFN in a gene-specific manner. Tretinoin 10-12 interferon alpha 1 Homo sapiens 82-85
26729628-2 2016 Studies show that this regulation is executed by a single protein, the nuclear isoform of FGFR1 (nFGFR1), which integrates signals from development-initiating factors, such as retinoic acid (RA), and operates at the interface of genomic and epigenomic information. Tretinoin 191-193 fibroblast growth factor receptor 1 Homo sapiens 90-95
26829212-3 2016 METHODS: Baseline and ATRA-induced expression of RIG-I in nine (3 wild type and 6 BRAF-mutant) melanoma cell lines was measured with Q-PCR and Western blot. Tretinoin 22-26 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 82-86
27101150-0 2016 RAF-1/MEK/ERK pathway regulates ATRA-induced differentiation in acute promyelocytic leukemia cells through C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 32-36 mitogen-activated protein kinase kinase 7 Homo sapiens 6-9
27101150-0 2016 RAF-1/MEK/ERK pathway regulates ATRA-induced differentiation in acute promyelocytic leukemia cells through C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 32-36 mitogen-activated protein kinase 1 Homo sapiens 10-13
27101150-2 2016 Recently, MEK/ERK cascade was reported to be involved in all-trans retinoic acid (ATRA) induced differentiation in acute promyelocytic leukemia (APL) cells. Tretinoin 67-80 mitogen-activated protein kinase kinase 7 Homo sapiens 10-13
27101150-2 2016 Recently, MEK/ERK cascade was reported to be involved in all-trans retinoic acid (ATRA) induced differentiation in acute promyelocytic leukemia (APL) cells. Tretinoin 67-80 mitogen-activated protein kinase 1 Homo sapiens 14-17
27101150-2 2016 Recently, MEK/ERK cascade was reported to be involved in all-trans retinoic acid (ATRA) induced differentiation in acute promyelocytic leukemia (APL) cells. Tretinoin 82-86 mitogen-activated protein kinase kinase 7 Homo sapiens 10-13
27101150-2 2016 Recently, MEK/ERK cascade was reported to be involved in all-trans retinoic acid (ATRA) induced differentiation in acute promyelocytic leukemia (APL) cells. Tretinoin 82-86 mitogen-activated protein kinase 1 Homo sapiens 14-17
27101150-5 2016 ATRA-enhanced protein levels of C/EBPbeta, C/EBPepsilon and PU.1, which were required for differentiation in APL cells, were suppressed by the specific inhibitor of MEK. Tretinoin 0-4 mitogen-activated protein kinase kinase 7 Homo sapiens 165-168
27101150-7 2016 Taken together, our study suggested that RAF-1/MEK/ERK cascade was involved in ATRA-induced differentiation in APL cells through enhancing the protein level of C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 79-83 mitogen-activated protein kinase kinase 7 Homo sapiens 47-50
27101150-7 2016 Taken together, our study suggested that RAF-1/MEK/ERK cascade was involved in ATRA-induced differentiation in APL cells through enhancing the protein level of C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 79-83 mitogen-activated protein kinase 1 Homo sapiens 51-54
27026484-7 2016 Expression analysis of specific genes after 7days of RA treatment, as examined by RT-PCR, proved positive for some germ cell markers such as CVH, STRA8, PLZF and some genes involved in spermatogonial stem cell maintenance like BCL6b and c-KIT. Tretinoin 53-55 stimulated by retinoic acid 8 Gallus gallus 146-151
27026484-8 2016 On the other hand, GDNF could additionally induce expression of POU5F1, and NANOG as well as other genes which were induced after RA treatment. Tretinoin 130-132 Nanog homeobox Gallus gallus 76-81
27146823-1 2016 BACKGROUND: Long noncoding RNA HOX antisense intergenic RNA myeloid 1 (HOTAIRM1) has been characterized as a critical factor in all-trans retinoic acid (ATRA)-induced differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 138-151 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 71-79
27146823-1 2016 BACKGROUND: Long noncoding RNA HOX antisense intergenic RNA myeloid 1 (HOTAIRM1) has been characterized as a critical factor in all-trans retinoic acid (ATRA)-induced differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 153-157 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 71-79
27146823-6 2016 The induction of HOTAIRM1 by ATRA was dependent on PU.1, and ectopic expression of PU.1 significantly up-regulated HOTAIRM1. Tretinoin 29-33 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 17-25
27082936-0 2016 [Retracted] Retinoic acid-incorporated glycol chitosan nanoparticles inhibit the expression of Ezh2 in U118 and U138 human glioma cells. Tretinoin 12-25 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 95-99
27082936-1 2016 We wish to retract our research article entitled "Retinoic acid-incorporated glycol chitosan nanoparticles inhibit Ezh2 expression in U118 and U138 human glioma cells" published in Molecular Medicine Reports 12: 6642-6648, 2015. Tretinoin 50-63 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 115-119
27182202-0 2016 Lyn, a tyrosine kinase closely linked to the differentiation status of primary acute myeloid leukemia blasts, associates with negative regulation of all-trans retinoic acid (ATRA) and dihydroxyvitamin D3 (VD3)-induced HL-60 cells differentiation. Tretinoin 159-172 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3
27182202-0 2016 Lyn, a tyrosine kinase closely linked to the differentiation status of primary acute myeloid leukemia blasts, associates with negative regulation of all-trans retinoic acid (ATRA) and dihydroxyvitamin D3 (VD3)-induced HL-60 cells differentiation. Tretinoin 174-178 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3
27146823-6 2016 The induction of HOTAIRM1 by ATRA was dependent on PU.1, and ectopic expression of PU.1 significantly up-regulated HOTAIRM1. Tretinoin 29-33 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 115-123
26829212-8 2016 RESULTS: Short-term ATRA pre-treatment increases the expression of RIG-I in BRAF-mutant melanoma cells. Tretinoin 20-24 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 76-80
26950191-0 2016 Loss-of-Function of HtrA1 Abrogates All-Trans Retinoic Acid-Induced Osteogenic Differentiation of Mouse Adipose-Derived Stromal Cells Through Deficiencies in p70S6K Activation. Tretinoin 46-59 HtrA serine peptidase 1 Mus musculus 20-25
26936961-4 2016 The endogenous level of RA is higher in visceral ASCs; this is associated with upregulation of the RA synthesis gene through the visceral-specific developmental factor WT1. Tretinoin 24-26 WT1 transcription factor Homo sapiens 168-171
26936961-4 2016 The endogenous level of RA is higher in visceral ASCs; this is associated with upregulation of the RA synthesis gene through the visceral-specific developmental factor WT1. Tretinoin 99-101 WT1 transcription factor Homo sapiens 168-171
26936961-5 2016 Excessive RA-mediated activity impedes the adipogenic capability of ASCs at early but not late stages of adipogenesis, which can be reversed by antagonism of RA receptors or knockdown of WT1. Tretinoin 10-12 WT1 transcription factor Homo sapiens 187-190
26937021-1 2016 Cytochrome P450 (CYP) 26A1 and 26B1 are heme-containing enzymes responsible for metabolizing all-trans retinoic acid (at-RA). Tretinoin 103-116 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-35
27022678-8 2016 These results indicate that ovarian de novo biosynthesis of RA is required for the follicular expression of Lhcgr in granulosa cells and their ability to respond to the ovulatory LH surge. Tretinoin 60-62 luteinizing hormone/choriogonadotropin receptor Mus musculus 108-113
25728212-8 2016 In addition, overexpression of GDF10 promotes DNA damage-induced apoptosis and sensitizes the response to all-trans retinoic acid (ATRA) and camptothecin (CPT). Tretinoin 116-129 growth differentiation factor 10 Homo sapiens 31-36
25728212-8 2016 In addition, overexpression of GDF10 promotes DNA damage-induced apoptosis and sensitizes the response to all-trans retinoic acid (ATRA) and camptothecin (CPT). Tretinoin 131-135 growth differentiation factor 10 Homo sapiens 31-36
26950191-3 2016 In this study, we assessed the influence of small interfering RNA (siRNA)-induced repression of HtrA1 production on mASC osteogenesis and examined its effects on ATRA-mediated mammalian target of rapamycin (mTOR) signaling. Tretinoin 162-166 mechanistic target of rapamycin kinase Homo sapiens 176-205
26950191-3 2016 In this study, we assessed the influence of small interfering RNA (siRNA)-induced repression of HtrA1 production on mASC osteogenesis and examined its effects on ATRA-mediated mammalian target of rapamycin (mTOR) signaling. Tretinoin 162-166 mechanistic target of rapamycin kinase Homo sapiens 207-211
26950191-5 2016 Western blot analyses revealed the rapid activation of Akt (Ser473) and p70S6K (Thr389) in ATRA-treated mASCs, and that levels of phosphorylated p70S6K were noticeably reduced in HtrA1-deficient mASCs. Tretinoin 91-95 thymoma viral proto-oncogene 1 Mus musculus 55-58
26950191-5 2016 Western blot analyses revealed the rapid activation of Akt (Ser473) and p70S6K (Thr389) in ATRA-treated mASCs, and that levels of phosphorylated p70S6K were noticeably reduced in HtrA1-deficient mASCs. Tretinoin 91-95 HtrA serine peptidase 1 Mus musculus 179-184
27074819-0 2016 The HER2 inhibitor TAK165 Sensitizes Human Acute Myeloid Leukemia Cells to Retinoic Acid-Induced Myeloid Differentiation by activating MEK/ERK mediated RARalpha/STAT1 axis. Tretinoin 75-88 erb-b2 receptor tyrosine kinase 2 Homo sapiens 4-8
27008339-11 2016 We demonstrate here that ATRA is absorbed by PDMS in a time-dependent manner and results in the concomitant reduced expression of CD38 on the cell surface of CB-derived CD34(+) cells. Tretinoin 25-29 CD34 molecule Homo sapiens 169-173
26979774-1 2016 AIMS: Retinoic acid has recently yielded promising results in the treatment of Cushing"s disease, i.e., excess cortisol secretion due to a pituitary corticotropin (ACTH)-secreting adenoma. Tretinoin 6-19 proopiomelanocortin Homo sapiens 164-168
26148230-7 2016 Together, the results suggest that FUS-ERG acts as a transcriptional repressor of the retinoic acid signaling pathway. Tretinoin 86-99 FUS RNA binding protein Homo sapiens 35-38
26148230-7 2016 Together, the results suggest that FUS-ERG acts as a transcriptional repressor of the retinoic acid signaling pathway. Tretinoin 86-99 ETS transcription factor ERG Homo sapiens 39-42
27074819-0 2016 The HER2 inhibitor TAK165 Sensitizes Human Acute Myeloid Leukemia Cells to Retinoic Acid-Induced Myeloid Differentiation by activating MEK/ERK mediated RARalpha/STAT1 axis. Tretinoin 75-88 mitogen-activated protein kinase kinase 7 Homo sapiens 135-138
27074819-0 2016 The HER2 inhibitor TAK165 Sensitizes Human Acute Myeloid Leukemia Cells to Retinoic Acid-Induced Myeloid Differentiation by activating MEK/ERK mediated RARalpha/STAT1 axis. Tretinoin 75-88 mitogen-activated protein kinase 1 Homo sapiens 139-142
27074819-4 2016 In this study, we showed that TAK165, a HER2 inhibitor, exhibited a strong synergy with ATRA to promote AML cell differentiation. Tretinoin 88-92 erb-b2 receptor tyrosine kinase 2 Homo sapiens 40-44
26818829-2 2016 We showed that atRA treatment increased VEGF-C, VEGF-D, and VEGFR3 protein and mRNA contents in dose-dependent manner. Tretinoin 15-19 vascular endothelial growth factor C Homo sapiens 40-46
27070801-6 2016 The addition of retinoic acid upregulates VE-cadherin expression, and results in a significant increase in transendothelial electrical resistance to physiological values. Tretinoin 16-29 cadherin 5 Homo sapiens 42-53
26239243-5 2016 Also, Bax activation and pro-apoptotic mitochondrial intermembrane space protein release, which are required to initiate the mitochondria-mediated apoptosis pathway, are more rapid in hPSCs than in retinoic-acid-differentiated hPSCs. Tretinoin 198-211 BCL2 associated X, apoptosis regulator Homo sapiens 6-9
26820774-3 2016 The livers of PTEN(+/-) mice also contained lower levels of retinoic acid (RA) than normal, similarly to human NAFLD patients. Tretinoin 60-73 phosphatase and tensin homolog Mus musculus 14-18
26820774-3 2016 The livers of PTEN(+/-) mice also contained lower levels of retinoic acid (RA) than normal, similarly to human NAFLD patients. Tretinoin 75-77 phosphatase and tensin homolog Mus musculus 14-18
27053772-3 2016 This methodology used timed administration of retinoic acid to FOXG1(+) neural precursor cells leading to differentiation of neuronal populations representative of the six cortical layers with both excitatory and inhibitory neuronal networks that were functional and homeostatically stable. Tretinoin 46-59 forkhead box G1 Homo sapiens 63-68
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 142-161 vascular endothelial growth factor C Homo sapiens 18-55
26893342-5 2016 We show that gdf6a mutant eyes exhibit expanded retinoic acid (RA) signalling and demonstrate that exogenous activation of this pathway in wild-type eyes inhibits retinal growth, generating small eyes with a reduced CMZ and fewer proliferating progenitors, similar to gdf6a mutants. Tretinoin 48-61 growth differentiation factor 6a Danio rerio 13-18
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 142-161 vascular endothelial growth factor C Homo sapiens 57-70
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 163-167 vascular endothelial growth factor C Homo sapiens 18-55
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 163-167 vascular endothelial growth factor C Homo sapiens 57-70
26903503-5 2016 Together, our data demonstrate that RA-induced osteoblast-to-preosteocyte transitioning has multiple effects on developing bone in Cyp26b1 mutants, ranging from gain to loss of bone, depending on the allelic strength, the developmental stage and the cellular context. Tretinoin 36-38 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 131-138
26893342-5 2016 We show that gdf6a mutant eyes exhibit expanded retinoic acid (RA) signalling and demonstrate that exogenous activation of this pathway in wild-type eyes inhibits retinal growth, generating small eyes with a reduced CMZ and fewer proliferating progenitors, similar to gdf6a mutants. Tretinoin 63-65 growth differentiation factor 6a Danio rerio 13-18
26893342-7 2016 Furthermore, reducing RA signalling in gdf6a mutants re-establishes appropriate timing of embryonic retinal neurogenesis and restores putative stem and progenitor cell populations in the CMZ. Tretinoin 22-24 growth differentiation factor 6a Danio rerio 39-44
26893342-8 2016 Together, our results support a model in which dorsally expressed gdf6a limits RA pathway activity to control the transition from proliferation to differentiation in the growing eye. Tretinoin 79-81 growth differentiation factor 6a Danio rerio 66-71
26678800-5 2016 Furthermore PEG-catalase inhibited the DCFH2 oxidation signal to a greater extent in the ATRA-treated cells (relative to controls) at 96h indicating that as the cells became more differentiated, steady-state levels of H2O2 increased in the absence of increases in peroxide-scavenging antioxidants (i.e., glutathione, glutathione peroxidase, and catalase). Tretinoin 89-93 catalase Homo sapiens 16-24
26863424-4 2016 RESULTS: At baseline, higher RA levels were inversely associated with the presence of MetS (odds ratio 0.61; 95% confidence interval [CI] 0.44-0.74, P < .001) after adjustment for age, gender, body mass index, the homeostasis model assessment index for insulin resistance (HOMA-IR), and other confounding factors. Tretinoin 29-31 insulin Homo sapiens 256-263
26863424-6 2016 Serum RA levels were inversely associated with 8-iso-prostaglandin F2alpha (P < .001), high-sensitivity C-reactive protein (P = .015), and IL-6 (P = .020) and positively correlated with high-density lipoprotein cholesterol (P = .038). Tretinoin 6-8 C-reactive protein Homo sapiens 107-125
26863424-6 2016 Serum RA levels were inversely associated with 8-iso-prostaglandin F2alpha (P < .001), high-sensitivity C-reactive protein (P = .015), and IL-6 (P = .020) and positively correlated with high-density lipoprotein cholesterol (P = .038). Tretinoin 6-8 interleukin 6 Homo sapiens 142-146
26678800-7 2016 Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression. Tretinoin 24-28 catalase Homo sapiens 75-83
26678800-7 2016 Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression. Tretinoin 94-98 catalase Homo sapiens 75-83
26678800-5 2016 Furthermore PEG-catalase inhibited the DCFH2 oxidation signal to a greater extent in the ATRA-treated cells (relative to controls) at 96h indicating that as the cells became more differentiated, steady-state levels of H2O2 increased in the absence of increases in peroxide-scavenging antioxidants (i.e., glutathione, glutathione peroxidase, and catalase). Tretinoin 89-93 catalase Homo sapiens 345-353
27011326-2 2016 However, expression of RARbeta is lowered in papillary thyroid carcinoma (PTC), contributing to promotion of tumor growth and inefficiency of retinoic acid and radioactive iodine treatment. Tretinoin 142-155 retinoic acid receptor beta Homo sapiens 23-30
27023064-7 2016 Moreover, cell exposure to all-trans-Retinoic acid (ATRA, 3 muM) reduces the binding of Nrf2 to the ARE sequences, decreases HO-1 induction and lowers GSH level increasing the efficacy of bortezomib. Tretinoin 27-50 NFE2 like bZIP transcription factor 2 Homo sapiens 88-92
27023064-7 2016 Moreover, cell exposure to all-trans-Retinoic acid (ATRA, 3 muM) reduces the binding of Nrf2 to the ARE sequences, decreases HO-1 induction and lowers GSH level increasing the efficacy of bortezomib. Tretinoin 52-56 NFE2 like bZIP transcription factor 2 Homo sapiens 88-92
27011326-1 2016 Retinoic acid is a promising tool in adjuvant cancer therapies, including refractory thyroid cancer, and its biological role is mediated by the retinoic acid receptor beta (RARbeta). Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 144-171
27011326-1 2016 Retinoic acid is a promising tool in adjuvant cancer therapies, including refractory thyroid cancer, and its biological role is mediated by the retinoic acid receptor beta (RARbeta). Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 173-180
26918322-1 2016 Cytochrome P450 CYP26 enzymes are responsible for all-trans-retinoic acid (atRA) clearance. Tretinoin 50-73 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 16-21
26918322-1 2016 Cytochrome P450 CYP26 enzymes are responsible for all-trans-retinoic acid (atRA) clearance. Tretinoin 75-79 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 16-21
26918322-2 2016 Inhibition of CYP26 enzymes will increase endogenous atRA concentrations and is an attractive therapeutic target. Tretinoin 53-57 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 14-19
26918322-3 2016 However, the selectivity and potency of the existing atRA metabolism inhibitors toward CYP26A1 and CYP26B1 is unknown, and no selective CYP26A1 or CYP26B1 inhibitors have been developed. Tretinoin 53-57 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 87-94
26918322-3 2016 However, the selectivity and potency of the existing atRA metabolism inhibitors toward CYP26A1 and CYP26B1 is unknown, and no selective CYP26A1 or CYP26B1 inhibitors have been developed. Tretinoin 53-57 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 99-106
27050967-0 2016 All-trans retinoic acid prevents the development of type 1 diabetes by affecting the levels of interferon gamma and interleukin 4 in streptozotocin-induced murine diabetes model. Tretinoin 10-23 interferon gamma Mus musculus 95-111
27050967-6 2016 Meanwhile, ATRA was shown to decrease the levels of IFN-gamma and increase the levels of IL-4 as well as the IFN-gamma/IL-4 ratio in STZ-treated animals (P < 0.05). Tretinoin 11-15 interferon gamma Mus musculus 52-61
26967733-7 2016 RESULTS: RARbeta mRNA levels significantly increased in the ARPE-19 cells treated with ATRA for 24h and 48h. Tretinoin 87-91 retinoic acid receptor beta Homo sapiens 9-16
27050967-6 2016 Meanwhile, ATRA was shown to decrease the levels of IFN-gamma and increase the levels of IL-4 as well as the IFN-gamma/IL-4 ratio in STZ-treated animals (P < 0.05). Tretinoin 11-15 interferon gamma Mus musculus 109-118
27050967-8 2016 This study demonstrated that ATRA effectively prevents the progression of T1DM in a murine model of the disease by reducing IFN-gamma levels and increasing IL-4 levels. Tretinoin 29-33 interferon gamma Mus musculus 124-133
26999080-3 2016 Furthermore, the docking capabilities of the model were assessed by docking of the natural substrate all-trans-retinoic acid (atRA), and a group of known azole- and tetralone-based CYP26A1 inhibitors. Tretinoin 126-130 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 181-188
26967733-10 2016 Western blot assay revealed that RARbeta protein levels were increased significantly in a time-dependent manner in ARPE-19 cells treated with 10-6 mol/l ATRA from 12 h to 72 h, with a marked increase observed at 24 h and 48 h. The upregulation of RARbeta and the ATRA-induced secretion in ARPE-19 cells could be inhibited by the RARbeta antagonist LE135. Tretinoin 153-157 retinoic acid receptor beta Homo sapiens 33-40
26967733-10 2016 Western blot assay revealed that RARbeta protein levels were increased significantly in a time-dependent manner in ARPE-19 cells treated with 10-6 mol/l ATRA from 12 h to 72 h, with a marked increase observed at 24 h and 48 h. The upregulation of RARbeta and the ATRA-induced secretion in ARPE-19 cells could be inhibited by the RARbeta antagonist LE135. Tretinoin 153-157 retinoic acid receptor beta Homo sapiens 247-254
26967733-10 2016 Western blot assay revealed that RARbeta protein levels were increased significantly in a time-dependent manner in ARPE-19 cells treated with 10-6 mol/l ATRA from 12 h to 72 h, with a marked increase observed at 24 h and 48 h. The upregulation of RARbeta and the ATRA-induced secretion in ARPE-19 cells could be inhibited by the RARbeta antagonist LE135. Tretinoin 153-157 retinoic acid receptor beta Homo sapiens 247-254
26967733-10 2016 Western blot assay revealed that RARbeta protein levels were increased significantly in a time-dependent manner in ARPE-19 cells treated with 10-6 mol/l ATRA from 12 h to 72 h, with a marked increase observed at 24 h and 48 h. The upregulation of RARbeta and the ATRA-induced secretion in ARPE-19 cells could be inhibited by the RARbeta antagonist LE135. Tretinoin 263-267 retinoic acid receptor beta Homo sapiens 33-40
26967733-11 2016 CONCLUSION: ATRA induced upregulation of RARbeta in ARPE-19 cells and stimulated these cells to secrete BMP-2 and MMP-2. Tretinoin 12-16 retinoic acid receptor beta Homo sapiens 41-48
26811260-6 2016 Retinoic acid significantly upregulated Piwil1 and Stra8 mRNA expression as well as Piwil1 levels in chicken PGCs. Tretinoin 0-13 stimulated by retinoic acid 8 Gallus gallus 51-56
26935534-0 2016 All trans-retinoic acid analogs promote cancer cell apoptosis through non-genomic Crabp1 mediating ERK1/2 phosphorylation. Tretinoin 4-23 mitogen-activated protein kinase 3 Homo sapiens 99-105
26329303-0 2016 Novel insights into a retinoic-acid-induced cleft palate based on Rac1 regulation of the fibronectin arrangement. Tretinoin 22-35 fibronectin 1 Homo sapiens 89-100
26329303-5 2016 Further analysis shows that RA treatment diminishes the region-distinctive expression of Rac1 within the palatal shelves, which reversely alters the fibrillar arrangement of FN. Tretinoin 28-30 fibronectin 1 Homo sapiens 174-176
26527258-3 2016 This study explored the rapid induction by TH of retinaldehyde dehydrogenase 1 (Raldh1), encoding a retinoic acid (RA)-synthesizing enzyme, as a gene specifically expressed in hypothalamic tanycytes, cells that mediate a number of actions of TH in the hypothalamus. Tretinoin 100-113 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 49-78
26459180-2 2016 We aim to improve ATRA therapy of AML by enhancing apoptosis through repression of the antiapoptotic proteins Bcl-2 and Mcl-1. Tretinoin 18-22 BCL2 apoptosis regulator Homo sapiens 110-115
26459180-5 2016 RESULTS: In differentiation-responsive AML cells, ATRA treatment induces long-lasting repression of Bcl-2 while first upmodulating and then reducing the Mcl-1 level. Tretinoin 50-54 BCL2 apoptosis regulator Homo sapiens 100-105
26459180-8 2016 Sorafenib blocks ATRA-induced Mcl-1 increase by reversing p90RSK activation and GSK3beta inactivation, maintains the repressed Bcl-2 level, and enhances ATRA induced apoptosis in non-APL AML cell lines and in primary AML cells. Tretinoin 17-21 BCL2 apoptosis regulator Homo sapiens 127-132
26459180-10 2016 ATRA and sorafenib can be developed as a novel drug combination therapy for AML patients because this drug combination augments apoptosis by inhibiting Bcl-2 and Mcl-1. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 152-157
26527258-3 2016 This study explored the rapid induction by TH of retinaldehyde dehydrogenase 1 (Raldh1), encoding a retinoic acid (RA)-synthesizing enzyme, as a gene specifically expressed in hypothalamic tanycytes, cells that mediate a number of actions of TH in the hypothalamus. Tretinoin 100-113 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 80-86
26527258-3 2016 This study explored the rapid induction by TH of retinaldehyde dehydrogenase 1 (Raldh1), encoding a retinoic acid (RA)-synthesizing enzyme, as a gene specifically expressed in hypothalamic tanycytes, cells that mediate a number of actions of TH in the hypothalamus. Tretinoin 115-117 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 49-78
26527258-3 2016 This study explored the rapid induction by TH of retinaldehyde dehydrogenase 1 (Raldh1), encoding a retinoic acid (RA)-synthesizing enzyme, as a gene specifically expressed in hypothalamic tanycytes, cells that mediate a number of actions of TH in the hypothalamus. Tretinoin 115-117 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 80-86
26271478-5 2016 Retinoic acid down regulates the expression of the adipogenic genes, srebf1a, srebf1c, pparg2, and cebpa; however, it did not down regulate the expression of cebpb, but it inhibited C/EBPbeta phosphorylation at Thr188, a critical step for the progression of the adipogenic program. Tretinoin 0-13 peroxisome proliferator activated receptor gamma Homo sapiens 87-93
26855507-0 2016 Changes of Apolipoprotein M Gene Expression During the Cell Differentiation and Apoptosis Induced by Simvastatin in Combination with All-Trans Retinoic Acid in Human Promyelocytic Leukemia Cell Line NB4. Tretinoin 143-156 apolipoprotein M Homo sapiens 11-27
26855507-7 2016 As expected 0.5 muM ATRA did not affect proliferation or apoptosis, strongly induced differentiation and decreased apoM expression. Tretinoin 20-24 apolipoprotein M Homo sapiens 115-119
26659823-12 2016 In addition, CDDP/ATRA co-treatment significantly increased RAR-alpha, RXR-alpha, fibrin, and iNOS protein expression compared to CDDP alone. Tretinoin 18-22 retinoid X receptor alpha Rattus norvegicus 71-80
26009309-1 2016 Retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to have increased expression levels in breast cancers and to effectively promote the survival of breast carcinoma cells, implying a potential oncogenic function. Tretinoin 0-13 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 39-46
26009309-1 2016 Retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to have increased expression levels in breast cancers and to effectively promote the survival of breast carcinoma cells, implying a potential oncogenic function. Tretinoin 15-17 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 39-46
26659823-12 2016 In addition, CDDP/ATRA co-treatment significantly increased RAR-alpha, RXR-alpha, fibrin, and iNOS protein expression compared to CDDP alone. Tretinoin 18-22 nitric oxide synthase 2 Rattus norvegicus 94-98
26566904-5 2016 We determined that RA is produced by pulmonary endothelial cells and regulates pulmonary angiogenesis and elastin synthesis by induction of VEGF-A and fibroblast growth factor (FGF)-18, respectively. Tretinoin 19-21 vascular endothelial growth factor A Homo sapiens 140-146
26902198-4 2016 Additionally, ATRA effectively upregulated the protein level of NIS, and reversed EMT phenotype in alcohol treated cells, with absence in epithelial expression of E-cadherin and cytokeratin 18, as well as abnormal expression of Vimentin, urinary plasminogen activator (uPA), uPAR and Fibronectin.Compared with alcohol-treated group, both in vitro proliferation and invasion potential of ATRA treated cells markedly decreased (all P<0.05), and iodine uptake in vitro increased about 3.5-folds (P=0.007). Tretinoin 14-18 cadherin 1 Homo sapiens 163-173
26902198-4 2016 Additionally, ATRA effectively upregulated the protein level of NIS, and reversed EMT phenotype in alcohol treated cells, with absence in epithelial expression of E-cadherin and cytokeratin 18, as well as abnormal expression of Vimentin, urinary plasminogen activator (uPA), uPAR and Fibronectin.Compared with alcohol-treated group, both in vitro proliferation and invasion potential of ATRA treated cells markedly decreased (all P<0.05), and iodine uptake in vitro increased about 3.5-folds (P=0.007). Tretinoin 14-18 plasminogen activator, urokinase Homo sapiens 269-272
26902198-4 2016 Additionally, ATRA effectively upregulated the protein level of NIS, and reversed EMT phenotype in alcohol treated cells, with absence in epithelial expression of E-cadherin and cytokeratin 18, as well as abnormal expression of Vimentin, urinary plasminogen activator (uPA), uPAR and Fibronectin.Compared with alcohol-treated group, both in vitro proliferation and invasion potential of ATRA treated cells markedly decreased (all P<0.05), and iodine uptake in vitro increased about 3.5-folds (P=0.007). Tretinoin 14-18 fibronectin 1 Homo sapiens 284-295
26886923-0 2016 Comparative Analysis of Protocols to Induce Human CD4+Foxp3+ Regulatory T Cells by Combinations of IL-2, TGF-beta, Retinoic Acid, Rapamycin and Butyrate. Tretinoin 115-128 CD4 molecule Homo sapiens 50-53
27019266-6 2016 The retinoic acid differentiated SH-S cell line (10 muM) shows a clear apoptosis when treated with H2O2 150 muM, with a Bax/Bcl-2 ratio of 3.75 (SD 0.80) in contrast to the differentiated control cells subjected to H2O2 and with extract, which have the same ratio of 1.02 (SD 0.01-0.03). Tretinoin 4-17 latexin Homo sapiens 52-55
27019266-6 2016 The retinoic acid differentiated SH-S cell line (10 muM) shows a clear apoptosis when treated with H2O2 150 muM, with a Bax/Bcl-2 ratio of 3.75 (SD 0.80) in contrast to the differentiated control cells subjected to H2O2 and with extract, which have the same ratio of 1.02 (SD 0.01-0.03). Tretinoin 4-17 latexin Homo sapiens 108-111
27019266-6 2016 The retinoic acid differentiated SH-S cell line (10 muM) shows a clear apoptosis when treated with H2O2 150 muM, with a Bax/Bcl-2 ratio of 3.75 (SD 0.80) in contrast to the differentiated control cells subjected to H2O2 and with extract, which have the same ratio of 1.02 (SD 0.01-0.03). Tretinoin 4-17 BCL2 associated X, apoptosis regulator Homo sapiens 120-123
27019266-6 2016 The retinoic acid differentiated SH-S cell line (10 muM) shows a clear apoptosis when treated with H2O2 150 muM, with a Bax/Bcl-2 ratio of 3.75 (SD 0.80) in contrast to the differentiated control cells subjected to H2O2 and with extract, which have the same ratio of 1.02 (SD 0.01-0.03). Tretinoin 4-17 BCL2 apoptosis regulator Homo sapiens 124-129
26923513-10 2016 However, expression of RARbeta in the kidney, which was induced in a retinoic acid-dependent manner, was downregulated by 90% (P < .01) in GK rats. Tretinoin 69-82 retinoic acid receptor, beta Rattus norvegicus 23-30
28219859-8 2016 CONCLUSION: ATRA can reduce the production of TNF-alpha and IL-17A and increase the production of IL-10 to alleviate the inflammation in rats with CIA. Tretinoin 12-16 tumor necrosis factor Rattus norvegicus 46-55
26892828-1 2016 Substantial evidence exists that during fetal ovarian development in mammals, retinoic acid (RA) induces germ cells to express the pre-meiotic marker Stra8 and enter meiosis, and that these effects are prevented in the fetal testis by the RA-degrading P450 enzyme CYP26B1. Tretinoin 78-91 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 264-271
26892828-1 2016 Substantial evidence exists that during fetal ovarian development in mammals, retinoic acid (RA) induces germ cells to express the pre-meiotic marker Stra8 and enter meiosis, and that these effects are prevented in the fetal testis by the RA-degrading P450 enzyme CYP26B1. Tretinoin 93-95 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 264-271
26566904-6 2016 Inhibition of RA synthesis in newborn mice decreased FGF-18 and elastin expression and impaired alveolarization. Tretinoin 14-16 fibroblast growth factor 18 Mus musculus 53-59
26773000-5 2016 Using chemical inhibitors to alter RA concentrations and morpholinos to knock-down Cdx4 function in zebrafish, we show that Cdx4 acts to prevent RA degradation in the presumptive spinal cord domain by suppressing expression of the RA degradation enzyme, Cyp26a1. Tretinoin 35-37 caudal type homeobox 4 Danio rerio 124-128
26773000-5 2016 Using chemical inhibitors to alter RA concentrations and morpholinos to knock-down Cdx4 function in zebrafish, we show that Cdx4 acts to prevent RA degradation in the presumptive spinal cord domain by suppressing expression of the RA degradation enzyme, Cyp26a1. Tretinoin 145-147 caudal type homeobox 4 Danio rerio 124-128
26566904-7 2016 Treatment with RA and vitamin A partially reversed the impaired vascular and alveolar development induced by VEGF inhibition. Tretinoin 15-17 vascular endothelial growth factor A Homo sapiens 109-113
26773000-5 2016 Using chemical inhibitors to alter RA concentrations and morpholinos to knock-down Cdx4 function in zebrafish, we show that Cdx4 acts to prevent RA degradation in the presumptive spinal cord domain by suppressing expression of the RA degradation enzyme, Cyp26a1. Tretinoin 145-147 caudal type homeobox 4 Danio rerio 124-128
26863504-8 2016 Besides XIB403, a tiol molecule that enhances GFRalpha family receptor signaling, existing drugs such as retinoic acid and amitriptyline should be considered for effective targeting of GDNF, at least in neuropathic pain. Tretinoin 105-118 glial cell derived neurotrophic factor Homo sapiens 185-189
26773000-6 2016 In the hindbrain, RA signaling modulates its own concentration by activating the expression of cyp26a1 and inhibiting the expansion of cdx4. Tretinoin 18-20 caudal type homeobox 4 Danio rerio 135-139
26773000-7 2016 Therefore, interactions between Cyp26a1 and Cdx4 modulate RA levels along the AP axis to segregate the posterior neural plate into the hindbrain and spinal cord territories. Tretinoin 58-60 caudal type homeobox 4 Danio rerio 44-48
26747727-7 2016 beta-catenin silencing abolished the stimulatory effect of ATRA on Wnt3A-induced alkaline phosphatase (ALP) activity and reversed its inhibitory effect on Cyp26a1 expression. Tretinoin 59-63 alkaline phosphatase, placental Homo sapiens 81-101
26747727-7 2016 beta-catenin silencing abolished the stimulatory effect of ATRA on Wnt3A-induced alkaline phosphatase (ALP) activity and reversed its inhibitory effect on Cyp26a1 expression. Tretinoin 59-63 alkaline phosphatase, placental Homo sapiens 103-106
26341094-7 2016 Retinoic acid, a morphogen known to interact with BMP-signaling during bone formation, was shown to down-regulate the expression of bmp2, bmp4 and bmp16, although to different extents. Tretinoin 0-13 bone morphogenetic protein 4 Danio rerio 138-142
26572536-6 2016 Here, we report atRA-mediated transcriptional upregulation of endogenous expression of a novel long intergenic noncoding RNA-rat brain expressed (LINC-RBE) in cultured primary hippocampal neurons from adult rat. Tretinoin 16-20 long intergenic non-protein coding RNA, rat brain expressed transcript Rattus norvegicus 146-154
26893773-0 2016 Changes in expression of WT1 during induced differentiation of the acute myeloid leukemia cell lines by treatment with 5-aza-2"-deoxycytidine and all-trans retinoic acid. Tretinoin 146-169 WT1 transcription factor Homo sapiens 25-28
26893773-1 2016 The aim of the present study was to investigate the effect of 5-aza-2"-deoxycytidine (decitabine; DAC) and all-trans retinoic acid (ATRA) on Wilms" tumor 1 (WT1) in acute myeloid leukemia (AML) in vitro. Tretinoin 117-130 WT1 transcription factor Homo sapiens 157-160
26893773-1 2016 The aim of the present study was to investigate the effect of 5-aza-2"-deoxycytidine (decitabine; DAC) and all-trans retinoic acid (ATRA) on Wilms" tumor 1 (WT1) in acute myeloid leukemia (AML) in vitro. Tretinoin 132-136 WT1 transcription factor Homo sapiens 157-160
26893773-9 2016 In conclusion, the combined treatment of DAC and ATRA has clinical therapeutic potential in acute monocytic leukemia patients with high WT1 expression and a poor response to standard induction chemotherapy. Tretinoin 49-53 WT1 transcription factor Homo sapiens 136-139
26747727-0 2016 All-trans retinoic acid modulates Wnt3A-induced osteogenic differentiation of mesenchymal stem cells via activating the PI3K/AKT/GSK3beta signalling pathway. Tretinoin 10-23 AKT serine/threonine kinase 1 Homo sapiens 125-128
26747727-6 2016 Additionally, Wnt3A attenuated ATRA-induced Cyp26a1 expression, inhibiting the degradation of ATRA into its oxidative forms. Tretinoin 31-35 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 44-51
26690704-6 2016 Importantly, TLR4-dependent Th17 polarization could be reversed by the enteral administration of retinoic acid, which induced Tregs and decreased NEC severity. Tretinoin 97-110 toll-like receptor 4 Mus musculus 13-17
26700766-0 2016 LZTFL1 Upregulated by All-Trans Retinoic Acid during CD4+ T Cell Activation Enhances IL-5 Production. Tretinoin 32-45 CD4 molecule Homo sapiens 53-56
26700766-2 2016 Because the molecular mechanism of regulation by retinoic acid is still not fully uncovered, we investigated the gene expression profile of all-trans retinoic acid (ATRA)-treated human CD4(+) T cells. Tretinoin 150-163 CD4 molecule Homo sapiens 185-188
26700766-2 2016 Because the molecular mechanism of regulation by retinoic acid is still not fully uncovered, we investigated the gene expression profile of all-trans retinoic acid (ATRA)-treated human CD4(+) T cells. Tretinoin 165-169 CD4 molecule Homo sapiens 185-188
26700766-7 2016 Knockdown of LZTFL1 reduced the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overexpression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important regulator of ATRA-induced T cell response. Tretinoin 43-47 CD4 molecule Homo sapiens 74-77
26551203-7 2016 The results revealed a marked increase in the NF-H and NeuN protein expression when treated with 8a, 8e, 8f, and 8k compared to undifferentiated and retinoic acid treated cells. Tretinoin 149-162 RNA binding fox-1 homolog 3 Homo sapiens 55-59
26518175-0 2016 All-trans-retinoic acid and retinol binding to the FA1 site of human serum albumin competitively inhibits heme-Fe(III) association. Tretinoin 0-23 albumin Homo sapiens 69-82
26981578-4 2016 Treatment with TGFbeta and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Tretinoin 42-44 transforming growth factor beta 1 Homo sapiens 15-22
27321378-3 2016 High MN1 expression confers poor prognosis to AML patients and induces resistance to cytarabine and alltrans-retinoic acid (ATRA) induced differentiation. Tretinoin 100-122 MN1 proto-oncogene, transcriptional regulator Homo sapiens 5-8
27321378-3 2016 High MN1 expression confers poor prognosis to AML patients and induces resistance to cytarabine and alltrans-retinoic acid (ATRA) induced differentiation. Tretinoin 124-128 MN1 proto-oncogene, transcriptional regulator Homo sapiens 5-8
26722220-4 2016 RA attenuated BSCB permeability and decreased the loss of tight junction (TJ) molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in Brain Microvascular Endothelial Cells (BMECs). Tretinoin 0-2 bromodomain containing 8 Rattus norvegicus 96-100
27014421-6 2016 In the present study, it has been investigated the expression pattern of WT1 isoforms in an in vitro model of neuroblastoma consisting in undifferentiated or all-trans retinoic acid (RA) differentiated cells. Tretinoin 168-181 WT1 transcription factor Homo sapiens 73-76
27014421-8 2016 Results have demonstrated that WT1.1-WT1.5, WT1.6-WT1.9, WT1.10 WT1.11-WT1.12 and WT1.13 isoforms are expressed in both groups of cells, but their levels are significantly increased after RA treatment. Tretinoin 188-190 WT1 transcription factor Homo sapiens 31-34
25691285-3 2016 Retinoic acid and calcitriol influenced, respectively, proliferation and differentiation of osteoblasts, and an increase in PPARgamma2 expression was observed following retinoic acid administration, whereas a decrease was observed following calcitriol administration. Tretinoin 0-13 peroxisome proliferator activated receptor gamma Homo sapiens 124-134
26548461-12 2016 The mRNA expression of mesenchymal markers N-cadherin, vimentin, snail and twist decreased, while expression of epithelial marker E-cadherin increased in hepa1-6 cells after treated with ATRA. Tretinoin 187-191 cadherin 1 Mus musculus 130-140
25691285-3 2016 Retinoic acid and calcitriol influenced, respectively, proliferation and differentiation of osteoblasts, and an increase in PPARgamma2 expression was observed following retinoic acid administration, whereas a decrease was observed following calcitriol administration. Tretinoin 169-182 peroxisome proliferator activated receptor gamma Homo sapiens 124-134
25465239-0 2016 Gene Expression Profile of NF-kappaB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid. Tretinoin 129-142 nuclear factor kappa B subunit 1 Homo sapiens 27-36
25465239-0 2016 Gene Expression Profile of NF-kappaB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid. Tretinoin 129-142 NFE2 like bZIP transcription factor 2 Homo sapiens 38-42
25465239-0 2016 Gene Expression Profile of NF-kappaB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid. Tretinoin 129-142 tumor protein p53 Homo sapiens 60-63
25465239-5 2016 We found that RA treatment increases levels of gene expression of NF-kappaB, glycolytic, and antioxidant pathway genes during neuronal differentiation of SH-SY5Y cells. Tretinoin 14-16 nuclear factor kappa B subunit 1 Homo sapiens 66-75
25465239-6 2016 We also found that ROS production induced by RA treatment in SH-SY5Y cells is involved in gene expression profile alterations, chiefly in NF-kappaB, and glycolytic pathways. Tretinoin 45-47 nuclear factor kappa B subunit 1 Homo sapiens 138-147
27780170-0 2016 Curcumin (Diferulolylmethane) Reduces Transglutaminase 2 Overexpression Induced by Retinoic Acid in Human Nervous Cell Lines. Tretinoin 83-96 transglutaminase 2 Homo sapiens 38-56
27780170-8 2016 METHODS: Human nervous cell lines were treated with curcumin alone or in association with retinoic acid in order to induce TG2 overexpression. Tretinoin 90-103 transglutaminase 2 Homo sapiens 123-126
27780170-10 2016 RESULTS: Curcumin was able to downregulate the expression of TG2 in human nervous cell lines, which was also the case after treatment with retinoic acid. Tretinoin 139-152 transglutaminase 2 Homo sapiens 61-64
27795714-10 2016 Moreover, pretreatment of cultured spermatogonia with the BMP4 antagonist Noggin could inhibit RA-induced expression of these two marker genes. Tretinoin 95-97 bone morphogenetic protein 4 Mus musculus 58-62
26456050-5 2016 Culture of hMSC with a combination of factors that induce photoreceptor differentiation of hMSC (FGF2, taurine, retinoic acid, and insulin-like growth factor type1; FTRI), markedly upregulated the expression of components of the canonical Wnt signaling pathway, including WNT2B, DKK1, and active beta-CATENIN. Tretinoin 112-125 Wnt family member 2B Homo sapiens 239-242
27431256-0 2016 Highly Efficient Neural Differentiation of CD34-Positive Hair-Follicle-Associated Pluripotent Stem Cells Induced by Retinoic Acid and Serum-Free Medium. Tretinoin 116-129 CD34 molecule Homo sapiens 43-47
27795714-11 2016 In conclusion, BMP4 may exert autocrine effects and act cooperatively with RA to induce the differentiation of spermatogonia in vivo. Tretinoin 75-77 bone morphogenetic protein 4 Mus musculus 15-19
26372689-4 2016 In RA-induced neuronal differentiation, the increased RIP140/LSD1 complex is recruited by RA-elevated Pit-1 to specifically reduce H3K4me2 modification on the Pax6 promoter, thereby repressing RA-induction of Pax6. Tretinoin 3-5 POU class 1 homeobox 1 Homo sapiens 102-107
26456050-5 2016 Culture of hMSC with a combination of factors that induce photoreceptor differentiation of hMSC (FGF2, taurine, retinoic acid, and insulin-like growth factor type1; FTRI), markedly upregulated the expression of components of the canonical Wnt signaling pathway, including WNT2B, DKK1, and active beta-CATENIN. Tretinoin 112-125 Wnt family member 2B Homo sapiens 272-277
26257239-7 2015 Furthermore, all-trans retinoic acid decreased AKT activity, reduced the epithelial cell adhesion molecule-positive cell population enriched by sorafenib, and potentiated the therapeutic effect of sorafenib in the patient-derived xenograft model. Tretinoin 23-36 AKT serine/threonine kinase 1 Homo sapiens 47-50
26483548-8 2015 The NRF2 inhibitor all-trans-retinoic acid reduced cellular NRF2 levels and increased the anti-proliferative and pro-apoptotic activities of bortezomib in resistant cells, while decreasing proteasome capacity. Tretinoin 19-42 NFE2 like bZIP transcription factor 2 Homo sapiens 4-8
26483548-8 2015 The NRF2 inhibitor all-trans-retinoic acid reduced cellular NRF2 levels and increased the anti-proliferative and pro-apoptotic activities of bortezomib in resistant cells, while decreasing proteasome capacity. Tretinoin 19-42 NFE2 like bZIP transcription factor 2 Homo sapiens 60-64
26637852-0 2015 Novel Nanoscale Delivery Particles Encapsulated with Anticancer Drugs, All-trans Retinoic Acid or Curcumin, Enhance Apoptosis in Lymphoma Cells Predominantly Expressing CD20 Antigen. Tretinoin 81-94 keratin 20 Homo sapiens 169-173
26108692-7 2015 In this work, we demonstrate that LiCl, a well-tolerated agent in humans, has antileukemic activity in APL and that it has the potential to restore RA-induced transcriptional activation and differentiation in RA-resistant APL cells in an MEK/ERK-dependent manner. Tretinoin 148-150 mitogen-activated protein kinase 1 Mus musculus 242-245
26411738-8 2015 Moreover, Nrf2 inhibitor all-trans-retinoic acid (ATRA) decreased remarkably their expressions. Tretinoin 25-48 NFE2 like bZIP transcription factor 2 Homo sapiens 10-14
26411738-8 2015 Moreover, Nrf2 inhibitor all-trans-retinoic acid (ATRA) decreased remarkably their expressions. Tretinoin 50-54 NFE2 like bZIP transcription factor 2 Homo sapiens 10-14
26618989-4 2015 We find that early embryonic rbp7a expression is negatively regulated by the Nodal/FoxH1-signaling pathway and we show that Nodal/FoxH1 activity has the opposite effect on aldh1a2, which encodes the major enzyme for early embryonic retinoic acid production. Tretinoin 232-245 retinol binding protein 7a, cellular Danio rerio 29-34
26708897-9 2015 Benzidine staining showed that ATRA could induce hemoglobin production in K562 cells with TBLR1-RARalpha fusion gene expression. Tretinoin 31-35 TBL1X/Y related 1 Homo sapiens 90-95
26481528-6 2015 RESULTS: Data showed an increasing wave of PPARgamma expression level when human neural progenitors (NPs) were formed upon retinoic acid treatment. Tretinoin 123-136 peroxisome proliferator activated receptor gamma Homo sapiens 43-52
26609166-0 2015 Retinoic Acid Signaling Mediates Hair Cell Regeneration by Repressing p27kip and sox2 in Supporting Cells. Tretinoin 0-13 SRY-box transcription factor 2 Danio rerio 81-85
26609166-7 2015 Moreover, in neuromast, RA pathway regulates the transcription of p27(kip) and sox2 in supporting cells but not fgf3. Tretinoin 24-26 SRY-box transcription factor 2 Danio rerio 79-83
26609166-15 2015 RA pathway is activated very early upon hair cell loss, promotes cell proliferation of progenitor cells, and regulates two key genes, p27(kip) and sox2. Tretinoin 0-2 SRY-box transcription factor 2 Danio rerio 147-151
26556479-6 2015 Suppression of pancreatic fibrosis upon administration of RA was confirmed based on reduction of histological damage, alpha-smooth muscle actin (alpha-SMA) expression and mRNA levels of beta-catenin, platelet-derived growth factor (PDGF)-Rbeta transforming growth factor (TGF)-betaRII and collagen 1alpha1 in vivo. Tretinoin 58-60 actin alpha 2, smooth muscle, aorta Mus musculus 118-143
26606046-6 2015 We focused on the tyrosine receptor kinase (Trk), G proteins, canonical Wnt2B/beta-catenin, genomic and non-genomic RA signaling transductions with Tyrosine hydroxylase (TH) gene expression as the differentiation endpoint. Tretinoin 116-118 tyrosine hydroxylase Homo sapiens 148-168
26604696-7 2015 The RA group exhibited more severe neurological dysfunction and lower levels of Nrf2 and HO-1 than the SFN and ICH groups. Tretinoin 4-6 NFE2 like bZIP transcription factor 2 Rattus norvegicus 80-84
26604696-9 2015 In conclusion, RA inhibits Nrf2 dissociation and translocation into nucleus, thereby suppressing the anti-inflammatory effect of Nrf2-ARE signaling pathway. Tretinoin 15-17 NFE2 like bZIP transcription factor 2 Rattus norvegicus 27-31
26604696-9 2015 In conclusion, RA inhibits Nrf2 dissociation and translocation into nucleus, thereby suppressing the anti-inflammatory effect of Nrf2-ARE signaling pathway. Tretinoin 15-17 NFE2 like bZIP transcription factor 2 Rattus norvegicus 129-133
26556479-6 2015 Suppression of pancreatic fibrosis upon administration of RA was confirmed based on reduction of histological damage, alpha-smooth muscle actin (alpha-SMA) expression and mRNA levels of beta-catenin, platelet-derived growth factor (PDGF)-Rbeta transforming growth factor (TGF)-betaRII and collagen 1alpha1 in vivo. Tretinoin 58-60 actin alpha 2, smooth muscle, aorta Mus musculus 145-154
26278034-4 2015 By examining late stage RA deficient embryos of Rdh10 mutant mice we show that SMG development requires RA in a dose-dependent manner. Tretinoin 104-106 retinol dehydrogenase 10 (all-trans) Mus musculus 48-53
26333706-14 2015 The levels of Foxp3, TGF-beta, and IL-10 mRNA, as well as the percentage of CD4+CD25+Foxp3+ T cells, were higher in the ATRA group than in theAR group. Tretinoin 120-124 interleukin 10 Mus musculus 35-40
26333706-15 2015 In the ATRA group the levels of IFN-gamma mRNA were higher, and the levels of GATA-3 and IL-4 mRNA, and ROR-gammat were lower. Tretinoin 7-11 interferon gamma Mus musculus 32-41
26416422-0 2015 Kruppel-like factor 2 suppresses mammary carcinoma growth by regulating retinoic acid signaling. Tretinoin 72-85 Kruppel like factor 2 Homo sapiens 0-21
26416422-3 2015 We show further that KLF2 suppresses tumor development by controlling the transcriptional activity of the vitamin A metabolite retinoic acid (RA). Tretinoin 127-140 Kruppel like factor 2 Homo sapiens 21-25
26416422-3 2015 We show further that KLF2 suppresses tumor development by controlling the transcriptional activity of the vitamin A metabolite retinoic acid (RA). Tretinoin 142-144 Kruppel like factor 2 Homo sapiens 21-25
26416422-6 2015 We show that KLF2 induces the expression of CRABP2 and RARgamma and inhibits the expression FABP5 and PPARbeta/delta thereby shifting RA signaling from the pro-carcinogenic FABP5/PPARbeta/delta to the growth-suppressing CRABP2/RAR path. Tretinoin 45-47 Kruppel like factor 2 Homo sapiens 13-17
26427713-8 2015 Induction of HWJMSCs with TCC in the presence of RA resulted in significant upregulation (P <= 0.05) of all germ cell-specific genes (c-Kit 2.6795 +- 0.75, DDX4 4.3188 +- 1.18, Piwil2 4.9962 +- 1.55, Dazl 6.1199 +- 0.78) compared to control and PCC + RA. Tretinoin 49-51 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 137-142
26427713-8 2015 Induction of HWJMSCs with TCC in the presence of RA resulted in significant upregulation (P <= 0.05) of all germ cell-specific genes (c-Kit 2.6795 +- 0.75, DDX4 4.3188 +- 1.18, Piwil2 4.9962 +- 1.55, Dazl 6.1199 +- 0.78) compared to control and PCC + RA. Tretinoin 49-51 DEAD-box helicase 4 Homo sapiens 159-163
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 14-16 interleukin 10 Mus musculus 57-62
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 14-16 interleukin 13 Mus musculus 102-107
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 154-156 interleukin 13 Mus musculus 102-107
26397153-4 2015 In the present study, we found that expression of C/EBPalpha, an important transcription factor for myeloid differentiation, was significantly suppressed in ATRA resistant APL cell line NB4-R1 compared with ATRA sensitive NB4 cells. Tretinoin 157-161 CCAAT enhancer binding protein alpha Homo sapiens 50-60
26397153-10 2015 Further upregulating of CD11b expression and differential morphological changes were found in NB4-R1 cells with restored C/EBPalpha P42 after ATRA treatment. Tretinoin 142-146 CCAAT enhancer binding protein alpha Homo sapiens 121-131
26256243-0 2015 All-trans retinoic acid modulates the balance of ADAMTS13 and VWF in human microvascular endothelial cells. Tretinoin 10-23 von Willebrand factor Homo sapiens 62-65
26256243-1 2015 PURPOSE: To better understand the antithrombotic property of All-trans retinoic acid (ATRA), we investigated whether ATRA may affect the balance between ADAMTS13 and von Willebrand factor (VWF) in human microvascular endothelial cell. Tretinoin 117-121 von Willebrand factor Homo sapiens 166-187
26256243-1 2015 PURPOSE: To better understand the antithrombotic property of All-trans retinoic acid (ATRA), we investigated whether ATRA may affect the balance between ADAMTS13 and von Willebrand factor (VWF) in human microvascular endothelial cell. Tretinoin 117-121 von Willebrand factor Homo sapiens 189-192
26256243-2 2015 METHODS: Compared to tumor necrosis factor-alpha (TNF-alpha), we observed the effects of ATRA on the expression of ADAMTS13 and VWF. Tretinoin 89-93 von Willebrand factor Homo sapiens 128-131
26256243-6 2015 ATRA could reverse the inhibition expression of ADAMTS13 by TNF-alpha. Tretinoin 0-4 tumor necrosis factor Homo sapiens 60-69
26256243-8 2015 CONCLUSIONS: This study provides the evidence that ATRA modulates the balance of ADAMTS13 and VWF in human microvascular endothelial cell, which might be a very relevant compartment for the antithrombotic property of ATRA. Tretinoin 51-55 von Willebrand factor Homo sapiens 94-97
26365710-2 2015 CYP26A1 enzyme, induced by ATRA in liver and target tissues, metabolizes ATRA into 4-hydroxyl-RA. Tretinoin 27-31 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
26351866-0 2015 Retinoic acid-incorporated glycol chitosan nanoparticles inhibit the expression of Ezh2 in U118 and U138 human glioma cells. Tretinoin 0-13 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 83-87
26351866-9 2015 The results also demonstrated that RA transfection resulted in the inhibition of cell proliferation, inhibition of the expression of Ezh2, and apoptosis through the mitochondrial signaling pathway by a decrease in membrane potential, the release of cytochrome c, and cell cycle arrest in the G0/G1 phase. Tretinoin 35-37 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 133-137
26351866-9 2015 The results also demonstrated that RA transfection resulted in the inhibition of cell proliferation, inhibition of the expression of Ezh2, and apoptosis through the mitochondrial signaling pathway by a decrease in membrane potential, the release of cytochrome c, and cell cycle arrest in the G0/G1 phase. Tretinoin 35-37 cytochrome c, somatic Homo sapiens 249-261
26403865-4 2015 mES exposed to retinoic acid +- 1 mug/L CYN differentiated into neural-like cells confirmed by morphological examination and RT-PCR for Oct4, Brachyury and Nestin. Tretinoin 15-28 brachyury, T-box transcription factor T Mus musculus 142-151
26044560-8 2015 The retinoic acid amide-treated tumors showed inhibition of JAK2/STAT3 activation and Bcl-XL expression. Tretinoin 4-17 signal transducer and activator of transcription 3 Homo sapiens 65-70
26044560-8 2015 The retinoic acid amide-treated tumors showed inhibition of JAK2/STAT3 activation and Bcl-XL expression. Tretinoin 4-17 BCL2 like 1 Homo sapiens 86-92
26446642-3 2015 In order to understand the mechanism of action for ATRA, we administrated ATRA to examine its inhibitory action on the production of transforming growth factor-beta1 (TGF-beta1), protein kinase C (PKC), and reactive oxidative stress (ROS) in cultured rat mesangial cells (RMCs). Tretinoin 74-78 transforming growth factor, beta 1 Rattus norvegicus 133-165
26446642-3 2015 In order to understand the mechanism of action for ATRA, we administrated ATRA to examine its inhibitory action on the production of transforming growth factor-beta1 (TGF-beta1), protein kinase C (PKC), and reactive oxidative stress (ROS) in cultured rat mesangial cells (RMCs). Tretinoin 74-78 transforming growth factor, beta 1 Rattus norvegicus 167-176
26446642-5 2015 After incubation of RMCs in media containing 30 or 5 mM of glucose, treatment with ATRA showed time- and dose-dependent decreases in TGF-beta1 levels and ROS. Tretinoin 83-87 transforming growth factor, beta 1 Rattus norvegicus 133-142
26446642-7 2015 CONCLUSION: ATRA treatment suppressed UAE and TGF-beta1 synthesis, which was mediated by significant reductions in PKC activity and ROS production. Tretinoin 12-16 transforming growth factor, beta 1 Rattus norvegicus 46-55
26365710-2 2015 CYP26A1 enzyme, induced by ATRA in liver and target tissues, metabolizes ATRA into 4-hydroxyl-RA. Tretinoin 73-77 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
26365710-4 2015 Herein, we describe the design, synthesis and biological evaluation of a series of new amide imidazole derivatives as retinoic acid metabolism blocking agents (RAMBAs) toward CYP26A1 enzyme. Tretinoin 118-131 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 175-182
26083127-7 2015 Mechanistically, ActA-dependent SMAD3 signaling modulated the expression of members of the retinoic acid (RA) system, including the RA degradation CYP26B1 enzyme and the RA receptors. Tretinoin 91-104 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 147-154
26251460-16 2015 In fetal testes, RA-treatment resulted in a decreased number of gonocytes (P < 0.05), a reduced percentage of proliferating gonocytes (P < 0.05), altered expression pattern of the somatic cell markers AMH and COUP-TFII, as well as disrupted seminiferous cord structure and testis morphology. Tretinoin 17-19 nuclear receptor subfamily 2 group F member 2 Homo sapiens 215-224
26181105-9 2015 Finally, increased ECS or RA activity ameliorated the reduced lipid abundance caused by peroxisome proliferator-activated receptor gamma (PPARgamma) inhibition. Tretinoin 26-28 peroxisome proliferator-activated receptor gamma Danio rerio 88-136
26181105-9 2015 Finally, increased ECS or RA activity ameliorated the reduced lipid abundance caused by peroxisome proliferator-activated receptor gamma (PPARgamma) inhibition. Tretinoin 26-28 peroxisome proliferator-activated receptor gamma Danio rerio 138-147
26362268-2 2015 However, RA may also induce the expression of resistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL). Tretinoin 9-11 homeobox B7 Homo sapiens 71-76
26276871-3 2015 By studying the regulatory networks known to drive these reactions, we revealed that RA enhances the expression of the plasma cell-generating transcription factors IFN regulatory factor (IRF)4 and Blimp1, and paradoxically also activation-induced deaminase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells. Tretinoin 85-87 PR/SET domain 1 Homo sapiens 197-203
25864619-0 2015 Protection of acute GVHD by all-trans retinoic acid through suppression of T cell expansion and induction of regulatory T cells through IL-2 signaling. Tretinoin 38-51 interleukin 2 Homo sapiens 136-140
25864619-7 2015 Injection of an anti-IL-2 antibody impaired the protection by atRA in aGVHD. Tretinoin 62-66 interleukin 2 Homo sapiens 21-25
24838400-0 2015 Involvement of protein kinase C alpha and delta activities on the induction of the retinoic acid system in mammary cancer cells. Tretinoin 83-96 protein kinase C alpha Homo sapiens 15-37
24838400-5 2015 ATRA also induced a remarkable increase in PKCalpha and PKCdelta expression and activity. Tretinoin 0-4 protein kinase C alpha Homo sapiens 43-51
24838400-6 2015 Interestingly, the pharmacological inhibition of these two PKC isoforms prevented the activation of retinoic acid receptors (RARs) by ATRA, indicating that both PKC isoforms are required for RARs activation. Tretinoin 134-138 protein kinase C alpha Homo sapiens 59-62
24838400-6 2015 Interestingly, the pharmacological inhibition of these two PKC isoforms prevented the activation of retinoic acid receptors (RARs) by ATRA, indicating that both PKC isoforms are required for RARs activation. Tretinoin 134-138 protein kinase C alpha Homo sapiens 161-164
24838400-10 2015 Besides inducing cell arrest, the activity of both PKC is necessary for the induction of the retinoic acid system. Tretinoin 93-106 protein kinase C alpha Homo sapiens 51-54
26394147-2 2015 Recent studies have demonstrated that RDH10 is a critical core component of the machinery that produces RA in mouse and Xenopus embryos. Tretinoin 104-106 retinol dehydrogenase 10 (all-trans) Mus musculus 38-43
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 53-66 deleted in azoospermia-like Mus musculus 99-103
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 68-70 deleted in azoospermia-like Mus musculus 99-103
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 162-164 deleted in azoospermia-like Mus musculus 99-103
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 162-164 deleted in azoospermia-like Mus musculus 99-103
26378784-7 2015 In the presence of Dazl, RA induces at least two pathways: one Stra8-independent, and one Stra8-dependent. Tretinoin 25-27 deleted in azoospermia-like Mus musculus 19-23
25975191-6 2015 Importantly, all-trans retinoic acid (ATRA) increased CD38 expression levels but also reduced expression of the complement-inhibitory proteins CD55 and CD59 in both cell lines and primary MM samples. Tretinoin 13-36 CD59 molecule (CD59 blood group) Homo sapiens 152-156
25975191-6 2015 Importantly, all-trans retinoic acid (ATRA) increased CD38 expression levels but also reduced expression of the complement-inhibitory proteins CD55 and CD59 in both cell lines and primary MM samples. Tretinoin 38-42 CD59 molecule (CD59 blood group) Homo sapiens 152-156
26524025-4 2015 RESULTS: After treatment of 8 courses, ALT and AST levels in As2O3+ ATRA group were significantly higher than those in As2O3and ATRA alone groups; the CK-MB and TnI-UI index increased in As2O3group (P < 0.05); as compared with As2O3group, the mortality and CR rate in As2O3+ ATRA group were no significant different, but the time of reaching CR was significantly shortened. Tretinoin 68-72 solute carrier family 17 member 5 Homo sapiens 47-50
26617752-0 2015 Effects of that ATRA inhibits Nrf2-ARE pathway on glial cells activation after intracerebral hemorrhage. Tretinoin 16-20 NFE2 like bZIP transcription factor 2 Homo sapiens 30-34
26240147-0 2015 All-trans-retinoic acid reduces BACE1 expression under inflammatory conditions via modulation of nuclear factor kappaB (NFkappaB) signaling. Tretinoin 0-23 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 97-118
26240147-0 2015 All-trans-retinoic acid reduces BACE1 expression under inflammatory conditions via modulation of nuclear factor kappaB (NFkappaB) signaling. Tretinoin 0-23 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 120-128
26240147-9 2015 Mutations of the NFkappaB binding site in BACE1 promoter abolished the suppressive effect of atRA. Tretinoin 93-97 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 17-25
26240147-10 2015 Furthermore, atRA disrupted LPS-induced nuclear translocation of NFkappaB and its binding to BACE1 promoter as well as promoting the recruitment of the corepressor NCoR. Tretinoin 13-17 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 65-73
26240147-11 2015 Our findings indicate that atRA represses BACE1 gene expression under inflammatory conditions via the modulation of NFkappaB signaling. Tretinoin 27-31 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 116-124
26368825-6 2015 Rdh10 mutants were found to lack RA activity during the early phase when somites are small, but at the 6-somite stage RA activity was detected in neural plate although not in presomitic mesoderm. Tretinoin 33-35 retinol dehydrogenase 10 (all-trans) Mus musculus 0-5
26368825-6 2015 Rdh10 mutants were found to lack RA activity during the early phase when somites are small, but at the 6-somite stage RA activity was detected in neural plate although not in presomitic mesoderm. Tretinoin 118-120 retinol dehydrogenase 10 (all-trans) Mus musculus 0-5
26352270-6 2015 Conserved Retinoic Acid Response Elements (RAREs) upstream of human ALDH1A3 and FOXN1 and in mouse Aldh1a3 and Foxn1 genes were revealed using bioinformatic approximation. Tretinoin 10-23 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 99-106
26617752-12 2015 ATRA significantly decreased total Nrf2 expression and increased binding Nrf2 expression in ATRA group compared to ICH group (P < 0.05). Tretinoin 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 35-39
26617752-12 2015 ATRA significantly decreased total Nrf2 expression and increased binding Nrf2 expression in ATRA group compared to ICH group (P < 0.05). Tretinoin 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77
26617752-12 2015 ATRA significantly decreased total Nrf2 expression and increased binding Nrf2 expression in ATRA group compared to ICH group (P < 0.05). Tretinoin 92-96 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77
26617752-13 2015 ATRA decreased anti-oxygen protein Nrf2 and HO-1, and increases inflammatory factors NF-kappaB and TNF-alpha. Tretinoin 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 35-39
26617752-13 2015 ATRA decreased anti-oxygen protein Nrf2 and HO-1, and increases inflammatory factors NF-kappaB and TNF-alpha. Tretinoin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 85-94
26617752-13 2015 ATRA decreased anti-oxygen protein Nrf2 and HO-1, and increases inflammatory factors NF-kappaB and TNF-alpha. Tretinoin 0-4 tumor necrosis factor Homo sapiens 99-108
26617752-14 2015 In conclusion, the application of ATRA could inhibit the neuro-protective function effectively by blocking the Nrf2-ARE pathway in glia cells. Tretinoin 34-38 NFE2 like bZIP transcription factor 2 Homo sapiens 111-115
25586558-4 2015 IL-21 and retinoic acid (RA) induce IgA(+) B-cell development and IgA production and drives autocrine TGFbeta1 production to initiate IgA CSR. Tretinoin 10-23 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 36-39
25586558-4 2015 IL-21 and retinoic acid (RA) induce IgA(+) B-cell development and IgA production and drives autocrine TGFbeta1 production to initiate IgA CSR. Tretinoin 10-23 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 66-69
25586558-4 2015 IL-21 and retinoic acid (RA) induce IgA(+) B-cell development and IgA production and drives autocrine TGFbeta1 production to initiate IgA CSR. Tretinoin 10-23 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 66-69
25971792-11 2015 Moreover, ATRA administration increased the expression and nuclear translocation of RXR-alpha in rat hepatocytes. Tretinoin 10-14 retinoid X receptor alpha Rattus norvegicus 84-93
26133502-3 2015 We have employed A549 and MCF7 cells to study the role of Nrf2 on DNA repair by inhibiting Nrf2 using all-trans retinoic acid (ATRA) or by knock down approach prior to radiation exposure (4 Gy). Tretinoin 102-125 NFE2 like bZIP transcription factor 2 Homo sapiens 91-95
26133502-10 2015 There was a significant reduction in the foci formation in cells treated with ATRA or shRNA against Nrf2 as compared to their respective radiation controls. Tretinoin 78-82 NFE2 like bZIP transcription factor 2 Homo sapiens 100-104
25826126-6 2015 These cells expressed anterior central nervous system fate markers OTX2 and GBX2 through at least seven passages, and responded to retinoic acid, promoting a more posterior fate (HOXB4+, OTX2-, and GBX2-). Tretinoin 131-144 HOXB4 Sus scrofa 179-184
26359103-9 2015 The levels of nestin, MAP2 and GFAP proteins in the ATRA group were significantly higher than those in both the brain slice co-culture group and the brain tissue homogenate supernatant group, but there was no significant difference between the brain slice co-culture group and the brain tissue homogenate supernatant group. Tretinoin 52-56 microtubule-associated protein 2 Mus musculus 22-26
26201974-0 2015 Retinoic acid induces macrophage cholesterol efflux and inhibits atherosclerotic plaque formation in apoE-deficient mice. Tretinoin 0-13 apolipoprotein E Mus musculus 101-105
26290227-0 2015 Retinoic Acid-Mediated Regulation of GLI3 Enables Efficient Motoneuron Derivation from Human ESCs in the Absence of Extrinsic SHH Activation. Tretinoin 0-13 GLI family zinc finger 3 Homo sapiens 37-41
26290227-5 2015 Using pharmacological and genetic strategies, we demonstrate that early RA treatment directs MN differentiation independently of extrinsic SHH activation by suppressing the induction of GLI3. Tretinoin 72-74 GLI family zinc finger 3 Homo sapiens 186-190
26290227-7 2015 Early RA treatment prevents this switch by direct binding of the RA receptor at the GLI3 promoter. Tretinoin 6-8 GLI family zinc finger 3 Homo sapiens 84-88
26290227-9 2015 Our data demonstrate that RA-mediated suppression of GLI3 is sufficient to generate MNs in an SHH-independent manner and that temporal changes in exposure to patterning factors such as RA affect chromatin state and competency of hESC-derived lineages to adopt specific neuronal fates. Tretinoin 26-28 GLI family zinc finger 3 Homo sapiens 53-57
26290227-13 2015 We show that early exposure to retinoic acid modulates the chromatin state of cells to be permissive for motoneuron generation and directly suppresses the induction of GLI3, a negative regulator of SHH signaling. Tretinoin 31-44 GLI family zinc finger 3 Homo sapiens 168-172
26713527-10 2015 The combination of RAD001 with ATRA significantly inhibited mTOR signaling downstream proteins P-P70S6K, P-4E-BP1 and enhanced autophagy-related protein LC3-II and Beclin 1. Tretinoin 31-35 mechanistic target of rapamycin kinase Homo sapiens 60-64
26167616-5 2015 In vitro all-trans retinoic acid-differentiated peripheral CD4 T cells (atRA-differentiated cells) were included as a comparison. Tretinoin 19-32 CD4 molecule Homo sapiens 59-62
26212321-0 2015 RA Acts in a Coherent Feed-Forward Mechanism with Tbx5 to Control Limb Bud Induction and Initiation. Tretinoin 0-2 T-box transcription factor 5 Homo sapiens 50-54
26263556-3 2015 To address the role of H3K27me3 in the retinoic acid (RA)-induced differentiation of the human carcinoma NCCIT cell line, we inhibited JMJD3 and UTX using the H3K27me3 demethylase inhibitor GSK-J4. Tretinoin 39-52 lysine demethylase 6A Homo sapiens 145-148
26263556-3 2015 To address the role of H3K27me3 in the retinoic acid (RA)-induced differentiation of the human carcinoma NCCIT cell line, we inhibited JMJD3 and UTX using the H3K27me3 demethylase inhibitor GSK-J4. Tretinoin 54-56 lysine demethylase 6A Homo sapiens 145-148
24612001-7 2015 The production of interferon-gamma and interleukin-17 was significantly reduced in all-trans retinoic acid-treated mice compared with vehicle-treated mice. Tretinoin 93-106 interferon gamma Mus musculus 18-34
26133921-3 2015 This study investigates whether combining all-trans retinoic acid (ATRA) and histone deacetylase inhibitor entinostat (ENT) can inhibit TICs and HER2 in AI-resistant cells and tumors. Tretinoin 52-65 erb-b2 receptor tyrosine kinase 2 Homo sapiens 145-149
26133921-3 2015 This study investigates whether combining all-trans retinoic acid (ATRA) and histone deacetylase inhibitor entinostat (ENT) can inhibit TICs and HER2 in AI-resistant cells and tumors. Tretinoin 67-71 erb-b2 receptor tyrosine kinase 2 Homo sapiens 145-149
26133921-4 2015 Modulation of cell viability and HER2 expression were assessed in AI-resistant cells treated with ATRA + ENT. Tretinoin 98-102 erb-b2 receptor tyrosine kinase 2 Homo sapiens 33-37
26133921-9 2015 Treatment with ATRA + ENT reduced HER2 expression and viability (P < 0.001) in AI-resistant cells, as well as decreased SP (P < 0.0001), mammosphere formation (P < 0.01), and expression of TIC molecular markers (P < 0.01) in LTLT-Ca. Tretinoin 15-19 erb-b2 receptor tyrosine kinase 2 Homo sapiens 34-38
26116962-0 2015 Retinoic acid inhibits tissue factor and HMGB1 via modulation of AMPK activity in TNF-alpha activated endothelial cells and LPS-injected mice. Tretinoin 0-13 tumor necrosis factor Mus musculus 82-91
26116962-3 2015 RESULTS: RA significantly increased AMPK and Akt phosphorylation in a time- and concentration-dependent manner in endothelial cells (EC). Tretinoin 9-11 thymoma viral proto-oncogene 1 Mus musculus 45-48
26116962-4 2015 RA downregulated TF expression at the transcriptional and translational levels in TNF-alpha activated ECs, which was reversed by the silencing of AMPK and transfection of DN-AMPK. Tretinoin 0-2 tumor necrosis factor Mus musculus 82-91
26116962-8 2015 In addition, RA reduced HMGB1 release in TNF-alpha activated ECs, which was reversed by both LY294001 and siAMPK. Tretinoin 13-15 tumor necrosis factor Mus musculus 41-50
26116962-10 2015 CONCLUSIONS: Taken together, the activation of PI3K/Akt by RA modulates AMPK activity in ECs and plays a crucial role in the inhibition of coagulatory factors such as TF, PAI-1, and HMGB1 in inflammatory conditions. Tretinoin 59-61 thymoma viral proto-oncogene 1 Mus musculus 52-55
25817574-0 2015 GW5074 and PP2 kinase inhibitors implicate nontraditional c-Raf and Lyn function as drivers of retinoic acid-induced maturation. Tretinoin 95-108 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 68-71
25817574-8 2015 This suggests that an interrelated kinase module involving c-Raf, PI3K, Lyn and perhaps Fgr functions in a nontraditional way during RA-induced maturation or during rescue of RA induction therapy using inhibitor co-treatment in RA-resistant leukemia cells. Tretinoin 133-135 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 72-75
25817574-8 2015 This suggests that an interrelated kinase module involving c-Raf, PI3K, Lyn and perhaps Fgr functions in a nontraditional way during RA-induced maturation or during rescue of RA induction therapy using inhibitor co-treatment in RA-resistant leukemia cells. Tretinoin 133-135 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 88-91
25817574-8 2015 This suggests that an interrelated kinase module involving c-Raf, PI3K, Lyn and perhaps Fgr functions in a nontraditional way during RA-induced maturation or during rescue of RA induction therapy using inhibitor co-treatment in RA-resistant leukemia cells. Tretinoin 175-177 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 72-75
25817574-8 2015 This suggests that an interrelated kinase module involving c-Raf, PI3K, Lyn and perhaps Fgr functions in a nontraditional way during RA-induced maturation or during rescue of RA induction therapy using inhibitor co-treatment in RA-resistant leukemia cells. Tretinoin 175-177 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 88-91
25987350-0 2015 Oral Delivery of Particulate Transforming Growth Factor Beta 1 and All-Trans Retinoic Acid Reduces Gut Inflammation in Murine Models of Inflammatory Bowel Disease. Tretinoin 77-90 retinol dehydrogenase 2 Mus musculus 67-76
25557231-7 2015 Co-treatment of cells with hydrogen peroxide and N-acetylcysteine or the Nrf2 inducer sulforaphane reduced hydrogen peroxide-induced damage in a similar fashion to baicalein, while the Nrf2 inhibitor retinoic acid blocked the protective effect of baicalein. Tretinoin 200-213 nuclear factor, erythroid derived 2, like 2 Mus musculus 185-189
26058854-0 2015 The retinoic acid-metabolizing enzyme CYP26A1 upregulates fascin and promotes the malignant behavior of breast carcinoma cells. Tretinoin 4-17 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 38-45
26058854-1 2015 The retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to efficiently enhance the oncogenic potential of breast cancer, suggesting a potential oncogenic function. Tretinoin 4-17 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 43-50
26058854-1 2015 The retinoic acid (RA)-metabolizing enzyme CYP26A1 has been shown to efficiently enhance the oncogenic potential of breast cancer, suggesting a potential oncogenic function. Tretinoin 19-21 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 43-50
26058854-9 2015 These data suggest that fascin expression is modulated by the intracellular RA status regulated by the expression of CYP26A1 and plays a significant role in the malignant behavior of CYP26A1-expressing breast carcinoma cells. Tretinoin 76-78 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 117-124
26035122-5 2015 RESULTS: Retinoic acid treatment reduces the expression of pancreatic stem cell markers CD24, CD44, CD133, and aldehyde dehydrogenase 1 but not c-Met. Tretinoin 9-22 CD24 molecule Homo sapiens 88-92
26225425-0 2015 All-Trans Retinoic Acid Induces TGF-beta2 in Intestinal Epithelial Cells via RhoA- and p38alpha MAPK-Mediated Activation of the Transcription Factor ATF2. Tretinoin 10-23 ras homolog family member A Homo sapiens 77-81
26225425-9 2015 CONCLUSIONS: AtRA induces TGF-beta2 expression in IECs via RhoA- and p38alpha MAPK-mediated activation of the transcription factor ATF2. Tretinoin 13-17 mitogen-activated protein kinase 14 Homo sapiens 69-77
26225425-0 2015 All-Trans Retinoic Acid Induces TGF-beta2 in Intestinal Epithelial Cells via RhoA- and p38alpha MAPK-Mediated Activation of the Transcription Factor ATF2. Tretinoin 10-23 mitogen-activated protein kinase 14 Homo sapiens 87-95
26225425-9 2015 CONCLUSIONS: AtRA induces TGF-beta2 expression in IECs via RhoA- and p38alpha MAPK-mediated activation of the transcription factor ATF2. Tretinoin 13-17 ras homolog family member A Homo sapiens 59-63
26187413-4 2015 CD127(+) ILC1 differentiated to ILC3 in the presence of interleukin-2 (IL-2), IL-23, and IL-1beta dependent on the transcription factor RORgammat, and this process was enhanced in the presence of retinoic acid. Tretinoin 196-209 interleukin 1 beta Homo sapiens 89-97
26186635-7 2015 The anti-apoptotic effects of ATRA were associated with partial inhibition of reactive oxygen species (ROS) production and significantly less phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, JNK, and ERK. Tretinoin 30-34 mitogen-activated protein kinase 1 Mus musculus 227-230
26018078-0 2015 All-trans-retinoic Acid Modulates the Plasticity and Inhibits the Motility of Breast Cancer Cells: ROLE OF NOTCH1 AND TRANSFORMING GROWTH FACTOR (TGFbeta). Tretinoin 0-23 notch receptor 1 Homo sapiens 107-113
26018078-0 2015 All-trans-retinoic Acid Modulates the Plasticity and Inhibits the Motility of Breast Cancer Cells: ROLE OF NOTCH1 AND TRANSFORMING GROWTH FACTOR (TGFbeta). Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 146-153
26018078-7 2015 Down-regulation of NOTCH1, an emerging EMT modulator, is involved in the inhibition of motility by ATRA. Tretinoin 99-103 notch receptor 1 Homo sapiens 19-25
26018078-10 2015 Stimulation of TGFbeta contributes to the anti-migratory effect of ATRA. Tretinoin 67-71 transforming growth factor beta 1 Homo sapiens 15-22
26018078-12 2015 Inhibition of the NOTCH1 pathway not only plays a role in the anti-migratory action of ATRA; it is relevant also for the anti-proliferative activity of the retinoid in HCC1599 breast cancer cells, which are addicted to NOTCH1 for growth/viability. Tretinoin 87-91 notch receptor 1 Homo sapiens 18-24
26018078-13 2015 This effect is enhanced by the combination of ATRA and the gamma-secretase inhibitor N-(N-(3,5-difluorophenacetyl)-l-alanyl)-S-phenylglycine t-butyl ester, supporting the concept that the two compounds act at the transcriptional and post-translational levels along the NOTCH1 pathway. Tretinoin 46-50 notch receptor 1 Homo sapiens 269-275
26186635-8 2015 Western blot analysis also revealed that ATRA pre-treatment increased a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (0.65 +- 0.20 vs. 0.41+-0.02 in vivo) and reduced the level of receptor for advanced glycation end-products (RAGE) (0.38 +- 0.17 vs. 0.52 +- 0.11 in vivo). Tretinoin 41-45 advanced glycosylation end product-specific receptor Mus musculus 218-262
26186635-8 2015 Western blot analysis also revealed that ATRA pre-treatment increased a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (0.65 +- 0.20 vs. 0.41+-0.02 in vivo) and reduced the level of receptor for advanced glycation end-products (RAGE) (0.38 +- 0.17 vs. 0.52 +- 0.11 in vivo). Tretinoin 41-45 advanced glycosylation end product-specific receptor Mus musculus 264-268
26186635-11 2015 One possible mechanism underlying these effects is that ATRA could increase ADAM10 expression and thus cleave RAGE, which is the main receptor up-stream of MAPKs in myocardial I/R injury, resulting in the down-regulation of MAPK signaling and protective role on myocardial I/R injury. Tretinoin 56-60 advanced glycosylation end product-specific receptor Mus musculus 110-114
26186635-11 2015 One possible mechanism underlying these effects is that ATRA could increase ADAM10 expression and thus cleave RAGE, which is the main receptor up-stream of MAPKs in myocardial I/R injury, resulting in the down-regulation of MAPK signaling and protective role on myocardial I/R injury. Tretinoin 56-60 mitogen-activated protein kinase 1 Mus musculus 156-160
26379840-6 2015 It appeared that retinoic acid nanoparticle conjugates were selectively taken and retained by the estrogen receptor alpha present in the plasma membrane. Tretinoin 17-30 estrogen receptor 1 Homo sapiens 98-121
26236584-0 2015 Inhibition of ASCT2 is essential in all-trans retinoic acid-induced reduction of adipogenesis in 3T3-L1 cells. Tretinoin 46-59 solute carrier family 1 (neutral amino acid transporter), member 5 Mus musculus 14-19
26173116-5 2015 We could show that in WERI-Rb1 cells RA/BMP-4 mediated cell death is at least partially caspase-dependent, whereby RA and BMP-4 additively increased (i) Apaf-1 mRNA levels, (ii) caspase-9 cleavage activity and (iii) the number of activated, cleaved caspase-3 positive cells. Tretinoin 37-39 caspase 3 Homo sapiens 249-258
26162091-4 2015 Moreover, RA modulated the DNA methylation of mESCs by altering the expression of epigenetic-associated genes such as Dnmt3b and Dnmt3l. Tretinoin 10-12 DNA methyltransferase 3B Mus musculus 118-124
26236584-3 2015 We found that ATRA suppressed up-regulation of the amino acid transporter, Asct2, in adipogenerating 3T3-L1 cells. Tretinoin 14-18 solute carrier family 1 (neutral amino acid transporter), member 5 Mus musculus 75-80
24797530-5 2015 We show that expression of BACE1 and the all-trans retinoic acid (RA)-degrading enzyme Cyp26B1 form DM-VL counter gradients in the olfactory epithelium. Tretinoin 51-64 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 87-94
26306150-7 2015 The data showed specific characteristics in favor of considering the differentiated cells as hepatocyte-like cells such as obtaining morphologic, functional, and alphaFP and HNF1-alpha expression patterns which in turn were higher in cells exposed to RA. Tretinoin 251-253 HNF1 homeobox A Homo sapiens 174-184
26040672-4 2015 One previous study alluded to a requirement for one of the RA degrading enzymes, CYP26B1, in Sertoli cells but no data exist to determine whether germ cells possess the ability to degrade RA. Tretinoin 59-61 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 81-88
24797530-5 2015 We show that expression of BACE1 and the all-trans retinoic acid (RA)-degrading enzyme Cyp26B1 form DM-VL counter gradients in the olfactory epithelium. Tretinoin 66-68 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 87-94
25827071-4 2015 The potential of ATRA to stabilize p53 was almost completely abolished by knock-down of p14 in HepG2 cells and was not observed in p14-negative A549 cells. Tretinoin 17-21 tumor protein p53 Homo sapiens 35-38
25959810-8 2015 RESULTS: Retinoic acid acted synergistically with IL-2 and other activating cytokines to induce expression of the gut-homing integrin alpha4beta7 in ILCs, as well as production of IL-5 and IL-13 in ILC2 cells, and IFN-gamma in ILC1 and ILC3 cells. Tretinoin 9-22 interleukin 13 Homo sapiens 189-194
25959810-8 2015 RESULTS: Retinoic acid acted synergistically with IL-2 and other activating cytokines to induce expression of the gut-homing integrin alpha4beta7 in ILCs, as well as production of IL-5 and IL-13 in ILC2 cells, and IFN-gamma in ILC1 and ILC3 cells. Tretinoin 9-22 interferon gamma Homo sapiens 214-223
25959810-10 2015 In contrast, RA completely inhibited the IL-2-induced expression of cutaneous lymphocyte antigen (CLA) in ILCs. Tretinoin 13-15 interleukin 2 Homo sapiens 41-45
25957888-0 2015 All-trans retinoic acid up-regulates the human CD2AP gene expression through Sp1/Sp3 binding sites. Tretinoin 10-23 Sp3 transcription factor Homo sapiens 81-84
25957888-5 2015 Chromatin immunoprecipitation assays revealed that ATRA activated the CD2AP transcription through enhancing the DNA-binding activity of Sp1 and Sp3 with the CD2AP promoter. Tretinoin 51-55 Sp3 transcription factor Homo sapiens 144-147
25827071-0 2015 All-trans retinoic acid induces p53-depenent apoptosis in human hepatocytes by activating p14 expression via promoter hypomethylation. Tretinoin 10-23 tumor protein p53 Homo sapiens 32-35
26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 140-159 tumor necrosis factor Homo sapiens 34-61
26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 140-159 tumor necrosis factor Homo sapiens 63-72
26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 161-165 tumor necrosis factor Homo sapiens 34-61
26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 161-165 tumor necrosis factor Homo sapiens 63-72
26146052-6 2015 CONCLUSION: TNF-alpha may have potential for strengthening the differentiation and apoptosis of acute promyelocytic leukemia cells induced by ATRA. Tretinoin 142-146 tumor necrosis factor Homo sapiens 12-21
25986924-5 2015 Importantly, ectopic Plzf expression in F9 cells suppressed retinoic acid (RA)-induced Stra8 activation, a gene required for meiosis initiation. Tretinoin 60-73 zinc finger and BTB domain containing 16 Mus musculus 21-25
25986924-5 2015 Importantly, ectopic Plzf expression in F9 cells suppressed retinoic acid (RA)-induced Stra8 activation, a gene required for meiosis initiation. Tretinoin 75-77 zinc finger and BTB domain containing 16 Mus musculus 21-25
25827071-2 2015 Here we found that ATRA induces apoptosis in p53-positive HepG2 cells, but not in p53-negative Hep3B cells. Tretinoin 19-23 tumor protein p53 Homo sapiens 45-48
25827071-7 2015 Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis. Tretinoin 91-95 tumor protein p53 Homo sapiens 121-124
25827071-7 2015 Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis. Tretinoin 91-95 tumor protein p53 Homo sapiens 144-147
25915157-3 2015 We showed that bone marrow (BM) stromal cytochrome P450 (CYP)26 enzymes protect normal hematopoietic stem cells (HSCs) from the pro-differentiation effects of retinoic acid. Tretinoin 159-172 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-63
25869623-12 2015 This led us to conclude that RA enhances Fndc5 expression through a non-genomic pathway via the ERK signaling pathway. Tretinoin 29-31 mitogen-activated protein kinase 3 Homo sapiens 96-99
26101153-5 2015 Among them we show that retinaldehyde dehydrogenase 2 (RALDH2) and lipocalin-type prostaglandin D2 synthase (LPGDS), which, respectively, regulate the synthesis and transport of RA, directly participate in the establishment of the PPR. Tretinoin 55-57 prostaglandin D2 synthase Homo sapiens 109-114
26065685-7 2015 However, CD11b expression induced by ATRA in HL60 cells was decreased by radotinib through upregulation of LYN. Tretinoin 37-41 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 107-110
25887398-6 2015 DRA mRNA levels were significantly elevated (~4-fold) in response to ATRA with induction starting as early as 8 h of incubation. Tretinoin 69-73 solute carrier family 26 member 3 Homo sapiens 0-3
25887398-0 2015 All-trans-retinoic Acid Increases SLC26A3 DRA (Down-regulated in Adenoma) Expression in Intestinal Epithelial Cells via HNF-1beta. Tretinoin 0-23 solute carrier family 26 member 3 Homo sapiens 42-45
25887398-0 2015 All-trans-retinoic Acid Increases SLC26A3 DRA (Down-regulated in Adenoma) Expression in Intestinal Epithelial Cells via HNF-1beta. Tretinoin 0-23 solute carrier family 26 member 3 Homo sapiens 47-72
25887398-0 2015 All-trans-retinoic Acid Increases SLC26A3 DRA (Down-regulated in Adenoma) Expression in Intestinal Epithelial Cells via HNF-1beta. Tretinoin 0-23 HNF1 homeobox B Homo sapiens 120-129
25887398-10 2015 Results obtained from agonist (CH-55) and antagonist (LE-135) studies further confirmed that ATRA exerts its effects through RAR-beta. Tretinoin 93-97 retinoic acid receptor beta Homo sapiens 125-133
25887398-11 2015 Furthermore, ATRA treatment resulted in a significant increase in HNF-1beta mRNA levels. Tretinoin 13-17 HNF1 homeobox B Homo sapiens 66-75
25887398-12 2015 The ability of ATRA to induce DRA expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression. Tretinoin 15-19 solute carrier family 26 member 3 Homo sapiens 30-33
25304492-9 2015 There are 15 human AKRs of these AKR1B1, AKR1C1-1C3, AKR1D1, and AKR1B10 have been implicated in diabetic complications, steroid hormone dependent malignancies, bile acid deficiency and defects in retinoic acid signaling, respectively. Tretinoin 197-210 aldo-keto reductase family 1 member B Homo sapiens 33-39
25887398-12 2015 The ability of ATRA to induce DRA expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression. Tretinoin 15-19 HNF1 homeobox B Homo sapiens 78-87
25887398-12 2015 The ability of ATRA to induce DRA expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression. Tretinoin 15-19 solute carrier family 26 member 3 Homo sapiens 151-154
25887398-12 2015 The ability of ATRA to induce DRA expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression. Tretinoin 127-131 solute carrier family 26 member 3 Homo sapiens 30-33
25887398-12 2015 The ability of ATRA to induce DRA expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression. Tretinoin 127-131 HNF1 homeobox B Homo sapiens 78-87
25887398-12 2015 The ability of ATRA to induce DRA expression was inhibited in the presence of HNF-1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression. Tretinoin 127-131 solute carrier family 26 member 3 Homo sapiens 151-154
25887398-13 2015 In conclusion, ATRA may act as an antidiarrheal agent by increasing DRA expression via the RAR-beta/HNF-1beta-dependent pathway. Tretinoin 15-19 solute carrier family 26 member 3 Homo sapiens 68-71
25887398-13 2015 In conclusion, ATRA may act as an antidiarrheal agent by increasing DRA expression via the RAR-beta/HNF-1beta-dependent pathway. Tretinoin 15-19 retinoic acid receptor beta Homo sapiens 91-99
25887398-13 2015 In conclusion, ATRA may act as an antidiarrheal agent by increasing DRA expression via the RAR-beta/HNF-1beta-dependent pathway. Tretinoin 15-19 HNF1 homeobox B Homo sapiens 100-109
25864124-4 2015 R-III treatment and albumin expression downregulated retinoic acid (RA) signaling which was involved in HSC activation. Tretinoin 53-66 albumin Homo sapiens 20-27
26047326-0 2015 All-Trans Retinoic Acid Activity in Acute Myeloid Leukemia: Role of Cytochrome P450 Enzyme Expression by the Microenvironment. Tretinoin 10-23 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 68-83
26047326-8 2015 Inhibition of CYP26 rescued atRA levels and AML cell sensitivity in the presence of stroma. Tretinoin 28-32 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 14-19
26047326-9 2015 Our data suggest that stromal CYP26 activity creates retinoid low sanctuaries in the BM that protect AML cells from systemic atRA therapy. Tretinoin 125-129 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 30-35
26047326-10 2015 Inhibition of CYP26 provides new opportunities to expand the clinical activity of atRA in both APL and non-APL AML. Tretinoin 82-86 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 14-19
25864124-4 2015 R-III treatment and albumin expression downregulated retinoic acid (RA) signaling which was involved in HSC activation. Tretinoin 68-70 albumin Homo sapiens 20-27
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein family, member 7 (cardiovascular) Mus musculus 53-58
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein 5 Mus musculus 269-274
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein family, member 7 (cardiovascular) Mus musculus 53-58
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein 5 Mus musculus 269-274
25592248-6 2015 Lastly, we observed that IFN-gamma and IL-17 production by ex vivo re-stimulated dLNs cells is greatly increased during rejection, which it turns depends on RA synthesis, as shown in experiments using a specific RALDH inhibitor. Tretinoin 157-159 interferon gamma Homo sapiens 25-34
25911751-4 2015 Regulatory functions can be corrected, even in T cells isolated from aged, diabetic mice, by a synergistic activity of retinoic acid, TGF-beta, and IL-2, which enhance connexin 43 and Foxp3 expression in T(regs) and restore the ability of conventional CD4(+) T cells to upregulate Foxp3 and generate peripherally derived T(regs). Tretinoin 119-132 gap junction protein, alpha 1 Mus musculus 168-179
25724388-5 2015 atRA levels increased with the low activity of CYP2E1 and decreased with high CYP26 activity in the UChB dorsal prostate. Tretinoin 0-4 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 47-53
25961594-1 2015 SKBR3-cells, characterized by ERBB2/RARA co-amplification, represent a subgroup of HER2+ breast-cancers sensitive to all-trans retinoic acid (ATRA) and Lapatinib. Tretinoin 127-140 erb-b2 receptor tyrosine kinase 2 Homo sapiens 83-87
25961594-1 2015 SKBR3-cells, characterized by ERBB2/RARA co-amplification, represent a subgroup of HER2+ breast-cancers sensitive to all-trans retinoic acid (ATRA) and Lapatinib. Tretinoin 142-146 erb-b2 receptor tyrosine kinase 2 Homo sapiens 83-87
25972084-2 2015 Restin was firstly cloned from HL-60 cells treated with all-trans retinoic acid (ATRA). Tretinoin 56-79 MAGE family member H1 Homo sapiens 0-6
26175847-0 2015 A novel all-trans retinoic acid derivative inhibits proliferation and induces differentiation of human gastric carcinoma xenografts via up-regulating retinoic acid receptor beta. Tretinoin 18-31 retinoic acid receptor beta Homo sapiens 150-177
25976364-0 2015 Retinoic acid homeostasis through aldh1a2 and cyp26a1 mediates meiotic entry in Nile tilapia (Oreochromis niloticus). Tretinoin 0-13 retinal dehydrogenase 2 Oreochromis niloticus 34-41
25972084-2 2015 Restin was firstly cloned from HL-60 cells treated with all-trans retinoic acid (ATRA). Tretinoin 81-85 MAGE family member H1 Homo sapiens 0-6
25725371-4 2015 Here, we demonstrate that human skin MCs display substantial susceptibility to RA by which they are instructed to increase pro-inflammatory mediators (IL-1beta, IL-8, TNF-alpha) but not histamine release. Tretinoin 79-81 interleukin 1 beta Homo sapiens 151-159
25725371-4 2015 Here, we demonstrate that human skin MCs display substantial susceptibility to RA by which they are instructed to increase pro-inflammatory mediators (IL-1beta, IL-8, TNF-alpha) but not histamine release. Tretinoin 79-81 C-X-C motif chemokine ligand 8 Homo sapiens 161-165
25725371-4 2015 Here, we demonstrate that human skin MCs display substantial susceptibility to RA by which they are instructed to increase pro-inflammatory mediators (IL-1beta, IL-8, TNF-alpha) but not histamine release. Tretinoin 79-81 tumor necrosis factor Homo sapiens 167-176
25515249-10 2015 The expression level of pulmonary surfactant C (SPC) was elevated after cells were exposed to RA for 24 and 72 h but was inhibited when cells were exposed to RA for 48 h. These results suggest that RA promotes fAECII proliferation by improving cell viability, promoting S phase entry and inhibiting apoptosis and RA promotes fAECIIs differentiation to alveolar epithelial type I cells (AECIs). Tretinoin 94-96 surfactant protein C Rattus norvegicus 48-51
25683251-8 2015 In the combination treatment using ATRA and sorafenib, increased apoptosis, followed by the activation of p38 MAPK and JNK, the upregulation and translocation of Bax to mitochondria, and the activation of caspase-3, was observed. Tretinoin 35-39 mitogen-activated protein kinase 14 Homo sapiens 106-109
25683251-8 2015 In the combination treatment using ATRA and sorafenib, increased apoptosis, followed by the activation of p38 MAPK and JNK, the upregulation and translocation of Bax to mitochondria, and the activation of caspase-3, was observed. Tretinoin 35-39 mitogen-activated protein kinase 8 Homo sapiens 119-122
25683251-8 2015 In the combination treatment using ATRA and sorafenib, increased apoptosis, followed by the activation of p38 MAPK and JNK, the upregulation and translocation of Bax to mitochondria, and the activation of caspase-3, was observed. Tretinoin 35-39 BCL2 associated X, apoptosis regulator Homo sapiens 162-165
25683251-8 2015 In the combination treatment using ATRA and sorafenib, increased apoptosis, followed by the activation of p38 MAPK and JNK, the upregulation and translocation of Bax to mitochondria, and the activation of caspase-3, was observed. Tretinoin 35-39 caspase 3 Homo sapiens 205-214
25858458-6 2015 In the present study, by combining fate analysis of pulse-labeled cells and a model of vitamin A deficiency, we demonstrate that retinoic acid (RA), which may periodically increase in concentration in the tubules during the seminiferous epithelial cycle, induced only NGN3(+) cells to differentiate. Tretinoin 129-142 neurogenin 3 Mus musculus 268-272
25858458-6 2015 In the present study, by combining fate analysis of pulse-labeled cells and a model of vitamin A deficiency, we demonstrate that retinoic acid (RA), which may periodically increase in concentration in the tubules during the seminiferous epithelial cycle, induced only NGN3(+) cells to differentiate. Tretinoin 144-146 neurogenin 3 Mus musculus 268-272
25515249-10 2015 The expression level of pulmonary surfactant C (SPC) was elevated after cells were exposed to RA for 24 and 72 h but was inhibited when cells were exposed to RA for 48 h. These results suggest that RA promotes fAECII proliferation by improving cell viability, promoting S phase entry and inhibiting apoptosis and RA promotes fAECIIs differentiation to alveolar epithelial type I cells (AECIs). Tretinoin 158-160 surfactant protein C Rattus norvegicus 48-51
25515249-10 2015 The expression level of pulmonary surfactant C (SPC) was elevated after cells were exposed to RA for 24 and 72 h but was inhibited when cells were exposed to RA for 48 h. These results suggest that RA promotes fAECII proliferation by improving cell viability, promoting S phase entry and inhibiting apoptosis and RA promotes fAECIIs differentiation to alveolar epithelial type I cells (AECIs). Tretinoin 158-160 surfactant protein C Rattus norvegicus 48-51
25515249-10 2015 The expression level of pulmonary surfactant C (SPC) was elevated after cells were exposed to RA for 24 and 72 h but was inhibited when cells were exposed to RA for 48 h. These results suggest that RA promotes fAECII proliferation by improving cell viability, promoting S phase entry and inhibiting apoptosis and RA promotes fAECIIs differentiation to alveolar epithelial type I cells (AECIs). Tretinoin 158-160 surfactant protein C Rattus norvegicus 48-51
25510432-4 2015 In contrast to other NUP98 fusions, cells transformed by the NUP98-RARG fusion were extremely sensitive to all-trans retinoic acid (ATRA) treatment. Tretinoin 132-136 nucleoporin 98 Mus musculus 21-26
25510432-4 2015 In contrast to other NUP98 fusions, cells transformed by the NUP98-RARG fusion were extremely sensitive to all-trans retinoic acid (ATRA) treatment. Tretinoin 132-136 nucleoporin 98 Mus musculus 61-66
25510432-4 2015 In contrast to other NUP98 fusions, cells transformed by the NUP98-RARG fusion were extremely sensitive to all-trans retinoic acid (ATRA) treatment. Tretinoin 117-130 nucleoporin 98 Mus musculus 21-26
25592076-0 2015 Synergistic effect of all-trans retinoic acid in combination with protein kinase C 412 in FMS-like tyrosine kinase 3-mutated acute myeloid leukemia cells. Tretinoin 32-45 fms related receptor tyrosine kinase 3 Homo sapiens 90-116
25510432-4 2015 In contrast to other NUP98 fusions, cells transformed by the NUP98-RARG fusion were extremely sensitive to all-trans retinoic acid (ATRA) treatment. Tretinoin 117-130 nucleoporin 98 Mus musculus 61-66
25592076-5 2015 The results indicated that the combined ATRA and PKC412 treatment exhibited additive or synergistic effects in FLT3-mutated AML cell lines. Tretinoin 40-44 fms related receptor tyrosine kinase 3 Homo sapiens 111-115
25896049-4 2015 The results showed that ATRA significantly induced apelin expression in a time- and dose-dependent manner in the VSMCs. Tretinoin 24-28 apelin Homo sapiens 51-57
25923916-2 2015 Using genome-wide sequencing and loss and gain of function experiments the present investigation reveals a mechanism that underlies global and direct gene regulation by the nuclear form of FGFR1, ensuring that pluripotent Embryonic Stem Cells differentiate into Neuronal Cells in response to Retinoic Acid. Tretinoin 292-305 fibroblast growth factor receptor 1 Homo sapiens 189-194
25896049-1 2015 This study was aimed to investigate the mechanism of all-trans retinoic acid (ATRA) up-regulating apelin expression in vascular smooth muscle cells (VSMCs). Tretinoin 57-76 apelin Homo sapiens 98-104
25896049-1 2015 This study was aimed to investigate the mechanism of all-trans retinoic acid (ATRA) up-regulating apelin expression in vascular smooth muscle cells (VSMCs). Tretinoin 78-82 apelin Homo sapiens 98-104
24909169-6 2015 Overexpression of non-SUMOylatable mutant CYLD in neuroblastoma cells reduced retinoic acid-induced NF-kappaB activation and differentiation of cells, but instead promoted cell death. Tretinoin 78-91 nuclear factor kappa B subunit 1 Homo sapiens 100-109
25896049-2 2015 The effect of ATRA on apelin expression in the VSMCs was investigated by RT-PCR, real-time PCR and Western blot analysis. Tretinoin 14-18 apelin Homo sapiens 22-28
25896049-3 2015 To further define whether retinoic acid receptor alpha (RARalpha) mediated the induction of apelin by ATRA, endogenous RARalpha was down regulated by transfection of siRNA against RARalpha (si-RARalpha) or RARalpha was over-expressed by infection of the adenovirus vector pAd-GFP-RARalpha in the VSMCs. Tretinoin 102-106 apelin Homo sapiens 92-98
25410880-8 2015 The mixed cells showed a significant increase in the CYP3A4 and ABCB1 reporter activities following treatment with 1,25(OH)2 D3, ATRA, and 9-cis RA. Tretinoin 129-133 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 53-59
25884658-6 2015 However, these effects were abolished by retinoic acid, Nrf2 inhibitor, in resveratrol and retinoic acid-treated and MG-induced mice. Tretinoin 41-54 nuclear factor, erythroid derived 2, like 2 Mus musculus 56-60
25884658-6 2015 However, these effects were abolished by retinoic acid, Nrf2 inhibitor, in resveratrol and retinoic acid-treated and MG-induced mice. Tretinoin 91-104 nuclear factor, erythroid derived 2, like 2 Mus musculus 56-60
25941627-8 2015 VAF347 augments RA-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47(phox). Tretinoin 16-18 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 46-49
25410880-8 2015 The mixed cells showed a significant increase in the CYP3A4 and ABCB1 reporter activities following treatment with 1,25(OH)2 D3, ATRA, and 9-cis RA. Tretinoin 129-133 ATP binding cassette subfamily B member 1 Homo sapiens 64-69
25614514-7 2015 RESULTS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs in a concentration- and time-dependent manner. Tretinoin 9-13 transforming growth factor beta 1 Homo sapiens 24-32
25485998-6 2015 Moreover, exogenous factors, such as ATP, retinoic acid, substance P, thioredoxin, inosine and laminin, can have cytoprotective effects against hyperoxia-induced cell damage, through promotion of ERK activation and/or limiting JNK and p38 involvement. Tretinoin 42-55 mitogen-activated protein kinase 1 Homo sapiens 196-199
25742746-8 2015 We conclude that ATRA downregulates ALDH1/FoxM1/Notch1 signalling and suppresses tumour formation in ovarian cancer cells. Tretinoin 17-21 notch receptor 1 Homo sapiens 48-54
25614514-9 2015 ATRA also stimulated TIMP-1 release from HTFs in the presence of TGF-beta. Tretinoin 0-4 TIMP metallopeptidase inhibitor 1 Homo sapiens 21-27
25614514-9 2015 ATRA also stimulated TIMP-1 release from HTFs in the presence of TGF-beta. Tretinoin 0-4 transforming growth factor beta 1 Homo sapiens 65-73
25614514-12 2015 CONCLUSIONS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, likely in part by attenuating the production of MMP-1 and MMP-3 and by stimulating the production of TIMP-1. Tretinoin 13-17 transforming growth factor beta 1 Homo sapiens 28-36
25614514-12 2015 CONCLUSIONS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, likely in part by attenuating the production of MMP-1 and MMP-3 and by stimulating the production of TIMP-1. Tretinoin 13-17 matrix metallopeptidase 3 Homo sapiens 146-151
25614514-12 2015 CONCLUSIONS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, likely in part by attenuating the production of MMP-1 and MMP-3 and by stimulating the production of TIMP-1. Tretinoin 13-17 TIMP metallopeptidase inhibitor 1 Homo sapiens 189-195
25631875-6 2015 ATRA treatment was associated with significantly increased Rb expression and decreased HER2 expression in gastric mucosa. Tretinoin 0-4 erb-b2 receptor tyrosine kinase 2 Homo sapiens 87-91
25578258-0 2015 Chronic all-trans retinoic acid administration induces CRF over-expression accompanied by AVP up-regulation and multiple CRF-controlling receptors disturbance in the hypothalamus of rats. Tretinoin 18-31 arginine vasopressin Rattus norvegicus 90-93
25826367-0 2015 Retinoic acid can exacerbate T cell intrinsic TLR2 activation to promote tolerance. Tretinoin 0-13 toll like receptor 2 Homo sapiens 46-50
25578258-5 2015 Here we show that ATRA-induced CRF over-expression is accompanied by arginine-vasopressin (AVP) up-regulation and apparent gene expression disturbances of CRF-controlling receptors. Tretinoin 18-22 arginine vasopressin Rattus norvegicus 69-89
25578258-5 2015 Here we show that ATRA-induced CRF over-expression is accompanied by arginine-vasopressin (AVP) up-regulation and apparent gene expression disturbances of CRF-controlling receptors. Tretinoin 18-22 arginine vasopressin Rattus norvegicus 91-94
25578258-7 2015 Chronic ATRA treatment induced significantly increased expression of CRF and AVP in the PVN. Tretinoin 8-12 arginine vasopressin Rattus norvegicus 77-80
26064333-5 2015 RESULTS: Combined treatment with ATRA and Genistein was able to reduce the expressions of Bcl-2, MUC1 and ICAM-1 and exerted synergistic effects to inhibit the invasion of A549 cells. Tretinoin 33-37 BCL2 apoptosis regulator Homo sapiens 90-95
25878769-0 2015 Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPbeta. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 63-94
25878769-2 2015 During adult skeletal myogenesis, TGFbeta signaling inhibits the differentiation of myoblasts, and this can be reversed by treatment with retinoic acid (RA). Tretinoin 138-151 transforming growth factor beta 1 Homo sapiens 34-41
26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 mitogen-activated protein kinase 3 Homo sapiens 161-167
26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 BCL2 associated X, apoptosis regulator Homo sapiens 201-204
26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 BCL2 apoptosis regulator Homo sapiens 209-214
25677622-3 2015 Here, we investigate how the overdose of retinoic acid (RA), which can induce cleft palate in mice and humans, regulates histone methyltransferase, Wolf-Hirschhorn syndrome candidate 1 (WHSC1) during palatal development in mice. Tretinoin 41-54 nuclear receptor binding SET domain protein 2 Homo sapiens 148-184
25677622-3 2015 Here, we investigate how the overdose of retinoic acid (RA), which can induce cleft palate in mice and humans, regulates histone methyltransferase, Wolf-Hirschhorn syndrome candidate 1 (WHSC1) during palatal development in mice. Tretinoin 41-54 nuclear receptor binding SET domain protein 2 Homo sapiens 186-191
25627686-0 2015 Insulin regulates retinol dehydrogenase expression and all-trans-retinoic acid biosynthesis through FoxO1. Tretinoin 65-78 insulin Homo sapiens 0-7
25805962-7 2015 RESULTS: ATRA (100 nM) induced granulocytic differentiation (upregulation of CD11b and downregulation of CD34) and the effect was potentiated by addition of G-CSF, while G-CSF alone had no effect on HT93A cells. Tretinoin 9-13 CD34 molecule Homo sapiens 105-109
25627686-0 2015 Insulin regulates retinol dehydrogenase expression and all-trans-retinoic acid biosynthesis through FoxO1. Tretinoin 65-78 forkhead box O1 Homo sapiens 100-105
25627686-9 2015 Thus, energy status via insulin and FoxO1 regulate Rdh expression and atRA biosynthesis. Tretinoin 70-74 insulin Homo sapiens 24-31
25627686-9 2015 Thus, energy status via insulin and FoxO1 regulate Rdh expression and atRA biosynthesis. Tretinoin 70-74 forkhead box O1 Homo sapiens 36-41
25627686-10 2015 These results reveal mechanisms for regulating atRA biosynthesis and the opposing effects of atRA and insulin on gluconeogenesis, and also suggest an interaction between atRA and insulin signaling related diseases, such as type II diabetes and cancer. Tretinoin 47-51 insulin Homo sapiens 179-186
25627686-10 2015 These results reveal mechanisms for regulating atRA biosynthesis and the opposing effects of atRA and insulin on gluconeogenesis, and also suggest an interaction between atRA and insulin signaling related diseases, such as type II diabetes and cancer. Tretinoin 93-97 insulin Homo sapiens 179-186
25627686-10 2015 These results reveal mechanisms for regulating atRA biosynthesis and the opposing effects of atRA and insulin on gluconeogenesis, and also suggest an interaction between atRA and insulin signaling related diseases, such as type II diabetes and cancer. Tretinoin 93-97 insulin Homo sapiens 179-186
25805962-10 2015 After 5 days" incubation with ATRA, the expression levels of signal transducer and activator of transcription (STAT) 3, and phosphorylated STAT3 and STAT5, were significantly reduced. Tretinoin 30-34 signal transducer and activator of transcription 3 Homo sapiens 61-118
25805962-10 2015 After 5 days" incubation with ATRA, the expression levels of signal transducer and activator of transcription (STAT) 3, and phosphorylated STAT3 and STAT5, were significantly reduced. Tretinoin 30-34 signal transducer and activator of transcription 3 Homo sapiens 139-144
25343668-7 2015 Our results demonstrated a novel function of RA in modulating the IFN-gamma expression by activated NKT cells. Tretinoin 45-47 interferon gamma Homo sapiens 66-75
25435432-4 2015 Our data revealed that ATRA treatment to HL-60 cells enhanced IkappaBalpha degradation and NF-kappaB nuclear translocation and the activated NF-kappaB potentiated the ability of ATRA for differentiation and switched differentiation to macrophages instead of granulocytes. Tretinoin 178-182 nuclear factor kappa B subunit 1 Homo sapiens 141-150
25435432-5 2015 Serum withdrawal and LPS treatment dampened IkappaBalpha expression via MAPK activation and reactive oxygen species generation leading to NF-kappaB nuclear translocation and ATRA treatment further corroborated these effects in myeloid leukemia cells. Tretinoin 174-178 NFKB inhibitor alpha Homo sapiens 44-56
25435432-6 2015 Activated NF-kappaB enhanced the degree of ATRA-induced differentiation of HL-60 cells to macrophages, rather than granulocytes, as assessed by morphologic examination and expressions of differentiation markers such as CD11b, CD38, CD68, MMP9 and Btg2. Tretinoin 43-47 nuclear factor kappa B subunit 1 Homo sapiens 10-19
25435432-7 2015 Employing LLnL or dominant negative IkappaBalpha attenuated NF-kappaB associated enhanced cell maturation and differentiation switch thus suggesting NF-kappaB as one of the factors that determines ATRA induced lineage specificity of myeloid leukemia cells. Tretinoin 197-201 NFKB inhibitor alpha Homo sapiens 36-48
25435432-7 2015 Employing LLnL or dominant negative IkappaBalpha attenuated NF-kappaB associated enhanced cell maturation and differentiation switch thus suggesting NF-kappaB as one of the factors that determines ATRA induced lineage specificity of myeloid leukemia cells. Tretinoin 197-201 nuclear factor kappa B subunit 1 Homo sapiens 60-69
25435432-7 2015 Employing LLnL or dominant negative IkappaBalpha attenuated NF-kappaB associated enhanced cell maturation and differentiation switch thus suggesting NF-kappaB as one of the factors that determines ATRA induced lineage specificity of myeloid leukemia cells. Tretinoin 197-201 nuclear factor kappa B subunit 1 Homo sapiens 149-158
25435432-9 2015 In summary, our present data demonstrate that activation of NF-kappaB directly affects differentiation program of promyelocytes to macrophages, rather than granulocyte, in response to ATRA treatment. Tretinoin 184-188 nuclear factor kappa B subunit 1 Homo sapiens 60-69
25239070-4 2015 Since retinoid is a potential patterning influence on the developing face, we have examined whether retinoic acid (RA) signaling regulated Lhx8, Msx1 and Msx2 transcription through fibroblast growth factor (FGF) signals in the maxillary prominence. Tretinoin 115-117 msh homeobox 2 Gallus gallus 154-158
25239070-8 2015 The downregulated Lhx8 was rescued by combined treatment with FGF-8b, which indicated a downstream of RA signaling. Tretinoin 102-104 fibroblast growth factor 10 Gallus gallus 62-65
25802994-5 2015 We have previously shown that the early phases of neural induction of these cells by RA involve the up-regulation of SOX3 gene expression. Tretinoin 85-87 SRY-box transcription factor 3 Homo sapiens 117-121
25802994-6 2015 Our goal was to compare RA-induced differentiation of NT2/D1 cells in serum-containing and serum-free media, by using SOX3 protein levels as a marker of differentiation. Tretinoin 24-26 SRY-box transcription factor 3 Homo sapiens 118-122
25802994-8 2015 However, six days of RA treatment resulted in a marked increase in SOX3 protein levels in serum-free media compared to serum-containing media, indicating that serum might have an inhibitory effect on the expression of this neural differentiation marker. Tretinoin 21-23 SRY-box transcription factor 3 Homo sapiens 67-71
25656823-8 2015 Exogenous RA also disrupts the expression of Shh in the zone of polarizing activity, and Fgf8 in the apical ectodermal ridge, and other genes with roles in the regulation of limb development and cell death. Tretinoin 10-12 sonic hedgehog protein Monodelphis domestica 45-48
25656823-8 2015 Exogenous RA also disrupts the expression of Shh in the zone of polarizing activity, and Fgf8 in the apical ectodermal ridge, and other genes with roles in the regulation of limb development and cell death. Tretinoin 10-12 fibroblast growth factor 8 Monodelphis domestica 89-93
25435432-0 2015 Stress-induced NF-kappaB activation differentiates promyelocytic leukemia cells to macrophages in response to all-trans-retinoic acid. Tretinoin 110-133 nuclear factor kappa B subunit 1 Homo sapiens 15-24
25435432-3 2015 We report here that NF-kappaB activation is critical for determining ATRA-induced lineage specific differentiation of myeloid leukemia cells. Tretinoin 69-73 nuclear factor kappa B subunit 1 Homo sapiens 20-29
25435432-4 2015 Our data revealed that ATRA treatment to HL-60 cells enhanced IkappaBalpha degradation and NF-kappaB nuclear translocation and the activated NF-kappaB potentiated the ability of ATRA for differentiation and switched differentiation to macrophages instead of granulocytes. Tretinoin 23-27 NFKB inhibitor alpha Homo sapiens 62-74
25435432-4 2015 Our data revealed that ATRA treatment to HL-60 cells enhanced IkappaBalpha degradation and NF-kappaB nuclear translocation and the activated NF-kappaB potentiated the ability of ATRA for differentiation and switched differentiation to macrophages instead of granulocytes. Tretinoin 23-27 nuclear factor kappa B subunit 1 Homo sapiens 91-100
25343668-0 2015 Retinoic acid modulates interferon-gamma production by hepatic natural killer T cells via phosphatase 2A and the extracellular signal-regulated kinase pathway. Tretinoin 0-13 interferon gamma Homo sapiens 24-40
25343668-0 2015 Retinoic acid modulates interferon-gamma production by hepatic natural killer T cells via phosphatase 2A and the extracellular signal-regulated kinase pathway. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 113-150
25343668-4 2015 We also found that RA reduced extracellular signal-regulated kinase (ERK) phosphorylation, but increased phosphatase 2A (PP2A) activity in TCR/CD28-stimulated NKT cells. Tretinoin 19-21 mitogen-activated protein kinase 1 Homo sapiens 30-67
25343668-4 2015 We also found that RA reduced extracellular signal-regulated kinase (ERK) phosphorylation, but increased phosphatase 2A (PP2A) activity in TCR/CD28-stimulated NKT cells. Tretinoin 19-21 mitogen-activated protein kinase 1 Homo sapiens 69-72
25541526-0 2015 Molecular recognition of CYP26A1 binding pockets and structure-activity relationship studies for design of potent and selective retinoic acid metabolism blocking agents. Tretinoin 128-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 25-32
25504116-3 2015 In ESCs, Snai1 does not respond to TGFbeta or BMP4 signaling but it is induced by retinoic acid treatment, which induces the binding, on the Snai1 promoter, of the retinoid receptors RARgamma and RXRalpha, the dissociation of the Polycomb repressor complex 2 which results in the decrease of H3K27me3, and the increase of histone H3K4me3. Tretinoin 82-95 snail family transcriptional repressor 1 Homo sapiens 9-14
25541526-2 2015 However, ATRA is very easy to be metabolized into 4-hydroxyl-RA in vivo by CYP26A1, an inducible cytochrome P450 enzyme, eventually into more polar metabolites. Tretinoin 9-13 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 75-82
25541526-3 2015 Therefore, it is vital to develop specific retinoic acid metabolism blocking agents (RAMBAs) to inhibit the metabolic enzyme CYP26A1 in the treatment of relevant diseases aforementioned. Tretinoin 43-56 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 125-132
25541526-4 2015 In this study, CYP26A1 and its interactions with retinoic acid-competitive metabolism blocking agents were investigated by a combined ligand- and structure-based approach. Tretinoin 49-62 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-22
25614230-3 2015 Following a 4 week treatment with retinoic acid (10muM), the human teratocarcinoma-derived NTera2/D1 cell line (NT2 cells) terminally differentiate into neurons which recapitulate many features of human fetal neurons. Tretinoin 34-47 latexin Homo sapiens 51-54
25577283-9 2015 DISCUSSION: Aldh1a3 is a novel marker for glycogen trophoblast cells and their precursors and may play a role in the differentiation of junctional zone cell types via production of a local source of RA. Tretinoin 199-201 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 12-19
25729271-0 2015 NgR1 Expressed in P19 Embryonal Carcinoma Cells Differentiated by Retinoic Acid Can Activate STAT3. Tretinoin 66-79 signal transducer and activator of transcription 3 Homo sapiens 93-98
25504116-3 2015 In ESCs, Snai1 does not respond to TGFbeta or BMP4 signaling but it is induced by retinoic acid treatment, which induces the binding, on the Snai1 promoter, of the retinoid receptors RARgamma and RXRalpha, the dissociation of the Polycomb repressor complex 2 which results in the decrease of H3K27me3, and the increase of histone H3K4me3. Tretinoin 82-95 snail family transcriptional repressor 1 Homo sapiens 141-146
25658587-11 2015 CYP26b1, a member of the cytochrome P450 superfamily, is involved in the degradation of RA. Tretinoin 88-90 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 0-7
25294494-9 2015 Moreover, increasing RA concentration (>=10 muM) leads to increased cell death in the cells, but a lower concentration of RA (1 muM) treatment results in a decrease in CD34-expressing stem cells. Tretinoin 21-23 latexin Homo sapiens 47-50
25605784-3 2015 FGF signaling, together with downstream nodal/activin signaling, promotes male differentiation in XY germ cells by suppressing retinoic acid (RA)-dependent meiotic entry and inducing male-specific genes. Tretinoin 127-140 fibroblast growth factor 9 Mus musculus 0-3
25605784-3 2015 FGF signaling, together with downstream nodal/activin signaling, promotes male differentiation in XY germ cells by suppressing retinoic acid (RA)-dependent meiotic entry and inducing male-specific genes. Tretinoin 142-144 fibroblast growth factor 9 Mus musculus 0-3
25294494-9 2015 Moreover, increasing RA concentration (>=10 muM) leads to increased cell death in the cells, but a lower concentration of RA (1 muM) treatment results in a decrease in CD34-expressing stem cells. Tretinoin 125-127 latexin Homo sapiens 131-134
25294494-9 2015 Moreover, increasing RA concentration (>=10 muM) leads to increased cell death in the cells, but a lower concentration of RA (1 muM) treatment results in a decrease in CD34-expressing stem cells. Tretinoin 125-127 CD34 molecule Homo sapiens 171-175
25451924-6 2015 Indeed, ectopic expression of miR-638 promoted phorbol 12-myristate 13-acetate- or all-trans-retinoic acid-induced differentiation of leukemic cell lines and primary AML blasts, whereas miR-638 inhibition caused an opposite phenotype. Tretinoin 93-106 microRNA 638 Homo sapiens 30-37
25078760-7 2015 In addition, AtRA influenced activation and phosphorylation of PTEN and Akt differently in wild-type and mutant SMCs, consistent with previous studies of perlecan-dependent SMC growth inhibition. Tretinoin 13-17 phosphatase and tensin homolog Mus musculus 63-67
25078760-7 2015 In addition, AtRA influenced activation and phosphorylation of PTEN and Akt differently in wild-type and mutant SMCs, consistent with previous studies of perlecan-dependent SMC growth inhibition. Tretinoin 13-17 thymoma viral proto-oncogene 1 Mus musculus 72-75
25673193-0 2015 Effect of retinoic acid on expression of LINGO-1 and neural regeneration after cerebral ischemia. Tretinoin 10-23 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 41-48
25673193-1 2015 The purpose of this study was to observe the expression of LINGO-1 after cerebral ischemia, investigate the effects of retinoic acid (RA) on the expression of LINGO-1 and GAP-43, and the number of synapses, and to emplore the repressive effect of LINGO-1 on neural regeneration after cerebral ischemia. Tretinoin 119-132 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 159-166
25673193-1 2015 The purpose of this study was to observe the expression of LINGO-1 after cerebral ischemia, investigate the effects of retinoic acid (RA) on the expression of LINGO-1 and GAP-43, and the number of synapses, and to emplore the repressive effect of LINGO-1 on neural regeneration after cerebral ischemia. Tretinoin 119-132 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 159-166
25673193-1 2015 The purpose of this study was to observe the expression of LINGO-1 after cerebral ischemia, investigate the effects of retinoic acid (RA) on the expression of LINGO-1 and GAP-43, and the number of synapses, and to emplore the repressive effect of LINGO-1 on neural regeneration after cerebral ischemia. Tretinoin 134-136 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 159-166
25673193-1 2015 The purpose of this study was to observe the expression of LINGO-1 after cerebral ischemia, investigate the effects of retinoic acid (RA) on the expression of LINGO-1 and GAP-43, and the number of synapses, and to emplore the repressive effect of LINGO-1 on neural regeneration after cerebral ischemia. Tretinoin 134-136 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 159-166
25673193-6 2015 The results showed that the expression level of LINGO-1 at 7th day after MCAO in sham, CI and RA groups was 0.266 +- 0.019, 1.215 +- 0.063 and 0.702 +- 0.081, respectively (P<0.01). Tretinoin 94-96 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 48-55
25673193-10 2015 It suggests that LINGO-1 may be involved in the pathogenesis of cerebral ischemia, which may provide an experimenal basis for LINGO-1 antogonist, RA, for the treatment of cerebral ischemia. Tretinoin 146-148 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 17-24
25673193-10 2015 It suggests that LINGO-1 may be involved in the pathogenesis of cerebral ischemia, which may provide an experimenal basis for LINGO-1 antogonist, RA, for the treatment of cerebral ischemia. Tretinoin 146-148 leucine rich repeat and Ig domain containing 1 Rattus norvegicus 126-133
26451280-4 2015 In addition, retinoic acid inhibited Klf4 and Klf5 expression but not that of Cebpb. Tretinoin 13-26 Kruppel-like factor 4 (gut) Mus musculus 37-41
26557664-0 2015 All-Trans Retinoic Acid Induces Proliferation, Survival, and Migration in A549 Lung Cancer Cells by Activating the ERK Signaling Pathway through a Transcription-Independent Mechanism. Tretinoin 10-23 mitogen-activated protein kinase 1 Homo sapiens 115-118
25413479-0 2015 Retinoic acid receptor-beta gene reexpression and biological activity in SHI-1 cells after combined treatment with 5-aza-2"-deoxycytidine and all-trans retinoic acid. Tretinoin 152-165 retinoic acid receptor beta Homo sapiens 0-27
25427901-3 2015 A loss of retinoic acid due to a CYP2E1-related enhanced degradation results in enhanced cellular proliferation and decreased cell differentiation. Tretinoin 10-23 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 33-39
25413479-6 2015 DAC, either alone or in combination with ATRA, induced demethylation of the genes p16 and RAR-beta, whereas ATRA alone had no effect on methylation. Tretinoin 41-45 cyclin dependent kinase inhibitor 2A Homo sapiens 82-85
25413479-6 2015 DAC, either alone or in combination with ATRA, induced demethylation of the genes p16 and RAR-beta, whereas ATRA alone had no effect on methylation. Tretinoin 41-45 retinoic acid receptor beta Homo sapiens 90-98
26233912-0 2015 Role of Retinoic Acid-Metabolizing Cytochrome P450s, CYP26, in Inflammation and Cancer. Tretinoin 8-21 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 53-58
26233912-3 2015 Concentrations of atRA are tightly regulated in tissues, predominantly by the availability of retinol, synthesis of atRA by ALDH1A enzymes and metabolism and clearance of atRA by CYP26 enzymes. Tretinoin 18-22 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 179-184
26233912-10 2015 Inhibition of the CYP26 enzymes to increase atRA concentrations and combat therapy resistance has been pursued as a drug target in these cancers. Tretinoin 44-48 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 18-23
26557664-3 2015 In this study, we demonstrate that treatment with ATRA can activate the ERK signaling pathway by a transcription-independent mechanism through a signaling cascade that involves RARalpha and PI3K, promoting growth, survival, and migration in lung cancer cells. Tretinoin 50-54 mitogen-activated protein kinase 1 Homo sapiens 72-75
26557664-5 2015 The inhibition of the ERK signaling pathway restores the beneficial effects of ATRA, reduces proliferation, increases apoptosis, and blocks the cell migration process in lung cancer cells. Tretinoin 79-83 mitogen-activated protein kinase 1 Homo sapiens 22-25
26295826-4 2015 Here we report that ouabain-induced signaling is altered under the action of 1 muM RA in human neuroblastoma SK-N-SH cells. Tretinoin 83-85 latexin Homo sapiens 79-82
26100049-8 2015 RESULTS: From a total of 868 interactions we were able to identify an interesting interaction between retinoic acid (i.e. Vitamin A) and the aromatase gene (i.e. CYP19A1). Tretinoin 102-115 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 162-169
26100049-9 2015 Our experimental results showed that retinoic acid at physiological concentration significantly influenced CYP19A1 gene expressions. Tretinoin 37-50 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 107-114
26295826-5 2015 RA increased the expression of p110alpha subunit of phosphoinositide 3-kinase (PI3K), Akt and beta1 subunit of Na(+)/K(+)-ATPase. Tretinoin 0-2 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 31-40
26295826-5 2015 RA increased the expression of p110alpha subunit of phosphoinositide 3-kinase (PI3K), Akt and beta1 subunit of Na(+)/K(+)-ATPase. Tretinoin 0-2 AKT serine/threonine kinase 1 Homo sapiens 86-89
25380237-11 2015 RA-induced gonocyte differentiation was significantly reduced by inhibiting SRC (v-src avian sarcoma [Schmidt-Ruppin A-2] viral oncogene) and JAK2/STAT5 (Janus kinase 2/signal transducer and activator of transcription 5) activities, implying that these signaling molecules play a role in gonocyte differentiation. Tretinoin 0-2 UDP glucuronosyltransferase 1 family, polypeptide A7C Rattus norvegicus 117-120
25380237-11 2015 RA-induced gonocyte differentiation was significantly reduced by inhibiting SRC (v-src avian sarcoma [Schmidt-Ruppin A-2] viral oncogene) and JAK2/STAT5 (Janus kinase 2/signal transducer and activator of transcription 5) activities, implying that these signaling molecules play a role in gonocyte differentiation. Tretinoin 0-2 signal transducer and activator of transcription 5A Rattus norvegicus 147-152
25446031-6 2015 We found that RA signaling utilized the PI3K/AKT/mTOR signaling pathway to induce the efficient translation of mRNAs for Kit, which are present but not translated in undifferentiated spermatogonia. Tretinoin 14-16 thymoma viral proto-oncogene 1 Mus musculus 45-48
25492813-0 2015 Induction of CYP26A1 by metabolites of retinoic acid: evidence that CYP26A1 is an important enzyme in the elimination of active retinoids. Tretinoin 39-52 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 13-20
25311225-1 2015 The vitamin A metabolite retinoic acid (RA) has been reported to suppress Th1 responses and enhance Th2 responses. Tretinoin 25-38 negative elongation factor complex member C/D, Th1l Mus musculus 74-77
25311225-1 2015 The vitamin A metabolite retinoic acid (RA) has been reported to suppress Th1 responses and enhance Th2 responses. Tretinoin 40-42 negative elongation factor complex member C/D, Th1l Mus musculus 74-77
25403801-6 2015 RESULTS: Increased mineralized nodule formation, ALP activity, osteocalcin, and osteopontin expression levels were detected in LPS + atRA-treated BMSCs after osteogenic induction, when compared with LPS-treated cells. Tretinoin 133-137 alkaline phosphatase, placental Homo sapiens 49-52
25403801-6 2015 RESULTS: Increased mineralized nodule formation, ALP activity, osteocalcin, and osteopontin expression levels were detected in LPS + atRA-treated BMSCs after osteogenic induction, when compared with LPS-treated cells. Tretinoin 133-137 bone gamma-carboxyglutamate protein Homo sapiens 63-74
25403801-7 2015 In addition, the high levels of tumor necrosis factor-alpha, interleukin-1beta, and receptor activator of nuclear factor-kappa B ligand (RANKL) expression induced by LPS were inhibited after treatment with atRA. Tretinoin 206-210 tumor necrosis factor Homo sapiens 32-59
25403801-7 2015 In addition, the high levels of tumor necrosis factor-alpha, interleukin-1beta, and receptor activator of nuclear factor-kappa B ligand (RANKL) expression induced by LPS were inhibited after treatment with atRA. Tretinoin 206-210 interleukin 1 beta Homo sapiens 61-78
25778325-12 2015 ATRA could enhance the expression of 67LR in U251 cells and this enhancement was dose-dependent. Tretinoin 0-4 ribosomal protein SA Homo sapiens 37-41
24957708-2 2015 Meningioma 1 (MN1) is overexpressed in AML patients and confers resistance to all-trans retinoic acid-induced differentiation. Tretinoin 88-101 MN1 proto-oncogene, transcriptional regulator Homo sapiens 0-12
24957708-2 2015 Meningioma 1 (MN1) is overexpressed in AML patients and confers resistance to all-trans retinoic acid-induced differentiation. Tretinoin 88-101 MN1 proto-oncogene, transcriptional regulator Homo sapiens 14-17
25537091-6 2015 Bmp3, egr3, and stra8 are stimulated after 1 d of RA treatment and then recover to normal after 3 d of RA treatment. Tretinoin 50-52 stimulated by retinoic acid 8 Bos taurus 16-21
25537091-6 2015 Bmp3, egr3, and stra8 are stimulated after 1 d of RA treatment and then recover to normal after 3 d of RA treatment. Tretinoin 103-105 stimulated by retinoic acid 8 Bos taurus 16-21
25944986-3 2015 Unstimulated Caco2 and HT-29 cells secreted CCL19, CCL21, and CCL22 chemokines, which could attract dendritic cells and macrophages and induced CCR7 receptor up-regulation by retinoic-acid resulting in dendritic cell migration. Tretinoin 175-188 C-C motif chemokine receptor 7 Homo sapiens 144-148
25944986-5 2015 In the presence of ATRA the supernatants of these cells induced CD103 expression on monocyte-derived dendritic cells and when conditioned by ATRA and cocultured with CD4(+) T-lymphocytes they reduced the proportion of Th17 T-cells. Tretinoin 19-23 CD4 molecule Homo sapiens 166-169
25492813-0 2015 Induction of CYP26A1 by metabolites of retinoic acid: evidence that CYP26A1 is an important enzyme in the elimination of active retinoids. Tretinoin 39-52 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 68-75
25492813-5 2015 After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers. Tretinoin 36-40 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 107-114
25492813-5 2015 After treatment of HepG2 cells with atRA, (4S)-OH-atRA, (4R)-OH-atRA, 4-oxo-atRA, and 18-OH-atRA, mRNAs of CYP26A1 and RARbeta were increased 300- to 3000-fold, with 4-oxo-atRA and atRA being the most potent inducers. Tretinoin 50-54 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 107-114
25492813-7 2015 In human hepatocytes, atRA, 4-OH-atRA, and 4-oxo-atRA induced CYP26A1 and 4-oxo-atRA formation was observed from 4-OH-atRA. Tretinoin 22-26 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 62-69
24909558-0 2014 Dickkopf-3 alters the morphological response to retinoic acid during neuronal differentiation of human embryonal carcinoma cells. Tretinoin 48-61 dickkopf WNT signaling pathway inhibitor 3 Homo sapiens 0-10
25473832-7 2014 This is surprisingly different from the earlier requirement for RA signalling in specification of non-neural fates via tbx1 expression, and highlights the shift in regulation that takes place between otic placode and vesicle stages in zebrafish. Tretinoin 64-66 T-box transcription factor 1 Danio rerio 119-123
24981688-0 2014 Internal tandem duplication of the FLT3 gene confers poor overall survival in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline-based chemotherapy: an International Consortium on Acute Promyelocytic Leukemia study. Tretinoin 144-157 fms related receptor tyrosine kinase 3 Homo sapiens 35-39
24981688-2 2014 Here, we screened for FLT3-ITD mutations in 171 APL patients, treated with all-trans retinoic acid (ATRA) and anthracycline-based chemotherapy. Tretinoin 85-98 fms related receptor tyrosine kinase 3 Homo sapiens 22-26
24981688-2 2014 Here, we screened for FLT3-ITD mutations in 171 APL patients, treated with all-trans retinoic acid (ATRA) and anthracycline-based chemotherapy. Tretinoin 100-104 fms related receptor tyrosine kinase 3 Homo sapiens 22-26
24981688-9 2014 In addition, FLT3-ITD may independently predict a shorter survival in patients with APL treated with ATRA and anthracycline-based chemotherapy. Tretinoin 101-105 fms related receptor tyrosine kinase 3 Homo sapiens 13-17
26278415-4 2015 OBJECTIVES: In our study, we aimed to investigate in vitro immunomodulatory effects of ATRA on inducible nitric oxide synthase (iNOS) expression and interleukin-17A production during AD. Tretinoin 87-91 nitric oxide synthase 2 Homo sapiens 95-126
26278415-4 2015 OBJECTIVES: In our study, we aimed to investigate in vitro immunomodulatory effects of ATRA on inducible nitric oxide synthase (iNOS) expression and interleukin-17A production during AD. Tretinoin 87-91 nitric oxide synthase 2 Homo sapiens 128-132
26278415-9 2015 Remarkably, ATRA treatment showed an important downregulatory effect on NO production and iNOS expression in patients. Tretinoin 12-16 nitric oxide synthase 2 Homo sapiens 90-94
26124839-6 2015 ATRA pretreatment increased interleukin-6 (IL-6) secretion of MSCs. Tretinoin 0-4 interleukin 6 Homo sapiens 28-41
26124839-6 2015 ATRA pretreatment increased interleukin-6 (IL-6) secretion of MSCs. Tretinoin 0-4 interleukin 6 Homo sapiens 43-47
26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 tumor necrosis factor Homo sapiens 91-118
26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 tumor necrosis factor Homo sapiens 120-129
26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 interferon gamma Homo sapiens 189-205
26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 interferon gamma Homo sapiens 207-216
24909558-5 2014 Gene silencing of Dkk-3 did not affect NT2 cell growth or differentiation but altered their response to RA in suspension cultures. Tretinoin 104-106 dickkopf WNT signaling pathway inhibitor 3 Homo sapiens 18-23
24909558-8 2014 These findings suggest that Dkk-3 plays a role in the regulation of cell interactions during RA-induced neuronal differentiation. Tretinoin 93-95 dickkopf WNT signaling pathway inhibitor 3 Homo sapiens 28-33
25450463-6 2014 Using bisulfite treatment, luciferase assay and chromatin immunoprecipitation we found that changes in S100A6 expression were DNA methylation independent but could be orchestrated by epidermal specific factors: the DeltaNp63 transcription factor and retinoic acid. Tretinoin 250-263 S100 calcium binding protein A6 Homo sapiens 103-109
24846581-1 2014 All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 4-23 retinoic acid receptor beta Homo sapiens 159-167
25040912-15 2014 The E2F3 repression, a novel target gene of miR-302b, was involved in ATRA-induced glioblastoma cell cytotoxicity. Tretinoin 70-74 E2F transcription factor 3 Homo sapiens 4-8
24846581-1 2014 All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 159-167
24846581-8 2014 Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-beta1 (all p < 0.05). Tretinoin 37-41 NPHS2 stomatin family member, podocin Homo sapiens 118-125
24846581-8 2014 Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-beta1 (all p < 0.05). Tretinoin 37-41 transforming growth factor beta 1 Homo sapiens 150-159
24846581-12 2014 In conclusion, RAR-alpha/gamma (and RAR-beta to a lesser degree) may be involved in the signal pathway of ATRA-induced differentiation in injured podocytes. Tretinoin 106-110 retinoic acid receptor beta Homo sapiens 36-44
25428027-7 2014 Both 6-BT and all-trans-retinoic-acid (ATRA) reduced canonical Wnt signaling and activated noncanonical Wnt/Ca2+ signaling in HL-60 cells. Tretinoin 14-37 Wnt family member 5A Homo sapiens 63-66
25428027-7 2014 Both 6-BT and all-trans-retinoic-acid (ATRA) reduced canonical Wnt signaling and activated noncanonical Wnt/Ca2+ signaling in HL-60 cells. Tretinoin 14-37 Wnt family member 5A Homo sapiens 104-107
25428027-7 2014 Both 6-BT and all-trans-retinoic-acid (ATRA) reduced canonical Wnt signaling and activated noncanonical Wnt/Ca2+ signaling in HL-60 cells. Tretinoin 39-43 Wnt family member 5A Homo sapiens 63-66
25428027-7 2014 Both 6-BT and all-trans-retinoic-acid (ATRA) reduced canonical Wnt signaling and activated noncanonical Wnt/Ca2+ signaling in HL-60 cells. Tretinoin 39-43 Wnt family member 5A Homo sapiens 104-107
25403085-9 2014 CONCLUSIONS: According to our modeling of metabolic and signalization pathways using differentially expressed genes we have identified a network with major nodes (including Sirt3, Il1b, Cpt1b and Pparg) likely to underlie the observed strain specific response to ATRA. Tretinoin 263-267 interleukin 1 beta Rattus norvegicus 180-184
25926859-1 2014 BACKGROUND: Members of the ALDH1 protein family, known as retinal dehydrogenases (RALDH), produce retinoic acid (RA), a metabolite of vitamin A, and may also oxidize other lipid aldehydes. Tretinoin 98-111 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 27-32
25926859-1 2014 BACKGROUND: Members of the ALDH1 protein family, known as retinal dehydrogenases (RALDH), produce retinoic acid (RA), a metabolite of vitamin A, and may also oxidize other lipid aldehydes. Tretinoin 82-84 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 27-32
25926859-4 2014 We hypothesized that ALDH1A1 may have a broad cellular distribution in the liver, and that its expression may be regulated by RA and perturbed by inflammation. Tretinoin 126-128 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 21-28
25926859-7 2014 RESULTS: Inflammation reduced ALDH1A1 mRNA in whole liver regardless of the level of vitamin A in the diet (P < 0.05), while treatment with RA reduced ALDH1A1 expression only in chow-fed rats. Tretinoin 143-145 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 154-161
25389900-6 2014 Retinoic acid, the main biologically active form of vitamin A, influences the expression of collagens, laminins, entactin, fibronectin, elastin and proteoglycans, which are the major components of the extracellular matrix. Tretinoin 0-13 fibronectin 1 Homo sapiens 123-134
25192658-0 2014 Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP. Tretinoin 20-24 interleukin 6 Homo sapiens 33-37
25192658-0 2014 Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP. Tretinoin 20-24 DNA damage inducible transcript 3 Homo sapiens 103-107
25192658-4 2014 Following treatment with ATRA, CHOP expression was increased and dimerized with LIP more preferentially than LAP to rescue function of LAP. Tretinoin 25-29 DNA damage inducible transcript 3 Homo sapiens 31-35
25192658-8 2014 Our results showed that oroxylin A decreased the level of IL-6 secretion of NB4 cells with or without ATRA treatment while the effect was eliminated by C/EBPbeta siRNA. Tretinoin 102-106 interleukin 6 Homo sapiens 58-62
25192658-9 2014 We conclude that oroxylin A possessed abilities of inhibiting the ATRA-induced IL-6 production via modulation of LAP/LIP/CHOP in leukemia cell lines, which could providing a therapeutic strategy for RAS. Tretinoin 66-70 interleukin 6 Homo sapiens 79-83
25192658-9 2014 We conclude that oroxylin A possessed abilities of inhibiting the ATRA-induced IL-6 production via modulation of LAP/LIP/CHOP in leukemia cell lines, which could providing a therapeutic strategy for RAS. Tretinoin 66-70 DNA damage inducible transcript 3 Homo sapiens 121-125
25305491-4 2014 We found localized RA activities in the diaphyseal portion of the growth plate cartilage were associated with the specific expression of Cyp26b1 in the epiphyseal portion in juvenile mice. Tretinoin 19-21 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 137-144
25371368-8 2014 Importantly, RA specifies and patterns the hindbrain territory by antagonizing the activity of the spinal cord specification gene cdx4; loss of Cdx4 rescues the defects associated with the loss of RA, including the reduction in hindbrain size and the loss of posterior rhombomeres. Tretinoin 13-15 caudal type homeobox 4 Danio rerio 130-134
25408532-4 2014 Here, using MTT assay and EB/AO staining as well as TUNEL assay we show that RA in a concentration-dependent manner induces apoptosis through upregulating Caspase expression and increasing Bax/Bcl2 ratio. Tretinoin 77-79 BCL2 associated X, apoptosis regulator Homo sapiens 189-192
25408532-4 2014 Here, using MTT assay and EB/AO staining as well as TUNEL assay we show that RA in a concentration-dependent manner induces apoptosis through upregulating Caspase expression and increasing Bax/Bcl2 ratio. Tretinoin 77-79 BCL2 apoptosis regulator Homo sapiens 193-197
25446614-11 2014 From the tested 11 compounds only all-trans-retinoic acid, an antioxidant and antiglycation agent, U0126, a MAP/ERK kinase inhibitor and aminoguanidine attenuated methylglyoxal-induced damage in hCMEC/D3 cells. Tretinoin 34-57 mitogen-activated protein kinase 1 Homo sapiens 112-115
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 cytochrome P450, family 7, subfamily a, polypeptide 1 Mus musculus 96-102
24722440-7 2014 Blocking retinoic acid signaling, which regulates wt1a, also prevented osr1 expression in podocyte progenitors. Tretinoin 9-22 WT1 transcription factor a Danio rerio 50-54
24722440-7 2014 Blocking retinoic acid signaling, which regulates wt1a, also prevented osr1 expression in podocyte progenitors. Tretinoin 9-22 odd-skipped related transcription factor 1 Mus musculus 71-75
25004394-7 2014 ATRA administration ameliorates DSS-induced colitis evidenced with decreased TNF level and CD68 expression, while LE135 leads to exacerbation of colitis. Tretinoin 0-4 tumor necrosis factor Mus musculus 77-80
25004394-8 2014 ATRA treatment in vitro dampens LPS induced NF-kappaB activation and TNF production of RAW 264.7 cells. Tretinoin 0-4 tumor necrosis factor Mus musculus 69-72
25531381-0 2014 [The anti-apoptotic effect of cytoplasmic alpha-fetoprotein in hepatoma cells induced by all-trans retinoic acid involves activation of the PI3K/AKT signaling pathway]. Tretinoin 99-112 alpha fetoprotein Homo sapiens 42-59
25531381-0 2014 [The anti-apoptotic effect of cytoplasmic alpha-fetoprotein in hepatoma cells induced by all-trans retinoic acid involves activation of the PI3K/AKT signaling pathway]. Tretinoin 99-112 AKT serine/threonine kinase 1 Homo sapiens 145-148
25531381-5 2014 PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src. Tretinoin 285-289 alpha fetoprotein Homo sapiens 69-72
25531381-5 2014 PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src. Tretinoin 285-289 alpha fetoprotein Homo sapiens 69-72
25531381-5 2014 PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src. Tretinoin 285-289 alpha fetoprotein Homo sapiens 69-72
25531381-5 2014 PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src. Tretinoin 285-289 alpha fetoprotein Homo sapiens 69-72
25531381-6 2014 CONCLUSION: AFP can activate transduction of the PI3K/AKT signal, and expression of AFP in hepatoma cells is a pivotal event for resisting ATRA-induced apoptosis. Tretinoin 139-143 AKT serine/threonine kinase 1 Homo sapiens 54-57
25531381-6 2014 CONCLUSION: AFP can activate transduction of the PI3K/AKT signal, and expression of AFP in hepatoma cells is a pivotal event for resisting ATRA-induced apoptosis. Tretinoin 139-143 alpha fetoprotein Homo sapiens 84-87
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 ATP-binding cassette, sub-family B (MDR/TAP), member 4 Mus musculus 112-116
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 ATP-binding cassette, sub-family B (MDR/TAP), member 11 Mus musculus 118-122
25148603-4 2014 Intrinsic drug binding properties of albumin to all-trans retinoic acid (atRA) are conserved through the partial denaturation process, as confirmed by fluorescence quenching. Tretinoin 52-71 albumin Homo sapiens 37-44
25175738-3 2014 Thus, RA can activate the FXR-mediated pathway as well. Tretinoin 6-8 nuclear receptor subfamily 1, group H, member 4 Mus musculus 26-29
25175738-7 2014 All-trans RA treatment reduced the gene expression levels of Cyp7a1, Cyp8b1, and Akr1d1, which are involved in bile acid synthesis. Tretinoin 10-12 cytochrome P450, family 7, subfamily a, polypeptide 1 Mus musculus 61-67
25175738-8 2014 All-trans RA also decreased the hepatic mRNA levels of Lrh-1 (Nr5a2) and Hnf4alpha (Nr2a1), which positively regulate the gene expression of Cyp7a1 and Cyp8b1. Tretinoin 10-12 cytochrome P450, family 7, subfamily a, polypeptide 1 Mus musculus 141-147
25175738-9 2014 Moreover, all-trans RA induced the gene expression levels of negative regulators of bile acid synthesis including hepatic Fgfr4, Fxr, and Shp (Nr0b2) as well as ileal Fgf15. Tretinoin 20-22 nuclear receptor subfamily 1, group H, member 4 Mus musculus 129-132
25175738-10 2014 All-trans RA also decreased the expression of Abcb11 and Slc51b, which have a role in bile acid transport. Tretinoin 10-12 ATP-binding cassette, sub-family B (MDR/TAP), member 11 Mus musculus 46-52
25175738-10 2014 All-trans RA also decreased the expression of Abcb11 and Slc51b, which have a role in bile acid transport. Tretinoin 10-12 solute carrier family 51, beta subunit Mus musculus 57-63
25175738-12 2014 The data suggest that all-trans RA-induced SHP may contribute to the inhibition of CYP7A1 and CYP8B1, which in turn reduces bile acid synthesis and affects lipid absorption in the gastrointestinal tract. Tretinoin 32-34 cytochrome P450, family 7, subfamily a, polypeptide 1 Mus musculus 83-89
25164008-5 2014 The breast cancer cell differentiation-inducing agent, all-trans retinoic acid, restored the miR20a-MICA/MICB axis and sensitized BCSC to NK cell-mediated killing, thereby reducing immune escape-associated BCSC metastasis. Tretinoin 65-78 microRNA 20a Homo sapiens 93-99
25148603-4 2014 Intrinsic drug binding properties of albumin to all-trans retinoic acid (atRA) are conserved through the partial denaturation process, as confirmed by fluorescence quenching. Tretinoin 73-77 albumin Homo sapiens 37-44
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 cell division cycle 25A Mus musculus 185-191
25294402-0 2014 Increased expression of the retinoic acid-metabolizing enzyme CYP26A1 during the progression of cervical squamous neoplasia and head and neck cancer. Tretinoin 28-41 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 62-69
25239423-8 2014 The best interpretative approach to ATRA-treated APL (CD34- or HLA-DR-) showed 100% sensitivity but limited specificity (73%). Tretinoin 36-40 CD34 molecule Homo sapiens 54-58
24973688-2 2014 Using differential display analysis, in this study, we demonstrate that gene expression of the serine protease inhibitor A3g (SerpinA3g) is specifically induced in 3T3-F442A preadipocytes by TNF-alpha but not by other adipogenic inhibitors, such as retinoic acid (RA) or transforming growth factor type beta (TGF-beta). Tretinoin 249-262 serine (or cysteine) peptidase inhibitor, clade A, member 3G Mus musculus 95-124
24973688-2 2014 Using differential display analysis, in this study, we demonstrate that gene expression of the serine protease inhibitor A3g (SerpinA3g) is specifically induced in 3T3-F442A preadipocytes by TNF-alpha but not by other adipogenic inhibitors, such as retinoic acid (RA) or transforming growth factor type beta (TGF-beta). Tretinoin 249-262 serine (or cysteine) peptidase inhibitor, clade A, member 3G Mus musculus 126-135
25088254-4 2014 BCL-2 family proteins regulate apoptosis and over-expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL-2) family proteins has been associated with chemotherapeutic resistance in APL including impairment of the ability of atRA to induce growth arrest and differentiation. Tretinoin 229-233 BCL2 apoptosis regulator Homo sapiens 0-5
25088254-4 2014 BCL-2 family proteins regulate apoptosis and over-expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL-2) family proteins has been associated with chemotherapeutic resistance in APL including impairment of the ability of atRA to induce growth arrest and differentiation. Tretinoin 229-233 BCL2 apoptosis regulator Homo sapiens 79-105
25088254-4 2014 BCL-2 family proteins regulate apoptosis and over-expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL-2) family proteins has been associated with chemotherapeutic resistance in APL including impairment of the ability of atRA to induce growth arrest and differentiation. Tretinoin 229-233 BCL2 apoptosis regulator Homo sapiens 107-112
25088254-5 2014 Here we investigated the novel BH3 domain mimetic, JY-1-106, which antagonizes the anti-apoptotic BCL-2 family members B-cell lymphoma-extra large (BCL-xL) and myeloid cell leukemia-1 (MCL-1) alone and in combination with retinoids including atRA, AM580 (RARalpha agonist), and SR11253 (RARgamma antagonist). Tretinoin 242-246 BCL2 apoptosis regulator Homo sapiens 98-103
25268355-5 2014 All-trans retinoic acid in vitro induced IL-10 in CD4(+)CD25(high)Foxp3(+) T cells; IL-10 and TGF-beta production in CD4(+)CD25-Foxp3- T cells, and IL-10 in monocytes isolated from healthy children. Tretinoin 10-23 transforming growth factor beta 1 Homo sapiens 94-102
25455157-11 2014 S1P antagonized the effect of ATRA on HT-29 cell proliferation, the ATRA-induced RARbeta expression, the arrest of cell cycle in G1-phase, and induction of apoptosis. Tretinoin 68-72 retinoic acid receptor beta Homo sapiens 81-88
24819304-1 2014 CYP26A1 expression is very highly induced by retinoic acid (RA) in the liver, compared to most other tissues, suggesting that a liver-enriched factor may be required for its physiological transcriptional response. Tretinoin 45-58 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
24819304-1 2014 CYP26A1 expression is very highly induced by retinoic acid (RA) in the liver, compared to most other tissues, suggesting that a liver-enriched factor may be required for its physiological transcriptional response. Tretinoin 60-62 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
24819304-3 2014 In this study, we hypothesized that HNF4alpha and RARs may cooperate in an RA-dependent manner to induce a high level of CYP26A1 expression in liver cells. Tretinoin 50-52 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 121-128
24819304-4 2014 Partial inhibition of endogenous HNF4alpha by siRNA reduced the level of RA-induced CYP26A1 mRNA in HepG2 cells. Tretinoin 73-75 hepatocyte nuclear factor 4 alpha Homo sapiens 33-42
24819304-4 2014 Partial inhibition of endogenous HNF4alpha by siRNA reduced the level of RA-induced CYP26A1 mRNA in HepG2 cells. Tretinoin 73-75 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 84-91
24819304-5 2014 Cotransfection of HNF4alpha, with or without RARs, demonstrated RA-dependent activation of a human CYP26A1 promoter-luciferase construct. Tretinoin 45-47 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 99-106
24819304-7 2014 In EMSA and ChIP analyses HNF4alpha and RARs binding in the proximal and distal CYP26A1 promoter regions was significantly higher in RA-treated cells. Tretinoin 40-42 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 80-87
24819304-9 2014 Our results indicate that HNF4alpha coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo. Tretinoin 53-55 hepatocyte nuclear factor 4 alpha Homo sapiens 26-35
24819304-9 2014 Our results indicate that HNF4alpha coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo. Tretinoin 53-55 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 103-110
24819304-9 2014 Our results indicate that HNF4alpha coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo. Tretinoin 64-66 hepatocyte nuclear factor 4 alpha Homo sapiens 26-35
24819304-9 2014 Our results indicate that HNF4alpha coordinates with RARs in an RA-dependent manner to strongly induce CYP26A1 gene expression in the liver, which may explain the high level of response to RA observed in vivo. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 103-110
24998947-6 2014 The treatment with atRA resulted in lower serum iron and transferrin concentrations, an increased iron concentration in the liver, a decreased iron concentration in the spleen and in the gut, and decreased hepatic Hamp mRNA levels. Tretinoin 19-23 transferrin Rattus norvegicus 57-68
24998947-6 2014 The treatment with atRA resulted in lower serum iron and transferrin concentrations, an increased iron concentration in the liver, a decreased iron concentration in the spleen and in the gut, and decreased hepatic Hamp mRNA levels. Tretinoin 19-23 hepcidin antimicrobial peptide Rattus norvegicus 214-218
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 3-23 retinoic acid receptor beta Homo sapiens 215-242
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 3-23 retinoic acid receptor beta Homo sapiens 244-252
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 215-242
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 244-252
25071154-2 2014 Stimulation with retinoic acid leads to the recruitment of UTX-containing complexes to HOX genes, which results in demethylation of histone H3 lysine 27 and concomitant methylation of histone H3 lysine 4. Tretinoin 17-30 lysine demethylase 6A Homo sapiens 59-62
25071154-3 2014 Here, we show that UTX interacts with the retinoic acid receptor alpha (RARalpha) and that this interaction is essential for proper differentiation of leukemic U937 cells in response to retinoic acid. Tretinoin 42-55 lysine demethylase 6A Homo sapiens 19-22
25071154-5 2014 Overexpression of UTX in promyelocytic NB4 cells results in enhanced cellular differentiation upon retinoic acid treatment. Tretinoin 99-112 lysine demethylase 6A Homo sapiens 18-21
24989326-7 2014 In addition, the PGC-like cells showed downregulation of DNA methylation and formed pluripotent stem cell colonies upon treatment with retinoic acid. Tretinoin 135-148 progastricsin (pepsinogen C) Mus musculus 17-20
25142465-2 2014 Fibroblast growth factor 9 and several members of the transforming growth factor beta superfamily are involved in this process in the foetal testis, counteracting the induction of meiosis by retinoic acid and activating germinal mitotic arrest. Tretinoin 191-204 fibroblast growth factor 9 Mus musculus 0-26
24800886-9 2014 Combined treatment with belinostat and RA dose dependently accelerated and reinforced granulocytic differentiation, accompanied by changes in the expression of CD11b, C/EBPalpha (CCAAT/enhancer binding protein-alpha), and C/EBPepsilon. Tretinoin 39-41 CCAAT enhancer binding protein alpha Homo sapiens 167-177
24800886-9 2014 Combined treatment with belinostat and RA dose dependently accelerated and reinforced granulocytic differentiation, accompanied by changes in the expression of CD11b, C/EBPalpha (CCAAT/enhancer binding protein-alpha), and C/EBPepsilon. Tretinoin 39-41 CCAAT enhancer binding protein alpha Homo sapiens 179-215
25212816-0 2014 PI3K/Akt pathway regulates retinoic acid-induced Hox gene expression in F9 cells. Tretinoin 27-40 thymoma viral proto-oncogene 1 Mus musculus 5-8
25212816-3 2014 The PI3K/Akt pathway was also reported to play an essential role in the process of RA-induced cell differentiation. Tretinoin 83-85 thymoma viral proto-oncogene 1 Mus musculus 9-12
25212816-5 2014 To examine the effect of PI3K/Akt signaling on RA-induced initiation of collinear expression of Hox genes, F9 cells were treated with RA in the presence or absence of PI3K inhibitor LY294002, and time-course gene expression profiles for all 39 Hox genes located in four different clusters-Hoxa, Hoxb, Hoxc, and Hoxd-were analyzed. Tretinoin 47-49 thymoma viral proto-oncogene 1 Mus musculus 30-33
25212816-7 2014 When LY294002 was applied along with RA, collinear expression induced by RA was delayed, suggesting that the PI3K/Akt signaling pathway somehow regulates RA-induced collinear expression of Hox genes in F9 cells. Tretinoin 37-39 thymoma viral proto-oncogene 1 Mus musculus 114-117
24926820-5 2014 Here we show that 9-cis RA induces a functional DRD2 in the pituitary corticotroph cell line AtT20, and increases cell sensitivity to Br via a mechanism only partially related to corticotroph-to-melanotroph transdifferentiation. Tretinoin 24-26 dopamine receptor D2 Mus musculus 48-52
24926820-7 2014 In nearly 45% of corticotropinoma-derived primary cultures, the combined administration of 9-cis RA and Br lowered the steady-state level of the ACTH precursor proopiomelanocortin (POMC) more efficiently than either of the drugs alone. Tretinoin 97-99 proopiomelanocortin Homo sapiens 145-149
24926820-7 2014 In nearly 45% of corticotropinoma-derived primary cultures, the combined administration of 9-cis RA and Br lowered the steady-state level of the ACTH precursor proopiomelanocortin (POMC) more efficiently than either of the drugs alone. Tretinoin 97-99 proopiomelanocortin Homo sapiens 181-185
24926820-8 2014 In conclusion, the effects of a combination of 9-cis RA and Br on ACTH synthesis/secretion and cell viability in AtT20, and on POMC transcriptional activity in human corticotropinomas might represent a suitable starting point for assessing the potential of this treatment regimen for ACTH-secreting pituitary adenomas. Tretinoin 53-55 proopiomelanocortin Homo sapiens 66-70
24914804-0 2014 A small-molecule targeting the microRNA binding domain of argonaute 2 improves the retinoic acid differentiation response of the acute promyelocytic leukemia cell line NB4. Tretinoin 83-96 argonaute RISC catalytic component 2 Homo sapiens 58-69
25691937-11 2014 Furthermore, aside from reducing NBT reduction and lymphocyte proliferation, Tretinoin markedly suppressed the secretion of interleukin-17 and conversely, increased the production of interleukin-10. Tretinoin 77-86 interleukin 10 Mus musculus 183-197
25691937-13 2014 CONCLUSION: The in vivo immunomudlatoty effects of Tretinoin may be partly due to immune deviation from pro-inflammatory cytokine interleukin-17 to anti-inflammatory cytokine interleukin-10, but not absolutely depend on the expansion of FoxP3(+)Treg cells. Tretinoin 51-60 interleukin 10 Mus musculus 175-189
25031298-0 2014 Effect of all-trans retinoic acid treatment on prohibitin and renin-angiotensin-aldosterone system expression in hypoxia-induced renal tubular epithelial cell injury. Tretinoin 20-33 renin Homo sapiens 62-67
25031298-5 2014 Therefore, the objective of this study was to investigate the effect of ATRA treatment on the renin-angiotensin-aldosterone system and expression of prohibitins to further understand its role in the processes leading to renal interstitial fibrosis. Tretinoin 72-76 renin Homo sapiens 94-99
25031298-11 2014 CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. Tretinoin 37-41 angiotensin I converting enzyme Homo sapiens 126-130
25031298-11 2014 CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. Tretinoin 37-41 angiotensinogen Homo sapiens 132-145
25031298-11 2014 CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. Tretinoin 37-41 angiotensinogen Homo sapiens 151-165
25003661-7 2014 In cells exposed to ATO plus ATRA, the Nrf2 nuclear translocation was prevented and cytotoxicity was enhanced. Tretinoin 29-33 NFE2 like bZIP transcription factor 2 Homo sapiens 39-43
24652806-3 2014 This impaired retinoic acid synthesis correlates with reduced renal expression of retinol dehydrogenase 9, which catalyzes the rate-limiting step of retinoic acid synthesis by converting retinol to retinal. Tretinoin 14-27 retinol dehydrogenase 9 Mus musculus 82-105
24652806-3 2014 This impaired retinoic acid synthesis correlates with reduced renal expression of retinol dehydrogenase 9, which catalyzes the rate-limiting step of retinoic acid synthesis by converting retinol to retinal. Tretinoin 149-162 retinol dehydrogenase 9 Mus musculus 82-105
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 0-23 retinoic acid receptor, beta Rattus norvegicus 104-131
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 0-23 retinoic acid receptor, beta Rattus norvegicus 133-141
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 25-29 retinoic acid receptor, beta Rattus norvegicus 104-131
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 25-29 retinoic acid receptor, beta Rattus norvegicus 133-141
24768685-9 2014 The treatment with vitamin A and ATRA reverted similarly the sensorial disturbances, which was associated with increased contents of NGF and RAR-beta expression. Tretinoin 33-37 retinoic acid receptor, beta Rattus norvegicus 141-149
25476428-0 2014 [Immunological effect of different doses of all-trans retinoic acid on ovalbumin allergic mice]. Tretinoin 54-67 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 71-80
25099355-4 2014 atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Tretinoin 0-4 interleukin 1 beta Homo sapiens 175-179
25099355-4 2014 atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Tretinoin 0-4 interleukin 6 Homo sapiens 184-188
25099355-5 2014 Interestingly, adoptive transfer of human nTregs pretreated with atRA significantly enhanced their suppressive effects on xenograft-vs.-host diseases (xGVHDs), and atRA- but not rapamycin-pretreated nTregs sustained the functional activity against xGVHD after stimulation with IL-1/IL-6. Tretinoin 65-69 interleukin 1 beta Homo sapiens 277-281
25099355-5 2014 Interestingly, adoptive transfer of human nTregs pretreated with atRA significantly enhanced their suppressive effects on xenograft-vs.-host diseases (xGVHDs), and atRA- but not rapamycin-pretreated nTregs sustained the functional activity against xGVHD after stimulation with IL-1/IL-6. Tretinoin 65-69 interleukin 6 Homo sapiens 282-286
24914804-3 2014 We report the identification of a chemical compound able to compete with Argonaute 2 miRNAs binding, and we demonstrate that this functional inhibition determines effects similar to Argonaute 2 shRNA-mediated down-regulation, favoring granulocytic differentiation of the acute promyelocytic leukemia cell line NB4 in response to retinoic acid. Tretinoin 329-342 argonaute RISC catalytic component 2 Homo sapiens 73-84
24954410-4 2014 In a microarray analysis, integrin-alpha1 and integrin-beta3 showed the largest variation in the ATRA-treated group compared with the controls. Tretinoin 97-101 integrin subunit beta 3 Homo sapiens 46-60
25119106-6 2014 Some retinoic acid target genes regulated by PML/RARA are involved in not only differentiation block but also hematopoietic cell self-renewal. Tretinoin 5-18 promyelocytic leukemia Mus musculus 45-48
25116125-6 2014 Celastrol"s effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. Tretinoin 32-36 mitogen-activated protein kinase 3 Homo sapiens 78-82
24954410-10 2014 In this study, it was shown that the differentiation-inducing effect on human alveolar epithelial stem cells by ATRA was induced by increased expression of integrin, and that the induced integrin enhanced phosphorylation signaling of AKT, resulting in inducing differentiations. Tretinoin 112-116 AKT serine/threonine kinase 1 Homo sapiens 234-237
24782508-8 2014 In the presence of pharmacologic doses of ATRA, TBLR1-RARalpha could be degraded, and its homodimerization was abrogated. Tretinoin 42-46 TBL1X/Y related 1 Homo sapiens 48-53
25065743-0 2014 WTIP interacts with ASXL2 and blocks ASXL2-mediated activation of retinoic acid signaling. Tretinoin 66-79 WT1 interacting protein Homo sapiens 0-4
25065743-8 2014 Together, these results implicate ASXL2 and WTIP in regulation of retinoic acid signaling during heart development. Tretinoin 66-79 WT1 interacting protein Homo sapiens 44-48
24782508-9 2014 Moreover, when treated with ATRA, TBLR1-RARalpha could mediate the dissociation and degradation of transcriptional corepressors, consequent transactivation of RARalpha target genes, and cell differentiation induction in a dose- and time-dependent manner. Tretinoin 28-32 TBL1X/Y related 1 Homo sapiens 34-39
24821725-6 2014 Importantly, RA treatment differentially mediates the removal of HDACs from the Hoxa1, Cyp26a1, and RARbeta2 genes and promotes the deposition of the H3K27ac mark at these genes. Tretinoin 13-15 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 87-94
24603314-13 2014 9-cis-RA antagonized Ang II-induced LKB1/AMPK and p70S6K activation changes in vitro. Tretinoin 0-8 angiotensinogen Rattus norvegicus 21-27
24603314-13 2014 9-cis-RA antagonized Ang II-induced LKB1/AMPK and p70S6K activation changes in vitro. Tretinoin 0-8 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 41-45
23913437-5 2014 We found that all-trans retinoic acid and its steroidal analogue EA-4 (a) provoke DNA migration due to DNA fragmentation as it is shown by the increased values of Comet parameters, and (b) induce significantly small-size fragmented genomic DNA as indicated by the quantification of necrotic/apoptotic small DNA segments in both cell systems. Tretinoin 24-37 erythrocyte antigen 4 Mus musculus 65-69
24648413-7 2014 RA increases the expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, Fzd2 and Fzd6), downstream signaling, and Tcf3 expression. Tretinoin 0-2 Wnt family member 5A Homo sapiens 86-92
24648413-7 2014 RA increases the expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, Fzd2 and Fzd6), downstream signaling, and Tcf3 expression. Tretinoin 0-2 frizzled class receptor 6 Homo sapiens 107-111
24648413-9 2014 We show that RA signaling increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Tretinoin 13-15 nuclear receptor subfamily 5 group A member 2 Homo sapiens 141-146
24648413-9 2014 We show that RA signaling increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Tretinoin 13-15 nuclear receptor subfamily 5 group A member 2 Homo sapiens 148-153
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 136-138 nuclear receptor subfamily 5 group A member 2 Homo sapiens 28-33
25072246-3 2014 Real-time PCR analyses demonstrated that the inductions of CD11b and CD11c and reductions in myeloperoxidase and c-myc by ATRA were significantly attenuated in NB4MTOE cells. Tretinoin 122-126 myeloperoxidase Homo sapiens 93-108
25072246-5 2014 Since G1 arrest is a hallmark of ATRA-induced NB4 cell differentiation, we observed a decrease in G1 accumulation, as well as decreases in p21WAF1/CIP1 and cyclin D1 inductions, by ATRA in NB4MTOE cells. Tretinoin 181-185 cyclin dependent kinase inhibitor 1A Homo sapiens 139-151
24962468-7 2014 RA-dependent expression in the ureteric trunk was also showed for the sodium channel subunit Scnn1b, which has been shown to be the marker gene of the collecting duct. Tretinoin 0-2 sodium channel, nonvoltage-gated 1 beta Mus musculus 93-99
24962468-11 2014 Our study thus identifies and characterizes RA-dependent up-regulated genes in kidney development, and suggests an involvement of NF-kappaB signaling in the branching morphogenesis. Tretinoin 44-46 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 130-139
24846415-1 2014 Src kinase-associated phosphoprotein 2 (Ra70/scap2), which was originally isolated as a retinoic acid (RA)-induced gene, associates with molecules that modulate integrin-survival signals. Tretinoin 88-101 src family associated phosphoprotein 2 Mus musculus 0-38
24846415-1 2014 Src kinase-associated phosphoprotein 2 (Ra70/scap2), which was originally isolated as a retinoic acid (RA)-induced gene, associates with molecules that modulate integrin-survival signals. Tretinoin 88-101 src family associated phosphoprotein 2 Mus musculus 40-44
24846415-1 2014 Src kinase-associated phosphoprotein 2 (Ra70/scap2), which was originally isolated as a retinoic acid (RA)-induced gene, associates with molecules that modulate integrin-survival signals. Tretinoin 88-101 src family associated phosphoprotein 2 Mus musculus 45-50
24846415-1 2014 Src kinase-associated phosphoprotein 2 (Ra70/scap2), which was originally isolated as a retinoic acid (RA)-induced gene, associates with molecules that modulate integrin-survival signals. Tretinoin 103-105 src family associated phosphoprotein 2 Mus musculus 0-38
24846415-1 2014 Src kinase-associated phosphoprotein 2 (Ra70/scap2), which was originally isolated as a retinoic acid (RA)-induced gene, associates with molecules that modulate integrin-survival signals. Tretinoin 103-105 src family associated phosphoprotein 2 Mus musculus 40-44
24846415-1 2014 Src kinase-associated phosphoprotein 2 (Ra70/scap2), which was originally isolated as a retinoic acid (RA)-induced gene, associates with molecules that modulate integrin-survival signals. Tretinoin 103-105 src family associated phosphoprotein 2 Mus musculus 45-50
24846415-3 2014 In the present study, we demonstrate that Ra70/scap2 mRNA is temporally expressed during the RA-induced neuronal differentiation of P19 embryonic carcinoma cells. Tretinoin 93-95 src family associated phosphoprotein 2 Mus musculus 42-46
24846415-3 2014 In the present study, we demonstrate that Ra70/scap2 mRNA is temporally expressed during the RA-induced neuronal differentiation of P19 embryonic carcinoma cells. Tretinoin 93-95 src family associated phosphoprotein 2 Mus musculus 47-52
25029539-1 2014 Stra8 (Stimulated by Retinoic Acid 8) is considered a meiotic gatekeeper gene. Tretinoin 21-34 stimulated by retinoic acid 8 Sus scrofa 0-5
24821728-3 2014 We found that PLZF-RARalpha can repress transcription of the p21WAF/CDKN1A gene, which encodes the negative cell cycle regulator p21 by binding to its proximal promoter Sp1-binding GC-boxes 3, 4, 5/6, a retinoic acid response element (RARE), and distal p53-responsive elements (p53REs). Tretinoin 203-216 cyclin dependent kinase inhibitor 1A Homo sapiens 68-74
24821728-3 2014 We found that PLZF-RARalpha can repress transcription of the p21WAF/CDKN1A gene, which encodes the negative cell cycle regulator p21 by binding to its proximal promoter Sp1-binding GC-boxes 3, 4, 5/6, a retinoic acid response element (RARE), and distal p53-responsive elements (p53REs). Tretinoin 203-216 cyclin dependent kinase inhibitor 1A Homo sapiens 61-64
24220301-0 2014 Retinoic acid prevents mesenteric lymph node dendritic cells from inducing IL-13-producing inflammatory Th2 cells. Tretinoin 0-13 interleukin 13 Mus musculus 75-80
24686085-4 2014 Cells treated with ATRA for 48h followed by one hour of PP2 incubation show SFK/Lyn kinase inhibition. Tretinoin 19-23 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 80-83
24686085-5 2014 We observed that Lyn inhibition blocked c-Cbl and p85/p55 PI3K phosphorylation driven by the anti-CD38 agonistic mAb IB4 in ATRA-treated HL-60 cells and untreated CD38+ transfectants. Tretinoin 124-128 extracellular matrix protein 1 Mus musculus 50-53
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 77-81 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 59-62
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 105-109 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 59-62
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 105-109 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 190-193
24686085-11 2014 Therefore, Lyn kinase activity is important for CD38-associated signaling that may drive ATRA-induced differentiation. Tretinoin 89-93 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 11-14
24908182-0 2014 Role of CX3CL1 in the chemotactic migration of all-trans retinoic acid-treated acute promyelocytic leukemic cells toward apoptotic cells. Tretinoin 57-70 C-X3-C motif chemokine ligand 1 Homo sapiens 8-14
24908182-5 2014 The current study investigated the role of CX3CL1 in the chemoattraction of all-trans retinoic acid (ATRA)-treated NB4 (ATRA-NB4) cells toward apoptotic cells. Tretinoin 86-99 C-X3-C motif chemokine ligand 1 Homo sapiens 43-49
24908182-5 2014 The current study investigated the role of CX3CL1 in the chemoattraction of all-trans retinoic acid (ATRA)-treated NB4 (ATRA-NB4) cells toward apoptotic cells. Tretinoin 101-105 C-X3-C motif chemokine ligand 1 Homo sapiens 43-49
24641925-0 2014 Atypical Clinical Presentation of ACTH-Dependent Cushing"s Syndrome in a Patient Treated with Retinoic Acid. Tretinoin 94-107 proopiomelanocortin Homo sapiens 34-38
24641925-3 2014 METHODS: We report an atypical presentation of adrenocorticotropic hormone (ACTH)-dependent CS in a patient treated with retinoic acid due to severe acne. Tretinoin 121-134 proopiomelanocortin Homo sapiens 47-74
24641925-3 2014 METHODS: We report an atypical presentation of adrenocorticotropic hormone (ACTH)-dependent CS in a patient treated with retinoic acid due to severe acne. Tretinoin 121-134 proopiomelanocortin Homo sapiens 76-80
24641925-11 2014 CONCLUSION: Retinoic acid treatment may alter the clinical presentation of ACTH-dependent CS and consequently delay the diagnosis. Tretinoin 12-25 proopiomelanocortin Homo sapiens 75-79
24220301-3 2014 This subset expressed homing receptors for skin and inflammatory sites, and was mainly induced by B220(-)CD8alpha(-)CD11b(+)CD103(-) MLN-DCs in an IL-6- and OX40 ligand-dependent manner, whereas RA inhibited this induction. Tretinoin 195-197 integrin alpha M Mus musculus 116-121
24220301-10 2014 These results suggest that RA inhibits allergic responses to oral antigens by preventing MLN-DCs from inducing IL-13-producing inflammatory Th2 cells. Tretinoin 27-29 interleukin 13 Mus musculus 111-116
25161869-9 2014 Finally, we analyzed the effect of retinoic acid (RA), a potent stimulator of keratinocyte proliferation, on AQP3 and AQP9 mRNA expression in differentiated NHEK. Tretinoin 50-52 aquaporin 9 Homo sapiens 118-122
24959230-0 2014 All-trans retinoic acid enhances the effect of 5-aza-2"-deoxycytidine on p16INK4a demethylation, and the two drugs synergistically activate retinoic acid receptor beta gene expression in the human erythroleukemia K562 cell line. Tretinoin 10-23 cyclin dependent kinase inhibitor 2A Homo sapiens 73-81
24959230-6 2014 DAC alone induced the demethylation of the p16 gene, and combination of DAC and ATRA demonstrated more evident demethylation of the p16 gene, however, ATRA alone had no effect on methylation. Tretinoin 80-84 cyclin dependent kinase inhibitor 2A Homo sapiens 132-135
24959230-8 2014 DAC in combination with ATRA appeared to produce a greater activation of the RAR-beta gene, which led to the upregulation of the RAR-beta expression level. Tretinoin 24-28 retinoic acid receptor beta Homo sapiens 77-85
24959230-8 2014 DAC in combination with ATRA appeared to produce a greater activation of the RAR-beta gene, which led to the upregulation of the RAR-beta expression level. Tretinoin 24-28 retinoic acid receptor beta Homo sapiens 129-137
24959230-9 2014 ATRA enhanced the effect of DAC on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression, which indicated that DAC used in combination with ATRA has clinical potential in the treatment of human erythroleukemia. Tretinoin 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 35-38
24959230-9 2014 ATRA enhanced the effect of DAC on p16 demethylation, and the combination of the two drugs was found to activate RAR-beta expression, which indicated that DAC used in combination with ATRA has clinical potential in the treatment of human erythroleukemia. Tretinoin 184-188 retinoic acid receptor beta Homo sapiens 113-121
25161869-9 2014 Finally, we analyzed the effect of retinoic acid (RA), a potent stimulator of keratinocyte proliferation, on AQP3 and AQP9 mRNA expression in differentiated NHEK. Tretinoin 35-48 aquaporin 9 Homo sapiens 118-122
25161869-10 2014 Stimulation with RA at 1 muM for 24 h augmented AQP3 expression and down-regulated AQP9 expression. Tretinoin 17-19 aquaporin 9 Homo sapiens 83-87
24677291-0 2014 Retinoic acid induces mouse bone marrow-derived CD15+, Oct4+ and CXCR4+ stem cells into male germ-like cells in a two-dimensional cell culture system. Tretinoin 0-13 fucosyltransferase 4 Mus musculus 48-52
24939938-5 2014 Loss-of-function analysis demonstrates that two lncRNAs, LL18/NANCI (Nkx2.1-associated noncoding intergenic RNA) and LL34, play distinct roles in endoderm development by controlling expression of critical developmental transcription factors and pathways, including retinoic acid signaling. Tretinoin 265-278 NK2 homeobox 1 Homo sapiens 69-75
24902847-10 2014 We also demonstrate that Hoxb1b regulates nucleosome organization at the hoxb1a promoter and that retinoic acid acts independently of hoxb1b to activate hoxb1a expression. Tretinoin 98-111 homeobox B1a Danio rerio 153-159
24902847-14 2014 Lastly, our data reveal independent regulation of hoxb1a expression by retinoic acid and Hoxb1b in zebrafish. Tretinoin 71-84 homeobox B1a Danio rerio 50-56
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 206-209
24894398-11 2014 CONCLUSIONS: All-trans-retinoic acid inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, most likely by attenuating the formation of actin stress fibers and focal adhesions as well as signaling by MAPKs, c-Jun, and Smads. Tretinoin 13-36 transforming growth factor beta 1 Homo sapiens 47-55
24959884-0 2014 Nuclear MEK1 sequesters PPARgamma and bisects MEK1/ERK signaling: a non-canonical pathway of retinoic acid inhibition of adipocyte differentiation. Tretinoin 93-106 mitogen-activated protein kinase 1 Homo sapiens 51-54
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 26-28 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 231-234
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 26-28 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 236-239
24894398-7 2014 RESULTS: All-trans-retinoic acid inhibited TGF-beta-induced collagen gel contraction mediated by HTFs in a concentration- and time-dependent manner. Tretinoin 9-32 transforming growth factor beta 1 Homo sapiens 43-51
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 43-51
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 mitogen-activated protein kinase 1 Homo sapiens 125-162
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 mitogen-activated protein kinase 1 Homo sapiens 164-167
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 mitogen-activated protein kinase 14 Homo sapiens 170-173
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 179-204
24646031-6 2014 ATRA and vitamin D3 can also downregulate expression of G1 CDKs, especially CDK2 and CDK6. Tretinoin 0-4 cyclin dependent kinase 6 Homo sapiens 85-89
24677291-1 2014 We have examined the effect of retinoic acid (RA) on differentiation of bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells. Tretinoin 31-44 fucosyltransferase 4 Mus musculus 92-96
24677291-1 2014 We have examined the effect of retinoic acid (RA) on differentiation of bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells. Tretinoin 46-48 fucosyltransferase 4 Mus musculus 92-96
24677291-11 2014 Thus RA can induce differentiation of mouse bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells in vitro. Tretinoin 5-7 fucosyltransferase 4 Mus musculus 64-68
24790153-8 2014 Thus, we conclude that ATRA enhances both Arg-1 and iNOS expression in IFN-gamma-treated DCs, resulting in a tolerogenic phenotype. Tretinoin 23-27 nitric oxide synthase 2, inducible Mus musculus 52-56
24790153-4 2014 Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Tretinoin 60-64 eukaryotic translation initiation factor 2 alpha kinase 4 Mus musculus 293-297
24720764-0 2014 Retinoic acid reduces migration of human breast cancer cells: role of retinoic acid receptor beta. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 70-97
24720764-5 2014 Administration of retinoic acid (RA) in breast cancer cells induced RARbeta gene expression that was greatest after 72 hrs with a concentration 1 muM. Tretinoin 18-31 retinoic acid receptor beta Homo sapiens 68-75
24720764-5 2014 Administration of retinoic acid (RA) in breast cancer cells induced RARbeta gene expression that was greatest after 72 hrs with a concentration 1 muM. Tretinoin 18-31 latexin Homo sapiens 146-149
24720764-5 2014 Administration of retinoic acid (RA) in breast cancer cells induced RARbeta gene expression that was greatest after 72 hrs with a concentration 1 muM. Tretinoin 33-35 retinoic acid receptor beta Homo sapiens 68-75
24720764-5 2014 Administration of retinoic acid (RA) in breast cancer cells induced RARbeta gene expression that was greatest after 72 hrs with a concentration 1 muM. Tretinoin 33-35 latexin Homo sapiens 146-149
24720764-6 2014 High concentrations of RA increased the expression of RARbeta causing an inhibition of the 60% in cell migration and significantly decreased the expression of migration-related proteins [moesin, c-Src and focal adhesion kinase (FAK)]. Tretinoin 23-25 retinoic acid receptor beta Homo sapiens 54-61
24720764-6 2014 High concentrations of RA increased the expression of RARbeta causing an inhibition of the 60% in cell migration and significantly decreased the expression of migration-related proteins [moesin, c-Src and focal adhesion kinase (FAK)]. Tretinoin 23-25 moesin Homo sapiens 187-193
24720764-6 2014 High concentrations of RA increased the expression of RARbeta causing an inhibition of the 60% in cell migration and significantly decreased the expression of migration-related proteins [moesin, c-Src and focal adhesion kinase (FAK)]. Tretinoin 23-25 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 195-200
24790153-8 2014 Thus, we conclude that ATRA enhances both Arg-1 and iNOS expression in IFN-gamma-treated DCs, resulting in a tolerogenic phenotype. Tretinoin 23-27 interferon gamma Mus musculus 71-80
24714214-7 2014 Treatment with ATRA and NaBu synergistically attenuated the expression of alpha-SMA and PCNA and reduced systolic blood pressure in Npr1(+/-) mice. Tretinoin 15-19 actin alpha 2, smooth muscle, aorta Mus musculus 74-83
24456325-2 2014 In the present study, we have investigated the neuroprotective effects of insulin on H2O2-induced toxicity of retinoic acid (RA)-differentiated SH-SY5Y cells. Tretinoin 110-123 insulin Homo sapiens 74-81
24484607-4 2014 Four-day ATRA treatment increases beta-secretase 1 (BACE1) level, Abeta1-42 production, and receptor for advanced glycation end-products (RAGE) expression. Tretinoin 9-13 beta-secretase 1 Homo sapiens 34-50
24484607-4 2014 Four-day ATRA treatment increases beta-secretase 1 (BACE1) level, Abeta1-42 production, and receptor for advanced glycation end-products (RAGE) expression. Tretinoin 9-13 beta-secretase 1 Homo sapiens 52-57
24484607-5 2014 RAGE is a well-recognized receptor for Abeta, and the block of both RAGE and Abeta1-42 with specific antibodies strongly impairs neurite formation in ATRA-treated cells. Tretinoin 150-154 amyloid beta precursor protein Homo sapiens 39-44
24680851-4 2014 The expression of E-cadherin, Occludin and Claudin-1 proteins were up-regulated after treatment with atRA for 6h to 48 h. We concluded that atRA could promote the epithelial barrier function of myopia RPE monolayer possibly by regulating expression of intercellular junction-associated proteins. Tretinoin 101-105 claudin-1 Cavia porcellus 43-52
24733397-4 2014 The RDH10-activated DHRS3 acts as a robust high affinity all-trans-retinaldehyde-specific reductase that effectively converts retinaldehyde back to retinol, decreasing the rate of retinoic acid biosynthesis. Tretinoin 180-193 retinol dehydrogenase 10 (all-trans) Mus musculus 4-9
24576537-2 2014 CYP26B1 is known to be a male sex-promoting factor that inactivates retinoic acid (RA) in somatic cells. Tretinoin 68-81 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-7
24576537-2 2014 CYP26B1 is known to be a male sex-promoting factor that inactivates retinoic acid (RA) in somatic cells. Tretinoin 83-85 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-7
24576537-3 2014 In CYP26B1-null XY gonads, germ cells are exposed to a higher level of RA than in normal XY gonads and this activates Stra8 to induce meiosis while male-specific gene expression is suppressed. Tretinoin 71-73 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 3-10
24576537-10 2014 Taken together, we conclude that inhibition of RA is one of the essential factors to promote male germ cell differentiation, and that CYP26B1 suppresses two distinct genetic programs induced by RA: a Stra8-dependent meiotic pathway, and a Stra8-independent mitotic pathway. Tretinoin 194-196 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 134-141
24680851-4 2014 The expression of E-cadherin, Occludin and Claudin-1 proteins were up-regulated after treatment with atRA for 6h to 48 h. We concluded that atRA could promote the epithelial barrier function of myopia RPE monolayer possibly by regulating expression of intercellular junction-associated proteins. Tretinoin 140-144 claudin-1 Cavia porcellus 43-52
24522204-0 2014 Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells. Tretinoin 71-84 AKT serine/threonine kinase 1 Homo sapiens 40-43
24657437-0 2014 MicroRNA-432 contributes to dopamine cocktail and retinoic acid induced differentiation of human neuroblastoma cells by targeting NESTIN and RCOR1 genes. Tretinoin 50-63 nestin Homo sapiens 130-136
24705138-7 2014 Upon differentiation into the parietal endoderm by retinoic acid and cAMP, Lrh-1 promoter activity and transcripts were markedly reduced within 24 h. At the same time, Sox2 and Gabp binding to the promoter region of Lrh-1 were decreased, followed by a reduction of their expression. Tretinoin 51-64 nuclear receptor subfamily 5 group A member 2 Homo sapiens 216-221
24606396-6 2014 Treatment with 5-HT significantly enhanced the ATRA-induced expression of nestin, a specific marker for NPC, and phosphorylation of cAMP response element-binding protein (CREB). Tretinoin 47-51 cAMP responsive element binding protein 1 Mus musculus 132-169
24606396-6 2014 Treatment with 5-HT significantly enhanced the ATRA-induced expression of nestin, a specific marker for NPC, and phosphorylation of cAMP response element-binding protein (CREB). Tretinoin 47-51 cAMP responsive element binding protein 1 Mus musculus 171-175
24606396-8 2014 These findings suggest that stimulation of 5-HT4 receptors may enhance ATRA-induced neural differentiation of mouse iPS cells through activation of PKA and CREB. Tretinoin 71-75 cAMP responsive element binding protein 1 Mus musculus 156-160
24711541-6 2014 Furthermore, HIF-1alpha levels increase upon treatment of APL cells with all-trans retinoic acid (ATRA). Tretinoin 73-96 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23
24711541-6 2014 Furthermore, HIF-1alpha levels increase upon treatment of APL cells with all-trans retinoic acid (ATRA). Tretinoin 98-102 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23
24522204-8 2014 Activation of nuclear AKT during ATRA-mediated differentiation results in the phosphorylation of several proteins, including PHB2, which may serve to coordinate nuclear-mitochondrial events during differentiation. Tretinoin 33-37 AKT serine/threonine kinase 1 Homo sapiens 22-25
24522204-2 2014 In the human acute promyelocytic leukemia cell line NB4, nuclear AKT activity increases during all-trans retinoic acid (ATRA)-mediated differentiation. Tretinoin 105-118 AKT serine/threonine kinase 1 Homo sapiens 65-68
24522204-2 2014 In the human acute promyelocytic leukemia cell line NB4, nuclear AKT activity increases during all-trans retinoic acid (ATRA)-mediated differentiation. Tretinoin 120-124 AKT serine/threonine kinase 1 Homo sapiens 65-68
24522204-3 2014 As nuclear AKT activity is associated with differentiation, we sought to identify the nuclear substrates of AKT that were phosphorylated after ATRA treatment. Tretinoin 143-147 AKT serine/threonine kinase 1 Homo sapiens 11-14
24522204-3 2014 As nuclear AKT activity is associated with differentiation, we sought to identify the nuclear substrates of AKT that were phosphorylated after ATRA treatment. Tretinoin 143-147 AKT serine/threonine kinase 1 Homo sapiens 108-111
24522204-4 2014 A proteomics-based search for nuclear substrates of AKT in ATRA-treated NB4 cells was undertaken by using 2D-electrophoresis/mass spectrometry (MS) in combination with an anti-AKT phospho-substrate antibody. Tretinoin 59-63 AKT serine/threonine kinase 1 Homo sapiens 52-55
24522204-4 2014 A proteomics-based search for nuclear substrates of AKT in ATRA-treated NB4 cells was undertaken by using 2D-electrophoresis/mass spectrometry (MS) in combination with an anti-AKT phospho-substrate antibody. Tretinoin 59-63 AKT serine/threonine kinase 1 Homo sapiens 176-179
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 CCAAT enhancer binding protein alpha Homo sapiens 105-115
25112011-5 2014 In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. Tretinoin 13-15 lin-28 homolog A Homo sapiens 180-185
25112011-8 2014 In addition, the expression of adipogenic differentiation marker C/EBPalpha was increased while the osteogenic differentiation marker OPN was decreased in EBs after RA treatment for 5 days. Tretinoin 165-167 CCAAT enhancer binding protein alpha Homo sapiens 65-75
24769642-4 2014 Taken together, we concluded that the combination of ATRA and staurosporine could overcome differentiation block via MEK/ERK signaling pathway in ATRA-resistant APL cell lines. Tretinoin 53-57 mitogen-activated protein kinase kinase 7 Homo sapiens 117-120
24769642-4 2014 Taken together, we concluded that the combination of ATRA and staurosporine could overcome differentiation block via MEK/ERK signaling pathway in ATRA-resistant APL cell lines. Tretinoin 53-57 mitogen-activated protein kinase 1 Homo sapiens 121-124
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 MLLT3 super elongation complex subunit Homo sapiens 140-143
24769646-4 2014 Combining ATRA with cytarabine had a synergistic antileukemic effect in MLL-AF9-positive cells in vitro. Tretinoin 10-14 MLLT3 super elongation complex subunit Homo sapiens 76-79
24656387-8 2014 We conclude that OFO-mediated teratogenesis is associated with disturbed RA metabolism in the dams and fetuses caused, at least in part, by modulation of PPARalpha and AhR transactivity by the oxidized components in OFO. Tretinoin 73-75 peroxisome proliferator activated receptor alpha Mus musculus 154-163
24399651-0 2014 The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma. Tretinoin 45-58 tumor protein p53 Homo sapiens 62-65
24399651-6 2014 The results showed that U87-p53(R273H) cells generated more rapid neurosphere growth than U87-p53(wt) but inhibition of neurosphere proliferation was seen with both ATO and ATRA. Tretinoin 173-177 tumor protein p53 Homo sapiens 28-31
24399651-7 2014 U87-p53(R273H) neurospheres showed resistance to differentiation into glial cells and neuronal cells with ATO and ATRA exposure. Tretinoin 114-118 tumor protein p53 Homo sapiens 4-7
24399651-8 2014 ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner. Tretinoin 132-136 tumor protein p53 Homo sapiens 74-77
24399651-8 2014 ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner. Tretinoin 132-136 tumor protein p53 Homo sapiens 90-93
24399651-9 2014 Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment. Tretinoin 113-117 tumor protein p53 Homo sapiens 21-24
24399651-9 2014 Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment. Tretinoin 113-117 tumor protein p53 Homo sapiens 52-55
25151738-5 2014 The mechanism of quercetin enhancing ability of retinoic acid on the induction of RARbeta, activating TPO, using as COX-2 and PDEs inhibitor was approved by biomolecular network and related literatures. Tretinoin 48-61 retinoic acid receptor, beta Rattus norvegicus 82-89
24599963-0 2014 Retinoic acid isomers facilitate apolipoprotein E production and lipidation in astrocytes through the retinoid X receptor/retinoic acid receptor pathway. Tretinoin 0-13 apolipoprotein E Mus musculus 33-49
24599963-0 2014 Retinoic acid isomers facilitate apolipoprotein E production and lipidation in astrocytes through the retinoid X receptor/retinoic acid receptor pathway. Tretinoin 122-135 apolipoprotein E Mus musculus 33-49
24599963-6 2014 Here, we report that retinoic acid (RA) isomers, including all-trans-RA, 9-cis-RA, and 13-cis-RA, significantly increase apoE secretion to ~4-fold of control through retinoid X receptor (RXR) and RA receptor. Tretinoin 21-34 apolipoprotein E Mus musculus 121-125
24599963-6 2014 Here, we report that retinoic acid (RA) isomers, including all-trans-RA, 9-cis-RA, and 13-cis-RA, significantly increase apoE secretion to ~4-fold of control through retinoid X receptor (RXR) and RA receptor. Tretinoin 36-38 apolipoprotein E Mus musculus 121-125
24599963-6 2014 Here, we report that retinoic acid (RA) isomers, including all-trans-RA, 9-cis-RA, and 13-cis-RA, significantly increase apoE secretion to ~4-fold of control through retinoid X receptor (RXR) and RA receptor. Tretinoin 59-71 apolipoprotein E Mus musculus 121-125
24694234-4 2014 We found that retinoic acid-inducible gene-I (RIG-1) is significantly elevated in the temporal cortex and plasma in patients with MCI. Tretinoin 14-27 phospholipase A and acyltransferase 4 Homo sapiens 46-51
24726878-5 2014 The retinoic-acid-degrading enzyme Cyp26b1 is highly expressed in skin fibroblasts, and its inhibition resulted in the upregulation of P2X7 on MCs. Tretinoin 4-17 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 35-42
24726878-5 2014 The retinoic-acid-degrading enzyme Cyp26b1 is highly expressed in skin fibroblasts, and its inhibition resulted in the upregulation of P2X7 on MCs. Tretinoin 4-17 purinergic receptor P2X 7 Homo sapiens 135-139
24726878-6 2014 We also noted the increased expression of P2X7 on skin MCs and consequent P2X7- and MC-dependent dermatitis (so-called retinoid dermatitis) in the presence of excessive amounts of retinoic acid. Tretinoin 180-193 purinergic receptor P2X 7 Homo sapiens 42-46
24739462-5 2014 The differentiation agent, retinoic acid, increases IKKalpha expression by suppressing EZH2-mediated H3K27 histone methylation, resulting in enhanced differentiation of NPC cells. Tretinoin 27-40 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 87-91
24410928-0 2014 All-trans-retinoic acid ameliorates the inflammation by inducing transforming growth factor beta 1 and interleukin 10 in mouse epididymitis. Tretinoin 0-23 interleukin 10 Mus musculus 103-117
24410928-7 2014 RESULTS: Our results demonstrate that atRA ameliorates the inflammation in mouse epididymitis by decreasing the expression of the pro-inflammatory cytokines and increasing the expression of anti-inflammatory factors including TGF-beta1 and IL-10. Tretinoin 38-42 interleukin 10 Mus musculus 240-245
24410928-8 2014 Our results show that the upregulating effect of atRA on TGF-beta1 was mediated by RARalpha, and the enhancing effect of atRA on IL-10 expression was mediated via RARbeta. Tretinoin 121-125 interleukin 10 Mus musculus 129-134
24667328-9 2014 Our results suggest that localized expression of Cyp26 enzymes cell non-autonomously defines the boundaries between the cardiac and VP fields within the ALPM through regulating RA levels, which ensures a proper balance of myocardial and endothelial lineages. Tretinoin 177-179 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 49-54
24496080-6 2014 RA was found to induce mRNA and protein expression of Patched 1 (Ptch1), the Hh ligand receptor and negative regulator of this pathway. Tretinoin 0-2 patched 1 Homo sapiens 54-63
24496080-6 2014 RA was found to induce mRNA and protein expression of Patched 1 (Ptch1), the Hh ligand receptor and negative regulator of this pathway. Tretinoin 0-2 patched 1 Homo sapiens 65-70
24496080-11 2014 Notably, this enhanced Ptch1 expression was preceded by induction of the homeobox transcription factor Meis1, a direct RA target. Tretinoin 119-121 patched 1 Homo sapiens 23-28
24496080-14 2014 Taken together, these findings reveal a previously unrecognized mechanism through which RA can inhibit the Hh pathway via Ptch1 induction. Tretinoin 88-90 patched 1 Homo sapiens 122-127
24635079-9 2014 In addition, ATRA significantly decreased the phosphorylation of ERK1/2 and JNK1/2, and inhibited AP-1 transcriptional activity. Tretinoin 13-17 mitogen-activated protein kinase 3 Homo sapiens 65-71
24635079-9 2014 In addition, ATRA significantly decreased the phosphorylation of ERK1/2 and JNK1/2, and inhibited AP-1 transcriptional activity. Tretinoin 13-17 mitogen-activated protein kinase 8 Homo sapiens 76-82
24635079-10 2014 CONCLUSIONS: ATRA induces cell-cycle arrest in human cSCC cells by inhibiting the mitogen-activated protein kinase (MAPK)-AP1 pathway, and could be effective in the prevention and chemotherapy of human cSCC. Tretinoin 13-17 mitogen-activated protein kinase 3 Homo sapiens 116-120
24667328-2 2014 RA levels in embryos are dampened by Cyp26 enzymes, which metabolize RA into easily degraded derivatives. Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 37-42
24667328-2 2014 RA levels in embryos are dampened by Cyp26 enzymes, which metabolize RA into easily degraded derivatives. Tretinoin 69-71 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 37-42
24334138-0 2014 Retinoic acid inhibits pancreatic cancer cell migration and EMT through the downregulation of IL-6 in cancer associated fibroblast cells. Tretinoin 0-13 interleukin 6 Homo sapiens 94-98
24334138-3 2014 We treated CAFs with RA and found that these cells became static due to the low expression of alpha-SMA, FAP, and IL-6 and decreased production of extracellular matrix (ECM). Tretinoin 21-23 interleukin 6 Homo sapiens 114-118
24334138-4 2014 Furthermore, we verified that the low secretion of IL-6 from CAFs was related to RA-induced inhibition of migration and epithelial-mesenchymal transition (EMT) of tumor cells. Tretinoin 81-83 interleukin 6 Homo sapiens 51-55
24791595-0 2014 The effect to IL-3Ralpha, downstream PI3k/Akt signaling of all-trans retinoic acid and arsenic trioxide in NB4 cells. Tretinoin 69-82 AKT serine/threonine kinase 1 Homo sapiens 42-45
24523292-4 2014 Retinoic acid treatment results in reduced wnt signaling, which leads to loss of the fmyhc2.1 domain. Tretinoin 0-13 myosin, heavy polypeptide 2, fast muscle specific Danio rerio 85-93
23190197-0 2014 Retinoic acid improves recovery after nephrectomy and decreases renal TGF-beta1 expression. Tretinoin 0-13 transforming growth factor, beta 1 Rattus norvegicus 70-79
23190197-16 2014 Glomerular expression of TGF-beta1 was lower in ATRA-treated animals than in controls. Tretinoin 48-52 transforming growth factor, beta 1 Rattus norvegicus 25-34
24492652-3 2014 Previous studies from our laboratory demonstrated that all-trans-retinoic acid (atRA) is a potent suppressor of CYP7A1, the rate-limiting enzyme in bile acid synthesis. Tretinoin 55-78 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 112-118
24492652-3 2014 Previous studies from our laboratory demonstrated that all-trans-retinoic acid (atRA) is a potent suppressor of CYP7A1, the rate-limiting enzyme in bile acid synthesis. Tretinoin 80-84 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 112-118
24316159-12 2014 Our findings indicate that topical application of ATRA can inhibit fibroblast proliferation, decrease TGF-beta1 and IL-6 expression level, and prevent epidural scar adhesion in rats. Tretinoin 50-54 transforming growth factor, beta 1 Rattus norvegicus 102-111
24316159-12 2014 Our findings indicate that topical application of ATRA can inhibit fibroblast proliferation, decrease TGF-beta1 and IL-6 expression level, and prevent epidural scar adhesion in rats. Tretinoin 50-54 interleukin 6 Rattus norvegicus 116-120
24637840-0 2014 Expression analysis of SOX14 during retinoic acid induced neural differentiation of embryonal carcinoma cells and assessment of the effect of its ectopic expression on SOXB members in HeLa cells. Tretinoin 36-49 SRY-box transcription factor 14 Homo sapiens 23-28
24642534-0 2014 NADPH-cytochrome P450 reductase is regulated by all-trans retinoic acid and by 1,25-dihydroxyvitamin D3 in human acute myeloid leukemia cells. Tretinoin 48-71 cytochrome p450 oxidoreductase Homo sapiens 0-31
24642534-3 2014 Inside the cells 1,25D is degraded to calcitrioic acid by a mitochondrial enzyme CYP24A1, while ATRA is degraded to several polar metabolites by CYP26. Tretinoin 96-100 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 145-150
24767374-6 2014 Additionally, an in vitro study demonstrated that the down-regulation of brain-derived neurotrophic factor (BDNF) gene expression by CRP treatment in retinoic acid (RA) differentiated SH-SY5Y neuroblastoma cells. Tretinoin 150-163 C-reactive protein Homo sapiens 133-136
24767374-6 2014 Additionally, an in vitro study demonstrated that the down-regulation of brain-derived neurotrophic factor (BDNF) gene expression by CRP treatment in retinoic acid (RA) differentiated SH-SY5Y neuroblastoma cells. Tretinoin 165-167 C-reactive protein Homo sapiens 133-136
24608339-4 2014 Immunohistochemistry was performed on the tissue microarray using monoclonal antibodies which we have developed to the retinoic acid metabolising enzymes CYP26A1, CYP26B1, CYP26C1 and lecithin retinol acyl transferase (LRAT) using a semi-quantitative scoring scheme to assess expression. Tretinoin 119-132 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 154-161
24618783-7 2014 T3 had opposing influences on retinoic acid synthesizing enzymes, increasing the expression of Aldh1a1, and decreasing Aldh1a3, while increasing the retinoic acid degrading enzyme Cyp26b1. Tretinoin 149-162 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 180-187
24608339-4 2014 Immunohistochemistry was performed on the tissue microarray using monoclonal antibodies which we have developed to the retinoic acid metabolising enzymes CYP26A1, CYP26B1, CYP26C1 and lecithin retinol acyl transferase (LRAT) using a semi-quantitative scoring scheme to assess expression. Tretinoin 119-132 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 163-170
24608339-12 2014 This study has shown that the retinoic acid metabolising enzymes CYP26A1, CYP26B1 and LRAT are significantly overexpressed in colorectal cancer and that CYP26B1 and LRAT are significantly associated with prognosis both in the total cohort and in those tumours which are mismatch repair proficient. Tretinoin 30-43 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 65-72
24608339-12 2014 This study has shown that the retinoic acid metabolising enzymes CYP26A1, CYP26B1 and LRAT are significantly overexpressed in colorectal cancer and that CYP26B1 and LRAT are significantly associated with prognosis both in the total cohort and in those tumours which are mismatch repair proficient. Tretinoin 30-43 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 74-81
24608339-12 2014 This study has shown that the retinoic acid metabolising enzymes CYP26A1, CYP26B1 and LRAT are significantly overexpressed in colorectal cancer and that CYP26B1 and LRAT are significantly associated with prognosis both in the total cohort and in those tumours which are mismatch repair proficient. Tretinoin 30-43 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 153-160
24406248-4 2014 ATRA at a therapeutic concentration (1 muM) induced granulocytic differentiation, followed by apoptosis. Tretinoin 0-4 latexin Homo sapiens 39-42
24374174-0 2014 Retinoic acid remodels extracellular matrix (ECM) of cultured human fetal palate mesenchymal cells (hFPMCs) through down-regulation of TGF-beta/Smad signaling. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 135-143
24374174-0 2014 Retinoic acid remodels extracellular matrix (ECM) of cultured human fetal palate mesenchymal cells (hFPMCs) through down-regulation of TGF-beta/Smad signaling. Tretinoin 0-13 SMAD family member 7 Homo sapiens 144-148
24374174-3 2014 RA dose-dependently inhibited cell proliferation and mRNA and protein levels of ECM components fibronectin, tenascin C and fibrillin-2. Tretinoin 0-2 fibronectin 1 Homo sapiens 95-106
24374174-6 2014 Because of the pivotal role of TGF-beta/Smad pathway in palatogenesis we therefore checked the effect of RA on TGF-beta/Smad signaling. Tretinoin 105-107 transforming growth factor beta 1 Homo sapiens 111-119
24374174-6 2014 Because of the pivotal role of TGF-beta/Smad pathway in palatogenesis we therefore checked the effect of RA on TGF-beta/Smad signaling. Tretinoin 105-107 SMAD family member 7 Homo sapiens 120-124
24374174-9 2014 In conclusion, these findings suggested that RA overexposure inhibited cell proliferation and disrupted the ECM network through down-regulation of TGF-beta/Smad pathway. Tretinoin 45-47 transforming growth factor beta 1 Homo sapiens 147-155
24374174-9 2014 In conclusion, these findings suggested that RA overexposure inhibited cell proliferation and disrupted the ECM network through down-regulation of TGF-beta/Smad pathway. Tretinoin 45-47 SMAD family member 7 Homo sapiens 156-160
24584857-4 2014 In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 96-109 CCAAT enhancer binding protein alpha Homo sapiens 22-27
24584857-4 2014 In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 111-115 CCAAT enhancer binding protein alpha Homo sapiens 22-27
24406248-5 2014 ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3beta. Tretinoin 0-4 caspase 3 Homo sapiens 39-48
24406248-5 2014 ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3beta. Tretinoin 0-4 poly(ADP-ribose) polymerase 1 Homo sapiens 65-69
24406248-5 2014 ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3beta. Tretinoin 0-4 AKT serine/threonine kinase 1 Homo sapiens 139-142
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 17-21 CD33 molecule Homo sapiens 147-150
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 172-176 CD33 molecule Homo sapiens 147-150
24500985-0 2014 Effects of all-trans retinoic acid on signal pathway of cyclooxygenase-2 and Smad3 in transforming growth factor-beta-stimulated glomerular mesangial cells. Tretinoin 11-34 SMAD family member 3 Rattus norvegicus 77-82
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2 Homo sapiens 95-101
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 ATP binding cassette subfamily G member 1 Homo sapiens 140-145
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 mitogen-activated protein kinase kinase 6 Homo sapiens 231-237
24451020-6 2014 Melanocytes after treatment with increasing concentrations of HQ, RA, SLS and urushiol showed significant increases in intracellular and extracellular S100B expression with reduced viable cell number and increased release of lactate dehydrogenase. Tretinoin 66-68 S100 calcium binding protein B Homo sapiens 151-156
24451020-9 2014 The numerical decrease in S100B/c-kit-double-positive melanocytes was also examined in human skin epidermis irritated by HQ or RA with stronger staining intensities of S100B. Tretinoin 127-129 S100 calcium binding protein B Homo sapiens 26-31
24500985-3 2014 In this study, the mRNA and protein of Smad3, Smad7, and COX-2 were detected by reverse transcription-polymerase chain reaction and Western blot, respectively, in mesangial cells stimulated by transforming growth factor-beta (TGF-beta) and treated with ATRA at various concentrations and times. Tretinoin 253-257 SMAD family member 3 Rattus norvegicus 39-44
24451020-9 2014 The numerical decrease in S100B/c-kit-double-positive melanocytes was also examined in human skin epidermis irritated by HQ or RA with stronger staining intensities of S100B. Tretinoin 127-129 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 32-37
24451020-9 2014 The numerical decrease in S100B/c-kit-double-positive melanocytes was also examined in human skin epidermis irritated by HQ or RA with stronger staining intensities of S100B. Tretinoin 127-129 S100 calcium binding protein B Homo sapiens 168-173
24500985-7 2014 The expression of Smad3, Smad7, and COX-2 mRNA and protein was increased by exogenous TGF-beta, but inhibited by pretreatment of ATRA, in dose and time-dependent manners. Tretinoin 129-133 SMAD family member 3 Rattus norvegicus 18-23
24500985-7 2014 The expression of Smad3, Smad7, and COX-2 mRNA and protein was increased by exogenous TGF-beta, but inhibited by pretreatment of ATRA, in dose and time-dependent manners. Tretinoin 129-133 SMAD family member 7 Rattus norvegicus 25-30
24500985-10 2014 Moreover, ATRA reversed the translocation of Smad3 and Smad7 induced by TGF-beta. Tretinoin 10-14 SMAD family member 3 Rattus norvegicus 45-50
24500985-10 2014 Moreover, ATRA reversed the translocation of Smad3 and Smad7 induced by TGF-beta. Tretinoin 10-14 SMAD family member 7 Rattus norvegicus 55-60
24500985-10 2014 Moreover, ATRA reversed the translocation of Smad3 and Smad7 induced by TGF-beta. Tretinoin 10-14 transforming growth factor, beta 1 Rattus norvegicus 72-80
24500985-12 2014 ATRA dose-dependently inhibited TGF-beta-induced cell proliferation, but had no significant effect on apoptosis in rat mesangial cells. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 32-40
24500985-13 2014 Therefore, ATRA repressed COX-2, PGE2, and TXA2 via the TGF-beta/Smad-signaling pathway and inhibited mesangial-cell proliferation, which might subsequently prevent renal fibrosis. Tretinoin 11-15 transforming growth factor, beta 1 Rattus norvegicus 56-64
24470498-3 2014 This study reports that blood and lymphatic murine endothelial cells produce chemerin following retinoic acid stimulation. Tretinoin 96-109 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 77-85
24287141-10 2014 Finally, administration of all-trans-retinoic acid (inhibitor of Nrf-2) significantly abrogated baicalein-mediated protection against WBI-induced mortality in mice. Tretinoin 27-50 nuclear factor, erythroid derived 2, like 2 Mus musculus 65-70
24398846-6 2014 In an additional analysis for the role of asparagine synthetase, ATRA-mediated HL-60 cell differentiation was enhanced when asparagine in the culture media was depleted by an addition of L-asparaginase, indicating that downregulation of asparagine synthetase gene expression may be involved in the enhanced cell differentiation by STL compounds. Tretinoin 65-69 asparaginase and isoaspartyl peptidase 1 Homo sapiens 187-201
24613594-0 2014 The ciliary proteins Meckelin and Jouberin are required for retinoic acid-dependent neural differentiation of mouse embryonic stem cells. Tretinoin 60-73 transmembrane protein 67 Mus musculus 21-29
24613594-0 2014 The ciliary proteins Meckelin and Jouberin are required for retinoic acid-dependent neural differentiation of mouse embryonic stem cells. Tretinoin 60-73 Abelson helper integration site 1 Mus musculus 34-42
24470498-9 2014 In conclusion, this study reports that retinoic acid-activated endothelial cells can promote myeloid and plasmacytoid dendritic cell transmigration across endothelial cell monolayers through the endogenous production of chemerin, the upregulation of CCRL2, and the activation of dendritic cell beta1 integrin affinity. Tretinoin 39-52 retinoic acid receptor responder (tazarotene induced) 2 Mus musculus 220-228
23834309-5 2014 The in vitro effect of ATRA on lipopolysaccharide (LPS)-induced TNF-alpha production by human peripheral blood mononuclear cells (PBMC) was assessed by ELISA and RT-PCR. Tretinoin 23-27 tumor necrosis factor Homo sapiens 64-73
24404978-8 2014 RK in the presence of ATRA also increased the levels of mRNAs of osteocalcin, alpha1(I) collagen, and TGF-betas (TGF-beta1, TGF-beta2, and TGF-beta3) compared with ATRA only. Tretinoin 22-26 transforming growth factor, beta 2 Mus musculus 124-133
23834309-9 2014 In vitro, ATRA pretreatment decreased the overproduction of TNF-alpha by LPS-stimulated PBMC of ALD patients. Tretinoin 10-14 tumor necrosis factor Homo sapiens 60-69
24398626-9 2014 ATRA, an inducer of apoptosis or differentiation, dramatically enhanced FOXO1 expression while it repressed QKI expression. Tretinoin 0-4 forkhead box O1 Homo sapiens 72-77
24398626-10 2014 Importantly, the ATRA-induced increase in FOXO1 expression was dependent on QKI-mediated post-transcriptional regulation. Tretinoin 17-21 forkhead box O1 Homo sapiens 42-47
24709904-5 2014 Expression of the i21-VEGFR-1 is upregulated by the Notch signaling pathway and repressed by miR-200c and retinoic acid in breast cancer cells. Tretinoin 106-119 fms related receptor tyrosine kinase 1 Homo sapiens 18-29
24318876-7 2014 Retinoic acid, an endogenous compound that induces SHP, exhibited decreased hepatic levels during pregnancy in Tg-CYP2D6 mice. Tretinoin 0-13 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 114-120
24318876-8 2014 Administration of all-trans-retinoic acid led to a significant decrease in the expression and activity of hepatic CYP2D6 in Tg-CYP2D6 mice. Tretinoin 18-41 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 114-120
24318876-8 2014 Administration of all-trans-retinoic acid led to a significant decrease in the expression and activity of hepatic CYP2D6 in Tg-CYP2D6 mice. Tretinoin 18-41 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 127-133
24527392-3 2014 Here, we show that retinoic acid (RA) regulates early human prostate epithelial differentiation by activating a tightly coexpressed set of 80 genes (e.g., TMPRSS2). Tretinoin 19-32 transmembrane serine protease 2 Homo sapiens 155-162
24503540-5 2014 We found that ASCs cultured with ATRA or transfected with miRNA let-7e expressed epithelial markers such as cytokeratin-18 and early renal organogenesis markers such as Pax2, Wt1, Wnt4 and megalin. Tretinoin 33-37 WT1 transcription factor Homo sapiens 175-178
24527392-3 2014 Here, we show that retinoic acid (RA) regulates early human prostate epithelial differentiation by activating a tightly coexpressed set of 80 genes (e.g., TMPRSS2). Tretinoin 34-36 transmembrane serine protease 2 Homo sapiens 155-162
24330068-0 2014 Nuclear Raf-1 kinase regulates the CXCR5 promoter by associating with NFATc3 to drive retinoic acid-induced leukemic cell differentiation. Tretinoin 86-99 nuclear factor of activated T cells 3 Homo sapiens 70-76
24395056-10 2014 The 2-nM retinoic acid exposure also led to alterations of neurobehavior- and optic nerve-related genes, with the transforming growth factor-beta signal transduction inhibitor noggin (nog) and the spinal cord marker homeobox c3a (hox) being underexpressed and the retinal G protein-coupled receptor a (rgr), the photoreceptor cell marker rhodopsin (rho), and the short wave-sensitive cone pigment opsin 1 (opn1sw1) being overexpressed. Tretinoin 9-22 homeobox C3a Danio rerio 216-228
24361262-3 2014 Here we identify a novel function for CYP26B1, an enzyme known to play a role in tissue morphogenesis by fine-tuning retinoic acid (RA) concentration, in regulating lymphangiogenesis. Tretinoin 117-130 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 38-45
24361262-3 2014 Here we identify a novel function for CYP26B1, an enzyme known to play a role in tissue morphogenesis by fine-tuning retinoic acid (RA) concentration, in regulating lymphangiogenesis. Tretinoin 132-134 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 38-45
24361262-4 2014 Cyp26b1-null mice, in which RA levels are elevated, exhibited an increased number of lymphatic endothelial progenitor cells in the cardinal veins, together with hyperplastic, blood filled lymph sacs and hyperplastic dermal lymphatic vessels. Tretinoin 28-30 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
24361262-6 2014 Our data suggest that RA clearance by CYP26B1 in the vicinity of lymphatic endothelial progenitor cells is important for determining the position and size of the progenitor pool specified. Tretinoin 22-24 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 38-45
24330068-6 2014 We find that nuclear pS621 Raf-1 associates with NFATc3 near its cognate binding site in the promoter of CXCR5, a gene that must be up-regulated to drive RA-induced differentiation. Tretinoin 154-156 nuclear factor of activated T cells 3 Homo sapiens 49-55
24330068-7 2014 NFATc3 becomes immunoprecipitable with anti-phosphoserine serum, and CXCR5 is transcriptionally up-regulated upon RA-induced differentiation. Tretinoin 114-116 nuclear factor of activated T cells 3 Homo sapiens 0-6
24330068-8 2014 Inhibiting the pS621 Raf-1/NFATc3 association with PD98059 inhibits these processes and cripples RA-induced differentiation. Tretinoin 97-99 nuclear factor of activated T cells 3 Homo sapiens 27-33
24394593-0 2014 A TDG/CBP/RARalpha ternary complex mediates the retinoic acid-dependent expression of DNA methylation-sensitive genes. Tretinoin 48-61 thymine DNA glycosylase Homo sapiens 2-5
24394593-0 2014 A TDG/CBP/RARalpha ternary complex mediates the retinoic acid-dependent expression of DNA methylation-sensitive genes. Tretinoin 48-61 CREB binding protein Homo sapiens 6-9
24300824-5 2014 In order to regulate the switch between osetogenesis and adipogenesis, we evaluated the effect of all-trans retinoic acid (ATRA) on BMP9-induced differentiation of preadipocytes. Tretinoin 108-121 growth differentiation factor 2 Homo sapiens 132-136
24369064-10 2014 We observed that ATRA inhibits NO production in BD both in active and inactive stages and inhibits NF-kappaB translocation. Tretinoin 17-21 nuclear factor kappa B subunit 1 Homo sapiens 99-108
24300824-0 2014 All-trans retinoic acid modulates bone morphogenic protein 9-induced osteogenesis and adipogenesis of preadipocytes through BMP/Smad and Wnt/beta-catenin signaling pathways. Tretinoin 10-23 growth differentiation factor 2 Homo sapiens 34-60
24300824-5 2014 In order to regulate the switch between osetogenesis and adipogenesis, we evaluated the effect of all-trans retinoic acid (ATRA) on BMP9-induced differentiation of preadipocytes. Tretinoin 123-127 growth differentiation factor 2 Homo sapiens 132-136
24300824-6 2014 We found that ATRA enhanced BMP9-induced osteogenic differentiation and blocked BMP9-induced adipogenic differentiation both in vitro and in vivo. Tretinoin 14-18 growth differentiation factor 2 Homo sapiens 28-32
24300824-6 2014 We found that ATRA enhanced BMP9-induced osteogenic differentiation and blocked BMP9-induced adipogenic differentiation both in vitro and in vivo. Tretinoin 14-18 growth differentiation factor 2 Homo sapiens 80-84
24300824-7 2014 Mechanistically, ATRA was shown to elevate BMP9 expression and activate BMP/Smad signaling. Tretinoin 17-21 growth differentiation factor 2 Homo sapiens 43-47
24300824-9 2014 Knockdown of beta-catenin abolished the stimulatory effect of ATRA on BMP9-induced alkaline phosphatase activity and reversed the inhibitory effect of ATRA on BMP9-induced adipogenesis in preadipocytes. Tretinoin 62-66 growth differentiation factor 2 Homo sapiens 70-74
24300824-9 2014 Knockdown of beta-catenin abolished the stimulatory effect of ATRA on BMP9-induced alkaline phosphatase activity and reversed the inhibitory effect of ATRA on BMP9-induced adipogenesis in preadipocytes. Tretinoin 151-155 growth differentiation factor 2 Homo sapiens 159-163
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 AKT serine/threonine kinase 1 Homo sapiens 117-120
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 AKT serine/threonine kinase 1 Homo sapiens 381-384
24300824-11 2014 Collectively, ATRA mediated BMP9-induced osteogenic or adipogenic differentiation of 3T3-L1 preadipocytes by BMP/Smad and Wnt/beta-catenin signaling. Tretinoin 14-18 growth differentiation factor 2 Homo sapiens 28-32
24317440-10 2014 Furthermore, in MNK-74 and SC-M1 cells treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) and 5 or 10 microM of ATPR significantly suppressed the activity of the AP-1 reporter as compared to treatment with ATRA (P<0.05). Tretinoin 211-215 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-171
24422634-10 2014 Finally, we found genes of the RA pathway (cyp26a1, raraa) the regulation of which by RA is highly robust and can even resist the knockdown of all RARs. Tretinoin 31-33 retinoic acid receptor, alpha a Danio rerio 52-57
24082012-0 2014 Differential role of all-trans retinoic acid in promoting the development of CD4+ and CD8+ regulatory T cells. Tretinoin 21-44 CD4 molecule Homo sapiens 77-80
24082012-1 2014 It is known that ATRA promotes the development of TGF-beta-induced CD4(+)Foxp3(+) iTregs, which play a vital role in the prevention of autoimmune diseases; however, the role of ATRA in facilitating the differentiation and function of CD8(+)Foxp3(+) iTregs remains elusive. Tretinoin 17-21 CD4 molecule Homo sapiens 67-70
24082012-2 2014 Using a head-to-head comparison, we found that ATRA promoted expression of Foxp3 and development of CD4(+) iTregs, but it did not promote Foxp3 expression on CD8(+) cells. Tretinoin 47-51 CD4 molecule Homo sapiens 100-103
24082012-7 2014 We have identified the differential role of ATRA in promoting Foxp3(+) Tregs in CD4(+) and CD8(+) cell populations. Tretinoin 44-48 CD4 molecule Homo sapiens 80-83
24422634-11 2014 This suggests that RA-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity. Tretinoin 19-21 retinoic acid receptor, alpha a Danio rerio 133-138
24422634-11 2014 This suggests that RA-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity. Tretinoin 90-92 retinoic acid receptor, alpha a Danio rerio 133-138
24551289-7 2014 Moreover, compared with the control group, lower expression of Bcl-2 and higher expression of BAX were found in the ATRA-exposed group in both mRNA and protein level. Tretinoin 116-120 BCL2, apoptosis regulator Rattus norvegicus 63-68
24412926-2 2014 APL is the only malignancy definitively cured by targeted therapies: retinoic acid (RA) and/or arsenic trioxide, which both trigger PML-RARA degradation through nonoverlapping pathways. Tretinoin 69-82 promyelocytic leukemia Mus musculus 132-135
24412926-2 2014 APL is the only malignancy definitively cured by targeted therapies: retinoic acid (RA) and/or arsenic trioxide, which both trigger PML-RARA degradation through nonoverlapping pathways. Tretinoin 84-86 promyelocytic leukemia Mus musculus 132-135
24412926-5 2014 Upon RA-induced PML-RARA degradation, normal Pml elicits NB reformation and induces a Trp53 response exhibiting features of senescence but not apoptosis, ultimately abrogating APL-initiating activity. Tretinoin 5-7 promyelocytic leukemia Mus musculus 16-19
24412926-5 2014 Upon RA-induced PML-RARA degradation, normal Pml elicits NB reformation and induces a Trp53 response exhibiting features of senescence but not apoptosis, ultimately abrogating APL-initiating activity. Tretinoin 5-7 promyelocytic leukemia Mus musculus 45-48
24076097-4 2014 In the fetal testis, CYP26B1 degrades RA, while FGF9 further antagonises RA signalling to suppress meiosis. Tretinoin 38-40 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 21-28
24465772-5 2014 Endogenous expression of NELL2 in the P19 cells increased in parallel with the neuronal differentiation induced by retinoic acid (RA). Tretinoin 115-128 NEL-like 2 Mus musculus 25-30
24465772-5 2014 Endogenous expression of NELL2 in the P19 cells increased in parallel with the neuronal differentiation induced by retinoic acid (RA). Tretinoin 130-132 NEL-like 2 Mus musculus 25-30
25118897-5 2014 These findings suggested that JAK2/STAT3, as well as PI3K/Akt, play important roles in mediating the survival and neurite growth response of RA-predifferentiated cells to CNTF. Tretinoin 141-143 signal transducer and activator of transcription 3 Homo sapiens 35-40
24416428-4 2014 ATRA rapidly activated p38-MSK (mitogen- and stress activated protein kinase) cascade to phosphorylate cAMP response element-binding protein (CREB). Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 23-30
24603149-3 2014 In this study, we investigated the role of CX3CL1 in the apo-MPs in the cell-cell interaction between alveolar macrophage NR8383 cells and apoptotic all-trans retinoic acid-treated NB4 (ATRA-NB4) cells. Tretinoin 159-172 C-X3-C motif chemokine ligand 1 Homo sapiens 43-49
24416428-7 2014 Moreover, ATRA-mediated Ape/Ref-1 upregulation was correlated with histone modification and activation of CBP/p300, an important cofactors for CREB transcriptional activity. Tretinoin 10-14 CREB binding protein Homo sapiens 106-114
24416428-8 2014 C646, a competitive CBP/p300 inhibitor, abolished the upregulation of Ape/Ref-1 induced by ATRA. Tretinoin 91-95 CREB binding protein Homo sapiens 20-28
24416428-10 2014 Hence, our study suggests the existence of a noncanonical mechanism involving p38-MSK-CREB cascade and CBP induction to mediate ATRA-induced Ape/Ref-1 expression and acquired chemoresistance in myeloma cells. Tretinoin 128-132 mitogen-activated protein kinase 14 Homo sapiens 78-81
24416428-10 2014 Hence, our study suggests the existence of a noncanonical mechanism involving p38-MSK-CREB cascade and CBP induction to mediate ATRA-induced Ape/Ref-1 expression and acquired chemoresistance in myeloma cells. Tretinoin 128-132 CREB binding protein Homo sapiens 103-106
25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 153-176 retinoic acid receptor beta Homo sapiens 249-256
25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 178-182 retinoic acid receptor beta Homo sapiens 249-256
25118897-5 2014 These findings suggested that JAK2/STAT3, as well as PI3K/Akt, play important roles in mediating the survival and neurite growth response of RA-predifferentiated cells to CNTF. Tretinoin 141-143 AKT serine/threonine kinase 1 Homo sapiens 58-61
23619123-0 2014 Expression of the novel all-trans retinoic acid-related resistance gene HA117 in pediatric solid tumors. Tretinoin 34-47 regulator of G protein signaling 6 Homo sapiens 72-77
23904188-0 2014 A truncated-Flt1 isoform of breast cancer cells is upregulated by Notch and downregulated by retinoic acid. Tretinoin 93-106 fms related receptor tyrosine kinase 1 Homo sapiens 12-16
23904188-9 2014 Retinoic acid interferes i21 Flt1 expression by downregulating Notch-3 and upregulating miR-200 expression. Tretinoin 0-13 fms related receptor tyrosine kinase 1 Homo sapiens 29-33
23904188-10 2014 Treatment of MDA-MB-231 breast cancer cells with both a gamma-secretase inhibitor and retinoic acid suppresses the expression of i21 Flt1, providing a new mechanism to explain the effectiveness of this therapeutic approach. Tretinoin 86-99 fms related receptor tyrosine kinase 1 Homo sapiens 133-137
24186946-8 2014 The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Ppardelta and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo. Tretinoin 13-15 peroxisome proliferator activator receptor delta Mus musculus 128-137
24186946-8 2014 The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Ppardelta and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo. Tretinoin 13-15 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 157-161
24186946-8 2014 The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Ppardelta and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo. Tretinoin 192-194 peroxisome proliferator activator receptor delta Mus musculus 128-137
24186946-8 2014 The elevated RA-responsive gene expression was associated with elevated hepatic triglyceride levels and decreased expression of Ppardelta and its downstream Pdk4 target, suggesting a role for RA in these processes in vivo. Tretinoin 192-194 pyruvate dehydrogenase kinase, isoenzyme 4 Mus musculus 157-161
24335929-11 2014 Hubs of these networks were as follows: P38 mitogen-activated protein kinases (P38 MAPK), p42/p44 MAP kinase (ERK1/2) and glutathione for Network 1; protein kinase B (Akt), nuclear factor kappa B (NFkB) and ERK for Network 2; and dexamethasone, tretinoin, and cyclosporin A for Network 3. Tretinoin 245-254 mitogen-activated protein kinase 3 Homo sapiens 110-116
23653115-0 2014 Interleukin-22 binding protein (IL-22BP) is constitutively expressed by a subset of conventional dendritic cells and is strongly induced by retinoic acid. Tretinoin 140-153 interleukin 22 receptor, alpha 2 Mus musculus 0-30
23653115-0 2014 Interleukin-22 binding protein (IL-22BP) is constitutively expressed by a subset of conventional dendritic cells and is strongly induced by retinoic acid. Tretinoin 140-153 interleukin 22 receptor, alpha 2 Mus musculus 32-39
24078252-2 2014 We performed genome-wide profiling of p53 chromatin interactions and target gene expression in human embryonic stem cells (hESCs) in response to early differentiation, induced by retinoic acid, versus DNA damage, caused by adriamycin. Tretinoin 179-192 tumor protein p53 Homo sapiens 38-41
25206741-1 2014 Glial cell line-derived neurotrophic factor recombinant adenovirus vector-transfected bone marrow mesenchymal stem cells were induced to differentiate into neuron-like cells using inductive medium containing retinoic acid and epidermal growth factor. Tretinoin 208-221 glial cell derived neurotrophic factor Homo sapiens 0-43
24335929-11 2014 Hubs of these networks were as follows: P38 mitogen-activated protein kinases (P38 MAPK), p42/p44 MAP kinase (ERK1/2) and glutathione for Network 1; protein kinase B (Akt), nuclear factor kappa B (NFkB) and ERK for Network 2; and dexamethasone, tretinoin, and cyclosporin A for Network 3. Tretinoin 245-254 mitogen-activated protein kinase 1 Homo sapiens 110-113
24111806-5 2013 ATRA significantly inhibited proliferation and expression of osteocalcin but enhanced the activity of alkaline phosphatase of BMSCs. Tretinoin 0-4 bone gamma-carboxyglutamate protein Rattus norvegicus 61-72
25140197-5 2014 Therefore, combination of ATRA with DAC and SAHA represents promising tool for therapy of leukemic disease with nonfunctional p53 signalization. Tretinoin 26-30 tumor protein p53 Homo sapiens 126-129
24824789-2 2014 Knockdown of HOTAIRM1 in the NB4 acute promyelocytic leukemia cell line retarded all-trans retinoid acid (ATRA)-induced granulocytic differentiation, resulting in a significantly larger population of immature and proliferating cells that maintained cell cycle progression from G1 to S phases. Tretinoin 106-110 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 13-21
25509416-5 2014 As induction of neuronal differentiation in the studied MSCs using differentiation medium containing B27 and N2 supplements, 5-azacytidine, retinoic acid, IBMX and dbcAMF caused changes in the cells morphology, the increased expression of beta-III-tubulin, and the appearance of neuronal markers GFAP, NF-H, NeuN and MAP2. Tretinoin 140-153 RNA binding fox-1 homolog 3 Homo sapiens 308-312
24391906-4 2013 In the present study we demonstrate that autocrine retinoic acid (RA) signaling in stromal cells is critical for their survival and patterning, and show that Extracellular matrix 1, Ecm1, a gene that in humans causes irritable bowel syndrome and lipoid proteinosis, is a novel RA-regulated target in the developing kidney, which is secreted from the cortical stromal cells surrounding the cap mesenchyme and ureteric bud. Tretinoin 51-64 extracellular matrix protein 1 Homo sapiens 182-186
24346134-9 2013 Additional in vitro studies confirmed that RA abolished GR-mediated glucocorticoid-induced suppression of CRH expression, indicating a negative cross-talk between RAR-alpha and GR signaling pathways. Tretinoin 43-45 corticotropin releasing hormone Rattus norvegicus 106-109
24346134-11 2013 We conclude that in addition to the "classic" RAR-alpha-mediated transcriptional control of CRH expression, disturbances in GR negative feedback constitute a novel pathway that underlies RA-induced HPA axis hyperactivity. Tretinoin 46-48 corticotropin releasing hormone Rattus norvegicus 92-95
24324637-10 2013 Immunohistochemistry and Western blot analysis demonstrated that RB1 significantly upregulated the protein expression of heme oxygenase-1 (HO-1) and Nrf2, which were attenuated by ATRA treatment. Tretinoin 180-184 heme oxygenase 1 Mus musculus 121-137
24324637-10 2013 Immunohistochemistry and Western blot analysis demonstrated that RB1 significantly upregulated the protein expression of heme oxygenase-1 (HO-1) and Nrf2, which were attenuated by ATRA treatment. Tretinoin 180-184 nuclear factor, erythroid derived 2, like 2 Mus musculus 149-153
24286429-0 2013 Tbx1 regulates the development of zebrafish neural crest cells by retinoic acid signaling. Tretinoin 66-79 T-box transcription factor 1 Danio rerio 0-4
25140197-0 2014 Decitabine and SAHA-induced apoptosis is accompanied by survivin downregulation and potentiated by ATRA in p53-deficient cells. Tretinoin 99-103 tumor protein p53 Homo sapiens 107-110
24340023-11 2013 Normal osteoblast differentiation involved up regulation of Cyp26b1, the major enzyme responsible for RA degradation, suggesting that a drop in RA signaling is required for osteogenesis analogous to what has been found for chondrogenesis. Tretinoin 102-104 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 60-67
24324637-4 2013 All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Tretinoin 0-23 nuclear factor, erythroid derived 2, like 2 Mus musculus 59-81
24324637-4 2013 All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Tretinoin 0-23 nuclear factor, erythroid derived 2, like 2 Mus musculus 83-87
24324637-4 2013 All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Tretinoin 25-29 nuclear factor, erythroid derived 2, like 2 Mus musculus 59-81
24324637-4 2013 All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Tretinoin 25-29 nuclear factor, erythroid derived 2, like 2 Mus musculus 83-87
24080087-2 2013 We provide evidence that the retinoic acid-producing enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) is an oncogene suppressor in specific splenic IgG1(+)/CD19(-) and IgG1(+)/CD19(+) B cell populations. Tretinoin 29-42 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 143-147
24080087-2 2013 We provide evidence that the retinoic acid-producing enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) is an oncogene suppressor in specific splenic IgG1(+)/CD19(-) and IgG1(+)/CD19(+) B cell populations. Tretinoin 29-42 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 163-167
24030392-7 2013 Our results demonstrate that the proline-rich region can also enhance cell proliferation and retinoic acid (RA)-induced neuronal differentiation and it is also involved in NEU4 interaction with Akt, as well as in substrate recognition, modifying directly or through the interaction with other protein(s) the enzyme specificity toward sialylated glycoprotein(s). Tretinoin 93-106 neuraminidase 4 Homo sapiens 172-176
24030392-7 2013 Our results demonstrate that the proline-rich region can also enhance cell proliferation and retinoic acid (RA)-induced neuronal differentiation and it is also involved in NEU4 interaction with Akt, as well as in substrate recognition, modifying directly or through the interaction with other protein(s) the enzyme specificity toward sialylated glycoprotein(s). Tretinoin 93-106 AKT serine/threonine kinase 1 Homo sapiens 194-197
24030392-7 2013 Our results demonstrate that the proline-rich region can also enhance cell proliferation and retinoic acid (RA)-induced neuronal differentiation and it is also involved in NEU4 interaction with Akt, as well as in substrate recognition, modifying directly or through the interaction with other protein(s) the enzyme specificity toward sialylated glycoprotein(s). Tretinoin 108-110 neuraminidase 4 Homo sapiens 172-176
24030392-7 2013 Our results demonstrate that the proline-rich region can also enhance cell proliferation and retinoic acid (RA)-induced neuronal differentiation and it is also involved in NEU4 interaction with Akt, as well as in substrate recognition, modifying directly or through the interaction with other protein(s) the enzyme specificity toward sialylated glycoprotein(s). Tretinoin 108-110 AKT serine/threonine kinase 1 Homo sapiens 194-197
24030392-8 2013 On the whole, our results suggest that N4L could be a downstream component of the PI3K/Akt signaling pathway required for RA-induced differentiation of neuroblastoma SK-N-BE cells. Tretinoin 122-124 AKT serine/threonine kinase 1 Homo sapiens 87-90
24042439-0 2013 All-transretinoic acid ameliorates bleomycin-induced lung fibrosis by downregulating the TGF-beta1/Smad3 signaling pathway in rats. Tretinoin 0-22 transforming growth factor, beta 1 Rattus norvegicus 89-98
24158695-10 2013 Consistent with these phenotypic data, we observed the diminishing effects of ATRA treatment on the production of proinflammatory mediators (e.g., TNF-alpha and IL-6) in hippocampal homogenates and LPS-stimulated BV2 cells, and these effects were dose-dependent. Tretinoin 78-82 interleukin 6 Mus musculus 161-165
24148305-4 2013 CAMSAP1L1 siRNA transfection of human SH-SY5Y neuroblastoma cells treated with or without retinoic acid reduced the CAMSAP1L1 protein level nearly 60% and stimulated neurite outgrowth, as measured by total length, number of processes and number of branches. Tretinoin 90-103 calmodulin regulated spectrin associated protein family member 2 Homo sapiens 0-9
24148305-4 2013 CAMSAP1L1 siRNA transfection of human SH-SY5Y neuroblastoma cells treated with or without retinoic acid reduced the CAMSAP1L1 protein level nearly 60% and stimulated neurite outgrowth, as measured by total length, number of processes and number of branches. Tretinoin 90-103 calmodulin regulated spectrin associated protein family member 2 Homo sapiens 116-125
23831118-10 2013 CONCLUSIONS: We identified RA-responsive genes which are regulated by retinoid signal and found that low-OTUD7B mRNA expression is associated with a poor prognosis for HCC patients. Tretinoin 27-29 OTU deubiquitinase 7B Homo sapiens 105-111
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 zinc finger E-box binding homeobox 2 Rattus norvegicus 203-207
24158695-10 2013 Consistent with these phenotypic data, we observed the diminishing effects of ATRA treatment on the production of proinflammatory mediators (e.g., TNF-alpha and IL-6) in hippocampal homogenates and LPS-stimulated BV2 cells, and these effects were dose-dependent. Tretinoin 78-82 tumor necrosis factor Mus musculus 147-156
24324457-6 2013 Vitamin A, which is metabolized to Retinoic Acid in Sertoli cells, controls both SSCs differentiation through KIT induction and NANOS2 inhibition, and meiotic entry of differentiating spermatogonia through STRA8 upregulation. Tretinoin 35-48 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 110-113
24324457-6 2013 Vitamin A, which is metabolized to Retinoic Acid in Sertoli cells, controls both SSCs differentiation through KIT induction and NANOS2 inhibition, and meiotic entry of differentiating spermatogonia through STRA8 upregulation. Tretinoin 35-48 nanos C2HC-type zinc finger 2 Homo sapiens 128-134
24045938-2 2013 During early embryonic development, atRA is synthesized from all-trans-retinal (atRAL) in an irreversible reaction mainly catalyzed by retinal dehydrogenase 2 (aldh1a2), whereas atRAL is converted from all-trans-retinol via reversible oxidation by retinol dehydrogenases, members of the short-chain dehydrogenase/reductase family. Tretinoin 36-40 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 160-167
24045938-7 2013 In embryos overexpressing aldh1a2 or retinol dehydrogenase 10 (rdh10) in the presence of their respective substrates, Dhrs3 counteracted the action of Aldh1a2 or Rdh10, indicating that retinoic acid signaling is attenuated. Tretinoin 185-198 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 26-33
24056063-10 2013 The localization of two enzymes, Raldh2 and Cyp26b1, which antagonistically control RA levels and whose abundance suggests the sites of RA synthesis and degradation respectively, showed two distinct expression patterns specific for (i) X. laevis, H. arborea, R. arvalis, R. temporaria and (ii) B. bombina, B. viridis. Tretinoin 84-86 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 33-39
24042439-0 2013 All-transretinoic acid ameliorates bleomycin-induced lung fibrosis by downregulating the TGF-beta1/Smad3 signaling pathway in rats. Tretinoin 0-22 SMAD family member 3 Rattus norvegicus 99-104
24056063-10 2013 The localization of two enzymes, Raldh2 and Cyp26b1, which antagonistically control RA levels and whose abundance suggests the sites of RA synthesis and degradation respectively, showed two distinct expression patterns specific for (i) X. laevis, H. arborea, R. arvalis, R. temporaria and (ii) B. bombina, B. viridis. Tretinoin 84-86 cytochrome P450 family 26 subfamily B member 1 L homeolog Xenopus laevis 44-51
24056063-10 2013 The localization of two enzymes, Raldh2 and Cyp26b1, which antagonistically control RA levels and whose abundance suggests the sites of RA synthesis and degradation respectively, showed two distinct expression patterns specific for (i) X. laevis, H. arborea, R. arvalis, R. temporaria and (ii) B. bombina, B. viridis. Tretinoin 136-138 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 33-39
24042439-2 2013 In the present study, we investigated if all-trans retinoic acid (ATRA) could attenuate fibrosis in bleomycin (BLM)-induced lung fibrosis in rats through regulating TGF-beta1/Smad3 signaling. Tretinoin 45-64 transforming growth factor, beta 1 Rattus norvegicus 165-174
24056063-10 2013 The localization of two enzymes, Raldh2 and Cyp26b1, which antagonistically control RA levels and whose abundance suggests the sites of RA synthesis and degradation respectively, showed two distinct expression patterns specific for (i) X. laevis, H. arborea, R. arvalis, R. temporaria and (ii) B. bombina, B. viridis. Tretinoin 136-138 cytochrome P450 family 26 subfamily B member 1 L homeolog Xenopus laevis 44-51
24056063-11 2013 Thus, RA, in correlation with specific expression patterns of Raldh2 and Cyp26b, induces meiosis during gonad development in anurans. Tretinoin 6-8 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 62-68
24042439-2 2013 In the present study, we investigated if all-trans retinoic acid (ATRA) could attenuate fibrosis in bleomycin (BLM)-induced lung fibrosis in rats through regulating TGF-beta1/Smad3 signaling. Tretinoin 45-64 SMAD family member 3 Rattus norvegicus 175-180
24042439-2 2013 In the present study, we investigated if all-trans retinoic acid (ATRA) could attenuate fibrosis in bleomycin (BLM)-induced lung fibrosis in rats through regulating TGF-beta1/Smad3 signaling. Tretinoin 66-70 transforming growth factor, beta 1 Rattus norvegicus 165-174
24042439-2 2013 In the present study, we investigated if all-trans retinoic acid (ATRA) could attenuate fibrosis in bleomycin (BLM)-induced lung fibrosis in rats through regulating TGF-beta1/Smad3 signaling. Tretinoin 66-70 SMAD family member 3 Rattus norvegicus 175-180
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 48-57
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 SMAD family member 3 Rattus norvegicus 58-63
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 123-132
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 SMAD family member 3 Rattus norvegicus 134-139
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 SMAD family member 3 Rattus norvegicus 134-139
24176856-6 2013 Furthermore, PI3K/Akt signaling was also involved in actions of RA. Tretinoin 64-66 thymoma viral proto-oncogene 1 Mus musculus 18-21
24004656-7 2013 In conclusion, mechanisms leading to neuroblastoma cell differentiation in response to As2O3 appear to involve the ERK pathway activation and PML-NB formation, which are observed in response to other differentiating molecules such as retinoic acid derivates. Tretinoin 234-247 mitogen-activated protein kinase 1 Homo sapiens 115-118
24148244-6 2013 Cell migration from EBs was significantly higher in DNP-treated EBs, and migrating cells were positive for nestin, ss-tubulin III and MAP2, similar to that observed with retinoic acid (RA)-treated EBs. Tretinoin 185-187 microtubule-associated protein 2 Mus musculus 134-138
24490503-0 2013 [Effects of retinoic acid on the expression of Cx43 and its gap juncion intercellular communication function in testicular cancer cell]. Tretinoin 12-25 gap junction protein, alpha 1 Mus musculus 47-51
24490503-1 2013 OBJECTIVE: To investigate the effects of retinoic acid (RA) on the expression of Cx43 and its gap junction intercellular communication function in testicular cancer cells. Tretinoin 41-54 gap junction protein, alpha 1 Mus musculus 81-85
24490503-1 2013 OBJECTIVE: To investigate the effects of retinoic acid (RA) on the expression of Cx43 and its gap junction intercellular communication function in testicular cancer cells. Tretinoin 56-58 gap junction protein, alpha 1 Mus musculus 81-85
24490503-5 2013 RESULTS: RA (2.5, 5.0, 10.0 micromol/L) markedly increased the expression of Cx43 in I-10 cells, the enhancement ratios were 43.14% +/- 2.1%, 58.09% +/- 1.8%, 143.13% +/- 1.6%, respectively. Tretinoin 9-11 gap junction protein, alpha 1 Mus musculus 77-81
24490503-6 2013 The result of immunofluorescence assay showed that RA (2.5, 5.0, 10.0 micromol/L) obviously increased the level of Cx43 located on the cellular membrane of I-10 cells. Tretinoin 51-53 gap junction protein, alpha 1 Mus musculus 115-119
24490503-8 2013 CONCLUSION: RA could enhance the gap junction intercellular communication by increasing the expression of Cx43 in I-10 cells. Tretinoin 12-14 gap junction protein, alpha 1 Mus musculus 106-110
24205241-8 2013 Consistent with a role of NKAIN2 in NB development, NKAIN2 was down-regulated during all-trans retinoic acid differentiation in two NB cell lines. Tretinoin 95-108 sodium/potassium transporting ATPase interacting 2 Homo sapiens 52-58
24205156-4 2013 MATERIALS AND METHODS: We applied 5 ng/ml or 50 ng/ml bone morphogenetic protein-2/7 to restore the osteoblastogenesis of pre-osteoblasts (MC3T3-E1 cell line) that was inhibited by 1 microM all-trans retinoic acid. Tretinoin 200-213 bone morphogenetic protein 2 Mus musculus 54-82
24161026-10 2013 The c-kit expression profiles in the testis and the spermatogonial stem cell lines vary after RA stimulation. Tretinoin 94-96 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 4-9
24075189-7 2013 We found that compared to the wild-type receptor, p.Arg387Ser and p.Arg387Cys altered RARB induced a 2- to 3-fold increase in transcriptional activity in response to retinoic acid ligands, suggesting a gain-of-function mechanism. Tretinoin 166-179 retinoic acid receptor beta Homo sapiens 86-90
23946489-3 2013 We show here that the cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying MN columnar subtypes. Tretinoin 72-95 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 45-52
23946489-3 2013 We show here that the cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying MN columnar subtypes. Tretinoin 97-99 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 45-52
23946489-3 2013 We show here that the cytochrome P450 enzyme Cyp26a1, which metabolizes all-trans-retinoic acid (RA) and thereby reduces RA levels, plays a crucial role in specifying MN columnar subtypes. Tretinoin 121-123 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 45-52
23830798-2 2013 A patient, with chemo- and trastuzumab-resistant HER2-overexpressing breast cancer, who presented concomitant acute promyelocytic leukemia, showed a response in her breast lesions to retinoic acid, arsenic, and aracytin. Tretinoin 183-196 erb-b2 receptor tyrosine kinase 2 Homo sapiens 49-53
23830798-10 2013 Gene expression arrays showed that ATRA-induced apoptosis in RARA-amplified cell lines was related to an increase in CASP1 and IRF1. Tretinoin 35-39 caspase 1 Homo sapiens 117-122
23830798-10 2013 Gene expression arrays showed that ATRA-induced apoptosis in RARA-amplified cell lines was related to an increase in CASP1 and IRF1. Tretinoin 35-39 interferon regulatory factor 1 Homo sapiens 127-131
23975865-4 2013 Genes involved in RA biosynthesis and metabolism, such as Adh1 and Raldh2, as well as RA receptors and IL-10, were induced in dendritic cells (DCs) via TLR2-dependent ERK signaling. Tretinoin 18-20 toll like receptor 2 Homo sapiens 152-156
23649634-4 2013 The increase in death of HOXA-AS2 knockdown cells was accompanied by an elevated TNF-related apoptosis-inducing ligand (TRAIL) levels, but ATRA-induced NB4 cells treated with TRAIL did show an increase in HOXA-AS2 expression. Tretinoin 139-143 TNF superfamily member 10 Homo sapiens 175-180
23649634-5 2013 These results demonstrate that ATRA induction of HOXA-AS2 suppresses ATRA-induced apoptosis, possibly through a TRAIL-mediated pathway. Tretinoin 31-35 TNF superfamily member 10 Homo sapiens 112-117
23649634-5 2013 These results demonstrate that ATRA induction of HOXA-AS2 suppresses ATRA-induced apoptosis, possibly through a TRAIL-mediated pathway. Tretinoin 69-73 TNF superfamily member 10 Homo sapiens 112-117
23851445-7 2013 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin 27-40 cyclin dependent kinase inhibitor 2A Homo sapiens 86-89
23851445-7 2013 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin 27-40 cyclin dependent kinase inhibitor 2A Homo sapiens 155-158
23851445-7 2013 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin 27-40 retinoic acid receptor beta Homo sapiens 210-217
23851445-7 2013 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin 42-46 cyclin dependent kinase inhibitor 2A Homo sapiens 86-89
23851445-7 2013 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin 42-46 retinoic acid receptor beta Homo sapiens 210-217
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 28-32 cyclin dependent kinase inhibitor 2A Homo sapiens 68-71
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 136-140 cyclin dependent kinase inhibitor 2A Homo sapiens 68-71
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 136-140 retinoic acid receptor beta Homo sapiens 212-219
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 136-140 cyclin dependent kinase inhibitor 2A Homo sapiens 220-223
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 136-140 cyclin dependent kinase inhibitor 2A Homo sapiens 260-263
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 136-140 cyclin dependent kinase inhibitor 2A Homo sapiens 264-269
23851445-8 2013 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin 136-140 tumor protein p53 Homo sapiens 275-278
23877261-11 2013 Expression of activated extracellular signal-regulated kinase 1/2 (pERK1/2) was enhanced following treatment with ATRA, independent of mTOR pathway inhibitors. Tretinoin 114-118 mitogen-activated protein kinase 1 Homo sapiens 24-65
23877261-15 2013 These findings indicate that ATRA-induced differentiation is mediated via the ERK1/2 pathway, and underscores the significance of including differentiating agents along with inhibitors of mTOR pathways in the treatment of GBM. Tretinoin 29-33 mitogen-activated protein kinase 3 Homo sapiens 78-84
23877261-15 2013 These findings indicate that ATRA-induced differentiation is mediated via the ERK1/2 pathway, and underscores the significance of including differentiating agents along with inhibitors of mTOR pathways in the treatment of GBM. Tretinoin 29-33 mechanistic target of rapamycin kinase Homo sapiens 188-192
23966631-2 2013 Mouse intestinal CD103+ dendritic cells (DCs) produce a high level of RA by highly expressing retinal dehydrogenase (RALDH)2, an enzyme that converts retinal to RA, and induce gut-homing T cells. Tretinoin 70-72 integrin alpha E, epithelial-associated Mus musculus 17-22
24043786-7 2013 The embryonic gonadal microenvironment has recently been shown to determine germ-cell fate by degrading RA through expression of the P450 retinoid-inactivating enzyme CYP26B1. Tretinoin 104-106 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 167-174
24043786-9 2013 Accordingly, we found that bone marrow stromal cell CYP26 was also able to inactivate retinoids in serum, preventing RA signaling. Tretinoin 117-119 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 52-57
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 33-46 cadherin 5 Homo sapiens 239-250
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 48-50 cadherin 5 Homo sapiens 239-250
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 161-209
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 211-220
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 15-17 peroxisome proliferator activator receptor delta Mus musculus 161-209
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 15-17 peroxisome proliferator activator receptor delta Mus musculus 211-220
23974111-0 2013 EGFR inhibitors exacerbate differentiation and cell cycle arrest induced by retinoic acid and vitamin D3 in acute myeloid leukemia cells. Tretinoin 76-89 epidermal growth factor receptor Homo sapiens 0-4
23974111-1 2013 By means of an unbiased, automated fluorescence microscopy-based screen, we identified the epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib as potent enhancers of the differentiation of HL-60 acute myeloid leukemia (AML) cells exposed to suboptimal concentrations of vitamin A (all-trans retinoic acid, ATRA) or vitamin D (1alpha,25-hydroxycholecalciferol, VD). Tretinoin 314-327 epidermal growth factor receptor Homo sapiens 91-123
23974111-1 2013 By means of an unbiased, automated fluorescence microscopy-based screen, we identified the epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib as potent enhancers of the differentiation of HL-60 acute myeloid leukemia (AML) cells exposed to suboptimal concentrations of vitamin A (all-trans retinoic acid, ATRA) or vitamin D (1alpha,25-hydroxycholecalciferol, VD). Tretinoin 314-327 epidermal growth factor receptor Homo sapiens 125-129
23974111-1 2013 By means of an unbiased, automated fluorescence microscopy-based screen, we identified the epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib as potent enhancers of the differentiation of HL-60 acute myeloid leukemia (AML) cells exposed to suboptimal concentrations of vitamin A (all-trans retinoic acid, ATRA) or vitamin D (1alpha,25-hydroxycholecalciferol, VD). Tretinoin 329-333 epidermal growth factor receptor Homo sapiens 91-123
23974111-1 2013 By means of an unbiased, automated fluorescence microscopy-based screen, we identified the epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib as potent enhancers of the differentiation of HL-60 acute myeloid leukemia (AML) cells exposed to suboptimal concentrations of vitamin A (all-trans retinoic acid, ATRA) or vitamin D (1alpha,25-hydroxycholecalciferol, VD). Tretinoin 329-333 epidermal growth factor receptor Homo sapiens 125-129
23974111-5 2013 If combined with the administration of ATRA or VD, the inhibition of p38(MAPK) or SFKs with specific pharmacological agents mimicked the pro-differentiation activity of erlotinib. Tretinoin 39-43 mitogen-activated protein kinase 14 Homo sapiens 69-72
27335827-11 2013 I discuss the roles of RA production in the development of insulin resistance in hepatocytes and proposes a mechanism by which RA production may contribute to hepatic insulin resistance. Tretinoin 23-25 insulin Homo sapiens 59-66
23960232-3 2013 We found that IL-4 and retinoic acid (RA) cotreatment of GM-CSF-differentiated IDCs synergistically induced the expression of aldehyde dehydrogenase family 1, subfamily A2, a rate-limiting enzyme for RA synthesis in DCs. Tretinoin 38-40 interleukin 4 Homo sapiens 14-18
23960232-3 2013 We found that IL-4 and retinoic acid (RA) cotreatment of GM-CSF-differentiated IDCs synergistically induced the expression of aldehyde dehydrogenase family 1, subfamily A2, a rate-limiting enzyme for RA synthesis in DCs. Tretinoin 200-202 interleukin 4 Homo sapiens 14-18
23960232-5 2013 IL-4 plus RA-treated IDCs strongly induced CD4+Foxp3+ regulatory T cell differentiation and suppressed Th1 and Th17 differentiation. Tretinoin 10-12 CD4 molecule Homo sapiens 43-46
23966631-9 2013 This study suggests that CD1c+ mDCs are a major human DC subset that produces RA in response to VD3 in the steady state. Tretinoin 78-80 chemokine (C-C motif) ligand 22 Mus musculus 32-34
23701916-0 2013 Increased production of IFN-gamma by natural killer cells triggered with bone marrow-derived dendritic cells cultured in the presence of retinoic acid. Tretinoin 137-150 interferon gamma Homo sapiens 24-33
23847298-8 2013 RA supplementation treatment restored corticosterone concentrations and 11beta-HSD1 expression to control levels. Tretinoin 0-2 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 72-83
23652568-2 2013 RECENT FINDINGS: Recombinant apoM can bind small lipids such as retinoic acid, oxidized phospholipids, and S1P. Tretinoin 64-77 apolipoprotein M Homo sapiens 29-33
23849428-0 2013 Calcium prevents retinoic acid-induced disruption of the spectrin-based cytoskeleton in keratinocytes through the Src/PI3K-p85alpha/AKT/PKCdelta/beta-adducin pathways. Tretinoin 17-30 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 114-117
23849428-0 2013 Calcium prevents retinoic acid-induced disruption of the spectrin-based cytoskeleton in keratinocytes through the Src/PI3K-p85alpha/AKT/PKCdelta/beta-adducin pathways. Tretinoin 17-30 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 123-131
23849428-0 2013 Calcium prevents retinoic acid-induced disruption of the spectrin-based cytoskeleton in keratinocytes through the Src/PI3K-p85alpha/AKT/PKCdelta/beta-adducin pathways. Tretinoin 17-30 AKT serine/threonine kinase 1 Homo sapiens 132-135
23849428-4 2013 Furthermore, RA substantially inhibited expression of both Src and PI3K-p85alpha and consequently the amounts of specific phosphorylation of both of these proteins. Tretinoin 13-15 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 59-62
23849428-4 2013 Furthermore, RA substantially inhibited expression of both Src and PI3K-p85alpha and consequently the amounts of specific phosphorylation of both of these proteins. Tretinoin 13-15 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 72-80
23849428-5 2013 RA also enhanced AKT expression and dramatically induced phosphorylation of AKT((Thr308)), accompanied by phosphorylation of both PKCdelta((Thr505)) and beta-adducin((Ser662)) and upregulated cyclin D2 and down-regulated cyclin B1. Tretinoin 0-2 AKT serine/threonine kinase 1 Homo sapiens 17-20
23849428-5 2013 RA also enhanced AKT expression and dramatically induced phosphorylation of AKT((Thr308)), accompanied by phosphorylation of both PKCdelta((Thr505)) and beta-adducin((Ser662)) and upregulated cyclin D2 and down-regulated cyclin B1. Tretinoin 0-2 AKT serine/threonine kinase 1 Homo sapiens 76-79
23849428-5 2013 RA also enhanced AKT expression and dramatically induced phosphorylation of AKT((Thr308)), accompanied by phosphorylation of both PKCdelta((Thr505)) and beta-adducin((Ser662)) and upregulated cyclin D2 and down-regulated cyclin B1. Tretinoin 0-2 cyclin D2 Homo sapiens 192-201
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 79-82
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 89-97
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 166-169
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 189-197
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 AKT serine/threonine kinase 1 Homo sapiens 232-235
23765990-3 2013 Previous studies on Raldh2-/- and Raldh3-/- mice demonstrated an RA requirement for gamma-aminobutyric acid (GABA)ergic and dopaminergic differentiation in forebrain basal ganglia, but no RA requirement was observed during early forebrain patterning or subsequent forebrain cortical expansion. Tretinoin 65-67 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 34-40
23765990-4 2013 However, other studies suggested that RA controls forebrain patterning, and analysis of ethylnitrosourea-induced Rdh10 mutants suggested that RA synthesized in the meninges stimulates forebrain cortical expansion. Tretinoin 142-144 retinol dehydrogenase 10 (all-trans) Mus musculus 113-118
23765990-5 2013 RESULTS: We generated Rdh10-/- mouse embryos that lack RA activity early in the head and later in the meninges. Tretinoin 55-57 retinol dehydrogenase 10 (all-trans) Mus musculus 22-27
23765990-8 2013 CONCLUSIONS: Rdh10-/- embryos demonstrate that RA controls hindbrain but not early forebrain patterning, while studies on retinaldehyde-rescued Rdh10-/- embryos show that meningeal RA synthesis is unnecessary to stimulate forebrain cortical expansion. Tretinoin 47-49 retinol dehydrogenase 10 (all-trans) Mus musculus 13-18
23526782-0 2013 RING finger protein 10 regulates retinoic acid-induced neuronal differentiation and the cell cycle exit of P19 embryonic carcinoma cells. Tretinoin 33-46 ring finger protein 10 Homo sapiens 0-22
23526782-3 2013 In this study, we observed that the mRNA levels and protein expression of Rnf10 increase significantly upon the retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 112-125 ring finger protein 10 Homo sapiens 74-79
23991089-0 2013 The retinoic acid-metabolizing enzyme Cyp26b1 regulates CD4 T cell differentiation and function. Tretinoin 4-17 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 38-45
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 11-34 peroxisome proliferator activator receptor delta Mus musculus 128-137
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 36-40 peroxisome proliferator activator receptor delta Mus musculus 128-137
23946634-0 2013 All-trans retinoic acid modulates mitogen-activated protein kinase pathway activation in human scleral fibroblasts through retinoic acid receptor beta. Tretinoin 10-23 retinoic acid receptor beta Homo sapiens 123-150
23946634-3 2013 The aim of the current study was to investigate whether changed activation of the MAPK pathway could be involved in the response of HSFs exposed to ATRA. Tretinoin 148-152 mitogen-activated protein kinase 3 Homo sapiens 82-86
23946634-7 2013 Western blot showed decreased activation of ERK 1/2 in the HSFs from 30 min (p=0.01) to 24 h (p<0.01) after the start of exposure to ATRA, and increased activation of the JNK protein from 10 to 30 min (p<0.01) after the start of exposure to ATRA. Tretinoin 136-140 mitogen-activated protein kinase 3 Homo sapiens 44-51
23946634-7 2013 Western blot showed decreased activation of ERK 1/2 in the HSFs from 30 min (p=0.01) to 24 h (p<0.01) after the start of exposure to ATRA, and increased activation of the JNK protein from 10 to 30 min (p<0.01) after the start of exposure to ATRA. Tretinoin 247-251 mitogen-activated protein kinase 8 Homo sapiens 174-177
23946634-8 2013 Indirect immunofluorescence confirmed changes in activation of ERK 1/2 and JNK in HSFs exposed to ATRA. Tretinoin 98-102 mitogen-activated protein kinase 3 Homo sapiens 63-70
23946634-8 2013 Indirect immunofluorescence confirmed changes in activation of ERK 1/2 and JNK in HSFs exposed to ATRA. Tretinoin 98-102 mitogen-activated protein kinase 8 Homo sapiens 75-78
23946634-10 2013 Pretreatment of the HSFs with LE135, an antagonist of retinoic acid receptor beta (RARbeta), abolished the ATRA-induced changes inactivation of ERK 1/2 and JNK. Tretinoin 107-111 retinoic acid receptor beta Homo sapiens 54-81
23946634-10 2013 Pretreatment of the HSFs with LE135, an antagonist of retinoic acid receptor beta (RARbeta), abolished the ATRA-induced changes inactivation of ERK 1/2 and JNK. Tretinoin 107-111 retinoic acid receptor beta Homo sapiens 83-90
23946634-10 2013 Pretreatment of the HSFs with LE135, an antagonist of retinoic acid receptor beta (RARbeta), abolished the ATRA-induced changes inactivation of ERK 1/2 and JNK. Tretinoin 107-111 mitogen-activated protein kinase 3 Homo sapiens 144-151
23946634-10 2013 Pretreatment of the HSFs with LE135, an antagonist of retinoic acid receptor beta (RARbeta), abolished the ATRA-induced changes inactivation of ERK 1/2 and JNK. Tretinoin 107-111 mitogen-activated protein kinase 8 Homo sapiens 156-159
23946634-11 2013 CONCLUSIONS: ATRA inhibits HSF proliferation by a mechanism associated with modulation of ERK 1/2 and JNK activation and depends on stimulation of retinoic acid receptor beta. Tretinoin 13-17 mitogen-activated protein kinase 3 Homo sapiens 90-97
23946634-11 2013 CONCLUSIONS: ATRA inhibits HSF proliferation by a mechanism associated with modulation of ERK 1/2 and JNK activation and depends on stimulation of retinoic acid receptor beta. Tretinoin 13-17 mitogen-activated protein kinase 8 Homo sapiens 102-105
23946634-11 2013 CONCLUSIONS: ATRA inhibits HSF proliferation by a mechanism associated with modulation of ERK 1/2 and JNK activation and depends on stimulation of retinoic acid receptor beta. Tretinoin 13-17 retinoic acid receptor beta Homo sapiens 147-174
23644172-3 2013 In human proximal tubular HK-2 cells, treatment with all-trans retinoic acid or prostaglandin E2 (PGE2) triggers the production of VEGF-A. Tretinoin 63-76 vascular endothelial growth factor A Homo sapiens 131-137
23644172-7 2013 We found that EGFR inhibitor AG1478 prevented the increase in VEGF-A production induced by PGE2- and all-trans retinoic acid. Tretinoin 111-124 epidermal growth factor receptor Homo sapiens 14-18
23644172-7 2013 We found that EGFR inhibitor AG1478 prevented the increase in VEGF-A production induced by PGE2- and all-trans retinoic acid. Tretinoin 111-124 vascular endothelial growth factor A Homo sapiens 62-68
23644172-9 2013 PGE2 and all-trans retinoic acid also increased EGFR phosphorylation and this effect was sensitive to antagonists of EP receptors. Tretinoin 9-32 epidermal growth factor receptor Homo sapiens 48-52
23644172-10 2013 The role of intracellular PGE2 was indicated by two facts; i) PGE2-induced EGFR phosphorylation was substantially prevented by inhibitor of prostaglandin uptake transporter bromocresol green and ii) all-trans retinoic acid treatment, which enhanced intracellular but not extracellular PGE2, had lower effect on EGFR phosphorylation upon pre-treatment with cyclooxygenase inhibitor diclofenac. Tretinoin 209-222 epidermal growth factor receptor Homo sapiens 75-79
23806210-4 2013 RA is produced by three different enzymes called retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3) that are all expressed in the developing bowel. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 98-104
23833249-6 2013 In our model of human mo-DCs, all three proteins (RDH10, RALDH2, and CRABP2) appeared to be required for ATRA production induced by activation of PPARgamma and therefore form a linear pathway. Tretinoin 105-109 peroxisome proliferator activated receptor gamma Homo sapiens 146-155
23726866-1 2013 Here, we tried to elucidate the possible role of autophagy against H2O2 and Amyloid beta (Abeta) induced neurotoxicity using retinoic acid differentiated SH-SY5Y cells. Tretinoin 125-138 amyloid beta precursor protein Homo sapiens 90-95
23861398-0 2013 beta-Transducin repeat-containing protein 1 (beta-TrCP1)-mediated silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) protein degradation promotes tumor necrosis factor alpha (TNFalpha)-induced inflammatory gene expression. Tretinoin 88-101 tumor necrosis factor Homo sapiens 167-194
23861398-0 2013 beta-Transducin repeat-containing protein 1 (beta-TrCP1)-mediated silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) protein degradation promotes tumor necrosis factor alpha (TNFalpha)-induced inflammatory gene expression. Tretinoin 88-101 tumor necrosis factor Homo sapiens 196-204
24137725-0 2013 Retraction notice to: Histone H2B ubquitination regulates retinoic acid signaling through the cooperation of ASXL1 and BAP1. Tretinoin 58-71 BRCA1 associated protein 1 Homo sapiens 119-123
23977348-0 2013 Polymorphism in the retinoic acid metabolizing enzyme CYP26B1 and the development of Crohn"s Disease. Tretinoin 20-33 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 54-61
23977348-2 2013 Cytochrome P450 26 B1 (CYP26B1) is involved in the degradation of retinoic acid and the polymorphism rs2241057 has an elevated catabolic function of retinoic acid, why we hypothesized that the rs2241057 polymorphism may affect the risk of Crohn"s disease (CD) and Ulcerative Colitis (UC). Tretinoin 66-79 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-21
23977348-2 2013 Cytochrome P450 26 B1 (CYP26B1) is involved in the degradation of retinoic acid and the polymorphism rs2241057 has an elevated catabolic function of retinoic acid, why we hypothesized that the rs2241057 polymorphism may affect the risk of Crohn"s disease (CD) and Ulcerative Colitis (UC). Tretinoin 66-79 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 23-30
23977348-2 2013 Cytochrome P450 26 B1 (CYP26B1) is involved in the degradation of retinoic acid and the polymorphism rs2241057 has an elevated catabolic function of retinoic acid, why we hypothesized that the rs2241057 polymorphism may affect the risk of Crohn"s disease (CD) and Ulcerative Colitis (UC). Tretinoin 149-162 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-21
23977348-2 2013 Cytochrome P450 26 B1 (CYP26B1) is involved in the degradation of retinoic acid and the polymorphism rs2241057 has an elevated catabolic function of retinoic acid, why we hypothesized that the rs2241057 polymorphism may affect the risk of Crohn"s disease (CD) and Ulcerative Colitis (UC). Tretinoin 149-162 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 23-30
23977348-7 2013 We suggest that homozygous carriers of the major (T) allele, relative to homozygous carriers of the minor (C) allele, of the CYP26B1 polymorphism rs2241057 may have an increased risk for the development of CD, which possibly may be due to elevated levels of retinoic acid. Tretinoin 258-271 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 125-132
23824578-3 2013 We show that RA acts early in the neurogenic pathway by inhibiting expression of neural progenitor markers Geminin and Foxd4l1, thereby promoting differentiation. Tretinoin 13-15 geminin, DNA replication inhibitor L homeolog Xenopus laevis 107-114
23824578-6 2013 We hypothesized that RA regulates primary neurogenesis by inducing Erf and Etv3l to antagonize proliferative signals. Tretinoin 21-23 ETS variant transcription factor 3 S homeolog Xenopus laevis 75-80
25436722-2 2013 Its main active metabolite is all trans-retinoic acid (atRA), which regulates gene expression through the activation of alpha, beta, and gamma isotypes of the nuclear atRA receptor (RAR). Tretinoin 34-53 RAB40B, member RAS oncogene family Homo sapiens 182-185
23242600-0 2013 Differential effects of rapamycin and retinoic acid on expansion, stability and suppressive qualities of human CD4(+)CD25(+)FOXP3(+) T regulatory cell subpopulations. Tretinoin 38-51 CD4 molecule Homo sapiens 111-114
25436722-2 2013 Its main active metabolite is all trans-retinoic acid (atRA), which regulates gene expression through the activation of alpha, beta, and gamma isotypes of the nuclear atRA receptor (RAR). Tretinoin 55-59 RAB40B, member RAS oncogene family Homo sapiens 182-185
23562973-7 2013 ATRA consistently and significantly inhibited LPS-induced release of the pro-inflammatory cytokines tumor necrosis factor, interleukin (IL)-6, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta. Tretinoin 0-4 interleukin 6 Homo sapiens 123-141
23562609-4 2013 METHODS: SIRPalpha was induced in SIRPalpha-negative promyelocytic cells by retinoic acid or phorbol 12-myristate 13-acetate, and the differential expression of miRNAs was assessed by means of microarray and quantitative RT-PCR assays. Tretinoin 76-89 signal regulatory protein alpha Homo sapiens 9-18
23562609-7 2013 During SIRPalpha induction, levels of these 3 miRNAs were all reduced, and their downregulation by retinoic acid or phorbol 12-myristate 13-acetate occurred through suppression of the c-Myc signaling pathway. Tretinoin 99-112 signal regulatory protein alpha Homo sapiens 7-16
23817628-0 2013 Induction and translocation of tissue transglutaminase isoforms increased phosphorylation in retinoic acid treated erythroleukemia cells. Tretinoin 93-106 transglutaminase 2 Homo sapiens 31-54
23998581-3 2013 ATRA could promote phosphorylation of AKT in NB4 cells at short time, but not had effect on phosphorylation of AKT in NB4-R1 cells; the curcumin could enhance the phosphorylation of AKT in NB4-1R cells, the curcumin combined with ATRA could further enhance the phosphorylation of AKT. Tretinoin 0-4 AKT serine/threonine kinase 1 Homo sapiens 38-41
23829413-5 2013 In this study, we examined whether the balance between CysLT(1)R and CysLT(2)R could be restored by treatment with the cancer chemopreventive agent all-trans retinoic acid (ATRA). Tretinoin 158-171 cysteinyl leukotriene receptor 1 Homo sapiens 55-64
23530929-7 2013 Treatment of cells with the specific ERK inhibitor PD98059 completely abolished RA-mediated inhibition of gamma-secretase. Tretinoin 80-82 mitogen-activated protein kinase 1 Mus musculus 37-40
23441952-3 2013 In addition, atRA could act in the cytoplasm by modulating the activity of mitogen-activated protein kinases (MAPK) ERK and p38, which also have a role in cell differentiation. Tretinoin 13-17 mitogen-activated protein kinase 14 Homo sapiens 124-127
23850490-0 2013 Retracted: Histone H2B ubquitination regulates retinoic acid signaling through the cooperation of ASXL1 and BAP1. Tretinoin 47-60 BRCA1 associated protein 1 Homo sapiens 108-112
23850490-7 2013 Both ASXL1 and BAP1 were downregulated during RA-induced P19 cell differentiation with concomitant increase of ubiquitinated H2B, leading to activation of Hox genes. Tretinoin 46-48 BRCA1 associated protein 1 Homo sapiens 15-19
23850490-8 2013 Our data demonstrate the critical role of ASXL1 cooperation with BAP1 in cell differentiation through the regulation of RA signaling associated with H2B ubiquitination. Tretinoin 120-122 BRCA1 associated protein 1 Homo sapiens 65-69
23752611-6 2013 Moreover, p38alpha in CD103(+) DCs was required for optimal expression of retinaldehyde dehydrogenase, a key enzyme for retinoic acid synthesis, which in turn imprinted gut-homing receptors on responding T cells. Tretinoin 120-133 mitogen-activated protein kinase 14 Homo sapiens 10-18
23837398-5 2013 The overlapping region included two genes, EXOC6B and CYP26B1, which are involved in exocytosis/Notch signaling and retinoic acid (RA) metabolism, respectively, and are of critical importance for early morphogenesis, symmetry as well as craniofacial, skeleton and brain development. Tretinoin 116-129 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 54-61
23829413-5 2013 In this study, we examined whether the balance between CysLT(1)R and CysLT(2)R could be restored by treatment with the cancer chemopreventive agent all-trans retinoic acid (ATRA). Tretinoin 173-177 cysteinyl leukotriene receptor 1 Homo sapiens 55-64
23666625-0 2013 Polycomb recruitment attenuates retinoic acid-induced transcription of the bivalent NR2F1 gene. Tretinoin 32-45 nuclear receptor subfamily 2 group F member 1 Homo sapiens 84-89
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 74-87 solute carrier family 5 member 5 Homo sapiens 172-175
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 74-87 solute carrier family 5 member 5 Homo sapiens 191-194
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 74-87 solute carrier family 5 member 5 Homo sapiens 191-194
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 74-87 solute carrier family 5 member 5 Homo sapiens 191-194
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 89-91 solute carrier family 5 member 5 Homo sapiens 172-175
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 89-91 solute carrier family 5 member 5 Homo sapiens 191-194
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 89-91 solute carrier family 5 member 5 Homo sapiens 191-194
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 89-91 solute carrier family 5 member 5 Homo sapiens 191-194
23571271-6 2013 The ATRA-treated BM2NFAT1 cells differentiated along monocyte/macrophage pathway as evidenced by changes in cell morphology, adherence, phagocytic and non-specific esterase activities, reactive oxygen species production, and vimentin expression. Tretinoin 4-8 vimentin Gallus gallus 225-233
23733880-4 2013 CD103(+) DCs, but not pDCs or lung macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key for the production of retinoic acid, a cofactor for TGF-beta for Foxp3 induction. Tretinoin 154-167 integrin alpha E, epithelial-associated Mus musculus 0-5
23874790-4 2013 The data suggest that, in response to RA, phospholipase A2-mediated release of AA and subsequent metabolism by lipoxygenases is important for cell survival. Tretinoin 38-40 phospholipase A2 group IB Homo sapiens 42-58
23829703-9 2013 Retinaldehyde dehydrogenase 3 (RALDH3) is the key enzyme required to generate retinoic acid within the olfactory epithelium. Tretinoin 78-91 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 0-29
23829703-9 2013 Retinaldehyde dehydrogenase 3 (RALDH3) is the key enzyme required to generate retinoic acid within the olfactory epithelium. Tretinoin 78-91 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 31-37
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 25-38 peroxisome proliferator activator receptor delta Mus musculus 117-125
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 25-38 peroxisome proliferator activator receptor delta Mus musculus 250-258
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 40-42 peroxisome proliferator activator receptor delta Mus musculus 117-125
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 40-42 peroxisome proliferator activator receptor delta Mus musculus 250-258
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 109-111 peroxisome proliferator activator receptor delta Mus musculus 250-258
23643326-2 2013 Since ATRA is metabolized by cytochrome P450 (CYP) enzymes, we sought to identify drug interactions that might be associated with a higher risk for the development of DS in addition to other predictive factors related to the incidence of DS. Tretinoin 6-10 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 29-44
23643326-2 2013 Since ATRA is metabolized by cytochrome P450 (CYP) enzymes, we sought to identify drug interactions that might be associated with a higher risk for the development of DS in addition to other predictive factors related to the incidence of DS. Tretinoin 6-10 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 46-49
23582512-9 2013 The TGF-beta type II receptor, responsible for binding TGF-beta during neuronal differentiation, was increased 14-fold in NT2 cells treated with RA (P < 0.001). Tretinoin 145-147 transforming growth factor beta 1 Homo sapiens 4-12
23600975-4 2013 PCDH11X and PCDH11Y, differentially regulated by retinoic acid, are highly expressed in the ventricular zone, subplate, and cortical plate of the developing cerebral cortex. Tretinoin 49-62 protocadherin 11 Y-linked Homo sapiens 12-19
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 7-20 thymoma viral proto-oncogene 1 Mus musculus 100-103
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 7-20 Kruppel-like factor 4 (gut) Mus musculus 216-220
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 7-20 Nanog homeobox Mus musculus 225-230
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 7-20 thymoma viral proto-oncogene 1 Mus musculus 247-250
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 22-24 thymoma viral proto-oncogene 1 Mus musculus 100-103
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 22-24 Kruppel-like factor 4 (gut) Mus musculus 216-220
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 22-24 Nanog homeobox Mus musculus 225-230
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 22-24 thymoma viral proto-oncogene 1 Mus musculus 247-250
23601821-0 2013 2-(2-Methylfuran-3-carboxamido)-3-phenylpropanoic acid, a potential CYP26A1 inhibitor to enhance all-trans retinoic acid-induced leukemia cell differentiation based on virtual screening and biological evaluation. Tretinoin 107-120 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 68-75
23711709-4 2013 RESULTS: Of them, 82 were mapped in proximity to known or previously predicted genes; 7 were randomly picked up for further confirmation by ChIP-PCR and 3 genes (GALM, ITPR2 and ORM2) were found to be specifically up-regulated in the ATRA-treated NB4 cells, indicating that they might be the down-stream target genes of ATRA. Tretinoin 234-238 galactose mutarotase Homo sapiens 162-166
23711709-4 2013 RESULTS: Of them, 82 were mapped in proximity to known or previously predicted genes; 7 were randomly picked up for further confirmation by ChIP-PCR and 3 genes (GALM, ITPR2 and ORM2) were found to be specifically up-regulated in the ATRA-treated NB4 cells, indicating that they might be the down-stream target genes of ATRA. Tretinoin 234-238 inositol 1,4,5-trisphosphate receptor type 2 Homo sapiens 168-173
23711709-4 2013 RESULTS: Of them, 82 were mapped in proximity to known or previously predicted genes; 7 were randomly picked up for further confirmation by ChIP-PCR and 3 genes (GALM, ITPR2 and ORM2) were found to be specifically up-regulated in the ATRA-treated NB4 cells, indicating that they might be the down-stream target genes of ATRA. Tretinoin 320-324 galactose mutarotase Homo sapiens 162-166
23711709-4 2013 RESULTS: Of them, 82 were mapped in proximity to known or previously predicted genes; 7 were randomly picked up for further confirmation by ChIP-PCR and 3 genes (GALM, ITPR2 and ORM2) were found to be specifically up-regulated in the ATRA-treated NB4 cells, indicating that they might be the down-stream target genes of ATRA. Tretinoin 320-324 inositol 1,4,5-trisphosphate receptor type 2 Homo sapiens 168-173
23601821-4 2013 Eight of them enhanced the ability of ATRA to induce differentiation at concentrations of 0.5 and 1 muM. Tretinoin 38-42 latexin Homo sapiens 100-103
23508548-11 2013 In addition, we found retinoic acid would decrease the expression of P53 and miR-34c, however, did not change the expression of c-Myc greatly. Tretinoin 22-35 microRNA 34c Capra hircus 77-84
23441061-6 2013 Finally, overexpression of SKI in human cells results in reduced levels of CYP26A1 mRNA, a known target of retinoic acid signaling. Tretinoin 107-120 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 75-82
23508548-3 2013 Recent studies demonstrated that Boule and stimulated by retinoic acid 8 (Stra8) played important roles in initiation meiosis in male germ cells. Tretinoin 57-70 stimulated by retinoic acid gene 8 protein homolog Capra hircus 74-79
23588680-0 2013 All-trans retinoic acid upregulates the expression of p53 via Axin and inhibits the proliferation of glioma cells. Tretinoin 10-23 tumor protein p53 Homo sapiens 54-57
23228968-0 2013 ATRA and the specific RARalpha agonist, NRX195183, have opposing effects on the clonogenicity of pre-leukemic murine AML1-ETO bone marrow cells. Tretinoin 0-4 RUNX1 translocation partner 1 Mus musculus 122-125
23228968-8 2013 In the ATRA-treated AE cells, gene expression analyses revealed functional networks involving SERPINE1 and bone morphogenetic protein 2; AKT phosphorylation was upregulated. Tretinoin 7-11 bone morphogenetic protein 2 Mus musculus 107-135
23228968-8 2013 In the ATRA-treated AE cells, gene expression analyses revealed functional networks involving SERPINE1 and bone morphogenetic protein 2; AKT phosphorylation was upregulated. Tretinoin 7-11 thymoma viral proto-oncogene 1 Mus musculus 137-140
23587393-7 2013 Retinoic acid-induced differentiation of MAC-T cells was associated with an increase in the mRNA expression of alphaS1-casein (3.9-fold), alphaS2-casein (4.5-fold), and beta-casein (4.4-fold) compared with the control group. Tretinoin 0-13 casein beta Bos taurus 169-180
23587393-8 2013 Expression of alphaS1-casein, alphaS2-casein, and beta-casein was increased 12.9-fold, 11.9-fold, and 19.3-fold, respectively, following treatment with RA and PRL combined compared with the control group. Tretinoin 152-154 casein beta Bos taurus 50-61
23588680-2 2013 In the present study, we demonstrated that ATRA activated the expression of p53 via Axin and induced cell cycle arrest at the G1/S phase and apoptosis of glioma cells. Tretinoin 43-47 tumor protein p53 Homo sapiens 76-79
23588680-6 2013 Furthermore, loss-of-function of Axin in glioma cells by RNAi blocked ATRA-induced cell cycle phase arrest and apoptosis via downregulation of p53. Tretinoin 70-74 tumor protein p53 Homo sapiens 143-146
23588859-0 2013 c-myc but not Hif-1alpha-dependent downregulation of VEGF influences the proliferation and differentiation of HL-60 cells induced by ATRA. Tretinoin 133-137 vascular endothelial growth factor A Homo sapiens 53-57
23588859-10 2013 In conclusion, our data demonstrate that VEGF plays an important role in the differentiation and proliferation of HL-60 cells; c-myc-dependent downregulation of VEGF induced by ATRA contributes to the differentiation of HL-60 cells. Tretinoin 177-181 vascular endothelial growth factor A Homo sapiens 161-165
23741453-7 2013 Furthermore, overexpression of the putative Wnt/beta-catenin target gene Atf3 phenocopied knockdown of Ndrg1a or inhibition of RA signaling, while Atf3 knockdown can rescue Ndrg1a knockdown phenotype. Tretinoin 127-129 activating transcription factor 3 Xenopus tropicalis 73-77
23131127-14 2013 Moreover, we found special interest in the literature to retinoic acid-related genes (e.g. FABP5/CRABP2) that might indicate abnormalities in post-partum tissue repair mechanisms. Tretinoin 57-70 fatty acid-binding protein 5 Bos taurus 91-96
23734084-8 2013 In Rpe65-/- Rho-/- explants, administration of 11-cis retinal, 11-cis retinol or retinoic acid (RA) reversed the opsin trafficking phenotype. Tretinoin 81-94 retinal pigment epithelium 65 Mus musculus 3-8
23734084-8 2013 In Rpe65-/- Rho-/- explants, administration of 11-cis retinal, 11-cis retinol or retinoic acid (RA) reversed the opsin trafficking phenotype. Tretinoin 96-98 retinal pigment epithelium 65 Mus musculus 3-8
23693014-0 2013 Activation of Akt pathway by transcription-independent mechanisms of retinoic acid promotes survival and invasion in lung cancer cells. Tretinoin 69-82 AKT serine/threonine kinase 1 Homo sapiens 14-17
23693014-6 2013 In this study, we explored the hypothesis that activation of the Akt pathway promotes resistance to ATRA treatment at the inhibition of cell survival and invasion in lung cancer. Tretinoin 100-104 AKT serine/threonine kinase 1 Homo sapiens 65-68
23693014-9 2013 We found that ATRA treatment promotes PI3k-Akt pathway activation through transcription-independent mechanisms. Tretinoin 14-18 AKT serine/threonine kinase 1 Homo sapiens 43-46
23693014-10 2013 Interestingly, ATRA treatment induces the translocation of RARalpha to the plasma membrane, where it colocalizes with Akt. Tretinoin 15-19 AKT serine/threonine kinase 1 Homo sapiens 118-121
23693014-12 2013 Activation of the PI3k-Akt pathway by ATRA promotes invasion through Rac-GTPase, whereas pretreatment with 15e (PI3k inhibitor) or over-expression of the inactive form of Akt blocks ATRA-induced invasion. Tretinoin 38-42 AKT serine/threonine kinase 1 Homo sapiens 23-26
23704880-2 2013 Mucosal CD103(+) dendritic cells are able to produce retinoic acid from retinal, however their role in vivo and how they are influenced by specific microbial species has been poorly described. Tretinoin 53-66 integrin alpha E, epithelial-associated Mus musculus 8-13
23693014-12 2013 Activation of the PI3k-Akt pathway by ATRA promotes invasion through Rac-GTPase, whereas pretreatment with 15e (PI3k inhibitor) or over-expression of the inactive form of Akt blocks ATRA-induced invasion. Tretinoin 182-186 AKT serine/threonine kinase 1 Homo sapiens 171-174
23693014-13 2013 We also found that treatment with ATRA induces cell survival, which is inhibited by 15e or over-expression of an inactive form of Akt, through a subsequent increase in the levels of the active form of caspase-3. Tretinoin 34-38 AKT serine/threonine kinase 1 Homo sapiens 130-133
23693014-13 2013 We also found that treatment with ATRA induces cell survival, which is inhibited by 15e or over-expression of an inactive form of Akt, through a subsequent increase in the levels of the active form of caspase-3. Tretinoin 34-38 caspase 3 Homo sapiens 201-210
23693014-15 2013 In contrast, over-expression of the inactive form of Akt restores RARbeta2 expression in cells treated with ATRA, indicating that activation of the PI3k-Akt pathway inhibits the expression of ATRA target genes. Tretinoin 108-112 AKT serine/threonine kinase 1 Homo sapiens 53-56
23693014-15 2013 In contrast, over-expression of the inactive form of Akt restores RARbeta2 expression in cells treated with ATRA, indicating that activation of the PI3k-Akt pathway inhibits the expression of ATRA target genes. Tretinoin 108-112 AKT serine/threonine kinase 1 Homo sapiens 153-156
23693014-16 2013 CONCLUSION: Our results demonstrate that rapid activation of Akt blocks transcription-dependent mechanism of ATRA, promotes invasion and cell survival and confers resistance to retinoic acid treatment in lung cancer cells. Tretinoin 109-113 AKT serine/threonine kinase 1 Homo sapiens 61-64
23693014-16 2013 CONCLUSION: Our results demonstrate that rapid activation of Akt blocks transcription-dependent mechanism of ATRA, promotes invasion and cell survival and confers resistance to retinoic acid treatment in lung cancer cells. Tretinoin 177-190 AKT serine/threonine kinase 1 Homo sapiens 61-64
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 26-45 enolase 2 Homo sapiens 209-232
23656719-12 2013 FICZ causes changes in signaling events that are known to drive differentiation, and notably augments the RA-induced sustained activation of the RAF/MEK/ERK axis of the mitogen-activated protein kinase (MAPK) cascade. Tretinoin 106-108 mitogen-activated protein kinase kinase 7 Homo sapiens 149-152
23656719-12 2013 FICZ causes changes in signaling events that are known to drive differentiation, and notably augments the RA-induced sustained activation of the RAF/MEK/ERK axis of the mitogen-activated protein kinase (MAPK) cascade. Tretinoin 106-108 mitogen-activated protein kinase 1 Homo sapiens 153-156
23656719-12 2013 FICZ causes changes in signaling events that are known to drive differentiation, and notably augments the RA-induced sustained activation of the RAF/MEK/ERK axis of the mitogen-activated protein kinase (MAPK) cascade. Tretinoin 106-108 mitogen-activated protein kinase 1 Homo sapiens 203-207
23423514-9 2013 Also, retinoic acid increased CRABPII, and decreased FABP5 and NF-kappaB expression in craniopharyngioma cells. Tretinoin 6-19 nuclear factor kappa B subunit 1 Homo sapiens 63-72
23423514-11 2013 Retinoic acid at pharmacological level induced craniopharyngioma cell apoptosis via increasing FABP5/CRABPII ratio and inhibiting NF-kappaB signaling pathway. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 130-139
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 110-117
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 chemokine (C-C motif) ligand 17 Mus musculus 138-143
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 chemokine (C-C motif) ligand 22 Mus musculus 148-153
23671444-0 2013 Adenovirus-mediated RAR-beta over-expression enhances ATRA-induced neuronal differentiation of rat mesenchymal stem cells. Tretinoin 54-58 retinoic acid receptor, beta Rattus norvegicus 20-28
23671444-2 2013 All-trans retinoic acid (ATRA) activates the RA signal by regulating RAR-beta in mesenchymal stem cell (MSC)-derived neuron cells. Tretinoin 0-23 retinoic acid receptor, beta Rattus norvegicus 69-77
23671444-2 2013 All-trans retinoic acid (ATRA) activates the RA signal by regulating RAR-beta in mesenchymal stem cell (MSC)-derived neuron cells. Tretinoin 25-29 retinoic acid receptor, beta Rattus norvegicus 69-77
23671444-2 2013 All-trans retinoic acid (ATRA) activates the RA signal by regulating RAR-beta in mesenchymal stem cell (MSC)-derived neuron cells. Tretinoin 27-29 retinoic acid receptor, beta Rattus norvegicus 69-77
23671444-16 2013 CONCLUSIONS: Our results have demonstrated that adenovirus-mediated RAR-beta over-expression could facilitate neuron cell types of MSCs in vitro, indicating that the RAR-beta-activated RA signal might be a vital factor in neuronal differentiation. Tretinoin 68-70 retinoic acid receptor, beta Rattus norvegicus 166-174
23507259-4 2013 We have examined at the molecular level the crosstalk between these nuclear receptors from the point of view of their control of cell growth and show here that RA reverts estrogen-stimulated transcription of the pivotal anti-apoptotic bcl-2 gene by preventing demethylation of dimethyl lysine 9 in histone H3 (HeK9me2). Tretinoin 160-162 BCL2 apoptosis regulator Homo sapiens 235-240
23710639-5 2013 Under the all-trans-retinoic acid (RA)-induced differentiation condition, spheroids extended neurites and further up-regulated the expression of synaptophysin, NSE, CAMs, and ECM proteins. Tretinoin 10-33 enolase 2 Homo sapiens 160-163
23710639-5 2013 Under the all-trans-retinoic acid (RA)-induced differentiation condition, spheroids extended neurites and further up-regulated the expression of synaptophysin, NSE, CAMs, and ECM proteins. Tretinoin 35-37 enolase 2 Homo sapiens 160-163
23833373-8 2013 Treatment with ATRA (5 mg/kg/p.o/4 days) and GW0742, a selective PPAR-beta/delta receptor agonist (0.1 mg/kg/i.p/4 days), significantly decreased the paw volume, mechanical and TH as compared to vehicle control. Tretinoin 15-19 peroxisome proliferator-activated receptor delta Rattus norvegicus 65-74
23833373-12 2013 CONCLUSION: From above findings, it can be concluded that ATRA exerts anti-inflammatory and anti-hyperalgesic effect, possibly through activation of PPAR-beta/delta and subsequent reduction of oxido-nitrosative stress. Tretinoin 58-62 peroxisome proliferator-activated receptor delta Rattus norvegicus 149-158
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 26-45 enolase 2 Homo sapiens 234-237
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 47-49 enolase 2 Homo sapiens 209-232
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 47-49 enolase 2 Homo sapiens 234-237
23593353-1 2013 This study indicates that embryonic stem cells [ESCs] cultured with retinoic acid and activin A significantly upregulate the miRNA let-7e. Tretinoin 68-81 sperm acrosome associated 6 Mus musculus 131-137
23588494-0 2013 Retinoic acid represses invasion and stem cell phenotype by induction of the metastasis suppressors RARRES1 and LXN. Tretinoin 0-13 retinoic acid receptor responder 1 Homo sapiens 100-107
23588494-0 2013 Retinoic acid represses invasion and stem cell phenotype by induction of the metastasis suppressors RARRES1 and LXN. Tretinoin 0-13 latexin Homo sapiens 112-115
23588494-4 2013 Here, we identified RARRES1 and LXN as highly significantly downregulated genes in human prostate SCs, whose expression was induced by the pro-differentiation agent all-trans retinoic acid (atRA). Tretinoin 175-188 retinoic acid receptor responder 1 Homo sapiens 20-27
23588494-4 2013 Here, we identified RARRES1 and LXN as highly significantly downregulated genes in human prostate SCs, whose expression was induced by the pro-differentiation agent all-trans retinoic acid (atRA). Tretinoin 175-188 latexin Homo sapiens 32-35
23588494-4 2013 Here, we identified RARRES1 and LXN as highly significantly downregulated genes in human prostate SCs, whose expression was induced by the pro-differentiation agent all-trans retinoic acid (atRA). Tretinoin 190-194 retinoic acid receptor responder 1 Homo sapiens 20-27
23588494-4 2013 Here, we identified RARRES1 and LXN as highly significantly downregulated genes in human prostate SCs, whose expression was induced by the pro-differentiation agent all-trans retinoic acid (atRA). Tretinoin 190-194 latexin Homo sapiens 32-35
23588494-7 2013 Expression of both RARRES1 and LXN was co-ordinately repressed by DNA methylation in prostate cancer cell lines and inhibition of RARRES1 and LXN increased the invasive capacity of primary prostate cultures, which also fully rescued an inhibitory effect induced by atRA. Tretinoin 265-269 retinoic acid receptor responder 1 Homo sapiens 19-26
23588494-7 2013 Expression of both RARRES1 and LXN was co-ordinately repressed by DNA methylation in prostate cancer cell lines and inhibition of RARRES1 and LXN increased the invasive capacity of primary prostate cultures, which also fully rescued an inhibitory effect induced by atRA. Tretinoin 265-269 latexin Homo sapiens 31-34
23428742-7 2013 Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. Tretinoin 37-39 fibronectin 1 Homo sapiens 145-191
23509325-1 2013 In PML/RARA-driven acute promyelocytic leukemia (APL), retinoic acid (RA) induces leukemia cell differentiation and transiently clears the disease. Tretinoin 55-68 promyelocytic leukemia Mus musculus 3-6
23509325-1 2013 In PML/RARA-driven acute promyelocytic leukemia (APL), retinoic acid (RA) induces leukemia cell differentiation and transiently clears the disease. Tretinoin 7-9 promyelocytic leukemia Mus musculus 3-6
23396089-9 2013 In contrast, ATRA increased the expression of SOSC2, BRAF, MEK, and ERK genes. Tretinoin 13-17 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 53-57
23396089-9 2013 In contrast, ATRA increased the expression of SOSC2, BRAF, MEK, and ERK genes. Tretinoin 13-17 mitogen-activated protein kinase kinase 7 Homo sapiens 59-62
23396089-9 2013 In contrast, ATRA increased the expression of SOSC2, BRAF, MEK, and ERK genes. Tretinoin 13-17 mitogen-activated protein kinase 1 Homo sapiens 68-71
23428742-7 2013 Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. Tretinoin 37-39 thrombospondin 1 Homo sapiens 193-209
23428742-7 2013 Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. Tretinoin 37-39 cadherin 1 Homo sapiens 286-296
23428742-7 2013 Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. Tretinoin 37-39 matrix metallopeptidase 3 Homo sapiens 301-305
23318218-5 2013 mRNA and protein levels of the neural-markers Nestin, NSE, MAP-2, Tau and Tuj1 were stronger in neural-like cells derived from all-trans retinoic acid-pretreated mesenchymal stem cells than in those not pre-induction. Tretinoin 137-150 enolase 2 Homo sapiens 54-57
23318218-12 2013 The neuronal differentiation promoting effects of all-trans retinoic acid on mesenchymal stem cells could be inhibited by siRNA silencing of retinoic acid receptor beta and by LE135, an inhibitor of retinoic acid receptor beta. Tretinoin 60-73 retinoic acid receptor beta Homo sapiens 141-168
23318218-12 2013 The neuronal differentiation promoting effects of all-trans retinoic acid on mesenchymal stem cells could be inhibited by siRNA silencing of retinoic acid receptor beta and by LE135, an inhibitor of retinoic acid receptor beta. Tretinoin 60-73 retinoic acid receptor beta Homo sapiens 199-226
23314291-10 2013 These data reveals that the effect of RA prevails in the presence of exogenous FGF-2 thus resulting in the direction of hESCs toward the ExE lineage. Tretinoin 38-40 fibroblast growth factor 2 Homo sapiens 79-84
23457382-8 2013 ATRA significantly increased intracellular IFN-gamma in cases but not in controls. Tretinoin 0-4 interferon gamma Homo sapiens 43-52
23404856-6 2013 We found that MEK inhibition decreased NIS protein levels in all-trans retinoic acid/hydrocortisone-treated MCF-7 cells as well as human breast cancer cells expressing exogenous NIS. Tretinoin 71-84 mitogen-activated protein kinase kinase 7 Homo sapiens 14-17
23385081-5 2013 Conversely, activated microglia showed increased protein expression of RA-degrading cytochromes CYP26A1, CYP26B1, CYP3A4 and CYP2C. Tretinoin 71-73 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 105-112
23352986-3 2013 Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5 muM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). Tretinoin 79-83 solute carrier family 22 member 1 Homo sapiens 245-279
23352986-3 2013 Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5 muM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). Tretinoin 79-83 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 356-388
23352986-3 2013 Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5 muM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). Tretinoin 79-83 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 390-394
23352986-5 2013 Some transporters such as OATP1B3 and the bile salt export pump (BSEP) were however down-regulated by atRA in primary human hepatocytes, but induced in HepaRG cells, thus pointing out discrepancies between these two liver cell models in terms of detoxifying protein regulation. Tretinoin 102-106 solute carrier organic anion transporter family member 1B3 Homo sapiens 26-33
23352986-6 2013 atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARalpha and RXRalpha through siRNA transfection in HepaRG cells. Tretinoin 0-4 solute carrier family 22 member 1 Homo sapiens 56-60
23001792-3 2013 Retinoic acid (RA) acts as a negative regulator of PcG actions in stem cells, but has shown limited therapeutic potential in some solid tumors, including colorectal cancer, in part because of retinoic acid receptor beta silencing. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 192-219
23018522-0 2013 Role of COUP-TFI during retinoic acid-induced differentiation of P19 cells to endodermal cells. Tretinoin 24-37 nuclear receptor subfamily 2 group F member 1 Gallus gallus 8-16
23018522-4 2013 RA treatment of wild type P19 cells results in a dramatic increase in the expression of COUP-TFI; however, COUP-TFI mRNA levels fail to be elevated upon RA treatment of AS cells indicating that PBX expression is required for elevation in COUP-TFI expression. Tretinoin 0-2 nuclear receptor subfamily 2 group F member 1 Gallus gallus 88-96
23457382-2 2013 The effect of all-transretinoic acid (ATRA) was studied on cultured CD4+ T cells of patients with AS compared to controls. Tretinoin 14-36 CD4 molecule Homo sapiens 68-71
23457382-2 2013 The effect of all-transretinoic acid (ATRA) was studied on cultured CD4+ T cells of patients with AS compared to controls. Tretinoin 38-42 CD4 molecule Homo sapiens 68-71
23531410-5 2013 Numerous genes belonging to specific signaling pathways (the Hedgehog, Notch, Wnt, FGF, TGFbeta/BMP, and retinoic acid pathways), and/or to the homeobox gene superfamily, were also uncovered when a less stringent fold change threshold was used. Tretinoin 105-118 transforming growth factor beta 1 Homo sapiens 88-95
23531410-9 2013 Two networks ERK1/2 kinases and tretinoin were involved in differential molar morphogenesis. Tretinoin 32-41 mitogen-activated protein kinase 3 Homo sapiens 13-19
23338237-2 2013 Most work on lymphoid cells has focused on the influence of RA on CD4 T cells. Tretinoin 60-62 CD4 molecule Homo sapiens 66-69
23334789-4 2013 Using genetic tools to label and interfere with T cell-development transcription factors, we found that CD4(+) T cells acquired the CD8-lineage transcription factor Runx3 and lost the CD4-lineage transcription factor ThPOK and their differentiation into the T(H)17 subset of helper T cells and colitogenic potential, in a manner dependent on transforming growth factor-beta (TGF-beta) and retinoic acid. Tretinoin 389-402 CD4 molecule Homo sapiens 104-107
23267795-13 2013 atRA not only activated distinct pathways to stimulate the expression of Scpep1, a retinoid-inducible gene, under normoxic conditions, but also acted as a CoCl(2)-mimicking hypoxia. Tretinoin 0-4 serine carboxypeptidase 1 Rattus norvegicus 73-79
23267795-14 2013 CONCLUSION: The protective effects of atRA against hypoxia-induced injury might be involved in suppression of VEGF expression via stimulating Scpep1 distinct pathways and inhibiting the NFkappaB pathway. Tretinoin 38-42 serine carboxypeptidase 1 Rattus norvegicus 142-148
23447598-8 2013 Enhanced hop isoform expression, elicited by in vitro treatment of E10.5 precursors with retinoic acid, correlated with sustained pro-mitogenic action of PACAP beyond the developmental switch. Tretinoin 89-102 adenylate cyclase activating polypeptide 1 Mus musculus 154-159
23382200-0 2013 8-CPT-cAMP/all-trans retinoic acid targets t(11;17) acute promyelocytic leukemia through enhanced cell differentiation and PLZF/RARalpha degradation. Tretinoin 11-34 zinc finger and BTB domain containing 16 Mus musculus 123-127
23382200-3 2013 Mechanistically, in combination with ATRA, 8-CPT-cAMP activates PKA, causing phosphorylation of PLZF/RARalpha at Ser765 and resulting in increased dissociation of the silencing mediator for retinoic acid and thyroid hormone receptors/nuclear receptor corepressor from PLZF/RARalpha. Tretinoin 37-41 zinc finger and BTB domain containing 16 Mus musculus 96-100
23382200-3 2013 Mechanistically, in combination with ATRA, 8-CPT-cAMP activates PKA, causing phosphorylation of PLZF/RARalpha at Ser765 and resulting in increased dissociation of the silencing mediator for retinoic acid and thyroid hormone receptors/nuclear receptor corepressor from PLZF/RARalpha. Tretinoin 37-41 zinc finger and BTB domain containing 16 Mus musculus 268-272
23382200-3 2013 Mechanistically, in combination with ATRA, 8-CPT-cAMP activates PKA, causing phosphorylation of PLZF/RARalpha at Ser765 and resulting in increased dissociation of the silencing mediator for retinoic acid and thyroid hormone receptors/nuclear receptor corepressor from PLZF/RARalpha. Tretinoin 190-203 zinc finger and BTB domain containing 16 Mus musculus 96-100
23382200-5 2013 Meanwhile, 8-CPT-cAMP also potentiated ATRA-induced degradation of PLZF/RARalpha through its Ser765 phosphorylation. Tretinoin 39-43 zinc finger and BTB domain containing 16 Mus musculus 67-71
23429425-0 2013 Expression of claudins -2 and -4 and cingulin is coordinated with the start of stratification and differentiation in corneal epithelial cells: retinoic acid reversibly disrupts epithelial barrier. Tretinoin 143-156 cingulin Oryctolagus cuniculus 37-45
23331247-8 2013 Suppressions of AGEs, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-beta) in serum of MG-induced rats were attenuated in the monascin administration group treated with retinoic acid (RA). Tretinoin 204-206 interleukin 1 beta Rattus norvegicus 67-84
23228856-5 2013 Here we show that under permissive epigenetic conditions, TNIP1 expression is induced by all trans retinoic acid (ATRA). Tretinoin 93-112 TNFAIP3 interacting protein 1 Homo sapiens 58-63
23228856-5 2013 Here we show that under permissive epigenetic conditions, TNIP1 expression is induced by all trans retinoic acid (ATRA). Tretinoin 114-118 TNFAIP3 interacting protein 1 Homo sapiens 58-63
23264745-5 2013 Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm"s tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARgamma(-/-) cells. Tretinoin 177-179 WT1 transcription factor Homo sapiens 81-84
23331247-8 2013 Suppressions of AGEs, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-beta) in serum of MG-induced rats were attenuated in the monascin administration group treated with retinoic acid (RA). Tretinoin 189-202 tumor necrosis factor Rattus norvegicus 22-49
23331247-8 2013 Suppressions of AGEs, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-beta) in serum of MG-induced rats were attenuated in the monascin administration group treated with retinoic acid (RA). Tretinoin 189-202 tumor necrosis factor Rattus norvegicus 51-60
23331247-8 2013 Suppressions of AGEs, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-beta) in serum of MG-induced rats were attenuated in the monascin administration group treated with retinoic acid (RA). Tretinoin 189-202 interleukin 1 beta Rattus norvegicus 67-84
23331247-9 2013 RA treatment resulted in Nrf2 inactivation by increasing RA receptor-alpha (RARalpha) activity, suggesting that RA acts as an inhibitor of Nrf2. Tretinoin 0-2 NFE2 like bZIP transcription factor 2 Rattus norvegicus 25-29
23331247-9 2013 RA treatment resulted in Nrf2 inactivation by increasing RA receptor-alpha (RARalpha) activity, suggesting that RA acts as an inhibitor of Nrf2. Tretinoin 0-2 NFE2 like bZIP transcription factor 2 Rattus norvegicus 139-143
23331247-9 2013 RA treatment resulted in Nrf2 inactivation by increasing RA receptor-alpha (RARalpha) activity, suggesting that RA acts as an inhibitor of Nrf2. Tretinoin 57-59 NFE2 like bZIP transcription factor 2 Rattus norvegicus 25-29
23331247-9 2013 RA treatment resulted in Nrf2 inactivation by increasing RA receptor-alpha (RARalpha) activity, suggesting that RA acts as an inhibitor of Nrf2. Tretinoin 57-59 NFE2 like bZIP transcription factor 2 Rattus norvegicus 139-143
23714660-11 2013 ATRA also promoted the CD44(+)CD24(-) subpopulation to differentiate. Tretinoin 0-4 CD24 molecule Homo sapiens 30-34
22733143-2 2013 Previous studies showed that retinoic acid (RA) as the vitamin A metabolite is crucial for controlling Stra8 (Stimulated by retinoic acid gene 8) expression in the gonad and to initiate meiosis; however, the mechanism by which retinoid-signaling acts has remained unclear. Tretinoin 29-42 stimulated by retinoic acid 8 Gallus gallus 103-108
22733143-2 2013 Previous studies showed that retinoic acid (RA) as the vitamin A metabolite is crucial for controlling Stra8 (Stimulated by retinoic acid gene 8) expression in the gonad and to initiate meiosis; however, the mechanism by which retinoid-signaling acts has remained unclear. Tretinoin 29-42 stimulated by retinoic acid 8 Gallus gallus 110-144
22733143-2 2013 Previous studies showed that retinoic acid (RA) as the vitamin A metabolite is crucial for controlling Stra8 (Stimulated by retinoic acid gene 8) expression in the gonad and to initiate meiosis; however, the mechanism by which retinoid-signaling acts has remained unclear. Tretinoin 44-46 stimulated by retinoic acid 8 Gallus gallus 103-108
22733143-2 2013 Previous studies showed that retinoic acid (RA) as the vitamin A metabolite is crucial for controlling Stra8 (Stimulated by retinoic acid gene 8) expression in the gonad and to initiate meiosis; however, the mechanism by which retinoid-signaling acts has remained unclear. Tretinoin 44-46 stimulated by retinoic acid 8 Gallus gallus 110-144
22733143-5 2013 It was observed from the increase in Raldh2 mRNA expression levels and decreases in Cyp26b1 (the enzyme for RA catabolism) expression levels during meiosis that requirement for RA accumulation is essential to sustain meiosis. Tretinoin 108-110 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 84-91
23178912-8 2013 Moreover, expression of these transcripts was further enhanced, if G93A-SOD1 cells were differentiated by retinoic acid (RA). Tretinoin 106-119 superoxide dismutase 1 Homo sapiens 72-76
23178912-8 2013 Moreover, expression of these transcripts was further enhanced, if G93A-SOD1 cells were differentiated by retinoic acid (RA). Tretinoin 121-123 superoxide dismutase 1 Homo sapiens 72-76
23221369-8 2013 Furthermore, undifferentiated spermatogonia overexpressing miR-221/222 are resistant to retinoic acid-induced transition to a KIT(+) state and are incapable of differentiation in vivo. Tretinoin 88-101 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 126-129
23221399-9 2013 When undifferentiated spermatogonia were exposed to RA, Mir146 was downregulated along with a marker for undifferentiated germ cells, zinc finger and BTB domain containing 16 (Zbtb16; Plzf); Kit was upregulated. Tretinoin 52-54 zinc finger and BTB domain containing 16 Mus musculus 176-182
23221399-9 2013 When undifferentiated spermatogonia were exposed to RA, Mir146 was downregulated along with a marker for undifferentiated germ cells, zinc finger and BTB domain containing 16 (Zbtb16; Plzf); Kit was upregulated. Tretinoin 52-54 zinc finger and BTB domain containing 16 Mus musculus 184-188
23237802-0 2013 B56alpha subunit of protein phosphatase 2A mediates retinoic acid-induced decreases in phosphorylation of endothelial nitric oxide synthase at serine 1179 and nitric oxide production in bovine aortic endothelial cells. Tretinoin 52-65 nitric oxide synthase 3 Bos taurus 106-139
23392891-0 2013 Differential regulation of TauT by calcitriol and retinoic acid via VDR/RXR in LLC-PK1 and MCF-7 cells. Tretinoin 50-63 vitamin D receptor Sus scrofa 68-71
23267101-8 2013 In contrast, adult Rdh10-deficient mice exhibit phenotypically normal spermatogenesis, indicating that during development a change occurs in either the cellular source of RA or the retinaldehyde dehydrogenase involved in RA synthesis. Tretinoin 221-223 retinol dehydrogenase 10 (all-trans) Mus musculus 19-24
23267101-8 2013 In contrast, adult Rdh10-deficient mice exhibit phenotypically normal spermatogenesis, indicating that during development a change occurs in either the cellular source of RA or the retinaldehyde dehydrogenase involved in RA synthesis. Tretinoin 171-173 retinol dehydrogenase 10 (all-trans) Mus musculus 19-24
21935707-4 2013 We aimed to evaluate the protein targets for transglutaminase 2 in cell response to NMDA-induced excitotoxic stress, using SH-SY5Y neuroblastoma cells which express high tranglutaminase 2 levels upon retinoic acid-driven differentiation toward neurons. Tretinoin 200-213 transglutaminase 2 Homo sapiens 45-63
23022267-0 2013 Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence. Tretinoin 46-59 mitogen-activated protein kinase 1 Homo sapiens 123-126
24648886-8 2013 Sox17, GATA6 and HNF4alpha were expressed after exposure a combination of oncostatin M, epidermal growth factor, retinoic acid, dexamethasone and ITS (OERDITS). Tretinoin 113-126 hepatocyte nuclear factor 4 alpha Homo sapiens 17-26
23022267-0 2013 Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence. Tretinoin 46-59 AKT serine/threonine kinase 1 Homo sapiens 132-135
23022267-0 2013 Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence. Tretinoin 46-59 tumor protein p53 Homo sapiens 147-150
24592121-0 2013 Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells. Tretinoin 61-74 BCL2 apoptosis regulator Homo sapiens 37-42
22982089-0 2013 Cellular retinoic acid binding protein I mediates rapid non-canonical activation of ERK1/2 by all-trans retinoic acid. Tretinoin 9-22 mitogen-activated protein kinase 3 Homo sapiens 84-90
22982089-2 2013 AtRA could also elicit certain non-canonical activities including, mostly, rapid activation of extracellular signal regulated kinase 1/2 (ERK1/2); but the mechanism was unclear. Tretinoin 0-4 mitogen-activated protein kinase 1 Homo sapiens 95-136
22982089-2 2013 AtRA could also elicit certain non-canonical activities including, mostly, rapid activation of extracellular signal regulated kinase 1/2 (ERK1/2); but the mechanism was unclear. Tretinoin 0-4 mitogen-activated protein kinase 3 Homo sapiens 138-144
22982089-3 2013 In this study, we have found that cellular retinoic acid binding protein I (CRABPI) mediates the non-canonical, RAR- and membrane signal-independent activation of ERK1/2 by atRA in various cellular backgrounds. Tretinoin 173-177 mitogen-activated protein kinase 3 Homo sapiens 163-169
23319320-4 2013 Western blotting showed a loss of NF-kappaB, Bcl-2 and p-Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA-treated AML-I preadipocytes. Tretinoin 114-118 nuclear factor kappa B subunit 1 Homo sapiens 34-43
23319320-4 2013 Western blotting showed a loss of NF-kappaB, Bcl-2 and p-Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA-treated AML-I preadipocytes. Tretinoin 114-118 BCL2 apoptosis regulator Homo sapiens 45-50
23319320-4 2013 Western blotting showed a loss of NF-kappaB, Bcl-2 and p-Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA-treated AML-I preadipocytes. Tretinoin 114-118 AKT serine/threonine kinase 1 Homo sapiens 57-60
23319320-4 2013 Western blotting showed a loss of NF-kappaB, Bcl-2 and p-Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA-treated AML-I preadipocytes. Tretinoin 114-118 AKT serine/threonine kinase 1 Homo sapiens 94-97
23319320-6 2013 Expression of fatty acid synthase (FAS) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) proteins was increased in ATRA-treated cells. Tretinoin 132-136 peroxisome proliferator activated receptor gamma Homo sapiens 44-92
23319320-6 2013 Expression of fatty acid synthase (FAS) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) proteins was increased in ATRA-treated cells. Tretinoin 132-136 peroxisome proliferator activated receptor gamma Homo sapiens 94-104
24592121-0 2013 Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells. Tretinoin 61-74 BCL2 associated X, apoptosis regulator Homo sapiens 48-51
24592121-6 2013 In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. Tretinoin 30-32 BCL2 apoptosis regulator Homo sapiens 65-70
24592121-6 2013 In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. Tretinoin 30-32 BCL2 associated X, apoptosis regulator Homo sapiens 75-78
24022014-8 2013 In addition, CCR7, which mediates homing to lymph nodes, was expressed by DCs differentiated in the presence of RA, and also to a lesser extent by the other DC types. Tretinoin 112-114 C-C motif chemokine receptor 7 Homo sapiens 13-17
22933113-5 2013 Estrogen decreased Aldh1a3 expression, limiting conversion of retinaldehyde (Rald) to RA. Tretinoin 86-88 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 19-26
23688132-5 2013 These inhibitors generally target the cytochrome P450 (CYP) enzymes because RA clearance is predominantly mediated by P450s. Tretinoin 76-78 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 38-53
23688132-5 2013 These inhibitors generally target the cytochrome P450 (CYP) enzymes because RA clearance is predominantly mediated by P450s. Tretinoin 76-78 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 55-58
23688132-6 2013 Since the initial identification of inhibitors of RA metabolism, CYP26 enzymes have been characterized as the main enzymes responsible for RA clearance. Tretinoin 50-52 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 65-70
23688132-6 2013 Since the initial identification of inhibitors of RA metabolism, CYP26 enzymes have been characterized as the main enzymes responsible for RA clearance. Tretinoin 139-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 65-70
23688132-8 2013 The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner. Tretinoin 74-76 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 38-43
23688132-8 2013 The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner. Tretinoin 74-76 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 131-136
23688132-8 2013 The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner. Tretinoin 194-196 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 38-43
23688132-8 2013 The basic principle of development of CYP26 inhibitors is that endogenous RA concentrations will be increased in the presence of a CYP26 inhibitor, thus, potentiating the activity of endogenous RA in a cell-type specific manner. Tretinoin 194-196 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 131-136
23142153-0 2013 Retinoic acid protects against proteasome inhibition associated cell death in SH-SY5Y cells via the AKT pathway. Tretinoin 0-13 AKT serine/threonine kinase 1 Homo sapiens 100-103
23554794-0 2013 All-trans retinoic acid upregulates VEGF expression in glioma cells in vitro. Tretinoin 10-23 vascular endothelial growth factor A Homo sapiens 36-40
23554794-3 2013 We examined the effect of ATRA on the expression of vascular endothelial growth factor (VEGF) in different glioma cell lines and investigated the underlying mechanism, intending to partially reveal the effects of ATRA on angiogenesis of glioma. Tretinoin 26-30 vascular endothelial growth factor A Homo sapiens 52-86
23554794-3 2013 We examined the effect of ATRA on the expression of vascular endothelial growth factor (VEGF) in different glioma cell lines and investigated the underlying mechanism, intending to partially reveal the effects of ATRA on angiogenesis of glioma. Tretinoin 26-30 vascular endothelial growth factor A Homo sapiens 88-92
23554794-7 2013 After treatment with 5 and 10 micromol/L ATRA, the VEGF mRNA transcript levels in glioma cells increased remarkably, compared with that in the control group, and the relative protein expression of VEGF was also up-regulated. Tretinoin 41-45 vascular endothelial growth factor A Homo sapiens 51-55
23554794-7 2013 After treatment with 5 and 10 micromol/L ATRA, the VEGF mRNA transcript levels in glioma cells increased remarkably, compared with that in the control group, and the relative protein expression of VEGF was also up-regulated. Tretinoin 41-45 vascular endothelial growth factor A Homo sapiens 197-201
23554794-9 2013 ATRA increases the expression of VEGF in glioma cells at both transcriptional and translational levels. Tretinoin 0-4 vascular endothelial growth factor A Homo sapiens 33-37
23014973-6 2013 The effects of RA were further enhanced by bone morphogenetic protein 2 (BMP2) and resultant Smad signaling. Tretinoin 15-17 bone morphogenetic protein 2 Mus musculus 43-71
23014973-6 2013 The effects of RA were further enhanced by bone morphogenetic protein 2 (BMP2) and resultant Smad signaling. Tretinoin 15-17 bone morphogenetic protein 2 Mus musculus 73-77
23014973-8 2013 In view of these findings, RA likely stimulates osteoblast differentiation through the BMP2-Smad-Runx2/Msx2 pathway. Tretinoin 27-29 bone morphogenetic protein 2 Mus musculus 87-91
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 bone morphogenetic protein 2 Mus musculus 35-39
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 CCAAT/enhancer binding protein (C/EBP), delta Mus musculus 211-221
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 CCAAT/enhancer binding protein (C/EBP), delta Mus musculus 272-282
23142153-8 2013 In addition, although RA activates both the AKT and ERK phosphorylation signaling pathways, only pretreatment with LY294002, an inhibitor of PI3-kinase in the AKT pathway, removed the protective effect of RA from the cells. Tretinoin 22-24 AKT serine/threonine kinase 1 Homo sapiens 44-47
23142153-8 2013 In addition, although RA activates both the AKT and ERK phosphorylation signaling pathways, only pretreatment with LY294002, an inhibitor of PI3-kinase in the AKT pathway, removed the protective effect of RA from the cells. Tretinoin 22-24 mitogen-activated protein kinase 1 Homo sapiens 52-55
23142153-8 2013 In addition, although RA activates both the AKT and ERK phosphorylation signaling pathways, only pretreatment with LY294002, an inhibitor of PI3-kinase in the AKT pathway, removed the protective effect of RA from the cells. Tretinoin 205-207 AKT serine/threonine kinase 1 Homo sapiens 159-162
23142153-9 2013 This finding implies that RA activation of the AKT signaling cascade takes precedence over its activation of ERK1/2 phosphorylation, and that this selective effect of RA is key to its protection of epoxomicin-treated cells. Tretinoin 26-28 AKT serine/threonine kinase 1 Homo sapiens 47-50
23129057-0 2013 Growth inhibition of Tax-activated human Jurkat leukemia T cells by all-trans retinoic acid requires JNK-1 inhibition. Tretinoin 90-103 mitogen-activated protein kinase 8 Homo sapiens 113-118
23909735-4 2013 Moreover, induction of megalin and Dab2 (protein and mRNA abundance) by all-trans-retinoic acid (RA) enhanced DBP uptake. Tretinoin 72-95 D-box binding PAR bZIP transcription factor Homo sapiens 110-113
23909735-4 2013 Moreover, induction of megalin and Dab2 (protein and mRNA abundance) by all-trans-retinoic acid (RA) enhanced DBP uptake. Tretinoin 97-99 D-box binding PAR bZIP transcription factor Homo sapiens 110-113
23909735-8 2013 Furthermore, DBP uptake was stimulated by low-dose RA supplementation in LNCaP, PC-3, and Caco-2 cells. Tretinoin 51-53 D-box binding PAR bZIP transcription factor Homo sapiens 13-16
23129057-2 2013 In this study, we report that all-trans retinoic acid (ATRA) decreases Jun N-terminal kinase 1 (JNK-1) activity, antagonizing the effect of the Tax protein in Jurkat leukemia T cells transiently transfected for expressing the Tax protein. Tretinoin 30-65 mitogen-activated protein kinase 8 Homo sapiens 83-106
23129057-2 2013 In this study, we report that all-trans retinoic acid (ATRA) decreases Jun N-terminal kinase 1 (JNK-1) activity, antagonizing the effect of the Tax protein in Jurkat leukemia T cells transiently transfected for expressing the Tax protein. Tretinoin 30-65 mitogen-activated protein kinase 8 Homo sapiens 108-113
23129057-2 2013 In this study, we report that all-trans retinoic acid (ATRA) decreases Jun N-terminal kinase 1 (JNK-1) activity, antagonizing the effect of the Tax protein in Jurkat leukemia T cells transiently transfected for expressing the Tax protein. Tretinoin 67-71 mitogen-activated protein kinase 8 Homo sapiens 83-106
23129057-2 2013 In this study, we report that all-trans retinoic acid (ATRA) decreases Jun N-terminal kinase 1 (JNK-1) activity, antagonizing the effect of the Tax protein in Jurkat leukemia T cells transiently transfected for expressing the Tax protein. Tretinoin 67-71 mitogen-activated protein kinase 8 Homo sapiens 108-113
23129057-4 2013 The decrease in JNK-1 activity was followed by a marked decrease in the expression of interleukin (IL)-2 and a weak increase in interferon (IFN)-gamma in Jurkat cells treated with ATRA in a dose-dependent manner, suggesting a correlation between the expression of JNK-1 and the activity of the Tax protein. Tretinoin 216-220 mitogen-activated protein kinase 8 Homo sapiens 28-33
23129057-4 2013 The decrease in JNK-1 activity was followed by a marked decrease in the expression of interleukin (IL)-2 and a weak increase in interferon (IFN)-gamma in Jurkat cells treated with ATRA in a dose-dependent manner, suggesting a correlation between the expression of JNK-1 and the activity of the Tax protein. Tretinoin 216-220 interleukin 2 Homo sapiens 98-128
23129057-4 2013 The decrease in JNK-1 activity was followed by a marked decrease in the expression of interleukin (IL)-2 and a weak increase in interferon (IFN)-gamma in Jurkat cells treated with ATRA in a dose-dependent manner, suggesting a correlation between the expression of JNK-1 and the activity of the Tax protein. Tretinoin 216-220 interferon gamma Homo sapiens 152-174
23129057-4 2013 The decrease in JNK-1 activity was followed by a marked decrease in the expression of interleukin (IL)-2 and a weak increase in interferon (IFN)-gamma in Jurkat cells treated with ATRA in a dose-dependent manner, suggesting a correlation between the expression of JNK-1 and the activity of the Tax protein. Tretinoin 216-220 mitogen-activated protein kinase 8 Homo sapiens 312-317
23129057-6 2013 In transfection studies using a luciferase reporter construct expressing the IL-2 promoter or a tandem repeat of AP-1 or NF-kappaB, the inhibitory effect of ATRA on the IL-2 promoter and AP-1 construct was confirmed at the transcriptional level. Tretinoin 181-185 interleukin 2 Homo sapiens 89-93
23129057-6 2013 In transfection studies using a luciferase reporter construct expressing the IL-2 promoter or a tandem repeat of AP-1 or NF-kappaB, the inhibitory effect of ATRA on the IL-2 promoter and AP-1 construct was confirmed at the transcriptional level. Tretinoin 181-185 nuclear factor kappa B subunit 1 Homo sapiens 133-142
23129057-6 2013 In transfection studies using a luciferase reporter construct expressing the IL-2 promoter or a tandem repeat of AP-1 or NF-kappaB, the inhibitory effect of ATRA on the IL-2 promoter and AP-1 construct was confirmed at the transcriptional level. Tretinoin 181-185 interleukin 2 Homo sapiens 193-197
23527272-0 2013 The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-beta. Tretinoin 105-118 CD79a molecule Homo sapiens 86-89
22576577-5 2013 The enhancer consists of at least 11 transcription factor binding sites and is responsive to various signal transduction pathways including cAMP, retinoic acid, endothelin-1, and cytokines, all of which are known to alter renin mRNA levels. Tretinoin 146-159 renin Homo sapiens 222-227
23527272-2 2013 Mucosal dendritic cells (DCs) are the primary antigen presenting cells driving TI IgA synthesis, by producing a proliferation-inducing ligand (APRIL), B cell activating factor (BAFF), Retinoic Acid (RA), TGF-beta or nitric oxide (NO). Tretinoin 199-201 CD79a molecule Homo sapiens 82-85
23409080-9 2013 Increased retinoic acid signaling in these cells was revealed by increased expression of the retinoic acid metabolizing cytochrome P450 (CYP26B1), a transcriptional target of retinoic acid signaling. Tretinoin 10-23 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 137-144
23554907-3 2013 However, RA-treated RA-resistant HL60 continue to exhibit sustained MEK/ERK activation, and one of the two sequentially emergent resistant lines retains RA-inducible CD38 expression. Tretinoin 9-11 mitogen-activated protein kinase kinase 7 Homo sapiens 68-71
23554907-3 2013 However, RA-treated RA-resistant HL60 continue to exhibit sustained MEK/ERK activation, and one of the two sequentially emergent resistant lines retains RA-inducible CD38 expression. Tretinoin 9-11 mitogen-activated protein kinase 1 Homo sapiens 72-75
23409080-9 2013 Increased retinoic acid signaling in these cells was revealed by increased expression of the retinoic acid metabolizing cytochrome P450 (CYP26B1), a transcriptional target of retinoic acid signaling. Tretinoin 93-106 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 137-144
23409080-9 2013 Increased retinoic acid signaling in these cells was revealed by increased expression of the retinoic acid metabolizing cytochrome P450 (CYP26B1), a transcriptional target of retinoic acid signaling. Tretinoin 93-106 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 137-144
23102850-3 2013 The objective was to elucidate the effects of exogenous RA and a RARalpha antagonist on gene expression of ALDH1, CYP26b1, RARalpha, cellular RA-binding protein II, and STRA8 in an in vitro organ culture model of canine testis. Tretinoin 56-58 stimulated by retinoic acid 8 Canis lupus familiaris 169-174
23135993-6 2013 One hundred fifty three protein spots with significantly different intensities were identified by MS. We detected alterations in the abundance of several proteins assigned to retinoic acid metabolism (e.g. retinal-binding protein 5) and the actin-cytoskeleton (e.g. vinculin and gelsolin). Tretinoin 175-188 vinculin Gallus gallus 266-274
23176567-3 2013 This investigation was performed to study the effect of ATRA in RIF rats and its effect on the TGF-beta1/Smad3 signaling pathway. Tretinoin 56-60 transforming growth factor, beta 1 Rattus norvegicus 95-104
23176567-3 2013 This investigation was performed to study the effect of ATRA in RIF rats and its effect on the TGF-beta1/Smad3 signaling pathway. Tretinoin 56-60 SMAD family member 3 Rattus norvegicus 105-110
23378917-3 2013 An essential step in this protocol was the generation of pancreatic precursor cell that express Pdx1 based on induction by a combination of 5-aza-2"-deoxycytidine, trichostatin A, retinoic acid, and a mix of insulin, transferrin and selenite. Tretinoin 180-193 pancreatic and duodenal homeobox 1 Rattus norvegicus 96-100
22947624-4 2013 Recent findings indicate that, in mice, the sex-specific timing of entry into meiosis is governed by the balance between 2 secreted signalling molecules, retinoic acid (RA), which promotes entry into meiosis, and fibroblast growth factor 9 (FGF9), which counteracts RA. Tretinoin 266-268 fibroblast growth factor 9 Mus musculus 241-245
23400919-9 2013 CYP2E1 also degrades retinoic acid and retinol to polar metabolites. Tretinoin 21-34 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 0-6
23102850-8 2013 In conclusion, exogenous RA decreased mRNA abundance of ALDH1 and increased mRNA abundance of RA signaling molecules and its downstream effectors (CYP26b1, CRABII, and STRA8), whereas treatment with a RARalpha antagonist effectively decreased RARalpha and RA metabolism molecules and its downstream effectors in canine testis. Tretinoin 25-27 stimulated by retinoic acid 8 Canis lupus familiaris 168-173
23105114-0 2012 Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RARs) and peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta). Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 89-136
23132926-10 2012 The anti-cytotoxic effects of retinoic acid were impaired in GPx3-inactivated myoblasts, which indicates that GPx3 regulates the antioxidative effects of retinoic acid. Tretinoin 30-43 glutathione peroxidase 3 Homo sapiens 61-65
23132926-10 2012 The anti-cytotoxic effects of retinoic acid were impaired in GPx3-inactivated myoblasts, which indicates that GPx3 regulates the antioxidative effects of retinoic acid. Tretinoin 30-43 glutathione peroxidase 3 Homo sapiens 110-114
23217322-4 2012 Therefore, for the first time, the hyphenated ACE with a high-sensitivity cell was developed and employed to investigate the binding of retinol and retinoic acid in nanomolars with human serum albumin (HSA) and bovine serum albumin (BSA) under physiological conditions. Tretinoin 148-161 albumin Homo sapiens 187-200
23217322-4 2012 Therefore, for the first time, the hyphenated ACE with a high-sensitivity cell was developed and employed to investigate the binding of retinol and retinoic acid in nanomolars with human serum albumin (HSA) and bovine serum albumin (BSA) under physiological conditions. Tretinoin 148-161 albumin Homo sapiens 218-231
23071109-2 2012 atRA is metabolized mainly by CYP26A1, but other P450 enzymes such as CYP2C8 and CYP3As also contribute to atRA 4-hydroxylation. Tretinoin 0-4 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 30-37
23071109-2 2012 atRA is metabolized mainly by CYP26A1, but other P450 enzymes such as CYP2C8 and CYP3As also contribute to atRA 4-hydroxylation. Tretinoin 0-4 peptidylprolyl isomerase F Homo sapiens 81-85
23071109-6 2012 This stereoselectivity was rationalized via docking of atRA in the active site of a CYP26A1 homology model. Tretinoin 55-59 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 84-91
23071109-9 2012 Interestingly, CYP3A7 and CYP2C8 preferentially formed (4S)-OH-RA from atRA. Tretinoin 71-75 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 15-21
23169621-3 2012 The mouse CMV MHC class I (MHC-I)-like m152/gp40 glycoprotein down-regulates retinoic acid early inducible-1 (RAE1) NKG2D ligands as well as host MHC-I. Tretinoin 77-90 epithelial cell adhesion molecule Mus musculus 44-48
23132926-10 2012 The anti-cytotoxic effects of retinoic acid were impaired in GPx3-inactivated myoblasts, which indicates that GPx3 regulates the antioxidative effects of retinoic acid. Tretinoin 154-167 glutathione peroxidase 3 Homo sapiens 61-65
23132926-10 2012 The anti-cytotoxic effects of retinoic acid were impaired in GPx3-inactivated myoblasts, which indicates that GPx3 regulates the antioxidative effects of retinoic acid. Tretinoin 154-167 glutathione peroxidase 3 Homo sapiens 110-114
23105114-0 2012 Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RARs) and peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta). Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 144-152
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 117-171
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 15-17 peroxisome proliferator activator receptor delta Mus musculus 117-171
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 peroxisome proliferator activator receptor delta Mus musculus 143-151
23105114-5 2012 Hence, RA-induced neuronal differentiation is mediated through RAR in the early stages and through PPARbeta/delta in the late stages of the process. Tretinoin 7-9 peroxisome proliferator activator receptor delta Mus musculus 99-107
23011350-5 2012 RESULTS: This study reveals, for the first time, that activin/TGF-beta signalling blocks pancreatic specification induced by retinoic acid while promoting hepatic specification in combination with bone morphogenetic protein and fibroblast growth factor. Tretinoin 125-138 transforming growth factor beta 1 Homo sapiens 62-70
23053054-2 2012 Cytochrome P450 26A1 (Cyp26a1), an RA-metabolizing enzyme, is involved in mammalian early pregnancy. Tretinoin 35-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-20
23053054-2 2012 Cytochrome P450 26A1 (Cyp26a1), an RA-metabolizing enzyme, is involved in mammalian early pregnancy. Tretinoin 35-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 22-29
22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Tretinoin 66-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 16-22
22434147-3 2012 Upregulation of CYP3A4 by modafinil was associated with increased retinoic acid (RA) degradation, which could be blocked by specific CYP3A4 inhibitor erythromycin. Tretinoin 66-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139
23543859-11 2012 These data demonstrate that the inhibition of ethanol-induced CYP2E1 as a key pathogenic factor can counteract the tumor-promoting action of ethanol by decreasing TNF-alpha expression, NF-kappaB activation, and oxidative DNA damage as well as restoring normal hepatic levels of retinoic acid in DEN-treated rats. Tretinoin 278-291 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 62-68
22542753-5 2012 Functionality of the co-cultures was assayed using as endpoints the retinol-dependent secretion of RBP4 and the retinoic acid-dependent induction of CYP26A1 in hepatocytes. Tretinoin 112-125 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 149-156
22981223-3 2012 We observed a significant increase of DRAM-1 expression during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of NB4 APL cells but not in ATRA-resistant NB4-R2 cells. Tretinoin 73-86 DNA damage regulated autophagy modulator 1 Homo sapiens 38-44
22981223-3 2012 We observed a significant increase of DRAM-1 expression during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of NB4 APL cells but not in ATRA-resistant NB4-R2 cells. Tretinoin 88-92 DNA damage regulated autophagy modulator 1 Homo sapiens 38-44
23268390-0 2012 [Role of aquaporin-1 gene in erythroid differentiation of erythroleukemia K562 cells induced by retinoic acid]. Tretinoin 96-109 aquaporin 1 (Colton blood group) Homo sapiens 9-20
23268390-1 2012 OBJECTIVE: To explore the role of aquaporin-1 (AQP1) gene in erythroid differentiation of erythroleukemia K562 cells induced by retinoic acid (RA). Tretinoin 128-141 aquaporin 1 (Colton blood group) Homo sapiens 34-45
23268390-1 2012 OBJECTIVE: To explore the role of aquaporin-1 (AQP1) gene in erythroid differentiation of erythroleukemia K562 cells induced by retinoic acid (RA). Tretinoin 128-141 aquaporin 1 (Colton blood group) Homo sapiens 47-51
23268390-1 2012 OBJECTIVE: To explore the role of aquaporin-1 (AQP1) gene in erythroid differentiation of erythroleukemia K562 cells induced by retinoic acid (RA). Tretinoin 143-145 aquaporin 1 (Colton blood group) Homo sapiens 34-45
23268390-1 2012 OBJECTIVE: To explore the role of aquaporin-1 (AQP1) gene in erythroid differentiation of erythroleukemia K562 cells induced by retinoic acid (RA). Tretinoin 143-145 aquaporin 1 (Colton blood group) Homo sapiens 47-51
23268390-4 2012 A retroviral expression vector of AQP1 small interfering RNA (pSUPER-retro-puro-shAQP1) was constructed and transfected into K562 cells to establish a K562 cell line with stable AQP1 down-regulation (K562-shAQP1), in which the changes in gamma-globin and hemoglobin expressions after RA treatment were detected. Tretinoin 284-286 aquaporin 1 (Colton blood group) Homo sapiens 34-38
23268390-5 2012 RESULTS: RA treatment significantly increased gamma-globin and hemoglobin expressions in K562 cells (P<0.01), causing also significantly enhanced AQP1 mRNA and protein expressions over time (P<0.01). Tretinoin 9-11 aquaporin 1 (Colton blood group) Homo sapiens 149-153
23268390-6 2012 Transfection with the recombinant plasmids pSuper-retro-puro-shAQP1 resulted in stable AQP1 suppression in K562 cells (P<0.01), which showed markedly reduced gamma-globin and hemoglobin expressions after RA induction as compared to the control K562 cells (P<0.01). Tretinoin 207-209 aquaporin 1 (Colton blood group) Homo sapiens 63-67
23268390-7 2012 CONCLUSION: K562 cells show a significant increase of AQP1 expression after RA-induced erythroid differentiation, and suppression of AQP1 expression can partially block the effect of RA, suggesting the important role of AQP1 in RA-induced erythroid differentiation of K562 cells. Tretinoin 76-78 aquaporin 1 (Colton blood group) Homo sapiens 54-58
23268390-7 2012 CONCLUSION: K562 cells show a significant increase of AQP1 expression after RA-induced erythroid differentiation, and suppression of AQP1 expression can partially block the effect of RA, suggesting the important role of AQP1 in RA-induced erythroid differentiation of K562 cells. Tretinoin 183-185 aquaporin 1 (Colton blood group) Homo sapiens 133-137
23268390-7 2012 CONCLUSION: K562 cells show a significant increase of AQP1 expression after RA-induced erythroid differentiation, and suppression of AQP1 expression can partially block the effect of RA, suggesting the important role of AQP1 in RA-induced erythroid differentiation of K562 cells. Tretinoin 183-185 aquaporin 1 (Colton blood group) Homo sapiens 133-137
23268390-7 2012 CONCLUSION: K562 cells show a significant increase of AQP1 expression after RA-induced erythroid differentiation, and suppression of AQP1 expression can partially block the effect of RA, suggesting the important role of AQP1 in RA-induced erythroid differentiation of K562 cells. Tretinoin 183-185 aquaporin 1 (Colton blood group) Homo sapiens 133-137
23268390-7 2012 CONCLUSION: K562 cells show a significant increase of AQP1 expression after RA-induced erythroid differentiation, and suppression of AQP1 expression can partially block the effect of RA, suggesting the important role of AQP1 in RA-induced erythroid differentiation of K562 cells. Tretinoin 183-185 aquaporin 1 (Colton blood group) Homo sapiens 133-137
22833419-3 2012 Here we show that NF-kappaB signaling is involved in cell fate determination during retinoic acid (RA) mediated differentiation of ESCs. Tretinoin 84-97 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 18-27
22833419-3 2012 Here we show that NF-kappaB signaling is involved in cell fate determination during retinoic acid (RA) mediated differentiation of ESCs. Tretinoin 99-101 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 18-27
23023919-6 2012 In conclusion, downregulation of the PHB gene may inhibit apoptosis of NB4-R1 cells, and it is speculated that this was at least partly due to the downregulation of caspase-3, and PHB may be a novel target for gene therapy for retinoic acid-resistant acute promyelocytic leukemia. Tretinoin 227-240 caspase 3 Homo sapiens 165-174
22708801-9 2012 Whereas, the overall outcome was negative, one of these cell lines demonstrated an up-regulation of DDX4 on RNA and protein level after 7 days of ATRA stimulation. Tretinoin 146-150 DEAD-box helicase 4 Homo sapiens 100-104
22906706-9 2012 We propose the differential response to RA in these populations is due to differential gene expression of Notch signaling members, CoupTF1 and CoupTF2, chromatin remodeling and histone modifying genes that render the small population resistant to RA differentiation. Tretinoin 40-42 nuclear receptor subfamily 2 group F member 1 Homo sapiens 131-138
23007396-3 2012 In the present study, we demonstrate that specific levels of RA, regulated by Cyp26b1, one of the RA-degrading enzymes, are required for hair follicle (hf) morphogenesis. Tretinoin 61-63 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 78-85
23007396-3 2012 In the present study, we demonstrate that specific levels of RA, regulated by Cyp26b1, one of the RA-degrading enzymes, are required for hair follicle (hf) morphogenesis. Tretinoin 98-100 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 78-85
23007396-4 2012 Mice with embryonic ablation of Cyp26b1 (Cyp26b1(-/-)) have excessive endogenous RA, resulting in arrest of hf growth at the hair germ stage. Tretinoin 81-83 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 32-39
23007396-4 2012 Mice with embryonic ablation of Cyp26b1 (Cyp26b1(-/-)) have excessive endogenous RA, resulting in arrest of hf growth at the hair germ stage. Tretinoin 81-83 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 41-48
23007396-7 2012 Conditional deficiency of Cyp26b1 in the dermis (En1Cre;Cyp26b1f/-) results in decreased hair follicle density and specific effect on hair type, indicating that RA levels also influence regulators of hair bending. Tretinoin 161-163 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 26-33
23007396-9 2012 To elucidate target gene pathways of RA, we performed microarray and RNA-Seq profiling of genes differentially expressed in Cyp26b1(-/-) skin and En1Cre;Cyp26b1f/- tissues. Tretinoin 37-39 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 124-131
23007396-9 2012 To elucidate target gene pathways of RA, we performed microarray and RNA-Seq profiling of genes differentially expressed in Cyp26b1(-/-) skin and En1Cre;Cyp26b1f/- tissues. Tretinoin 37-39 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 153-160
23155234-4 2012 We report that in HL-60 cells, by using a highly quantitative analysis of a set of genes found to be abnormally expressed in AML, polymerase chain reaction (PCR)-amplified p16 gene promoter molecules (each with 15 CpG sites), exhibited a CpG methylation level of 0-4% in untreated cells, which increased to 4-21% after treatment with ATRA for seven days. Tretinoin 334-338 cyclin dependent kinase inhibitor 2A Homo sapiens 172-175
23063977-0 2012 All-trans retinoic acid combined with 5-Aza-2"-deoxycitidine induces C/EBPalpha expression and growth inhibition in MLL-AF9-positive leukemic cells. Tretinoin 0-23 CCAAT enhancer binding protein alpha Homo sapiens 69-79
23063977-0 2012 All-trans retinoic acid combined with 5-Aza-2"-deoxycitidine induces C/EBPalpha expression and growth inhibition in MLL-AF9-positive leukemic cells. Tretinoin 0-23 MLLT3 super elongation complex subunit Homo sapiens 120-123
23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 43-56 CCAAT enhancer binding protein alpha Homo sapiens 168-204
23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 43-56 CCAAT enhancer binding protein alpha Homo sapiens 206-216
23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 58-62 CCAAT enhancer binding protein alpha Homo sapiens 168-204
23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 58-62 CCAAT enhancer binding protein alpha Homo sapiens 206-216
23063977-3 2012 These findings indicate that MLL-AF9-expressing cells are more sensitive to ATRA and 5-Aza, indicating that different MLL fusion proteins possess different epigenetic properties associated with retinoic acid pathway inactivation. Tretinoin 76-80 MLLT3 super elongation complex subunit Homo sapiens 33-36
23063977-3 2012 These findings indicate that MLL-AF9-expressing cells are more sensitive to ATRA and 5-Aza, indicating that different MLL fusion proteins possess different epigenetic properties associated with retinoic acid pathway inactivation. Tretinoin 194-207 MLLT3 super elongation complex subunit Homo sapiens 33-36
23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 estrogen receptor 1 Homo sapiens 243-266
23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 estrogen receptor 1 Homo sapiens 268-275
22972661-0 2012 The regulation of endogenous retinoic acid level through CYP26B1 is required for elevation of palatal shelves. Tretinoin 29-42 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 57-64
22972661-2 2012 In the present study, we deleted Cyp26b1, one of the RA-degrading enzymes, to further study the effects of excess RA in the normal developing palate and to understand how endogenous levels of RA are regulated. Tretinoin 53-55 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 33-40
22972661-10 2012 The regulation of RA signaling through CYP26B1 is also necessary for the development of tongue musculature and for tongue depression. Tretinoin 18-20 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 39-46
22640830-7 2012 ATRA suppressed the expression of the stem cell markers Oct4, Sox2, Nestin and CD44 in HNSC CSCs and inhibited the proliferation of HNSC CSCs in vitro and in vivo. Tretinoin 0-4 nestin Homo sapiens 68-74
22871568-3 2012 Exposure to all-trans RA (ATRA) up-regulated the expression of carnitine palmitoyl transferase-1 (CPT1-L) in HepG2 cells in a dose- and time-dependent manner, and increased cellular oxidation rate of exogenously added radiolabeled palmitate. Tretinoin 22-24 carnitine palmitoyltransferase 1A Homo sapiens 98-104
22820162-0 2012 Retinoic acid and tumor necrosis factor-alpha induced monocytic cell gene expression is regulated in part by induction of transcription factor MafB. Tretinoin 0-13 MAF bZIP transcription factor B Homo sapiens 143-147
22820162-2 2012 In the present study, we investigated RA in the regulation of MafB, a basic leucine-zipper transcription factor with broad roles in embryonic development, hematopoiesis and monocyte-macrophage differentiation. Tretinoin 38-40 MAF bZIP transcription factor B Homo sapiens 62-66
22689466-3 2012 Diffusion of RA from the meninges potentially creates a gradient of RA across the infrapyramidal and suprapyramidal blades of the dentate gyrus, enhanced by the expression of the RA catabolic enzyme Cyp26B1 between the blades, and an infrapyramidal and suprapyramidal blade difference is evident in RA-regulated transcription. Tretinoin 13-15 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 199-206
22689466-3 2012 Diffusion of RA from the meninges potentially creates a gradient of RA across the infrapyramidal and suprapyramidal blades of the dentate gyrus, enhanced by the expression of the RA catabolic enzyme Cyp26B1 between the blades, and an infrapyramidal and suprapyramidal blade difference is evident in RA-regulated transcription. Tretinoin 68-70 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 199-206
22871568-3 2012 Exposure to all-trans RA (ATRA) up-regulated the expression of carnitine palmitoyl transferase-1 (CPT1-L) in HepG2 cells in a dose- and time-dependent manner, and increased cellular oxidation rate of exogenously added radiolabeled palmitate. Tretinoin 26-30 carnitine palmitoyltransferase 1A Homo sapiens 98-104
22871568-5 2012 CPT1-L gene expression was synergistically induced in HepG2 cells simultaneously exposed to ATRA and a selective peroxisome proliferator-activated receptor alpha agonist. Tretinoin 92-96 carnitine palmitoyltransferase 1A Homo sapiens 0-6
22344541-0 2012 All-trans retinoic acid inhibits mesangial cell proliferation by up-regulating p21Waf1/Cip1 and p27Kip1 and down-regulating Skp2. Tretinoin 10-23 S-phase kinase associated protein 2 Rattus norvegicus 124-128
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 36-46
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 S-phase kinase associated protein 2 Rattus norvegicus 153-157
22989911-2 2012 The use of ATRA or prodrugs as pharmacological agents is limited by a short half-life in vivo resulting from the activity of specific ATRA hydroxylases, CYP26 enzymes, induced by ATRA in liver and target tissues. Tretinoin 11-15 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 153-158
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 36-47
22344541-10 2012 CONCLUSION: ATRA inhibited TGF-beta(1)-induced mesangial cell proliferation by up-regulating p21(Waf1/Cip1) mRNA and protein levels, and p27(Kip1) protein level, and down-regulating Skp2 mRNA and protein levels, but it had no significant effect on apoptosis in rat mesangial cells. Tretinoin 12-16 transforming growth factor, beta 1 Rattus norvegicus 27-37
22344541-10 2012 CONCLUSION: ATRA inhibited TGF-beta(1)-induced mesangial cell proliferation by up-regulating p21(Waf1/Cip1) mRNA and protein levels, and p27(Kip1) protein level, and down-regulating Skp2 mRNA and protein levels, but it had no significant effect on apoptosis in rat mesangial cells. Tretinoin 12-16 S-phase kinase associated protein 2 Rattus norvegicus 182-186
22940758-8 2012 ATRA induced expression of aquaporin-9 (AQP9), a transmembrane transporter recognized as a major pathway of arsenic uptake, in a time- and dose-dependent manner. Tretinoin 0-4 aquaporin 9 Homo sapiens 27-38
22940758-8 2012 ATRA induced expression of aquaporin-9 (AQP9), a transmembrane transporter recognized as a major pathway of arsenic uptake, in a time- and dose-dependent manner. Tretinoin 0-4 aquaporin 9 Homo sapiens 40-44
22985482-3 2012 The results show that in the model of the full-length CYP26B1, the protein is capable of distinguishing between the natural substrate (atRA), R115866, and the tetralone derivatives. Tretinoin 135-139 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 54-61
22966203-8 2012 Importantly, while depletion of SNAPC1 had a small effect on basal transcription, it diminished the transcriptional responsiveness of a large number of genes to two distinct extracellular stimuli, epidermal growth factor (EGF) and retinoic acid (RA). Tretinoin 231-244 small nuclear RNA activating complex polypeptide 1 Homo sapiens 32-38
22966203-8 2012 Importantly, while depletion of SNAPC1 had a small effect on basal transcription, it diminished the transcriptional responsiveness of a large number of genes to two distinct extracellular stimuli, epidermal growth factor (EGF) and retinoic acid (RA). Tretinoin 246-248 small nuclear RNA activating complex polypeptide 1 Homo sapiens 32-38
22888005-2 2012 In this study, we found that CaMKII induced by Wnt5a remarkably reduced the protein stability of the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), a co-repressor of Notch signaling, through proteasomal degradation. Tretinoin 123-136 Wnt family member 5A Homo sapiens 47-52
23000165-2 2012 LRH-1 and OCT4 are co-expressed in undifferentiated NCCIT cells and decreased during retinoic acid-induced differentiation. Tretinoin 85-98 nuclear receptor subfamily 5 group A member 2 Homo sapiens 0-5
22911456-9 2012 Subsequent evaluation showed that RA concentrations were significantly elevated by an average of ~3-fold in adrenergic-deficient (Dbh(-/-)) embryos compared with controls, thereby suggesting that RA may be an important downstream mediator of adrenergic action during embryonic heart development. Tretinoin 34-36 dopamine beta hydroxylase Mus musculus 130-133
22911456-9 2012 Subsequent evaluation showed that RA concentrations were significantly elevated by an average of ~3-fold in adrenergic-deficient (Dbh(-/-)) embryos compared with controls, thereby suggesting that RA may be an important downstream mediator of adrenergic action during embryonic heart development. Tretinoin 196-198 dopamine beta hydroxylase Mus musculus 130-133
22945948-14 2012 Because RBP1 is involved in retinoic acid synthesis, our results suggest that dysregulation of retinoic acid metabolism may contribute to glioma formation along the IDH1/IDH2-mutant pathway. Tretinoin 95-108 isocitrate dehydrogenase (NADP(+)) 2 Homo sapiens 170-174
22851491-2 2012 Experimental data have recently shown that retinoic acid restrains ACTH secretion by tumoral corticotropes. Tretinoin 43-56 proopiomelanocortin Homo sapiens 67-71
22531980-8 2012 In agreement with these observations, in vitro experiments showed that in the presence of leptin, ATRA directly induced LEPR gene expression through RARalpha, resulting in enhancement of STAT3 and insulin-induced insulin receptor substrate 1 phosphorylation. Tretinoin 98-102 signal transducer and activator of transcription 3 Mus musculus 187-192
23076176-5 2012 RESULTS: Compared with the normal control cells, ATRA treatment resulted in a significantly increased expression of total Cx43 protein in the astrocytes (P<0.01), and oleamide significantly suppressed its expression (P<0.01). Tretinoin 49-53 gap junction protein, alpha 1 Rattus norvegicus 122-126
23076176-8 2012 CONCLUSION: ATRA and oleamide can modulate gap junction intercellular communication of the astrocytes possibly by regulating the expression of Cx43 protein. Tretinoin 12-16 gap junction protein, alpha 1 Rattus norvegicus 143-147
22910408-0 2012 All-trans retinoic acid activates E-cadherin expression via promoter hypomethylation in the human colon carcinoma HCT116 cells. Tretinoin 10-23 cadherin 1 Homo sapiens 34-44
22378655-8 2012 In patients who received ATRA (C9710 or CCG-2911, n = 8), those with FLT3/Mut had an induction death rate of 30% (7/23) compared to 3% (1/35) in FLT3/WT patients (P = 0.005). Tretinoin 25-29 fms related receptor tyrosine kinase 3 Homo sapiens 69-73
22378655-8 2012 In patients who received ATRA (C9710 or CCG-2911, n = 8), those with FLT3/Mut had an induction death rate of 30% (7/23) compared to 3% (1/35) in FLT3/WT patients (P = 0.005). Tretinoin 25-29 fms related receptor tyrosine kinase 3 Homo sapiens 145-149
22797253-6 2012 In conclusion, consecutive treatment with ATRA and polyI:C results in strong, TLR3/MDA5-mediated chemokine and IFN responses in cultured human melanoma cells, which triggers a functional migratory response in professional antigen-presenting cells. Tretinoin 42-46 interferon alpha 1 Homo sapiens 111-114
22734072-6 2012 These exploratory results suggest that differing PRalpha/LBD+ activities may interact with FLT3-ITD+ or ACA, that FLT3-ITD+ and ACA are associated with different intrinsic disease progression pathways manifest at relapse Off-ATRA, and that these different pathways may be short-circuited by ATRA-selectable defects at relapse On-ATRA. Tretinoin 291-295 fms related receptor tyrosine kinase 3 Homo sapiens 114-118
22734072-1 2012 Mutations in the all-trans retinoic acid (ATRA)-targeted ligand binding domain of PML-RARalpha (PRalpha/LBD+) have been implicated in the passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease relapse. Tretinoin 159-163 S100 calcium binding protein A6 Homo sapiens 96-103
22734072-1 2012 Mutations in the all-trans retinoic acid (ATRA)-targeted ligand binding domain of PML-RARalpha (PRalpha/LBD+) have been implicated in the passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease relapse. Tretinoin 27-40 S100 calcium binding protein A6 Homo sapiens 96-103
22734072-1 2012 Mutations in the all-trans retinoic acid (ATRA)-targeted ligand binding domain of PML-RARalpha (PRalpha/LBD+) have been implicated in the passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease relapse. Tretinoin 42-46 S100 calcium binding protein A6 Homo sapiens 96-103
22734072-2 2012 Among 45 relapse patients from the ATRA/chemotherapy arm of intergroup protocol C9710, 18 patients harbored PRalpha/LBD+ (40%), 7 of whom (39%) relapsed Off-ATRA selection pressure, suggesting a possible active role of PRalpha/LBD+. Tretinoin 35-39 S100 calcium binding protein A6 Homo sapiens 108-115
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 197-201 fms related receptor tyrosine kinase 3 Homo sapiens 48-77
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 197-201 fms related receptor tyrosine kinase 3 Homo sapiens 117-121
22681667-4 2012 In this study, we show that functionally suppressive, alloantigen-specific CD8(+) Foxp3(+) T cells can be induced and significantly expanded by stimulating naive CD8(+) T cells with donor dendritic cells in the presence of IL-2, TGF-beta1 and retinoic acid. Tretinoin 243-256 interleukin 2 Homo sapiens 223-227
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 246-250 fms related receptor tyrosine kinase 3 Homo sapiens 48-77
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 246-250 fms related receptor tyrosine kinase 3 Homo sapiens 117-121
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 246-250 S100 calcium binding protein A6 Homo sapiens 171-178
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 246-250 fms related receptor tyrosine kinase 3 Homo sapiens 48-77
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 246-250 fms related receptor tyrosine kinase 3 Homo sapiens 117-121
22734072-3 2012 Of 41 relapse patients coanalyzed, 15 (37%) had FMS-related tyrosine kinase 3 internal tandem duplication mutations (FLT3-ITD+), which were differentially associated with PRalpha/LBD+ depending on ATRA treatment status at relapse: positively, On-ATRA; negatively, Off-ATRA. Tretinoin 246-250 S100 calcium binding protein A6 Homo sapiens 171-178
22734072-6 2012 These exploratory results suggest that differing PRalpha/LBD+ activities may interact with FLT3-ITD+ or ACA, that FLT3-ITD+ and ACA are associated with different intrinsic disease progression pathways manifest at relapse Off-ATRA, and that these different pathways may be short-circuited by ATRA-selectable defects at relapse On-ATRA. Tretinoin 225-229 S100 calcium binding protein A6 Homo sapiens 49-56
22734072-6 2012 These exploratory results suggest that differing PRalpha/LBD+ activities may interact with FLT3-ITD+ or ACA, that FLT3-ITD+ and ACA are associated with different intrinsic disease progression pathways manifest at relapse Off-ATRA, and that these different pathways may be short-circuited by ATRA-selectable defects at relapse On-ATRA. Tretinoin 225-229 fms related receptor tyrosine kinase 3 Homo sapiens 114-118
22734072-6 2012 These exploratory results suggest that differing PRalpha/LBD+ activities may interact with FLT3-ITD+ or ACA, that FLT3-ITD+ and ACA are associated with different intrinsic disease progression pathways manifest at relapse Off-ATRA, and that these different pathways may be short-circuited by ATRA-selectable defects at relapse On-ATRA. Tretinoin 291-295 S100 calcium binding protein A6 Homo sapiens 49-56
22734072-6 2012 These exploratory results suggest that differing PRalpha/LBD+ activities may interact with FLT3-ITD+ or ACA, that FLT3-ITD+ and ACA are associated with different intrinsic disease progression pathways manifest at relapse Off-ATRA, and that these different pathways may be short-circuited by ATRA-selectable defects at relapse On-ATRA. Tretinoin 291-295 fms related receptor tyrosine kinase 3 Homo sapiens 114-118
22734072-6 2012 These exploratory results suggest that differing PRalpha/LBD+ activities may interact with FLT3-ITD+ or ACA, that FLT3-ITD+ and ACA are associated with different intrinsic disease progression pathways manifest at relapse Off-ATRA, and that these different pathways may be short-circuited by ATRA-selectable defects at relapse On-ATRA. Tretinoin 291-295 S100 calcium binding protein A6 Homo sapiens 49-56
22801367-3 2012 Here, we report that the H3K9 methyltransferase G9a negatively regulated JAK2 transcription in histone methyltransferase activity and in a YY1-dependent manner during ATRA-mediated leukemia cell differentiation. Tretinoin 167-171 YY1 transcription factor Homo sapiens 139-142
22790594-0 2012 DHRS3, a retinal reductase, is differentially regulated by retinoic acid and lipopolysaccharide-induced inflammation in THP-1 cells and rat liver. Tretinoin 59-72 GLI family zinc finger 2 Homo sapiens 120-125
22790594-2 2012 In the present study, DHRS3, previously shown to possess retinal reductase activity, was identified by microarray analysis of THP-1 monocytes as a possible gene target of all-trans-retinoic acid (RA). Tretinoin 171-194 dehydrogenase/reductase 3 Rattus norvegicus 22-27
22790594-2 2012 In the present study, DHRS3, previously shown to possess retinal reductase activity, was identified by microarray analysis of THP-1 monocytes as a possible gene target of all-trans-retinoic acid (RA). Tretinoin 171-194 GLI family zinc finger 2 Homo sapiens 126-131
22790594-2 2012 In the present study, DHRS3, previously shown to possess retinal reductase activity, was identified by microarray analysis of THP-1 monocytes as a possible gene target of all-trans-retinoic acid (RA). Tretinoin 196-198 dehydrogenase/reductase 3 Rattus norvegicus 22-27
22790594-2 2012 In the present study, DHRS3, previously shown to possess retinal reductase activity, was identified by microarray analysis of THP-1 monocytes as a possible gene target of all-trans-retinoic acid (RA). Tretinoin 196-198 GLI family zinc finger 2 Homo sapiens 126-131
22790594-9 2012 To evaluate whether DHRS3 is regulated in the liver by RA and/or inflammatory stimuli, we treated rats for 6 h with RA or LPS or both. Tretinoin 55-57 dehydrogenase/reductase 3 Rattus norvegicus 20-25
22790594-10 2012 DHRS3 mRNA was doubled by RA but reduced by >90% after treatment with LPS in the absence and presence of RA. Tretinoin 26-28 dehydrogenase/reductase 3 Rattus norvegicus 0-5
22548301-7 2012 A strong up-regulation of mkp3 occurs in response to exogenous RA. Tretinoin 63-65 dual specificity phosphatase 6 L homeolog Xenopus laevis 26-30
22548301-11 2012 Functional interactions between RA and FGF rather take place at the level of the transcriptional regulation of mkp3, indicating that RA may antagonise FGF signalling at the level of the extracellular signal-regulated kinase (Erk) pathway. Tretinoin 133-135 dual specificity phosphatase 6 L homeolog Xenopus laevis 111-115
22761456-7 2012 Furthermore, VD(3) enhanced all-trans retinoic acid (ATRA)-induced CYP11A1 gene expression and PROG production. Tretinoin 32-51 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 67-74
22761456-7 2012 Furthermore, VD(3) enhanced all-trans retinoic acid (ATRA)-induced CYP11A1 gene expression and PROG production. Tretinoin 53-57 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 67-74
22539306-2 2012 We show that nuclear accumulation of FGFR1 is a common response to retinoic acid (RA) in pluripotent embryonic stem cells (ESC) and neural progenitors and is both necessary and sufficient for neuronal-like differentiation and accompanying neuritic outgrowth. Tretinoin 67-80 fibroblast growth factor receptor 1 Homo sapiens 37-42
22539306-2 2012 We show that nuclear accumulation of FGFR1 is a common response to retinoic acid (RA) in pluripotent embryonic stem cells (ESC) and neural progenitors and is both necessary and sufficient for neuronal-like differentiation and accompanying neuritic outgrowth. Tretinoin 82-84 fibroblast growth factor receptor 1 Homo sapiens 37-42
22539306-3 2012 Dominant negative nuclear FGFR1, which lacks the tyrosine kinase domain, prevents RA-induced differentiation while full-length nuclear FGFR1 elicits differentiation in the absence of RA. Tretinoin 82-84 fibroblast growth factor receptor 1 Homo sapiens 26-31
22539306-6 2012 RXR and FGFR1 co-associate with 5"-Fluorouridine-labeled transcription sites and with RA Responsive Elements (RARE). Tretinoin 86-88 fibroblast growth factor receptor 1 Homo sapiens 8-13
22539306-7 2012 RA activation of neuronal (tyrosine hydroxylase) and neurogenic (fgf-2 and fgfr1) genes is accompanied by increased FGFR1, Nur, and histone H3.3 binding to their regulatory sequences. Tretinoin 0-2 fibroblast growth factor 2 Homo sapiens 65-70
22539306-7 2012 RA activation of neuronal (tyrosine hydroxylase) and neurogenic (fgf-2 and fgfr1) genes is accompanied by increased FGFR1, Nur, and histone H3.3 binding to their regulatory sequences. Tretinoin 0-2 fibroblast growth factor receptor 1 Homo sapiens 75-80
22539306-7 2012 RA activation of neuronal (tyrosine hydroxylase) and neurogenic (fgf-2 and fgfr1) genes is accompanied by increased FGFR1, Nur, and histone H3.3 binding to their regulatory sequences. Tretinoin 0-2 fibroblast growth factor receptor 1 Homo sapiens 116-121
22750642-5 2012 Retinoic acid is a potent NIS inducer in some breast cancer cells. Tretinoin 0-13 solute carrier family 5 member 5 Homo sapiens 26-29
23159076-2 2012 METHODS: VEGF gene expression in myeloma cell line U266 cells was analyzed by semi-quantitative RT-PCR after incubation with RGZ, ATRA, or RGZ + ATRA for 24 h. Myeloma xenograft was established by subcutaneous injection of 10(7) U266 cells in the scapula area of 4-week old nude mice. Tretinoin 130-134 vascular endothelial growth factor A Homo sapiens 9-13
23159076-2 2012 METHODS: VEGF gene expression in myeloma cell line U266 cells was analyzed by semi-quantitative RT-PCR after incubation with RGZ, ATRA, or RGZ + ATRA for 24 h. Myeloma xenograft was established by subcutaneous injection of 10(7) U266 cells in the scapula area of 4-week old nude mice. Tretinoin 145-149 vascular endothelial growth factor A Homo sapiens 9-13
21633925-3 2012 In the present study, we show that retinoic acid enhances the cytostatic and apoptogenic properties of the novel adamantyl retinoid ST1926 in a panel of neuroblastoma cells with different p53 status and caspase 8 expression, resulting in synergistic effects as assessed by Combination Index and Isobologram analysis. Tretinoin 35-48 tumor protein p53 Homo sapiens 188-191
22214285-7 2012 We further demonstrate that the differential RA response was mediated by the RA-degrading enzyme cytochrome P450 oxidase b1 Cyp26b1. Tretinoin 45-47 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 124-131
22214285-7 2012 We further demonstrate that the differential RA response was mediated by the RA-degrading enzyme cytochrome P450 oxidase b1 Cyp26b1. Tretinoin 77-79 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 124-131
22214285-8 2012 Lumbar cells express high levels of Cyp26b1 and low levels of the RA-synthesizing enzyme retinaldehyde dehydrogenase Raldh2, resulting in limited activation of the RA signaling pathway in these cells. Tretinoin 164-166 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 36-43
22214285-9 2012 In contrast, low Cyp26b1 expression in cervical spinal cord progenitor cells allows RA signaling to be readily activated upon RA treatment. Tretinoin 84-86 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 17-24
22214285-9 2012 In contrast, low Cyp26b1 expression in cervical spinal cord progenitor cells allows RA signaling to be readily activated upon RA treatment. Tretinoin 126-128 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 17-24
22791509-2 2012 Moreover, the characterisation of specific molecular abnormalities provides the basis for targeted therapies, such as all trans retinoic acid (ATRA) and arsenic trioxide treatment in acute promyelocytic leukaemia or tyrosine kinase inhibitors in AML with FLT3 mutations. Tretinoin 122-141 fms related receptor tyrosine kinase 3 Homo sapiens 255-259
22791509-2 2012 Moreover, the characterisation of specific molecular abnormalities provides the basis for targeted therapies, such as all trans retinoic acid (ATRA) and arsenic trioxide treatment in acute promyelocytic leukaemia or tyrosine kinase inhibitors in AML with FLT3 mutations. Tretinoin 143-147 fms related receptor tyrosine kinase 3 Homo sapiens 255-259
22766505-0 2012 PI3K/AKT and ERK regulate retinoic acid-induced neuroblastoma cellular differentiation. Tretinoin 26-39 mitogen-activated protein kinase 1 Homo sapiens 13-16
22766505-6 2012 The protein levels of cyclin-dependent kinase inhibitors, p21 and p27(Kip), which inhibit cell proliferation by blocking cell cycle progression at G1/S phase, increased after RA treatment. Tretinoin 175-177 zinc ribbon domain containing 2 Homo sapiens 66-69
22766505-8 2012 Importantly, we found that the PI3K/AKT pathway is required for RA-induced neuroblastoma cell differentiation. Tretinoin 64-66 AKT serine/threonine kinase 1 Homo sapiens 36-39
22548360-7 2012 Treatment with RA increased expression of NF-kappaB and decreased IkappaBalpha (inhibitory kappaBalpha) expression, which were inhibited by SN50. Tretinoin 15-17 NFKB inhibitor alpha Gallus gallus 66-78
21633925-8 2012 Although not modulated, p53 appeared to enhance cells responsiveness to retinoid/ATRA combination. Tretinoin 81-85 tumor protein p53 Homo sapiens 24-27
22521346-6 2012 An assay of hepatocyte cell lines of differing AFP expression showed that cytoplasmic AFP is able to block ATRA-induced nuclear translocation of RAR and expression of the Fn14 gene. Tretinoin 107-111 alpha fetoprotein Homo sapiens 86-89
22299829-3 2012 Once secreted, L-PGDS functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Tretinoin 83-106 prostaglandin D2 synthase Homo sapiens 15-21
22299829-3 2012 Once secreted, L-PGDS functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Tretinoin 108-110 prostaglandin D2 synthase Homo sapiens 15-21
22299829-4 2012 L-PGDS, therefore, may possess pleiotropic functions in the skin through PGD(2) and RA. Tretinoin 85-87 prostaglandin D2 synthase Homo sapiens 0-6
22681644-6 2012 In parallel to this shift in RA synthesis, cell proliferation in the third ventricle was found to be lowest during long days when RA was highest, implying that RALDH1 synthesized RA may regulate neural stem cell proliferation. Tretinoin 29-31 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 160-166
22681644-6 2012 In parallel to this shift in RA synthesis, cell proliferation in the third ventricle was found to be lowest during long days when RA was highest, implying that RALDH1 synthesized RA may regulate neural stem cell proliferation. Tretinoin 130-132 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 160-166
22681644-6 2012 In parallel to this shift in RA synthesis, cell proliferation in the third ventricle was found to be lowest during long days when RA was highest, implying that RALDH1 synthesized RA may regulate neural stem cell proliferation. Tretinoin 130-132 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 160-166
23197867-8 2012 Screening of paracrine or endocrine factors in the skin indicated that all-trans retinoic acid (atRA) upregulated Wnt10b gene expression, although synergistic upregulation (combined atRA and VD(3)) was not seen. Tretinoin 81-94 Wnt family member 10B Homo sapiens 114-120
22354283-3 2012 Here, we provide evidence that pharmacological inhibition of the mitogen-activated protein kinase, p38alpha, or silencing of the corresponding gene sensitizes APL and AML cell lines, as well as primary cultures of AML blasts to the anti-proliferative and cyto-differentiating activity of ATRA and synthetic retinoids. Tretinoin 288-292 mitogen-activated protein kinase 14 Homo sapiens 99-107
22614235-10 2012 Differentiation induction with all-trans retinoic acid induced the upregulation of Reelin and DAB1. Tretinoin 41-54 DAB adaptor protein 1 Homo sapiens 94-98
23197867-8 2012 Screening of paracrine or endocrine factors in the skin indicated that all-trans retinoic acid (atRA) upregulated Wnt10b gene expression, although synergistic upregulation (combined atRA and VD(3)) was not seen. Tretinoin 96-100 Wnt family member 10B Homo sapiens 114-120
22056878-5 2012 In estrogen-receptor-negative cellular models showing coamplification of ERBB2 and RARA, simultaneous targeting of the corresponding gene products with combinations of lapatinib and ATRA causes synergistic growth inhibition, cyto-differentiation and apoptosis. Tretinoin 182-186 erb-b2 receptor tyrosine kinase 2 Homo sapiens 73-78
22056878-9 2012 Induction of the retinoid-dependent RARRES3 protein by ATRA stabilizes the effect of lapatinib inhibiting ERBB2 phosphorylation. Tretinoin 55-59 phospholipase A and acyltransferase 4 Homo sapiens 36-43
22056878-9 2012 Induction of the retinoid-dependent RARRES3 protein by ATRA stabilizes the effect of lapatinib inhibiting ERBB2 phosphorylation. Tretinoin 55-59 erb-b2 receptor tyrosine kinase 2 Homo sapiens 106-111
22771034-5 2012 Furthermore, we show that Ajuba binds Isl1, represses its transcriptional activity, and is also required for autorepression of Isl1 expression in an RA-dependent manner. Tretinoin 149-151 ajuba LIM protein Danio rerio 26-31
22771034-5 2012 Furthermore, we show that Ajuba binds Isl1, represses its transcriptional activity, and is also required for autorepression of Isl1 expression in an RA-dependent manner. Tretinoin 149-151 ISL LIM homeobox 1a Danio rerio 127-131
22771034-6 2012 Lack of Ajuba abrogates the RA-dependent restriction of Isl1(+) cardiac cells. Tretinoin 28-30 ajuba LIM protein Danio rerio 8-13
22771034-6 2012 Lack of Ajuba abrogates the RA-dependent restriction of Isl1(+) cardiac cells. Tretinoin 28-30 ISL LIM homeobox 1a Danio rerio 56-60
22771034-7 2012 We conclude that Ajuba plays a central role in regulating the SHF during heart development by linking RA signaling to the function of Isl1, a key transcription factor in cardiac progenitor cells. Tretinoin 102-104 ajuba LIM protein Danio rerio 17-22
22771034-7 2012 We conclude that Ajuba plays a central role in regulating the SHF during heart development by linking RA signaling to the function of Isl1, a key transcription factor in cardiac progenitor cells. Tretinoin 102-104 ISL LIM homeobox 1a Danio rerio 134-138
22806070-8 2012 42: 1685-1694] show that RA ameliorates Con A-induced murine hepatitis by selectively downmodulating IFN-gamma and IL-4 production in disease-causing NKT cells in the liver. Tretinoin 25-27 interferon gamma Mus musculus 101-110
22727372-3 2012 RA metabolism inhibitors (RAMBAs or CYP26 inhibitors) are attracting increasing interest as an alternative method for enhancing endogenous levels of retinoic acid in the treatment of hyperproliferative disease. Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 36-41
22727372-3 2012 RA metabolism inhibitors (RAMBAs or CYP26 inhibitors) are attracting increasing interest as an alternative method for enhancing endogenous levels of retinoic acid in the treatment of hyperproliferative disease. Tretinoin 149-162 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 36-41
22728880-5 2012 Ectopic supplementation of RA induced hairy2 in a short time period, with simultaneous transient activation of Erk/MAPK, Akt/PI3K and Gli3 intracellular pathways. Tretinoin 27-29 GLI family zinc finger 3 Gallus gallus 134-138
22585464-5 2012 In correlation with cytokine levels in serum, RA regulated the production of IFN-gamma and IL-4 but not TNF-alpha by NKT cells without influencing the NKT-cell activation status. Tretinoin 46-48 interferon gamma Homo sapiens 77-86
22585464-5 2012 In correlation with cytokine levels in serum, RA regulated the production of IFN-gamma and IL-4 but not TNF-alpha by NKT cells without influencing the NKT-cell activation status. Tretinoin 46-48 interleukin 4 Homo sapiens 91-95
22585464-6 2012 However, RA did not alleviate alpha-GalCer-induced liver injury, even though it reduced IFN-gamma and IL-4 but not TNF-alpha levels in serum. Tretinoin 9-11 interferon gamma Homo sapiens 88-97
22585464-6 2012 However, RA did not alleviate alpha-GalCer-induced liver injury, even though it reduced IFN-gamma and IL-4 but not TNF-alpha levels in serum. Tretinoin 9-11 interleukin 4 Homo sapiens 102-106
22696440-10 2012 Moreover, ATRA downregulated the expression of receptor activator of NF-kappaB ligand, the leading player of osteoclastogenesis, in the CD4(+) T cells and fibroblast-like synoviocytes from patients with RA. Tretinoin 10-14 CD4 molecule Homo sapiens 136-139
22826360-3 2012 The phosphorylation of signal transducer and activator of transcription (STAT) factors 1 and 3 are involved in DNA synthesis and cyclin D1 expression after PH, which is stimulated by production of retinoic acid (RA). Tretinoin 197-210 cyclin D1 Rattus norvegicus 129-138
22826360-3 2012 The phosphorylation of signal transducer and activator of transcription (STAT) factors 1 and 3 are involved in DNA synthesis and cyclin D1 expression after PH, which is stimulated by production of retinoic acid (RA). Tretinoin 212-214 cyclin D1 Rattus norvegicus 129-138
22193544-10 2012 Conversely, RNAi-mediated knockdown of WWOX in retinoic acid (RA)-differentiated SH-SY5Y cells inhibited neurite outgrowth. Tretinoin 47-60 WW domain containing oxidoreductase Homo sapiens 39-43
22568433-6 2012 Retinoic acid-induced differentiation of human precursor NT2 cells into dopaminergic cells increased expression of TH, NURR1, D2 R and SRY. Tretinoin 0-13 tyrosine hydroxylase Homo sapiens 115-117
22261335-0 2012 Sphingosine 1-phosphate antagonizes the effect of all-trans retinoic acid (ATRA) in a human colon cancer cell line by modulation of RARbeta expression. Tretinoin 50-73 retinoic acid receptor beta Homo sapiens 132-139
22261335-0 2012 Sphingosine 1-phosphate antagonizes the effect of all-trans retinoic acid (ATRA) in a human colon cancer cell line by modulation of RARbeta expression. Tretinoin 75-79 retinoic acid receptor beta Homo sapiens 132-139
22261335-4 2012 S1P treatment or transient co-transfection with SphK2 expression vector antagonized ATRA-induced RARbeta promoter activity. Tretinoin 84-88 retinoic acid receptor beta Homo sapiens 97-104
22261335-6 2012 Overall, S1P antagonized ATRA"s inhibitory effects by down-regulating RARbeta expression, likely via the proteasome-dependent pathway. Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 70-77
22333881-9 2012 However, in combination with ATRA, VPA synergized for PML-RARA degradation and LIC eradication in vivo. Tretinoin 29-33 promyelocytic leukemia Mus musculus 54-57
22659417-4 2012 In addition, LMP1 suppressed ATRA-mediated activation of Caspase 9, Caspase 3, and PARP but not Caspase 8 in Ad-AH cells, suggesting that LMP1 acts by blocking the activation of intrinsic apoptosis pathway by ATRA. Tretinoin 29-33 caspase 3 Homo sapiens 68-77
22193544-10 2012 Conversely, RNAi-mediated knockdown of WWOX in retinoic acid (RA)-differentiated SH-SY5Y cells inhibited neurite outgrowth. Tretinoin 62-64 WW domain containing oxidoreductase Homo sapiens 39-43
22193544-12 2012 In summary, our data reveal a novel mechanism by which WWOX promotes neuronal differentiation in response to RA. Tretinoin 109-111 WW domain containing oxidoreductase Homo sapiens 55-59
22204820-8 2012 IL-13 suppressed the ATRA induced PTGES expression at both mRNA and protein level in MDM and BAL cells. Tretinoin 21-25 interleukin 13 Homo sapiens 0-5
22619388-5 2012 Of the four zebrafish Crabps, Crabp2a is uniquely RA inducible and depletion or overexpression of Crabp2a makes embryos hypersensitive to exogenous RA. Tretinoin 50-52 cellular retinoic acid binding protein 2, a Danio rerio 30-37
22619388-5 2012 Of the four zebrafish Crabps, Crabp2a is uniquely RA inducible and depletion or overexpression of Crabp2a makes embryos hypersensitive to exogenous RA. Tretinoin 148-150 cellular retinoic acid binding protein 2, a Danio rerio 30-37
22619388-5 2012 Of the four zebrafish Crabps, Crabp2a is uniquely RA inducible and depletion or overexpression of Crabp2a makes embryos hypersensitive to exogenous RA. Tretinoin 148-150 cellular retinoic acid binding protein 2, a Danio rerio 98-105
22619388-7 2012 Exploration of signaling parameters in our models suggests that the ability of Crabp2a to transport RA to Cyp26 enzymes for degradation is a major factor in promoting robustness. Tretinoin 100-102 cellular retinoic acid binding protein 2, a Danio rerio 79-86
22464761-9 2012 Concomitant with these effects on day 14, CD38, CD11b, and F4/80 were higher on macrophages from RA-treated mice versus controls. Tretinoin 97-99 integrin alpha M Mus musculus 48-53
21882191-6 2012 Notably, the non-dyplastic metaplasia-derived cell line (CP-A) expressed reduced squamous cytokeratins and enhanced columnar cytokeratins upon ATRA treatment. Tretinoin 143-147 carboxypeptidase A1 Homo sapiens 57-61
22607296-7 2012 Topical application of a PPARalpha agonist improved the stratum corneum structure and function, reduced mRNA expression of interleukin (IL)-1alpha, tumor necrosis factor-alpha and IL-8, and inhibited ear edema induced by retinoic acid or retinyl retinoate. Tretinoin 221-234 peroxisome proliferator activated receptor alpha Mus musculus 25-34
22182854-11 2012 This is the first evidence suggesting SFK inhibitors enhance ATRA-induced differentiation through a possible feedback loop involving KSR1-scaffolded c-Raf and ERK complexed with Lyn and CK2. Tretinoin 61-65 mitogen-activated protein kinase 1 Homo sapiens 159-162
21938722-8 2012 Our findings provide the first evidence on the identification and differential transcription of the two TSSs of the mouse Gap43 gene, and the preferential distribution of their protein products in the specific stages of RA induced P19 differentiation. Tretinoin 220-222 growth associated protein 43 Mus musculus 122-127
22349414-2 2012 In this study, the induction/activation of C/EBPalpha in myelomonocytic AML was investigated using a combination of all-trans retinoic acid (ATRA) and RAD001 (Everolimus), a mammalian target of rapamycin complex 1 (mTORC1) inhibitor. Tretinoin 126-139 CCAAT enhancer binding protein alpha Homo sapiens 43-53
22349414-2 2012 In this study, the induction/activation of C/EBPalpha in myelomonocytic AML was investigated using a combination of all-trans retinoic acid (ATRA) and RAD001 (Everolimus), a mammalian target of rapamycin complex 1 (mTORC1) inhibitor. Tretinoin 141-145 CCAAT enhancer binding protein alpha Homo sapiens 43-53
22182854-11 2012 This is the first evidence suggesting SFK inhibitors enhance ATRA-induced differentiation through a possible feedback loop involving KSR1-scaffolded c-Raf and ERK complexed with Lyn and CK2. Tretinoin 61-65 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 178-181
22182854-0 2012 Src inhibitors, PP2 and dasatinib, increase retinoic acid-induced association of Lyn and c-Raf (S259) and enhance MAPK-dependent differentiation of myeloid leukemia cells. Tretinoin 44-57 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 0-3
22182854-0 2012 Src inhibitors, PP2 and dasatinib, increase retinoic acid-induced association of Lyn and c-Raf (S259) and enhance MAPK-dependent differentiation of myeloid leukemia cells. Tretinoin 44-57 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 81-84
22405964-6 2012 To further understand how retinoic acid regulates upper lip and palate morphogenesis we searched for genes downregulated in response to RARgamma inhibition in orofacial tissue, and uncovered homeobox genes lhx8 and msx2. Tretinoin 26-39 msh homeobox 2 L homeolog Xenopus laevis 215-219
22182854-6 2012 PP2 and dasatinib increased the ATRA-induced expression of Lyn and c-Raf (total and c-RafpS259) and their interaction. Tretinoin 32-36 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 59-62
22182854-11 2012 This is the first evidence suggesting SFK inhibitors enhance ATRA-induced differentiation through a possible feedback loop involving KSR1-scaffolded c-Raf and ERK complexed with Lyn and CK2. Tretinoin 61-65 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 38-41
22182854-11 2012 This is the first evidence suggesting SFK inhibitors enhance ATRA-induced differentiation through a possible feedback loop involving KSR1-scaffolded c-Raf and ERK complexed with Lyn and CK2. Tretinoin 61-65 kinase suppressor of ras 1 Homo sapiens 133-137
22525672-1 2012 F9 embryonic carcinoma (EC) cells undergo extra-embryonic endodermal (ExE) differentiation in response to retinoic acid (RA) treatment, which induces the expression of two isoforms (p96 and p67) of the adaptor protein, Disabled-2 (Dab2). Tretinoin 106-119 CD33 molecule Homo sapiens 190-193
22525672-1 2012 F9 embryonic carcinoma (EC) cells undergo extra-embryonic endodermal (ExE) differentiation in response to retinoic acid (RA) treatment, which induces the expression of two isoforms (p96 and p67) of the adaptor protein, Disabled-2 (Dab2). Tretinoin 121-123 CD33 molecule Homo sapiens 190-193
21735106-6 2012 We treated hESCs with retinoic acid (RA) and found an enhancement of skeletal myogenesis, and the expression of the myogenic regulatory factors (MRFs) MyoD and myogenin by day 25. Tretinoin 22-35 myogenic differentiation 1 Homo sapiens 151-155
21735106-7 2012 Furthermore, we found that RA treatment expanded the muscle progenitor pool, which occurred as a distinct Pax3(+ve) population prior to MRF expression. Tretinoin 27-29 paired box 3 Homo sapiens 106-110
22415012-0 2012 A CYP26B1 polymorphism enhances retinoic acid catabolism and may aggravate atherosclerosis. Tretinoin 32-45 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 2-9
22415012-1 2012 All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment. Tretinoin 10-23 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 39-65
22415012-1 2012 All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment. Tretinoin 10-23 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 67-72
22415012-3 2012 We found that CYP26B1 mRNA was induced by retinoic acid in human atherosclerotic arteries, and CYP26B1 and the macrophage marker CD68 were colocalized in human atherosclerotic lesions. Tretinoin 42-55 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 14-21
22415012-10 2012 In summary, this study identifies the first CYP26B1 polymorphism that alters CYP26B1 capacity to metabolize retinoic acid. Tretinoin 108-121 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 44-51
22415012-10 2012 In summary, this study identifies the first CYP26B1 polymorphism that alters CYP26B1 capacity to metabolize retinoic acid. Tretinoin 108-121 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 77-84
22415012-11 2012 CYP26B1 was expressed in macrophage-rich areas of human atherosclerotic lesions, induced by retinoic acid and increased in murine atherosclerosis. Tretinoin 92-105 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-7
24130925-0 2012 Transglutaminase-2 Is Involved in All-Trans Retinoic Acid-Induced Invasion and Matrix Metalloproteinases Expression of SH-SY5Y Neuroblastoma Cells via NF-kappaB Pathway. Tretinoin 44-57 transglutaminase 2 Homo sapiens 0-18
24130925-0 2012 Transglutaminase-2 Is Involved in All-Trans Retinoic Acid-Induced Invasion and Matrix Metalloproteinases Expression of SH-SY5Y Neuroblastoma Cells via NF-kappaB Pathway. Tretinoin 44-57 nuclear factor kappa B subunit 1 Homo sapiens 151-160
24130925-2 2012 It has been reported that short-term ATRA treatment induces migration and invasion of SH-SY5Y via transglutaminase-2 (Tgase-2). Tretinoin 37-41 transglutaminase 2 Homo sapiens 98-116
24130925-2 2012 It has been reported that short-term ATRA treatment induces migration and invasion of SH-SY5Y via transglutaminase-2 (Tgase-2). Tretinoin 37-41 transglutaminase 2 Homo sapiens 118-125
24130925-9 2012 To confirm the involvement of Tgase-2, gene silencing of Tgase-2 was performed in the ATRA-induced invasion of the SH-SH5Y cells. Tretinoin 86-90 transglutaminase 2 Homo sapiens 57-64
24130925-12 2012 Therefore the relationship of Tgase-2 and NF-kappaB in the ATRA-induced invasion of the SH-SY5Y cells was examined using siRNA and CTM. Tretinoin 59-63 transglutaminase 2 Homo sapiens 30-37
24130925-12 2012 Therefore the relationship of Tgase-2 and NF-kappaB in the ATRA-induced invasion of the SH-SY5Y cells was examined using siRNA and CTM. Tretinoin 59-63 nuclear factor kappa B subunit 1 Homo sapiens 42-51
24130925-13 2012 ATRA induced the activation of NF-kappaB in the SH-SY5Y cells and CTM suppressed the activation of NF-kappaB. Tretinoin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 31-40
24130925-14 2012 Gene silencing of Tgase-2 suppressed the MMP expression by ATRA. Tretinoin 59-63 transglutaminase 2 Homo sapiens 18-25
24130925-15 2012 These results suggested that Tgase-2 might be a new target for controlling the ATRA-induced invasion of NBs. Tretinoin 79-83 transglutaminase 2 Homo sapiens 29-36
22387209-11 2012 Reduced retinoic acid synthesis altered the expression of genes involved in retinoic acid homeostasis and also demonstrated that retinoic acid signaling is required for Tbx3 expression, whereas high levels of retinoic acid signaling inhibited Bmp4 expression and repressed Wnt signaling. Tretinoin 8-21 bone morphogenetic protein 4 Mus musculus 243-247
22387209-11 2012 Reduced retinoic acid synthesis altered the expression of genes involved in retinoic acid homeostasis and also demonstrated that retinoic acid signaling is required for Tbx3 expression, whereas high levels of retinoic acid signaling inhibited Bmp4 expression and repressed Wnt signaling. Tretinoin 8-21 wingless-type MMTV integration site family, member 10B Mus musculus 273-276
22405964-9 2012 These results suggest a model whereby retinoic acid signaling regulates Lhx8 and Msx2, which together direct the tissue growth and differentiation necessary for the upper lip and primary palate morphogenesis. Tretinoin 38-51 msh homeobox 2 L homeolog Xenopus laevis 81-85
22380620-0 2012 Retinoic acid mediates the expression of glutamate transporter-1 in rat astrocytes through genomic RXR action and non-genomic protein kinase C signaling pathway. Tretinoin 0-13 solute carrier family 1 member 2 Rattus norvegicus 41-64
22969967-11 2012 IFN-gamma in combination with ATRA not only strengthens the induction differentiation effect of ATRA on NB4 cells, but also can partially induce the maturation of NB4-R1 cells with ATRA resistance. Tretinoin 96-100 interferon gamma Homo sapiens 0-9
22969967-11 2012 IFN-gamma in combination with ATRA not only strengthens the induction differentiation effect of ATRA on NB4 cells, but also can partially induce the maturation of NB4-R1 cells with ATRA resistance. Tretinoin 96-100 interferon gamma Homo sapiens 0-9
22366926-0 2012 The p85alpha regulatory subunit of PI3K mediates cAMP-PKA and retinoic acid biological effects on MCF7 cell growth and migration. Tretinoin 62-75 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 4-12
22366926-6 2012 We demonstrated that p85alphaPI3KSer83 is crucial for the synergistic enhancement of RARalpha/p85alphaPI3K binding induced by cAMP/RA co-treatment in MCF7 cells. Tretinoin 85-87 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 21-38
22366926-8 2012 Wound healing and transwell experiments demonstrated that p85alphaPI3KSer83 was also essential both for the control of migratory behaviour and for the reduction of motility induced by RA. Tretinoin 184-186 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 58-75
22969967-0 2012 Interferon-gamma enhances promyelocytic leukemia protein expression in acute promyelocytic cells and cooperates with all-trans-retinoic acid to induce maturation of NB4 and NB4-R1 cells. Tretinoin 117-140 interferon gamma Homo sapiens 0-16
22969967-10 2012 Together, IFN-gamma augments the proliferation inhibition effect of ATRA on NB4 and NB4-R1 cells through enhancing the expression of PML protein. Tretinoin 68-72 interferon gamma Homo sapiens 10-19
22504302-7 2012 Setdb1 co-immunoprecipitated with Oct4 in mESCs, and Setdb1 expression was markedly reduced upon retinoic acid-induced differentiation. Tretinoin 97-110 SET domain, bifurcated 1 Mus musculus 0-6
22504302-7 2012 Setdb1 co-immunoprecipitated with Oct4 in mESCs, and Setdb1 expression was markedly reduced upon retinoic acid-induced differentiation. Tretinoin 97-110 SET domain, bifurcated 1 Mus musculus 53-59
22380620-4 2012 RA applied at submicromolar concentrations for 24 h significantly reduced GLT-1 mRNA and membrane levels in astrocytes and dibutyryl cAMP (dbcAMP)-primed astrocytes. Tretinoin 0-2 solute carrier family 1 member 2 Rattus norvegicus 74-79
22380620-5 2012 An RXR agonist reduced astrocytic GLT-1 mRNA expression, whereas an RXR antagonist blocked the effects of RA on the reduction of astrocytic GLT-1 mRNA expression. Tretinoin 106-108 solute carrier family 1 member 2 Rattus norvegicus 140-145
22380620-7 2012 RA-induced reduction in GLT-1 mRNA expression was also observed in dbcAMP-primed astrocytes. Tretinoin 0-2 solute carrier family 1 member 2 Rattus norvegicus 24-29
22380620-8 2012 Through lentivirus-mediated astrocytic over-expression of rat GLT-1, levels of GLT-1 in the processes of dbcAMP-treated astrocytes were attenuated by exposure to RA. Tretinoin 162-164 solute carrier family 1 member 2 Rattus norvegicus 62-67
22380620-8 2012 Through lentivirus-mediated astrocytic over-expression of rat GLT-1, levels of GLT-1 in the processes of dbcAMP-treated astrocytes were attenuated by exposure to RA. Tretinoin 162-164 solute carrier family 1 member 2 Rattus norvegicus 79-84
22380620-9 2012 The protein kinase C inhibitor, Bis I, restored GLT-1 distribution in the processes of RA-treated dbcAMP-primed astrocytes. Tretinoin 87-89 solute carrier family 1 member 2 Rattus norvegicus 48-53
22380620-10 2012 These results suggest that RA reduces astrocytic GLT-1 levels through both RXR-mediated inhibition at the transcriptional level and triggering activation of protein kinase C which reduces cell surface GLT-1 levels. Tretinoin 27-29 solute carrier family 1 member 2 Rattus norvegicus 49-54
22380620-10 2012 These results suggest that RA reduces astrocytic GLT-1 levels through both RXR-mediated inhibition at the transcriptional level and triggering activation of protein kinase C which reduces cell surface GLT-1 levels. Tretinoin 27-29 solute carrier family 1 member 2 Rattus norvegicus 201-206
22916501-0 2012 [Recombinant adenovirus expressing siRNA is generated to inhibit the expression of RARbeta in rat mesenchymal stem cells treated by all-trans retinoic acid]. Tretinoin 142-155 retinoic acid receptor, beta Rattus norvegicus 83-90
22471368-5 2012 Specificity of hPPARgamma activity was determined by dual luciferase reporter assay of co-transfected cells exposed to PPARgamma agonist rosiglitazone, PPARalpha agonist WY14643 and retinoic acid receptor alpha (RARalpha) agonist all-trans-retinoic acid (ATRA). Tretinoin 234-253 peroxisome proliferator activated receptor gamma Homo sapiens 15-25
22471368-5 2012 Specificity of hPPARgamma activity was determined by dual luciferase reporter assay of co-transfected cells exposed to PPARgamma agonist rosiglitazone, PPARalpha agonist WY14643 and retinoic acid receptor alpha (RARalpha) agonist all-trans-retinoic acid (ATRA). Tretinoin 234-253 peroxisome proliferator activated receptor gamma Homo sapiens 16-25
22471368-5 2012 Specificity of hPPARgamma activity was determined by dual luciferase reporter assay of co-transfected cells exposed to PPARgamma agonist rosiglitazone, PPARalpha agonist WY14643 and retinoic acid receptor alpha (RARalpha) agonist all-trans-retinoic acid (ATRA). Tretinoin 255-259 peroxisome proliferator activated receptor gamma Homo sapiens 15-25
22471368-5 2012 Specificity of hPPARgamma activity was determined by dual luciferase reporter assay of co-transfected cells exposed to PPARgamma agonist rosiglitazone, PPARalpha agonist WY14643 and retinoic acid receptor alpha (RARalpha) agonist all-trans-retinoic acid (ATRA). Tretinoin 255-259 peroxisome proliferator activated receptor gamma Homo sapiens 16-25
22916501-1 2012 To construct the recombinant adenovirus vector expressing specific siRNA for rat retinoic acid receptor-beta (RARbeta) gene, and to detect its effect on RARbeta expression and neuronal differentiation of all-trans retinoic acid (ATRA) treated mesenchymal stem cells (MSCs). Tretinoin 81-94 retinoic acid receptor, beta Rattus norvegicus 110-117
22916501-11 2012 Therefore, we successfully constructed the recombinant adenovirus vector containing siRNA for rat RARP gene, adenovirus could effectively infect MSCs and inhibit the expression of induced RARbeta in ATRA treated MSCs, then inhibit neuronal differentiation of MSCs. Tretinoin 199-203 retinoic acid receptor, beta Rattus norvegicus 188-195
22190708-4 2012 Translation of RHOX13 coincides with initiation of RA signaling in both male and female gonads in vivo but occurs precociously in neonatal testes exposed to RA in vitro or in fetal male germ cells when NANOS2 is absent in vivo. Tretinoin 51-53 reproductive homeobox 13 Mus musculus 15-21
22190708-4 2012 Translation of RHOX13 coincides with initiation of RA signaling in both male and female gonads in vivo but occurs precociously in neonatal testes exposed to RA in vitro or in fetal male germ cells when NANOS2 is absent in vivo. Tretinoin 157-159 reproductive homeobox 13 Mus musculus 15-21
22387108-0 2012 c-Jun N-terminal kinase controls a negative loop in the regulation of glial fibrillary acidic protein expression by retinoic acid. Tretinoin 116-129 mitogen-activated protein kinase 8 Homo sapiens 0-23
22387108-3 2012 Here, we extend our previous work and show that retinoic acid also activates specifically the c-Jun N-terminal kinase (JNK) phosphorylation pathway, which in turn inhibits GFAP expression. Tretinoin 48-61 mitogen-activated protein kinase 8 Homo sapiens 94-117
22387108-3 2012 Here, we extend our previous work and show that retinoic acid also activates specifically the c-Jun N-terminal kinase (JNK) phosphorylation pathway, which in turn inhibits GFAP expression. Tretinoin 48-61 mitogen-activated protein kinase 8 Homo sapiens 119-122
22306363-6 2012 These results confirmed that PGE(2) mediates the effects of ATRA on HIF-1alpha expression; iii) Prostaglandin uptake transporter inhibitor bromocresol green blocked the increase in HIF-1alpha expression induced by PGE(2) or by PGE(2)-increasing cytokine interleukin-1beta, but not by ATRA. Tretinoin 60-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 68-78
22306363-0 2012 Retinoic acid increases hypoxia-inducible factor-1alpha through intracrine prostaglandin E(2) signaling in human renal proximal tubular cells HK-2. Tretinoin 0-13 hypoxia inducible factor 1 subunit alpha Homo sapiens 24-55
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 44-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 88-98
22532966-7 2012 We found that melatonin in combination with all-trans retinoic acid and somatostatin potentiated the effects of melatonin alone on MCF-7 cell viability and growth inhibition; this phenomenon was associated with altered conductance through Ca2+ and voltage-activated K+ (BK) channels, and with substantial impairments of Notch-1 and epidermal growth factor (EGF)-mediated signaling. Tretinoin 54-67 notch receptor 1 Homo sapiens 320-327
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 44-48 hypoxia inducible factor 1 subunit alpha Homo sapiens 100-131
22306363-6 2012 These results confirmed that PGE(2) mediates the effects of ATRA on HIF-1alpha expression; iii) Prostaglandin uptake transporter inhibitor bromocresol green blocked the increase in HIF-1alpha expression induced by PGE(2) or by PGE(2)-increasing cytokine interleukin-1beta, but not by ATRA. Tretinoin 60-64 hypoxia inducible factor 1 subunit alpha Homo sapiens 181-191
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 44-48 vascular endothelial growth factor A Homo sapiens 203-209
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 44-48 vascular endothelial growth factor A Homo sapiens 211-247
22306363-6 2012 These results confirmed that PGE(2) mediates the effects of ATRA on HIF-1alpha expression; iii) Prostaglandin uptake transporter inhibitor bromocresol green blocked the increase in HIF-1alpha expression induced by PGE(2) or by PGE(2)-increasing cytokine interleukin-1beta, but not by ATRA. Tretinoin 284-288 hypoxia inducible factor 1 subunit alpha Homo sapiens 181-191
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 50-73 hypoxia inducible factor 1 subunit alpha Homo sapiens 88-98
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 50-73 hypoxia inducible factor 1 subunit alpha Homo sapiens 100-131
22309941-9 2012 In conclusion, bFGF suppresses RA-induced entry of germ cells into meiosis to ensure embryonic ovarian germ cells to maintain at undifferentiated status and accelerate germ cell proliferation by binding with FGFR1 involving PKC activation in the chicken. Tretinoin 31-33 fibroblast growth factor receptor 1 Gallus gallus 208-213
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 50-73 vascular endothelial growth factor A Homo sapiens 203-209
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 50-73 vascular endothelial growth factor A Homo sapiens 211-247
22306363-2 2012 Here we investigated the role of COXs (cyclooxygenases) in these effects and we found that, i) ATRA increased the expression of COX-1 and COX-2 mRNA and protein and the intracellular levels (but not the extracellular ones) of PGE(2). Tretinoin 95-99 mitochondrially encoded cytochrome c oxidase II Homo sapiens 138-143
22306363-3 2012 Furthermore, inhibitors of COX isoenzymes blocked ATRA-induced increase in intracellular PGE(2), HIF-1alpha up-regulation and increased VEGF-A production. Tretinoin 50-54 hypoxia inducible factor 1 subunit alpha Homo sapiens 97-107
22306363-3 2012 Furthermore, inhibitors of COX isoenzymes blocked ATRA-induced increase in intracellular PGE(2), HIF-1alpha up-regulation and increased VEGF-A production. Tretinoin 50-54 vascular endothelial growth factor A Homo sapiens 136-142
22306363-5 2012 These results indicated that COX activity is critical for ATRA-induced HIF-1alpha up-regulation and suggested that intracellular PGE(2) could mediate the effects of ATRA; ii) Treatment with PGE(2) analog 16,16-dimethyl-PGE(2) resulted in up-regulation of HIF-1alpha and antagonists of EP1-4 receptors inhibited 16,16-dimethyl-PGE(2)- and ATRA-induced HIF-1alpha up-regulation. Tretinoin 58-62 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-81
22306363-5 2012 These results indicated that COX activity is critical for ATRA-induced HIF-1alpha up-regulation and suggested that intracellular PGE(2) could mediate the effects of ATRA; ii) Treatment with PGE(2) analog 16,16-dimethyl-PGE(2) resulted in up-regulation of HIF-1alpha and antagonists of EP1-4 receptors inhibited 16,16-dimethyl-PGE(2)- and ATRA-induced HIF-1alpha up-regulation. Tretinoin 58-62 hypoxia inducible factor 1 subunit alpha Homo sapiens 255-265
22306363-5 2012 These results indicated that COX activity is critical for ATRA-induced HIF-1alpha up-regulation and suggested that intracellular PGE(2) could mediate the effects of ATRA; ii) Treatment with PGE(2) analog 16,16-dimethyl-PGE(2) resulted in up-regulation of HIF-1alpha and antagonists of EP1-4 receptors inhibited 16,16-dimethyl-PGE(2)- and ATRA-induced HIF-1alpha up-regulation. Tretinoin 58-62 hypoxia inducible factor 1 subunit alpha Homo sapiens 255-265
22353356-3 2012 All-trans retinoic acid (ATRA), an RAR ligand, increased ABCG1 protein levels and apoA-I/HDL-mediated cholesterol efflux from the macrophages. Tretinoin 0-23 ATP binding cassette subfamily G member 1 Homo sapiens 57-62
22353356-3 2012 All-trans retinoic acid (ATRA), an RAR ligand, increased ABCG1 protein levels and apoA-I/HDL-mediated cholesterol efflux from the macrophages. Tretinoin 0-23 apolipoprotein A1 Homo sapiens 82-88
22353356-3 2012 All-trans retinoic acid (ATRA), an RAR ligand, increased ABCG1 protein levels and apoA-I/HDL-mediated cholesterol efflux from the macrophages. Tretinoin 25-29 ATP binding cassette subfamily G member 1 Homo sapiens 57-62
22353356-3 2012 All-trans retinoic acid (ATRA), an RAR ligand, increased ABCG1 protein levels and apoA-I/HDL-mediated cholesterol efflux from the macrophages. Tretinoin 25-29 apolipoprotein A1 Homo sapiens 82-88
22353356-5 2012 The stimulatory effects of ATRA on ABCG1 expression were completely abolished in the presence of RAR/RXR antagonists but were only partially canceled in the presence of an LXR antagonist. Tretinoin 27-31 ATP binding cassette subfamily G member 1 Homo sapiens 35-40
22366455-0 2012 Increased retinoic acid levels through ablation of Cyp26b1 determine the processes of embryonic skin barrier formation and peridermal development. Tretinoin 10-23 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 51-58
21678401-0 2012 Role of SF-1 and DAX-1 during differentiation of P19 cells by retinoic acid. Tretinoin 62-75 nuclear receptor subfamily 0 group B member 1 Homo sapiens 17-22
22248690-3 2012 Wild-type P19 embryonal carcinoma cells or cells stably expressing shRNAs targeting P2X2 or P2X7 receptor expression were induced to differentiate into neurons and glial cells in the presence of retinoic acid. Tretinoin 195-208 purinergic receptor P2X 7 Homo sapiens 92-105
22366455-5 2012 Absence of cytochrome P450, family 26, subfamily b, polypeptide 1 (Cyp26b1), a retinoic-acid-degrading enzyme, results in aberrant epidermal differentiation and filaggrin expression, defective cornified envelopes and skin barrier formation, in conjunction with peridermal retention. Tretinoin 79-92 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 11-50
22366455-5 2012 Absence of cytochrome P450, family 26, subfamily b, polypeptide 1 (Cyp26b1), a retinoic-acid-degrading enzyme, results in aberrant epidermal differentiation and filaggrin expression, defective cornified envelopes and skin barrier formation, in conjunction with peridermal retention. Tretinoin 79-92 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 67-74
22366455-6 2012 We show that these alterations are RA dependent because administration of exogenous RA in vivo and to organotypic skin cultures phenocopy Cyp26b1(-/-) skin abnormalities. Tretinoin 35-37 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 138-145
22366455-6 2012 We show that these alterations are RA dependent because administration of exogenous RA in vivo and to organotypic skin cultures phenocopy Cyp26b1(-/-) skin abnormalities. Tretinoin 84-86 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 138-145
22366036-6 2012 Importantly, knockout of ACS4 in ES cells markedly attenuated neuronal differentiation induced by NGF and all-trans retinoic acids (RA). Tretinoin 116-130 acyl-CoA synthetase long-chain family member 4 Rattus norvegicus 25-29
22116806-2 2012 The miRNA expression profiles of THY1(+)-enriched undifferentiated spermatogonia were characterized, and members of Mir-17-92 (Mirc1) and its paralog Mir-106b-25 (Mirc3) clusters are significantly downregulated during retinoic acid-induced spermatogonial differentiation, both in vitro and in vivo. Tretinoin 218-231 thymus cell antigen 1, theta Mus musculus 33-37
22245250-0 2012 The retinoic acid-induced up-regulation of insulin-like growth factor 1 and 2 is associated with prolidase-dependent collagen synthesis in UVA-irradiated human dermal equivalents. Tretinoin 4-17 insulin like growth factor 1 Homo sapiens 43-77
22357617-6 2012 Next, we used an inducible expression system to silence MECP2 in neuroblastoma cells before and after the induction of neural differentiation via retinoic acid treatment. Tretinoin 146-159 methyl-CpG binding protein 2 Homo sapiens 56-61
22116806-3 2012 The repression of microRNA clusters Mir-17-92 (Mirc1) and Mir-106b-25 (Mirc3) by retinoic acid in turn potentially upregulates the expression of Bim, Kit, Socs3, and Stat3. Tretinoin 81-94 signal transducer and activator of transcription 3 Mus musculus 166-171
22366036-6 2012 Importantly, knockout of ACS4 in ES cells markedly attenuated neuronal differentiation induced by NGF and all-trans retinoic acids (RA). Tretinoin 132-134 acyl-CoA synthetase long-chain family member 4 Rattus norvegicus 25-29
22229477-0 2012 Combination of valproic acid and ATRA restores RARbeta2 expression and induces differentiation in cervical cancer through the PI3K/Akt pathway. Tretinoin 33-37 AKT serine/threonine kinase 1 Homo sapiens 131-134
22330803-7 2012 Immunocytochemistry revealed that 48 +- 11% of ATRA-treated cells were positive for tyrosine hydroxylase (TH), and 36 +- 9% of cells were positive for dopamine transporter (DAT). Tretinoin 47-51 tyrosine hydroxylase Homo sapiens 84-104
22406747-6 2012 Furthermore, initiation of ATRA plus TCP treatment 15 d after engraftment of human AML cells in NOD-SCID gamma (with interleukin-2 (IL-2) receptor gamma chain deficiency) mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect that was superior to treatment with either drug alone. Tretinoin 27-31 interleukin 2 Homo sapiens 117-130
22406747-6 2012 Furthermore, initiation of ATRA plus TCP treatment 15 d after engraftment of human AML cells in NOD-SCID gamma (with interleukin-2 (IL-2) receptor gamma chain deficiency) mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect that was superior to treatment with either drug alone. Tretinoin 27-31 interleukin 2 Homo sapiens 132-136
22406747-6 2012 Furthermore, initiation of ATRA plus TCP treatment 15 d after engraftment of human AML cells in NOD-SCID gamma (with interleukin-2 (IL-2) receptor gamma chain deficiency) mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect that was superior to treatment with either drug alone. Tretinoin 194-198 interleukin 2 Homo sapiens 117-130
22406747-6 2012 Furthermore, initiation of ATRA plus TCP treatment 15 d after engraftment of human AML cells in NOD-SCID gamma (with interleukin-2 (IL-2) receptor gamma chain deficiency) mice also revealed the ATRA plus TCP drug combination to have a potent anti-leukemic effect that was superior to treatment with either drug alone. Tretinoin 194-198 interleukin 2 Homo sapiens 132-136
22355136-4 2012 We previously demonstrated that retinoic acid (RAR-RXR) and vitamin D3 receptors (VDR-RXR) heterodimers recruit only one coactivator molecule asymmetrically without steric hindrance for the binding of a second cofactor. Tretinoin 32-45 RAB40B, member RAS oncogene family Homo sapiens 47-50
22127979-5 2012 We found dynamic patterns of gene expression for the RA-synthesizing enzyme, Raldh2, and for the RA-catabolizing enzyme, Cyp26b1, during GT development. Tretinoin 97-99 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 121-128
22250783-15 2012 ATRA may ease the bleomycin-induced pulmonary fibrosis by inhibiting the expression of IL-6 and TGF-beta, shifting the Treg/Th17 ratio and reducing the secretion of IL-17A. Tretinoin 0-4 interleukin 6 Mus musculus 87-91
22293198-5 2012 In a monolayer culture, RA significantly induced both the expression of the early germ-specific genes, Stra8, Dazl and Mvh, and prolonged activation of Smad1/5 (for at least 24h). Tretinoin 24-26 deleted in azoospermia-like Mus musculus 110-114
22357317-3 2012 In a set of retinoic-acid (RA) and carotenoic-acid (CA) sensitizers, having n conjugated double bonds, CA7 gave rise to the highest performance, which was reduced toward RA5 and CA13. Tretinoin 12-25 carbonic anhydrase 7 Homo sapiens 103-106
22357317-3 2012 In a set of retinoic-acid (RA) and carotenoic-acid (CA) sensitizers, having n conjugated double bonds, CA7 gave rise to the highest performance, which was reduced toward RA5 and CA13. Tretinoin 12-25 carbonic anhydrase 13 Homo sapiens 178-182
22357317-3 2012 In a set of retinoic-acid (RA) and carotenoic-acid (CA) sensitizers, having n conjugated double bonds, CA7 gave rise to the highest performance, which was reduced toward RA5 and CA13. Tretinoin 27-29 carbonic anhydrase 7 Homo sapiens 103-106
22357317-3 2012 In a set of retinoic-acid (RA) and carotenoic-acid (CA) sensitizers, having n conjugated double bonds, CA7 gave rise to the highest performance, which was reduced toward RA5 and CA13. Tretinoin 27-29 carbonic anhydrase 13 Homo sapiens 178-182
21365646-5 2012 The level of GADD153 was gradually elevated as the effect of AFP was counteracted by increasing dose or prolonging treatment time with ATRA in HepG2 cells. Tretinoin 135-139 DNA damage inducible transcript 3 Homo sapiens 13-20
21365646-5 2012 The level of GADD153 was gradually elevated as the effect of AFP was counteracted by increasing dose or prolonging treatment time with ATRA in HepG2 cells. Tretinoin 135-139 alpha fetoprotein Homo sapiens 61-64
22127979-7 2012 Excessive RA signaling in Cyp26b1(-/-) mutants leads to abnormal extents of cell proliferation and differentiation during GT development, and also upregulates expression of growth factor signalings. Tretinoin 10-12 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 26-33
22127979-9 2012 RA signaling positively regulatesShh and Bmp4 expression during GT development as testified also by the experiment of RA administration and analyses of loss-of-function of RA signaling mutants. Tretinoin 0-2 bone morphogenetic protein 4 Mus musculus 41-45
20686816-1 2012 Unlike its cytotoxicity in p53-functional cell lines, Nutlin-1, the small-molecule inhibitor of murine double minute (MDM2), significantly enhanced the differentiation-inducing activity of all-trans retinoic acid (ATRA) in HL60 and NB4 cells (p53-nonfunctional) but not in U937 cells (p53 wild-type). Tretinoin 214-218 tumor protein p53 Homo sapiens 243-246
22009938-7 2012 Finally, we showed that CNG channel activity regulated expression of the retinoic acid-degrading enzyme Cyp26B1. Tretinoin 73-86 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 104-111
21993673-10 2012 CONCLUSIONS: The combination of all-trans-retinoic acid and just two cycles of idarubicin followed by triple maintenance produced durable remissions in most patients, but patients with high-risk disease, especially those with FLT3 mutations, require additional agents or alternative treatment approaches. Tretinoin 32-55 fms related receptor tyrosine kinase 3 Homo sapiens 226-230
20686816-0 2012 Nutlin-1 strengthened anti-proliferation and differentiation-inducing activity of ATRA in ATRA-treated p-glycoprotein deregulated human myelocytic leukemia cells. Tretinoin 82-86 ATP binding cassette subfamily B member 1 Homo sapiens 103-117
22197381-2 2012 We report the complexation of bovine serum albumin (BSA) with retinol and retinoic acid at physiological conditions, using constant protein concentration and various retinoid contents. Tretinoin 74-87 albumin Homo sapiens 37-50
22107969-0 2012 UTF1 deficiency promotes retinoic acid-induced neuronal differentiation in P19 embryonal carcinoma cells. Tretinoin 25-38 undifferentiated embryonic cell transcription factor 1 Homo sapiens 0-4
22107969-3 2012 Consistent with this result, suppression of UTF1 expression in P19 cells by RNA interference enhanced retinoic acid (RA)-induced neuronal differentiation. Tretinoin 102-115 undifferentiated embryonic cell transcription factor 1 Homo sapiens 44-48
22107969-3 2012 Consistent with this result, suppression of UTF1 expression in P19 cells by RNA interference enhanced retinoic acid (RA)-induced neuronal differentiation. Tretinoin 117-119 undifferentiated embryonic cell transcription factor 1 Homo sapiens 44-48
22107969-5 2012 Interestingly, the growth rates of UTF1-deficient P19 cells did not differ from that of parental cells in adherent cultures, but were increased in embryoid bodies during RA-induced differentiation. Tretinoin 170-172 undifferentiated embryonic cell transcription factor 1 Homo sapiens 35-39
20686816-0 2012 Nutlin-1 strengthened anti-proliferation and differentiation-inducing activity of ATRA in ATRA-treated p-glycoprotein deregulated human myelocytic leukemia cells. Tretinoin 90-94 ATP binding cassette subfamily B member 1 Homo sapiens 103-117
20686816-1 2012 Unlike its cytotoxicity in p53-functional cell lines, Nutlin-1, the small-molecule inhibitor of murine double minute (MDM2), significantly enhanced the differentiation-inducing activity of all-trans retinoic acid (ATRA) in HL60 and NB4 cells (p53-nonfunctional) but not in U937 cells (p53 wild-type). Tretinoin 214-218 tumor protein p53 Homo sapiens 243-246
20686816-2 2012 Moreover, we demonstrated that the synergistic differentiation-inducing activity of Nutlin-1 combined with ATRA appeared in a p53-independent manner. Tretinoin 107-111 tumor protein p53 Homo sapiens 126-129
20686816-3 2012 In the present study, we found that ATRA could selectively induce expression of p-glycoprotein (p-gp) in HL60 and NB4 cells but not in U937 cells. Tretinoin 36-40 ATP binding cassette subfamily B member 1 Homo sapiens 80-94
20686816-3 2012 In the present study, we found that ATRA could selectively induce expression of p-glycoprotein (p-gp) in HL60 and NB4 cells but not in U937 cells. Tretinoin 36-40 ATP binding cassette subfamily B member 1 Homo sapiens 96-100
20686816-8 2012 Nutlin-1 might be a useful adjuvant with ATRA for patients with retinoid-resistant leukemia induced by overexpression of p-gp. Tretinoin 41-45 ATP binding cassette subfamily B member 1 Homo sapiens 121-125
22325386-0 2012 Prenatal retinoic acid upregulates connexin 43 (Cx43) gene expression in pulmonary hypoplasia in the nitrofen-induced congenital diaphragmatic hernia rat model. Tretinoin 9-22 gap junction protein, alpha 1 Rattus norvegicus 35-46
22325386-0 2012 Prenatal retinoic acid upregulates connexin 43 (Cx43) gene expression in pulmonary hypoplasia in the nitrofen-induced congenital diaphragmatic hernia rat model. Tretinoin 9-22 gap junction protein, alpha 1 Rattus norvegicus 48-52
22325386-5 2012 We hypothesized that gene expression of Cx43 is downregulated during alveologenesis and that administration of RA upregulates Cx43 expression in the nitrofen-induced PH. Tretinoin 111-113 gap junction protein, alpha 1 Rattus norvegicus 126-130
22325386-11 2012 On D21, expression levels of Cx43 were significantly upregulated in nitrofen+RA and control+RA compared with those in nitrofen group. Tretinoin 77-79 gap junction protein, alpha 1 Rattus norvegicus 29-33
22391160-4 2012 The results demonstrated that in ATRA-induced differentiation, the transcriptional level of CD44v6 was dominantly down-regulated, the translational level of CD44v6 did not change and the PI3K/Akt signal axis was activated. Tretinoin 33-37 AKT serine/threonine kinase 1 Homo sapiens 192-195
22325386-11 2012 On D21, expression levels of Cx43 were significantly upregulated in nitrofen+RA and control+RA compared with those in nitrofen group. Tretinoin 92-94 gap junction protein, alpha 1 Rattus norvegicus 29-33
22325386-14 2012 Upregulation of Cx43 pulmonary gene expression after RA treatment may promote lung growth by stimulating alveologenesis in nitrofen-induced PH. Tretinoin 53-55 gap junction protein, alpha 1 Rattus norvegicus 16-20
21611753-6 2012 Our study also implies that RA induced to express Wnt antagonist Dickkopf-1 (Dkk-1) for neural differentiation. Tretinoin 28-30 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 65-75
21611753-6 2012 Our study also implies that RA induced to express Wnt antagonist Dickkopf-1 (Dkk-1) for neural differentiation. Tretinoin 28-30 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 77-82
22135230-4 2012 In this article, we report that, by suppressing CAK phosphorylation of RARalpha, RA induces FGF8f to mediate osteosarcoma U2OS cell differentiation in an autocrine manner. Tretinoin 71-73 cyclin dependent kinase 7 Homo sapiens 48-51
22391160-2 2012 This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 54-77 AKT serine/threonine kinase 1 Homo sapiens 213-216
22391160-2 2012 This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 79-83 AKT serine/threonine kinase 1 Homo sapiens 213-216
22209845-5 2012 For stage II induction, the addition of retinoic acid (R) in the continuous presence of A4L during days 6-8 was most effective to induce nephrogenic intermediate mesodermal markers, such as Pax2 and Lim1. Tretinoin 40-53 paired box 2 Mus musculus 190-194
22116818-11 2012 Notably, RA was required to more fully differentiate SMC from VEGFR2+ cells and completely blocked differentiation of cardiomyocytes from VEGFR2+/PDGFRalpha+ cells. Tretinoin 9-11 platelet derived growth factor receptor, alpha polypeptide Mus musculus 146-156
21995425-7 2012 The latter result could be mimicked by the addition of retinoic acid to the C2C12 cell tissue culture medium, a treatment which caused a significant reduction of RyR1 expression. Tretinoin 55-68 ryanodine receptor 1, skeletal muscle Mus musculus 162-166
22197812-12 2012 In H9 cells treated with RA for 29 days, GRP78/Bip, XBP-1 and Bcl2 were all upregulated. Tretinoin 25-27 heat shock protein family A (Hsp70) member 5 Homo sapiens 41-46
22197812-12 2012 In H9 cells treated with RA for 29 days, GRP78/Bip, XBP-1 and Bcl2 were all upregulated. Tretinoin 25-27 heat shock protein family A (Hsp70) member 5 Homo sapiens 47-50
22197812-12 2012 In H9 cells treated with RA for 29 days, GRP78/Bip, XBP-1 and Bcl2 were all upregulated. Tretinoin 25-27 BCL2 apoptosis regulator Homo sapiens 62-66
23383387-5 2012 In sporadic ALS, the cytoplasmic binding protein that facilitates nuclear translocation of retinoic acid, cellular retinoic acid binding protein-II (CRABP-II), was localized to the nucleus and retinoic acid receptor beta (RARbeta) was significantly increased in motor neuron nuclei when compared to either familial ALS patients or non-neurologic disease controls. Tretinoin 91-104 retinoic acid receptor beta Homo sapiens 193-220
22490698-1 2012 OBJECTIVE: To explore the relationship between interferon (IFN) alpha and all-trans retinoic acid (ATRA)-induced signaling pathways in the expression of retinoic acid-induced gene G (RIG-G). Tretinoin 84-97 interferon alpha 1 Homo sapiens 47-69
22490698-1 2012 OBJECTIVE: To explore the relationship between interferon (IFN) alpha and all-trans retinoic acid (ATRA)-induced signaling pathways in the expression of retinoic acid-induced gene G (RIG-G). Tretinoin 99-103 interferon alpha 1 Homo sapiens 47-69
22125274-4 2012 RESULTS: The authors demonstrated in vivo that pitx2 is a key downstream target of retinoic acid (RA) in craniofacial development, and this pathway is required for coordinating neural crest, mesoderm, and ocular development. Tretinoin 83-96 paired like homeodomain 2 Homo sapiens 47-52
22125274-4 2012 RESULTS: The authors demonstrated in vivo that pitx2 is a key downstream target of retinoic acid (RA) in craniofacial development, and this pathway is required for coordinating neural crest, mesoderm, and ocular development. Tretinoin 98-100 paired like homeodomain 2 Homo sapiens 47-52
23383387-5 2012 In sporadic ALS, the cytoplasmic binding protein that facilitates nuclear translocation of retinoic acid, cellular retinoic acid binding protein-II (CRABP-II), was localized to the nucleus and retinoic acid receptor beta (RARbeta) was significantly increased in motor neuron nuclei when compared to either familial ALS patients or non-neurologic disease controls. Tretinoin 91-104 retinoic acid receptor beta Homo sapiens 222-229
22020119-2 2012 The cytochrome P450 enzymes CYP26 are believed to partially regulate cellular concentrations of atRA via oxidative metabolism and hence affect retinoid homeostasis and signaling. Tretinoin 96-100 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 28-33
21515404-7 2012 A point mutation in Rdh10 generated by ethylnitrosourea has demonstrated that RDH10 generates much of the retinaldehyde needed for RA synthesis during embryonic development. Tretinoin 131-133 retinol dehydrogenase 10 (all-trans) Mus musculus 20-25
21515404-7 2012 A point mutation in Rdh10 generated by ethylnitrosourea has demonstrated that RDH10 generates much of the retinaldehyde needed for RA synthesis during embryonic development. Tretinoin 131-133 retinol dehydrogenase 10 (all-trans) Mus musculus 78-83
22020119-8 2012 Qualitatively, recombinant CYP26A1 and CYP26B1 formed the same primary and sequential metabolites from atRA. Tretinoin 103-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 27-34
22020119-8 2012 Qualitatively, recombinant CYP26A1 and CYP26B1 formed the same primary and sequential metabolites from atRA. Tretinoin 103-107 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 39-46
22020119-10 2012 The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested. Tretinoin 10-14 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 81-88
21669299-2 2012 Treatment with retinoic acid, in particular, has been shown to reduce body fat and improve insulin sensitivity in lean and obese rodents by enhancing fat mobilization and energy utilization systemically, in tissues including brown and white adipose tissues, skeletal muscle and the liver. Tretinoin 15-28 insulin Homo sapiens 91-98
22020119-10 2012 The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested. Tretinoin 10-14 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 93-100
22020119-10 2012 The major atRA metabolites 4-OH-RA, 18-OH-RA and 4-oxo-RA were all substrates of CYP26A1 and CYP26B1, and CYP26A1 had a 2-10-fold higher catalytic activity towards all substrates tested. Tretinoin 10-14 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 106-113
22020119-12 2012 CYP26A1 has higher catalytic activity than CYP26B1 and seems to be responsible for metabolism of atRA in tissues that function as a barrier for atRA exposure. Tretinoin 97-101 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
22020119-12 2012 CYP26A1 has higher catalytic activity than CYP26B1 and seems to be responsible for metabolism of atRA in tissues that function as a barrier for atRA exposure. Tretinoin 97-101 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 43-50
21954838-10 2012 The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Tretinoin 83-87 tight junction protein 1 Homo sapiens 127-131
21898109-7 2012 We further explored the role of genistein on countering the ATRA-induced VEGF expression. Tretinoin 60-64 vascular endothelial growth factor A Homo sapiens 73-77
21898109-10 2012 Finally, expression of VEGF (both mRNA and protein) was diminished in A549 cells exposed to both ATRA and genistein. Tretinoin 97-101 vascular endothelial growth factor A Homo sapiens 23-27
21898109-11 2012 In conclusion, our results demonstrate that genistein effectively enhances anti-cancer effects of ATRA, particularly, by countering the ATRA-induced up-regulation of VEGF. Tretinoin 98-102 vascular endothelial growth factor A Homo sapiens 166-170
21898109-11 2012 In conclusion, our results demonstrate that genistein effectively enhances anti-cancer effects of ATRA, particularly, by countering the ATRA-induced up-regulation of VEGF. Tretinoin 136-140 vascular endothelial growth factor A Homo sapiens 166-170
22701192-7 2012 Concomitant administration of medications such as triazole antifungals which influence the cytochrome P-450 system can exacerbate this potential complication of ATRA. Tretinoin 161-165 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 91-107
22129829-0 2012 The Osr1 and Osr2 genes act in the pronephric anlage downstream of retinoic acid signaling and upstream of Wnt2b to maintain pectoral fin development. Tretinoin 67-80 odd-skipped related transcription factor 1 Danio rerio 4-8
22037423-6 2012 Moreover, there is concurrent induction of TRIAD1 and UBCH8 upon combinatorial treatment of acute promyelocytic leukemia cells with the pro-apoptotic epigenetic modulator valproic acid and the differentiation inducing agent all-trans retinoic acid. Tretinoin 234-247 ariadne RBR E3 ubiquitin protein ligase 2 Homo sapiens 43-49
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 16-29 retinoic acid receptor beta Homo sapiens 164-171
22096078-4 2012 We show that RA signaling is upregulated within the first few hours after fin amputation in the stump mesenchyme, where it controls Fgf, Wnt/beta-catenin and Igf signaling. Tretinoin 13-15 catenin (cadherin-associated protein), beta 1 Danio rerio 141-153
22096078-7 2012 In addition, RA signaling maintains blastema proliferation through the activation of growth-stimulatory signals mediated by Fgf and Wnt/beta-catenin signaling, as well as by reducing signaling through the growth-inhibitory non-canonical Wnt pathway. Tretinoin 13-15 catenin (cadherin-associated protein), beta 1 Danio rerio 136-148
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 31-33 retinoic acid receptor beta Homo sapiens 164-171
23304206-6 2012 Furthermore, RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown. Tretinoin 13-15 caspase 3 Homo sapiens 26-35
22293114-6 2012 TGIF overexpression downregulates SOX3 promoter activity and decreases endogenous SOX3 protein expression in both uninduced and retinoic acid (RA)-induced NT2/D1 cells. Tretinoin 128-141 TGFB induced factor homeobox 1 Homo sapiens 0-4
22562199-0 2012 xCOUP-TF-B regulates xCyp26 transcription and modulates retinoic acid signaling for anterior neural patterning in Xenopus. Tretinoin 56-69 nuclear receptor subfamily 2 group F member 2 L homeolog Xenopus laevis 0-10
22562199-5 2012 Analysis of brain marker gene expression revealed that xCOUP-TF-B injection induced slight anteriorization in embryos and attenuated the effects of RA treatment. Tretinoin 148-150 nuclear receptor subfamily 2 group F member 2 L homeolog Xenopus laevis 55-65
22562199-6 2012 This anteriorization effect was enhanced when xCOUP-TF-B was co-injected with xCyp26A or xCyp26C, which are known RA metabolizing factors. Tretinoin 114-116 nuclear receptor subfamily 2 group F member 2 L homeolog Xenopus laevis 46-56
22942771-7 2012 All-trans retinoic acid modulated secretion of RARRES1 in a dose dependent manner. Tretinoin 10-23 retinoic acid receptor responder 1 Homo sapiens 47-54
22293114-6 2012 TGIF overexpression downregulates SOX3 promoter activity and decreases endogenous SOX3 protein expression in both uninduced and retinoic acid (RA)-induced NT2/D1 cells. Tretinoin 143-145 TGFB induced factor homeobox 1 Homo sapiens 0-4
23259068-3 2012 ATRA and ATO induce Ser-51 phosphorylation (inactivation) of eIF2alpha, through the induction of protein kinase C delta (PKCdelta) and PKR, but not other eIF2alpha kinases, such as GCN2 and PERK in APL (NB4) and AML cells (HL60, U937, and THP-1). Tretinoin 0-4 GLI family zinc finger 2 Homo sapiens 239-244
21836606-7 2012 Moreover, ectopic expression of PIG7 could sensitize these cell lines to PB or all-trans retinoic acid, respectively, which could then be abrogated by downregulation of PIG7 expression. Tretinoin 89-102 lipopolysaccharide induced TNF factor Homo sapiens 32-36
22577255-3 2012 CA strongly suppressed the production of IL-6, IL-8, and MCP-1 from keratinocyte HaCaT cells stimulated with sodium lauryl sulfate (SLS) and retinoic acid (RA). Tretinoin 141-154 mast cell protease 1 Mus musculus 57-62
22577255-3 2012 CA strongly suppressed the production of IL-6, IL-8, and MCP-1 from keratinocyte HaCaT cells stimulated with sodium lauryl sulfate (SLS) and retinoic acid (RA). Tretinoin 156-158 mast cell protease 1 Mus musculus 57-62
22218901-1 2012 Murine Prickle2 but not Prickle1 gene expression was induced in C1300 neuroblastoma cell line during neurite-like process formation induced by all trans-retinoic acid (RA). Tretinoin 147-166 prickle planar cell polarity protein 2 Mus musculus 7-15
22218901-1 2012 Murine Prickle2 but not Prickle1 gene expression was induced in C1300 neuroblastoma cell line during neurite-like process formation induced by all trans-retinoic acid (RA). Tretinoin 168-170 prickle planar cell polarity protein 2 Mus musculus 7-15
22218901-2 2012 Overexpression of Prickle1 or Prickle2 in C1300 cells induced striking neurite-like process formation without RA. Tretinoin 110-112 prickle planar cell polarity protein 2 Mus musculus 30-38
23077538-9 2012 A similar correlation between the increase of miR-223/Ago2 association and the resistance of miR-223 against RNaseA was observed during all trans retinoic acid (ATRA)-induced cell differentiation of promyelocytic HL60 cells. Tretinoin 146-159 argonaute RISC catalytic component 2 Homo sapiens 54-58
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 35-58 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 231-236
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 60-64 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 231-236
23152790-6 2012 PML/RARalpha without the "coiled-coil" fails to block differentiation and mediates an all-trans retinoic acid-response. Tretinoin 96-109 promyelocytic leukemia Mus musculus 0-3
21833538-4 2012 Menin expression is induced in P19 cell aggregates by retinoic acid (RA). Tretinoin 54-67 multiple endocrine neoplasia 1 Mus musculus 0-5
21833538-4 2012 Menin expression is induced in P19 cell aggregates by retinoic acid (RA). Tretinoin 69-71 multiple endocrine neoplasia 1 Mus musculus 0-5
21833538-6 2012 RA induced cell death in aggregated menin over-expressing cells. Tretinoin 0-2 multiple endocrine neoplasia 1 Mus musculus 36-41
21833538-8 2012 Menin"s ability to induce endodermal differentiation in specific populations of the aggregated cells in the absence of RA implied that menin could substitute RA by inducing a set of target genes that are RA responsive. Tretinoin 158-160 multiple endocrine neoplasia 1 Mus musculus 0-5
21833538-8 2012 Menin"s ability to induce endodermal differentiation in specific populations of the aggregated cells in the absence of RA implied that menin could substitute RA by inducing a set of target genes that are RA responsive. Tretinoin 158-160 multiple endocrine neoplasia 1 Mus musculus 0-5
21842375-7 2012 Zebularine alone or in sequential combination with RA decreased expression of DNMT1, caused fast and time-dependent expression of pan-cadherin and partial demethylation of E-cadherin but not tumor suppressor p15. Tretinoin 51-53 cadherin 1 Homo sapiens 172-182
23010996-3 2012 During development of rhombomeres in the zebrafish hindbrain, the morphogen retinoic acid (RA) induces expression of hoxb1a in rhombomere 4 (r4) and krox20 in r3 and r5. Tretinoin 76-89 homeobox B1a Danio rerio 117-123
23010996-3 2012 During development of rhombomeres in the zebrafish hindbrain, the morphogen retinoic acid (RA) induces expression of hoxb1a in rhombomere 4 (r4) and krox20 in r3 and r5. Tretinoin 76-89 early growth response 2a Danio rerio 149-155
23107969-6 2012 RESULTS: Compared to diseased animals receiving vehicle, ATRA statistically significantly increased the number of glomerular transition cells, defined as cells double-staining for PAX2 and WT-1, in membranous nephropathy at weeks 2, 5 and 16, and in FSGS at weeks 1 and 2. Tretinoin 57-61 paired box 2 Rattus norvegicus 180-184
22389628-4 2012 In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24. Tretinoin 15-28 tumor protein p53 Homo sapiens 50-53
22389628-7 2012 Induction of p53 levels is a key step: RNA-interference-mediated knockdown of p53 delays differentiation, whereas depletion of negative regulators of p53 or ectopic expression of p53 yields spontaneous differentiation of hESCs, independently of retinoic acid. Tretinoin 245-258 tumor protein p53 Homo sapiens 13-16
23077538-9 2012 A similar correlation between the increase of miR-223/Ago2 association and the resistance of miR-223 against RNaseA was observed during all trans retinoic acid (ATRA)-induced cell differentiation of promyelocytic HL60 cells. Tretinoin 161-165 argonaute RISC catalytic component 2 Homo sapiens 54-58
22319578-0 2012 RDH10 oxidation of Vitamin A is a critical control step in synthesis of retinoic acid during mouse embryogenesis. Tretinoin 72-85 retinol dehydrogenase 10 (all-trans) Mus musculus 0-5
22693611-8 2012 Chromatin immunoprecipitation revealed COUP-TFII occupancy of the RARB2 promoter was increased by all-trans retinoic acid (atRA). Tretinoin 98-121 nuclear receptor subfamily 2 group F member 2 Homo sapiens 39-48
22693611-8 2012 Chromatin immunoprecipitation revealed COUP-TFII occupancy of the RARB2 promoter was increased by all-trans retinoic acid (atRA). Tretinoin 123-127 nuclear receptor subfamily 2 group F member 2 Homo sapiens 39-48
22666329-4 2012 The present study describes the molecular cloning, characterization and function of atRA-induced expression of a spliced variant of the CYP26B1 gene. Tretinoin 84-88 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 136-143
22666329-5 2012 METHODOLOGY/PRINCIPAL FINDINGS: The coding region of the spliced CYP26B1 lacking exon 2 was amplified from cDNA synthesized from atRA-treated human aortic smooth muscle cells and sequenced. Tretinoin 129-133 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 65-72
22666329-7 2012 atRA induced both variants of CYP26B1 in cultured vascular cells. Tretinoin 0-4 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 30-37
22666329-10 2012 Transfection of COS-1 and THP-1 cells with the CYP26B1 spliced variant indicated either an increase or a decrease in the catabolism of atRA, probably depending on the expression of other atRA catabolizing enzymes in the cells. Tretinoin 135-139 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 47-54
22470433-0 2012 The colocalization potential of HIV-specific CD8+ and CD4+ T-cells is mediated by integrin beta7 but not CCR6 and regulated by retinoic acid. Tretinoin 127-140 CD4 molecule Homo sapiens 54-57
22363502-3 2012 RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. Tretinoin 0-2 GATA binding protein 2a Danio rerio 92-97
23028851-14 2012 The elevated hepatic expression of Raldh1 in ZF rats may cause the excessive RA production from retinol, and in turn, result in higher Srebp-1c expression. Tretinoin 77-79 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 35-41
22319578-9 2012 Here we describe a new targeted knockout of Rdh10 in which RA synthesis is severely impaired, particularly at critical early embryonic stages. Tretinoin 59-61 retinol dehydrogenase 10 (all-trans) Mus musculus 44-49
22319578-13 2012 We also show that reduced RA production results in upregulation of Rdh10. Tretinoin 26-28 retinol dehydrogenase 10 (all-trans) Mus musculus 67-72
22319578-14 2012 These data demonstrate that RDH10 plays a critical role in mediating the rate limiting RDH step of Vitamin A metabolism and functions as a nodal point in feedback regulation of RA synthesis. Tretinoin 177-179 retinol dehydrogenase 10 (all-trans) Mus musculus 28-33
22085718-2 2011 We first examined the expression of PRC1 genes during all-trans retinoic acid (ATRA)-mediated differentiation of human HL-60 cells, and identified PCGF2 as a gene down-regulated by ATRA in a time-dependent manner. Tretinoin 64-77 polycomb group ring finger 2 Homo sapiens 147-152
22079989-6 2011 Consistent with this finding, retinoic acid-inducible gene I- and TBK1-induced phosphorylation of IFN regulatory factor 3 was significantly diminished when MIP-T3 was overexpressed. Tretinoin 30-43 interferon alpha 1 Homo sapiens 98-101
22079989-6 2011 Consistent with this finding, retinoic acid-inducible gene I- and TBK1-induced phosphorylation of IFN regulatory factor 3 was significantly diminished when MIP-T3 was overexpressed. Tretinoin 30-43 TRAF3 interacting protein 1 Homo sapiens 156-162
21910960-12 2011 The effect of typical effectors (retinoic acid and interferon-gamma) on tTG expression could be demonstrated. Tretinoin 33-46 transglutaminase 2 Homo sapiens 72-75
22085718-2 2011 We first examined the expression of PRC1 genes during all-trans retinoic acid (ATRA)-mediated differentiation of human HL-60 cells, and identified PCGF2 as a gene down-regulated by ATRA in a time-dependent manner. Tretinoin 79-83 polycomb group ring finger 2 Homo sapiens 147-152
22069185-4 2011 We also provide evidence that RA pathway activation can modulate Gli function in a Hh ligand-independent manner. Tretinoin 30-32 gli Danio rerio 65-68
22069189-3 2011 Previously, we have demonstrated that Pitx3(-/-) embryos lack the expression of the retinoic acid (RA)-generating enzyme Ahd2, which is normally selectively expressed in the Pitx3-dependent DA neurons of the SNc. Tretinoin 84-97 paired like homeodomain 3 Homo sapiens 38-43
22069189-3 2011 Previously, we have demonstrated that Pitx3(-/-) embryos lack the expression of the retinoic acid (RA)-generating enzyme Ahd2, which is normally selectively expressed in the Pitx3-dependent DA neurons of the SNc. Tretinoin 84-97 paired like homeodomain 3 Homo sapiens 174-179
22069189-3 2011 Previously, we have demonstrated that Pitx3(-/-) embryos lack the expression of the retinoic acid (RA)-generating enzyme Ahd2, which is normally selectively expressed in the Pitx3-dependent DA neurons of the SNc. Tretinoin 99-101 paired like homeodomain 3 Homo sapiens 38-43
22069189-3 2011 Previously, we have demonstrated that Pitx3(-/-) embryos lack the expression of the retinoic acid (RA)-generating enzyme Ahd2, which is normally selectively expressed in the Pitx3-dependent DA neurons of the SNc. Tretinoin 99-101 paired like homeodomain 3 Homo sapiens 174-179
22069189-4 2011 Restoring RA signaling in Pitx3(-/-) embryos revealed a selective dependence of SNc neurons on the presence of RA for differentiation into Th-positive neurons and maintenance throughout embryonic development. Tretinoin 10-12 paired like homeodomain 3 Homo sapiens 26-31
22069189-4 2011 Restoring RA signaling in Pitx3(-/-) embryos revealed a selective dependence of SNc neurons on the presence of RA for differentiation into Th-positive neurons and maintenance throughout embryonic development. Tretinoin 111-113 paired like homeodomain 3 Homo sapiens 26-31
22069189-6 2011 In the search for genes that were affected in Pitx3-deficient mdDA neurons and restored upon embryonic RA treatment, we provide evidence that Delta-like 1, D2R (Drd2) and Th are regulated by Pitx3 and RA signaling, which influences the mdDA terminal differentiated phenotype. Tretinoin 103-105 paired like homeodomain 3 Homo sapiens 191-196
22069189-7 2011 Furthermore, we show that regulation of Ahd2-mediated RA signaling represents only one aspect of the Pitx3 downstream cascade, as Vmat2, Dat, Ahd2 (Aldh1a1), En1, En2 and Cck were unaffected by RA treatment and are (subset) specifically modulated by Pitx3. Tretinoin 54-56 paired like homeodomain 3 Homo sapiens 101-106
22069189-8 2011 In conclusion, our data reveal several RA-dependent and -independent aspects of the Pitx3-regulated gene cascade, suggesting that Pitx3 acts on multiple levels in the molecular subset-specification of mdDA neurons. Tretinoin 39-41 paired like homeodomain 3 Homo sapiens 84-89
22069189-8 2011 In conclusion, our data reveal several RA-dependent and -independent aspects of the Pitx3-regulated gene cascade, suggesting that Pitx3 acts on multiple levels in the molecular subset-specification of mdDA neurons. Tretinoin 39-41 paired like homeodomain 3 Homo sapiens 130-135
22071108-3 2011 Upon meiosis initiation, Msx1 and Msx2 genes are strongly expressed in the foetal ovary, possibly stimulated by soluble factors found there: bone morphogenetic proteins Bmp2 and Bmp4, and retinoic acid. Tretinoin 188-201 msh homeobox 2 Homo sapiens 34-38
21735090-0 2011 In vitro optimization of retinoic acid-induced neuritogenesis and TH endogenous expression in human SH-SY5Y neuroblastoma cells by the antioxidant Trolox. Tretinoin 25-38 tyrosine hydroxylase Homo sapiens 66-68
21905773-6 2011 The first group of U-CH1 cells was exposed to drugs only and the second group of cells was exposed to the simultaneous treatment of 1 muM all-trans retinoic acid (ATRA) and chemotherapeutic agents in differentiation therapy. Tretinoin 138-161 latexin Homo sapiens 134-137
21905773-6 2011 The first group of U-CH1 cells was exposed to drugs only and the second group of cells was exposed to the simultaneous treatment of 1 muM all-trans retinoic acid (ATRA) and chemotherapeutic agents in differentiation therapy. Tretinoin 163-167 latexin Homo sapiens 134-137
21740303-0 2011 Interferon regulatory factor-1 binds c-Cbl, enhances mitogen activated protein kinase signaling and promotes retinoic acid-induced differentiation of HL-60 human myelo-monoblastic leukemia cells. Tretinoin 109-122 interferon regulatory factor 1 Homo sapiens 0-30
21740303-4 2011 RA induces MAPK-dependent expression of IRF-1. Tretinoin 0-2 mitogen-activated protein kinase 1 Homo sapiens 11-15
21740303-4 2011 RA induces MAPK-dependent expression of IRF-1. Tretinoin 0-2 interferon regulatory factor 1 Homo sapiens 40-45
21740303-6 2011 Ectopic IRF-1 expression causes CD38 expression and activation of the Raf/MEK/ERK axis, and enhances RA-induced differentiation by augmenting CD38, CD11b, respiratory burst and G0 arrest. Tretinoin 101-103 interferon regulatory factor 1 Homo sapiens 8-13
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 71-73 interferon regulatory factor 1 Homo sapiens 166-171
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 124-126 interferon regulatory factor 1 Homo sapiens 166-171
22184266-0 2011 Effect of all-trans retinoic acid (ATRA) on viability, proliferation, activation and lineage-specific transcription factors of CD4+ T cells. Tretinoin 10-33 CD4 molecule Homo sapiens 127-130
22184266-0 2011 Effect of all-trans retinoic acid (ATRA) on viability, proliferation, activation and lineage-specific transcription factors of CD4+ T cells. Tretinoin 35-39 CD4 molecule Homo sapiens 127-130
22184266-2 2011 This study was performed to evaluate the effect of ATRA on viability, proliferation, activation and lineage-specific transcription factors of CD4+ T cells. Tretinoin 51-55 CD4 molecule Homo sapiens 142-145
22184266-7 2011 High doses of ATRA (0.1-1 mM) caused extensive cell death in both PBMCs and CD4+ T cells. Tretinoin 14-18 CD4 molecule Homo sapiens 76-79
22184266-11 2011 This study showed that doses of ATRA up to 10 microM are safe when using with CD4+ T cells in terms of cell viability, proliferation and activation. Tretinoin 32-36 CD4 molecule Homo sapiens 78-81
20635168-1 2011 The novel gene HA117 is a multidrug resistance (MDR) gene in all-trans retinoic acid resistance HL-60 cells. Tretinoin 71-84 regulator of G protein signaling 6 Homo sapiens 15-20
22179182-0 2011 Enhanced expression of retinoic acid-metabolizing enzyme CYP26A1 in sunlight-damaged human skin. Tretinoin 23-36 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 57-64
22179182-2 2011 CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, has been shown to result in a state of functional VAD of the cell. Tretinoin 103-116 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
22179182-2 2011 CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, has been shown to result in a state of functional VAD of the cell. Tretinoin 118-120 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
21735090-3 2011 Our results show a significant enhancement of RA (10 muM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 muM) for 7 days. Tretinoin 46-48 latexin Homo sapiens 53-56
21735090-3 2011 Our results show a significant enhancement of RA (10 muM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 muM) for 7 days. Tretinoin 46-48 tyrosine hydroxylase Homo sapiens 85-87
21735090-3 2011 Our results show a significant enhancement of RA (10 muM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 muM) for 7 days. Tretinoin 46-48 latexin Homo sapiens 155-158
22019272-5 2011 We have identified human null and hypomorphic mutations in the gene encoding the RA-degrading enzyme CYP26B1 that lead to skeletal and craniofacial anomalies, including fusions of long bones, calvarial bone hypoplasia, and craniosynostosis. Tretinoin 81-83 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 101-108
21964460-8 2011 Concomitant up regulation of ERalpha, VEGF, cyclin D1, CDK4 and Ki-67 was also observed to be more prominent for ATRA-treated rats as compared to the rats that were allowed to recover naturally for 56 days. Tretinoin 113-117 cyclin D1 Rattus norvegicus 44-53
21964460-8 2011 Concomitant up regulation of ERalpha, VEGF, cyclin D1, CDK4 and Ki-67 was also observed to be more prominent for ATRA-treated rats as compared to the rats that were allowed to recover naturally for 56 days. Tretinoin 113-117 cyclin-dependent kinase 4 Rattus norvegicus 55-59
21803488-0 2011 All-trans retinoic acid induces cellular senescence via upregulation of p16, p21, and p27. Tretinoin 10-23 cyclin dependent kinase inhibitor 2A Homo sapiens 72-75
21803488-0 2011 All-trans retinoic acid induces cellular senescence via upregulation of p16, p21, and p27. Tretinoin 10-23 dynactin subunit 6 Homo sapiens 86-89
21803488-3 2011 ATRA also upregulated levels of p16, p21, and p27 which lead to activation of Rb and subsequent inactivation of E2F1. Tretinoin 0-4 cyclin dependent kinase inhibitor 2A Homo sapiens 32-35
21803488-3 2011 ATRA also upregulated levels of p16, p21, and p27 which lead to activation of Rb and subsequent inactivation of E2F1. Tretinoin 0-4 dynactin subunit 6 Homo sapiens 46-49
22027263-4 2011 We quantified RA by electrochemical analysis and examined the effect of RA supplementation on TNF-induced ileitis using histologic, coculture, and suppression assays and flow cytometry. Tretinoin 72-74 tumor necrosis factor Mus musculus 94-97
22148010-6 2011 RA significantly decreased DSG1 and DSC1 expression at the mRNA and protein levels in keratinocytes that were cultured in both low- and high-calcium media. Tretinoin 0-2 desmocollin 1 Homo sapiens 36-40
22148010-9 2011 CONCLUSION: Our results indicate that DSG1 and DSC1 downregulation by RA could be related to the increased degradation of corneodesmosomes and consequent desquamation induced by retinoids. Tretinoin 70-72 desmocollin 1 Homo sapiens 47-51
21807577-0 2011 Retinoic acid drives aryl hydrocarbon receptor expression and is instrumental to dioxin-induced toxicity during palate development. Tretinoin 0-13 aryl-hydrocarbon receptor Mus musculus 21-46
22027263-7 2011 IECs responded to reduced levels of RA by up-regulating RALDH3 in vivo and in vitro. Tretinoin 36-38 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 56-62
22027263-8 2011 Net tissue levels of RA remained lower in TNF+ARE than wild-type mice, indicating that epithelial up-regulation of RALDH3 could not maintain adequate concentrations of RA, probably because of loss of IEC mass. Tretinoin 21-23 tumor necrosis factor Mus musculus 42-45
22027263-8 2011 Net tissue levels of RA remained lower in TNF+ARE than wild-type mice, indicating that epithelial up-regulation of RALDH3 could not maintain adequate concentrations of RA, probably because of loss of IEC mass. Tretinoin 21-23 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 115-121
22027263-8 2011 Net tissue levels of RA remained lower in TNF+ARE than wild-type mice, indicating that epithelial up-regulation of RALDH3 could not maintain adequate concentrations of RA, probably because of loss of IEC mass. Tretinoin 115-117 tumor necrosis factor Mus musculus 42-45
22027263-9 2011 RA supplementation significantly attenuated disease by increasing the number and function of CD103+ DCs and Tregs and reducing Th17 cells. Tretinoin 0-2 integrin alpha E, epithelial-associated Mus musculus 93-98
22027263-11 2011 RA supplementation attenuates ileitis through its effects on CD103+ DCs, Tregs, and Th17 cells. Tretinoin 0-2 integrin alpha E, epithelial-associated Mus musculus 61-66
22019586-6 2011 Specifically, NOD-derived APCs showed increased production of pro-Th17 mediators and dysregulation of the retinoic acid (RA) signaling pathway compared with APCs from NOD.Idd3 and NOD.Il21r-deficient mice. Tretinoin 106-119 amyloid P component, serum Mus musculus 26-30
21384111-0 2011 Retinoic acid inhibits NFATc1 expression and osteoclast differentiation. Tretinoin 0-13 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1 Mus musculus 23-29
21384111-7 2011 These results suggest that RA blocks in vitro RANKL-mediated osteoclastogenesis by decreasing NFATc1 function. Tretinoin 27-29 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1 Mus musculus 94-100
22019586-6 2011 Specifically, NOD-derived APCs showed increased production of pro-Th17 mediators and dysregulation of the retinoic acid (RA) signaling pathway compared with APCs from NOD.Idd3 and NOD.Il21r-deficient mice. Tretinoin 121-123 amyloid P component, serum Mus musculus 26-30
21895658-3 2011 We found retinoic acid to potently inhibit cell migration in slice preparations of embryonic mouse forebrains, which was reversed by an antagonist of the dopamine-D(2) receptor, whose gene is transcriptionally regulated by retinoic acid. Tretinoin 9-22 dopamine receptor D2 Mus musculus 154-176
22055260-10 2011 Two muM retinoic acid reduced MMP-1 but did not significantly affect skin structure. Tretinoin 8-21 latexin Homo sapiens 4-7
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 50-63 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 34-39
21906690-9 2011 DISCUSSION: CYP26 enzymes are functionally expressed in microsomal fractions of insect cells and stably bind radiolabeled RA isomers with affinities respecting their substrate specificities. Tretinoin 122-124 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 12-17
21895658-3 2011 We found retinoic acid to potently inhibit cell migration in slice preparations of embryonic mouse forebrains, which was reversed by an antagonist of the dopamine-D(2) receptor, whose gene is transcriptionally regulated by retinoic acid. Tretinoin 223-236 dopamine receptor D2 Mus musculus 154-176
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 50-63 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 102-109
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 50-63 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 111-118
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 65-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 34-39
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 65-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 102-109
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 65-67 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 111-118
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 173-175 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 34-39
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 173-175 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 102-109
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 173-175 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 111-118
22173253-11 2011 The data suggests that genotypes of the ACE gene are linked to certain haplotypes, which could influence IgAN patients" response to ACEI/ATRA therapy. Tretinoin 137-141 angiotensin I converting enzyme Homo sapiens 40-43
21801775-0 2011 Retinoic acid-induced upregulation of the metalloendopeptidase nardilysin is accelerated by co-expression of the brain-specific protein p42(IP4) (centaurin alpha 1; ADAP1) in neuroblastoma cells. Tretinoin 0-13 nardilysin convertase Homo sapiens 63-73
21801775-8 2011 Furthermore, we report that differentiation of SH-SY5Y cells by stimulation with 10muM retinoic acid (RA) results in upregulation of NRD protein levels, with a 6-fold rise after 15 days. Tretinoin 87-100 nardilysin convertase Homo sapiens 133-136
21801775-8 2011 Furthermore, we report that differentiation of SH-SY5Y cells by stimulation with 10muM retinoic acid (RA) results in upregulation of NRD protein levels, with a 6-fold rise after 15 days. Tretinoin 102-104 nardilysin convertase Homo sapiens 133-136
21801775-9 2011 NRD is expressed in the neurites of RA-stimulated SH-SY5Y cells, and localized in vesicular structures. Tretinoin 36-38 nardilysin convertase Homo sapiens 0-3
21801775-11 2011 Interestingly, SH-SY5Y cells, which we stably transfected with GFP-tagged-p42(IP4) showed an enhanced NRD protein expression already at an earlier time point after RA stimulation. Tretinoin 164-166 nardilysin convertase Homo sapiens 102-105
21685470-0 2011 Prognostic value of FLT3 mutations in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline monochemotherapy. Tretinoin 104-117 fms related receptor tyrosine kinase 3 Homo sapiens 20-24
21907828-0 2011 All-trans retinoic acid can regulate the expressions of gelatinases and apolipoprotein E in glomerulosclerosis rats. Tretinoin 10-23 apolipoprotein E Rattus norvegicus 72-88
21757499-1 2011 Sex determination in fetal germ cells depends on a balance between exposure to retinoic acid (RA) and the degradation of RA achieved by the testis-specific expression of the catabolic cytochrome P450 enzyme, CYP26B1. Tretinoin 121-123 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 208-215
21838328-4 2011 Compounds with CYP26 inhibitory IC(50) values <=50 nM enhanced the biological activity of exogenous ATRA, as evidenced by a 3.7-5.8-fold increase in CYP26A1 mRNA in SH-SY5Y neuroblastoma cells as compared with ATRA alone. Tretinoin 103-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-20
21838328-4 2011 Compounds with CYP26 inhibitory IC(50) values <=50 nM enhanced the biological activity of exogenous ATRA, as evidenced by a 3.7-5.8-fold increase in CYP26A1 mRNA in SH-SY5Y neuroblastoma cells as compared with ATRA alone. Tretinoin 103-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 152-159
21838328-4 2011 Compounds with CYP26 inhibitory IC(50) values <=50 nM enhanced the biological activity of exogenous ATRA, as evidenced by a 3.7-5.8-fold increase in CYP26A1 mRNA in SH-SY5Y neuroblastoma cells as compared with ATRA alone. Tretinoin 213-217 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-20
21803036-0 2011 Restraint of Fgf8 signaling by retinoic acid signaling is required for proper heart and forelimb formation. Tretinoin 31-44 fibroblast growth factor 8a Danio rerio 13-17
21803036-8 2011 Together, these results are the first to directly support the hypothesis that RA signaling is required shortly after gastrulation in the forelimb field to temper Fgf8a signaling in the cardiac field, thus coordinating the development of the heart and forelimb. Tretinoin 78-80 fibroblast growth factor 8a Danio rerio 162-167
21685470-2 2011 DESIGN AND METHODS: We evaluated FLT3-internal tandem duplication and FLT3-D835 mutations in patients treated with all-trans retinoic acid and anthracycline-based chemotherapy enrolled in two subsequent trials of the Programa de Estudio y Tratamiento de las Hemopatias Malignas (PETHEMA) and Hemato-Oncologie voor Volwassenen Nederland (HOVON) groups between 1996 and 2005. Tretinoin 125-138 fms related receptor tyrosine kinase 3 Homo sapiens 33-37
21685470-9 2011 CONCLUSIONS: FLT3-internal tandem duplication mutations are associated with several hematologic features in acute promyelocytic leukemia, in particular with high white blood cell counts, but we were unable to demonstrate an independent prognostic value in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline-based regimens. Tretinoin 322-335 fms related receptor tyrosine kinase 3 Homo sapiens 13-17
21768647-6 2011 Moreover, together with Rara, Trim24 bound to the retinoic acid-responsive element of the Stat1 promoter and repressed its retinoic acid-induced transcription. Tretinoin 50-63 tripartite motif-containing 24 Mus musculus 30-36
21618588-6 2011 In spite of its lower potency, increased Hoxa1 gene expression was detected 30 min after retinol exposure and increased 40-fold by 2 h. Rdh10 and Aldh1a2/Raldh2, which together convert retinol to atRA in the embryo, were the predominant alcohol and aldehyde dehydrogenases expressed in P19 cells. Tretinoin 196-200 retinol dehydrogenase 10 (all-trans) Mus musculus 136-141
22145115-0 2011 Study on cytochrome p-450 dependent retinoic Acid metabolism and its inhibitors as potential agents for cancer therapy. Tretinoin 36-49 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 9-25
21672580-3 2011 This review focuses on the role of carotenoids like retinoic acid (RA), all trans retinoic acid (ATRA), lycopene and beta-carotene in prevention of AD symptoms primarily through inhibition of amyloid beta (Abeta) formation, deposition and fibril formation either by reducing the levels of p35 or inhibiting corresponding enzymes. Tretinoin 52-65 amyloid beta precursor protein Homo sapiens 192-204
21719597-7 2011 Knockdown of NPM1 also sensitized OCI-AML3 to all-trans retinoic acid (ATRA) and cytarabine. Tretinoin 46-69 RUNX family transcription factor 2 Homo sapiens 38-42
21719597-7 2011 Knockdown of NPM1 also sensitized OCI-AML3 to all-trans retinoic acid (ATRA) and cytarabine. Tretinoin 71-75 RUNX family transcription factor 2 Homo sapiens 38-42
21843507-0 2011 All-trans retinoic acid induces cellular senescence by up-regulating levels of p16 and p21 via promoter hypomethylation. Tretinoin 10-23 cyclin dependent kinase inhibitor 2A Homo sapiens 79-82
21843507-1 2011 All-trans retinoic acid (ATRA) induces cellular senescence via up-regulation of p16 and p21; however, the action mechanism of ATRA is unknown. Tretinoin 0-23 cyclin dependent kinase inhibitor 2A Homo sapiens 80-83
21843507-1 2011 All-trans retinoic acid (ATRA) induces cellular senescence via up-regulation of p16 and p21; however, the action mechanism of ATRA is unknown. Tretinoin 25-29 cyclin dependent kinase inhibitor 2A Homo sapiens 80-83
21865574-3 2011 ATRA (20 mg/kg PO) was administered for 15 days in groups C and E. We evaluated neuropathy and nerve regeneration-related morphologic changes in sciatic nerve, the concentration of nerve growth factor (NGF), and retinoic acid receptor (RAR)-alpha and RAR-beta expression. Tretinoin 0-4 nerve growth factor Homo sapiens 181-200
21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 cyclin dependent kinase inhibitor 2A Homo sapiens 60-63
21865574-7 2011 Treatment with ATRA reversed sensorial changes and nerve morphology; this was associated with increased NGF levels and RAR-beta expression. Tretinoin 15-19 nerve growth factor Homo sapiens 104-107
21865574-7 2011 Treatment with ATRA reversed sensorial changes and nerve morphology; this was associated with increased NGF levels and RAR-beta expression. Tretinoin 15-19 retinoic acid receptor beta Homo sapiens 119-127
21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 endothelin 1 Homo sapiens 157-163
21865574-10 2011 CONCLUSIONS: ATRA reduced chemotherapy-induced experimental neuropathy, increased NGF levels, and induced RAR-beta expression in nerve. Tretinoin 13-17 nerve growth factor Homo sapiens 82-85
21865574-10 2011 CONCLUSIONS: ATRA reduced chemotherapy-induced experimental neuropathy, increased NGF levels, and induced RAR-beta expression in nerve. Tretinoin 13-17 retinoic acid receptor beta Homo sapiens 106-114
21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 cyclin dependent kinase inhibitor 2A Homo sapiens 171-174
21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 tumor protein p53 Homo sapiens 188-191
21878116-7 2011 RESULTS: Human neuroblastoma SH-SY5Y cells with stably silenced TDP-43 showed a significant reduction of neurite outgrowth induced by retinoic acid and brain-derived neurotrophic factor. Tretinoin 134-147 TAR DNA binding protein Homo sapiens 64-70
21623752-0 2011 High-concentration all-trans retinoic acid induces dermal inflammation and reduces the accumulation of type I procollagen in human skin in vivo. Tretinoin 19-42 collagen type I alpha 2 chain Homo sapiens 103-121
21623752-5 2011 RESULTS: Topical RA regardless of concentration increased type I procollagen expression in human skin in vivo after 2 weeks. Tretinoin 17-19 collagen type I alpha 2 chain Homo sapiens 58-76
21623752-6 2011 However, only 0 01% RA continuously increased type I procollagen expression up to 8 weeks. Tretinoin 20-22 collagen type I alpha 2 chain Homo sapiens 46-64
21336564-5 2011 These results demonstrate that, although the combination of PI3K inhibitor and rapamycin is more effective in inhibiting proliferation of AML, the concomitant inhibition of PI3K and mTOR by LY 294002 and rapamycin has more inhibitory effects on ATRA-mediated differentiation than the presence of PI3K-inhibitor alone, and diminishes positive effects of rapamycin on leukemia cell differentiation. Tretinoin 245-249 mechanistic target of rapamycin kinase Homo sapiens 182-186
22040429-3 2011 We have explored the anticancer effect of ATRA in ESCC, and in this study, the effects of ATRA on levels and patterns of expression of the vascular endothelial growth factor (VEGF) signal transduction pathway in transplantable tumor growth of the human ESCC cell line, EC9706, in nude mice. Tretinoin 90-94 vascular endothelial growth factor A Homo sapiens 139-173
22040429-3 2011 We have explored the anticancer effect of ATRA in ESCC, and in this study, the effects of ATRA on levels and patterns of expression of the vascular endothelial growth factor (VEGF) signal transduction pathway in transplantable tumor growth of the human ESCC cell line, EC9706, in nude mice. Tretinoin 90-94 vascular endothelial growth factor A Homo sapiens 175-179
21270509-9 2011 CONCLUSIONS: The findings of differential expression of CRABP1 in prolactinomas and of RERG in NFPA compared to normal pituitary suggests that retinoic acid and estrogen receptor, respectively, could be involved in the tumorigenesis of these adenomas subtypes. Tretinoin 143-156 RAS like estrogen regulated growth inhibitor Homo sapiens 87-91
21816185-5 2011 Suppression of retinoic acid-inducible gene-I (RIG-I) expression using siRNA significantly reduced IFN-lambda1 production in RSV-infected hTERT-NECs, while suppression of melanoma differentiation-associated gene 5 (MDA5) expression did not. Tretinoin 15-28 interferon alpha 1 Homo sapiens 99-102
21878116-8 2011 Re-transfection with TDP-43 as well as HDAC6 rescued retinoic acid-induced neurite outgrowth. Tretinoin 53-66 TAR DNA binding protein Homo sapiens 21-27
21878116-8 2011 Re-transfection with TDP-43 as well as HDAC6 rescued retinoic acid-induced neurite outgrowth. Tretinoin 53-66 histone deacetylase 6 Homo sapiens 39-44
21529158-5 2011 The CYP26A1 gene is regulated by multiple RA response elements. Tretinoin 42-44 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-11
21859847-5 2011 Conditional ablation of RA signaling in T cells significantly interferes with CD4(+) T cell effector function, migration, and polarity. Tretinoin 24-26 CD4 molecule Homo sapiens 78-81
21859847-6 2011 These findings provide a new perspective of the role of RA as a mediator directly controlling CD4(+) T cell differentiation and immunity. Tretinoin 56-58 CD4 molecule Homo sapiens 94-97
21529158-7 2011 Enzyme kinetic studies have demonstrated that several CYP proteins are capable of metabolizing at-RA; however, it is likely that CYP26A1 plays a major role in RA clearance. Tretinoin 98-100 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 129-136
21808038-1 2011 NADPH-cytochrome P450 oxidoreductase (CYPOR) is essential for electron donation to microsomal cytochrome P450-mediated monooxygenation in such diverse physiological processes as drug metabolism (approximately 85-90% of therapeutic drugs), steroid biosynthesis, and bioactive metabolite production (vitamin D and retinoic acid metabolites). Tretinoin 312-325 cytochrome p450 oxidoreductase Homo sapiens 0-36
21663736-0 2011 WT1 regulates epicardial epithelial to mesenchymal transition through beta-catenin and retinoic acid signaling pathways. Tretinoin 87-100 WT1 transcription factor Homo sapiens 0-3
21663736-12 2011 Wnt5a, a prototypic non-canonical Wnt with enriched epicardial expression, and Raldh2, a key regulator of retinoic acid signaling confined to the epicardium, were also markedly downregulated in Wt1(KO) epicardium. Tretinoin 106-119 WT1 transcription factor Homo sapiens 194-201
21663736-15 2011 Collectively, our study shows that Wt1 regulates epicardial EMT and heart development through canonical Wnt, non-canonical Wnt, and retinoic acid signaling pathways. Tretinoin 132-145 WT1 transcription factor Homo sapiens 35-38
21808038-1 2011 NADPH-cytochrome P450 oxidoreductase (CYPOR) is essential for electron donation to microsomal cytochrome P450-mediated monooxygenation in such diverse physiological processes as drug metabolism (approximately 85-90% of therapeutic drugs), steroid biosynthesis, and bioactive metabolite production (vitamin D and retinoic acid metabolites). Tretinoin 312-325 cytochrome p450 oxidoreductase Homo sapiens 38-43
21295138-5 2011 The biological and physiological implications of PXR activation are broad, ranging from drug metabolism and drug-drug interactions to the homeostasis of numerous endobiotics, such as glucose, lipids, steroids, bile acids, bilirubin, retinoic acid, and bone minerals. Tretinoin 233-246 nuclear receptor subfamily 1 group I member 2 Homo sapiens 49-52
21807937-1 2011 Cyp26b1, a retinoic acid (RA)-metabolising enzyme, is expressed in the developing limb bud, and Cyp26b1(-/-) mice present with severe limb defects. Tretinoin 11-24 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
21807937-1 2011 Cyp26b1, a retinoic acid (RA)-metabolising enzyme, is expressed in the developing limb bud, and Cyp26b1(-/-) mice present with severe limb defects. Tretinoin 26-28 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
21807937-5 2011 We systematically examined the role of endogenous RA signalling in chondrogenesis and found that Cyp26b1(-/-) cells and limb mesenchymal cells treated with a CYP inhibitor, are maintained in a pre-chondrogenic state, exhibit reduced chondroblast differentiation and have modestly accelerated chondrocyte hypertrophy. Tretinoin 50-52 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 97-104
21685476-0 2011 Retinoic acid enhances TRAIL-induced apoptosis in cancer cells by upregulating TRAIL receptor 1 expression. Tretinoin 0-13 TNF superfamily member 10 Homo sapiens 23-28
21685476-8 2011 Consistent with this observation, RAR binding to DR-11, but not to Pal-17, was detected by chromatin immunoprecipitation assay in ATRA-treated cells, arguing that DR-11 was responsible for ATRA-mediated activation of the TRAIL-R1 gene. Tretinoin 130-134 WD repeat domain 11 Homo sapiens 49-54
21685476-8 2011 Consistent with this observation, RAR binding to DR-11, but not to Pal-17, was detected by chromatin immunoprecipitation assay in ATRA-treated cells, arguing that DR-11 was responsible for ATRA-mediated activation of the TRAIL-R1 gene. Tretinoin 130-134 WD repeat domain 11 Homo sapiens 163-168
21685476-8 2011 Consistent with this observation, RAR binding to DR-11, but not to Pal-17, was detected by chromatin immunoprecipitation assay in ATRA-treated cells, arguing that DR-11 was responsible for ATRA-mediated activation of the TRAIL-R1 gene. Tretinoin 189-193 WD repeat domain 11 Homo sapiens 49-54
21685476-8 2011 Consistent with this observation, RAR binding to DR-11, but not to Pal-17, was detected by chromatin immunoprecipitation assay in ATRA-treated cells, arguing that DR-11 was responsible for ATRA-mediated activation of the TRAIL-R1 gene. Tretinoin 189-193 WD repeat domain 11 Homo sapiens 163-168
21685476-9 2011 ATRA augmented TRAIL-induced apoptosis of cancer cells, and this activity was attenuated by a blockade to upregulation of TRAIL-R1 expression. Tretinoin 0-4 TNF superfamily member 10 Homo sapiens 15-20
21851243-4 2011 2-E2 antigen expression drastically decreased in retinoic acid-induced differentiated hESCs. Tretinoin 49-62 CD99 molecule (Xg blood group) Homo sapiens 2-12
21659316-9 2011 We found increased levels of CYP26B1, responsible for RA metabolism. Tretinoin 54-56 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 29-36
21554977-6 2011 In human proximal tubular HK-2 cells we have found that: (i) ATRA treatment induces HIF-1alpha under normoxic conditions and also synergizes with hypoxia leading to the over-expression of HIF-1alpha and vascular endothelial growth factor-A, a HIF-1alpha-regulated renal protector. Tretinoin 61-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 84-94
21554977-6 2011 In human proximal tubular HK-2 cells we have found that: (i) ATRA treatment induces HIF-1alpha under normoxic conditions and also synergizes with hypoxia leading to the over-expression of HIF-1alpha and vascular endothelial growth factor-A, a HIF-1alpha-regulated renal protector. Tretinoin 61-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 188-198
21554977-6 2011 In human proximal tubular HK-2 cells we have found that: (i) ATRA treatment induces HIF-1alpha under normoxic conditions and also synergizes with hypoxia leading to the over-expression of HIF-1alpha and vascular endothelial growth factor-A, a HIF-1alpha-regulated renal protector. Tretinoin 61-65 vascular endothelial growth factor A Homo sapiens 203-239
21554977-6 2011 In human proximal tubular HK-2 cells we have found that: (i) ATRA treatment induces HIF-1alpha under normoxic conditions and also synergizes with hypoxia leading to the over-expression of HIF-1alpha and vascular endothelial growth factor-A, a HIF-1alpha-regulated renal protector. Tretinoin 61-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 188-198
21554977-7 2011 ATRA-induced HIF-1alpha expression involved stabilization of HIF-1alpha mRNA but not of HIF-1alpha protein. Tretinoin 0-4 hypoxia inducible factor 1 subunit alpha Homo sapiens 13-23
21554977-7 2011 ATRA-induced HIF-1alpha expression involved stabilization of HIF-1alpha mRNA but not of HIF-1alpha protein. Tretinoin 0-4 hypoxia inducible factor 1 subunit alpha Homo sapiens 61-71
21554977-7 2011 ATRA-induced HIF-1alpha expression involved stabilization of HIF-1alpha mRNA but not of HIF-1alpha protein. Tretinoin 0-4 hypoxia inducible factor 1 subunit alpha Homo sapiens 61-71
21554977-9 2011 Transfection with HIF-1alpha siRNA abolished the induction by ATRA of the expression of both RARbeta mRNA and protein while treatment with HIF-1alpha inhibitor YC-1 results in the abolishment of ATRA-induced activity of a retinoic acid-response element (RARE) construct from the RARbeta promoter. Tretinoin 62-66 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-28
21554977-9 2011 Transfection with HIF-1alpha siRNA abolished the induction by ATRA of the expression of both RARbeta mRNA and protein while treatment with HIF-1alpha inhibitor YC-1 results in the abolishment of ATRA-induced activity of a retinoic acid-response element (RARE) construct from the RARbeta promoter. Tretinoin 62-66 retinoic acid receptor beta Homo sapiens 93-100
21554977-9 2011 Transfection with HIF-1alpha siRNA abolished the induction by ATRA of the expression of both RARbeta mRNA and protein while treatment with HIF-1alpha inhibitor YC-1 results in the abolishment of ATRA-induced activity of a retinoic acid-response element (RARE) construct from the RARbeta promoter. Tretinoin 62-66 retinoic acid receptor beta Homo sapiens 279-286
21554977-9 2011 Transfection with HIF-1alpha siRNA abolished the induction by ATRA of the expression of both RARbeta mRNA and protein while treatment with HIF-1alpha inhibitor YC-1 results in the abolishment of ATRA-induced activity of a retinoic acid-response element (RARE) construct from the RARbeta promoter. Tretinoin 222-235 hypoxia inducible factor 1 subunit alpha Homo sapiens 18-28
21554977-9 2011 Transfection with HIF-1alpha siRNA abolished the induction by ATRA of the expression of both RARbeta mRNA and protein while treatment with HIF-1alpha inhibitor YC-1 results in the abolishment of ATRA-induced activity of a retinoic acid-response element (RARE) construct from the RARbeta promoter. Tretinoin 222-235 retinoic acid receptor beta Homo sapiens 93-100
21554977-9 2011 Transfection with HIF-1alpha siRNA abolished the induction by ATRA of the expression of both RARbeta mRNA and protein while treatment with HIF-1alpha inhibitor YC-1 results in the abolishment of ATRA-induced activity of a retinoic acid-response element (RARE) construct from the RARbeta promoter. Tretinoin 222-235 hypoxia inducible factor 1 subunit alpha Homo sapiens 139-149
21554977-11 2011 In contrast to ATRA-induced RARbeta up-regulation, induction of RARbeta expression by ATRA did not involve transcriptional up-regulation as hypoxia did not increase the expression of RARbeta mRNA or the activity of the RARE construct. Tretinoin 15-19 retinoic acid receptor beta Homo sapiens 28-35
21722948-4 2011 TDG is necessary for recruiting p300 to retinoic acid (RA)-regulated promoters, protection of CpG islands from hypermethylation, and active demethylation of tissue-specific developmentally and hormonally regulated promoters and enhancers. Tretinoin 40-53 thymine DNA glycosylase Homo sapiens 0-3
22093791-0 2011 [Effects of simvastatin plus all-trans retinoic acid on WT1/hDMP1 gene expression profiles of human promyelocytic leukemia cell line NB4]. Tretinoin 39-52 WT1 transcription factor Homo sapiens 56-59
22093791-1 2011 OBJECTIVE: To investigate the effects of simvastatin (SV) plus all-trans retinoic acid (ATRA) on the proliferation, differentiation, apoptosis and WT1/hDMP1 gene expression profiles of human promyelocytic leukemia cell line NB4. Tretinoin 88-92 WT1 transcription factor Homo sapiens 147-150
21184786-10 2011 At the molecular level, SRC-3 interacts with retinoic receptor alpha (RARalpha) to activate COUP-TFII expression under all-trans retinoic acid (ARTA) treatment. Tretinoin 129-142 nuclear receptor subfamily 2 group F member 2 Homo sapiens 92-101
21184786-10 2011 At the molecular level, SRC-3 interacts with retinoic receptor alpha (RARalpha) to activate COUP-TFII expression under all-trans retinoic acid (ARTA) treatment. Tretinoin 144-148 nuclear receptor subfamily 2 group F member 2 Homo sapiens 92-101
21521770-2 2011 The hepatic clearance of atRA is mediated primarily by CYP26A1, but design of CYP26A1 inhibitors is hindered by lack of information on CYP26A1 structure and structure-activity relationships of its ligands. Tretinoin 25-29 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 55-62
21521770-3 2011 The aim of this study was to identify the primary metabolites of atRA formed by CYP26A1 and to characterize the ligand selectivity and ligand interactions of CYP26A1. Tretinoin 65-69 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 80-87
21521770-3 2011 The aim of this study was to identify the primary metabolites of atRA formed by CYP26A1 and to characterize the ligand selectivity and ligand interactions of CYP26A1. Tretinoin 65-69 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 158-165
21684256-6 2011 In Stage 2, the cells were treated with all-trans retinoic acid which promoted the transition to cells that expressed gut tube endoderm mRNA marker HNF1b. Tretinoin 50-63 HNF1 homeobox B Homo sapiens 148-153
21722948-4 2011 TDG is necessary for recruiting p300 to retinoic acid (RA)-regulated promoters, protection of CpG islands from hypermethylation, and active demethylation of tissue-specific developmentally and hormonally regulated promoters and enhancers. Tretinoin 55-57 thymine DNA glycosylase Homo sapiens 0-3
21539831-0 2011 Hmx4 regulates Sonic hedgehog signaling through control of retinoic acid synthesis during forebrain patterning. Tretinoin 59-72 H6 family homeobox 4 Danio rerio 0-4
21705183-1 2011 In the present report, we investigated the action of retinoic acid (RA) on the transactivation of the epidermal growth factor receptor (EGFR) gene promoter. Tretinoin 53-66 epidermal growth factor receptor Homo sapiens 102-134
21705183-1 2011 In the present report, we investigated the action of retinoic acid (RA) on the transactivation of the epidermal growth factor receptor (EGFR) gene promoter. Tretinoin 53-66 epidermal growth factor receptor Homo sapiens 136-140
21705183-1 2011 In the present report, we investigated the action of retinoic acid (RA) on the transactivation of the epidermal growth factor receptor (EGFR) gene promoter. Tretinoin 68-70 epidermal growth factor receptor Homo sapiens 102-134
21705183-1 2011 In the present report, we investigated the action of retinoic acid (RA) on the transactivation of the epidermal growth factor receptor (EGFR) gene promoter. Tretinoin 68-70 epidermal growth factor receptor Homo sapiens 136-140
21705183-7 2011 Our results suggest that the interference with the activity of Sp1 on the EGFR promoter could be related to the observed RA-mediated growth suppression of breast cancer cells. Tretinoin 121-123 epidermal growth factor receptor Homo sapiens 74-78
21344672-0 2011 Effects of retinoic acid and butyric acid on the expression of prestin and Gata-3 in organotypic cultures of the organ of corti of newborn rats. Tretinoin 11-24 GATA binding protein 3 Rattus norvegicus 75-81
21344672-3 2011 We studied the effects of the application of retinoic acid, a ligand of a nuclear receptor, and of butyric acid, an inhibitor of histone deacetylase activity, on the expression of mRNA of prestin and Gata-3 in the organotypic culture of the organ of Corti of newborn rats using RT-PCR. Tretinoin 45-58 GATA binding protein 3 Rattus norvegicus 200-206
21594951-5 2011 Here we show that in chick embryo brain development: (1) E-CSF helps to control RA synthesis in the IsO by means of the RBP and all-trans-retinol it contains; (2) E-CSF has retinoic acid activity, which suggests it may act as a diffusion pathway for RA; and (3) the influence of E-CSF on embryonic brain neurogenesis is to a large extent due to its involvement in RA synthesis. Tretinoin 80-82 riboflavin binding protein Gallus gallus 120-123
21539831-2 2011 We demonstrate that zebrafish Hmx4 regulates the signaling of two morphogens critical for neural development, retinoic acid (RA) and Sonic hedgehog (Shh). Tretinoin 110-123 H6 family homeobox 4 Danio rerio 30-34
21539831-2 2011 We demonstrate that zebrafish Hmx4 regulates the signaling of two morphogens critical for neural development, retinoic acid (RA) and Sonic hedgehog (Shh). Tretinoin 125-127 H6 family homeobox 4 Danio rerio 30-34
21539831-7 2011 Loss of RA is the primary defect in Hmx4-depleted embryos, as RA treatment rescues a number of the neural patterning defects. Tretinoin 8-10 H6 family homeobox 4 Danio rerio 36-40
21539831-7 2011 Loss of RA is the primary defect in Hmx4-depleted embryos, as RA treatment rescues a number of the neural patterning defects. Tretinoin 62-64 H6 family homeobox 4 Danio rerio 36-40
21539831-9 2011 We propose that Hmx4 is a critical regulator of retinoic acid synthesis in a developing embryo, and that this regulation is essential for controlling Shh signaling and forebrain development. Tretinoin 48-61 H6 family homeobox 4 Danio rerio 16-20
21289617-4 2011 Consistent with this, SI-LP CD103(+) DCs constitutively received RA signals in vivo at significantly higher levels than did colonic CD103(+) DCs. Tretinoin 65-67 integrin alpha E, epithelial-associated Mus musculus 28-33
21455565-0 2011 Silencing of the icb-1 gene inhibits the induction of differentiation-associated genes by vitamin D3 and all-trans retinoic acid in gynecological cancer cells. Tretinoin 115-128 thymocyte selection associated family member 2 Homo sapiens 17-22
21455565-4 2011 Induction of E-cadherin expression by all-trans retinoic acid (ATRA) was also blocked in both cell lines expressing icb-1 siRNA. Tretinoin 38-61 cadherin 1 Homo sapiens 13-23
21297158-3 2011 The cascade starts with the RA-induced phosphorylation of a serine residue located in the ligand-binding domain, S(LBD), allowing the recruitment of the cdk7/cyclin H/MAT1 subcomplex of TFIIH through the docking of cyclin H. Tretinoin 28-30 cyclin-dependent kinase 7 Danio rerio 153-157
21672091-0 2011 Transcriptional regulation of the CADM1 gene by retinoic acid during the neural differentiation of murine embryonal carcinoma P19 cells. Tretinoin 48-61 cell adhesion molecule 1 Mus musculus 34-39
21672091-2 2011 The expression of the Cadm1 gene is induced during the neural differentiation of murine embryonal carcinoma P19 cells by treatment with retinoic acid (RA). Tretinoin 136-149 cell adhesion molecule 1 Mus musculus 22-27
21672091-2 2011 The expression of the Cadm1 gene is induced during the neural differentiation of murine embryonal carcinoma P19 cells by treatment with retinoic acid (RA). Tretinoin 151-153 cell adhesion molecule 1 Mus musculus 22-27
21672091-3 2011 Here, we show that the suppression of CADM1 expression using RNAi interfered with P19 cell aggregation and reduced cell populations expressing MAP2 after RA treatment. Tretinoin 154-156 cell adhesion molecule 1 Mus musculus 38-43
21672091-3 2011 Here, we show that the suppression of CADM1 expression using RNAi interfered with P19 cell aggregation and reduced cell populations expressing MAP2 after RA treatment. Tretinoin 154-156 microtubule-associated protein 2 Mus musculus 143-147
21672091-5 2011 A luciferase assay of a series of deletion mutants of the CADM1 promoter localized an RA-responsive cis-acting element to an approximately 90-bp fragment upstream of the translational start site. Tretinoin 86-88 cell adhesion molecule 1 Mus musculus 58-63
21672091-9 2011 These results suggest that Sp1 plays a critical role in RA-induced CADM1 expression through possible interaction with RARalpha in the neural differentiation of P19. Tretinoin 56-58 cell adhesion molecule 1 Mus musculus 67-72
21455565-4 2011 Induction of E-cadherin expression by all-trans retinoic acid (ATRA) was also blocked in both cell lines expressing icb-1 siRNA. Tretinoin 38-61 thymocyte selection associated family member 2 Homo sapiens 116-121
21455565-4 2011 Induction of E-cadherin expression by all-trans retinoic acid (ATRA) was also blocked in both cell lines expressing icb-1 siRNA. Tretinoin 63-67 cadherin 1 Homo sapiens 13-23
21455565-4 2011 Induction of E-cadherin expression by all-trans retinoic acid (ATRA) was also blocked in both cell lines expressing icb-1 siRNA. Tretinoin 63-67 thymocyte selection associated family member 2 Homo sapiens 116-121
21455565-6 2011 In MCF-7 cells, silencing of the icb-1 gene inhibited the ATRA- and the vitamin D3-induced up-regulation of lactoferrin and estrogen receptor beta expression. Tretinoin 58-62 thymocyte selection associated family member 2 Homo sapiens 33-38
21455565-7 2011 The data of our knockdown study suggest that icb-1 may act as a mediator of differentiation signals in breast cancer cells induced by ATRA or vitamin D3. Tretinoin 134-138 thymocyte selection associated family member 2 Homo sapiens 45-50
21321999-4 2011 Results from 2-DE PAGE and MS showed that hnRNP A2/B1 is involved with components of nuclear matrix proteins of SK-N-SH cells, and that its expression level is down-regulated after retinoic acid (RA) treatment. Tretinoin 181-194 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 42-53
21321999-4 2011 Results from 2-DE PAGE and MS showed that hnRNP A2/B1 is involved with components of nuclear matrix proteins of SK-N-SH cells, and that its expression level is down-regulated after retinoic acid (RA) treatment. Tretinoin 196-198 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 42-53
21321999-6 2011 Immunofluorescence microscopy observation showed that hnRNP A2/B1 localized in nuclear matrix of SK-N-SH cells and its distribution regions were altered after RA treatment. Tretinoin 159-161 heterogeneous nuclear ribonucleoprotein A2/B1 Homo sapiens 54-65
21708033-0 2011 Defective response of CD4(+) T cells to retinoic acid and TGFbeta in systemic lupus erythematosus. Tretinoin 40-53 CD4 molecule Homo sapiens 22-25
21471848-6 2011 RESULTS: Enhanced expression of NIS mRNA and protein was observed in FTC-133 cells treated with ATRA and tributyrin, which further resulted in significant higher levels of radioiodine uptake than that of untreated control cells and cells treated with ATRA alone. Tretinoin 251-255 solute carrier family 5 member 5 Homo sapiens 32-35
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 14-27 retinoic acid receptor beta Homo sapiens 71-79
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 71-79
21690307-6 2011 Furthermore, we confirm in vivo that RA treatment after a dorsal column overhemisection injury inhibited Lingo-1 expression, specifically through RAR-beta. Tretinoin 37-39 retinoic acid receptor beta Homo sapiens 146-154
21471848-2 2011 We investigated the effects of all-trans retinoic acid (ATRA) combined with histone deacetylase inhibitor, tributyrin on sodium-iodide symporter (NIS) expression, radioiodine uptake, and inhibition of cell proliferation in a poorly differentiated follicular thyroid carcinoma (FTC-133) in vitro. Tretinoin 31-54 solute carrier family 5 member 5 Homo sapiens 146-149
21471848-3 2011 METHODS: FTC-133 cells were cultured in the presence of ATRA and tributyrin either as a single agent or in combinations for 48 h. The expression of NIS mRNA and protein was, respectively, detected by quantitative real-time polymerase chain reaction and western blot. Tretinoin 56-60 solute carrier family 5 member 5 Homo sapiens 148-151
21471848-6 2011 RESULTS: Enhanced expression of NIS mRNA and protein was observed in FTC-133 cells treated with ATRA and tributyrin, which further resulted in significant higher levels of radioiodine uptake than that of untreated control cells and cells treated with ATRA alone. Tretinoin 96-100 solute carrier family 5 member 5 Homo sapiens 32-35
21708033-1 2011 INTRODUCTION: CD25(+) FOXP3(+) CD4(+) regulatory T cells (Tregs) are induced by transforming growth factor beta (TGFbeta) and further expanded by retinoic acid (RA). Tretinoin 146-159 CD4 molecule Homo sapiens 31-34
21708033-1 2011 INTRODUCTION: CD25(+) FOXP3(+) CD4(+) regulatory T cells (Tregs) are induced by transforming growth factor beta (TGFbeta) and further expanded by retinoic acid (RA). Tretinoin 161-163 CD4 molecule Homo sapiens 31-34
21555530-5 2011 NO antagonized IL-6 to block TGF-beta-directed Th17 differentiation, and together with IL-6, NO suppressed Treg development induced by TGF-beta and retinoic acid. Tretinoin 148-161 interleukin 6 Homo sapiens 87-91
21527557-6 2011 In agreement with neuroblastomas becoming more differentiated after treatment, we show that retinoic acid-induced differentiation of human neuroblastoma cells in vitro also leads to a strong decrease in MMSET levels. Tretinoin 92-105 nuclear receptor binding SET domain protein 2 Homo sapiens 203-208
21385580-0 2011 All-trans retinoic acid regulates the expression of apolipoprotein E in rats with glomerulosclerosis induced by Adriamycin. Tretinoin 10-23 apolipoprotein E Rattus norvegicus 52-68
21605549-0 2011 Retinoic acid inhibits BMP4-induced C3H10T1/2 stem cell commitment to adipocyte via downregulating Smad/p38MAPK signaling. Tretinoin 0-13 bone morphogenetic protein 4 Mus musculus 23-27
21605549-3 2011 We examined potential role of retinoic acid (RA) in inhibiting the BMP4 induction of MSC commitment toward adipocyte. Tretinoin 30-43 bone morphogenetic protein 4 Mus musculus 67-71
21605549-3 2011 We examined potential role of retinoic acid (RA) in inhibiting the BMP4 induction of MSC commitment toward adipocyte. Tretinoin 45-47 bone morphogenetic protein 4 Mus musculus 67-71
21605549-5 2011 This could be inhibited by RA exposure during the BMP4 treatment stage (commitment stage before adipogenic hormonal inducers were given), as was observed by reductions in key adipogenic genes/transcription factors (C/EBPalpha, PPARgamma, aP2), lipogenic genes (LPL, FAS, GLUT4), and lipid accumulation. Tretinoin 27-29 bone morphogenetic protein 4 Mus musculus 50-54
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 mitogen-activated protein kinase 8 Homo sapiens 122-149
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 mitogen-activated protein kinase 8 Homo sapiens 151-154
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 mitogen-activated protein kinase 1 Homo sapiens 160-163
21605549-5 2011 This could be inhibited by RA exposure during the BMP4 treatment stage (commitment stage before adipogenic hormonal inducers were given), as was observed by reductions in key adipogenic genes/transcription factors (C/EBPalpha, PPARgamma, aP2), lipogenic genes (LPL, FAS, GLUT4), and lipid accumulation. Tretinoin 27-29 solute carrier family 2 (facilitated glucose transporter), member 4 Mus musculus 271-276
21605549-8 2011 These data suggest that RA has inhibitory effects on the BMP4 induction of C3H10T1/2 adipocytic commitment via downregulating Smad/p38MAPK signaling. Tretinoin 24-26 bone morphogenetic protein 4 Mus musculus 57-61
21555266-0 2011 Inhibition of Smad signaling is implicated in cleft palate induced by all-trans retinoic acid. Tretinoin 80-93 SMAD family member 7 Homo sapiens 14-18
21555266-2 2011 Compared with control group, the atRA-treated group (1 muM and 5 muM) had more medial edge epithelium (ME) remaining within the midline epithelial seam (MES). Tretinoin 33-37 latexin Homo sapiens 55-58
21555266-2 2011 Compared with control group, the atRA-treated group (1 muM and 5 muM) had more medial edge epithelium (ME) remaining within the midline epithelial seam (MES). Tretinoin 33-37 latexin Homo sapiens 65-68
21555266-4 2011 Cell death detection by TUNEL and laminin immunohistochemistry demonstrated that atRA (5 muM) induced apoptosis in mesenchyme and inhibited degradation of basal lamina within MES. Tretinoin 81-85 latexin Homo sapiens 89-92
21555266-8 2011 In contrast, atRA treatment abrogated phosphorylation of Smad2 and Smad3 and inducible expression of Smad7 in ME. Tretinoin 13-17 SMAD family member 7 Homo sapiens 101-106
21555266-9 2011 From these data, it is assumed that inhibition of Smad pathway by atRA in ME may play a critical role in abrogation of the ME cell apoptosis and degradation of the basal laminin, which might contribute to failure of palatal fusion. Tretinoin 66-70 SMAD family member 7 Homo sapiens 50-54
21471300-2 2011 We show here that CD1d, a major histocompatibility complex class I-like molecule that presents lipid antigens, is expressed in the mouse spleen B cells and is increased by RA. Tretinoin 172-174 CD1d1 antigen Mus musculus 18-22
21471300-3 2011 Thus, we hypothesized that RA and the CD1d ligand, alpha-galactosylceramide (alphaGalCer), could interact to promote the differentiation, maturation, and antibody response of antigen-activated B cells. Tretinoin 27-29 CD1d1 antigen Mus musculus 38-42
21471300-7 2011 In vivo, wild-type mice treated with RA and/or alphaGalCer during primary immunization with tetanus toxoid produced a higher serum anti-tetanus IgG response and had more bone marrow anti-tetanus antibody-secreting cells as determined by enzyme-linked immunospot assay (P < 0.05) in the secondary response, a finding indicative of heightened long-term memory; however, the increased antibody secretion after alphaGalCer treatment was abolished in CD1d-null mice. Tretinoin 37-39 CD1d1 antigen Mus musculus 449-453
21385580-2 2011 We conducted this investigation to explore whether all-trans retinoic acid (ATRA) could regulate the apoE expression in the pathological process of GS. Tretinoin 51-74 apolipoprotein E Rattus norvegicus 101-105
21385580-2 2011 We conducted this investigation to explore whether all-trans retinoic acid (ATRA) could regulate the apoE expression in the pathological process of GS. Tretinoin 76-80 apolipoprotein E Rattus norvegicus 101-105
21385580-11 2011 In conclusion, ATRA can regulate the expression of apoE, reduce the accumulation of extracellular matrix (ECM) and step down the progression of GS. Tretinoin 15-19 apolipoprotein E Rattus norvegicus 51-55
20685100-4 2011 Retinol (ROH) and all-trans retinoic acid (ATRA) significantly inhibited aromatase activity in a concentration-dependent manner in microsomes isolated from JEG-3 human placental carcinoma cells, whereas 9-cis and 13-cis retinoic acid had significant inhibitory activity only at the highest concentrations tested. Tretinoin 18-41 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 73-82
21325480-0 2011 Hepatitis B virus X protein overcomes all-trans retinoic acid-induced cellular senescence by downregulating levels of p16 and p21 via DNA methylation. Tretinoin 48-61 cyclin dependent kinase inhibitor 2A Homo sapiens 118-121
21325480-4 2011 In addition, HBx suppressed ATRA-mediated induction of p16 and p21 in HepG2 cells via promoter hypermethylation, resulting in inactivation of retinoblastoma protein. Tretinoin 28-32 cyclin dependent kinase inhibitor 2A Homo sapiens 55-58
20685100-4 2011 Retinol (ROH) and all-trans retinoic acid (ATRA) significantly inhibited aromatase activity in a concentration-dependent manner in microsomes isolated from JEG-3 human placental carcinoma cells, whereas 9-cis and 13-cis retinoic acid had significant inhibitory activity only at the highest concentrations tested. Tretinoin 43-47 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 73-82
21431284-7 2011 Finally, AML cells collected during in vivo ATRA therapy showed increased calreticulin exposure during spontaneous in vitro apoptosis, suggesting that in vivo pharmacotherapy can modulate the apoptotic phenotype. Tretinoin 44-48 calreticulin Homo sapiens 74-86
21531907-3 2011 Germ line inactivation of TRIM24 in mice deregulates RA-signaling in hepatocytes leading to the development of hepatocellular carcinoma (HCC). Tretinoin 53-55 tripartite motif-containing 24 Mus musculus 26-32
21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 49-62 transforming growth factor beta 1 Homo sapiens 103-111
21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 49-62 transforming growth factor beta 1 Homo sapiens 159-167
21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 64-66 transforming growth factor beta 1 Homo sapiens 103-111
21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 64-66 transforming growth factor beta 1 Homo sapiens 159-167
21514413-6 2011 Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. Tretinoin 21-23 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 214-221
21573179-1 2011 BACKGROUND: In the intestine, the integrin CD103 is expressed on a subset of T regulatory (T(reg)) cells and a population of dendritic cells (DCs) that produce retinoic acid and promote immune homeostasis. Tretinoin 160-173 integrin alpha E, epithelial-associated Mus musculus 43-48
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 262-275 retinol binding protein 2 Homo sapiens 96-102
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 277-279 retinol binding protein 2 Homo sapiens 59-94
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 262-275 retinol binding protein 2 Homo sapiens 59-94
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 277-279 retinol binding protein 2 Homo sapiens 96-102
21471156-0 2011 SHH propagates distal limb bud development by enhancing CYP26B1-mediated retinoic acid clearance via AER-FGF signalling. Tretinoin 73-86 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 56-63
21360789-3 2011 Using embryos carrying the RARE-lacZ RA-reporter transgene, we show that endogenous RA activity in Rdh10(trex/trex) mutants is detected in neuroectoderm but not limbs during initiation and patterning. Tretinoin 27-29 retinol dehydrogenase 10 (all-trans) Mus musculus 99-104
21360789-4 2011 Treatment of Rdh10 mutants with 25 nM RA restores RARE-lacZ activity to limb mesoderm, validating RARE-lacZ and verifying that RA is absent in mutant limbs. Tretinoin 38-40 retinol dehydrogenase 10 (all-trans) Mus musculus 13-18
21360789-4 2011 Treatment of Rdh10 mutants with 25 nM RA restores RARE-lacZ activity to limb mesoderm, validating RARE-lacZ and verifying that RA is absent in mutant limbs. Tretinoin 50-52 retinol dehydrogenase 10 (all-trans) Mus musculus 13-18
21360789-6 2011 Later in development, Rdh10 mutants lack interdigital RA activity and accordingly fail to exhibit normal loss of interdigital mesenchyme. Tretinoin 54-56 retinol dehydrogenase 10 (all-trans) Mus musculus 22-27
21471156-5 2011 In particular, retinoic acid (RA) target genes were upregulated proximally, while the expression of the RA-inactivating Cyp26b1 enzyme was downregulated distally, pointing to increased RA activity in Shh-deficient mouse limb buds. Tretinoin 104-106 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 120-127
21354561-1 2011 OBJECTIVE: To detect changes induced by all-trans-retinoic acid (ATRA) on the expression and activation of target proteins of the retinoic acid (RA) and PI3K/Akt pathways involved in leiomyoma growth. Tretinoin 40-63 AKT serine/threonine kinase 1 Homo sapiens 158-161
21471156-5 2011 In particular, retinoic acid (RA) target genes were upregulated proximally, while the expression of the RA-inactivating Cyp26b1 enzyme was downregulated distally, pointing to increased RA activity in Shh-deficient mouse limb buds. Tretinoin 104-106 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 120-127
21471156-7 2011 During initiation of limb bud outgrowth, the activation of Cyp26b1 expression creates a distal "RA-free" domain, as indicated by complementary downregulation of a transcriptional sensor of RA activity. Tretinoin 96-98 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 59-66
21471156-7 2011 During initiation of limb bud outgrowth, the activation of Cyp26b1 expression creates a distal "RA-free" domain, as indicated by complementary downregulation of a transcriptional sensor of RA activity. Tretinoin 189-191 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 59-66
21471156-11 2011 In summary, SHH promotes distal progression of limb development by enhancing CYP26B1-mediated RA clearance as part of a signalling network linking the SHH/GREM1/AER-FGF feedback loop to the newly identified AER-FGF/CYP26B1/RA module. Tretinoin 94-96 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 77-84
21471156-11 2011 In summary, SHH promotes distal progression of limb development by enhancing CYP26B1-mediated RA clearance as part of a signalling network linking the SHH/GREM1/AER-FGF feedback loop to the newly identified AER-FGF/CYP26B1/RA module. Tretinoin 94-96 gremlin 1, DAN family BMP antagonist Mus musculus 155-160
21471156-11 2011 In summary, SHH promotes distal progression of limb development by enhancing CYP26B1-mediated RA clearance as part of a signalling network linking the SHH/GREM1/AER-FGF feedback loop to the newly identified AER-FGF/CYP26B1/RA module. Tretinoin 94-96 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 215-222
21509899-4 2011 Our data indicate that RA is synthesised by Raldh2 in proximal cells during limb bud outgrowth. Tretinoin 23-25 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 44-50
21354561-1 2011 OBJECTIVE: To detect changes induced by all-trans-retinoic acid (ATRA) on the expression and activation of target proteins of the retinoic acid (RA) and PI3K/Akt pathways involved in leiomyoma growth. Tretinoin 65-69 AKT serine/threonine kinase 1 Homo sapiens 158-161
21354561-1 2011 OBJECTIVE: To detect changes induced by all-trans-retinoic acid (ATRA) on the expression and activation of target proteins of the retinoic acid (RA) and PI3K/Akt pathways involved in leiomyoma growth. Tretinoin 50-63 AKT serine/threonine kinase 1 Homo sapiens 158-161
22977519-12 2011 In conclusion, the combination of RSG and ATRA reduced the expression of COX-2, MMP-7 and TIMP-1, caused cell cycle arrest at the G1 phase and induced apoptosis, which resulted in the inhibition of cell proliferation in the HCT-15 human colorectal cancer cell line. Tretinoin 42-46 mitochondrially encoded cytochrome c oxidase II Homo sapiens 73-78
22977519-12 2011 In conclusion, the combination of RSG and ATRA reduced the expression of COX-2, MMP-7 and TIMP-1, caused cell cycle arrest at the G1 phase and induced apoptosis, which resulted in the inhibition of cell proliferation in the HCT-15 human colorectal cancer cell line. Tretinoin 42-46 TIMP metallopeptidase inhibitor 1 Homo sapiens 90-96
21354561-1 2011 OBJECTIVE: To detect changes induced by all-trans-retinoic acid (ATRA) on the expression and activation of target proteins of the retinoic acid (RA) and PI3K/Akt pathways involved in leiomyoma growth. Tretinoin 67-69 AKT serine/threonine kinase 1 Homo sapiens 158-161
21354561-6 2011 MAIN OUTCOME MEASURE(S): The effect of ATRA was examined on the expression and phosphorylation of relevant RA, PI3K/Akt, and Bcl2 proteins (immunochemical analysis), cell proliferation, cell cycle distribution, and apoptosis. Tretinoin 39-43 BCL2 apoptosis regulator Homo sapiens 125-129
21354561-7 2011 RESULT(S): Applying our cell culture model, we demonstrated that ATRA induced changes in the expression and activation of the RA and PI3K/Akt pathway proteins in leiomyoma cells, with significant increases of alcohol dehydrogenase 1 and cyclin D2 protein levels. Tretinoin 65-69 AKT serine/threonine kinase 1 Homo sapiens 138-141
21354561-7 2011 RESULT(S): Applying our cell culture model, we demonstrated that ATRA induced changes in the expression and activation of the RA and PI3K/Akt pathway proteins in leiomyoma cells, with significant increases of alcohol dehydrogenase 1 and cyclin D2 protein levels. Tretinoin 65-69 cyclin D2 Homo sapiens 237-246
21354561-8 2011 In part of the leiomyoma cells, ATRA induced a relative increase of Bax (proapoptotic) as well as a relative decrease of phosphorylated glycogen synthase kinase 3beta (proapoptotic). Tretinoin 32-36 BCL2 associated X, apoptosis regulator Homo sapiens 68-71
21388746-2 2011 As human alpha-fetoprotein binds retinoids and inhibits estrogen-dependent cancer cell proliferation, and because retinoic acid (a retinol metabolite) and estradiol (an estrogen) can both initiate cellular gene transcription, it is hypothesized here that alpha-fetoprotein functions during critical gestational periods to prevent retinoic acid and maternal estradiol from inappropriately stimulating gene expression in developing brain regions which are sensitive to these chemicals. Tretinoin 114-127 alpha fetoprotein Homo sapiens 255-272
21437295-10 2011 The ensemble of models also correctly predicted Rb and p47phox regulation and the correlation between p21-CDK4-cyclin D formation and G1/0-arrest following exposure to RA. Tretinoin 168-170 cyclin dependent kinase inhibitor 1A Homo sapiens 102-105
21388746-4 2011 It will be shown how each of these risk factors may initiate expression of genes which are sensitive to retinoic acid and/or estradiol - whether by direct promotion or by reducing production of alpha-fetoprotein. Tretinoin 104-117 alpha fetoprotein Homo sapiens 194-211
21436255-10 2011 This loss of RA-producing enzymes was accompanied by 70% decreased expression of ZFP423, PPARgamma, and Fabp4 in visceral fat of Aldh1a1(-/-) vs. wild-type mice and by the predominant loss of visceral fat. Tretinoin 13-15 zinc finger protein 423 Mus musculus 81-87
21436255-11 2011 Subcutaneous fat of Aldh1a1(-/-) mice expressed Aldh1a3 for RA production that was sufficient to maintain expression of ZFP423 and PPARgamma and sc fat mass. Tretinoin 60-62 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 48-55
21436255-11 2011 Subcutaneous fat of Aldh1a1(-/-) mice expressed Aldh1a3 for RA production that was sufficient to maintain expression of ZFP423 and PPARgamma and sc fat mass. Tretinoin 60-62 zinc finger protein 423 Mus musculus 120-126
21436255-12 2011 Our data suggest a paradigm for regulation of fat depots through the concerted action of Aldh1 enzymes that establish RA-dependent tandem regulation of transcription factors ZFP423 and PPARgamma in a depot-specific manner. Tretinoin 118-120 zinc finger protein 423 Mus musculus 174-180
21385898-7 2011 Further, retinoic acid and other differentiation- inducing stimuli upregulated CAMTA1 expression in neuroblastoma cells. Tretinoin 9-22 calmodulin binding transcription activator 1 Homo sapiens 79-85
21428449-2 2011 The induction of CYP26A1 mRNA was used to evaluate the ability of the compounds to enhance the biological effects of all-trans retinoic acid (ATRA) in a retinoid-responsive neuroblastoma cell line. Tretinoin 142-146 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-24
21237205-4 2011 Furthermore, when stimulated with flagellin, ATRA-induced THP-1 cells expressed multiple cytokines, including TNF-alpha, IL-1beta, and IL-12p40, and several co-stimulatory molecules, such as CD40, CD80, CD86, and MHC class I and II. Tretinoin 45-49 tumor necrosis factor Homo sapiens 110-119
21237205-4 2011 Furthermore, when stimulated with flagellin, ATRA-induced THP-1 cells expressed multiple cytokines, including TNF-alpha, IL-1beta, and IL-12p40, and several co-stimulatory molecules, such as CD40, CD80, CD86, and MHC class I and II. Tretinoin 45-49 interleukin 1 beta Homo sapiens 121-129
21518431-3 2011 RESULTS: Six microRNAs were upregulated by ATRA treatment, miR-663, miR-494, miR-145, miR-22, miR-363* and miR-223; and three microRNAs were downregulated, miR-10a, miR-181 and miR-612. Tretinoin 43-47 microRNA 22 Homo sapiens 86-92
21146490-7 2011 By use of this assay, tTG in several cell lines and the stimulatory effect of retinoic acid on tTG expression could be demonstrated. Tretinoin 78-91 transglutaminase 2 Homo sapiens 95-98
21310922-4 2011 In the present study we show for the first time that the plasminogen receptor, S100A10, is present on the extracellular surface of APL cells and is rapidly down-regulated in response to all-trans retinoic acid. Tretinoin 196-209 S100 calcium binding protein A10 Homo sapiens 79-86
21427174-4 2011 The role of PML in the retinoic acid pathway that drives GMPs to granulopoiesis is documented in the literature. Tretinoin 23-36 promyelocytic leukemia Mus musculus 12-15
21221725-5 2011 qPCR results showed that ATRA upregulated endogenous expression of Nkx2.2 in C6 cells. Tretinoin 25-29 NK2 homeobox 2 Homo sapiens 67-73
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 major facilitator superfamily domain containing 2A Homo sapiens 155-159
21352343-0 2011 Retinoic acids exhibit anti-fibrotic activity through the inhibition of 5-lipoxygenase expression in scleroderma fibroblasts. Tretinoin 0-14 arachidonate 5-lipoxygenase Homo sapiens 72-86
21352343-5 2011 Cultured skin fibroblasts from patients with scleroderma were treated with RA and their effect on the expression of 5-lipoxygenase (LOX), transforming growth factor (TGF)-beta1, connective tissue growth factor (CTGF), type I and type III collagen was tested by reverse transcription polymerase chain reaction (RT-PCR) and western immunoblotting. Tretinoin 75-77 arachidonate 5-lipoxygenase Homo sapiens 116-130
21352343-5 2011 Cultured skin fibroblasts from patients with scleroderma were treated with RA and their effect on the expression of 5-lipoxygenase (LOX), transforming growth factor (TGF)-beta1, connective tissue growth factor (CTGF), type I and type III collagen was tested by reverse transcription polymerase chain reaction (RT-PCR) and western immunoblotting. Tretinoin 75-77 arachidonate 5-lipoxygenase Homo sapiens 132-135
21352343-5 2011 Cultured skin fibroblasts from patients with scleroderma were treated with RA and their effect on the expression of 5-lipoxygenase (LOX), transforming growth factor (TGF)-beta1, connective tissue growth factor (CTGF), type I and type III collagen was tested by reverse transcription polymerase chain reaction (RT-PCR) and western immunoblotting. Tretinoin 75-77 transforming growth factor beta 1 Homo sapiens 138-176
21352343-8 2011 RA significantly inhibited the expression of 5-LOX and of TGF-beta1, CTGF, type I and type III collagen. Tretinoin 0-2 arachidonate 5-lipoxygenase Homo sapiens 45-50
21352343-8 2011 RA significantly inhibited the expression of 5-LOX and of TGF-beta1, CTGF, type I and type III collagen. Tretinoin 0-2 transforming growth factor beta 1 Homo sapiens 58-67
21352343-10 2011 In vitro, RA reduced 5-LOX expression in scleroderma fibroblasts and downregulated TGF-beta1 and CTGF expression, leading to the inhibition of type I and type III collagen synthesis. Tretinoin 10-12 arachidonate 5-lipoxygenase Homo sapiens 23-26
21352343-10 2011 In vitro, RA reduced 5-LOX expression in scleroderma fibroblasts and downregulated TGF-beta1 and CTGF expression, leading to the inhibition of type I and type III collagen synthesis. Tretinoin 10-12 transforming growth factor beta 1 Homo sapiens 83-92
21352343-11 2011 Our results indicate that the clinical effects of RA on scleroderma are, at least in part, attributable to the reduction of 5-LOX expression and the subsequent suppression of TGF-beta1 and CTGF expression that results in the blockade of collagenogenesis. Tretinoin 50-52 arachidonate 5-lipoxygenase Homo sapiens 126-129
21352343-11 2011 Our results indicate that the clinical effects of RA on scleroderma are, at least in part, attributable to the reduction of 5-LOX expression and the subsequent suppression of TGF-beta1 and CTGF expression that results in the blockade of collagenogenesis. Tretinoin 50-52 transforming growth factor beta 1 Homo sapiens 175-184
21307853-5 2011 Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. Tretinoin 124-137 mitogen-activated protein kinase 8 Homo sapiens 182-185
21357440-7 2011 TRA-8 combined with AT-101 or BH3I-2", inhibitors of antiapoptotic Bcl-2 proteins, produced synergistic cytotoxicity against ZR-75-1, BT-474, and T47D cells. Tretinoin 0-3 BCL2 apoptosis regulator Homo sapiens 67-72
21532733-2 2011 Here, analysis of retinaldehyde dehydrogenase mutant mouse embryos lacking RA synthesis demonstrates that RA generated by Raldh3 in the subventricular zone of the basal ganglia is required for GABAergic differentiation, whereas RA generated by Raldh2 in the meninges is unnecessary for development of the adjacent cortex. Tretinoin 106-108 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 122-128
21532733-2 2011 Here, analysis of retinaldehyde dehydrogenase mutant mouse embryos lacking RA synthesis demonstrates that RA generated by Raldh3 in the subventricular zone of the basal ganglia is required for GABAergic differentiation, whereas RA generated by Raldh2 in the meninges is unnecessary for development of the adjacent cortex. Tretinoin 106-108 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 122-128
21419664-0 2011 Essential role for retinoic acid in the promotion of CD4(+) T cell effector responses via retinoic acid receptor alpha. Tretinoin 19-32 CD4 molecule Homo sapiens 53-56
21419664-2 2011 Here we showed RA was also required to elicit proinflammatory CD4(+) helper T cell responses to infection and mucosal vaccination. Tretinoin 15-17 CD4 molecule Homo sapiens 62-65
21262915-4 2011 RA effects are mediated by RAR/RXR receptors that we show are modified by interactions with the aryl hydrocarbon receptor (AhR), a protein functioning both as a transcription factor and a ligand-dependent adaptor in an ubiquitin ligase complex. Tretinoin 0-2 RAB40B, member RAS oncogene family Homo sapiens 27-30
21307853-5 2011 Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. Tretinoin 124-137 mitogen-activated protein kinase 8 Homo sapiens 201-206
21423769-2 2011 We report that from all inductive signals tested, retinoic acid (RA) and platelet derived growth factor (PDGF(BB)) are the most effective agents in guiding the differentiation of CD34(+) cells into smooth muscle progenitor cells (SMPCs) characterized by the expression of SMC genes and proteins, secretion of SMC-related cytokines, contraction in response to depolarization agents and vasoactive peptides and expression of SMC-related genes in a 3D environment. Tretinoin 50-63 CD34 molecule Homo sapiens 179-183
21423769-2 2011 We report that from all inductive signals tested, retinoic acid (RA) and platelet derived growth factor (PDGF(BB)) are the most effective agents in guiding the differentiation of CD34(+) cells into smooth muscle progenitor cells (SMPCs) characterized by the expression of SMC genes and proteins, secretion of SMC-related cytokines, contraction in response to depolarization agents and vasoactive peptides and expression of SMC-related genes in a 3D environment. Tretinoin 65-67 CD34 molecule Homo sapiens 179-183
20717697-9 2011 The proliferating effect of RA on PGCs was further confirmed by increased mRNA expression of cyclins, CCND1 and CCNE1, and cyclin-dependent kinases 6 and 2, which are critical for G1-S progression in cell cycle. Tretinoin 28-30 cyclin D1 Gallus gallus 102-107
21061155-4 2011 Laser confocal microscopy results reveal that PHB colocalized with the expression products of c-myc, c-fos, p53, and Rb, but the colocalization region was altered after RA treatment. Tretinoin 169-171 tumor protein p53 Homo sapiens 108-111
21343363-0 2011 Wt1 controls retinoic acid signalling in embryonic epicardium through transcriptional activation of Raldh2. Tretinoin 13-26 WT1 transcription factor Homo sapiens 0-3
21343363-6 2011 Using a RA-responsive reporter, we have confirmed that Wt1-null epicardial cells actually show reduced synthesis of RA. Tretinoin 8-10 WT1 transcription factor Homo sapiens 55-58
21343363-6 2011 Using a RA-responsive reporter, we have confirmed that Wt1-null epicardial cells actually show reduced synthesis of RA. Tretinoin 116-118 WT1 transcription factor Homo sapiens 55-58
21343363-9 2011 PDGFRalpha and PDGFRbeta mRNA and protein levels are downregulated in the absence of Wt1, but only Pdgfra expression is rescued by the addition of RA to Wt1-null epicardial cells. Tretinoin 147-149 platelet derived growth factor receptor alpha Homo sapiens 0-10
21343363-9 2011 PDGFRalpha and PDGFRbeta mRNA and protein levels are downregulated in the absence of Wt1, but only Pdgfra expression is rescued by the addition of RA to Wt1-null epicardial cells. Tretinoin 147-149 platelet derived growth factor receptor alpha Homo sapiens 99-105
21343363-9 2011 PDGFRalpha and PDGFRbeta mRNA and protein levels are downregulated in the absence of Wt1, but only Pdgfra expression is rescued by the addition of RA to Wt1-null epicardial cells. Tretinoin 147-149 WT1 transcription factor Homo sapiens 153-156
21343363-11 2011 Taken together, our results indicate that Wt1 critically regulates epicardial RA signalling via direct activation of the Raldh2 gene, and identify a role for Wt1 in the regulation of morphogen receptors involved in the proliferation, migration, and differentiation of epicardial and epicardially-derived cells (EPDC). Tretinoin 78-80 WT1 transcription factor Homo sapiens 42-45
21425409-2 2011 Generation of NKX2.1-GFP(+) cells was dependent on the concentration, timing, and duration of retinoic acid treatment during differentiation. Tretinoin 94-107 NK2 homeobox 1 Homo sapiens 14-20
20952403-6 2011 Moreover, ChIP experiments demonstrated that EZH2 and MeCP2 repressor complexes were associated to the heavily methylated enhancer region in the absence of RA while both complexes were displaced during RA stimulation. Tretinoin 202-204 methyl-CpG binding protein 2 Homo sapiens 54-59
21298309-9 2011 Enhancement of putative epithelial progenitor commitment was observed when cultured in KCM with BMP-4 following pretreatment of RA and BMP-4. Tretinoin 128-130 bone morphogenetic protein 4 Mus musculus 96-101
21482329-4 2011 In human alveolar epithelial cells (lines A549), RAR beta (induced by retinoic acid) was quantified, after treatment by retinol, by q-PCR at 24h and 48 h. RESULTS: The expression of the RNA of ADH3, RALDH1 and CYP26B1 was detected for each of the four stages studied and in the A549 cell line. Tretinoin 70-83 retinoic acid receptor beta Homo sapiens 49-57
21138835-7 2011 siRNA knockdown indicates that Rdh10, Rdh2 (mRdh1), and Raldh1, -2, and -3 contribute to atRA production. Tretinoin 89-93 retinol dehydrogenase 16 Rattus norvegicus 38-42
21138835-7 2011 siRNA knockdown indicates that Rdh10, Rdh2 (mRdh1), and Raldh1, -2, and -3 contribute to atRA production. Tretinoin 89-93 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 56-74
21138835-8 2011 Knockdown of the Rdh Dhrs9 increased atRA synthesis ~40% by increasing Raldh1 expression. Tretinoin 37-41 dehydrogenase/reductase 9 Rattus norvegicus 21-26
21138835-8 2011 Knockdown of the Rdh Dhrs9 increased atRA synthesis ~40% by increasing Raldh1 expression. Tretinoin 37-41 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 71-77
21138835-12 2011 Observation of cross-talk between Dhrs9 and Raldh1 provides a novel mechanism of regulating atRA biosynthesis. Tretinoin 92-96 dehydrogenase/reductase 9 Rattus norvegicus 34-39
21138835-12 2011 Observation of cross-talk between Dhrs9 and Raldh1 provides a novel mechanism of regulating atRA biosynthesis. Tretinoin 92-96 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 44-50
21303978-1 2011 Even though it is among the most commonly methylated loci in multiple cancers, the retinoic acid-induced tumor suppressor retinoic acid receptor responder 1 (RARRES1) has no known function. Tretinoin 83-96 retinoic acid receptor responder 1 Homo sapiens 158-165
21173077-6 2011 The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibited both RA + TPA and RA + TGF-beta-stimulated secretion of VEGF, as well as RA-induced ROS production. Tretinoin 94-96 transforming growth factor beta 1 Homo sapiens 99-107
21173077-0 2011 Retinoic acid stimulation of VEGF secretion from human endometrial stromal cells is mediated by production of reactive oxygen species. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 29-33
21426646-4 2011 VEGF concentrations in the SY5Y cell culture supernatants were measured using ELISA after the treatment with ATRA, BDNF, tyrosine kinase inhibitor K252a and PI3k inhibitor LY294002. Tretinoin 109-113 vascular endothelial growth factor A Homo sapiens 0-4
21426646-8 2011 VEGF concentrations in the group treated with ATRA+BDNF were significantly higher than those in the untreated control and the ATRA alone treatment groups (P<0.01). Tretinoin 46-50 vascular endothelial growth factor A Homo sapiens 0-4
21426646-9 2011 VEGF concentrations in the K252a pretreated ATRA+BDNF group were significantly lower than those in the group treated with ATRA+BDNF (P<0.05). Tretinoin 44-48 vascular endothelial growth factor A Homo sapiens 0-4
21426646-10 2011 VEGF concentrations in the LY294002 treatment group (ATRA+LY294002+BDNF group) were also significantly lower than those in the group treated with ATRA+BDNF (P<0.01). Tretinoin 53-57 vascular endothelial growth factor A Homo sapiens 0-4
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 19-32 vascular endothelial growth factor A Homo sapiens 156-160
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 19-32 transforming growth factor beta 1 Homo sapiens 172-180
21173077-6 2011 The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibited both RA + TPA and RA + TGF-beta-stimulated secretion of VEGF, as well as RA-induced ROS production. Tretinoin 94-96 vascular endothelial growth factor A Homo sapiens 132-136
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 19-32 interleukin 1 beta Homo sapiens 182-190
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 19-32 vascular endothelial growth factor A Homo sapiens 210-214
21173077-7 2011 Treatment of cells with RA resulted in a shift in the glutathione (GSH) redox potential to a more oxidative state, suggesting that the transduction pathway leading to increased VEGF secretion is at least partially mediated through the antioxidant capacity of GSH couples. Tretinoin 24-26 vascular endothelial growth factor A Homo sapiens 177-181
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 34-36 vascular endothelial growth factor A Homo sapiens 156-160
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 34-36 transforming growth factor beta 1 Homo sapiens 172-180
21427903-5 2011 RESULTS: (1) Gene-chip analysis showed that in RA-induced cleft palate group wnt8a and fgf9 were down-regulated, wnt3 and fgf10 were up-regulated in conversely. Tretinoin 47-49 fibroblast growth factor 9 Mus musculus 87-91
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 34-36 interleukin 1 beta Homo sapiens 182-190
21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 34-36 vascular endothelial growth factor A Homo sapiens 210-214
21173077-3 2011 We have now determined that this stimulation of VEGF by RA is mediated through an increased production of cellular reactive oxygen species (ROS). Tretinoin 56-58 vascular endothelial growth factor A Homo sapiens 48-52
21173077-4 2011 Results indicated that RA, but not TPA or TGF-beta, directly increases ROS production in endometrial stromal cells and that the co-stimulating activity of RA on VEGF secretion can be mimicked by direct addition of H2O2. Tretinoin 155-157 vascular endothelial growth factor A Homo sapiens 161-165
21173077-5 2011 Importantly, co-treatment of RA with TPA or TGF-beta further stimulated ROS production in a fashion that positively correlated with levels of VEGF secretion. Tretinoin 29-31 transforming growth factor beta 1 Homo sapiens 44-52
21173077-5 2011 Importantly, co-treatment of RA with TPA or TGF-beta further stimulated ROS production in a fashion that positively correlated with levels of VEGF secretion. Tretinoin 29-31 vascular endothelial growth factor A Homo sapiens 142-146
21205785-0 2011 Her9 represses neurogenic fate downstream of Tbx1 and retinoic acid signaling in the inner ear. Tretinoin 54-67 hairy-related 9 Danio rerio 0-4
21205785-7 2011 Third, we have identified retinoic acid (RA) signaling as the upstream patterning signal of otic posterolateral genes such as tbx1 and her9. Tretinoin 26-39 T-box transcription factor 1 Danio rerio 126-130
21205785-7 2011 Third, we have identified retinoic acid (RA) signaling as the upstream patterning signal of otic posterolateral genes such as tbx1 and her9. Tretinoin 26-39 hairy-related 9 Danio rerio 135-139
21274875-10 2011 atRA alone or in combination with UDCA greatly repressed CYP7A1 expression in human hepatocytes and significantly inhibited COL1A1, MMP2, and alpha-SMA expression and/or activity in primary human hepatic stellate cells and LX-2 cells. Tretinoin 0-4 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 57-63
20473866-4 2011 Knockdown of AFP mRNA or inhibition of AFP expression by all trans-retinoic acid resulted in enhancement of the PTEN level with a synchronous decrease in phosphorylated AKT. Tretinoin 61-80 alpha fetoprotein Homo sapiens 39-42
21187378-6 2011 We demonstrate that injection of all-trans retinoic acid induces the expression of NFATc1, particularly from the constitutive P2 promoter, and leads to the increase of the B1 cells. Tretinoin 43-56 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1 Mus musculus 83-89
21068381-7 2011 Importantly, both retinol and retinoic acid are able to promote TR4 to recruit coactivators and to activate a TR4-regulated reporter. Tretinoin 30-43 nuclear receptor subfamily 2 group C member 2 Homo sapiens 64-67
21068381-7 2011 Importantly, both retinol and retinoic acid are able to promote TR4 to recruit coactivators and to activate a TR4-regulated reporter. Tretinoin 30-43 nuclear receptor subfamily 2 group C member 2 Homo sapiens 110-113
21171566-5 2011 Retinoic acid-loaded nanoparticles increase the number of neuronal nuclear protein (NeuN)-positive neurons and functional neurons responding to depolarization with KCl and expressing NMDA receptor subunit type 1 (NR1). Tretinoin 0-13 RNA binding fox-1 homolog 3 Homo sapiens 58-82
21171566-5 2011 Retinoic acid-loaded nanoparticles increase the number of neuronal nuclear protein (NeuN)-positive neurons and functional neurons responding to depolarization with KCl and expressing NMDA receptor subunit type 1 (NR1). Tretinoin 0-13 RNA binding fox-1 homolog 3 Homo sapiens 84-88
21171566-5 2011 Retinoic acid-loaded nanoparticles increase the number of neuronal nuclear protein (NeuN)-positive neurons and functional neurons responding to depolarization with KCl and expressing NMDA receptor subunit type 1 (NR1). Tretinoin 0-13 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 183-216
21148038-0 2011 Retinoic acid-induced CCR9 expression requires transient TCR stimulation and cooperativity between NFATc2 and the retinoic acid receptor/retinoid X receptor complex. Tretinoin 0-13 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2 Mus musculus 99-105
20838376-3 2011 Although we know much about the molecular basis of TRAIL-mediated cell killing, the mechanism responsible for TRAIL inhibition in tumors remains elusive because (a) TRAIL can be regulated by retinoic acid (RA); (b) the tumor antigen preferentially expressed antigen of melanoma (PRAME) was shown to inhibit transcription of RA receptor target genes through the polycomb protein, enhancer of zeste homolog 2 (EZH2); and (c) we have found that TRAIL is inversely correlated with BCR-ABL in chronic myeloid leukemia (CML) patients. Tretinoin 191-204 TNF superfamily member 10 Homo sapiens 110-115
20838376-3 2011 Although we know much about the molecular basis of TRAIL-mediated cell killing, the mechanism responsible for TRAIL inhibition in tumors remains elusive because (a) TRAIL can be regulated by retinoic acid (RA); (b) the tumor antigen preferentially expressed antigen of melanoma (PRAME) was shown to inhibit transcription of RA receptor target genes through the polycomb protein, enhancer of zeste homolog 2 (EZH2); and (c) we have found that TRAIL is inversely correlated with BCR-ABL in chronic myeloid leukemia (CML) patients. Tretinoin 191-204 TNF superfamily member 10 Homo sapiens 110-115
20838376-3 2011 Although we know much about the molecular basis of TRAIL-mediated cell killing, the mechanism responsible for TRAIL inhibition in tumors remains elusive because (a) TRAIL can be regulated by retinoic acid (RA); (b) the tumor antigen preferentially expressed antigen of melanoma (PRAME) was shown to inhibit transcription of RA receptor target genes through the polycomb protein, enhancer of zeste homolog 2 (EZH2); and (c) we have found that TRAIL is inversely correlated with BCR-ABL in chronic myeloid leukemia (CML) patients. Tretinoin 191-204 TNF superfamily member 10 Homo sapiens 110-115
21224842-1 2011 Sex-specific initiation of meiosis in the fetal ovary has been suggested to require retinoic acid (RA) for induction of Stra8, with expression of the RA-degrading enzyme Cyp26b1 in fetal testis delaying meiosis until postnatal development. Tretinoin 150-152 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 170-177
21224842-4 2011 Ketoconazole inhibition of Cyp26b1 in Raldh2(-/-) testis allows RA-independent induction of Stra8, but only when the mesonephros remains attached, pointing to a non-RA signal from the mesonephros that induces Stra8 in the adjacent gonad. Tretinoin 64-66 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 27-34
20376700-2 2011 We found that in AN(3)CA and F9 cells, this hCOX-2 DR1 mediates responsiveness to all-trans-retinoic acid (tRA) or 9-cis-retinoic acid (9cRA), but this effect was suppressed by PPARdelta. Tretinoin 82-105 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-50
20376700-2 2011 We found that in AN(3)CA and F9 cells, this hCOX-2 DR1 mediates responsiveness to all-trans-retinoic acid (tRA) or 9-cis-retinoic acid (9cRA), but this effect was suppressed by PPARdelta. Tretinoin 107-110 mitochondrially encoded cytochrome c oxidase II Homo sapiens 44-50
21247419-8 2011 Rasd1 inhibited transcriptional repression by Ear2 on a renin promoter-luciferase reporter construct both in the presence and absence of all-trans-retinoic acid. Tretinoin 137-160 RAS, dexamethasone-induced 1 Mus musculus 0-5
21148038-8 2011 NFATc2 directly bound to RARalpha and RXRalpha, and it enhanced the binding of RARalpha to the RA response element half-site. Tretinoin 25-27 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 2 Mus musculus 0-6
21187378-7 2011 Thus, the retinoic acid-dependent pathway is critical for regulating NFATc1 expression and for maintenance of the natural memory B cell compartment. Tretinoin 10-23 nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1 Mus musculus 69-75
21187396-1 2011 Retinoic acid is a potent differentiation and antiproliferative agent of breast cancer cells, and one of its receptors, retinoic acid receptor beta (RARbeta), has been proposed to act as a tumor suppressor. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 120-147
21187396-1 2011 Retinoic acid is a potent differentiation and antiproliferative agent of breast cancer cells, and one of its receptors, retinoic acid receptor beta (RARbeta), has been proposed to act as a tumor suppressor. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 149-156
21249211-0 2011 Cyp26b1 regulates retinoic acid-dependent signals in T cells and its expression is inhibited by transforming growth factor-beta. Tretinoin 18-31 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
21045116-5 2011 After acute treatment with RA, the same genes were rapidly and concomitantly induced, preceding retinoic acid receptor (RAR)beta, a classical direct target of RA. Tretinoin 27-29 retinoic acid receptor, beta Rattus norvegicus 120-128
21206504-0 2011 Amelioration of glomerulosclerosis with all-trans retinoic acid is linked to decreased plasminogen activator inhibitor-1 and alpha-smooth muscle actin. Tretinoin 50-63 serpin family E member 1 Rattus norvegicus 87-120
21206504-10 2011 Treatment with atRA significantly reduced the expressions of PAI-1 and alpha-SMA. Tretinoin 15-19 serpin family E member 1 Rattus norvegicus 61-66
21249211-8 2011 Accordingly, physiological levels of RA (1-10 nM) could induce Cyp26b1 expression in naive T cells upon activation in vitro, but could not do so in the presence of TGF-beta. Tretinoin 37-39 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 63-70
22056434-4 2011 When the differentiation of Th17 cells was inhibited by all tarans retinoic acid (ATRA) which induces regulatory T cell (Treg) differentiation under Th17 differentiation conditions, expression of Acvr2a was also inhibited. Tretinoin 67-80 activin A receptor type 2A Homo sapiens 196-202
22056434-4 2011 When the differentiation of Th17 cells was inhibited by all tarans retinoic acid (ATRA) which induces regulatory T cell (Treg) differentiation under Th17 differentiation conditions, expression of Acvr2a was also inhibited. Tretinoin 82-86 activin A receptor type 2A Homo sapiens 196-202
21249211-9 2011 Overexpression of Cyp26b1 significantly suppressed the RA effect to induce expression of the gut-homing receptor CCR9 on T cells. Tretinoin 55-57 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 18-25
21249211-11 2011 CONCLUSIONS/SIGNIFICANCE: Our data demonstrate a role for CYP26B1 in regulating RA-dependent signals in activated T cells but not during TGF-beta-dependent differentiation to Foxp3+ regulatory T cells. Tretinoin 80-82 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 58-65
21148184-4 2011 In particular, we detected an expansion of the expression domains of the RA-catabolizing enzymes Cyp26a1 and Cyp26c1, and a downregulation of the RA-synthesizing enzyme Raldh3. Tretinoin 146-148 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 169-175
20300827-2 2011 Recently, we reported significant stimulation of all-trans retinoic acid (atRA)-induced NIS expression in the estrogen-receptor positive human breast cancer cell line MCF-7 by dexamethasone (Dex) in vitro and in vivo, which might offer the potential to image and treat breast cancer with radioiodine. Tretinoin 53-72 estrogen receptor 1 Homo sapiens 110-127
20300827-2 2011 Recently, we reported significant stimulation of all-trans retinoic acid (atRA)-induced NIS expression in the estrogen-receptor positive human breast cancer cell line MCF-7 by dexamethasone (Dex) in vitro and in vivo, which might offer the potential to image and treat breast cancer with radioiodine. Tretinoin 74-78 estrogen receptor 1 Homo sapiens 110-127
20300827-3 2011 In this study, based on its known interaction with the pregnane-X-receptor (PXR) forming a heterodimer with the retinoid-X-receptor (RXR), we examined the effect of carbamazepine (CBZ), a potent activator of PXR, on atRA-induced NIS expression and therapeutic efficacy of (131)I in MCF-7 cells. Tretinoin 216-220 nuclear receptor subfamily 1 group I member 2 Homo sapiens 76-79
22178948-2 2011 We describe differences in the regulation of UCP-1 mRNA expression between rat and mouse brown adipocytes in culture, using norepinephrine (NE), triiodothyronine (T3), insulin and retinoic acid (RA). Tretinoin 180-193 uncoupling protein 1 Rattus norvegicus 45-50
22178948-2 2011 We describe differences in the regulation of UCP-1 mRNA expression between rat and mouse brown adipocytes in culture, using norepinephrine (NE), triiodothyronine (T3), insulin and retinoic acid (RA). Tretinoin 195-197 uncoupling protein 1 Rattus norvegicus 45-50
21212668-3 2011 Furthermore, the relationship of IGF-I with RA-induced decrement in cell viability has yet to be elucidated. Tretinoin 44-46 insulin like growth factor 1 Homo sapiens 33-38
21212668-9 2011 RESULTS: We showed that RA treatment resulted in a dose- and time-dependent decrease in the secretion and synthesis of IGF-I. Tretinoin 24-26 insulin like growth factor 1 Homo sapiens 119-124
21212668-12 2011 The combination of RA treatment with IGF-I or IRS-1 small interfering RNA resulted in an additive decrease in cell viability. Tretinoin 19-21 insulin like growth factor 1 Homo sapiens 37-42
21212668-13 2011 CONCLUSION: These results indicate that IGF-I plays an important role in the effect of RA and that suppression of IGF-I is implicated in the RA-induced inhibition of cell viability in MCF-7 cells. Tretinoin 87-89 insulin like growth factor 1 Homo sapiens 40-45
21084447-4 2011 The gene most strongly inhibited by activin was Cyp26b1, which encodes a P450 cytochrome enzyme that degrades retinoic acid (RA). Tretinoin 110-123 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 48-55
21084447-4 2011 The gene most strongly inhibited by activin was Cyp26b1, which encodes a P450 cytochrome enzyme that degrades retinoic acid (RA). Tretinoin 125-127 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 48-55
20606468-0 2011 CYP26B1 plays a major role in the regulation of all-trans-retinoic acid metabolism and signaling in human aortic smooth muscle cells. Tretinoin 52-71 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 0-7
22117966-5 2011 FLT3 siRNA treatment also reduced cyclin D1 and Bcl-2 protein levels, and increased the nuclear level of silencing mediator for retinoic acid and thyroid hormone receptors protein both in vitro and in vivo. Tretinoin 128-141 fms related receptor tyrosine kinase 3 Homo sapiens 0-4
21811022-6 2011 A fluorescence peak of retinoic acid was greatly restrained in the presence of Abeta25-35, and retinoic acid inhibited aggregation of Abeta25-35, but not of Abeta1-16, which suggest the specific binding of retinoic acid to the C-terminal portion of Abeta. Tretinoin 23-36 amyloid beta precursor protein Homo sapiens 79-84
20606468-1 2011 AIM: The cytochrome P450 enzymes of the CYP26 family are involved in the catabolism of the biologically active retinoid all-trans-retinoic acid (atRA). Tretinoin 120-143 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-45
20606468-1 2011 AIM: The cytochrome P450 enzymes of the CYP26 family are involved in the catabolism of the biologically active retinoid all-trans-retinoic acid (atRA). Tretinoin 145-149 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-45
20606468-2 2011 Since it is possible that an increased local CYP26 activity would reduce the effects of retinoids in vascular injury, we investigated the role of CYP26 in the regulation of atRA levels in human aortic smooth muscle cells (AOSMCs). Tretinoin 173-177 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 146-151
20606468-5 2011 RESULTS: AOSMCs expressed CYP26B1 constitutively and atRA exposure augmented CYP26B1 mRNA levels. Tretinoin 53-57 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 77-84
20606468-6 2011 Silencing of the CYP26B1 gene expression or reduction of CYP26B1 enzymatic activity by using siRNA or the inhibitor R115866, respectively, increased atRA-mediated signaling and resulted in decreased cell proliferation. Tretinoin 149-153 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 17-24
20606468-6 2011 Silencing of the CYP26B1 gene expression or reduction of CYP26B1 enzymatic activity by using siRNA or the inhibitor R115866, respectively, increased atRA-mediated signaling and resulted in decreased cell proliferation. Tretinoin 149-153 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 57-64
20606468-7 2011 The CYP26 inhibitor also induced expression of atRA-responsive genes. Tretinoin 47-51 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-9
20606468-8 2011 Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop. Tretinoin 11-15 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 24-29
20606468-8 2011 Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop. Tretinoin 11-15 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 105-110
20606468-8 2011 Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop. Tretinoin 53-57 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 24-29
20606468-8 2011 Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop. Tretinoin 53-57 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 105-110
22110742-10 2011 Mechanistically, RA sensitization by MLN4924 was mediated via enhanced apoptosis, likely through accumulation of pro-apoptotic proteins NOXA and c-JUN, two well-known substrates of SAG-SCF E3 ligase. Tretinoin 17-19 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 136-140
21777018-3 2011 This review is focused on the retinoic acid induced regulation of SOX3 gene expression, with particular emphasis on the involvement of retinoid receptors. Tretinoin 30-43 SRY-box transcription factor 3 Homo sapiens 66-70
22087283-0 2011 The proteasome inhibitor bortezomib enhances ATRA-induced differentiation of neuroblastoma cells via the JNK mitogen-activated protein kinase pathway. Tretinoin 45-49 mitogen-activated protein kinase 8 Homo sapiens 105-108
22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Tretinoin 34-38 retinoic acid receptor beta Homo sapiens 131-138
22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Tretinoin 34-38 mitogen-activated protein kinase 8 Homo sapiens 152-155
21287335-4 2011 Furthermore, we also address methods in order to achieve TGFbeta-dependent Treg conversion in vitro, thereby mainly focusing on the role of retinoic acid (RA) to enhance TGFbeta-dependent conversion into Tregs. Tretinoin 140-153 transforming growth factor beta 1 Homo sapiens 170-177
21931644-2 2011 Moderate ectopic expression of GRIM-1 caused growth inhibition and sensitized cells to retinoic acid (RA)/IFN-induced cell death while high expression caused apoptosis. Tretinoin 87-100 SHQ1, H/ACA ribonucleoprotein assembly factor Homo sapiens 31-37
22125642-5 2011 The physiological actions of ATRA are mediated by binding to all three isoforms of the nuclear retinoic acid receptors (RARs): RARalpha, RARbeta, and RARgamma. Tretinoin 29-33 retinoic acid receptor beta Homo sapiens 137-144
22022577-3 2011 The present study further demonstrated that GRP75 translocates into the nucleus and physically interacts with retinoid receptors (RARalpha and RXRalpha) to augment RA-elicited neuronal differentiation. Tretinoin 130-132 heat shock protein family A (Hsp70) member 9 Homo sapiens 44-49
22022577-4 2011 GRP75 was required for RARalpha/RXRalpha-mediated transcriptional regulation and was shown to reduce the proteasome-mediated degradation of RARalpha/RXRalphain a RA-dependent manner. Tretinoin 23-25 heat shock protein family A (Hsp70) member 9 Homo sapiens 0-5
22022577-7 2011 The present findings reveal a novel function of nucleus-localized GRP75 in actively promoting neuronal differentiation, delineating the mode of action for the differentiation therapy of NB by RA. Tretinoin 192-194 heat shock protein family A (Hsp70) member 9 Homo sapiens 66-71
21931644-2 2011 Moderate ectopic expression of GRIM-1 caused growth inhibition and sensitized cells to retinoic acid (RA)/IFN-induced cell death while high expression caused apoptosis. Tretinoin 102-104 SHQ1, H/ACA ribonucleoprotein assembly factor Homo sapiens 31-37
21695257-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: In the present study, differential gene expression profiling revealed a faster silencing of pluripotency-associated genes, like Nanog, Oct4, and Lin28, during retinoic acid-induced neuronal differentiation of LRRK2-deficient mouse embryonic stem cells compared to wildtype cultures. Tretinoin 191-204 Nanog homeobox Mus musculus 160-165
21228620-1 2011 Talarozole is a new highly potent and selective azole derivative which inhibits cytochrome-P450-dependent all-trans-retinoic acid catabolism. Tretinoin 110-129 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 80-95
20850503-5 2010 Increased viability occurred also after the administration of retinoic acid (RA), a pro-differentiative agent able to activate both JNK/Sapk and ERK1/2. Tretinoin 62-75 mitogen-activated protein kinase 8 Homo sapiens 132-140
21963974-4 2011 The Western blot assay indicated that the expression of Bcl-2 was decreased more in A549 cells treated with N-(3-trifluoromethylphenyl) retinamide than that in A549 cells treated with ATRA. Tretinoin 184-188 BCL2 apoptosis regulator Homo sapiens 56-61
21280163-0 2011 Distinct roles for Wnt-4 and Wnt-11 during retinoic acid-induced neuronal differentiation. Tretinoin 43-56 Wnt family member 11 Homo sapiens 29-35
21280163-3 2011 Retinoic acid treatment inhibited beta-catenin/Tcf activity in NTERA-2 cells but not in 2102Ep cells. Tretinoin 0-13 hepatocyte nuclear factor 4 alpha Homo sapiens 47-50
21280163-6 2011 Retinoic acid treatment of NTERA-2 cells induced the expression of Wnt-4 and Wnt-11, both of which were able to inhibit beta-catenin/Tcf activity. Tretinoin 0-13 Wnt family member 11 Homo sapiens 77-83
21280163-6 2011 Retinoic acid treatment of NTERA-2 cells induced the expression of Wnt-4 and Wnt-11, both of which were able to inhibit beta-catenin/Tcf activity. Tretinoin 0-13 hepatocyte nuclear factor 4 alpha Homo sapiens 133-136
21280163-9 2011 Gene expression analysis of NTERA-2 cells stably overexpressing Wnt-11 suggested that Wnt-11 potentiates retinoic acid induction of early neurogenesis. Tretinoin 105-118 Wnt family member 11 Homo sapiens 64-70
21280163-9 2011 Gene expression analysis of NTERA-2 cells stably overexpressing Wnt-11 suggested that Wnt-11 potentiates retinoic acid induction of early neurogenesis. Tretinoin 105-118 Wnt family member 11 Homo sapiens 86-92
21280163-10 2011 Consistent with this, overexpression of Wnt-11 maintained a population of proliferating progenitor cells in cultures treated with retinoic acid for several weeks. Tretinoin 130-143 Wnt family member 11 Homo sapiens 40-46
20850503-5 2010 Increased viability occurred also after the administration of retinoic acid (RA), a pro-differentiative agent able to activate both JNK/Sapk and ERK1/2. Tretinoin 62-75 mitogen-activated protein kinase 3 Homo sapiens 145-151
20850503-5 2010 Increased viability occurred also after the administration of retinoic acid (RA), a pro-differentiative agent able to activate both JNK/Sapk and ERK1/2. Tretinoin 77-79 mitogen-activated protein kinase 8 Homo sapiens 132-140
20850503-5 2010 Increased viability occurred also after the administration of retinoic acid (RA), a pro-differentiative agent able to activate both JNK/Sapk and ERK1/2. Tretinoin 77-79 mitogen-activated protein kinase 3 Homo sapiens 145-151
21159206-0 2010 All-trans retinoic acid inhibits KIT activity and induces apoptosis in gastrointestinal stromal tumor GIST-T1 cell line by affecting on the expression of survivin and Bax protein. Tretinoin 10-23 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 33-36
21159206-0 2010 All-trans retinoic acid inhibits KIT activity and induces apoptosis in gastrointestinal stromal tumor GIST-T1 cell line by affecting on the expression of survivin and Bax protein. Tretinoin 10-23 BCL2 associated X, apoptosis regulator Homo sapiens 167-170
21159206-10 2010 In further examination, we found that the ATRA-induced apoptosis in GIST-T1 cells was accompanied by the down-regulated expression of survivin and up-regulated expression of Bax protein. Tretinoin 42-46 BCL2 associated X, apoptosis regulator Homo sapiens 174-177
21179414-5 2010 METHODOLOGY/PRINCIPAL FINDINGS: The addition of the vitamin A metabolite, all-trans retinoic acid (atRA) to human naive CD4+ cells suboptimally activated with IL-2 and TGF-beta enhanced and stabilized FOXP3 expression, and accelerated their maturation to protective regulatory T cells. Tretinoin 84-97 interleukin 2 Homo sapiens 159-163
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 45-58 interleukin 1 beta Mus musculus 143-151
21179414-5 2010 METHODOLOGY/PRINCIPAL FINDINGS: The addition of the vitamin A metabolite, all-trans retinoic acid (atRA) to human naive CD4+ cells suboptimally activated with IL-2 and TGF-beta enhanced and stabilized FOXP3 expression, and accelerated their maturation to protective regulatory T cells. Tretinoin 99-103 CD4 molecule Homo sapiens 120-123
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 45-58 tumor necrosis factor Mus musculus 166-174
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 60-62 interleukin 1 beta Mus musculus 143-151
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 60-62 tumor necrosis factor Mus musculus 166-174
20724538-0 2010 Olfactomedin 4 is a novel target gene of retinoic acids and 5-aza-2"-deoxycytidine involved in human myeloid leukemia cell growth, differentiation, and apoptosis. Tretinoin 41-55 olfactomedin 4 Homo sapiens 0-14
21057085-8 2010 Moreover, trichostatin A and retinoic acid enhanced the generation of iTregs synergistically with PPARalpha and PPARgamma agonists. Tretinoin 29-42 peroxisome proliferator activated receptor gamma Homo sapiens 112-121
20724538-8 2010 Thus, our study demonstrates that OLFM4 plays an important role in myeloid leukemia cellular functions and induction of OLFM4-mediated effects may contribute to the therapeutic value of ATRA. Tretinoin 186-190 olfactomedin 4 Homo sapiens 34-39
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 25-38 olfactomedin 4 Homo sapiens 152-157
20724538-8 2010 Thus, our study demonstrates that OLFM4 plays an important role in myeloid leukemia cellular functions and induction of OLFM4-mediated effects may contribute to the therapeutic value of ATRA. Tretinoin 186-190 olfactomedin 4 Homo sapiens 120-125
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 25-38 olfactomedin 4 Homo sapiens 242-247
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 184-203 olfactomedin 4 Homo sapiens 152-157
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 184-203 olfactomedin 4 Homo sapiens 242-247
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 205-209 olfactomedin 4 Homo sapiens 152-157
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 205-209 olfactomedin 4 Homo sapiens 242-247
20724538-6 2010 Conversely, down-regulation of endogenous OLFM4 in acute myeloid leukemia-193 cells compromised ATRA-induced growth inhibition, differentiation, and apoptosis. Tretinoin 96-100 olfactomedin 4 Homo sapiens 42-47
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 olfactomedin 4 Homo sapiens 18-23
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 olfactomedin 4 Homo sapiens 188-193
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 olfactomedin 4 Homo sapiens 188-193
21187470-0 2010 All-trans retinoic acid modulates cancer stem cells of glioblastoma multiforme in an MAPK-dependent manner. Tretinoin 10-23 mitogen-activated protein kinase 3 Homo sapiens 85-89
21187470-4 2010 CSCs differentiated into glial and neuronal lineages at low concentrations of ATRA (10 muM). Tretinoin 78-82 latexin Homo sapiens 87-90
21187470-5 2010 Proliferation and self renewal of neurospheres were reduced following ATRA, although ATRA induced apopotsis at higher (40 muM) concentrations. Tretinoin 85-89 latexin Homo sapiens 122-125
21187470-6 2010 Analysis of mitogen-activated protein kinase signaling pathways, specifically extracellular signal-regulated kinases (ERK1/2), showed that ATRA-induced alterations in ERK1/2 were associated with regulation of differentiation, proliferation and apoptosis. Tretinoin 139-143 mitogen-activated protein kinase 3 Homo sapiens 118-124
21187470-6 2010 Analysis of mitogen-activated protein kinase signaling pathways, specifically extracellular signal-regulated kinases (ERK1/2), showed that ATRA-induced alterations in ERK1/2 were associated with regulation of differentiation, proliferation and apoptosis. Tretinoin 139-143 mitogen-activated protein kinase 3 Homo sapiens 167-173
20846163-4 2010 We reported recently that two substances (ATRA and thalidomide) have preventive effects on pulmonary fibrosis by inhibiting IL-6-dependent proliferation and TGF-beta1-dependent transdifferentiation of lung fibroblasts. Tretinoin 42-46 interleukin 6 Mus musculus 124-128
20864529-3 2010 The present study was conducted to examine the interactive roles of all-trans retinoic acid (ATRA), Ets-1, Sp1, and histone acetylation on the transcriptional regulation and function of the Npr1 gene. Tretinoin 78-91 natriuretic peptide receptor 1 Homo sapiens 190-194
20659790-6 2010 Furthermore, the mRNA expression of corticotropin release factor (CRF) and retinoic acid receptor-alpha (RAR-alpha) in the hypothalamus was both markedly increased in ATRA-treated rats compared with vehicle. Tretinoin 167-171 corticotropin releasing hormone Rattus norvegicus 36-64
20869113-3 2010 We found that TRH and all the tested analogues at concentrations 0.1-50 muM attenuated cell damage induced by MPP(+) (2 mM), 3-nitropropionate (10 mM), hydrogen peroxide (0.5 mM), homocysteine (250 muM) and beta-amyloid (20muM) in retinoic acid differentiated SH-SY5Y cells. Tretinoin 231-244 latexin Homo sapiens 72-75
20632143-9 2010 These results indicate that ATRA within a certain range of concentration could reversibly induce the expression of FR-beta in a dosage- and cell type-dependent manner, and its action in KG-1 cells might be associated with the signal transduction of retinoid receptor RARalpha and RARgamma, rather than RARbeta and RXRs. Tretinoin 28-32 retinoic acid receptor beta Homo sapiens 302-309
20655952-8 2010 ATRA further suppressed IL-6R, whereas 1,25D3 did not. Tretinoin 0-4 interleukin 6 receptor Homo sapiens 24-29
21086135-3 2010 We show that PKC activates telomerase and is, itself, activated following VD3- or ATRA-induced differentiation of HL60 cells, as was observed for PI3K/Akt. Tretinoin 82-86 protein kinase C alpha Homo sapiens 13-16
21086135-3 2010 We show that PKC activates telomerase and is, itself, activated following VD3- or ATRA-induced differentiation of HL60 cells, as was observed for PI3K/Akt. Tretinoin 82-86 AKT serine/threonine kinase 1 Homo sapiens 151-154
21086135-7 2010 In addition, in cells induced to differentiate by ATRA or VD3, Nitroblue-tetrazolium (NBT) reduction and esterase activity, were blocked either by LY294002, a PI3K inhibitor, or by BIM, a PKC inhibitor, without affecting cell surface markers such as CD11b or CD14. Tretinoin 50-54 protein kinase C alpha Homo sapiens 188-191
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 transforming growth factor, beta 1 Rattus norvegicus 187-198
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 serpin family E member 1 Rattus norvegicus 229-234
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 transforming growth factor, beta 1 Rattus norvegicus 230-241
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 serpin family E member 1 Rattus norvegicus 272-277
20864529-3 2010 The present study was conducted to examine the interactive roles of all-trans retinoic acid (ATRA), Ets-1, Sp1, and histone acetylation on the transcriptional regulation and function of the Npr1 gene. Tretinoin 93-97 natriuretic peptide receptor 1 Homo sapiens 190-194
20864529-4 2010 Deletion analysis of the Npr1 promoter and luciferase assays showed that ATRA enhanced a 16-fold Npr1 promoter activity and greatly stimulated guanylyl cyclase (GC) activity of the receptor protein in both atrial natriuretic peptide (ANP)-dependent and -independent manner. Tretinoin 73-77 natriuretic peptide receptor 1 Homo sapiens 25-29
20864529-4 2010 Deletion analysis of the Npr1 promoter and luciferase assays showed that ATRA enhanced a 16-fold Npr1 promoter activity and greatly stimulated guanylyl cyclase (GC) activity of the receptor protein in both atrial natriuretic peptide (ANP)-dependent and -independent manner. Tretinoin 73-77 natriuretic peptide receptor 1 Homo sapiens 97-101
20864529-5 2010 As confirmed by gel shift and chromatin immunoprecipitation assays, ATRA enhanced the binding of both Ets-1 and Sp1 to the Npr1 promoter. Tretinoin 68-72 natriuretic peptide receptor 1 Homo sapiens 123-127
20864529-7 2010 Interestingly, ATRA also increased the acetylation of histones H3 and H4 and enhanced their recruitment to Ets-1 and Sp1 binding sites within the Npr1 promoter. Tretinoin 15-19 natriuretic peptide receptor 1 Homo sapiens 146-150
20956305-0 2010 Retinoic acid regulates bone morphogenic protein signal duration by promoting the degradation of phosphorylated Smad1. Tretinoin 0-13 SMAD family member 1 Gallus gallus 112-117
20974140-0 2010 Evidence for a dynamic role of the linker histone variant H1x during retinoic acid-induced differentiation of NT2 cells. Tretinoin 69-82 H1.10 linker histone Homo sapiens 58-61
20813103-7 2010 Upon differentiation of ESCs by retinoic acid treatment or LIF deprivation, PDCD2 levels declined. Tretinoin 32-45 programmed cell death 2 Homo sapiens 76-81
20944006-5 2010 RA promoted bone marrow-derived DC production of bioactive TGF-beta by inhibiting suppressor of cytokine signaling 3 expression and thereby enhancing STAT3 activation. Tretinoin 0-2 signal transducer and activator of transcription 3 Mus musculus 150-155
20736048-8 2010 In contrast, intraperitoneal RA rendered a 60%, 35% and 58% reduction of IL-1beta, IL-6 and TNFalpha mRNA levels, respectively. Tretinoin 29-31 interleukin 1 beta Rattus norvegicus 73-81
20736048-8 2010 In contrast, intraperitoneal RA rendered a 60%, 35% and 58% reduction of IL-1beta, IL-6 and TNFalpha mRNA levels, respectively. Tretinoin 29-31 interleukin 6 Rattus norvegicus 83-87
20736048-8 2010 In contrast, intraperitoneal RA rendered a 60%, 35% and 58% reduction of IL-1beta, IL-6 and TNFalpha mRNA levels, respectively. Tretinoin 29-31 tumor necrosis factor Rattus norvegicus 92-100
20739659-0 2010 Tissue transglutaminase contributes to the all-trans-retinoic acid-induced differentiation syndrome phenotype in the NB4 model of acute promyelocytic leukemia. Tretinoin 53-66 transglutaminase 2 Homo sapiens 0-23
20739659-7 2010 CC chemokines CCL2, CCL3, CCL22, CCL24, and cytokines IL1B and IL8 involved in the development of differentiation syndrome are expressed at significantly lower level in TG2-KD NB4 than in wild-type NB4 cells upon ATRA treatment. Tretinoin 213-217 transglutaminase 2 Homo sapiens 169-172
20956305-3 2010 Here, we show that RA represses BMP signal duration by reducing the level of phosphorylated Smad1 (pSmad1). Tretinoin 19-21 SMAD family member 1 Gallus gallus 92-97
21043051-2 2010 All-trans-retinol dehydrogenase (RDH8) is an important enzyme of retinoic acid metabolism. Tretinoin 65-78 retinol dehydrogenase 8 Homo sapiens 33-37
20650878-7 2010 The RA-degrading enzyme, CYP26B1, was found to have germ cell localization and nonuniform distribution between tubules via immunohistochemistry. Tretinoin 4-6 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 25-32
21061289-6 2010 BMPR-IB and Smad5 mRNA levels increased significantly in cells cultured in OM and declined following treatment with ATRA, whereas the expression of the BMPR-IA mRNA was up-regulated by ATRA. Tretinoin 116-120 bone morphogenetic protein receptor, type 1B Mus musculus 0-7
20921526-3 2010 The myeloid-differentiating agents all-trans retinoic acid/PMA and histamine, the inflammatory mediator that inhibits promonocyte proliferation, induced an intracellular Ca(2+)-mediated PMV (as opposed to exosome) release from THP-1 promonocytes. Tretinoin 45-58 GLI family zinc finger 2 Homo sapiens 227-232
20921526-8 2010 Our in vitro findings support a model in which TGF-beta1-bearing PMVs, released from promonocytic leukemia cells (THP-1) or primary peripheral blood monocytes on exposure to sublytic complement or after treatment with a differentiation therapy agent, such as all-trans retinoic acid, significantly reduce proliferation of THP-1 cells. Tretinoin 269-282 transforming growth factor beta 1 Homo sapiens 47-56
21327094-7 2010 During in vitro granulopoiesis induced with retinoic acid, the LBR knockdown cells retain an ovoid shaped nucleus with reduced levels of lamin A/C; while, the parent cells develop highly lobulated nuclei. Tretinoin 44-57 lamin B receptor Homo sapiens 63-66
21180254-1 2010 Both retinoic acid (RA) and oxidative stress (H2O2) increased transcription and cleavage of membrane-bound sterol regulatory element-binding protein (SREBP)-1, leading to enhanced transcription of fatty acid synthase (FAS) in hepatoma cells. Tretinoin 5-18 fatty acid synthase Mus musculus 197-216
21180254-1 2010 Both retinoic acid (RA) and oxidative stress (H2O2) increased transcription and cleavage of membrane-bound sterol regulatory element-binding protein (SREBP)-1, leading to enhanced transcription of fatty acid synthase (FAS) in hepatoma cells. Tretinoin 5-18 fatty acid synthase Mus musculus 218-221
21180254-1 2010 Both retinoic acid (RA) and oxidative stress (H2O2) increased transcription and cleavage of membrane-bound sterol regulatory element-binding protein (SREBP)-1, leading to enhanced transcription of fatty acid synthase (FAS) in hepatoma cells. Tretinoin 20-22 fatty acid synthase Mus musculus 197-216
21180254-1 2010 Both retinoic acid (RA) and oxidative stress (H2O2) increased transcription and cleavage of membrane-bound sterol regulatory element-binding protein (SREBP)-1, leading to enhanced transcription of fatty acid synthase (FAS) in hepatoma cells. Tretinoin 20-22 fatty acid synthase Mus musculus 218-221
21180254-4 2010 RA (1 microM) treatment suppressed expression of SREBP-1a and FAS genes and lipid accumulation. Tretinoin 0-2 fatty acid synthase Mus musculus 62-65
20623292-0 2010 Prenatal retinoic acid upregulates pulmonary gene expression of PI3K and AKT in nitrofen-induced pulmonary hypoplasia. Tretinoin 9-22 AKT serine/threonine kinase 1 Rattus norvegicus 73-76
20943360-5 2010 Increased mRNA levels of GPx 1 were also observed in cells treated with insulin and hydrocortisone or with retinoic acid. Tretinoin 107-120 glutathione peroxidase 1 Bos taurus 25-30
20623292-6 2010 We hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PI3K and AKT in the nitrofen-induced hypoplastic lung. Tretinoin 48-50 AKT serine/threonine kinase 1 Rattus norvegicus 101-104
20711222-8 2010 ATRA increased the interaction of KLF4 with p300 by inducing KLF4 phosphorylation via activation of JNK and p38 MAPK signaling. Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 108-111
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 transforming growth factor beta 1 Homo sapiens 97-128
20623292-12 2010 RESULTS: The pulmonary gene expression levels of PI3K and AKT were significantly upregulated in nitrofen + RA group compared to nitrofen group and control + RA group (p < 0.05), whereas there were no significant differences between controls and control + RA group. Tretinoin 107-109 AKT serine/threonine kinase 1 Rattus norvegicus 58-61
20623292-12 2010 RESULTS: The pulmonary gene expression levels of PI3K and AKT were significantly upregulated in nitrofen + RA group compared to nitrofen group and control + RA group (p < 0.05), whereas there were no significant differences between controls and control + RA group. Tretinoin 157-159 AKT serine/threonine kinase 1 Rattus norvegicus 58-61
20623292-12 2010 RESULTS: The pulmonary gene expression levels of PI3K and AKT were significantly upregulated in nitrofen + RA group compared to nitrofen group and control + RA group (p < 0.05), whereas there were no significant differences between controls and control + RA group. Tretinoin 157-159 AKT serine/threonine kinase 1 Rattus norvegicus 58-61
20623292-13 2010 Immunoreactivity of PI3K and AKT was markedly increased in nitrofen + RA lungs compared to nitrofen-induced hypoplastic lungs. Tretinoin 70-72 AKT serine/threonine kinase 1 Rattus norvegicus 29-32
20623292-14 2010 CONCLUSIONS: Upregulation of PI3K and AKT genes after prenatal treatment with RA in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential in modulating lung alveologenesis by stimulating epithelial-mesenchymal interaction via PI3K-AKT signaling. Tretinoin 78-80 AKT serine/threonine kinase 1 Rattus norvegicus 38-41
20623292-14 2010 CONCLUSIONS: Upregulation of PI3K and AKT genes after prenatal treatment with RA in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential in modulating lung alveologenesis by stimulating epithelial-mesenchymal interaction via PI3K-AKT signaling. Tretinoin 78-80 AKT serine/threonine kinase 1 Rattus norvegicus 265-268
20623292-14 2010 CONCLUSIONS: Upregulation of PI3K and AKT genes after prenatal treatment with RA in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential in modulating lung alveologenesis by stimulating epithelial-mesenchymal interaction via PI3K-AKT signaling. Tretinoin 136-138 AKT serine/threonine kinase 1 Rattus norvegicus 38-41
20623292-14 2010 CONCLUSIONS: Upregulation of PI3K and AKT genes after prenatal treatment with RA in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential in modulating lung alveologenesis by stimulating epithelial-mesenchymal interaction via PI3K-AKT signaling. Tretinoin 136-138 AKT serine/threonine kinase 1 Rattus norvegicus 265-268
21129240-4 2010 Expression of CD59 on NB4 cells was determined by flow cytometry before and after treating with all trans retinoic acid (ATRA). Tretinoin 100-119 CD59 molecule (CD59 blood group) Homo sapiens 14-18
21129240-4 2010 Expression of CD59 on NB4 cells was determined by flow cytometry before and after treating with all trans retinoic acid (ATRA). Tretinoin 121-125 CD59 molecule (CD59 blood group) Homo sapiens 14-18
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 transforming growth factor beta 1 Homo sapiens 130-138
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 transforming growth factor beta 1 Homo sapiens 301-309
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 transforming growth factor beta 1 Homo sapiens 97-128
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 transforming growth factor beta 1 Homo sapiens 130-138
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 transforming growth factor beta 1 Homo sapiens 301-309
20682464-0 2010 Multiple retinoic acid response elements cooperate to enhance the inducibility of CYP26A1 gene expression in liver. Tretinoin 9-22 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 82-89
20513361-0 2010 The relative importance of CYP26A1 in hepatic clearance of all-trans retinoic acid. Tretinoin 69-82 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 27-34
20513361-2 2010 Several P450 enzymes including CYP26A1, CYP2C8, and CYP3A4 have been proposed to be responsible for RA clearance in the liver but their quantitative importance has not been demonstrated. Tretinoin 100-102 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 31-38
20513361-2 2010 Several P450 enzymes including CYP26A1, CYP2C8, and CYP3A4 have been proposed to be responsible for RA clearance in the liver but their quantitative importance has not been demonstrated. Tretinoin 100-102 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-58
20513361-6 2010 CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA. Tretinoin 46-48 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 8-14
20513361-6 2010 CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA. Tretinoin 46-48 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 16-22
20513361-6 2010 CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA. Tretinoin 46-48 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 27-33
20513361-6 2010 CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA. Tretinoin 46-48 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 168-175
20513361-7 2010 Simulations performed for livers with varying P450 expression levels over a range of RA concentrations demonstrated that at both endogenous and therapeutic concentrations of RA, CYP26A1 is the primary enzyme responsible for 4-OH RA formation clearance. Tretinoin 85-87 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 178-185
20513361-7 2010 Simulations performed for livers with varying P450 expression levels over a range of RA concentrations demonstrated that at both endogenous and therapeutic concentrations of RA, CYP26A1 is the primary enzyme responsible for 4-OH RA formation clearance. Tretinoin 174-176 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 178-185
20513361-8 2010 HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8. Tretinoin 37-39 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 178-185
20513361-8 2010 HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8. Tretinoin 37-39 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 187-193
20513361-8 2010 HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8. Tretinoin 37-39 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 199-205
20513361-10 2010 These findings suggest that CYP26A1 is the P450 isoform that should be targeted when designing RA metabolism blocking agents. Tretinoin 95-97 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 28-35
20682464-7 2010 The results support a cooperative model in which the functioning of multiple RAREs may account for the strong inducibility of CYP26A1 in liver, which, in turn, may be important physiologically for restoring retinoid homeostasis when the concentration of RA rises. Tretinoin 77-79 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 126-133
20682464-1 2010 CYP26A1, which catalyzes the oxidation of all-trans (at)-retinoic acid (RA), is induced moderately by RA in numerous tissues, but is highly responsive in liver. Tretinoin 52-70 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
20682464-1 2010 CYP26A1, which catalyzes the oxidation of all-trans (at)-retinoic acid (RA), is induced moderately by RA in numerous tissues, but is highly responsive in liver. Tretinoin 72-74 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
20682464-1 2010 CYP26A1, which catalyzes the oxidation of all-trans (at)-retinoic acid (RA), is induced moderately by RA in numerous tissues, but is highly responsive in liver. Tretinoin 102-104 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
20833365-2 2010 Previous studies have established that retinoic acid (RA) triggers ovarian germ cells to enter meiosis and thereby commit to oogenesis, whereas in the developing testis, the enzyme CYP26B1 degrades RA and germ cells are not induced to enter meiosis. Tretinoin 39-52 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 181-188
20679534-4 2010 We found that nTregs treated with atRA were resistant to Th17 and other Th cell conversion and maintained Foxp3 expression and suppressive activity in the presence of IL-6 in vitro. Tretinoin 34-38 interleukin 6 Mus musculus 167-171
20844755-6 2010 We show that hMSC treated for five days with retinoic acid (RA) in the absence of serum undergo several transcriptional changes causing an inhibition of ERK related pathways. Tretinoin 45-58 mitogen-activated protein kinase 1 Homo sapiens 153-156
20844755-6 2010 We show that hMSC treated for five days with retinoic acid (RA) in the absence of serum undergo several transcriptional changes causing an inhibition of ERK related pathways. Tretinoin 60-62 mitogen-activated protein kinase 1 Homo sapiens 153-156
20844755-8 2010 We also found that RA inhibits cell cycle progression in the presence of proliferating signals such as epidermal growth factor (EGF) combined with basic fibroblast growth factor (bFGF). Tretinoin 19-21 fibroblast growth factor 2 Homo sapiens 147-177
20844755-8 2010 We also found that RA inhibits cell cycle progression in the presence of proliferating signals such as epidermal growth factor (EGF) combined with basic fibroblast growth factor (bFGF). Tretinoin 19-21 fibroblast growth factor 2 Homo sapiens 179-183
20496179-7 2010 The results showed that celecoxib enhanced the inhibitory effect of ATRA in both COX-2 high-expressing HT-29 and COX-2 low-expressing SW480 cell lines. Tretinoin 68-72 mitochondrially encoded cytochrome c oxidase II Homo sapiens 81-86
20496179-7 2010 The results showed that celecoxib enhanced the inhibitory effect of ATRA in both COX-2 high-expressing HT-29 and COX-2 low-expressing SW480 cell lines. Tretinoin 68-72 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118
20496179-11 2010 In conclusion, celecoxib increased the expression of RARbeta and the level of cellular ATRA sensitivity through COX-2-independent mechanisms. Tretinoin 87-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 112-117
20679534-3 2010 In this study, we report a vital role of atRA in sustaining the stability and functionality of nTregs in the presence of IL-6. Tretinoin 41-45 interleukin 6 Mus musculus 121-125
20564173-3 2010 Moreover, ELF-MF- and ATRA-treated cells showed more differentiated morphological traits (a higher neurite number/cell, an increased neurite length), together with a significant increase of mRNA levels of p21(WAF1/CIP1) and cdk5 genes, both involved in neuronal differentiation. Tretinoin 22-26 cyclin dependent kinase inhibitor 1A Homo sapiens 205-208
20564173-3 2010 Moreover, ELF-MF- and ATRA-treated cells showed more differentiated morphological traits (a higher neurite number/cell, an increased neurite length), together with a significant increase of mRNA levels of p21(WAF1/CIP1) and cdk5 genes, both involved in neuronal differentiation. Tretinoin 22-26 cyclin dependent kinase inhibitor 1A Homo sapiens 209-213
20564173-3 2010 Moreover, ELF-MF- and ATRA-treated cells showed more differentiated morphological traits (a higher neurite number/cell, an increased neurite length), together with a significant increase of mRNA levels of p21(WAF1/CIP1) and cdk5 genes, both involved in neuronal differentiation. Tretinoin 22-26 cyclin dependent kinase inhibitor 1A Homo sapiens 214-218
20564173-4 2010 In addition, the expression of cyp19 gene, which is involved both in neuronal differentiation and stress response, was evaluated; cyp19 gene expression was enhanced by ATRA treatment and significantly enhanced further by ELF-MF exposure combined with ATRA. Tretinoin 168-172 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 31-36
20564173-4 2010 In addition, the expression of cyp19 gene, which is involved both in neuronal differentiation and stress response, was evaluated; cyp19 gene expression was enhanced by ATRA treatment and significantly enhanced further by ELF-MF exposure combined with ATRA. Tretinoin 168-172 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 130-135
20564173-4 2010 In addition, the expression of cyp19 gene, which is involved both in neuronal differentiation and stress response, was evaluated; cyp19 gene expression was enhanced by ATRA treatment and significantly enhanced further by ELF-MF exposure combined with ATRA. Tretinoin 251-255 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 31-36
20564173-4 2010 In addition, the expression of cyp19 gene, which is involved both in neuronal differentiation and stress response, was evaluated; cyp19 gene expression was enhanced by ATRA treatment and significantly enhanced further by ELF-MF exposure combined with ATRA. Tretinoin 251-255 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 130-135
20615082-4 2010 ATO augmented ATRA-induced RAF/MEK/ERK axis signaling, expression of CD11b and p47(PHOX), and inducible oxidative metabolism. Tretinoin 14-18 mitogen-activated protein kinase 1 Homo sapiens 35-38
20615082-4 2010 ATO augmented ATRA-induced RAF/MEK/ERK axis signaling, expression of CD11b and p47(PHOX), and inducible oxidative metabolism. Tretinoin 14-18 mitogen-activated protein kinase kinase 7 Homo sapiens 31-34
20735826-11 2010 Interestingly, we find that Gsx2, which is necessary for normal RA signaling during LGE development, is also required for Nolz1 expression, which is lost in Gsx2 knockout mice. Tretinoin 64-66 GS homeobox 2 Mus musculus 28-32
20735826-12 2010 These findings suggest that Nolz1 might act downstream of Gsx2 to regulate RA-induced neurogenesis. Tretinoin 75-77 GS homeobox 2 Mus musculus 58-62
20562004-0 2010 All-trans retinoic acid enhances the transport of phase II metabolites of benzo[a]pyrene by inducing the Breast Cancer Resistance Protein expression in Caco-2 cells. Tretinoin 10-23 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 105-137
20727175-0 2010 Retinoic acid accelerates downregulation of the Xist repressor, Oct4, and increases the likelihood of Xist activation when Tsix is deficient. Tretinoin 0-13 TSIX transcript, XIST antisense RNA Homo sapiens 123-127
20727175-7 2010 RESULTS: We compared suspension and cell-adhesion cultures in the presence or absence of RA and find that RA significantly impacts Xist expression in Tsix-mutant male cells. Tretinoin 106-108 TSIX transcript, XIST antisense RNA Homo sapiens 150-154
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 27-29 TSIX transcript, XIST antisense RNA Homo sapiens 125-129
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 41-43 TSIX transcript, XIST antisense RNA Homo sapiens 125-129
20562004-5 2010 Pre-treatment of the cells with atRA resulted in enhanced apical excretion of B[a]P-3-sulfate, a phase II metabolite of B[a]P. Gene expression analysis revealed that the Breast Cancer Resistance Protein (BCRP), an ABC-transporter known to be involved in B[a]P-3-sulfate excretion, was strongly stimulated already at low concentrations of atRA. Tretinoin 32-36 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 170-202
20562004-5 2010 Pre-treatment of the cells with atRA resulted in enhanced apical excretion of B[a]P-3-sulfate, a phase II metabolite of B[a]P. Gene expression analysis revealed that the Breast Cancer Resistance Protein (BCRP), an ABC-transporter known to be involved in B[a]P-3-sulfate excretion, was strongly stimulated already at low concentrations of atRA. Tretinoin 32-36 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 204-208
20562004-5 2010 Pre-treatment of the cells with atRA resulted in enhanced apical excretion of B[a]P-3-sulfate, a phase II metabolite of B[a]P. Gene expression analysis revealed that the Breast Cancer Resistance Protein (BCRP), an ABC-transporter known to be involved in B[a]P-3-sulfate excretion, was strongly stimulated already at low concentrations of atRA. Tretinoin 338-342 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 170-202
20562004-5 2010 Pre-treatment of the cells with atRA resulted in enhanced apical excretion of B[a]P-3-sulfate, a phase II metabolite of B[a]P. Gene expression analysis revealed that the Breast Cancer Resistance Protein (BCRP), an ABC-transporter known to be involved in B[a]P-3-sulfate excretion, was strongly stimulated already at low concentrations of atRA. Tretinoin 338-342 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 204-208
20562004-7 2010 Thus, atRA was shown to induce BCRP gene expression probably via the RAR/RXR signalling pathway, resulting in effective removal of B[a]P metabolites from intestinal cells. Tretinoin 6-10 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 31-35
19845755-2 2010 Retinoids such as retinoic acid and synthetic analogues have long been used alone or in combination with other therapies for CTCL. Tretinoin 18-31 TSPY like 2 Homo sapiens 125-129
20511343-0 2010 All-trans retinoic acid mediates DUOX2 expression and function in respiratory tract epithelium. Tretinoin 10-23 dual oxidase 2 Homo sapiens 33-38
20511343-4 2010 By comparing a respiratory tract cell line, HBE1, with primary tracheobronchial epithelial (TBE) cells, we determined that DUOX2 was significantly expressed only in cell conditions that included all-trans retinoic acid (ATRA). Tretinoin 205-218 dual oxidase 2 Homo sapiens 123-128
20511343-4 2010 By comparing a respiratory tract cell line, HBE1, with primary tracheobronchial epithelial (TBE) cells, we determined that DUOX2 was significantly expressed only in cell conditions that included all-trans retinoic acid (ATRA). Tretinoin 220-224 dual oxidase 2 Homo sapiens 123-128
20511343-5 2010 In HBE1 cells, DUOX2 mRNA increased 6-fold after ATRA treatment. Tretinoin 49-53 dual oxidase 2 Homo sapiens 15-20
20511343-6 2010 Similarly, ATRA induced a 19-fold increase in DUOX2 mRNA expression in primary TBE cells with parallel increases in DUOX protein and DUOX-mediated H(2)O(2) production as well. Tretinoin 11-15 dual oxidase 2 Homo sapiens 46-51
20511343-7 2010 In addition, DUOX2 induction by rhinovirus required the presence of ATRA. Tretinoin 68-72 dual oxidase 2 Homo sapiens 13-18
20403807-1 2010 Lipocalin-type prostaglandin D synthase (L-PGDS) catalyses the formation of prostaglandin D(2) (PGD(2)) and also functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Tretinoin 184-197 prostaglandin D2 synthase Homo sapiens 0-39
20403807-1 2010 Lipocalin-type prostaglandin D synthase (L-PGDS) catalyses the formation of prostaglandin D(2) (PGD(2)) and also functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Tretinoin 184-197 prostaglandin D2 synthase Homo sapiens 41-47
20403807-1 2010 Lipocalin-type prostaglandin D synthase (L-PGDS) catalyses the formation of prostaglandin D(2) (PGD(2)) and also functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Tretinoin 199-201 prostaglandin D2 synthase Homo sapiens 0-39
20403807-1 2010 Lipocalin-type prostaglandin D synthase (L-PGDS) catalyses the formation of prostaglandin D(2) (PGD(2)) and also functions as a transporter for lipophilic ligands, including all-trans retinoic acid (RA). Tretinoin 199-201 prostaglandin D2 synthase Homo sapiens 41-47
20403807-5 2010 Treatment with RA decreased the proliferation of L-PGDS-expressing cells by 20%, but not mock-transfected cell lines lacking L-PGDS expression. Tretinoin 15-17 prostaglandin D2 synthase Homo sapiens 49-55
20403807-6 2010 RA induced expression of a cyclin-dependent kinase inhibitor p21(Cip1) in L-PGDS-expressing cells, but not mock-transfected cells. Tretinoin 0-2 cyclin dependent kinase inhibitor 1A Homo sapiens 61-64
20403807-6 2010 RA induced expression of a cyclin-dependent kinase inhibitor p21(Cip1) in L-PGDS-expressing cells, but not mock-transfected cells. Tretinoin 0-2 cyclin dependent kinase inhibitor 1A Homo sapiens 65-69
20403807-6 2010 RA induced expression of a cyclin-dependent kinase inhibitor p21(Cip1) in L-PGDS-expressing cells, but not mock-transfected cells. Tretinoin 0-2 prostaglandin D2 synthase Homo sapiens 74-80
20403807-7 2010 Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Tretinoin 10-12 prostaglandin D2 synthase Homo sapiens 106-112
20403807-7 2010 Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Tretinoin 10-12 prostaglandin D2 synthase Homo sapiens 247-253
20403807-7 2010 Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Tretinoin 80-82 prostaglandin D2 synthase Homo sapiens 106-112
20403807-7 2010 Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Tretinoin 80-82 prostaglandin D2 synthase Homo sapiens 247-253
20403807-7 2010 Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Tretinoin 80-82 prostaglandin D2 synthase Homo sapiens 106-112
20403807-7 2010 Moreover, RA increased the transient expression of a reporter gene carrying the RA-responsive elements in L-PGDS-expressing cell lines (at least 5-fold activation), compared to the 2-fold activation in mock-transfected cell lines, suggesting that L-PGDS may increase the sensitivity to RA. Tretinoin 80-82 prostaglandin D2 synthase Homo sapiens 247-253
20403807-8 2010 Lastly, the knockdown of L-PGDS expression by RNA interference was associated with the restoration of the RA-mediated decrease in proliferation of human and mouse melanocytes. Tretinoin 106-108 prostaglandin D2 synthase Homo sapiens 25-31
20403807-9 2010 In conclusion, L-PGDS may fine-tune the RA signalling in melanocytes. Tretinoin 40-42 prostaglandin D2 synthase Homo sapiens 15-21
20338915-0 2010 Retinoic acid represses CYP7A1 expression in human hepatocytes and HepG2 cells by FXR/RXR-dependent and independent mechanisms. Tretinoin 0-13 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 24-30
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 32-38
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 265-275
20447390-9 2010 In MDA-MB-231 cells, only 2CdA, F-ara-A, and ATRA induced RAR beta 2 expression without any notable effects in combined treatment. Tretinoin 45-49 retinoic acid receptor beta Homo sapiens 58-66
20689858-2 2010 Expression of proteoglycans and tenascin-C increased after retinoic acid induction of SSEA1-positive ES (embryonic stem) cells to nestin-positive neural stem cells, and after neural differentiation, proteoglycans and tenascin-C are expressed by both neurons and astrocytes, where they surround cell bodies and processes and in certain cases show distinctive expression patterns. Tretinoin 59-72 fucosyltransferase 4 Homo sapiens 86-91
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 0-23 tumor necrosis factor Mus musculus 199-208
20655465-7 2010 Inhibition of MEK signaling downstream of NF1 restores responsiveness to RA, suggesting a therapeutic strategy to overcome RA resistance in NF1-deficient neuroblastomas. Tretinoin 73-75 neurofibromin 1 Homo sapiens 42-45
20655465-7 2010 Inhibition of MEK signaling downstream of NF1 restores responsiveness to RA, suggesting a therapeutic strategy to overcome RA resistance in NF1-deficient neuroblastomas. Tretinoin 123-125 mitogen-activated protein kinase kinase 7 Homo sapiens 14-17
20655465-7 2010 Inhibition of MEK signaling downstream of NF1 restores responsiveness to RA, suggesting a therapeutic strategy to overcome RA resistance in NF1-deficient neuroblastomas. Tretinoin 123-125 neurofibromin 1 Homo sapiens 42-45
20642825-1 2010 BACKGROUND: The novel gene HA117 is a multidrug resistance (MDR) gene expressed by all-trans retinoic acid-resistant HL-60 cells. Tretinoin 93-106 regulator of G protein signaling 6 Homo sapiens 27-32
20643338-3 2010 We showed here that direct stimulation of FDCs by bacterial products and retinoic acid synergistically enhanced the expression of the chemokine CXCL13, the survival factor BAFF, and molecules that facilitate the secretion and activation of the cytokine TGF-beta1. Tretinoin 73-86 transforming growth factor beta 1 Homo sapiens 253-262
20655465-0 2010 NF1 is a tumor suppressor in neuroblastoma that determines retinoic acid response and disease outcome. Tretinoin 59-72 neurofibromin 1 Homo sapiens 0-3
20655465-3 2010 Using a large-scale RNAi genetic screen, we identify crosstalk between the tumor suppressor NF1 and retinoic acid-induced differentiation in neuroblastoma. Tretinoin 100-113 neurofibromin 1 Homo sapiens 92-95
20655465-7 2010 Inhibition of MEK signaling downstream of NF1 restores responsiveness to RA, suggesting a therapeutic strategy to overcome RA resistance in NF1-deficient neuroblastomas. Tretinoin 73-75 mitogen-activated protein kinase kinase 7 Homo sapiens 14-17
20410509-4 2010 Treatment with an inhibitor of RA biosynthesis or a retinoic acid receptor antagonist increases gata1(+) erythroid progenitors in the posterior mesoderm of wild-type embryos and anemic cdx4(-/-) mutants, indicating a link between the cdx-hox signaling pathway and RA. Tretinoin 31-33 caudal type homeobox 4 Danio rerio 185-189
20410509-7 2010 Taken together, these data indicate that RA inhibits the commitment of mesodermal cells to hematopoietic fates, functioning downstream of cdx4 and upstream of scl. Tretinoin 41-43 caudal type homeobox 4 Danio rerio 138-142
20644631-0 2010 All-trans retinoic acid directs urothelial specification of murine embryonic stem cells via GATA4/6 signaling mechanisms. Tretinoin 10-23 GATA binding protein 4 Mus musculus 92-97
20644631-4 2010 Upon stimulation with micromolar concentrations of RA, ESCs significantly downregulated the pluripotency factor OCT-4 but markedly upregulated UP1A, UP1B, UP2, UP3A, and UP3B mRNA levels in comparison to naive ESCs and spontaneously differentiating controls. Tretinoin 51-53 uroplakin 1B Mus musculus 149-153
20644631-4 2010 Upon stimulation with micromolar concentrations of RA, ESCs significantly downregulated the pluripotency factor OCT-4 but markedly upregulated UP1A, UP1B, UP2, UP3A, and UP3B mRNA levels in comparison to naive ESCs and spontaneously differentiating controls. Tretinoin 51-53 uroplakin 3A Mus musculus 160-164
20644631-7 2010 GATA4-/- and GATA6-/- transgenic ESC lines revealed substantial attenuation of RA-mediated UP expression in comparison to wild type controls. Tretinoin 79-81 GATA binding protein 4 Mus musculus 0-5
20644631-8 2010 In addition, EMSA analysis revealed that RA treatment induced formation of transcriptional complexes containing GATA4/6 on both UP1B and UP2 promoter fragments containing putative GATA factor binding sites. Tretinoin 41-43 GATA binding protein 4 Mus musculus 112-117
20644631-8 2010 In addition, EMSA analysis revealed that RA treatment induced formation of transcriptional complexes containing GATA4/6 on both UP1B and UP2 promoter fragments containing putative GATA factor binding sites. Tretinoin 41-43 uroplakin 1B Mus musculus 128-132
20644631-9 2010 Collectively, these data suggest that RA mediates ESC specification toward a urothelial lineage via GATA4/6-dependent processes. Tretinoin 38-40 GATA binding protein 4 Mus musculus 100-105
20661723-2 2010 In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Tretinoin 117-130 Nanog homeobox Mus musculus 45-50
20661723-2 2010 In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Tretinoin 117-130 thymoma viral proto-oncogene 1 Mus musculus 98-101
20661723-2 2010 In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Tretinoin 132-134 Nanog homeobox Mus musculus 45-50
20661723-2 2010 In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Tretinoin 132-134 thymoma viral proto-oncogene 1 Mus musculus 98-101
20661723-3 2010 Nanog protein expression was transiently upregulated up to 6 h after RA treatment and then declined. Tretinoin 69-71 Nanog homeobox Mus musculus 0-5
20661723-5 2010 RA treatment of F9 cells also led to a transient and parallel increase in both Akt and glycogen synthase kinase 3beta phosphorylations. Tretinoin 0-2 thymoma viral proto-oncogene 1 Mus musculus 79-82
20661723-7 2010 These data suggest that RA-induced PI3K/Akt activation in the early stage of differentiation is required for Nanog expression, which becomes independent of PI3K/Akt signaling once the differentiation is established. Tretinoin 24-26 thymoma viral proto-oncogene 1 Mus musculus 40-43
20661723-7 2010 These data suggest that RA-induced PI3K/Akt activation in the early stage of differentiation is required for Nanog expression, which becomes independent of PI3K/Akt signaling once the differentiation is established. Tretinoin 24-26 Nanog homeobox Mus musculus 109-114
20661723-7 2010 These data suggest that RA-induced PI3K/Akt activation in the early stage of differentiation is required for Nanog expression, which becomes independent of PI3K/Akt signaling once the differentiation is established. Tretinoin 24-26 thymoma viral proto-oncogene 1 Mus musculus 161-164
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 25-29 tumor necrosis factor Mus musculus 199-208
20577838-5 2010 These data suggested that miR-146a might influence proliferation of APL cells through TGF-beta1/Smad signal transduction pathway during ATRA induction. Tretinoin 136-140 transforming growth factor beta 1 Homo sapiens 86-95
20456496-5 2010 Addition of ATRA to the medium for 48 h caused a dose-dependent increase in KRT4/KRT13 and a down-regulation of KRT2 mRNA. Tretinoin 12-16 keratin 2 Homo sapiens 112-116
20559758-4 2010 EA activated the caspase-3 pathway and enhanced the expressions of myeloid differentiation markers (CD11b, MRP-14 protein, granulocytic morphology) induced by ATRA treatment. Tretinoin 159-163 caspase 3 Homo sapiens 17-26
20432234-1 2010 Intestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naive CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). Tretinoin 160-173 integrin alpha E, epithelial-associated Mus musculus 11-16
20432234-1 2010 Intestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naive CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). Tretinoin 175-177 integrin alpha E, epithelial-associated Mus musculus 11-16
20438866-0 2010 Retinoic acid attenuates lipopolysaccharide-induced inflammatory responses by suppressing TLR4/NF-kappaB expression in rat mammary tissue. Tretinoin 0-13 toll-like receptor 4 Rattus norvegicus 90-94
20438866-3 2010 In the present study, an LPS-induced rat mastitis model and primary cultures of rat mammary epithelial cells were used to investigate the effect of retinoic acid on the TLR4/NF-kappaB signaling pathway. Tretinoin 148-161 toll-like receptor 4 Rattus norvegicus 169-173
20438866-4 2010 The data indicated that toll-like receptor 4 (TLR4) gene expression reached its peak value earlier in retinoic acid-treated rats than in the control group, and that retinoic acid significantly decreased NF-kappaB DNA binding activity and the level of IL-1beta in the mammary gland. Tretinoin 102-115 toll-like receptor 4 Rattus norvegicus 24-44
20438866-4 2010 The data indicated that toll-like receptor 4 (TLR4) gene expression reached its peak value earlier in retinoic acid-treated rats than in the control group, and that retinoic acid significantly decreased NF-kappaB DNA binding activity and the level of IL-1beta in the mammary gland. Tretinoin 102-115 toll-like receptor 4 Rattus norvegicus 46-50
20593513-4 2010 All-trans retinoic acid increased the expression of myocardin, caldesmon, 22-kDa smooth muscle cell-specific protein (SM22alpha), and SM-myosin heavy chains in rabbit bone marrow-derived mesenchymal stem cells, as detected by reverse transcription polymerase chain reaction (PCR). Tretinoin 10-23 myocardin Oryctolagus cuniculus 52-61
20438866-4 2010 The data indicated that toll-like receptor 4 (TLR4) gene expression reached its peak value earlier in retinoic acid-treated rats than in the control group, and that retinoic acid significantly decreased NF-kappaB DNA binding activity and the level of IL-1beta in the mammary gland. Tretinoin 102-115 interleukin 1 beta Rattus norvegicus 251-259
20438866-4 2010 The data indicated that toll-like receptor 4 (TLR4) gene expression reached its peak value earlier in retinoic acid-treated rats than in the control group, and that retinoic acid significantly decreased NF-kappaB DNA binding activity and the level of IL-1beta in the mammary gland. Tretinoin 165-178 toll-like receptor 4 Rattus norvegicus 24-44
20438866-4 2010 The data indicated that toll-like receptor 4 (TLR4) gene expression reached its peak value earlier in retinoic acid-treated rats than in the control group, and that retinoic acid significantly decreased NF-kappaB DNA binding activity and the level of IL-1beta in the mammary gland. Tretinoin 165-178 toll-like receptor 4 Rattus norvegicus 46-50
20438866-4 2010 The data indicated that toll-like receptor 4 (TLR4) gene expression reached its peak value earlier in retinoic acid-treated rats than in the control group, and that retinoic acid significantly decreased NF-kappaB DNA binding activity and the level of IL-1beta in the mammary gland. Tretinoin 165-178 interleukin 1 beta Rattus norvegicus 251-259
20438866-6 2010 TLR4 protein expression and NF-kappaB DNA binding activity were significantly decreased in primary rat mammary epithelial cells pretreated with 1mumol/l retinoic acid at 1h post-LPS stimulation. Tretinoin 153-166 toll-like receptor 4 Rattus norvegicus 0-4
20438866-8 2010 These findings demonstrate that direct action by retinoic acid leads to attenuation of the LPS-induced inflammatory response by suppression of the TLR4/NF-kappaB signalling system, thereby providing a novel explanation for the underlying effect proposed for retinoic acid in the protection of mammary tissue during LPS-induced acute mastitis. Tretinoin 49-62 toll-like receptor 4 Rattus norvegicus 147-151
20438866-8 2010 These findings demonstrate that direct action by retinoic acid leads to attenuation of the LPS-induced inflammatory response by suppression of the TLR4/NF-kappaB signalling system, thereby providing a novel explanation for the underlying effect proposed for retinoic acid in the protection of mammary tissue during LPS-induced acute mastitis. Tretinoin 258-271 toll-like receptor 4 Rattus norvegicus 147-151
20147703-0 2010 Liver-specific cytochrome P450 CYP2C22 is a direct target of retinoic acid and a retinoic acid-metabolizing enzyme in rat liver. Tretinoin 61-74 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 15-30
20147703-0 2010 Liver-specific cytochrome P450 CYP2C22 is a direct target of retinoic acid and a retinoic acid-metabolizing enzyme in rat liver. Tretinoin 81-94 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 15-30
20147703-1 2010 Several cytochrome P450 (CYP) enzymes catalyze the C4-hydroxylation of retinoic acid (RA), a potent inducer of cell differentiation and an agent in the treatment of several diseases. Tretinoin 71-84 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 8-23
20147703-1 2010 Several cytochrome P450 (CYP) enzymes catalyze the C4-hydroxylation of retinoic acid (RA), a potent inducer of cell differentiation and an agent in the treatment of several diseases. Tretinoin 71-84 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 25-28
20147703-1 2010 Several cytochrome P450 (CYP) enzymes catalyze the C4-hydroxylation of retinoic acid (RA), a potent inducer of cell differentiation and an agent in the treatment of several diseases. Tretinoin 86-88 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 8-23
20147703-1 2010 Several cytochrome P450 (CYP) enzymes catalyze the C4-hydroxylation of retinoic acid (RA), a potent inducer of cell differentiation and an agent in the treatment of several diseases. Tretinoin 86-88 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 25-28
20575083-4 2010 According to published reports, factors such as the proper selection of feeder cells, including ovarian granulosa cells and those which could secrete bone morphogenic protein-4 (BMP4), and the addition of retinoic acid into culture medium, could to some extent establish and improve the microenvironment ES cells rely on for differentiation into germ cells. Tretinoin 205-218 bone morphogenetic protein 4 Mus musculus 178-182
20409737-1 2010 CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA). Tretinoin 153-166 cytochrome p450 oxidoreductase Homo sapiens 9-39
20409737-1 2010 CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA). Tretinoin 153-166 cytochrome p450 oxidoreductase Homo sapiens 41-44
20409737-1 2010 CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA). Tretinoin 153-166 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 109-114
20409737-1 2010 CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA). Tretinoin 168-172 cytochrome p450 oxidoreductase Homo sapiens 9-39
20409737-1 2010 CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA). Tretinoin 168-172 cytochrome p450 oxidoreductase Homo sapiens 41-44
20409737-1 2010 CONTEXT: Cytochrome P450 oxidoreductase (POR) is an electron donor for all microsomal P450 enzymes including CYP26 involved in inactivation of all-trans retinoic acid (atRA). Tretinoin 168-172 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 109-114
20598227-0 2010 Role of acetylated p53 in regulating the expression of map2 in retinoic acid-induced P19 cells. Tretinoin 63-76 tumor protein p53 Homo sapiens 19-22
20565948-0 2010 Expression of a retinoic acid signature in circulating CD34 cells from coronary artery disease patients. Tretinoin 16-29 CD34 molecule Homo sapiens 55-59
20565948-8 2010 CONCLUSIONS: The altered gene expression profile of CD34+ cells in CAD patients was related to activation/differentiation by a retinoic acid-induced differentiation program. Tretinoin 127-140 CD34 molecule Homo sapiens 52-56
20565948-9 2010 These results suggest that circulating CD34+ cells in CAD patients are programmed by retinoic acid, leading to a reduced capacity to migrate to ischemic tissues. Tretinoin 85-98 CD34 molecule Homo sapiens 39-43
20488794-1 2010 Retinoic acid (RA), a well-known vitamin A metabolite, mediates inhibition of the IL-6-driven induction of proinflammatory Th17 cells and promotes anti-inflammatory regulatory T cell generation in the presence of TGF-beta, which is mainly regulated by dendritic cells. Tretinoin 0-13 interleukin 6 Mus musculus 82-86
20488794-1 2010 Retinoic acid (RA), a well-known vitamin A metabolite, mediates inhibition of the IL-6-driven induction of proinflammatory Th17 cells and promotes anti-inflammatory regulatory T cell generation in the presence of TGF-beta, which is mainly regulated by dendritic cells. Tretinoin 15-17 interleukin 6 Mus musculus 82-86
19965837-6 2010 In vivo-primed draining lymph node cells from vehicle-treated or ATRA-treated mice were stimulated with IRBP(1-20) and the culture supernatant fraction was harvested for assay of interferon (IFN)-gamma and IL-17 by ELISA. Tretinoin 65-69 interferon gamma Mus musculus 179-201
19965837-7 2010 RESULTS: ATRA synergised with TGF-beta to induce Foxp3(+) T regulatory cells (Treg) and reciprocally inhibited development of IL-17-producing T helper cells (Th17) induced by TGF-beta and IL-6. Tretinoin 9-13 interleukin 6 Mus musculus 188-192
19965837-8 2010 ATRA treatment reduced the severity of EAU clinically, and IFN-gamma and IL-17 production were significantly reduced in ATRA-treated mice. Tretinoin 120-124 interferon gamma Mus musculus 59-68
19965837-9 2010 CONCLUSION: These findings demonstrate that ATRA treatment ameliorates severity of EAU and reduces the Th1/Th17 responses. Tretinoin 44-48 negative elongation factor complex member C/D, Th1l Mus musculus 103-106
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 208-210 tumor protein p53 Homo sapiens 66-69
19651460-5 2010 In vitro co-culture experiments showed that RA treated THP-1 cells were more stimulatory for CD4(+) than for CD8(+) T cells, as determined by CFSE loss, in comparison to untreated THP-1 cells. Tretinoin 44-46 CD4 molecule Homo sapiens 93-96
20507357-9 2010 However, at 24 h after ATRA treatment, the expression of RARbeta, not RARalpha or RARgamma, increased significantly. Tretinoin 23-27 retinoic acid receptor, beta Rattus norvegicus 57-64
20507357-11 2010 ATRA treatment upregulated the expression of Vimentin and Stra13, while it downregulated the expression of Brachyury in MSCs. Tretinoin 0-4 T-box transcription factor T Rattus norvegicus 107-116
20484817-5 2010 We demonstrated that activation of Wnt signaling required for lung formation was dependent on local repression of its antagonist, Dickkopf homolog 1 (Dkk1), by endogenous RA. Tretinoin 171-173 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 130-148
19538480-4 2010 RA induced t-PA mRNA and proteins in a time-dependent manner in amniotic membrane explants and Wistar Institute Susan Hayflick (WISH) cells. Tretinoin 0-2 plasminogen activator, tissue type Homo sapiens 11-15
19538480-6 2010 Gene reporter assays confirmed that the RA-induced t-PA gene expression occurred through interactions of retinoid receptors (RARs and RXRs) with a DR5 response element located at -7 kb from the transcription site. Tretinoin 40-42 plasminogen activator, tissue type Homo sapiens 51-55
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 plasminogen activator, tissue type Homo sapiens 84-88
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 retinoic acid receptor beta Homo sapiens 199-207
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 119-121 plasminogen activator, tissue type Homo sapiens 84-88
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 119-121 retinoic acid receptor beta Homo sapiens 199-207
19538480-10 2010 Altogether, our results established that the RA-mediated regulation of t-PA in human foetal membranes occurred through two steps, with a major role played by RAR-beta. Tretinoin 45-47 plasminogen activator, tissue type Homo sapiens 71-75
19538480-10 2010 Altogether, our results established that the RA-mediated regulation of t-PA in human foetal membranes occurred through two steps, with a major role played by RAR-beta. Tretinoin 45-47 retinoic acid receptor beta Homo sapiens 158-166
20455087-7 2010 The RA/arsenic trioxide association, which dramatically synergizes for PML/RARA degradation but not for differentiation, rapidly clears LIC in a proteasome-dependent manner, resulting in APL eradication in murine models and patients. Tretinoin 4-6 promyelocytic leukemia Mus musculus 71-74
20512933-7 2010 The expression of i(21)VEGFR-1 in MDA-MB-231 cells was inhibited by retinoic acid. Tretinoin 68-81 fms related receptor tyrosine kinase 1 Homo sapiens 23-30
20512933-8 2010 Both, activation of Src and downregulation by retinoic acid, have been reported in other intracellular members of the Fms/Kit/PDGFR family of tyrosine kinases, particularly in the intracellular isoform of c-kit, analogous structurally to i(21)VEGFR-1 and frequently expressed in cancer cells. Tretinoin 46-59 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 205-210
20512933-8 2010 Both, activation of Src and downregulation by retinoic acid, have been reported in other intracellular members of the Fms/Kit/PDGFR family of tyrosine kinases, particularly in the intracellular isoform of c-kit, analogous structurally to i(21)VEGFR-1 and frequently expressed in cancer cells. Tretinoin 46-59 fms related receptor tyrosine kinase 1 Homo sapiens 243-250
20484817-5 2010 We demonstrated that activation of Wnt signaling required for lung formation was dependent on local repression of its antagonist, Dickkopf homolog 1 (Dkk1), by endogenous RA. Tretinoin 171-173 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 150-154
20187766-0 2010 All-trans retinoic acid ameliorates trinitrobenzene sulfonic acid-induced colitis by shifting Th1 to Th2 profile. Tretinoin 0-23 negative elongation factor complex member C/D, Th1l Mus musculus 94-97
20187766-2 2010 Recently, all-trans retinoic acid has been shown that can lead T-cell response by suppressing Th17 development via retinoic acid receptor (RAR), but it is still unknown whether all-trans retinoic acid can modulate Th1 response of inflammatory bowel disease. Tretinoin 10-33 negative elongation factor complex member C/D, Th1l Mus musculus 94-97
19937743-9 2010 Thus, the specific defects in spermiogenesis in RARalpha-deficient testes may correlate with a disrupted cyclic expression of RA-responsive structural components, including vimentin, a downregulation of connexin-40 in spermatogenic cells, and delayed assembly of ZO-1 into Sertoli cell tight junctions. Tretinoin 48-50 tight junction protein 1 Mus musculus 263-267
21204008-6 2010 Knockdown of PGRN in SH-SY5Y cells impaired retinoic acid induced differentiation and reduced the level of phosphorylated GSK-3beta. Tretinoin 44-57 granulin precursor Homo sapiens 13-17
20123735-3 2010 All-trans-retinoic acid (tRA) is a potent ligand that enhances NIS expression in a subset of breast cancer cell lines and in experimental breast cancer models. Tretinoin 0-23 solute carrier family 5 member 5 Homo sapiens 63-66
20123735-3 2010 All-trans-retinoic acid (tRA) is a potent ligand that enhances NIS expression in a subset of breast cancer cell lines and in experimental breast cancer models. Tretinoin 25-28 solute carrier family 5 member 5 Homo sapiens 63-66
20215638-2 2010 We investigated ATRA-induced cellular responses mediated by the transcription factor FOXO3A in APL cells. Tretinoin 16-20 forkhead box O3 Homo sapiens 85-91
20428830-5 2010 These results were paralleled with the pattern of p21 Waf1/Cip1 induction by the treatment of RA in combination with ionizing radiation (IR). Tretinoin 94-96 cyclin dependent kinase inhibitor 1A Homo sapiens 59-63
20421479-3 2010 In this study, we show that Ag-specific memory Th cells were redifferentiated into Foxp3(+) T cells by TGF-beta when stimulated in the presence of all-trans retinoic acid and rapamycin. Tretinoin 157-170 transforming growth factor beta 1 Homo sapiens 103-111
20348100-4 2010 Forkhead family member Foxa1 is activated by retinoic acid treatment of embryonic stem cells, binds its DNA consensus site within the short interspersed transposable/medium reiterated sequence 1 elements, and displaces linker histone H1 from silent Afp chromatin. Tretinoin 45-58 alpha fetoprotein Homo sapiens 249-252
20215638-4 2010 Upon treating the cells with ATRA, FOXO3A phosphorylation was reduced and FOXO3A translocated into the nucleus. Tretinoin 29-33 forkhead box O3 Homo sapiens 35-41
20215638-4 2010 Upon treating the cells with ATRA, FOXO3A phosphorylation was reduced and FOXO3A translocated into the nucleus. Tretinoin 29-33 forkhead box O3 Homo sapiens 74-80
20215638-6 2010 As expected, transfection of a short hairpin RNA (shRNA) oligonucleotide specific for FOXO3A significantly inhibited ATRA-induced granulocytic differentiation and apoptosis in NB4 cells. Tretinoin 117-121 forkhead box O3 Homo sapiens 86-92
20215638-9 2010 We conclude that activation of FOXO3A is an essential event for ATRA-induced cellular responses in NB4 cells. Tretinoin 64-68 forkhead box O3 Homo sapiens 31-37
20215638-10 2010 FOXO3A is a promising target for therapeutic approaches to overcome ATRA resistance in APL. Tretinoin 68-72 forkhead box O3 Homo sapiens 0-6
20225234-7 2010 The inhibition of the PI3K/Akt pathway by Ly294002 abrogated the protective effects induced by either Epo or atRA. Tretinoin 109-113 AKT serine/threonine kinase 1 Homo sapiens 27-30
20074641-4 2010 Retinoic acid induces neuronal differentiation as revealed by the increased expression of MAP2, the decreased cell doubling rate, and the gain in neuronal morphological features and these events are accompanied by the increased expression level of PKC delta and p67(phox), one of the components of NADPH oxidase. Tretinoin 0-13 CD33 molecule Homo sapiens 262-265
20074641-6 2010 Moreover, using rottlerin to inhibit PKC delta or transfection experiments to overexpress it, we show that retinoic acid acts through this enzyme to induce MAP2 expression and to increase p67(phox) membrane translocation leading to NADPH oxidase activation. Tretinoin 107-120 CD33 molecule Homo sapiens 188-191
20439172-4 2010 Activation of adenosine monophosphate-activated kinase (AMPK) induced by retinoic acid in differentiating cells was blocked by As. Tretinoin 73-86 protein kinase, AMP-activated, alpha 1 catalytic subunit Mus musculus 56-60
20225234-8 2010 The effect of atRA was mediated by an increased expression of Bcl-2 whereas the Epo treatment upregulated not only Bcl-2 but also Bcl-xL. Tretinoin 14-18 BCL2 apoptosis regulator Homo sapiens 62-67
20225234-13 2010 The results allow us to suggest that this differential cell behavior can be ascribed to the interaction between atRA and the signaling pathways mediated by Epo. Tretinoin 112-116 erythropoietin Homo sapiens 156-159
20032991-8 2010 A protein induced by both p-DDAP and RA was identified as cytokeratin 16. Tretinoin 37-39 keratin 16 Mus musculus 58-72
20032991-11 2010 An increase in cytokeratin 16 expression might be essential for the effects of both p-DDAP and RA in skin healing and maintenance. Tretinoin 95-97 keratin 16 Mus musculus 15-29
20106871-6 2010 Wnt-4 may control meiosis via these proteins since the Cyp26b1 enzyme is known to degrade retinoic acid (RA) and inhibit meiosis in the male embryo, and Stra8 induces meiosis in the female through RA. Tretinoin 90-103 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 55-62
20346917-0 2010 Curcumin dramatically enhances retinoic acid-induced superoxide generating activity via accumulation of p47-phox and p67-phox proteins in U937 cells. Tretinoin 31-44 CD33 molecule Homo sapiens 117-120
20060826-9 2010 In retinoic acid-induced granulocytic differentiation, the activation of ERK and upregulation of tescalcin occurs slowly (16-48 h). Tretinoin 3-16 mitogen-activated protein kinase 1 Homo sapiens 73-76
20134361-8 2010 RESULTS: Mouse sutures were found to express genes necessary for retinoic acid synthesis, binding, and signal transduction, demonstrated by quantitative real-time polymerase chain reaction (Raldh1, Raldh2, Raldh3, and Rbp4). Tretinoin 65-78 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 206-212
20172853-0 2010 All-trans-retinoic acid promotes trafficking of human concentrative nucleoside transporter-3 (hCNT3) to the plasma membrane by a TGF-beta1-mediated mechanism. Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 129-138
20346917-6 2010 On the other hand, immunoblot analysis revealed that co-treatment with RA and curcumin caused remarkable accumulation of protein levels of p47-phox (to 7-fold) and p67-phox (to 4-fold) compared with those of the RA-treatment alone. Tretinoin 71-73 CD33 molecule Homo sapiens 164-167
20346917-7 2010 These results suggested that curcumin dramatically enhances RA-induced O(2)(-)-generating activity via accumulation of cytosolic p47-phox and p67-phox proteins in U937 cells. Tretinoin 60-62 CD33 molecule Homo sapiens 142-145
20179325-5 2010 Using preadipocytes and mesenchymal stem cell models, we show that RA specifically blocks the occupancy of C/EBPbeta of the Cebpa promoter, thereby abrogating the differentiation process. Tretinoin 67-69 CCAAT enhancer binding protein alpha Homo sapiens 124-129
24281085-2 2010 Midkine (MK), a plasma secreted protein, was initially identified in embryonal carcinoma cells at early stages of retinoic acid-induced differentiation. Tretinoin 114-127 midkine Homo sapiens 0-7
24281085-2 2010 Midkine (MK), a plasma secreted protein, was initially identified in embryonal carcinoma cells at early stages of retinoic acid-induced differentiation. Tretinoin 114-127 midkine Homo sapiens 9-11
20106871-6 2010 Wnt-4 may control meiosis via these proteins since the Cyp26b1 enzyme is known to degrade retinoic acid (RA) and inhibit meiosis in the male embryo, and Stra8 induces meiosis in the female through RA. Tretinoin 105-107 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 55-62
19914251-0 2010 Lack of retinoic acid leads to increased langerin-expressing dendritic cells in gut-associated lymphoid tissues. Tretinoin 8-21 CD207 antigen Mus musculus 41-49
20405022-0 2010 All-trans retinoic acid regulates the expression of the extracellular matrix protein fibulin-1 in the guinea pig sclera and human scleral fibroblasts. Tretinoin 10-23 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 85-94
20405022-3 2010 Our purpose was to confirm the presence of fibulin-1 protein in guinea pig sclera and investigate the effect of RA on the expression of fibulin-1 in guinea pig sclera in vivo and in cultured human scleral fibroblasts (HSFs). Tretinoin 112-114 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 136-145
20405022-5 2010 The effects of RA (from 10(-9) to 10(-5) M) on fibulin-1 expression in HSFs were observed by immunohistochemistry and assayed by real-time PCR and western blot analysis. Tretinoin 15-17 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 47-56
20405022-7 2010 Upregulation of fibulin-1 in scleral tissue was observed after feeding with RA. Tretinoin 76-78 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 16-25
20405022-8 2010 In vitro, the level of Fbln1 mRNA was increased after treatment of HSFs with RA (at concentrations of 10(-8) to 10(-6) M; p<0.001), with a maximum effect at 10(-7) M. Fibulin-1 protein levels were significantly increased after treatment of HSFs with 10(-7) M of RA for 24 or 48 h (p<0.05). Tretinoin 77-79 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 23-28
20405022-8 2010 In vitro, the level of Fbln1 mRNA was increased after treatment of HSFs with RA (at concentrations of 10(-8) to 10(-6) M; p<0.001), with a maximum effect at 10(-7) M. Fibulin-1 protein levels were significantly increased after treatment of HSFs with 10(-7) M of RA for 24 or 48 h (p<0.05). Tretinoin 77-79 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 170-179
20405022-8 2010 In vitro, the level of Fbln1 mRNA was increased after treatment of HSFs with RA (at concentrations of 10(-8) to 10(-6) M; p<0.001), with a maximum effect at 10(-7) M. Fibulin-1 protein levels were significantly increased after treatment of HSFs with 10(-7) M of RA for 24 or 48 h (p<0.05). Tretinoin 265-267 LOW QUALITY PROTEIN: fibulin-1 Cavia porcellus 23-28
20386594-0 2010 Retinoic acid mediates regulation of network formation by COUP-TFII and VE-cadherin expression by TGFbeta receptor kinase in breast cancer cells. Tretinoin 0-13 nuclear receptor subfamily 2 group F member 2 Homo sapiens 58-67
20386594-0 2010 Retinoic acid mediates regulation of network formation by COUP-TFII and VE-cadherin expression by TGFbeta receptor kinase in breast cancer cells. Tretinoin 0-13 cadherin 5 Homo sapiens 72-83
20386594-0 2010 Retinoic acid mediates regulation of network formation by COUP-TFII and VE-cadherin expression by TGFbeta receptor kinase in breast cancer cells. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 98-105
20386594-3 2010 Our previous studies showed that retinoic acid (RA) treatment converts a subset of breast cancer cells into cells with significant endothelial genotypic and phenotypic elements including marked induction of VE-cadherin, which was responsible for some but not all morphological changes. Tretinoin 33-46 cadherin 5 Homo sapiens 207-218
20386594-3 2010 Our previous studies showed that retinoic acid (RA) treatment converts a subset of breast cancer cells into cells with significant endothelial genotypic and phenotypic elements including marked induction of VE-cadherin, which was responsible for some but not all morphological changes. Tretinoin 48-50 cadherin 5 Homo sapiens 207-218
20386594-4 2010 The present study demonstrates that of the endothelial-related genes induced by RA treatment, only a few were affected by knockdown of VE-cadherin, ruling it out as a regulator of the RA-induced endothelial genotypic switch. Tretinoin 184-186 cadherin 5 Homo sapiens 135-146
20386594-6 2010 Two pan-kinase inhibitors markedly blocked RA-induced VE-cadherin expression and cell fusion. Tretinoin 43-45 cadherin 5 Homo sapiens 54-65
20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 63-65 transforming growth factor beta 1 Homo sapiens 21-28
20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 135-137 transforming growth factor beta 1 Homo sapiens 21-28
20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 135-137 transforming growth factor beta 1 Homo sapiens 98-105
20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 135-137 cadherin 5 Homo sapiens 146-157
20386594-9 2010 Together these data indicate a role for the TGFbeta pathway and COUP-TFII in mediating the endothelial transdifferentiating properties of RA. Tretinoin 138-140 transforming growth factor beta 1 Homo sapiens 44-51
20386594-9 2010 Together these data indicate a role for the TGFbeta pathway and COUP-TFII in mediating the endothelial transdifferentiating properties of RA. Tretinoin 138-140 nuclear receptor subfamily 2 group F member 2 Homo sapiens 64-73
20096012-8 2010 Pretreatment of AML cells with ATRA, causing downregulation of 67LR, rendered these cells resistant to EGCG-mediated cell death. Tretinoin 31-35 ribosomal protein SA Homo sapiens 63-67
20096012-9 2010 In summary, it was found that (i) DAPK2 is essential for EGCG-induced cell death in AML cells, (ii) ATRA and EGCG cotreatment significantly boosted neutrophil differentiation, and 67LR expression correlates with susceptibility of AML cells to EGCG. Tretinoin 100-104 ribosomal protein SA Homo sapiens 180-184
19778331-0 2010 Changes in cell characteristics due to retinoic acid; specifically, a decrease in the expression of claudin-1 and increase in claudin-4 within tight junctions in stratified oral keratinocytes. Tretinoin 39-52 claudin 4 Homo sapiens 126-135
19932628-5 2010 The silencing of PKC-delta prevented the RA-induced inhibition of the secretion and synthesis of IGF-I and cell viability (p<0.05). Tretinoin 41-43 insulin like growth factor 1 Homo sapiens 97-102
19932628-8 2010 These antioxidants also reversed the RA-induced inhibition of the secretion and synthesis of IGF-I and cell viability to control levels (p<0.05). Tretinoin 37-39 insulin like growth factor 1 Homo sapiens 93-98
19932628-10 2010 These results indicate that the anticancer effects of RA are mediated by inhibition of the secretion and synthesis of IGF-I, and involve a PKC-delta-dependent mechanism, and they provide evidence of an interaction between PKC-delta and reactive oxygen species. Tretinoin 54-56 insulin like growth factor 1 Homo sapiens 118-123
19932628-0 2010 Oxidative stress in MCF-7 cells is involved in the effects of retinoic acid-induced activation of protein kinase C-delta on insulin-like growth factor-I secretion and synthesis. Tretinoin 62-75 insulin like growth factor 1 Homo sapiens 124-152
19932628-4 2010 RA at 10(-8)M and 10(-7)M increased PKC-delta phosphorylation (the ratio of phosphorylated to total PKC-delta) (p<0.05) and decreased the secretion and synthesis of IGF-I (p<0.05) compared to control, with the effects peaking for treatment with 10(-7)M RA for 72h. Tretinoin 0-2 insulin like growth factor 1 Homo sapiens 168-173
19778331-6 2010 The RT-PCR showed that retinoic acid significantly reduced the expression of claudin-1 mRNA, whereas it dramatically enhanced expression of claudin-4 mRNA. Tretinoin 23-36 claudin 4 Homo sapiens 140-149
19778331-8 2010 In the culture with retinoic acid, the flattened uppermost cells were absent and there claudin-1 was less present, but claudin-4 was prominently present in all layers. Tretinoin 20-33 claudin 4 Homo sapiens 119-128
19778331-10 2010 Along with the change of claudin species, the expressions of keratin 7, keratin 8 and keratin 18, as markers for the simple epithelium, were clearly stimulated by retinoic acid. Tretinoin 163-176 keratin 7 Homo sapiens 61-70
19778331-11 2010 CONCLUSION: Retinoic acid changed the expression of tight junction constituent molecules, such as claudin-1 and claudin-4, in oral keratinocytes. Tretinoin 12-25 claudin 4 Homo sapiens 112-121
20197308-0 2010 Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways. Tretinoin 91-104 insulin Homo sapiens 0-10
19883939-6 2010 DCs cultured with ATRA induced the differentiation of naive T cells towards a helper T cell type 2 (Th2) response and expansion of CD4(+)CD25(+)Foxp3(+) regulatory T cells. Tretinoin 18-22 CD4 molecule Homo sapiens 131-134
19882109-8 2010 We assessed the involvement of protein kinases and found that p38 signaling was activated in undifferentiated after nucleotide stimulation, but abolished by the differentiating RA pretreatment. Tretinoin 177-179 mitogen-activated protein kinase 14 Homo sapiens 62-65
19882109-10 2010 Taken together, our results suggest that RA treatment of human SH-SY5Y cells leads to decreased P2X(7) nucleotide receptor protein expression thus protecting differentiated cells from extracellular nucleotide-induced neuronal death, and p38 signaling pathway is critically involved in this protection of RA-differentiated cells. Tretinoin 41-43 mitogen-activated protein kinase 14 Homo sapiens 237-240
20200558-6 2010 Co-treatment with a pharmacologic inhibitor of PRKCD and RA resulted in the induction of an RA responsive reporter construct, as well as the endogenous RA target genes, CEBPE, CYP26A1 and RIG-I. Tretinoin 57-59 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 176-183
20197308-0 2010 Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways. Tretinoin 91-104 insulin Homo sapiens 11-20
20197308-0 2010 Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways. Tretinoin 91-104 transforming growth factor beta 1 Homo sapiens 60-69
20197308-10 2010 We confirmed a role for RA in reversal of TGF-beta1-induced changes associated with epithelial-mesenchymal transition, including expression changes in Snail, E-cadherin, vimetin, and redistribution of beta-catenin. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 42-51
20197308-10 2010 We confirmed a role for RA in reversal of TGF-beta1-induced changes associated with epithelial-mesenchymal transition, including expression changes in Snail, E-cadherin, vimetin, and redistribution of beta-catenin. Tretinoin 24-26 snail family transcriptional repressor 1 Homo sapiens 151-156
20197308-10 2010 We confirmed a role for RA in reversal of TGF-beta1-induced changes associated with epithelial-mesenchymal transition, including expression changes in Snail, E-cadherin, vimetin, and redistribution of beta-catenin. Tretinoin 24-26 cadherin 1 Homo sapiens 158-168
20118242-6 2010 To determine the molecular mechanism through which retinoic acid induced miR-10a expression, a consensus NF-kappaB element was identified in the miR-10a gene promoter by bioinformatics analysis, and chromatin immunoprecipitation assay confirmed that NF-kappaB could bind to this element. Tretinoin 51-64 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 105-114
20118242-6 2010 To determine the molecular mechanism through which retinoic acid induced miR-10a expression, a consensus NF-kappaB element was identified in the miR-10a gene promoter by bioinformatics analysis, and chromatin immunoprecipitation assay confirmed that NF-kappaB could bind to this element. Tretinoin 51-64 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 250-259
20167204-5 2010 In animal cap explant assay, we further demonstrated that mkrn2(s)-7 not only inhibits activin and retinoic acid-induced animal cap neuralization and the expression of a pan-neural marker neural cell adhesion molecule, but also induces GSK-3beta expression. Tretinoin 99-112 glycogen synthase kinase 3 beta L homeolog Xenopus laevis 236-245
20212135-2 2010 We now describe an experimental system in which the pluripotency genes Sox2 and Oct4 are repressed in retinoic acid-treated ES cells but are reprogrammed up to 100% within 24 h by injection of nuclei into the germinal vesicle (GV) of growing Xenopus oocytes. Tretinoin 102-115 SRY-box 2 L homeolog Xenopus laevis 71-75
20179094-3 2010 Retinoic acid also induces differentiation in many cellular contexts, but its mechanism of action in relation to Fgf/Erk signalling in ES cells is poorly understood. Tretinoin 0-13 mitogen-activated protein kinase 1 Mus musculus 117-120
20026169-5 2010 The role of Nrf2 was confirmed using retinoic acid as an inhibitor of Nrf2. Tretinoin 37-50 NFE2 like bZIP transcription factor 2 Homo sapiens 12-16
20026169-5 2010 The role of Nrf2 was confirmed using retinoic acid as an inhibitor of Nrf2. Tretinoin 37-50 NFE2 like bZIP transcription factor 2 Homo sapiens 70-74
20043900-2 2010 Exogenous RA produces a teratogenic effect on limb morphology; similarly, changes in the endogenous distribution of RA following genetic ablation of the RA-metabolizing enzyme, CYP26B1, result in phocomelia accompanied by changes in expression of proximo-distal (P-D) patterning genes, increased cell death, and delayed chondrocyte maturation. Tretinoin 116-118 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 177-184
20043900-2 2010 Exogenous RA produces a teratogenic effect on limb morphology; similarly, changes in the endogenous distribution of RA following genetic ablation of the RA-metabolizing enzyme, CYP26B1, result in phocomelia accompanied by changes in expression of proximo-distal (P-D) patterning genes, increased cell death, and delayed chondrocyte maturation. Tretinoin 116-118 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 177-184
20043900-5 2010 This model reveals two genetically separable effects of RA in the limb: an apoptotic effect mediated by RARgamma in the presence of ectopic RA, and a P-D patterning defect which is uncovered following the loss of both CYP26B1 and RARgamma. Tretinoin 56-58 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 218-225
20171952-5 2010 When these cells were cultured with adding retinoic acid, expression of odd-skipped related 1 (Osr1), which is essential to IM differentiation, was enhanced. Tretinoin 43-56 odd-skipped related transcription factor 1 Mus musculus 72-93
20171952-5 2010 When these cells were cultured with adding retinoic acid, expression of odd-skipped related 1 (Osr1), which is essential to IM differentiation, was enhanced. Tretinoin 43-56 odd-skipped related transcription factor 1 Mus musculus 95-99
20068222-0 2010 Skin-draining lymph nodes contain dermis-derived CD103(-) dendritic cells that constitutively produce retinoic acid and induce Foxp3(+) regulatory T cells. Tretinoin 102-115 integrin alpha E, epithelial-associated Mus musculus 49-54
20068222-1 2010 Small intestinal CD103(+) dendritic cells (DCs) have the selective ability to promote de novo generation of regulatory T cells via the production of retinoic acid (RA). Tretinoin 149-162 integrin alpha E, epithelial-associated Mus musculus 17-22
20068222-1 2010 Small intestinal CD103(+) dendritic cells (DCs) have the selective ability to promote de novo generation of regulatory T cells via the production of retinoic acid (RA). Tretinoin 164-166 integrin alpha E, epithelial-associated Mus musculus 17-22
20068222-5 2010 Unexpectedly, the production of RA by skin DCs was restricted to CD103(-) DCs, indicating that CD103 expression does not constitute a "universal" marker for RA-producing mouse DCs. Tretinoin 32-34 integrin alpha E, epithelial-associated Mus musculus 65-70
20043900-0 2010 Analysis of Cyp26b1/Rarg compound-null mice reveals two genetically separable effects of retinoic acid on limb outgrowth. Tretinoin 89-102 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 12-19
20179094-6 2010 However, more gradual repression of Fgf4 by retinoic acid is accompanied by an overall reduction in Erk activity on day 2, and the acquisition of neural and non-neural fates is now advanced by inhibition of Fgf signalling. Tretinoin 44-57 fibroblast growth factor 4 Mus musculus 36-40
19957374-6 2010 Positional cloning indicated that the hio mutation affects the raldh2 gene encoding retinaldehyde dehydrogenase type2 (RALDH2), the enzyme principally responsible for retinoic acid (RA) biosynthesis. Tretinoin 167-180 retinal dehydrogenase 2 Oryzias latipes 63-69
19957374-0 2010 Retinoic acid signaling positively regulates liver specification by inducing wnt2bb gene expression in medaka. Tretinoin 0-13 wingless-type MMTV integration site family, member 2Bb Oryzias latipes 77-83
19957374-6 2010 Positional cloning indicated that the hio mutation affects the raldh2 gene encoding retinaldehyde dehydrogenase type2 (RALDH2), the enzyme principally responsible for retinoic acid (RA) biosynthesis. Tretinoin 167-180 retinal dehydrogenase 2 Oryzias latipes 84-117
19957374-6 2010 Positional cloning indicated that the hio mutation affects the raldh2 gene encoding retinaldehyde dehydrogenase type2 (RALDH2), the enzyme principally responsible for retinoic acid (RA) biosynthesis. Tretinoin 167-180 retinal dehydrogenase 2 Oryzias latipes 119-125
19957374-6 2010 Positional cloning indicated that the hio mutation affects the raldh2 gene encoding retinaldehyde dehydrogenase type2 (RALDH2), the enzyme principally responsible for retinoic acid (RA) biosynthesis. Tretinoin 119-121 retinal dehydrogenase 2 Oryzias latipes 63-69
19957374-6 2010 Positional cloning indicated that the hio mutation affects the raldh2 gene encoding retinaldehyde dehydrogenase type2 (RALDH2), the enzyme principally responsible for retinoic acid (RA) biosynthesis. Tretinoin 119-121 retinal dehydrogenase 2 Oryzias latipes 84-117
19957374-9 2010 CONCLUSION: Our data reveal the unexpected finding that RA signaling positively regulates the wnt2bb gene expression required for liver specification in medaka. Tretinoin 56-58 wingless-type MMTV integration site family, member 2Bb Oryzias latipes 94-100
19935721-2 2010 Here, we found that CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, is highly expressed in 42% (27/65) of primary breast cancers. Tretinoin 123-136 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 20-27
20450766-0 2010 [Alteration of the expression ratio between WT1 gene and its isomers during all-trans retinoic acid-induced differentiation of HL-60 cells]. Tretinoin 86-99 WT1 transcription factor Homo sapiens 44-47
20450766-1 2010 OBJECTIVE: To explore expression ratio alteration between WT1 gene and its isomers during differentiation of leukemia cell line HL-60 induced by all-trans retinoic acid (ATRA) and the relationship existed between them. Tretinoin 155-168 WT1 transcription factor Homo sapiens 58-61
20450766-1 2010 OBJECTIVE: To explore expression ratio alteration between WT1 gene and its isomers during differentiation of leukemia cell line HL-60 induced by all-trans retinoic acid (ATRA) and the relationship existed between them. Tretinoin 170-174 WT1 transcription factor Homo sapiens 58-61
19935721-2 2010 Here, we found that CYP26A1, the gene encoding a cytochrome P450 enzyme specifically involved in metabolic inactivation of retinoic acid (RA), the most active vitamin A derivative, is highly expressed in 42% (27/65) of primary breast cancers. Tretinoin 138-140 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 20-27
19935721-5 2010 Suppression of CYP26A1 significantly reversed the CYP26A1-mediated oncogenic characteristics, suggesting a direct link between intracellular RA status and tumorigenicity. Tretinoin 141-143 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-22
19935721-5 2010 Suppression of CYP26A1 significantly reversed the CYP26A1-mediated oncogenic characteristics, suggesting a direct link between intracellular RA status and tumorigenicity. Tretinoin 141-143 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 50-57
19960509-4 2010 In GnT-V-AS/7721 cells with ATRA treatment, a significant elevation of intracellular homocysteine levels suggests that ATRA perturbs homocysteine metabolism in GnT-V-AS/7721 cells and, therefore, sensitizes the cells to homocysteine-induced ER stress. Tretinoin 28-32 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 3-8
19960509-0 2010 All-trans-retinoic acid intensifies endoplasmic reticulum stress in N-acetylglucosaminyltransferase V repressed human hepatocarcinoma cells by perturbing homocysteine metabolism. Tretinoin 0-23 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 68-101
20164929-5 2010 Furthermore, the knockdown of Nr2f2 and/or Rere decreases retinoic acid signalling, suggesting that this complex is required to promote transcriptional activation of retinoic acid targets. Tretinoin 58-71 nuclear receptor subfamily 2 group F member 2 Homo sapiens 30-35
20164929-5 2010 Furthermore, the knockdown of Nr2f2 and/or Rere decreases retinoic acid signalling, suggesting that this complex is required to promote transcriptional activation of retinoic acid targets. Tretinoin 166-179 nuclear receptor subfamily 2 group F member 2 Homo sapiens 30-35
20164929-6 2010 The asymmetrical expression of Nr2f2 in the presomitic mesoderm overlaps with the asymmetry of the retinoic acid signalling response, supporting its implication in the control of somitic symmetry. Tretinoin 99-112 nuclear receptor subfamily 2 group F member 2 Homo sapiens 31-36
19960509-1 2010 We previously reported that all-trans-retinoic acid (ATRA) induced apoptosis in N-acetylglucosaminyltransferase V (GnT-V) repressed human hepatocarcinoma 7721 (GnT-V-AS/7721) cells via endoplasmic reticulum (ER) stress. Tretinoin 28-51 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 80-113
19960509-1 2010 We previously reported that all-trans-retinoic acid (ATRA) induced apoptosis in N-acetylglucosaminyltransferase V (GnT-V) repressed human hepatocarcinoma 7721 (GnT-V-AS/7721) cells via endoplasmic reticulum (ER) stress. Tretinoin 28-51 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 115-120
19960509-1 2010 We previously reported that all-trans-retinoic acid (ATRA) induced apoptosis in N-acetylglucosaminyltransferase V (GnT-V) repressed human hepatocarcinoma 7721 (GnT-V-AS/7721) cells via endoplasmic reticulum (ER) stress. Tretinoin 28-51 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 160-165
19960509-1 2010 We previously reported that all-trans-retinoic acid (ATRA) induced apoptosis in N-acetylglucosaminyltransferase V (GnT-V) repressed human hepatocarcinoma 7721 (GnT-V-AS/7721) cells via endoplasmic reticulum (ER) stress. Tretinoin 53-57 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 80-113
19960509-1 2010 We previously reported that all-trans-retinoic acid (ATRA) induced apoptosis in N-acetylglucosaminyltransferase V (GnT-V) repressed human hepatocarcinoma 7721 (GnT-V-AS/7721) cells via endoplasmic reticulum (ER) stress. Tretinoin 53-57 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 115-120
19960509-1 2010 We previously reported that all-trans-retinoic acid (ATRA) induced apoptosis in N-acetylglucosaminyltransferase V (GnT-V) repressed human hepatocarcinoma 7721 (GnT-V-AS/7721) cells via endoplasmic reticulum (ER) stress. Tretinoin 53-57 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 160-165
19960509-2 2010 In addition to confirming these findings, we further found that ATRA repressed the expression of betaine-homocysteine methyltransferase (BHMT) and cystathionine-beta-synthase (CBS), which are key enzymes that are involved in homocysteine metabolism, increased the level of intracellular homocysteine, and decreased the glutathione (GSH) level in GnT-V-AS/7721 cells. Tretinoin 64-68 cystathionine beta-synthase Homo sapiens 147-174
19960509-2 2010 In addition to confirming these findings, we further found that ATRA repressed the expression of betaine-homocysteine methyltransferase (BHMT) and cystathionine-beta-synthase (CBS), which are key enzymes that are involved in homocysteine metabolism, increased the level of intracellular homocysteine, and decreased the glutathione (GSH) level in GnT-V-AS/7721 cells. Tretinoin 64-68 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 346-351
19960509-4 2010 In GnT-V-AS/7721 cells with ATRA treatment, a significant elevation of intracellular homocysteine levels suggests that ATRA perturbs homocysteine metabolism in GnT-V-AS/7721 cells and, therefore, sensitizes the cells to homocysteine-induced ER stress. Tretinoin 28-32 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 160-165
19960509-4 2010 In GnT-V-AS/7721 cells with ATRA treatment, a significant elevation of intracellular homocysteine levels suggests that ATRA perturbs homocysteine metabolism in GnT-V-AS/7721 cells and, therefore, sensitizes the cells to homocysteine-induced ER stress. Tretinoin 119-123 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 3-8
19960509-4 2010 In GnT-V-AS/7721 cells with ATRA treatment, a significant elevation of intracellular homocysteine levels suggests that ATRA perturbs homocysteine metabolism in GnT-V-AS/7721 cells and, therefore, sensitizes the cells to homocysteine-induced ER stress. Tretinoin 119-123 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 160-165
19960509-6 2010 Furthermore, we observed that ATRA blunted the homocysteine-induced increase of GSH only in GnT-V-AS/7721 cells. Tretinoin 30-34 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 92-97
19960509-7 2010 These results demonstrate that ATRA intensifies ER stress and induces apoptosis in GnT-V-AS/7721 cells by disturbing homocysteine metabolism through the down-regulation of CBS and BHMT, depleting the cellular GSH and, in turn, altering the cellular redox status. Tretinoin 31-35 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 83-88
20034106-2 2010 Here, we report that the RA-generating enzyme retinaldehyde dehydrogenase-2 (Raldh2) is expressed in the interdigital mesenchyme whereas Cyp26b1, controlling RA degradation, is expressed in digits, limiting autopodal RA action to the interdigital zones. Tretinoin 158-160 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 137-144
20034106-2 2010 Here, we report that the RA-generating enzyme retinaldehyde dehydrogenase-2 (Raldh2) is expressed in the interdigital mesenchyme whereas Cyp26b1, controlling RA degradation, is expressed in digits, limiting autopodal RA action to the interdigital zones. Tretinoin 158-160 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 137-144
20034106-0 2010 Retinoic acid controls expression of tissue remodeling genes Hmgn1 and Fgf18 at the digit-interdigit junction. Tretinoin 0-13 fibroblast growth factor 18 Mus musculus 71-76
20155467-9 2010 After treatment of Walker-256 cell lines with ATRA, the expression of Fas mRNA was significantly up-regulated and the Bcl-2 mRNA was significantly down-regulated by ATRA at the concentration of 10 mumol/L as compared with the control group (P<0.05). Tretinoin 46-50 BCL2, apoptosis regulator Rattus norvegicus 118-123
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 44-57 cyclin dependent kinase inhibitor 2A Homo sapiens 126-129
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 44-57 dynactin subunit 6 Homo sapiens 139-142
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 59-61 cyclin dependent kinase inhibitor 2A Homo sapiens 126-129
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 59-61 dynactin subunit 6 Homo sapiens 139-142
20155467-9 2010 After treatment of Walker-256 cell lines with ATRA, the expression of Fas mRNA was significantly up-regulated and the Bcl-2 mRNA was significantly down-regulated by ATRA at the concentration of 10 mumol/L as compared with the control group (P<0.05). Tretinoin 165-169 BCL2, apoptosis regulator Rattus norvegicus 118-123
20009537-3 2010 Meiotic suppression in embryonic male germ cells is believed to result from sex-specific differences in CYP26B1-catalyzed RA metabolism in the developing gonads. Tretinoin 122-124 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 104-111
20137113-2 2010 The results showed that the expression of STAT2, IRF-9 and IRF-1 could be upregulated by ATRA with different kinetics in NB4 cells. Tretinoin 89-93 interferon regulatory factor 9 Homo sapiens 49-54
20137113-2 2010 The results showed that the expression of STAT2, IRF-9 and IRF-1 could be upregulated by ATRA with different kinetics in NB4 cells. Tretinoin 89-93 interferon regulatory factor 1 Homo sapiens 59-64
20137113-5 2010 It is concluded that during ATRA-induced APL cell differentiation, IRF-1 is first upregulated by ATRA, and then IRF-1 increases the protein levels of IRF-9 and STAT2 with the downregulation of C/EBPalpha. Tretinoin 28-32 interferon regulatory factor 1 Homo sapiens 67-72
20137113-5 2010 It is concluded that during ATRA-induced APL cell differentiation, IRF-1 is first upregulated by ATRA, and then IRF-1 increases the protein levels of IRF-9 and STAT2 with the downregulation of C/EBPalpha. Tretinoin 28-32 interferon regulatory factor 1 Homo sapiens 112-117
20137113-5 2010 It is concluded that during ATRA-induced APL cell differentiation, IRF-1 is first upregulated by ATRA, and then IRF-1 increases the protein levels of IRF-9 and STAT2 with the downregulation of C/EBPalpha. Tretinoin 28-32 interferon regulatory factor 9 Homo sapiens 150-155
20137113-5 2010 It is concluded that during ATRA-induced APL cell differentiation, IRF-1 is first upregulated by ATRA, and then IRF-1 increases the protein levels of IRF-9 and STAT2 with the downregulation of C/EBPalpha. Tretinoin 28-32 CCAAT enhancer binding protein alpha Homo sapiens 193-203
20102612-11 2010 CONCLUSIONS: This study shows an important role for the NF-kappaB pathway in retinoic acid signaling and retinoic acid-mediated resistance to cancer therapy-mediated apoptosis in breast cancer cells, independently of cIAP2. Tretinoin 77-90 nuclear factor kappa B subunit 1 Homo sapiens 56-65
20102612-11 2010 CONCLUSIONS: This study shows an important role for the NF-kappaB pathway in retinoic acid signaling and retinoic acid-mediated resistance to cancer therapy-mediated apoptosis in breast cancer cells, independently of cIAP2. Tretinoin 105-118 nuclear factor kappa B subunit 1 Homo sapiens 56-65
20102612-0 2010 Retinoic acid protects human breast cancer cells against etoposide-induced apoptosis by NF-kappaB-dependent but cIAP2-independent mechanisms. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 88-97
19965687-7 2010 Our results demonstrate that DNA vaccination with ATRA confers the effective boosting of interferon-gamma-producing and cytotoxic T cells in the leukemic mice. Tretinoin 50-54 interferon gamma Mus musculus 89-105
20150637-2 2010 PATIENTS AND METHODS: With the aim of increasing patient"s lymphocyte count and reducing VEGF, wich could translate into an improved immune function and a better clinical outcome, patients with HRBC, received HDCT, PBPCT and immunotherapy with interleukin-2 (IL-2) and 13-cis retinoic acid (RA). Tretinoin 291-293 vascular endothelial growth factor A Homo sapiens 89-93
19918205-5 2010 Cdh1 was upregulated, whereas Id2 (one downstream substrate of Cdh1-APC) was downregulated when primary neural stem cells were induced to differentiate into neurons by all-trans retinoic acid. Tretinoin 178-191 cadherin 1 Homo sapiens 63-67
20150637-7 2010 CONCLUSION: These data show that IL-2 and RA administration after HDCT and PBPCT is feasible and, as well as giving a statistically significant improvement in lymphocyte count and a decrease of VEGF, also seems to improve the expected clinical outcome. Tretinoin 42-44 vascular endothelial growth factor A Homo sapiens 194-198
20040491-1 2010 Tgif1 and Tgif2 are transcriptional co-repressors that limit the response to TGFbeta signaling and play a role in regulating retinoic-acid-mediated gene expression. Tretinoin 125-138 TGFB induced factor homeobox 1 Homo sapiens 0-5
20511711-8 2010 In the liver, RA treatment triggered an increase in the mRNA expression levels of peroxisome proliferator-activated receptor alpha, retinoid X receptor alpha, uncoupling protein 2, liver-type carnitine palmitoyltransferase 1, and carnitine/acylcarnitine carrier, and a reduction in the mRNA expression levels of sterol regulatory element binding protein 1c and fatty acid synthase. Tretinoin 14-16 peroxisome proliferator activated receptor alpha Mus musculus 82-157
20511711-8 2010 In the liver, RA treatment triggered an increase in the mRNA expression levels of peroxisome proliferator-activated receptor alpha, retinoid X receptor alpha, uncoupling protein 2, liver-type carnitine palmitoyltransferase 1, and carnitine/acylcarnitine carrier, and a reduction in the mRNA expression levels of sterol regulatory element binding protein 1c and fatty acid synthase. Tretinoin 14-16 fatty acid synthase Mus musculus 361-380
20696059-6 2010 RESULTS: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Tretinoin 77-90 erb-b2 receptor tyrosine kinase 2 Homo sapiens 12-16
20696059-6 2010 RESULTS: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Tretinoin 77-90 estrogen receptor 1 Homo sapiens 13-15
20696059-6 2010 RESULTS: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Tretinoin 92-96 erb-b2 receptor tyrosine kinase 2 Homo sapiens 12-16
20696059-6 2010 RESULTS: In HER2-overexpressing/ER-positive BT474 cells, combining all-trans retinoic acid (atRA) with tamoxifen or trastuzumab synergistically inhibited cell growth, and altered cell differentiation and cell cycle. Tretinoin 92-96 estrogen receptor 1 Homo sapiens 13-15
20040494-6 2010 Together, these studies suggest that renal development depends on paracrine RA signaling between stromal mesenchyme and ureteric bud cells that regulates Ret expression both during ureteric bud formation and within the developing collecting duct system. Tretinoin 76-78 ret proto-oncogene Mus musculus 154-157
19757389-5 2010 We show by loss of function using the inhibitor citral, that RA signalling within the limb bud is required to maintain Pax3 and Meox2 in the progenitor and Myf5 and MyoD in the differentiating myoblasts. Tretinoin 61-63 myogenic factor 5 Gallus gallus 156-160
19812349-3 2010 Transrepression of many genes by retinoic acids is mediated by interactions between retinoid receptors and the activator protein 1 (AP-1) complex. Tretinoin 33-47 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 111-130
19812349-3 2010 Transrepression of many genes by retinoic acids is mediated by interactions between retinoid receptors and the activator protein 1 (AP-1) complex. Tretinoin 33-47 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-136
20501978-9 2010 We propose other candidates such as STRA6, LRAT, CRBP1, CRBP2 and CRABP1 are directly implicated in retinoic acid metabolism. Tretinoin 100-113 retinol binding protein 2 Homo sapiens 56-61
20563989-1 2010 Two new components of the retinoic acid (RA) synthetic pathway, the cell surface receptor for retinol, Stra6, and the enzyme converting retinol into retinal, Rdh10, have recently been described. Tretinoin 26-39 retinol dehydrogenase 10 (all-trans) Gallus gallus 158-163
20563989-1 2010 Two new components of the retinoic acid (RA) synthetic pathway, the cell surface receptor for retinol, Stra6, and the enzyme converting retinol into retinal, Rdh10, have recently been described. Tretinoin 41-43 retinol dehydrogenase 10 (all-trans) Gallus gallus 158-163
19909807-6 2010 Treatment of retinoic acid induced the expression of XPteg in the pronephric field without protein synthesis. Tretinoin 13-26 pdzk1 interacting protein 1 S homeolog Xenopus laevis 53-58
19858186-4 2010 This stimulation was accompanied by increased gene expression of Wnt proteins and receptors and was inhibited by co-treatment with Dickkopf-related protein-1, an extracellular inhibitor of Wnt/beta-catenin signaling, suggesting that RA modulates Wnt signaling at Wnt cell surface receptor level. Tretinoin 233-235 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 131-157
19903244-0 2010 ATRA inhibits ceramide kinase transcription in a human neuroblastoma cell line, SH-SY5Y cells: the role of COUP-TFI. Tretinoin 0-4 nuclear receptor subfamily 2 group F member 1 Homo sapiens 107-115
19903244-9 2010 The electrophoresis mobility shift assay revealed that ATRA produced two retarded bands, which were erased by antibody against chicken ovalbumin upstream promoter transcription factor I (COUP-TFI), RARalpha, and RXRalpha, respectively. Tretinoin 55-59 nuclear receptor subfamily 2 group F member 1 Gallus gallus 127-185
19903244-9 2010 The electrophoresis mobility shift assay revealed that ATRA produced two retarded bands, which were erased by antibody against chicken ovalbumin upstream promoter transcription factor I (COUP-TFI), RARalpha, and RXRalpha, respectively. Tretinoin 55-59 nuclear receptor subfamily 2 group F member 1 Gallus gallus 187-195
20042001-0 2010 Retinoic acid activation of peroxisome proliferation-activated receptor delta represses obesity and insulin resistance. Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 28-77
19910455-0 2010 Retinoic acid is a cofactor for translational regulation of vascular endothelial growth factor in human endometrial stromal cells. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 60-94
19910455-3 2010 Retinoic acid (RA) has been reported to regulate VEGF in a variety of cell types. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 49-53
19910455-3 2010 Retinoic acid (RA) has been reported to regulate VEGF in a variety of cell types. Tretinoin 15-17 vascular endothelial growth factor A Homo sapiens 49-53
19910455-4 2010 Because localized RA synthesis occurs within the periimplantation endometrium, we tested the possibility that RA regulates VEGF production in endometrial stromal cells. Tretinoin 110-112 vascular endothelial growth factor A Homo sapiens 123-127
19910455-7 2010 Analysis of retinoids in secretory phase endometrial biopsies indicated that endogenous RA accumulated at concentrations sufficient to induce VEGF secretion. Tretinoin 88-90 vascular endothelial growth factor A Homo sapiens 142-146
19910455-9 2010 Although the precise mechanism(s) of the RA effect remains to be defined, it appears to be mediated by reactive oxygen species; the antioxidant N-acetylcysteine inhibited RA+TPA-stimulated secretion of VEGF by more than 80%. Tretinoin 41-43 vascular endothelial growth factor A Homo sapiens 202-206
19910455-9 2010 Although the precise mechanism(s) of the RA effect remains to be defined, it appears to be mediated by reactive oxygen species; the antioxidant N-acetylcysteine inhibited RA+TPA-stimulated secretion of VEGF by more than 80%. Tretinoin 171-173 vascular endothelial growth factor A Homo sapiens 202-206
19800972-2 2010 Retinoic acid (RA) can stimulate neurite outgrowth in vitro of both the embryonic central and peripheral nervous system, via activation of the retinoic acid receptor (RAR) beta2. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 167-170
19800972-2 2010 Retinoic acid (RA) can stimulate neurite outgrowth in vitro of both the embryonic central and peripheral nervous system, via activation of the retinoic acid receptor (RAR) beta2. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 167-170
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 48-97
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 0-13 peroxisome proliferator activator receptor delta Mus musculus 99-108
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 15-17 peroxisome proliferator activator receptor delta Mus musculus 48-97
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 15-17 peroxisome proliferator activator receptor delta Mus musculus 99-108
20042001-2 2010 Carrier proteins that move the RA from the cytosol into the nucleus are the fatty acid-binding protein 5 (FABP5), activating PPARdelta, and the cellular retinoic acid-binding protein II (CRABPII), activating RAR. Tretinoin 31-33 peroxisome proliferator activator receptor delta Mus musculus 125-134
20042001-4 2010 By activating PPARdelta, RA was found to induce expression of genes affecting lipid and glucose homeostasis, in particular, leading to expression of the insulin-signaling gene PDK1 and improvement of insulin action. Tretinoin 25-27 peroxisome proliferator activator receptor delta Mus musculus 14-23
20042001-4 2010 By activating PPARdelta, RA was found to induce expression of genes affecting lipid and glucose homeostasis, in particular, leading to expression of the insulin-signaling gene PDK1 and improvement of insulin action. Tretinoin 25-27 pyruvate dehydrogenase kinase, isoenzyme 1 Mus musculus 176-180
20042001-7 2010 RA implantation into obese mice has caused upregulation of levels of PPARdelta and consequent weight loss as well as increased expression of PPARdelta target genes, including the insulin-signaling gene PDK1. Tretinoin 0-2 peroxisome proliferator activator receptor delta Mus musculus 69-78
20042001-7 2010 RA implantation into obese mice has caused upregulation of levels of PPARdelta and consequent weight loss as well as increased expression of PPARdelta target genes, including the insulin-signaling gene PDK1. Tretinoin 0-2 peroxisome proliferator activator receptor delta Mus musculus 141-150
20042001-7 2010 RA implantation into obese mice has caused upregulation of levels of PPARdelta and consequent weight loss as well as increased expression of PPARdelta target genes, including the insulin-signaling gene PDK1. Tretinoin 0-2 pyruvate dehydrogenase kinase, isoenzyme 1 Mus musculus 202-206
19526345-4 2010 The expression of the orphan nuclear receptor COUP-TFI antagonizes retinoic acid signaling and has been shown to be expressed in normal corticotroph cells, but absent in corticotroph tumor cell lines. Tretinoin 67-80 nuclear receptor subfamily 2 group F member 1 Homo sapiens 46-54
19799567-5 2009 By functional analysis we also showed that mutations of the PBX1/MEIS1-binding sites resulted in profound reduction of SOX3 promoter responsiveness to RA. Tretinoin 151-153 SRY-box transcription factor 3 Homo sapiens 119-123
20942599-5 2010 Our results show that treatment with ATRA (10-11 M) and VPA (2 x 10-3 M) induces megakaryopoiesis of MEG-01 cells as estimated by polyploidy, formation of characteristic proplatelets and elevated expression of the megakaryocytic markers CD41 and CD61. Tretinoin 37-41 integrin subunit beta 3 Homo sapiens 246-250
19855079-5 2009 RA induced the differentiation of PLZF-RARalpha-transformed murine hematopoietic cells and reduced the frequency of clonogenic progenitors, concomitant with c-Myc down-regulation. Tretinoin 0-2 zinc finger and BTB domain containing 16 Mus musculus 34-38
19855079-6 2009 Surviving RA-treated cells retained the ability to be replated and this was associated with sustained c-Myc expression and repression of Dusp6, suggesting a role for these genes in maintaining a self-renewal pathway triggered by PLZF-RARalpha. Tretinoin 10-12 zinc finger and BTB domain containing 16 Mus musculus 229-233
19858209-2 2009 GPS2 potently represses basal transcription, with the repression domain mapped to the N-terminal silencing mediator of retinoic acid and thyroid hormone receptor (SMRT)-interacting domain. Tretinoin 119-132 G protein pathway suppressor 2 Homo sapiens 0-4
21189168-9 2010 The expression levels of GATA-4 and AFP were the highest after induction of differentiation with retinoic acid. Tretinoin 97-110 GATA binding protein 4 Mus musculus 25-31
19808863-11 2010 Downregulation of SSEA1 paralleled betaIII-tubulin upregulation in an RA concentration-dependent manner. Tretinoin 70-72 fucosyltransferase 4 Homo sapiens 18-23
19808863-13 2010 However, low molar nitrite prevented RA-induced SSEA1 downregulation and decreased betaIII-tubulin appearance. Tretinoin 37-39 fucosyltransferase 4 Homo sapiens 48-53
19788910-2 2009 Prickle2 but not Prickle1 gene expression was induced in C1300 neuroblastoma cells during neurite-like process formation induced by retinoic acid (RA). Tretinoin 132-145 prickle planar cell polarity protein 2 Mus musculus 0-8
19788910-2 2009 Prickle2 but not Prickle1 gene expression was induced in C1300 neuroblastoma cells during neurite-like process formation induced by retinoic acid (RA). Tretinoin 147-149 prickle planar cell polarity protein 2 Mus musculus 0-8
19788910-3 2009 Over-expression of Prickle1 or Prickle2 in C1300 cells induced striking neurite-like process formation in the absence of RA. Tretinoin 121-123 prickle planar cell polarity protein 2 Mus musculus 31-39
19799861-3 2009 Systematic yeast two-hybrid assays showed that in the presence of RA, TGR interacts with RAR via the LxxLL motif (NR box) located between the Grx and TrxR domains of TGR. Tretinoin 66-68 thioredoxin reductase 3 Mus musculus 70-73
19799861-3 2009 Systematic yeast two-hybrid assays showed that in the presence of RA, TGR interacts with RAR via the LxxLL motif (NR box) located between the Grx and TrxR domains of TGR. Tretinoin 66-68 thioredoxin reductase 3 Mus musculus 166-169
19850744-6 2009 In the presence of ATRA, lysine 166 (K166) and K171 of RARA were modified at a physiological concentration of SUMO-2, whereas in the absence of ATRA, K399 was the only site that was modified, but at a higher SUMO-2 concentration. Tretinoin 19-23 small ubiquitin-like modifier 2 Mus musculus 110-116
19966493-5 2009 Gene expression levels of Toll-like receptor (TLR)1, TLR2, TLR4, TLR6 and dectin-1 in HL-60 cells were additionally affected by retinoic acid or DMSO and by co-culturing with S. cerevisiae or C. albicans. Tretinoin 128-141 toll like receptor 1 Homo sapiens 46-51
19966493-5 2009 Gene expression levels of Toll-like receptor (TLR)1, TLR2, TLR4, TLR6 and dectin-1 in HL-60 cells were additionally affected by retinoic acid or DMSO and by co-culturing with S. cerevisiae or C. albicans. Tretinoin 128-141 toll like receptor 2 Homo sapiens 53-57
19966493-5 2009 Gene expression levels of Toll-like receptor (TLR)1, TLR2, TLR4, TLR6 and dectin-1 in HL-60 cells were additionally affected by retinoic acid or DMSO and by co-culturing with S. cerevisiae or C. albicans. Tretinoin 128-141 toll like receptor 6 Homo sapiens 65-69
19766701-2 2009 This study sought to determine the detailed kinetic properties of 2 mouse RALDHs, namely RALDH3 and 4, for retinal isomer substrates, to better define their specificities in RA isomer synthesis. Tretinoin 74-76 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 89-101
19850744-6 2009 In the presence of ATRA, lysine 166 (K166) and K171 of RARA were modified at a physiological concentration of SUMO-2, whereas in the absence of ATRA, K399 was the only site that was modified, but at a higher SUMO-2 concentration. Tretinoin 19-23 small ubiquitin-like modifier 2 Mus musculus 208-214
21351468-7 2009 The results showed that celecoxib enhanced the inhibitory effect of ATRA in both COX-2 high-expressing HT-29 and COX-2 low-expressing SW480 cell lines. Tretinoin 68-72 mitochondrially encoded cytochrome c oxidase II Homo sapiens 81-86
19699159-2 2009 TGIF is expressed in hematopoietic stem cells and modulates TGF-beta and retinoic acid (RA) signaling, both of which play an important role in hematopoiesis. Tretinoin 73-86 TGFB induced factor homeobox 1 Homo sapiens 0-4
19744992-4 2009 Treatment with ATRA (10 muM) induced a 4.9-fold increase in the expression of the cytochrome P450scc (CYP11A1) gene, the product of which cleaves the cholesterol side chain, a rate-limiting step during steroidogenesis. Tretinoin 15-19 latexin Homo sapiens 24-27
19744992-4 2009 Treatment with ATRA (10 muM) induced a 4.9-fold increase in the expression of the cytochrome P450scc (CYP11A1) gene, the product of which cleaves the cholesterol side chain, a rate-limiting step during steroidogenesis. Tretinoin 15-19 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 102-109
21351468-7 2009 The results showed that celecoxib enhanced the inhibitory effect of ATRA in both COX-2 high-expressing HT-29 and COX-2 low-expressing SW480 cell lines. Tretinoin 68-72 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118
19501957-3 2009 AFP may inhibit translocation of RAR-beta into the nucleus via competitive binding to RAR-beta with ATRA, which was reversed by AFP-siRNA transfection. Tretinoin 100-104 alpha fetoprotein Homo sapiens 0-3
20078939-0 2009 [Role of Ezh2 in the all-trans retinoic acid induced P19 neural differentiation]. Tretinoin 31-44 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 9-13
20193324-11 2009 The expression of p27(Kip1) and p21(Waf1) in myeloma cells was up-regulated by RGZ and this change was more apparent when RGZ was used in combination with ATRA. Tretinoin 155-159 cyclin dependent kinase inhibitor 1A Homo sapiens 32-35
20193324-11 2009 The expression of p27(Kip1) and p21(Waf1) in myeloma cells was up-regulated by RGZ and this change was more apparent when RGZ was used in combination with ATRA. Tretinoin 155-159 cyclin dependent kinase inhibitor 1A Homo sapiens 36-40
19501957-3 2009 AFP may inhibit translocation of RAR-beta into the nucleus via competitive binding to RAR-beta with ATRA, which was reversed by AFP-siRNA transfection. Tretinoin 100-104 retinoic acid receptor beta Homo sapiens 33-41
19501957-3 2009 AFP may inhibit translocation of RAR-beta into the nucleus via competitive binding to RAR-beta with ATRA, which was reversed by AFP-siRNA transfection. Tretinoin 100-104 retinoic acid receptor beta Homo sapiens 86-94
19501957-3 2009 AFP may inhibit translocation of RAR-beta into the nucleus via competitive binding to RAR-beta with ATRA, which was reversed by AFP-siRNA transfection. Tretinoin 100-104 alpha fetoprotein Homo sapiens 128-131
19211146-5 2009 Moreover, the animals receiving ATRA exhibited reduced Th1/Th17 response and nitric oxide (NO) production in the peripheral lymphoid tissues, thus shifting the balance towards the anti-inflammatory cytokines. Tretinoin 32-36 negative elongation factor complex member C/D, Th1l Mus musculus 55-58
19443527-4 2009 Previously, it was reported that all-trans-retinoic acid (ATRA) inhibited the production and function of IL-6 and transforming growth factor (TGF)-beta1 in experiments using lung fibroblasts. Tretinoin 33-56 interleukin 6 Mus musculus 105-109
19443527-4 2009 Previously, it was reported that all-trans-retinoic acid (ATRA) inhibited the production and function of IL-6 and transforming growth factor (TGF)-beta1 in experiments using lung fibroblasts. Tretinoin 58-62 interleukin 6 Mus musculus 105-109
19597529-6 2009 However, addition of ATRA, but not 13-cis RA, to a liposomal formulation containing the Toll-like receptor-4 agonist monophosphoryl lipid A resulted in a fourfold enhancement of serum anti-peptide IgG titers as compared with a formulation containing lipid A alone (P=0.00039). Tretinoin 21-25 toll-like receptor 4 Mus musculus 88-108
19597529-6 2009 However, addition of ATRA, but not 13-cis RA, to a liposomal formulation containing the Toll-like receptor-4 agonist monophosphoryl lipid A resulted in a fourfold enhancement of serum anti-peptide IgG titers as compared with a formulation containing lipid A alone (P=0.00039). Tretinoin 23-25 toll-like receptor 4 Mus musculus 88-108
19726747-0 2009 Retinoic acid-induced nNOS expression depends on a novel PI3K/Akt/DAX1 pathway in human TGW-nu-I neuroblastoma cells. Tretinoin 0-13 AKT serine/threonine kinase 1 Homo sapiens 62-65
19726747-0 2009 Retinoic acid-induced nNOS expression depends on a novel PI3K/Akt/DAX1 pathway in human TGW-nu-I neuroblastoma cells. Tretinoin 0-13 nuclear receptor subfamily 0 group B member 1 Homo sapiens 66-70
19726747-8 2009 RA treatment increases DAX1 expression via PI3K/Akt signaling. Tretinoin 0-2 nuclear receptor subfamily 0 group B member 1 Homo sapiens 23-27
19726747-8 2009 RA treatment increases DAX1 expression via PI3K/Akt signaling. Tretinoin 0-2 AKT serine/threonine kinase 1 Homo sapiens 48-51
19843176-7 2009 Augmentation of the retinoic acid response by EVI1 was also observed for the endogenous RARbeta gene. Tretinoin 20-33 retinoic acid receptor beta Homo sapiens 88-95
19843631-0 2009 UNC45A confers resistance to histone deacetylase inhibitors and retinoic acid. Tretinoin 64-77 unc-45 myosin chaperone A Homo sapiens 0-6
19843631-7 2009 Expression of UNC45A inhibits retinoic acid-induced proliferation arrest and differentiation of human neuroblastoma cells and inhibits the induction of endogenous retinoic acid receptor target genes. Tretinoin 30-43 unc-45 myosin chaperone A Homo sapiens 14-20
19843631-8 2009 These data establish an unexpected role for UNC45A in causing resistance to both HDACI drugs and retinoic acid. Tretinoin 97-110 unc-45 myosin chaperone A Homo sapiens 44-50
19838304-3 2009 In mice, retinoic acid (RA) signaling has been implicated in controlling entry into meiosis in germ cells, as meiosis in male embryonic germ cells is blocked by the activity of a RA-catabolizing enzyme, CYP26B1. Tretinoin 9-22 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 203-210
19340880-2 2009 Recent studies have revealed that retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (Treg) cells. Tretinoin 34-47 transforming growth factor beta 1 Homo sapiens 106-143
19814781-0 2009 Retinoic acid enhances skeletal muscle progenitor formation and bypasses inhibition by bone morphogenetic protein 4 but not dominant negative beta-catenin. Tretinoin 0-13 bone morphogenetic protein 4 Mus musculus 87-115
19814781-4 2009 Thus, the purpose of this study is to examine the molecular mechanisms by which RA enhances skeletal myogenesis and interacts with Wnt and BMP4 signalling during P19 or mouse embryonic stem (ES) cell differentiation. Tretinoin 80-82 bone morphogenetic protein 4 Mus musculus 139-143
19814781-5 2009 RESULTS: Treatment of P19 or mouse ES cells with low levels of RA led to an enhancement of skeletal myogenesis by upregulating the expression of the mesodermal marker, Wnt3a, the skeletal muscle progenitor factors Pax3 and Meox1, and the myogenic regulatory factors (MRFs) MyoD and myogenin. Tretinoin 63-65 paired box 3 Mus musculus 214-218
19814781-10 2009 Furthermore, RA downregulated BMP4 expression and upregulated the BMP4 inhibitor, Tob1. Tretinoin 13-15 bone morphogenetic protein 4 Mus musculus 30-34
19814781-10 2009 Furthermore, RA downregulated BMP4 expression and upregulated the BMP4 inhibitor, Tob1. Tretinoin 13-15 bone morphogenetic protein 4 Mus musculus 66-70
19789299-0 2009 All-trans retinoic acid suppresses Stat3 signaling during skin carcinogenesis. Tretinoin 10-23 signal transducer and activator of transcription 3 Mus musculus 35-40
19789299-2 2009 We have determined the effects of all-trans retinoic acid (ATRA), a naturally occurring chemopreventive retinoid, on signal transducer and activator of transcription 3 (Stat3) signaling during the development of skin SCC. Tretinoin 44-57 signal transducer and activator of transcription 3 Mus musculus 117-167
19789299-2 2009 We have determined the effects of all-trans retinoic acid (ATRA), a naturally occurring chemopreventive retinoid, on signal transducer and activator of transcription 3 (Stat3) signaling during the development of skin SCC. Tretinoin 44-57 signal transducer and activator of transcription 3 Mus musculus 169-174
19789299-2 2009 We have determined the effects of all-trans retinoic acid (ATRA), a naturally occurring chemopreventive retinoid, on signal transducer and activator of transcription 3 (Stat3) signaling during the development of skin SCC. Tretinoin 59-63 signal transducer and activator of transcription 3 Mus musculus 117-167
19789299-2 2009 We have determined the effects of all-trans retinoic acid (ATRA), a naturally occurring chemopreventive retinoid, on signal transducer and activator of transcription 3 (Stat3) signaling during the development of skin SCC. Tretinoin 59-63 signal transducer and activator of transcription 3 Mus musculus 169-174
19789299-5 2009 ATRA is a highly efficient suppressor of tumor formation in the two-stage mouse skin carcinogenesis model and we have shown that this effect correlates with the suppression of the B-Raf/Mek/Erk signaling pathway. Tretinoin 0-4 mitogen-activated protein kinase 1 Mus musculus 190-193
19789299-8 2009 Using Western blotting and immunohistochemical staining with phosphospecific antibodies, we show that coadministration of ATRA suppressed the 12-O-tetradecanoylphorbol-13-acetate-induced phosphorylation of Stat3 in both models, but was only able to suppress tumor formation in the SENCAR mice. Tretinoin 122-126 signal transducer and activator of transcription 3 Mus musculus 206-211
19789299-10 2009 We hypothesize that ATRA blocks tumor formation, at least in part, by targeting events upstream of Stat3, such as the B-Raf/Mek/Erk pathway, and that in the K5.Stat3C mice, in which Stat3 activity is constitutive, it cannot suppress tumor formation. Tretinoin 20-24 signal transducer and activator of transcription 3 Mus musculus 99-104
19789299-10 2009 We hypothesize that ATRA blocks tumor formation, at least in part, by targeting events upstream of Stat3, such as the B-Raf/Mek/Erk pathway, and that in the K5.Stat3C mice, in which Stat3 activity is constitutive, it cannot suppress tumor formation. Tretinoin 20-24 mitogen-activated protein kinase 1 Mus musculus 128-131
19789299-10 2009 We hypothesize that ATRA blocks tumor formation, at least in part, by targeting events upstream of Stat3, such as the B-Raf/Mek/Erk pathway, and that in the K5.Stat3C mice, in which Stat3 activity is constitutive, it cannot suppress tumor formation. Tretinoin 20-24 signal transducer and activator of transcription 3 Mus musculus 160-165
19853565-8 2009 Concomitant regulation of Cyp26a1 expression, restraining retinoic acid signaling away from the posterior growth zone, may likewise play a role in timing the trunk-tail transition. Tretinoin 58-71 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-33
19507250-0 2009 Inhibition of mammalian target of rapamycin signaling potentiates the effects of all-trans retinoic acid to induce growth arrest and differentiation of human acute myelogenous leukemia cells. Tretinoin 91-104 mechanistic target of rapamycin kinase Homo sapiens 14-43
19507250-1 2009 Our study explored the drug interaction of all-trans retinoic acid (ATRA) and RAD001 (everolimus), the inhibitor of mammalian target of rapamycin complex 1 (mTORC1), in acute myelogenous leukemia (AML) NB4 and HL60 cells. Tretinoin 53-66 mechanistic target of rapamycin kinase Homo sapiens 116-145
19507250-1 2009 Our study explored the drug interaction of all-trans retinoic acid (ATRA) and RAD001 (everolimus), the inhibitor of mammalian target of rapamycin complex 1 (mTORC1), in acute myelogenous leukemia (AML) NB4 and HL60 cells. Tretinoin 68-72 mechanistic target of rapamycin kinase Homo sapiens 116-145
19507250-5 2009 Notably, RAD001 (10 nM) significantly augmented ATRA-induced expression of CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) and p27(kip1) and downregulated levels of c-Myc in these cells. Tretinoin 48-52 dynactin subunit 6 Homo sapiens 133-136
19340880-2 2009 Recent studies have revealed that retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (Treg) cells. Tretinoin 49-51 transforming growth factor beta 1 Homo sapiens 106-143
19595764-4 2009 Since retinoic acid is known to pattern many tissues during development, and RALDH2, the enzyme primarily responsible for retinoic acid synthesis, is expressed in the anterior and dorsal LPM, we hypothesized that retinoic acid is necessary for correct patterning of the LPM. Tretinoin 122-135 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 77-83
19853750-0 2009 Prenatal retinoic acid up-regulates pulmonary gene expression of COUP-TFII, FOG2, and GATA4 in pulmonary hypoplasia. Tretinoin 9-22 GATA binding protein 4 Rattus norvegicus 86-91
19853750-13 2009 RESULTS: The relative mRNA expression levels of COUP-TFII, FOG2, and GATA4 were significantly increased in CDH + RA lungs compared to control, control + RA, and CDH (P < .05). Tretinoin 113-115 GATA binding protein 4 Rattus norvegicus 69-74
19853750-13 2009 RESULTS: The relative mRNA expression levels of COUP-TFII, FOG2, and GATA4 were significantly increased in CDH + RA lungs compared to control, control + RA, and CDH (P < .05). Tretinoin 153-155 GATA binding protein 4 Rattus norvegicus 69-74
19853750-14 2009 CONCLUSIONS: Up-regulation of pulmonary gene expression of COUP-TFII, FOG2, and GATA4 after prenatal treatment with retinoic acid in the nitrofen model of CDH suggests that RA may have a therapeutic potential in modulating lung growth. Tretinoin 116-129 GATA binding protein 4 Rattus norvegicus 80-85
19853750-14 2009 CONCLUSIONS: Up-regulation of pulmonary gene expression of COUP-TFII, FOG2, and GATA4 after prenatal treatment with retinoic acid in the nitrofen model of CDH suggests that RA may have a therapeutic potential in modulating lung growth. Tretinoin 173-175 GATA binding protein 4 Rattus norvegicus 80-85
19595764-4 2009 Since retinoic acid is known to pattern many tissues during development, and RALDH2, the enzyme primarily responsible for retinoic acid synthesis, is expressed in the anterior and dorsal LPM, we hypothesized that retinoic acid is necessary for correct patterning of the LPM. Tretinoin 122-135 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 77-83
19595764-7 2009 After altering retinoic acid signaling in a temporally restricted window, the displaced anterior-posterior pattern is maintained until gut looping, as demonstrated by permanently altered Hand1, FoxF1, xHoxC-10, and Pitx2 expression domains. Tretinoin 15-28 homeobox C10 L homeolog Xenopus laevis 201-209
19729514-9 2009 We also demonstrated that retinoic-acid-inducible gene I, and not melanoma differentiation associated gene 5 or toll-like receptor 3, is the cytoplasmic sensor for intracellularly expressed shRNAs that trigger IFN activation. Tretinoin 26-39 interferon alpha 1 Homo sapiens 210-213
19573594-4 2009 Retinoic acid (RA) and 12-O-tetradecanoylphorbol 13-acetate, two well-studied inducers of neuronal differentiation, are able to induce Nrf2 and its target gene NAD(P)H quinone oxidoreductase 1 in a dose- and time-dependent manner. Tretinoin 0-13 NFE2 like bZIP transcription factor 2 Homo sapiens 135-139
19633294-5 2009 This is evidenced by RA-dependent induction of the cell cycle inhibitor p21/Cip1 (Cdk-interacting protein 1) and cell cycle arrest, induction of the neuroblastic marker doublecortin and of the neuron-specific intermediate filament protein, peripherin, and by RA-stimulated extension of neuritic processes. Tretinoin 21-23 cyclin dependent kinase inhibitor 1A Homo sapiens 72-75
19633294-5 2009 This is evidenced by RA-dependent induction of the cell cycle inhibitor p21/Cip1 (Cdk-interacting protein 1) and cell cycle arrest, induction of the neuroblastic marker doublecortin and of the neuron-specific intermediate filament protein, peripherin, and by RA-stimulated extension of neuritic processes. Tretinoin 21-23 cyclin dependent kinase inhibitor 1A Homo sapiens 76-80
19633294-5 2009 This is evidenced by RA-dependent induction of the cell cycle inhibitor p21/Cip1 (Cdk-interacting protein 1) and cell cycle arrest, induction of the neuroblastic marker doublecortin and of the neuron-specific intermediate filament protein, peripherin, and by RA-stimulated extension of neuritic processes. Tretinoin 21-23 cyclin dependent kinase inhibitor 1A Homo sapiens 82-107
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 0-2 cyclin dependent kinase inhibitor 1A Homo sapiens 282-285
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 0-2 cyclin dependent kinase inhibitor 1A Homo sapiens 286-290
19573594-4 2009 Retinoic acid (RA) and 12-O-tetradecanoylphorbol 13-acetate, two well-studied inducers of neuronal differentiation, are able to induce Nrf2 and its target gene NAD(P)H quinone oxidoreductase 1 in a dose- and time-dependent manner. Tretinoin 0-13 NAD(P)H quinone dehydrogenase 1 Homo sapiens 160-192
19573594-4 2009 Retinoic acid (RA) and 12-O-tetradecanoylphorbol 13-acetate, two well-studied inducers of neuronal differentiation, are able to induce Nrf2 and its target gene NAD(P)H quinone oxidoreductase 1 in a dose- and time-dependent manner. Tretinoin 15-17 NFE2 like bZIP transcription factor 2 Homo sapiens 135-139
19573594-4 2009 Retinoic acid (RA) and 12-O-tetradecanoylphorbol 13-acetate, two well-studied inducers of neuronal differentiation, are able to induce Nrf2 and its target gene NAD(P)H quinone oxidoreductase 1 in a dose- and time-dependent manner. Tretinoin 15-17 NAD(P)H quinone dehydrogenase 1 Homo sapiens 160-192
19573594-5 2009 RA-induced Nrf2 up-regulation is accompanied by neurite outgrowth and an induction of two neuronal differentiation markers, neurofilament-M and microtubule-associated protein 2. Tretinoin 0-2 NFE2 like bZIP transcription factor 2 Homo sapiens 11-15
19717521-0 2009 De novo generation and enhanced suppression of human CD4+CD25+ regulatory T cells by retinoic acid. Tretinoin 85-98 CD4 molecule Homo sapiens 53-56
19486889-0 2009 All-trans retinoic acid increases KLF4 acetylation by inducing HDAC2 phosphorylation and its dissociation from KLF4 in vascular smooth muscle cells. Tretinoin 0-23 histone deacetylase 2 Homo sapiens 63-68
19486889-3 2009 Here, we show that ATRA-induced histone deacetylase 2 (HDAC2) phosphorylation at Ser424 in VSMCs and inhibited the interaction of HDAC2 with KLF4. Tretinoin 19-23 histone deacetylase 2 Homo sapiens 32-53
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 84-88 mitogen-activated protein kinase 8 Homo sapiens 11-14
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 84-88 histone deacetylase 2 Homo sapiens 97-102
19556237-9 2009 Furthermore, cadmium inhibited the expression of Cyp26a1 and Cyp26b1, which are involved in retinoic acid degradation. Tretinoin 92-105 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 61-68
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 84-88 histone deacetylase 2 Homo sapiens 179-184
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 132-136 mitogen-activated protein kinase 8 Homo sapiens 11-14
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 132-136 histone deacetylase 2 Homo sapiens 179-184
19486889-3 2009 Here, we show that ATRA-induced histone deacetylase 2 (HDAC2) phosphorylation at Ser424 in VSMCs and inhibited the interaction of HDAC2 with KLF4. Tretinoin 19-23 histone deacetylase 2 Homo sapiens 55-60
19486889-3 2009 Here, we show that ATRA-induced histone deacetylase 2 (HDAC2) phosphorylation at Ser424 in VSMCs and inhibited the interaction of HDAC2 with KLF4. Tretinoin 19-23 histone deacetylase 2 Homo sapiens 130-135
19619546-2 2009 In the epithelial cell membrane, we show that manipulation of tgase2 function by monodansylcadaverine or retinoic acid (RA) alters the activity of a membrane-bound protein kinase, nucleoside diphosphate kinase (NDPK, nm23-H1/H2) that is known to control G-protein function. Tretinoin 105-118 transglutaminase 2 Homo sapiens 62-68
19486889-5 2009 We further demonstrated that HDAC2 directly deacetylated KLF4, and that KLF4 acetylation and binding activity of KLF4 to the SM22alpha promoter were significantly increased in ATRA-treated VSMCs. Tretinoin 176-180 histone deacetylase 2 Homo sapiens 29-34
19486889-6 2009 Collectively, our results indicate that ATRA induces HDAC2 phosphorylation mediated by JNK signaling, and thus causes HDAC2 dissociation from KLF4, subsequently leading to the increase in KLF4 acetylation. Tretinoin 40-44 histone deacetylase 2 Homo sapiens 53-58
19486889-6 2009 Collectively, our results indicate that ATRA induces HDAC2 phosphorylation mediated by JNK signaling, and thus causes HDAC2 dissociation from KLF4, subsequently leading to the increase in KLF4 acetylation. Tretinoin 40-44 mitogen-activated protein kinase 8 Homo sapiens 87-90
19486889-6 2009 Collectively, our results indicate that ATRA induces HDAC2 phosphorylation mediated by JNK signaling, and thus causes HDAC2 dissociation from KLF4, subsequently leading to the increase in KLF4 acetylation. Tretinoin 40-44 histone deacetylase 2 Homo sapiens 118-123
19619546-2 2009 In the epithelial cell membrane, we show that manipulation of tgase2 function by monodansylcadaverine or retinoic acid (RA) alters the activity of a membrane-bound protein kinase, nucleoside diphosphate kinase (NDPK, nm23-H1/H2) that is known to control G-protein function. Tretinoin 120-122 transglutaminase 2 Homo sapiens 62-68
19450544-5 2009 Moreover, the ATRA-dependent induction of Slc1a1 mRNA required the synthesis of a protein intermediate and was not associated with changes in the messenger half-life. Tretinoin 14-18 solute carrier family 1 member 1 Homo sapiens 42-48
19584707-6 2009 Growth inhibitory concentrations of HCQ and ATRA stimulated purified p300/CBP-associated factor, where CBP is the cAMP-response element binding protein, HAT activity. Tretinoin 44-48 CREB binding protein Homo sapiens 74-77
19584707-6 2009 Growth inhibitory concentrations of HCQ and ATRA stimulated purified p300/CBP-associated factor, where CBP is the cAMP-response element binding protein, HAT activity. Tretinoin 44-48 CREB binding protein Homo sapiens 103-106
19450544-6 2009 ATRA treatment induced the expression of both Rarb mRNA and RARbeta protein several hours before the induction of Slc1a1, while the mRNA for RFX1, a transcription factor recently involved in Slc1a1 transcription, was unchanged. Tretinoin 0-4 retinoic acid receptor beta Homo sapiens 46-50
19450544-6 2009 ATRA treatment induced the expression of both Rarb mRNA and RARbeta protein several hours before the induction of Slc1a1, while the mRNA for RFX1, a transcription factor recently involved in Slc1a1 transcription, was unchanged. Tretinoin 0-4 retinoic acid receptor beta Homo sapiens 60-67
19450544-6 2009 ATRA treatment induced the expression of both Rarb mRNA and RARbeta protein several hours before the induction of Slc1a1, while the mRNA for RFX1, a transcription factor recently involved in Slc1a1 transcription, was unchanged. Tretinoin 0-4 solute carrier family 1 member 1 Homo sapiens 114-120
19450544-8 2009 We conclude that in C6 glioma cells the induction of Slc1a1 by ATRA requires the synthesis of RARbeta, suggesting that the receptor is involved in the regulation of the transporter gene. Tretinoin 63-67 solute carrier family 1 member 1 Homo sapiens 53-59
19450544-8 2009 We conclude that in C6 glioma cells the induction of Slc1a1 by ATRA requires the synthesis of RARbeta, suggesting that the receptor is involved in the regulation of the transporter gene. Tretinoin 63-67 retinoic acid receptor beta Homo sapiens 94-101
19700620-7 2009 By contrast, a ;fusion-resistant" gene, Raldh3 (also known as Aldh1a3), that encodes a retinoic acid-synthesizing enzyme is ectopically expressed in the upper lip primordia of Lrp6-deficient embryos, indicating a region-specific role of the Wnt/beta-catenin signaling pathway in repressing retinoic acid signaling. Tretinoin 87-100 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 40-46
19388084-0 2009 Smad2/3 is involved in growth inhibition of mouse embryonic palate mesenchymal cells induced by all-trans retinoic acid. Tretinoin 106-119 SMAD family member 2 Mus musculus 0-7
19388084-8 2009 The protein expression levels of p21, Smad2/3, phospho-Smad2, and phospho-Smad3 were increased, while phospho-Rb was decreased in MEPM after atRA treatment on GD 10. Tretinoin 141-145 SMAD family member 2 Mus musculus 38-45
19388084-8 2009 The protein expression levels of p21, Smad2/3, phospho-Smad2, and phospho-Smad3 were increased, while phospho-Rb was decreased in MEPM after atRA treatment on GD 10. Tretinoin 141-145 SMAD family member 2 Mus musculus 38-43
19388084-13 2009 Our study demonstrated that Smad2/3 regulation of p21 was partly required for atRA-induced cell cycle perturbations in MEPM cells. Tretinoin 78-82 SMAD family member 2 Mus musculus 28-33
19585150-4 2009 The present data demonstrate that retinoic acid (RA) treatment and the activation of Wnt signaling induce Hoxa2 and Hoxd9 expression, respectively, in mouse mesencephalic neural crest cells, which never express Hox genes in vivo. Tretinoin 34-47 homeobox A2 Mus musculus 106-111
19700620-7 2009 By contrast, a ;fusion-resistant" gene, Raldh3 (also known as Aldh1a3), that encodes a retinoic acid-synthesizing enzyme is ectopically expressed in the upper lip primordia of Lrp6-deficient embryos, indicating a region-specific role of the Wnt/beta-catenin signaling pathway in repressing retinoic acid signaling. Tretinoin 87-100 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 62-69
19700620-7 2009 By contrast, a ;fusion-resistant" gene, Raldh3 (also known as Aldh1a3), that encodes a retinoic acid-synthesizing enzyme is ectopically expressed in the upper lip primordia of Lrp6-deficient embryos, indicating a region-specific role of the Wnt/beta-catenin signaling pathway in repressing retinoic acid signaling. Tretinoin 290-303 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 40-46
19700620-7 2009 By contrast, a ;fusion-resistant" gene, Raldh3 (also known as Aldh1a3), that encodes a retinoic acid-synthesizing enzyme is ectopically expressed in the upper lip primordia of Lrp6-deficient embryos, indicating a region-specific role of the Wnt/beta-catenin signaling pathway in repressing retinoic acid signaling. Tretinoin 290-303 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 62-69
19467017-12 2009 Caspase-3 activity was increased upon exposure to RGZ in both U266 and RPMI-8226 cells while combination of RGZ and ATRA brought out more effective activation of caspase-3. Tretinoin 116-120 caspase 3 Homo sapiens 162-171
19539783-5 2009 Following loss of RA signaling, the caudal expression domains of Fgf8, Wnt8a, and Wnt3a expand anteriorly into the trunk, but no change is observed in caudal expression of Fgf4 or Fgf17 plus caudal expression of Fgf18 and Cdx1 is reduced. Tretinoin 18-20 fibroblast growth factor 18 Mus musculus 212-217
19671662-6 2009 Subsequent treatment with retinoic acid and taurine induces photoreceptors that express recoverin, rhodopsin and genes involved in phototransduction. Tretinoin 26-39 rhodopsin Homo sapiens 99-108
19594405-6 2009 CYP1A2 and CYP3A4 appear to be the major P450 enzymes catalyzing the oxidation of all-trans-retinol to all-trans-retinoic acid in human liver, and CYP3A4 is one of the vitamin D3 25-hydroxylases. Tretinoin 103-126 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 11-17
19623614-3 2009 In the current review, we summarize recent data showing that PITX2, a homeodomain transcription factor, integrates retinoic acid and canonical Wnt/beta-catenin signaling during anterior segment development. Tretinoin 115-128 paired like homeodomain 2 Homo sapiens 61-66
19623614-4 2009 Because the requirements for retinoic acid signaling, canonical Wnt/beta-catenin signaling, and PITX2 are not unique to the eye, this newly identified pathway may have relevance elsewhere during development and in tissue homeostasis. Tretinoin 29-42 paired like homeodomain 2 Homo sapiens 96-101
19666820-0 2009 A highly conserved retinoic acid responsive element controls wt1a expression in the zebrafish pronephros. Tretinoin 19-32 WT1 transcription factor a Danio rerio 61-65
18926686-0 2009 Retinoic acid dampens LPS-induced NF-kappaB activity: results from human monoblasts and in vivo imaging of NF-kappaB reporter mice. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 34-43
18926686-0 2009 Retinoic acid dampens LPS-induced NF-kappaB activity: results from human monoblasts and in vivo imaging of NF-kappaB reporter mice. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 107-116
18926686-2 2009 In the present study, we demonstrate that retinoic acid inhibits LPS-induced activation in transgenic reporter mice and human monoblasts through inhibition of nuclear factor kappaB (NF-kappaB). Tretinoin 42-55 nuclear factor kappa B subunit 1 Homo sapiens 174-180
18926686-2 2009 In the present study, we demonstrate that retinoic acid inhibits LPS-induced activation in transgenic reporter mice and human monoblasts through inhibition of nuclear factor kappaB (NF-kappaB). Tretinoin 42-55 nuclear factor kappa B subunit 1 Homo sapiens 182-191
18926686-3 2009 By using noninvasive molecular imaging of NF-kappaB luciferase reporter mice, we showed that administration of retinoic acid repressed LPS-induced whole-body luminescence, demonstrating in vivo the dynamics of retinoic acid"s ability to repress physiologic response to LPS. Tretinoin 111-124 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 42-51
18926686-3 2009 By using noninvasive molecular imaging of NF-kappaB luciferase reporter mice, we showed that administration of retinoic acid repressed LPS-induced whole-body luminescence, demonstrating in vivo the dynamics of retinoic acid"s ability to repress physiologic response to LPS. Tretinoin 210-223 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 42-51
18926686-4 2009 Retinoic acid also inhibited LPS-induced NF-kappaB activity in the human myeloblastic cell line U937. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 41-50
18926686-6 2009 Retinoic acid also repressed LPS-induced transcription of NF-kappaB target genes such as IL-6, MCP-1 and COX-2. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 58-67
18926686-6 2009 Retinoic acid also repressed LPS-induced transcription of NF-kappaB target genes such as IL-6, MCP-1 and COX-2. Tretinoin 0-13 interleukin 6 Homo sapiens 89-93
18926686-6 2009 Retinoic acid also repressed LPS-induced transcription of NF-kappaB target genes such as IL-6, MCP-1 and COX-2. Tretinoin 0-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 105-110
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 14-27 nuclear factor kappa B subunit 1 Homo sapiens 329-338
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 245-258 nuclear factor kappa B subunit 1 Homo sapiens 329-338
19723072-5 2009 Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites. Tretinoin 94-96 tumor protein p53 Homo sapiens 186-189
19950589-1 2009 OBJECTIVE: To evaluate the synergism of Tanshinone II A (Tan II A) and arsenic trioxide (As2O3) on the apoptosis of retinoic acid resistant acute promyelocytic leukemia (APL) cell line (MR2), and to investigate its effect on the expression of P-glycoprotein (Pgp) of MR2 cells. Tretinoin 116-129 ATP binding cassette subfamily B member 1 Homo sapiens 243-257
19950589-1 2009 OBJECTIVE: To evaluate the synergism of Tanshinone II A (Tan II A) and arsenic trioxide (As2O3) on the apoptosis of retinoic acid resistant acute promyelocytic leukemia (APL) cell line (MR2), and to investigate its effect on the expression of P-glycoprotein (Pgp) of MR2 cells. Tretinoin 116-129 ATP binding cassette subfamily B member 1 Homo sapiens 259-262
19502291-8 2009 One week after completion of RA treatment, alphaSMA expression was detected in interstitial fibroblasts, supporting the concept that RA-initiated realveolarization recapitulates aspects of septation that occur during normal lung development. Tretinoin 29-31 actin alpha 2, smooth muscle, aorta Mus musculus 43-51
19502291-8 2009 One week after completion of RA treatment, alphaSMA expression was detected in interstitial fibroblasts, supporting the concept that RA-initiated realveolarization recapitulates aspects of septation that occur during normal lung development. Tretinoin 133-135 actin alpha 2, smooth muscle, aorta Mus musculus 43-51
19854382-1 2009 Chronic, excessive ethanol intake can increase retinoic acid (RA) catabolism by inducing cytochrome P450 2E1 (CYP2E1). Tretinoin 47-60 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 89-108
19854382-1 2009 Chronic, excessive ethanol intake can increase retinoic acid (RA) catabolism by inducing cytochrome P450 2E1 (CYP2E1). Tretinoin 47-60 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 110-116
19854382-1 2009 Chronic, excessive ethanol intake can increase retinoic acid (RA) catabolism by inducing cytochrome P450 2E1 (CYP2E1). Tretinoin 62-64 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 89-108
19854382-1 2009 Chronic, excessive ethanol intake can increase retinoic acid (RA) catabolism by inducing cytochrome P450 2E1 (CYP2E1). Tretinoin 62-64 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 110-116
19561324-1 2009 Forced expression of MN1 in primitive mouse hematopoietic cells causes acute myeloid leukemia and impairs all-trans retinoic acid-induced granulocytic differentiation. Tretinoin 116-129 MN1 proto-oncogene, transcriptional regulator Homo sapiens 21-24
19519282-4 2009 The CYP26 enzymes have been shown to metabolize RA efficiently and they are also inducible by RA in selected systems. Tretinoin 94-96 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-9
19294396-4 2009 RA induced the expression of CYP26 enzymes already after 8 h, whereas LRAT exhibited a later response and peaked at 48 h, indicating a feedback induction of retinol esterification. Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 29-34
19294396-6 2009 The mRNA expression of RA-regulated genes (KRT2, KRT4, CRABPII and HBEGF) was altered within 24 h after RA exposure. Tretinoin 23-25 keratin 2 Homo sapiens 43-47
19294396-6 2009 The mRNA expression of RA-regulated genes (KRT2, KRT4, CRABPII and HBEGF) was altered within 24 h after RA exposure. Tretinoin 23-25 retinol binding protein 2 Homo sapiens 55-62
19294396-8 2009 Cellular accumulation of exogenous [3H]RA was higher after talarozole than after liarozole, probably indicating a greater CYP26-inhibitory potency of the former drug. Tretinoin 39-41 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 122-127
19294396-9 2009 The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis. Tretinoin 89-91 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 29-36
19294396-9 2009 The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis. Tretinoin 89-91 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 29-34
19294396-9 2009 The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis. Tretinoin 117-119 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 29-36
19294396-9 2009 The present study shows that CYP26A1 expression is extremely sensitive to both exogenous RA and increased endogenous RA levels, i.e. due to CYP26 inhibition, and thus an excellent biomarker for retinoid signalling in organotypic epidermis. Tretinoin 117-119 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 29-34
19519282-4 2009 The CYP26 enzymes have been shown to metabolize RA efficiently and they are also inducible by RA in selected systems. Tretinoin 48-50 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-9
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 20-33 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 202-207
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 35-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 202-207
19519282-0 2009 The role of CYP26 enzymes in retinoic acid clearance. Tretinoin 29-42 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 12-17
19519282-3 2009 It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA. Tretinoin 120-122 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-51
19519282-3 2009 It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA. Tretinoin 120-122 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 53-58
19519282-3 2009 It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA. Tretinoin 139-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-51
19519282-3 2009 It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA. Tretinoin 139-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 53-58
19519282-3 2009 It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA. Tretinoin 139-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-51
19519282-8 2009 To further the understanding of how CYP26 enzymes contribute to the regulation of RA homeostasis, structural information of the CYP26s, commercially available recombinant enzymes and good specific and sensitive antibodies are needed. Tretinoin 82-84 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 36-41
19519282-3 2009 It has been proposed that cytochrome P450 family 26 (CYP26) enzymes have a role in determining the cellular exposure to RA by inactivating RA in cells that do not need RA. Tretinoin 139-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 53-58
19401386-0 2009 PPARgamma regulates retinoic acid-mediated DC induction of Tregs. Tretinoin 20-33 peroxisome proliferator activated receptor gamma Homo sapiens 0-9
19477923-4 2009 RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. Tretinoin 0-2 splicing factor proline and glutamine rich Homo sapiens 196-199
19574996-7 2009 RESULTS: We obtained a high percentage of MAP2-positive neurons derived from embryoid bodies (EBs) induced by RA by administering 1 mmol/L NAC at differentiation day 0. Tretinoin 110-112 microtubule-associated protein 2 Mus musculus 42-46
19642999-8 2009 ERK phosphorylation was enhanced in RA-treated cultures at the early stage of differentiation. Tretinoin 36-38 mitogen-activated protein kinase 1 Mus musculus 0-3
19642999-10 2009 This effect depends on RA signaling and its crosstalk with the ERK and Wnt pathways. Tretinoin 23-25 mitogen-activated protein kinase 1 Mus musculus 63-66
19578722-4 2009 When treated with ATRA for 72 h, the EZH2 and SUZ12 mRNA levels were decreased to 35% and 38% of the control group, respectively. Tretinoin 18-22 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 37-41
19571399-0 2009 Silencing mediator of retinoic acid and thyroid hormone receptor regulates enhanced activation of signal transducer and activator of transcription 3 by epstein-barr virus-derived epstein-barr nuclear antigen 2. Tretinoin 22-35 signal transducer and activator of transcription 3 Homo sapiens 98-148
19688019-8 2009 The pre-induced cells after 2 days of RA exposure showed the expression of neuroblastic markers of nestin and NF68 (81.56 +/- 2.64% and 82.12 +/- 2.65%, respectively). Tretinoin 38-40 neurofilament light chain Rattus norvegicus 110-114
19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 41-43 caspase 3 Homo sapiens 107-116
19267404-4 2009 Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL. Tretinoin 209-222 caspase 3 Homo sapiens 0-9
20016705-5 2009 Treatment of RA isomers inhibited cell viability and induced apoptosis of MCF-7 cells as a result of increased caspase activity in cytoplasm and cytochrome C released from mitochondria. Tretinoin 13-15 cytochrome c, somatic Homo sapiens 145-157
20016705-8 2009 In addition, activities of antioxidant enzymes such as catalase and glutathione peroxidase were decreased effectively after treatment of RA in MCF-7 cells, whereas SOD activity was rarely affected. Tretinoin 137-139 catalase Homo sapiens 55-63
19528322-0 2009 Zic-associated holoprosencephaly: zebrafish Zic1 controls midline formation and forebrain patterning by regulating Nodal, Hedgehog, and retinoic acid signaling. Tretinoin 136-149 zic family member 1 (odd-paired homolog, Drosophila) Danio rerio 44-48
19528322-6 2009 Strikingly, we were able to show that Zic1 is also required for maintaining early forebrain expression of the retinoic acid (RA)-degrading enzyme cyp26a1. Tretinoin 110-123 zic family member 1 (odd-paired homolog, Drosophila) Danio rerio 38-42
19528322-6 2009 Strikingly, we were able to show that Zic1 is also required for maintaining early forebrain expression of the retinoic acid (RA)-degrading enzyme cyp26a1. Tretinoin 125-127 zic family member 1 (odd-paired homolog, Drosophila) Danio rerio 38-42
19528322-7 2009 Zic1 LOF leads to increased RA levels in the forebrain, subsequent ventralization of the optic vesicle and down-regulation of genes involved in dorsal BMP signaling. Tretinoin 28-30 zic family member 1 (odd-paired homolog, Drosophila) Danio rerio 0-4
19267404-4 2009 Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL. Tretinoin 224-228 caspase 3 Homo sapiens 0-9
19364826-1 2009 Many biological activities of all-trans-retinoic acid (RA) are mediated by the ligand-activated transcription factors termed retinoic acid receptors (RARs), but this hormone can also activate the nuclear receptor peroxisome proliferation-activated receptor beta/delta (PPARbeta/delta). Tretinoin 40-53 peroxisome proliferator activator receptor delta Mus musculus 269-277
19179438-4 2009 Here, we investigated whether RA might counteract glucocorticoid effects in skeletal muscle cells by lowering 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1)-dependent local glucocorticoid activation and/or activation of glucocorticoid receptor (GR). Tretinoin 30-32 nuclear receptor subfamily 3, group C, member 1 Mus musculus 230-253
19179438-4 2009 Here, we investigated whether RA might counteract glucocorticoid effects in skeletal muscle cells by lowering 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1)-dependent local glucocorticoid activation and/or activation of glucocorticoid receptor (GR). Tretinoin 30-32 nuclear receptor subfamily 3, group C, member 1 Mus musculus 255-257
19524524-5 2009 RA then facilitates the recruitment of a histone acetyltransferase CBP to the Ngn2/RAR-complex, markedly inducing histone H3/H4-acetylation. Tretinoin 0-2 CREB binding protein Homo sapiens 67-70
19385050-0 2009 Functional decreases in P2X7 receptors are associated with retinoic acid-induced neuronal differentiation of Neuro-2a neuroblastoma cells. Tretinoin 59-72 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 24-28
19385050-2 2009 Recently, P2X7 receptor has been shown to sustain growth of human neuroblastoma cells but its role during neuronal differentiation remains unexamined.We characterized the role of P2X7 receptors in the retinoic acid (RA)-differentiated N2a cells. Tretinoin 201-214 purinergic receptor P2X 7 Homo sapiens 10-23
19385050-2 2009 Recently, P2X7 receptor has been shown to sustain growth of human neuroblastoma cells but its role during neuronal differentiation remains unexamined.We characterized the role of P2X7 receptors in the retinoic acid (RA)-differentiated N2a cells. Tretinoin 201-214 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 10-14
19385050-2 2009 Recently, P2X7 receptor has been shown to sustain growth of human neuroblastoma cells but its role during neuronal differentiation remains unexamined.We characterized the role of P2X7 receptors in the retinoic acid (RA)-differentiated N2a cells. Tretinoin 216-218 purinergic receptor P2X 7 Homo sapiens 10-23
19385050-2 2009 Recently, P2X7 receptor has been shown to sustain growth of human neuroblastoma cells but its role during neuronal differentiation remains unexamined.We characterized the role of P2X7 receptors in the retinoic acid (RA)-differentiated N2a cells. Tretinoin 216-218 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 10-14
19385050-3 2009 RA induced N2a cells differentiation into neurite bearing and neuronal specific proteins, microtubule-associated protein 2 (MAP2) and neuronal specific nuclear protein (NeuN), expressing neuronal-like cells. Tretinoin 0-2 microtubule-associated protein 2 Mus musculus 90-122
19385050-3 2009 RA induced N2a cells differentiation into neurite bearing and neuronal specific proteins, microtubule-associated protein 2 (MAP2) and neuronal specific nuclear protein (NeuN), expressing neuronal-like cells. Tretinoin 0-2 microtubule-associated protein 2 Mus musculus 124-128
19385050-4 2009 Interestingly, the RA-induced neuronal differentiation was associated with decreases in the expression and function of P2X7 receptors. Tretinoin 19-21 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 119-123
19385050-6 2009 In addition, RA and oATP treatment stimulated the expression of neuron-specific class III beta-tubulin (TuJ1), and knockdown of P2X7 receptor expression by siRNA induced neurite outgrowth. Tretinoin 13-15 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 128-141
19332534-6 2009 Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. Tretinoin 110-114 interleukin-1 beta Sus scrofa 25-29
19364826-1 2009 Many biological activities of all-trans-retinoic acid (RA) are mediated by the ligand-activated transcription factors termed retinoic acid receptors (RARs), but this hormone can also activate the nuclear receptor peroxisome proliferation-activated receptor beta/delta (PPARbeta/delta). Tretinoin 55-57 peroxisome proliferator activator receptor delta Mus musculus 269-277
19364826-2 2009 We show here that adipocyte differentiation is accompanied by a shift in RA signaling which, in mature adipocytes, allows RA to activate both RARs and PPARbeta/delta, thereby enhancing lipolysis and depleting lipid stores. Tretinoin 73-75 peroxisome proliferator activator receptor delta Mus musculus 151-165
22666666-8 2009 Conditioned media from SCF, NGF or RA-treated HMC-1 cells, and SCF, NGF, DMSO or RA-treated THP-1 cells enhanced immune complex transport via enhancing the expression of the CD23 in HT29 cells and the release of inflammatory mediator TNF-alpha. Tretinoin 81-83 tumor necrosis factor Homo sapiens 234-243
19364826-4 2009 RA treatment of obese mice induced expression of PPARbeta/delta and RAR target genes involved in regulation of lipid homeostasis, leading to weight loss and improved insulin responsiveness. Tretinoin 0-2 peroxisome proliferator activator receptor delta Mus musculus 49-57
19364826-5 2009 RA treatment also restored adipose PPARbeta/delta expression. Tretinoin 0-2 peroxisome proliferator activator receptor delta Mus musculus 35-43
19364826-6 2009 The data indicate that suppression of obesity and insulin resistance by RA is largely mediated by PPARbeta/delta and is further enhanced by activation of RARs. Tretinoin 72-74 peroxisome proliferator activator receptor delta Mus musculus 98-106
19324018-0 2009 All-trans retinoic acid induces Thrombospondin-1 expression in acute promyelocytic leukemia cells though down-regulation of its transcription repressor, c-MYC oncoprotein. Tretinoin 10-23 thrombospondin 1 Homo sapiens 32-48
19324018-1 2009 Thrombospondin-1 (TSP-1) was found to mediate the therapeutic effects of all-trans retinoic acid (ATRA) for leukemia. Tretinoin 73-96 thrombospondin 1 Homo sapiens 0-16
19324018-1 2009 Thrombospondin-1 (TSP-1) was found to mediate the therapeutic effects of all-trans retinoic acid (ATRA) for leukemia. Tretinoin 73-96 thrombospondin 1 Homo sapiens 18-23
19324018-1 2009 Thrombospondin-1 (TSP-1) was found to mediate the therapeutic effects of all-trans retinoic acid (ATRA) for leukemia. Tretinoin 98-102 thrombospondin 1 Homo sapiens 0-16
19324018-1 2009 Thrombospondin-1 (TSP-1) was found to mediate the therapeutic effects of all-trans retinoic acid (ATRA) for leukemia. Tretinoin 98-102 thrombospondin 1 Homo sapiens 18-23
19324018-2 2009 The aim of the present study was to evaluate the role of c-MYC, a key transcription factor that contributes to the genesis of many human tumors, in TSP-1 induction by ATRA in acute promyelocytic leukemia (APL). Tretinoin 167-171 thrombospondin 1 Homo sapiens 148-153
19324018-3 2009 ATRA treatment markedly increased TSP-1 level and inhibited c-MYC expression in NB4 APL leukemic cells compared with controls. Tretinoin 0-4 thrombospondin 1 Homo sapiens 34-39
19324018-5 2009 c-MYC recruitment to TSP-1 promoter was dramatically decreased in NB4 cells following ATRA treatment. Tretinoin 86-90 thrombospondin 1 Homo sapiens 21-26
19324018-7 2009 Moreover, transient over-expression of c-MYC totally abolished TSP-1 induction by ATRA in NB4 cells. Tretinoin 82-86 thrombospondin 1 Homo sapiens 63-68
19324018-8 2009 Collectively, our results indicate that ATRA induces TSP-1 expression in APL cells though down-regulation of its transcription repressor, c-MYC oncoprotein. Tretinoin 40-44 thrombospondin 1 Homo sapiens 53-58
19147277-8 2009 The effect of EBBP on retinoid-responsive transcription appeared to be limited to genes with the retinoic acid response element (betaRARE) regulatory sequence, such as CYP26A1. Tretinoin 97-110 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 168-175
19432991-0 2009 Identification of the B-Raf/Mek/Erk MAP kinase pathway as a target for all-trans retinoic acid during skin cancer promotion. Tretinoin 81-94 mitogen-activated protein kinase 1 Mus musculus 32-35
19432991-8 2009 The counter-regulated genes have been clustered into functional categories and bioinformatic analysis has identified the B-Raf/Mek/Erk branch of the MAP kinase pathway as one containing several genes whose upregulation by TPA is blocked by ATRA. Tretinoin 240-244 mitogen-activated protein kinase 1 Mus musculus 131-134
19181377-1 2009 Polyethyleneimine (PEI)-g-All-trans-retinoic acid (ATRA) (designated as PRA) was synthesized as a gene carrier. Tretinoin 51-55 S100 calcium binding protein A6 Homo sapiens 72-75
19181377-4 2009 The resulting nanosized and positively charged PRA/pDNA complexes showed lower transfection efficiency than the PEI/pDNA complexes (N/P=10) against NIH3T3 which is less sensitive to ATRA in cell growth and more sensitive HeLa cells. Tretinoin 182-186 S100 calcium binding protein A6 Homo sapiens 47-50
19279407-0 2009 Mechanisms underlying the induction of the putative human tumor suppressor GPRC5A by retinoic acid. Tretinoin 85-98 G protein-coupled receptor class C group 5 member A Homo sapiens 75-81
19040532-6 2009 There was a major distinction between ERG rearranged and non-rearranged cancers that involves the levels of expression of genes linked to exposure to beta-oestradiol, and to retinoic acid. Tretinoin 174-187 ETS transcription factor ERG Homo sapiens 38-41
19279407-2 2009 Herein, we investigated the mechanism by which retinoic acid induces the expression of the human tumor suppressor GPRC5A. Tretinoin 47-60 G protein-coupled receptor class C group 5 member A Homo sapiens 114-120
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 0-4 integrin subunit beta 3 Homo sapiens 63-77
19131575-7 2009 Mechanism dissection suggests that TR2 and TR4 may affect the Oct-3/4 gene by binding to a direct repeat-1 element located in its promoter region, which is influenced by retinoic acid. Tretinoin 170-183 nuclear receptor subfamily 2 group C member 2 Homo sapiens 43-46
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 0-4 integrin subunit beta 3 Homo sapiens 160-174
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 0-4 integrin subunit beta 3 Homo sapiens 160-174
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 0-4 integrin subunit beta 3 Homo sapiens 160-174
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 249-253 integrin subunit beta 3 Homo sapiens 160-174
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 249-253 integrin subunit beta 3 Homo sapiens 160-174
19094985-8 2009 atRA treatment significantly suppressed the gene expression of integrin beta3 but not alphaV subunit, and effectively inhibited the tyrosine phosphorylation of integrin beta3 at residue 747 in RPE cells grown on laminin-coated dish, suggesting that atRA may suppress the RPE contractility through either inhibiting integrin beta3 expression or abrogating the integrin beta3-mediated signaling. Tretinoin 249-253 integrin subunit beta 3 Homo sapiens 160-174
19415779-6 2009 Nestin transcription is also mediated by treatment with retinoic acid, again in the absence of DNA demethylation. Tretinoin 56-69 nestin Homo sapiens 0-6
19461187-0 2009 A case of acute promyelocytic leukemia showing transient thrombocytosis caused by increased interleukin-6 and thrombopoietin after treatment with all-trans retinoic acid and chemotherapy. Tretinoin 156-169 interleukin 6 Homo sapiens 92-105
19461187-0 2009 A case of acute promyelocytic leukemia showing transient thrombocytosis caused by increased interleukin-6 and thrombopoietin after treatment with all-trans retinoic acid and chemotherapy. Tretinoin 156-169 thrombopoietin Homo sapiens 110-124
19461187-5 2009 These findings suggest that in APL patients, thrombocytosis after treatment with ATRA and or chemotherapy may be caused by increased plasma levels of both of IL-6 and TPO. Tretinoin 81-85 interleukin 6 Homo sapiens 158-170
19118439-6 2009 To induce granulocytic differentiation, HL-60 cells were treated for 5 d with ATRA and differentiation was confirmed by examining superoxide anion production, nuclear morphology, and changes in the expression of CD11b, CD13, and CD15. Tretinoin 78-82 fucosyltransferase 4 Homo sapiens 229-233
19260055-5 2009 The Raldh3 expression pattern delimited totally or partially the Bmp4-positive presumptive territories of vestibular sensory epithelia by stage 24 and the basilar papilla at stage 34, suggesting a possible involvement of RA in their specification. Tretinoin 221-223 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 4-10
19380800-7 2009 The defective polarization into effector cells was associated with impaired induction of T-bet, GATA3, MAF, and retinoic acid-related orphan nuclear hormone receptor (RORC). Tretinoin 112-125 RAR related orphan receptor C Homo sapiens 167-171
19476501-5 2009 Furthermore, ATRA demonstrates substrate specificity for beta-site amyloid precursor protein-cleaving enzyme (BACE) 1 over nonamyloidogenic BACE2 in beta-secretase regulation, which probably promotes competition for amyloid precursor protein between ADAM17 and BACE1. Tretinoin 13-17 beta-secretase 1 Homo sapiens 57-117
19476501-5 2009 Furthermore, ATRA demonstrates substrate specificity for beta-site amyloid precursor protein-cleaving enzyme (BACE) 1 over nonamyloidogenic BACE2 in beta-secretase regulation, which probably promotes competition for amyloid precursor protein between ADAM17 and BACE1. Tretinoin 13-17 amyloid beta precursor protein Homo sapiens 67-92
19476501-5 2009 Furthermore, ATRA demonstrates substrate specificity for beta-site amyloid precursor protein-cleaving enzyme (BACE) 1 over nonamyloidogenic BACE2 in beta-secretase regulation, which probably promotes competition for amyloid precursor protein between ADAM17 and BACE1. Tretinoin 13-17 beta-secretase 1 Homo sapiens 261-266
19363708-6 2009 These results indicate that the upregulation of TGF-beta1 pathway plays an important role in NB4 cells differentiation induced by ATRA. Tretinoin 130-134 transforming growth factor beta 1 Homo sapiens 48-57
19143025-8 2009 Interestingly, in another 6 patients with high-risk NT, diarrhea occurred at the time of chemotherapy or retinoic acid therapy ("Secondary VIP secreting NTs"). Tretinoin 105-118 vasoactive intestinal peptide Homo sapiens 139-142
19371709-0 2009 Retinoic acid can directly promote TGF-beta-mediated Foxp3(+) Treg cell conversion of naive T cells. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 35-43
19504631-6 2009 RESULT: RA up-regulated the mRNA expression of Mtap2 and Nefm, especially Mtap2 increased by 1.27 times, which was consistent with the morphological alteration. Tretinoin 8-10 microtubule-associated protein 2 Mus musculus 47-52
19504631-6 2009 RESULT: RA up-regulated the mRNA expression of Mtap2 and Nefm, especially Mtap2 increased by 1.27 times, which was consistent with the morphological alteration. Tretinoin 8-10 microtubule-associated protein 2 Mus musculus 74-79
19351818-7 2009 Moreover, the induction of RIG-G by retinoic acid in NB4 cells resulted, to some extent, from an IFNalpha autocrine pathway, a finding that suggests a novel mechanism for the signal cross-talk between IFNalpha and retinoic acid. Tretinoin 36-49 interferon alpha 1 Homo sapiens 97-105
19351818-7 2009 Moreover, the induction of RIG-G by retinoic acid in NB4 cells resulted, to some extent, from an IFNalpha autocrine pathway, a finding that suggests a novel mechanism for the signal cross-talk between IFNalpha and retinoic acid. Tretinoin 36-49 interferon alpha 1 Homo sapiens 201-209
19351818-7 2009 Moreover, the induction of RIG-G by retinoic acid in NB4 cells resulted, to some extent, from an IFNalpha autocrine pathway, a finding that suggests a novel mechanism for the signal cross-talk between IFNalpha and retinoic acid. Tretinoin 214-227 interferon alpha 1 Homo sapiens 97-105
19351850-9 2009 Treatment with LY294002, the PI3K inhibitor, or p85alpha knockdown with siRNA abolished tRA-induced NIS expression. Tretinoin 88-91 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 48-56
19731824-8 2009 Caspase-3 activity increased substantially with the increase of RGZ concentration and the addition of RGZ + ATRA in the culture medium showed similar synergism effect on caspase-3 activation (P < 0.01). Tretinoin 108-112 caspase 3 Homo sapiens 0-9
19285077-5 2009 FOXO3a deacetylation was increased by ATRA and blocked by nicotinamide. Tretinoin 38-42 forkhead box O3 Homo sapiens 0-6
19285077-6 2009 SIRT1 and FOXO3a siRNA inhibited ATRA-induced up-regulation of TH and differentiation. Tretinoin 33-37 forkhead box O3 Homo sapiens 10-16
19285077-6 2009 SIRT1 and FOXO3a siRNA inhibited ATRA-induced up-regulation of TH and differentiation. Tretinoin 33-37 tyrosine hydroxylase Homo sapiens 63-65
19285077-7 2009 Taken together, these results indicate that SIRT1 is involved in ATRA-induced differentiation of neuroblastoma cells via FOXO3a. Tretinoin 65-69 forkhead box O3 Homo sapiens 121-127
19252500-5 2009 Retinoic acid acted on DCs to induce suppressor of cytokine signaling-3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory cytokines. Tretinoin 0-13 mitogen-activated protein kinase 14 Homo sapiens 115-118
19351818-1 2009 Retinoic acid-induced gene G (RIG-G), a gene originally identified in all-trans retinoic acid-treated NB4 acute promyelocytic leukemia cells, is also induced by IFNalpha in various hematopoietic and solid tumor cells. Tretinoin 80-93 interferon alpha 1 Homo sapiens 161-169
18778286-2 2009 We have previously reported that all-trans retinoic acid (atRA) enhances the secretion of IL-2 from human peripheral blood T cells in vitro, followed by increased proliferation and inhibition of spontaneous cell death. Tretinoin 33-56 interleukin 2 Homo sapiens 90-94
18778286-2 2009 We have previously reported that all-trans retinoic acid (atRA) enhances the secretion of IL-2 from human peripheral blood T cells in vitro, followed by increased proliferation and inhibition of spontaneous cell death. Tretinoin 58-62 interleukin 2 Homo sapiens 90-94
18778286-4 2009 In contrast to the observations in human T cells, we found an overall reduction in luciferase-reported IL-2 gene expression in mice treated with atRA. Tretinoin 145-149 interleukin 2 Homo sapiens 103-107
18830878-0 2009 Ca2+/calmodulin-dependent protein kinase II mediates apoptosis of P19 cells expressing human tau during neural differentiation with retinoic acid treatment. Tretinoin 132-145 calmodulin 1 Homo sapiens 5-15
19151787-3 2009 A preliminary report suggested that adding all-trans retinoic acid (ATRA) to ESAs may improve their erythroid response, particularly in patients with high endogenous erythropoietin (EPO) level, and may improve other cytopenias. Tretinoin 43-66 erythropoietin Homo sapiens 166-180
19151787-3 2009 A preliminary report suggested that adding all-trans retinoic acid (ATRA) to ESAs may improve their erythroid response, particularly in patients with high endogenous erythropoietin (EPO) level, and may improve other cytopenias. Tretinoin 43-66 erythropoietin Homo sapiens 182-185
19151787-3 2009 A preliminary report suggested that adding all-trans retinoic acid (ATRA) to ESAs may improve their erythroid response, particularly in patients with high endogenous erythropoietin (EPO) level, and may improve other cytopenias. Tretinoin 68-72 erythropoietin Homo sapiens 166-180
19151787-3 2009 A preliminary report suggested that adding all-trans retinoic acid (ATRA) to ESAs may improve their erythroid response, particularly in patients with high endogenous erythropoietin (EPO) level, and may improve other cytopenias. Tretinoin 68-72 erythropoietin Homo sapiens 182-185
19731824-8 2009 Caspase-3 activity increased substantially with the increase of RGZ concentration and the addition of RGZ + ATRA in the culture medium showed similar synergism effect on caspase-3 activation (P < 0.01). Tretinoin 108-112 caspase 3 Homo sapiens 170-179
18831967-2 2009 The final step in the conversion of retinol to retinoic acid is carried out by three retinaldehyde dehydrogenases encoded by Raldh1 (Aldh1a1), Raldh2 (Aldh1a2), and Raldh3 (Aldh1a3). Tretinoin 47-60 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 165-171
19144644-6 2009 However, when present in excess amounts, SUG-1 blocks the activation of RARalpha target genes and the degradation of RARalpha that occurs in response to RA, via its ability to interfere with the recruitment of SRC-3 and other coregulators at the AF-2 domain of RARalpha. Tretinoin 72-74 proteasome 26S subunit, ATPase 5 Homo sapiens 41-46
18831967-2 2009 The final step in the conversion of retinol to retinoic acid is carried out by three retinaldehyde dehydrogenases encoded by Raldh1 (Aldh1a1), Raldh2 (Aldh1a2), and Raldh3 (Aldh1a3). Tretinoin 47-60 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 173-180
19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 ETS variant transcription factor 6 Homo sapiens 410-413
19014918-7 2009 In addition, we demonstrate here that enzymatic activity of AKR1B1 and AKR1B10 lowers all-trans- and 9-cis-retinoic acid-dependent trans-activation in living cells, indicating that both enzymes may contribute to pre-receptor regulation of retinoic acid and retinoid X nuclear receptors. Tretinoin 107-120 aldo-keto reductase family 1 member B Homo sapiens 60-66
19014918-7 2009 In addition, we demonstrate here that enzymatic activity of AKR1B1 and AKR1B10 lowers all-trans- and 9-cis-retinoic acid-dependent trans-activation in living cells, indicating that both enzymes may contribute to pre-receptor regulation of retinoic acid and retinoid X nuclear receptors. Tretinoin 239-252 aldo-keto reductase family 1 member B Homo sapiens 60-66
19120344-0 2009 The CYP26 inhibitor R115866 potentiates the effects of all-trans retinoic acid on cultured human epidermal keratinocytes. Tretinoin 65-78 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-9
19184071-7 2009 Topical application of all-trans retinoic acid (RA), a known regulator of keratinocyte differentiation and proliferation, induced comparable expression of differentiation marker proteins in wildtype and AQP3 null epidermis, though with impaired RA-induced proliferation in AQP3 null mice. Tretinoin 23-46 aquaporin 3 Mus musculus 203-207
19184071-7 2009 Topical application of all-trans retinoic acid (RA), a known regulator of keratinocyte differentiation and proliferation, induced comparable expression of differentiation marker proteins in wildtype and AQP3 null epidermis, though with impaired RA-induced proliferation in AQP3 null mice. Tretinoin 23-46 aquaporin 3 Mus musculus 273-277
19184071-7 2009 Topical application of all-trans retinoic acid (RA), a known regulator of keratinocyte differentiation and proliferation, induced comparable expression of differentiation marker proteins in wildtype and AQP3 null epidermis, though with impaired RA-induced proliferation in AQP3 null mice. Tretinoin 48-50 aquaporin 3 Mus musculus 203-207
19184071-7 2009 Topical application of all-trans retinoic acid (RA), a known regulator of keratinocyte differentiation and proliferation, induced comparable expression of differentiation marker proteins in wildtype and AQP3 null epidermis, though with impaired RA-induced proliferation in AQP3 null mice. Tretinoin 48-50 aquaporin 3 Mus musculus 273-277
19144990-6 2009 Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes. Tretinoin 45-47 HOXA transcript antisense RNA, myeloid-specific 1 Homo sapiens 13-21
19144990-6 2009 Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes. Tretinoin 45-47 integrin subunit beta 2 Homo sapiens 235-239
19120344-4 2009 R115866 is a specific inhibitor of the cytochrome P450 isoform CYP26, which is involved in the metabolic inactivation pathway of RA. Tretinoin 129-131 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 63-68
19120344-8 2009 RESULTS: RA induced HB-EGF and involucrin expression in a concentration-dependent manner, whereas it inhibited keratin 10 expression. Tretinoin 9-11 involucrin Homo sapiens 31-41
19120344-10 2009 However, when R115866 was combined with low concentrations of RA, HB-EGF and involucrin expression was induced. Tretinoin 62-64 involucrin Homo sapiens 77-87
19235731-1 2009 Cyp26b1 encodes a cytochrome-P450 enzyme that catabolizes retinoic acid (RA), a vitamin A derived signaling molecule. Tretinoin 58-71 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
19235731-1 2009 Cyp26b1 encodes a cytochrome-P450 enzyme that catabolizes retinoic acid (RA), a vitamin A derived signaling molecule. Tretinoin 73-75 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 10-23 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 135-140
19171200-7 2009 Thus CYP26B1 appears essential for RA catabolism under physiological conditions, whereas CYP26A1 might play a greater role during RA excess. Tretinoin 35-37 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 5-12
19112091-3 2009 The effect of RA was dose-dependent, and at the optimal concentration of 1 muM, repression of Fas-induced cell death by the mitogens 12-O-tetradecanoylphorbol 13-acetate (TPA) or Con A was reversed by approximately 50% and 30%, respectively. Tretinoin 14-16 latexin Homo sapiens 75-78
19171200-7 2009 Thus CYP26B1 appears essential for RA catabolism under physiological conditions, whereas CYP26A1 might play a greater role during RA excess. Tretinoin 130-132 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 89-96
19050858-7 2009 Moreover, cerebral ischemic induction of cyclooxygenase-2 (COX-2) and CCAAT/enhancer binding protein beta (C/EBPbeta), which binds to the COX-2 promoter, was also inhibited by RA. Tretinoin 176-178 prostaglandin-endoperoxide synthase 2 Homo sapiens 138-143
19050858-8 2009 These results suggest that RA can reduce ischemia-induced cerebral injury by an anti-inflammatory action, which may be effected via inhibition of C/EBPbeta-mediated COX-2 induction. Tretinoin 27-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170
19177594-3 2009 Injection of poly I:C/D-GalN into mice could promote tumor necrosis factor-alpha production and surface retinoic acid early inducible-1 (Rae1) protein expression by Kupffer cells, which then activated NK cells to produce interferon-gamma via NKG2D-Rae1 recognition. Tretinoin 104-117 galanin and GMAP prepropeptide Mus musculus 24-28
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 25-27 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 135-140
19171200-4 2009 RA (1 microM) induced CYP26A1, CYP26B1, CYP2S1, CRABPII and LRAT mRNA. Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 22-29
19171200-4 2009 RA (1 microM) induced CYP26A1, CYP26B1, CYP2S1, CRABPII and LRAT mRNA. Tretinoin 0-2 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 31-38
19171200-5 2009 The CYP26 inhibitor talarozole altered CYP26A1 and LRAT mRNA expression in a similar way as RA, increased the cellular accumulation of [(3)H]RA, and induced a punctate CRABPII staining, also observed after siRNA knock-down of CYP26B1 (but not after RA exposure). Tretinoin 52-54 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-9
19050858-7 2009 Moreover, cerebral ischemic induction of cyclooxygenase-2 (COX-2) and CCAAT/enhancer binding protein beta (C/EBPbeta), which binds to the COX-2 promoter, was also inhibited by RA. Tretinoin 176-178 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-57
19050858-7 2009 Moreover, cerebral ischemic induction of cyclooxygenase-2 (COX-2) and CCAAT/enhancer binding protein beta (C/EBPbeta), which binds to the COX-2 promoter, was also inhibited by RA. Tretinoin 176-178 prostaglandin-endoperoxide synthase 2 Homo sapiens 59-64
19112091-6 2009 However, analyses of ERK and NF-kappaB activities and expression of target genes indicated that RA-mediated counteraction of the protective effect of TPA did not involve negative crosstalk with ERK or NF-kappaB survival pathways. Tretinoin 96-98 nuclear factor kappa B subunit 1 Homo sapiens 29-38
19112091-7 2009 RA-induced cell death was accompanied by enhanced cleavage of procaspase-3, -6, and -8, as well as enhanced cleavage of DNA fragmentation factor 45. Tretinoin 0-2 caspase 3 Homo sapiens 62-86
19135033-6 2009 In addition, we demonstrate that the RA-mediated activation of Galanin promoter activity and Brn-3a N-terminal transcriptional activity are both blocked by pan-MEK inhibitors, and show that the expression of a constitutively-active mutant of MEK1, but not MEK5, is sufficient to increase Brn-3a activity. Tretinoin 37-39 mitogen-activated protein kinase kinase 7 Homo sapiens 160-163
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 caspase 3 Homo sapiens 127-136
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 poly(ADP-ribose) polymerase 1 Homo sapiens 156-160
19135033-6 2009 In addition, we demonstrate that the RA-mediated activation of Galanin promoter activity and Brn-3a N-terminal transcriptional activity are both blocked by pan-MEK inhibitors, and show that the expression of a constitutively-active mutant of MEK1, but not MEK5, is sufficient to increase Brn-3a activity. Tretinoin 37-39 mitogen-activated protein kinase kinase 5 Homo sapiens 256-260
19135033-7 2009 These results reveal an important role for the ERK1/2 pathway in Brn-3a regulation during RA-mediated neuronal differentiation and define the neuropeptide Galanin as a novel target of this transcription factor. Tretinoin 90-92 mitogen-activated protein kinase 3 Homo sapiens 47-53
18986761-0 2009 Enhanced interleukin-2 diphtheria toxin conjugate-induced growth suppression in retinoic acid-treated hypoxic hepatocellular carcinoma cells. Tretinoin 80-93 interleukin 2 Homo sapiens 9-22
19097998-4 2009 We show that the ability of P19 cells to undergo the transition from an Oct3/4-positive, undifferentiated status to microtubule-associated protein 2-positive neurons and glial fibrillary acidic protein-positive astrocytes, upon treatment with retinoic acid (RA), requires RA-induced activation of Cdc42 during the neural cell lineage specification phase. Tretinoin 243-256 microtubule-associated protein 2 Mus musculus 116-148
18986761-2 2009 Hypoxia and retinoic acid (RA) may also induce interleukin-2 (IL-2) receptor expression, and thus we evaluated if RA and IL-2 receptor-targeted therapy are indicated in hypoxic HCCs. Tretinoin 12-25 interleukin 2 Homo sapiens 47-60
18986761-2 2009 Hypoxia and retinoic acid (RA) may also induce interleukin-2 (IL-2) receptor expression, and thus we evaluated if RA and IL-2 receptor-targeted therapy are indicated in hypoxic HCCs. Tretinoin 12-25 interleukin 2 Homo sapiens 62-66
18986761-2 2009 Hypoxia and retinoic acid (RA) may also induce interleukin-2 (IL-2) receptor expression, and thus we evaluated if RA and IL-2 receptor-targeted therapy are indicated in hypoxic HCCs. Tretinoin 27-29 interleukin 2 Homo sapiens 47-60
18986761-2 2009 Hypoxia and retinoic acid (RA) may also induce interleukin-2 (IL-2) receptor expression, and thus we evaluated if RA and IL-2 receptor-targeted therapy are indicated in hypoxic HCCs. Tretinoin 27-29 interleukin 2 Homo sapiens 62-66
18986761-3 2009 RA induced IL-2 receptor expression (R alpha, R beta, R gamma) in HCC cells, whereas hypoxia specifically induced IL-2 R gamma expression. Tretinoin 0-2 interleukin 2 Homo sapiens 11-15
19115248-0 2009 Effect of tamoxifen and retinoic acid on bradykinin induced proliferation in MCF-7 cells. Tretinoin 24-37 kininogen 1 Homo sapiens 41-51
19100254-6 2009 We further show that fibroblast growth factor (FGF) signalling, induces the expression of the retinoic acid degrading enzyme cytochrome P450 (cyp) 26a1, and that one of its products, 4-oxo-RA, mimics the action of the RARalpha agonist in the differentiation of the NPCs into cholinergic neurons. Tretinoin 94-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 125-151
19216755-11 2009 Also, Chmp1A silencing diminished the increase of Chmp1A, P53 and phospho-P53 protein expression induced by ATRA. Tretinoin 108-112 tumor protein p53 Homo sapiens 58-61
19115248-2 2009 The combined action of tamoxifen/all-trans retinoic acid was advantageous in MCF-7 cells, reducing cell proliferation, Bcl-2 and c-Myc protein levels and increasing E-Cadherin protein levels and Gap junctional Intercellular Communication. Tretinoin 43-56 BCL2 apoptosis regulator Homo sapiens 119-124
19115248-2 2009 The combined action of tamoxifen/all-trans retinoic acid was advantageous in MCF-7 cells, reducing cell proliferation, Bcl-2 and c-Myc protein levels and increasing E-Cadherin protein levels and Gap junctional Intercellular Communication. Tretinoin 43-56 cadherin 1 Homo sapiens 165-175
19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 kininogen 1 Homo sapiens 21-31
19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 mitogen-activated protein kinase 3 Homo sapiens 111-117
19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 BCL2 apoptosis regulator Homo sapiens 139-144
19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 kininogen 1 Homo sapiens 157-167
19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 cadherin 1 Homo sapiens 217-227
19115248-6 2009 We showed that the anti-tumoral effect of tamoxifen/all-trans retinoic acid is beneficial in MCF-7 breast cancer cells grown in a bradykinin-pro-mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2-bradykinin receptor inhibition. Tretinoin 62-75 kininogen 1 Homo sapiens 130-140
19115248-6 2009 We showed that the anti-tumoral effect of tamoxifen/all-trans retinoic acid is beneficial in MCF-7 breast cancer cells grown in a bradykinin-pro-mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2-bradykinin receptor inhibition. Tretinoin 62-75 mitogen-activated protein kinase 3 Homo sapiens 223-227
19216755-11 2009 Also, Chmp1A silencing diminished the increase of Chmp1A, P53 and phospho-P53 protein expression induced by ATRA. Tretinoin 108-112 tumor protein p53 Homo sapiens 74-77
18629627-0 2009 DIXDC1 promotes retinoic acid-induced neuronal differentiation and inhibits gliogenesis in P19 cells. Tretinoin 16-29 DIX domain containing 1 Homo sapiens 0-6
19204112-0 2009 Contrasting roles for all-trans retinoic acid in TGF-beta-mediated induction of Foxp3 and Il10 genes in developing regulatory T cells. Tretinoin 32-45 interleukin 10 Mus musculus 90-94
18629627-8 2009 Thus, our finding suggested that DIXDC1 might play an important role during neurogenesis, overexpression of DIXDC1 in embryonic carcinoma P19 cells promoted neuronal differentiation, and inhibited gliogenesis induced by retinoic acid. Tretinoin 220-233 DIX domain containing 1 Homo sapiens 108-114
19015161-4 2009 The radius of gyration was estimated to be 19.4 A for L-PGDS, and 18.8 A for L-PGDS/RA, 17.3 A for L-PGDS/BR and 17.8 A for L-PGDS/BV complexes, indicating that L-PGDS became compact after binding of these ligands. Tretinoin 84-86 prostaglandin D2 synthase Homo sapiens 77-83
19176369-2 2009 ATRA-induced phosphorylation of the Akt kinase and ribosomal S6 protein in APL cells was sensitive to class I PI3K, and p110beta or p110delta inhibitors, and to the mammalian target of rapamycin (mTOR) inhibitor rapamycin. Tretinoin 0-4 mechanistic target of rapamycin kinase Homo sapiens 165-194
19176369-2 2009 ATRA-induced phosphorylation of the Akt kinase and ribosomal S6 protein in APL cells was sensitive to class I PI3K, and p110beta or p110delta inhibitors, and to the mammalian target of rapamycin (mTOR) inhibitor rapamycin. Tretinoin 0-4 mechanistic target of rapamycin kinase Homo sapiens 196-200
18945876-6 2009 Treatment with all-trans retinoic acid (ATRA) increased both the expression of ACER2 and the generation of sphingosine in HeLa cells and inhibited beta1 maturation. Tretinoin 15-38 alkaline ceramidase 2 Homo sapiens 79-84
18945876-6 2009 Treatment with all-trans retinoic acid (ATRA) increased both the expression of ACER2 and the generation of sphingosine in HeLa cells and inhibited beta1 maturation. Tretinoin 15-38 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 147-152
18945876-6 2009 Treatment with all-trans retinoic acid (ATRA) increased both the expression of ACER2 and the generation of sphingosine in HeLa cells and inhibited beta1 maturation. Tretinoin 40-44 alkaline ceramidase 2 Homo sapiens 79-84
18945876-6 2009 Treatment with all-trans retinoic acid (ATRA) increased both the expression of ACER2 and the generation of sphingosine in HeLa cells and inhibited beta1 maturation. Tretinoin 40-44 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 147-152
18945876-7 2009 ACER2 knockdown attenuated the inhibitory effects of ATRA on both beta1 maturation and cell adhesion. Tretinoin 53-57 alkaline ceramidase 2 Homo sapiens 0-5
18945876-7 2009 ACER2 knockdown attenuated the inhibitory effects of ATRA on both beta1 maturation and cell adhesion. Tretinoin 53-57 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 66-71
19015161-4 2009 The radius of gyration was estimated to be 19.4 A for L-PGDS, and 18.8 A for L-PGDS/RA, 17.3 A for L-PGDS/BR and 17.8 A for L-PGDS/BV complexes, indicating that L-PGDS became compact after binding of these ligands. Tretinoin 84-86 prostaglandin D2 synthase Homo sapiens 77-83
19015161-4 2009 The radius of gyration was estimated to be 19.4 A for L-PGDS, and 18.8 A for L-PGDS/RA, 17.3 A for L-PGDS/BR and 17.8 A for L-PGDS/BV complexes, indicating that L-PGDS became compact after binding of these ligands. Tretinoin 84-86 prostaglandin D2 synthase Homo sapiens 77-83
19015161-4 2009 The radius of gyration was estimated to be 19.4 A for L-PGDS, and 18.8 A for L-PGDS/RA, 17.3 A for L-PGDS/BR and 17.8 A for L-PGDS/BV complexes, indicating that L-PGDS became compact after binding of these ligands. Tretinoin 84-86 prostaglandin D2 synthase Homo sapiens 77-83
19246282-1 2009 OBJECTIVE: To investigate the molecular mechanism of dermal damage in heat shock-induced skin aging by observing the expressions of metalloproteinase-1 (MMP-1) and tissue inhibitor of MMP-1 (TIMP-1) in retinoic acid-treated cultured human fibroblasts with heat shock. Tretinoin 202-215 TIMP metallopeptidase inhibitor 1 Homo sapiens 164-189
19091570-7 2009 There was stable down-regulation of MDM2 and UGB as well as overexpression of SOD2, CSTB, and G3BP when RA-treated SHG-44 was compared with normal SHG-44. Tretinoin 104-106 cystatin B Homo sapiens 84-88
19246282-5 2009 CONCLUSION: Retinoic acid can reduce the expression of MMP-1 and increase the expression of TIMP-1 in cultured human fibroblasts, suggesting its therapeutic potential for heat shock-induced skin aging. Tretinoin 12-25 TIMP metallopeptidase inhibitor 1 Homo sapiens 92-98
18987662-5 2009 U-937 cells overexpressing VEGF were resistant to all-trans-retinoic acid-(ATRA) or camptothecin-induced apoptosis. Tretinoin 50-74 vascular endothelial growth factor A Homo sapiens 27-31
18987662-5 2009 U-937 cells overexpressing VEGF were resistant to all-trans-retinoic acid-(ATRA) or camptothecin-induced apoptosis. Tretinoin 75-79 vascular endothelial growth factor A Homo sapiens 27-31
19246282-1 2009 OBJECTIVE: To investigate the molecular mechanism of dermal damage in heat shock-induced skin aging by observing the expressions of metalloproteinase-1 (MMP-1) and tissue inhibitor of MMP-1 (TIMP-1) in retinoic acid-treated cultured human fibroblasts with heat shock. Tretinoin 202-215 TIMP metallopeptidase inhibitor 1 Homo sapiens 191-197
26238624-5 2009 Specific PTMs of TR2 could differentially regulate its biological activity mediated by multiple signaling pathways including one elicited by the nongenomic action of retinoic acid. Tretinoin 166-179 parathymosin Mus musculus 9-13
19152448-9 2009 Expression of vascular endothelial growth factor (VEGF) mRNA in PANC-1 cells, which were treated with 15d-PGJ(2) or 9-cis-RA at various concentrations or different duration, was detected by semi-quantitative RT-PCR. Tretinoin 116-124 vascular endothelial growth factor A Homo sapiens 14-48
18804386-5 2009 Here, we discuss the role of RA in the imprinting of gut-homing ASC and the evidence linking RA with the generation of intestinal IgA-ASCs. Tretinoin 29-31 PYD and CARD domain containing Homo sapiens 64-67
18809338-2 2009 Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 68-99
18809338-2 2009 Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 101-109
18809338-3 2009 This review will focus on the role of RA in the reciprocal TGF-beta-driven differentiation of T(H)17 and Treg and on the importance of such regulatory mechanism to control a functional immune system, in particular at the mucosal interface of the intestine. Tretinoin 38-40 transforming growth factor beta 1 Homo sapiens 59-67
19317219-9 2009 We demonstrated that histone acetylation by the PPARgamma agonist CDDO, RAR/RXR agonist ATRA, and/or histone deacetylase inhibitors (HDACIs) reversed the silenced RARbeta and MDR1 genes in acute promyelocytic leukemia, and that HDACI induced apoptosis with phagocytosis through the induction of Annexin A1 in AML1/ETO-positive acute myelocytic leukemia (AML) cells. Tretinoin 88-92 RAB40B, member RAS oncogene family Homo sapiens 72-75
19317219-9 2009 We demonstrated that histone acetylation by the PPARgamma agonist CDDO, RAR/RXR agonist ATRA, and/or histone deacetylase inhibitors (HDACIs) reversed the silenced RARbeta and MDR1 genes in acute promyelocytic leukemia, and that HDACI induced apoptosis with phagocytosis through the induction of Annexin A1 in AML1/ETO-positive acute myelocytic leukemia (AML) cells. Tretinoin 88-92 retinoic acid receptor beta Homo sapiens 163-170
19152444-1 2009 Midkine (MK) is a heparin-binding growth factor with its gene first identified in embryonal carcinoma cells at early stages of retinoic acid-induced differentiation. Tretinoin 127-140 midkine Homo sapiens 0-7
19152444-1 2009 Midkine (MK) is a heparin-binding growth factor with its gene first identified in embryonal carcinoma cells at early stages of retinoic acid-induced differentiation. Tretinoin 127-140 midkine Homo sapiens 9-11
19152448-9 2009 Expression of vascular endothelial growth factor (VEGF) mRNA in PANC-1 cells, which were treated with 15d-PGJ(2) or 9-cis-RA at various concentrations or different duration, was detected by semi-quantitative RT-PCR. Tretinoin 116-124 vascular endothelial growth factor A Homo sapiens 50-54
19255510-4 2009 We found that atRA suppressed chondrogenesis and Smad2/3 phosphorylation regardless of the presence of TGF-beta3. Tretinoin 14-18 SMAD family member 2 Mus musculus 49-56
18992716-0 2009 Retinoic acid modulates retinaldehyde dehydrogenase 1 gene expression through the induction of GADD153-C/EBPbeta interaction. Tretinoin 0-13 DNA damage inducible transcript 3 Homo sapiens 95-102
18992716-7 2009 Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box. Tretinoin 15-17 DNA damage inducible transcript 3 Homo sapiens 28-35
18992716-7 2009 Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box. Tretinoin 15-17 DNA damage inducible transcript 3 Homo sapiens 40-47
18992716-8 2009 These data support a model in which high RA levels inhibit Raldh1 gene expression by sequestering C/EBPbeta through its interaction to GADD153. Tretinoin 41-43 DNA damage inducible transcript 3 Homo sapiens 135-142
18992717-3 2009 Enzymes in the CYP26 family are thought to be responsible for the elimination of RA, and CYP26A1 appears to serve the most critical functions in this family. Tretinoin 81-83 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 89-96
18992717-6 2009 Heme incorporation was determined by carbon monoxide difference spectrum and a type 1 spectrum was observed with RA binding to CYP26A1. Tretinoin 113-115 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 127-134
18992717-7 2009 We found that RA is a tight binding ligand of CYP26A1 with low nM binding affinity. Tretinoin 14-16 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 46-53
18992717-8 2009 CYP26A1 oxidized RA efficiently (depletion K(m) 9.4+/-3.3nM and V(max) 11.3+/-4.3pmolesmin(-1)pmoleP450(-1)) when supplemented with P450 oxidoreductase and NADPH but was independent of cytochrome b5. Tretinoin 17-19 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18992717-10 2009 4-OH-RA was further metabolized by CYP26A1 to more polar metabolites and this sequential metabolism of RA occurred in part without 4-OH-RA leaving the active site of CYP26A1. Tretinoin 5-7 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 35-42
18992717-10 2009 4-OH-RA was further metabolized by CYP26A1 to more polar metabolites and this sequential metabolism of RA occurred in part without 4-OH-RA leaving the active site of CYP26A1. Tretinoin 5-7 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 166-173
18992717-11 2009 The high efficiency of CYP26A1 in eliminating both RA and its potentially active metabolites supports the major role of this enzyme in regulating RA clearance in vivo. Tretinoin 51-53 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 23-30
18992717-11 2009 The high efficiency of CYP26A1 in eliminating both RA and its potentially active metabolites supports the major role of this enzyme in regulating RA clearance in vivo. Tretinoin 146-148 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 23-30
19010342-10 2009 Chemical and immuno-inhibition metabolism studies suggested that Cyp26a1, Cyp2b, and Cyp3a, but not Cyp1a1 proteins were involved in atRA metabolism. Tretinoin 133-137 cytochrome P450, family 2, subfamily b, polypeptide 10 Mus musculus 74-79
20429413-11 2009 For example, retinoic acid, produced by the dendritic cells and epithelial cells in the intestine, works together with TGF-beta1 and promotes generation of small intestine-homing FOXP3 T-cells by upregulating the expression ofFOXP3 and gut homing receptors. Tretinoin 13-26 transforming growth factor beta 1 Homo sapiens 119-128
19016711-1 2009 BACKGROUND: An alternative approach to retinoid therapy is to inhibit the cytochrome P450 (CYP)-mediated catabolism of endogenous all-trans retinoic acid in the skin by applying retinoic acid metabolism blocking agents such as talarozole (R115866). Tretinoin 130-153 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 74-89
19016711-1 2009 BACKGROUND: An alternative approach to retinoid therapy is to inhibit the cytochrome P450 (CYP)-mediated catabolism of endogenous all-trans retinoic acid in the skin by applying retinoic acid metabolism blocking agents such as talarozole (R115866). Tretinoin 130-153 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 91-94
19016711-1 2009 BACKGROUND: An alternative approach to retinoid therapy is to inhibit the cytochrome P450 (CYP)-mediated catabolism of endogenous all-trans retinoic acid in the skin by applying retinoic acid metabolism blocking agents such as talarozole (R115866). Tretinoin 140-153 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 74-89
19016711-1 2009 BACKGROUND: An alternative approach to retinoid therapy is to inhibit the cytochrome P450 (CYP)-mediated catabolism of endogenous all-trans retinoic acid in the skin by applying retinoic acid metabolism blocking agents such as talarozole (R115866). Tretinoin 140-153 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 91-94
19540457-0 2009 Retinoic acid inhibits dendritic cell differentiation driven by interleukin-4. Tretinoin 0-13 interleukin 4 Homo sapiens 64-77
19540457-9 2009 In fact, atRA was detrimental on IL-4 property as a DC inductor. Tretinoin 9-13 interleukin 4 Homo sapiens 33-37
19255510-5 2009 Functional assays indicated that TGF-beta3 treatment or co-transfection of expressing Smad2/3 vectors suppressed atRA-induced RARE-tk-Luc activity. Tretinoin 113-117 SMAD family member 2 Mus musculus 86-93
18984738-0 2009 All-trans retinoic acid inhibits type 1 diabetes by T regulatory (Treg)-dependent suppression of interferon-gamma-producing T-cells without affecting Th17 cells. Tretinoin 10-23 interferon gamma Mus musculus 97-113
18984738-9 2009 CONCLUSIONS: These results demonstrate that ATRA treatment promoted in vivo expansion of Treg cells and induced Treg cell-dependent immune tolerance by suppressing IFN-gamma-producing T-cells, without affecting Th17 cells. Tretinoin 44-48 interferon gamma Mus musculus 164-173
18929555-6 2009 In addition, the alpha subclass (raraa, rarab) is RA inducible, and of these only raraa expression is RA-dependent, suggesting that these receptors establish a region of particularly high RA signaling through positive-feedback. Tretinoin 50-52 retinoic acid receptor, alpha a Danio rerio 33-38
19056829-3 2009 Here we show that RA signals induce expression of the NET transcriptional regulator Nolz1 in differentiated chick MNs, where it regulates the progressive specification of prospective Lim3-negative motor columns. Tretinoin 18-20 LIM homeobox 3 Gallus gallus 183-187
18929555-6 2009 In addition, the alpha subclass (raraa, rarab) is RA inducible, and of these only raraa expression is RA-dependent, suggesting that these receptors establish a region of particularly high RA signaling through positive-feedback. Tretinoin 50-52 retinoic acid receptor, alpha b Danio rerio 40-45
18929555-6 2009 In addition, the alpha subclass (raraa, rarab) is RA inducible, and of these only raraa expression is RA-dependent, suggesting that these receptors establish a region of particularly high RA signaling through positive-feedback. Tretinoin 102-104 retinoic acid receptor, alpha a Danio rerio 82-87
18929555-6 2009 In addition, the alpha subclass (raraa, rarab) is RA inducible, and of these only raraa expression is RA-dependent, suggesting that these receptors establish a region of particularly high RA signaling through positive-feedback. Tretinoin 102-104 retinoic acid receptor, alpha a Danio rerio 82-87
20067883-14 2009 Docetaxel and estradiol increased the percentage of apoptotic cells (71% apoptotic cells after administration of 10 muM all-trans retinoic acid combined with 0.01 muM estradiol, p<0.0001). Tretinoin 120-143 latexin Homo sapiens 116-119
20067883-15 2009 beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined. Tretinoin 38-51 BCL2 apoptosis regulator Homo sapiens 134-139
20067883-15 2009 beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined. Tretinoin 38-51 tumor protein p53 Homo sapiens 144-147
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 61-63 iodothyronine deiodinase 3 Homo sapiens 109-111
19636436-9 2009 However, expression of E-cadherin, RAR, and CRABP increased upon ATRA treatment. Tretinoin 65-69 cadherin 1 Homo sapiens 23-33
19636436-9 2009 However, expression of E-cadherin, RAR, and CRABP increased upon ATRA treatment. Tretinoin 65-69 RAB40B, member RAS oncogene family Homo sapiens 35-38
19636436-10 2009 Binding of cells to extra cellular matrix (ECM) protein fibronectin reduced significantly after ATRA treatment. Tretinoin 96-100 fibronectin 1 Homo sapiens 56-67
19636436-14 2009 This study is focused on the effect of ATRA on MMP, MMP-integrin-E-cadherin interrelationship, and also the effect of the drug on different signaling molecules which may involve in the progression of malignant tumor development. Tretinoin 39-43 cadherin 1 Homo sapiens 65-75
19075394-0 2009 Mutant Hoxd13 induces extra digits in a mouse model of synpolydactyly directly and by decreasing retinoic acid synthesis. Tretinoin 97-110 homeobox D13 Mus musculus 7-13
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 86-99 homeobox D13 Mus musculus 140-146
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 86-99 homeobox D13 Mus musculus 201-205
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 101-103 homeobox D13 Mus musculus 140-146
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 173-175 homeobox D13 Mus musculus 140-146
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 173-175 homeobox D13 Mus musculus 201-205
19075394-6 2009 Intrauterine treatment with RA restored pentadactyly in Spdh/Spdh mice. Tretinoin 28-30 homeobox D13 Mus musculus 56-60
19075394-6 2009 Intrauterine treatment with RA restored pentadactyly in Spdh/Spdh mice. Tretinoin 28-30 homeobox D13 Mus musculus 61-65
19075394-9 2009 Thus, we propose that mutated Hoxd13 causes polydactyly in SPD by inducing extraneous interdigital chondrogenesis, both directly and indirectly, via a reduction in RA levels. Tretinoin 164-166 homeobox D13 Mus musculus 30-36
19784600-3 2009 The Taqman Array results show that (1) stimulation with the liver-X-receptor and retinoid-X-receptor ligands T0901317 and 9-cis retinoic acid induces several genes of lipid metabolism, (2) lipopolysaccharide (LPS) and interferon-g (Ifn-g) strongly repress lipid-related genes, and (3) coincubation with docosahexaenoic acid dampens the repressing effect of LPS. Tretinoin 128-141 interferon gamma Homo sapiens 218-230
19784600-3 2009 The Taqman Array results show that (1) stimulation with the liver-X-receptor and retinoid-X-receptor ligands T0901317 and 9-cis retinoic acid induces several genes of lipid metabolism, (2) lipopolysaccharide (LPS) and interferon-g (Ifn-g) strongly repress lipid-related genes, and (3) coincubation with docosahexaenoic acid dampens the repressing effect of LPS. Tretinoin 128-141 interferon gamma Homo sapiens 232-237
19056420-7 2009 While undifferentiated SH-SY5Y cells were susceptible to 6-OHDA and MPP+, RA-differentiation conferred SH-SY5Y cells higher tolerance, potentially by up-regulating survival signaling, including Akt pathway as inhibition of Akt removed RA-induced neuroprotection against 6-OHDA. Tretinoin 74-76 AKT serine/threonine kinase 1 Homo sapiens 194-197
19056420-7 2009 While undifferentiated SH-SY5Y cells were susceptible to 6-OHDA and MPP+, RA-differentiation conferred SH-SY5Y cells higher tolerance, potentially by up-regulating survival signaling, including Akt pathway as inhibition of Akt removed RA-induced neuroprotection against 6-OHDA. Tretinoin 74-76 AKT serine/threonine kinase 1 Homo sapiens 223-226
19127080-1 2009 Nicotinamide, the amide derivative of vitamin B(3), cooperates with retinoic acid (RA), a form of vitamin A, and 1,25-dihydroxyvitamin D(3) (D3), to regulate cell differentiation and proliferation of human myeloblastic leukemia cells. Tretinoin 83-85 iodothyronine deiodinase 3 Homo sapiens 141-143
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 184-186 iodothyronine deiodinase 3 Homo sapiens 67-69
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 184-186 iodothyronine deiodinase 3 Homo sapiens 109-111
19127080-6 2009 Nicotinamide induced ERK activation and further enhanced the RA-induced ERK activation, but the D3-induced ERK activation was diminished by nicotinamide, although levels still exceeded those induced by RA, suggesting lineage-specific nicotinamide responses. Tretinoin 61-63 mitogen-activated protein kinase 1 Homo sapiens 72-75
19127080-6 2009 Nicotinamide induced ERK activation and further enhanced the RA-induced ERK activation, but the D3-induced ERK activation was diminished by nicotinamide, although levels still exceeded those induced by RA, suggesting lineage-specific nicotinamide responses. Tretinoin 61-63 mitogen-activated protein kinase 1 Homo sapiens 72-75
19127080-6 2009 Nicotinamide induced ERK activation and further enhanced the RA-induced ERK activation, but the D3-induced ERK activation was diminished by nicotinamide, although levels still exceeded those induced by RA, suggesting lineage-specific nicotinamide responses. Tretinoin 202-204 iodothyronine deiodinase 3 Homo sapiens 96-98
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 24-47 mitogen-activated protein kinase 1 Homo sapiens 82-121
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 24-47 mitogen-activated protein kinase 1 Homo sapiens 123-127
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 49-53 mitogen-activated protein kinase 1 Homo sapiens 82-121
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 49-53 mitogen-activated protein kinase 1 Homo sapiens 123-127
18976680-11 2009 The results show that the two RA-related molecules (TGF-beta1 and CRABPI) are altered by FON exposure in vitro. Tretinoin 30-32 transforming growth factor, beta 1 Rattus norvegicus 52-61
18845239-0 2008 NRF2 as a determinant of cellular resistance in retinoic acid cytotoxicity. Tretinoin 48-61 nuclear factor, erythroid derived 2, like 2 Mus musculus 0-4
19018263-4 2008 In vitro treatment with PPARgamma agonist, 15-Deoxy-Delta(12,14)-Prostaglandin J(2) (15d-PGJ2) or all-trans retinoic acid resulted in a reversible inhibition of gliosphere formation in culture. Tretinoin 108-121 peroxisome proliferator activated receptor gamma Homo sapiens 24-33
18845239-2 2008 Recently, RA at relatively low concentrations was shown to inhibit NRF2 and the expression of its target antioxidative genes. Tretinoin 10-12 nuclear factor, erythroid derived 2, like 2 Mus musculus 67-71
18845239-8 2008 Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA. Tretinoin 82-86 mitogen-activated protein kinase 1 Mus musculus 19-22
18845239-4 2008 Using in vitro cell and in vivo mouse models, we report that RA, specifically all-trans-RA (atRA) at concentrations implicated in toxicity, can activate NRF2 and induce NRF2 target genes, particularly the subunits of the rate-limiting enzyme of glutathione biosynthesis, glutamate cysteine ligase (GCLM/GCLC). Tretinoin 92-96 nuclear factor, erythroid derived 2, like 2 Mus musculus 153-157
18845239-8 2008 Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA. Tretinoin 82-86 nuclear factor, erythroid derived 2, like 2 Mus musculus 95-99
18845239-8 2008 Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA. Tretinoin 84-86 mitogen-activated protein kinase 1 Mus musculus 19-22
18845239-4 2008 Using in vitro cell and in vivo mouse models, we report that RA, specifically all-trans-RA (atRA) at concentrations implicated in toxicity, can activate NRF2 and induce NRF2 target genes, particularly the subunits of the rate-limiting enzyme of glutathione biosynthesis, glutamate cysteine ligase (GCLM/GCLC). Tretinoin 92-96 nuclear factor, erythroid derived 2, like 2 Mus musculus 169-173
18845239-8 2008 Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA. Tretinoin 84-86 nuclear factor, erythroid derived 2, like 2 Mus musculus 95-99
18845239-9 2008 NRF2-silenced cells were vulnerable to atRA-induced mitochondrial toxicity and apoptosis. Tretinoin 39-43 nuclear factor, erythroid derived 2, like 2 Mus musculus 0-4
18845239-5 2008 RNA interference-mediated silencing of NRF2, but not of retinoid X receptor-alpha and -beta, reduced basal and atRA-induced GCLM/GCLC gene expression. Tretinoin 111-115 nuclear factor, erythroid derived 2, like 2 Mus musculus 39-43
18845239-10 2008 In conclusion, toxic RA activates NRF2, thereby triggering an adaptive response against the resultant oxidative stress. Tretinoin 21-23 nuclear factor, erythroid derived 2, like 2 Mus musculus 34-38
18845239-6 2008 Moreover, RA increased nuclear accumulation of NRF2, antioxidant response element (ARE) reporter activity, and NRF2 occupancy at AREs. Tretinoin 10-12 nuclear factor, erythroid derived 2, like 2 Mus musculus 47-51
18845239-6 2008 Moreover, RA increased nuclear accumulation of NRF2, antioxidant response element (ARE) reporter activity, and NRF2 occupancy at AREs. Tretinoin 10-12 nuclear factor, erythroid derived 2, like 2 Mus musculus 111-115
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 15-17 GLI family zinc finger 2 Homo sapiens 109-114
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 0-13 GLI family zinc finger 2 Homo sapiens 109-114
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 0-13 CCAAT enhancer binding protein alpha Homo sapiens 206-216
18930031-6 2008 During retinoic acid-induced neuronal differentiation, Cyclin D2 protein but not mRNA expression is strongly increased, concurrent with the down-regulation of miR-302b and Oct4. Tretinoin 7-20 cyclin D2 Homo sapiens 55-64
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 15-17 CCAAT enhancer binding protein alpha Homo sapiens 206-216
19029830-7 2008 This result, along with the observation that in response to pharmacological inhibition of the RA signaling, hepatocytes lacking Trim24 loose their ability to proliferate, strongly implicates Rara as a proto-oncogene in hepatocytes and demonstrates that overactivated RA signaling is deleterious to liver homeostasis. Tretinoin 94-96 tripartite motif-containing 24 Mus musculus 128-134
18767146-7 2008 Differential expression of the retinoic acid target genes, RARB, CRABP1, and CRABP2, indicated that deletion of TBL1XR1 compromised the function of SMRT/N-CoR in the appropriate control of gene expression. Tretinoin 31-44 retinoic acid receptor beta Homo sapiens 59-63
18767146-7 2008 Differential expression of the retinoic acid target genes, RARB, CRABP1, and CRABP2, indicated that deletion of TBL1XR1 compromised the function of SMRT/N-CoR in the appropriate control of gene expression. Tretinoin 31-44 TBL1X/Y related 1 Homo sapiens 112-119
19017957-6 2008 RA-induced eosinophil survival appears to be associated with down-regulation of caspase 3 and inhibition of its enzymatic activity. Tretinoin 0-2 caspase 3 Homo sapiens 80-89
18786169-2 2008 We have previously shown that early phases of differentiation and neural induction of NT2/D1 embryonal carcinoma cells by retinoic acid (RA) involve up-regulation of the SOX3 gene expression. Tretinoin 122-135 SRY-box transcription factor 3 Homo sapiens 170-174
18786169-2 2008 We have previously shown that early phases of differentiation and neural induction of NT2/D1 embryonal carcinoma cells by retinoic acid (RA) involve up-regulation of the SOX3 gene expression. Tretinoin 137-139 SRY-box transcription factor 3 Homo sapiens 170-174
18786169-3 2008 Here, we present identification of a novel positive regulatory promoter element involved in RA-dependent activation of the SOX3 gene expression in NT2/D1 cells. Tretinoin 92-94 SRY-box transcription factor 3 Homo sapiens 123-127
18786169-5 2008 It is capable of independently mediating the RA effect in a heterologous promoter context and its disruption caused significant reduction of RA/RXR transactivation of the SOX3 promoter. Tretinoin 45-47 SRY-box transcription factor 3 Homo sapiens 171-175
18786169-6 2008 Furthermore, by using synthetic antagonists of retinoid receptors, we have shown for the first time, that RA-induced SOX3 gene expression could be significantly down-regulated by the synthetic antagonist of RXR. Tretinoin 106-108 SRY-box transcription factor 3 Homo sapiens 117-121
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 28-32 mitogen-activated protein kinase 1 Homo sapiens 209-212
18989765-9 2008 The effects of ATRA on mitogen-activated protein kinase (MAPK) and NFkb were evaluated with Western blotting. Tretinoin 15-19 mitogen-activated protein kinase 1 Homo sapiens 57-61
18989765-13 2008 Furthermore, ATRA suppressed the expression of LPS-stimulated c-Raf, MKK1/2 and ERK expression of THP-1 cells. Tretinoin 13-17 mitogen-activated protein kinase 1 Homo sapiens 80-83
18989765-14 2008 In conclusion, ATRA suppressed Th2- and Th1-related chemokines expression in THP-1 cells, at least in part via the c-Raf-MKK1/2-ERK/MAPK pathway. Tretinoin 15-19 mitogen-activated protein kinase 1 Homo sapiens 128-131
18989765-14 2008 In conclusion, ATRA suppressed Th2- and Th1-related chemokines expression in THP-1 cells, at least in part via the c-Raf-MKK1/2-ERK/MAPK pathway. Tretinoin 15-19 mitogen-activated protein kinase 1 Homo sapiens 132-136
18642056-4 2008 Bax expression in the leukemic cells was increased by treatment with ATRA, alpha-TS, and their combination to 40%, 240%, and 320%, respectively, without any change in Bcl2 and p53 expression. Tretinoin 69-73 BCL2 associated X, apoptosis regulator Homo sapiens 0-3
19029980-1 2008 Retinoic acid and arsenic trioxide target the protein stability and transcriptional repression activity of the fusion oncoprotein PML-RARA, resulting in regression of acute promyelocytic leukemia (APL). Tretinoin 0-13 promyelocytic leukemia Mus musculus 130-133
19029980-3 2008 Here we show that retinoic acid also triggers growth arrest of leukemia-initiating cells (LICs) ex vivo and their clearance in PML-RARA mouse APL in vivo. Tretinoin 18-31 promyelocytic leukemia Mus musculus 127-130
19029980-4 2008 Retinoic acid treatment of mouse APLs expressing the fusion protein PLZF-RARA triggers full differentiation, but not LIC loss or disease remission, establishing that differentiation and LIC loss can be uncoupled. Tretinoin 0-13 zinc finger and BTB domain containing 16 Mus musculus 68-72
19029980-5 2008 Although retinoic acid and arsenic synergize to clear LICs through cooperative PML-RARA degradation, this combination does not enhance differentiation. Tretinoin 9-22 promyelocytic leukemia Mus musculus 79-82
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 28-32 mitogen-activated protein kinase 1 Homo sapiens 239-242
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 209-212
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 239-242
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 209-212
18809380-3 2008 The MMP-9 activity of certain cell lines was significantly inhibited with retinoic acid treatment, and this effect was reversed in the presence of a TGase 2 inhibitor. Tretinoin 74-87 transglutaminase 2 Homo sapiens 149-156
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 239-242
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 209-212
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 239-242
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 209-212
19099631-3 2008 The results showed that the ATRA in 0.01-01 micromol/L inhibited the proliferation of NB4 cells in time-and dose-dependent manner and induced the differentiation of NB4 cells into myeloid; the ATRA stimulated ERK activity in this process; ERK inhibitor PD98059 could partially block ATRA effect, specific inhibitor of p38MAPK, SB203580, combined with ATRA also could partially block the effects of ATRA on inhibition of NB4 growth and induction of differentiation. Tretinoin 193-197 mitogen-activated protein kinase 1 Homo sapiens 239-242
19099631-4 2008 It is concluded that the ATRA stimulates ERK and p38MAPK pathway in the process inducing differentiation of NB4 cells, the ERK and P38MAPK may be necessary for the ATRA-induced differentiation in NB4 cells. Tretinoin 25-29 mitogen-activated protein kinase 1 Homo sapiens 41-44
19099631-4 2008 It is concluded that the ATRA stimulates ERK and p38MAPK pathway in the process inducing differentiation of NB4 cells, the ERK and P38MAPK may be necessary for the ATRA-induced differentiation in NB4 cells. Tretinoin 164-168 mitogen-activated protein kinase 1 Homo sapiens 41-44
19099631-4 2008 It is concluded that the ATRA stimulates ERK and p38MAPK pathway in the process inducing differentiation of NB4 cells, the ERK and P38MAPK may be necessary for the ATRA-induced differentiation in NB4 cells. Tretinoin 164-168 mitogen-activated protein kinase 1 Homo sapiens 123-126
19067490-0 2008 Exdpf is a key regulator of exocrine pancreas development controlled by retinoic acid and ptf1a in zebrafish. Tretinoin 72-85 pancreatic progenitor cell differentiation and proliferation factor a Danio rerio 0-5
19006694-2 2008 Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. Tretinoin 15-17 transforming growth factor beta 1 Homo sapiens 29-37
19004786-6 2008 miR-138 functioned partially by repressing the retinoic acid synthesis enzyme, aldehyde dehydrogenase-1a2, in the ventricle. Tretinoin 47-60 microRNA 138 Danio rerio 0-7
18975307-10 2008 Tumor necrosis factor alpha and retinoic acid also stimulated release of neoepitope, and this was also suppressed by FGF-2. Tretinoin 32-45 fibroblast growth factor 2 Homo sapiens 117-122
19006694-0 2008 Retinoic acid enhances Foxp3 induction indirectly by relieving inhibition from CD4+CD44hi Cells. Tretinoin 0-13 CD4 molecule Homo sapiens 79-82
19006694-2 2008 Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 29-37
19076350-3 2008 Intersecting the rapidly emerging field of T(reg) function, has been the discovery that retinoic acid (RA) controls both the homing and differentiation of T(reg). Tretinoin 88-101 regenerating family member 1 alpha Homo sapiens 45-48
19076350-3 2008 Intersecting the rapidly emerging field of T(reg) function, has been the discovery that retinoic acid (RA) controls both the homing and differentiation of T(reg). Tretinoin 88-101 regenerating family member 1 alpha Homo sapiens 157-160
19076350-3 2008 Intersecting the rapidly emerging field of T(reg) function, has been the discovery that retinoic acid (RA) controls both the homing and differentiation of T(reg). Tretinoin 103-105 regenerating family member 1 alpha Homo sapiens 45-48
19076350-3 2008 Intersecting the rapidly emerging field of T(reg) function, has been the discovery that retinoic acid (RA) controls both the homing and differentiation of T(reg). Tretinoin 103-105 regenerating family member 1 alpha Homo sapiens 157-160
19076350-6 2008 Now these findings can be interpreted in light of the revelations that RA controls leukocyte homing and T(reg) function. Tretinoin 71-73 regenerating family member 1 alpha Homo sapiens 106-109
18724384-7 2008 Signalling kinases PKC and ERK were involved in the ATRA-induced differentiation enhanced by all of the effective sesquiterpene lactones, but JNK and PI3-K were involved in the ATRA-induced differentiation enhanced by costunolide and parthenolide. Tretinoin 52-56 mitogen-activated protein kinase 1 Homo sapiens 27-30
18974118-9 2008 RA-induced differentiation can thus be propelled by c-Cbl and by CD38, both of which bind together, enhance the expression of each other, and cause MAPK signaling. Tretinoin 0-2 mitogen-activated protein kinase 3 Homo sapiens 148-152
18724384-7 2008 Signalling kinases PKC and ERK were involved in the ATRA-induced differentiation enhanced by all of the effective sesquiterpene lactones, but JNK and PI3-K were involved in the ATRA-induced differentiation enhanced by costunolide and parthenolide. Tretinoin 177-181 mitogen-activated protein kinase 8 Homo sapiens 142-145
18771528-2 2008 Recently, many synthetic retinoids have been developed and among them, a novel synthetic retinoid, Am80 (Tamibarotene) is an RARalpha- and RARbeta-specific retinoid expected to overcome ATRA resistance. Tretinoin 186-190 retinoic acid receptor beta Homo sapiens 139-146
18368492-5 2008 Retinoic acid induces expression of a marker of intestinal differentiation, MUC2, in these cells. Tretinoin 0-13 mucin 2, oligomeric mucus/gel-forming Homo sapiens 76-80
18368492-7 2008 The ability of retinoic acid to induce MUC2 expression may be relevant to the pathogenesis of Barrett"s esophagus. Tretinoin 15-28 mucin 2, oligomeric mucus/gel-forming Homo sapiens 39-43
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 interleukin 6 Mus musculus 100-104
18637026-9 2008 In addition, RA treatment enhanced expression of endodermal markers GATA4 and AFP but inhibited expression of primitive ectodermal marker Fgf-5 and mesodermal marker Brachyury. Tretinoin 13-15 GATA binding protein 4 Mus musculus 68-73
18637026-9 2008 In addition, RA treatment enhanced expression of endodermal markers GATA4 and AFP but inhibited expression of primitive ectodermal marker Fgf-5 and mesodermal marker Brachyury. Tretinoin 13-15 fibroblast growth factor 5 Mus musculus 138-143
18949372-7 2008 The results indicated that VIP reduced MYCN mRNA and protein expression, especially in the MYCN-amplified IMR-32 cells, with a maximal and transient decrease by approximately 50% after few hours of treatment with VIP at 10(-6) M. This effect was compared to that of RA at 10(-5) M, which induced a diminution of MYCN mRNA expression by approximately 25% after few days of treatment. Tretinoin 266-268 vasoactive intestinal peptide Homo sapiens 27-30
18949372-7 2008 The results indicated that VIP reduced MYCN mRNA and protein expression, especially in the MYCN-amplified IMR-32 cells, with a maximal and transient decrease by approximately 50% after few hours of treatment with VIP at 10(-6) M. This effect was compared to that of RA at 10(-5) M, which induced a diminution of MYCN mRNA expression by approximately 25% after few days of treatment. Tretinoin 266-268 vasoactive intestinal peptide Homo sapiens 213-216
18615582-0 2008 S10 phosphorylation of p27 mediates atRA induced growth arrest in ovarian carcinoma cell lines. Tretinoin 36-40 dynactin subunit 6 Homo sapiens 23-26
18615582-1 2008 All trans retinoic acid (atRA) has been shown to inhibit the growth of CAOV3 ovarian carcinoma cells and to elevate the level of p27 cyclin-dependent kinase inhibitor. Tretinoin 4-23 dynactin subunit 6 Homo sapiens 129-132
18615582-1 2008 All trans retinoic acid (atRA) has been shown to inhibit the growth of CAOV3 ovarian carcinoma cells and to elevate the level of p27 cyclin-dependent kinase inhibitor. Tretinoin 25-29 dynactin subunit 6 Homo sapiens 129-132
18615582-2 2008 We report here that phosphorylation at S10 residue is an important event in mediating p27 role in atRA induced growth arrest. Tretinoin 98-102 dynactin subunit 6 Homo sapiens 86-89
18615582-3 2008 atRA treatment of atRA sensitive CAOV3 cells increases the levels of S10 phospho-p27 in both nuclear and cytoplasmic cell compartments. Tretinoin 0-4 dynactin subunit 6 Homo sapiens 81-84
18615582-7 2008 Overexpression of A10-p27 mutant renders CAOV3 cells more resistant to atRA treatment and reverses the effect that atRA has on p27 binding to CDKs, on CDK activity, and on the expression of S phase genes. Tretinoin 71-75 dynactin subunit 6 Homo sapiens 22-25
18615582-7 2008 Overexpression of A10-p27 mutant renders CAOV3 cells more resistant to atRA treatment and reverses the effect that atRA has on p27 binding to CDKs, on CDK activity, and on the expression of S phase genes. Tretinoin 115-119 dynactin subunit 6 Homo sapiens 22-25
18615582-7 2008 Overexpression of A10-p27 mutant renders CAOV3 cells more resistant to atRA treatment and reverses the effect that atRA has on p27 binding to CDKs, on CDK activity, and on the expression of S phase genes. Tretinoin 115-119 dynactin subunit 6 Homo sapiens 127-130
18243243-7 2008 Administration of ATRA attenuated irradiation-induced intestinal fibrosis and reduced mRNA of interleukin-6 and transforming growth factor-beta(1). Tretinoin 18-22 interleukin 6 Mus musculus 94-146
18927157-4 2008 Here, based on the positional cloning of the dolphin mutation, we have studied the role of the RA-oxidizing enzyme Cyp26b1 during cartilage and bone development in zebrafish. Tretinoin 95-97 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 115-122
18927157-8 2008 Together with data on the expression of osteoblast markers, our results indicate that temporal and spatial restriction of RA signaling by Cyp26 enzymes is required to attenuate osteoblast maturation and/or activity in vivo. Tretinoin 122-124 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 138-143
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 interleukin 6 Mus musculus 191-195
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 interleukin 6 Mus musculus 191-195
18959816-4 2008 Protein levels of NF-kappaB p65 and relB were clearly enhanced during retinoic acid-induced differentiation. Tretinoin 70-83 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 18-27
18621984-7 2008 The effect of CRABP2 silencing on elastin and RAR-beta expression in response to ATRA was measured in MRC5 lung fibroblasts. Tretinoin 81-85 retinoic acid receptor beta Homo sapiens 46-54
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 142-146 MN1 proto-oncogene, transcriptional regulator Homo sapiens 107-110
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 cyclin dependent kinase inhibitor 2A Homo sapiens 115-118
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 dynactin subunit 6 Homo sapiens 129-132
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 cyclin dependent kinase inhibitor 2A Homo sapiens 115-118
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 dynactin subunit 6 Homo sapiens 129-132
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 40-53 MN1 proto-oncogene, transcriptional regulator Homo sapiens 107-110
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 55-59 MN1 proto-oncogene, transcriptional regulator Homo sapiens 107-110
18632758-8 2008 MN1 inhibited DHRS9 expression and completely abolished its induction by ATRA. Tretinoin 73-77 MN1 proto-oncogene, transcriptional regulator Homo sapiens 0-3
18816858-3 2008 RA-degrading enzymes (Cyp26a1 and Cyp26b1) were expressed at early stages of normal tongue development, but exogenous RA perturbed their expression in the fetal tongue. Tretinoin 0-2 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 34-41
18715948-10 2008 Finally, we find that retinoic acid signalling activates both Irx1 and Irx3 genes in the pronephros. Tretinoin 22-35 iroquois homeobox 3 L homeolog Xenopus laevis 71-75
18718172-8 2008 CONCLUSION: These results indicate that atRA inhibits the increases in fibronectin that are induced by TGF-beta1 and Ang II in cultured glomerular mesangial cells. Tretinoin 40-44 transforming growth factor, beta 1 Rattus norvegicus 103-112
18728026-0 2008 Accumulation of hypoxia-inducible factor-1 alpha protein and its role in the differentiation of myeloid leukemic cells induced by all-trans retinoic acid. Tretinoin 140-153 hypoxia inducible factor 1 subunit alpha Homo sapiens 16-48
18728026-7 2008 RESULTS: all-trans retinoic acid rapidly increased endogenous and inducible expressed or CoCl(2)-stabilized HIF-1 alpha protein in leukemic cells under normoxia. Tretinoin 19-32 hypoxia inducible factor 1 subunit alpha Homo sapiens 108-119
18728026-8 2008 Importantly, suppression of HIF-1 alpha expression by specific short hairpin RNA partially but significantly inhibited all-trans retinoic acid-induced differentiation of the U937 cell line. Tretinoin 129-142 hypoxia inducible factor 1 subunit alpha Homo sapiens 28-39
18728026-9 2008 Reciprocally, the differentiation induced by all-trans retinoic acid was significantly enhanced by conditional HIF-1 alpha induction and HIF-1 alpha-stabilizing CoCl(2) treatment. Tretinoin 55-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 111-122
18728026-9 2008 Reciprocally, the differentiation induced by all-trans retinoic acid was significantly enhanced by conditional HIF-1 alpha induction and HIF-1 alpha-stabilizing CoCl(2) treatment. Tretinoin 55-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 137-148
18728026-11 2008 CONCLUSIONS: This work provides the first demonstration that HIF-1 alpha, a protein rapidly responsive to all-trans retinoic acid, plays a role in all-trans retinoic acid-induced differentiation of leukemic cells. Tretinoin 116-129 hypoxia inducible factor 1 subunit alpha Homo sapiens 61-72
18728026-11 2008 CONCLUSIONS: This work provides the first demonstration that HIF-1 alpha, a protein rapidly responsive to all-trans retinoic acid, plays a role in all-trans retinoic acid-induced differentiation of leukemic cells. Tretinoin 157-170 hypoxia inducible factor 1 subunit alpha Homo sapiens 61-72
18768840-4 2008 However, P2X7 was highly up-regulated on CD8(+) T cells from spleen and lymph nodes when T cells were activated in the presence of retinoic acid. Tretinoin 131-144 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 9-13
18718172-0 2008 All-trans retinoic acid inhibits the increases in fibronectin and PAI-1 induced by TGF-beta1 and Ang II in rat mesangial cells. Tretinoin 10-23 serpin family E member 1 Rattus norvegicus 66-71
18718172-0 2008 All-trans retinoic acid inhibits the increases in fibronectin and PAI-1 induced by TGF-beta1 and Ang II in rat mesangial cells. Tretinoin 10-23 transforming growth factor, beta 1 Rattus norvegicus 83-92
18718172-0 2008 All-trans retinoic acid inhibits the increases in fibronectin and PAI-1 induced by TGF-beta1 and Ang II in rat mesangial cells. Tretinoin 10-23 angiotensinogen Rattus norvegicus 97-103
18692045-10 2008 There is thus a membrane localized estrogen receptor in HL-60 myeloblastic leukemia cells that can cause ERK activation and modulates the response of these cells to retinoic acid, indicating crosstalk between the membrane estrogen and retinoic acid evoked pathways relevant to propulsion of cell differentiation. Tretinoin 165-178 estrogen receptor 1 Homo sapiens 35-52
18692045-10 2008 There is thus a membrane localized estrogen receptor in HL-60 myeloblastic leukemia cells that can cause ERK activation and modulates the response of these cells to retinoic acid, indicating crosstalk between the membrane estrogen and retinoic acid evoked pathways relevant to propulsion of cell differentiation. Tretinoin 235-248 estrogen receptor 1 Homo sapiens 35-52
18846337-14 2008 In comparison with group A, the mRNA levels of TGF-beta1 and CTGF in ATRA-treated CBDL groups were significantly decreased (P<0.05). Tretinoin 69-73 transforming growth factor, beta 1 Rattus norvegicus 47-56
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 transforming growth factor, beta 1 Rattus norvegicus 110-119
18799012-10 2008 In particular, the retinoic acid-synthesising enzyme, RALDH2, is expressed in the left ovarian cortex at the time of STRA8 up-regulation, prior to meiosis. Tretinoin 19-32 stimulated by retinoic acid 8 Gallus gallus 117-122
18798693-8 2008 Although the concentration needed is higher than the physiological levels of retinoic acids, these findings demonstrate that COUP-TFII is a ligand-regulated nuclear receptor, in which ligands activate the receptor by releasing it from the autorepressed conformation. Tretinoin 77-91 nuclear receptor subfamily 2 group F member 2 Homo sapiens 125-134
18718172-2 2008 METHODS: Subconfluent glomerular mesangial cells were serum-starved for 48 h and pretreated with atRA with subsequent stimulation of TGF-beta1 and Ang II. Tretinoin 97-101 transforming growth factor, beta 1 Rattus norvegicus 133-142
18718172-2 2008 METHODS: Subconfluent glomerular mesangial cells were serum-starved for 48 h and pretreated with atRA with subsequent stimulation of TGF-beta1 and Ang II. Tretinoin 97-101 angiotensinogen Rattus norvegicus 147-153
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 107-117
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 angiotensinogen Rattus norvegicus 121-127
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 138-148
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 serpin family E member 1 Rattus norvegicus 160-165
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 serpin family E member 1 Rattus norvegicus 238-243
18718172-8 2008 CONCLUSION: These results indicate that atRA inhibits the increases in fibronectin that are induced by TGF-beta1 and Ang II in cultured glomerular mesangial cells. Tretinoin 40-44 angiotensinogen Rattus norvegicus 117-123
18718172-9 2008 The data also suggest that this effect of atRA is associated with a change in PAI-1 levels. Tretinoin 42-46 serpin family E member 1 Rattus norvegicus 78-83
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 138-148
18437159-6 2008 In addition, we have demonstrated that some genes, similarly regulated by both inhibitors (upregulated as Bcl2, Id2, Cd24a or downregulated as Nodal), are bona fide p38alpha targets involved in neurogenesis and found a correlation with their expression profiles and the onset of neuronal differentiation triggered upon retinoic acid treatment. Tretinoin 319-332 B cell leukemia/lymphoma 2 Mus musculus 106-110
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 serpin family E member 1 Rattus norvegicus 238-243
18722776-4 2008 Incubation of SH-SY5Y human neuroblastoma cells with the imidazole aryl derivative 8, and the imidazole heteroaryl derivatives 16 and 17 potentiated the atRA-induced expression of CYP26B1. Tretinoin 153-157 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 180-187
18248652-8 2008 Exposure of leiomyoma cells to ATRA resulted in a dose-dependent inhibition of templates for specific ECM protein production including collagen 1, collagen 4, fibronectin and versican. Tretinoin 31-35 fibronectin 1 Homo sapiens 159-170
18248652-13 2008 CONCLUSION: Exposure of leiomyomas to ATRA down-regulated cell proliferation, ECM formation, RA metabolism and TGF-beta regulation, suggesting that RA exposure can alter the leiomyoma phenotype to one that more closely approximates normal myometrium. Tretinoin 40-42 transforming growth factor beta 1 Homo sapiens 111-119
18807137-2 2008 We previously demonstrated that a retinoic acid-synthesizing enzyme, retinaldehyde dehydrogenase 1 (RALDH1), is expressed in prolactin cells of adult rats and that estrogen suppressed RALDH1 expression. Tretinoin 34-47 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 69-98
18511450-9 2008 These results indicate that retinoylated proteins in HL60 cells can be recognized by ARMAs and that alpha-actinin modified by RA may play a significant role in RA-induced differentiation, including the promotion of cytomorphology changes. Tretinoin 126-128 actinin alpha 1 Homo sapiens 100-113
18511450-9 2008 These results indicate that retinoylated proteins in HL60 cells can be recognized by ARMAs and that alpha-actinin modified by RA may play a significant role in RA-induced differentiation, including the promotion of cytomorphology changes. Tretinoin 160-162 actinin alpha 1 Homo sapiens 100-113
18511453-7 2008 Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22alpha and alpha-SMA expression and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration. Tretinoin 110-114 tumor protein p53 Homo sapiens 118-121
18807137-2 2008 We previously demonstrated that a retinoic acid-synthesizing enzyme, retinaldehyde dehydrogenase 1 (RALDH1), is expressed in prolactin cells of adult rats and that estrogen suppressed RALDH1 expression. Tretinoin 34-47 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 100-106
18807137-2 2008 We previously demonstrated that a retinoic acid-synthesizing enzyme, retinaldehyde dehydrogenase 1 (RALDH1), is expressed in prolactin cells of adult rats and that estrogen suppressed RALDH1 expression. Tretinoin 34-47 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 184-190
18664493-6 2008 Instead, we demonstrate a novel role for P311 in an alternative pathway of lipid-droplet accumulation that is induced by the regeneration-inducing molecule retinoic acid. Tretinoin 156-169 neuronal regeneration related protein Mus musculus 41-45
18684916-0 2008 Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 102-110
18664493-0 2008 P311 functions in an alternative pathway of lipid accumulation that is induced by retinoic acid. Tretinoin 82-95 neuronal regeneration related protein Mus musculus 0-4
18684916-0 2008 Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression. Tretinoin 0-13 interleukin 6 Homo sapiens 149-153
18458045-0 2008 Retinoic acid induces PGI synthase expression in human endothelial cells. Tretinoin 0-13 prostaglandin I2 synthase Homo sapiens 22-34
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 106-119 mitogen-activated protein kinase kinase 7 Homo sapiens 275-278
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 121-125 mitogen-activated protein kinase 1 Homo sapiens 161-200
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 121-125 mitogen-activated protein kinase 1 Homo sapiens 202-206
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 121-125 mitogen-activated protein kinase kinase 7 Homo sapiens 234-273
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 121-125 mitogen-activated protein kinase kinase 7 Homo sapiens 275-278
18636178-0 2008 Nicotinamide attenuates aquaporin 3 overexpression induced by retinoic acid through inhibition of EGFR/ERK in cultured human skin keratinocytes. Tretinoin 62-75 epidermal growth factor receptor Homo sapiens 98-102
18636178-0 2008 Nicotinamide attenuates aquaporin 3 overexpression induced by retinoic acid through inhibition of EGFR/ERK in cultured human skin keratinocytes. Tretinoin 62-75 mitogen-activated protein kinase 1 Homo sapiens 103-106
18458045-11 2008 Furthermore, RA increased PGIS transcriptional activity in transient transfection assays, an effect that was prevented by an RAR antagonist. Tretinoin 13-15 prostaglandin I2 synthase Homo sapiens 26-30
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 106-119 mitogen-activated protein kinase 1 Homo sapiens 161-200
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 106-119 mitogen-activated protein kinase 1 Homo sapiens 202-206
18682553-2 2008 In the present study, we identify a signaling pathway initiated from the nongenomic activity of all-trans retinoic acid (atRA) to stimulate complex formation of extracellular signal-regulated kinase 2 (ERK2) with its upstream kinase, mitogen-activated protein kinase kinase (MEK). Tretinoin 106-119 mitogen-activated protein kinase kinase 7 Homo sapiens 234-273
18636178-7 2008 atRA treatment induces EGFR and ERK activation. Tretinoin 0-4 epidermal growth factor receptor Homo sapiens 23-27
18636178-7 2008 atRA treatment induces EGFR and ERK activation. Tretinoin 0-4 mitogen-activated protein kinase 1 Homo sapiens 32-35
18636178-8 2008 PD153035, an EGFR inhibitor, and U0126, an ERK inhibitor, inhibit atRA-induced upregulation of AQP3. Tretinoin 66-70 epidermal growth factor receptor Homo sapiens 13-17
18636178-8 2008 PD153035, an EGFR inhibitor, and U0126, an ERK inhibitor, inhibit atRA-induced upregulation of AQP3. Tretinoin 66-70 mitogen-activated protein kinase 1 Homo sapiens 43-46
18636178-9 2008 Nicotinamide also inhibits atRA-induced activation of EGFR/ERK signal transduction and decreases water permeability by downregulating AQP3 expression. Tretinoin 27-31 epidermal growth factor receptor Homo sapiens 54-58
18636178-9 2008 Nicotinamide also inhibits atRA-induced activation of EGFR/ERK signal transduction and decreases water permeability by downregulating AQP3 expression. Tretinoin 27-31 mitogen-activated protein kinase 1 Homo sapiens 59-62
18636178-10 2008 Collectively, our results indicate that the effect of atRA on AQP3 expression is at least partly mediated by EGFR/ERK signaling in cultured human skin keratinocytes. Tretinoin 54-58 epidermal growth factor receptor Homo sapiens 109-113
18636178-10 2008 Collectively, our results indicate that the effect of atRA on AQP3 expression is at least partly mediated by EGFR/ERK signaling in cultured human skin keratinocytes. Tretinoin 54-58 mitogen-activated protein kinase 1 Homo sapiens 114-117
18636178-11 2008 Nicotinamide attenuates atRA-induced AQP3 expression through inhibition of EGFR/ERK signal transduction and eventually decreases water permeability and water loss. Tretinoin 24-28 epidermal growth factor receptor Homo sapiens 75-79
18636178-11 2008 Nicotinamide attenuates atRA-induced AQP3 expression through inhibition of EGFR/ERK signal transduction and eventually decreases water permeability and water loss. Tretinoin 24-28 mitogen-activated protein kinase 1 Homo sapiens 80-83
18458045-8 2008 In contrast, RA induced PGI synthase (PGIS) activity and expression in terms of mRNA and protein determined by real-time PCR and Western blotting, respectively. Tretinoin 13-15 prostaglandin I2 synthase Homo sapiens 24-36
18458045-8 2008 In contrast, RA induced PGI synthase (PGIS) activity and expression in terms of mRNA and protein determined by real-time PCR and Western blotting, respectively. Tretinoin 13-15 prostaglandin I2 synthase Homo sapiens 38-42
18458045-9 2008 Results from experiments with several species of RA and with retinoic acid receptor (RAR) and retinoid X receptor (RXR) antagonists showed that the effect of RA on PGIS expression was mediated by RAR. Tretinoin 49-51 prostaglandin I2 synthase Homo sapiens 164-168
18458045-9 2008 Results from experiments with several species of RA and with retinoic acid receptor (RAR) and retinoid X receptor (RXR) antagonists showed that the effect of RA on PGIS expression was mediated by RAR. Tretinoin 85-87 prostaglandin I2 synthase Homo sapiens 164-168
18458045-10 2008 Actinomycin D and cycloheximide both inhibited RA-induced PGIS expression. Tretinoin 47-49 prostaglandin I2 synthase Homo sapiens 58-62
18474417-0 2008 Retinoic acid induces apoptosis by a non-classical mechanism of ERK1/2 activation. Tretinoin 0-13 mitogen-activated protein kinase 3 Homo sapiens 64-70
18564368-5 2008 Surprisingly, RA promoted astrogliogenesis at E17 but inhibited astrogliogenesis induced by ciliary neurotrophic factor (CNTF) at E13. Tretinoin 14-16 ciliary neurotrophic factor Rattus norvegicus 92-119
18564368-5 2008 Surprisingly, RA promoted astrogliogenesis at E17 but inhibited astrogliogenesis induced by ciliary neurotrophic factor (CNTF) at E13. Tretinoin 14-16 ciliary neurotrophic factor Rattus norvegicus 121-125
18440196-0 2008 Retinol and retinoic acid modulate catalase activity in Sertoli cells by distinct and gene expression-independent mechanisms. Tretinoin 12-25 catalase Homo sapiens 35-43
18495661-1 2008 All-trans-retinoic acid stimulates dendritic growth in hippocampal neurons within minutes by activating mitogen-activated protein kinase and mTOR and increasing dendritic translation of calcium calmodulin-dependent protein kinase II alpha and the alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate receptor subunit GluR1. Tretinoin 0-23 mechanistic target of rapamycin kinase Homo sapiens 141-145
18440196-4 2008 The aim of this study was to investigate the effects of retinol and its major biologically active metabolite, all-trans retinoic acid (RA), on CAT regulation. Tretinoin 110-133 catalase Homo sapiens 143-146
18571505-4 2008 In the present work we evaluated the effects of RA therapy in the presence of PDGFR inhibitor, AG1296. Tretinoin 48-50 platelet derived growth factor receptor beta Homo sapiens 78-83
18571505-7 2008 Inhibiting PDGFR enhanced RA-induced expression of integrin. Tretinoin 26-28 platelet derived growth factor receptor beta Homo sapiens 11-16
18571505-5 2008 Adding AG1296 with RA increased secretion of TNF-alpha, IL-8, and MMP-9 expression. Tretinoin 19-21 tumor necrosis factor Homo sapiens 45-54
18571505-5 2008 Adding AG1296 with RA increased secretion of TNF-alpha, IL-8, and MMP-9 expression. Tretinoin 19-21 C-X-C motif chemokine ligand 8 Homo sapiens 56-60
18628953-5 2008 RA induces expression of many endothelial genes including vascular endothelial (VE) cadherin. Tretinoin 0-2 cadherin 5 Homo sapiens 58-92
18628953-6 2008 VE-cadherin was also induced by RA in a number of other breast cancer cells. Tretinoin 32-34 cadherin 5 Homo sapiens 0-11
18628953-7 2008 We show that RA-induced VE-cadherin is responsible for the RA-induced morphological changes. Tretinoin 13-15 cadherin 5 Homo sapiens 24-35
18628953-7 2008 We show that RA-induced VE-cadherin is responsible for the RA-induced morphological changes. Tretinoin 59-61 cadherin 5 Homo sapiens 24-35
18628953-8 2008 RA rapidly induced the expression of Sox-9 and ER81, which in turn form a complex on the VE-cadherin promoter and are required to mediate the transcriptional regulation of VE-cadherin by RA. Tretinoin 0-2 ETS variant transcription factor 1 Homo sapiens 47-51
18628953-8 2008 RA rapidly induced the expression of Sox-9 and ER81, which in turn form a complex on the VE-cadherin promoter and are required to mediate the transcriptional regulation of VE-cadherin by RA. Tretinoin 0-2 cadherin 5 Homo sapiens 89-100
18628953-8 2008 RA rapidly induced the expression of Sox-9 and ER81, which in turn form a complex on the VE-cadherin promoter and are required to mediate the transcriptional regulation of VE-cadherin by RA. Tretinoin 0-2 cadherin 5 Homo sapiens 172-183
18491231-0 2008 Death-associated protein 5 (DAP5/p97/NAT1) contributes to retinoic acid-induced granulocytic differentiation and arsenic trioxide-induced apoptosis in acute promyelocytic leukemia. Tretinoin 58-71 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 0-26
18491231-3 2008 We found that ATRA markedly induced DAP5/p97 protein and gene expression and nuclear translocation during terminal differentiation of APL (NB4) and HL60 cells but not differentiation-resistant cells (NB4.R1 and HL60R), which express very low levels of DAP5/p97. Tretinoin 14-18 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 36-40
18491231-0 2008 Death-associated protein 5 (DAP5/p97/NAT1) contributes to retinoic acid-induced granulocytic differentiation and arsenic trioxide-induced apoptosis in acute promyelocytic leukemia. Tretinoin 58-71 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 28-32
18491231-3 2008 We found that ATRA markedly induced DAP5/p97 protein and gene expression and nuclear translocation during terminal differentiation of APL (NB4) and HL60 cells but not differentiation-resistant cells (NB4.R1 and HL60R), which express very low levels of DAP5/p97. Tretinoin 14-18 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 41-44
18491231-3 2008 We found that ATRA markedly induced DAP5/p97 protein and gene expression and nuclear translocation during terminal differentiation of APL (NB4) and HL60 cells but not differentiation-resistant cells (NB4.R1 and HL60R), which express very low levels of DAP5/p97. Tretinoin 14-18 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 252-256
18491231-0 2008 Death-associated protein 5 (DAP5/p97/NAT1) contributes to retinoic acid-induced granulocytic differentiation and arsenic trioxide-induced apoptosis in acute promyelocytic leukemia. Tretinoin 58-71 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 33-36
18491231-3 2008 We found that ATRA markedly induced DAP5/p97 protein and gene expression and nuclear translocation during terminal differentiation of APL (NB4) and HL60 cells but not differentiation-resistant cells (NB4.R1 and HL60R), which express very low levels of DAP5/p97. Tretinoin 14-18 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 257-260
18491231-6 2008 ATRA and ATO-induced expression of DAP5/p97 was associated with inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Tretinoin 0-4 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 35-39
18478160-0 2008 Expression of the retinoic acid-metabolizing enzymes RALDH2 and CYP26b1 during mouse postnatal testis development. Tretinoin 18-31 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 64-71
18491231-6 2008 ATRA and ATO-induced expression of DAP5/p97 was associated with inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Tretinoin 0-4 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 40-43
18491231-6 2008 ATRA and ATO-induced expression of DAP5/p97 was associated with inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Tretinoin 0-4 AKT serine/threonine kinase 1 Homo sapiens 119-122
18491231-8 2008 Finally, knockdown of DAP5/p97 expression by small interfering RNA inhibited ATRA-induced granulocytic differentiation and ATO-induced apoptosis. Tretinoin 77-81 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 22-26
18491231-8 2008 Finally, knockdown of DAP5/p97 expression by small interfering RNA inhibited ATRA-induced granulocytic differentiation and ATO-induced apoptosis. Tretinoin 77-81 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 27-30
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 52-56 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 40-44
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 52-56 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 45-48
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 52-56 AKT serine/threonine kinase 1 Homo sapiens 169-172
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 52-56 mechanistic target of rapamycin kinase Homo sapiens 173-177
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 206-210 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 40-44
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 206-210 eukaryotic translation initiation factor 4 gamma 2 Homo sapiens 45-48
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 206-210 AKT serine/threonine kinase 1 Homo sapiens 169-172
18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Tretinoin 206-210 mechanistic target of rapamycin kinase Homo sapiens 173-177
18394023-9 2008 RA counteracted the inflammatory regulation of cyclooxygenase (COX)-2 mRNA and protein in astrocytes and thereby reduced the synthesis of PGE(2) by approximately 60%. Tretinoin 0-2 mitochondrially encoded cytochrome c oxidase II Homo sapiens 47-69
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 58-77 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 131-138
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 58-77 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 144-151
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 79-83 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 144-151
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 184-188 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 131-138
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 184-188 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 144-151
18485106-0 2008 Phosphatidylinositide 3-kinase and protein kinase C zeta mediate retinoic acid induction of DARPP-32 in medium size spiny neurons in vitro. Tretinoin 65-78 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 92-100
18798497-0 2008 [Effects of all-trans retinoic acid on the expression of TGF-beta 1 and COL-I in rat model of peritoneal dialysis]. Tretinoin 22-35 transforming growth factor, beta 1 Rattus norvegicus 57-67
18485106-2 2008 Cell extrinsic molecules that increase DARPP-32 mRNA and/or protein levels include retinoic acid (RA), brain-derived neurotrophic factor, and estrogen (E(2)). Tretinoin 83-96 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 39-47
18485106-2 2008 Cell extrinsic molecules that increase DARPP-32 mRNA and/or protein levels include retinoic acid (RA), brain-derived neurotrophic factor, and estrogen (E(2)). Tretinoin 98-100 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 39-47
18485106-3 2008 We now demonstrate that RA regulates DARPP-32 mRNA and protein in primary striatal neuronal cultures. Tretinoin 24-26 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 37-45
18485106-4 2008 Furthermore, DARPP-32 induction by RA in vitro requires phosphatidylinositide 3-kinase, but is independent of tropomyosin-related kinase B, cyclin-dependent kinase 5, and protein kinase B. Tretinoin 35-37 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 13-21
18485106-5 2008 Using pharmacologic inhibitors of various isoforms of protein kinase C (PKC), we also demonstrate that DARPP-32 induction by RA in vitro is dependent on PKC zeta (PKCzeta). Tretinoin 125-127 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 103-111
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 132-151 D-box binding PAR bZIP transcription factor Homo sapiens 243-246
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 153-155 D-box binding PAR bZIP transcription factor Homo sapiens 243-246
18443043-5 2008 CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. Tretinoin 160-162 CREB binding protein Homo sapiens 0-20
18443043-5 2008 CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. Tretinoin 160-162 CREB binding protein Homo sapiens 22-25
18798497-1 2008 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA) on the expression of transforming growth factor-beta 1 (TGF-beta 1) and collagen I (COL-I )in rat model of peritoneal dialysis, which may relate to the prevention peritoneal fibrosis. Tretinoin 45-64 transforming growth factor, beta 1 Rattus norvegicus 93-126
18798497-1 2008 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA) on the expression of transforming growth factor-beta 1 (TGF-beta 1) and collagen I (COL-I )in rat model of peritoneal dialysis, which may relate to the prevention peritoneal fibrosis. Tretinoin 45-64 transforming growth factor, beta 1 Rattus norvegicus 128-138
18798497-1 2008 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA) on the expression of transforming growth factor-beta 1 (TGF-beta 1) and collagen I (COL-I )in rat model of peritoneal dialysis, which may relate to the prevention peritoneal fibrosis. Tretinoin 66-70 transforming growth factor, beta 1 Rattus norvegicus 93-126
18798497-1 2008 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA) on the expression of transforming growth factor-beta 1 (TGF-beta 1) and collagen I (COL-I )in rat model of peritoneal dialysis, which may relate to the prevention peritoneal fibrosis. Tretinoin 66-70 transforming growth factor, beta 1 Rattus norvegicus 128-138
18798497-8 2008 The expression of TGF-beta 1 and COL-I of peritoneum was increased significantly in the rats model, but the levels in the two ATRA treated groups were lower than those of the untreated group. Tretinoin 126-130 transforming growth factor, beta 1 Rattus norvegicus 18-28
19035179-6 2008 Western blot displayed that ATRA could decrease the expression of cyclin A, up-regulate the expression of p21 and p27, and down-regulate the expression of p27 related proteins Skp2. Tretinoin 28-32 cyclin A2 Homo sapiens 66-74
18399539-3 2008 The activity of RALDHs is known to be crucial for RA synthesis; however, recently a retinol dehydrogenase (RDH10) has been shown to represent a new limiting factor in this synthesis. Tretinoin 16-18 retinol dehydrogenase 10 (all-trans) Mus musculus 107-112
19035179-6 2008 Western blot displayed that ATRA could decrease the expression of cyclin A, up-regulate the expression of p21 and p27, and down-regulate the expression of p27 related proteins Skp2. Tretinoin 28-32 cyclin dependent kinase inhibitor 1A Homo sapiens 106-109
18420480-2 2008 For bone differentiation of mouse ASCs (mASCs), retinoic-acid mediated upregulation of BMPR-IB has been found to be necessary. Tretinoin 48-61 bone morphogenetic protein receptor, type 1B Mus musculus 87-94
18614847-4 2008 The differences were found in the gene expression of importin alpha3 and exportin 6 between the cells after treatments with DVD and ATRA. Tretinoin 132-136 exportin 6 Homo sapiens 73-83
18420480-4 2008 In this report, we investigated the molecular mechanisms underlying FGF-2 mediated osteogenic inhibition, demonstrating that addition of exogenous FGF-2 to mASCs antagonizes upregulation of BMPR-IB gene expression in response to retinoic acid. Tretinoin 229-242 bone morphogenetic protein receptor, type 1B Mus musculus 190-197
18420480-7 2008 Collectively, our data therefore indicate that FGF-2 antagonizes the response of mASCs to retinoic acid and also suggest that threshold levels of BMPR-IB may play a crucial role both in counteracting the inhibitory role of FGF-2 and in promoting osteogenic differentiation of ASCs in the absence of retinoic acid. Tretinoin 299-312 bone morphogenetic protein receptor, type 1B Mus musculus 146-153
18082883-0 2008 Retinoid X receptor alpha is highly phosphorylated in retinoic acid-resistant HL-60R cells and the combination of 9-cis retinoic acid plus MEK inhibitor induces apoptosis in the cells. Tretinoin 54-67 mitogen-activated protein kinase kinase 7 Homo sapiens 139-142
26621242-0 2008 Homology Models and Molecular Modeling of Human Retinoic Acid Metabolizing Enzymes Cytochrome P450 26A1 (CYP26A1) and P450 26B1 (CYP26B1). Tretinoin 48-61 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 83-103
26621242-0 2008 Homology Models and Molecular Modeling of Human Retinoic Acid Metabolizing Enzymes Cytochrome P450 26A1 (CYP26A1) and P450 26B1 (CYP26B1). Tretinoin 48-61 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 105-112
26621242-0 2008 Homology Models and Molecular Modeling of Human Retinoic Acid Metabolizing Enzymes Cytochrome P450 26A1 (CYP26A1) and P450 26B1 (CYP26B1). Tretinoin 48-61 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 129-136
26621242-6 2008 Residues involved in hydrophobic interactions with atRA were Pro113, Phe222, Phe299, Val370, Pro371, and Phe374 in CYP26A1 and Leu88, Pro118, Phe222, Phe295, Ile368, and Tyr272 in CYP26B1. Tretinoin 51-55 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 115-122
26621242-6 2008 Residues involved in hydrophobic interactions with atRA were Pro113, Phe222, Phe299, Val370, Pro371, and Phe374 in CYP26A1 and Leu88, Pro118, Phe222, Phe295, Ile368, and Tyr272 in CYP26B1. Tretinoin 51-55 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 180-187
18354491-0 2008 Arsenic trioxide inhibits ATRA-induced prostaglandin E2 and cyclooxygenase-1 in NB4 cells, a model of acute promyelocytic leukemia. Tretinoin 26-30 prostaglandin-endoperoxide synthase 1 Homo sapiens 60-76
18354491-4 2008 We have recently demonstrated that ATRA induces cyclooxygenase-1 (COX-1) expression and prostaglandin synthesis in NB4 cells and in blasts from patients with APL. Tretinoin 35-39 prostaglandin-endoperoxide synthase 1 Homo sapiens 48-64
18082883-3 2008 However, when the HL-60R cells were treated with the combination of 9-cis RA plus PD98059, MEK inhibitor, the p-RXR alpha and RXR alpha proteins all markedly decreased. Tretinoin 74-76 mitogen-activated protein kinase kinase 7 Homo sapiens 91-94
18354491-4 2008 We have recently demonstrated that ATRA induces cyclooxygenase-1 (COX-1) expression and prostaglandin synthesis in NB4 cells and in blasts from patients with APL. Tretinoin 35-39 prostaglandin-endoperoxide synthase 1 Homo sapiens 66-71
18354491-6 2008 Arsenic treatment of NB4 cells resulted in a partial but significant reduction of ATRA-dependent induction of COX-1 expression and activity. Tretinoin 82-86 prostaglandin-endoperoxide synthase 1 Homo sapiens 110-115
18059332-9 2008 CYP26A1 expression was increased synergistically by RA and lithocholic acid (P<0.05). Tretinoin 52-54 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
19031739-7 2008 2) Phosphatase assay showed a decrease in PP2A phosphatase activity [(534 +/- 43) pmol x min(-1) x microg protein(-1)] in NB4 after ATRA treatment, accompanied with that activity [(959 +/- 83) pmol x min(-1) x microg protein(-1)] in untreated NB4 cells. Tretinoin 132-136 CD59 molecule (CD59 blood group) Homo sapiens 89-95
19031739-7 2008 2) Phosphatase assay showed a decrease in PP2A phosphatase activity [(534 +/- 43) pmol x min(-1) x microg protein(-1)] in NB4 after ATRA treatment, accompanied with that activity [(959 +/- 83) pmol x min(-1) x microg protein(-1)] in untreated NB4 cells. Tretinoin 132-136 CD59 molecule (CD59 blood group) Homo sapiens 200-206
18084321-4 2008 We report that nanomolar concentrations of all-trans retinoic acid (ATRA) amplify TNFalpha-induced apoptosis in APL cells expressing a specific repressor of NF-kappaB activation. Tretinoin 53-66 tumor necrosis factor Homo sapiens 82-90
18084321-4 2008 We report that nanomolar concentrations of all-trans retinoic acid (ATRA) amplify TNFalpha-induced apoptosis in APL cells expressing a specific repressor of NF-kappaB activation. Tretinoin 68-72 tumor necrosis factor Homo sapiens 82-90
18084321-10 2008 This study also suggests that inclusion of nanomolar doses of ATRA could be clinically beneficial in amplifying TNFalpha-induced antitumor signals. Tretinoin 62-66 tumor necrosis factor Homo sapiens 112-120
18212744-0 2008 Retinoic acid downregulates Rae1 leading to APC(Cdh1) activation and neuroblastoma SH-SY5Y differentiation. Tretinoin 0-13 cadherin 1 Homo sapiens 48-52
18212744-1 2008 In neuroblastoma cells, retinoic acid induces cell cycle arrest and differentiation through degradation of the F-box protein, Skp2, and stabilization of cyclin-dependent kinase inhibitor, p27. Tretinoin 24-37 zinc ribbon domain containing 2 Homo sapiens 188-191
18212744-4 2008 We found that retinoic acid induced the nuclear accumulation of Cdh1 that paralleled Skp2 destabilization and p27 accumulation. Tretinoin 14-27 cadherin 1 Homo sapiens 64-68
18212744-4 2008 We found that retinoic acid induced the nuclear accumulation of Cdh1 that paralleled Skp2 destabilization and p27 accumulation. Tretinoin 14-27 zinc ribbon domain containing 2 Homo sapiens 110-113
18212744-5 2008 The mRNA and protein abundance of Rae1-a nuclear export factor that limits APC(Cdh1) activity in mitosis-decreased upon retinoic acid-induced inhibition of neuroblastoma cell proliferation. Tretinoin 120-133 cadherin 1 Homo sapiens 79-83
18212744-6 2008 Furthermore, either Rae1 overexpression or Cdh1 inhibition promoted Skp2 accumulation, p27 destabilization and prevented retinoic acid-induced cell cycle arrest and differentiation. Tretinoin 121-134 cadherin 1 Homo sapiens 43-47
18059332-0 2008 A novel role for the retinoic acid-catabolizing enzyme CYP26A1 in Barrett"s associated adenocarcinoma. Tretinoin 21-34 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 55-62
18059332-1 2008 Vitamin A deficiency is associated with carcinogenesis, and upregulation of CYP26A1, a major retinoic acid (RA)-catabolizing enzyme, has recently been shown in cancer. Tretinoin 93-106 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 76-83
18059332-1 2008 Vitamin A deficiency is associated with carcinogenesis, and upregulation of CYP26A1, a major retinoic acid (RA)-catabolizing enzyme, has recently been shown in cancer. Tretinoin 108-110 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 76-83
18059332-8 2008 RA levels decreased progressively with the degree of dysplasia (P<0.05) and were inversely correlated with CYP26A1 gene levels and activity (P<0.01). Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 110-117
19035249-15 2008 After the ATRA treatment, cells were stained strongly positive, strongly positive and moderately positive by NSE, vimentin and GFAP antibodies, respectively. Tretinoin 10-14 enolase 2 Homo sapiens 109-112
18084321-0 2008 A PARP-1/JNK1 cascade participates in the synergistic apoptotic effect of TNFalpha and all-trans retinoic acid in APL cells. Tretinoin 97-110 poly(ADP-ribose) polymerase 1 Homo sapiens 2-8
18084321-0 2008 A PARP-1/JNK1 cascade participates in the synergistic apoptotic effect of TNFalpha and all-trans retinoic acid in APL cells. Tretinoin 97-110 mitogen-activated protein kinase 8 Homo sapiens 9-13
18212744-8 2008 Thus, retinoic acid downregulates Rae1, hence facilitating APC(Cdh1)-mediated Skp2 degradation leading to the arrest of cell cycle progression and neuroblastoma differentiation. Tretinoin 6-19 cadherin 1 Homo sapiens 63-67
18059332-12 2008 Overexpression of CYP26A1 causes intracellular RA depletion and drives the cell into a highly proliferative and invasive state with induction of other known oncogenes. Tretinoin 47-49 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 18-25
18064629-10 2008 We conclude that atRA protects against UV-induced down-regulation AQP3 and decrease in water permeability, reduction in cell migration and delayed in vitro wound healing via trans-activation of EGFR and inhibition on ROS-mediated MEK/ERK pathway. Tretinoin 17-21 epidermal growth factor receptor Homo sapiens 194-198
18291094-0 2008 Interleukin-1beta mediates LPS-induced inhibition of apoptosis in retinoic acid-differentiated HL-60 cells. Tretinoin 66-79 interleukin 1 beta Homo sapiens 0-17
18383274-3 2008 During embryoid body (EB) differentiation, the level of active cyclic AMP response element-binding protein (CREB) was relatively high when 5 microM RA treatment was performed. Tretinoin 148-150 cAMP responsive element binding protein 1 Mus musculus 63-106
18383274-3 2008 During embryoid body (EB) differentiation, the level of active cyclic AMP response element-binding protein (CREB) was relatively high when 5 microM RA treatment was performed. Tretinoin 148-150 cAMP responsive element binding protein 1 Mus musculus 108-112
18383274-5 2008 Moreover, RA increased the expression of active CREB by enhancing the activity of JNK. Tretinoin 10-12 cAMP responsive element binding protein 1 Mus musculus 48-52
18383274-6 2008 Our research suggests that CREB plays a role in RA-induced NPC differentiation by increasing the expression of active JNK. Tretinoin 48-50 cAMP responsive element binding protein 1 Mus musculus 27-31
18386821-6 2008 Furthermore, retinoic acid is likely to act directly on BAMBI as induction occurs in the presence of cycloheximide. Tretinoin 13-26 BMP and activin membrane bound inhibitor Homo sapiens 56-61
18393306-2 2008 This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Tretinoin 20-43 bone morphogenetic protein 4 Mus musculus 213-241
18393306-2 2008 This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Tretinoin 20-43 bone morphogenetic protein 4 Mus musculus 243-247
18393306-2 2008 This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Tretinoin 45-47 bone morphogenetic protein 4 Mus musculus 213-241
18393306-2 2008 This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Tretinoin 45-47 bone morphogenetic protein 4 Mus musculus 243-247
18374307-7 2008 However, a cystamine-mediated significant inhibition of transglutaminase activity (70%) was accompanied by a drastically reduced NF-kappaB activation only in cells exposed to NGF following retinoic acid treatment. Tretinoin 189-202 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 129-138
18241033-4 2008 The study revealed that expression of GLI1 and its direct transcriptional target Patched (PTCH) is downregulated in the early stages of retinoic acid-induced neuronal differentiation of NT2 cells. Tretinoin 136-149 patched 1 Homo sapiens 81-88
18241033-4 2008 The study revealed that expression of GLI1 and its direct transcriptional target Patched (PTCH) is downregulated in the early stages of retinoic acid-induced neuronal differentiation of NT2 cells. Tretinoin 136-149 patched 1 Homo sapiens 90-94
18064629-10 2008 We conclude that atRA protects against UV-induced down-regulation AQP3 and decrease in water permeability, reduction in cell migration and delayed in vitro wound healing via trans-activation of EGFR and inhibition on ROS-mediated MEK/ERK pathway. Tretinoin 17-21 mitogen-activated protein kinase kinase 7 Homo sapiens 230-233
18064629-10 2008 We conclude that atRA protects against UV-induced down-regulation AQP3 and decrease in water permeability, reduction in cell migration and delayed in vitro wound healing via trans-activation of EGFR and inhibition on ROS-mediated MEK/ERK pathway. Tretinoin 17-21 mitogen-activated protein kinase 1 Homo sapiens 234-237
18270252-0 2008 Retinoic acid (RA) regulates 17beta-hydroxysteroid dehydrogenase type 2 expression in endometrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. Tretinoin 0-13 Sp1 transcription factor Homo sapiens 132-158
18183617-5 2008 Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. Tretinoin 15-38 nitric oxide synthase 2 Rattus norvegicus 138-142
18270252-0 2008 Retinoic acid (RA) regulates 17beta-hydroxysteroid dehydrogenase type 2 expression in endometrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. Tretinoin 0-13 Sp3 transcription factor Homo sapiens 159-162
18270252-0 2008 Retinoic acid (RA) regulates 17beta-hydroxysteroid dehydrogenase type 2 expression in endometrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. Tretinoin 15-17 Sp1 transcription factor Homo sapiens 132-158
18270252-0 2008 Retinoic acid (RA) regulates 17beta-hydroxysteroid dehydrogenase type 2 expression in endometrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. Tretinoin 15-17 Sp3 transcription factor Homo sapiens 159-162
18270252-10 2008 Small interfering RNA ablation of SP1 and SP3 expression markedly decreased HSD17B2 basal expression and blocked RA-induced expression. Tretinoin 113-115 Sp3 transcription factor Homo sapiens 42-45
18270252-11 2008 Finally, immunoprecipitationimmunoblotting demonstrated RA-induced interactions between RARalpha/RXRalpha and SP1/SP3 in intact endometrial cells. Tretinoin 56-58 Sp1 transcription factor Homo sapiens 110-117
18270252-12 2008 CONCLUSIONS: In endometrial epithelial cells, RA stimulates formation of a multimeric complex comprised of RARalpha/RXRalpha tethered to transcription factors SP1 and SP3 on the HSD17B2 promoter. Tretinoin 46-48 Sp3 transcription factor Homo sapiens 167-170
18058943-4 2008 RAGE knockdown inhibited retinoic acid-induced activation and blocked nuclear translocation of NF-kappaB, suggesting RAGE regulates activation of NF-kappaB. Tretinoin 25-38 nuclear factor kappa B subunit 1 Homo sapiens 95-104
18058943-4 2008 RAGE knockdown inhibited retinoic acid-induced activation and blocked nuclear translocation of NF-kappaB, suggesting RAGE regulates activation of NF-kappaB. Tretinoin 25-38 nuclear factor kappa B subunit 1 Homo sapiens 146-155
18319322-0 2008 Retinoic acid stimulation of the sodium/iodide symporter in MCF-7 breast cancer cells is mediated by the insulin growth factor-I/phosphatidylinositol 3-kinase and p38 mitogen-activated protein kinase signaling pathways. Tretinoin 0-13 mitogen-activated protein kinase 14 Homo sapiens 163-166
18183617-5 2008 Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. Tretinoin 40-44 nitric oxide synthase 2 Rattus norvegicus 138-142
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 47-70 interleukin 4 Homo sapiens 121-125
18280804-2 2008 We have previously shown that all-trans-retinoic acid (ATRA) induces mTOR-mediated activation of the p70 S6 kinase, suggesting the existence of a mechanism by which retinoids may regulate mRNA translation. Tretinoin 30-53 mechanistic target of rapamycin kinase Homo sapiens 69-73
18280804-2 2008 We have previously shown that all-trans-retinoic acid (ATRA) induces mTOR-mediated activation of the p70 S6 kinase, suggesting the existence of a mechanism by which retinoids may regulate mRNA translation. Tretinoin 55-59 mechanistic target of rapamycin kinase Homo sapiens 69-73
18280804-4 2008 We also show that siRNA-mediated inhibition of 4E-BP1 expression enhances ATRA-dependent upregulation of p21(Waf1/Cip1), a protein that plays a key role in the induction of retinoid-dependent responses. Tretinoin 74-78 cyclin dependent kinase inhibitor 1A Homo sapiens 105-108
18280804-4 2008 We also show that siRNA-mediated inhibition of 4E-BP1 expression enhances ATRA-dependent upregulation of p21(Waf1/Cip1), a protein that plays a key role in the induction of retinoid-dependent responses. Tretinoin 74-78 cyclin dependent kinase inhibitor 1A Homo sapiens 109-113
18280804-4 2008 We also show that siRNA-mediated inhibition of 4E-BP1 expression enhances ATRA-dependent upregulation of p21(Waf1/Cip1), a protein that plays a key role in the induction of retinoid-dependent responses. Tretinoin 74-78 cyclin dependent kinase inhibitor 1A Homo sapiens 114-118
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 47-70 interleukin 13 Homo sapiens 136-141
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 47-70 interferon gamma Homo sapiens 170-179
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 47-70 tumor necrosis factor Homo sapiens 184-193
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 72-76 interleukin 4 Homo sapiens 121-125
18280257-6 2008 Nuclear levels of the NF-kappaB proteins p50 and p65 increased within 24 h of ATRA administration. Tretinoin 78-82 nuclear factor kappa B subunit 1 Homo sapiens 41-44
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 72-76 interleukin 13 Homo sapiens 136-141
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 72-76 interferon gamma Homo sapiens 170-179
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 72-76 tumor necrosis factor Homo sapiens 184-193
18416830-2 2008 Here, we have demonstrated that the observed effects using ATRA and 9-cis RA are shared with the clinically useful RAR ligand, 13-cis retinoic acid (13-cis RA), and the retinoic acid receptor-alpha (RAR-alpha)-selective agonist, AM580 but not with the RAR-beta/gamma ligand, 4-hydroxyphenylretinamide (4-HPR). Tretinoin 59-63 retinoic acid receptor beta Homo sapiens 252-260
17941088-0 2008 All-trans retinoic acid prevents angiotensin II- and mechanical stretch-induced reactive oxygen species generation and cardiomyocyte apoptosis. Tretinoin 0-23 angiotensinogen Homo sapiens 33-47
18234667-6 2008 Additionally, retinoic acid treatment reduced the binding of histone deacetylase-1 and REST to neuronal genes. Tretinoin 14-27 histone deacetylase 1 Homo sapiens 61-82
18355041-6 2008 The effect of t-RA exposure on cell adhesion to vascular cell adhesion molecule-1 (VCAM-1), a well-established integrin counter receptor involved in immunity, and to nonconventional ADAM integrin ligands was assessed. Tretinoin 14-18 vascular cell adhesion molecule 1 Homo sapiens 48-81
18355041-6 2008 The effect of t-RA exposure on cell adhesion to vascular cell adhesion molecule-1 (VCAM-1), a well-established integrin counter receptor involved in immunity, and to nonconventional ADAM integrin ligands was assessed. Tretinoin 14-18 vascular cell adhesion molecule 1 Homo sapiens 83-89
18355041-7 2008 We show for the first time that t-RA potently induces B cell adhesion in an integrin-independent manner to both VCAM-1 and select ADAM disintegrin domains. Tretinoin 32-36 vascular cell adhesion molecule 1 Homo sapiens 112-118
18358086-9 2008 The ratio of Bax/Bcl-2 decreased in arterial duct VSMC after RA treatment due to the significant inhibition of Bax expression. Tretinoin 61-63 BCL2 associated X, apoptosis regulator Homo sapiens 13-16
18358086-9 2008 The ratio of Bax/Bcl-2 decreased in arterial duct VSMC after RA treatment due to the significant inhibition of Bax expression. Tretinoin 61-63 BCL2 apoptosis regulator Homo sapiens 17-22
18358086-9 2008 The ratio of Bax/Bcl-2 decreased in arterial duct VSMC after RA treatment due to the significant inhibition of Bax expression. Tretinoin 61-63 BCL2 associated X, apoptosis regulator Homo sapiens 111-114
17941088-2 2008 All-trans retinoic acid (RA), a bioactive vitamin A derivative, prevents stretch- and angiotensin II (Ang II)-induced cardiac hypertrophy. Tretinoin 0-23 angiotensinogen Homo sapiens 86-100
17941088-2 2008 All-trans retinoic acid (RA), a bioactive vitamin A derivative, prevents stretch- and angiotensin II (Ang II)-induced cardiac hypertrophy. Tretinoin 0-23 angiotensinogen Homo sapiens 102-108
17941088-2 2008 All-trans retinoic acid (RA), a bioactive vitamin A derivative, prevents stretch- and angiotensin II (Ang II)-induced cardiac hypertrophy. Tretinoin 25-27 angiotensinogen Homo sapiens 86-100
17941088-2 2008 All-trans retinoic acid (RA), a bioactive vitamin A derivative, prevents stretch- and angiotensin II (Ang II)-induced cardiac hypertrophy. Tretinoin 25-27 angiotensinogen Homo sapiens 102-108
17941088-4 2008 Here, we demonstrate that stretch- and Ang II-induced apoptosis is prevented by RA in neonatal cardiomyocytes. Tretinoin 80-82 angiotensinogen Homo sapiens 39-45
17941088-5 2008 RA improved mitochondrial function by inhibiting the stretch- and Ang II-induced reduction in mitochondrial membrane potential, cytochrome c release and by increasing the Bcl2/Bax ratio. Tretinoin 0-2 angiotensinogen Homo sapiens 66-72
17941088-5 2008 RA improved mitochondrial function by inhibiting the stretch- and Ang II-induced reduction in mitochondrial membrane potential, cytochrome c release and by increasing the Bcl2/Bax ratio. Tretinoin 0-2 cytochrome c, somatic Homo sapiens 128-140
17941088-5 2008 RA improved mitochondrial function by inhibiting the stretch- and Ang II-induced reduction in mitochondrial membrane potential, cytochrome c release and by increasing the Bcl2/Bax ratio. Tretinoin 0-2 BCL2 apoptosis regulator Homo sapiens 171-175
17941088-5 2008 RA improved mitochondrial function by inhibiting the stretch- and Ang II-induced reduction in mitochondrial membrane potential, cytochrome c release and by increasing the Bcl2/Bax ratio. Tretinoin 0-2 BCL2 associated X, apoptosis regulator Homo sapiens 176-179
17941088-6 2008 RA inhibited stretch- and Ang II-induced intracellular reactive oxygen species (ROS) generation and upregulated the SOD2 level. Tretinoin 0-2 angiotensinogen Homo sapiens 26-32
17941088-11 2008 Our data provide the first evidence that RA prevents Ang II and stretch induced apoptosis, by inhibiting ROS generation and increasing the anti-oxidant defense system, suggesting that RA-mediated signaling may provide a new therapeutic target for the prevention of the cardiac remodeling process. Tretinoin 41-43 angiotensinogen Homo sapiens 53-59
17941088-11 2008 Our data provide the first evidence that RA prevents Ang II and stretch induced apoptosis, by inhibiting ROS generation and increasing the anti-oxidant defense system, suggesting that RA-mediated signaling may provide a new therapeutic target for the prevention of the cardiac remodeling process. Tretinoin 184-186 angiotensinogen Homo sapiens 53-59
18241852-3 2008 CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 139-146
17943186-3 2008 All-trans RA treatment of organotypic REK cultures (10 days) increased the synthesis of hyaluronan, the expression of hyaluronan synthases Has2 and Has3, and the CD44 receptor, with hyperplasia of the epidermis. Tretinoin 10-12 hyaluronan synthase 2 Rattus norvegicus 139-143
17943186-3 2008 All-trans RA treatment of organotypic REK cultures (10 days) increased the synthesis of hyaluronan, the expression of hyaluronan synthases Has2 and Has3, and the CD44 receptor, with hyperplasia of the epidermis. Tretinoin 10-12 hyaluronan synthase 3 Rattus norvegicus 148-152
17943186-5 2008 These effects were consistent with the findings that all-trans RA upregulated heparin-binding epidermal growth factor-like growth factor mRNA expression and increased the phosphorylation of EGFR and extracellular signal-regulated kinase 1/2 (ERK1/2). Tretinoin 63-65 heparin-binding EGF-like growth factor Rattus norvegicus 78-136
18060600-4 2008 Retinoic acid acts by transcriptionally activating bone morphogenetic protein-2 (BMP-2) and SAHA facilitates transcriptional activity through chromatin accessibility. Tretinoin 0-13 bone morphogenetic protein 2 Mus musculus 51-79
18060600-4 2008 Retinoic acid acts by transcriptionally activating bone morphogenetic protein-2 (BMP-2) and SAHA facilitates transcriptional activity through chromatin accessibility. Tretinoin 0-13 bone morphogenetic protein 2 Mus musculus 81-86
18060600-6 2008 EXPERIMENTAL DESIGN: RA + SAHA induction of BMP-2 transcription and apoptosis in medulloblastoma cultures was evaluated. Tretinoin 21-23 bone morphogenetic protein 2 Mus musculus 44-49
18060600-13 2008 CONCLUSIONS: RA + SAHA additively induce BMP-2 transcription and medulloblastoma apoptosis. Tretinoin 13-15 bone morphogenetic protein 2 Mus musculus 41-46
18241852-0 2008 CYP26A1 knockout embryonic stem cells exhibit reduced differentiation and growth arrest in response to retinoic acid. Tretinoin 103-116 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18241852-1 2008 CYP26A1, a cytochrome P450 enzyme, metabolizes all-trans-retinoic acid (RA) into polar metabolites, e.g. 4-oxo-RA and 4-OH-RA. Tretinoin 47-70 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18241852-1 2008 CYP26A1, a cytochrome P450 enzyme, metabolizes all-trans-retinoic acid (RA) into polar metabolites, e.g. 4-oxo-RA and 4-OH-RA. Tretinoin 72-74 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18241852-3 2008 CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18241852-3 2008 CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells. Tretinoin 65-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18241852-3 2008 CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells. Tretinoin 65-67 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 139-146
18241852-3 2008 CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 139-146
18241852-3 2008 CYP26a1(-/-) ES cells had a 11.0+/-3.2-fold higher intracellular RA concentration than Wt ES cells after RA treatment for 48 h. RA-treated CYP26A1(-/-) ES cells exhibited 2-3 fold higher mRNA levels of Hoxa1, a primary RA target gene, than Wt ES cells. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
18241852-4 2008 Despite increased intracellular RA levels, CYP26a1(-/-) ES cells were more resistant than Wt ES cells to RA-induced proliferation arrest. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 43-50
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 45-52
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 caldesmon 1 Homo sapiens 271-281
18241852-7 2008 In contrast, genes involved in the stress response (e.g. Tlr2, Stk2, Fcgr2b, Bnip3, Pdk1) were expressed at higher levels in CYP26A1(-/-) than in Wt ES cells without RA. Tretinoin 166-168 toll like receptor 2 Homo sapiens 57-61
18241852-7 2008 In contrast, genes involved in the stress response (e.g. Tlr2, Stk2, Fcgr2b, Bnip3, Pdk1) were expressed at higher levels in CYP26A1(-/-) than in Wt ES cells without RA. Tretinoin 166-168 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 125-132
18241852-8 2008 Collectively, our results show that CYP26A1 activity regulates intracellular RA levels, cell proliferation, transcriptional regulation of primary RA target genes, and ES cell differentiation to parietal endoderm. Tretinoin 77-79 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 36-43
18026954-8 2008 Clinically, BP1 levels were elevated in all pretreatment APL patients tested, while BP1 expression was decreased in 91% of patients after combined ATRA and chemotherapy treatment. Tretinoin 147-151 BP1 Homo sapiens 84-87
18063688-6 2008 Treatment of cardiomyocytes with ciglitazone, a PPARgamma agonist, or 9-cis retinoic acid (RA), a RXR agonist, increased insulin- and metabolic stress-stimulated glucose transport, whereas agonists of PPARalpha or PPARbeta/delta had no effect. Tretinoin 91-93 peroxisome proliferator-activated receptor delta Rattus norvegicus 214-222
18026954-0 2008 Overexpression of BP1, a homeobox gene, is associated with resistance to all-trans retinoic acid in acute promyelocytic leukemia cells. Tretinoin 83-96 BP1 Homo sapiens 18-21
18026954-4 2008 NB4 and R4 cells express BP1, bcl-2, and c-myc; the expression of all three genes was repressed after ATRA treatment of NB4 cells but not R4 cells. Tretinoin 102-106 BP1 Homo sapiens 25-28
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 growth arrest specific 1 Mus musculus 153-157
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 fructose bisphosphatase 2 Mus musculus 175-179
18256537-2 2008 Retinoic acid (RA) is degraded by Cyp26b1 in the embryonic testis but not in the ovary where it initiates the mitosis/meiosis transition. Tretinoin 0-13 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 34-41
18256537-2 2008 Retinoic acid (RA) is degraded by Cyp26b1 in the embryonic testis but not in the ovary where it initiates the mitosis/meiosis transition. Tretinoin 15-17 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 34-41
18256537-8 2008 At this stage, RA delayed SSEA-1 extinction, p63gamma expression and DNA hypermethylation which normally occur in male mitotic arrested germ cells. Tretinoin 15-17 fucosyltransferase 4 Mus musculus 26-32
18234725-10 2008 Cdx4 might function to block pancreatic identity by preventing retinoic acid (RA) signal transduction in posterior endoderm. Tretinoin 63-76 caudal type homeobox 4 Danio rerio 0-4
18202528-4 2008 The oxidation of retinal to RA is catalyzed by the retinaldehyde dehydrogenases (RALDHs), including RALDH1, RALDH2 and RALDH3. Tretinoin 28-30 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 100-106
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 129-131 retinoic acid receptor, alpha a Danio rerio 186-191
23675063-8 2008 However, addition of retinoic acid (RA) to the nef transfected cells caused even a slight increase in neuron formation as compared to control ESC treated with RA. Tretinoin 21-34 S100 calcium binding protein B Homo sapiens 47-50
17998248-0 2008 Zebrafish model of holoprosencephaly demonstrates a key role for TGIF in regulating retinoic acid metabolism. Tretinoin 84-97 TGFB induced factor homeobox 1 Homo sapiens 65-69
18239600-4 2008 RESULTS: ATRA treatment triggered a dose-dependent increase in the muscle mRNA expression levels of selected enzymes, transporters and transcription factors involved in fatty-acid oxidation, respiration, and thermogenesis namely: muscle-type carnitine palmitoyltransferase 1, acyl CoA oxidase 1, subunit II of cytochrome oxidase, uncoupling protein 3, peroxisome proliferator-activated receptor-gamma co-activator -1alpha and peroxisome proliferator-activated receptor-delta (PPARdelta). Tretinoin 9-13 peroxisome proliferator activator receptor delta Mus musculus 426-474
18239600-4 2008 RESULTS: ATRA treatment triggered a dose-dependent increase in the muscle mRNA expression levels of selected enzymes, transporters and transcription factors involved in fatty-acid oxidation, respiration, and thermogenesis namely: muscle-type carnitine palmitoyltransferase 1, acyl CoA oxidase 1, subunit II of cytochrome oxidase, uncoupling protein 3, peroxisome proliferator-activated receptor-gamma co-activator -1alpha and peroxisome proliferator-activated receptor-delta (PPARdelta). Tretinoin 9-13 peroxisome proliferator activator receptor delta Mus musculus 476-485
18239600-6 2008 Skeletal muscle protein levels of PPARdelta and retinoid X receptor gamma, a partner for many nuclear receptors involved in lipid metabolism, were increased after ATRA treatment. Tretinoin 163-167 peroxisome proliferator activator receptor delta Mus musculus 34-43
18239600-6 2008 Skeletal muscle protein levels of PPARdelta and retinoid X receptor gamma, a partner for many nuclear receptors involved in lipid metabolism, were increased after ATRA treatment. Tretinoin 163-167 retinoid X receptor gamma Mus musculus 48-73
18093970-7 2008 Moreover, in the case of excessive maternal dietary vitamin A intake, LRAT acts together with Cyp26A1, one of the enzymes that catalyze the degradation of retinoic acid, and possibly with STRA6, the recently identified cell surface receptor for retinol-RBP, in maintaining adequate levels of retinoids in embryonic and extraembryonic tissues. Tretinoin 155-168 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 94-101
18207650-7 2008 Compared with untreated cells, ATRA-treated C6 cells express less Slc1a3 mRNA, for the transporter GLAST, but significantly higher levels of Slc1a2 mRNA, for the transporter GLT-1, although no expression of either protein is detected with Western blot in both untreated and ATRA-treated cells. Tretinoin 31-35 solute carrier family 1 member 2 Rattus norvegicus 141-147
18207650-7 2008 Compared with untreated cells, ATRA-treated C6 cells express less Slc1a3 mRNA, for the transporter GLAST, but significantly higher levels of Slc1a2 mRNA, for the transporter GLT-1, although no expression of either protein is detected with Western blot in both untreated and ATRA-treated cells. Tretinoin 31-35 solute carrier family 1 member 2 Rattus norvegicus 174-179
18006504-4 2008 Unlike wild-type parental cells, RA-treated BLR1 knock-out cells failed to show RAF and consequential MEK and ERK phosphorylation, failed to accumulate CDK inhibitors that control G(1)/S transition, and failed to differentiate and arrest in response to RA, whereas ectopically overexpressing BLR1 enhanced MAPK signaling and caused accelerated RA-induced differentiation and arrest. Tretinoin 33-35 mitogen-activated protein kinase 1 Homo sapiens 306-310
18006504-6 2008 Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. Tretinoin 26-28 mitogen-activated protein kinase 1 Homo sapiens 110-114
18006504-6 2008 Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. Tretinoin 26-28 mitogen-activated protein kinase 1 Homo sapiens 199-203
18006504-7 2008 Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. Tretinoin 16-18 mitogen-activated protein kinase 1 Homo sapiens 96-100
18006504-7 2008 Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. Tretinoin 16-18 mitogen-activated protein kinase 1 Homo sapiens 213-217
18006504-7 2008 Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. Tretinoin 239-241 mitogen-activated protein kinase 1 Homo sapiens 96-100
18006504-7 2008 Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. Tretinoin 239-241 mitogen-activated protein kinase 1 Homo sapiens 213-217
17998248-8 2008 We demonstrate in zebrafish that Tgif plays a key role in regulating RA signaling, and is essential to properly pattern the forebrain. Tretinoin 69-71 TGFB-induced factor homeobox 1 Danio rerio 33-37
17998248-9 2008 Tgif is necessary for normal initiation of genes that control RA synthesis and degradation, resulting in defects in RA-dependent central nervous system patterning in Tgif-depleted embryos. Tretinoin 62-64 TGFB induced factor homeobox 1 Homo sapiens 0-4
17998248-9 2008 Tgif is necessary for normal initiation of genes that control RA synthesis and degradation, resulting in defects in RA-dependent central nervous system patterning in Tgif-depleted embryos. Tretinoin 116-118 TGFB induced factor homeobox 1 Homo sapiens 0-4
17998248-9 2008 Tgif is necessary for normal initiation of genes that control RA synthesis and degradation, resulting in defects in RA-dependent central nervous system patterning in Tgif-depleted embryos. Tretinoin 116-118 TGFB induced factor homeobox 1 Homo sapiens 166-170
17998248-10 2008 The loss of the forebrain-specific RA-degrading enzyme cyp26a1 causes a forebrain phenotype that mimics tgif morphants. Tretinoin 35-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 55-62
17998248-10 2008 The loss of the forebrain-specific RA-degrading enzyme cyp26a1 causes a forebrain phenotype that mimics tgif morphants. Tretinoin 35-37 TGFB induced factor homeobox 1 Homo sapiens 104-108
18006504-0 2008 A MAPK-positive feedback mechanism for BLR1 signaling propels retinoic acid-triggered differentiation and cell cycle arrest. Tretinoin 62-75 mitogen-activated protein kinase 1 Homo sapiens 2-6
18006504-1 2008 MAPK signaling is required for retinoic acid (RA)-triggered G(0) cell cycle arrest and cell differentiation, but the mechanism is not well defined. Tretinoin 31-44 mitogen-activated protein kinase 1 Homo sapiens 0-4
18006504-1 2008 MAPK signaling is required for retinoic acid (RA)-triggered G(0) cell cycle arrest and cell differentiation, but the mechanism is not well defined. Tretinoin 46-48 mitogen-activated protein kinase 1 Homo sapiens 0-4
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 36-40
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 mitogen-activated protein kinase kinase 7 Homo sapiens 89-92
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 96-99
18281459-1 2008 In mouse fetal gonads, retinoic acid (RA) induces meiosis in the female germ cells, whereas the male germ cells never enter meiosis due to Cyp26b1-mediated RA metabolism. Tretinoin 156-158 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 139-146
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 114-118
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 cyclin dependent kinase inhibitor 1A Homo sapiens 145-148
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 cyclin dependent kinase inhibitor 1A Homo sapiens 149-153
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 cyclin dependent kinase inhibitor 1A Homo sapiens 154-158
18269766-0 2008 Retinoic acid decreases ATF-2 phosphorylation and sensitizes melanoma cells to taxol-mediated growth inhibition. Tretinoin 0-13 activating transcription factor 2 Mus musculus 24-29
18269766-5 2008 In the course of determining how retinoic acid (RA) stimulates activating protein-1 (AP-1) activity in B16 melanoma, we discovered that this retinoid decreased the phosphorylation of ATF-2. Tretinoin 33-46 activating transcription factor 2 Mus musculus 183-188
18269766-5 2008 In the course of determining how retinoic acid (RA) stimulates activating protein-1 (AP-1) activity in B16 melanoma, we discovered that this retinoid decreased the phosphorylation of ATF-2. Tretinoin 48-50 activating transcription factor 2 Mus musculus 183-188
18269766-6 2008 It appears that this effect is mediated through p38 MAPK, because RA decreased p38 phosphorylation, and a selective inhibitor of p38 MAPK (SB203580) also inhibited the phosphorylation of ATF-2. Tretinoin 66-68 activating transcription factor 2 Mus musculus 187-192
18269766-7 2008 Since ATF-2 activity appears to be involved in resistance of melanoma to chemotherapy, we tested the hypothesis that treatment of the melanoma cells with RA would sensitize them to the growth-inhibitory effect of taxol. Tretinoin 154-156 activating transcription factor 2 Mus musculus 6-11
18269766-9 2008 On the basis of these findings and our previous work on AP-1, we propose a model in which treatment of B16 cells with RA decreases the phosphorylation of ATF-2, which results in less dimer formation with Jun. Tretinoin 118-120 activating transcription factor 2 Mus musculus 154-159
18269766-11 2008 Shifting the balance from predominantly ATF-2:Jun dimers to a higher amount of Jun:Fos dimers could lead a change in target gene expression that reduces resistance to chemotherapeutic drugs and contributes to the pathway by which RA arrests proliferation and induces differentiation. Tretinoin 230-232 activating transcription factor 2 Mus musculus 40-45
18156191-7 2008 RA restored the ratio of Bcl-2 to Bax, inhibited cleavage of caspase-3 and -9, and prevented the decreases in the levels of SOD-1 and SOD-2. Tretinoin 0-2 BCL2, apoptosis regulator Rattus norvegicus 25-30
18156191-7 2008 RA restored the ratio of Bcl-2 to Bax, inhibited cleavage of caspase-3 and -9, and prevented the decreases in the levels of SOD-1 and SOD-2. Tretinoin 0-2 superoxide dismutase 1 Rattus norvegicus 124-129
18156191-9 2008 The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Tretinoin 76-78 angiotensin I converting enzyme Rattus norvegicus 113-142
18156191-9 2008 The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Tretinoin 76-78 angiotensinogen Rattus norvegicus 219-234
18156191-9 2008 The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Tretinoin 76-78 angiotensinogen Rattus norvegicus 44-58
18156191-9 2008 The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Tretinoin 76-78 angiotensin I converting enzyme Rattus norvegicus 144-147
18327422-3 2008 We have shown earlier that vitamin D(3) and retinoic acid (RA) down-regulate TACO gene transcription in a dose-dependent manner. Tretinoin 44-57 coronin 1A Homo sapiens 77-81
17951529-0 2008 Retinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathway. Tretinoin 0-13 signal transducer and activator of transcription 3 Homo sapiens 81-87
17951529-4 2008 Conversely, inhibition of retinoic acid signaling constrains transforming growth factor beta (TGF-beta1) induction of FoxP3. Tretinoin 26-39 transforming growth factor beta 1 Homo sapiens 94-103
17951529-5 2008 The effect of ATRA is mediated independently of IL-2, signal transducer and activator of transcription 5 (Stat5) and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. Tretinoin 14-18 interleukin 2 Homo sapiens 48-52
17951529-5 2008 The effect of ATRA is mediated independently of IL-2, signal transducer and activator of transcription 5 (Stat5) and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. Tretinoin 14-18 signal transducer and activator of transcription 3 Homo sapiens 117-122
18199582-4 2008 Asymmetric PITX2 expression in the left presumptive gonad leads to the asymmetric expression of the retinoic-acid (RA)-synthesizing enzyme, RALDH2, in the right presumptive gonad. Tretinoin 100-113 paired like homeodomain 2 Gallus gallus 11-16
18199582-4 2008 Asymmetric PITX2 expression in the left presumptive gonad leads to the asymmetric expression of the retinoic-acid (RA)-synthesizing enzyme, RALDH2, in the right presumptive gonad. Tretinoin 115-117 paired like homeodomain 2 Gallus gallus 11-16
18293192-0 2008 Activation of TGF-beta1 through up-regulation of TSP-1 by retinoic acid in retinal pigment epithelial cells. Tretinoin 58-71 transforming growth factor beta 1 Homo sapiens 14-23
18293192-0 2008 Activation of TGF-beta1 through up-regulation of TSP-1 by retinoic acid in retinal pigment epithelial cells. Tretinoin 58-71 thrombospondin 1 Homo sapiens 49-54
18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 9-22 transforming growth factor beta 1 Homo sapiens 54-87
18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 9-22 transforming growth factor beta 1 Homo sapiens 89-98
18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 54-87
18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 89-98
18293192-3 2008 Since TSP-1 activates TGF-beta1, we investigated whether RA stimulates the activation of TGF-beta1 through up-regulation of TSP-1 in RPE cells. Tretinoin 57-59 transforming growth factor beta 1 Homo sapiens 89-98
18293192-3 2008 Since TSP-1 activates TGF-beta1, we investigated whether RA stimulates the activation of TGF-beta1 through up-regulation of TSP-1 in RPE cells. Tretinoin 57-59 thrombospondin 1 Homo sapiens 124-129
18293192-6 2008 RESULTS: The active form of TGF-beta1 was increased dose-dependently by RA or TSP-1. Tretinoin 72-74 transforming growth factor beta 1 Homo sapiens 28-37
18293192-7 2008 The activation of TGF-beta1 by RA was significantly hampered by an anti-TSP-1 antibody. Tretinoin 31-33 transforming growth factor beta 1 Homo sapiens 18-27
18293192-7 2008 The activation of TGF-beta1 by RA was significantly hampered by an anti-TSP-1 antibody. Tretinoin 31-33 thrombospondin 1 Homo sapiens 72-77
18293192-9 2008 CONCLUSIONS: These findings suggest that, in RPE cells, RA increases the activation of TGF-beta1 via up-regulation of TSP-1, and integrins such as alphavbeta3 and alphavbeta5 are essential in this activation step. Tretinoin 56-58 transforming growth factor beta 1 Homo sapiens 87-96
18293192-9 2008 CONCLUSIONS: These findings suggest that, in RPE cells, RA increases the activation of TGF-beta1 via up-regulation of TSP-1, and integrins such as alphavbeta3 and alphavbeta5 are essential in this activation step. Tretinoin 56-58 thrombospondin 1 Homo sapiens 118-123
17828768-4 2008 Treatment of SH-SY5Y cells, differentiated by long-term exposure to 10 microM retinoic acid with a neutralizing anti-alpha1-integrin antibody significantly reduced A beta-induced neuronal death. Tretinoin 78-91 amyloid beta precursor protein Homo sapiens 164-170
18327422-3 2008 We have shown earlier that vitamin D(3) and retinoic acid (RA) down-regulate TACO gene transcription in a dose-dependent manner. Tretinoin 59-61 coronin 1A Homo sapiens 77-81
18327422-6 2008 RESULTS: TACO gene down-regulation observed with vitamin D(3)/RA treatment occurred through modulation of this gene via the VDR/RXR response sequence present in the promoter region of TACO gene. Tretinoin 62-64 coronin 1A Homo sapiens 9-13
18327422-6 2008 RESULTS: TACO gene down-regulation observed with vitamin D(3)/RA treatment occurred through modulation of this gene via the VDR/RXR response sequence present in the promoter region of TACO gene. Tretinoin 62-64 coronin 1A Homo sapiens 184-188
17561254-7 2008 On HL60 cells, ATRA induced expression of CD38, CD43 and CD45RO and repressed CD117, while the converse was true on NB4 cells that contain chimeric PML-RARalpha. Tretinoin 15-19 sialophorin Homo sapiens 48-52
18039708-0 2008 Retinoic acid modulates chromatin to potentiate tumor necrosis factor alpha signaling on the DIF2 promoter. Tretinoin 0-13 tumor necrosis factor Homo sapiens 48-75
18039708-0 2008 Retinoic acid modulates chromatin to potentiate tumor necrosis factor alpha signaling on the DIF2 promoter. Tretinoin 0-13 immediate early response 3 Homo sapiens 93-97
18039708-4 2008 We show a functional RA response element in the DIF2 promoter, which is constitutively bound by PML/RARalpha in APL cells. Tretinoin 21-23 immediate early response 3 Homo sapiens 48-52
17888423-8 2008 When cocultured with mouse cardiomyocytes, Retinoic Acid-treated skeletal muscle stem cells expressed connexin43 and when transplanted into ischemic heart were detectable even 5 weeks after injection. Tretinoin 43-56 gap junction protein, alpha 1 Mus musculus 102-112
17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 cyclin dependent kinase 6 Homo sapiens 221-225
17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 dynactin subunit 6 Homo sapiens 275-278
17997979-4 2008 The retinoic acid derivative also reverses an early liver fibrosis, as assayed by liver contents of hydroxyproline, alpha-smooth muscle actin (alpha-SMA), and collagen 1A2, in an early liver fibrosis model we established previously where an inducible expression vector containing a TGF-beta gene was hydrodynamically transferred into a testing animal. Tretinoin 4-17 transforming growth factor, beta 1 Rattus norvegicus 282-290
17997979-0 2008 Antagonizing TGF-beta induced liver fibrosis by a retinoic acid derivative through regulation of ROS and calcium influx. Tretinoin 50-63 transforming growth factor, beta 1 Rattus norvegicus 13-21
17109394-4 2008 Here we discuss the evidence for non-chordate RA signaling systems in the light of recent advances in our understanding of carotene (pro-Vitamin A) metabolism and of the identification of potential RARs and members of the NR1 family in echinoderms and lophotrochozoan trematodes, respectively. Tretinoin 46-48 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 222-225
18089289-8 2008 According to the possible role of Nanos3 in inhibiting spermatogonia cell differentiation, we show that treatment with the differentiating factor all-trans retinoic acid induces a dramatic down-regulation of its expression. Tretinoin 156-169 nanos C2HC-type zinc finger 3 Mus musculus 34-40
19068145-12 2008 CONCLUSIONS: Among RAR and RXR agonists, only ATRA inhibited IL-1-induced IL-6 expression in rat synovial fibroblasts by inhibiting ERK1/2 pathway and subsequent activation of AP-1 and NF-IL-6 independently of RAR. Tretinoin 46-50 interleukin 6 Rattus norvegicus 74-78
17986385-0 2008 PI3-K- and PKC-dependent up-regulation of APP processing enzymes by retinoic acid. Tretinoin 68-81 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha Homo sapiens 0-14
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 40-63 matrix metallopeptidase 3 Homo sapiens 93-98
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 65-69 matrix metallopeptidase 3 Homo sapiens 93-98
19068145-0 2008 All-trans retinoic acid suppresses interleukin-6 expression in interleukin-1-stimulated synovial fibroblasts by inhibition of ERK1/2 pathway independently of RAR activation. Tretinoin 10-23 interleukin 6 Rattus norvegicus 35-48
19068145-8 2008 In IL-1-stimulated cells, ATRA, but not BMS-649, reduced IL-6 expression whereas selective RAR agonists were inactive. Tretinoin 26-30 interleukin 6 Rattus norvegicus 57-61
19068145-9 2008 The inhibitory effect of ATRA on IL-6 was not affected by the silencing of RAR subtypes. Tretinoin 25-29 interleukin 6 Rattus norvegicus 33-37
18182117-2 2008 Tumour necrosis factor (TNF)-alpha, found in arthritic joints, activates nuclear factor-kappaB (NF-kappaB), whereas retinoic acid receptors (RARs) are activated by retinoid agonists, including all-trans retinoic acid (atRA). Tretinoin 218-222 tumor necrosis factor Rattus norvegicus 0-34
18224398-5 2008 ATRA decreased the expression of PKCalpha, as well as reduced ERK MAPK phosphorylation, and consequently caused G(1) arrest. Tretinoin 0-4 protein kinase C alpha Homo sapiens 33-41
18836242-4 2008 ATRA (300 or 1000 nM) inhibited IL-1-induced expression of iNOS and nitrites level in both species, although the NO pathway was induced maximally in rat cells. Tretinoin 0-4 nitric oxide synthase 2 Rattus norvegicus 59-63
18296860-2 2008 ATRA enhanced the production of IL-2 stimulated by TPA, but suppressed that stimulated by PHA. Tretinoin 0-4 interleukin 2 Homo sapiens 32-36
18296860-0 2008 Different effects of all-trans-retinoic acid on phorbol ester-stimulated and phytohemagglutinin-stimulated interleukin-2 expression in human T-cell lymphoma HUT-78 cells. Tretinoin 21-44 interleukin 2 Homo sapiens 107-120
18296860-7 2008 These results suggest that ATRA affects the production of IL-2 by T-lymphocytes in a stimulus-dependent manner. Tretinoin 27-31 interleukin 2 Homo sapiens 58-62
17712061-5 2008 In synaptoneurosomes, atRA rapidly increased phosphorylation of ERK1/2, its target 4E-BP, and p70S6K, and its substrate, ribosome protein S6, indicating activation of MAPK and mammalian target of rapamycin (mTOR). Tretinoin 22-26 mitogen-activated protein kinase 3 Homo sapiens 64-70
18781947-5 2008 Lasting recent years it has become clear that human skin cells express various CYP enzymes, including CYP26AI which is responsible for the metabolism of retinoic acid in skin cells. Tretinoin 153-166 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 79-82
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 RUNX family transcription factor 2 Homo sapiens 86-91
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 RUNX family transcription factor 2 Homo sapiens 92-97
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 bone gamma-carboxyglutamate protein Homo sapiens 177-188
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 CCAAT enhancer binding protein alpha Homo sapiens 291-301
17949889-1 2008 OBJECTIVE: The roles of phosphatidylinositol 3 (PI3K) and mitogen-activated protein kinases (MAPK) have been widely studied in terms of the differentiation process induced by several drugs (phorbol ester, vitamin D-3, retinoic acid, etc. Tretinoin 218-231 mitogen-activated protein kinase 1 Homo sapiens 93-97
17712061-5 2008 In synaptoneurosomes, atRA rapidly increased phosphorylation of ERK1/2, its target 4E-BP, and p70S6K, and its substrate, ribosome protein S6, indicating activation of MAPK and mammalian target of rapamycin (mTOR). Tretinoin 22-26 mitogen-activated protein kinase 3 Homo sapiens 167-171
17712061-5 2008 In synaptoneurosomes, atRA rapidly increased phosphorylation of ERK1/2, its target 4E-BP, and p70S6K, and its substrate, ribosome protein S6, indicating activation of MAPK and mammalian target of rapamycin (mTOR). Tretinoin 22-26 mechanistic target of rapamycin kinase Homo sapiens 176-205
17712061-5 2008 In synaptoneurosomes, atRA rapidly increased phosphorylation of ERK1/2, its target 4E-BP, and p70S6K, and its substrate, ribosome protein S6, indicating activation of MAPK and mammalian target of rapamycin (mTOR). Tretinoin 22-26 mechanistic target of rapamycin kinase Homo sapiens 207-211
17928352-9 2008 The interaction between U95 and GRIM-19 is thus functionally and metabolically significant in HHV-6B-infected cells and may be a means through which HHV-6B modulates cell death signals by interferon and retinoic acid. Tretinoin 203-216 small nucleolar RNA, C/D box 95 Homo sapiens 24-27
17828619-4 2008 In in vitro culture, all-transretinoic acid promoted the maturation from CD4+CD8+ cells to CD4+ cells but inhibited the differentiation from CD4+CD8+ cells to CD8+ cells. Tretinoin 25-43 CD4 molecule Homo sapiens 73-76
17828619-4 2008 In in vitro culture, all-transretinoic acid promoted the maturation from CD4+CD8+ cells to CD4+ cells but inhibited the differentiation from CD4+CD8+ cells to CD8+ cells. Tretinoin 25-43 CD4 molecule Homo sapiens 91-94
17828619-4 2008 In in vitro culture, all-transretinoic acid promoted the maturation from CD4+CD8+ cells to CD4+ cells but inhibited the differentiation from CD4+CD8+ cells to CD8+ cells. Tretinoin 25-43 CD4 molecule Homo sapiens 91-94
18001002-8 2008 In addition, intravenous injection of ATRA-lipoplexes inhibited the activation of NFkappaB in liver, and subsequently suppressed the serum levels of tumor necrosis factor-alpha (TNF-alpha) and alanine aminotransferase (ALT) compared with lipoplexes. Tretinoin 38-42 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 82-90
18001002-8 2008 In addition, intravenous injection of ATRA-lipoplexes inhibited the activation of NFkappaB in liver, and subsequently suppressed the serum levels of tumor necrosis factor-alpha (TNF-alpha) and alanine aminotransferase (ALT) compared with lipoplexes. Tretinoin 38-42 tumor necrosis factor Mus musculus 149-176
18001002-8 2008 In addition, intravenous injection of ATRA-lipoplexes inhibited the activation of NFkappaB in liver, and subsequently suppressed the serum levels of tumor necrosis factor-alpha (TNF-alpha) and alanine aminotransferase (ALT) compared with lipoplexes. Tretinoin 38-42 tumor necrosis factor Mus musculus 178-187
18773862-6 2008 Consistent with the inhibition effect and G1 arrest, ATRA and SB, alone or in combination, induced the expression of G1 phase markers cyclin-dependent kinase (CDK) 6, p21, and p27; inhibited the expression of S-G2 phase proteins CDK2; and decreased Rb phosphorylation. Tretinoin 53-57 cyclin dependent kinase 6 Homo sapiens 159-165
18773862-6 2008 Consistent with the inhibition effect and G1 arrest, ATRA and SB, alone or in combination, induced the expression of G1 phase markers cyclin-dependent kinase (CDK) 6, p21, and p27; inhibited the expression of S-G2 phase proteins CDK2; and decreased Rb phosphorylation. Tretinoin 53-57 cyclin dependent kinase inhibitor 1A Homo sapiens 167-170
18791934-3 2008 Evidence was obtained that this interaction depends on histone deactylase one (HDAC1) inhibition by butyrate and retinoic acid receptor alpha (RARalpha) activation by ATRA. Tretinoin 167-171 histone deacetylase 1 Homo sapiens 79-84
18773862-6 2008 Consistent with the inhibition effect and G1 arrest, ATRA and SB, alone or in combination, induced the expression of G1 phase markers cyclin-dependent kinase (CDK) 6, p21, and p27; inhibited the expression of S-G2 phase proteins CDK2; and decreased Rb phosphorylation. Tretinoin 53-57 dynactin subunit 6 Homo sapiens 176-179
18773862-9 2008 These results indicate that the growth inhibition and G1 arrest of oral squamous carcinoma cells in response to ATRA and/or SB correlates with the induction of G1 phase cell cycle regulatory proteins CDK6, p21, and p27 and the inhibition of S-G2 phase cell cycle regulatory protein CDK2. Tretinoin 112-116 cyclin dependent kinase 6 Homo sapiens 200-204
18773862-9 2008 These results indicate that the growth inhibition and G1 arrest of oral squamous carcinoma cells in response to ATRA and/or SB correlates with the induction of G1 phase cell cycle regulatory proteins CDK6, p21, and p27 and the inhibition of S-G2 phase cell cycle regulatory protein CDK2. Tretinoin 112-116 cyclin dependent kinase inhibitor 1A Homo sapiens 206-209
18773862-9 2008 These results indicate that the growth inhibition and G1 arrest of oral squamous carcinoma cells in response to ATRA and/or SB correlates with the induction of G1 phase cell cycle regulatory proteins CDK6, p21, and p27 and the inhibition of S-G2 phase cell cycle regulatory protein CDK2. Tretinoin 112-116 dynactin subunit 6 Homo sapiens 215-218
17938173-5 2007 IL-1alpha and retinoic acid stimulated radiolabeled aggrecan loss from wild-type and ADAMTS-4 Deltacat cartilage, but there was little effect on ADAMTS-5 cartilage. Tretinoin 14-27 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 4 Mus musculus 85-93
17938173-8 2007 Retinoic acid, but not IL-1alpha, stimulated radiolabeled aggrecan loss from ADAMTS-4/-5 Deltacat cartilage explants. Tretinoin 0-13 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 4 Mus musculus 77-85
17938173-9 2007 Even though there was a 300% increase in aggrecan loss from ADAMTS-4/-5 Deltacat cartilage stimulated with retinoic acid, the loss was not associated with aggrecanase cleavage but with the release of predominantly intact aggrecan consistent with the phenotype of the ADAMTS-4/-5 Deltacat mouse. Tretinoin 107-120 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 4 Mus musculus 60-68
18052213-0 2007 Galactomutarotase and other galactose-related genes are rapidly induced by retinoic acid in human myeloid cells. Tretinoin 75-88 galactose mutarotase Homo sapiens 0-17
18052213-3 2007 We report herein that all-trans-retinoic acid (RA), an active metabolite of vitamin A that is known to induce myeloid lineage cell differentiation into macrophage-like cells, induces a rapid and robust regulation of GALM mRNA expression in human myeloid cells. Tretinoin 22-45 galactose mutarotase Homo sapiens 216-220
18052213-3 2007 We report herein that all-trans-retinoic acid (RA), an active metabolite of vitamin A that is known to induce myeloid lineage cell differentiation into macrophage-like cells, induces a rapid and robust regulation of GALM mRNA expression in human myeloid cells. Tretinoin 47-49 galactose mutarotase Homo sapiens 216-220
18052213-7 2007 The increase in GALM mRNA by RA was blocked by pretreating THP-1 cells with actinomycin D but not by cycloheximide. Tretinoin 29-31 galactose mutarotase Homo sapiens 16-20
18052213-10 2007 Thus, the results of this study identify RA as a significant regulator of GALM and other galactose-related genes in myeloid-monocytic cells, which could affect energy utilization and synthesis of cell-surface glycoproteins or glycolipids involved in cell motility, adhesion, and/or functional properties. Tretinoin 41-43 galactose mutarotase Homo sapiens 74-78
18079182-8 2007 Upon retinoic acid-induced transcriptional activation of HoxA2 in a cell model of neuronal differentiation, PRMT6 recruitment and H3 R2 methylation are diminished and H3 K4 trimethylation increases at the gene. Tretinoin 5-18 protein arginine methyltransferase 6 Homo sapiens 108-113
18157915-0 2007 On the role of transforming growth factor-beta in the growth inhibitory effects of retinoic acid in human pancreatic cancer cells. Tretinoin 83-96 transforming growth factor beta 1 Homo sapiens 15-46
18157915-9 2007 A TGF-beta neutralizing antibody blocked the growth inhibitory effects of retinoic acid in Capan-2 cells and partially inhibitory the effects in Hs766T cells. Tretinoin 74-87 transforming growth factor beta 1 Homo sapiens 2-10
18157915-11 2007 Furthermore, it demonstrates the fundamental role of TGF-beta in growth inhibition in response to retinoic acid treatment is preserved in vitro. Tretinoin 98-111 transforming growth factor beta 1 Homo sapiens 53-61
18476539-1 2007 OBJECTIVE: To study the reactivation of retinoic acid receptor beta (RARbeta) expression in myeloid leukemia cells by a combination of all-trans retinoic acid (ATRA) with a DNA demethylating agent, decitabine (DAC), and valproic acid (VPA, a histone deacetylase inhibitor),and their effects on cell differentiation and proliferation. Tretinoin 40-53 retinoic acid receptor beta Homo sapiens 69-76
18476539-1 2007 OBJECTIVE: To study the reactivation of retinoic acid receptor beta (RARbeta) expression in myeloid leukemia cells by a combination of all-trans retinoic acid (ATRA) with a DNA demethylating agent, decitabine (DAC), and valproic acid (VPA, a histone deacetylase inhibitor),and their effects on cell differentiation and proliferation. Tretinoin 160-164 retinoic acid receptor beta Homo sapiens 40-67
18476539-1 2007 OBJECTIVE: To study the reactivation of retinoic acid receptor beta (RARbeta) expression in myeloid leukemia cells by a combination of all-trans retinoic acid (ATRA) with a DNA demethylating agent, decitabine (DAC), and valproic acid (VPA, a histone deacetylase inhibitor),and their effects on cell differentiation and proliferation. Tretinoin 160-164 retinoic acid receptor beta Homo sapiens 69-76
18476539-8 2007 Chromatin immuno-precipitation assay (ChIP) was used to analyze the acetylated histone 3 bound to the retinoic acid response element (RARE) at the promoter region of RARbeta. Tretinoin 102-115 retinoic acid receptor beta Homo sapiens 166-173
18476539-10 2007 The expression of RARbeta in U937 cells was up-regulated after treatment with ATRA (1 micromol/L) plus DAC (1 micromol/L) or VPA (0.5 mmol/L) for 72 hours, especially when the three drugs were used together. Tretinoin 78-82 retinoic acid receptor beta Homo sapiens 18-25
18476539-14 2007 CONCLUSION: The repressed expression of RARbeta in myeloid leukemia cells is closely related to both DNA hypermethylation and histone deacetylation, and a combination of ATRA with epigenetic modulators can be beneficial in the treatment of myeloid malignancies. Tretinoin 170-174 retinoic acid receptor beta Homo sapiens 40-47
18509255-0 2008 Claudin 2 mRNA and protein are present in human keratinocytes and may be regulated by all-trans-retinoic acid. Tretinoin 90-109 claudin 2 Homo sapiens 0-9
18509255-6 2008 Further, we show that all-trans-retinoic acid increases the expression of claudin 2 in keratinocytes in a dose-dependent manner. Tretinoin 22-45 claudin 2 Homo sapiens 74-83
18048326-0 2007 Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha. Tretinoin 18-31 NFE2 like bZIP transcription factor 2 Homo sapiens 72-76
18048326-2 2007 Using a human mammary MCF7-derived AREc32 reporter cell line, we now report that all-trans retinoic acid (ATRA), and other retinoic acid receptor alpha (RARalpha) agonists, markedly reduces the ability of Nrf2 to mediate induction of ARE-driven genes by cancer chemopreventive agents including the metabolite of butylated hydroxyanisole, tert-butylhydroquinone (tBHQ). Tretinoin 91-104 NFE2 like bZIP transcription factor 2 Homo sapiens 205-209
18048326-2 2007 Using a human mammary MCF7-derived AREc32 reporter cell line, we now report that all-trans retinoic acid (ATRA), and other retinoic acid receptor alpha (RARalpha) agonists, markedly reduces the ability of Nrf2 to mediate induction of ARE-driven genes by cancer chemopreventive agents including the metabolite of butylated hydroxyanisole, tert-butylhydroquinone (tBHQ). Tretinoin 106-110 NFE2 like bZIP transcription factor 2 Homo sapiens 205-209
18048326-7 2007 In MCF7 cells, ATRA did not block the nuclear accumulation of Nrf2 but reduced the binding of Nrf2 to the ARE enhancer as a consequence of forming a complex with RARalpha. Tretinoin 15-19 NFE2 like bZIP transcription factor 2 Homo sapiens 94-98
18075836-8 2007 We found that retinol and retinoic acid induced ERK1/2 phosphorylation, but only retinol-increased MMP-2 activity was inhibited by UO126, an ERK1/2 phosphorylation inhibitor. Tretinoin 26-39 mitogen-activated protein kinase 3 Homo sapiens 48-54
18345250-2 2007 Both retinoids and rexinoids are either natural or synthetic compounds related to retinoic acids that act through interaction with two basic types of nuclear receptors belonging to the nuclear receptor superfamily: All-trans retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 82-96 retinoic acid receptor beta Homo sapiens 260-267
18075297-0 2007 PPARgamma-active triterpenoid CDDO enhances ATRA-induced differentiation in APL. Tretinoin 44-48 peroxisome proliferator activated receptor gamma Homo sapiens 0-9
18075297-5 2007 Using ATRA sensitive NB4 and ATRA-resistant derivative MR2 cell lines, we demonstrate that PPARgamma ligand 2-cyano-3, 12-dioxooleana-1, 9-dien-28-oic acid (CDDO) enhances pro-apoptotic and differentiating effects of ATRA in ATRA-sensitive NB4 cells and partially reverses ATRA resistance in MR2 cells. Tretinoin 6-10 peroxisome proliferator activated receptor gamma Homo sapiens 91-100
18075297-5 2007 Using ATRA sensitive NB4 and ATRA-resistant derivative MR2 cell lines, we demonstrate that PPARgamma ligand 2-cyano-3, 12-dioxooleana-1, 9-dien-28-oic acid (CDDO) enhances pro-apoptotic and differentiating effects of ATRA in ATRA-sensitive NB4 cells and partially reverses ATRA resistance in MR2 cells. Tretinoin 29-33 peroxisome proliferator activated receptor gamma Homo sapiens 91-100
18075297-5 2007 Using ATRA sensitive NB4 and ATRA-resistant derivative MR2 cell lines, we demonstrate that PPARgamma ligand 2-cyano-3, 12-dioxooleana-1, 9-dien-28-oic acid (CDDO) enhances pro-apoptotic and differentiating effects of ATRA in ATRA-sensitive NB4 cells and partially reverses ATRA resistance in MR2 cells. Tretinoin 29-33 peroxisome proliferator activated receptor gamma Homo sapiens 91-100
18075297-5 2007 Using ATRA sensitive NB4 and ATRA-resistant derivative MR2 cell lines, we demonstrate that PPARgamma ligand 2-cyano-3, 12-dioxooleana-1, 9-dien-28-oic acid (CDDO) enhances pro-apoptotic and differentiating effects of ATRA in ATRA-sensitive NB4 cells and partially reverses ATRA resistance in MR2 cells. Tretinoin 29-33 peroxisome proliferator activated receptor gamma Homo sapiens 91-100
18075297-5 2007 Using ATRA sensitive NB4 and ATRA-resistant derivative MR2 cell lines, we demonstrate that PPARgamma ligand 2-cyano-3, 12-dioxooleana-1, 9-dien-28-oic acid (CDDO) enhances pro-apoptotic and differentiating effects of ATRA in ATRA-sensitive NB4 cells and partially reverses ATRA resistance in MR2 cells. Tretinoin 29-33 peroxisome proliferator activated receptor gamma Homo sapiens 91-100
18075297-7 2007 RARbeta2 MrNA induction by CDDO/ATRA was mediated in part by enhanced H3-Lys9 acetylation in the RARbeta2 promoter which in turn increased the affinity of RARbeta for betaRARE. Tretinoin 32-36 retinoic acid receptor beta Homo sapiens 0-7
18029484-8 2007 This inhibition of IRP RNA-binding activity by atRA supplementation was also associated with a 40% reduction in transferrin receptor abundance. Tretinoin 47-51 transferrin Rattus norvegicus 112-123
17931360-3 2007 The treatment of rat astrocytes with retinoic acid and dibutyryl cAMP, which induce apolipoprotein E (apoE) synthesis and HDL-like lipoprotein formation, stimulated extracellular S1P accumulation in the presence of its precursor sphingosine. Tretinoin 37-50 apolipoprotein E Rattus norvegicus 84-100
17931360-3 2007 The treatment of rat astrocytes with retinoic acid and dibutyryl cAMP, which induce apolipoprotein E (apoE) synthesis and HDL-like lipoprotein formation, stimulated extracellular S1P accumulation in the presence of its precursor sphingosine. Tretinoin 37-50 apolipoprotein E Rattus norvegicus 102-106
17509854-9 2007 Inhibition of ERK5 significantly decreased atRA-induced pJluc expression (P<.01). Tretinoin 43-47 mitogen-activated protein kinase 7 Rattus norvegicus 14-18
17509854-10 2007 The activity of ERK5 but not ERK1 was induced by atRA. Tretinoin 49-53 mitogen-activated protein kinase 7 Rattus norvegicus 16-20
17509854-11 2007 Furthermore, atRA promoted the nuclear translocation of ERK5 but not ERK1. Tretinoin 13-17 mitogen-activated protein kinase 7 Rattus norvegicus 56-60
18055984-6 2007 In addition, CD54 and CD18 knock-out mice were injected with NB4 cells and concomitantly treated with ATRA. Tretinoin 102-106 integrin beta 2 Mus musculus 22-26
18055984-10 2007 PB and G-CSF had no effect, but the latter potentiated ATRA-induced CD18 up-regulation. Tretinoin 55-59 integrin subunit beta 2 Homo sapiens 68-72
18029486-4 2007 CD4-positive and CD8-positive T cells, natural killer cells, and CD163-positive macrophages increased (P < 0.05) in the infected lung tissues of RA-treated rats. Tretinoin 148-150 CD163 molecule Rattus norvegicus 65-70
17616812-0 2007 Combination of all-trans retinoic acid and interferon-gamma suppressed PI3K/Akt survival pathway in glioblastoma T98G cells whereas NF-kappaB survival signaling in glioblastoma U87MG cells for induction of apoptosis. Tretinoin 25-38 AKT serine/threonine kinase 1 Homo sapiens 76-79
18026104-4 2007 Using pharmacological approaches, we show that inhibition of retinoic acid signaling markedly reduces hepatocyte proliferation in Trim24-/- mice. Tretinoin 61-74 tripartite motif-containing 24 Mus musculus 130-136
18026104-5 2007 We further show that deletion of a single retinoic acid receptor alpha (Rara) allele in a Trim24-null background suppresses HCC development and restores wild-type expression of retinoic acid-responsive genes in the liver, thus demonstrating that in this genetic background Rara expresses an oncogenic activity correlating with a dysregulation of the retinoic acid signaling pathway. Tretinoin 42-55 tripartite motif-containing 24 Mus musculus 90-96
18026104-5 2007 We further show that deletion of a single retinoic acid receptor alpha (Rara) allele in a Trim24-null background suppresses HCC development and restores wild-type expression of retinoic acid-responsive genes in the liver, thus demonstrating that in this genetic background Rara expresses an oncogenic activity correlating with a dysregulation of the retinoic acid signaling pathway. Tretinoin 177-190 tripartite motif-containing 24 Mus musculus 90-96
18065491-0 2007 Inhibition of Src family kinases enhances retinoic acid induced gene expression and myeloid differentiation. Tretinoin 42-55 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 14-17
18065491-8 2007 These studies provide the first demonstration that SFKs act to negatively regulate RA-induced gene expression and myeloid differentiation and suggest that the combination of SFK inhibition and RA treatment may be therapeutically beneficial in AML. Tretinoin 83-85 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 51-54
18065491-8 2007 These studies provide the first demonstration that SFKs act to negatively regulate RA-induced gene expression and myeloid differentiation and suggest that the combination of SFK inhibition and RA treatment may be therapeutically beneficial in AML. Tretinoin 193-195 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 51-54
17676389-5 2007 Our recent study demonstrated that combination of the chemotherapeutic agent all-trans retinoic acid (ATRA) and the immunotherapeutic agent interferon-gamma (IFN-gamma) could concurrently induce differentiation, apoptotic death, and immune components in two different human glioblastoma cell lines. Tretinoin 87-100 interferon gamma Homo sapiens 158-167
17616812-5 2007 Treatment with ATRA plus IFN-gamma stimulated PTEN expression and suppressed Akt activation in T98G cells, whereas no PTEN expression but Akt activation in U87MG cells under the same conditions. Tretinoin 15-19 AKT serine/threonine kinase 1 Homo sapiens 77-80
17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 interferon gamma Homo sapiens 60-69
17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 BCL2 associated X, apoptosis regulator Homo sapiens 131-134
17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 BCL2 apoptosis regulator Homo sapiens 135-140
17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 cytochrome c, somatic Homo sapiens 173-185
17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 caspase 3 Homo sapiens 191-200
18000064-2 2007 We show that CRABPI (encoding cellular retinoic acid binding protein I) is a target of PLZF, which is fused to RARalpha by the t(11;17)(q23;q21) translocation associated with retinoic acid (RA)-resistant acute promyelocytic leukemia (APL). Tretinoin 39-52 zinc finger and BTB domain containing 16 Mus musculus 87-91
18000064-2 2007 We show that CRABPI (encoding cellular retinoic acid binding protein I) is a target of PLZF, which is fused to RARalpha by the t(11;17)(q23;q21) translocation associated with retinoic acid (RA)-resistant acute promyelocytic leukemia (APL). Tretinoin 14-16 zinc finger and BTB domain containing 16 Mus musculus 87-91
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 zinc finger and BTB domain containing 16 Mus musculus 53-57
18000218-0 2007 Identification of the retinoic acid-inducible Gprc5a as a new lung tumor suppressor gene. Tretinoin 22-35 G protein-coupled receptor class C group 5 member A Homo sapiens 46-52
17992631-2 2007 AOX1 is well-described as xenobiotic metabolizing enzyme, which upon oxidation of acetaldehyde and retinaldehyde to acetic acid and retinoic acid generates reactive oxygen species. Tretinoin 132-145 aldehyde oxidase 1 Homo sapiens 0-4
17890117-9 2007 These results suggest that the postnatal induction of BCMO1 gene expression in the chick duodenum may be caused by the elevation of serum HC levels and may contribute to the RALDH1-mediated RA synthetic pathway. Tretinoin 174-176 beta-carotene oxygenase 1 Gallus gallus 54-59
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 zinc finger and BTB domain containing 16 Mus musculus 76-80
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 promyelocytic leukemia Mus musculus 156-159
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 58-60 zinc finger and BTB domain containing 16 Mus musculus 53-57
18000064-6 2007 RARalpha-PLZF confers RA resistance to a retinoid-sensitive acute myeloid leukemia (AML) cell line in a CRABPI-dependent fashion. Tretinoin 0-2 zinc finger and BTB domain containing 16 Mus musculus 9-13
17910945-7 2007 Further, our results indicate that these elements can be recognized as modulators of retinoic acid induced activation of SOX3 expression. Tretinoin 85-98 SRY-box transcription factor 3 Homo sapiens 121-125
17646067-6 2007 These cultures can be expanded in vitro for several months and differentiating markers such as ATOH1/HATH1 and POU4F3/BRN3C can be induced by manipulating the culture conditions using specific growth factors such as bFGF, EGF and retinoic acid. Tretinoin 230-243 POU class 4 homeobox 3 Homo sapiens 118-123
17881122-2 2007 Synergistic effects with brain-derived neurotrophic factor suggested that RA influences neurotrophin signaling. Tretinoin 74-76 brain derived neurotrophic factor Gallus gallus 25-58
17656367-4 2007 Structural overlap of a retinoic acid response element with these retinoid X response elements led to a high affinity binding of retinoic acid receptor/RXR heterodimer to the retinoic acid response element, resulting in the prevention of RXR ligand-mediated p21 transactivation. Tretinoin 24-37 cyclin dependent kinase inhibitor 1A Homo sapiens 258-261
17656367-4 2007 Structural overlap of a retinoic acid response element with these retinoid X response elements led to a high affinity binding of retinoic acid receptor/RXR heterodimer to the retinoic acid response element, resulting in the prevention of RXR ligand-mediated p21 transactivation. Tretinoin 129-142 cyclin dependent kinase inhibitor 1A Homo sapiens 258-261
17726077-2 2007 Moreover, protein C inhibitor (PCI), which specifically binds retinoic acid, was found to be increased in myocardial infarction survivors who are also insulin resistant. Tretinoin 62-75 insulin Homo sapiens 151-158
17875935-3 2007 p160 and Pbx1 compete for Prep1 in vitro, and p160 inhibits Prep1-dependent HoxB2 expression in retinoic acid-treated NT2-D1 cells. Tretinoin 96-109 MYB binding protein 1a Homo sapiens 46-50
17917245-7 2007 Introduction of siRNA against GATA-1 markedly reduced the ATRA-induced differentiation markers including CD11b and CCR3, as well as reduced eotaxin-2/CCL24 production. Tretinoin 58-62 GATA binding protein 1 Homo sapiens 30-36
17917245-6 2007 During the ATRA-induced differentiation, expression of a transcriptional factor, GATA-1 was significantly increased. Tretinoin 11-15 GATA binding protein 1 Homo sapiens 81-87
17673467-0 2007 Retinoic acid inhibits beta-catenin through suppression of Cox-2: a role for truncated adenomatous polyposis coli. Tretinoin 0-13 catenin (cadherin-associated protein), beta 1 Danio rerio 23-35
17673467-3 2007 Here we showed that treatment of zebrafish expressing a truncated form of Apc with either retinoic acid or a selective COX-2 inhibitor decreased beta-catenin protein levels and downstream signaling events. Tretinoin 90-103 catenin (cadherin-associated protein), beta 1 Danio rerio 145-157
17673467-5 2007 These findings support roles for retinoic acid and Cox-2 in regulating the stability of beta-catenin following Apc loss. Tretinoin 33-46 catenin (cadherin-associated protein), beta 1 Danio rerio 88-100
17917245-8 2007 Finally, ATRA-induced differentiation and eotaxin-2/CCL24 production were greatly enhanced in the GATA-1-overexpressed clones. Tretinoin 9-13 GATA binding protein 1 Homo sapiens 98-104
17652913-1 2007 The mRNA expression of GPRC5B, an orphan G protein-coupled receptor, is induced by retinoic acid (RA). Tretinoin 83-96 G protein-coupled receptor, family C, group 5, member B Mus musculus 23-29
17854312-3 2007 Growth, viability and differentiation patterns were maintained, but the expression of the FUS antisense construct in both the cell lines altered the response to ATRA: the previously ATRA-sensitive NB4 cells exhibited resistance; whilst the previously resistant NB4R2 cells showed a differentiation response to treatment. Tretinoin 161-165 FUS RNA binding protein Homo sapiens 90-93
17854312-3 2007 Growth, viability and differentiation patterns were maintained, but the expression of the FUS antisense construct in both the cell lines altered the response to ATRA: the previously ATRA-sensitive NB4 cells exhibited resistance; whilst the previously resistant NB4R2 cells showed a differentiation response to treatment. Tretinoin 182-186 FUS RNA binding protein Homo sapiens 90-93
17854312-0 2007 FUS expression alters the differentiation response to all-trans retinoic acid in NB4 and NB4R2 cells. Tretinoin 64-77 FUS RNA binding protein Homo sapiens 0-3
17584971-1 2007 Cyp26b1 encodes a retinoic acid (RA) metabolizing cytochrome P450 enzyme that is expressed in embryonic tissues undergoing morphogenesis, including the testes. Tretinoin 18-31 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
17584971-1 2007 Cyp26b1 encodes a retinoic acid (RA) metabolizing cytochrome P450 enzyme that is expressed in embryonic tissues undergoing morphogenesis, including the testes. Tretinoin 33-35 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 0-7
17584971-2 2007 We have generated transgenic mice lacking Cyp26b1 and have observed increased RA levels in embryonic testes. Tretinoin 78-80 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 42-49
17584971-8 2007 These results provide evidence that CYP26B1 maintains low levels of RA in the developing testes that blocks entry into meiosis and acts as a survival factor to prevent apoptosis of male germ cells. Tretinoin 68-70 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 36-43
17652913-1 2007 The mRNA expression of GPRC5B, an orphan G protein-coupled receptor, is induced by retinoic acid (RA). Tretinoin 98-100 G protein-coupled receptor, family C, group 5, member B Mus musculus 23-29
17652913-9 2007 These findings indicate that GPRC5B is involved in RA-dependent morphogenesis/angiogenesis and regulation of extracellular matrix synthesis in the murine placenta and yolk sac. Tretinoin 51-53 G protein-coupled receptor, family C, group 5, member B Mus musculus 29-35
17622583-1 2007 The retinoic acid receptor beta (RARbeta) is a retinoic acid (RA)-inducible tumor suppressor, which plays an important role in the arrest of neuroblastoma cell growth. Tretinoin 4-17 retinoic acid receptor beta Homo sapiens 33-40
17595318-2 2007 Here we show that RA activates PI3K and ERK1/2 MAPK signaling pathways through a rapid, nongenomic mechanism that does not require new gene transcription or newly synthesized proteins. Tretinoin 18-20 mitogen-activated protein kinase 3 Homo sapiens 40-46
17595318-2 2007 Here we show that RA activates PI3K and ERK1/2 MAPK signaling pathways through a rapid, nongenomic mechanism that does not require new gene transcription or newly synthesized proteins. Tretinoin 18-20 mitogen-activated protein kinase 3 Homo sapiens 47-51
17622583-1 2007 The retinoic acid receptor beta (RARbeta) is a retinoic acid (RA)-inducible tumor suppressor, which plays an important role in the arrest of neuroblastoma cell growth. Tretinoin 33-35 retinoic acid receptor beta Homo sapiens 4-31
17622583-3 2007 Our results show that HDACi cooperated with RA to increase RARbeta mRNA levels and to activate the RARbeta2 promoter in transient transfection assays. Tretinoin 44-46 retinoic acid receptor beta Homo sapiens 59-66
17646388-3 2007 In the present study, we further demonstrated that this nonclassical signaling of RA on the activation of CREB plays a critical role in regulating the expression of airway epithelial cell differentiation markers, the MUC2, MUC5AC, and MUC5B genes. Tretinoin 82-84 mucin 2, oligomeric mucus/gel-forming Homo sapiens 217-221
17646388-4 2007 We found that RA rapidly activates the protein kinase Calpha isozyme and transmits the activation signal to CREB via the Raf/MEK/extracellular signal-regulated kinase/p90 ribosomal S6 kinase (RSK) pathway. Tretinoin 14-16 mitogen-activated protein kinase kinase 7 Homo sapiens 125-128
17514648-3 2007 The purpose was to test if thalidomide can inhibit 13-cis RA-induced HOXB7 expression and whether thalidomide may enhance the antiproliferative effect of 13-cis RA in U343MG glioblastoma cells. Tretinoin 58-60 homeobox B7 Homo sapiens 69-74
17646388-4 2007 We found that RA rapidly activates the protein kinase Calpha isozyme and transmits the activation signal to CREB via the Raf/MEK/extracellular signal-regulated kinase/p90 ribosomal S6 kinase (RSK) pathway. Tretinoin 14-16 ribosomal protein S6 kinase A2 Homo sapiens 192-195
17938259-4 2007 We and others have previously reported that IFN-gamma synergistically potentiates retinoic acid (RA)-induced sympathetic differentiation and growth inhibition in neuroblastoma cells. Tretinoin 82-95 interferon gamma Homo sapiens 44-53
17938259-4 2007 We and others have previously reported that IFN-gamma synergistically potentiates retinoic acid (RA)-induced sympathetic differentiation and growth inhibition in neuroblastoma cells. Tretinoin 97-99 interferon gamma Homo sapiens 44-53
17628022-3 2007 We previously found that in myeloid leukemia cells, the lack of RA-induced RAR alpha-CAK dissociation and MAT1 degradation suppresses cell differentiation by inhibiting CAK-dependent G(1) exit and sustaining CAK hyperphosphorylation of RAR alpha. Tretinoin 64-66 cyclin dependent kinase 7 Homo sapiens 85-88
17628022-3 2007 We previously found that in myeloid leukemia cells, the lack of RA-induced RAR alpha-CAK dissociation and MAT1 degradation suppresses cell differentiation by inhibiting CAK-dependent G(1) exit and sustaining CAK hyperphosphorylation of RAR alpha. Tretinoin 64-66 cyclin dependent kinase 7 Homo sapiens 169-172
17628022-3 2007 We previously found that in myeloid leukemia cells, the lack of RA-induced RAR alpha-CAK dissociation and MAT1 degradation suppresses cell differentiation by inhibiting CAK-dependent G(1) exit and sustaining CAK hyperphosphorylation of RAR alpha. Tretinoin 64-66 cyclin dependent kinase 7 Homo sapiens 169-172
17628022-6 2007 These studies suggest that the subversion of RAR alpha-CAK signaling during normal granulopoiesis is crucial to myeloid leukemogenesis and challenges the current paradigm that RA induces cell differentiation solely by transactivating target genes. Tretinoin 45-47 cyclin dependent kinase 7 Homo sapiens 55-58
17514648-7 2007 It is concluded that thalidomide inhibits the RA-induced HOXB7 expression in glioblastoma cells and that 13-cis RA/thalidomide combinations can in principle enhance cytotoxicity. Tretinoin 46-48 homeobox B7 Homo sapiens 57-62
17663992-0 2007 Retinoid regulated association of transcriptional co-regulators and the polycomb group protein SUZ12 with the retinoic acid response elements of Hoxa1, RARbeta(2), and Cyp26A1 in F9 embryonal carcinoma cells. Tretinoin 110-123 retinoic acid receptor beta Homo sapiens 152-159
17785784-4 2007 In this study, we show that monocyte-derived DCs pretreated with the vitamin A derivative all-trans retinoic acid (RA) indeed acquired several attributes characteristic of mucosal DC: secretion of TGF-beta and IL-6 and the capacity to augment mucosal homing receptor expression and IgA responses in cocultured lymphocytes. Tretinoin 100-113 interleukin 6 Homo sapiens 210-214
17785784-4 2007 In this study, we show that monocyte-derived DCs pretreated with the vitamin A derivative all-trans retinoic acid (RA) indeed acquired several attributes characteristic of mucosal DC: secretion of TGF-beta and IL-6 and the capacity to augment mucosal homing receptor expression and IgA responses in cocultured lymphocytes. Tretinoin 115-117 interleukin 6 Homo sapiens 210-214
17785809-4 2007 Retinoic acid can promote TGF-beta1-dependent generation of FoxP3+ regulatory T cells but decrease the TGF-beta1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Tretinoin 0-13 interleukin 6 Mus musculus 118-122
17663992-0 2007 Retinoid regulated association of transcriptional co-regulators and the polycomb group protein SUZ12 with the retinoic acid response elements of Hoxa1, RARbeta(2), and Cyp26A1 in F9 embryonal carcinoma cells. Tretinoin 110-123 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 168-175
17706616-0 2007 Distribution of the cellular retinoic acid binding protein CRABP-I in the developing chick optic tectum. Tretinoin 29-42 cellular retinoic acid binding protein 1 Gallus gallus 59-66
17706616-5 2007 While the precise role of CRABP-I is still unknown, this is an intracellular transport protein for RA, which tends to be expressed in cells that are responsive to retinoic acid. Tretinoin 163-176 cellular retinoic acid binding protein 1 Gallus gallus 26-33
17723172-6 2007 The ability of retinoids to induce RARb has been consistently shown to correlate with the response of cells and tissues to retinoic acid, but few other biomarkers have been certified as indicators of retinoid activity. Tretinoin 123-136 retinoic acid receptor beta Homo sapiens 35-39
17804711-7 2007 Overexpression of RARbeta strongly enhances RA responsiveness, and knocking down RARbeta expression abolishes RA-mediated induction of HOXA5 expression in breast cancer cells. Tretinoin 44-46 retinoic acid receptor beta Homo sapiens 18-25
17494859-5 2007 MN1 increased resistance to all-trans retinoic acid (ATRA)-induced cell-cycle arrest and differentiation by more than 3000-fold in vitro. Tretinoin 38-51 MN1 proto-oncogene, transcriptional regulator Homo sapiens 0-3
17494859-5 2007 MN1 increased resistance to all-trans retinoic acid (ATRA)-induced cell-cycle arrest and differentiation by more than 3000-fold in vitro. Tretinoin 53-57 MN1 proto-oncogene, transcriptional regulator Homo sapiens 0-3
17494859-7 2007 We then evaluated whether MN1 expression levels in patients with AML (excluding M3-AML) correlated with resistance to ATRA treatment in elderly patients uniformly treated within treatment protocol AMLHD98-B. Tretinoin 118-122 MN1 proto-oncogene, transcriptional regulator Homo sapiens 26-29
17494859-8 2007 Strikingly, patients with low MN1 expression who received ATRA had a significantly prolonged event-free (P = .008) and overall (P = .04) survival compared with patients with either low MN1 expression and no ATRA, or high MN1 expression with or without ATRA. Tretinoin 58-62 MN1 proto-oncogene, transcriptional regulator Homo sapiens 30-33
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 transforming growth factor beta 1 Homo sapiens 36-44
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 CD4 molecule Homo sapiens 120-123
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 interleukin 6 Homo sapiens 283-287
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 transforming growth factor beta 1 Homo sapiens 36-44
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 CD4 molecule Homo sapiens 120-123
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 interleukin 6 Homo sapiens 283-287
18063853-1 2007 In the present work, the effects of colchicine (COL) and/or all-trans retinoic acid (ATRA) on expression of rexinoid receptors (RXRs) (alpha, beta, gamma), thyroid hormone receptor alpha and coregulators N-CoR, SMRT and SRC-1 mRNA in primary rat hepatocytes as a model of no-proliferating cells were investigated. Tretinoin 70-83 thyroid hormone receptor alpha Rattus norvegicus 134-186
18063853-1 2007 In the present work, the effects of colchicine (COL) and/or all-trans retinoic acid (ATRA) on expression of rexinoid receptors (RXRs) (alpha, beta, gamma), thyroid hormone receptor alpha and coregulators N-CoR, SMRT and SRC-1 mRNA in primary rat hepatocytes as a model of no-proliferating cells were investigated. Tretinoin 85-89 thyroid hormone receptor alpha Rattus norvegicus 134-186
17699781-1 2007 Here, we show that the platelet-derived growth factor receptor (PDGFR) regulates myeloid and monocytic differentiation of HL-60 myeloblastic leukemia cells in response to retinoic acid (RA) and vitamin D3 (D3), respectively. Tretinoin 171-184 platelet derived growth factor receptor beta Homo sapiens 23-62
17714122-1 2007 BACKGROUND: R115866 (Rambazole) is a new generation all-trans retinoic acid metabolism blocking agent, highly specific against the retinoic acid 4-hydroxylase. Tretinoin 62-75 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 131-158
17923756-4 2007 However, retinoic acid receptor beta(RAR beta) expression was up-regulated on H460 and H1299 cells treated with 1 microM of ATRA, 13-cis RA, or 9-cis RA. Tretinoin 124-128 retinoic acid receptor beta Homo sapiens 9-36
17923756-4 2007 However, retinoic acid receptor beta(RAR beta) expression was up-regulated on H460 and H1299 cells treated with 1 microM of ATRA, 13-cis RA, or 9-cis RA. Tretinoin 124-128 retinoic acid receptor beta Homo sapiens 37-45
17923756-4 2007 However, retinoic acid receptor beta(RAR beta) expression was up-regulated on H460 and H1299 cells treated with 1 microM of ATRA, 13-cis RA, or 9-cis RA. Tretinoin 37-39 retinoic acid receptor beta Homo sapiens 9-36
17923756-4 2007 However, retinoic acid receptor beta(RAR beta) expression was up-regulated on H460 and H1299 cells treated with 1 microM of ATRA, 13-cis RA, or 9-cis RA. Tretinoin 126-128 retinoic acid receptor beta Homo sapiens 9-36
17923756-4 2007 However, retinoic acid receptor beta(RAR beta) expression was up-regulated on H460 and H1299 cells treated with 1 microM of ATRA, 13-cis RA, or 9-cis RA. Tretinoin 126-128 retinoic acid receptor beta Homo sapiens 37-45
17923756-6 2007 In particular, sequential treatment with 1 microM ATRA or 13-cis RA and 4-HPR markedly inhibited H1703 cell growth; these cells exhibited no basal RAR beta expression and were refractory to 4-HPR. Tretinoin 50-54 retinoic acid receptor beta Homo sapiens 147-155
17923756-7 2007 However, in NSCLC cell lines that expressed RAR beta, the expressional levels of RAR beta were up-regulated by ATRA alone and by sequential treatment with ATRA and 4-HPR. Tretinoin 111-115 retinoic acid receptor beta Homo sapiens 44-52
17923756-7 2007 However, in NSCLC cell lines that expressed RAR beta, the expressional levels of RAR beta were up-regulated by ATRA alone and by sequential treatment with ATRA and 4-HPR. Tretinoin 111-115 retinoic acid receptor beta Homo sapiens 81-89
17923756-7 2007 However, in NSCLC cell lines that expressed RAR beta, the expressional levels of RAR beta were up-regulated by ATRA alone and by sequential treatment with ATRA and 4-HPR. Tretinoin 155-159 retinoic acid receptor beta Homo sapiens 44-52
17923756-7 2007 However, in NSCLC cell lines that expressed RAR beta, the expressional levels of RAR beta were up-regulated by ATRA alone and by sequential treatment with ATRA and 4-HPR. Tretinoin 155-159 retinoic acid receptor beta Homo sapiens 81-89
17591692-0 2007 The silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressor is required for full estrogen receptor alpha transcriptional activity. Tretinoin 26-39 estrogen receptor 1 Homo sapiens 109-132
17599952-3 2007 To gain insights into Atxn1 function, we have analysed the cerebellar gene expression profiles by microarray analysis in Atxn1-null mice, and identified alterations in expression of genes regulated by Sp1-dependent transcription, including the dopamine receptor D2 (Drd2), retinoic acid/thyroid hormone and Wnt-signalling. Tretinoin 273-286 dopamine receptor D2 Mus musculus 244-264
17453147-11 2007 Expression of RARbeta, a mediator of the action of retinoids, was also induced by RA in DAOY cells, implying that RAR-beta might also be involved in the mechanism of RA-induced cell cycle arrest. Tretinoin 14-16 retinoic acid receptor beta Homo sapiens 114-122
17453147-11 2007 Expression of RARbeta, a mediator of the action of retinoids, was also induced by RA in DAOY cells, implying that RAR-beta might also be involved in the mechanism of RA-induced cell cycle arrest. Tretinoin 82-84 retinoic acid receptor beta Homo sapiens 14-21
17453147-11 2007 Expression of RARbeta, a mediator of the action of retinoids, was also induced by RA in DAOY cells, implying that RAR-beta might also be involved in the mechanism of RA-induced cell cycle arrest. Tretinoin 82-84 retinoic acid receptor beta Homo sapiens 114-122
17699781-1 2007 Here, we show that the platelet-derived growth factor receptor (PDGFR) regulates myeloid and monocytic differentiation of HL-60 myeloblastic leukemia cells in response to retinoic acid (RA) and vitamin D3 (D3), respectively. Tretinoin 171-184 platelet derived growth factor receptor beta Homo sapiens 64-69
17666827-4 2007 Among the four PUFAs examined (linoleic acid, gamma-linolenic acid, retinoic acid, and docosahexaenoic acid; DHA), the highest inhibitory effect of CYP3A-catalyzed testosterone metabolism was observed with DHA, which inhibited testosterone metabolism by 94%. Tretinoin 68-81 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 148-153
17620364-2 2007 New studies support this idea by showing that the catalysis of vitamin A into retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (T reg) cells and also directs T reg cell homing to the gut. Tretinoin 78-91 transforming growth factor beta 1 Homo sapiens 150-187
17620364-2 2007 New studies support this idea by showing that the catalysis of vitamin A into retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (T reg) cells and also directs T reg cell homing to the gut. Tretinoin 93-95 transforming growth factor beta 1 Homo sapiens 150-187
17634193-6 2007 RA rescue of the lung phenotype was associated with low levels of Smad2 phosphorylation and downregulation of Tgfbeta targets in Raldh2-null foreguts. Tretinoin 0-2 SMAD family member 2 Mus musculus 66-71
17538947-5 2007 This result has pointed the way toward the detailed study of Raf/Mek/Erk pathway signaling in skin cancer development and its potential as a target pathway for chemoprevention by ATRA and other chemopreventive drugs. Tretinoin 179-183 zinc fingers and homeoboxes 2 Mus musculus 61-64
17438145-6 2007 We show that blockage of retinoic acid signaling by the pan-RAR antagonist AGN193109 prevents glia-induced neuron formation by noncommitted stem cells. Tretinoin 25-38 RAB40B, member RAS oncogene family Homo sapiens 60-63
17525477-8 2007 Intrinsic tryptophan fluorescence of both apoM variants revealed that retinol, all-trans-retinoic acid, and 9-cis-retinoic acid bound (dissociation constant = 2-3 microM), whereas other tested substances (e.g., cholesterol, vitamin K, and arachidonic acid) did not. Tretinoin 79-102 apolipoprotein M Homo sapiens 42-46
17525477-9 2007 The intrinsic fluorescence of two apoM mutants carrying single tryptophans was quenched by retinol and retinoic acid to the same extent as wild-type apoM, indicating that the environment of both tryptophans was affected by the binding. Tretinoin 103-116 apolipoprotein M Homo sapiens 34-38
17525477-10 2007 In conclusion, the binding of retinol and retinoic acid supports the hypothesis that apoM is a lipocalin. Tretinoin 42-55 apolipoprotein M Homo sapiens 85-89
17562868-3 2007 This finding has been explained, at least in part, by the lack of PML action to modulate retinoic acid-differentiating activities. Tretinoin 89-102 promyelocytic leukemia Mus musculus 66-69
17538947-5 2007 This result has pointed the way toward the detailed study of Raf/Mek/Erk pathway signaling in skin cancer development and its potential as a target pathway for chemoprevention by ATRA and other chemopreventive drugs. Tretinoin 179-183 mitogen-activated protein kinase 1 Mus musculus 69-72
17297443-3 2007 GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. Tretinoin 99-101 interferon alpha 1 Homo sapiens 70-73
17784835-4 2007 However, when SNUhES3 cells were induced to differentiate by retinoic acid, expression levels of NF-kappaB significantly increased compared to undifferentiated SNUhES3 cells. Tretinoin 61-74 nuclear factor kappa B subunit 1 Homo sapiens 97-106
17784840-0 2007 Neurospheres derived from human embryoid bodies treated with retinoic Acid show an increase in nestin and ngn2 expression that correlates with the proportion of tyrosine hydroxylase-positive cells. Tretinoin 61-74 nestin Homo sapiens 95-101
17784840-6 2007 Our results show that treatment of embryoid bodies (EBs) with retinoic acid (RA) leads to the greatest proportion of tyrosine hydroxylase (TH)-positive cells followed by vasoactive intestinal peptide (VIP)-treated EBs as compared to untreated EBs. Tretinoin 62-75 vasoactive intestinal peptide Homo sapiens 201-204
17784840-6 2007 Our results show that treatment of embryoid bodies (EBs) with retinoic acid (RA) leads to the greatest proportion of tyrosine hydroxylase (TH)-positive cells followed by vasoactive intestinal peptide (VIP)-treated EBs as compared to untreated EBs. Tretinoin 77-79 vasoactive intestinal peptide Homo sapiens 201-204
17784840-8 2007 Neurospheres derived from RA-treated EBs contained many nestin-positive cells within regions that expressed Ngn2. Tretinoin 26-28 nestin Homo sapiens 56-62
17475324-0 2007 RXRalpha regulates the pregnancy-specific glycoprotein 5 gene transcription through a functional retinoic acid responsive element. Tretinoin 97-110 pregnancy specific beta-1-glycoprotein 5 Homo sapiens 23-56
17420285-0 2007 RNAi screen identifies UBE2D3 as a mediator of all-trans retinoic acid-induced cell growth arrest in human acute promyelocytic NB4 cells. Tretinoin 57-70 ubiquitin conjugating enzyme E2 D3 Homo sapiens 23-29
17662308-2 2007 In vitro, hNT neurons express tyrosine hydroxylase (TH), depending on the length of time they are exposed to retinoic acid. Tretinoin 109-122 tyrosine hydroxylase Homo sapiens 30-50
17420285-7 2007 One of these proteins, the ubiquitin-conjugating enzyme UBE2D3, is up-regulated in ATRA-treated acute promyelocytic NB4 cells. Tretinoin 83-87 ubiquitin conjugating enzyme E2 D3 Homo sapiens 56-62
17420285-8 2007 UBE2D3 is physically associated with cyclin D1 and mediates ATRA-induced cyclin D1 degradation. Tretinoin 60-64 ubiquitin conjugating enzyme E2 D3 Homo sapiens 0-6
17420285-9 2007 Knocking down UBE2D3 by RNA interference (RNAi) leads to blockage of ATRA-induced cyclin D1 degradation and cell-cycle arrest. Tretinoin 69-73 ubiquitin conjugating enzyme E2 D3 Homo sapiens 14-20
19262136-4 2007 A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation. Tretinoin 24-37 transforming growth factor beta 1 Homo sapiens 90-97
17569825-4 2007 We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-beta-dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory T(H)17 cells and promoting anti-inflammatory Treg cell differentiation. Tretinoin 39-52 transforming growth factor beta 1 Homo sapiens 75-83
17569825-4 2007 We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-beta-dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory T(H)17 cells and promoting anti-inflammatory Treg cell differentiation. Tretinoin 39-52 interleukin 6 Homo sapiens 138-142
17510468-5 2007 A key enzyme is the all-trans retinoic acid-degrading enzyme cytochrome p450 isoform 26 (CYP26). Tretinoin 20-43 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 61-87
17510468-5 2007 A key enzyme is the all-trans retinoic acid-degrading enzyme cytochrome p450 isoform 26 (CYP26). Tretinoin 20-43 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 89-94
19262136-4 2007 A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation. Tretinoin 39-41 transforming growth factor beta 1 Homo sapiens 90-97
17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 85-98 BCL2 associated X, apoptosis regulator Homo sapiens 262-265
17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 85-98 BCL2 apoptosis regulator Homo sapiens 323-328
17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 85-98 BCL2 like 1 Homo sapiens 333-341
17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 100-104 BCL2 associated X, apoptosis regulator Homo sapiens 262-265
17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 100-104 BCL2 apoptosis regulator Homo sapiens 323-328
17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 100-104 BCL2 like 1 Homo sapiens 333-341
17467687-4 2007 Furthermore, the striking similarity between some of the hereby observed Hox/Gli3-dependent morphogenetic defects and those displayed by fetuses with severely altered retinoic acid metabolism suggests a tight connection between these various pathways. Tretinoin 167-180 GLI family zinc finger 3 Homo sapiens 77-81
17510468-6 2007 Thus, an alternative approach to exogenous retinoid administration could be to increase the intracellular level of all-trans retinoic acid by blocking CYP26-mediated degradation of retinoids. Tretinoin 125-138 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 151-156
17510468-8 2007 Although medial cells remained unaffected, treatment with the CYP26-inhibitor R115866 significantly increased cellular levels of all-trans retinoic acid in intimal SMCs. Tretinoin 139-152 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 62-67
17521827-4 2007 The cytoprotective effect of ATRA was observed not only in cornu ammonis (CA) 1 but also in CA2 and dentate gyrus (DG), and was attenuated by selective antagonists for RAR or RXR. Tretinoin 29-33 carbonic anhydrase 2 Rattus norvegicus 92-95
17467165-7 2007 The relevant nuclear receptor gene that was differentially expressed in the VAD liver was that encoding the peroxisome proliferator-activated receptor (PPAR) alpha, the mRNA levels for which were decreased in VAD liver and increased with all-trans RA treatment. Tretinoin 248-250 peroxisome proliferator activated receptor alpha Mus musculus 108-163
17213810-3 2007 We report that in both cell lines, RA signalling pathways are functional, as transactivation of an exogenous RARbeta2 promoter is effective in the presence of pharmacological concentrations of all-trans RA, and enhanced in RA-resistant FTC238 cells after ectopical expression of RARbeta, suggesting a defective endogenous RARbeta2 promoter in these cells. Tretinoin 35-37 retinoic acid receptor beta Homo sapiens 109-116
17213810-5 2007 Incubation with a histone deacetylase inhibitor, alone or in combination with RA, restored histone acetylation levels and reactivated RARbeta and differentiation marker Na+/I- symporter gene expression. Tretinoin 78-80 retinoic acid receptor beta Homo sapiens 134-141
19746216-6 2007 RESULTS: All-trans retinoic acid and 13-cis retinoic acid induced a reduction of NF-kappaB activity up to 64% and 65%, respectively, compared to the control. Tretinoin 9-32 nuclear factor kappa B subunit 1 Homo sapiens 81-90
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 integrin subunit beta 3 Rattus norvegicus 219-235
17332158-4 2007 Here, we show differential regulation of MMPs in cultured chondrocytes from chickens and turkeys; retinoic acid (RA) elevated MMP-2 activity in both species, but only in chicken did it induce MMP-9 activity. Tretinoin 98-111 72 kDa type IV collagenase Meleagris gallopavo 126-131
19746216-7 2007 For the treatment of the human transfectant cells with chemical carcinogens, all-trans retinoic acid (5 mM) and 13-cis retinoic acid (5 mM) downregulated the cellular NF-kappaB activation up to 83% and 85% compared to the NF-kappaB activity that was upregulated by NMU (5microM) and NEU (5microM), respectively. Tretinoin 87-100 nuclear factor kappa B subunit 1 Homo sapiens 167-176
19746216-7 2007 For the treatment of the human transfectant cells with chemical carcinogens, all-trans retinoic acid (5 mM) and 13-cis retinoic acid (5 mM) downregulated the cellular NF-kappaB activation up to 83% and 85% compared to the NF-kappaB activity that was upregulated by NMU (5microM) and NEU (5microM), respectively. Tretinoin 87-100 nuclear factor kappa B subunit 1 Homo sapiens 222-231
17551590-3 2007 Recent results suggest that RA could act on the endoderm of the first pharyngeal arch (1stPA), through a RARbeta-dependent mechanism. Tretinoin 28-30 retinoic acid receptor beta Homo sapiens 105-112
17551590-5 2007 We provide evidence showing that RA acts on the signalling epithelium of the 1(st) PA, gradually reducing the expression of endothelin-1 and Fgf8. Tretinoin 33-35 endothelin 1 Homo sapiens 124-136
17335046-5 2007 RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Tretinoin 53-55 bone morphogenetic protein 4 Mus musculus 211-215
17451684-8 2007 Following RA induction, quantitative RT-PCR analysis demonstrated downregulation of nestin, PAX-6, thy1.1, and PKCalpha, and upregulation of rhodopsin, glial fibrillary acidic protein (GFAP), and CrX. Tretinoin 10-12 cone-rod homeobox Rattus norvegicus 196-199
17507413-2 2007 FGF protects tail-end stem zone cells from precocious differentiation by inhibiting retinoid synthesis, whereas later-produced retinoic acid (RA) attenuates FGF signalling and drives differentiation. Tretinoin 127-140 fibroblast growth factor 10 Gallus gallus 157-160
17507413-2 2007 FGF protects tail-end stem zone cells from precocious differentiation by inhibiting retinoid synthesis, whereas later-produced retinoic acid (RA) attenuates FGF signalling and drives differentiation. Tretinoin 142-144 fibroblast growth factor 10 Gallus gallus 157-160
17507413-7 2007 Furthermore, although FGF inhibition of neuronal differentiation involves repression of the RA-responsive gene, retinoic acid receptor beta (RARbeta), Wnt signals are weaker repressors of neuron production and do not interfere with RA signal transduction. Tretinoin 92-94 fibroblast growth factor 10 Gallus gallus 22-25
17507413-9 2007 This study identifies a directional signalling relay that leads from FGF to retinoid signalling and demonstrates that Wnt signals serve, as cells leave the stem zone, to permit and promote RA activity, providing a mechanism to control the timing of the FGF-RA differentiation switch. Tretinoin 189-191 fibroblast growth factor 10 Gallus gallus 253-256
17276435-7 2007 Cytochrome P450 (CYP 26A1), which is responsible for retinoic acid metabolism, was highly up-regulated in leiomyomas (+5.4- +/- 0.53-fold). Tretinoin 53-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-25
17369494-0 2007 Catalase potentiates retinoic acid-induced THP-1 monocyte differentiation into macrophage through inhibition of peroxisome proliferator-activated receptor gamma. Tretinoin 21-34 catalase Homo sapiens 0-8
17286282-4 2007 The ErbB-1 inhibitor PD153035 cooperates with retinoic acid during growth inhibition and induces retinoic acid receptor-beta suggesting that ErbB-1 controls retinoic acid receptor-beta. Tretinoin 46-59 epidermal growth factor receptor Homo sapiens 4-10
17286282-4 2007 The ErbB-1 inhibitor PD153035 cooperates with retinoic acid during growth inhibition and induces retinoic acid receptor-beta suggesting that ErbB-1 controls retinoic acid receptor-beta. Tretinoin 46-59 epidermal growth factor receptor Homo sapiens 4-8
17286282-4 2007 The ErbB-1 inhibitor PD153035 cooperates with retinoic acid during growth inhibition and induces retinoic acid receptor-beta suggesting that ErbB-1 controls retinoic acid receptor-beta. Tretinoin 46-59 retinoic acid receptor beta Homo sapiens 157-184
17369494-0 2007 Catalase potentiates retinoic acid-induced THP-1 monocyte differentiation into macrophage through inhibition of peroxisome proliferator-activated receptor gamma. Tretinoin 21-34 GLI family zinc finger 2 Homo sapiens 43-48
17369494-0 2007 Catalase potentiates retinoic acid-induced THP-1 monocyte differentiation into macrophage through inhibition of peroxisome proliferator-activated receptor gamma. Tretinoin 21-34 peroxisome proliferator activated receptor gamma Homo sapiens 112-160
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 76-89 GLI family zinc finger 2 Homo sapiens 13-18
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 76-89 catalase Homo sapiens 30-38
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 91-95 GLI family zinc finger 2 Homo sapiens 13-18
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 91-95 catalase Homo sapiens 30-38
17369494-8 2007 Therefore, these data indicate that catalase is able to potentiate ATRA-induced macrophage differentiation by inhibition of PPARgamma activity, underscoring an important interplay between H(2)O(2), RA, and PPARgamma in macrophages. Tretinoin 67-71 catalase Homo sapiens 36-44
17369494-8 2007 Therefore, these data indicate that catalase is able to potentiate ATRA-induced macrophage differentiation by inhibition of PPARgamma activity, underscoring an important interplay between H(2)O(2), RA, and PPARgamma in macrophages. Tretinoin 67-71 peroxisome proliferator activated receptor gamma Homo sapiens 124-133
17369494-8 2007 Therefore, these data indicate that catalase is able to potentiate ATRA-induced macrophage differentiation by inhibition of PPARgamma activity, underscoring an important interplay between H(2)O(2), RA, and PPARgamma in macrophages. Tretinoin 67-71 peroxisome proliferator activated receptor gamma Homo sapiens 206-215
17325034-3 2007 CSK overexpression inhibited RA-mediated neurite outgrowth, a result which correlated with the inhibition of the SFK c-SRC. Tretinoin 29-31 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 117-122
17325034-5 2007 The conversion of GDP-RAC1 to GTP-RAC1 parallels the activation of c-SRC as early as 15 min following all-trans-retinoic acid treatment in LA-N-5 cells. Tretinoin 106-125 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 67-72
17325034-11 2007 We have elucidated a nongenomic extranuclear signal mediated by the RAR-SRC interaction that is negatively regulated by CSK and is required for RA-induced neuronal differentiation. Tretinoin 68-70 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 72-75
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 16-29 microtubule-associated protein 2 Mus musculus 131-136
17512406-1 2007 Transcriptional activation of the nuclear receptor RAR by retinoic acid (RA) often leads to inhibition of cell growth. Tretinoin 58-71 RAB40B, member RAS oncogene family Homo sapiens 51-54
17512406-5 2007 These proteins specifically deliver RA from the cytosol to nuclear RAR and PPARbeta/delta, respectively, thereby selectively enhancing the transcriptional activity of their cognate receptors. Tretinoin 36-38 RAB40B, member RAS oncogene family Homo sapiens 67-70
17512406-6 2007 Consequently, RA functions through RAR and is a proapoptotic agent in cells with high CRABP-II/FABP5 ratio, but it signals through PPARbeta/delta and promotes survival in cells that highly express FABP5. Tretinoin 14-16 RAB40B, member RAS oncogene family Homo sapiens 35-38
17350151-6 2007 Activation of ERK1/2 by RA was increased more in MeHg-treated differentiating cells, comparing with only RA-treated groups. Tretinoin 24-26 mitogen-activated protein kinase 3 Homo sapiens 14-20
17350151-6 2007 Activation of ERK1/2 by RA was increased more in MeHg-treated differentiating cells, comparing with only RA-treated groups. Tretinoin 105-107 mitogen-activated protein kinase 3 Homo sapiens 14-20
17350151-8 2007 Thus, it indicates that the neuronal differentiation with RA was mediated by the ERK1/2 and PKC related pathway and MeHg resulted in neurotoxic influences through the disturbance in steps of differentiation by this pathway. Tretinoin 58-60 mitogen-activated protein kinase 3 Homo sapiens 81-87
17350151-9 2007 These results suggest that MeHg inhibits RA-induced differentiation in SH-SY5Y cells by a pathway dependent ERK1/2 and PKC. Tretinoin 41-43 mitogen-activated protein kinase 3 Homo sapiens 108-114
17218384-0 2007 Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity. Tretinoin 128-141 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 74-79
17218384-5 2007 In opposition, only high-sensitive blasts expressed the CYP26A1 gene, encoding the p450 cytochrome which is known to be involved in retinoic acid catabolism. Tretinoin 132-145 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 56-63
17218384-6 2007 In NB4 cells, ATRA treatment activates a novel signaling pathway, whereby interleukin-8 stimulates the expression of the homeobox transcription factor HOXA10v2, an effective enhancer of CYP26A1 transcription. Tretinoin 14-18 C-X-C motif chemokine ligand 8 Homo sapiens 74-87
17218384-6 2007 In NB4 cells, ATRA treatment activates a novel signaling pathway, whereby interleukin-8 stimulates the expression of the homeobox transcription factor HOXA10v2, an effective enhancer of CYP26A1 transcription. Tretinoin 14-18 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 186-193
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 71-84 apolipoprotein B Homo sapiens 53-57
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 86-88 apolipoprotein B Homo sapiens 53-57
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 31-33 microtubule-associated protein 2 Mus musculus 131-136
17473173-8 2007 Thus, we show that the first oxidative step of Vitamin A metabolism, which is catalyzed in large part by the retinol dehydrogenase RDH10, is critical for the spatiotemporal synthesis of RA. Tretinoin 186-188 retinol dehydrogenase 10 (all-trans) Mus musculus 131-136
17209053-5 2007 Of importance, RA increased the CpG-induced phosphorylation of ERK1/2, p38MAPK, and IkappaB as early as 30 minutes after stimulation. Tretinoin 15-17 mitogen-activated protein kinase 3 Homo sapiens 63-69
17209053-6 2007 By using specific inhibitors, all the RA-mediated events, including proliferation, cyclin D3 expression, IL-10 secretion, and Ig secretion, were shown to be dependent on p38MAPK. Tretinoin 38-40 cyclin D3 Homo sapiens 83-92
17531122-13 2007 CONCLUSIONS: Berbamine induces caspase-3-dependent apoptosis of leukemia NB4 cells via survivin-mediated pathway, suggesting that berbamine may be a novel potential agent against APL with a mechanism distinct from that of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 232-245 caspase 3 Homo sapiens 31-40
17531122-13 2007 CONCLUSIONS: Berbamine induces caspase-3-dependent apoptosis of leukemia NB4 cells via survivin-mediated pathway, suggesting that berbamine may be a novel potential agent against APL with a mechanism distinct from that of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 247-251 caspase 3 Homo sapiens 31-40
16947022-6 2007 Treatment of glioblastoma cells with ATRA alone prevented cell proliferation and induced astrocytic differentiation, while IFN-gamma alone induced apoptosis and modulated expression of human leukocyte antigen (HLA) class II molecules such as HLA-DRalpha, HLA-DR complex, invariant chain (Ii), HLA-DM (an important catalyst of the class II-peptide loading), and gamma interferon-inducible lysosomal thiol-reductase (GILT). Tretinoin 37-41 IFI30 lysosomal thiol reductase Homo sapiens 361-413
16947022-6 2007 Treatment of glioblastoma cells with ATRA alone prevented cell proliferation and induced astrocytic differentiation, while IFN-gamma alone induced apoptosis and modulated expression of human leukocyte antigen (HLA) class II molecules such as HLA-DRalpha, HLA-DR complex, invariant chain (Ii), HLA-DM (an important catalyst of the class II-peptide loading), and gamma interferon-inducible lysosomal thiol-reductase (GILT). Tretinoin 37-41 IFI30 lysosomal thiol reductase Homo sapiens 415-419
16947022-7 2007 Interestingly, both T98G and U87MG cells showed more increase in apoptosis with expression of the HLA class II components for an effective immune response following treatment with ATRA plus IFN-gamma than with IFN-gamma alone. Tretinoin 180-184 interferon gamma Homo sapiens 210-219
17303670-9 2007 Similarly, treatment of postnatal d 3 rat gonocytes with RA induced a dose-dependent increase in V1-PDGFRbeta expression together with an increase in c-kit and Stra8, markers of more differentiated germ cells and a concomitant decrease in GFRalpha1, a marker of spermatogonial stem cells. Tretinoin 57-59 GDNF family receptor alpha 1 Rattus norvegicus 239-248
17393500-1 2007 UNLABELLED: The HCV nonstructural protein (NS)3/4A serine protease is not only involved in viral polyprotein processing but also efficiently blocks the retinoic-acid-inducible gen I and Toll-like receptor 3 signaling pathways and contributes to virus persistence by enabling HCV to escape the interferon antiviral response. Tretinoin 152-165 coagulation factor II, thrombin Homo sapiens 51-66
17387344-6 2007 Retinoic acid metabolism blocking agents induced cell differentiation as determined by increased expression of cytokeratin 8/18 and oestrogen receptor-alpha (ER-alpha). Tretinoin 0-13 estrogen receptor 1 Homo sapiens 158-166
17452250-9 2007 Furthermore, SEMA3B was upregulated in the SK-N-BE neuroblastoma cell line following induction of differentiation with retinoic acid. Tretinoin 119-132 semaphorin 3B Homo sapiens 13-19
17184834-0 2007 Retinol and retinoic acid bind human serum albumin: stability and structural features. Tretinoin 12-25 albumin Homo sapiens 37-50
17184834-4 2007 The aim of present study was to examine the interaction of retinol and retinoic acid with human serum albumin in aqueous solution at physiological conditions using constant protein concentration and various retinoid contents. Tretinoin 71-84 albumin Homo sapiens 96-109
17289015-7 2007 Each of these subtypes was detected in differentiated trophoblast stem cell cultures and can be differentially regulated; treatment with retinoic acid induces Pl1/Plf+ TGCs preferentially. Tretinoin 137-150 prolactin family 3, subfamily d, member 1 Mus musculus 159-162
17663352-5 2007 After treated with different concentrations of retinoic acid, ALP activity of PDLCs was increased than that of the control, and its mRNA signals were enhanced, especially in 5 x 10(-6) mol/L. Tretinoin 47-60 alkaline phosphatase, placental Homo sapiens 62-65
17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 mitogen-activated protein kinase 1 Homo sapiens 57-60
17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 AKT serine/threonine kinase 1 Homo sapiens 77-80
17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 BCL2 apoptosis regulator Homo sapiens 98-103
17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 BCL2 associated X, apoptosis regulator Homo sapiens 104-107
17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 tumor protein p53 Homo sapiens 142-145
17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 mitogen-activated protein kinase 1 Homo sapiens 166-169
17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 AKT serine/threonine kinase 1 Homo sapiens 174-177
17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 BCL2 apoptosis regulator Homo sapiens 289-294
17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 BCL2 associated X, apoptosis regulator Homo sapiens 295-298
17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 tumor protein p53 Homo sapiens 337-340
16920192-0 2007 Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome. Tretinoin 0-13 interferon gamma Homo sapiens 74-90
16920192-0 2007 Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome. Tretinoin 0-13 interleukin 1 beta Homo sapiens 91-108
17310502-7 2007 In keeping with these observations, VEGF expression was found in human neuroblastoma SH-SY5Y cells during differentiation after retinoic acid treatment. Tretinoin 128-141 vascular endothelial growth factor A Homo sapiens 36-40
17706063-0 2007 [Effect of external retinoic acid on Tbx1 gene during zebrafish embryogenesis]. Tretinoin 20-33 T-box transcription factor 1 Danio rerio 37-41
16920192-4 2007 In the present study, we found that RA treatment induces the expression of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in peripheral blast cells from APL patients. Tretinoin 36-38 interferon gamma Homo sapiens 75-91
16920192-4 2007 In the present study, we found that RA treatment induces the expression of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in peripheral blast cells from APL patients. Tretinoin 36-38 interferon gamma Homo sapiens 93-102
16920192-4 2007 In the present study, we found that RA treatment induces the expression of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in peripheral blast cells from APL patients. Tretinoin 36-38 interleukin 1 beta Homo sapiens 108-125
16920192-4 2007 In the present study, we found that RA treatment induces the expression of interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta) in peripheral blast cells from APL patients. Tretinoin 36-38 interleukin 1 beta Homo sapiens 127-135
17706063-5 2007 However, the interaction between RA and Tbx1 has not been fully investigated. Tretinoin 33-35 T-box transcription factor 1 Danio rerio 40-44
17706063-13 2007 RA treatment led to a distinct spatio-temporal expression pattern for Tbx1 from that in wild type embryo. Tretinoin 0-2 T-box transcription factor 1 Danio rerio 70-74
17706063-14 2007 The real-time PCR analysis showed that Tbx1 expression levels were markedly reduced by RA treatment. Tretinoin 87-89 T-box transcription factor 1 Danio rerio 39-43
17706063-16 2007 In contrast to 5 x 10(-8) mol/L RA-treated groups, 10(-7) mol/L RA caused a more severe effect on the Tbx1 expression level. Tretinoin 64-66 T-box transcription factor 1 Danio rerio 102-106
17706063-18 2007 RA could produce an altered Tbx1 expression pattern in zebrafish. Tretinoin 0-2 T-box transcription factor 1 Danio rerio 28-32
17706063-19 2007 RA may regulate the Tbx1 expression in a dose-dependant manner. Tretinoin 0-2 T-box transcription factor 1 Danio rerio 20-24
17706063-20 2007 RA could represent a major epigenetic factor to cause abnormal expression of Tbx1, secondarily, disrupt the pharyngeal arch and heart development. Tretinoin 0-2 T-box transcription factor 1 Danio rerio 77-81
17207476-0 2007 Role of retinoic acid during forebrain development begins late when Raldh3 generates retinoic acid in the ventral subventricular zone. Tretinoin 8-21 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 68-74
17244623-7 2007 Furthermore, BZLF1 expression in AGS cells is sufficient to activate DHRS9 gene expression and increases the ability of retinol to induce the RA-responsive gene, CYP26A1. Tretinoin 142-144 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 162-169
16824629-8 2007 Upon culture in a cell differentiation medium containing fetal bovine serum (1%) and retinoic acid (10 nM), both the activity and mRNA expression of ENT-1 increased 3-fold, however, ENT-2 was unaffected. Tretinoin 85-98 solute carrier family 29 member 1 Rattus norvegicus 149-154
16740359-2 2007 This study investigates the individual and combined effects of PML, when overexpressed by the recombinant PML adenovirus, and all-trans-retinoic acid on the proliferation of human estrogen-receptor negative SKBR-3 and estrogen-receptor positive MCF-7 breast cancer cell lines. Tretinoin 126-149 estrogen receptor 1 Homo sapiens 180-197
16740359-2 2007 This study investigates the individual and combined effects of PML, when overexpressed by the recombinant PML adenovirus, and all-trans-retinoic acid on the proliferation of human estrogen-receptor negative SKBR-3 and estrogen-receptor positive MCF-7 breast cancer cell lines. Tretinoin 126-149 estrogen receptor 1 Homo sapiens 218-235
16740359-5 2007 We concluded that PML and all-trans-retinoic acid cause cell death by different pathways: PML activates ERK1/2, p38 MAPK, and p21; arrests the cell cycle; and later causes cell death; and all-trans-retinoic acid activates proteasome function, caspase cleavage, and apoptosis. Tretinoin 26-49 mitogen-activated protein kinase 3 Homo sapiens 104-110
16740359-5 2007 We concluded that PML and all-trans-retinoic acid cause cell death by different pathways: PML activates ERK1/2, p38 MAPK, and p21; arrests the cell cycle; and later causes cell death; and all-trans-retinoic acid activates proteasome function, caspase cleavage, and apoptosis. Tretinoin 188-211 mitogen-activated protein kinase 3 Homo sapiens 104-110
17207476-0 2007 Role of retinoic acid during forebrain development begins late when Raldh3 generates retinoic acid in the ventral subventricular zone. Tretinoin 85-98 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 68-74
17207476-1 2007 Retinoic acid (RA) synthesized by Raldh3 in the frontonasal surface ectoderm of chick embryos has been suggested to function in early forebrain patterning by regulating Fgf8, Shh, and Meis2 expression. Tretinoin 0-13 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 34-40
17090780-0 2007 Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Tretinoin 80-93 stromal interaction molecule 1 Rattus norvegicus 14-19
17209049-2 2007 Cell extrinsic molecules that increase DARPP-32 mRNA and/or protein levels include brain-derived neurotrophic factor (BDNF), retinoic acid, and estrogen. Tretinoin 125-138 protein phosphatase 1 regulatory inhibitor subunit 1B Homo sapiens 39-47
17293044-4 2007 Treatment of the cells with all trans retinoic acid (RA) generates a neuron-like, morphological change of differentiation, and results in the activation of ERK and Akt pathways, an inhibition of the nuclear translocation of p53 induced by GA, and induces higher resistance to the GA-induced apoptosis. Tretinoin 38-51 mitogen-activated protein kinase 1 Homo sapiens 156-159
17293044-4 2007 Treatment of the cells with all trans retinoic acid (RA) generates a neuron-like, morphological change of differentiation, and results in the activation of ERK and Akt pathways, an inhibition of the nuclear translocation of p53 induced by GA, and induces higher resistance to the GA-induced apoptosis. Tretinoin 38-51 AKT serine/threonine kinase 1 Homo sapiens 164-167
17293044-4 2007 Treatment of the cells with all trans retinoic acid (RA) generates a neuron-like, morphological change of differentiation, and results in the activation of ERK and Akt pathways, an inhibition of the nuclear translocation of p53 induced by GA, and induces higher resistance to the GA-induced apoptosis. Tretinoin 38-51 tumor protein p53 Homo sapiens 224-227
17090780-5 2007 In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1. Tretinoin 92-94 stromal interaction molecule 1 Rattus norvegicus 106-111
17090780-11 2007 Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production. Tretinoin 54-56 stromal interaction molecule 1 Rattus norvegicus 18-23
17090780-12 2007 The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells. Tretinoin 53-55 stromal interaction molecule 1 Rattus norvegicus 175-180
17235257-0 2007 Role of interleukin-8 and growth-regulated oncogene-alpha in the chemotactic migration of all-trans retinoic acid-treated promyelocytic leukemic cells toward alveolar epithelial cells. Tretinoin 100-113 C-X-C motif chemokine ligand 8 Homo sapiens 8-21
17491551-1 2007 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RARalpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as ligand-activated, DNA-binding, transacting, transcription-modulating proteins involved in a general molecular mechanism responsible for transcriptional responses in target genes. Tretinoin 57-70 retinoic acid receptor beta Homo sapiens 178-185
17235257-15 2007 CONCLUSIONS: IL-8 and GRO-alpha secreted from alveolar epithelial cells play an important role in the cell-cell interaction involved in the chemotactic transmigration of ATRA-treated APL cells toward alveolar epithelial cells. Tretinoin 170-174 C-X-C motif chemokine ligand 8 Homo sapiens 13-17
17235257-2 2007 We investigated the role of interleukin (IL)-8 and growth-regulated oncogene (GRO)-alpha in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4) APL cells toward A549 alveolar epithelial cells. Tretinoin 126-130 C-X-C motif chemokine ligand 8 Homo sapiens 28-46
17235257-10 2007 Only A549 cells constitutively secreted GRO-alpha, and both A549 and NB4 cells constitutively secreted IL-8, which was enhanced by ATRA. Tretinoin 131-135 C-X-C motif chemokine ligand 8 Homo sapiens 103-107
16713227-6 2007 PPARalpha binding to the upstream retinoic acid response element is decreased in the vitamin A-deficient liver, when compared to the vitamin A-sufficient state. Tretinoin 34-47 peroxisome proliferator activated receptor alpha Mus musculus 0-9
17170094-9 2007 The ATRA-induced tube formation was completely abolished by coincubation with vascular endothelial growth factor (VEGF) neutralizing antibody or with VEGF receptor (VEGFR)-2 (KDR) neutralizing antibody, but not VEGFR-1 (Flt-1) neutralizing antibody. Tretinoin 4-8 vascular endothelial growth factor A Homo sapiens 78-112
17170094-9 2007 The ATRA-induced tube formation was completely abolished by coincubation with vascular endothelial growth factor (VEGF) neutralizing antibody or with VEGF receptor (VEGFR)-2 (KDR) neutralizing antibody, but not VEGFR-1 (Flt-1) neutralizing antibody. Tretinoin 4-8 vascular endothelial growth factor A Homo sapiens 114-118
17170094-9 2007 The ATRA-induced tube formation was completely abolished by coincubation with vascular endothelial growth factor (VEGF) neutralizing antibody or with VEGF receptor (VEGFR)-2 (KDR) neutralizing antibody, but not VEGFR-1 (Flt-1) neutralizing antibody. Tretinoin 4-8 fms related receptor tyrosine kinase 1 Homo sapiens 220-225
17039240-8 2007 In contrast, the steroid dexamethasone and all-trans retinoic acid slightly stimulated rip4 expression. Tretinoin 43-66 receptor interacting serine/threonine kinase 4 Homo sapiens 87-91
17170094-10 2007 ATRA and Am80 induced VEGF secretion in the coculture as well as VEGF secretion/mRNA expression in NHDFs. Tretinoin 0-4 vascular endothelial growth factor A Homo sapiens 22-26
17170094-11 2007 Transcription activity of human VEGF gene promoter in NHDFs was stimulated by ATRA, which was augmented by RAR overexpression. Tretinoin 78-82 vascular endothelial growth factor A Homo sapiens 32-36
17170094-14 2007 Taken together, ATRA may have induced angiogenesis via RAR mainly by stimulation of HUVEC proliferation and enhancement of endogenous VEGF signaling and in part by induction of hepatocyte growth factor and angiopoietin-2 production. Tretinoin 16-20 vascular endothelial growth factor A Homo sapiens 134-138
17339181-7 2007 Here we compared the effects of ATRA and arsenic on PML/RARalpha-positive stem cell compartments. Tretinoin 32-36 promyelocytic leukemia Mus musculus 52-55
17253143-0 2007 Retinoic acid enhances the production of IL-10 while reducing the synthesis of IL-12 and TNF-alpha from LPS-stimulated monocytes/macrophages. Tretinoin 0-13 tumor necrosis factor Homo sapiens 89-98
17253143-5 2007 The effects of atRA on LPS-induced mRNA expression of IL-10, IL-12p40, TNF-alpha, IL-18, and TGF-beta in the THP-1 monocyte/macrophage cell line and in cord blood mononuclear cells were measured by competitive RT-PCR. Tretinoin 15-19 GLI family zinc finger 2 Homo sapiens 109-114
17253143-7 2007 The addition of atRA to cell cultures potentiated the LPS-induced IL-10 mRNA expression and the number of IL-10 secreting cells from THP-1 cells and cord blood mononuclear cells. Tretinoin 16-20 GLI family zinc finger 2 Homo sapiens 133-138
17253143-8 2007 In contrast, the addition of atRA inhibited the LPS-induced TNF-alpha and IL-12p40 mRNA expression, and the number of ELISPOT positive cells for TNF-alpha. Tretinoin 29-33 tumor necrosis factor Homo sapiens 60-69
17253143-8 2007 In contrast, the addition of atRA inhibited the LPS-induced TNF-alpha and IL-12p40 mRNA expression, and the number of ELISPOT positive cells for TNF-alpha. Tretinoin 29-33 tumor necrosis factor Homo sapiens 145-154
17253143-11 2007 While atRA downregulated the proinflammatory cytokines, e.g., IL-12 and TNF-alpha, the production of an immune modulating cytokine, IL-10 was enhanced by atRA. Tretinoin 6-10 tumor necrosis factor Homo sapiens 72-81
17332617-2 2007 We investigated the effect of retinoic acid on adenovirus-mediated expression of the human NIS gene in the MCF-7 breast cancer cell line. Tretinoin 30-43 solute carrier family 5 member 5 Homo sapiens 91-94
17332617-6 2007 After incubation with 10(-6) mol/L ATRA, the mRNA level in Rad-NIS-infected MCF-7 cells increased to 118.5 times that of wild-type MCF-7 cells, whereas the mRNA level in wild-type MCF-7 cells showed only a 2.1-fold increase. Tretinoin 35-39 solute carrier family 5 member 5 Homo sapiens 63-66
17332617-7 2007 Western blot, immunocytochemical staining, and flow cytometry analyses showed that NIS protein expression in MCF-7 cells infected with Rad-NIS increased after ATRA treatment. Tretinoin 159-163 solute carrier family 5 member 5 Homo sapiens 83-86
17332617-7 2007 Western blot, immunocytochemical staining, and flow cytometry analyses showed that NIS protein expression in MCF-7 cells infected with Rad-NIS increased after ATRA treatment. Tretinoin 159-163 solute carrier family 5 member 5 Homo sapiens 139-142
17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 87-100 estrogen receptor 1 Homo sapiens 152-175
17332617-11 2007 Treatment of Rad-NIS-infected cells with 10(-8), 10(-7), and 10(-6) mol/L ATRA increased (125)I uptake by 4.9-, 8.2-, and 27.6-fold, respectively, compared with wild-type MCF-7 cells. Tretinoin 74-78 solute carrier family 5 member 5 Homo sapiens 17-20
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 86-90 solute carrier family 5 member 5 Homo sapiens 13-16
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 86-90 solute carrier family 5 member 5 Homo sapiens 35-38
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 86-90 solute carrier family 5 member 5 Homo sapiens 35-38
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 188-192 solute carrier family 5 member 5 Homo sapiens 13-16
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 188-192 solute carrier family 5 member 5 Homo sapiens 35-38
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 188-192 solute carrier family 5 member 5 Homo sapiens 35-38
17332617-13 2007 CONCLUSION: Retinoic acid increases adenovirus-mediated NIS expression in MCF-7 cells. Tretinoin 12-25 solute carrier family 5 member 5 Homo sapiens 56-59
17332617-14 2007 Our results indicate that improved efficiency of NIS gene therapy or reporter imaging in breast cancer may be possible with retinoic acid treatment. Tretinoin 124-137 solute carrier family 5 member 5 Homo sapiens 49-52
17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 87-100 estrogen receptor 1 Homo sapiens 177-184
17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 102-104 estrogen receptor 1 Homo sapiens 152-175
17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 102-104 estrogen receptor 1 Homo sapiens 177-184
17460545-0 2007 The discovery of new coding alleles of human CYP26A1 that are potentially defective in the metabolism of all-trans retinoic acid and their assessment in a recombinant cDNA expression system. Tretinoin 115-128 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 45-52
17460545-3 2007 We sequenced CYP26A1 in racially diverse individuals and assessed the metabolism of retinoic acid by newly identified coding alleles of CYP26A1 in a recombinant system. Tretinoin 84-97 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 136-143
17460545-10 2007 Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites. Tretinoin 42-61 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 10-17
17460545-10 2007 Wild type CYP26A1 protein metabolized all-trans-retinoic acid (at-RA) to 4-oxo-RA, 4-OH-RA as well as water-soluble metabolites. Tretinoin 63-68 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 10-17
17343783-0 2007 [Experimental study of IFN-alpha and IFN-gamma on reversing ATRA-resistance in MR2 cell line]. Tretinoin 60-64 interferon alpha 1 Homo sapiens 23-32
17124010-6 2007 Embryonal carcinoma cells treated with retinoic acid undergo differentiation and lose the TRA-1-60/TRA-1-81 markers from their plasma membrane surface. Tretinoin 39-52 transformation/transcription domain associated protein Homo sapiens 90-95
17124010-6 2007 Embryonal carcinoma cells treated with retinoic acid undergo differentiation and lose the TRA-1-60/TRA-1-81 markers from their plasma membrane surface. Tretinoin 39-52 transformation/transcription domain associated protein Homo sapiens 99-104
17124010-7 2007 We show that podocalyxin is modified in the retinoic acid-treated cells and has an apparent molecular mass of 170 kDa on protein blots as compared with the apparent 200-kDa molecular weight form of podocalyxin expressed in untreated cells. Tretinoin 44-57 podocalyxin like Homo sapiens 13-24
17343783-0 2007 [Experimental study of IFN-alpha and IFN-gamma on reversing ATRA-resistance in MR2 cell line]. Tretinoin 60-64 interferon gamma Homo sapiens 37-46
17343783-1 2007 AIM: To explore the possibility and the possible mechanism of reversing ATRA-resistance in MR2 cells by using IFN-alpha and IFN-gamma in combination with all-trans retinoic acid (ATRA). Tretinoin 72-76 interferon alpha 1 Homo sapiens 110-119
17343783-5 2007 The effects were more obviously in both IFN-alpha+ATRA group and IFN-gamma+ATRA group. Tretinoin 75-79 interferon gamma Homo sapiens 65-74
17343783-1 2007 AIM: To explore the possibility and the possible mechanism of reversing ATRA-resistance in MR2 cells by using IFN-alpha and IFN-gamma in combination with all-trans retinoic acid (ATRA). Tretinoin 72-76 interferon gamma Homo sapiens 124-133
17031849-2 2007 In the present study, we report that ATRA-induced apoptosis in GnT-V-AS/7721 cells is mediated through ER stress. Tretinoin 37-41 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 63-68
17031849-0 2007 Apoptosis induced by all-trans retinoic acid in N-acetylglucosaminyltransferase V repressed human hepatocarcinoma cells is mediated through endoplasmic reticulum stress. Tretinoin 21-44 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 48-81
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 43-48
17031849-1 2007 We previously demonstrated that endoplasmic reticulum (ER) stress was triggered in human hepatocarcinoma 7721 cells transfected with antisense cDNA of N-acetylglucosaminyltransferase V (GnT-V-AS/7721) which were more susceptible to apoptosis induced by all-trans retinoic acid (ATRA). Tretinoin 263-276 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 151-184
17031849-1 2007 We previously demonstrated that endoplasmic reticulum (ER) stress was triggered in human hepatocarcinoma 7721 cells transfected with antisense cDNA of N-acetylglucosaminyltransferase V (GnT-V-AS/7721) which were more susceptible to apoptosis induced by all-trans retinoic acid (ATRA). Tretinoin 263-276 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 186-191
17031849-1 2007 We previously demonstrated that endoplasmic reticulum (ER) stress was triggered in human hepatocarcinoma 7721 cells transfected with antisense cDNA of N-acetylglucosaminyltransferase V (GnT-V-AS/7721) which were more susceptible to apoptosis induced by all-trans retinoic acid (ATRA). Tretinoin 278-282 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 151-184
17031849-1 2007 We previously demonstrated that endoplasmic reticulum (ER) stress was triggered in human hepatocarcinoma 7721 cells transfected with antisense cDNA of N-acetylglucosaminyltransferase V (GnT-V-AS/7721) which were more susceptible to apoptosis induced by all-trans retinoic acid (ATRA). Tretinoin 278-282 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 186-191
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 heat shock protein family A (Hsp70) member 5 Homo sapiens 141-146
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 heat shock protein family A (Hsp70) member 5 Homo sapiens 147-150
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 DNA damage inducible transcript 3 Homo sapiens 152-179
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 DNA damage inducible transcript 3 Homo sapiens 181-185
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 DNA damage inducible transcript 3 Homo sapiens 201-208
17031849-4 2007 Additionally, activation of caspase-12, caspase-9, and -3 was detected, and apoptosis morphology was observed in GnT-V-AS/7721 cells with ATRA treatment. Tretinoin 138-142 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 113-118
17031849-5 2007 These results suggest that ATRA enhances the ER stress triggered in GnT-V-AS/7721 cells, which represents a novel mechanism of ATRA to induce apoptosis. Tretinoin 27-31 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 68-73
17031849-5 2007 These results suggest that ATRA enhances the ER stress triggered in GnT-V-AS/7721 cells, which represents a novel mechanism of ATRA to induce apoptosis. Tretinoin 127-131 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 68-73
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 140-144 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 25-30
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 140-144 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 105-110
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 140-144 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 105-110
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 140-144 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 105-110
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 204-208 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 25-30
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 204-208 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 105-110
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 204-208 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 105-110
17031849-6 2007 We further observed that GnT-V was significantly repressed and the structure of N-glycans was changed in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, suggesting that repression of GnT-V by ATRA causes the enhanced ER stress and ER stress-mediated apoptosis in GnT-V-AS/7721 cells. Tretinoin 204-208 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 105-110
17101211-8 2007 In vitro, thyroid cancer cell lines responded to RA with reduced proliferation, ranging from 26 to 34% after 2 weeks of treatment and with up to 80% reduced secretion of VEGF. Tretinoin 49-51 vascular endothelial growth factor A Homo sapiens 170-174
17239557-6 2007 It is presumed that these cells release RA in a paracrine fashion in the region of the wound; however, the RALDH2/NG2-immunoreactive cells expressed the retinoid receptors RARalpha, RARbeta, RXRalpha and RXRbeta, suggesting that RA also serves an autocrine function. Tretinoin 107-109 chondroitin sulfate proteoglycan 4 Homo sapiens 114-117
17239557-6 2007 It is presumed that these cells release RA in a paracrine fashion in the region of the wound; however, the RALDH2/NG2-immunoreactive cells expressed the retinoid receptors RARalpha, RARbeta, RXRalpha and RXRbeta, suggesting that RA also serves an autocrine function. Tretinoin 107-109 retinoic acid receptor beta Homo sapiens 182-189
17242174-7 2007 The CACCC element has also been shown to be important for induction of the IGFBP5 promoter by retinoic acid (RA) and progesterone (Pg). Tretinoin 94-107 insulin like growth factor binding protein 5 Homo sapiens 75-81
17242174-7 2007 The CACCC element has also been shown to be important for induction of the IGFBP5 promoter by retinoic acid (RA) and progesterone (Pg). Tretinoin 109-111 insulin like growth factor binding protein 5 Homo sapiens 75-81
17242174-9 2007 On the other hand, we show that induction of the promoter by RA depends on co-expressed MN1 in Hep3B cells. Tretinoin 61-63 MN1 proto-oncogene, transcriptional regulator Homo sapiens 88-91
16752155-3 2007 RA treatment resulted in an increase of p21, p27 and p53 protein levels and G1 arrest in UM cells, which correlated with significant down-modulation of surface Her2/neu proto-oncogene expression. Tretinoin 0-2 tumor protein p53 Homo sapiens 53-56
16752155-3 2007 RA treatment resulted in an increase of p21, p27 and p53 protein levels and G1 arrest in UM cells, which correlated with significant down-modulation of surface Her2/neu proto-oncogene expression. Tretinoin 0-2 erb-b2 receptor tyrosine kinase 2 Homo sapiens 160-168
17261132-1 2007 OBJECTIVE: To determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and vascular endothelial growth factor (VEGF) expression in the human gastric cancer cell line BGC-823 in vitro. Tretinoin 50-73 vascular endothelial growth factor A Homo sapiens 112-146
17261132-1 2007 OBJECTIVE: To determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and vascular endothelial growth factor (VEGF) expression in the human gastric cancer cell line BGC-823 in vitro. Tretinoin 75-79 vascular endothelial growth factor A Homo sapiens 112-146
17261132-8 2007 CONCLUSION: The anti-tumor effects of ATRA on human gastric cancer cells are associated with G0/G1 phase arrest and decreased VEGF expression. Tretinoin 38-42 vascular endothelial growth factor A Homo sapiens 126-130
17393088-1 2007 Restin, belonging to the melanoma-associated antigen superfamily, was firstly cloned from the differentiated HL-60 cells when induced by all-trans retinoic acid (ATRA) in our lab. Tretinoin 147-160 MAGE family member H1 Homo sapiens 0-6
17393088-1 2007 Restin, belonging to the melanoma-associated antigen superfamily, was firstly cloned from the differentiated HL-60 cells when induced by all-trans retinoic acid (ATRA) in our lab. Tretinoin 162-166 MAGE family member H1 Homo sapiens 0-6
17184907-3 2007 Several peptides including D22, PGC1alpha, SRC3-2, PRIP/RAP250 and SRC1-4 also formed a complex with RXRbeta LBD in the presence of all-trans retinoic acid (at-RA) and the fatty acids, phytanic acid (PA) and docosahexaenoic acid (DHA). Tretinoin 142-155 PPARG coactivator 1 alpha Homo sapiens 32-41
17184907-3 2007 Several peptides including D22, PGC1alpha, SRC3-2, PRIP/RAP250 and SRC1-4 also formed a complex with RXRbeta LBD in the presence of all-trans retinoic acid (at-RA) and the fatty acids, phytanic acid (PA) and docosahexaenoic acid (DHA). Tretinoin 142-155 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 67-73
17101211-14 2007 It demonstrates a decrease of in vitro VEGF accumulation and reduction of VSD in experimental undifferentiated thyroid carcinoma, suggesting that reduced angiogenesis may be an important mechanism responsible for the therapeutic effect of RA in thyroid cancer. Tretinoin 239-241 vascular endothelial growth factor A Homo sapiens 39-43
16968895-7 2007 Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3. Tretinoin 63-76 aquaporin 9 Homo sapiens 97-101
16968895-7 2007 Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3. Tretinoin 78-82 aquaporin 9 Homo sapiens 97-101
16968895-7 2007 Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3. Tretinoin 254-258 aquaporin 9 Homo sapiens 97-101
17098229-4 2007 The negative growth factor-transforming growth factor beta (TGFbeta) was secreted by RA and/or tamoxifen treatment and was studies as a potential mediator of the synergistic effects of RA and tamoxifen in apoptosis. Tretinoin 185-187 transforming growth factor beta 1 Homo sapiens 60-67
17234770-5 2007 Expression array analyses revealed that RA induces the expression of several genes involved in cell cycle regulation, including the p53-controlled antiproliferative gene B-cell translocation gene, member 2 (Btg2) and the BTG family member Tob1. Tretinoin 40-42 tumor protein p53 Homo sapiens 132-135
17107666-6 2007 Our results demonstrated that ATRA suppressed NF-kappaB activity and prevented IkappaBalpha degradation in a dose-dependent way, inhibited IFN-gamma production and gene expression of granzyme B and NKp46. Tretinoin 30-34 nuclear factor kappa B subunit 1 Homo sapiens 46-55
17098223-10 2007 Strikingly, expression of the RA-degrading enzyme cyp26a1 in the tailbud was controlled by Su(H) activity, and morpholino knockdown of cyp26a1 alone caused asymmetric cyclic dlc expression, suggesting that excess RA in the tailbud may contribute to the cyclic asymmetries. Tretinoin 30-32 recombination signal binding protein for immunoglobulin kappa J region a Danio rerio 91-96
17098223-12 2007 Our observations indicate that one element of the Notch signalling pathway, Su(H), is required for control of RA metabolism in the tailbud and that this regulation is involved in bilateral symmetry of cyclic gene expression and somitogenesis. Tretinoin 110-112 recombination signal binding protein for immunoglobulin kappa J region a Danio rerio 76-81
17098229-4 2007 The negative growth factor-transforming growth factor beta (TGFbeta) was secreted by RA and/or tamoxifen treatment and was studies as a potential mediator of the synergistic effects of RA and tamoxifen in apoptosis. Tretinoin 85-87 transforming growth factor beta 1 Homo sapiens 60-67
17134824-12 2007 IL-6 was down-regulated in all three cell lines by all-trans-retinoic acid treatment. Tretinoin 61-74 interleukin 6 Homo sapiens 0-4
17107666-6 2007 Our results demonstrated that ATRA suppressed NF-kappaB activity and prevented IkappaBalpha degradation in a dose-dependent way, inhibited IFN-gamma production and gene expression of granzyme B and NKp46. Tretinoin 30-34 NFKB inhibitor alpha Homo sapiens 79-91
17107666-6 2007 Our results demonstrated that ATRA suppressed NF-kappaB activity and prevented IkappaBalpha degradation in a dose-dependent way, inhibited IFN-gamma production and gene expression of granzyme B and NKp46. Tretinoin 30-34 interferon gamma Homo sapiens 139-148
17204142-0 2007 All-trans retinoic acid induces COX-2 and prostaglandin E2 synthesis in SH-SY5Y human neuroblastoma cells: involvement of retinoic acid receptors and extracellular-regulated kinase 1/2. Tretinoin 10-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 32-37
17204142-3 2007 Since ATRA also up-regulated COX-2 expression in SH-SY5Y human neuroblastoma cells, the current study was undertaken to analyze in these cells the mechanism through which ATRA increases COX activity. Tretinoin 6-10 mitochondrially encoded cytochrome c oxidase II Homo sapiens 29-34
17204142-10 2007 RESULTS: ATRA induced a significant increase of COX-2 expression in a dose- and time-dependent manner in SH-SY5Y human neuroblastoma cells, while COX-1 expression remained unchanged. Tretinoin 9-13 mitochondrially encoded cytochrome c oxidase II Homo sapiens 48-53
17204142-15 2007 Pre-incubation of SH-SY5Y human neuroblastoma cells with either RAR-pan-antagonist LE540 or MAP kinase kinase 1 (MEK-1) inhibitor PD98059 resulted in the abolition of ATRA-induced COX-2 promoter activity, COX-2 protein expression and PGE2 production whereas the retinoid X receptor pan-antagonist HX531, the p38 MAPK inhibitor SB203580 or the c-Jun kinase inhibitor SP600125 did not have any effect. Tretinoin 167-171 mitochondrially encoded cytochrome c oxidase II Homo sapiens 180-185
17204142-15 2007 Pre-incubation of SH-SY5Y human neuroblastoma cells with either RAR-pan-antagonist LE540 or MAP kinase kinase 1 (MEK-1) inhibitor PD98059 resulted in the abolition of ATRA-induced COX-2 promoter activity, COX-2 protein expression and PGE2 production whereas the retinoid X receptor pan-antagonist HX531, the p38 MAPK inhibitor SB203580 or the c-Jun kinase inhibitor SP600125 did not have any effect. Tretinoin 167-171 mitochondrially encoded cytochrome c oxidase II Homo sapiens 205-210
17204142-17 2007 CONCLUSION: These results highlight the importance of RAR-dependent and kinase-dependent mechanisms for ATRA-induced COX-2 expression and activity. Tretinoin 104-108 mitochondrially encoded cytochrome c oxidase II Homo sapiens 117-122
17217039-10 2007 The activation of both pathways of transcriptional regulation by the myeloid lineage-specific transcription factor C/EBPalpha (CCAAT/enhancer-binding protein-alpha), and posttranscriptional regulation by miR-223 appears essential for granulocytic differentiation and clinical response of acute promyelocytic leukemia (APL) blasts to all-trans retinoic acid (ATRA). Tretinoin 343-356 CCAAT enhancer binding protein alpha Homo sapiens 115-125
17546709-0 2007 Atom-transfer radical addition (ATRA) and cyclization (ATRC) reactions catalyzed by a mixture of [RuCl(2)Cp*(PPh3)] and Magnesium. Tretinoin 32-36 caveolin 1 Homo sapiens 109-113
17506718-6 2007 TGFbeta was depressed at 28 days by MCT, an effect reversed by a combination of captopril and RA. Tretinoin 94-96 transforming growth factor, beta 1 Rattus norvegicus 0-7
16935849-0 2007 All trans-retinoic acid induces apoptosis via p38 and caspase pathways in metaplastic Barrett"s cells. Tretinoin 4-23 mitogen-activated protein kinase 14 Homo sapiens 46-49
16935849-6 2007 ATRA induced apoptosis and increased the expression of p53 protein in a dose-dependent fashion. Tretinoin 0-4 tumor protein p53 Homo sapiens 55-58
16935849-7 2007 The apoptotic effect of ATRA was abolished by treatment with inhibitors of both p38 and caspase, but not by p53 interfering RNA (RNAi). Tretinoin 24-28 mitogen-activated protein kinase 14 Homo sapiens 80-83
16935849-8 2007 Inhibition of p38 also prevented expression of cleaved caspase-3, suggesting that ATRA activates p38 upstream of the caspase cascade. Tretinoin 82-86 mitogen-activated protein kinase 14 Homo sapiens 14-17
16935849-8 2007 Inhibition of p38 also prevented expression of cleaved caspase-3, suggesting that ATRA activates p38 upstream of the caspase cascade. Tretinoin 82-86 mitogen-activated protein kinase 14 Homo sapiens 97-100
16935849-10 2007 ATRA induces apoptosis in Barrett"s epithelial cells and sensitizes them to apoptosis induced by UV-B irradiation via activation of p38 and the caspase cascade, but not through p53. Tretinoin 0-4 mitogen-activated protein kinase 14 Homo sapiens 132-135
17217039-10 2007 The activation of both pathways of transcriptional regulation by the myeloid lineage-specific transcription factor C/EBPalpha (CCAAT/enhancer-binding protein-alpha), and posttranscriptional regulation by miR-223 appears essential for granulocytic differentiation and clinical response of acute promyelocytic leukemia (APL) blasts to all-trans retinoic acid (ATRA). Tretinoin 358-362 CCAAT enhancer binding protein alpha Homo sapiens 115-125
17976305-4 2007 Here we demonstrate that pro-neural effects of LIF and partially also of retinoic acid are abolished by inhibition of the JAK2->STAT3 signalling pathway. Tretinoin 73-86 signal transducer and activator of transcription 3 Mus musculus 131-136
17164423-0 2007 Cyp26 enzymes generate the retinoic acid response pattern necessary for hindbrain development. Tretinoin 27-40 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
17164423-4 2007 Here, we show that the cytochrome p450 enzymes of the Cyp26 class, which metabolize RA into polar derivatives, function redundantly to shape RA-dependent gene-expression domains during hindbrain development. Tretinoin 84-86 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 54-59
17164423-4 2007 Here, we show that the cytochrome p450 enzymes of the Cyp26 class, which metabolize RA into polar derivatives, function redundantly to shape RA-dependent gene-expression domains during hindbrain development. Tretinoin 141-143 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 54-59
17164423-5 2007 In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain. Tretinoin 143-145 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 70-75
17164423-5 2007 In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain. Tretinoin 143-145 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 82-89
17164423-5 2007 In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain. Tretinoin 143-145 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 91-98
17164423-6 2007 Furthermore, we show that Cyp26 enzymes are essential for exogenous RA to rescue hindbrain patterning in RA-depleted embryos. Tretinoin 68-70 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-31
17164423-6 2007 Furthermore, we show that Cyp26 enzymes are essential for exogenous RA to rescue hindbrain patterning in RA-depleted embryos. Tretinoin 105-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 26-31
17124510-4 2007 Furthermore, in the absence of RA signalling, normal asymmetric Snail1 expression in the lateral mesoderm is extended to the PSM, desynchronizing somitogenesis. Tretinoin 31-33 snail family transcriptional repressor 1 Homo sapiens 64-70
17124510-5 2007 Thus, Snail1 is the first cue corrected by RA in the PSM to ensure synchronized bilateral segmentation. Tretinoin 43-45 snail family transcriptional repressor 1 Homo sapiens 6-12
17976305-6 2007 These results suggest that in neurogenic regions, cooperative action of LIF and other neuro-differentiation-inducing factors, such as retinoic acid, may be mediated by the STAT3 signalling pathway. Tretinoin 134-147 signal transducer and activator of transcription 3 Mus musculus 172-177
17433757-5 2007 Lastly, its involvement in a retinoic acid-induced tumor-specific apoptosis program mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Tretinoin 29-42 TNF superfamily member 10 Homo sapiens 96-151
17433757-5 2007 Lastly, its involvement in a retinoic acid-induced tumor-specific apoptosis program mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Tretinoin 29-42 TNF superfamily member 10 Homo sapiens 153-158
17182884-10 2007 Furthermore, both atRA and forskolin suppressed HIV-induced mitogen-activated protein kinase 1 and 2 and Stat3 phosphorylation. Tretinoin 18-22 mitogen-activated protein kinase 1 Homo sapiens 60-100
17182884-10 2007 Furthermore, both atRA and forskolin suppressed HIV-induced mitogen-activated protein kinase 1 and 2 and Stat3 phosphorylation. Tretinoin 18-22 signal transducer and activator of transcription 3 Homo sapiens 105-110
17064353-0 2007 Expression of the Wnt inhibitor Dickkopf-1 is required for the induction of neural markers in mouse embryonic stem cells differentiating in response to retinoic acid. Tretinoin 152-165 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 32-42
17035595-6 2007 This RA-mediated enhancement of barrier function is potentially associated with the increased expression of TJ-associated genes such as occludin, claudin-1, claudin-4, and zonula occludens-1. Tretinoin 5-7 occludin Mus musculus 136-144
17035595-6 2007 This RA-mediated enhancement of barrier function is potentially associated with the increased expression of TJ-associated genes such as occludin, claudin-1, claudin-4, and zonula occludens-1. Tretinoin 5-7 claudin 4 Mus musculus 157-166
17064353-2 2007 A 4-day treatment with retinoic acid (RA), which promoted neural differentiation of EBs, substantially increased the expression of the Wnt antagonist Dkk-1, and induced the synthesis of the Wnt/Dkk-1 co-receptor LRP6. Tretinoin 23-36 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 150-155
17064353-2 2007 A 4-day treatment with retinoic acid (RA), which promoted neural differentiation of EBs, substantially increased the expression of the Wnt antagonist Dkk-1, and induced the synthesis of the Wnt/Dkk-1 co-receptor LRP6. Tretinoin 23-36 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 194-199
17064353-2 2007 A 4-day treatment with retinoic acid (RA), which promoted neural differentiation of EBs, substantially increased the expression of the Wnt antagonist Dkk-1, and induced the synthesis of the Wnt/Dkk-1 co-receptor LRP6. Tretinoin 38-40 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 150-155
17064353-2 2007 A 4-day treatment with retinoic acid (RA), which promoted neural differentiation of EBs, substantially increased the expression of the Wnt antagonist Dkk-1, and induced the synthesis of the Wnt/Dkk-1 co-receptor LRP6. Tretinoin 38-40 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 194-199
17064353-3 2007 Recombinant Dkk-1 applied to EBs behaved like RA in inducing the expression of the neural markers nestin and distal-less homeobox gene (Dlx-2). Tretinoin 46-48 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 12-17
17064353-5 2007 Remarkably, the antisense- or small interfering RNA-induced knockdown of Dkk-1 largely reduced the expression of Dlx-2, and the neuronal marker beta-III tubulin in EBs exposed to RA. Tretinoin 179-181 dickkopf WNT signaling pathway inhibitor 1 Mus musculus 73-78
17158062-3 2007 In the Pax6-deficient cortex the expression levels of various transcription factors involved in neurogenesis (like Satb2, Nfia, AP-2gamma, NeuroD6, Ngn2, Tbr2, Bhlhb5) and the retinoic acid signalling molecule Rlbp1 were reduced. Tretinoin 176-189 paired box 6 Mus musculus 7-11
17546008-3 2007 Treatment with retinoic acid causes these ES cells to essentially become neural progenitors with the characteristics of Pax6-positive radial glial cells. Tretinoin 15-28 paired box 6 Mus musculus 120-124
17259349-3 2007 Expression of PDCD4 was markedly up-regulated during all-trans retinoic acid (ATRA)-induced granulocytic differentiation in NB4 and HL60 AML cell lines and in primary human promyelocytic leukemia (AML-M3) and CD34(+) hematopoietic progenitor cells but not in differentiation-resistant NB4.R1 and HL60R cells. Tretinoin 78-82 CD34 molecule Homo sapiens 209-213
17023731-8 2006 In vitro studies disclosed that the administration of ATRA reduced (1) irradiation-induced production of IL-6, TGF-beta(1), and collagen from IMR90 cells, and (2) IL-6-dependent proliferation and TGF-beta(1)-dependent transdifferentiation of the cells, which could be the mechanism underlying the preventive effect of ATRA on lung fibrosis. Tretinoin 54-58 interleukin 6 Homo sapiens 105-109
17337438-4 2007 During retinoic-acid-induced P19 stem cell differentiation, the expression of CoAA undergoes a rapid switch to its dominant negative splice variant CoAM in the cavity of the embryoid body. Tretinoin 7-20 RNA binding motif protein 14 Homo sapiens 78-82
17159378-1 2007 All-trans retinoic acid (ATRA) increases the expression of COX-1 and COX-2 and the production of PGE2, a prostaglandin with anti-inflammatory effects in human mesangial cells (MC). Tretinoin 0-23 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74
17159378-1 2007 All-trans retinoic acid (ATRA) increases the expression of COX-1 and COX-2 and the production of PGE2, a prostaglandin with anti-inflammatory effects in human mesangial cells (MC). Tretinoin 25-29 mitochondrially encoded cytochrome c oxidase II Homo sapiens 69-74
17023731-4 2006 OBJECTIVES: Previously, we reported that all-trans-retinoic acid (ATRA) reduced both irradiation-induced interleukin (IL)-6 production in lung fibroblasts and IL-6-dependent cell growth, and also directly inhibited the proliferation of lung fibroblasts after irradiation. Tretinoin 41-64 interleukin 6 Mus musculus 105-123
17023731-4 2006 OBJECTIVES: Previously, we reported that all-trans-retinoic acid (ATRA) reduced both irradiation-induced interleukin (IL)-6 production in lung fibroblasts and IL-6-dependent cell growth, and also directly inhibited the proliferation of lung fibroblasts after irradiation. Tretinoin 41-64 interleukin 6 Mus musculus 159-163
17023731-4 2006 OBJECTIVES: Previously, we reported that all-trans-retinoic acid (ATRA) reduced both irradiation-induced interleukin (IL)-6 production in lung fibroblasts and IL-6-dependent cell growth, and also directly inhibited the proliferation of lung fibroblasts after irradiation. Tretinoin 66-70 interleukin 6 Mus musculus 105-123
17023731-4 2006 OBJECTIVES: Previously, we reported that all-trans-retinoic acid (ATRA) reduced both irradiation-induced interleukin (IL)-6 production in lung fibroblasts and IL-6-dependent cell growth, and also directly inhibited the proliferation of lung fibroblasts after irradiation. Tretinoin 66-70 interleukin 6 Mus musculus 159-163
17069763-0 2006 Bidirectional CLOCK/BMAL1-dependent circadian gene regulation by retinoic acid in vitro. Tretinoin 65-78 circadian locomotor output cycles kaput Mus musculus 14-19
17023731-8 2006 In vitro studies disclosed that the administration of ATRA reduced (1) irradiation-induced production of IL-6, TGF-beta(1), and collagen from IMR90 cells, and (2) IL-6-dependent proliferation and TGF-beta(1)-dependent transdifferentiation of the cells, which could be the mechanism underlying the preventive effect of ATRA on lung fibrosis. Tretinoin 54-58 interleukin 6 Homo sapiens 163-167
17023731-8 2006 In vitro studies disclosed that the administration of ATRA reduced (1) irradiation-induced production of IL-6, TGF-beta(1), and collagen from IMR90 cells, and (2) IL-6-dependent proliferation and TGF-beta(1)-dependent transdifferentiation of the cells, which could be the mechanism underlying the preventive effect of ATRA on lung fibrosis. Tretinoin 318-322 interleukin 6 Homo sapiens 163-167
17166369-10 2006 CONCLUSIONS: ATRA and 1,25(OH)2D3 could inhibit growth and induce apoptosis of HepG2 cells, and the molecular basis of the cell cycle blockade by 1,25(OH)2D3 may be associated with the up-regulation of CDK inhibitors p21(WAF/CIP1) and p27(KIP1), which mediate G1 arrest. Tretinoin 13-17 cyclin dependent kinase inhibitor 1A Homo sapiens 217-220
17313834-7 2006 RA alone did not significantly promote the proliferation of the A549 cells, but weakened the inhibitory effect of TNF-alpha on the proliferation of the A549 cells. Tretinoin 0-2 tumor necrosis factor Homo sapiens 114-123
17313834-9 2006 CONCLUSION: RA relieves the injury of alveolar epithelial cells and protects the pulmonary surfactant by inhibiting the destruction of TNF-alpha to type II lung alveolar epithelial cells. Tretinoin 12-14 tumor necrosis factor Homo sapiens 135-144
17313834-0 2006 [Retinoic acid inhibits tumor necrosis factor-alpha induced injury in human lung epithelial cells]. Tretinoin 1-14 tumor necrosis factor Homo sapiens 24-51
17166369-10 2006 CONCLUSIONS: ATRA and 1,25(OH)2D3 could inhibit growth and induce apoptosis of HepG2 cells, and the molecular basis of the cell cycle blockade by 1,25(OH)2D3 may be associated with the up-regulation of CDK inhibitors p21(WAF/CIP1) and p27(KIP1), which mediate G1 arrest. Tretinoin 13-17 cyclin dependent kinase inhibitor 1A Homo sapiens 225-229
17166369-10 2006 CONCLUSIONS: ATRA and 1,25(OH)2D3 could inhibit growth and induce apoptosis of HepG2 cells, and the molecular basis of the cell cycle blockade by 1,25(OH)2D3 may be associated with the up-regulation of CDK inhibitors p21(WAF/CIP1) and p27(KIP1), which mediate G1 arrest. Tretinoin 13-17 zinc ribbon domain containing 2 Homo sapiens 235-238
16959849-2 2006 IL-1beta can repress renin transcription under both baseline and retinoic acid-stimulated conditions in As4.1 cells, a renin-expressing cell line derived from the kidney. Tretinoin 65-78 interleukin 1 beta Mus musculus 0-8
17384263-3 2006 We previously reported that ATRA-induced NF-kappaB activation in APL cells is not essential for granulocytic differentiation, but prolongs the life span of mature cells. Tretinoin 28-32 nuclear factor kappa B subunit 1 Homo sapiens 41-50
17384263-6 2006 As2O3 antagonizes ATRA-induced degradation of the NF-kappaB inhibitor IkappaB and consequently decreases NF-kappaB activation. Tretinoin 18-22 nuclear factor kappa B subunit 1 Homo sapiens 50-59
17384263-6 2006 As2O3 antagonizes ATRA-induced degradation of the NF-kappaB inhibitor IkappaB and consequently decreases NF-kappaB activation. Tretinoin 18-22 nuclear factor kappa B subunit 1 Homo sapiens 105-114
17384263-7 2006 Also, cotreatment of NB4 cells with ATRA and As2O3 results in a higher JNK activation than treatment with ATRA alone. Tretinoin 36-40 mitogen-activated protein kinase 8 Homo sapiens 71-74
17384263-7 2006 Also, cotreatment of NB4 cells with ATRA and As2O3 results in a higher JNK activation than treatment with ATRA alone. Tretinoin 106-110 mitogen-activated protein kinase 8 Homo sapiens 71-74
17118012-1 2006 Using a subtracted Xenopus cDNA library based on the differential sensitivity of anterior and posterior genes to retinoic acid, we isolated a novel Xenopus nuclear GTP-binding protein (XGB). Tretinoin 113-126 GTP binding protein 4 L homeolog Xenopus laevis 148-183
17118012-1 2006 Using a subtracted Xenopus cDNA library based on the differential sensitivity of anterior and posterior genes to retinoic acid, we isolated a novel Xenopus nuclear GTP-binding protein (XGB). Tretinoin 113-126 GTP binding protein 4 L homeolog Xenopus laevis 185-188
16959849-4 2006 Three tandem copies of the retinoic acid response element is sufficient to attenuate the retinoic acid-response by IL-1beta. Tretinoin 89-102 interleukin 1 beta Mus musculus 115-123
16959849-5 2006 The decrease in retinoic acid-induced renin promoter activity in response to IL-1beta was blocked with the general tyrosine kinase inhibitor Genistein. Tretinoin 16-29 interleukin 1 beta Mus musculus 77-85
16959849-8 2006 PD98059 partially reversed the IL-1beta effect on retinoic acid-mediated transcription. Tretinoin 50-63 interleukin 1 beta Mus musculus 31-39
16959849-4 2006 Three tandem copies of the retinoic acid response element is sufficient to attenuate the retinoic acid-response by IL-1beta. Tretinoin 27-40 interleukin 1 beta Mus musculus 115-123
17035043-2 2006 During neuronal differentiation, both the control and Olig2-induced groups produced a similar proportion of HB9-expressing motoneurons in the presence of retinoic acid (RA) and sonic hedgehog (SHH), but both generated few motoneurons in the absence of SHH. Tretinoin 154-167 oligodendrocyte transcription factor 2 Mus musculus 54-59
16810296-0 2006 All-trans retinoic acid antagonizes UV-induced VEGF production and angiogenesis via the inhibition of ERK activation in human skin keratinocytes. Tretinoin 10-23 vascular endothelial growth factor A Homo sapiens 47-51
16810296-0 2006 All-trans retinoic acid antagonizes UV-induced VEGF production and angiogenesis via the inhibition of ERK activation in human skin keratinocytes. Tretinoin 10-23 mitogen-activated protein kinase 1 Homo sapiens 102-105
17082780-7 2006 A chromatin immunoprecipitation assay revealed occupancy of the human C/EBPalpha promoter in vivo by Max and Myc under cellular settings and by C/EBPalpha and Max under retinoic acid induced granulocytic differentiation. Tretinoin 169-182 CCAAT enhancer binding protein alpha Homo sapiens 70-80
16732315-1 2006 Gene associated with retinoid interferon-induced mortality (GRIM)-19, an inhibitor of transcription factor STAT3, was originally identified as a critical regulatory protein in a genetic screen that was designed to identify the gene products necessary for Interferon (IFN)-beta- and retinoic acid-induced cell death. Tretinoin 282-295 signal transducer and activator of transcription 3 Homo sapiens 107-112
17005281-0 2006 Mapping of the RXRalpha binding elements involved in retinoic acid induced transcriptional activation of the human SOX3 gene. Tretinoin 53-66 SRY-box transcription factor 3 Homo sapiens 115-119
17005281-9 2006 Since it is proven that Sox3 is critical determinant of neurogenesis our data may help in providing new insight into complex regulatory networks involved in retinoic acid induced neural differentiation of NT2/D1 cells. Tretinoin 157-170 SRY-box transcription factor 3 Homo sapiens 24-28
17110582-4 2006 However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Tretinoin 9-11 interleukin 6 Mus musculus 68-72
17110582-4 2006 However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Tretinoin 9-11 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 92-95
17110582-5 2006 Consequently, mice deficient in the RA precursor vitamin A lacked IgA-secreting cells in the small intestine. Tretinoin 36-38 CD79A antigen (immunoglobulin-associated alpha) Mus musculus 66-69
17055661-5 2006 Following addition of 20 microM retinoic acid (RA), a stimulus for differentiation that enhances neurite growth and differentiation, Sox11 level rises. Tretinoin 32-45 SRY (sex determining region Y)-box 11 Mus musculus 133-138
17055661-5 2006 Following addition of 20 microM retinoic acid (RA), a stimulus for differentiation that enhances neurite growth and differentiation, Sox11 level rises. Tretinoin 47-49 SRY (sex determining region Y)-box 11 Mus musculus 133-138
16841329-6 2006 Furthermore, beta-cryptoxanthin transactivated RAR-mediated transcription activity of the retinoic acid response element. Tretinoin 90-103 retinoic acid receptor beta Homo sapiens 47-50
16732322-4 2006 Specifically, we show that 1,25D selectively increases the expression of the gene encoding kinase suppressor of Ras-1 (KSR-1) in HL60 cells, while other differentiation-inducing agents such as 12-O-tetradecanoylphorbol-13-acetate, retinoic acid or dimethyl sulfoxide do not significantly increase KSR-1 expression. Tretinoin 231-244 kinase suppressor of ras 1 Homo sapiens 91-117
16732322-4 2006 Specifically, we show that 1,25D selectively increases the expression of the gene encoding kinase suppressor of Ras-1 (KSR-1) in HL60 cells, while other differentiation-inducing agents such as 12-O-tetradecanoylphorbol-13-acetate, retinoic acid or dimethyl sulfoxide do not significantly increase KSR-1 expression. Tretinoin 231-244 kinase suppressor of ras 1 Homo sapiens 119-124
16778795-2 2006 Metabolic transformation of all-trans RA to 4-hydroxylated RA appears to be primarily catalyzed by the cytochrome P450 (CYP) 26AI. Tretinoin 38-40 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 103-118
16778795-2 2006 Metabolic transformation of all-trans RA to 4-hydroxylated RA appears to be primarily catalyzed by the cytochrome P450 (CYP) 26AI. Tretinoin 38-40 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 120-123
16778795-2 2006 Metabolic transformation of all-trans RA to 4-hydroxylated RA appears to be primarily catalyzed by the cytochrome P450 (CYP) 26AI. Tretinoin 59-61 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 103-118
16778795-2 2006 Metabolic transformation of all-trans RA to 4-hydroxylated RA appears to be primarily catalyzed by the cytochrome P450 (CYP) 26AI. Tretinoin 59-61 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 120-123
16778795-9 2006 In light of our prior studies documenting the functional activity of RA metabolites, expression of CYP26 in the sebaceous gland epithelium supports the suggestion that altered RA metabolism may be involved in the pathogenesis of acne. Tretinoin 176-178 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 99-104
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 73-77 prostaglandin-endoperoxide synthase 2 Homo sapiens 147-163
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 73-77 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 58-71 prostaglandin-endoperoxide synthase 2 Homo sapiens 147-163
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 58-71 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 108-121 prostaglandin-endoperoxide synthase 2 Homo sapiens 147-163
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 108-121 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170
16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 174-178 prostaglandin-endoperoxide synthase 2 Homo sapiens 31-36
16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 174-178 retinoic acid receptor beta Homo sapiens 115-122
16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 92-105 retinoic acid receptor beta Homo sapiens 115-122
16956736-5 2006 We examined the effects of RA on PDGF-C and its receptor PDGFR-alpha expressions. Tretinoin 27-29 platelet derived growth factor receptor, alpha polypeptide Mus musculus 57-68
17051635-0 2006 Profilin 1 obtained by proteomic analysis in all-trans retinoic acid-treated hepatocarcinoma cell lines is involved in inhibition of cell proliferation and migration. Tretinoin 55-68 profilin 1 Homo sapiens 0-10
17051635-6 2006 The PFN1 expression was increased in response to ATRA in a dose- and time-dependent manner. Tretinoin 49-53 profilin 1 Homo sapiens 4-8
17051635-11 2006 Furthermore, RNAi-based PFN1 knockdown could rescue the inhibitory effect of ATRA on cell proliferation and migration. Tretinoin 77-81 profilin 1 Homo sapiens 24-28
17051635-12 2006 In conclusion, ATRA inhibited cell proliferation and migration through up-regulation of PFN1. Tretinoin 15-19 profilin 1 Homo sapiens 88-92
17050680-7 2006 Considering that IFN-alpha and ATRA synergistically inhibit growth along the intracellular pathways triggered by the two compounds in many cell types, we suggest that Rig-G may also represent one of the key molecular nodes of signaling cross-talk between ATRA and IFN-alpha. Tretinoin 31-35 interferon alpha 1 Homo sapiens 264-273
17050680-7 2006 Considering that IFN-alpha and ATRA synergistically inhibit growth along the intracellular pathways triggered by the two compounds in many cell types, we suggest that Rig-G may also represent one of the key molecular nodes of signaling cross-talk between ATRA and IFN-alpha. Tretinoin 255-259 interferon alpha 1 Homo sapiens 17-26
16956736-6 2006 We demonstrated that administration of RA to mouse embryos resulted in dramatic losses of PDGF-C and its receptor PDGFR-alpha. Tretinoin 39-41 platelet derived growth factor receptor, alpha polypeptide Mus musculus 114-125
16932348-6 2006 Reduced expression of PRDX2 validated at the mRNA and protein level, in topo IIbeta-deficient cells correlated with increased accumulation of reactive oxygen species (ROS) following ATRA-induced differentiation. Tretinoin 182-186 peroxiredoxin 2 Homo sapiens 22-27
16935935-4 2006 We previously found that ATRA-induced cell differentiation accompanies ubiquitination-proteolysis of menage a trois 1 (MAT1), an assembly factor and targeting subunit of cyclin-dependent kinase (CDK)-activating kinase (CAK) that regulates G1 exit. Tretinoin 25-29 cyclin dependent kinase 7 Homo sapiens 219-222
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 cyclin dependent kinase 7 Homo sapiens 54-57
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 cyclin dependent kinase 7 Homo sapiens 113-116
16619265-7 2006 AtRA also inhibited endothelin-1 (ET-1) expression in a time-dependent manner. Tretinoin 0-4 endothelin 1 Rattus norvegicus 20-32
16619265-7 2006 AtRA also inhibited endothelin-1 (ET-1) expression in a time-dependent manner. Tretinoin 0-4 endothelin 1 Rattus norvegicus 34-38
16982809-0 2006 PPARgamma controls CD1d expression by turning on retinoic acid synthesis in developing human dendritic cells. Tretinoin 49-62 peroxisome proliferator activated receptor gamma Homo sapiens 0-9
16982809-4 2006 Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 (RALDH2). Tretinoin 45-58 peroxisome proliferator activated receptor gamma Homo sapiens 25-34
16982809-5 2006 PPARgamma-regulated expression of these enzymes leads to an increase in the intracellular generation of all-trans retinoic acid (ATRA) from retinol. Tretinoin 114-127 peroxisome proliferator activated receptor gamma Homo sapiens 0-9
16982809-5 2006 PPARgamma-regulated expression of these enzymes leads to an increase in the intracellular generation of all-trans retinoic acid (ATRA) from retinol. Tretinoin 129-133 peroxisome proliferator activated receptor gamma Homo sapiens 0-9
17069899-0 2006 Transcriptional regulation of the human Sia-alpha2,3-Gal-beta1,4-GlcNAc-R:alpha2,8-sialyltransferase (hST8Sia III) by retinoic acid in human glioblastoma tumor cell line. Tretinoin 118-131 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 40-100
17069899-0 2006 Transcriptional regulation of the human Sia-alpha2,3-Gal-beta1,4-GlcNAc-R:alpha2,8-sialyltransferase (hST8Sia III) by retinoic acid in human glioblastoma tumor cell line. Tretinoin 118-131 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 102-113
17069899-1 2006 In this study, we have shown the transcriptional regulation of the human Sia-alpha2,3-Gal-beta1,4-GlcNAc-R:alpha2,8-sialyltransferase (hST8Sia III) induced by retinoic acid (RA), a potent neuronal cell regulator in glioblastoma cell line (U-87MG). Tretinoin 159-172 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 73-133
17069899-1 2006 In this study, we have shown the transcriptional regulation of the human Sia-alpha2,3-Gal-beta1,4-GlcNAc-R:alpha2,8-sialyltransferase (hST8Sia III) induced by retinoic acid (RA), a potent neuronal cell regulator in glioblastoma cell line (U-87MG). Tretinoin 159-172 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 135-146
17069899-1 2006 In this study, we have shown the transcriptional regulation of the human Sia-alpha2,3-Gal-beta1,4-GlcNAc-R:alpha2,8-sialyltransferase (hST8Sia III) induced by retinoic acid (RA), a potent neuronal cell regulator in glioblastoma cell line (U-87MG). Tretinoin 174-176 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 73-133
17069899-1 2006 In this study, we have shown the transcriptional regulation of the human Sia-alpha2,3-Gal-beta1,4-GlcNAc-R:alpha2,8-sialyltransferase (hST8Sia III) induced by retinoic acid (RA), a potent neuronal cell regulator in glioblastoma cell line (U-87MG). Tretinoin 174-176 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 135-146
17069899-2 2006 The induction of hST8Sia III by RA is regulated at the transcriptional level in a dose- and time-dependent manner, as evidenced by reverse transcription-polymerase chain reaction (RT-PCR). Tretinoin 32-34 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 17-28
17069899-5 2006 Site-directed mutagenesis indicated that the RA binding site at -996 to -991 is crucial for the RA-induced expression of the hST8Sia III in U-87MG cells. Tretinoin 45-47 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 125-136
17069899-5 2006 Site-directed mutagenesis indicated that the RA binding site at -996 to -991 is crucial for the RA-induced expression of the hST8Sia III in U-87MG cells. Tretinoin 96-98 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 125-136
17069899-6 2006 In addition, the transcriptional activity of hST8Sia III induced by RA in U-87MG cells was strongly inhibited by SP600125, c-Jun N-terminal Kinase (JNK) inhibitor, as determined by RT-PCR and luciferase assay of hST8Sia III promoter containing the -1194 to -816 regions. Tretinoin 68-70 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 45-56
17069899-6 2006 In addition, the transcriptional activity of hST8Sia III induced by RA in U-87MG cells was strongly inhibited by SP600125, c-Jun N-terminal Kinase (JNK) inhibitor, as determined by RT-PCR and luciferase assay of hST8Sia III promoter containing the -1194 to -816 regions. Tretinoin 68-70 mitogen-activated protein kinase 8 Homo sapiens 148-151
17069899-7 2006 These results suggest that RA markedly modulates transcriptional regulation of hST8Sia III gene expression through JNK signal pathway in U-87MG cells. Tretinoin 27-29 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 3 Homo sapiens 79-90
17069899-7 2006 These results suggest that RA markedly modulates transcriptional regulation of hST8Sia III gene expression through JNK signal pathway in U-87MG cells. Tretinoin 27-29 mitogen-activated protein kinase 8 Homo sapiens 115-118
16932348-7 2006 Overexpression of PRDX2 in topo IIbeta-deficient cells led to reduced accumulation of ROS and partially reversed ATRA-induced apoptosis. Tretinoin 113-117 peroxiredoxin 2 Homo sapiens 18-23
16932348-10 2006 Thus, suppression of topo IIbeta and/or PRDX2 levels in myeloid leukemia cells provides a novel approach for improving ATRA-based differentiation therapy. Tretinoin 119-123 peroxiredoxin 2 Homo sapiens 40-45
16847436-11 2006 The expression of COX-2 enzyme, but not COX-1, was significantly higher in animals treated with ATRA. Tretinoin 96-100 cytochrome c oxidase I, mitochondrial Rattus norvegicus 40-45
17045167-2 2006 It has been shown that retinoic acid (RA) alters NIS gene expression in thyroid carcinoma lines and stimulates their iodide uptake. Tretinoin 23-36 solute carrier family 5 member 5 Homo sapiens 49-52
17045167-2 2006 It has been shown that retinoic acid (RA) alters NIS gene expression in thyroid carcinoma lines and stimulates their iodide uptake. Tretinoin 38-40 solute carrier family 5 member 5 Homo sapiens 49-52
17045167-4 2006 However, a 1-microM all-trans retinoic acid (tRA) treatment significantly increased this 125I uptake up to approximately approximately 6.5-fold on Day 3. tRA also elevated NIS mRNA expression in ARO-NIS cells, with peaks of expression being observed on Day 3. Tretinoin 20-43 solute carrier family 5 member 5 Homo sapiens 172-175
17045167-4 2006 However, a 1-microM all-trans retinoic acid (tRA) treatment significantly increased this 125I uptake up to approximately approximately 6.5-fold on Day 3. tRA also elevated NIS mRNA expression in ARO-NIS cells, with peaks of expression being observed on Day 3. Tretinoin 20-43 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 195-198
17045167-4 2006 However, a 1-microM all-trans retinoic acid (tRA) treatment significantly increased this 125I uptake up to approximately approximately 6.5-fold on Day 3. tRA also elevated NIS mRNA expression in ARO-NIS cells, with peaks of expression being observed on Day 3. Tretinoin 20-43 solute carrier family 5 member 5 Homo sapiens 199-202
17045167-4 2006 However, a 1-microM all-trans retinoic acid (tRA) treatment significantly increased this 125I uptake up to approximately approximately 6.5-fold on Day 3. tRA also elevated NIS mRNA expression in ARO-NIS cells, with peaks of expression being observed on Day 3. Tretinoin 45-48 solute carrier family 5 member 5 Homo sapiens 172-175
17045167-4 2006 However, a 1-microM all-trans retinoic acid (tRA) treatment significantly increased this 125I uptake up to approximately approximately 6.5-fold on Day 3. tRA also elevated NIS mRNA expression in ARO-NIS cells, with peaks of expression being observed on Day 3. Tretinoin 45-48 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 195-198
17045167-4 2006 However, a 1-microM all-trans retinoic acid (tRA) treatment significantly increased this 125I uptake up to approximately approximately 6.5-fold on Day 3. tRA also elevated NIS mRNA expression in ARO-NIS cells, with peaks of expression being observed on Day 3. Tretinoin 45-48 solute carrier family 5 member 5 Homo sapiens 199-202
17045167-6 2006 Of 1152, genes spotted onto the microarray membrane, 18 were up-regulated (z ratio>2.0) and 33 were down-regulated (z ratio<-2.0) in ARO-NIS cells after 3 days of tRA treatment. Tretinoin 169-172 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 139-142
17045167-6 2006 Of 1152, genes spotted onto the microarray membrane, 18 were up-regulated (z ratio>2.0) and 33 were down-regulated (z ratio<-2.0) in ARO-NIS cells after 3 days of tRA treatment. Tretinoin 169-172 solute carrier family 5 member 5 Homo sapiens 143-146
16982775-11 2006 During the IL-2 treatment, the ATRA effect was completely eliminated. Tretinoin 31-35 interleukin 2 Homo sapiens 11-15
16960373-3 2006 We found that the addition of all-trans-retinoic acid to the fructose-based medium improved the growth and monoclonal antibody production of hybridoma cell lines by up-regulation of fructose incorporation that represented increased expression of the fructose transporter, GLUT5. Tretinoin 30-53 solute carrier family 2 member 5 Homo sapiens 272-277
16894348-0 2006 Kinase-dependent, retinoic acid receptor-independent up-regulation of cyclooxygenase-2 by all-trans retinoic acid in human mesangial cells. Tretinoin 90-113 prostaglandin-endoperoxide synthase 2 Homo sapiens 70-86
16894348-1 2006 BACKGROUND AND PURPOSE: Preliminary results in human mesangial cells (MC) suggested that all-trans retinoic acid (ATRA) increased the expression of COX-2 and the production of prostaglandin E2 (PGE2), a PG with anti-inflammatory effects in MC. Tretinoin 89-112 mitochondrially encoded cytochrome c oxidase II Homo sapiens 148-153
16894348-1 2006 BACKGROUND AND PURPOSE: Preliminary results in human mesangial cells (MC) suggested that all-trans retinoic acid (ATRA) increased the expression of COX-2 and the production of prostaglandin E2 (PGE2), a PG with anti-inflammatory effects in MC. Tretinoin 114-118 mitochondrially encoded cytochrome c oxidase II Homo sapiens 148-153
16894348-2 2006 The aim of this work is to confirm that ATRA increases the expression of COX-2 in MC and to examine the mechanisms involved. Tretinoin 40-44 mitochondrially encoded cytochrome c oxidase II Homo sapiens 73-78
16894348-8 2006 COX-2 up-regulation by ATRA was due to transcriptional mechanisms as pre-incubation with actinomycin D abolished it and ATRA increased the expression of COX-2 mRNA and the activity of a human COX-2 promoter construct, whereas post-transcriptional mechanisms were not found. Tretinoin 23-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5
16842746-0 2006 Suppression of PTEN expression during aggregation with retinoic acid in P19 mouse embryonal carcinoma cells. Tretinoin 55-68 phosphatase and tensin homolog Mus musculus 15-19
16842746-6 2006 Our results suggest that RA attenuates the induction of apoptosis during the aggregation phase of P19 EC cells, probably by suppressing PTEN expression. Tretinoin 25-27 phosphatase and tensin homolog Mus musculus 136-140
16740975-4 2006 We recorded a significant reduction in plasma ACTH and alpha-MSH, and also in the cortisol/creatinine urine ratio, of the dogs treated with retinoic acid. Tretinoin 140-153 proopiomelanocortin Canis lupus familiaris 46-50
16922813-8 2006 Western blot analysis revealed that ATRA caused increased expression of JWA in HeLa cells in a dose- and time-dependent manner, accompanied by activation of extracellular signal-regulated kinase (ERK) 1/2 phosphorylation. Tretinoin 36-40 mitogen-activated protein kinase 3 Homo sapiens 157-204
16922813-9 2006 However, ERK1/2 phosphorylation induced by ATRA was inhibited in JWA-deficient HeLa cells. Tretinoin 43-47 mitogen-activated protein kinase 3 Homo sapiens 9-15
16894348-8 2006 COX-2 up-regulation by ATRA was due to transcriptional mechanisms as pre-incubation with actinomycin D abolished it and ATRA increased the expression of COX-2 mRNA and the activity of a human COX-2 promoter construct, whereas post-transcriptional mechanisms were not found. Tretinoin 23-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158
16894348-8 2006 COX-2 up-regulation by ATRA was due to transcriptional mechanisms as pre-incubation with actinomycin D abolished it and ATRA increased the expression of COX-2 mRNA and the activity of a human COX-2 promoter construct, whereas post-transcriptional mechanisms were not found. Tretinoin 23-27 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158
16894348-8 2006 COX-2 up-regulation by ATRA was due to transcriptional mechanisms as pre-incubation with actinomycin D abolished it and ATRA increased the expression of COX-2 mRNA and the activity of a human COX-2 promoter construct, whereas post-transcriptional mechanisms were not found. Tretinoin 120-124 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5
16894348-8 2006 COX-2 up-regulation by ATRA was due to transcriptional mechanisms as pre-incubation with actinomycin D abolished it and ATRA increased the expression of COX-2 mRNA and the activity of a human COX-2 promoter construct, whereas post-transcriptional mechanisms were not found. Tretinoin 120-124 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158
16894348-8 2006 COX-2 up-regulation by ATRA was due to transcriptional mechanisms as pre-incubation with actinomycin D abolished it and ATRA increased the expression of COX-2 mRNA and the activity of a human COX-2 promoter construct, whereas post-transcriptional mechanisms were not found. Tretinoin 120-124 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158
16894348-10 2006 Instead ATRA might act through a sustained activation of extracellular signal-regulated kinase 1/2 (ERK1/2) since up-regulation of COX-2 was prevented by inhibition of the activation of ERK1/2 with PD098059. Tretinoin 8-12 mitogen-activated protein kinase 1 Homo sapiens 57-98
16894348-10 2006 Instead ATRA might act through a sustained activation of extracellular signal-regulated kinase 1/2 (ERK1/2) since up-regulation of COX-2 was prevented by inhibition of the activation of ERK1/2 with PD098059. Tretinoin 8-12 mitogen-activated protein kinase 3 Homo sapiens 100-106
16894348-10 2006 Instead ATRA might act through a sustained activation of extracellular signal-regulated kinase 1/2 (ERK1/2) since up-regulation of COX-2 was prevented by inhibition of the activation of ERK1/2 with PD098059. Tretinoin 8-12 mitochondrially encoded cytochrome c oxidase II Homo sapiens 131-136
16894348-10 2006 Instead ATRA might act through a sustained activation of extracellular signal-regulated kinase 1/2 (ERK1/2) since up-regulation of COX-2 was prevented by inhibition of the activation of ERK1/2 with PD098059. Tretinoin 8-12 mitogen-activated protein kinase 3 Homo sapiens 186-192
16740975-8 2006 Retinoic acid treatment controls ACTH and cortisol hyperactivity and tumor size in dogs with ACTH-secreting tumors, leading to resolution of the clinical phenotype. Tretinoin 0-13 proopiomelanocortin Canis lupus familiaris 33-37
16954431-11 2006 Retinoic acid has been used to stimulate NIS expression in both thyroid and breast cancer. Tretinoin 0-13 solute carrier family 5 member 5 Homo sapiens 41-44
16740975-8 2006 Retinoic acid treatment controls ACTH and cortisol hyperactivity and tumor size in dogs with ACTH-secreting tumors, leading to resolution of the clinical phenotype. Tretinoin 0-13 proopiomelanocortin Canis lupus familiaris 93-97
16740975-9 2006 This study highlights the possibility of using retinoic acid as a novel therapy in the treatment of ACTH-secreting tumors in humans with Cushing"s disease. Tretinoin 47-60 proopiomelanocortin Canis lupus familiaris 100-104
16920920-0 2006 All-trans retinoic acid stimulates IL-2-mediated proliferation of human T lymphocytes: early induction of cyclin D3. Tretinoin 10-23 interleukin 2 Homo sapiens 35-39
16598785-3 2006 Retinoic acid or 1,25-dihydroxyvitamin D3 enhanced TGF-beta-induced VEGF release in a concentration-dependent manner, whereas dexamethasone or corticosterone suppressed TGF-beta-induced VEGF release. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 68-72
16598785-3 2006 Retinoic acid or 1,25-dihydroxyvitamin D3 enhanced TGF-beta-induced VEGF release in a concentration-dependent manner, whereas dexamethasone or corticosterone suppressed TGF-beta-induced VEGF release. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 186-190
16598785-7 2006 These results indicate that retinoic acid, 1,25-dihydroxyvitamin D3, and glucocorticoids affect TGF-beta-stimulated VEGF release from aortic smooth muscle cells. Tretinoin 28-41 vascular endothelial growth factor A Homo sapiens 116-120
16920920-0 2006 All-trans retinoic acid stimulates IL-2-mediated proliferation of human T lymphocytes: early induction of cyclin D3. Tretinoin 10-23 cyclin D3 Homo sapiens 106-115
16920920-2 2006 In this study, we show that an active metabolite of vitamin A, all-trans retinoic acid (RA), potently stimulates T cell proliferation by modulating IL-2-mediated signaling downstream of IL-2R and independent of the induction of IL-2. Tretinoin 73-86 interleukin 2 Homo sapiens 148-152
16920920-2 2006 In this study, we show that an active metabolite of vitamin A, all-trans retinoic acid (RA), potently stimulates T cell proliferation by modulating IL-2-mediated signaling downstream of IL-2R and independent of the induction of IL-2. Tretinoin 73-86 interleukin 2 Homo sapiens 186-190
16568081-10 2006 This may provide a new therapeutic strategy against the ATRA-resistant and aggressive neuroblastomas by combining treatment with ATRA and a Bcl-2 inhibitor. Tretinoin 56-60 BCL2 apoptosis regulator Homo sapiens 140-145
17017984-9 2006 There were time and dose dependent increases in alkaline phosphatase activity (ALP), an indicator of cell differentiation, upon treatment with ATRA when compared to controls. Tretinoin 143-147 alkaline phosphatase, placental Homo sapiens 79-82
16918696-7 2006 In contrast, ATRA-induced expression of PU.1, C/EBPalpha, C/EBPbeta and IRF-1 was unaffected. Tretinoin 13-17 CCAAT enhancer binding protein alpha Homo sapiens 46-56
16918696-7 2006 In contrast, ATRA-induced expression of PU.1, C/EBPalpha, C/EBPbeta and IRF-1 was unaffected. Tretinoin 13-17 interferon regulatory factor 1 Homo sapiens 72-77
16568081-0 2006 Bcl-2 is a key regulator for the retinoic acid-induced apoptotic cell death in neuroblastoma. Tretinoin 33-46 BCL2 apoptosis regulator Homo sapiens 0-5
16568081-5 2006 ATRA-mediated apoptosis in CHP134 and NB-39-nu cells was associated with a significant activation of caspase-9 and caspase-3 as well as cytoplasmic release of cytochrome c from mitochondria in a p53-independent manner. Tretinoin 0-4 caspase 3 Homo sapiens 115-124
16724269-3 2006 Exposure of SN56 cholinergic neuroblastoma cells to dibutyryl cAMP and retinoic acid for 3 days caused their morphologic differentiation along with the increase in choline acetyltransferase activity, acetylcholine content and release, calcium content, and the expression of p75 neurotrophin receptors. Tretinoin 71-84 nerve growth factor receptor (TNFR superfamily, member 16) Mus musculus 274-277
16712891-0 2006 atRA-induced apoptosis of mouse embryonic palate mesenchymal cells involves activation of MAPK pathway. Tretinoin 0-4 mitogen-activated protein kinase 1 Mus musculus 90-94
16568081-5 2006 ATRA-mediated apoptosis in CHP134 and NB-39-nu cells was associated with a significant activation of caspase-9 and caspase-3 as well as cytoplasmic release of cytochrome c from mitochondria in a p53-independent manner. Tretinoin 0-4 cytochrome c, somatic Homo sapiens 159-171
16568081-5 2006 ATRA-mediated apoptosis in CHP134 and NB-39-nu cells was associated with a significant activation of caspase-9 and caspase-3 as well as cytoplasmic release of cytochrome c from mitochondria in a p53-independent manner. Tretinoin 0-4 tumor protein p53 Homo sapiens 195-198
16568081-6 2006 Enforced expression of Bcl-2 significantly inhibited ATRA-mediated apoptosis in CHP134 cells. Tretinoin 53-57 BCL2 apoptosis regulator Homo sapiens 23-28
16568081-7 2006 In addition, treatment of RTBM1 cells with a Bcl-2 inhibitor, HA14-1, enhanced apoptotic response induced by ATRA. Tretinoin 109-113 BCL2 apoptosis regulator Homo sapiens 45-50
16894153-4 2006 Western blot analysis revealed that retinoic acid enhanced levels of BMPR-IB protein during the first 7 days of osteogenic differentiation and that RNAi-mediated suppression of BMPR-IB dramatically impaired the ability of ADAS to form bone in vitro. Tretinoin 36-49 bone morphogenetic protein receptor, type 1B Mus musculus 69-76
16894153-6 2006 Our data therefore demonstrate that the osteogenic commitment of multipotent mouse ADAS requires retinoic acid, which enhances expression of the critical BMPR-IB isoform. Tretinoin 97-110 bone morphogenetic protein receptor, type 1B Mus musculus 154-161
16712891-5 2006 atRA-induced apoptosis was associated with upregulation of bcl-2, translocation of bax protein to the mitochondria from the cytosol, activation of caspase-3 and cytochrome c release into cytosol. Tretinoin 0-4 B cell leukemia/lymphoma 2 Mus musculus 59-64
16712891-7 2006 In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase (p38), as well as an early but transient activation of extracellular signal-regulated kinase (ERK). Tretinoin 13-17 mitogen-activated protein kinase 1 Mus musculus 172-209
16712891-7 2006 In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase (p38), as well as an early but transient activation of extracellular signal-regulated kinase (ERK). Tretinoin 13-17 mitogen-activated protein kinase 1 Mus musculus 211-214
16565789-9 2006 Cell treatment with lycopene and atRA inhibited IGF-I-stimulated cell cycle progression from G1 to S phase and decreased retinoblastoma protein (pRb) phosphorylation. Tretinoin 33-37 insulin like growth factor 1 Homo sapiens 48-53
16565789-13 2006 CONCLUSIONS: Our findings suggest that attenuation of cyclin Dl levels by lycopene and atRA is an important mechanism for the reduction of the mitogenic action of IGF-I. Tretinoin 87-91 insulin like growth factor 1 Homo sapiens 163-168
16608438-4 2006 ChIP (chromatin immunoprecipitation) assays revealed that in vivo binding of C/EBPalpha to the region markedly decreases upon incubation with ATRA, whereas ATRA treatment marginally increases the recruitment of C/EBPbeta. Tretinoin 142-146 CCAAT enhancer binding protein alpha Homo sapiens 77-87
16872382-5 2006 In addition, all-trans-retinoic acid-treated dendritic cells could drive T cells towards T-helper cell type 2 responses with decreased secretion of interleukin-12, interferon-gamma, and increased production of interleukin-10 and interleukin-4. Tretinoin 13-36 interferon gamma Homo sapiens 164-180
16872382-5 2006 In addition, all-trans-retinoic acid-treated dendritic cells could drive T cells towards T-helper cell type 2 responses with decreased secretion of interleukin-12, interferon-gamma, and increased production of interleukin-10 and interleukin-4. Tretinoin 13-36 interleukin 4 Homo sapiens 229-242
17059167-0 2006 Homology model of human retinoic acid metabolising enzyme cytochrome P450 26A1 (CYP26A1): active site architecture and ligand binding. Tretinoin 24-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 58-78
17059167-0 2006 Homology model of human retinoic acid metabolising enzyme cytochrome P450 26A1 (CYP26A1): active site architecture and ligand binding. Tretinoin 24-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 80-87
16467367-0 2006 Retinoic acid and oncostatin M combine to promote cartilage degradation via matrix metalloproteinase-13 expression in bovine but not human chondrocytes. Tretinoin 0-13 matrix metallopeptidase 13 Bos taurus 76-103
16928318-3 2006 After treated with ATRA at 0.01, 0.1, or 1 micromol/L, expression of intercellular adhesion molecule-1 (ICAM-1) protein and vascular adhesion molecule-1 (VCAM-1) protein were detected by flow cytometry, and soluble ICAM-1 (sICAM-1) protein was determined by using radioimmunoassay. Tretinoin 19-23 vascular cell adhesion molecule 1 Homo sapiens 124-152
16928318-3 2006 After treated with ATRA at 0.01, 0.1, or 1 micromol/L, expression of intercellular adhesion molecule-1 (ICAM-1) protein and vascular adhesion molecule-1 (VCAM-1) protein were detected by flow cytometry, and soluble ICAM-1 (sICAM-1) protein was determined by using radioimmunoassay. Tretinoin 19-23 vascular cell adhesion molecule 1 Homo sapiens 154-160
16699180-0 2006 The adenomatous polyposis coli tumor suppressor gene regulates expression of cyclooxygenase-2 by a mechanism that involves retinoic acid. Tretinoin 123-136 prostaglandin-endoperoxide synthase 2 Homo sapiens 77-93
16699180-4 2006 We report that COX-2 is up-regulated in APC mutant zebrafish because of a deficiency in retinoic acid biosynthesis. Tretinoin 88-101 prostaglandin-endoperoxide synthase 2 Homo sapiens 15-20
16699180-5 2006 Treatment of both APC mutant zebrafish and human carcinoma cell lines with retinoic acid significantly reduces COX-2 expression. Tretinoin 75-88 prostaglandin-endoperoxide synthase 2 Homo sapiens 111-116
16699180-6 2006 Retinoic acid regulates COX-2 levels by a mechanism that involves participation of the transcription factor C/EBP-beta. Tretinoin 0-13 prostaglandin-endoperoxide synthase 2 Homo sapiens 24-29
16608438-7 2006 In conclusion, we propose a novel model for down-regulation of the albumin gene, in which ATRA triggers an increase in the translation of C/EBPbeta-LIP that antagonizes C/EBP transactivators by interacting with their binding sites in the albumin promoter. Tretinoin 90-94 CCAAT enhancer binding protein alpha Homo sapiens 138-143
16928291-10 2006 CD117- CD11b+ phenotype was detected in all patients recovering from APL with CD117+ CD11b- phenotype at diagnosis and after treatment with all-trans-retinoic acid (ARTA) for 2 months. Tretinoin 140-163 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 0-5
16928291-10 2006 CD117- CD11b+ phenotype was detected in all patients recovering from APL with CD117+ CD11b- phenotype at diagnosis and after treatment with all-trans-retinoic acid (ARTA) for 2 months. Tretinoin 165-169 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 0-5
16849523-0 2006 An autocrine loop involving ret and glial cell-derived neurotrophic factor mediates retinoic acid-induced neuroblastoma cell differentiation. Tretinoin 84-97 glial cell derived neurotrophic factor Homo sapiens 36-74
16819187-4 2006 MDR1 mRNA up-regulation was found in a colorectal adenocarcinoma cell line, HCT-15, after treatment with two typical differentiating agents, sodium butyrate and all-trans retinoic acid, suggesting its involvement in the cellular events, resulting in differentiation without malignant transformation. Tretinoin 171-184 ATP binding cassette subfamily B member 1 Homo sapiens 0-4
16497480-0 2006 Inhibition of growth and increase of alkaline phosphatase activity in cultured human oral cancer cells by all-trans retinoic acid. Tretinoin 106-129 alkaline phosphatase, placental Homo sapiens 37-57
16497480-1 2006 In this study, the effects of all-trans retinoic acid (ATRA) on human oral cancer cells with regard to cell growth, the cell cycle, and alkaline phosphatase (ALP) activity were evaluated. Tretinoin 55-59 alkaline phosphatase, placental Homo sapiens 136-156
16497480-8 2006 These findings suggest that the anti-tumour effects of ATRA on human oral cancer are associated with G0/G1 phase arrest and an increase in ALP activity. Tretinoin 55-59 alkaline phosphatase, placental Homo sapiens 139-142
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 150-154 CCAAT enhancer binding protein alpha Homo sapiens 77-82
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 150-154 CCAAT enhancer binding protein alpha Homo sapiens 122-132
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 150-154 CCAAT enhancer binding protein alpha Homo sapiens 224-234
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 249-253 CCAAT enhancer binding protein alpha Homo sapiens 77-82
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 249-253 CCAAT enhancer binding protein alpha Homo sapiens 122-132
16226872-5 2006 In addition, the association of retinoblastoma protein (pRb) and c/EBPalpha after treatment with ATRA was seen in HL-60/Vect cells but not in HL-60/FAK cells. Tretinoin 97-101 CCAAT enhancer binding protein alpha Homo sapiens 65-75
16226872-7 2006 Finally, the introduction of FAK siRNA into HL-60/FAK cells resulted in the recovery of sensitivity to ATRA-induced differentiation, confirming that the inhibition of HL-60/FAK differentiation resulted from both the induction of pRb hyperphosphorylation and the inhibition of association of pRb and c/EBPalpha. Tretinoin 103-107 CCAAT enhancer binding protein alpha Homo sapiens 299-309
16836633-3 2006 This band of cortex, which is distinguished by the retinoic acid-synthesizing enzyme RALDH3, exhibits signs of delayed maturation and enhanced plasticity compared to the surrounding cortex, as indicated by suppression of parvalbumin, neurofilament, cytochrome oxidase and perineuronal net maturation, and persistence of the embryonic, polysialated form of the neural cell-adhesion molecule PSA-NCAM. Tretinoin 51-64 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 85-91
16469417-6 2006 However, after induction of neuronal differentiation by retinoic acid the previously ineffective NCAM signals activated extracellular signal-regulated kinase (ERK) and promoted neuritogenesis. Tretinoin 56-69 mitogen-activated protein kinase 1 Homo sapiens 120-157
16469417-6 2006 However, after induction of neuronal differentiation by retinoic acid the previously ineffective NCAM signals activated extracellular signal-regulated kinase (ERK) and promoted neuritogenesis. Tretinoin 56-69 mitogen-activated protein kinase 1 Homo sapiens 159-162
16449964-1 2006 Retinoic acid (RA), used as first-line therapy for acute promyelocytic leukemia (APL), exerts its antileukemic activity by inducing blast differentiation and activating tumor-selective TNF-related apoptosis-inducing ligand (TRAIL) signaling. Tretinoin 0-13 TNF superfamily member 10 Homo sapiens 185-222
16292516-0 2006 All-trans-retinoic acid suppresses interferon-gamma and tumor necrosis factor-alpha; a possible therapeutic agent for rheumatoid arthritis. Tretinoin 0-23 interferon gamma Homo sapiens 35-83
16292516-7 2006 In contrast, ATRA suppressed the production of IFN-gamma and TNF-alpha significantly. Tretinoin 13-17 interferon gamma Homo sapiens 47-56
16292516-7 2006 In contrast, ATRA suppressed the production of IFN-gamma and TNF-alpha significantly. Tretinoin 13-17 tumor necrosis factor Homo sapiens 61-70
16292516-9 2006 CONCLUSIONS: ATRA was demonstrated to affect the cytokine production of IFN-gamma and TNF-alpha. Tretinoin 13-17 interferon gamma Homo sapiens 72-81
16292516-9 2006 CONCLUSIONS: ATRA was demonstrated to affect the cytokine production of IFN-gamma and TNF-alpha. Tretinoin 13-17 tumor necrosis factor Homo sapiens 86-95
16834973-11 2006 The Cdk4 mRNA was transcripted at a high level in embryonic neural tube in the GASP-treated plus ATRA-induced group, but the Cdk2 mRNA was not detected in this group. Tretinoin 97-101 cyclin-dependent kinase 4 Mus musculus 4-8
16531051-3 2006 Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Tretinoin 73-86 retinoic acid receptor, beta Rattus norvegicus 149-156
16531051-3 2006 Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Tretinoin 88-90 retinoic acid receptor, beta Rattus norvegicus 149-156
16765349-4 2006 Upregulated p21 by RA accompanies caspase-3 activation and precedes the occurrence of apoptosis. Tretinoin 19-21 caspase 3 Homo sapiens 34-43
16449964-1 2006 Retinoic acid (RA), used as first-line therapy for acute promyelocytic leukemia (APL), exerts its antileukemic activity by inducing blast differentiation and activating tumor-selective TNF-related apoptosis-inducing ligand (TRAIL) signaling. Tretinoin 0-13 TNF superfamily member 10 Homo sapiens 224-229
16449964-1 2006 Retinoic acid (RA), used as first-line therapy for acute promyelocytic leukemia (APL), exerts its antileukemic activity by inducing blast differentiation and activating tumor-selective TNF-related apoptosis-inducing ligand (TRAIL) signaling. Tretinoin 15-17 TNF superfamily member 10 Homo sapiens 185-222
16449964-1 2006 Retinoic acid (RA), used as first-line therapy for acute promyelocytic leukemia (APL), exerts its antileukemic activity by inducing blast differentiation and activating tumor-selective TNF-related apoptosis-inducing ligand (TRAIL) signaling. Tretinoin 15-17 TNF superfamily member 10 Homo sapiens 224-229
16449964-8 2006 Whereas knocking down RAM expression by RNA interference promoted RA-induced differentiation and TRAIL-triggered apoptosis of PLB985 and WY-1 cells, overexpression of the predicted 109 amino-acid RAM open reading frame did not alter RA signaling in PLB985 cells. Tretinoin 22-24 TNF superfamily member 10 Homo sapiens 97-102
16449964-10 2006 Our study demonstrates that RA induction of the TRAIL pathway is also operative in leukemia cells lacking an RARalpha oncofusion protein and identifies RAM as a novel RA-dependent modulator of myeloid differentiation and death. Tretinoin 28-30 TNF superfamily member 10 Homo sapiens 48-53
16456186-11 2006 ATRA suppressed PDGF-induced Akt activation without influencing ERK activation. Tretinoin 0-4 AKT serine/threonine kinase 1 Homo sapiens 29-32
16456186-13 2006 These results suggest that retinoic acid inhibits airway SMC migration through the modulation of the PI3K/Akt pathway. Tretinoin 27-40 AKT serine/threonine kinase 1 Homo sapiens 106-109
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 85-98 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 12-19
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 85-98 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 35-42
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 100-102 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 12-19
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 100-102 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 35-42
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 215-217 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 12-19
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 215-217 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 35-42
16617325-2 2006 However, several studies demonstrated the activation of PI3K in the nuclei of all-trans-retinoic acid (ATRA) - differentiated HL-60 cells, raising the possibility that PI3K/Akt-inhibitors may block antitumor properties of retinoids. Tretinoin 78-101 AKT serine/threonine kinase 1 Homo sapiens 173-176
16534781-2 2006 In vitro studies have shown that TGIF can repress transcription mediated by either of two signaling pathways: TGF-beta and retinoic acid signaling. Tretinoin 123-136 TGFB induced factor homeobox 1 Homo sapiens 33-37
16723453-2 2006 This investigation was conducted to identify UV activated signaling pathways in pterygium epithelial cells (PECs) that mediate cytokine and growth factor production and to determine whether these pathways are sensitive to blockade by anti-inflammatory agents such as retinoic acid (RA) and interferon (IFN)-alpha. Tretinoin 267-280 interferon alpha 1 Homo sapiens 290-312
16572199-0 2006 Upregulation of Bfl-1/A1 in leukemia cells undergoing differentiation by all-trans retinoic acid treatment attenuates chemotherapeutic agent-induced apoptosis. Tretinoin 83-96 BCL2 related protein A1 Homo sapiens 16-21
16572199-4 2006 The level of Bcl-2 protein is decreased by ATRA treatment in NB4, HL-60 and HL-60/Res cells. Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 13-18
16572199-6 2006 Bfl-1/A1 mRNA is not expressed in these cell lines, however, its expression is markedly induced by ATRA treatment in NB4 and HL-60 cells, but not in R4 or HL-60/Res cells, which correlates with inhibition of apoptosis. Tretinoin 99-103 BCL2 related protein A1 Homo sapiens 0-5
16617325-2 2006 However, several studies demonstrated the activation of PI3K in the nuclei of all-trans-retinoic acid (ATRA) - differentiated HL-60 cells, raising the possibility that PI3K/Akt-inhibitors may block antitumor properties of retinoids. Tretinoin 103-107 AKT serine/threonine kinase 1 Homo sapiens 173-176
16572199-7 2006 Inhibiting Bfl-1/A1 mRNA upregulation in ATRA-pretreated NB4 cells using small interfering RNA (siRNA) partly recovers cell sensitivity to Dox-induced apoptosis. Tretinoin 41-45 BCL2 related protein A1 Homo sapiens 11-16
16572199-8 2006 These data demonstrate that ATRA induction of Bfl-1/A1 in differentiated NB4 and HL-60 cells contributes to a loss of sensitivity to chemotherapy-induced apoptosis. Tretinoin 28-32 BCL2 related protein A1 Homo sapiens 46-51
16617325-3 2006 The aim of the present study was to investigate the possible activation of nuclear Akt in ATRA-treated cells and to test the effects of Akt-inhibitors on ATRA-mediated differentiation. Tretinoin 90-94 AKT serine/threonine kinase 1 Homo sapiens 83-86
16617325-3 2006 The aim of the present study was to investigate the possible activation of nuclear Akt in ATRA-treated cells and to test the effects of Akt-inhibitors on ATRA-mediated differentiation. Tretinoin 154-158 AKT serine/threonine kinase 1 Homo sapiens 136-139
16617325-5 2006 The down-modulation of the expression of Akt protein in HL-60 cells using siRNA reduces the CD11b expression in ATRA-treated cells. Tretinoin 112-116 AKT serine/threonine kinase 1 Homo sapiens 41-44
16617325-6 2006 The treatment of both cell lines with the commercially available Akt inhibitors inhibited the growth of both control and ATRA-treated cells. Tretinoin 121-125 AKT serine/threonine kinase 1 Homo sapiens 65-68
16617325-8 2006 In contrast, the presence of Akt inhibitors reduced the expression of CD11b in ATRA-treated NB4 cells. Tretinoin 79-83 AKT serine/threonine kinase 1 Homo sapiens 29-32
16800923-12 2006 It is concluded that an aminopeptidase inhibitor bestatin can potentiate ATRA-inducing differentiation of NB4 cells, possibly by down-regulating c-myc expression in synergy with ATRA. Tretinoin 73-77 carboxypeptidase Q Homo sapiens 24-38
16813970-0 2006 Pathogenesis of bronchopulmonary dysplasia: the role of interleukin 1beta in the regulation of inflammation-mediated pulmonary retinoic acid pathways in transgenic mice. Tretinoin 127-140 interleukin 1 beta Mus musculus 56-73
16800923-12 2006 It is concluded that an aminopeptidase inhibitor bestatin can potentiate ATRA-inducing differentiation of NB4 cells, possibly by down-regulating c-myc expression in synergy with ATRA. Tretinoin 178-182 carboxypeptidase Q Homo sapiens 24-38
16800923-0 2006 [Effect of aminopeptidase inhibitor on differentiation induction activity of all-trans retinoic acid in human acute promyelocytic leukemia NB4 cells and its mechanism]. Tretinoin 87-100 carboxypeptidase Q Homo sapiens 11-25
16800923-1 2006 This study was purposed to investigate whether aminopeptidase inhibitor, bestatin, can potentiate all-trans retinoic acid (ATRA)-inducing differentiation in NB4 cells, and to explore its mechanism. Tretinoin 98-121 carboxypeptidase Q Homo sapiens 47-61
16496360-0 2006 The Rho-family guanine nucleotide exchange factor GEFT enhances retinoic acid- and cAMP-induced neurite outgrowth. Tretinoin 64-77 Rho guanine nucleotide exchange factor (GEF) 25 Mus musculus 50-54
16800923-1 2006 This study was purposed to investigate whether aminopeptidase inhibitor, bestatin, can potentiate all-trans retinoic acid (ATRA)-inducing differentiation in NB4 cells, and to explore its mechanism. Tretinoin 123-127 carboxypeptidase Q Homo sapiens 47-61
16574066-1 2006 RESTIN, a member of the melanoma-associated antigen superfamily, is a nuclear protein induced by atRA (all-trans retinoic acid) in HL60 cells. Tretinoin 97-101 MAGE family member H1 Homo sapiens 0-6
16574066-1 2006 RESTIN, a member of the melanoma-associated antigen superfamily, is a nuclear protein induced by atRA (all-trans retinoic acid) in HL60 cells. Tretinoin 103-126 MAGE family member H1 Homo sapiens 0-6
16574066-4 2006 In this study, we observed that up-regulation of restin was present during the atRA-induced HL60 cell differentiation process, suggesting the functional relevance between RESTIN and atRA-induced cellular effects. Tretinoin 79-83 MAGE family member H1 Homo sapiens 49-55
16574066-4 2006 In this study, we observed that up-regulation of restin was present during the atRA-induced HL60 cell differentiation process, suggesting the functional relevance between RESTIN and atRA-induced cellular effects. Tretinoin 79-83 MAGE family member H1 Homo sapiens 171-177
16574066-4 2006 In this study, we observed that up-regulation of restin was present during the atRA-induced HL60 cell differentiation process, suggesting the functional relevance between RESTIN and atRA-induced cellular effects. Tretinoin 182-186 MAGE family member H1 Homo sapiens 49-55
16574066-7 2006 Interestingly, restin promoter containing several potential consensus-binding sites of STAT-1alpha was activated by atRA in ER(+) MCF-7 cells but not in ER(-) MDA-MB-231 cells, over-expression of STAT-1alpha in latter rescued the activation effect of restin promoter in response to atRA and IFNgamma. Tretinoin 116-120 MAGE family member H1 Homo sapiens 4-10
16574066-7 2006 Interestingly, restin promoter containing several potential consensus-binding sites of STAT-1alpha was activated by atRA in ER(+) MCF-7 cells but not in ER(-) MDA-MB-231 cells, over-expression of STAT-1alpha in latter rescued the activation effect of restin promoter in response to atRA and IFNgamma. Tretinoin 116-120 MAGE family member H1 Homo sapiens 15-21
16574066-8 2006 Our evidence supported that STAT-1alpha plays an important role in the atRA-induced transcriptional up-regulation of restin, which was associated with the atRA-induced HL60 cell differentiation and potentially mediated the downstream effects of atRA signal pathway via STAT-1alpha in some cancer cells. Tretinoin 71-75 MAGE family member H1 Homo sapiens 117-123
16496360-3 2006 Here we demonstrate that GEFT protein is highly expressed in all regions of the brain and is highly up-regulated upon treatment of Neuro2A cells with retinoic acid and dibutyric cAMP, which promote dendrite and axon-like neurite extensions, respectively. Tretinoin 150-163 Rho guanine nucleotide exchange factor (GEF) 25 Mus musculus 25-29
16496360-4 2006 Within retinoic acid-induced neurite extensions, GEFT is localized to actin-enriched regions in the primary neurites, with little or no expression from secondary branches. Tretinoin 7-20 Rho guanine nucleotide exchange factor (GEF) 25 Mus musculus 49-53
16611695-4 2006 Here, we report Raldh1, Raldh2 and Raldh3 single, double and triple null mice exhibiting progressively less or no RA synthesis in the eye. Tretinoin 114-116 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 35-41
16538685-10 2006 These findings support the hypothesis that RA is synthesized in the postnatal OE (catalyzed by RALDH 1) and underlying LP (differentially catalyzed by RALDH 1 and RALDH 2) at sites that could influence the development, maturation, targeting, and/or turnover of olfactory receptor neurons throughout the olfactory organ. Tretinoin 43-45 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 95-102
16538685-10 2006 These findings support the hypothesis that RA is synthesized in the postnatal OE (catalyzed by RALDH 1) and underlying LP (differentially catalyzed by RALDH 1 and RALDH 2) at sites that could influence the development, maturation, targeting, and/or turnover of olfactory receptor neurons throughout the olfactory organ. Tretinoin 43-45 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 151-158
16647867-0 2006 Retinoic acid-induced protein ISGylation is dependent on interferon signal transduction. Tretinoin 0-13 interferon alpha 1 Homo sapiens 57-67
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 199-212 interferon alpha 1 Homo sapiens 258-261
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 236-249 interferon alpha 1 Homo sapiens 258-261
16647867-4 2006 In this study, we examined a possible link between IFN signaling and retinoic acid-induced ISG15 conjugation. Tretinoin 69-82 interferon alpha 1 Homo sapiens 51-54
16647867-6 2006 By sandwich ELISA, we detected increased IFN secretion into cell culture media following retinoic acid treatment. Tretinoin 89-102 interferon alpha 1 Homo sapiens 41-44
16647867-7 2006 Blockade of the type I IFN receptor with a neutralizing antibody blocked retinoic acid induced ISG15 expression and ISG15 conjugation. Tretinoin 73-86 interferon alpha 1 Homo sapiens 23-26
16647867-8 2006 Taken together, these data suggested that retinoic acid-induced secretion of IFN plays a fundamental role in retinoic acid promoted ISGylation. Tretinoin 42-55 interferon alpha 1 Homo sapiens 77-80
16647867-8 2006 Taken together, these data suggested that retinoic acid-induced secretion of IFN plays a fundamental role in retinoic acid promoted ISGylation. Tretinoin 109-122 interferon alpha 1 Homo sapiens 77-80
16611695-7 2006 At early stages, Raldh2 expressed in mesenchyme and Raldh3 expressed in the retinal pigmented epithelium generate RA that delivers an essential signal to the neural retina required for morphogenetic movements that lead to ventral invagination of the optic cup. Tretinoin 114-116 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 52-58
16611695-8 2006 At later stages, Raldh1 expressed in dorsal neural retina and Raldh3 expressed in ventral neural retina (plus weaker expression of each in lens/corneal ectoderm) generates RA that travels to surrounding mesenchyme, where it is needed to limit the anterior invasion of perioptic mesenchyme during the formation of corneal mesenchyme and eyelids. Tretinoin 172-174 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 62-68
16636307-9 2006 With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. Tretinoin 53-57 NPHS2 stomatin family member, podocin Rattus norvegicus 97-104
16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Tretinoin 88-92 NPHS2 stomatin family member, podocin Rattus norvegicus 198-205
16636311-0 2006 Retinoic acid exerts dual regulatory actions on the expression and nuclear localization of interferon regulatory factor-1. Tretinoin 0-13 interferon regulatory factor 1 Homo sapiens 91-121
16636311-1 2006 Interferon regulatory factor-1 (IRF-1), a transcription factor and tumor suppressor involved in cell growth regulation and immune responses, has been shown to be induced by all-trans retinoic acid (ATRA). Tretinoin 173-196 interferon regulatory factor 1 Homo sapiens 0-30
16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Tretinoin 88-92 actinin alpha 4 Rattus norvegicus 218-233
16636311-1 2006 Interferon regulatory factor-1 (IRF-1), a transcription factor and tumor suppressor involved in cell growth regulation and immune responses, has been shown to be induced by all-trans retinoic acid (ATRA). Tretinoin 173-196 interferon regulatory factor 1 Homo sapiens 32-37
16636311-1 2006 Interferon regulatory factor-1 (IRF-1), a transcription factor and tumor suppressor involved in cell growth regulation and immune responses, has been shown to be induced by all-trans retinoic acid (ATRA). Tretinoin 198-202 interferon regulatory factor 1 Homo sapiens 0-30
16242776-0 2006 Transforming growth factor-beta1 inhibits all-trans retinoic acid-induced apoptosis. Tretinoin 52-65 transforming growth factor beta 1 Homo sapiens 0-32
16636311-1 2006 Interferon regulatory factor-1 (IRF-1), a transcription factor and tumor suppressor involved in cell growth regulation and immune responses, has been shown to be induced by all-trans retinoic acid (ATRA). Tretinoin 198-202 interferon regulatory factor 1 Homo sapiens 32-37
16636311-4 2006 Following initial treatment with ATRA, IRF-1 mRNA and protein were induced within 2 hrs, reached a peak (>30-fold induction) at 8 hrs, and declined afterwards. Tretinoin 33-37 interferon regulatory factor 1 Homo sapiens 39-44
16636311-6 2006 Although a second dose of ATRA or Am580 (a related retinoid selective for retinoic acid receptor-alpha [RARalpha]), given 16 hrs after the first dose, restimulated IRF-1 mRNA and protein levels to a similar level to that obtained by the first dose, IRF-1 was predominantly concentrated in the nucleus after restimulation. Tretinoin 26-30 interferon regulatory factor 1 Homo sapiens 164-169
16636311-6 2006 Although a second dose of ATRA or Am580 (a related retinoid selective for retinoic acid receptor-alpha [RARalpha]), given 16 hrs after the first dose, restimulated IRF-1 mRNA and protein levels to a similar level to that obtained by the first dose, IRF-1 was predominantly concentrated in the nucleus after restimulation. Tretinoin 26-30 interferon regulatory factor 1 Homo sapiens 249-254
16477621-2 2006 This study was undertaken to investigate the expression of CB1 and CB2 cannabinoid receptors in neurons that develop from retinoic acid (RA)-primed mouse P19 embryonal carcinoma cells. Tretinoin 122-135 cannabinoid receptor 2 (macrophage) Mus musculus 67-70
16477621-2 2006 This study was undertaken to investigate the expression of CB1 and CB2 cannabinoid receptors in neurons that develop from retinoic acid (RA)-primed mouse P19 embryonal carcinoma cells. Tretinoin 137-139 cannabinoid receptor 2 (macrophage) Mus musculus 67-70
16477621-3 2006 Both undifferentiated P19 cells and RA-treated P19 neurons were positive, by using reverse transcription-polymerase chain reaction (RT-PCR), for CB1 (but not CB2) mRNA. Tretinoin 36-38 cannabinoid receptor 2 (macrophage) Mus musculus 158-161
16242776-2 2006 In this study, we demonstrated that a combination treatment with all-trans retinoic acid (ATRA) and TGF-beta1 led to the enhancement of ATRA-induced suppression of cell proliferation, which is accompanied by inhibition of ATRA-induced apoptosis in human leukemia HL-60 cells. Tretinoin 136-140 transforming growth factor beta 1 Homo sapiens 100-109
16242776-2 2006 In this study, we demonstrated that a combination treatment with all-trans retinoic acid (ATRA) and TGF-beta1 led to the enhancement of ATRA-induced suppression of cell proliferation, which is accompanied by inhibition of ATRA-induced apoptosis in human leukemia HL-60 cells. Tretinoin 136-140 transforming growth factor beta 1 Homo sapiens 100-109
16473406-0 2006 ATRA can enhance apoptosis that is induced by Flt3 tyrosine kinase inhibition in Flt3-ITD positive cells. Tretinoin 0-4 fms related receptor tyrosine kinase 3 Homo sapiens 46-50
16473406-0 2006 ATRA can enhance apoptosis that is induced by Flt3 tyrosine kinase inhibition in Flt3-ITD positive cells. Tretinoin 0-4 fms related receptor tyrosine kinase 3 Homo sapiens 81-85
16242776-4 2006 Inhibition of ATRA-induced apoptosis by TGF-beta1 was associated with an increased level of Mcl-1 protein, an anti-apoptotic member of Bcl-2 family, but not with inhibition of mitochondrial membrane depolarization. Tretinoin 14-18 transforming growth factor beta 1 Homo sapiens 40-49
16473406-4 2006 The combined treatment with ATRA and D-65476 also led to a pronounced down-regulation of surviv in on mRNA and protein level in Flt3-ITD but not in Flt3 wildtype expressing cells (THP-1). Tretinoin 28-32 fms related receptor tyrosine kinase 3 Homo sapiens 128-132
16242776-4 2006 Inhibition of ATRA-induced apoptosis by TGF-beta1 was associated with an increased level of Mcl-1 protein, an anti-apoptotic member of Bcl-2 family, but not with inhibition of mitochondrial membrane depolarization. Tretinoin 14-18 BCL2 apoptosis regulator Homo sapiens 135-140
16473406-4 2006 The combined treatment with ATRA and D-65476 also led to a pronounced down-regulation of surviv in on mRNA and protein level in Flt3-ITD but not in Flt3 wildtype expressing cells (THP-1). Tretinoin 28-32 fms related receptor tyrosine kinase 3 Homo sapiens 148-152
16473406-4 2006 The combined treatment with ATRA and D-65476 also led to a pronounced down-regulation of surviv in on mRNA and protein level in Flt3-ITD but not in Flt3 wildtype expressing cells (THP-1). Tretinoin 28-32 GLI family zinc finger 2 Homo sapiens 180-185
16473406-7 2006 We suggest that regulation of inhibitors of apoptosis might play a crucial role how ATRA can increase the proapoptotic effect of Flt3 inhibitors in myeloid leukemia cells expressing Flt3-ITD. Tretinoin 84-88 fms related receptor tyrosine kinase 3 Homo sapiens 129-133
16242776-6 2006 Upregulation of c-FLIP(L) protein, an inhibitor of apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), correspond with inhibition of ATRA-induced (autocrine TRAIL-mediated) caspase-8 activation and apoptosis. Tretinoin 167-171 CASP8 and FADD like apoptosis regulator Homo sapiens 16-25
16242776-6 2006 Upregulation of c-FLIP(L) protein, an inhibitor of apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), correspond with inhibition of ATRA-induced (autocrine TRAIL-mediated) caspase-8 activation and apoptosis. Tretinoin 167-171 TNF superfamily member 10 Homo sapiens 72-127
16242776-6 2006 Upregulation of c-FLIP(L) protein, an inhibitor of apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), correspond with inhibition of ATRA-induced (autocrine TRAIL-mediated) caspase-8 activation and apoptosis. Tretinoin 167-171 TNF superfamily member 10 Homo sapiens 129-134
16242776-6 2006 Upregulation of c-FLIP(L) protein, an inhibitor of apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), correspond with inhibition of ATRA-induced (autocrine TRAIL-mediated) caspase-8 activation and apoptosis. Tretinoin 167-171 TNF superfamily member 10 Homo sapiens 191-196
16473406-7 2006 We suggest that regulation of inhibitors of apoptosis might play a crucial role how ATRA can increase the proapoptotic effect of Flt3 inhibitors in myeloid leukemia cells expressing Flt3-ITD. Tretinoin 84-88 fms related receptor tyrosine kinase 3 Homo sapiens 182-186
16246418-4 2006 Concomitantly, treatment of HL-60 cells with the combination of TGFbeta1 and the retinoid partially suppresses ATRA-dependent induction of TRAIL. Tretinoin 111-115 transforming growth factor beta 1 Homo sapiens 64-72
16246418-4 2006 Concomitantly, treatment of HL-60 cells with the combination of TGFbeta1 and the retinoid partially suppresses ATRA-dependent induction of TRAIL. Tretinoin 111-115 TNF superfamily member 10 Homo sapiens 139-144
16352814-4 2006 ATRA-induced activation was mediated by a region in the PU.1 promoter to which CEBPB and OCT-1 binding were induced. Tretinoin 0-4 solute carrier family 22 member 1 Homo sapiens 89-94
16638120-9 2006 In NB4 cells undergoing retinoic acid mediated differentiation, the level of endogenous hARD1 and NATH protein decreases while the level of hARD2 protein is stable. Tretinoin 24-37 N-alpha-acetyltransferase 15, NatA auxiliary subunit Homo sapiens 98-102
16680587-10 2006 Retinoic acid x10(-5) M completely abrogated the proliferative actions of IGF II (70.2% +/- 9.7%, P < 0.05) but had no significant effect on the IGF I response (P > 0.05). Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 74-79
16581781-7 2006 Expression of the PNT domain, alone, disrupts the GABPalpha-p300 interaction and decreases the RA responsiveness of the CD18 proximal promoter. Tretinoin 95-97 integrin subunit beta 2 Homo sapiens 120-124
16609697-6 2006 Treatment of Xenopus embryos with lithium chloride (LiCl), ultraviolet irradiation (UV), or retinoic acid (RA) revealed that MT3-MMP levels increased with LiCl-dorsalizing treatments and decreased with UV-ventralizing and RA-anterior neural truncating treatments. Tretinoin 92-105 matrix metallopeptidase 16 L homeolog Xenopus laevis 125-132
16609697-6 2006 Treatment of Xenopus embryos with lithium chloride (LiCl), ultraviolet irradiation (UV), or retinoic acid (RA) revealed that MT3-MMP levels increased with LiCl-dorsalizing treatments and decreased with UV-ventralizing and RA-anterior neural truncating treatments. Tretinoin 107-109 matrix metallopeptidase 16 L homeolog Xenopus laevis 125-132
16581781-1 2006 Expression of CD18, the beta chain of the leukocyte integrins, is transcriptionally regulated by retinoic acid (RA) in myeloid cells. Tretinoin 97-110 integrin subunit beta 2 Homo sapiens 14-18
16581781-1 2006 Expression of CD18, the beta chain of the leukocyte integrins, is transcriptionally regulated by retinoic acid (RA) in myeloid cells. Tretinoin 112-114 integrin subunit beta 2 Homo sapiens 14-18
16581781-2 2006 Full RA responsiveness of the CD18 gene requires its proximal promoter, which lacks a retinoic acid response element (RARE). Tretinoin 5-7 integrin subunit beta 2 Homo sapiens 30-34
16581781-3 2006 Rather, RA responsiveness of the CD18 proximal promoter requires ets sites that are bound by GA-binding protein (GABP). Tretinoin 8-10 integrin subunit beta 2 Homo sapiens 33-37
16539842-0 2006 All-trans retinoic acid inhibited angiotensin II-induced increase in cell growth and collagen secretion of neonatal cardiac fibroblasts. Tretinoin 10-23 angiotensinogen Rattus norvegicus 34-48
16539842-1 2006 AIM: To determine whether all-trans retinoic acid (atRA) acts to modulate angiotensin II (Ang II)-induced cardiac fibroblast cell growth and collagen secretion. Tretinoin 36-49 angiotensinogen Rattus norvegicus 74-88
16539842-1 2006 AIM: To determine whether all-trans retinoic acid (atRA) acts to modulate angiotensin II (Ang II)-induced cardiac fibroblast cell growth and collagen secretion. Tretinoin 51-55 angiotensinogen Rattus norvegicus 74-88
16539842-1 2006 AIM: To determine whether all-trans retinoic acid (atRA) acts to modulate angiotensin II (Ang II)-induced cardiac fibroblast cell growth and collagen secretion. Tretinoin 51-55 angiotensinogen Rattus norvegicus 90-96
16539842-4 2006 RESULTS: atRA (10(-7) to 10(-5) mol/L) inhibited the Ang II-induced increase in cell growth of CF (P<0.05). Tretinoin 9-13 angiotensinogen Rattus norvegicus 53-59
16539842-7 2006 Exposure of CF to atRA (10(-5) mol/L) attenuated the Ang II-induced increase in the secretion of collagen types I and III (P<0.05). Tretinoin 18-22 angiotensinogen Rattus norvegicus 53-59
16539842-8 2006 atRA (10(-5) mol/L) also blocked the Ang II-induced increase in the expression of TGF-beta1. Tretinoin 0-4 angiotensinogen Rattus norvegicus 37-43
16539842-8 2006 atRA (10(-5) mol/L) also blocked the Ang II-induced increase in the expression of TGF-beta1. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 82-91
16539842-9 2006 CONCLUSION: atRA inhibits the Ang II-induced increase in cell growth and collagen secretion of neonatal rat CF. Tretinoin 12-16 angiotensinogen Rattus norvegicus 30-36
16539842-10 2006 The effect of atRA is possibly mediated by lowering the TGF-beta1 level. Tretinoin 14-18 transforming growth factor, beta 1 Rattus norvegicus 56-65
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 47-60 epidermal growth factor receptor Homo sapiens 75-79
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 62-65 epidermal growth factor receptor Homo sapiens 75-79
16581781-9 2006 A dominant negative p300 construct disrupts enhanceosome formation and reduces the RA responsiveness of CD18. Tretinoin 83-85 integrin subunit beta 2 Homo sapiens 104-108
16581781-10 2006 Thus, proteins on the CD18 proximal promoter recruit the distal RARE in the presence of RA. Tretinoin 64-66 integrin subunit beta 2 Homo sapiens 22-26
16581781-11 2006 This is the first description of an RA-induced enhanceosome and demonstrates that GABP and p300 are essential components of CD18 RA responsiveness in myeloid cells. Tretinoin 36-38 integrin subunit beta 2 Homo sapiens 124-128
16581781-11 2006 This is the first description of an RA-induced enhanceosome and demonstrates that GABP and p300 are essential components of CD18 RA responsiveness in myeloid cells. Tretinoin 129-131 integrin subunit beta 2 Homo sapiens 124-128
16875555-1 2006 OBJECTIVE: To explore the biological effect on NB4 cells proliferation, all-trans retinoic acid (ATRA) inducing differentiation and resistance to apoptosis by vascular endothelial growth factor (VEGF)-C cDNA transfection. Tretinoin 72-95 vascular endothelial growth factor A Homo sapiens 159-193
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 WT1 transcription factor Homo sapiens 343-346
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 BCL2 apoptosis regulator Homo sapiens 348-353
16875555-1 2006 OBJECTIVE: To explore the biological effect on NB4 cells proliferation, all-trans retinoic acid (ATRA) inducing differentiation and resistance to apoptosis by vascular endothelial growth factor (VEGF)-C cDNA transfection. Tretinoin 72-95 vascular endothelial growth factor A Homo sapiens 195-199
16875555-1 2006 OBJECTIVE: To explore the biological effect on NB4 cells proliferation, all-trans retinoic acid (ATRA) inducing differentiation and resistance to apoptosis by vascular endothelial growth factor (VEGF)-C cDNA transfection. Tretinoin 97-101 vascular endothelial growth factor A Homo sapiens 159-193
16875555-1 2006 OBJECTIVE: To explore the biological effect on NB4 cells proliferation, all-trans retinoic acid (ATRA) inducing differentiation and resistance to apoptosis by vascular endothelial growth factor (VEGF)-C cDNA transfection. Tretinoin 97-101 vascular endothelial growth factor A Homo sapiens 195-199
16875555-10 2006 The expression level of C/EBPalpha gene of NB4/VEGF-C cells on ATRA treatment was only 1/32 that of NB4/pcDNA3.1 cells. Tretinoin 63-67 CCAAT enhancer binding protein alpha Homo sapiens 24-34
16875555-10 2006 The expression level of C/EBPalpha gene of NB4/VEGF-C cells on ATRA treatment was only 1/32 that of NB4/pcDNA3.1 cells. Tretinoin 63-67 vascular endothelial growth factor A Homo sapiens 47-51
16875555-13 2006 CONCLUSION: The VEGF-C via VEGFR-3 signaling pathway could promote the proliferation of leukemic cells by autocrine pathway and inhibit the cell differentiation mediated by ATRA and chemotherapy-induced apoptosis. Tretinoin 173-177 vascular endothelial growth factor C Homo sapiens 16-22
16288212-0 2006 The phosphoinositide 3-kinase/Akt pathway is essential for the retinoic acid-induced differentiation of F9 cells. Tretinoin 63-76 thymoma viral proto-oncogene 1 Mus musculus 30-33
16288212-3 2006 We report that, in mouse embryocarcinoma cells (F9 cells), RA induces an early activation of PI3K and Akt via an increase in the expression of the p85alpha regulatory subunit. Tretinoin 59-61 thymoma viral proto-oncogene 1 Mus musculus 102-105
16288212-6 2006 We propose a model through which RA induces a biphasic regulation of Akt with an activation participating to the differentiation process, followed by an inhibition, which has been correlated to the RA-induced growth arrest. Tretinoin 33-35 thymoma viral proto-oncogene 1 Mus musculus 69-72
16288212-6 2006 We propose a model through which RA induces a biphasic regulation of Akt with an activation participating to the differentiation process, followed by an inhibition, which has been correlated to the RA-induced growth arrest. Tretinoin 198-200 thymoma viral proto-oncogene 1 Mus musculus 69-72
16508168-5 2006 The ATPase activity and P-gp mRNA expression in Caco-2 cells were induced by all-trans-retinoic acid, digoxin and levothyroxine, but not dexamethasone or rifampicin. Tretinoin 77-100 ATP binding cassette subfamily B member 1 Homo sapiens 24-28
16352598-4 2006 The forced expression of the alpha-variant RNA caused the down-regulation of oct-3/4 and nanog mRNA expression during the 12-48 h of the late-early stages of neural differentiation and was sufficient to convert P19 cells into neurons (but not glial cells) when the cells were cultured in aggregated form without retinoic acid. Tretinoin 312-325 Nanog homeobox Mus musculus 89-94
16257998-0 2006 All-trans retinoic acid modulates radiation-induced proliferation of lung fibroblasts via IL-6/IL-6R system. Tretinoin 10-23 interleukin 6 Homo sapiens 90-94
16257998-0 2006 All-trans retinoic acid modulates radiation-induced proliferation of lung fibroblasts via IL-6/IL-6R system. Tretinoin 10-23 interleukin 6 receptor Homo sapiens 95-100
16257998-6 2006 Irradiation also increased the levels of mRNA for IL-6R and gp130, which were blocked by coexisting ATRA. Tretinoin 100-104 interleukin 6 receptor Homo sapiens 50-55
16257998-7 2006 Furthermore, IL-6 stimulated cell proliferation in dose-dependent manner but was overcome by pharmacological concentration of ATRA. Tretinoin 126-130 interleukin 6 Homo sapiens 13-17
16257998-9 2006 Finally, we demonstrated that IL-6 transcripts in the lung were upregulated at 2 mo after irradiation, and the effect was inhibited by the intraperitoneal administration of ATRA. Tretinoin 173-177 interleukin 6 Homo sapiens 30-34
16757381-0 2006 Retinoic acids and trichostatin A (TSA), a histone deacetylase inhibitor, induce human pyruvate dehydrogenase kinase 4 (PDK4) gene expression. Tretinoin 0-14 pyruvate dehydrogenase kinase 4 Homo sapiens 87-118
16757381-0 2006 Retinoic acids and trichostatin A (TSA), a histone deacetylase inhibitor, induce human pyruvate dehydrogenase kinase 4 (PDK4) gene expression. Tretinoin 0-14 pyruvate dehydrogenase kinase 4 Homo sapiens 120-124
16554478-5 2006 In addition, we find that nuclear retinoid signaling is required for the expression of a retinoic acid-degrading enzyme, Cyp26B1, in a small fraction of mature neurons. Tretinoin 89-102 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 121-128
16304046-5 2006 Conversely, separate blockage of the Akt/mTor-signaling pathway was a prerequisite for overcoming apoptosis resistance to VPA/ATRA in FLT3-ITD cells, and primary AML blasts (n = 9). Tretinoin 126-130 AKT serine/threonine kinase 1 Homo sapiens 37-40
16304046-2 2006 We here show that BCR/ABL-, but not FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD)-transformed 32D cells or primary acute myeloid leukemia (AML) blasts undergo apoptosis after treatment with the HDI valproic acid (VPA) plus all-trans retinoic acid (VPA/ATRA). Tretinoin 255-268 BCR activator of RhoGEF and GTPase Mus musculus 18-21
16757381-2 2006 We report here that retinoic acids (RA) as well as Trichostatin A (TSA), an inhibitor of histone deacetylase (HDAC), regulate PDK4 gene expression. Tretinoin 20-34 pyruvate dehydrogenase kinase 4 Homo sapiens 126-130
16757381-2 2006 We report here that retinoic acids (RA) as well as Trichostatin A (TSA), an inhibitor of histone deacetylase (HDAC), regulate PDK4 gene expression. Tretinoin 36-38 pyruvate dehydrogenase kinase 4 Homo sapiens 126-130
16757381-3 2006 Two retinoic acid response elements (RAREs) to which retinoid X receptor alpha (RXRalpha) and retinoic acid receptor alpha (RARalpha) bind and activate transcription are present in the human PDK4 (hPDK4) proximal promoter. Tretinoin 4-17 pyruvate dehydrogenase kinase 4 Homo sapiens 191-195
16757381-3 2006 Two retinoic acid response elements (RAREs) to which retinoid X receptor alpha (RXRalpha) and retinoic acid receptor alpha (RARalpha) bind and activate transcription are present in the human PDK4 (hPDK4) proximal promoter. Tretinoin 4-17 pyruvate dehydrogenase kinase 4 Homo sapiens 197-202
16757381-6 2006 By the chromatin immunoprecipitation assay, RA and TSA increase acetylation of histones bound to the proximal promoter as well as occupancy of CBP and Sp1. Tretinoin 44-46 CREB binding protein Homo sapiens 143-146
16757381-8 2006 The p300/CBP may enhance acetylation of histones bound to the hPDK4 promoter and cooperate with Sp1 and CBF to stimulate transcription of the hPDK4 gene in response to RA and TSA. Tretinoin 168-170 CREB binding protein Homo sapiens 9-12
16757381-8 2006 The p300/CBP may enhance acetylation of histones bound to the hPDK4 promoter and cooperate with Sp1 and CBF to stimulate transcription of the hPDK4 gene in response to RA and TSA. Tretinoin 168-170 pyruvate dehydrogenase kinase 4 Homo sapiens 62-67
16757381-8 2006 The p300/CBP may enhance acetylation of histones bound to the hPDK4 promoter and cooperate with Sp1 and CBF to stimulate transcription of the hPDK4 gene in response to RA and TSA. Tretinoin 168-170 pyruvate dehydrogenase kinase 4 Homo sapiens 142-147
16304046-2 2006 We here show that BCR/ABL-, but not FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD)-transformed 32D cells or primary acute myeloid leukemia (AML) blasts undergo apoptosis after treatment with the HDI valproic acid (VPA) plus all-trans retinoic acid (VPA/ATRA). Tretinoin 274-278 BCR activator of RhoGEF and GTPase Mus musculus 18-21
16360957-8 2006 The enhanced expression of TIG3 mRNA tumor suppressor gene by ATRA incorporation into DOTAP/cholesterol liposomes might partly explain the mechanism of enhanced cytotoxicity and/or apoptosis. Tretinoin 62-66 phospholipase A and acyltransferase 4 Homo sapiens 27-31
16322068-0 2006 All-trans retinoic acid inhibits vascular endothelial growth factor expression in a cell model of neutrophil activation. Tretinoin 10-23 vascular endothelial growth factor A Homo sapiens 33-67
16322068-8 2006 Examination of the regulation of VEGF using differentiated HL-60 cells as a model, revealed that atRA induced a dose- and time-dependent suppression of VEGF mRNA and protein. Tretinoin 97-101 vascular endothelial growth factor A Homo sapiens 33-37
16322068-8 2006 Examination of the regulation of VEGF using differentiated HL-60 cells as a model, revealed that atRA induced a dose- and time-dependent suppression of VEGF mRNA and protein. Tretinoin 97-101 vascular endothelial growth factor A Homo sapiens 152-156
16322068-10 2006 Because retinoic acid is synthesized de novo in endometrial cells under the influence of progesterone, our findings suggest that the up-regulated VEGF and angiogenesis in tissue from women with endometriosis may reflect failure of neutrophil differentiation in these cases, and provide a rationale for retinoid therapy in this condition. Tretinoin 8-21 vascular endothelial growth factor A Homo sapiens 146-150
16530516-0 2006 All-trans retinoic acid induces XAF1 expression through an interferon regulatory factor-1 element in colon cancer. Tretinoin 10-23 XIAP associated factor 1 Mus musculus 32-36
16530516-3 2006 The aim of this study was to determine the effect and mechanism of ATRA on XAF1 expression and the role of XAF1 in ATRA-induced growth inhibition in colon cancer. Tretinoin 67-71 XIAP associated factor 1 Mus musculus 75-79
16530516-11 2006 ATRA induces XAF1 expression both in vitro and in vivo through interaction with IRF-E-XAF1. Tretinoin 0-4 XIAP associated factor 1 Mus musculus 13-17
16530516-11 2006 ATRA induces XAF1 expression both in vitro and in vivo through interaction with IRF-E-XAF1. Tretinoin 0-4 XIAP associated factor 1 Mus musculus 86-90
16530516-12 2006 Overexpression of XAF1 increases cell susceptibility to ATRA-induced growth suppression both in vitro and in vivo. Tretinoin 56-60 XIAP associated factor 1 Mus musculus 18-22
16522742-1 2006 Farnesoid X receptor (FXR), the receptor for bile acids, including chenodeoxycholic acid (CDCA), is a member of the nuclear receptor superfamily, which also includes the receptors for retinoic acid, vitamin D (D3), thyroid hormone, thiazolidinedione and 22(R)-hydroxycholesterol. Tretinoin 184-197 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 10-20
16411021-0 2006 Down regulation of N-acetylglucosaminyltransferase V facilitates all-transretinoic acid to induce apoptosis of human hepatocarcinoma cells. Tretinoin 69-87 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 19-52
16411021-1 2006 After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80 microM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. Tretinoin 205-227 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 6-39
16411021-1 2006 After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80 microM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. Tretinoin 205-227 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 41-46
16411021-1 2006 After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80 microM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. Tretinoin 229-233 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 6-39
16411021-1 2006 After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80 microM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. Tretinoin 229-233 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 41-46
16411021-1 2006 After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80 microM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. Tretinoin 258-262 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 6-39
16411021-1 2006 After N-acetylglucosaminyltransferase V (GnT-V) activity was down-regulated by the transfection of its antisense cDNA(GnTV-AS), apoptosis of H7721 cells was appeared and the apoptosis induced by 80 microM all-transretinoic acid (ATRA) was facilitated, while ATRA itself could not induce apparent apoptosis in mock cells transfected with the vector. Tretinoin 258-262 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 41-46
16274701-4 2006 Similarly, the increase of Akt activation, as well as PTEN inactivation, was accompanied both by a decrease of CKIepsilon expression induced by all-trans retinoic acid and by the addition of a specific inhibitor for CKIepsilon in HL-60 cells. Tretinoin 154-167 AKT serine/threonine kinase 1 Homo sapiens 27-30
16456540-2 2006 Here we show that during RA-dependent activation of the RARalpha isotype, the p160 coactivator pCIP/ACTR/AIB-1/RAC-3/TRAM-1/SRC-3 is phosphorylated by p38MAPK. Tretinoin 25-27 MYB binding protein 1a Homo sapiens 78-82
16456540-2 2006 Here we show that during RA-dependent activation of the RARalpha isotype, the p160 coactivator pCIP/ACTR/AIB-1/RAC-3/TRAM-1/SRC-3 is phosphorylated by p38MAPK. Tretinoin 25-27 Rac family small GTPase 3 Homo sapiens 111-116
16456540-2 2006 Here we show that during RA-dependent activation of the RARalpha isotype, the p160 coactivator pCIP/ACTR/AIB-1/RAC-3/TRAM-1/SRC-3 is phosphorylated by p38MAPK. Tretinoin 25-27 translocation associated membrane protein 1 Homo sapiens 117-123
16223781-0 2006 Up-regulation of MDR1 and induction of doxorubicin resistance by histone deacetylase inhibitor depsipeptide (FK228) and ATRA in acute promyelocytic leukemia cells. Tretinoin 120-124 ATP binding cassette subfamily B member 1 Homo sapiens 17-21
16463413-1 2006 BACKGROUND: The retinoic acid (RA)-catabolizing enzyme Cyp26a1 plays an important role in protecting tailbud tissues from inappropriate exposure to RA. Tretinoin 16-29 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 55-62
16463413-1 2006 BACKGROUND: The retinoic acid (RA)-catabolizing enzyme Cyp26a1 plays an important role in protecting tailbud tissues from inappropriate exposure to RA. Tretinoin 31-33 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 55-62
16463413-1 2006 BACKGROUND: The retinoic acid (RA)-catabolizing enzyme Cyp26a1 plays an important role in protecting tailbud tissues from inappropriate exposure to RA. Tretinoin 148-150 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 55-62
16397143-5 2006 Interestingly, inactivation of RhoA with C3-exoenzyme or treatment with ROK inhibitors strongly inhibited myocardin mRNA expression in retinoic acid-treated A404 cells or human iliac vein SMCs. Tretinoin 135-148 ras homolog family member A Homo sapiens 31-35
16410076-8 2006 Further study showed that atRA inhibited phosphorylation of Smad2 and Smad3 and increased Smad7 expression. Tretinoin 26-30 SMAD family member 2 Mus musculus 60-65
16223781-3 2006 The combination of ATRA and the novel histone deacetylase inhibitor (HDACI) depsipeptide (FK228) induced P-gp expression and prevented growth inhibition and apoptosis in NB4 APL cells subsequently exposed to doxorubicin (DOX). Tretinoin 19-23 ATP binding cassette subfamily B member 1 Homo sapiens 105-109
16223781-5 2006 Both agents, ATRA or FK228, induced MDR1 mRNA. Tretinoin 13-17 ATP binding cassette subfamily B member 1 Homo sapiens 36-40
16223781-6 2006 This effect was significantly enhanced by ATRA/FK228 administered in combination, due in part to increased H4 and H3-Lys9 acetylation of the MDR1 promoter and recruitment of the nuclear transcription factor Y alpha (NFYA) transcription activator to the CCAAT box. Tretinoin 42-46 ATP binding cassette subfamily B member 1 Homo sapiens 141-145
16223781-7 2006 Cotreatment with specific P-gp inhibitor PSC833 reversed cytoprotective effects of ATRA/FK228. Tretinoin 83-87 ATP binding cassette subfamily B member 1 Homo sapiens 26-30
16223781-8 2006 G1 cell-cycle arrest and p21 mRNA induction were also observed in response to ATRA/FK228, which may restrict DOX-induced apoptosis of cells in G2 phase. Tretinoin 78-82 cyclin dependent kinase inhibitor 1A Homo sapiens 25-28
16223781-9 2006 These results indicate that epigenetic mechanisms involving NF-YA transcription factor recruitment and histone acetylation are activated by ATRA and HDACI, induce MDR1 in APL cells, and point to the critical importance of mechanism-based sequential therapy in future clinical trials that combine HDAC inhibitors, ATRA, and anthracyclines. Tretinoin 140-144 ATP binding cassette subfamily B member 1 Homo sapiens 163-167
16509872-2 2006 The aim of the present study was to determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and alkaline phosphatase (ALP) activity in the human pancreatic cancer cell line PANC-1 in vitro. Tretinoin 72-95 alkaline phosphatase, placental Homo sapiens 134-154
16439309-0 2006 Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 75-78
16439309-1 2006 Retinoic acid (RA) is known to cause MAPK signaling which propels G0 arrest and myeloid differentiation of HL-60 human myeloblastic leukemia cells. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 37-41
16439309-1 2006 Retinoic acid (RA) is known to cause MAPK signaling which propels G0 arrest and myeloid differentiation of HL-60 human myeloblastic leukemia cells. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 37-41
16439309-7 2006 SLP-76 now enhanced RA-induced ERK activation, compared to parental c-FMS transfectants. Tretinoin 20-22 mitogen-activated protein kinase 1 Homo sapiens 31-34
16439309-10 2006 A triple Y to F mutant SLP-76 known to be a dominant negative in T-cell receptor signaling failed to enhance RA-induced paxillin expression, but enhanced RA-induced ERK activation, differentiation and G0 arrest essentially as well as wild-type SLP-76. Tretinoin 154-156 mitogen-activated protein kinase 1 Homo sapiens 165-168
16509872-2 2006 The aim of the present study was to determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and alkaline phosphatase (ALP) activity in the human pancreatic cancer cell line PANC-1 in vitro. Tretinoin 72-95 alkaline phosphatase, placental Homo sapiens 156-159
16509872-2 2006 The aim of the present study was to determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and alkaline phosphatase (ALP) activity in the human pancreatic cancer cell line PANC-1 in vitro. Tretinoin 97-101 alkaline phosphatase, placental Homo sapiens 134-154
16509872-2 2006 The aim of the present study was to determine the inhibitory effects of all-trans-retinoic acid (ATRA) on cell growth, cell cycle and alkaline phosphatase (ALP) activity in the human pancreatic cancer cell line PANC-1 in vitro. Tretinoin 97-101 alkaline phosphatase, placental Homo sapiens 156-159
16509872-7 2006 The ALP activity of PANC-1 cells was significantly increased by 1-50 micromol/L ATRA. Tretinoin 80-84 alkaline phosphatase, placental Homo sapiens 4-7
16509872-8 2006 CONCLUSIONS: The antitumor effects of ATRA on human pancreatic cancer cells are associated with G2/M phase arrest and increased ALP activity. Tretinoin 38-42 alkaline phosphatase, placental Homo sapiens 128-131
16385345-6 2006 However, the effects of all-trans retinoic acid (RA) on cellular expression of VEGF are determined by both cell type and genotype. Tretinoin 34-47 vascular endothelial growth factor A Homo sapiens 79-83
16385345-6 2006 However, the effects of all-trans retinoic acid (RA) on cellular expression of VEGF are determined by both cell type and genotype. Tretinoin 49-51 vascular endothelial growth factor A Homo sapiens 79-83
16406367-3 2006 Conversely, the downregulation of GnT-V expression by small interfering RNA resulted in a decrease in the susceptibility to cell apoptosis induced by retinoic acid in NBL cells accompanied by morphological change. Tretinoin 150-163 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 34-39
16385345-7 2006 RA inhibits KC production of VEGF in a genotype-dependent manner (P < 0.005) whereas RA stimulates PBMCs production irrespective of VEGF genotype (P < 0.001). Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 29-33
16280361-7 2006 Inhibition of protein kinase C (PKC) or extracellular regulated kinase (ERK1/2) blocked the RA-mediated activation of CREB. Tretinoin 92-94 mitogen-activated protein kinase 3 Homo sapiens 72-78
16280361-9 2006 Altogether, this study provides the first evidence that RA rapidly activates CREB transcription factor via PKC, ERK, and RSK in a retinoid receptor-independent manner in normal bronchial epithelial cells. Tretinoin 56-58 mitogen-activated protein kinase 1 Homo sapiens 112-115
16280361-9 2006 Altogether, this study provides the first evidence that RA rapidly activates CREB transcription factor via PKC, ERK, and RSK in a retinoid receptor-independent manner in normal bronchial epithelial cells. Tretinoin 56-58 ribosomal protein S6 kinase A2 Homo sapiens 121-124
16454184-3 2006 The stains on pancreas of Wistar rat at STZ induced diabetes, which was subcutaneous administered nanoegg -atRA 6 mg/head/week for 141 days, showed not only the expression of PDX-1 but also the presence of beta cell in islet of Langerhans. Tretinoin 107-111 pancreatic and duodenal homeobox 1 Rattus norvegicus 175-180
16158052-0 2006 Retinoic acid receptors and tissue-transglutaminase mediate short-term effect of retinoic acid on migration and invasion of neuroblastoma SH-SY5Y cells. Tretinoin 81-94 transglutaminase 2 Homo sapiens 28-51
16158052-3 2006 RA induces expression of tissue-transglutaminase (TGase) and promotes migration and invasion after 24 h of treatment in SH-SY5Y cells, but not in IMR-32 cells. Tretinoin 0-2 transglutaminase 2 Homo sapiens 25-48
16158052-9 2006 Overexpression of TGase has no effect on migration or invasion, while overexpression of antisense TGase blocks RA-induced migration and invasion, indicating that other molecules along with TGase mediate RA effects. Tretinoin 111-113 transglutaminase 2 Homo sapiens 98-103
16158052-9 2006 Overexpression of TGase has no effect on migration or invasion, while overexpression of antisense TGase blocks RA-induced migration and invasion, indicating that other molecules along with TGase mediate RA effects. Tretinoin 111-113 transglutaminase 2 Homo sapiens 98-103
16158052-3 2006 RA induces expression of tissue-transglutaminase (TGase) and promotes migration and invasion after 24 h of treatment in SH-SY5Y cells, but not in IMR-32 cells. Tretinoin 0-2 transglutaminase 2 Homo sapiens 50-55
16158052-9 2006 Overexpression of TGase has no effect on migration or invasion, while overexpression of antisense TGase blocks RA-induced migration and invasion, indicating that other molecules along with TGase mediate RA effects. Tretinoin 203-205 transglutaminase 2 Homo sapiens 98-103
17361080-0 2006 Epidermal growth factor-, transforming growth factor-beta-, retinoic acid- and 1,25-dihydroxyvitamin D3-regulated expression of the novel protein PTPIP51 in keratinocytes. Tretinoin 60-73 regulator of microtubule dynamics 3 Homo sapiens 146-153
16158052-9 2006 Overexpression of TGase has no effect on migration or invasion, while overexpression of antisense TGase blocks RA-induced migration and invasion, indicating that other molecules along with TGase mediate RA effects. Tretinoin 203-205 transglutaminase 2 Homo sapiens 98-103
16178820-6 2006 Accordingly, the addition of retinoic acid uncouples the respiration of the UCP1-expressing clone, but not that of the UCP3-expressing ones. Tretinoin 29-42 mitochondrial brown fat uncoupling protein 1 Cricetulus griseus 76-80
17168722-6 2006 It is also interesting to note that basal and RA-induced RARbeta mRNA levels tend to increase with senescence of normal cells. Tretinoin 46-48 retinoic acid receptor beta Homo sapiens 57-64
16430309-17 2006 CYP3A7 has a specific role in hydroxylation of retinoic acid and 16alpha-hydroxylation of steroids, and is therefore of relevance both to normal development and carcinogenesis.CYP3A43 is the most recently discovered CYP3A isoform. Tretinoin 47-60 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 0-6
16430309-17 2006 CYP3A7 has a specific role in hydroxylation of retinoic acid and 16alpha-hydroxylation of steroids, and is therefore of relevance both to normal development and carcinogenesis.CYP3A43 is the most recently discovered CYP3A isoform. Tretinoin 47-60 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-5
16323078-7 2006 Tbx1 expression was obviously reduced, even lost, in the pharyngeal arch and outflow tract in RA treated groups. Tretinoin 94-96 T-box transcription factor 1 Danio rerio 0-4
16316642-0 2006 Retinoic acid activates myogenesis in vivo through Fgf8 signalling. Tretinoin 0-13 fibroblast growth factor 8a Danio rerio 51-55
16316642-5 2006 The expression dynamics of myf5 in presomitic and somitic mesoderm suggest that RA promotes muscle differentiation, a role supported by the fact that RA activates expression of fast myosin, while DEAB represses it. Tretinoin 80-82 myogenic factor 5 Danio rerio 27-31
16316642-5 2006 The expression dynamics of myf5 in presomitic and somitic mesoderm suggest that RA promotes muscle differentiation, a role supported by the fact that RA activates expression of fast myosin, while DEAB represses it. Tretinoin 150-152 myogenic factor 5 Danio rerio 27-31
16316642-8 2006 We propose that, in the developing embryo, localised synthesis of RA by Raldh2 in the anterior psm and in somites activates fgf8 expression which in turn induces the expression of myogenic genes and fast muscle differentiation. Tretinoin 66-68 fibroblast growth factor 8a Danio rerio 124-128
16195406-0 2006 Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action. Tretinoin 83-96 bone morphogenetic protein 4 Mus musculus 0-28
16195406-7 2006 Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do not respond to BMP-4. Tretinoin 8-21 bone morphogenetic protein 4 Mus musculus 35-40
16195406-8 2006 Therefore, retinoic acid induces BMP-4, which participates in the antiproliferative effects of retinoic acid. Tretinoin 11-24 bone morphogenetic protein 4 Mus musculus 33-38
16195406-8 2006 Therefore, retinoic acid induces BMP-4, which participates in the antiproliferative effects of retinoic acid. Tretinoin 95-108 bone morphogenetic protein 4 Mus musculus 33-38
16409128-7 2006 Finally, using the BAC system, we constructed an HSV vector that expressed an inducible human superoxide dismutase-1 (SOD1) gene for delivery into differentiated human NT-neurons (cells of the human embryonal carcinoma cell line NT2, which differentiate irreversibly into postmitotic neuron-like cells after treatment with retinoic acid). Tretinoin 323-336 superoxide dismutase 1 Homo sapiens 118-122
16323078-0 2006 TBX1, a DiGeorge syndrome candidate gene, is inhibited by retinoic acid. Tretinoin 58-71 T-box transcription factor 1 Danio rerio 0-4
16323078-3 2006 Based on these similarities, the effects of RA on Tbx1 expression pattern were explored during pharyngeal arch development in zebrafish. Tretinoin 44-46 T-box transcription factor 1 Danio rerio 50-54
16323078-11 2006 The results suggested that RA could produce an altered Tbx1 expression pattern in zebrafish. Tretinoin 27-29 T-box transcription factor 1 Danio rerio 55-59
16323078-12 2006 In addition, RA could repress Tbx1 expression in a dose-dependent manner. Tretinoin 13-15 T-box transcription factor 1 Danio rerio 30-34
16365604-2 2006 We have previously shown that low-dose interleukin (IL)-2 and 13-cis retinoic acid (RA) decreased VEGF and improved the immune function of patients with advanced tumors treated with chemotherapy. Tretinoin 84-86 vascular endothelial growth factor A Homo sapiens 98-102
16850740-13 2006 Western blotting showed that the amounts of JNK, p38 and ERK proteins in hyperoxia-exposure or RA-treated lung tissues were same as those in untreated lung tissues (P>0.05), whereas activation of these MAPKs was markedly altered by hyperoxia and RA. Tretinoin 95-97 Eph receptor B1 Rattus norvegicus 57-60
16804330-3 2006 In all-trans-retinoic acid (atRA)-treated human aortic smooth muscle cells (AOSMC), significant increases in IL-1beta levels were observed, compared with untreated cells. Tretinoin 3-26 interleukin 1 beta Homo sapiens 109-117
16804330-3 2006 In all-trans-retinoic acid (atRA)-treated human aortic smooth muscle cells (AOSMC), significant increases in IL-1beta levels were observed, compared with untreated cells. Tretinoin 28-32 interleukin 1 beta Homo sapiens 109-117
16804330-5 2006 The results show that atRA-treated AOSMC express both the precursor (33 kDa) and the active form (17 kDa) of the IL-1beta protein. Tretinoin 22-26 interleukin 1 beta Homo sapiens 113-121
16804330-6 2006 atRA-treated carotid lesions showed significantly elevated IL-1beta mRNA levels (2.9 +/- 2.33) compared with untreated lesions (2.0 +/- 1.77; p < 0.05). Tretinoin 0-4 interleukin 1 beta Homo sapiens 59-67
16837774-8 2006 Furthermore, the retinoic acid-catabolizing enzyme CYP26A1 is expressed at higher levels in medial SMCs compared to intimal SMCs. Tretinoin 17-30 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 51-58
16297713-4 2005 A growing evidence indicated that RARbeta(2) was required for the growth inhibitory effect of retinoic acid (RA). Tretinoin 94-107 retinoic acid receptor beta Homo sapiens 34-41
16249966-7 2006 DLEC cells are sensitive to substances known to induce differentiation of mammalian cells such as retinoic acid and phorbol esters. Tretinoin 98-111 C-type lectin domain family 4 member C Homo sapiens 0-4
16289102-6 2005 Moreover, the ATRA-induced expression of RARbeta was also mediated by RARalpha. Tretinoin 14-18 retinoic acid receptor beta Homo sapiens 41-48
16309824-7 2005 In sharp contrast to our previous observations that atRA supplementation enhances IFN-gamma expression and NOS2 pathway activation in LPS-challenged rats [Devaux, Y., Grosjean, S., Seguin, C., David, C., Dousset, B., Zannad, F., Meistelman, C., de Talance, N., Mertes, P.M., Ungureanu-Longrois, D., 2000. Tretinoin 52-56 nitric oxide synthase 2 Rattus norvegicus 107-111
16125842-2 2005 However, we report here that GDNF and neurturin blocked the growth inhibitory and neuritogenic effects of all-trans-retinoic acid in neuroblastoma cells in vitro. Tretinoin 106-129 glial cell derived neurotrophic factor Homo sapiens 29-33
16050810-2 2005 We previously showed that RA inhibited cellular proliferation in part by decreasing expression of the mitogen activated protein kinase ERK1 (extracellular signal regulated kinase 1). Tretinoin 26-28 mitogen-activated protein kinase 3 Homo sapiens 135-139
16050810-2 2005 We previously showed that RA inhibited cellular proliferation in part by decreasing expression of the mitogen activated protein kinase ERK1 (extracellular signal regulated kinase 1). Tretinoin 26-28 mitogen-activated protein kinase 3 Homo sapiens 141-180
16050810-7 2005 CBP clones expressed higher ERK1 protein levels, proliferated faster in culture and were resistant to RA-mediated growth inhibition. Tretinoin 102-104 CREB binding protein Homo sapiens 0-3
16050810-12 2005 CBP and PCAF occupancy of the proximal ERK1 promoter was dramatically decreased by RA treatment. Tretinoin 83-85 CREB binding protein Homo sapiens 0-3
16050810-12 2005 CBP and PCAF occupancy of the proximal ERK1 promoter was dramatically decreased by RA treatment. Tretinoin 83-85 mitogen-activated protein kinase 3 Homo sapiens 39-43
16251210-6 2005 RA signaling was found to play a role in regulating the expression of EphB2, EphB3 and ephrin B2, three molecules whose graded expression in the retina along the DV axis is important for establishing the correct retinotectal map. Tretinoin 0-2 EPH receptor B2 Gallus gallus 70-75
16325577-3 2005 The two factors compete for binding to the miR-223 promoter: NFI-A maintains miR-223 at low levels, whereas its replacement by C/EBPalpha, following retinoic acid (RA)-induced differentiation, upregulates miR-223 expression. Tretinoin 149-162 CCAAT enhancer binding protein alpha Homo sapiens 127-137
16325577-3 2005 The two factors compete for binding to the miR-223 promoter: NFI-A maintains miR-223 at low levels, whereas its replacement by C/EBPalpha, following retinoic acid (RA)-induced differentiation, upregulates miR-223 expression. Tretinoin 164-166 CCAAT enhancer binding protein alpha Homo sapiens 127-137
16105978-7 2005 In in vitro differentiation assays using primary APL blasts (n = 6), the FLT3 inhibitor CEP-701 had a greater effect on cell survival/proliferation in FLT3/ITD+ cells, but this inhibition was reduced in the presence of ATRA. Tretinoin 219-223 fms related receptor tyrosine kinase 3 Homo sapiens 73-77
16105978-8 2005 Furthermore, in the presence of CEP-701, ATRA-induced differentiation was reduced in FLT3/ITD+ cells. Tretinoin 41-45 fms related receptor tyrosine kinase 3 Homo sapiens 85-89
16149052-6 2005 MEK1/2 inhibitors, such as PD98059 and U0126, reduced RA-induced ERK1/2 activity, but could not block the genistein effects. Tretinoin 54-56 mitogen-activated protein kinase 3 Homo sapiens 65-71
16303967-14 2005 Furthermore, ketoconazole, all-trans retinoic acid, and cyclosporine inhibited CYP3A6 mediated [3H]testosterone 6beta hydroxylation in a concentration-dependent manner, with IC50 ranging from 3.73 to 435 microM. Tretinoin 27-50 cytochrome P450 3A6 Oryctolagus cuniculus 79-85
16102944-8 2005 RESULTS: EGCG, like RA, decreased the level of MMPs production and increased TIMP-1 expression level. Tretinoin 20-22 TIMP metallopeptidase inhibitor 1 Homo sapiens 77-83
16149052-4 2005 Additionally, genistein enhanced RA-induced neuronal differentiation by increasing the activation of extracellular signal-related kinase 1/2 (ERK1/2) via phosphorylation at Thr183 and Tyr185 in 3-7 days. Tretinoin 33-35 mitogen-activated protein kinase 3 Homo sapiens 101-140
16149052-4 2005 Additionally, genistein enhanced RA-induced neuronal differentiation by increasing the activation of extracellular signal-related kinase 1/2 (ERK1/2) via phosphorylation at Thr183 and Tyr185 in 3-7 days. Tretinoin 33-35 mitogen-activated protein kinase 3 Homo sapiens 142-148
16102944-10 2005 RA decreased the MMP-1 and MMP-3 expression levels to a greater extent than EGCG. Tretinoin 0-2 matrix metallopeptidase 3 Homo sapiens 27-32
16386082-0 2005 Retinoic acid induces VEGF gene expression in human retinal pigment epithelial cells (ARPE-19). Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 22-26
16386082-1 2005 PURPOSE: The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells. Tretinoin 122-135 vascular endothelial growth factor A Homo sapiens 65-99
16386082-1 2005 PURPOSE: The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells. Tretinoin 122-135 vascular endothelial growth factor A Homo sapiens 101-105
16126938-8 2005 The NR ligands, vitamin D(3), trans/cis RA, glucocorticoids, and thiazolidines, induce dramatic changes in the physiology of cells harboring high Wnt/beta-catenin/Tcf activity. Tretinoin 40-42 hepatocyte nuclear factor 4 alpha Homo sapiens 163-166
16386082-1 2005 PURPOSE: The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells. Tretinoin 137-139 vascular endothelial growth factor A Homo sapiens 65-99
16386082-1 2005 PURPOSE: The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells. Tretinoin 137-139 vascular endothelial growth factor A Homo sapiens 101-105
16386082-5 2005 RESULTS: All-trans retinoic acid (atRA) time-dependently increased VEGF mRNA levels. Tretinoin 19-32 vascular endothelial growth factor A Homo sapiens 67-71
16386082-6 2005 The effect of atRA was dose-dependent in a range between 10(-7) M and 10(-6) M. Treatment with actinomycin D revealed that atRA induces the VEGF gene at the transcriptional level. Tretinoin 14-18 vascular endothelial growth factor A Homo sapiens 140-144
16386082-6 2005 The effect of atRA was dose-dependent in a range between 10(-7) M and 10(-6) M. Treatment with actinomycin D revealed that atRA induces the VEGF gene at the transcriptional level. Tretinoin 123-127 vascular endothelial growth factor A Homo sapiens 140-144
16386082-7 2005 Of the various RAs tested, atRA was the most potent inducer of the VEGF gene. Tretinoin 27-31 vascular endothelial growth factor A Homo sapiens 67-71
16386082-8 2005 CONCLUSIONS: We demonstrated that atRA stimulates the induction of the VEGF gene in ARPE-19 cells, suggesting a novel pathway for the development of age-related macular degeneration. Tretinoin 34-38 vascular endothelial growth factor A Homo sapiens 71-75
16116481-0 2005 Vascular endothelial growth factor acts in an autocrine manner in rhabdomyosarcoma cell lines and can be inhibited with all-trans-retinoic acid. Tretinoin 120-143 vascular endothelial growth factor A Homo sapiens 0-34
16403252-7 2005 HDAC inhibitors such as trichostatin A, in combination with ATRA, induce differentiation of the blast/promyelocytic cells from PLZF-RARa/RARa-PLZF double TM, but not ATRA alone. Tretinoin 60-64 zinc finger and BTB domain containing 16 Mus musculus 127-131
16279770-0 2005 Novel tetralone-derived retinoic acid metabolism blocking agents: synthesis and in vitro evaluation with liver microsomal and MCF-7 CYP26A1 cell assays. Tretinoin 24-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 132-139
16403252-7 2005 HDAC inhibitors such as trichostatin A, in combination with ATRA, induce differentiation of the blast/promyelocytic cells from PLZF-RARa/RARa-PLZF double TM, but not ATRA alone. Tretinoin 60-64 zinc finger and BTB domain containing 16 Mus musculus 142-146
16403261-3 2005 By treatment of 1 micromol/L ATRA, cell differentiation antigen CD11b was gradually increased ([chi = 47.002, P = 0.000) and CD33 was gradually decreased (chi = 1.614, P = 0.806) with time. Tretinoin 29-33 CD33 molecule Homo sapiens 125-129
16122834-4 2005 In this study, we have investigated a possible role for NTE in the all-trans retinoic acid-induced differentiation of neuroblastoma cells. Tretinoin 77-90 patatin like phospholipase domain containing 6 Homo sapiens 56-59
15959780-0 2005 Hyperacetylation enhances the growth-inhibitory effect of all-trans retinoic acid by the restoration of retinoic acid receptor beta expression in head and neck squamous carcinoma (HNSCC) cells. Tretinoin 68-81 retinoic acid receptor beta Homo sapiens 104-131
16044154-2 2005 Since an activation of the transcription factor NF-kappaB occurs during ATRA-induced maturation of APL cells, a mechanistic link between these two processes was investigated. Tretinoin 72-76 nuclear factor kappa B subunit 1 Homo sapiens 48-57
16044154-7 2005 Furthermore, impairment of NF-kappaB activation resulted in increased levels of reactive oxygen species (ROS) upon ATRA treatment. Tretinoin 115-119 nuclear factor kappa B subunit 1 Homo sapiens 27-36
16044154-8 2005 ROS accumulation was suppressed by the antioxidant butylated hydroxyanisol, which also abolished ATRA-induced JNK activation and apoptosis. Tretinoin 97-101 mitogen-activated protein kinase 8 Homo sapiens 110-113
16044154-9 2005 Altogether, our results demonstrate an anti-apoptotic effect of NF-kappaB activation during ATRA-induced differentiation of NB4 cells and identify repression of ROS-mediated JNK activation as a mechanism for this effect. Tretinoin 92-96 nuclear factor kappa B subunit 1 Homo sapiens 64-73
15975960-6 2005 Percent of remodeling GST-P positive PNL was increased (P < 0.05) in 9cRA (92 +/- 1), ROL (96 +/- 1) and betaC (93 +/- 1) groups, but not (P > 0.05) in AtRA group (90 +/- 2), compared with the CO group (86 +/- 1). Tretinoin 158-162 glutathione S-transferase pi 1 Rattus norvegicus 22-27
15959780-1 2005 The chemotherapeutic effects of all-trans-retinoic acid (atRA) are mediated by the retinoic acid receptor beta (RARbeta), but RARbeta expression is reduced in a number of head and neck carcinoma (HNSCC) cells which causes resistance to RA treatment in half the patients with HNSCC. Tretinoin 32-55 retinoic acid receptor beta Homo sapiens 83-110
15959780-1 2005 The chemotherapeutic effects of all-trans-retinoic acid (atRA) are mediated by the retinoic acid receptor beta (RARbeta), but RARbeta expression is reduced in a number of head and neck carcinoma (HNSCC) cells which causes resistance to RA treatment in half the patients with HNSCC. Tretinoin 32-55 retinoic acid receptor beta Homo sapiens 112-119
15959780-1 2005 The chemotherapeutic effects of all-trans-retinoic acid (atRA) are mediated by the retinoic acid receptor beta (RARbeta), but RARbeta expression is reduced in a number of head and neck carcinoma (HNSCC) cells which causes resistance to RA treatment in half the patients with HNSCC. Tretinoin 57-61 retinoic acid receptor beta Homo sapiens 83-110
15959780-1 2005 The chemotherapeutic effects of all-trans-retinoic acid (atRA) are mediated by the retinoic acid receptor beta (RARbeta), but RARbeta expression is reduced in a number of head and neck carcinoma (HNSCC) cells which causes resistance to RA treatment in half the patients with HNSCC. Tretinoin 57-61 retinoic acid receptor beta Homo sapiens 112-119
15959780-5 2005 SqCC/Y1 cells resistant to atRA showed methylated and unmethylated forms in the RARbeta promoter region. Tretinoin 27-31 retinoic acid receptor beta Homo sapiens 80-87
15959780-7 2005 Also, treatment with TSA and atRA combined synergistically increased the growth-inhibitory effect and highly induced the transcriptional activation of the RARbeta promoter compared to atRA treatment in HNSCC cells. Tretinoin 29-33 retinoic acid receptor beta Homo sapiens 155-162
16085646-9 2005 In addition, atRA pretreatment affected the transcriptional functions of IFNgamma-induced IRF-1, increasing its nuclear localization and DNA binding activity as well as the transcript levels of IRF-1 target genes. Tretinoin 13-17 interferon gamma Homo sapiens 73-81
16205117-4 2005 TAF4 is however essential in the retinoic acid and cAMP signalling pathways acting as a cofactor for CREB and the retinoic acid receptor, but is a negative regulator of the ATF7 transcription factor. Tretinoin 33-46 Taf4p Saccharomyces cerevisiae S288C 0-4
16207763-1 2005 Using genetic approaches in the mouse, we show that the primary target tissue of retinoic acid (RA) action during eye morphogenesis is not the retina nor the corneal ectoderm, which both express RA-synthesizing retinaldehyde dehydrogenases (RALDH1 and RALDH3), but the neural crest cell-derived periocular mesenchyme (POM), which is devoid of RALDH. Tretinoin 81-94 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 252-258
16207763-1 2005 Using genetic approaches in the mouse, we show that the primary target tissue of retinoic acid (RA) action during eye morphogenesis is not the retina nor the corneal ectoderm, which both express RA-synthesizing retinaldehyde dehydrogenases (RALDH1 and RALDH3), but the neural crest cell-derived periocular mesenchyme (POM), which is devoid of RALDH. Tretinoin 96-98 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 252-258
16085646-3 2005 In this study, we have used the human lung epithelial cell line A549 to examine the effect of atRA on IFNgamma-induced expression of IFN regulatory factor-1 (IRF-1), an important transcription factor involved in cell growth and apoptosis, differentiation, and antiviral and antibacterial immune responses. Tretinoin 94-98 interferon gamma Homo sapiens 102-110
16085646-3 2005 In this study, we have used the human lung epithelial cell line A549 to examine the effect of atRA on IFNgamma-induced expression of IFN regulatory factor-1 (IRF-1), an important transcription factor involved in cell growth and apoptosis, differentiation, and antiviral and antibacterial immune responses. Tretinoin 94-98 interferon regulatory factor 1 Homo sapiens 133-156
16085646-3 2005 In this study, we have used the human lung epithelial cell line A549 to examine the effect of atRA on IFNgamma-induced expression of IFN regulatory factor-1 (IRF-1), an important transcription factor involved in cell growth and apoptosis, differentiation, and antiviral and antibacterial immune responses. Tretinoin 94-98 interferon regulatory factor 1 Homo sapiens 158-163
16085646-4 2005 At least 4 h of pretreatment with atRA followed by suboptimal concentrations of IFNgamma induced a faster, higher, and more stable expression of IRF-1 than IFNgamma alone. Tretinoin 34-38 interferon regulatory factor 1 Homo sapiens 145-150
16085646-4 2005 At least 4 h of pretreatment with atRA followed by suboptimal concentrations of IFNgamma induced a faster, higher, and more stable expression of IRF-1 than IFNgamma alone. Tretinoin 34-38 interferon gamma Homo sapiens 156-164
16305955-5 2005 atRA could induce the expression of RARbeta mRNA in a dose- and time-dependent manner. Tretinoin 0-4 retinoic acid receptor, beta Rattus norvegicus 36-43
16305955-6 2005 CONCLUSION: atRA can accelerate differentiation of NSCs into neuron-likes cells and up-regulate the expression of RAR-beta mRNA in neonatal rat striatal NSCs. Tretinoin 12-16 retinoic acid receptor, beta Rattus norvegicus 114-122
16085646-9 2005 In addition, atRA pretreatment affected the transcriptional functions of IFNgamma-induced IRF-1, increasing its nuclear localization and DNA binding activity as well as the transcript levels of IRF-1 target genes. Tretinoin 13-17 interferon regulatory factor 1 Homo sapiens 90-95
16085646-9 2005 In addition, atRA pretreatment affected the transcriptional functions of IFNgamma-induced IRF-1, increasing its nuclear localization and DNA binding activity as well as the transcript levels of IRF-1 target genes. Tretinoin 13-17 interferon regulatory factor 1 Homo sapiens 194-199
15964596-7 2005 These results suggest that the possible perinatal RA production by RALDHs might regulate various RA-target genes including CRBPII and RARalpha through RXRalpha or HNF-4 in the small intestine. Tretinoin 50-52 retinoid X receptor alpha Rattus norvegicus 151-159
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 124-128 interferon regulatory factor 1 Homo sapiens 286-291
15925444-5 2005 As retinoic acid (RA) plays a major role in the neural crest induction and differentiation, we showed that RA reverses the aberrant negative regulation of Wnt-5a in metastatic neuroblasts. Tretinoin 3-16 Wnt family member 5A Homo sapiens 155-161
16134180-1 2005 BACKGROUND: Hypermethylation of CpG islands has been associated with silencing of various tumor suppressor genes, and the retinoid acid receptor beta (RARbeta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) genes have been associated with retinoic acid signaling. Tretinoin 274-287 retinoic acid receptor responder 1 Homo sapiens 209-234
16134180-1 2005 BACKGROUND: Hypermethylation of CpG islands has been associated with silencing of various tumor suppressor genes, and the retinoid acid receptor beta (RARbeta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) genes have been associated with retinoic acid signaling. Tretinoin 274-287 retinoic acid receptor responder 1 Homo sapiens 236-240
16142401-6 2005 RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. Tretinoin 97-101 C-X-C motif chemokine ligand 16 Homo sapiens 43-49
16054129-3 2005 To elucidate possible mechanisms of RA-mediated downmodulation of telomerase activity, we measured the kinetics of concentration changes of several transcription regulators by using standard biochemical techniques at low (10 muM) and high (100 muM) RA concentrations. Tretinoin 36-38 latexin Homo sapiens 225-228
16054129-3 2005 To elucidate possible mechanisms of RA-mediated downmodulation of telomerase activity, we measured the kinetics of concentration changes of several transcription regulators by using standard biochemical techniques at low (10 muM) and high (100 muM) RA concentrations. Tretinoin 36-38 latexin Homo sapiens 244-247
16142401-0 2005 All-trans retinoic acid regulates CXCL16/SR-PSOX expression. Tretinoin 10-23 C-X-C motif chemokine ligand 16 Homo sapiens 34-40
16142401-0 2005 All-trans retinoic acid regulates CXCL16/SR-PSOX expression. Tretinoin 10-23 C-X-C motif chemokine ligand 16 Homo sapiens 41-48
16166633-6 2005 Loss of repression of ES cell marker genes Oct4, Nanog, Sox2, FGF4, and Stella was observed upon treatment of GCNF-/- ES cells with retinoic acid. Tretinoin 132-145 Nanog homeobox Mus musculus 49-54
16142401-3 2005 We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Tretinoin 27-50 C-X-C motif chemokine ligand 16 Homo sapiens 61-67
16142401-3 2005 We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Tretinoin 27-50 C-X-C motif chemokine ligand 16 Homo sapiens 68-75
16142401-3 2005 We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Tretinoin 52-56 C-X-C motif chemokine ligand 16 Homo sapiens 61-67
16142401-3 2005 We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Tretinoin 52-56 C-X-C motif chemokine ligand 16 Homo sapiens 68-75
16194896-1 2005 The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels. Tretinoin 24-37 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 78-85
16194896-1 2005 The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels. Tretinoin 39-41 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 78-85
16194896-1 2005 The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels. Tretinoin 156-179 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 78-85
16194896-1 2005 The recently identified retinoic acid (RA)-metabolizing cytochrome P450RAI-1 (CYP26A1) has been implicated in accelerated metabolism and rapid clearance of all-trans-retinoic acid (ATRA) during prolonged oral administration in patients with acute promyelocytic leukemia (APL), leading to a progressive decline in plasma drug levels. Tretinoin 181-185 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 78-85
16194896-3 2005 ATRA rapidly induced upregulation of CYP26A1 mRNA expression in a dose-dependent manner. Tretinoin 0-4 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 37-44
16194896-5 2005 CYP26A1 mRNA expression in HepG2 cells returned to baseline in 48 h upon removal of ATRA from the culture medium, suggesting that the expression is reversible and requires the presence of ATRA. Tretinoin 84-88 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
16194896-5 2005 CYP26A1 mRNA expression in HepG2 cells returned to baseline in 48 h upon removal of ATRA from the culture medium, suggesting that the expression is reversible and requires the presence of ATRA. Tretinoin 188-192 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-7
16194896-6 2005 In endothelial cells, however, a higher concentration of ATRA (10 microM) was required to induce expression of CYP26A1. Tretinoin 57-61 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 111-118
16194896-7 2005 A specific RA receptor-alpha antagonist totally inhibited ATRA-induced expression of CYP26A1, indicating that RA receptor-alpha plays a major role in CYP26A1 expression in HepG2 cells. Tretinoin 58-62 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 85-92
16194896-7 2005 A specific RA receptor-alpha antagonist totally inhibited ATRA-induced expression of CYP26A1, indicating that RA receptor-alpha plays a major role in CYP26A1 expression in HepG2 cells. Tretinoin 58-62 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 150-157
16194896-10 2005 L-ATRA induced lower CYP26A1 expression and metabolic activity in HepG2 and NB4 cells when compared with free ATRA. Tretinoin 2-6 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 21-28
16194896-12 2005 Our data suggest that upregulation of CYP26A1 expression in intestinal, endothelial, liver, and APL cells and metabolism of ATRA may play a role in rapid clearance of ATRA after continuous oral administration. Tretinoin 167-171 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 38-45
15976015-8 2005 Treatment with the TPA/ATRA combination resulted in a substantially decreased ratio of the percentage of mitotic cells to the percentage of caspase-3-positive cells in the tumors compared with tumors from the vehicle-treated control animals. Tretinoin 23-27 caspase 3 Homo sapiens 140-149
16166633-6 2005 Loss of repression of ES cell marker genes Oct4, Nanog, Sox2, FGF4, and Stella was observed upon treatment of GCNF-/- ES cells with retinoic acid. Tretinoin 132-145 fibroblast growth factor 4 Mus musculus 62-66
16051514-2 2005 The exposed RNA template of hTR is an ideal target for antisense oligonucleotides (As-ODN); while recent findings indicate all-trans retinoid acid (ATRA) could effectively inhibit the expression of catalytic subunit-hTERT. Tretinoin 148-152 telomerase RNA component Homo sapiens 28-31
16051514-6 2005 Tca8113 cells displayed significant growth inhibition during the 9-day exposure to ATRA/As-ODN, especially to a combination of As-ODN-hTR and 5muM ATRA, correlating with the inhibition of telomerase expression. Tretinoin 83-87 telomerase RNA component Homo sapiens 134-137
16087156-0 2005 Knockdown of p53 by RNAi in ES cells facilitates RA-induced differentiation into muscle cells. Tretinoin 49-51 tumor protein p53 Homo sapiens 13-16
16087156-5 2005 With RA treatment, silencing of p53 by RNAi in ES cells leads to dominant muscle cell production but lack of neuronal cell, indicating that p53 indeed plays a role during muscle and neuronal fate commitment. Tretinoin 5-7 tumor protein p53 Homo sapiens 32-35
16087156-5 2005 With RA treatment, silencing of p53 by RNAi in ES cells leads to dominant muscle cell production but lack of neuronal cell, indicating that p53 indeed plays a role during muscle and neuronal fate commitment. Tretinoin 5-7 tumor protein p53 Homo sapiens 140-143
16277846-2 2005 By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively. Tretinoin 111-115 fucosyltransferase 4 Homo sapiens 41-45
16277846-6 2005 In ATRA and TPA group, the change of HSP70 had positive correlation with JWA, and negative correlation with Bcl-2. Tretinoin 3-7 BCL2 apoptosis regulator Homo sapiens 108-113
16007204-6 2005 Interestingly, while the upregulation of STAT-1 by IFNgamma is partially inhibited by RA, IFNgamma is shown to repress RA-driven TGFbeta-2 induction, pointing to the involvement of alternative mechanism(s) in IFNgamma-RA synergism. Tretinoin 86-88 interferon gamma Homo sapiens 51-59
16083855-5 2005 When a dominant negative form of NDRF protein was expressed during retinoic acid-induced neuronal differentiation of P19 cells, the BLBP gene, but not the Id1 gene, was potently repressed. Tretinoin 67-80 neurogenic differentiation 2 Mus musculus 33-37
16166294-9 2005 Specifically, overexpression of CRABP-II, in the absence of RA, up-regulated the expression of Apaf1 and triggered caspase 7 and caspase 9 cleavage. Tretinoin 33-35 apoptotic peptidase activating factor 1 Homo sapiens 95-100
16140954-7 2005 The differentiation effect of NSC656243 was associated with enhanced ATRA-mediated up-regulation of cell cycle regulatory proteins p21waf1 and p27kip1, retinoblastoma dephosphorylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation of the myeloperoxidase (MPO) gene. Tretinoin 69-73 lymphocyte antigen 6 family member E Homo sapiens 200-205
16128742-2 2005 Retinoic acid receptor-beta (RAR-beta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) have been linked to retinoic acid signaling. Tretinoin 141-154 retinoic acid receptor responder 1 Homo sapiens 115-119
16128742-2 2005 Retinoic acid receptor-beta (RAR-beta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) have been linked to retinoic acid signaling. Tretinoin 141-154 retinoic acid receptor beta Homo sapiens 0-27
16128742-2 2005 Retinoic acid receptor-beta (RAR-beta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) have been linked to retinoic acid signaling. Tretinoin 141-154 retinoic acid receptor beta Homo sapiens 29-37
16128742-2 2005 Retinoic acid receptor-beta (RAR-beta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) have been linked to retinoic acid signaling. Tretinoin 141-154 retinoic acid receptor responder 1 Homo sapiens 88-113
16140954-7 2005 The differentiation effect of NSC656243 was associated with enhanced ATRA-mediated up-regulation of cell cycle regulatory proteins p21waf1 and p27kip1, retinoblastoma dephosphorylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation of the myeloperoxidase (MPO) gene. Tretinoin 69-73 myeloperoxidase Homo sapiens 284-299
16140954-7 2005 The differentiation effect of NSC656243 was associated with enhanced ATRA-mediated up-regulation of cell cycle regulatory proteins p21waf1 and p27kip1, retinoblastoma dephosphorylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation of the myeloperoxidase (MPO) gene. Tretinoin 69-73 myeloperoxidase Homo sapiens 301-304
16143075-5 2005 RESULTS: Either IFN-alpha or ATRA induced HL-60 cell differentiation and apoptosis, which was enhanced when combining ATRA with IFN-alpha. Tretinoin 29-33 interferon alpha 1 Homo sapiens 128-137
16040207-3 2005 The study revealed that chenodeoxycholic acid (CDCA), either alone or in combination with retinoic acid (RA), had the inherent capacity to downregulate TACO gene transcription in a dose-dependent fashion. Tretinoin 90-103 coronin 1A Homo sapiens 152-156
16040207-3 2005 The study revealed that chenodeoxycholic acid (CDCA), either alone or in combination with retinoic acid (RA), had the inherent capacity to downregulate TACO gene transcription in a dose-dependent fashion. Tretinoin 105-107 coronin 1A Homo sapiens 152-156
16188211-6 2005 We have used LA-N-1 cell cultures to study activities of PLA2, C, and D during retinoic acid (RA)-mediated differentiation. Tretinoin 79-92 phospholipase A2 group IB Homo sapiens 57-61
16188211-6 2005 We have used LA-N-1 cell cultures to study activities of PLA2, C, and D during retinoic acid (RA)-mediated differentiation. Tretinoin 94-96 phospholipase A2 group IB Homo sapiens 57-61
16188211-7 2005 The treatment of LA-N-1 cells with RA produces an increase in PLA2 activity in the nuclear fraction. Tretinoin 35-37 phospholipase A2 group IB Homo sapiens 62-66
16188211-8 2005 This increase in PLA2 activity can be prevented with BMS493, a pan retinoic acid receptor antagonist, suggesting that RA-induced stimulation of PLA2 activity is a RA receptor-mediated process. Tretinoin 118-120 phospholipase A2 group IB Homo sapiens 17-21
16188211-8 2005 This increase in PLA2 activity can be prevented with BMS493, a pan retinoic acid receptor antagonist, suggesting that RA-induced stimulation of PLA2 activity is a RA receptor-mediated process. Tretinoin 118-120 phospholipase A2 group IB Homo sapiens 144-148
16188211-13 2005 RA stimulates the oleate-dependent isoform of PLD, whereas RA does not stimulate the TPA-dependent isoform. Tretinoin 0-2 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 46-49
16143075-6 2005 The level of ATRA and the expression of CYP26 were higher in HL-60 cells treated with both ATRA and IFN-alpha than in the cells treated with ATRA alone. Tretinoin 13-17 interferon alpha 1 Homo sapiens 100-109
16143075-7 2005 CONCLUSION: ATRA has remarkable synergic effect with IFN-alpha on HL-60 cells, probably because IFN-alpha inhibits CYP26 mRNA expression and thus reduces the metabolism of ATRA. Tretinoin 12-16 interferon alpha 1 Homo sapiens 96-105
16143075-7 2005 CONCLUSION: ATRA has remarkable synergic effect with IFN-alpha on HL-60 cells, probably because IFN-alpha inhibits CYP26 mRNA expression and thus reduces the metabolism of ATRA. Tretinoin 12-16 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 115-120
16350840-7 2005 In this system, RA upregulates the mRNA level of Runx2/Cbfa1 (type II), a positive regulator for mineralization, and downregulates the mRNA of Indian hedgehog (Ihh), parathyroid hormone related protein (PTHrP), negative regulators for terminal differentiation. Tretinoin 16-18 parathyroid hormone-like peptide Mus musculus 166-201
16350840-7 2005 In this system, RA upregulates the mRNA level of Runx2/Cbfa1 (type II), a positive regulator for mineralization, and downregulates the mRNA of Indian hedgehog (Ihh), parathyroid hormone related protein (PTHrP), negative regulators for terminal differentiation. Tretinoin 16-18 parathyroid hormone-like peptide Mus musculus 203-208
16041241-8 2005 The relatively high level of CYP3A7 protein expression detected in a subset of adult livers may be relevant with respect to the metabolism of exogenous and endogenous substrates, such as retinoic acid and dehydroepiandrosterone. Tretinoin 187-200 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 29-35
16143075-5 2005 RESULTS: Either IFN-alpha or ATRA induced HL-60 cell differentiation and apoptosis, which was enhanced when combining ATRA with IFN-alpha. Tretinoin 118-122 interferon alpha 1 Homo sapiens 16-25
16043647-0 2005 Upregulation of nitric oxide production in vascular endothelial cells by all-trans retinoic acid through the phosphoinositide 3-kinase/Akt pathway. Tretinoin 83-96 AKT serine/threonine kinase 1 Homo sapiens 135-138
16114872-2 2005 We demonstrate that atRA is able to modulate the activity of protein kinase C alpha (PKCalpha), which is related to tumor development. Tretinoin 20-24 protein kinase C alpha Homo sapiens 61-83
16114872-2 2005 We demonstrate that atRA is able to modulate the activity of protein kinase C alpha (PKCalpha), which is related to tumor development. Tretinoin 20-24 protein kinase C alpha Homo sapiens 85-93
16114872-3 2005 In vitro, it was found that atRA activated PKCalpha in the presence of Ca(2+) and in the absence of phosphatidylserine, although such activity is considerably inhibited in mutations affecting residues D246 and D248 and also residue N189, all of which are known to be essential for the interaction with Ca(2+) and phosphatidylserine in the C2 domain. Tretinoin 28-32 protein kinase C alpha Homo sapiens 43-51
16114872-5 2005 However, atRA had a biphasic effect on PKCalpha activity in the presence of activating phospholipids, such as phosphatidylserine and phosphatidylinositol 4,5-bisphosphate, yielding activation at low concentrations but inactivation at higher ones. Tretinoin 9-13 protein kinase C alpha Homo sapiens 39-47
16114872-9 2005 It was concluded that whereas atRA may activate PKCalpha through the Ca(2+)-phosphatidylserine-binding site of the C2 domain, it may also inhibit the activity of this enzyme when displacing the phospholipid from the Lys-rich cluster also located in the C2 domain. Tretinoin 30-34 protein kinase C alpha Homo sapiens 48-56
15919153-3 2005 MGF enhanced Fas expression in NT2/D1 cells and prevented the decrease of Fas expression when RA was also added. Tretinoin 94-96 insulin like growth factor 1 Homo sapiens 0-3
15919153-7 2005 MGF slightly induced neurofilament-medium size (NF-M) synthesis in NT2/D1 cells that RA induced in the cells. Tretinoin 85-87 insulin like growth factor 1 Homo sapiens 0-3
15897880-4 2005 Several genes like RARRES1, RARRES3, CTGF, CKS2, CCNA2, IGFBP3, UBE2C, CCL2 or ITM2B that were previously found to be deregulated in advanced tumors exhibited opposite expression changes after ATRA treatment. Tretinoin 193-197 retinoic acid receptor responder 1 Homo sapiens 19-26
15897880-4 2005 Several genes like RARRES1, RARRES3, CTGF, CKS2, CCNA2, IGFBP3, UBE2C, CCL2 or ITM2B that were previously found to be deregulated in advanced tumors exhibited opposite expression changes after ATRA treatment. Tretinoin 193-197 phospholipase A and acyltransferase 4 Homo sapiens 28-35
15897880-4 2005 Several genes like RARRES1, RARRES3, CTGF, CKS2, CCNA2, IGFBP3, UBE2C, CCL2 or ITM2B that were previously found to be deregulated in advanced tumors exhibited opposite expression changes after ATRA treatment. Tretinoin 193-197 ubiquitin conjugating enzyme E2 C Homo sapiens 64-69
15967793-5 2005 Knockdown of rdh1l results in a robust RA-deficient phenotype including lack of intestinal differentiation, which can be rescued by the addition of exogenous retinoic acid. Tretinoin 158-171 dehydrogenase/reductase (SDR family) member 9 Danio rerio 13-18
15967793-8 2005 These results provide genetic evidence that retinoic acid is required for vertebrate gut development and that the tumor suppressor APC controls the production of RA in the gut by regulating the expression of the retinol dehydrogenase, rdh1l. Tretinoin 162-164 dehydrogenase/reductase (SDR family) member 9 Danio rerio 235-240
15897880-5 2005 In addition to enhanced retinoid signaling, the transforming growth factor-beta (TGFbeta) pathway was strongly activated by ATRA treatment of Wilms tumor cells. Tretinoin 124-128 transforming growth factor beta 1 Homo sapiens 48-79
16043647-16 2005 CONCLUSIONS: ATRA increases NO production by eNOS phosphorylation through RAR-mediated PI3K/Akt pathway activation in vascular ECs and possibly plays beneficial roles in vascular endothelium. Tretinoin 13-17 AKT serine/threonine kinase 1 Homo sapiens 92-95
15897880-5 2005 In addition to enhanced retinoid signaling, the transforming growth factor-beta (TGFbeta) pathway was strongly activated by ATRA treatment of Wilms tumor cells. Tretinoin 124-128 transforming growth factor beta 1 Homo sapiens 81-88
16109552-1 2005 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA), acitretin and tazarotene on apoptosis and Bax/Bcl-2 protein expressions of human melanoma A375 cells. Tretinoin 41-64 BCL2 associated X, apoptosis regulator Homo sapiens 115-118
16109552-1 2005 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA), acitretin and tazarotene on apoptosis and Bax/Bcl-2 protein expressions of human melanoma A375 cells. Tretinoin 66-70 BCL2 associated X, apoptosis regulator Homo sapiens 115-118
16109552-1 2005 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA), acitretin and tazarotene on apoptosis and Bax/Bcl-2 protein expressions of human melanoma A375 cells. Tretinoin 66-70 BCL2 apoptosis regulator Homo sapiens 119-124
16024653-4 2005 Retinoic acid increased cyclin D2, decreased cyclin D3 and had no effect on cyclin D1 mRNA expression. Tretinoin 0-13 cyclin D2 Homo sapiens 24-33
16055936-5 2005 We hypothesized that RA alters IGFBP-2 and -3 in hyperoxia-exposed neonatal lung and alters collagen production. Tretinoin 21-23 insulin-like growth factor binding protein 2 Rattus norvegicus 31-45
16055936-13 2005 In conclusion, RA modulates the secreted IGFBP-2 and -3 during O(2) exposure and inhibits the increase in collagen that occurs during lung injury. Tretinoin 15-17 insulin-like growth factor binding protein 2 Rattus norvegicus 41-55
16055936-14 2005 We speculate that RA protects against O(2)-induced neonatal lung injury through modulation of the IGFBPs. Tretinoin 18-20 insulin-like growth factor binding protein 2 Rattus norvegicus 98-104
16129031-3 2005 In order to assess the alternation of VEGF gene expression in the process of all-trans retinoic acid (ATRA)-induced differentiation of NB4 acute promyelocytic leukemia cell line, and a competitor DNA fragment, VEGF gene competative template (T-VEGFDelta) was constructed by using gene recombinant technologies, and a competitive quantitative reverse transcriptase-polymerase chain reaction (cQRT-PCR) method was developed. Tretinoin 87-100 vascular endothelial growth factor A Homo sapiens 38-42
16129031-3 2005 In order to assess the alternation of VEGF gene expression in the process of all-trans retinoic acid (ATRA)-induced differentiation of NB4 acute promyelocytic leukemia cell line, and a competitor DNA fragment, VEGF gene competative template (T-VEGFDelta) was constructed by using gene recombinant technologies, and a competitive quantitative reverse transcriptase-polymerase chain reaction (cQRT-PCR) method was developed. Tretinoin 102-106 vascular endothelial growth factor A Homo sapiens 38-42
16129031-7 2005 The number of VEGF gene transcripts detected by means of cQRT-PCR assay was 42.3 x 10(5), 12.6 x 10(5), 3.6 x 10(5), and less than 1.0 x 10(5)/microg total RNA at 0, 12, 24 and 48 hours after ATRA treatment, respectively. Tretinoin 192-196 vascular endothelial growth factor A Homo sapiens 14-18
16129031-8 2005 This rapid down-regulation of VEGF gene expression, during ATRA-induced NB4 cell differentiation, was accompanied by the up-regulation of CD11b expression and an increased NBT reduction rate. Tretinoin 59-63 vascular endothelial growth factor A Homo sapiens 30-34
16129031-9 2005 In conclusion, cQRT-PCR method was successtully constructed, confirming that ATRA efficiently repressed VEGF, at the same time, the ATRA might exert an antileukemic effect, other than induction of differentiation via inhibition of angiogenesis. Tretinoin 77-81 vascular endothelial growth factor A Homo sapiens 104-108
16009726-0 2005 A novel role for Gab2 in bFGF-mediated cell survival during retinoic acid-induced neuronal differentiation. Tretinoin 60-73 GRB2 associated binding protein 2 Homo sapiens 17-21
16009726-0 2005 A novel role for Gab2 in bFGF-mediated cell survival during retinoic acid-induced neuronal differentiation. Tretinoin 60-73 fibroblast growth factor 2 Homo sapiens 25-29
16009726-4 2005 RA treatment induces apoptosis, countered by basic FGF (bFGF). Tretinoin 0-2 fibroblast growth factor 2 Homo sapiens 45-54
16009726-4 2005 RA treatment induces apoptosis, countered by basic FGF (bFGF). Tretinoin 0-2 fibroblast growth factor 2 Homo sapiens 56-60
16009726-5 2005 In EC cells, Gab2 silencing results in hypersensitivity to RA-induced apoptosis and abrogates the protection by bFGF. Tretinoin 59-61 GRB2 associated binding protein 2 Homo sapiens 13-17
15946654-6 2005 We showed that both MMP-1 and MMP-13 mRNA expression, protein production and enzyme activity induced by either IL-1 or TNF-alpha were suppressed by t-RA or different retinoid derivatives. Tretinoin 148-152 matrix metallopeptidase 13 Homo sapiens 30-36
15946654-6 2005 We showed that both MMP-1 and MMP-13 mRNA expression, protein production and enzyme activity induced by either IL-1 or TNF-alpha were suppressed by t-RA or different retinoid derivatives. Tretinoin 148-152 tumor necrosis factor Homo sapiens 119-128
15946654-9 2005 Furthermore, we showed that t-RA could reduce IL-1-induced TNF-alpha production in chondrocytes. Tretinoin 28-32 tumor necrosis factor Homo sapiens 59-68
16012770-3 2005 Using P19 teratocarcinoma cells differentiated by retinoic acid treatment, we observed an induction of Ret mRNA accompanied by a decrease of SP1 binding due to its proteolytic cleavage. Tretinoin 50-63 ret proto-oncogene Mus musculus 103-106
16080579-11 2005 CONCLUSION: These data show that low-dose IL-2 and oral RA is more effective than IL-2 alone in improving all known prognostically significant parameters in a variety of solid tumors, including an increase of lymphocytes and a decrease of VEGF. Tretinoin 56-58 vascular endothelial growth factor A Homo sapiens 239-243
16024653-4 2005 Retinoic acid increased cyclin D2, decreased cyclin D3 and had no effect on cyclin D1 mRNA expression. Tretinoin 0-13 cyclin D3 Homo sapiens 45-54
16024653-5 2005 Retinoic acid decreased cyclin D1 and cyclin D3 protein expression. Tretinoin 0-13 cyclin D3 Homo sapiens 38-47
16024653-7 2005 Proteasomal inhibition prevented the early cyclin D3 degradation by retinoic acid. Tretinoin 68-81 cyclin D3 Homo sapiens 43-52
16024653-11 2005 Expression of cyclin D1 and cyclin D3 was deregulated in retinoic acid-resistant HBE cells, directly implicating these species in retinoic acid response. Tretinoin 57-70 cyclin D3 Homo sapiens 28-37
16024653-11 2005 Expression of cyclin D1 and cyclin D3 was deregulated in retinoic acid-resistant HBE cells, directly implicating these species in retinoic acid response. Tretinoin 130-143 cyclin D3 Homo sapiens 28-37
16024653-15 2005 Thus, retinoic acid repressed cyclin D1 and cyclin D3 through distinct mechanisms. Tretinoin 6-19 cyclin D3 Homo sapiens 44-53
16002375-10 2005 Similar to the T3 response, the PCB-mediated effect on oligodendrocyte formation was blocked by retinoic acid and the thyroid hormone receptor antagonist NH-3. Tretinoin 96-109 pyruvate carboxylase Homo sapiens 32-35
15978261-5 2005 STAT3 activation was detected in the outermost retina layer in response to CNTF, LIF, FGF1, and IFN-alpha 24 hr after stimulation in postnatal day 1 (PN1) explants, but not FGF2, EGF, IFN-gamma, and retinoic acid (RA). Tretinoin 214-216 signal transducer and activator of transcription 3 Mus musculus 0-5
15978261-5 2005 STAT3 activation was detected in the outermost retina layer in response to CNTF, LIF, FGF1, and IFN-alpha 24 hr after stimulation in postnatal day 1 (PN1) explants, but not FGF2, EGF, IFN-gamma, and retinoic acid (RA). Tretinoin 199-212 signal transducer and activator of transcription 3 Mus musculus 0-5
15927671-1 2005 We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA. Tretinoin 102-115 C-X-C motif chemokine ligand 8 Homo sapiens 40-53
16233856-7 2005 When stimulated with retinoic acid (an inducer of differentiation into neurons), EBs on the PC surface expressed Pax6. Tretinoin 21-34 paired box 6 Mus musculus 113-117
15927671-1 2005 We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA. Tretinoin 102-115 C-X-C motif chemokine ligand 8 Homo sapiens 55-59
15927671-1 2005 We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA. Tretinoin 117-121 C-X-C motif chemokine ligand 8 Homo sapiens 40-53
15927671-1 2005 We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA. Tretinoin 117-121 C-X-C motif chemokine ligand 8 Homo sapiens 55-59
15927671-1 2005 We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA. Tretinoin 343-347 C-X-C motif chemokine ligand 8 Homo sapiens 40-53
15927671-1 2005 We previously reported the induction of interleukin-8 (IL-8), one of the CXC chemokines, by all-trans retinoic acid (ATRA) in PL-21 and NB4 human myeloid leukemia cells, which may be implicated in APL differentiation syndrome that is a relatively frequent complication in patients with acute promyelocytic leukemia (APL) during treatment with ATRA. Tretinoin 343-347 C-X-C motif chemokine ligand 8 Homo sapiens 55-59
15927671-5 2005 APL cells prepared from two APL patients showed gene expression of chemokines, such as IL-8, MCP-1, MIP-1alpha, and MIP-1beta when stimulated with ATRA in vitro. Tretinoin 147-151 C-X-C motif chemokine ligand 8 Homo sapiens 87-91
15927671-6 2005 Furthermore, serum levels of IL-8, MIP-1beta and RANTES were increased during the course of ATRA treatment in both APL patients who developed APL differentiation syndrome. Tretinoin 92-96 C-X-C motif chemokine ligand 8 Homo sapiens 29-33
15949696-1 2005 The effects of fatty acids and retinoic acid (carotene) on brown adipose tissue differentiation are mediated by activation of the transcription factors PPARgamma and PPARalpha in combination with RXR. Tretinoin 31-44 peroxisome proliferator activated receptor gamma Homo sapiens 152-161
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 132-145 transforming growth factor beta 1 Homo sapiens 216-224
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 147-149 transforming growth factor beta 1 Homo sapiens 216-224
15850806-0 2005 Identification and characterization of the retinoic acid response elements in the human RIG1 gene promoter. Tretinoin 43-56 phospholipase A and acyltransferase 4 Homo sapiens 88-92
15850806-5 2005 The present study was designed to study the molecular mechanism underlying the all-trans retinoic acid (atRA)-mediated induction of RIG1 gene expression. Tretinoin 79-102 phospholipase A and acyltransferase 4 Homo sapiens 132-136
15850806-5 2005 The present study was designed to study the molecular mechanism underlying the all-trans retinoic acid (atRA)-mediated induction of RIG1 gene expression. Tretinoin 104-108 phospholipase A and acyltransferase 4 Homo sapiens 132-136
15885502-5 2005 Northern analysis of GRWD1 message levels in the myeloid cell line HL-60 undergoing differentiation induced by vitamin D(3) or retinoic acid demonstrate downregulation coincident with slowing of cellular proliferation. Tretinoin 127-140 glutamate rich WD repeat containing 1 Homo sapiens 21-26
15955085-9 2005 After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Tretinoin 13-17 transforming growth factor beta 1 Homo sapiens 29-37
15843825-3 2005 In the present study, we observed that NF-kappaB transcriptional activity as well as cell growth decreased significantly in HTLV-1-positive T-cell lines in the presence of ATRA. Tretinoin 172-176 nuclear factor kappa B subunit 1 Homo sapiens 39-48
16092758-1 2005 Restin, a member of melanoma-associated antigen superfamily gene, was first cloned from differentiated leukemia cell induced by all trans-retinoic acid, and was able to inhibit cell proliferation, but the molecular mechanism was not clear. Tretinoin 132-151 MAGE family member H1 Homo sapiens 0-6
15949692-5 2005 It is shown that RA reduces RB expression and enhances RB phosphorylation by a mechanism that involves down-regulation of the cyclin-dependent kinase inhibitor (CKI) p21(Cip1), having this fact as important consequences for both the cell cycle progression and the adipocyte differentiation process. Tretinoin 17-19 cyclin dependent kinase inhibitor 1A Homo sapiens 166-169
15949692-5 2005 It is shown that RA reduces RB expression and enhances RB phosphorylation by a mechanism that involves down-regulation of the cyclin-dependent kinase inhibitor (CKI) p21(Cip1), having this fact as important consequences for both the cell cycle progression and the adipocyte differentiation process. Tretinoin 17-19 cyclin dependent kinase inhibitor 1A Homo sapiens 170-174
16295569-0 2005 Induction of type I collagen and osteocalcin in human dental pulp cells by retinoic acid. Tretinoin 75-88 bone gamma-carboxyglutamate protein Homo sapiens 33-44
16295569-3 2005 The effects of retinoic acid on human dental pulp cells in terms of type I collagen and osteocalcin induction were investigated in vitro. Tretinoin 15-28 bone gamma-carboxyglutamate protein Homo sapiens 88-99
16295569-7 2005 Retinoic acid at concentrations of 10(-5), 10(-6), 10(-7) M was able to induce type I collagen and osteocalcin production in human dental pulp cells within 12 hours of exposure. Tretinoin 0-13 bone gamma-carboxyglutamate protein Homo sapiens 99-110
16295569-9 2005 A two-fold increase in osteocalcin level was detected after exposed to 10(-5) M retinoic acid within 24 hours. Tretinoin 80-93 bone gamma-carboxyglutamate protein Homo sapiens 23-34
16295569-10 2005 Our data suggest that retinoic acid at concentrations of 10(-5), 10(-6), 10(-7) M has the ability to induce type I collagen and osteocalcin secretions in human dental pulp cells in vitro. Tretinoin 22-35 bone gamma-carboxyglutamate protein Homo sapiens 128-139
15914280-0 2005 All-trans retinoic acid inhibits the cell proliferation but enhances the cell invasion through up-regulation of c-met in pancreatic cancer cells. Tretinoin 10-23 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 112-117
15914280-3 2005 Also, the effects of ATRA on c-Met expression in pancreatic cancer have never been addressed so far. Tretinoin 21-25 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 29-34
15914280-5 2005 In addition, the expression of c-Met in pancreatic cancer cell lines treated with ATRA was investigated by real-time PCR and western blotting. Tretinoin 82-86 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 31-36
15914280-12 2005 In addition, ATRA also increased the protein level of c-Met. Tretinoin 13-17 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 54-59
21190613-0 2005 [Experimental study of effects of retinoic acid on IL-1beta and IFN-gamma induced C3 and factor B secretion in lung cancer cell line]. Tretinoin 34-47 interleukin 1 beta Homo sapiens 51-59
21190613-0 2005 [Experimental study of effects of retinoic acid on IL-1beta and IFN-gamma induced C3 and factor B secretion in lung cancer cell line]. Tretinoin 34-47 interferon gamma Homo sapiens 64-73
21190613-2 2005 The aim of this study is to investigate the regulated effects of retinoic acid (RA) on IL-1beta and IFN-gamma induced C3 and factor B secretion in human lung cancer cell line A549. Tretinoin 65-78 interleukin 1 beta Homo sapiens 87-95
21190613-2 2005 The aim of this study is to investigate the regulated effects of retinoic acid (RA) on IL-1beta and IFN-gamma induced C3 and factor B secretion in human lung cancer cell line A549. Tretinoin 65-78 interferon gamma Homo sapiens 100-109
21190613-2 2005 The aim of this study is to investigate the regulated effects of retinoic acid (RA) on IL-1beta and IFN-gamma induced C3 and factor B secretion in human lung cancer cell line A549. Tretinoin 80-82 interleukin 1 beta Homo sapiens 87-95
21190613-2 2005 The aim of this study is to investigate the regulated effects of retinoic acid (RA) on IL-1beta and IFN-gamma induced C3 and factor B secretion in human lung cancer cell line A549. Tretinoin 80-82 interferon gamma Homo sapiens 100-109
21190613-6 2005 CONCLUSIONS: RA can up-regulate C3 and factor B secretion induced by IL-1beta and IFN-gamma in human lung cancer cell A549. Tretinoin 13-15 interleukin 1 beta Homo sapiens 69-77
21190613-6 2005 CONCLUSIONS: RA can up-regulate C3 and factor B secretion induced by IL-1beta and IFN-gamma in human lung cancer cell A549. Tretinoin 13-15 interferon gamma Homo sapiens 82-91
15896339-2 2005 Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells. Tretinoin 46-50 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 82-102
15896339-2 2005 Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells. Tretinoin 46-50 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 104-111
15896339-2 2005 Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells. Tretinoin 67-71 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 82-102
15896339-2 2005 Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells. Tretinoin 67-71 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 104-111
15896339-4 2005 CYP26A1 constitutive expression was barely detectable in NB4 cells, but ATRA could induce high levels of CYP26A1 expression, which reached a maximum at 72h. Tretinoin 72-76 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 105-112
15872003-2 2005 Hoxb1 expression requires 3" and 5" RA response elements for widespread induction up to r4 and for r3/r5 repression, but RA has previously been detected only from r5-r8, and vHnf1 is required for repression of Hoxb1 posterior to r4 in zebrafish. Tretinoin 36-38 homeobox B1a Danio rerio 0-5
15843825-7 2005 Moreover, AZT inhibited proviral DNA but not NF-kappaB transcriptional activity, and sIL-2R on HTLV-1; however, ATRA inhibited of NF-kappaB, proviral DNA and sIL-2R on HTLV-1. Tretinoin 112-116 nuclear factor kappa B subunit 1 Homo sapiens 130-139
15843825-8 2005 These results suggested that the decrease in sIL-2R induced by ATRA may be caused by the actions of a NF-kappaB inhibitor acting on the NF-kappaB/sIL-2R signal pathway. Tretinoin 63-67 nuclear factor kappa B subunit 1 Homo sapiens 102-111
15843825-8 2005 These results suggested that the decrease in sIL-2R induced by ATRA may be caused by the actions of a NF-kappaB inhibitor acting on the NF-kappaB/sIL-2R signal pathway. Tretinoin 63-67 nuclear factor kappa B subunit 1 Homo sapiens 136-145
15843825-9 2005 These results suggested that ATRA could have two roles, as a NF-kappaB inhibitor and as an RT inhibitor. Tretinoin 29-33 nuclear factor kappa B subunit 1 Homo sapiens 61-70
16029656-1 2005 OBJECTIVE: To investigate the effect of all-trans retinoic acid (ATRA) on the expression of connexin 26, 32 and 43 genes and the alteration of gap junction communication function in human hepatocellular carcinoma cells. Tretinoin 40-63 gap junction protein beta 2 Homo sapiens 92-103
16029656-1 2005 OBJECTIVE: To investigate the effect of all-trans retinoic acid (ATRA) on the expression of connexin 26, 32 and 43 genes and the alteration of gap junction communication function in human hepatocellular carcinoma cells. Tretinoin 65-69 gap junction protein beta 2 Homo sapiens 92-103
16029656-6 2005 CX26 mRNA and CX32 mRNA were not expressed in the cell lines BEL-7404, however, expression of CX26 mRNA and expression of CX32 mRNA were found 48 hours after induction by ATRA. Tretinoin 171-175 gap junction protein beta 2 Homo sapiens 0-4
16029656-6 2005 CX26 mRNA and CX32 mRNA were not expressed in the cell lines BEL-7404, however, expression of CX26 mRNA and expression of CX32 mRNA were found 48 hours after induction by ATRA. Tretinoin 171-175 gap junction protein beta 2 Homo sapiens 94-98
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 30-32 hypoxia inducible factor 1 subunit alpha Homo sapiens 145-150
15910691-9 2005 All-trans-retinoic acid (ATRA) induced Pgp activity in two of three infectants to a larger extent than in parental cells. Tretinoin 0-23 ATP binding cassette subfamily B member 1 Homo sapiens 39-42
15910691-9 2005 All-trans-retinoic acid (ATRA) induced Pgp activity in two of three infectants to a larger extent than in parental cells. Tretinoin 25-29 ATP binding cassette subfamily B member 1 Homo sapiens 39-42
15910691-10 2005 CONCLUSION: The data show that RARalpha regulates MDR1/ Pgp activity in human leukemic cells, in the first place, Pgp activity induced by ATRA. Tretinoin 138-142 ATP binding cassette subfamily B member 1 Homo sapiens 50-54
15910691-10 2005 CONCLUSION: The data show that RARalpha regulates MDR1/ Pgp activity in human leukemic cells, in the first place, Pgp activity induced by ATRA. Tretinoin 138-142 ATP binding cassette subfamily B member 1 Homo sapiens 56-59
15910691-10 2005 CONCLUSION: The data show that RARalpha regulates MDR1/ Pgp activity in human leukemic cells, in the first place, Pgp activity induced by ATRA. Tretinoin 138-142 ATP binding cassette subfamily B member 1 Homo sapiens 114-117
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 15-28 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-76
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 15-28 hypoxia inducible factor 1 subunit alpha Homo sapiens 145-150
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 30-32 CREB binding protein Homo sapiens 178-181
15857604-7 2005 Possible underlying mechanisms of these AhR responses are discussed, including enhanced metabolism of retinoic acid which attenuates TGFbeta-mediated apoptosis and interaction of the Ah receptor with the hypophosphorylated retinoblastoma tumor suppressor protein. Tretinoin 102-115 aryl-hydrocarbon receptor Mus musculus 40-43
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 15-28 CREB binding protein Homo sapiens 178-181
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 30-32 hypoxia inducible factor 1 subunit alpha Homo sapiens 71-76
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 35-48 TSPY like 2 Homo sapiens 141-146
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 191-204 TSPY like 2 Homo sapiens 246-251
15823505-7 2005 Transient transfection studies showed that ectopic DENTT expression significantly increased TGF-beta1-responsive 3TP-Lux and CAGA12-Lux reporter transcription in 12MBr6 and NCI-H727 cells with TGF-beta1 addition, while ectopic DENTT expression had no significant effect on the transcription of a retinoic acid-responsive element reporter in the presence of retinoic acid or TGF-beta1. Tretinoin 296-309 TSPY like 2 Homo sapiens 51-56
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 35-48 transforming growth factor beta 1 Homo sapiens 167-176
15823505-7 2005 Transient transfection studies showed that ectopic DENTT expression significantly increased TGF-beta1-responsive 3TP-Lux and CAGA12-Lux reporter transcription in 12MBr6 and NCI-H727 cells with TGF-beta1 addition, while ectopic DENTT expression had no significant effect on the transcription of a retinoic acid-responsive element reporter in the presence of retinoic acid or TGF-beta1. Tretinoin 296-309 transforming growth factor beta 1 Homo sapiens 92-101
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 35-48 TSPY like 2 Homo sapiens 246-251
15823505-7 2005 Transient transfection studies showed that ectopic DENTT expression significantly increased TGF-beta1-responsive 3TP-Lux and CAGA12-Lux reporter transcription in 12MBr6 and NCI-H727 cells with TGF-beta1 addition, while ectopic DENTT expression had no significant effect on the transcription of a retinoic acid-responsive element reporter in the presence of retinoic acid or TGF-beta1. Tretinoin 357-370 TSPY like 2 Homo sapiens 51-56
15823505-7 2005 Transient transfection studies showed that ectopic DENTT expression significantly increased TGF-beta1-responsive 3TP-Lux and CAGA12-Lux reporter transcription in 12MBr6 and NCI-H727 cells with TGF-beta1 addition, while ectopic DENTT expression had no significant effect on the transcription of a retinoic acid-responsive element reporter in the presence of retinoic acid or TGF-beta1. Tretinoin 357-370 transforming growth factor beta 1 Homo sapiens 92-101
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 35-48 transforming growth factor beta 1 Homo sapiens 167-176
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 191-204 transforming growth factor beta 1 Homo sapiens 22-31
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 191-204 TSPY like 2 Homo sapiens 246-251
15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 191-204 transforming growth factor beta 1 Homo sapiens 22-31
15970678-8 2005 Cotreatment with the RAR-alpha antagonist, Ro41-5253 or pan-TGF-beta neutralizing antibody abolished the phenotypic and antiproliferative effects of all-trans retinoic acid. Tretinoin 159-172 transforming growth factor beta 1 Homo sapiens 60-68
15921376-8 2005 Before, during and after retinoic acid treatment APL cells are TRAIL-resistant. Tretinoin 25-38 TNF superfamily member 10 Homo sapiens 63-68
15867224-6 2005 Also, shcB was hardly expressed in neuroblastoma cell lines, but its expression in RT-BM-1 cells was enhanced after all-trans-retinoic acid-induced differentiation, and it was highly expressed in low-stage tumors (P = 0.0095). Tretinoin 126-139 SHC adaptor protein 2 Homo sapiens 6-10
15921376-9 2005 The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression. Tretinoin 57-70 TNF superfamily member 10 Homo sapiens 111-116
15836616-0 2005 Activation of Rac1 by phosphatidylinositol 3-kinase in vivo: role in activation of mitogen-activated protein kinase (MAPK) pathways and retinoic acid-induced neuronal differentiation of SH-SY5Y cells. Tretinoin 136-149 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 22-51
15824860-11 2005 Experimental ERK1/2 inhibition led to a severe drop in baseline and RA-stimulated CTGF expression, whereas p38 inhibition increased it markedly. Tretinoin 68-70 cellular communication network factor 2 Gallus gallus 82-86
15824860-13 2005 Tests with Noggin showed that RA induction of CTGF expression was negatively influenced by BMP signaling, whereas induction of collagen X expression was BMP-dependent. Tretinoin 30-32 cellular communication network factor 2 Gallus gallus 46-50
15836616-5 2005 RA-induced activation of Rac1 is mediated by phosphatidylinositol 3-kinase (PI3K), probably because of phosphorylation of the p85 regulatory subunit by Src kinases. Tretinoin 0-2 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 45-74
15836616-2 2005 Using an in vitro cell culture model of neuroblastoma SH-SY5Y cells, we demonstrated previously that RhoA is an in vivo substrate of tissue transglutaminase (TGase) and retinoic acid (RA) promoted activation of RhoA by transamidation. Tretinoin 169-182 ras homolog family member A Homo sapiens 101-105
15836616-2 2005 Using an in vitro cell culture model of neuroblastoma SH-SY5Y cells, we demonstrated previously that RhoA is an in vivo substrate of tissue transglutaminase (TGase) and retinoic acid (RA) promoted activation of RhoA by transamidation. Tretinoin 169-182 ras homolog family member A Homo sapiens 211-215
15836616-2 2005 Using an in vitro cell culture model of neuroblastoma SH-SY5Y cells, we demonstrated previously that RhoA is an in vivo substrate of tissue transglutaminase (TGase) and retinoic acid (RA) promoted activation of RhoA by transamidation. Tretinoin 184-186 ras homolog family member A Homo sapiens 101-105
15836616-2 2005 Using an in vitro cell culture model of neuroblastoma SH-SY5Y cells, we demonstrated previously that RhoA is an in vivo substrate of tissue transglutaminase (TGase) and retinoic acid (RA) promoted activation of RhoA by transamidation. Tretinoin 184-186 transglutaminase 2 Homo sapiens 133-156
15836616-2 2005 Using an in vitro cell culture model of neuroblastoma SH-SY5Y cells, we demonstrated previously that RhoA is an in vivo substrate of tissue transglutaminase (TGase) and retinoic acid (RA) promoted activation of RhoA by transamidation. Tretinoin 184-186 ras homolog family member A Homo sapiens 211-215
15812311-3 2005 Cyclooxygenase-2-765G-->C constructs, when transfected into human neural cells, exhibited a 1.4-fold higher level of basal expression, while the proinflammatory factors interleukin-1beta and 9-cis retinoic acid synergistically induced polymorphic promoter activity 2.4-fold over wild type. Tretinoin 200-213 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16
15857687-2 2005 We have previously shown that bone morphogenetic protein-2 (BMP2) and retinoic acid synergistically induce the responsiveness of developing sympathetic neurons to neurotrophic factors, neurotrophin 3 (NT-3), and GDNF by upregulating corresponding receptors concomitantly with the induction of other neuron-specific genes including BRINP1, a neuron-specific cell-cycle regulatory protein. Tretinoin 70-83 glial cell derived neurotrophic factor Homo sapiens 212-216
15703382-0 2005 Expression of the retinoic acid-metabolizing enzyme CYP26A1 limits programmed cell death. Tretinoin 18-31 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 52-59
15703382-3 2005 On the other hand, we show here that various cell lines overexpressing CYP26A1, a cytochrome P450 enzyme specifically involved in the catabolic inactivation of RA, exhibit increased resistance to various apoptogenic factors, including death receptor ligands such as tumor necrosis factor-related apoptosis-inducing ligand. Tretinoin 160-162 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 71-78
15929660-5 2005 Type I 5"-deiodinase, another selenoprotein that catalyzes thyroid hormone metabolism, was detectable only in cell lysates by enzyme assay and Western blot, and responded to stimulation by both Na(2)SeO(3) and retinoic acid. Tretinoin 210-223 iodothyronine deiodinase 1 Homo sapiens 0-20
15908778-13 2005 Caspase 3-like activity was induced by the apoptotic concentrations of atRA at late time points. Tretinoin 71-75 caspase 3 Homo sapiens 0-9
15777798-3 2005 We found that IGFBP-5 expression increased during retinoic acid (RA)-mediated differentiation of NB cells. Tretinoin 50-63 insulin like growth factor binding protein 5 Homo sapiens 14-21
15777798-3 2005 We found that IGFBP-5 expression increased during retinoic acid (RA)-mediated differentiation of NB cells. Tretinoin 65-67 insulin like growth factor binding protein 5 Homo sapiens 14-21
15777798-5 2005 We defined the shortest region of the human IGFBP-5 promoter (from nucleotide -83 to +53) which is sensitive to RA. Tretinoin 112-114 insulin like growth factor binding protein 5 Homo sapiens 44-51
15777798-7 2005 DNA Affinity Precipitation Assays (DAPA) and chromatin immunoprecipitation demonstrated that the binding of C/EBPalpha and beta to the C/EBP site decreased upon treatment with RA. Tretinoin 176-178 CCAAT enhancer binding protein alpha Homo sapiens 108-118
15777798-7 2005 DNA Affinity Precipitation Assays (DAPA) and chromatin immunoprecipitation demonstrated that the binding of C/EBPalpha and beta to the C/EBP site decreased upon treatment with RA. Tretinoin 176-178 CCAAT enhancer binding protein alpha Homo sapiens 108-113
15799023-6 2005 RESULTS: Endogenous TGFbetaRII and Smad2 are downregulated in the inner ear following in utero atRA treatment. Tretinoin 95-99 SMAD family member 2 Mus musculus 35-40
16054987-7 2005 Moreover, this alcohol-impaired retinoic acid homeostasis interferes with (1) retinoic acid signaling (e.g., down-regulates retinoid target gene expression) and (2) retinoic acid "cross-talk" with the mitogen-activated protein kinase [(MAPK), including Jun N-terminal kinase, extracellular signal-regulated kinase, and p38 kinase] signaling pathway. Tretinoin 32-45 mitogen-activated protein kinase 14 Homo sapiens 319-322
15781332-5 2005 RESULTS: All-trans retinoic acid (1 mumol/L) reduced expansion of CD34+CD38-Lin- TNC and CFUs after 2 to 5 weeks of culture. Tretinoin 9-32 CD34 molecule Homo sapiens 66-70
15736225-3 2005 Moreover, among all retinoic acid receptors (RARs) and retinoid X receptors (RXRs), RARbeta was strongly induced by retinoic acid in the ventral telencephalon, suggesting that RARbeta might be involved in retinoid signaling competence. Tretinoin 20-33 retinoic acid receptor beta Homo sapiens 84-91
15736225-3 2005 Moreover, among all retinoic acid receptors (RARs) and retinoid X receptors (RXRs), RARbeta was strongly induced by retinoic acid in the ventral telencephalon, suggesting that RARbeta might be involved in retinoid signaling competence. Tretinoin 20-33 retinoic acid receptor beta Homo sapiens 176-183
15817924-0 2005 Differential effects of all-trans-retinoic acid (RA) on Erk1/2 phosphorylation and cAMP accumulation in normal and malignant human prostate epithelial cells: Erk1/2 inhibition restores RA-induced decrease of cell growth in malignant prostate cells. Tretinoin 24-47 mitogen-activated protein kinase 3 Homo sapiens 56-62
15817924-0 2005 Differential effects of all-trans-retinoic acid (RA) on Erk1/2 phosphorylation and cAMP accumulation in normal and malignant human prostate epithelial cells: Erk1/2 inhibition restores RA-induced decrease of cell growth in malignant prostate cells. Tretinoin 24-47 mitogen-activated protein kinase 3 Homo sapiens 158-164
15817924-0 2005 Differential effects of all-trans-retinoic acid (RA) on Erk1/2 phosphorylation and cAMP accumulation in normal and malignant human prostate epithelial cells: Erk1/2 inhibition restores RA-induced decrease of cell growth in malignant prostate cells. Tretinoin 49-51 mitogen-activated protein kinase 3 Homo sapiens 56-62
15817924-0 2005 Differential effects of all-trans-retinoic acid (RA) on Erk1/2 phosphorylation and cAMP accumulation in normal and malignant human prostate epithelial cells: Erk1/2 inhibition restores RA-induced decrease of cell growth in malignant prostate cells. Tretinoin 49-51 mitogen-activated protein kinase 3 Homo sapiens 158-164
15817924-0 2005 Differential effects of all-trans-retinoic acid (RA) on Erk1/2 phosphorylation and cAMP accumulation in normal and malignant human prostate epithelial cells: Erk1/2 inhibition restores RA-induced decrease of cell growth in malignant prostate cells. Tretinoin 185-187 mitogen-activated protein kinase 3 Homo sapiens 158-164
15817924-4 2005 Then we have verified the effect of the inhibition of Erk1/2 on RA-induced growth arrest and apoptosis in malignant cells. Tretinoin 64-66 mitogen-activated protein kinase 3 Homo sapiens 54-60
15817924-5 2005 RESULTS: In NPEC and in EPN treated with RA for up to 24 h, Western blot analyses of Erk1/2 phosphorylation show that RA causes a rapid activation of Erk1/2 within 5 min, which is maintained for 30 min, followed by a return to basal levels. Tretinoin 41-43 mitogen-activated protein kinase 3 Homo sapiens 85-91
15817924-5 2005 RESULTS: In NPEC and in EPN treated with RA for up to 24 h, Western blot analyses of Erk1/2 phosphorylation show that RA causes a rapid activation of Erk1/2 within 5 min, which is maintained for 30 min, followed by a return to basal levels. Tretinoin 41-43 mitogen-activated protein kinase 3 Homo sapiens 150-156
15817924-5 2005 RESULTS: In NPEC and in EPN treated with RA for up to 24 h, Western blot analyses of Erk1/2 phosphorylation show that RA causes a rapid activation of Erk1/2 within 5 min, which is maintained for 30 min, followed by a return to basal levels. Tretinoin 118-120 mitogen-activated protein kinase 3 Homo sapiens 85-91
15817924-5 2005 RESULTS: In NPEC and in EPN treated with RA for up to 24 h, Western blot analyses of Erk1/2 phosphorylation show that RA causes a rapid activation of Erk1/2 within 5 min, which is maintained for 30 min, followed by a return to basal levels. Tretinoin 118-120 mitogen-activated protein kinase 3 Homo sapiens 150-156
15623821-0 2005 All-trans-retinoic acid treatment inhibits the growth of retinoic acid receptor beta messenger ribonucleic acid expressing thyroid cancer cell lines but does not reinduce the expression of thyroid-specific genes. Tretinoin 0-23 retinoic acid receptor beta Homo sapiens 57-84
15790450-4 2005 The objective of this study was to determine if p53 is involved in the mechanism of RA radiosensitization. Tretinoin 84-86 tumor protein p53 Homo sapiens 48-51
15790450-6 2005 RESULTS: RA (5 microM 9-cis-RA) radiosensitized the SiHa and CC-1 cell lines that contain HPV-degraded p53, but did not radiosensitize the SW962 cell line, which is HPV negative and contains wild-type p53, nor the C33a cell line, which contains mutant p53 (R273C). Tretinoin 9-11 tumor protein p53 Homo sapiens 103-106
15790450-6 2005 RESULTS: RA (5 microM 9-cis-RA) radiosensitized the SiHa and CC-1 cell lines that contain HPV-degraded p53, but did not radiosensitize the SW962 cell line, which is HPV negative and contains wild-type p53, nor the C33a cell line, which contains mutant p53 (R273C). Tretinoin 9-11 tumor protein p53 Homo sapiens 201-204
15790450-6 2005 RESULTS: RA (5 microM 9-cis-RA) radiosensitized the SiHa and CC-1 cell lines that contain HPV-degraded p53, but did not radiosensitize the SW962 cell line, which is HPV negative and contains wild-type p53, nor the C33a cell line, which contains mutant p53 (R273C). Tretinoin 9-11 tumor protein p53 Homo sapiens 201-204
15602748-0 2005 Retinoic acid inhibits expression of TNF-alpha and iNOS in activated rat microglia. Tretinoin 0-13 tumor necrosis factor Rattus norvegicus 37-46
15602748-0 2005 Retinoic acid inhibits expression of TNF-alpha and iNOS in activated rat microglia. Tretinoin 0-13 nitric oxide synthase 2 Rattus norvegicus 51-55
15602748-2 2005 As all-trans-retinoic acid (RA) has been reported to exert anti-inflammatory actions in various cell types, we have examined its effects on the expression of TNF-alpha and inducible nitric oxide synthase (iNOS) in microglia activated by beta-amyloid peptide (Abeta) and lipopolysaccharide (LPS). Tretinoin 3-26 nitric oxide synthase 2 Rattus norvegicus 205-209
15602748-2 2005 As all-trans-retinoic acid (RA) has been reported to exert anti-inflammatory actions in various cell types, we have examined its effects on the expression of TNF-alpha and inducible nitric oxide synthase (iNOS) in microglia activated by beta-amyloid peptide (Abeta) and lipopolysaccharide (LPS). Tretinoin 28-30 tumor necrosis factor Rattus norvegicus 158-167
15602748-2 2005 As all-trans-retinoic acid (RA) has been reported to exert anti-inflammatory actions in various cell types, we have examined its effects on the expression of TNF-alpha and inducible nitric oxide synthase (iNOS) in microglia activated by beta-amyloid peptide (Abeta) and lipopolysaccharide (LPS). Tretinoin 28-30 nitric oxide synthase 2 Rattus norvegicus 172-203
15602748-2 2005 As all-trans-retinoic acid (RA) has been reported to exert anti-inflammatory actions in various cell types, we have examined its effects on the expression of TNF-alpha and inducible nitric oxide synthase (iNOS) in microglia activated by beta-amyloid peptide (Abeta) and lipopolysaccharide (LPS). Tretinoin 28-30 nitric oxide synthase 2 Rattus norvegicus 205-209
15602748-4 2005 RA acted in a dose-dependent manner (0.1-10 microM) by attenuating both TNF-alpha (29-97%) and iNOS (61-96%) mRNA expression in microglia exposed to Abeta or LPS. Tretinoin 0-2 tumor necrosis factor Rattus norvegicus 72-81
15602748-4 2005 RA acted in a dose-dependent manner (0.1-10 microM) by attenuating both TNF-alpha (29-97%) and iNOS (61-96%) mRNA expression in microglia exposed to Abeta or LPS. Tretinoin 0-2 nitric oxide synthase 2 Rattus norvegicus 95-99
15602748-5 2005 RA-induced inhibition of TNF-alpha and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-alpha proteins as revealed by nitrite assay and ELISA, respectively. Tretinoin 0-2 tumor necrosis factor Rattus norvegicus 25-34
15602748-5 2005 RA-induced inhibition of TNF-alpha and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-alpha proteins as revealed by nitrite assay and ELISA, respectively. Tretinoin 0-2 nitric oxide synthase 2 Rattus norvegicus 39-43
15602748-5 2005 RA-induced inhibition of TNF-alpha and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-alpha proteins as revealed by nitrite assay and ELISA, respectively. Tretinoin 0-2 nitric oxide synthase 2 Rattus norvegicus 142-146
15602748-5 2005 RA-induced inhibition of TNF-alpha and iNOS mRNA expression in activated microglia was accompanied by the concomitant reduction in release of iNOS and TNF-alpha proteins as revealed by nitrite assay and ELISA, respectively. Tretinoin 0-2 tumor necrosis factor Rattus norvegicus 151-160
15602748-6 2005 The anti-inflammatory effects of RA were correlated with the enhanced expression of retinoic acid receptor-beta, and transforming growth factor-beta1 as well as the inhibition of NF-kappaB translocation. Tretinoin 33-35 retinoic acid receptor, beta Rattus norvegicus 84-111
15602748-6 2005 The anti-inflammatory effects of RA were correlated with the enhanced expression of retinoic acid receptor-beta, and transforming growth factor-beta1 as well as the inhibition of NF-kappaB translocation. Tretinoin 33-35 transforming growth factor, beta 1 Rattus norvegicus 117-149
15745819-1 2005 A series of [2-imidazol-1-yl-2-(6-alkoxy-naphthalen-2-yl)-1-methyl-ethyl]-dimethyl-amines were designed and synthesized as CYP26 inhibitors, serving as retinoic acid metabolic blocking agents (RAMBA"s). Tretinoin 152-165 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 123-128
16010971-4 2005 In this study we have investigated a possible role for NTE in the all-trans retinoic acid (ATRA)-induced differentiation of neuroblastoma cells by antisense RNA. Tretinoin 66-89 patatin like phospholipase domain containing 6 Homo sapiens 55-58
16010971-4 2005 In this study we have investigated a possible role for NTE in the all-trans retinoic acid (ATRA)-induced differentiation of neuroblastoma cells by antisense RNA. Tretinoin 91-95 patatin like phospholipase domain containing 6 Homo sapiens 55-58
16010971-8 2005 ATRA-induced differentiation of the neuroblastoma cells with lowered NTE activity revealed that inhibition of NTE expression does not affect neural differentiation in SK-N-SH cells. Tretinoin 0-4 patatin like phospholipase domain containing 6 Homo sapiens 69-72
16010971-8 2005 ATRA-induced differentiation of the neuroblastoma cells with lowered NTE activity revealed that inhibition of NTE expression does not affect neural differentiation in SK-N-SH cells. Tretinoin 0-4 patatin like phospholipase domain containing 6 Homo sapiens 110-113
15816857-5 2005 The human secretin gene in SH-SY5Y cells is controlled by the (Sp1 + Sp4)/Sp3 ratio and the RA-induced activation is a partial result of a decrease in Sp3 levels. Tretinoin 92-94 Sp3 transcription factor Homo sapiens 151-154
15816857-10 2005 We conclude that RA induction of the secretin gene in neuronal cells is regulated by the combined actions of reducing Sp3 and increasing NFI-C expression. Tretinoin 17-19 Sp3 transcription factor Homo sapiens 118-121
15816857-10 2005 We conclude that RA induction of the secretin gene in neuronal cells is regulated by the combined actions of reducing Sp3 and increasing NFI-C expression. Tretinoin 17-19 nuclear factor I C Homo sapiens 137-142
15807274-4 2005 RESULTS: After 15 days of induction by retinoic acid, the serum E2 and BGP contents of rats were obviously decreased, the activities of AKP and TRAP were significantly increased, and the levels of BMD were lowered. Tretinoin 39-52 dihydrolipoamide S-succinyltransferase Rattus norvegicus 64-74
15707588-2 2005 In this study, using luciferase assay of a reporter gene containing PPAR response element (PPRE), we found PPRE transactivity was additively induced by PPAR gamma activator (15dPGJ2) and RXR activator (9-cis retinoic acid, 9-cis RA). Tretinoin 208-221 peroxisome proliferator activated receptor gamma Homo sapiens 152-162
15590754-9 2005 BPI gene expression in Sertoli and promyelocytic cells was enhanced several-fold by all-trans retinoic acid. Tretinoin 94-107 bactericidal permeablility increasing protein Mus musculus 0-3
15868907-2 2005 In this study, we showed that the amount of TSP-1 secreted by two human leukemia cell lines, HL-60 and NB4, increased markedly during differentiation of these cells by all-trans retinoic acid (ATRA) (10(-7) M), reaching about 100 ng/10(6) cells after 3 days. Tretinoin 178-191 thrombospondin 1 Homo sapiens 44-49
15868907-2 2005 In this study, we showed that the amount of TSP-1 secreted by two human leukemia cell lines, HL-60 and NB4, increased markedly during differentiation of these cells by all-trans retinoic acid (ATRA) (10(-7) M), reaching about 100 ng/10(6) cells after 3 days. Tretinoin 193-197 thrombospondin 1 Homo sapiens 44-49
15749674-1 2005 The levels of expression of WT1 gene and WT1+17AA isoforms rapidly decreased during the differentiation of NB4 cells induced by all-trans retinoic acid; this decrease was conversely related to the dynamic changes of CD11b positive cells, indicating that the abnormally high expression of WT1 gene and WT1+17AA isoforms was associated with a block of NB4 cell differentiation. Tretinoin 138-151 WT1 transcription factor Homo sapiens 28-31
15749674-1 2005 The levels of expression of WT1 gene and WT1+17AA isoforms rapidly decreased during the differentiation of NB4 cells induced by all-trans retinoic acid; this decrease was conversely related to the dynamic changes of CD11b positive cells, indicating that the abnormally high expression of WT1 gene and WT1+17AA isoforms was associated with a block of NB4 cell differentiation. Tretinoin 138-151 WT1 transcription factor Homo sapiens 41-44
15749674-1 2005 The levels of expression of WT1 gene and WT1+17AA isoforms rapidly decreased during the differentiation of NB4 cells induced by all-trans retinoic acid; this decrease was conversely related to the dynamic changes of CD11b positive cells, indicating that the abnormally high expression of WT1 gene and WT1+17AA isoforms was associated with a block of NB4 cell differentiation. Tretinoin 138-151 WT1 transcription factor Homo sapiens 41-44
15749674-1 2005 The levels of expression of WT1 gene and WT1+17AA isoforms rapidly decreased during the differentiation of NB4 cells induced by all-trans retinoic acid; this decrease was conversely related to the dynamic changes of CD11b positive cells, indicating that the abnormally high expression of WT1 gene and WT1+17AA isoforms was associated with a block of NB4 cell differentiation. Tretinoin 138-151 WT1 transcription factor Homo sapiens 41-44
15883744-0 2005 Retinoic acid inhibits CD40 plus IL-4 mediated IgE production through alterations of sCD23, sCD54 and IL-6 production. Tretinoin 0-13 interleukin 4 Homo sapiens 33-37
15883744-0 2005 Retinoic acid inhibits CD40 plus IL-4 mediated IgE production through alterations of sCD23, sCD54 and IL-6 production. Tretinoin 0-13 interleukin 6 Homo sapiens 102-106
15883744-1 2005 BACKGROUND: All-trans retinoic acid (ATRA) inhibits IgE synthesis from anti-CD40 plus IL-4 stimulated human B lymphocytes. Tretinoin 12-35 interleukin 4 Homo sapiens 86-90
15883744-1 2005 BACKGROUND: All-trans retinoic acid (ATRA) inhibits IgE synthesis from anti-CD40 plus IL-4 stimulated human B lymphocytes. Tretinoin 37-41 interleukin 4 Homo sapiens 86-90
15883744-10 2005 Cytokine analysis showed that IL-6 secretion was significantly inhibited by ATRA (53.6 +/- 0.6%) and also IL-6 mRNA synthesis was reduced (66.3 +/- 11.6%). Tretinoin 76-80 interleukin 6 Homo sapiens 30-34
15883744-11 2005 The observed inhibition of IgE production mediated by ATRA was significantly reversed to 90.5 +/- 12% by the addition of 100 pg/mL recombinant IL-6. Tretinoin 54-58 interleukin 6 Homo sapiens 143-147
15883744-12 2005 CONCLUSIONS: ATRA interferes through several pathways with the anti-CD40 plus IL-4 mediated B cell activation, namely IL-6, CD23 and CD54. Tretinoin 13-17 interleukin 4 Homo sapiens 78-82
15883744-12 2005 CONCLUSIONS: ATRA interferes through several pathways with the anti-CD40 plus IL-4 mediated B cell activation, namely IL-6, CD23 and CD54. Tretinoin 13-17 interleukin 6 Homo sapiens 118-122
15728448-4 2005 Treatment of primary human monocytes with ATRA led to the down-regulation of TLR2 as well as its coreceptor CD14, but not TLR1 or TLR4. Tretinoin 42-46 toll like receptor 2 Homo sapiens 77-81
15728448-5 2005 The ability of a TLR2/1 ligand to trigger monocyte cytokine release was inhibited by pre- and cotreatment with ATRA; however, TLR4 activation was affected by cotreatment only. Tretinoin 111-115 toll like receptor 2 Homo sapiens 17-23
15728448-7 2005 These data indicate that ATRA exerts an anti-inflammatory effect on monocytes via two pathways, one specifically affecting TLR2/1 and CD14 expression and one independent of TLR expression. Tretinoin 25-29 toll like receptor 2 Homo sapiens 123-129
15713534-2 2005 The silencing mediator of retinoic acid and thyroid hormone (SMRT) and other members of the corepressor complex are enriched in spherical intranuclear foci, and repress estrogen receptor alpha (ERalpha)-dependent transcriptional activity. Tretinoin 26-39 estrogen receptor 1 Homo sapiens 169-192
15713534-2 2005 The silencing mediator of retinoic acid and thyroid hormone (SMRT) and other members of the corepressor complex are enriched in spherical intranuclear foci, and repress estrogen receptor alpha (ERalpha)-dependent transcriptional activity. Tretinoin 26-39 estrogen receptor 1 Homo sapiens 194-201
15714209-7 2005 Both ATRA and 13cisRA dramatically induced the expression of CYP26A1 in SH-SY5Y cells, and treatment with R116010, but not acitretin, potentiated the RA-induced expression of a reporter gene and CYP26A1. Tretinoin 5-9 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 61-68
15714209-7 2005 Both ATRA and 13cisRA dramatically induced the expression of CYP26A1 in SH-SY5Y cells, and treatment with R116010, but not acitretin, potentiated the RA-induced expression of a reporter gene and CYP26A1. Tretinoin 5-9 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 195-202
15674351-2 2005 We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity. Tretinoin 134-147 tumor protein p53 Homo sapiens 30-33
15674351-2 2005 We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity. Tretinoin 134-147 tumor protein p53 Homo sapiens 176-179
15674351-2 2005 We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity. Tretinoin 149-151 tumor protein p53 Homo sapiens 30-33
15674351-2 2005 We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity. Tretinoin 149-151 tumor protein p53 Homo sapiens 176-179
15674351-11 2005 While RA alone had no effect on p53-NRD activity, cotreatment with RA and the histone deacetylase inhibitor trichostatin-A (TSA) completely relieved p53-NRD-mediated repression. Tretinoin 67-69 tumor protein p53 Homo sapiens 149-152
15664402-6 2005 CONCLUSIONS: Chronic atRA treatment activates gene and protein expression of APJ and apelin and reduces blood pressure in SHR, suggesting that atRA may regulate the balance between apelin-APJ and angiotensin II-AT(1) signaling and have potential clinical value in the prevention and treatment of human hypertension. Tretinoin 21-25 angiotensinogen Homo sapiens 196-210
15471950-3 2005 RA treatment of sensitive cell lines resulted in phosphorylation/activation of mTOR and downstream induction of p70 S6 kinase activity. Tretinoin 0-2 mechanistic target of rapamycin kinase Homo sapiens 79-83
15471950-6 2005 RA treatment of leukemia cells also resulted in an mTOR-mediated phosphorylation of the 4E-BP1 repressor of mRNA translation, to induce its deactivation and dissociation from the eukaryotic initiation factor-4E (eIF-4E) complex. Tretinoin 0-2 mechanistic target of rapamycin kinase Homo sapiens 51-55
15474987-6 2005 Pharmacological studies using PD098059 (a MEK inhibitor), SB203580 (a p38 MAPK inhibitor) and SP600125 (a JNK inhibitor) suggested that the MEK pathway was important for VD3 and ATRA-induced differentiation and also its enhancement by MG or HK, the p38 MAPK pathway had a inhibitory effect and the JNK pathway had little influence. Tretinoin 178-182 mitogen-activated protein kinase kinase 7 Homo sapiens 140-143
15574421-6 2005 Human SHBG transcripts were found within their Sertoli cells, primary cultures of which secrete human SHBG, and this was increased by treatment with follicle-stimulating hormone, retinoic acid, and estradiol but not testosterone. Tretinoin 179-192 sex hormone binding globulin Homo sapiens 6-10
15574421-6 2005 Human SHBG transcripts were found within their Sertoli cells, primary cultures of which secrete human SHBG, and this was increased by treatment with follicle-stimulating hormone, retinoic acid, and estradiol but not testosterone. Tretinoin 179-192 sex hormone binding globulin Homo sapiens 102-106
15592517-7 2005 Our study highlights, for the first time, the involvement of Wnt-5a, which has a role in embryonic and morphogenetic processes, in the response of malignant neuroblasts to RA. Tretinoin 172-174 Wnt family member 5A Homo sapiens 61-67
15592517-8 2005 In conclusion, we demonstrated that RA, which is used in the treatment of high-risk NB patients with recurrent/residual disease in the bone marrow, is able to upregulate Wnt-5a gene expression. Tretinoin 36-38 Wnt family member 5A Homo sapiens 170-176
15694019-1 2005 BACKGROUND & OBJECTIVE: apr-1 was cloned by improved polymerase chain reaction (PCR)-based subtractive hybridization from all-trans retinoic acid (ATRA)-induced apoptotic leukemia HL-60 cells in 1999. Tretinoin 136-149 MAGE family member H1 Homo sapiens 28-33
15694019-1 2005 BACKGROUND & OBJECTIVE: apr-1 was cloned by improved polymerase chain reaction (PCR)-based subtractive hybridization from all-trans retinoic acid (ATRA)-induced apoptotic leukemia HL-60 cells in 1999. Tretinoin 151-155 MAGE family member H1 Homo sapiens 28-33
15466927-0 2005 The t-PA -7351C>T enhancer polymorphism decreases Sp1 and Sp3 protein binding affinity and transcriptional responsiveness to retinoic acid. Tretinoin 125-138 plasminogen activator, tissue type Homo sapiens 4-8
15466927-0 2005 The t-PA -7351C>T enhancer polymorphism decreases Sp1 and Sp3 protein binding affinity and transcriptional responsiveness to retinoic acid. Tretinoin 125-138 Sp3 transcription factor Homo sapiens 58-61
15466927-1 2005 We have previously identified a common polymorphism at the tissue-type plasminogen activator (t-PA) locus (-7351C>T), located within a GC-box in the retinoic acid (RA) and steroid hormone responsive t-PA enhancer. Tretinoin 149-162 plasminogen activator, tissue type Homo sapiens 59-92
15466927-1 2005 We have previously identified a common polymorphism at the tissue-type plasminogen activator (t-PA) locus (-7351C>T), located within a GC-box in the retinoic acid (RA) and steroid hormone responsive t-PA enhancer. Tretinoin 149-162 plasminogen activator, tissue type Homo sapiens 94-98
15466927-1 2005 We have previously identified a common polymorphism at the tissue-type plasminogen activator (t-PA) locus (-7351C>T), located within a GC-box in the retinoic acid (RA) and steroid hormone responsive t-PA enhancer. Tretinoin 164-166 plasminogen activator, tissue type Homo sapiens 59-92
15466927-1 2005 We have previously identified a common polymorphism at the tissue-type plasminogen activator (t-PA) locus (-7351C>T), located within a GC-box in the retinoic acid (RA) and steroid hormone responsive t-PA enhancer. Tretinoin 164-166 plasminogen activator, tissue type Homo sapiens 94-98
15466927-6 2005 Further EMSAs showed that RA treatment enhanced Sp1/Sp3 binding to the GC-box. Tretinoin 26-28 Sp3 transcription factor Homo sapiens 52-55
15661642-3 2005 cDNA transfection assays showed that like human cyp26b1, zebrafish cyp26b1 is involved in limiting the activity of retinoic acid. Tretinoin 115-128 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 48-55
15661643-9 2005 Whole mount in situ hybridization detected crabp2b and crabp2a mRNA in a number of structures known to require retinoic acid signaling during embryonic development. Tretinoin 111-124 cellular retinoic acid binding protein 2, a Danio rerio 55-62
15645120-2 2005 Treatment of SCC25 oral squamous carcinoma cells with sodium butyrate (SB) at 0.5-5 mM or all-trans retinoic acid (ATRA) at 3-300 microM inhibited cell growth and induced apoptosis in a dose-dependent manner with concomittant increases in expression of keratin 13, p21WAF1/Cip1 and p27Kip1 and decreases in expression of COX-2. Tretinoin 115-119 cyclin dependent kinase inhibitor 1A Homo sapiens 273-277
15645120-2 2005 Treatment of SCC25 oral squamous carcinoma cells with sodium butyrate (SB) at 0.5-5 mM or all-trans retinoic acid (ATRA) at 3-300 microM inhibited cell growth and induced apoptosis in a dose-dependent manner with concomittant increases in expression of keratin 13, p21WAF1/Cip1 and p27Kip1 and decreases in expression of COX-2. Tretinoin 115-119 mitochondrially encoded cytochrome c oxidase II Homo sapiens 321-326
15537748-9 2005 Furthermore, atRA treatment reduced phosphorylated Rb and decreased cdk2 and cdk4 kinase activity. Tretinoin 13-17 cyclin-dependent kinase 4 Mus musculus 77-81
15607369-0 2005 The Notch ligand, Delta-1, alters retinoic acid (RA)-induced neutrophilic differentiation into monocytic and reduces RA-induced apoptosis in NB4 cells. Tretinoin 34-47 delta like non-canonical Notch ligand 1 Homo sapiens 18-25
15607369-0 2005 The Notch ligand, Delta-1, alters retinoic acid (RA)-induced neutrophilic differentiation into monocytic and reduces RA-induced apoptosis in NB4 cells. Tretinoin 49-51 delta like non-canonical Notch ligand 1 Homo sapiens 18-25
15607369-0 2005 The Notch ligand, Delta-1, alters retinoic acid (RA)-induced neutrophilic differentiation into monocytic and reduces RA-induced apoptosis in NB4 cells. Tretinoin 117-119 delta like non-canonical Notch ligand 1 Homo sapiens 18-25
15607369-6 2005 RA treatment induced cleavage of caspase-8 and PARP in NB4. Tretinoin 0-2 poly(ADP-ribose) polymerase 1 Homo sapiens 47-51
15607369-7 2005 Delta-1 suppressed the RA-induced cleavage of them, which may be a possible mechanism through which Delta-1 suppressed the RA-induced apoptosis. Tretinoin 23-25 delta like non-canonical Notch ligand 1 Homo sapiens 0-7
15607369-7 2005 Delta-1 suppressed the RA-induced cleavage of them, which may be a possible mechanism through which Delta-1 suppressed the RA-induced apoptosis. Tretinoin 23-25 delta like non-canonical Notch ligand 1 Homo sapiens 100-107
15657432-8 2005 JNK inhibition in a human lung cancer cell line enhanced RARalpha levels, ligand-induced activity of RXR-RAR dimers, and growth inhibition by RA. Tretinoin 57-59 mitogen-activated protein kinase 8 Homo sapiens 0-3
15596294-3 2005 In this study, we used a model system of matched primary and metastatic melanoma cells to investigate whether expression of Id1 and p16 proteins were involved in atRA-induced apoptosis and cell cycle re-distribution. Tretinoin 162-166 cyclin dependent kinase inhibitor 2A Homo sapiens 132-135
15607726-0 2005 Retinoic acid decreases nitric oxide production in endothelial cells: a role of phosphorylation of endothelial nitric oxide synthase at Ser(1179). Tretinoin 0-13 nitric oxide synthase 3 Bos taurus 99-132
15695403-0 2005 Retinoic acid inhibits the proliferative response induced by CD40 activation and interleukin-4 in mantle cell lymphoma. Tretinoin 0-13 interleukin 4 Homo sapiens 81-94
15695403-7 2005 Notably, RA isomers, and particularly 9-cis-RA, also inhibited the growth-promoting effect induced in primary MCL cells by CD40 activation alone or in combination with interleukin-4. Tretinoin 9-11 interleukin 4 Homo sapiens 168-181
15596294-7 2005 Expression level of Id1 protein was decreased and the p16 was increased in a dose- and time-dependent (P<0.05) manner after treatment with atRA. Tretinoin 142-146 cyclin dependent kinase inhibitor 2A Homo sapiens 54-57
15596294-0 2005 Expression profiles of Id1 and p16 proteins in all-trans-retinoic acid-induced apoptosis and cell cycle re-distribution in melanoma. Tretinoin 57-70 cyclin dependent kinase inhibitor 2A Homo sapiens 31-34
15596294-9 2005 These data suggested that the alterations of Id1 and/or p16 proteins were involved in atRA-induced apoptosis and cell cycle re-distribution in melanoma. Tretinoin 86-90 cyclin dependent kinase inhibitor 2A Homo sapiens 56-59
15667595-5 2005 The present investigation evaluates the role of retinoic acid on the expression of aryl sulfotransferase IV and hydroxysteroid sulfotransferase a in male and female Sprague-Dawley rat liver and intestine. Tretinoin 48-61 sulfotransferase family 1A member 1 Rattus norvegicus 83-107
15591039-3 2005 Here, we report the upregulation of core 2 beta1,6 N-acetylglucosaminyltransferase (C2GnT) activity both by all-trans retinoic acid (RA) and by IL-4 and IL-13 in the H292 airway epithelial cell line. Tretinoin 133-135 interleukin 13 Homo sapiens 153-158
15667595-8 2005 Retinoic acid induced aryl sulfotransferase IV in liver of female rats and sulfotransferase a in liver of male rats. Tretinoin 0-13 sulfotransferase family 1A member 1 Rattus norvegicus 22-46
15667595-9 2005 Intestinal rat aryl sulfotransferase IV and sulfotransferase a in male rats and intestinal aryl sulfotransferase IV in female rats were also induced after retinoic acid treatment. Tretinoin 155-168 sulfotransferase family 1A member 1 Rattus norvegicus 15-39
15667595-9 2005 Intestinal rat aryl sulfotransferase IV and sulfotransferase a in male rats and intestinal aryl sulfotransferase IV in female rats were also induced after retinoic acid treatment. Tretinoin 155-168 sulfotransferase family 1A member 1 Rattus norvegicus 91-115
15492114-2 2005 Studies were done to address the question whether ATRA-induced apoptosis is a consequence of destabilization of bcl-2 mRNA and decreased cellular levels of the anti-apoptotic protein, bcl-2. Tretinoin 50-54 BCL2 apoptosis regulator Homo sapiens 184-189
15621532-4 2005 Here, we show that Fgf9, Fgf16, and Fgf20 are expressed in the endocardium and epicardium and that RA can induce epicardial expression of Fgf9. Tretinoin 99-101 fibroblast growth factor 9 Mus musculus 138-142
15727050-3 2005 Components of the TGFbeta signal transduction machinery are discussed in relation to regulation of transcription, cell division and tissue differentiation in developing orofacial tissue, as evidence for a functional linkage between the TGFbeta and retinoic acid signal transduction pathways during orofacial development. Tretinoin 248-261 transforming growth factor beta 1 Homo sapiens 18-25
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 interleukin 1 beta Homo sapiens 122-139
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 vascular cell adhesion molecule 1 Homo sapiens 148-181
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 vascular cell adhesion molecule 1 Homo sapiens 183-189
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 192-208
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 210-215
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 retinoic acid receptor beta Homo sapiens 226-253
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 12-35 retinoic acid receptor beta Homo sapiens 255-263
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 interleukin 1 beta Homo sapiens 122-139
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 vascular cell adhesion molecule 1 Homo sapiens 148-181
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 vascular cell adhesion molecule 1 Homo sapiens 183-189
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 prostaglandin-endoperoxide synthase 2 Homo sapiens 192-208
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 prostaglandin-endoperoxide synthase 2 Homo sapiens 210-215
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 retinoic acid receptor beta Homo sapiens 226-253
15830921-1 2005 UNLABELLED: All-trans-retinoic acid (tRA) modulates in human mesangial cells (MC) antioxidant defenses, the expression of interleukin-1beta-induced vascular cell-adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and the retinoic acid-receptor-beta (RAR-beta). Tretinoin 37-40 retinoic acid receptor beta Homo sapiens 255-263
15912649-0 2005 [All-trans retinoic acid induces apoptosis in human mesangial cells: involvement of stress activated p38 kinase]. Tretinoin 1-24 mitogen-activated protein kinase 14 Homo sapiens 101-104
15912649-7 2005 Therefore we focussed on the stress activated p38 kinase, the third member of the MAPK family, to investigate its involvement in AR-t induced apoptosis. Tretinoin 129-133 mitogen-activated protein kinase 14 Homo sapiens 46-49
15912649-7 2005 Therefore we focussed on the stress activated p38 kinase, the third member of the MAPK family, to investigate its involvement in AR-t induced apoptosis. Tretinoin 129-133 mitogen-activated protein kinase 1 Homo sapiens 82-86
16390259-4 2005 RA treatment during EB formation induced osteoblastic marker genes, such as collagen type 1, osteopontin, and Cbfa1. Tretinoin 0-2 RUNX family transcription factor 2 Homo sapiens 110-115
16026305-5 2005 Recent studies have shown that RA can induce in vitro re-differentiation of thyroid carcinoma cell lines, as suggested by increased expression of the sodium/iodide symporter (NIS), type I iodothyronine deiodinase, alkaline phosphatase and by the increment of cellular (131)I uptake. Tretinoin 31-33 iodothyronine deiodinase 1 Homo sapiens 181-212
15652522-5 2005 RA increased the release of TSP-1 and PEDF, but not that of VEGF, from human RPE cells in vitro. Tretinoin 0-2 thrombospondin 1 Homo sapiens 28-33
15545507-6 2005 The enhancer consists of at least 11 transcription factor-binding sites and is responsive to various signal transduction pathways, including cAMP, retinoic acid, endothelin-1, and cytokines, to alter renin mRNA levels. Tretinoin 147-160 renin Homo sapiens 200-205
15968585-5 2005 XTRAP-gamma morpholinos also inhibited differentiation of the pronephros in activin/retinoic acid-treated animal caps. Tretinoin 84-97 signal sequence receptor, gamma (translocon-associated protein gamma) S homeolog Xenopus laevis 0-11
15389595-9 2005 In the ATRA-treated cells, TGF-beta2 stimulated a significant increase in chemotaxis only at the highest concentration tested. Tretinoin 7-11 transforming growth factor, beta 2 Mus musculus 27-36
15795517-0 2005 All-trans-retinoic acid inhibits the development of mesangial proliferative glomerulonephritis in interleukin-6 transgenic mice. Tretinoin 0-23 interleukin 6 Mus musculus 98-111
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 0-23 interleukin 6 Mus musculus 85-98
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 0-23 interleukin 6 Mus musculus 100-104
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 0-23 interleukin 6 receptor, alpha Mus musculus 141-154
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 0-23 interleukin 6 receptor, alpha Mus musculus 156-161
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 25-29 interleukin 6 Mus musculus 85-98
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 25-29 interleukin 6 Mus musculus 100-104
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 25-29 interleukin 6 receptor, alpha Mus musculus 141-154
15795517-1 2005 All-trans-retinoic acid (ATRA), a vitamin A derivative, was reported to suppress the interleukin-6 (IL-6) production and to downregulate the IL-6 receptor (IL-6R) and/or its signal transducer glycoprotein 130. Tretinoin 25-29 interleukin 6 receptor, alpha Mus musculus 156-161
15795517-2 2005 We investigated the in vivo antinephritic effect of ATRA on IL-6 transgenic mice which had developed mesangial proliferative glomerulonephritis (PGN) as well as its in vitro inhibitory effect on the proliferation of rat mesangial cells. Tretinoin 52-56 interleukin 6 Mus musculus 60-64
15795517-3 2005 In vivo experiments on IL-6 transgenic mice showed that ATRA administration suppressed proteinuria and hematuria and reduced the IL-6 concentrations; furthermore, histological examination demonstrated that it improved PGN. Tretinoin 56-60 interleukin 6 Mus musculus 23-27
15795517-3 2005 In vivo experiments on IL-6 transgenic mice showed that ATRA administration suppressed proteinuria and hematuria and reduced the IL-6 concentrations; furthermore, histological examination demonstrated that it improved PGN. Tretinoin 56-60 interleukin 6 Mus musculus 129-133
15795517-4 2005 In vitro experiments using rat mesangial cells demonstrated that ATRA inhibited cell growth in a dose-dependent manner within a range from 10(-4) to 10(-6) M. This inhibition by ATRA was partially counteracted by the addition of IL-6. Tretinoin 65-69 interleukin 6 Mus musculus 229-233
15795517-4 2005 In vitro experiments using rat mesangial cells demonstrated that ATRA inhibited cell growth in a dose-dependent manner within a range from 10(-4) to 10(-6) M. This inhibition by ATRA was partially counteracted by the addition of IL-6. Tretinoin 178-182 interleukin 6 Mus musculus 229-233
15795517-6 2005 These findings indicate that, by blocking of the IL-6 function, ATRA may be therapeutically effective in PGN. Tretinoin 64-68 interleukin 6 Mus musculus 49-53
15939542-4 2005 Using the ribonuclease protection assay, we found that both all-trans retinoic acid and 9-cis retinoic acid significantly up-regulated dopamine D1 receptor, heterotrimeric G protein olfactory, adenylyl cyclase type V and dopamine- and cyclic adenosine 3":5"-monophosphate-regulated phosphoprotein mRNAs in the lateral ganglionic eminence culture. Tretinoin 70-83 adenylate cyclase 5 Rattus norvegicus 193-216
15492114-3 2005 ATRA induced differentiation of HL-60 cells along the granulocytic pathway within 48 h. The half-lives of bcl-2 mRNA in HL-60 cells incubated with ATRA for 48 or 72 h were reduced to 39 and 7% of the corresponding untreated control values, respectively. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 106-111
15492114-3 2005 ATRA induced differentiation of HL-60 cells along the granulocytic pathway within 48 h. The half-lives of bcl-2 mRNA in HL-60 cells incubated with ATRA for 48 or 72 h were reduced to 39 and 7% of the corresponding untreated control values, respectively. Tretinoin 147-151 BCL2 apoptosis regulator Homo sapiens 106-111
15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 99-103 BCL2 apoptosis regulator Homo sapiens 13-18
15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 99-103 BCL2 apoptosis regulator Homo sapiens 202-207
15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 279-283 BCL2 apoptosis regulator Homo sapiens 13-18
15492114-6 2005 However, when recombinant nucleolin was added to extracts of ATRA-treated cells, the rate of bcl-2 mRNA decay was similar to the rate in extracts of untreated cells. Tretinoin 61-65 BCL2 apoptosis regulator Homo sapiens 93-98
15492114-7 2005 These results provide evidence that ATRA-induced apoptosis is a consequence of cellular differentiation, which leads to nucleolin down-regulation and bcl-2 mRNA instability. Tretinoin 36-40 BCL2 apoptosis regulator Homo sapiens 150-155
15589975-6 2005 In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid. Tretinoin 103-116 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 66-74
15717849-4 2005 Moreover, not only neural (Mash-1) and neuroectodermal (Pax-6), but also endodermal (GATA-4, alpha-fetoprotein) genes are expressed at early stages of differentiation driven by RA under serum-free conditions. Tretinoin 177-179 paired box 6 Mus musculus 56-61
15717849-4 2005 Moreover, not only neural (Mash-1) and neuroectodermal (Pax-6), but also endodermal (GATA-4, alpha-fetoprotein) genes are expressed at early stages of differentiation driven by RA under serum-free conditions. Tretinoin 177-179 GATA binding protein 4 Mus musculus 85-91
15589975-6 2005 In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid. Tretinoin 103-116 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 76-84
15589975-6 2005 In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid. Tretinoin 208-221 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 66-74
15589975-6 2005 In addition, organochlorine pesticides strongly induce cytochrome P450RAI1 (P450RAI1), a key factor of retinoic acid level regulation in many tissues and whose expression and activity are strongly induced by retinoic acid. Tretinoin 208-221 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 76-84
15541384-5 2004 When the embryoid bodies were treated with retinoic acid, Wnt11 expression decreased in parallel with the decreased expression of cardiac genes. Tretinoin 43-56 Wnt family member 11 Homo sapiens 58-63
15597047-3 2004 Injections of all-trans RA suppressed the expression of dorsal signals Tbx5, BMP4 and to a lesser extent of ephrinB1, whereas the injection of citral, an inhibitor of RA synthesis, enhanced the expression of BMP4 and Tbx5. Tretinoin 24-26 ephrin B1 Gallus gallus 108-116
15494319-3 2004 Utilizing neonatal cardiomyocytes, we demonstrated that RA suppressed the hypertrophic features induced by cyclic stretch or angiotensin II (Ang II). Tretinoin 56-58 angiotensinogen Homo sapiens 125-139
15494319-3 2004 Utilizing neonatal cardiomyocytes, we demonstrated that RA suppressed the hypertrophic features induced by cyclic stretch or angiotensin II (Ang II). Tretinoin 56-58 angiotensinogen Homo sapiens 141-147
15494319-4 2004 Cyclic stretch- or Ang II-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAP kinase) was dose- and time-dependently inhibited by RA. Tretinoin 229-231 angiotensinogen Homo sapiens 19-25
15494319-4 2004 Cyclic stretch- or Ang II-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAP kinase) was dose- and time-dependently inhibited by RA. Tretinoin 229-231 mitogen-activated protein kinase 1 Homo sapiens 48-89
15494319-4 2004 Cyclic stretch- or Ang II-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAP kinase) was dose- and time-dependently inhibited by RA. Tretinoin 229-231 mitogen-activated protein kinase 14 Homo sapiens 135-171
15494319-8 2004 RA up-regulated the expression level of MAP kinase phosphatase-1 (MKP-1) and MKP-2, and the time course was correlated with the inhibitory effect of RA on activation of MAP kinases. Tretinoin 0-2 dual specificity phosphatase 1 Homo sapiens 40-64
15494319-8 2004 RA up-regulated the expression level of MAP kinase phosphatase-1 (MKP-1) and MKP-2, and the time course was correlated with the inhibitory effect of RA on activation of MAP kinases. Tretinoin 0-2 dual specificity phosphatase 1 Homo sapiens 66-71
15494319-8 2004 RA up-regulated the expression level of MAP kinase phosphatase-1 (MKP-1) and MKP-2, and the time course was correlated with the inhibitory effect of RA on activation of MAP kinases. Tretinoin 149-151 dual specificity phosphatase 1 Homo sapiens 40-64
15494319-8 2004 RA up-regulated the expression level of MAP kinase phosphatase-1 (MKP-1) and MKP-2, and the time course was correlated with the inhibitory effect of RA on activation of MAP kinases. Tretinoin 149-151 dual specificity phosphatase 1 Homo sapiens 66-71
15308577-3 2004 All-trans retinoic acid (ATRA) induced a biphasic expression of CHOP mRNA in the NB4 and HL60 AML cell lines. Tretinoin 0-23 DNA damage inducible transcript 3 Homo sapiens 64-68
15454112-7 2004 The addition of cytokines alone, such as GM-CSF or CD40 ligand, did not affect the expression of CD83 in untreated NB4 cells but they up-regulated CD83 in ATRA-treated cells. Tretinoin 155-159 CD40 ligand Homo sapiens 51-62
15308577-3 2004 All-trans retinoic acid (ATRA) induced a biphasic expression of CHOP mRNA in the NB4 and HL60 AML cell lines. Tretinoin 25-29 DNA damage inducible transcript 3 Homo sapiens 64-68
15308577-4 2004 Levels of CHOP expression increased within 1 hour of exposure to ATRA. Tretinoin 65-69 DNA damage inducible transcript 3 Homo sapiens 10-14
15308577-11 2004 RA signaling in granulocytic differentiation involves regulated expression of CHOP and C/EBPepsilon in a coordinated fashion. Tretinoin 0-2 DNA damage inducible transcript 3 Homo sapiens 78-82
15358764-5 2004 To examine the relationship between APC and retinoic acid biosynthesis in normal enterocytes, we have identified two novel zebrafish retinol dehydrogenases, termed zRDHA and zRDHB, that show strong expression within the gut of developing zebrafish embryos. Tretinoin 44-57 dehydrogenase/reductase (SDR family) member 9 Danio rerio 164-169
15604252-0 2004 A novel RARbeta isoform directed by a distinct promoter P3 and mediated by retinoic acid in breast cancer cells. Tretinoin 75-88 retinoic acid receptor beta Homo sapiens 8-15
15530851-2 2004 Previously, we demonstrated that RA-induced growth arrest of T-47D HBC cells required the activity of the RA-induced protein kinase, protein kinase Calpha (PKCalpha) [J. Tretinoin 33-35 protein kinase C alpha Homo sapiens 133-154
15530851-2 2004 Previously, we demonstrated that RA-induced growth arrest of T-47D HBC cells required the activity of the RA-induced protein kinase, protein kinase Calpha (PKCalpha) [J. Tretinoin 33-35 protein kinase C alpha Homo sapiens 156-164
15530851-8 2004 Inhibiting the activity of PKCalpha, a retinoic acid-induced target gene, prevented the effects of RA on cell proliferation and EGF signaling. Tretinoin 99-101 protein kinase C alpha Homo sapiens 27-35
15530851-10 2004 RA treatment increased steady-state levels of the protein tyrosine phosphatase PTP-1C and all measured effects of RA on EGF receptor function were reversed by the tyrosine phosphate inhibitor orthovanadate. Tretinoin 114-116 epidermal growth factor receptor Homo sapiens 120-132
15530851-11 2004 These results indicate that RA-induced target genes, particularly PKCalpha, prevent sustained growth factor signaling, uncoupling activated receptor tyrosine kinases and nuclear targets that are required for cell cycle progression. Tretinoin 28-30 protein kinase C alpha Homo sapiens 66-74
15650232-9 2004 We show that the effect of RA on the IGFBP-5 promoter is exerted, at least in part, through a proximal 5"-CACCC-3" tandem repeat (-147 bp to -137 bp from the transcription start site) that has previously been described as a cis-acting element involved in the progesterone-mediated response in osteoblasts. Tretinoin 27-29 insulin like growth factor binding protein 5 Homo sapiens 37-44
15650232-7 2004 RA-induced differentiation causes a sharp increase of IGFBP-5. Tretinoin 0-2 insulin like growth factor binding protein 5 Homo sapiens 54-61
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 0-23 RNA binding fox-1 homolog 3 Homo sapiens 180-184
15309027-0 2004 Pharmacological doses of all-trans retinoic acid promote G0/G1 transition and G1 arrest of normal human marrow CD34+ cells. Tretinoin 35-48 CD34 molecule Homo sapiens 111-115
15597402-9 2004 In addition to these inhibitors of CYP5, CYP17, and CYP19, liarozole, known to be a potent inhibitor of CYP26 (retinoic acid-4-hydroxylase) and ATRA (all-trans-retinoic acid) metabolism, was able to reduce tumor cell adhesion to 51% of the initial rate. Tretinoin 144-148 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 52-57
15597402-9 2004 In addition to these inhibitors of CYP5, CYP17, and CYP19, liarozole, known to be a potent inhibitor of CYP26 (retinoic acid-4-hydroxylase) and ATRA (all-trans-retinoic acid) metabolism, was able to reduce tumor cell adhesion to 51% of the initial rate. Tretinoin 150-173 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 52-57
15610140-6 2004 Treatment with RA had only a slight effect on the mRNA expression of the tight junction-associated proteins occludin, ZO-1, claudin-1, -3, and -4, but enhanced the expression of claudin-2, which was recently suggested to form a paracellular ion channel. Tretinoin 15-17 tight junction protein 1 Homo sapiens 118-122
15610140-6 2004 Treatment with RA had only a slight effect on the mRNA expression of the tight junction-associated proteins occludin, ZO-1, claudin-1, -3, and -4, but enhanced the expression of claudin-2, which was recently suggested to form a paracellular ion channel. Tretinoin 15-17 claudin 2 Homo sapiens 178-187
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 25-27 RNA binding fox-1 homolog 3 Homo sapiens 180-184
15567713-2 2004 Here, we describe the distribution of four enzymes of the RA synthetic pathway (aldehyde dehydrogenases ALDH1A1-3 and ALDH8A1) and two enzymes of the degradative pathway (CYP26A1 and CYP26B1) in the developing rat metanephros. Tretinoin 58-60 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 104-111
15567713-2 2004 Here, we describe the distribution of four enzymes of the RA synthetic pathway (aldehyde dehydrogenases ALDH1A1-3 and ALDH8A1) and two enzymes of the degradative pathway (CYP26A1 and CYP26B1) in the developing rat metanephros. Tretinoin 58-60 aldehyde dehydrogenase 8 family, member A1 Rattus norvegicus 118-125
15610518-10 2004 In summary, ATRA induces IL-8 production in both NF-kappaB- and p38 MAPK-dependent manners in normal human keratinocytes. Tretinoin 12-16 C-X-C motif chemokine ligand 8 Homo sapiens 25-29
15815076-0 2004 Retinoic acid increased expression of the Na+/Ca2+ exchanger in the heart and brain. Tretinoin 0-13 solute carrier family 8 member A1 Rattus norvegicus 42-60
15815076-3 2004 We report here that binding of retinoic acid enhances expression of the NCX1 in the rat cardiac atria, brain stem and hypothalamus, but not in cerebellum. Tretinoin 31-44 solute carrier family 8 member A1 Rattus norvegicus 72-76
15815076-4 2004 Differences in the regulation of the NCX1 by retinoic acid might suggest that GATA4-retinoic acid inducible transcription factor is activated in the hypothalamus and brain stem, but not in the cerebellum. Tretinoin 45-58 solute carrier family 8 member A1 Rattus norvegicus 37-41
15815076-4 2004 Differences in the regulation of the NCX1 by retinoic acid might suggest that GATA4-retinoic acid inducible transcription factor is activated in the hypothalamus and brain stem, but not in the cerebellum. Tretinoin 45-58 GATA binding protein 4 Rattus norvegicus 78-83
15610518-0 2004 All-trans-retinoic acid induces interleukin-8 via the nuclear factor-kappaB and p38 mitogen-activated protein kinase pathways in normal human keratinocytes. Tretinoin 0-23 C-X-C motif chemokine ligand 8 Homo sapiens 32-45
15610518-0 2004 All-trans-retinoic acid induces interleukin-8 via the nuclear factor-kappaB and p38 mitogen-activated protein kinase pathways in normal human keratinocytes. Tretinoin 0-23 mitogen-activated protein kinase 14 Homo sapiens 80-116
15610518-3 2004 To test this hypothesis, we investigated whether all-trans-retinoic acid (ATRA) induced IL-8 production in normal human keratinocytes. Tretinoin 49-72 C-X-C motif chemokine ligand 8 Homo sapiens 88-92
15610518-3 2004 To test this hypothesis, we investigated whether all-trans-retinoic acid (ATRA) induced IL-8 production in normal human keratinocytes. Tretinoin 74-78 C-X-C motif chemokine ligand 8 Homo sapiens 88-92
15371543-0 2004 Rapid effects of retinoic acid on CREB and ERK phosphorylation in neuronal cells. Tretinoin 17-30 Eph receptor B1 Rattus norvegicus 43-46
15610518-4 2004 Stimulation with 10(-7) M ATRA enhanced IL-8 mRNA expression and induced IL-8 production. Tretinoin 26-30 C-X-C motif chemokine ligand 8 Homo sapiens 40-44
15610518-4 2004 Stimulation with 10(-7) M ATRA enhanced IL-8 mRNA expression and induced IL-8 production. Tretinoin 26-30 C-X-C motif chemokine ligand 8 Homo sapiens 73-77
15610518-5 2004 We also studied the intracellular signaling mechanisms of ATRA-induced IL-8 production in keratinocytes. Tretinoin 58-62 C-X-C motif chemokine ligand 8 Homo sapiens 71-75
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 RELB proto-oncogene, NF-kB subunit Homo sapiens 45-49
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 nuclear factor kappa B subunit 2 Homo sapiens 80-83
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 nuclear factor kappa B subunit 1 Homo sapiens 102-105
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 NFKB inhibitor alpha Homo sapiens 176-208
15610518-7 2004 Introduction of a dominant-negative mutant of IkappaBalpha completely abolished ATRA-induced IL-8 production, which indicates that this process is NF-kappaB-dependent. Tretinoin 80-84 NFKB inhibitor alpha Homo sapiens 46-58
15610518-7 2004 Introduction of a dominant-negative mutant of IkappaBalpha completely abolished ATRA-induced IL-8 production, which indicates that this process is NF-kappaB-dependent. Tretinoin 80-84 C-X-C motif chemokine ligand 8 Homo sapiens 93-97
15610518-9 2004 ATRA phosphorylated the p38 MAPK, and SB202180 inhibited ATRA-induced IL-8 production, which indicates that the p38 MAPK is also involved in ATRA-induced IL-8 production. Tretinoin 0-4 C-X-C motif chemokine ligand 8 Homo sapiens 154-158
15610518-9 2004 ATRA phosphorylated the p38 MAPK, and SB202180 inhibited ATRA-induced IL-8 production, which indicates that the p38 MAPK is also involved in ATRA-induced IL-8 production. Tretinoin 57-61 C-X-C motif chemokine ligand 8 Homo sapiens 70-74
15610518-9 2004 ATRA phosphorylated the p38 MAPK, and SB202180 inhibited ATRA-induced IL-8 production, which indicates that the p38 MAPK is also involved in ATRA-induced IL-8 production. Tretinoin 57-61 C-X-C motif chemokine ligand 8 Homo sapiens 154-158
15610518-9 2004 ATRA phosphorylated the p38 MAPK, and SB202180 inhibited ATRA-induced IL-8 production, which indicates that the p38 MAPK is also involved in ATRA-induced IL-8 production. Tretinoin 57-61 C-X-C motif chemokine ligand 8 Homo sapiens 70-74
15610518-9 2004 ATRA phosphorylated the p38 MAPK, and SB202180 inhibited ATRA-induced IL-8 production, which indicates that the p38 MAPK is also involved in ATRA-induced IL-8 production. Tretinoin 57-61 C-X-C motif chemokine ligand 8 Homo sapiens 154-158
15256426-0 2004 Combination of retinoic acid and tumor necrosis factor overcomes the maturation block in a variety of retinoic acid-resistant acute promyelocytic leukemia cells. Tretinoin 102-115 tumor necrosis factor Homo sapiens 33-54
15541024-0 2004 All trans-retinoic acid (ATRA) elevated eukaryotic translation initiation factor 4A1 (eIF4A1) mRNA in ATRA-responsive vitiliginous epidermis. Tretinoin 4-23 eukaryotic translation initiation factor 4A1 Homo sapiens 40-84
15541024-0 2004 All trans-retinoic acid (ATRA) elevated eukaryotic translation initiation factor 4A1 (eIF4A1) mRNA in ATRA-responsive vitiliginous epidermis. Tretinoin 4-23 eukaryotic translation initiation factor 4A1 Homo sapiens 86-92
15541024-0 2004 All trans-retinoic acid (ATRA) elevated eukaryotic translation initiation factor 4A1 (eIF4A1) mRNA in ATRA-responsive vitiliginous epidermis. Tretinoin 25-29 eukaryotic translation initiation factor 4A1 Homo sapiens 40-84
15541024-0 2004 All trans-retinoic acid (ATRA) elevated eukaryotic translation initiation factor 4A1 (eIF4A1) mRNA in ATRA-responsive vitiliginous epidermis. Tretinoin 25-29 eukaryotic translation initiation factor 4A1 Homo sapiens 86-92
15541024-0 2004 All trans-retinoic acid (ATRA) elevated eukaryotic translation initiation factor 4A1 (eIF4A1) mRNA in ATRA-responsive vitiliginous epidermis. Tretinoin 102-106 eukaryotic translation initiation factor 4A1 Homo sapiens 40-84
15541024-0 2004 All trans-retinoic acid (ATRA) elevated eukaryotic translation initiation factor 4A1 (eIF4A1) mRNA in ATRA-responsive vitiliginous epidermis. Tretinoin 102-106 eukaryotic translation initiation factor 4A1 Homo sapiens 86-92
15541024-8 2004 Of those mRNAs, the level of eIF4A1 mRNA showed a clinical correlation; The expression of eIF4A1 mRNA, examined by real-time PCR, was elevated in four patients who showed a favorable clinical response to ATRA, whereas no change or a decrease occurred in three patients whose clinical responses did not differ between ATRA and vehicle treatment. Tretinoin 204-208 eukaryotic translation initiation factor 4A1 Homo sapiens 29-35
15541024-8 2004 Of those mRNAs, the level of eIF4A1 mRNA showed a clinical correlation; The expression of eIF4A1 mRNA, examined by real-time PCR, was elevated in four patients who showed a favorable clinical response to ATRA, whereas no change or a decrease occurred in three patients whose clinical responses did not differ between ATRA and vehicle treatment. Tretinoin 204-208 eukaryotic translation initiation factor 4A1 Homo sapiens 90-96
15541024-8 2004 Of those mRNAs, the level of eIF4A1 mRNA showed a clinical correlation; The expression of eIF4A1 mRNA, examined by real-time PCR, was elevated in four patients who showed a favorable clinical response to ATRA, whereas no change or a decrease occurred in three patients whose clinical responses did not differ between ATRA and vehicle treatment. Tretinoin 317-321 eukaryotic translation initiation factor 4A1 Homo sapiens 29-35
15541024-8 2004 Of those mRNAs, the level of eIF4A1 mRNA showed a clinical correlation; The expression of eIF4A1 mRNA, examined by real-time PCR, was elevated in four patients who showed a favorable clinical response to ATRA, whereas no change or a decrease occurred in three patients whose clinical responses did not differ between ATRA and vehicle treatment. Tretinoin 317-321 eukaryotic translation initiation factor 4A1 Homo sapiens 90-96
15541024-9 2004 The eIF4A1 protein expression from the other two patients, one of them with a favorable response to ATRA, also showed a clinical correlation. Tretinoin 100-104 eukaryotic translation initiation factor 4A1 Homo sapiens 4-10
15556610-4 2004 Non-transfected K562 cells showed the increase of membrane-bound-TG2 level after 3 days in the response to Hemin and all trans-retinoic acid (tRA), indicating that membrane recruitment of TG2 is occurred during the erythroid differentiation. Tretinoin 121-140 transglutaminase 2 Homo sapiens 65-68
15556610-4 2004 Non-transfected K562 cells showed the increase of membrane-bound-TG2 level after 3 days in the response to Hemin and all trans-retinoic acid (tRA), indicating that membrane recruitment of TG2 is occurred during the erythroid differentiation. Tretinoin 142-145 transglutaminase 2 Homo sapiens 65-68
15556610-4 2004 Non-transfected K562 cells showed the increase of membrane-bound-TG2 level after 3 days in the response to Hemin and all trans-retinoic acid (tRA), indicating that membrane recruitment of TG2 is occurred during the erythroid differentiation. Tretinoin 142-145 transglutaminase 2 Homo sapiens 188-191
15256426-5 2004 Here, we report that combining TNF with RA leads to maturation of several RA-resistant APL cells along a monocytic pathway, whereas UF-1, a patient-derived RA-resistant cell line, showed characteristics of granulocytic differentiation. Tretinoin 74-76 tumor necrosis factor Homo sapiens 31-34
15256426-5 2004 Here, we report that combining TNF with RA leads to maturation of several RA-resistant APL cells along a monocytic pathway, whereas UF-1, a patient-derived RA-resistant cell line, showed characteristics of granulocytic differentiation. Tretinoin 74-76 tumor necrosis factor Homo sapiens 31-34
15451545-1 2004 All trans-retinoic acid (RA) plays a role in regulation of P450RAI gene expression. Tretinoin 4-23 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 59-66
15381082-0 2004 Modulation of the retinoic acid-induced cell apoptosis and differentiation by the human TR4 orphan nuclear receptor. Tretinoin 18-31 nuclear receptor subfamily 2 group C member 2 Homo sapiens 88-91
15313475-0 2004 Increased expression of N-acetylglucosaminyltransferase-V in human hepatoma cells by retinoic acid and 1alpha,25-dihydroxyvitamin D3. Tretinoin 85-98 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 24-57
15485494-3 2004 In this study we newly found that RA treatment of SK-N-BE(2)C, human neuroblastoma cells, increased the expression of Cdk5 and its neuron specific activator p35 through the extracellular-signal-regulated kinase1/2 (ERK1/2) and cAMP-dependent protein kinase A (PKA) pathway. Tretinoin 34-36 mitogen-activated protein kinase 1 Homo sapiens 173-213
15485494-3 2004 In this study we newly found that RA treatment of SK-N-BE(2)C, human neuroblastoma cells, increased the expression of Cdk5 and its neuron specific activator p35 through the extracellular-signal-regulated kinase1/2 (ERK1/2) and cAMP-dependent protein kinase A (PKA) pathway. Tretinoin 34-36 mitogen-activated protein kinase 3 Homo sapiens 215-221
15485494-6 2004 In addition, a transcription factor early growth response 1 (Egr-1) was induced by RA through the ERK1/2 pathway, suggesting its possible involvement in the p35 induction. Tretinoin 83-85 mitogen-activated protein kinase 3 Homo sapiens 98-104
15485494-7 2004 RA treatment also induced c-fos mediated AP-1 binding, and cAMP-responsive element binding protein (CREB) mediated CRE binding via ERK1/2 and PKA pathway, respectively, in the Cdk5 promoter region, resulting in the induction of Cdk5. Tretinoin 0-2 mitogen-activated protein kinase 3 Homo sapiens 131-137
15485494-8 2004 Our results suggest that ERK1/2 and PKA-induced regulation of Cdk5 activity possibly through Egr-1, c-fos, and CREB plays a critical role in the RA-induced neuronal differentiation. Tretinoin 145-147 mitogen-activated protein kinase 3 Homo sapiens 25-31
15284334-6 2004 The fact that binding of RXR-RAR on DR3 is not observed suggests that contrary to RA-induced granulocytic differentiation, 1 alpha,25-dihydroxyvitamin D(3)-mediated monocytic differentiation requires positive and negative transcriptional controls both likely mediated by the RXR-VDR heterodimer. Tretinoin 29-31 TNF receptor superfamily member 25 Homo sapiens 36-39
15347642-8 2004 There was a significant decline in homocysteine concentrations in diabetic rats, owing in part to a 38% increase in the abundance of the transsulfuration enzyme cystathionine beta-synthase; treatment of diabetic rats with RA prevented cystathionine beta-synthase induction. Tretinoin 222-224 cystathionine beta synthase Rattus norvegicus 161-188
15347642-8 2004 There was a significant decline in homocysteine concentrations in diabetic rats, owing in part to a 38% increase in the abundance of the transsulfuration enzyme cystathionine beta-synthase; treatment of diabetic rats with RA prevented cystathionine beta-synthase induction. Tretinoin 222-224 cystathionine beta synthase Rattus norvegicus 235-262
15482329-7 2004 RA significantly decreased the transcript levels of keratin 13, keratin 14, desmoglein 1, and desmocollin 1 in a dose-dependent manner. Tretinoin 0-2 desmocollin 1 Homo sapiens 94-107
15482329-9 2004 CONCLUSION: These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. Tretinoin 41-43 desmocollin 1 Homo sapiens 118-131
15555458-1 2004 AIM: To explore the expression and role of Notch1 gene in the differentiation of the human embryonic neural stem cells to neurons induced by all-trans-retinoic-acid(ATRA). Tretinoin 141-164 notch receptor 1 Homo sapiens 43-49
15555458-1 2004 AIM: To explore the expression and role of Notch1 gene in the differentiation of the human embryonic neural stem cells to neurons induced by all-trans-retinoic-acid(ATRA). Tretinoin 165-169 notch receptor 1 Homo sapiens 43-49
15555458-10 2004 The expression of Notch1 gene decreased significantly after being treated with ATRA(P<0.001). Tretinoin 79-83 notch receptor 1 Homo sapiens 18-24
15347642-10 2004 In contrast, RA treatment attenuated the streptozotocin-mediated increase in betaine-homocysteine S-methyltransferase, whereas methionine synthase activity remained diminished. Tretinoin 13-15 betaine-homocysteine S-methyltransferase Rattus norvegicus 77-117
15381082-1 2004 In our previous studies, the TR4 orphan nuclear receptor (TR4) has been demonstrated to suppress retinoic acid (RA)-induced transactivation via a negative feedback control mechanism and in situ analysis showed that TR4 is extensively expressed in mouse brain, especially in regions where the cells are proliferating. Tretinoin 97-110 nuclear receptor subfamily 2 group C member 2 Homo sapiens 29-32
15381082-1 2004 In our previous studies, the TR4 orphan nuclear receptor (TR4) has been demonstrated to suppress retinoic acid (RA)-induced transactivation via a negative feedback control mechanism and in situ analysis showed that TR4 is extensively expressed in mouse brain, especially in regions where the cells are proliferating. Tretinoin 97-110 nuclear receptor subfamily 2, group C, member 2 Mus musculus 58-61
15381082-1 2004 In our previous studies, the TR4 orphan nuclear receptor (TR4) has been demonstrated to suppress retinoic acid (RA)-induced transactivation via a negative feedback control mechanism and in situ analysis showed that TR4 is extensively expressed in mouse brain, especially in regions where the cells are proliferating. Tretinoin 97-110 nuclear receptor subfamily 2, group C, member 2 Mus musculus 58-61
15381082-1 2004 In our previous studies, the TR4 orphan nuclear receptor (TR4) has been demonstrated to suppress retinoic acid (RA)-induced transactivation via a negative feedback control mechanism and in situ analysis showed that TR4 is extensively expressed in mouse brain, especially in regions where the cells are proliferating. Tretinoin 112-114 nuclear receptor subfamily 2 group C member 2 Homo sapiens 29-32
15381082-1 2004 In our previous studies, the TR4 orphan nuclear receptor (TR4) has been demonstrated to suppress retinoic acid (RA)-induced transactivation via a negative feedback control mechanism and in situ analysis showed that TR4 is extensively expressed in mouse brain, especially in regions where the cells are proliferating. Tretinoin 112-114 nuclear receptor subfamily 2, group C, member 2 Mus musculus 58-61
15193143-7 2004 Our findings suggest that opposing actions of CRBP1 and ADH1 enable a large fraction of liver retinol to remain esterified due to CRBP1 action, while continuously allowing some retinol to be oxidized to retinoic acid by ADH1 for degradative retinoid turnover under any dietary vitamin A conditions. Tretinoin 203-216 alcohol dehydrogenase 1 (class I) Mus musculus 56-60
15381082-1 2004 In our previous studies, the TR4 orphan nuclear receptor (TR4) has been demonstrated to suppress retinoic acid (RA)-induced transactivation via a negative feedback control mechanism and in situ analysis showed that TR4 is extensively expressed in mouse brain, especially in regions where the cells are proliferating. Tretinoin 112-114 nuclear receptor subfamily 2, group C, member 2 Mus musculus 58-61
15193143-7 2004 Our findings suggest that opposing actions of CRBP1 and ADH1 enable a large fraction of liver retinol to remain esterified due to CRBP1 action, while continuously allowing some retinol to be oxidized to retinoic acid by ADH1 for degradative retinoid turnover under any dietary vitamin A conditions. Tretinoin 203-216 alcohol dehydrogenase 1 (class I) Mus musculus 220-224
15381082-3 2004 The results indicated that the expression of TR4 reduced by doxycycline anti-sense TR4 would alter the retinoic acid-induced differentiation pathway that results in the changes of cell morphology and cell cycle profile. Tretinoin 103-116 nuclear receptor subfamily 2 group C member 2 Homo sapiens 45-48
15381082-3 2004 The results indicated that the expression of TR4 reduced by doxycycline anti-sense TR4 would alter the retinoic acid-induced differentiation pathway that results in the changes of cell morphology and cell cycle profile. Tretinoin 103-116 nuclear receptor subfamily 2 group C member 2 Homo sapiens 83-86
15381082-4 2004 Unexpectedly, our data further indicated that the RA-induced apoptosis, judging by DNA fragmentation, could also be altered by the induction of anti-sense TR4. Tretinoin 50-52 nuclear receptor subfamily 2 group C member 2 Homo sapiens 155-158
15381082-5 2004 Together, these findings provide the first in vivo evidence that an orphan nuclear receptor, such as TR4, may play major roles in the RA-mediated apoptosis or differentiation in P19 cells. Tretinoin 134-136 nuclear receptor subfamily 2 group C member 2 Homo sapiens 101-104
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 261-274 protein disulfide isomerase family A member 2 Homo sapiens 65-103
15369820-3 2004 Thus, ADH1 and ADH4 provide a metabolic pathway for the synthesis of the corresponding retinoic acids. Tretinoin 87-101 alcohol dehydrogenase 4 (class II), pi polypeptide Homo sapiens 15-19
15369700-6 2004 Transglutaminase 2 expression was increased by either all-trans retinoic acid or EGF, and further up-regulated by the simultaneous addition of both substances. Tretinoin 64-77 transglutaminase 2 Homo sapiens 0-18
15366004-1 2004 Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. Tretinoin 138-151 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 61-67
15366004-1 2004 Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. Tretinoin 153-155 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 61-67
15366004-5 2004 Both mutants retain RA activity in the lens placode associated with Raldh3 expression, but this RA activity is insufficient to induce optic cup formation. Tretinoin 20-22 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 68-74
15366004-8 2004 Thus, RA signaling initiates in the optic vesicle in response to Raldh2 but can be maintained during optic cup formation by a gene other than Raldh1, most likely Raldh3. Tretinoin 6-8 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 162-168
15465489-5 2004 In the present study, four discrete DNA elements within the 1.6 kbp promoter fragment are shown by electrophoretic mobility shift assays (EMSA) to exhibit sequence specific interactions with proteins present in nuclear extracts from P19 EC cells induced to express Pax3 by treatment with retinoic acid (RA). Tretinoin 288-301 paired box 3 Mus musculus 265-269
15465489-5 2004 In the present study, four discrete DNA elements within the 1.6 kbp promoter fragment are shown by electrophoretic mobility shift assays (EMSA) to exhibit sequence specific interactions with proteins present in nuclear extracts from P19 EC cells induced to express Pax3 by treatment with retinoic acid (RA). Tretinoin 303-305 paired box 3 Mus musculus 265-269
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 261-274 protein disulfide isomerase family A member 2 Homo sapiens 105-109
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 276-278 protein disulfide isomerase family A member 2 Homo sapiens 65-103
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 276-278 protein disulfide isomerase family A member 2 Homo sapiens 105-109
15306824-0 2004 The expression of immediate early gene X-1 (IEX-1) is differentially induced by retinoic acids in NB4 and KG1 cells: possible implication in the distinct phenotype of retinoic acid-responsive and -resistant leukemic cells. Tretinoin 80-93 immediate early response 3 Homo sapiens 44-49
15375546-7 2004 All-trans retinoic acid (atRA), 9-cis retinoic acid (9cRA), and 4-(hydroxyphenyl) retinamide (4-HPR) induced RARbeta2 protein expression exclusively in the benign MCF10A cells and the former two retinoids, mRNA expression in MCF10A and MCF10AT cells, but not in malignant, MCF10CA1a cells, suggesting that the loss of inducible RARbeta expression is associated with the progression and malignant transformation of MCF10A cells. Tretinoin 0-23 retinoic acid receptor beta Homo sapiens 109-116
15375546-7 2004 All-trans retinoic acid (atRA), 9-cis retinoic acid (9cRA), and 4-(hydroxyphenyl) retinamide (4-HPR) induced RARbeta2 protein expression exclusively in the benign MCF10A cells and the former two retinoids, mRNA expression in MCF10A and MCF10AT cells, but not in malignant, MCF10CA1a cells, suggesting that the loss of inducible RARbeta expression is associated with the progression and malignant transformation of MCF10A cells. Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 109-116
15306824-0 2004 The expression of immediate early gene X-1 (IEX-1) is differentially induced by retinoic acids in NB4 and KG1 cells: possible implication in the distinct phenotype of retinoic acid-responsive and -resistant leukemic cells. Tretinoin 80-94 immediate early response 3 Homo sapiens 18-42
15306824-0 2004 The expression of immediate early gene X-1 (IEX-1) is differentially induced by retinoic acids in NB4 and KG1 cells: possible implication in the distinct phenotype of retinoic acid-responsive and -resistant leukemic cells. Tretinoin 80-94 immediate early response 3 Homo sapiens 44-49
15306824-0 2004 The expression of immediate early gene X-1 (IEX-1) is differentially induced by retinoic acids in NB4 and KG1 cells: possible implication in the distinct phenotype of retinoic acid-responsive and -resistant leukemic cells. Tretinoin 80-93 immediate early response 3 Homo sapiens 18-42
15306824-2 2004 The present study demonstrates that, in the two acute promyelocytic leukemia (APL) cell lines NB4 and KG1, exhibiting distinct responsiveness to retinoic acids (RAs), IEX-1 expression is rapidly (30-60 min) induced by all-trans- or cis-RA and independently of other signal transduction mediators, such as TNFalpha, NF-kappaB or MAP kinases. Tretinoin 145-159 immediate early response 3 Homo sapiens 167-172
15306824-5 2004 Furthermore, two functional RA-response elements in the IEX-1 promoter were identified by gel shift and luciferase reporter gene assays. Tretinoin 28-30 immediate early response 3 Homo sapiens 56-61
15375520-1 2004 We showed that the HER2/Grb2/Akt pathway induces all-trans retinoic acid (ATRA) resistance in breast cancer cells by suppressing the DNA binding activity of retinoic acid receptors (RAR). Tretinoin 59-72 erb-b2 receptor tyrosine kinase 2 Homo sapiens 19-23
15486192-7 2004 A combination of PPAR gamma ligands with a retinoid X receptor agonist (i.e., LG100268) or a retinoic acid receptor agonist (i.e., all trans-retinoic acid) enhanced differentiating and growth-inhibitory effects. Tretinoin 135-154 peroxisome proliferator activated receptor gamma Homo sapiens 17-27
15375520-1 2004 We showed that the HER2/Grb2/Akt pathway induces all-trans retinoic acid (ATRA) resistance in breast cancer cells by suppressing the DNA binding activity of retinoic acid receptors (RAR). Tretinoin 59-72 growth factor receptor bound protein 2 Homo sapiens 24-28
15375520-1 2004 We showed that the HER2/Grb2/Akt pathway induces all-trans retinoic acid (ATRA) resistance in breast cancer cells by suppressing the DNA binding activity of retinoic acid receptors (RAR). Tretinoin 59-72 AKT serine/threonine kinase 1 Homo sapiens 29-32
15375520-1 2004 We showed that the HER2/Grb2/Akt pathway induces all-trans retinoic acid (ATRA) resistance in breast cancer cells by suppressing the DNA binding activity of retinoic acid receptors (RAR). Tretinoin 74-78 erb-b2 receptor tyrosine kinase 2 Homo sapiens 19-23
15375520-1 2004 We showed that the HER2/Grb2/Akt pathway induces all-trans retinoic acid (ATRA) resistance in breast cancer cells by suppressing the DNA binding activity of retinoic acid receptors (RAR). Tretinoin 74-78 growth factor receptor bound protein 2 Homo sapiens 24-28
15375520-1 2004 We showed that the HER2/Grb2/Akt pathway induces all-trans retinoic acid (ATRA) resistance in breast cancer cells by suppressing the DNA binding activity of retinoic acid receptors (RAR). Tretinoin 74-78 AKT serine/threonine kinase 1 Homo sapiens 29-32
15375520-3 2004 Here, we determined whether AP-1 binding activity is correlated with ATRA resistance in HER2-overexpressing cells. Tretinoin 69-73 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-32
15375520-3 2004 Here, we determined whether AP-1 binding activity is correlated with ATRA resistance in HER2-overexpressing cells. Tretinoin 69-73 erb-b2 receptor tyrosine kinase 2 Homo sapiens 88-92
15325130-5 2004 A similar increase in PrPres was observed in another prion-infected cell line, scrapie-mouse brain (SMB) cells, treated with retinoic acid while retinoic acid increased the amount of PrPC in non-infected cells. Tretinoin 145-158 prion protein Homo sapiens 183-187
15326479-5 2004 Conversely, in these cells, TRAIL-induced cell death is magnified by all-trans retinoic acid (ATRA) treatment, independently of telomerase activity on telomeres. Tretinoin 79-92 TNF superfamily member 10 Homo sapiens 28-33
15328022-5 2004 Furthermore, we show that RA activity is essential in the lung field to maintain lung cell identity in the endoderm; RAR antagonism disrupts expression of thyroid transcription factor 1 (Ttf1), an early marker of the respiratory region in the endoderm, and surfactant protein C (Sp-C) mRNAs. Tretinoin 26-28 surfactant protein C Rattus norvegicus 257-277
15326479-5 2004 Conversely, in these cells, TRAIL-induced cell death is magnified by all-trans retinoic acid (ATRA) treatment, independently of telomerase activity on telomeres. Tretinoin 94-98 TNF superfamily member 10 Homo sapiens 28-33
15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 54-67 estrogen receptor 1 Homo sapiens 12-29
15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 54-67 estrogen receptor 1 Homo sapiens 31-33
15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 69-71 estrogen receptor 1 Homo sapiens 12-29
15273718-2 2004 In general, estrogen receptor (ER)-positive cells are retinoic acid (RA) sensitive, whereas ER-negative cells are resistant. Tretinoin 69-71 estrogen receptor 1 Homo sapiens 31-33
15273718-5 2004 We found that RA+GF induce apoptosis, as shown by an increase in fragmented DNA, Annexin-V-positive cells and caspase-3 activation. Tretinoin 14-16 caspase 3 Homo sapiens 110-119
15273718-10 2004 In support of this novel finding, the ability of other PKC inhibitors to cause apoptosis in combination with RA correlates with ability to cause sustained activation of ERK. Tretinoin 109-111 mitogen-activated protein kinase 1 Homo sapiens 169-172
15273724-7 2004 Introduction of the dominant-negative form of CBP into Ewing"s sarcoma cells sensitizes these cells against genotoxic or retinoic-acid induced apoptosis. Tretinoin 121-134 CREB binding protein Homo sapiens 46-49
15328022-5 2004 Furthermore, we show that RA activity is essential in the lung field to maintain lung cell identity in the endoderm; RAR antagonism disrupts expression of thyroid transcription factor 1 (Ttf1), an early marker of the respiratory region in the endoderm, and surfactant protein C (Sp-C) mRNAs. Tretinoin 26-28 surfactant protein C Rattus norvegicus 279-283
15358106-6 2004 A significant upregulation of the mAM mRNA was observed in monkey cells exposed to low oxygen tension conditions, TGF-beta1, all-trans-retinoic acid, and dexamethasone. Tretinoin 125-148 activating transcription factor 7 interacting protein Mus musculus 34-37
15374966-8 2004 Inhibition of p53 and caspases with alpha-pifithrin and z-Val-Ala-Asp-fluoromethyl ketone, respectively, blocked UVB- and doxorubicin-induced apoptosis in ATRA-treated KCs. Tretinoin 155-159 tumor protein p53 Homo sapiens 14-17
15374966-9 2004 Analogous to the observed ATRA effects in monolayer cultures, in vitro-generated organotypic skin cultures reacted with up-regulation of p53 and proapoptotic caspases and displayed increased sensitivity to UVB-induced apoptosis. Tretinoin 26-30 tumor protein p53 Homo sapiens 137-140
15337319-4 2004 The obtained results indicate that transcriptional activity of dopamine D2 receptor gene promoter was dose-dependently increased by retinoic acid, forskolin, rolipram and phorbol 12 myristate 13-acetate, as well as by DMI, CIT and MIA. Tretinoin 132-145 dopamine receptor D2 Mus musculus 63-83
15374966-0 2004 Retinoic acid increases the expression of p53 and proapoptotic caspases and sensitizes keratinocytes to apoptosis: a possible explanation for tumor preventive action of retinoids. Tretinoin 0-13 tumor protein p53 Homo sapiens 42-45
15374966-4 2004 In contrast, when the cells were treated with 1 micromol/L ATRA for 6 days and subsequently irradiated with different doses of UVB, they underwent massive apoptosis as assessed by morphology, expression of activated caspase-3, and DNA fragmentation. Tretinoin 59-63 caspase 3 Homo sapiens 216-225
15374966-6 2004 Analysis by real-time PCR and Western blot revealed that ATRA treatment strongly increased the mRNA and protein expression of p53 and caspase-3, -6, -7, and -9, which are key regulators of apoptosis. Tretinoin 57-61 tumor protein p53 Homo sapiens 126-129
15374966-6 2004 Analysis by real-time PCR and Western blot revealed that ATRA treatment strongly increased the mRNA and protein expression of p53 and caspase-3, -6, -7, and -9, which are key regulators of apoptosis. Tretinoin 57-61 caspase 3 Homo sapiens 134-159
15374966-7 2004 UVB irradiation of ATRA-treated cells but not of control cells led to the accumulation of p53 protein and of its target gene Noxa. Tretinoin 19-23 tumor protein p53 Homo sapiens 90-93
15374966-7 2004 UVB irradiation of ATRA-treated cells but not of control cells led to the accumulation of p53 protein and of its target gene Noxa. Tretinoin 19-23 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 125-129
15340050-0 2004 Transcription factor Nkx-2.5 induces sodium/iodide symporter gene expression and participates in retinoic acid- and lactation-induced transcription in mammary cells. Tretinoin 97-110 NK2 homeobox 5 Homo sapiens 21-28
15304092-0 2004 Differential gene induction of human beta-defensins (hBD-1, -2, -3, and -4) in keratinocytes is inhibited by retinoic acid. Tretinoin 109-122 defensin beta 1 Homo sapiens 53-74
15304092-6 2004 Furthermore, the differential induction of hBD-2, -3, and -4 gene expression in keratinocytes by proinflammatory cytokines, phorbol-myristate-acetate (PMA), and bacteria was inhibited by more than 90% when the keratinocytes were pre-incubated with RA. Tretinoin 248-250 defensin beta 4A Homo sapiens 43-60
15327395-0 2004 Retinoic acid treatment protects MRL/lpr lupus mice from the development of glomerular disease. Tretinoin 0-13 Fas (TNF receptor superfamily member 6) Mus musculus 37-40
15327395-12 2004 Adoptively transferred T cells from vehicle-treated to tRA-treated MRL/lpr mice did not induce renal lesions or proteinuria. Tretinoin 55-58 Fas (TNF receptor superfamily member 6) Mus musculus 71-74
15554945-6 2004 However, in the present study, we show that the RA-induced expression of endodermal markers such as EndoA, collagen IV, and t-PA are inhibited by exogenous MyoR expression and that the level of inhibition of these markers correlates with the level of MyoR expressed. Tretinoin 48-50 plasminogen activator, tissue type Homo sapiens 124-128
15340050-6 2004 Interestingly, coincident with NIS expression, Nkx-2.5 mRNA and protein were present in lactating, but not virgin, mammary glands in two human breast cancer samples and in all-trans retinoic acid (tRA)-stimulated MCF-7 breast cancer cells. Tretinoin 182-195 NK2 homeobox 5 Homo sapiens 47-54
15340050-6 2004 Interestingly, coincident with NIS expression, Nkx-2.5 mRNA and protein were present in lactating, but not virgin, mammary glands in two human breast cancer samples and in all-trans retinoic acid (tRA)-stimulated MCF-7 breast cancer cells. Tretinoin 197-200 NK2 homeobox 5 Homo sapiens 47-54
15218018-2 2004 We have previously reported that the activation of c-Jun amino-terminal kinase (JNK) is required for the retinoic acid-induced neural differentiation of P19 cells. Tretinoin 105-118 mitogen-activated protein kinase 8 Homo sapiens 80-83
15332090-2 2004 We report here that selection of highly proliferative stem cells followed by treatment with retinoic acid generated essentially pure precursors that markers identified as Pax-6-positive radial glial cells. Tretinoin 92-105 paired box 6 Mus musculus 171-176
15627897-7 2004 Moreover, retinoic acid and PD98059, which inhibited the AP-1 activity, abolished the TPA-induced transformation. Tretinoin 10-23 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-61
15383262-5 2004 The expression of Bcl-2 was higher in the Bugu Mixture group than that in the all-trans retinoic acid (ATRA) induced group, and the expression of Bax was lower in the Bugu Mixture group than that in the ATRA induced group. Tretinoin 88-101 BCL2, apoptosis regulator Rattus norvegicus 18-23
15383262-5 2004 The expression of Bcl-2 was higher in the Bugu Mixture group than that in the all-trans retinoic acid (ATRA) induced group, and the expression of Bax was lower in the Bugu Mixture group than that in the ATRA induced group. Tretinoin 103-107 BCL2, apoptosis regulator Rattus norvegicus 18-23
15241475-2 2004 We show that in both acute promyelocytic leukemia and breast cancer cells the retinoic acid (RA) and interferon signaling pathways converge on the promoter of the tumoricidal death ligand TRAIL. Tretinoin 78-91 TNF superfamily member 10 Homo sapiens 188-193
15241475-2 2004 We show that in both acute promyelocytic leukemia and breast cancer cells the retinoic acid (RA) and interferon signaling pathways converge on the promoter of the tumoricidal death ligand TRAIL. Tretinoin 93-95 TNF superfamily member 10 Homo sapiens 188-193
15241475-5 2004 In coculture experiments, pre-exposure of breast cancer cells to RA and IFNgamma induced a dramatic TRAIL-dependent apoptosis in heterologous cancer cells in a paracrine mode of action, while normal cells were not affected. Tretinoin 65-67 TNF superfamily member 10 Homo sapiens 100-105
15262180-9 2004 These results strongly suggest that retinoic acid stimulates the release of VEGF in a p44/p42 MAP kinase-dependent manner in aortic smooth muscle cells. Tretinoin 36-49 vascular endothelial growth factor A Homo sapiens 76-80
15268896-8 2004 BMP"s stimulatory effects on SOST were further enhanced by retinoic acid or 1,25-dihydroxyvitamin D3. Tretinoin 59-72 sclerostin Homo sapiens 29-33
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 0-13 collagen type I alpha 2 chain Homo sapiens 30-49
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 110-137
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 139-147
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 0-13 collagen type I alpha 2 chain Homo sapiens 230-249
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 15-17 collagen type I alpha 2 chain Homo sapiens 30-49
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 110-137
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 139-147
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 15-17 collagen type I alpha 2 chain Homo sapiens 230-249
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 139-141 collagen type I alpha 2 chain Homo sapiens 30-49
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 139-141 retinoic acid receptor beta Homo sapiens 110-137
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 139-141 collagen type I alpha 2 chain Homo sapiens 230-249
15234273-4 2004 In the presence of RA, the coactivators SRC-1 and GRIP-1 formed complexes with RAR beta and RXR alpha which are bound to an oligonucleotide specifying a RARE site in the promoter. Tretinoin 19-21 retinoic acid receptor beta Homo sapiens 79-87
15234273-5 2004 In conclusion, this study shows that in the presence of retinoic acid, the coactivators SRC-1 and GRIP-1 augment, while the corepressor N-CoR abolishes, the suppressive effects of RAR beta and RXR alpha on alpha 2(I) collagen promoter activity. Tretinoin 56-69 retinoic acid receptor beta Homo sapiens 180-188
15234273-5 2004 In conclusion, this study shows that in the presence of retinoic acid, the coactivators SRC-1 and GRIP-1 augment, while the corepressor N-CoR abolishes, the suppressive effects of RAR beta and RXR alpha on alpha 2(I) collagen promoter activity. Tretinoin 56-69 collagen type I alpha 2 chain Homo sapiens 206-225
15262180-0 2004 Possible involvement of p44/p42 MAP kinase in retinoic acid-stimulated vascular endothelial growth factor release in aortic smooth muscle cells. Tretinoin 46-59 vascular endothelial growth factor A Homo sapiens 71-105
15262180-3 2004 In the present study, we investigated whether retinoic acid induces VEGF release in aortic smooth muscle A10 cells and if so, the mechanism of VEGF release. Tretinoin 46-59 vascular endothelial growth factor A Homo sapiens 68-72
15262180-4 2004 Retinoic acid stimulated VEGF release dose-dependently over the range 0.1 nM-0.1 microM. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 25-29
15262180-5 2004 The retinoic acid-stimulated VEGF release was significantly reduced by actinomycin D. Tretinoin 4-17 vascular endothelial growth factor A Homo sapiens 29-33
15262180-8 2004 The retinoic acid-stimulated release of VEGF was significantly reduced by PD98059 and U0126, specific MEK inhibitors, which attenuated the retinoic acid-induced phosphorylation of p44/p42 MAP kinase. Tretinoin 4-17 vascular endothelial growth factor A Homo sapiens 40-44
15262180-8 2004 The retinoic acid-stimulated release of VEGF was significantly reduced by PD98059 and U0126, specific MEK inhibitors, which attenuated the retinoic acid-induced phosphorylation of p44/p42 MAP kinase. Tretinoin 139-152 vascular endothelial growth factor A Homo sapiens 40-44
15180954-5 2004 The administration of all-trans retinoic acid to VAD mice resulted in a transient reduction in NF-kappaB activity and, conversely, a single dose of the RAR-pan-antagonist, AGN 194310, administered to control mice, led to a marked, transient induction of whole-body luminescence. Tretinoin 32-45 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 95-104
15269172-3 2004 We show that the expression of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Aldh1a3), is reduced in the lateral ganglionic eminence (LGE) of Gsh2 mutants. Tretinoin 35-48 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 72-101
15269172-3 2004 We show that the expression of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Aldh1a3), is reduced in the lateral ganglionic eminence (LGE) of Gsh2 mutants. Tretinoin 35-48 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 103-109
15269172-3 2004 We show that the expression of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Aldh1a3), is reduced in the lateral ganglionic eminence (LGE) of Gsh2 mutants. Tretinoin 35-48 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 125-132
15269172-3 2004 We show that the expression of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Aldh1a3), is reduced in the lateral ganglionic eminence (LGE) of Gsh2 mutants. Tretinoin 50-52 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 72-101
15269172-3 2004 We show that the expression of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Aldh1a3), is reduced in the lateral ganglionic eminence (LGE) of Gsh2 mutants. Tretinoin 50-52 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 103-109
15269172-3 2004 We show that the expression of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Aldh1a3), is reduced in the lateral ganglionic eminence (LGE) of Gsh2 mutants. Tretinoin 50-52 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 125-132
15269172-10 2004 Indeed, RA supplementation of Gsh2 mutants, during the period of striatal neurogenesis, results in a significant increase in DARPP-32 expression. Tretinoin 8-10 protein phosphatase 1, regulatory inhibitor subunit 1B Mus musculus 125-133
15254726-5 2004 Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. Tretinoin 106-110 tumor protein p53 Homo sapiens 14-17
15254726-5 2004 Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. Tretinoin 106-110 BCL2 associated X, apoptosis regulator Homo sapiens 27-30
15254726-0 2004 Expression profiles of p53, p21, bax and bcl-2 proteins in all-trans-retinoic acid treated primary and metastatic melanoma cells. Tretinoin 69-82 tumor protein p53 Homo sapiens 23-26
15254726-0 2004 Expression profiles of p53, p21, bax and bcl-2 proteins in all-trans-retinoic acid treated primary and metastatic melanoma cells. Tretinoin 69-82 BCL2 apoptosis regulator Homo sapiens 41-46
15254726-3 2004 In this study, we used a similar cell culture model system of matched primary and metastatic melanoma cells from the same patient to investigate whether p53 and bcl-2 family proteins were involved in atRA-induced apoptosis. Tretinoin 200-204 tumor protein p53 Homo sapiens 153-156
15254726-3 2004 In this study, we used a similar cell culture model system of matched primary and metastatic melanoma cells from the same patient to investigate whether p53 and bcl-2 family proteins were involved in atRA-induced apoptosis. Tretinoin 200-204 BCL2 apoptosis regulator Homo sapiens 161-166
15304040-5 2004 ATRA treatment was associated with a significant decrease in TF gene expression in bone marrow cells during the first 30 days of treatment, whereas IL-1 beta gene expression, which decreased in the cells of six patients treated with either chemotherapy or ATRA, actually increased in the remaining six patients treated with either chemotherapy or ATRA. Tretinoin 256-260 interleukin 1 beta Homo sapiens 148-157
15304040-5 2004 ATRA treatment was associated with a significant decrease in TF gene expression in bone marrow cells during the first 30 days of treatment, whereas IL-1 beta gene expression, which decreased in the cells of six patients treated with either chemotherapy or ATRA, actually increased in the remaining six patients treated with either chemotherapy or ATRA. Tretinoin 256-260 interleukin 1 beta Homo sapiens 148-157
15219855-3 2004 We previously showed, using P19 cells as a model system, that the lamin A/C promoter has a retinoic acid-responsive element (L-RARE), and that Sp1 and Sp3 bind the CACCC box of the L-RARE. Tretinoin 91-104 Sp3 transcription factor Homo sapiens 151-154
15219855-4 2004 In this study, we report that Sp1, Sp3, and c-Jun increase transactivation of the L-RARE during RA treatment. Tretinoin 84-86 Sp3 transcription factor Homo sapiens 35-38
15219855-5 2004 Sp1 and Sp3 regulate the lamin A/C promoter in Sp1-deficient SL2 cells and contribute to RA-dependent activation in GAL4-based transcriptional assays. Tretinoin 89-91 Sp3 transcription factor Homo sapiens 8-11
15219855-9 2004 Our data suggest that Sp1, Sp3, and c-Jun play an important role in gene expression through the L-RARE during RA treatment. Tretinoin 98-100 Sp3 transcription factor Homo sapiens 27-30
15281009-0 2004 The effect of cellular retinoic acid binding protein-I expression on the CYP26-mediated catabolism of all-trans retinoic acid and cell proliferation in head and neck squamous cell carcinoma. Tretinoin 23-36 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 73-78
15254719-1 2004 Peroxisome proliferator activated receptor-gamma (PPARgamma) belongs to a family of nuclear receptors and acts as a receptor for peroxisome proliferators, steroids, retinoic acids and polyunsaturated fatty acids. Tretinoin 165-179 peroxisome proliferator activated receptor gamma Homo sapiens 0-48
15254719-1 2004 Peroxisome proliferator activated receptor-gamma (PPARgamma) belongs to a family of nuclear receptors and acts as a receptor for peroxisome proliferators, steroids, retinoic acids and polyunsaturated fatty acids. Tretinoin 165-179 peroxisome proliferator activated receptor gamma Homo sapiens 50-59
15173175-7 2004 Importantly, tamalin was endogenously phosphorylated and associated with Syk in retinoic acid-treated P19 embryonal carcinoma cells that undergo neuron-like differentiation. Tretinoin 80-93 trafficking regulator and scaffold protein tamalin Rattus norvegicus 13-20
15254726-5 2004 Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. Tretinoin 106-110 BCL2 apoptosis regulator Homo sapiens 50-55
15254726-8 2004 These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Tretinoin 75-79 tumor protein p53 Homo sapiens 25-28
15254726-8 2004 These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Tretinoin 75-79 BCL2 associated X, apoptosis regulator Homo sapiens 35-38
15254726-8 2004 These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Tretinoin 75-79 BCL2 apoptosis regulator Homo sapiens 43-48
15254731-0 2004 Retinoic acid inhibits IL-6-dependent but not constitutive STAT3 activation in Epstein-Barr virus-immortalized B lymphocytes. Tretinoin 0-13 interleukin 6 Homo sapiens 23-27
15254731-5 2004 RA-induced modulation of IL-6 receptor components did not abolish IL-6-mediated phosphorylation of gp130, whereas JAK1 and STAT3 phosphorylation and activation induced by IL-6 were markedly inhibited. Tretinoin 0-2 interleukin 6 Homo sapiens 25-29
15254731-6 2004 Overall, the effects of RA resulted in the induction of a complete resistance of LCLs to IL-6-mediated growth promotion. Tretinoin 24-26 interleukin 6 Homo sapiens 89-93
15254731-8 2004 The finding that RA severely impairs IL-6-dependent signalings in LCLs and inhibits their growth despite the presence of constitutively active JAK/STAT and MAPK cascades provide additional support for a role of RA in the prevention and treatment of EBV-related lymphoproliferative disorders of immunosuppressed patients. Tretinoin 17-19 interleukin 6 Homo sapiens 37-41
15238214-4 2004 The HL60 cells, which were differentiated into PMN-like shapes by treatment with all-trans-retinoic acid (RA), also expressed CYP4F3, CYP4F3B and CYP4F12. Tretinoin 81-104 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 126-132
15225593-14 2004 NF-kappaB activity is elevated in mice fed a Vitamin A deficient (VAD) diet, and suppressed by surplus doses of retinoic acid (RA). Tretinoin 112-125 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 0-9
15225593-14 2004 NF-kappaB activity is elevated in mice fed a Vitamin A deficient (VAD) diet, and suppressed by surplus doses of retinoic acid (RA). Tretinoin 127-129 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 0-9
15238214-4 2004 The HL60 cells, which were differentiated into PMN-like shapes by treatment with all-trans-retinoic acid (RA), also expressed CYP4F3, CYP4F3B and CYP4F12. Tretinoin 81-104 cytochrome P450 family 4 subfamily F member 12 Homo sapiens 146-153
15238214-4 2004 The HL60 cells, which were differentiated into PMN-like shapes by treatment with all-trans-retinoic acid (RA), also expressed CYP4F3, CYP4F3B and CYP4F12. Tretinoin 106-108 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 126-132
15238214-4 2004 The HL60 cells, which were differentiated into PMN-like shapes by treatment with all-trans-retinoic acid (RA), also expressed CYP4F3, CYP4F3B and CYP4F12. Tretinoin 106-108 cytochrome P450 family 4 subfamily F member 12 Homo sapiens 146-153
15207915-3 2004 In the present study, we examined the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid (RA)-differentiated human SH-SY5Y neuroblastoma cells. Tretinoin 106-119 forkhead box O3 Homo sapiens 52-58
15207915-3 2004 In the present study, we examined the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid (RA)-differentiated human SH-SY5Y neuroblastoma cells. Tretinoin 121-123 forkhead box O3 Homo sapiens 52-58
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 calmin Homo sapiens 202-208
15025563-14 2004 Re-expression of these proteins restored calcium- and RA (retinoic acid)-responsive involucrin expression in these cells. Tretinoin 58-71 involucrin Homo sapiens 84-94
15256728-3 2004 The expression of p21 and p27 among the CDK inhibitors we examined increased during the differentiation induced with ATRA. Tretinoin 117-121 cyclin dependent kinase inhibitor 1A Homo sapiens 18-21
15256728-6 2004 These results suggest that increased expression of CDK inhibitors, p21 and p27, is necessary for the differentiation of HL-60 cells induced with ATRA. Tretinoin 145-149 cyclin dependent kinase inhibitor 1A Homo sapiens 67-70
15312521-0 2004 [Effects of retinoic acid on the signal transduction of beta-catenin /Tcf of cultured bronchial epithelial cells]. Tretinoin 12-25 hepatocyte nuclear factor 4 alpha Homo sapiens 70-73
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 ephrin B2 Homo sapiens 221-230
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 homeobox D10 Homo sapiens 232-238
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 80-93 ephrin B2 Homo sapiens 221-230
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 80-93 homeobox D10 Homo sapiens 232-238
15523539-5 2004 Its absence in AhR null mice, results in severe phenotypic abnormalities, such as liver half size with fibrosis, accumulation of retinoic acid and immune system insufficiency. Tretinoin 129-142 aryl-hydrocarbon receptor Mus musculus 15-18
15026310-0 2004 Retinoic acid controls blood vessel formation by modulating endothelial and mural cell interaction via suppression of Tie2 signaling in vascular progenitor cells. Tretinoin 0-13 TEK receptor tyrosine kinase Mus musculus 118-122
15026310-4 2004 In both atRA-treated VPC cultures and CAM tissues underneath the chorionic epithelial layer, the expression of angiopoietin-2 (Ang-2; competitor for Ang-1) was enhanced, whereas that of Tie2 (a receptor for Angs) was reduced. Tretinoin 8-12 angiopoietin 1 Mus musculus 149-154
15026310-4 2004 In both atRA-treated VPC cultures and CAM tissues underneath the chorionic epithelial layer, the expression of angiopoietin-2 (Ang-2; competitor for Ang-1) was enhanced, whereas that of Tie2 (a receptor for Angs) was reduced. Tretinoin 8-12 TEK receptor tyrosine kinase Mus musculus 186-190
15301109-5 2004 After induction of RA, PKCalpha was present in significantly lower levers in induced ESC as compared with that in ES-D3 cells at first, then PKCalpha isoform was found in slightly higher amounts and resumed on 14th day. Tretinoin 19-21 protein kinase C, alpha Mus musculus 23-31
15196951-4 2004 In contrast, inhibition of RA signaling differentially modulated XMeis3 activity. Tretinoin 27-29 Meis homeobox 3 L homeolog Xenopus laevis 65-71
15196951-5 2004 Target genes that are jointly activated by either RA or XMeis3 activities could not be efficiently induced by XMeis3 when RA signaling was inhibited. Tretinoin 122-124 Meis homeobox 3 L homeolog Xenopus laevis 56-62
15196951-10 2004 To pattern the hindbrain, RA requires functional XMeis3 protein activity. Tretinoin 26-28 Meis homeobox 3 L homeolog Xenopus laevis 49-55
15246743-0 2004 Protective effect of retinoic acid on interleukin-1 beta-induced cytotoxicity of pancreatic beta-cells. Tretinoin 21-34 interleukin 1 beta Rattus norvegicus 38-56
15246743-4 2004 The molecular mechanism, by which RA inhibited iNOS gene expression, appeared to involve the inhibition of NF-kappa B activation. Tretinoin 34-36 nitric oxide synthase 2 Rattus norvegicus 47-51
15210303-0 2004 Retinoic acid-mediated phospholipase A2 signaling in the nucleus. Tretinoin 0-13 phospholipase A2 group IB Homo sapiens 23-39
15210303-7 2004 The treatment of LA-N-1 cells with retinoic acid produces an increase in phospholipase A2 activity in the nuclear fraction. Tretinoin 35-48 phospholipase A2 group IB Homo sapiens 73-89
15210303-9 2004 This suggests that retinoic acid-induced stimulation of phospholipase A2 activity is a retinoic acid receptor-mediated process. Tretinoin 19-32 phospholipase A2 group IB Homo sapiens 56-72
15210303-9 2004 This suggests that retinoic acid-induced stimulation of phospholipase A2 activity is a retinoic acid receptor-mediated process. Tretinoin 87-100 phospholipase A2 group IB Homo sapiens 56-72
15210303-10 2004 LA-N-1 cell nuclei also have phospholipase C and phospholipase D (PLD) activities that are stimulated by retinoic acid. Tretinoin 105-118 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 49-64
15210303-10 2004 LA-N-1 cell nuclei also have phospholipase C and phospholipase D (PLD) activities that are stimulated by retinoic acid. Tretinoin 105-118 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 66-69
15194426-5 2004 Concomitantly, RA increased the level of the cyclin-dependent kinase inhibitor p27 (Kip-1). Tretinoin 15-17 dynactin subunit 6 Homo sapiens 79-82
15301109-5 2004 After induction of RA, PKCalpha was present in significantly lower levers in induced ESC as compared with that in ES-D3 cells at first, then PKCalpha isoform was found in slightly higher amounts and resumed on 14th day. Tretinoin 19-21 protein kinase C, alpha Mus musculus 141-149
15301109-6 2004 CONCLUSION: This study was characterized the PKCalpha isoenzyme profile in RA-induced differentiation of ESC into neuron-like cells and suggests that PKCalpha may play a very important role in differentiation of mouse ESC along the neuronal pathway. Tretinoin 75-77 protein kinase C, alpha Mus musculus 45-53
15301109-6 2004 CONCLUSION: This study was characterized the PKCalpha isoenzyme profile in RA-induced differentiation of ESC into neuron-like cells and suggests that PKCalpha may play a very important role in differentiation of mouse ESC along the neuronal pathway. Tretinoin 75-77 protein kinase C, alpha Mus musculus 150-158
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 0-13 cyclin dependent kinase 7 Homo sapiens 116-119
15069081-8 2004 Our findings indicate the existence of an early phase of RA signaling acting upstream of Tbx5, Meis2, and dHand, followed by a late phase of RA signaling needed to expand AER structure fully along the distal ectoderm. Tretinoin 57-59 T-box transcription factor 5 Homo sapiens 89-93
15159275-14 2004 These findings suggest not only that AF induces caspase-3-dependent apoptosis via a mechanism involving ROS, but also that the combined treatment with AF and ATRA induces differentiation of NB4 cells. Tretinoin 158-162 caspase 3 Homo sapiens 48-57
15354417-10 2004 We also observed a reduction in expression of the telomerase components, hTERT and hTR in ATRA treated ovarian carcinoma cells. Tretinoin 90-94 telomerase RNA component Homo sapiens 83-86
15135888-3 2004 Exposure of retinoic acid-differentiated human SH-SY5Y neuroblastoma cells to 270 microM hydrogen peroxide caused activation of caspase 3 and significant neuronal death. Tretinoin 12-25 caspase 3 Homo sapiens 128-137
15227730-1 2004 Retinoic acid receptor-beta (RAR-beta) is induced by and mediates the growth-inhibitory and apoptotic effects of retinoic acid (RA), suggesting that loss of RAR-beta expression may be one of the critical events involved in the carcinogenesis/ progression of non-small cell lung cancer (NSCLC) and in the responsiveness to retinoid chemotherapy. Tretinoin 113-126 retinoic acid receptor beta Homo sapiens 0-27
15227730-1 2004 Retinoic acid receptor-beta (RAR-beta) is induced by and mediates the growth-inhibitory and apoptotic effects of retinoic acid (RA), suggesting that loss of RAR-beta expression may be one of the critical events involved in the carcinogenesis/ progression of non-small cell lung cancer (NSCLC) and in the responsiveness to retinoid chemotherapy. Tretinoin 113-126 retinoic acid receptor beta Homo sapiens 29-37
15227730-1 2004 Retinoic acid receptor-beta (RAR-beta) is induced by and mediates the growth-inhibitory and apoptotic effects of retinoic acid (RA), suggesting that loss of RAR-beta expression may be one of the critical events involved in the carcinogenesis/ progression of non-small cell lung cancer (NSCLC) and in the responsiveness to retinoid chemotherapy. Tretinoin 113-126 retinoic acid receptor beta Homo sapiens 157-165
15227730-1 2004 Retinoic acid receptor-beta (RAR-beta) is induced by and mediates the growth-inhibitory and apoptotic effects of retinoic acid (RA), suggesting that loss of RAR-beta expression may be one of the critical events involved in the carcinogenesis/ progression of non-small cell lung cancer (NSCLC) and in the responsiveness to retinoid chemotherapy. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 0-27
15227730-1 2004 Retinoic acid receptor-beta (RAR-beta) is induced by and mediates the growth-inhibitory and apoptotic effects of retinoic acid (RA), suggesting that loss of RAR-beta expression may be one of the critical events involved in the carcinogenesis/ progression of non-small cell lung cancer (NSCLC) and in the responsiveness to retinoid chemotherapy. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 157-165
15206958-13 2004 Our results suggest that RA decreases proliferation of lung mesenchyme via a G(i)-protein and the erk-1/2 signaling cascade. Tretinoin 25-27 mitogen-activated protein kinase 3 Homo sapiens 98-105
15242250-4 2004 All-trans retinoic acid, taxol and okadiac acid induce downregulation or inactivation of nucleolin, which destabilizes bcl-2 mRNA and triggers apoptosis. Tretinoin 10-23 BCL2 apoptosis regulator Homo sapiens 119-124
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 0-13 cyclin dependent kinase 7 Homo sapiens 160-163
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 15-17 cyclin dependent kinase 7 Homo sapiens 116-119
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 15-17 cyclin dependent kinase 7 Homo sapiens 160-163
15040006-6 2004 Messenger RNA levels of p27/Kip1 do not change in CAOV3 cells following ATRA treatment, however, we have shown that p27/Kip1 mRNA is more stable in ATRA treated CAOV3 cells. Tretinoin 148-152 zinc ribbon domain containing 2 Homo sapiens 24-27
15040006-0 2004 p27/Kip1 mediates retinoic acid-induced suppression of ovarian carcinoma cell growth. Tretinoin 18-31 zinc ribbon domain containing 2 Homo sapiens 0-3
15040006-6 2004 Messenger RNA levels of p27/Kip1 do not change in CAOV3 cells following ATRA treatment, however, we have shown that p27/Kip1 mRNA is more stable in ATRA treated CAOV3 cells. Tretinoin 148-152 zinc ribbon domain containing 2 Homo sapiens 116-119
15040006-3 2004 We have found that treatment of CAOV3 cells with ATRA causes a 5-10 fold increase in the protein level of the cyclin dependent kinase inhibitor p27/Kip1. Tretinoin 49-53 zinc ribbon domain containing 2 Homo sapiens 144-147
15040006-5 2004 The increase in p27/Kip1 is detected by day 3 of ATRA treatment of CAOV3 cells, and is maximal by day 5. Tretinoin 49-53 zinc ribbon domain containing 2 Homo sapiens 16-19
15040006-9 2004 We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Tretinoin 28-32 zinc ribbon domain containing 2 Homo sapiens 55-58
15095411-0 2004 Retinoic acid regulates the expression of PBX1, PBX2, and PBX3 in P19 cells both transcriptionally and post-translationally. Tretinoin 0-13 pre B cell leukemia homeobox 3 Mus musculus 58-62
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 139-143 zinc ribbon domain containing 2 Homo sapiens 61-64
15095411-3 2004 In this report, we demonstrate that PBX1a, PBX1b, PBX2, and PBX3 mRNAs and PBX1/2/3 proteins are induced during endodermal and neuronal differentiation of P19 cells in a RAR-dependent subtype-unspecific manner following RA treatment. Tretinoin 170-172 pre B cell leukemia homeobox 3 Mus musculus 60-64
15095411-4 2004 The increases in both PBX1 mRNA and PBX3 mRNA levels are secondary responses to RA treatment requiring new proteins synthesis while the increase in PBX2 mRNA is a primary response. Tretinoin 80-82 pre B cell leukemia homeobox 3 Mus musculus 36-40
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 139-143 zinc ribbon domain containing 2 Homo sapiens 120-123
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 216-220 zinc ribbon domain containing 2 Homo sapiens 61-64
15040006-11 2004 Taken together our data suggest ATRA-induced growth inhibition in CAOV3 ovarian carcinoma cells involves modulation of the CDK inhibitor p27/kip1. Tretinoin 32-36 zinc ribbon domain containing 2 Homo sapiens 137-140
15189689-14 2004 Expression of mRNA for IL-12p35, IL-12p40, IFN-gamma in the cells that had been incubated with RA declined, but IL-10, IL-4 increased significantly. Tretinoin 95-97 interferon gamma Homo sapiens 43-52
15291362-6 2004 Based on these findings, combined treatment with ATRA and TSA may be clinically useful in therapy for acute leukemia displaying MLL-AF9 fusion gene. Tretinoin 49-53 MLLT3 super elongation complex subunit Homo sapiens 132-135
15228095-3 2004 All-trans retinoic acid (ATRA) and antisense cDNA of N-acetylglucosaminyltransferase-V (GnT-V) were used to suppress the expression of GnT-V and decreased the GlcNAc beta1,6-branching or tri-/tetra-antennary structure of surface N-glycans. Tretinoin 3-23 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 135-140
15228095-3 2004 All-trans retinoic acid (ATRA) and antisense cDNA of N-acetylglucosaminyltransferase-V (GnT-V) were used to suppress the expression of GnT-V and decreased the GlcNAc beta1,6-branching or tri-/tetra-antennary structure of surface N-glycans. Tretinoin 25-29 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 135-140
15291358-4 2004 We treated HL-60 and ATRA-resistant HL-60 (HL-60R) cells that express mutated RARalpha and very low levels of RARbeta, RARgamma and RXRalpha with 4-HPR (2 microM) for 3 days. Tretinoin 21-25 retinoic acid receptor beta Homo sapiens 110-117
15291358-8 2004 Although ATRA and 4-HPR induced expression of CYP26, an ATRA-inducible gene encoding a cytochrome P450 enzyme, in HL-60 cells, both retinoids failed to induce CYP26 in HL-60R cells. Tretinoin 9-13 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 46-51
15291358-8 2004 Although ATRA and 4-HPR induced expression of CYP26, an ATRA-inducible gene encoding a cytochrome P450 enzyme, in HL-60 cells, both retinoids failed to induce CYP26 in HL-60R cells. Tretinoin 56-60 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 46-51
15093674-3 2004 All-trans retinoic acid (t-RA) and all-trans retinol significantly inhibited a LPS-induced PGE(2) production as assessed by enzyme-linked immunosorbant assay (ELISA) and COX-2 protein expression as assessed by Western blot assay in mouse peritoneal macrophages, after knocking out the COX-1 activity by aspirin. Tretinoin 0-23 cytochrome c oxidase I, mitochondrial Mus musculus 285-290
15093674-4 2004 All-trans retinoic acid, but not all-trans retinol, inhibited LPS-induced TNF-alpha release as assessed by ELISA in rat PBMC. Tretinoin 10-23 tumor necrosis factor Rattus norvegicus 74-83
15093674-3 2004 All-trans retinoic acid (t-RA) and all-trans retinol significantly inhibited a LPS-induced PGE(2) production as assessed by enzyme-linked immunosorbant assay (ELISA) and COX-2 protein expression as assessed by Western blot assay in mouse peritoneal macrophages, after knocking out the COX-1 activity by aspirin. Tretinoin 25-29 cytochrome c oxidase I, mitochondrial Mus musculus 285-290
15020229-0 2004 Retinoic acid-induced differentiation into astrocytes and glutamatergic neurons is associated with expression of functional and activable phospholipase D. Tretinoin 0-13 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 138-153
14757762-8 2004 A conserved Sp1 site contributes to the retinoic acid responsiveness of the Bmp2 promoter, which lacks a classical retinoic acid response element. Tretinoin 40-53 bone morphogenetic protein 2 Mus musculus 76-80
14757762-8 2004 A conserved Sp1 site contributes to the retinoic acid responsiveness of the Bmp2 promoter, which lacks a classical retinoic acid response element. Tretinoin 115-128 bone morphogenetic protein 2 Mus musculus 76-80
14742427-6 2004 Furthermore we demonstrated that PBX proteins regulate the RA-dependent induction in the mRNA levels of bone morphogenetic protein 4 (BMP4) and Decorin (DCN) in P19 cells using both PBX1b-AS cells and PBX1 small interfering RNA. Tretinoin 59-61 bone morphogenetic protein 4 Mus musculus 104-132
14742427-6 2004 Furthermore we demonstrated that PBX proteins regulate the RA-dependent induction in the mRNA levels of bone morphogenetic protein 4 (BMP4) and Decorin (DCN) in P19 cells using both PBX1b-AS cells and PBX1 small interfering RNA. Tretinoin 59-61 bone morphogenetic protein 4 Mus musculus 134-138
14742427-7 2004 Chromatin immunoprecipitation assays further demonstrated that PBX proteins directly bind to the promoter of Bmp4 and Dcn in vivo in a RA-dependent fashion. Tretinoin 135-137 bone morphogenetic protein 4 Mus musculus 109-113
15020229-3 2004 Retinoic acid (RA)-induced differentiation increased PLD1 and PLD2 mRNA levels and PLD activity that was responsive to phorbol myristate acetate. Tretinoin 0-13 phospholipase D1 Homo sapiens 53-57
15020229-3 2004 Retinoic acid (RA)-induced differentiation increased PLD1 and PLD2 mRNA levels and PLD activity that was responsive to phorbol myristate acetate. Tretinoin 0-13 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 53-56
15020229-3 2004 Retinoic acid (RA)-induced differentiation increased PLD1 and PLD2 mRNA levels and PLD activity that was responsive to phorbol myristate acetate. Tretinoin 15-17 phospholipase D1 Homo sapiens 53-57
15020229-3 2004 Retinoic acid (RA)-induced differentiation increased PLD1 and PLD2 mRNA levels and PLD activity that was responsive to phorbol myristate acetate. Tretinoin 15-17 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 53-56
15020229-7 2004 These results indicate upregulation of PLD gene expression associated with RA-induced neural differentiation. Tretinoin 75-77 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 39-42
14660485-0 2004 Retinoic acid inhibits interleukin-4-induced eotaxin production in a human bronchial epithelial cell line. Tretinoin 0-13 interleukin 4 Homo sapiens 23-36
14660485-0 2004 Retinoic acid inhibits interleukin-4-induced eotaxin production in a human bronchial epithelial cell line. Tretinoin 0-13 C-C motif chemokine ligand 11 Homo sapiens 45-52
14660485-3 2004 We investigated whether RA can alter expression of eotaxin, a potent eosinophil chemoattractant that is regulated by the transcription factors signal transducer and activator of transcription 6 (STAT6) and NF-kappaB. Tretinoin 24-26 C-C motif chemokine ligand 11 Homo sapiens 51-58
14660485-4 2004 We examined the effects of RA on eotaxin expression in a human bronchial epithelial cell line BEAS-2B. Tretinoin 27-29 C-C motif chemokine ligand 11 Homo sapiens 33-40
14660485-5 2004 ATRA and its stereodimer 9-cis retinoic acid (9-cis RA) inhibited IL-4-induced release of eotaxin at 10(-6) M by 78.0 and 52.0%, respectively (P < 0.05). Tretinoin 0-4 interleukin 4 Homo sapiens 66-70
14660485-5 2004 ATRA and its stereodimer 9-cis retinoic acid (9-cis RA) inhibited IL-4-induced release of eotaxin at 10(-6) M by 78.0 and 52.0%, respectively (P < 0.05). Tretinoin 0-4 C-C motif chemokine ligand 11 Homo sapiens 90-97
14660485-5 2004 ATRA and its stereodimer 9-cis retinoic acid (9-cis RA) inhibited IL-4-induced release of eotaxin at 10(-6) M by 78.0 and 52.0%, respectively (P < 0.05). Tretinoin 2-4 interleukin 4 Homo sapiens 66-70
14660485-5 2004 ATRA and its stereodimer 9-cis retinoic acid (9-cis RA) inhibited IL-4-induced release of eotaxin at 10(-6) M by 78.0 and 52.0%, respectively (P < 0.05). Tretinoin 2-4 C-C motif chemokine ligand 11 Homo sapiens 90-97
14660485-6 2004 ATRA and 9-cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10(-6) M by 52.3 and 53.5%, respectively (P < 0.05). Tretinoin 0-4 interleukin 4 Homo sapiens 47-51
14660485-6 2004 ATRA and 9-cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10(-6) M by 52.3 and 53.5%, respectively (P < 0.05). Tretinoin 0-4 C-C motif chemokine ligand 11 Homo sapiens 60-67
14660485-6 2004 ATRA and 9-cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10(-6) M by 52.3 and 53.5%, respectively (P < 0.05). Tretinoin 2-4 interleukin 4 Homo sapiens 47-51
14660485-6 2004 ATRA and 9-cis RA also significantly inhibited IL-4-induced eotaxin mRNA expression at 10(-6) M by 52.3 and 53.5%, respectively (P < 0.05). Tretinoin 2-4 C-C motif chemokine ligand 11 Homo sapiens 60-67
14660485-8 2004 In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Tretinoin 93-97 C-C motif chemokine ligand 11 Homo sapiens 30-37
14660485-8 2004 In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Tretinoin 93-97 interleukin 4 Homo sapiens 101-105
14660485-8 2004 In transfection studies using eotaxin promoter luciferase plasmids, the inhibitory effect of ATRA on IL-4-induced eotaxin production was confirmed at the transcriptional level. Tretinoin 93-97 C-C motif chemokine ligand 11 Homo sapiens 114-121
14660485-11 2004 The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. Tretinoin 42-46 interleukin 4 Homo sapiens 50-54
14660485-11 2004 The mechanism of the inhibitory effect of ATRA on IL-4-induced eotaxin production in human bronchial epithelial cells has not been elucidated but does not appear to be due to an effect on STAT6 activation. Tretinoin 42-46 C-C motif chemokine ligand 11 Homo sapiens 63-70
15024057-3 2004 Exposure to retinoic acid (RA), a differentiation agent in many cell types, causes an upregulation of neurotrophin receptor TrkB and the cyclin kinase inhibitor p21(Cip1) at a transcriptional level. Tretinoin 12-25 cyclin dependent kinase inhibitor 1A Homo sapiens 161-164
15160951-1 2004 All-trans retinoic acid (ATRA) is a derivative of vitamin A. ATRA inhibits the growth of human myeloma cell lines and freshly isolated myeloma cells in vitro mainly by down-regulating interleukin-6 receptor. Tretinoin 0-23 interleukin 6 receptor Homo sapiens 184-206
15160951-1 2004 All-trans retinoic acid (ATRA) is a derivative of vitamin A. ATRA inhibits the growth of human myeloma cell lines and freshly isolated myeloma cells in vitro mainly by down-regulating interleukin-6 receptor. Tretinoin 25-29 interleukin 6 receptor Homo sapiens 184-206
15160951-4 2004 The purpose of the combination therapy was to sensitize the myeloma cells with ATRA to chemotherapy by blocking the growth-promoting effect of IL-6. Tretinoin 79-83 interleukin 6 Homo sapiens 143-147
15160951-10 2004 There may be some beneficial effect of ATRA in combination chemotherapy in selected patients who have activated IL-6 signaling. Tretinoin 39-43 interleukin 6 Homo sapiens 112-116
15059893-3 2004 Because TIG1 has been proposed to act as a tumor suppressor, we tested the hypothesis that cytosine methylation of the TIG1 promoter suppresses its expression and causes a loss of responsiveness to retinoic acid in some neoplastic cells. Tretinoin 198-211 retinoic acid receptor responder 1 Homo sapiens 8-12
15059893-3 2004 Because TIG1 has been proposed to act as a tumor suppressor, we tested the hypothesis that cytosine methylation of the TIG1 promoter suppresses its expression and causes a loss of responsiveness to retinoic acid in some neoplastic cells. Tretinoin 198-211 retinoic acid receptor responder 1 Homo sapiens 119-123
15059893-8 2004 TIG1 expression was also inducible by treatment with 1 micro M all-trans-retinoic acid for 3 days except in densely methylated cell lines. Tretinoin 63-86 retinoic acid receptor responder 1 Homo sapiens 0-4
15059893-10 2004 These findings indicate that silencing of TIG1 promoter by hypermethylation is common in human cancers and may contribute to the loss of retinoic acid responsiveness in some neoplastic cells. Tretinoin 137-150 retinoic acid receptor responder 1 Homo sapiens 42-46
14754907-8 2004 Specific RAR and RXR agonists were used to identify the nuclear receptor responsible for LPLA(2) induction by retinoic acid. Tretinoin 110-123 phospholipase A2 group XV Homo sapiens 89-96
14754907-13 2004 Thus, an RXR-dependent pathway controls LPLA(2) gene activation by retinoic acid in THP-1 cells. Tretinoin 67-80 phospholipase A2 group XV Homo sapiens 40-47
15024057-3 2004 Exposure to retinoic acid (RA), a differentiation agent in many cell types, causes an upregulation of neurotrophin receptor TrkB and the cyclin kinase inhibitor p21(Cip1) at a transcriptional level. Tretinoin 12-25 cyclin dependent kinase inhibitor 1A Homo sapiens 165-169
15024057-3 2004 Exposure to retinoic acid (RA), a differentiation agent in many cell types, causes an upregulation of neurotrophin receptor TrkB and the cyclin kinase inhibitor p21(Cip1) at a transcriptional level. Tretinoin 27-29 cyclin dependent kinase inhibitor 1A Homo sapiens 161-164
15024057-3 2004 Exposure to retinoic acid (RA), a differentiation agent in many cell types, causes an upregulation of neurotrophin receptor TrkB and the cyclin kinase inhibitor p21(Cip1) at a transcriptional level. Tretinoin 27-29 cyclin dependent kinase inhibitor 1A Homo sapiens 165-169
15024057-5 2004 As reported for other E-box-regulated promoters, ectopic expression of E47 and E12 basic helix-loop-helix (bHLH) proteins enhances RA-dependent expression of TrkB and p21(Cip1), whereas the inhibitory HLH Id2 exerts opposite effects. Tretinoin 131-133 cyclin dependent kinase inhibitor 1A Homo sapiens 167-170
15024057-5 2004 As reported for other E-box-regulated promoters, ectopic expression of E47 and E12 basic helix-loop-helix (bHLH) proteins enhances RA-dependent expression of TrkB and p21(Cip1), whereas the inhibitory HLH Id2 exerts opposite effects. Tretinoin 131-133 cyclin dependent kinase inhibitor 1A Homo sapiens 171-175
15157320-1 2004 In order to investigate the effect of non-medullar toxicity drug - all trans retinoid acid (ATRA) and cancer preventive trace element-selenium compound - sodium selenite (Na(2)SeO(3)) on the expression of vascular endothelial growth factor (VEGF) and its receptor in HL-60 cells, the expression of VEGF and its receptor in HL-60 cells were detected by ELISA technique and flow cytometry before and after treatment with two drugs. Tretinoin 92-96 vascular endothelial growth factor A Homo sapiens 205-239
15157320-2 2004 The results showed that the mean VEGF concentrations in the cultural supernatant of 5 and 10 micro mol/L ATRA-treated HL-60 cells for 48 and 72 hours were lower than those of the control group without adding ATRA. Tretinoin 105-109 vascular endothelial growth factor A Homo sapiens 33-37
15157320-6 2004 In conclusion, ATRA could inhibit the expression of VEGF and its receptor in HL-60 cell. Tretinoin 15-19 vascular endothelial growth factor A Homo sapiens 52-56
14980522-5 2004 In F9 Wt cells, cyclin D1, D3, and cyclin E protein levels decreased, while cyclin D2 and p27 levels increased after RA treatment. Tretinoin 117-119 cyclin D2 Homo sapiens 76-85
15469694-4 2004 Immunostaining and Western blot analysis showed the tTGase expression by RA treatment. Tretinoin 73-75 transglutaminase 2 Homo sapiens 52-58
15469694-5 2004 TNF-alpha or C(2) ceramide, a cell permeable ceramide analog, induced cell death in normal cells, but cell death was largely inhibited by the RA treatment. Tretinoin 142-144 tumor necrosis factor Homo sapiens 0-9
15469694-6 2004 The inhibition of tTGase by the tTGase inhibitors, monodansylcadaverine and cystamine, eliminated the protective role of RA-treatment in the cell death that is caused by TNF-alpha or C(2)-ceramide. Tretinoin 121-123 transglutaminase 2 Homo sapiens 18-24
15469694-6 2004 The inhibition of tTGase by the tTGase inhibitors, monodansylcadaverine and cystamine, eliminated the protective role of RA-treatment in the cell death that is caused by TNF-alpha or C(2)-ceramide. Tretinoin 121-123 transglutaminase 2 Homo sapiens 32-38
15469694-6 2004 The inhibition of tTGase by the tTGase inhibitors, monodansylcadaverine and cystamine, eliminated the protective role of RA-treatment in the cell death that is caused by TNF-alpha or C(2)-ceramide. Tretinoin 121-123 tumor necrosis factor Homo sapiens 170-179
15469694-9 2004 These results suggest that tTGase expressed by RA treatment plays an important role in the protection of cell death caused by TNF-alpha and ceramide. Tretinoin 47-49 transglutaminase 2 Homo sapiens 27-33
15469694-9 2004 These results suggest that tTGase expressed by RA treatment plays an important role in the protection of cell death caused by TNF-alpha and ceramide. Tretinoin 47-49 tumor necrosis factor Homo sapiens 126-135
15035668-5 2004 Using Line 1 tumor cells as a model for signal regulation of metastatic gene expression, we investigated the reciprocal interactions between NFkappaB and RARs in response to the pan-RAR agonist, all-trans retinoic acid (at-RA) and the pan-RAR antagonist, AGN193109. Tretinoin 205-218 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 141-149
15008977-0 2004 Retinoic acid enhances the gene expression of human polymeric immunoglobulin receptor (pIgR) by TNF-alpha. Tretinoin 0-13 tumor necrosis factor Homo sapiens 96-105
14604978-6 2004 This suggests that ATRA-mediated differentiation of EPRO-Gr cells occurs via a RARE-dependent, STAT3-independent pathway, while G-CSF-mediated differentiation occurs via a RARE-independent, STAT3-dependent pathway. Tretinoin 19-23 signal transducer and activator of transcription 3 Homo sapiens 95-100
14604978-10 2004 The addition of G-CSF with ATRA during NB4 induction resulted in STAT3 phosphorylation but did not enhance differentiation. Tretinoin 27-31 signal transducer and activator of transcription 3 Homo sapiens 65-70
15014026-8 2004 The demethylating agent 5-aza-2"-deoxycytidine (5-aza-CdR) restored RAR-beta(2) inducibility by all-trans-retinoic acid (ATRA) in some of the cell lines, which posses a methylated RAR-beta(2) promoter. Tretinoin 100-119 retinoic acid receptor beta Homo sapiens 68-76
15008977-2 2004 Expression of the pIgR by tumour necrosis factor (TNF-alpha) was enhanced by the addition of all-trans retinoic acid (ATRA) or 9-cis retinoic acid (9CRA). Tretinoin 93-116 tumor necrosis factor Homo sapiens 50-59
15014026-8 2004 The demethylating agent 5-aza-2"-deoxycytidine (5-aza-CdR) restored RAR-beta(2) inducibility by all-trans-retinoic acid (ATRA) in some of the cell lines, which posses a methylated RAR-beta(2) promoter. Tretinoin 121-125 retinoic acid receptor beta Homo sapiens 68-76
15014026-8 2004 The demethylating agent 5-aza-2"-deoxycytidine (5-aza-CdR) restored RAR-beta(2) inducibility by all-trans-retinoic acid (ATRA) in some of the cell lines, which posses a methylated RAR-beta(2) promoter. Tretinoin 121-125 retinoic acid receptor beta Homo sapiens 180-188
15008977-2 2004 Expression of the pIgR by tumour necrosis factor (TNF-alpha) was enhanced by the addition of all-trans retinoic acid (ATRA) or 9-cis retinoic acid (9CRA). Tretinoin 118-122 tumor necrosis factor Homo sapiens 50-59
15014026-10 2004 CONCLUSIONS: RAR-beta(2) silencing by methylation is an early event in head and neck carcinogenesis; 5-Aza-CdR can restore RAR-beta(2) inducibility by ATRA in most cell lines, and the combination of 5-aza-CdR and ATRA is more effective in growth inhibition than single agents. Tretinoin 151-155 retinoic acid receptor beta Homo sapiens 123-131
15030763-2 2004 We have studied the role of RA in mouse limb development by focusing on CYP26B1, a cytochrome P450 enzyme that inactivates RA. Tretinoin 123-125 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 72-79
15161092-8 2004 These results reveal specific tissue- and cellular expression patterns of RA synthesizing and catabolizing enzymes in the pre-natal inner ear, and suggest that a precise control of RA concentrations in various cell types of the inner ear is achieved by the balance between RALDHs and CYP26B1 activities. Tretinoin 74-76 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 284-291
14978018-0 2004 Survival of activated human T lymphocytes is promoted by retinoic acid via induction of IL-2. Tretinoin 57-70 interleukin 2 Homo sapiens 88-92
14978018-10 2004 Strikingly, we found that the ability of atRA to inhibit apoptosis was significantly correlated with its ability to increase the production of IL-2. Tretinoin 41-45 interleukin 2 Homo sapiens 143-147
14978018-12 2004 Together, these results suggest that retinoic acid inhibits spontaneous apoptosis of activated T lymphocytes through a RAR-dependent increase in IL-2 production. Tretinoin 37-50 interleukin 2 Homo sapiens 145-149
15030763-4 2004 The lack of CYP26B1 resulted in spreading of the RA signal toward the distal end of the developing limb and induced proximodistal patterning defects characterized by expansion of proximal identity and restriction of distal identity. Tretinoin 49-51 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 12-19
15030763-6 2004 Wild-type embryos exposed to excess RA phenocopied the limb defects of Cyp26b1(-/-) mice. Tretinoin 36-38 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 71-78
15086536-1 2004 Retinoic acid-inducible gene-1 was originally identified as an orphan G-protein coupled receptor induced by retinoic acid. Tretinoin 108-121 phospholipase A and acyltransferase 4 Homo sapiens 0-30
14985558-8 2004 Moreover, worsening of emphysema was observed in TNF-alpha transgenic mice treated with all-trans-retinoic acid. Tretinoin 88-111 tumor necrosis factor Mus musculus 49-58
15086536-6 2004 The differentiation-inducer, all-trans retinoic acid, induces GPRC5D expression in cultured hair bulb cells. Tretinoin 39-52 G protein-coupled receptor class C group 5 member D Homo sapiens 62-68
14749706-7 2004 The gene expression levels of CXC chemokines (MIP-2 and KC) and ICAM-1 were increased in the lung and heart by the ATRA administration. Tretinoin 115-119 chemokine (C-X-C motif) ligand 2 Mus musculus 46-51
14976384-5 2004 The copresence of NAG with either of two retinoids, retinoic acid (RA) or retinol, exerted a synergistic effect on HA production. Tretinoin 52-65 N-acetyl-alpha-glucosaminidase Homo sapiens 18-21
14976384-5 2004 The copresence of NAG with either of two retinoids, retinoic acid (RA) or retinol, exerted a synergistic effect on HA production. Tretinoin 67-69 N-acetyl-alpha-glucosaminidase Homo sapiens 18-21
14985558-9 2004 The level of keratinocyte chemoattractant (KC), a CXC chemokine, in bronchoalveolar lavage fluid was increased in TNF-alpha transgenic mice following retinoic acid treatment. Tretinoin 150-163 tumor necrosis factor Mus musculus 114-123
14988021-10 2004 Moreover, E-cadherin, a major cell adhesion molecule of wild-type P19, was strongly induced by Sox6, resulting in cellular aggregation without RA. Tretinoin 143-145 cadherin 1 Homo sapiens 10-20
15182588-1 2004 OBJECTIVE: To investigate the expression of VEGF mRNA and secretion of VEGF protein in NB4 and HL-60 cells affected by all-trans retinoic acid (ATRA) and daunorubincin (DNR) respectively. Tretinoin 129-142 vascular endothelial growth factor A Homo sapiens 44-48
15182588-1 2004 OBJECTIVE: To investigate the expression of VEGF mRNA and secretion of VEGF protein in NB4 and HL-60 cells affected by all-trans retinoic acid (ATRA) and daunorubincin (DNR) respectively. Tretinoin 129-142 vascular endothelial growth factor A Homo sapiens 71-75
15182588-1 2004 OBJECTIVE: To investigate the expression of VEGF mRNA and secretion of VEGF protein in NB4 and HL-60 cells affected by all-trans retinoic acid (ATRA) and daunorubincin (DNR) respectively. Tretinoin 144-148 vascular endothelial growth factor A Homo sapiens 44-48
15182588-1 2004 OBJECTIVE: To investigate the expression of VEGF mRNA and secretion of VEGF protein in NB4 and HL-60 cells affected by all-trans retinoic acid (ATRA) and daunorubincin (DNR) respectively. Tretinoin 144-148 vascular endothelial growth factor A Homo sapiens 71-75
14711804-7 2004 Exposure to RA for 12 days but not 4 days restored resistance and elastance to control (VAS) levels. Tretinoin 12-14 arginine vasopressin Rattus norvegicus 88-91
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 enolase 2 Homo sapiens 237-260
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 enolase 2 Homo sapiens 262-265
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 RNA binding fox-1 homolog 3 Homo sapiens 312-316
14733912-6 2004 Promyelocytic HL60 cells transfected with a RELMgamma expression plasmid have an increased proliferation rate compared to mock-transfected cells and display an altered response to retinoic acid-induced granulocytic differentiation. Tretinoin 180-193 resistin like gamma Mus musculus 44-53
14960275-5 2004 RA also activates Thylacine1 expression in the caudal PSM indirectly by inducing the expression of MKP3, an inhibitor of the FGF signaling pathway. Tretinoin 0-2 dual specificity phosphatase 6 L homeolog Xenopus laevis 99-103
14736747-8 2004 In addition, a Tead2-Engrailed fusion protein is able to repress retinoic acid-induced Pax3 expression in P19 cells and in vivo. Tretinoin 65-78 paired box 3 Mus musculus 87-91
14871833-11 2004 In the hormone-independent and highly malignant Nb2-SFJCD1 subline, the constitutive expression of HRPAP20 was markedly reduced by exposure of the cells to dietary differentiating agents (butyrate, retinoic acid, and vitamin D(3)). Tretinoin 198-211 NADH:ubiquinone oxidoreductase complex assembly factor 4 Rattus norvegicus 99-106
14871833-15 2004 Exposure of the cells to butyrate or retinoic acid reduced HRPAP20 expression, similar to the effects of these substances in the malignant rat lymphoma. Tretinoin 37-50 NADH:ubiquinone oxidoreductase complex assembly factor 4 Rattus norvegicus 59-66
14603524-5 2004 We demonstrate that RA-induced differentiation of CCE ES cells is associated with (1) downregulation of the LIF receptor (LIFR); (2) decreased tyrosine phosphorylation of signal transducer and activator of transcription 3 protein (Stat3); and (3) increased activation of extracellular regulated kinase (Erk1/2). Tretinoin 20-22 signal transducer and activator of transcription 3 Mus musculus 171-221
14603524-5 2004 We demonstrate that RA-induced differentiation of CCE ES cells is associated with (1) downregulation of the LIF receptor (LIFR); (2) decreased tyrosine phosphorylation of signal transducer and activator of transcription 3 protein (Stat3); and (3) increased activation of extracellular regulated kinase (Erk1/2). Tretinoin 20-22 signal transducer and activator of transcription 3 Mus musculus 231-236
14603524-6 2004 We conclude that RA induces CCE ES cell differentiation in the presence of LIF, in part, by disrupting signaling between the LIFR/gp130 receptor and nuclear targets that are required to prevent ES cell differentiation. Tretinoin 17-19 interleukin 6 signal transducer Mus musculus 130-135
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 43-56 bone morphogenetic protein 4 Mus musculus 123-151
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 43-56 bone morphogenetic protein 4 Mus musculus 153-157
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 58-62 bone morphogenetic protein 4 Mus musculus 123-151
15006160-0 2004 Retinoic acid induces corneal epithelial CYP4B1 gene expression and stimulates the synthesis of inflammatory 12-hydroxyeicosanoids. Tretinoin 0-13 cytochrome P450 family 4 subfamily B member 1 Homo sapiens 41-47
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 58-62 bone morphogenetic protein 4 Mus musculus 153-157
15006160-10 2004 The finding that retinoic acid increases the expression of the CYP4B1 gene and enhances production of the inflammatory 12-hydroxyeicosanoids in the corneal epithelium may provide a linkage between wound healing and inflammation in the ocular surface. Tretinoin 17-30 cytochrome P450 family 4 subfamily B member 1 Homo sapiens 63-69
14585838-8 2004 Human neuronal precursor NT2/D1 cells expressed apoE constitutively; however, after treatment of these cells with retinoic acid to induce differentiation, apoE expression diminished. Tretinoin 114-127 apolipoprotein E Homo sapiens 48-52
14585838-8 2004 Human neuronal precursor NT2/D1 cells expressed apoE constitutively; however, after treatment of these cells with retinoic acid to induce differentiation, apoE expression diminished. Tretinoin 114-127 apolipoprotein E Homo sapiens 155-159
14729653-2 2004 We recently demonstrated that all-trans retinoic acid (tRA) induces both NIS gene expression and iodide accumulation in vitro in well-differentiated human breast cancer cells (MCF-7). Tretinoin 40-53 solute carrier family 5 member 5 Homo sapiens 73-76
14623888-2 2004 Livers of aryl hydrocarbon receptor (AHR)-null mice have high levels of retinoic acid (RA), retinol, and retinyl palmitate. Tretinoin 87-89 aryl-hydrocarbon receptor Mus musculus 10-35
14623888-2 2004 Livers of aryl hydrocarbon receptor (AHR)-null mice have high levels of retinoic acid (RA), retinol, and retinyl palmitate. Tretinoin 87-89 aryl-hydrocarbon receptor Mus musculus 37-40
14724571-0 2004 All-trans retinoic acid potentiates Taxotere-induced cell death mediated by Jun N-terminal kinase in breast cancer cells. Tretinoin 10-23 mitogen-activated protein kinase 8 Homo sapiens 76-97
14532297-4 2004 We have previously identified two cytochrome P450s, P450RAI-1 and P450RAI-2 (herein named CYP26A1 and CYP26B1), which were shown to be responsible for catabolism of atRA both in the embryo and the adult. Tretinoin 165-169 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 52-61
14532297-4 2004 We have previously identified two cytochrome P450s, P450RAI-1 and P450RAI-2 (herein named CYP26A1 and CYP26B1), which were shown to be responsible for catabolism of atRA both in the embryo and the adult. Tretinoin 165-169 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 66-75
14532297-4 2004 We have previously identified two cytochrome P450s, P450RAI-1 and P450RAI-2 (herein named CYP26A1 and CYP26B1), which were shown to be responsible for catabolism of atRA both in the embryo and the adult. Tretinoin 165-169 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 90-97
14532297-4 2004 We have previously identified two cytochrome P450s, P450RAI-1 and P450RAI-2 (herein named CYP26A1 and CYP26B1), which were shown to be responsible for catabolism of atRA both in the embryo and the adult. Tretinoin 165-169 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 102-109
14532297-9 2004 Specifically, CYP26C1 can also recognize and metabolize 9-cis-RA and is much less sensitive than the other CYP26 family members to the inhibitory effects of ketoconazole. Tretinoin 56-64 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 14-19
14623888-2 2004 Livers of aryl hydrocarbon receptor (AHR)-null mice have high levels of retinoic acid (RA), retinol, and retinyl palmitate. Tretinoin 72-85 aryl-hydrocarbon receptor Mus musculus 10-35
14623888-2 2004 Livers of aryl hydrocarbon receptor (AHR)-null mice have high levels of retinoic acid (RA), retinol, and retinyl palmitate. Tretinoin 72-85 aryl-hydrocarbon receptor Mus musculus 37-40
14705145-0 2004 Retinoic acid-induced neuritogenesis of human neuroblastoma SH-SY5Y cells is ERK independent and PKC dependent. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 77-80
14705145-3 2004 From immunoblotting experiments, we observed that RA induced delayed but persistent ERK1 and ERK2 phosphorylation (until 96 hr) that was reduced significantly by the specific mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor U0126. Tretinoin 50-52 mitogen-activated protein kinase 3 Homo sapiens 84-88
14705145-3 2004 From immunoblotting experiments, we observed that RA induced delayed but persistent ERK1 and ERK2 phosphorylation (until 96 hr) that was reduced significantly by the specific mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor U0126. Tretinoin 50-52 mitogen-activated protein kinase 1 Homo sapiens 93-97
14705145-3 2004 From immunoblotting experiments, we observed that RA induced delayed but persistent ERK1 and ERK2 phosphorylation (until 96 hr) that was reduced significantly by the specific mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor U0126. Tretinoin 50-52 mitogen-activated protein kinase 3 Homo sapiens 209-213
14705145-3 2004 From immunoblotting experiments, we observed that RA induced delayed but persistent ERK1 and ERK2 phosphorylation (until 96 hr) that was reduced significantly by the specific mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor U0126. Tretinoin 50-52 mitogen-activated protein kinase 1 Homo sapiens 84-87
14705145-7 2004 Our results suggest that RA-induced ERK phosphorylation does not follow the classic Raf kinase-dependent pathway. Tretinoin 25-27 mitogen-activated protein kinase 1 Homo sapiens 36-39
14729653-2 2004 We recently demonstrated that all-trans retinoic acid (tRA) induces both NIS gene expression and iodide accumulation in vitro in well-differentiated human breast cancer cells (MCF-7). Tretinoin 55-58 solute carrier family 5 member 5 Homo sapiens 73-76
14725900-6 2004 RESULTS: TPO mRNA expression was up-regulated by approximately 2.9 times 8 hours after stimulation with 10(-6) M ATRA in KM101 cells. Tretinoin 113-117 thrombopoietin Homo sapiens 9-12
15500294-3 2004 Results showed that retinoic acid treatment increases the amount of beta-catenin bound to E-cadherin by decreasing its tyrosine-phosphorylation level. Tretinoin 20-33 cadherin 1 Homo sapiens 90-100
14725900-10 2004 In addition, [gamma-32P]-labeled TPO-RARE probe bound to KM101 nuclear protein extract was supershifted by anti-RARalpha antibody and modified by treatment with ATRA. Tretinoin 161-165 thrombopoietin Homo sapiens 33-36
14725900-0 2004 All-trans retinoic acid directly up-regulates thrombopoietin transcription in human bone marrow stromal cells. Tretinoin 10-23 thrombopoietin Homo sapiens 46-60
14725900-12 2004 CONCLUSION: These data support the direct up-regulation of TPO transcription by ATRA stimulation in human bone marrow stromal cells and propose one of the mechanisms of thrombocytosis during ATRA therapy for APL. Tretinoin 80-84 thrombopoietin Homo sapiens 59-62
14592536-0 2004 Distinct role and functional mode of TR3 and RARalpha in mediating ATRA-induced signalling pathway in breast and gastric cancer cells. Tretinoin 67-71 nuclear receptor subfamily 4 group A member 1 Homo sapiens 37-40
14702176-2 2004 Previous studies on mature somatic cell types showed that RA exerted inhibitory effects on inducible nitric oxide synthase (iNOS) production. Tretinoin 58-60 nitric oxide synthase 2, inducible Mus musculus 91-122
14702176-2 2004 Previous studies on mature somatic cell types showed that RA exerted inhibitory effects on inducible nitric oxide synthase (iNOS) production. Tretinoin 58-60 nitric oxide synthase 2, inducible Mus musculus 124-128
14702176-3 2004 For the first time, our study has shown that RA actually stimulates significant expression of iNOS at specific zones of the affected embryonic palatal tissues at three consecutive stages, from gestation day 13 (GD13) to day 16 (GD16). Tretinoin 45-47 nitric oxide synthase 2, inducible Mus musculus 94-98
14592536-4 2004 In the present study, we found that formation of TR3/RXRalpha heterodimers in the nucleus and their subsequent translocation into the cytoplasm, in association with regulation of apoptosis-related proteins Bcl-2, Bcl-xl and Bax, was critical for apoptosis induction by ATRA in breast cancer cells MCF-7. Tretinoin 269-273 nuclear receptor subfamily 4 group A member 1 Homo sapiens 49-52
14592536-8 2004 Furthermore, we demonstrated that the effects of ATRA depend on the relative levels of TR3, RARalpha and RXRalpha expression in cancer cells. Tretinoin 49-53 nuclear receptor subfamily 4 group A member 1 Homo sapiens 87-90
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 nuclear receptor subfamily 4 group A member 1 Homo sapiens 46-49
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 nuclear receptor subfamily 4 group A member 1 Homo sapiens 75-78
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 nuclear receptor subfamily 4 group A member 1 Homo sapiens 75-78
15641681-8 2004 It was indicated that retinoic acid could increase beta-catenin level of the whole cell protein and decrease nuclear beta-catenin, downregulating beta-cat/TCF signaling activity and reducing target gene cyclinD1 protein level. Tretinoin 22-35 hepatocyte nuclear factor 4 alpha Homo sapiens 155-158
14654966-0 2004 Retinoic acid delays keratinocyte senescence by suppression of betaig-h3 and p16 expression and induction of telomerase activity. Tretinoin 0-13 cyclin dependent kinase inhibitor 2A Homo sapiens 77-80
14654966-4 2004 The levels of betaig-h3 and p16 in 1 nM of RA-treated cells remained significantly lower than that of the vehicle control at all population doublings. Tretinoin 43-45 cyclin dependent kinase inhibitor 2A Homo sapiens 28-31
14704332-6 2004 Additionally, an RA-inducible cytochrome P450, P450RAI or CYP26, is down-regulated in liver during vitamin A deficiency and up-regulated dose-dependently by dietary vitamin A and exogenous RA. Tretinoin 17-19 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 47-54
14704332-6 2004 Additionally, an RA-inducible cytochrome P450, P450RAI or CYP26, is down-regulated in liver during vitamin A deficiency and up-regulated dose-dependently by dietary vitamin A and exogenous RA. Tretinoin 17-19 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 58-63
15587392-7 2004 ATRA inhibited the mRNA expression of CDK6, CDK4, cyclinD3 and cyclinD1. Tretinoin 0-4 cyclin dependent kinase 6 Homo sapiens 38-42
15587392-7 2004 ATRA inhibited the mRNA expression of CDK6, CDK4, cyclinD3 and cyclinD1. Tretinoin 0-4 cyclin D3 Homo sapiens 50-58
15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin dependent kinase 6 Homo sapiens 58-62
15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin D2 Homo sapiens 86-94
15641681-9 2004 As a result, retinoic acid can downregulate beta-catenin/TCF pathway in porcine tracheobronchial epithelial cell, suggesting that retinoic acid can inhibit the proliferation and accelerate differentiation of tracheobronchial epithelial cells. Tretinoin 13-26 hepatocyte nuclear factor 4 alpha Homo sapiens 57-60
15641681-9 2004 As a result, retinoic acid can downregulate beta-catenin/TCF pathway in porcine tracheobronchial epithelial cell, suggesting that retinoic acid can inhibit the proliferation and accelerate differentiation of tracheobronchial epithelial cells. Tretinoin 130-143 hepatocyte nuclear factor 4 alpha Homo sapiens 57-60
14701740-5 2004 As a consequence of C/EBPalpha phosphorylation, induction of granulocyte differentiation by C/EBPalpha or retinoic acid is inhibited. Tretinoin 106-119 CCAAT enhancer binding protein alpha Homo sapiens 20-30
15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin D3 Homo sapiens 99-107
15013071-5 2004 Expression of Hox-b1 and Krox20 (markers of specific rhombomeres) was altered after FLUCO and RA exposure. Tretinoin 94-96 early growth response 2 Rattus norvegicus 25-31
14694446-12 2004 Paired related homeobox gene 2 (Prx2)/S8 homeobox, and retinoic acid (RA)-regulated nur77 and cellular retinoic acid-binding protein II (CRABPII) transcription factors are expressed preferentially in P- cells. Tretinoin 70-72 paired related homeobox 2 Homo sapiens 0-30
14694446-12 2004 Paired related homeobox gene 2 (Prx2)/S8 homeobox, and retinoic acid (RA)-regulated nur77 and cellular retinoic acid-binding protein II (CRABPII) transcription factors are expressed preferentially in P- cells. Tretinoin 70-72 paired related homeobox 2 Homo sapiens 32-36
14680805-3 2003 Treatment of the antisense BAG-1-transfected cells with the anti-cancer drugs staurosporine, paclitaxel, all-trans retinoic acid (ATRA), and N-(4-hydroxyphenyl) retinamide (4-HPR) resulted in significantly enhanced apoptosis and reduced cell viability relative to vector-transfected cells. Tretinoin 105-128 BAG cochaperone 1 Homo sapiens 27-32
15110184-6 2004 In this context, particularly interesting is that retinoic acid induces a member of the tumor necrosis factor family, tumor necrosis factor-related apoptosis inducing ligand (TRAIL) or Apo2L. Tretinoin 50-63 TNF superfamily member 10 Homo sapiens 118-173
15110184-6 2004 In this context, particularly interesting is that retinoic acid induces a member of the tumor necrosis factor family, tumor necrosis factor-related apoptosis inducing ligand (TRAIL) or Apo2L. Tretinoin 50-63 TNF superfamily member 10 Homo sapiens 175-180
15110184-6 2004 In this context, particularly interesting is that retinoic acid induces a member of the tumor necrosis factor family, tumor necrosis factor-related apoptosis inducing ligand (TRAIL) or Apo2L. Tretinoin 50-63 TNF superfamily member 10 Homo sapiens 185-190
15263793-9 2004 CONCLUSIONS: ATRA provides a slightly stronger direct antineoplastic effect on human renal cancer cells than 13-cRA, and acts synergistically with IFN-alpha. Tretinoin 13-17 interferon alpha 1 Homo sapiens 147-156
14530287-7 2003 A specific antibody against RARP1 recognized a 110-kDa protein, which accumulates after incubation of HL-60 cells with ATRA. Tretinoin 119-123 amyloid beta precursor protein binding family B member 1 interacting protein Homo sapiens 28-33
14675751-2 2003 Here we report that the N-terminal inhibitory domain of tissue inhibitor of metalloproteinases 3 (N-TIMP-3), but not TIMP-1 or TIMP-2, inhibits glycosaminoglycan release from bovine nasal and porcine articular cartilage explants stimulated with interleukin-1alpha or retinoic acid in a dose-dependent manner. Tretinoin 267-280 TIMP metallopeptidase inhibitor 3 Bos taurus 56-96
14680805-3 2003 Treatment of the antisense BAG-1-transfected cells with the anti-cancer drugs staurosporine, paclitaxel, all-trans retinoic acid (ATRA), and N-(4-hydroxyphenyl) retinamide (4-HPR) resulted in significantly enhanced apoptosis and reduced cell viability relative to vector-transfected cells. Tretinoin 130-134 BAG cochaperone 1 Homo sapiens 27-32
14675751-2 2003 Here we report that the N-terminal inhibitory domain of tissue inhibitor of metalloproteinases 3 (N-TIMP-3), but not TIMP-1 or TIMP-2, inhibits glycosaminoglycan release from bovine nasal and porcine articular cartilage explants stimulated with interleukin-1alpha or retinoic acid in a dose-dependent manner. Tretinoin 267-280 TIMP metallopeptidase inhibitor 3 Bos taurus 100-106
14652353-6 2003 In support of this finding, the hepatic activity of methionine synthase, the folate-dependent enzyme required for homocysteine remethylation, was elevated 40% in ATRA-treated rats. Tretinoin 162-166 5-methyltetrahydrofolate-homocysteine methyltransferase Rattus norvegicus 52-71
14635200-0 2003 Runx2/Cbfa1 stimulation by retinoic acid is potentiated by BMP2 signaling through interaction with Smad1 on the collagen X promoter in chondrocytes. Tretinoin 27-40 SMAD family member 1 Gallus gallus 99-104
14713576-5 2003 The retinoic acid-sensitive cell line HTB35 was transfected for inducible CRABP I overexpression to test the role of this protein in modulating the sensitivity to retinoic acid and radiation as well as in regulating RAR-beta 2 and cyclin D1 expression. Tretinoin 4-17 retinoic acid receptor beta Homo sapiens 216-224
14668793-4 2003 In this report, we show that in NB4 cells and in two RA-resistant NB4-derived cell lines, NB4-R1 and NB4-R2, IFNalpha or IFNgamma combined with 0.1 microM As2O3 lead to an increased maturation effect. Tretinoin 53-55 interferon alpha 1 Homo sapiens 109-117
14612949-0 2003 HER2/neu uses Akt to suppress retinoic acid response element binding activity in MDA-MB-453 breast cancer cells. Tretinoin 30-43 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-4
14612949-0 2003 HER2/neu uses Akt to suppress retinoic acid response element binding activity in MDA-MB-453 breast cancer cells. Tretinoin 30-43 erb-b2 receptor tyrosine kinase 2 Homo sapiens 5-8
14612949-0 2003 HER2/neu uses Akt to suppress retinoic acid response element binding activity in MDA-MB-453 breast cancer cells. Tretinoin 30-43 AKT serine/threonine kinase 1 Homo sapiens 14-17
14612949-1 2003 We previously demonstrated that HER2/neu prevents all trans-retinoic acid (ATRA) from inducing growth inhibition in MDA-MB-453 breast cancer cells. Tretinoin 54-73 erb-b2 receptor tyrosine kinase 2 Homo sapiens 32-36
14612949-1 2003 We previously demonstrated that HER2/neu prevents all trans-retinoic acid (ATRA) from inducing growth inhibition in MDA-MB-453 breast cancer cells. Tretinoin 54-73 erb-b2 receptor tyrosine kinase 2 Homo sapiens 37-40
14612949-1 2003 We previously demonstrated that HER2/neu prevents all trans-retinoic acid (ATRA) from inducing growth inhibition in MDA-MB-453 breast cancer cells. Tretinoin 75-79 erb-b2 receptor tyrosine kinase 2 Homo sapiens 32-36
14612949-1 2003 We previously demonstrated that HER2/neu prevents all trans-retinoic acid (ATRA) from inducing growth inhibition in MDA-MB-453 breast cancer cells. Tretinoin 75-79 erb-b2 receptor tyrosine kinase 2 Homo sapiens 37-40
14646967-2 2003 Retinoic acid has been demonstrated to be produced from retinol via a two step oxidation pathway in which alcohol dehydrogenase isozymes have roles. Tretinoin 0-13 aldo-keto reductase family 1 member A1 Rattus norvegicus 106-127
14646967-6 2003 The all-trans retinoic acid formation was hampered by addition of ethanol, another substrate of alcohol dehydrogenase, and some histamine 2 receptor antagonists, inhibitors of alcohol dehydrogenase. Tretinoin 14-27 aldo-keto reductase family 1 member A1 Rattus norvegicus 96-117
14646967-6 2003 The all-trans retinoic acid formation was hampered by addition of ethanol, another substrate of alcohol dehydrogenase, and some histamine 2 receptor antagonists, inhibitors of alcohol dehydrogenase. Tretinoin 14-27 aldo-keto reductase family 1 member A1 Rattus norvegicus 176-197
14646967-7 2003 CONCLUSIONS: These results suggest that rat esophagus has an nicotinamide adenine dinucleotide-dependent all-trans retinoic acid formation pathway in which alcohol dehydrogenase is involved. Tretinoin 105-128 aldo-keto reductase family 1 member A1 Rattus norvegicus 156-177
14649730-3 2003 Exposure of retinoic acid (RA)-differentiated SH-SY5Y cells to MPP+ (1 mM, 72 h) also resulted in a decrease in RMB3 expression and an increase in GADD153 expression. Tretinoin 12-25 DNA damage inducible transcript 3 Homo sapiens 147-154
14649730-3 2003 Exposure of retinoic acid (RA)-differentiated SH-SY5Y cells to MPP+ (1 mM, 72 h) also resulted in a decrease in RMB3 expression and an increase in GADD153 expression. Tretinoin 27-29 DNA damage inducible transcript 3 Homo sapiens 147-154
13679204-8 2003 ATRA treatment resulted in enhanced expression of p21(cip1/waf1), nuclear translocation of retinoic acid receptors and apoptotic cell death. Tretinoin 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 50-53
13679204-8 2003 ATRA treatment resulted in enhanced expression of p21(cip1/waf1), nuclear translocation of retinoic acid receptors and apoptotic cell death. Tretinoin 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 54-58
13679204-8 2003 ATRA treatment resulted in enhanced expression of p21(cip1/waf1), nuclear translocation of retinoic acid receptors and apoptotic cell death. Tretinoin 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 59-63
14647461-5 2003 In THP-1 cells differentiated to mature macrophage-like cells by PMA/TPA or ATRA, MLL-AF9 expression was downregulated. Tretinoin 76-80 MLLT3 super elongation complex subunit Homo sapiens 86-89
12968026-5 2003 Retinoic acid dramatically increased the expression of JSAP1 and JNK3, which were co-precipitated with anti-JNK3 in the neuroectoderm of wild type but not JSAP1-null embryoid bodies. Tretinoin 0-13 mitogen-activated protein kinase 8 interacting protein 3 Mus musculus 55-60
14623956-2 2003 We demonstrate that Raldh3 knockout in mouse suppresses RA synthesis and causes malformations restricted to ocular and nasal regions, which are similar to those observed in vitamin A-deficient fetuses and/or in retinoid receptor mutants. Tretinoin 56-58 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 20-26
12975341-7 2003 Xrx1 is required for anterior neural plate proliferation and, when overexpressed, induces proliferation, inhibits X-ngnr-1, X-Delta-1 and N-tubulin and counteracts X-ngnr-1- and retinoic acid-mediated differentiation. Tretinoin 178-191 retina and anterior neural fold homeobox S homeolog Xenopus laevis 0-4
15058751-1 2003 The effect of all-trans retinoid acid (ATRA) on the expression of Notch1 gene by real-time reverse transcriptase polymerase chain reaction (RT-PCR) in acute promyelocytic leukemia cells (APL), NB4, and HL-60 lacking t(15;17) was studied. Tretinoin 39-43 notch receptor 1 Homo sapiens 66-72
14605041-0 2003 All-trans retinoic acid modulates the balance of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in patients with emphysema. Tretinoin 0-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 80-119
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 50-73 TIMP metallopeptidase inhibitor 1 Homo sapiens 138-177
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 50-73 TIMP metallopeptidase inhibitor 1 Homo sapiens 179-185
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 75-79 TIMP metallopeptidase inhibitor 1 Homo sapiens 138-177
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 75-79 TIMP metallopeptidase inhibitor 1 Homo sapiens 179-185
14605041-3 2003 DESIGN AND SETTING: As part of a clinical study, ATRA was administered to 20 patients with emphysema for 12 weeks and evaluated for its effects on plasma levels of MMP-9 and TIMP-1. Tretinoin 49-53 TIMP metallopeptidase inhibitor 1 Homo sapiens 174-180
14605041-6 2003 MEASUREMENTS AND RESULTS: Administration of ATRA to patients with emphysema produced a 45 +/- 14% reduction (mean +/- SEM) in plasma MMP-9 by enzyme-linked immunosorbent assay and a similar reduction in MMP-9 enzyme activity, while having little effect on TIMP-1 levels. Tretinoin 44-48 TIMP metallopeptidase inhibitor 1 Homo sapiens 256-262
14581379-10 2003 All-trans-retinoic acid, a prototypic AP-1 antagonist, blocked bryostatin-mediated induction of COX-2. Tretinoin 0-23 prostaglandin-endoperoxide synthase 2 Homo sapiens 96-101
14686729-9 2003 In addition, apoptosis occurred in both cell lines treated with either PGZ or ATRA, which was associated with a downregulation of bcl-2 and an upregulation of bax proteins. Tretinoin 78-82 BCL2 apoptosis regulator Homo sapiens 130-135
14686729-9 2003 In addition, apoptosis occurred in both cell lines treated with either PGZ or ATRA, which was associated with a downregulation of bcl-2 and an upregulation of bax proteins. Tretinoin 78-82 BCL2 associated X, apoptosis regulator Homo sapiens 159-162
14686729-11 2003 Furthermore, treatment of fresh glioblastoma tissue from patients with PGZ, either alone or in combination with ATRA, induced a significant level of tumor cell apoptosis together with a downregulation of bcl-2 protein level as compared with untreated control brain tissue. Tretinoin 112-116 BCL2 apoptosis regulator Homo sapiens 204-209
14587095-3 2003 Using the estrogen receptor-negative, retinoid receptor-positive breast cancer cell line SKRB-3, we found that treatment with ATRA significantly decreased the expression of PKCalpha, as well as reducing ERK MAPK phosphorylation. Tretinoin 126-130 protein kinase C alpha Homo sapiens 173-181
14587095-5 2003 Marked changes in the expression of cyclins (particularly cyclins A and E) were observed in SKBR-3 cells treated with ATRA. Tretinoin 118-122 cyclin A2 Homo sapiens 58-73
14587095-6 2003 Using a series of pharmacological and molecular approaches, we found evidence that ATRA-induced SKBR-3 cell growth inhibition involves the deregulation of the PKCalpha-MAPK pathway. Tretinoin 83-87 protein kinase C alpha Homo sapiens 159-167
12963727-7 2003 We demonstrate that while RA does not activate PPARalpha and PPARgamma, it binds to PPARbeta/delta with nanomolar affinity, modulates the conformation of the receptor, promotes interaction with the coactivator SRC-1, and efficiently activates PPARbeta/delta-mediated transcription. Tretinoin 26-28 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 210-215
14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 0-23 BCL2 apoptosis regulator Homo sapiens 76-81
14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 25-29 BCL2 apoptosis regulator Homo sapiens 76-81
14560020-6 2003 Dose-response experiments with ATRA in mouse primary macrophages showed that other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXRalpha). Tretinoin 31-35 nuclear receptor subfamily 1, group H, member 3 Mus musculus 83-86
14646600-4 2003 Effect of the ATRA treatment was demonstrated by the concomitant induction of cd14 and il1beta genes in four patients. Tretinoin 14-18 interleukin 1 beta Homo sapiens 87-94
14550285-3 2003 Such a study revealed that synergistic action of vitamin D(3) and retinoic acid (RA) had inherent ability to down-regulate TACO gene transcription in human macrophages. Tretinoin 66-79 coronin 1A Homo sapiens 123-127
14550285-3 2003 Such a study revealed that synergistic action of vitamin D(3) and retinoic acid (RA) had inherent ability to down-regulate TACO gene transcription in human macrophages. Tretinoin 81-83 coronin 1A Homo sapiens 123-127
12971996-0 2003 Expression of the retinoic acid catabolising enzyme CYP26B1 in the chick embryo and its regulation by retinoic acid. Tretinoin 18-31 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 52-59
12841847-11 2003 In addition, we documented for the first time that human breast cancer cells express FGF-4 protein, and its expression could be inhibited by all- trans -retinoic acid. Tretinoin 141-166 fibroblast growth factor 4 Homo sapiens 85-90
12971996-6 2003 Adding back RA rescues Cyp26B1 expression. Tretinoin 12-14 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 23-30
14559157-6 2003 Treatment of the Schwann cells isolated from the sciatic nerve with combination of BMP2 and retinoic acid (RA) dramatically induced GDNF-mRNA, while BMP2 or RA alone had no effect. Tretinoin 92-105 glial cell derived neurotrophic factor Homo sapiens 132-136
14559157-6 2003 Treatment of the Schwann cells isolated from the sciatic nerve with combination of BMP2 and retinoic acid (RA) dramatically induced GDNF-mRNA, while BMP2 or RA alone had no effect. Tretinoin 107-109 glial cell derived neurotrophic factor Homo sapiens 132-136
12971996-0 2003 Expression of the retinoic acid catabolising enzyme CYP26B1 in the chick embryo and its regulation by retinoic acid. Tretinoin 102-115 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 52-59
12971996-1 2003 We have cloned a fragment of Cyp26B1, a novel retinoic acid (RA) catabolising enzyme, and examined its expression pattern during early stages of chick embryogenesis. Tretinoin 46-59 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 29-36
12971996-1 2003 We have cloned a fragment of Cyp26B1, a novel retinoic acid (RA) catabolising enzyme, and examined its expression pattern during early stages of chick embryogenesis. Tretinoin 61-63 cytochrome P450 family 26 subfamily B member 1 Gallus gallus 29-36
12851412-0 2003 Genetic evidence that retinaldehyde dehydrogenase Raldh1 (Aldh1a1) functions downstream of alcohol dehydrogenase Adh1 in metabolism of retinol to retinoic acid. Tretinoin 146-159 alcohol dehydrogenase 1 (class I) Mus musculus 113-117
12851412-2 2003 Previous genetic studies have revealed that alcohol dehydrogenase Adh1 is required for efficient clearance of excess retinol to prevent toxicity, thus demonstrating that the mechanism involves oxidation of excess retinol to retinoic acid (RA). Tretinoin 224-237 alcohol dehydrogenase 1 (class I) Mus musculus 66-70
12851412-5 2003 Serum RA levels following a 50 mg/kg dose of retinol were reduced 72% in Raldh1-/- mice and 82% in Adh1-/- mice. Tretinoin 6-8 alcohol dehydrogenase 1 (class I) Mus musculus 99-103
12851412-2 2003 Previous genetic studies have revealed that alcohol dehydrogenase Adh1 is required for efficient clearance of excess retinol to prevent toxicity, thus demonstrating that the mechanism involves oxidation of excess retinol to retinoic acid (RA). Tretinoin 239-241 alcohol dehydrogenase 1 (class I) Mus musculus 66-70
12866036-1 2003 Peroxisome-proliferator activated receptor-gamma (PPARgamma) belongs to a family of nuclear receptors and acts as receptor for peroxisome-proliferators, steroids, retinoic acids, and polyunsaturated fatty acids. Tretinoin 163-177 peroxisome proliferator activated receptor gamma Homo sapiens 0-48
14519626-0 2003 All-trans-retinoic acid-induced apoptosis in human medulloblastoma: activation of caspase-3/poly(ADP-ribose) polymerase 1 pathway. Tretinoin 0-23 caspase 3 Homo sapiens 82-121
12866036-1 2003 Peroxisome-proliferator activated receptor-gamma (PPARgamma) belongs to a family of nuclear receptors and acts as receptor for peroxisome-proliferators, steroids, retinoic acids, and polyunsaturated fatty acids. Tretinoin 163-177 peroxisome proliferator activated receptor gamma Homo sapiens 50-59
14519626-7 2003 We also demonstrate that the ATRA-induced decrease in cell viability was due to increased cell death by apoptosis, which was accompanied by a 20-fold induction of caspase-3 activity in the most sensitive cell line, D458. Tretinoin 29-33 caspase 3 Homo sapiens 163-172
14519626-9 2003 Furthermore, ATRA-induced cell death in D283, D425, and D458 cells was accompanied by activation of caspase-3, a key executioner of apoptosis. Tretinoin 13-17 caspase 3 Homo sapiens 100-109
14519626-11 2003 Pretreatment with a specific caspase-3 inhibitor, DEVD-CHO, significantly reduced ATRA-induced apoptotic cell death. Tretinoin 82-86 caspase 3 Homo sapiens 29-38
14519626-12 2003 Thus, we demonstrate for the first time that low concentrations of ATRA inhibit MB cell proliferation and induce apoptotic cell death in part by activating caspase-3/poly(ADP-ribose) polymerase 1 effector pathway, and we show that retinoic acids and novel retinoids are potential antitumor agents in MB therapy. Tretinoin 67-71 caspase 3 Homo sapiens 156-195
14519626-12 2003 Thus, we demonstrate for the first time that low concentrations of ATRA inhibit MB cell proliferation and induce apoptotic cell death in part by activating caspase-3/poly(ADP-ribose) polymerase 1 effector pathway, and we show that retinoic acids and novel retinoids are potential antitumor agents in MB therapy. Tretinoin 231-245 caspase 3 Homo sapiens 156-195
12941614-6 2003 Using embryonic ectoderm analogous stem cells, we demonstrate that in these nonmuscle cells, as in skeletal muscle precursor cells, expression of MyoR is inversely correlated with the extent of cellular differentiation as induced by retinoic acid. Tretinoin 233-246 musculin Mus musculus 146-150
12941614-7 2003 Our preliminary results indicate that overexpression of exogenous MyoR inhibits retinoic-acid-induced differentiation in EC cells and is lethal to early mouse embryos. Tretinoin 80-93 musculin Mus musculus 66-70
12941622-4 2003 At all sites, expression of additional RA signaling molecules (RARalpha, RARbeta, RXR, CRABP1) depends on M/E interactions. Tretinoin 39-41 retinoic acid receptor beta Homo sapiens 73-80
12914961-4 2003 Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway. Tretinoin 43-56 glial cell derived neurotrophic factor Homo sapiens 98-102
14708942-0 2003 HB-GAM/Pleiotrophin and Midkine are differently expressed and distributed during retinoic acid-induced neural differentiation of P19 cells. Tretinoin 81-94 pleiotrophin Homo sapiens 0-6
12933640-5 2003 We used real-time RT-PCR to examine the effects of these factors on the expression of mRNA encoding the Id proteins, demonstrating an increase in Id2 and Id3 expression in Sertoli cells treated with thyroid hormone, retinoic acid, or testosterone. Tretinoin 216-229 inhibitor of DNA binding 3, HLH protein Rattus norvegicus 154-157
14693485-0 2003 Effect of topical tretinoin, chemical peeling and dermabrasion on p53 expression in facial skin. Tretinoin 18-27 tumor protein p53 Homo sapiens 66-69
14693485-6 2003 Topical tretinoin therapy was found to induce a significant decrease in the expression of p53 up to 6 months of therapy followed by a significant increase after 10 months of therapy. Tretinoin 8-17 tumor protein p53 Homo sapiens 90-93
14708942-0 2003 HB-GAM/Pleiotrophin and Midkine are differently expressed and distributed during retinoic acid-induced neural differentiation of P19 cells. Tretinoin 81-94 pleiotrophin Homo sapiens 7-19
14708942-0 2003 HB-GAM/Pleiotrophin and Midkine are differently expressed and distributed during retinoic acid-induced neural differentiation of P19 cells. Tretinoin 81-94 midkine Homo sapiens 24-31
14708942-2 2003 Using the P19 cell which is a model to study the events associated with early development, we examined the expression and cellular localization of HB-GAM and MK during neural differentiation of P19 cells induced by retinoic acid (RA). Tretinoin 215-228 pleiotrophin Homo sapiens 147-153
14708942-2 2003 Using the P19 cell which is a model to study the events associated with early development, we examined the expression and cellular localization of HB-GAM and MK during neural differentiation of P19 cells induced by retinoic acid (RA). Tretinoin 230-232 pleiotrophin Homo sapiens 147-153
14708942-5 2003 More interestingly, HB-GAM which was not detected in untreated P19 cells was strongly expressed after 2 days of RA treatment and this expression persists throughout the duration of the culture suggesting that it could be involved in different aspects of this differentiation process. Tretinoin 112-114 pleiotrophin Homo sapiens 20-26
12970779-0 2003 A new selective AKT pharmacological inhibitor reduces resistance to chemotherapeutic drugs, TRAIL, all-trans-retinoic acid, and ionizing radiation of human leukemia cells. Tretinoin 99-122 AKT serine/threonine kinase 1 Homo sapiens 16-19
12929139-5 2003 Differentiation by cAMP and retinoic acid caused an increase of choline acetyltransferase activity and decrease of acetyl-CoA levels in both cell lines. Tretinoin 28-41 HPS3, biogenesis of lysosomal organelles complex 2 subunit 1 Mus musculus 122-125
14582708-2 2003 We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. Tretinoin 37-50 GLI family zinc finger 2 Homo sapiens 103-108
14582708-2 2003 We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. Tretinoin 52-56 GLI family zinc finger 2 Homo sapiens 103-108
12970779-9 2003 Our findings demonstrate that, at a concentration which does not affect PI3K activity, the Akt inhibitor markedly reduced resistance of HL60AR cells to etoposide, cytarabine, TRAIL, ATRA, and ionizing radiation. Tretinoin 182-186 AKT serine/threonine kinase 1 Homo sapiens 91-94
12970919-9 2003 The inhibition of telomerase activity and the activation of Caspase-3 may be the key steps through which ATRA inhibits the proliferation of SMMC-7721 cell line. Tretinoin 105-109 caspase 3 Homo sapiens 60-69
12858358-0 2003 Stable expression of full length human androgen receptor in PC-3 prostate cancer cells enhances sensitivity to retinoic acid but not to 1alpha,25-dihydroxyvitamin D3. Tretinoin 111-124 androgen receptor Homo sapiens 39-56
12920340-8 2003 Those cultured in the medium with retinoic acid expressed HPC-1 and calbindin, but not Thy-1. Tretinoin 34-47 calbindin 1 Rattus norvegicus 68-77
12970919-7 2003 Besides, ATRA could inhibit the activity of telomerase, promote the expression of Caspase-3 and its activation. Tretinoin 9-13 caspase 3 Homo sapiens 82-91
12930800-6 2003 Further regulation of RA signaling is provided by the presence of a RA sink in the form of the CYP26B1 RA catabolic enzyme expressed in deeper regions of the brain. Tretinoin 22-24 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 95-102
12930800-6 2003 Further regulation of RA signaling is provided by the presence of a RA sink in the form of the CYP26B1 RA catabolic enzyme expressed in deeper regions of the brain. Tretinoin 68-70 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 95-102
12930800-6 2003 Further regulation of RA signaling is provided by the presence of a RA sink in the form of the CYP26B1 RA catabolic enzyme expressed in deeper regions of the brain. Tretinoin 68-70 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 95-102
12930299-5 2003 Interestingly, insulin-like growth factor-II (IGF-II, 50 ng/ml) was able to significantly (67.3%; P < 0.05) reduce RA effects, whereas IGF-I (50 ng/ml) and insulin (75 ng/ml) were without effect. Tretinoin 118-120 insulin like growth factor 1 Homo sapiens 46-51
12915124-5 2003 Here, we report that Western blots of lysates from retinoic-acid-differentiated P19 cells and bovine endothelial cells indicate the presence of a 45-kDa Wnt-1 protein. Tretinoin 51-64 Wnt family member 1 Homo sapiens 153-158
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 CREB binding protein Homo sapiens 160-180
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 CREB binding protein Homo sapiens 182-185
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 MYB binding protein 1a Homo sapiens 196-200
12912909-4 2003 We find that hydroxynonenal and structurally related compounds (such as trans-retinoic acid, trans-retinal and other 2-alkenals) specifically induce uncoupling of mitochondria through the uncoupling proteins UCP1, UCP2 and UCP3 and the adenine nucleotide translocase (ANT). Tretinoin 72-91 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 214-218
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 CREB binding protein Homo sapiens 160-180
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 CREB binding protein Homo sapiens 182-185
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 MYB binding protein 1a Homo sapiens 196-200
14535629-2 2003 In order to investigate the relationship of CBP to the RA signaling in a human salivary gland (HSG) adenocarcinoma cell line, we examined the expression of CBP in the cells. Tretinoin 55-57 CREB binding protein Homo sapiens 44-47
14535629-6 2003 Co-transfection with a CBP-expression plasmid and the luciferase reporter gene enhanced the RA-dependent transcription activation approximately 10-fold. Tretinoin 92-94 CREB binding protein Homo sapiens 23-26
14535629-9 2003 These findings indicate that CBP expressed in HSG cells mediates the RA-inducible growth and differentiation-regulating transcription activation in concert with the retinoic acid receptors. Tretinoin 69-71 CREB binding protein Homo sapiens 29-32
12935977-7 2003 RESULTS: ATRA significantly inhibited TNFalpha-induced TF expression in HMEC-1 as well as HUVEC. Tretinoin 9-13 tumor necrosis factor Homo sapiens 38-46
12935977-8 2003 ATRA increased t-PA antigen without significantly affecting PAI-1 expression, and counteracted the TNFalpha-induced t-PA decrease in both types of EC. Tretinoin 0-4 plasminogen activator, tissue type Homo sapiens 15-19
12935977-8 2003 ATRA increased t-PA antigen without significantly affecting PAI-1 expression, and counteracted the TNFalpha-induced t-PA decrease in both types of EC. Tretinoin 0-4 tumor necrosis factor Homo sapiens 99-107
12935977-8 2003 ATRA increased t-PA antigen without significantly affecting PAI-1 expression, and counteracted the TNFalpha-induced t-PA decrease in both types of EC. Tretinoin 0-4 plasminogen activator, tissue type Homo sapiens 116-120
12935977-9 2003 Accordingly, t-PA activity was significantly increased by ATRA, even in the presence of TNFalpha. Tretinoin 58-62 plasminogen activator, tissue type Homo sapiens 13-17
12930299-5 2003 Interestingly, insulin-like growth factor-II (IGF-II, 50 ng/ml) was able to significantly (67.3%; P < 0.05) reduce RA effects, whereas IGF-I (50 ng/ml) and insulin (75 ng/ml) were without effect. Tretinoin 118-120 insulin Homo sapiens 15-22
12935977-10 2003 Finally, ATRA upregulated TM, and prevented TNFalpha-induced TM downregulation. Tretinoin 9-13 tumor necrosis factor Homo sapiens 44-52
12743114-2 2003 Treatment of human neuroblastoma SH-SY5Y cells with retinoic acid results in increased tTG expression, which is both necessary and sufficient for differentiation. Tretinoin 52-65 transglutaminase 2 Homo sapiens 87-90
12882839-0 2003 Retinoic acids exert direct effects on T cells to suppress Th1 development and enhance Th2 development via retinoic acid receptors. Tretinoin 0-14 negative elongation factor complex member C/D, Th1l Mus musculus 59-62
12882839-1 2003 The vitamin A metabolite, retinoic acid (RA), affects Th1 and Th2 development. Tretinoin 26-39 negative elongation factor complex member C/D, Th1l Mus musculus 54-57
12882839-1 2003 The vitamin A metabolite, retinoic acid (RA), affects Th1 and Th2 development. Tretinoin 41-43 negative elongation factor complex member C/D, Th1l Mus musculus 54-57
12877989-3 2003 The treatment of LA-N-1 cell cultures with all-trans retinoic acid (atRA) results in time- and dose-dependent stimulation of PlsEtn-PLA2 and PtdEtn-PLA2 activities in the nuclear fraction. Tretinoin 53-66 phospholipase A2 group IB Homo sapiens 132-136
12877989-3 2003 The treatment of LA-N-1 cell cultures with all-trans retinoic acid (atRA) results in time- and dose-dependent stimulation of PlsEtn-PLA2 and PtdEtn-PLA2 activities in the nuclear fraction. Tretinoin 53-66 phospholipase A2 group IB Homo sapiens 148-152
12877989-3 2003 The treatment of LA-N-1 cell cultures with all-trans retinoic acid (atRA) results in time- and dose-dependent stimulation of PlsEtn-PLA2 and PtdEtn-PLA2 activities in the nuclear fraction. Tretinoin 68-72 phospholipase A2 group IB Homo sapiens 132-136
12877989-3 2003 The treatment of LA-N-1 cell cultures with all-trans retinoic acid (atRA) results in time- and dose-dependent stimulation of PlsEtn-PLA2 and PtdEtn-PLA2 activities in the nuclear fraction. Tretinoin 68-72 phospholipase A2 group IB Homo sapiens 148-152
12877989-7 2003 However, atRA-mediated stimulation of PLA2 activities in LA-N-1 cell nuclei is partially inhibited by cycloheximide indicating that this decrease in PLA2 activity is due to a general decreased protein synthesis. Tretinoin 9-13 phospholipase A2 group IB Homo sapiens 38-42
12877989-7 2003 However, atRA-mediated stimulation of PLA2 activities in LA-N-1 cell nuclei is partially inhibited by cycloheximide indicating that this decrease in PLA2 activity is due to a general decreased protein synthesis. Tretinoin 9-13 phospholipase A2 group IB Homo sapiens 149-153
12877989-8 2003 Our results also support earlier studies in which atRA induces morphologic differentiation through the stimulation of PLA2-generated second messengers such as arachidonic acid and eicosanoids. Tretinoin 50-54 phospholipase A2 group IB Homo sapiens 118-122
12882839-10 2003 The RA receptor (RAR) antagonists, LE540 and LE135, but not the retinoic X receptor (RXR) antagonist, PA452, inhibited the effect of RA on Th1/Th2 development. Tretinoin 4-6 negative elongation factor complex member C/D, Th1l Mus musculus 139-142
12882839-13 2003 These results indicate that, via RAR, RA directly suppresses Th1 development and directly enhances Th2 development with its timely addition. Tretinoin 33-35 negative elongation factor complex member C/D, Th1l Mus musculus 61-64
12873138-0 2003 Retinoic acid binds to the C2-domain of protein kinase C(alpha). Tretinoin 0-13 protein kinase C alpha Homo sapiens 40-63
12873138-2 2003 PKC activity is known to be modulated by all-trans retinoic acid (atRA), although neither the action mechanism nor even the possible binding to PKCs has been established. Tretinoin 41-64 protein kinase C alpha Homo sapiens 0-3
12873138-2 2003 PKC activity is known to be modulated by all-trans retinoic acid (atRA), although neither the action mechanism nor even the possible binding to PKCs has been established. Tretinoin 66-70 protein kinase C alpha Homo sapiens 0-3
12873138-3 2003 Crystals of the C2-domain of PKC(alpha), a regulatory module in the protein that binds Ca(2+) and acidic phospholipids, have now been obtained by cocrystallization with atRA. Tretinoin 169-173 protein kinase C alpha Homo sapiens 29-39
12873138-9 2003 Competition between atRA and acidic phospholipids to bind to PKC is a possible mechanism for modulating PKC(alpha) activity. Tretinoin 20-24 protein kinase C alpha Homo sapiens 61-64
12873138-9 2003 Competition between atRA and acidic phospholipids to bind to PKC is a possible mechanism for modulating PKC(alpha) activity. Tretinoin 20-24 protein kinase C alpha Homo sapiens 104-114
12879006-0 2003 Induction of TIG3, a putative class II tumor suppressor gene, by retinoic acid in head and neck and lung carcinoma cells and its association with suppression of the transformed phenotype. Tretinoin 65-78 phospholipase A and acyltransferase 4 Homo sapiens 13-17
12879006-5 2003 We examined the constitutive and all-trans retinoic acid (ATRA)-inducible expression of TIG3 mRNA in five head and neck squamous cell carcinoma (HNSCC) and five nonsmall cell lung carcinoma (NSCLC) cell lines to determine whether it is associated with their responsiveness to ATRA. Tretinoin 43-56 phospholipase A and acyltransferase 4 Homo sapiens 88-92
12879006-5 2003 We examined the constitutive and all-trans retinoic acid (ATRA)-inducible expression of TIG3 mRNA in five head and neck squamous cell carcinoma (HNSCC) and five nonsmall cell lung carcinoma (NSCLC) cell lines to determine whether it is associated with their responsiveness to ATRA. Tretinoin 58-62 phospholipase A and acyltransferase 4 Homo sapiens 88-92
12879006-9 2003 ATRA (1 microM; 48 h) increased TIG3 mRNA in 4/5 HNSCCs and 3/5 NSCLCs and RARbeta mRNA in some of the same cell lines, but also in cells that did not show TIG3 induction. Tretinoin 0-4 phospholipase A and acyltransferase 4 Homo sapiens 32-36
12879006-9 2003 ATRA (1 microM; 48 h) increased TIG3 mRNA in 4/5 HNSCCs and 3/5 NSCLCs and RARbeta mRNA in some of the same cell lines, but also in cells that did not show TIG3 induction. Tretinoin 0-4 retinoic acid receptor beta Homo sapiens 75-82
12879006-9 2003 ATRA (1 microM; 48 h) increased TIG3 mRNA in 4/5 HNSCCs and 3/5 NSCLCs and RARbeta mRNA in some of the same cell lines, but also in cells that did not show TIG3 induction. Tretinoin 0-4 phospholipase A and acyltransferase 4 Homo sapiens 156-160
12879006-11 2003 ATRA concentrations required for TIG3 induction ranged from 1 to 500 nM depending on the cell line. Tretinoin 0-4 phospholipase A and acyltransferase 4 Homo sapiens 33-37
12879006-12 2003 The pan-RAR antagonists AGN193109 and the RARalpha antagonist Ro 41-5253 blocked TIG3 induction by ATRA. Tretinoin 99-103 phospholipase A and acyltransferase 4 Homo sapiens 81-85
12767074-2 2003 Retinoic acid receptor beta (RARbeta) is itself a retinoid target gene with a retinoic acid response element (betaRARE) in the 5" untranslated region of the RARbeta2 gene. Tretinoin 78-91 retinoic acid receptor beta Homo sapiens 0-27
12767074-2 2003 Retinoic acid receptor beta (RARbeta) is itself a retinoid target gene with a retinoic acid response element (betaRARE) in the 5" untranslated region of the RARbeta2 gene. Tretinoin 78-91 retinoic acid receptor beta Homo sapiens 29-36
12842195-8 2003 Interestingly, the COX-2 protein and COX-2 mRNA were not detected in U937 cells, and their levels remained undetectable during the entire course of RA treatment. Tretinoin 148-150 mitochondrially encoded cytochrome c oxidase II Homo sapiens 19-24
12586626-4 2003 Here we show that TNF can synergize with ATRA to induce differentiation, showing monocytic characteristics more typical of differentiation mediated by TNF than by ATRA. Tretinoin 41-45 tumor necrosis factor Homo sapiens 151-154
12586626-9 2003 We propose that ATRA can prime cancer cells for differentiation triggered by TNF and suggest that targeting the TNF pathway in combination with ATRA may represent a novel route to treat leukemias. Tretinoin 16-20 tumor necrosis factor Homo sapiens 77-80
12586626-4 2003 Here we show that TNF can synergize with ATRA to induce differentiation, showing monocytic characteristics more typical of differentiation mediated by TNF than by ATRA. Tretinoin 163-167 tumor necrosis factor Homo sapiens 18-21
12586626-9 2003 We propose that ATRA can prime cancer cells for differentiation triggered by TNF and suggest that targeting the TNF pathway in combination with ATRA may represent a novel route to treat leukemias. Tretinoin 16-20 tumor necrosis factor Homo sapiens 112-115
12586626-6 2003 Underlying this response was an increase in TNF-induced nuclear factor-kappaB (NF-kappaB) DNA binding within 2 hours in the presence of ATRA and activation of NF-kappaB DNA binding and transcriptional activity in response to ATRA alone within 48 hours of ATRA treatment. Tretinoin 136-140 tumor necrosis factor Homo sapiens 44-47
12586626-6 2003 Underlying this response was an increase in TNF-induced nuclear factor-kappaB (NF-kappaB) DNA binding within 2 hours in the presence of ATRA and activation of NF-kappaB DNA binding and transcriptional activity in response to ATRA alone within 48 hours of ATRA treatment. Tretinoin 225-229 tumor necrosis factor Homo sapiens 44-47
12586626-6 2003 Underlying this response was an increase in TNF-induced nuclear factor-kappaB (NF-kappaB) DNA binding within 2 hours in the presence of ATRA and activation of NF-kappaB DNA binding and transcriptional activity in response to ATRA alone within 48 hours of ATRA treatment. Tretinoin 225-229 tumor necrosis factor Homo sapiens 44-47
12839938-4 2003 Gel shift analysis indicated that PPAR gamma, in the presence of RXR, formed a strong complex with a retinoic acid response element (beta retinoic acid response element) in the RAR beta promoter. Tretinoin 101-114 retinoic acid receptor beta Homo sapiens 177-185
12839938-4 2003 Gel shift analysis indicated that PPAR gamma, in the presence of RXR, formed a strong complex with a retinoic acid response element (beta retinoic acid response element) in the RAR beta promoter. Tretinoin 133-151 peroxisome proliferator activated receptor gamma Homo sapiens 34-44
12839938-4 2003 Gel shift analysis indicated that PPAR gamma, in the presence of RXR, formed a strong complex with a retinoic acid response element (beta retinoic acid response element) in the RAR beta promoter. Tretinoin 133-151 retinoic acid receptor beta Homo sapiens 177-185
12839938-4 2003 Gel shift analysis indicated that PPAR gamma, in the presence of RXR, formed a strong complex with a retinoic acid response element (beta retinoic acid response element) in the RAR beta promoter. Tretinoin 101-114 peroxisome proliferator activated receptor gamma Homo sapiens 34-44
12759464-2 2003 Recently, retinoic acids were reported to inhibit Th1 cytokine production. Tretinoin 10-24 negative elongation factor complex member C/D, Th1l Mus musculus 50-53
12753752-1 2003 The aim of this study was to develop an intravenous delivery of all-trans retinoic acid (ATRA) for the treatment of cancer. Tretinoin 89-93 retinol dehydrogenase 2 Mus musculus 64-73
12846418-3 2003 9-cis retinoic acid (9-cis RA), a ligand for both retinoic acid receptor (RAR)/retinoic X receptor (RXR) heterodimers as well as RXR/RXR homodimers, markedly induced NIS mRNA expression in MCF-7 breast cancer cells in a dose- and time-dependent fashion, with maximal levels occurring at 12 h. All-trans retinoic acid, ATRA, a RAR specific ligand had a similar potency. Tretinoin 6-19 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 88-98
12866655-6 2003 A tyrosine phosphorylation of PLC-gamma1 was observed in concomitance with the ATRA-induced maximal functional activity. Tretinoin 79-83 phospholipase C gamma 1 Homo sapiens 30-40
12866655-7 2003 An increased expression of PLC-beta3 and PKC-alpha and -beta2 was also evidentiated at the longer time points explored, when the effects of ATRA in preservation of the differentiated morphology were maximal. Tretinoin 140-144 protein kinase C alpha Homo sapiens 41-50
12761879-8 2003 Blockage of the RA + Tx-induced GJIC with 18-beta-glycyrrhetinic acid (beta-Gly) prevented in 34% the inhibition of MCF-7 proliferation and the E-cadherin increment in 30% at 96 h of culture. Tretinoin 16-18 cadherin 1 Homo sapiens 144-154
12799182-1 2003 RA175, a new immunoglobulin superfamily member, is preferentially expressed during differentiation of P19 embryonic carcinoma (EC) cells induced by retinoic acid. Tretinoin 148-161 cell adhesion molecule 1 Mus musculus 0-5
12943740-2 2003 We have previously shown that re-expression of ERalpha in ER-negative cells stimulates the transcriptional and growth inhibitory effects of all-trans-retinoic acid (tRA) by a mechanism that is independent of the ER ligands estradiol and tamoxifen. Tretinoin 140-163 estrogen receptor 1 Homo sapiens 47-54
12943740-2 2003 We have previously shown that re-expression of ERalpha in ER-negative cells stimulates the transcriptional and growth inhibitory effects of all-trans-retinoic acid (tRA) by a mechanism that is independent of the ER ligands estradiol and tamoxifen. Tretinoin 165-168 estrogen receptor 1 Homo sapiens 47-54
12813000-7 2003 In another set of experiments, cells treated for 10-12 days with vehicle (ethanol) or retinoic acid were challenged with ET-1 or sarafotoxin S6c, and various determinations were made at 24 h. 3 Retinoic acid inhibited transformation and proliferation of HSC as assessed by morphological characteristics, expression of alpha-sma, bromodeoxyuridine incorporation and cell count. Tretinoin 194-207 endothelin 1 Rattus norvegicus 121-125
12813000-11 2003 The presence of retinoic acid in the medium during treatment with ET-1 caused further reduction in the expression of alpha-smooth muscle actin. Tretinoin 16-29 endothelin 1 Rattus norvegicus 66-70
12813000-12 2003 ET-1 and sarafotoxin S6c stimulated total protein synthesis in vehicle- and retinoic acid-treated cells, but collagen synthesis only in the latter. Tretinoin 76-89 endothelin 1 Rattus norvegicus 0-4
12746314-0 2003 Retinoic acid stimulates chondrocyte differentiation and enhances bone morphogenetic protein effects through induction of Smad1 and Smad5. Tretinoin 0-13 SMAD family member 1 Gallus gallus 122-127
12746314-7 2003 RA did not increase the expression of the type IA BMP receptor but did markedly up-regulate the expression of Smad1 and Smad5 proteins, important participants in the BMP pathway. Tretinoin 0-2 SMAD family member 5 Homo sapiens 120-125
12746314-8 2003 Inhibition of RA signaling, with the selective inhibitor AGN 193109, blocked RA-mediated induction of the Smad proteins and chondrocyte differentiation. Tretinoin 14-16 SMAD family member 1 Gallus gallus 106-110
12759464-8 2003 We conclude that treatment with ATRA in SLE-prone NZB/W F(1) mice significantly alleviates autoimmune renal disorder and prolongs survival; this may thus represent a novel approach to the treatment of patients with lupus nephritis. Tretinoin 32-36 TP53 regulated inhibitor of apoptosis 1 Mus musculus 54-60
12808116-9 2003 In addition, treatment with RA-induced expression of the platelet-derived growth factor receptor-alpha. Tretinoin 28-30 platelet derived growth factor receptor alpha Homo sapiens 57-102
12841584-6 2003 In this study it is shown for the first time that the retinoic acid-induced neuronal differentiation of NTERA2 cells is accompanied by down-regulation of SOX2 and up-regulation of SOX3 gene during early phases of induction. Tretinoin 54-67 SRY-box transcription factor 3 Homo sapiens 180-184
12955881-4 2003 We demonstrate that RA induces growth arrest and differentiation in HepG2 cells by influencing the activities of cyclin-cdk complexes involved in the regulation of G1/S transition and S-phase progression, in particular by modifying the binding of these complexes to p21 and p27 inhibitors. Tretinoin 20-22 cyclin dependent kinase inhibitor 1A Homo sapiens 266-269
12955881-5 2003 In fetal cells, however, the induction of apoptosis and differentiation by RA was obtained via inhibition of cyclin D1-cdk4 activity, as result of an increased binding to the p16 inhibitor. Tretinoin 75-77 cyclin dependent kinase inhibitor 2A Homo sapiens 175-178
12955881-6 2003 Retinoic acid also modulates c-myc and Bcl-2 expression. Tretinoin 0-13 BCL2 apoptosis regulator Homo sapiens 39-44
12841584-7 2003 These data suggest that the effects of retinoic acid on neural differentiation of NTERA2 EC cells might be mediated by modulation of SOX2 and SOX3 gene expression. Tretinoin 39-52 SRY-box transcription factor 3 Homo sapiens 142-146
12870655-0 2003 Transcript profiling of cytochrome P450 genes in HL-60 human leukemic cells: upregulation of CYP1B1 by all-trans-retinoic acid. Tretinoin 103-126 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 24-39
12776186-0 2003 Retinoic acid-induced growth arrest of MCF-7 cells involves the selective regulation of the IRS-1/PI 3-kinase/AKT pathway. Tretinoin 0-13 AKT serine/threonine kinase 1 Homo sapiens 110-113
12870655-2 2003 The biotransformation of this drug is catalyzed by various cytochrome P450 (CYP) enzymes, but relatively little is known about the effect of ATRA on CYP enzyme expression in leukemic cells. Tretinoin 141-145 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 149-152
12870655-6 2003 The same ATRA treatment also resulted in the detection of CYP26A1 but not CYP1A1, CYP2B6, CYP2C8, CY2C9, CYP3A4, or CYP3A5 mRNA. Tretinoin 9-13 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 58-65
12704731-9 2003 As both RARalpha and RXRalpha are present in fetal and neonatal gonocytes, we suggest that retinoic acid exerts its effects on gonocytes via a RARalpha-RXRalpha heterodimer, with RARalpha functioning as an active partner and RXRalpha as a passive partner. Tretinoin 91-104 retinoid X receptor alpha Rattus norvegicus 21-29
12704731-9 2003 As both RARalpha and RXRalpha are present in fetal and neonatal gonocytes, we suggest that retinoic acid exerts its effects on gonocytes via a RARalpha-RXRalpha heterodimer, with RARalpha functioning as an active partner and RXRalpha as a passive partner. Tretinoin 91-104 retinoid X receptor alpha Rattus norvegicus 152-160
12704731-9 2003 As both RARalpha and RXRalpha are present in fetal and neonatal gonocytes, we suggest that retinoic acid exerts its effects on gonocytes via a RARalpha-RXRalpha heterodimer, with RARalpha functioning as an active partner and RXRalpha as a passive partner. Tretinoin 91-104 retinoid X receptor alpha Rattus norvegicus 152-160
12644474-4 2003 We observed growth arrest and apoptosis, upon decreasing Bcl-2 protein and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bcl-2. Tretinoin 177-190 BCL2 apoptosis regulator Homo sapiens 57-62
12644474-4 2003 We observed growth arrest and apoptosis, upon decreasing Bcl-2 protein and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bcl-2. Tretinoin 177-190 BCL2 apoptosis regulator Homo sapiens 98-103
12644474-4 2003 We observed growth arrest and apoptosis, upon decreasing Bcl-2 protein and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bcl-2. Tretinoin 177-190 BCL2 apoptosis regulator Homo sapiens 98-103
12644474-6 2003 In stable clones expressing ectopic Par-4 and in ATRA-treated cells, we observed decreased Bcl-2 protein and transcript. Tretinoin 49-53 BCL2 apoptosis regulator Homo sapiens 91-96
12776186-6 2003 Downstream signaling events were also selectively reduced, as RA abrogated IGF-I-stimulated AKT activation but did not alter erk1/2 activation. Tretinoin 62-64 insulin like growth factor 1 Homo sapiens 75-80
12776186-6 2003 Downstream signaling events were also selectively reduced, as RA abrogated IGF-I-stimulated AKT activation but did not alter erk1/2 activation. Tretinoin 62-64 AKT serine/threonine kinase 1 Homo sapiens 92-95
12776186-9 2003 This suggests that RA-mediated growth inhibition requires the selective downregulation of IRS-1 and AKT. Tretinoin 19-21 AKT serine/threonine kinase 1 Homo sapiens 100-103
12776186-10 2003 Therapeutic agents targeting the IRS-1/PI 3-kinase/AKT pathway may enhance the cytostatic effects of RA in breast cancer, since overexpression of IRS-1 and AKT have been reported in primary breast tumors. Tretinoin 101-103 AKT serine/threonine kinase 1 Homo sapiens 51-54
12776186-10 2003 Therapeutic agents targeting the IRS-1/PI 3-kinase/AKT pathway may enhance the cytostatic effects of RA in breast cancer, since overexpression of IRS-1 and AKT have been reported in primary breast tumors. Tretinoin 101-103 AKT serine/threonine kinase 1 Homo sapiens 156-159
12802179-0 2003 JNK pathway is required for retinoic acid-induced neurite outgrowth of human neuroblastoma, SH-SY5Y. Tretinoin 28-41 mitogen-activated protein kinase 8 Homo sapiens 0-3
12606540-6 2003 We treated chondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATRA), which promotes endochondral chondrocyte hypertrophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endochondral development. Tretinoin 95-108 interleukin 1 beta Mus musculus 57-66
12606540-6 2003 We treated chondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATRA), which promotes endochondral chondrocyte hypertrophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endochondral development. Tretinoin 110-114 interleukin 1 beta Mus musculus 57-66
12706826-0 2003 Retinoic acid specifically activates an oleate-dependent phospholipase D in the nuclei of LA-N-1 neuroblastoma cells. Tretinoin 0-13 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 57-72
12604597-0 2003 Activation of the Ras-ERK pathway inhibits retinoic acid-induced stimulation of tissue transglutaminase expression in NIH3T3 cells. Tretinoin 43-56 mitogen-activated protein kinase 1 Mus musculus 22-25
12604597-4 2003 Activation of the Ras-ERK pathway by EGF was sufficient to elicit this effect, since continuous Ras signaling mimicked the actions of EGF and inhibited RA-induced TGase expression, whereas blocking ERK activity in these same cells restored the ability of RA to up-regulate TGase expression. Tretinoin 152-154 mitogen-activated protein kinase 1 Mus musculus 22-25
12604597-4 2003 Activation of the Ras-ERK pathway by EGF was sufficient to elicit this effect, since continuous Ras signaling mimicked the actions of EGF and inhibited RA-induced TGase expression, whereas blocking ERK activity in these same cells restored the ability of RA to up-regulate TGase expression. Tretinoin 255-257 mitogen-activated protein kinase 1 Mus musculus 22-25
12604597-8 2003 These findings demonstrate that TGase may serve as a survival factor and RA-induced TGase expression requires the activation of PI3K but is antagonized by the Ras-ERK pathway. Tretinoin 73-75 mitogen-activated protein kinase 1 Mus musculus 163-166
12736759-9 2003 CONCLUSIONS: The ATRA-induced increase in cytotoxicity of ara-C was, in part, the result of an increase in the functional expression of nucleoside transporters, and a role for bcl-2 was also indicated. Tretinoin 17-21 BCL2 apoptosis regulator Homo sapiens 176-181
14613334-1 2003 Both retinoic acid (RA) and transforming growth factor (TGF)-beta1 are known to be influential in the development of insulin cells. Tretinoin 5-18 insulin Gallus gallus 117-124
14613334-1 2003 Both retinoic acid (RA) and transforming growth factor (TGF)-beta1 are known to be influential in the development of insulin cells. Tretinoin 20-22 insulin Gallus gallus 117-124
14613334-3 2003 The aim of this study was to define the action of RA in the presence of decreased levels of TGF-beta1, as are found in growth factor-reduced Matrigel (GFRM), on the proportion of insulin cells. Tretinoin 50-52 insulin Gallus gallus 179-186
14613334-5 2003 Retinoic acid (10(-6) M) was added to Ham"s F12 culture medium containing insulin (5 microg/ml), transferrin (5 microg/ml), and selenium (10(-10) M) (F12.ITS). Tretinoin 0-13 insulin Gallus gallus 74-81
14613334-8 2003 Medium containing RA or DMSO increased the proportion of insulin cells significantly compared with the proportion in the explants cultured in F12.ITS medium alone. Tretinoin 18-20 insulin Gallus gallus 57-64
12754300-7 2003 Low concentrations of RA (20 nM) increased proliferation of SCC lines by epidermal growth factor (EGF) activation of the mitogen-activated protein kinase ERK1. Tretinoin 22-24 mitogen-activated protein kinase 3 Homo sapiens 154-158
12754300-9 2003 In contrast, higher doses of RA (40 nM to 1 micro M) inhibited ERK1 expression, caused accumulation of G(1) phase cyclins and cdks, decreased Rb phosphorylation, and increased Rb/E2F-1 association. Tretinoin 29-31 mitogen-activated protein kinase 3 Homo sapiens 63-67
12754300-10 2003 Overexpression of ERK1 or dominant negative ERK1 was sufficient to reproduce the effects of low- and high-dose RA, respectively. Tretinoin 111-113 mitogen-activated protein kinase 3 Homo sapiens 18-22
12754300-10 2003 Overexpression of ERK1 or dominant negative ERK1 was sufficient to reproduce the effects of low- and high-dose RA, respectively. Tretinoin 111-113 mitogen-activated protein kinase 3 Homo sapiens 44-48
12754300-12 2003 We concluded that low-dose RA induced proliferation by increased EGF signaling while higher concentrations inhibited cell division by decreasing ERK1 activation. Tretinoin 27-29 mitogen-activated protein kinase 3 Homo sapiens 145-149
12759628-3 2003 The effects of ATRA can be potentiated by inhibition of cytochrome P-450, which is known to occur with certain drugs. Tretinoin 15-19 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 56-72
12841631-0 2003 Retinoic acid inhibits the growth of bone marrow mesenchymal stem cells and induces p27Kip1 and p16INK4A up-regulation. Tretinoin 0-13 cyclin dependent kinase inhibitor 2A Homo sapiens 96-104
12706826-2 2003 Now we demonstrate that retinoic acid, a cellular differentiation inducing agent, activates a nuclear oleate-dependent PLD in LA-N-1 cells. Tretinoin 24-37 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 119-122
12601690-4 2003 Undifferentiated HL-60 cells expressed Scar1 and WASP, and differentiation to neutrophils, induced by retinoic acid or non-retinoid agent treatments, led to a decrease in the level of expression of Scar1, whereas WASP expression was unaffected. Tretinoin 102-115 WASP family member 1 Homo sapiens 198-203
12515727-0 2003 A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657. Tretinoin 51-64 fms related receptor tyrosine kinase 3 Homo sapiens 20-24
12515727-11 2003 Our findings also indicate that APL patients with FLT3 mutations may benefit from combination therapy with all-trans retinoic acid plus an FLT3 inhibitor. Tretinoin 117-130 fms related receptor tyrosine kinase 3 Homo sapiens 50-54
12569559-8 2003 Retinoic acid-treated hepatoma cells induced IFN gamma production from cocultured NK cells and rendered themselves more susceptible to NK cells. Tretinoin 0-13 interferon gamma Homo sapiens 45-54
12711469-7 2003 We showed that all-trans retinoic acid is metabolised by CYP2S1, which has higher cutaneous expression than CYP26, previously described as the specific cutaneous P450 retinoic-acid-metabolising enzyme. Tretinoin 25-38 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 108-113
12711469-7 2003 We showed that all-trans retinoic acid is metabolised by CYP2S1, which has higher cutaneous expression than CYP26, previously described as the specific cutaneous P450 retinoic-acid-metabolising enzyme. Tretinoin 167-180 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 108-113
12658066-8 2003 Plasma bradykinin levels were increased and B(2) receptors were synergistically upregulated in CHF groups treated with combined ATRA and ACEI compared with those treated with ATRA or ACEI alone. Tretinoin 128-132 kininogen 1 Canis lupus familiaris 7-17
12666199-0 2003 Differential expression of decorin and biglycan genes during palatogenesis in normal and retinoic acid-treated mice. Tretinoin 89-102 biglycan Mus musculus 39-47
12666199-11 2003 On the other hand, biglycan in the retinoic acid-treated mice did not show remarkable change in its distribution patterns compared with that in the control mice. Tretinoin 35-48 biglycan Mus musculus 19-27
12658066-10 2003 Thus, endogenous bradykinin partially contributes to the synergistic improvement of cardiovascular function in CHF with additional treatment with ATRA to ACEI. Tretinoin 146-150 kininogen 1 Canis lupus familiaris 17-27
12522100-6 2003 Although Nif3l1 was mainly detected in the cytoplasm, the translocation of Nif3l1 into the nuclei was observed in retinoic acid-primed neural differentiation of P19 cells and enhanced by the enforced expression of Trip15/CSN2. Tretinoin 114-127 NGG1 interacting factor 3 like 1 Homo sapiens 75-81
12769347-10 2003 The results suggest that while in normal hematopoietic cells and in PML CD34 - cells induction of CD38 antigen expression by RA results in terminal differentiation along the myeloid lineage, in early myeloblastic leukemic CD34 + cells, induction of CD38 and differentiation are not functionally related. Tretinoin 125-127 CD34 molecule Homo sapiens 72-76
12769347-10 2003 The results suggest that while in normal hematopoietic cells and in PML CD34 - cells induction of CD38 antigen expression by RA results in terminal differentiation along the myeloid lineage, in early myeloblastic leukemic CD34 + cells, induction of CD38 and differentiation are not functionally related. Tretinoin 125-127 CD34 molecule Homo sapiens 222-226
12679911-12 2003 The activity of AFP gene promoter was significantly suppressed by addition of 1 x 10(-7)M retinoic acid (P<0.05, P=0.003, t=6.488). Tretinoin 90-103 alpha fetoprotein Homo sapiens 16-19
12531222-3 2003 All-trans retinoic acid (ATRA) down-regulates bcl-2 expression and heightens AML sensitivity to cytosine arabinoside (ara-C)-induced apoptosis in vitro. Tretinoin 0-23 BCL2 apoptosis regulator Homo sapiens 46-51
12531222-3 2003 All-trans retinoic acid (ATRA) down-regulates bcl-2 expression and heightens AML sensitivity to cytosine arabinoside (ara-C)-induced apoptosis in vitro. Tretinoin 25-29 BCL2 apoptosis regulator Homo sapiens 46-51
12640113-0 2003 Retinoic acid repression of bone morphogenetic protein 4 in inner ear development. Tretinoin 0-13 bone morphogenetic protein 4 Mus musculus 28-56
12640113-3 2003 We demonstrate that retinoic acid directly down-regulates BMP4 transcription in a mouse inner ear-derived cell line, and we identify a novel promoter in the second intron of the BMP4 gene that is a target of this regulation both in the cell line and in the mouse embryonic inner ear in vivo. Tretinoin 20-33 bone morphogenetic protein 4 Mus musculus 58-62
12640113-3 2003 We demonstrate that retinoic acid directly down-regulates BMP4 transcription in a mouse inner ear-derived cell line, and we identify a novel promoter in the second intron of the BMP4 gene that is a target of this regulation both in the cell line and in the mouse embryonic inner ear in vivo. Tretinoin 20-33 bone morphogenetic protein 4 Mus musculus 178-182
12646247-5 2003 Antisense suppression of CBP/p300 in HMECs resulted in decreased retinoic acid response element reporter trans-activation and decreased ATRA-mediated growth arrest. Tretinoin 65-78 CREB binding protein Homo sapiens 25-33
12646247-0 2003 CBP/p300 induction is required for retinoic acid sensitivity in human mammary cells. Tretinoin 35-48 CREB binding protein Homo sapiens 0-8
12646247-5 2003 Antisense suppression of CBP/p300 in HMECs resulted in decreased retinoic acid response element reporter trans-activation and decreased ATRA-mediated growth arrest. Tretinoin 136-140 CREB binding protein Homo sapiens 25-33
12646247-6 2003 Thus, in human mammary epithelial cells, CBP/p300 were both modulated by an ATRA signaling pathway and were required for a normal response to ATRA. Tretinoin 76-80 CREB binding protein Homo sapiens 41-49
12618289-0 2003 Retinoic acid downregulates the expression of ciliary neurotrophic factor in rat Schwann cells. Tretinoin 0-13 ciliary neurotrophic factor Rattus norvegicus 46-73
12618289-4 2003 Using quantitative reverse transcription-polymerase chain reaction, we have investigated the effect of RA on the expression of CNTF in these cells. Tretinoin 103-105 ciliary neurotrophic factor Rattus norvegicus 127-131
12516107-9 2003 Our results indicate that recombinant adenovirus-mediated p21(sdi1) gene transfer could be potentially useful for the local induction of RA sensitivity in human premalignant and malignant lesions lacking appropriate RARbeta expression. Tretinoin 137-139 cyclin dependent kinase inhibitor 1A Homo sapiens 58-61
12594055-6 2003 Likewise, retinoic acid inhibited caspase 3 activity in BEAS-2B cells and A549 cells induced by elastase, as well as proteolytic activity of elastase. Tretinoin 10-23 caspase 3 Homo sapiens 34-43
12594055-8 2003 These findings suggest that retinoic acid may inhibit elastase-induced lung epithelial cell injury partly through the inhibition of proteolytic activity of elastase and through the inhibition of caspase 3 activity by elastase. Tretinoin 28-41 caspase 3 Homo sapiens 195-204
12616482-3 2003 As evidenced by flow cytometry, ATRA (at 1 microM) clearly and donor-independently suppressed the expression of all integrin chains investigated (CD11a, CD11b, CD11c, and CD18), most strikingly of CD11a. Tretinoin 32-36 integrin subunit beta 2 Homo sapiens 171-175
12820386-5 2003 When compared with undifferentiated controls, ATRA induced Bcl-2 expression, while loss of Bax expression was observed only in cells differentiated by ATRA + BMP-6. Tretinoin 46-50 BCL2 apoptosis regulator Homo sapiens 59-64
12820386-6 2003 The high Bcl-2/Bax ratio in cells differentiated by ATRA and ATRA + BMP-6, respectively, correlated with the survival of these cells in serum-free media. Tretinoin 52-56 BCL2 apoptosis regulator Homo sapiens 9-14
12820386-6 2003 The high Bcl-2/Bax ratio in cells differentiated by ATRA and ATRA + BMP-6, respectively, correlated with the survival of these cells in serum-free media. Tretinoin 52-56 BCL2 associated X, apoptosis regulator Homo sapiens 15-18
12820386-6 2003 The high Bcl-2/Bax ratio in cells differentiated by ATRA and ATRA + BMP-6, respectively, correlated with the survival of these cells in serum-free media. Tretinoin 61-65 BCL2 apoptosis regulator Homo sapiens 9-14
12820386-6 2003 The high Bcl-2/Bax ratio in cells differentiated by ATRA and ATRA + BMP-6, respectively, correlated with the survival of these cells in serum-free media. Tretinoin 61-65 BCL2 associated X, apoptosis regulator Homo sapiens 15-18
12579317-0 2003 Differential effects of retinoic acid on the growth of isogenic metastatic and non-metastatic breast cancer cell lines and their association with distinct expression of retinoic acid receptor beta isoforms 2 and 4. Tretinoin 24-37 retinoic acid receptor beta Homo sapiens 169-196
12579317-1 2003 The human retinoic acid receptor beta (RARbeta) has three isoforms (beta1, beta2, and beta4), which play important, distinct roles in mediating the effects of retinoic acid on cell growth and apoptosis. Tretinoin 10-23 retinoic acid receptor beta Homo sapiens 39-46
12516107-9 2003 Our results indicate that recombinant adenovirus-mediated p21(sdi1) gene transfer could be potentially useful for the local induction of RA sensitivity in human premalignant and malignant lesions lacking appropriate RARbeta expression. Tretinoin 137-139 cyclin dependent kinase inhibitor 1A Homo sapiens 62-66
12579317-1 2003 The human retinoic acid receptor beta (RARbeta) has three isoforms (beta1, beta2, and beta4), which play important, distinct roles in mediating the effects of retinoic acid on cell growth and apoptosis. Tretinoin 10-23 adaptor related protein complex 4 subunit beta 1 Homo sapiens 86-91
12482873-4 2003 Cyclin D3 interacted with CRABPII in a ligand-independent manner and equally bound RAR alpha, but not RXR alpha, and only in the presence of RA. Tretinoin 27-29 cyclin D3 Homo sapiens 0-9
12579317-7 2003 ATRA treatment of NM-2C5 cells increased the protein levels of the histone acetyl transferases p300 and CBP, suppressed the level of histone deacetylase and increased the level of acetylated histone H4. Tretinoin 0-4 CREB binding protein Homo sapiens 104-107
12579317-10 2003 These results suggest that the effects of ATRA on the growth of the metastatic and non-metastatic breast cancer cell lines depend on the expression of RARbeta isoforms and that the expression of RARbeta4 may contribute to metastatic properties. Tretinoin 42-46 retinoic acid receptor beta Homo sapiens 151-158
12642900-10 2003 These results explained that retinoic acids differentially affected the action of MRFs according to their types and RXRalpha specially elevates the expression of muscle specific genes by stimulating the action of MRF4. Tretinoin 29-43 myogenic factor 6 Homo sapiens 213-217
12601020-9 2003 The cell-cycle-arrest stage correlated with the observed microarray results in which the RA treatment downregulated critical genes such as cyclins (cyclin E, cyclin D3) and cyclin-dependent kinases (CDK5, CDK10). Tretinoin 89-91 cyclin D3 Homo sapiens 158-167
12795836-6 2003 Curcumin, a JNK blocker, blocked the apoptosis and the growth inhibition induced by ATRA. Tretinoin 84-88 mitogen-activated protein kinase 8 Homo sapiens 12-15
12795836-8 2003 CONCLUSION: ATRA can induce the apoptosis in Y79 cells by phosphorylation of JNK, which suggests that ATRA may have clinical application prospects for treatment of retinoblastoma. Tretinoin 12-16 mitogen-activated protein kinase 8 Homo sapiens 77-80
12795836-8 2003 CONCLUSION: ATRA can induce the apoptosis in Y79 cells by phosphorylation of JNK, which suggests that ATRA may have clinical application prospects for treatment of retinoblastoma. Tretinoin 102-106 mitogen-activated protein kinase 8 Homo sapiens 77-80
12446691-10 2003 Interestingly, the cytosolic calcium chelator BAPTA-AM and K-201 protected RA-treated chondrocytes from undergoing apoptotic changes, as indicated by higher bcl-2 gene expression, reduced caspase-3 activity, and the percentage of TUNEL-positive cells. Tretinoin 75-77 BCL2 apoptosis regulator Homo sapiens 157-162
12401132-8 2003 Moreover, the tTG inducer retinoic acid was also able to cause increased expression and ubiquitination of tTG in H1355 cells. Tretinoin 26-39 transglutaminase 2 Homo sapiens 14-17
12401132-8 2003 Moreover, the tTG inducer retinoic acid was also able to cause increased expression and ubiquitination of tTG in H1355 cells. Tretinoin 26-39 transglutaminase 2 Homo sapiens 106-109
12584566-3 2003 In gel-shift assays, NuMA-RARalpha bound to retinoic acid response elements (RAREs) both as a homodimer and as a heterodimer with RXRalpha. Tretinoin 44-57 nuclear mitotic apparatus protein 1 Homo sapiens 21-25
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 nuclear mitotic apparatus protein 1 Homo sapiens 30-34
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 nuclear mitotic apparatus protein 1 Homo sapiens 110-114
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 translocation associated membrane protein 1 Homo sapiens 235-241
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 nuclear mitotic apparatus protein 1 Homo sapiens 30-34
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 nuclear mitotic apparatus protein 1 Homo sapiens 110-114
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 translocation associated membrane protein 1 Homo sapiens 235-241
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 254-258 nuclear mitotic apparatus protein 1 Homo sapiens 30-34
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 254-258 nuclear mitotic apparatus protein 1 Homo sapiens 110-114
12446691-10 2003 Interestingly, the cytosolic calcium chelator BAPTA-AM and K-201 protected RA-treated chondrocytes from undergoing apoptotic changes, as indicated by higher bcl-2 gene expression, reduced caspase-3 activity, and the percentage of TUNEL-positive cells. Tretinoin 75-77 caspase 3 Homo sapiens 188-197
12569142-12 2003 After adjustment for years of smoking, packs/day smoked, and metaplasia, treatment with 9-cis-RA, but not with 13-cis-RA + AT, led to a statistically significant increase in RAR-beta expression compared with placebo (P =.03). Tretinoin 88-96 retinoic acid receptor beta Homo sapiens 174-182
12569362-6 2003 A search for a bound DNA sequence revealed that MN1 has affinity for retinoic acid responsive elements. Tretinoin 69-82 MN1 proto-oncogene, transcriptional regulator Homo sapiens 48-51
12627849-6 2003 Cell surface expression of the chemotactic peptide receptors CD33 and CD10 but not of CD11b and CD11c was up-regulated by ATRA plus G-CSF far more profoundly than by ATRA alone. Tretinoin 122-126 CD33 molecule Homo sapiens 61-65
26680915-0 2003 Correlation between Retinoic Acid Sensitivity and IGFBP-3, AFP Protein Expression in Hepatoma Cell Lines. Tretinoin 20-33 alpha fetoprotein Homo sapiens 59-62
26680915-9 2003 We supposed that RA-induced cell growth inhibition may be related to the expressions of IGFBP-3 and AFP, but no exact correlation exists between the growth inhibition and receptor expression status in hepatoma cell lines. Tretinoin 17-19 alpha fetoprotein Homo sapiens 100-103
12604207-6 2003 Kinetic and genetic studies support the proposal that ADH4 may play two important physiological roles, i.e., as a major contributor to first-pass metabolism of ethanol in stomach as well as involvement in the synthesis of retinoic acid, a hormonal ligand controlling a nuclear receptor signaling pathway that regulates growth, development, and epithelial maintenance. Tretinoin 222-235 alcohol dehydrogenase 4 (class II), pi polypeptide Homo sapiens 54-58
12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 dynactin subunit 6 Homo sapiens 37-40
12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 dynactin subunit 6 Homo sapiens 92-95
12700651-10 2003 However, RA also decreases Skp2 levels thus impairing the ability of p27 to be ubiquitinated. Tretinoin 9-11 dynactin subunit 6 Homo sapiens 69-72
12700651-11 2003 Thus, RA induces both N-myc-dependent and -independent mechanisms to minimize the degradation of p27 and arrest NB cell growth. Tretinoin 6-8 dynactin subunit 6 Homo sapiens 97-100
12655154-7 2003 Moreover, levels of SGP-2 and/or TF were significantly elevated in the cells treatment with sodium butyrate and retinoic acid, inducers of cellular differentiation. Tretinoin 112-125 transferrin Rattus norvegicus 33-35
12627849-6 2003 Cell surface expression of the chemotactic peptide receptors CD33 and CD10 but not of CD11b and CD11c was up-regulated by ATRA plus G-CSF far more profoundly than by ATRA alone. Tretinoin 122-126 membrane metalloendopeptidase Homo sapiens 70-74
12494454-9 2003 The ability of RA to induce RARbeta and PKCalpha expression was retained in A-fos clones, suggesting that A-fos was not interfering with RAR transcription activation functions. Tretinoin 15-17 protein kinase C, alpha Mus musculus 40-48
12687724-1 2003 Retinoic acid (RA) is produced via two sequential reactions of retinol dehydrogenases (RDHs) and retinal dehydrogenases (RALDHs). Tretinoin 0-13 retinol dehydrogenase 19 Mus musculus 63-85
12494454-10 2003 We tested whether the RA-induced AP-1 activity might be mediated by the ERK1/2 MAPK pathway. Tretinoin 22-24 mitogen-activated protein kinase 1 Mus musculus 79-83
12592339-4 2003 We observed that induction of granulocytic differentiation by retinoic acid led to robust activation of the executioner protease caspase-3, and early onset of apoptosis. Tretinoin 62-75 caspase 3 Homo sapiens 129-138
12615366-5 2003 This suppression is similar to our previous report showing TR4 orphan nuclear receptor (TR4) can suppress RA-induced transactivation. Tretinoin 106-108 nuclear receptor subfamily 2 group C member 2 Homo sapiens 59-62
12615366-5 2003 This suppression is similar to our previous report showing TR4 orphan nuclear receptor (TR4) can suppress RA-induced transactivation. Tretinoin 106-108 nuclear receptor subfamily 2 group C member 2 Homo sapiens 88-91
12687724-1 2003 Retinoic acid (RA) is produced via two sequential reactions of retinol dehydrogenases (RDHs) and retinal dehydrogenases (RALDHs). Tretinoin 0-13 retinol dehydrogenase 19 Mus musculus 87-91
12414803-0 2003 Rosiglitazone and retinoic acid induce uncoupling protein-1 (UCP-1) in a p38 mitogen-activated protein kinase-dependent manner in fetal primary brown adipocytes. Tretinoin 18-31 uncoupling protein 1 Rattus norvegicus 39-66
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 26-39 retinoic acid receptor beta Homo sapiens 96-103
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 41-43 retinoic acid receptor beta Homo sapiens 96-103
12401808-0 2003 Tissue transglutaminase mediates activation of RhoA and MAP kinase pathways during retinoic acid-induced neuronal differentiation of SH-SY5Y cells. Tretinoin 83-96 transglutaminase 2 Homo sapiens 0-23
12401808-0 2003 Tissue transglutaminase mediates activation of RhoA and MAP kinase pathways during retinoic acid-induced neuronal differentiation of SH-SY5Y cells. Tretinoin 83-96 ras homolog family member A Homo sapiens 47-51
12401808-3 2003 Here we report that RA-induced neuronal differentiation of SH-SY5Y cells is coupled with increased expression/activation of TGase and in vivo transamidation and activation of RhoA. Tretinoin 20-22 ras homolog family member A Homo sapiens 175-179
12401808-4 2003 In addition, RA promotes formation of stress fibers and focal adhesion complexes, and activation of ERK1/2, JNK1, and p38alpha/beta/gamma MAP kinases. Tretinoin 13-15 mitogen-activated protein kinase 3 Homo sapiens 100-106
12401808-4 2003 In addition, RA promotes formation of stress fibers and focal adhesion complexes, and activation of ERK1/2, JNK1, and p38alpha/beta/gamma MAP kinases. Tretinoin 13-15 mitogen-activated protein kinase 8 Homo sapiens 108-112
12401808-4 2003 In addition, RA promotes formation of stress fibers and focal adhesion complexes, and activation of ERK1/2, JNK1, and p38alpha/beta/gamma MAP kinases. Tretinoin 13-15 mitogen-activated protein kinase 14 Homo sapiens 118-126
12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 57-80 transforming growth factor beta 1 Homo sapiens 43-52
12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 57-80 transforming growth factor beta 1 Homo sapiens 278-287
12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 82-86 transforming growth factor beta 1 Homo sapiens 43-52
12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 82-86 transforming growth factor beta 1 Homo sapiens 278-287
12393416-6 2003 Addition of the inhibitor-of-protein serine/threonine phosphatases, okadaic acid, blocks the ATRA-mediated reduction in TGF-beta-induced phospho-Smad2 and shifts the differentiation toward monocytic end points. Tretinoin 93-97 transforming growth factor beta 1 Homo sapiens 120-128
12401808-8 2003 The results of our studies suggest a novel mechanism of RA signaling, which involves activation of TGase and transamidation of RhoA. Tretinoin 56-58 ras homolog family member A Homo sapiens 127-131
12842099-0 2003 Stimulation of lipocalin-type prostaglandin D synthase by retinoic acid coincides with inhibition of cell proliferation in human 3AO ovarian cancer cells. Tretinoin 58-71 prostaglandin D2 synthase Homo sapiens 15-54
14515147-1 2003 In the retinoic acid-differentiated neuroblastoma SH-SY5Y cells, IL-1 induced binding activity of NFkappaB and up-regulated the expression and activity of MnSOD. Tretinoin 7-20 nuclear factor kappa B subunit 1 Homo sapiens 98-106
12485937-0 2003 GA-binding protein (GABP) and Sp1 are required, along with retinoid receptors, to mediate retinoic acid responsiveness of CD18 (beta 2 leukocyte integrin): a novel mechanism of transcriptional regulation in myeloid cells. Tretinoin 90-103 integrin subunit beta 2 Homo sapiens 122-126
12485937-1 2003 CD18 (beta(2) leukocyte integrin) is transcriptionally regulated in myeloid cells, but the mechanisms that increase its expression in response to retinoic acid (RA) have not been defined. Tretinoin 146-159 integrin subunit beta 2 Homo sapiens 0-4
12485937-1 2003 CD18 (beta(2) leukocyte integrin) is transcriptionally regulated in myeloid cells, but the mechanisms that increase its expression in response to retinoic acid (RA) have not been defined. Tretinoin 161-163 integrin subunit beta 2 Homo sapiens 0-4
12485937-2 2003 The CD18 promoter was activated by RA treatment in stably transfected U937 myeloid cells. Tretinoin 35-37 integrin subunit beta 2 Homo sapiens 4-8
12485937-3 2003 We identified a retinoic acid response element (RARE) that lies nearly 900 nucleotides upstream of the CD18 transcriptional start site that was bound by the RA receptors, retinoic acid receptor (RAR) and retinoic X receptor (RXR). Tretinoin 16-29 integrin subunit beta 2 Homo sapiens 103-107
12485937-3 2003 We identified a retinoic acid response element (RARE) that lies nearly 900 nucleotides upstream of the CD18 transcriptional start site that was bound by the RA receptors, retinoic acid receptor (RAR) and retinoic X receptor (RXR). Tretinoin 16-29 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 213-223
12485937-4 2003 This RARE accounted for one half of the RA responsiveness of CD18. Tretinoin 5-7 integrin subunit beta 2 Homo sapiens 61-65
12485937-5 2003 However, unexpectedly, one half of the dynamic response to RA was mediated by the 96-nucleotide CD18 minimal promoter, which lacks a recognizable RARE. Tretinoin 59-61 integrin subunit beta 2 Homo sapiens 96-100
12485937-6 2003 Binding sites for the ets transcription factor, GA-binding protein (GABP), and Sp1 were required for full RA responsiveness of both the CD18 minimal promoter and the full-length promoter. Tretinoin 106-108 integrin subunit beta 2 Homo sapiens 136-140
12680251-0 2003 All-trans-retinoic acid activates caspase-1 in a dose-dependent manner in cervical squamous carcinoma cells. Tretinoin 0-23 caspase 1 Homo sapiens 34-43
12680251-2 2003 Suppression of growth required sustained activation of interferon regulatory factor 1 (IRF-1), which was achieved by high-dose (10(-4) M), but not low-dose (10(-6) M), ATRA treatment. Tretinoin 168-172 interferon regulatory factor 1 Homo sapiens 55-85
12680251-2 2003 Suppression of growth required sustained activation of interferon regulatory factor 1 (IRF-1), which was achieved by high-dose (10(-4) M), but not low-dose (10(-6) M), ATRA treatment. Tretinoin 168-172 interferon regulatory factor 1 Homo sapiens 87-92
12680251-3 2003 In this paper we examine the role of IRF-1 in cell death that accompanied the growth suppression in high-dose ATRA-treated cells. Tretinoin 110-114 interferon regulatory factor 1 Homo sapiens 37-42
12680251-4 2003 We found that high-dose, but not low-dose, ATRA treatment activated caspase-1 in those cervical carcinoma cells. Tretinoin 43-47 caspase 1 Homo sapiens 68-77
12680251-5 2003 Transient transfection of an antisense-IRF-1 construct diminished high-dose ATRA-mediated caspase-1 activation. Tretinoin 76-80 interferon regulatory factor 1 Homo sapiens 39-44
12680251-5 2003 Transient transfection of an antisense-IRF-1 construct diminished high-dose ATRA-mediated caspase-1 activation. Tretinoin 76-80 caspase 1 Homo sapiens 90-99
12680251-7 2003 These results suggested the importance of both IRF-1 and STAT1 in high-dose ATRA-induced activation of caspase-1. Tretinoin 76-80 interferon regulatory factor 1 Homo sapiens 47-52
12680251-7 2003 These results suggested the importance of both IRF-1 and STAT1 in high-dose ATRA-induced activation of caspase-1. Tretinoin 76-80 caspase 1 Homo sapiens 103-112
12680256-4 2003 We found that, as with the induction of IRF-1, levels of p21WAF1 were similarly dose-dependently induced by ATRA. Tretinoin 108-112 interferon regulatory factor 1 Homo sapiens 40-45
12680256-6 2003 We concluded that activation of STAT1 and IRF-1 is crucial for the growth inhibitory action of ATRA, which is associated with the activation of p21WAF1. Tretinoin 95-99 interferon regulatory factor 1 Homo sapiens 42-47
12842099-4 2003 To determine whether there is a relationship between retinoid and LPGDS in ovarian tumors, we examined the regulation of the gene encoding LPGDS by all-trans retinoic acid (RA). Tretinoin 158-171 prostaglandin D2 synthase Homo sapiens 139-144
12842099-4 2003 To determine whether there is a relationship between retinoid and LPGDS in ovarian tumors, we examined the regulation of the gene encoding LPGDS by all-trans retinoic acid (RA). Tretinoin 173-175 prostaglandin D2 synthase Homo sapiens 139-144
12842099-5 2003 Real-time quantitative RT-PCR analysis showed that RA strongly induced the accumulation of LPGDS mRNA in human 3AO ovarian cancer cells. Tretinoin 51-53 prostaglandin D2 synthase Homo sapiens 91-96
12842099-6 2003 Furthermore, treatment of the cells with RA induced the synthesis and secretion of LPGDS into the culture medium. Tretinoin 41-43 prostaglandin D2 synthase Homo sapiens 83-88
14756522-9 2003 In contrast, the remarkably elevated MMP-13 mRNA expression in the keloid group was significantly suppressed, with the peak suppression at 12 h after addition of tretinoin, while MMP-13 mRNA expression in the control group was not significantly changed. Tretinoin 162-171 matrix metallopeptidase 13 Homo sapiens 37-43
12507292-1 2003 Midkine (MK) is a heparin-binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 127-140 midkine Homo sapiens 0-7
12507292-1 2003 Midkine (MK) is a heparin-binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 127-140 midkine Homo sapiens 9-11
14502257-0 2003 Downregulation of Bcl-xL and activation of caspases during retinoic acid-induced apoptosis in an adult T-cell leukemia cell line. Tretinoin 59-72 BCL2 like 1 Homo sapiens 18-24
14502257-0 2003 Downregulation of Bcl-xL and activation of caspases during retinoic acid-induced apoptosis in an adult T-cell leukemia cell line. Tretinoin 59-72 caspase 1 Homo sapiens 43-51
14502257-13 2003 CONCLUSION: These results suggest that the RA-induced apoptotic signals were transduced via downregulation of Bcl-xL and the decrease in the mitochondrial membrane function leading to caspase-3 activation. Tretinoin 43-45 BCL2 like 1 Homo sapiens 110-116
14502257-13 2003 CONCLUSION: These results suggest that the RA-induced apoptotic signals were transduced via downregulation of Bcl-xL and the decrease in the mitochondrial membrane function leading to caspase-3 activation. Tretinoin 43-45 caspase 3 Homo sapiens 184-193
12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 233-246 transforming growth factor beta 1 Homo sapiens 87-94
12514310-13 2003 These data suggest that PKCalpha either works through a nonenzymatic protein-protein mechanism or may interfere with the enzymatic function of another isozyme of PKC to mediate the actions of RA in B16 melanoma cells. Tretinoin 192-194 protein kinase C, alpha Mus musculus 24-32
12514310-13 2003 These data suggest that PKCalpha either works through a nonenzymatic protein-protein mechanism or may interfere with the enzymatic function of another isozyme of PKC to mediate the actions of RA in B16 melanoma cells. Tretinoin 192-194 protein kinase C, alpha Mus musculus 24-27
12927207-0 2003 Induction of tyrosine kinase receptor b by retinoic acid allows brain-derived neurotrophic factor-induced amyloid precursor protein gene expression in human SH-SY5Y neuroblastoma cells. Tretinoin 43-56 amyloid beta precursor protein Homo sapiens 106-131
12927207-3 2003 In these cells, RA regulates the expression of the beta-amyloid precursor protein. Tretinoin 16-18 amyloid beta precursor protein Homo sapiens 51-81
14529416-2 2003 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RAR alpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 57-70 retinoic acid receptor beta Homo sapiens 179-186
12556562-0 2003 The phosphoinositide 3-kinase/AKT1 pathway involvement in drug and all-trans-retinoic acid resistance of leukemia cells. Tretinoin 71-90 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 4-29
12556562-0 2003 The phosphoinositide 3-kinase/AKT1 pathway involvement in drug and all-trans-retinoic acid resistance of leukemia cells. Tretinoin 71-90 AKT serine/threonine kinase 1 Homo sapiens 30-34
12556562-6 2003 Resistant cells overexpressing either dominant negative PI3K or dominant negative AKT1 became sensitive to drugs and ATRA. Tretinoin 117-121 AKT serine/threonine kinase 1 Homo sapiens 82-86
12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 248-250 transforming growth factor beta 1 Homo sapiens 87-94
12468040-4 2002 Cell differentiation due to TGF-beta1 treatment is accompanied by an increase in tyrosine hydroxylase (TH) expression, more pronounced in the presence of TPA or RA and counteracted by BMP-2. Tretinoin 161-163 transforming growth factor beta 1 Homo sapiens 28-37
12468040-4 2002 Cell differentiation due to TGF-beta1 treatment is accompanied by an increase in tyrosine hydroxylase (TH) expression, more pronounced in the presence of TPA or RA and counteracted by BMP-2. Tretinoin 161-163 tyrosine hydroxylase Homo sapiens 81-101
12427543-2 2002 Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of retinal to retinoic acid (RA), a metabolite of vitamin A important for embryogenesis and tissue differentiation. Tretinoin 76-89 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 0-28
12427543-2 2002 Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of retinal to retinoic acid (RA), a metabolite of vitamin A important for embryogenesis and tissue differentiation. Tretinoin 76-89 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 30-36
12393181-3 2002 In Tera-2 embryonal carcinoma cells, PDGFRA expression is strongly enhanced upon differentiation induced by retinoic acid and cAMP treatment. Tretinoin 108-121 platelet derived growth factor receptor alpha Homo sapiens 37-43
12427543-2 2002 Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of retinal to retinoic acid (RA), a metabolite of vitamin A important for embryogenesis and tissue differentiation. Tretinoin 30-32 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 0-28
12492429-10 2002 These data suggest that SK-N-SH cells differentiated by brief treatment with RA may represent an unlimited source of neuron-like cells suitable for studying molecular events associated with activation of human NR1/NR2B receptors. Tretinoin 77-79 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 210-213
12526099-3 2002 Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Tretinoin 47-70 tumor necrosis factor Homo sapiens 24-27
12468615-5 2002 Without exogenous cytokines, atRA addition significantly inhibited the interferon (IFN)-gamma response but did not alter the interleukin (IL)-4 response. Tretinoin 29-33 interferon gamma Mus musculus 71-93
12468615-6 2002 With Th1 polarizing cytokines, atRA enhanced the IFN-gamma response, with no effect on the IL-4 response. Tretinoin 31-35 interferon gamma Mus musculus 49-58
12429992-6 2002 WNT3A, WNT8A, WNT8B, WNT10B and WNT11 are down-regulated in NT2 cells after ATRA treatment, while WNT2, WNT7B and WNT14B are up-regulated. Tretinoin 76-80 Wnt family member 10B Homo sapiens 21-27
12429992-6 2002 WNT3A, WNT8A, WNT8B, WNT10B and WNT11 are down-regulated in NT2 cells after ATRA treatment, while WNT2, WNT7B and WNT14B are up-regulated. Tretinoin 76-80 Wnt family member 11 Homo sapiens 32-37
12429992-6 2002 WNT3A, WNT8A, WNT8B, WNT10B and WNT11 are down-regulated in NT2 cells after ATRA treatment, while WNT2, WNT7B and WNT14B are up-regulated. Tretinoin 76-80 Wnt family member 9B Homo sapiens 114-120
12775111-7 2002 When VA-deficient rats received a single injection of retinoic acid (2 mg/rat), tissue IGF-I and IGF-IR gene expression did not change after 4 or 8 h, while the expression of IGF-II, IGFBP-4, and IGFBP-6 mRNAs in some tissues increased rapidly. Tretinoin 54-67 insulin-like growth factor binding protein 6 Rattus norvegicus 196-203
12526099-0 2002 Retinoic acid inhibits inducible nitric oxide synthase expression in 3T3-L1 adipocytes. Tretinoin 0-13 nitric oxide synthase 2 Homo sapiens 23-54
12526099-3 2002 Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Tretinoin 47-70 nitric oxide synthase 2 Homo sapiens 137-141
12526099-3 2002 Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Tretinoin 72-74 tumor necrosis factor Homo sapiens 24-27
12526099-3 2002 Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Tretinoin 72-74 nitric oxide synthase 2 Homo sapiens 137-141
12526099-5 2002 The inhibitory effect of RA on TNF-induced iNOS induction was reversible, completely recovered after 2 days, and was exerted through the inhibition of NF-kappaB activation. Tretinoin 25-27 tumor necrosis factor Homo sapiens 31-34
12526099-5 2002 The inhibitory effect of RA on TNF-induced iNOS induction was reversible, completely recovered after 2 days, and was exerted through the inhibition of NF-kappaB activation. Tretinoin 25-27 nitric oxide synthase 2 Homo sapiens 43-47
12526099-7 2002 RA could not reverse the TNF- induced LPL suppression at RA levels causing near complete inhibition of the TNF-induced NO production. Tretinoin 0-2 tumor necrosis factor Homo sapiens 107-110
12421932-0 2002 Retinoic acid stimulates the cell cycle machinery in normal T cells: involvement of retinoic acid receptor-mediated IL-2 secretion. Tretinoin 0-13 interleukin 2 Homo sapiens 116-120
12393712-9 2002 In addition, a specific JNK inhibitor blocks the enhancing effect of ST1346 on ATRA-induced maturation of NB4 cells. Tretinoin 79-83 mitogen-activated protein kinase 8 Homo sapiens 24-27
12421932-5 2002 The presence of atRA led to elevated levels of cyclin D3, -E, and -A, decreased levels of p27(Kip1), increased activity of cyclin-dependent kinase 2, and enhanced phosphorylation of the retinoblastoma protein (pRB). Tretinoin 16-20 cyclin D3 Homo sapiens 47-56
12421932-10 2002 A retinoic acid receptor (RAR)-selective agonist and 9-cis-RA had the same potency as atRA on T cell proliferation and IL-2 secretion, whereas a retinoid X receptor-selective agonist had only marginal effects. Tretinoin 86-90 interleukin 2 Homo sapiens 119-123
12421932-12 2002 Taken together, these results suggest that atRA stimulates the cell cycle machinery and proliferation of normal human T cells by increasing IL-2 secretion through mechanisms involving RARs. Tretinoin 43-47 interleukin 2 Homo sapiens 140-144
12457868-0 2002 Down-regulation of androgen receptor expression and inhibition of lacrimal gland cell proliferation by retinoic acid. Tretinoin 103-116 androgen receptor Oryctolagus cuniculus 19-36
12381680-6 2002 In [35S]-GTPgammaS exchange assays, membranes from cells cultured with retinoic acid (4-6 days) were the most responsive to activation by MIP-1alpha and MPIF-1. Tretinoin 71-84 C-C motif chemokine ligand 23 Homo sapiens 153-159
12404122-3 2002 We report here that B-myb expression does not decrease, cyclin A and Sp1 levels remain constant while p21 levels increase continuously upon retinoic acid-induced differentiation of the LAN-5 neuroblastoma cell line. Tretinoin 140-153 cyclin dependent kinase inhibitor 1A Homo sapiens 102-105
12404122-5 2002 Luciferase assays of promoter activity indicate that B-myb-dependent transactivation is enhanced in LAN-5 cells treated with retinoic acid (RA) for 24 h. The enhancement is independent from cyclin A but is suppressed by a degradation-resistant mutant form of cyclin D1. Tretinoin 125-138 cyclin A2 Homo sapiens 190-198
12404122-5 2002 Luciferase assays of promoter activity indicate that B-myb-dependent transactivation is enhanced in LAN-5 cells treated with retinoic acid (RA) for 24 h. The enhancement is independent from cyclin A but is suppressed by a degradation-resistant mutant form of cyclin D1. Tretinoin 140-142 cyclin A2 Homo sapiens 190-198
12409228-6 2002 VIP-induced differentiation effects were potentiated by retinoic acid. Tretinoin 56-69 vasoactive intestinal peptide Homo sapiens 0-3
12457868-4 2002 Exposure of primary lacrimal acinar cells in culture to 10(-10)-10(-6)M all-trans retinoic acid for 4-24hr causes an approximately 50% decrease in AR mRNA expression. Tretinoin 72-95 androgen receptor Oryctolagus cuniculus 147-149
12457868-6 2002 Exposure of the primary cells to 10(-6)M retinoic acid for 24hr caused a 40% decrease in AR protein levels as determined by measurement of binding of(3) [H]-dihydrotestosterone (DHT) to cells in culture and Scatchard analysis. Tretinoin 41-54 androgen receptor Oryctolagus cuniculus 89-91
12353227-9 2002 In the HeLa cells, both 4HPR and ATRA caused a 2- to 4-fold stimulation of the promoter activity of gadd153, but similar to the CNE3 cells, ATRA was incapable of upregulating the protein level of gadd153. Tretinoin 33-37 DNA damage inducible transcript 3 Homo sapiens 100-107
12392597-0 2002 A phosphorylation defective retinoic acid receptor mutant mimics the effects of retinoic acid on EGFR mediated AP-1 expression and cancer cell proliferation. Tretinoin 28-41 epidermal growth factor receptor Homo sapiens 97-101
12385002-0 2002 Retinoic acid induces expression of the interleukin-1beta gene in cultured normal human mammary epithelial cells and in human breast carcinoma lines. Tretinoin 0-13 interleukin 1 beta Homo sapiens 40-57
12445205-5 2002 By contrast, the expression of the caspases 3 and 8, which are both activated during conventional apoptosis, was increased and unchanged, respectively, after retinoic acid treatment. Tretinoin 158-171 caspase 3 Homo sapiens 35-51
12445205-6 2002 In addition to inhibition of differentiation in skin equivalents, retinoic acid treatment led to keratinocyte apoptosis and activation of caspase-3, both of which were undetectable in differentiated control skin equivalents. Tretinoin 66-79 caspase 3 Homo sapiens 138-147
12537770-1 2002 In vitro, cells derived from Ewing sarcoma (ES) with the characteristic somatic rearrangement between the genes EWS and FLII can be induced to differentiate toward a neuronal phenotype by exposure to agents such as dibutyryl cyclic AMP (db cAMP) or retinoic acid. Tretinoin 249-262 FLII actin remodeling protein Homo sapiens 120-124
12397630-7 2002 In addition to the two PBX1 isoforms, the mRNA level of the other two subtypes (PBX2 and PBX3) and the level of PBX1/2/3 protein were also found to be elevated in limb buds after RA treatment. Tretinoin 179-181 pre B cell leukemia homeobox 3 Mus musculus 89-93
12171913-6 2002 Collectively, enhanced binding of Sp1 to promoter I of the KOR gene as a result of inhibiting the ERK pathway contributes to RA induction of this gene in P19. Tretinoin 125-127 mitogen-activated protein kinase 1 Mus musculus 98-101
12379805-6 2002 Retinoic acid inhibited adipose conversion and cooperated with BMP-2 to enhance proliferation, inhibit adipogenesis, and promote early osteoblastic differentiation. Tretinoin 0-13 bone morphogenetic protein 2 Mus musculus 63-68
12186877-7 2002 The antiapoptotic effect of t-RA on H(2)O(2)-induced apoptosis in several cell types was correlated with the inducibility of MKP-1 by t-RA. Tretinoin 28-32 dual specificity phosphatase 1 Homo sapiens 125-130
12186877-7 2002 The antiapoptotic effect of t-RA on H(2)O(2)-induced apoptosis in several cell types was correlated with the inducibility of MKP-1 by t-RA. Tretinoin 134-138 dual specificity phosphatase 1 Homo sapiens 125-130
12186877-8 2002 Inhibition of MKP-1 by vanadate enhanced JNK phosphorylation and attenuated the antiapoptotic effect of t-RA. Tretinoin 104-108 dual specificity phosphatase 1 Homo sapiens 14-19
12401501-2 2002 The aim of this study was to investigate the effect of TGF-beta2 gene deletion on susceptibility to RA-induced teratogenesis in a mouse model. Tretinoin 100-102 transforming growth factor, beta 2 Mus musculus 55-64
12401501-4 2002 The incidence of RA-induced cleft palate (CP) was 48% in wild-type embryos from wild-type dams, increasing to 71% in TGF-beta2 heterozygous littermates. Tretinoin 17-19 transforming growth factor, beta 2 Mus musculus 117-126
12401501-5 2002 Wild-type and TGF-beta2 heterozygous embryos from heterozygous dams exhibited a CP incidence of 74 and 77% respectively, following treatment with RA. Tretinoin 146-148 transforming growth factor, beta 2 Mus musculus 14-23
12401501-7 2002 We conclude that the genotype of the dam and embryo with respect to TGF-beta2 affects the incidence of RA-induced teratogenesis. Tretinoin 103-105 transforming growth factor, beta 2 Mus musculus 68-77
12392597-5 2002 RESULTS: We have determined that RA inhibits cyclin H and cdk7 expression thereby decreasing levels of phosphorylated RARalpha in human cancer cell lines. Tretinoin 33-35 cyclin dependent kinase 7 Homo sapiens 58-62
12237846-0 2002 p16(ink4a) and retinoic acid modulate rhoA and GFAP expression during induction of a stellate phenotype in U343 MG-A astrocytoma cells. Tretinoin 15-28 ras homolog family member A Homo sapiens 38-42
12239173-7 2002 Cotreatment with ATRA and TSA restored RARbeta gene expression in NB4-MRA1 cells, whose PML/RARalpha mutation is in helix 12 of the LBD, but not in an APL cell line harboring the patient-derived PML/RARalpha mutation, which was between helix 5 and 6. Tretinoin 17-21 retinoic acid receptor beta Homo sapiens 39-46
12239173-8 2002 Furthermore, ATRA combined with TSA increases histone 4 acetylation on the RARbeta promoter only in NB4-MRA1 cells. Tretinoin 13-17 retinoic acid receptor beta Homo sapiens 75-82
12376465-0 2002 Dual roles of Nur77 in selective regulation of apoptosis and cell cycle by TPA and ATRA in gastric cancer cells. Tretinoin 83-87 nuclear receptor subfamily 4 group A member 1 Homo sapiens 14-19
12376465-7 2002 Although all-trans retinoic acid (ATRA) could not induce apoptosis in BGC-823 cells due to failure of stimulating Nur77 translocation, expression of Nur77 in the nucleus was required for cell growth inhibition by ATRA. Tretinoin 213-217 nuclear receptor subfamily 4 group A member 1 Homo sapiens 149-154
12376465-10 2002 Taken together, the data revealed the dual functioning mechanisms of Nur77 in gastric cancer cells in response to TPA and ATRA. Tretinoin 122-126 nuclear receptor subfamily 4 group A member 1 Homo sapiens 69-74
12356739-0 2002 Mammalian Rcd1 is a novel transcriptional cofactor that mediates retinoic acid-induced cell differentiation. Tretinoin 65-78 RCD1 Homo sapiens 10-14
12356739-2 2002 Here we show that mammalian Rcd1 is a novel transcriptional cofactor and is critically involved in the commitment step in the retinoic acid-induced differentiation of F9 mouse teratocarcinoma cells, at least in part, via forming complexes with retinoic acid receptor and activation transcription factor-2 (ATF-2). Tretinoin 126-139 RCD1 Homo sapiens 28-32
12356739-2 2002 Here we show that mammalian Rcd1 is a novel transcriptional cofactor and is critically involved in the commitment step in the retinoic acid-induced differentiation of F9 mouse teratocarcinoma cells, at least in part, via forming complexes with retinoic acid receptor and activation transcription factor-2 (ATF-2). Tretinoin 126-139 activating transcription factor 2 Mus musculus 271-304
12356739-2 2002 Here we show that mammalian Rcd1 is a novel transcriptional cofactor and is critically involved in the commitment step in the retinoic acid-induced differentiation of F9 mouse teratocarcinoma cells, at least in part, via forming complexes with retinoic acid receptor and activation transcription factor-2 (ATF-2). Tretinoin 126-139 activating transcription factor 2 Mus musculus 306-311
12431242-2 2002 ATRA induced apoptosis in all the B-CLL samples tested, and this was accompanied by a specific reduction in Bcl-2 and Mcl-1 protein expression in the apoptotic cells. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 108-113
12431242-4 2002 Caspase-3 activation was shown to be a prerequisite for ATRA-induced apoptosis, which was inhibited by the pan-caspase inhibitor Z-VAD-FMK and the caspase-9 inhibitor Z-LEHD-FMK. Tretinoin 56-60 caspase 3 Homo sapiens 0-9
12392082-9 2002 Treatment with the histone deacetvlase inhibitor trichostatin A (TSA) increased both basal and RA-induced betaRARE activity in DLD-1, indicating that histone deacetylase is involved in the regulation of RARbeta gene expression. Tretinoin 95-97 retinoic acid receptor beta Homo sapiens 203-210
12237846-1 2002 We previously showed that the expression of p16(ink4a) (p16), in conjunction with retinoic acid (RA) treatment in the p16-deficient astrocytoma cell line, U343 MG-A, induced a potent cell cycle arrest in G(1) associated with changes in morphology. Tretinoin 82-95 cyclin dependent kinase inhibitor 2A Homo sapiens 44-47
12237846-1 2002 We previously showed that the expression of p16(ink4a) (p16), in conjunction with retinoic acid (RA) treatment in the p16-deficient astrocytoma cell line, U343 MG-A, induced a potent cell cycle arrest in G(1) associated with changes in morphology. Tretinoin 97-99 cyclin dependent kinase inhibitor 2A Homo sapiens 44-53
12237846-1 2002 We previously showed that the expression of p16(ink4a) (p16), in conjunction with retinoic acid (RA) treatment in the p16-deficient astrocytoma cell line, U343 MG-A, induced a potent cell cycle arrest in G(1) associated with changes in morphology. Tretinoin 97-99 cyclin dependent kinase inhibitor 2A Homo sapiens 44-47
12237846-5 2002 p16 induction in combination with RA treatment resulted in a decreased expression and activation of rhoA as determined by immunocytochemistry and Western blot analysis of soluble and insoluble fractions of cell lysates. Tretinoin 34-36 ras homolog family member A Homo sapiens 100-104
12237846-7 2002 Introduction of a dominant active rhoA mutant into p16-induced, RA-treated U343 MG-A astrocytoma cells was associated with the loss of long astrocytic processes and stellate morphology. Tretinoin 64-66 ras homolog family member A Homo sapiens 34-38
12237846-7 2002 Introduction of a dominant active rhoA mutant into p16-induced, RA-treated U343 MG-A astrocytoma cells was associated with the loss of long astrocytic processes and stellate morphology. Tretinoin 64-66 cyclin dependent kinase inhibitor 2A Homo sapiens 51-54
12383199-2 2002 While RA (10(-8) m) alone did not alter STAT-1 activation or expression in THP-1 cells, RA enhanced or prolonged STAT-1 activation (tyrosine 701 phosphorylation) and gene expression (mRNA and protein) induced by either IFN-beta or IFN-gamma. Tretinoin 88-90 interferon gamma Homo sapiens 231-240
12383199-4 2002 These results imply that RA can significantly rebalance STAT-1-dependent responses, and that one of the mechanisms may be through the inhibition of the NFkappaB pathway. Tretinoin 25-27 nuclear factor kappa B subunit 1 Homo sapiens 152-160
12242694-7 2002 Inhibition of RAR function in HMECs by DNRAR suppressed expression of CBP/p300 and expression of RARbeta2 in MCF-7 cells promoted induction of CBP/p300 when cells were treated with 1.0 microM all-trans-retinoic acid (ATRA). Tretinoin 192-215 CREB binding protein Homo sapiens 70-78
12364474-9 2002 However, in vitro treatments with retinoic acid and TGF beta restored the ability of progesterone to suppress MMPs in vitro and prevented the establishment of experimental disease. Tretinoin 34-47 matrix metallopeptidase 3 Homo sapiens 110-114
12242694-7 2002 Inhibition of RAR function in HMECs by DNRAR suppressed expression of CBP/p300 and expression of RARbeta2 in MCF-7 cells promoted induction of CBP/p300 when cells were treated with 1.0 microM all-trans-retinoic acid (ATRA). Tretinoin 192-215 CREB binding protein Homo sapiens 70-73
12242694-7 2002 Inhibition of RAR function in HMECs by DNRAR suppressed expression of CBP/p300 and expression of RARbeta2 in MCF-7 cells promoted induction of CBP/p300 when cells were treated with 1.0 microM all-trans-retinoic acid (ATRA). Tretinoin 217-221 CREB binding protein Homo sapiens 70-78
12118004-9 2002 These findings demonstrate an antagonistic role for RARbeta" in signaling by retinoic acid. Tretinoin 77-90 retinoic acid receptor beta Homo sapiens 52-60
12513735-0 2002 [Study on telomerase activity and expression of hTERT, c-myc and bcl-2 during terminal differentiation of HL-60 cells induced by retinoic acid]. Tretinoin 129-142 BCL2 apoptosis regulator Homo sapiens 65-70
12513735-4 2002 It is concluded that the telomerase activity is related to decrease expression of hTERT, c-myc and bcl-2 mRNA during HL-60 cell differentiation induced by ATRA. Tretinoin 155-159 BCL2 apoptosis regulator Homo sapiens 99-104
12239602-0 2002 Expression and regulation of WNT10B in human cancer: up-regulation of WNT10B in MCF-7 cells by beta-estradiol and down-regulation of WNT10B in NT2 cells by retinoic acid. Tretinoin 156-169 Wnt family member 10B Homo sapiens 29-35
12132038-0 2002 Mechanism of retinoic acid induced attenuation of PTH action in UMR 106-01 cells. Tretinoin 13-26 parathyroid hormone Rattus norvegicus 50-53
12234625-19 2002 In contrast, long-term culture with RA resulted in a reduction in the cAMP response to PTH (Days 7 and 14) with no effect on PTH/PTH-rp receptor mRNA expression. Tretinoin 36-38 parathyroid hormone Homo sapiens 87-90
12169446-0 2002 Enhancement of the inducible NO synthase activation by retinoic acid is mimicked by RARalpha agonist in vivo. Tretinoin 55-68 nitric oxide synthase 2 Rattus norvegicus 19-40
12132038-1 2002 Studies from our laboratory in osteoblast-like cells have shown that the increase in EGF receptor expression in response to PTH was cyclic AMP mediated and was blocked by treatment with retinoic acid (RA). Tretinoin 186-199 parathyroid hormone Rattus norvegicus 124-127
12132038-1 2002 Studies from our laboratory in osteoblast-like cells have shown that the increase in EGF receptor expression in response to PTH was cyclic AMP mediated and was blocked by treatment with retinoic acid (RA). Tretinoin 201-203 parathyroid hormone Rattus norvegicus 124-127
12132038-2 2002 The present studies investigate the mechanism for this effect of RA on PTH actions. Tretinoin 65-67 parathyroid hormone Rattus norvegicus 71-74
12132038-4 2002 cAMP production in response to PTH was markedly decreased by RA (25.1 +/- 1.6% of control) whereas there was only a slight decrease in PTH binding in response to RA. Tretinoin 61-63 parathyroid hormone Rattus norvegicus 31-34
12132038-4 2002 cAMP production in response to PTH was markedly decreased by RA (25.1 +/- 1.6% of control) whereas there was only a slight decrease in PTH binding in response to RA. Tretinoin 162-164 parathyroid hormone Rattus norvegicus 135-138
12132038-6 2002 Treatment with RA decreased PTH-stimulated adenylate cyclase activity; however, forskolin-stimulated enzyme activity was unchanged. Tretinoin 15-17 parathyroid hormone Rattus norvegicus 28-31
12132038-11 2002 These data indicate that RA impairs the response to PTH in intact cells. Tretinoin 25-27 parathyroid hormone Rattus norvegicus 52-55
12132038-13 2002 The RA-induced alterations of enzymes involved in the GTP biosynthetic pathway in a direction that favors a decrease in GTP biosynthesis provide an explanation for the inhibitory effect of RA on PTH actions. Tretinoin 4-6 parathyroid hormone Rattus norvegicus 195-198
12132038-13 2002 The RA-induced alterations of enzymes involved in the GTP biosynthetic pathway in a direction that favors a decrease in GTP biosynthesis provide an explanation for the inhibitory effect of RA on PTH actions. Tretinoin 189-191 parathyroid hormone Rattus norvegicus 195-198
12065601-3 2002 Induction with Me(2)SO or retinoic acid reduced levels of calreticulin protein by approximately 60% within 4 days. Tretinoin 26-39 calreticulin Homo sapiens 58-70
12204966-0 2002 Suppression of growth by all-trans retinoic acid requires prolonged induction of interferon regulatory factor 1 in cervical squamous carcinoma (SiHa) cells. Tretinoin 35-48 interferon regulatory factor 1 Homo sapiens 81-111
12204966-4 2002 The growth inhibition by high-dose (10(-4) M) ATRA was associated with a sustained activation of interferon regulatory factor 1 (IRF-1), while a low dose (10(-6) M) of ATRA activated IRF-1 only transiently. Tretinoin 46-50 interferon regulatory factor 1 Homo sapiens 97-127
12204966-4 2002 The growth inhibition by high-dose (10(-4) M) ATRA was associated with a sustained activation of interferon regulatory factor 1 (IRF-1), while a low dose (10(-6) M) of ATRA activated IRF-1 only transiently. Tretinoin 46-50 interferon regulatory factor 1 Homo sapiens 129-134
12204966-4 2002 The growth inhibition by high-dose (10(-4) M) ATRA was associated with a sustained activation of interferon regulatory factor 1 (IRF-1), while a low dose (10(-6) M) of ATRA activated IRF-1 only transiently. Tretinoin 46-50 interferon regulatory factor 1 Homo sapiens 183-188
12204966-4 2002 The growth inhibition by high-dose (10(-4) M) ATRA was associated with a sustained activation of interferon regulatory factor 1 (IRF-1), while a low dose (10(-6) M) of ATRA activated IRF-1 only transiently. Tretinoin 168-172 interferon regulatory factor 1 Homo sapiens 183-188
12204966-5 2002 Antisense IRF-1 inhibited the high-dose (10(-4) M), ATRA-mediated growth arrest; forced expression of IRF-1 caused a significant reduction in cell growth. Tretinoin 52-56 interferon regulatory factor 1 Homo sapiens 10-15
12204966-6 2002 High-dose (10(-4) M) ATRA increased binding of NF-kappaB and STAT1 proteins to sequences that originated from the IRF-1 promoter region, while low-dose (10(-6) M) ATRA induced only NF-kappaB binding. Tretinoin 21-25 interferon regulatory factor 1 Homo sapiens 114-119
12204966-6 2002 High-dose (10(-4) M) ATRA increased binding of NF-kappaB and STAT1 proteins to sequences that originated from the IRF-1 promoter region, while low-dose (10(-6) M) ATRA induced only NF-kappaB binding. Tretinoin 163-167 interferon regulatory factor 1 Homo sapiens 114-119
12009305-0 2002 Anticancer effect of retinoic acid via AP-1 activity repression is mediated by retinoic acid receptor alpha and beta in gastric cancer cells. Tretinoin 21-34 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-43
12009305-1 2002 To uncover the mechanisms relating to the anticancer effect of retinoic acids in gastric cancer cells, the mediation of activator protein-1 (AP-1) activity repression by retinoic acid receptors (RARs) was investigated. Tretinoin 63-77 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 141-145
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 10-23 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 41-45
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 10-23 retinoic acid receptor beta Homo sapiens 86-93
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 25-29 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 41-45
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 86-93
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 25-29 retinoic acid receptor beta Homo sapiens 138-145
12009305-5 2002 Transient transfection of RARalpha into MKN-45 cells however, displayed receptor concentration-dependent AP-1 activity inhibition only in the presence of ATRA. Tretinoin 154-158 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-109
12009305-7 2002 For AP-1 binding activity induced by TPA, the repressive effect of ATRA was only observed in BGC-823 and RARalpha and RARbeta stably transfected MKN-45 cells, but not in intact MKN-45 cells. Tretinoin 67-71 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8
12009305-7 2002 For AP-1 binding activity induced by TPA, the repressive effect of ATRA was only observed in BGC-823 and RARalpha and RARbeta stably transfected MKN-45 cells, but not in intact MKN-45 cells. Tretinoin 67-71 retinoic acid receptor beta Homo sapiens 118-125
12165812-9 2002 WNT5A and WNT5B were expressed together in 5 embryonal tumor cell lines, and were slightly down-regulated by all-trans retinoic acid in NT2 cells. Tretinoin 119-132 Wnt family member 5A Homo sapiens 0-5
12595744-4 2002 At 1.3 micro M concentration (a clinically pharmacologically achievable dose), 4HPR increased ATRA sensitivity synergistically in HER2/NEU-overexpressing BT-474, MDA-MB-453, and MCF-7/Her2 breast cancer cells. Tretinoin 94-98 erb-b2 receptor tyrosine kinase 2 Homo sapiens 130-134
12595744-7 2002 Combining 4HPR with ATRA may lead to a novel, selective therapeutic or chemopreventive strategy against HER2/NEU-overexpressing breast tumors. Tretinoin 20-24 erb-b2 receptor tyrosine kinase 2 Homo sapiens 104-108
12070176-8 2002 For RAR beta, the EC(50) values increased as follows: 4-oxo-RA (8 nM), ATRA (9 nM), 18-OH-RA (14 nM), 5,6-epoxy-RA (35 nM), 13-cis-RA (47 nM), 4-OH-RA (64 nM), and 9-cis-RA (173 nM). Tretinoin 71-75 retinoic acid receptor beta Homo sapiens 4-12
12070176-8 2002 For RAR beta, the EC(50) values increased as follows: 4-oxo-RA (8 nM), ATRA (9 nM), 18-OH-RA (14 nM), 5,6-epoxy-RA (35 nM), 13-cis-RA (47 nM), 4-OH-RA (64 nM), and 9-cis-RA (173 nM). Tretinoin 164-172 retinoic acid receptor beta Homo sapiens 4-12
12186855-3 2002 Consistent with a role in neural promotion, REN overexpression induced neuronal differentiation as well as growth arrest and p27Kip1 expression in CNS and PNS neural progenitor cell lines, and its inhibition impaired retinoic acid induction of neurogenin-1 and NeuroD expression. Tretinoin 217-230 renin 1 structural Mus musculus 44-47
12186855-5 2002 We propose that REN represents a novel component of the neurogenic signaling cascade induced by retinoic acid, EGF, and NGF, and is both a marker and a regulator of neuronal differentiation. Tretinoin 96-109 renin 1 structural Mus musculus 16-19
12165850-5 2002 Differentiation induced by retinoic acid results in the gain of ERK-dependent control of cyclin D1 expression and of S phase progression. Tretinoin 27-40 mitogen-activated protein kinase 1 Mus musculus 64-67
12595744-1 2002 We previously reported that overexpression of the HER2/NEU oncogene induces all-TRANS retinoic acid (ATRA) resistance in breast cancer cells. Tretinoin 76-99 erb-b2 receptor tyrosine kinase 2 Homo sapiens 50-58
12595744-1 2002 We previously reported that overexpression of the HER2/NEU oncogene induces all-TRANS retinoic acid (ATRA) resistance in breast cancer cells. Tretinoin 101-105 erb-b2 receptor tyrosine kinase 2 Homo sapiens 50-58
12595744-2 2002 N-(4-hydroxyphenyl)-retinamide (4HPR), a synthetic analogue of ATRA, has been shown to repress the expression of HER2/neu and its family member, epidermal growth factor receptor (EGFR). Tretinoin 63-67 erb-b2 receptor tyrosine kinase 2 Homo sapiens 113-117
12595744-2 2002 N-(4-hydroxyphenyl)-retinamide (4HPR), a synthetic analogue of ATRA, has been shown to repress the expression of HER2/neu and its family member, epidermal growth factor receptor (EGFR). Tretinoin 63-67 erb-b2 receptor tyrosine kinase 2 Homo sapiens 118-121
12595744-2 2002 N-(4-hydroxyphenyl)-retinamide (4HPR), a synthetic analogue of ATRA, has been shown to repress the expression of HER2/neu and its family member, epidermal growth factor receptor (EGFR). Tretinoin 63-67 epidermal growth factor receptor Homo sapiens 145-177
12595744-2 2002 N-(4-hydroxyphenyl)-retinamide (4HPR), a synthetic analogue of ATRA, has been shown to repress the expression of HER2/neu and its family member, epidermal growth factor receptor (EGFR). Tretinoin 63-67 epidermal growth factor receptor Homo sapiens 179-183
12149644-0 2002 Her2/neu induces all-trans retinoic acid (ATRA) resistance in breast cancer cells. Tretinoin 27-40 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-4
12080040-1 2002 All-trans-retinoic acid has been shown to have an antiproliferative effect in the estrogen receptor alpha-positive breast cancer cell line MCF-7. Tretinoin 0-23 estrogen receptor 1 Homo sapiens 82-105
12080040-11 2002 This finding indicates that Hairy and Enhancer of Split homologue-1 is a mediator of the antiproliferative effect of all-trans-retinoic acid in estrogen receptor alpha-positive breast cancer cell lines. Tretinoin 117-140 estrogen receptor 1 Homo sapiens 144-167
12149644-0 2002 Her2/neu induces all-trans retinoic acid (ATRA) resistance in breast cancer cells. Tretinoin 27-40 erb-b2 receptor tyrosine kinase 2 Homo sapiens 5-8
12149644-0 2002 Her2/neu induces all-trans retinoic acid (ATRA) resistance in breast cancer cells. Tretinoin 42-46 erb-b2 receptor tyrosine kinase 2 Homo sapiens 0-4
12149644-0 2002 Her2/neu induces all-trans retinoic acid (ATRA) resistance in breast cancer cells. Tretinoin 42-46 erb-b2 receptor tyrosine kinase 2 Homo sapiens 5-8
12149644-2 2002 This suggests that Her2/neu causes breast cancer cells to be resistant to the growth inhibitory effects of ATRA. Tretinoin 107-111 erb-b2 receptor tyrosine kinase 2 Homo sapiens 19-27
12149644-5 2002 We then determined whether Her2/neu uses Grb2 and Akt proteins to induce ATRA resistance. Tretinoin 73-77 erb-b2 receptor tyrosine kinase 2 Homo sapiens 27-35
12149644-5 2002 We then determined whether Her2/neu uses Grb2 and Akt proteins to induce ATRA resistance. Tretinoin 73-77 growth factor receptor bound protein 2 Homo sapiens 41-45
12149644-5 2002 We then determined whether Her2/neu uses Grb2 and Akt proteins to induce ATRA resistance. Tretinoin 73-77 AKT serine/threonine kinase 1 Homo sapiens 50-53
12149644-7 2002 When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Tretinoin 66-70 growth factor receptor bound protein 2 Homo sapiens 22-26
12149644-7 2002 When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Tretinoin 66-70 AKT serine/threonine kinase 1 Homo sapiens 54-57
12149644-7 2002 When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Tretinoin 66-70 erb-b2 receptor tyrosine kinase 2 Homo sapiens 82-86
12149644-7 2002 When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Tretinoin 132-136 growth factor receptor bound protein 2 Homo sapiens 22-26
12149644-7 2002 When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Tretinoin 132-136 AKT serine/threonine kinase 1 Homo sapiens 54-57
12149644-7 2002 When incubated with L-Grb2 or transfected with the DN AKT mutant, ATRA-resistant, Her2/neu-overexpressing cells became sensitive to ATRA. Tretinoin 132-136 erb-b2 receptor tyrosine kinase 2 Homo sapiens 82-86
12149644-8 2002 Our results indicate that Her2/neu utilizes Grb2 and Akt proteins to induce ATRA resistance in breast cancer cells. Tretinoin 76-80 erb-b2 receptor tyrosine kinase 2 Homo sapiens 26-34
12149644-8 2002 Our results indicate that Her2/neu utilizes Grb2 and Akt proteins to induce ATRA resistance in breast cancer cells. Tretinoin 76-80 growth factor receptor bound protein 2 Homo sapiens 44-48
12149644-8 2002 Our results indicate that Her2/neu utilizes Grb2 and Akt proteins to induce ATRA resistance in breast cancer cells. Tretinoin 76-80 AKT serine/threonine kinase 1 Homo sapiens 53-56
12139723-0 2002 Superior effect of 9-cis retinoic acid (RA) compared with all-trans RA and 13-cis RA on the inhibition of clonogenic cell growth and the induction of apoptosis in OCI/AML-2 subclones: is the p53 pathway involved? Tretinoin 40-42 tumor protein p53 Homo sapiens 191-194
12139723-1 2002 In the present study, the effects of 9-cis retinoic acid (RA) and 13-cis RA on acute myeloblastic leukaemia (AML) cell growth and the induction of apoptosis as well as its relationship with bcl-2 and p53 were compared with those of all-trans RA (ATRA). Tretinoin 58-60 tumor protein p53 Homo sapiens 200-203
12139723-4 2002 In addition, Western blotting revealed the most obvious translocation of p53 from cytosol to nucleus in the case of 9-cis RA, which was the only retinoid able to change the conformation of p53 from mutational to wild type, as demonstrated by flow cytometry. Tretinoin 122-124 tumor protein p53 Homo sapiens 73-76
12139742-1 2002 All-trans retinoic acid (ATRA) is a specific inducer of CD38 antigen on marrow CD34+ cells as well as on blast cells in acute promyelocytic and myeloblastic leukaemia. Tretinoin 0-23 CD34 molecule Homo sapiens 79-83
12139723-4 2002 In addition, Western blotting revealed the most obvious translocation of p53 from cytosol to nucleus in the case of 9-cis RA, which was the only retinoid able to change the conformation of p53 from mutational to wild type, as demonstrated by flow cytometry. Tretinoin 122-124 tumor protein p53 Homo sapiens 189-192
12139742-1 2002 All-trans retinoic acid (ATRA) is a specific inducer of CD38 antigen on marrow CD34+ cells as well as on blast cells in acute promyelocytic and myeloblastic leukaemia. Tretinoin 25-29 CD34 molecule Homo sapiens 79-83
12130515-8 2002 As2O3 in combination with tRA induces gene (Bfl-1/A1 and C/EBPepsilon) expression and partial differentiation. Tretinoin 26-29 BCL2 related protein A1 Homo sapiens 44-49
12139725-0 2002 Simultaneous induction of matrix metalloproteinase-9 and interleukin 8 by all-trans retinoic acid in human PL-21 and NB4 myeloid leukaemia cells. Tretinoin 84-97 C-X-C motif chemokine ligand 8 Homo sapiens 57-70
12139742-6 2002 Interestingly, PI3-K activity was also necessary for CD38 expression on normal marrow CD34+ cells and for the ATRA-induced upregulation of CD157, a CD38-related antigen. Tretinoin 110-114 bone marrow stromal cell antigen 1 Homo sapiens 139-144
12139725-8 2002 ATRA can induce interleukin 8 (IL-8) in APL cells. Tretinoin 0-4 C-X-C motif chemokine ligand 8 Homo sapiens 16-29
12139725-8 2002 ATRA can induce interleukin 8 (IL-8) in APL cells. Tretinoin 0-4 C-X-C motif chemokine ligand 8 Homo sapiens 31-35
12139725-9 2002 IL-8, chemokine for neutrophils and a potent inducer of MMP-9, was also induced by ATRA in PL-21 cells. Tretinoin 83-87 C-X-C motif chemokine ligand 8 Homo sapiens 0-4
12139725-12 2002 These observations suggest that ATRA can induce both MMP-9 and IL-8, but IL-8 is not involved in ATRA-induced MMP-9 expression. Tretinoin 32-36 C-X-C motif chemokine ligand 8 Homo sapiens 63-67
12139725-13 2002 As MMP-9 can truncate and activate IL-8, simultaneous induction of MMP-9 and IL-8 by ATRA could activate leucocytes excessively, causing the hyper-inflammatory events in retinoic acid syndrome. Tretinoin 85-89 C-X-C motif chemokine ligand 8 Homo sapiens 35-39
12139725-13 2002 As MMP-9 can truncate and activate IL-8, simultaneous induction of MMP-9 and IL-8 by ATRA could activate leucocytes excessively, causing the hyper-inflammatory events in retinoic acid syndrome. Tretinoin 85-89 C-X-C motif chemokine ligand 8 Homo sapiens 77-81
12139741-6 2002 Treatment with all-trans retinoic acid (ATRA) reduced Bcl-2 and Bcl-X(L) expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara-C). Tretinoin 15-38 BCL2 apoptosis regulator Homo sapiens 54-59
12139741-6 2002 Treatment with all-trans retinoic acid (ATRA) reduced Bcl-2 and Bcl-X(L) expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara-C). Tretinoin 15-38 BCL2 like 1 Homo sapiens 64-72
12139741-6 2002 Treatment with all-trans retinoic acid (ATRA) reduced Bcl-2 and Bcl-X(L) expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara-C). Tretinoin 40-44 BCL2 apoptosis regulator Homo sapiens 54-59
12139741-6 2002 Treatment with all-trans retinoic acid (ATRA) reduced Bcl-2 and Bcl-X(L) expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara-C). Tretinoin 40-44 BCL2 like 1 Homo sapiens 64-72
12269787-4 2002 Retinoic acid had an inhibitory effect on the level of oocyte eNOS mRNA in a dose-dependent manner if COCs were exposed to retinoic acid before FSH stimulation. Tretinoin 0-13 nitric oxide synthase 3 Homo sapiens 62-66
12269787-0 2002 Retinoic acid suppression of endothelial nitric oxide synthase in porcine oocyte. Tretinoin 0-13 nitric oxide synthase 3 Homo sapiens 29-62
12269787-4 2002 Retinoic acid had an inhibitory effect on the level of oocyte eNOS mRNA in a dose-dependent manner if COCs were exposed to retinoic acid before FSH stimulation. Tretinoin 123-136 nitric oxide synthase 3 Homo sapiens 62-66
12269787-2 2002 The present study was designed to determine the effect of retinoic acid on eNOS regulation in porcine oocytes during follicle-stimulating hormone (FSH) stimulation. Tretinoin 58-71 nitric oxide synthase 3 Homo sapiens 75-79
12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 36-38 nuclear factor kappa B subunit 1 Homo sapiens 289-292
12269787-6 2002 eNOS protein also decreased to approximately 50% of the control after exposure to 10 microM retinoic acid. Tretinoin 92-105 nitric oxide synthase 3 Homo sapiens 0-4
12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 36-38 nuclear factor kappa B subunit 1 Homo sapiens 320-329
12269787-8 2002 These results suggest that retinoic acid has a strong inhibitory action on eNOS mRNA level and NO synthesis in the porcine oocyte. Tretinoin 27-40 nitric oxide synthase 3 Homo sapiens 75-79
12363040-6 2002 The appearance of CD10 on the cell surface was blocked by preincubation of the cells with the monocytic/macrophage-differentiating agents vitamin D3 and phorbol 12-myristate 13-acetate, but not by the granulocytic differentiating agents retinoic acid or dimethyl sulfoxide. Tretinoin 237-250 membrane metalloendopeptidase Homo sapiens 18-22
12191570-1 2002 When cells were incubated in the presence of both interferon-gamma (IFN-gamma) and all-trans retinoic acid (ATRA), the concentration of IFN-gamma required to induce apoptosis of B-cell lymphoma cells was much lower than that required for myeloid or erythroid cell lines. Tretinoin 93-106 interferon gamma Homo sapiens 136-145
12191570-1 2002 When cells were incubated in the presence of both interferon-gamma (IFN-gamma) and all-trans retinoic acid (ATRA), the concentration of IFN-gamma required to induce apoptosis of B-cell lymphoma cells was much lower than that required for myeloid or erythroid cell lines. Tretinoin 108-112 interferon gamma Homo sapiens 136-145
12191572-3 2002 We report the up-regulation of icb-1 transcript levels in HL-60 promyelocytic leukemia cells during their in vitro differentiation induced by all-trans retinoic acid, vitamin D(3) or DMSO. Tretinoin 152-165 thymocyte selection associated family member 2 Homo sapiens 31-36
18759029-1 2002 In the present study, a new member of melanoma associated antigens (Mage), named Restin (219 amino acids), was identified from HL-60 cell induced by all-trans-retinoic acid (ATRA) by PCR-based subtractive hybridization. Tretinoin 149-172 MAGE family member H1 Homo sapiens 81-87
18759029-1 2002 In the present study, a new member of melanoma associated antigens (Mage), named Restin (219 amino acids), was identified from HL-60 cell induced by all-trans-retinoic acid (ATRA) by PCR-based subtractive hybridization. Tretinoin 174-178 MAGE family member H1 Homo sapiens 81-87
12127961-5 2002 But when the proliferation of breast cancer cells was inhibited by tamoxifen or all-trans retinoic acid (ATRA), WT1 protein expression decreased. Tretinoin 80-103 WT1 transcription factor Homo sapiens 112-115
12223147-5 2002 RESULTS: Transfection of RAR-beta gene and treatment with ligand ATRA could increase the expression of RAR-beta protein for at least 144h and inhibit the proliferation and the expression of alpha-SMA and desmin in PDGF-activated HSC. Tretinoin 65-69 retinoic acid receptor, beta Rattus norvegicus 103-111
12127961-5 2002 But when the proliferation of breast cancer cells was inhibited by tamoxifen or all-trans retinoic acid (ATRA), WT1 protein expression decreased. Tretinoin 105-109 WT1 transcription factor Homo sapiens 112-115
12115542-7 2002 Owing to a decrease in the secretion of MCP-1 and transforming growth factor-beta 1 (TGF-beta 1), tumor cells treated with RA were unable to induce peripheral blood monocyte (PBM) chemotaxis. Tretinoin 123-125 transforming growth factor beta 1 Homo sapiens 50-83
12000751-1 2002 We have previously found that retinoic acid stimulates the expression of protein kinase C alpha (PKC) in B16 mouse melanoma cells. Tretinoin 30-43 protein kinase C, alpha Mus musculus 73-95
12011051-5 2002 Previous reports have concluded that retinoic acid and superoxide activate proton transport by UCP2. Tretinoin 37-50 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 95-99
12115542-7 2002 Owing to a decrease in the secretion of MCP-1 and transforming growth factor-beta 1 (TGF-beta 1), tumor cells treated with RA were unable to induce peripheral blood monocyte (PBM) chemotaxis. Tretinoin 123-125 transforming growth factor beta 1 Homo sapiens 85-95
12115542-11 2002 Finally, RA decreased the ability of tumor-activated macrophages to secrete IL-8 and VEGF. Tretinoin 9-11 C-X-C motif chemokine ligand 8 Homo sapiens 76-80
12115542-11 2002 Finally, RA decreased the ability of tumor-activated macrophages to secrete IL-8 and VEGF. Tretinoin 9-11 vascular endothelial growth factor A Homo sapiens 85-89
12032135-0 2002 Down-regulation of the phosphatidylinositol 3-kinase/Akt pathway is involved in retinoic acid-induced phosphorylation, degradation, and transcriptional activity of retinoic acid receptor gamma 2. Tretinoin 80-93 AKT serine/threonine kinase 1 Homo sapiens 53-56
12124324-5 2002 Treatment with 5-aza-2"-deoxycytidine restored RA response in two of the seven cell lines with RARbeta promoter methylation (29%). Tretinoin 47-49 retinoic acid receptor beta Homo sapiens 95-102
12124324-6 2002 RA treatment increased acetylation of histones H3 and H4 on chromatin of the RARbeta promoter in RA-responsive cells. Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 77-84
12000752-0 2002 Activation of the phosphatidylinositol 3-kinase/Akt signaling pathway by retinoic acid is required for neural differentiation of SH-SY5Y human neuroblastoma cells. Tretinoin 73-86 AKT serine/threonine kinase 1 Homo sapiens 48-51
12000752-7 2002 RA treatment activates the PI3K/Akt signaling pathway, resulting in increased PI3K activity in extracts from RA-treated cells and a rapid increase in phosphorylation of Akt in Ser-473. Tretinoin 0-2 AKT serine/threonine kinase 1 Homo sapiens 32-35
12000752-7 2002 RA treatment activates the PI3K/Akt signaling pathway, resulting in increased PI3K activity in extracts from RA-treated cells and a rapid increase in phosphorylation of Akt in Ser-473. Tretinoin 0-2 AKT serine/threonine kinase 1 Homo sapiens 169-172
12000752-7 2002 RA treatment activates the PI3K/Akt signaling pathway, resulting in increased PI3K activity in extracts from RA-treated cells and a rapid increase in phosphorylation of Akt in Ser-473. Tretinoin 109-111 AKT serine/threonine kinase 1 Homo sapiens 32-35
12000752-9 2002 We propose that RA, by activating the PI3K/Akt signaling pathway, plays an important role in the regulation of neuronal cell survival. Tretinoin 16-18 AKT serine/threonine kinase 1 Homo sapiens 43-46
12000762-6 2002 RA also reduces the activity of an AP-1 and TCF-sensitive cyclin D1 reporter in SKBR3 cells in a manner that is independent of the TCF site. Tretinoin 0-2 hepatocyte nuclear factor 4 alpha Homo sapiens 44-47
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 57-59 RAB40B, member RAS oncogene family Homo sapiens 217-220
12032135-3 2002 We show here that this RA-induced phosphorylation of RARgamma2 resulted from the down-regulation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Tretinoin 23-25 AKT serine/threonine kinase 1 Homo sapiens 141-144
12032135-4 2002 By overexpressing Akt and by using agents that activated or inhibited the PI3K/Akt pathway, we also demonstrated that the RA-induced down-regulation of the PI3K/Akt pathway targeted not only the phosphorylation of RARgamma2 but also the turnover and transcriptional activity of the receptor. Tretinoin 122-124 AKT serine/threonine kinase 1 Homo sapiens 18-21
12032135-4 2002 By overexpressing Akt and by using agents that activated or inhibited the PI3K/Akt pathway, we also demonstrated that the RA-induced down-regulation of the PI3K/Akt pathway targeted not only the phosphorylation of RARgamma2 but also the turnover and transcriptional activity of the receptor. Tretinoin 122-124 AKT serine/threonine kinase 1 Homo sapiens 79-82
12032135-4 2002 By overexpressing Akt and by using agents that activated or inhibited the PI3K/Akt pathway, we also demonstrated that the RA-induced down-regulation of the PI3K/Akt pathway targeted not only the phosphorylation of RARgamma2 but also the turnover and transcriptional activity of the receptor. Tretinoin 122-124 AKT serine/threonine kinase 1 Homo sapiens 79-82
12032135-5 2002 Altogether these data indicate that the PI3K/Akt pathway plays an important role in retinoic acid signaling. Tretinoin 84-97 AKT serine/threonine kinase 1 Homo sapiens 45-48
12174890-3 2002 HBD-2 was extracted from tissue samples in the presence of retinoic acid and subjected to reversed-phase HPLC. Tretinoin 59-72 defensin beta 4A Homo sapiens 0-5
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 57-59 hepatocyte nuclear factor 4 alpha Homo sapiens 249-252
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 171-173 RAB40B, member RAS oncogene family Homo sapiens 217-220
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 171-173 hepatocyte nuclear factor 4 alpha Homo sapiens 249-252
12150978-1 2002 We previously reported that DAN, a founding member of the DAN family of secreted proteins, acts as an inhibitor of cell cycle progression and is closely involved in retinoic acid-induced neuroblastoma differentiation. Tretinoin 165-178 NBL1, DAN family BMP antagonist Homo sapiens 28-31
12150978-1 2002 We previously reported that DAN, a founding member of the DAN family of secreted proteins, acts as an inhibitor of cell cycle progression and is closely involved in retinoic acid-induced neuroblastoma differentiation. Tretinoin 165-178 NBL1, DAN family BMP antagonist Homo sapiens 58-61
12100164-0 2002 All-trans retinoic acid prevents apoptosis of human marrow CD34+ cells deprived of haematopoietic growth factors. Tretinoin 10-23 CD34 molecule Homo sapiens 59-63
12100164-3 2002 We studied the effects of pharmacological doses of all-transretinoic acid (ATRA) on the apoptosis of human adult marrow CD34+ progenitor cells cultured for 7 d in a serum-free medium. Tretinoin 51-73 CD34 molecule Homo sapiens 120-124
12100164-3 2002 We studied the effects of pharmacological doses of all-transretinoic acid (ATRA) on the apoptosis of human adult marrow CD34+ progenitor cells cultured for 7 d in a serum-free medium. Tretinoin 75-79 CD34 molecule Homo sapiens 120-124
12100164-7 2002 Exposure to ATRA partially prevented the decrease in viable CD34+, without a concomitant effect on the clonogenic and more immature progenitors. Tretinoin 12-16 CD34 molecule Homo sapiens 60-64
12100164-8 2002 ATRA-treated CD34+ cells displayed changes in apoptotic status compared with control cultures, particularly in lower annexin V-binding. Tretinoin 0-4 CD34 molecule Homo sapiens 13-17
12186376-5 2002 However, only MCF-7, MDA-MB-231, and ZR-75-1 cells, which expressed a high level of bcl-2 protein, underwent apoptosis when exposed to the combination of TGZ and either ATRA or 9-cis-RA. Tretinoin 169-173 BCL2 apoptosis regulator Homo sapiens 84-89
12063559-12 2002 Western blot analysis revealed that ATRA induced an increase in RARbeta expression and a decrease in RARgamma expression, while 9cisRA down-regulated RXRalpha expression. Tretinoin 36-40 retinoic acid receptor beta Homo sapiens 64-71
12186376-5 2002 However, only MCF-7, MDA-MB-231, and ZR-75-1 cells, which expressed a high level of bcl-2 protein, underwent apoptosis when exposed to the combination of TGZ and either ATRA or 9-cis-RA. Tretinoin 177-185 BCL2 apoptosis regulator Homo sapiens 84-89
12111213-7 2002 RA treatment also affects the morphogenetic process of the palp formation and also disturbs the precise patterning of the surrounding epidermis, which may contribute to the regulation of RTEN development. Tretinoin 0-2 alkaline phosphatase, placental Homo sapiens 59-63
12063559-13 2002 These data demonstrate that ATRA and 9cisRA may inhibit HER-2/neu induced aberrant proliferation in part by retarding cell cycle progression, down-regulating HER-2/neu-mediated signal transduction and inducing Bcl-2-dependent apoptosis through a retinoid receptor-mediated mechanism. Tretinoin 28-32 erb-b2 receptor tyrosine kinase 2 Homo sapiens 56-65
12063559-13 2002 These data demonstrate that ATRA and 9cisRA may inhibit HER-2/neu induced aberrant proliferation in part by retarding cell cycle progression, down-regulating HER-2/neu-mediated signal transduction and inducing Bcl-2-dependent apoptosis through a retinoid receptor-mediated mechanism. Tretinoin 28-32 erb-b2 receptor tyrosine kinase 2 Homo sapiens 56-61
12063559-13 2002 These data demonstrate that ATRA and 9cisRA may inhibit HER-2/neu induced aberrant proliferation in part by retarding cell cycle progression, down-regulating HER-2/neu-mediated signal transduction and inducing Bcl-2-dependent apoptosis through a retinoid receptor-mediated mechanism. Tretinoin 28-32 erb-b2 receptor tyrosine kinase 2 Homo sapiens 62-65
12063559-13 2002 These data demonstrate that ATRA and 9cisRA may inhibit HER-2/neu induced aberrant proliferation in part by retarding cell cycle progression, down-regulating HER-2/neu-mediated signal transduction and inducing Bcl-2-dependent apoptosis through a retinoid receptor-mediated mechanism. Tretinoin 28-32 BCL2 apoptosis regulator Homo sapiens 210-215
12052862-6 2002 Importantly, CBP and ERKs were excluded from the promoter in the presence of atRA. Tretinoin 77-81 CREB binding protein Homo sapiens 13-16
12097159-7 2002 On the other hand, growth inhibition and tTGase expression and activity are potentiated by retinoic acid, a tTGase inducer. Tretinoin 91-104 transglutaminase 2 Homo sapiens 41-47
12097159-7 2002 On the other hand, growth inhibition and tTGase expression and activity are potentiated by retinoic acid, a tTGase inducer. Tretinoin 91-104 transglutaminase 2 Homo sapiens 108-114
12164942-2 2002 In this study, we have shown that bovine serum albumin, an extracellular binding protein for 13-cis retinoic acid, plays an important part in the uptake of 13-cis retinoic acid in human sebocytes, its intracellular isomerization to all-trans retinoic acid, and the induction of its anti-proliferative effect. Tretinoin 100-113 albumin Homo sapiens 41-54
12164942-3 2002 The addition of highly concentrated bovine serum albumin (20 mg per ml) to the serum-free maintenance medium resulted in a rather controlled uptake of constant levels of 13-cis and all-trans retinoic acid into the cells over the 72 h of treatment. Tretinoin 191-204 albumin Homo sapiens 43-56
12101269-5 2002 However, upon differentiation of THP-1 monocytes to macrophages, through treatment with retinoic acid and interferon-gamma (IFN-gamma), wortmannin and PD98059 blocked Fc receptor-mediated phagocytosis efficiently. Tretinoin 88-101 GLI family zinc finger 2 Homo sapiens 33-38
12074569-0 2002 Involvement of CCAAT/enhancer-binding protein alpha in haptoglobin gene expression by all-trans-retinoic acid. Tretinoin 86-109 CCAAT enhancer binding protein alpha Homo sapiens 15-51
12218287-5 2002 All-trans-retinoic acid, dithranol and the p38 mitogen-activated protein (MAP) kinase inhibitor SB220025 displayed a strong inhibitory effect on SKALP expression while cyclosporin A, dexamethasone, the vitamin D(3) derivative calcipotriol and the p38 MAP kinase inhibitor SB203580 showed only moderate inhibition. Tretinoin 0-23 mitogen-activated protein kinase 14 Homo sapiens 247-261
12074569-0 2002 Involvement of CCAAT/enhancer-binding protein alpha in haptoglobin gene expression by all-trans-retinoic acid. Tretinoin 86-109 haptoglobin Homo sapiens 55-66
12074569-2 2002 Recently, we found that Hp gene expression is up-regulated by all-trans-retinoic acid (ATRA) in the extrahepatic monocytic cell line, THP-1. Tretinoin 62-85 GLI family zinc finger 2 Homo sapiens 134-139
12074569-2 2002 Recently, we found that Hp gene expression is up-regulated by all-trans-retinoic acid (ATRA) in the extrahepatic monocytic cell line, THP-1. Tretinoin 87-91 GLI family zinc finger 2 Homo sapiens 134-139
12074569-4 2002 Western blot analysis showed that treatment with ATRA increased C/EBPalpha and beta expression, but decreased that of C/EBPdelta. Tretinoin 49-53 CCAAT enhancer binding protein alpha Homo sapiens 64-74
12074569-6 2002 Furthermore, when ATRA-dependent Hp induction was inhibited by sodium butyrate or auranofin, induction of C/EBPalpha, but not C/EBPbeta, was also diminished. Tretinoin 18-22 CCAAT enhancer binding protein alpha Homo sapiens 106-116
12123542-0 2002 Retinoic acid receptor beta is required for anti-activator protein-1 activity by retinoic acid in gastric cancer cells. Tretinoin 81-94 retinoic acid receptor beta Homo sapiens 0-27
11960985-7 2002 RA produced in Adh1-null mutant mice following a 50-mg/kg dose of retinol was reduced 82% relative to wild-type mice, thus similar to wild-type mice pretreated with ethanol. Tretinoin 0-2 alcohol dehydrogenase 1 (class I) Mus musculus 15-19
11960985-8 2002 Reduced RA production was associated with increased retinol levels in both ethanol-treated wild-type mice and Adh1-null mutant mice, indicating reduced clearance of the retinol dose. Tretinoin 8-10 alcohol dehydrogenase 1 (class I) Mus musculus 110-114
11960985-9 2002 RA degradation following a dose of RA (10 mg/kg) was increased only 42% by ethanol pretreatment (3.5 g/kg) and only 26% in Adh1-null mutant mice relative to wild-type mice. Tretinoin 0-2 alcohol dehydrogenase 1 (class I) Mus musculus 123-127
12069693-2 2002 METHOD: In this study, we examined the interactions between T and retinoic acid (RA) in cell growth of human prostate carcinoma cells, LNCaP, and their relationship with the expression of RAR and epidermal growth factor receptor (EGF-R). Tretinoin 66-79 epidermal growth factor receptor Homo sapiens 196-228
12069693-2 2002 METHOD: In this study, we examined the interactions between T and retinoic acid (RA) in cell growth of human prostate carcinoma cells, LNCaP, and their relationship with the expression of RAR and epidermal growth factor receptor (EGF-R). Tretinoin 81-83 epidermal growth factor receptor Homo sapiens 196-228
12069693-10 2002 The opposite effects of T and RA on the expression of RAR and EGF-R suggest that signal events of these receptors might be involved in the interaction between T and RA in the control of LNCaP cell growth. Tretinoin 30-32 epidermal growth factor receptor Homo sapiens 62-67
12016134-2 2002 Previous studies have shown that retinoic acid upregulates endogenous human CRBP II gene expression in differentiated Caco-2 cells. Tretinoin 33-46 retinol binding protein 2 Homo sapiens 76-83
12016134-6 2002 The results indicate that the retinoic acid responsiveness of the human CRBP II promoter is mediated by an indirect mechanism and that this mechanism is associated with enterocyte differentiation. Tretinoin 30-43 retinol binding protein 2 Homo sapiens 72-79
11979502-0 2002 Monoamine oxidase A and B activities in embryonic chick hepatocytes: differential regulation by retinoic acid. Tretinoin 96-109 monoamine oxidase A Gallus gallus 0-25
11979502-6 2002 RA stimulated MAO B but not MAO A activity, in a dose- and time-dependent way, and only in the presence of serum. Tretinoin 0-2 monoamine oxidase A Gallus gallus 28-33
12123542-6 2002 The stable transfection of the RARbeta gene into MKN-45 cells led to cell growth inhibition and colony formation inhibition by ATRA. Tretinoin 127-131 retinoic acid receptor beta Homo sapiens 31-38
12123542-8 2002 CONCLUSION: RARbeta might be required for anti-AP-1 activity, and contribute to growth inhibition of gastric cancer cells by ATRA. Tretinoin 125-129 retinoic acid receptor beta Homo sapiens 12-19
11934895-2 2002 We recently reported that the expression of orphan receptor chicken ovalbumin upstream promoter-transcription factor (COUP-TF) plays a role in mediating the growth inhibitory effect of trans-retinoic acid (trans-RA) in cancer cells. Tretinoin 185-204 nuclear receptor subfamily 2 group F member 1 Homo sapiens 118-125
12069693-0 2002 Androgen and retinoic acid interaction in LNCaP cells, effects on cell proliferation and expression of retinoic acid receptors and epidermal growth factor receptor. Tretinoin 13-26 epidermal growth factor receptor Homo sapiens 131-163
12123542-0 2002 Retinoic acid receptor beta is required for anti-activator protein-1 activity by retinoic acid in gastric cancer cells. Tretinoin 81-94 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-68
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 110-133 retinoic acid receptor beta Homo sapiens 38-65
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 110-133 retinoic acid receptor beta Homo sapiens 67-74
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 110-133 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-163
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 110-133 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-169
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 135-139 retinoic acid receptor beta Homo sapiens 38-65
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 135-139 retinoic acid receptor beta Homo sapiens 67-74
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 135-139 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-163
12123542-1 2002 OBJECTIVE: To investigate the role of retinoic acid receptor beta (RARbeta) in mediating inhibitory effect of all-trans retinoic acid (ATRA) on activator protein-1 (AP-1) activity in gastric cancer cells. Tretinoin 135-139 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-169
12123542-3 2002 RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA. Tretinoin 240-244 retinoic acid receptor beta Homo sapiens 35-42
12123542-3 2002 RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA. Tretinoin 240-244 retinoic acid receptor beta Homo sapiens 95-102
12123542-3 2002 RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA. Tretinoin 240-244 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 141-145
12012012-5 2002 Bcl-2 over-expression inhibited both delay in S-phase exit and CDDP-induced apoptosis in ATRA-pretreated cells. Tretinoin 89-93 BCL2 apoptosis regulator Homo sapiens 0-5
12042033-6 2002 We previously reported that induction of MUC2, MUC5AC, and MUC5B gene expressions by retinoic acid is mediated by the retinoic acid receptor (RARalpha), and inhibited by the specific RARalpha antagonist Ro 41-5253. Tretinoin 85-98 mucin 2, oligomeric mucus/gel-forming Homo sapiens 41-45
12012012-7 2002 Our results indicate that ATRA-pretreatment modified the CDDP-induced regulation of CDK2 activity by the CDK inhibitors p21 and p27. Tretinoin 26-30 cyclin dependent kinase inhibitor 1A Homo sapiens 120-123
12012012-8 2002 Taken together, our findings suggest that ATRA potentiates the apoptosis induced by CDDP in ovarian carcinoma cells and that this action is sustained by modulation of the activity of CDK2/cyclin A. Tretinoin 42-46 cyclin A2 Homo sapiens 188-196
12051745-0 2002 Induction of human aquaporin-1 gene by retinoic acid in human erythroleukemia HEL cells. Tretinoin 39-52 aquaporin 1 (Colton blood group) Homo sapiens 19-30
12054474-1 2002 A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA. Tretinoin 8-21 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 54-62
12054474-1 2002 A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA. Tretinoin 8-21 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 66-71
12054474-1 2002 A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA. Tretinoin 23-25 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 54-62
12054474-1 2002 A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA. Tretinoin 23-25 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 66-71
12054474-1 2002 A novel retinoic acid (RA)-inducible cytochrome P450 (P450 RAI or CYP26), previously cloned from human, zebra fish, and mouse, functions in the metabolism of all-trans-RA to polar metabolites including 4-hydroxy-RA and 4-oxo-RA. Tretinoin 59-61 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 66-71
12175512-4 2002 The expression of HIN-1 is up-regulated during retinoic acid induced differentiation of bronchial epithelial cells. Tretinoin 47-60 secretoglobin, family 3A, member 1 Mus musculus 18-23
11986218-6 2002 After up-regulation of t-PA synthesis either by vascular endothelial growth factor (VEGF) and retinoic acid or by sodium butyrate, there was a large increase in t-PA-positive cells. Tretinoin 94-107 plasminogen activator, tissue type Homo sapiens 23-27
12051745-2 2002 We report here that aquaporin-1 (AQP1) is specifically induced by retinoic acid (RA) in human erythroleukemia HEL cells. Tretinoin 66-79 aquaporin 1 (Colton blood group) Homo sapiens 20-31
12051745-2 2002 We report here that aquaporin-1 (AQP1) is specifically induced by retinoic acid (RA) in human erythroleukemia HEL cells. Tretinoin 66-79 aquaporin 1 (Colton blood group) Homo sapiens 33-37
12051745-2 2002 We report here that aquaporin-1 (AQP1) is specifically induced by retinoic acid (RA) in human erythroleukemia HEL cells. Tretinoin 81-83 aquaporin 1 (Colton blood group) Homo sapiens 20-31
12051745-2 2002 We report here that aquaporin-1 (AQP1) is specifically induced by retinoic acid (RA) in human erythroleukemia HEL cells. Tretinoin 81-83 aquaporin 1 (Colton blood group) Homo sapiens 33-37
12051745-5 2002 To identify the RA response element (RARE) in the human AQP1 promoter, the 5(")-flanking region of AQP1 promoter was isolated and transient transfection experiment in HEL cells was performed. Tretinoin 16-18 aquaporin 1 (Colton blood group) Homo sapiens 56-60
11875072-5 2002 As in rodents, PGC-1 is involved in the transcriptional regulation of the UCP1 gene in humans and mediates the effects of PPARalpha and PPARgamma agonists and retinoic acid. Tretinoin 159-172 PPARG coactivator 1 alpha Homo sapiens 15-20
11875072-7 2002 Furthermore, inhibition of p38 MAPK signaling, known to regulate the PGC-1/repressor interaction, decreases the stimulatory effect of PPARalpha agonist treatment without reducing the response to thiazolidinedione or retinoic acid. Tretinoin 216-229 mitogen-activated protein kinase 14 Homo sapiens 27-30
12051745-5 2002 To identify the RA response element (RARE) in the human AQP1 promoter, the 5(")-flanking region of AQP1 promoter was isolated and transient transfection experiment in HEL cells was performed. Tretinoin 16-18 aquaporin 1 (Colton blood group) Homo sapiens 99-103
11959834-4 2002 Conditional rescue of Raldh2(-/-) embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Tretinoin 62-64 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 235-241
11994980-0 2002 all-trans-Retinoic acid-induced expression and regulation of retinoic acid 4-hydroxylase (CYP26) in human promyelocytic leukemia. Tretinoin 0-23 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 61-88
11994980-0 2002 all-trans-Retinoic acid-induced expression and regulation of retinoic acid 4-hydroxylase (CYP26) in human promyelocytic leukemia. Tretinoin 0-23 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 90-95
11994980-4 2002 We found that treatment of NB4 cells with a pharmacological concentration of ATRA (1 microM) induced rapid and dose-dependent expression of CYP26 mRNA. Tretinoin 77-81 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 140-145
11994980-5 2002 The CYP26 expression returned to pretreatment levels in both cells after ATRA was removed from the media. Tretinoin 73-77 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 4-9
11994980-6 2002 Retinoic acid receptor-alpha (RARalpha) specific antagonist (CD2503) totally abolished the ATRA-induced expression of CYP26 mRNA in HL-60 and NB4 cells. Tretinoin 91-95 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 118-123
11994980-8 2002 ATRA-induced expression of CYP26 was restored in HL-60R cells retrovirally transduced with RARalpha, but not in those cells transduced with the other retinoid receptors. Tretinoin 0-4 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 27-32
11994980-9 2002 In conclusion, ATRA induces expression of CYP26 in myeloid and promyelocytic leukemia cells and this expression is modulated by RARalpha. Tretinoin 15-19 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 42-47
11994980-10 2002 The induction of CYP26 expression by ATRA treatment might be related to a substrate-driven feedback mechanism to regulate intracellular concentrations of ATRA and its over expression in some clones may be partly responsible for reduced sensitivity or resistance to ATRA therapy. Tretinoin 37-41 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-22
11994980-10 2002 The induction of CYP26 expression by ATRA treatment might be related to a substrate-driven feedback mechanism to regulate intracellular concentrations of ATRA and its over expression in some clones may be partly responsible for reduced sensitivity or resistance to ATRA therapy. Tretinoin 154-158 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-22
11994980-10 2002 The induction of CYP26 expression by ATRA treatment might be related to a substrate-driven feedback mechanism to regulate intracellular concentrations of ATRA and its over expression in some clones may be partly responsible for reduced sensitivity or resistance to ATRA therapy. Tretinoin 154-158 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-22
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 15-28 prostaglandin-endoperoxide synthase 2 Homo sapiens 204-220
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 15-28 prostaglandin-endoperoxide synthase 2 Homo sapiens 222-227
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 30-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 204-220
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 30-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 222-227
11980644-5 2002 Because AP-1 binding was unaffected by RA, we investigated whether RA inhibited COX-2 transcription via effects on the coactivator CBP/p300. Tretinoin 67-69 prostaglandin-endoperoxide synthase 2 Homo sapiens 80-85
11980644-6 2002 Treatment with RA stimulated an interaction between RA receptor-alpha and CBP/p300; a corresponding decrease in the interaction between CBP/p300 and c-Jun was observed. Tretinoin 15-17 CREB binding protein Homo sapiens 74-82
11980644-6 2002 Treatment with RA stimulated an interaction between RA receptor-alpha and CBP/p300; a corresponding decrease in the interaction between CBP/p300 and c-Jun was observed. Tretinoin 15-17 CREB binding protein Homo sapiens 74-77
11980644-7 2002 Importantly, overexpressing CBP/p300 or dominant-negative RA receptor-alpha relieved the suppressive effect of RA on PMA-mediated stimulation of the COX-2 promoter. Tretinoin 58-60 prostaglandin-endoperoxide synthase 2 Homo sapiens 149-154
11959834-4 2002 Conditional rescue of Raldh2(-/-) embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Tretinoin 166-168 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 235-241
11959834-9 2002 These novel RA-generating activities in the neural tube and heart fill gaps in our knowledge of how RA is generated spatiotemporally and may, along with Raldh1 and Raldh3, contribute to rescue of Raldh2(-/-) embryos by producing RA locally. Tretinoin 12-14 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 164-170
11912557-0 2002 Retinoic acid 4-hydroxylase-mediated catabolism of all-trans retinoic acid and the cell proliferation in head and neck squamous cell carcinoma. Tretinoin 61-74 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-27
12027900-3 2002 Following an acute dose of retinol (50 mg.kg(-1)), metabolism of retinol to retinoic acid in liver was reduced 10-fold in Adh1 mutants and 3.8-fold in Adh3 mutants, but was not significantly reduced in Adh4 mutants. Tretinoin 76-89 alcohol dehydrogenase 1 (class I) Mus musculus 122-126
12027900-3 2002 Following an acute dose of retinol (50 mg.kg(-1)), metabolism of retinol to retinoic acid in liver was reduced 10-fold in Adh1 mutants and 3.8-fold in Adh3 mutants, but was not significantly reduced in Adh4 mutants. Tretinoin 76-89 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 202-206
12027900-9 2002 Our results also show that retinoic acid is not the toxic moiety during vitamin A excess, as Adh1 mutants have less retinoic acid production while experiencing increased toxicity. Tretinoin 116-129 alcohol dehydrogenase 1 (class I) Mus musculus 93-97
12027902-0 2002 Interaction between p21-activated protein kinase and Rac during differentiation of HL-60 human promyelocytic leukemia cell induced by all-trans-retinoic acid. Tretinoin 134-157 AKT serine/threonine kinase 1 Homo sapiens 53-56
12027902-5 2002 The amount of Rac identified in the two fractions was also markedly enhanced by ATRA- induced differentiation. Tretinoin 80-84 AKT serine/threonine kinase 1 Homo sapiens 14-17
11980848-0 2002 Induction of VEGF gene expression by retinoic acid through Sp1-binding sites in retinoblastoma Y79 cells. Tretinoin 37-50 vascular endothelial growth factor A Homo sapiens 13-17
11980848-3 2002 In this study, we investigated the effects of atRA on expression of the VEGF gene in retinoblastoma Y79 cells. Tretinoin 46-50 vascular endothelial growth factor A Homo sapiens 72-76
11980848-13 2002 Pharmacologic intervention that inhibits the signals elicited by atRA may be effective in treating VEGF-mediated retinopathies. Tretinoin 65-69 vascular endothelial growth factor A Homo sapiens 99-103
11986958-4 2002 PrPc messenger ribonucleic acid (mRNA) and protein are down-regulated upon ATRA-induced differentiation of HL60 cells. Tretinoin 75-79 prion protein Homo sapiens 0-4
11986958-6 2002 In ATRA-induced maturation of NB4 cells, down-regulation of PrPc mRNA and protein were observed. Tretinoin 3-7 prion protein Homo sapiens 60-64
11880314-0 2002 Protective role of retinoic acid from antiproliferative action of TNF-alpha on lung epithelial cells. Tretinoin 19-32 tumor necrosis factor Homo sapiens 66-75
11880314-8 2002 Interestingly, we observed that RA abrogated TNF-alpha-induced growth arrest and that this effect was associated with a dramatic decrease in IGFBP-2 expression. Tretinoin 32-34 tumor necrosis factor Homo sapiens 45-54
11880314-9 2002 These results suggest a protective role of RA from TNF-alpha antiproliferative action, through mechanisms involving modulation of IGFBP-2 production. Tretinoin 43-45 tumor necrosis factor Homo sapiens 51-60
12207051-0 2002 Expression of selected apoptosis related genes, MIF, IGIF and TNF alpha, during retinoic acid-induced neural differentiation in murine embryonic stem cells. Tretinoin 80-93 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 48-51
12207051-0 2002 Expression of selected apoptosis related genes, MIF, IGIF and TNF alpha, during retinoic acid-induced neural differentiation in murine embryonic stem cells. Tretinoin 80-93 tumor necrosis factor Mus musculus 62-71
12207051-7 2002 Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Tretinoin 66-79 caspase 6 Mus musculus 43-52
12207051-7 2002 Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Tretinoin 66-79 caspase 6 Mus musculus 112-120
12207051-7 2002 Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Tretinoin 147-160 caspase 6 Mus musculus 43-52
12207051-7 2002 Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Tretinoin 147-160 caspase 6 Mus musculus 112-120
12207051-8 2002 Increase in the expression of TNF alpha and macrophage migration inhibitory factor (MIF) was noted in retinoic acid-treated cells on day 14. Tretinoin 102-115 tumor necrosis factor Mus musculus 30-39
12207051-8 2002 Increase in the expression of TNF alpha and macrophage migration inhibitory factor (MIF) was noted in retinoic acid-treated cells on day 14. Tretinoin 102-115 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 44-82
12207051-8 2002 Increase in the expression of TNF alpha and macrophage migration inhibitory factor (MIF) was noted in retinoic acid-treated cells on day 14. Tretinoin 102-115 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 84-87
12153175-8 2002 However, ATRA-induced upregulation of CRABPII did significantly correlate with the ATRA sensitivity (p < 0.005) as well as with ATRA-induced upregulation of the retinoid receptor RARbeta (p < 0.05). Tretinoin 9-13 retinoic acid receptor beta Homo sapiens 182-189
11960970-0 2002 Effects of all-trans retinoic acid on angiotensin II-induced myocyte hypertrophy. Tretinoin 11-34 angiotensinogen Rattus norvegicus 38-52
11960970-1 2002 We used cultured neonatal rat cardiac myocytes to test the hypothesis that all-trans retinoic acid (atRA) may act to modulate ANG II actions in inducing myocyte hypertrophy. Tretinoin 75-98 angiotensinogen Rattus norvegicus 126-132
11960970-1 2002 We used cultured neonatal rat cardiac myocytes to test the hypothesis that all-trans retinoic acid (atRA) may act to modulate ANG II actions in inducing myocyte hypertrophy. Tretinoin 100-104 angiotensinogen Rattus norvegicus 126-132
11960970-3 2002 1) atRA (10(-7) to approximately 10(-5) M ) inhibited ANG II-induced hyperplasia of fibroblasts in a dose-dependent manner. Tretinoin 3-7 angiotensinogen Rattus norvegicus 54-60
11960970-8 2002 Our results show that atRA inhibits some effects of ANG II on neonatal rat cardiac myocytes and suggest that atRA may be a therapeutic candidate for the prevention and therapy of cardiac hypertrophy and remodeling. Tretinoin 22-26 angiotensinogen Rattus norvegicus 52-58
11970994-2 2002 To identify a potential mechanism(s) underlying this in vivo activity of vitamin A, we examined the effects of all-trans and 9-cis RA on development of Th1 and Th2 cell populations using in vitro stimulation of Ag-naive Th0 cells from the DO11.10 TCR-transgenic mouse. Tretinoin 131-133 negative elongation factor complex member C/D, Th1l Mus musculus 152-155
11953746-4 2002 Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration, indicating that human CYP26A1 may be essential in controlling retinoic acid levels during development. Tretinoin 100-113 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 152-159
11953746-4 2002 Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration, indicating that human CYP26A1 may be essential in controlling retinoic acid levels during development. Tretinoin 192-205 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 152-159
11854287-4 2002 It was found that RA stimulation of NIH3T3 cells activated ERK and phosphoinositide 3-kinase (PI3K); however, only PI3K activation was necessary for RA-induced TGase expression. Tretinoin 18-20 mitogen-activated protein kinase 1 Mus musculus 59-62
11836246-1 2002 The ability of class I alcohol dehydrogenase (ADH1) and class IV alcohol dehydrogenase (ADH4) to metabolize retinol to retinoic acid is supported by genetic studies in mice carrying Adh1 or Adh4 gene disruptions. Tretinoin 119-132 alcohol dehydrogenase 1 (class I) Mus musculus 15-44
11836246-1 2002 The ability of class I alcohol dehydrogenase (ADH1) and class IV alcohol dehydrogenase (ADH4) to metabolize retinol to retinoic acid is supported by genetic studies in mice carrying Adh1 or Adh4 gene disruptions. Tretinoin 119-132 alcohol dehydrogenase 1 (class I) Mus musculus 46-50
11836246-1 2002 The ability of class I alcohol dehydrogenase (ADH1) and class IV alcohol dehydrogenase (ADH4) to metabolize retinol to retinoic acid is supported by genetic studies in mice carrying Adh1 or Adh4 gene disruptions. Tretinoin 119-132 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 88-92
11836246-1 2002 The ability of class I alcohol dehydrogenase (ADH1) and class IV alcohol dehydrogenase (ADH4) to metabolize retinol to retinoic acid is supported by genetic studies in mice carrying Adh1 or Adh4 gene disruptions. Tretinoin 119-132 alcohol dehydrogenase 1 (class I) Mus musculus 182-186
11836246-1 2002 The ability of class I alcohol dehydrogenase (ADH1) and class IV alcohol dehydrogenase (ADH4) to metabolize retinol to retinoic acid is supported by genetic studies in mice carrying Adh1 or Adh4 gene disruptions. Tretinoin 119-132 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 190-194
11836246-5 2002 Following administration of a 50-mg/kg dose of retinol to examine retinol turnover, Adh1 and Adh1/4 mutants exhibit similar 10-fold decreases in retinoic acid production, whereas Adh4 mutants have only a slight decrease. Tretinoin 145-158 alcohol dehydrogenase 1 (class I) Mus musculus 84-88
11836246-5 2002 Following administration of a 50-mg/kg dose of retinol to examine retinol turnover, Adh1 and Adh1/4 mutants exhibit similar 10-fold decreases in retinoic acid production, whereas Adh4 mutants have only a slight decrease. Tretinoin 145-158 alcohol dehydrogenase 1 (class I) Mus musculus 93-97
12207051-11 2002 The function of TNF alpha, IGIF/IL-18 and MIF in all-trans-retinoic acid-treated cells during ES differentiation and apoptosis is still speculatory. Tretinoin 59-72 tumor necrosis factor Mus musculus 16-25
12207051-11 2002 The function of TNF alpha, IGIF/IL-18 and MIF in all-trans-retinoic acid-treated cells during ES differentiation and apoptosis is still speculatory. Tretinoin 59-72 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 42-45
11960350-6 2002 Pretreatment of cells with 5 microM of the MEK-1/-2-specific inhibitor U0126 abrogated PMA- or RA-induced activation of ERK-1/MAPK and ERK-2/MAPK. Tretinoin 95-97 mitogen-activated protein kinase 3 Homo sapiens 120-125
11960350-6 2002 Pretreatment of cells with 5 microM of the MEK-1/-2-specific inhibitor U0126 abrogated PMA- or RA-induced activation of ERK-1/MAPK and ERK-2/MAPK. Tretinoin 95-97 mitogen-activated protein kinase 1 Homo sapiens 135-140
11912557-5 2002 The sensitivity to RA was variable by the amount of CYP26, and the rapid catabolism by CYP26 made AMC-HN-6 resistant to RA in vitro. Tretinoin 19-21 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 52-57
11912557-5 2002 The sensitivity to RA was variable by the amount of CYP26, and the rapid catabolism by CYP26 made AMC-HN-6 resistant to RA in vitro. Tretinoin 120-122 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 87-92
11912557-7 2002 Conclusively, the CYP26 activity might be one essential factor for the RA sensitivity, but in cells showing induction of CYP26, the RA sensitivity is inversely related to the rate of RA catabolism. Tretinoin 71-73 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 18-23
11912557-7 2002 Conclusively, the CYP26 activity might be one essential factor for the RA sensitivity, but in cells showing induction of CYP26, the RA sensitivity is inversely related to the rate of RA catabolism. Tretinoin 132-134 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 121-126
11912557-7 2002 Conclusively, the CYP26 activity might be one essential factor for the RA sensitivity, but in cells showing induction of CYP26, the RA sensitivity is inversely related to the rate of RA catabolism. Tretinoin 132-134 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 121-126
11912557-2 2002 The aim of this study was to confirm if retinoic acid 4-hydroxylase (CYP26) is a P450 induced by RA and to investigate the role of cellular RA binding proteins (CRABPs), using a slow catabolizer, AMC-HN-4, and a rapid catabolizer, AMC-HN-6. Tretinoin 97-99 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-67
11912557-2 2002 The aim of this study was to confirm if retinoic acid 4-hydroxylase (CYP26) is a P450 induced by RA and to investigate the role of cellular RA binding proteins (CRABPs), using a slow catabolizer, AMC-HN-4, and a rapid catabolizer, AMC-HN-6. Tretinoin 97-99 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 69-74
11788605-2 2002 We found that ATRA induced the 4-fold elevation of acid sphingomyelinase (ASMase) activity 24 h after treatment in NB4 cells, but not in NB4/RA cells. Tretinoin 14-18 sphingomyelin phosphodiesterase 1 Homo sapiens 51-72
12039073-1 2002 It was shown previously that hNIS mRNA expression is stimulated by retinoic acid (RA) in human follicular thyroid carcinoma cell lines FTC-133 and FTC-238, and patients with thyroid carcinomas lacking iodide uptake respond to RA treatment with increased radioiodide transport. Tretinoin 67-80 solute carrier family 5 member 5 Homo sapiens 29-33
12039073-1 2002 It was shown previously that hNIS mRNA expression is stimulated by retinoic acid (RA) in human follicular thyroid carcinoma cell lines FTC-133 and FTC-238, and patients with thyroid carcinomas lacking iodide uptake respond to RA treatment with increased radioiodide transport. Tretinoin 82-84 solute carrier family 5 member 5 Homo sapiens 29-33
12039073-1 2002 It was shown previously that hNIS mRNA expression is stimulated by retinoic acid (RA) in human follicular thyroid carcinoma cell lines FTC-133 and FTC-238, and patients with thyroid carcinomas lacking iodide uptake respond to RA treatment with increased radioiodide transport. Tretinoin 226-228 solute carrier family 5 member 5 Homo sapiens 29-33
12039073-2 2002 Here, in transient transfection experiments using FTC-238 cells, hNIS promoter/luciferase reporter constructs showed an up to 2.5-fold increase in transcriptional activity after incubation with 1 microM RA. Tretinoin 203-205 solute carrier family 5 member 5 Homo sapiens 65-69
12039073-7 2002 Thus, RA redifferentiation of advanced thyroid carcinomas may reinduce iodide uptake by stimulating hNIS expression and thereby make tumours accessible for radioiodide therapy again. Tretinoin 6-8 solute carrier family 5 member 5 Homo sapiens 100-104
12165291-3 2002 We investigated patients with APL receiving all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)) treatment, contributing to the downregulation of the expression of annexin II on APL cells, and decreasing the generation of plasmin by tissue plasminogen activator (t-PA). Tretinoin 44-67 plasminogen activator, tissue type Homo sapiens 243-277
12165291-3 2002 We investigated patients with APL receiving all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)) treatment, contributing to the downregulation of the expression of annexin II on APL cells, and decreasing the generation of plasmin by tissue plasminogen activator (t-PA). Tretinoin 69-73 plasminogen activator, tissue type Homo sapiens 243-277
11788590-5 2002 Interleukin 6 and interleukin 11, known to activate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at least partially mediated through interactions between STAT3 and retinoid nuclear receptor enhanceosome proteins in pulmonary epithelial cells. Tretinoin 118-131 interleukin 6 Homo sapiens 0-13
11788590-5 2002 Interleukin 6 and interleukin 11, known to activate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at least partially mediated through interactions between STAT3 and retinoid nuclear receptor enhanceosome proteins in pulmonary epithelial cells. Tretinoin 118-131 signal transducer and activator of transcription 3 Homo sapiens 52-57
11788590-5 2002 Interleukin 6 and interleukin 11, known to activate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at least partially mediated through interactions between STAT3 and retinoid nuclear receptor enhanceosome proteins in pulmonary epithelial cells. Tretinoin 118-131 signal transducer and activator of transcription 3 Homo sapiens 199-204
11948401-9 2002 The transcriptional activities of full-length JunB and full-length Fra-1, but not the transactivation domain fusions, were increased by TPA treatment and suppressed by RA. Tretinoin 168-170 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-50
11948401-10 2002 Since these full-length fusions have bzip domains, the results suggest that JunB and/or Fra-1-containing dimers may constitute one target of RA for transrepression of AP-1. Tretinoin 141-143 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 76-80
11788605-2 2002 We found that ATRA induced the 4-fold elevation of acid sphingomyelinase (ASMase) activity 24 h after treatment in NB4 cells, but not in NB4/RA cells. Tretinoin 14-18 sphingomyelin phosphodiesterase 1 Homo sapiens 74-80
11788605-4 2002 Upon treatment with ATRA, ceramide, the product of an ASMase reaction, accumulated in NB4 cells. Tretinoin 20-24 sphingomyelin phosphodiesterase 1 Homo sapiens 54-60
11788605-5 2002 Northern blot analysis showed a marked elevation of the ASMase mRNA 8 h after ATRA treatment, reaching a plateau at 24 h. Regulation of ASMase gene expression was studied by a promoter analysis using luciferase reporter assay. Tretinoin 78-82 sphingomyelin phosphodiesterase 1 Homo sapiens 56-62
11788605-5 2002 Northern blot analysis showed a marked elevation of the ASMase mRNA 8 h after ATRA treatment, reaching a plateau at 24 h. Regulation of ASMase gene expression was studied by a promoter analysis using luciferase reporter assay. Tretinoin 78-82 sphingomyelin phosphodiesterase 1 Homo sapiens 136-142
11877298-3 2002 In this study, we show that the onset of ATRA-induced G(0)/G(1) arrest of human monoblastic U-937 cells is linked to a sharp down-regulation of c-Myc and cyclin E levels and an increase in p21(WAF1/CIP1) expression. Tretinoin 41-45 cyclin dependent kinase inhibitor 1A Homo sapiens 189-192
11877298-3 2002 In this study, we show that the onset of ATRA-induced G(0)/G(1) arrest of human monoblastic U-937 cells is linked to a sharp down-regulation of c-Myc and cyclin E levels and an increase in p21(WAF1/CIP1) expression. Tretinoin 41-45 cyclin dependent kinase inhibitor 1A Homo sapiens 193-197
11877298-3 2002 In this study, we show that the onset of ATRA-induced G(0)/G(1) arrest of human monoblastic U-937 cells is linked to a sharp down-regulation of c-Myc and cyclin E levels and an increase in p21(WAF1/CIP1) expression. Tretinoin 41-45 cyclin dependent kinase inhibitor 1A Homo sapiens 198-202
12894880-1 2002 OBJECTIVE: To illuminate the regulating effect of all-trans retinoic acid (ATRA) on gap junctional intercellular communication (GJIC) and connexin 43 (Cx43) gene expression in glioma cells, which is tissue- and organ-specific. Tretinoin 54-73 gap junction protein, alpha 1 Rattus norvegicus 138-149
12014653-1 2002 BACKGROUND: The retinoid-inducible gene I (RIG1), belonging to the family of type II tumor suppressor genes, was isolated from human gastric cancer cells treated with all-trans retinoic acid. Tretinoin 177-190 phospholipase A and acyltransferase 4 Homo sapiens 43-47
12894880-1 2002 OBJECTIVE: To illuminate the regulating effect of all-trans retinoic acid (ATRA) on gap junctional intercellular communication (GJIC) and connexin 43 (Cx43) gene expression in glioma cells, which is tissue- and organ-specific. Tretinoin 75-79 gap junction protein, alpha 1 Rattus norvegicus 138-149
12894880-3 2002 The effect of ATRA on Cx43 gene expression was measured with semiquantitative reverse transcription polymerase chain reaction (RT-PCR) 24 hours after ATRA exposure. Tretinoin 14-18 gap junction protein, alpha 1 Rattus norvegicus 22-26
11739380-7 2002 Interestingly, the survival of the neuroblastoma cells treated with retinoic acid was partly dependent on the expression of RAGE, and inhibition of RAGE function partially blocked the increase in anti-apoptotic protein Bcl-2 following retinoic acid treatment. Tretinoin 68-81 BCL2 apoptosis regulator Homo sapiens 219-224
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 BCL2 apoptosis regulator Homo sapiens 293-298
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 interleukin 6 Homo sapiens 114-127
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 interleukin 6 Homo sapiens 129-133
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 interleukin 6 Homo sapiens 135-139
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 interleukin 6 receptor Homo sapiens 150-155
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 cyclin dependent kinase inhibitor 1A Homo sapiens 195-198
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 cyclin dependent kinase inhibitor 1A Homo sapiens 199-203
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 BCL2 apoptosis regulator Homo sapiens 293-298
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 interleukin 6 Homo sapiens 114-127
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 interleukin 6 Homo sapiens 129-133
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 interleukin 6 Homo sapiens 135-139
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 interleukin 6 receptor Homo sapiens 150-155
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 cyclin dependent kinase inhibitor 1A Homo sapiens 195-198
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 cyclin dependent kinase inhibitor 1A Homo sapiens 199-203
11739380-7 2002 Interestingly, the survival of the neuroblastoma cells treated with retinoic acid was partly dependent on the expression of RAGE, and inhibition of RAGE function partially blocked the increase in anti-apoptotic protein Bcl-2 following retinoic acid treatment. Tretinoin 235-248 BCL2 apoptosis regulator Homo sapiens 219-224
11891779-0 2002 Retinoic acid increases proliferation rate of GL-15 glioma cells, involving activation of STAT-3 transcription factor. Tretinoin 0-13 signal transducer and activator of transcription 3 Homo sapiens 90-96
12058867-1 2002 Our previous studies demonstrated retinoic acid (RA) inhibition of activation protein-1 (AP-1) formation in TNF-alpha-treated osteoblastic MC3T3-E1 cells via c-fos suppression. Tretinoin 34-47 tumor necrosis factor Mus musculus 108-117
12058867-8 2002 The present study suggests a regulatory interference by 1alpha25(OH)2D3 for RA inhibition of TNF-alpha-induced AP-1 activity in osteoblasts. Tretinoin 76-78 tumor necrosis factor Mus musculus 93-102
12058867-1 2002 Our previous studies demonstrated retinoic acid (RA) inhibition of activation protein-1 (AP-1) formation in TNF-alpha-treated osteoblastic MC3T3-E1 cells via c-fos suppression. Tretinoin 49-51 tumor necrosis factor Mus musculus 108-117
12058867-2 2002 In the present study, we observed that 1alpha25(OH)2D3 was able to interfere at the transcriptional level with RA inhibition of TNF-alpha-induced c-fos gene expression in cells when the cells were incubated with the vitamin for 24 hr before the RA treatment. Tretinoin 111-113 tumor necrosis factor Mus musculus 128-137
12058867-2 2002 In the present study, we observed that 1alpha25(OH)2D3 was able to interfere at the transcriptional level with RA inhibition of TNF-alpha-induced c-fos gene expression in cells when the cells were incubated with the vitamin for 24 hr before the RA treatment. Tretinoin 245-247 tumor necrosis factor Mus musculus 128-137
11802792-0 2002 Retinoic acid activation of the ERK pathway is required for embryonic stem cell commitment into the adipocyte lineage. Tretinoin 0-13 mitogen-activated protein kinase 1 Mus musculus 32-35
11927016-7 2002 Both ATRA and 5-FU activated c-Jun N-terminal kinase (JNK) 1 and the combination of both agents resulted in additive or synergistic activation of JNK1, and also enhanced the induction of apoptosis. Tretinoin 5-9 mitogen-activated protein kinase 8 Homo sapiens 146-150
11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Tretinoin 208-212 epidermal growth factor receptor Homo sapiens 33-65
11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Tretinoin 208-212 epidermal growth factor receptor Homo sapiens 67-71
11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Tretinoin 208-212 signal transducer and activator of transcription 3 Homo sapiens 73-123
11927016-8 2002 The YCU-H891 cells, in which the epidermal growth factor receptor (EGFR)-signal transducer and activator of transcription 3 (Stat3) pathway is constitutively activated, were more resistant to treatments with ATRA, 5-FU and the combination of both agents than YCU-N861 cells. Tretinoin 208-212 signal transducer and activator of transcription 3 Homo sapiens 125-130
11802792-6 2002 Furthermore, we show that ERK activation is required only during RA treatment. Tretinoin 65-67 mitogen-activated protein kinase 1 Mus musculus 26-29
11927016-0 2002 The roles of JNK1 and Stat3 in the response of head and neck cancer cell lines to combined treatment with all-trans-retinoic acid and 5-fluorouracil. Tretinoin 106-129 mitogen-activated protein kinase 8 Homo sapiens 13-17
11927016-0 2002 The roles of JNK1 and Stat3 in the response of head and neck cancer cell lines to combined treatment with all-trans-retinoic acid and 5-fluorouracil. Tretinoin 106-129 signal transducer and activator of transcription 3 Homo sapiens 22-27
11927016-6 2002 With YCU-N861 cells, ATRA also caused a decrease in Bcl-2 and Bcl-X(L) and an increase in Bax. Tretinoin 21-25 BCL2 apoptosis regulator Homo sapiens 52-57
11927016-6 2002 With YCU-N861 cells, ATRA also caused a decrease in Bcl-2 and Bcl-X(L) and an increase in Bax. Tretinoin 21-25 BCL2 like 1 Homo sapiens 62-70
11927016-6 2002 With YCU-N861 cells, ATRA also caused a decrease in Bcl-2 and Bcl-X(L) and an increase in Bax. Tretinoin 21-25 BCL2 associated X, apoptosis regulator Homo sapiens 90-93
11927016-7 2002 Both ATRA and 5-FU activated c-Jun N-terminal kinase (JNK) 1 and the combination of both agents resulted in additive or synergistic activation of JNK1, and also enhanced the induction of apoptosis. Tretinoin 5-9 mitogen-activated protein kinase 8 Homo sapiens 29-60
11804877-0 2002 Stimulation of vascular endothelial growth factor gene transcription by all trans retinoic acid through Sp1 and Sp3 sites in human bronchioloalveolar carcinoma cells. Tretinoin 82-95 vascular endothelial growth factor A Homo sapiens 15-49
11804877-0 2002 Stimulation of vascular endothelial growth factor gene transcription by all trans retinoic acid through Sp1 and Sp3 sites in human bronchioloalveolar carcinoma cells. Tretinoin 82-95 Sp3 transcription factor Homo sapiens 112-115
11804963-11 2002 It is likely that PGDS, which has a structure similar to that of lipocalin, functions as a lipophilic carrier protein, because we have shown that epididymal PGDS binds retinoic acid and testosterone in vitro. Tretinoin 168-181 prostaglandin D2 synthase Homo sapiens 18-22
11802792-4 2002 Treatment of ES cell-derived embryoid bodies with RA resulted in a prolonged activation of the ERK pathway, but not the c-Jun N-terminal kinase, p38 mitogen-activated protein kinase or phosphoinositide 3-kinase pathways. Tretinoin 50-52 mitogen-activated protein kinase 1 Mus musculus 95-98
11802792-5 2002 To investigate the role of ERK activation, co-treatment of RA with PD98059, a specific inhibitor of the ERK signalling pathway, prevented both adipocyte formation and expression of the adipogenic markers, adipocyte lipid-binding protein and peroxisome-proliferator-activated receptor gamma. Tretinoin 59-61 mitogen-activated protein kinase 1 Mus musculus 27-30
11802792-5 2002 To investigate the role of ERK activation, co-treatment of RA with PD98059, a specific inhibitor of the ERK signalling pathway, prevented both adipocyte formation and expression of the adipogenic markers, adipocyte lipid-binding protein and peroxisome-proliferator-activated receptor gamma. Tretinoin 59-61 mitogen-activated protein kinase 1 Mus musculus 104-107
11792692-0 2002 Retinoic acids repress constitutive active receptor-mediated induction by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene of the CYP2B10 gene in mouse primary hepatocytes. Tretinoin 0-14 cytochrome P450, family 2, subfamily b, polypeptide 10 Mus musculus 124-131
11792692-4 2002 Both retinoic acids also repressed TCPOBOP-induced NR1 enhancer activity in both transfected hepatocytes and HepG2 cells. Tretinoin 5-19 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 51-54
11836298-0 2002 Divergent effects of retinoic acids on the expression of ERalpha and 17beta-hydroxysteroid dehydrogenase type 2 in endometrial carcinoma cells (RL 95-2). Tretinoin 21-35 estrogen receptor 1 Homo sapiens 57-64
11788904-4 2002 WNT3 and WNT3A mRNAs were co-expressed in an embryonal carcinoma cell line NT2, which is reported to differentiate into postmitotic CNS neurons by treatment with retinoic acid for two weeks. Tretinoin 162-175 Wnt family member 3 Homo sapiens 0-4
11807825-10 2002 We further show that RA specifically upregulates expression of osteocalcin via activation of BMP-7 mRNA and protein in vitro. Tretinoin 21-23 bone gamma-carboxyglutamate protein Homo sapiens 63-74
11786923-3 2002 WNT14B gene is clustered with WNT3 gene in human chromosome 17q21, and mRNA expression of WNT14B is significantly up-regulated by retinoic acid during the early phase of neuronal differentiation in human NT2 cells. Tretinoin 130-143 Wnt family member 9B Homo sapiens 0-6
11786923-3 2002 WNT14B gene is clustered with WNT3 gene in human chromosome 17q21, and mRNA expression of WNT14B is significantly up-regulated by retinoic acid during the early phase of neuronal differentiation in human NT2 cells. Tretinoin 130-143 Wnt family member 9B Homo sapiens 90-96
11842302-7 2002 Similarly, ATRA (10(-6) mol/L) inhibited eosinophil-basophil differentiation of cord blood CD34(+) cells in liquid culture, whereas neutrophil differentiation proceeded without impediment. Tretinoin 11-15 CD34 molecule Homo sapiens 91-95
11842302-8 2002 Most importantly, these effects of ATRA (10(-8) to 10(-6) mol/L) on CD34(+) cells were associated with a dose-dependent inhibition of IL-5Ralpha but no change in GM-CSF receptor expression, as detected with flow cytometry. Tretinoin 35-39 CD34 molecule Homo sapiens 68-72
11777343-5 2002 All-trans-retinoic acid (ATRA) treatment of HPV-immortalized HEN-16-2 cells and transformed/MDR HEN-16-2/CDDP cells inhibited telomerase activity and downregulated expression of hTERT mRNAs containing full-length functional and a defective RT motif, but there were no changes in hTR and TP1 expression. Tretinoin 0-23 telomerase RNA component Homo sapiens 279-282
11777343-5 2002 All-trans-retinoic acid (ATRA) treatment of HPV-immortalized HEN-16-2 cells and transformed/MDR HEN-16-2/CDDP cells inhibited telomerase activity and downregulated expression of hTERT mRNAs containing full-length functional and a defective RT motif, but there were no changes in hTR and TP1 expression. Tretinoin 25-29 telomerase RNA component Homo sapiens 279-282
11841795-10 2002 RAR-beta was induced in a dose-dependent manner in SH SY 5Y cells following incubation with ATRA, whereas a weaker and delayed induction was observed with 13-cis RA. Tretinoin 92-96 retinoic acid receptor beta Homo sapiens 0-8
11853001-8 2002 This study demonstrates that: (1) both RA and DEX can inhibit cell growth and induce morphologic and functional differentiation of HOS-8603 cells; (2) telomerase is an enzyme system regulated during induced differentiation of HOS-8603 cells; (3) significantly decreased telomerase activity may be an indicator of differentiation but does not parallel the expression level of hTR; and (4) the regulation of telomerase is directly linked to cell differentiation not cell cycle. Tretinoin 39-41 telomerase RNA component Homo sapiens 375-378
11841792-0 2002 Matrix and serine protease expression during leukemic cell differentiation induced by aclacinomycin and all-trans-retinoic acid. Tretinoin 104-127 coagulation factor II, thrombin Homo sapiens 11-26
11841792-7 2002 Use of Batimastat and aprotinin suggests that ATRA was active by modulating the uPA system while ACLA interfered with MMP expression. Tretinoin 46-50 plasminogen activator, urokinase Homo sapiens 80-83
12053118-7 2002 The anti-apoptotic effect of RA is mediated by both nuclear receptor dependent and nuclear receptor independent mechanisms and is, at least in part, mediated by induction of mitogen-activated protein kinase phosphatase 1. Tretinoin 29-31 dual specificity phosphatase 1 Homo sapiens 174-220
11801540-6 2002 RA effects on epidermal growth factor (EGF) induction of EGFR-phosphotyrosine levels, cyclin D1 expression and mitogenesis were examined in BEAS-2B cells. Tretinoin 0-2 epidermal growth factor receptor Homo sapiens 57-61
11801540-8 2002 RA treatment repressed EGFR expression and reporter plasmid activity in these cells. Tretinoin 0-2 epidermal growth factor receptor Homo sapiens 23-27
11801540-11 2002 Notably, RA treatment prevented transformation as well as outgrowth of EGFR overexpressing bronchial epithelial cells, despite NNK exposure. Tretinoin 9-11 epidermal growth factor receptor Homo sapiens 71-75
12622418-4 2002 A variety of extracellular regulators including TGFbeta, retinoic acid and butyrate stimulate ZBP-89 gene expression. Tretinoin 57-70 zinc finger protein 148 Homo sapiens 94-100
12203032-9 2002 Several cDNAs representing genes with previously unrecognized RA responsiveness were identified by this comparison, including the receptor for bone morphogenetic proteins 2 and 4 (Bmp2/Bmp4) and hemoglobin Y. Tretinoin 62-64 bone morphogenetic protein 2 Mus musculus 143-178
12244570-9 2002 We find that RA strongly suppresses Ihh, but enhances expression of Shh in this system. Tretinoin 13-15 indian hedgehog Gallus gallus 36-39
12203032-9 2002 Several cDNAs representing genes with previously unrecognized RA responsiveness were identified by this comparison, including the receptor for bone morphogenetic proteins 2 and 4 (Bmp2/Bmp4) and hemoglobin Y. Tretinoin 62-64 bone morphogenetic protein 2 Mus musculus 180-184
12203032-9 2002 Several cDNAs representing genes with previously unrecognized RA responsiveness were identified by this comparison, including the receptor for bone morphogenetic proteins 2 and 4 (Bmp2/Bmp4) and hemoglobin Y. Tretinoin 62-64 bone morphogenetic protein 4 Mus musculus 185-189
12397600-9 2002 On the other hand, okadaic acid (310 nM) and all trans-retinoic acid (1 micro M) significantly increased (3)H-MPP(+) uptake and inhibited ecto-ALP activity. Tretinoin 49-68 alkaline phosphatase, placental Homo sapiens 143-146
12025892-2 2002 Because ATRA has effects (increase in apoptosis, suppression of bcl-2), it has also been used for the treatment of other French-American-British (FAB) subtypes of acute myelogenous leukemia (AML). Tretinoin 8-12 BCL2 apoptosis regulator Homo sapiens 64-69
11851873-0 2002 All-trans retinoic acid induces differentiation and apoptosis of murine melanocyte precursors with induction of the microphthalmia-associated transcription factor. Tretinoin 10-23 melanogenesis associated transcription factor Mus musculus 116-162
11851873-7 2002 Reverse transcription polymerase chain reaction analysis revealed a marked increase in expression of microphthalmia-associated transcription factor mRNA after all-trans retinoic acid treatment, suggesting that microphthalmia-associated transcription factor may be the key molecule in this event. Tretinoin 169-182 melanogenesis associated transcription factor Mus musculus 101-147
11851873-7 2002 Reverse transcription polymerase chain reaction analysis revealed a marked increase in expression of microphthalmia-associated transcription factor mRNA after all-trans retinoic acid treatment, suggesting that microphthalmia-associated transcription factor may be the key molecule in this event. Tretinoin 169-182 melanogenesis associated transcription factor Mus musculus 210-256
11851873-11 2002 All-trans retinoic acid upregulated caspase-3 and downregulated bcl-2. Tretinoin 10-23 B cell leukemia/lymphoma 2 Mus musculus 64-69
11734301-0 2002 Augmented expression of P-gp/multi-drug resistance gene by all-trans retinoic acid in monocytic leukemic cells. Tretinoin 69-82 ATP binding cassette subfamily B member 1 Homo sapiens 24-28
11734301-13 2002 However, P-gp/MDR1 expression augmented by ATRA, which was observed in monocytic AML, was recognized as a functional molecule of mature monocyte/macrophage, because CD34 expression decreased and CD13 expression increased by ATRA. Tretinoin 43-47 ATP binding cassette subfamily B member 1 Homo sapiens 9-13
11734301-13 2002 However, P-gp/MDR1 expression augmented by ATRA, which was observed in monocytic AML, was recognized as a functional molecule of mature monocyte/macrophage, because CD34 expression decreased and CD13 expression increased by ATRA. Tretinoin 43-47 ATP binding cassette subfamily B member 1 Homo sapiens 14-18
11734301-13 2002 However, P-gp/MDR1 expression augmented by ATRA, which was observed in monocytic AML, was recognized as a functional molecule of mature monocyte/macrophage, because CD34 expression decreased and CD13 expression increased by ATRA. Tretinoin 43-47 CD34 molecule Homo sapiens 165-169
11786372-0 2002 Retinoic acids promote the action of aromatase and 17beta-hydroxysteroid dehydrogenase type 1 on the biosynthesis of 17beta-estradiol in placental cells. Tretinoin 0-14 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 51-93
11786372-3 2002 In the present study, the effects of retinoic acids (RAs) on P450arom and 17HSD1 expression in placental cells were investigated. Tretinoin 37-51 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 61-69
11744377-1 2002 Three retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3), which catalyze the oxidation of retinaldehyde into retinoic acid, have been shown to be differentially expressed during early embryogenesis. Tretinoin 115-128 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 55-61
11744378-0 2002 Differential expression of the retinoic acid-metabolizing enzymes CYP26A1 and CYP26B1 during murine organogenesis. Tretinoin 31-44 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 78-85
11744378-1 2002 We recently cloned the murine homologue of Cyp26B1, a novel retinoic acid (RA)-metabolizing enzyme and showed that its gene expression pattern is unique from that of Cyp26A1 during early embryogenesis. Tretinoin 60-73 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 43-50
11744378-1 2002 We recently cloned the murine homologue of Cyp26B1, a novel retinoic acid (RA)-metabolizing enzyme and showed that its gene expression pattern is unique from that of Cyp26A1 during early embryogenesis. Tretinoin 75-77 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 43-50
11744378-8 2002 In addition, Cyp26B1 was expressed at specific levels of the differentiating upper and lower thoracic spinal cord, adjacent to the cervical and lumbar regions that express the RA-synthesizing enzyme RALDH-2. Tretinoin 176-178 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 13-20
12025892-10 2002 Logistic regression analysis revealed that ATRA administration was the important factor in CR, among other potential factors including age, white blood count, bcl-2 expression, and the uptake and efflux of Rh123 (p = 0.05). Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 159-164
11746830-0 2001 Decreased mitogenic response to epidermal growth factor in human squamous cell carcinoma lines overexpressing epidermal growth factor receptor owing to limiting amounts of the adaptor protein Grb2: rescue by retinoic acid treatment. Tretinoin 208-221 epidermal growth factor receptor Homo sapiens 110-142
11748484-0 2002 Retinoic acid inhibits fibronectin and laminin synthesis and cell migration of human pleural mesothelioma in vitro. Tretinoin 0-13 fibronectin 1 Homo sapiens 23-34
11730831-0 2001 Retinoic acid suppresses endothelin-1 gene expression at the transcription level in endothelial cells. Tretinoin 0-13 endothelin 1 Homo sapiens 25-37
11730831-4 2001 All-trans retinoic acid (ATRA) suppressed ET-1 mRNA expression in cultured endothelial cells. Tretinoin 0-23 endothelin 1 Homo sapiens 42-46
11730831-4 2001 All-trans retinoic acid (ATRA) suppressed ET-1 mRNA expression in cultured endothelial cells. Tretinoin 25-29 endothelin 1 Homo sapiens 42-46
11748135-5 2001 As we demonstrate that the repression of Otx2 by retinoic acid is dependent on an induction of Gbx2 in the anterior brain, molecules other than retinoic acid must regulate the initial expression of Otx2 in vivo. Tretinoin 49-62 gastrulation brain homeobox 2 Mus musculus 95-99
11750096-9 2001 Despite an enhanced tendency to accumulate in G(0)/G(1), p16(INK4A)-overexpressing cells were less sensitive to induction of differentiation with vitamin D(3) or ATRA than control cells. Tretinoin 162-166 cyclin dependent kinase inhibitor 2A Homo sapiens 57-60
11750096-9 2001 Despite an enhanced tendency to accumulate in G(0)/G(1), p16(INK4A)-overexpressing cells were less sensitive to induction of differentiation with vitamin D(3) or ATRA than control cells. Tretinoin 162-166 cyclin dependent kinase inhibitor 2A Homo sapiens 61-66
11831438-0 2001 Effects of all-trans-retinoic acid (atRA) on inducible nitric oxide synthase (iNOS) activity and transforming growth factor beta-1 production in experimental anti-GBM antibody-mediated glomerulonephritis. Tretinoin 36-40 nitric oxide synthase 2 Rattus norvegicus 45-76
11831438-3 2001 The present study employed all-trans retinoic acid (atRA) which is known to have anti-inflammatory effects and to modulate expression of iNOS and TGF-beta1, in order to explore its effect on iNOS enzyme activity and TGF-beta1 production in anti-GBM antibody induced glomerulonephritis. Tretinoin 37-50 nitric oxide synthase 2 Rattus norvegicus 137-141
11831438-3 2001 The present study employed all-trans retinoic acid (atRA) which is known to have anti-inflammatory effects and to modulate expression of iNOS and TGF-beta1, in order to explore its effect on iNOS enzyme activity and TGF-beta1 production in anti-GBM antibody induced glomerulonephritis. Tretinoin 37-50 transforming growth factor, beta 1 Rattus norvegicus 146-155
11831438-3 2001 The present study employed all-trans retinoic acid (atRA) which is known to have anti-inflammatory effects and to modulate expression of iNOS and TGF-beta1, in order to explore its effect on iNOS enzyme activity and TGF-beta1 production in anti-GBM antibody induced glomerulonephritis. Tretinoin 52-56 nitric oxide synthase 2 Rattus norvegicus 137-141
11831438-3 2001 The present study employed all-trans retinoic acid (atRA) which is known to have anti-inflammatory effects and to modulate expression of iNOS and TGF-beta1, in order to explore its effect on iNOS enzyme activity and TGF-beta1 production in anti-GBM antibody induced glomerulonephritis. Tretinoin 52-56 transforming growth factor, beta 1 Rattus norvegicus 146-155
11831438-3 2001 The present study employed all-trans retinoic acid (atRA) which is known to have anti-inflammatory effects and to modulate expression of iNOS and TGF-beta1, in order to explore its effect on iNOS enzyme activity and TGF-beta1 production in anti-GBM antibody induced glomerulonephritis. Tretinoin 52-56 nitric oxide synthase 2 Rattus norvegicus 191-195
11831438-10 2001 Glomerular iNOS activity in atRA treated nephritic animals was attenuated in comparison to that in nephritic controls that were not. Tretinoin 28-32 nitric oxide synthase 2 Rattus norvegicus 11-15
11831438-12 2001 Levels of TGF-beta1 were increased in glomeruli of atRA treated nephritic animals. Tretinoin 51-55 transforming growth factor, beta 1 Rattus norvegicus 10-19
11831438-16 2001 The failure of atRA treatment to reduce proteinuria could be due to the increase in TGF-beta1 levels and to inhibition of iNOS-driven NO production. Tretinoin 15-19 transforming growth factor, beta 1 Rattus norvegicus 84-93
11831438-16 2001 The failure of atRA treatment to reduce proteinuria could be due to the increase in TGF-beta1 levels and to inhibition of iNOS-driven NO production. Tretinoin 15-19 nitric oxide synthase 2 Rattus norvegicus 122-126
12865629-11 2002 Retinoic acid induces osteoblastic differentiation, i.e. osteocalcin expression and alkaline phosphatase production. Tretinoin 0-13 bone gamma-carboxyglutamate protein Homo sapiens 57-68
11795492-6 2001 Pretreatment of JNK specific inhibitors, curcumin and all trans-retinoic acid, decreased the basal motility of DAR-ECV cells in a dose-dependent manner. Tretinoin 58-77 mitogen-activated protein kinase 8 Homo sapiens 16-19
11748248-3 2001 We have found that all-trans retinoic acid (RA), which usually downregulates MMPs, strongly induces collagenase-3 expression in cultures of embryonic metatarsal cartilage rudiments and in chondrocytic cells. Tretinoin 29-42 matrix metallopeptidase 13 Homo sapiens 77-81
11748248-3 2001 We have found that all-trans retinoic acid (RA), which usually downregulates MMPs, strongly induces collagenase-3 expression in cultures of embryonic metatarsal cartilage rudiments and in chondrocytic cells. Tretinoin 29-42 matrix metallopeptidase 13 Homo sapiens 100-113
11748248-3 2001 We have found that all-trans retinoic acid (RA), which usually downregulates MMPs, strongly induces collagenase-3 expression in cultures of embryonic metatarsal cartilage rudiments and in chondrocytic cells. Tretinoin 44-46 matrix metallopeptidase 13 Homo sapiens 77-81
11748248-3 2001 We have found that all-trans retinoic acid (RA), which usually downregulates MMPs, strongly induces collagenase-3 expression in cultures of embryonic metatarsal cartilage rudiments and in chondrocytic cells. Tretinoin 44-46 matrix metallopeptidase 13 Homo sapiens 100-113
11748248-5 2001 Analysis of the signal transduction mechanisms underlying the upregulating effect of RA on collagenase-3 expression demonstrated that this factor acts through a signaling pathway involving p38 mitogen-activated protein kinase. Tretinoin 85-87 matrix metallopeptidase 13 Homo sapiens 91-104
11748248-6 2001 RA treatment of chondrocytic cells also induces the production of MT1-MMP, a membrane-bound metalloproteinase essential for skeletal formation, which participates in a proteolytic cascade with collagenase-3. Tretinoin 0-2 matrix metallopeptidase 13 Homo sapiens 193-206
11748248-7 2001 The production of these MMPs is concomitant with the development of an RA-induced differentiation program characterized by formation of a mineralized bone matrix, downregulation of chondrocyte markers like type II collagen, and upregulation of osteoblastic markers such as osteocalcin. Tretinoin 71-73 matrix metallopeptidase 13 Homo sapiens 24-28
11748248-7 2001 The production of these MMPs is concomitant with the development of an RA-induced differentiation program characterized by formation of a mineralized bone matrix, downregulation of chondrocyte markers like type II collagen, and upregulation of osteoblastic markers such as osteocalcin. Tretinoin 71-73 bone gamma-carboxyglutamate protein Homo sapiens 273-284
11748248-9 2001 RA treatment also resulted in the upregulation of Cbfa1, a transcription factor responsible for collagenase-3 and osteocalcin induction in osteoblastic cells. Tretinoin 0-2 RUNX family transcription factor 2 Homo sapiens 50-55
11748248-9 2001 RA treatment also resulted in the upregulation of Cbfa1, a transcription factor responsible for collagenase-3 and osteocalcin induction in osteoblastic cells. Tretinoin 0-2 matrix metallopeptidase 13 Homo sapiens 96-109
11748248-9 2001 RA treatment also resulted in the upregulation of Cbfa1, a transcription factor responsible for collagenase-3 and osteocalcin induction in osteoblastic cells. Tretinoin 0-2 bone gamma-carboxyglutamate protein Homo sapiens 114-125
11766909-4 2001 RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA. Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 56-61
11766909-4 2001 RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA. Tretinoin 98-100 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 56-61
11766909-4 2001 RA also induces the expression in liver of the mRNA for CYP26, the enzyme that disposes of excess RA by oxidizing RA to 4-oxo-RA. Tretinoin 98-100 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 56-61
11746830-0 2001 Decreased mitogenic response to epidermal growth factor in human squamous cell carcinoma lines overexpressing epidermal growth factor receptor owing to limiting amounts of the adaptor protein Grb2: rescue by retinoic acid treatment. Tretinoin 208-221 growth factor receptor bound protein 2 Homo sapiens 192-196
11746830-9 2001 RA inhibited expression of EGFR and proteins in the MAPK signaling pathway. Tretinoin 0-2 epidermal growth factor receptor Homo sapiens 27-31
11733135-8 2001 Most notably, AhR, HNF-3 and N-Oct3 have already been shown to respond to RA treatment of EC cells, while E47, HNF-3, MAZ, N-Oct3 and Pit-1a have been implicated in embryonic, muscle or neural development. Tretinoin 74-76 POU class 3 homeobox 2 Homo sapiens 29-35
11698455-3 2001 In retinoic acid-differentiated HL-60 cells, cross-linking of FcgammaRs resulted in a marked increase in the tyrosine phosphorylation of FcgammaRIIa, p58(lyn), and p120(c-cbl), which was inhibited by a specific inhibitor of Src family protein tyrosine kinases. Tretinoin 3-16 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 154-157
11753676-4 2001 However, RA sensitive CA-OV3 cells expressed higher levels of p53, p27, p21, and p16 compared to RA resistant SK-OV3 cells. Tretinoin 9-11 tumor protein p53 Homo sapiens 62-65
11753676-4 2001 However, RA sensitive CA-OV3 cells expressed higher levels of p53, p27, p21, and p16 compared to RA resistant SK-OV3 cells. Tretinoin 9-11 dynactin subunit 6 Homo sapiens 67-70
11753676-4 2001 However, RA sensitive CA-OV3 cells expressed higher levels of p53, p27, p21, and p16 compared to RA resistant SK-OV3 cells. Tretinoin 9-11 cyclin dependent kinase inhibitor 2A Homo sapiens 81-84
11753676-6 2001 Also, RA treatment increased expression of the cdk inhibitor p27 and decreased activity of cdk 2, cdk 4 and cdk 6. Tretinoin 6-8 dynactin subunit 6 Homo sapiens 61-64
11753676-6 2001 Also, RA treatment increased expression of the cdk inhibitor p27 and decreased activity of cdk 2, cdk 4 and cdk 6. Tretinoin 6-8 cyclin dependent kinase 6 Homo sapiens 108-113
11720446-5 2001 Conversely, we found that the same NB tumour cell line overexpressing the full-length MRP1 cDNA in sense orientation (MRP-S) demonstrated resistance to the neuritogenic effect of the differentiating agent, all-trans-retinoic acid. Tretinoin 210-229 ATP binding cassette subfamily C member 1 Homo sapiens 86-90
11602520-8 2001 The retinoic acid receptor ligand all-trans-retinoic acid augmented the 1,25-(OH)(2)-D(3)-mediated induction of CYP3A4 catalytic activity up to 2-fold in Caco-2 cells, while having no demonstrable effect on levels of CYP3A4 mRNA or protein. Tretinoin 34-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-118
11766235-0 2001 [Effect of retinoic acid on the cytogenetic remission in the first chronic phase of chronic myeloid leukemia treated with interferon]. Tretinoin 11-24 interferon alpha 1 Homo sapiens 122-132
11713105-8 2001 Retinoic acid attenuated the induction and activation of MMP-1 and MMP-3. Tretinoin 0-13 matrix metallopeptidase 3 Homo sapiens 67-72
11602520-8 2001 The retinoic acid receptor ligand all-trans-retinoic acid augmented the 1,25-(OH)(2)-D(3)-mediated induction of CYP3A4 catalytic activity up to 2-fold in Caco-2 cells, while having no demonstrable effect on levels of CYP3A4 mRNA or protein. Tretinoin 34-57 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 217-223
11606945-2 2001 Presented is a summary of recent research that examines the role of some of the enzymes involved in RA distribution, particularly those involved in RA catabolism (P450RAI). Tretinoin 100-102 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 163-170
11604992-11 2001 WNT14B mRNA was significantly up-regulated by all-trans retinoic acid in NT2 cells. Tretinoin 56-69 Wnt family member 9B Homo sapiens 0-6
11604992-12 2001 These results strongly suggest that WNT14B might be implicated in the early process of neuronal differentiation of NT2 cells induced by retinoic acid. Tretinoin 136-149 Wnt family member 9B Homo sapiens 36-42
11696577-6 2001 In cells from PLZF-RAR alpha/RAR alpha-PLZF transgenic mice and cells harboring t(15;17), HDACIs induced apoptosis and dramatic growth inhibition, effects that could be potentiated by RA. Tretinoin 19-21 zinc finger and BTB domain containing 16 Mus musculus 39-43
11675406-5 2001 Urinary TGF-beta 1 excretion was 60% lower in all-trans retinoic acid-treated animals with Thy-GN (P < 0.025). Tretinoin 56-69 transforming growth factor, beta 1 Rattus norvegicus 8-18
11675406-6 2001 The increase of cortical TGF-beta 1 gene expression in Thy-GN rats was significantly attenuated with all-trans retinoic acid and even more with isotretinoin treatment as compared with untreated animals (P < 0.025). Tretinoin 111-124 transforming growth factor, beta 1 Rattus norvegicus 25-35
11675406-8 2001 In all-trans retinoic acid-treated animals with Thy-GN, the increase of glomerular TGF-beta 1 protein (P < 0.008) and TGF-beta 1 (P < 0.025) and TGF receptor II mRNA (P < 0.015) was significantly less. Tretinoin 13-26 transforming growth factor, beta 1 Rattus norvegicus 83-93
11675406-8 2001 In all-trans retinoic acid-treated animals with Thy-GN, the increase of glomerular TGF-beta 1 protein (P < 0.008) and TGF-beta 1 (P < 0.025) and TGF receptor II mRNA (P < 0.015) was significantly less. Tretinoin 13-26 transforming growth factor, beta 1 Rattus norvegicus 121-131
11675406-9 2001 Immunohistochemistry revealed less glomerular staining for TGF-beta 1 and TGF receptor II in the presence of all-trans retinoic acid. Tretinoin 119-132 transforming growth factor, beta 1 Rattus norvegicus 59-69
11696577-6 2001 In cells from PLZF-RAR alpha/RAR alpha-PLZF transgenic mice and cells harboring t(15;17), HDACIs induced apoptosis and dramatic growth inhibition, effects that could be potentiated by RA. Tretinoin 19-21 zinc finger and BTB domain containing 16 Mus musculus 14-18
11690641-8 2001 This study indicates that food compounds such as phytanic acid and DHA that are RXR-agonists and have an impact on intestinal CYP26 gene expression and metabolism of all-trans-RA in intestinal cells. Tretinoin 176-178 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 126-131
11584082-7 2001 The RA + LPS-mediated increase in PGE(2) was significantly attenuated (97%) by aminoguanidine (AG), a relatively specific inhibitor of the inducible nitric oxide synthase (NOS2), consistent with the previously reported synergistic effect of RA and LPS on NOS2 expression and activity. Tretinoin 4-6 nitric oxide synthase 2 Rattus norvegicus 172-176
11859704-8 2001 The level of P-gp expression in ATRA-treated cells was increased from 54.2% +/- 8.6% up to 98.5% +/- 1.4% (P < 0.01), but IL-4 markedly inhibited expression of P-gp down to 25.4% +/- 7.3% (P < 0.01). Tretinoin 32-36 ATP binding cassette subfamily B member 1 Homo sapiens 13-17
11859704-8 2001 The level of P-gp expression in ATRA-treated cells was increased from 54.2% +/- 8.6% up to 98.5% +/- 1.4% (P < 0.01), but IL-4 markedly inhibited expression of P-gp down to 25.4% +/- 7.3% (P < 0.01). Tretinoin 32-36 interleukin 4 Homo sapiens 125-129
11859704-8 2001 The level of P-gp expression in ATRA-treated cells was increased from 54.2% +/- 8.6% up to 98.5% +/- 1.4% (P < 0.01), but IL-4 markedly inhibited expression of P-gp down to 25.4% +/- 7.3% (P < 0.01). Tretinoin 32-36 ATP binding cassette subfamily B member 1 Homo sapiens 163-167
11668484-0 2001 Interferon-gamma cooperates with retinoic acid and phorbol ester to induce differentiation and growth inhibition of human neuroblastoma cells. Tretinoin 33-46 interferon gamma Homo sapiens 0-16
12536483-3 2001 After infected with HCMV and/or treated with ATRA, the expressions of HOXB7 and HOXB8 were up-regulated and the expression of HOXB7 lasted the fourth generation, while HOXB8 was up-regulated only in the second generation. Tretinoin 45-49 homeobox B7 Homo sapiens 70-75
12536483-3 2001 After infected with HCMV and/or treated with ATRA, the expressions of HOXB7 and HOXB8 were up-regulated and the expression of HOXB7 lasted the fourth generation, while HOXB8 was up-regulated only in the second generation. Tretinoin 45-49 homeobox B7 Homo sapiens 126-131
11600826-11 2001 Elevated retinoic acid levels might be responsible for retinoid-like or other adverse effects due to alterations in the expression of retinoic acid-responsive genes. Tretinoin 9-22 G protein-coupled receptor class C group 5 member A Homo sapiens 134-158
11694457-8 2001 Analysis of p21(CIP1), an inhibitor of CDK, revealed an increased expression in O(2)-exposed cells that was no longer observed in cells treated with RA. Tretinoin 149-151 cyclin dependent kinase inhibitor 1A Homo sapiens 12-15
11694457-8 2001 Analysis of p21(CIP1), an inhibitor of CDK, revealed an increased expression in O(2)-exposed cells that was no longer observed in cells treated with RA. Tretinoin 149-151 cyclin dependent kinase inhibitor 1A Homo sapiens 16-20
11694457-9 2001 These effects were associated with a reduced association of p21(CIP1) with cyclin E-CDK2 complexes in the presence of RA. Tretinoin 118-120 cyclin dependent kinase inhibitor 1A Homo sapiens 60-63
11694457-9 2001 These effects were associated with a reduced association of p21(CIP1) with cyclin E-CDK2 complexes in the presence of RA. Tretinoin 118-120 cyclin dependent kinase inhibitor 1A Homo sapiens 64-68
11589695-9 2001 Moreover, the involvement of ADH in the synthesis of retinoic acid suggests a role for the enzyme in the regulation of adult brain functions. Tretinoin 53-66 aldo-keto reductase family 1 member A1 Rattus norvegicus 29-32
11732841-13 2001 This observation suggests that retinoic acid plays an important role in the regulation of XMLP. Tretinoin 31-44 MARCKS-like 1 S homeolog Xenopus laevis 90-94
11602619-2 2001 We found that retinoic acid inhibits the transcriptional activity of AP-1 and the orphan receptors Nur77 and Nurr1 in ACTH-secreting tumor cells. Tretinoin 14-27 nuclear receptor subfamily 4 group A member 1 Homo sapiens 99-104
11602619-2 2001 We found that retinoic acid inhibits the transcriptional activity of AP-1 and the orphan receptors Nur77 and Nurr1 in ACTH-secreting tumor cells. Tretinoin 14-27 proopiomelanocortin Homo sapiens 118-122
11602619-3 2001 Retinoic acid treatment resulted in reduced pro-opiomelanocortin transcription and ACTH production. Tretinoin 0-13 proopiomelanocortin Homo sapiens 44-64
11602619-3 2001 Retinoic acid treatment resulted in reduced pro-opiomelanocortin transcription and ACTH production. Tretinoin 0-13 proopiomelanocortin Homo sapiens 83-87
11602619-6 2001 COUP-TFI expression in ACTH-secreting tumor cells blocked retinoic acid action. Tretinoin 58-71 nuclear receptor subfamily 2 group F member 1 Homo sapiens 0-8
11602619-6 2001 COUP-TFI expression in ACTH-secreting tumor cells blocked retinoic acid action. Tretinoin 58-71 proopiomelanocortin Homo sapiens 23-27
11602619-7 2001 Retinoic acid also inhibited cell proliferation and, after prolonged treatment, increased caspase-3 activity and induced cell death in ACTH-secreting cells. Tretinoin 0-13 caspase 3 Homo sapiens 90-99
11602619-7 2001 Retinoic acid also inhibited cell proliferation and, after prolonged treatment, increased caspase-3 activity and induced cell death in ACTH-secreting cells. Tretinoin 0-13 proopiomelanocortin Homo sapiens 135-139
11584082-7 2001 The RA + LPS-mediated increase in PGE(2) was significantly attenuated (97%) by aminoguanidine (AG), a relatively specific inhibitor of the inducible nitric oxide synthase (NOS2), consistent with the previously reported synergistic effect of RA and LPS on NOS2 expression and activity. Tretinoin 4-6 nitric oxide synthase 2 Rattus norvegicus 255-259
11584082-7 2001 The RA + LPS-mediated increase in PGE(2) was significantly attenuated (97%) by aminoguanidine (AG), a relatively specific inhibitor of the inducible nitric oxide synthase (NOS2), consistent with the previously reported synergistic effect of RA and LPS on NOS2 expression and activity. Tretinoin 241-243 nitric oxide synthase 2 Rattus norvegicus 172-176
11676881-8 2001 CONCLUSIONS: Up-regulation of p16 and p21 on post-transcriptional level may contribute, in part, to retinoic acid inhibition of transforming growth factor beta 1-initiated rat hepatic stellate cells activation in vitro. Tretinoin 100-113 transforming growth factor, beta 1 Rattus norvegicus 128-161
11642546-3 2001 ATRA or IL-6 induced a dose-dependent increase of TSP-1 protein and mRNA levels in PAE cells, while they negatively regulated TSP-1 expression in the Hep3B and SK-HEP-1 cells. Tretinoin 0-4 thrombospondin 1 Homo sapiens 50-55
11642546-3 2001 ATRA or IL-6 induced a dose-dependent increase of TSP-1 protein and mRNA levels in PAE cells, while they negatively regulated TSP-1 expression in the Hep3B and SK-HEP-1 cells. Tretinoin 0-4 thrombospondin 1 Homo sapiens 126-131
11447226-4 2001 Expression of RISC is low in cultured SMC but progressively increases over a 5-day time-course treatment with all-trans-retinoic acid. Tretinoin 110-133 serine carboxypeptidase 1 Rattus norvegicus 14-18
11642546-7 2001 Possible TSP-1 promoter-mediated responses by ATRA, IL-6, IFN-gamma, or PMA in Hep3B and PAE cells examined with luciferase activity of TSP-LUC reporter plasmid showed that levels of TSP-1 promoter activity were lower than that of the expressed TSP-1 protein and mRNA levels. Tretinoin 46-50 thrombospondin 1 Homo sapiens 9-14
11438548-4 2001 In attempting to discover the underlying biochemical activities that might account for these cellular effects, we found that monodansylcadaverine (MDC), which binds to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and in fact caused RA to become an apoptotic factor, suggesting that the ability of RA to protect against apoptosis is linked to the expression of active TGase. Tretinoin 253-255 transglutaminase 2 Homo sapiens 209-232
11525643-0 2001 Protein kinase Calpha expression confers retinoic acid sensitivity on MDA-MB-231 human breast cancer cells. Tretinoin 41-54 protein kinase C alpha Homo sapiens 0-21
11525643-1 2001 Retinoic acid activation of retinoic acid receptor alpha (RARalpha) induces protein kinase Calpha (PKCalpha) expression and inhibits proliferation of the hormone-dependent T-47D breast cancer cell line. Tretinoin 0-13 protein kinase C alpha Homo sapiens 76-97
11525643-1 2001 Retinoic acid activation of retinoic acid receptor alpha (RARalpha) induces protein kinase Calpha (PKCalpha) expression and inhibits proliferation of the hormone-dependent T-47D breast cancer cell line. Tretinoin 0-13 protein kinase C alpha Homo sapiens 99-107
11525643-4 2001 Constitutive expression of PKCalpha did not affect proliferation of MDA-MB-231 cells but did result in partial retinoic acid sensitivity. Tretinoin 111-124 protein kinase C alpha Homo sapiens 27-35
11525643-5 2001 Retinoic acid treatment of PKCalpha-MDA-MB-231 cells decreased proliferation (by approximately 40%) and inhibited serum activation of MAP kinases and induction of c-fos. Tretinoin 0-13 protein kinase C alpha Homo sapiens 27-35
11525643-7 2001 Expression of RARalpha in PKCalpha expressing MDA-MB-231 cells resulted in even greater retinoic acid responses, as measured by effects on cell proliferation, inhibition of serum signaling, and transactivation of an RARE-CAT reporter plasmid. Tretinoin 88-101 protein kinase C alpha Homo sapiens 26-34
11438548-4 2001 In attempting to discover the underlying biochemical activities that might account for these cellular effects, we found that monodansylcadaverine (MDC), which binds to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and in fact caused RA to become an apoptotic factor, suggesting that the ability of RA to protect against apoptosis is linked to the expression of active TGase. Tretinoin 305-307 transglutaminase 2 Homo sapiens 209-232
11438548-4 2001 In attempting to discover the underlying biochemical activities that might account for these cellular effects, we found that monodansylcadaverine (MDC), which binds to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and in fact caused RA to become an apoptotic factor, suggesting that the ability of RA to protect against apoptosis is linked to the expression of active TGase. Tretinoin 305-307 transglutaminase 2 Homo sapiens 209-232
11780391-6 2001 ATRA might induce p21WAF1/CIP1 expression in ATRA-sensitive cell lines through p53-dependent and p53-independent pathways. Tretinoin 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 26-30
11500296-0 2001 Destabilization of TNF-alpha mRNA by retinoic acid in hepatic macrophages: implications for alcoholic liver disease. Tretinoin 37-50 tumor necrosis factor Rattus norvegicus 19-28
11500296-3 2001 The aim of the present study was to determine the mechanism of RA-induced inhibition of HM tumor necrosis factor (TNF)-alpha expression and the relevance of this regulation to ALD. Tretinoin 63-65 tumor necrosis factor Rattus norvegicus 114-124
11500296-7 2001 RA did not alter LPS-stimulated NF-kB and activation protein-1 binding but significantly decreased TNF-alpha mRNA stability in HM. Tretinoin 0-2 tumor necrosis factor Rattus norvegicus 99-108
11500296-10 2001 These results demonstrate the RA-induced destabilization of TNF-alpha mRNA by cultured HM and the association of RA depletion with increased TNF-alpha mRNA stability in HM from experimental ALD. Tretinoin 30-32 tumor necrosis factor Rattus norvegicus 60-69
11500296-10 2001 These results demonstrate the RA-induced destabilization of TNF-alpha mRNA by cultured HM and the association of RA depletion with increased TNF-alpha mRNA stability in HM from experimental ALD. Tretinoin 113-115 tumor necrosis factor Rattus norvegicus 141-150
11780391-6 2001 ATRA might induce p21WAF1/CIP1 expression in ATRA-sensitive cell lines through p53-dependent and p53-independent pathways. Tretinoin 0-4 tumor protein p53 Homo sapiens 79-82
11780391-6 2001 ATRA might induce p21WAF1/CIP1 expression in ATRA-sensitive cell lines through p53-dependent and p53-independent pathways. Tretinoin 0-4 tumor protein p53 Homo sapiens 97-100
11683923-8 2001 Western blot for Bcl-2 family also performed in neutrophilic differentiated HL-60 cells by all-trans-retinoic acid. Tretinoin 91-114 BCL2 apoptosis regulator Homo sapiens 17-22
11675933-3 2001 Previous experiments have shown that IGF-I, tamoxifen, retinoic acid and tangeretin are able to upregulate the function of this complex in MCF-7/6 cells. Tretinoin 55-68 insulin like growth factor 1 Homo sapiens 37-42
11520679-2 2001 The RA-metabolizing enzymes Cyp26A1 and Cyp26B1 are believed to play important roles in protecting certain embryonic tissues from inappropriate RA signaling. Tretinoin 144-146 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 40-47
11675954-8 2001 In contrast, ATRA strongly suppressed the pRb kinase activities of the cyclin-dependent kinases (Cdks) Cdk4, Cdk6, and Cdk2. Tretinoin 13-17 cyclin-dependent kinase 4 Rattus norvegicus 103-107
11675954-8 2001 In contrast, ATRA strongly suppressed the pRb kinase activities of the cyclin-dependent kinases (Cdks) Cdk4, Cdk6, and Cdk2. Tretinoin 13-17 cyclin-dependent kinase 6 Rattus norvegicus 109-113
11675954-9 2001 ATRA did not influence the expressions of Cip/Kip family Cdk inhibitors or those of cyclins D1 and D2, whereas it strongly inhibited the expressions of cyclins D3 and E, Cdk4, Cdk6, and Cdk2. Tretinoin 0-4 cyclin D3 Rattus norvegicus 152-168
11675954-9 2001 ATRA did not influence the expressions of Cip/Kip family Cdk inhibitors or those of cyclins D1 and D2, whereas it strongly inhibited the expressions of cyclins D3 and E, Cdk4, Cdk6, and Cdk2. Tretinoin 0-4 cyclin-dependent kinase 4 Rattus norvegicus 170-174
11675954-9 2001 ATRA did not influence the expressions of Cip/Kip family Cdk inhibitors or those of cyclins D1 and D2, whereas it strongly inhibited the expressions of cyclins D3 and E, Cdk4, Cdk6, and Cdk2. Tretinoin 0-4 cyclin-dependent kinase 6 Rattus norvegicus 176-180
11718225-6 2001 The results indicated that Fn binding prevented the cells from apoptosis induced by atRA, in contrast to L-poly-lysine binding. Tretinoin 84-88 fibronectin 1 Homo sapiens 27-29
11520679-0 2001 Cloning of a novel retinoic-acid metabolizing cytochrome P450, Cyp26B1, and comparative expression analysis with Cyp26A1 during early murine development. Tretinoin 19-32 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 63-70
11758167-0 2001 [Influence of suppressor gene p16 on retinoic acid inducing lung cancer cell A549 differentiation]. Tretinoin 37-50 cyclin dependent kinase inhibitor 2A Homo sapiens 30-33
11520679-2 2001 The RA-metabolizing enzymes Cyp26A1 and Cyp26B1 are believed to play important roles in protecting certain embryonic tissues from inappropriate RA signaling. Tretinoin 4-6 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 40-47
11520048-4 2001 In DMS-treated cells, 9-cis retinoic acid (RA) further enhanced HNF-4alpha and albumin expression but it inhibited AFP accumulation. Tretinoin 43-45 hepatocyte nuclear factor 4 alpha Homo sapiens 64-74
11520048-4 2001 In DMS-treated cells, 9-cis retinoic acid (RA) further enhanced HNF-4alpha and albumin expression but it inhibited AFP accumulation. Tretinoin 43-45 alpha fetoprotein Homo sapiens 115-118
11758167-1 2001 OBJECTIVE: To investigate the role of suppressor gene p16 in the process of differential regulation of retinoic acid (RA) on the A549 lung cancer cells. Tretinoin 103-116 cyclin dependent kinase inhibitor 2A Homo sapiens 54-57
11758167-1 2001 OBJECTIVE: To investigate the role of suppressor gene p16 in the process of differential regulation of retinoic acid (RA) on the A549 lung cancer cells. Tretinoin 118-120 cyclin dependent kinase inhibitor 2A Homo sapiens 54-57
11758167-2 2001 METHODS: Tumor suppressor gene p16 was transfered into A549 cells and the cells were treated with all-trans retinoic acid (ATRA) at the dosage of 5 x 10(-6) mol/L for 4 d. After that, the proliferation and differentiation of A549 cells were examined by growth curve and cytometry analysis, the change of lung lineage-specific marker MUC1 was tested by immunohistochemical staining. Tretinoin 108-121 cyclin dependent kinase inhibitor 2A Homo sapiens 31-34
11758167-2 2001 METHODS: Tumor suppressor gene p16 was transfered into A549 cells and the cells were treated with all-trans retinoic acid (ATRA) at the dosage of 5 x 10(-6) mol/L for 4 d. After that, the proliferation and differentiation of A549 cells were examined by growth curve and cytometry analysis, the change of lung lineage-specific marker MUC1 was tested by immunohistochemical staining. Tretinoin 123-127 cyclin dependent kinase inhibitor 2A Homo sapiens 31-34
11758167-3 2001 Meanwhile, Western blot was used to observe the change of p16 protein expression in A549 cells treated with ATRA. Tretinoin 108-112 cyclin dependent kinase inhibitor 2A Homo sapiens 58-61
11758167-4 2001 RESULTS: ATRA could obviously inhibit the growth and induce the differentiation of A549 cells that were transfered with p16 gene. Tretinoin 9-13 cyclin dependent kinase inhibitor 2A Homo sapiens 120-123
11758167-6 2001 The expression of p16 protein was up-regulated in A549 cells treated with ATRA. Tretinoin 74-78 cyclin dependent kinase inhibitor 2A Homo sapiens 18-21
11513861-0 2001 Activation of c-Jun amino-terminal kinase is required for retinoic acid-induced neural differentiation of P19 embryonal carcinoma cells. Tretinoin 58-71 mitogen-activated protein kinase 8 Homo sapiens 14-41
11478838-3 2001 Immunoblotting analyses and capillary zone electrophoresis demonstrated that following RA treatment: lamins A/C and B1, and vimentin decreased to negligible amounts; LAP2 beta, lamin B2 and emerin remained essentially unchanged; lamin B receptor (LBR) increased markedly; histone subtypes H1.4 and 1.5 exhibited dephosphorylation. Tretinoin 87-89 lamin B receptor Homo sapiens 229-245
11478838-3 2001 Immunoblotting analyses and capillary zone electrophoresis demonstrated that following RA treatment: lamins A/C and B1, and vimentin decreased to negligible amounts; LAP2 beta, lamin B2 and emerin remained essentially unchanged; lamin B receptor (LBR) increased markedly; histone subtypes H1.4 and 1.5 exhibited dephosphorylation. Tretinoin 87-89 lamin B receptor Homo sapiens 247-250
11513861-2 2001 Concomitant with this RA-induced neural differentiation, we observed an activation of the c-Jun amino-terminal kinase (JNK). Tretinoin 22-24 mitogen-activated protein kinase 8 Homo sapiens 119-122
11513861-3 2001 JNK was required for the RA-induced neural differentiation, because dominant-negative JNK blocked the differentiation. Tretinoin 25-27 mitogen-activated protein kinase 8 Homo sapiens 0-3
11513861-3 2001 JNK was required for the RA-induced neural differentiation, because dominant-negative JNK blocked the differentiation. Tretinoin 25-27 mitogen-activated protein kinase 8 Homo sapiens 86-89
11603003-0 2001 13cis- and all-trans retinoic acid have antiproliferative effects on CML cells and render IFN alpha antiproliferative potency after combined treatment in vitro. Tretinoin 21-34 interferon alpha 1 Homo sapiens 90-99
11479234-10 2001 These results suggest that an RXR-selective retinoic acid decreases SCCHN proliferation in part by interfering with TGF-alpha/EGFR autocrine signaling. Tretinoin 44-57 epidermal growth factor receptor Homo sapiens 126-130
26680805-9 2001 CONCLUSION: We found that only radioresistant cell line (UMSCC-11B) showed synergistic radiosensitivity effect by t-RA and this mechanism may be through RAR-beta expression induction. Tretinoin 114-118 retinoic acid receptor beta Homo sapiens 153-161
11446778-0 2001 Retinoic acid-dependent transgene expression is regulated by RARbeta expression in the retina. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 61-68
11697504-1 2001 Here the relationship between all-trans retinoic acid (ATRA)-resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) is discussed in acute promyelocytic leukemia (APL). Tretinoin 30-53 ATP binding cassette subfamily B member 1 Homo sapiens 76-90
11683493-0 2001 Retinoic acid causes MEK-dependent RAF phosphorylation through RARalpha plus RXR activation in HL-60 cells. Tretinoin 0-13 mitogen-activated protein kinase kinase 7 Homo sapiens 21-24
11683493-1 2001 Retinoic acid (RA) is known to cause the myeloid differentiation of HL-60 human myeloblastic leukemia cells in a process requiring MEK-dependent ERK2 activation. Tretinoin 0-13 mitogen-activated protein kinase kinase 7 Homo sapiens 131-134
11683493-1 2001 Retinoic acid (RA) is known to cause the myeloid differentiation of HL-60 human myeloblastic leukemia cells in a process requiring MEK-dependent ERK2 activation. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 145-149
11683493-1 2001 Retinoic acid (RA) is known to cause the myeloid differentiation of HL-60 human myeloblastic leukemia cells in a process requiring MEK-dependent ERK2 activation. Tretinoin 15-17 mitogen-activated protein kinase kinase 7 Homo sapiens 131-134
11506967-5 2001 COX-2 inhibitors also inhibited the differentiation of these cells induced by interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and retinoic acid (RA). Tretinoin 153-166 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5
11506967-5 2001 COX-2 inhibitors also inhibited the differentiation of these cells induced by interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and retinoic acid (RA). Tretinoin 168-170 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5
11694025-0 2001 Inhibitory effect of retinoic acid on expression of inducible nitric oxide synthase gene in l929 cells. Tretinoin 21-34 nitric oxide synthase 2, inducible Mus musculus 52-83
11694025-5 2001 All-trans-retinoic acid significantly inhibited NO synthesis and iNOS gene expression in a dose-dependent manner. Tretinoin 0-23 nitric oxide synthase 2, inducible Mus musculus 65-69
11683493-1 2001 Retinoic acid (RA) is known to cause the myeloid differentiation of HL-60 human myeloblastic leukemia cells in a process requiring MEK-dependent ERK2 activation. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 145-149
11683493-2 2001 This RA-induced ERK2 activation appears after approximately 4 h and persists until the cells are differentiated and G0 arrested (Yen et al, 1998). Tretinoin 5-7 mitogen-activated protein kinase 1 Homo sapiens 16-20
11683493-3 2001 This motivates the question of whether RA also activated RAF as part of a typical RAF/MEK/MAPK cascade. Tretinoin 39-41 mitogen-activated protein kinase kinase 7 Homo sapiens 86-89
11683493-10 2001 RA-induced MEK-dependent RAF phosphorylation is not due to changes in the amount of cellular MEK. Tretinoin 0-2 mitogen-activated protein kinase kinase 7 Homo sapiens 11-14
11683493-13 2001 In summary, RA induces a MEK-dependent prolonged RAF activation, whose slow onset occurs after ERK2 activation but still well before cell cycle arrest and cell differentiation. Tretinoin 12-14 mitogen-activated protein kinase kinase 7 Homo sapiens 25-28
11683493-13 2001 In summary, RA induces a MEK-dependent prolonged RAF activation, whose slow onset occurs after ERK2 activation but still well before cell cycle arrest and cell differentiation. Tretinoin 12-14 mitogen-activated protein kinase 1 Homo sapiens 95-99
11561905-9 2001 Furthermore, treating Bcl-2 cultures with ceramide (10 microM), a second messenger mediating the RA-initiated death signal in parental cells, no longer caused DNA laddering. Tretinoin 97-99 BCL2 apoptosis regulator Homo sapiens 22-27
11568584-0 2001 All-trans-retinoic acid enhances the effect of adenovirus-mediated wild-type p53 gene transfer in head and neck squamous cell carcinoma. Tretinoin 0-23 tumor protein p53 Homo sapiens 77-80
11697504-1 2001 Here the relationship between all-trans retinoic acid (ATRA)-resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) is discussed in acute promyelocytic leukemia (APL). Tretinoin 30-53 ATP binding cassette subfamily B member 1 Homo sapiens 92-96
11697504-1 2001 Here the relationship between all-trans retinoic acid (ATRA)-resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) is discussed in acute promyelocytic leukemia (APL). Tretinoin 55-59 ATP binding cassette subfamily B member 1 Homo sapiens 76-90
11697504-1 2001 Here the relationship between all-trans retinoic acid (ATRA)-resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) is discussed in acute promyelocytic leukemia (APL). Tretinoin 55-59 ATP binding cassette subfamily B member 1 Homo sapiens 92-96
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 31-33 cyclin dependent kinase inhibitor 2A Homo sapiens 123-126
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 31-33 cyclin dependent kinase inhibitor 2A Homo sapiens 127-132
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 31-33 cyclin dependent kinase inhibitor 2C Homo sapiens 168-171
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 147-149 cyclin dependent kinase inhibitor 2A Homo sapiens 123-126
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 147-149 cyclin dependent kinase inhibitor 2C Homo sapiens 168-171
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 147-149 cyclin dependent kinase inhibitor 2C Homo sapiens 172-177
11451739-7 2001 tRA-induced apoptosis associated with an increased ratio of bax to bcl-2 by bax overexpression and cleavage of caspase-3. Tretinoin 0-3 BCL2, apoptosis regulator Rattus norvegicus 67-72
11331281-8 2001 IFN/all-trans-retinoic acid-induced cytochrome c release from the mitochondrion was promoted in the presence of wild type and was inhibited in the presence of mutant TR. Tretinoin 4-27 interferon alpha 1 Homo sapiens 0-3
11331281-8 2001 IFN/all-trans-retinoic acid-induced cytochrome c release from the mitochondrion was promoted in the presence of wild type and was inhibited in the presence of mutant TR. Tretinoin 4-27 cytochrome c, somatic Homo sapiens 36-48
11399650-4 2001 We found that ADP-ribosyl cyclase, a CD38-like enzyme that catalyzes cADPR synthesis, is upregulated in MC by tumor necrosis factor-alpha, interleukin-1beta, and all-trans retinoic acid (atRA). Tretinoin 172-185 CD38 molecule Rattus norvegicus 37-41
11399650-4 2001 We found that ADP-ribosyl cyclase, a CD38-like enzyme that catalyzes cADPR synthesis, is upregulated in MC by tumor necrosis factor-alpha, interleukin-1beta, and all-trans retinoic acid (atRA). Tretinoin 187-191 CD38 molecule Rattus norvegicus 37-41
11399650-4 2001 We found that ADP-ribosyl cyclase, a CD38-like enzyme that catalyzes cADPR synthesis, is upregulated in MC by tumor necrosis factor-alpha, interleukin-1beta, and all-trans retinoic acid (atRA). Tretinoin 187-191 tumor necrosis factor Rattus norvegicus 110-137
11437442-12 2001 Conversely, treatment of wild-type embryos with retinoic acid greatly expands the periotic domains of expression of fgf3, fgf8, and pax8 and leads to formation of supernumerary and ectopic otic vesicles. Tretinoin 48-61 fibroblast growth factor 8a Danio rerio 122-126
11437442-12 2001 Conversely, treatment of wild-type embryos with retinoic acid greatly expands the periotic domains of expression of fgf3, fgf8, and pax8 and leads to formation of supernumerary and ectopic otic vesicles. Tretinoin 48-61 paired box 8 Danio rerio 132-136
11437448-5 2001 During TS cell differentiation into trophoblast subtypes induced by withdrawal of FGF4, RA treatment further illustrated its role in the specification of cell fate by the promotion of differentiation into giant cells and the suppression of spongiotrophoblast formation. Tretinoin 88-90 fibroblast growth factor 4 Homo sapiens 82-86
11470254-5 2001 Furthermore, indomethacin potentiated apoptosis in cells treated with a differentiating agent, all-trans retinoic acid, which induces resistance to TNF-alpha. Tretinoin 105-118 tumor necrosis factor Homo sapiens 148-157
11471143-0 2001 Differential expression of chicken CYP26 in anterior versus posterior limb bud in response to retinoic acid. Tretinoin 94-107 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 35-40
11720243-6 2001 PRL (20 ng/mL) stimulated its expression, reaching maximal levels within 12 h. Expression of XIAP was also evaluated in Nb2-SFJCD1 cells subsequent to treatment with differentiating agents (sodium butyrate [2 mM, 72 h], all trans-retinoic acid [10 microM, 72 h], or 1,25-dihydroxycholecalciferol [100 nM, 24 h]). Tretinoin 224-243 prolactin Rattus norvegicus 0-3
11471143-4 2001 Recently, enzymes capable of catabolizing RA were found to constitute a new family, called CYP26, within the cytochrome P450 superfamily. Tretinoin 42-44 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 91-96
11274148-9 2001 RAR DBD greatly enhanced TTF-1 homeodomain DNA binding activity to a hSP-B enhancer oligonucleotide, in which retinoic acid-responsive element and TTF-1 DNA binding sites overlap. Tretinoin 110-123 NK2 homeobox 1 Homo sapiens 25-30
11454993-2 2001 Retinoic acid suppresses cancer cell growth through binding to RARs, especially RARbeta, indicating a critical role in mediating anticancer effects. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 80-87
11369141-0 2001 Proteolysis of integrin alpha5 and beta1 subunits involved in retinoic acid-induced apoptosis in human hepatoma Hep3B cells. Tretinoin 62-75 integrin subunit alpha 5 Homo sapiens 15-30
11369141-6 2001 Results from the adhesion assay indicated that the cell attachment to fibronectin was significantly inhibited by ATRA. Tretinoin 113-117 fibronectin 1 Homo sapiens 70-81
11369141-7 2001 Treatment with perturbing antibody against integrin alpha5 or beta1 subunits resulted in promotion of ATRA-induced apoptosis. Tretinoin 102-106 integrin subunit alpha 5 Homo sapiens 43-58
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 145-158 NK2 homeobox 1 Homo sapiens 47-52
11435494-0 2001 Potentiation of interferon-gamma-stimulated nitric oxide production by retinoic acid in RAW 264.7 cells. Tretinoin 71-84 interferon gamma Mus musculus 16-32
11435494-5 2001 The RA-potentiated production of NO was positively correlated with inducible NO synthase (iNOS) protein (r =0.94, P <0.002), although the expression of iNOS mRNA was not altered. Tretinoin 4-6 nitric oxide synthase 2, inducible Mus musculus 67-88
11435494-5 2001 The RA-potentiated production of NO was positively correlated with inducible NO synthase (iNOS) protein (r =0.94, P <0.002), although the expression of iNOS mRNA was not altered. Tretinoin 4-6 nitric oxide synthase 2, inducible Mus musculus 90-94
11435494-5 2001 The RA-potentiated production of NO was positively correlated with inducible NO synthase (iNOS) protein (r =0.94, P <0.002), although the expression of iNOS mRNA was not altered. Tretinoin 4-6 nitric oxide synthase 2, inducible Mus musculus 155-159
11518283-10 2001 Northern blot analysis showed that expression of CD-RAP mRNA was suppressed by bFGF, IL-1beta and retinoic acid in coordination with type II collagen mRNA. Tretinoin 98-111 MIA SH3 domain containing Homo sapiens 49-55
11518283-12 2001 In chondrocytes dedifferentiated with retinoic acid, IGF-1 induced re-expression of both CD-RAP and type II collagen mRNAs. Tretinoin 38-51 insulin like growth factor 1 Homo sapiens 53-58
11518283-12 2001 In chondrocytes dedifferentiated with retinoic acid, IGF-1 induced re-expression of both CD-RAP and type II collagen mRNAs. Tretinoin 38-51 MIA SH3 domain containing Homo sapiens 89-95
11396964-0 2001 Induction of haptoglobin by all-trans retinoic acid in THP-1 human monocytic cell line. Tretinoin 28-51 haptoglobin Homo sapiens 13-24
11274148-10 2001 Chromatin immunoprecipitation assay demonstrated that retinoic acid treatment of H441 cells greatly stimulated both RAR and TTF-1 DNA binding to the hSP-B enhancer region in H441 cells. Tretinoin 54-67 NK2 homeobox 1 Homo sapiens 124-129
11384110-7 2001 We conclude that ATRA synergistically enhances docetaxel toxicity by down-regulating Bcl-2 expression and partially reverses the docetaxel-induced G2/M arrest by inhibiting docetaxel-induced cdc2 phosphorylation in a pathway that is dependent on MAPK. Tretinoin 17-21 BCL2 apoptosis regulator Homo sapiens 85-90
11389035-11 2001 Finally, quantitative assays showed that ATRA treatment resulted in the abrogation of VEGF production by the NB4 cells. Tretinoin 41-45 vascular endothelial growth factor A Homo sapiens 86-90
11389035-12 2001 These results show that there is increased angiogenesis and VEGF production in APL and that ATRA therapy inhibits VEGF production and suppresses angiogenesis. Tretinoin 92-96 vascular endothelial growth factor A Homo sapiens 114-118
11429697-6 2001 Retinoic acid treatment of vector-transfected clones resulted in Bax protein activation as assessed by exposure of the NH(2)-terminus of Bax but the proportion of cells containing activated Bax was increased in cyclin D-expressing cells treated with retinoic acid. Tretinoin 0-13 BCL2 associated X, apoptosis regulator Homo sapiens 65-68
11429697-6 2001 Retinoic acid treatment of vector-transfected clones resulted in Bax protein activation as assessed by exposure of the NH(2)-terminus of Bax but the proportion of cells containing activated Bax was increased in cyclin D-expressing cells treated with retinoic acid. Tretinoin 0-13 BCL2 associated X, apoptosis regulator Homo sapiens 137-140
11429697-6 2001 Retinoic acid treatment of vector-transfected clones resulted in Bax protein activation as assessed by exposure of the NH(2)-terminus of Bax but the proportion of cells containing activated Bax was increased in cyclin D-expressing cells treated with retinoic acid. Tretinoin 0-13 BCL2 associated X, apoptosis regulator Homo sapiens 137-140
11429697-8 2001 Retinoic acid markedly decreased the Bcl-2 levels in MCF-7 and ZR-75 cells. Tretinoin 0-13 BCL2 apoptosis regulator Homo sapiens 37-42
11429697-9 2001 Accordingly, coexpression of Bcl-2 and cyclin D1 rendered the cells resistant to retinoic acid-induced apoptosis. Tretinoin 81-94 BCL2 apoptosis regulator Homo sapiens 29-34
11429697-10 2001 We conclude that constitutive expression of cyclin D1 sensitizes ER-positive breast cancer cells to a retinoic acid-induced mitochondrial death pathway involving Bax activation, cytochrome c release and caspase-9 cleavage. Tretinoin 102-115 BCL2 associated X, apoptosis regulator Homo sapiens 162-165
11429697-10 2001 We conclude that constitutive expression of cyclin D1 sensitizes ER-positive breast cancer cells to a retinoic acid-induced mitochondrial death pathway involving Bax activation, cytochrome c release and caspase-9 cleavage. Tretinoin 102-115 cytochrome c, somatic Homo sapiens 178-190
11384110-3 2001 ATRA enhanced docetaxel-induced apoptosis and combined treatment with ATRA and docetaxel resulted in down-regulation of Bcl-2. Tretinoin 70-74 BCL2 apoptosis regulator Homo sapiens 120-125
11465510-3 2001 In order to determine if the genotype of the p53 donor or the genotype of the sp donor determined the binding efficiency, p53 expression was induced by retinoic acid and sp synthesis by bleomycin. Tretinoin 152-165 tumor protein p53 Homo sapiens 122-125
11385504-4 2001 In the leukemic blasts of freshly diagnosed acute promyelocytic leukemia patients, retinoic-acid-induced expression of TRAIL most likely caused blast apoptosis. Tretinoin 83-96 TNF superfamily member 10 Homo sapiens 119-124
11397877-4 2001 We also then examined the effects of retinoic acid on the expression of 17 beta-HSD type 2 in cell lines derived from endometrial carcinoma using Northern blotting analysis to examine the possible roles of retinoids in in situ endometrial estrogen metabolism. Tretinoin 37-50 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 72-83
11397877-10 2001 In the endometrial carcinoma cell line, RL95-2, retinoic acid markedly increased the level of 17 beta-HSD type 2 messenger RNA in a time- and dose-dependent manner. Tretinoin 48-61 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 94-105
11397877-11 2001 These results all suggest that retinoic acids may be involved in modulation of in situ estrogen metabolism in both normal and neoplastic human endometrium possibly through RXR gamma by stimulating the expression of 17 beta-HSD type 2. Tretinoin 31-45 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 215-226
11385504-0 2001 Retinoic acid-induced apoptosis in leukemia cells is mediated by paracrine action of tumor-selective death ligand TRAIL. Tretinoin 0-13 TNF superfamily member 10 Homo sapiens 114-119
11319755-4 2001 We have observed that the TGF-beta-induced, but not the retinoic acid-induced, alpha-smooth muscle actin expression is associated with a modulation of endogenous TGF-beta and TGF-beta receptors, suggesting that the action of retinoic acid on alpha-smooth muscle actin expression is not mediated by TGF-beta. Tretinoin 225-238 transforming growth factor, beta 1 Rattus norvegicus 26-34
11319755-4 2001 We have observed that the TGF-beta-induced, but not the retinoic acid-induced, alpha-smooth muscle actin expression is associated with a modulation of endogenous TGF-beta and TGF-beta receptors, suggesting that the action of retinoic acid on alpha-smooth muscle actin expression is not mediated by TGF-beta. Tretinoin 225-238 transforming growth factor, beta 1 Rattus norvegicus 162-170
11319755-4 2001 We have observed that the TGF-beta-induced, but not the retinoic acid-induced, alpha-smooth muscle actin expression is associated with a modulation of endogenous TGF-beta and TGF-beta receptors, suggesting that the action of retinoic acid on alpha-smooth muscle actin expression is not mediated by TGF-beta. Tretinoin 225-238 transforming growth factor, beta 1 Rattus norvegicus 162-170
11319755-4 2001 We have observed that the TGF-beta-induced, but not the retinoic acid-induced, alpha-smooth muscle actin expression is associated with a modulation of endogenous TGF-beta and TGF-beta receptors, suggesting that the action of retinoic acid on alpha-smooth muscle actin expression is not mediated by TGF-beta. Tretinoin 225-238 transforming growth factor, beta 1 Rattus norvegicus 162-170
11385504-3 2001 In a paracrine mode of action, TRAIL killed NB4 as well as heterologous and retinoic-acid-resistant cells. Tretinoin 76-89 TNF superfamily member 10 Homo sapiens 31-36
11434680-5 2001 Myo-inositol uptake and PKC activity increased in cells induced to differentiate by ATRA but the retinoid did not affect cAMP levels or PKA activity. Tretinoin 84-88 proline rich transmembrane protein 2 Homo sapiens 24-27
11434680-7 2001 Our results show that the effects of ATRA and dbcAMP on promyelocytic cells are closely related, respectively, to the PLC/IP/PKC and the cAMP/PKA pathways. Tretinoin 37-41 proline rich transmembrane protein 2 Homo sapiens 125-128
11434680-8 2001 In cells induced to differentiate by ATRA, CD11b expression seems more closely related to inositol uptake than to PKC activity while the expression of TF and TM show the opposite pattern, which suggests cellular events regulated at a different level within a common signal transduction pathway. Tretinoin 37-41 proline rich transmembrane protein 2 Homo sapiens 114-117
11358845-0 2001 Overexpression of the retinoic acid-responsive gene Stra6 in human cancers and its synergistic induction by Wnt-1 and retinoic acid. Tretinoin 22-35 Wnt family member 1 Homo sapiens 108-113
12578618-0 2001 [Change of WT1 Gene Expression during Induction of Differentiation of NB4 Cell Line] In order to study the relation between WT1 gene expression and differentiation of NB4 leukemic cells, a competitive RT-PCR method was established by using recombinant DNA technique to detect the expression of WT1 gene quantitatively during differentiation of NB4 leukemic cells induced by retinoic acid. Tretinoin 374-387 WT1 transcription factor Homo sapiens 11-14
12578618-3 2001 The molecular number of WT1 gene in 1 micro g total RNA was 4 x 10(6), 1.56 x 10(6) and 0.4 x 10(6), respectively, prior to and at 12 or 24 hours after exposure to retinoic acid, and it was in accordance with the change of CD11b. Tretinoin 164-177 WT1 transcription factor Homo sapiens 24-27
11278931-6 2001 Osteoblast OCIL mRNA expression was enhanced by parathyroid hormone, calcitriol, interleukin-1alpha and -11, and retinoic acid. Tretinoin 113-126 C-type lectin domain family 2, member d Mus musculus 11-15
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 0-13 ras homolog family member A Homo sapiens 170-174
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 15-17 ras homolog family member A Homo sapiens 170-174
11369496-0 2001 Retinoic acid reduces apoptosis and oxidative stress by preservation of SOD protein level. Tretinoin 0-13 superoxide dismutase 1 Rattus norvegicus 72-75
11369496-2 2001 In this study, we determined the effect of RA on the mRNA and protein levels of the Cu-,Zn-superoxide dismutase (SOD-1) and Mn-superoxide dismutase (SOD-2) during staurosporine-induced apoptosis in primary cultures from neonatal rat hippocampus. Tretinoin 43-45 superoxide dismutase 1 Rattus norvegicus 113-118
11369496-7 2001 Compared with staurosporine-exposed controls, RA (10 nM)-treated cultures showed a significant increase in neuronal survival, a reduced neuronal ROS content, and enhanced protein levels of SOD-1 and SOD-2 24 and 48 h after the start of the exposure to staurosporine. Tretinoin 46-48 superoxide dismutase 1 Rattus norvegicus 189-194
11369496-8 2001 The results suggest that RA reduced staurosporine-induced oxidative stress and apoptosis by preventing the decrease in the protein levels of SOD-1 and SOD-2, and thus supported the antioxidant defense system. Tretinoin 25-27 superoxide dismutase 1 Rattus norvegicus 141-146
11279655-3 2001 Although the differentiating effects of ATRA on promyelocytes have been well established, in vitro studies have shown that less-differentiated APL blasts (CD34(+)) demonstrate a variable responsiveness to ATRA. Tretinoin 205-209 CD34 molecule Homo sapiens 155-159
11313272-7 2001 Conversely, all-trans retinoic acid significantly decreased survivin protein levels in HL-60, OCI-AML3, and NB-4 cells within 96 hours, parallel to the induction of myelomonocytic differentiation. Tretinoin 22-35 RUNX family transcription factor 2 Homo sapiens 98-102
11465095-3 2001 Both processes are dependent on new mRNA and protein synthesis, involve up-regulation of nur77, and can be inhibited by retinoic acids (RA). Tretinoin 136-138 nuclear receptor subfamily 4 group A member 1 Homo sapiens 89-94
11302942-0 2001 Effects of receptor-selective retinoids on CYP26 gene expression and metabolism of all-trans-retinoic acid in intestinal cells. Tretinoin 86-106 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 43-48
11519864-6 2001 Both 1,25(OH)2D3 and ATRA individually induced an accumulation of MCF-7 cells in the G1 phase of the cell cycle and an associated increase in p21WAFI/CiP1, p27KiP1 and a dephosphorylation of Rb but the effects were not additive. Tretinoin 21-25 cyclin dependent kinase inhibitor 1A Homo sapiens 150-154
11350127-6 2001 Interestingly, the (HSA)SEMA6B transcript was downregulated in two different human glioblastoma cell lines (T98G and A172) upon prolonged treatment with all-trans-retinoic acid, an anti-tumor and differentiation-inducing agent. Tretinoin 153-176 semaphorin 6B Homo sapiens 24-30
11376874-8 2001 Retinoic acid elicited synergistic effects on the CNP secretion rate from HL-60 cells when administered with lipopolysaccharide, interferon-gamma, interleukin-1beta, tumor necrosis factor-alpha, or phorbol ester. Tretinoin 0-13 interferon gamma Homo sapiens 129-145
11376874-8 2001 Retinoic acid elicited synergistic effects on the CNP secretion rate from HL-60 cells when administered with lipopolysaccharide, interferon-gamma, interleukin-1beta, tumor necrosis factor-alpha, or phorbol ester. Tretinoin 0-13 interleukin 1 beta Homo sapiens 147-193
11348470-7 2001 As tested in a chromogenic plasminogen activation assay, incubation with 10 microM all-trans retinoic acid caused a marked induction of cell-associated plasminogen activity after 24 h, and this induction was blocked by neutralizing anti-urokinase-type plasminogen activator antibodies, but not anti-tissue-type plasminogen activator antibodies. Tretinoin 83-106 plasminogen activator, urokinase Homo sapiens 237-273
11295114-4 2001 Despite a previous report that retinoic acid (RA) induced the mac25 gene, the mac25 gene did not increase in U937 cells treated with RA but did increase in the cells treated with 1alpha,25(OH)2-D3. Tretinoin 31-44 insulin like growth factor binding protein 7 Homo sapiens 62-67
11295114-4 2001 Despite a previous report that retinoic acid (RA) induced the mac25 gene, the mac25 gene did not increase in U937 cells treated with RA but did increase in the cells treated with 1alpha,25(OH)2-D3. Tretinoin 46-48 insulin like growth factor binding protein 7 Homo sapiens 62-67
11504380-7 2001 Retinol and retinoic acid also inhibited proliferation of cells growth-stimulated by insulin and other growth factors from the IGF growth factor family (des(1-3)IGF-I and IGF-II), as well as growth factors from the epidermal growth factor family (EGF and TGF-alpha), with retinoic acid being more effective than retinol. Tretinoin 12-25 transforming growth factor alpha Bos taurus 255-264
11504380-9 2001 The growth-stimulating effect of insulin, EGF and TGF-alpha was inhibited 42-64% by retinol and retinoic acid at 100 ng/ml, and 64-84% at 10,000 ng/ml. Tretinoin 96-109 transforming growth factor alpha Bos taurus 50-59
11348470-8 2001 All-trans retinoic acid lead to a strong increase in urokinase-type plasminogen activator (enzyme-linked immunosorbent assay) and urokinase-type plasminogen activator receptor cell surface expression (flow cytometry) after 24 h. At this time-point, tissue-type plasminogen activator and plasminogen activator inhibitor-1 and -2 proteins were not or only slightly increased. Tretinoin 10-23 plasminogen activator, urokinase Homo sapiens 53-89
11348470-8 2001 All-trans retinoic acid lead to a strong increase in urokinase-type plasminogen activator (enzyme-linked immunosorbent assay) and urokinase-type plasminogen activator receptor cell surface expression (flow cytometry) after 24 h. At this time-point, tissue-type plasminogen activator and plasminogen activator inhibitor-1 and -2 proteins were not or only slightly increased. Tretinoin 10-23 plasminogen activator, urokinase Homo sapiens 130-166
11348470-9 2001 Northern blot analyses revealed that all-trans retinoic acid caused an early and short-lived increase of plasminogen activator inhibitor-1, but a prolonged induction of urokinase-type plasminogen activator and urokinase-type plasminogen activator receptor mRNA levels. Tretinoin 47-60 plasminogen activator, urokinase Homo sapiens 169-205
11348470-9 2001 Northern blot analyses revealed that all-trans retinoic acid caused an early and short-lived increase of plasminogen activator inhibitor-1, but a prolonged induction of urokinase-type plasminogen activator and urokinase-type plasminogen activator receptor mRNA levels. Tretinoin 47-60 plasminogen activator, urokinase Homo sapiens 210-246
11358989-4 2001 In contrast, ATRA treatment induced resistance to TNF-alpha-induced apoptosis. Tretinoin 13-17 tumor necrosis factor Homo sapiens 50-59
11343416-0 2001 Retinoic acid attenuates inducible nitric oxide synthase (NOS2) activation in cultured rat cardiac myocytes and microvascular endothelial cells. Tretinoin 0-13 nitric oxide synthase 2 Rattus norvegicus 25-56
11343416-0 2001 Retinoic acid attenuates inducible nitric oxide synthase (NOS2) activation in cultured rat cardiac myocytes and microvascular endothelial cells. Tretinoin 0-13 nitric oxide synthase 2 Rattus norvegicus 58-62
11343416-2 2001 Retinoic Acid Attenuates Inducible Nitric Oxide Synthase (NOS2) Activation in Cultured Rat Cardiac Myocytes and Microvascular Endothelial Cells. Tretinoin 0-13 nitric oxide synthase 2 Rattus norvegicus 25-56
11343416-2 2001 Retinoic Acid Attenuates Inducible Nitric Oxide Synthase (NOS2) Activation in Cultured Rat Cardiac Myocytes and Microvascular Endothelial Cells. Tretinoin 0-13 nitric oxide synthase 2 Rattus norvegicus 58-62
11343416-5 2001 Several natural (endogenous) hormones such as retinoic acid, the active metabolite of vitamin A, have the ability to attenuate NOS2 activation in inflammatory cells. Tretinoin 46-59 nitric oxide synthase 2 Rattus norvegicus 127-131
11343416-10 2001 In CMEC and ARVM stimulated with a combination of LPS and/or cytokines, atRA (10(-6), 10(-5)M) significantly (P<0.05) attenuated NOS2 mRNA and protein expression, enzymatic activity and reduced supernatant nitrite concentration. Tretinoin 72-76 nitric oxide synthase 2 Rattus norvegicus 132-136
11369412-8 2001 All the parameters were restored to normal ranges after complete remission (CR) except elevation of TF and TAT in both groups, as well as PC:A, PS, and t-PA in the ATRA group. Tretinoin 164-168 plasminogen activator, tissue type Homo sapiens 152-156
11430695-0 2001 Retinoic acid specifically downregulates Fgf4 and inhibits posterior cell proliferation in the developing mouse autopod. Tretinoin 0-13 fibroblast growth factor 4 Mus musculus 41-45
11430695-4 2001 The reduction in Fgf4 expression is not accompanied by downregulation of Shh, nor of its receptor and downstream target gene Ptc, suggesting that the skeletal reduction defects induced by retinoic acid are mediated specifically by FGF4-induced skeletogenic mesenchymal cell proliferation. Tretinoin 188-201 fibroblast growth factor 4 Mus musculus 17-21
11430695-4 2001 The reduction in Fgf4 expression is not accompanied by downregulation of Shh, nor of its receptor and downstream target gene Ptc, suggesting that the skeletal reduction defects induced by retinoic acid are mediated specifically by FGF4-induced skeletogenic mesenchymal cell proliferation. Tretinoin 188-201 fibroblast growth factor 4 Mus musculus 231-235
11335000-11 2001 The third RA-synthesizing activity (pI 6.0-6.3) was limited to the ventral retina, and likely corresponded to mouse RALDH-3. Tretinoin 10-12 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 116-123
11309353-5 2001 Furthermore, the mRNA expression of the RA-specific 4-hydroxylase, CYP26A1, was dramatically increased after RA-induction in the two HNSCC cell lines with the highest metabolism, was undetectable in normal keratinocytes, and was not inducible by RA. Tretinoin 40-42 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 67-74
11335102-7 2001 Levels of YY1 DNA binding activity and protein decrease in NT2 cells as they are differentiated with retinoic acid. Tretinoin 101-114 YY1 transcription factor Homo sapiens 10-13
11313141-2 2001 The Adh4 gene product may play an important role in differentiation and development because of its capacity to metabolize retinol to retinoic acid. Tretinoin 133-146 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 4-8
11277867-8 2001 The transduced hepatocytes were shown to secrete immunoreactive proinsulin/insulin, which were stimulated by the concentrations of retinoic acid, dexamethasone and dbcAMP in the culture medium. Tretinoin 131-144 insulin Homo sapiens 64-74
11277867-8 2001 The transduced hepatocytes were shown to secrete immunoreactive proinsulin/insulin, which were stimulated by the concentrations of retinoic acid, dexamethasone and dbcAMP in the culture medium. Tretinoin 131-144 insulin Homo sapiens 67-74
11278809-10 2001 Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Tretinoin 46-50 mitogen-activated protein kinase 8 Homo sapiens 28-31
11284723-6 2001 During the differentiation of HL60 cells induced by all-trans-retinoic acid or 1alpha,25-dihydroxyvitamin D3, there is increased conversion of 17beta-oestradiol into oestrone by an oxidative 17beta-hydroxysteroid dehydrogenase. Tretinoin 52-75 hydroxysteroid 17-beta dehydrogenase 7 Homo sapiens 191-226
11309353-5 2001 Furthermore, the mRNA expression of the RA-specific 4-hydroxylase, CYP26A1, was dramatically increased after RA-induction in the two HNSCC cell lines with the highest metabolism, was undetectable in normal keratinocytes, and was not inducible by RA. Tretinoin 109-111 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 67-74
11309353-6 2001 Next, introduction of CYP26A1 cDNA in a low-metabolizing HNSCC cell line resulted in an 11-fold higher turnover rate of RA and a 12-fold increase in the amount of polar metabolites, but it did not change sensitivity to RA. Tretinoin 120-122 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 22-29
11306173-6 2001 A marked reduction of VEGF-C mRNA expression was also found when HB2 cells were treated with agonists of peroxisome proliferator-activated receptor gamma (PPARgamma, troglitazone), retinoic acid receptor (RAR, all-trans retinoic acid) and retinoid X receptor (RXR, 9-cis retinoic acid). Tretinoin 181-194 vascular endothelial growth factor C Mus musculus 22-28
11338296-6 2001 RESULTS: Gingival and periodontal fibroblasts showed expression of KGF transcripts in vitro, and the degree of expression was markedly influenced by the presence of retinoic acid, an agent known to influence patterns of epithelial differentiation. Tretinoin 165-178 fibroblast growth factor 7 Homo sapiens 67-70
11338296-10 2001 The effects of retinoic acid (RA) on KGF expression in vitro provide an indirect mechanism by which RA may regulate the growth and differentiation of gingival epithelia. Tretinoin 15-28 fibroblast growth factor 7 Homo sapiens 37-40
11338296-10 2001 The effects of retinoic acid (RA) on KGF expression in vitro provide an indirect mechanism by which RA may regulate the growth and differentiation of gingival epithelia. Tretinoin 30-32 fibroblast growth factor 7 Homo sapiens 37-40
11338296-10 2001 The effects of retinoic acid (RA) on KGF expression in vitro provide an indirect mechanism by which RA may regulate the growth and differentiation of gingival epithelia. Tretinoin 100-102 fibroblast growth factor 7 Homo sapiens 37-40
11471571-0 2001 All trans-retinoic acid selectively down-regulates matrix metalloproteinase-9 (MMP-9) and up-regulates tissue inhibitor of metalloproteinase-1 (TIMP-1) in human bronchoalveolar lavage cells. Tretinoin 4-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 103-142
11471571-0 2001 All trans-retinoic acid selectively down-regulates matrix metalloproteinase-9 (MMP-9) and up-regulates tissue inhibitor of metalloproteinase-1 (TIMP-1) in human bronchoalveolar lavage cells. Tretinoin 4-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 144-150
11471571-4 2001 We therefore have analyzed the effects of free and liposomal all trans-retinoic acid (ATRA) on the expression of MMP-9 and TIMP-1 in bronchoalveolar lavage (BAL) cells from patients with COPD and patients with other lung diseases. Tretinoin 65-84 TIMP metallopeptidase inhibitor 1 Homo sapiens 123-129
11471571-4 2001 We therefore have analyzed the effects of free and liposomal all trans-retinoic acid (ATRA) on the expression of MMP-9 and TIMP-1 in bronchoalveolar lavage (BAL) cells from patients with COPD and patients with other lung diseases. Tretinoin 86-90 TIMP metallopeptidase inhibitor 1 Homo sapiens 123-129
11471571-7 2001 RESULTS: We demonstrate that either liposomal or free ATRA selectively down-regulates MMP-9 and up-regulates TIMP-1. Tretinoin 54-58 TIMP metallopeptidase inhibitor 1 Homo sapiens 109-115
11282899-5 2001 Long-term exposure to 1 micromol/L all-trans retinoic acid (RA) dose-dependently inhibited Ang II-induced cell proliferation (P<0.005) as well as DNA and protein synthesis (P<0.001). Tretinoin 35-58 angiotensinogen Homo sapiens 91-97
11282899-5 2001 Long-term exposure to 1 micromol/L all-trans retinoic acid (RA) dose-dependently inhibited Ang II-induced cell proliferation (P<0.005) as well as DNA and protein synthesis (P<0.001). Tretinoin 60-62 angiotensinogen Homo sapiens 91-97
11346880-0 2001 Retinoic acid-induced expression of autotaxin in N-myc-amplified neuroblastoma cells. Tretinoin 0-13 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 36-45
11346880-3 2001 We identified autotaxin (ATX), which encodes an autocrine tumor motility-stimulating factor, as a gene whose expression is significantly induced by retinoic acid in neuroblastoma cells. Tretinoin 148-161 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 14-23
11346880-3 2001 We identified autotaxin (ATX), which encodes an autocrine tumor motility-stimulating factor, as a gene whose expression is significantly induced by retinoic acid in neuroblastoma cells. Tretinoin 148-161 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 25-28
11346880-6 2001 ATX induction by retinoic acid was due to increased transcription and required new protein synthesis. Tretinoin 17-30 ectonucleotide pyrophosphatase/phosphodiesterase 2 Homo sapiens 0-3
11396227-2 2001 PATIENTS AND METHODS: Between November 1994 and October 1996, 38 patients with advanced squamous cell carcinoma were enrolled in a phase II study to investigate an association of low-dose all-trans-retinoic acid (tRA) (40 mg/m2/day, 84 days), interferon-alpha (IFN-alpha) (6.10(6) UI/day, 84 days s.c.) and cisplatin (40 mg/m2/day, day 1, 28 and 56, i.v.). Tretinoin 213-216 interferon alpha 1 Homo sapiens 261-270
11246122-3 2001 Mucous differentiation and expression of MUC2, MUC5AC, MUC5B and MUC7, but not MUCi, MUC4, and MUC8 mucin genes, were shown to be retinoic acid- (RA) or retinol-dependent. Tretinoin 130-143 mucin 2, oligomeric mucus/gel-forming Homo sapiens 41-45
11246122-3 2001 Mucous differentiation and expression of MUC2, MUC5AC, MUC5B and MUC7, but not MUCi, MUC4, and MUC8 mucin genes, were shown to be retinoic acid- (RA) or retinol-dependent. Tretinoin 146-148 mucin 2, oligomeric mucus/gel-forming Homo sapiens 41-45
11171635-0 2001 Interleukin-1beta enhances retinoic acid-mediated expression of bone-type alkaline phosphatase in rat IEC-6 cells. Tretinoin 27-40 interleukin 1 beta Rattus norvegicus 0-17
11171635-4 2001 In contrast, IL-1beta markedly increased the activity, protein, and mRNA of the bone-type ALP only when RA was present. Tretinoin 104-106 interleukin 1 beta Rattus norvegicus 13-21
12733354-0 2001 [Effects of retinoic acid on secretion of apolipoproteins A I, A II, B100, C III and E by cultured HepG2 cells]. Tretinoin 12-25 NLR family pyrin domain containing 3 Homo sapiens 42-80
11320653-8 2001 Notably, an increase in Id3 during RA-induced differentiation of NT2/D1 cells was observed, while Id2 levels increased during BMP-2 and -4 treatment of NT2/D1 cells and during the induction of an endodermal-like differentiation program in the cell line, 27X-1. Tretinoin 35-37 inhibitor of DNA binding 3, HLH protein Homo sapiens 24-27
12733354-2 2001 METHODS: We observed the effect of retinoic acid on the secretion of apolipoproteins A I, A II, C III, B100 and E by cultured HepG2 cells. Tretinoin 35-48 NLR family pyrin domain containing 3 Homo sapiens 69-107
12733354-5 2001 RESULTS: Retinoic acid increased the secretion of apoA I, B100, C III and A II, and it inhibited the secretion of apoE. Tretinoin 9-22 apolipoprotein A1 Homo sapiens 50-56
12733354-5 2001 RESULTS: Retinoic acid increased the secretion of apoA I, B100, C III and A II, and it inhibited the secretion of apoE. Tretinoin 9-22 NLR family pyrin domain containing 3 Homo sapiens 64-78
12733354-5 2001 RESULTS: Retinoic acid increased the secretion of apoA I, B100, C III and A II, and it inhibited the secretion of apoE. Tretinoin 9-22 apolipoprotein E Homo sapiens 114-118
12733354-7 2001 When the concentration of retinoic acid in cultured media was 2 x 10(-4) mol/l, the secretion of apoA I, A II, B100 and C III increased by 14.3% (P < 0.01), 23.8% (P < 0.05), 16.1% (P < 0.01) and 47.6% (P < 0.01) respectively, and the secretion of apoE decreased by 37.2% (P < 0.01). Tretinoin 26-39 apolipoprotein A1 Homo sapiens 97-103
12733354-7 2001 When the concentration of retinoic acid in cultured media was 2 x 10(-4) mol/l, the secretion of apoA I, A II, B100 and C III increased by 14.3% (P < 0.01), 23.8% (P < 0.05), 16.1% (P < 0.01) and 47.6% (P < 0.01) respectively, and the secretion of apoE decreased by 37.2% (P < 0.01). Tretinoin 26-39 NLR family pyrin domain containing 3 Homo sapiens 105-109
12733354-7 2001 When the concentration of retinoic acid in cultured media was 2 x 10(-4) mol/l, the secretion of apoA I, A II, B100 and C III increased by 14.3% (P < 0.01), 23.8% (P < 0.05), 16.1% (P < 0.01) and 47.6% (P < 0.01) respectively, and the secretion of apoE decreased by 37.2% (P < 0.01). Tretinoin 26-39 apolipoprotein E Homo sapiens 260-264
11231062-8 2001 Taken together, our data support the notion that XRALDH2 plays an important role in RA homeostasis by the creation of a critical RA concentration gradient along the anteroposterior axis of early embryos, which is essential for proper patterning of the central nervous system in Xenopus. Tretinoin 84-86 aldehyde dehydrogenase 1 family member A2 L homeolog Xenopus laevis 49-56
11176527-10 2001 All-trans-retinoic acid and 4HPR induced retinoic acid receptor beta expression in 1 bladder cancer cell line. Tretinoin 0-23 retinoic acid receptor beta Homo sapiens 41-68
11176527-14 2001 Lack of retinoic acid receptor beta expression may be responsible for cell resistance to all-trans-retinoic acid but not to the other retinoids. Tretinoin 93-112 retinoic acid receptor beta Homo sapiens 8-35
11242046-10 2001 The expression of GTRAP3-18 can be upregulated by retinoic acid, which results in a specific reduction of EAAC1-mediated glutamate transport. Tretinoin 50-63 solute carrier family 1 member 1 Homo sapiens 106-111
11261782-8 2001 Increased ICAM-3 expression was of functional significance, such that processes stimulated or co-stimulated via ICAM-3 (homotypic aggregation, IL-8 secretion) were clearly enhanced upon RA pretreatment, suggesting that RA may contribute via hitherto unrecognized pathways to immune function and host defense. Tretinoin 186-188 C-X-C motif chemokine ligand 8 Homo sapiens 143-147
11060298-0 2001 Activation of Rac1 and the p38 mitogen-activated protein kinase pathway in response to all-trans-retinoic acid. Tretinoin 87-110 mitogen-activated protein kinase 14 Homo sapiens 27-30
11092879-7 2001 It is proposed that in an RA-induced P19 differentiation model, RA elevates Ik-1 expression, which recruits histone deacetylase to intron 1 of the KOR gene and silences KOR gene promoters. Tretinoin 26-28 potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4 Mus musculus 76-80
11060298-2 2001 In the present study we provide evidence that the p38 MAP kinase pathway is activated in a RA-dependent manner in the NB-4, acute pro-myelocytic leukemia, and the MCF-7, breast carcinoma, cell lines. Tretinoin 91-93 mitogen-activated protein kinase 14 Homo sapiens 50-53
11060298-9 2001 Altogether, our findings demonstrate that the Rac1/p38 MAP kinase pathway is activated in a RA-dependent manner and exhibits negative regulatory effects on the induction of differentiation. Tretinoin 92-94 mitogen-activated protein kinase 14 Homo sapiens 51-54
11060298-3 2001 RA treatment of cells induces a time- and dose-dependent phosphorylation of p38, and such phosphorylation results in activation of its catalytic domain. Tretinoin 0-2 mitogen-activated protein kinase 14 Homo sapiens 76-79
11780200-3 2001 RESULTS: Significant upregulation of IGF-I, IGF-IR and IGF-IIR mRNA was found at 6-24 hours in CBL incubated with physiologic concentrations of RA as compared to those without RA. Tretinoin 144-146 insulin like growth factor 1 Homo sapiens 37-42
11314001-3 2001 This investigation reports that IL-6 protected cells against apoptosis induced by a variety of agents including, TGF-beta, UV and retinoic acid (RA) in Hep3B cells, suggesting that IL-6 is a fundamental determinant of hepatic cell survival. Tretinoin 130-143 interleukin 6 Homo sapiens 32-36
11314001-3 2001 This investigation reports that IL-6 protected cells against apoptosis induced by a variety of agents including, TGF-beta, UV and retinoic acid (RA) in Hep3B cells, suggesting that IL-6 is a fundamental determinant of hepatic cell survival. Tretinoin 130-143 interleukin 6 Homo sapiens 181-185
11314001-3 2001 This investigation reports that IL-6 protected cells against apoptosis induced by a variety of agents including, TGF-beta, UV and retinoic acid (RA) in Hep3B cells, suggesting that IL-6 is a fundamental determinant of hepatic cell survival. Tretinoin 145-147 interleukin 6 Homo sapiens 32-36
11314001-3 2001 This investigation reports that IL-6 protected cells against apoptosis induced by a variety of agents including, TGF-beta, UV and retinoic acid (RA) in Hep3B cells, suggesting that IL-6 is a fundamental determinant of hepatic cell survival. Tretinoin 145-147 interleukin 6 Homo sapiens 181-185
11234892-8 2001 A 24-h exposure to ATRA increased the expression of RAR alpha, RAR beta, RAR gamma, and RXR alpha in 46%, 77%, 30%, and 38% of the samples, respectively. Tretinoin 19-23 retinoic acid receptor beta Homo sapiens 63-71
11234892-10 2001 There was a significant correlation between an increase in RAR beta expression in response to ATRA and sensitivity to ATRA (P < 0.014). Tretinoin 94-98 retinoic acid receptor beta Homo sapiens 59-67
11234892-10 2001 There was a significant correlation between an increase in RAR beta expression in response to ATRA and sensitivity to ATRA (P < 0.014). Tretinoin 118-122 retinoic acid receptor beta Homo sapiens 59-67
11234892-13 2001 We conclude that RAR alpha, RAR beta, RAR gamma, and RXR alpha are expressed in non-M3 AML blast cells and that ATRA-induced expression of RAR beta may be a marker for retinoid sensitivity. Tretinoin 112-116 retinoic acid receptor beta Homo sapiens 28-36
11780200-3 2001 RESULTS: Significant upregulation of IGF-I, IGF-IR and IGF-IIR mRNA was found at 6-24 hours in CBL incubated with physiologic concentrations of RA as compared to those without RA. Tretinoin 176-178 insulin like growth factor 1 Homo sapiens 37-42
11332745-0 2001 Nongenomic vitamin D3 analogs activating ERK2 in HL-60 cells show that retinoic acid-induced differentiation and cell cycle arrest require early concurrent MAPK and RAR and RXR activation. Tretinoin 71-84 mitogen-activated protein kinase 1 Homo sapiens 41-45
11234892-13 2001 We conclude that RAR alpha, RAR beta, RAR gamma, and RXR alpha are expressed in non-M3 AML blast cells and that ATRA-induced expression of RAR beta may be a marker for retinoid sensitivity. Tretinoin 112-116 retinoic acid receptor beta Homo sapiens 139-147
11161715-4 2001 We show that RA induces the TJ structure and expression of several TJ-associated molecules, such as ZO-1, occludin, claudin-6, and claudin-7, as well as a barrier function in the genetically engineered cell line F9:rtTA:Cre-ER(T) L32T2, which allows sophisticated genetic manipulations simply by addition of ligands (H. Chiba et al., 2000, Exp. Tretinoin 13-15 occludin Mus musculus 106-114
11172606-8 2001 RA also induced ets-1 expression, a transcription factor known to be phosphorylated by ERK1, in RA sensitive but not RA resistant lines. Tretinoin 0-2 mitogen-activated protein kinase 3 Homo sapiens 87-91
11172606-8 2001 RA also induced ets-1 expression, a transcription factor known to be phosphorylated by ERK1, in RA sensitive but not RA resistant lines. Tretinoin 96-98 mitogen-activated protein kinase 3 Homo sapiens 87-91
11172606-11 2001 The results of these experiments indicate that induction of hypophosphorylated ets-1 as the result of RA and ECM mediated decreases in ERK1 activity represents a novel mechanism by which RA regulates MMP-9 gene expression. Tretinoin 102-104 mitogen-activated protein kinase 3 Homo sapiens 135-139
11172606-11 2001 The results of these experiments indicate that induction of hypophosphorylated ets-1 as the result of RA and ECM mediated decreases in ERK1 activity represents a novel mechanism by which RA regulates MMP-9 gene expression. Tretinoin 187-189 mitogen-activated protein kinase 3 Homo sapiens 135-139
11332745-0 2001 Nongenomic vitamin D3 analogs activating ERK2 in HL-60 cells show that retinoic acid-induced differentiation and cell cycle arrest require early concurrent MAPK and RAR and RXR activation. Tretinoin 71-84 RAB40B, member RAS oncogene family Homo sapiens 165-168
11181829-0 2001 Antisense inhibition of BCL-2 expression induces retinoic acid-mediated cell death during differentiation of human NT2N neurons. Tretinoin 49-62 BCL2 apoptosis regulator Homo sapiens 24-29
11181829-5 2001 This concentration of retinoic acid was not toxic to undifferentiated NT2/D1 cells but was sufficient to up-regulate the BCL-2 protein in 6 days. Tretinoin 22-35 BCL2 apoptosis regulator Homo sapiens 121-126
11181829-7 2001 Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. Tretinoin 151-164 BCL2 apoptosis regulator Homo sapiens 45-50
11181829-7 2001 Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. Tretinoin 151-164 BCL2 apoptosis regulator Homo sapiens 97-102
11181829-10 2001 The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40-80 microM) of retinoic acid. Tretinoin 32-45 BCL2 apoptosis regulator Homo sapiens 15-20
11181829-10 2001 The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40-80 microM) of retinoic acid. Tretinoin 241-254 BCL2 apoptosis regulator Homo sapiens 15-20
11181829-11 2001 Furthermore, down-regulation of BCL-2 levels by an antisense oligonucleotide in neuronally differentiated NT2/D1 cells increased their susceptibility to retinoic acid-induced apoptosis. Tretinoin 153-166 BCL2 apoptosis regulator Homo sapiens 32-37
11181829-12 2001 These results indicate that one function of the up-regulation of endogenous BCL-2 during neuronal differentiation is to regulate the sensitivity of young post-mitotic neurons to retinoic acid-mediated apoptosis. Tretinoin 178-191 BCL2 apoptosis regulator Homo sapiens 76-81
11036068-7 2001 Upon treatment of the cells with RA, time-dependent increases in the ratio of RARbeta to RXRalpha and the phosphorylated form of Sp1 were observed. Tretinoin 33-35 retinoic acid receptor beta Homo sapiens 78-85
11306066-5 2001 However, if the K(m) for ethanol were smaller, as for human ADH4, the rate of retinol oxidation and formation of retinoic acid would be significantly decreased during metabolism of 50 mM ethanol. Tretinoin 113-126 alcohol dehydrogenase 4 (class II), pi polypeptide Homo sapiens 60-64
11306068-6 2001 When adult mice were examined for production of retinoic acid following retinol administration, Adh1 knockout mice exhibited 10-fold lower retinoic acid levels in liver compared with wild-type, whereas Adh4 knockout mice differed from wild-type by less than 2-fold. Tretinoin 48-61 alcohol dehydrogenase 1 (class I) Mus musculus 96-100
11306068-6 2001 When adult mice were examined for production of retinoic acid following retinol administration, Adh1 knockout mice exhibited 10-fold lower retinoic acid levels in liver compared with wild-type, whereas Adh4 knockout mice differed from wild-type by less than 2-fold. Tretinoin 139-152 alcohol dehydrogenase 1 (class I) Mus musculus 96-100
11306068-7 2001 Thus, Adh1 plays a major role in the metabolism of a large dose of retinol to retinoic acid in adults, whereas Adh4 plays a role in maintaining sufficient retinol metabolism for development during retinol deficiency. Tretinoin 78-91 alcohol dehydrogenase 1 (class I) Mus musculus 6-10
11306068-12 2001 Overall, these studies provide genetic evidence that Adh1, Adh4, Raldh1, and Raldh2 encode retinoid dehydrogenases involved in retinoic acid synthesis in vivo. Tretinoin 127-140 alcohol dehydrogenase 1 (class I) Mus musculus 53-57
11306066-4 2001 Simulations of the oxidation of retinol to retinoic acid with mouse ADH4 and human aldehyde dehydrogenase (ALDH1), using rate constants estimated for all steps in the mechanism, suggest that ethanol (50 mM) would modestly decrease production of retinoic acid. Tretinoin 43-56 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 68-72
11042181-0 2001 Molecular characterization and developmental expression of NORPEG, a novel gene induced by retinoic acid. Tretinoin 91-104 retinoic acid induced 14 Homo sapiens 59-65
11163789-1 2001 The Lewis X (Le(x)) bearing glycolipids were noticeably increased in amounts during the course of neural differentiation of P19 EC cells induced by retinoic acid (RA, all-trans form). Tretinoin 148-161 fucosyltransferase 4 Mus musculus 4-11
11313967-5 2001 When SN-1 cells were treated with MLL-CBP antisense oligonucleotide, the cells were induced to differentiate by ATRA or VD3, suggesting that the MLL-CBP fusion gene dominant-negatively suppresses ATRA- or VD3-induced differentiation. Tretinoin 112-116 CREB binding protein Homo sapiens 38-41
11313967-5 2001 When SN-1 cells were treated with MLL-CBP antisense oligonucleotide, the cells were induced to differentiate by ATRA or VD3, suggesting that the MLL-CBP fusion gene dominant-negatively suppresses ATRA- or VD3-induced differentiation. Tretinoin 112-116 CREB binding protein Homo sapiens 149-152
11313967-8 2001 These findings suggest that RXR agonists or a clinically applicable combination of ATRA and butyrate derivatives might be useful for differentiation therapy in leukemia patients with the MLL-CBP fusion gene. Tretinoin 83-87 CREB binding protein Homo sapiens 191-194
11163789-1 2001 The Lewis X (Le(x)) bearing glycolipids were noticeably increased in amounts during the course of neural differentiation of P19 EC cells induced by retinoic acid (RA, all-trans form). Tretinoin 163-165 fucosyltransferase 4 Mus musculus 4-11
11176716-8 2001 Tretinoin-treated normal fibroblasts secreted more bFGF than did controls at 24 hours (P<.05). Tretinoin 0-9 fibroblast growth factor 2 Homo sapiens 51-55
11179692-19 2001 Since SLAP is transcriptionally regulated by retinoic acid and by activation of B cells, the cloning of its promoter region will permit a detailed analysis of the elements required for its transcriptional regulation. Tretinoin 45-58 Src like adaptor Homo sapiens 6-10
11205873-14 2001 The treatment of retinoic acid induced expression of mucin and CFTR, whereas it inhibited expression of cornifin. Tretinoin 17-30 CF transmembrane conductance regulator Homo sapiens 63-67
11176716-9 2001 Tretinoin-treated keloid-producing fibroblasts secreted more TGF-beta1 than did controls at 120 hours (P<.05). Tretinoin 0-9 transforming growth factor beta 1 Homo sapiens 61-70
11176716-11 2001 CONCLUSIONS: Normal fibroblasts treated with tretinoin produced more bFGF than did controls, and this might partially explain the clinically observed tightening effects of tretinoin. Tretinoin 45-54 fibroblast growth factor 2 Homo sapiens 69-73
11176716-11 2001 CONCLUSIONS: Normal fibroblasts treated with tretinoin produced more bFGF than did controls, and this might partially explain the clinically observed tightening effects of tretinoin. Tretinoin 172-181 fibroblast growth factor 2 Homo sapiens 69-73
11285139-0 2001 Coordinate regulation of RARgamma2, TBP, and TAFII135 by targeted proteolysis during retinoic acid-induced differentiation of F9 embryonal carcinoma cells. Tretinoin 85-98 TATA box binding protein Mus musculus 36-39
11245337-9 2001 In T-47D breast cancer cells, which express RARalpha, RXRalpha and ER, 17beta-HSD reductive activity increased 1.76-fold (p < 0.001), five days following treatment with 10 nM retinoic acid. Tretinoin 178-191 hydroxysteroid 17-beta dehydrogenase 7 Homo sapiens 71-81
11211936-0 2001 Retinoic acid-induced blr1 expression requires RARalpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 91-95
11340260-4 2001 The aim of this study was to define the action of retinoic acid (RA) in combination with IGF-1 on the proportion of insulin cells. Tretinoin 50-63 insulin Gallus gallus 116-123
11340260-4 2001 The aim of this study was to define the action of retinoic acid (RA) in combination with IGF-1 on the proportion of insulin cells. Tretinoin 65-67 insulin Gallus gallus 116-123
11914476-6 2001 Since retinoic acid inhibits the secretion of parathyroid hormone and CRABP I is thought to play a key role in regulating the amount of retinoic acid available to interact with specific nuclear receptors, these data may suggest impaired transport of retinoic acid to cell nuclei, thus contributing to the development of hyperparathyroidism. Tretinoin 6-19 parathyroid hormone Homo sapiens 46-65
11522124-11 2001 One known morphogen, retinoic acid, has the enzymes retinal dehydrogenase (RALDH) and CYP26 maintaining its actions, the former responsible for its generation and the latter for its elimination. Tretinoin 21-34 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 86-91
11211936-0 2001 Retinoic acid-induced blr1 expression requires RARalpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation. Tretinoin 0-13 mitogen-activated protein kinase 8 Homo sapiens 104-112
11211936-2 2001 RA-induced myeloid differentiation and G1/G0 growth arrest of HL-60 cells is known to require the activation of the RARalpha and RXR retinoid receptors, as well as activation of the MAPK, ERK2. Tretinoin 0-2 mitogen-activated protein kinase 1 Homo sapiens 188-192
11243576-6 2001 During HL60 cell differentiation, atRA induced RARbeta mRNA, while the RXR had no effect. Tretinoin 34-38 retinoic acid receptor beta Homo sapiens 47-54
11424001-10 2001 ATRA also inhibited CD34+ JCML monocytic growth and GM-CSF hypersensitivity. Tretinoin 0-4 CD34 molecule Homo sapiens 20-24
11424005-12 2001 While ATRA alone had no effect on Tax and IkappaB-alpha protein levels, ATRA increased the As-induced Tax degradation and the up-regulation of IkappaB-alpha protein. Tretinoin 72-76 NFKB inhibitor alpha Homo sapiens 143-156
11208727-3 2001 However, the role of the major ethanol-induced CYP, CYP2E1, in the metabolism of RA has not been defined. Tretinoin 81-83 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 52-58
11208727-8 2001 The enhancement of RA catabolism by ethanol was inhibited by both CYP2E1 antibody and specific inhibitors (allyl sulfide and chlormethiazole) in a dose-dependent fashion, whereas the metabolism of RA into polar metabolites was abolished completely by nonspecific CYP inhibitors (disulfiram and liarozole). Tretinoin 19-21 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 66-72
11208727-10 2001 CONCLUSIONS: Ethanol-induced CYP2E1 plays a major role in the degradation of RA, which may provide a possible biochemical mechanism for chronic and excessive ethanol intake as a risk for both hepatic and extrahepatic cell proliferation and carcinogenesis. Tretinoin 77-79 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 29-35
11306982-6 2001 Similarly, ATRA inhibited eosinophil/basophil differentiation of cord blood CD34+ cells, while neutrophil differentiation proceeded without impediment. Tretinoin 11-15 CD34 molecule Homo sapiens 76-80
11358286-0 2001 Effect of retinoic acid on the Ca2+-independent phospholipase A2 in nuclei of LA-N-1 neuroblastoma cells. Tretinoin 10-23 phospholipase A2 group IB Homo sapiens 48-64
11464863-0 2001 Retinoic acid-induced apoptosis of the CHP134 neuroblastoma cell line is associated with nuclear accumulation of p53 and is rescued by the GDNF/Ret signal. Tretinoin 0-13 tumor protein p53 Homo sapiens 113-116
11464863-0 2001 Retinoic acid-induced apoptosis of the CHP134 neuroblastoma cell line is associated with nuclear accumulation of p53 and is rescued by the GDNF/Ret signal. Tretinoin 0-13 glial cell derived neurotrophic factor Homo sapiens 139-143
11464863-11 2001 The present results suggest that the RA-induced apoptosis of NBL cells is associated with activation of both the caspase cascade and the p53-mediated pathway with its nuclear translocation. Tretinoin 37-39 tumor protein p53 Homo sapiens 137-140
11169731-3 2001 15 min) but transient activation of ERK1/2 has been reported following induction of macrophage/monocyte differentiation by phorbol esters, or by very high (10(-6) M) concentrations of 1,25-dihydroxyvitamin D(3) (1,25D3), while retinoic acid-induced granulocytic differentiation was accompanied by sustained activation of ERK1/2. Tretinoin 227-240 mitogen-activated protein kinase 3 Homo sapiens 36-42
11516830-4 2001 We show here that in rat primary hippocampal astrocyte cultures, dibutyryl-cAMP increased apolipoprotein E secretion with time in a dose-dependent manner (to 177% at 48 h) and that retinoic acid potentiated this effect (to 298% at 48 h). Tretinoin 181-194 apolipoprotein E Rattus norvegicus 90-106
11166134-2 2001 Further, treatment of human neuroblastoma SH-SY5Y cells with retinoic acid results in the cells withdrawing from the cell cycle and extending neurites, in the same time frame that tissue transglutaminase expression significantly increases. Tretinoin 61-74 transglutaminase 2 Homo sapiens 180-203
11166134-7 2001 In addition, increased tissue transglutaminase expression in response to retinoic acid was abolished in the antisense tissue transglutaminase cells, and antisense and mutant tissue transglutaminase expressing cells did not extend neurites in response to retinoic acid. Tretinoin 73-86 transglutaminase 2 Homo sapiens 23-46
11141033-2 2000 There are few studies on the ability of retinoic acid to affect ADH expression in vivo and none on its effects on alcohol metabolic rate. Tretinoin 40-53 aldo-keto reductase family 1 member A1 Rattus norvegicus 64-67
11104676-1 2000 Activation of mitogen-activated protein kinases (MAPKs), their upstream activators MAPK kinases (MAPKKs or MEKs) and induction of MKP-1 (CL100/3CH134) and MKP-3 (Pyst1/rVH6) dual-specificity MAPK phosphatases (MKPs) were studied in the mouse embryonic stem cell line P19 during the 7 day induction of neuronal differentiation triggered by aggregation and retinoic acid. Tretinoin 355-368 mitogen-activated protein kinase 1 Mus musculus 49-53
11114157-11 2000 Overall, the results indicate that RA modulates horizontal cell electrical synapses by activation of novel nonnuclear RAR(beta)(/gamma)-like sites either directly on, or intimately associated with, gap junction channels. Tretinoin 35-37 retinoic acid receptor beta Homo sapiens 118-127
11162441-0 2000 Regulation of CYP4F2 leukotriene B4 omega-hydroxylase by retinoic acids in HepG2 cells. Tretinoin 57-71 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 14-20
11162441-6 2000 Three regions in the CYP4F2 gene are responsive to retinoic acid with the DR1 RARE element (CCTCCT G TGACCT) at -708 able to bind RXRalpha/RARalpha heterodimers and mediate the repressive response of ATRA. Tretinoin 51-64 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 21-27
11162441-7 2000 These results indicate that retinoic acid can regulate CYP4F2 gene activity with RXRalpha heterodimers stimulating while RARalpha functioning to repress CYP4F2 gene expression. Tretinoin 28-41 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 55-61
11162441-7 2000 These results indicate that retinoic acid can regulate CYP4F2 gene activity with RXRalpha heterodimers stimulating while RARalpha functioning to repress CYP4F2 gene expression. Tretinoin 28-41 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 153-159
11076800-0 2000 Retinoic acid reduces p11 protein levels in bronchial epithelial cells by a posttranslational mechanism. Tretinoin 0-13 S100 calcium binding protein A10 Homo sapiens 22-25
11060239-10 2000 Several manipulations of the chick limb bud show that cux2 expression is regulated by retinoic acid, Sonic hedgehog and the posterior AER. Tretinoin 86-99 cut like homeobox 2 Gallus gallus 54-58
11076800-3 2000 The addition of 10(-6) M RA resulted in reduced p11 protein levels at 4 days, with the greatest effect observed on days 6 and 7. Tretinoin 25-27 S100 calcium binding protein A10 Homo sapiens 48-51
11076800-7 2000 Treatment with RA reduced p11 levels in control cells and in cells transfected with a p11 expression vector, suggesting a posttranslational mechanism. Tretinoin 15-17 S100 calcium binding protein A10 Homo sapiens 26-29
11076800-7 2000 Treatment with RA reduced p11 levels in control cells and in cells transfected with a p11 expression vector, suggesting a posttranslational mechanism. Tretinoin 15-17 S100 calcium binding protein A10 Homo sapiens 86-89
11076800-8 2000 Lactacystin (10(-6) M), an inhibitor of the human 26S proteasome, blocked the decrease in p11 observed with RA treatment. Tretinoin 108-110 S100 calcium binding protein A10 Homo sapiens 90-93
11085906-4 2000 The presence of apoE was investigated in undifferentiated human teratocarcinoma NT2/D1 (NT2) cells and during their differentiation into postmitotic hNT neurons induced by retinoic acid (RA) treatment. Tretinoin 172-185 apolipoprotein E Homo sapiens 16-20
11084658-4 2000 However, when synthesis of retinoic acid was inhibited by disulfiram, or when the function of the retinoid receptors was impaired by using a RAR antagonist, the process of lens regeneration was dramatically affected. Tretinoin 27-40 RAB40B, member RAS oncogene family Homo sapiens 141-144
11098153-7 2000 These results indicate that ARX transduces signals that up-regulate HES-1 gene expression in response to RA-treatment. Tretinoin 105-107 aristaless related homeobox Homo sapiens 28-31
11115359-11 2000 Treatment with retinoic acid caused cytoplasmic PKC-alpha to increase concomitant with a decrease in PKC-alpha in the membrane. Tretinoin 15-28 protein kinase C alpha Homo sapiens 48-57
11115359-11 2000 Treatment with retinoic acid caused cytoplasmic PKC-alpha to increase concomitant with a decrease in PKC-alpha in the membrane. Tretinoin 15-28 protein kinase C alpha Homo sapiens 101-110
11082432-10 2000 The specific retinoic acid metabolizing CYP26 was induced after RA treatment in Caco-2 cells. Tretinoin 13-26 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-45
11082432-10 2000 The specific retinoic acid metabolizing CYP26 was induced after RA treatment in Caco-2 cells. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 40-45
11169062-1 2000 BACKGROUND/AIMS: Midkine (MK) is a novel heparin-binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 150-163 midkine Homo sapiens 17-24
11169062-1 2000 BACKGROUND/AIMS: Midkine (MK) is a novel heparin-binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 150-163 midkine Homo sapiens 26-28
11426618-5 2000 Increased expression of the leukocyte integrins CD11b and CD18 as well as down-regulation of the anti-apoptotic gene bcl-2 are associated with late stage differentiation of the myeloid lineage and retinoic acid induced maturation of acute myeloid leukemic cells. Tretinoin 197-210 integrin subunit beta 2 Homo sapiens 58-62
11117523-3 2000 We have studied the functional involvement of COUP-TFI in retinoic acid (RA)-induced neuronal differentiation of P19 embryonal carcinoma cells through two complementary approaches: 1) deregulated expression of COUP-TFI, and 2) inactivation of endogenous COUP-TFs by means of a dominant-negative COUP-TFI mutant. Tretinoin 58-71 nuclear receptor subfamily 2 group F member 1 Gallus gallus 46-54
11426618-5 2000 Increased expression of the leukocyte integrins CD11b and CD18 as well as down-regulation of the anti-apoptotic gene bcl-2 are associated with late stage differentiation of the myeloid lineage and retinoic acid induced maturation of acute myeloid leukemic cells. Tretinoin 197-210 BCL2 apoptosis regulator Homo sapiens 117-122
11117523-3 2000 We have studied the functional involvement of COUP-TFI in retinoic acid (RA)-induced neuronal differentiation of P19 embryonal carcinoma cells through two complementary approaches: 1) deregulated expression of COUP-TFI, and 2) inactivation of endogenous COUP-TFs by means of a dominant-negative COUP-TFI mutant. Tretinoin 73-75 nuclear receptor subfamily 2 group F member 1 Gallus gallus 46-54
11117523-4 2000 Low levels of wild-type (wt)COUP-TFI transgene expression did not inhibit neural cell fate and primarily enhanced neuron outgrowth from RA-treated P19 aggregates. Tretinoin 136-138 nuclear receptor subfamily 2 group F member 1 Gallus gallus 28-36
11117523-5 2000 In contrast, high COUP-TFI expression impeded the neuronal differentiation of P19 cells induced with RA, resulting in cell cultures lacking neurons. Tretinoin 101-103 nuclear receptor subfamily 2 group F member 1 Gallus gallus 18-26
11117523-7 2000 The dominant-negative COUP-TFI mutant induced cell packing after RA treatment and inhibited neurite extension and neuron outgrowth from aggregates. Tretinoin 65-67 nuclear receptor subfamily 2 group F member 1 Gallus gallus 22-30
11058790-0 2000 Effect of retinoic acid and ethanol on retinoic acid receptor beta and glial fibrillary acidic protein mRNA expression in human astrocytoma cells. Tretinoin 10-23 retinoic acid receptor beta Homo sapiens 39-66
11819702-0 2000 Effects of retinoic acid on proliferation, phenotype and expression of cyclin-dependent kinase inhibitors in TGF-beta1-stimulated rat hepatic stellate cells. Tretinoin 11-24 transforming growth factor, beta 1 Rattus norvegicus 109-118
11819702-1 2000 AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA. Tretinoin 41-54 transforming growth factor, beta 1 Rattus norvegicus 220-253
11819702-1 2000 AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA. Tretinoin 41-54 transforming growth factor, beta 1 Rattus norvegicus 255-264
11819702-1 2000 AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA. Tretinoin 41-54 transforming growth factor, beta 1 Rattus norvegicus 357-366
11211053-4 2000 By northern blot analysis, the expression of BACE mRNA composed of five distinct transcripts (>8.0, 7.0, 6.0, 4.4 and 2.6 kb) was elevated markedly in NTera2 teratocarcinoma cells following retinoic acid-induced neuronal differentiation. Tretinoin 190-203 beta-secretase 1 Homo sapiens 45-49
11071654-4 2000 Consistent with the hypothesis, the HIV-1 protease inhibitors enhanced the ability of ATRA to inhibit growth and induce differentiation of HL-60 and NB4 myeloid leukemia cells, as measured by expression of CD11b and CD66b cell surface antigens, as well as reduction of nitroblue tetrazolium. Tretinoin 86-90 CEA cell adhesion molecule 8 Homo sapiens 216-221
11087670-0 2000 Characterization of the adrenoleukodystrophy-related (ALDR, ABCD2) gene promoter: inductibility by retinoic acid and forskolin. Tretinoin 99-112 ATP binding cassette subfamily D member 2 Homo sapiens 54-58
11087670-0 2000 Characterization of the adrenoleukodystrophy-related (ALDR, ABCD2) gene promoter: inductibility by retinoic acid and forskolin. Tretinoin 99-112 ATP binding cassette subfamily D member 2 Homo sapiens 60-65
11068028-4 2000 We have now examined the effects of all-trans-retinoic acid and 9-cis-retinoic acid on the bradykinin B1 receptor-sensitized responses in human umbilical vein. Tretinoin 36-59 bradykinin receptor B1 Homo sapiens 91-113
11150643-9 2000 These results suggest that RA may inhibit lung cancer growth by down-regulating VPAC(1) receptor and TGF-beta 3 mRNA but up-regulating TGF-beta 2 mRNA. Tretinoin 27-29 vasoactive intestinal peptide receptor 1 Homo sapiens 80-96
10924505-5 2000 After a 7-day treatment with retinoic acid (20 microm), N2a transformants (N2a-Cx43 and N2a-Cx43.GFP) maintained the expression of Cx43 and Cx43.GFP. Tretinoin 29-42 gap junction protein, alpha 1 Mus musculus 79-83
10924505-5 2000 After a 7-day treatment with retinoic acid (20 microm), N2a transformants (N2a-Cx43 and N2a-Cx43.GFP) maintained the expression of Cx43 and Cx43.GFP. Tretinoin 29-42 gap junction protein, alpha 1 Mus musculus 92-96
10924505-5 2000 After a 7-day treatment with retinoic acid (20 microm), N2a transformants (N2a-Cx43 and N2a-Cx43.GFP) maintained the expression of Cx43 and Cx43.GFP. Tretinoin 29-42 gap junction protein, alpha 1 Mus musculus 92-96
10924505-5 2000 After a 7-day treatment with retinoic acid (20 microm), N2a transformants (N2a-Cx43 and N2a-Cx43.GFP) maintained the expression of Cx43 and Cx43.GFP. Tretinoin 29-42 gap junction protein, alpha 1 Mus musculus 92-96
11054636-14 2000 Immunofluorescence, however, revealed enhanced organisation of E-cadherin along the cell membrane by RA treatment. Tretinoin 101-103 cadherin 1 Homo sapiens 63-73
11074878-14 2000 Oral all-trans-retinoic acid enhanced collagen deposition, TGF-beta and IGF-I levels over normal chow fed control animals (P<.05). Tretinoin 5-28 transforming growth factor beta 1 Homo sapiens 59-67
11074878-14 2000 Oral all-trans-retinoic acid enhanced collagen deposition, TGF-beta and IGF-I levels over normal chow fed control animals (P<.05). Tretinoin 5-28 insulin like growth factor 1 Homo sapiens 72-77
11027432-7 2000 Function of the receptors was retained in terms of the ability of both oestradiol and retinoic acid to upregulate pS2 gene expression, but there was reduced ability to upregulate transiently transfected ERE- and RRE-linked reporter genes. Tretinoin 86-99 taste 2 receptor member 64 pseudogene Homo sapiens 114-117
11052959-2 2000 In vitro studies have suggested that retinoic acid decreases inducible NO synthase (NOS2, or iNOS) expression, a component of innate immunity, in several cell types stimulated with lipopolysaccharide (LPS) or cytokines. Tretinoin 37-50 nitric oxide synthase 2 Rattus norvegicus 84-88
11052959-2 2000 In vitro studies have suggested that retinoic acid decreases inducible NO synthase (NOS2, or iNOS) expression, a component of innate immunity, in several cell types stimulated with lipopolysaccharide (LPS) or cytokines. Tretinoin 37-50 nitric oxide synthase 2 Rattus norvegicus 93-97
11052959-3 2000 This study investigated the effect of retinoic acid on LPS-stimulated NOS2 expression in vivo. Tretinoin 38-51 nitric oxide synthase 2 Rattus norvegicus 70-74
11052959-6 2000 In sharp contrast to previous in vitro study reports, RA significantly enhanced NOS2 mRNA, protein expression, and plasma nitrate/nitrite concentration in LPS-injected rats but not in saline-injected rats. Tretinoin 54-56 nitric oxide synthase 2 Rattus norvegicus 80-84
11052959-10 2000 These results demonstrate for the first time that RA supplementation in vivo enhances activation of the LPS-triggered NOS2 pathway. Tretinoin 50-52 nitric oxide synthase 2 Rattus norvegicus 118-122
11050012-0 2000 Retinoic acid stimulates erythropoietin gene transcription in embryonal carcinoma cells through the direct repeat of a steroid/thyroid hormone receptor response element half-site in the hypoxia-response enhancer. Tretinoin 0-13 erythropoietin Homo sapiens 25-39
11050012-2 2000 This study identifies retinoic acid (RA) as an inducer for Epo production in the embryonal carcinoma cell lines P19 and F9. Tretinoin 22-35 erythropoietin Homo sapiens 59-62
11050012-2 2000 This study identifies retinoic acid (RA) as an inducer for Epo production in the embryonal carcinoma cell lines P19 and F9. Tretinoin 37-39 erythropoietin Homo sapiens 59-62
11050012-3 2000 RA induced Epo production through the transcriptional activation of the Epo gene in an oxygen-independent manner. Tretinoin 0-2 erythropoietin Homo sapiens 11-14
11050012-3 2000 RA induced Epo production through the transcriptional activation of the Epo gene in an oxygen-independent manner. Tretinoin 0-2 erythropoietin Homo sapiens 72-75
11050012-6 2000 In human hepatoma Hep3B cells, an orphan receptor, hepatocyte nuclear factor-4, strongly augmented hypoxic induction of the Epo gene in cooperation with hypoxia-inducible factor-1 (HIF-1) by binding to DR-2, whereas in P19 cells, the interaction of RA receptors with DR-2 was sufficient for RA-induced transcriptional activation of the Epo gene without the requirement of the HIF-1 site. Tretinoin 249-251 erythropoietin Homo sapiens 124-127
11050012-6 2000 In human hepatoma Hep3B cells, an orphan receptor, hepatocyte nuclear factor-4, strongly augmented hypoxic induction of the Epo gene in cooperation with hypoxia-inducible factor-1 (HIF-1) by binding to DR-2, whereas in P19 cells, the interaction of RA receptors with DR-2 was sufficient for RA-induced transcriptional activation of the Epo gene without the requirement of the HIF-1 site. Tretinoin 249-251 hypoxia inducible factor 1 subunit alpha Homo sapiens 181-186
11029503-9 2000 Retinoic acid receptor (RAR)-alpha was not affected by treatment and RAR-alpha was moderately influenced whereas RAR-beta (concomitantly with transforming growth factor-beta) was induced in 33% of patients by ATRA alone. Tretinoin 209-213 retinoic acid receptor beta Homo sapiens 113-121
11025452-8 2000 Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor. Tretinoin 7-9 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 42-49
11025452-8 2000 Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor. Tretinoin 7-9 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 51-56
11025452-8 2000 Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor. Tretinoin 7-9 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 293-300
11025452-8 2000 Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor. Tretinoin 27-29 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 42-49
11025452-8 2000 Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor. Tretinoin 27-29 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 51-56
11025452-8 2000 Strong RA induction of the RA hydroxylase P450RAI (CYP26) was confined to ERalpha-positive T47D and MCF-7 breast cancer cells and did not appear to explain the lack of detectable RA levels in these cells since RA remained undetectable when the cells were treated with 5-10 microM liarozole, a P450RAI inhibitor. Tretinoin 27-29 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 293-300
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 127-140 HNF1 homeobox A Homo sapiens 29-38
11069616-2 2000 In addition, keratin 6 expression is inducible in interfollicular epidermis and the outer root sheath of the follicle, in response to wounding stimuli, phorbol esters, or retinoic acid. Tretinoin 171-184 keratin 6 Mus musculus 13-22
11120388-0 2000 Interaction of ethanol with retinol and retinoic acid in RAR beta and GAP-43 expression. Tretinoin 40-53 retinoic acid receptor beta Homo sapiens 57-65
11120388-2 2000 In LAN-5 neuroblastoma cells, retinol (10(-6) M) and retinoic acid (RA; 10(-5)-10(-6) M) increased RAR beta mRNA expression. Tretinoin 53-66 retinoic acid receptor beta Homo sapiens 99-107
11120388-2 2000 In LAN-5 neuroblastoma cells, retinol (10(-6) M) and retinoic acid (RA; 10(-5)-10(-6) M) increased RAR beta mRNA expression. Tretinoin 68-70 retinoic acid receptor beta Homo sapiens 99-107
11120388-4 2000 RAR beta mRNA expression was decreased by ethanol in the presence of 10(-6) M RA, but not 10(-5) M RA. Tretinoin 78-80 retinoic acid receptor beta Homo sapiens 0-8
11120388-5 2000 With cycloheximide (CX), RA still stimulated RAR beta mRNA, but the effect of ethanol was abolished. Tretinoin 25-27 retinoic acid receptor beta Homo sapiens 45-53
10938282-10 2000 The TGF-beta-neutralizing antibody blocked the RA-induced as well as TGF-beta2-mediated MUC4 expression. Tretinoin 47-49 transforming growth factor beta 1 Homo sapiens 4-12
11069026-4 2000 In contrast, following treatment of HL-60 cells with retinoic acid (RA) which results in a granulocytic differentiation of these cells, 4E-BP1 protein expression is decreased whereas 4E-BP2 protein expression is strongly increased. Tretinoin 53-66 eukaryotic translation initiation factor 4E binding protein 2 Homo sapiens 183-189
11069026-4 2000 In contrast, following treatment of HL-60 cells with retinoic acid (RA) which results in a granulocytic differentiation of these cells, 4E-BP1 protein expression is decreased whereas 4E-BP2 protein expression is strongly increased. Tretinoin 68-70 eukaryotic translation initiation factor 4E binding protein 2 Homo sapiens 183-189
11069026-6 2000 RA treatment resulted in a decrease in 4E-BP1 protein and mRNA expression and concomitant increase in 4E-BP2 protein expression, in NB4 cells, but not in NB4-R1 and NB4-R2 cells. Tretinoin 0-2 eukaryotic translation initiation factor 4E binding protein 2 Homo sapiens 102-108
12212112-4 2000 Treated with all-trans retinoic acid (ATRA), the expression of HOXB7 in HEL cells infected by HCMV was significantly increased. Tretinoin 13-36 homeobox B7 Homo sapiens 63-68
12212112-4 2000 Treated with all-trans retinoic acid (ATRA), the expression of HOXB7 in HEL cells infected by HCMV was significantly increased. Tretinoin 38-42 homeobox B7 Homo sapiens 63-68
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 127-140 hepatocyte nuclear factor 4 alpha Homo sapiens 50-59
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 142-144 HNF1 homeobox A Homo sapiens 29-38
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 142-144 hepatocyte nuclear factor 4 alpha Homo sapiens 50-59
11027556-3 2000 Transient transfection experiments showed that RA increased the promoter activity of the HNF1alpha and HNF4alpha genes in Hep3B cells. Tretinoin 47-49 HNF1 homeobox A Homo sapiens 89-98
11027556-3 2000 Transient transfection experiments showed that RA increased the promoter activity of the HNF1alpha and HNF4alpha genes in Hep3B cells. Tretinoin 47-49 hepatocyte nuclear factor 4 alpha Homo sapiens 103-112
11027556-8 2000 These data suggest that the differentiation effect of RA on hepatocyte may be due to direct interaction of RXRalpha with the RA-responsive elements on the HNF1alpha and HNF4alpha genes. Tretinoin 54-56 HNF1 homeobox A Homo sapiens 155-164
11027556-8 2000 These data suggest that the differentiation effect of RA on hepatocyte may be due to direct interaction of RXRalpha with the RA-responsive elements on the HNF1alpha and HNF4alpha genes. Tretinoin 54-56 hepatocyte nuclear factor 4 alpha Homo sapiens 169-178
11027556-8 2000 These data suggest that the differentiation effect of RA on hepatocyte may be due to direct interaction of RXRalpha with the RA-responsive elements on the HNF1alpha and HNF4alpha genes. Tretinoin 125-127 HNF1 homeobox A Homo sapiens 155-164
11027556-8 2000 These data suggest that the differentiation effect of RA on hepatocyte may be due to direct interaction of RXRalpha with the RA-responsive elements on the HNF1alpha and HNF4alpha genes. Tretinoin 125-127 hepatocyte nuclear factor 4 alpha Homo sapiens 169-178
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 12-25 lysozyme Homo sapiens 77-85
11003584-9 2000 In addition, decreasing TGF-betaRI expression by treatment with retinoic acid not only decreased TGF-beta-mediated growth inhibition in normal cells but also prevented the increased sensitivity to exogenous TGF-beta in polyamine-deficient cells. Tretinoin 64-77 transforming growth factor, beta 1 Rattus norvegicus 24-32
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 12-25 mucin 2, oligomeric mucus/gel-forming Homo sapiens 121-126
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 27-29 lysozyme Homo sapiens 77-85
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 27-29 mucin 2, oligomeric mucus/gel-forming Homo sapiens 121-126
11003584-9 2000 In addition, decreasing TGF-betaRI expression by treatment with retinoic acid not only decreased TGF-beta-mediated growth inhibition in normal cells but also prevented the increased sensitivity to exogenous TGF-beta in polyamine-deficient cells. Tretinoin 64-77 transforming growth factor, beta 1 Rattus norvegicus 97-105
11023996-10 2000 We conclude that CYP26 expression and RA metabolism are regulated in adult liver not only acutely by RA administration, as may be relevant to retinoid therapy, but under chronic dietary conditions relevant to vitamin A nutrition in humans. Tretinoin 101-103 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-22
11089918-2 2000 Also CD38, a homologous gene to CD157, is upregulated in promyelocytic HL-60 cells by the monocyte and granulocyte differentiation-inducing 1alpha,25dihydroxyvitamin D3 (VD3) and all-trans retinoic acid (ATRA), respectively. Tretinoin 189-202 bone marrow stromal cell antigen 1 Homo sapiens 32-37
11089918-2 2000 Also CD38, a homologous gene to CD157, is upregulated in promyelocytic HL-60 cells by the monocyte and granulocyte differentiation-inducing 1alpha,25dihydroxyvitamin D3 (VD3) and all-trans retinoic acid (ATRA), respectively. Tretinoin 204-208 bone marrow stromal cell antigen 1 Homo sapiens 32-37
10962451-6 2000 The aim of our study was to determine and compare the effects of retinoic acid and palm oil carotenoids on growth of and oestrone sulphatase and E(2)DH activities in the oestrogen receptor positive, MCF-7 and oestrogen receptor negative, MDA-MB-231 breast cancer cell lines. Tretinoin 65-78 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 145-151
11126425-4 2000 Protease inhibitors are hypothesized to cause this syndrome by impairing conversion of retinoic acid to cis-9-retinoic acid (leading to impaired peripheral fat storage, sequestration of body fat to central adipocytes, and hyperlipidemia) and by inhibiting low-density lipoprotein receptor-related protein (LRP), thus preventing postprandial chylomicron clearance and further contributing to hyperlipidemia. Tretinoin 87-100 LDL receptor related protein 1 Homo sapiens 306-309
11025231-0 2000 RALDH3, a retinaldehyde dehydrogenase that generates retinoic acid, is expressed in the ventral retina, otic vesicle and olfactory pit during mouse development. Tretinoin 53-66 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 0-6
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 0-13 RAB40B, member RAS oncogene family Homo sapiens 74-77
11048798-1 2000 Midkine (MK) is a novel heparin-binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 133-146 midkine Homo sapiens 0-7
11048798-1 2000 Midkine (MK) is a novel heparin-binding growth factor whose gene has been identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 133-146 midkine Homo sapiens 9-11
11000524-5 2000 In contrast, NGF inhibited invasion and reverted the effect of retinoic acid. Tretinoin 63-76 nerve growth factor Homo sapiens 13-16
11030153-8 2000 We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Tretinoin 98-102 dynactin subunit 6 Homo sapiens 46-49
11030153-8 2000 We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Tretinoin 98-102 H3 histone pseudogene 12 Homo sapiens 65-68
11030153-8 2000 We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Tretinoin 98-102 cyclin D3 Homo sapiens 132-141
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 0-13 RAB40B, member RAS oncogene family Homo sapiens 147-150
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 15-17 RAB40B, member RAS oncogene family Homo sapiens 74-77
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 15-17 RAB40B, member RAS oncogene family Homo sapiens 147-150
10996843-9 2000 Both MMP-1 and MMP-13 were detected and appear to be involved in IL-1 + RetA induced bovine cartilage destruction. Tretinoin 72-76 matrix metallopeptidase 13 Bos taurus 15-21
10999756-11 2000 Pharmacological dietary RA stimulated RARalpha, RARbeta, and RARgamma as early as day 1 by 2-, 4-, and 2.1-fold, respectively, without effect on lung RARs. Tretinoin 24-26 retinoic acid receptor, beta Rattus norvegicus 48-55
10950848-0 2000 Catalysis of the 4-hydroxylation of retinoic acids by cyp3a7 in human fetal hepatic tissues. Tretinoin 36-50 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 54-60
10950848-2 2000 In this study, we investigated the 4-hydroxylation of highly embryotoxic and teratogenic retinoic acids (RA) as catalyzed by human fetal liver microsomes (HFLM) and demonstrated that CYP3A7 is an efficient RA hydroxylase. Tretinoin 105-107 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 183-189
10950848-11 2000 Because 4-hydroxylated metabolites of RA are much less potent embryotoxins and teratogens, the results indicated that the 4-hydroxylation of RA, catalyzed prenatally by CYP3A7, might play an important role in protecting the human fetus against RA-induced embryotoxicity. Tretinoin 38-40 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 169-175
10950848-11 2000 Because 4-hydroxylated metabolites of RA are much less potent embryotoxins and teratogens, the results indicated that the 4-hydroxylation of RA, catalyzed prenatally by CYP3A7, might play an important role in protecting the human fetus against RA-induced embryotoxicity. Tretinoin 141-143 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 169-175
10950848-11 2000 Because 4-hydroxylated metabolites of RA are much less potent embryotoxins and teratogens, the results indicated that the 4-hydroxylation of RA, catalyzed prenatally by CYP3A7, might play an important role in protecting the human fetus against RA-induced embryotoxicity. Tretinoin 141-143 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 169-175
10936200-4 2000 This biphasic response may be related to the different expression of TNF-alpha receptors (TNFRs); a significant increase in the density of TNFR1 was in fact observed following RA-induced differentiation. Tretinoin 176-178 tumor necrosis factor Homo sapiens 69-78
10884590-6 2000 1 cells, a murine macrophage cell line, was used to study the effects of RA on the production of NO, TNFalpha and IL-1beta. Tretinoin 73-75 interleukin 1 beta Mus musculus 114-122
10884590-9 2000 NO production and subsequent nitrite accumulation in the media peaked at 24 h, plateaued at 48 h, and remained at the same level through 72 h. The presence of RA decreased TNFalpha levels, measured by both bioassay and enzyme-linked immunosorbent assay (ELISA), but these did not correlate with increased mRNA expression measured by reverse-transcriptase polymerase chain reaction at 6 h after LPS stimulation. Tretinoin 159-161 tumor necrosis factor Mus musculus 172-180
10884590-10 2000 IL-1beta protein production measured by both ELISA and bioassay decreased with RA treatment. Tretinoin 79-81 interleukin 1 beta Mus musculus 0-8
10974645-0 2000 Opposite effects of feeding a vitamin A-deficient diet and retinoic acid treatment on brown adipose tissue uncoupling protein 1 (UCP1), UCP2 and leptin expression. Tretinoin 59-72 uncoupling protein 2 (mitochondrial, proton carrier) Mus musculus 136-140
10953040-9 2000 The induction of CYP26 correlated with increased metabolism of RA into 18-hydroxy-, 4-oxo-, and 4-hydroxy-RA. Tretinoin 63-65 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 17-22
10964585-0 2000 Retinoic acid selectively inhibits the vascular permeabilizing effect of VPF/VEGF, an early step in the angiogenic cascade. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 73-76
10964585-0 2000 Retinoic acid selectively inhibits the vascular permeabilizing effect of VPF/VEGF, an early step in the angiogenic cascade. Tretinoin 0-13 vascular endothelial growth factor A Homo sapiens 77-81
10964585-5 2000 To investigate further the mechanisms by which RA inhibits angiogenesis, we evaluated the effects of RA on VPF/VEGF-induced angiogenesis and microvascular permeability. Tretinoin 101-103 vascular endothelial growth factor A Homo sapiens 107-110
10964585-6 2000 RA selectively inhibited the angiogenic response induced by VPF/VEGF, but not that induced by fibroblast growth factor-2 (FGF-2), in the CAM assay. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 60-63
10964585-6 2000 RA selectively inhibited the angiogenic response induced by VPF/VEGF, but not that induced by fibroblast growth factor-2 (FGF-2), in the CAM assay. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 64-68
10964585-7 2000 RA and two of its isomers also inhibited the vascular permeabilizing effect of VPF/VEGF but not that induced by histamine. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 79-82
10964585-7 2000 RA and two of its isomers also inhibited the vascular permeabilizing effect of VPF/VEGF but not that induced by histamine. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 83-87
10964585-8 2000 The vascular permeabilization induced by VPF/VEGF and blocked by RA takes place within 1-15 min, too short a time frame for RA to act by modulating transcription through classic retinoid receptors. Tretinoin 124-126 vascular endothelial growth factor A Homo sapiens 41-44
10964585-8 2000 The vascular permeabilization induced by VPF/VEGF and blocked by RA takes place within 1-15 min, too short a time frame for RA to act by modulating transcription through classic retinoid receptors. Tretinoin 124-126 vascular endothelial growth factor A Homo sapiens 45-49
10964585-9 2000 RA also inhibited VPF/VEGF-induced phosphorylation of PLC-gamma and synthesis of cGMP but actually increased VPF/VEGF binding to cultured endothelial cells. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 18-21
10964585-9 2000 RA also inhibited VPF/VEGF-induced phosphorylation of PLC-gamma and synthesis of cGMP but actually increased VPF/VEGF binding to cultured endothelial cells. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 22-26
10964585-9 2000 RA also inhibited VPF/VEGF-induced phosphorylation of PLC-gamma and synthesis of cGMP but actually increased VPF/VEGF binding to cultured endothelial cells. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 109-112
10964585-9 2000 RA also inhibited VPF/VEGF-induced phosphorylation of PLC-gamma and synthesis of cGMP but actually increased VPF/VEGF binding to cultured endothelial cells. Tretinoin 0-2 vascular endothelial growth factor A Homo sapiens 113-117
10964585-10 2000 Taken together, these findings indicate that RA selectively blocks VPF/VEGF-induced microvascular permeability and angiogenesis and also identify VPF/VEGF as a major target of RA action. Tretinoin 45-47 vascular endothelial growth factor A Homo sapiens 67-70
10964585-10 2000 Taken together, these findings indicate that RA selectively blocks VPF/VEGF-induced microvascular permeability and angiogenesis and also identify VPF/VEGF as a major target of RA action. Tretinoin 45-47 vascular endothelial growth factor A Homo sapiens 71-75
10964585-10 2000 Taken together, these findings indicate that RA selectively blocks VPF/VEGF-induced microvascular permeability and angiogenesis and also identify VPF/VEGF as a major target of RA action. Tretinoin 176-178 vascular endothelial growth factor A Homo sapiens 67-70
10964585-10 2000 Taken together, these findings indicate that RA selectively blocks VPF/VEGF-induced microvascular permeability and angiogenesis and also identify VPF/VEGF as a major target of RA action. Tretinoin 176-178 vascular endothelial growth factor A Homo sapiens 146-149
10964585-10 2000 Taken together, these findings indicate that RA selectively blocks VPF/VEGF-induced microvascular permeability and angiogenesis and also identify VPF/VEGF as a major target of RA action. Tretinoin 176-178 vascular endothelial growth factor A Homo sapiens 150-154
10964585-11 2000 The selectivity of RA"s action suggests that other, RA-independent pathways must exist for the angiogenesis induced by FGF-2 and the vascular permeabilizing effect of histamine. Tretinoin 19-21 fibroblast growth factor 2 Homo sapiens 119-124
10978779-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human chronic myelogenous leukemia K562 cells. Tretinoin 31-44 nerve growth factor Homo sapiens 113-132
10978779-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human chronic myelogenous leukemia K562 cells. Tretinoin 31-44 nerve growth factor Homo sapiens 134-137
10978779-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human chronic myelogenous leukemia K562 cells. Tretinoin 46-48 nerve growth factor Homo sapiens 113-132
10978779-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human chronic myelogenous leukemia K562 cells. Tretinoin 46-48 nerve growth factor Homo sapiens 134-137
10953040-2 2000 In HTBE cells, retinoic acid (RA) inhibits squamous differentiation and induces mucous cell differentiation as indicated by the suppression of transglutaminase I and increased expression of the mucin gene MUC2. Tretinoin 15-28 mucin 2, oligomeric mucus/gel-forming Homo sapiens 205-209
10953040-2 2000 In HTBE cells, retinoic acid (RA) inhibits squamous differentiation and induces mucous cell differentiation as indicated by the suppression of transglutaminase I and increased expression of the mucin gene MUC2. Tretinoin 30-32 mucin 2, oligomeric mucus/gel-forming Homo sapiens 205-209
10953040-4 2000 RA is required but not sufficient to induce RARbeta, CYP26, and MUC2 mRNA because induction is only observed in confluent but not in logarithmic cultures, suggesting that additional factors are critical in their regulation. Tretinoin 0-2 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 53-58
10953040-4 2000 RA is required but not sufficient to induce RARbeta, CYP26, and MUC2 mRNA because induction is only observed in confluent but not in logarithmic cultures, suggesting that additional factors are critical in their regulation. Tretinoin 0-2 mucin 2, oligomeric mucus/gel-forming Homo sapiens 64-68
10874126-0 2000 Identification of human cytochrome P450 isoforms that contribute to all-trans-retinoic acid 4-hydroxylation. Tretinoin 78-91 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 24-39
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 0-13 promyelocytic leukemia Mus musculus 169-172
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 0-13 zinc finger and BTB domain containing 16 Mus musculus 186-190
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 15-17 promyelocytic leukemia Mus musculus 169-172
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 15-17 zinc finger and BTB domain containing 16 Mus musculus 186-190
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 35-37 promyelocytic leukemia Mus musculus 122-125
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 35-37 zinc finger and BTB domain containing 16 Mus musculus 138-142
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 42-44 promyelocytic leukemia Mus musculus 122-125
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 42-44 zinc finger and BTB domain containing 16 Mus musculus 138-142
10874126-1 2000 The role of specific human cytochrome P450 (CYP) isoforms in the oxidative metabolism of all-trans-retinoic acid was investigated by studies in human liver microsomes using isoform-specific chemical inhibitors and inhibitory antibodies. Tretinoin 89-112 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 27-42
10874126-1 2000 The role of specific human cytochrome P450 (CYP) isoforms in the oxidative metabolism of all-trans-retinoic acid was investigated by studies in human liver microsomes using isoform-specific chemical inhibitors and inhibitory antibodies. Tretinoin 89-112 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 44-47
10874126-4 2000 Using inhibition studies and correlation analysis, we also concluded that CYP2C8 was the major all-trans-retinoic acid 4-hydroxylating cytochrome P450 in human liver microsomes, though CYP3A4 and, to a lesser extent CYP2C9, also made a contribution. Tretinoin 95-118 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 135-150
10944551-1 2000 BACKGROUND: Retinoic acid plays an important role in lung development and differentiation, acting primarily via nuclear receptors encoded by the retinoic acid receptor-beta (RARbeta) gene. Tretinoin 12-25 retinoic acid receptor beta Homo sapiens 145-172
10933889-0 2000 Role of Ser(289) in RARgamma and its homologous amino acid residue of RARalpha and RARbeta in the binding of retinoic acid. Tretinoin 109-122 retinoic acid receptor beta Homo sapiens 83-90
10933889-4 2000 Here we have examined the role of the hydroxyl group of RARgamma Ser(289) and its homologous amino acid residues in RARalpha (Ser(287)) and RARbeta (Ser(280)) alone and in conjunction with their respective RARgamma Arg(278) homologs for RA binding and RA-dependent transactivation activity. Tretinoin 56-58 retinoic acid receptor beta Homo sapiens 140-147
10933889-7 2000 Alternatively, strong synergism was observed in RARbeta between Ser(280) and Arg(269) for RA-binding and RA-dependent transactivation activity. Tretinoin 90-92 retinoic acid receptor beta Homo sapiens 48-55
10969765-2 2000 Midkine (MK) is a newly identified heparin-binding growth factor that is transiently expressed in the early stages of retinoic acid-induced differentiation of embryonal carcinoma cells. Tretinoin 118-131 midkine Homo sapiens 0-7
10969765-2 2000 Midkine (MK) is a newly identified heparin-binding growth factor that is transiently expressed in the early stages of retinoic acid-induced differentiation of embryonal carcinoma cells. Tretinoin 118-131 midkine Homo sapiens 9-11
10944551-1 2000 BACKGROUND: Retinoic acid plays an important role in lung development and differentiation, acting primarily via nuclear receptors encoded by the retinoic acid receptor-beta (RARbeta) gene. Tretinoin 12-25 retinoic acid receptor beta Homo sapiens 174-181
10913361-3 2000 The enhanced synthesis of proteoglycan induced at all ages by TGF-beta1 was down-regulated by IL-1 beta and retinoic acid. Tretinoin 108-121 transforming growth factor beta 1 Equus caballus 62-71
10807916-4 2000 Expression of the constitutively active form of either MEKK1 or MEKK4 mimicked the action of retinoic acid, inducing these embryonal carcinoma cells to primitive endoderm. Tretinoin 93-106 mitogen-activated protein kinase kinase kinase 1 Rattus norvegicus 55-60
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin A2 Homo sapiens 146-154
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 cyclin dependent kinase inhibitor 1A Homo sapiens 202-205
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 cyclin dependent kinase inhibitor 1A Homo sapiens 206-210
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin dependent kinase 6 Homo sapiens 273-277
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 cyclin dependent kinase inhibitor 1A Homo sapiens 211-215
10896783-4 2000 Furthermore, RA-induced growth arrest of CH27 cells was also associated with increased retinoic acid receptor beta (RARbeta) and reduced c-Myc expression. Tretinoin 13-15 retinoic acid receptor beta Homo sapiens 87-114
10896783-4 2000 Furthermore, RA-induced growth arrest of CH27 cells was also associated with increased retinoic acid receptor beta (RARbeta) and reduced c-Myc expression. Tretinoin 13-15 retinoic acid receptor beta Homo sapiens 116-123
10942234-8 2000 However, addition of ATRA to cultures containing IFN-alpha reversed the selective inhibition of CML CFU-GM replating seen in cultures containing IFN-alpha alone. Tretinoin 21-25 interferon alpha 1 Homo sapiens 49-58
11032179-5 2000 The inhibitory effect of RA on branching is strongly decreased in RARbeta null lungs, while enhancement of budding by the pan-RAR antagonist is not affected by an RARgamma null mutation. Tretinoin 25-27 retinoic acid receptor, beta Rattus norvegicus 66-73
11032179-8 2000 They also suggest that at the pseudoglandular stage, RA signaling through RARbeta, but not RARgamma, inhibits distal bud formation thereby promoting the formation of conducting airways. Tretinoin 53-55 retinoic acid receptor, beta Rattus norvegicus 74-81
10946899-10 2000 Moreover, all-trans-retinoic acid increased the mRNA expression of thyroglobulin and decreased both the mRNA expression and secretion of interleukin-6 and leukemia inhibitory factor while significantly stimulating growth. Tretinoin 10-33 interleukin 6 Homo sapiens 137-150
10954918-3 2000 Exposure to LPS resulted in the maximum release of soluble TNF-alpha by 2 h. Electrophoretic mobility shift assays (EMSA) using the TAC element as a probe showed a unique pattern for LPS-activated cells: the disappearance of the upper band of a doublet seen in untreated and all-trans retinoic acid (ATRA)-treated cells. Tretinoin 285-298 tumor necrosis factor Homo sapiens 59-68
10954918-3 2000 Exposure to LPS resulted in the maximum release of soluble TNF-alpha by 2 h. Electrophoretic mobility shift assays (EMSA) using the TAC element as a probe showed a unique pattern for LPS-activated cells: the disappearance of the upper band of a doublet seen in untreated and all-trans retinoic acid (ATRA)-treated cells. Tretinoin 300-304 tumor necrosis factor Homo sapiens 59-68
10942234-8 2000 However, addition of ATRA to cultures containing IFN-alpha reversed the selective inhibition of CML CFU-GM replating seen in cultures containing IFN-alpha alone. Tretinoin 21-25 interferon alpha 1 Homo sapiens 145-154
10942234-12 2000 Thus we conclude that combining IFN-alpha with Ara-C or ATRA neutralises the effect of IFN-alpha on CML CFU-GM. Tretinoin 56-60 interferon alpha 1 Homo sapiens 87-96
10748087-7 2000 At pharmacological concentrations (10 micrometer), atRA decreased PKCalpha activity through the competition with PS but not phorbol-12-myristate-13-acetate, diacylglycerol, or Ca(2+). Tretinoin 51-55 protein kinase C alpha Homo sapiens 66-74
10931510-3 2000 The way in which RA modulates secondary neurulation is unclear but probably involves RA-regulated downstream genes such midkine (MK), which encodes a growth factor implicated in tail bud mesenchymal-neuroepithelial conversion. Tretinoin 17-19 midkine (neurite growth-promoting factor 2) Gallus gallus 120-127
10931510-3 2000 The way in which RA modulates secondary neurulation is unclear but probably involves RA-regulated downstream genes such midkine (MK), which encodes a growth factor implicated in tail bud mesenchymal-neuroepithelial conversion. Tretinoin 17-19 midkine (neurite growth-promoting factor 2) Gallus gallus 129-131
10931510-3 2000 The way in which RA modulates secondary neurulation is unclear but probably involves RA-regulated downstream genes such midkine (MK), which encodes a growth factor implicated in tail bud mesenchymal-neuroepithelial conversion. Tretinoin 85-87 midkine (neurite growth-promoting factor 2) Gallus gallus 120-127
10931510-3 2000 The way in which RA modulates secondary neurulation is unclear but probably involves RA-regulated downstream genes such midkine (MK), which encodes a growth factor implicated in tail bud mesenchymal-neuroepithelial conversion. Tretinoin 85-87 midkine (neurite growth-promoting factor 2) Gallus gallus 129-131
10931510-7 2000 Competitive RT-PCR was used to examine the effects of excess RA and RA deficiency due to citral on the expression of MK mRNA. Tretinoin 61-63 midkine (neurite growth-promoting factor 2) Gallus gallus 117-119
10931510-11 2000 Competitive RT-PCR showed that excess RA decreased MK expression by 60%. Tretinoin 38-40 midkine (neurite growth-promoting factor 2) Gallus gallus 51-53
10931510-14 2000 While excess RA decreased MK expression, RA deficiency had minimal effects. Tretinoin 13-15 midkine (neurite growth-promoting factor 2) Gallus gallus 26-28
10748087-0 2000 Direct interaction of all-trans-retinoic acid with protein kinase C (PKC). Tretinoin 22-45 protein kinase C alpha Homo sapiens 69-72
10748087-3 2000 All-trans-retinoic acid (atRA) modulates PKC activity, but the mechanism of this regulation is unknown. Tretinoin 0-23 protein kinase C alpha Homo sapiens 41-44
10748087-3 2000 All-trans-retinoic acid (atRA) modulates PKC activity, but the mechanism of this regulation is unknown. Tretinoin 25-29 protein kinase C alpha Homo sapiens 41-44
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 56-69 protein kinase C alpha Homo sapiens 134-137
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 56-69 protein kinase C alpha Homo sapiens 191-194
10910994-7 2000 Retinoic acid induction of tissue transglutaminase displayed a lag phase of >24 h, indicating that the induction has an indirect component. Tretinoin 0-13 transglutaminase 2 Homo sapiens 27-50
10956204-2 2000 The derivative of butyric acid (BA) and all-trans-retinoic acid (ATRA)-retinoyloxymethyl butyrate (RN1)-acting as a mutual prodrug was a more potent inducer of cancer cell differentiation and inhibitor of proliferation than the parent acids. Tretinoin 40-63 renin 1 structural Mus musculus 99-102
10956204-2 2000 The derivative of butyric acid (BA) and all-trans-retinoic acid (ATRA)-retinoyloxymethyl butyrate (RN1)-acting as a mutual prodrug was a more potent inducer of cancer cell differentiation and inhibitor of proliferation than the parent acids. Tretinoin 65-69 renin 1 structural Mus musculus 99-102
10748087-8 2000 These results let us hypothesize that in vivo, pharmacological concentrations of atRA may hamper binding of PS to PKCalpha and prevent PKCalpha activation. Tretinoin 81-85 protein kinase C alpha Homo sapiens 114-122
10748087-8 2000 These results let us hypothesize that in vivo, pharmacological concentrations of atRA may hamper binding of PS to PKCalpha and prevent PKCalpha activation. Tretinoin 81-85 protein kinase C alpha Homo sapiens 135-143
10748087-9 2000 Thus, this study provides the first evidence for direct binding of atRA to PKC isozymes and suggests the existence of a general mechanism for regulation of PKC activity during exposure to retinoids, as in retinoid-based cancer therapy. Tretinoin 67-71 protein kinase C alpha Homo sapiens 75-78
10748087-9 2000 Thus, this study provides the first evidence for direct binding of atRA to PKC isozymes and suggests the existence of a general mechanism for regulation of PKC activity during exposure to retinoids, as in retinoid-based cancer therapy. Tretinoin 67-71 protein kinase C alpha Homo sapiens 156-159
10887139-6 2000 Both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486, indicating that all of these effects were mediated by GR. Tretinoin 19-21 nuclear receptor subfamily 3 group C member 1 Homo sapiens 117-140
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 71-73 protein kinase C alpha Homo sapiens 134-137
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 71-73 protein kinase C alpha Homo sapiens 191-194
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 112-116 protein kinase C alpha Homo sapiens 134-137
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 112-116 protein kinase C alpha Homo sapiens 191-194
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 166-170 protein kinase C alpha Homo sapiens 134-137
10748087-4 2000 Amino acid alignments and crystal structure analysis of retinoic acid (RA)-binding proteins revealed a putative atRA-binding motif in PKC, suggesting existence of an atRA binding site on the PKC molecule. Tretinoin 166-170 protein kinase C alpha Homo sapiens 191-194
10748087-6 2000 Photoaffinity labeling demonstrated strong competition between atRA and phosphatidylserine (PS) for binding to PKCalpha, a slight competition with phorbol-12-myristate-13-acetate, and none with diacylglycerol, fatty acids, or Ca(2+). Tretinoin 63-67 protein kinase C alpha Homo sapiens 111-119
10887139-6 2000 Both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486, indicating that all of these effects were mediated by GR. Tretinoin 19-21 nuclear receptor subfamily 3 group C member 1 Homo sapiens 142-144
10866818-0 2000 Mechanisms of induction of human tissue inhibitor of metalloproteinases-1 (TIMP-1) gene expression by all-trans retinoic acid in combination with basic fibroblast growth factor. Tretinoin 112-125 TIMP metallopeptidase inhibitor 1 Homo sapiens 33-73
10862743-6 2000 We show that this phenotype likely results from RA interfering with the establishment of a distal signaling center, altering levels and distribution of Fgf10 and Bmp4, genes that are essential for distal lung formation. Tretinoin 48-50 fibroblast growth factor 10 Homo sapiens 152-157
10862743-7 2000 Furthermore, RA upregulates P450RAI expression, suggesting the presence of feedback mechanisms controlling RA availability. Tretinoin 13-15 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 28-35
10874003-5 2000 Mutant mice deficient in aryl hydrocarbon receptor (AHR) accumulate retinyl palmitate, retinol and retinoic acid. Tretinoin 99-112 aryl-hydrocarbon receptor Mus musculus 25-50
10874003-5 2000 Mutant mice deficient in aryl hydrocarbon receptor (AHR) accumulate retinyl palmitate, retinol and retinoic acid. Tretinoin 99-112 aryl-hydrocarbon receptor Mus musculus 52-55
10866818-0 2000 Mechanisms of induction of human tissue inhibitor of metalloproteinases-1 (TIMP-1) gene expression by all-trans retinoic acid in combination with basic fibroblast growth factor. Tretinoin 112-125 TIMP metallopeptidase inhibitor 1 Homo sapiens 75-81
10866818-1 2000 The addition of all-trans retinoic acid (ATRA) in combination with basic fibroblast growth factor (bFGF) to human fibroblasts results in a synergistic induction of tissue inhibitor of metalloproteinases-1 (TIMP-1) protein production. Tretinoin 16-39 TIMP metallopeptidase inhibitor 1 Homo sapiens 164-204
10866818-1 2000 The addition of all-trans retinoic acid (ATRA) in combination with basic fibroblast growth factor (bFGF) to human fibroblasts results in a synergistic induction of tissue inhibitor of metalloproteinases-1 (TIMP-1) protein production. Tretinoin 16-39 TIMP metallopeptidase inhibitor 1 Homo sapiens 206-212
10866818-1 2000 The addition of all-trans retinoic acid (ATRA) in combination with basic fibroblast growth factor (bFGF) to human fibroblasts results in a synergistic induction of tissue inhibitor of metalloproteinases-1 (TIMP-1) protein production. Tretinoin 41-45 TIMP metallopeptidase inhibitor 1 Homo sapiens 164-204
10866818-1 2000 The addition of all-trans retinoic acid (ATRA) in combination with basic fibroblast growth factor (bFGF) to human fibroblasts results in a synergistic induction of tissue inhibitor of metalloproteinases-1 (TIMP-1) protein production. Tretinoin 41-45 TIMP metallopeptidase inhibitor 1 Homo sapiens 206-212
10866818-2 2000 The synergistic stimulation of TIMP-1 protein by ATRA and bFGF increased across 72 h. An incubation of 10 min to 12 h with bFGF alone followed by ATRA gave a similar synergistic induction of TIMP-1 protein to that seen with both agents together. Tretinoin 49-53 TIMP metallopeptidase inhibitor 1 Homo sapiens 31-37
10866818-2 2000 The synergistic stimulation of TIMP-1 protein by ATRA and bFGF increased across 72 h. An incubation of 10 min to 12 h with bFGF alone followed by ATRA gave a similar synergistic induction of TIMP-1 protein to that seen with both agents together. Tretinoin 49-53 fibroblast growth factor 2 Homo sapiens 123-127
10866818-2 2000 The synergistic stimulation of TIMP-1 protein by ATRA and bFGF increased across 72 h. An incubation of 10 min to 12 h with bFGF alone followed by ATRA gave a similar synergistic induction of TIMP-1 protein to that seen with both agents together. Tretinoin 49-53 TIMP metallopeptidase inhibitor 1 Homo sapiens 191-197
10866818-4 2000 Expression of RARbeta mRNA was induced by ATRA alone, but not further induced by ATRA and bFGF; expression of RARgamma mRNA was induced by both ATRA or bFGF alone, and further induced by both reagents together; expression of RXRgamma was repressed by ATRA alone, but not by ATRA in combination with bFGF. Tretinoin 42-46 retinoic acid receptor beta Homo sapiens 14-21
10861789-0 2000 Retinoic acid potentiated the protective effect of NGF against staurosporine-induced apoptosis in cultured chick neurons by increasing the trkA protein expression. Tretinoin 0-13 nerve growth factor Gallus gallus 51-54
11100817-7 2000 Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53. Tretinoin 20-33 tumor protein p53 Homo sapiens 152-155
11100817-7 2000 Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53. Tretinoin 35-37 tumor protein p53 Homo sapiens 152-155
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 290-303 retinoic acid receptor beta Homo sapiens 69-76
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 retinoic acid receptor beta Homo sapiens 69-76
10945465-8 2000 In addition, expression of RAIG-2 and RAIG-3 mRNA was increased following treatment with all-trans-retinoic acid in a manner similar to that previously described for RAIG-1. Tretinoin 92-112 phospholipase A and acyltransferase 4 Homo sapiens 166-172
10945465-10 2000 These results suggest that RAIG-1, RAIG-2, and RAIG-3 represent a novel family of retinoic acid-inducible receptors, most closely related to the type 3 GPCR subfamily, and provide further evidence for a linkage between retinoic acid and G-protein-coupled receptor signal transduction pathways. Tretinoin 82-95 phospholipase A and acyltransferase 4 Homo sapiens 27-33
10941258-0 2000 Retinoic acid induces the degradation of the leukemogenic protein encoded by the promyelocytic leukemia gene fused to the retinoic acid receptor alpha gene. Tretinoin 0-13 promyelocytic leukemia Mus musculus 81-103
10941258-3 2000 All-trans-retinoic acid (atRA) induces the proteolytic degradation of PML/RAR alpha by ubiquitination and proteolysis. Tretinoin 0-23 promyelocytic leukemia Mus musculus 70-83
10941258-3 2000 All-trans-retinoic acid (atRA) induces the proteolytic degradation of PML/RAR alpha by ubiquitination and proteolysis. Tretinoin 25-29 promyelocytic leukemia Mus musculus 70-83
10860554-0 2000 Promoter activity and regulation of the CYP4F2 leukotriene B(4) omega-hydroxylase gene by peroxisomal proliferators and retinoic acid in HepG2 cells. Tretinoin 120-133 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 40-46
10860554-0 2000 Promoter activity and regulation of the CYP4F2 leukotriene B(4) omega-hydroxylase gene by peroxisomal proliferators and retinoic acid in HepG2 cells. Tretinoin 120-133 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 47-81
10860554-13 2000 Therefore, the CYP4F2 gene is repressed by peroxisomal proliferators and induced by retinoic acid, with RAR/RXRalpha mediating the induction while PPARalpha/RXR functions neither in the repression nor in the induction by peroxisomal proliferators or retinoic acid. Tretinoin 84-97 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 15-21
10860554-13 2000 Therefore, the CYP4F2 gene is repressed by peroxisomal proliferators and induced by retinoic acid, with RAR/RXRalpha mediating the induction while PPARalpha/RXR functions neither in the repression nor in the induction by peroxisomal proliferators or retinoic acid. Tretinoin 250-263 cytochrome P450 family 4 subfamily F member 2 Homo sapiens 15-21
10861789-3 2000 In the presence of retinoic acid (RA, 5 microM), however, NGF (20 pg/ml) reduced staurosporine-induced damage to 42% apoptotic neurons compared to 58% in the presence of RA (5 icroM) alone. Tretinoin 19-32 nerve growth factor Gallus gallus 58-61
10861789-3 2000 In the presence of retinoic acid (RA, 5 microM), however, NGF (20 pg/ml) reduced staurosporine-induced damage to 42% apoptotic neurons compared to 58% in the presence of RA (5 icroM) alone. Tretinoin 34-36 nerve growth factor Gallus gallus 58-61
10861789-3 2000 In the presence of retinoic acid (RA, 5 microM), however, NGF (20 pg/ml) reduced staurosporine-induced damage to 42% apoptotic neurons compared to 58% in the presence of RA (5 icroM) alone. Tretinoin 170-172 nerve growth factor Gallus gallus 58-61
10861789-5 2000 The antiapoptotic effect caused by RA and NGF was abolished by the tyrosine kinase inhibitor K-252a, as well as by anti-trkA antibodies and anti-NGF antibodies suggesting that the increase in trkA protein expression contributed to its mechanism of action. Tretinoin 35-37 nerve growth factor Gallus gallus 145-148
10861789-6 2000 In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Tretinoin 13-15 nerve growth factor Gallus gallus 286-289
10861789-6 2000 In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Tretinoin 116-118 nerve growth factor Gallus gallus 286-289
10747926-3 2000 However, in some of these cells (e.g. H157 human squamous cell carcinoma cells), RARbeta can be induced by retinoids (e.g. all-trans-retinoic acid, ATRA) because its promoter contains a retinoic acid response element. Tretinoin 123-146 retinoic acid receptor beta Homo sapiens 81-88
10861789-6 2000 In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Tretinoin 116-118 nerve growth factor Gallus gallus 286-289
10823918-0 2000 Identification of the human cytochrome P450, P450RAI-2, which is predominantly expressed in the adult cerebellum and is responsible for all-trans-retinoic acid metabolism. Tretinoin 140-159 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 45-54
10747926-3 2000 However, in some of these cells (e.g. H157 human squamous cell carcinoma cells), RARbeta can be induced by retinoids (e.g. all-trans-retinoic acid, ATRA) because its promoter contains a retinoic acid response element. Tretinoin 148-152 retinoic acid receptor beta Homo sapiens 81-88
10747926-3 2000 However, in some of these cells (e.g. H157 human squamous cell carcinoma cells), RARbeta can be induced by retinoids (e.g. all-trans-retinoic acid, ATRA) because its promoter contains a retinoic acid response element. Tretinoin 133-146 retinoic acid receptor beta Homo sapiens 81-88
10747926-4 2000 To examine the hypothesis that RARbeta induction is important for inhibition of cell proliferation by retinoids, we blocked ATRA-induced RARbeta expression in H157 cells using a retroviral vector harboring multiple copies of antisense RARbeta2 sequences. Tretinoin 124-128 retinoic acid receptor beta Homo sapiens 31-38
10747926-4 2000 To examine the hypothesis that RARbeta induction is important for inhibition of cell proliferation by retinoids, we blocked ATRA-induced RARbeta expression in H157 cells using a retroviral vector harboring multiple copies of antisense RARbeta2 sequences. Tretinoin 124-128 retinoic acid receptor beta Homo sapiens 137-144
10747926-5 2000 Antisense RARbeta-transfected cells showed not only decreased expression of ATRA-induced RARbeta protein but also reduced ATRA-induced RARE binding activity and transactivation. Tretinoin 76-80 retinoic acid receptor beta Homo sapiens 10-17
10747926-5 2000 Antisense RARbeta-transfected cells showed not only decreased expression of ATRA-induced RARbeta protein but also reduced ATRA-induced RARE binding activity and transactivation. Tretinoin 76-80 retinoic acid receptor beta Homo sapiens 89-96
10747926-5 2000 Antisense RARbeta-transfected cells showed not only decreased expression of ATRA-induced RARbeta protein but also reduced ATRA-induced RARE binding activity and transactivation. Tretinoin 122-126 retinoic acid receptor beta Homo sapiens 10-17
10816444-12 2000 In a search for the mechanism by which Bcl-2 affects growth regulation, we found that p21 gene expression was more prominent in SC-M1/Bcl2 cells than in SC-M1/neo cells in the presence of RA, but when RA was removed, p21 gene expression levels in SC-M1/Bcl2 cells were also reduced earlier than in SC-M1/neo cells. Tretinoin 201-203 BCL2 apoptosis regulator Homo sapiens 39-44
10816444-0 2000 Bcl-2 accelerates retinoic acid-induced growth arrest and recovery in human gastric cancer cells. Tretinoin 18-31 BCL2 apoptosis regulator Homo sapiens 0-5
10835519-1 2000 CONTEXT: Midkine (MK) is a novel heparin-binding growth factor whose gene was identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 137-150 midkine Homo sapiens 9-16
10835519-1 2000 CONTEXT: Midkine (MK) is a novel heparin-binding growth factor whose gene was identified in embryonal carcinoma cells in early stages of retinoic acid-induced differentiation. Tretinoin 137-150 midkine Homo sapiens 18-20
10816444-12 2000 In a search for the mechanism by which Bcl-2 affects growth regulation, we found that p21 gene expression was more prominent in SC-M1/Bcl2 cells than in SC-M1/neo cells in the presence of RA, but when RA was removed, p21 gene expression levels in SC-M1/Bcl2 cells were also reduced earlier than in SC-M1/neo cells. Tretinoin 201-203 cyclin dependent kinase inhibitor 1A Homo sapiens 86-89
10799735-3 2000 RA-induced Hep3B-cell death was associated with inhibited expression of the hepatocyte nuclear factor 4 (HNF-4) gene. Tretinoin 0-2 hepatocyte nuclear factor 4 alpha Homo sapiens 76-103
10821786-6 2000 The in vivo administration of 9-cis-RA resulted in the inhibition of IL-12 production by macrophages stimulated in vitro with either LPS or HKL, leading to the inhibition of Th1 cytokine profile (decreased IFN-gamma and increased IL-4 production) in CD4(+) T cells. Tretinoin 30-38 interferon gamma Mus musculus 206-215
10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 BCL2 apoptosis regulator Homo sapiens 43-47
10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 BCL2 apoptosis regulator Homo sapiens 109-114
10816444-7 2000 This indicates that Bcl-2 accelerates RA-induced growth arrest. Tretinoin 38-40 BCL2 apoptosis regulator Homo sapiens 20-25
10816444-8 2000 In addition to the accelerated growth arrest, RA-treated SC-M1/Bcl2 cells also recovered from growth arrest two days faster than SC-M1/neo cells after the removal of RA. Tretinoin 46-48 BCL2 apoptosis regulator Homo sapiens 63-67
10816444-9 2000 Previously, we had identified the cyclin-dependent kinase inhibitor p21((WAF1/CIP1)) (p21) as a mediator of RA-induced growth arrest [Tsao, Li, Kuo, Liu and Chen (1996) Biochem. Tretinoin 108-110 cyclin dependent kinase inhibitor 1A Homo sapiens 68-83
10816444-9 2000 Previously, we had identified the cyclin-dependent kinase inhibitor p21((WAF1/CIP1)) (p21) as a mediator of RA-induced growth arrest [Tsao, Li, Kuo, Liu and Chen (1996) Biochem. Tretinoin 108-110 cyclin dependent kinase inhibitor 1A Homo sapiens 68-71
10816444-12 2000 In a search for the mechanism by which Bcl-2 affects growth regulation, we found that p21 gene expression was more prominent in SC-M1/Bcl2 cells than in SC-M1/neo cells in the presence of RA, but when RA was removed, p21 gene expression levels in SC-M1/Bcl2 cells were also reduced earlier than in SC-M1/neo cells. Tretinoin 188-190 BCL2 apoptosis regulator Homo sapiens 39-44
10816444-12 2000 In a search for the mechanism by which Bcl-2 affects growth regulation, we found that p21 gene expression was more prominent in SC-M1/Bcl2 cells than in SC-M1/neo cells in the presence of RA, but when RA was removed, p21 gene expression levels in SC-M1/Bcl2 cells were also reduced earlier than in SC-M1/neo cells. Tretinoin 188-190 cyclin dependent kinase inhibitor 1A Homo sapiens 86-89
10799735-3 2000 RA-induced Hep3B-cell death was associated with inhibited expression of the hepatocyte nuclear factor 4 (HNF-4) gene. Tretinoin 0-2 hepatocyte nuclear factor 4 alpha Homo sapiens 105-110
10799735-4 2000 Palmitoyl-CoA ((C16:0)-CoA), the reported HNF-4 ligand, prevented RA-induced apoptosis. Tretinoin 66-68 hepatocyte nuclear factor 4 alpha Homo sapiens 42-47
10799735-8 2000 Investigating the possible role of HNF-4 in apoptosis, the reported HNF-4 antagonist (C18:0)-CoA was employed, and it also prevented RA-induced apoptosis. Tretinoin 133-135 hepatocyte nuclear factor 4 alpha Homo sapiens 35-40
10799735-8 2000 Investigating the possible role of HNF-4 in apoptosis, the reported HNF-4 antagonist (C18:0)-CoA was employed, and it also prevented RA-induced apoptosis. Tretinoin 133-135 hepatocyte nuclear factor 4 alpha Homo sapiens 68-73
10816385-0 2000 Retinoic acid affects the EGF-R signaling pathway during differentiation induction of human endometrial adenocarcinoma cells. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 26-31
10816385-7 2000 We evaluated the possibility that the differentiating effects of retinoids are due to retinoic-acid-induced decreases in phosphorylation of EGF-R and changes in downstream effector proteins. Tretinoin 86-99 epidermal growth factor receptor Homo sapiens 140-145
10816385-8 2000 Retinoic acid caused a decrease in tyrosine phosphorylation of EGF-R. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 63-68
10816385-11 2000 Retinoic acid induced a relocalization and decrease in the amount of Shc protein, another actin-binding protein which is an adaptor protein for EGF-R signaling. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 144-149
10816385-14 2000 These results are consistent with the idea that retinoic acid induces differentiation of RL95-2 cells by interfering with the EGF-R signaling pathway. Tretinoin 48-61 epidermal growth factor receptor Homo sapiens 126-131
10965999-1 2000 It has been established that melatonin (Mlt) and retinoic acid, individually, inhibit the proliferation of the estrogen receptor-alpha (ER alpha)-positive MCF-7 breast cancer cell line. Tretinoin 49-62 estrogen receptor 1 Homo sapiens 111-134
10965999-1 2000 It has been established that melatonin (Mlt) and retinoic acid, individually, inhibit the proliferation of the estrogen receptor-alpha (ER alpha)-positive MCF-7 breast cancer cell line. Tretinoin 49-62 estrogen receptor 1 Homo sapiens 136-144
10825004-3 2000 Furthermore, growth inhibition of esophageal cancer cell lines by all-trans retinoic acid has been associated with the constitutive and induced expression of RARB. Tretinoin 76-89 retinoic acid receptor beta Homo sapiens 158-162
10820192-4 2000 Retinoic acid-mediated differentiation of NT2 precursor cells to the neuronal phenotype resulted in five- to 15-fold increases in the expression of PLC-beta1, PLC-beta4, and Galpha(q/11) (the prime G protein activator of these isozymes). Tretinoin 0-13 phospholipase C beta 4 Homo sapiens 159-168
10928048-7 2000 Furthermore, immunohistochemical analysis showed that the differentiation-inducing agent, all-trans retinoic acid, can up-regulate E-cadherin expression in esophageal SCC cells in vitro. Tretinoin 100-113 cadherin 1 Homo sapiens 131-141
10902971-1 2000 AIMS/BACKGROUND: Midkine (MK) is a novel heparin-binding growth factor whose gene was identified in embryonal carcinoma cells in the early stages of retinoic acid-induced differentiation. Tretinoin 149-162 midkine Homo sapiens 17-24
10902971-1 2000 AIMS/BACKGROUND: Midkine (MK) is a novel heparin-binding growth factor whose gene was identified in embryonal carcinoma cells in the early stages of retinoic acid-induced differentiation. Tretinoin 149-162 midkine Homo sapiens 26-28
10929428-14 2000 Mutant p53 expression was more decreased in the EJ cells treated with RA or Ni(RA)2.3H2O than in the control. Tretinoin 70-72 tumor protein p53 Homo sapiens 7-10
10841350-2 2000 We have studied by immunocytochemistry, Western blotting and RT-PCR the expression pattern of Bcl-xL, Bcl-2 and BAX in the in vitro model of neuronal differentiation constituted by retinoic acid (RA)-treated NTera-2/D1 (NT2/D1) cells. Tretinoin 181-194 BCL2 like 1 Homo sapiens 94-100
10841350-2 2000 We have studied by immunocytochemistry, Western blotting and RT-PCR the expression pattern of Bcl-xL, Bcl-2 and BAX in the in vitro model of neuronal differentiation constituted by retinoic acid (RA)-treated NTera-2/D1 (NT2/D1) cells. Tretinoin 181-194 BCL2 associated X, apoptosis regulator Homo sapiens 112-115
10837911-10 2000 AATYK-induced differentiation was in the same range as the differentiation induced by agents like all-trans retinoic acid (RA), 12-O-Tetradecanoyl phorbol 13-acetate (TPA) and IGF-I. Tretinoin 108-121 apoptosis associated tyrosine kinase Homo sapiens 0-5
10837911-10 2000 AATYK-induced differentiation was in the same range as the differentiation induced by agents like all-trans retinoic acid (RA), 12-O-Tetradecanoyl phorbol 13-acetate (TPA) and IGF-I. Tretinoin 123-125 apoptosis associated tyrosine kinase Homo sapiens 0-5
10837916-2 2000 The levels of p27 mRNA and protein increased within 24 h of treatment with ATRA, reaching a plateau 4-5 days later prior to neurite formation. Tretinoin 75-79 zinc ribbon domain containing 2 Homo sapiens 14-17
10837916-5 2000 In a mutant P19 cell line, RAC65, treatment with ATRA induced neither p27 accumulation nor neuronal differentiation, but p21 mRNA expression increased markedly. Tretinoin 49-53 zinc ribbon domain containing 2 Homo sapiens 70-73
10837916-8 2000 Luciferase reporter assays showed that p27 promoter activity increased in ATRA-treated cells, consistent with the elevation of p27 mRNA levels. Tretinoin 74-78 zinc ribbon domain containing 2 Homo sapiens 39-42
10837916-8 2000 Luciferase reporter assays showed that p27 promoter activity increased in ATRA-treated cells, consistent with the elevation of p27 mRNA levels. Tretinoin 74-78 zinc ribbon domain containing 2 Homo sapiens 127-130
10704935-7 2000 Of the PIs tested, only indinavir stimulated ATRA-dependent ALP activity and altered stem cell morphology; the effects of indinavir occurred in the presence of ATRA, but not in its absence. Tretinoin 45-49 alkaline phosphatase, placental Homo sapiens 60-63
10772788-8 2000 These results implicate retinoid signaling in lens formation and show that RA signaling in the developing eye is dependent upon Pax-6. Tretinoin 75-77 paired box 6 Mus musculus 128-133
10812241-10 2000 NB4 cell line and five of seven leukemic samples displayed undetectable or very low level of p15(INK4B) that rapidly increased during retinoic acid-induced differentiation. Tretinoin 134-147 cyclin dependent kinase inhibitor 2B Homo sapiens 93-96
10785230-0 2000 Retinoic acid suppresses interleukin-6 production in human endometrial cells. Tretinoin 0-13 interleukin 6 Homo sapiens 25-38
10785230-1 2000 OBJECTIVE: To determine whether retinoic acid (RA) can regulate the expression of interleukin (IL)-6 in human endometrial cells in a manner that might be beneficial to women with endometriosis. Tretinoin 32-45 interleukin 6 Homo sapiens 82-100
10785230-1 2000 OBJECTIVE: To determine whether retinoic acid (RA) can regulate the expression of interleukin (IL)-6 in human endometrial cells in a manner that might be beneficial to women with endometriosis. Tretinoin 47-49 interleukin 6 Homo sapiens 82-100
10785230-7 2000 RESULT(S): Using a human endometrial cell line (EM42), as well as primary stromal and epithelial endometrial cells, we demonstrated that RA suppresses IL-6 protein and messenger RNA expression in a time- and dose-dependent fashion, showing maximal effects at pharmacologically achievable blood serum concentrations (micromoles per liter). Tretinoin 137-139 interleukin 6 Homo sapiens 151-155
10785230-8 2000 Retinoic acid specifically inhibited the activity of IL-6-promoter reporter constructs that were transiently transfected into EM42 cells. Tretinoin 0-13 interleukin 6 Homo sapiens 53-57
10772826-0 2000 Retinoic acid and its receptors repress the expression and transactivation functions of Nur77: a possible mechanism for the inhibition of apoptosis by retinoic acid. Tretinoin 0-13 nuclear receptor subfamily 4 group A member 1 Homo sapiens 88-93
10772826-0 2000 Retinoic acid and its receptors repress the expression and transactivation functions of Nur77: a possible mechanism for the inhibition of apoptosis by retinoic acid. Tretinoin 151-164 nuclear receptor subfamily 4 group A member 1 Homo sapiens 88-93
10772826-3 2000 To illustrate the mechanism of the inhibition, we examined the effects of retinoic acid (RA) on the expression and transactivation functions of Nur77 in the human peripheral blood mononuclear cells and the human T-cell leukemia, Jurkat. Tretinoin 74-87 nuclear receptor subfamily 4 group A member 1 Homo sapiens 144-149
10772826-3 2000 To illustrate the mechanism of the inhibition, we examined the effects of retinoic acid (RA) on the expression and transactivation functions of Nur77 in the human peripheral blood mononuclear cells and the human T-cell leukemia, Jurkat. Tretinoin 89-91 nuclear receptor subfamily 4 group A member 1 Homo sapiens 144-149
10772826-8 2000 Taken all together, we demonstrated that RA repressed Nur77 function through multiple mechanisms that may provide the basis for RA inhibition on the apoptosis of activated T-lymphocytes. Tretinoin 41-43 nuclear receptor subfamily 4 group A member 1 Homo sapiens 54-59
10772826-8 2000 Taken all together, we demonstrated that RA repressed Nur77 function through multiple mechanisms that may provide the basis for RA inhibition on the apoptosis of activated T-lymphocytes. Tretinoin 128-130 nuclear receptor subfamily 4 group A member 1 Homo sapiens 54-59
10785230-9 2000 Mutational analysis of reporter constructs indicated that RA suppression of IL-6 expression was mediated, at least in part, through the nuclear factor IL-6 binding site located in the IL-6 promoter. Tretinoin 58-60 interleukin 6 Homo sapiens 76-80
10785230-9 2000 Mutational analysis of reporter constructs indicated that RA suppression of IL-6 expression was mediated, at least in part, through the nuclear factor IL-6 binding site located in the IL-6 promoter. Tretinoin 58-60 interleukin 6 Homo sapiens 151-155
10785230-9 2000 Mutational analysis of reporter constructs indicated that RA suppression of IL-6 expression was mediated, at least in part, through the nuclear factor IL-6 binding site located in the IL-6 promoter. Tretinoin 58-60 interleukin 6 Homo sapiens 151-155
10812241-10 2000 NB4 cell line and five of seven leukemic samples displayed undetectable or very low level of p15(INK4B) that rapidly increased during retinoic acid-induced differentiation. Tretinoin 134-147 cyclin dependent kinase inhibitor 2B Homo sapiens 97-102
10812241-11 2000 Two leukemic samples (both collected from two patients developing all-trans retinoic acid syndrome) showed high basal levels of p15(INK4B), which was not modified by retinoic acid treatment. Tretinoin 76-89 cyclin dependent kinase inhibitor 2B Homo sapiens 128-131
10812241-11 2000 Two leukemic samples (both collected from two patients developing all-trans retinoic acid syndrome) showed high basal levels of p15(INK4B), which was not modified by retinoic acid treatment. Tretinoin 76-89 cyclin dependent kinase inhibitor 2B Homo sapiens 132-137
10812241-13 2000 In acute promyelocytic leukemic blasts, p15(INK4B), which is detectable at a very low level, is promptly increased by retinoic acid. Tretinoin 118-131 cyclin dependent kinase inhibitor 2B Homo sapiens 40-43
10812241-13 2000 In acute promyelocytic leukemic blasts, p15(INK4B), which is detectable at a very low level, is promptly increased by retinoic acid. Tretinoin 118-131 cyclin dependent kinase inhibitor 2B Homo sapiens 44-49
10812241-14 2000 In contrast, two acute promyelocytic leukemia samples obtained from patients who developed all-trans retinoic acid syndrome showed high basal levels of p15(INK4B) that did not increase further during all-trans retinoic acid-induced differentiation. Tretinoin 101-114 cyclin dependent kinase inhibitor 2B Homo sapiens 152-155
10812241-14 2000 In contrast, two acute promyelocytic leukemia samples obtained from patients who developed all-trans retinoic acid syndrome showed high basal levels of p15(INK4B) that did not increase further during all-trans retinoic acid-induced differentiation. Tretinoin 101-114 cyclin dependent kinase inhibitor 2B Homo sapiens 156-161
10717330-1 2000 Retinoic acid receptor beta is the retinoid receptor most frequently associated with the growth suppressive effects of retinoic acid in various epithelial tumor-derived cell lines. Tretinoin 119-132 retinoic acid receptor beta Homo sapiens 0-27
10753851-10 2000 Retinoic acid induces binding of the co-activator protein RAC3. Tretinoin 0-13 Rac family small GTPase 3 Homo sapiens 58-62
10751444-5 2000 Consequently, we found that RA alone induced the responsiveness of SCG neurons specifically to GDNF by upregulating the ligand-specifying receptor for GDNF (GFRalpha-1) at both the mRNA and protein levels. Tretinoin 28-30 GDNF family receptor alpha 1 Rattus norvegicus 157-167
10751444-7 2000 Although the upregulation of signal-transducing receptor Ret by the RA treatment was rather small, this treatment significantly increased the efficacy of tyrosine phosphorylation of Ret by GDNF. Tretinoin 68-70 ret proto-oncogene Rattus norvegicus 57-60
10803520-0 2000 All-trans-retinoic acid effects the growth, differentiation and apoptosis of normal human myeloid progenitors derived from purified CD34+ bone marrow cells. Tretinoin 0-23 CD34 molecule Homo sapiens 132-136
10803520-2 2000 In this study, we further characterized the effect of ATRA on the growth of CFU-GM stimulated by individual cytokines from multiple samples of CD34+ enriched or purified human bone marrow cells. Tretinoin 54-58 CD34 molecule Homo sapiens 143-147
10803520-6 2000 In 14 days liquid cultures of purified CD34+ cells with IL-3, ATRA increased the number of myeloid differentiated cells to 91-95%, compared to 37-70% with IL-3 alone. Tretinoin 62-66 CD34 molecule Homo sapiens 39-43
10772914-0 2000 Retinoic acid inhibits nitric oxide synthase-2 expression through the retinoic acid receptor-alpha. Tretinoin 0-13 nitric oxide synthase 2 Rattus norvegicus 23-46
10772914-2 2000 We have explored the mechanisms by which retinoic acid (RA) regulates NO production in rat aortic smooth muscle cells (VSMC), which express NOS2 in response to proinflammatory cytokines. Tretinoin 41-54 nitric oxide synthase 2 Rattus norvegicus 140-144
10772914-2 2000 We have explored the mechanisms by which retinoic acid (RA) regulates NO production in rat aortic smooth muscle cells (VSMC), which express NOS2 in response to proinflammatory cytokines. Tretinoin 56-58 nitric oxide synthase 2 Rattus norvegicus 140-144
10815802-0 2000 All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-kappaB, activated protein-1 and apoptosis in human lung cancer cells. Tretinoin 0-23 tumor necrosis factor Homo sapiens 36-39
10815802-0 2000 All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-kappaB, activated protein-1 and apoptosis in human lung cancer cells. Tretinoin 0-23 tumor necrosis factor Homo sapiens 66-69
10815802-2 2000 In this study, we investigated the effect of all-trans-retinoic acid (ATRA) on the cell surface expression of TNF receptors and receptor-mediated signaling in various human lung cancer cell lines. Tretinoin 45-68 tumor necrosis factor Homo sapiens 110-113
10815802-2 2000 In this study, we investigated the effect of all-trans-retinoic acid (ATRA) on the cell surface expression of TNF receptors and receptor-mediated signaling in various human lung cancer cell lines. Tretinoin 70-74 tumor necrosis factor Homo sapiens 110-113
10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor protein p53 Homo sapiens 47-50
10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor protein p53 Homo sapiens 76-79
10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor protein p53 Homo sapiens 76-79
10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor necrosis factor Homo sapiens 134-137
10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor necrosis factor Homo sapiens 203-206
10815802-9 2000 Treatment of these cells with as little as 0.5 microM ATRA was effective in converting TNF-resistant cells to TNF-sensitive. Tretinoin 54-58 tumor necrosis factor Homo sapiens 87-90
10815802-9 2000 Treatment of these cells with as little as 0.5 microM ATRA was effective in converting TNF-resistant cells to TNF-sensitive. Tretinoin 54-58 tumor necrosis factor Homo sapiens 110-113
10815802-10 2000 Overall our results indicate that ATRA induces the TNF receptors in human lung cancer cells, which sensitizes them to TNF-induced signaling leading to activation of NF-kappaB, AP-1 and apoptosis. Tretinoin 34-38 tumor necrosis factor Homo sapiens 51-54
10815802-10 2000 Overall our results indicate that ATRA induces the TNF receptors in human lung cancer cells, which sensitizes them to TNF-induced signaling leading to activation of NF-kappaB, AP-1 and apoptosis. Tretinoin 34-38 tumor necrosis factor Homo sapiens 118-121
10751444-7 2000 Although the upregulation of signal-transducing receptor Ret by the RA treatment was rather small, this treatment significantly increased the efficacy of tyrosine phosphorylation of Ret by GDNF. Tretinoin 68-70 ret proto-oncogene Rattus norvegicus 182-185
10751444-9 2000 On the other hand, BMP2, which had no significant effect by itself on the GDNF responsiveness, promoted the action of RA to upregulate GFRalpha-1 and enhance the GDNF responsiveness. Tretinoin 118-120 GDNF family receptor alpha 1 Rattus norvegicus 135-145
10852350-0 2000 Retinoic acid increases amount of phosphorylated RAF; ectopic expression of cFMS reveals that retinoic acid-induced differentiation is more strongly dependent on ERK2 signaling than induced GO arrest is. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 162-166
10783262-5 2000 Promoter analysis reveals a consensus retinoic acid response element and several potential binding sites for transcription factors Crx and Nrl, which correlates with the retina-specific expression of FSCN2 mRNA. Tretinoin 38-51 fascin actin-bundling protein 2, retinal Homo sapiens 200-205
10745031-0 2000 A novel mechanism of retinoic acid-enhanced interleukin-8 gene expression in airway epithelium. Tretinoin 21-34 C-X-C motif chemokine ligand 8 Homo sapiens 44-57
10745031-1 2000 A 3- to 8-fold stimulation of interleukin (IL)-8 gene expression by all-trans-retinoic acid (ATRA) was demonstrated in primary cultures of human and monkey tracheobronchial epithelial cells and BEAS-2B serum-sensitive cell line. Tretinoin 71-91 C-X-C motif chemokine ligand 8 Homo sapiens 30-48
10745031-1 2000 A 3- to 8-fold stimulation of interleukin (IL)-8 gene expression by all-trans-retinoic acid (ATRA) was demonstrated in primary cultures of human and monkey tracheobronchial epithelial cells and BEAS-2B serum-sensitive cell line. Tretinoin 93-97 C-X-C motif chemokine ligand 8 Homo sapiens 30-48
10745031-2 2000 The effect of ATRA on IL-8 gene expression is dose- and time-dependent. Tretinoin 14-18 C-X-C motif chemokine ligand 8 Homo sapiens 22-26
10745031-5 2000 A difference in nuclear run-on activity suggests that a transcriptional mechanism is involved in ATRA-enhanced IL-8 gene expression. Tretinoin 97-101 C-X-C motif chemokine ligand 8 Homo sapiens 111-115
10745031-13 2000 Taking these data together, a novel mechanism is proposed in which ATRA activates promoter activity of IL-8 gene through TRX-dependent NF-kappaB activation. Tretinoin 67-71 C-X-C motif chemokine ligand 8 Homo sapiens 103-107
10766196-8 2000 Pretreatment of MCF-7 cells with either 1,25(OH)2D3 or ATRA increased the phosphorylation of Bcl-2 by variable concentrations of paclitaxel. Tretinoin 55-59 BCL2 apoptosis regulator Homo sapiens 93-98
10733907-5 2000 RT-PCR results showed that RA (10 microM) decreased the expression of Bcl-2 mRNA. Tretinoin 27-29 BCL2, apoptosis regulator Rattus norvegicus 70-75
10733907-6 2000 These results suggest that fat cell loss by apoptosis can be regulated, in part, by RA (10 microM) which increases caspase 3 activity and decreases Bcl-2 expression in rat S-V cells. Tretinoin 84-86 BCL2, apoptosis regulator Rattus norvegicus 148-153
10766166-4 2000 The B94 gene (TNFAIP2; Unigene Hs.101382), originally identified as a tumor necrosis factor alpha-inducible gene in endothelial cells, was one of several genes found to be induced by RA specifically in TF1-PR cells, but not in TF1-neo (control) cells. Tretinoin 183-185 tumor necrosis factor Homo sapiens 70-97
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 mitogen-activated protein kinase 1 Homo sapiens 205-209
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 mitogen-activated protein kinase 1 Homo sapiens 371-375
10852350-13 2000 Ectopic expression of cFMS and differential sensitivity to ERK2 inhibition thus reveal that retinoic acid-induced HL-60 cell differentiation and G1/0 arrest are differentially dependent on ERK2 and can be uncoupled. Tretinoin 92-105 mitogen-activated protein kinase 1 Homo sapiens 59-63
10852350-13 2000 Ectopic expression of cFMS and differential sensitivity to ERK2 inhibition thus reveal that retinoic acid-induced HL-60 cell differentiation and G1/0 arrest are differentially dependent on ERK2 and can be uncoupled. Tretinoin 92-105 mitogen-activated protein kinase 1 Homo sapiens 189-193
10852350-14 2000 A significant unanticipated finding was that retinoic acid caused a MEK-dependent increase in the amount of phosphorylated RAF. Tretinoin 45-58 mitogen-activated protein kinase kinase 7 Homo sapiens 68-71
10852350-0 2000 Retinoic acid increases amount of phosphorylated RAF; ectopic expression of cFMS reveals that retinoic acid-induced differentiation is more strongly dependent on ERK2 signaling than induced GO arrest is. Tretinoin 94-107 mitogen-activated protein kinase 1 Homo sapiens 162-166
10852350-1 2000 Retinoic acid is known to cause the myeloid differentiation and G1/0 cell cycle arrest of HL-60 cells in a process that requires mitogen-activated protein/extracellular signal regulated kinase (MEK)-dependent extracellular signal regulated kinase (ERK)2 activation. Tretinoin 0-13 mitogen-activated protein kinase kinase 7 Homo sapiens 194-197
10852350-1 2000 Retinoic acid is known to cause the myeloid differentiation and G1/0 cell cycle arrest of HL-60 cells in a process that requires mitogen-activated protein/extracellular signal regulated kinase (MEK)-dependent extracellular signal regulated kinase (ERK)2 activation. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 248-253
10852350-4 2000 The present data show that the ectopic expression of cFMS results in the differential loss of sensitivity of retinoic acid-induced differentiation or G1/0 arrest to inhibition of ERK2 activation. Tretinoin 109-122 mitogen-activated protein kinase 1 Homo sapiens 179-183
10852350-10 2000 Retinoic acid increased the amount of activated ERK2 and phosphorylated RAF in both cell lines. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 48-52
10852350-11 2000 But PD98059 eliminated detectable ERK2 activation, as well as inhibited RAF phosphorylation, in untreated and retinoic acid-treated wild-type HL-60 and cFMS transfectants, consistent with MEK or ERK feedback-regulation of RAF, in all four cases. Tretinoin 110-123 mitogen-activated protein kinase kinase 7 Homo sapiens 188-191
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 mitogen-activated protein kinase kinase 7 Homo sapiens 197-200
10727725-1 2000 CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development. Tretinoin 36-49 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
10734183-3 2000 This study identifies R115866 as a novel inhibitor of the cytochrome P450 (CYP)-mediated metabolism of RA. Tretinoin 103-105 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 58-73
10734183-3 2000 This study identifies R115866 as a novel inhibitor of the cytochrome P450 (CYP)-mediated metabolism of RA. Tretinoin 103-105 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 75-78
10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 82-86 BCL2 apoptosis regulator Homo sapiens 19-24
10698704-5 2000 After vitamin-induced differentiation in vitro with retinoic acid (RA) and 1,25-dihydroxy vitamin D(3) (VD), termed RA/VD, we observed that THP1 RA/VD cells became more resistant to NO-mediated cytotoxicity whereas the susceptibility of U937 cells was not modified. Tretinoin 52-65 GLI family zinc finger 2 Homo sapiens 140-144
10734315-1 2000 Retinoic acid (RA)-resistance in breast cancer cells has been associated with irreversible loss of retinoic acid receptor beta, RARbeta, gene expression. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 99-126
10734315-1 2000 Retinoic acid (RA)-resistance in breast cancer cells has been associated with irreversible loss of retinoic acid receptor beta, RARbeta, gene expression. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 128-135
10734315-1 2000 Retinoic acid (RA)-resistance in breast cancer cells has been associated with irreversible loss of retinoic acid receptor beta, RARbeta, gene expression. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 99-126
10734315-1 2000 Retinoic acid (RA)-resistance in breast cancer cells has been associated with irreversible loss of retinoic acid receptor beta, RARbeta, gene expression. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 128-135
10713328-0 2000 All trans retinoic acid induces apoptosis in acute promyelocytic NB4 cells when combined with isoquinolinediol, a poly(ADP-ribose) polymerase inhibitor. Tretinoin 10-23 poly(ADP-ribose) polymerase 1 Homo sapiens 114-141
10713328-3 2000 Here we show that NB4 cells simultaneously treated with ATRA and isoquinolinediol (Iso-Q), a specific PARP inhibitor, fail to differentiate into neutrophils. Tretinoin 56-60 poly(ADP-ribose) polymerase 1 Homo sapiens 102-106
10713328-5 2000 NB4 cells treated with ATRA and Iso-Q instead showed features of apoptosis including nuclear condensation, DNA fragmentation, and PARP cleavage yielding a 85 kDa fragment. Tretinoin 23-27 poly(ADP-ribose) polymerase 1 Homo sapiens 130-134
10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 82-86 BCL2 apoptosis regulator Homo sapiens 235-240
10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 91-95 BCL2 apoptosis regulator Homo sapiens 19-24
10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 91-95 BCL2 apoptosis regulator Homo sapiens 235-240
10694435-7 2000 To study PS2 expression during differentiation, mouse embryonic carcinoma P19 cells were treated with retinoic acid. Tretinoin 102-115 presenilin 2 Mus musculus 9-12
10694435-10 2000 The differential expression of PS1 and PS2 within the P19 cells following retinoic acid treatment indicates different utilization or temporal requirements for these proteins during neuronal differentiation. Tretinoin 74-87 presenilin 2 Mus musculus 39-42
10727725-1 2000 CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development. Tretinoin 36-49 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 7-14
10727725-1 2000 CYP26 (P450RAI) catalyzes catabolic retinoic acid (RA) hydroxylation and thereby appears to play a critical role in retinoid signaling pathways during development. Tretinoin 11-13 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
10692469-3 2000 Previously, we have shown that the Oct-3/4 promoter harbors an RA-responsive element, RAREoct, which functions in EC cells as a binding site for positive regulators of transcription, such as RAR and RXR. Tretinoin 63-65 RAB40B, member RAS oncogene family Homo sapiens 86-89
10702227-7 2000 mAKRa mRNA levels decreased later in the differentiation process particularly when the EML cells were cultured with granulocyte/macrophage colony-stimulating factor and retinoic acid to induce terminal granulocytic maturation. Tretinoin 169-182 aldo-keto reductase family 1, member C12 Mus musculus 0-5
10702227-8 2000 mAKRa mRNA levels decreased during retinoic acid-induced terminal granulocytic differentiation of the MPRO promyelocyte cell line. Tretinoin 35-48 aldo-keto reductase family 1, member C12 Mus musculus 0-5
10702251-9 2000 We also propose that atRA induces its own oxidative metabolism via a cytochrome P450 (CYP26) and is further biotransformed into glucuronides via UGT-mediated pathways. Tretinoin 21-25 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 86-91
10686319-0 2000 Down-regulation of fibronectin in rainbow trout gonadal cells exposed to retinoic acid. Tretinoin 73-86 fibronectin 1 Homo sapiens 19-30
10686319-3 2000 In vitro studies with mammalian cells have demonstrated a relationship between exposure to RA and expression of the extracellular matrix protein, fibronectin (FN); a protein critical for cell migration, adhesion, and transformation. Tretinoin 91-93 fibronectin 1 Homo sapiens 146-157
10686319-3 2000 In vitro studies with mammalian cells have demonstrated a relationship between exposure to RA and expression of the extracellular matrix protein, fibronectin (FN); a protein critical for cell migration, adhesion, and transformation. Tretinoin 91-93 fibronectin 1 Homo sapiens 159-161
10686319-4 2000 In this study, in vitro exposures of rainbow trout gonadal cells (RTG-2) to RA reduced levels of FN in culture medium; as measured using SDS-PAGE and immunoblot analysis with antisera prepared against RTG-2 cellular fibronectin. Tretinoin 76-78 fibronectin 1 Homo sapiens 216-227
10792293-8 2000 When HL-60 cells were differentiated to mature granulocytes with all-trans retinoic acid, ENX-1 was down-regulated. Tretinoin 75-88 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 90-95
10677255-3 2000 Exogenous retinoic acid or transplantation of normal chick embryo anterior endoderm is sufficient to rescue apoptosis as well as GATA-4 expression and results in normal development and heart tube morphogenesis. Tretinoin 10-23 GATA binding protein 4 Gallus gallus 129-135
10704257-0 2000 Retinoic acid suppresses interleukin 6 production in normal human osteoblasts. Tretinoin 0-13 interleukin 6 Homo sapiens 25-38
10704257-7 2000 The production of bone specific markers, alkaline phosphatase and osteocalcin, was also reduced in RA-treated cultures. Tretinoin 99-101 bone gamma-carboxyglutamate protein Homo sapiens 66-77
10704257-9 2000 Within 24 h, RA at all four concentrations reduced Il-6 production from normal human osteoblasts. Tretinoin 13-15 interleukin 6 Homo sapiens 51-55
10704257-10 2000 The pharmacological concentration of 10(-5) M RA suppressed 90% of IL-6 production. Tretinoin 46-48 interleukin 6 Homo sapiens 67-71
10704257-11 2000 The present study shows for the first time that RA profoundly inhibits IL-6 production in normal human osteoblasts within 24 h and in a dose-dependent manner. Tretinoin 48-50 interleukin 6 Homo sapiens 71-75
10704257-12 2000 RA was shown previously to inhibit IL-6 production in several other normal and malignant human cell types. Tretinoin 0-2 interleukin 6 Homo sapiens 35-39
10691970-7 2000 Whereas dexamethasone conferred no significant effect on TNAP activity, retinoic acid was shown to inhibit IAP activity by approximately 50%. Tretinoin 72-85 alkaline phosphatase, intestinal Homo sapiens 107-110
10704257-14 2000 Thus, RA inhibition of IL-6 production in normal human osteoblasts may contribute to the bone abnormalities seen after systemic long-term retinoid therapy in some patients. Tretinoin 6-8 interleukin 6 Homo sapiens 23-27
10681373-0 2000 Human cytochrome P-450 metabolism of retinals to retinoic acids. Tretinoin 49-63 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 6-22
10694373-2 2000 We also reported that retinoic acid (RA) increases UCP1 mRNA in BAT. Tretinoin 22-35 uncoupling protein 1 Rattus norvegicus 51-55
10660115-0 2000 Differential effects of retinoic acid on growth and apoptosis in human colon cancer cell lines associated with the induction of retinoic acid receptor beta. Tretinoin 24-37 retinoic acid receptor beta Homo sapiens 128-155
10772242-6 2000 In agarose cultures of bovine and porcine chondrocytes HAS2 mRNA was present in control, IL-1 and retinoic acid treated cultures, whereas HAS3 mRNA was only detected in IL-1 stimulated cultures. Tretinoin 98-111 hyaluronan synthase 2 Bos taurus 55-59
10772242-8 2000 HAS2 and HAS3 mRNAs were also expressed by bovine chondrocytes isolated from either the superficial or deep zone of articular cartilage, and by human chondrocytes cultured either in the absence or presence of IL-1 and retinoic acid. Tretinoin 218-231 hyaluronan synthase 2 Bos taurus 0-4
10694373-2 2000 We also reported that retinoic acid (RA) increases UCP1 mRNA in BAT. Tretinoin 37-39 uncoupling protein 1 Rattus norvegicus 51-55
10694373-7 2000 RA (7.5 mg/kg) increased UCP1 mRNA but decreased UCP2 and UCP3 mRNA by 50%, whereas methylprednisolone (65 mg/kg, two doses 24 h apart) suppressed all three uncoupling proteins by greater than 60%. Tretinoin 0-2 uncoupling protein 1 Rattus norvegicus 25-29
11776647-9 2000 Interferon alpha (IFN-alpha) and PGE1 could significantly inhibit proliferation of ATRA-resistant HL60 cells and restore cell differentiation induced by ATRA. Tretinoin 83-87 interferon alpha 1 Homo sapiens 18-27
11776647-9 2000 Interferon alpha (IFN-alpha) and PGE1 could significantly inhibit proliferation of ATRA-resistant HL60 cells and restore cell differentiation induced by ATRA. Tretinoin 153-157 interferon alpha 1 Homo sapiens 18-27
10699467-10 2000 The decrease in GnT-V and the corresponding increase in GnT-III activities were also found after the cells were treated with all-trans retinoic acid (ATRA), and the mechanism of this might be different from that in the cell cycle. Tretinoin 135-148 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 16-21
10699467-10 2000 The decrease in GnT-V and the corresponding increase in GnT-III activities were also found after the cells were treated with all-trans retinoic acid (ATRA), and the mechanism of this might be different from that in the cell cycle. Tretinoin 150-154 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 16-21
10679192-0 2000 Retinoic acid extends the in vitro life span of normal human oral keratinocytes by decreasing p16(INK4A) expression and maintaining telomerase activity. Tretinoin 0-13 cyclin dependent kinase inhibitor 2A Homo sapiens 94-97
10679192-0 2000 Retinoic acid extends the in vitro life span of normal human oral keratinocytes by decreasing p16(INK4A) expression and maintaining telomerase activity. Tretinoin 0-13 cyclin dependent kinase inhibitor 2A Homo sapiens 98-103
10679192-4 2000 Since the replicative senescence of human epithelial cells is associated with a steady increase of p16(INK4A) and a loss of telomerase activity, we expected that RA could delay the replicative senescence of oral keratinocytes by decreasing p16(INK4A) expression and/or inhibiting the loss of telomerase activity. Tretinoin 162-164 cyclin dependent kinase inhibitor 2A Homo sapiens 99-102
10679192-4 2000 Since the replicative senescence of human epithelial cells is associated with a steady increase of p16(INK4A) and a loss of telomerase activity, we expected that RA could delay the replicative senescence of oral keratinocytes by decreasing p16(INK4A) expression and/or inhibiting the loss of telomerase activity. Tretinoin 162-164 cyclin dependent kinase inhibitor 2A Homo sapiens 103-108
10679192-4 2000 Since the replicative senescence of human epithelial cells is associated with a steady increase of p16(INK4A) and a loss of telomerase activity, we expected that RA could delay the replicative senescence of oral keratinocytes by decreasing p16(INK4A) expression and/or inhibiting the loss of telomerase activity. Tretinoin 162-164 cyclin dependent kinase inhibitor 2A Homo sapiens 240-243
10679192-4 2000 Since the replicative senescence of human epithelial cells is associated with a steady increase of p16(INK4A) and a loss of telomerase activity, we expected that RA could delay the replicative senescence of oral keratinocytes by decreasing p16(INK4A) expression and/or inhibiting the loss of telomerase activity. Tretinoin 162-164 cyclin dependent kinase inhibitor 2A Homo sapiens 244-249
10679192-6 2000 The protein level of cellular p16(INK4A) in the RA-treated oral keratinocytes was gradually but significantly enhanced by an increased PDL number; however, the level was significantly lower than that of the vehicle control at all of the same PDL numbers. Tretinoin 48-50 cyclin dependent kinase inhibitor 2A Homo sapiens 30-33
10706136-5 2000 Exposure of SN-1 cells to ATRA hardly affected cell growth and differentiation, whereas the growth of HL-60 and NB4 cells treated with ATRA was effectively inhibited, and differentiation into mature granulocytes was induced. Tretinoin 26-30 solute carrier family 38 member 3 Homo sapiens 12-16
10679192-6 2000 The protein level of cellular p16(INK4A) in the RA-treated oral keratinocytes was gradually but significantly enhanced by an increased PDL number; however, the level was significantly lower than that of the vehicle control at all of the same PDL numbers. Tretinoin 48-50 cyclin dependent kinase inhibitor 2A Homo sapiens 34-39
10679192-8 2000 Summarizing, these results indicate that RA induces the in vitro life-span extension of oral keratinocytes, which is linked to a decreased cellular level of p16(INK4A) and the maintenance of telomerase activity. Tretinoin 41-43 cyclin dependent kinase inhibitor 2A Homo sapiens 157-160
10679192-8 2000 Summarizing, these results indicate that RA induces the in vitro life-span extension of oral keratinocytes, which is linked to a decreased cellular level of p16(INK4A) and the maintenance of telomerase activity. Tretinoin 41-43 cyclin dependent kinase inhibitor 2A Homo sapiens 161-166
10648421-1 2000 When bcl-2 is immunoprecipitated from (32)P-labeled cell extracts of all-trans retinoic acid (ATRA)-treated acute myeloblastic leukemia (AML) blasts, a phosphorylated protein of approximately 30 kd is coprecipitated. Tretinoin 79-92 BCL2 apoptosis regulator Homo sapiens 5-10
10642512-0 2000 Induction of Myc-intron-binding polypeptides MIBP1 and RFX1 during retinoic acid-mediated differentiation of haemopoietic cells. Tretinoin 67-80 regulatory factor X1 Homo sapiens 55-59
10642512-4 2000 In addition, we show that treatment with retinoic acid induces both MIBP1 and RFX1 protein, as well as their DNA-binding activity, upon granulocytic differentiation of HL60 cells, with a gel mobility pattern identical to that of HeLa cells. Tretinoin 41-54 regulatory factor X1 Homo sapiens 78-82
10642512-6 2000 We also show that the time course of MIBP1 and RFX1 induction is inversely correlated with the down-regulation of c-myc levels during the treatment of HL60 cells with retinoic acid. Tretinoin 167-180 regulatory factor X1 Homo sapiens 47-51
10716617-8 2000 Exposure to retinoic acid delayed the formation of the condensation and decreased BMP-2,4,5 mRNA dramatically in mesenchyme from E13 to E15. Tretinoin 12-25 bone morphogenetic protein 2 Mus musculus 82-89
10648421-1 2000 When bcl-2 is immunoprecipitated from (32)P-labeled cell extracts of all-trans retinoic acid (ATRA)-treated acute myeloblastic leukemia (AML) blasts, a phosphorylated protein of approximately 30 kd is coprecipitated. Tretinoin 94-98 BCL2 apoptosis regulator Homo sapiens 5-10
10640427-9 2000 The early expression of blr1 mRNA during differentiation, its ability to increase ERK2 activation, and its enhancement of retinoic acid-induced differentiation suggest that blr1 expression may be involved in retinoic acid-induced HL-60 differentiation. Tretinoin 208-221 mitogen-activated protein kinase 1 Homo sapiens 82-86
10695998-0 2000 IL-6 enhanced the retinoic acid-induced differentiation of human acute promyelocytic leukemia cells. Tretinoin 18-31 interleukin 6 Homo sapiens 0-4
10695998-1 2000 It has been shown that retinoic acid (RA) induced the expression of interleukin-6 (IL-6) in human acute promyelocytic leukemia HL-60 cells. Tretinoin 23-36 interleukin 6 Homo sapiens 68-81
10695998-1 2000 It has been shown that retinoic acid (RA) induced the expression of interleukin-6 (IL-6) in human acute promyelocytic leukemia HL-60 cells. Tretinoin 23-36 interleukin 6 Homo sapiens 83-87
10695998-1 2000 It has been shown that retinoic acid (RA) induced the expression of interleukin-6 (IL-6) in human acute promyelocytic leukemia HL-60 cells. Tretinoin 38-40 interleukin 6 Homo sapiens 68-81
10695998-1 2000 It has been shown that retinoic acid (RA) induced the expression of interleukin-6 (IL-6) in human acute promyelocytic leukemia HL-60 cells. Tretinoin 38-40 interleukin 6 Homo sapiens 83-87
10695998-2 2000 In the present study, we examined the ability of RA to induce the expression of gp130, the signal-transducing receptor component for IL-6, in HL-60 and a RA-supersensitive cell line HL-60/S4. Tretinoin 49-51 interleukin 6 Homo sapiens 133-137
10695998-5 2000 Furthermore, activation of the RA-induced gp130 by exogenous IL-6 potentiated the differentiating effects of RA. Tretinoin 31-33 interleukin 6 Homo sapiens 61-65
10695998-7 2000 Our findings suggest that the differentiating effects of RA may partially be mediated by the up-regulation of IL-6/gp130 signaling in HL-60 and HL-60/S4 cells. Tretinoin 57-59 interleukin 6 Homo sapiens 110-114
10640427-0 2000 Retinoic acid-induced blr1 expression promotes ERK2 activation and cell differentiation in HL-60 cells. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 47-51
10646501-9 2000 The addition of TNFalpha or PMA potentiated RA-induced MMP-9 expression with a synergic maximal effect at day 14 of RA exposure. Tretinoin 44-46 tumor necrosis factor Homo sapiens 16-24
10664247-7 2000 These results reveal that the metastasis-preventing effect of ATRA may partly result from the up-regulation of nm23-H1, and the metastasis-promoting effects of EGF and c-erbB-2/neu were probably mediated in part by the down-regulation of nm23-H1. Tretinoin 62-66 erb-b2 receptor tyrosine kinase 2 Homo sapiens 177-180
10784405-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human myeloid leukemia KG-1 cells. Tretinoin 31-44 nerve growth factor Homo sapiens 113-132
10657000-4 2000 When RA was used in combination with 2 mM NaB, the treatment induced substantial morphological changes, apoptosis-independent growth arrest, up-regulation of tissue transglutaminase (tTGase), and down-regulation of beta and gamma RA receptor (RAR) mRNA expression. Tretinoin 5-7 transglutaminase 2 Homo sapiens 158-181
10657000-4 2000 When RA was used in combination with 2 mM NaB, the treatment induced substantial morphological changes, apoptosis-independent growth arrest, up-regulation of tissue transglutaminase (tTGase), and down-regulation of beta and gamma RA receptor (RAR) mRNA expression. Tretinoin 5-7 transglutaminase 2 Homo sapiens 183-189
10651997-6 2000 Furthermore, the RAR-beta,gamma antagonist CD2665 antagonized the suppressive effects of all-trans retinoic acid, adapalene, and CD2043 on both cell growth and differentiation. Tretinoin 89-112 retinoic acid receptor, beta Rattus norvegicus 17-25
10784405-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human myeloid leukemia KG-1 cells. Tretinoin 31-44 nerve growth factor Homo sapiens 134-137
10629053-0 2000 Orphan receptor COUP-TF is required for induction of retinoic acid receptor beta, growth inhibition, and apoptosis by retinoic acid in cancer cells. Tretinoin 53-66 nuclear receptor subfamily 2 group F member 1 Homo sapiens 16-23
10629053-2 2000 Expression of RARbeta is highly induced by retinoic acid (RA) through a RA response element (betaRARE) that is activated by heterodimers of RARs and retinoid X receptors (RXRs). Tretinoin 43-56 retinoic acid receptor beta Homo sapiens 14-21
10784405-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human myeloid leukemia KG-1 cells. Tretinoin 46-48 nerve growth factor Homo sapiens 113-132
10629053-2 2000 Expression of RARbeta is highly induced by retinoic acid (RA) through a RA response element (betaRARE) that is activated by heterodimers of RARs and retinoid X receptors (RXRs). Tretinoin 58-60 retinoic acid receptor beta Homo sapiens 14-21
10784405-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human myeloid leukemia KG-1 cells. Tretinoin 46-48 nerve growth factor Homo sapiens 134-137
10784405-4 2000 Furthermore, activation of the induced trkA receptor by exogenous NGF potentiated the differentiating effects of RA and NaBut. Tretinoin 113-115 nerve growth factor Homo sapiens 66-69
10687848-8 2000 All-trans retinoic acid increased the level of RIG1 mRNA in a time- and concentration-dependent manner in SC-M1 CL23 gastric cancer cells. Tretinoin 10-23 phospholipase A and acyltransferase 4 Homo sapiens 47-51
10623473-6 2000 Employing bcl-2-overexpressing HL-60 cells permitted demonstration of nuclear lobulation, ELCS formation, and centrosome-MT movement concomitantly during RA-induced differentiation, implying independence between the cellular reorganization and apoptotic programs. Tretinoin 154-156 BCL2 apoptosis regulator Homo sapiens 10-15
10629091-4 2000 Transfection of HeLa cells with RARbeta expression plasmids resulted in reduced clonal cell growth in the presence of retinoic acid (RA). Tretinoin 118-131 retinoic acid receptor beta Homo sapiens 32-39
10629091-5 2000 RA-induced growth inhibition in HeLa x fibroblast hybrid cells was partially relieved by a dominant-negative RARbeta mutant. Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 109-116
10629091-7 2000 Anchorage-independent growth of the HeLa(RARbeta) lines was indistinguishable from that of control cells in the absence of RA, but strongly impaired after RA treatment. Tretinoin 123-125 retinoic acid receptor beta Homo sapiens 41-48
10645889-0 2000 Retinoic acid-induced proliferation of lung alveolar epithelial cells is linked to p21(CIP1) downregulation. Tretinoin 0-13 cyclin dependent kinase inhibitor 1A Homo sapiens 83-86
10940651-0 2000 p53 pathway in apoptosis induced by all-trans-retinoic acid in acute myeloblastic leukaemia cells. Tretinoin 36-59 tumor protein p53 Homo sapiens 0-3
10940651-1 2000 The role of the p53 pathway in apoptosis induced by all-trans-retinoic acid (ATRA) was studied in 5 human acute myeloid leukaemia (AML) cell lines, OU-AML-3, -4, -5, -7 and -8, previously established and characterized by the authors. Tretinoin 52-75 tumor protein p53 Homo sapiens 16-19
10940651-1 2000 The role of the p53 pathway in apoptosis induced by all-trans-retinoic acid (ATRA) was studied in 5 human acute myeloid leukaemia (AML) cell lines, OU-AML-3, -4, -5, -7 and -8, previously established and characterized by the authors. Tretinoin 77-81 tumor protein p53 Homo sapiens 16-19
10940651-8 2000 On the basis of these results, ATRA-induced apoptosis in these AML cell lines is independent of the p53 pathway, although it is associated with the down-regulation of bcl-2. Tretinoin 31-35 BCL2 apoptosis regulator Homo sapiens 167-172
10645889-0 2000 Retinoic acid-induced proliferation of lung alveolar epithelial cells is linked to p21(CIP1) downregulation. Tretinoin 0-13 cyclin dependent kinase inhibitor 1A Homo sapiens 87-91
10645889-14 2000 Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Tretinoin 104-106 cyclin dependent kinase inhibitor 2B Homo sapiens 13-16
10645889-14 2000 Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Tretinoin 104-106 cyclin dependent kinase inhibitor 1A Homo sapiens 17-20
10645889-14 2000 Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Tretinoin 104-106 cyclin dependent kinase inhibitor 1A Homo sapiens 21-25
10645889-14 2000 Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Tretinoin 151-153 cyclin dependent kinase inhibitor 2B Homo sapiens 13-16
10645889-14 2000 Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Tretinoin 151-153 cyclin dependent kinase inhibitor 1A Homo sapiens 17-20
10645889-14 2000 Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Tretinoin 151-153 cyclin dependent kinase inhibitor 1A Homo sapiens 21-25
10651729-0 2000 Role of P-glycoprotein in all-trans retinoic acid (ATRA) resistance in acute promyelocytic leukaemia cells: analysis of intracellular concentration of ATRA. Tretinoin 26-49 ATP binding cassette subfamily B member 1 Homo sapiens 8-22
10620339-2 2000 Treatment with FSH produced a substantial increase in LH-R mRNA level, as was expected, while concurrent treatment with increasing concentrations of RA brought about dose-dependent decreases in FSH-induced LH-R mRNA. Tretinoin 149-151 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 206-210
10620339-6 2000 The effect of RA on LH-R mRNA stability was determined by measuring the decay of LH receptor mRNA under conditions known to inhibit transcription. Tretinoin 14-16 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 20-24
10620339-6 2000 The effect of RA on LH-R mRNA stability was determined by measuring the decay of LH receptor mRNA under conditions known to inhibit transcription. Tretinoin 14-16 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 81-92
10620339-8 2000 It may be possible that RA not only inhibits FSH-induced transcription but also stimulates the production of destabilizing factors for the LH-R mRNA. Tretinoin 24-26 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 139-143
10651729-0 2000 Role of P-glycoprotein in all-trans retinoic acid (ATRA) resistance in acute promyelocytic leukaemia cells: analysis of intracellular concentration of ATRA. Tretinoin 51-55 ATP binding cassette subfamily B member 1 Homo sapiens 8-22
10651729-1 2000 We analysed the relationship between all-trans retinoic acid (ATRA) resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) in acute promyelocytic leukaemia (APL). Tretinoin 37-60 ATP binding cassette subfamily B member 1 Homo sapiens 83-97
10651729-1 2000 We analysed the relationship between all-trans retinoic acid (ATRA) resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) in acute promyelocytic leukaemia (APL). Tretinoin 37-60 ATP binding cassette subfamily B member 1 Homo sapiens 99-103
10651729-1 2000 We analysed the relationship between all-trans retinoic acid (ATRA) resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) in acute promyelocytic leukaemia (APL). Tretinoin 62-66 ATP binding cassette subfamily B member 1 Homo sapiens 83-97
10620339-0 2000 Retinoic acid (RA) represses follicle stimulating hormone (FSH)-induced luteinizing hormone (LH) receptor in rat granulosa cells. Tretinoin 0-13 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 72-105
10620339-0 2000 Retinoic acid (RA) represses follicle stimulating hormone (FSH)-induced luteinizing hormone (LH) receptor in rat granulosa cells. Tretinoin 15-17 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 72-105
10620339-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on the luteinizing hormone receptor (LH-R) in rat granulosa cells. Tretinoin 85-98 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 111-139
10620339-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on the luteinizing hormone receptor (LH-R) in rat granulosa cells. Tretinoin 85-98 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 141-145
10620339-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on the luteinizing hormone receptor (LH-R) in rat granulosa cells. Tretinoin 100-102 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 111-139
10620339-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on the luteinizing hormone receptor (LH-R) in rat granulosa cells. Tretinoin 100-102 luteinizing hormone/choriogonadotropin receptor Rattus norvegicus 141-145
10651729-1 2000 We analysed the relationship between all-trans retinoic acid (ATRA) resistance and P-glycoprotein (P-gp)-associated multidrug resistance (MDR) in acute promyelocytic leukaemia (APL). Tretinoin 62-66 ATP binding cassette subfamily B member 1 Homo sapiens 99-103
11059564-0 2000 Inhibition of the cytochrome P-450 modulates all-trans-retinoic acid-induced differentiation and apoptosis of HL-60 cells. Tretinoin 55-68 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 18-34
11059564-6 2000 Moreover, proadifen weakened ATRA-induced downregulation of the Bcl-2 protein. Tretinoin 29-33 BCL2 apoptosis regulator Homo sapiens 64-69
11399583-6 2000 After a week with ATRA treatment, fibrinogen level improved and "D" dimers decreased, so as observed slowly maturation of leukemic leucocytes. Tretinoin 18-22 fibrinogen beta chain Homo sapiens 34-44
10634641-5 2000 The expression of CD34 correlated to a higher sensitivity to ATRA (P = 0.003). Tretinoin 61-65 CD34 molecule Homo sapiens 18-22
10642314-0 2000 Downregulation of angiotensin II type 1 receptor by all-trans retinoic acid in vascular smooth muscle cells. Tretinoin 62-75 angiotensin II receptor, type 1b Rattus norvegicus 18-48
10642314-4 2000 atRA (1 micromol/L) decreased the AT(1)-R mRNA level by 50% after 24 hours; AT(1)-R number was also reduced to the same extent after 48 hours. Tretinoin 0-4 angiotensin II receptor, type 1b Rattus norvegicus 34-41
10642314-6 2000 Cycloheximide blocked the atRA-induced decrease in AT(1)-R mRNA expression, suggesting that this process requires de novo protein synthesis. Tretinoin 26-30 angiotensin II receptor, type 1b Rattus norvegicus 51-58
10642314-7 2000 Simultaneous treatment with an agonist (Ro40-6055) specific for retinoic acid receptor (RAR) and an agonist (Ro25-7836) specific for retinoid X receptor (RXR) suppressed the AT(1)-R mRNA expression comparable to that with treatment with atRA, suggesting that the RAR/RXR heterodimer mediates the effect of atRA in AT(1)-R downregulation. Tretinoin 237-241 angiotensin II receptor, type 1b Rattus norvegicus 174-181
10642314-7 2000 Simultaneous treatment with an agonist (Ro40-6055) specific for retinoic acid receptor (RAR) and an agonist (Ro25-7836) specific for retinoid X receptor (RXR) suppressed the AT(1)-R mRNA expression comparable to that with treatment with atRA, suggesting that the RAR/RXR heterodimer mediates the effect of atRA in AT(1)-R downregulation. Tretinoin 306-310 angiotensin II receptor, type 1b Rattus norvegicus 174-181
10649440-9 2000 The dephosphorylating properties of ecto-ALP are induced by RA, suggesting a specific function in differentiating P19 teratocarcinoma and HL-60 myeloblastic leukemia cells. Tretinoin 60-62 alkaline phosphatase, placental Homo sapiens 41-44
10691036-0 2000 The effect of retinoic acid on the proportion of insulin cells in the developing chick pancreas. Tretinoin 14-27 insulin Gallus gallus 49-56
10691036-3 2000 Retinoic acid (10(-6) or 10(-5) M) was added to a standard serum-free medium, Ham"s F12 containing insulin, transferrin and selenium (F12.ITS). Tretinoin 0-13 insulin Gallus gallus 99-106
10691036-8 2000 Retinoic acid had a dose-related effect; the proportion of insulin cells in explants treated with the lower dose of retinoic acid (10(-6) M) was more than twice the proportion of insulin cells in explants treated with the higher dose (10(-5) M) of retinoic acid and more than three times that of the control grafts. Tretinoin 0-13 insulin Gallus gallus 59-66
10691036-8 2000 Retinoic acid had a dose-related effect; the proportion of insulin cells in explants treated with the lower dose of retinoic acid (10(-6) M) was more than twice the proportion of insulin cells in explants treated with the higher dose (10(-5) M) of retinoic acid and more than three times that of the control grafts. Tretinoin 0-13 insulin Gallus gallus 179-186
10691036-8 2000 Retinoic acid had a dose-related effect; the proportion of insulin cells in explants treated with the lower dose of retinoic acid (10(-6) M) was more than twice the proportion of insulin cells in explants treated with the higher dose (10(-5) M) of retinoic acid and more than three times that of the control grafts. Tretinoin 116-129 insulin Gallus gallus 59-66
10649440-0 2000 Ecto-alkaline phosphatase activity identified at physiological pH range on intact P19 and HL-60 cells is induced by retinoic acid. Tretinoin 116-129 alkaline phosphatase, placental Homo sapiens 5-25
10649440-7 2000 After its autophosphorylation by ecto-kinase activity, a 98-kDa membrane protein in P19 cells was found to be sensitive to ecto-ALP, and protein dephosphorylation increased after incubation of cells with RA for 24 h and 48 h. Orthovanadate, an inhibitor of all phosphatase activities, blocked the levamisole-sensitive dephosphorylation of the membrane phosphoproteins, while (R)-(-)-epinephrine reversed the effect by complexation of the inhibitor. Tretinoin 204-206 alkaline phosphatase, placental Homo sapiens 128-131
10649274-5 2000 RESULTS: After a mean observation period of 27 +/- 15 months (mean +/- standard deviation) under treatment with IFN-alpha +/- tretinoin, local control was seen in 11 of 13 patients (85%). Tretinoin 126-135 interferon alpha 1 Homo sapiens 112-121
10649274-8 2000 CONCLUSIONS: The data of this retrospective, nonrandomized study on therapy with IFN-alpha +/- tretinoin suggest that such treatment may be effective in prolonging the disease-free interval of patients after intralesional or marginal surgery. Tretinoin 95-104 interferon alpha 1 Homo sapiens 81-90
10607566-6 1999 Here, we shown that retinoic acid (RA) decreases the activity of the beta-catenin-LEF/TCF signaling pathway. Tretinoin 20-33 hepatocyte nuclear factor 4 alpha Homo sapiens 86-89
11142098-8 2000 In contrast to the carotenoids, the 9-cis isomer of retinoic acid was approximately 10-fold more active in suppressing neoplastic transformation and inducing connexin 43 expression in both cell types than the all-trans isomer. Tretinoin 52-65 gap junction protein, alpha 1 Mus musculus 158-169
10626844-5 1999 The expression of the two NPRAP mRNA variants was dramatically induced even prior to the terminal neuronal and glial differentiation of P19 cells after retinoic acid treatment. Tretinoin 152-165 catenin (cadherin associated protein), delta 2 Mus musculus 26-31
10718618-0 2000 Synergistic effects of 8-Cl-cAMP and retinoic acids in the inhibition of growth and induction of apoptosis in ovarian cancer cells: induction of retinoic acid receptor beta. Tretinoin 37-51 retinoic acid receptor beta Homo sapiens 145-172
10840075-6 2000 A similar marked increase in the soluble adhesion molecules ICAM-1, and to a lesser extent VCAM-1, released from the four-week bone marrow stroma was observed after RA treatment. Tretinoin 165-167 vascular cell adhesion molecule 1 Homo sapiens 91-97
10840075-7 2000 IL-6 has been implicated in the inhibitory effect of RA in several human hemopoietic and nonhemopoietic cells. Tretinoin 53-55 interleukin 6 Homo sapiens 0-4
10840075-10 2000 The profound and rapid 7.5-fold increase in the natural antagonist of human IL-6 cytokine family after RA treatment could abrogate the gp130 signaling required for proliferation and/or expansion of human primitive hemopoietic stem cells and lead to the observed inhibitory effect of RA on CAFC. Tretinoin 103-105 interleukin 6 Homo sapiens 76-80
10840075-10 2000 The profound and rapid 7.5-fold increase in the natural antagonist of human IL-6 cytokine family after RA treatment could abrogate the gp130 signaling required for proliferation and/or expansion of human primitive hemopoietic stem cells and lead to the observed inhibitory effect of RA on CAFC. Tretinoin 283-285 interleukin 6 Homo sapiens 76-80
10714240-2 2000 The biological action of retinoic acid and synthetic analogs, referred to as retinoids, is mediated by RAR alpha, RAR beta, or RAR gamma and/or by RXR alpha, RXR beta, or RXR gamma, all being nuclear receptors. Tretinoin 25-38 retinoic acid receptor beta Homo sapiens 114-122
10607566-6 1999 Here, we shown that retinoic acid (RA) decreases the activity of the beta-catenin-LEF/TCF signaling pathway. Tretinoin 35-37 hepatocyte nuclear factor 4 alpha Homo sapiens 86-89
10607566-10 1999 The data suggest that direct regulation of beta-catenin-LEF/TCF signaling is one mechanism whereby RA influences development, cell differentiation and cancer. Tretinoin 99-101 hepatocyte nuclear factor 4 alpha Homo sapiens 60-63
10863413-0 1999 Effects of all-trans retinoic acid and interferon-gamma on expression of RAR beta gene in Tca8113 cells. Tretinoin 21-34 retinoic acid receptor beta Homo sapiens 73-81
10863413-9 1999 The expression of RAR beta increased 12 times after treatment with combined ATRA and IFN gamma treatment. Tretinoin 76-80 retinoic acid receptor beta Homo sapiens 18-26
10518116-10 1999 The opposite alteration of Bcl-2 (anti-apoptotic) and p53 (apoptotic) contents in SH-SY5Y cells with retinoic acid and staurosporine are attributed to the changes in cell vulnerability. Tretinoin 101-114 BCL2 apoptosis regulator Homo sapiens 27-32
10588863-9 1999 Regulatory mechanisms altered by excess RA must function normally to limit GATA-4/5/6 expression levels, to define the region of Nkx2.5 expression and regulate myocardial differentiation. Tretinoin 40-42 GATA binding protein 4 L homeolog Xenopus laevis 75-81
10601968-0 1999 Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in prepubertal pig sertoli cells. Tretinoin 20-33 insulin like growth factor binding protein 4 Sus scrofa 58-102
10601968-2 1999 A significant dose-dependent increase in IGFBP-4 mRNA levels was observed in Sertoli cells cultured in the presence of physiological concentrations of T(3) or RA. Tretinoin 159-161 insulin like growth factor binding protein 4 Sus scrofa 41-48
10601968-5 1999 Our data establish an important direct role for T(3) and RA in regulating IGFBP-4 expression and consequently IGF activity at the testis level. Tretinoin 57-59 insulin like growth factor binding protein 4 Sus scrofa 74-81
10611763-4 1999 In addition, enhanced levels of circulating endogenous TGF-beta appear to be an instrument of suppression during the development of oral tolerance, cyclosporin treatment, and following administration of retinoic acid. Tretinoin 203-216 transforming growth factor beta 1 Homo sapiens 55-63
10597280-0 1999 The induction and activation of STAT1 by all-trans-retinoic acid are mediated by RAR beta signaling pathways in breast cancer cells. Tretinoin 41-64 retinoic acid receptor beta Homo sapiens 81-89
10597280-4 1999 First, by using different receptor-selective retinoids, we demonstrated that RAR beta induction in MCF-7 cells by all-trans-retinoic acid (atRA) was associated with the activation of STAT1 gene transcription. Tretinoin 114-137 retinoic acid receptor beta Homo sapiens 77-85
10597280-4 1999 First, by using different receptor-selective retinoids, we demonstrated that RAR beta induction in MCF-7 cells by all-trans-retinoic acid (atRA) was associated with the activation of STAT1 gene transcription. Tretinoin 139-143 retinoic acid receptor beta Homo sapiens 77-85
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 38-42 retinoic acid receptor beta Homo sapiens 26-34
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 38-42 retinoic acid receptor beta Homo sapiens 146-154
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 38-42 retinoic acid receptor beta Homo sapiens 146-154
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 retinoic acid receptor beta Homo sapiens 26-34
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 retinoic acid receptor beta Homo sapiens 146-154
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 retinoic acid receptor beta Homo sapiens 146-154
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 retinoic acid receptor beta Homo sapiens 26-34
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 retinoic acid receptor beta Homo sapiens 146-154
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 retinoic acid receptor beta Homo sapiens 146-154
10597280-6 1999 In addition, we showed that STAT1 was phosphorylated/activated under atRA treatment of MCF-7 cells; this process required the involvement of RAR beta and protein synthesis. Tretinoin 69-73 retinoic acid receptor beta Homo sapiens 141-149
10583214-8 1999 To establish whether ATRA-induced changes influenced the fibrinolytic process, we evaluated the effect of MNC stimulated with ATRA on u-PA-induced degradation of diluted plasma clots. Tretinoin 126-130 plasminogen activator, urokinase Homo sapiens 134-138
10583214-9 1999 ATRA-treated cells markedly inhibited clot lysis induced by low concentrations of u-PA. Tretinoin 0-4 plasminogen activator, urokinase Homo sapiens 82-86
10583214-10 1999 The effect was due to enhanced extracellular PAI-2 accumulation since it was observed with conditioned medium from ATRA-treated cells; it was abolished by the addition of neutralizing anti-PAI-2 antibodies and was negligible when single-chain t-PA was used instead of u-PA. Tretinoin 115-119 plasminogen activator, tissue type Homo sapiens 243-247
10583214-10 1999 The effect was due to enhanced extracellular PAI-2 accumulation since it was observed with conditioned medium from ATRA-treated cells; it was abolished by the addition of neutralizing anti-PAI-2 antibodies and was negligible when single-chain t-PA was used instead of u-PA. Tretinoin 115-119 plasminogen activator, urokinase Homo sapiens 268-272
10525374-6 1999 The binding of SiHa cells to ECM proteins (fibronectin, vitronectin, laminin, collagen IV) was drastically reduced when cells were treated with ATRA at 10 microM for 96 h in culture. Tretinoin 144-148 fibronectin 1 Homo sapiens 43-54
10525374-7 1999 Interestingly, when ATRA-treated (10 microM, 96 h) SiHa cells were allowed to grow for 15 days in ATRA-free complete medium the binding of SiHa cells to fibronectin and vitronectin was inhibited, even after 15 days of drug withdrawal, whereas cell adhesion to laminin and collagen IV returned to normal within 3-7 days. Tretinoin 20-24 fibronectin 1 Homo sapiens 153-164
10525374-7 1999 Interestingly, when ATRA-treated (10 microM, 96 h) SiHa cells were allowed to grow for 15 days in ATRA-free complete medium the binding of SiHa cells to fibronectin and vitronectin was inhibited, even after 15 days of drug withdrawal, whereas cell adhesion to laminin and collagen IV returned to normal within 3-7 days. Tretinoin 98-102 fibronectin 1 Homo sapiens 153-164
10602416-6 1999 Unexpectedly, all primary acute promyelocytic leukemia (APL) samples lacked IRF-1 protein and most exhibited accelerated exon skipping; furthermore, IRF-1 could not be induced by IFNgamma or all-trans retinoic acid (ATRA) which both induce IRF-1 in the NB4 APL cell line. Tretinoin 216-220 interferon regulatory factor 1 Homo sapiens 149-154
10602416-6 1999 Unexpectedly, all primary acute promyelocytic leukemia (APL) samples lacked IRF-1 protein and most exhibited accelerated exon skipping; furthermore, IRF-1 could not be induced by IFNgamma or all-trans retinoic acid (ATRA) which both induce IRF-1 in the NB4 APL cell line. Tretinoin 216-220 interferon regulatory factor 1 Homo sapiens 149-154
10619646-0 1999 Retinoic acid increases BDNF-dependent regeneration of chick retinal ganglion cells in vitro. Tretinoin 0-13 brain derived neurotrophic factor Gallus gallus 24-28
10582693-6 1999 A PPARgamma agonist, troglitazone, was given to guinea pigs along with estradiol and all-trans retinoic acid and produced the largest leiomyomata seen to date in this model. Tretinoin 95-108 peroxisome proliferator activated receptor gamma Homo sapiens 2-11
10550308-1 1999 We recently observed that growth inhibition of esophageal cancer cells by retinoic acid (RA) was associated with both constitutive expression and RA-induced up-regulation of RA receptor beta (RAR-beta). Tretinoin 74-87 retinoic acid receptor beta Homo sapiens 192-200
10550308-1 1999 We recently observed that growth inhibition of esophageal cancer cells by retinoic acid (RA) was associated with both constitutive expression and RA-induced up-regulation of RA receptor beta (RAR-beta). Tretinoin 89-91 retinoic acid receptor beta Homo sapiens 192-200
10550308-1 1999 We recently observed that growth inhibition of esophageal cancer cells by retinoic acid (RA) was associated with both constitutive expression and RA-induced up-regulation of RA receptor beta (RAR-beta). Tretinoin 146-148 retinoic acid receptor beta Homo sapiens 192-200
10583214-2 1999 We investigated the in vitro effect of all-trans-retinoic acid (ATRA) on the production of two major fibrinolytic components, urokinase-type plasminogen activator (u-PA) and PA inhibitor 2 (PAI-2), by human blood mononuclear cells (MNC). Tretinoin 39-62 plasminogen activator, urokinase Homo sapiens 126-162
10583214-2 1999 We investigated the in vitro effect of all-trans-retinoic acid (ATRA) on the production of two major fibrinolytic components, urokinase-type plasminogen activator (u-PA) and PA inhibitor 2 (PAI-2), by human blood mononuclear cells (MNC). Tretinoin 64-68 plasminogen activator, urokinase Homo sapiens 126-162
10520221-11 1999 Retinoic acid increased integrin alpha( V) expression by primary and immortalized cells 1.3-fold and 3-fold, respectively, and caused a slight increase in integrin alpha(6) expression by primary cells. Tretinoin 0-13 integrin alpha-6 Oryctolagus cuniculus 155-172
10518116-8 1999 The expression of the proteins of the protooncogene Bcl-2 and the tumor suppressor gene p53 following staurosporine or retinoic acid treatment was assessed by Western blot and immunocytochemistry. Tretinoin 119-132 BCL2 apoptosis regulator Homo sapiens 52-57
10518116-8 1999 The expression of the proteins of the protooncogene Bcl-2 and the tumor suppressor gene p53 following staurosporine or retinoic acid treatment was assessed by Western blot and immunocytochemistry. Tretinoin 119-132 tumor protein p53 Homo sapiens 88-91
10518116-9 1999 Retinoic acid increased Bcl-2 and decreased p53 levels, whereas staurosporine decreased Bcl-2 and increased p53 levels. Tretinoin 0-13 BCL2 apoptosis regulator Homo sapiens 24-29
10518116-9 1999 Retinoic acid increased Bcl-2 and decreased p53 levels, whereas staurosporine decreased Bcl-2 and increased p53 levels. Tretinoin 0-13 tumor protein p53 Homo sapiens 44-47
10518116-10 1999 The opposite alteration of Bcl-2 (anti-apoptotic) and p53 (apoptotic) contents in SH-SY5Y cells with retinoic acid and staurosporine are attributed to the changes in cell vulnerability. Tretinoin 101-114 tumor protein p53 Homo sapiens 54-57
10557066-0 1999 Expression of Bcl-2-related genes in normal and AML progenitors: changes induced by chemotherapy and retinoic acid. Tretinoin 101-114 BCL2 apoptosis regulator Homo sapiens 14-19
10609785-1 1999 Preclinical data have shown that all-trans retinoic acid (ATRA) with interferon-alpha (IFN-alpha) can exert significant suppressive effects on Philadelphia-chromosome (Ph)-positive cells. Tretinoin 33-56 interferon alpha 1 Homo sapiens 87-96
10557066-10 1999 Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C. Tretinoin 57-61 BCL2 apoptosis regulator Homo sapiens 18-23
10609785-1 1999 Preclinical data have shown that all-trans retinoic acid (ATRA) with interferon-alpha (IFN-alpha) can exert significant suppressive effects on Philadelphia-chromosome (Ph)-positive cells. Tretinoin 58-62 interferon alpha 1 Homo sapiens 87-96
10609785-2 1999 The aim of this study combining IFN-alpha, low-dose cytosine arabinoside (ara-C) and ATRA was to increase the proportion of patients achieving a major cytogenetic response, in comparison with a group of 140 patients previously treated with IFN-alpha plus low-dose ara-C. Tretinoin 85-89 interferon alpha 1 Homo sapiens 240-249
10557066-10 1999 Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C. Tretinoin 104-108 BCL2 apoptosis regulator Homo sapiens 18-23
10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tretinoin 6-14 mitogen-activated protein kinase 8 Homo sapiens 82-85
10531331-7 1999 By using different retinoic acid reporter systems, it is demonstrated that RIP140 strongly suppresses retinoic acid induction of reporter activities, but coactivator SRC-1 enhances it. Tretinoin 19-32 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 166-171
10529394-6 1999 The GnT-V-AS/7721 cells were more susceptible to the apoptosis induced by ATRA than the mock-transfected cells. Tretinoin 74-78 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 4-9
10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tretinoin 6-14 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90
10477294-5 1999 Thus, retinoic acid and hedgehog signaling have opposite effects on the prepattern genes Gli3 and Zic2 and on other genes acting downstream in the neurogenesis cascade. Tretinoin 6-19 Zic family member 2 S homeolog Xenopus laevis 98-102
10518034-3 1999 Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) signalling pathways by the pro-angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. Tretinoin 71-84 mitogen-activated protein kinase 8 Homo sapiens 116-139
10518034-3 1999 Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) signalling pathways by the pro-angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. Tretinoin 71-84 mitogen-activated protein kinase 8 Homo sapiens 141-144
10518034-3 1999 Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) signalling pathways by the pro-angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. Tretinoin 71-84 mitogen-activated protein kinase 1 Homo sapiens 150-180
10518034-3 1999 Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) signalling pathways by the pro-angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. Tretinoin 71-84 mitogen-activated protein kinase 1 Homo sapiens 182-185
10518034-3 1999 Here we show that the synthetic glucocorticoid dexamethasone (Dex) and retinoic acid (RA) inhibit the activation of c-Jun N-terminal kinase (JNK) and extracellular-regulated kinase (ERK) signalling pathways by the pro-angiogenic agents tumor necrosis factor and vascular endothelial growth factor in endothelial cells. Tretinoin 71-84 vascular endothelial growth factor A Homo sapiens 262-296
10477294-3 1999 We show that retinoic acid expands the N-tubulin, X-ngnr-1, X-MyT1, X-&Dgr;-1 and Gli3 domains and inhibits the expression of Zic2 and sonic hedgehog in the neural ectoderm, whereas a retinoid antagonist produces opposite changes. Tretinoin 13-26 Zic family member 2 S homeolog Xenopus laevis 130-134
10548434-0 1999 Retinoic acid selectively activates the ERK2 but not JNK/SAPK or p38 MAP kinases when inducing myeloid differentiation. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 40-44
10548434-0 1999 Retinoic acid selectively activates the ERK2 but not JNK/SAPK or p38 MAP kinases when inducing myeloid differentiation. Tretinoin 0-13 mitogen-activated protein kinase 8 Homo sapiens 53-56
10548434-1 1999 Among the three major mitogen-activated protein kinase (MAPK) cascades--the extracellular signal regulated kinase (ERK) pathway, the c-JUN N-terminal/stress-activated protein kinase (JNK/SAPK) pathway, and the reactivating kinase (p38) pathway--retinoic acid selectively utilizes ERK but not JNK/SAPK or p38 when inducing myeloid differentiation of HL-60 human myeloblastic leukemia cells. Tretinoin 245-258 mitogen-activated protein kinase 1 Homo sapiens 56-60
10548434-2 1999 Retinoic acid is known to activate ERK2. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 35-39
10548434-5 1999 Presumably because it activates relevant signaling pathways including MAPK, the polyoma middle T antigen, as well as certain transformation defective mutants thereof, is known to promote retinoic acid-induced differentiation, although the mechanism of action is not well understood. Tretinoin 187-200 mitogen-activated protein kinase 1 Homo sapiens 70-74
10548434-8 1999 Polyoma-activated MAPK signaling relevant to retinoic acid-induced differentiation is thus restricted to ERK2 and does not involve JNK/SAPK or p38. Tretinoin 45-58 mitogen-activated protein kinase 1 Homo sapiens 18-22
10548434-8 1999 Polyoma-activated MAPK signaling relevant to retinoic acid-induced differentiation is thus restricted to ERK2 and does not involve JNK/SAPK or p38. Tretinoin 45-58 mitogen-activated protein kinase 1 Homo sapiens 105-109
10548434-9 1999 Taken together, the data indicate that among the three parallel MAPK pathways, retinoic acid-induced HL-60 myeloid differentiation selectively depends on activating ERK but not the other two MAPK pathways, JNK/SAPK or p38, with no apparent cross talk between pathways. Tretinoin 79-92 mitogen-activated protein kinase 1 Homo sapiens 64-68
10573135-5 1999 These results suggest that hypophosphorylation of pRB and repression of cyclin D3 and cdc25A are induced synergistically by treatment with ATRA plus GM-CSF in ML-1 cells. Tretinoin 139-143 cyclin D3 Homo sapiens 72-81
10548434-9 1999 Taken together, the data indicate that among the three parallel MAPK pathways, retinoic acid-induced HL-60 myeloid differentiation selectively depends on activating ERK but not the other two MAPK pathways, JNK/SAPK or p38, with no apparent cross talk between pathways. Tretinoin 79-92 mitogen-activated protein kinase 1 Homo sapiens 165-168
10548434-9 1999 Taken together, the data indicate that among the three parallel MAPK pathways, retinoic acid-induced HL-60 myeloid differentiation selectively depends on activating ERK but not the other two MAPK pathways, JNK/SAPK or p38, with no apparent cross talk between pathways. Tretinoin 79-92 mitogen-activated protein kinase 8 Homo sapiens 206-209
10548434-9 1999 Taken together, the data indicate that among the three parallel MAPK pathways, retinoic acid-induced HL-60 myeloid differentiation selectively depends on activating ERK but not the other two MAPK pathways, JNK/SAPK or p38, with no apparent cross talk between pathways. Tretinoin 79-92 mitogen-activated protein kinase 9 Homo sapiens 210-214
10548434-9 1999 Taken together, the data indicate that among the three parallel MAPK pathways, retinoic acid-induced HL-60 myeloid differentiation selectively depends on activating ERK but not the other two MAPK pathways, JNK/SAPK or p38, with no apparent cross talk between pathways. Tretinoin 79-92 mitogen-activated protein kinase 1 Homo sapiens 218-221
10548434-10 1999 Furthermore, the striking ability of polyoma middle T antigens to promote retinoic acid-induced differentiation appears to utilize ERK, but not JNK/SPK or p38 signaling. Tretinoin 74-87 mitogen-activated protein kinase 1 Homo sapiens 131-134
10493748-6 1999 Exogenous application of retinoic acid induced NRTN responsiveness and Ret protein expression from E9 vestibular ganglion neurons, suggesting that retinoic acid can regulate Ret protein expression in peripheral sensory neurons in vitro. Tretinoin 25-38 neurturin Gallus gallus 47-51
10493748-6 1999 Exogenous application of retinoic acid induced NRTN responsiveness and Ret protein expression from E9 vestibular ganglion neurons, suggesting that retinoic acid can regulate Ret protein expression in peripheral sensory neurons in vitro. Tretinoin 147-160 neurturin Gallus gallus 47-51
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 nerve growth factor Homo sapiens 164-183
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 nerve growth factor Homo sapiens 185-188
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 AKT serine/threonine kinase 1 Homo sapiens 255-258
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 mitogen-activated protein kinase 1 Homo sapiens 267-320
10540859-5 1999 A refined control mechanism for intracellular level of retinoic acid is also discussed with retinal dehydrogenase II and cytochrome P450 RAI (CYP26). Tretinoin 55-68 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 142-147
10498893-1 1999 The retinoic acid (RA) receptor beta isoform (RARbeta) plays an important role in RA-induced differentiation of human neuroblastoma. Tretinoin 19-21 retinoic acid receptor beta Homo sapiens 46-53
10493812-3 1999 Treatment of cells with 9-cis retinoic acid enhanced accessibility to cisplatin on the retinoic acid receptor beta gene promoter region, but not on the coding regions of that gene nor on the dihydrofolate reductase gene promoter or coding regions, where accessibilities to cisplatin remained 2-4 times lower than on the activated retinoic acid receptor beta gene promoter. Tretinoin 30-43 retinoic acid receptor beta Homo sapiens 87-114
10493812-3 1999 Treatment of cells with 9-cis retinoic acid enhanced accessibility to cisplatin on the retinoic acid receptor beta gene promoter region, but not on the coding regions of that gene nor on the dihydrofolate reductase gene promoter or coding regions, where accessibilities to cisplatin remained 2-4 times lower than on the activated retinoic acid receptor beta gene promoter. Tretinoin 30-43 retinoic acid receptor beta Homo sapiens 330-357
10935488-4 1999 Retinoid X receptor alpha (RXRalpha), a 9-cis-retinoic acid stimulated (9-cis-RA) heterodimeric partner of PPARgamma, was also co-expressed in all TCCa tissues and cell lines. Tretinoin 72-80 peroxisome proliferator activated receptor gamma Homo sapiens 107-116
10526130-0 1999 pRb phosphorylation is regulated differentially by cyclin-dependent kinase (Cdk) 2 and Cdk4 in retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 95-108 cyclin-dependent kinase 4 Mus musculus 87-91
10526130-7 1999 Cdk4 kinase activity was almost undetectable in undifferentiated P19 cells, but was strongly activated on exposure to RA. Tretinoin 118-120 cyclin-dependent kinase 4 Mus musculus 0-4
10526130-9 1999 These observations suggest that Cdk2 and Cdk4 may phosphorylate different sites of pRb in vivo and that the two sites of pRb examined here are newly phosphorylated during RA-induced neuronal differentiation in P19 cells. Tretinoin 171-173 cyclin-dependent kinase 4 Mus musculus 41-45
10486248-0 1999 Cloning and characterization of the murine PKC alpha promoter: identification of a retinoic acid response element. Tretinoin 83-96 protein kinase C, alpha Mus musculus 43-52
10479456-5 1999 P19 embryonal carcinoma (EC) cell lines stably expressing hCYP26 undergo extensive and rapid neuronal differentiation in monolayer at already low concentrations of RA, while normally P19 cells under these conditions differentiate only in endoderm-like cells. Tretinoin 164-166 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 58-64
10480883-6 1999 The induction of RA metabolism in the F9 RARbeta(2)-/- cells following differentiation was not impaired. Tretinoin 17-19 retinoic acid receptor beta Homo sapiens 41-48
10486248-2 1999 We have previously demonstrated that levels of PKC alpha mRNA, protein, and enzyme activity in B16 melanoma cells can be modulated by retinoic acid. Tretinoin 134-147 protein kinase C, alpha Mus musculus 47-56
10486248-12 1999 These results suggest that retinoic acid increases PKC alpha gene expression in B16 cells, at least in part, through direct transcriptional stimulation of its promoter. Tretinoin 27-40 protein kinase C, alpha Mus musculus 51-60
10479651-4 1999 In human THP-1 monocytic leukemia cells cultured with RA (0.05 to 500 nmol/L), MCP-1 expression was induced rapidly, significantly, and dose-dependently by as much as 165-fold. Tretinoin 54-56 GLI family zinc finger 2 Homo sapiens 9-14
10440729-10 1999 Collectively, our results suggest that BMP-4 can overcome the neuralizing action of retinoic acid to enhance mesodermal differentiation of murine ES cells. Tretinoin 84-97 bone morphogenetic protein 4 Mus musculus 39-44
10479651-6 1999 Expression of PPARgamma, a heterodimer partner of RXR, is also markedly induced by RA in THP-1 cells. Tretinoin 83-85 peroxisome proliferator activated receptor gamma Homo sapiens 14-23
10479651-6 1999 Expression of PPARgamma, a heterodimer partner of RXR, is also markedly induced by RA in THP-1 cells. Tretinoin 83-85 GLI family zinc finger 2 Homo sapiens 89-94
10438723-0 1999 Retinoic acid prevents phosphorylation of pRB in normal human B lymphocytes: regulation of cyclin E, cyclin A, and p21(Cip1). Tretinoin 0-13 cyclin A2 Homo sapiens 101-109
10509805-6 1999 Both retinoic acid isomers and PPAR agonists, specific for either PPARalpha or PPARgamma, regulate expression of each PPAR subtype gene in the opposite way: they up-regulate PPARalpha and down-regulate PPARgamma. Tretinoin 5-18 peroxisome proliferator activated receptor gamma Homo sapiens 79-88
10509805-6 1999 Both retinoic acid isomers and PPAR agonists, specific for either PPARalpha or PPARgamma, regulate expression of each PPAR subtype gene in the opposite way: they up-regulate PPARalpha and down-regulate PPARgamma. Tretinoin 5-18 peroxisome proliferator activated receptor gamma Homo sapiens 202-211
10583049-11 1999 These studies also indicate that as yet unknown isoforms of cytochrome P450 may be involved in RA metabolism in keratinocytes. Tretinoin 95-97 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 60-75
10485269-0 1999 All-trans retinoic acid at low concentration directly stimulates normal adult megakaryocytopoiesis in the presence of thrombopoietin or combined cytokines. Tretinoin 0-23 thrombopoietin Homo sapiens 118-132
10485269-3 1999 On the other hand, 10(-12) M ATRA significantly promoted the growth of CFU-meg, in the presence either of thrombopoietin or of IL-3+ GM-CSF, and induced a reproducible stimulation of the immature CD34+DR- subset. Tretinoin 29-33 thrombopoietin Homo sapiens 106-120
10485269-3 1999 On the other hand, 10(-12) M ATRA significantly promoted the growth of CFU-meg, in the presence either of thrombopoietin or of IL-3+ GM-CSF, and induced a reproducible stimulation of the immature CD34+DR- subset. Tretinoin 29-33 CD34 molecule Homo sapiens 196-200
10438723-0 1999 Retinoic acid prevents phosphorylation of pRB in normal human B lymphocytes: regulation of cyclin E, cyclin A, and p21(Cip1). Tretinoin 0-13 cyclin dependent kinase inhibitor 1A Homo sapiens 115-118
10438723-0 1999 Retinoic acid prevents phosphorylation of pRB in normal human B lymphocytes: regulation of cyclin E, cyclin A, and p21(Cip1). Tretinoin 0-13 cyclin dependent kinase inhibitor 1A Homo sapiens 119-123
10438723-5 1999 Based on our results, we suggest that the rapid effect of retinoic acid on pRB phosphorylation is due primarily to the reduced expression of cyclin E and cyclin A in late G1. Tretinoin 58-71 cyclin A2 Homo sapiens 154-162
10438723-6 1999 This could lead to the diminished cyclin E- and cyclin A-associated kinase activities noted as early as 2 hours after addition of retinoic acid. Tretinoin 130-143 cyclin A2 Homo sapiens 48-56
10438723-8 1999 Thus, retinoic acid induced a rapid, but transient increased binding of p21(Cip1) to CDK2. Tretinoin 6-19 cyclin dependent kinase inhibitor 1A Homo sapiens 72-75
10438723-8 1999 Thus, retinoic acid induced a rapid, but transient increased binding of p21(Cip1) to CDK2. Tretinoin 6-19 cyclin dependent kinase inhibitor 1A Homo sapiens 76-80
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 4-17 cyclin dependent kinase inhibitor 1A Homo sapiens 166-169
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 4-17 cyclin dependent kinase inhibitor 1A Homo sapiens 170-174
10427161-3 1999 Insulin, tri-iodothyronine (T(3)) and norepinephrine, the main regulators of brown adipose tissue function, upregulated GAPDH mRNA levels, whereas retinoic acid inhibited them. Tretinoin 147-160 insulin Homo sapiens 0-7
10442638-0 1999 ZPK inhibits PKA induced transcriptional activation by CREB and blocks retinoic acid induced neuronal differentiation. Tretinoin 71-84 mitogen-activated protein kinase kinase kinase 12 Homo sapiens 0-3
10442638-4 1999 Overexpression of ZPK in NTera-2 human teratocarcinoma cells results in inhibition of PKA induced transcriptional activation by CREB and prevents retinoic acid induced differentiation of the cells to neurons. Tretinoin 146-159 mitogen-activated protein kinase kinase kinase 12 Homo sapiens 18-21
10442642-7 1999 Moreover, induction of differentiation of mouse F9 line by retinoic acid leads to the inhibition of both POMp100 and TLS/POMp75 activities. Tretinoin 59-72 splicing factor proline and glutamine rich Homo sapiens 105-112
10442642-7 1999 Moreover, induction of differentiation of mouse F9 line by retinoic acid leads to the inhibition of both POMp100 and TLS/POMp75 activities. Tretinoin 59-72 FUS RNA binding protein Homo sapiens 121-127
10573118-6 1999 To determine whether activation of RAR-dependent gene transcription by atRA is necessary for growth inhibition, we tested the growth suppressive effect of a retinoid (BMS453) which binds RAR receptors and transrepresses AP-1 but does not activate RAR-dependent gene expression. Tretinoin 71-75 RAB40B, member RAS oncogene family Homo sapiens 35-38
10470856-6 1999 After incubation with RA with aggregation, the Evi1 clones expressed microtubule-associated protein-2 continuously but did not express glial fibrillary acidic protein as an astrocyte marker protein until 12 days of culture. Tretinoin 22-24 microtubule-associated protein 2 Mus musculus 69-101
10432387-11 1999 At this concentration, ATRA attenuated iNOS expression (mRNA and protein levels) and enzyme activity. Tretinoin 23-27 nitric oxide synthase 2, inducible Mus musculus 39-43
10428509-0 1999 Two pathways of apoptosis induced with all-trans retinoic acid and etoposide in the myeloid cell line P39. Tretinoin 49-62 cyclin dependent kinase 5 regulatory subunit 2 Homo sapiens 102-105
10428509-10 1999 ATRA-induced apoptosis caused actin cleavage, which was not affected by G-CSF, and Bcl-2 downregulation. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 83-88
10450744-7 1999 In various cell lines, including those derived from APL, RA induces directly the expression of two transcription factors, Stat1 and IRF-1 which play central roles in the IFN signal transduction. Tretinoin 57-59 interferon regulatory factor 1 Homo sapiens 132-137
10450744-7 1999 In various cell lines, including those derived from APL, RA induces directly the expression of two transcription factors, Stat1 and IRF-1 which play central roles in the IFN signal transduction. Tretinoin 57-59 interferon alpha 1 Homo sapiens 170-173
10450744-8 1999 In addition, RA induces IFN-alpha synthesis and enhances the IFN-induced Stat activation. Tretinoin 13-15 interferon alpha 1 Homo sapiens 24-33
10450744-8 1999 In addition, RA induces IFN-alpha synthesis and enhances the IFN-induced Stat activation. Tretinoin 13-15 interferon alpha 1 Homo sapiens 24-27
10456672-0 1999 Effect of all-trans retinoic acid on chemotherapy induced apoptosis and down-regulation of Bcl-2 in human myeloid leukaemia CD34 positive cells. Tretinoin 20-33 BCL2 apoptosis regulator Homo sapiens 91-96
10456672-0 1999 Effect of all-trans retinoic acid on chemotherapy induced apoptosis and down-regulation of Bcl-2 in human myeloid leukaemia CD34 positive cells. Tretinoin 20-33 CD34 molecule Homo sapiens 124-128
10456672-4 1999 Recently, all-trans retinoic acid (RA) has been reported to enhance cytarabine-induced apoptosis and downregulate Bcl-2 in several human myeloid leukaemia CD34 negative cells. Tretinoin 10-33 BCL2 apoptosis regulator Homo sapiens 114-119
10456672-4 1999 Recently, all-trans retinoic acid (RA) has been reported to enhance cytarabine-induced apoptosis and downregulate Bcl-2 in several human myeloid leukaemia CD34 negative cells. Tretinoin 10-33 CD34 molecule Homo sapiens 155-159
10456672-4 1999 Recently, all-trans retinoic acid (RA) has been reported to enhance cytarabine-induced apoptosis and downregulate Bcl-2 in several human myeloid leukaemia CD34 negative cells. Tretinoin 35-37 BCL2 apoptosis regulator Homo sapiens 114-119
10456672-4 1999 Recently, all-trans retinoic acid (RA) has been reported to enhance cytarabine-induced apoptosis and downregulate Bcl-2 in several human myeloid leukaemia CD34 negative cells. Tretinoin 35-37 CD34 molecule Homo sapiens 155-159
10456672-6 1999 Thus, the efficacy of RA in enhancing cytrabine- and fludarabine-induced apoptosis and overcoming the resistance was examined in both KG1 (CD34+CD7-) and KGla (CD34+CD7+) human myeloid leukaemia cells in the present study. Tretinoin 22-24 CD34 molecule Homo sapiens 139-143
10456672-10 1999 However, RA enhanced cytarabine- or fludarabine-induced apoptosis and inhibition of proliferation in KG1 CD34+CD7- but not in KGla CD34+CD7+ myeloid leukaemia cells. Tretinoin 9-11 CD34 molecule Homo sapiens 105-109
10456672-11 1999 As single agents, RA, cytarabine and fludarabine reduced Bcl-2 expression in a dose dependent manner in both cell types. Tretinoin 18-20 BCL2 apoptosis regulator Homo sapiens 57-62
10456672-13 1999 The addition of RA to cytarabine enhanced its induced reduction of Bcl-2 in KG1 CD34+CD7- but not in KGla CD34+CD7+ human myeloid leukaemia cells. Tretinoin 16-18 BCL2 apoptosis regulator Homo sapiens 67-72
10456672-13 1999 The addition of RA to cytarabine enhanced its induced reduction of Bcl-2 in KG1 CD34+CD7- but not in KGla CD34+CD7+ human myeloid leukaemia cells. Tretinoin 16-18 CD34 molecule Homo sapiens 80-84
10456672-15 1999 In conclusion, the present results suggest a potential role for the combination of RA and cytarabine in the treatment of refractory and/or relapsed AML patients with CD34+CD7- but not CD34+CD7+ blast cells. Tretinoin 83-85 CD34 molecule Homo sapiens 166-170
10504054-4 1999 In this study, we examined the effect of retinoic acid (RA) on uPA and tPA secretion in the highly metastatic C8161 and the poorly metastatic Hs294T human melanoma cell lines using a specific enzyme-linked immunosorbent assay (ELISA) detection system, and correlated this production with RA receptor (RAR) expression. Tretinoin 41-54 plasminogen activator, urokinase Homo sapiens 63-66
10504054-4 1999 In this study, we examined the effect of retinoic acid (RA) on uPA and tPA secretion in the highly metastatic C8161 and the poorly metastatic Hs294T human melanoma cell lines using a specific enzyme-linked immunosorbent assay (ELISA) detection system, and correlated this production with RA receptor (RAR) expression. Tretinoin 41-54 plasminogen activator, tissue type Homo sapiens 71-74
10504054-4 1999 In this study, we examined the effect of retinoic acid (RA) on uPA and tPA secretion in the highly metastatic C8161 and the poorly metastatic Hs294T human melanoma cell lines using a specific enzyme-linked immunosorbent assay (ELISA) detection system, and correlated this production with RA receptor (RAR) expression. Tretinoin 56-58 plasminogen activator, urokinase Homo sapiens 63-66
10504054-4 1999 In this study, we examined the effect of retinoic acid (RA) on uPA and tPA secretion in the highly metastatic C8161 and the poorly metastatic Hs294T human melanoma cell lines using a specific enzyme-linked immunosorbent assay (ELISA) detection system, and correlated this production with RA receptor (RAR) expression. Tretinoin 56-58 plasminogen activator, tissue type Homo sapiens 71-74
10504054-6 1999 On exposure of the cells to RA (10(-10)-10(-5) M) for 4 days, uPA secretion was increased 3.4-fold in the C8161 cell line and 1.6-fold in the Hs294T cell line using 10(-8) M RA. Tretinoin 28-30 plasminogen activator, urokinase Homo sapiens 62-65
10504054-6 1999 On exposure of the cells to RA (10(-10)-10(-5) M) for 4 days, uPA secretion was increased 3.4-fold in the C8161 cell line and 1.6-fold in the Hs294T cell line using 10(-8) M RA. Tretinoin 174-176 plasminogen activator, urokinase Homo sapiens 62-65
10504054-7 1999 In addition, tPA expression was increased in both cell lines by 3.7-fold in the C8161 cells and 3.8-fold in the Hs294T cells with 10(-6) M RA treatment. Tretinoin 139-141 plasminogen activator, tissue type Homo sapiens 13-16
10504054-10 1999 This suggests that another mechanism must exist to regulate the RA modulation of tPA and uPA secretion in these cell lines that does not require RAR alpha expression. Tretinoin 64-66 plasminogen activator, tissue type Homo sapiens 81-84
10504054-10 1999 This suggests that another mechanism must exist to regulate the RA modulation of tPA and uPA secretion in these cell lines that does not require RAR alpha expression. Tretinoin 64-66 plasminogen activator, urokinase Homo sapiens 89-92
10432387-0 1999 Retinoic acids inhibit inducible nitric oxide synthase expression in mesangial cells. Tretinoin 0-14 nitric oxide synthase 2, inducible Mus musculus 23-54
10432387-4 1999 METHODS: Expression of iNOS was evaluated by NO production (nitrite analysis), protein (Western blot analysis) and mRNA (RT-PCR analysis) levels in mesangial cells stimulated by a combination of lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma) in the presence and absence of all-trans-retinoic acid (ATRA) or its active metabolite, 13-cis-retinoic acid (13-cis-RA). Tretinoin 284-307 nitric oxide synthase 2, inducible Mus musculus 23-27
10432387-4 1999 METHODS: Expression of iNOS was evaluated by NO production (nitrite analysis), protein (Western blot analysis) and mRNA (RT-PCR analysis) levels in mesangial cells stimulated by a combination of lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma) in the presence and absence of all-trans-retinoic acid (ATRA) or its active metabolite, 13-cis-retinoic acid (13-cis-RA). Tretinoin 309-313 nitric oxide synthase 2, inducible Mus musculus 23-27
10432387-12 1999 ATRA also reduced nuclear levels of both subunits (p50 and p65) of NF-kappaB. Tretinoin 0-4 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 51-54
10432387-13 1999 TGF-beta1 levels in mesangial cells stimulated with LPS/IFN-gamma in presence of ATRA or 13-cis-RA were also reduced indicating that TGF-beta1 did not mediate the suppressive effect of retinoids on iNOS. Tretinoin 81-85 toll-like receptor 4 Mus musculus 52-55
10432387-14 1999 CONCLUSIONS: Our studies demonstrate that the retinoids ATRA and 13-cis-RA attenuate iNOS expression and activity in cytokine-stimulated murine mesangial cells. Tretinoin 56-60 nitric oxide synthase 2, inducible Mus musculus 85-89
10400643-12 1999 The anti-apoptotic action of t-RA was ascribed, at least in part, to dual suppression of the cell death pathway mediated by JNK and AP-1. Tretinoin 29-33 mitogen-activated protein kinase 8 Homo sapiens 124-127
10452548-0 1999 Involvement of Sp1 in basal and retinoic acid induced transcription of the human tissue-type plasminogen activator gene. Tretinoin 32-45 plasminogen activator, tissue type Homo sapiens 81-114
10407146-10 1999 These findings suggest that ADH1B has a limited capacity to metabolize retinols, but that ADH4 is well suited to function in the metabolism of many diverse retinols and is predicted to participate in the synthesis of the active ligands all-trans-retinoic acid, 9-cis-retinoic acid, 3, 4-didehydroretinoic acid, 4-oxo-retinoic acid, and 4-hydroxy-retinoic acid. Tretinoin 240-259 alcohol dehydrogenase 4 (class II), pi polypeptide Homo sapiens 90-94
10416619-7 1999 These findings suggest that, in SqCC/Y1 cells, RARbeta mediates suppression of squamous differentiation by ATRA without enhancing its growth-inhibitory effects. Tretinoin 107-111 retinoic acid receptor beta Homo sapiens 47-54
10395942-4 1999 Northern blot analysis revealed that RA repressed the expression of c-fos and c-jun at 15 and 30 min with the up-regulation of retinoic acid receptor gamma (RARgamma) and RARbeta at 2 h after PH. Tretinoin 37-39 retinoic acid receptor, beta Rattus norvegicus 171-178
10395947-7 1999 The mouse Drg1 homologous protein was up-regulated by retinoic acid in C2 myogenic cells. Tretinoin 54-67 developmentally regulated GTP binding protein 1 Mus musculus 10-14
10652610-6 1999 Interestingly, RA treatment up-regulated RAR beta proteins but not RAR alpha proteins, suggesting post-transcriptional regulations of RAR transcripts in glioma cells. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 41-49
10435617-0 1999 Retinoic acid resistance in NB4 APL cells is associated with lack of interferon alpha synthesis Stat1 and p48 induction. Tretinoin 0-13 interferon regulatory factor 9 Homo sapiens 106-109
10381520-0 1999 Growth inhibition of a human myeloma cell line by all-trans retinoic acid is not mediated through downregulation of interleukin-6 receptors but through upregulation of p21(WAF1). Tretinoin 60-73 cyclin dependent kinase inhibitor 1A Homo sapiens 168-171
10394471-5 1999 Furthermore, there are at least two mouse mutations--in the Pax-6 and Gli-3 genes--that cause peripheral malformations and specifically disrupt neural crest mediated, RA-dependent induction and differentiation in the forebrain. Tretinoin 167-169 paired box 6 Mus musculus 60-65
10381520-0 1999 Growth inhibition of a human myeloma cell line by all-trans retinoic acid is not mediated through downregulation of interleukin-6 receptors but through upregulation of p21(WAF1). Tretinoin 60-73 cyclin dependent kinase inhibitor 1A Homo sapiens 172-176
10381520-10 1999 Pretreatment with ATRA greatly reduced IL-6-induced gp130 phosphorylation in OPM-2 cells, reflecting a reduction in cellular IL-6Ralpha. Tretinoin 18-22 interleukin 6 Homo sapiens 39-43
10381520-10 1999 Pretreatment with ATRA greatly reduced IL-6-induced gp130 phosphorylation in OPM-2 cells, reflecting a reduction in cellular IL-6Ralpha. Tretinoin 18-22 interleukin 6 receptor Homo sapiens 125-135
10381520-13 1999 ATRA was further shown to upregulate p21(WAF1) expression and cause dephosphorylation of the retinoblastoma protein (pRB) in both OPM-2 and C5 cells. Tretinoin 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 37-40
10381520-13 1999 ATRA was further shown to upregulate p21(WAF1) expression and cause dephosphorylation of the retinoblastoma protein (pRB) in both OPM-2 and C5 cells. Tretinoin 0-4 cyclin dependent kinase inhibitor 1A Homo sapiens 41-45
10381520-15 1999 Thus, the growth inhibitory activity of ATRA is not mediated through cellular IL-6Ralpha downregulation and is likely to result from a direct upregulation of p21(WAF1) and consequent dephosphorylation of pRB. Tretinoin 40-44 cyclin dependent kinase inhibitor 1A Homo sapiens 158-161
10381520-15 1999 Thus, the growth inhibitory activity of ATRA is not mediated through cellular IL-6Ralpha downregulation and is likely to result from a direct upregulation of p21(WAF1) and consequent dephosphorylation of pRB. Tretinoin 40-44 cyclin dependent kinase inhibitor 1A Homo sapiens 162-166
10456660-3 1999 ATRA acts by down-regulating IL-6-receptor-alpha or gp130 on the surface of the myeloma cells. Tretinoin 0-4 interleukin 6 Mus musculus 29-33
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 212-225 retinoic acid receptor beta Homo sapiens 0-27
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 212-225 retinoic acid receptor beta Homo sapiens 29-37
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 212-225 retinoic acid receptor beta Homo sapiens 295-303
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 0-27
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 295-303
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 227-229 retinoic acid receptor beta Homo sapiens 0-27
10430067-1 1999 Retinoic acid receptor-beta (RAR-beta) mRNA is not expressed by retinoid-resistant renal cancer cell lines but is present in retinoid-sensitive SK-RC-06 renal cancer cells and increases following incubation with retinoic acid (RA), suggesting that the antitumor action of RA is mediated through RAR-beta (A. D. Hoffman et al., Clin. Tretinoin 227-229 retinoic acid receptor beta Homo sapiens 29-37
10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 C-X-C motif chemokine ligand 8 Homo sapiens 68-72
10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 interleukin 1 beta Homo sapiens 74-82
10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 tumor necrosis factor Homo sapiens 84-93
10400422-2 1999 In this study, we found that in APL patients receiving ATRA or As2O3 treatment, the improvement in hypercoagulobility and hyperfibrinolysis paralleled the correction of plasma fibrinogen level and amelioration of bleeding symptoms. Tretinoin 55-59 fibrinogen beta chain Homo sapiens 176-186
10512193-6 1999 BMP-4 was repressed by RA-treatment as well, both in embryos and in F9 teratocarcinoma cells. Tretinoin 23-25 bone morphogenetic protein 4 Mus musculus 0-5
10512193-7 1999 Our data suggest that both goosecoid and BMP-4 function as mediators of RA teratogenicity in mouse embryos. Tretinoin 72-74 bone morphogenetic protein 4 Mus musculus 41-46
10430097-0 1999 Synergistic effects of retinoic acid and 8-chloro-adenosine 3",5"-cyclic monophosphate on the regulation of retinoic acid receptor beta and apoptosis: involvement of mitochondria. Tretinoin 23-36 retinoic acid receptor beta Homo sapiens 108-135
10385706-0 1999 Levels of retinoic acid and retinaldehyde dehydrogenase expression in eyes of the Mitf-vit mouse model of retinal degeneration. Tretinoin 10-23 melanogenesis associated transcription factor Mus musculus 82-86
10406468-0 1999 Identification of a retinoic acid-inducible element in the murine PTH/PTHrP (parathyroid hormone/parathyroid hormone-related peptide) receptor gene. Tretinoin 20-33 parathyroid hormone-like peptide Mus musculus 70-75
10406468-4 1999 The data show that RA-induced expression of the PTH/ PTHrP-receptor gene is mediated by the downstream P2 promoter. Tretinoin 19-21 parathyroid hormone-like peptide Mus musculus 53-58
10422847-1 1999 Triad1 was recently identified as a nuclear RING finger protein, which is up-regulated during retinoic acid induced granulocytic differentiation of acute leukemia cells. Tretinoin 94-107 ariadne RBR E3 ubiquitin protein ligase 2 Homo sapiens 0-6
10385706-5 1999 It is possible that retinoic acid (RA) modulates the retinal degeneration observed in the Mitf(vit) mice. Tretinoin 20-33 melanogenesis associated transcription factor Mus musculus 90-94
10385706-5 1999 It is possible that retinoic acid (RA) modulates the retinal degeneration observed in the Mitf(vit) mice. Tretinoin 35-37 melanogenesis associated transcription factor Mus musculus 90-94
10364250-3 1999 By using an RARalpha-selective antagonist (Ro 41-5253), we demonstrated that RARbeta expression was induced by atRA through an RARalpha-dependent signaling pathway and that RARbeta induction was correlated with IGFBP-3 induction. Tretinoin 111-115 retinoic acid receptor beta Homo sapiens 77-84
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 78-82 retinoic acid receptor beta Homo sapiens 29-36
10364268-0 1999 Retinoic acid confers resistance to p53-dependent apoptosis in SH-SY5Y neuroblastoma cells by modulating nuclear import of p53. Tretinoin 0-13 tumor protein p53 Homo sapiens 36-39
10364268-0 1999 Retinoic acid confers resistance to p53-dependent apoptosis in SH-SY5Y neuroblastoma cells by modulating nuclear import of p53. Tretinoin 0-13 tumor protein p53 Homo sapiens 123-126
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 78-82 retinoic acid receptor beta Homo sapiens 127-134
10364268-3 1999 We examine here the possible contribution of the p53 pathway to the chemoresistance response associated with the RA treatment in NB cells. Tretinoin 113-115 tumor protein p53 Homo sapiens 49-52
10364268-4 1999 Upon treatment with RA (1-10 microM) for 4 days, the human NB cells, SH-SY5Y, developed resistance selectively to p53-dependent apoptotic stimuli including gamma-irradiation, etoposide, and 1-(5-isoquinolinyl sulfonyl)-2-methylpiperazine (H-7). Tretinoin 20-22 tumor protein p53 Homo sapiens 114-117
10364268-5 1999 Interestingly, RA affected the ability of H-7 to induce nuclear accumulation of the p53 protein without altering its effect on elevating the steady-state level of p53, suggesting that drug-induced up-regulation and nuclear accumulation of the wild-type p53 protein are separable processes. Tretinoin 15-17 tumor protein p53 Homo sapiens 84-87
10364268-6 1999 The modulation of nuclear import of p53 protein by RA may thus represent a potential mechanism by which certain tumor cells with the wild-type p53 gene develop resistance to chemotherapeutic agents. Tretinoin 51-53 tumor protein p53 Homo sapiens 36-39
10364268-6 1999 The modulation of nuclear import of p53 protein by RA may thus represent a potential mechanism by which certain tumor cells with the wild-type p53 gene develop resistance to chemotherapeutic agents. Tretinoin 51-53 tumor protein p53 Homo sapiens 143-146
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 197-201 retinoic acid receptor beta Homo sapiens 29-36
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 197-201 retinoic acid receptor beta Homo sapiens 127-134
10364250-7 1999 Finally, we showed that atRA-induced IGFBP-3 is functionally active in modulating the growth-promoting effect of IGF-I. Tretinoin 24-28 insulin like growth factor 1 Homo sapiens 113-118
10361124-1 1999 Induction of urokinase plasminogen activator (uPA) by retinoic acid (RA) is the initial event preceding certain subsequent biological changes in vascular endothelial cells. Tretinoin 54-67 plasminogen activator, urokinase Homo sapiens 13-44
10361124-1 1999 Induction of urokinase plasminogen activator (uPA) by retinoic acid (RA) is the initial event preceding certain subsequent biological changes in vascular endothelial cells. Tretinoin 54-67 plasminogen activator, urokinase Homo sapiens 46-49
10366424-5 1999 In precrisis pCol2SV-transfected chondrocytes, all-trans-retinoic acid, a down-regulator of col2a1 expression, induced apoptosis, strongly suggesting the strict control of T Ag expression by col2a1 regulatory sequences. Tretinoin 47-70 collagen alpha-1(II) chain Oryctolagus cuniculus 92-98
10361124-3 1999 Upon stimulation with RA, mRNA levels of RARalpha and beta transiently increased in parallel with the induction of uPA, and this increase was inhibited by cycloheximide. Tretinoin 22-24 plasminogen activator, urokinase Homo sapiens 115-118
10361124-10 1999 These results suggest that (1) RA induces RARs mainly via RARalpha and that (2) RAR/RXR physically and functionally interact with Sp1, resulting in a potentiation of uPA transcription. Tretinoin 31-33 plasminogen activator, urokinase Homo sapiens 166-169
10366424-5 1999 In precrisis pCol2SV-transfected chondrocytes, all-trans-retinoic acid, a down-regulator of col2a1 expression, induced apoptosis, strongly suggesting the strict control of T Ag expression by col2a1 regulatory sequences. Tretinoin 47-70 collagen alpha-1(II) chain Oryctolagus cuniculus 191-197
10361124-1 1999 Induction of urokinase plasminogen activator (uPA) by retinoic acid (RA) is the initial event preceding certain subsequent biological changes in vascular endothelial cells. Tretinoin 69-71 plasminogen activator, urokinase Homo sapiens 13-44
10366424-8 1999 In these postcrisis cells, T Ag remained at least partially under the control of functional col2a1 regulatory elements as assessed by all-trans-retinoic acid down-regulation. Tretinoin 134-157 collagen alpha-1(II) chain Oryctolagus cuniculus 92-98
10361124-1 1999 Induction of urokinase plasminogen activator (uPA) by retinoic acid (RA) is the initial event preceding certain subsequent biological changes in vascular endothelial cells. Tretinoin 69-71 plasminogen activator, urokinase Homo sapiens 46-49
10358083-6 1999 The GATA binding site mediates the retinoic acid/dibutyryl cyclic AMP stimulation of transcription and correlates with the binding of Gata-4 which is induced by retinoic acid in differentiating F9 cells. Tretinoin 35-48 GATA binding protein 4 Mus musculus 134-140
10358022-1 1999 Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. Tretinoin 85-98 alcohol dehydrogenase 1 (class I) Mus musculus 21-25
10358022-2 1999 Targeting of mouse alcohol dehydrogenase genes Adh1, Adh3, and Adh4 resulted in null mutant mice that all developed and reproduced apparently normally but differed markedly in clearance of ethanol and formaldehyde plus metabolism of retinol to the signaling molecule retinoic acid. Tretinoin 267-280 alcohol dehydrogenase 1 (class I) Mus musculus 47-51
10358022-7 1999 Retinoic acid production following retinol administration was reduced 4.8-fold in Adh1 -/- mice and 8.5-fold in Adh4 -/- mice. Tretinoin 0-13 alcohol dehydrogenase 1 (class I) Mus musculus 82-86
10358022-9 1999 Redundant roles for Adh1 and Adh4 in retinoic acid production may explain the apparent normal development of mutant mice. Tretinoin 37-50 alcohol dehydrogenase 1 (class I) Mus musculus 20-24
10358083-6 1999 The GATA binding site mediates the retinoic acid/dibutyryl cyclic AMP stimulation of transcription and correlates with the binding of Gata-4 which is induced by retinoic acid in differentiating F9 cells. Tretinoin 161-174 GATA binding protein 4 Mus musculus 134-140
10362099-0 1999 Induction of matrix metalloprotease-1 gene expression by retinoic acid in the human pancreatic tumour cell line Dan-G. We have investigated the effects of retinoic acid (RA) on matrix metalloprotease-1 (MMP-1) gene expression in the human pancreatic tumour cell line Dan-G. 13-cis RA results in a time- and dose-dependent increase of MMP-1 protein concentration. Tretinoin 57-70 NBL1, DAN family BMP antagonist Homo sapiens 112-115
10421060-8 1999 [3H]Retinoic acid showed a more rapid metabolism to 4-hydroxy/4-keto-retinoic acid in HaCaT cells than in HEK, which could be explained by a higher expression of cytochrome p450RAI in the former cells. Tretinoin 4-17 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 162-180
10392906-6 1999 Additionally, ATRA induced significant and lasting stimulation of mitogen-activated protein kinase/Erk2 activity. Tretinoin 14-18 mitogen-activated protein kinase 1 Homo sapiens 99-103
10429942-9 1999 For the MMPs, IL-1 treatment resulted in an approximately two to threefold increase in human and porcine MMP-3 and MMP-13 mRNAs, while retinoic acid treatment caused a statistically significant increase in human MMP-3 mRNA levels, but no significant change in transcript levels for porcine MMP-3 nor human or porcine MMP-13. Tretinoin 135-148 matrix metallopeptidase 3 Homo sapiens 212-217
10502453-7 1999 Retinoic acid with TNFalpha and IFN-gamma had a marked inhibitory effect (P<0.05) which was similarly reversed by increasing concentrations of IGFBP-3 antibody. Tretinoin 0-13 tumor necrosis factor Homo sapiens 19-27
10502453-7 1999 Retinoic acid with TNFalpha and IFN-gamma had a marked inhibitory effect (P<0.05) which was similarly reversed by increasing concentrations of IGFBP-3 antibody. Tretinoin 0-13 interferon gamma Homo sapiens 32-41
10502453-8 1999 The present data support the hypothesis that the combination of TNFalpha and IFN-gamma with retinoic acid exert their anti-proliferative effect on HSG cells by reducing the mitogenic effect of IGF-I due to a shift in IGF-I from the free to the IGFBP-3-bound form. Tretinoin 92-105 interferon gamma Homo sapiens 77-86
10502453-8 1999 The present data support the hypothesis that the combination of TNFalpha and IFN-gamma with retinoic acid exert their anti-proliferative effect on HSG cells by reducing the mitogenic effect of IGF-I due to a shift in IGF-I from the free to the IGFBP-3-bound form. Tretinoin 92-105 insulin like growth factor 1 Homo sapiens 193-198
10502453-8 1999 The present data support the hypothesis that the combination of TNFalpha and IFN-gamma with retinoic acid exert their anti-proliferative effect on HSG cells by reducing the mitogenic effect of IGF-I due to a shift in IGF-I from the free to the IGFBP-3-bound form. Tretinoin 92-105 insulin like growth factor 1 Homo sapiens 217-222
10503991-5 1999 MtT/E-2 secretes growth hormone which is, interestingly, regulated by retinoic acid and dexamethasone rather than thyroid hormones. Tretinoin 70-83 dihydrolipoamide S-succinyltransferase Rattus norvegicus 4-7
10228952-0 1999 Activation of Rb and decline in androgen receptor protein precede retinoic acid-induced apoptosis in androgen-dependent LNCaP cells and their androgen-independent derivative. Tretinoin 66-79 androgen receptor Homo sapiens 32-49
10318760-2 1999 The putative transcriptional mediator TIF1alpha is a nuclear protein kinase that has been identified via its interaction with liganded nuclear receptors, including retinoic acid (RAR), retinoid X (RXR) and estrogen (ER) receptors. Tretinoin 164-177 tripartite motif-containing 24 Mus musculus 38-47
10429942-9 1999 For the MMPs, IL-1 treatment resulted in an approximately two to threefold increase in human and porcine MMP-3 and MMP-13 mRNAs, while retinoic acid treatment caused a statistically significant increase in human MMP-3 mRNA levels, but no significant change in transcript levels for porcine MMP-3 nor human or porcine MMP-13. Tretinoin 135-148 matrix metallopeptidase 3 Homo sapiens 212-217
10371506-2 1999 Differentiation therapy in AML has recently raised interest because the survival of AML3 patients has been greatly improved using the differentiating agent retinoic acid. Tretinoin 156-169 RUNX family transcription factor 2 Homo sapiens 84-88
10429942-9 1999 For the MMPs, IL-1 treatment resulted in an approximately two to threefold increase in human and porcine MMP-3 and MMP-13 mRNAs, while retinoic acid treatment caused a statistically significant increase in human MMP-3 mRNA levels, but no significant change in transcript levels for porcine MMP-3 nor human or porcine MMP-13. Tretinoin 135-148 matrix metallopeptidase 13 Homo sapiens 317-323
10429942-10 1999 The mRNA levels for ADAM-15 were elevated in human monolayer chondrocytes exposed to IL-1 or retinoic acid, while transcripts levels for TNF-alpha converting enzyme were increased in response to retinoic acid. Tretinoin 93-106 ADAM metallopeptidase domain 15 Homo sapiens 20-27
12548778-4 1999 In RA-sensitive cell lines, ATRA-induced G0/G1 arrest is associated with down regulaton of c-myc and hyperphosphorylated Rb expression, and up regulation of p21WAF1/CIP1 and p53 expression. Tretinoin 28-32 cyclin dependent kinase inhibitor 1A Homo sapiens 157-169
12548778-4 1999 In RA-sensitive cell lines, ATRA-induced G0/G1 arrest is associated with down regulaton of c-myc and hyperphosphorylated Rb expression, and up regulation of p21WAF1/CIP1 and p53 expression. Tretinoin 28-32 tumor protein p53 Homo sapiens 174-177
10359529-5 1999 RA-treatment induced two peaks of p21 synthesis: early (from the 2nd to the 6th hour), dependent on PML/RAR alpha expression and associated with G1-S transition and high CDK activity; late (from 3rd to the 4th day), independent from PML/RAR alpha and associated with G1 block and low CDK activity. Tretinoin 0-2 cyclin dependent kinase inhibitor 1A Homo sapiens 34-37
10328956-0 1999 Retinoic acid alters the mechanism of attachment of malignant astrocytoma and neuroblastoma cells to thrombospondin-1. Tretinoin 0-13 thrombospondin 1 Homo sapiens 101-117
10328956-1 1999 Based on the hypothesis that the attachment of neuroectodermal cells to thrombospondin-1 (TSP-1) may affect tumor spread and play a role in the anti-tumor effects of retinoic acid, we investigated the expression of TSP-1 in these cells in situ and the effect of retinoic acid on the morphology of TSP-1-adherent neuroblastoma (SK-N-SH) and malignant astrocytoma (U-251MG) cells in vitro. Tretinoin 166-179 thrombospondin 1 Homo sapiens 72-88
10328956-1 1999 Based on the hypothesis that the attachment of neuroectodermal cells to thrombospondin-1 (TSP-1) may affect tumor spread and play a role in the anti-tumor effects of retinoic acid, we investigated the expression of TSP-1 in these cells in situ and the effect of retinoic acid on the morphology of TSP-1-adherent neuroblastoma (SK-N-SH) and malignant astrocytoma (U-251MG) cells in vitro. Tretinoin 166-179 thrombospondin 1 Homo sapiens 90-95
10328956-1 1999 Based on the hypothesis that the attachment of neuroectodermal cells to thrombospondin-1 (TSP-1) may affect tumor spread and play a role in the anti-tumor effects of retinoic acid, we investigated the expression of TSP-1 in these cells in situ and the effect of retinoic acid on the morphology of TSP-1-adherent neuroblastoma (SK-N-SH) and malignant astrocytoma (U-251MG) cells in vitro. Tretinoin 262-275 thrombospondin 1 Homo sapiens 72-88
10328956-1 1999 Based on the hypothesis that the attachment of neuroectodermal cells to thrombospondin-1 (TSP-1) may affect tumor spread and play a role in the anti-tumor effects of retinoic acid, we investigated the expression of TSP-1 in these cells in situ and the effect of retinoic acid on the morphology of TSP-1-adherent neuroblastoma (SK-N-SH) and malignant astrocytoma (U-251MG) cells in vitro. Tretinoin 262-275 thrombospondin 1 Homo sapiens 90-95
10328956-2 1999 TSP-1-adherent SK-N-SH cells demonstrated process outgrowth, with further neuronal differentiation after retinoic acid treatment, consistent with the in situ studies showing that TSP-1 expression occurs in a differentiation-specific manner in neuroblastic tumors. Tretinoin 105-118 thrombospondin 1 Homo sapiens 0-5
10328956-3 1999 TSP-1-adherent U-251MG cells failed to spread; however, after retinoic acid treatment the cells demonstrated broad lamellipodia containing radial actin fibers and organization of integrins alpha3beta1 and alpha5beta1 in clusters in lamellipodia and filopodia. Tretinoin 62-75 thrombospondin 1 Homo sapiens 0-5
10328956-8 1999 Treatment with a pharmacologic dosage of retinoic acid altered the TSP-1 cell adhesion mechanism in both cell lines in that neither heparin nor micromolar concentrations of the RGD peptide inhibited attachment; after treatment, attachment was inhibited by the CSVTCG peptide located in the type I repeat domain of TSP-1 and a recombinant adhesion domain (CLESH-1) from CD36. Tretinoin 41-54 thrombospondin 1 Homo sapiens 67-72
10328956-8 1999 Treatment with a pharmacologic dosage of retinoic acid altered the TSP-1 cell adhesion mechanism in both cell lines in that neither heparin nor micromolar concentrations of the RGD peptide inhibited attachment; after treatment, attachment was inhibited by the CSVTCG peptide located in the type I repeat domain of TSP-1 and a recombinant adhesion domain (CLESH-1) from CD36. Tretinoin 41-54 thrombospondin 1 Homo sapiens 314-319
10328956-10 1999 These data indicate that neuroectodermally derived cells utilize several mechanisms to attach to TSP-1, and these are differentially modulated by treatment with retinoic acid. Tretinoin 161-174 thrombospondin 1 Homo sapiens 97-102
10336422-3 1999 Both LE135 and LE540 inhibited retinoic acid (RA)-induced transcriptional activation of RARbeta, but not RARalpha, RARgamma or retinoid X receptor alpha (RXRalpha), on a variety of RA response elements. Tretinoin 31-44 retinoic acid receptor beta Homo sapiens 88-95
10336422-3 1999 Both LE135 and LE540 inhibited retinoic acid (RA)-induced transcriptional activation of RARbeta, but not RARalpha, RARgamma or retinoid X receptor alpha (RXRalpha), on a variety of RA response elements. Tretinoin 46-48 retinoic acid receptor beta Homo sapiens 88-95
10336422-5 1999 In ZR-75-1 human breast cancer cells, cotreatment of LE135 and LE540 with all-trans-RA inhibited all-trans-RA-induced apoptosis of the cells, further demonstrating that RARbeta plays a role in RA-induced apoptosis of breast cancer cells. Tretinoin 84-86 retinoic acid receptor beta Homo sapiens 169-176
10359529-6 1999 Increased p21 in PML/RAR alpha cells during G1-S had no effect on the cell cycle while an antisense p21 prevented RA-induced differentiation without altering G1-S transition and the late G1 block. Tretinoin 21-23 cyclin dependent kinase inhibitor 1A Homo sapiens 10-13
10383375-2 1999 Recently, we reported that retinoic acids are efficient repressors of c-erbB-2 and -3, but not of c-erbB-1 gene expresson. Tretinoin 27-41 erb-b2 receptor tyrosine kinase 2 Homo sapiens 70-85
10329401-1 1999 The transcriptional regulation of the human cholesteryl ester transfer protein (CETP) gene by retinoic acid was investigated by a transient transfection assay. Tretinoin 94-107 cholesteryl ester transfer protein Homo sapiens 44-78
10329401-1 1999 The transcriptional regulation of the human cholesteryl ester transfer protein (CETP) gene by retinoic acid was investigated by a transient transfection assay. Tretinoin 94-107 cholesteryl ester transfer protein Homo sapiens 80-84
10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 90-98
10381637-5 1999 The expression of tissue transglutaminase (tTG), an enzyme proposed to play a role in apoptosis was induced with RA, as shown by both enzymatic assay and in situ immunofluorescence detection. Tretinoin 113-115 transglutaminase 2 Homo sapiens 18-41
10381637-5 1999 The expression of tissue transglutaminase (tTG), an enzyme proposed to play a role in apoptosis was induced with RA, as shown by both enzymatic assay and in situ immunofluorescence detection. Tretinoin 113-115 transglutaminase 2 Homo sapiens 43-46
10381637-9 1999 Interestingly, Dex also inhibited the RA-dependent induction of tTG. Tretinoin 38-40 transglutaminase 2 Homo sapiens 64-67
10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 156-164
10222145-8 1999 Since retinoic acid increases ERK2 activation, which is necessary for differentiation, the data suggest that mutant and wild-type middle T enhanced the retinoic acid effects by increasing basal levels of ERK2 activation. Tretinoin 6-19 mitogen-activated protein kinase 1 Homo sapiens 30-34
10222145-8 1999 Since retinoic acid increases ERK2 activation, which is necessary for differentiation, the data suggest that mutant and wild-type middle T enhanced the retinoic acid effects by increasing basal levels of ERK2 activation. Tretinoin 6-19 mitogen-activated protein kinase 1 Homo sapiens 204-208
10222145-8 1999 Since retinoic acid increases ERK2 activation, which is necessary for differentiation, the data suggest that mutant and wild-type middle T enhanced the retinoic acid effects by increasing basal levels of ERK2 activation. Tretinoin 152-165 mitogen-activated protein kinase 1 Homo sapiens 204-208
10222145-9 1999 Consistent with this, the polyoma-induced foreshortening of the time for differentiation coincided with the time for retinoic acid to significantly increase ERK2 activation. Tretinoin 117-130 mitogen-activated protein kinase 1 Homo sapiens 157-161
10222145-12 1999 Polyoma middle T and these transformation-defective mutants thus enhanced ERK2 activation to have an early effect in promoting retinoic acid-induced differentiation without a strong dependence on activating PLCgamma, PI-3 kinase, or src-like kinase. Tretinoin 127-140 mitogen-activated protein kinase 1 Homo sapiens 74-78
10207061-3 1999 Nevertheless, relatively high, pharmacological concentrations of RA (1 to 10 microM) overcome these differentiation blocks and induce terminal granulocytic differentiation of the MPRO promyelocytes while potentiating interleukin-3 (IL-3)-induced commitment of EML cells to the granulocyte/monocyte lineage. Tretinoin 65-67 interleukin 3 Mus musculus 217-230
10224151-1 1999 All-trans-retinoic acid (RA), an active metabolite of vitamin A, induces the gene expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) and suppresses leptin gene expression in white adipose tissue (WAT) when given as an acute dose. Tretinoin 0-23 uncoupling protein 1 Rattus norvegicus 96-116
10224151-1 1999 All-trans-retinoic acid (RA), an active metabolite of vitamin A, induces the gene expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) and suppresses leptin gene expression in white adipose tissue (WAT) when given as an acute dose. Tretinoin 0-23 uncoupling protein 1 Rattus norvegicus 118-122
10320523-7 1999 Expression of B-CK increased slightly over 15 days in mineralizing, retinoic acid-treated cephalic chondrocytes, but it decreased in nonmineralizing caudal chondrocytes, while there was little expression of M-CK. Tretinoin 68-81 creatine kinase B Gallus gallus 14-18
10215635-5 1999 The IL-2-mediated c-myc overexpression and CYP down-regulation were prevented by 1) genistein (a tyrosine kinase inhibitor that blocks the initial transduction of the IL-2R signal), 2) retinoic acid, butyric acid, or dimethyl sulfoxide (three agents that block c-myc transcription), or 3) an antisense c-myc oligonucleotide (which may cause rapid degradation of the c-myc transcript). Tretinoin 185-198 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 43-46
10207061-3 1999 Nevertheless, relatively high, pharmacological concentrations of RA (1 to 10 microM) overcome these differentiation blocks and induce terminal granulocytic differentiation of the MPRO promyelocytes while potentiating interleukin-3 (IL-3)-induced commitment of EML cells to the granulocyte/monocyte lineage. Tretinoin 65-67 interleukin 3 Mus musculus 232-236
10194425-1 1999 Preclinical data suggest that retinoids, eg, all-trans retinoic acid (ATRA), lower concentrations of antiapoptotic proteins such as bcl-2, possibly thereby improving the outcome of anti-acute myeloid leukemia (AML) chemotherapy. Tretinoin 45-68 BCL2 apoptosis regulator Homo sapiens 132-137
10356361-4 1999 We showed in this study that PML/RARalpha increased the transcription of p21WAF1/CIP1 gene and the activation was further induced by RA treatment. Tretinoin 33-35 cyclin dependent kinase inhibitor 1A Homo sapiens 81-85
10356361-7 1999 These results suggest that the induction of APL cells differentiation by RA may be a result of the activation of p21WAF1/CIP1 by PML/RARalpha. Tretinoin 73-75 cyclin dependent kinase inhibitor 1A Homo sapiens 121-125
10194425-1 1999 Preclinical data suggest that retinoids, eg, all-trans retinoic acid (ATRA), lower concentrations of antiapoptotic proteins such as bcl-2, possibly thereby improving the outcome of anti-acute myeloid leukemia (AML) chemotherapy. Tretinoin 70-74 BCL2 apoptosis regulator Homo sapiens 132-137
10190895-1 1999 In acute promyelocytic leukemia (APL) patients, retinoic acid (RA) triggers differentiation while arsenic trioxide (arsenic) induces both a partial differentiation and apoptosis. Tretinoin 48-61 promyelocytic leukemia Mus musculus 9-32
10094816-0 1999 Induction of p21(CIP1/Waf1) and activation of p34(cdc2) involved in retinoic acid-induced apoptosis in human hepatoma Hep3B cells. Tretinoin 68-81 cyclin dependent kinase inhibitor 1A Homo sapiens 13-16
10094816-0 1999 Induction of p21(CIP1/Waf1) and activation of p34(cdc2) involved in retinoic acid-induced apoptosis in human hepatoma Hep3B cells. Tretinoin 68-81 cyclin dependent kinase inhibitor 1A Homo sapiens 17-21
10094816-0 1999 Induction of p21(CIP1/Waf1) and activation of p34(cdc2) involved in retinoic acid-induced apoptosis in human hepatoma Hep3B cells. Tretinoin 68-81 general transcription factor IIH subunit 3 Homo sapiens 46-49
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 tumor protein p53 Homo sapiens 45-48
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 cyclin dependent kinase inhibitor 1A Homo sapiens 89-92
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 cyclin dependent kinase inhibitor 1A Homo sapiens 98-102
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 BCL2 associated X, apoptosis regulator Homo sapiens 108-111
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 general transcription factor IIH subunit 3 Homo sapiens 147-150
10216260-2 1999 We used differential display reverse transcriptase polymerase chain reaction (RT-PCR) to identify RA-responsive genes expressed in embryonic stem (ES) cells and found that murine folate receptor-alpha (FR-alpha) expression is rapidly induced by RA treatment. Tretinoin 98-100 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 202-210
10216260-2 1999 We used differential display reverse transcriptase polymerase chain reaction (RT-PCR) to identify RA-responsive genes expressed in embryonic stem (ES) cells and found that murine folate receptor-alpha (FR-alpha) expression is rapidly induced by RA treatment. Tretinoin 245-247 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 202-210
10216260-3 1999 The observed increase in FR-alpha expression occurs within 3h, is independent of protein synthesis and does not occur when ES cells are differentiated by removal of leukaemia inhibitory factor (LIF), evidence that the response to RA is both direct and specific. Tretinoin 230-232 rabaptin, RAB GTPase binding effector protein 2 Mus musculus 25-33
10094816-6 1999 Olomoucine, a potent p34(cdc2) and Cdk2 inhibitor, effectively blocked RA-mediated p34(cdc2) kinase activation and prevented RA-induced apoptosis. Tretinoin 71-73 general transcription factor IIH subunit 3 Homo sapiens 83-86
10094816-7 1999 Furthermore, antisense oligonucleotide complementary to p21(CIP2/Waf1) and p34(cdc2) mRNA significantly rescued RA-induced apoptosis. Tretinoin 112-114 cyclin dependent kinase inhibitor 1A Homo sapiens 56-59
10094816-7 1999 Furthermore, antisense oligonucleotide complementary to p21(CIP2/Waf1) and p34(cdc2) mRNA significantly rescued RA-induced apoptosis. Tretinoin 112-114 cyclin dependent kinase inhibitor 1A Homo sapiens 65-69
10094816-7 1999 Furthermore, antisense oligonucleotide complementary to p21(CIP2/Waf1) and p34(cdc2) mRNA significantly rescued RA-induced apoptosis. Tretinoin 112-114 general transcription factor IIH subunit 3 Homo sapiens 75-78
10094816-11 1999 These findings suggest that inappropriate regulation of the cell cycle regulators p21(CIP2/Waf1) and p34(cdc2) is coupled with induction of Bax and involved in cell death with apoptosis when Hep3B cells are exposed to RA. Tretinoin 218-220 cyclin dependent kinase inhibitor 1A Homo sapiens 82-85
10094816-11 1999 These findings suggest that inappropriate regulation of the cell cycle regulators p21(CIP2/Waf1) and p34(cdc2) is coupled with induction of Bax and involved in cell death with apoptosis when Hep3B cells are exposed to RA. Tretinoin 218-220 cyclin dependent kinase inhibitor 1A Homo sapiens 91-95
10094816-11 1999 These findings suggest that inappropriate regulation of the cell cycle regulators p21(CIP2/Waf1) and p34(cdc2) is coupled with induction of Bax and involved in cell death with apoptosis when Hep3B cells are exposed to RA. Tretinoin 218-220 general transcription factor IIH subunit 3 Homo sapiens 101-104
10094816-11 1999 These findings suggest that inappropriate regulation of the cell cycle regulators p21(CIP2/Waf1) and p34(cdc2) is coupled with induction of Bax and involved in cell death with apoptosis when Hep3B cells are exposed to RA. Tretinoin 218-220 BCL2 associated X, apoptosis regulator Homo sapiens 140-143
10320034-1 1999 Phosphorylation of the mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1 (ERK1) and extracellular signal-regulated kinase 2 (ERK2), induced by resveratrol, a natural antioxidant present in grapes and wine, has been studied in vitro on undifferentiated and differentiated (induction by retinoic acid) SH-SY5Y human neuroblastoma cells. Tretinoin 316-329 mitogen-activated protein kinase 1 Homo sapiens 64-103
10320034-1 1999 Phosphorylation of the mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1 (ERK1) and extracellular signal-regulated kinase 2 (ERK2), induced by resveratrol, a natural antioxidant present in grapes and wine, has been studied in vitro on undifferentiated and differentiated (induction by retinoic acid) SH-SY5Y human neuroblastoma cells. Tretinoin 316-329 mitogen-activated protein kinase 3 Homo sapiens 105-109
10320034-1 1999 Phosphorylation of the mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1 (ERK1) and extracellular signal-regulated kinase 2 (ERK2), induced by resveratrol, a natural antioxidant present in grapes and wine, has been studied in vitro on undifferentiated and differentiated (induction by retinoic acid) SH-SY5Y human neuroblastoma cells. Tretinoin 316-329 mitogen-activated protein kinase 1 Homo sapiens 115-154
10320034-1 1999 Phosphorylation of the mitogen-activated protein (MAP) kinases, extracellular signal-regulated kinase 1 (ERK1) and extracellular signal-regulated kinase 2 (ERK2), induced by resveratrol, a natural antioxidant present in grapes and wine, has been studied in vitro on undifferentiated and differentiated (induction by retinoic acid) SH-SY5Y human neuroblastoma cells. Tretinoin 316-329 mitogen-activated protein kinase 1 Homo sapiens 156-160
10320034-4 1999 In retinoic acid (RA) differentiated cells resveratrol (1 microM) induced an evident increase in ERK1 and ERK2 phosphorylation. Tretinoin 3-16 mitogen-activated protein kinase 3 Homo sapiens 97-101
10320034-4 1999 In retinoic acid (RA) differentiated cells resveratrol (1 microM) induced an evident increase in ERK1 and ERK2 phosphorylation. Tretinoin 3-16 mitogen-activated protein kinase 1 Homo sapiens 106-110
10100988-0 1999 Lysozyme expression during metaplastic squamous differentiation of retinoic acid-deficient human tracheobronchial epithelial cells. Tretinoin 67-80 lysozyme Homo sapiens 0-8
10100988-8 1999 14:104-112) that retinoic acid (RA)-deprived cultures of normal human tracheobronchial epithelial (NHTBE) cells became squamous, failed to produce mucin, and instead secreted or released large amounts of lysozyme (LZ). Tretinoin 17-30 lysozyme Homo sapiens 204-212
10320034-4 1999 In retinoic acid (RA) differentiated cells resveratrol (1 microM) induced an evident increase in ERK1 and ERK2 phosphorylation. Tretinoin 18-20 mitogen-activated protein kinase 3 Homo sapiens 97-101
10320034-4 1999 In retinoic acid (RA) differentiated cells resveratrol (1 microM) induced an evident increase in ERK1 and ERK2 phosphorylation. Tretinoin 18-20 mitogen-activated protein kinase 1 Homo sapiens 106-110
10201524-0 1999 Induction of TR4 orphan receptor by retinoic acid in human HaCaT keratinocytes. Tretinoin 36-49 nuclear receptor subfamily 2 group C member 2 Homo sapiens 13-16
10100988-8 1999 14:104-112) that retinoic acid (RA)-deprived cultures of normal human tracheobronchial epithelial (NHTBE) cells became squamous, failed to produce mucin, and instead secreted or released large amounts of lysozyme (LZ). Tretinoin 17-30 lysozyme Homo sapiens 214-216
10100988-8 1999 14:104-112) that retinoic acid (RA)-deprived cultures of normal human tracheobronchial epithelial (NHTBE) cells became squamous, failed to produce mucin, and instead secreted or released large amounts of lysozyme (LZ). Tretinoin 32-34 lysozyme Homo sapiens 204-212
10100988-8 1999 14:104-112) that retinoic acid (RA)-deprived cultures of normal human tracheobronchial epithelial (NHTBE) cells became squamous, failed to produce mucin, and instead secreted or released large amounts of lysozyme (LZ). Tretinoin 32-34 lysozyme Homo sapiens 214-216
10100988-11 1999 Between Days 10 and 18 of culture, cellular LZ levels were more than 10 times higher in RA-deficient than in RA-sufficient cultures. Tretinoin 88-90 lysozyme Homo sapiens 44-46
10100988-15 1999 When RA-deficient cultures were treated on Day 7 with 10(-6) M RA, intracellular LZ levels did not substantially decrease until 3 d later, coinciding with a marked increase in mucin secretion. Tretinoin 5-7 lysozyme Homo sapiens 81-83
10100988-17 1999 We concluded that RA does not directly regulate LZ, and that the excessive accumulation of LZ in RA-deprived NHTBE cells is a consequence of vitamin A deficiency-induced abnormal differentiation. Tretinoin 97-99 lysozyme Homo sapiens 91-93
10090931-0 1999 1,25-Dihydroxyvitamin D3 induces differentiation of a retinoic acid-resistant acute promyelocytic leukemia cell line (UF-1) associated with expression of p21(WAF1/CIP1) and p27(KIP1). Tretinoin 54-67 cyclin dependent kinase inhibitor 1A Homo sapiens 158-162
10090931-0 1999 1,25-Dihydroxyvitamin D3 induces differentiation of a retinoic acid-resistant acute promyelocytic leukemia cell line (UF-1) associated with expression of p21(WAF1/CIP1) and p27(KIP1). Tretinoin 54-67 cyclin dependent kinase inhibitor 1A Homo sapiens 163-167
10233362-5 1999 Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation. Tretinoin 237-250 GLI family zinc finger 2 Homo sapiens 39-44
10233362-5 1999 Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation. Tretinoin 252-254 GLI family zinc finger 2 Homo sapiens 39-44
10233386-5 1999 The efflux of mitochondrial cytochrome c to cytosol was notable in Western blotting after 48 h exposure of the cells to ATRA and was observed before the drop in the mitochondrial membrane potential, which only took place after 72 h exposure, when measured by flow cytometry and a JC-1 probe. Tretinoin 120-124 cytochrome c, somatic Homo sapiens 28-40
10233386-8 1999 However, both of the cell lines showed progressive down-regulation of bcl-2, which began after 12-24 h exposure of the cells to ATRA as determined by ELISA, Western blotting and flow cytometry. Tretinoin 128-132 BCL2 apoptosis regulator Homo sapiens 70-75
10233386-9 1999 The present results show that mitochondria have a role in ATRA-induced apoptosis in AML cells and down-regulation of bcl-2 is related to it. Tretinoin 58-62 BCL2 apoptosis regulator Homo sapiens 117-122
10210322-9 1999 Moreover, RA induced apoptosis of CD34+ cells and CD34+CD71+ cells stimulated with erythropoietin. Tretinoin 10-12 CD34 molecule Homo sapiens 34-38
10210322-9 1999 Moreover, RA induced apoptosis of CD34+ cells and CD34+CD71+ cells stimulated with erythropoietin. Tretinoin 10-12 CD34 molecule Homo sapiens 50-54
10210322-9 1999 Moreover, RA induced apoptosis of CD34+ cells and CD34+CD71+ cells stimulated with erythropoietin. Tretinoin 10-12 erythropoietin Homo sapiens 83-97
10503735-8 1999 A second observation is that ATRA treated cells are, only apparently, less sensitive to lysis by lymphocytes activated by IL-2, as determined by means of a standard 51Cr release assay. Tretinoin 29-33 interleukin 2 Homo sapiens 122-126
10319996-0 1999 Retinoic acid is able to induce interferon regulatory factor 1 in squamous carcinoma cells via a STAT-1 independent signalling pathway. Tretinoin 0-13 interferon regulatory factor 1 Homo sapiens 32-62
10319996-4 1999 IRF-1 expression correlates with the IFN-alpha-induced apoptosis phenomenon and, surprisingly, with the RA-induced apoptosis phenomenon. Tretinoin 104-106 interferon regulatory factor 1 Homo sapiens 0-5
10319996-6 1999 We provide evidence indicating that RA-induced IRF-1 gene expression is independent of the STAT-1 activation pathway, despite the presence of the IFN-gamma activated sequence element in the gene promoter, but involves nuclear factor-kappaB activation. Tretinoin 36-38 interferon regulatory factor 1 Homo sapiens 47-52
10319996-6 1999 We provide evidence indicating that RA-induced IRF-1 gene expression is independent of the STAT-1 activation pathway, despite the presence of the IFN-gamma activated sequence element in the gene promoter, but involves nuclear factor-kappaB activation. Tretinoin 36-38 interferon gamma Homo sapiens 146-155
10210322-0 1999 Retinoic acid induces apoptosis of human CD34+ hematopoietic progenitor cells: involvement of retinoic acid receptors and retinoid X receptors depends on lineage commitment of the hematopoietic progenitor cells. Tretinoin 0-13 CD34 molecule Homo sapiens 41-45
10210322-2 1999 In this study we explored the effects of retinoic acid (RA) on apoptosis of human CD34+ hematopoietic progenitor cells isolated from normal bone marrow. Tretinoin 41-54 CD34 molecule Homo sapiens 82-86
10210322-2 1999 In this study we explored the effects of retinoic acid (RA) on apoptosis of human CD34+ hematopoietic progenitor cells isolated from normal bone marrow. Tretinoin 56-58 CD34 molecule Homo sapiens 82-86
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 CD34 molecule Homo sapiens 80-84
10199796-0 1999 Changes in tissue transglutaminase activity and expression during retinoic acid-induced growth arrest and apoptosis in primary cultures of human epithelial prostate cells. Tretinoin 66-79 transglutaminase 2 Homo sapiens 11-34
10199796-1 1999 We treated primary epithelial cells from human normal prostate (NEPC) and prostate cancer (CEPC) with all-trans-retinoic acid (RA) to study whether it regulates the activity of tissue transglutaminase (tTGase), an enzyme that accumulates in cells undergoing apoptosis. Tretinoin 102-125 transglutaminase 2 Homo sapiens 177-200
10199796-1 1999 We treated primary epithelial cells from human normal prostate (NEPC) and prostate cancer (CEPC) with all-trans-retinoic acid (RA) to study whether it regulates the activity of tissue transglutaminase (tTGase), an enzyme that accumulates in cells undergoing apoptosis. Tretinoin 102-125 transglutaminase 2 Homo sapiens 202-208
10199796-3 1999 After 72-96 h of 10(-6) mol/L RA treatment, cell growth inhibition and apoptosis were associated with increased tTGase activity in both NEPC and CEPC, and with increased tTGase protein and messenger ribonucleic acid levels only in NEPC. Tretinoin 30-32 transglutaminase 2 Homo sapiens 112-118
10199796-3 1999 After 72-96 h of 10(-6) mol/L RA treatment, cell growth inhibition and apoptosis were associated with increased tTGase activity in both NEPC and CEPC, and with increased tTGase protein and messenger ribonucleic acid levels only in NEPC. Tretinoin 30-32 transglutaminase 2 Homo sapiens 170-176
10199796-5 1999 Our results suggest that RA induces tTGase gene expression and enzyme activity in normal prostate cells, and that RA-regulated pathways are impaired in cancer cells. Tretinoin 25-27 transglutaminase 2 Homo sapiens 36-42
10334392-9 1999 The IFN-y-inducing effect of ATRA and 13-cis-retinoic acid could be abrogated by addition of anti-IL-12 antibodies, suggesting that IL-12 plays a role in the synergistic upregulation of IFN-gamma. Tretinoin 29-33 interferon gamma Homo sapiens 186-195
10201524-3 1999 Using a chloramphenicol acetyl-transferase reporter gene assay, it was shown that TR4 can suppress retinoic acid-induced transactivation by 47.3% in human HaCaT keratinocytes. Tretinoin 99-112 nuclear receptor subfamily 2 group C member 2 Homo sapiens 82-85
10201524-4 1999 Electrophoretic mobility shift assay indicated that this suppression may be due to TR4 binding with higher affinity to the retinoic acid response element than retinoid receptors. Tretinoin 123-136 nuclear receptor subfamily 2 group C member 2 Homo sapiens 83-86
10201524-5 1999 Western blot analysis further suggested that retinoic acid can increase the expression of TR4 protein in human HaCaT keratinocytes, indicating that TR4 acts as a negative feedback modulator for retinoic acid action. Tretinoin 45-58 nuclear receptor subfamily 2 group C member 2 Homo sapiens 90-93
10201524-5 1999 Western blot analysis further suggested that retinoic acid can increase the expression of TR4 protein in human HaCaT keratinocytes, indicating that TR4 acts as a negative feedback modulator for retinoic acid action. Tretinoin 45-58 nuclear receptor subfamily 2 group C member 2 Homo sapiens 148-151
10201524-5 1999 Western blot analysis further suggested that retinoic acid can increase the expression of TR4 protein in human HaCaT keratinocytes, indicating that TR4 acts as a negative feedback modulator for retinoic acid action. Tretinoin 194-207 nuclear receptor subfamily 2 group C member 2 Homo sapiens 90-93
10201524-5 1999 Western blot analysis further suggested that retinoic acid can increase the expression of TR4 protein in human HaCaT keratinocytes, indicating that TR4 acts as a negative feedback modulator for retinoic acid action. Tretinoin 194-207 nuclear receptor subfamily 2 group C member 2 Homo sapiens 148-151
10024510-1 1999 To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). Tretinoin 84-97 mucin 2, oligomeric mucus/gel-forming Homo sapiens 122-126
10074929-1 1999 Human lung cancer cells, including small cell lung carcinoma (SCLC), frequently lose expression of retinoic acid receptor beta (RAR-beta) and are resistant to the growth inhibitory activity of all-trans retinoic acid (RA). Tretinoin 99-112 retinoic acid receptor beta Homo sapiens 128-136
10074929-1 1999 Human lung cancer cells, including small cell lung carcinoma (SCLC), frequently lose expression of retinoic acid receptor beta (RAR-beta) and are resistant to the growth inhibitory activity of all-trans retinoic acid (RA). Tretinoin 128-130 retinoic acid receptor beta Homo sapiens 99-126
10074929-5 1999 RA treatment of H209-RAR-beta cells was also accompanied by increased expression of the cdk inhibitor p27Kip1, whereas no differences in the expression of L-myc or p27Kip1 were detected upon RA treatment of parental H209 cells. Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 21-29
10074929-8 1999 Our observations indicate that RAR-beta gene transfer can restore RA sensitivity in SCLC cells and suggest that myc and p27Kip1 may represent critical mediators of the RA-induced cell cycle arrest in SCLC cells expressing RAR-beta. Tretinoin 31-33 retinoic acid receptor beta Homo sapiens 222-230
10074929-8 1999 Our observations indicate that RAR-beta gene transfer can restore RA sensitivity in SCLC cells and suggest that myc and p27Kip1 may represent critical mediators of the RA-induced cell cycle arrest in SCLC cells expressing RAR-beta. Tretinoin 66-68 retinoic acid receptor beta Homo sapiens 31-39
10082969-4 1999 In density-arrested NRK cells, ET-1 and LPA induce phenotypic transformation rapidly, with similar kinetics as retinoic acid (RA) and transforming growth factor (TGF)-beta, while BK and PGF2alpha only do so with delayed kinetics. Tretinoin 111-124 endothelin 1 Rattus norvegicus 31-35
10082969-4 1999 In density-arrested NRK cells, ET-1 and LPA induce phenotypic transformation rapidly, with similar kinetics as retinoic acid (RA) and transforming growth factor (TGF)-beta, while BK and PGF2alpha only do so with delayed kinetics. Tretinoin 126-128 endothelin 1 Rattus norvegicus 31-35
10208436-0 1999 Synergistic effects of retinoic acid and 8-Cl-cAMP on apoptosis require caspase-3 activation in human ovarian cancer cells. Tretinoin 23-36 caspase 3 Homo sapiens 72-81
10086995-4 1999 In addition, we show that tretinoin prevents the cytotoxicity of H2O2 in cultured human MCs by increasing both the catalase activity and the reduced glutathione content, which are dose- and time-dependent changes. Tretinoin 26-35 catalase Homo sapiens 115-123
10086995-6 1999 An enhanced gene transcription is the most likely mechanism involved in the tretinoin-induced stimulation of MC antioxidant defense systems because 1) preincubation of MCs with actinomycin D or cycloheximide fully abolished it; 2) tretinoin-incubated MCs showed increased levels of catalase mRNA and gamma-glutamyl-cysteine synthetase (catalytic subunit) mRNA, the latter being the rate-limiting step in de novo reduced glutathione synthesis; and 3) the stability of both mRNA was unchanged by tretinoin. Tretinoin 76-85 catalase Rattus norvegicus 282-290
10092805-7 1999 In contrast, treatment of HL-60 cells with retinoic acid or DMSO, which results in a granulocytic differentiation of these cells, decreases 4E-BP1 amount without affecting its phosphorylation and strongly increases 4E-BP2 amount. Tretinoin 43-56 eukaryotic translation initiation factor 4E binding protein 2 Homo sapiens 215-221
10024510-1 1999 To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). Tretinoin 99-101 mucin 2, oligomeric mucus/gel-forming Homo sapiens 122-126
17023940-11 1999 Another study has shown that retinoic acid increases the mRNA level of the cellular retinol binding protein II and the rate of retinol uptake by Caco-2 intestinal epithelial cells. Tretinoin 29-42 retinol binding protein 2 Homo sapiens 75-110
10192429-0 1999 Increased adhesion of the promyelocytic leukaemia cell line, NB4, to fibronectin and thrombospondin upon all-trans-retinoic acid treatment. Tretinoin 109-128 fibronectin 1 Homo sapiens 69-80
10192429-6 1999 Preincubation of RA-treated cells with blocking antibodies demonstrated a role for alpha4beta1 and alpha5beta1 in cell adhesion to fibronectin and alpha5beta1, alpha(IIb)beta3, CD36 and CD47 in cell adhesion to thrombospondin. Tretinoin 17-19 fibronectin 1 Homo sapiens 131-142
10192429-9 1999 Our results indicate that increase in NB4 cell adhesion to fibronectin and thrombospondin upon RA treatment is likely to occur through a modulation of the functional state of several receptors for these proteins. Tretinoin 95-97 fibronectin 1 Homo sapiens 59-70
10067845-3 1999 In the current study, we have investigated the mechanism by which 1,25-(OH)2D3 regulates AR gene expression and the involvement of AR in the 1,25-(OH)2D3- and 9-cis retinoic acid (RA)-mediated growth inhibition of LNCaP cells. Tretinoin 180-182 androgen receptor Homo sapiens 131-133
10067828-5 1999 The level of the mRNA expression induced by PTH, PTHrP, and (Bu)2cAMP was as high as that by retinoic acid (RA), known as a potent inducer of RBP in hepatoma cells. Tretinoin 93-106 retinol-binding protein 4 Oryctolagus cuniculus 142-145
10067845-13 1999 These antiproliferative effects of 1,25-(OH)2D3 and 9-cis RA, alone or in combination, were blocked by the pure AR antagonist, Casodex. Tretinoin 58-60 androgen receptor Homo sapiens 112-114
10067828-5 1999 The level of the mRNA expression induced by PTH, PTHrP, and (Bu)2cAMP was as high as that by retinoic acid (RA), known as a potent inducer of RBP in hepatoma cells. Tretinoin 108-110 retinol-binding protein 4 Oryctolagus cuniculus 142-145
10067828-7 1999 Both RBP and PTH/PTHrP inhibited the dedifferentiative activity of RA on growth plate chondrocytes when added to the culture medium. Tretinoin 67-69 retinol-binding protein 4 Oryctolagus cuniculus 5-8
10067828-8 1999 These results demonstrate that chondrocytes synthesize and secrete RBP in vivo and in vitro and suggest that PTH/PTHrP modulates the effect of RA by means of RBP production in chondrocytes. Tretinoin 143-145 retinol-binding protein 4 Oryctolagus cuniculus 67-70
10067828-8 1999 These results demonstrate that chondrocytes synthesize and secrete RBP in vivo and in vitro and suggest that PTH/PTHrP modulates the effect of RA by means of RBP production in chondrocytes. Tretinoin 143-145 retinol-binding protein 4 Oryctolagus cuniculus 158-161
10067845-14 1999 In conclusion, our results demonstrate that growth inhibition of LNCaP cells by 1,25-(OH)2D3 and 9-cis RA is mediated by an AR-dependent mechanism and preceded by the induction of AR gene expression. Tretinoin 103-105 androgen receptor Homo sapiens 124-126
10067845-14 1999 In conclusion, our results demonstrate that growth inhibition of LNCaP cells by 1,25-(OH)2D3 and 9-cis RA is mediated by an AR-dependent mechanism and preceded by the induction of AR gene expression. Tretinoin 103-105 androgen receptor Homo sapiens 180-182
10022522-6 1999 Tumor necrosis factor-alpha, which enhances the posttranscriptional action of retinoic acid, reduced U1 70K mRNA expression, while an inhibition of retinoic acid action by transforming growth factor-beta was associated with a marked increase in U1 70K mRNA levels. Tretinoin 78-91 tumor necrosis factor Homo sapiens 0-27
10103089-5 1999 Moreover, treatment with retinoic acid led to the appearance of an inward rectifying potassium channel with electrophysiological properties similar to IRK1. Tretinoin 25-38 potassium inwardly-rectifying channel, subfamily J, member 2 Mus musculus 151-155
10103089-7 1999 However, Northern analysis with a murine cDNA probe indicated that IRK1 mRNA was induced by retinoic acid at a similar level in both kinds of cells. Tretinoin 92-105 potassium inwardly-rectifying channel, subfamily J, member 2 Mus musculus 67-71
10022522-6 1999 Tumor necrosis factor-alpha, which enhances the posttranscriptional action of retinoic acid, reduced U1 70K mRNA expression, while an inhibition of retinoic acid action by transforming growth factor-beta was associated with a marked increase in U1 70K mRNA levels. Tretinoin 148-161 tumor necrosis factor Homo sapiens 0-27
10022884-2 1999 We previously observed that JNK activity is suppressed by all-trans-retinoic acid (t-RA), a ligand for retinoic acid nuclear receptors (RARs), in normal human bronchial epithelial cells, which are growth inhibited by t-RA. Tretinoin 58-81 mitogen-activated protein kinase 8 Homo sapiens 28-31
10022884-2 1999 We previously observed that JNK activity is suppressed by all-trans-retinoic acid (t-RA), a ligand for retinoic acid nuclear receptors (RARs), in normal human bronchial epithelial cells, which are growth inhibited by t-RA. Tretinoin 83-87 mitogen-activated protein kinase 8 Homo sapiens 28-31
10022884-2 1999 We previously observed that JNK activity is suppressed by all-trans-retinoic acid (t-RA), a ligand for retinoic acid nuclear receptors (RARs), in normal human bronchial epithelial cells, which are growth inhibited by t-RA. Tretinoin 217-221 mitogen-activated protein kinase 8 Homo sapiens 28-31
10022884-3 1999 In this study, we investigated the mechanism by which t-RA inhibits JNK and the possibility that this signaling event is blocked in non-small cell lung cancer (NSCLC) cells. Tretinoin 54-58 mitogen-activated protein kinase 8 Homo sapiens 68-71
10022884-5 1999 We found that in NSCLC cells expressing functional retinoid receptors, serum-induced JNK phosphorylation and activity were inhibited by t-RA in a bimodal pattern, transiently within 30 min and in a sustained fashion beginning at 12 h. Retinoid receptor transcriptional activation was required for the late, but not the early, suppression of JNK activity. Tretinoin 136-140 mitogen-activated protein kinase 8 Homo sapiens 85-88
10022884-5 1999 We found that in NSCLC cells expressing functional retinoid receptors, serum-induced JNK phosphorylation and activity were inhibited by t-RA in a bimodal pattern, transiently within 30 min and in a sustained fashion beginning at 12 h. Retinoid receptor transcriptional activation was required for the late, but not the early, suppression of JNK activity. Tretinoin 136-140 mitogen-activated protein kinase 8 Homo sapiens 341-344
10022884-7 1999 This effect of t-RA was phosphatase dependent and involved an increase in the expression of the dual-specificity MAP kinase phosphatase 1 (MKP-1). Tretinoin 15-19 dual specificity phosphatase 1 Homo sapiens 139-144
10077004-0 1999 Defective retinoic acid regulation of the Pit-1 gene enhancer: a novel mechanism of combined pituitary hormone deficiency. Tretinoin 10-23 POU class 1 homeobox 1 Homo sapiens 42-47
10077004-3 1999 Pit-1 is also necessary for retinoic acid induction of its own gene during development through a Pit-1-dependent enhancer. Tretinoin 28-41 POU class 1 homeobox 1 Homo sapiens 0-5
10047453-9 1999 beta4 and alpha6A are also mainly localized in the VE but they are undetectable in undifferentiated aggregates and their expression is induced by RA treatment. Tretinoin 146-148 adaptor related protein complex 4 subunit beta 1 Homo sapiens 0-5
10077004-3 1999 Pit-1 is also necessary for retinoic acid induction of its own gene during development through a Pit-1-dependent enhancer. Tretinoin 28-41 POU class 1 homeobox 1 Homo sapiens 97-102
10077004-5 1999 In the present report, we provide in vivo evidence that retinoic acid induction of the Pit-1 gene can be impaired by a Pit-1 gene mutation, suggesting a new molecular mechanism for combined pituitary hormone deficiency in man. Tretinoin 56-69 POU class 1 homeobox 1 Homo sapiens 87-92
10077004-5 1999 In the present report, we provide in vivo evidence that retinoic acid induction of the Pit-1 gene can be impaired by a Pit-1 gene mutation, suggesting a new molecular mechanism for combined pituitary hormone deficiency in man. Tretinoin 56-69 POU class 1 homeobox 1 Homo sapiens 119-124
10051769-4 1999 In contrast, brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) decrease ionic current activity, and the addition of RA with the neurotrophins enhances this inhibitory response in an age-dependent manner. Tretinoin 133-135 brain derived neurotrophic factor Gallus gallus 48-52
10221781-3 1999 Co-treatment of Sertoli cells with the optimal dose of retinoic acid (RA, a potent inducer of transferrin) and TNFalpha induced a stimulation of transferrin that was significantly higher than the FIRT combination, a well known mixture of transferrin activators. Tretinoin 55-68 transferrin Rattus norvegicus 94-105
10221781-3 1999 Co-treatment of Sertoli cells with the optimal dose of retinoic acid (RA, a potent inducer of transferrin) and TNFalpha induced a stimulation of transferrin that was significantly higher than the FIRT combination, a well known mixture of transferrin activators. Tretinoin 55-68 transferrin Rattus norvegicus 145-156
10221781-3 1999 Co-treatment of Sertoli cells with the optimal dose of retinoic acid (RA, a potent inducer of transferrin) and TNFalpha induced a stimulation of transferrin that was significantly higher than the FIRT combination, a well known mixture of transferrin activators. Tretinoin 55-68 transferrin Rattus norvegicus 145-156
10221781-3 1999 Co-treatment of Sertoli cells with the optimal dose of retinoic acid (RA, a potent inducer of transferrin) and TNFalpha induced a stimulation of transferrin that was significantly higher than the FIRT combination, a well known mixture of transferrin activators. Tretinoin 70-72 transferrin Rattus norvegicus 94-105
10221781-3 1999 Co-treatment of Sertoli cells with the optimal dose of retinoic acid (RA, a potent inducer of transferrin) and TNFalpha induced a stimulation of transferrin that was significantly higher than the FIRT combination, a well known mixture of transferrin activators. Tretinoin 70-72 transferrin Rattus norvegicus 145-156
10221781-3 1999 Co-treatment of Sertoli cells with the optimal dose of retinoic acid (RA, a potent inducer of transferrin) and TNFalpha induced a stimulation of transferrin that was significantly higher than the FIRT combination, a well known mixture of transferrin activators. Tretinoin 70-72 transferrin Rattus norvegicus 145-156
10221781-6 1999 Moreover pre-treatment with RA, while greatly increasing the amount of transferrin produced, did not modify Sertoli cell responsiveness to TNFalpha. Tretinoin 28-30 transferrin Rattus norvegicus 71-82
10082656-0 1999 Retinoic acid potentiates TNF-alpha-induced ICAM-1 expression in normal human epidermal keratinocytes. Tretinoin 0-13 tumor necrosis factor Homo sapiens 26-35
10082656-7 1999 RA potentiated the TNF-alpha-induced ICAM-1 response in all Ca2+-concentrations. Tretinoin 0-2 tumor necrosis factor Homo sapiens 19-28
10082656-9 1999 In summary, our results establish retinoic acid as an enhancer of TNF-alpha-induced ICAM-1 levels in NHK. Tretinoin 34-47 tumor necrosis factor Homo sapiens 66-75
18031118-7 1999 The broad spectrum of antineoplastic drugs whose activity can be enhanced by IFNalpha argues for multiple levels of drug-drug interactions: protein binding (cisplatin), alteration in cellular uptake, modulation of drug target enzymes (dihydropyrimidine hydrogenase) and changes in biotransformation (tretinoin) or excretion. Tretinoin 300-309 interferon alpha 1 Homo sapiens 77-85
10051751-1 1999 Expression of the growth-associated protein of 43-kDa (GAP-43), which is described as a postmitotic, neuron-specific major protein kinase C (PKC) substrate, was investigated in the murine embryonic carcinoma cell line PCC7-Mz1 which develops into a brain-tissue-like pattern of neuronal, fibroblast-like and astroglial cells upon stimulation with all-trans retinoic acid (RA). Tretinoin 357-370 growth associated protein 43 Mus musculus 18-53
10051751-1 1999 Expression of the growth-associated protein of 43-kDa (GAP-43), which is described as a postmitotic, neuron-specific major protein kinase C (PKC) substrate, was investigated in the murine embryonic carcinoma cell line PCC7-Mz1 which develops into a brain-tissue-like pattern of neuronal, fibroblast-like and astroglial cells upon stimulation with all-trans retinoic acid (RA). Tretinoin 357-370 growth associated protein 43 Mus musculus 55-61
10051751-1 1999 Expression of the growth-associated protein of 43-kDa (GAP-43), which is described as a postmitotic, neuron-specific major protein kinase C (PKC) substrate, was investigated in the murine embryonic carcinoma cell line PCC7-Mz1 which develops into a brain-tissue-like pattern of neuronal, fibroblast-like and astroglial cells upon stimulation with all-trans retinoic acid (RA). Tretinoin 372-374 growth associated protein 43 Mus musculus 18-53
10051751-1 1999 Expression of the growth-associated protein of 43-kDa (GAP-43), which is described as a postmitotic, neuron-specific major protein kinase C (PKC) substrate, was investigated in the murine embryonic carcinoma cell line PCC7-Mz1 which develops into a brain-tissue-like pattern of neuronal, fibroblast-like and astroglial cells upon stimulation with all-trans retinoic acid (RA). Tretinoin 372-374 growth associated protein 43 Mus musculus 55-61
10051751-3 1999 While the P1 promoter of the GAP-43 gene gave rise to a 1.6-kb mRNA and was already active at a very low level in PCC7-Mz1 stem cells, transcription of the P2 promoter, which resulted in a 1.4-kb mRNA, was completely blocked in stem cells but increased rapidly after RA treatment. Tretinoin 267-269 growth associated protein 43 Mus musculus 29-35
10051751-9 1999 In PCC7-Mz1 cultures, 2 days after addition of RA, GAP-43 became phosphorylated upon activation of PKC, and colocalized specifically with the novel PKC isoform eta. Tretinoin 47-49 growth associated protein 43 Mus musculus 51-57
9973197-0 1999 Phosphoinositide 3-kinase activity is essential for all-trans-retinoic acid-induced granulocytic differentiation of HL-60 cells. Tretinoin 62-75 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 0-25
9973197-1 1999 Phosphoinositide 3-kinase (PI 3-K) activity increases in HL-60 cells that are induced to granulocytic differentiation by all-trans-retinoic acid. Tretinoin 121-144 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 0-25
10088603-6 1999 Moreover, tapasin expression was found to be induced by dimethyl sulfoxide and by retinoic acid in HL-60 cells. Tretinoin 82-95 TAP binding protein Homo sapiens 10-17
10225671-0 1999 Acute myelogenous leukemia with a t(2;17;4)(p13;q21;p16) aberration: effective treatment with all-trans retinoic acid and granulocyte colony-stimulating factor. Tretinoin 104-117 cyclin dependent kinase inhibitor 2A Homo sapiens 52-55
9924183-10 1999 Indeed, DEX also enhanced the RA-dependent increase in RARbeta mRNA in a cycloheximide-sensitive manner. Tretinoin 30-32 retinoic acid receptor, beta Rattus norvegicus 55-62
9920792-0 1999 Carcinoma cell lines resistant for growth inhibition and apoptosis to retinoic acid are responsive to 4-hydroxy-phenyl-retinamide: correlation with tissue transglutaminase. Tretinoin 70-83 transglutaminase 2 Homo sapiens 148-171
9920669-1 1999 We have studied the effect of retinoic acid on the expression of the neurotrophin receptors trkA, trkC, and p75 by neuroblasts and neurons at different axial levels along the embryonic mouse paravertebral sympathetic chain. Tretinoin 30-43 nerve growth factor receptor (TNFR superfamily, member 16) Mus musculus 108-111
9920024-1 1999 OBJECTIVE: To determine the role of matrix metalloproteinases (MMPs) in retinoic acid (RetA)-induced degradation of type II collagen in cartilage. Tretinoin 72-85 matrix metallopeptidase 8 Bos taurus 63-67
9890568-1 1999 Retinoic acid exerts pleiotropic effects by acting through two families of nuclear receptors, RAR and RXR. Tretinoin 0-13 RAB40B, member RAS oncogene family Homo sapiens 94-97
9920024-1 1999 OBJECTIVE: To determine the role of matrix metalloproteinases (MMPs) in retinoic acid (RetA)-induced degradation of type II collagen in cartilage. Tretinoin 87-91 matrix metallopeptidase 8 Bos taurus 63-67
10668629-0 1999 Inhibition of retinoic acid-inducible transcription by COUP-TFI in human salivary gland adenocarcinoma cell line HSG. Tretinoin 14-27 nuclear receptor subfamily 2 group F member 1 Homo sapiens 55-63
9950218-6 1999 Increased expression of p53 protein is observed in ATRA-treated HMECs at 72 h; however, initiation of G1-S-phase arrest starts at 24 h, suggesting that this observed induction of p53 is a secondary event. Tretinoin 51-55 tumor protein p53 Homo sapiens 24-27
9864179-6 1999 C-Jun amino-terminal kinase (JNK) was not tyrosine-phosphorylated by any cytokine despite the existence of JNK proteins in human neutrophils, whereas it was tyrosine-phosphorylated by TNF in undifferentiated and all-trans retinoic acid-differentiated HL-60 cells. Tretinoin 222-235 mitogen-activated protein kinase 8 Homo sapiens 29-32
9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 82-95 estrogen receptor 1 Homo sapiens 13-30
9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 82-95 estrogen receptor 1 Homo sapiens 32-34
9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 82-95 fibronectin 1 Homo sapiens 154-165
9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 97-99 estrogen receptor 1 Homo sapiens 13-30
9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 97-99 estrogen receptor 1 Homo sapiens 32-34
9892191-1 1999 Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. Tretinoin 97-99 fibronectin 1 Homo sapiens 154-165
9892191-3 1999 Western blot analysis showed that tyrosine phosphorylation of two major bands at Mr 125,000 and Mr 68,000 was induced by RA in ER+ MCF-7 human breast carcinoma cells. Tretinoin 121-123 estrogen receptor 1 Homo sapiens 127-129
9892191-4 1999 However, this induction was a late phenomenon detectable at 12 and 24 h, but not within 3 h. A similar increase of tyrosine phosphorylation by RA was observed in ER+ human breast cancer cell lines T-47D and ZR-75-1, but not in the ER- cell lines MDA-MB-231, MDA-MB-453, and MDA-MB-468. Tretinoin 143-145 estrogen receptor 1 Homo sapiens 162-164
9892191-4 1999 However, this induction was a late phenomenon detectable at 12 and 24 h, but not within 3 h. A similar increase of tyrosine phosphorylation by RA was observed in ER+ human breast cancer cell lines T-47D and ZR-75-1, but not in the ER- cell lines MDA-MB-231, MDA-MB-453, and MDA-MB-468. Tretinoin 143-145 estrogen receptor 1 Homo sapiens 231-233
9950218-6 1999 Increased expression of p53 protein is observed in ATRA-treated HMECs at 72 h; however, initiation of G1-S-phase arrest starts at 24 h, suggesting that this observed induction of p53 is a secondary event. Tretinoin 51-55 tumor protein p53 Homo sapiens 179-182
10352886-0 1999 Modulation of alpha-actin and alpha-actinin proteins in cardiomyocytes by retinoic acid during development. Tretinoin 74-87 actinin, alpha 4 Gallus gallus 30-43
9950218-13 1999 Our results emphasize the chemotherapeutic potential of ATRA and antiestrogens, particularly for suppressing the growth of tumors lacking functional p53. Tretinoin 56-60 tumor protein p53 Homo sapiens 149-152
20426546-11 1999 However, ATRA inhibited colony formation, reduced the expansion of CFC and accelerated the loss of CD34 expression at doses required for the induction of CD38 expression. Tretinoin 9-13 CD34 molecule Homo sapiens 99-103
10234809-4 1999 All-trans-retinoic acid (tRA) or 13-cis-RA increased RAR beta and decreased K1 and TGase I mRNA levels in serum-free medium. Tretinoin 0-23 retinoic acid receptor beta Homo sapiens 53-61
10473956-4 1999 METHODS: The effects of different concentrations of retinoids (all-trans-retinal and all-trans-retinoic acid) on VEGF production by cultured human skin keratinocytes in both cell extracts and supernatants were determined. Tretinoin 89-108 vascular endothelial growth factor A Homo sapiens 113-117
10473956-6 1999 RESULTS: The amount of cell-associated and secreted VEGF strongly decreased with retinoid concentration (e.g. 48, 69% inhibition at 0.1 microM all-trans-retinal and -retinoic acid, respectively, in the supernatants). Tretinoin 166-179 vascular endothelial growth factor A Homo sapiens 52-56
10234809-4 1999 All-trans-retinoic acid (tRA) or 13-cis-RA increased RAR beta and decreased K1 and TGase I mRNA levels in serum-free medium. Tretinoin 25-28 retinoic acid receptor beta Homo sapiens 53-61
10565546-4 1999 A potential retinoic acid response element (RARE) and a possible cAMP response element are located in the putative promoter region, suggesting a role for retinoic acid and cAMP in the induction of thrombomodulin gene expression. Tretinoin 12-25 thrombomodulin Rattus norvegicus 197-211
9914484-9 1999 L-FABP binds two fatty acids per molecule but Lb-FABP displays a fatty-acid-conformation-dependent binding stoichiometry; L-FABP shows a higher affinity for fatty acids, especially oleic acid, while Lb-FABP has a higher affinity for other hydrophobic ligands, especially retinoic acid. Tretinoin 271-284 fatty acid binding protein 1 Homo sapiens 122-128
10565546-4 1999 A potential retinoic acid response element (RARE) and a possible cAMP response element are located in the putative promoter region, suggesting a role for retinoic acid and cAMP in the induction of thrombomodulin gene expression. Tretinoin 154-167 thrombomodulin Rattus norvegicus 197-211
9886825-4 1999 However, the transcriptional coactivator, CREB-binding protein (CBP) coactivates expression of this gene through an indirect interaction with the HNF-4-binding site, and overexpression of CBP in HepG2 cells eliminates retinoic acid repression of reporter gene expression driven by the HGFL promoter. Tretinoin 218-231 CREB binding protein Homo sapiens 42-62
9886825-4 1999 However, the transcriptional coactivator, CREB-binding protein (CBP) coactivates expression of this gene through an indirect interaction with the HNF-4-binding site, and overexpression of CBP in HepG2 cells eliminates retinoic acid repression of reporter gene expression driven by the HGFL promoter. Tretinoin 218-231 CREB binding protein Homo sapiens 64-67
9886825-4 1999 However, the transcriptional coactivator, CREB-binding protein (CBP) coactivates expression of this gene through an indirect interaction with the HNF-4-binding site, and overexpression of CBP in HepG2 cells eliminates retinoic acid repression of reporter gene expression driven by the HGFL promoter. Tretinoin 218-231 hepatocyte nuclear factor 4 alpha Homo sapiens 146-151
9886825-4 1999 However, the transcriptional coactivator, CREB-binding protein (CBP) coactivates expression of this gene through an indirect interaction with the HNF-4-binding site, and overexpression of CBP in HepG2 cells eliminates retinoic acid repression of reporter gene expression driven by the HGFL promoter. Tretinoin 218-231 CREB binding protein Homo sapiens 188-191
9886825-5 1999 Overexpression of CBP also protects the endogenous HGFL gene from down-regulation by retinoic acid. Tretinoin 85-98 CREB binding protein Homo sapiens 18-21
10052016-3 1999 stimulated splenic ALA-S activity, whereas co-administration of tin-metalloporphyrins with RA antagonised the RA mediated induction of ALA-S. Tretinoin 91-93 5'-aminolevulinate synthase 1 Rattus norvegicus 135-140
27426845-6 1999 After a week with ATRA treatment, fibrinogen level improved and "D" dimers decreased, so as observed slowly maturation of leukemic leucocytes. Tretinoin 18-22 fibrinogen beta chain Homo sapiens 34-44
10052016-3 1999 stimulated splenic ALA-S activity, whereas co-administration of tin-metalloporphyrins with RA antagonised the RA mediated induction of ALA-S. Tretinoin 110-112 5'-aminolevulinate synthase 1 Rattus norvegicus 135-140
10052016-4 1999 In the other tissues viz., liver, heart and lung our results showed a diminution of ALA-S activity on RA administration, the level of repression was further attenuated when tin-metalloporphyrins were co-administered with RA. Tretinoin 102-104 5'-aminolevulinate synthase 1 Rattus norvegicus 84-89
10052016-4 1999 In the other tissues viz., liver, heart and lung our results showed a diminution of ALA-S activity on RA administration, the level of repression was further attenuated when tin-metalloporphyrins were co-administered with RA. Tretinoin 221-223 5'-aminolevulinate synthase 1 Rattus norvegicus 84-89
10052016-5 1999 This marked suppression of ALA-S brought forth by concurrent administration of RA and tin-metalloporphyrins is suggestive of the beneficial effect of this formulation in acute attacks of porphyria, similar to heme. Tretinoin 79-81 5'-aminolevulinate synthase 1 Rattus norvegicus 27-32
9831819-6 1999 RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. Tretinoin 0-2 ornithine decarboxylase Bos taurus 61-84
10027563-5 1999 An accompanying effect of RA was to sustain or up-regulate trkA, trkB, trkC, and p75NGFR expression. Tretinoin 26-28 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 65-69
9831819-6 1999 RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. Tretinoin 0-2 ornithine decarboxylase Bos taurus 86-89
10780452-2 1999 In this report, we examined levels of p300 protein and the related protein, CREB binding protein (CBP), during the retinoic acid (RA)-induced differentiation of F9 cell. Tretinoin 115-128 CREB binding protein Homo sapiens 76-96
9831819-7 1999 The putrescine content was significantly increased in RA-treated RPE cells up until 24 h, while spermidine, spermine and N1-acetylspermidine contents were significantly increased until 16 h. Our findings suggest that RA treatment increases the intracellular polyamine concentration of RPE cells via activation of ODC, SAMDC and SAT and that this results in the promotion of RPE cell growth until the cells reach full confluency. Tretinoin 217-219 ornithine decarboxylase Bos taurus 313-316
10780452-2 1999 In this report, we examined levels of p300 protein and the related protein, CREB binding protein (CBP), during the retinoic acid (RA)-induced differentiation of F9 cell. Tretinoin 115-128 CREB binding protein Homo sapiens 98-101
10780452-2 1999 In this report, we examined levels of p300 protein and the related protein, CREB binding protein (CBP), during the retinoic acid (RA)-induced differentiation of F9 cell. Tretinoin 130-132 CREB binding protein Homo sapiens 76-96
9857033-5 1998 Induction of RAIG1 expression by ATRA is rapid (within 2 h) and dose-dependent in the range between 1 nM to 1 microM. Tretinoin 33-37 phospholipase A and acyltransferase 4 Homo sapiens 13-18
10780452-2 1999 In this report, we examined levels of p300 protein and the related protein, CREB binding protein (CBP), during the retinoic acid (RA)-induced differentiation of F9 cell. Tretinoin 130-132 CREB binding protein Homo sapiens 98-101
10780480-2 1999 In this study, we investigated functions of p300 and CBP during the retinoic acid (RA) induced F9 cell differentiation using hammerhead ribozymes. Tretinoin 68-81 CREB binding protein Homo sapiens 53-56
10780480-2 1999 In this study, we investigated functions of p300 and CBP during the retinoic acid (RA) induced F9 cell differentiation using hammerhead ribozymes. Tretinoin 83-85 CREB binding protein Homo sapiens 53-56
10821537-3 1999 Western analyses showed that continuous exposure for 48 h of HL-60 cells to the differentiation-inducing agents, all-trans retinoic acid, 1,25-dihydroxyvitamin D3, or N-methylformamide, resulted in decreases in mitochondrial HSP70 (mtHSP70), with little change in the levels of HSP70, HSC70, and GRP78. Tretinoin 123-136 heat shock protein family A (Hsp70) member 9 Homo sapiens 232-239
10821537-3 1999 Western analyses showed that continuous exposure for 48 h of HL-60 cells to the differentiation-inducing agents, all-trans retinoic acid, 1,25-dihydroxyvitamin D3, or N-methylformamide, resulted in decreases in mitochondrial HSP70 (mtHSP70), with little change in the levels of HSP70, HSC70, and GRP78. Tretinoin 123-136 heat shock protein family A (Hsp70) member 5 Homo sapiens 296-301
9857033-6 1998 The constitutive RAIG1 mRNA levels, which were low in three of five head and neck and four of six lung cancer cell lines, increased after ATRA treatment in most cell lines. Tretinoin 138-142 phospholipase A and acyltransferase 4 Homo sapiens 17-22
9860927-8 1998 AHR may directly or indirectly control levels of a cytochrome P450 that is responsible for catabolizing retinoic acid. Tretinoin 104-117 aryl-hydrocarbon receptor Mus musculus 0-3
9852056-3 1998 Previously we have demonstrated the importance for RA binding and RA-dependent transactivation of Arg276 of RARalpha alone and in RARbeta Arg269 in conjunction with Lys220. Tretinoin 66-68 retinoic acid receptor beta Homo sapiens 130-137
9852056-8 1998 It is likely that Lys236 in RARgamma and its homologs in RARalpha and RARbeta are solvent exposed rather than pointing into the RA-binding pocket. Tretinoin 28-30 retinoic acid receptor beta Homo sapiens 70-77
9874511-8 1998 IL-6 completely abolished detectable expression of BMP-2 mRNA, which was also greatly reduced by IL-1beta, retinoic acid and 1,25(OH)2 vitamin D3. Tretinoin 107-120 interleukin 6 Homo sapiens 0-4
9797132-4 1998 Four of 5 rhabdomyosarcoma cell lines expressed the mRNA for SCF receptor c-kit, while the 5th cell line became weakly positive for c-kit mRNA only after stimulation with retinoic acid. Tretinoin 171-184 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 132-137
9889406-0 1998 Apoptosis and growth inhibition of squamous carcinoma cells treated with interferon-alpha, IFN-beta and retinoic acid are associated with induction of the cyclin-dependent kinase inhibitor p21. Tretinoin 104-117 cyclin dependent kinase inhibitor 1A Homo sapiens 189-192
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 10-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 90-96
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 10-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 233-239
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 10-23 interleukin 6 Homo sapiens 254-257
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 176-178 TIMP metallopeptidase inhibitor 1 Homo sapiens 90-96
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 176-178 TIMP metallopeptidase inhibitor 1 Homo sapiens 233-239
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 176-178 interleukin 6 Homo sapiens 254-257
18505519-4 1998 The extent of variations obtained on MMP-1 and TIMP-1 levels, when HSF culture medium was supplemented with 10-5 m RA, could be obtained using a 100-fold lower concentration of RA encapsulated into CER vesicles. Tretinoin 115-117 TIMP metallopeptidase inhibitor 1 Homo sapiens 47-53
18505519-4 1998 The extent of variations obtained on MMP-1 and TIMP-1 levels, when HSF culture medium was supplemented with 10-5 m RA, could be obtained using a 100-fold lower concentration of RA encapsulated into CER vesicles. Tretinoin 177-179 TIMP metallopeptidase inhibitor 1 Homo sapiens 47-53
10098724-3 1998 Treatment with RA for periods longer than 1 h resulted in enhanced binding of the non-competitive NMDA-receptor antagonist, TCP, by embryonic and fetal (E17, E18) cells, but not by cells derived from perinatal (E19, P0) forebrains. Tretinoin 15-17 serine peptidase inhibitor Kazal type 1 Homo sapiens 124-127
10098724-4 1998 As TCP binding-sites are localised within the channel-complex, treatment with RA was thought to result in an opening of the NMDA receptor channel. Tretinoin 78-80 serine peptidase inhibitor Kazal type 1 Homo sapiens 3-6
9822698-2 1998 Also during retinoic acid (RA)-dependent embryonal carcinoma (EC) cell differentiation, RARbeta expression is initially up-regulated, while in later phases of differentiation expression is down-regulated, by an unknown mechanism. Tretinoin 12-25 retinoic acid receptor beta Homo sapiens 88-95
9822698-2 1998 Also during retinoic acid (RA)-dependent embryonal carcinoma (EC) cell differentiation, RARbeta expression is initially up-regulated, while in later phases of differentiation expression is down-regulated, by an unknown mechanism. Tretinoin 27-29 retinoic acid receptor beta Homo sapiens 88-95
9828104-9 1998 RA induced the appearance of low-molecular-weight LBR-related proteins. Tretinoin 0-2 lamin B receptor Homo sapiens 50-53
9823320-5 1998 However, stable expression of ER increased retinoid activation of transcription of a retinoic acid (RA) response elements from the low level in MDA-MB-231 to approach the level of MCF-7. Tretinoin 85-98 estrogen receptor 1 Homo sapiens 30-32
9823320-5 1998 However, stable expression of ER increased retinoid activation of transcription of a retinoic acid (RA) response elements from the low level in MDA-MB-231 to approach the level of MCF-7. Tretinoin 100-102 estrogen receptor 1 Homo sapiens 30-32
9929163-4 1998 Retinoic acid treatment which can effectively suppress p21 gene expression did not prevent apoptosis. Tretinoin 0-13 cyclin dependent kinase inhibitor 1A Homo sapiens 55-58
18505519-4 1998 The extent of variations obtained on MMP-1 and TIMP-1 levels, when HSF culture medium was supplemented with 10-5 m RA, could be obtained using a 100-fold lower concentration of RA encapsulated into CER vesicles. Tretinoin 177-179 interleukin 6 Homo sapiens 67-70
18505519-6 1998 The rate of internalization of RA into HSF was increased when used in its CER encapsulated form. Tretinoin 31-33 interleukin 6 Homo sapiens 39-42
9865605-0 1998 A parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 by retinoic acid in mouse embryonal carcinoma F9 cells. Tretinoin 108-121 lectin, galactose binding, soluble 3 Mus musculus 94-104
9792724-0 1998 Retinoic acid mediates down-regulation of the alpha-fetoprotein gene through decreased expression of hepatocyte nuclear factors. Tretinoin 0-13 alpha fetoprotein Homo sapiens 46-63
9792724-6 1998 Gel mobility shift assays for factors binding to key elements in the AFP promoter region demonstrated that hepatocyte nuclear factor (HNF) 1 binding was diminished in nuclear extracts from RA-treated cells. Tretinoin 189-191 alpha fetoprotein Homo sapiens 69-72
9792724-6 1998 Gel mobility shift assays for factors binding to key elements in the AFP promoter region demonstrated that hepatocyte nuclear factor (HNF) 1 binding was diminished in nuclear extracts from RA-treated cells. Tretinoin 189-191 HNF1 homeobox A Homo sapiens 107-140
9865605-5 1998 On the other hand, RA inhibited expression of galectin-3 in the wild-type line but had no effect on the RA-3-10 line. Tretinoin 19-21 lectin, galactose binding, soluble 3 Mus musculus 46-56
9827903-0 1998 All-trans-retinoic acid up-regulates CD38 but not c-Kit antigens on human marrow CD34+ cells without recruitment into cell cycle. Tretinoin 0-23 CD34 molecule Homo sapiens 81-85
9779827-0 1998 Evidence of a direct role for Bcl-2 in the regulation of articular chondrocyte apoptosis under the conditions of serum withdrawal and retinoic acid treatment. Tretinoin 134-147 BCL2 apoptosis regulator Homo sapiens 30-35
9827903-10 1998 Contrary to steady-state cells, CD34+ cells treated with pharmacological doses of ATRA alone displayed CD38 over-expression without change in c-Kit levels and cycle status, suggesting an absence of maturation pressure. Tretinoin 82-86 CD34 molecule Homo sapiens 32-36
9809989-0 1998 Retinoic acid down-regulates the expression of the vasoactive intestinal polypeptide receptor type-1 in human breast carcinoma cell lines. Tretinoin 0-13 vasoactive intestinal peptide receptor 1 Homo sapiens 51-100
9809989-2 1998 In all four cell lines, retinoic acid (RA) treatment caused a fast and marked decrease in VIP-R1 mRNA level as examined by Northern blots. Tretinoin 24-37 vasoactive intestinal peptide receptor 1 Homo sapiens 90-96
9809989-2 1998 In all four cell lines, retinoic acid (RA) treatment caused a fast and marked decrease in VIP-R1 mRNA level as examined by Northern blots. Tretinoin 39-41 vasoactive intestinal peptide receptor 1 Homo sapiens 90-96
9825862-1 1998 Mammalian alcohol dehydrogenases ADH1 (class I ADH) and ADH4 (class IV ADH) function as retinol dehydrogenases contributing to the synthesis of retinoic acid, the active form of vitamin A involved in growth and development. Tretinoin 144-157 alcohol dehydrogenase 1 Xenopus laevis 33-37
9779827-2 1998 Here we demonstrate the importance of Bcl-2 in regulating articular chondrocyte apoptosis in response to both serum withdrawal and retinoic acid treatment. Tretinoin 131-144 BCL2 apoptosis regulator Homo sapiens 38-43
9779827-8 1998 In contrast, chondrocytes overexpressing Bcl-2 were resistant to apoptosis induced by both serum withdrawal and retinoic acid treatment. Tretinoin 112-125 BCL2 apoptosis regulator Homo sapiens 41-46
9823948-3 1998 Here, we show that retinoic acid (RA)-induced JEM-1 expression is biphasic (peaks at 6 h and 48 h) and associated with the later stages of maturation. Tretinoin 19-32 basic leucine zipper nuclear factor 1 Homo sapiens 46-51
9804359-3 1998 All-trans retinoic acid (RA), 13-cis RA, and all-trans retinol reduced VEGF/VPF secretion by KC in primary cultures by a mean +/- SD of 58 +/- 25%, 46 +/- 21%, and 54 +/- 20%, respectively, compared with control values. Tretinoin 10-23 vascular endothelial growth factor A Homo sapiens 71-75
9804359-3 1998 All-trans retinoic acid (RA), 13-cis RA, and all-trans retinol reduced VEGF/VPF secretion by KC in primary cultures by a mean +/- SD of 58 +/- 25%, 46 +/- 21%, and 54 +/- 20%, respectively, compared with control values. Tretinoin 10-23 vascular endothelial growth factor A Homo sapiens 76-79
9804359-3 1998 All-trans retinoic acid (RA), 13-cis RA, and all-trans retinol reduced VEGF/VPF secretion by KC in primary cultures by a mean +/- SD of 58 +/- 25%, 46 +/- 21%, and 54 +/- 20%, respectively, compared with control values. Tretinoin 25-27 vascular endothelial growth factor A Homo sapiens 71-75
9804359-3 1998 All-trans retinoic acid (RA), 13-cis RA, and all-trans retinol reduced VEGF/VPF secretion by KC in primary cultures by a mean +/- SD of 58 +/- 25%, 46 +/- 21%, and 54 +/- 20%, respectively, compared with control values. Tretinoin 25-27 vascular endothelial growth factor A Homo sapiens 76-79
9804359-3 1998 All-trans retinoic acid (RA), 13-cis RA, and all-trans retinol reduced VEGF/VPF secretion by KC in primary cultures by a mean +/- SD of 58 +/- 25%, 46 +/- 21%, and 54 +/- 20%, respectively, compared with control values. Tretinoin 37-39 vascular endothelial growth factor A Homo sapiens 71-75
9808636-7 1998 Among these receptor mRNAs, RARbeta mRNA quickly responded to RA treatment, and the level was doubled within 4 h. Gel mobility shift assay showed that RA induced an RXRE-binding activity in IEC-6 cells. Tretinoin 62-64 retinoic acid receptor, beta Rattus norvegicus 28-35
9783809-0 1998 Retinoic acid differentially regulates interleukin-1beta and interleukin-1 receptor antagonist production by human alveolar macrophages. Tretinoin 0-13 interleukin 1 beta Homo sapiens 39-56
9783809-4 1998 In the present study, we examined the effect of RA on IL-1beta and IL-1ra production by human alveolar macrophages in order to clarify the mechanism in pulmonary infiltration of neutrophils, since IL-1 has been shown to initiate neutrophil recruitment into the lung through up-regulated expression of adhesion molecules on vascular endothelium. Tretinoin 48-50 interleukin 1 beta Homo sapiens 54-62
9783809-4 1998 In the present study, we examined the effect of RA on IL-1beta and IL-1ra production by human alveolar macrophages in order to clarify the mechanism in pulmonary infiltration of neutrophils, since IL-1 has been shown to initiate neutrophil recruitment into the lung through up-regulated expression of adhesion molecules on vascular endothelium. Tretinoin 48-50 interleukin 1 beta Homo sapiens 54-58
9783809-5 1998 RA enhanced IL-1beta and inhibited IL-1ra production by 4beta phorbol 12beta-myristate-13alpha acetate (PMA)- and lipopolysaccharide (LPS)-stimulated human alveolar macrophages. Tretinoin 0-2 interleukin 1 beta Homo sapiens 12-20
9774664-6 1998 Overexpression of RARgamma1 neutralizes the effects of RA on RARbeta induction. Tretinoin 18-20 retinoic acid receptor beta Homo sapiens 61-68
9839358-12 1998 The increases in mRNA steady-state levels for TGF-beta 2 and TGF-beta 3, as for TGF-beta 1, were rapid and transient in nature, again arguing for direct mediation by RA. Tretinoin 166-168 transforming growth factor, beta 2 Mus musculus 46-56
9791009-5 1998 All-trans (ATRA) and 9-cis retinoic acid (9cRA) reduce c-erbB-1 protein to 50-100%, c-erbB-2 to 20-30%, and c-erbB-3 to 10-50% of control, depending on the concentration, respectively, without influencing the tyrosine phosphorylation status. Tretinoin 11-15 erb-b2 receptor tyrosine kinase 2 Homo sapiens 84-92
9791009-7 1998 Retinoic acid-mediated down-regulation of growth and c-erbB-2 and -3 expression was also seen in MCF-7 cells. Tretinoin 0-13 erb-b2 receptor tyrosine kinase 2 Homo sapiens 53-68
9791009-8 1998 We conclude that retinoic acids are efficient repressors of c-erbB-2 and -3 gene expression, whereas c-erbB-1 is not markedly affected. Tretinoin 17-31 erb-b2 receptor tyrosine kinase 2 Homo sapiens 60-75
9804359-3 1998 All-trans retinoic acid (RA), 13-cis RA, and all-trans retinol reduced VEGF/VPF secretion by KC in primary cultures by a mean +/- SD of 58 +/- 25%, 46 +/- 21%, and 54 +/- 20%, respectively, compared with control values. Tretinoin 37-39 vascular endothelial growth factor A Homo sapiens 76-79
9823948-3 1998 Here, we show that retinoic acid (RA)-induced JEM-1 expression is biphasic (peaks at 6 h and 48 h) and associated with the later stages of maturation. Tretinoin 34-36 basic leucine zipper nuclear factor 1 Homo sapiens 46-51
9823948-6 1998 RA treatment induced an increase in the level of JEM-1 mRNA, as detected by a semi-quantitative PCR. Tretinoin 0-2 basic leucine zipper nuclear factor 1 Homo sapiens 49-54
9823948-11 1998 This work identifies JEM-1 as a novel ubiquitous gene whose expression is low in APL cells, but can be restored by RA treatment, concomitant with cell maturation. Tretinoin 115-117 basic leucine zipper nuclear factor 1 Homo sapiens 21-26
9770378-7 1998 Treatment of ECE16-1 and ECE16-D1 cells with retinoic acid suppresses proliferation, EGFR level, EGFR mRNA level, and EGFR promoter activity. Tretinoin 45-58 epidermal growth factor receptor Homo sapiens 85-89
9765286-2 1998 In contrast, after expression of the pituitary-specific transcription factor GHF-1, thyroid hormone and retinoic acid produce a stimulation similar to that found in pituitary cells. Tretinoin 104-117 POU class 1 homeobox 1 Rattus norvegicus 77-82
9770378-7 1998 Treatment of ECE16-1 and ECE16-D1 cells with retinoic acid suppresses proliferation, EGFR level, EGFR mRNA level, and EGFR promoter activity. Tretinoin 45-58 epidermal growth factor receptor Homo sapiens 97-101
9770378-7 1998 Treatment of ECE16-1 and ECE16-D1 cells with retinoic acid suppresses proliferation, EGFR level, EGFR mRNA level, and EGFR promoter activity. Tretinoin 45-58 epidermal growth factor receptor Homo sapiens 97-101
9770378-12 1998 Nevertheless expression of E6/E7 proteins did not confer retinoic acid regulation, as EGFR promoter activity remained elevated in normal cells cotransfected with pHPVE6/E7 and treated with retinoic acid. Tretinoin 189-202 epidermal growth factor receptor Homo sapiens 86-90
9770378-13 1998 These results suggest that human papillomavirus and retinoic acid regulate EGFR levels by independent effects on the EGFR promoter. Tretinoin 52-65 epidermal growth factor receptor Homo sapiens 75-79
9770378-13 1998 These results suggest that human papillomavirus and retinoic acid regulate EGFR levels by independent effects on the EGFR promoter. Tretinoin 52-65 epidermal growth factor receptor Homo sapiens 117-121
9716607-4 1998 Metabolic labeling experiments using 32Pi showed that, while control bcl-2 was labeled, incorporation was greatly increased when cells were treated with ATRA. Tretinoin 153-157 BCL2 apoptosis regulator Homo sapiens 69-74
9731743-6 1998 RA also increased TGF-beta2 mRNA expression; we have previously shown that RA upregulates TGF-beta3 mRNA in these cells. Tretinoin 0-2 transforming growth factor, beta 2 Mus musculus 18-27
9731743-9 1998 Coincubation of heat-activated CM from RA-treated MEPM cells with pan-specific or TGF-beta2 or beta3-specific neutralizing antibodies partially relieved the inhibitory effect on 3H-thymidine incorporation, suggesting that this proliferative response was due to RA-induced TGF-beta. Tretinoin 39-41 transforming growth factor, beta 2 Mus musculus 82-91
9842508-2 1998 Since retinoic acid (RA) has been shown as a potent inducer of TNSALP expression in various osteoblastic and fibroblastic cells, we investigated the effects of RA on the level of ALP activity and expression of TNSALP mRNAs in HPDL cells. Tretinoin 6-19 alkaline phosphatase, placental Homo sapiens 66-69
9842508-2 1998 Since retinoic acid (RA) has been shown as a potent inducer of TNSALP expression in various osteoblastic and fibroblastic cells, we investigated the effects of RA on the level of ALP activity and expression of TNSALP mRNAs in HPDL cells. Tretinoin 21-23 alkaline phosphatase, placental Homo sapiens 66-69
9842508-6 1998 After treatment with RA (10(-6) M) for 4 d, there was a significant increase in the ALP activity of HPDL cells. Tretinoin 21-23 alkaline phosphatase, placental Homo sapiens 84-87
9734662-3 1998 Accumulating data support the concept that glucocorticoids down-regulate IL-6, whereas retinoic acid derivatives (RA) down-regulate IL-6R in myeloma. Tretinoin 87-100 interleukin 6 receptor Homo sapiens 132-137
9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 cyclin dependent kinase 6 Homo sapiens 167-171
9778049-4 1998 LCLs arrested in G0/G1 by RA also showed a significant decrease in the protein levels of cyclins D2, D3 and A, together with a reduction in the amount of cyclin D associated with CDK4 and CDK6, probably accounting for the inhibition of the relative kinase activity. Tretinoin 26-28 cyclin dependent kinase 6 Homo sapiens 188-192
9778049-9 1998 Overall, these results demonstrate that RA treatment of EBV-immortalized B lymphocytes is associated with multiple effects on G1 regulatory proteins, including p27Kip1 up-regulation, decreased levels of cyclins D2, D3 and A, and inhibition of CDK2, CDK4 and CDK6 activity, which ultimately result in reduced pRb phosphorylation and G0/G1 growth arrest. Tretinoin 40-42 cyclin dependent kinase 6 Homo sapiens 258-262
9892899-11 1998 RA produced a greater reduction in desmocollin 1 staining compared with SDS (P < 0.001). Tretinoin 0-2 desmocollin 1 Homo sapiens 35-48
9766444-7 1998 In contrast, the differentiation response of p53-negative U-937 cells to 1,25-dihydroxychole-calciferol or all-trans retinoic acid was enhanced by cAMP-inducing agents at optimal concentrations and inhibited at higher concentrations. Tretinoin 107-130 tumor protein p53 Homo sapiens 45-48
9716600-0 1998 Retinoic acid inhibits CD40 + interleukin-4-mediated IgE production in vitro. Tretinoin 0-13 interleukin 4 Homo sapiens 30-43
9716600-2 1998 Anti-CD40 + IL-4-mediated proliferation of PBMC and B cells was inhibited by RA in a dose-dependent manner, with maximal inhibition of 62% +/- 5% in PBMC and 55% +/- 4.4% in B cells by all-trans RA, and 58% +/- 6.7% and 51% +/- 4.7%, respectively by 13-cis RA. Tretinoin 77-79 interleukin 4 Homo sapiens 12-16
9716600-2 1998 Anti-CD40 + IL-4-mediated proliferation of PBMC and B cells was inhibited by RA in a dose-dependent manner, with maximal inhibition of 62% +/- 5% in PBMC and 55% +/- 4.4% in B cells by all-trans RA, and 58% +/- 6.7% and 51% +/- 4.7%, respectively by 13-cis RA. Tretinoin 195-197 interleukin 4 Homo sapiens 12-16
9716600-10 1998 Taken together, this study shows that RA inhibits IgE production of anti-CD40 + IL-4-stimulated B cells in vitro. Tretinoin 38-40 interleukin 4 Homo sapiens 80-84
9716607-0 1998 Phosphorylation of BCL-2 after exposure of human leukemic cells to retinoic acid. Tretinoin 67-80 BCL2 apoptosis regulator Homo sapiens 19-24
9716607-2 1998 We report here that bcl-2 is phosphorylated on serine in acute myeloblastic leukemia (AML) blasts exposed to all trans retinoic acid (ATRA). Tretinoin 119-132 BCL2 apoptosis regulator Homo sapiens 20-25
9716607-2 1998 We report here that bcl-2 is phosphorylated on serine in acute myeloblastic leukemia (AML) blasts exposed to all trans retinoic acid (ATRA). Tretinoin 134-138 BCL2 apoptosis regulator Homo sapiens 20-25
9716607-5 1998 A comparison of bcl-2 from blasts treated with ATRA or taxol showed that bcl-2 was phosphorylated on serine in cells treated with either agent; however, both qualitative and quantitative differences were seen. Tretinoin 47-51 BCL2 apoptosis regulator Homo sapiens 16-21
9733106-2 1998 Alcohol dehydrogenases ADH1 (class I ADH) and ADH4 (class IV ADH) function as retinol dehydrogenases in the oxidation of retinol, a necessary step in the synthesis of retinoic acid from vitamin A. Tretinoin 167-180 alcohol dehydrogenase 1 (class I) Mus musculus 23-27
9733106-2 1998 Alcohol dehydrogenases ADH1 (class I ADH) and ADH4 (class IV ADH) function as retinol dehydrogenases in the oxidation of retinol, a necessary step in the synthesis of retinoic acid from vitamin A. Tretinoin 167-180 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 46-50
9733106-10 1998 The presence of both ADH1 and ADH4 retinol dehydrogenases during the earliest stages of adrenal gland development, combined with our earlier findings of high levels of retinoic acid in the embryonic adrenal gland, suggests that one of the earliest functions of ADH may be to provide an embryonic endocrine source of retinoic acid for growth and development. Tretinoin 168-181 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 30-34
9733106-10 1998 The presence of both ADH1 and ADH4 retinol dehydrogenases during the earliest stages of adrenal gland development, combined with our earlier findings of high levels of retinoic acid in the embryonic adrenal gland, suggests that one of the earliest functions of ADH may be to provide an embryonic endocrine source of retinoic acid for growth and development. Tretinoin 316-329 alcohol dehydrogenase 1 (class I) Mus musculus 21-25
9733106-10 1998 The presence of both ADH1 and ADH4 retinol dehydrogenases during the earliest stages of adrenal gland development, combined with our earlier findings of high levels of retinoic acid in the embryonic adrenal gland, suggests that one of the earliest functions of ADH may be to provide an embryonic endocrine source of retinoic acid for growth and development. Tretinoin 316-329 alcohol dehydrogenase 4 (class II), pi polypeptide Mus musculus 30-34
9737723-1 1998 The nuclear receptors for thyroid hormone (TRs) and retinoic acid (RARs and RXRs) cooperate with the pituitary-specific transcription factor GHF-1 to activate the rat growth hormone (GH) gene. Tretinoin 52-65 POU class 1 homeobox 1 Rattus norvegicus 141-146
9716607-5 1998 A comparison of bcl-2 from blasts treated with ATRA or taxol showed that bcl-2 was phosphorylated on serine in cells treated with either agent; however, both qualitative and quantitative differences were seen. Tretinoin 47-51 BCL2 apoptosis regulator Homo sapiens 73-78
9716607-7 1998 Quantitatively, all bcl-2 from ATRA-treated cells was in the phosphorylated isoform, while after taxol, both phosphorylated and native bcl-2 was present; incorporation of 32Pi into bcl-2 was stimulated to greater extent in ATRA-treated compared with taxol-treated cells. Tretinoin 31-35 BCL2 apoptosis regulator Homo sapiens 20-25
9716607-8 1998 We used immunoprecipitation experiments to ask if bcl-2 phosphorylated after ATRA or taxol had altered capacity to dimerize with bax. Tretinoin 77-81 BCL2 apoptosis regulator Homo sapiens 50-55
9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 87-91 BCL2 apoptosis regulator Homo sapiens 18-23
9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 121-125 BCL2 apoptosis regulator Homo sapiens 18-23
9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 121-125 BCL2 apoptosis regulator Homo sapiens 93-98
9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 121-125 BCL2 apoptosis regulator Homo sapiens 93-98
9716607-11 1998 The ATRA or taxol-induced phosphorylation of bcl-2 can also be seen in blast cells obtained from AML patients. Tretinoin 4-8 BCL2 apoptosis regulator Homo sapiens 45-50
9846167-6 1998 In contrast, RA abolished the collagen-induced increase in ALP mRNA and PTH/PTHrP receptor mRNA. Tretinoin 13-15 parathyroid hormone Rattus norvegicus 72-75
9891902-7 1998 RESULTS: Tretinoin showed very potent inhibition of PMA-stimulated IL-6 (interleukin 6) release by A431 cells. Tretinoin 9-18 interleukin 6 Homo sapiens 67-71
10921031-5 1998 During ATRA treatment, serum IL-6 changes were correlated with WBC changes. Tretinoin 7-11 interleukin 6 Homo sapiens 29-33
9891902-7 1998 RESULTS: Tretinoin showed very potent inhibition of PMA-stimulated IL-6 (interleukin 6) release by A431 cells. Tretinoin 9-18 interleukin 6 Homo sapiens 73-86
9891902-9 1998 Tretinoin very potently stimulated IL-5 release, and inhibited IFN gamma release by SEB-stimulated human PBMCs. Tretinoin 0-9 interferon gamma Homo sapiens 63-72
10921031-8 1998 CONCLUSION: Serum levels of IL-6, sgp130, IL-8 may reflect patient"s responsiveness to ATRA treatment, predict hyperleukocytosis and intercurrent infection. Tretinoin 87-91 interleukin 6 Homo sapiens 28-32
10921031-8 1998 CONCLUSION: Serum levels of IL-6, sgp130, IL-8 may reflect patient"s responsiveness to ATRA treatment, predict hyperleukocytosis and intercurrent infection. Tretinoin 87-91 C-X-C motif chemokine ligand 8 Homo sapiens 42-46
9710432-6 1998 Activation of mitogenesis, seen in the presence of ATRA alone, was independent of extracellular signal-regulated kinase activation but correlated well with increased expression of cyclin D1 mRNA and protein. Tretinoin 51-55 cyclin D1 Rattus norvegicus 180-189
9743471-3 1998 To gain some insight into the role of Bax in the molecular mechanisms of apoptosis of myeloid cells, we inhibited this gene in all-trans-retinoic acid (ATRA)-treated HL60 cells using the methodology of antisense oligodeoxynucleotides (AS-ODN). Tretinoin 130-150 BCL2 associated X, apoptosis regulator Homo sapiens 38-41
9715277-4 1998 Human neuroblastoma cells transfected with a vector expressing RAR beta demonstrated irreversible growth arrest following a 1 week exposure to all-transretinoic acid, whereas control cells continued to proliferate. Tretinoin 147-165 retinoic acid receptor beta Homo sapiens 63-71
9715277-5 1998 In the absence of additional retinoid, RAR beta transfectants demonstrated a higher proportion of cells in the G0/G1 phase of the cell cycle, increased p21WAF1/CIP1 expression and specific binding to a retinoic acid response element. Tretinoin 202-215 retinoic acid receptor beta Homo sapiens 39-47
9715278-0 1998 FGF4 dissociates anti-tumorigenic from differentiation signals of retinoic acid in human embryonal carcinomas. Tretinoin 66-79 fibroblast growth factor 4 Homo sapiens 0-4
9715278-5 1998 All-trans-retinoic acid (RA)-treatment of these cells induces a neuronal phenotype and represses tumorigenicity and FGF4 expression. Tretinoin 0-23 fibroblast growth factor 4 Homo sapiens 116-120
9715278-5 1998 All-trans-retinoic acid (RA)-treatment of these cells induces a neuronal phenotype and represses tumorigenicity and FGF4 expression. Tretinoin 25-27 fibroblast growth factor 4 Homo sapiens 116-120
9715278-10 1998 RA-treatment repressed endogenous but not exogenous FGF4 expression. Tretinoin 0-2 fibroblast growth factor 4 Homo sapiens 52-56
9715278-14 1998 Despite RA-treatment, this repressed tumorigenicity was overcome in all the transfectants over-expressing FGF4. Tretinoin 8-10 fibroblast growth factor 4 Homo sapiens 106-110
9743471-3 1998 To gain some insight into the role of Bax in the molecular mechanisms of apoptosis of myeloid cells, we inhibited this gene in all-trans-retinoic acid (ATRA)-treated HL60 cells using the methodology of antisense oligodeoxynucleotides (AS-ODN). Tretinoin 152-156 BCL2 associated X, apoptosis regulator Homo sapiens 38-41
9716180-6 1998 The RA-induced CYP26 was shown to be highly specific for the hydroxylation of all-trans-RA and did not recognize the 13-cis and 9-cis isomers. Tretinoin 4-6 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-20
9716179-10 1998 RXR-gamma expression produced significant reduction in levels of RA-responsive genes including the cyclin-dependent kinase inhibitors p21Cip1/WAF1 and p27Kip1, resulting in increased cdc2 and cdk2 kinase activity and RB phosphorylation. Tretinoin 65-67 cyclin dependent kinase inhibitor 1A Homo sapiens 134-141
9716179-10 1998 RXR-gamma expression produced significant reduction in levels of RA-responsive genes including the cyclin-dependent kinase inhibitors p21Cip1/WAF1 and p27Kip1, resulting in increased cdc2 and cdk2 kinase activity and RB phosphorylation. Tretinoin 65-67 cyclin dependent kinase inhibitor 1A Homo sapiens 142-146
9679985-1 1998 Retinoic acid (RA) activated the extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid differentiation and cell cycle arrest associated with hypophosphorylation of the retinoblastoma (RB) tumor suppressor protein. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 33-70
9716180-1 1998 We report on the isolation of a cytochrome P450 (CYP)-like retinoic acid (RA) 4-hydroxylase cDNA from T-47D human breast cancer cells that is identical to the recently cloned hCYP26, which is involved in the metabolic breakdown of RA. Tretinoin 74-76 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 175-181
9716180-2 1998 Northern analysis showed that this novel human CYP26 is induced within 1 h upon RA treatment in RA-sensitive T-47D breast carcinoma cells but not in RA-resistant MDA-MB-231 breast cancer cells and HCT 116 colon cancer cells. Tretinoin 80-82 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 47-52
9716180-2 1998 Northern analysis showed that this novel human CYP26 is induced within 1 h upon RA treatment in RA-sensitive T-47D breast carcinoma cells but not in RA-resistant MDA-MB-231 breast cancer cells and HCT 116 colon cancer cells. Tretinoin 96-98 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 47-52
9716180-3 1998 Stable introduction of different RA receptor (RAR) subtypes in HCT 116 cells showed that CYP26 expression is dependent on RARalpha and RARgamma and, to a lesser extent, on RARbeta and closely paralleled RA metabolism, suggesting that it represents the major RA 4-hydroxylase in these human cells. Tretinoin 33-35 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 89-94
9716180-5 1998 Interestingly, CYP26 activity was efficiently inhibited by liarozole, an inhibitor of RA metabolism, leading to enhanced growth inhibition by RA. Tretinoin 86-88 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-20
9716180-5 1998 Interestingly, CYP26 activity was efficiently inhibited by liarozole, an inhibitor of RA metabolism, leading to enhanced growth inhibition by RA. Tretinoin 142-144 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 15-20
9679985-0 1998 Retinoic acid induced mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase-dependent MAP kinase activation needed to elicit HL-60 cell differentiation and growth arrest. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 54-91
9679985-0 1998 Retinoic acid induced mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase-dependent MAP kinase activation needed to elicit HL-60 cell differentiation and growth arrest. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 93-96
9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 98-103
9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 139-144
9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 181-185 BCL2 apoptosis regulator Homo sapiens 98-103
9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 181-185 BCL2 apoptosis regulator Homo sapiens 139-144
9674702-8 1998 Northern analysis confirmed induction of Wnt-13 as a 2.4 kb mRNA during the early phases of retinoic acid-induced differentiation, and during differentiation along a non-neural pathway induced by hexamethylene bisacetamide (HMBA), but not in the terminally differentiated neurons. Tretinoin 92-105 Wnt family member 2B Homo sapiens 41-47
9679985-1 1998 Retinoic acid (RA) activated the extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid differentiation and cell cycle arrest associated with hypophosphorylation of the retinoblastoma (RB) tumor suppressor protein. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 72-75
9679985-1 1998 Retinoic acid (RA) activated the extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid differentiation and cell cycle arrest associated with hypophosphorylation of the retinoblastoma (RB) tumor suppressor protein. Tretinoin 0-13 mitogen-activated protein kinase 1 Homo sapiens 113-117
9679985-1 1998 Retinoic acid (RA) activated the extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid differentiation and cell cycle arrest associated with hypophosphorylation of the retinoblastoma (RB) tumor suppressor protein. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 33-70
9679985-1 1998 Retinoic acid (RA) activated the extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid differentiation and cell cycle arrest associated with hypophosphorylation of the retinoblastoma (RB) tumor suppressor protein. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 72-75
9679985-1 1998 Retinoic acid (RA) activated the extracellular signal-regulated kinase (ERK) 2 mitogen-activated protein kinase (MAPK) of HL-60 human myeloblastic leukemia cells before causing myeloid differentiation and cell cycle arrest associated with hypophosphorylation of the retinoblastoma (RB) tumor suppressor protein. Tretinoin 15-17 mitogen-activated protein kinase 1 Homo sapiens 113-117
9679985-2 1998 ERK2 activation by mitogen-activated protein/ERK kinase (MEK) was necessary for RA-induced differentiation in studies using PD98059 to block MEK phosphorylation. Tretinoin 80-82 mitogen-activated protein kinase 1 Homo sapiens 0-4
9679985-2 1998 ERK2 activation by mitogen-activated protein/ERK kinase (MEK) was necessary for RA-induced differentiation in studies using PD98059 to block MEK phosphorylation. Tretinoin 80-82 mitogen-activated protein kinase 1 Homo sapiens 0-3
9679985-2 1998 ERK2 activation by mitogen-activated protein/ERK kinase (MEK) was necessary for RA-induced differentiation in studies using PD98059 to block MEK phosphorylation. Tretinoin 80-82 mitogen-activated protein kinase kinase 7 Homo sapiens 57-60
9679985-2 1998 ERK2 activation by mitogen-activated protein/ERK kinase (MEK) was necessary for RA-induced differentiation in studies using PD98059 to block MEK phosphorylation. Tretinoin 80-82 mitogen-activated protein kinase kinase 7 Homo sapiens 141-144
9679985-4 1998 Activation of ERK2 by RA occurred within hours and persisted until the onset of RB hypophosphorylation, differentiation, and arrest. Tretinoin 22-24 mitogen-activated protein kinase 1 Homo sapiens 14-18
9679985-5 1998 ERK2 activation was probably needed early, because delaying the addition of PD98059 relative to that of RA restored most of the RA-induced cellular response. Tretinoin 104-106 mitogen-activated protein kinase 1 Homo sapiens 0-4
9679985-5 1998 ERK2 activation was probably needed early, because delaying the addition of PD98059 relative to that of RA restored most of the RA-induced cellular response. Tretinoin 128-130 mitogen-activated protein kinase 1 Homo sapiens 0-4
9679985-7 1998 This is consistent with the need for a nuclear retinoid receptor function in RA-induced ERK2 activation. Tretinoin 77-79 mitogen-activated protein kinase 1 Homo sapiens 88-92
9679985-11 1998 The results thus show that RA augments MEK-dependent ERK2 activation that is needed for subsequent RB hypophosphorylation, cell differentiation, and G0 arrest. Tretinoin 27-29 mitogen-activated protein kinase kinase 7 Homo sapiens 39-42
9679985-11 1998 The results thus show that RA augments MEK-dependent ERK2 activation that is needed for subsequent RB hypophosphorylation, cell differentiation, and G0 arrest. Tretinoin 27-29 mitogen-activated protein kinase 1 Homo sapiens 53-57
9642228-6 1998 RA exerted a synergistic effect when administered with TPA, LPS, or IFN-gamma, whereas IFN-gamma completely suppressed AM production in RAW 264.7 cells stimulated with LPS. Tretinoin 0-2 interferon gamma Mus musculus 68-77
9688937-7 1998 Using conditioned media from RA-treated cells, we provided evidence that the proliferative response of type 2 cells to RA was mediated through production of growth factor(s) distinct from IGF-I. Tretinoin 29-31 insulin like growth factor 1 Homo sapiens 188-193
9692544-1 1998 The results reported here indicate that retinoic acid (RA) induces growth arrest and differentiation only in MyoD-expressing muscle cells. Tretinoin 40-53 myogenic differentiation 1 Homo sapiens 109-113
9692544-1 1998 The results reported here indicate that retinoic acid (RA) induces growth arrest and differentiation only in MyoD-expressing muscle cells. Tretinoin 55-57 myogenic differentiation 1 Homo sapiens 109-113
9692544-2 1998 Transient transfection assays reveal a functional interaction between MyoD, a key myogenic regulator and RA-receptors, principal mediators of RA actions. Tretinoin 105-107 myogenic differentiation 1 Homo sapiens 70-74
9642262-0 1998 Interaction of BAG-1 with retinoic acid receptor and its inhibition of retinoic acid-induced apoptosis in cancer cells. Tretinoin 26-39 BAG cochaperone 1 Homo sapiens 15-20
9642262-3 1998 Gel retardation assays demonstrated that in vitro translated BAG-1 protein could effectively inhibit the binding of RAR but not retinoid X receptor (RXR) to a number of retinoic acid (RA) response elements (RAREs). Tretinoin 169-182 BAG cochaperone 1 Homo sapiens 61-66
9642262-3 1998 Gel retardation assays demonstrated that in vitro translated BAG-1 protein could effectively inhibit the binding of RAR but not retinoid X receptor (RXR) to a number of retinoic acid (RA) response elements (RAREs). Tretinoin 116-118 BAG cochaperone 1 Homo sapiens 61-66
9642262-8 1998 In addition, RA-induced suppression of Bcl-2 expression was abrogated by overexpression of BAG-1. Tretinoin 13-15 BCL2 apoptosis regulator Homo sapiens 39-44
9642262-8 1998 In addition, RA-induced suppression of Bcl-2 expression was abrogated by overexpression of BAG-1. Tretinoin 13-15 BAG cochaperone 1 Homo sapiens 91-96
9688937-8 1998 We also showed that RA was able to reduce the decrease in cell number observed when type 2 cells were treated with transforming growth factor (TGF)-beta1. Tretinoin 20-22 transforming growth factor beta 1 Homo sapiens 115-153
9688937-9 1998 These results together with the known stimulatory effect of TGF-beta1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-beta1 pathway. Tretinoin 112-114 transforming growth factor beta 1 Homo sapiens 60-69
9688937-9 1998 These results together with the known stimulatory effect of TGF-beta1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-beta1 pathway. Tretinoin 112-114 transforming growth factor beta 1 Homo sapiens 204-213
9639524-6 1998 IL-7 and IL-15 also supported the growth of SeAx cells in the presence of the apoptosis inducing agents dexamethasone and retinoic acid. Tretinoin 122-135 interleukin 7 Homo sapiens 0-4
9696418-3 1998 It was clearly demonstrated that two structurally different inhibitors of 5-lipoxygenase metabolism, i.e., 3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-di methyl propanoic acid (MK-886) and esculetin, significantly potentiated the HL-60 cell differentiation induced by retinoic acid or DMSO. Tretinoin 288-301 arachidonate 5-lipoxygenase Homo sapiens 74-88
9662255-0 1998 Effects of retinoic acid and fenretinide on the c-erbB-2 expression, growth and cisplatin sensitivity of breast cancer cells. Tretinoin 11-24 erb-b2 receptor tyrosine kinase 2 Homo sapiens 48-56
9662255-1 1998 We investigated the effects of all-trans retinoic acid (ATRA) and fenretinide (4-HPR) on c-erbB-2 expression in SK-BR-3, BT-474 and MCF-7 breast cancer cells and on the growth, differentiation, apoptosis and cisplatin (CDDP) sensitivity of SK-BR-3 cells. Tretinoin 41-54 erb-b2 receptor tyrosine kinase 2 Homo sapiens 89-97
9662255-1 1998 We investigated the effects of all-trans retinoic acid (ATRA) and fenretinide (4-HPR) on c-erbB-2 expression in SK-BR-3, BT-474 and MCF-7 breast cancer cells and on the growth, differentiation, apoptosis and cisplatin (CDDP) sensitivity of SK-BR-3 cells. Tretinoin 56-60 erb-b2 receptor tyrosine kinase 2 Homo sapiens 89-97
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 70-83 interleukin 4 Homo sapiens 156-169
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 70-83 interleukin 4 Homo sapiens 171-175
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 70-83 interferon gamma Homo sapiens 181-197
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 70-83 interferon gamma Homo sapiens 199-208
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 85-87 interleukin 4 Homo sapiens 156-169
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 85-87 interleukin 4 Homo sapiens 171-175
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 85-87 interferon gamma Homo sapiens 181-197
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 85-87 interferon gamma Homo sapiens 199-208
11189515-0 1998 [Expression of interleukin-8 and its receptor in acute promyelocytic leukemia under all-trans retinoic acid treatment]. Tretinoin 94-107 C-X-C motif chemokine ligand 8 Homo sapiens 15-28
11189515-1 1998 OBJECTIVE: To evaluate the clinical significance of expression of interleukin-(IL-8) and its type A receptor(IL-8RA) in acute promyelocytic leukemia(APL) patients under all trans-retinoic acid(ATRA) induction. Tretinoin 173-192 C-X-C motif chemokine ligand 8 Homo sapiens 79-83
11189515-1 1998 OBJECTIVE: To evaluate the clinical significance of expression of interleukin-(IL-8) and its type A receptor(IL-8RA) in acute promyelocytic leukemia(APL) patients under all trans-retinoic acid(ATRA) induction. Tretinoin 193-197 C-X-C motif chemokine ligand 8 Homo sapiens 79-83
11189515-9 1998 CONCLUSION: ATRA inhibited IL-8 secretion of APL cells while increased the expression of IL-8RA. Tretinoin 12-16 C-X-C motif chemokine ligand 8 Homo sapiens 27-31
9696418-9 1998 The results implied that either modulation of 5-lipoxygenase metabolism or a certain type of imbalance in arachidonic acid metabolism could modulate the effects of retinoic acid or DMSO on myeloid cell differentiation. Tretinoin 164-177 arachidonate 5-lipoxygenase Homo sapiens 46-60
9667638-6 1998 Treatment with cytotoxic drug (colchicine) or retinoic acid (RA) resulted in a slight increase in P-gp activity in the parental and RAR alpha-infected melanoma cells, whereas the increase in P-gp function in the infected hepatoma cells (both human and rat) was very prominent. Tretinoin 46-59 ATP binding cassette subfamily B member 1 Homo sapiens 98-102
9667638-6 1998 Treatment with cytotoxic drug (colchicine) or retinoic acid (RA) resulted in a slight increase in P-gp activity in the parental and RAR alpha-infected melanoma cells, whereas the increase in P-gp function in the infected hepatoma cells (both human and rat) was very prominent. Tretinoin 46-59 ATP binding cassette subfamily B member 1 Homo sapiens 191-195
9667638-6 1998 Treatment with cytotoxic drug (colchicine) or retinoic acid (RA) resulted in a slight increase in P-gp activity in the parental and RAR alpha-infected melanoma cells, whereas the increase in P-gp function in the infected hepatoma cells (both human and rat) was very prominent. Tretinoin 61-63 ATP binding cassette subfamily B member 1 Homo sapiens 98-102
9667638-6 1998 Treatment with cytotoxic drug (colchicine) or retinoic acid (RA) resulted in a slight increase in P-gp activity in the parental and RAR alpha-infected melanoma cells, whereas the increase in P-gp function in the infected hepatoma cells (both human and rat) was very prominent. Tretinoin 61-63 ATP binding cassette subfamily B member 1 Homo sapiens 191-195
9667638-8 1998 These data imply that the activation of the RA-controlled signalling pathway up-regulates MDR1 gene expression. Tretinoin 44-46 ATP binding cassette subfamily B member 1 Homo sapiens 90-94
9664142-8 1998 The most striking difference between the cell lines was a strong downregulation of transforming growth factor-beta (TGF-beta) expression in cell lines derived from metastases when treated with RA in contrast to cell lines from primary melanomas. Tretinoin 193-195 transforming growth factor beta 1 Homo sapiens 83-114
9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 BCL2 apoptosis regulator Homo sapiens 185-190
9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 BCL2 associated X, apoptosis regulator Homo sapiens 205-208
9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 transforming growth factor beta 1 Homo sapiens 213-246
9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 transforming growth factor beta 1 Homo sapiens 248-257
9649125-1 1998 The potent mitogenic activity of insulin-like growth factor I (IGF-I) on breast epithelium is inhibited by retinoic acid in oestrogen receptor-positive (ER+) breast cancer cell lines. Tretinoin 107-120 insulin like growth factor 1 Homo sapiens 33-61
9649125-1 1998 The potent mitogenic activity of insulin-like growth factor I (IGF-I) on breast epithelium is inhibited by retinoic acid in oestrogen receptor-positive (ER+) breast cancer cell lines. Tretinoin 107-120 insulin like growth factor 1 Homo sapiens 63-68
9669677-5 1998 We have shown that ATRA activates IRF-1 gene expression in several myeloid leukemia cell lines (HL-60, NB4, THP-1, U937), all of which respond to ATRA by growth inhibition. Tretinoin 19-23 interferon regulatory factor 1 Homo sapiens 34-39
9669677-5 1998 We have shown that ATRA activates IRF-1 gene expression in several myeloid leukemia cell lines (HL-60, NB4, THP-1, U937), all of which respond to ATRA by growth inhibition. Tretinoin 19-23 GLI family zinc finger 2 Homo sapiens 108-113
9669677-5 1998 We have shown that ATRA activates IRF-1 gene expression in several myeloid leukemia cell lines (HL-60, NB4, THP-1, U937), all of which respond to ATRA by growth inhibition. Tretinoin 146-150 interferon regulatory factor 1 Homo sapiens 34-39
9669677-5 1998 We have shown that ATRA activates IRF-1 gene expression in several myeloid leukemia cell lines (HL-60, NB4, THP-1, U937), all of which respond to ATRA by growth inhibition. Tretinoin 146-150 GLI family zinc finger 2 Homo sapiens 108-113
9669677-6 1998 In addition, during ATRA-induced myeloid differentiation, gene expression of STAT1, STAT2, and p48 was upregulated. Tretinoin 20-24 interferon regulatory factor 9 Homo sapiens 95-98
9620283-2 1998 Several investigators have recently reported that ATRA downregulates the production of interleukin-6 (IL-6) and the expression of IL-6 receptor (IL-6R) and also inhibits the proliferation of myeloma cells. Tretinoin 50-54 interleukin 6 Homo sapiens 87-100
9620283-2 1998 Several investigators have recently reported that ATRA downregulates the production of interleukin-6 (IL-6) and the expression of IL-6 receptor (IL-6R) and also inhibits the proliferation of myeloma cells. Tretinoin 50-54 interleukin 6 Homo sapiens 102-106
9620283-2 1998 Several investigators have recently reported that ATRA downregulates the production of interleukin-6 (IL-6) and the expression of IL-6 receptor (IL-6R) and also inhibits the proliferation of myeloma cells. Tretinoin 50-54 interleukin 6 receptor Homo sapiens 130-143
9620283-2 1998 Several investigators have recently reported that ATRA downregulates the production of interleukin-6 (IL-6) and the expression of IL-6 receptor (IL-6R) and also inhibits the proliferation of myeloma cells. Tretinoin 50-54 interleukin 6 receptor Homo sapiens 145-150
9620283-7 1998 Flow cytometry analysis revealed that the mean fluorescence intensity of bcl-2 protein was slightly decreased in cells treated with ATRA. Tretinoin 132-136 BCL2 apoptosis regulator Homo sapiens 73-78
9620283-8 1998 These results indicate that in U266B1 cells, combined treatment with anti-Fas mAb and ATRA enhances the induction of apoptosis by modulating the expression of Fas and bcl-2 by ATRA. Tretinoin 86-90 BCL2 apoptosis regulator Homo sapiens 167-172
9603996-2 1998 They were induced and colocalized in the cytoplasm and in lesser amounts in the nucleus when THP-1 and HL-60 cells were induced to differentiate by 1alpha,25-dihydroxyvitamin D3 or retinoic acid. Tretinoin 181-194 GLI family zinc finger 2 Homo sapiens 93-98
9664142-8 1998 The most striking difference between the cell lines was a strong downregulation of transforming growth factor-beta (TGF-beta) expression in cell lines derived from metastases when treated with RA in contrast to cell lines from primary melanomas. Tretinoin 193-195 transforming growth factor beta 1 Homo sapiens 116-124
9607768-0 1998 Distinct roles of the co-activators p300 and CBP in retinoic-acid-induced F9-cell differentiation. Tretinoin 52-65 CREB binding protein Homo sapiens 45-48
9593676-7 1998 Furthermore, treatment of F9 murine teratocarcinoma (F9) cells with 10(-6) M all-trans-retinoic acid increased TR4 mRNA levels, and this change was accompanied by an increased amount of endogenous TR4 protein that can bind to RXRE in electrophoretic mobility shift assay. Tretinoin 81-100 nuclear receptor subfamily 2, group C, member 2 Mus musculus 111-114
9593676-7 1998 Furthermore, treatment of F9 murine teratocarcinoma (F9) cells with 10(-6) M all-trans-retinoic acid increased TR4 mRNA levels, and this change was accompanied by an increased amount of endogenous TR4 protein that can bind to RXRE in electrophoretic mobility shift assay. Tretinoin 81-100 nuclear receptor subfamily 2, group C, member 2 Mus musculus 197-200
9593676-8 1998 Our data therefore strongly suggest that the retinoid signal pathway can be regulated by TR4 in a negative feedback control mechanism, which may restrict retinoic acid signaling to certain elements in a cell-specific fashion. Tretinoin 154-167 nuclear receptor subfamily 2 group C member 2 Homo sapiens 89-92
9633525-1 1998 The heparin-binding growth-associated molecule HB-GAM (also named pleiotrophin) and the retinoic acid-induced heparin-binding protein RIHB (chicken midkine) are developmentally regulated proteins forming a new family of heparin-binding molecules with putative functions during cell growth and differentiation. Tretinoin 88-101 midkine (neurite growth-promoting factor 2) Gallus gallus 134-138
9607768-7 1998 Similarly, retinoic-acid-induced transcriptional upregulation of the cell-cycle inhibitor p21Cip1 required normal levels of p300, but not CBP, whereas the reverse was true for p27Kip1. Tretinoin 11-24 cyclin dependent kinase inhibitor 1A Homo sapiens 90-97
9607768-7 1998 Similarly, retinoic-acid-induced transcriptional upregulation of the cell-cycle inhibitor p21Cip1 required normal levels of p300, but not CBP, whereas the reverse was true for p27Kip1. Tretinoin 11-24 CREB binding protein Homo sapiens 138-141
9605760-0 1998 Glial cell line-derived neurotrophic factor/neurturin-induced differentiation and its enhancement by retinoic acid in primary human neuroblastomas expressing c-Ret, GFR alpha-1, and GFR alpha-2. Tretinoin 101-114 glial cell derived neurotrophic factor Homo sapiens 0-43
9617548-0 1998 Modulation of basic fibroblast growth factor effect by retinoic acid in cultured retinal pigment epithelium. Tretinoin 55-68 fibroblast growth factor 2 Homo sapiens 14-44
9619634-0 1998 Contrasting levels of p21ras activation and expression of neurofibromin in peripheral primitive neuroectodermal tumour and neuroblastoma cells, and their response to retinoic acid. Tretinoin 166-179 neurofibromin 1 Homo sapiens 58-71
9619634-8 1998 Retinoic acid (RA)-induced differentiation and growth inhibition of neuroblastoma cells was associated with an increase in type 1 GAP120 and neurofibromin mRNA, and a decrease in p21ras-GTP. Tretinoin 0-13 neurofibromin 1 Homo sapiens 141-154
9619634-8 1998 Retinoic acid (RA)-induced differentiation and growth inhibition of neuroblastoma cells was associated with an increase in type 1 GAP120 and neurofibromin mRNA, and a decrease in p21ras-GTP. Tretinoin 15-17 neurofibromin 1 Homo sapiens 141-154
9606960-0 1998 Characterization of the cytochrome P450 CYP2J4: expression in rat small intestine and role in retinoic acid biotransformation from retinal. Tretinoin 94-107 cytochrome P450, family 2, subfamily j, polypeptide 4 Rattus norvegicus 40-46
9606960-6 1998 We determined that purified, heterologously expressed CYP2J4 is active toward all-trans- and 9-cis-retinal in reconstituted systems, producing the corresponding retinoic acids as the major products. Tretinoin 161-175 cytochrome P450, family 2, subfamily j, polypeptide 4 Rattus norvegicus 54-60
9606960-9 1998 Rat enterocyte microsomes were also active with all-trans-retinal to produce all-trans-retinoic acid in the presence of NADPH, and the majority of retinoic acid synthesis activity was inhibited by the polyclonal anti-CYP2J4 antibody. Tretinoin 77-100 cytochrome P450, family 2, subfamily j, polypeptide 4 Rattus norvegicus 217-223
9606960-10 1998 These findings suggest that CYP2J4 plays a major role in intestinal microsomal metabolism of retinal to retinoic acid and may be involved in the maintenance of retinoid homeostasis in the small intestine in vivo. Tretinoin 104-117 cytochrome P450, family 2, subfamily j, polypeptide 4 Rattus norvegicus 28-34
9558392-6 1998 ATRA treatment also led to downregulation of bcl-2 and endogenous RARalpha in PML-RARalpha-expressing cells, but had little effect on the level of exogenously expressed PML-RARalpha. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 45-50
9558392-7 1998 We conclude that (1) subtle differences exist in the biologic activities of the L and S isoforms of PML-RARalpha, and (2) both isoforms are capable of transducing an ATRA-mediated signal that leads to downregulation of bcl-2 and induction of programmed cell death. Tretinoin 166-170 BCL2 apoptosis regulator Homo sapiens 219-224
9617548-1 1998 PURPOSE: We investigated the effect of retinoic acid (RA) on basic fibroblast growth factor (bFGF)-stimulated proliferation of cultured human retinal pigment epithelial (hRPE) cells and of 125I-bFGF-binding to the bFGF plasma membrane receptors of hRPE. Tretinoin 39-52 fibroblast growth factor 2 Homo sapiens 61-91
9617548-1 1998 PURPOSE: We investigated the effect of retinoic acid (RA) on basic fibroblast growth factor (bFGF)-stimulated proliferation of cultured human retinal pigment epithelial (hRPE) cells and of 125I-bFGF-binding to the bFGF plasma membrane receptors of hRPE. Tretinoin 39-52 fibroblast growth factor 2 Homo sapiens 93-97
9617548-1 1998 PURPOSE: We investigated the effect of retinoic acid (RA) on basic fibroblast growth factor (bFGF)-stimulated proliferation of cultured human retinal pigment epithelial (hRPE) cells and of 125I-bFGF-binding to the bFGF plasma membrane receptors of hRPE. Tretinoin 54-56 fibroblast growth factor 2 Homo sapiens 61-91
9617548-1 1998 PURPOSE: We investigated the effect of retinoic acid (RA) on basic fibroblast growth factor (bFGF)-stimulated proliferation of cultured human retinal pigment epithelial (hRPE) cells and of 125I-bFGF-binding to the bFGF plasma membrane receptors of hRPE. Tretinoin 54-56 fibroblast growth factor 2 Homo sapiens 93-97
9617548-5 1998 RA inhibited bFGF-stimulated 3H-thymidine incorporation in the presence or absence of heparin. Tretinoin 0-2 fibroblast growth factor 2 Homo sapiens 13-17
9635256-8 1998 During the early stages of differentiation, expression of iNOS (RA+) and eNOS (RA-) was very low, indicating that the expression of these two isoforms was not only dependent on the presence or absence of RA, but also on the degree of differentiation. Tretinoin 64-66 nitric oxide synthase 2 Homo sapiens 58-62
9635256-10 1998 Four days of RA treatment of RA- cultures, which reverses the squamous phenotype and restores mucous differentiation, induced iNOS expression in a concentration-dependent manner. Tretinoin 13-15 nitric oxide synthase 2 Homo sapiens 126-130
9579536-4 1998 The induction of the human PLC-gamma1 VDRE by 1,25(OH)2D3 was synergistic with all-trans retinoic acid in normal human keratinocytes, but none of the constructs was induced by 1,25(OH)2D3 and/or all-trans retinoic acid in SCC4 and SCC12B2 cells. Tretinoin 89-102 phospholipase C gamma 1 Homo sapiens 27-37
9659296-9 1998 However, retinoic acid (10(-6) M) stimulated both IGFBP-2 and IGFBP-6 protein and mRNA levels, but it decreased IGFBP-3 mRNA levels relative to controls. Tretinoin 9-22 insulin like growth factor binding protein 2 Bos taurus 50-57
9659296-18 1998 In addition, the differential regulation of IGFBP-2, -3 and -6 by retinoic acid (which inhibits proliferation) and IGF-I (which stimulates proliferation) suggests that these forms of IGFBP have different roles in regulating mammary epithelial cell physiology. Tretinoin 66-79 insulin like growth factor binding protein 2 Bos taurus 44-62
9659296-18 1998 In addition, the differential regulation of IGFBP-2, -3 and -6 by retinoic acid (which inhibits proliferation) and IGF-I (which stimulates proliferation) suggests that these forms of IGFBP have different roles in regulating mammary epithelial cell physiology. Tretinoin 66-79 insulin like growth factor binding protein 2 Bos taurus 44-49
9659286-0 1998 Differential effects of retinoic acid on uncoupling protein-1 and leptin gene expression. Tretinoin 24-37 uncoupling protein 1 Rattus norvegicus 41-61
9659286-1 1998 All-trans-retinoic acid (RA), one of the active metabolites of vitamin A, can increase the expression of uncoupling protein-1 (UCP1) gene. Tretinoin 0-23 uncoupling protein 1 Rattus norvegicus 105-131
9659286-1 1998 All-trans-retinoic acid (RA), one of the active metabolites of vitamin A, can increase the expression of uncoupling protein-1 (UCP1) gene. Tretinoin 25-27 uncoupling protein 1 Rattus norvegicus 105-131
9659286-7 1998 RA treatment also significantly increased UCP1 mRNA levels but to a lesser extent than CGP 12177. Tretinoin 0-2 uncoupling protein 1 Rattus norvegicus 42-46
9659286-13 1998 This involvement of RA in positive regulation of UCP1 mRNA and negative regulation of leptin mRNA suggests a contrasting role for RA in energy homeostasis. Tretinoin 20-22 uncoupling protein 1 Rattus norvegicus 49-53
9579536-4 1998 The induction of the human PLC-gamma1 VDRE by 1,25(OH)2D3 was synergistic with all-trans retinoic acid in normal human keratinocytes, but none of the constructs was induced by 1,25(OH)2D3 and/or all-trans retinoic acid in SCC4 and SCC12B2 cells. Tretinoin 205-218 phospholipase C gamma 1 Homo sapiens 27-37
9531596-4 1998 We show that ATRA selectively inhibited LPS induction of TF expression in human monocytes and monocytic THP-1 cells without affecting LPS induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8). Tretinoin 13-17 C-X-C motif chemokine ligand 8 Homo sapiens 210-214
9609098-6 1998 Pretreatment of both control and experimental groups with RA enhanced epidermal growth factor-induced proliferation despite RA-dependent downregulation of epidermal growth factor receptor expression. Tretinoin 124-126 epidermal growth factor receptor Homo sapiens 155-187
9555083-9 1998 Furthermore, they demonstrate that RA can directly act on hepatocytes and differently affect Apo A-I and Apo A-II gene expression. Tretinoin 35-37 apolipoprotein A2 Rattus norvegicus 105-113
9599015-3 1998 Retinoic acid exerted synergistic effects on AM secretion from THP-1 and HL-60 cells when administered with tumor necrosis factor-alpha, lipopolysaccharide or 12-O-tetradecanoyl phorbol-13-acetate. Tretinoin 0-13 GLI family zinc finger 2 Homo sapiens 63-68
9599015-3 1998 Retinoic acid exerted synergistic effects on AM secretion from THP-1 and HL-60 cells when administered with tumor necrosis factor-alpha, lipopolysaccharide or 12-O-tetradecanoyl phorbol-13-acetate. Tretinoin 0-13 tumor necrosis factor Homo sapiens 108-135
9502726-6 1998 The in vitro differentiation with retinoic acid and cAMP led to a 5- to 10-fold induction of flk-1, von Willebrand Factor (vWF), TM, GATA-4 and GATA-6. Tretinoin 34-47 GATA binding protein 4 Mus musculus 133-139
9516142-9 1998 Finally, treatment with atRA or the combination of CD367 and CD2425, but not with CD367 or CD2425 alone, was also shown to trigger apoptosis in RPMI 8226 cells, with prominent accumulation of TGase II immunoreactivity in apoptotic cells. Tretinoin 24-28 C-type lectin domain family 4 member A Homo sapiens 51-56
9516145-0 1998 Restoration of retinoid sensitivity by MDR1 ribozymes in retinoic acid-resistant myeloid leukemic cells. Tretinoin 57-70 ATP binding cassette subfamily B member 1 Homo sapiens 39-43
9516145-8 1998 Interestingly, RA inhibited cellular proliferation and induced differentiation of HL-60R/196Rz cells in a dose-dependent manner, suggesting reversal of drug resistance in HL-60R cells by the MDR1 ribozyme. Tretinoin 15-17 ATP binding cassette subfamily B member 1 Homo sapiens 191-195
9516145-9 1998 These data are direct evidence that P-glycoprotein/MDR1 is responsible in part for acquired resistance to RA in myeloid leukemic cells. Tretinoin 106-108 ATP binding cassette subfamily B member 1 Homo sapiens 51-55
9752294-7 1998 RA causes the induction and secretion of IFN alpha. Tretinoin 0-2 interferon alpha 1 Homo sapiens 41-50
9516142-1 1998 In this study, we show that both all-trans-retinoic acid (atRA) and 9-cis-retinoic acid (9-cis-RA) are potent inducers of tissue transglutaminase (TGase II), an enzyme involved in apoptosis, at the level of both enzyme activity and mRNA in the human myeloma cell line RPMI 8226. Tretinoin 33-56 transglutaminase 2 Homo sapiens 122-145
9516142-1 1998 In this study, we show that both all-trans-retinoic acid (atRA) and 9-cis-retinoic acid (9-cis-RA) are potent inducers of tissue transglutaminase (TGase II), an enzyme involved in apoptosis, at the level of both enzyme activity and mRNA in the human myeloma cell line RPMI 8226. Tretinoin 58-62 transglutaminase 2 Homo sapiens 122-145
9516142-6 1998 Moreover, when used in combination with atRA, CD367 partially inhibited the atRA-dependent induction of TGase II, whereas CD2425 enhanced it. Tretinoin 76-80 C-type lectin domain family 4 member A Homo sapiens 46-51
9492050-6 1998 However, the retinoic acid response of the 716-bp dio1 5" flanking region is unaffected by elimination of TRE2 but is lost with mutations in TRE1. Tretinoin 13-26 iodothyronine deiodinase 1 Homo sapiens 50-54
9579827-3 1998 Liarozole-fumarate is an anti-tumour drug that inhibits the cytochrome P450-dependent catabolism of ATRA. Tretinoin 100-104 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 60-75
9507016-0 1998 All-trans-retinoic acid inhibits Jun N-terminal kinase-dependent signaling pathways. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 33-54
9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 41-62
9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 0-23 mitogen-activated protein kinase 8 Homo sapiens 64-67
9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 25-29 mitogen-activated protein kinase 8 Homo sapiens 41-62
9507016-5 1998 All-trans-retinoic acid (t-RA) inhibited Jun N-terminal kinase (JNK) and, to a lesser extent, extracellular signal-regulated kinase activity in normal HBE cells. Tretinoin 25-29 mitogen-activated protein kinase 8 Homo sapiens 64-67
9488655-3 1998 PML function was essential for the tumor-growth-suppressive activity of retinoic acid (RA) and for its ability to induce terminal myeloid differentiation of precursor cells. Tretinoin 72-85 promyelocytic leukemia Mus musculus 0-3
9488655-3 1998 PML function was essential for the tumor-growth-suppressive activity of retinoic acid (RA) and for its ability to induce terminal myeloid differentiation of precursor cells. Tretinoin 87-89 promyelocytic leukemia Mus musculus 0-3
9488655-4 1998 PML was needed for the RA-dependent transactivation of the p21WAF1/CIP1 gene, which regulates cell cycle progression and cellular differentiation. Tretinoin 23-25 promyelocytic leukemia Mus musculus 0-3
9533531-13 1998 Declines in the serum insulin-like growth factor I concentrations observed in patients treated with tamoxifen and ATRA were similar to those observed in patients treated with tamoxifen alone. Tretinoin 114-118 insulin like growth factor 1 Homo sapiens 22-50
9488655-5 1998 These results indicate that PML is a critical component of the RA pathway and that disruption of its activity by the PML-RARalpha fusion protein may be important in APL pathogenesis. Tretinoin 63-65 promyelocytic leukemia Mus musculus 28-31
9473220-6 1998 In vitro retinoic acid-induced differentiation of the premyeloid line HL-60 into granulocyte-like cells mimics the suppression of PrPC in granulocyte differentiation, as both PrPC mRNA and protein are downregulated. Tretinoin 9-22 prion protein Homo sapiens 130-134
9473220-6 1998 In vitro retinoic acid-induced differentiation of the premyeloid line HL-60 into granulocyte-like cells mimics the suppression of PrPC in granulocyte differentiation, as both PrPC mRNA and protein are downregulated. Tretinoin 9-22 prion protein Homo sapiens 175-179
9473220-8 1998 Additionally, retinoic acid-induced extinction of PrPC expression in HL-60 cells provides a potential model to study PrP gene regulation and protein function. Tretinoin 14-27 prion protein Homo sapiens 50-54
9473220-8 1998 Additionally, retinoic acid-induced extinction of PrPC expression in HL-60 cells provides a potential model to study PrP gene regulation and protein function. Tretinoin 14-27 prion protein Homo sapiens 50-53
9533545-6 1998 The combined effects of 8-Cl-cAMP and RA on the induction of growth arrest at the G0-G1 stage of the cell cycle, apoptosis, down-regulation of RIalpha, and cleavage of poly(ADP-ribose) polymerase were synergistic. Tretinoin 38-40 poly(ADP-ribose) polymerase 1 Homo sapiens 168-195
9566306-5 1998 Here we report that the level of tyrosine-phosphorylated Stat3 decreases rapidly during differentiation induced by treatment of ES1 cells either with retinoic acid (RA) or by withdrawal of LIF. Tretinoin 150-163 signal transducer and activator of transcription 3 Mus musculus 57-62
9533957-5 1998 Further, we show that XAG-2 signaling depends on an intact fibroblast growth factor (FGF) signal transduction pathway and that XAG-2-induced anterior neural fate of ectodermal cells can be transformed to a more posterior character by retinoic acid. Tretinoin 234-247 anterior gradient 1 L homeolog Xenopus laevis 22-27
9619915-5 1998 ATRA enhanced neutrophilic maturation in liquid cultures of both normal and myelodysplastic CD34 + ve cells, as detected by conventional morphology and acquisition of CD15. Tretinoin 0-4 CD34 molecule Homo sapiens 92-96
9619915-5 1998 ATRA enhanced neutrophilic maturation in liquid cultures of both normal and myelodysplastic CD34 + ve cells, as detected by conventional morphology and acquisition of CD15. Tretinoin 0-4 fucosyltransferase 4 Homo sapiens 167-171
9533957-5 1998 Further, we show that XAG-2 signaling depends on an intact fibroblast growth factor (FGF) signal transduction pathway and that XAG-2-induced anterior neural fate of ectodermal cells can be transformed to a more posterior character by retinoic acid. Tretinoin 234-247 anterior gradient 1 L homeolog Xenopus laevis 127-132
9564181-0 1998 The cloning and characterization of a novel cytochrome P450 family, CYP26, with specificity toward retinoic acid. Tretinoin 99-112 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 68-73
9564181-2 1998 CYP26 displays specificity toward retinoic acid and it may function as an important regulator or differentiation and a possible modulator of disease states by controlling retinoid concentration and homeostasis. Tretinoin 34-47 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
9511735-4 1998 In contrast, NaPA was able to specifically activate a reporter gene construct (delta SV beta RE-CAT) which contains a retinoic acid response element (RARE beta) that is located in the RAR beta promoter. Tretinoin 118-131 retinoic acid receptor beta Homo sapiens 184-192
9500212-8 1998 The results demonstrated that expression of the RARbeta gene resulted in increased sensitivity of the hepatoma cells to the antiproliferative effect of retinoic acid (RA). Tretinoin 152-165 retinoic acid receptor, beta Rattus norvegicus 48-55
9505268-6 1998 In addition, RA inhibited several features of DEX-induced accelerated maturation, such as: 1) the increased levels of SP-A, SP-B, and CC10 mRNAs; 2) the attenuation of mesenchymal tissue; and 3) the mature distribution of cells expressing SP-C mRNA. Tretinoin 13-15 surfactant protein A1 Rattus norvegicus 118-122
9505268-6 1998 In addition, RA inhibited several features of DEX-induced accelerated maturation, such as: 1) the increased levels of SP-A, SP-B, and CC10 mRNAs; 2) the attenuation of mesenchymal tissue; and 3) the mature distribution of cells expressing SP-C mRNA. Tretinoin 13-15 secretoglobin family 1A member 1 Rattus norvegicus 134-138
9505268-6 1998 In addition, RA inhibited several features of DEX-induced accelerated maturation, such as: 1) the increased levels of SP-A, SP-B, and CC10 mRNAs; 2) the attenuation of mesenchymal tissue; and 3) the mature distribution of cells expressing SP-C mRNA. Tretinoin 13-15 surfactant protein C Rattus norvegicus 239-243
9610845-0 1998 Retinoic acid suppresses interleukin-6 synthesis induced by prostaglandins in osteoblasts. Tretinoin 0-13 interleukin 6 Mus musculus 25-38
9610845-2 1998 Retinoic acid inhibited the IL-6 synthesis induced by PGF2alpha or PGE1 in a dose-dependent manner in the range between 0.1 and 10 nM. Tretinoin 0-13 interleukin 6 Mus musculus 28-32
9610845-3 1998 Retinoic acid also suppressed the IL-6 synthesis stimulated by 12-O-tetradecanoylphorbol-13-acetate, an activator of protein kinase C. The IL-6 synthesis induced by cholera toxin, forskolin or dibutyryl cAMP was inhibited by retinoic acid. Tretinoin 0-13 interleukin 6 Mus musculus 34-38
9610845-3 1998 Retinoic acid also suppressed the IL-6 synthesis stimulated by 12-O-tetradecanoylphorbol-13-acetate, an activator of protein kinase C. The IL-6 synthesis induced by cholera toxin, forskolin or dibutyryl cAMP was inhibited by retinoic acid. Tretinoin 0-13 interleukin 6 Mus musculus 139-143
9610845-3 1998 Retinoic acid also suppressed the IL-6 synthesis stimulated by 12-O-tetradecanoylphorbol-13-acetate, an activator of protein kinase C. The IL-6 synthesis induced by cholera toxin, forskolin or dibutyryl cAMP was inhibited by retinoic acid. Tretinoin 225-238 interleukin 6 Mus musculus 139-143
9610845-5 1998 These results indicate that retinoic acid inhibits IL-6 synthesis induced by prostaglandins in osteoblasts as follows: the inhibitory effect on the PGE1-induced IL-6 synthesis is exerted at a point downstream from cAMP, and the inhibitory effect on the PGF2alpha-induced IL-6 synthesis is exerted at a point downstream from protein kinase C. Tretinoin 28-41 interleukin 6 Mus musculus 51-55
9610845-5 1998 These results indicate that retinoic acid inhibits IL-6 synthesis induced by prostaglandins in osteoblasts as follows: the inhibitory effect on the PGE1-induced IL-6 synthesis is exerted at a point downstream from cAMP, and the inhibitory effect on the PGF2alpha-induced IL-6 synthesis is exerted at a point downstream from protein kinase C. Tretinoin 28-41 interleukin 6 Mus musculus 161-165
9610845-5 1998 These results indicate that retinoic acid inhibits IL-6 synthesis induced by prostaglandins in osteoblasts as follows: the inhibitory effect on the PGE1-induced IL-6 synthesis is exerted at a point downstream from cAMP, and the inhibitory effect on the PGF2alpha-induced IL-6 synthesis is exerted at a point downstream from protein kinase C. Tretinoin 28-41 interleukin 6 Mus musculus 161-165
9500977-0 1998 Ectopic expression of DAN enhances the retinoic acid-induced neuronal differentiation in human neuroblastoma cell lines. Tretinoin 39-52 NBL1, DAN family BMP antagonist Homo sapiens 22-25
9500977-6 1998 The forced expression of DAN gene enhanced the neurite extension in the presence of RA, suggesting that DAN gene product might contain some regulatory role(s) in the RA-induced cellular differentiation in neuroblastoma cells. Tretinoin 84-86 NBL1, DAN family BMP antagonist Homo sapiens 25-28
9511735-6 1998 Taken together, our findings suggest that induction of RAR beta by NaPA is regulated at the level of transcription and mediated through the retinoic acid response element, RARE beta. Tretinoin 140-153 retinoic acid receptor beta Homo sapiens 55-63
9486851-4 1998 Constitutive expression of PKCalpha or inhibition of PKCbeta expression in F9 stem cells enhanced RA induced differentiation, both by increasing total expression and accelerating RA-induced expression of laminins A, B1, B2, and type IV collagen. Tretinoin 98-100 protein kinase C alpha Homo sapiens 27-35
9484784-5 1998 Although U937 cells expressing WT1 were hampered in their ability to differentiate on incubation with retinoic acid and vitamin D3, the induced G1/G0-accumulation was similar to differentiating control cells treated with inducers. Tretinoin 102-115 WT1 transcription factor Homo sapiens 31-34
9473310-0 1998 Human MDR1 and mouse mdr1a P-glycoprotein alter the cellular retention and disposition of erythromycin, but not of retinoic acid or benzo(a)pyrene. Tretinoin 115-128 ATP-binding cassette, sub-family B (MDR/TAP), member 1B Mus musculus 6-10
9486851-4 1998 Constitutive expression of PKCalpha or inhibition of PKCbeta expression in F9 stem cells enhanced RA induced differentiation, both by increasing total expression and accelerating RA-induced expression of laminins A, B1, B2, and type IV collagen. Tretinoin 179-181 protein kinase C alpha Homo sapiens 27-35
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen activator, urokinase Homo sapiens 138-141
9645394-1 1998 When differentiated into mature macrophages by the combination of all-trans retinoic acid and 1,25-dihydroxyvitamin D3, the human promonocytic cell lines U937 and THP-1 expressed inducible nitric oxide synthase (iNOS) transcripts. Tretinoin 76-89 GLI family zinc finger 2 Homo sapiens 163-168
9645394-1 1998 When differentiated into mature macrophages by the combination of all-trans retinoic acid and 1,25-dihydroxyvitamin D3, the human promonocytic cell lines U937 and THP-1 expressed inducible nitric oxide synthase (iNOS) transcripts. Tretinoin 76-89 nitric oxide synthase 2 Homo sapiens 179-210
9458362-0 1998 Retinoic acid suppresses insulin-induced cell growth and cyclin D1 gene expression in human breast cancer cells. Tretinoin 0-13 insulin Homo sapiens 25-32
9458362-1 1998 We examined the effects of all-trans retinoic acid (RA) on the insulin-induced cell growth, cell cycle progression and cyclin D1 gene expression in breast cancer cells. Tretinoin 37-50 insulin Homo sapiens 63-70
9458362-1 1998 We examined the effects of all-trans retinoic acid (RA) on the insulin-induced cell growth, cell cycle progression and cyclin D1 gene expression in breast cancer cells. Tretinoin 52-54 insulin Homo sapiens 63-70
9458362-2 1998 RA exerted a dose-dependent growth inhibition on insulin-induced proliferation in T47D and MCF-7 hormone-dependent cell lines, whereas MDA-MB231 hormone-independent cells were not affected. Tretinoin 0-2 insulin Homo sapiens 49-56
9458362-3 1998 The RA antagonism of insulin growth effect was associated with an inhibition of cell cycle progression and a suppression of insulin-induced cyclin D1 mRNA. Tretinoin 4-6 insulin Homo sapiens 21-28
9458362-4 1998 The effect of RA on cyclin D1 mRNA was dose-dependent and was observed within 5 h of treatment when insulin response was maximal. Tretinoin 14-16 insulin Homo sapiens 100-107
9478049-6 1998 This phenomenon is due to changing levels of the retinoic acid precursor retinaldehyde, which is released from illuminated rhodopsin, thus providing a mechanism by which light can directly influence gene expression. Tretinoin 49-62 rhodopsin Homo sapiens 123-132
9478049-8 1998 The light-induced release of retinaldehyde from rhodopsin, which occurs only in vertebrate but not invertebrate photoreceptors, may have accelerated the rapid evolution of retinoic acid-mediated transcriptional regulation at the transition from invertebrates to vertebrates, and it may explain the prominent role of retinoic acid in the eye. Tretinoin 172-185 rhodopsin Homo sapiens 48-57
9478049-8 1998 The light-induced release of retinaldehyde from rhodopsin, which occurs only in vertebrate but not invertebrate photoreceptors, may have accelerated the rapid evolution of retinoic acid-mediated transcriptional regulation at the transition from invertebrates to vertebrates, and it may explain the prominent role of retinoic acid in the eye. Tretinoin 316-329 rhodopsin Homo sapiens 48-57
9519778-4 1998 In our earlier study we found that treatment of APL cells with RA results in changes in urokinase (uPA) production. Tretinoin 63-65 plasminogen activator, urokinase Homo sapiens 99-102
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen activator, urokinase Homo sapiens 213-216
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 192-194 plasminogen activator, urokinase Homo sapiens 213-216
9462740-0 1998 Distinct interactions of PML-RARalpha and PLZF-RARalpha with co-repressors determine differential responses to RA in APL. Tretinoin 29-31 promyelocytic leukemia Mus musculus 25-28
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 192-194 plasminogen activator, urokinase Homo sapiens 213-216
9462740-2 1998 We have generated PML-RARA and PLZF-RARA transgenic mice and show here that these fusion proteins play a critical role in leukaemogenesis and in determining responses to RA in APL, because PLZF-RARA transgenic mice develop RA-resistant leukaemia, while PML-RARA mice are responsive to RA treatment. Tretinoin 22-24 promyelocytic leukemia Mus musculus 18-21
9462740-2 1998 We have generated PML-RARA and PLZF-RARA transgenic mice and show here that these fusion proteins play a critical role in leukaemogenesis and in determining responses to RA in APL, because PLZF-RARA transgenic mice develop RA-resistant leukaemia, while PML-RARA mice are responsive to RA treatment. Tretinoin 24-26 promyelocytic leukemia Mus musculus 18-21
9511764-7 1998 Further, we demonstrate a decrease in the activity of the isolated human IP3R-I promoter and of the endogenous IP3R-I promoter after 48 h of treatment with retinoic acid. Tretinoin 156-169 inositol 1,4,5-trisphosphate receptor type 1 Homo sapiens 73-79
9462740-4 1998 PLZF-RARalpha, but not PML-RARalpha, can form, via its PLZF moiety, co-repressor complexes which are insensitive to RA. Tretinoin 5-7 zinc finger and BTB domain containing 16 Mus musculus 0-4
9462740-4 1998 PLZF-RARalpha, but not PML-RARalpha, can form, via its PLZF moiety, co-repressor complexes which are insensitive to RA. Tretinoin 5-7 zinc finger and BTB domain containing 16 Mus musculus 55-59
9462740-5 1998 Histone deacetylase inhibitors such as Trichostatin A (TSA), in combination with RA, can overcome the transcriptional repressor activity of PML-RARalpha and PLZF-RARalpha as well as the unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA. Tretinoin 81-83 promyelocytic leukemia Mus musculus 140-143
9462740-5 1998 Histone deacetylase inhibitors such as Trichostatin A (TSA), in combination with RA, can overcome the transcriptional repressor activity of PML-RARalpha and PLZF-RARalpha as well as the unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA. Tretinoin 81-83 zinc finger and BTB domain containing 16 Mus musculus 157-161
9462740-5 1998 Histone deacetylase inhibitors such as Trichostatin A (TSA), in combination with RA, can overcome the transcriptional repressor activity of PML-RARalpha and PLZF-RARalpha as well as the unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA. Tretinoin 81-83 zinc finger and BTB domain containing 16 Mus musculus 206-210
9511764-7 1998 Further, we demonstrate a decrease in the activity of the isolated human IP3R-I promoter and of the endogenous IP3R-I promoter after 48 h of treatment with retinoic acid. Tretinoin 156-169 inositol 1,4,5-trisphosphate receptor type 1 Homo sapiens 111-117
9442073-4 1998 Treatment of human neuroblastoma SH-SY5Y cells with retinoic acid (RA) resulted in a significant increase in tTG levels and in vitro TG activity. Tretinoin 52-65 transglutaminase 2 Homo sapiens 109-112
9442029-5 1998 The interaction between eIF-5A and TGase is specific for the GDP-bound form of the TGase and is not detected when the TGase is pre-loaded with GTP gamma S. The TGase-eIF-5A interaction also is promoted by Ca2+, Mg2+, and RA treatment of HeLa cells. Tretinoin 221-223 coagulation factor XIII A chain Homo sapiens 35-40
9442029-5 1998 The interaction between eIF-5A and TGase is specific for the GDP-bound form of the TGase and is not detected when the TGase is pre-loaded with GTP gamma S. The TGase-eIF-5A interaction also is promoted by Ca2+, Mg2+, and RA treatment of HeLa cells. Tretinoin 221-223 coagulation factor XIII A chain Homo sapiens 83-88
9442029-5 1998 The interaction between eIF-5A and TGase is specific for the GDP-bound form of the TGase and is not detected when the TGase is pre-loaded with GTP gamma S. The TGase-eIF-5A interaction also is promoted by Ca2+, Mg2+, and RA treatment of HeLa cells. Tretinoin 221-223 coagulation factor XIII A chain Homo sapiens 83-88
9442029-5 1998 The interaction between eIF-5A and TGase is specific for the GDP-bound form of the TGase and is not detected when the TGase is pre-loaded with GTP gamma S. The TGase-eIF-5A interaction also is promoted by Ca2+, Mg2+, and RA treatment of HeLa cells. Tretinoin 221-223 coagulation factor XIII A chain Homo sapiens 83-88
9442029-6 1998 In the presence of retinoic acid, millimolar levels of Ca2+ are no longer required for the TGase-eIF-5A interaction. Tretinoin 19-32 coagulation factor XIII A chain Homo sapiens 91-96
9442029-8 1998 The interaction between TGase and eIF-5A and its sensitivity to the nucleotide-occupied state of the TGase provides a potentially interesting connection between RA signaling and protein synthesis and/or RNA trafficking activities. Tretinoin 161-163 coagulation factor XIII A chain Homo sapiens 24-29
9442029-8 1998 The interaction between TGase and eIF-5A and its sensitivity to the nucleotide-occupied state of the TGase provides a potentially interesting connection between RA signaling and protein synthesis and/or RNA trafficking activities. Tretinoin 161-163 coagulation factor XIII A chain Homo sapiens 101-106
9442073-4 1998 Treatment of human neuroblastoma SH-SY5Y cells with retinoic acid (RA) resulted in a significant increase in tTG levels and in vitro TG activity. Tretinoin 67-69 transglutaminase 2 Homo sapiens 109-112
9457077-11 1998 By super-shift assays using specific anti-RAR and -RXR antibodies, RA treatment decreased the amount of RXR alpha while increasing the amount RAR beta bound to retinoic acid response element-DR1 (direct repeat with spacer of one nucleotide), indicating the levels of RAR/RXR heterodimer, RXR/RXR homodimer, or RAR/RAR homodimers were altered upon RA treatment of Hep3B cells. Tretinoin 42-44 retinoic acid receptor beta Homo sapiens 142-150
9436983-7 1998 The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. Tretinoin 157-170 protein kinase C alpha Homo sapiens 92-114
9436983-7 1998 The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. Tretinoin 157-170 protein kinase C alpha Homo sapiens 116-125
9436983-7 1998 The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. Tretinoin 172-174 protein kinase C alpha Homo sapiens 92-114
9436983-7 1998 The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. Tretinoin 172-174 protein kinase C alpha Homo sapiens 116-125
9457077-1 1998 Retinoic acid (RA) up-regulates retinoic acid receptor beta (RAR beta) gene expression in a variety of cell lines. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 32-59
9457077-1 1998 Retinoic acid (RA) up-regulates retinoic acid receptor beta (RAR beta) gene expression in a variety of cell lines. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 61-69
9462716-8 1998 Exposure to the combination of IFN-gamma plus retinoic acid significantly up-regulated (in an additive manner) HLA-Class-I and ICAM-1 molecules as compared with the levels obtainable after exposure to IFN-gamma alone. Tretinoin 46-59 interferon gamma Homo sapiens 201-210
9464546-5 1998 Furthermore, the RA-inducible expression of MyoD gene is lost in C2-dnRXR but not in C2-dnRAR cells, indicating that each family of retinoid receptors RAR and RXR may regulate distinct subsets of RA-responsive genes. Tretinoin 17-19 myogenic differentiation 1 Homo sapiens 44-48
9457077-1 1998 Retinoic acid (RA) up-regulates retinoic acid receptor beta (RAR beta) gene expression in a variety of cell lines. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 32-59
9488162-3 1998 Treatment of cultured cardiomyocytes and retinal and ciliary ganglion neurons with retinoic acid resulted in increased expression of receptors for the neuropoietic cytokine, CNTF. Tretinoin 83-96 ciliary neurotrophic factor Gallus gallus 174-178
9457077-1 1998 Retinoic acid (RA) up-regulates retinoic acid receptor beta (RAR beta) gene expression in a variety of cell lines. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 61-69
9457077-3 1998 In F9 teratocarcinoma cell line, RA-induced differentiation is accompanied by increased expression of the RAR beta, RXR alpha, and alpha-fetoprotein (AFP) genes. Tretinoin 33-35 retinoic acid receptor beta Homo sapiens 106-114
9457077-3 1998 In F9 teratocarcinoma cell line, RA-induced differentiation is accompanied by increased expression of the RAR beta, RXR alpha, and alpha-fetoprotein (AFP) genes. Tretinoin 33-35 alpha fetoprotein Homo sapiens 131-148
9457077-3 1998 In F9 teratocarcinoma cell line, RA-induced differentiation is accompanied by increased expression of the RAR beta, RXR alpha, and alpha-fetoprotein (AFP) genes. Tretinoin 33-35 alpha fetoprotein Homo sapiens 150-153
9457077-6 1998 In this paper, we have examined the RA-mediated regulation of the RAR, RXR, peroxisome proliferator-activated receptor (PPAR), and AFP genes in Hep3B cells. Tretinoin 36-38 alpha fetoprotein Homo sapiens 131-134
9488162-4 1998 All-trans-retinoic acid induced as much as a 3-fold increase in CNTF receptor alpha subunit mRNA in a time and concentration dependent manner and resulted in an enhanced CNTF-induced tyrosine phosphorylation of the transcription factor, STAT3. Tretinoin 0-23 ciliary neurotrophic factor Gallus gallus 64-68
9488162-4 1998 All-trans-retinoic acid induced as much as a 3-fold increase in CNTF receptor alpha subunit mRNA in a time and concentration dependent manner and resulted in an enhanced CNTF-induced tyrosine phosphorylation of the transcription factor, STAT3. Tretinoin 0-23 ciliary neurotrophic factor Gallus gallus 170-174
9488162-4 1998 All-trans-retinoic acid induced as much as a 3-fold increase in CNTF receptor alpha subunit mRNA in a time and concentration dependent manner and resulted in an enhanced CNTF-induced tyrosine phosphorylation of the transcription factor, STAT3. Tretinoin 0-23 signal transducer and activator of transcription 3 Gallus gallus 237-242
9488162-5 1998 These results indicate that neurons and myocytes expressing CNTF receptors are responsive to retinoic acid and suggest that retinoids may regulate cell sensitivity to cytokines during development. Tretinoin 93-106 ciliary neurotrophic factor Gallus gallus 60-64
9588080-0 1998 [Production of IL-8 by the THP-1 monocyte cell line is regulated differently by cyclosporin and retinoic acid]. Tretinoin 96-109 C-X-C motif chemokine ligand 8 Homo sapiens 15-19
9458794-7 1998 Despite Dex, RA increased both RAR-beta and SP-C mRNA. Tretinoin 13-15 sparse coat Mus musculus 44-48
9588080-0 1998 [Production of IL-8 by the THP-1 monocyte cell line is regulated differently by cyclosporin and retinoic acid]. Tretinoin 96-109 GLI family zinc finger 2 Homo sapiens 27-32
9443626-8 1998 RESULTS: After 14 days of ATRA therapy, the activities of CYP2E1 (chlorzoxazone hydroxylase) and N-acetyltransferase (in fast acetylators only) were increased by 83% and 29% (P < 0.05), respectively. Tretinoin 26-30 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 58-64
9588080-7 1998 The aim of the experiment was to find out CsA effect and RA effect on production of IL-8 by THP-1 cell line. Tretinoin 57-59 C-X-C motif chemokine ligand 8 Homo sapiens 84-88
9588080-7 1998 The aim of the experiment was to find out CsA effect and RA effect on production of IL-8 by THP-1 cell line. Tretinoin 57-59 GLI family zinc finger 2 Homo sapiens 92-97
9588080-12 1998 RA promotes IL-8 production by stimulated THP-1 monocyte cell line in dose dependence course. Tretinoin 0-2 C-X-C motif chemokine ligand 8 Homo sapiens 12-16
9588080-12 1998 RA promotes IL-8 production by stimulated THP-1 monocyte cell line in dose dependence course. Tretinoin 0-2 GLI family zinc finger 2 Homo sapiens 42-47
9438427-4 1998 We have previously identified a 10 bp element, called CE2, which is located approximately 3 kilobases 3" of the Hoxa1 coding region in the RAIDR5 enhancer, and which binds to an approximately 170 kd protein in retinoic acid treated P19 embryonal carcinoma cells. Tretinoin 210-223 catalase activity, kidney Mus musculus 54-57
9792954-0 1998 Regulation of renal parathyroid hormone receptor expression by 1, 25-dihydroxyvitamin D3 and retinoic acid. Tretinoin 93-106 parathyroid hormone Homo sapiens 20-39
9857269-4 1998 Recently, a novel cytochrome P450 enzyme (CYP26) with specific RA 4-hydroxylase activity, which is rapidly induced by RA, has been cloned from man, mouse and zebra fish, fullfilling all requirements of an enzyme which could be of crucial importance in controlling steady-state levels of active retinoids in cells and target tissues, thus protecting against excessive exposure. Tretinoin 63-65 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 42-47
9600389-3 1998 In this study we investigated whether the well-known retinoic acid-induced differentiation of ES cells into neurons (identified by immunostaining for neuron-specific enolase and synaptophysin) was accompanied by cells expressing astroglial (GFAP), oligodendroglial (O4), and microglial (5C6, galectin-3) markers. Tretinoin 53-66 lectin, galactose binding, soluble 3 Mus musculus 292-302
9865544-6 1998 NIS mRNA expression can be up-regulated by retinoic acid in human thyroid carcinoma cell lines whereas retinoic acid treatment decreases NIS expression and function in differentiated rat thyroid FRTL-5 cells. Tretinoin 43-56 solute carrier family 5 member 5 Homo sapiens 0-3
9865544-6 1998 NIS mRNA expression can be up-regulated by retinoic acid in human thyroid carcinoma cell lines whereas retinoic acid treatment decreases NIS expression and function in differentiated rat thyroid FRTL-5 cells. Tretinoin 103-116 solute carrier family 5 member 5 Homo sapiens 137-140
9597752-0 1998 Forced expression of hic-5, a senescence-related gene, potentiates a differentiation process of RCT-1 cells induced by retinoic acid. Tretinoin 119-132 transforming growth factor beta 1 induced transcript 1 Rattus norvegicus 21-26
9597752-2 1998 Previous studies of rat calvarial cells stimulated to differentiate by addition of retinoic acid (R.A.) showed a four-fold increase in hic-5 expression which preceded an increase in the expression of the differentiation markers, alkaline phosphatase and alpha (I) pro-collagen mRNA. Tretinoin 83-96 transforming growth factor beta 1 induced transcript 1 Rattus norvegicus 135-140
9434781-0 1997 Midkine, a retinoic acid-inducible heparin-binding cytokine, is a novel regulator of intracellular calcium in human neutrophils. Tretinoin 11-24 midkine Homo sapiens 0-7
9613452-7 1998 Treating SUIT-2 cells with retinoic acid also induced the upregulation of E-cadherin expression. Tretinoin 27-40 cadherin 1 Homo sapiens 74-84
9701452-4 1998 In vitro studies have reported that ATRA caused downregulation of tissue factor and upregulation of thrombomodulin (TM) on endothelial cells as well as APL cells. Tretinoin 36-40 thrombomodulin Rattus norvegicus 100-114
9701452-4 1998 In vitro studies have reported that ATRA caused downregulation of tissue factor and upregulation of thrombomodulin (TM) on endothelial cells as well as APL cells. Tretinoin 36-40 thrombomodulin Rattus norvegicus 116-118
9701452-9 1998 Fibrin deposition in renal glomeruli was inhibited by ATRA administration, with an increase in the intensity of immunohistochemical TM staining. Tretinoin 54-58 thrombomodulin Rattus norvegicus 132-134
9397150-7 1998 A similar pattern was observed for TGase protein, but, RA, which, by itself, reduced INV, markedly enhanced the ability of 1,25(OH)2D3 to raise INV levels, possibly by inhibiting 1,25(OH)2D3-stimulated TGase activity and cross-linking of soluble INV into the insoluble cornified envelope (CE). Tretinoin 55-57 involucrin Homo sapiens 85-88
9397150-7 1998 A similar pattern was observed for TGase protein, but, RA, which, by itself, reduced INV, markedly enhanced the ability of 1,25(OH)2D3 to raise INV levels, possibly by inhibiting 1,25(OH)2D3-stimulated TGase activity and cross-linking of soluble INV into the insoluble cornified envelope (CE). Tretinoin 55-57 involucrin Homo sapiens 144-147
9397150-7 1998 A similar pattern was observed for TGase protein, but, RA, which, by itself, reduced INV, markedly enhanced the ability of 1,25(OH)2D3 to raise INV levels, possibly by inhibiting 1,25(OH)2D3-stimulated TGase activity and cross-linking of soluble INV into the insoluble cornified envelope (CE). Tretinoin 55-57 involucrin Homo sapiens 144-147
9718082-8 1998 An increase in the level of immunophenotypic expression of wild type p53 was also noted after treatment with all trans retinoic acid and 9-cis retinoic acid. Tretinoin 119-132 tumor protein p53 Homo sapiens 69-72
9769475-0 1998 Cytoskeletal reorganization induced by retinoic acid treatment of human endometrial adenocarcinoma (RL95-2) cells is correlated with alterations in protein kinase C-alpha. Tretinoin 39-52 protein kinase C alpha Homo sapiens 148-170
9769475-7 1998 We then investigated whether retinoic acid affected the subcellular localization of PKC-alpha. Tretinoin 29-42 protein kinase C alpha Homo sapiens 84-93
9769475-9 1998 Retinoic acid treatment dramatically altered PKC-alpha localization, since a more distinct cytoplasmic and perinuclear staining pattern was apparent. Tretinoin 0-13 protein kinase C alpha Homo sapiens 45-54
9769475-10 1998 Western blot analysis confirmed these results, since the amount of cytosolic PKC-alpha increased following retinoic acid treatment. Tretinoin 107-120 protein kinase C alpha Homo sapiens 77-86
9769475-11 1998 Thus, retinoic-acid-induced endometrial differentiation may be associated with alterations in PKC-alpha localization and signaling. Tretinoin 6-19 protein kinase C alpha Homo sapiens 94-103
9425271-5 1997 GD3 synthase (alpha 2,8-sialyltransferase, SAT-II) and GD3 synthase mRNA, as analyzed by Northern blotting, were also markedly present in aggregates and neurons induced by RA. Tretinoin 172-174 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 Mus musculus 0-12
9405615-7 1997 We demonstrate here that the D2 receptor promoter contains a functional retinoic acid response element. Tretinoin 72-85 dopamine receptor D2 Mus musculus 29-40
9570357-4 1997 Our previous work has shown that RA works synergistically with other agents, such as interferon-gamma (IFN-gamma), to down-regulate N-myc expression and induce differentiation. Tretinoin 33-35 interferon gamma Homo sapiens 85-101
9570357-4 1997 Our previous work has shown that RA works synergistically with other agents, such as interferon-gamma (IFN-gamma), to down-regulate N-myc expression and induce differentiation. Tretinoin 33-35 interferon gamma Homo sapiens 103-112
9425271-5 1997 GD3 synthase (alpha 2,8-sialyltransferase, SAT-II) and GD3 synthase mRNA, as analyzed by Northern blotting, were also markedly present in aggregates and neurons induced by RA. Tretinoin 172-174 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 Mus musculus 14-41
9425271-5 1997 GD3 synthase (alpha 2,8-sialyltransferase, SAT-II) and GD3 synthase mRNA, as analyzed by Northern blotting, were also markedly present in aggregates and neurons induced by RA. Tretinoin 172-174 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 Mus musculus 55-67
9425271-8 1997 On the other hand, the level of GQ1b synthase (alpha 2,8-sialyltransferase, SAT-V) in RA-induced aggregates was significantly higher than that in neurons. Tretinoin 86-88 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 Mus musculus 47-74
9425271-9 1997 These results show that RA but not DMSO induces the expression of GM3, GD3, GT1b and GQ1b synthases, and particularly GD3 synthase mRNA, in the ganglioside biosynthetic pathway during the neural differentiation of embryonic carcinoma P19 cells. Tretinoin 24-26 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 Mus musculus 118-130
9441693-7 1997 In addition, we demonstrate that the FGF-4-/- ES cells can differentiate in vitro after exposure to retinoic acid; however, the growth and/or survival of the differentiated cells is severely compromised. Tretinoin 100-113 fibroblast growth factor 4 Mus musculus 37-42
9389530-4 1997 IGF-1 also decreased PRL and GH-mRNA response to T3, retinoic acid, and Fk in GH3 cells. Tretinoin 53-66 prolactin Rattus norvegicus 21-24
9428648-0 1997 Evidence for a posttranscriptional effect of retinoic acid on connexin43 gene expression via the 3"-untranslated region. Tretinoin 45-58 gap junction protein, alpha 1 Mus musculus 62-72
9398535-8 1997 These results indicate that RI58 is induced by retinoic acid stimulation through autocrinally secreted IFN-alpha from NB4 cells. Tretinoin 47-60 interferon alpha 1 Homo sapiens 103-112
16465284-9 1997 Treatment with IFN-gamma+TNF induced GI-LI-N cells to show only a late and remarkable increase of alpha1/beta1 heterodimer; on the contrary, RA treatment caused a decrease in all integrin chains. Tretinoin 141-143 interferon gamma Homo sapiens 15-24
16465284-9 1997 Treatment with IFN-gamma+TNF induced GI-LI-N cells to show only a late and remarkable increase of alpha1/beta1 heterodimer; on the contrary, RA treatment caused a decrease in all integrin chains. Tretinoin 141-143 tumor necrosis factor Homo sapiens 25-28
9559292-6 1997 Chromogranin A was expressed by TM87-16 only after treatment with either TPA or RA. Tretinoin 80-82 chromogranin A Homo sapiens 0-14
9428648-1 1997 All-trans retinoic acid (10(-7) M) induces cell-cell communication and the expression of the gap junction protein connexin43 in mouse F9 teratocarcinoma cells. Tretinoin 10-23 gap junction protein, alpha 1 Mus musculus 114-124
9420627-1 1997 The expression of the major histocompatibility complex (MHC) class I antigens is suppressed in early post-implantation embryonic cells as well as in embryonal carcinoma (EC) cells, but could be upregulated by treatment with interferon (IFN)-gamma or retinoic acid. Tretinoin 250-263 interferon gamma Homo sapiens 224-246
9447832-0 1997 Induction of thrombospondin-1 by all-trans retinoic acid modulates growth and differentiation of HL-60 myeloid leukemia cells. Tretinoin 43-56 thrombospondin 1 Homo sapiens 13-29
9447832-2 1997 The expression of TSP was studied in the human myeloid leukemia cell line, HL-60, upon differentiation into monocytes by phorbol-13-monoacetate (PMA) or into granulocytes by all-trans retinoic acid (RA). Tretinoin 184-197 thrombospondin 1 Homo sapiens 18-21
9447832-2 1997 The expression of TSP was studied in the human myeloid leukemia cell line, HL-60, upon differentiation into monocytes by phorbol-13-monoacetate (PMA) or into granulocytes by all-trans retinoic acid (RA). Tretinoin 199-201 thrombospondin 1 Homo sapiens 18-21
9447832-4 1997 In contrast, RA at 10(-7) M induced a 5- to 10-fold increase in TSP secreted by HL-60 cells during their differentiation into granulocytes over a 5 day period. Tretinoin 13-15 thrombospondin 1 Homo sapiens 64-67
9447832-5 1997 The role of secreted TSP in RA-dependent cessation of growth and differentiation was examined using blocking anti-TSP antibodies. Tretinoin 28-30 thrombospondin 1 Homo sapiens 21-24
9447832-6 1997 In the presence of the polyclonal anti-TSP antibody R5 (25 microg/ml), growth of RA-treated HL-60 cells was maintained at control levels for up to 3 days and a concomitant delay in granulocytic differentiation was observed. Tretinoin 81-83 thrombospondin 1 Homo sapiens 39-42
9504902-7 1997 Serum levels of TNF-alpha 1 h after LPS administration were significantly lower in the ATRA-treated group (60.5+/-7.0 ng/mL) as compared with the control group (105.2+/-39.3 ng/mL; P< 0.05). Tretinoin 87-91 tumor necrosis factor Rattus norvegicus 16-25
11039015-7 1997 The relation between the elevation of PC-PLD and protein kinases was further studied and discovered that ATRA decreased both the specific activities of membrane bound and cytosolic protein kinase C (PKC) as well as tyrosine protein kinase (TPK) either in 2nd or 4th day of cell culture, which indicated that the increasing effect of ATRA on membrane bound PC-PLD was not resulted from the stimulating effect of PKC and TPK on PC-PLD, and its mechanism remains to be further investigated. Tretinoin 105-109 proline rich transmembrane protein 2 Homo sapiens 199-202
11039015-7 1997 The relation between the elevation of PC-PLD and protein kinases was further studied and discovered that ATRA decreased both the specific activities of membrane bound and cytosolic protein kinase C (PKC) as well as tyrosine protein kinase (TPK) either in 2nd or 4th day of cell culture, which indicated that the increasing effect of ATRA on membrane bound PC-PLD was not resulted from the stimulating effect of PKC and TPK on PC-PLD, and its mechanism remains to be further investigated. Tretinoin 105-109 proline rich transmembrane protein 2 Homo sapiens 411-422
9398056-0 1997 Retinoic acid-enhanced invasion through reconstituted basement membrane by human SK-N-SH neuroblastoma cells involves membrane-associated tissue-type plasminogen activator. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 138-171
11039015-7 1997 The relation between the elevation of PC-PLD and protein kinases was further studied and discovered that ATRA decreased both the specific activities of membrane bound and cytosolic protein kinase C (PKC) as well as tyrosine protein kinase (TPK) either in 2nd or 4th day of cell culture, which indicated that the increasing effect of ATRA on membrane bound PC-PLD was not resulted from the stimulating effect of PKC and TPK on PC-PLD, and its mechanism remains to be further investigated. Tretinoin 333-337 proline rich transmembrane protein 2 Homo sapiens 199-202
9398654-3 1997 However, in follicular thyroid carcinoma cell lines FTC-133 and FTC-238, treatment with 1 microM all-trans retinoic acid (RA) markedly increased NIS mRNA levels. Tretinoin 107-120 solute carrier family 5 member 5 Rattus norvegicus 145-148
9398654-3 1997 However, in follicular thyroid carcinoma cell lines FTC-133 and FTC-238, treatment with 1 microM all-trans retinoic acid (RA) markedly increased NIS mRNA levels. Tretinoin 122-124 solute carrier family 5 member 5 Rattus norvegicus 145-148
9398056-2 1997 In contrast to basal invasion, which was urokinase (uPA)- and plasmin-dependent, RA-enhanced invasion was dependent on tissue-type plasminogen activator (t-PA) and plasmin activity. Tretinoin 81-83 plasminogen activator, tissue type Homo sapiens 119-152
9398056-2 1997 In contrast to basal invasion, which was urokinase (uPA)- and plasmin-dependent, RA-enhanced invasion was dependent on tissue-type plasminogen activator (t-PA) and plasmin activity. Tretinoin 81-83 plasminogen activator, tissue type Homo sapiens 154-158
9398056-6 1997 RA stimulated the association of t-PA with the external cell membrane surface, which could be inhibited by heparin sulphate but not by mannose sugars or chelators of divalent cations, consistent with a role for amphoterin. Tretinoin 0-2 plasminogen activator, tissue type Homo sapiens 33-37
9393879-7 1997 RA also inhibits vesicular stomatitis virus replication and induces a higher antiviral state and growth inhibition when combined with IFN. Tretinoin 0-2 interferon alpha 1 Homo sapiens 134-137
9371251-0 1997 Retinoic acid conjugates as potential antitumor agents: synthesis and biological activity of conjugates with Ara-A, Ara-C, 3(2H)-furanone, and aniline mustard moieties. Tretinoin 0-13 ATP binding cassette subfamily C member 6 Homo sapiens 109-112
9371251-0 1997 Retinoic acid conjugates as potential antitumor agents: synthesis and biological activity of conjugates with Ara-A, Ara-C, 3(2H)-furanone, and aniline mustard moieties. Tretinoin 0-13 ATP binding cassette subfamily C member 6 Homo sapiens 116-119
9439808-5 1997 In this study we used the SK-N-AS human neuroblastoma cell line as a model system to study LRP expression during cellular differentiation induced by phorbol esters, retinoic acid and interferon gamma. Tretinoin 165-178 LDL receptor related protein 1 Homo sapiens 91-94
9367872-7 1997 Interestingly, the bfp is induced during retinoic acid-mediated differentiation of P19 embryonal carcinoma cells into neural cells. Tretinoin 41-54 ring finger protein 112 Rattus norvegicus 19-22
9393879-9 1997 Additional mechanisms could be involved as RA increases the level of signal transducing activators of transcription (STAT) proteins, and enhances the IFN-induced STAT activation, suggesting that cooperative effects by RA and IFN are mediated through multiple pathways. Tretinoin 43-45 interferon alpha 1 Homo sapiens 150-154
9393879-9 1997 Additional mechanisms could be involved as RA increases the level of signal transducing activators of transcription (STAT) proteins, and enhances the IFN-induced STAT activation, suggesting that cooperative effects by RA and IFN are mediated through multiple pathways. Tretinoin 43-45 interferon alpha 1 Homo sapiens 150-153
9393879-9 1997 Additional mechanisms could be involved as RA increases the level of signal transducing activators of transcription (STAT) proteins, and enhances the IFN-induced STAT activation, suggesting that cooperative effects by RA and IFN are mediated through multiple pathways. Tretinoin 218-220 interferon alpha 1 Homo sapiens 150-154
9393879-9 1997 Additional mechanisms could be involved as RA increases the level of signal transducing activators of transcription (STAT) proteins, and enhances the IFN-induced STAT activation, suggesting that cooperative effects by RA and IFN are mediated through multiple pathways. Tretinoin 218-220 interferon alpha 1 Homo sapiens 150-153
9366521-1 1997 We have characterized the expression and activity of the cell cycle regulatory machinery and the organization of the cytoskeleton of the p16(Ink4a)-deficient astrocytoma cell line, U343 MG-a (U343), following retinoic acid (RA) treatment. Tretinoin 209-222 cyclin dependent kinase inhibitor 2A Homo sapiens 137-140
9365097-7 1997 Retinoic acid, an agent which induces autodigestion of cartilage in vitro, stimulated only the expression of MMP-13. Tretinoin 0-13 matrix metallopeptidase 13 Homo sapiens 109-115
9815594-7 1997 The expression of Bcl-2 relative to Bax decreased more after combined treatment with cisplatin and ATRA than after either drug alone. Tretinoin 99-103 BCL2 apoptosis regulator Homo sapiens 18-23
9815594-7 1997 The expression of Bcl-2 relative to Bax decreased more after combined treatment with cisplatin and ATRA than after either drug alone. Tretinoin 99-103 BCL2 associated X, apoptosis regulator Homo sapiens 36-39
9367678-3 1997 We isolated mouse and human DDOST cDNAs from retinoic acid-treated mouse P19 EC cells and human NT-2 cells, respectively. Tretinoin 45-58 dolichyl-diphosphooligosaccharide--protein glycosyltransferase non-catalytic subunit Homo sapiens 28-33
9392425-3 1997 The time course of the effect of 10 microM all-trans retinoic acid (at-RA) on apoA-I mRNA levels and protein secretion were comparable, i.e., minor increases were observed after a 24-h incubation and mRNA levels were increased 2.2- and 3.5-fold after 48 h and 72 h, respectively. Tretinoin 43-66 apolipoprotein A1 Homo sapiens 78-84
10322910-0 1997 Tretinoin or retinol enhancement of lymphokine-activated killer cell proliferation and cytotoxicity against human bladder cancer cells in vitro. Tretinoin 0-9 interleukin 2 Homo sapiens 36-46
10322910-1 1997 AIM: To study the effect of tretinoin (Tre) or retinol (Ret) on the proliferation of lymphokine-activated killer (LAK) cells in patients with transitional cell cancer of bladder and their cytolysis to bladder tumor cells. Tretinoin 28-37 interleukin 2 Homo sapiens 85-95
9395064-4 1997 The results demonstrated that among several PTP genes expressed in P19 cells, a cytosolic Src homology region 2 domain-containing PTP, SHP-1, is expressed highly in undifferentiated P19 cells, but is reduced to an undetectable level at day 3 after replating in the presence of RA. Tretinoin 277-279 protein tyrosine phosphatase, receptor type, U Mus musculus 44-47
9395064-4 1997 The results demonstrated that among several PTP genes expressed in P19 cells, a cytosolic Src homology region 2 domain-containing PTP, SHP-1, is expressed highly in undifferentiated P19 cells, but is reduced to an undetectable level at day 3 after replating in the presence of RA. Tretinoin 277-279 protein tyrosine phosphatase, receptor type, U Mus musculus 130-133
9334271-3 1997 Accordingly, Hoxb-8 expression is rapidly induced by retinoic acid (RA) treatment in the anterior of the forelimb in a spatial and temporal manner that is consistent with the induction of Shh and formation of the ZPA. Tretinoin 53-66 homeobox B8 Gallus gallus 13-19
9334271-3 1997 Accordingly, Hoxb-8 expression is rapidly induced by retinoic acid (RA) treatment in the anterior of the forelimb in a spatial and temporal manner that is consistent with the induction of Shh and formation of the ZPA. Tretinoin 68-70 homeobox B8 Gallus gallus 13-19
9334271-4 1997 Furthermore, inhibition of RA synthesis in the flank downregulates the expression of endogenous Hoxb-8 and results in the loss of Shh expression. Tretinoin 27-29 homeobox B8 Gallus gallus 96-102
9334271-8 1997 The anterior AER also secretes an inhibitory factor, preventing RA-induced or already established Hoxb-8 expression in the cells immediately underneath the AER. Tretinoin 64-66 homeobox B8 Gallus gallus 98-104
9404004-1 1997 We have found that the MAL gene, which encodes a membrane proteolipid expressed during the late stages of T-lymphocyte maturation, is also activated during neuronal differentiation of NTERA2 human embryonal carcinoma cells following induction with retinoic acid. Tretinoin 248-261 mal, T cell differentiation protein Homo sapiens 23-26
9404004-3 1997 PCR and Northern blot analysis with a cloned MAL cDNA as a probe confirmed that MAL is not expressed by undifferentiated NTERA2 EC cells, but is expressed, predominantly as a 1.1 kb transcript, within 7 days of retinoic acid-induced differentiation and later in the post-mitotic neurons arising in such cultures. Tretinoin 211-224 mal, T cell differentiation protein Homo sapiens 80-83
9367833-0 1997 Retinoic acid inhibits cell growth in HPV negative cervical carcinoma cells by induction of insulin-like growth factor binding protein-5 (IGFBP-5) secretion. Tretinoin 0-13 insulin like growth factor binding protein 5 Homo sapiens 92-136
9367833-0 1997 Retinoic acid inhibits cell growth in HPV negative cervical carcinoma cells by induction of insulin-like growth factor binding protein-5 (IGFBP-5) secretion. Tretinoin 0-13 insulin like growth factor binding protein 5 Homo sapiens 138-145
9367833-5 1997 Since RA has been shown to modulate the expression of insulin-like growth factor binding proteins (IGFBPs) in many cells, we examined RA regulated expression of IGFBPs in medium isolated from RA treated C33A cells. Tretinoin 6-8 insulin like growth factor binding protein 5 Homo sapiens 99-105
9367833-6 1997 IGFBP-5 was detectable in medium from C33A cells exposed to RA, and addition of purified exogenous IGFBP-5 resulted in growth inhibition of C33A cells. Tretinoin 60-62 insulin like growth factor binding protein 5 Homo sapiens 0-7
9367833-7 1997 These results indicate that RA exerts it"s anti-neoplastic effect in HPV negative cervical carcinoma cells via the overproduction of IGFBP-5. Tretinoin 28-30 insulin like growth factor binding protein 5 Homo sapiens 133-140
9366521-1 1997 We have characterized the expression and activity of the cell cycle regulatory machinery and the organization of the cytoskeleton of the p16(Ink4a)-deficient astrocytoma cell line, U343 MG-a (U343), following retinoic acid (RA) treatment. Tretinoin 209-222 cyclin dependent kinase inhibitor 2A Homo sapiens 141-146
9366521-1 1997 We have characterized the expression and activity of the cell cycle regulatory machinery and the organization of the cytoskeleton of the p16(Ink4a)-deficient astrocytoma cell line, U343 MG-a (U343), following retinoic acid (RA) treatment. Tretinoin 224-226 cyclin dependent kinase inhibitor 2A Homo sapiens 137-140
9366521-1 1997 We have characterized the expression and activity of the cell cycle regulatory machinery and the organization of the cytoskeleton of the p16(Ink4a)-deficient astrocytoma cell line, U343 MG-a (U343), following retinoic acid (RA) treatment. Tretinoin 224-226 cyclin dependent kinase inhibitor 2A Homo sapiens 141-146
9326242-0 1997 Retinoic acid induces aggregation of the acute promyelocytic leukemia cell line NB-4 by utilization of LFA-1 and ICAM-2. Tretinoin 0-13 integrin subunit beta 2 Homo sapiens 103-108
9357979-0 1997 Distinct patterns of all-trans retinoic acid dependent expression of HOXB and HOXC homeogenes in human embryonal and small-cell lung carcinoma cell lines. Tretinoin 31-44 homeobox C cluster Homo sapiens 78-82
9357979-1 1997 The expression patterns of the class I homeogenes HOXB and HOXC clusters in the presence of retinoic acid (RA) were studied in two human small-cell lung cancer (SCLC) cell lines and compared to that of NT2/D1 embryonal carcinoma cells. Tretinoin 92-105 homeobox C cluster Homo sapiens 59-63
9357979-1 1997 The expression patterns of the class I homeogenes HOXB and HOXC clusters in the presence of retinoic acid (RA) were studied in two human small-cell lung cancer (SCLC) cell lines and compared to that of NT2/D1 embryonal carcinoma cells. Tretinoin 107-109 homeobox C cluster Homo sapiens 59-63
9362447-9 1997 RA treatment dramatically induced a DR5-binding RXRalpha-RARbeta heterodimer. Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 57-64
9402847-0 1997 In vitro down-regulation of bcl-2 expression by all-trans retinoic acid in AML blasts. Tretinoin 58-71 BCL2 apoptosis regulator Homo sapiens 28-33
9402847-1 1997 Using flow cytometry, we have investigated the effects of 0.5 microM all-trans-retinoic acid (ATRA) on bcl-2 expression in the blast cells of 25 acute myeloblastic leukemia (AML) patients and the HL-60 cell line after incubation for 6 days. Tretinoin 69-92 BCL2 apoptosis regulator Homo sapiens 103-108
9402847-1 1997 Using flow cytometry, we have investigated the effects of 0.5 microM all-trans-retinoic acid (ATRA) on bcl-2 expression in the blast cells of 25 acute myeloblastic leukemia (AML) patients and the HL-60 cell line after incubation for 6 days. Tretinoin 94-98 BCL2 apoptosis regulator Homo sapiens 103-108
9402847-2 1997 We observed a significant decrease of bcl-2 expression after treatment with ATRA in 12 of 25 AML samples and the HL-60 cells. Tretinoin 76-80 BCL2 apoptosis regulator Homo sapiens 38-43
9402847-3 1997 The mean fluorescence intensity (MFI) ratio for the bcl-2 levels of the ATRA responders (n = 12) was reduced to 7.9 +/- 4.8 following incubation with ATRA compared with 10.9 +/- 6.5 (mean +/- SD) for control samples incubated without ATRA (p = 0.011). Tretinoin 72-76 BCL2 apoptosis regulator Homo sapiens 52-57
9402847-9 1997 Because many chemotherapeutic agents also operate through the activation of programmed cell death and bcl-2 levels are positively associated with resistance to apoptosis, ATRA can be used in combination chemotherapy to increase the chemosensitivity of some patients with AML. Tretinoin 171-175 BCL2 apoptosis regulator Homo sapiens 102-107
9444384-5 1997 The PKC antagonists (H7, sphingosine) as well as RA downregulated the IFN-gamma-induced PNA-reactive gps, whereas staurosporine and TPA upregulated their expression. Tretinoin 49-51 interferon gamma Homo sapiens 70-79
9337135-7 1997 Moreover, if Hoxa-2 is concomitantly induced by retinoic acid in the first branchial arch, the proximal derivatives of this arch are also affected. Tretinoin 48-61 homeobox A2 Mus musculus 13-19
14555966-6 1997 In these stably transfected HeLa cells both the endogenous tissue transglutaminase gene and transfected mouse tissue transglutaminase promoter are activated by all-trans retinoic acid and by retinoic acid receptor (RAR)-specific and retinoid X receptor (RXR)-specific retinoids. Tretinoin 170-183 transglutaminase 2 Homo sapiens 59-82
9328313-7 1997 In in vivo rat models, an RA analog accelerated the porcine serum-induced fibrosis by enhancing TGF-beta contents and, thus, collagen levels in the liver, although the RA analog alone was not fibrogenic. Tretinoin 26-28 transforming growth factor, beta 1 Rattus norvegicus 96-104
9328313-8 1997 These results suggest that RA exacerbated liver fibrosis, at least in part, by inducing the activation and production of latent TGF-beta in liver SCs. Tretinoin 27-29 transforming growth factor, beta 1 Rattus norvegicus 128-136
9414661-0 1997 All-trans-retinoic acid-dependent inhibition of E-cadherin-based cell adhesion with concomitant dephosphorylation of beta-catenin in metastatic human renal carcinoma cells. Tretinoin 0-23 cadherin 1 Homo sapiens 48-58
9414661-5 1997 The clustering induced by ATRA was virtually blocked in the presence of anti-E cadherin antibody. Tretinoin 26-30 cadherin 1 Homo sapiens 77-87
9414661-6 1997 E-Cadherin and beta-catenin were each localized mainly at the cell-cell adherent junctions of colonizing cell populations that had been treated with ATRA. Tretinoin 149-153 cadherin 1 Homo sapiens 0-10
9284950-0 1997 Retinoic acid induced growth arrest of human breast carcinoma cells requires protein kinase C alpha expression and activity. Tretinoin 0-13 protein kinase C alpha Homo sapiens 77-99
9305907-7 1997 Thus, both Galpha12 and Galpha13 are essential to stimulation of cell differentiation by retinoic acid. Tretinoin 89-102 guanine nucleotide binding protein, alpha 12 Mus musculus 11-19
9305908-0 1997 c-Jun amino-terminal kinase is regulated by Galpha12/Galpha13 and obligate for differentiation of P19 embryonal carcinoma cells by retinoic acid. Tretinoin 131-144 guanine nucleotide binding protein, alpha 12 Mus musculus 44-52
9305908-1 1997 Retinoic acid induces P19 mouse embryonal carcinoma cells to differentiate to endoderm and increases expression of the heterotrimeric G-protein subunits Galpha12 and Galpha13. Tretinoin 0-13 guanine nucleotide binding protein, alpha 12 Mus musculus 153-161
9305908-3 1997 Much like retinoic acid, expression of constitutively active forms of Galpha12 and Galpha13 induced differentiation and constitutive activation of c-Jun amino-terminal kinase. Tretinoin 10-23 guanine nucleotide binding protein, alpha 12 Mus musculus 70-78
9305908-5 1997 These data implicate c-Jun amino-terminal kinase as a downstream element of activation of Galpha12 or Galpha13 obligate for retinoic acid-induced differentiation. Tretinoin 124-137 guanine nucleotide binding protein, alpha 12 Mus musculus 90-98
9349427-3 1997 Addition of all-trans retinoic acid increased GJIC in tumor cell lines, augmented expression of connexin 43, and was associated with more efficient GCV-induced in vitro bystander killing in cells transduced with HSVtk via either retrovirus or adenovirus vectors. Tretinoin 22-35 gap junction protein, alpha 1 Mus musculus 96-107
9305907-0 1997 Galpha12 and Galpha13 mediate differentiation of P19 mouse embryonal carcinoma cells in response to retinoic acid. Tretinoin 100-113 guanine nucleotide binding protein, alpha 12 Mus musculus 0-8
9305907-3 1997 The Galpha12 and Galpha13 subunits of heterotrimeric G-proteins are expressed in the embryonal P19 cells and stimulated in response to retinoic acid as the cells differentiate to endodermal or neuroectodermal phenotypes. Tretinoin 135-148 guanine nucleotide binding protein, alpha 12 Mus musculus 4-12
9436034-5 1997 In the present study, all-trans-retionic acid (ATRA) elevated the level of AFP and inhibited the growth of KU-MT cells in vitro. Tretinoin 47-51 alpha fetoprotein Homo sapiens 75-78
9436034-6 1997 ATRA also arrested the cell cycle in G1 and reduced the percentage of the S phase cell in terms of wild type p53, leading to apoptosis in part. Tretinoin 0-4 tumor protein p53 Homo sapiens 109-112
9284950-4 1997 Retinoic acid arrested T-47D proliferation, induced PKC alpha expression and concomitantly repressed PKC zeta expression. Tretinoin 0-13 protein kinase C alpha Homo sapiens 52-61
9284950-5 1997 The changes in PKC alpha and PKC zeta reflect retinoic acid-induced changes in mRNA. Tretinoin 46-59 protein kinase C alpha Homo sapiens 15-24
9379127-5 1997 Retinoids (all-trans-retinoic acid or the isomer 9-cis-retinoic acid) were less effective in limiting MCF-7 cell responsiveness to IGF-I but, in combination with EB1089, a co-operative effect was achieved. Tretinoin 11-34 insulin like growth factor 1 Homo sapiens 131-136
9302644-2 1997 Retinoic acid inhibited cell proliferation one half of control at the concentration 10(-5) M. Retinoic acid exhibited stimulatory effect on elastin synthesis with a maximum stimulation of 2.0-fold at the concentration of 10(-6) M for 24 h treatment. Tretinoin 94-107 elastin Gallus gallus 140-147
9302644-0 1997 Elastin expression is up-regulated by retinoic acid but not by retinol in chick embryonic skin fibroblasts. Tretinoin 38-51 elastin Gallus gallus 0-7
9302644-1 1997 Effects of retinoid derivatives (retinol and retinoic acid) on elastin expression and cell proliferation in chick embryonic skin fibroblasts were studied. Tretinoin 45-58 elastin Gallus gallus 63-70
9302644-2 1997 Retinoic acid inhibited cell proliferation one half of control at the concentration 10(-5) M. Retinoic acid exhibited stimulatory effect on elastin synthesis with a maximum stimulation of 2.0-fold at the concentration of 10(-6) M for 24 h treatment. Tretinoin 0-13 elastin Gallus gallus 140-147
9302644-3 1997 Elastin level detected by Western blot analysis in the pooled conditioned medium was compatible with the increase of elastin synthesis by retinoic acid treatment. Tretinoin 138-151 elastin Gallus gallus 0-7
9302644-3 1997 Elastin level detected by Western blot analysis in the pooled conditioned medium was compatible with the increase of elastin synthesis by retinoic acid treatment. Tretinoin 138-151 elastin Gallus gallus 117-124
9280059-0 1997 Expression of the parathyroid hormone-related peptide gene in retinoic acid-induced differentiation: involvement of ETS and Sp1. Tretinoin 62-75 parathyroid hormone-like peptide Mus musculus 18-53
9302644-4 1997 Comparable increase in elastin mRNA level was observed by retinoic acid treatment. Tretinoin 58-71 elastin Gallus gallus 23-30
9271417-11 1997 In addition, ERR alpha efficiently represses retinoic acid induction mediated by NRRE-1. Tretinoin 45-58 estrogen related receptor alpha Homo sapiens 13-22
9210065-10 1997 CONCLUSION: These results suggest: a) a therapeutic effect of ATRA in combination with cytosine arabinoside in patients with relapsing malignant gliomas b) that intratumoral calcifications are related to the effects of ATRA on differentiation and/or on endothelial t-PA production and that these effects explain the tumor progression arrest in responder patients. Tretinoin 62-66 plasminogen activator, tissue type Homo sapiens 265-269
9280059-1 1997 Differentiation of P19 embryonal carcinoma (EC) and embryonal stem (ES)-5 cells with retinoic acid (RA) induces expression of PTH-related peptide (PTHrP) mRNA. Tretinoin 85-98 parathyroid hormone-like peptide Mus musculus 126-145
9280059-1 1997 Differentiation of P19 embryonal carcinoma (EC) and embryonal stem (ES)-5 cells with retinoic acid (RA) induces expression of PTH-related peptide (PTHrP) mRNA. Tretinoin 85-98 parathyroid hormone-like peptide Mus musculus 147-152
9280059-1 1997 Differentiation of P19 embryonal carcinoma (EC) and embryonal stem (ES)-5 cells with retinoic acid (RA) induces expression of PTH-related peptide (PTHrP) mRNA. Tretinoin 100-102 parathyroid hormone-like peptide Mus musculus 126-145
9280059-1 1997 Differentiation of P19 embryonal carcinoma (EC) and embryonal stem (ES)-5 cells with retinoic acid (RA) induces expression of PTH-related peptide (PTHrP) mRNA. Tretinoin 100-102 parathyroid hormone-like peptide Mus musculus 147-152
9280059-7 1997 Mutations in either of the Ets-binding sites or the Sp1-binding site completely abolished RA-induced expression of PTHrP promoter reporter constructs, indicating that the RA effect was dependent on the simultaneous action of both Ets- and Sp1-like activities. Tretinoin 90-92 parathyroid hormone-like peptide Mus musculus 115-120
9280059-7 1997 Mutations in either of the Ets-binding sites or the Sp1-binding site completely abolished RA-induced expression of PTHrP promoter reporter constructs, indicating that the RA effect was dependent on the simultaneous action of both Ets- and Sp1-like activities. Tretinoin 171-173 parathyroid hormone-like peptide Mus musculus 115-120
9281352-8 1997 We have also studied the effect of the selective RA analogs on tTG activity. Tretinoin 49-51 transglutaminase 2 Homo sapiens 63-66
9276450-1 1997 The role of retinoic acids (RA) on liver fatty acid-binding protein (L-FABP) expression was investigated in the well differentiated FAO rat hepatoma cell line. Tretinoin 12-26 fatty acid binding protein 1 Rattus norvegicus 35-67
9261178-11 1997 Furthermore, we demonstrated, using mouse P19 embryonal carcinoma cells, that this 371-base pair sequence is likely to be sufficient to confer the transcriptional activation of the ERK2 promoter during the retinoic acid-induced differentiation of P19 cells. Tretinoin 206-219 mitogen-activated protein kinase 1 Mus musculus 181-185
9264555-4 1997 Addition of TIMP or L-758,354 to the culture media inhibited IL-1beta-induced loss of tissue GAG by 40 and 65%, respectively, and inhibited RA-induced GAG loss by 35 and 65%, respectively. Tretinoin 140-142 TIMP metallopeptidase inhibitor 1 Homo sapiens 12-16
9296372-1 1997 We have previously shown that thyroid stimulating hormone-beta (TSHbeta) mRNA levels are modulated by vitamin A status in vivo and using transient transfection, that suppression of rat TSHbeta gene promoter activity by all-trans retinoic acid (RA) requires RA receptor (RAR) and retinoid X receptor (RXR). Tretinoin 229-242 thyroid stimulating hormone subunit beta Rattus norvegicus 30-62
9296372-1 1997 We have previously shown that thyroid stimulating hormone-beta (TSHbeta) mRNA levels are modulated by vitamin A status in vivo and using transient transfection, that suppression of rat TSHbeta gene promoter activity by all-trans retinoic acid (RA) requires RA receptor (RAR) and retinoid X receptor (RXR). Tretinoin 229-242 thyroid stimulating hormone subunit beta Rattus norvegicus 64-71
9296372-1 1997 We have previously shown that thyroid stimulating hormone-beta (TSHbeta) mRNA levels are modulated by vitamin A status in vivo and using transient transfection, that suppression of rat TSHbeta gene promoter activity by all-trans retinoic acid (RA) requires RA receptor (RAR) and retinoid X receptor (RXR). Tretinoin 229-242 thyroid stimulating hormone subunit beta Rattus norvegicus 185-192
9296372-1 1997 We have previously shown that thyroid stimulating hormone-beta (TSHbeta) mRNA levels are modulated by vitamin A status in vivo and using transient transfection, that suppression of rat TSHbeta gene promoter activity by all-trans retinoic acid (RA) requires RA receptor (RAR) and retinoid X receptor (RXR). Tretinoin 244-246 thyroid stimulating hormone subunit beta Rattus norvegicus 30-62
9296372-1 1997 We have previously shown that thyroid stimulating hormone-beta (TSHbeta) mRNA levels are modulated by vitamin A status in vivo and using transient transfection, that suppression of rat TSHbeta gene promoter activity by all-trans retinoic acid (RA) requires RA receptor (RAR) and retinoid X receptor (RXR). Tretinoin 244-246 thyroid stimulating hormone subunit beta Rattus norvegicus 64-71
9296372-1 1997 We have previously shown that thyroid stimulating hormone-beta (TSHbeta) mRNA levels are modulated by vitamin A status in vivo and using transient transfection, that suppression of rat TSHbeta gene promoter activity by all-trans retinoic acid (RA) requires RA receptor (RAR) and retinoid X receptor (RXR). Tretinoin 244-246 thyroid stimulating hormone subunit beta Rattus norvegicus 185-192
9285688-2 1997 TDGF-1 is highly expressed in the undifferentiated embryonal carcinoma stem cell line NTERA2 clone D1 (NT2/D1) and its expression is downregulated in response to differentiating agents such as retinoic acid (RA) and hexamethylen-bisacetamide (HMBA). Tretinoin 193-206 teratocarcinoma-derived growth factor 1 Homo sapiens 0-6
9276475-8 1997 De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis. Tretinoin 165-178 caspase 1 Homo sapiens 118-121
9276475-8 1997 De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis. Tretinoin 165-178 caspase 3 Homo sapiens 137-142
9276450-1 1997 The role of retinoic acids (RA) on liver fatty acid-binding protein (L-FABP) expression was investigated in the well differentiated FAO rat hepatoma cell line. Tretinoin 12-26 fatty acid binding protein 1 Rattus norvegicus 69-75
9276450-1 1997 The role of retinoic acids (RA) on liver fatty acid-binding protein (L-FABP) expression was investigated in the well differentiated FAO rat hepatoma cell line. Tretinoin 28-30 fatty acid binding protein 1 Rattus norvegicus 35-67
9276450-1 1997 The role of retinoic acids (RA) on liver fatty acid-binding protein (L-FABP) expression was investigated in the well differentiated FAO rat hepatoma cell line. Tretinoin 28-30 fatty acid binding protein 1 Rattus norvegicus 69-75
9276450-4 1997 RA also enhanced further both L-FABP mRNA levels and cytosolic L-FABP protein content induced by oleic acid. Tretinoin 0-2 fatty acid binding protein 1 Rattus norvegicus 30-36
9276450-4 1997 RA also enhanced further both L-FABP mRNA levels and cytosolic L-FABP protein content induced by oleic acid. Tretinoin 0-2 fatty acid binding protein 1 Rattus norvegicus 63-69
9258346-7 1997 In contrast, 48 h exposure to retinoic acid increased IGF II polypeptide levels, possible due to increased levels of IGF binding protein-6. Tretinoin 30-43 insulin-like growth factor binding protein 6 Rattus norvegicus 117-138
9260895-1 1997 We have investigated the regulation of transcription factors HNF-3alpha and HNF-3beta during the retinoic acid-mediated differentiation of mouse P19 cells. Tretinoin 97-110 forkhead box A2 Mus musculus 76-85
9260895-9 1997 In comparison to HNF-3alpha, HNF-3beta induction is a subsequent event and detectable levels of HNF-3beta mRNA materialize approximately 1 day after addition of retinoic acid to P19 stem cells. Tretinoin 161-174 forkhead box A2 Homo sapiens 96-105
9260895-11 1997 This temporal pattern is consistent with HNF-3beta being a secondary target for retinoic acid. Tretinoin 80-93 forkhead box A2 Homo sapiens 41-50
9260897-2 1997 RA did not affect cyclins D1, A, and E and cyclin-dependent kinase 2 (CDK2) expression, but significantly reduced cyclin D3 and CDK4 expression after 24 h. RA also inhibited cyclin B1 and CDC2 expression, possibly responsible for the reduction of the proportion of cells in G2 + M and S phases. Tretinoin 0-2 cyclin D3 Homo sapiens 114-123
9341974-5 1997 As determined by anion exchange chromatography and HPLC analysis, HaCaT keratinocytes treated with 1 microM RA for up to 72 h showed a marked decrease in Ins(1,4,5)P3 release upon stimulation with 10 microM bradykinin or 10 microM ionomycin. Tretinoin 108-110 kininogen 1 Homo sapiens 207-217
9242550-9 1997 Moreover, two different high-affinity 9-cis-RA binding sites (Kd = 0.45 and 0.075 nmol/L) were detectable in the bcr3-PML/RAR alpha product but not in the bcr1-PML/RAR alpha product (Kd = 0.77 nmol/L). Tretinoin 38-46 BCR pseudogene 3 Homo sapiens 113-117
9277051-3 1997 CD15 and CD11b were expressed on the APL cells in vivo as neutrophil maturation markers, while growth activity of the cells was decreased during ATRA administration. Tretinoin 145-149 fucosyltransferase 4 Homo sapiens 0-4
9258346-13 1997 These changes in the IGF/IGFBP axis may be relevant to the mechanism of action of retinoic acid in bone. Tretinoin 82-95 insulin-like growth factor binding protein 6 Rattus norvegicus 25-30
9378726-0 1997 Midkine, a retinoic acid-inducible heparin-binding cytokine in inflammatory responses: chemotactic activity to neutrophils and association with inflammatory synovitis. Tretinoin 11-24 midkine Homo sapiens 0-7
9228017-11 1997 In this paper, we describe the cloning and characterization of the first mammalian retinoic acid-inducible retinoic acid-metabolizing cytochrome P450 (hP450RAI), which belongs to a novel class of cytochromes (CYP26). Tretinoin 83-96 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 145-159
9261338-5 1997 The differentiation effects of TGF-beta 1 alone and especially of its combination with MK-886 were most pronounced when the cells were pretreated with dimethyl sulfoxide or all-trans-retinoic acid. Tretinoin 173-196 transforming growth factor beta 1 Homo sapiens 31-41
9228017-0 1997 cDNA cloning of human retinoic acid-metabolizing enzyme (hP450RAI) identifies a novel family of cytochromes P450. Tretinoin 22-35 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 57-65
9228017-13 1997 We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 18-26
9228041-0 1997 CYP26, a novel mammalian cytochrome P450, is induced by retinoic acid and defines a new family. Tretinoin 56-69 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-5
9228017-13 1997 We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 19-26
9228017-13 1997 We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 18-26
9228017-13 1997 We also show that hP450RAI mRNA expression is highly induced by RA in certain human tumor cell lines and further show that RA-inducible RA metabolism may correlate with P450RAI expression. Tretinoin 64-66 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 19-26
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, ionotropic, kainate 3 Mus musculus 297-303
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, ionotropic, AMPA4 (alpha 4) Mus musculus 391-397
9230197-4 1997 Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Tretinoin 26-49 prostaglandin-endoperoxide synthase 2 Homo sapiens 140-145
9230184-0 1997 Aryl hydrocarbon receptor knockout mice (AHR-/-) exhibit liver retinoid accumulation and reduced retinoic acid metabolism. Tretinoin 97-110 aryl-hydrocarbon receptor Mus musculus 0-25
9230184-0 1997 Aryl hydrocarbon receptor knockout mice (AHR-/-) exhibit liver retinoid accumulation and reduced retinoic acid metabolism. Tretinoin 97-110 aryl-hydrocarbon receptor Mus musculus 41-44
9230184-1 1997 Livers from aryl hydrocarbon receptor-null mice showed a 3-fold increase in retinoids and a 65% decrease in retinoic acid metabolism. Tretinoin 108-121 aryl-hydrocarbon receptor Mus musculus 12-37
9230197-4 1997 Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Tretinoin 26-49 prostaglandin-endoperoxide synthase 2 Homo sapiens 176-181
9230197-4 1997 Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Tretinoin 51-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 140-145
9230197-4 1997 Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Tretinoin 51-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 176-181
9230197-4 1997 Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Tretinoin 66-74 prostaglandin-endoperoxide synthase 2 Homo sapiens 140-145
9230197-4 1997 Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Tretinoin 66-74 prostaglandin-endoperoxide synthase 2 Homo sapiens 176-181
9266702-1 1997 Retinoic acid stimulates the expression of tissue-type plasminogen activator (t-PA) in vascular endothelial cells in vitro and enhances t-PA levels in plasma and tissues in vivo. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 43-76
9218601-4 1997 However, when IGF-I is added to RA-treated cells, the proportion of CD11b-positive cells increases to a level similar to that in RA-treated cells cultured in serum-containing medium. Tretinoin 32-34 insulin like growth factor 1 Homo sapiens 14-19
9218601-4 1997 However, when IGF-I is added to RA-treated cells, the proportion of CD11b-positive cells increases to a level similar to that in RA-treated cells cultured in serum-containing medium. Tretinoin 129-131 insulin like growth factor 1 Homo sapiens 14-19
9218601-7 1997 However, addition of IGF-I to RA-treated cells prevents the appearance of this apoptotic population and increases phosphatidylinositol 3"-kinase (PI 3-kinase) activity by fivefold. Tretinoin 30-32 insulin like growth factor 1 Homo sapiens 21-26
9218601-9 1997 These data demonstrate that IGF-I acts on RA-treated progenitors to promote their differentiation along the granulocytic lineage. Tretinoin 42-44 insulin like growth factor 1 Homo sapiens 28-33
9266702-12 1997 In the presence of the most potent retinoic acid metabolism inhibitor in endothelial cells, liarozole, at least 10-fold lower all-trans-retinoic acid concentrations were required than in the absence of the inhibitor to obtain the same induction of t-PA. Tretinoin 130-149 plasminogen activator, tissue type Homo sapiens 248-252
9266702-1 1997 Retinoic acid stimulates the expression of tissue-type plasminogen activator (t-PA) in vascular endothelial cells in vitro and enhances t-PA levels in plasma and tissues in vivo. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 78-82
9266702-14 1997 The rapid metabolism of retinoic acid explains the relatively high concentrations of retinoic acid required to induce t-PA in cultured endothelial cells. Tretinoin 24-37 plasminogen activator, tissue type Homo sapiens 118-122
9266702-1 1997 Retinoic acid stimulates the expression of tissue-type plasminogen activator (t-PA) in vascular endothelial cells in vitro and enhances t-PA levels in plasma and tissues in vivo. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 136-140
9266702-14 1997 The rapid metabolism of retinoic acid explains the relatively high concentrations of retinoic acid required to induce t-PA in cultured endothelial cells. Tretinoin 85-98 plasminogen activator, tissue type Homo sapiens 118-122
9266702-2 1997 Compared with the in vivo situation, high retinoic acid concentrations are required to induce optimally t-PA expression in vitro. Tretinoin 42-55 plasminogen activator, tissue type Homo sapiens 104-108
9266702-12 1997 In the presence of the most potent retinoic acid metabolism inhibitor in endothelial cells, liarozole, at least 10-fold lower all-trans-retinoic acid concentrations were required than in the absence of the inhibitor to obtain the same induction of t-PA. Tretinoin 35-48 plasminogen activator, tissue type Homo sapiens 248-252
9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 40-53 transforming growth factor beta 1 Homo sapiens 195-205
9207452-10 1997 Antiproliferative cytokines such as transforming growth factor-beta1 and high concentrations of all-trans-retinoic acid in cytokine-supported CD34+ cultures downmodulated telomerase activity. Tretinoin 99-119 CD34 molecule Homo sapiens 142-146
9259183-8 1997 In contrast, Pax-2 gene expression was suppressed by treating PTC with retinoic acid (10 mM), a well-described differentiating factor, and with TGF-beta 1 (10 ng/ml), a recognized antiproliferative agent for these cells, which suggests that Pax-2 has a role in renal cell proliferation. Tretinoin 71-84 paired box protein Pax-2 Oryctolagus cuniculus 13-18
9259183-8 1997 In contrast, Pax-2 gene expression was suppressed by treating PTC with retinoic acid (10 mM), a well-described differentiating factor, and with TGF-beta 1 (10 ng/ml), a recognized antiproliferative agent for these cells, which suggests that Pax-2 has a role in renal cell proliferation. Tretinoin 71-84 paired box protein Pax-2 Oryctolagus cuniculus 241-246
9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 279-293 transforming growth factor beta 1 Homo sapiens 195-205
9199351-3 1997 We demonstrate that RA and its synthetic analogs inhibit the proliferation of KS cells by inhibiting the mRNA and protein levels of interleukin-6 (IL-6), an autocrine growth factor for KS cells. Tretinoin 20-22 interleukin 6 Homo sapiens 132-145
9256344-0 1997 Induction of yolk sac endoderm in GATA-4-deficient embryoid bodies by retinoic acid. Tretinoin 70-83 GATA binding protein 4 Mus musculus 34-40
9256344-5 1997 We show that differentiation of Gata4 -/- embryoid bodies in the presence of retinoic acid results in formation of visceral endoderm, while differentiation of Gata4 -/- embryoid bodies in the presence of retinoic acid plus dbcAMP causes parietal endoderm formation. Tretinoin 77-90 GATA binding protein 4 Mus musculus 32-37
9256344-7 1997 Treatment of Gata4 -/- embryoid bodies with retinoic acid induces expression of another GATA-binding protein, GATA-6, in both visceral and parietal endoderm cells. Tretinoin 44-57 GATA binding protein 4 Mus musculus 13-18
9199351-3 1997 We demonstrate that RA and its synthetic analogs inhibit the proliferation of KS cells by inhibiting the mRNA and protein levels of interleukin-6 (IL-6), an autocrine growth factor for KS cells. Tretinoin 20-22 interleukin 6 Homo sapiens 147-151
9188476-4 1997 All-trans-retinoic acid inhibited the enzyme activity in a noncompetitive manner, suggesting that it binds to the same hydrophobic pocket as prostaglandin H2, the substrate for prostaglandin D synthase, but at a different site in this pocket. Tretinoin 0-23 prostaglandin D2 synthase Homo sapiens 177-201
9191101-5 1997 When neuroblastoma Neuro 2a cells were treated with retinoic acid to induce differentiation, p24 mRNA increased but the p24 protein was not detected. Tretinoin 52-65 cytochrome P450, family 2, subfamily b, polypeptide 10 Mus musculus 93-96
11038749-0 1997 [Inhibition of estrogen receptor-positive human breast carcinoma cell growth by retinoic acid]. Tretinoin 80-93 estrogen receptor 1 Homo sapiens 15-32
15624332-6 1997 9-cis RA was more potent than all-trans retinoic acid (ATRA) did in inducing terminal differentiation associated apoptosis and in downregulation of Bcl-2 expression. Tretinoin 40-53 BCL2 apoptosis regulator Homo sapiens 148-153
15624332-6 1997 9-cis RA was more potent than all-trans retinoic acid (ATRA) did in inducing terminal differentiation associated apoptosis and in downregulation of Bcl-2 expression. Tretinoin 55-59 BCL2 apoptosis regulator Homo sapiens 148-153
9191474-5 1997 Removal of RA from the media caused a drastic decrease in mucin secretion and a decrease in expression of the mucin genes MUC2 and MUC5AC.LZ and SLPI secretions were increased in these cultures. Tretinoin 11-13 mucin 2, oligomeric mucus/gel-forming Homo sapiens 122-126
9191474-5 1997 Removal of RA from the media caused a drastic decrease in mucin secretion and a decrease in expression of the mucin genes MUC2 and MUC5AC.LZ and SLPI secretions were increased in these cultures. Tretinoin 11-13 lysozyme Homo sapiens 138-140
9191474-5 1997 Removal of RA from the media caused a drastic decrease in mucin secretion and a decrease in expression of the mucin genes MUC2 and MUC5AC.LZ and SLPI secretions were increased in these cultures. Tretinoin 11-13 secretory leukocyte peptidase inhibitor Homo sapiens 145-149
9191101-5 1997 When neuroblastoma Neuro 2a cells were treated with retinoic acid to induce differentiation, p24 mRNA increased but the p24 protein was not detected. Tretinoin 52-65 cytochrome P450, family 2, subfamily b, polypeptide 10 Mus musculus 120-123
9368678-7 1997 However, in contrast to TGF-beta 2, high concentrations of RA (1 microM) negatively regulated IGFBP-5 expression, with IGFBP-5 mRNA levels downregulated to 20% of that of the control, and protein levels were decreased by 50%. Tretinoin 59-61 insulin like growth factor binding protein 5 Homo sapiens 94-101
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 175-188 interferon alpha 1 Homo sapiens 53-56
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 175-188 interferon regulatory factor 9 Homo sapiens 158-161
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 190-194 interferon alpha 1 Homo sapiens 53-56
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 190-194 interferon regulatory factor 9 Homo sapiens 158-161
9186002-7 1997 However, during ATRA-induced differentiation, steady-state STAT1, STAT2, and especially p48 mRNA and corresponding protein levels were elevated both in NB4 and U937 cells, apparently correlating to an enhanced responsiveness of these cells to IFNs. Tretinoin 16-20 interferon regulatory factor 9 Homo sapiens 88-91
9186002-8 1997 ATRA treatment of NB4 cells sensitized them to IFN action as seen by increased IFN-gamma activation site DNA-binding activity or by efficient formation of IFN-alpha-specific ISGF3 complex and subsequent oligoadenylate synthetase and MxB gene expression. Tretinoin 0-4 interferon alpha 1 Homo sapiens 47-50
9186002-8 1997 ATRA treatment of NB4 cells sensitized them to IFN action as seen by increased IFN-gamma activation site DNA-binding activity or by efficient formation of IFN-alpha-specific ISGF3 complex and subsequent oligoadenylate synthetase and MxB gene expression. Tretinoin 0-4 interferon gamma Homo sapiens 79-88
9186002-8 1997 ATRA treatment of NB4 cells sensitized them to IFN action as seen by increased IFN-gamma activation site DNA-binding activity or by efficient formation of IFN-alpha-specific ISGF3 complex and subsequent oligoadenylate synthetase and MxB gene expression. Tretinoin 0-4 interferon alpha 1 Homo sapiens 155-164
9186002-0 1997 Retinoic acid induces signal transducer and activator of transcription (STAT) 1, STAT2, and p48 expression in myeloid leukemia cells and enhances their responsiveness to interferons. Tretinoin 0-13 interferon regulatory factor 9 Homo sapiens 92-95
9279512-4 1997 Retinoic acid enhanced the expression of alkaline phosphatase and type I collagen, and reduced TGF-beta receptors in these cells. Tretinoin 0-13 transforming growth factor, beta 1 Rattus norvegicus 95-103
9279512-6 1997 Because TGF-beta inhibits osteoblastic differentiation, the changes described here may contribute to the osteoblastic differentiation by retinoic acid. Tretinoin 137-150 transforming growth factor, beta 1 Rattus norvegicus 8-16
9368687-8 1997 Conversely, all-trans retinoic acid, which attenuates progesterone-dependent decidualization, significantly (p < 0.05) decreased both prolactin secretion and cAMP levels. Tretinoin 12-35 prolactin Homo sapiens 137-146
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 55-63
9138088-0 1997 Effects of TPA, bryostatin 1, and retinoic acid on PO-B, AP-1, and AP-2 DNA binding during HL-60 differentiation. Tretinoin 34-47 ER membrane protein complex subunit 3 Homo sapiens 51-55
9138088-3 1997 We now report that PO-B DNA-binding in HL-60 cells is similarly induced during differentiation to the granulocytic lineage (with either retinoic acid or dimethylsulfoxide). Tretinoin 136-149 ER membrane protein complex subunit 3 Homo sapiens 19-23
9220339-6 1997 To test whether this acceleration of cardiac differentiation and RA-induced increase of the MLC-2v promotor/beta-galactosidase activity reflects an increase of cardiac- and ventricle-specific gene expression, a semi-quantitative RT-PCR analysis was performed for alpha-cardiac myosin heavy chain (alpha-MHC) and MLC-2v genes. Tretinoin 65-67 myosin heavy chain 6 Homo sapiens 263-295
9220339-6 1997 To test whether this acceleration of cardiac differentiation and RA-induced increase of the MLC-2v promotor/beta-galactosidase activity reflects an increase of cardiac- and ventricle-specific gene expression, a semi-quantitative RT-PCR analysis was performed for alpha-cardiac myosin heavy chain (alpha-MHC) and MLC-2v genes. Tretinoin 65-67 myosin heavy chain 6 Homo sapiens 297-306
11039029-0 1997 [Changes of PKC isoforms in induced differentiation of HL-60 cells by ATRA and PMA]. Tretinoin 70-74 proline rich transmembrane protein 2 Homo sapiens 12-15
11039029-3 1997 The results showed that ATRA led to 5.0, 2.8 and 4.2 times increase of PKC alpha, beta I and beta II isoforms respectively as compared with the undifferentiated control levels and translocation of PKC from membrane to cytosol. Tretinoin 24-28 protein kinase C alpha Homo sapiens 71-80
11039029-3 1997 The results showed that ATRA led to 5.0, 2.8 and 4.2 times increase of PKC alpha, beta I and beta II isoforms respectively as compared with the undifferentiated control levels and translocation of PKC from membrane to cytosol. Tretinoin 24-28 proline rich transmembrane protein 2 Homo sapiens 71-74
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 25-29 transforming growth factor beta 1 Homo sapiens 55-63
9139741-1 1997 Retinoic acid (RA) induces differentiation of B16 mouse melanoma cells, which is accompanied by an increase in protein kinase Calpha (PKCalpha) as well as a selective enrichment of nuclear PKCalpha. Tretinoin 0-13 protein kinase C, alpha Mus musculus 111-132
9139741-1 1997 Retinoic acid (RA) induces differentiation of B16 mouse melanoma cells, which is accompanied by an increase in protein kinase Calpha (PKCalpha) as well as a selective enrichment of nuclear PKCalpha. Tretinoin 0-13 protein kinase C, alpha Mus musculus 134-142
9139741-1 1997 Retinoic acid (RA) induces differentiation of B16 mouse melanoma cells, which is accompanied by an increase in protein kinase Calpha (PKCalpha) as well as a selective enrichment of nuclear PKCalpha. Tretinoin 0-13 protein kinase C, alpha Mus musculus 189-197
9139741-1 1997 Retinoic acid (RA) induces differentiation of B16 mouse melanoma cells, which is accompanied by an increase in protein kinase Calpha (PKCalpha) as well as a selective enrichment of nuclear PKCalpha. Tretinoin 15-17 protein kinase C, alpha Mus musculus 111-132
9139741-1 1997 Retinoic acid (RA) induces differentiation of B16 mouse melanoma cells, which is accompanied by an increase in protein kinase Calpha (PKCalpha) as well as a selective enrichment of nuclear PKCalpha. Tretinoin 15-17 protein kinase C, alpha Mus musculus 134-142
9139741-1 1997 Retinoic acid (RA) induces differentiation of B16 mouse melanoma cells, which is accompanied by an increase in protein kinase Calpha (PKCalpha) as well as a selective enrichment of nuclear PKCalpha. Tretinoin 15-17 protein kinase C, alpha Mus musculus 189-197
9234591-1 1997 The in vitro inhibitory effect of all-trans retinoic acid (ATRA) on myeloma cell growth may be synergistically potentiated by the activity of dexamethasone (DEX) and alpha-interferon (IFN). Tretinoin 34-57 interferon alpha 1 Homo sapiens 166-188
9160172-6 1997 The most favoured explanation is that continuous tretinoin treatment acts to induce drug catabolism by cytochrome P450 (CYP) enzymes. Tretinoin 49-58 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 103-118
9160172-6 1997 The most favoured explanation is that continuous tretinoin treatment acts to induce drug catabolism by cytochrome P450 (CYP) enzymes. Tretinoin 49-58 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 120-123
9174604-0 1997 CD43 (leukosialin, sialophorin) expression is differentially regulated by retinoic acids. Tretinoin 74-88 sialophorin Homo sapiens 0-4
9174604-0 1997 CD43 (leukosialin, sialophorin) expression is differentially regulated by retinoic acids. Tretinoin 74-88 sialophorin Homo sapiens 19-30
9174604-4 1997 CD43 expression was also enhanced in response to retinoic acids on isolated human skin mast cells and human monocytes, but not on cells of the basophilic cell line KU-812 and promyelocytic HL-60 cells, indicating that these agents might act in a cell-type specific manner. Tretinoin 49-63 sialophorin Homo sapiens 0-4
9174604-6 1997 Possibly, vitamin A metabolites act directly on the CD43 gene, since putative retinoic acid response elements have been detected within its regulatory regions. Tretinoin 78-91 sialophorin Homo sapiens 52-56
9135005-5 1997 Thus, induction of tissue transglutaminase by all-trans-RA and, surprisingly, 9-cis-RA was enhanced 5-fold over and above the level of induction in control cells (SC115), and activation of a RA response element reporter was enhanced 3-fold (MDA-MB-231). Tretinoin 55-58 transglutaminase 2 Homo sapiens 19-42
9135005-5 1997 Thus, induction of tissue transglutaminase by all-trans-RA and, surprisingly, 9-cis-RA was enhanced 5-fold over and above the level of induction in control cells (SC115), and activation of a RA response element reporter was enhanced 3-fold (MDA-MB-231). Tretinoin 56-58 transglutaminase 2 Homo sapiens 19-42
9234591-1 1997 The in vitro inhibitory effect of all-trans retinoic acid (ATRA) on myeloma cell growth may be synergistically potentiated by the activity of dexamethasone (DEX) and alpha-interferon (IFN). Tretinoin 59-63 interferon alpha 1 Homo sapiens 166-188
9130512-6 1997 The effects of RA on IL-2-alpha receptor expression was determined by flow cytometry on T cells. Tretinoin 15-17 interleukin 2 Homo sapiens 21-25
9130512-7 1997 CONCLUSION: These studies suggest that RA can augment IL-2 mRNA production by T cells with a possible paracrine effect on IL-2R-alpha expression. Tretinoin 39-41 interleukin 2 Homo sapiens 54-58
9130512-0 1997 Retinoic acid-induced modulation of IL-2 mRNA production and IL-2 receptor expression on T cells. Tretinoin 0-13 interleukin 2 Homo sapiens 36-40
9175709-4 1997 Both the human myeloid cell line HL-60, when differentiated by treatment with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid, and human blood leukocytes, adhered to myeloperoxidase; however, undifferentiated HL-60 cells showed only minimal adhesion. Tretinoin 125-138 myeloperoxidase Homo sapiens 179-194
9108446-5 1997 Loss of RA inducibility of RAR beta gene expression is assumed to play a role in the development of several types of human carcinomas, including carcinomas of the uterine cervix. Tretinoin 8-10 retinoic acid receptor beta Homo sapiens 27-35
9225073-0 1997 Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells. Tretinoin 56-69 tumor protein p53 Homo sapiens 14-17
9225073-0 1997 Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells. Tretinoin 56-69 cyclin dependent kinase inhibitor 1A Homo sapiens 19-23
9225073-0 1997 Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells. Tretinoin 56-69 cyclin dependent kinase inhibitor 1A Homo sapiens 24-27
9225073-0 1997 Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells. Tretinoin 56-69 BCL2 apoptosis regulator Homo sapiens 32-37
9111026-6 1997 In addition, Arg276 of RARalpha, like its homologous residue Arg269 of RARbeta, was found to play an important role in the binding of RA most likely by interacting with the carboxylate group of RA. Tretinoin 23-25 retinoic acid receptor beta Homo sapiens 71-78
9128293-2 1997 We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants. Tretinoin 97-120 surfactant protein C Homo sapiens 70-74
9128293-2 1997 We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants. Tretinoin 122-124 surfactant protein C Homo sapiens 70-74
9128293-7 1997 Human fetal lung explants were treated with 9-cis-RA for 6 d. 9-cis-RA did not significantly increase SP-B mRNA levels, significantly inhibited SP-A mRNA levels at all concentrations tested, and significantly inhibited SP-C mRNA levels at 10(-6) M in the human fetal lung explants. Tretinoin 62-70 surfactant protein C Homo sapiens 219-223
9108446-7 1997 The results show that the RAR beta mRNA levels are high and RA inducible in the primary keratinocytes, whereas they are low and not inducible or only slightly inducible by RA in all of the cervical carcinoma cell lines analyzed. Tretinoin 60-62 retinoic acid receptor beta Homo sapiens 26-34
9130647-0 1997 Chemoattractant receptors for interleukin-8 and C5a: expression on peripheral blood leukocytes and differential regulation on HL-60 and AML-193 cells by vitamin D3 and all-trans retinoic acid. Tretinoin 178-191 C-X-C motif chemokine ligand 8 Homo sapiens 30-43
9130647-0 1997 Chemoattractant receptors for interleukin-8 and C5a: expression on peripheral blood leukocytes and differential regulation on HL-60 and AML-193 cells by vitamin D3 and all-trans retinoic acid. Tretinoin 178-191 complement C5a receptor 1 Homo sapiens 48-51
9130711-0 1997 Modulation of retinoic acid sensitivity in lung cancer cells through dynamic balance of orphan receptors nur77 and COUP-TF and their heterodimerization. Tretinoin 14-27 nuclear receptor subfamily 4 group A member 1 Homo sapiens 105-110
9130711-0 1997 Modulation of retinoic acid sensitivity in lung cancer cells through dynamic balance of orphan receptors nur77 and COUP-TF and their heterodimerization. Tretinoin 14-27 nuclear receptor subfamily 2 group F member 1 Homo sapiens 115-122
9130647-10 1997 In contrast, all-trans retinoic acid (0.1 microM, 7 days), which induces differentiation into the granulocytic phenotype, led to an up-regulation of IL-8RB in AML-193 cells and to an expression of IL-8RB and C5aR in HL-60 cells. Tretinoin 23-36 complement C5a receptor 1 Homo sapiens 208-212
9130711-3 1997 Previously, it was demonstrated that the RA response is regulated by the COUP-TF orphan receptors. Tretinoin 41-43 nuclear receptor subfamily 2 group F member 1 Homo sapiens 73-80
9130711-5 1997 Expression of nur77 enhances ligand-independent transactivation of RA response elements (RAREs) and desensitizes their RA responsiveness. Tretinoin 67-69 nuclear receptor subfamily 4 group A member 1 Homo sapiens 14-19
9126480-8 1997 Retinoic acid, which inhibits squamous differentiation, represses CL-20 expression in normal human bronchial epithelial cells. Tretinoin 0-13 epithelial membrane protein 1 Homo sapiens 66-71
9130711-6 1997 Conversely, expression of COUP-TF sensitizes RA responsiveness of RAREs by repressing their basal transactivation activity. Tretinoin 45-47 nuclear receptor subfamily 2 group F member 1 Homo sapiens 26-33
9130711-10 1997 In human lung cancer cell lines, COUP-TF is highly expressed in RA-sensitive cell lines while nur77 expression is associated with RA resistance. Tretinoin 64-66 nuclear receptor subfamily 2 group F member 1 Homo sapiens 33-40
9130711-12 1997 These observations demonstrate that a dynamic equilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness of human lung cancer cells. Tretinoin 158-160 nuclear receptor subfamily 4 group A member 1 Homo sapiens 83-88
9130711-12 1997 These observations demonstrate that a dynamic equilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness of human lung cancer cells. Tretinoin 158-160 nuclear receptor subfamily 2 group F member 1 Homo sapiens 93-100
9130711-12 1997 These observations demonstrate that a dynamic equilibrium between orphan receptors nur77 and COUP-TF, through their heterodimerization that regulates COUP-TF RARE binding, is critical for RA responsiveness of human lung cancer cells. Tretinoin 158-160 nuclear receptor subfamily 2 group F member 1 Homo sapiens 150-157
10743138-2 1997 The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased. Tretinoin 53-55 BCL2 apoptosis regulator Homo sapiens 221-226
9138077-0 1997 Retinoic acid stimulates growth hormone synthesis in human somatotropic adenoma cells: characterization of its nuclear receptors. Tretinoin 0-13 growth hormone 1 Homo sapiens 25-39
9079631-6 1997 Its mRNA level is induced by transforming growth factor beta-1 and indomethacin and inhibited by phorbol ester and retinoic acid. Tretinoin 115-128 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 56-62
10743138-2 1997 The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased. Tretinoin 53-55 tumor protein p53 Homo sapiens 274-277
9067275-5 1997 Retinoids [all-trans-retinoic acid (RA), 13-cis-RA, and retinyl acetate] markedly suppressed PMA-mediated increases in amounts of cyclooxygenase-2 (Cox-2) and the production of PGE2. Tretinoin 11-34 prostaglandin-endoperoxide synthase 2 Homo sapiens 130-146
9067275-5 1997 Retinoids [all-trans-retinoic acid (RA), 13-cis-RA, and retinyl acetate] markedly suppressed PMA-mediated increases in amounts of cyclooxygenase-2 (Cox-2) and the production of PGE2. Tretinoin 11-34 prostaglandin-endoperoxide synthase 2 Homo sapiens 148-153
9067275-5 1997 Retinoids [all-trans-retinoic acid (RA), 13-cis-RA, and retinyl acetate] markedly suppressed PMA-mediated increases in amounts of cyclooxygenase-2 (Cox-2) and the production of PGE2. Tretinoin 36-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 130-146
9067275-5 1997 Retinoids [all-trans-retinoic acid (RA), 13-cis-RA, and retinyl acetate] markedly suppressed PMA-mediated increases in amounts of cyclooxygenase-2 (Cox-2) and the production of PGE2. Tretinoin 36-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 148-153
9050783-7 1997 However, in Pax6(Sey-Neu)/ Pax6(Sey-Neu) embryos, retinoic acid (RA) is not produced by the frontonasal mesenchyme, which normally provides local retinoid signals to the placode and forebrain. Tretinoin 50-63 paired box 6 Mus musculus 17-20
9093912-4 1997 Specifically, when proteoglycan synthesis was blocked by treatment with 10(-10) M retinoic acid, extensive mineral deposition occurred on a matrix devoid of both proteoglycans and cartilage nodules. Tretinoin 82-95 versican Gallus gallus 19-31
9050783-7 1997 However, in Pax6(Sey-Neu)/ Pax6(Sey-Neu) embryos, retinoic acid (RA) is not produced by the frontonasal mesenchyme, which normally provides local retinoid signals to the placode and forebrain. Tretinoin 50-63 paired box 6 Mus musculus 32-35
9032283-4 1997 In studies of normal preadipocytes, RA does not prevent C/EBPbeta induction but blocks induction of PPARgamma, C/EBPalpha, and adipogenesis. Tretinoin 36-38 peroxisome proliferator activated receptor gamma Homo sapiens 100-109
9124579-9 1997 These results demonstrate diminished RA signaling in HSC from cholestatic liver fibrosis, which appeared to have resulted from RA deficiency and suppressed expression of RAR-beta and RXR-alpha. Tretinoin 37-39 retinoic acid receptor, beta Rattus norvegicus 170-178
9124579-9 1997 These results demonstrate diminished RA signaling in HSC from cholestatic liver fibrosis, which appeared to have resulted from RA deficiency and suppressed expression of RAR-beta and RXR-alpha. Tretinoin 37-39 retinoid X receptor alpha Rattus norvegicus 183-192
9124579-10 1997 Furthermore, the reciprocal enhancement of AP-1 activity and coordinately increased expression of an AP-1 responsive gene, TGF-beta1, suggest a permissive role of the diminished RA signaling in promoting AP-1 activity and TGF-beta1 expression. Tretinoin 178-180 transforming growth factor, beta 1 Rattus norvegicus 123-132
9124579-10 1997 Furthermore, the reciprocal enhancement of AP-1 activity and coordinately increased expression of an AP-1 responsive gene, TGF-beta1, suggest a permissive role of the diminished RA signaling in promoting AP-1 activity and TGF-beta1 expression. Tretinoin 178-180 transforming growth factor, beta 1 Rattus norvegicus 222-231
9060998-2 1997 Addition of either 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) or retinoic acid (RA) to HL-60 cells for 2 h inhibited PMA-stimulated PLA2 activity measured by [3H]AA release. Tretinoin 61-74 phospholipase A2 group IB Homo sapiens 128-132
9060998-2 1997 Addition of either 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) or retinoic acid (RA) to HL-60 cells for 2 h inhibited PMA-stimulated PLA2 activity measured by [3H]AA release. Tretinoin 76-78 phospholipase A2 group IB Homo sapiens 128-132
9057102-0 1997 Retinoic acid abolishes the calcitonin gene-related peptide autocrine system in F9 teratocarcinoma cells. Tretinoin 0-13 calcitonin related polypeptide alpha Homo sapiens 28-59
9057102-2 1997 We analyzed the effect of retinoic acid (RA)-induced differentiation of F9 cells into primitive parietal endoderm-like cells, on CGRP production and the CGRP responsiveness of these cells. Tretinoin 26-39 calcitonin related polypeptide alpha Homo sapiens 129-133
9057102-2 1997 We analyzed the effect of retinoic acid (RA)-induced differentiation of F9 cells into primitive parietal endoderm-like cells, on CGRP production and the CGRP responsiveness of these cells. Tretinoin 26-39 calcitonin related polypeptide alpha Homo sapiens 153-157
9057102-2 1997 We analyzed the effect of retinoic acid (RA)-induced differentiation of F9 cells into primitive parietal endoderm-like cells, on CGRP production and the CGRP responsiveness of these cells. Tretinoin 41-43 calcitonin related polypeptide alpha Homo sapiens 129-133
9057102-6 1997 RA treatment also reduced CGRP secretion by F9 cells; the effect was maximal at 3 days and remained stable thereafter. Tretinoin 0-2 calcitonin related polypeptide alpha Homo sapiens 26-30
9057102-7 1997 Similarly, RA rapidly reduced adenylate cyclase responsiveness to chicken CGRP (cCGRP) and human CGRP (hCGRP). Tretinoin 11-13 calcitonin Gallus gallus 74-78
9057102-7 1997 Similarly, RA rapidly reduced adenylate cyclase responsiveness to chicken CGRP (cCGRP) and human CGRP (hCGRP). Tretinoin 11-13 calcitonin related polypeptide alpha Homo sapiens 81-85
9057102-8 1997 An 80% fall in cAMP release into the culture medium in the presence of CGRP was observed after 24 h of RA treatment. Tretinoin 103-105 calcitonin related polypeptide alpha Homo sapiens 71-75
9057102-9 1997 These results demonstrate that RA rapidly abolishes the CGRP autocrine system involved in the proliferation of F9 cells, at the same time inducing their differentiation into primitive parietal endoderm. Tretinoin 31-33 calcitonin related polypeptide alpha Homo sapiens 56-60
9125129-0 1997 Wortmannin enhances CPP32-like activity during neuronal differentiation of P19 embryonal carcinoma cells induced by retinoic acid. Tretinoin 116-129 caspase 3 Homo sapiens 20-25
9125129-2 1997 Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. Tretinoin 74-87 caspase 3 Homo sapiens 4-9
9125129-2 1997 Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. Tretinoin 74-87 caspase 3 Homo sapiens 26-31
9125129-5 1997 Wortmannin, PI-3K inhibitor, enhances the CPP32-like activity of the retinoic acid-treated P19 EC cells. Tretinoin 69-82 caspase 3 Homo sapiens 42-47
9032283-4 1997 In studies of normal preadipocytes, RA does not prevent C/EBPbeta induction but blocks induction of PPARgamma, C/EBPalpha, and adipogenesis. Tretinoin 36-38 CCAAT enhancer binding protein alpha Homo sapiens 111-121
9070291-0 1997 Retinoic acids differentially regulate NOR-1 and its closely related orphan nuclear receptor genes in breast cancer cell line MCF-7. Tretinoin 0-14 nuclear receptor subfamily 4 group A member 3 Homo sapiens 39-44
9056414-10 1997 These differences in the differentiation and RA response in vitro may be related to inherent stage-specific differences between fetal and neonatal keratinocytes in RA-signaling pathways including expression of the retinoic acid receptor, RARbeta. Tretinoin 45-47 retinoic acid receptor beta Homo sapiens 238-245
9070291-5 1997 In the presence of cycloheximide, all-trans retinoic acid superinduced NOR-1 mRNA, whereas all-trans and 9-cis retinoic acids strongly suppressed the NGFI-B mRNA accumulation. Tretinoin 44-57 nuclear receptor subfamily 4 group A member 3 Homo sapiens 71-76
9070291-5 1997 In the presence of cycloheximide, all-trans retinoic acid superinduced NOR-1 mRNA, whereas all-trans and 9-cis retinoic acids strongly suppressed the NGFI-B mRNA accumulation. Tretinoin 111-125 nuclear receptor subfamily 4 group A member 1 Homo sapiens 150-156
9022083-0 1997 Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells. Tretinoin 0-13 vascular cell adhesion molecule 1 Homo sapiens 51-84
9045990-0 1997 Alterations in Msx 1 and Msx 2 expression correlate with inhibition of outgrowth of chick facial primordia induced by retinoic acid. Tretinoin 118-131 msh homeobox 2 Gallus gallus 25-30
9028332-5 1997 Treatment of NB4 cells with ATRA is associated with a remarkable upregulation of the two IFN-responsive genes IFN-responsive factor 1 and 2"-5" oligoadenylate synthetase, as well as with an augmentation in the levels of IFN alpha secretion. Tretinoin 28-32 interferon alpha 1 Homo sapiens 89-92
9028332-5 1997 Treatment of NB4 cells with ATRA is associated with a remarkable upregulation of the two IFN-responsive genes IFN-responsive factor 1 and 2"-5" oligoadenylate synthetase, as well as with an augmentation in the levels of IFN alpha secretion. Tretinoin 28-32 interferon alpha 1 Homo sapiens 110-113
9028332-5 1997 Treatment of NB4 cells with ATRA is associated with a remarkable upregulation of the two IFN-responsive genes IFN-responsive factor 1 and 2"-5" oligoadenylate synthetase, as well as with an augmentation in the levels of IFN alpha secretion. Tretinoin 28-32 interferon alpha 1 Homo sapiens 220-229
9028332-6 1997 Our data show that ATRA is capable of modulating the amounts and the state of activation of some of the components of the IFN intracellular signaling pathways. Tretinoin 19-23 interferon alpha 1 Homo sapiens 122-125
9040946-4 1997 The maximal induction of MMP-13 mRNAs by TNF-alpha was noted after a 6-h incubation, whereas with TGF-beta, the maximal stimulation was observed after 24 h. The up-regulation of MMP-13 mRNA abundance by TNF-alpha and TGF-beta was dependent on protein synthesis and was prevented partially by dexamethasone and retinoic acid. Tretinoin 310-323 matrix metallopeptidase 13 Homo sapiens 25-31
9040946-4 1997 The maximal induction of MMP-13 mRNAs by TNF-alpha was noted after a 6-h incubation, whereas with TGF-beta, the maximal stimulation was observed after 24 h. The up-regulation of MMP-13 mRNA abundance by TNF-alpha and TGF-beta was dependent on protein synthesis and was prevented partially by dexamethasone and retinoic acid. Tretinoin 310-323 matrix metallopeptidase 13 Homo sapiens 178-184
9040946-4 1997 The maximal induction of MMP-13 mRNAs by TNF-alpha was noted after a 6-h incubation, whereas with TGF-beta, the maximal stimulation was observed after 24 h. The up-regulation of MMP-13 mRNA abundance by TNF-alpha and TGF-beta was dependent on protein synthesis and was prevented partially by dexamethasone and retinoic acid. Tretinoin 310-323 tumor necrosis factor Homo sapiens 203-212
9113387-0 1997 All-trans retinoic acid inhibits dexamethasone-induced ALP activity and mineralization in human osteoblastic cell line SV HFO. Tretinoin 0-23 alkaline phosphatase, placental Homo sapiens 55-58
9113387-3 1997 RA inhibited the mineralization, coincident with the inhibition of alkaline phosphatase (ALP). Tretinoin 0-2 alkaline phosphatase, placental Homo sapiens 67-87
9113387-3 1997 RA inhibited the mineralization, coincident with the inhibition of alkaline phosphatase (ALP). Tretinoin 0-2 alkaline phosphatase, placental Homo sapiens 89-92
9113387-4 1997 On the other hand, RA induced osteocalcin secretion and had no effect on the expression of the other osteoblastic markers such as type I collagen and osteonectin. Tretinoin 19-21 bone gamma-carboxyglutamate protein Homo sapiens 30-41
9113387-8 1997 These results suggested that the inhibitory effect of RA on the mineralization of human osteoblasts is mediated by the activation of RAR alpha and/or RAR beta and that RAR gamma preferentially regulates the expression of osteocalcin without influence on mineralization. Tretinoin 54-56 retinoic acid receptor beta Homo sapiens 150-158
9028736-2 1997 Retinoic acid (RA) inhibition of estrogen receptor (ER)-positive breast carcinoma seems to be mediated through RAR alpha. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 33-50
9028736-2 1997 Retinoic acid (RA) inhibition of estrogen receptor (ER)-positive breast carcinoma seems to be mediated through RAR alpha. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 52-54
9022083-4 1997 Pretreatment with t-RA specifically prevented TNFalpha-induced VCAM-1 expression, but not ICAM-1 and E-selectin induction. Tretinoin 18-22 tumor necrosis factor Homo sapiens 46-54
9022083-4 1997 Pretreatment with t-RA specifically prevented TNFalpha-induced VCAM-1 expression, but not ICAM-1 and E-selectin induction. Tretinoin 18-22 vascular cell adhesion molecule 1 Homo sapiens 63-69
9022083-7 1997 In transcriptional activation studies, the TNFalpha-mediated activation of the human VCAM-1 promoter was inhibited after t-RA treatment, while the ICAM-1 promoter activation was unaffected, indicating that the selective inhibition of CAM expression is regulated in part at the level of gene transcription. Tretinoin 121-125 tumor necrosis factor Homo sapiens 43-51
9022083-7 1997 In transcriptional activation studies, the TNFalpha-mediated activation of the human VCAM-1 promoter was inhibited after t-RA treatment, while the ICAM-1 promoter activation was unaffected, indicating that the selective inhibition of CAM expression is regulated in part at the level of gene transcription. Tretinoin 121-125 vascular cell adhesion molecule 1 Homo sapiens 85-91
9022083-3 1997 To determine modes of retinoid action in the modulation of inflammatory responses, we explored effects of all-trans-retinoic acid (t-RA) on the TNFalpha-induced expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin in cultured human dermal microvascular endothelial cells. Tretinoin 109-129 tumor necrosis factor Homo sapiens 144-152
8993032-2 1997 In P19 EC cells RA treatment stimulates induction of the RAR beta gene, while it represses Oct3/4 gene expression. Tretinoin 16-18 retinoic acid receptor beta Homo sapiens 57-65
8999891-2 1997 In cell lysate and in vitro reconstitution system, phospholipase D (PLD) activity in response to guanosine 5"-O-(3-thiotriphosphate) (GTPgammaS) was up-regulated by dbcAMP or all-trans retinoic acid treatment. Tretinoin 185-198 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 51-66
8999891-2 1997 In cell lysate and in vitro reconstitution system, phospholipase D (PLD) activity in response to guanosine 5"-O-(3-thiotriphosphate) (GTPgammaS) was up-regulated by dbcAMP or all-trans retinoic acid treatment. Tretinoin 185-198 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 68-71
9121703-0 1997 Increased gene expression of beta-amyloid precursor protein and its homologues APLP1 and APLP2 in human neuroblastoma cells in response to retinoic acid. Tretinoin 139-152 amyloid beta precursor protein Homo sapiens 29-59
8985093-6 1997 Exposure to ATRA in vitro (1 microM for 48 to 96 hr) increased the adhesiveness of APL cells; this effect was particularly evident in the case of sub-endothelial matrix and fibronectin. Tretinoin 12-16 fibronectin 1 Homo sapiens 173-184
8995359-6 1997 Only modification of Cys228 is necessary to inhibit RA binding when RARbeta is modified by reagents which transfer large bulky groups while both Cys228 and Cys267 must be modified when a small functional group is transferred. Tretinoin 52-54 retinoic acid receptor beta Homo sapiens 68-75
9013706-0 1997 Modulation of the retinoic acid and retinoid X receptor signaling pathways in P19 embryonal carcinoma cells by calreticulin. Tretinoin 18-31 calreticulin Homo sapiens 111-123
8995310-7 1997 The amplitude of the synergistic response to dexamethasone and RA increased by reducing the distance between the enhancer and the proximal t-PA promoter. Tretinoin 63-65 plasminogen activator, tissue type Homo sapiens 139-143
8993838-0 1997 Retinoic acid and IFN inhibition of cell proliferation is associated with apoptosis in squamous carcinoma cell lines: role of IRF-1 and TGase II-dependent pathways. Tretinoin 0-13 interferon regulatory factor 1 Homo sapiens 126-131
9551182-5 1997 To investigate the relationships between the spatial distribution of retinoid signalling and the regulation of retinoid target genes, we studied the downregulation by retinoic acid of two genes expressed in anterior regions of the embryo, goosecoid and otx1. Tretinoin 167-180 goosecoid Danio rerio 239-248
9551182-7 1997 Interestingly, a significant downregulation of goosecoid expression by retinoic acid was observed only during midgastrulation but not in earlier stages. Tretinoin 71-84 goosecoid Danio rerio 47-56
9020066-0 1997 Expression of Src-like adapter protein mRNA is induced by all-trans retinoic acid. Tretinoin 68-81 Src like adaptor Homo sapiens 14-38
9049834-8 1997 2) As there are indications that expression of NF-1 type II is related to the state of differentiation, we tried to shift expression of NF-1 from type I to type II by treatment of the neuroblastoma cells with retinoic acid. Tretinoin 209-222 neurofibromin 1 Homo sapiens 47-51
9067636-3 1997 Treatment with retinoic acid (RA, 1 microM) or 1,250(OH)2-vitamin D3 (1,25-D3, 10 nM) increased the expression of the monocytic surface antigens CD11b plus CD11c, and CD11b, CD11c, CD14 plus CD18, respectively. Tretinoin 15-28 integrin subunit beta 2 Homo sapiens 191-195
8989665-3 1997 Cells treated for 24 h with retinoic acid (10 microM) showed a threefold increase in 125I-CNTF binding sites and were up to five times more sensitive to CNTF than untreated cells in stimulating the tyrosine phosphorylation of the transcription factor STAT3. Tretinoin 28-41 signal transducer and activator of transcription 3 Homo sapiens 251-256
9027555-8 1997 Following a 24-h exposure of porcine preadipocytes to retinoic acid at d 1, Northern blot analysis showed that there was a decrease in lipoprotein lipase and adipsin mRNA levels. Tretinoin 54-67 lipoprotein lipase Sus scrofa 135-153
9040537-0 1997 Retinoic acid increases cellular retinol binding protein II mRNA and retinol uptake in the human intestinal Caco-2 cell line. Tretinoin 0-13 retinol binding protein 2 Homo sapiens 24-59
9040537-7 1997 Thus, retinoic acid may regulate CRBPII expression directly or by selectively changing levels of nuclear receptors or other factors. Tretinoin 6-19 retinol binding protein 2 Homo sapiens 33-39
9040537-8 1997 These studies are the first to demonstrate that retinoic acid can modulate endogenous CRBPII mRNA levels and retinol absorption in Caco-2 cells and suggest that human intestinal vitamin A absorption may be regulated by retinoids. Tretinoin 48-61 retinol binding protein 2 Homo sapiens 86-92
9049834-8 1997 2) As there are indications that expression of NF-1 type II is related to the state of differentiation, we tried to shift expression of NF-1 from type I to type II by treatment of the neuroblastoma cells with retinoic acid. Tretinoin 209-222 neurofibromin 1 Homo sapiens 136-140
9049835-2 1997 We have used this model system to study the modulation of the transcriptional expression of putative processing enzymes, two novel metallopeptidases; i.e. N-arginine dibasic convertase (NRD convertase; EC 3.4,24,61) and an aminopeptidase-B after exposure of the cells either to retinoic acid or to synthetic retinoid analogs. Tretinoin 278-291 nardilysin convertase Homo sapiens 186-200
9049837-5 1997 In addition, expression of IL-6 mRNA and peptide was increased by retinoic acid. Tretinoin 66-79 interleukin 6 Homo sapiens 27-31
9285932-0 1997 Retinoic acid regulation of the VIP and PACAP autocrine ligand and receptor system in human neuroblastoma cell lines. Tretinoin 0-13 vasoactive intestinal peptide Homo sapiens 32-35
9285932-3 1997 We sought to determine which receptor gene subtypes are expressed in selected human neuroblastoma cell lines (SH-SY5Y, IMR-32, and LA-N-5), and the effect of RA on the VIP/PACAP ligand/receptor system. Tretinoin 158-160 vasoactive intestinal peptide Homo sapiens 168-171
9285932-6 1997 In contrast to RA upregulation of VIP binding (confirmed here in IMR-32 cells), levels of both receptor mRNAs were reduced after RA treatment. Tretinoin 15-17 vasoactive intestinal peptide Homo sapiens 34-37
9285932-8 1997 The studies indicate that several components of the VIP/PACAP autocrine system are regulated in neuroblastoma cell lines during RA differentiation. Tretinoin 128-130 vasoactive intestinal peptide Homo sapiens 52-55
8940169-3 1996 A search for retinoic acid response elements in the ucp gene enhancer was undertaken using mutagenesis and transfection of cultured cells with chloramphenicol acetyltransferase constructs. Tretinoin 13-26 uncoupling protein 1 Rattus norvegicus 52-55
9493287-4 1997 Addition of RA to lympho-stromal cell co-culture results in the enhancement of IL4 and IL7 expression in thymocytes while in thymic epithelial cells IL1 alpha decreased and IL6 and IL7 increased. Tretinoin 12-14 interleukin 4 Homo sapiens 79-82
9493287-4 1997 Addition of RA to lympho-stromal cell co-culture results in the enhancement of IL4 and IL7 expression in thymocytes while in thymic epithelial cells IL1 alpha decreased and IL6 and IL7 increased. Tretinoin 12-14 interleukin 7 Homo sapiens 87-90
9493287-4 1997 Addition of RA to lympho-stromal cell co-culture results in the enhancement of IL4 and IL7 expression in thymocytes while in thymic epithelial cells IL1 alpha decreased and IL6 and IL7 increased. Tretinoin 12-14 interleukin 6 Homo sapiens 173-176
9493287-4 1997 Addition of RA to lympho-stromal cell co-culture results in the enhancement of IL4 and IL7 expression in thymocytes while in thymic epithelial cells IL1 alpha decreased and IL6 and IL7 increased. Tretinoin 12-14 interleukin 7 Homo sapiens 181-184
8940196-6 1996 In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene"s promoter which is required to confer RA induction through RAR.RXR heterodimers. Tretinoin 67-69 cyclin dependent kinase inhibitor 1A Homo sapiens 53-56
8940196-6 1996 In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene"s promoter which is required to confer RA induction through RAR.RXR heterodimers. Tretinoin 123-125 cyclin dependent kinase inhibitor 1A Homo sapiens 53-56
8922411-4 1996 We now report that the activity of the proximal apoE promoter in astrocytes is upregulated by cAMP and retinoic acid, which act synergistically. Tretinoin 103-116 apolipoprotein E Homo sapiens 48-52
8940196-7 1996 These results correlate the RA induction of monocytic differentiation of U937 cells with the transcriptional activation of the p21 gene and suggest a role for this cyclin/cyclin-dependent kinase complex inhibitor in facilitating this differentiation pathway. Tretinoin 28-30 cyclin dependent kinase inhibitor 1A Homo sapiens 127-130
8959336-8 1996 RA addition causes an up-regulation of receptor type IIA expression. Tretinoin 0-2 ATPase, class II, type 9A Mus musculus 53-56
8959344-0 1996 Regulation of involucrin gene expression by retinoic acid and glucocorticoids. Tretinoin 44-57 involucrin Homo sapiens 14-24
8959344-3 1996 Dexamethasone enhanced, and retinoic acid decreased, endogenous involucrin mRNA expression in cells treated with these ligands. Tretinoin 28-41 involucrin Homo sapiens 64-74
8959344-4 1996 Functional interactions between each ligand were observed; all-trans or 9-cis retinoic acid reduced dexamethasone enhancement of involucrin expression. Tretinoin 78-91 involucrin Homo sapiens 129-139
8959344-11 1996 Based on these data, we suggest that suppression of involucrin promoter activity by retinoic acid may be mediated through interaction with the AP1 transcriptional complex. Tretinoin 84-97 involucrin Homo sapiens 52-62
8975882-1 1996 Interferon-gamma (IFN-gamma), vitamin D3 (VD), and retinoic acid (RA) induce differentiation of human monoblastic leukemia U937 cells to macrophage-like cells with potential superoxide anion-generating activity upon further stimulation. Tretinoin 66-68 interferon gamma Homo sapiens 0-16
8975882-1 1996 Interferon-gamma (IFN-gamma), vitamin D3 (VD), and retinoic acid (RA) induce differentiation of human monoblastic leukemia U937 cells to macrophage-like cells with potential superoxide anion-generating activity upon further stimulation. Tretinoin 66-68 interferon gamma Homo sapiens 18-27
8922411-5 1996 Sequence analysis of the apoE promoter indicated the presence of several AP-2 consensus sequences that could mediate the stimulatory effect of cAMP and retinoic acid. Tretinoin 152-165 apolipoprotein E Homo sapiens 25-29
8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 46-48 transforming growth factor beta 1 Homo sapiens 119-127
8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 46-48 transforming growth factor beta 1 Homo sapiens 154-162
8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 223-225 transforming growth factor beta 1 Homo sapiens 119-127
8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 223-225 transforming growth factor beta 1 Homo sapiens 154-162
8946934-7 1996 These data show that, in combination with IL-3, RA additionally stimulates quiescent bone marrow progenitors in a simultaneous way, and that it increases sensitivity of the progenitors to the inhibitory action of TGF-beta. Tretinoin 48-50 transforming growth factor beta 1 Homo sapiens 213-221
8944731-3 1996 Exposure of fetal rat lung explants to all trans-retinoic acid for 4 h resulted in a significant dose-dependent increase in SP-A, -B, and -C mRNA with markedly different dose-response characteristics. Tretinoin 43-62 surfactant protein A1 Rattus norvegicus 124-140
9027335-5 1996 Elements allowing regulation by vitamin D3, pituitary-specific factors and Pit-1-dependent response to retinoic acid are well conserved. Tretinoin 103-116 POU class 1 homeobox 1 Rattus norvegicus 75-80
8941706-0 1996 Analysis of connexin43 gene expression induced by retinoic acid in F9 teratocarcinoma cells. Tretinoin 50-63 gap junction protein, alpha 1 Mus musculus 12-22
8941706-1 1996 All-trans retinoic acid (10(-7) M) induces cell-cell communication and expression of the gap junction protein connexin43 in mouse F9 teratocarcinoma cells. Tretinoin 0-23 gap junction protein, alpha 1 Mus musculus 110-120
8941706-2 1996 Northern blot analysis revealed an increase of connexin43 mRNA after treatment with retinoic acid, accompanied by an increase of the mRNA of collagen IV, a differentiation marker. Tretinoin 84-97 gap junction protein, alpha 1 Mus musculus 47-57
8941706-5 1996 Therefore, we postulate a post-transcriptional mechanism responsible for the regulation of connexin43 mRNA levels by retinoic acid. Tretinoin 117-130 gap junction protein, alpha 1 Mus musculus 91-101
8934535-0 1996 Mechanism of all-trans-retinoic acid-mediated L-myc gene regulation in small cell lung cancer. Tretinoin 13-36 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 46-51
8934535-2 1996 We have previously reported that all-trans-retinoic acid (RA) inhibits the growth of NCI-H82 SCLC cells in association with increased neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression. Tretinoin 33-56 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 176-181
8934535-2 1996 We have previously reported that all-trans-retinoic acid (RA) inhibits the growth of NCI-H82 SCLC cells in association with increased neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression. Tretinoin 58-60 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 176-181
8934535-3 1996 In the present report, the mechanism of RA-mediated L-myc up-regulation in NCI-H82 SCLC cells was determined by analysing transcriptional and post-transcriptional control of L-myc gene expression. Tretinoin 40-42 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 52-57
8934535-3 1996 In the present report, the mechanism of RA-mediated L-myc up-regulation in NCI-H82 SCLC cells was determined by analysing transcriptional and post-transcriptional control of L-myc gene expression. Tretinoin 40-42 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 174-179
8934535-4 1996 Increases in steady-state levels of L-myc mRNA occurred in a dose-dependent manner after exposure to RA at a time-point prior to discernible changes in cellular morphology or growth. Tretinoin 101-103 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 36-41
8934535-5 1996 By nuclear run-on analysis, there was a clear increase in L-myc transcript initiation in NCI-H82 cells treated with 1 microM RA, but no alteration was noted in the baseline degree of transcript attenuation when compared to control cells. Tretinoin 125-127 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 58-63
8934535-8 1996 We conclude that RA-mediated up-regulation of L-myc gene expression occurs through stimulation of transcript initiation and that the biological effects of RA in SCLC cells may be mediated through RARbeta-dependent pathways. Tretinoin 17-19 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 46-51
8934535-8 1996 We conclude that RA-mediated up-regulation of L-myc gene expression occurs through stimulation of transcript initiation and that the biological effects of RA in SCLC cells may be mediated through RARbeta-dependent pathways. Tretinoin 155-157 retinoic acid receptor beta Homo sapiens 196-203
8945961-2 1996 Of three compounds known to stimulate t-PA synthesis in cultured human endothelial cells, i.e., retinoic acid, the protein kinase C activator 4 beta-phorbol 12-myristate 13-acetate (PMA), and sodium butyrate, only butyrate (1 mM) caused about a threefold increase in t-PA synthesis and mRNA expression in HMC after 24 h of incubation, without markedly affecting PAI-1 synthesis. Tretinoin 96-109 plasminogen activator, tissue type Homo sapiens 38-42
8944731-4 1996 The maximal (2.5x) increase in SP-A mRNA was observed with 10(-10) M retinoic acid, whereas treatment with 10(-5) M resulted in a tendency to decreased levels. Tretinoin 69-82 surfactant protein A1 Rattus norvegicus 31-35
8944731-5 1996 In contrast, maximal stimulation of SP-C (6x) was noted at 10(-5) M retinoic acid and that of SP-B (2x) at 10(-7) to 10(-5) M retinoic acid. Tretinoin 68-81 surfactant protein C Rattus norvegicus 36-40
8944731-7 1996 A retinoic acid response element consensus sequence was identified in the rat SP-A gene; we hypothesize that retinoic acid-receptor complexes act directly on the SP-A gene via this response element. Tretinoin 2-15 surfactant protein A1 Rattus norvegicus 78-82
8944731-7 1996 A retinoic acid response element consensus sequence was identified in the rat SP-A gene; we hypothesize that retinoic acid-receptor complexes act directly on the SP-A gene via this response element. Tretinoin 2-15 surfactant protein A1 Rattus norvegicus 162-166
8977666-3 1996 Five weeks of topical RA led to thickening of the spinous and granular compartments, induction of keratins K6, K16 and K17, and suppression of filaggrin expression. Tretinoin 22-24 keratin 16 Mus musculus 111-114
8945636-10 1996 CAT assays demonstrated that overexpression of RXRalpha conferred the best RA response, consistent with our previous observation that 9-cis-RA is more potent than all-trans-RA for inducing the expression of the AFP gene. Tretinoin 75-77 retinoid X receptor alpha Rattus norvegicus 47-55
8930166-2 1996 The following agents inhibited phorbol 12-myristate 13-acetate-stimulated O2- generation significantly in the all-trans retinoic acid-treated HL-60 cells (expressed as percentage of control, P < .05): 1) PKC inhibitors: staurosporine (100 nM, 3 +/- 1%); Ro 31-8220 (1 microM, 3 +/- 2%); sphingosine (100 microM, 15 +/- 7%); 2) PSP 1 and 2a inhibitors, okadaic acid (10 microM, 35 +/- 1%); calyculin A (10 microM, 73 +/- 1%); 3) MAPK inhibitor: SB-203580 (100 microM, 62 +/- 1%); 4) PTP inhibitors: phenylarsine oxide (1 microM, 12 +/- 9%); diamide (1 mM, 21 +/- 11%); and 5) secretory phospholipase A2 inhibitors: manoalide (1 microM, 24 +/- 10%); scalaradial (1 microM, 11 +/- 4%). Tretinoin 120-133 phospholipase A2 group IB Homo sapiens 588-604
8908199-2 1996 This inhibition results, at least in part, from RA-induced decreases in the mRNA for the transactivators Fos and Jun (with concominant increases in RAR mRNA) and by sequestration of Fos/Jun by RARs/RXRs. Tretinoin 48-50 arginine--tRNA ligase, cytoplasmic Oryctolagus cuniculus 193-197
8900159-0 1996 Retinoic acid-induced transcriptional modulation of the human interferon-gamma promoter. Tretinoin 0-13 interferon gamma Homo sapiens 62-78
8900159-2 1996 In particular, IFN-gamma gene expression is significantly affected by vitamin A and/or its derivatives (e.g. retinoic acid (RA)). Tretinoin 109-122 interferon gamma Homo sapiens 15-24
8900159-2 1996 In particular, IFN-gamma gene expression is significantly affected by vitamin A and/or its derivatives (e.g. retinoic acid (RA)). Tretinoin 124-126 interferon gamma Homo sapiens 15-24
8900159-3 1996 Here, we analyze the effect of retinoic acid on IFN-gamma transcription. Tretinoin 31-44 interferon gamma Homo sapiens 48-57
8900159-4 1996 Transient transfection assays in the human T lymphoblastoid cell line Jurkat demonstrated that the activation of the IFN-gamma promoter was significantly down-regulated in the presence of RA. Tretinoin 188-190 interferon gamma Homo sapiens 117-126
9387294-2 1996 It was found that RA could only inhibit the growth of ER-positive but not ER-negative breast cancer cells. Tretinoin 18-20 estrogen receptor 1 Homo sapiens 54-56
9387294-5 1996 When, RAR alpha cDNA was introduced and ixpressed in RA-resistant, ER-negative MDA-MB-231 breast cancer cell line, its growth was strongly inhibited by RA. Tretinoin 6-8 estrogen receptor 1 Homo sapiens 67-69
8900181-6 1996 Electrophoretic mobility shift assays with nuclear extracts of A3 cells showed that stimulation with ATRA and TNF-alpha for more than 16 h resulted in enhanced NF-kappaB binding compared to that induced by TNF-alpha alone. Tretinoin 101-105 nuclear factor kappa B subunit 1 Homo sapiens 160-169
8900181-6 1996 Electrophoretic mobility shift assays with nuclear extracts of A3 cells showed that stimulation with ATRA and TNF-alpha for more than 16 h resulted in enhanced NF-kappaB binding compared to that induced by TNF-alpha alone. Tretinoin 101-105 tumor necrosis factor Homo sapiens 206-215
8900181-7 1996 The simultaneous treatment with ATRA and TNF-alpha also resulted in changes in the composition of NF-kappaB complexes bound to the IL-8 NF-kappaB site, preventing the formation of two TNF-alpha-inducible binding activities. Tretinoin 32-36 nuclear factor kappa B subunit 1 Homo sapiens 98-107
8900181-7 1996 The simultaneous treatment with ATRA and TNF-alpha also resulted in changes in the composition of NF-kappaB complexes bound to the IL-8 NF-kappaB site, preventing the formation of two TNF-alpha-inducible binding activities. Tretinoin 32-36 C-X-C motif chemokine ligand 8 Homo sapiens 131-135
8900181-7 1996 The simultaneous treatment with ATRA and TNF-alpha also resulted in changes in the composition of NF-kappaB complexes bound to the IL-8 NF-kappaB site, preventing the formation of two TNF-alpha-inducible binding activities. Tretinoin 32-36 nuclear factor kappa B subunit 1 Homo sapiens 136-145
8900181-7 1996 The simultaneous treatment with ATRA and TNF-alpha also resulted in changes in the composition of NF-kappaB complexes bound to the IL-8 NF-kappaB site, preventing the formation of two TNF-alpha-inducible binding activities. Tretinoin 32-36 tumor necrosis factor Homo sapiens 184-193
8830674-3 1996 We show here that bax protein also declined with a time course similar to the downregulation of bcl-2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 198-211 BCL2 associated X, apoptosis regulator Homo sapiens 18-21
8830674-3 1996 We show here that bax protein also declined with a time course similar to the downregulation of bcl-2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 198-211 BCL2 apoptosis regulator Homo sapiens 96-101
8830674-3 1996 We show here that bax protein also declined with a time course similar to the downregulation of bcl-2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 213-215 BCL2 associated X, apoptosis regulator Homo sapiens 18-21
8830674-3 1996 We show here that bax protein also declined with a time course similar to the downregulation of bcl-2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 213-215 BCL2 apoptosis regulator Homo sapiens 96-101
8898244-2 1996 We previously reported that, in P19 embryonal carcinoma cells, the expression of kinase-negative EGFR inhibits retinoic acid (RA)-induced differentiation to nervous tissue, suggesting that EGFR plays a role in differentiation (J.-X. Tretinoin 111-124 epidermal growth factor receptor Homo sapiens 97-101
8875981-0 1996 Constitutive expression of the Wilms tumor suppressor gene WT1 in F9 embryonal carcinoma cells induces apoptotic cell death in response to retinoic acid. Tretinoin 139-152 WT1 transcription factor Homo sapiens 59-62
8875981-2 1996 To elucidate the function of WT1 in cellular differentiation, we examined the changes in the level of WT1 expression during retinoic acid induced-differentiation of embryonal carcinoma F9 cells into parietal endoderm cells. Tretinoin 124-137 WT1 transcription factor Homo sapiens 102-105
8875981-3 1996 We found that, in response to retinoic acid addition, the expression of WT1 increased significantly after 12--24 h of incubation, then decreased and finally disappeared after 4 days, by which time most of the cells had differentiated into primitive endoderm cells. Tretinoin 30-43 WT1 transcription factor Homo sapiens 72-75
8898244-2 1996 We previously reported that, in P19 embryonal carcinoma cells, the expression of kinase-negative EGFR inhibits retinoic acid (RA)-induced differentiation to nervous tissue, suggesting that EGFR plays a role in differentiation (J.-X. Tretinoin 111-124 epidermal growth factor receptor Homo sapiens 189-193
8898244-2 1996 We previously reported that, in P19 embryonal carcinoma cells, the expression of kinase-negative EGFR inhibits retinoic acid (RA)-induced differentiation to nervous tissue, suggesting that EGFR plays a role in differentiation (J.-X. Tretinoin 126-128 epidermal growth factor receptor Homo sapiens 97-101
8898244-2 1996 We previously reported that, in P19 embryonal carcinoma cells, the expression of kinase-negative EGFR inhibits retinoic acid (RA)-induced differentiation to nervous tissue, suggesting that EGFR plays a role in differentiation (J.-X. Tretinoin 126-128 epidermal growth factor receptor Homo sapiens 189-193
8811066-15 1996 EBV-transformed B-cell clones incubated with RA for 6 days produced a 20- to 45-fold increase in IL-6. Tretinoin 45-47 interleukin 6 Homo sapiens 97-101
8841418-0 1996 Retinoic acid stimulates the transcription of insulin-like growth factor binding protein-6 in skeletal cells. Tretinoin 0-13 insulin-like growth factor binding protein 6 Rattus norvegicus 46-90
8841418-4 1996 In fibroblasts, IGFBP-6 levels are regulated by retinoic acid, and we postulated that retinoic acid may regulate IGF II in bone by altering IGFBP-6 synthesis. Tretinoin 48-61 insulin-like growth factor binding protein 6 Rattus norvegicus 16-23
8841418-4 1996 In fibroblasts, IGFBP-6 levels are regulated by retinoic acid, and we postulated that retinoic acid may regulate IGF II in bone by altering IGFBP-6 synthesis. Tretinoin 86-99 insulin-like growth factor binding protein 6 Rattus norvegicus 140-147
8841418-5 1996 We examined the effect of retinoic acid on IGFBP-6 expression in cultures of osteoblast-enriched cells from 22-day fetal rat calvariae (Ob cells). Tretinoin 26-39 insulin-like growth factor binding protein 6 Rattus norvegicus 43-50
8841418-6 1996 Retinoic acid caused a time- and dose-dependent increase in IGFBP-6 mRNA levels, as determined by Northern blot analysis. Tretinoin 0-13 insulin-like growth factor binding protein 6 Rattus norvegicus 60-67
8841418-8 1996 Retinoic acid increased IGFBP-6 polypeptide levels in the culture medium, as determined by Western immunoblot analysis. Tretinoin 0-13 insulin-like growth factor binding protein 6 Rattus norvegicus 24-31
8841418-10 1996 The decay of IGFBP-6 mRNA in transcriptionally arrested Ob cells was similar in control and retinoic acid-treated cells, and retinoic acid increased the rates of IGFBP-6 transcription, as determined by nuclear run on assays. Tretinoin 92-105 insulin-like growth factor binding protein 6 Rattus norvegicus 13-20
8841418-10 1996 The decay of IGFBP-6 mRNA in transcriptionally arrested Ob cells was similar in control and retinoic acid-treated cells, and retinoic acid increased the rates of IGFBP-6 transcription, as determined by nuclear run on assays. Tretinoin 125-138 insulin-like growth factor binding protein 6 Rattus norvegicus 162-169
8841418-11 1996 In conclusion, retinoic acid enhances IGFBP-6 expression in Ob cells by transcriptional mechanisms. Tretinoin 15-28 insulin-like growth factor binding protein 6 Rattus norvegicus 38-45
8841418-12 1996 Since IGFBP-6 prevents the effects of IGF II, increased synthesis of IGFBP-6 could mediate selected actions of retinoic acid in bone. Tretinoin 111-124 insulin-like growth factor binding protein 6 Rattus norvegicus 69-76
8823154-0 1996 Involvement of alcohol dehydrogenase, short-chain dehydrogenase/reductase, aldehyde dehydrogenase, and cytochrome P450 in the control of retinoid signaling by activation of retinoic acid synthesis. Tretinoin 173-186 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 103-118
8982293-3 1996 After 5 d exposure to ATRA 10(-6) M APL-treated samples showed a significant reduction of IL-6 (p = 0.008) and GM-CSF (p = 0.03) and a significant increase of IL-1 alpha (p = 0.01) production, if compared to untreated APL samples. Tretinoin 22-26 interleukin 6 Homo sapiens 90-94
8877104-7 1996 Stimulation by RA resulted in increased RAR beta/RXR DNA binding, activated RARE-dependent transcription, and increased expression of RAR-beta. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 40-48
8877104-7 1996 Stimulation by RA resulted in increased RAR beta/RXR DNA binding, activated RARE-dependent transcription, and increased expression of RAR-beta. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 134-142
8877104-8 1996 Concomitant stimulation by VitD3 inhibited the RA-stimulated formation of RAR beta/RXR heterodimers, favoring VDR/RXR binding to the RARE. Tretinoin 47-49 retinoic acid receptor beta Homo sapiens 74-82
8875075-4 1996 To determine whether these retinoic acid-induced changes in lung development were linked to alterations in pattern-related genes, we characterized the expression of Hoxa-2, Hoxb-6, and Sonic hedgehog mRNAs in vivo and in vitro, with or without 10(-5)M retinoic acid, by in situ hybridization and quantitative polymerase chain reaction. Tretinoin 27-40 homeo box A2 Rattus norvegicus 165-171
9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 191-204 estrogen receptor 1 Homo sapiens 35-52
9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 191-204 estrogen receptor 1 Homo sapiens 54-56
9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 191-204 estrogen receptor 1 Homo sapiens 122-124
9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 206-208 estrogen receptor 1 Homo sapiens 35-52
9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 206-208 estrogen receptor 1 Homo sapiens 54-56
9387397-3 1996 Recently studies demonstrated that estrogen receptor (ER)-positive human breast cancer (HBC) cell lines are sensitive and ER-negative cell lines are resistant to growth inhibitory effects of retinoic acid (RA). Tretinoin 206-208 estrogen receptor 1 Homo sapiens 122-124
8906581-5 1996 12-0-Tetradecanoylphorbol 13-acetate (TPA) stimulation activated a phospholipase D (PLD) specific for phosphatidylcholine (PtdCho) in proliferating cells and a phospholipase C (PLC) specific for phosphatidylethanolamine (PtdEtn) in retinoic acid (RA) differentiated cells. Tretinoin 232-245 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 67-82
8884182-1 1996 Liarozole inhibits cytochrome P-450-dependent enzymes that play a key role in all-trans-retinoic acid (ATRA) catabolism. Tretinoin 82-101 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 19-35
8884182-1 1996 Liarozole inhibits cytochrome P-450-dependent enzymes that play a key role in all-trans-retinoic acid (ATRA) catabolism. Tretinoin 103-107 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 19-35
8826891-0 1996 Down-regulation of bcl-2 in AML blasts by all-trans retinoic acid and its relationship to CD34 antigen expression. Tretinoin 52-65 BCL2 apoptosis regulator Homo sapiens 19-24
8826891-3 1996 All-trans retinoic acid (ATRA) has been reported to increase the sensitivity of AML cell lines to Ara-C and to induce differentiation in the HL60 promyelocytic cell line, with both effects being accompanied by a decrease in bcl-2 expression. Tretinoin 0-23 BCL2 apoptosis regulator Homo sapiens 224-229
8826891-3 1996 All-trans retinoic acid (ATRA) has been reported to increase the sensitivity of AML cell lines to Ara-C and to induce differentiation in the HL60 promyelocytic cell line, with both effects being accompanied by a decrease in bcl-2 expression. Tretinoin 25-29 BCL2 apoptosis regulator Homo sapiens 224-229
8826891-4 1996 Using flow cytometry and a monoclonal antibody to bcl-2, we have investigated the effects of ATRA (1 microM) on bcl-2 expression in the blast cells of 25 AML patients and the K562 cell line after incubation for 72 or 24 h, respectively. Tretinoin 93-97 BCL2 apoptosis regulator Homo sapiens 112-117
8826891-5 1996 Using Kolmogorov-Smirnov statistical analysis where a D value of > 0.12 was statistically significant, we found that in 8/25 AML samples and the K562 cells there was a significant decrease in bcl-2 protein expression after incubation with ATRA (D value range 0.14-0.44). Tretinoin 242-246 BCL2 apoptosis regulator Homo sapiens 195-200
8826891-6 1996 The mean peak fluorescence (MPF) values for the bcl-2 levels of the ATRA responders (n = 8) was reduced to 35.5 +/- 6.9 following incubation with ATRA compared to 47.6 +/- 8.2 (mean +/- SEM) for control samples incubated in the absence of ATRA (P = 0.014). Tretinoin 68-72 BCL2 apoptosis regulator Homo sapiens 48-53
8826891-6 1996 The mean peak fluorescence (MPF) values for the bcl-2 levels of the ATRA responders (n = 8) was reduced to 35.5 +/- 6.9 following incubation with ATRA compared to 47.6 +/- 8.2 (mean +/- SEM) for control samples incubated in the absence of ATRA (P = 0.014). Tretinoin 146-150 BCL2 apoptosis regulator Homo sapiens 48-53
8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 23-28
8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 43-47 CD34 molecule Homo sapiens 81-85
8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 154-158 BCL2 apoptosis regulator Homo sapiens 23-28
8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 154-158 BCL2 apoptosis regulator Homo sapiens 178-183
8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 154-158 CD34 molecule Homo sapiens 196-200
8826891-9 1996 Our data suggest that the addition of ATRA to combination chemotherapy would increase the chemosensitivity of some patients with AML, particularly CD34-negative AML, due to down-regulation of bcl-2 expression. Tretinoin 38-42 CD34 molecule Homo sapiens 147-151
8826891-9 1996 Our data suggest that the addition of ATRA to combination chemotherapy would increase the chemosensitivity of some patients with AML, particularly CD34-negative AML, due to down-regulation of bcl-2 expression. Tretinoin 38-42 BCL2 apoptosis regulator Homo sapiens 192-197
8906581-5 1996 12-0-Tetradecanoylphorbol 13-acetate (TPA) stimulation activated a phospholipase D (PLD) specific for phosphatidylcholine (PtdCho) in proliferating cells and a phospholipase C (PLC) specific for phosphatidylethanolamine (PtdEtn) in retinoic acid (RA) differentiated cells. Tretinoin 232-245 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 84-87
8906581-5 1996 12-0-Tetradecanoylphorbol 13-acetate (TPA) stimulation activated a phospholipase D (PLD) specific for phosphatidylcholine (PtdCho) in proliferating cells and a phospholipase C (PLC) specific for phosphatidylethanolamine (PtdEtn) in retinoic acid (RA) differentiated cells. Tretinoin 247-249 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 67-82
8906581-5 1996 12-0-Tetradecanoylphorbol 13-acetate (TPA) stimulation activated a phospholipase D (PLD) specific for phosphatidylcholine (PtdCho) in proliferating cells and a phospholipase C (PLC) specific for phosphatidylethanolamine (PtdEtn) in retinoic acid (RA) differentiated cells. Tretinoin 247-249 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 84-87
9639813-7 1996 Addition of suitable amount of anti-TGF-beta 1 monoclonal antibody IgG (TB21) to the culture medium of embryoid bodies of ES-T6 cells could effectively abolish the formation of vessel-like structures induced by retinoic acid. Tretinoin 211-224 transforming growth factor beta 1 Homo sapiens 36-46
8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 interleukin 1 beta Homo sapiens 123-141
8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 82-105 estrogen receptor 1 Homo sapiens 14-31
8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 82-105 estrogen receptor 1 Homo sapiens 33-35
8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 107-109 estrogen receptor 1 Homo sapiens 14-31
8702769-1 1996 The growth of estrogen receptor (ER)-positive breast cancer cells is inhibited by all-trans-retinoic acid (RA). Tretinoin 107-109 estrogen receptor 1 Homo sapiens 33-35
8702769-2 1996 In the present study, estrogen (E2) induction of pS2 mRNA levels was significantly reduced within 6 h following cotreatment with RA. Tretinoin 129-131 taste 2 receptor member 64 pseudogene Homo sapiens 49-52
8753804-0 1996 The opposing effects of retinoic acid and phorbol esters converge to a common response element in the promoter of the rat cholesterol 7 alpha-hydroxylase gene (CYP7A). Tretinoin 24-37 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 122-153
8753812-0 1996 Production of granulocyte colony-stimulating factor by THP-1 cells in response to retinoic acid and phorbol ester is mediated through the autocrine production of interleukin-1. Tretinoin 82-95 GLI family zinc finger 2 Homo sapiens 55-60
8806447-7 1996 In addition, treatment of Rcho-1 cells with retinoic acid for 7 days upregulated expression of cx43 transcript, but no protein could be found. Tretinoin 44-57 gap junction protein, alpha 1 Rattus norvegicus 95-99
8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 interleukin 1 beta Homo sapiens 143-152
8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 interleukin 1 beta Homo sapiens 178-187
8765131-0 1996 Characteristic properties of a retinoic acid synthetic cytochrome P-450 purified from liver microsomes of 3-methylcholanthrene-induced rats. Tretinoin 31-44 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 55-71
8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 67-69 GLI family zinc finger 2 Homo sapiens 103-108
8765131-1 1996 An inducible cytochrome P-450 (P-450) catalyzing retinoic acid synthesis was purified from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats, based on the activity of all-trans-retinoic acid formation from all-trans-retinal. Tretinoin 49-62 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 13-29
8765131-1 1996 An inducible cytochrome P-450 (P-450) catalyzing retinoic acid synthesis was purified from liver microsomes of 3-methylcholanthrene (3-MC)-treated rats, based on the activity of all-trans-retinoic acid formation from all-trans-retinal. Tretinoin 182-201 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 13-29
8765131-2 1996 We previously reported that the retinoic acid synthesis by microsomes was catalyzed by a cytochrome P-450-linked monooxygenase system (Tomita et al. Tretinoin 32-45 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 89-105
8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 162-164 interleukin 1 beta Homo sapiens 37-41
8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 162-164 GLI family zinc finger 2 Homo sapiens 103-108
8753812-6 1996 Finally, we demonstrated that RA can also enhance IL-1-induced G-CSF production in primary monocytes of human peripheral blood. Tretinoin 30-32 interleukin 1 beta Homo sapiens 50-54
8760353-2 1996 Here we show that all-trans-retinoic acid (RA) treatment prevented the growth restriction of HFL 6-2 cells at 39 degrees C. In the presence of RA, HFL 6-2 cells proliferated into sizeable colonies even at 39 degrees C. [3H]Thymidine incorporation and flow cytometry analysis revealed that cells exposed to RA maintained DNA synthesis at 39 degrees C. Prevention of growth restriction by RA was correlated with a lack of induction of p21 at the transcription level. Tretinoin 18-41 cyclin dependent kinase inhibitor 1A Homo sapiens 433-436
8702454-7 1996 This study documents in vivo the ability of all-trans-retinoic acid to down-regulate the release of IL-6, IL-1 beta, and TNF alpha, and illustrates its potential as a therapeutic agent in conditions associated with chronic overproduction of proinflammatory cytokines. Tretinoin 44-67 interleukin 1 beta Homo sapiens 106-115
8702454-7 1996 This study documents in vivo the ability of all-trans-retinoic acid to down-regulate the release of IL-6, IL-1 beta, and TNF alpha, and illustrates its potential as a therapeutic agent in conditions associated with chronic overproduction of proinflammatory cytokines. Tretinoin 44-67 tumor necrosis factor Homo sapiens 121-130
8702454-5 1996 Serum levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), and IL-1 beta normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. Tretinoin 152-161 interleukin 6 Homo sapiens 16-29
8702454-5 1996 Serum levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), and IL-1 beta normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. Tretinoin 152-161 tumor necrosis factor Homo sapiens 38-65
8702454-5 1996 Serum levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), and IL-1 beta normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. Tretinoin 152-161 tumor necrosis factor Homo sapiens 67-76
8702454-5 1996 Serum levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), and IL-1 beta normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. Tretinoin 152-161 interleukin 1 beta Homo sapiens 83-92
8702454-7 1996 This study documents in vivo the ability of all-trans-retinoic acid to down-regulate the release of IL-6, IL-1 beta, and TNF alpha, and illustrates its potential as a therapeutic agent in conditions associated with chronic overproduction of proinflammatory cytokines. Tretinoin 44-67 interleukin 6 Homo sapiens 100-104
8760353-2 1996 Here we show that all-trans-retinoic acid (RA) treatment prevented the growth restriction of HFL 6-2 cells at 39 degrees C. In the presence of RA, HFL 6-2 cells proliferated into sizeable colonies even at 39 degrees C. [3H]Thymidine incorporation and flow cytometry analysis revealed that cells exposed to RA maintained DNA synthesis at 39 degrees C. Prevention of growth restriction by RA was correlated with a lack of induction of p21 at the transcription level. Tretinoin 43-45 cyclin dependent kinase inhibitor 1A Homo sapiens 433-436
8760353-2 1996 Here we show that all-trans-retinoic acid (RA) treatment prevented the growth restriction of HFL 6-2 cells at 39 degrees C. In the presence of RA, HFL 6-2 cells proliferated into sizeable colonies even at 39 degrees C. [3H]Thymidine incorporation and flow cytometry analysis revealed that cells exposed to RA maintained DNA synthesis at 39 degrees C. Prevention of growth restriction by RA was correlated with a lack of induction of p21 at the transcription level. Tretinoin 143-145 cyclin dependent kinase inhibitor 1A Homo sapiens 433-436
8760353-2 1996 Here we show that all-trans-retinoic acid (RA) treatment prevented the growth restriction of HFL 6-2 cells at 39 degrees C. In the presence of RA, HFL 6-2 cells proliferated into sizeable colonies even at 39 degrees C. [3H]Thymidine incorporation and flow cytometry analysis revealed that cells exposed to RA maintained DNA synthesis at 39 degrees C. Prevention of growth restriction by RA was correlated with a lack of induction of p21 at the transcription level. Tretinoin 143-145 cyclin dependent kinase inhibitor 1A Homo sapiens 433-436
8760353-2 1996 Here we show that all-trans-retinoic acid (RA) treatment prevented the growth restriction of HFL 6-2 cells at 39 degrees C. In the presence of RA, HFL 6-2 cells proliferated into sizeable colonies even at 39 degrees C. [3H]Thymidine incorporation and flow cytometry analysis revealed that cells exposed to RA maintained DNA synthesis at 39 degrees C. Prevention of growth restriction by RA was correlated with a lack of induction of p21 at the transcription level. Tretinoin 143-145 cyclin dependent kinase inhibitor 1A Homo sapiens 433-436
8760353-3 1996 These observations suggest that RA may prevent the senescence process by repressing p21 gene expression, and perturb the growth regulation of somatic cells. Tretinoin 32-34 cyclin dependent kinase inhibitor 1A Homo sapiens 84-87
8754738-8 1996 With T3 (10 nM) together with RA (3, 10, or 100 nM), the maximal SHBG responses were reduced to 193 +/- 24%, 151 +/- 5% and 132 +/- 30%, respectively. Tretinoin 30-32 sex hormone binding globulin Homo sapiens 65-69
8687982-6 1996 IGF1 and anti-EGF antibody diminished the effects of RA on PPi elaboration. Tretinoin 53-55 insulin like growth factor 1 Homo sapiens 0-4
8687982-8 1996 As some RA effects are mediated through increased activity of TGFbeta, a known PPi stimulant, we examined the effect of anti-TGFbeta antibody on RA-induced PPi elaboration. Tretinoin 145-147 transforming growth factor beta 1 Homo sapiens 125-132
8754760-0 1996 Differential growth regulation by all-trans retinoic acid is determined by protein kinase C alpha in human pancreatic carcinoma cells. Tretinoin 44-57 protein kinase C alpha Homo sapiens 75-97
8754760-1 1996 We have investigated the role of protein kinase C (PKC) isoenzymes in the differential growth regulation of human pancreatic carcinoma cell lines by all-trans retinoic acid (RA). Tretinoin 159-172 protein kinase C alpha Homo sapiens 51-54
8754760-1 1996 We have investigated the role of protein kinase C (PKC) isoenzymes in the differential growth regulation of human pancreatic carcinoma cell lines by all-trans retinoic acid (RA). Tretinoin 174-176 protein kinase C alpha Homo sapiens 51-54
8754760-5 1996 Incubation with RA in the growth-stimulated AsPc1 cell line resulted in induction of PKC alpha expression, whereas PKC alpha expression was decreased by RA in the growth-inhibited Capan 2 cell line. Tretinoin 16-18 protein kinase C alpha Homo sapiens 85-94
8754778-0 1996 A complex retinoic acid response element in the uncoupling protein gene defines a novel role for retinoids in thermogenesis. Tretinoin 10-23 uncoupling protein 1 Rattus norvegicus 48-66
8844688-2 1996 The FGF-4 gene is expressed in EC cells and ES cells, but it is repressed in their retinoic acid (RA)-induced differentiated counterparts. Tretinoin 83-96 fibroblast growth factor 4 Mus musculus 4-9
8754778-2 1996 We report here the molecular bases for a metabolic role of RA, by showing that the expression of the uncoupling protein (UCP), the key element in brown adipose tissue (BAT) thermogenesis, is stimulated by retinoic acid (RA). Tretinoin 59-61 uncoupling protein 1 Rattus norvegicus 101-119
8754778-2 1996 We report here the molecular bases for a metabolic role of RA, by showing that the expression of the uncoupling protein (UCP), the key element in brown adipose tissue (BAT) thermogenesis, is stimulated by retinoic acid (RA). Tretinoin 59-61 uncoupling protein 1 Rattus norvegicus 121-124
8754778-2 1996 We report here the molecular bases for a metabolic role of RA, by showing that the expression of the uncoupling protein (UCP), the key element in brown adipose tissue (BAT) thermogenesis, is stimulated by retinoic acid (RA). Tretinoin 205-218 uncoupling protein 1 Rattus norvegicus 101-119
8754778-2 1996 We report here the molecular bases for a metabolic role of RA, by showing that the expression of the uncoupling protein (UCP), the key element in brown adipose tissue (BAT) thermogenesis, is stimulated by retinoic acid (RA). Tretinoin 205-218 uncoupling protein 1 Rattus norvegicus 121-124
8754778-2 1996 We report here the molecular bases for a metabolic role of RA, by showing that the expression of the uncoupling protein (UCP), the key element in brown adipose tissue (BAT) thermogenesis, is stimulated by retinoic acid (RA). Tretinoin 220-222 uncoupling protein 1 Rattus norvegicus 101-119
8754778-2 1996 We report here the molecular bases for a metabolic role of RA, by showing that the expression of the uncoupling protein (UCP), the key element in brown adipose tissue (BAT) thermogenesis, is stimulated by retinoic acid (RA). Tretinoin 220-222 uncoupling protein 1 Rattus norvegicus 121-124
8754778-4 1996 Transient transfection experiments in HIB-1B cells, a BAT-derived cell line, identified the sequence -2399/-2490 (called R90) as the RA-responsive sequence in the rat UCP gene. Tretinoin 133-135 uncoupling protein 1 Rattus norvegicus 167-170
8754778-7 1996 RA effect was also less when chloramphenicol acetyl transferase gene was driven by a heterologous promoter instead of the UCP minimal promoter. Tretinoin 0-2 uncoupling protein 1 Rattus norvegicus 122-125
8757760-3 1996 Retinoic acid 4-hydroxylase activity induced in vivo by 4 d treatment with retinoic acid (0.1%) was inhibited in vitro by liarozole in a concentration-dependent manner. Tretinoin 75-88 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 0-27
8754760-5 1996 Incubation with RA in the growth-stimulated AsPc1 cell line resulted in induction of PKC alpha expression, whereas PKC alpha expression was decreased by RA in the growth-inhibited Capan 2 cell line. Tretinoin 153-155 protein kinase C alpha Homo sapiens 115-124
8754760-11 1996 These data, therefore, suggest that differential regulation of PKC alpha expression plays a central role in determining the bidirectional effects of RA on growth in pancreatic carcinoma cells. Tretinoin 149-151 protein kinase C alpha Homo sapiens 63-72
8768885-0 1996 Vitamin A and retinoic acid stimulate within minutes cAMP release and growth hormone secretion in human pituitary cells. Tretinoin 14-27 growth hormone 1 Homo sapiens 70-84
8869596-1 1996 We have previously shown that the response of osteoblasts to parathyroid hormone (PTH) can be influenced at the receptor level by growth on the physiological substrate, type I collagen, or by treatment with retinoic acid. Tretinoin 207-220 parathyroid hormone Rattus norvegicus 61-80
8869596-1 1996 We have previously shown that the response of osteoblasts to parathyroid hormone (PTH) can be influenced at the receptor level by growth on the physiological substrate, type I collagen, or by treatment with retinoic acid. Tretinoin 207-220 parathyroid hormone Rattus norvegicus 82-85
8869596-3 1996 The aim of this study was therefore to examine the effect of retinoic acid and growth on type I collagen on PTH/PTH-related protein (PTHrP) receptor mRNA expression in the osteosarcoma osteoblast-like cell line UMR 106-06. Tretinoin 61-74 parathyroid hormone Rattus norvegicus 108-111
8869596-3 1996 The aim of this study was therefore to examine the effect of retinoic acid and growth on type I collagen on PTH/PTH-related protein (PTHrP) receptor mRNA expression in the osteosarcoma osteoblast-like cell line UMR 106-06. Tretinoin 61-74 parathyroid hormone Rattus norvegicus 112-115
8844688-2 1996 The FGF-4 gene is expressed in EC cells and ES cells, but it is repressed in their retinoic acid (RA)-induced differentiated counterparts. Tretinoin 98-100 fibroblast growth factor 4 Mus musculus 4-9
8755574-3 1996 Clinical remissions induced with all-trans retinoic acid (RA) treatment in acute promyelocytic leukemia are linked to PML/RARalpha expression in leukemic cells. Tretinoin 43-56 promyelocytic leukemia Mus musculus 118-121
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 37-50 retinoic acid receptor beta Homo sapiens 0-8
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 37-50 retinoic acid receptor beta Homo sapiens 208-216
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 208-216
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 52-54 retinoic acid receptor beta Homo sapiens 0-8
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 52-54 retinoic acid receptor beta Homo sapiens 208-216
8707417-5 1996 We report here that severe reduction of RA-induced RAR-beta mRNA levels is a general feature of tumorigenic HeLa x fibroblast segregants. Tretinoin 40-42 retinoic acid receptor beta Homo sapiens 51-59
8707417-7 1996 Remarkably, maximal RA inducibility in 444 cells required the integrity of the complete RAR-beta upstream region. Tretinoin 20-22 retinoic acid receptor beta Homo sapiens 88-96
8707417-13 1996 Similar defects may be responsible for the loss of RA responsiveness of RAR-beta gene expression in other human tumors. Tretinoin 51-53 retinoic acid receptor beta Homo sapiens 72-80
8713132-7 1996 Furthermore, RA induced bcl-2 but prevented the processing of actin, whereas 4-HPR had little effect on bcl-2 but increased the specific processing of actin. Tretinoin 13-15 BCL2 apoptosis regulator Homo sapiens 24-29
8713132-8 1996 These results suggest that RA promotes neutrophil differentiation and the establishment of a semi apoptosis-resistant state, possibly through the overexpression of the bcl-2 gene. Tretinoin 27-29 BCL2 apoptosis regulator Homo sapiens 168-173
8755574-15 1996 Retinoic acid treatment of irradiated PML/RARalpha mice enhanced granulocyte recovery. Tretinoin 0-13 promyelocytic leukemia Mus musculus 38-41
8704165-0 1996 Retinoic acid activates interferon regulatory factor-1 gene expression in myeloid cells. Tretinoin 0-13 interferon regulatory factor 1 Homo sapiens 24-54
8695801-0 1996 Stimulation of tissue-type plasminogen activator expression by retinoic acid in human endothelial cells requires retinoic acid receptor beta 2 induction. Tretinoin 63-76 plasminogen activator, tissue type Homo sapiens 15-48
8686749-4 1996 Although retinoic-acid-treated and untreated tumor cells make the same amount of interleukin-8, the major inducer of neovascularization produced by such tumor lines, they vary in production of inhibitory activity. Tretinoin 9-22 C-X-C motif chemokine ligand 8 Homo sapiens 81-94
8702428-0 1996 Retinoic acid regulates differentially the expression of IL-1 beta and IL-1 receptor antagonist (IL-1ra) in PMA-activated human monocytes. Tretinoin 0-13 interleukin 1 beta Homo sapiens 57-66
8702428-3 1996 In this study, we examined the effect of RA on expression of IL-1 beta and IL-ra in phorbol-myristate-acetate (PMA)-activated human monocytes. Tretinoin 41-43 interleukin 1 beta Homo sapiens 61-70
8702428-4 1996 RA enhanced gene expression and production of IL-1 beta in PMA-activated monocytes. Tretinoin 0-2 interleukin 1 beta Homo sapiens 46-55
8704182-6 1996 NB4 cells treated with ATRA in suspension or on laminin acquired the equivalent ability to reduce nitroblue tetrazolium or cytochrome C. Tretinoin 23-27 cytochrome c, somatic Homo sapiens 123-135
8704165-6 1996 We show that ATRA directly activates IRF-1 gene expression, followed by activation of IRF-2 and 2"-5" oligoadenylate synthetase (OAS) gene expression with slower kinetics. Tretinoin 13-17 interferon regulatory factor 1 Homo sapiens 37-42
8704165-6 1996 We show that ATRA directly activates IRF-1 gene expression, followed by activation of IRF-2 and 2"-5" oligoadenylate synthetase (OAS) gene expression with slower kinetics. Tretinoin 13-17 interferon regulatory factor 2 Homo sapiens 86-91
8704165-7 1996 In addition to NB4 cells, ATRA also activated IRF-1 gene expression in HL-60, U937, and THP-1 cells, which all respond to ATRA by growth inhibition. Tretinoin 26-30 interferon regulatory factor 1 Homo sapiens 46-51
8704165-10 1996 The ATRA-induced expression of IRF-1, an activator of transcription and repressor of transformation, may be one of the molecular mechanisms of ATRA-induced growth inhibition, and the basis for the synergistic actions of ATRA and IFNs in myeloid leukemia cells. Tretinoin 4-8 interferon regulatory factor 1 Homo sapiens 31-36
8704165-10 1996 The ATRA-induced expression of IRF-1, an activator of transcription and repressor of transformation, may be one of the molecular mechanisms of ATRA-induced growth inhibition, and the basis for the synergistic actions of ATRA and IFNs in myeloid leukemia cells. Tretinoin 143-147 interferon regulatory factor 1 Homo sapiens 31-36
8704165-10 1996 The ATRA-induced expression of IRF-1, an activator of transcription and repressor of transformation, may be one of the molecular mechanisms of ATRA-induced growth inhibition, and the basis for the synergistic actions of ATRA and IFNs in myeloid leukemia cells. Tretinoin 143-147 interferon regulatory factor 1 Homo sapiens 31-36
8801170-6 1996 The chick RARbeta2, like the mammalian RAR, binds to [3H]atRA with high affinity (Kd=0.7-2 nM). Tretinoin 57-61 RAB40B, member RAS oncogene family Homo sapiens 10-13
8666983-2 1996 WHen the cells were treated with 12-O-tetradecanoylphorbol 13-acetate (TPA) or retinoic acid, the level of Bcl-2 protein was increased compared with the control. Tretinoin 79-92 BCL2 apoptosis regulator Homo sapiens 107-112
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 0-13 NLR family pyrin domain containing 3 Homo sapiens 67-71
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 0-13 NLR family pyrin domain containing 3 Homo sapiens 120-124
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 0-13 NLR family pyrin domain containing 3 Homo sapiens 120-124
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 15-17 NLR family pyrin domain containing 3 Homo sapiens 67-71
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 15-17 NLR family pyrin domain containing 3 Homo sapiens 120-124
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 15-17 NLR family pyrin domain containing 3 Homo sapiens 120-124
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 105-107 NLR family pyrin domain containing 3 Homo sapiens 120-124
8668150-2 1996 Retinoic acid (RA) derivatives have a direct effect on hepatic apo A-II production, since all-trans (at) RA induces apo A-II mRNA levels and apo A-II secretion in primary cultures of human hepatocytes. Tretinoin 105-107 NLR family pyrin domain containing 3 Homo sapiens 120-124
8880870-11 1996 At least in vitro, insulin-like growth factor-I, retinoic acid, tangeretin and tamoxifen were shown to upregulate the functions of the E-cadherin/catenin complex including inhibition of invasion. Tretinoin 49-62 cadherin 1 Homo sapiens 135-145
8673928-3 1996 Differentiation of these teratocarcinoma cells with retinoic acid results in a marked decrease in p53 protein levels but is accompanied by a marked increase in p53-mediated transcriptional activity. Tretinoin 52-65 tumor protein p53 Homo sapiens 98-101
8673928-3 1996 Differentiation of these teratocarcinoma cells with retinoic acid results in a marked decrease in p53 protein levels but is accompanied by a marked increase in p53-mediated transcriptional activity. Tretinoin 52-65 tumor protein p53 Homo sapiens 160-163
8819158-7 1996 Therefore, cpl1-expressing cells will secrete the precursors of active retinoids such as retinoic acid isomers. Tretinoin 89-102 LOC108698139 Xenopus laevis 11-15
8841765-3 1996 The retinol-binding proteins CRBP I and CRBP II appear to play an essential role in retinyl ester hydrolysis and formation and in retinoic acid formation. Tretinoin 130-143 retinol binding protein 2 Homo sapiens 40-47
8655595-9 1996 Pretreatment of B16 cells with cyclic AMP prior to RA addition dramatically reduced induction of PKC alpha, an early marker of RA-induced cell differentiation. Tretinoin 51-53 protein kinase C, alpha Mus musculus 97-106
8662962-6 1996 Here we report that overexpression of the calreticulin gene in B16 mouse melanoma cells resulted in a decrease in retinoic acid (RA)-stimulated reporter gene expression. Tretinoin 114-127 calreticulin Mus musculus 42-54
8662962-6 1996 Here we report that overexpression of the calreticulin gene in B16 mouse melanoma cells resulted in a decrease in retinoic acid (RA)-stimulated reporter gene expression. Tretinoin 129-131 calreticulin Mus musculus 42-54
8662962-7 1996 Gel shift analysis showed that purified calreticulin inhibited the binding of endogenous RAR to a beta-RA response element oligonucleotide, only if added prior to the addition of the oligonucleotide. Tretinoin 98-105 calreticulin Mus musculus 40-52
8662962-9 1996 Transfection of the calreticulin gene into B16 cells inhibited the RA induction of protein kinase Calpha, a marker of RA-induced differentiation. Tretinoin 67-69 calreticulin Mus musculus 20-32
8662930-0 1996 An Alu element in the myeloperoxidase promoter contains a composite SP1-thyroid hormone-retinoic acid response element. Tretinoin 88-101 myeloperoxidase Homo sapiens 22-37
8652371-0 1996 Nuclear translocation of protein kinase C-alpha and -zeta isoforms in HL-60 cells induced to differentiate along the granulocytic lineage by all-trans retinoic acid. Tretinoin 151-164 protein kinase C alpha Homo sapiens 25-57
8652371-1 1996 We investigated whether members of the protein kinase C (PKC) family of enzymes were involved in the nuclear events underlying granulocytic differentiation induced by 10(-6) M all-trans retinoic acid (ATRA) in HL-60 cells. Tretinoin 176-199 protein kinase C alpha Homo sapiens 57-60
8652371-1 1996 We investigated whether members of the protein kinase C (PKC) family of enzymes were involved in the nuclear events underlying granulocytic differentiation induced by 10(-6) M all-trans retinoic acid (ATRA) in HL-60 cells. Tretinoin 201-205 protein kinase C alpha Homo sapiens 57-60
8652371-4 1996 The level of PKC catalytic activity in the nuclei of HL-60 cells significantly (P < 0.01) and progressively increased from 1 h of ATRA treatment onwards. Tretinoin 133-137 protein kinase C alpha Homo sapiens 13-16
8652371-5 1996 Consistently, PKC-alpha and -zeta showed a striking and selective accumulation inside the nucleus upon treatment with ATRA. Tretinoin 118-122 protein kinase C alpha Homo sapiens 14-33
8652371-7 1996 The remaining PKC isoforms were not detectable inside the nucleus and showed only modest and non-significant variations, also in whole cell homogenates, upon ATRA treatment, except PKC-delta which showed a progressive down-regulation. Tretinoin 158-162 protein kinase C alpha Homo sapiens 14-17
8650192-0 1996 RIG-E, a human homolog of the murine Ly-6 family, is induced by retinoic acid during the differentiation of acute promyelocytic leukemia cell. Tretinoin 64-77 lymphocyte antigen 6 family member E Homo sapiens 0-5
8645577-6 1996 Addition of all-trans-retinoic acid increased the amount of RAR-alpha mRNA in the three cell lines and induced RAR-beta mRNA in Capan 1 and Capan 2 cells. Tretinoin 12-35 retinoic acid receptor beta Homo sapiens 111-119
8661485-10 1996 Additional studies revealed that retinoic acid decreased PTH-stimulated cAMP generation in a dose-dependent manner. Tretinoin 33-46 parathyroid hormone Rattus norvegicus 57-60
8646757-0 1996 Regulation of differentiation and keratin 10 expression by all-trans retinoic acid during the estrous cycle in the rat vaginal epithelium. Tretinoin 69-82 keratin 10 Rattus norvegicus 34-44
8646757-5 1996 Retinoic acid suppressed estrogen-induced vaginal keratinization and cytokeratin K10 expression (a biochemical marker of terminal differentiation). Tretinoin 0-13 keratin 10 Rattus norvegicus 81-84
8655603-10 1996 Inhibition of proliferation by RA was associated with increased levels of IGFBP-2 in conditioned media and in plasma membrane preparations. Tretinoin 31-33 insulin like growth factor binding protein 2 Bos taurus 74-81
8655603-13 1996 Thus, RA is a potent but transient inhibitor of bovine mammary epithelial cell proliferation, and this growth inhibition is correlated with increased IGFBP-2 accumulation and inhibition of IGF-I stimulated IGFBP-3 protein secretion. Tretinoin 6-8 insulin like growth factor binding protein 2 Bos taurus 150-157
8655595-9 1996 Pretreatment of B16 cells with cyclic AMP prior to RA addition dramatically reduced induction of PKC alpha, an early marker of RA-induced cell differentiation. Tretinoin 127-129 protein kinase C, alpha Mus musculus 97-106
8738758-1 1996 Controlled exposure to retinoic acid (RA) induces the murine embryonal carcinoma cell line P19S18O1A1 (P19) to differentiate into a variety of cell types. Tretinoin 23-36 stathmin 1 Mus musculus 91-101
8738758-1 1996 Controlled exposure to retinoic acid (RA) induces the murine embryonal carcinoma cell line P19S18O1A1 (P19) to differentiate into a variety of cell types. Tretinoin 23-36 stathmin 1 Mus musculus 91-94
8738758-1 1996 Controlled exposure to retinoic acid (RA) induces the murine embryonal carcinoma cell line P19S18O1A1 (P19) to differentiate into a variety of cell types. Tretinoin 38-40 stathmin 1 Mus musculus 91-101
8738758-1 1996 Controlled exposure to retinoic acid (RA) induces the murine embryonal carcinoma cell line P19S18O1A1 (P19) to differentiate into a variety of cell types. Tretinoin 38-40 stathmin 1 Mus musculus 91-94
8738758-3 1996 In this study we use Northern blot analysis, double-label immunocytochemistry, and single cell RNA analysis using polymerase chain reaction to show that RA-treated P19 cells with neuronal-like morphology also express neuronal nicotinic acetylcholine receptor (nAChR) subunits alpha 3, alpha 4, and beta 2. Tretinoin 153-155 cyclin dependent kinase inhibitor 2A Homo sapiens 164-167
8738758-3 1996 In this study we use Northern blot analysis, double-label immunocytochemistry, and single cell RNA analysis using polymerase chain reaction to show that RA-treated P19 cells with neuronal-like morphology also express neuronal nicotinic acetylcholine receptor (nAChR) subunits alpha 3, alpha 4, and beta 2. Tretinoin 153-155 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 260-265
8738758-4 1996 Greater than 80% of RA-treated P19 cells with a neuronal-like phenotype express nAChR alpha 4 subunit transcripts and both alpha 4 and beta 2 protein. Tretinoin 20-22 cyclin dependent kinase inhibitor 2A Homo sapiens 31-34
8738758-4 1996 Greater than 80% of RA-treated P19 cells with a neuronal-like phenotype express nAChR alpha 4 subunit transcripts and both alpha 4 and beta 2 protein. Tretinoin 20-22 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 80-85
8738758-7 1996 The appearance of nAChR subunits also coincides with RA-induced expression of high affinity [3H]-nicotine binding receptors. Tretinoin 53-55 cholinergic receptor nicotinic alpha 4 subunit Homo sapiens 18-23
8752654-5 1996 As a consequence, RA derivatives also reduced the production of tumor necrosis factor alpha by these cells by 70%. Tretinoin 18-20 tumor necrosis factor Homo sapiens 64-91
8752654-8 1996 Therefore, RA derivatives downregulate tumor necrosis factor-alpha release and the NO-transduction pathway through the inhibition of inducible NO synthase transcription. Tretinoin 11-13 tumor necrosis factor Homo sapiens 39-66
8626717-0 1996 Lyn and Fgr protein-tyrosine kinases prevent apoptosis during retinoic acid-induced granulocytic differentiation of HL-60 cells. Tretinoin 62-75 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 0-3
8804707-1 1996 The effect of all-trans retinoic acid (RA) on chicken ovalbumin upstream promoter-transcription factor (COUP-TF) I and COUP-TF II expression in the developing cervical spinal cord and telencephalon was examined using embryonic day 11 and 13 mice. Tretinoin 39-41 nuclear receptor subfamily 2 group F member 1 Gallus gallus 104-114
8626717-0 1996 Lyn and Fgr protein-tyrosine kinases prevent apoptosis during retinoic acid-induced granulocytic differentiation of HL-60 cells. Tretinoin 62-75 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 8-11
8626717-3 1996 Accompanying the RA-induced differentiation, activities of src family PTKs Lyn and Fgr became detected and reached a plateau 2 days after the stimulation. Tretinoin 17-19 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 59-62
8626717-3 1996 Accompanying the RA-induced differentiation, activities of src family PTKs Lyn and Fgr became detected and reached a plateau 2 days after the stimulation. Tretinoin 17-19 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 75-78
8626717-3 1996 Accompanying the RA-induced differentiation, activities of src family PTKs Lyn and Fgr became detected and reached a plateau 2 days after the stimulation. Tretinoin 17-19 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 83-86
9019245-8 1996 RA-treated embryos were subsequently analyzed for appropriate cardiac myocyte differentiation using antibody staining and ELISA analysis to detect sarcomeric myosin heavy chain, tropomyosin, titin, and alpha-actinin protein expression. Tretinoin 0-2 actinin, alpha 4 Gallus gallus 202-215
8732669-0 1996 Retinoic acid-induced transition from protein kinase C beta to protein kinase C alpha in differentiated F9 cells: correlation with altered regulation of proto-oncogene expression by phorbol esters. Tretinoin 0-13 protein kinase C alpha Homo sapiens 63-85
8732669-3 1996 Since AP1 activity is a target for protein kinase C (PKC)-regulated changes in gene expression, we have examined the effects of RA on the expression and function of the PKC isozymes. Tretinoin 128-130 protein kinase C alpha Homo sapiens 169-172
8732669-5 1996 RA-induced differentiation to primitive endoderm led to a transition from PKC beta to PKC alpha expression. Tretinoin 0-2 protein kinase C alpha Homo sapiens 86-95
8732669-13 1996 Together, our data demonstrate that the RA-induced (and dbcAMP-induced) changes in conventional PKC expression alters gene expression during parietal endoderm formation. Tretinoin 40-42 protein kinase C alpha Homo sapiens 96-99
9019245-9 1996 Alpha-actinin expression was significantly decreased in RA-treated embryos, as compared to DMSO-treated controls. Tretinoin 56-58 actinin, alpha 4 Gallus gallus 0-13
8630327-0 1996 Uptake and metabolism of [3H]retinoic acid delivered to human foreskin keratinocytes either bound to serum albumin or added directly to the culture medium. Tretinoin 29-42 albumin Homo sapiens 101-114
8612709-2 1996 In the present study we demonstrate that in P19 embryonal carcinoma cells both the induction of the activin responsive 3TP-lux reporter construct and the inhibition of retinoic acid-induced neuronal differentiation by activin are blocked by expression of a truncated activin receptor. Tretinoin 168-181 activin A receptor type 2B S homeolog Xenopus laevis 267-283
8734361-8 1996 Polyclonal rabbit anti-IL-6 antibodies were used to block the augmenting effects of RA on Ig synthesis of adenoidal B cells. Tretinoin 84-86 interleukin 6 Homo sapiens 23-27
8734361-9 1996 RA-induced augmentation in IgG and IgA synthesis was blocked 58 and 29%, respectively, by anti-IL-6 antibodies. Tretinoin 0-2 interleukin 6 Homo sapiens 95-99
8734361-10 1996 These studies suggest that the enhancing effects of RA on Ig synthesis are mediated, at least in part, by the autocrine or paracrine effects of IL-6 on B-cell differentiation. Tretinoin 52-54 interleukin 6 Homo sapiens 144-148
8881437-7 1996 This process is dependent upon an IL6-autocrine differentiation pathway which may be modulated by some drugs such as interferons or all trans retinoic acid. Tretinoin 142-155 interleukin 6 Homo sapiens 34-37
8639429-3 1996 To explore this we used a functional assay to study the effect of ATRA treatment on the adhesion of blast cells to cultured human endothelial cells (EC), endothelial cell matrix (ECM), and interleukin 1beta-activated EC (IL1 + EC). Tretinoin 66-70 interleukin 1 beta Homo sapiens 189-206
8639429-3 1996 To explore this we used a functional assay to study the effect of ATRA treatment on the adhesion of blast cells to cultured human endothelial cells (EC), endothelial cell matrix (ECM), and interleukin 1beta-activated EC (IL1 + EC). Tretinoin 66-70 interleukin 1 beta Homo sapiens 221-224
8639429-7 1996 Preincubation of ATRA-treated NB4 cells with MoAbs anti-VLA4 and anti-LFA1, the VCAM-1 and ICAM-1 counter-receptors respectively, resulted in a significant inhibition of adhesion. Tretinoin 17-21 integrin subunit beta 2 Homo sapiens 70-74
8639429-7 1996 Preincubation of ATRA-treated NB4 cells with MoAbs anti-VLA4 and anti-LFA1, the VCAM-1 and ICAM-1 counter-receptors respectively, resulted in a significant inhibition of adhesion. Tretinoin 17-21 vascular cell adhesion molecule 1 Homo sapiens 80-86
8630327-1 1996 Retinoic acid (RA), a potent modulator of cell proliferation and differentiation is present in plasma bound to serum albumin. Tretinoin 0-13 albumin Homo sapiens 111-124
8630327-1 1996 Retinoic acid (RA), a potent modulator of cell proliferation and differentiation is present in plasma bound to serum albumin. Tretinoin 15-17 albumin Homo sapiens 111-124
8609382-3 1996 The retinol metabolite retinoic acid inhibited the IFN-gamma stimulatory activity of APCs, enhanced Th2 cell differentiation, and inhibited Th1 cell IFN-gamma synthesis. Tretinoin 23-36 interferon gamma Mus musculus 51-60
8609382-3 1996 The retinol metabolite retinoic acid inhibited the IFN-gamma stimulatory activity of APCs, enhanced Th2 cell differentiation, and inhibited Th1 cell IFN-gamma synthesis. Tretinoin 23-36 negative elongation factor complex member C/D, Th1l Mus musculus 140-143
8609382-9 1996 Retinoic acid inhibited IFN-gamma synthesis when the CD28 costimulatory pathway was activated in addition to the TCR/CD3 pathway, suggesting it blocks some step in the CD28 pathway. Tretinoin 0-13 interferon gamma Mus musculus 24-33
8609382-3 1996 The retinol metabolite retinoic acid inhibited the IFN-gamma stimulatory activity of APCs, enhanced Th2 cell differentiation, and inhibited Th1 cell IFN-gamma synthesis. Tretinoin 23-36 interferon gamma Mus musculus 149-158
8609382-4 1996 Here we focus on the mechanism for retinoic acid inhibition of IFN-gamma synthesis in myelin basic protein-specific MM4 Th1 cells. Tretinoin 35-48 interferon gamma Mus musculus 63-72
8609382-4 1996 Here we focus on the mechanism for retinoic acid inhibition of IFN-gamma synthesis in myelin basic protein-specific MM4 Th1 cells. Tretinoin 35-48 negative elongation factor complex member C/D, Th1l Mus musculus 120-123
8609382-5 1996 Physiologic amounts of all-trans-retinoic acid directly and specifically down-regulated the MM4 Th1 cell IFN-gamma secretion rate in vitro without affecting cell growth, viability, or overall protein synthesis. Tretinoin 23-46 negative elongation factor complex member C/D, Th1l Mus musculus 96-99
8609382-5 1996 Physiologic amounts of all-trans-retinoic acid directly and specifically down-regulated the MM4 Th1 cell IFN-gamma secretion rate in vitro without affecting cell growth, viability, or overall protein synthesis. Tretinoin 23-46 interferon gamma Mus musculus 105-114
8611626-1 1996 A 2.4 kilobase (kb) cDNA encoding a new form of human tissue transglutaminase homologue (TGH2) was isolated from retinoic acid-induced human erythroleukemia cell (HEL) library. Tretinoin 113-126 transglutaminase 2 Homo sapiens 54-77
8790944-0 1996 Induction of mcl1/EAT, Bcl-2 related gene, by retinoic acid or heat shock in the human embryonal carcinoma cells, NCR-G3. Tretinoin 46-59 BCL2 apoptosis regulator Homo sapiens 23-28
8624378-12 1996 This pilot study demonstrates that treatment with ATRA/G-CSF/EPO/tocopherol is well tolerated, leading to normalization of neutrophil counts in most, and to improvement of platelets and red blood cells in a significant subgroup of patients. Tretinoin 50-54 erythropoietin Homo sapiens 61-64
8790944-7 1996 The expression of mcl1/EAT, the Bcl-2 related gene, was increased at an early stage of the retinoic acid-induced differentiation and preceded the up-regulation of cytokeratin and hCG genes after ratinoic acid treatment. Tretinoin 91-104 BCL2 apoptosis regulator Homo sapiens 32-37
8620841-2 1996 Expression of Cek-8 in distal mesenchyme is regulated by apical ridge- and FGF-polarising signals and retinoic acid, and is uniform across the anteroposterior axis in talpid3 mutants. Tretinoin 102-115 EPH receptor A4 Gallus gallus 14-19
8603522-0 1996 Retinoic acid modulates the in vivo and in vitro growth of IL-6 autocrine human myeloma cell lines via induction of apoptosis. Tretinoin 0-13 interleukin 6 Homo sapiens 59-63
8603522-7 1996 RA-mediated interruption of the IL-6 autocrine loop was associated with a decrease of bcl-2 oncoprotein expression and apoptosis of the myeloma cells which was RA concentration- and time-dependent. Tretinoin 0-2 interleukin 6 Homo sapiens 32-36
8603522-7 1996 RA-mediated interruption of the IL-6 autocrine loop was associated with a decrease of bcl-2 oncoprotein expression and apoptosis of the myeloma cells which was RA concentration- and time-dependent. Tretinoin 0-2 BCL2 apoptosis regulator Homo sapiens 86-91
8603522-7 1996 RA-mediated interruption of the IL-6 autocrine loop was associated with a decrease of bcl-2 oncoprotein expression and apoptosis of the myeloma cells which was RA concentration- and time-dependent. Tretinoin 160-162 interleukin 6 Homo sapiens 32-36
8603522-11 1996 Our study indicate that long-term RA treatment interferes in vivo and in vitro with IL-6 autocrine growth of myeloma cell lines, leading to apoptosis. Tretinoin 34-36 interleukin 6 Homo sapiens 84-88
8741221-0 1996 Retinoic acid-induced heparin binding (RIHB, chicken midkine) factor expression by cultured chondrocytes is strongly enhanced by ascorbic acid. Tretinoin 0-13 midkine (neurite growth-promoting factor 2) Gallus gallus 39-43
8657131-6 1996 Remarkably, RA inhibited differentiation when added after PPARgamma1 and PPARgamma2 proteins had already been expressed and resulted in the loss of PPARgamma proteins from cells. Tretinoin 12-14 peroxisome proliferator activated receptor gamma Homo sapiens 58-67
8626114-1 1996 The purpose of this study was to determine whether all-trans-retinoic acid (RA) can inhibit the growth of cervical neoplastic cells by inducing differentiation or by increasing the secretion of transforming growth factor-beta (TGF-beta). Tretinoin 51-74 transforming growth factor beta 1 Homo sapiens 227-235
8626114-1 1996 The purpose of this study was to determine whether all-trans-retinoic acid (RA) can inhibit the growth of cervical neoplastic cells by inducing differentiation or by increasing the secretion of transforming growth factor-beta (TGF-beta). Tretinoin 76-78 transforming growth factor beta 1 Homo sapiens 227-235
8626114-9 1996 Secretion of either TGF-beta 1 or TGF-beta 2 is significantly increased (P<0.05) in response to RA, both in RA-sensitive and in RA-resistant cells. Tretinoin 99-101 transforming growth factor beta 1 Homo sapiens 20-30
8726400-3 1996 In vitro treatment with ATRA dramatically modifies the adhesion phenotype of APL blast cells, promoting a consistently striking up-regulation of CD11b, CD11c, CD15, CD65, CD54, and CD38. Tretinoin 24-28 fucosyltransferase 4 Homo sapiens 159-163
8630001-0 1996 Retinoic acid-stimulated liver stellate cells suppress the production of albumin from parenchymal cells via TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Rattus norvegicus 108-116
8630001-2 1996 Both TGF-beta added exogenously to the culture medium, and TGF-beta produced endogenously from SCs after stimulation with retinoic acid (RA), suppressed the production and secretion of albumin from PCs. Tretinoin 122-135 transforming growth factor, beta 1 Rattus norvegicus 59-67
8630001-2 1996 Both TGF-beta added exogenously to the culture medium, and TGF-beta produced endogenously from SCs after stimulation with retinoic acid (RA), suppressed the production and secretion of albumin from PCs. Tretinoin 137-139 transforming growth factor, beta 1 Rattus norvegicus 59-67
9627689-6 1996 Retinoic acid, which is known to interfere with vitamin D3 signaling, slightly decreased the levels of secreted TGF-beta 1 protein in BT-20 cells, but did not significantly affect the vitamin D3-induced increase. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 112-122
8616017-4 1996 Interestingly, 50% of cases with acute promyelocytic leukaemia expressed SCFR and this molecule was heterogenously regulated by in vitro treatment with all-trans retinoic acid. Tretinoin 162-175 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 73-77
8649839-1 1996 mac25, a retinoic acid-inducible gene that is expressed at high levels in senescent epithelial cells, was initially cloned as a gene that is differentially expressed in meningioma. Tretinoin 9-22 insulin-like growth factor binding protein 7 Mus musculus 0-5
8616045-0 1996 Proteolysis of von Willebrand factor is decreased in acute promyelocytic leukaemia by treatment with all-trans-retinoic acid. Tretinoin 101-124 von Willebrand factor Homo sapiens 15-36
8634418-4 1996 Erythroid colony growth was also inhibited when CD34+ progenitors were seeded at one cell per well, suggesting a direct action of RA. Tretinoin 130-132 CD34 molecule Homo sapiens 48-52
8616045-12 1996 Therefore, improvement of VWF after ATRA administration might explain in part the effectiveness of this drug in reducing haemorrhagic complications. Tretinoin 36-40 von Willebrand factor Homo sapiens 26-29
8641674-0 1996 [Alterations of protein phosphatases, PP2A and PP1, during retinoic acid-induced differentiation of HL-60 cells]. Tretinoin 59-72 inorganic pyrophosphatase 1 Homo sapiens 47-50
8634442-3 1996 This induction correlated with t-RA-induced growth arrest, granulocytic differentiation, and upregulation of the leukocyte adherence receptor beta subunit (CD18) gene expression. Tretinoin 31-35 integrin subunit beta 2 Homo sapiens 156-160
8603611-7 1996 The levels of the 24-, 29- to 32-, and 38- to 42 kDa IGFBPs in the conditioned medium of RA-treated cultures increased, as determined by ligand blot analysis, whereas the amount of IGFBP-5 was reduced, as determined by RIA. Tretinoin 89-91 insulin like growth factor binding protein 5 Homo sapiens 181-188
8603611-8 1996 Cycloheximide abolished the RA-stimulated increase in IGFBP-6 mRNA and reduced baseline IGFBP-5 mRNA levels, but did not affect RA-modulated mRNA levels of the other IGFBPs. Tretinoin 28-30 insulin like growth factor binding protein 5 Homo sapiens 88-95
8603611-9 1996 RA modestly increased the stabilities of all four IGFBP mRNAs, which could contribute to the observed increases in IGFBP-3 and IGFBP-4 mRNA levels; however, the 217% increase in the IGFBP-5 mRNA half- life in the presence of RA could not contribute to the reduction in mRNA levels. Tretinoin 0-2 insulin like growth factor binding protein 5 Homo sapiens 182-189
8603611-9 1996 RA modestly increased the stabilities of all four IGFBP mRNAs, which could contribute to the observed increases in IGFBP-3 and IGFBP-4 mRNA levels; however, the 217% increase in the IGFBP-5 mRNA half- life in the presence of RA could not contribute to the reduction in mRNA levels. Tretinoin 225-227 insulin like growth factor binding protein 5 Homo sapiens 182-189
8603611-11 1996 These data suggest that RA stimulated changes in IGFBP-5 and -6 mRNA levels may in part be mediated by alterations in transcription or other early posttranscription regulatory mechanisms. Tretinoin 24-26 insulin like growth factor binding protein 5 Homo sapiens 49-56
8717447-5 1996 Growth was decreased to a greater extent by deletion of growth factors from medium with KGF versus EGF, and retinoic acid was 10-fold more potent at inducing growth inhibition and differentiation-associated keratin with KGF compared with EGF. Tretinoin 108-121 fibroblast growth factor 7 Homo sapiens 220-223
8774652-2 1996 Results of [3H]thymidine uptake assays showed that exposure to pharmacologic concentrations of interferon-alpha (IFN-alpha) and all-trans-retinoic acid (RA) for 72 hr inhibited growth of the cervical cancer cell lines ME-180, 283, SiHa, C33-A, 621, CaSki, HeLa, and B132, CaSki and SiHa cells continuously exposed to IFN-alpha or RA or both for 9 days developed resistance to growth inhibition, and growth resumed at a rate comparable to control after removal of agents. Tretinoin 138-151 interferon alpha 1 Homo sapiens 317-326
8774652-2 1996 Results of [3H]thymidine uptake assays showed that exposure to pharmacologic concentrations of interferon-alpha (IFN-alpha) and all-trans-retinoic acid (RA) for 72 hr inhibited growth of the cervical cancer cell lines ME-180, 283, SiHa, C33-A, 621, CaSki, HeLa, and B132, CaSki and SiHa cells continuously exposed to IFN-alpha or RA or both for 9 days developed resistance to growth inhibition, and growth resumed at a rate comparable to control after removal of agents. Tretinoin 153-155 interferon alpha 1 Homo sapiens 317-326
8641674-8 1996 PP1 activity determined with MBP was transiently increased between 27 and 36 h of the incubation of cells without retinoic acid. Tretinoin 114-127 inorganic pyrophosphatase 1 Homo sapiens 0-3
8641674-9 1996 The increase was strongly suppressed in the cells incubated with retinoic acid, suggesting a role of PP1 in the cell proliferation, the activity of which was also inhibited by retinoic acid. Tretinoin 65-78 inorganic pyrophosphatase 1 Homo sapiens 101-104
8641674-9 1996 The increase was strongly suppressed in the cells incubated with retinoic acid, suggesting a role of PP1 in the cell proliferation, the activity of which was also inhibited by retinoic acid. Tretinoin 176-189 inorganic pyrophosphatase 1 Homo sapiens 101-104
8603926-0 1996 Bcl-2 inhibits retinoic acid-induced apoptosis during the neural differentiation of embryonal stem cells. Tretinoin 15-28 B cell leukemia/lymphoma 2 Mus musculus 0-5
8622658-0 1996 Retinoic acid receptor beta mediates the growth-inhibitory effect of retinoic acid by promoting apoptosis in human breast cancer cells. Tretinoin 69-82 retinoic acid receptor beta Homo sapiens 0-27
8642855-6 1996 We found that the half-life of bcl-2 protein is markedly shortened after treatment with ATRA. Tretinoin 88-92 BCL2 apoptosis regulator Homo sapiens 31-36
8622679-3 1996 In support of this idea, expression of vHNF1 but not HNF1 is induced upon treatment of the embryonal carcinoma cell line F9 with retinoic acid. Tretinoin 129-142 HNF1 homeobox B Homo sapiens 39-44
8622679-3 1996 In support of this idea, expression of vHNF1 but not HNF1 is induced upon treatment of the embryonal carcinoma cell line F9 with retinoic acid. Tretinoin 129-142 HNF1 homeobox A Homo sapiens 40-44
8622658-5 1996 In addition, RA sensitivity of hormone-dependent cells was inhibited by a RAR beta-selective antagonist and the expression of RAR beta antisense RNA. Tretinoin 13-15 retinoic acid receptor beta Homo sapiens 74-82
8622658-5 1996 In addition, RA sensitivity of hormone-dependent cells was inhibited by a RAR beta-selective antagonist and the expression of RAR beta antisense RNA. Tretinoin 13-15 retinoic acid receptor beta Homo sapiens 126-134
8622658-6 1996 Introduction of RAR alpha also restored RA sensitivity in hormone-independent cells, but this restoration was accomplished by the induction of endogenous RAR beta expression. Tretinoin 16-18 retinoic acid receptor beta Homo sapiens 154-162
8635492-0 1996 The relationship between susceptibility to retinoic acid treatment and protein kinase C alpha expression in murine melanoma cell lines. Tretinoin 43-56 protein kinase C, alpha Mus musculus 71-93
8635481-8 1996 The RAR beta 2-expressing cell lines are inhibited further by the addition of exogenous all-trans-retinoic acid. Tretinoin 88-111 retinoic acid receptor beta Homo sapiens 4-12
9238678-6 1996 RA treatment significantly (P < 0.05) suppressed prolactin and IGFBP-1 production associated with stromal cells decidualization. Tretinoin 0-2 prolactin Homo sapiens 52-61
9238678-12 1996 Addition of 50 microM dibutyryl cAMP to stromal cells treated with MPA and oestradiol only partially reversed the suppression of decidualization and prolactin release by RA. Tretinoin 170-172 prolactin Homo sapiens 149-158
8641447-3 1996 In these two conditions, there was an increase in reactive oxygen species and antioxidants such as catalase, superoxide dismutase or phenol prevented ATRA-induced cell death. Tretinoin 150-154 catalase Homo sapiens 99-107
8635481-9 1996 Finally, soft agar assays show that the RAR beta 2-expressing cell lines also demonstrate an inhibition of growth in soft agar, when compared to the parent growth cell lines, and are inhibited further in the presence of added all-trans-retinoic acid. Tretinoin 230-249 retinoic acid receptor beta Homo sapiens 40-48
8635492-1 1996 Retinoic acid (RA)-induced differentiation of B16 mouse melanoma cells is accompanied by a large increase in the amount of PKCalpha protein. Tretinoin 0-13 protein kinase C, alpha Mus musculus 123-131
8657191-3 1996 In studying how retinoid sensitivity is lost in cancer cells, we have found that lack of the retinoic acid receptor beta (RAR beta) gene expression and its abnormal regulation by retinoic acid (RA) are common features in human lung cancer and breast cancer cells. Tretinoin 93-106 retinoic acid receptor beta Homo sapiens 122-130
8657191-3 1996 In studying how retinoid sensitivity is lost in cancer cells, we have found that lack of the retinoic acid receptor beta (RAR beta) gene expression and its abnormal regulation by retinoic acid (RA) are common features in human lung cancer and breast cancer cells. Tretinoin 122-124 retinoic acid receptor beta Homo sapiens 93-120
8603731-3 1996 The major MMP expressed by chondrocytes stimulated with retinoic acid to degrade their matrix is collagenase-3 or MMP-13. Tretinoin 56-69 matrix metallopeptidase 13 Homo sapiens 97-110
8603731-3 1996 The major MMP expressed by chondrocytes stimulated with retinoic acid to degrade their matrix is collagenase-3 or MMP-13. Tretinoin 56-69 matrix metallopeptidase 13 Homo sapiens 114-120
8603335-11 1996 Thus, the selection of DOX resistance in two sublines of HL-60 cells which differ in their response to retinoic acid-induced myeloid differentiation is reproducibly associated with overexpression of mdr-1 versus MRP. Tretinoin 103-116 ATP binding cassette subfamily B member 1 Homo sapiens 199-204
8603335-11 1996 Thus, the selection of DOX resistance in two sublines of HL-60 cells which differ in their response to retinoic acid-induced myeloid differentiation is reproducibly associated with overexpression of mdr-1 versus MRP. Tretinoin 103-116 ATP binding cassette subfamily C member 1 Homo sapiens 212-215
8564960-4 1996 The role of TGF-beta in RA-dependent differentiation and cessation of growth was examined by adding neutralizing anti-TGF-beta IgG to RA-treated HL-60 cells, followed by assessing cell growth and markers of granulocytic differentiation over 5 days. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 12-20
8564960-9 1996 Similar levels of total TGF-beta were observed between control and RA-treated cells. Tretinoin 67-69 transforming growth factor beta 1 Homo sapiens 24-32
8564960-11 1996 Activation of endogenous latent TGF-beta by RA-treated cells occurred through a plasmin-independent mechanism. Tretinoin 44-46 transforming growth factor beta 1 Homo sapiens 32-40
8564960-0 1996 Effects of endogenously activated transforming growth factor-beta on growth and differentiation of retinoic acid-treated HL-60 cells. Tretinoin 99-112 transforming growth factor beta 1 Homo sapiens 34-65
9816167-8 1996 ATRA also induced significant down-regulation of myeloma IL-6 receptors and inhibited IL-6 autosecretion by myeloma cells. Tretinoin 0-4 interleukin 6 Homo sapiens 57-61
9816167-8 1996 ATRA also induced significant down-regulation of myeloma IL-6 receptors and inhibited IL-6 autosecretion by myeloma cells. Tretinoin 0-4 interleukin 6 Homo sapiens 86-90
8601734-1 1996 Application of all-trans retinoic acid to human skin for 4 d under occlusion produces a marked increase in retinoic acid 4-hydroxylase activity. Tretinoin 25-38 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 107-134
8645624-3 1996 Dex, by enhancing 4-hydroxylation of RA, reduces its intracellular concentration thereby leading to a decreased expression of RARs, since RARbeta, the main type of RARs in liver, are known to be up-regulated by RA. Tretinoin 37-39 retinoic acid receptor, beta Rattus norvegicus 138-145
8652410-0 1996 Developmental expression and differential regulation by retinoic acid of Xenopus COUP-TF-A and COUP-TF-B. Tretinoin 56-69 nuclear receptor subfamily 2 group F member 2 L homeolog Xenopus laevis 95-104
8780165-5 1996 Clinically achievable doses of RA rapidly caused large- and small-vessel endothelial cells to become refractory to stimulation of migration either by tumor-conditioned media or purified angiogenic factors (a-fibroblast growth factor (aFGF), bFGF, vascular endothelial GF, platelet-derived GF, TGF beta-1, and IL-8). Tretinoin 31-33 transforming growth factor, beta 1 Rattus norvegicus 293-303
8919301-1 1996 Chronic exposure of all-trans-retinoic acid-differentiated SH-SY5Y cells to morphine (10 mu M; 2 days) results in sensitization of adenylate cyclase as characterized by a significant increase in both PGE1 receptor-mediated as well as receptor-independent (NaF, 10 mM; forskolin, 100 mu M) stimulation of effector activity. Tretinoin 24-43 C-X-C motif chemokine ligand 8 Homo sapiens 256-259
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 79-92 interferon gamma Homo sapiens 26-42
8570219-6 1996 Our results show that RXR alpha restores the response to RA in this subclone with respect to AP1 inhibition and growth arrest. Tretinoin 57-59 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-96
8555483-10 1996 These data indicate that ATRA increases the promyelocyte-induced EC TF, partly through increased IL-1 beta production. Tretinoin 25-29 interleukin 1 beta Homo sapiens 97-106
8567689-4 1996 Furthermore, in Nulli-SSC1 cells, the beta isoform is induced by the morphogen retinoic acid. Tretinoin 79-92 aquaporin 9 Homo sapiens 22-26
8555497-7 1996 After isolation of microsomes, measurements showed that levels of cytochrome P450 activities in both wild-type and RA-resistant HL-60 cells were almost comparable. Tretinoin 115-117 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 66-81
8555497-11 1996 Possible mechanisms for accelerated clearance of RA include the induction of non-CYP1A1 cytochrome P450 enzymes and P-glycoprotein. Tretinoin 49-51 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 88-103
8555497-11 1996 Possible mechanisms for accelerated clearance of RA include the induction of non-CYP1A1 cytochrome P450 enzymes and P-glycoprotein. Tretinoin 49-51 ATP binding cassette subfamily B member 1 Homo sapiens 116-130
8534481-8 1996 In contrast, secretion of lysozyme, lactoferrin, and SLPI was significantly increased in RA-depleted cultures. Tretinoin 89-91 secretory leukocyte peptidase inhibitor Homo sapiens 53-57
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 79-92 interferon gamma Homo sapiens 44-53
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 79-92 interferon gamma Homo sapiens 99-108
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 94-96 interferon gamma Homo sapiens 26-42
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 94-96 interferon gamma Homo sapiens 44-53
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 94-96 interferon gamma Homo sapiens 99-108
8615638-7 1996 In contrast with SKBR-3 and BT-20 cells a combination of ATRA with IFN-alpha markedly reduced ATRA mediated CRABP II induction. Tretinoin 94-98 interferon alpha 1 Homo sapiens 67-76
8615638-8 1996 These results suggest that two factors may be responsible for synergistic action of RA and IFN-alpha: the inhibition of the CRABP II expression and an IFN-alpha/RA mediated upregulation of RAR-gamma. Tretinoin 84-86 interferon alpha 1 Homo sapiens 151-160
8615638-8 1996 These results suggest that two factors may be responsible for synergistic action of RA and IFN-alpha: the inhibition of the CRABP II expression and an IFN-alpha/RA mediated upregulation of RAR-gamma. Tretinoin 125-127 interferon alpha 1 Homo sapiens 91-100
8931954-7 1996 Following 4 days of maturation with ATRA, the cells would increase F-actin content in response to interleukin-8, ingest latex beads, migrate in a chemotaxis chamber, reduce NBT, and express CD11b. Tretinoin 36-40 C-X-C motif chemokine ligand 8 Homo sapiens 98-111
8546684-1 1996 Retinoic acid (RA) treatment of a suspension of quail chondrocytes inhibits the expression of cartilage collagens and induces cell adhesion along with fibronectin expression. Tretinoin 0-13 fibronectin 1 Homo sapiens 151-162
8546684-1 1996 Retinoic acid (RA) treatment of a suspension of quail chondrocytes inhibits the expression of cartilage collagens and induces cell adhesion along with fibronectin expression. Tretinoin 15-17 fibronectin 1 Homo sapiens 151-162
8547658-0 1996 Inhibition of myeloma cell growth by dexamethasone and all-trans retinoic acid: synergy through modulation of interleukin-6 autocrine loop at multiple sites. Tretinoin 65-78 interleukin 6 Homo sapiens 110-123
8547658-2 1996 We investigated the effect of dexamethasone and all-trans retinoic acid, previously shown to modulate IL-6/IL-6R, on the in vitro growth of a human myeloma cell line, OPM-2. Tretinoin 58-71 interleukin 6 Homo sapiens 102-106
8547658-2 1996 We investigated the effect of dexamethasone and all-trans retinoic acid, previously shown to modulate IL-6/IL-6R, on the in vitro growth of a human myeloma cell line, OPM-2. Tretinoin 58-71 interleukin 6 receptor Homo sapiens 107-112
8547658-8 1996 Dexamethasone increased, while all-trans retinoic acid reduced, IL-6R but not gp130 mRNA expression. Tretinoin 41-54 interleukin 6 receptor Homo sapiens 64-69
8723391-4 1996 Human thyroid hormone, retinoic acid, vitamin D, and several orphan receptors prefer to work as heterodimers with retinoic X receptor (RXR). Tretinoin 23-36 xenotropic and polytropic retrovirus receptor 1 Homo sapiens 123-133
8788037-11 1996 In contrast, PARP overexpression blocked the appearance of phenotypic markers of terminally differentiated neutrophils in 85% of the transfected population in response to 1 microM ATRA. Tretinoin 180-184 poly(ADP-ribose) polymerase 1 Homo sapiens 13-17
8788037-13 1996 These data suggest that overexpression of PARP arrests APL cells and blocks ATRA-induced terminal neutrophilic differentiation. Tretinoin 76-80 poly(ADP-ribose) polymerase 1 Homo sapiens 42-46
8792611-5 1996 Following retinoic acid treatment on both day 11 and day 12, the normal downregulation of Hoxd-11 and Hoxd-13 in the digital mesenchymal condensations was retarded. Tretinoin 10-23 homeobox D13 Mus musculus 102-109
8792611-8 1996 There was a good correlation between the effects of retinoic acid on Hoxd-11 and Hoxd-13 expression and delay of skeletal differentiation, suggesting that this may be a direct effect. Tretinoin 52-65 homeobox D13 Mus musculus 81-88
8931990-3 1996 Col1a1 mRNA became detectable by RNase protection assay after 3 days of RA treatment and, after 6 days, reached a level comparable to that in NIH 3T3 fibroblasts. Tretinoin 72-74 collagen, type I, alpha 1 Mus musculus 0-6
8603034-6 1996 Cytochrome P450-dependent enzymes are involved in the synthesis and/or degradation of many endogenous compounds, such as steroids and retinoic acid. Tretinoin 134-147 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-15
8835319-0 1996 Altered distribution of the nuclear receptor RAR beta accompanies proliferation and differentiation changes caused by retinoic acid in Caco-2 cells. Tretinoin 118-131 retinoic acid receptor beta Homo sapiens 45-53
8835319-7 1996 Retinoic acid in intestinal cells acts through its nuclear receptor, RAR beta. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 69-77
8835319-9 1996 In this study, we show that RAR beta responds to increasing concentrations of retinoic acid with a shift to the nuclear membrane in undifferentiated cells and progressive aggregation, diffusion, and loss in differentiated cells. Tretinoin 78-91 retinoic acid receptor beta Homo sapiens 28-36
8835319-10 1996 We conclude that retinoic acid can inhibit proliferation and stimulate differentiation in Caco-2 cells depending on concentration and cell stage, and that these effects are accompanied by changes in distribution, as well as by the loss of RAR beta. Tretinoin 17-30 retinoic acid receptor beta Homo sapiens 239-247
9145335-0 1996 Differential expression of protein kinase C isozymes and small GTP-binding proteins during HL60 cell differentiation by retinoic acid and cyclic AMP: relation with phospholipase D (PLD) activation. Tretinoin 120-133 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 164-179
9145335-0 1996 Differential expression of protein kinase C isozymes and small GTP-binding proteins during HL60 cell differentiation by retinoic acid and cyclic AMP: relation with phospholipase D (PLD) activation. Tretinoin 120-133 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 181-184
8557772-3 1996 In this study the role of the transforming growth factor-beta (TGF-beta) growth inhibitors, in promoting the biological activities of all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) was studied in NRP-152 cells, a nontumorigenic epithelial line derived from rat dorsal-lateral prostate. Tretinoin 134-157 transforming growth factor, beta 1 Rattus norvegicus 63-71
8557772-3 1996 In this study the role of the transforming growth factor-beta (TGF-beta) growth inhibitors, in promoting the biological activities of all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) was studied in NRP-152 cells, a nontumorigenic epithelial line derived from rat dorsal-lateral prostate. Tretinoin 159-161 transforming growth factor, beta 1 Rattus norvegicus 63-71
8557772-4 1996 Inhibition of growth by nanomolar concentrations of RA was associated with an increase in both mRNA and protein for all three TGF-beta isoforms, with greater and much earlier increases for TGF-beta s 2 and 3 (5.5 h) than for TGF-beta 1 (24 h). Tretinoin 52-54 transforming growth factor, beta 1 Rattus norvegicus 126-134
8557772-4 1996 Inhibition of growth by nanomolar concentrations of RA was associated with an increase in both mRNA and protein for all three TGF-beta isoforms, with greater and much earlier increases for TGF-beta s 2 and 3 (5.5 h) than for TGF-beta 1 (24 h). Tretinoin 52-54 transforming growth factor, beta 1 Rattus norvegicus 189-197
8557772-4 1996 Inhibition of growth by nanomolar concentrations of RA was associated with an increase in both mRNA and protein for all three TGF-beta isoforms, with greater and much earlier increases for TGF-beta s 2 and 3 (5.5 h) than for TGF-beta 1 (24 h). Tretinoin 52-54 transforming growth factor, beta 1 Rattus norvegicus 225-235
8557772-5 1996 A monoclonal antibody against TGF-beta and TGF-beta 1 latency associated peptide (LAP), both of which neutralize all three TGF-beta isoforms, each block the ability of RA to inhibit growth of NRP-152 cells by > 95%. Tretinoin 168-170 transforming growth factor, beta 1 Rattus norvegicus 30-38
8557772-5 1996 A monoclonal antibody against TGF-beta and TGF-beta 1 latency associated peptide (LAP), both of which neutralize all three TGF-beta isoforms, each block the ability of RA to inhibit growth of NRP-152 cells by > 95%. Tretinoin 168-170 transforming growth factor, beta 1 Rattus norvegicus 43-51
8557772-5 1996 A monoclonal antibody against TGF-beta and TGF-beta 1 latency associated peptide (LAP), both of which neutralize all three TGF-beta isoforms, each block the ability of RA to inhibit growth of NRP-152 cells by > 95%. Tretinoin 168-170 transforming growth factor, beta 1 Rattus norvegicus 43-51
8557772-9 1996 Thus, autocrine production of TGF-beta s may be a significant part of the mechanisms by which RA and 1,25-(OH)2D3 promote cellular differentiation. Tretinoin 94-96 transforming growth factor, beta 1 Rattus norvegicus 30-38
8557779-0 1996 Effect of retinoic acid in combination with platelet-derived growth factor-BB or transforming growth factor-beta on tissue inhibitor of metalloproteinases and collagenase secretion from human skin and synovial fibroblasts. Tretinoin 10-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 116-154
8557779-1 1996 This report shows for the first time that platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta (TGF-beta) can interact in a synergistic manner with retinoic acid to stimulate the production of tissue inhibitor of metalloproteinases (TIMP) from human skin and synovial fibroblasts. Tretinoin 175-188 transforming growth factor beta 1 Homo sapiens 90-121
8557779-1 1996 This report shows for the first time that platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta (TGF-beta) can interact in a synergistic manner with retinoic acid to stimulate the production of tissue inhibitor of metalloproteinases (TIMP) from human skin and synovial fibroblasts. Tretinoin 175-188 transforming growth factor beta 1 Homo sapiens 123-131
8557779-1 1996 This report shows for the first time that platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta (TGF-beta) can interact in a synergistic manner with retinoic acid to stimulate the production of tissue inhibitor of metalloproteinases (TIMP) from human skin and synovial fibroblasts. Tretinoin 175-188 TIMP metallopeptidase inhibitor 1 Homo sapiens 220-258
8557779-1 1996 This report shows for the first time that platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta (TGF-beta) can interact in a synergistic manner with retinoic acid to stimulate the production of tissue inhibitor of metalloproteinases (TIMP) from human skin and synovial fibroblasts. Tretinoin 175-188 TIMP metallopeptidase inhibitor 1 Homo sapiens 260-264
8557779-2 1996 When cells are treated with 1, 10, and 100 ng/ml of either of these growth factors in combination with 10(-5) M retinoic acid, this results in a dose-dependent synergistic induction of TIMP protein secretion which is greater than the additive effect of the agents by up to fourfold. Tretinoin 112-125 TIMP metallopeptidase inhibitor 1 Homo sapiens 185-189
8869967-0 1996 The antiproliferative effect of trans-retinoic acid is associated with selective induction of interleukin-1 beta, a cytokine that directly inhibits growth of lung cancer cells. Tretinoin 32-51 interleukin 1 beta Homo sapiens 94-112
8869967-7 1996 Growth inhibition similar to that following RA treatment could be reproduced by exposing cells to exogeneous IL-1 beta alone. Tretinoin 44-46 interleukin 1 beta Homo sapiens 109-118
8845574-7 1995 Finally, in the next years, there will be a wider diffusion of biotherapies in MM that should take into account the roles that IL-1 beta and TNF alpha play in myeloma cell proliferation and bone destruction and the finding that retinoic acid is capable of inhibiting the growth of human myeloma cells in vitro through modulation of IL-6 and its receptor. Tretinoin 228-241 interleukin 6 Homo sapiens 332-336
8762455-0 1996 [Induction of expression of MDR 1 gene by retinoic acid and DMSO and effects on rhodamine-123 efflux in HL-60 cell lines and resistant sublines]. Tretinoin 42-55 ATP binding cassette subfamily B member 1 Homo sapiens 28-33
8762455-5 1996 The results suggest that RA can induce the expression of MDR1 gene but perhaps inhibit the function of pump glycoprotein 170 (Pgp-170) through phosphorylation/dephosphorylation pathway. Tretinoin 25-27 ATP binding cassette subfamily B member 1 Homo sapiens 57-61
8537382-4 1995 Transient cellular transfections demonstrate that TGIF inhibits the 9-cis-retinoic acid-dependent RXR alpha transcription activation of the retinoic acid responsive element. Tretinoin 74-87 TGFB induced factor homeobox 1 Homo sapiens 50-54
7497526-3 1995 RA induced the expression of IL-5 and TGF-beta 2 mRNAs in the LPS-stimulated cells. Tretinoin 0-2 transforming growth factor, beta 2 Mus musculus 38-48
8519658-0 1995 Activation of the E-cadherin/catenin complex in human MCF-7 breast cancer cells by all-trans-retinoic acid. Tretinoin 83-106 cadherin 1 Homo sapiens 18-28
8519658-1 1995 All-trans-retinoic acid (RA), like insulin-like growth factor I (IGF-I) and tamoxifen, inhibit invasion of human MCF-7/6 mammary cancer cells in vitro. Tretinoin 0-23 insulin like growth factor 1 Homo sapiens 35-63
8519658-1 1995 All-trans-retinoic acid (RA), like insulin-like growth factor I (IGF-I) and tamoxifen, inhibit invasion of human MCF-7/6 mammary cancer cells in vitro. Tretinoin 0-23 insulin like growth factor 1 Homo sapiens 65-70
8519658-1 1995 All-trans-retinoic acid (RA), like insulin-like growth factor I (IGF-I) and tamoxifen, inhibit invasion of human MCF-7/6 mammary cancer cells in vitro. Tretinoin 25-27 insulin like growth factor 1 Homo sapiens 35-63
8519658-3 1995 We did a series of experiments to determine whether the anti-invasive effect of RA also implicated the invasion-suppressor E-cadherin/catenin complex. Tretinoin 80-82 cadherin 1 Homo sapiens 123-133
8519658-9 1995 RA up-regulates the function of the invasion-suppressor complex E-cadherin/catenin. Tretinoin 0-2 cadherin 1 Homo sapiens 64-74
7588287-0 1995 Retinoic acid induces expression of the transcription factor GHF-1/Pit-1 in pituitary prolactin- and growth hormone-producing cell lines. Tretinoin 0-13 POU class 1 homeobox 1 Rattus norvegicus 61-66
7588287-0 1995 Retinoic acid induces expression of the transcription factor GHF-1/Pit-1 in pituitary prolactin- and growth hormone-producing cell lines. Tretinoin 0-13 POU class 1 homeobox 1 Rattus norvegicus 67-72
7588278-5 1995 Moreover, using rats of various retinoid status, we investigated whether the expression of target genes for vitamin A (RAR beta and CRBP-I) is regulated by retinoic acid (RA) in the adult rat tibia. Tretinoin 156-169 retinoic acid receptor, beta Rattus norvegicus 119-127
7588287-2 1995 We have examined the effects of retinoic acid (RA) on the expression of the GHF-1/Pit-1 gene. Tretinoin 32-45 POU class 1 homeobox 1 Rattus norvegicus 76-81
7588287-2 1995 We have examined the effects of retinoic acid (RA) on the expression of the GHF-1/Pit-1 gene. Tretinoin 32-45 POU class 1 homeobox 1 Rattus norvegicus 82-87
7588287-2 1995 We have examined the effects of retinoic acid (RA) on the expression of the GHF-1/Pit-1 gene. Tretinoin 47-49 POU class 1 homeobox 1 Rattus norvegicus 76-81
7588287-2 1995 We have examined the effects of retinoic acid (RA) on the expression of the GHF-1/Pit-1 gene. Tretinoin 47-49 POU class 1 homeobox 1 Rattus norvegicus 82-87
8601031-0 1995 Sequence and expression pattern of the Stra7 (Gbx-2) homeobox-containing gene induced by retinoic acid in P19 embryonal carcinoma cells. Tretinoin 89-102 gastrulation brain homeobox 2 Mus musculus 39-44
7588287-3 1995 RA induced a time- and dose-dependent increase in GHF-1/Pit-1 messenger RNA in the PRL-producing cell line 235-1. Tretinoin 0-2 POU class 1 homeobox 1 Rattus norvegicus 50-55
8601031-0 1995 Sequence and expression pattern of the Stra7 (Gbx-2) homeobox-containing gene induced by retinoic acid in P19 embryonal carcinoma cells. Tretinoin 89-102 gastrulation brain homeobox 2 Mus musculus 46-51
8601031-1 1995 The cDNA sequence of Stra7, a retinoic acid (RA)-inducible gene in P19 embryonal carcinoma (EC) cells, was determined. Tretinoin 30-43 gastrulation brain homeobox 2 Mus musculus 21-26
7588287-3 1995 RA induced a time- and dose-dependent increase in GHF-1/Pit-1 messenger RNA in the PRL-producing cell line 235-1. Tretinoin 0-2 POU class 1 homeobox 1 Rattus norvegicus 56-61
8601031-1 1995 The cDNA sequence of Stra7, a retinoic acid (RA)-inducible gene in P19 embryonal carcinoma (EC) cells, was determined. Tretinoin 45-47 gastrulation brain homeobox 2 Mus musculus 21-26
7588287-5 1995 The level of the transcription factor determined by both Western blotting and gel retardation analysis with a GHF-1/Pit-1-binding site was increased in RA-treated cells compared to that in control cells. Tretinoin 152-154 POU class 1 homeobox 1 Rattus norvegicus 110-115
8601038-0 1995 Differential effects of retinoic acid and a retinoid antagonist on the spatial distribution of the homeoprotein Hoxb-7 in vertebrate embryos. Tretinoin 24-37 homeobox B7 L homeolog Xenopus laevis 112-118
8601038-11 1995 Treatment of X. laevis embryos with retinoic acid during gastrulation induced an anterior shift of the Hoxb-7 expression domain and was correlated with an enlargement of rhombomere r7. Tretinoin 36-49 homeobox B7 L homeolog Xenopus laevis 103-109
7588287-5 1995 The level of the transcription factor determined by both Western blotting and gel retardation analysis with a GHF-1/Pit-1-binding site was increased in RA-treated cells compared to that in control cells. Tretinoin 152-154 POU class 1 homeobox 1 Rattus norvegicus 116-121
7588287-8 1995 Both CREs are required for RA induction, as deletion of either CRE abolished the response to the retinoid RA also induced GHF-1/Pit-1 gene expression in GH4C1 cells, which produce both PRL and GH. Tretinoin 27-29 POU class 1 homeobox 1 Rattus norvegicus 122-127
7588287-8 1995 Both CREs are required for RA induction, as deletion of either CRE abolished the response to the retinoid RA also induced GHF-1/Pit-1 gene expression in GH4C1 cells, which produce both PRL and GH. Tretinoin 27-29 POU class 1 homeobox 1 Rattus norvegicus 128-133
7588287-8 1995 Both CREs are required for RA induction, as deletion of either CRE abolished the response to the retinoid RA also induced GHF-1/Pit-1 gene expression in GH4C1 cells, which produce both PRL and GH. Tretinoin 106-108 POU class 1 homeobox 1 Rattus norvegicus 122-127
7588287-8 1995 Both CREs are required for RA induction, as deletion of either CRE abolished the response to the retinoid RA also induced GHF-1/Pit-1 gene expression in GH4C1 cells, which produce both PRL and GH. Tretinoin 106-108 POU class 1 homeobox 1 Rattus norvegicus 128-133
8608343-0 1995 tPA of human keratinocytes: contribution to cell surface-associated plasminogen activation and upregulation by retinoic acid. Tretinoin 111-124 plasminogen activator, tissue type Homo sapiens 0-3
7493637-0 1995 Retinoic acid specifically increases nuclear PKC alpha and stimulates AP-1 transcriptional activity in B16 mouse melanoma cells. Tretinoin 0-13 protein kinase C, alpha Mus musculus 45-54
7493637-4 1995 The purpose of the study reported here was to determine the subcellular distribution of the RA-induced PKC alpha, whether the RA-induced increase in PKC alpha protein levels was accompanied by an increase in in situ enzyme activity, and whether RA altered AP-1 transcriptional activity. Tretinoin 92-94 protein kinase C, alpha Mus musculus 103-112
7493637-4 1995 The purpose of the study reported here was to determine the subcellular distribution of the RA-induced PKC alpha, whether the RA-induced increase in PKC alpha protein levels was accompanied by an increase in in situ enzyme activity, and whether RA altered AP-1 transcriptional activity. Tretinoin 126-128 protein kinase C, alpha Mus musculus 149-158
7493637-4 1995 The purpose of the study reported here was to determine the subcellular distribution of the RA-induced PKC alpha, whether the RA-induced increase in PKC alpha protein levels was accompanied by an increase in in situ enzyme activity, and whether RA altered AP-1 transcriptional activity. Tretinoin 126-128 protein kinase C, alpha Mus musculus 149-158
7493637-5 1995 We found that RA treatment increased PKC alpha protein levels in all subcellular compartments examined, but it also induced a selective enrichment in nuclear-associated PKC alpha levels. Tretinoin 14-16 protein kinase C, alpha Mus musculus 37-46
7493637-5 1995 We found that RA treatment increased PKC alpha protein levels in all subcellular compartments examined, but it also induced a selective enrichment in nuclear-associated PKC alpha levels. Tretinoin 14-16 protein kinase C, alpha Mus musculus 169-178
7493637-7 1995 RA also increased PKC enzymatic activity in intact cells as determined by phosphorylation of the PKC-specific endogenous substrate MARCKS. Tretinoin 0-2 protein kinase C, alpha Mus musculus 18-21
8608343-8 1995 Finally, we demonstrate that tPA secretion of HaCaT 44 cells can be induced by retinoic acid, most likely via interaction of retinoic acid with nuclear-associated retinoic acid-receptor(s). Tretinoin 79-92 plasminogen activator, tissue type Homo sapiens 29-32
7493637-7 1995 RA also increased PKC enzymatic activity in intact cells as determined by phosphorylation of the PKC-specific endogenous substrate MARCKS. Tretinoin 0-2 protein kinase C, alpha Mus musculus 97-100
7493637-8 1995 However, while RA induced a five- to eightfold increase in total cellular PKC alpha protein levels, it only increased MARCKS phosphorylation by twofold. Tretinoin 15-17 protein kinase C, alpha Mus musculus 74-83
8608343-8 1995 Finally, we demonstrate that tPA secretion of HaCaT 44 cells can be induced by retinoic acid, most likely via interaction of retinoic acid with nuclear-associated retinoic acid-receptor(s). Tretinoin 125-138 plasminogen activator, tissue type Homo sapiens 29-32
7493637-11 1995 These results suggest a hypothesis whereby RA-induced nuclear PKC alpha might lead to increased AP-1 activity and show that RA-induced growth inhibition and differentiation are not always accompanied by an inhibition of AP-1 activity as has been proposed by other investigators. Tretinoin 43-45 protein kinase C, alpha Mus musculus 62-71
7593223-4 1995 Treatment of RAR beta-transfected MDA-MB-231 cells with 1 microM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RAR beta. Tretinoin 65-88 retinoic acid receptor beta Homo sapiens 13-21
7593223-4 1995 Treatment of RAR beta-transfected MDA-MB-231 cells with 1 microM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RAR beta. Tretinoin 65-88 retinoic acid receptor beta Homo sapiens 174-182
7593223-4 1995 Treatment of RAR beta-transfected MDA-MB-231 cells with 1 microM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RAR beta. Tretinoin 13-15 retinoic acid receptor beta Homo sapiens 174-182
7593223-6 1995 Addition of 1 microM RA stimulated colony size and number in the RAR beta-transfected MDA-MB-231 cells. Tretinoin 21-23 retinoic acid receptor beta Homo sapiens 65-73
7595558-6 1995 When embryonic day 14 fetal midbrain neurons, previously exposed to 1 microM retinoic acid (a compound that severely reduces the number of fetal midbrain dopamine neurons), were treated with dbcAMP, the levels of dopamine and the number of TH-immunoreactive cells returned to normal levels. Tretinoin 77-90 tyrosine hydroxylase Homo sapiens 240-242
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 174-187 retinoic acid receptor beta Homo sapiens 81-89
8609716-7 1995 After incubation with ATRA, cell survival was not altered and was correlated with a concomitant absence of apoptosis, despite a significant decrease of the BcL-2 protein in APL differentiated cells. Tretinoin 22-26 BCL2 apoptosis regulator Homo sapiens 156-161
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 65-67 retinoic acid receptor beta Homo sapiens 81-89
7579340-7 1995 Concomitant with the loss of major basic protein and fast green staining, surface expression of CD16 becomes detectable and is maximum by 10 days after ATRA. Tretinoin 152-156 Fc receptor, IgG, low affinity III Mus musculus 96-100
8614400-0 1995 Coordination of transcription of the human 17 beta-hydroxysteroid dehydrogenase type 1 gene (EDH17B2) by a cell-specific enhancer and a silencer: identification of a retinoic acid response element. Tretinoin 166-179 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 43-86
8614400-0 1995 Coordination of transcription of the human 17 beta-hydroxysteroid dehydrogenase type 1 gene (EDH17B2) by a cell-specific enhancer and a silencer: identification of a retinoic acid response element. Tretinoin 166-179 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 93-100
8614400-8 1995 The retinoic acid responsive element, which was located between bases -503 and -487 in the EDH17B2 enhancer, bound retinoid acid receptor alpha retinoid X receptor alpha complex and transmitted retinoic acid induction on transcription in JEG-3 and T-47D cells. Tretinoin 4-17 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 91-98
8614400-8 1995 The retinoic acid responsive element, which was located between bases -503 and -487 in the EDH17B2 enhancer, bound retinoid acid receptor alpha retinoid X receptor alpha complex and transmitted retinoic acid induction on transcription in JEG-3 and T-47D cells. Tretinoin 194-207 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 91-98
8614404-10 1995 Therefore, our data suggest that TOR, similar to COUP-TF, can negatively regulate retinoic acid and thyroid hormone signals. Tretinoin 82-95 RAR related orphan receptor C Homo sapiens 33-36
8614404-10 1995 Therefore, our data suggest that TOR, similar to COUP-TF, can negatively regulate retinoic acid and thyroid hormone signals. Tretinoin 82-95 nuclear receptor subfamily 2 group F member 1 Homo sapiens 49-56
7565739-2 1995 For ligand-induced activation by the retinoic acid receptor-retinoid X receptor (RAR-RXR) heterodimer, the RAR beta 2 promoter is dependent on the presence of E1A or E1A-like activity, since this promoter is activated by retinoic acid only in cells expressing such proteins. Tretinoin 37-50 retinoic acid receptor beta Homo sapiens 107-115
7579461-10 1995 In the presence of ATRA, all parameters (except u-PA) decreased during the culture time. Tretinoin 19-23 plasminogen activator, urokinase Homo sapiens 48-52
8591087-1 1995 BACKGROUND: Liarozole binds to the cytochrome P-450-dependent hydroxylating enzymes involved in steroid biosynthesis and retinoic acid catabolism. Tretinoin 121-134 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 35-51
8656080-10 1995 The CYP7 promoter activity was induced nearly 5-fold by all-trans-retinoic acid through sequences in the region from -200 to -129. Tretinoin 66-79 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 4-8
8656080-12 1995 Our results revealed that the -416 fragment of the rat CYP7 gene confers the activation by glucocorticoids and retinoic acid, and inhibition by insulin, phorbol esters and cAMP. Tretinoin 111-124 cytochrome P450 family 7 subfamily A member 1 Rattus norvegicus 55-59
7565739-4 1995 We now show that direct interaction between RAR and E1A is a requirement for retinoic acid-induced RAR beta 2 activation. Tretinoin 77-90 retinoic acid receptor beta Homo sapiens 99-107
7479394-4 1995 Trans retinoic acid (RA) also induced uPA mRNA and protein production in a dose-dependent manner (10(-6) to 10(-9) M). Tretinoin 0-19 proline rich acidic protein 1 Homo sapiens 38-41
7479394-4 1995 Trans retinoic acid (RA) also induced uPA mRNA and protein production in a dose-dependent manner (10(-6) to 10(-9) M). Tretinoin 21-23 proline rich acidic protein 1 Homo sapiens 38-41
7589553-5 1995 Overexpression of NSCL1 in F9 cells blocks the downregulation of Id2 gene expression during retinoic acid induced differentiation. Tretinoin 92-105 nescient helix loop helix 1 Mus musculus 18-23
7578267-0 1995 Cooperative effects of interferon-gamma on the induction of NADPH oxidase by retinoic acid or 1,25(OH)2-vitamin D3 in monocytic U937 cells. Tretinoin 77-90 interferon gamma Homo sapiens 23-39
7559612-1 1995 Retinoic acid exerts its many biological effects by interaction with a nuclear protein, the retinoic acid receptor (RAR). Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 116-119
7583541-4 1995 In HepG2 cells, maximal stimulation (twofold) of fibrinogen secretion was obtained when cells were incubated in the presence of 1 mumol/L all-trans retinoic acid (T-RA) for 24 hours. Tretinoin 138-161 fibrinogen beta chain Homo sapiens 49-59
7553653-6 1995 Marked induction of bcl-2 in NB cells followed RA-induced differentiation, whereas in cell lines failing to differentiate, bcl-2 was not detected. Tretinoin 47-49 BCL2 apoptosis regulator Homo sapiens 20-25
7548195-5 1995 Treatment of 7800C1 cells with 100 microM all-trans-retinoic acid resulted in inductions of catalase (160% above the control activity) and carnitine acetyltransferase (140% above the control activity) activities. Tretinoin 42-65 catalase Rattus norvegicus 92-100
7548195-5 1995 Treatment of 7800C1 cells with 100 microM all-trans-retinoic acid resulted in inductions of catalase (160% above the control activity) and carnitine acetyltransferase (140% above the control activity) activities. Tretinoin 42-65 carnitine O-acetyltransferase Rattus norvegicus 139-166
7583541-4 1995 In HepG2 cells, maximal stimulation (twofold) of fibrinogen secretion was obtained when cells were incubated in the presence of 1 mumol/L all-trans retinoic acid (T-RA) for 24 hours. Tretinoin 163-167 fibrinogen beta chain Homo sapiens 49-59
7583541-6 1995 In primary cultures of human hepatocytes, treatment with 1 mumol/L T-RA for 72 hours also gave a twofold increase in fibrinogen production. Tretinoin 67-71 fibrinogen beta chain Homo sapiens 117-127
7583541-10 1995 The ED50 of the different retinoids on fibrinogen secretion by HepG2 cells was 25 nmol/L for T-RA, 4 nmol/L for 9-cis retinoic acid, 11 nmol/L for the synthetic RXR agonist, and > 500 nmol/L for the RAR alpha agonist. Tretinoin 93-97 fibrinogen beta chain Homo sapiens 39-49
7564522-1 1995 We studied tissue transglutaminase (TGase) expression in human myelomonocytic leukemia cells treated by combinations of all-trans retinoic acid (RA) and 1,25 dihydroxyvitamin D3 (VD). Tretinoin 130-143 transglutaminase 2 Homo sapiens 11-34
7564507-0 1995 Direct evidence for the participation of bcl-2 in the regulation by retinoic acid of the Ara-C sensitivity of leukemic stem cells. Tretinoin 68-81 BCL2 apoptosis regulator Homo sapiens 41-46
7670094-4 1995 Calcitriol, 9 cis-RA, and sodium butyrate increase interleukin-8 (IL-8) mRNA expression, and pretreatment with these agents or RA potentiates the stimulation of IL-8 by phorbol ester (TPA). Tretinoin 18-20 C-X-C motif chemokine ligand 8 Homo sapiens 51-64
7670094-4 1995 Calcitriol, 9 cis-RA, and sodium butyrate increase interleukin-8 (IL-8) mRNA expression, and pretreatment with these agents or RA potentiates the stimulation of IL-8 by phorbol ester (TPA). Tretinoin 18-20 C-X-C motif chemokine ligand 8 Homo sapiens 66-70
7670094-4 1995 Calcitriol, 9 cis-RA, and sodium butyrate increase interleukin-8 (IL-8) mRNA expression, and pretreatment with these agents or RA potentiates the stimulation of IL-8 by phorbol ester (TPA). Tretinoin 18-20 C-X-C motif chemokine ligand 8 Homo sapiens 161-165
7670094-4 1995 Calcitriol, 9 cis-RA, and sodium butyrate increase interleukin-8 (IL-8) mRNA expression, and pretreatment with these agents or RA potentiates the stimulation of IL-8 by phorbol ester (TPA). Tretinoin 127-129 C-X-C motif chemokine ligand 8 Homo sapiens 51-64
7670094-4 1995 Calcitriol, 9 cis-RA, and sodium butyrate increase interleukin-8 (IL-8) mRNA expression, and pretreatment with these agents or RA potentiates the stimulation of IL-8 by phorbol ester (TPA). Tretinoin 127-129 C-X-C motif chemokine ligand 8 Homo sapiens 66-70
7670094-4 1995 Calcitriol, 9 cis-RA, and sodium butyrate increase interleukin-8 (IL-8) mRNA expression, and pretreatment with these agents or RA potentiates the stimulation of IL-8 by phorbol ester (TPA). Tretinoin 127-129 C-X-C motif chemokine ligand 8 Homo sapiens 161-165
8574976-0 1995 Effect of retinoic acid on expression of transforming growth factor-beta by retinal pigment epithelial cells in culture. Tretinoin 10-23 transforming growth factor beta 1 Homo sapiens 41-72
8574976-1 1995 OBJECTIVE: To study the effect of retinoic acid on the expression of transforming growth factor-beta (TGF-beta) by human retinal pigment epithelial (RPE) cells in culture. Tretinoin 34-47 transforming growth factor beta 1 Homo sapiens 69-100
8574976-1 1995 OBJECTIVE: To study the effect of retinoic acid on the expression of transforming growth factor-beta (TGF-beta) by human retinal pigment epithelial (RPE) cells in culture. Tretinoin 34-47 transforming growth factor beta 1 Homo sapiens 102-110
8574976-5 1995 Densitometry showed that retinoic acid reduced the level of TGF-beta 1 mRNA expression by 41% compared with control samples. Tretinoin 25-38 transforming growth factor beta 1 Homo sapiens 60-70
8574976-6 1995 ELISA showed that retinoic acid inhibited TGF-beta expression when compared with the baseline level of TGF-beta in media from RPE cells in culture. Tretinoin 18-31 transforming growth factor beta 1 Homo sapiens 42-50
7559803-0 1995 Insulin-like growth factors modulate the growth inhibitory effects of retinoic acid on MCF-7 breast cancer cells. Tretinoin 70-83 insulin Homo sapiens 0-7
7559803-5 1995 Pharmacologic doses of RA (> or = 10(-6) M) completely inhibit IGF-I-stimulated MCF-7 cell growth. Tretinoin 23-25 insulin like growth factor 1 Homo sapiens 66-71
7559803-9 1995 Treatment with the IGF-I receptor blocking antibody, alpha IR-3, restores RA-induced growth inhibition of IGF-I-treated or IGF-II-overexpressing MCF-7 cells, indicating that the IGF-I receptor is mediating these effects. Tretinoin 74-76 insulin like growth factor 1 Homo sapiens 19-24
7559803-9 1995 Treatment with the IGF-I receptor blocking antibody, alpha IR-3, restores RA-induced growth inhibition of IGF-I-treated or IGF-II-overexpressing MCF-7 cells, indicating that the IGF-I receptor is mediating these effects. Tretinoin 74-76 insulin like growth factor 1 Homo sapiens 106-111
7559803-11 1995 These results indicate that RA action on MCF-7 cells is biphasic in the presence of IGF-I or insulin with 10(-9) - 10(-7) M RA enhancing cell proliferation and > or = 10(-6) M RA causing growth inhibition. Tretinoin 28-30 insulin like growth factor 1 Homo sapiens 84-89
7559803-11 1995 These results indicate that RA action on MCF-7 cells is biphasic in the presence of IGF-I or insulin with 10(-9) - 10(-7) M RA enhancing cell proliferation and > or = 10(-6) M RA causing growth inhibition. Tretinoin 28-30 insulin Homo sapiens 93-100
7559803-11 1995 These results indicate that RA action on MCF-7 cells is biphasic in the presence of IGF-I or insulin with 10(-9) - 10(-7) M RA enhancing cell proliferation and > or = 10(-6) M RA causing growth inhibition. Tretinoin 124-126 insulin Homo sapiens 93-100
7559803-11 1995 These results indicate that RA action on MCF-7 cells is biphasic in the presence of IGF-I or insulin with 10(-9) - 10(-7) M RA enhancing cell proliferation and > or = 10(-6) M RA causing growth inhibition. Tretinoin 124-126 insulin Homo sapiens 93-100
7564507-7 1995 The effect of ATRA on bcl-2 expression was compared in sense-transfected cells and their parents; by Northern blotting it was shown that the endogenous but not the transfected genes were down-regulated after ATRA exposure. Tretinoin 14-18 BCL2 apoptosis regulator Homo sapiens 22-27
7564507-7 1995 The effect of ATRA on bcl-2 expression was compared in sense-transfected cells and their parents; by Northern blotting it was shown that the endogenous but not the transfected genes were down-regulated after ATRA exposure. Tretinoin 208-212 BCL2 apoptosis regulator Homo sapiens 22-27
7564507-10 1995 We conclude that data from the transfectants provides evidence that expression of bcl-2 is a determinant of sensitivity to Ara-C and H2O2; and that the effect of ATRA on sensitivity requires the presence of bcl-2 genes in association with regulatory elements. Tretinoin 162-166 BCL2 apoptosis regulator Homo sapiens 207-212
7564522-1 1995 We studied tissue transglutaminase (TGase) expression in human myelomonocytic leukemia cells treated by combinations of all-trans retinoic acid (RA) and 1,25 dihydroxyvitamin D3 (VD). Tretinoin 145-147 transglutaminase 2 Homo sapiens 11-34
7564522-2 1995 We found that in U937 cells, as in HL-60 and THP-1 cells, RA alone caused an early induction of enzyme activity, correlated with increased mRNA expression. Tretinoin 58-60 GLI family zinc finger 2 Homo sapiens 45-50
7554078-0 1995 Liarozole potentiates the cancer chemopreventive activity of and the up-regulation of gap junctional communication and connexin43 expression by retinoic acid and beta-carotene in 10T1/2 cells. Tretinoin 144-157 gap junction protein, alpha 1 Mus musculus 119-129
8578537-6 1995 The enhanced activity was inhibited by anti-uPA IgG and by pretreatment with phosphatidylinositol-specific phospholipase C. These findings suggest that retinoic acid increases the amount of receptor-bound uPA via de novo synthesis, and that it plays an important role in modulating cell-associated plasminogen activation. Tretinoin 152-165 proline rich acidic protein 1 Homo sapiens 44-47
8578537-6 1995 The enhanced activity was inhibited by anti-uPA IgG and by pretreatment with phosphatidylinositol-specific phospholipase C. These findings suggest that retinoic acid increases the amount of receptor-bound uPA via de novo synthesis, and that it plays an important role in modulating cell-associated plasminogen activation. Tretinoin 152-165 proline rich acidic protein 1 Homo sapiens 205-208
7668224-2 1995 Blast cells from this patient showed a striking response to all-trans-retinoic acid (ATRA)-induced differentiation as evaluated by CD15 expression following in vitro exposure to this inducer. Tretinoin 60-83 fucosyltransferase 4 Homo sapiens 131-135
7668224-2 1995 Blast cells from this patient showed a striking response to all-trans-retinoic acid (ATRA)-induced differentiation as evaluated by CD15 expression following in vitro exposure to this inducer. Tretinoin 85-89 fucosyltransferase 4 Homo sapiens 131-135
8584140-0 1995 Modulation of CCK mRNA in cell lines in response to isoproterenol and retinoic acid. Tretinoin 70-83 cholecystokinin Homo sapiens 14-17
8584140-11 1995 CCK mRNA levels in SK-N-MCIXC cells treated with retinoic acid combined with either isoproterenol or phorbol-12-myristate-13 acetate, were not significantly different from cells treated with retinoic acid alone. Tretinoin 49-62 cholecystokinin Homo sapiens 0-3
7554078-4 1995 Simultaneous treatment with Liarozole (10(-5) M) potentiated by a factor of 1000 the ability of low concentrations of retinoic acid (10(-10) M) to inhibit carcinogen-induced neoplastic transformation, to up-regulate gap junctional communication and to increase connexin43 expression. Tretinoin 118-131 gap junction protein, alpha 1 Mus musculus 261-271
7581951-6 1995 Retinoic acid at 10(-8) mol/l also increased the level of osteocalcin mRNA on day 12. Tretinoin 0-13 bone gamma-carboxyglutamate protein Rattus norvegicus 58-69
8519684-3 1995 RAR beta-transduced clones underwent growth inhibition associated with G1 arrest when treated with 1 microM all-trans-retinoic acid (RA). Tretinoin 108-131 retinoic acid receptor beta Homo sapiens 0-8
7581951-8 1995 At a high concentration (10(-6) mol/l), RA increased the level of osteopontin mRNA on day 6 and decreased the levels of ALP and osteocalcin mRNA irrespective of culture period. Tretinoin 40-42 bone gamma-carboxyglutamate protein Rattus norvegicus 128-139
7556191-7 1995 Exposure of HUVEC to 1 microM retinoic acid or the retinobenzoic acid, Ch55, led to the induction of the two RAR-beta mRNAs, RXR-alpha mRNA and CRBP-I mRNA, whereas the expression of the other receptor and CRABP-I transcripts did not change appreciably. Tretinoin 30-43 retinoic acid receptor beta Homo sapiens 109-117
7656983-0 1995 Retinoic acid induces gene expression of fibroblast growth factor-9 during induction of neuronal differentiation of mouse embryonal carcinoma P19 cells. Tretinoin 0-13 fibroblast growth factor 9 Mus musculus 41-67
7656983-1 1995 We have found that the gene expression of the ninth member of the fibroblast growth factor (FGF) family, FGF9 was induced during retinoic acid(RA)-induced neuronal differentiation of murine embryonal carcinoma P19 cells. Tretinoin 129-142 fibroblast growth factor 9 Mus musculus 105-109
7629162-1 1995 Retinoic acid receptor-beta (RAR-beta) specifically binds retinoic acid (RA) and functions as a RA-inducible transcriptional regulatory factor. Tretinoin 58-71 retinoic acid receptor beta Homo sapiens 0-27
7500381-9 1995 P19 cells induced with retinoic acid and plated in N2 were exposed to bFGF and EGF, which are known to be mitogens for neuronal precursor cells. Tretinoin 23-36 fibroblast growth factor 2 Homo sapiens 70-74
7629162-1 1995 Retinoic acid receptor-beta (RAR-beta) specifically binds retinoic acid (RA) and functions as a RA-inducible transcriptional regulatory factor. Tretinoin 58-71 retinoic acid receptor beta Homo sapiens 29-37
7629162-1 1995 Retinoic acid receptor-beta (RAR-beta) specifically binds retinoic acid (RA) and functions as a RA-inducible transcriptional regulatory factor. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 0-27
7629162-2 1995 Simultaneous mutation of Arg269 and Lys220 of RAR-beta to Ala results in a dramatic reduction in both transactivation and affinity for RA along with creating a RA concentration-dependent dominant negative mutant. Tretinoin 135-137 retinoic acid receptor beta Homo sapiens 46-54
7629162-6 1995 Taken together, these results suggest that Arg269 and Lys220 lie within the ligand binding pocket of RAR-beta and Lys220 lie within the ligand binding pocket of RAR-beta and that these two amino acid residues play an important role in determining retinoid specificity most likely by directly interacting with the carboxylate group of RA. Tretinoin 101-103 retinoic acid receptor beta Homo sapiens 161-169
7639703-0 1995 Identification and characterization of a functional retinoic acid/thyroid hormone-response element upstream of the human insulin gene enhancer. Tretinoin 52-65 insulin Homo sapiens 121-128
7639703-11 1995 In human islets of Langerhans, retinoic acid was shown to stimulate insulin mRNA levels. Tretinoin 31-44 insulin Homo sapiens 68-75
7615640-8 1995 Finally, Notch expression in dental mesenchyme is upregulated in a region surrounding beads soaked in retinoic acid (50-100 micrograms/ml) but not in fibroblast growth factor-2 (100-250 micrograms/ml). Tretinoin 102-115 Notch Drosophila melanogaster 9-14
7581005-0 1995 Study of retinoic acid effect upon retinoic acid receptors beta (RAR-beta) in C6 cultured glioma cells. Tretinoin 9-22 retinoic acid receptor, beta Rattus norvegicus 65-73
7581005-3 1995 After a treatment for 48 h with retinoic acid 10 microM, the 55 kDa form was enhanced, while no effect was observed either on RAR-alpha isoforms from C6 cells and on both RAR-alpha and RAR-beta forms from neuroblastoma SKN SH SY5Y used as a control. Tretinoin 32-45 retinoic acid receptor, beta Rattus norvegicus 185-193
7581005-5 1995 These results suggest that retinoic acid treatment of C6 cells led to a partial differentiation, the enhancement of the heavy form of RAR-beta being a marker of this phenomenon. Tretinoin 27-40 retinoic acid receptor, beta Rattus norvegicus 134-142
7636535-13 1995 Northern blot analysis showed that expression of retinoic acid receptor-beta (RAR-beta) was repressed and not induced by retinoic acid in retinoic acid-insensitive RCC lines. Tretinoin 49-62 retinoic acid receptor beta Homo sapiens 78-86
7636535-14 1995 However, RAR-beta expression was induced by retinoic acid in SK-RC-06 cells. Tretinoin 44-57 retinoic acid receptor beta Homo sapiens 9-17
7606736-9 1995 Although RA per se has no effect on the 2-5A synthetase expression, when it is combined with IFN-alpha-2b it appears to be able to potentiate the IFN-induced 2-5A synthetase expression. Tretinoin 9-11 interferon alpha 1 Homo sapiens 146-149
7628539-9 1995 In previous studies, we have demonstrated that retinoic acid induces the expression of RAR beta and RAR gamma in human dermal fibroblasts. Tretinoin 47-60 retinoic acid receptor beta Homo sapiens 87-95
7669674-2 1995 We studied the effect of interferon-alpha 2a (IFN) on ATRA pharmacokinetics in two patients with acute promyelocytic leukaemia (APL) in complete remission maintained by alternating 15 d of IFN and 15 d of ATRA. Tretinoin 54-58 interferon alpha 1 Homo sapiens 46-49
7669674-3 1995 Day 15 ATRA levels obtained during IFN+ATRA treatment were significantly higher than those observed in patients maintained on ATRA alone. Tretinoin 7-11 interferon alpha 1 Homo sapiens 35-38
7669674-5 1995 In our two patients IFN substantially reduced the induction of ATRA catabolism, indicating a potential role for IFN in modulating ATRA pharmacokinetics. Tretinoin 63-67 interferon alpha 1 Homo sapiens 20-23
7669674-5 1995 In our two patients IFN substantially reduced the induction of ATRA catabolism, indicating a potential role for IFN in modulating ATRA pharmacokinetics. Tretinoin 130-134 interferon alpha 1 Homo sapiens 20-23
7669674-5 1995 In our two patients IFN substantially reduced the induction of ATRA catabolism, indicating a potential role for IFN in modulating ATRA pharmacokinetics. Tretinoin 130-134 interferon alpha 1 Homo sapiens 112-115
7649373-0 1995 Efficient cloning of cDNAs of retinoic acid-responsive genes in P19 embryonal carcinoma cells and characterization of a novel mouse gene, Stra1 (mouse LERK-2/Eplg2). Tretinoin 30-43 ephrin B1 Mus musculus 158-163
7649373-9 1995 We also report the sequence and expression pattern in mouse embryos and adult tissues of one of these novel RA-inducible genes, Stra1, and show that it corresponds to the mouse ligand for the Cek5 receptor protein-tyrosine kinase. Tretinoin 108-110 ephrin B1 Mus musculus 128-133
11725062-0 1995 Retinoic Acid Modulates Epidermal Growth Factor Receptor Expression in Human Lung Epithelial Cancer Cells. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 24-56
11725062-1 1995 In human lung epithelial cancer cell line H460, an accumulation of epidermal growth factor receptors (EGF-R) was observed following treatment with 1 &mgr;M retinoic acid. Tretinoin 160-173 epidermal growth factor receptor Homo sapiens 67-100
11725062-1 1995 In human lung epithelial cancer cell line H460, an accumulation of epidermal growth factor receptors (EGF-R) was observed following treatment with 1 &mgr;M retinoic acid. Tretinoin 160-173 epidermal growth factor receptor Homo sapiens 102-107
11725062-3 1995 Transiently increased autophosphorylation of EGF-R after 48 h of retinoic acid treatment correlated with enhancement of EGF binding capacity on the H460 cell surface. Tretinoin 65-78 epidermal growth factor receptor Homo sapiens 45-50
11725062-4 1995 Nuclear run-on analysis indicated that retinoic acid upregulates transcription of the EGF-R gene, reaching a maximum at 48 h and decreasing after 72 h of treatment. Tretinoin 39-52 epidermal growth factor receptor Homo sapiens 86-91
11725062-5 1995 When retinoic acid-treated cells were chased in drug-free medium, the increased EGF-R transcript level remained unchanged. Tretinoin 5-18 epidermal growth factor receptor Homo sapiens 80-85
11725062-7 1995 The results demonstrate that retinoic acid induces EGF-R synthesis in human lung cancer cells. Tretinoin 29-42 epidermal growth factor receptor Homo sapiens 51-56
9816041-0 1995 Retinoic acid modulates extracellular urokinase-type plasminogen activator activity in DU-145 human prostatic carcinoma cells. Tretinoin 0-13 plasminogen activator, urokinase Homo sapiens 38-74
9816041-1 1995 Effects of all-trans retinoic acid (RA) on the net enzymatic activity of secreted, extracellular urokinase-type plasminogen activator (u-PA) in DU-145 human prostatic carcinoma cells were examined to assess the potential use of retinoids in human prostate cancer prevention and treatment. Tretinoin 11-34 plasminogen activator, urokinase Homo sapiens 97-133
9816041-1 1995 Effects of all-trans retinoic acid (RA) on the net enzymatic activity of secreted, extracellular urokinase-type plasminogen activator (u-PA) in DU-145 human prostatic carcinoma cells were examined to assess the potential use of retinoids in human prostate cancer prevention and treatment. Tretinoin 36-38 plasminogen activator, urokinase Homo sapiens 97-133
9816041-1 1995 Effects of all-trans retinoic acid (RA) on the net enzymatic activity of secreted, extracellular urokinase-type plasminogen activator (u-PA) in DU-145 human prostatic carcinoma cells were examined to assess the potential use of retinoids in human prostate cancer prevention and treatment. Tretinoin 36-38 plasminogen activator, urokinase Homo sapiens 135-139
9816041-8 1995 A 48-h treatment with 1.0 micrometer RA reduced u-PA activity in conditioned medium to 51.6% of control. Tretinoin 37-39 plasminogen activator, urokinase Homo sapiens 48-52
9816041-9 1995 A 50% reduction in free u-PA antigen level, as compared to control, was further demonstrated at 1.0 micrometer RA by Western blot analysis and densitometry. Tretinoin 111-113 plasminogen activator, urokinase Homo sapiens 24-28
9816042-9 1995 However, treatment of cultures with 1 microM all-trans retinoic acid (RA) for 48 h reduced the ability of serum-free conditioned medium to cause u-PA-mediated degradation of fibronectin and laminin. Tretinoin 45-68 plasminogen activator, urokinase Homo sapiens 145-149
9816042-9 1995 However, treatment of cultures with 1 microM all-trans retinoic acid (RA) for 48 h reduced the ability of serum-free conditioned medium to cause u-PA-mediated degradation of fibronectin and laminin. Tretinoin 45-68 fibronectin 1 Homo sapiens 174-185
9816042-9 1995 However, treatment of cultures with 1 microM all-trans retinoic acid (RA) for 48 h reduced the ability of serum-free conditioned medium to cause u-PA-mediated degradation of fibronectin and laminin. Tretinoin 70-72 plasminogen activator, urokinase Homo sapiens 145-149
9816042-9 1995 However, treatment of cultures with 1 microM all-trans retinoic acid (RA) for 48 h reduced the ability of serum-free conditioned medium to cause u-PA-mediated degradation of fibronectin and laminin. Tretinoin 70-72 fibronectin 1 Homo sapiens 174-185
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 interleukin 1 beta Homo sapiens 216-234
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 interleukin 1 beta Homo sapiens 236-245
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 tumor necrosis factor Homo sapiens 252-279
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 tumor necrosis factor Homo sapiens 281-290
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 interleukin 1 beta Homo sapiens 216-234
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 interleukin 1 beta Homo sapiens 236-245
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 tumor necrosis factor Homo sapiens 252-279
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 tumor necrosis factor Homo sapiens 281-290
7615640-10 1995 These data suggest that Notch genes may be involved in mediating some of the biological effects of retinoic acid during normal development and after teratogenic exposure. Tretinoin 99-112 Notch Drosophila melanogaster 24-29
7797528-7 1995 In contrast, differentiation to a neural lineage, by aggregation and exposure to retinoic acid, was associated with the induction of predominantly ETB. Tretinoin 81-94 endothelin receptor type B Homo sapiens 147-150
7791800-2 1995 One of the earliest events following the exposure of bronchial epithelial cells to RA is the strong induction of RA receptor beta (RAR beta) mRNA. Tretinoin 83-85 retinoic acid receptor beta Homo sapiens 131-139
7630193-10 1995 NB4 cells treated with either all-trans or 9-cis retinoic acid (1 microM) were induced to differentiate and the level of Bcl-2 protein decreased to undetectable levels during terminal maturation when only a few apoptotic cells were detected. Tretinoin 49-62 BCL2 apoptosis regulator Homo sapiens 121-126
7797489-3 1995 Additionally, COUP-TF I enhanced retinoic acid response element-dependent reporter gene expression in 3T3 fibroblasts, indicating that COUP-TF I can modulate transcriptional activation in these cells. Tretinoin 33-46 nuclear receptor subfamily 2 group F member 1 Gallus gallus 14-23
7797489-3 1995 Additionally, COUP-TF I enhanced retinoic acid response element-dependent reporter gene expression in 3T3 fibroblasts, indicating that COUP-TF I can modulate transcriptional activation in these cells. Tretinoin 33-46 nuclear receptor subfamily 2 group F member 1 Gallus gallus 135-144
7757990-4 1995 However, in the RA-resistant line SK-N-AS, TGF-beta 1 is constitutively secreted at levels that are unchanged after RA treatment, and although TBRI and TBRIII mRNA is expressed in untreated SK-N-AS cells, levels of TBRI and TBRIII protein and TBRII mRNA decrease after RA treatment. Tretinoin 16-18 transforming growth factor beta 1 Homo sapiens 43-53
7540854-0 1995 All-trans retinoic acid shows multiple effects on the survival, proliferation and differentiation of human fetal CD34+ haemopoietic progenitor cells. Tretinoin 10-23 CD34 molecule Homo sapiens 113-117
7540854-2 1995 RA, at both physiological (10(-11) and 10(-12)M) and pharmacological (10(-6) and 10(-7)M) concentrations, significantly (P < 0.01) promoted the survival of fetal CD34+ cells in liquid cultures from day 3 onwards, by suppressing apoptosis induced by serum and growth factor deprivation. Tretinoin 0-2 CD34 molecule Homo sapiens 165-169
7780141-1 1995 Because retinoids are known to modulate the growth and differentiation effects of tumor necrosis factor (TNF), we investigated the effect of all-trans-retinoic acid (RA) on the cell surface expression of TNF receptors in human histiocytic lymphoma U-937 cells. Tretinoin 141-164 tumor necrosis factor Homo sapiens 204-207
7780141-1 1995 Because retinoids are known to modulate the growth and differentiation effects of tumor necrosis factor (TNF), we investigated the effect of all-trans-retinoic acid (RA) on the cell surface expression of TNF receptors in human histiocytic lymphoma U-937 cells. Tretinoin 166-168 tumor necrosis factor Homo sapiens 204-207
7780141-2 1995 RA decreased the specific binding of 125I-labeled TNF to these cells in a dose- and time-dependent manner. Tretinoin 0-2 tumor necrosis factor Homo sapiens 50-53
7780141-8 1995 RA treatment also decreased TNF receptors on acute monocytic leukemia cell line THP-1. Tretinoin 0-2 tumor necrosis factor Homo sapiens 28-31
7780141-8 1995 RA treatment also decreased TNF receptors on acute monocytic leukemia cell line THP-1. Tretinoin 0-2 GLI family zinc finger 2 Homo sapiens 80-85
7780141-11 1995 The downregulation of TNF receptors by RA correlated with the downmodulation of the antiproliferative effects of TNF against U-937 cells. Tretinoin 39-41 tumor necrosis factor Homo sapiens 22-25
7780141-11 1995 The downregulation of TNF receptors by RA correlated with the downmodulation of the antiproliferative effects of TNF against U-937 cells. Tretinoin 39-41 tumor necrosis factor Homo sapiens 113-116
7780141-12 1995 Overall, our results indicate that RA downmodulates both the p60 and p80 form of the TNF receptor on cells of myeloid origin, which correlates with the cellular response. Tretinoin 35-37 tumor necrosis factor Homo sapiens 85-88
7786028-7 1995 In contrast, all-trans RA and 9-cis RA are equally effective in the induction of RAR beta transcript and inhibition of cell proliferation. Tretinoin 23-25 retinoic acid receptor beta Homo sapiens 81-89
7757990-0 1995 Induction of transforming growth factor beta 1 and its receptors during all-trans-retinoic acid (RA) treatment of RA-responsive human neuroblastoma cell lines. Tretinoin 76-95 transforming growth factor beta 1 Homo sapiens 13-46
7757990-0 1995 Induction of transforming growth factor beta 1 and its receptors during all-trans-retinoic acid (RA) treatment of RA-responsive human neuroblastoma cell lines. Tretinoin 97-99 transforming growth factor beta 1 Homo sapiens 13-46
7757990-0 1995 Induction of transforming growth factor beta 1 and its receptors during all-trans-retinoic acid (RA) treatment of RA-responsive human neuroblastoma cell lines. Tretinoin 114-116 transforming growth factor beta 1 Homo sapiens 13-46
7757990-1 1995 Recent work on a variety of normal and malignant cell lines has shown that induction and secretion of biologically active TGF-beta may occur after exposure to all-trans-retinoic acid (RA), coincident with decreased growth rate and/or differentiation. Tretinoin 163-182 transforming growth factor beta 1 Homo sapiens 122-130
7757990-1 1995 Recent work on a variety of normal and malignant cell lines has shown that induction and secretion of biologically active TGF-beta may occur after exposure to all-trans-retinoic acid (RA), coincident with decreased growth rate and/or differentiation. Tretinoin 184-186 transforming growth factor beta 1 Homo sapiens 122-130
7757990-5 1995 Thus, in RA-sensitive neuroblastoma cells, RA treatment may result in the induction of a negative autocrine TGF-beta 1 growth regulatory loop. Tretinoin 9-11 transforming growth factor beta 1 Homo sapiens 108-118
7584721-1 1995 Midkine (MK) is a novel heparin-binding growth factor whose expression is regulated by retinoic acid. Tretinoin 87-100 midkine Homo sapiens 0-7
7600989-12 1995 Treatment with retinoic acid alters this Hox code to that of a more proximal region by the rapid and differential downregulation of HoxA13, at the same time that expression of HoxA9 is unaffected. Tretinoin 15-28 homeobox A13 Gallus gallus 132-138
7600989-12 1995 Treatment with retinoic acid alters this Hox code to that of a more proximal region by the rapid and differential downregulation of HoxA13, at the same time that expression of HoxA9 is unaffected. Tretinoin 15-28 homeobox A9 Gallus gallus 176-181
7775578-5 1995 RA inhibited MLC-CAT transgene but not alpha sk actin-CAT transgene expression in primary cultures from these mice. Tretinoin 0-2 catalase Mus musculus 17-20
7775578-6 1995 Analysis of MLC-CAT expression in transgenic mouse primary cultures and in stably transfected C2C12 cells demonstrated that repression of MLC-CAT activity by RA was dependent upon diffusible factors in chick embryo extract. Tretinoin 158-160 catalase Mus musculus 16-19
7775578-6 1995 Analysis of MLC-CAT expression in transgenic mouse primary cultures and in stably transfected C2C12 cells demonstrated that repression of MLC-CAT activity by RA was dependent upon diffusible factors in chick embryo extract. Tretinoin 158-160 catalase Mus musculus 142-145
7651608-17 1995 The effects of retinoic acid on PHF-1 immunofluorescence were modifiable by fibronectin, which can be released by some neuroblastoma cell lines [Ciccarone V. et al. Tretinoin 15-28 fibronectin 1 Homo sapiens 76-87
7614995-6 1995 Dietary all-trans-retinoic acid supplementation down-regulated the level of constitutive IL-12 and IFN-gamma transcripts. Tretinoin 12-31 interferon gamma Mus musculus 99-108
7614995-9 1995 The inducible IFN-gamma was largely from CD8+ T cells and all-trans-retinoic acid addition in vitro inhibited IFN-gamma production at the transcript level. Tretinoin 62-81 interferon gamma Mus musculus 14-23
7614995-9 1995 The inducible IFN-gamma was largely from CD8+ T cells and all-trans-retinoic acid addition in vitro inhibited IFN-gamma production at the transcript level. Tretinoin 62-81 interferon gamma Mus musculus 110-119
7614995-10 1995 Retinoic acid addition in vitro also decreased natural killer cell IFN-gamma synthesis at the transcript level. Tretinoin 0-13 interferon gamma Mus musculus 67-76
7584721-1 1995 Midkine (MK) is a novel heparin-binding growth factor whose expression is regulated by retinoic acid. Tretinoin 87-100 midkine Homo sapiens 9-11
7755585-3 1995 The affinity and specificity of retinoic acid receptors for all-trans-retinoic acid encouraged us to express both the entire human retinoic acid receptor beta (RAR-beta) and two versions of its retinoic acid-binding domain in Escherichia coli in the hope that these recombinant proteins might be used as binders in a ligand-binding assay for all-trans-retinoic acid. Tretinoin 32-45 retinoic acid receptor beta Homo sapiens 131-158
7763262-0 1995 Regulation of interleukin-8 gene expression by all-trans retinoic acid. Tretinoin 57-70 C-X-C motif chemokine ligand 8 Homo sapiens 14-27
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 140-153 C-X-C motif chemokine ligand 8 Homo sapiens 41-54
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 140-153 C-X-C motif chemokine ligand 8 Homo sapiens 56-60
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 155-159 C-X-C motif chemokine ligand 8 Homo sapiens 41-54
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 155-159 C-X-C motif chemokine ligand 8 Homo sapiens 56-60
7763262-2 1995 Both IL-1 alpha and IL-8 protein release were enhanced by treatment with ATRA and TNF-alpha after 48 h exposure. Tretinoin 73-77 C-X-C motif chemokine ligand 8 Homo sapiens 20-24
7763262-3 1995 Blocking of IL-1 alpha activity in HOC-7 cells with either IL-1 receptor antagonist (IL-1ra) or a neutralizing antibody directed against IL-1 alpha resulted in a dose-dependent decrease of IL-8 release by ATRA, TNF-alpha and IL-1 alpha treated HOC-7 cells. Tretinoin 205-209 C-X-C motif chemokine ligand 8 Homo sapiens 189-193
7755585-3 1995 The affinity and specificity of retinoic acid receptors for all-trans-retinoic acid encouraged us to express both the entire human retinoic acid receptor beta (RAR-beta) and two versions of its retinoic acid-binding domain in Escherichia coli in the hope that these recombinant proteins might be used as binders in a ligand-binding assay for all-trans-retinoic acid. Tretinoin 32-45 retinoic acid receptor beta Homo sapiens 160-168
7755585-7 1995 RAR-beta-(V7-Q448) and RAR-beta-(E149-Q448) had similar Kd values for all-trans-retinoic acid (1.4 and 0.6 nmol/l respectively) whereas RAR-beta-(P193-Q448) bound all-trans-retinoic acid less avidly (Kd 9.6 nmol/l). Tretinoin 74-93 retinoic acid receptor beta Homo sapiens 0-8
7755585-7 1995 RAR-beta-(V7-Q448) and RAR-beta-(E149-Q448) had similar Kd values for all-trans-retinoic acid (1.4 and 0.6 nmol/l respectively) whereas RAR-beta-(P193-Q448) bound all-trans-retinoic acid less avidly (Kd 9.6 nmol/l). Tretinoin 74-93 retinoic acid receptor beta Homo sapiens 23-31
7755585-7 1995 RAR-beta-(V7-Q448) and RAR-beta-(E149-Q448) had similar Kd values for all-trans-retinoic acid (1.4 and 0.6 nmol/l respectively) whereas RAR-beta-(P193-Q448) bound all-trans-retinoic acid less avidly (Kd 9.6 nmol/l). Tretinoin 74-93 retinoic acid receptor beta Homo sapiens 23-31
7769841-16 1995 Left unexplained are the action of HC, which does not affect bcl-2 expression and the mechanism by which ara-C prevents down-regulation of bcl-2 by ATRA. Tretinoin 148-152 BCL2 apoptosis regulator Homo sapiens 139-144
7771807-0 1995 All-trans-retinoic acid interacts synergistically with basic fibroblast growth factor and epidermal growth factor to stimulate the production of tissue inhibitor of metalloproteinases from fibroblasts. Tretinoin 0-23 fibroblast growth factor 2 Homo sapiens 55-85
7771807-0 1995 All-trans-retinoic acid interacts synergistically with basic fibroblast growth factor and epidermal growth factor to stimulate the production of tissue inhibitor of metalloproteinases from fibroblasts. Tretinoin 0-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 145-183
7771807-1 1995 This report examines the effect of all-trans-retinoic acid in combination with basic fibroblast growth factor (bFGF) or epidermal growth factor (EGF) on collagenase and tissue inhibitor of metalloproteinases (TIMP) production from human foreskin and synovial fibroblasts. Tretinoin 35-58 TIMP metallopeptidase inhibitor 1 Homo sapiens 169-207
7771807-1 1995 This report examines the effect of all-trans-retinoic acid in combination with basic fibroblast growth factor (bFGF) or epidermal growth factor (EGF) on collagenase and tissue inhibitor of metalloproteinases (TIMP) production from human foreskin and synovial fibroblasts. Tretinoin 35-58 TIMP metallopeptidase inhibitor 1 Homo sapiens 209-213
7771807-2 1995 When 10(-5) M retinoic acid is applied in combination with 1, 10, and 100 ng/ml of either FGF or EGF to foreskin or synovial fibroblasts, this results in a dose-dependent synergistic increase in TIMP protein production which is greater than the additive effect of the agents by up to fourfold. Tretinoin 14-27 TIMP metallopeptidase inhibitor 1 Homo sapiens 195-199
7771807-4 1995 We have also found that retinoic acid potently inhibits bFGF- and EGF-stimulated collagenase protein production in both skin and synovial fibroblasts. Tretinoin 24-37 fibroblast growth factor 2 Homo sapiens 56-60
7742011-4 1995 We found that retinoic acid interferes, in a dose-dependent fashion, with the expression of epithelial genes that are found in distal segments of the fetal lung (surfactant-associated proteins SP-A, SP-B, and SP-C). Tretinoin 14-27 surfactant protein C Homo sapiens 209-213
7668385-3 1995 This technique was successfully applied to evaluate differences in glucocorticoid receptor expression in U937 cells before and after the addition of potent differentiation inducers: 12-O-tetradecanoylphorbol 13-acetate (TPA) and a combination of all-trans retinoic acid (RA) and 1,25-dihydroxyvitamin D2 (VD). Tretinoin 256-269 nuclear receptor subfamily 3 group C member 1 Homo sapiens 67-90
8589272-2 1995 Upon granulocytic differentiation with all-trans retinoic acid (ATRA) or the combination of ATRA and granulocyte-colony-stimulating factor (G-CSF), significant amounts of IL-1 beta and IL-8 mRNAs accumulated in both cell types. Tretinoin 49-62 interleukin 1 beta Homo sapiens 171-180
8589272-2 1995 Upon granulocytic differentiation with all-trans retinoic acid (ATRA) or the combination of ATRA and granulocyte-colony-stimulating factor (G-CSF), significant amounts of IL-1 beta and IL-8 mRNAs accumulated in both cell types. Tretinoin 49-62 C-X-C motif chemokine ligand 8 Homo sapiens 185-189
8589272-2 1995 Upon granulocytic differentiation with all-trans retinoic acid (ATRA) or the combination of ATRA and granulocyte-colony-stimulating factor (G-CSF), significant amounts of IL-1 beta and IL-8 mRNAs accumulated in both cell types. Tretinoin 64-68 interleukin 1 beta Homo sapiens 171-180
8589272-2 1995 Upon granulocytic differentiation with all-trans retinoic acid (ATRA) or the combination of ATRA and granulocyte-colony-stimulating factor (G-CSF), significant amounts of IL-1 beta and IL-8 mRNAs accumulated in both cell types. Tretinoin 64-68 C-X-C motif chemokine ligand 8 Homo sapiens 185-189
7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 44-57 BCL2 apoptosis regulator Homo sapiens 118-123
7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 59-82 BCL2 apoptosis regulator Homo sapiens 118-123
7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 84-88 BCL2 apoptosis regulator Homo sapiens 118-123
7769841-5 1995 The down-regulation could be prevented by exposing the cells to ara-C either before or after ATRA; decrease in bcl-2 protein was moderate and only obvious after 36 h of ATRA treatment. Tretinoin 93-97 BCL2 apoptosis regulator Homo sapiens 111-116
7769841-5 1995 The down-regulation could be prevented by exposing the cells to ara-C either before or after ATRA; decrease in bcl-2 protein was moderate and only obvious after 36 h of ATRA treatment. Tretinoin 169-173 BCL2 apoptosis regulator Homo sapiens 111-116
7538673-0 1995 Enhanced expression of an insulin growth factor-like binding protein (mac25) in senescent human mammary epithelial cells and induced expression with retinoic acid. Tretinoin 149-162 insulin like growth factor binding protein 7 Homo sapiens 70-75
7538673-7 1995 We found that mac25 accumulates in senescent cells and is up-regulated in normal, growing mammary epithelial cells by all-trans-retinoic acid or the synthetic retinoid fenretinide. Tretinoin 118-141 insulin like growth factor binding protein 7 Homo sapiens 14-19
7737975-3 1995 Upon retinoic acid-induced differentiation of P19 cells, there was an early and rapid 10-fold increase in NHE1 transcription. Tretinoin 5-18 solute carrier family 9 (sodium/hydrogen exchanger), member 1 Mus musculus 106-110
7674376-8 1995 These results suggest that COUP-TF I plays an important role in regulating RA-induced neuronal differentiation. Tretinoin 75-77 nuclear receptor subfamily 2 group F member 1 Gallus gallus 27-36
7714611-6 1995 In addition, cell lines with the highest EGFR levels were also more resistant to the growth-suppressive effects of retinoic acid when maintained in soft agar. Tretinoin 115-128 epidermal growth factor receptor Homo sapiens 41-45
7714611-7 1995 These observations suggest that even though the overexpression of the EGFR did not confer a distinct growth advantage to glioma cells cultured on flat culture dishes, the ability of these cells to maintain anchorage-independent growth in soft agar especially in response to EGF and retinoic acid is facilitated. Tretinoin 282-295 epidermal growth factor receptor Homo sapiens 70-74
7769841-15 1995 ATRA regulates ara-C toxicity by its action on bcl-2. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 47-52
7717974-3 1995 Northern-blot analysis indicates that transcripts encoding GATA-4 and J6 increase in parallel during retinoic acid-induced differentiation of F9 cells. Tretinoin 101-114 GATA binding protein 4 Mus musculus 59-65
7739519-2 1995 We report here on the effects of exogenous TNF-alpha on SK-N-MC human neuroblastoma cells differentiated to a neuronal phenotype with retinoic acid, TNF-alpha caused a dose-dependent loss of viability and a corresponding increase in apoptosis in differentiated SK-N-MC cells but not in undifferentiated cultures. Tretinoin 134-147 tumor necrosis factor Homo sapiens 43-52
7739519-2 1995 We report here on the effects of exogenous TNF-alpha on SK-N-MC human neuroblastoma cells differentiated to a neuronal phenotype with retinoic acid, TNF-alpha caused a dose-dependent loss of viability and a corresponding increase in apoptosis in differentiated SK-N-MC cells but not in undifferentiated cultures. Tretinoin 134-147 tumor necrosis factor Homo sapiens 149-158
21597757-1 1995 Retinoic acid transiently induced expression of high levels of epidermal growth factor receptor (EGFR) in the human non-small cell lung carcinoma cell line H460a. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 63-95
21597757-1 1995 Retinoic acid transiently induced expression of high levels of epidermal growth factor receptor (EGFR) in the human non-small cell lung carcinoma cell line H460a. Tretinoin 0-13 epidermal growth factor receptor Homo sapiens 97-101
21597757-2 1995 Scatchard analysis revealed a 40-fold increase in the expression of EGFR on the cell surface of H460a cells within 48 h of treatment with 5 mu M concentrations of retinoic acid. Tretinoin 163-176 epidermal growth factor receptor Homo sapiens 68-72
21597757-3 1995 RNase protection and nuclear run-off assays established that increases in EGFR expression in retinoic acid-treated cells were not the result of increased promoter activity of EGFR gene, but were more likely the result of a posttranscriptional mechanism. Tretinoin 93-106 epidermal growth factor receptor Homo sapiens 74-78
21597757-4 1995 Immune complex kinase assays demonstrated that the EGFR induced by retinoic acid was functionally active. Tretinoin 67-80 epidermal growth factor receptor Homo sapiens 51-55
21597757-5 1995 We conclude that retinoic acid exerts its control over expression of the EGFR in H460a cells through a posttranscriptional mechanism. Tretinoin 17-30 epidermal growth factor receptor Homo sapiens 73-77
21597757-6 1995 Moreover, elevated EGFR might play a role in the increased tumorigenic potential exhibited by retinoic acid-treated H460a cells. Tretinoin 94-107 epidermal growth factor receptor Homo sapiens 19-23
7731708-4 1995 Using NTera2/clone D1 (NT2/D1) human embryonal carcinoma cells as a model, we report that the RA induced terminal differentiation of these cells into a neuronal phenotype is characterized by an increase in expression of RAR alpha, RAR beta, RAR gamma, and a slight induction of RXR alpha. Tretinoin 94-96 retinoic acid receptor beta Homo sapiens 231-239
7704904-1 1995 The effects of retinoids (all-trans-retinoic acid (RA) and vitamin A) and hydrocortisone (HC) on the IL-4-dependent IgE and IgG1 response by mouse whole spleen cells and splenic B cells were studied. Tretinoin 26-49 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 124-128
7721805-0 1995 Tumor necrosis factor alpha facilitates nuclear actions of retinoic acid to regulate expression of the alkaline phosphatase gene in preosteoblasts. Tretinoin 59-72 tumor necrosis factor Rattus norvegicus 0-27
7721805-2 1995 In this cell line, alkaline phosphatase mRNA was not constitutively expressed but was progressively induced by treatment with 1 microM retinoic acid, detectable by 6 h. Combining retinoic acid with 0.6 nM TNF alpha resulted in alkaline phosphatase mRNA appearing by 2 h, as well as enhanced expression above that observed with retinoic acid alone at 6, 12, and 24 h. Nuclear run-on analysis showed constitutive transcription of the alkaline phosphatase gene in control and TNF alpha-treated cells. Tretinoin 135-148 tumor necrosis factor Rattus norvegicus 205-214
7721805-2 1995 In this cell line, alkaline phosphatase mRNA was not constitutively expressed but was progressively induced by treatment with 1 microM retinoic acid, detectable by 6 h. Combining retinoic acid with 0.6 nM TNF alpha resulted in alkaline phosphatase mRNA appearing by 2 h, as well as enhanced expression above that observed with retinoic acid alone at 6, 12, and 24 h. Nuclear run-on analysis showed constitutive transcription of the alkaline phosphatase gene in control and TNF alpha-treated cells. Tretinoin 135-148 tumor necrosis factor Rattus norvegicus 473-482
7721805-2 1995 In this cell line, alkaline phosphatase mRNA was not constitutively expressed but was progressively induced by treatment with 1 microM retinoic acid, detectable by 6 h. Combining retinoic acid with 0.6 nM TNF alpha resulted in alkaline phosphatase mRNA appearing by 2 h, as well as enhanced expression above that observed with retinoic acid alone at 6, 12, and 24 h. Nuclear run-on analysis showed constitutive transcription of the alkaline phosphatase gene in control and TNF alpha-treated cells. Tretinoin 179-192 tumor necrosis factor Rattus norvegicus 473-482
7721805-2 1995 In this cell line, alkaline phosphatase mRNA was not constitutively expressed but was progressively induced by treatment with 1 microM retinoic acid, detectable by 6 h. Combining retinoic acid with 0.6 nM TNF alpha resulted in alkaline phosphatase mRNA appearing by 2 h, as well as enhanced expression above that observed with retinoic acid alone at 6, 12, and 24 h. Nuclear run-on analysis showed constitutive transcription of the alkaline phosphatase gene in control and TNF alpha-treated cells. Tretinoin 179-192 tumor necrosis factor Rattus norvegicus 473-482
7721805-7 1995 Adding TNF alpha with retinoic acid greatly enhanced this effect, which was observed after 4 h, prior to any detectable interaction between TNF alpha and retinoic acid on gene transcription. Tretinoin 22-35 tumor necrosis factor Rattus norvegicus 7-16
7655621-1 1995 All-trans retinoic acid (all-trans RA), the active metabolite of vitamin A, has been demonstrated to be an efficient alternative to chemotherapy in the treatment of acute promyelocytic leukemia (APL), the AML3 subtype of the FAB cytological classification. Tretinoin 0-23 RUNX family transcription factor 2 Homo sapiens 205-209
7592548-0 1995 A retinoic acid-responsive element in human midkine gene. Tretinoin 2-15 midkine Homo sapiens 44-51
7537232-6 1995 BMP 4 and FGF 2 can also maintain Msx-1 expression in limb mesenchyme as well as retinoic acid which is usually associated with polarizing activity in the early limb. Tretinoin 81-94 bone morphogenetic protein 4 Mus musculus 0-5
7729568-0 1995 Galectin-7, a human 14-kDa S-lectin, specifically expressed in keratinocytes and sensitive to retinoic acid. Tretinoin 94-107 galectin 7 Homo sapiens 0-10
7729568-8 1995 This effect of retinoic acid on a keratinocyte cell type marker such as galectin-7 is more reminiscent of its metaplasiogenic effect in vivo than of its inhibitory effect on terminal epidermal differentiation in vitro. Tretinoin 15-28 galectin 7 Homo sapiens 72-82
7706255-0 1995 Retinoic acid induction of human tissue-type plasminogen activator gene expression via a direct repeat element (DR5) located at -7 kilobases. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 33-66
7706767-0 1995 Differential regulation of decorin and biglycan gene expression by dexamethasone and retinoic acid in cultured human skin fibroblasts. Tretinoin 85-98 biglycan Homo sapiens 39-47
7706767-2 1995 We have studied the regulation of gene expression of two small extracellular matrix chondroitin/dermatan sulfate proteoglycans, decorin and biglycan, by dexamethasone and retinoic acid in cultured human skin fibroblasts. Tretinoin 171-184 biglycan Homo sapiens 140-148
7602313-7 1995 Unlike hypoxia, however, cAMP analogs also stimulated neurofilament (NF 68 or NF 160 kD) expression and neurite outgrowth in glomus cells, and these properties were enhanced by retinoic acid. Tretinoin 177-190 neurofilament light chain Rattus norvegicus 69-87
7706255-2 1995 In HT1080 fibrosarcoma cells, induction of t-PA-related antigen secretion and t-PA mRNA steady state levels by RA were found to depend on de novo protein and mRNA synthesis. Tretinoin 111-113 plasminogen activator, tissue type Homo sapiens 43-47
7706255-2 1995 In HT1080 fibrosarcoma cells, induction of t-PA-related antigen secretion and t-PA mRNA steady state levels by RA were found to depend on de novo protein and mRNA synthesis. Tretinoin 111-113 plasminogen activator, tissue type Homo sapiens 78-82
7706255-5 1995 A functional retinoic acid response element (RARE), consisting of a direct repeat of the GGGTCA motif spaced by 5 nucleotides (t-PA/DR5), was localized at -7.3 kilobases. Tretinoin 13-26 plasminogen activator, tissue type Homo sapiens 127-131
7706255-6 1995 The t-PA/DR5 element interacted with the heterodimer composed of retinoic acid receptor alpha and retinoid X receptor alpha in vitro, whereas its mutation abolished induction by RA in transient expression. Tretinoin 178-180 plasminogen activator, tissue type Homo sapiens 4-8
7890721-3 1995 Addition of retinoic acid (RA) for the last 24 h during dimethyl sulfoxide (Me2SO)-induced differentiation enhanced fMLP-dependent signals and interaction between fMLP receptor and G(i). Tretinoin 12-25 formyl peptide receptor 1 Homo sapiens 116-120
7890721-3 1995 Addition of retinoic acid (RA) for the last 24 h during dimethyl sulfoxide (Me2SO)-induced differentiation enhanced fMLP-dependent signals and interaction between fMLP receptor and G(i). Tretinoin 12-25 formyl peptide receptor 1 Homo sapiens 163-167
7890721-3 1995 Addition of retinoic acid (RA) for the last 24 h during dimethyl sulfoxide (Me2SO)-induced differentiation enhanced fMLP-dependent signals and interaction between fMLP receptor and G(i). Tretinoin 27-29 formyl peptide receptor 1 Homo sapiens 116-120
7890721-3 1995 Addition of retinoic acid (RA) for the last 24 h during dimethyl sulfoxide (Me2SO)-induced differentiation enhanced fMLP-dependent signals and interaction between fMLP receptor and G(i). Tretinoin 27-29 formyl peptide receptor 1 Homo sapiens 163-167
7890689-3 1995 Retinoic acid (RA) increased UCP mRNA levels severalfold in brown adipocytes differentiated in culture. Tretinoin 0-13 uncoupling protein 1 Rattus norvegicus 29-32
7890689-3 1995 Retinoic acid (RA) increased UCP mRNA levels severalfold in brown adipocytes differentiated in culture. Tretinoin 15-17 uncoupling protein 1 Rattus norvegicus 29-32
7890689-8 1995 The RA-responsive region in the ucp gene was located at -2469/-2318 and contains three motifs (between -2357 and -2330) of the consensus half-sites characteristic of retinoic acid response elements. Tretinoin 4-6 uncoupling protein 1 Rattus norvegicus 32-35
7890689-8 1995 The RA-responsive region in the ucp gene was located at -2469/-2318 and contains three motifs (between -2357 and -2330) of the consensus half-sites characteristic of retinoic acid response elements. Tretinoin 166-179 uncoupling protein 1 Rattus norvegicus 32-35
7873195-4 1995 To test this hypothesis, we determined whether all-trans retinoic acid (RA) and several other retinoid compounds regulate the production of types I and III collagen by unstimulated and TGF-beta 1-stimulated human lung fibroblasts. Tretinoin 72-74 transforming growth factor beta 1 Homo sapiens 185-195
7873195-7 1995 RA preincubation also totally abrogated the collagen inductive effects of TGF-beta 1. Tretinoin 0-2 transforming growth factor beta 1 Homo sapiens 74-84
7763006-4 1995 Analysis of cellular inducible pathways demonstrated that RA augmented levels of gene expression: (i) induced by IFN-alpha such as 2"-5"-oligoadenylate synthetase, mRNA 561 and mRNA 6-16; (ii) induced by IFN-gamma such as 2A and P56; and (iii) induced by both IFN-alpha and IFN-gamma such as mRNA 1-8. Tretinoin 58-60 interferon alpha 1 Homo sapiens 113-122
7763006-4 1995 Analysis of cellular inducible pathways demonstrated that RA augmented levels of gene expression: (i) induced by IFN-alpha such as 2"-5"-oligoadenylate synthetase, mRNA 561 and mRNA 6-16; (ii) induced by IFN-gamma such as 2A and P56; and (iii) induced by both IFN-alpha and IFN-gamma such as mRNA 1-8. Tretinoin 58-60 interferon gamma Homo sapiens 204-213
7873195-8 1995 At 10(-5) M, RA preincubation caused a 97% decrease in the stimulation of type I collagen and a 115% decrease in the stimulation of type III collagen caused by TGF-beta 1. Tretinoin 13-15 transforming growth factor beta 1 Homo sapiens 160-170
7763006-4 1995 Analysis of cellular inducible pathways demonstrated that RA augmented levels of gene expression: (i) induced by IFN-alpha such as 2"-5"-oligoadenylate synthetase, mRNA 561 and mRNA 6-16; (ii) induced by IFN-gamma such as 2A and P56; and (iii) induced by both IFN-alpha and IFN-gamma such as mRNA 1-8. Tretinoin 58-60 interferon alpha 1 Homo sapiens 260-269
7763006-4 1995 Analysis of cellular inducible pathways demonstrated that RA augmented levels of gene expression: (i) induced by IFN-alpha such as 2"-5"-oligoadenylate synthetase, mRNA 561 and mRNA 6-16; (ii) induced by IFN-gamma such as 2A and P56; and (iii) induced by both IFN-alpha and IFN-gamma such as mRNA 1-8. Tretinoin 58-60 interferon gamma Homo sapiens 274-283
7720192-0 1995 Retinoic acid enhances connexin43 expression at the post-transcriptional level in rat liver epithelial cells. Tretinoin 0-13 gap junction protein, alpha 1 Rattus norvegicus 23-33
7763006-6 1995 Co-treatment of NB-4 cells by IFN-gamma plus RA induced a sub-set of IFN-induced genes which were not induced by either IFN-gamma or RA alone. Tretinoin 45-47 interferon gamma Homo sapiens 120-129
7720192-3 1995 When RA, at 0.1 microM for 24-48 h, enhanced the dye transfer in IAR203 cells (x 1.4), it increased the amount of connexin43 (Cx43) in the cell-cell contact regions of the plasma membrane, as evidenced by analysis by Western blot and by immunofluorescence. Tretinoin 5-7 gap junction protein, alpha 1 Rattus norvegicus 114-124
7720192-3 1995 When RA, at 0.1 microM for 24-48 h, enhanced the dye transfer in IAR203 cells (x 1.4), it increased the amount of connexin43 (Cx43) in the cell-cell contact regions of the plasma membrane, as evidenced by analysis by Western blot and by immunofluorescence. Tretinoin 5-7 gap junction protein, alpha 1 Rattus norvegicus 126-130
7720192-6 1995 We conclude that, in IAR203 cells, RA stimulates GJIC by acting at the post-transcriptional level of Cx43 regulation. Tretinoin 35-37 gap junction protein, alpha 1 Rattus norvegicus 101-105
7720192-7 1995 The possibility that RA acts indirectly on the regulation of Cx43 expression, and increases the half-life of Cx43 by inducing adhesion molecules is discussed. Tretinoin 21-23 gap junction protein, alpha 1 Rattus norvegicus 61-65
7720192-7 1995 The possibility that RA acts indirectly on the regulation of Cx43 expression, and increases the half-life of Cx43 by inducing adhesion molecules is discussed. Tretinoin 21-23 gap junction protein, alpha 1 Rattus norvegicus 109-113
7867602-0 1995 Retinoic acid and thyroid hormone regulate placental lactogen expression in human trophoblast cells. Tretinoin 0-13 chorionic somatomammotropin hormone 2 Homo sapiens 43-61
7532580-11 1995 Increased IGFBP-3 and -6 production in response to RA + forskolin was accompanied by a decrease in IGF-stimulated thymidine incorporation into DNA; by contrast, the bioactivity of an IGF analog that does not bind with IGFBPs, [Gln3, Ala4, Tyr15, Leu16]IGF-I, was unchanged under these conditions. Tretinoin 51-53 insulin like growth factor 1 Homo sapiens 252-257
7867602-1 1995 In this study, we have demonstrated that retinoic acid (RA) and thyroid hormone (T3) stimulate the synthesis and release of human placental lactogen (hPL), one of the major secretory products of syncytiotrophoblast cells. Tretinoin 41-54 chorionic somatomammotropin hormone 2 Homo sapiens 130-148
7758830-3 1995 At the myoblast stage, treatment with 1 microM retinoic acid for 24 h increased both 1 h and 8 h insulin stimulated uptake of 2-deoxyglucose by more than twofold. Tretinoin 47-60 insulin Homo sapiens 97-104
7533818-0 1995 Retinoic acid inhibits basal and interferon-gamma-induced expression of intercellular adhesion molecule 1 in monocytic cells. Tretinoin 0-13 interferon gamma Homo sapiens 33-49
7533818-5 1995 In contrast, suppression of IFN-gamma-induced ICAM-1 expression by RA was only partly reversible by indomethacin, suggesting that inhibition of IFN-gamma stimulation was not completely due to cyclooxygenase induction. Tretinoin 67-69 interferon gamma Homo sapiens 28-37
7533818-8 1995 RA also blocked ICAM-1 induction by IFN-gamma in isolated human blood monocytes. Tretinoin 0-2 interferon gamma Homo sapiens 36-45
7758830-4 1995 A dose and time dependent effect of retinoic acid on 8 h insulin stimulated 2-deoxyglucose uptake was observed at both the myoblast and myocyte stage. Tretinoin 36-49 insulin Homo sapiens 57-64
7758830-6 1995 In myoblast cells, retinoic acid increased the content of GLUT4 mRNA in a dose and time dependent manner, an effect that was partially attenuated by insulin. Tretinoin 19-32 insulin Homo sapiens 149-156
7532115-6 1995 The level of HPV16 transcript encoding E6/E7 is not significantly suppressed by 1 microM RA in ECE16-1 cells, but is suppressed in ECE16-D1 and ECE16-D2 cells. Tretinoin 89-91 protein E6*;transforming protein E6 Human papillomavirus type 16 39-44
7829265-7 1995 Thus among its varied effects on LA-N-5 cells, NaPA appears to interact with the RA pathway at the nuclear level by up-regulating RAR beta expression. Tretinoin 81-83 retinoic acid receptor beta Homo sapiens 130-138
7530503-5 1995 Constitutive overexpression of HOX B7 in the HL60 cell line inhibited the granulocytic differentiation associated with stimulation with DMSO or retinoic acid, but had no effect on the monocytic differentiation induced by vitamin D3. Tretinoin 144-157 homeobox B7 Homo sapiens 31-37
7532115-7 1995 In addition, an increase in HPV transcripts encoding E6/E7 is observed at intermediate (10 and 100 nM) retinoic acid concentrations in ECE16-1 and ECE16-D2 cells, but not in ECE16-D1 cells. Tretinoin 103-116 protein E6*;transforming protein E6 Human papillomavirus type 16 53-58
7837814-0 1995 Functional properties of HL60 cells matured with all-trans-retinoic acid and DMSO: differences in response to interleukin-8 and fMLP. Tretinoin 49-72 C-X-C motif chemokine ligand 8 Homo sapiens 110-123
7742777-6 1995 All-trans retinoic acid (RA) decreased collagenase expression and stimulated TIMP-1 expression. Tretinoin 0-23 TIMP metallopeptidase inhibitor 1 Homo sapiens 77-83
7742777-6 1995 All-trans retinoic acid (RA) decreased collagenase expression and stimulated TIMP-1 expression. Tretinoin 25-27 TIMP metallopeptidase inhibitor 1 Homo sapiens 77-83
7730147-6 1995 All-trans retinoic acid (all-trans RA) at 1 nM or granulocyte macrophage colony-stimulating factor (GM-CSF) at 35 pM inhibited the wt-p53-induced apoptosis over a 42-h treatment. Tretinoin 10-23 tumor protein p53 Homo sapiens 134-137
7823919-5 1995 Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. Tretinoin 48-50 nuclear receptor subfamily 2 group F member 2 Homo sapiens 91-96
7823919-5 1995 Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. Tretinoin 48-50 nuclear receptor subfamily 2 group F member 2 Homo sapiens 97-106
7823919-5 1995 Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. Tretinoin 48-50 nuclear receptor subfamily 2 group F member 1 Homo sapiens 111-116
7823919-5 1995 Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. Tretinoin 48-50 nuclear receptor subfamily 2 group F member 1 Homo sapiens 97-105
7823919-13 1995 We have shown that RA treatment of EC cells results in up-regulation of ARP-1/COUP-TFII and EAR-3/COUP-TFI expression. Tretinoin 19-21 nuclear receptor subfamily 2 group F member 2 Homo sapiens 72-77
7823919-13 1995 We have shown that RA treatment of EC cells results in up-regulation of ARP-1/COUP-TFII and EAR-3/COUP-TFI expression. Tretinoin 19-21 nuclear receptor subfamily 2 group F member 2 Homo sapiens 78-87
7823919-13 1995 We have shown that RA treatment of EC cells results in up-regulation of ARP-1/COUP-TFII and EAR-3/COUP-TFI expression. Tretinoin 19-21 nuclear receptor subfamily 2 group F member 1 Homo sapiens 92-97
7823919-13 1995 We have shown that RA treatment of EC cells results in up-regulation of ARP-1/COUP-TFII and EAR-3/COUP-TFI expression. Tretinoin 19-21 nuclear receptor subfamily 2 group F member 1 Homo sapiens 78-86
7823919-14 1995 Most interestingly, in RA-treated EC cells, the kinetics of Oct-3/4 repression inversely correlates with the kinetics of ARP-1/COUP-TFII and EAR-3/COUP-TFI activation. Tretinoin 23-25 nuclear receptor subfamily 2 group F member 2 Homo sapiens 121-126
7823919-14 1995 Most interestingly, in RA-treated EC cells, the kinetics of Oct-3/4 repression inversely correlates with the kinetics of ARP-1/COUP-TFII and EAR-3/COUP-TFI activation. Tretinoin 23-25 nuclear receptor subfamily 2 group F member 2 Homo sapiens 127-136
7823919-14 1995 Most interestingly, in RA-treated EC cells, the kinetics of Oct-3/4 repression inversely correlates with the kinetics of ARP-1/COUP-TFII and EAR-3/COUP-TFI activation. Tretinoin 23-25 nuclear receptor subfamily 2 group F member 1 Homo sapiens 141-146
7823919-14 1995 Most interestingly, in RA-treated EC cells, the kinetics of Oct-3/4 repression inversely correlates with the kinetics of ARP-1/COUP-TFII and EAR-3/COUP-TFI activation. Tretinoin 23-25 nuclear receptor subfamily 2 group F member 1 Homo sapiens 127-135
7818524-0 1995 Effects of retinoic acid (vitamin A) on tumor necrosis factor cytolytic action. Tretinoin 11-24 tumor necrosis factor Mus musculus 40-61
7818524-6 1995 We present evidence that both the cis- and trans- forms of RA and to a lesser extent, the RA precursor beta-carotene, can inhibit recombinant human TNF cytolytic activity in mouse L-929 cells. Tretinoin 59-61 tumor necrosis factor Homo sapiens 148-151
7818524-6 1995 We present evidence that both the cis- and trans- forms of RA and to a lesser extent, the RA precursor beta-carotene, can inhibit recombinant human TNF cytolytic activity in mouse L-929 cells. Tretinoin 90-92 tumor necrosis factor Homo sapiens 148-151
7645423-11 1995 Growth inhibition by RA may be mediated through the cytokine transforming growth factor-beta (TGF-beta), a potent inhibitor of epithelial cell proliferation. Tretinoin 21-23 transforming growth factor beta 1 Homo sapiens 94-102
7645423-13 1995 Also, Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced TGF-beta 1 and TGF-beta 2 expression about 3- and 50-fold, respectively. Tretinoin 79-81 transforming growth factor beta 1 Homo sapiens 100-110
7833269-0 1995 Hypercalcaemia and increased serum interleukin-6 levels induced by all-trans retinoic acid in patients with multiple myeloma. Tretinoin 77-90 interleukin 6 Homo sapiens 35-48
7833269-1 1995 All-trans retinoic acid (ATRA) inhibits human myeloma cell growth in vitro, presumably through the down-regulation of interleukin 6 receptors (IL-6R). Tretinoin 0-23 interleukin 6 receptor Homo sapiens 118-141
7833269-1 1995 All-trans retinoic acid (ATRA) inhibits human myeloma cell growth in vitro, presumably through the down-regulation of interleukin 6 receptors (IL-6R). Tretinoin 0-23 interleukin 6 receptor Homo sapiens 143-148
7833269-1 1995 All-trans retinoic acid (ATRA) inhibits human myeloma cell growth in vitro, presumably through the down-regulation of interleukin 6 receptors (IL-6R). Tretinoin 25-29 interleukin 6 receptor Homo sapiens 118-141
7833269-1 1995 All-trans retinoic acid (ATRA) inhibits human myeloma cell growth in vitro, presumably through the down-regulation of interleukin 6 receptors (IL-6R). Tretinoin 25-29 interleukin 6 receptor Homo sapiens 143-148
7833269-3 1995 We report that three out of six treated patients developed severe hypercalcaemia following administration of ATRA, which was accompanied by a significant rise in serum IL-6 levels. Tretinoin 109-113 interleukin 6 Homo sapiens 168-172
7851655-7 1995 Retinoic acid strongly induced HoxA1 and HoxD1 throughout the ectoderm and mesendoderm of gastrula stages, while in older embryos retinoids induced ectopic expression of these genes in more limited regions. Tretinoin 0-13 homeobox A1 L homeolog Xenopus laevis 31-36
8536058-0 1995 Effect of retinoic acid on the proliferation and alkaline phosphatase activity of osteoblastic MC3T3-E1 cells by modulating the release of local regulators from monocytes. Tretinoin 10-23 alkaline phosphatase, placental Homo sapiens 49-69
8536058-3 1995 Treatment of MC3T3-E1 cells with retinoic acid (10(-8) to 10(-6) M) caused an inhibition of TdR in a dose-dependent manner and an inhibition of ALP activity at 10(-6) M. Conditioned medium from monocytes untreated with retinoic acid caused a stimulation of TdR and an inhibition of ALP activity in these cells. Tretinoin 33-46 alkaline phosphatase, placental Homo sapiens 144-147
8536058-3 1995 Treatment of MC3T3-E1 cells with retinoic acid (10(-8) to 10(-6) M) caused an inhibition of TdR in a dose-dependent manner and an inhibition of ALP activity at 10(-6) M. Conditioned medium from monocytes untreated with retinoic acid caused a stimulation of TdR and an inhibition of ALP activity in these cells. Tretinoin 33-46 alkaline phosphatase, placental Homo sapiens 282-285
8536058-3 1995 Treatment of MC3T3-E1 cells with retinoic acid (10(-8) to 10(-6) M) caused an inhibition of TdR in a dose-dependent manner and an inhibition of ALP activity at 10(-6) M. Conditioned medium from monocytes untreated with retinoic acid caused a stimulation of TdR and an inhibition of ALP activity in these cells. Tretinoin 219-232 alkaline phosphatase, placental Homo sapiens 144-147
8536058-4 1995 In contrast, treatment of monocytes with retinoic acid (10(-8) or 10(-6) M) abolished both stimulation of DNA synthesis and inhibition of ALP activity induced by CM. Tretinoin 41-54 alkaline phosphatase, placental Homo sapiens 138-141
8536058-5 1995 The present study suggested that retinoic acid modulated osteoblast proliferation and ALP activity not only directly but also indirectly, presumably through modulating the release of local regulators as to bone remodeling from monocytes. Tretinoin 33-46 alkaline phosphatase, placental Homo sapiens 86-89
7775379-1 1995 Effects of retinoid derivatives (retinol, retinal, retinoic acid, and etretinate) on elastin expression and cell proliferation in chick embryonic vascular smooth muscle cells were compared. Tretinoin 51-64 elastin Gallus gallus 85-92
7775379-4 1995 Retinoic acid exhibited the most pronounced stimulatory effect on elastin synthesis with a maximum stimulation of 2.8-fold at the concentration of 10(-6) M for 24-48 h treatment. Tretinoin 0-13 elastin Gallus gallus 66-73
7775379-5 1995 A comparable increase in elastin mRNA level was observed in the case of retinoic acid treatment. Tretinoin 72-85 elastin Gallus gallus 25-32
7775379-7 1995 Retinoic acid reversed this decline of elastin synthesis. Tretinoin 0-13 elastin Gallus gallus 39-46
7837814-10 1995 The 2 h migration for ATRA induced cells was 124 microns in response to IL-8, 107 microns with fMLP, and 105 microns in buffer. Tretinoin 22-26 C-X-C motif chemokine ligand 8 Homo sapiens 72-76
7837814-10 1995 The 2 h migration for ATRA induced cells was 124 microns in response to IL-8, 107 microns with fMLP, and 105 microns in buffer. Tretinoin 22-26 formyl peptide receptor 1 Homo sapiens 95-99
7837814-13 1995 In summary, HL60 cells cultured in ATRA develop greater functional maturity than those cultured in DMSO, and a greater responsiveness to IL-8 than fMLP, a finding distinct from previously reported work in neutrophils. Tretinoin 35-39 C-X-C motif chemokine ligand 8 Homo sapiens 137-141
7537564-4 1995 Differentiation of B16-F1 metastatic melanoma cells with retinoic acid resulted in an elevation in c-SRC activity, protein and mRNA. Tretinoin 57-70 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 99-104
7537564-5 1995 The increase in c-SRC was detectable after about 48 h of retinoic acid treatment, as were changes in cellular morphology and growth rate. Tretinoin 57-70 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 16-21
7733631-6 1995 On the molecular level, exposure to RA resulted in a moderate increase in RAR a mRNA expression, whereas CRABP mRNA remained constant. Tretinoin 36-38 RAB40B, member RAS oncogene family Homo sapiens 74-77
7576943-0 1995 Retinoic acid and cAMP differentially regulate human chromogranin A promoter activity during differentiation of neuroblastoma cells. Tretinoin 0-13 chromogranin A Homo sapiens 53-67
7576943-1 1995 We report the first evidence that differential transcriptional regulation of human chromogranin A (CHGA) gene expression occurs during in vitro treatment of tumorigenic neuroblastoma (NB) cells with retinoic acid (5 microM) and/or dibutyryl-cAMP (1 mM). Tretinoin 199-212 chromogranin A Homo sapiens 83-97
7576943-1 1995 We report the first evidence that differential transcriptional regulation of human chromogranin A (CHGA) gene expression occurs during in vitro treatment of tumorigenic neuroblastoma (NB) cells with retinoic acid (5 microM) and/or dibutyryl-cAMP (1 mM). Tretinoin 199-212 chromogranin A Homo sapiens 99-103
7576949-6 1995 Differentiation induced by RA resulted in an increase in both type I GAP120 and neurofibromin mRNAs. Tretinoin 27-29 neurofibromin 1 Homo sapiens 62-93
7576949-9 1995 However, the GTPase activating proteins type I GAP120 and neurofibromin may have effector functions in RA-induced differentiation of neuroblastoma. Tretinoin 103-105 neurofibromin 1 Homo sapiens 58-71
7813633-4 1995 The effects of LPA are compared with all-trans-retinoic acid (RA), a structurally unrelated lipid that has previously been shown to induce both TGF alpha and TGF beta and have pronounced effects on keratinocyte proliferation and differentiation. Tretinoin 62-64 transforming growth factor beta 1 Homo sapiens 158-166
7813633-8 1995 LPA and RA also induced both the active and latent forms TGF beta from cultured keratinocytes. Tretinoin 8-10 transforming growth factor beta 1 Homo sapiens 57-65
7538894-4 1995 Retinoic acid reduced the response to IL-6 of alpha-2-macroglobulin but enhanced that of alpha-1-acid glycoprotein and especially of C3 complement. Tretinoin 0-13 interleukin 6 Rattus norvegicus 38-42
7531260-3 1995 In vivo ATRA therapy induces a rapid correction of both low fibrinogen level and bleeding tendency, but no clear explanation of this beneficial effect has been proposed. Tretinoin 8-12 fibrinogen beta chain Homo sapiens 60-70
7531260-8 1995 Moreover, was observed a rapid simultaneous correction of low fibrinogen levels and plasmin activation markers in APL patients undergoing ATRA therapy (before day 5), but a more prolonged persistence of DIC markers (until day 14). Tretinoin 138-142 fibrinogen beta chain Homo sapiens 62-72
7531260-11 1995 In vivo differentiation ATRA therapy induces a rapid decrease in the plasmin activation and a normalization of fibrinogen level, while DIC may in vivo persist for several weeks. Tretinoin 24-28 fibrinogen beta chain Homo sapiens 111-121
7845008-1 1995 All-trans retinoic acid (ATRA) has been demonstrated to be an efficient alternative to chemotherapy in the treatment of acute promyelocytic leukemia (APL or AML3). Tretinoin 0-23 RUNX family transcription factor 2 Homo sapiens 157-161
7845008-1 1995 All-trans retinoic acid (ATRA) has been demonstrated to be an efficient alternative to chemotherapy in the treatment of acute promyelocytic leukemia (APL or AML3). Tretinoin 25-29 RUNX family transcription factor 2 Homo sapiens 157-161
7837814-0 1995 Functional properties of HL60 cells matured with all-trans-retinoic acid and DMSO: differences in response to interleukin-8 and fMLP. Tretinoin 49-72 formyl peptide receptor 1 Homo sapiens 128-132
7534188-4 1994 All-trans-retinoic acid (all-trans-RA, 0.1-10 microM) and its active analogues produced concentration-dependent inhibition of IL-1 beta (0.1-10 ng ml-1)-induced nitrite production in cultured VSM cells. Tretinoin 0-23 interleukin 1 beta Rattus norvegicus 126-135
8817658-2 1995 IGF I increases IGFBP-5 mRNA levels in both cell types, whereas retinoic acid stimulates IGFBP-5 mRNA expression in calvaria but suppresses it in Saos-2 cells. Tretinoin 64-77 insulin like growth factor binding protein 5 Homo sapiens 89-96
7811238-0 1994 On the induction of 5-lipoxygenase expression and activity in HL-60 cells: effects of vitamin D3, retinoic acid, DMSO and TGF beta. Tretinoin 98-111 arachidonate 5-lipoxygenase Homo sapiens 20-34
7988722-3 1994 Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of trkA mRNA and induced the expression of trkB mRNA. Tretinoin 122-135 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 238-242
7988722-3 1994 Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of trkA mRNA and induced the expression of trkB mRNA. Tretinoin 137-139 neurotrophic receptor tyrosine kinase 2 Rattus norvegicus 238-242
8534359-5 1995 Dexamethasone alone increased the release of both peptides within 6 d. However, when cells were treated simultaneously with estradiol and 1 mumol/l dexamethasone, the addition of retinoic acid blunted both the CT and CGRP secretions induced by dexamethasone. Tretinoin 179-192 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 217-221
8534359-6 1995 These results showed that the positive effects of 17 beta-estradiol on both CT and CGRP secretions were modulated by dexamethasone and retinoic acid. Tretinoin 135-148 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 83-87
7534188-4 1994 All-trans-retinoic acid (all-trans-RA, 0.1-10 microM) and its active analogues produced concentration-dependent inhibition of IL-1 beta (0.1-10 ng ml-1)-induced nitrite production in cultured VSM cells. Tretinoin 25-37 interleukin 1 beta Rattus norvegicus 126-135
7861122-4 1994 The inhibition of PKC by sphingosine or by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) at high concentration greatly reduced the mean axonal length of spinal neurons cultured in medium conditioned by cerebellar astroglia (SCn-CBg), while activation of PKC by TPA at low concentration, or by retinoic acid, was not additive to the glial effect. Tretinoin 308-321 proline rich transmembrane protein 2 Homo sapiens 18-21
7898304-7 1994 Retinoic acid and dexamethasone, respectively, increased activity of the RC3 promoter in neuroblastoma cells when a deletion construct containing the retinoic acid and the glucocorticoid responsive elements was cotransfected with retinoic acid receptor or glucocorticoid receptor expression vectors. Tretinoin 0-13 nuclear receptor subfamily 3 group C member 1 Homo sapiens 256-279
7861122-5 1994 The activation of PKC by TPA or retinoic acid promoted axon growth of spinal neurons cultured in medium conditioned by spinal astroglia (SCn-SCg), which otherwise would not be as supportive for axon growth as cerebellar astroglia. Tretinoin 32-45 proline rich transmembrane protein 2 Homo sapiens 18-21
7961696-4 1994 When the cells were treated with retinoic acid either alone or in the presence of cAMP for 120 h, PKC alpha mRNA and protein levels increased, whereas those of PKC beta and PKC gamma became undetectable. Tretinoin 33-46 protein kinase C alpha Homo sapiens 98-107
7877718-5 1994 We have measured the effect of RA on the metabolism of dopa and expression of tyrosine hydroxylase and DDC in human neuroblastoma cell lines, CHP-126, CHP-134, IMR-32, NB-69, and LA-N-5. Tretinoin 31-33 dopa decarboxylase Homo sapiens 103-106
7877718-7 1994 The RA treatment modulated the activities of tyrosine hydroxylase and DDC, but does not increase DDC relative to tyrosine hydroxylase. Tretinoin 4-6 dopa decarboxylase Homo sapiens 70-73
7986828-0 1994 Vitamin D-dependent rickets type II: regulation of human osteocalcin gene expression in cells with defective vitamin D receptors by 1,25-dihydroxyvitamin D-3, retinoic acid, and triiodothyronine. Tretinoin 159-172 bone gamma-carboxyglutamate protein Homo sapiens 57-68
7998926-2 1994 RAR-beta and CRABP II mRNA was induced by both all-trans and 9-cis retinoic acid in SH SY 5Y cells. Tretinoin 67-80 retinoic acid receptor beta Homo sapiens 0-8
7998926-4 1994 Time-courses of induction for RAR-beta and CRABP II differed: RAR-beta mRNA levels reached a maximum 4-6 h after adding all-trans or 9-cis retinoic acid, whereas CRABP II mRNA levels increased over at least 18 h. These differences were attributed to the longer half-life of CRABP II mRNA (20 h) compared with RAR-beta mRNA (3.9 h). Tretinoin 139-152 retinoic acid receptor beta Homo sapiens 62-70
7998926-4 1994 Time-courses of induction for RAR-beta and CRABP II differed: RAR-beta mRNA levels reached a maximum 4-6 h after adding all-trans or 9-cis retinoic acid, whereas CRABP II mRNA levels increased over at least 18 h. These differences were attributed to the longer half-life of CRABP II mRNA (20 h) compared with RAR-beta mRNA (3.9 h). Tretinoin 139-152 retinoic acid receptor beta Homo sapiens 62-70
7998926-7 1994 The induction of RAR-beta and CRABP II by all-trans retinoic acid was maintained in the subsequent absence of all-trans retinoic acid, whereas induction by 9-cis retinoic acid was dependent on its continued presence in the culture medium. Tretinoin 52-65 retinoic acid receptor beta Homo sapiens 17-25
7998926-7 1994 The induction of RAR-beta and CRABP II by all-trans retinoic acid was maintained in the subsequent absence of all-trans retinoic acid, whereas induction by 9-cis retinoic acid was dependent on its continued presence in the culture medium. Tretinoin 120-133 retinoic acid receptor beta Homo sapiens 17-25
7958454-3 1994 Analysis of the mRNA accumulation profiles for Wnt genes during retinoic acid (RA)-induced neural differentiation of P19 cells showed that nine Wnt family members were expressed in a regulated manner during this process. Tretinoin 64-77 Wnt family member 1 Homo sapiens 47-50
7949175-0 1994 Inhibitory effect of all-trans retinoic acid on the growth of freshly isolated myeloma cells via interference with interleukin-6 signal transduction. Tretinoin 31-44 interleukin 6 Homo sapiens 115-128
7949175-2 1994 ATRA downregulated the cell surface expression of interleukin-6 receptor (IL-6R) and/or glycoprotein (gp) 130. Tretinoin 0-4 interleukin 6 receptor Homo sapiens 50-72
7949175-2 1994 ATRA downregulated the cell surface expression of interleukin-6 receptor (IL-6R) and/or glycoprotein (gp) 130. Tretinoin 0-4 interleukin 6 receptor Homo sapiens 74-79
7949175-4 1994 Furthermore, ATRA inhibited the production of IL-6 from both myeloma cells and marrow stromal cells, and recombinant IL-6 (rIL-6) could partially recover the myeloma cell growth that had been inhibited by ATRA. Tretinoin 13-17 interleukin 6 Homo sapiens 46-50
7949175-4 1994 Furthermore, ATRA inhibited the production of IL-6 from both myeloma cells and marrow stromal cells, and recombinant IL-6 (rIL-6) could partially recover the myeloma cell growth that had been inhibited by ATRA. Tretinoin 205-209 interleukin 6 Homo sapiens 117-121
7949175-4 1994 Furthermore, ATRA inhibited the production of IL-6 from both myeloma cells and marrow stromal cells, and recombinant IL-6 (rIL-6) could partially recover the myeloma cell growth that had been inhibited by ATRA. Tretinoin 205-209 interleukin 6 Rattus norvegicus 123-128
7949175-5 1994 These data suggest that ATRA may inhibit the proliferation of myeloma cells both by the downregulation of IL-6R and gp130 expression on myeloma cells and by the inhibition of IL-6 production from myeloma and stromal cells. Tretinoin 24-28 interleukin 6 receptor Homo sapiens 106-111
7949175-5 1994 These data suggest that ATRA may inhibit the proliferation of myeloma cells both by the downregulation of IL-6R and gp130 expression on myeloma cells and by the inhibition of IL-6 production from myeloma and stromal cells. Tretinoin 24-28 interleukin 6 Homo sapiens 106-110
7695840-4 1994 Retinoic acid increased the effect of IL-6 on alpha-1-antichymotrypsin (ACT) and fibrinogen (FBG) on the level of both proteins and mRNAs. Tretinoin 0-13 interleukin 6 Homo sapiens 38-42
7695840-4 1994 Retinoic acid increased the effect of IL-6 on alpha-1-antichymotrypsin (ACT) and fibrinogen (FBG) on the level of both proteins and mRNAs. Tretinoin 0-13 fibrinogen beta chain Homo sapiens 81-91
7695840-4 1994 Retinoic acid increased the effect of IL-6 on alpha-1-antichymotrypsin (ACT) and fibrinogen (FBG) on the level of both proteins and mRNAs. Tretinoin 0-13 fibrinogen beta chain Homo sapiens 93-96
7524761-0 1994 All-trans retinoic acid directly inhibits granulocyte colony-stimulating factor-induced proliferation of CD34+ human hematopoietic progenitor cells. Tretinoin 10-23 CD34 molecule Homo sapiens 105-109
7923214-3 1994 Due to the presence of a RARE (beta RARE) in its promoter, the expression of the RAR beta 2 is markedly increased in response to RA in most epithelial tissues, including lung. Tretinoin 25-27 retinoic acid receptor beta Homo sapiens 81-89
7958454-3 1994 Analysis of the mRNA accumulation profiles for Wnt genes during retinoic acid (RA)-induced neural differentiation of P19 cells showed that nine Wnt family members were expressed in a regulated manner during this process. Tretinoin 64-77 Wnt family member 1 Homo sapiens 144-147
7958454-3 1994 Analysis of the mRNA accumulation profiles for Wnt genes during retinoic acid (RA)-induced neural differentiation of P19 cells showed that nine Wnt family members were expressed in a regulated manner during this process. Tretinoin 79-81 Wnt family member 1 Homo sapiens 47-50
7958454-3 1994 Analysis of the mRNA accumulation profiles for Wnt genes during retinoic acid (RA)-induced neural differentiation of P19 cells showed that nine Wnt family members were expressed in a regulated manner during this process. Tretinoin 79-81 Wnt family member 1 Homo sapiens 144-147
7956930-4 1994 RXR alpha-RF formed, like recombinant RXR alpha, heterodimers on DNA with vitamin D and retinoic acid but not estrogen receptors. Tretinoin 88-101 retinoid X receptor alpha Rattus norvegicus 0-9
7958454-6 1994 In the presence of ectopic Wnt-1, expression of other endogenous Wnt genes, which serve as early differentiation markers in this system, were induced without RA, which is normally required for appearance of these gene products. Tretinoin 158-160 Wnt family member 1 Homo sapiens 27-32
7958454-6 1994 In the presence of ectopic Wnt-1, expression of other endogenous Wnt genes, which serve as early differentiation markers in this system, were induced without RA, which is normally required for appearance of these gene products. Tretinoin 158-160 Wnt family member 1 Homo sapiens 27-30
7958454-8 1994 Similarly to the parental cell line, addition of RA to P19 cells overexpressing Wnt-1 induced the neuroectodermal pathway, but expression of cell type-specific markers such as MASH-1, HNK-1, and GAP-43 was diminished and the morphology of neuronal processes, stained with an antibody to neurofilament, was abnormal. Tretinoin 49-51 Wnt family member 1 Homo sapiens 80-85
7958454-8 1994 Similarly to the parental cell line, addition of RA to P19 cells overexpressing Wnt-1 induced the neuroectodermal pathway, but expression of cell type-specific markers such as MASH-1, HNK-1, and GAP-43 was diminished and the morphology of neuronal processes, stained with an antibody to neurofilament, was abnormal. Tretinoin 49-51 beta-1,3-glucuronyltransferase 1 Homo sapiens 184-189
7958454-9 1994 These data suggest that Wnt-1 itself can induce some aspects of early neuroectodermal differentiation and, furthermore, that the correct timing of Wnt-1 expression is necessary for proper RA-induced expression of the neural phenotype. Tretinoin 188-190 Wnt family member 1 Homo sapiens 24-29
7958454-9 1994 These data suggest that Wnt-1 itself can induce some aspects of early neuroectodermal differentiation and, furthermore, that the correct timing of Wnt-1 expression is necessary for proper RA-induced expression of the neural phenotype. Tretinoin 188-190 Wnt family member 1 Homo sapiens 147-152
7967734-4 1994 In vitro treatment with ATRA consistently increased the expression of CD15, CD11b, and CD45R0 on leukemic promyelocytes; these changes were paralleled by a decrease of CD45RA display. Tretinoin 24-28 fucosyltransferase 4 Homo sapiens 70-74
7877619-0 1994 Characterization of retinoic acid- and cell-dependent sequences which regulate zif268 gene expression in osteoblastic cells. Tretinoin 20-33 early growth response 1 Rattus norvegicus 79-85
7859922-7 1994 Furthermore, RA treatment led to a concentration-dependent decrease in the amount of EGFR protein expression. Tretinoin 13-15 epidermal growth factor receptor Homo sapiens 85-89
7877619-1 1994 We have previously shown that retinoic acid (RA) induces differentiation in an osteoblastic cell line derived from embryonic rat calvaria and that RA has selective effects on zif268 gene expression in these preosteoblastic cells,distinct from those in more mature osteoblasts. Tretinoin 147-149 early growth response 1 Rattus norvegicus 175-181
7877619-2 1994 In this study we demonstrate that the RA-dependent transcriptional increase in zif268 gene expression is mediated by the interaction of RA receptors (RARs) with a 17 base pair sequence in the zif268 promoter containing a single half-site motif (GTTCA), identical to each of the direct repeats seen in the RAR beta 2 gene. Tretinoin 38-40 early growth response 1 Rattus norvegicus 79-85
7877619-2 1994 In this study we demonstrate that the RA-dependent transcriptional increase in zif268 gene expression is mediated by the interaction of RA receptors (RARs) with a 17 base pair sequence in the zif268 promoter containing a single half-site motif (GTTCA), identical to each of the direct repeats seen in the RAR beta 2 gene. Tretinoin 38-40 early growth response 1 Rattus norvegicus 192-198
7877619-3 1994 The sequence appears relatively RA-specific, since the zif268 RA-responsive element is not activated by 1,25-dihydroxyvitamin D3 or thyroid hormone (T3). Tretinoin 32-34 early growth response 1 Rattus norvegicus 55-61
7877619-3 1994 The sequence appears relatively RA-specific, since the zif268 RA-responsive element is not activated by 1,25-dihydroxyvitamin D3 or thyroid hormone (T3). Tretinoin 62-64 early growth response 1 Rattus norvegicus 55-61
7877619-5 1994 Extensive mutagenesis of the zif268 promoter region containing the RA response element (RARE) motif confirms that the transactivation and nuclear protein binding activity of this region requires only the half-site motif. Tretinoin 67-69 early growth response 1 Rattus norvegicus 29-35
7877619-7 1994 In addition, we found that cell-specific suppression of RA-stimulated zif268 gene expression can be attributed to a 29 base pair nucleotide sequence, located downstream of the RA-responsive region in the zif268 gene. Tretinoin 56-58 early growth response 1 Rattus norvegicus 70-76
7877619-7 1994 In addition, we found that cell-specific suppression of RA-stimulated zif268 gene expression can be attributed to a 29 base pair nucleotide sequence, located downstream of the RA-responsive region in the zif268 gene. Tretinoin 56-58 early growth response 1 Rattus norvegicus 204-210
7936668-4 1994 mda-6 gene expression in HL-60 cells is induced within 1 to 3 h during differentiation along the macrophage/monocyte pathway evoked by 12-0-tetradecanoyl phorbol-13-acetate (TPA) or 1,25-dihydroxyvitamin D3 (Vit D3) or the granulocytic pathway produced by retinoic acid (RA) or dimethylsulfoxide (DMSO). Tretinoin 256-269 cyclin dependent kinase inhibitor 1A Homo sapiens 0-5
7877619-9 1994 The presence of this sequence in cis to the zif268 RARE or the consensus beta RARE completely blocks the RA-responsiveness of the zif268 gene in differentiated osteoblasts. Tretinoin 51-53 early growth response 1 Rattus norvegicus 44-50
7877619-9 1994 The presence of this sequence in cis to the zif268 RARE or the consensus beta RARE completely blocks the RA-responsiveness of the zif268 gene in differentiated osteoblasts. Tretinoin 51-53 early growth response 1 Rattus norvegicus 130-136
7945240-5 1994 Retinoic acid showed opposing effects with dexamethasone on the expression of alkaline phosphatase. Tretinoin 0-13 alkaline phosphatase, placental Homo sapiens 78-98
7918317-11 1994 These results therefore show additional regulatory effects of RA on apoA-I gene expression in vivo and raise questions about the usefulness of RA in the treatment of atherosclerosis. Tretinoin 62-64 apolipoprotein A1 Homo sapiens 68-74
7918317-0 1994 Opposite in vitro and in vivo regulation of hepatic apolipoprotein A-I gene expression by retinoic acid. Tretinoin 90-103 apolipoprotein A1 Homo sapiens 52-70
7918317-3 1994 In HepG2 cells, addition of all-trans retinoic acid (RA) doubled apoA-I mRNA within 24 hours and protein secreted in the culture medium after 48 hours. Tretinoin 38-51 apolipoprotein A1 Homo sapiens 65-71
7918317-3 1994 In HepG2 cells, addition of all-trans retinoic acid (RA) doubled apoA-I mRNA within 24 hours and protein secreted in the culture medium after 48 hours. Tretinoin 53-55 apolipoprotein A1 Homo sapiens 65-71
7918317-4 1994 The induction of apoA-I mRNA by RA was completely blocked by actinomycin D, suggesting that RA acts at the transcriptional level in HepG2 cells. Tretinoin 32-34 apolipoprotein A1 Homo sapiens 17-23
7918317-4 1994 The induction of apoA-I mRNA by RA was completely blocked by actinomycin D, suggesting that RA acts at the transcriptional level in HepG2 cells. Tretinoin 92-94 apolipoprotein A1 Homo sapiens 17-23
7918317-6 1994 Similar changes in apoA-I mRNA were observed with 9-cis RA. Tretinoin 56-58 apolipoprotein A1 Homo sapiens 19-25
7918317-7 1994 However, in vivo, hepatic apoA-I mRNA levels decreased after a single administration of RA at 10 mg/kg and remained low after prolonged treatment or at a higher dose, and serum apoA-I concentrations did not change. Tretinoin 88-90 apolipoprotein A1 Homo sapiens 26-32
7918317-10 1994 In conclusion, RA treatment selectively induces apoA-I and not apoA-II expression in vitro but not in vivo. Tretinoin 15-17 apolipoprotein A1 Homo sapiens 48-54
7945240-6 1994 Retinoic acid (RA) and phorbol 12-myristate 13-acetate also substantially reduced the dexamethasone-induced expression of ALP. Tretinoin 0-13 alkaline phosphatase, placental Homo sapiens 122-125
7945240-6 1994 Retinoic acid (RA) and phorbol 12-myristate 13-acetate also substantially reduced the dexamethasone-induced expression of ALP. Tretinoin 15-17 alkaline phosphatase, placental Homo sapiens 122-125
7945240-9 1994 Analysis of the degradation of BC-M1 ALP mRNA showed a similar half-life of 27 h in the untreated and in dexamethasone- or RA-treated cells. Tretinoin 123-125 alkaline phosphatase, placental Homo sapiens 37-40
7925107-0 1994 Characterization of the effects of retinoic acid on vasoactive intestinal polypeptide gene expression in neuroblastoma cells. Tretinoin 35-48 vasoactive intestinal peptide Homo sapiens 52-85
7803267-9 1994 In APL cases ATRA generated an asynchronous phenotype (CD15+, CDw65+, CD11b+, CD11a-), undetectable on normally maturing myeloid cells, but consistent with the concept that incomplete differentiation, in terms of surface molecule expression, can be sufficient to obtain therapeutic results. Tretinoin 13-17 fucosyltransferase 4 Homo sapiens 55-59
7925107-2 1994 Here we present data on the effects of retinoic acid (RA), a known modulator of neuronal differentiation, on VIP gene expression in the human neuroblastoma cell line NB-1. Tretinoin 39-52 vasoactive intestinal peptide Homo sapiens 109-112
7925107-2 1994 Here we present data on the effects of retinoic acid (RA), a known modulator of neuronal differentiation, on VIP gene expression in the human neuroblastoma cell line NB-1. Tretinoin 54-56 vasoactive intestinal peptide Homo sapiens 109-112
7881185-12 1994 The combined data suggest that 5" exons in the Mgat-1 gene are differentially utilized by tissue-specific promoters and that transcription factor(s) which specify production of the approximately 3.3 kb Mgat-1 mRNA are induced by retinoic acid treatment of P19 EC cells. Tretinoin 229-242 mannoside acetylglucosaminyltransferase 1 Mus musculus 47-53
7925656-0 1994 Delayed activation of HNF-3 beta upon retinoic acid-induced teratocarcinoma cell differentiation. Tretinoin 38-51 forkhead box A2 Mus musculus 22-32
7925656-1 1994 We have investigated the retinoic acid-mediated activation of the transcriptional regulator HNF-3 beta during differentiation of mouse F9 embryonal carcinoma cells. Tretinoin 25-38 forkhead box A2 Mus musculus 92-102
7925656-4 1994 Addition of retinoic acid to F9 stem cells results in delayed activation of HNF-3 beta mRNA which can be detected 1-2 days after the initiation of differentiation. Tretinoin 12-25 forkhead box A2 Mus musculus 76-86
7881185-12 1994 The combined data suggest that 5" exons in the Mgat-1 gene are differentially utilized by tissue-specific promoters and that transcription factor(s) which specify production of the approximately 3.3 kb Mgat-1 mRNA are induced by retinoic acid treatment of P19 EC cells. Tretinoin 229-242 mannoside acetylglucosaminyltransferase 1 Mus musculus 202-208
7853357-5 1994 The dissociation constants (Kd) for RA were 1.4 nM for GST-hRAR alpha, 1.4 nM for GST-hRAR beta, and 3.3 nM for GST-mRAR gamma, respectively. Tretinoin 36-38 retinoic acid receptor beta Homo sapiens 86-95
7817811-4 1994 Furthermore, TGF-beta 1 decreased osteocalcin synthesis modulated negatively by dexamethasone or positively by retinoic acid. Tretinoin 111-124 transforming growth factor beta 1 Homo sapiens 13-23
7817811-4 1994 Furthermore, TGF-beta 1 decreased osteocalcin synthesis modulated negatively by dexamethasone or positively by retinoic acid. Tretinoin 111-124 bone gamma-carboxyglutamate protein Homo sapiens 34-45
7931079-1 1994 The differentiating agent retinoic acid (RA) has been previously reported to interfere with 12-O-tetradecanoyl-phorbol-13-acetate (TPA)/Ca2+-induced signals for the regulation of the -96 to -66-bp octamer motif found in the enhancer for the interleukin (IL)-2 gene, which encodes a major T lymphocyte growth factor. Tretinoin 26-39 interleukin 2 Homo sapiens 241-259
7931079-1 1994 The differentiating agent retinoic acid (RA) has been previously reported to interfere with 12-O-tetradecanoyl-phorbol-13-acetate (TPA)/Ca2+-induced signals for the regulation of the -96 to -66-bp octamer motif found in the enhancer for the interleukin (IL)-2 gene, which encodes a major T lymphocyte growth factor. Tretinoin 41-43 interleukin 2 Homo sapiens 241-259
8083995-0 1994 Synergistic activation of simian immunodeficiency virus and human immunodeficiency virus type 1 transcription by retinoic acid and phorbol ester through an NF-kappa B-independent mechanism. Tretinoin 113-126 nuclear factor kappa B subunit 1 Homo sapiens 156-166
7523800-0 1994 Modulation of IL-8, IL-1 beta, and G-CSF secretion by all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 64-77 C-X-C motif chemokine ligand 8 Homo sapiens 14-18
7523800-0 1994 Modulation of IL-8, IL-1 beta, and G-CSF secretion by all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 64-77 interleukin 1 beta Homo sapiens 20-29
7523800-9 1994 Interestingly, the increase of IL-1 beta and G-CSF production in the presence of ATRA was highly correlated to an increase in APL cell count in vitro and in vivo hyperleukocytosis, resulting in fatal outcome. Tretinoin 81-85 interleukin 1 beta Homo sapiens 31-40
7854351-13 1994 Treatment of AtT-20 cells with all-trans retinoic acid gave different kinetics for GR and c-jun mRNA regulation than obtained with TA; however, the GR and c-jun mRNA levels were still coordinately regulated after retinoic acid treatment. Tretinoin 41-54 nuclear receptor subfamily 3, group C, member 1 Mus musculus 83-85
7934172-2 1994 All-trans retinoic acid (ATRA) induces terminal differentiation of acute promyelocytic leukemia cells (AML3 subtype). Tretinoin 0-23 RUNX family transcription factor 2 Homo sapiens 103-107
7934172-2 1994 All-trans retinoic acid (ATRA) induces terminal differentiation of acute promyelocytic leukemia cells (AML3 subtype). Tretinoin 25-29 RUNX family transcription factor 2 Homo sapiens 103-107
7945203-6 1994 Northern-blot analysis of HL-60 cell differentiation along the neutrophilic lineage induced by retinoic acid or dimethylsulphoxide showed an accompanying enhanced expression of InsP3R1 mRNA. Tretinoin 95-108 inositol 1,4,5-trisphosphate receptor type 1 Homo sapiens 177-184
7935379-5 1994 In keeping with these findings, transfection of neuroblastoma cells with an expression vector containing segments of the human tTG cDNA in antisense orientation resulted in a pronounced decrease of both spontaneous and retinoic acid (RA)-induced apoptosis. Tretinoin 219-232 transglutaminase 2 Homo sapiens 127-130
7935379-5 1994 In keeping with these findings, transfection of neuroblastoma cells with an expression vector containing segments of the human tTG cDNA in antisense orientation resulted in a pronounced decrease of both spontaneous and retinoic acid (RA)-induced apoptosis. Tretinoin 234-236 transglutaminase 2 Homo sapiens 127-130
7716736-2 1994 Since retinoic acid (RA) is teratogenic to some parts of the embryo, stimulatory to other parts, and has no effect on others it may be that the distribution of cytoplasmic proteins such as CRABP I and II plays some role in this differential activity. Tretinoin 6-19 cellular retinoic acid binding protein 1 Gallus gallus 189-196
7716736-2 1994 Since retinoic acid (RA) is teratogenic to some parts of the embryo, stimulatory to other parts, and has no effect on others it may be that the distribution of cytoplasmic proteins such as CRABP I and II plays some role in this differential activity. Tretinoin 21-23 cellular retinoic acid binding protein 1 Gallus gallus 189-196
8083217-1 1994 Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tretinoin 0-13 interleukin 1 beta Homo sapiens 160-169
8083217-1 1994 Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tretinoin 15-17 interleukin 1 beta Homo sapiens 160-169
7925417-8 1994 Analysis of the promoter activity suggests an indirect regulation of transcription by retinoic acid and demonstrates a high degree of complexity of the regulation of the RIHB gene. Tretinoin 86-99 midkine (neurite growth-promoting factor 2) Gallus gallus 170-174
7878635-3 1994 TM antigen and cofactor activity for thrombin-dependent protein C activation were not detected in untreated HL-60 cells and the cells cultured with DMSO, but were expressed in a time-dependent manner in the cells cultured with ATRA. Tretinoin 227-231 coagulation factor II, thrombin Homo sapiens 37-45
8091645-8 1994 Treatment with TPA or retinoic acid led to enhanced expression of the IE2 gene and the early genes encoding pp65 (UL83) and p52 (UL44). Tretinoin 22-35 nuclear factor kappa B subunit 2 Homo sapiens 124-127
7929091-4 1994 Moreover, a positive effect of retinoic acid on ucp mRNA levels in immortalized brown adipocytes was observed. Tretinoin 31-44 uncoupling protein 1 Rattus norvegicus 48-51
7945224-9 1994 RA induced the expression of CAT activity in preadipocytes and adipocytes transfected with pPL1-CAT, but had no effect in cells transfected with pPL9-CAT. Tretinoin 0-2 catalase Mus musculus 29-32
7945224-9 1994 RA induced the expression of CAT activity in preadipocytes and adipocytes transfected with pPL1-CAT, but had no effect in cells transfected with pPL9-CAT. Tretinoin 0-2 catalase Mus musculus 96-99
8069853-1 1994 To elucidate the regulation of protein phosphatases types 1 (PP1) and 2A (PP2A) during all-trans retinoic acid (ATRA)-induced granulocytic differentiation of HL-60 cells, the phosphatase activity, proteins, and gene expressions of PP1 and PP2A were examined. Tretinoin 97-110 inorganic pyrophosphatase 1 Homo sapiens 61-64
8062253-6 1994 Both 9cRA and all-trans-retinoic acid induce the expression of the adhesion molecule, E-cadherin, in the SK-BR-3 cell line. Tretinoin 14-37 cadherin 1 Homo sapiens 86-96
8069853-1 1994 To elucidate the regulation of protein phosphatases types 1 (PP1) and 2A (PP2A) during all-trans retinoic acid (ATRA)-induced granulocytic differentiation of HL-60 cells, the phosphatase activity, proteins, and gene expressions of PP1 and PP2A were examined. Tretinoin 112-116 inorganic pyrophosphatase 1 Homo sapiens 61-64
8080040-9 1994 Activity was elevated in the RA-treated tissues and this was due to increased amounts of both urokinase-type plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA). Tretinoin 29-31 plasminogen activator, urokinase Homo sapiens 94-130
8080040-9 1994 Activity was elevated in the RA-treated tissues and this was due to increased amounts of both urokinase-type plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA). Tretinoin 29-31 plasminogen activator, urokinase Homo sapiens 132-136
8080040-9 1994 Activity was elevated in the RA-treated tissues and this was due to increased amounts of both urokinase-type plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA). Tretinoin 29-31 plasminogen activator, tissue type Homo sapiens 142-175
8080040-9 1994 Activity was elevated in the RA-treated tissues and this was due to increased amounts of both urokinase-type plasminogen activator (u-PA) and tissue-type plasminogen activator (t-PA). Tretinoin 29-31 plasminogen activator, tissue type Homo sapiens 177-181
7819135-0 1994 Activation of interleukin-1 beta gene expression during retinoic acid-induced granulocytic differentiation of promyeloid leukemia cells. Tretinoin 56-69 interleukin 1 beta Homo sapiens 14-32
8082729-7 1994 As a first step in determining sites of retinoic acid-mediated transcriptional activation in the skin and its appendages, we developed a transgenic model in which the retinoic acid response element (RARE) of the RAR beta 2 isoform is linked to a beta-galactosidase reporter gene. Tretinoin 40-53 retinoic acid receptor beta Homo sapiens 212-220
8082729-7 1994 As a first step in determining sites of retinoic acid-mediated transcriptional activation in the skin and its appendages, we developed a transgenic model in which the retinoic acid response element (RARE) of the RAR beta 2 isoform is linked to a beta-galactosidase reporter gene. Tretinoin 167-180 retinoic acid receptor beta Homo sapiens 212-220
8082749-0 1994 Transient stabilization of p53 in non-small cell lung carcinoma cultures arrested for growth by retinoic acid. Tretinoin 96-109 tumor protein p53 Homo sapiens 27-30
8082749-3 1994 Levels of p53 transcripts remained unchanged during the time of increases in protein expression in retinoic acid-treated H460a cells, suggesting that a post-translational mechanism was involved in the increased expression of the protein. Tretinoin 99-112 tumor protein p53 Homo sapiens 10-13
8082749-4 1994 Pulse-chase analysis demonstrated that wild-type p53 was significantly more stabile in H460a cells treated with retinoic acid, exhibiting a half-life greater than 6 h, in contrast to 3 h for the protein in untreated control cells. Tretinoin 112-125 tumor protein p53 Homo sapiens 49-52
8082749-5 1994 The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid. Tretinoin 4-17 tumor protein p53 Homo sapiens 61-64
8082749-5 1994 The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid. Tretinoin 4-17 tumor protein p53 Homo sapiens 93-96
8082749-5 1994 The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid. Tretinoin 189-202 tumor protein p53 Homo sapiens 61-64
8082749-5 1994 The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid. Tretinoin 189-202 tumor protein p53 Homo sapiens 93-96
8082749-6 1994 We conclude that retinoic acid induces stabilization of wild-type p53 in NSCLC cells by a post-translational mechanism. Tretinoin 17-30 tumor protein p53 Homo sapiens 66-69
8082749-7 1994 Furthermore, increases in expression of p53 were not responsible for the retinoic acid-induced transient inhibition of growth of NSCLC cells, since the growth of H358 p53-null cells also was inhibited by retinoic acid. Tretinoin 204-217 tumor protein p53 Homo sapiens 167-170
8077363-2 1994 Basal and retinoic acid (RA)-induced type I 5"-deiodinase (5"DI) activities were studied in human thyroid carcinoma cell lines. Tretinoin 10-23 iodothyronine deiodinase 1 Homo sapiens 37-57
8077293-2 1994 The capacity of F9 cells to bind 125I-basic FGF (FGF-2) increased upon induction of differentiation with dibutyryl cAMP and retinoic acid. Tretinoin 124-137 fibroblast growth factor 2 Homo sapiens 44-47
8077293-2 1994 The capacity of F9 cells to bind 125I-basic FGF (FGF-2) increased upon induction of differentiation with dibutyryl cAMP and retinoic acid. Tretinoin 124-137 fibroblast growth factor 2 Homo sapiens 49-54
8090031-8 1994 On treatment with various biomodulators, only all-trans retinoic acid significantly upregulated MSE message and protein levels but could not induce new MSE expression in several leukemia cell lines; lipopolysaccharide and interferon-gamma increased MSE expression in normal monocytes. Tretinoin 56-69 interferon gamma Homo sapiens 222-238
8077363-2 1994 Basal and retinoic acid (RA)-induced type I 5"-deiodinase (5"DI) activities were studied in human thyroid carcinoma cell lines. Tretinoin 25-27 iodothyronine deiodinase 1 Homo sapiens 37-57
7519122-10 1994 These results indicate that in both U937 and NB4 cells high level PML/RAR alpha expression inhibits the monocytic terminal differentiation program triggered by D3 or D3 plus TGF-beta 1, whereas RA treatment effectively antagonizes this inhibitory PML-RAR alpha action and restores the D3 differentiative effect. Tretinoin 70-72 transforming growth factor beta 1 Homo sapiens 174-184
8063765-0 1994 Retinoic acid suppression of c-fos gene inhibits expression of tumor necrosis factor-alpha-induced monocyte chemoattractant JE/MCP-1 in clonal osteoblastic MC3T3-E1 cells. Tretinoin 0-13 tumor necrosis factor Mus musculus 63-90
8063765-8 1994 RA pretreatment transcriptionally suppressed the expression of the c-fos gene but not that of the c-jun gene in TNF-alpha-treated cells. Tretinoin 0-2 tumor necrosis factor Mus musculus 112-121
8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tretinoin 13-15 tumor necrosis factor Mus musculus 143-152
8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tretinoin 170-172 tumor necrosis factor Mus musculus 143-152
7949394-9 1994 Treatment of parallel 3-week-old cultures with RA (10-100 nM) rapidly increased expression of the APase, ON, and OP genes severalfold. Tretinoin 47-49 secreted phosphoprotein 1 Gallus gallus 113-115
7915087-1 1994 Spontaneous and all-trans-retinoic acid (RA)-induced differentiation of normal human monocytes and of leukemic THP-1 monocytes into macrophages resulted in a progressive loss of adenosine 3",5"-cyclic monophosphate production induced by histamine via typical H2 receptors (H2R). Tretinoin 16-39 GLI family zinc finger 2 Homo sapiens 111-116
7915087-1 1994 Spontaneous and all-trans-retinoic acid (RA)-induced differentiation of normal human monocytes and of leukemic THP-1 monocytes into macrophages resulted in a progressive loss of adenosine 3",5"-cyclic monophosphate production induced by histamine via typical H2 receptors (H2R). Tretinoin 41-43 GLI family zinc finger 2 Homo sapiens 111-116
7915087-2 1994 In THP-1 cells and in HL-60 human acute myelocytic leukemia cells, RA treatment increased the abundance of the 4.5-kb messenger RNA of the H2R gene fourfold, suggesting transcriptional control by a RA response element. Tretinoin 67-69 GLI family zinc finger 2 Homo sapiens 3-8
7913411-0 1994 Retinoic acid-stimulated intercellular adhesion molecule-1 expression on SK-N-SH cells: calcium/calmodulin-dependent pathway. Tretinoin 0-13 calmodulin 1 Homo sapiens 96-106
7913411-3 1994 In the present study, we investigated the role of calcium (Ca2+) and calmodulin (CaM) in the retinoic acid and gamma-interferon (IFN-gamma) signaling in the human neuroblastoma cell line SK-N-SH for up-regulating ICAM-1 expression. Tretinoin 93-106 calmodulin 1 Homo sapiens 69-79
7913411-3 1994 In the present study, we investigated the role of calcium (Ca2+) and calmodulin (CaM) in the retinoic acid and gamma-interferon (IFN-gamma) signaling in the human neuroblastoma cell line SK-N-SH for up-regulating ICAM-1 expression. Tretinoin 93-106 calmodulin 1 Homo sapiens 81-84
7913411-7 1994 Using calmodulin inhibitors (W7 and calmidazolium), we found that retinoic acid-stimulated, A23187-stimulated, and thapsigargin-stimulated but not FIN-gamma-stimulated ICAM-1 were inhibited. Tretinoin 66-79 calmodulin 1 Homo sapiens 6-16
7913411-8 1994 Calmodulin signaling elicited by retinoic acid was an early event occurring within the first h of retinoic acid treatment, providing evidence that they may both be coupled to regulate gene expression. Tretinoin 33-46 calmodulin 1 Homo sapiens 0-10
7913411-8 1994 Calmodulin signaling elicited by retinoic acid was an early event occurring within the first h of retinoic acid treatment, providing evidence that they may both be coupled to regulate gene expression. Tretinoin 98-111 calmodulin 1 Homo sapiens 0-10
7913411-9 1994 Using a novel CaM kinase II inhibitor, KN-62, we demonstrated that retinoic acid stimulated ICAM-1 expression in a CaM kinase II-dependent fashion. Tretinoin 67-80 calmodulin 1 Homo sapiens 14-17
7913411-9 1994 Using a novel CaM kinase II inhibitor, KN-62, we demonstrated that retinoic acid stimulated ICAM-1 expression in a CaM kinase II-dependent fashion. Tretinoin 67-80 calmodulin 1 Homo sapiens 115-118
7989498-7 1994 In addition, the response of the two cell types to retinoic acid differs: RAR-beta is induced in stromal cells treated with all-trans retinoic acid but not in epithelial cells. Tretinoin 51-64 retinoic acid receptor beta Homo sapiens 74-82
8050571-1 1994 Retinoic acid (RA) stimulated the production of erythropoietin (Epo) in a human hepatoma cell line, HepG2 cells. Tretinoin 0-13 erythropoietin Homo sapiens 48-62
8050571-1 1994 Retinoic acid (RA) stimulated the production of erythropoietin (Epo) in a human hepatoma cell line, HepG2 cells. Tretinoin 0-13 erythropoietin Homo sapiens 64-67
8050571-1 1994 Retinoic acid (RA) stimulated the production of erythropoietin (Epo) in a human hepatoma cell line, HepG2 cells. Tretinoin 15-17 erythropoietin Homo sapiens 48-62
8050571-1 1994 Retinoic acid (RA) stimulated the production of erythropoietin (Epo) in a human hepatoma cell line, HepG2 cells. Tretinoin 15-17 erythropoietin Homo sapiens 64-67
8050571-3 1994 The Epo production in HepG2 cells was also dependent on O2 tension for cell culture but the enhancement of Epo production by RA was independent of O2 tension, indicating that RA exerts its effect through a pathway different from O2. Tretinoin 125-127 erythropoietin Homo sapiens 107-110
8050571-5 1994 These results suggest that RA up-regulates EPO production in vivo as well as in vitro. Tretinoin 27-29 erythropoietin Homo sapiens 43-46
7989498-7 1994 In addition, the response of the two cell types to retinoic acid differs: RAR-beta is induced in stromal cells treated with all-trans retinoic acid but not in epithelial cells. Tretinoin 134-147 retinoic acid receptor beta Homo sapiens 74-82
17180006-6 1994 In this study we isolated RA-resistant 15N cell lines and analyzed their growth properties and changes in cell cycle related (cdc2, cdk2, cyclins A, B, D and E) and early response (fos and jun) gene expression to evaluate the role IGF2 may play in mediating RA resistance. Tretinoin 26-28 cyclin A2 Homo sapiens 138-159
7518821-12 1994 These results suggest that RA may act to inhibit cervical cell growth by increasing IGFBP-3 levels and reducing the extracellular concentration of free insulin-like growth factor I (IGFI) and/or alternatively, IGFBP-3 may inhibit cell growth by direct effects on the cell, independent of IGFI. Tretinoin 27-29 insulin like growth factor 1 Homo sapiens 152-180
8034042-1 1994 Rae-30, one of the retinoic acid (RA)-inducible cDNA clones in mouse embryonal carcinoma F9 cells, was sequenced and the deduced RAE-30 protein showed about a 70% homology to mammalian fructose 1,6-bisphosphatase (EC 3.1.3.11) (FBPase), in comparison to over 85% homology observed among the previously documented rat liver, pig kidney and human leukemic HL-60 cell FBPases. Tretinoin 34-36 fructose bisphosphatase 2 Mus musculus 129-135
7979182-4 1994 In the H460a and H226b cell lines, p110 showed some conversion to the underphosphorylated p105 form after 24 h of retinoic acid treatment. Tretinoin 114-127 nuclear factor kappa B subunit 1 Homo sapiens 90-94
7979182-8 1994 In these cells, both p110 and p105 were induced within 8 h of retinoic acid treatment. Tretinoin 62-75 nuclear factor kappa B subunit 1 Homo sapiens 30-34
7950360-2 1994 TPA induced only slight reductions, whereas retinoic acid and doxorubicin caused an increase in invasiveness, enzymatic activity and differentiation in the clone showing low invasivity, low urokinase-type plasminogen activator levels and high differentiation. Tretinoin 44-57 plasminogen activator, urokinase Homo sapiens 190-226
8034721-10 1994 Taken together these data demonstrate the importance of both Arg269 and Lys220 of RAR-beta for the binding of RA, possibly by interacting with the negatively charged carboxyl group of RA. Tretinoin 110-112 retinoic acid receptor beta Homo sapiens 82-90
8034042-1 1994 Rae-30, one of the retinoic acid (RA)-inducible cDNA clones in mouse embryonal carcinoma F9 cells, was sequenced and the deduced RAE-30 protein showed about a 70% homology to mammalian fructose 1,6-bisphosphatase (EC 3.1.3.11) (FBPase), in comparison to over 85% homology observed among the previously documented rat liver, pig kidney and human leukemic HL-60 cell FBPases. Tretinoin 19-32 fructose bisphosphatase 2 Mus musculus 0-6
8034042-1 1994 Rae-30, one of the retinoic acid (RA)-inducible cDNA clones in mouse embryonal carcinoma F9 cells, was sequenced and the deduced RAE-30 protein showed about a 70% homology to mammalian fructose 1,6-bisphosphatase (EC 3.1.3.11) (FBPase), in comparison to over 85% homology observed among the previously documented rat liver, pig kidney and human leukemic HL-60 cell FBPases. Tretinoin 34-36 fructose bisphosphatase 2 Mus musculus 0-6
8025957-0 1994 Upregulation of tumor necrosis factor-alpha production by retrovirally transduced human tumor-infiltrating lymphocytes using trans-retinoic acid. Tretinoin 125-144 tumor necrosis factor Homo sapiens 16-43
8025957-1 1994 The ability of retinoic acid (RA) to upregulate gene expression in human tumor-infiltrating lymphocytes (TIL) transduced with a Moloney murine leukemia virus containing the cDNA encoding tumor necrosis factor (TNF) has been studied. Tretinoin 15-28 tumor necrosis factor Homo sapiens 210-213
8207257-8 1994 Together these data suggest that FN/VLA-4 interaction may be an important component of stromal cell-dependent thymocyte phenotypic differentiation and that this interaction can be one of the targets for the influence of RA in T cell development. Tretinoin 220-222 fibronectin 1 Homo sapiens 33-35
8013376-2 1994 The control of 17 beta HSD expression by all-trans-retinoic acid (RA) in T47D breast cancer cells was examined using a specific 17 beta HSD complementary DNA probe. Tretinoin 45-64 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 15-26
8013376-2 1994 The control of 17 beta HSD expression by all-trans-retinoic acid (RA) in T47D breast cancer cells was examined using a specific 17 beta HSD complementary DNA probe. Tretinoin 66-68 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 15-26
8013376-7 1994 Whereas RA increased 17 beta HSD reductive activity, it had no effect on oxidative activity. Tretinoin 8-10 hydroxysteroid 17-beta dehydrogenase 1 Homo sapiens 21-32
8207257-0 1994 Modulation of fibronectin and thymic stromal cell-dependent thymocyte maturation by retinoic acid. Tretinoin 84-97 fibronectin 1 Homo sapiens 14-25
8061571-1 1994 Northern hybridizations were used to evaluate the modulated action of retinoic acid (R.A.) in presence of dexamethasone (Dex) and/or calcitriol (1,25-(OH)2D3) on calcitonin (CT) and calcitonin gene-related peptide (CGRP) mRNA steady state levels in the murine CA-77 C cell line. Tretinoin 70-83 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 182-213
8022710-2 1994 Since the proliferation of prostate cells is highly dependent on androgen stimulation, presumably via its cognate receptor, we investigated the effects of RA on the expression of the androgen receptor and other androgen-regulated genes in the human prostatic adenocarcinoma cell line LNCaP. Tretinoin 155-157 androgen receptor Homo sapiens 183-200
8022710-7 1994 Consistent with this finding, androgen induction of PSA glycoprotein was also repressed by RA, with maximal inhibition occurring at 10(-5) M. These data suggest that the suppression of proliferation and function of prostatic cells by RA may be via modulatory effects on the AR. Tretinoin 234-236 androgen receptor Homo sapiens 274-276
7943653-3 1994 This study demonstrates that therapeutic doses of RA (0.1-10 microM) significantly increase transforming growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic cells, and in human peripheral blood monocytes. Tretinoin 50-52 transforming growth factor beta 1 Homo sapiens 92-123
7943653-3 1994 This study demonstrates that therapeutic doses of RA (0.1-10 microM) significantly increase transforming growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic cells, and in human peripheral blood monocytes. Tretinoin 50-52 transforming growth factor beta 1 Homo sapiens 125-133
7943653-3 1994 This study demonstrates that therapeutic doses of RA (0.1-10 microM) significantly increase transforming growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic cells, and in human peripheral blood monocytes. Tretinoin 50-52 GLI family zinc finger 2 Homo sapiens 154-159
7943653-5 1994 Combination of RA stimulation with acute in vitro ethanol treatment, however, resulted in significantly lower M theta TGF beta production than TGF beta levels induced by RA alone (p < 0.003). Tretinoin 15-17 transforming growth factor beta 1 Homo sapiens 118-126
7943653-5 1994 Combination of RA stimulation with acute in vitro ethanol treatment, however, resulted in significantly lower M theta TGF beta production than TGF beta levels induced by RA alone (p < 0.003). Tretinoin 170-172 transforming growth factor beta 1 Homo sapiens 143-151
7943653-6 1994 Down-regulation of M theta TGF beta production by ethanol was tested at the concentration range of 25-150 mM and occurred both at high and low RA concentrations (10-0.1 microM). Tretinoin 143-145 transforming growth factor beta 1 Homo sapiens 27-35
7943653-7 1994 In contrast to its inhibitory effect on RA-induced M theta TGF beta production, ethanol augmented TGF beta production induced by muramyl dipeptide (20 micrograms/ml), suggesting that ethanol can either up- or down-regulate M theta TGF beta production, depending on the costimulatory factors. Tretinoin 40-42 transforming growth factor beta 1 Homo sapiens 59-67
7943653-8 1994 RA also induced a moderate increase in M theta tumor necrosis factor-alpha (TNF alpha) production, which was down-regulated by ethanol both at the level of secreted and cell-associated TNF alpha. Tretinoin 0-2 tumor necrosis factor Homo sapiens 76-85
7943653-8 1994 RA also induced a moderate increase in M theta tumor necrosis factor-alpha (TNF alpha) production, which was down-regulated by ethanol both at the level of secreted and cell-associated TNF alpha. Tretinoin 0-2 tumor necrosis factor Homo sapiens 185-194
7943653-9 1994 In addition to regulation of cytokine production, both RA and ethanol decreased expression of CD4 on THP-1 cells. Tretinoin 55-57 CD4 molecule Homo sapiens 94-97
7943653-9 1994 In addition to regulation of cytokine production, both RA and ethanol decreased expression of CD4 on THP-1 cells. Tretinoin 55-57 GLI family zinc finger 2 Homo sapiens 101-106
7943653-10 1994 The degree of inhibition of CD4 expression by RA was more significant than by ethanol, but RA-induced decrease in CD4 expression was not significantly affected by the combined stimulation with ethanol. Tretinoin 46-48 CD4 molecule Homo sapiens 28-31
7943653-10 1994 The degree of inhibition of CD4 expression by RA was more significant than by ethanol, but RA-induced decrease in CD4 expression was not significantly affected by the combined stimulation with ethanol. Tretinoin 91-93 CD4 molecule Homo sapiens 114-117
8061571-1 1994 Northern hybridizations were used to evaluate the modulated action of retinoic acid (R.A.) in presence of dexamethasone (Dex) and/or calcitriol (1,25-(OH)2D3) on calcitonin (CT) and calcitonin gene-related peptide (CGRP) mRNA steady state levels in the murine CA-77 C cell line. Tretinoin 70-83 calcitonin/calcitonin-related polypeptide, alpha Mus musculus 215-219
8089852-0 1994 Antagonistic effects of retinoic acid and thyroid hormone on the expression of the tissue-specific splicing protein SmN in a clonal cell line derived from rat heart. Tretinoin 24-37 survival of motor neuron 1, telomeric Rattus norvegicus 116-119
7516397-0 1994 Retinoic acid suppression of loricrin expression in reconstituted human skin cultured at the liquid-air interface. Tretinoin 0-13 loricrin cornified envelope precursor protein Homo sapiens 29-37
7516397-4 1994 Retinoic acid (10(-6) M) suppressed loricrin expression in skin cultures as determined by both protein and mRNA analysis. Tretinoin 0-13 loricrin cornified envelope precursor protein Homo sapiens 36-44
8089852-4 1994 In particular thyroid hormone and retinoic acid exhibit antagonistic effects on SmN expression with thyroid hormone treatment producing large increases in expression whilst retinoic acid treatment virtually abolishes expression. Tretinoin 34-47 survival of motor neuron 1, telomeric Rattus norvegicus 80-83
8089852-4 1994 In particular thyroid hormone and retinoic acid exhibit antagonistic effects on SmN expression with thyroid hormone treatment producing large increases in expression whilst retinoic acid treatment virtually abolishes expression. Tretinoin 173-186 survival of motor neuron 1, telomeric Rattus norvegicus 80-83
8207983-1 1994 The current treatment of acute promyelocytic leukemia (APL, also called AML3 subtype) is focused on differentiating agents such as the vitamin A derivative all-trans retinoic acid (ATRA). Tretinoin 166-179 RUNX family transcription factor 2 Homo sapiens 72-76
7919958-4 1994 Retinoic acid, which inhibits cell proliferation and down-regulates the mts1 gene, reduced heat shock protein expression in the ML8-B16 variant line. Tretinoin 0-13 S100 calcium binding protein A4 Mus musculus 72-76
8207983-1 1994 The current treatment of acute promyelocytic leukemia (APL, also called AML3 subtype) is focused on differentiating agents such as the vitamin A derivative all-trans retinoic acid (ATRA). Tretinoin 181-185 RUNX family transcription factor 2 Homo sapiens 72-76
8207983-6 1994 We have demonstrated that AML3 patients" cells (from four patients) at relapse show high levels of CRABP, a cytosolic retinoic acid binding protein and this protein was not detected prior to ATRA therapy. Tretinoin 191-195 RUNX family transcription factor 2 Homo sapiens 26-30
8207983-9 1994 This induced ATRA hypercatabolytic state should be monitored during consolidation therapy and at relapse by evaluating CRABP and RA metabolite levels, in order to detect ATRA resistance in patients with AML3. Tretinoin 13-17 RUNX family transcription factor 2 Homo sapiens 203-207
8195142-1 1994 The orphan receptor chicken ovalbumin upstream promoter transcription factor I (COUP-TF I) fully prevented not only the activation of the oxytocin gene by retinoic acid and thyroid hormone but also completely repressed the estrogen-dependent stimulation in transfected P19 EC cells. Tretinoin 155-168 nuclear receptor subfamily 2 group F member 1 Gallus gallus 80-89
7925248-1 1994 A novel protein (p34) was observed in polyacrylamide gel fluorographs of gestation day 13 embryonic mouse brain following retinoic acid dosing of dams. Tretinoin 122-135 alpha- and gamma-adaptin binding protein Mus musculus 17-20
7521152-6 1994 Although GM-CSF, IL-3 and IL-1 significantly modulated the ATRA-induced morphological changes, they did not induce CD14 expression, a typical marker of monocytic differentiation. Tretinoin 59-63 interleukin 1 beta Homo sapiens 26-30
7521152-7 1994 In the presence of ATRA, GM-CSF potentiated production and secretion of tumor necrosis factor-alpha (TNF) in response to lipopolysaccharide, as well as interferon-gamma which is a potent inducer of monocytic differentiation in APL cells. Tretinoin 19-23 tumor necrosis factor Homo sapiens 72-99
7521152-7 1994 In the presence of ATRA, GM-CSF potentiated production and secretion of tumor necrosis factor-alpha (TNF) in response to lipopolysaccharide, as well as interferon-gamma which is a potent inducer of monocytic differentiation in APL cells. Tretinoin 19-23 tumor necrosis factor Homo sapiens 101-104
7521152-8 1994 On the other hand, production of TNF in ATRA-treated cells was not affected by G-CSF which significantly enhanced granulocytic differentiation. Tretinoin 40-44 tumor necrosis factor Homo sapiens 33-36
8168086-10 1994 TPA and retinoic acid generally down-regulated MSH receptors but had no effect on HBL cells. Tretinoin 8-21 proopiomelanocortin Homo sapiens 47-50
8174790-12 1994 Exposure to retinoic acid influenced the morphology of the cells and the profile of members of the placental PRL family expressed by in vitro differentiated cells. Tretinoin 12-25 prolactin Rattus norvegicus 109-112
8032951-2 1994 Here we show that the degree of apoptosis can also be enhanced by agents which activate protein kinase C (PKC) and that such agents synergize with RA in inducing apoptosis. Tretinoin 147-149 proline rich transmembrane protein 2 Homo sapiens 106-109
8163572-0 1994 Inhibition of the chondrocyte phenotype by retinoic acid involves upregulation of metalloprotease genes independent of TGF-beta. Tretinoin 43-56 transforming growth factor beta 1 Homo sapiens 119-127
7918098-1 1994 The cDNAs encoding the zebrafish homologs of retinoic acid receptor alpha(zRAR alpha) and gamma (zRAR gamma) were isolated and their expression studied in normal and retinoic acid (RA) treated embryos. Tretinoin 45-58 retinoic acid receptor, alpha a Danio rerio 74-84
8032951-3 1994 In contrast chronic down regulation of PKC dramatically reduces the ability of RA to induce apoptosis whilst ND7 cell lines selected for resistance to RA-induced apoptosis are also resistant to apoptosis induced by PKC activation. Tretinoin 79-81 proline rich transmembrane protein 2 Homo sapiens 39-42
8157664-5 1994 Nedd1 mRNA is strongly expressed in early embryonic brain, but it can be detected at low levels in a number of adult tissues as well as cell lines and is up-regulated in an embryonal carcinoma cell line upon retinoic acid-induced differentiation. Tretinoin 208-221 NEDD1 gamma-tubulin ring complex targeting factor Homo sapiens 0-5
7512841-5 1994 Exposure to all-trans retinoic acid down-regulated c-kit mRNA levels, while simultaneously causing morphologic alterations in all four cell lines. Tretinoin 22-35 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 51-56
7511050-10 1994 Following culture with ATRA, increased CD38 protein levels were also observed in normal CD34+ bone marrow cells, but not on normal circulating granulocytes. Tretinoin 23-27 CD34 molecule Homo sapiens 88-92
8161786-7 1994 The IL-6R was no more detectable on cells from patients with MGUS after 2 days of treatment with RA and slightly downregulated in patients with WM. Tretinoin 97-99 interleukin 6 receptor Homo sapiens 4-9
8161792-5 1994 After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Tretinoin 51-64 BCL2 apoptosis regulator Homo sapiens 25-29
8161792-5 1994 After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Tretinoin 51-64 BCL2 apoptosis regulator Homo sapiens 91-95
8142654-4 1994 When HL60 cells were induced to differentiate to granulocytes by dimethyl sulfoxide (DMSO) or retinoic acid (RA), a marked downregulation in the levels of wt1 transcripts was found. Tretinoin 94-107 WT1 transcription factor Homo sapiens 155-158
7912076-4 1994 In B16-ML8 cells, retinoic acid reduced mts1 expression together with a reduction of p53 positivity. Tretinoin 18-31 cyclin dependent kinase inhibitor 2A Mus musculus 40-44
8149483-5 1994 In a more detailed time course, application of 20 nmol of TPA to mouse skin led to 20, 36, 92 and 0% decrease in the binding of [3H]RA to mouse epidermal RAR at 2, 4, 12 and 72 h after treatment respectively. Tretinoin 132-134 promotion susceptibility QTL 1 Mus musculus 58-61
8149483-1 1994 During studies to determine the mechanism of tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA), we found that TPA downregulates mouse epidermal retinoic acid nuclear receptors (RAR), a superfamily of nuclear steroid/thyroid receptors implicated in mediating effects of retinoic acid (RA). Tretinoin 156-169 promotion susceptibility QTL 1 Mus musculus 102-105
8149483-1 1994 During studies to determine the mechanism of tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA), we found that TPA downregulates mouse epidermal retinoic acid nuclear receptors (RAR), a superfamily of nuclear steroid/thyroid receptors implicated in mediating effects of retinoic acid (RA). Tretinoin 156-169 promotion susceptibility QTL 1 Mus musculus 122-125
8149483-1 1994 During studies to determine the mechanism of tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA), we found that TPA downregulates mouse epidermal retinoic acid nuclear receptors (RAR), a superfamily of nuclear steroid/thyroid receptors implicated in mediating effects of retinoic acid (RA). Tretinoin 189-191 promotion susceptibility QTL 1 Mus musculus 122-125
8149483-2 1994 Application of TPA to mouse skin decreased the binding of [3H]RA to RAR from mouse epidermal nuclear extracts. Tretinoin 62-64 promotion susceptibility QTL 1 Mus musculus 15-18
8149483-3 1994 In this experiment, 20 nmol of TPA was applied to mouse skin and 3.5 h later binding of [3H]RA to RAR was analyzed by chromatography on a size-exclusion column. Tretinoin 92-94 promotion susceptibility QTL 1 Mus musculus 31-34
8149483-4 1994 TPA treatment resulted in an approximately 67% decrease in the specific binding of [3H]RA to RAR. Tretinoin 87-89 promotion susceptibility QTL 1 Mus musculus 0-3
8018987-1 1994 The Adh-1 gene product, ADH-A2, the only known murine class I alcohol dehydrogenase, is able to oxidize retinol (vitamin A) into retinaldehyde, the first enzymatic step in the conversion of retinol into its biologically active metabolite retinoic acid. Tretinoin 238-251 alcohol dehydrogenase 1 (class I) Mus musculus 4-9
8056839-4 1994 We demonstrate that transient overexpression of RAR-beta in the presence, but not absence, of all-trans retinoic acid results in a dramatic suppression of cell proliferation. Tretinoin 104-117 retinoic acid receptor beta Homo sapiens 48-56
8038727-2 1994 Albumin has two kinds of binding sites for retinoic acid with an affinity constant of 10(5) M-1 and 10(4) M-1 respectively. Tretinoin 43-56 myoregulin Homo sapiens 92-109
7512079-2 1994 In addition to PMA, cells of the THP-1 myeloid leukemia cell line acquire macrophage-like characteristics after treatment with all-trans retinoic acid (RA). Tretinoin 137-150 GLI family zinc finger 2 Homo sapiens 33-38
8119774-3 1994 In this study, we show that in human neuroblastoma, a cell type exceptionally sensitive to RA-induced differentiation, RAR alpha as well as RAR beta is markedly up-regulated by RA treatment. Tretinoin 91-93 retinoic acid receptor beta Homo sapiens 140-148
8018987-9 1994 This highly regulated expression of Adh-1 is discussed with respect to the local synthesis of retinoic acid during development. Tretinoin 94-107 alcohol dehydrogenase 1 (class I) Mus musculus 36-41
8018987-1 1994 The Adh-1 gene product, ADH-A2, the only known murine class I alcohol dehydrogenase, is able to oxidize retinol (vitamin A) into retinaldehyde, the first enzymatic step in the conversion of retinol into its biologically active metabolite retinoic acid. Tretinoin 238-251 alcohol dehydrogenase 1 (class I) Mus musculus 24-30
8018987-1 1994 The Adh-1 gene product, ADH-A2, the only known murine class I alcohol dehydrogenase, is able to oxidize retinol (vitamin A) into retinaldehyde, the first enzymatic step in the conversion of retinol into its biologically active metabolite retinoic acid. Tretinoin 238-251 alcohol dehydrogenase 1 (class I) Mus musculus 54-83
8125154-9 1994 TGF-beta treatment was able to at least partially overcome the inhibitory effects of retinoic acid. Tretinoin 85-98 transforming growth factor beta 1 Homo sapiens 0-8
8125161-0 1994 Retinoic acid inhibition of insulin-like growth factor I stimulation of c-fos mRNA levels in a breast carcinoma cell line. Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 28-56
8125154-6 1994 Treatment of chondrocytes with retinoic acid for the first 3 days of culture, prior to use in attachment assays, resulted in a decrease in the attachment to collagen but not to fibronectin or MGP. Tretinoin 31-44 fibronectin 1 Homo sapiens 177-188
8125154-7 1994 Seven days of retinoic acid treatment resulted in decreased attachment to fibronectin, MGP, and collagen. Tretinoin 14-27 fibronectin 1 Homo sapiens 74-85
8125161-1 1994 Retinoic acid (RA) inhibits insulin-like growth factor I (IGF-I)-stimulated growth of the human breast carcinoma cell line MCF-7. Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 28-56
8125161-1 1994 Retinoic acid (RA) inhibits insulin-like growth factor I (IGF-I)-stimulated growth of the human breast carcinoma cell line MCF-7. Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 58-63
8125161-1 1994 Retinoic acid (RA) inhibits insulin-like growth factor I (IGF-I)-stimulated growth of the human breast carcinoma cell line MCF-7. Tretinoin 15-17 insulin like growth factor 1 Homo sapiens 28-56
8125161-1 1994 Retinoic acid (RA) inhibits insulin-like growth factor I (IGF-I)-stimulated growth of the human breast carcinoma cell line MCF-7. Tretinoin 15-17 insulin like growth factor 1 Homo sapiens 58-63
8125161-2 1994 RA-mediated inhibition of IGF-I-stimulated growth is not associated with either a decrease in IGF-I receptor number or affinity. Tretinoin 0-2 insulin like growth factor 1 Homo sapiens 26-31
8125161-5 1994 Pretreatment of MCF-7 cells with 1 microM RA blocked IGF-I-mediated enhancement of c-fos mRNA levels by approximately 70%. Tretinoin 42-44 insulin like growth factor 1 Homo sapiens 53-58
8125161-6 1994 The maximal RA effect (80% inhibition) on IGF-I stimulation of c-fos mRNA levels was noted within 2 h of exposure to RA. Tretinoin 12-14 insulin like growth factor 1 Homo sapiens 42-47
8125161-6 1994 The maximal RA effect (80% inhibition) on IGF-I stimulation of c-fos mRNA levels was noted within 2 h of exposure to RA. Tretinoin 117-119 insulin like growth factor 1 Homo sapiens 42-47
8125161-10 1994 We conclude that RA-mediated inhibition of IGF-I stimulation of c-fos mRNA may represent a potential mechanism by which RA inhibits IGF-I stimulation of growth. Tretinoin 17-19 insulin like growth factor 1 Homo sapiens 43-48
8125161-10 1994 We conclude that RA-mediated inhibition of IGF-I stimulation of c-fos mRNA may represent a potential mechanism by which RA inhibits IGF-I stimulation of growth. Tretinoin 17-19 insulin like growth factor 1 Homo sapiens 132-137
8125161-10 1994 We conclude that RA-mediated inhibition of IGF-I stimulation of c-fos mRNA may represent a potential mechanism by which RA inhibits IGF-I stimulation of growth. Tretinoin 120-122 insulin like growth factor 1 Homo sapiens 43-48
8125161-10 1994 We conclude that RA-mediated inhibition of IGF-I stimulation of c-fos mRNA may represent a potential mechanism by which RA inhibits IGF-I stimulation of growth. Tretinoin 120-122 insulin like growth factor 1 Homo sapiens 132-137
8125162-3 1994 Recently, three nuclear receptors specific for retinoic acid (RAR alpha, RAR beta, and RAR gamma) have been cloned and all are members of a large multigene family of ligand-inducible transcription enhancer factors. Tretinoin 47-60 retinoic acid receptor beta Homo sapiens 73-81
8125162-6 1994 When treated with 1 microM RA, the messenger RNAs for both RAR beta and RAR gamma are induced. Tretinoin 27-29 retinoic acid receptor beta Homo sapiens 59-67
8016390-9 1994 Induction of eicosanoid synthesis by RA was further confirmed in THP-1 cells. Tretinoin 37-39 GLI family zinc finger 2 Homo sapiens 65-70
8120450-5 1994 Of the various retinoids studied, all-trans-retinoic acid (RA) was most potent; it almost completely inhibited the production of TNF by macrophages activated with endotoxin and interferon-gamma. Tretinoin 34-57 tumor necrosis factor Mus musculus 129-132
8120450-5 1994 Of the various retinoids studied, all-trans-retinoic acid (RA) was most potent; it almost completely inhibited the production of TNF by macrophages activated with endotoxin and interferon-gamma. Tretinoin 34-57 interferon gamma Mus musculus 177-193
8016390-10 1994 These data indicate that RA most effectively induced cyclooxygenase activity and stimulus-dependent eicosanoid formation in U937 and THP-1 cells. Tretinoin 25-27 GLI family zinc finger 2 Homo sapiens 133-138
8298127-0 1994 Retinoic acid downmodulates erythroid differentiation and GATA1 expression in purified adult-progenitor culture. Tretinoin 0-13 GATA binding protein 1 Homo sapiens 58-63
7906679-7 1994 Of the agents which inhibit the growth of T47D and ZR75.1 cells--Pg, Prl, cAMP, RA and TPA--only Pg and cAMP caused an increase in the erbB-2 protein level. Tretinoin 80-82 erb-b2 receptor tyrosine kinase 2 Homo sapiens 135-141
8107809-4 1994 Calreticulin can also inhibit androgen receptor and retinoic acid receptor transcriptional activities in vivo, as well as retinoic acid-induced neuronal differentiation. Tretinoin 52-65 calreticulin Homo sapiens 0-12
8120366-7 1994 The APC from deficient mice stimulated greater IFN-gamma release than control APC and retinoic acid addition in vitro decreased this activity 50%. Tretinoin 86-99 interferon gamma Mus musculus 47-56
8027277-2 1994 We have previously shown that all three RAR types are expressed in human endometrial stromal cells in vitro and that RAR-beta expression is induced in response to retinoic acid. Tretinoin 163-176 retinoic acid receptor beta Homo sapiens 117-125
8180126-6 1994 RAR-beta gene expression is induced both by retinoic acid and by fenretinide in normal cells, but tumor cells fail to respond to either. Tretinoin 44-57 retinoic acid receptor beta Homo sapiens 0-8
8027277-5 1994 Furthermore, the retinoic acid-mediated induction of RAR-beta was not affected by oestradiol or progesterone, and was dependent on the continued presence of retinoic acid. Tretinoin 17-30 retinoic acid receptor beta Homo sapiens 53-61
8027277-5 1994 Furthermore, the retinoic acid-mediated induction of RAR-beta was not affected by oestradiol or progesterone, and was dependent on the continued presence of retinoic acid. Tretinoin 157-170 retinoic acid receptor beta Homo sapiens 53-61
8301142-0 1994 Retinoic acid inhibition of IL-1-induced IL-6 production by human lung fibroblasts. Tretinoin 0-13 interleukin 6 Homo sapiens 41-45
8309256-3 1994 ATRA is strikingly effective in acute promyelocytic leukemia (the AML3 subtype) inducing a high incidence of complete remissions. Tretinoin 0-4 RUNX family transcription factor 2 Homo sapiens 66-70
8294940-8 1994 Further studies of transcriptional regulation showed that cerebral endothelium was responsive to apo A-I-inducing agents, such as cholesterol, insulin, and retinoic acid, as previously shown in human hepatoma HepG2 cells. Tretinoin 156-169 apolipoprotein A1 Homo sapiens 97-104
8089767-1 1994 A nuclear component interacting with a retinoic acid response element (RARE-beta) derived from the all-trans-retinoic acid receptor beta (RAR beta) gene promoter was detected in the rat liver by gel-shift assay. Tretinoin 39-52 retinoic acid receptor, beta Rattus norvegicus 138-146
7508403-1 1994 Expression of the oct-2 gene was studied in mouse tissues and during in vitro differentiation of embryocarcinoma PCC4, mouse neuroblastoma Neuro2A and NB41A3 cells in the presence of retinoic acid (RA) or 1% DMSO. Tretinoin 183-196 POU domain, class 2, transcription factor 2 Mus musculus 18-23
7904998-5 1994 The action of IFN-gamma on the expression of squamous cell-specific genes is antagonized by retinoic acid and transforming growth factor beta 1. Tretinoin 92-105 interferon gamma Homo sapiens 14-23
8286746-5 1994 In order to measure PKC expression associated with the reversal of TPA resistance by ATRA, we exposed HL-525 cells to ATRA and analyzed PKC-mRNA and protein levels. Tretinoin 85-89 protein kinase C alpha Homo sapiens 20-23
8286746-7 1994 ATRA treatment was also associated with an increase in PKC activity and an induction of cytosolic PKC beta protein levels. Tretinoin 0-4 protein kinase C alpha Homo sapiens 55-58
8286746-8 1994 These findings are consistent with the hypothesis that ATRA reverses TPA resistance in HL-525 cells by enhancing the expression of PKC. Tretinoin 55-59 protein kinase C alpha Homo sapiens 131-134
8143931-0 1994 All-trans-retinoic acid and hexamethylene bisacetamide (HMBA) regulate TGF-alpha and Hst-1/kFGF expression in differentiation sensitive but not in resistant human teratocarcinomas. Tretinoin 0-23 fibroblast growth factor 4 Homo sapiens 85-90
8123593-4 1994 We now report that treatment of NCI-H82 cells with 1 microM all-trans-retinoic acid resulted in decreased cellular growth, decreased c-myc mRNA levels, and increased L-myc mRNA levels. Tretinoin 60-83 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 166-171
8123593-7 1994 These data show that all-trans-retinoic acid, a clinically relevant compound, inhibits small cell lung cancer progression in our in vitro model and alters the expression of the c-myc and L-myc oncogenes. Tretinoin 21-44 MYCL proto-oncogene, bHLH transcription factor Homo sapiens 187-192
8067288-7 1994 We found that only PKC-alpha is expressed in these cells, and this is the form that is induced by retinoic acid. Tretinoin 98-111 protein kinase C, alpha Mus musculus 19-28
8067288-8 1994 The retinoic acid-induced increased in PKC-alpha is found at both the RNA and protein level. Tretinoin 4-17 protein kinase C, alpha Mus musculus 39-48
8067288-18 1994 In summary, these finding suggest a key role for PKC-alpha in the pathway by which retinoic acid induces B16 mouse melanoma differentiation. Tretinoin 83-96 protein kinase C, alpha Mus musculus 49-58
7905817-0 1994 Modulation of EGF receptor and CD15 (Lewisx) antigen on the cell surface of breast carcinoma cell lines induced by cytokines, retinoic acid, 12-O-tetradecanoylphorbol 13-acetate and 1,25(OH)2-vitamin D3. Tretinoin 126-139 epidermal growth factor receptor Homo sapiens 14-26
7905817-0 1994 Modulation of EGF receptor and CD15 (Lewisx) antigen on the cell surface of breast carcinoma cell lines induced by cytokines, retinoic acid, 12-O-tetradecanoylphorbol 13-acetate and 1,25(OH)2-vitamin D3. Tretinoin 126-139 fucosyltransferase 4 Homo sapiens 31-35
8143931-0 1994 All-trans-retinoic acid and hexamethylene bisacetamide (HMBA) regulate TGF-alpha and Hst-1/kFGF expression in differentiation sensitive but not in resistant human teratocarcinomas. Tretinoin 0-23 fibroblast growth factor 4 Homo sapiens 91-95
7987085-4 1994 Combination of retinoic acid with interferon-gamma increased the down-regulation of specific binding sites of interferon-gamma. Tretinoin 15-28 interferon gamma Homo sapiens 34-50
7987085-4 1994 Combination of retinoic acid with interferon-gamma increased the down-regulation of specific binding sites of interferon-gamma. Tretinoin 15-28 interferon gamma Homo sapiens 110-126
7994082-0 1994 Effects of retinoic acid and dexamethasone on proliferation, differentiation, and glucocorticoid receptor expression in cultured human osteosarcoma cells. Tretinoin 11-24 nuclear receptor subfamily 3 group C member 1 Homo sapiens 82-105
7505280-5 1994 We have previously demonstrated that retinoic acid (RA) inhibition of IGF-I-stimulated MCF-7 cell proliferation is associated with increased IGFBP-3 levels in the conditioned media. Tretinoin 37-50 insulin like growth factor 1 Homo sapiens 70-75
7893379-3 1994 The pharmacological effects of RA on the cultures and their relation to catecholamine and acetylcholine neurotransmission were evaluated according the levels of catecholamines, tyrosine hydroxylase (TH) activity, TH immunostaining, and choline acetyltransferase (CAT) activity, respectively. Tretinoin 31-33 tyrosine hydroxylase Homo sapiens 199-201
7815831-1 1994 The current treatment of acute promyelocytic leukemia (APL, also called AML3 subtype) is focused on differentiating agents such as the vitamin A derivative all-trans retinoic acid (ATRA). Tretinoin 166-179 RUNX family transcription factor 2 Homo sapiens 72-76
7815831-1 1994 The current treatment of acute promyelocytic leukemia (APL, also called AML3 subtype) is focused on differentiating agents such as the vitamin A derivative all-trans retinoic acid (ATRA). Tretinoin 181-185 RUNX family transcription factor 2 Homo sapiens 72-76
7815831-6 1994 We have demonstrated that AML3 patients" cells (from four patients) at relapse show high levels of CRABP, a cytosolic retinoic acid binding protein and this protein was not detected prior to ATRA therapy. Tretinoin 191-195 RUNX family transcription factor 2 Homo sapiens 26-30
7815831-9 1994 This induced ATRA hypercatabolytic state should be monitored during consolidation therapy and at relapse by evaluating CRABP and RA metabolite levels, in order to detect ATRA resistance in patients with AML3. Tretinoin 13-17 RUNX family transcription factor 2 Homo sapiens 203-207
7815843-4 1994 In vitro treatment with ATRA consistently increased the expression of CD15, CD11b, and CD45R0 on leukemic promyelocytes; these changes were paralleled by a decrease of CD45RA display. Tretinoin 24-28 fucosyltransferase 4 Homo sapiens 70-74
7893379-4 1994 RA reduces catecholamine levels and TH activity in NB69 cells and the number of dopamine neurons in cultures derived from rat fetal mid brain. Tretinoin 0-2 tyrosine hydroxylase Homo sapiens 36-38
7893379-5 1994 The detrimental effect of RA on mid brain neurons is dose- dependent; limited to TH+ cells at low concentrations (100 to 500 nM) and toxic for all types of cells at high concentrations (1 to 2 microM). Tretinoin 26-28 tyrosine hydroxylase Homo sapiens 81-83
7904822-0 1994 Brn-3.2: a Brn-3-related transcription factor with distinctive central nervous system expression and regulation by retinoic acid. Tretinoin 115-128 POU class 4 homeobox 2 Homo sapiens 0-7
7904822-2 1994 Brn-3.2 exhibits DNA binding properties similar to those of Brn-3.0, but its expression is uniquely regulated by retinoic acid in teratocarcinoma and neuroblastoma cells. Tretinoin 113-126 POU class 4 homeobox 2 Homo sapiens 0-7
7972200-2 1994 The results indicate that retinoic acid and forskolin were able to activate the human MDR1 pp in a dose dependent manner after transfection of the MDR1pp- CAT constructs in the 2 cell models tested, i.e., SK-N-SH and IGR-N-91, a new human neuroblastoma cell line. Tretinoin 26-39 ATP binding cassette subfamily B member 1 Homo sapiens 86-90
8262244-3 1993 The physiological function of aldehyde oxidase appears to be the synthesis of retinoic acid from retinal. Tretinoin 78-91 aldehyde oxidase 1 Homo sapiens 30-46
7972200-0 1994 Retinoic acid and forskolin activate the human MDR1 gene promoter in differentiated neuroblasts. Tretinoin 0-13 ATP binding cassette subfamily B member 1 Homo sapiens 47-51
8129853-1 1993 CYP3A proteins are P450 monooxygenases involved in the metabolism of steroids, retinoic acid and several important drugs. Tretinoin 79-92 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 0-5
8262951-0 1993 Retinol bound to cellular retinol-binding protein is a substrate for cytosolic retinoic acid synthesis. Tretinoin 79-92 retinol binding protein 1 Bos taurus 17-49
8262951-1 1993 Retinol bound to cellular retinol-binding protein (CRBP) was found to be oxidized to retinoic acid by a soluble activity from calf liver. Tretinoin 85-98 retinol binding protein 1 Bos taurus 17-49
8262951-1 1993 Retinol bound to cellular retinol-binding protein (CRBP) was found to be oxidized to retinoic acid by a soluble activity from calf liver. Tretinoin 85-98 retinol binding protein 1 Bos taurus 51-55
8262951-2 1993 Cytosolic retinoic acid synthesis from retinol-CRBP was strictly dependent on the exogenous supply of either NAD or NADP. Tretinoin 10-23 retinol binding protein 1 Bos taurus 47-51
8262951-5 1993 Since the dissociation constant of the bovine retinol-CRBP complex is less than 10(-8) M, whereas the Km for retinol-CRBP is of the same order as the Km for free retinol, synthesis of retinoic acid from retinol-CRBP does not rely on prior dissociation of retinol. Tretinoin 184-197 retinol binding protein 1 Bos taurus 54-58
8262951-5 1993 Since the dissociation constant of the bovine retinol-CRBP complex is less than 10(-8) M, whereas the Km for retinol-CRBP is of the same order as the Km for free retinol, synthesis of retinoic acid from retinol-CRBP does not rely on prior dissociation of retinol. Tretinoin 184-197 retinol binding protein 1 Bos taurus 117-121
8262951-5 1993 Since the dissociation constant of the bovine retinol-CRBP complex is less than 10(-8) M, whereas the Km for retinol-CRBP is of the same order as the Km for free retinol, synthesis of retinoic acid from retinol-CRBP does not rely on prior dissociation of retinol. Tretinoin 184-197 retinol binding protein 1 Bos taurus 117-121
8262951-6 1993 ApoCRBP proved to be a specific inhibitor of retinoic acid synthesis from CRBP-bound retinol. Tretinoin 45-58 retinol binding protein 1 Bos taurus 3-7
8262951-9 1993 These results indicate that the protein moiety of holoCRBP is specifically recognized by the cytosolic enzyme system that catalyzes retinoic acid synthesis from CRBP-bound retinol. Tretinoin 132-145 retinol binding protein 1 Bos taurus 54-58
7503983-8 1993 RA action was independent of cell density, serum, or PDGF but was partially inhibited by bFGF. Tretinoin 0-2 fibroblast growth factor 2 Homo sapiens 89-93
8250033-0 1993 Regulation of epidermal growth factor receptor expression and growth by protein kinase C and retinoic acid in LLC-PK1 cells. Tretinoin 93-106 epidermal growth factor receptor Sus scrofa 14-46
8280157-5 1993 However, the expression of POMC mRNA and of immunoreactive beta-endorphin was reduced within a few hours of treatment of these cell lines with retinoic acid. Tretinoin 143-156 proopiomelanocortin Homo sapiens 27-31
8280157-5 1993 However, the expression of POMC mRNA and of immunoreactive beta-endorphin was reduced within a few hours of treatment of these cell lines with retinoic acid. Tretinoin 143-156 proopiomelanocortin Homo sapiens 59-73
8281940-2 1993 In addition, IGF-I reverses the inhibitory effects of dexamethasone and enhances the effects of retinoic acid on osteocalcin synthesis. Tretinoin 96-109 insulin like growth factor 1 Homo sapiens 13-18
8281940-2 1993 In addition, IGF-I reverses the inhibitory effects of dexamethasone and enhances the effects of retinoic acid on osteocalcin synthesis. Tretinoin 96-109 bone gamma-carboxyglutamate protein Homo sapiens 113-124
8274426-6 1993 Comparing all-trans- with 9-cis-RA, the latter was more effective in inhibiting tumor cell growth and in inducing synergism with interferon-gamma. Tretinoin 26-34 interferon gamma Homo sapiens 129-145
8243317-7 1993 Treatment of cultured ES cells with retinoic acid (100 nM) for 6 days increased GH-receptor mRNA levels (P < 0.01). Tretinoin 36-49 growth hormone receptor Mus musculus 80-91
8243317-12 1993 In conclusion, we have in the present study shown that germline competent ES cells and preimplantation mouse embryos express the GH receptor transcript and that this transcription is increased by retinoic acid in ES cells. Tretinoin 196-209 growth hormone receptor Mus musculus 129-140
8300756-0 1993 Estrogen receptor-negative breast cancer cells transfected with the estrogen receptor exhibit increased RAR alpha gene expression and sensitivity to growth inhibition by retinoic acid. Tretinoin 170-183 estrogen receptor 1 Homo sapiens 0-17
8300756-0 1993 Estrogen receptor-negative breast cancer cells transfected with the estrogen receptor exhibit increased RAR alpha gene expression and sensitivity to growth inhibition by retinoic acid. Tretinoin 170-183 estrogen receptor 1 Homo sapiens 68-85
8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 41-54 estrogen receptor 1 Homo sapiens 95-112
8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 41-54 estrogen receptor 1 Homo sapiens 114-116
8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 56-58 estrogen receptor 1 Homo sapiens 95-112
8300756-1 1993 We and others have shown previously that retinoic acid (RA) selectively inhibits the growth of estrogen receptor (ER)-positive human breast carcinoma (HBC) cells and ER-negative cells are refractory to RA inhibition of growth. Tretinoin 56-58 estrogen receptor 1 Homo sapiens 114-116
8300756-2 1993 The ER-negative cells inherently express lower levels of RAR alpha and retinoic acid response element (RARE)-mediated RA-induced CAT activity. Tretinoin 71-84 estrogen receptor 1 Homo sapiens 4-6
8300756-2 1993 The ER-negative cells inherently express lower levels of RAR alpha and retinoic acid response element (RARE)-mediated RA-induced CAT activity. Tretinoin 57-59 estrogen receptor 1 Homo sapiens 4-6
8300756-3 1993 In this study we report that when ER-negative MDA-MB-231 cells were transfected with the ER gene they not only expressed higher levels of RAR alpha and RARE-mediated RA-induced CAT gene expression, but their growth was not inhibited by RA. Tretinoin 138-140 estrogen receptor 1 Homo sapiens 34-36
7504151-5 1993 In cells in which TGF beta inhibited DNA synthesis, it also inhibited RA-induced granulocytic differentiation of APL cells and, to a greater degree, granulocytic differentiation induced by RA plus G-CSF. Tretinoin 70-72 transforming growth factor beta 1 Homo sapiens 18-26
8247127-2 1993 The pleiotropic effects of retinoids may be explained by the existence of complex signal transduction pathways involving diverse nuclear receptors of the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families, and at least two types of cellular retinoic acid binding proteins (CRABP-I and -II). Tretinoin 154-167 retinoic acid receptor beta Homo sapiens 178-181
8108182-0 1993 Induction of interleukin-8 expression in neuroblastoma cells by retinoic acid: implication of leukocyte chemotaxis and activation. Tretinoin 64-77 C-X-C motif chemokine ligand 8 Homo sapiens 13-26
8108182-6 1993 RA-treated but not untreated SK-N-SH cells expressed IL-8 mRNA in a time- and dose-dependent fashion. Tretinoin 0-2 C-X-C motif chemokine ligand 8 Homo sapiens 53-57
8108182-7 1993 As determined by ELISA, IL-8 levels were detectable in the culture supernatants from RA-treated, but not untreated, neuroblastoma cells (2.65 +/- 0.43 versus 0.05 +/- 0.04 ng/mL). Tretinoin 85-87 C-X-C motif chemokine ligand 8 Homo sapiens 24-28
8108182-10 1993 These results suggest that RA-induced neuroblastoma cell differentiation is associated with production of functional IL-8, which may be involved in the leukocyte infiltration and activation resulting in tumor regression. Tretinoin 27-29 C-X-C motif chemokine ligand 8 Homo sapiens 117-121
8308393-0 1993 [Midkine (MK): a retinoic acid-responsive, heparin-binding growth factor in relationship with differentiation, development, cancer and neural function]. Tretinoin 17-30 midkine Homo sapiens 1-8
8241133-4 1993 Following purification and thrombin cleavage, a predominant monomeric (stokes radius = 2.3 nm, molecular mass of 32 kDa) [3H]retinoic acid hRAR alpha LBD complex was characterized by high-performance size-exclusion chromatography. Tretinoin 125-138 coagulation factor II, thrombin Homo sapiens 27-35
8145770-7 1993 However, direct in vitro phosphorylation of hRAR alpha by PKC diminished its ability to form heterodimeric or homodimeric complexes on a retinoic acid response element, suggesting that the DNA-binding capacity of hRAR alpha in intact cells is indirectly controlled by a PKC-dependent mechanism. Tretinoin 137-150 protein kinase C alpha Homo sapiens 58-61
8121610-2 1993 We have examined the expression of retinoic acid receptors (RARs) in relation to neuroblastoma differentiation and show that short term exposure of SK N SH, SH SY 5Y AND GI LI N cells to physiological concentrations of retinoic acid results in induction of RAR-beta, particularly the lower transcript. Tretinoin 35-48 retinoic acid receptor beta Homo sapiens 257-265
8404646-10 1993 Retinoic acid reduced SP-A mRNA levels in a concentration-dependent manner (ANOVA, P < 0.02) and reduced SP-C mRNA levels at 3 microM. Tretinoin 0-13 surfactant protein C Homo sapiens 108-112
8218362-6 1993 In these studies a constitutively active PKC-gamma augmented the RA-mediated transactivation of a luciferase reporter containing the native RAR-beta promoter which has a retinoic-acid-response element (RARE). Tretinoin 65-67 retinoic acid receptor beta Homo sapiens 140-148
7521344-0 1993 Regulation of insulin-like growth factor (IGF) binding protein-5 in the T47D human breast carcinoma cell line by IGF-I and retinoic acid. Tretinoin 123-136 insulin like growth factor binding protein 5 Homo sapiens 14-64
7521344-9 1993 The inhibitory effect of RA, on the other hand, appears to be due primarily to regulation of IGFBP-5 mRNA levels. Tretinoin 25-27 insulin like growth factor binding protein 5 Homo sapiens 93-100
8216205-3 1993 In transient transfection assays, expression of COL1A2-CAT, a chimeric gene bearing 3500 bp upstream the bone/tendon transcription start site from the human alpha 2(I) gene fused to the CAT gene, is stimulated severalfold in RA-treated chondrocytes. Tretinoin 225-227 catalase Homo sapiens 55-58
8402688-10 1993 Conversely, stimulation of this I-type clone with retinoic acid resulted in an accumulation of N-type cells (which are thought to represent embryonic precursors of sympathetic neurons), decreased vimentin and beta-2-microglobulin, increased neurofilament-M, and a marked elevation in p26-Bcl-2. Tretinoin 50-63 BCL2 apoptosis regulator Homo sapiens 288-293
8216300-0 1993 Effects of synthetic retinoids and retinoic acid isomers on the expression of alkaline phosphatase in F9 teratocarcinoma cells. Tretinoin 35-48 alkaline phosphatase, placental Homo sapiens 78-98
8216300-1 1993 Expression of ALP in F9 teratocarcinoma cells is induced by all-trans retinoic acid (ATRA) (Gianni" et al., Biochem. Tretinoin 63-83 alkaline phosphatase, placental Homo sapiens 14-17
8216300-1 1993 Expression of ALP in F9 teratocarcinoma cells is induced by all-trans retinoic acid (ATRA) (Gianni" et al., Biochem. Tretinoin 85-89 alkaline phosphatase, placental Homo sapiens 14-17
8216205-3 1993 In transient transfection assays, expression of COL1A2-CAT, a chimeric gene bearing 3500 bp upstream the bone/tendon transcription start site from the human alpha 2(I) gene fused to the CAT gene, is stimulated severalfold in RA-treated chondrocytes. Tretinoin 225-227 catalase Homo sapiens 186-189
8216205-3 1993 In transient transfection assays, expression of COL1A2-CAT, a chimeric gene bearing 3500 bp upstream the bone/tendon transcription start site from the human alpha 2(I) gene fused to the CAT gene, is stimulated severalfold in RA-treated chondrocytes. Tretinoin 225-227 collagen type I alpha 2 chain Homo sapiens 48-54
8408229-5 1993 Retinoic acid at 10(-7) M, however, enhanced TNF-stimulated hepatocyte DNA synthesis and even more effectively the growth response to EGF. Tretinoin 0-13 tumor necrosis factor Mus musculus 45-48
8400267-1 1993 All-trans retinoic acid (ATRA) induces leukemic cell differentiation and complete remission (CR) in a high proportion of patients with acute promyelocytic leukemia (AML3 subtype). Tretinoin 0-23 RUNX family transcription factor 2 Homo sapiens 165-169
8400267-1 1993 All-trans retinoic acid (ATRA) induces leukemic cell differentiation and complete remission (CR) in a high proportion of patients with acute promyelocytic leukemia (AML3 subtype). Tretinoin 25-29 RUNX family transcription factor 2 Homo sapiens 165-169
8402622-0 1993 Human papillomavirus 16 immortalization of normal human ectocervical epithelial cells alters retinoic acid regulation of cell growth and epidermal growth factor receptor expression. Tretinoin 93-106 epidermal growth factor receptor Homo sapiens 137-169
8269032-0 1993 Involvement of transforming growth factor-alpha and its receptor in the growth response of cultured human epidermal cells to retinoic acid. Tretinoin 125-138 tumor necrosis factor Homo sapiens 15-47
8375477-7 1993 These results suggest that the mechanism of differentiation induced with NaB differs from that of RA; the former may be mediated by the junB gene and the latter by c-jun. Tretinoin 98-100 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 136-140
8395912-9 1993 Differentiation induced by protein kinase C activators 12-O-tetradecanoylphorbol 13-acetate and Bryostatin 1 or by all-trans retinoic acid was associated with a decrease in MPO mRNA in all 7 initially positive cell lines studied, even leading to the complete absence of transcripts, but the enzymatic activity of the differentiated cells was only slightly less than that of unstimulated cells. Tretinoin 125-138 myeloperoxidase Homo sapiens 173-176
8413217-0 1993 Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 133-143
8413217-0 1993 Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers. Tretinoin 0-13 nuclear factor kappa B subunit 1 Homo sapiens 145-148
8413217-4 1993 Region I binding activity was not present in undifferentiated NT2 cells, but binding of an NF-kappa B heterodimer, p50-p65, was induced following RA treatment. Tretinoin 146-148 nuclear factor kappa B subunit 1 Homo sapiens 91-101
8413217-4 1993 Region I binding activity was not present in undifferentiated NT2 cells, but binding of an NF-kappa B heterodimer, p50-p65, was induced following RA treatment. Tretinoin 146-148 nuclear factor kappa B subunit 1 Homo sapiens 115-118
8413217-6 1993 Region II binding activity was present in undifferentiated cells at low levels but was greatly augmented by RA treatment because of activation of a nuclear hormone receptor heterodimer composed of the retinoid X receptor (RXR beta) and the RA receptor (RAR beta). Tretinoin 108-110 retinoic acid receptor beta Homo sapiens 253-261
8243888-4 1993 This finding was extended with transient co-transfection experiments using a PKC-alpha expression vector which revealed that the PKC pathway can augment the activation of RAR-beta by RA. Tretinoin 171-173 protein kinase C alpha Homo sapiens 77-86
8243888-4 1993 This finding was extended with transient co-transfection experiments using a PKC-alpha expression vector which revealed that the PKC pathway can augment the activation of RAR-beta by RA. Tretinoin 171-173 protein kinase C alpha Homo sapiens 77-80
8243888-9 1993 In summary, these studies show that stimulation of the PKC second messenger pathway can modulate tumor differentiation and transcriptional activation of a retinoid receptor associated with RA response. Tretinoin 189-191 protein kinase C alpha Homo sapiens 55-58
8244449-0 1993 Retinoic acid induces changes in c-fgr proto-oncogene mRNA levels in Burkitt"s lymphoma cells. Tretinoin 0-13 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 33-38
8292531-0 1993 Localization of RIHB (retinoic acid-induced heparin-binding factor) transcript and protein during early chicken embryogenesis and in the developing wing. Tretinoin 22-35 midkine (neurite growth-promoting factor 2) Gallus gallus 16-20
8339256-3 1993 Neutrophilic granulocytes obtained by the addition of dimethyl sulfoxide or retinoic acid to the culture medium showed only slight changes in cellular glucocorticoid receptor levels and receptor-specific mRNA as compared to undifferentiated control cells. Tretinoin 76-89 nuclear receptor subfamily 3 group C member 1 Homo sapiens 151-174
8344391-0 1993 Retinoic acid-induced heparin-binding factor (RIHB) mRNA and protein are strongly induced in chick embryo chondrocytes treated with retinoic acid. Tretinoin 132-145 midkine (neurite growth-promoting factor 2) Gallus gallus 0-44
8344391-0 1993 Retinoic acid-induced heparin-binding factor (RIHB) mRNA and protein are strongly induced in chick embryo chondrocytes treated with retinoic acid. Tretinoin 132-145 midkine (neurite growth-promoting factor 2) Gallus gallus 46-50
8344391-2 1993 We have examined the induction of RIHB by retinoic acid in chondrocytes isolated from the sterna of Day 15 chick embryos and the effects of exogenous RIHB on these cells. Tretinoin 42-55 midkine (neurite growth-promoting factor 2) Gallus gallus 34-38
8344391-3 1993 There is an induction of RIHB mRNA in chondrocytes which is dose dependent, with maximal levels of expression observed with concentrations of retinoic acid in the 10(-6) M range. Tretinoin 142-155 midkine (neurite growth-promoting factor 2) Gallus gallus 25-29
8241025-0 1993 Retroviral gene transfer of epidermal growth factor receptor into HL60 cells results in a partial block of retinoic acid-induced granulocytic differentiation. Tretinoin 107-120 epidermal growth factor receptor Homo sapiens 28-60
8241025-12 1993 We found that these HL60-EGFR cells responded to retinoic acid differently from the HL60-control cells. Tretinoin 49-62 epidermal growth factor receptor Homo sapiens 25-29
8394351-4 1993 In several steps we converted the retinoid specific response element of the human retinoic acid receptor beta promoter into the vitamin D/retinoic acid response element of the human osteocalcin promoter. Tretinoin 82-95 bone gamma-carboxyglutamate protein Homo sapiens 182-193
8394351-7 1993 The responsiveness of the osteocalcin element to all-trans-retinoic acid is mediated neither by RAR homodimers nor by RAR-RXR heterodimers. Tretinoin 49-72 bone gamma-carboxyglutamate protein Homo sapiens 26-37
8394351-8 1993 However, a VDR-RAR heterodimer binds to the osteocalcin response element and mediates activation by all-trans-retinoic acid. Tretinoin 100-123 bone gamma-carboxyglutamate protein Homo sapiens 44-55
8244449-3 1993 In this paper we show that treatment of EBV-negative and EBV-positive BL cell lines with all-trans retinoic acid also stimulates an increase in c-fgr mRNA levels, varying between 2- and 13-fold depending on the cell line. Tretinoin 99-112 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 144-149
8244449-4 1993 An increase is detectable 12 to 48 h after treatment, depending on the cell line, suggesting that the c-fgr gene is not regulated directly by retinoic acid but responds to other retinoic acid-induced changes in the cell. Tretinoin 142-155 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 102-107
8244449-4 1993 An increase is detectable 12 to 48 h after treatment, depending on the cell line, suggesting that the c-fgr gene is not regulated directly by retinoic acid but responds to other retinoic acid-induced changes in the cell. Tretinoin 178-191 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 102-107
8393790-4 1993 In this work, we study the modulation by adrenergic stimuli, cAMP effectors and retinoic acid on the induction produced by insulin and 3,5,3"-triiodothyronine on malic-enzyme-gene expression. Tretinoin 80-93 insulin Homo sapiens 123-130
7689128-0 1993 Alkaline phosphatase activity in the human promyelocytic leukemia cell line, HL-60, induced by retinoic acid and recombinant human granulocyte colony-stimulating factor. Tretinoin 95-108 alkaline phosphatase, placental Homo sapiens 0-20
21573366-2 1993 The mutant (NR1-6) is aberrant in respect to morphology, tumorigenicity and response to retinoic acid (RA). Tretinoin 88-101 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 12-17
21573366-2 1993 The mutant (NR1-6) is aberrant in respect to morphology, tumorigenicity and response to retinoic acid (RA). Tretinoin 103-105 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 12-17
8360592-4 1993 RA differentially modulated the expression of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 mRNAs depending on the inducing stimulus. Tretinoin 0-2 interleukin 1 beta Homo sapiens 46-64
8360592-4 1993 RA differentially modulated the expression of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 mRNAs depending on the inducing stimulus. Tretinoin 0-2 interleukin 1 beta Homo sapiens 66-75
8360592-4 1993 RA differentially modulated the expression of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 mRNAs depending on the inducing stimulus. Tretinoin 0-2 interleukin 6 Homo sapiens 78-82
8360592-4 1993 RA differentially modulated the expression of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 mRNAs depending on the inducing stimulus. Tretinoin 0-2 C-X-C motif chemokine ligand 8 Homo sapiens 88-92
8360592-7 1993 IL-1-induced de novo synthesis of IL-6 protein and secretion of biologically active IL-6 were also inhibited by RA. Tretinoin 112-114 interleukin 1 beta Homo sapiens 0-4
8360592-7 1993 IL-1-induced de novo synthesis of IL-6 protein and secretion of biologically active IL-6 were also inhibited by RA. Tretinoin 112-114 interleukin 6 Homo sapiens 34-38
8360592-7 1993 IL-1-induced de novo synthesis of IL-6 protein and secretion of biologically active IL-6 were also inhibited by RA. Tretinoin 112-114 interleukin 6 Homo sapiens 84-88
8360592-8 1993 The inhibition pattern of RA was different from that of dexamethasone, which inhibited both IL-1 and LPS effects. Tretinoin 26-28 interleukin 1 beta Homo sapiens 92-96
8100485-0 1993 Interactions between interferon gamma and retinoic acid with transforming growth factor beta in the induction of immune recognition molecules. Tretinoin 42-55 transforming growth factor beta 1 Homo sapiens 61-92
8100485-15 1993 In contrast to IFN gamma-induced ICAM-1 expression, retinoic-acid-induced ICAM-1 expression was inhibited by TGF beta on two of the three responsive lines. Tretinoin 52-65 transforming growth factor beta 1 Homo sapiens 109-117
8392478-1 1993 Recently, we have shown that receptors for vitamin D3 (VDR), thyroid hormone (TR), and retinoic acid (RAR) activate preferentially through direct repeats (DRs) spaced by 3, 4, and 5 nucleotides, respectively. Tretinoin 87-100 RAB40B, member RAS oncogene family Homo sapiens 102-105
8391258-5 1993 This effect of RA on GSTP1 expression is mediated by the human beta-type RA receptor, hRAR beta, but not the chicken retinoid X receptor, cRXR. Tretinoin 15-17 retinoic acid receptor beta Homo sapiens 86-95
8506950-12 1993 Although RA by itself failed to stimulate extracellular matrix production, the addition of 3 mumol/L RA to basal medium containing 1.4 mmol/L Ca2+ led to a further increase in fibronectin production over that seen in the presence of 1.4 mmol/L Ca2+ alone. Tretinoin 101-103 fibronectin 1 Homo sapiens 176-187
8344702-0 1993 Effect of retinoic acid and vitamin D on the expression of interleukin-1 beta, tumour necrosis factor-alpha and interleukin-6 in the human monocytic cell line U937. Tretinoin 10-23 interleukin 1 beta Homo sapiens 59-77
7689318-3 1993 AFP has been shown to bind various ligands in vitro including fatty acids, estrogens, thyroid hormones and retinoic acids. Tretinoin 107-121 alpha fetoprotein Homo sapiens 0-3
7689318-8 1993 The presence of nine such hydrophobic repeats in the third domain of the AFP molecule mimics the heptad dimerization repeats found in the retinoic acid, thyroid, c-erbA and other members of the nuclear receptor superfamily. Tretinoin 138-151 alpha fetoprotein Homo sapiens 73-76
8504933-6 1993 Unexpectedly, the major retinoic acid response element is absolutely dependent on Pit-1 for retinoic acid receptor function. Tretinoin 24-37 POU domain, class 1, transcription factor 1 Mus musculus 82-87
8344702-0 1993 Effect of retinoic acid and vitamin D on the expression of interleukin-1 beta, tumour necrosis factor-alpha and interleukin-6 in the human monocytic cell line U937. Tretinoin 10-23 interleukin 6 Homo sapiens 112-125
8388633-7 1993 Differentiation by exposure to 1 microM retinoic acid for 6 days caused a 15-fold increase in the synthesis of the NHE-1 protein. Tretinoin 40-53 solute carrier family 9 member A1 Homo sapiens 115-120
7684042-12 1993 The addition of RA also blocked IGF-I stimulation of IGFBP-2 and IGFBP-5 levels. Tretinoin 16-18 insulin like growth factor 1 Homo sapiens 32-37
7684042-12 1993 The addition of RA also blocked IGF-I stimulation of IGFBP-2 and IGFBP-5 levels. Tretinoin 16-18 insulin like growth factor binding protein 5 Homo sapiens 65-72
8497061-2 1993 Exposure to HBV suppressed the ability of HL-60 cells to differentiate into granulocytes after treatment with retinoic acid (RA) or dimethyl sulfoxide (DMSO), and RA-induced activation of the monocytic cell line THP-1 was also suppressed. Tretinoin 163-165 GLI family zinc finger 2 Homo sapiens 212-217
8481912-7 1993 We investigated the ability of liposomal ATRA (L-ATRA) to induce differentiation of human myeloid leukemia cell lines (HL-60, KG-1, and THP-1). Tretinoin 41-45 GLI family zinc finger 2 Homo sapiens 136-141
8395280-2 1993 The expressed recombinant RARs (rRARs: rRAR alpha/E, rRAR beta/E and rRAR gamma) showed nearly the same magnitude of binding affinity toward [3H]retinoic acid (RA) as hRARs extracted from human cells (Ka values: 6.0 x 10(9) M-1 for rRAR alpha/E and 2.7 x 10(10) M-1 for both rRAR beta/E and rRAR gamma). Tretinoin 145-158 retinoic acid receptor, beta Rattus norvegicus 53-62
8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 320-333 transforming growth factor beta 1 Homo sapiens 28-61
8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 320-333 transforming growth factor beta 1 Homo sapiens 63-73
8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 335-337 transforming growth factor beta 1 Homo sapiens 28-61
8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 335-337 transforming growth factor beta 1 Homo sapiens 63-73
8476634-0 1993 Retinoic acid and calcium regulation of p53, transforming growth factor-beta 1, and transforming growth factor-alpha gene expression and growth in adenovirus 12-SV40-transformed human tracheal gland epithelial cells. Tretinoin 0-13 tumor protein p53 Homo sapiens 40-43
8476634-0 1993 Retinoic acid and calcium regulation of p53, transforming growth factor-beta 1, and transforming growth factor-alpha gene expression and growth in adenovirus 12-SV40-transformed human tracheal gland epithelial cells. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 45-78
8476634-0 1993 Retinoic acid and calcium regulation of p53, transforming growth factor-beta 1, and transforming growth factor-alpha gene expression and growth in adenovirus 12-SV40-transformed human tracheal gland epithelial cells. Tretinoin 0-13 tumor necrosis factor Homo sapiens 84-116
8476634-10 1993 RA inhibited both cell proliferation and AIG growth, which was accompanied by enhanced expression of p53. Tretinoin 0-2 tumor protein p53 Homo sapiens 101-104
8386680-4 1993 The mRNA level of PP2A beta was markedly decreased within 5 h after addition of ATRA, but there was only a slight increase in the mRNA level of PP2A alpha. Tretinoin 80-84 protein phosphatase 2 catalytic subunit beta Homo sapiens 18-27
8386680-5 1993 Selective down-regulation of PP2A beta mRNA clearly preceded the cell differentiation induced by ATRA treatment. Tretinoin 97-101 protein phosphatase 2 catalytic subunit beta Homo sapiens 29-38
8476634-12 1993 These results demonstrate that RA regulates growth of HTGE cells mainly by upregulating the p53 gene; Ca2+, which enhances TGF-beta 1 expression, had no effect on growth. Tretinoin 31-33 tumor protein p53 Homo sapiens 92-95
8385674-2 1993 This study compared the effects of TGF-beta 1 and BMP 4 on the gene expression of a retinoic acid (RA) responsive rat clonal preosteoblast cell line, UMR 201, as well as the way in which these proteins interact with RA in these cells. Tretinoin 84-97 transforming growth factor, beta 1 Rattus norvegicus 35-45
8384988-1 1993 The retinoic acid (RA) receptor-beta (RAR beta) gene is dramatically up-regulated by RA in F9 teratocarcinoma cells due to the presence of an RA-responsive element (RARE) in its promoter. Tretinoin 19-21 retinoic acid receptor, beta Rattus norvegicus 38-46
8384988-1 1993 The retinoic acid (RA) receptor-beta (RAR beta) gene is dramatically up-regulated by RA in F9 teratocarcinoma cells due to the presence of an RA-responsive element (RARE) in its promoter. Tretinoin 38-40 retinoic acid receptor, beta Rattus norvegicus 4-36
8385674-2 1993 This study compared the effects of TGF-beta 1 and BMP 4 on the gene expression of a retinoic acid (RA) responsive rat clonal preosteoblast cell line, UMR 201, as well as the way in which these proteins interact with RA in these cells. Tretinoin 99-101 transforming growth factor, beta 1 Rattus norvegicus 35-45
8455608-5 1993 Retinoic acid-induced differentiation of mouse F9 cells into visceral or parietal endoderm is accompanied by increased expression of GATA-4 mRNA and protein. Tretinoin 0-13 GATA binding protein 4 Mus musculus 133-139
8455608-7 1993 We conclude that GATA-4 is a tissue-specific, retinoic acid-inducible, and developmentally regulated transcription factor. Tretinoin 46-59 GATA binding protein 4 Mus musculus 17-23
8466530-0 1993 Effect of retinoic acid on osteocalcin gene expression in human osteoblasts. Tretinoin 10-23 bone gamma-carboxyglutamate protein Homo sapiens 27-38
8385052-5 1993 Northern blot hybridization demonstrated a moderate induction of u-PA and u-PAR mRNA in bovine aortic endothelial cells after treatment with 10 nM and 1 microM retinoic acid for 8 hours. Tretinoin 160-173 plasminogen activator, urokinase receptor Bos taurus 74-79
8466530-3 1993 Our studies, carried out on primary cultures of human osteoblasts, have demonstrated for the first time the activation of the osteocalcin gene expression by retinoic acid. Tretinoin 157-170 bone gamma-carboxyglutamate protein Homo sapiens 126-137
8383004-0 1993 Lipid hydroperoxides greatly increase the rate of oxidative catabolism of all-trans-retinoic acid by human cell culture microsomes genetically enriched in specified cytochrome P-450 isoforms. Tretinoin 74-97 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 165-181
8383004-1 1993 Cytochrome P-450 enzymes have been implicated in the oxidative catabolism of all-trans-retinoic acid (RA), a process that is accelerated by exposure to RA in cultured cells and rodents, and also in patients receiving RA as treatment for cancer (J.F.R. Tretinoin 80-100 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-16
8384124-3 1993 Spontaneous and RA-induced differentiation into normal and leukemic macrophages induced a progressive loss of cAMP production and regulation of superoxide anion production by VIP and related peptides. Tretinoin 16-18 vasoactive intestinal peptide Homo sapiens 175-178
8383004-1 1993 Cytochrome P-450 enzymes have been implicated in the oxidative catabolism of all-trans-retinoic acid (RA), a process that is accelerated by exposure to RA in cultured cells and rodents, and also in patients receiving RA as treatment for cancer (J.F.R. Tretinoin 102-104 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-16
8383004-1 1993 Cytochrome P-450 enzymes have been implicated in the oxidative catabolism of all-trans-retinoic acid (RA), a process that is accelerated by exposure to RA in cultured cells and rodents, and also in patients receiving RA as treatment for cancer (J.F.R. Tretinoin 152-154 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-16
8383004-1 1993 Cytochrome P-450 enzymes have been implicated in the oxidative catabolism of all-trans-retinoic acid (RA), a process that is accelerated by exposure to RA in cultured cells and rodents, and also in patients receiving RA as treatment for cancer (J.F.R. Tretinoin 152-154 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-16
7680579-8 1993 Results on CD34+ BM fractions (substantially reduced in accessory cells) demonstrate that the described effects can probably be attributed to the direct action of RA on these progenitors; single progenitor (CD34+) cell liquid cultures further prove this point. Tretinoin 163-165 CD34 molecule Homo sapiens 11-15
8445950-6 1993 The results also demonstrate that ATRA-induced c-fms expression is potentiated by exposure to tumor necrosis factor alpha (TNF alpha) or dibutyryl cyclic adenosine monophosphate (cAMP). Tretinoin 34-38 tumor necrosis factor Homo sapiens 94-121
8445950-6 1993 The results also demonstrate that ATRA-induced c-fms expression is potentiated by exposure to tumor necrosis factor alpha (TNF alpha) or dibutyryl cyclic adenosine monophosphate (cAMP). Tretinoin 34-38 tumor necrosis factor Homo sapiens 123-132
8094032-9 1993 A 24-h incubation in the presence of retinoic acid or IFN-gamma strongly inhibited activation and translocation of PKC by PMA. Tretinoin 37-50 proline rich transmembrane protein 2 Homo sapiens 115-118
8453995-2 1993 The RAR-beta and MK genes were induced specifically by RA treatment, which indicates that these two genes are solely RA responsive. Tretinoin 55-57 retinoic acid receptor beta Homo sapiens 4-12
7680553-4 1993 A substantial decrease in binding of K-FGF was found to occur upon RA-induced differentiation of the cells. Tretinoin 67-69 fibroblast growth factor 4 Homo sapiens 37-42
7679109-0 1993 The long terminal repeat of VL30 retrotransposons contains sequences that determine retinoic acid-induced transcription in cultured keratinocytes. Tretinoin 84-97 RIKEN cDNA A130040M12 gene Mus musculus 28-32
7679109-2 1993 We show that cultured mouse keratinocytes (Balb/MK) responded to RA with induced expression of VL30 retrotransposons. Tretinoin 65-67 RIKEN cDNA A130040M12 gene Mus musculus 95-99
7679109-4 1993 The long terminal repeat of a VL30 retrotransposon, expressed in mouse epidermis in vivo, was found to contain two RA-responsive elements (RREs) that independently conferred RA responsiveness on a heterologous promoter in both cultured Balb/MK cells and normal human keratinocytes. Tretinoin 115-117 RIKEN cDNA A130040M12 gene Mus musculus 30-34
7679109-4 1993 The long terminal repeat of a VL30 retrotransposon, expressed in mouse epidermis in vivo, was found to contain two RA-responsive elements (RREs) that independently conferred RA responsiveness on a heterologous promoter in both cultured Balb/MK cells and normal human keratinocytes. Tretinoin 174-176 RIKEN cDNA A130040M12 gene Mus musculus 30-34
7680579-8 1993 Results on CD34+ BM fractions (substantially reduced in accessory cells) demonstrate that the described effects can probably be attributed to the direct action of RA on these progenitors; single progenitor (CD34+) cell liquid cultures further prove this point. Tretinoin 163-165 CD34 molecule Homo sapiens 207-211
8382032-4 1993 Exposure of LA1-15n cells to RA leads to the induction of a approximately 2.9-kb RAR beta mRNA, whereas the expression of transcripts for RARs alpha and gamma does not change appreciably. Tretinoin 29-31 retinoic acid receptor beta Homo sapiens 81-89
8382032-14 1993 They also demonstrate that RA markedly influences the expression of steady-state levels of mRNA for one of its own receptors, the RAR beta. Tretinoin 27-29 retinoic acid receptor beta Homo sapiens 130-138
8382035-6 1993 RA competed with the binding of CD 367 to CRABP-I and CRABP-II with IC50 values of 20.0 and 90.0 nM, respectively. Tretinoin 0-2 C-type lectin domain family 4 member A Homo sapiens 32-38
8382035-7 1993 Retinoid analogs competed with the binding of CD 367 to CRABP-I and CRABP-II in the following order: (p-[(E)-2-(5,6,7,8-tetrahydro-5,5,8,8- tetramethyl-2-naphtyl)-1-propenyl]-benzoic acid (TTNPB) > 4-oxo-RA > 4-OH-RA > 13-cis-RA = 9-cis-RA. Tretinoin 57-59 C-type lectin domain family 4 member A Homo sapiens 46-52
8425196-10 1993 Retinoic acid, dexamethasone, or forskolin inhibits induction of anchorage independence by tumor necrosis factor alpha, interleukin 1 alpha, and transfected v-jun. Tretinoin 0-13 tumor necrosis factor Mus musculus 91-118
8382933-8 1993 These RA effects on ER and VDR seem to be specific, since glucocorticoid receptor quantities were not affected by RA treatment. Tretinoin 6-8 nuclear receptor subfamily 3, group C, member 1 Mus musculus 58-81
8381540-9 1993 Together with the known effects of retinoic acid on differentiation and carcinogenesis, our results support the hypothesis that RAR beta functions as a tumor suppressor gene in epidermoid lung tumorigenesis. Tretinoin 35-48 retinoic acid receptor beta Homo sapiens 128-136
7748347-6 1993 Retinoic acid treatment was able to induce Adh-1 mRNA in 10.5-day mouse embryos and also in mouse F9 embryonal carcinoma cells. Tretinoin 0-13 alcohol dehydrogenase 1 (class I) Mus musculus 43-48
8440324-2 1993 Exposure of such cells to transforming growth factor-beta 1 (TGF-beta 1) in secondary culture under serum-free and RA-free, defined conditions led to reexpression of the differentiated phenotype. Tretinoin 115-117 LOW QUALITY PROTEIN: transforming growth factor beta-1 Oryctolagus cuniculus 26-59
8440324-2 1993 Exposure of such cells to transforming growth factor-beta 1 (TGF-beta 1) in secondary culture under serum-free and RA-free, defined conditions led to reexpression of the differentiated phenotype. Tretinoin 115-117 LOW QUALITY PROTEIN: transforming growth factor beta-1 Oryctolagus cuniculus 61-71
8385738-8 1993 Furthermore, BMP-2 and -4 expression are decreased after treatment with retinoic acid, whereas vgr-1/BMP-6 expression is induced in C26 cells, but decreased in 10T1/2 cells. Tretinoin 72-85 bone morphogenetic protein 2 Mus musculus 13-25
8096334-0 1993 VIP potentiates retinoic-acid effect on tissue transglutaminase activity in human neuroblastoma, the SK-N-SH cells. Tretinoin 16-29 vasoactive intestinal peptide Homo sapiens 0-3
8096334-0 1993 VIP potentiates retinoic-acid effect on tissue transglutaminase activity in human neuroblastoma, the SK-N-SH cells. Tretinoin 16-29 transglutaminase 2 Homo sapiens 40-63
8096334-1 1993 Tissue transglutaminase (tTG) activity was used to test the potent regulatory role of vasoactive intestinal peptide (VIP) on Retinoic Acid-induced effect in human neuroblastoma cell line. Tretinoin 125-138 vasoactive intestinal peptide Homo sapiens 117-120
8096334-3 1993 VIP alone was a potent differentiating agent in SK-N-SH cells but in the presence of retinoic acid (RA), this peptide rather potentiates RA-induced tTG activity which is now considered as an apoptosis marker in neuroblastoma cell line. Tretinoin 137-139 vasoactive intestinal peptide Homo sapiens 0-3
8096334-3 1993 VIP alone was a potent differentiating agent in SK-N-SH cells but in the presence of retinoic acid (RA), this peptide rather potentiates RA-induced tTG activity which is now considered as an apoptosis marker in neuroblastoma cell line. Tretinoin 137-139 transglutaminase 2 Homo sapiens 148-151
8380989-3 1993 Differentiation of HL-60 cells into granulocyte-like cells with dimethyl sulphoxide (Me2SO), retinoic acid or dibutyryl cyclic AMP (Bt2-cAMP) resulted in a 2-3-fold increase in 5-lipoxygenase enzyme activity and a 4-fold increase in leukotriene B4 synthesis. Tretinoin 93-106 arachidonate 5-lipoxygenase Homo sapiens 177-191
7678784-1 1993 It was previously demonstrated that retinoic acid (RA) can enhance the functional responses of human T lymphocytes by increasing surface IL-2R alpha chain protein expression on proliferating T blasts, resulting in augmented IL-2-dependent growth. Tretinoin 36-49 interleukin 2 Homo sapiens 137-141
7682522-8 1993 However, this does not represent a general defect in positive regulation of gene expression by retinoids, since in a transient transfection assay trans-retinoic acid positively regulates a reporter plasmid containing the retinoid response element from the retinoic acid receptor-beta gene. Tretinoin 146-165 retinoic acid receptor beta Homo sapiens 256-283
7678784-1 1993 It was previously demonstrated that retinoic acid (RA) can enhance the functional responses of human T lymphocytes by increasing surface IL-2R alpha chain protein expression on proliferating T blasts, resulting in augmented IL-2-dependent growth. Tretinoin 51-53 interleukin 2 Homo sapiens 137-141
7678784-2 1993 In the present study, we used IL-2-maintained lymphoblasts generated from human thymocytes to show that RA enhancement of IL-2R alpha is accompanied by an increase in steady-state levels of IL-2R alpha mRNA. Tretinoin 104-106 interleukin 2 Homo sapiens 30-34
7678784-6 1993 In addition to inducing IL-2R alpha expression, RA also increased the surface expression and mRNA levels of IL-2R beta, the 75-kDa component of the IL-2 receptor that mediates IL-2 signal transduction. Tretinoin 48-50 interleukin 2 Homo sapiens 24-28
7678784-6 1993 In addition to inducing IL-2R alpha expression, RA also increased the surface expression and mRNA levels of IL-2R beta, the 75-kDa component of the IL-2 receptor that mediates IL-2 signal transduction. Tretinoin 48-50 interleukin 2 Homo sapiens 108-112
7678784-7 1993 These new findings showing regulation by RA of both IL-2R alpha and IL-2R beta suggest multiple pathways by which this retinoid can modulate functional IL-2 receptors. Tretinoin 41-43 interleukin 2 Homo sapiens 52-56
8418375-16 1993 Further prospective studies are needed in order to confirm the persistence of thrombin activation in course of ATRA therapy. Tretinoin 111-115 coagulation factor II, thrombin Homo sapiens 78-86
8382939-8 1993 delta 1 receptor message is increased on amputation, but does not exhibit a pronounced differential distribution along the proximal-distal axis in normal and regenerating limbs, nor does it show a persistent alteration in expression levels following a dose of retinoic acid sufficient to respecify position. Tretinoin 260-273 delta like non-canonical Notch ligand 1 Homo sapiens 0-7
8502130-0 1993 Alkaline phosphatase activity during sphinganine potentiation of retinoic acid-induced differentiation of human promyelocytic leukemia cell line, HL-60. Tretinoin 65-78 alkaline phosphatase, placental Homo sapiens 0-20
8502130-3 1993 In cells exposed to RA alone for only a period of 24h, the ALP activity could still increase and reach a similar maximum ALP activity (8.5-10.0 units/mg protein) at 48h as it was under continuous RA treatment. Tretinoin 20-22 alkaline phosphatase, placental Homo sapiens 59-62
8502130-3 1993 In cells exposed to RA alone for only a period of 24h, the ALP activity could still increase and reach a similar maximum ALP activity (8.5-10.0 units/mg protein) at 48h as it was under continuous RA treatment. Tretinoin 20-22 alkaline phosphatase, placental Homo sapiens 121-124
8502130-3 1993 In cells exposed to RA alone for only a period of 24h, the ALP activity could still increase and reach a similar maximum ALP activity (8.5-10.0 units/mg protein) at 48h as it was under continuous RA treatment. Tretinoin 196-198 alkaline phosphatase, placental Homo sapiens 59-62
8502130-3 1993 In cells exposed to RA alone for only a period of 24h, the ALP activity could still increase and reach a similar maximum ALP activity (8.5-10.0 units/mg protein) at 48h as it was under continuous RA treatment. Tretinoin 196-198 alkaline phosphatase, placental Homo sapiens 121-124
8502130-4 1993 In all cells with longer exposures (24-96h) to RA, SP pre-treatment increased ALP activity to more or less the same higher maximum (14.0-15.5 units/mg protein). Tretinoin 47-49 alkaline phosphatase, placental Homo sapiens 78-81
8350952-0 1993 Modulation of leukosialin (sialophorin, CD43 antigen) on the cell surface of human hematopoietic cell lines induced by cytokins, retinoic acid and 1,25(OH)2-vitamin D3. Tretinoin 129-142 sialophorin Homo sapiens 27-38
7507222-3 1993 All-trans retinoic acid weakly down-regulated cell surface protectin on K-562, while 1,25(OH)2-vitamin D3 produced such effect on HL-60 cells. Tretinoin 10-23 CD59 molecule (CD59 blood group) Homo sapiens 59-68
7691069-9 1993 By contrast, RAR beta was expressed in only seven RA-resistant cell lines (Saos-2, ACHN, 293, A549, A-375, A673, and PA-1), and its level was enhanced by RA in some cases. Tretinoin 13-15 PAXIP1 associated glutamate rich protein 1 Homo sapiens 117-121
7691069-9 1993 By contrast, RAR beta was expressed in only seven RA-resistant cell lines (Saos-2, ACHN, 293, A549, A-375, A673, and PA-1), and its level was enhanced by RA in some cases. Tretinoin 50-52 retinoic acid receptor beta Homo sapiens 13-21
8350952-0 1993 Modulation of leukosialin (sialophorin, CD43 antigen) on the cell surface of human hematopoietic cell lines induced by cytokins, retinoic acid and 1,25(OH)2-vitamin D3. Tretinoin 129-142 sialophorin Homo sapiens 40-44
8350952-4 1993 Retinoic acid down-regulated leukosialin on both U-937 monocyte-like cells and the CALLA+ ALL cell line REH. Tretinoin 0-13 membrane metalloendopeptidase Homo sapiens 83-88
8489769-3 1993 Radioimmunoassay showed that after stimulation by RA, the IL-1 beta intracellular level is predominantly increased, with no significant modification of IL-1 alpha expression. Tretinoin 50-52 interleukin 1 beta Homo sapiens 58-67
8489769-4 1993 The addition of hydrocortisone in the culture medium resulted in a decrease in RA-induced IL-1 beta overexpression, without notable modifications in untreated cultures. Tretinoin 79-81 interleukin 1 beta Homo sapiens 90-99
8489769-6 1993 The overexpression of IL-1 beta in control and RA-treated cultures mainly concerned the 52- and 31- to 36-kD biologically inactive precursor forms. Tretinoin 47-49 interleukin 1 beta Homo sapiens 22-31
8489769-8 1993 These findings indicate that in cultured keratinocytes intracellular IL-1 beta is preferentially increased by RA but in its immature forms. Tretinoin 110-112 interleukin 1 beta Homo sapiens 69-78
1428232-0 1992 Regulation of androgen receptor gene expression by steroids and retinoic acid in human breast-cancer cells. Tretinoin 64-77 androgen receptor Homo sapiens 14-31
1330076-3 1992 The approximate 50% downregulation of TM antigen and cofactor activity induced by TNF-alpha (10 U/mL for 24 hours) was completely prevented when the cells were coincubated with both TNF-alpha and 10 mumol/L RA. Tretinoin 207-209 tumor necrosis factor Homo sapiens 82-91
1330076-4 1992 In accordance with changes in cell surface TM antigen levels, the 70% decrease in TM messenger RNA (mRNA) induced by TNF-alpha was also prevented by 10 mumol/L RA. Tretinoin 160-162 tumor necrosis factor Homo sapiens 117-126
1330076-7 1992 The effects of RA on the regulation of TM and TF expression in the cells exposed to TNF-alpha was dose-dependent from 0.01 to 10 mumol/L RA. Tretinoin 15-17 tumor necrosis factor Homo sapiens 84-93
1330076-7 1992 The effects of RA on the regulation of TM and TF expression in the cells exposed to TNF-alpha was dose-dependent from 0.01 to 10 mumol/L RA. Tretinoin 137-139 tumor necrosis factor Homo sapiens 84-93
1330076-8 1992 The present results suggest that RA may affect on the mRNA level to alter TM and TF expression, effectively counteracting expression of prothrombotic properties of endothelial cells induced by inflammatory cytokines such as TNF-alpha. Tretinoin 33-35 tumor necrosis factor Homo sapiens 224-233
1361214-4 1992 Here we follow the changes induced by retinoic acid to hindbrain segmentation and the branchial arches using transgenic mice which contain lacZ reporter genes that reveal the endogenous segment-restricted expression of the Hox-B1 (Hox-2.9), Hox-B2(Hox-2.8) and Krox-20 genes. Tretinoin 38-51 homeobox B2 Mus musculus 241-247
1361214-4 1992 Here we follow the changes induced by retinoic acid to hindbrain segmentation and the branchial arches using transgenic mice which contain lacZ reporter genes that reveal the endogenous segment-restricted expression of the Hox-B1 (Hox-2.9), Hox-B2(Hox-2.8) and Krox-20 genes. Tretinoin 38-51 homeobox B2 Mus musculus 248-255
1280130-0 1992 Insulin-like growth factor binding protein-5 gene expression is differentially regulated at a post-transcriptional level in retinoic acid-sensitive and resistant MCF-7 human breast carcinoma cells. Tretinoin 124-137 insulin like growth factor binding protein 5 Homo sapiens 0-44
1446821-8 1992 Treatment of TM4 cells with retinoic acid (RA) increases the level of LNGFR mRNA twofold, while testosterone treatment results in a tenfold decrease. Tretinoin 28-41 nerve growth factor receptor (TNFR superfamily, member 16) Mus musculus 70-75
1446821-8 1992 Treatment of TM4 cells with retinoic acid (RA) increases the level of LNGFR mRNA twofold, while testosterone treatment results in a tenfold decrease. Tretinoin 43-45 nerve growth factor receptor (TNFR superfamily, member 16) Mus musculus 70-75
1362830-4 1992 Treatment of normal skin with retinoic acid, increasing epidermal thickness in some subjects, led to an increased expression of loricrin. Tretinoin 30-43 loricrin cornified envelope precursor protein Homo sapiens 128-136
1428232-3 1992 Dexamethasone (Dex), Organon 2058 (Org 2058), dihydrotestosterone (DHT), and all-trans-retinoic acid (RA) down-regulated AR mRNA levels in T-47D (ER+, PR+) cells 6 hr after treatment, whereas oestradiol (E2) had no effect. Tretinoin 77-100 androgen receptor Homo sapiens 121-123
1428232-3 1992 Dexamethasone (Dex), Organon 2058 (Org 2058), dihydrotestosterone (DHT), and all-trans-retinoic acid (RA) down-regulated AR mRNA levels in T-47D (ER+, PR+) cells 6 hr after treatment, whereas oestradiol (E2) had no effect. Tretinoin 102-104 androgen receptor Homo sapiens 121-123
1428232-7 1992 The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. Tretinoin 36-38 androgen receptor Homo sapiens 23-25
1428232-7 1992 The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. Tretinoin 36-38 androgen receptor Homo sapiens 171-173
1428232-7 1992 The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. Tretinoin 184-186 androgen receptor Homo sapiens 23-25
1428232-7 1992 The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. Tretinoin 184-186 androgen receptor Homo sapiens 171-173
1332684-8 1992 The RA metabolites 4-hydroxy-RA and 4-oxo-RA were poor competitors for [3H]CD367 binding to recombinant RAR-gamma 1 (K(i) > 1 microM), indicating that 4-oxidation of RA greatly reduces its affinity for RAR-gamma 1. Tretinoin 29-31 C-type lectin domain family 4 member A Homo sapiens 75-80
1332684-8 1992 The RA metabolites 4-hydroxy-RA and 4-oxo-RA were poor competitors for [3H]CD367 binding to recombinant RAR-gamma 1 (K(i) > 1 microM), indicating that 4-oxidation of RA greatly reduces its affinity for RAR-gamma 1. Tretinoin 4-6 C-type lectin domain family 4 member A Homo sapiens 75-80
1363506-5 1992 U937 cells exposed to retinoic acid (RA) for 4 days or to phorbol myristate acetate (PMA) for 2 days acquired characteristics of macrophages, including the capacity to produce superoxide (O2-), responsiveness to formyl-methionyl-leucyl-phenylalanine (fMLP) and reduced proliferation. Tretinoin 22-35 formyl peptide receptor 1 Homo sapiens 251-255
1363506-5 1992 U937 cells exposed to retinoic acid (RA) for 4 days or to phorbol myristate acetate (PMA) for 2 days acquired characteristics of macrophages, including the capacity to produce superoxide (O2-), responsiveness to formyl-methionyl-leucyl-phenylalanine (fMLP) and reduced proliferation. Tretinoin 37-39 formyl peptide receptor 1 Homo sapiens 251-255
1384800-0 1992 Retinoic acid inhibits interleukin-6-induced macrophage differentiation and apoptosis in a murine hematopoietic cell line, Y6. Tretinoin 0-13 interleukin 6 Mus musculus 23-36
1384800-3 1992 Retinoic acid (RA) inhibited such effects of IL-6 on Y6 cells. Tretinoin 0-13 interleukin 6 Mus musculus 45-49
1332684-10 1992 RAR-gamma 1 species expressed from recombinant baculovirus (in Sf9 cells) and vaccinia virus (in HeLa cells) exhibited similar affinities for RA and CD367 and had comparable DNA-binding properties in gel-retardation experiments. Tretinoin 0-2 C-type lectin domain family 4 member A Homo sapiens 149-154
1384800-3 1992 Retinoic acid (RA) inhibited such effects of IL-6 on Y6 cells. Tretinoin 15-17 interleukin 6 Mus musculus 45-49
1384800-4 1992 The inhibitory effect of RA on the effects of IL-6 was not caused by the downregulation of the IL-6 receptor, because RA neither affected the expression of IL-6 receptor mRNA nor the expression of IL-6 receptor molecule on the cell surface. Tretinoin 25-27 interleukin 6 Mus musculus 46-50
1334692-0 1992 Retinoic acid induces secretion of latent transforming growth factor beta 1 and beta 2 in normal and human papillomavirus type 16-immortalized human keratinocytes. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 42-73
1384800-6 1992 IL-6-induced macrophage differentiation of Y6 cells was preceded by the downregulation of the c-myc gene, which was also prevented by RA. Tretinoin 134-136 interleukin 6 Mus musculus 0-4
1384800-7 1992 Because the inhibitory effect of RA on Y6 cells was reversible and seemed not to require de novo protein synthesis, the RA receptor by itself might be directly involved in the inhibition of the IL-6 signal transduction pathway. Tretinoin 33-35 interleukin 6 Mus musculus 194-198
1334692-2 1992 We investigated the ability of RA to modulate the production of TGF-beta in normal human keratinocytes (HKc) and HKc lines immortalized by transfection with human papillomavirus type 16 DNA (HKc/HPV16). Tretinoin 31-33 transforming growth factor beta 1 Homo sapiens 64-72
1334692-3 1992 RA treatment of both normal HKc and HKc/HPV16 resulted in a 2-3-fold induction in secreted levels of latent TGF-beta. Tretinoin 0-2 transforming growth factor beta 1 Homo sapiens 108-116
1334692-4 1992 The induction in TGF-beta secretion by RA was dose dependent, with significant increases observed with RA concentrations as low as 1-10 nM, and time dependent, with maximal induction occurring about 3 days after initiation of RA exposure. Tretinoin 39-41 transforming growth factor beta 1 Homo sapiens 17-25
1334692-4 1992 The induction in TGF-beta secretion by RA was dose dependent, with significant increases observed with RA concentrations as low as 1-10 nM, and time dependent, with maximal induction occurring about 3 days after initiation of RA exposure. Tretinoin 103-105 transforming growth factor beta 1 Homo sapiens 17-25
1334692-4 1992 The induction in TGF-beta secretion by RA was dose dependent, with significant increases observed with RA concentrations as low as 1-10 nM, and time dependent, with maximal induction occurring about 3 days after initiation of RA exposure. Tretinoin 103-105 transforming growth factor beta 1 Homo sapiens 17-25
1334692-5 1992 In addition, RA induced intracellular levels of TGF-beta almost 5-fold. Tretinoin 13-15 transforming growth factor beta 1 Homo sapiens 48-56
1334692-8 1992 Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced specific transcripts for TGF-beta 1 and TGF-beta 2 about 3- and 50-fold, respectively. Tretinoin 73-75 transforming growth factor beta 1 Homo sapiens 119-127
1334692-8 1992 Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced specific transcripts for TGF-beta 1 and TGF-beta 2 about 3- and 50-fold, respectively. Tretinoin 73-75 transforming growth factor beta 1 Homo sapiens 134-142
1334692-11 1992 These studies indicate that RA may regulate growth control in both normal HKc and HKc/HPV16 by enhancing TGF-beta 1 and TGF-beta 2 production, which, after activation at the cell surface, could inhibit cellular proliferation in an autocrine and/or paracrine manner. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 105-113
1334692-11 1992 These studies indicate that RA may regulate growth control in both normal HKc and HKc/HPV16 by enhancing TGF-beta 1 and TGF-beta 2 production, which, after activation at the cell surface, could inhibit cellular proliferation in an autocrine and/or paracrine manner. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 120-128
1430209-0 1992 Induction of thrombospondin 1 by retinoic acid is important during differentiation of neuroblastoma cells. Tretinoin 33-46 thrombospondin 1 Homo sapiens 13-29
1478921-6 1992 PKC inhibitor H7 inhibited MRP synthesis in HL-60 cells treated with RA and 1 alpha,25(OH)2D3. Tretinoin 69-71 ATP binding cassette subfamily C member 1 Homo sapiens 27-30
1430209-8 1992 A functional role for TSP in SMH-KCNR differentiation was established in experiments which showed that exposure to anti-TSP monoclonal antibodies delay retinoic acid differentiation for 48 h. At the time the cells overcome the effects of TSP inhibition, laminin production becomes maximal. Tretinoin 152-165 thrombospondin 1 Homo sapiens 22-25
1430209-4 1992 Using the human neuroblastoma cell line SMH-KCNR, we have investigated the role of the extracellular matrix protein thrombospondin in retinoic acid induced neuroblastoma differentiation. Tretinoin 134-147 thrombospondin 1 Homo sapiens 116-130
1430209-8 1992 A functional role for TSP in SMH-KCNR differentiation was established in experiments which showed that exposure to anti-TSP monoclonal antibodies delay retinoic acid differentiation for 48 h. At the time the cells overcome the effects of TSP inhibition, laminin production becomes maximal. Tretinoin 152-165 thrombospondin 1 Homo sapiens 120-123
1430209-8 1992 A functional role for TSP in SMH-KCNR differentiation was established in experiments which showed that exposure to anti-TSP monoclonal antibodies delay retinoic acid differentiation for 48 h. At the time the cells overcome the effects of TSP inhibition, laminin production becomes maximal. Tretinoin 152-165 thrombospondin 1 Homo sapiens 120-123
1430209-5 1992 Treatment with retinoic acid results in a rapid induction (within 4 h) of thrombospondin (TSP) message which is independent of intervening protein synthesis and superinducible in the presence of cycloheximide. Tretinoin 15-28 thrombospondin 1 Homo sapiens 74-88
1430209-5 1992 Treatment with retinoic acid results in a rapid induction (within 4 h) of thrombospondin (TSP) message which is independent of intervening protein synthesis and superinducible in the presence of cycloheximide. Tretinoin 15-28 thrombospondin 1 Homo sapiens 90-93
1430209-7 1992 A concomitant increase in both cell associated and soluble forms of TSP protein can be detected within 24 h of retinoic acid treatment. Tretinoin 111-124 thrombospondin 1 Homo sapiens 68-71
1284912-0 1992 [The effects of retinoic acid and recombinant human granulocyte colony-stimulating factor on alkaline phosphatase activity of HL-60 cells]. Tretinoin 16-29 alkaline phosphatase, placental Homo sapiens 93-113
1358983-6 1992 Topical RA also prevented UV light from reducing the density of both LC and Thy-1+ dendritic epidermal cells (Thy-1+ dEC). Tretinoin 8-10 thymus cell antigen 1, theta Mus musculus 76-81
1358983-6 1992 Topical RA also prevented UV light from reducing the density of both LC and Thy-1+ dendritic epidermal cells (Thy-1+ dEC). Tretinoin 8-10 thymus cell antigen 1, theta Mus musculus 110-115
1406664-1 1992 The retinoic acid-induced differentiation of F9 cells into parietal endoderm-like cells activates transcription of the endogenous mouse retrovirus, the intracisternal A-particle (IAP). Tretinoin 4-17 intracisternal A particle, Eya1 linked Mus musculus 179-182
1284912-4 1992 Protein kinase C inhibitors (H-7 and staurosporine) but not a protein kinase A inhibitor (HA1004) significantly suppressed the ALP activity induced by the simultaneous treatment with RA and rhG-CSF. Tretinoin 183-185 alkaline phosphatase, placental Homo sapiens 127-130
1284912-1 1992 We examined alkaline phosphatase (ALP) activity in the HL-60 cell induced by retinoic acid (RA) and recombinant human granulocyte colony-stimulating factor (rhG-CSF). Tretinoin 77-90 alkaline phosphatase, placental Homo sapiens 12-32
1284912-1 1992 We examined alkaline phosphatase (ALP) activity in the HL-60 cell induced by retinoic acid (RA) and recombinant human granulocyte colony-stimulating factor (rhG-CSF). Tretinoin 77-90 alkaline phosphatase, placental Homo sapiens 34-37
1284912-1 1992 We examined alkaline phosphatase (ALP) activity in the HL-60 cell induced by retinoic acid (RA) and recombinant human granulocyte colony-stimulating factor (rhG-CSF). Tretinoin 92-94 alkaline phosphatase, placental Homo sapiens 12-32
1284912-1 1992 We examined alkaline phosphatase (ALP) activity in the HL-60 cell induced by retinoic acid (RA) and recombinant human granulocyte colony-stimulating factor (rhG-CSF). Tretinoin 92-94 alkaline phosphatase, placental Homo sapiens 34-37
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 26-54
1328196-4 1992 The retinoic acid-induced activation was 3-4-fold higher with RXR alpha than with either RAR alpha or RAR beta. Tretinoin 4-17 retinoic acid receptor beta Homo sapiens 102-110
1363087-5 1992 The Hox-2.9 and Hox-2.8 genes were induced anteriorly in the neurectoderm in response to RA on day 7 but not at later stages. Tretinoin 89-91 homeobox B2 Mus musculus 16-23
1363087-12 1992 The ectopic anterior expression of Hox-2.8 and Hox-2.9 induced by RA on day 7 was persistent to day 8, as was the altered expression of Krox-20. Tretinoin 66-68 homeobox B2 Mus musculus 35-42
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 56-61
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 15-17 insulin like growth factor 1 Homo sapiens 26-54
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 15-17 insulin like growth factor 1 Homo sapiens 56-61
1328857-10 1992 In addition, we found that the previously identified COUP-TF binding site in the ovalbumin gene functions in vitro as an RA response element that is repressed in the presence of COUP. Tretinoin 121-123 nuclear receptor subfamily 2 group F member 1 Homo sapiens 53-60
1328295-0 1992 Human skin levels of retinoic acid and cytochrome P-450-derived 4-hydroxyretinoic acid after topical application of retinoic acid in vivo compared to concentrations required to stimulate retinoic acid receptor-mediated transcription in vitro. Tretinoin 73-86 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 39-55
1328295-1 1992 Metabolism of retinoic acid to a less active metabolite, 4-hydroxyretinoic acid, occurs via cytochrome P-450 isozyme(s). Tretinoin 14-27 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 92-108
1284131-6 1992 When the cells were incubated with both 10(-6) M RA and 10(-8) M 1,25-(OH)2D3, basal [Ca2+]i was higher and FMLP caused a greater increase in [Ca2+]i than when only RA or 1,25-(OH)2D3 was added. Tretinoin 49-51 formyl peptide receptor 1 Homo sapiens 108-112
1284131-6 1992 When the cells were incubated with both 10(-6) M RA and 10(-8) M 1,25-(OH)2D3, basal [Ca2+]i was higher and FMLP caused a greater increase in [Ca2+]i than when only RA or 1,25-(OH)2D3 was added. Tretinoin 165-167 formyl peptide receptor 1 Homo sapiens 108-112
1329717-2 1992 Although vitamin A deficiency caused no significant changes in the levels of RAR alpha and RAR gamma mRNAs, the level of RAR beta transcripts was greatly decreased in various tissues of vitamin A-deficient rats, but was restored rapidly to a normal level after administration of retinoic acid. Tretinoin 279-292 retinoic acid receptor, beta Rattus norvegicus 121-129
1329717-6 1992 Moreover, we found that administration of retinol and retinoic acid to normal rats caused the overexpression of RAR beta transcripts (2-15-fold) when compared with the control levels of RAR beta mRNA, although the levels of RAR alpha and RAR gamma mRNAs were not affected. Tretinoin 54-67 retinoic acid receptor, beta Rattus norvegicus 112-120
1329717-6 1992 Moreover, we found that administration of retinol and retinoic acid to normal rats caused the overexpression of RAR beta transcripts (2-15-fold) when compared with the control levels of RAR beta mRNA, although the levels of RAR alpha and RAR gamma mRNAs were not affected. Tretinoin 54-67 retinoic acid receptor, beta Rattus norvegicus 186-194
1325286-2 1992 This study examined the effect of RA on the level of a cell surface receptor (M(r) 78,000) (gp78) for an autocrine motility factor, which has been implicated in invasion and metastasis. Tretinoin 34-36 autocrine motility factor receptor Mus musculus 92-96
1483388-5 1992 NeuN can also be detected in neurons in primary cerebellar cultures and in retinoic acid-stimulated P19 embryonal carcinoma cells. Tretinoin 75-88 RNA binding fox-1 homolog 3 Homo sapiens 0-4
1325286-3 1992 Treatment of murine melanoma cell lines S91-C2, B16-F1, and K1735-P with RA (10 microM) for 5 days decreased the level of gp78 by 37, 72, and 92%, respectively, as revealed by immunoblotting with monoclonal antibodies raised against gp78. Tretinoin 73-75 autocrine motility factor receptor Mus musculus 122-126
1325286-3 1992 Treatment of murine melanoma cell lines S91-C2, B16-F1, and K1735-P with RA (10 microM) for 5 days decreased the level of gp78 by 37, 72, and 92%, respectively, as revealed by immunoblotting with monoclonal antibodies raised against gp78. Tretinoin 73-75 autocrine motility factor receptor Mus musculus 233-237
1325286-5 1992 Further studies with K1735-P, the most sensitive cell line with respect to modulation of gp78, showed that the decrease in gp78 level required at least 1 microM RA and 4 to 5 days of treatment. Tretinoin 161-163 autocrine motility factor receptor Mus musculus 123-127
1325286-6 1992 The binding of anti-gp78 antibodies to the surface of intact RA-treated cells and to intracellular gp78 in permeabilized cells was also lower than in untreated cells. Tretinoin 61-63 autocrine motility factor receptor Mus musculus 20-24
1355009-7 1992 Analysis of the distribution in the melanoma cell lines of retinoic acid receptors (RARs) showed a relationship between susceptibility to a RA-mediated increase of ICAM-1 expression and RAR beta expression, suggesting that the latter receptor may play a role in the phenomenon. Tretinoin 84-86 retinoic acid receptor beta Homo sapiens 186-194
1324146-0 1992 Posttranscriptional regulation of the human prolactin gene in IM-9-P3 cells by retinoic acid. Tretinoin 79-92 prolactin Homo sapiens 44-53
1324146-2 1992 Here we describe regulation of hPRL gene expression in members of the IM-9-P3 family by retinoic acid (RA). Tretinoin 88-101 prolactin Homo sapiens 31-35
1324146-2 1992 Here we describe regulation of hPRL gene expression in members of the IM-9-P3 family by retinoic acid (RA). Tretinoin 103-105 prolactin Homo sapiens 31-35
1325286-7 1992 Furthermore, RA treatment decreased the induction of cell motility, on colloidal gold-coated glass coverslips, by anti-gp78 antibodies, which mimic the effect of autocrine motility factor. Tretinoin 13-15 autocrine motility factor receptor Mus musculus 119-123
1325286-8 1992 The RA-induced decrease in antibody-enhanced cell motility was similar to the time- and RA concentration-dependent decrease in the amount of gp78, suggesting that the two events are related. Tretinoin 4-6 autocrine motility factor receptor Mus musculus 141-145
1325286-8 1992 The RA-induced decrease in antibody-enhanced cell motility was similar to the time- and RA concentration-dependent decrease in the amount of gp78, suggesting that the two events are related. Tretinoin 88-90 autocrine motility factor receptor Mus musculus 141-145
1381704-0 1992 Phenotype-specific "tissue" transglutaminase regulation in human neuroblastoma cells in response to retinoic acid: correlation with cell death by apoptosis. Tretinoin 100-113 transglutaminase 2 Homo sapiens 19-44
1381704-3 1992 However, we recently showed that, during the RA treatment, a subset of SK-N-BE(2) cells undergo apoptosis; these cells specifically express a high "tissue" transglutaminase (tTG) level. Tretinoin 45-47 transglutaminase 2 Homo sapiens 147-172
1381704-3 1992 However, we recently showed that, during the RA treatment, a subset of SK-N-BE(2) cells undergo apoptosis; these cells specifically express a high "tissue" transglutaminase (tTG) level. Tretinoin 45-47 transglutaminase 2 Homo sapiens 174-177
1381704-7 1992 In fact, RA treatment enhanced tTG expression and apoptotic index in the flat substrate-adherent variant, whereas, in cells expressing the neural phenotype, very low tTG expression and apoptosis were found. Tretinoin 9-11 transglutaminase 2 Homo sapiens 31-34
1381704-9 1992 An increase in tTG mRNA major transcript levels (3.7 kb) occurred within a few hours of exposure to RA in both the phenotypic variants. Tretinoin 100-102 transglutaminase 2 Homo sapiens 15-18
1381704-10 1992 By contrast, tTG protein level was very low in the cell expressing the neuronal phenotype, even after prolonged exposure to RA. Tretinoin 124-126 transglutaminase 2 Homo sapiens 13-16
1324146-3 1992 When cells were incubated in medium supplemented with fetal calf serum that had been treated with dextran-coated charcoal, the addition of RA caused a 2-fold stimulation of hPRL secretion in the low hPRL-producing clone IM-9-P31 and the moderate producer IM-9-P32 (ED50, 0.53 and 0.13 nM, respectively), but not in the high hPRL-producing IM-9-P33 clone. Tretinoin 139-141 prolactin Homo sapiens 173-177
1324146-3 1992 When cells were incubated in medium supplemented with fetal calf serum that had been treated with dextran-coated charcoal, the addition of RA caused a 2-fold stimulation of hPRL secretion in the low hPRL-producing clone IM-9-P31 and the moderate producer IM-9-P32 (ED50, 0.53 and 0.13 nM, respectively), but not in the high hPRL-producing IM-9-P33 clone. Tretinoin 139-141 prolactin Homo sapiens 199-203
1324146-3 1992 When cells were incubated in medium supplemented with fetal calf serum that had been treated with dextran-coated charcoal, the addition of RA caused a 2-fold stimulation of hPRL secretion in the low hPRL-producing clone IM-9-P31 and the moderate producer IM-9-P32 (ED50, 0.53 and 0.13 nM, respectively), but not in the high hPRL-producing IM-9-P33 clone. Tretinoin 139-141 prolactin Homo sapiens 199-203
1324146-9 1992 This receptor subtype was absent from hPRL-negative members of the IM-9-P family, strongly induced by RA in the RA-responsive IM-9-P31 and IM-9-P32 cell lines via rapid transcriptional up-regulation, and only slightly induced in the RA-resistant IM-9-P33 cell line, suggesting a function in mediation of the effect of RA on hPRL gene expression. Tretinoin 102-104 prolactin Homo sapiens 38-42
1324146-9 1992 This receptor subtype was absent from hPRL-negative members of the IM-9-P family, strongly induced by RA in the RA-responsive IM-9-P31 and IM-9-P32 cell lines via rapid transcriptional up-regulation, and only slightly induced in the RA-resistant IM-9-P33 cell line, suggesting a function in mediation of the effect of RA on hPRL gene expression. Tretinoin 112-114 prolactin Homo sapiens 38-42
1324146-9 1992 This receptor subtype was absent from hPRL-negative members of the IM-9-P family, strongly induced by RA in the RA-responsive IM-9-P31 and IM-9-P32 cell lines via rapid transcriptional up-regulation, and only slightly induced in the RA-resistant IM-9-P33 cell line, suggesting a function in mediation of the effect of RA on hPRL gene expression. Tretinoin 112-114 prolactin Homo sapiens 324-328
1453015-5 1992 ATRA increased the number of these colonies in a concentration-dependent manner, with maximal stimulation (3.5-fold) occurring at 30 nM in the presence of 5.5 ng/ml IL-3, 0.1 mM hemin, 3.0 U/ml Epo and 30 nM IGF-I. Tretinoin 0-4 erythropoietin Homo sapiens 194-197
1453015-5 1992 ATRA increased the number of these colonies in a concentration-dependent manner, with maximal stimulation (3.5-fold) occurring at 30 nM in the presence of 5.5 ng/ml IL-3, 0.1 mM hemin, 3.0 U/ml Epo and 30 nM IGF-I. Tretinoin 0-4 insulin like growth factor 1 Homo sapiens 208-213
1520304-0 1992 Retinoic acid ambivalently regulates the expression of MyoD1 in the myogenic cells in the limb buds of the early developmental stages. Tretinoin 0-13 myogenic differentiation 1 Homo sapiens 55-60
1520304-1 1992 The expression of MyoD1 in myogenic cells located in the muscle prospective region of the limb bud at stage 20-22 was highly sensitive to retinoic acid. Tretinoin 138-151 myogenic differentiation 1 Homo sapiens 18-23
1520304-2 1992 Unlike RAR-beta, the expression of MyoD1 mRNA in the muscle precursor cells was significantly increased by retinoic acid at lower concentrations (0.1-10 nM), but inhibited by it at higher concentrations (0.1-1 microM). Tretinoin 107-120 myogenic differentiation 1 Homo sapiens 35-40
1322787-5 1992 Using cyclic AMP and RA in combination, we found that RA inhibited expression of adrenal gland specific gene pG2 and induced a neuronal phenotype. Tretinoin 54-56 delta like non-canonical Notch ligand 1 Homo sapiens 109-112
1525046-2 1992 Mono- and polyunsaturated fatty acids markedly decreased the affinity of both 25-OHD3 and 1,25-(OH)2D3 for DBP, whereas saturated fatty acids (stearic and arachidic acid), cholesterol, cholesterol esters, retinol, retinoic acid and prostaglandins (A1 and E1) did not affect the apparent affinity. Tretinoin 214-227 D-box binding PAR bZIP transcription factor Homo sapiens 107-110
1360694-0 1992 Polyamines are involved in retinoic acid-mediated induction of tissue transglutaminase in human peripheral blood monocytes. Tretinoin 27-40 transglutaminase 2 Homo sapiens 63-86
1360694-2 1992 Retinoic acid (RA) addition to 5-day-old cultured monocytes, 36 h later induced about 5-folds increase of TGc content. Tretinoin 0-13 transglutaminase 2 Homo sapiens 106-109
1360694-2 1992 Retinoic acid (RA) addition to 5-day-old cultured monocytes, 36 h later induced about 5-folds increase of TGc content. Tretinoin 15-17 transglutaminase 2 Homo sapiens 106-109
1360694-3 1992 The preliminary exposure of cultured monocytes to alpha-difluoromethylornithine (DFMO) significantly reduced TGc induction caused by RA. Tretinoin 133-135 transglutaminase 2 Homo sapiens 109-112
1360694-8 1992 We conclude that TGc induction by RA during in vitro maturation of monocytes to macrophages may be modulated by polyamine availability. Tretinoin 34-36 transglutaminase 2 Homo sapiens 17-20
1323347-5 1992 Histamine and thrombin also synergized with t-RA. Tretinoin 44-48 coagulation factor II, thrombin Homo sapiens 14-22
1323613-0 1992 Retinoic acid and phorbol ester synergistically up-regulate IL-8 expression and specifically modulate protein kinase C-epsilon in human skin fibroblasts. Tretinoin 0-13 C-X-C motif chemokine ligand 8 Homo sapiens 60-64
1323613-1 1992 Phorbol ester (TPA) and retinoic acid (RA) are two potent immunomodulatory agents whose actions are mediated through distinct signal transduction pathways involving protein kinase C (PKC) and nuclear RA receptors, respectively. Tretinoin 24-37 protein kinase C alpha Homo sapiens 183-186
1323613-1 1992 Phorbol ester (TPA) and retinoic acid (RA) are two potent immunomodulatory agents whose actions are mediated through distinct signal transduction pathways involving protein kinase C (PKC) and nuclear RA receptors, respectively. Tretinoin 39-41 protein kinase C alpha Homo sapiens 183-186
1323613-3 1992 TPA (as previously reported) and RA both induced IL-8 mRNA and protein in a time- and dose-dependent manner. Tretinoin 33-35 C-X-C motif chemokine ligand 8 Homo sapiens 49-53
1323613-4 1992 IL-8 mRNA induction by TPA (10 nM) was maximal (15-fold) within 6 h, and returned to baseline within 24 h of treatment, although maximal induction (10-fold) by RA (1 microM) did not occur until 24 h posttreatment. Tretinoin 160-162 C-X-C motif chemokine ligand 8 Homo sapiens 0-4
1323613-4 1992 IL-8 mRNA induction by TPA (10 nM) was maximal (15-fold) within 6 h, and returned to baseline within 24 h of treatment, although maximal induction (10-fold) by RA (1 microM) did not occur until 24 h posttreatment. Tretinoin 160-162 plasminogen activator, tissue type Homo sapiens 23-26
1323613-6 1992 In contrast, induction of IL-8 by RA was inhibited by both 1-(5-isoquinoline sulfonamide and N-(2-gamidinoethyl)-5-isoquinoline sulfonamide, suggesting the participation of PKA in the induction of IL-8 by RA. Tretinoin 34-36 C-X-C motif chemokine ligand 8 Homo sapiens 26-30
1323613-6 1992 In contrast, induction of IL-8 by RA was inhibited by both 1-(5-isoquinoline sulfonamide and N-(2-gamidinoethyl)-5-isoquinoline sulfonamide, suggesting the participation of PKA in the induction of IL-8 by RA. Tretinoin 34-36 C-X-C motif chemokine ligand 8 Homo sapiens 197-201
1323613-6 1992 In contrast, induction of IL-8 by RA was inhibited by both 1-(5-isoquinoline sulfonamide and N-(2-gamidinoethyl)-5-isoquinoline sulfonamide, suggesting the participation of PKA in the induction of IL-8 by RA. Tretinoin 205-207 C-X-C motif chemokine ligand 8 Homo sapiens 26-30
1323613-8 1992 Induction of IL-8 by RA also did not appear to be mediated indirectly through induction of IL-1, because addition of IL-1R antagonist did not block IL-8 induction by RA. Tretinoin 21-23 C-X-C motif chemokine ligand 8 Homo sapiens 13-17
1323613-9 1992 RA and TPA added in combination synergistically enhanced expression of IL-8 mRNA, measured at 6 (2-fold) and 24 h (10-fold) posttreatment. Tretinoin 0-2 C-X-C motif chemokine ligand 8 Homo sapiens 71-75
1323613-11 1992 TPA, either alone or together with RA, but not RA alone, stimulated phosphorylation of an endogenous 80-kDa PKC substrate. Tretinoin 35-37 protein kinase C alpha Homo sapiens 108-111
1510669-4 1992 In a cloned human neuroblastoma cell line, Be(2)C, lyn mRNA levels increased during neuronal differentiation induced by retinoic acid. Tretinoin 120-133 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 51-54
1510669-6 1992 Retinoic acid-induced glial differentiation was associated with a reduction of lyn transcripts in a clonal I-type neuroblastoma cell line, SH-IN, which shares properties of both neuronal- and glial-type clones. Tretinoin 0-13 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 79-82
1527804-14 1992 This effect of TPA in altering the distribution of labeling of the cytosolic and lipid components was not demonstrable with cells grown in the presence of 10(-5) M retinoic acid. Tretinoin 164-177 plasminogen activator, tissue type Homo sapiens 15-18
1365641-12 1992 In contrast, retinoic acid strongly increased phorbol myristate acetate-induced MCP-1 expression and potentiated the effects of IL-1 and LPS. Tretinoin 13-26 interleukin 1 beta Homo sapiens 128-140
1639854-5 1992 Using a basement membrane invasion assay, we found that the mutant cells, differentiated in low concentrations of serum with retinoic acid, were more invasive than their normal cell counterparts, and that this was specifically reversed by adding exogenous TIMP-1 protein. Tretinoin 125-138 TIMP metallopeptidase inhibitor 1 Homo sapiens 256-262
1328588-5 1992 Intracellular and extracellular levels of VIP were also shown to increase significantly during the retinoic acid-induced differentiation of these cells. Tretinoin 99-112 vasoactive intestinal peptide Homo sapiens 42-45
1328588-8 1992 It is concluded that VIP is a normal autoregulator of neuroblastoma cell growth and differentiation, and that retinoic acid-mediated differentiation may be, in part, due to endogenous VIP. Tretinoin 110-123 vasoactive intestinal peptide Homo sapiens 184-187
1618838-0 1992 Increased expression of protein kinase C alpha plays a key role in retinoic acid-induced melanoma differentiation. Tretinoin 67-80 protein kinase C, alpha Mus musculus 24-46
1319834-8 1992 Retinoic acid treatment suppressed by greater than 80% both the basal and estradiol-induced pS2 mRNA expression. Tretinoin 0-13 trefoil factor 1 Homo sapiens 92-95
1319834-9 1992 Retinoic acid modulation of the estrogen receptor gene mRNA was not responsible for the retinoic acid inhibition of the stimulation of pS2 and TGF-alpha gene expression by estradiol, since estrogen receptor gene expression was increased rather than decreased in the presence of retinoic acid. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 32-49
1319834-12 1992 These results indicate that retinoic acid can inhibit estradiol-induced TGF-alpha and pS2 mRNA expression in MCF-7 cells. Tretinoin 28-41 trefoil factor 1 Homo sapiens 86-89
1321332-0 1992 Repression by ARP-1 sensitizes apolipoprotein AI gene responsiveness to RXR alpha and retinoic acid. Tretinoin 86-99 apolipoprotein A1 Homo sapiens 31-48
1321332-4 1992 In a more recent series of experiments, we found that site A is a retinoic acid (RA) response element that responds preferentially to the recently identified RA-responsive receptor RXR alpha over the previously characterized RA receptors RAR alpha and RAR beta. Tretinoin 66-79 retinoic acid receptor beta Homo sapiens 252-260
1321332-4 1992 In a more recent series of experiments, we found that site A is a retinoic acid (RA) response element that responds preferentially to the recently identified RA-responsive receptor RXR alpha over the previously characterized RA receptors RAR alpha and RAR beta. Tretinoin 81-83 retinoic acid receptor beta Homo sapiens 252-260
1321332-6 1992 Transient transfection assays showed that site A is necessary and sufficient for RXR alpha-mediated transactivation of the apoAI gene basal promoter in human hepatoma HepG2 cells in the presence of RA and that this transactivation is abolished by increasing amounts of cotransfected ARP-1. Tretinoin 198-200 apolipoprotein A1 Homo sapiens 123-128
1618838-1 1992 Differentiation of B16 mouse melanoma cells induced by retinoic acid (RA) is preceded by a large increase in protein kinase C alpha (PKC alpha) mRNA and protein. Tretinoin 55-68 protein kinase C, alpha Mus musculus 109-131
1618838-1 1992 Differentiation of B16 mouse melanoma cells induced by retinoic acid (RA) is preceded by a large increase in protein kinase C alpha (PKC alpha) mRNA and protein. Tretinoin 55-68 protein kinase C, alpha Mus musculus 133-142
1618838-1 1992 Differentiation of B16 mouse melanoma cells induced by retinoic acid (RA) is preceded by a large increase in protein kinase C alpha (PKC alpha) mRNA and protein. Tretinoin 70-72 protein kinase C, alpha Mus musculus 109-131
1618838-1 1992 Differentiation of B16 mouse melanoma cells induced by retinoic acid (RA) is preceded by a large increase in protein kinase C alpha (PKC alpha) mRNA and protein. Tretinoin 70-72 protein kinase C, alpha Mus musculus 133-142
1618838-7 1992 These findings, combined with the fact that phorbol esters down-regulate PKC and antagonize RA action suggest that PKC alpha plays a key role in the RA-induced melanoma differentiation. Tretinoin 92-94 protein kinase C, alpha Mus musculus 115-124
1618838-7 1992 These findings, combined with the fact that phorbol esters down-regulate PKC and antagonize RA action suggest that PKC alpha plays a key role in the RA-induced melanoma differentiation. Tretinoin 149-151 protein kinase C, alpha Mus musculus 115-124
1611098-5 1992 PK-C alpha mRNA decreases as HL-60 cells mature to a neutrophil phenotype in response to retinoic acid, but its abundance does not change during monocytic differentiation in response to vitamin D3. Tretinoin 89-102 protein kinase C alpha Homo sapiens 0-10
1342293-8 1992 Retinoic acid appears to be a specific inducer of t-PA synthesis in human endothelial cells in culture and may constitute a model for the development of drugs that stimulate endogenous t-PA synthesis. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 50-54
1342293-8 1992 Retinoic acid appears to be a specific inducer of t-PA synthesis in human endothelial cells in culture and may constitute a model for the development of drugs that stimulate endogenous t-PA synthesis. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 185-189
1354431-4 1992 Neuroblastoma cell lines induced to differentiate in vitro by retinoic acid showed a decline of the activities of DNA polymerase alpha, DNA polymerase delta/epsilon, uracil-DNA glycosylase and thymidine kinase similar to that observed during in vivo differentiation. Tretinoin 62-75 uracil DNA glycosylase Homo sapiens 166-188
1534272-6 1992 In contrast, cells exposed to RA contained larger amounts of alpha-actinin, vinculin, talin, lipocortin I, and lipocortin II, as determined with their respective antibodies followed by flow cytometric analysis as described above. Tretinoin 30-32 actinin alpha 1 Homo sapiens 61-74
1431336-5 1992 Treatment of LoVo/Dx with differentiating agents (dimethylformamide and retinoic acid) led to a decreased expression of the adhesion molecules, including NCA, accompanied by increased resistance to LAK-mediated lysis. Tretinoin 72-85 CEA cell adhesion molecule 4 Homo sapiens 154-157
1324421-6 1992 RXR alpha complexes with RAR alpha, RAR beta, and RAR gamma bound selectively to retinoic acid responsive elements from the human RAR beta 2 gene (hRAR beta 2), the gene of the rat cellular retinol binding protein I and the human apolipoprotein A1 gene. Tretinoin 81-94 retinoic acid receptor beta Homo sapiens 36-44
1324421-6 1992 RXR alpha complexes with RAR alpha, RAR beta, and RAR gamma bound selectively to retinoic acid responsive elements from the human RAR beta 2 gene (hRAR beta 2), the gene of the rat cellular retinol binding protein I and the human apolipoprotein A1 gene. Tretinoin 81-94 retinoic acid receptor beta Homo sapiens 130-138
1324421-6 1992 RXR alpha complexes with RAR alpha, RAR beta, and RAR gamma bound selectively to retinoic acid responsive elements from the human RAR beta 2 gene (hRAR beta 2), the gene of the rat cellular retinol binding protein I and the human apolipoprotein A1 gene. Tretinoin 81-94 apolipoprotein A1 Homo sapiens 230-247
1358448-11 1992 Acetylcholinesterase activity was significantly stimulated by retinoic acid and by gamma-interferon. Tretinoin 62-75 acetylcholinesterase (Cartwright blood group) Homo sapiens 0-20
1623557-7 1992 Retinoic acid-differentiated F9 cells and P19 cells expressing H-2 antigen after exposure to MAF (IFN-gamma) were sensitive to the killing by nonactivated macrophages. Tretinoin 0-13 histocompatibility-2, MHC Mus musculus 63-66
1623557-7 1992 Retinoic acid-differentiated F9 cells and P19 cells expressing H-2 antigen after exposure to MAF (IFN-gamma) were sensitive to the killing by nonactivated macrophages. Tretinoin 0-13 interferon gamma Mus musculus 98-107
1317749-5 1992 Recently, differentiation therapy of acute promyelocytic leukemias (AML3 subtype) with all-trans-retinoic acid has been shown to be an efficient alternative to chemotherapy. Tretinoin 87-110 RUNX family transcription factor 2 Homo sapiens 68-72
1317749-10 1992 However, detectable binding to a cytosolic protein corresponding to cellular retinoic acid-binding protein (M(r) 15,000, Kd 3 nM) was observed in the bone marrow cells of AML3 patients undergoing all-trans-retinoic acid therapy. Tretinoin 77-90 RUNX family transcription factor 2 Homo sapiens 171-175
1534272-9 1992 An RA-resistant clone, designated HL-60/R3, constitutively expressed larger amounts of alpha-actinin, vinculin, lipocortin I, and lipocortin II than parental HL-60 cells. Tretinoin 3-5 actinin alpha 1 Homo sapiens 87-100
1375906-0 1992 Retinoic acid regulates insulin-like growth factor II expression in a neuroblastoma cell line. Tretinoin 0-13 insulin like growth factor 2 Gallus gallus 24-53
1318198-2 1992 Since retinoic acid (RA) is a key regulator of epithelial cell differentiation and a growth inhibitor in vitro of HPV18-positive HeLa cervical carcinoma cells, we have used HeLa and HeLa hybrid cells in order to analyse the effects of RA on expression of the HPV18 E6 and E7 oncogenes and of the cellular RA receptor genes RAR-beta and -gamma. Tretinoin 6-19 retinoic acid receptor beta Homo sapiens 323-331
1318198-2 1992 Since retinoic acid (RA) is a key regulator of epithelial cell differentiation and a growth inhibitor in vitro of HPV18-positive HeLa cervical carcinoma cells, we have used HeLa and HeLa hybrid cells in order to analyse the effects of RA on expression of the HPV18 E6 and E7 oncogenes and of the cellular RA receptor genes RAR-beta and -gamma. Tretinoin 21-23 retinoic acid receptor beta Homo sapiens 323-331
1318198-5 1992 RA treatment resulted in induction of RAR-beta mRNA levels in non-tumorigenic HeLa hybrid cells, but not in tumorigenic hybrid segregants nor in HeLa cells. Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 38-46
1599493-2 1992 The expression of lyn, a src-related tyrosine kinase, was studied by analysis of the steady-state levels of its transcript during the cell differentiation process induced by retinoic acid, phorbol 12-myristate 13-acetate and 1,25-dihydroxyvitamin D3. Tretinoin 174-187 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 18-21
1376696-0 1992 Differential regulation of insulin-like growth factor binding protein (IGFBP)-2 mRNA in liver and bone cells by insulin and retinoic acid in vitro. Tretinoin 124-137 insulin-like growth factor binding protein 2 Rattus norvegicus 27-79
1376696-4 1992 Retinoic acid stimulates IGFBP-2 production by liver cells. Tretinoin 0-13 insulin-like growth factor binding protein 2 Rattus norvegicus 25-32
1376696-5 1992 Insulin suppresses both basal and retinoic acid-induced IGFBP-2 mRNA expression in hepatocytes and has no such effect on osteoblasts. Tretinoin 34-47 insulin-like growth factor binding protein 2 Rattus norvegicus 56-63
1376696-6 1992 Retinoic acid and insulin regulate IGFBP-2 expression in a tissue-specific manner. Tretinoin 0-13 insulin-like growth factor binding protein 2 Rattus norvegicus 35-42
1316917-1 1992 Expression of the two known receptors for TNF was studied in the promyelocytic leukemia cell line HL-60 before and after differentiation of the cells along the granulocyte lineage (induced by incubation with retinoic acid), or along the macrophage lineage (induced by incubation with the phorbol diester, PMA). Tretinoin 208-221 tumor necrosis factor Homo sapiens 42-45
1319016-2 1992 An approximate 4-fold increase in vasoactive intestinal peptide (VIP) mRNA concentration was observed after differentiation with retinoic acid, whereas no change in VIP mRNA concentration was observed after differentiation with dBcAMP or PMA. Tretinoin 129-142 vasoactive intestinal peptide Homo sapiens 34-63
1319016-2 1992 An approximate 4-fold increase in vasoactive intestinal peptide (VIP) mRNA concentration was observed after differentiation with retinoic acid, whereas no change in VIP mRNA concentration was observed after differentiation with dBcAMP or PMA. Tretinoin 129-142 vasoactive intestinal peptide Homo sapiens 65-68
1632803-0 1992 Expression of pS2 gene in human breast cancer cell line MCF-7 is controlled by retinoic acid. Tretinoin 79-92 taste 2 receptor member 64 pseudogene Homo sapiens 14-17
1632803-2 1992 Expression of the pS2 gene, which is transcriptionally induced by estrogen in breast cancer cell line MCF-7 cells, can be repressed by retinoic acid (RA) in unstimulated cells. Tretinoin 135-148 taste 2 receptor member 64 pseudogene Homo sapiens 18-21
1323569-8 1992 Retinoic acid at low concentrations (10(-10) to 10(-9) M) rapidly induced the expression of RAR-beta. Tretinoin 0-13 retinoic acid receptor beta Homo sapiens 92-100
1639750-0 1992 Genomic structure of human midkine (MK), a retinoic acid-responsive growth/differentiation factor. Tretinoin 43-56 midkine Homo sapiens 27-34
1639750-0 1992 Genomic structure of human midkine (MK), a retinoic acid-responsive growth/differentiation factor. Tretinoin 43-56 midkine Homo sapiens 36-38
1638993-5 1992 Exposure of early neural plate stage embryos to retinoic acid caused reduced expression of TGF beta 1 and TGF beta 2 proteins but had no effect on TGF beta 3. Tretinoin 48-61 transforming growth factor, beta 2 Mus musculus 106-116
1379266-3 1992 The abundance of RAR-beta transcripts was elevated by treating the cells with retinoic acid, but there was no effect on the level of expression of RAR-alpha and RAR-gamma. Tretinoin 78-91 retinoic acid receptor beta Homo sapiens 17-25
1379266-4 1992 The induction of RAR-beta by retinoic acid was detectable within 4 h and at low concentrations of retinoic acid (10(-10) M). Tretinoin 29-42 retinoic acid receptor beta Homo sapiens 17-25
1379266-4 1992 The induction of RAR-beta by retinoic acid was detectable within 4 h and at low concentrations of retinoic acid (10(-10) M). Tretinoin 98-111 retinoic acid receptor beta Homo sapiens 17-25
1564559-5 1992 We also compared four retinoids for IgG1 response restoration in vitro; 1 nmol/L retinoic acid fully repleted A- cell IgG1 responses and helper T cell frequencies to the unsupplemented A+ control levels. Tretinoin 81-94 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 36-40
1374473-1 1992 Liarozole is an imidazole-containing compound that inhibits the cytochrome P-450-dependent metabolism of all-trans-retinoic acid (RA). Tretinoin 105-128 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 64-80
1374473-1 1992 Liarozole is an imidazole-containing compound that inhibits the cytochrome P-450-dependent metabolism of all-trans-retinoic acid (RA). Tretinoin 130-132 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 64-80
1564559-5 1992 We also compared four retinoids for IgG1 response restoration in vitro; 1 nmol/L retinoic acid fully repleted A- cell IgG1 responses and helper T cell frequencies to the unsupplemented A+ control levels. Tretinoin 81-94 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 118-122
1581328-0 1992 The ionization behavior of retinoic acid in aqueous environments and bound to serum albumin. Tretinoin 27-40 albumin Homo sapiens 78-91
1315406-10 1992 In H-4-II-E cells, retinoic acid increased the expression of retinoic acid receptor beta and gamma gene. Tretinoin 19-32 retinoic acid receptor, beta Rattus norvegicus 61-88
1581328-1 1992 The ionization behavior of retinoic acid (RA) in an aqueous phase and when bound to bovine serum albumin was studied. Tretinoin 27-40 albumin Homo sapiens 91-104
1581328-1 1992 The ionization behavior of retinoic acid (RA) in an aqueous phase and when bound to bovine serum albumin was studied. Tretinoin 42-44 albumin Homo sapiens 91-104
1315521-0 1992 Transcriptional regulation of transferrin and albumin genes by retinoic acid in human hepatoma cell line Hep3B. Tretinoin 63-76 transferrin Homo sapiens 30-41
1581328-9 1992 Titration of RA in the presence of bovine serum albumin revealed the presence of a heterogeneous population comprised of three distinct microenvironments for RA associated with this protein. Tretinoin 158-160 albumin Homo sapiens 42-55
1315521-0 1992 Transcriptional regulation of transferrin and albumin genes by retinoic acid in human hepatoma cell line Hep3B. Tretinoin 63-76 albumin Homo sapiens 46-53
1315521-1 1992 Transferrin and albumin, which are both secreted from the human hepatoma cell line Hep3B, were regulated transcriptionally by retinoic acid (RA) in a dose-dependent manner. Tretinoin 126-139 transferrin Homo sapiens 0-11
1315521-1 1992 Transferrin and albumin, which are both secreted from the human hepatoma cell line Hep3B, were regulated transcriptionally by retinoic acid (RA) in a dose-dependent manner. Tretinoin 126-139 albumin Homo sapiens 16-23
1315521-1 1992 Transferrin and albumin, which are both secreted from the human hepatoma cell line Hep3B, were regulated transcriptionally by retinoic acid (RA) in a dose-dependent manner. Tretinoin 141-143 transferrin Homo sapiens 0-11
1315521-1 1992 Transferrin and albumin, which are both secreted from the human hepatoma cell line Hep3B, were regulated transcriptionally by retinoic acid (RA) in a dose-dependent manner. Tretinoin 141-143 albumin Homo sapiens 16-23
1315521-3 1992 The treatment of Hep3B cells with RA (10 microM for 48 h) resulted in an 8-fold increase in transferrin protein synthesis, a 10-fold increase in the steady-state transferrin mRNA level, and a 5-fold increase in its transcriptional rate. Tretinoin 34-36 transferrin Homo sapiens 92-103
1315521-3 1992 The treatment of Hep3B cells with RA (10 microM for 48 h) resulted in an 8-fold increase in transferrin protein synthesis, a 10-fold increase in the steady-state transferrin mRNA level, and a 5-fold increase in its transcriptional rate. Tretinoin 34-36 transferrin Homo sapiens 162-173
1315521-5 1992 Cycloheximide and actinomycin D blocked the action of RA, suggesting that RA may regulate transferrin and albumin gene expression indirectly in human liver cells. Tretinoin 54-56 transferrin Homo sapiens 90-101
1315521-5 1992 Cycloheximide and actinomycin D blocked the action of RA, suggesting that RA may regulate transferrin and albumin gene expression indirectly in human liver cells. Tretinoin 54-56 albumin Homo sapiens 106-113
1315521-5 1992 Cycloheximide and actinomycin D blocked the action of RA, suggesting that RA may regulate transferrin and albumin gene expression indirectly in human liver cells. Tretinoin 74-76 transferrin Homo sapiens 90-101
1315521-5 1992 Cycloheximide and actinomycin D blocked the action of RA, suggesting that RA may regulate transferrin and albumin gene expression indirectly in human liver cells. Tretinoin 74-76 albumin Homo sapiens 106-113
1313791-5 1992 Furthermore, the expression of follistatin in P19 cells is subject to dynamic fluctuations in response to retinoic acid treatment. Tretinoin 106-119 follistatin Homo sapiens 31-42
1584225-1 1992 The epidermal growth factor (EGF) receptor (EGFR) promoter is negatively regulated by thyroid hormone and retinoic acid. Tretinoin 106-119 epidermal growth factor receptor Homo sapiens 4-42
1550338-1 1992 We have previously shown that the retinoic acid (RA)-induced growth arrest and differentiation of B16 mouse melanoma cells is accompanied by a large increase in the amount and activity of protein kinase C (PKC). Tretinoin 34-47 protein kinase C, alpha Mus musculus 206-209
1550338-1 1992 We have previously shown that the retinoic acid (RA)-induced growth arrest and differentiation of B16 mouse melanoma cells is accompanied by a large increase in the amount and activity of protein kinase C (PKC). Tretinoin 49-51 protein kinase C, alpha Mus musculus 206-209
1550338-2 1992 Since PKC is a multigene family, we investigated which isoforms were expressed in control and RA-treated B16 melanoma cells, and characterized the manner by which RA regulates PKC gene expression. Tretinoin 163-165 protein kinase C, alpha Mus musculus 6-9
1550338-2 1992 Since PKC is a multigene family, we investigated which isoforms were expressed in control and RA-treated B16 melanoma cells, and characterized the manner by which RA regulates PKC gene expression. Tretinoin 163-165 protein kinase C, alpha Mus musculus 176-179
1550338-3 1992 We found that RA treatment of B16 cells resulted in an increase in PKC alpha mRNA beginning at 4-8 h and reached a maximum of 10- to 12-fold over control levels by 48 h. There was also a small amount of PKC gamma mRNA, present only in 48-h RA-treated cells, but no PKC beta mRNA was detected. Tretinoin 14-16 protein kinase C, alpha Mus musculus 67-76
1550338-4 1992 The effect of RA on PKC alpha mRNA induction was not direct since the induction was abolished when cycloheximide was included in the incubation medium. Tretinoin 14-16 protein kinase C, alpha Mus musculus 20-29
1550338-5 1992 Nuclear run-on experiments showed that the RA-induced increase in PKC alpha steady-state mRNA was not entirely due to an increase in transcriptional activity, as the increase in PKC alpha transcription was only 2- to 3-fold over control, which is not enough to account for the 10- to 15-fold increase in steady state levels. Tretinoin 43-45 protein kinase C, alpha Mus musculus 66-75
1550338-5 1992 Nuclear run-on experiments showed that the RA-induced increase in PKC alpha steady-state mRNA was not entirely due to an increase in transcriptional activity, as the increase in PKC alpha transcription was only 2- to 3-fold over control, which is not enough to account for the 10- to 15-fold increase in steady state levels. Tretinoin 43-45 protein kinase C, alpha Mus musculus 178-187
1550338-7 1992 The 10.9-kb PKC alpha message in both control and RA-treated cells was less stable than the 3.8-kb PKC alpha message. Tretinoin 50-52 protein kinase C, alpha Mus musculus 12-21
1350944-5 1992 In addition, CD4 mRNA was evaluated in two NB cell lines induced to differentiate in vitro with retinoic acid (RA) or 1-(5-isoquinolinyl-sulfonyl)-2-methyl piperazine (H7), a protein kinase C inhibitor. Tretinoin 96-109 CD4 molecule Homo sapiens 13-16
1380592-1 1992 Retinoic acid induces tissue-type plasminogen activator (t-PA) but not plasminogen activator inhibitor-1 (PAI-1) expression in cultured human umbilical vein endothelial cells (HUVEC). Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 22-55
1380592-1 1992 Retinoic acid induces tissue-type plasminogen activator (t-PA) but not plasminogen activator inhibitor-1 (PAI-1) expression in cultured human umbilical vein endothelial cells (HUVEC). Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 57-61
1380592-4 1992 Group 1 showed little induction (0.9- to 1.9-fold after 48 h) at concentrations between 10(-8) and 10(-6) M. Group 2, which includes all-trans-retinoic acid, induced t-PA threefold to fivefold at 10(-6) M but had little effect at 10(-8) M (less than threefold). Tretinoin 137-156 plasminogen activator, tissue type Homo sapiens 166-170
1374482-0 1992 Retinoic acid-regulated expression of proteolipid protein and myelin-associated glycoprotein genes in C6 glioma cells. Tretinoin 0-13 myelin-associated glycoprotein Rattus norvegicus 62-92
1374482-1 1992 The effect of retinoic acid (RA) on the expression of myelin-specific genes, i.e., proteolipid protein (PLP) and myelin-associated glycoprotein (MAG) in rat glioma C6 cells, was analyzed by Northern blot hybridization. Tretinoin 14-27 myelin-associated glycoprotein Rattus norvegicus 113-143
1374482-1 1992 The effect of retinoic acid (RA) on the expression of myelin-specific genes, i.e., proteolipid protein (PLP) and myelin-associated glycoprotein (MAG) in rat glioma C6 cells, was analyzed by Northern blot hybridization. Tretinoin 29-31 myelin-associated glycoprotein Rattus norvegicus 113-143
1584225-1 1992 The epidermal growth factor (EGF) receptor (EGFR) promoter is negatively regulated by thyroid hormone and retinoic acid. Tretinoin 106-119 epidermal growth factor receptor Homo sapiens 44-48
1584226-1 1992 The immortalized rat calvarial bone cell line RCT-1 responds to treatment with retinoic acid (RA) by increased expression of osteoblast phenotype-related features, including the induction of liver/bone/kidney alkaline phosphatase (ALP) activity. Tretinoin 79-92 alkaline phosphatase, placental Homo sapiens 231-234
1584226-1 1992 The immortalized rat calvarial bone cell line RCT-1 responds to treatment with retinoic acid (RA) by increased expression of osteoblast phenotype-related features, including the induction of liver/bone/kidney alkaline phosphatase (ALP) activity. Tretinoin 94-96 alkaline phosphatase, placental Homo sapiens 231-234
1584226-2 1992 ALP mRNA could not be demonstrated in unstimulated cells, but was first detected in cells treated for 6 h with 1 microM RA. Tretinoin 120-122 alkaline phosphatase, placental Homo sapiens 0-3
1584226-4 1992 This was confirmed by nuclear run-on assays, which demonstrated a 2.5-fold increase in the abundance of ALP transcripts after 6 h of RA treatment. Tretinoin 133-135 alkaline phosphatase, placental Homo sapiens 104-107
1372988-1 1992 Retinoic acid (RA) exerts potent suppressive and upregulatory effects on human immunodeficiency virus (HIV) expression in mononuclear phagocytes, strikingly similar to the effects of the cytokine transforming growth factor beta (TGF-beta). Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 229-237
1313565-2 1992 RAR-beta 4 is expressed under the control of the same retinoic acid-responsive promoter as RAR-beta 2. Tretinoin 54-67 retinoic acid receptor beta Homo sapiens 0-8
1515368-0 1992 Transcriptional control of epidermal growth factor receptor by retinoic acid. Tretinoin 63-76 epidermal growth factor receptor Homo sapiens 27-59
1515368-5 1992 There is evidence for functional interactions between RA and the EGF receptor (EGFR). Tretinoin 54-56 epidermal growth factor receptor Homo sapiens 65-77
1515368-5 1992 There is evidence for functional interactions between RA and the EGF receptor (EGFR). Tretinoin 54-56 epidermal growth factor receptor Homo sapiens 79-83
1515368-6 1992 RA enhances the proliferative response of cultured keratinocytes to EGF, increases the number of EGFRs on the surface of some cells, and induces EGFR promoter activity in most cells. Tretinoin 0-2 epidermal growth factor receptor Homo sapiens 97-101
1515368-7 1992 In contrast, immunoprecipitation, Northern blot, and nuclear run-on analysis described in this paper show that RA suppresses EGFR synthesis at the transcriptional level in human epidermoid carcinoma ME180 cells. Tretinoin 111-113 epidermal growth factor receptor Homo sapiens 125-129
1372028-0 1992 Acute or chronic topical retinoic acid treatment of human skin in vivo alters the expression of epidermal transglutaminase, loricrin, involucrin, filaggrin, and keratins 6 and 13 but not keratins 1, 10, and 14. Tretinoin 25-38 loricrin cornified envelope precursor protein Homo sapiens 124-132
1590919-1 1992 Treatment of the human esophageal cancer cell line EC8712 with retinoic acid (RA) stopped the cell growth significantly and gave rise to terminal differentiation of the cells characterized by increased expression of involucrin gene. Tretinoin 63-76 involucrin Homo sapiens 216-226
1590919-1 1992 Treatment of the human esophageal cancer cell line EC8712 with retinoic acid (RA) stopped the cell growth significantly and gave rise to terminal differentiation of the cells characterized by increased expression of involucrin gene. Tretinoin 78-80 involucrin Homo sapiens 216-226
1311101-0 1992 Retinoid X receptor-COUP-TF interactions modulate retinoic acid signaling. Tretinoin 50-63 nuclear receptor subfamily 2 group F member 1 Homo sapiens 20-27
1545145-3 1992 Immunochemical methods have shown an increase in TGF-beta 1 and, to a lesser extent, of TGF-beta 2 in the epidermis following retinoic acid treatment. Tretinoin 126-139 transforming growth factor, beta 2 Mus musculus 88-98
1309985-3 1992 The site in HL-60 cells remained unmethylated after retinoic acid- or 12-O-tetradecanoyl-phorbol-13-acetate-induced differentiation that arrests myeloperoxidase synthesis. Tretinoin 52-65 myeloperoxidase Homo sapiens 145-160
1542003-5 1992 The ability of pure hCRBP(II) to bind all-trans-retinol, retinal and retinoic acid was examined by competitive binding assay and compared with the binding specificity of pure human cellular retinol-binding protein (hCRBP). Tretinoin 69-82 retinol binding protein 2 Homo sapiens 20-29
1737056-0 1992 Effect of iron and retinoic acid on the control of transferrin receptor and ferritin in the human promonocytic cell line U937. Tretinoin 19-32 transferrin Homo sapiens 51-62
1731642-6 1992 Treatment of the cultures with retinoic acid elevated levels of TGF-beta 2 synthesis, but not TGF-beta 1. Tretinoin 31-44 transforming growth factor beta 2 Bos taurus 64-74
1731642-7 1992 While the role of the newly synthesized TGF-beta 2 in the set of events elicited by retinoic acid in articular cartilage is unclear, the results establish an intrinsic metabolic link between the isoprenoid and TGF-beta in articular cartilage. Tretinoin 84-97 transforming growth factor beta 2 Bos taurus 40-50
1734039-0 1992 Differential regulation of the expression of transforming growth factor-beta mRNAs by growth factors and retinoic acid in chicken embryo chondrocytes, myocytes, and fibroblasts. Tretinoin 105-118 transforming growth factor beta 1 Homo sapiens 45-76
1346252-4 1992 Transcription of CD18 is highly tissue-specific, hormonally inducible (by retinoic acid [RA]), and coordinately regulated with leukocyte integrin alpha-chains. Tretinoin 74-87 integrin subunit beta 2 Homo sapiens 17-21
1346252-4 1992 Transcription of CD18 is highly tissue-specific, hormonally inducible (by retinoic acid [RA]), and coordinately regulated with leukocyte integrin alpha-chains. Tretinoin 89-91 integrin subunit beta 2 Homo sapiens 17-21
1531473-0 1992 Induction of phosphatidylinositol-glycan-linked Fc gamma RIII in human monocytic THP-1 cells by transforming growth factor-beta 1 and retinoic acid. Tretinoin 134-147 GLI family zinc finger 2 Homo sapiens 81-86
1569050-7 1992 These results suggest that while the increases in the activities of PKC alpha and beta isoforms are common in the differentiation program initiated by several inducers, including retinoic acid, the emergence of an unclassified PKC isoform is a retinoic acid-specific process. Tretinoin 244-257 protein kinase C alpha Homo sapiens 68-71
1531473-6 1992 These results indicated that TGF-beta 1 could induce phosphatidylinositol-glycan-linked Fc gamma RIII (Fc gamma RIII-I) in THP-1 cells in the presence of RA. Tretinoin 154-156 transforming growth factor beta 1 Homo sapiens 29-39
1531473-6 1992 These results indicated that TGF-beta 1 could induce phosphatidylinositol-glycan-linked Fc gamma RIII (Fc gamma RIII-I) in THP-1 cells in the presence of RA. Tretinoin 154-156 GLI family zinc finger 2 Homo sapiens 123-128
1569050-4 1992 When retinoic acid was used as the inducer, in addition to PKC alpha and beta, a third PKC isoform appeared. Tretinoin 5-18 protein kinase C alpha Homo sapiens 59-68
1569050-4 1992 When retinoic acid was used as the inducer, in addition to PKC alpha and beta, a third PKC isoform appeared. Tretinoin 5-18 protein kinase C alpha Homo sapiens 59-62
1569050-7 1992 These results suggest that while the increases in the activities of PKC alpha and beta isoforms are common in the differentiation program initiated by several inducers, including retinoic acid, the emergence of an unclassified PKC isoform is a retinoic acid-specific process. Tretinoin 179-192 protein kinase C alpha Homo sapiens 68-77
1569050-7 1992 These results suggest that while the increases in the activities of PKC alpha and beta isoforms are common in the differentiation program initiated by several inducers, including retinoic acid, the emergence of an unclassified PKC isoform is a retinoic acid-specific process. Tretinoin 179-192 protein kinase C alpha Homo sapiens 68-71
1734039-8 1992 Our results indicate a complex pattern of regulation of the different TGF-beta genes by themselves as well as by PDGF, EGF, IL-1, dexamethasone, TPA, and retinoic acid in chicken embryo cells. Tretinoin 154-167 transforming growth factor beta 1 Homo sapiens 70-78
1734039-7 1992 Retinoic acid also has contrasting effects on chondrocytes and myocytes either increasing or decreasing, respectively, expression of TGF-beta s 2 and 3 mRNAs and TGF-beta 2 protein. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 133-141
1378029-0 1992 Expression of loricrin is negatively controlled by retinoic acid in human epidermis reconstructed in vitro. Tretinoin 51-64 loricrin cornified envelope precursor protein Homo sapiens 14-22
1734863-1 1992 The differentiation of HL-60 promyelocytic cells toward mature myelocytic cells induced by retinoic acid (RA) was accompanied by a quantitative similar increase in alkaline phosphatase (ALP) activity. Tretinoin 91-104 alkaline phosphatase, placental Homo sapiens 186-189
1734863-3 1992 The combination of RA and sphinganine increased in parallel the percentage of mature cells and the ALP activities. Tretinoin 19-21 alkaline phosphatase, placental Homo sapiens 99-102
1734863-4 1992 Short exposures (4-8h) of HL-60 cells to RA promoted differentiation and ALP activity to a fraction (about 50%) of their maximums which were achieved in cells after 24h or longer RA exposure. Tretinoin 41-43 alkaline phosphatase, placental Homo sapiens 73-76
1370462-9 1992 Retinoic acid treatment of endothelial cells results in down-regulation of GATA-2 expression as well as down-regulation of PPET-1 gene expression. Tretinoin 0-13 endothelin 1 Homo sapiens 123-129
1309742-5 1992 Retinoic acid (but not retinal or retinol) was capable of inhibiting dbcAMP-dependent expression of FPR mRNA half-life. Tretinoin 0-13 formyl peptide receptor 1 Homo sapiens 100-103
1309742-6 1992 Dexamethasone enhanced the effects of dbcAMP and blocked the inhibitory effect of retinoic acid on expression of FPR and FPR transcripts. Tretinoin 82-95 formyl peptide receptor 1 Homo sapiens 113-116
1309742-6 1992 Dexamethasone enhanced the effects of dbcAMP and blocked the inhibitory effect of retinoic acid on expression of FPR and FPR transcripts. Tretinoin 82-95 formyl peptide receptor 1 Homo sapiens 121-124
1730652-6 1992 Although most of the total PKC activity (97%) was detected in the cytosol fraction, the increase in PKC activity was attributed to an increased enzyme activity in both cytosol and membrane fractions, and shown to be RA dose-dependent. Tretinoin 216-218 protein kinase C, alpha Mus musculus 100-103
1730652-7 1992 Kinetics study revealed that the increase in PKC was a time-dependent process and the enhancement was detectable as early as 8 h after the addition of RA to LAK cell culture. Tretinoin 151-153 protein kinase C, alpha Mus musculus 45-48
1730652-9 1992 RA further increased the expression of PKC alpha. Tretinoin 0-2 protein kinase C, alpha Mus musculus 39-48
1730652-10 1992 The enhanced expression of alpha isozyme of PKC by RA was also in a dose and time dependent manner. Tretinoin 51-53 protein kinase C, alpha Mus musculus 44-47
1730652-11 1992 Taken together, these results indicate that the mechanism of the augmentation of LAK cell activity by RA may in part result from the increase in PKC, especially PKC alpha isozyme. Tretinoin 102-104 protein kinase C, alpha Mus musculus 145-148
1730652-11 1992 Taken together, these results indicate that the mechanism of the augmentation of LAK cell activity by RA may in part result from the increase in PKC, especially PKC alpha isozyme. Tretinoin 102-104 protein kinase C, alpha Mus musculus 161-170
1378029-4 1992 The reactivities for both loricrin and loricrin mRNAs were abolished by a treatment of the cultures with a retinoic acid concentration (10(-6) M) provoking a complete inhibition of terminal epidermal differentiation (parakeratosis). Tretinoin 107-120 loricrin cornified envelope precursor protein Homo sapiens 26-34
1378029-4 1992 The reactivities for both loricrin and loricrin mRNAs were abolished by a treatment of the cultures with a retinoic acid concentration (10(-6) M) provoking a complete inhibition of terminal epidermal differentiation (parakeratosis). Tretinoin 107-120 loricrin cornified envelope precursor protein Homo sapiens 39-47
12106426-0 1992 Accelerated Differentiation in Response to Retinoic Acid After Retrovirally Mediated Gene Transfer of GAP-43 into Mouse Neuroblastoma Cells. Tretinoin 43-56 growth associated protein 43 Mus musculus 102-108
1727694-1 1992 The objective of this study was to investigate the possible regulation of the vitamin K-dependent matrix Gla (gamma-carboxyglutamic acid) protein (MGP) by retinoic acid, a regulation suggested by the recent observation that the human MGP promoter has a perfect direct repeat which is nearly identical to the retinoic acid-responsive element in the retinoic acid receptor-beta gene. Tretinoin 155-168 retinoic acid receptor beta Homo sapiens 348-375
12106426-4 1992 However, overexpression of GAP-43 results in a marked acceleration of neurite formation in response to RA. Tretinoin 103-105 growth associated protein 43 Mus musculus 27-33
12106426-5 1992 We propose that while GAP-43 does not trigger the initiation of neurite extension, its expression is rate-limiting for neurite outgrowth in response to differentiation agents such as RA. Tretinoin 183-185 growth associated protein 43 Mus musculus 22-28
1741160-6 1992 Upon retinoic acid-induced differentiation of the LA-N-5 neuroblastoma cell line, the level of p53 protein declined, as did the level of p53 mRNA, but the half-life of the protein remained unchanged. Tretinoin 5-18 tumor protein p53 Homo sapiens 95-98
1728634-0 1992 Differential modulation of transforming growth factor-beta 1 expression and mucin deposition by retinoic acid and sodium lauryl sulfate in human skin. Tretinoin 96-109 transforming growth factor beta 1 Homo sapiens 27-60
1728634-3 1992 The modulation of transforming growth factor-beta 1 expression by retinoic acid occurred in the absence of any change in its mRNA level. Tretinoin 66-79 transforming growth factor beta 1 Homo sapiens 18-51
1728634-5 1992 Similar changes in TGF-beta 1 and TGF-beta 2 immunoreactivity and mRNA levels, as observed in retinoic acid-treated skin, were observed in skin following topical application of the irritant sodium lauryl sulfate, indicating that the alterations induced by retinoic acid were not specific. Tretinoin 94-107 transforming growth factor beta 1 Homo sapiens 19-29
1728634-5 1992 Similar changes in TGF-beta 1 and TGF-beta 2 immunoreactivity and mRNA levels, as observed in retinoic acid-treated skin, were observed in skin following topical application of the irritant sodium lauryl sulfate, indicating that the alterations induced by retinoic acid were not specific. Tretinoin 256-269 transforming growth factor beta 1 Homo sapiens 19-29
1728634-8 1992 Treatment of keratinocytes with retinoic acid resulted in a 50% induction of transforming growth factor-beta 1 protein, without any detectable change in transforming growth factor-beta 2. Tretinoin 32-45 transforming growth factor beta 1 Homo sapiens 77-110
1728634-10 1992 Whereas alterations in transforming growth factor-beta 1 expression were observed in both retinoic acid- and sodium lauryl sulfate-treated skin, accumulation of mucin was specific to retinoic acid-treated skin. Tretinoin 90-103 transforming growth factor beta 1 Homo sapiens 23-56
1635422-0 1992 Protein kinase C activity during sphinganine potentiation of retinoic acid-induced differentiation in a human leukemia cell line (HL-60). Tretinoin 61-74 proline rich transmembrane protein 2 Homo sapiens 0-16
1373794-5 1992 A further correlation was made between retinoic acid and alpha-fetoprotein synthesis. Tretinoin 39-52 alpha fetoprotein Homo sapiens 57-74
1389683-0 1992 Suppression by retinoic acid of epidermal growth factor receptor autophosphorylation and glycosylation in cultured human head and neck squamous carcinoma cells. Tretinoin 15-28 epidermal growth factor receptor Homo sapiens 32-64
1389683-3 1992 Here we examined the effects of RA on the expression and function of EGF-R in two HNSCC cell lines, 1483 and 183, which exhibit distinct states of squamous cell differentiation, EGF-R mRNA levels, and responses to the growth inhibitory effects of RA. Tretinoin 32-34 epidermal growth factor receptor Homo sapiens 69-74
1389683-4 1992 Treatment with RA (1 microM, 7 days) of the RA-sensitive 1483 cells decreased the level of EGF-R mRNA two- to four-fold and the binding of 125I-EGF to the cell surface by 30%-35%. Tretinoin 15-17 epidermal growth factor receptor Homo sapiens 91-96
1389683-6 1992 Other effects of RA on EGF-R structure and function were similar in both cell lines. Tretinoin 17-19 epidermal growth factor receptor Homo sapiens 23-28
1389683-8 1992 More important, RA treatment of both cell lines decreased EGF-R autophosphorylation activity detected in immune-complex-kinase assay by about three- and five-fold in the 1483 and 183 cells, respectively. Tretinoin 16-18 epidermal growth factor receptor Homo sapiens 58-63
1389683-9 1992 Likewise, RA decreased the glycosylation of EGF-R in both cell lines. Tretinoin 10-12 epidermal growth factor receptor Homo sapiens 44-49
1389683-11 1992 These results demonstrate that RA can modify the structure of the EGF-R by decreasing its glycosylation and suggest that these changes may suppress the autophosphorylation activity of the receptor kinase. Tretinoin 31-33 epidermal growth factor receptor Homo sapiens 66-71
1389683-12 1992 The RA-induced changes in EGF-R do not correlate with the effect of RA on the growth of the cells but may be related to the suppression of squamous cell differentiation in the 1483 cells. Tretinoin 4-6 epidermal growth factor receptor Homo sapiens 26-31
1635422-1 1992 The differentiation of HL-60 promyelocytic cells toward mature granulocytic cells induced by retinoic acid (RA) was accompanied by a decrease in protein kinase C (PKC) activity. Tretinoin 93-106 proline rich transmembrane protein 2 Homo sapiens 145-161
1635422-1 1992 The differentiation of HL-60 promyelocytic cells toward mature granulocytic cells induced by retinoic acid (RA) was accompanied by a decrease in protein kinase C (PKC) activity. Tretinoin 93-106 proline rich transmembrane protein 2 Homo sapiens 163-166
1635422-1 1992 The differentiation of HL-60 promyelocytic cells toward mature granulocytic cells induced by retinoic acid (RA) was accompanied by a decrease in protein kinase C (PKC) activity. Tretinoin 108-110 proline rich transmembrane protein 2 Homo sapiens 145-161
1635422-3 1992 Kinetically, PKC activity during RA-induced differentiation without SP decreased to its lowest (75% of the control) after 48h; about 50% of the reduction was observed at 24h. Tretinoin 33-35 proline rich transmembrane protein 2 Homo sapiens 13-16
1635422-4 1992 In the presence of SP, PKC activity decreased more rapidly to its lowest (60% of the control) within 24h of incubation of RA. Tretinoin 122-124 proline rich transmembrane protein 2 Homo sapiens 23-26
1635422-5 1992 SP, added 24h before or concomitantly with the addition of RA, could potentiate the RA-induced differentiation and the reduction of PKC activity. Tretinoin 59-61 proline rich transmembrane protein 2 Homo sapiens 132-135
1635422-6 1992 Our results indicate that the effect of SP and the role of PKC during RA-induced differentiation may be critical at the early stages of induction of differentiation (within 24h of RA exposure). Tretinoin 70-72 proline rich transmembrane protein 2 Homo sapiens 59-62
1635422-6 1992 Our results indicate that the effect of SP and the role of PKC during RA-induced differentiation may be critical at the early stages of induction of differentiation (within 24h of RA exposure). Tretinoin 180-182 proline rich transmembrane protein 2 Homo sapiens 59-62
1741160-6 1992 Upon retinoic acid-induced differentiation of the LA-N-5 neuroblastoma cell line, the level of p53 protein declined, as did the level of p53 mRNA, but the half-life of the protein remained unchanged. Tretinoin 5-18 tumor protein p53 Homo sapiens 137-140
1742485-5 1991 Similar time-related increases in COX metabolites were observed in THP-1 cells induced to differentiate with retinoic acid. Tretinoin 109-122 GLI family zinc finger 2 Homo sapiens 67-72
1315557-1 1992 From a series of naphthalene and benzoic acid derivatives we have identified synthetic retinoic acid analogues exhibiting high selectivity for the nuclear retinoic acid receptors RAR alpha (Am 580), RAR beta (CD 2019) and RAR gamma (CD 437) as well as ligands sharing high affinities for all RAR subtypes (CD 367). Tretinoin 87-100 retinoic acid receptor beta Homo sapiens 199-207
1315557-1 1992 From a series of naphthalene and benzoic acid derivatives we have identified synthetic retinoic acid analogues exhibiting high selectivity for the nuclear retinoic acid receptors RAR alpha (Am 580), RAR beta (CD 2019) and RAR gamma (CD 437) as well as ligands sharing high affinities for all RAR subtypes (CD 367). Tretinoin 87-100 C-type lectin domain family 4 member A Homo sapiens 306-312
1660713-0 1991 Specific down-regulation of parathyroid hormone (PTH) receptors and responses to PTH by tumour necrosis factor alpha and retinoic acid in UMR 106-06 osteoblast-like osteosarcoma cells. Tretinoin 121-134 parathyroid hormone Rattus norvegicus 28-47
1661164-0 1991 The secretion of the tissue inhibitor of metalloproteinases (TIMP) by human synovial fibroblasts is modulated by all-trans-retinoic acid. Tretinoin 113-136 TIMP metallopeptidase inhibitor 1 Homo sapiens 21-59
1661164-0 1991 The secretion of the tissue inhibitor of metalloproteinases (TIMP) by human synovial fibroblasts is modulated by all-trans-retinoic acid. Tretinoin 113-136 TIMP metallopeptidase inhibitor 1 Homo sapiens 61-65
1661164-4 1991 The production of the highly specific tissue inhibitor of metalloproteinases (TIMP) by connective tissue cells may be crucial in the regulation of connective tissue breakdown and this present study was undertaken to determine if retinoic acid (RA) could modulate TIMP and collagenase production by synovial fibroblasts. Tretinoin 229-242 TIMP metallopeptidase inhibitor 1 Homo sapiens 38-76
1661164-4 1991 The production of the highly specific tissue inhibitor of metalloproteinases (TIMP) by connective tissue cells may be crucial in the regulation of connective tissue breakdown and this present study was undertaken to determine if retinoic acid (RA) could modulate TIMP and collagenase production by synovial fibroblasts. Tretinoin 229-242 TIMP metallopeptidase inhibitor 1 Homo sapiens 78-82
1661164-4 1991 The production of the highly specific tissue inhibitor of metalloproteinases (TIMP) by connective tissue cells may be crucial in the regulation of connective tissue breakdown and this present study was undertaken to determine if retinoic acid (RA) could modulate TIMP and collagenase production by synovial fibroblasts. Tretinoin 229-242 TIMP metallopeptidase inhibitor 1 Homo sapiens 263-267
1660713-0 1991 Specific down-regulation of parathyroid hormone (PTH) receptors and responses to PTH by tumour necrosis factor alpha and retinoic acid in UMR 106-06 osteoblast-like osteosarcoma cells. Tretinoin 121-134 parathyroid hormone Rattus norvegicus 49-52
1660713-0 1991 Specific down-regulation of parathyroid hormone (PTH) receptors and responses to PTH by tumour necrosis factor alpha and retinoic acid in UMR 106-06 osteoblast-like osteosarcoma cells. Tretinoin 121-134 parathyroid hormone Rattus norvegicus 81-84
1797449-0 1991 Recombinant human interleukin-6 enhances the antiproliferation and differentiation inducing effects of retinoic acid in HL-60 human myeloid leukaemic cells. Tretinoin 103-116 interleukin 6 Homo sapiens 18-31
1797449-6 1991 The addition of interleukin-6 to all-trans retinoic acid-treated cultures of HL-60 human myeloid leukaemia cells significantly enhanced the desired antiproliferation effect of all-trans retinoic acid. Tretinoin 43-56 interleukin 6 Homo sapiens 16-29
1797449-6 1991 The addition of interleukin-6 to all-trans retinoic acid-treated cultures of HL-60 human myeloid leukaemia cells significantly enhanced the desired antiproliferation effect of all-trans retinoic acid. Tretinoin 186-199 interleukin 6 Homo sapiens 16-29
1797449-8 1991 The combination of interleukin-6 with all-trans retinoic acid reduced the doses of all-trans retinoic acid required to induce the same differentiation of HL-60 cells as single agent by between 1.7- and 4.8-fold; that is, the efficacy of all-trans retinoic acid in inducing the differentiation of human myeloid leukaemia HL-60 cells was increased up to 4.8 times by its combination with interleukin-6. Tretinoin 48-61 interleukin 6 Homo sapiens 386-399
1797449-8 1991 The combination of interleukin-6 with all-trans retinoic acid reduced the doses of all-trans retinoic acid required to induce the same differentiation of HL-60 cells as single agent by between 1.7- and 4.8-fold; that is, the efficacy of all-trans retinoic acid in inducing the differentiation of human myeloid leukaemia HL-60 cells was increased up to 4.8 times by its combination with interleukin-6. Tretinoin 93-106 interleukin 6 Homo sapiens 19-32
1797449-8 1991 The combination of interleukin-6 with all-trans retinoic acid reduced the doses of all-trans retinoic acid required to induce the same differentiation of HL-60 cells as single agent by between 1.7- and 4.8-fold; that is, the efficacy of all-trans retinoic acid in inducing the differentiation of human myeloid leukaemia HL-60 cells was increased up to 4.8 times by its combination with interleukin-6. Tretinoin 93-106 interleukin 6 Homo sapiens 386-399
1797449-8 1991 The combination of interleukin-6 with all-trans retinoic acid reduced the doses of all-trans retinoic acid required to induce the same differentiation of HL-60 cells as single agent by between 1.7- and 4.8-fold; that is, the efficacy of all-trans retinoic acid in inducing the differentiation of human myeloid leukaemia HL-60 cells was increased up to 4.8 times by its combination with interleukin-6. Tretinoin 93-106 interleukin 6 Homo sapiens 19-32
1797449-8 1991 The combination of interleukin-6 with all-trans retinoic acid reduced the doses of all-trans retinoic acid required to induce the same differentiation of HL-60 cells as single agent by between 1.7- and 4.8-fold; that is, the efficacy of all-trans retinoic acid in inducing the differentiation of human myeloid leukaemia HL-60 cells was increased up to 4.8 times by its combination with interleukin-6. Tretinoin 93-106 interleukin 6 Homo sapiens 386-399
1661301-1 1991 We have recently demonstrated that all-trans retinoic acid (RA), the active metabolite of vitamin A, is an efficient alternative to chemotherapy in the treatment of acute promyelocytic leukemia (AML3). Tretinoin 35-58 RUNX family transcription factor 2 Homo sapiens 195-199
1802719-3 1991 Furthermore, it has been demonstrated that retinoic acid-dedifferentiated chondrocytes can reexpress type II collagen if treated by the microfilament disruptive drug dihydrocytochalasin B, without a return to the spherical shape. Tretinoin 43-56 collagen type II alpha 1 chain Gallus gallus 101-117
1725165-5 1991 Exposure to 10(-6) M RA increases the levels of RAR beta and K19 mRNA; conversely, complete removal of RA from the medium results in reduced levels of these messages. Tretinoin 21-23 retinoic acid receptor beta Homo sapiens 48-56
1661301-1 1991 We have recently demonstrated that all-trans retinoic acid (RA), the active metabolite of vitamin A, is an efficient alternative to chemotherapy in the treatment of acute promyelocytic leukemia (AML3). Tretinoin 60-62 RUNX family transcription factor 2 Homo sapiens 195-199
1661301-4 1991 The PLM-RAR alpha protein may account for the impairment of differentiation and thus leukemogenesis, but not for the paradoxical efficacy of RA in these cells. Tretinoin 8-10 FXYD domain containing ion transport regulator 1 Homo sapiens 4-7
1659820-0 1991 Gs alpha availability to cholera toxin-catalysed ADP-ribosylation is decreased in membranes of retinoic acid-treated leukemic cell lines HL-60 and THP-1. Tretinoin 95-108 GNAS complex locus Homo sapiens 0-8
1774953-1 1991 It has been shown that patients with acute promyelocytic leukemia (AML3 subtype) treated with all-trans retinoic acid (all-trans RA), 45 mg/m2/day, achieve complete remission through differentiation of the leukemic clone to mature myeloid cells, which die spontaneously. Tretinoin 104-117 RUNX family transcription factor 2 Homo sapiens 67-71
1659820-0 1991 Gs alpha availability to cholera toxin-catalysed ADP-ribosylation is decreased in membranes of retinoic acid-treated leukemic cell lines HL-60 and THP-1. Tretinoin 95-108 GLI family zinc finger 2 Homo sapiens 147-152
1659820-2 1991 Retinoic acid (RA) induces HL-60 and THP-1 leukemic cell lines to differentiate into granulocyte-like and monocyte-like cells. Tretinoin 0-13 GLI family zinc finger 2 Homo sapiens 37-42
1659820-2 1991 Retinoic acid (RA) induces HL-60 and THP-1 leukemic cell lines to differentiate into granulocyte-like and monocyte-like cells. Tretinoin 15-17 GLI family zinc finger 2 Homo sapiens 37-42
1667243-4 1991 Both retinoids (1-100 microM) also inhibited, in a dose-dependent way, degranulation induced by fMLP (upto 85% at the highest concentration of RA). Tretinoin 143-145 formyl peptide receptor 1 Homo sapiens 96-100
1717193-0 1991 Retinoic acid potentiates interleukin-1- and fibroblast growth factor-induced human synovial fibroblast proliferation. Tretinoin 0-13 fibroblast growth factor 1 Homo sapiens 45-69
1667243-3 1991 Incubation of PMN with RAc or RA (1-100 microM) caused a dose-dependent inhibition (upto 90%) in O2- production and chemiluminescence induced by phorbol myristate acetate (PMA), N-formyl-methionyl-leucyl-phenylanaline (fMLP), opsonized zymosan or ionophore A23187. Tretinoin 23-25 formyl peptide receptor 1 Homo sapiens 219-223
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 4-23 fibroblast growth factor 1 Homo sapiens 279-303
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 4-23 fibroblast growth factor 1 Homo sapiens 305-309
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 4-23 fibroblast growth factor 2 Homo sapiens 311-315
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 25-29 fibroblast growth factor 1 Homo sapiens 279-303
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 25-29 fibroblast growth factor 1 Homo sapiens 305-309
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 25-29 fibroblast growth factor 2 Homo sapiens 311-315
1717193-4 1991 The mechanism by which ATRA enhances IL-1-induced HSN proliferation does not appear mediated by changes in the affinity or number of IL-1 receptors expressed by HSN; however, treatment with dexamethasone (DEX, 10(-6)M) resulted in a twofold increase in IL-1 receptor number. Tretinoin 23-27 interleukin 1 beta Homo sapiens 37-41
1717193-5 1991 ATRA inhibited both IL-1 beta- and TNF alpha-induced secretion of prostaglandin-E2 (PGE2), a potent feedback inhibitor of cytokine-stimulated HSN proliferation. Tretinoin 0-4 interleukin 1 beta Homo sapiens 20-29
1717193-5 1991 ATRA inhibited both IL-1 beta- and TNF alpha-induced secretion of prostaglandin-E2 (PGE2), a potent feedback inhibitor of cytokine-stimulated HSN proliferation. Tretinoin 0-4 tumor necrosis factor Homo sapiens 35-44
1717193-6 1991 However, the synergistic effect of ATRA on IL-1- or FGF-induced proliferation did not appear related to the secretion of cyclooxygenase products since ATRA had no effect on TNF alpha-induced HSN proliferation and indomethacin was included in all HSN proliferation experiments. Tretinoin 35-39 interleukin 1 beta Homo sapiens 43-47
1934258-1 1991 Previous work from our laboratory showed that tumor promoters such as phorbol ester (TPA) stimulated the release of fibronectin (FN) from the surface of several cell types in culture, and that this stimulation was counteracted by retinoic acid. Tretinoin 230-243 fibronectin 1 Homo sapiens 116-127
1685145-4 1991 In this study we show that topical all-trans-retinoic acid (RA) and an orally administered retinoid, temarotene, protect both LC and Thy-1+ DEC from being depleted by UV light. Tretinoin 35-58 thymus cell antigen 1, theta Mus musculus 133-138
1685145-4 1991 In this study we show that topical all-trans-retinoic acid (RA) and an orally administered retinoid, temarotene, protect both LC and Thy-1+ DEC from being depleted by UV light. Tretinoin 60-62 thymus cell antigen 1, theta Mus musculus 133-138
1661427-0 1991 Induction of CAT gene expression on a plasmid vector (L factor) by retinoic acid in mouse embryonal carcinoma (F9) cells. Tretinoin 67-80 catalase Mus musculus 13-16
1661427-3 1991 When such plasmid-bearing cells were treated with retinoic acid, the CAT gene was inducibly expressed. Tretinoin 50-63 catalase Homo sapiens 69-72
1657172-8 1991 The results indicate that RA can influence the levels of hepatic cytochrome P-450 and can modulate the stimulation of heme oxygenase activity by thyroid hormone in vivo. Tretinoin 26-28 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 65-81
1935958-0 1991 Effect of retinoic acid on the synthesis of tissue-type plasminogen activator and plasminogen activator inhibitor-1 in human endothelial cells. Tretinoin 10-23 plasminogen activator, tissue type Homo sapiens 44-77
1935958-2 1991 The present study evaluates the effect of retinoic acid on the synthesis of tissue-type plasminogen activator (t-PA) and of plasminogen activator inhibitor-1 (PAI-1) by cultured human umbilical vein endothelial cells (HUVEC). Tretinoin 42-55 plasminogen activator, tissue type Homo sapiens 76-109
1935958-2 1991 The present study evaluates the effect of retinoic acid on the synthesis of tissue-type plasminogen activator (t-PA) and of plasminogen activator inhibitor-1 (PAI-1) by cultured human umbilical vein endothelial cells (HUVEC). Tretinoin 42-55 plasminogen activator, tissue type Homo sapiens 111-115
1935958-3 1991 Retinoic acid produced a time- and concentration-dependent increase in the secretion of t-PA-related antigen but not of PAI-1 related antigen into the culture medium. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 88-92
1935958-4 1991 A maximal sevenfold increase of t-PA antigen after 24 h was observed with 10 microM and a half-maximal increase with 0.1 microM retinoic acid. Tretinoin 128-141 plasminogen activator, tissue type Homo sapiens 32-36
1935958-5 1991 Retinoic acid induced a time-dependent increase of the t-PA mRNA, with a maximum at 8 h and returning to normal at 24 h. The protein kinase inhibitor H7 decreased the t-PA antigen induced by both retinoic acid and phorbol 12-myristate 13-acetate. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 55-59
1935958-5 1991 Retinoic acid induced a time-dependent increase of the t-PA mRNA, with a maximum at 8 h and returning to normal at 24 h. The protein kinase inhibitor H7 decreased the t-PA antigen induced by both retinoic acid and phorbol 12-myristate 13-acetate. Tretinoin 0-13 plasminogen activator, tissue type Homo sapiens 167-171
1935958-5 1991 Retinoic acid induced a time-dependent increase of the t-PA mRNA, with a maximum at 8 h and returning to normal at 24 h. The protein kinase inhibitor H7 decreased the t-PA antigen induced by both retinoic acid and phorbol 12-myristate 13-acetate. Tretinoin 196-209 plasminogen activator, tissue type Homo sapiens 55-59
1935958-5 1991 Retinoic acid induced a time-dependent increase of the t-PA mRNA, with a maximum at 8 h and returning to normal at 24 h. The protein kinase inhibitor H7 decreased the t-PA antigen induced by both retinoic acid and phorbol 12-myristate 13-acetate. Tretinoin 196-209 plasminogen activator, tissue type Homo sapiens 167-171
1935958-6 1991 These results suggest that treatment of HUVEC with retinoic acid increases t-PA production by a pathway which, at some level, involves protein kinases. Tretinoin 51-64 plasminogen activator, tissue type Homo sapiens 75-79
1935958-7 1991 Thus, retinoic acid induces t-PA synthesis in the absence of altered PAI-1 synthesis, which may enhance the fibrinolytic potential of the endothelium. Tretinoin 6-19 plasminogen activator, tissue type Homo sapiens 28-32
1661245-5 1991 Response elements for retinoic acid have so far been identified for the rat growth hormone and phosphoenolpyruvate carboxykinase, the mouse complement H and laminin B1, the human and mouse retinoic acid receptor beta, the human osteocalcin, and the human alcohol dehydrogenase genes. Tretinoin 22-35 bone gamma-carboxyglutamate protein Homo sapiens 228-239
1934258-1 1991 Previous work from our laboratory showed that tumor promoters such as phorbol ester (TPA) stimulated the release of fibronectin (FN) from the surface of several cell types in culture, and that this stimulation was counteracted by retinoic acid. Tretinoin 230-243 fibronectin 1 Homo sapiens 129-131
1934258-3 1991 To show that the release of FN is related to activation of PKC, we tested the action of DAGs on FN release from human lung fibroblasts and its counteraction by retinoic acid. Tretinoin 160-173 fibronectin 1 Homo sapiens 28-30
1934258-6 1991 Retinoic acid reversed the action of DAG with respect to stimulation of FN release and inhibited this release even in the absence of DAG. Tretinoin 0-13 fibronectin 1 Homo sapiens 72-74
1654565-8 1991 When retinol-deficient rats were orally administered 1 dose of retinoic acid (100 micrograms per rat), lung RAR-beta mRNA levels started to increase after 1 hr and reached a 16-fold higher level after 4 hr; after 4 hr these retinoic acid-fed rats also showed a 7-fold increase in liver RAR-beta mRNA levels as compared with levels in the retinol-deficient rats. Tretinoin 63-76 retinoic acid receptor, beta Rattus norvegicus 108-116
1749528-1 1991 The gene of the bone protein osteocalcin has a promoter region recognized by the receptors for 1,25-dihydroxyvitamin D3 and retinoic acid, both of which stimulate transcription. Tretinoin 124-137 bone gamma-carboxyglutamate protein Homo sapiens 29-40
1656191-1 1991 Biological effects of retinoic acid (RA) are mediated through its binding to three closely related nuclear receptors (RAR alpha, RAR beta, and RAR gamma) belonging to the steroid-thyroid nuclear receptor family. Tretinoin 22-35 retinoic acid receptor beta Homo sapiens 129-137
1656191-1 1991 Biological effects of retinoic acid (RA) are mediated through its binding to three closely related nuclear receptors (RAR alpha, RAR beta, and RAR gamma) belonging to the steroid-thyroid nuclear receptor family. Tretinoin 37-39 retinoic acid receptor beta Homo sapiens 129-137
1717924-3 1991 Normally, RAR-beta is expressed as two transcripts, of sizes 3.1 kb and 2.8 kb, which are strongly induced by retinoic acid. Tretinoin 110-123 retinoic acid receptor beta Homo sapiens 10-18
1656958-4 1991 In response to retinoic acid, the three hybrid receptors ER-RAR alpha, ER-RAR beta and ER-RAR gamma exhibited the same induction profile as the corresponding wild type receptors RAR alpha, RAR beta, and RAR gamma. Tretinoin 15-28 retinoic acid receptor beta Homo sapiens 74-82
1656958-4 1991 In response to retinoic acid, the three hybrid receptors ER-RAR alpha, ER-RAR beta and ER-RAR gamma exhibited the same induction profile as the corresponding wild type receptors RAR alpha, RAR beta, and RAR gamma. Tretinoin 15-28 retinoic acid receptor beta Homo sapiens 189-197
1654565-8 1991 When retinol-deficient rats were orally administered 1 dose of retinoic acid (100 micrograms per rat), lung RAR-beta mRNA levels started to increase after 1 hr and reached a 16-fold higher level after 4 hr; after 4 hr these retinoic acid-fed rats also showed a 7-fold increase in liver RAR-beta mRNA levels as compared with levels in the retinol-deficient rats. Tretinoin 63-76 retinoic acid receptor, beta Rattus norvegicus 286-294
1654565-8 1991 When retinol-deficient rats were orally administered 1 dose of retinoic acid (100 micrograms per rat), lung RAR-beta mRNA levels started to increase after 1 hr and reached a 16-fold higher level after 4 hr; after 4 hr these retinoic acid-fed rats also showed a 7-fold increase in liver RAR-beta mRNA levels as compared with levels in the retinol-deficient rats. Tretinoin 224-237 retinoic acid receptor, beta Rattus norvegicus 108-116
1654565-11 1991 These results show tissue diversity in the rapid induction of RAR-beta and RAR-gamma by retinoic acid in the adult animal and suggest distinct roles for the various receptor isoforms in the control of the retinoid response. Tretinoin 88-101 retinoic acid receptor, beta Rattus norvegicus 62-70
1651173-2 1991 We provide evidence that expression of the gene for cellular retinol-binding protein type II (CRBPII), a key protein in the intestinal absorption of vitamin A, is dramatically up-regulated by retinoic acid in the presence of RXR but not RAR. Tretinoin 192-205 retinol binding protein 2 Homo sapiens 52-92
1652063-0 1991 Retinoic acid-induced down-regulation of the interleukin-2 promoter via cis-regulatory sequences containing an octamer motif. Tretinoin 0-13 interleukin 2 Homo sapiens 45-58
1652063-4 1991 RA-induced down-regulation of the IL-2 enhancer is mediated by RAR, since overexpression of transfected RARs increased RA sensitivity of the IL-2 promoter. Tretinoin 0-2 interleukin 2 Homo sapiens 34-38
1652063-4 1991 RA-induced down-regulation of the IL-2 enhancer is mediated by RAR, since overexpression of transfected RARs increased RA sensitivity of the IL-2 promoter. Tretinoin 0-2 interleukin 2 Homo sapiens 141-145
1652063-5 1991 Functional analysis of chloramphenicol acetyltransferase vectors containing either internal deletion mutants of the region from -317 to +47 bp of the IL-2 enhancer or multimerized cis-regulatory elements showed that the RA-responsive element in the IL-2 promoter mapped to sequences containing an octamer motif. Tretinoin 220-222 interleukin 2 Homo sapiens 150-154
1652063-5 1991 Functional analysis of chloramphenicol acetyltransferase vectors containing either internal deletion mutants of the region from -317 to +47 bp of the IL-2 enhancer or multimerized cis-regulatory elements showed that the RA-responsive element in the IL-2 promoter mapped to sequences containing an octamer motif. Tretinoin 220-222 interleukin 2 Homo sapiens 249-253
1715692-2 1991 The cells responded to retinoic acid with a significant induction of tissue transglutaminase expression but no alterations in the expression of beta-retinoic acid receptor transcripts. Tretinoin 23-36 transglutaminase 2 Homo sapiens 69-92
1923522-7 1991 Furthermore, the expression pattern of type I and type II NF1-GRD mRNA immediately changed in SH-SY5Y neuroblastoma cells when neuronal differentiation programs were induced by retinoic acid treatment. Tretinoin 177-190 neurofibromin 1 Homo sapiens 58-61
1907993-4 1991 Retinoic acid supplementation in vitro decreased IFN-gamma secretion from A- T cells, indicating that IFN-gamma production is retinoid-responsive. Tretinoin 0-13 interferon gamma Mus musculus 49-58
1907993-4 1991 Retinoic acid supplementation in vitro decreased IFN-gamma secretion from A- T cells, indicating that IFN-gamma production is retinoid-responsive. Tretinoin 0-13 interferon gamma Mus musculus 102-111
1907993-6 1991 Adding retinoic acid to the cultures either at initiation, or 48 h later, fully restored IgG1 production by A- cultures to the level of A+ control cultures. Tretinoin 7-20 immunoglobulin heavy constant gamma 1 (G1m marker) Mus musculus 89-93
1713586-8 1991 We demonstrate that serum deprivation; placement of cells into primary culture; and growth factors such as transforming growth factor beta 1, retinoic acid, and 1,25-dihydroxyvitamin D3 can all change the alternative splicing of fibronectin pre-mRNA in the ED-A, ED-B, and type III connecting sequence exons. Tretinoin 142-155 transforming growth factor, beta 1 Rattus norvegicus 107-140
1651173-2 1991 We provide evidence that expression of the gene for cellular retinol-binding protein type II (CRBPII), a key protein in the intestinal absorption of vitamin A, is dramatically up-regulated by retinoic acid in the presence of RXR but not RAR. Tretinoin 192-205 retinol binding protein 2 Homo sapiens 94-100
2065662-0 1991 Independent regulation of HNF-1 alpha and HNF-1 beta by retinoic acid in F9 teratocarcinoma cells. Tretinoin 56-69 HNF1 homeobox A Homo sapiens 26-37
1677311-0 1991 Enhancement by retinoic acid and dibutyryl cyclic adenosine 3":5"-monophosphate of the differentiation and gene expression of human neuroblastoma cells induced by interferon. Tretinoin 15-28 interferon alpha 1 Homo sapiens 163-173
2065662-0 1991 Independent regulation of HNF-1 alpha and HNF-1 beta by retinoic acid in F9 teratocarcinoma cells. Tretinoin 56-69 HNF1 homeobox B Homo sapiens 42-52
2065662-3 1991 During retinoic acid (RA) induced differentiation of F9 embryonal carcinoma (EC) cells, which stimulates aspects of pre-implantation embryogenesis, both HNF-1 beta mRNA and immunoreactive DNA-binding activity are strongly induced approximately 24 h post RA-treatment. Tretinoin 7-20 HNF1 homeobox B Homo sapiens 153-163
2065662-3 1991 During retinoic acid (RA) induced differentiation of F9 embryonal carcinoma (EC) cells, which stimulates aspects of pre-implantation embryogenesis, both HNF-1 beta mRNA and immunoreactive DNA-binding activity are strongly induced approximately 24 h post RA-treatment. Tretinoin 22-24 HNF1 homeobox B Homo sapiens 153-163
2065662-3 1991 During retinoic acid (RA) induced differentiation of F9 embryonal carcinoma (EC) cells, which stimulates aspects of pre-implantation embryogenesis, both HNF-1 beta mRNA and immunoreactive DNA-binding activity are strongly induced approximately 24 h post RA-treatment. Tretinoin 254-256 HNF1 homeobox B Homo sapiens 153-163
1657566-0 1991 Retinoic acid induces NGF-dependent survival response and high-affinity NGF receptors in immature chick sympathetic neurons. Tretinoin 0-13 nerve growth factor Gallus gallus 22-25
1880152-4 1991 Moreover, treatment with EGF diminishes the levels of TGF-beta 2, while RA decreases the levels of TGF-beta 1 in both cell lines. Tretinoin 72-74 transforming growth factor, beta 1 Rattus norvegicus 99-109
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 32-34 transforming growth factor, beta 1 Rattus norvegicus 65-75
1657566-0 1991 Retinoic acid induces NGF-dependent survival response and high-affinity NGF receptors in immature chick sympathetic neurons. Tretinoin 0-13 nerve growth factor Gallus gallus 72-75
1657566-3 1991 We found that retinoic acid (RA) induces the ability of these cells to survive in the presence of NGF. Tretinoin 14-27 nerve growth factor Gallus gallus 98-101
1657566-3 1991 We found that retinoic acid (RA) induces the ability of these cells to survive in the presence of NGF. Tretinoin 29-31 nerve growth factor Gallus gallus 98-101
1657566-6 1991 These findings suggest that the induction of high-affinity NGF receptors may be sufficient to activate the survival response in sympathetic neurons and imply an important role for RA during neuron differentiation in the peripheral nervous system. Tretinoin 180-182 nerve growth factor Gallus gallus 59-62
1648223-5 1991 However, the v-myc-associated block of phorbol 12-myristate 13-acetate-, 1 alpha,25-dihydroxycholecalciferol-, and retinoic acid-induced differentiation retinoic acid-induced differentiation can be overcome by adding interferon gamma as a costimulatory factor. Tretinoin 115-128 interferon gamma Homo sapiens 217-233
1646397-0 1991 A retinoic acid-responsive element in the apolipoprotein AI gene distinguishes between two different retinoic acid response pathways. Tretinoin 2-15 apolipoprotein A1 Homo sapiens 42-59
1675998-8 1991 Treatment of HBE and RbTE cells with 100 nM retinoic acid increased RAR beta mRNA expression but did not change the levels of RAR alpha and RAR gamma. Tretinoin 44-57 retinoic acid receptor beta Homo sapiens 68-76
1675998-9 1991 In contrast, retinoic acid suppressed in these cells the level of involucrin, transglutaminase Type I, and SQ37 mRNA. Tretinoin 13-26 involucrin Homo sapiens 66-76
1646841-0 1991 Retinoic acid enhances IL-1 beta expression in myeloid leukemia cells and in human monocytes. Tretinoin 0-13 interleukin 1 beta Homo sapiens 23-32
1646841-1 1991 We have examined the role of retinoic acid (RA), the biologically active metabolite of vitamin A, in expression of the IL-1 beta gene in the human myeloid leukemia cell line THP-1 and in human monocytes. Tretinoin 29-42 interleukin 1 beta Homo sapiens 119-128
1646841-1 1991 We have examined the role of retinoic acid (RA), the biologically active metabolite of vitamin A, in expression of the IL-1 beta gene in the human myeloid leukemia cell line THP-1 and in human monocytes. Tretinoin 29-42 GLI family zinc finger 2 Homo sapiens 174-179
1646841-1 1991 We have examined the role of retinoic acid (RA), the biologically active metabolite of vitamin A, in expression of the IL-1 beta gene in the human myeloid leukemia cell line THP-1 and in human monocytes. Tretinoin 44-46 interleukin 1 beta Homo sapiens 119-128
1646841-1 1991 We have examined the role of retinoic acid (RA), the biologically active metabolite of vitamin A, in expression of the IL-1 beta gene in the human myeloid leukemia cell line THP-1 and in human monocytes. Tretinoin 44-46 GLI family zinc finger 2 Homo sapiens 174-179
1646841-3 1991 Physiologic RA concentrations alone were not able to induce any IL-1 beta production, but they strongly enhanced the PMA-induced IL-1 beta protein production and mRNA accumulation in both human monocytes and in THP-1 cells. Tretinoin 12-14 interleukin 1 beta Homo sapiens 129-138
1646841-3 1991 Physiologic RA concentrations alone were not able to induce any IL-1 beta production, but they strongly enhanced the PMA-induced IL-1 beta protein production and mRNA accumulation in both human monocytes and in THP-1 cells. Tretinoin 12-14 GLI family zinc finger 2 Homo sapiens 211-216
1646841-5 1991 RA also slightly potentiated LPS-induced IL-1 beta expression in THP-1 cells but not in human monocytes. Tretinoin 0-2 interleukin 1 beta Homo sapiens 41-50
1646841-5 1991 RA also slightly potentiated LPS-induced IL-1 beta expression in THP-1 cells but not in human monocytes. Tretinoin 0-2 GLI family zinc finger 2 Homo sapiens 65-70
1648223-5 1991 However, the v-myc-associated block of phorbol 12-myristate 13-acetate-, 1 alpha,25-dihydroxycholecalciferol-, and retinoic acid-induced differentiation retinoic acid-induced differentiation can be overcome by adding interferon gamma as a costimulatory factor. Tretinoin 153-166 interferon gamma Homo sapiens 217-233
1708092-0 1991 Retinoic acid increases zif268 early gene expression in rat preosteoblastic cells. Tretinoin 0-13 early growth response 1 Rattus norvegicus 24-30
2033252-0 1991 Retinoic acid-induced growth inhibition of a human myeloma cell line via down-regulation of IL-6 receptors. Tretinoin 0-13 interleukin 6 Homo sapiens 92-96
2033252-1 1991 In this report we demonstrate that retinoic acid (RA) down-regulated the number of IL-6R on human leukocyte cell lines, including the myeloma cell line AF10, and two B cell hybridomas that correspond to cells at earlier stages of B cell development. Tretinoin 35-48 interleukin 6 receptor Homo sapiens 83-88
2033252-1 1991 In this report we demonstrate that retinoic acid (RA) down-regulated the number of IL-6R on human leukocyte cell lines, including the myeloma cell line AF10, and two B cell hybridomas that correspond to cells at earlier stages of B cell development. Tretinoin 50-52 interleukin 6 receptor Homo sapiens 83-88
2033252-2 1991 Using AF10 cells, whose growth was determined to be mediated by the autocrine action of IL-6, we found that RA reduction of IL-6R was concentration-dependent over a range of 10(-11) to 10(-5) M and corresponded to the ability of the retinoid to inhibit cell proliferation. Tretinoin 108-110 interleukin 6 Homo sapiens 88-92
2033252-2 1991 Using AF10 cells, whose growth was determined to be mediated by the autocrine action of IL-6, we found that RA reduction of IL-6R was concentration-dependent over a range of 10(-11) to 10(-5) M and corresponded to the ability of the retinoid to inhibit cell proliferation. Tretinoin 108-110 interleukin 6 receptor Homo sapiens 124-129
2033252-3 1991 The down-regulation of IL-6R number by RA was accompanied by reduced IL-6R mRNA expression. Tretinoin 39-41 interleukin 6 receptor Homo sapiens 23-28
2033252-3 1991 The down-regulation of IL-6R number by RA was accompanied by reduced IL-6R mRNA expression. Tretinoin 39-41 interleukin 6 receptor Homo sapiens 69-74
2033252-5 1991 However, addition of exogenous rIL-6 could overcome RA-induced growth inhibition. Tretinoin 52-54 interleukin 6 Rattus norvegicus 31-36
2033252-8 1991 These findings suggest the possibility that down-regulation of IL-6R is a means by which RA can modulate immune function. Tretinoin 89-91 interleukin 6 receptor Homo sapiens 63-68
1827123-0 1991 Influence of thyroid hormone and retinoic acid on slow sarcoplasmic reticulum Ca2+ ATPase and myosin heavy chain alpha gene expression in cardiac myocytes. Tretinoin 33-46 carbonic anhydrase 2 Rattus norvegicus 78-89
1827123-3 1991 We show here that this effect of T3 can be mimicked in primary neonatal rat cardiocytes, both in serum-containing and in serum-free media; the expression of SR Ca2+ ATPase mRNA is myocyte-specific and is also modulated by retinoic acid (RA). Tretinoin 222-235 carbonic anhydrase 2 Rattus norvegicus 160-171
1827123-3 1991 We show here that this effect of T3 can be mimicked in primary neonatal rat cardiocytes, both in serum-containing and in serum-free media; the expression of SR Ca2+ ATPase mRNA is myocyte-specific and is also modulated by retinoic acid (RA). Tretinoin 237-239 carbonic anhydrase 2 Rattus norvegicus 160-171
1827123-5 1991 The induction of Ca2+ ATPase mRNA is sensitive to T3 (EC50 approximately 30 pM) and less sensitive to RA (EC50 approximately 2 nM). Tretinoin 102-104 carbonic anhydrase 2 Rattus norvegicus 17-28
1849825-2 1991 Conversion of poly(ADP-ribose) polymerase activity to NAD-glycohydrolase during retinoic acid-induced differentiation of HL60 cells. Tretinoin 80-93 poly(ADP-ribose) polymerase 1 Homo sapiens 14-41
1849825-3 1991 Two enzymatic activities of the nuclear enzyme poly(ADP-ribose) polymerase or transferase (ADPRT, EC 2.4.2.30), a DNA-associating abundant nuclear protein with multiple molecular activities, have been determined in HL60 cells prior to and after their exposure to 1 microM retinoic acid, which results in the induction of differentiation to mature granulocytes in 4-5 days. Tretinoin 272-285 poly(ADP-ribose) polymerase 1 Homo sapiens 47-89
1849825-3 1991 Two enzymatic activities of the nuclear enzyme poly(ADP-ribose) polymerase or transferase (ADPRT, EC 2.4.2.30), a DNA-associating abundant nuclear protein with multiple molecular activities, have been determined in HL60 cells prior to and after their exposure to 1 microM retinoic acid, which results in the induction of differentiation to mature granulocytes in 4-5 days. Tretinoin 272-285 poly(ADP-ribose) polymerase 1 Homo sapiens 91-96
1849825-7 1991 During the decrease in in vitro poly(ADP-ribose) polymerase activity of nuclei following retinoic acid treatment, the quantity of endogenously poly(ADP-ribosylated) ADPRT significantly increased, as determined by chromatographic isolation of this modified protein by the boronate affinity technique, followed by gel electrophoresis and immunotransblot. Tretinoin 89-102 poly(ADP-ribose) polymerase 1 Homo sapiens 32-59
1849825-7 1991 During the decrease in in vitro poly(ADP-ribose) polymerase activity of nuclei following retinoic acid treatment, the quantity of endogenously poly(ADP-ribosylated) ADPRT significantly increased, as determined by chromatographic isolation of this modified protein by the boronate affinity technique, followed by gel electrophoresis and immunotransblot. Tretinoin 89-102 poly(ADP-ribose) polymerase 1 Homo sapiens 165-170
1849825-9 1991 Since results of in vivo and in vitro experiments coincide, it appears that in retinoic acid-induced differentiated cells (granulocytes) the autopoly(ADP-ribosylated) ADPRT performs a predominantly, if not exclusively, NAD glycohydrolase function. Tretinoin 79-92 poly(ADP-ribose) polymerase 1 Homo sapiens 167-172
1674864-3 1991 On the other hand, pretreatment of MKN-45 cells with retinoic acid (RA) significantly enhanced histamine-induced increase of cyclic AMP production, although the cyclic AMP response to either forskolin or NaF was not affected. Tretinoin 68-70 C-X-C motif chemokine ligand 8 Homo sapiens 204-207
1903722-2 1991 We here report that both D factor/LIF and IL-6 inhibit the differentiation of mouse teratocarcinoma F9 cells induced by retinoic acid alone or combined with dibutyryl cAMP. Tretinoin 120-133 interleukin 6 Mus musculus 42-46
1908141-3 1991 We report that retinoic acid (vitamin A acid) and other retinoids rather specifically stimulate the production of t-PA by cultured human umbilical vein endothelial cells. Tretinoin 15-28 plasminogen activator, tissue type Homo sapiens 114-118
1908141-3 1991 We report that retinoic acid (vitamin A acid) and other retinoids rather specifically stimulate the production of t-PA by cultured human umbilical vein endothelial cells. Tretinoin 30-44 plasminogen activator, tissue type Homo sapiens 114-118
1850696-2 1991 Here we have shown by gel retardation assay that all three retinoic acid receptors (RARs) alpha, beta and gamma expressed in Cos cells can bind directly to the previously characterized retinoic acid response element (RARE) of the LB1 promoter, albeit with a weaker affinity than to the RAR-beta gene RARE. Tretinoin 59-72 retinoic acid receptor beta Homo sapiens 286-294
1708092-1 1991 In this study we demonstrate that retinoic acid (RA) increases the expression of transcription factor zif268 mRNA in primary cultures of fetal rat calvarial cells and in simian virus 40-immortalized clonal rat calvarial preosteoblastic cells (RCT-1), which differentiate in response to RA, but not in the more differentiated RCT-3 and ROS 17/2.8 cells. Tretinoin 34-47 early growth response 1 Rattus norvegicus 102-108
1708092-1 1991 In this study we demonstrate that retinoic acid (RA) increases the expression of transcription factor zif268 mRNA in primary cultures of fetal rat calvarial cells and in simian virus 40-immortalized clonal rat calvarial preosteoblastic cells (RCT-1), which differentiate in response to RA, but not in the more differentiated RCT-3 and ROS 17/2.8 cells. Tretinoin 49-51 early growth response 1 Rattus norvegicus 102-108
1708092-1 1991 In this study we demonstrate that retinoic acid (RA) increases the expression of transcription factor zif268 mRNA in primary cultures of fetal rat calvarial cells and in simian virus 40-immortalized clonal rat calvarial preosteoblastic cells (RCT-1), which differentiate in response to RA, but not in the more differentiated RCT-3 and ROS 17/2.8 cells. Tretinoin 286-288 early growth response 1 Rattus norvegicus 102-108
1708092-3 1991 The relative stimulation of zif268 mRNA by RA was much larger than that of other early genes, including c-fos, c-jun, and junB. Tretinoin 43-45 early growth response 1 Rattus norvegicus 28-34
1708092-5 1991 Moreover, RA stimulated the transcriptional activity of a Zif268CAT (chloramphenicol acetyltransferase) plasmid containing 632 bp of zif268 5" regulatory sequences in RCT-1 cells but not in the more differentiated RCT-3 cells. Tretinoin 10-12 early growth response 1 Rattus norvegicus 133-139
1708092-6 1991 These in vitro data support the in vivo observations which localize zif268 and RA receptor-gamma transcripts to bone and cartilage during development, suggesting that both RA and zif268 may play a role in osteoblast differentiation. Tretinoin 79-81 early growth response 1 Rattus norvegicus 179-185
1673449-6 1991 Reversal of IFN-gamma"s ability to influence neuroblastoma cell growth as well as potentiate the anti-tumor effects of RA was obtained in the presence of an antibody against the IFN-gamma receptor, implying receptor-mediated physiological events. Tretinoin 119-121 interferon gamma Homo sapiens 12-21
1673449-6 1991 Reversal of IFN-gamma"s ability to influence neuroblastoma cell growth as well as potentiate the anti-tumor effects of RA was obtained in the presence of an antibody against the IFN-gamma receptor, implying receptor-mediated physiological events. Tretinoin 119-121 interferon gamma Homo sapiens 178-187
1868031-2 1991 It has previously been shown that protein kinase C (PKC) isozymes are modulated during granulocytic differentiation of HL-60 cells induced by dimethyl sulfoxide or retinoic acid (M. Makowske, R. Ballester, Y. Cayre, and O.M. Tretinoin 164-177 proline rich transmembrane protein 2 Homo sapiens 34-50
1826464-2 1991 TH1 clones are very sensitive to ATRA-mediated inhibition of DNA synthesis while TH2 clones are very resistant, but both TH1 and TH2 clones show significant down-modulation of surface transferrin receptors after ATRA exposure. Tretinoin 33-37 transferrin Homo sapiens 184-195
1826464-2 1991 TH1 clones are very sensitive to ATRA-mediated inhibition of DNA synthesis while TH2 clones are very resistant, but both TH1 and TH2 clones show significant down-modulation of surface transferrin receptors after ATRA exposure. Tretinoin 212-216 transferrin Homo sapiens 184-195
1868031-2 1991 It has previously been shown that protein kinase C (PKC) isozymes are modulated during granulocytic differentiation of HL-60 cells induced by dimethyl sulfoxide or retinoic acid (M. Makowske, R. Ballester, Y. Cayre, and O.M. Tretinoin 164-177 proline rich transmembrane protein 2 Homo sapiens 52-55
1820970-5 1991 In the present study, the regulation of osteocalcin synthesis by other hormones of the steroid-thyroid hormone family (retinoic acid, 17 beta-estradiol, triiodothyronine, and dexamethasone) was examined. Tretinoin 119-132 bone gamma-carboxyglutamate protein Homo sapiens 40-51
1679009-6 1991 Immunocytochemistry and cell cloning of SK-N-BE(2) line demonstrated that tTG was absent in cells showing neurite outgrowth, indicating that the enzyme expression is not associated with neural differentiation, even though both phenomena are elicited by retinoic acid. Tretinoin 253-266 transglutaminase 2 Homo sapiens 74-77
2030332-0 1991 The effect of retinoic acid on parathyroid hormone- and parathyroid hormone-related peptide-induced intracellular calcium in a rat osteosarcoma cell line, UMR106. Tretinoin 14-27 parathyroid hormone Rattus norvegicus 31-50
1879351-0 1991 Complex regulation of TGF beta expression by retinoic acid in the vitamin A-deficient rat. Tretinoin 45-58 transforming growth factor, beta 1 Rattus norvegicus 22-30
1879351-1 1991 We report the results of a histochemical study, using polyclonal antipeptide antibodies to the different TGF beta isoforms, which demonstrates that retinoic acid regulates the expression of TGF beta 2 in the vitamin A-deficient rat. Tretinoin 148-161 transforming growth factor, beta 1 Rattus norvegicus 105-113
1879351-3 1991 Treatment with retinoic acid caused a rapid and transient induction of TGF beta 2 and TGF beta 3 in the epidermis, tracheobronchial and alveolar epithelium, and intestinal mucosa. Tretinoin 15-28 transforming growth factor, beta 3 Rattus norvegicus 86-96
1879351-5 1991 In contrast to these epithelia, expression of the three TGF beta isoforms increased in vaginal epithelium during vitamin A deficiency, and decreased following systemic administration of retinoic acid. Tretinoin 186-199 transforming growth factor, beta 1 Rattus norvegicus 56-64
1879351-6 1991 Our results show for the first time the widespread regulation of TGF beta expression by retinoic acid in vivo, and suggest a possible mechanism by which retinoics regulate the functions of both normal and pre-neoplastic epithelia. Tretinoin 88-101 transforming growth factor, beta 1 Rattus norvegicus 65-73
2007780-0 1991 Transcription of the human loricrin gene in vitro is induced by calcium and cell density and suppressed by retinoic acid. Tretinoin 107-120 loricrin cornified envelope precursor protein Homo sapiens 27-35
2007780-5 1991 Retinoic acid (RA) at 10(-7) to 10(-9) M completely blocked Ca+(+)-induced loricrin mRNA synthesis when applied simultaneously. Tretinoin 0-13 loricrin cornified envelope precursor protein Homo sapiens 75-83
2007780-5 1991 Retinoic acid (RA) at 10(-7) to 10(-9) M completely blocked Ca+(+)-induced loricrin mRNA synthesis when applied simultaneously. Tretinoin 15-17 loricrin cornified envelope precursor protein Homo sapiens 75-83
2007780-6 1991 Furthermore, addition of RA to cultures already exposed to higher Ca++ levels resulted in the complete loss of loricrin mRNA within 48-72 h. So far, no other components of the CE have been shown to be suppressed by RA. Tretinoin 25-27 loricrin cornified envelope precursor protein Homo sapiens 111-119
1820970-9 1991 In contrast, the combination of 1,25(OH)2D3 with retinoic acid resulted in an increased medium osteocalcin concentration. Tretinoin 49-62 bone gamma-carboxyglutamate protein Homo sapiens 95-106
1848114-0 1991 Induction of transforming growth factor-beta 1 (TGF-beta 1), receptor expression and TGF-beta 1 protein production in retinoic acid-treated HL-60 cells: possible TGF-beta 1-mediated autocrine inhibition. Tretinoin 118-131 transforming growth factor beta 1 Homo sapiens 85-95
2013316-7 1991 One cell line expressing high levels of both PKC-alpha mRNA was treated with 10(-5) M retinoic acid (RA). Tretinoin 86-99 protein kinase C alpha Homo sapiens 45-54
2013316-7 1991 One cell line expressing high levels of both PKC-alpha mRNA was treated with 10(-5) M retinoic acid (RA). Tretinoin 101-103 protein kinase C alpha Homo sapiens 45-54
2005128-8 1991 Manipulation of culture conditions to produce more adhesive chondrocytes (treatment with hyaluronidase, transformation with Rous sarcoma virus, and treatment with retinoic acid) increases the amount of fibronectin mRNA containing exon IIIA. Tretinoin 163-176 fibronectin 1 Homo sapiens 202-213
1848114-0 1991 Induction of transforming growth factor-beta 1 (TGF-beta 1), receptor expression and TGF-beta 1 protein production in retinoic acid-treated HL-60 cells: possible TGF-beta 1-mediated autocrine inhibition. Tretinoin 118-131 transforming growth factor beta 1 Homo sapiens 85-95
1848114-3 1991 Although TGF-beta 1 alone had little effect on proliferation or differentiation of HL-60 cells, addition of TGF-beta 1 to HL-60 cells treated with a suboptimum concentration of RA (1.0 nmol/L) resulted in a marked decrease in proliferation with no effect on granulocytic differentiation. Tretinoin 177-179 transforming growth factor beta 1 Homo sapiens 108-118
1848114-4 1991 Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 39-47
1848114-4 1991 Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 127-137
1848114-4 1991 Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Tretinoin 235-237 transforming growth factor beta 1 Homo sapiens 39-47
1848114-5 1991 Maximum induction was achieved after treatment with 10 nmol/L RA and consisted predominantly of the 65-Kd TGF-beta 1 receptor type. Tretinoin 62-64 transforming growth factor beta 1 Homo sapiens 106-116
2018506-0 1991 Molecular cloning of RI-HB, a heparin binding protein regulated by retinoic acid. Tretinoin 67-80 midkine (neurite growth-promoting factor 2) Gallus gallus 21-26
1848114-6 1991 Moreover, RA treatment also resulted in a dose-dependent increase in both TGF-beta 1 steady-state mRNA expression and production of active TGF-beta with maximum induction at 10 nmol/LRA. Tretinoin 10-12 transforming growth factor beta 1 Homo sapiens 74-84
2018506-1 1991 RI-HB is an extracellular heparin binding protein regulated by retinoic acid and essentially expressed during embryogenesis. Tretinoin 63-76 midkine (neurite growth-promoting factor 2) Gallus gallus 0-5
1848114-6 1991 Moreover, RA treatment also resulted in a dose-dependent increase in both TGF-beta 1 steady-state mRNA expression and production of active TGF-beta with maximum induction at 10 nmol/LRA. Tretinoin 10-12 transforming growth factor beta 1 Homo sapiens 74-82
2018506-5 1991 Northern blot analysis indicates that RI-HB mRNA is strongly expressed during early chicken embryogenesis and that it is induced by retinoic acid treatment of chicken fibroblasts and myotubes in culture. Tretinoin 132-145 midkine (neurite growth-promoting factor 2) Gallus gallus 38-43
1848114-8 1991 These data suggest that the effects of RA may be mediated by a TGF-beta 1-mediated autocrine antiproliferative loop during differentiation of HL-60 cells. Tretinoin 39-41 transforming growth factor beta 1 Homo sapiens 63-73
1988285-2 1991 The treatment of NIH-3T3 cells with RA for 2 days also caused a reproducible increase in the binding of the lectin Phaseolus vulgaris leukoagglutinin (PHA-L) to a glycoprotein of molecular weight 130,000 (gp130) as judged by SDS-PAGE analysis. Tretinoin 36-38 interleukin 6 signal transducer Mus musculus 205-210
1650576-5 1991 Upon transient assays in P19 EC cells CAT activity is enhanced rapidly by RA, to more than 100-fold in a concentration-dependent fashion. Tretinoin 74-76 catalase Homo sapiens 38-41
1650576-6 1991 On the contrary no activity can be observed in the RA-resistant RAC65 cells; however, co-transfection of hRAR alpha, hRAR beta or hRAR gamma 1 restores the RA-dependent induction of CAT activity. Tretinoin 51-53 catalase Homo sapiens 182-185
1847657-6 1991 TGF-beta was synergistic with retinoic acid, a known anti-tumor promoter, in inhibiting the PMA-induced transformation of JB6 cells. Tretinoin 30-43 transforming growth factor beta 1 Homo sapiens 0-8
1847657-8 1991 TGF-beta, therefore, appears to function as an incomplete antipromoter whose action can be permitted and/or complemented by retinoic acid. Tretinoin 124-137 transforming growth factor beta 1 Homo sapiens 0-8
1703480-5 1991 Retinoic acid (RA; 1 microM) completely blocked the effect of IGF-I (50 ng/ml) on enhancing proliferation of MCF-7 cells in culture. Tretinoin 0-13 insulin like growth factor 1 Homo sapiens 62-67
1703480-5 1991 Retinoic acid (RA; 1 microM) completely blocked the effect of IGF-I (50 ng/ml) on enhancing proliferation of MCF-7 cells in culture. Tretinoin 15-17 insulin like growth factor 1 Homo sapiens 62-67
1998963-1 1991 Calcyclin gene expression was evaluated in different neuroblastoma cell lines and during neuronal differentiation induced by retinoic acid. Tretinoin 125-138 S100 calcium binding protein A6 Homo sapiens 0-9
1998963-4 1991 LAN-5 cell (neuronal type) differentiation experiments showed that calcyclin gene is detectable after 4 days of retinoic acid treatment, which induces G1 phase accumulation (as detected by cytofluorometric analysis), and cell growth arrest. Tretinoin 112-125 S100 calcium binding protein A6 Homo sapiens 67-76
1998963-7 1991 This bivalent role of the calcyclin gene, which is normally expressed in the G1 phase of the cell cycle but also expressed during retinoic acid-induced neuroblastoma cell differentiation, suggests that (at least in neuroblastoma cells) the gene is subject to a complex transcriptional regulation. Tretinoin 130-143 S100 calcium binding protein A6 Homo sapiens 26-35
1988285-5 1991 Similar to RA, 13-cis-RA and 3,5-di-tert-butyl-4-chalcone carboxylic acid, a synthetic retinoid, also increased PHA-L binding to gp130; they also enhanced cell adhesiveness and inhibited cell growth. Tretinoin 11-13 interleukin 6 signal transducer Mus musculus 129-134
1670759-6 1991 In addition, these RA-treated cells exhibit downregulation of the CD15 surface antigen and a slight increase in hemoglobin production but manifest no other evidence of significant erythroid, megakaryocytic, or myeloid differentiation. Tretinoin 19-21 fucosyltransferase 4 Homo sapiens 66-70
1987282-8 1991 The granulocytic differentiation of the cells treated with retinoic acid was accompanied by intense expression of fgr, but weak or no expression of lyn and fyn gene. Tretinoin 59-72 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 148-151
1987282-8 1991 The granulocytic differentiation of the cells treated with retinoic acid was accompanied by intense expression of fgr, but weak or no expression of lyn and fyn gene. Tretinoin 59-72 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 114-117
1657330-6 1991 Compared with 1,25(OH)2D3, the combination of 1,25(OH)2D3 and retinoic acid resulted an increased synthesis of osteocalcin. Tretinoin 62-75 bone gamma-carboxyglutamate protein Homo sapiens 111-122
1932206-6 1991 Two nuclear matrix proteins, p52 and p55, incorporated [3H] retinoic acid rapidly, were cell-cycle-related, and disappeared within 12 h of dosing. Tretinoin 60-73 nuclear factor kappa B subunit 2 Homo sapiens 29-32
1822401-3 1991 Its synthesis and that of the RIHB mRNA are induced by retinoic acid in chicken myoblasts cell culture. Tretinoin 55-68 midkine (neurite growth-promoting factor 2) Gallus gallus 30-34
1822392-3 1991 In addition, the inhibitory effect of retinoic acid was not observed for genes regulated by the progesterone receptor and the glucocorticoid receptor. Tretinoin 38-51 nuclear receptor subfamily 3 group C member 1 Homo sapiens 126-149
1822394-1 1991 We have previously shown that all-trans retinoic acid therapy is an alternative therapy for acute promyelocytic leukemia (AML3) via differentiation of the leukemic cells. Tretinoin 40-53 RUNX family transcription factor 2 Homo sapiens 122-126
1702702-3 1991 RA stimulated hCG and hCG-alpha secretion in a dose-dependent fashion by each of the three cell lines. Tretinoin 0-2 chromogranin A Homo sapiens 22-31
1903636-5 1991 Retinoic acid treatment, in a time- and concentration-dependent manner, led to a decrease in phospholipase C activity when stimulated with either GTP gamma S or NaF, both of which activate the enzyme via the G-protein. Tretinoin 0-13 C-X-C motif chemokine ligand 8 Homo sapiens 161-164
1879193-1 1991 When the leukemia cells in 14 patients with acute promyelocytic leukemia (APL) were induced by all-trans retinoic acid (RA) treatment, the activity of protein kinase C (PKC) increased with the differentiation. Tretinoin 99-118 proline rich transmembrane protein 2 Homo sapiens 151-167
1879193-1 1991 When the leukemia cells in 14 patients with acute promyelocytic leukemia (APL) were induced by all-trans retinoic acid (RA) treatment, the activity of protein kinase C (PKC) increased with the differentiation. Tretinoin 99-118 proline rich transmembrane protein 2 Homo sapiens 169-172
1702702-5 1991 Cycloheximide (1 microM) abolished the effect of RA on hCG and hCG-alpha secretion in the BeWo cell line. Tretinoin 49-51 chromogranin A Homo sapiens 63-72
1702702-10 1991 RA in physiologic concentrations stimulates hCG and hCG-alpha secretion by three choriocarcinoma cell lines in vitro. Tretinoin 0-2 chromogranin A Homo sapiens 52-61
2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 14-27 tumor necrosis factor Homo sapiens 69-90
1710463-7 1991 Three cell lines with an adult phenotype (high albumin and low alpha-fetoprotein) were inhibited by RA, two undifferentiated lines showed moderate growth stimulation, and two of three cell lines that had high levels of alpha-fetoprotein were markedly stimulated by RA. Tretinoin 100-102 alpha fetoprotein Homo sapiens 63-80
2068137-2 1991 The expression of POMC mRNA decreases when the cell lines are differentiated with retinoic acid or alpha-difluoromethylornithine. Tretinoin 82-95 proopiomelanocortin Homo sapiens 18-22
2176462-3 1990 RA binding to the wild-type and truncated forms of the receptor was identical for both RAR alpha and RAR beta, indicating that the ligand-binding domains have retained the binding characteristics of the intact receptors. Tretinoin 0-2 retinoic acid receptor beta Homo sapiens 101-109
2176462-4 1990 Furthermore, RA bound with the same affinity to both RAR alpha and RAR beta. Tretinoin 13-15 retinoic acid receptor beta Homo sapiens 67-75
2100255-12 1990 The results suggest (1) a role for retinoic acid in controlling the early development of the inner ear and (2) that this control is effected through the regulation of the proto-oncogene c-fos. Tretinoin 35-48 Fos proto-oncogene, AP-1 transcription factor subunit Gallus gallus 171-191
1980476-4 1990 RA activates expression of the posterior gene XlHbox 6, but not of XlHbox 1. Tretinoin 0-2 homeobox A9 S homeolog Xenopus laevis 46-54
1768439-9 1991 Retinoic acid induced the expression of HBNF and MK 6- and 11-fold, respectively, in this cell line. Tretinoin 0-13 pleiotrophin Homo sapiens 40-44
1705636-6 1991 RA in addition to G-CSF synergistically increased FMLP binding to HL-60 cells, accompanied by increased NBT reduction in response to FMLP. Tretinoin 0-2 formyl peptide receptor 1 Homo sapiens 50-54
1705636-6 1991 RA in addition to G-CSF synergistically increased FMLP binding to HL-60 cells, accompanied by increased NBT reduction in response to FMLP. Tretinoin 0-2 formyl peptide receptor 1 Homo sapiens 133-137
1705636-7 1991 RA in addition to GM-CSF markedly increased FMLP binding to HL-60 cells more than that induced by RA alone, but the combined treatment with RA and GM-CSF did not increase FMLP-stimulated NBT reduction more than that induced by RA alone. Tretinoin 0-2 formyl peptide receptor 1 Homo sapiens 44-48
1768424-0 1991 Binding of synthetic analogues of retinol and retinoic acid (CD-270 derivatives) to retinoid-binding proteins. Tretinoin 46-59 TNF receptor superfamily member 14 Homo sapiens 61-67
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 41-54 TNF receptor superfamily member 14 Homo sapiens 103-109
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 204-217 TNF receptor superfamily member 14 Homo sapiens 103-109
2257974-4 1990 After formation of parietal endoderm-like cells by addition of retinoic acid (RA) to BRL-CM, the 1.8-kb transcript of TGF beta 1 and PDGF-A expression were reduced, IGF II mRNA and a single TGF beta 3 transcript of 3.8 kb were induced while PDGF-B and TGF beta 4 remained virtually unchanged. Tretinoin 63-76 transforming growth factor, beta 1 Rattus norvegicus 118-128
2257974-4 1990 After formation of parietal endoderm-like cells by addition of retinoic acid (RA) to BRL-CM, the 1.8-kb transcript of TGF beta 1 and PDGF-A expression were reduced, IGF II mRNA and a single TGF beta 3 transcript of 3.8 kb were induced while PDGF-B and TGF beta 4 remained virtually unchanged. Tretinoin 63-76 transforming growth factor, beta 3 Rattus norvegicus 190-200
2087681-12 1990 RA exposure altered the expression of TFG-alpha, TGF-beta 1, and TGF-beta 2, but significant effects on EGF were not found. Tretinoin 0-2 transforming growth factor, beta 2 Mus musculus 65-75
2122968-5 1990 Treatment of F9 cells with retinoic acid (1 microM) for 5 days resulted in a 20-fold increase in steady-state levels of a 2.0-kilobase Gs alpha mRNA. Tretinoin 27-40 GNAS complex locus Homo sapiens 135-143
2122968-7 1990 Gs alpha mRNA increases within 24 h of exposure to retinoic acid, whereas the expression of alpha 1 (IV) collagen, a marker for F9 differentiation, did not increase until 48 h of treatment. Tretinoin 51-64 GNAS complex locus Homo sapiens 0-8
2122968-8 1990 In the presence of retinoic acid, exogenous human PTHrP-(1-34)-amide (20 nM) produced a further 2-fold increase in Gs alpha mRNA. Tretinoin 19-32 GNAS complex locus Homo sapiens 115-123
2122968-11 1990 These data demonstrate that a marked increase in Gs alpha expression accompanies F9 differentiation induced by retinoic acid and PTHrP, and that the regulation is predominantly transcriptional. Tretinoin 111-124 GNAS complex locus Homo sapiens 49-57
2224120-3 1990 All-trans retinoic acid induces leukemic cells from patients with acute promyelocytic leukemia (M3) to differentiate in vitro to mature granulocytes which express the CD15 antigen and are capable of respiratory burst function. Tretinoin 10-23 fucosyltransferase 4 Homo sapiens 167-171
2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 14-27 tumor necrosis factor Homo sapiens 92-95
2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 29-31 tumor necrosis factor Homo sapiens 69-90
2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 29-31 tumor necrosis factor Homo sapiens 92-95
2230595-5 1990 Addition of RA (0.5 microM) to DLS restored LPS-induced TNF release by HPBM, and supplementation with ROH (1.0 microM) resulted in release of TNF-like activity, but only after 3 days of in vitro culture. Tretinoin 12-14 tumor necrosis factor Homo sapiens 56-59
2230595-6 1990 The maintenance of TNF release by the addition of exogenous RA after 3 days of in vitro culture suggested that depletion of endogenous RA was partially responsible for loss of TNF-like activity. Tretinoin 60-62 tumor necrosis factor Homo sapiens 19-22
2230595-6 1990 The maintenance of TNF release by the addition of exogenous RA after 3 days of in vitro culture suggested that depletion of endogenous RA was partially responsible for loss of TNF-like activity. Tretinoin 135-137 tumor necrosis factor Homo sapiens 19-22
2167670-6 1990 Cytosol from monocytes cultured for 6 days is immunochemically deficient in p47 but not p67, while cytosol from HL-60 cells induced with retinoic acid for 3 days is deficient in p67 but not p47. Tretinoin 137-150 CD33 molecule Homo sapiens 178-181
2206968-4 1990 Immunoblot patterns of epidermal extracts revealed both the mature form of IL-1 (17 kDa) and the precursor (36 kDa) and were identical in amounts whether the specimens were from controls or from RA- or corticosteroid-treated skin. Tretinoin 195-197 interleukin 1 beta Homo sapiens 75-79
2164926-12 1990 Similarly, PTH also inhibited heterologous up-regulation of VDR and VDR mRNA induced by retinoic acid. Tretinoin 88-101 parathyroid hormone Rattus norvegicus 11-14
2379178-7 1990 The degree of suppression correlated with the concentration of VIP, and the effect was indistinguishable, on a molar basis, from that seen when cells were treated with retinoic acid. Tretinoin 168-181 vasoactive intestinal peptide Homo sapiens 63-66
2379178-8 1990 Similarly, the morphological changes seen in the VIP-treated cells were the same as those seen in retinoic acid-treated ones. Tretinoin 98-111 vasoactive intestinal peptide Homo sapiens 49-52
2379178-9 1990 The effects of VIP on both cell lines, like those of retinoic acid, are reversible. Tretinoin 53-66 vasoactive intestinal peptide Homo sapiens 15-18
2394926-0 1990 Increase in carcinoembryonic antigen release from cancer cells by combined treatment with retinoic acid and low-temperature hyperthermia. Tretinoin 90-103 CEA cell adhesion molecule 3 Homo sapiens 12-36
2164735-4 1990 Retinoic acid-treated EC cell extracts provided three completely protected regions, each containing sequences with homology to nuclear factor 1 (NF1) binding motifs and the partially protected TATA box. Tretinoin 0-13 neurofibromin 1 Homo sapiens 145-148
2272312-6 1990 Cells induced with RA for 12 hr and subsequently recultured in liquid culture gradually expressed the differentiated phenotype and lost transferrin receptor expression. Tretinoin 19-21 transferrin Homo sapiens 136-147
2394926-1 1990 The growth of a human gastric adenocarcinoma cell line, MKN-45, was inhibited and the amount of carcinoembryonic antigen (CEA) in both the culture medium and the cell extract was increased in the presence of retinoic acid at a concentration of 75 (1.5x)-125 microM (1.9x), which did not substantially affect cell survival. Tretinoin 208-221 CEA cell adhesion molecule 3 Homo sapiens 96-120
2394926-1 1990 The growth of a human gastric adenocarcinoma cell line, MKN-45, was inhibited and the amount of carcinoembryonic antigen (CEA) in both the culture medium and the cell extract was increased in the presence of retinoic acid at a concentration of 75 (1.5x)-125 microM (1.9x), which did not substantially affect cell survival. Tretinoin 208-221 CEA cell adhesion molecule 3 Homo sapiens 122-125
2394926-2 1990 Treatment using a combination of retinoic acid (125 microM) and low-temperature hyperthermia (40 degrees C, 30 min) was more effective in increasing CEA compared with retinoic acid alone (extracellular 1.9-2.4x, intracellular 1.5-1.9x). Tretinoin 33-46 CEA cell adhesion molecule 3 Homo sapiens 149-152
2394926-4 1990 Cells treated with both retinoic acid and (low-temperature) hyperthermia, however, could be induced to release a significant amount of CEA at about 48 h after retinoic acid removal. Tretinoin 24-37 CEA cell adhesion molecule 3 Homo sapiens 135-138
2394926-4 1990 Cells treated with both retinoic acid and (low-temperature) hyperthermia, however, could be induced to release a significant amount of CEA at about 48 h after retinoic acid removal. Tretinoin 159-172 CEA cell adhesion molecule 3 Homo sapiens 135-138
2394926-6 1990 These results suggest that retinoic acid, used alone or in combination with hyperthermia, enhances the production and release of CEA in human gastric cancer cells. Tretinoin 27-40 CEA cell adhesion molecule 3 Homo sapiens 129-132
2371287-8 1990 The presence of retinoic acid was required for maximal PUFA-dependent growth inhibition of A549 or B16 cells by TGF-beta 1 under some, but not all, conditions. Tretinoin 16-29 transforming growth factor beta 1 Homo sapiens 112-122
2401528-3 1990 RA pretreatment of human blood platelets resulted in an increase in the activities of catalase and GPx, two important radical scavenging enzymes, with significant decrease in MDA formation when compared with ADP alone. Tretinoin 0-2 catalase Homo sapiens 86-94
2355021-9 1990 Ribonuclease protection, RNA blotting, and primer extension revealed that MK2-type RNA was the major MK RNA in retinoic acid-treated embryonal carcinoma cells. Tretinoin 111-124 MAP kinase-activated protein kinase 2 Mus musculus 74-77
2340496-0 1990 Epidermal growth factor receptor expression in a retinoic acid-treated human melanoma cell line. Tretinoin 49-62 epidermal growth factor receptor Homo sapiens 0-32
2158037-5 1990 Three growth factors were markedly down-regulated following RA treatment: Hst-1/kFGF and TGF-alpha expression became undetectable by Northern analysis and bFGF expression was substantially reduced. Tretinoin 60-62 fibroblast growth factor 4 Homo sapiens 74-79
2161434-0 1990 Retinoic acid inhibits calmodulin binding to human erythrocyte membranes and reduces membrane Ca2(+)-adenosine triphosphatase activity. Tretinoin 0-13 calmodulin 1 Homo sapiens 23-33
2161434-4 1990 Purified calmodulin (up to 500 ng/ml, 3 X 10(-8) M) added to red cell membranes, in the presence of inhibitory concentrations of retinoic acid, only partially restored Ca2(+)-ATPase activity. Tretinoin 129-142 calmodulin 1 Homo sapiens 9-19
2161434-5 1990 125I-Calmodulin bound to red cell membranes was displaced by unlabeled retinoic acid (50% reduction at 10(-8) M retinoic acid), as effectively as by unlabeled calmodulin. Tretinoin 71-84 calmodulin 1 Homo sapiens 5-15
2161434-5 1990 125I-Calmodulin bound to red cell membranes was displaced by unlabeled retinoic acid (50% reduction at 10(-8) M retinoic acid), as effectively as by unlabeled calmodulin. Tretinoin 112-125 calmodulin 1 Homo sapiens 5-15
2161434-8 1990 Thus, retinoic acid inhibits calmodulin binding to red cell membranes, reducing calmodulin-stimulable Ca2(+)-ATPase activity. Tretinoin 6-19 calmodulin 1 Homo sapiens 29-39
2161434-8 1990 Thus, retinoic acid inhibits calmodulin binding to red cell membranes, reducing calmodulin-stimulable Ca2(+)-ATPase activity. Tretinoin 6-19 calmodulin 1 Homo sapiens 80-90
2161434-9 1990 Retinoic acid does not directly interact with calmodulin, but rather exerts its effect by interfering with calmodulin access to the membrane enzyme. Tretinoin 0-13 calmodulin 1 Homo sapiens 46-56
2161434-9 1990 Retinoic acid does not directly interact with calmodulin, but rather exerts its effect by interfering with calmodulin access to the membrane enzyme. Tretinoin 0-13 calmodulin 1 Homo sapiens 107-117
2170809-6 1990 Because retinoic acid is known to regulate the transcription of target genes crucial for cellular growth and differentiation, it is most probable that consequent to the HBV insertion, hap, usually transcribed at a very low level in normal hepatocytes, became inappropriately expressed as an altered chimaeric retinoic acid receptor, thus contributing to the cell transformation. Tretinoin 8-21 retinoic acid receptor beta Homo sapiens 184-187
2162058-2 1990 Addition of retinoic acid to F9 cell medium caused a dose-dependent increase in RAR-beta mRNA within 3 hr that reached 5- to 30-fold greater than the constitutively expressed mRNA by 24 hr. Tretinoin 12-25 retinoic acid receptor beta Homo sapiens 80-88
2162058-4 1990 N6,O2"-Dibutyryl-cAMP attenuated the retinoic acid-induced increase in RAR-beta mRNA by a post-transcriptional mechanism. Tretinoin 37-50 retinoic acid receptor beta Homo sapiens 71-79
1970751-3 1990 When combined with human recombinant interleukin-2 (IL-2), retinoic acid augmented LAK cell activity in both a dose- and time-dependent manner. Tretinoin 59-72 interleukin 2 Homo sapiens 37-50
1970751-3 1990 When combined with human recombinant interleukin-2 (IL-2), retinoic acid augmented LAK cell activity in both a dose- and time-dependent manner. Tretinoin 59-72 interleukin 2 Homo sapiens 52-56
2159384-1 1990 We present evidence that the vitamin D response element in the human osteocalcin gene confers responsiveness to the vitamin A metabolite, retinoic acid. Tretinoin 138-151 bone gamma-carboxyglutamate protein Homo sapiens 69-80
2324527-8 1990 Concentrations of all-trans retinoic acid that stimulated proliferation also induced increased production of fibronectin as indicated by biosynthetic labeling/immunoprecipitation and by enzyme-linked immunosorbent assay. Tretinoin 28-41 fibronectin 1 Homo sapiens 109-120
2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 132-149
2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 0-13 estrogen receptor 1 Homo sapiens 151-153
2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 15-17 estrogen receptor 1 Homo sapiens 132-149
2317786-1 1990 Retinoic acid (RA) inhibits proliferation of numerous breast carcinoma cells and prevents estrogen stimulation of growth of several estrogen receptor (ER)-positive cell lines. Tretinoin 15-17 estrogen receptor 1 Homo sapiens 151-153
2317786-2 1990 RA inhibition of human breast carcinoma cell proliferation is associated with marked inhibition of the synthesis of a Mr 39,000 protein in the ER-positive human breast carcinoma cell lines investigated. Tretinoin 0-2 estrogen receptor 1 Homo sapiens 143-145
2172793-4 1990 Dose-dependent profiles upon trans-activation of the reporter indicate that apparent sensitivity to retinoic acid of this protein is approximately 10-fold higher than that of human RAR alpha and is comparable to that of the second human RAR, RAR beta. Tretinoin 100-113 retinoic acid receptor beta Homo sapiens 242-250
2150351-6 1990 Treatment of M phi with retinoic acid strongly inhibited LPS-induced TNF-alpha mRNA expression, whereas trifluoperazine had an opposite effect. Tretinoin 24-37 toll-like receptor 4 Mus musculus 57-60
2150351-6 1990 Treatment of M phi with retinoic acid strongly inhibited LPS-induced TNF-alpha mRNA expression, whereas trifluoperazine had an opposite effect. Tretinoin 24-37 tumor necrosis factor Mus musculus 69-78
1692330-5 1990 Unexpectedly, AFP mRNA is detectable in only a subset of the outer cells of F9 cell aggregates grown 15 d in the presence of RA. Tretinoin 125-127 alpha fetoprotein Homo sapiens 14-17
1692330-7 1990 RA-5-1 cells exhibit four- to sixfold less of the mRNAs encoding two visceral endoderm proteins, AFP and H19, than wild-type F9 cells after RA treatment of RA-5-1 aggregates. Tretinoin 0-2 alpha fetoprotein Homo sapiens 97-100
2199088-2 1990 The strongest differentiation inducing activity on promyelocytic HL60 cells and histiocytic U937 cells was obtained by combining recombinant tumor necrosis factor (rTNF), interferon-gamma (IFN-gamma), retinoic acid (RA), and 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3). Tretinoin 216-218 tumor necrosis factor Homo sapiens 141-162
2352289-2 1990 Tyrosine hydroxylase (TH) activity of the LA-N-1 cells was increased in the RA-treated cells compared with control cultures at day 4 and remained elevated. Tretinoin 76-78 tyrosine hydroxylase Homo sapiens 0-20
2177844-6 1990 However, differentiation of these cells to parietal endoderm, either spontaneously (PSA-1) or by treatment with retinoic acid and dibutyryl cAMP (F9), resulted in expression of the 1.4-kilobase PLP message. Tretinoin 112-125 parathyroid hormone-like peptide Mus musculus 194-197
2177844-10 1990 In the presence of retinoic acid, exogenous PLP substituted for dibutyryl cAMP in a concentration-dependent fashion in promoting the differentiation of F9 cells to parietal endoderm. Tretinoin 19-32 parathyroid hormone-like peptide Mus musculus 44-47
2158037-5 1990 Three growth factors were markedly down-regulated following RA treatment: Hst-1/kFGF and TGF-alpha expression became undetectable by Northern analysis and bFGF expression was substantially reduced. Tretinoin 60-62 fibroblast growth factor 4 Homo sapiens 80-84
2158037-5 1990 Three growth factors were markedly down-regulated following RA treatment: Hst-1/kFGF and TGF-alpha expression became undetectable by Northern analysis and bFGF expression was substantially reduced. Tretinoin 60-62 fibroblast growth factor 2 Homo sapiens 155-159
2307713-0 1990 Inhibition of epidermal growth factor receptor activity by retinoic acid in glioma cells. Tretinoin 59-72 epidermal growth factor receptor Homo sapiens 14-46
1692794-8 1990 Since GRP78 is expressed during mouse embryogenesis and the promoter is also active in F9 cells treated with retinoic acid, the GRP78 promoter may be useful for the efficient expression of heterologous genes in undifferentiated and differentiated mouse embryonal cells. Tretinoin 109-122 heat shock protein 5 Mus musculus 128-133
1693606-6 1990 Pharmacological modulators of LPS-induced IL-1 production were identified: glucocorticoids were inhibitors whereas retinoic acid and 1.25-dihydroxy-vitamin D3 had no effects and prostaglandin E2 and IBMX were weak inhibitors. Tretinoin 115-128 interleukin 1 beta Homo sapiens 42-46
2307713-2 1990 The protein tyrosine kinase activity of epidermal growth factor receptor (EGF-receptor) appeared to parallel the cell"s growth responsiveness to RA. Tretinoin 145-147 epidermal growth factor receptor Homo sapiens 40-72
2307713-2 1990 The protein tyrosine kinase activity of epidermal growth factor receptor (EGF-receptor) appeared to parallel the cell"s growth responsiveness to RA. Tretinoin 145-147 epidermal growth factor receptor Homo sapiens 74-86
2307713-3 1990 Cells sensitive to RA-induced growth inhibition exhibited a dose-dependent decrease in EGF-receptor activity, whereas RA-resistant cells showed no alterations in EGF-receptor protein tyrosine kinase activity or expression. Tretinoin 19-21 epidermal growth factor receptor Homo sapiens 87-99
2307713-4 1990 The modulation of EGF-receptor by RA was further examined with RA-sensitive (LG) and -resistant (NG-1) cell lines. Tretinoin 34-36 epidermal growth factor receptor Homo sapiens 18-30
2307713-8 1990 These results suggest RA-induced growth inhibition in sensitive cells may arise, at least in part, through alterations in EGF-receptor and structure. Tretinoin 22-24 epidermal growth factor receptor Homo sapiens 122-134
2176907-5 1990 In differentiated HL-60 and U 937 cells, the oxidative metabolism increases in parallel with Cyt b specific contents, both being enhanced by the addition of IFN gamma to the RA treatment. Tretinoin 174-176 interferon gamma Homo sapiens 157-166
2152801-5 1990 Treatment of the chondrocytes with retinoic acid (0.2 microM) inhibited the parathyroid hormone and phorbol ester-induced increase in intracellular ionized calcium and the increase in proteoglycan synthesis. Tretinoin 35-48 parathyroid hormone Homo sapiens 76-95
2124549-0 1990 Effect of retinol and retinoic acid supplemented diets on cytochrome P-450 content and UDP glucuronosyltransferase activities in vitamin A-deficient rat liver. Tretinoin 22-35 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 58-74
2337474-0 1990 Transforming growth factor beta (TGF-beta) potentiates the inhibitory effect of retinoic acid on human breast carcinoma (MCF-7) cell proliferation. Tretinoin 80-93 transforming growth factor beta 1 Homo sapiens 0-31
2337474-0 1990 Transforming growth factor beta (TGF-beta) potentiates the inhibitory effect of retinoic acid on human breast carcinoma (MCF-7) cell proliferation. Tretinoin 80-93 transforming growth factor beta 1 Homo sapiens 33-41
2337474-5 1990 These results demonstrate that although TGF-beta does not inhibit the growth of MCF-7 cells, it potentiates the antiproliferative effect of RA, suggesting that it may play a part, albeit indirect, in the regulation of MCF-7 cell growth. Tretinoin 140-142 transforming growth factor beta 1 Homo sapiens 40-48
2403946-4 1990 Retinoic acid (RA) addition and/or deprivation of the differentiation inhibiting activity of feeder cells resulted in the appearance of TGF beta 2 transcripts within 2 days. Tretinoin 0-13 transforming growth factor, beta 2 Mus musculus 136-146
2403946-4 1990 Retinoic acid (RA) addition and/or deprivation of the differentiation inhibiting activity of feeder cells resulted in the appearance of TGF beta 2 transcripts within 2 days. Tretinoin 15-17 transforming growth factor, beta 2 Mus musculus 136-146
2295827-0 1990 Trans retinoic acid enhances the growth response of epidermal keratinocytes to epidermal growth factor and transforming growth factor beta. Tretinoin 6-19 transforming growth factor beta 1 Homo sapiens 107-138
2295827-4 1990 Transforming growth factor beta (TGF beta) inhibited the EGF-induced DNA synthesis in a dose-dependent manner, and the inhibition was greatly enhanced by a low dose of RA. Tretinoin 168-170 transforming growth factor beta 1 Homo sapiens 0-31
2295827-4 1990 Transforming growth factor beta (TGF beta) inhibited the EGF-induced DNA synthesis in a dose-dependent manner, and the inhibition was greatly enhanced by a low dose of RA. Tretinoin 168-170 transforming growth factor beta 1 Homo sapiens 33-41
2295827-6 1990 A low concentration of RA also enhanced the inhibitory effect of TGF beta on growth-factor-induced DNA synthesis and cell growth in hKC. Tretinoin 23-25 transforming growth factor beta 1 Homo sapiens 65-73
2293618-3 1990 Down-regulation of PKC in cells induced to differentiate by retinoic acid (1 microM) was less pronounced, whereas it was undetected in cells induced to differentiate by nerve growth factor (100 ng/ml). Tretinoin 60-73 proline rich transmembrane protein 2 Homo sapiens 19-22
2293618-7 1990 The present studies suggested that PKC and its 80-kilodalton substrate protein were likely involved in initiation and/or progression of LA-N-5 cell differentiation induced by TPA and that separate PKC-independent pathways might also be involved in the differentiating effect of retinoic acid or nerve growth factor. Tretinoin 278-291 proline rich transmembrane protein 2 Homo sapiens 35-38
2293618-7 1990 The present studies suggested that PKC and its 80-kilodalton substrate protein were likely involved in initiation and/or progression of LA-N-5 cell differentiation induced by TPA and that separate PKC-independent pathways might also be involved in the differentiating effect of retinoic acid or nerve growth factor. Tretinoin 278-291 proline rich transmembrane protein 2 Homo sapiens 197-200
2172660-0 1990 Difference in effects of interferon-alpha and interferon-gamma on the induction of differentiation of retinoic acid-treated acute myeloid leukemia cells in primary culture. Tretinoin 102-115 interferon gamma Homo sapiens 46-62
2299598-0 1990 Effects of cytochrome P-450 inhibitors on the in vivo metabolism of all-trans-retinoic acid in rats. Tretinoin 68-91 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 11-27
2299598-1 1990 This study examines the effects of ketoconazole, R 75 251 and some other cytochrome P-450 inhibitors on the in vivo metabolism of all-trans-retinoic acid (RA) in normal rats. Tretinoin 130-153 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 73-89
2299598-10 1990 These data are indicative of the important contribution of the cytochrome P-450 enzyme system to the in vivo metabolic process of RA. Tretinoin 130-132 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 63-79
2172660-3 1990 In particular, interferon-alpha enhanced granulocytic differentiation and interferon-gamma induced mono-macrophage differentiation of promyelocytic leukemic cells in the presence of RA. Tretinoin 182-184 interferon gamma Homo sapiens 74-90
33972395-0 2021 Erf affects commitment and differentiation of osteoprogenitor cells in cranial sutures via the retinoic acid pathway. Tretinoin 95-108 ETS2 repressor factor Homo sapiens 0-3
1966875-3 1990 The NADPH-DPR activity was increased by the treatment of the cells with RA+dBcAMP+NGF and with RA+dBcAMP by about 2.2-fold and 1.8-fold, respectively, of that detected in the control (untreated) cells. Tretinoin 72-74 nerve growth factor Homo sapiens 82-85
1966875-6 1990 These results suggest that the cells acquire responsiveness to NGF by the treatment with RA and dBcAMP and that NADPH-DPR may play some regulatory role in tetrahydrobiopterin regeneration from its quinonoid-dihydro form. Tretinoin 89-91 nerve growth factor Homo sapiens 63-66
2250947-2 1990 We report here that retinoic acid and its synthetic analog, CBS-211 A (10(-8)-10(-7) M), enhance the mitogenic effect of EGF on cultured bovine corneal endothelial cells (BCEC). Tretinoin 20-33 LOC521832 Bos taurus 121-124
33972395-6 2021 Elevated retinoic acid catabolism due to increased levels of the cytochrome P450 superfamily member Cyp26b1 as a result of decreased Erf levels appears to be the underlying mechanism leading to defective differentiation. Tretinoin 9-22 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 100-107
32858178-5 2021 After that, retinoic acid (RA), as a master regulator, promotes A1 spg formation with its helpers and Sall4. Tretinoin 12-25 spalt like transcription factor 4 Mus musculus 102-107
19525031-3 2009 However, 13-cis RA can isomerize to tRA, which can then be metabolized by CYP26. Tretinoin 16-18 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 74-79
30309678-5 2018 mRNA expression of Oct4 and Dazl were downregulated in embryonic stem cells by the retinoic acid group, whereas Mvh transcription was reduced by retinoic acid and estrogen group in these cells compared to the control group. Tretinoin 83-96 deleted in azoospermia-like Mus musculus 28-32
25360083-5 2014 We report that ATRA-BDNF induced significant increases in expression of key synaptic genes, brain-specific miRNA and miRNA biogenesis machinery, and in AChE activity, compared with ATRA alone. Tretinoin 15-19 acetylcholinesterase (Cartwright blood group) Homo sapiens 152-156
25284716-0 2015 GTF2I-RARA is a novel fusion transcript in a t(7;17) variant of acute promyelocytic leukaemia with clinical resistance to retinoic acid. Tretinoin 122-135 general transcription factor IIi Homo sapiens 0-10
22693486-4 2012 We recently observed that cPA negatively regulates PPARgamma function by stabilizing the binding of the corepressor protein, silencing mediator of retinoic acid and thyroid hormone receptor. Tretinoin 147-160 peroxisome proliferator activated receptor gamma Homo sapiens 51-60
19525031-5 2009 We then investigated whether response to oral 13-cis RA among patients with acne correlates with variability in CYP26 expression. Tretinoin 53-55 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 112-117
17166370-4 2006 This study was to explore the possibility and the possible mechanism of treating ATRA-resistant APL with IFN in combination with ATRA. Tretinoin 81-85 interferon alpha 1 Homo sapiens 105-108
8070357-8 1994 All-trans-retinoic acid and 9-cis-retinoic acid increased CG secretion and CG alpha and CG beta mRNAs, but clofibric acid blunted these stimulatory effects. Tretinoin 0-23 chromogranin A Homo sapiens 75-83
34921867-8 2022 Coupled with ATRA or GSK3beta inhibitor treatment, genetic or pharmacological inhibition of Skp2 strikingly induces JunB expression by accelerating the degradation of PML-RARalpha, which contributes to the eradication of APL. Tretinoin 13-17 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-120
34415562-0 2022 Retinoic acid attenuates nuclear factor kappaB mediated induction of NLRP3 inflammasome. Tretinoin 0-13 NLR family pyrin domain containing 3 Homo sapiens 69-74
34415562-13 2022 The addition of RA also significantly reduced the effect of carbachol on NLRP3 inflammasomes. Tretinoin 16-18 NLR family pyrin domain containing 3 Homo sapiens 73-78
34415562-14 2022 CONCLUSIONS: Our current study suggests that carbachol induces NLRP3 inflammasome activation through mAChR and NF-kB, and that RA abolishes the inflammatory response. Tretinoin 127-129 NLR family pyrin domain containing 3 Homo sapiens 63-68
34546543-5 2022 Three samples in which CD11b increased in response to ATRA had an inversion of chromosome 16 as well as the CBFB-MYH11 fusion gene, and the fourth sample was from a patient with KMT2A-rearranged, therapy-related AML. Tretinoin 54-58 myosin heavy chain 11 Homo sapiens 113-118
34546543-6 2022 In conclusion, we identified a subgroup of non-APL AML patients with inv(16) and CBFB-MYH11 as the most sensitive to ATRA-mediated differentiation in vitro, and our results can help identify patients who may benefit from ATRA treatment. Tretinoin 117-121 myosin heavy chain 11 Homo sapiens 86-91
34994166-0 2021 Initiation of oogenesis and meiosis in the fetal ovary depends on Dennd1a-mediated production of Wnt5a and retinoic acid from the somatic niches. Tretinoin 107-120 DENN/MADD domain containing 1A Mus musculus 66-73
34632533-0 2022 Protective effects of all-trans retinoic acid against gastric premalignant lesions by repressing exosomal LncHOXA10-pyruvate carboxylase axis. Tretinoin 22-45 pyruvate carboxylase Homo sapiens 116-136
34973477-10 2022 Moreover, LKB1DeltaIEC mice showed impaired conversion of retinol to retinoic acids in the SI ileum. Tretinoin 69-83 serine/threonine kinase 11 Mus musculus 10-22
34944824-5 2021 Somewhat unexpectedly, TGFbeta treatment resulted in an increase in intracellular levels of retinoic acid (RA) that in turn resulted in increased levels of extracellular matrix (ECM) proteins including fibronectin (FN) and collagen (COL1). Tretinoin 92-105 fibronectin 1 Homo sapiens 202-213
34944824-5 2021 Somewhat unexpectedly, TGFbeta treatment resulted in an increase in intracellular levels of retinoic acid (RA) that in turn resulted in increased levels of extracellular matrix (ECM) proteins including fibronectin (FN) and collagen (COL1). Tretinoin 92-105 fibronectin 1 Homo sapiens 215-217
34945773-1 2021 BACKGROUND: Recent reports indicate the potential role of the stimulated by retinoic acid 6 (STRA6) protein in developing insulin resistance. Tretinoin 76-89 insulin Homo sapiens 122-129
34880391-6 2021 Moreover, somatic expression of TEX12 is aberrantly activated via retinoic acid signalling, which is commonly disregulated in cancer. Tretinoin 66-79 testis expressed 12 Homo sapiens 32-37
34784434-8 2021 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin 44-46 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-169
34836491-1 2021 In the present study, we determined the effects of the Src family kinase (SFK) inhibitor, Bosutinib, and the engineered loss of the Lyn SFK on all-trans retinoic acid-induced leukemic cell differentiation. Tretinoin 153-166 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 74-77
34836491-1 2021 In the present study, we determined the effects of the Src family kinase (SFK) inhibitor, Bosutinib, and the engineered loss of the Lyn SFK on all-trans retinoic acid-induced leukemic cell differentiation. Tretinoin 153-166 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 132-135
34836491-1 2021 In the present study, we determined the effects of the Src family kinase (SFK) inhibitor, Bosutinib, and the engineered loss of the Lyn SFK on all-trans retinoic acid-induced leukemic cell differentiation. Tretinoin 153-166 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 136-139
34836491-4 2021 Using either Bosutinib or loss of Lyn expression due to shRNA promoted RA-induced phenotypic differentiation, G0 arrest, and respiratory burst (functional differentiation) of HL-60 cells. Tretinoin 71-73 LYN proto-oncogene, Src family tyrosine kinase Homo sapiens 34-37
34784434-8 2021 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin 48-52 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-169
34988552-8 2021 Antioxidants, such as Retinoic acid and Oxytocin, can reduce activation of the NF-kappaB pathway by neutralizing stimulatory reactive oxygen species (ROS). Tretinoin 22-35 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 79-88
34713889-6 2021 Further research revealed that retinoic acid-related orphan receptor C (RORC) directly targeted stigmasterol in lung cancer. Tretinoin 31-44 RAR related orphan receptor C Homo sapiens 72-76
34519134-7 2021 This regulation pattern of PARylation was found to be associated with the protective effect of BOS against SIN1 on the viability of retinoic acid-differentiated SH-SY5Y cells. Tretinoin 132-145 MAPK associated protein 1 Homo sapiens 107-111
34676874-0 2021 All-trans retinoic acid promotes macrophage phagocytosis and decreases inflammation via inhibiting CD14/TLR4 in acute lung injury. Tretinoin 0-23 CD14 molecule Rattus norvegicus 99-103
34355652-2 2021 In the present study, a clinically achievable concentration of trametinib, a highly selective inhibitor of MEK, enhanced ATRA-induced differentiation in AML cell lines, HL-60 and U937 as well as AML primary cells. Tretinoin 121-125 mitogen-activated protein kinase kinase 7 Homo sapiens 107-110
34355652-6 2021 Therefore, STAT3, Akt, and JNK signaling pathways were involved in tra-ATRA-induced differentiation in HL-60, U937, and HL-60Res cells, respectively. Tretinoin 67-70 signal transducer and activator of transcription 3 Homo sapiens 11-16
34355652-6 2021 Therefore, STAT3, Akt, and JNK signaling pathways were involved in tra-ATRA-induced differentiation in HL-60, U937, and HL-60Res cells, respectively. Tretinoin 67-70 AKT serine/threonine kinase 1 Homo sapiens 18-21
34355652-6 2021 Therefore, STAT3, Akt, and JNK signaling pathways were involved in tra-ATRA-induced differentiation in HL-60, U937, and HL-60Res cells, respectively. Tretinoin 67-70 mitogen-activated protein kinase 8 Homo sapiens 27-30
34355652-6 2021 Therefore, STAT3, Akt, and JNK signaling pathways were involved in tra-ATRA-induced differentiation in HL-60, U937, and HL-60Res cells, respectively. Tretinoin 71-75 signal transducer and activator of transcription 3 Homo sapiens 11-16
34355652-6 2021 Therefore, STAT3, Akt, and JNK signaling pathways were involved in tra-ATRA-induced differentiation in HL-60, U937, and HL-60Res cells, respectively. Tretinoin 71-75 AKT serine/threonine kinase 1 Homo sapiens 18-21
34355652-6 2021 Therefore, STAT3, Akt, and JNK signaling pathways were involved in tra-ATRA-induced differentiation in HL-60, U937, and HL-60Res cells, respectively. Tretinoin 71-75 mitogen-activated protein kinase 8 Homo sapiens 27-30
34676874-0 2021 All-trans retinoic acid promotes macrophage phagocytosis and decreases inflammation via inhibiting CD14/TLR4 in acute lung injury. Tretinoin 0-23 toll-like receptor 4 Rattus norvegicus 104-108
34676874-10 2021 Macrophages were treated with IAXO-102 (TLR4 inhibitor) to verify the involvement of CD14/TLR4 in the effect of ATRA on ALI. Tretinoin 112-116 CD14 molecule Rattus norvegicus 85-89
34676874-10 2021 Macrophages were treated with IAXO-102 (TLR4 inhibitor) to verify the involvement of CD14/TLR4 in the effect of ATRA on ALI. Tretinoin 112-116 toll-like receptor 4 Rattus norvegicus 90-94
34676874-13 2021 Mechanically, ATRA inhibited CD14 and TLR4 expression and NF-kappaB pathway activation. Tretinoin 14-18 CD14 molecule Rattus norvegicus 29-33
34676874-13 2021 Mechanically, ATRA inhibited CD14 and TLR4 expression and NF-kappaB pathway activation. Tretinoin 14-18 toll-like receptor 4 Rattus norvegicus 38-42
34676874-14 2021 ATRA enhanced macrophage phagocytosis and reduced inflammation by inhibiting the CD14/TLR4-NF-kappaB pathway in LPS-induced ALI. Tretinoin 0-4 CD14 molecule Rattus norvegicus 81-85
34676874-14 2021 ATRA enhanced macrophage phagocytosis and reduced inflammation by inhibiting the CD14/TLR4-NF-kappaB pathway in LPS-induced ALI. Tretinoin 0-4 toll-like receptor 4 Rattus norvegicus 86-90
34676874-15 2021 In summary, ATRA inactivated the NF-kappaB pathway by inhibiting the expression of CD14/TLR4 receptor in the alveolar macrophages of rats, thus enhancing the phagocytic function of macrophages in ALI rats, improving the activity of macrophages, inhibiting apoptosis, reducing the levels of inflammatory factors, and consequently playing a protective role in ALI model rats. Tretinoin 12-16 CD14 molecule Rattus norvegicus 83-87
34676874-15 2021 In summary, ATRA inactivated the NF-kappaB pathway by inhibiting the expression of CD14/TLR4 receptor in the alveolar macrophages of rats, thus enhancing the phagocytic function of macrophages in ALI rats, improving the activity of macrophages, inhibiting apoptosis, reducing the levels of inflammatory factors, and consequently playing a protective role in ALI model rats. Tretinoin 12-16 toll-like receptor 4 Rattus norvegicus 88-92
33820492-10 2021 ATRA treatment reduced TGF-beta1, Col-IV and FN expressions and improved Angpt-1 expression compared with the UUO group. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 23-32
34579932-0 2021 Expression of concern: "Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence" Cancer Letters, Volume 328, Issue 1, 1 January 2013, Pages 44-54. Tretinoin 70-83 mitogen-activated protein kinase 1 Homo sapiens 147-150
34579932-0 2021 Expression of concern: "Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence" Cancer Letters, Volume 328, Issue 1, 1 January 2013, Pages 44-54. Tretinoin 70-83 AKT serine/threonine kinase 1 Homo sapiens 156-159
34579932-0 2021 Expression of concern: "Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence" Cancer Letters, Volume 328, Issue 1, 1 January 2013, Pages 44-54. Tretinoin 70-83 tumor protein p53 Homo sapiens 171-174
34087410-7 2021 Calcitriol and retinoic acid together impaired the recruitment of HDAC1 to the Il9 gene without impacting Gcn5 recruitment. Tretinoin 15-28 histone deacetylase 1 Homo sapiens 66-71
34840990-9 2021 Moreover, retinoic acid (RA) released from TLR5+ LPDCs could play a key role in modulating TH1 polarization. Tretinoin 10-23 negative elongation factor complex member C/D, Th1l Mus musculus 91-94
34840990-9 2021 Moreover, retinoic acid (RA) released from TLR5+ LPDCs could play a key role in modulating TH1 polarization. Tretinoin 25-27 negative elongation factor complex member C/D, Th1l Mus musculus 91-94
34783423-8 2022 DRA was associated with higher percentage of PF (97.2% vs. 78.5% in TRA group, p < 0.0001) and reduced time-to-hemostasis (147 +- 99 min vs. 285 +- 138 min, p < 0.0001). Tretinoin 68-71 solute carrier family 26 member 3 Homo sapiens 0-3
34827649-0 2021 Similarities in DSG1 and KRT3 Downregulation through Retinoic Acid Treatment and PAX6 Knockdown Related Expression Profiles: Does PAX6 Affect RA Signaling in Limbal Epithelial Cells? Tretinoin 53-66 keratin 3 Homo sapiens 25-29
34731634-7 2021 In a proof-of-principle approach, we use these datasets to show that MEK signaling is required for M2-type polarization by promoting peroxisome proliferator-activated receptor-gamma (PPARgamma)-induced retinoic acid signaling. Tretinoin 202-215 mitogen-activated protein kinase kinase 7 Homo sapiens 69-72
34731634-7 2021 In a proof-of-principle approach, we use these datasets to show that MEK signaling is required for M2-type polarization by promoting peroxisome proliferator-activated receptor-gamma (PPARgamma)-induced retinoic acid signaling. Tretinoin 202-215 peroxisome proliferator activated receptor gamma Homo sapiens 133-181
34731634-7 2021 In a proof-of-principle approach, we use these datasets to show that MEK signaling is required for M2-type polarization by promoting peroxisome proliferator-activated receptor-gamma (PPARgamma)-induced retinoic acid signaling. Tretinoin 202-215 peroxisome proliferator activated receptor gamma Homo sapiens 183-192
34579532-13 2021 This work presents a new paradigm for addressing chemotherapy-induced side effects via degradation of Pin1 induced by tumor-targeted delivery of DOX and ATRA. Tretinoin 153-157 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 102-106
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 281-285 interleukin 7 Mus musculus 247-251
34769078-4 2021 We found that the coagulation system and retinoic acid signaling were most highly affected by SEPHS1 deficiency throughout gastrulation. Tretinoin 41-54 selenophosphate synthetase 1 Mus musculus 94-100
34744762-5 2021 L-PGDS binds retinoic acids and retinal with high affinities (Kd < 100 nM) and diverse small lipophilic substances, such as thyroids, gangliosides, bilirubin and biliverdin, heme, NAD(P)H, and PGD2, acting as an extracellular carrier of these substances. Tretinoin 13-27 prostaglandin D2 synthase Homo sapiens 0-6
34379517-0 2021 Retinoic Acid Inducible Gene-I like Receptors Activate Snail to Limit RNA Viral Infections. Tretinoin 0-13 snail family transcriptional repressor 1 Homo sapiens 55-60
34625492-4 2021 VIP is also required for postnatal formation of lymphoid tissues as well as the maintenance of local populations of retinoic acid (RA)-producing dendritic cells, with RA up-regulating gut-homing receptor CCR9 expression by ILC3s. Tretinoin 116-129 vasoactive intestinal polypeptide Mus musculus 0-3
34625492-4 2021 VIP is also required for postnatal formation of lymphoid tissues as well as the maintenance of local populations of retinoic acid (RA)-producing dendritic cells, with RA up-regulating gut-homing receptor CCR9 expression by ILC3s. Tretinoin 131-133 vasoactive intestinal polypeptide Mus musculus 0-3
34625492-5 2021 Correspondingly, mice deficient in VIP or VPAC1 suffer a paucity of intestinal ILC3s along with impaired production of the cytokine IL-22, rendering them highly susceptible to the enteric pathogen Citrobacter rodentium This heightened susceptibility to C. rodentium infection was ameliorated by RA supplementation, adoptive transfer of ILC3s, or by recombinant IL-22. Tretinoin 295-297 vasoactive intestinal polypeptide Mus musculus 35-38
34625492-5 2021 Correspondingly, mice deficient in VIP or VPAC1 suffer a paucity of intestinal ILC3s along with impaired production of the cytokine IL-22, rendering them highly susceptible to the enteric pathogen Citrobacter rodentium This heightened susceptibility to C. rodentium infection was ameliorated by RA supplementation, adoptive transfer of ILC3s, or by recombinant IL-22. Tretinoin 295-297 vasoactive intestinal peptide receptor 1 Mus musculus 42-47
34660779-4 2021 Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels. Tretinoin 23-27 tumor protein p53 Homo sapiens 102-105
34816580-6 2022 NAV2 is a retinoic-acid responsive novel disease gene candidate with biological roles in neurite outgrowth and cerebellar dysgenesis in mouse models. Tretinoin 10-23 neuron navigator 2 Mus musculus 0-4
34832966-9 2021 Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells. Tretinoin 153-166 tumor protein p53 Homo sapiens 245-249
34832966-10 2021 Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2). Tretinoin 46-48 tumor protein p53 Homo sapiens 59-62
34830120-9 2021 Furthermore, RA and stress can increase Crabp1 level, which would up-regulate FKBP5 thereby de-sensitizing feedback inhibition of HPA axis (by decreasing GR signaling) and increasing the risk of stress-related disorders. Tretinoin 13-15 nuclear receptor subfamily 3, group C, member 1 Mus musculus 154-156
34872261-0 2021 All-trans retinoic acid inhibits epithelial-to-mesenchymal transition (EMT) through the down-regulation of IL-6 in endometriosis. Tretinoin 3-23 interleukin 6 Homo sapiens 107-111
34872261-10 2021 After ATRA treatment, the expression of IL-6 was significantly reduced, accompanied by a decrease in the migration, invasion, and EMT of large endometriotic stromal CFUs. Tretinoin 6-10 interleukin 6 Homo sapiens 40-44
34872261-11 2021 In addition, the inhibition of ATRA was mediated by IL-6. Tretinoin 31-35 interleukin 6 Homo sapiens 52-56
34872261-13 2021 ATRA may be a promising therapeutic strategy aimed at IL-6 for the stem-cell treatment of EMs. Tretinoin 0-4 interleukin 6 Homo sapiens 54-58
34579532-0 2021 All-Trans Retinoic Acid and Doxorubicin Delivery by Folic Acid Modified Polymeric Micelles for the Modulation of Pin1-Mediated DOX-Induced Breast Cancer Stemness and Metastasis. Tretinoin 0-23 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 113-117
34579532-7 2021 ATRA, a newly identified Pin1 inhibitor, can abolish several oncogenic pathways by effectively inhibiting and degrading overexpressed Pin1. Tretinoin 0-4 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 25-29
34579532-7 2021 ATRA, a newly identified Pin1 inhibitor, can abolish several oncogenic pathways by effectively inhibiting and degrading overexpressed Pin1. Tretinoin 0-4 peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1 Mus musculus 134-138
34092372-0 2021 Reactivation of silenced alpha-N-catenin induces retinoic acid sensitivity in neuroblastoma cells. Tretinoin 49-62 catenin alpha 2 Homo sapiens 25-40
34092372-3 2021 A subset of neuroblastoma tumors that lack alpha-N-catenin are resistant to all-trans retinoic acid. Tretinoin 86-99 catenin alpha 2 Homo sapiens 43-58
34092372-12 2021 Re-expression of alpha-N-catenin enhanced the sensitivity to retinoic acid-induced cell growth arrest and downregulated key cell survival pathways in both cell lines. Tretinoin 61-74 catenin alpha 2 Homo sapiens 17-32
34092372-14 2021 CONCLUSION: Re-expression of alpha-N-catenin in retinoic acid-resistant cells induced sensitivity to retinoic acid treatment and is controlled epigenetically via histone deacetylase. Tretinoin 48-61 catenin alpha 2 Homo sapiens 29-44
34092372-14 2021 CONCLUSION: Re-expression of alpha-N-catenin in retinoic acid-resistant cells induced sensitivity to retinoic acid treatment and is controlled epigenetically via histone deacetylase. Tretinoin 101-114 catenin alpha 2 Homo sapiens 29-44
34092372-15 2021 alpha-N-catenin is a potential biomarker for retinoic acid sensitivity and combination treatment with Trichostatin A and retinoic acid may improve survival among children with high-risk, retinoic acid-resistant neuroblastoma. Tretinoin 45-58 catenin alpha 2 Homo sapiens 0-15
34092372-15 2021 alpha-N-catenin is a potential biomarker for retinoic acid sensitivity and combination treatment with Trichostatin A and retinoic acid may improve survival among children with high-risk, retinoic acid-resistant neuroblastoma. Tretinoin 121-134 catenin alpha 2 Homo sapiens 0-15
34092372-15 2021 alpha-N-catenin is a potential biomarker for retinoic acid sensitivity and combination treatment with Trichostatin A and retinoic acid may improve survival among children with high-risk, retinoic acid-resistant neuroblastoma. Tretinoin 187-200 catenin alpha 2 Homo sapiens 0-15
34768994-0 2021 Helicobacter pylori Neutrophil-Activating Protein Directly Interacts with and Activates Toll-like Receptor 2 to Induce the Secretion of Interleukin-8 from Neutrophils and ATRA-Induced Differentiated HL-60 Cells. Tretinoin 171-175 toll like receptor 2 Homo sapiens 88-108
34768994-4 2021 HP-NAP-induced ROS production in ATRA-induced differentiated HL-60 cells is mediated by the PTX-sensitive heterotrimeric G protein-dependent activation of extracellular signal-regulated kinase 1/2 and p38-mitogen-activated protein kinase, which is consistent with the findings reported for human neutrophils. Tretinoin 33-37 mitogen-activated protein kinase 3 Homo sapiens 155-196
34768994-4 2021 HP-NAP-induced ROS production in ATRA-induced differentiated HL-60 cells is mediated by the PTX-sensitive heterotrimeric G protein-dependent activation of extracellular signal-regulated kinase 1/2 and p38-mitogen-activated protein kinase, which is consistent with the findings reported for human neutrophils. Tretinoin 33-37 mitogen-activated protein kinase 14 Homo sapiens 201-237
34768994-9 2021 Thus, HP-NAP directly interacts with and activates TLR2 to induce IL-8 secretion in neutrophils and ATRA-induced differentiated HL-60 cells. Tretinoin 100-104 toll like receptor 2 Homo sapiens 51-55
34417282-8 2021 Other affected components of RA signaling include selective increases in AI animals in hippocampal synthesis (RALDH1) and catabolism of RA (CYP26B1), RA receptor alpha, the RA regulated ionotropic glutamate receptor (GluR1), as well as fragile X mental retardation protein. Tretinoin 29-31 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 110-116
34599305-5 2021 Furthermore, retinoic acid signalling is largely confined to the prospective PFC by CYP26B1, a retinoic-acid-catabolizing enzyme, which is upregulated in the prospective motor cortex. Tretinoin 13-26 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 84-91
34599305-6 2021 Genetic deletions in mice revealed that retinoic acid signalling through the retinoic acid receptors RXRG and RARB, as well as CYP26B1-dependent catabolism, are involved in proper molecular patterning of prefrontal and motor areas, development of PFC-mediodorsal thalamus connectivity, intra-PFC dendritic spinogenesis and expression of the layer 4 marker RORB. Tretinoin 40-53 retinoid X receptor gamma Mus musculus 101-105
34599306-5 2021 Moreover, we found that species differences in level of expression and laminar distribution of CBLN2 are, at least in part, due to Hominini-specific deletions containing SOX5-binding sites within a retinoic acid-responsive CBLN2 enhancer. Tretinoin 198-211 cerebellin 2 precursor Homo sapiens 95-100
34599306-5 2021 Moreover, we found that species differences in level of expression and laminar distribution of CBLN2 are, at least in part, due to Hominini-specific deletions containing SOX5-binding sites within a retinoic acid-responsive CBLN2 enhancer. Tretinoin 198-211 SRY-box transcription factor 5 Homo sapiens 170-174
34599306-5 2021 Moreover, we found that species differences in level of expression and laminar distribution of CBLN2 are, at least in part, due to Hominini-specific deletions containing SOX5-binding sites within a retinoic acid-responsive CBLN2 enhancer. Tretinoin 198-211 cerebellin 2 precursor Homo sapiens 223-228
34650910-10 2021 In vitro, treatment with the EGFR inhibitor gefitinib (ZD1839) reduced cell proliferation and survival of NB4 (ATRA-sensitive) and NB4-R2 (ATRA-resistant) cells. Tretinoin 111-115 epidermal growth factor receptor Homo sapiens 29-33
34557995-0 2022 Hypoxia-Inducible Factor-1alpha (HIF-1alpha) Inhibition Impairs Retinoic Acid-Induced Differentiation in SH-SY5Y Neuroblastoma Cells, Leading to Reduced Neurite Length and Diminished Gene Expression Related to Cell Differentiation. Tretinoin 64-77 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-31
34557995-0 2022 Hypoxia-Inducible Factor-1alpha (HIF-1alpha) Inhibition Impairs Retinoic Acid-Induced Differentiation in SH-SY5Y Neuroblastoma Cells, Leading to Reduced Neurite Length and Diminished Gene Expression Related to Cell Differentiation. Tretinoin 64-77 hypoxia inducible factor 1 subunit alpha Homo sapiens 33-43
34557995-5 2022 This work aims to investigate the effects of the selective inhibition of HIF-1alpha on the differentiation induced by retinoic acid in human neuroblastoma cells from the SH-SY5Y lineage to clarify its role in cell differentiation. Tretinoin 118-131 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-83
34557995-6 2022 Our results indicate that HIF-1alpha inhibition impairs RA-induced differentiation by reducing neuron-like phenotype and diminished immunolabeling and expression of differentiation markers. Tretinoin 56-58 hypoxia inducible factor 1 subunit alpha Homo sapiens 26-36
34557995-7 2022 HIF1A is involved in Retinoic Acid (RA) induced differentiation in SH-SY5Y neuroblastoma cells. Tretinoin 21-34 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5
34557995-7 2022 HIF1A is involved in Retinoic Acid (RA) induced differentiation in SH-SY5Y neuroblastoma cells. Tretinoin 36-38 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-5
34557995-8 2022 siRNA HIF1A gene silencing leads to a weaker response to RA, demonstrated by changes in the neuro-like phenotype and diminished expression of differentiation markers. Tretinoin 57-59 hypoxia inducible factor 1 subunit alpha Homo sapiens 6-11
34417282-8 2021 Other affected components of RA signaling include selective increases in AI animals in hippocampal synthesis (RALDH1) and catabolism of RA (CYP26B1), RA receptor alpha, the RA regulated ionotropic glutamate receptor (GluR1), as well as fragile X mental retardation protein. Tretinoin 29-31 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 217-222
34292881-4 2021 Reduction in RA signaling activity severely affects the ability of the uterus to achieve receptive status and decidualize, partially through dampening follistatin expression and downstream activin B/BMP2 signaling. Tretinoin 13-15 follistatin Homo sapiens 151-162
34160123-1 2021 Retinoic acid exposures as well as defects in the retinoic acid-degrading enzyme CYP26B1 have teratogenic effects on both limb and craniofacial skeleton. Tretinoin 50-63 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 81-88
34282811-7 2021 LP22A3 induced TGF-beta secretion from the IECs of the small intestine with retinoic acid production probably through TLR2, resulting in an increase in CD103+ DCs and the Foxp3+ Treg population. Tretinoin 76-89 integrin alpha E, epithelial-associated Mus musculus 152-157
34288263-8 2021 Moreover, all-trans-retinoic acid, which enhances CD38 expression and induces cell differentiation in myeloma cells, reduced B-cell marker expression and the BCL2/BCL2L1 ratio in myeloma cell lines, leading to reduced efficacy of venetoclax. Tretinoin 10-33 BCL2 apoptosis regulator Homo sapiens 158-162
34288263-8 2021 Moreover, all-trans-retinoic acid, which enhances CD38 expression and induces cell differentiation in myeloma cells, reduced B-cell marker expression and the BCL2/BCL2L1 ratio in myeloma cell lines, leading to reduced efficacy of venetoclax. Tretinoin 10-33 BCL2 like 1 Homo sapiens 163-169
34403508-8 2021 All trans retinoic acid, an IL-6 inhibitor, also decreased the secretion of IL-6 and reduced the paracrine effect of senescent cells on healthy cells. Tretinoin 4-23 interleukin 6 Bos taurus 28-32
34403508-8 2021 All trans retinoic acid, an IL-6 inhibitor, also decreased the secretion of IL-6 and reduced the paracrine effect of senescent cells on healthy cells. Tretinoin 4-23 interleukin 6 Bos taurus 76-80
34410954-7 2021 CONCLUSION: Combined ATRA and IM therapy was shown to be effective in decreasing BCR-ABL and ABCB1 genes, possibly through the differentiation of blast cells, demonstrating that the therapy could be potentially effective in the blast crisis of the disease and for those patients who develop resistance to available CML treatments. Tretinoin 21-25 ATP binding cassette subfamily B member 1 Homo sapiens 93-98
34410954-0 2021 Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model. Tretinoin 20-24 ATP binding cassette subfamily B member 1 Homo sapiens 69-74
34410954-0 2021 Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model. Tretinoin 20-24 ATP binding cassette subfamily B member 1 Homo sapiens 75-79
34410954-3 2021 MATERIALS AND METHODS: K562 cells were treated with IM and with the combined therapy of ATRA together with IM for 48 and 72 h. The expression of BCR-ABL gene and multidrug resistance gene ABCB1 were evaluated using RT-qPCR. Tretinoin 88-92 ATP binding cassette subfamily B member 1 Homo sapiens 188-193
34324169-5 2021 The objective of this study is to employ JAK1 inhibition (JAK1i) in the presence of ATRA as a potential therapy in non-M3 acute myeloid leukemia (AML). Tretinoin 84-88 Janus kinase 1 Homo sapiens 41-45
34419449-17 2021 We conclude that Rdh10/RA affects whole body energy use and insulin resistance partially through sexual dimorphic effects on skeletal muscle gene expression, structure, and mitochondria activity. Tretinoin 23-25 insulin Homo sapiens 60-67
34166781-6 2021 Moreover, Smad2 was found to interact directly with Meg3, and atRA treatment significantly enriched Meg3 in Smad2-immunoprecipitated samples. Tretinoin 62-66 SMAD family member 2 Mus musculus 108-113
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 76-80 retinoid X receptor alpha Rattus norvegicus 0-8
34324169-0 2021 Selective Inhibition of JAK1 Primes STAT5-Driven Human Leukemia Cells for ATRA-Induced Differentiation. Tretinoin 74-78 Janus kinase 1 Homo sapiens 24-28
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 76-80 retinoid X receptor alpha Rattus norvegicus 117-125
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 301-305 retinoid X receptor alpha Rattus norvegicus 0-8
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 301-305 retinoid X receptor alpha Rattus norvegicus 117-125
34458260-5 2021 We suggest RA signaling-mediated regulation of VIPR1 and KRT7 as the underlying mechanism for lumen formation, rather than apoptosis in the organoid culture system. Tretinoin 11-13 vasoactive intestinal peptide receptor 1 Mus musculus 47-52
34389675-5 2021 There were two unexpected findings: 1) a strong induction of CYPs involved in activation of fatty acids (CYP4), and in inactivation of calcitriol (CYP24A1) and retinoic acid (CYP26A1); and 2) a marked down-regulation of FOS, FRA1, and JUN, known tethering partners of ERbeta. Tretinoin 160-173 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 175-182
34389675-5 2021 There were two unexpected findings: 1) a strong induction of CYPs involved in activation of fatty acids (CYP4), and in inactivation of calcitriol (CYP24A1) and retinoic acid (CYP26A1); and 2) a marked down-regulation of FOS, FRA1, and JUN, known tethering partners of ERbeta. Tretinoin 160-173 estrogen receptor 1 Homo sapiens 268-274
34422216-8 2021 To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated PTZ toxicity. Tretinoin 69-92 NFE2 like bZIP transcription factor 2 Rattus norvegicus 57-61
34422216-8 2021 To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated PTZ toxicity. Tretinoin 94-98 NFE2 like bZIP transcription factor 2 Rattus norvegicus 57-61
34430707-11 2021 The rescue experiments verified that recovery of miR-130a-3p in HAGLR-overexpressing SH-SY5Y cells could successfully overcome the RA-induced SH-SY5Y differentiation by targeting MeCP2. Tretinoin 131-133 methyl-CpG binding protein 2 Homo sapiens 179-184
34244292-4 2021 Mutations of two SUMO-acceptor lysines of Satb2 (Satb2 K R ) or knockout of Zfp451 impair the ability of ESCs to silence pluripotency genes and activate differentiation-associated genes in response to retinoic acid (RA) treatment. Tretinoin 202-215 SATB homeobox 2 Homo sapiens 42-47
34244292-4 2021 Mutations of two SUMO-acceptor lysines of Satb2 (Satb2 K R ) or knockout of Zfp451 impair the ability of ESCs to silence pluripotency genes and activate differentiation-associated genes in response to retinoic acid (RA) treatment. Tretinoin 217-219 SATB homeobox 2 Homo sapiens 42-47
34244292-6 2021 Upon RA treatment of Satb2 wt ESCs, SATB2 interacts with ZFP451 and the LSD1/CoREST complex and gains binding at differentiation genes, which is not observed in RA-treated Satb2 K R cells. Tretinoin 5-7 SATB homeobox 2 Homo sapiens 21-26
34244292-6 2021 Upon RA treatment of Satb2 wt ESCs, SATB2 interacts with ZFP451 and the LSD1/CoREST complex and gains binding at differentiation genes, which is not observed in RA-treated Satb2 K R cells. Tretinoin 5-7 SATB homeobox 2 Homo sapiens 36-41
34244292-6 2021 Upon RA treatment of Satb2 wt ESCs, SATB2 interacts with ZFP451 and the LSD1/CoREST complex and gains binding at differentiation genes, which is not observed in RA-treated Satb2 K R cells. Tretinoin 161-163 SATB homeobox 2 Homo sapiens 172-177
34122632-2 2021 Our previous study demonstrated that sphingosine 1-phosphate attenuated the effects of ATRA on human colon cancer cells by blocking the expression of retinoic acid receptor beta. Tretinoin 87-91 retinoic acid receptor beta Homo sapiens 150-177
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 88-92 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 297-317
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 88-92 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 319-326
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 275-279 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 297-317
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 275-279 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 319-326
34113673-10 2021 Treatment with RA for 14 days increased the expression of DAZL and FRAGILIS and maintained the mRNA levels of STRA8 in bovine fetal AT-MSCs transfected with bi-cistronic and tri-cistronic vectors. Tretinoin 15-17 stimulated by retinoic acid 8 Bos taurus 110-115
34116057-4 2021 We observed that assembly of the CSB-Elongin ubiquitin ligase is induced not just by DNA damage, but also by a variety of signals that activate RNAPII-mediated transcription, including endoplasmic reticulum (ER) stress, amino acid starvation, retinoic acid, glucocorticoids, and doxycycline treatment of cells carrying several copies of a doxycycline-inducible reporter. Tretinoin 243-256 excision repair cross-complementing rodent repair deficiency, complementation group 6 Mus musculus 33-36
34188166-5 2021 In activated PSC, PTX3 secretion could be downregulated by rendering PSC quiescent using all-trans-retinoic acid (ATRA). Tretinoin 89-112 pentraxin related gene Mus musculus 18-22
34188166-5 2021 In activated PSC, PTX3 secretion could be downregulated by rendering PSC quiescent using all-trans-retinoic acid (ATRA). Tretinoin 114-118 pentraxin related gene Mus musculus 18-22
34188166-8 2021 However, in STARPAC clinical trial (NCT03307148), stromal modulation by ATRA even at first dose is accompanied with serum PTX3 response in patients who later go on to demonstrate disease control but not those in whom the disease progresses. Tretinoin 72-76 pentraxin 3 Homo sapiens 122-126
34136084-5 2021 Addition of RA induces the expression of Fgr. Tretinoin 12-14 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 41-44
34136084-8 2021 If RA-induced Fgr expression is ablated by a CRISPR-KO; then the RA-induced (p-tyr) phosphorylation of NUMB and enhanced NUMB-binding and (p-tyr)phosphorylation of select signalosome components are lost. Tretinoin 3-5 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 14-17
34136084-8 2021 If RA-induced Fgr expression is ablated by a CRISPR-KO; then the RA-induced (p-tyr) phosphorylation of NUMB and enhanced NUMB-binding and (p-tyr)phosphorylation of select signalosome components are lost. Tretinoin 65-67 FGR proto-oncogene, Src family tyrosine kinase Homo sapiens 14-17
34169421-3 2021 The aim of this study was to analyze the prognostic impact of FLT3-ITD on APL patients who received remission induction with ATRA, idarubicin (IDA) and/or ATO, followed by ATRA plus ATO along with anthracycline, as consolidation therapy. Tretinoin 125-129 fms related receptor tyrosine kinase 3 Homo sapiens 62-66
34169421-3 2021 The aim of this study was to analyze the prognostic impact of FLT3-ITD on APL patients who received remission induction with ATRA, idarubicin (IDA) and/or ATO, followed by ATRA plus ATO along with anthracycline, as consolidation therapy. Tretinoin 172-176 fms related receptor tyrosine kinase 3 Homo sapiens 62-66
34233909-2 2021 In this study, we investigated the role of the redundant cation channels TMEM176A and TMEM176B (TMEM176A/B) in retinoic acid-related orphan receptor gammat+ cells and conventional dendritic cells (DCs) using germline and conditional double knockout mice. Tretinoin 111-124 transmembrane protein 176B Mus musculus 86-94
34233909-2 2021 In this study, we investigated the role of the redundant cation channels TMEM176A and TMEM176B (TMEM176A/B) in retinoic acid-related orphan receptor gammat+ cells and conventional dendritic cells (DCs) using germline and conditional double knockout mice. Tretinoin 111-124 transmembrane protein 176B Mus musculus 96-106
34253781-2 2021 Recent clinical trials revealed therapeutic potential of both all-trans and 9-cis retinoic acid in patients with cortisol excess due to a pituitary ACTH-secreting adenoma and indicated that retinoids might act also on the adrenal. Tretinoin 82-95 proopiomelanocortin Homo sapiens 148-152
34253781-8 2021 ACTH itself increased ligand-induced retinoic acid receptor expression, possibly enhancing sensitivity to retinoic acid. Tretinoin 106-119 proopiomelanocortin Homo sapiens 0-4
34148507-11 2021 Also, retinoic acid inhibits Nrf2 activation via DMF and increases inflammatory factors in hypoperfused rats" hippocampus compared with the CCH group (P<0.001). Tretinoin 6-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 29-33
34723044-5 2021 T cells and T cell-derived IFN-gamma are crucial for increasing inflammatory macrophage levels in IR and RA treated tumors. Tretinoin 105-107 interferon gamma Homo sapiens 27-36
34723044-6 2021 Notably, whereas CD8+ T cells are required for the antitumor response to IR, CD4+ T cells are required for the effectiveness of the IR and RA combination. Tretinoin 139-141 CD4 molecule Homo sapiens 77-80
34178631-4 2021 We also aimed to investigate the effect of the FDA approved drug rapamycin and the vitamin A metabolite retinoic acid (RA) in cell lines with TSC mutation. Tretinoin 104-117 TSC complex subunit 1 Homo sapiens 142-145
34178631-4 2021 We also aimed to investigate the effect of the FDA approved drug rapamycin and the vitamin A metabolite retinoic acid (RA) in cell lines with TSC mutation. Tretinoin 119-121 TSC complex subunit 1 Homo sapiens 142-145
34085926-0 2021 Canonical NF-kappaB signaling maintains corneal epithelial integrity and prevents corneal aging via retinoic acid. Tretinoin 100-113 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 10-19
34136389-0 2021 Retinoic Acid Downregulates HSPB8 Gene Expression in Human Breast Cancer Cells MCF-7. Tretinoin 0-13 heat shock protein family B (small) member 8 Homo sapiens 28-33
34072457-1 2021 Cytochrome P450 3A7 (CYP3A7) is a fetal/neonatal liver enzyme that participates in estriol synthesis, clearance of all-trans retinoic acid, and xenobiotic metabolism. Tretinoin 125-138 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 0-19
34072457-1 2021 Cytochrome P450 3A7 (CYP3A7) is a fetal/neonatal liver enzyme that participates in estriol synthesis, clearance of all-trans retinoic acid, and xenobiotic metabolism. Tretinoin 125-138 cytochrome P450 family 3 subfamily A member 7 Homo sapiens 21-27
34113673-11 2021 Moreover, RA treatment repressed the expression of OCT4 and NANOG in these cells. Tretinoin 10-12 POU domain, class 5, transcription factor 1 Bos taurus 51-55
35001679-5 2022 More important, expanded Shh signaling in the ventral forebrain, as well as partial abrogation of midfacial defects in Rdh10 mutants via inhibition of Hh signaling, indicates that misregulation of Shh signaling underlies the pathogenesis of reduced RA signaling-associated midfacial defects. Tretinoin 249-251 retinol dehydrogenase 10 (all-trans) Mus musculus 119-124
35364055-10 2022 We show that loss of Cyp26b1 results in upregulation of retinoic acid (RA) target genes, supporting the observation that Cyp26b1 has RA-dependent roles. Tretinoin 56-69 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 21-28
35364055-10 2022 We show that loss of Cyp26b1 results in upregulation of retinoic acid (RA) target genes, supporting the observation that Cyp26b1 has RA-dependent roles. Tretinoin 56-69 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 121-128
35364055-10 2022 We show that loss of Cyp26b1 results in upregulation of retinoic acid (RA) target genes, supporting the observation that Cyp26b1 has RA-dependent roles. Tretinoin 71-73 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 21-28
35364055-10 2022 We show that loss of Cyp26b1 results in upregulation of retinoic acid (RA) target genes, supporting the observation that Cyp26b1 has RA-dependent roles. Tretinoin 71-73 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 121-128
35364055-10 2022 We show that loss of Cyp26b1 results in upregulation of retinoic acid (RA) target genes, supporting the observation that Cyp26b1 has RA-dependent roles. Tretinoin 133-135 cytochrome P450, family 26, subfamily b, polypeptide 1 Mus musculus 121-128
35503261-8 2022 Based on a previous study showing that FUS::ERG binds to the retinoic acid-responsive elements (RARE) and that All-trans retinoic acid (ATRA) induced cell differentiation of AML cells, we support the clinical evaluation of an APL-like therapeutic regimen for AML with ERG rearrangement. Tretinoin 136-140 FUS RNA binding protein Homo sapiens 39-42
34782578-6 2022 All-trans retinoic acid, an Nrf2 inhibitor, reversed the effects of lithium. Tretinoin 0-23 NFE2 like bZIP transcription factor 2 Rattus norvegicus 28-32
35464301-0 2022 All-trans-retinoic acid induces RARB-dependent apoptosis via ROS induction and enhances cisplatin sensitivity by NRF2 downregulation in cholangiocarcinoma cells. Tretinoin 0-23 retinoic acid receptor beta Homo sapiens 32-36
35464301-14 2022 ATRA also suppressed cisplatin-induced NRF2 expression, suggesting that the enhancement of cisplatin cytotoxicity by ATRA may be associated with the downregulation of NRF2 signaling. Tretinoin 117-121 NFE2 like bZIP transcription factor 2 Homo sapiens 167-171
35464301-0 2022 All-trans-retinoic acid induces RARB-dependent apoptosis via ROS induction and enhances cisplatin sensitivity by NRF2 downregulation in cholangiocarcinoma cells. Tretinoin 0-23 NFE2 like bZIP transcription factor 2 Homo sapiens 113-117
35464301-10 2022 Furthermore, when the cytotoxicity of ATRA against retinoic acid receptor (RAR)-deficient cells was assessed, it was revealed that ATRA cytotoxicity was RARB-dependent. Tretinoin 38-42 retinoic acid receptor beta Homo sapiens 75-78
35464301-10 2022 Furthermore, when the cytotoxicity of ATRA against retinoic acid receptor (RAR)-deficient cells was assessed, it was revealed that ATRA cytotoxicity was RARB-dependent. Tretinoin 38-42 retinoic acid receptor beta Homo sapiens 153-157
35464301-10 2022 Furthermore, when the cytotoxicity of ATRA against retinoic acid receptor (RAR)-deficient cells was assessed, it was revealed that ATRA cytotoxicity was RARB-dependent. Tretinoin 131-135 retinoic acid receptor beta Homo sapiens 75-78
35464301-10 2022 Furthermore, when the cytotoxicity of ATRA against retinoic acid receptor (RAR)-deficient cells was assessed, it was revealed that ATRA cytotoxicity was RARB-dependent. Tretinoin 131-135 retinoic acid receptor beta Homo sapiens 153-157
35464301-13 2022 Furthermore, following ATRA treatment, an increase in cellular ROS content was associated with suppressing nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2) and NRF2-downstream active genes. Tretinoin 23-27 NFE2 like bZIP transcription factor 2 Homo sapiens 107-150
35464301-13 2022 Furthermore, following ATRA treatment, an increase in cellular ROS content was associated with suppressing nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2) and NRF2-downstream active genes. Tretinoin 23-27 NFE2 like bZIP transcription factor 2 Homo sapiens 152-158
35464301-13 2022 Furthermore, following ATRA treatment, an increase in cellular ROS content was associated with suppressing nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2) and NRF2-downstream active genes. Tretinoin 23-27 NFE2 like bZIP transcription factor 2 Homo sapiens 162-166
35464301-13 2022 Furthermore, following ATRA treatment, an increase in cellular ROS content was associated with suppressing nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2) and NRF2-downstream active genes. Tretinoin 23-27 NFE2 like bZIP transcription factor 2 Homo sapiens 172-176
35464301-14 2022 ATRA also suppressed cisplatin-induced NRF2 expression, suggesting that the enhancement of cisplatin cytotoxicity by ATRA may be associated with the downregulation of NRF2 signaling. Tretinoin 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 39-43
35464301-14 2022 ATRA also suppressed cisplatin-induced NRF2 expression, suggesting that the enhancement of cisplatin cytotoxicity by ATRA may be associated with the downregulation of NRF2 signaling. Tretinoin 0-4 NFE2 like bZIP transcription factor 2 Homo sapiens 167-171
35464301-14 2022 ATRA also suppressed cisplatin-induced NRF2 expression, suggesting that the enhancement of cisplatin cytotoxicity by ATRA may be associated with the downregulation of NRF2 signaling. Tretinoin 117-121 NFE2 like bZIP transcription factor 2 Homo sapiens 39-43
35588039-10 2022 However, all-trans-retinoic acid (ATRA), an Nrf2 inhibitor, reversed the effects on AEPS to activation of Nrf2, enhancement of antioxidant, alleviation of kidney injury, restoration of kidney function, prevention of apoptotic, and facilitation of lead exclusion. Tretinoin 9-32 nuclear factor, erythroid derived 2, like 2 Mus musculus 44-48
35588039-10 2022 However, all-trans-retinoic acid (ATRA), an Nrf2 inhibitor, reversed the effects on AEPS to activation of Nrf2, enhancement of antioxidant, alleviation of kidney injury, restoration of kidney function, prevention of apoptotic, and facilitation of lead exclusion. Tretinoin 9-32 nuclear factor, erythroid derived 2, like 2 Mus musculus 106-110
35588039-10 2022 However, all-trans-retinoic acid (ATRA), an Nrf2 inhibitor, reversed the effects on AEPS to activation of Nrf2, enhancement of antioxidant, alleviation of kidney injury, restoration of kidney function, prevention of apoptotic, and facilitation of lead exclusion. Tretinoin 34-38 nuclear factor, erythroid derived 2, like 2 Mus musculus 44-48
35588039-10 2022 However, all-trans-retinoic acid (ATRA), an Nrf2 inhibitor, reversed the effects on AEPS to activation of Nrf2, enhancement of antioxidant, alleviation of kidney injury, restoration of kidney function, prevention of apoptotic, and facilitation of lead exclusion. Tretinoin 34-38 nuclear factor, erythroid derived 2, like 2 Mus musculus 106-110
35532157-4 2022 We employed all-trans retinoic acid (ATRA) as an inducer of profilin expression and showed that profilin induces autophagy through mTOR inhibition, autophagy-activating kinase ULK1 upregulation, and AMPK stabilization as well as its activation. Tretinoin 12-35 mechanistic target of rapamycin kinase Homo sapiens 131-135
35562751-6 2022 In this study, we investigated whether retinoic acid regulates the expression of deubiquitinating enzymes ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in cerebral ischemic injury. Tretinoin 39-52 OTU deubiquitinase, ubiquitin aldehyde binding 1 Rattus norvegicus 147-175
35562751-16 2022 CONCLUSIONS: These findings suggest that retinoic acid regulates ubiquitin- and proteasome-related proteins including ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in a brain ischemia model. Tretinoin 41-54 OTU deubiquitinase, ubiquitin aldehyde binding 1 Rattus norvegicus 159-187
35545255-6 2022 In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner. Tretinoin 37-41 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 99-105
35545255-6 2022 In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner. Tretinoin 37-41 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 136-142
35585420-0 2022 Retinoic acid increases the cellular cholesterol predominantly in a mTOR-independent manner. Tretinoin 0-13 mechanistic target of rapamycin kinase Homo sapiens 68-72
35594692-4 2022 In a 3D culture system, RA promoted capillary sprout development and promoted the subsequent adipogenesis of intramuscular SVF cells by activating VEGFA/VEGFR2 signaling. Tretinoin 24-26 vascular endothelial growth factor A Homo sapiens 147-152
35594692-5 2022 However, during terminal adipogenesis, RA downregulated PPARgamma, C/EBPalpha and inhibited lipid accumulation. Tretinoin 39-41 peroxisome proliferator activated receptor gamma Homo sapiens 56-65
35594692-5 2022 However, during terminal adipogenesis, RA downregulated PPARgamma, C/EBPalpha and inhibited lipid accumulation. Tretinoin 39-41 CCAAT enhancer binding protein alpha Homo sapiens 67-77
35594692-6 2022 In conclusion, vitamin A/RA upregulate VEGFA and stimulate intramuscular vascular capillary development, which increases intramuscular adipose progenitors and contributes to adipocyte formation. Tretinoin 25-27 vascular endothelial growth factor A Homo sapiens 39-44
35532157-4 2022 We employed all-trans retinoic acid (ATRA) as an inducer of profilin expression and showed that profilin induces autophagy through mTOR inhibition, autophagy-activating kinase ULK1 upregulation, and AMPK stabilization as well as its activation. Tretinoin 37-41 mechanistic target of rapamycin kinase Homo sapiens 131-135
35278669-0 2022 ATRA-mediated-crosstalk between stellate cells and Kupffer cells inhibits autophagy and promotes NLRP3 activation in acute liver injury. Tretinoin 0-4 NLR family pyrin domain containing 3 Homo sapiens 97-102
35523143-4 2022 Ablating PDGFRalpha in the LTBR stromal lineage demonstrates that PDGFRalpha has a major impact on the lineage fate and function, inducing a transcriptomic switch from prostemness genes, such as Rspo3 and Grem1, to prodifferentiation factors, including BMPs, retinoic acid, and laminins, and on spatial organization within the crypt-villus and repair responses. Tretinoin 259-272 platelet derived growth factor receptor, alpha polypeptide Mus musculus 9-19
35523143-4 2022 Ablating PDGFRalpha in the LTBR stromal lineage demonstrates that PDGFRalpha has a major impact on the lineage fate and function, inducing a transcriptomic switch from prostemness genes, such as Rspo3 and Grem1, to prodifferentiation factors, including BMPs, retinoic acid, and laminins, and on spatial organization within the crypt-villus and repair responses. Tretinoin 259-272 platelet derived growth factor receptor, alpha polypeptide Mus musculus 66-76
35523143-4 2022 Ablating PDGFRalpha in the LTBR stromal lineage demonstrates that PDGFRalpha has a major impact on the lineage fate and function, inducing a transcriptomic switch from prostemness genes, such as Rspo3 and Grem1, to prodifferentiation factors, including BMPs, retinoic acid, and laminins, and on spatial organization within the crypt-villus and repair responses. Tretinoin 259-272 R-spondin 3 Mus musculus 195-200
35523143-4 2022 Ablating PDGFRalpha in the LTBR stromal lineage demonstrates that PDGFRalpha has a major impact on the lineage fate and function, inducing a transcriptomic switch from prostemness genes, such as Rspo3 and Grem1, to prodifferentiation factors, including BMPs, retinoic acid, and laminins, and on spatial organization within the crypt-villus and repair responses. Tretinoin 259-272 gremlin 1, DAN family BMP antagonist Mus musculus 205-210
35278669-7 2022 ATRA also blocked autophagic flow by activating the AKT/mTOR pathway, leading to an excessive accumulation of ROS, which further activated the NLRP3 inflammasome. Tretinoin 0-4 AKT serine/threonine kinase 1 Homo sapiens 52-55
35278669-7 2022 ATRA also blocked autophagic flow by activating the AKT/mTOR pathway, leading to an excessive accumulation of ROS, which further activated the NLRP3 inflammasome. Tretinoin 0-4 mechanistic target of rapamycin kinase Homo sapiens 56-60
35278669-7 2022 ATRA also blocked autophagic flow by activating the AKT/mTOR pathway, leading to an excessive accumulation of ROS, which further activated the NLRP3 inflammasome. Tretinoin 0-4 NLR family pyrin domain containing 3 Homo sapiens 143-148
35278669-9 2022 In conclusion, we have uncovered a novel crosstalk pattern between HSCs and KCs, and ATRA-mediated-crosstalk between HSCs and KCs inhibits autophagy and promotes NLRP3 activation to aggravate acute liver injury. Tretinoin 85-89 NLR family pyrin domain containing 3 Homo sapiens 162-167
35147911-0 2022 All-Trans Retinoic Acid-Preconditioned Mesenchymal Stem Cells Improve Motor Function and Alleviate Tissue Damage After Spinal Cord Injury by Inhibition of HMGB1/NF-kappaB/NLRP3 Pathway Through Autophagy Activation. Tretinoin 0-23 nuclear factor kappa B subunit 1 Homo sapiens 161-170
35147911-0 2022 All-Trans Retinoic Acid-Preconditioned Mesenchymal Stem Cells Improve Motor Function and Alleviate Tissue Damage After Spinal Cord Injury by Inhibition of HMGB1/NF-kappaB/NLRP3 Pathway Through Autophagy Activation. Tretinoin 0-23 NLR family pyrin domain containing 3 Homo sapiens 171-176
35147911-4 2022 To this end, we examined the effects of intrathecal injection of all-trans retinoic acid (ATRA)-preconditioned bone marrow mesenchymal stem cells (BM-MSCs) (ATRA-MSCs) on autophagy activity and the HMGB1/NF-kappaB/NLRP3 inflammatory pathway in an SCI rat model. Tretinoin 157-161 nuclear factor kappa B subunit 1 Homo sapiens 204-213
35147911-4 2022 To this end, we examined the effects of intrathecal injection of all-trans retinoic acid (ATRA)-preconditioned bone marrow mesenchymal stem cells (BM-MSCs) (ATRA-MSCs) on autophagy activity and the HMGB1/NF-kappaB/NLRP3 inflammatory pathway in an SCI rat model. Tretinoin 157-161 NLR family, pyrin domain containing 3 Rattus norvegicus 214-219
35467087-3 2022 However, silencing HoxC9 promoter by EZH2-induced H3K27me3 hypermethylation can lead to RA resistance. Tretinoin 88-90 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 37-41
35490242-0 2022 The MYCN inhibitor BGA002 restores the retinoic acid response leading to differentiation or apoptosis by the mTOR block in MYCN-amplified neuroblastoma. Tretinoin 39-52 mechanistic target of rapamycin kinase Homo sapiens 109-113
35467087-5 2022 OBJECTIVES: In our study, we attempted to obtain some insight into the mechanisms of differentiation of RA-resistant NB cells by detecting the expressions of HoxC9 and EZH2 in NB cells treated with ATO, so as to provide a basis for the subsequent treatment of RA-resistant NB by ATO. Tretinoin 104-106 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 168-172
35467087-14 2022 CONCLUSIONS: Arsenic trioxide may reactivate the expression of HoxC9 by downregulating EZH2, which leads to restoring RA sensitivity and promoting the differentiation and apoptosis of RA-resistant NB cells. Tretinoin 118-120 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 87-91
35468223-4 2022 We find that ATRA treatment in combination with inhibition of PI3K (ZSTK474), mTOR (WYE132) or PI3K/mTOR (BEZ235, dactolisib) drastically reduces protein levels of the proto-oncogene MYC. Tretinoin 13-17 mechanistic target of rapamycin kinase Homo sapiens 78-82
35467087-14 2022 CONCLUSIONS: Arsenic trioxide may reactivate the expression of HoxC9 by downregulating EZH2, which leads to restoring RA sensitivity and promoting the differentiation and apoptosis of RA-resistant NB cells. Tretinoin 184-186 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 87-91
35468223-4 2022 We find that ATRA treatment in combination with inhibition of PI3K (ZSTK474), mTOR (WYE132) or PI3K/mTOR (BEZ235, dactolisib) drastically reduces protein levels of the proto-oncogene MYC. Tretinoin 13-17 mechanistic target of rapamycin kinase Homo sapiens 100-104
35078784-0 2022 Targeting S100A9-ALDH1A1-retinoic acid signaling to suppress brain relapse in EGFR-mutant lung cancer. Tretinoin 25-38 epidermal growth factor receptor Homo sapiens 78-82
35436742-0 2022 All-trans retinoic acid inhibits the osteogenesis of periodontal ligament stem cells by promoting IL-1beta production via NF-kappaB signaling. Tretinoin 0-23 nuclear factor kappa B subunit 1 Homo sapiens 122-131
35436742-12 2022 Levels of interleukin-1beta (IL-1beta) were increased at varied time points after ATRA treatment. Tretinoin 82-86 interleukin 1 beta Homo sapiens 10-27
35436742-15 2022 Taken together, our results demonstrate that ATRA disrupts the osteogenesis and mineralizationof PDLSCs by promoting IL-1beta expression via activating NF-kappaB signaling and NLRP3 inflammasome, which may offer a new method for improving the ATRA-induced disruption of osteoblast differentiation. Tretinoin 45-49 nuclear factor kappa B subunit 1 Homo sapiens 152-161
35436742-15 2022 Taken together, our results demonstrate that ATRA disrupts the osteogenesis and mineralizationof PDLSCs by promoting IL-1beta expression via activating NF-kappaB signaling and NLRP3 inflammasome, which may offer a new method for improving the ATRA-induced disruption of osteoblast differentiation. Tretinoin 45-49 NLR family pyrin domain containing 3 Homo sapiens 176-181
35458115-0 2022 Retinoic Acid: Sexually Dimorphic, Anti-Insulin and Concentration-Dependent Effects on Energy. Tretinoin 0-13 insulin Homo sapiens 40-47
35465310-4 2022 An acute induction of Ppargamma expression by atRA under cycloheximide treatment indicated a direct regulation of Ppargamma by atRA. Tretinoin 46-50 peroxisome proliferator activated receptor gamma Homo sapiens 22-31
35465310-4 2022 An acute induction of Ppargamma expression by atRA under cycloheximide treatment indicated a direct regulation of Ppargamma by atRA. Tretinoin 46-50 peroxisome proliferator activated receptor gamma Homo sapiens 114-123
35465310-4 2022 An acute induction of Ppargamma expression by atRA under cycloheximide treatment indicated a direct regulation of Ppargamma by atRA. Tretinoin 127-131 peroxisome proliferator activated receptor gamma Homo sapiens 22-31
35465310-4 2022 An acute induction of Ppargamma expression by atRA under cycloheximide treatment indicated a direct regulation of Ppargamma by atRA. Tretinoin 127-131 peroxisome proliferator activated receptor gamma Homo sapiens 114-123
35465310-6 2022 At high levels of Ppargamma by atRA, BADGE, an antagonist of Ppargamma, inhibited, and rosiglitazone, an agonist of Ppargamma, further enhanced atRA-induced transdifferentiation. Tretinoin 31-35 peroxisome proliferator activated receptor gamma Homo sapiens 18-27
35465310-6 2022 At high levels of Ppargamma by atRA, BADGE, an antagonist of Ppargamma, inhibited, and rosiglitazone, an agonist of Ppargamma, further enhanced atRA-induced transdifferentiation. Tretinoin 144-148 peroxisome proliferator activated receptor gamma Homo sapiens 116-125
35465310-8 2022 These data suggest that the induction of Ppargamma expression by atRA is an essential molecular event in myoblasts for atRA-induced transdifferentiation into adipocytes. Tretinoin 65-69 peroxisome proliferator activated receptor gamma Homo sapiens 41-50
35465310-8 2022 These data suggest that the induction of Ppargamma expression by atRA is an essential molecular event in myoblasts for atRA-induced transdifferentiation into adipocytes. Tretinoin 119-123 peroxisome proliferator activated receptor gamma Homo sapiens 41-50
35565751-0 2022 CRABPs Alter all-trans-Retinoic Acid Metabolism by CYP26A1 via Protein-Protein Interactions. Tretinoin 13-36 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 51-58
35565751-3 2022 We hypothesized that CRABP1 and CRABP2 also alter atRA metabolism and clearance by CYP26A1, the third key atRA-metabolizing enzyme in the CYP26 family. Tretinoin 50-54 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 83-90
35565751-3 2022 We hypothesized that CRABP1 and CRABP2 also alter atRA metabolism and clearance by CYP26A1, the third key atRA-metabolizing enzyme in the CYP26 family. Tretinoin 106-110 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 83-90
35565751-5 2022 The unbound atRA Km values for 4-OH-atRA formation by CYP26A1 were 4.7 +- 0.8 nM with atRA, 6.8 +- 1.7 nM with holo-CRABP1 and 6.1 +- 2.7 nM with holo-CRABP2 as a substrate. Tretinoin 86-90 cytochrome P450 family 26 subfamily A member 1 Homo sapiens 54-61
35394008-8 2022 Our study suggests that NANOS3 plays an important role in timing progenitor expansion to adjust to the proper differentiation timing by blocking the retinoic acid (RA) signaling pathway. Tretinoin 149-162 nanos C2HC-type zinc finger 3 Mus musculus 24-30
35394008-8 2022 Our study suggests that NANOS3 plays an important role in timing progenitor expansion to adjust to the proper differentiation timing by blocking the retinoic acid (RA) signaling pathway. Tretinoin 164-166 nanos C2HC-type zinc finger 3 Mus musculus 24-30
35418672-0 2022 The role of retinoic acid in the production of immunoglobulin A. Tretinoin 12-25 CD79a molecule Homo sapiens 47-63
35418672-4 2022 Here, we describe the contribution of RA to IgA class switching in tissues including the lamina propria, mesenteric lymph nodes, Peyer"s patches and isolated lymphoid follicles. Tretinoin 38-40 CD79a molecule Homo sapiens 44-47
35418672-6 2022 IgA levels in healthy individuals are under the control of the metabolism of vitamin A, providing a steady supply of RA. Tretinoin 117-119 CD79a molecule Homo sapiens 0-3
35406024-14 2022 In deed, those closest in size to the C-20 retinoids-namely, beta-apo-14"-carotenoids (C-22) and beta-apo-13-carotenone (C-18) bind with high affinity to purified retinoid receptors and function as retinoic acid antagonists in transactivation assays and in retinoic acid induction of target genes. Tretinoin 198-211 Bardet-Biedl syndrome 9 Homo sapiens 121-125
35409392-10 2022 When ALDH1A3 was up regulated by retinoic acid treatment in OMECS, Pax-6 expression was down regulated, suggesting a decrease in regenerative capacity when ALDH enzymes are up regulated. Tretinoin 33-46 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 5-12
35248720-2 2022 Retinoic acid receptor beta (RARbeta) functions as a tumor suppressor gene and is associated with the proliferation inhibition to retinoic acid. Tretinoin 130-143 retinoic acid receptor beta Homo sapiens 0-27
35406024-14 2022 In deed, those closest in size to the C-20 retinoids-namely, beta-apo-14"-carotenoids (C-22) and beta-apo-13-carotenone (C-18) bind with high affinity to purified retinoid receptors and function as retinoic acid antagonists in transactivation assays and in retinoic acid induction of target genes. Tretinoin 257-270 Bardet-Biedl syndrome 9 Homo sapiens 121-125
35241664-5 2022 Tig1 encodes a conserved cell surface molecule, is regulated by retinoic acid and exhibits a graded expression along the proximo-distal axis of the limb. Tretinoin 64-77 retinoic acid receptor responder 1 Homo sapiens 0-4
35402250-7 2022 The addition of tretinoin significantly improved the efficacy of anti-CTLA4/anti-PD-L1 combination therapy, and staggered scheduling was more efficacious than concomitant scheduling, in a dose-dependent manner. Tretinoin 16-25 CD274 antigen Mus musculus 81-86
35402250-8 2022 The positive effects of tretinoin could be extended to ICT antibodies targeting OX40, GITR and CTLA4 monotherapy in multiple cancer models. Tretinoin 24-33 tumor necrosis factor receptor superfamily, member 18 Mus musculus 86-90
35294045-0 2022 EZH2 modulates retinoic acid signaling to ensure myotube formation during development. Tretinoin 15-28 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 0-4
35294045-5 2022 We observed elevated retinoic acid (RA) signaling in the prospective myocytes in the Ezh2 mutants (E8.5-MusEzh2 ), and its inhibition can partially rescue the myocyte differentiation defect. Tretinoin 21-34 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 85-89
35294045-5 2022 We observed elevated retinoic acid (RA) signaling in the prospective myocytes in the Ezh2 mutants (E8.5-MusEzh2 ), and its inhibition can partially rescue the myocyte differentiation defect. Tretinoin 36-38 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 85-89
35294045-6 2022 Together, our data demonstrate a new role for PRC2-EZH2 during myocyte differentiation into myotubes by modulating RA signaling. Tretinoin 115-117 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 51-55
35295720-8 2022 To further elaborate our hypothesis, we employed all-trans retinoic acid (ATRA), an Nrf2 inhibitor, and we found that ATRA exaggerated LPS-induced depressive-like effects associated with elevated neuroinflammatory markers. Tretinoin 49-72 NFE2 like bZIP transcription factor 2 Rattus norvegicus 84-88
35295720-8 2022 To further elaborate our hypothesis, we employed all-trans retinoic acid (ATRA), an Nrf2 inhibitor, and we found that ATRA exaggerated LPS-induced depressive-like effects associated with elevated neuroinflammatory markers. Tretinoin 74-78 NFE2 like bZIP transcription factor 2 Rattus norvegicus 84-88
35295720-8 2022 To further elaborate our hypothesis, we employed all-trans retinoic acid (ATRA), an Nrf2 inhibitor, and we found that ATRA exaggerated LPS-induced depressive-like effects associated with elevated neuroinflammatory markers. Tretinoin 118-122 NFE2 like bZIP transcription factor 2 Rattus norvegicus 84-88
35066375-2 2022 For this effect, ATRA downregulated both protein and enzyme activity levels of DNA methyltransferase 1 and 3b and activated E6AP expression via promoter hypomethylation in HepG2 cells but not in Hep3B cells, in which p53 was absent. Tretinoin 17-21 tumor protein p53 Homo sapiens 217-220
35225106-8 2022 Consistently, in the GPL rat model, we observed a similar disorder; however, ATRA supplementation significantly not only corrected the disorder by increasing Rdh10, Aldh1a1 and decreasing Cyp26b1, but also reduced claudin-18 (P < 0.05). Tretinoin 77-81 aldehyde dehydrogenase 1 family, member A1 Rattus norvegicus 165-172
35066375-3 2022 Ectopic p53 expression but not E6AP overexpression restored the ability of ATRA to downregulate HCV Core levels in Hep3B cells, suggesting a direct role of p53 in the E6AP-mediated ubiquitination of HCV Core. Tretinoin 75-79 tumor protein p53 Homo sapiens 8-11
35066375-3 2022 Ectopic p53 expression but not E6AP overexpression restored the ability of ATRA to downregulate HCV Core levels in Hep3B cells, suggesting a direct role of p53 in the E6AP-mediated ubiquitination of HCV Core. Tretinoin 75-79 tumor protein p53 Homo sapiens 156-159
35204227-7 2022 ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Tretinoin 0-4 caspase 3 Sus scrofa 107-116
35007564-3 2022 MATERIALS AND METHODS: ChIP-seq was utilized to identify binding sites of DDX5 and DDX17 in both human pluripotent stem cell (hPSC) line NTERA2 and their retinoic acid-induced neural derivatives. Tretinoin 154-167 DEAD-box helicase 17 Homo sapiens 83-88
35149723-4 2022 Results suggested that elevated Pax6 expression was driven by the increased activity of the RA signaling pathway in the Rybp-/- neural cultures. Tretinoin 92-94 paired box 6 Mus musculus 32-36
35204227-7 2022 ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Tretinoin 0-4 caspase 8 Sus scrofa 180-189
35204227-7 2022 ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Tretinoin 0-4 caspase 9 Sus scrofa 226-235
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 superoxide dismutase 1 Homo sapiens 201-204
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 catalase Homo sapiens 206-209
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 superoxide dismutase 1 Homo sapiens 287-291
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 catalase Homo sapiens 293-296
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 glutamate-cysteine ligase modifier subunit Homo sapiens 308-312
35197751-0 2022 Impact of preconditioning stem cells with all-trans retinoic acid signaling pathway on cisplatin-induced nephrotoxicity by down-regulation of TGFbeta1, IL-6, and caspase-3 and up-regulation of HIF1alpha and VEGF. Tretinoin 52-65 transforming growth factor, beta 1 Rattus norvegicus 142-150
35198449-4 2022 In this report, we identified THRAP3 as novel RARA fusion in resembling APL, which was resistant to all-trans retinoic acid (ATRA) combined arsenic trioxide (ATO) chemotherapy. Tretinoin 100-123 thyroid hormone receptor associated protein 3 Homo sapiens 30-36
35198449-4 2022 In this report, we identified THRAP3 as novel RARA fusion in resembling APL, which was resistant to all-trans retinoic acid (ATRA) combined arsenic trioxide (ATO) chemotherapy. Tretinoin 125-129 thyroid hormone receptor associated protein 3 Homo sapiens 30-36
35197751-6 2022 ATRA also supported ADMSCs by a significant down-regulation of caspase-3, il-6 and TGFbeta1, and a significant up-regulation of HIF1, VEGF and CD31 compared to group of cisplatin which reversed the cisplatin effect. Tretinoin 0-4 interleukin 6 Rattus norvegicus 74-78
35197751-6 2022 ATRA also supported ADMSCs by a significant down-regulation of caspase-3, il-6 and TGFbeta1, and a significant up-regulation of HIF1, VEGF and CD31 compared to group of cisplatin which reversed the cisplatin effect. Tretinoin 0-4 transforming growth factor, beta 1 Rattus norvegicus 83-91
35197751-6 2022 ATRA also supported ADMSCs by a significant down-regulation of caspase-3, il-6 and TGFbeta1, and a significant up-regulation of HIF1, VEGF and CD31 compared to group of cisplatin which reversed the cisplatin effect. Tretinoin 0-4 platelet and endothelial cell adhesion molecule 1 Rattus norvegicus 143-147
35197751-0 2022 Impact of preconditioning stem cells with all-trans retinoic acid signaling pathway on cisplatin-induced nephrotoxicity by down-regulation of TGFbeta1, IL-6, and caspase-3 and up-regulation of HIF1alpha and VEGF. Tretinoin 52-65 interleukin 6 Rattus norvegicus 152-156
35205034-5 2022 The treatment with 10 muM of retinoic acid (RA) for 6 days resulted in neuronal differentiation that was accompanied by a remarkable increase in ASIC1a expression, while ASIC2 expression remained almost unaltered. Tretinoin 44-46 acid sensing ion channel subunit 2 Homo sapiens 170-175
35204719-9 2022 ATRA or UDP-4 treatment significantly upregulated ENO2 and NF1 expression, indicating neuronal differentiation. Tretinoin 0-4 enolase 2 Homo sapiens 50-54
35204719-9 2022 ATRA or UDP-4 treatment significantly upregulated ENO2 and NF1 expression, indicating neuronal differentiation. Tretinoin 0-4 neurofibromin 1 Homo sapiens 59-62
35086406-8 2022 By immunofluorescence, we verified the positive expression of HSD17B3, GDNF, ACRV-1, and TRIM-36, indicating their differentiation using RA in vitro, reinforcing the possibility of EB in male germ cell differentiation. Tretinoin 137-139 hydroxysteroid (17-beta) dehydrogenase 3 Rattus norvegicus 62-69
35173714-0 2022 All-Trans Retinoic Acid Attenuates Transmissible Gastroenteritis Virus-Induced Inflammation in IPEC-J2 Cells via Suppressing the RLRs/NF-kappaB Signaling Pathway. Tretinoin 0-23 nuclear factor kappa B subunit 1 Homo sapiens 134-143
35173714-6 2022 However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1beta, IL-6, IL-8 and TNF-alpha. Tretinoin 9-13 interleukin 6 Homo sapiens 137-141
35173714-6 2022 However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1beta, IL-6, IL-8 and TNF-alpha. Tretinoin 9-13 C-X-C motif chemokine ligand 8 Homo sapiens 143-147
35173714-6 2022 However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1beta, IL-6, IL-8 and TNF-alpha. Tretinoin 9-13 tumor necrosis factor Homo sapiens 152-161
35173714-7 2022 ATRA also significantly reversed the reduction of ZO-1 and Occludin protein levels induced by TGEV infection and maintained epithelial barrier integrity. Tretinoin 0-4 tight junction protein 1 Homo sapiens 50-54
35173714-8 2022 Moreover, ATRA treatment significantly prevented the upregulation of IkBalpha and NF-kappaB p65 phosphorylation levels and the nuclear translocation of NF-kB p65 induced by TGEV. Tretinoin 10-14 nuclear factor kappa B subunit 1 Homo sapiens 82-91
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 toll like receptor 7 Homo sapiens 103-107
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 TIR domain containing adaptor molecule 1 Homo sapiens 180-184
35173714-12 2022 Our results indicated that ATRA attenuated TGEV-induced IPEC-J2 cells damage via suppressing inflammatory response, the mechanism of which is associated with the inhibition of TGEV-mediated activation of the RLRs/NF-kappaB signaling pathway. Tretinoin 27-31 nuclear factor kappa B subunit 1 Homo sapiens 213-222
35080452-0 2022 Correction for Vedagiri et al., "Retinoic Acid-Inducible Gene I-Like Receptors Activate Snail To Limit RNA Viral Infections". Tretinoin 33-46 snail family transcriptional repressor 1 Homo sapiens 88-93
35205034-5 2022 The treatment with 10 muM of retinoic acid (RA) for 6 days resulted in neuronal differentiation that was accompanied by a remarkable increase in ASIC1a expression, while ASIC2 expression remained almost unaltered. Tretinoin 29-42 acid sensing ion channel subunit 2 Homo sapiens 170-175
35159132-3 2022 Retinol is first converted to retinaldehyde by retinol dehydrogenase 10 (RDH10) and then to RA by all three retinaldehyde dehydrogenases (ALDH1A1, ALDH1A2, and ALDH1A3). Tretinoin 92-94 aldehyde dehydrogenase family 1, subfamily A3 Mus musculus 160-167
35013142-9 2022 The RNA-seq studies performed in parental NB4 cells and a NB4-derived cell population, characterized by silencing of the autophagy mediator, ATG5, provide insights into the mechanisms underlying the differentiating action of ATRA. Tretinoin 225-229 autophagy related 5 Homo sapiens 141-145
34954769-2 2022 METHODS: A rat SCI model was established and treated with ginsenoside Rg1 and nuclear factor erythroid 2-related factor2(Nrf2) inhibitor all-trans retinoic acid (ATRA). Tretinoin 137-160 NFE2 like bZIP transcription factor 2 Rattus norvegicus 78-120
34954769-2 2022 METHODS: A rat SCI model was established and treated with ginsenoside Rg1 and nuclear factor erythroid 2-related factor2(Nrf2) inhibitor all-trans retinoic acid (ATRA). Tretinoin 137-160 NFE2 like bZIP transcription factor 2 Rattus norvegicus 121-125
34954769-2 2022 METHODS: A rat SCI model was established and treated with ginsenoside Rg1 and nuclear factor erythroid 2-related factor2(Nrf2) inhibitor all-trans retinoic acid (ATRA). Tretinoin 162-166 NFE2 like bZIP transcription factor 2 Rattus norvegicus 78-120
34954769-2 2022 METHODS: A rat SCI model was established and treated with ginsenoside Rg1 and nuclear factor erythroid 2-related factor2(Nrf2) inhibitor all-trans retinoic acid (ATRA). Tretinoin 162-166 NFE2 like bZIP transcription factor 2 Rattus norvegicus 121-125
34954769-7 2022 Furthermore, western blot and RT-qPCR also suggested that ginsenoside Rg1 could activate the protein expression of Nrf2 and heme oxygenase-1 (HO-1) after SCI, and the inhibition of ATRA on these improvements further verified the neuroprotective effect of Nrf2 and HO-1 in ginsenoside Rg1 on SCI. Tretinoin 181-185 NFE2 like bZIP transcription factor 2 Rattus norvegicus 255-259
2508757-2 1989 Liver and kidney microsomal uridine diphosphoglucuronosyltransferase (UDPGT) activity toward all-trans-retinoic acid was increased 3.7- and 2.6-fold, respectively, ten days following exposure to TCDD. Tretinoin 93-116 UDP glucuronosyltransferase family 1 member A1 Rattus norvegicus 28-68
34706256-5 2022 We show that HSCs rely on Cyp26b1, an enzyme conventionally considered to limit RA effects in the cell. Tretinoin 80-82 cytochrome P450 family 26 subfamily B member 1 Homo sapiens 26-33
2556699-0 1989 A retinoic acid-responsive element is present in the 5" flanking region of the laminin B1 gene. Tretinoin 2-15 laminin B1 Mus musculus 79-89
2556699-5 1989 Through the use of deletion and mutation analyses, the RA-responsive element (RARE) of the murine laminin B1 gene has been defined as a 46-base-pair element between -477 and -432 of the laminin B1 5" flanking region. Tretinoin 55-57 laminin B1 Mus musculus 98-108
2556699-5 1989 Through the use of deletion and mutation analyses, the RA-responsive element (RARE) of the murine laminin B1 gene has been defined as a 46-base-pair element between -477 and -432 of the laminin B1 5" flanking region. Tretinoin 55-57 laminin B1 Mus musculus 186-196
2556699-8 1989 This suggests that the laminin B1 gene is activated by RA but not by thyroid hormone in vivo. Tretinoin 55-57 laminin B1 Mus musculus 23-33
2508757-2 1989 Liver and kidney microsomal uridine diphosphoglucuronosyltransferase (UDPGT) activity toward all-trans-retinoic acid was increased 3.7- and 2.6-fold, respectively, ten days following exposure to TCDD. Tretinoin 93-116 UDP glucuronosyltransferase family 1 member A1 Rattus norvegicus 70-75
2702640-3 1989 Transferrin receptor down-regulation which occurs during granulocytic differentiation by dimethyl sulfoxide, retinoic acid, or aclacinomycin A appears to be kinetically compatible with reduced biosynthesis resulting from reductions in the level of steady-state mRNA. Tretinoin 109-122 transferrin receptor Homo sapiens 0-20
2543582-1 1989 Retinoic acid (RA) is bound intracellularly by a specific, low molecular weight protein (CRABP), that is unrelated to its nuclear receptor and whose function and regulation are still unknown. Tretinoin 0-13 cellular retinoic acid binding protein 1 Homo sapiens 89-94
2543582-1 1989 Retinoic acid (RA) is bound intracellularly by a specific, low molecular weight protein (CRABP), that is unrelated to its nuclear receptor and whose function and regulation are still unknown. Tretinoin 15-17 cellular retinoic acid binding protein 1 Homo sapiens 89-94
2543582-3 1989 We found increased CRABP after daily application during 4 days of natural or synthetic retinoids (RA, acitretin, isotretinoin, Ro137410, retinol), that have either a high affinity to CRABP or can be transformed into RA. Tretinoin 20-22 cellular retinoic acid binding protein 1 Homo sapiens 183-188
2542775-0 1989 Differentiation-responsive elements in the 5" region of the mouse tissue plasminogen activator gene confer two-stage regulation by retinoic acid and cyclic AMP in teratocarcinoma cells. Tretinoin 131-144 plasminogen activator, tissue Mus musculus 66-94
2472150-10 1989 Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells. Tretinoin 131-144 colony stimulating factor 1 receptor Rattus norvegicus 59-64
2472150-10 1989 Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells. Tretinoin 131-144 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 80-85
2513840-1 1989 The effects of biologic response modifiers such as interferon-gamma, tumor necrosis factor alpha (TNF), and retinoic acid on the human chorionic gonadotropin (hCG) secretion of cultured choriocarcinoma cells (JAR) and term placenta have been studied. Tretinoin 108-121 chorionic gonadotropin subunit beta 5 Homo sapiens 159-162
2513840-2 1989 Although the proliferation of JAR cells was not inhibited by these agents, retinoic acid and TNF markedly increased both the intracellular levels as well as the secreted amounts of hCG. Tretinoin 75-88 chorionic gonadotropin subunit beta 5 Homo sapiens 181-184
2513840-3 1989 In the case of the term placenta, only retinoic acid increased the hCG secretion into the culture medium, whereas interferon-gamma and TNF both markedly reduced secretion. Tretinoin 39-52 chorionic gonadotropin subunit beta 5 Homo sapiens 67-70
3180083-0 1988 Changes in c-myc, c-fms, and N-ras proto-oncogene expression associated with retinoic acid-induced monocytic differentiation of human leukemia HL60/MRI cells. Tretinoin 77-90 colony stimulating factor 1 receptor Homo sapiens 18-23
2842791-1 1988 Down-regulation of Myc expression is the earliest documented change in gene expression in retinoic acid-induced differentiation of murine F9 teratocarcinoma cells. Tretinoin 90-103 myelocytomatosis oncogene Mus musculus 19-22
2842791-4 1988 In contrast, when F9 cells are transfected with a plasmid expressing Myc under control of the SV40 early promoter, resulting cell clones are resistant to differentiation by retinoic acid as shown by the lack of induction of plasminogen activator. Tretinoin 173-186 myelocytomatosis oncogene Mus musculus 69-72
2842348-0 1988 Protein synthesis inhibitors prevent the induction of laminin B1, collagen IV (alpha 1), and other differentiation-specific mRNAs by retinoic acid in F9 teratocarcinoma cells. Tretinoin 133-146 laminin B1 Mus musculus 54-64
2826484-7 1988 When F9 cells are induced to differentiate with retinoic acid and dibutyryl cyclic AMP, tPA mRNA accumulates. Tretinoin 48-61 plasminogen activator, tissue Mus musculus 88-91
3365571-9 1988 One explanation of these results is that only well differentiated cells have functional cellular retinoic acid-binding protein (cRABP), and that certain actions of retinoic acid (inhibition of anchorage-dependent growth) are independent of the presence of cRABP. Tretinoin 97-110 cellular retinoic acid binding protein 1 Homo sapiens 128-133
2856163-1 1988 In order to better understand the respective roles of the nuclear retinoic acid receptors (RARs) and the cytosolic retinoic acid binding protein (CRABP) in the mode of action of retinoic acid (RA), several types of RA analogs have been synthesized. Tretinoin 147-149 cellular retinoic acid binding protein 1 Homo sapiens 105-144
2856164-8 1988 The RA metabolism in rat epidermal microsomes shows the typical characteristics of a cytochrome-P-450 (P450)-dependent enzyme system, i.e. a requirement for NADPH and oxygen and inhibition by CO and SKF-525A. Tretinoin 4-6 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 103-107
2856164-9 1988 Ketoconazole and miconazole, imidazole antifungal agents and inhibitors of some fungal and mammalian P450-dependent enzymes, inhibit in vitro RA metabolism by rat epidermal microsomes. Tretinoin 142-144 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 101-105
2856164-13 1988 Our data show a P450-dependent RA metabolism in rat epidermal microsomes and suggest that ketoconazole may prove to be effective in maintaining biologically active levels of RA in epidermal cells. Tretinoin 31-33 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 16-20
2825608-4 1987 A third intracellular protein, cellular retinoic acid-binding protein (CRABP) also is structurally similar but binds only retinoic acid. Tretinoin 40-53 cellular retinoic acid binding protein 1 Homo sapiens 71-76
2820396-1 1987 Cellular retinoic acid-binding protein (CRABP) is the putative mediator of the biological effects of retinoic acid in the control of epithelial differentiation and tumorigenesis. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 40-45
3496961-3 1987 Addition of the differentiation agents N,N-dimethylformamide (DMF) or retinoic acid simultaneously with TGF-beta blocked the ability of TGF-beta to induce mitogenesis. Tretinoin 70-83 transforming growth factor, beta 1 Mus musculus 136-144
3566738-0 1987 Phorbol ester, retinoic acid and diacylglycerol decrease ecto- but increase total basal-protein kinase activity of human fibroblasts. Tretinoin 15-28 tripartite motif containing 33 Homo sapiens 57-61
3566738-2 1987 The ecto-kinase reaction of the HLF-cells was cAMP-independent, showed an apparent Km for ATP of 6.99 +/- 0.35 (microM) and was substantially inhibited by TPA and RA. Tretinoin 163-165 tripartite motif containing 33 Homo sapiens 4-8
3566738-5 1987 RA was the most potent retinoid in reducing ecto-kinase activity. Tretinoin 0-2 tripartite motif containing 33 Homo sapiens 44-48
3566738-7 1987 The drop in ecto-kinase activity of HLF-cells in situ caused by TPA, RA and the diacylglycerols was accompanied by an increase in total basal-(Mg++-dependent) protein kinase activity present in extracts of treated cells. Tretinoin 69-71 tripartite motif containing 33 Homo sapiens 12-16
3566738-8 1987 The results suggest an important role of ecto-kinase in the response of intact cells to TPA and RA. Tretinoin 96-98 tripartite motif containing 33 Homo sapiens 41-45
2833143-2 1987 Studies on CRBP and CRABP suggest that both retinol and retinoic acid are involved in maintaining testicular function. Tretinoin 56-69 retinol binding protein 1 Homo sapiens 11-15
2833143-2 1987 Studies on CRBP and CRABP suggest that both retinol and retinoic acid are involved in maintaining testicular function. Tretinoin 56-69 cellular retinoic acid binding protein 1 Homo sapiens 20-25
2427007-3 1986 Cultured Y-79 human retinoblastoma cells, however, can be induced to differentiate to a more "normal" stage in development through the use of several naturally occurring agents, such as butyrate, cyclic AMP, and retinoic acid. Tretinoin 212-225 RB transcriptional corepressor 1 Homo sapiens 20-34
3002611-8 1986 Agents which induced granulocytic differentiation, such as 160 mM dimethyl sulfoxide and 100 nM retinoic acid, significantly decreased insulin receptor expression compared to monocytic inducing agents. Tretinoin 96-109 insulin receptor Homo sapiens 135-151
2427593-4 1986 Since psoriatic plaques are particularly responsive to systemic retinoids, specifically to retinoic acid analogues, our results suggest for the first time a link between the levels of CRABP and the responsiveness of a nonneoplastic hyperproliferative tissue to systemic administration of retinoids in the human. Tretinoin 91-104 cellular retinoic acid binding protein 1 Homo sapiens 184-189
4053280-0 1985 Dose and schedule of oral retinoic acid and indomethacin needed to effectively inhibit phorbol ester-induced epidermal ornithine decarboxylase activity. Tretinoin 26-39 ornithine decarboxylase 1 Homo sapiens 119-142
4053280-5 1985 Using this system we evaluated the doses and dose schedules of retinoic acid and indomethacin needed to effectively inhibit ornithine decarboxylase activity. Tretinoin 63-76 ornithine decarboxylase 1 Homo sapiens 124-147
3931632-5 1985 Retinoic acid stimulated IL 1 release by P388D1 cells in a dose-related fashion, starting at 10(-9) M and maximally at 10(-8)-10(-6) M. With peripheral blood mononuclear cells a maximal stimulation of IL 1 release was observed with 10(-7) M-retinoic acid. Tretinoin 0-13 interleukin 1 complex Mus musculus 25-29
3931632-5 1985 Retinoic acid stimulated IL 1 release by P388D1 cells in a dose-related fashion, starting at 10(-9) M and maximally at 10(-8)-10(-6) M. With peripheral blood mononuclear cells a maximal stimulation of IL 1 release was observed with 10(-7) M-retinoic acid. Tretinoin 0-13 interleukin 1 complex Mus musculus 201-205
3931632-5 1985 Retinoic acid stimulated IL 1 release by P388D1 cells in a dose-related fashion, starting at 10(-9) M and maximally at 10(-8)-10(-6) M. With peripheral blood mononuclear cells a maximal stimulation of IL 1 release was observed with 10(-7) M-retinoic acid. Tretinoin 241-254 interleukin 1 complex Mus musculus 25-29
3931632-8 1985 These results show that retinoic acid, in physiological concentrations, exerts selective effects on interleukin production in vitro, and this stimulation of IL 1 and IL 3 release may explain some of the immunostimulatory effects of retinoids in vivo. Tretinoin 24-37 interleukin 1 complex Mus musculus 157-178
2995045-1 1985 The cellular content of receptors for retinol (CRBP) and retinoic acid (CRABP) was measured in 148 human mammary carcinomas. Tretinoin 57-70 cellular retinoic acid binding protein 1 Homo sapiens 72-77
3924406-1 1985 The relationships between replicative DNA synthesis and retinoic acid (RA)-induced differentiation of human promyelocytic leukaemic (HL-60) cells are evaluated with the use of Aphidicolin, a specific and reversible inhibitor of DNA polymerase alpha (alpha). Tretinoin 71-73 DNA polymerase alpha 1, catalytic subunit Homo sapiens 228-248
3857122-1 1985 Two recently derived human myeloid leukemia cell lines, ML-1 and ML-2, were induced to differentiate by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or with retinoic acid for 5 to 12 days. Tretinoin 170-183 interleukin 17F Homo sapiens 56-60
4044668-3 1985 We show here that P10 cells rapidly differentiate into a cell type resembling extraembryonic endoderm when cultured in the presence of retinoic acid. Tretinoin 135-148 S100 calcium binding protein A10 (calpactin) Mus musculus 18-21
6489452-5 1984 Cells treated for 4 or 8 days with TPA or a combination of TPA and RA had a low ODC activity which could not be induced by fresh medium. Tretinoin 67-69 ornithine decarboxylase 1 Homo sapiens 80-83
6489452-6 1984 However, RA-treated (and thus growth-inhibited) cells still responded to a change of medium by exhibiting an ODC activity of the same magnitude and duration as in medium-stimulated control cells. Tretinoin 9-11 ornithine decarboxylase 1 Homo sapiens 109-112
6334100-2 1984 The C3b receptor (C3bR) of the human promyelocytic leukemia cell line (HL-60) was induced by incubating these cells with dimethylsulfoxide (DMSO) or retinoic acid. Tretinoin 149-162 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 4-16
6334100-2 1984 The C3b receptor (C3bR) of the human promyelocytic leukemia cell line (HL-60) was induced by incubating these cells with dimethylsulfoxide (DMSO) or retinoic acid. Tretinoin 149-162 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 18-22
6090748-7 1984 These results indicate that RA resistance in these sublines is not secondary to a defect of RA uptake or of binding of RA to cRABP; the resistance may result from a defect distal to binding to cRABP, or alternatively, cRABP may not mediate this effect of RA. Tretinoin 28-30 cellular retinoic acid binding protein 1 Homo sapiens 193-198
6090748-7 1984 These results indicate that RA resistance in these sublines is not secondary to a defect of RA uptake or of binding of RA to cRABP; the resistance may result from a defect distal to binding to cRABP, or alternatively, cRABP may not mediate this effect of RA. Tretinoin 28-30 cellular retinoic acid binding protein 1 Homo sapiens 193-198
6205395-6 1984 Treatment of epidermal cells with arotinoid Ro 13-6298, a potent synthetic analog of retinoic acid, increased the abundance of mRNA for keratin 13 by 25-fold and for keratin 19 by greater than 40-fold but had no effect on the abundance of mRNA for keratins 5 and 6. Tretinoin 85-98 keratin 19 Homo sapiens 166-176
6582309-2 1984 Untreated and RA-treated cells were labeled either metabolically with radioactive precursors or by oxidation of externally exposed cell membrane glycoprotein(s) (GP) by treatment with NalO4 or neuraminidase and galactose oxidase followed by reduction with NaB[3H]4. Tretinoin 14-16 neuraminidase 1 Homo sapiens 193-206
6310582-8 1983 Thus, although CRABP is not necessarily correlated with growth inhibition in monolayer culture, it is associated with retinoic acid"s ability to inhibit neuroblastoma colony formation in soft agar. Tretinoin 118-131 cellular retinoic acid binding protein 1 Homo sapiens 15-20
6188622-0 1983 Formation of vinculin plaques precedes other cytoskeletal changes during retinoic acid-induced teratocarcinoma cell differentiation. Tretinoin 73-86 vinculin Homo sapiens 13-21
6188622-8 1983 This sequence of changes suggests that the vinculin-containing adhesion plaques may be important in the mechanism of RA-induced differentiation of EC cells. Tretinoin 117-119 vinculin Homo sapiens 43-51
6684744-6 1983 CRBP and CRABP are assumed to be mediating factors for the retinol and retinoic acid action. Tretinoin 71-84 retinol binding protein 1 Homo sapiens 0-4
6684744-6 1983 CRBP and CRABP are assumed to be mediating factors for the retinol and retinoic acid action. Tretinoin 71-84 cellular retinoic acid binding protein 1 Homo sapiens 9-14
6684744-7 1983 Since the presence of CRABP is a constant finding, we propose that retinoic acid and its synthetic derivatives with high affinity for CRABP could be appropriate antineoplastic drugs in these tissues. Tretinoin 67-80 cellular retinoic acid binding protein 1 Homo sapiens 22-27
6684744-7 1983 Since the presence of CRABP is a constant finding, we propose that retinoic acid and its synthetic derivatives with high affinity for CRABP could be appropriate antineoplastic drugs in these tissues. Tretinoin 67-80 cellular retinoic acid binding protein 1 Homo sapiens 134-139
6299278-1 1982 Cellular retinoic acid-binding protein (CRABP) was detected in the nuclear fraction of N-methyl-N-nitrosourea-induced mammary cancers after the incubation of cytosol containing [3H]retinoic acid (RA)-bound CRABP with isolated nuclei. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 40-45
6299278-1 1982 Cellular retinoic acid-binding protein (CRABP) was detected in the nuclear fraction of N-methyl-N-nitrosourea-induced mammary cancers after the incubation of cytosol containing [3H]retinoic acid (RA)-bound CRABP with isolated nuclei. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 206-211
6950518-2 1982 It also inhibited increases in ornithine decarboxylase activity associated with the phorbol ester-induced conversion of promyelocytic HL-60 cells to monocyte-like cells and the retinoic acid-induced conversion to granulocyte-like cells. Tretinoin 177-190 ornithine decarboxylase 1 Homo sapiens 31-54
7172413-8 1982 In addition, the inhibitory effect of retinoic acid on TPA-induced ODC activity remained unaffected by some of the above treatments, suggesting that retinoic acid is unlikely to interfere with TPA interactions at the plasma membrane level. Tretinoin 38-51 ornithine decarboxylase 1 Homo sapiens 67-70
6942700-9 1981 A number of tissues of rats, humans, and other species contain soluble proteins with binding specificity for retinol (CRBP) or for retinoic acid (CRABP). Tretinoin 131-144 cellular retinoic acid binding protein 1 Homo sapiens 146-151
34051632-5 2021 RESULTS: In CLP model, ATRA was found to reduce frequency of MDSCs in spleen of mice and inhibit activity of MDSCs by regulating the generation and activity of arginase-1 and iNOS, and the secretion of immune-supressive cytokines. Tretinoin 23-27 arginase, liver Mus musculus 160-170
33454316-0 2021 Changes in the levels of alpha-actinin-4 in differentiating human myeloid leukemia cells induced by retinoic acid. Tretinoin 100-113 actinin alpha 4 Homo sapiens 25-40
33454316-3 2021 Herein, we elucidated the effects of RA on alpha-actinin-4 expression during cell differentiation. Tretinoin 37-39 actinin alpha 4 Homo sapiens 43-58
33454316-4 2021 RA increased the levels of alpha-actinin-4 protein significantly, while mRNA expression remained unchanged. Tretinoin 0-2 actinin alpha 4 Homo sapiens 27-42
2684957-9 1989 Purified rALBP exhibited stoichiometric, saturable binding of oleic acid (n = 1.0, K0.5 approximately 100 microM) and retinoic acid (n = 1.0, K0.5 approximately 170 microM). Tretinoin 118-131 fatty acid binding protein 4 Rattus norvegicus 9-14
2573410-0 1989 Cholinergic differentiation of clonal rat pheochromocytoma cells (PC12) induced by retinoic acid: increase of choline acetyltransferase activity and decrease of tyrosine hydroxylase activity. Tretinoin 83-96 tyrosine hydroxylase Rattus norvegicus 161-181
2573410-3 1989 In PC12 cells cultured in the presence of 10 microM RA for 8 days, the specific activity of choline acetyltransferase (ChAT) was increased 2-fold, while the specific activity of tyrosine hydroxylase (TH) was decreased 0.5-fold compared with cells cultured in the absence of RA. Tretinoin 52-54 tyrosine hydroxylase Rattus norvegicus 178-198
2573410-6 1989 RA inhibited the increase of TH activity induced by nerve growth factor (NGF), an adrenergic neuronotrophic factor on PC12 cells. Tretinoin 0-2 tyrosine hydroxylase Rattus norvegicus 29-31
2613750-6 1989 Similarly, retinoic acid treatment also enhanced in a time- and dose-dependent manner the TGF alpha-dependent response of EGF receptor mRNA and acted synergistically with TGF beta 1. Tretinoin 11-24 transforming growth factor alpha Homo sapiens 90-99
2553481-3 1989 RA induced a rapid accumulation of RAR alpha within 2 h and this was followed by an increase in the RAR beta mRNA. Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 100-108
2478272-2 1989 Induction of differentiation with either retinoic acid, dimethylsulfoxide, dibutyryl cAMP or dihydroxy-vitamin D3 resulted in a decrease of the cellular content of ODC RNA. Tretinoin 41-54 ornithine decarboxylase 1 Homo sapiens 164-167
2551727-3 1989 The retinoic acid-induced differentiation of HL-60 cells was, but the Bt2cAMP- or PMA-induced one was not, inhibited by prior exposure of the cells to islet-activating protein (IAP), pertussis toxin. Tretinoin 4-17 islet amyloid polypeptide Homo sapiens 177-180
2551727-5 1989 Thus, the IAP-substrate GTP-binding protein appears to be involved in the retinoic acid-induced differentiation of HL-60 cells. Tretinoin 74-87 islet amyloid polypeptide Homo sapiens 10-13
2518451-1 1989 Evidence from expression studies using transfected F9 teratocarcinoma stem cells indicates that the synthesis of the H1(0) histone is turned on very soon after the cells have been treated with retinoic acid, which causes them to differentiate into murine parietal endoderm. Tretinoin 193-206 H1.0 linker histone Mus musculus 117-130
2743337-3 1989 These biological actions of retinoic acid have been shown to be accompanied by an increase in the amount of cyclic AMP-dependent protein kinase and an induction of a new isozyme form (RII beta). Tretinoin 28-41 protein kinase, cAMP dependent regulatory, type II beta Mus musculus 184-192
2526689-1 1989 Prior work has suggested that Mabs against the transferrin receptor (ATRAs) may function as selective inhibitors of lymphocyte activation and that T cell activation protocols may be more sensitive to ATRA-mediated inhibition than B cell activation protocols. Tretinoin 69-73 transferrin receptor Homo sapiens 47-67
2716850-5 1989 We therefore examined whether the effects of RA on growth could be related to changes in the expression of the growth hormone gene which is known to be transcriptionally regulated by both thyroid and glucocorticoid hormones. Tretinoin 45-47 gonadotropin releasing hormone receptor Rattus norvegicus 111-125
2716850-6 1989 Our results show that RA controls growth hormone production in pituitary GH1 cells and that its effect is synergistic with that caused by these hormones. Tretinoin 22-24 gonadotropin releasing hormone receptor Rattus norvegicus 34-48
2546063-6 1989 1) Induction of CRBP occurred at lower concentrations of RA (10(-9) M) than did that of CRABP (10(-8)-10(-7) M). Tretinoin 57-59 retinol binding protein 1 Homo sapiens 16-20
2546063-7 1989 2) CRBP induction was an early response (within 3 h) to RA treatment, whereas CRABP induction occurred at a later time (12-24 h). Tretinoin 56-58 retinol binding protein 1 Homo sapiens 3-7
2546063-14 1989 Taken together, our results suggest that CRBP induction may be a direct response to RA and represent a general event in RA-induced cell differentiation, whereas CRABP induction may be an indirect response and represent a later event restricted to only certain differentiation pathways. Tretinoin 84-86 retinol binding protein 1 Homo sapiens 41-45
2657391-4 1989 The time course and retinoic acid dose dependence of int-1 expression suggest that the gene is specifically expressed during early neural differentiation. Tretinoin 20-33 wingless-type MMTV integration site family, member 1 Mus musculus 53-58
2610595-5 1989 Furthermore, higher antiviral activity was consistently obtained when RA (0.1-10 microM) was added prior to either IFN-alpha or IFN-beta comparing to cultures with IFN alone. Tretinoin 70-72 interferon beta 1 Homo sapiens 128-136
3183386-4 1988 In the assay for cytokine, a few of the hybridomas produced a novel tumor-killing factor (TKF) after stimulation with PMA, polypeptone, and retinoic acid. Tretinoin 140-153 fibroblast growth factor receptor 4 Homo sapiens 68-88
3183386-4 1988 In the assay for cytokine, a few of the hybridomas produced a novel tumor-killing factor (TKF) after stimulation with PMA, polypeptone, and retinoic acid. Tretinoin 140-153 fibroblast growth factor receptor 4 Homo sapiens 90-93
2458954-4 1988 In contrast, P19 cells showed increased levels of both mRNAs both mRNAs when induced to differentiate along the neural pathway by retinoic acid, whereas differentiation along the muscle pathway by dimethyl sulfoxide resulted in decreased levels of c-abl expression. Tretinoin 130-143 interleukin 23, alpha subunit p19 Mus musculus 13-16
3165863-1 1988 Monocytic differentiation of U937 cells induced by retinoic acid is accompanied by a 0.2-pH-unit cell alkalinisation. Tretinoin 51-64 glucose-6-phosphate isomerase Homo sapiens 89-91
3165863-2 1988 The effect of retinoic acid on intracellular pH (pHi) develops slowly and it precedes the differentiation of the cells by 24 h. Heterogeneity in cellular pHi values was assessed using flow cytometry. Tretinoin 14-27 glucose-6-phosphate isomerase Homo sapiens 45-47
3165863-2 1988 The effect of retinoic acid on intracellular pH (pHi) develops slowly and it precedes the differentiation of the cells by 24 h. Heterogeneity in cellular pHi values was assessed using flow cytometry. Tretinoin 14-27 glucose-6-phosphate isomerase Homo sapiens 49-52
3165863-2 1988 The effect of retinoic acid on intracellular pH (pHi) develops slowly and it precedes the differentiation of the cells by 24 h. Heterogeneity in cellular pHi values was assessed using flow cytometry. Tretinoin 14-27 glucose-6-phosphate isomerase Homo sapiens 154-157
2842235-8 1988 The presence of cRABP suggest that retinoic acid may have a role to play in the function of the pancreas. Tretinoin 35-48 cellular retinoic acid binding protein 1 Homo sapiens 16-21
2837484-3 1988 Two retinoic acid-binding peaks were resolved at the DEAE-cellulose step, with CRABP-I in the major peak and CRABP-II in the minor peak. Tretinoin 4-17 cellular retinoic acid binding protein 1 Rattus norvegicus 79-86
3139405-8 1988 Hyperphosphorylation of the nucleolin fragment (N-60) was suppressed by anti-tumour promoter retinoic acid. Tretinoin 93-106 nucleolin Homo sapiens 28-37
2903078-0 1988 Characteristics of cyclic AMP enhancement of retinoic acid induction of increased transglutaminase activity in HL60 cells. Tretinoin 45-58 transglutaminase 1 Homo sapiens 82-98
2903078-1 1988 When the human myeloid leukemia cell line (HL60) is induced to differentiate with retinoic acid (RA), there is a concentration-dependent increase in transglutaminase (TGase) activity which peaks on day 5. Tretinoin 82-95 transglutaminase 1 Homo sapiens 149-165
2903078-1 1988 When the human myeloid leukemia cell line (HL60) is induced to differentiate with retinoic acid (RA), there is a concentration-dependent increase in transglutaminase (TGase) activity which peaks on day 5. Tretinoin 82-95 transglutaminase 1 Homo sapiens 167-172
2903078-1 1988 When the human myeloid leukemia cell line (HL60) is induced to differentiate with retinoic acid (RA), there is a concentration-dependent increase in transglutaminase (TGase) activity which peaks on day 5. Tretinoin 97-99 transglutaminase 1 Homo sapiens 149-165
2903078-1 1988 When the human myeloid leukemia cell line (HL60) is induced to differentiate with retinoic acid (RA), there is a concentration-dependent increase in transglutaminase (TGase) activity which peaks on day 5. Tretinoin 97-99 transglutaminase 1 Homo sapiens 167-172
2903078-3 1988 Maximal increases in TGase activity (2- to 10-fold) were observed with 10(-4)-10(-7) M RA and when db-cAMP was present from 24 to 48 h after the addition of RA. Tretinoin 87-89 transglutaminase 1 Homo sapiens 21-26
2903078-3 1988 Maximal increases in TGase activity (2- to 10-fold) were observed with 10(-4)-10(-7) M RA and when db-cAMP was present from 24 to 48 h after the addition of RA. Tretinoin 157-159 transglutaminase 1 Homo sapiens 21-26
2903078-9 1988 cAMP potentiates RA-induced TGase activity in HL60 cells and the combination appears to be associated with enhanced RA-induced differentiation. Tretinoin 17-19 transglutaminase 1 Homo sapiens 28-33
2850450-5 1988 This decrease of BB-1 was blocked by the additional treatment with retinoic acid, an inhibitor of virus replication. Tretinoin 67-80 CD80 molecule Homo sapiens 17-21
3426588-5 1987 It seems, therefore, that RA may influence nerve cell differentiation by promoting both the synthesis of the neurotrophic factor and the responsiveness of target cells. Tretinoin 26-28 glial cell line derived neurotrophic factor Mus musculus 109-128
2825608-9 1987 Like CRBP, CRABP can deliver its ligand retinoic acid to specific binding sites within the nucleus, sites different from those for retinol. Tretinoin 40-53 retinol binding protein 1 Homo sapiens 5-9
2825608-9 1987 Like CRBP, CRABP can deliver its ligand retinoic acid to specific binding sites within the nucleus, sites different from those for retinol. Tretinoin 40-53 cellular retinoic acid binding protein 1 Homo sapiens 11-16
3655940-0 1987 Induction of ceruloplasmin synthesis by retinoic acid in rats: influence of dietary copper and vitamin A status. Tretinoin 40-53 ceruloplasmin Rattus norvegicus 13-26
3655940-3 1987 With daily injections of retinoic acid, the ceruloplasmin activity continued to increase for at least 4 d. After 4 d, the activity was four times control levels. Tretinoin 25-38 ceruloplasmin Rattus norvegicus 44-57
2820396-2 1987 Omega-6 fatty acids such as linoleic acid and arachidonic acid, precursors of prostaglandin synthesis, caused inhibition of retinoic acid binding to CRABP. Tretinoin 124-137 cellular retinoic acid binding protein 1 Homo sapiens 149-154
2820396-6 1987 Competition by omega-6 fatty acids with retinoic acid for CRABP may neutralize the binding protein-mediated biological functions of retinoic acid, and could thereby enhance tumor production. Tretinoin 40-53 cellular retinoic acid binding protein 1 Homo sapiens 58-63
2820396-6 1987 Competition by omega-6 fatty acids with retinoic acid for CRABP may neutralize the binding protein-mediated biological functions of retinoic acid, and could thereby enhance tumor production. Tretinoin 132-145 cellular retinoic acid binding protein 1 Homo sapiens 58-63
33454316-5 2021 In addition, RA treatment altered the intracellular localization of alpha-actinin-4 from the nucleus to the cytoplasm. Tretinoin 13-15 actinin alpha 4 Homo sapiens 68-83
33454316-6 2021 Cells pretreated with RA, maintained alpha-actinin-4 protein levels after cycloheximide treatment as compared with control cells. Tretinoin 22-24 actinin alpha 4 Homo sapiens 37-52
33454316-7 2021 The amount of ubiquitylated alpha-actinin-4 protein in RA-treated cells was less than in control cells. Tretinoin 55-57 actinin alpha 4 Homo sapiens 28-43
33454316-8 2021 These results indicate that RA may inhibit nuclei transport and proteasomal degradation of alpha-actinin-4 protein. Tretinoin 28-30 actinin alpha 4 Homo sapiens 91-106
33454316-9 2021 alpha-Actinin-4 may play a significant role in RA-induced differentiation, including the promotion of cytomorphology changes. Tretinoin 47-49 actinin alpha 4 Homo sapiens 0-15
33933435-2 2021 Here, a series of amphiphilic retinoyl-bPEI conjugates (RP-1, RP-2 and RP-3) has been synthesized by allowing the reaction between bPEI (1.8 kDa) and a bioactive and hydrophobic vitamin A metabolite, all-trans-retinoic acid (ATRA), in varying amounts. Tretinoin 200-223 RP1 axonemal microtubule associated Homo sapiens 56-60
33933435-2 2021 Here, a series of amphiphilic retinoyl-bPEI conjugates (RP-1, RP-2 and RP-3) has been synthesized by allowing the reaction between bPEI (1.8 kDa) and a bioactive and hydrophobic vitamin A metabolite, all-trans-retinoic acid (ATRA), in varying amounts. Tretinoin 225-229 RP1 axonemal microtubule associated Homo sapiens 56-60
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 dihydropyrimidinase-like 3 Mus musculus 107-113
2673546-5 1989 Induction of differentiation in several human leukemia cell lines by treatment with phorbol ester or retinoic acid leads to dephosphorylation of RB. Tretinoin 101-114 RB transcriptional corepressor 1 Homo sapiens 145-147
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin D2 Bos taurus 169-174
33551168-7 2021 Additionally, ATRA (0.2, 2, and 20 nM) supplementation also inhibited differentiation of postconfluent preadipocytes through downregulation of protein abundance of PPARgamma and C/EBPalpha. Tretinoin 14-18 peroxisome proliferator activated receptor gamma Bos taurus 164-173
33551168-7 2021 Additionally, ATRA (0.2, 2, and 20 nM) supplementation also inhibited differentiation of postconfluent preadipocytes through downregulation of protein abundance of PPARgamma and C/EBPalpha. Tretinoin 14-18 CCAAT/enhancer-binding protein alpha Bos taurus 178-188
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 164-177 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 250-254
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 179-181 Yes1 associated transcriptional regulator Homo sapiens 32-35
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 179-181 leucine rich repeat containing G protein-coupled receptor 5 Homo sapiens 250-254
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 193-195 Yes1 associated transcriptional regulator Homo sapiens 32-35
3555769-1 1987 Previous studies have shown that treatment of S91-C2 murine melanoma cells with beta-all-trans-retinoic acid (RA) results in growth inhibition, enhanced activity of sialyltransferase, and increased glycosylation of a Mr 160,000 cell surface sialoglycoprotein (gp160). Tretinoin 110-112 leucyl/cystinyl aminopeptidase Mus musculus 260-265
3555769-3 1987 These findings suggest that modulation by RA of gp160 might be related causally to growth inhibition. Tretinoin 42-44 leucyl/cystinyl aminopeptidase Mus musculus 48-53
3555769-7 1987 Rabbits were immunized with this material and immunoblotting revealed that their sera contained antibodies that bound specifically to gp160 in extracts of untreated or RA-treated S91-C2 cells. Tretinoin 168-170 leucyl/cystinyl aminopeptidase Mus musculus 134-139
3555769-8 1987 Indirect immunofluorescence staining followed by fluorescence-activated cell sorter analysis demonstrated that the anti-gp160 antibodies bound to the surface of both untreated and RA-treated S91-C2 cells and that the treated cells bound more of the antibodies than untreated ones. Tretinoin 180-182 leucyl/cystinyl aminopeptidase Mus musculus 120-125
3031026-1 1987 F9 teratocarcinoma cells contain a cellular retinoic acid-binding protein (CRABP) that may mediate the retinoic acid-induced differentiation of this cell line. Tretinoin 44-57 cellular retinoic acid binding protein 1 Homo sapiens 75-80
3031026-2 1987 Specific [3H]retinoic acid binding to CRABP in F9 stem cell cytosol is protein-dependent, reaches equilibrium within 4 h at 4 degrees C, and yields 643 +/- 105 fmol of [3H]retinoic acid per mg of protein with an apparent dissociation constant of 9.2 +/- 1.1 nM. Tretinoin 13-26 cellular retinoic acid binding protein 1 Homo sapiens 38-43
3031026-2 1987 Specific [3H]retinoic acid binding to CRABP in F9 stem cell cytosol is protein-dependent, reaches equilibrium within 4 h at 4 degrees C, and yields 643 +/- 105 fmol of [3H]retinoic acid per mg of protein with an apparent dissociation constant of 9.2 +/- 1.1 nM. Tretinoin 172-185 cellular retinoic acid binding protein 1 Homo sapiens 38-43
3031026-4 1987 The effect of these drugs on CRABP activity is both time and concentration-dependent, resulting in an increase in the number of binding sites for [3H]retinoic acid with no change in their affinity. Tretinoin 150-163 cellular retinoic acid binding protein 1 Homo sapiens 29-34
2484657-7 1989 Treatment of P19 cells with retinoic acid resulted in a decrease in the expression of Thy-1 antigen which preceded changes in morphology of the cells. Tretinoin 28-41 interleukin 23, alpha subunit p19 Mus musculus 13-16
2450799-9 1987 The treatment of basal cells with retinoic acid at pharmacological concentrations prevented the expression of K1 and K10 when cells were challenged by 1.4 mM Ca2+. Tretinoin 34-47 endothelin receptor type B modifier 1 Mus musculus 117-120
33360628-5 2021 The cell-binding efficiencies of substrates modified with anti-CD13 and anti-CD11b decreased and increased, respectively, with increasing duration of cell culture in medium containing differentiation-inducing agents, including all-trans retinoic acid. Tretinoin 237-250 alanyl aminopeptidase, membrane Homo sapiens 63-67
2674852-2 1989 P19 cells are induced to differentiate into neurons, astrocytes and fibroblast-like cells following exposure to retinoic acid (RA). Tretinoin 112-125 interleukin 23, alpha subunit p19 Mus musculus 0-3
33668324-0 2021 FOXC1 Downregulates Nanog Expression by Recruiting HDAC2 to Its Promoter in F9 Cells Treated by Retinoic Acid. Tretinoin 96-109 forkhead box C1 Homo sapiens 0-5
33668324-2 2021 FOXC1 is up-regulated in retinoic acid-induced differentiation of F9 Embryonal Carcinoma (EC) cells; furthermore, FOXC1 specifically inhibits the core pluripotency factor Nanog by binding to the proximal promoter. Tretinoin 25-38 forkhead box C1 Homo sapiens 0-5
3595420-2 1987 The aggregates of P19, a mouse EC cell line, undergo differentiation and rapidly lose its colony-forming ability in culture with retinoic acid (RA) or DMSO. Tretinoin 129-142 interleukin 23, alpha subunit p19 Mus musculus 18-21
3595420-2 1987 The aggregates of P19, a mouse EC cell line, undergo differentiation and rapidly lose its colony-forming ability in culture with retinoic acid (RA) or DMSO. Tretinoin 144-146 interleukin 23, alpha subunit p19 Mus musculus 18-21
33668324-2 2021 FOXC1 is up-regulated in retinoic acid-induced differentiation of F9 Embryonal Carcinoma (EC) cells; furthermore, FOXC1 specifically inhibits the core pluripotency factor Nanog by binding to the proximal promoter. Tretinoin 25-38 forkhead box C1 Homo sapiens 114-119
2674852-2 1989 P19 cells are induced to differentiate into neurons, astrocytes and fibroblast-like cells following exposure to retinoic acid (RA). Tretinoin 127-129 interleukin 23, alpha subunit p19 Mus musculus 0-3
2674852-4 1989 Northern blot analysis showed that int-1 RNA was not present in the EC cells but appeared 48 h after RA exposure and could be detected for at least the next 8 days. Tretinoin 101-103 wingless-type MMTV integration site family, member 1 Mus musculus 35-40
2674852-6 1989 Nuclear run-on transcription assays showed that int-1 expression in RA-treated P19 cells was induced at the transcriptional level. Tretinoin 68-70 wingless-type MMTV integration site family, member 1 Mus musculus 48-53
2428876-11 1986 Retinoic acid stimulated myeloid differentiation of HL-60 cells and induced expression of both Mac-1 and p150,95. Tretinoin 0-13 chromatin assembly factor 1 subunit A Homo sapiens 105-109
2674852-6 1989 Nuclear run-on transcription assays showed that int-1 expression in RA-treated P19 cells was induced at the transcriptional level. Tretinoin 68-70 interleukin 23, alpha subunit p19 Mus musculus 79-82
2546152-4 1989 Using a transient transfection assay in HeLa cells and a reporter gene harboring a synthetic RA responsive element, we demonstrate that hRAR-gamma cDNA indeed encodes a RA-inducible transcriptional trans-activator. Tretinoin 93-95 retinoic acid receptor gamma Homo sapiens 136-146
3021829-4 1986 In several tumor cells, including human promyelocytic leukemia, human and murine neuroblastoma, and murine teratocarcinoma, retinoic acid induces terminal differentiation, accompanied by suppression of the expression of either the c-myc or the N-myc gene. Tretinoin 124-137 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 231-236
3021829-6 1986 We have shown that retinoic acid greatly inhibits the anchorage-independent growth of a rat fibroblast cell line that has been transfected with the c-myc gene, particularly when these cells are stimulated by the combination of platelet-derived growth factor and transforming growth factor-beta. Tretinoin 19-32 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 148-153
33605051-8 2021 Remarkably, the cleavage site on the RNA helicases MDA5 and LGP2, two relevant immune sensors of the retinoic acid-inducible gene-I (RIG-I)-like receptors family, resembles the L target site of Gemin5 and Daxx, and similar cleavage sites have been reported in ISG15 and TBK1, two proteins involved in type I interferon response and signaling pathway, respectively. Tretinoin 101-114 death domain associated protein Homo sapiens 205-209
33605051-8 2021 Remarkably, the cleavage site on the RNA helicases MDA5 and LGP2, two relevant immune sensors of the retinoic acid-inducible gene-I (RIG-I)-like receptors family, resembles the L target site of Gemin5 and Daxx, and similar cleavage sites have been reported in ISG15 and TBK1, two proteins involved in type I interferon response and signaling pathway, respectively. Tretinoin 101-114 ISG15 ubiquitin like modifier Homo sapiens 260-265
2470609-0 1989 Keratin 13 expression is linked to squamous differentiation in rabbit tracheal epithelial cells and down-regulated by retinoic acid. Tretinoin 118-131 keratin, type I cytoskeletal 13 Oryctolagus cuniculus 0-10
3773529-1 1986 ABP levels in the testes and epididymides of vitamin A deficient-retinoic acid maintained rats were only 20 and 6% respectively as compared with those in normal rats. Tretinoin 65-78 sex hormone binding globulin Rattus norvegicus 0-3
2542775-1 1989 F9 cells induced to differentiate with retinoic acid (RA) increase transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 39-52 plasminogen activator, tissue Mus musculus 88-116
33832420-1 2021 Retinoic acid (RA) binding proteins, CRABP1 and CRABP2, are molecular chaperones that mediate intracellular activity of RA, the key promoter of cell differentiation with tumor suppressor activity. Tretinoin 0-13 cellular retinoic acid binding protein 1 Homo sapiens 37-43
33832420-1 2021 Retinoic acid (RA) binding proteins, CRABP1 and CRABP2, are molecular chaperones that mediate intracellular activity of RA, the key promoter of cell differentiation with tumor suppressor activity. Tretinoin 15-17 cellular retinoic acid binding protein 1 Homo sapiens 37-43
2542775-1 1989 F9 cells induced to differentiate with retinoic acid (RA) increase transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 39-52 plasminogen activator, tissue Mus musculus 118-122
33832420-3 2021 The functions of CRABP1 are less studied but are apparently associated with sequestration of RA in cytoplasm and limitation of its transcriptional activity, suggesting involvement of this protein in the development of RA resistance. Tretinoin 93-95 cellular retinoic acid binding protein 1 Homo sapiens 17-23
33832420-8 2021 Moreover, suppression of the CRABP1 level in both RA-sensitive and RA-resistant cells was shown in the cells with cells with knockdown of CRABP2 gene. Tretinoin 50-52 cellular retinoic acid binding protein 1 Homo sapiens 29-35
3461785-0 1986 Dimethylsulfoxide, retinoic acid and 12-O-tetradecanoylphorbol-13-acetate induce a selective decrease in the phosphorylation of P150, a surface membrane phosphoprotein of HL60 cells resistant to adriamycin. Tretinoin 19-32 chromatin assembly factor 1 subunit A Homo sapiens 128-132
2542775-1 1989 F9 cells induced to differentiate with retinoic acid (RA) increase transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 54-56 plasminogen activator, tissue Mus musculus 88-116
33044585-12 2021 Meanwhile, ATRA could reduce the interaction between KLF5 and RARalpha, thereby inhibiting the function of cis-elements of KLF5. Tretinoin 11-15 Kruppel like factor 5 Homo sapiens 123-127
2542775-1 1989 F9 cells induced to differentiate with retinoic acid (RA) increase transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 54-56 plasminogen activator, tissue Mus musculus 118-122
33044585-13 2021 KLF5-induced inducible nitric oxide synthase (iNOS) expression activation could be significantly inhibited by ATRA. Tretinoin 110-114 Kruppel like factor 5 Homo sapiens 0-4
2536892-4 1989 Both FSH and (Bu)2cAMP increased the steady-state level of tPA mRNA and tPA production without affecting those of uPA in stages VII-IX in vitro, whereas retinoic acid treatment selectively increased the concentration uPA mRNA and uPA production in stages II-VI. Tretinoin 153-166 plasminogen activator, urokinase Rattus norvegicus 217-220
3085092-4 1986 Certain drugs irreversibly (glutaraldehyde, 1-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline) or reversibly (retinoic acid) abolish dependence of gj on pHi without appreciably affecting kinetic properties of voltage dependence or the shape of the steady-state Vj-gj relation. Tretinoin 107-120 glucose-6-phosphate isomerase Homo sapiens 150-153
2536892-4 1989 Both FSH and (Bu)2cAMP increased the steady-state level of tPA mRNA and tPA production without affecting those of uPA in stages VII-IX in vitro, whereas retinoic acid treatment selectively increased the concentration uPA mRNA and uPA production in stages II-VI. Tretinoin 153-166 plasminogen activator, urokinase Rattus norvegicus 217-220
2645590-4 1989 Human skin extracts incubated with either [3H]retinol or [3H]retinoic acid and analyzed by PAGE is a novel technique for the study of cellular retinol-(CRBP) and retinoic acid-(CRABP) binding proteins; it allows one to more specifically analyse these binding proteins and differentiate them from RBP. Tretinoin 61-74 retinol binding protein 1 Homo sapiens 152-156
3007486-0 1986 Transforming growth factor-beta and retinoic acid modulate phenotypic transformation of normal rat kidney cells induced by epidermal growth factor and platelet-derived growth factor. Tretinoin 36-49 epidermal growth factor like 1 Rattus norvegicus 123-146
33181146-9 2021 Manipulation of the retinoic acid pathway specifically in the NAcSh of male rats via viral vector-mediated RNA interference targeting fatty acid binding protein 5 (FABP5) decreased cocaine self-administration and modulates excitability of medium spiny neurons in the NAcSh. Tretinoin 20-33 fatty acid binding protein 5 Rattus norvegicus 134-162
33181146-9 2021 Manipulation of the retinoic acid pathway specifically in the NAcSh of male rats via viral vector-mediated RNA interference targeting fatty acid binding protein 5 (FABP5) decreased cocaine self-administration and modulates excitability of medium spiny neurons in the NAcSh. Tretinoin 20-33 fatty acid binding protein 5 Rattus norvegicus 164-169
2645590-4 1989 Human skin extracts incubated with either [3H]retinol or [3H]retinoic acid and analyzed by PAGE is a novel technique for the study of cellular retinol-(CRBP) and retinoic acid-(CRABP) binding proteins; it allows one to more specifically analyse these binding proteins and differentiate them from RBP. Tretinoin 61-74 cellular retinoic acid binding protein 1 Homo sapiens 177-182
33479039-0 2021 Pretreatment of aged mice with retinoic acid supports alveolar regeneration via upregulation of reciprocal PDGFA signalling. Tretinoin 31-44 platelet derived growth factor, alpha Mus musculus 107-112
33479039-10 2021 CONCLUSIONS: Our data support the concept that RA indirectly induces reciprocal PDGFA signalling, which activates regenerative fibroblasts that support alveolar epithelial cell differentiation and repair, providing a potential therapeutic strategy to influence the pathogenesis of IPF. Tretinoin 47-49 platelet derived growth factor, alpha Mus musculus 80-85
3015289-2 1986 Intracellular metabolism is complex and involves the binding to specific receptors for retinol (CRBP) and retinoic acid (CRABP) followed by a nuclear translocation. Tretinoin 106-119 cellular retinoic acid binding protein 1 Homo sapiens 121-126
2645590-4 1989 Human skin extracts incubated with either [3H]retinol or [3H]retinoic acid and analyzed by PAGE is a novel technique for the study of cellular retinol-(CRBP) and retinoic acid-(CRABP) binding proteins; it allows one to more specifically analyse these binding proteins and differentiate them from RBP. Tretinoin 162-175 cellular retinoic acid binding protein 1 Homo sapiens 177-182
2645590-6 1989 When the ability of some synthetic analogs of retinoic acid to compete with [3H]retinoic acid binding on human skin CRABP was studied, two important observations were made: (1) the analogs that, when given to human subjects were pharmacologically active, were found to be good competitors and vice-versa, (2) no strict correlation was found between the IC50 and the pharmacological potency of the retinoid. Tretinoin 46-59 cellular retinoic acid binding protein 1 Homo sapiens 116-121
2645590-6 1989 When the ability of some synthetic analogs of retinoic acid to compete with [3H]retinoic acid binding on human skin CRABP was studied, two important observations were made: (1) the analogs that, when given to human subjects were pharmacologically active, were found to be good competitors and vice-versa, (2) no strict correlation was found between the IC50 and the pharmacological potency of the retinoid. Tretinoin 80-93 cellular retinoic acid binding protein 1 Homo sapiens 116-121
2997185-0 1985 An increase in prolyl-4-hydroxylase activity occurs during the retinoic acid-induced differentiation of mouse teratocarcinoma stem cell lines F9 and P19. Tretinoin 63-76 interleukin 23, alpha subunit p19 Mus musculus 149-152
2997185-1 1985 Monolayer cultures of F9 teratocarcinoma stem cells and P19 stem cells differentiate into endoderm, and fibroblast-like cells, respectively, when treated with retinoic acid. Tretinoin 159-172 interleukin 23, alpha subunit p19 Mus musculus 56-59
3078960-1 1988 Mouse embryonal carcinoma (EC) cells of the P19 line can be induced to differentiate into neurons, astrocytes and fibroblasts by exposure to retinoic acid (RA), whereas treatment of the EC cells with dimethyl sulfoxide (DMSO) leads to differentiation into mesodermal tissues, including cardiac and skeletal muscle. Tretinoin 141-154 interleukin 23, alpha subunit p19 Mus musculus 44-47
2998367-1 1985 Retinoic acid (RA) caused a reduction in the level of 1,25(OH)2D3 receptors to 1/3 of control in rat osteoblast-like cells (ROB) while increasing the receptor level to 3-fold the control in mouse osteoblast-like cells (MOB). Tretinoin 0-13 sphingomyelin synthase 1 Mus musculus 219-222
2998367-1 1985 Retinoic acid (RA) caused a reduction in the level of 1,25(OH)2D3 receptors to 1/3 of control in rat osteoblast-like cells (ROB) while increasing the receptor level to 3-fold the control in mouse osteoblast-like cells (MOB). Tretinoin 15-17 sphingomyelin synthase 1 Mus musculus 219-222
33428669-5 2021 We found that BMP antagonism and activation of retinoic acid signaling at stage 2 (from definitive endoderm to primitive gut tube) effectively suppressed NKX6.1 expression at later stages. Tretinoin 47-60 NK6 homeobox 1 Homo sapiens 154-160
33428669-6 2021 Using two different hPSCs lines, treatment with BMP signaling inhibitor (LDN193189) and retinoic acid agonist (EC23) at Stage 2 reduced NKX6.1 expression and allowed differentiation of almost all cells into pancreatic alpha cells in vivo after transplantation under a kidney capsule. Tretinoin 88-101 NK6 homeobox 1 Homo sapiens 136-142
33428669-7 2021 Our study demonstrated that the cell fate of pancreatic cells can be controlled by adjusting the expression level of NKX6.1 with proper timing of BMP antagonism and activation of retinoic acid signaling during the pancreatic differentiation process. Tretinoin 179-192 NK6 homeobox 1 Homo sapiens 117-123
3078960-1 1988 Mouse embryonal carcinoma (EC) cells of the P19 line can be induced to differentiate into neurons, astrocytes and fibroblasts by exposure to retinoic acid (RA), whereas treatment of the EC cells with dimethyl sulfoxide (DMSO) leads to differentiation into mesodermal tissues, including cardiac and skeletal muscle. Tretinoin 156-158 interleukin 23, alpha subunit p19 Mus musculus 44-47
3136932-6 1988 Thus, RA enhancement of thymocyte responses appears to be mediated by an increase in IL-2-receptor expression on thymocyte blasts, resulting in augmented IL-2-dependent growth. Tretinoin 6-8 interleukin 2 receptor subunit beta Homo sapiens 85-98
33473264-4 2021 Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 (CPSF6)-RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine. Tretinoin 150-154 retinoic acid receptor gamma Homo sapiens 115-119
2993004-5 1985 We show here that retinoic acid (RA) has no effect on the growth rate of the cells or the synthesis of EGF receptor and colligin, but stimulates the synthesis of transferrin receptor. Tretinoin 18-31 transferrin receptor Homo sapiens 162-182
2993004-5 1985 We show here that retinoic acid (RA) has no effect on the growth rate of the cells or the synthesis of EGF receptor and colligin, but stimulates the synthesis of transferrin receptor. Tretinoin 33-35 transferrin receptor Homo sapiens 162-182
32469071-1 2021 BACKGROUND: All-trans retinoic acid (RA) plays a crucial role in promoting Foxp3+ Treg generation while reciprocally inhibiting Th1/Th17 generation. Tretinoin 12-35 forkhead box P3 Homo sapiens 75-80
2457503-2 1988 In the present study the levels of cellular retinoic acid (CRABP)- and retinol (CRBP)-binding proteins were measured in cultured normal human epidermal keratinocytes. Tretinoin 44-57 cellular retinoic acid binding protein 1 Homo sapiens 59-64
32469071-1 2021 BACKGROUND: All-trans retinoic acid (RA) plays a crucial role in promoting Foxp3+ Treg generation while reciprocally inhibiting Th1/Th17 generation. Tretinoin 37-39 forkhead box P3 Homo sapiens 75-80
32469071-7 2021 We also found that RA negatively correlated with IL-9, thereby reinstating our previous finding that RA inhibits Th9 differentiation. Tretinoin 19-21 interleukin 9 Homo sapiens 49-53
32469071-7 2021 We also found that RA negatively correlated with IL-9, thereby reinstating our previous finding that RA inhibits Th9 differentiation. Tretinoin 101-103 interleukin 9 Homo sapiens 49-53
2864293-0 1985 Transglutaminase activity increases in HL60 cells induced to differentiate with retinoic acid and TPA but not with DMSO. Tretinoin 80-93 transglutaminase 1 Homo sapiens 0-16
2864293-1 1985 HL60 cells induced to differentiate into myeloid cells by retinoic acid exhibited a 300-fold increase in transglutaminase (TGase) activity which peaked on day 5. Tretinoin 58-71 transglutaminase 1 Homo sapiens 105-121
2864293-1 1985 HL60 cells induced to differentiate into myeloid cells by retinoic acid exhibited a 300-fold increase in transglutaminase (TGase) activity which peaked on day 5. Tretinoin 58-71 transglutaminase 1 Homo sapiens 123-128
2864293-4 1985 Elevation of TGase activity appears to be characteristic of monocyte differentiation and retinoic acid-induced myeloid differentiation but not of myeloid differentiation in response to DMSO. Tretinoin 89-102 transglutaminase 1 Homo sapiens 13-18
6322983-0 1984 Antagonistic actions of retinoic acid and dexamethasone on anchorage-independent growth and epidermal growth factor binding of normal rat kidney cells. Tretinoin 24-37 epidermal growth factor like 1 Rattus norvegicus 92-115
6322983-2 1984 Retinoic acid by itself has no effect on colony formation; but at concentrations of 10(-9) M or greater, it can greatly enhance the response of the cells to EGF and TGF-beta, as measured by colony growth in soft agar and expression of a transformed morphology in monolayer culture. Tretinoin 0-13 epidermal growth factor like 1 Rattus norvegicus 157-160
6322983-5 1984 Retinoic acid and dexamethasone also have opposite and antagonistic effects on the binding of 125I-labeled EGF to normal rat kidney cells. Tretinoin 0-13 epidermal growth factor like 1 Rattus norvegicus 107-110
33241756-6 2021 In addition, we found that HOTAIR promoted ATRA-induced differentiation via the regulation of the cell cycle regulator p21 via miR-17-5p. Tretinoin 43-47 microRNA 17 Homo sapiens 127-136
2906112-0 1988 Early retinoic acid-induced F9 teratocarcinoma stem cell gene ERA-1: alternate splicing creates transcripts for a homeobox-containing protein and one lacking the homeobox. Tretinoin 6-19 homeobox A1 Mus musculus 62-67
6322983-6 1984 Retinoic acid enhances the binding of EGF up to 6-fold, while dexamethasone reduces the binding to 50 to 60% of control levels. Tretinoin 0-13 epidermal growth factor like 1 Rattus norvegicus 38-41
6322983-9 1984 It can be concluded that the abilities of retinoic acid and dexamethasone to alter expression of the transformed phenotype induced by treatment of normal rat kidney cells with TGF-beta and EGF are mediated at least in part through their effects on the EGF receptor. Tretinoin 42-55 epidermal growth factor like 1 Rattus norvegicus 189-192
6322983-9 1984 It can be concluded that the abilities of retinoic acid and dexamethasone to alter expression of the transformed phenotype induced by treatment of normal rat kidney cells with TGF-beta and EGF are mediated at least in part through their effects on the EGF receptor. Tretinoin 42-55 epidermal growth factor like 1 Rattus norvegicus 252-255
32881426-5 2020 AIMS: We have previously shown that ATRA stimulates transactivation of RARgamma at sub-nanomolar concentrations (EC50 0.24 nM), whereas an 80-fold higher concentration was required for RARalpha-mediated transactivation (EC50 19.3 nM). Tretinoin 36-40 retinoic acid receptor gamma Homo sapiens 71-79
2906112-2 1988 As an initial step toward understanding the molecular mechanism(s) by which RA exerts these effects, we previously isolated cDNA clones for a gene, ERA-1, which has the characteristics of an early, direct target for RA. Tretinoin 76-78 homeobox A1 Mus musculus 148-153
32881426-7 2020 These findings, together with the low level of ATRA in PC, led us to hypothesize that RARgamma plays a role in PC pathogenesis and that RARgamma-selective antagonism may be an effective treatment. Tretinoin 47-51 retinoic acid receptor gamma Homo sapiens 136-144
32881426-8 2020 METHODS AND RESULTS: We found that concentrations of 10-9 M and below of ATRA promoted survival/proliferation and opposed adipogenic differentiation of human PC cell lines by a mechanism that involves RARgamma. Tretinoin 73-77 retinoic acid receptor gamma Homo sapiens 201-209
6199027-1 1984 Regulation of the biosynthesis of alpha-fetoprotein and albumin was studied in a temperature-sensitive fetal rat hepatocyte line (RLA209-15) which exhibits a differentiated phenotype when grown at 40 degrees C. Retinoic acid inhibited alpha-fetoprotein production but increased albumin production. Tretinoin 211-224 alpha-fetoprotein Rattus norvegicus 34-51
2906112-3 1988 We demonstrated that RA causes a rapid, dose-dependent, and protein synthesis-independent expression of the ERA-1 gene (G. J. LaRosa and L. J. Gudas, Proc. Tretinoin 21-23 homeobox A1 Mus musculus 108-113
2906112-9 1988 The data indicate that the RA-induced 2.2- to 2.4-kilobase ERA-1 RNA species that we previously detected consists of two alternately spliced messages. Tretinoin 27-29 homeobox A1 Mus musculus 59-64
2842348-9 1988 Both cycloheximide and puromycin inhibited the RA induction of the collagen IV (alpha 1), laminin B1, and J6 mRNAs. Tretinoin 47-49 laminin B1 Mus musculus 90-100
2455658-2 1988 12-O-Tetradecanoyl phorbol-13-acetate (PMA), butyrate, interferon, retinoic acid and 1,25-dihydroxyvitamin D3 all increased pHi. Tretinoin 67-80 glucose-6-phosphate isomerase Homo sapiens 124-127
6315022-6 1983 Mitogenic responses induced by the TGF-beta-EGF combination were prevented by all-trans-retinoic acid but not by indomethacin or dexamethasone. Tretinoin 78-101 pro-epidermal growth factor Oryctolagus cuniculus 44-47
6310582-4 1983 All five lines contain significant levels of cytosolic CRABP (2.5-7.5 pmol/mg of protein), which display typical properties of specific high affinity retinoic acid binding, a sedimentation coefficient of 2 S, and inhibition by PCMBS. Tretinoin 150-163 cellular retinoic acid binding protein 1 Homo sapiens 55-60
33174611-4 2020 The results demonstrated that in retinoic acid-resistant NB4-R1 cells, the protein expression of cofilin-1 was markedly increased compared with that in the drug-sensitive NB4 cells. Tretinoin 33-46 cofilin 1 Homo sapiens 97-106
33148658-5 2020 Mechanistically, LSD1 tightly controls retinoic acid signaling through regulation of Aldh1a2 expression level. Tretinoin 39-52 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 85-92
33148658-6 2020 The increased retinoic acid signaling in LSD1-deficient mice suppressed SOX9 expression and impeded the cartilaginous callus formation during fracture repair. Tretinoin 14-27 SRY (sex determining region Y)-box 9 Mus musculus 72-76
2839288-1 1988 Binding proteins for retinoic acid (cellular retinoid acid binding protein, CRABP), and for vitamin A (cellular retinol binding protein, CRBP) have been demonstrated in various cell types; these binding proteins display the characteristics of receptors. Tretinoin 21-34 cellular retinoic acid binding protein 1 Homo sapiens 76-81
32959699-0 2021 All-Trans Retinoic Acid Rescues the Tumor Suppressive Role of RAR-beta by Inhibiting LncHOXA10 Expression in Gastric Tumorigenesis. Tretinoin 10-23 homeobox A10 Homo sapiens 85-94
32959699-9 2021 Finally, we showed that ATRA can reverse the pro-cancerous function of LncHOXA10. Tretinoin 24-28 homeobox A10 Homo sapiens 71-80
32959699-11 2021 Furthermore, ATRA can inhibit the role of LncHOXA10 in gastric tumorigenesis. Tretinoin 13-17 homeobox A10 Homo sapiens 42-51
6306117-7 1983 Retinoic acid, which binds to CRABP but not CRBP, induces differentiation of teratocarcinoma cells. Tretinoin 0-13 cellular retinoic acid binding protein 1 Homo sapiens 30-35
6356262-5 1983 RB SF81 cells were treated with retinoic acid, a known stimulator of differentiation (optimal concentration 5 X 10(-8) M). Tretinoin 32-45 RB transcriptional corepressor 1 Homo sapiens 0-2
6356262-7 1983 RB SF81 treated with retinoic acid showed a significant, persistent increase in HLA levels by 24 hours compared with controls. Tretinoin 21-34 RB transcriptional corepressor 1 Homo sapiens 0-2
2453513-2 1988 It belongs to a family of fatty acid binding proteins and shows a 72% amino acid sequence similarity to aP2/422, the adipocyte lipid binding protein, a 58% sequence similarity to rat heart fatty acid binding protein, and a 40% sequence similarity to cellular retinoic acid binding protein. Tretinoin 259-272 fatty acid binding protein 4 Rattus norvegicus 104-111
6356262-9 1983 Developmental parallels between embryonic retina and in vitro retinoblastoma treated with retinoic acid exist. Tretinoin 90-103 RB transcriptional corepressor 1 Homo sapiens 62-76
6125941-6 1982 In mouse melanoma cells, retinoic acid plus MSH markedly enhanced the activity of the initial TGase peak compared to MSH alone. Tretinoin 25-38 transglutaminase 1 Homo sapiens 94-99
6125941-6 1982 In mouse melanoma cells, retinoic acid plus MSH markedly enhanced the activity of the initial TGase peak compared to MSH alone. Tretinoin 25-38 pro-opiomelanocortin-alpha Mus musculus 117-120
32955735-5 2021 Moreover, in SH-SY5Y cells differentiated into neurons by exposure to retinoic acid (10 microM), overexpression of GSK3beta and tau provokes an imbalance in cholinergic activity with a decrease in the neurotransmitter acetylcholine in the cell (45 +- 10%). Tretinoin 70-83 glycogen synthase kinase 3 alpha Homo sapiens 115-123
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoic acid receptor gamma Homo sapiens 126-154
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoic acid receptor gamma Homo sapiens 156-160
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoid X receptor beta Homo sapiens 223-247
6125941-7 1982 Retinoic acid alone also increased TGase activity biphasically in these cells without the addition of MSH. Tretinoin 0-13 transglutaminase 1 Homo sapiens 35-40
6176589-6 1982 The simultaneous addition of retinoic acid along with 8BrcAMP, cholera toxin, or MIX gave additive induction for hCG and hCG alpha. Tretinoin 29-42 glycoprotein hormones, alpha polypeptide Homo sapiens 113-130
2830014-10 1988 IRBP RNA transcripts in Y-79 cells were below the limits of detectability but appeared at low levels after induction of differentiation of Y-79 by 10(-6) M retinoic acid. Tretinoin 156-169 retinol binding protein 3 Homo sapiens 0-4
6793526-0 1981 Antagonistic action of retinoic acid and teleocidin on the proliferation and epidermal growth factor binding of rat hepatoma cells. Tretinoin 23-36 epidermal growth factor like 1 Rattus norvegicus 77-100
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoid X receptor beta Homo sapiens 249-253
2832311-0 1988 Induction of a beta-1,3-D-glucan receptor in P388D1 cells treated with retinoic acid or 1,25-dihydroxyvitamin D3. Tretinoin 71-84 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 15-23
32823855-4 2020 In this review, we mostly focus on emerging RA-regulated epigenetic mechanisms involving RA receptor alpha (RARA) and Annexin A8 (ANXA8), which is a member of the Annexin family, as well as ANXA8 regulatory microRNAs (miRNAs). Tretinoin 44-46 annexin A8 Homo sapiens 118-128
32823855-4 2020 In this review, we mostly focus on emerging RA-regulated epigenetic mechanisms involving RA receptor alpha (RARA) and Annexin A8 (ANXA8), which is a member of the Annexin family, as well as ANXA8 regulatory microRNAs (miRNAs). Tretinoin 44-46 annexin A8 Homo sapiens 130-135
32823855-4 2020 In this review, we mostly focus on emerging RA-regulated epigenetic mechanisms involving RA receptor alpha (RARA) and Annexin A8 (ANXA8), which is a member of the Annexin family, as well as ANXA8 regulatory microRNAs (miRNAs). Tretinoin 44-46 annexin A8 Homo sapiens 190-195
32823855-5 2020 The first cancer showing ANXA8 upregulation was reported in acute promyelocytic leukemia (APL), which induces the differentiation arrest of promyelocytes due to defective RA signaling caused by RARA fusion genes as the PML-RARA gene. Tretinoin 171-173 annexin A8 Homo sapiens 25-30
6793526-2 1981 In this low serum culture, retinoic acid inhibited the cell proliferation and enhanced the number of receptors for epidermal growth factor (EGF). Tretinoin 27-40 epidermal growth factor like 1 Rattus norvegicus 115-138
6793526-2 1981 In this low serum culture, retinoic acid inhibited the cell proliferation and enhanced the number of receptors for epidermal growth factor (EGF). Tretinoin 27-40 epidermal growth factor like 1 Rattus norvegicus 140-143
6793526-5 1981 Retinoic acid inhibited the mitogenic action of teleocidin, while teleocidin suppressed the retinoic-acid enhancement of the number of EGF receptors. Tretinoin 92-105 epidermal growth factor like 1 Rattus norvegicus 135-138
6258773-1 1980 Blinded analyses of the concentrations of binding proteins for retinol and retinoic acid (CRABP) in homogenates of cancer and normal tissue aliquots obtained from human cervix, endometrium, ovary, breast, and lung were carried out by the sucrose gradient ultracentrifugation technique. Tretinoin 75-88 cellular retinoic acid binding protein 1 Homo sapiens 90-95
6258776-3 1980 This technique allows, after incubation with tritiated retinoic acid (RA) overnight, the separation of the specific CRABP activity from the nonspecific serum-originated binding activity and from the free RA. Tretinoin 55-68 cellular retinoic acid binding protein 1 Homo sapiens 116-121
3133373-6 1988 Am 80 and Am 580 inhibited the specific binding of 3H-retinoic acid to CRABP, but also showed less affinity than authentic unlabeled retinoic acid and compound 19. Tretinoin 54-67 cellular retinoic acid binding protein 1 Homo sapiens 71-76
6258776-3 1980 This technique allows, after incubation with tritiated retinoic acid (RA) overnight, the separation of the specific CRABP activity from the nonspecific serum-originated binding activity and from the free RA. Tretinoin 70-72 cellular retinoic acid binding protein 1 Homo sapiens 116-121
89058-4 1979 In addition to cellular retinol-binding protein (CRBP) and retinoic acid-binding protein (CRABP), a new molecular species having affinity for both retinol and retinoic acid was detected in the cytosols obtained from hepatocellular carcinoma as well as glioma by means of gel filtration on Sephadex G-75. Tretinoin 59-72 cellular retinoic acid binding protein 1 Homo sapiens 90-95
32540366-3 2020 In order to identify signaling pathways responsible for this autophagy defect, we performed an unbiased screen using RNA sequencing (RNA-Seq) of wild-type or VPS35 D620N-expressing retinoic acid-differentiated SH-SY5Y cells. Tretinoin 181-194 VPS35 retromer complex component Homo sapiens 158-163
32556644-8 2020 We then evaluated the effect of all-trans retinoic acid (ATRA), which is a retinoic acid receptor (RAR)alpha, RARbeta and RARgamma agonist, on the differentiation from the hiPSC-derived foregut. Tretinoin 57-61 retinoic acid receptor gamma Homo sapiens 122-130
32032659-0 2020 Roscovitine enhances All-trans retinoic acid (ATRA)-induced leukemia cell differentiation: Novel effects on signaling molecules for a putative Cdk2 inhibitor. Tretinoin 46-50 cyclin dependent kinase 2 Homo sapiens 143-147
2856164-13 1988 Our data show a P450-dependent RA metabolism in rat epidermal microsomes and suggest that ketoconazole may prove to be effective in maintaining biologically active levels of RA in epidermal cells. Tretinoin 174-176 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 16-20
984876-4 1976 In resting yeast cells, both substances failed to exert any significant influence on oxygen consumption.--Pure G-6-PDH was inhibited by retinoic acid and retinoid in concentrations as low as 5 mug/ml. Tretinoin 136-149 hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase Homo sapiens 111-118
3435894-1 1987 Retinoic acid (RA) inhibits the growth of mouse S91-C2 melanoma cells and enhances the glycosylation of a cell surface sialoglycoprotein (gp160). Tretinoin 0-13 leucyl/cystinyl aminopeptidase Mus musculus 138-143
4101-0 1976 The effect of retinol and retinoic acid on the testicular phospholipase a activity in retinol-deficient rats. Tretinoin 26-39 phospholipase A and acyltransferase 1 Rattus norvegicus 58-73
3435894-1 1987 Retinoic acid (RA) inhibits the growth of mouse S91-C2 melanoma cells and enhances the glycosylation of a cell surface sialoglycoprotein (gp160). Tretinoin 15-17 leucyl/cystinyl aminopeptidase Mus musculus 138-143
32583043-8 2021 Surprisingly, a significant increase of invasive ability was observed in SK-N-SH cells with overexpression of CA8-S100P as compared with those with overexpression of WT CA8 under retinoic acid (RA) treatment. Tretinoin 194-196 carbonic anhydrase 8 Homo sapiens 110-113
3435894-6 1987 In contrast, desialylation made possible the binding of RCAI to RA-gp160. Tretinoin 64-66 leucyl/cystinyl aminopeptidase Mus musculus 67-72
3655940-5 1987 Actinomycin D blocked the retinoic acid-induced stimulation of ceruloplasmin activity in copper-sufficient rats, but in copper-deficient rats only about half of the increase was blocked when the rats were given copper or copper and retinoic acid. Tretinoin 26-39 ceruloplasmin Rattus norvegicus 63-76
33986873-7 2021 Finally, the induction through to terminal differentiation of the keratinocyte by all-trans retinoic acid on parental ESCC cell lines led to the upregulation of the terminal differentiation marker Involucrin and a decrease in cell viability similar to that observed in ZNF750-overexpressing ESCC cells. Tretinoin 92-105 involucrin Mus musculus 197-207
3655940-6 1987 By use of pulse-labeling techniques, ceruloplasmin synthesis was shown to increase 1.5-fold after retinoic acid and this increase was blocked by actinomycin D. Tretinoin 98-111 ceruloplasmin Rattus norvegicus 37-50
3609538-2 1987 The purpose of this investigation was to obtain preliminary in vivo toxicity data on SMR-2(analog of RO) and SMR-6 (analog of RA), arotinoids with promising activity (ED50"s of 20 X 10(-11) and 5 X 10(-11) M, respectively; ED50 of RA = 1 X 10(-11) M) for reversal of keratinization in tracheal organ culture. Tretinoin 126-128 Scm-like with four mbt domains 1 Mus musculus 109-112
34058077-0 2021 Cross-talk between hnRNP K and SET in ATRA-induced differentiation in acute promyelocytic leukemia. Tretinoin 38-42 heterogeneous nuclear ribonucleoprotein K Homo sapiens 19-26
34058077-3 2021 The objective of this study was to characterize the participation of hnRNP K and SET proteins in ATRA-induced differentiation in APL. Tretinoin 97-101 heterogeneous nuclear ribonucleoprotein K Homo sapiens 69-76
34058077-5 2021 hnRNP K knockdown using short hairpin RNA led to cell death in ATRA-sensitive NB4 and resistant NB4-R2 cells by apoptosis with SET cleavage. Tretinoin 63-67 heterogeneous nuclear ribonucleoprotein K Homo sapiens 0-7
34058077-6 2021 In addition, hnRNP K knockdown increased granulocytic differentiation in APL cells, mainly in NB4-R2 with ATRA. Tretinoin 106-110 heterogeneous nuclear ribonucleoprotein K Homo sapiens 13-20
34058077-10 2021 Therefore, hnRNP K/SET and ERK are potential therapeutic targets for both anti-neoplastic leukemia therapy and relapsed APL patients with ATRA resistance. Tretinoin 138-142 heterogeneous nuclear ribonucleoprotein K Homo sapiens 11-18
32587277-4 2020 Here, we show that reduced levels of NTAL were associated with increased all-trans retinoic acid (ATRA)-induced differentiation, generation of reactive oxygen species, and mitochondrial dysfunction. Tretinoin 83-96 linker for activation of T cells family member 2 Homo sapiens 37-41
32587277-4 2020 Here, we show that reduced levels of NTAL were associated with increased all-trans retinoic acid (ATRA)-induced differentiation, generation of reactive oxygen species, and mitochondrial dysfunction. Tretinoin 98-102 linker for activation of T cells family member 2 Homo sapiens 37-41
32587277-7 2020 A retrospective analysis of NTAL expression in a cohort of patients treated with ATRA and anthracyclines, revealed that NTAL overexpression was associated with a high leukocyte count (P = 0.007) and was independently associated with shorter overall survival (Hazard Ratio: 3.6; 95% Confidence Interval: 1.17-11.28; P = 0.026). Tretinoin 81-85 linker for activation of T cells family member 2 Homo sapiens 28-32
3035450-1 1987 Binding proteins for retinoic acid (cellular retinoic acid binding protein, CRABP) have been demonstrated in various cell types, and display the characteristics of receptors. Tretinoin 21-34 cellular retinoic acid binding protein 1 Homo sapiens 76-81
32513696-4 2020 Herein, we identified a number of RIG-I-binding endogenous RNAs in APL cells following ATRA treatment, including the tripartite motif-containing protein 25 (TRIM25) messenger RNA (mRNA). Tretinoin 87-91 tripartite motif containing 25 Homo sapiens 117-155
32513696-4 2020 Herein, we identified a number of RIG-I-binding endogenous RNAs in APL cells following ATRA treatment, including the tripartite motif-containing protein 25 (TRIM25) messenger RNA (mRNA). Tretinoin 87-91 tripartite motif containing 25 Homo sapiens 157-163
32587903-7 2020 This was accompanied by increased expression of mitochondrial electron transport chain subunit genes and the retinoic acid biosynthetic enzyme gene Raldh2. Tretinoin 109-122 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 148-154
34030475-0 2021 Two Enhancers Regulate HoxB Genes Expression During Retinoic Acid-Induced Early Embryonic Stem Cells Differentiation Through Long-Range Chromatin Interactions. Tretinoin 52-65 homeobox B cluster Homo sapiens 23-27
34030475-1 2021 Homeobox B cluster (HoxB) genes play important roles in retinoic acid (RA)-induced early embryonic stem cells (ESCs) differentiation. Tretinoin 56-69 homeobox B cluster Homo sapiens 0-18
34030475-1 2021 Homeobox B cluster (HoxB) genes play important roles in retinoic acid (RA)-induced early embryonic stem cells (ESCs) differentiation. Tretinoin 56-69 homeobox B cluster Homo sapiens 20-24
34030475-1 2021 Homeobox B cluster (HoxB) genes play important roles in retinoic acid (RA)-induced early embryonic stem cells (ESCs) differentiation. Tretinoin 71-73 homeobox B cluster Homo sapiens 0-18
34030475-1 2021 Homeobox B cluster (HoxB) genes play important roles in retinoic acid (RA)-induced early embryonic stem cells (ESCs) differentiation. Tretinoin 71-73 homeobox B cluster Homo sapiens 20-24
34030475-3 2021 In this study, we identified two enhancers that were activated by RA treatment and 4C data showed long-range interactions between HoxB genes and the two enhancers. Tretinoin 66-68 homeobox B cluster Homo sapiens 130-134
34030475-4 2021 CRISPR/Cas9-mediated individual or compound deletion of the two enhancers significantly inhibits HoxB gene expression, and transcriptome analysis revealed that RA-induced early ESCs differentiation was blocked in the enhancer KO cells. Tretinoin 160-162 homeobox B cluster Homo sapiens 97-101
3539326-3 1987 In this study the presence of nucleolar antigen p145 was examined in the human promyelocytic tumor cell line HL-60 which was induced to differentiate by retinoic acid. Tretinoin 153-166 POM121 transmembrane nucleoporin Homo sapiens 48-52
34030475-5 2021 We propose new mechanism by which two enhancers regulate HoxB gene expression by different regulation modes during RA-induced early ESCs differentiation through long-range chromatin interactions. Tretinoin 115-117 homeobox B cluster Homo sapiens 57-61
34001245-15 2021 During the reversal process of ATRA, the expression of retinoic acid receptor beta (RARbeta) was elevated. Tretinoin 31-35 retinoic acid receptor, beta Mus musculus 55-82
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 nucleophosmin 1 Homo sapiens 17-21
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 factor interacting with PAPOLA and CPSF1 Homo sapiens 39-45
33959758-0 2021 Roles of Stra8 and Tcerg1l in retinoic acid induced spermatogonial differentiation in mouse. Tretinoin 30-43 transcription elongation regulator 1-like Mus musculus 19-26
32527063-3 2020 Retinoic acid (RA)/sonic hedgehog (Shh)-induced embryonic stem cells differentiation into motor neurons are employed to study up-regulation of Crabp1 by Shh. Tretinoin 0-13 cellular retinoic acid binding protein 1 Homo sapiens 143-149
32527063-3 2020 Retinoic acid (RA)/sonic hedgehog (Shh)-induced embryonic stem cells differentiation into motor neurons are employed to study up-regulation of Crabp1 by Shh. Tretinoin 15-17 cellular retinoic acid binding protein 1 Homo sapiens 143-149
32125053-0 2020 RXRalpha and MRTF-A have a synergistic effect in the retinoic acid-induced neural-like differentiation of adult bone marrow-derived mesenchymal stem cells. Tretinoin 53-66 myocardin related transcription factor A Homo sapiens 13-19
3539326-6 1987 Nucleolar antigen p145 in HL-60 cells was undetectable after 132 h of treatment with retinoic acid. Tretinoin 85-98 POM121 transmembrane nucleoporin Homo sapiens 18-22
33899766-1 2021 ABSTRACT: Preferentially expressed antigen in melanoma (PRAME) is a tumor-associated repressor of retinoic acid signaling which is expressed in melanoma and has emerged as a potential biomarker for malignant behavior in melanocytic neoplasms. Tretinoin 98-111 PRAME nuclear receptor transcriptional regulator Homo sapiens 56-61
2425004-2 1986 A 200% increase in CRABP levels, measured by the ability of the protein to bind retinoic acid, was observed in the normal skin during treatment. Tretinoin 80-93 cellular retinoic acid binding protein 1 Homo sapiens 19-24
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 164-177 Yes1 associated transcriptional regulator Homo sapiens 32-35
33165749-0 2021 Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA). Tretinoin 112-135 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
33165749-0 2021 Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA). Tretinoin 137-141 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
33165749-5 2021 We demonstrated here that Vav1 sustains the maturation to beta-cells of the normal precursors human Biliary Tree Stem/progenitor Cells (hBTSCs) induced by a differentiation medium containing ATRA and that, in the mature normal pancreas, insulin-producing cells express variable levels of Vav1. Tretinoin 191-195 vav guanine nucleotide exchange factor 1 Homo sapiens 26-30
33165749-6 2021 Using pancreatic ductal adenocarcinoma (PDAC)-derived cells, we also revealed that the ATRA induced up-modulation of Vav1 is essential for the retinoid-induced trans-differentiation of neoplastic cells into insulin producing cells. Tretinoin 87-91 vav guanine nucleotide exchange factor 1 Homo sapiens 117-121
33165749-7 2021 The results of this study identify Vav1 as crucial molecule in ATRA induced maturation of insulin producing cells and suggest this protein as a marker for new strategies ended to restore functional beta-cells. Tretinoin 63-67 vav guanine nucleotide exchange factor 1 Homo sapiens 35-39
32125053-4 2020 Here, we show that RXRalpha collaborated with myocardin-related transcription factor-A (MRTF-A) to strongly promote the RA-induced process as evidenced by the increase in NF-H expression and NF-H promoter transcription activity. Tretinoin 120-122 myocardin related transcription factor A Homo sapiens 46-86
32125053-4 2020 Here, we show that RXRalpha collaborated with myocardin-related transcription factor-A (MRTF-A) to strongly promote the RA-induced process as evidenced by the increase in NF-H expression and NF-H promoter transcription activity. Tretinoin 120-122 myocardin related transcription factor A Homo sapiens 88-94
32125053-7 2020 These findings reveal the important roles of RXRalpha and MRTF-A signaling in RA-induced neural-like differentiation of MSCs and describe a new mechanism underlying the synergistic interaction of RXRalpha and MRTF-A. Tretinoin 78-80 myocardin related transcription factor A Homo sapiens 58-64
32125053-7 2020 These findings reveal the important roles of RXRalpha and MRTF-A signaling in RA-induced neural-like differentiation of MSCs and describe a new mechanism underlying the synergistic interaction of RXRalpha and MRTF-A. Tretinoin 78-80 myocardin related transcription factor A Homo sapiens 209-215
3962900-4 1986 The identity of retinoyl beta-glucuronide was confirmed by its conversion to retinoic acid by the action of beta-glucuronidase and by study of the mass spectrum of the methylated derivative. Tretinoin 77-90 glucuronidase beta Homo sapiens 108-126
33531433-0 2021 Retinoic acid production, regulation, and containment through Zic1, Pitx2c and Cyp26c1 control cranial placode specification. Tretinoin 0-13 Zic family member 1 S homeolog Xenopus laevis 62-66
33531433-0 2021 Retinoic acid production, regulation, and containment through Zic1, Pitx2c and Cyp26c1 control cranial placode specification. Tretinoin 0-13 cytochrome P450 family 26 subfamily C member 1 S homeolog Xenopus laevis 79-86
33531433-2 2021 In Xenopus, Zic1 non-cell autonomously regulates PPR formation by activating retinoic acid (RA) production. Tretinoin 77-90 Zic family member 1 S homeolog Xenopus laevis 12-16
33531433-2 2021 In Xenopus, Zic1 non-cell autonomously regulates PPR formation by activating retinoic acid (RA) production. Tretinoin 92-94 Zic family member 1 S homeolog Xenopus laevis 12-16
33531433-3 2021 Here we identified two Zic1 targets, the RA catabolizing enzyme Cyp26c1 and the transcription factor Pitx2c, expressed in the vicinity of the PPR as crucially required for maintaining low RA levels in a spatially restricted, PPR-adjacent domain. Tretinoin 41-43 Zic family member 1 S homeolog Xenopus laevis 23-27
33531433-3 2021 Here we identified two Zic1 targets, the RA catabolizing enzyme Cyp26c1 and the transcription factor Pitx2c, expressed in the vicinity of the PPR as crucially required for maintaining low RA levels in a spatially restricted, PPR-adjacent domain. Tretinoin 41-43 cytochrome P450 family 26 subfamily C member 1 S homeolog Xenopus laevis 64-71
3714826-0 1986 Lack of inhibition of ultraviolet radiation-induced ornithine decarboxylase activity by retinoic acid. Tretinoin 88-101 ornithine decarboxylase 1 Homo sapiens 52-75
33531433-3 2021 Here we identified two Zic1 targets, the RA catabolizing enzyme Cyp26c1 and the transcription factor Pitx2c, expressed in the vicinity of the PPR as crucially required for maintaining low RA levels in a spatially restricted, PPR-adjacent domain. Tretinoin 188-190 Zic family member 1 S homeolog Xenopus laevis 23-27
33531433-3 2021 Here we identified two Zic1 targets, the RA catabolizing enzyme Cyp26c1 and the transcription factor Pitx2c, expressed in the vicinity of the PPR as crucially required for maintaining low RA levels in a spatially restricted, PPR-adjacent domain. Tretinoin 188-190 cytochrome P450 family 26 subfamily C member 1 S homeolog Xenopus laevis 64-71
33531433-7 2021 We propose that Zic1 anteriorly establishes a program of RA containment and regulation through activation of Cyp26c1 and Pitx2c that cooperates to promote PPR specification in a spatially restricted domain. Tretinoin 57-59 Zic family member 1 S homeolog Xenopus laevis 16-20
33576062-10 2021 Additionally, FSK and ATRA ameliorated oxidative stress and inflammation, reduced TGF-beta1 levels and reversed the effect of BLM on the mRNA expression of Ptch-1, Smo and Gli-2. Tretinoin 22-26 patched 1 Rattus norvegicus 156-162
3007157-3 1986 The presence of cellular retinoic acid binding protein (cRABP) was indicated by the cellular uptake of [3H]all-trans-retinoic acid. Tretinoin 110-130 cellular retinoic acid binding protein 1 Homo sapiens 16-54
33581110-4 2021 CRISPR-Cas9-mediated deletion of CBE+47 significantly upregulated HoxA expression and enhanced early ESC differentiation induced by retinoic acid (RA) relative to wild-type cells. Tretinoin 147-149 homeobox A cluster Homo sapiens 66-70
33581110-7 2021 Furthermore, deletion of those adjacent enhancers synergistically inhibited HoxA activation, suggesting that these enhancers serve as an EEIC required for RA-induced HoxA activation. Tretinoin 155-157 homeobox A cluster Homo sapiens 76-80
33581110-7 2021 Furthermore, deletion of those adjacent enhancers synergistically inhibited HoxA activation, suggesting that these enhancers serve as an EEIC required for RA-induced HoxA activation. Tretinoin 155-157 homeobox A cluster Homo sapiens 166-170
33581110-8 2021 Collectively, these results provide new insight into RA-induced HoxA expression during early ESC differentiation, also highlight precise regulatory roles of the CTCF-binding element in orchestrating high-order chromatin structure. Tretinoin 53-55 homeobox A cluster Homo sapiens 64-68
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 0-13 cytochrome P450, family 3, subfamily A, polypeptide 65 Danio rerio 24-31
3007157-3 1986 The presence of cellular retinoic acid binding protein (cRABP) was indicated by the cellular uptake of [3H]all-trans-retinoic acid. Tretinoin 110-130 cellular retinoic acid binding protein 1 Homo sapiens 56-61
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 0-13 ELOVL fatty acid elongase 6 Danio rerio 73-79
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 151-164 cytochrome P450, family 3, subfamily A, polypeptide 65 Danio rerio 24-31
3099098-7 1986 The changes in PK-C activity in TPA + RA-treated cells were accompanied by Ca2+/phospholipid(PL)-dependent phosphorylation in vitro of pp38 which is characteristic of treatment with RA alone, as well as the Ca2+/PL-independent phosphorylation in vitro of pp82 and pp130 (vinculin) which is prevalent in cells treated continuously with TPA alone and is absent in RA-treated cells. Tretinoin 38-40 vinculin Homo sapiens 271-279
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 151-164 ELOVL fatty acid elongase 6 Danio rerio 73-79
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 187-200 cytochrome P450, family 3, subfamily A, polypeptide 65 Danio rerio 24-31
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 187-200 ELOVL fatty acid elongase 6 Danio rerio 73-79
3161611-8 1985 Cells treated with DMSO and RA also exhibited a PL-Ca-dependent pp21 which was barely evident in 1,25(OH)2D3-treated cells and thus represented a myeloid cell marker. Tretinoin 28-30 transcription elongation factor A like 1 Homo sapiens 64-68
33044585-12 2021 Meanwhile, ATRA could reduce the interaction between KLF5 and RARalpha, thereby inhibiting the function of cis-elements of KLF5. Tretinoin 11-15 Kruppel like factor 5 Homo sapiens 53-57
33585479-7 2021 Importantly, a miR-4680-3p-specific inhibitor normalized cell proliferation and altered expression of ERBB2 and JADE1 in cells treated with atRA. Tretinoin 140-144 jade family PHD finger 1 Homo sapiens 112-117
33585479-8 2021 Taken together, our results suggest that upregulation of miR-4680-3p induced by atRA may cause cleft palate through suppression of ERBB2 and JADE1. Tretinoin 80-84 jade family PHD finger 1 Homo sapiens 141-146
33495541-0 2021 Intracellular alpha-fetoprotein interferes with all-trans retinoic acid induced ATG7 expression and autophagy in hepatocellular carcinoma cells. Tretinoin 58-71 autophagy related 7 Homo sapiens 80-84
33495541-7 2021 The results showed that ATRA dosage and time-dependently induced high levels of cell autophagy in both the PLC/PRF/5 and HLE cells, which was accompanied with up-regulation of ATG7. Tretinoin 24-28 autophagy related 7 Homo sapiens 176-180
33495541-9 2021 Impairment of ATG7 induction or blockade of autophagy with chloroquine aggravated ATRA induced apoptosis of HCC cells. Tretinoin 82-86 autophagy related 7 Homo sapiens 14-18
2581807-2 1985 Histamine H2 receptor activity (cAMP generation) has been characterized in U-937 cells before and after retinoic acid-induced differentiation into monocyte-/macrophage-like cells. Tretinoin 104-117 histamine receptor H2 Homo sapiens 0-21
33495541-11 2021 Knockdown of AFP in PLC/PRF/5 cells augmented the up-regulation of ATG7 by ATRA while overexpression of AFP in HLE cells attenuated ATRA induced ATG7 expression and autophagy. Tretinoin 75-79 autophagy related 7 Homo sapiens 67-71
33495541-11 2021 Knockdown of AFP in PLC/PRF/5 cells augmented the up-regulation of ATG7 by ATRA while overexpression of AFP in HLE cells attenuated ATRA induced ATG7 expression and autophagy. Tretinoin 132-136 autophagy related 7 Homo sapiens 145-149
33495541-12 2021 Thus, ATRA induced ATG7 and autophagy participated in its cytotoxicity on HCC cells and AFP interfere with the induction of ATG7 and autophagy through forming complex with RAR. Tretinoin 6-10 autophagy related 7 Homo sapiens 19-23
33495541-12 2021 Thus, ATRA induced ATG7 and autophagy participated in its cytotoxicity on HCC cells and AFP interfere with the induction of ATG7 and autophagy through forming complex with RAR. Tretinoin 6-10 autophagy related 7 Homo sapiens 124-128
2992894-6 1985 Retinol and RA might be translocated to nuclei by their respective binding proteins [cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP)]: isolated EC nuclei have specific, independent binding sites for both holoproteins but not their ligands. Tretinoin 12-14 retinol binding protein 1 Homo sapiens 85-117
33177108-8 2021 Supplementation with RA could significantly delay tumor growth, with reduced arginase 1-expressing myeloid cells, increased CD8P+P and granzyme BP+P T cells in both colitis-associated and implanted MC38 mouse CRC models. Tretinoin 21-23 arginase, liver Mus musculus 77-87
2992894-6 1985 Retinol and RA might be translocated to nuclei by their respective binding proteins [cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP)]: isolated EC nuclei have specific, independent binding sites for both holoproteins but not their ligands. Tretinoin 12-14 retinol binding protein 1 Homo sapiens 119-123
33006416-5 2021 Previous studies using murine brown/beige adipocytes revealed that Ucp1 expression levels are directly increased by forskolin and all-trans retinoic acid (RA). Tretinoin 130-153 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 67-71
2992894-6 1985 Retinol and RA might be translocated to nuclei by their respective binding proteins [cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP)]: isolated EC nuclei have specific, independent binding sites for both holoproteins but not their ligands. Tretinoin 12-14 cellular retinoic acid binding protein 1 Homo sapiens 129-167
33006416-5 2021 Previous studies using murine brown/beige adipocytes revealed that Ucp1 expression levels are directly increased by forskolin and all-trans retinoic acid (RA). Tretinoin 155-157 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 67-71
2992894-6 1985 Retinol and RA might be translocated to nuclei by their respective binding proteins [cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP)]: isolated EC nuclei have specific, independent binding sites for both holoproteins but not their ligands. Tretinoin 12-14 cellular retinoic acid binding protein 1 Homo sapiens 169-174
6322972-1 1984 We investigated the ability of retinoic acid (RA) to alter the binding of epidermal growth factor (EGF) to Rat-1 and Swiss mouse 3T3 cells, the EGF-related induction of ornithine decarboxylase (ODC) activity and DNA synthesis. Tretinoin 31-44 epidermal growth factor like 1 Rattus norvegicus 74-97
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 240-263 high mobility group box 1 Homo sapiens 129-134
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 265-269 high mobility group box 1 Homo sapiens 129-134
6322972-1 1984 We investigated the ability of retinoic acid (RA) to alter the binding of epidermal growth factor (EGF) to Rat-1 and Swiss mouse 3T3 cells, the EGF-related induction of ornithine decarboxylase (ODC) activity and DNA synthesis. Tretinoin 31-44 epidermal growth factor like 1 Rattus norvegicus 99-102
6603411-3 1983 Passage of SPA255-26 placental cells in medium containing retinoic acid induced a stable altered phenotype characterized by elevated levels of HCG and PS beta G and a reduced level of HCG alpha. Tretinoin 58-71 surfactant protein A1 Homo sapiens 11-14
33969133-0 2021 Retinoic Acid Correlates with Reduced Serum IL-10 And TGF-beta in Allergic Rhinitis. Tretinoin 0-13 transforming growth factor alpha Homo sapiens 54-62
33969133-1 2021 Background: Retinoic acid (RA) plays a key role in naive T cell differentiation into FOXP3+ Treg cell in the respiratory airways. Tretinoin 12-25 forkhead box P3 Homo sapiens 85-90
33969133-1 2021 Background: Retinoic acid (RA) plays a key role in naive T cell differentiation into FOXP3+ Treg cell in the respiratory airways. Tretinoin 27-29 forkhead box P3 Homo sapiens 85-90
6279709-4 1982 A number of tissues of rats, humans, and other species contain soluble binding proteins with specificity for either retinol (cellular retinol-binding protein, CRBP) or retinoic acid (cellular retinoic acid-binding protein, CRABP). Tretinoin 168-181 cellular retinoic acid binding protein 1 Homo sapiens 223-228
33969133-7 2021 Conclusion: Our data suggest that RA may influence AR risk via affecting the TGF-beta and IL-10 production. Tretinoin 34-36 transforming growth factor alpha Homo sapiens 77-85
33378690-7 2021 RESULTS: PN induced a unique gene expression profile in mDC, including the gene that encodes retinaldehyde dehydrogenase 2 (RALDH2), a rate-limiting enzyme in the retinoic acid (RA)-producing pathway. Tretinoin 163-176 decorin Mus musculus 56-59
33378690-7 2021 RESULTS: PN induced a unique gene expression profile in mDC, including the gene that encodes retinaldehyde dehydrogenase 2 (RALDH2), a rate-limiting enzyme in the retinoic acid (RA)-producing pathway. Tretinoin 124-126 decorin Mus musculus 56-59
33378690-10 2021 Naive Th cells co-cultured with PN-stimulated mDC showed an RA-dependent 4-fold increase in production of IL-5 and expression of integrin alpha4beta7. Tretinoin 60-62 decorin Mus musculus 46-49
32771670-10 2020 While treatment with all-trans retinoic acid (ATRA), epidermal growth factor (EGF), and basic fibroblast growth factor (FGF) significantly induced NeuN expression in the differentiated NPCs (P < 0.01), the addition of ox-LDL significantly inhibited the NeuN expression (P < 0.05). Tretinoin 21-44 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 147-151
32771670-10 2020 While treatment with all-trans retinoic acid (ATRA), epidermal growth factor (EGF), and basic fibroblast growth factor (FGF) significantly induced NeuN expression in the differentiated NPCs (P < 0.01), the addition of ox-LDL significantly inhibited the NeuN expression (P < 0.05). Tretinoin 21-44 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 253-257
32771670-10 2020 While treatment with all-trans retinoic acid (ATRA), epidermal growth factor (EGF), and basic fibroblast growth factor (FGF) significantly induced NeuN expression in the differentiated NPCs (P < 0.01), the addition of ox-LDL significantly inhibited the NeuN expression (P < 0.05). Tretinoin 46-50 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 147-151
32771670-10 2020 While treatment with all-trans retinoic acid (ATRA), epidermal growth factor (EGF), and basic fibroblast growth factor (FGF) significantly induced NeuN expression in the differentiated NPCs (P < 0.01), the addition of ox-LDL significantly inhibited the NeuN expression (P < 0.05). Tretinoin 46-50 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 253-257
33459508-1 2020 BACKGROUND: To investigate whether folic acid (FA) can rescue anorectal malformations (ARMs) induced by all-trans retinoic acid (ATRA) in rats. Tretinoin 104-127 glycogen synthase kinase 3 beta Rattus norvegicus 47-49
33459508-1 2020 BACKGROUND: To investigate whether folic acid (FA) can rescue anorectal malformations (ARMs) induced by all-trans retinoic acid (ATRA) in rats. Tretinoin 129-133 glycogen synthase kinase 3 beta Rattus norvegicus 47-49
33459508-12 2020 CONCLUSION: Taken together, FA rescued ARMs induced by ATRA in rats. Tretinoin 55-59 glycogen synthase kinase 3 beta Rattus norvegicus 28-30
33255695-5 2020 This effect was significantly higher when cells were treated with retinoic acid (RA) to induce neuroectodermal lineage, studied through the gene and protein expression of nestin, an undifferentiated progenitor marker from the neuroectoderm lineage, as established by nestin mRNA and protein regulation. Tretinoin 66-79 nestin Rattus norvegicus 171-177
33255695-5 2020 This effect was significantly higher when cells were treated with retinoic acid (RA) to induce neuroectodermal lineage, studied through the gene and protein expression of nestin, an undifferentiated progenitor marker from the neuroectoderm lineage, as established by nestin mRNA and protein regulation. Tretinoin 66-79 nestin Rattus norvegicus 267-273
32949975-16 2020 We detected several affected genes, most notably, the Cyp26 enzymes that control endogenous ATRA concentration, which documents an effect on retinoid signalling. Tretinoin 92-96 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 54-59
32964418-7 2020 ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO). Tretinoin 0-4 high mobility group box 1 Mus musculus 89-94
32569741-10 2020 Besides, the mRNA level of Spp1, were down-regulated at E16.5 and the protein were down-regulated at E15.5 and E16.5 in all-trans retinoic acid group, suggesting that atRA may involve in palatal bone formation by regulating Spp1. Tretinoin 130-143 secreted phosphoprotein 1 Mus musculus 27-31
33113971-6 2020 Among the genes that were affected by TCDD, there are functionally related gene groups that suggest an interplay between retinoic acid, AhR, and Wnt signaling pathways. Tretinoin 121-134 aryl hydrocarbon receptor Homo sapiens 136-139
32638255-0 2020 All-trans retinoic acid increases NF-kappaB activity in PMA-stimulated THP-1 cells upon unmethylated CpG challenge by enhancing cell surface TLR9 expression. Tretinoin 0-23 toll like receptor 9 Homo sapiens 141-145
32638255-6 2020 To determine the mechanism involved in increasing in the NF-kappaB activity of stimulated THP-1 cells, we examined the effects of PMA and ATRA on the expression of TLR9 (a receptor of ODN2006) in THP-1 cells. Tretinoin 138-142 toll like receptor 9 Homo sapiens 164-168
32638255-8 2020 However, ATRA synergistically enhanced the cell surface TLR9 expression of PMA-differentiated cells. Tretinoin 9-13 toll like receptor 9 Homo sapiens 56-60
32638255-9 2020 To determine whether the ATRA-enhanced NF-kappaB activity is due to the enhanced cell surface TLR9 expression, we examined NF-kappaB activity after treatment with anti-TLR9 blocking antibody. Tretinoin 25-29 toll like receptor 9 Homo sapiens 94-98
32638255-9 2020 To determine whether the ATRA-enhanced NF-kappaB activity is due to the enhanced cell surface TLR9 expression, we examined NF-kappaB activity after treatment with anti-TLR9 blocking antibody. Tretinoin 25-29 toll like receptor 9 Homo sapiens 168-172
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 86-90 toll like receptor 9 Homo sapiens 31-35
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 86-90 toll like receptor 9 Homo sapiens 210-214
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 136-140 toll like receptor 9 Homo sapiens 31-35
32638255-10 2020 Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-kappaB activity, suggesting that ATRA enhances NF-kappaB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. Tretinoin 136-140 toll like receptor 9 Homo sapiens 210-214
32785847-6 2020 Glioma cells treated with retinoic acid increased the differentiation status with concomitant increased expression of brachyury. Tretinoin 26-39 T-box transcription factor 1 Homo sapiens 118-127
32785847-8 2020 We observed that both exogenous and endogenous brachyury activation, through overexpression and retinoic acid treatment, are associated with TMZ sensitization in glioma-resistant cell lines. Tretinoin 96-109 T-box transcription factor 1 Homo sapiens 47-56
31820845-8 2020 In addition, ATRA induced ISG15 gene expression in NB4 APL cells, leading to increased levels of both free ISG15 protein and ISG15 conjugates. Tretinoin 13-17 ISG15 ubiquitin like modifier Homo sapiens 26-31
31820845-8 2020 In addition, ATRA induced ISG15 gene expression in NB4 APL cells, leading to increased levels of both free ISG15 protein and ISG15 conjugates. Tretinoin 13-17 ISG15 ubiquitin like modifier Homo sapiens 107-112
31820845-8 2020 In addition, ATRA induced ISG15 gene expression in NB4 APL cells, leading to increased levels of both free ISG15 protein and ISG15 conjugates. Tretinoin 13-17 ISG15 ubiquitin like modifier Homo sapiens 107-112
31820845-9 2020 UBE2L6 depletion attenuated ATRA-induced ISG15 conjugation. Tretinoin 28-32 ISG15 ubiquitin like modifier Homo sapiens 41-46
31820845-10 2020 Knockdown of ISG15 in NB4 APL cells inhibited ISGylation and also attenuated ATRA-induced differentiation. Tretinoin 77-81 ISG15 ubiquitin like modifier Homo sapiens 13-18
32017313-1 2020 Preferentially expressed antigen in melanoma (PRAME) is cancer/testis antigen and a transcriptional repressor, inhibiting the signaling of retinoic acid through the retinoic acid receptor (RAR) for promoting cell proliferation and preventing cell apoptosis in cancer cells. Tretinoin 139-152 PRAME like, X-linked 1 Mus musculus 46-51
32017313-1 2020 Preferentially expressed antigen in melanoma (PRAME) is cancer/testis antigen and a transcriptional repressor, inhibiting the signaling of retinoic acid through the retinoic acid receptor (RAR) for promoting cell proliferation and preventing cell apoptosis in cancer cells. Tretinoin 165-178 PRAME like, X-linked 1 Mus musculus 46-51
32397071-10 2020 The mRNA levels of IL-6, IL-1beta, TNF-alpha, and autophagy-related genes were detected after adding niacin, shRNA, compound C, trans retinoic acid, 3-methyladenine to BMECs. Tretinoin 134-147 interferon beta-2 Bos taurus 19-23
32384653-6 2020 ATRA induces a non-canonical type of viral mimicry, which results in increased expression of the IRF1 (Interferon Responsive Factor 1) transcription factor and the DTX3L (Deltex-E3-Ubiquitin-Ligase-3L) downstream effector. Tretinoin 0-4 deltex E3 ubiquitin ligase 3L Homo sapiens 164-169
32384653-6 2020 ATRA induces a non-canonical type of viral mimicry, which results in increased expression of the IRF1 (Interferon Responsive Factor 1) transcription factor and the DTX3L (Deltex-E3-Ubiquitin-Ligase-3L) downstream effector. Tretinoin 0-4 deltex E3 ubiquitin ligase 3L Homo sapiens 171-200
32384653-7 2020 Functional knockdown studies indicate that IRF1 and DTX3L are part of a negative feedback loop controlling ATRA-dependent growth inhibition of breast cancer cells. Tretinoin 107-111 deltex E3 ubiquitin ligase 3L Homo sapiens 52-57
32431691-4 2020 ATRA also increased IL-4 induced phosphorylation of signal transducer and activator of transcription 6 (STAT6) and mRNA expression of the chloride channel, calcium activated, family member 1 (CLCA1), important for mucus formation, and chemokine (C-C motif) ligand 26 (CCL26), a potent eosinophil chemoattractant. Tretinoin 0-4 chloride channel accessory 1 Homo sapiens 138-190
32431691-5 2020 We extended these findings to human Mphi THP-1 cells and showed that ATRA synergistically increased IL-4-induced CCL2, CCL13, and CCL26 mRNA and protein levels. Tretinoin 69-73 C-C motif chemokine ligand 13 Homo sapiens 119-124
7193082-1 1980 Human colon adenocarcinomas and adjacent non-cancerous, normal colon from the same patient were assayed for the presence and amounts of cellular binding proteins for retinol (CRBP) and retinoic acid (CRABP) by sucrose gradient analysis. Tretinoin 185-198 cellular retinoic acid binding protein 1 Homo sapiens 200-205
32075938-15 2020 These IRF5-deficient cells exhibited impaired influenza-induced cytokine production and revealed that IRF5 acts downstream of Toll-like receptor 7 and possibly retinoic acid-inducible gene-I. Tretinoin 160-173 interferon regulatory factor 5 Homo sapiens 6-10
32075938-15 2020 These IRF5-deficient cells exhibited impaired influenza-induced cytokine production and revealed that IRF5 acts downstream of Toll-like receptor 7 and possibly retinoic acid-inducible gene-I. Tretinoin 160-173 interferon regulatory factor 5 Homo sapiens 102-106
984876-5 1976 In human skin homogenates, LDH-, GAPDH-, and G-6-PDH-activities were inhibited by retinoic acid whereas GOT-, LAP-, and ALD-activites remained practically unchanged following an incubation with retinoic acid in concentrations between 1 and 100 mug/ml for 60 min.--The data collected in this study were briefly discussed with regard to the use of retinoic acid and its derivatives in psoriasis. Tretinoin 82-95 hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase Homo sapiens 45-52
32020743-0 2020 Regulation of Gdnf expression by retinoic acid in Sertoli cells. Tretinoin 33-46 glial cell line derived neurotrophic factor Mus musculus 14-18
33757404-8 2021 RA shifted the polarization away from the M1 state by negative regulation of IKKalpha/beta, p65, and miR-21. Tretinoin 0-2 RELA proto-oncogene, NF-kB subunit Homo sapiens 92-95
32020743-2 2020 During the cycle of the seminiferous epithelium, their relative concentration oscillates with lower GDNF levels in stages where RA levels are high. Tretinoin 128-130 glial cell line derived neurotrophic factor Mus musculus 100-104
32020743-3 2020 It has been recently shown that RA negatively regulates Gdnf expression but the mechanisms behind are so far unknown. Tretinoin 32-34 glial cell line derived neurotrophic factor Mus musculus 56-60
32020743-4 2020 Here, we show that RA directly downregulates Gdnf mRNA levels in primary murine Sertoli cells through binding of RARalpha to a novel DR5-RARE on Gdnf promoter. Tretinoin 19-21 glial cell line derived neurotrophic factor Mus musculus 45-49
32020743-4 2020 Here, we show that RA directly downregulates Gdnf mRNA levels in primary murine Sertoli cells through binding of RARalpha to a novel DR5-RARE on Gdnf promoter. Tretinoin 19-21 glial cell line derived neurotrophic factor Mus musculus 145-149
32020743-5 2020 Pharmacological inhibition and chromatin immunoprecipitation-quantitative polymerase chain reaction analysis suggested that the underlying mechanism involved histone deacetylase activity and epigenetic repression of Gdnf promoter upon RA treatment. Tretinoin 235-237 glial cell line derived neurotrophic factor Mus musculus 216-220
33757404-9 2021 RA hindered the phosphorylation of IKKalpha/beta, translocation of p65 into the nucleus, and the subsequent upregulation of miR-21. Tretinoin 0-2 RELA proto-oncogene, NF-kB subunit Homo sapiens 67-70
31953222-9 2020 Reduced retinoic acid receptor (RXRalpha) signaling also increases conjunctival monocyte infiltration, IFN-gamma expression and goblet cell loss. Tretinoin 8-21 retinoid X receptor alpha Mus musculus 32-40
33988253-7 2021 Among the other relevant CNVs, a deletion encompassing HSD17B6, a gene connected with the retinoic acid signaling pathway, whose dysregulation has been implicated in craniofacial malformations, was also identified. Tretinoin 90-103 hydroxysteroid 17-beta dehydrogenase 6 Homo sapiens 55-62
32109521-0 2020 Retinoic acid induced cytokines are selectively modulated by liver X receptor activation in zebrafish. Tretinoin 0-13 nuclear receptor subfamily 1, group H, member 3 Danio rerio 61-77
33991687-9 2021 Also, RPPA data, combined with results of transcriptome profiling, uncovered defects in the retinoic acid (RA) metabolism pathway in FRDA samples. Tretinoin 92-105 frataxin Homo sapiens 133-137
32256976-3 2020 Using the HL-60 human non-APL AML model where ATRA causes nuclear enrichment of c-Raf that drives differentiation/G0-arrest, we now observe that roscovitine enhanced nuclear enrichment of certain traditionally cytoplasmic signaling molecules and enhanced differentiation and cell cycle arrest. Tretinoin 46-50 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 80-85
32256976-4 2020 Roscovitine upregulated ATRA-induced nuclear c-Raf phosphorylation at S259 and S289/296/301. Tretinoin 24-28 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 45-50
32256976-6 2020 ATRA-induced loss of pS608RB with cell cycle arrest was associated with loss of RB-sequestered c-Raf, thereby coupling cell cycle arrest and increased availability of c-Raf to promote differentiation. Tretinoin 0-4 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 95-100
33556379-4 2021 RA-differentiation induced an upregulation of ace2 and tmprss2 gene expression while inducing downregulation of ctsb and ctsl. Tretinoin 0-2 angiotensin converting enzyme 2 Homo sapiens 46-50
33616147-2 2021 Herein, we report a nano-educator (NE) that when loaded with all trans retinoic acid (ATRA) and anti-PD-1 antibodies (aPD-1) instructs myeloid cells to assist T cells towards revitalizing anti-PD-1 therapy. Tretinoin 65-84 programmed cell death 1 Homo sapiens 119-123
31811682-0 2020 All-trans retinoic acid (ATRA)-induced TFEB expression is required for myeloid differentiation in acute promyelocytic leukemia (APL). Tretinoin 0-23 transcription factor EB Homo sapiens 39-43
31811682-0 2020 All-trans retinoic acid (ATRA)-induced TFEB expression is required for myeloid differentiation in acute promyelocytic leukemia (APL). Tretinoin 25-29 transcription factor EB Homo sapiens 39-43
31811682-9 2020 CONCLUSIONS: We show for the first time that TFEB plays an important role in ATRA-induced autophagy during myeloid differentiation and that autophagy induction potentiates leukemic cell differentiation (Note: this study includes data obtained from NCT00195156, https://clinicaltrials.gov/show/NCT00195156). Tretinoin 77-81 transcription factor EB Homo sapiens 45-49
33616147-3 2021 In vivo, ATRA converts myeloid-derived suppressor cells (MDSCs) into dendritic cells (DCs), which are essential for anti-PD-1 therapy, while intervening in the polarization of macrophages. Tretinoin 9-13 programmed cell death 1 Homo sapiens 121-125
33631212-4 2021 The homeodomain transcription factor ISX controls the activity of the vitamin A-forming enzyme BCO1 in intestinal enterocytes in response to increasing concentration of the vitamin A metabolite retinoic acid. Tretinoin 194-207 beta-carotene oxygenase 1 Mus musculus 95-99
32194732-11 2020 Furthermore, ADH7 and CYP26B1 were enriched in the retinoic acid metabolic process and the retinol metabolism pathway. Tretinoin 51-64 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 13-17
33531433-7 2021 We propose that Zic1 anteriorly establishes a program of RA containment and regulation through activation of Cyp26c1 and Pitx2c that cooperates to promote PPR specification in a spatially restricted domain. Tretinoin 57-59 cytochrome P450 family 26 subfamily C member 1 S homeolog Xenopus laevis 109-116
32190725-1 2020 We investigated the expression of OCC-1 at mRNA level during retinoic acid (RA) induced differentiation of mouse embryonic carcinoma P19 pluripotent cancer cells by quantitative real time PCR (qPCR). Tretinoin 61-74 RIKEN cDNA 1500009L16 gene Mus musculus 34-39
32190725-1 2020 We investigated the expression of OCC-1 at mRNA level during retinoic acid (RA) induced differentiation of mouse embryonic carcinoma P19 pluripotent cancer cells by quantitative real time PCR (qPCR). Tretinoin 76-78 RIKEN cDNA 1500009L16 gene Mus musculus 34-39
32190725-5 2020 Data analysis revealed that the expression of OCC-1 was reduced by about 69% after 4-day treatment with RA, when significant down-regulation of key pluripotency factors, including OCT4 and Nanog was observed [1]. Tretinoin 104-106 RIKEN cDNA 1500009L16 gene Mus musculus 46-51
32190725-5 2020 Data analysis revealed that the expression of OCC-1 was reduced by about 69% after 4-day treatment with RA, when significant down-regulation of key pluripotency factors, including OCT4 and Nanog was observed [1]. Tretinoin 104-106 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 180-184
32918369-9 2021 We also presented evidence that Chd1 is regulated by retinoic acid signaling during craniofacial development. Tretinoin 53-66 chromodomain helicase DNA binding protein 1 Homo sapiens 32-36
33506002-0 2020 Administration of All-Trans Retinoic Acid to Pregnant Sows Improves the Developmental Defects of Hoxa1-/- Fetal Pigs. Tretinoin 18-41 homeobox A1 Sus scrofa 97-102
32149119-6 2020 Among them, NTRK2 is the only one that was dramatically upregulated in the RT-qPCR test that we performed on ATRA-treated SH-SY5Y-A cells. Tretinoin 109-113 neurotrophic receptor tyrosine kinase 2 Homo sapiens 12-17
31913463-3 2020 We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1.Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. Tretinoin 291-304 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 218-225
33506002-1 2020 Hoxa1 mutation adversely affect fetal pig development, but whether all-trans retinoic acid (ATRA) administration to Hoxa1+/- pregnant sows can improve Hoxa1-/- fetal pig development defects has not been reported. Tretinoin 67-90 homeobox A1 Sus scrofa 116-121
33506002-1 2020 Hoxa1 mutation adversely affect fetal pig development, but whether all-trans retinoic acid (ATRA) administration to Hoxa1+/- pregnant sows can improve Hoxa1-/- fetal pig development defects has not been reported. Tretinoin 67-90 homeobox A1 Sus scrofa 116-121
31841694-1 2020 As a member of tumor necrosis factor receptor (TNFR)-associated factor (TRAF) family, TRAF3 is an important regulator of NF-kappaB and type I interferon (IFN) activation, especially in Toll-like receptors (TLRs)- and retinoic acid inducible gene I (RIG-I)-like receptors (RLRs)-mediated signaling pathway. Tretinoin 217-230 TNF receptor-associated factor 3 Larimichthys crocea 86-91
33506002-1 2020 Hoxa1 mutation adversely affect fetal pig development, but whether all-trans retinoic acid (ATRA) administration to Hoxa1+/- pregnant sows can improve Hoxa1-/- fetal pig development defects has not been reported. Tretinoin 92-96 homeobox A1 Sus scrofa 116-121
31959382-0 2020 Regulation of skin fibrosis by RALDH1-producing dermal dendritic cells via retinoic acid-mediated regulatory T cell induction: A role in scleroderma. Tretinoin 75-88 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 31-37
33506002-1 2020 Hoxa1 mutation adversely affect fetal pig development, but whether all-trans retinoic acid (ATRA) administration to Hoxa1+/- pregnant sows can improve Hoxa1-/- fetal pig development defects has not been reported. Tretinoin 92-96 homeobox A1 Sus scrofa 116-121
31959382-10 2020 Importantly, RALDH1/ALDH1A1 enzyme oxidizing retinaldehyde to retinoic acid, an inducer of Tregs, was preferentially expressed by CD11b-CD103- DCs and its expression levels were elevated in bleomycin-injected skin lesions, to a greater extent in Cd103-/- mice than in wild-type mice. Tretinoin 62-75 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 13-19
33506002-3 2020 ATRA was orally administered to pregnant sows at the doses of 0, 4, 5, or 6 mg/kg maternal body weight on 12, 13, and 14 days post coitum (dpc), respectively, and a total of 146 live piglets were delivered including 37 Hoxa1-/- piglets and 109 non-Hoxa1-/- piglets. Tretinoin 0-4 homeobox A1 Sus scrofa 219-224
31959382-10 2020 Importantly, RALDH1/ALDH1A1 enzyme oxidizing retinaldehyde to retinoic acid, an inducer of Tregs, was preferentially expressed by CD11b-CD103- DCs and its expression levels were elevated in bleomycin-injected skin lesions, to a greater extent in Cd103-/- mice than in wild-type mice. Tretinoin 62-75 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 20-27
33506002-3 2020 ATRA was orally administered to pregnant sows at the doses of 0, 4, 5, or 6 mg/kg maternal body weight on 12, 13, and 14 days post coitum (dpc), respectively, and a total of 146 live piglets were delivered including 37 Hoxa1-/- piglets and 109 non-Hoxa1-/- piglets. Tretinoin 0-4 homeobox A1 Sus scrofa 248-253
33506002-6 2020 The time of ATRA administration significantly affected Hoxa1-/- fetal development (P < 0.05). Tretinoin 12-16 homeobox A1 Sus scrofa 55-60
33506002-7 2020 Administration of ATRA to Hoxa1+/- pregnant sows at 4 mg/kg body weight on 14 dpc can effectively improve the birth liveweight and ear defects of Hoxa1-/- piglets. Tretinoin 18-22 homeobox A1 Sus scrofa 26-31
32089684-3 2020 All-trans retinoic acid (atRA, the active form of vitamin A) inhibits the adipogenic differentiation of BMSCs through its receptor RARG. Tretinoin 0-23 retinoic acid receptor gamma Homo sapiens 131-135
33506002-7 2020 Administration of ATRA to Hoxa1+/- pregnant sows at 4 mg/kg body weight on 14 dpc can effectively improve the birth liveweight and ear defects of Hoxa1-/- piglets. Tretinoin 18-22 homeobox A1 Sus scrofa 146-151
32089684-3 2020 All-trans retinoic acid (atRA, the active form of vitamin A) inhibits the adipogenic differentiation of BMSCs through its receptor RARG. Tretinoin 25-29 retinoic acid receptor gamma Homo sapiens 131-135
32089684-11 2020 The results supported the conclusion that atRA inhibits BMSC adipogenesis partially through the RARG-FRA1-PPARG2 or the CEBPA axis or both. Tretinoin 42-46 retinoic acid receptor gamma Homo sapiens 96-100
32818607-5 2021 The mRNA expressions of amh and sycp3 were downregulated, the retinoic acid content increased at later stage of starvation through the transcriptional regulation of aldh1a2 and cyp26a1. Tretinoin 62-75 aldehyde dehydrogenase 1 family, member A2 Danio rerio 165-172
31735076-10 2020 The membrane fraction from MYL4-/- human embryonic stem cell derived atrial cells demonstrated increased phospho-Cx43, which was further accentuated by retinoic acid treatment and by the presence of risk alleles at the Pitx2 locus. Tretinoin 152-165 myosin light chain 4 Homo sapiens 27-31
31735076-10 2020 The membrane fraction from MYL4-/- human embryonic stem cell derived atrial cells demonstrated increased phospho-Cx43, which was further accentuated by retinoic acid treatment and by the presence of risk alleles at the Pitx2 locus. Tretinoin 152-165 gap junction protein alpha 1 Homo sapiens 113-117
32818607-5 2021 The mRNA expressions of amh and sycp3 were downregulated, the retinoic acid content increased at later stage of starvation through the transcriptional regulation of aldh1a2 and cyp26a1. Tretinoin 62-75 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 177-184
33215509-10 2020 RA acted synergistically with insulin to phosphorylate glycogen synthase kinase 3beta, and dephosphorylate glycogen synthase (GS), which was associated with increases in the protein and mRNA levels of GS. Tretinoin 0-2 glycogen synthase kinase 3 beta Rattus norvegicus 55-85
31813960-7 2020 Transcript and protein analyses indicate an enhanced production of retinol and reduced conversion the retinoic acids (unchanged LRAT, Pnpla2/ATGL and Pnpla3 up, Cyp26a1 down) in L-G6pc-/- mice. Tretinoin 102-116 glucose-6-phosphatase, catalytic Mus musculus 180-184
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 protein tyrosine phosphatase, non-receptor type 11 Mus musculus 33-37
32424865-10 2020 Mechanistically, RA could activate the AKT/GSK3beta/beta-catenin pathway during the process of iPSCs osteogenesis. Tretinoin 17-19 glycogen synthase kinase 3 alpha Homo sapiens 43-51
32868073-6 2020 However, massive cell death was observed after retinoic acid treatment, suggesting a role of Ulk1-induced p53 activation in the elimination of defective pluripotent cells prior to differentiation. Tretinoin 47-60 unc-51 like kinase 1 Mus musculus 93-97
32970669-8 2020 Importantly, inhibition of retinoic acid signaling by the aldehyde dehydrogenase (Aldh) and retinoic acid receptor inhibitors promoted Pou4f3 expression in the cochlear tissue and suppressed the progression of hearing loss in the mutant mice. Tretinoin 27-40 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 58-80
32970669-8 2020 Importantly, inhibition of retinoic acid signaling by the aldehyde dehydrogenase (Aldh) and retinoic acid receptor inhibitors promoted Pou4f3 expression in the cochlear tissue and suppressed the progression of hearing loss in the mutant mice. Tretinoin 27-40 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 82-86
32569741-10 2020 Besides, the mRNA level of Spp1, were down-regulated at E16.5 and the protein were down-regulated at E15.5 and E16.5 in all-trans retinoic acid group, suggesting that atRA may involve in palatal bone formation by regulating Spp1. Tretinoin 167-171 secreted phosphoprotein 1 Mus musculus 27-31
32588086-6 2020 Prednisolone inhibited AKR1C3 with an IC50 of 41.73 microM, while ATRA decreased the activity of AKR1B10 (IC50 = 78.33 microM) and AKR1C3 (IC50 = 1.17 microM). Tretinoin 66-70 aldo-keto reductase family 1 member B10 Homo sapiens 97-104
32569741-10 2020 Besides, the mRNA level of Spp1, were down-regulated at E16.5 and the protein were down-regulated at E15.5 and E16.5 in all-trans retinoic acid group, suggesting that atRA may involve in palatal bone formation by regulating Spp1. Tretinoin 167-171 secreted phosphoprotein 1 Mus musculus 224-228
32588086-6 2020 Prednisolone inhibited AKR1C3 with an IC50 of 41.73 microM, while ATRA decreased the activity of AKR1B10 (IC50 = 78.33 microM) and AKR1C3 (IC50 = 1.17 microM). Tretinoin 66-70 aldo-keto reductase family 1 member C3 Homo sapiens 131-137
32588086-7 2020 Subsequent studies showed that AKR1C3 inhibition mediated by ATRA exhibited tight binding (Kiapp = 0.54 microM). Tretinoin 61-65 aldo-keto reductase family 1 member C3 Homo sapiens 31-37
33120845-13 2020 LESSONS: APL patients with STAT5B-RARa is not only resistant to ATRA, but also to conventional combination chemotherapy such as daunorubicin and cytarabine/idarubicin and cytarabine or other regimens. Tretinoin 64-68 signal transducer and activator of transcription 5B Homo sapiens 27-33
32588086-8 2020 Further, the combination of 1 microM ATRA with different concentrations of Dau demonstrated synergistic effects in HCT116 and KG1a human cells expressing AKR1C3. Tretinoin 37-41 aldo-keto reductase family 1 member C3 Homo sapiens 154-160
32588086-9 2020 Our results suggest that ATRA-mediated inhibition of AKR1C3 can contribute to the mechanisms that are hidden beyond the beneficial clinical outcome of the ATRA-Dau combination. Tretinoin 25-29 aldo-keto reductase family 1 member C3 Homo sapiens 53-59
32588086-9 2020 Our results suggest that ATRA-mediated inhibition of AKR1C3 can contribute to the mechanisms that are hidden beyond the beneficial clinical outcome of the ATRA-Dau combination. Tretinoin 155-159 aldo-keto reductase family 1 member C3 Homo sapiens 53-59
32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 nucleoporin 98 and 96 precursor Homo sapiens 113-118
32932813-7 2020 In parallel, the addition of RA to either CD3/CD28 or phorbol myristate acetate (PMA)/ionomycin during QVOA and TILDA, respectively, was shown to augment reactivation of the replication-competent viral reservoir in anti-retroviral therapy (ART)-suppressed RMs as shown by a greater than 2.3-fold increase for QVOA and 1 to 2-fold increments for multi-spliced RNA per million CD4+ T cells. Tretinoin 29-31 CD28 molecule Macaca mulatta 46-50
32329577-8 2020 RESULTS: NOX4, as a novel target of miR-322, was upregulated in ATRA-induced mouse model of NTDs. Tretinoin 64-68 NADPH oxidase 4 Mus musculus 9-13
32932813-9 2020 In addition, flow cytometry analysis revealed that RA improved estimates of various viral reservoir assays by eliciting broad CD4 T-cell activation as demonstrated by elevated CD25 and CD38 but reduced CD69 and PD-1 expressing cells. Tretinoin 51-53 CD69 molecule Sus scrofa 202-206
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 239-252 FERM domain containing 6 Homo sapiens 37-43
31676951-8 2020 Furthermore, CYP26A1 a retinoic acid receptor-specific target was revealed as a new player mediating the suppressive effect of fish oil-supplemented diet on SCD1 and ELOVL6 hepatic gene expression. Tretinoin 23-36 ELOVL family member 6, elongation of long chain fatty acids (yeast) Mus musculus 166-172
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 239-252 FERM domain containing 6 Homo sapiens 44-49
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 254-256 FERM domain containing 6 Homo sapiens 37-43
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 254-256 FERM domain containing 6 Homo sapiens 44-49
32909215-7 2020 CRBP-1+ showed reduced proliferation and viability in basal condition and after atRA treatment when compared to empty-transfected H460 cells. Tretinoin 80-84 retinol binding protein 1 Homo sapiens 0-6
32458204-2 2020 Human SH-SY5Y neuroblastoma-derived cell line is widely used in neuroscience research and is known to undergo neurodifferentiation in the presence of all-trans retinoic acid by upregulating the expression of TrkB, making cells responsive to BDNF. Tretinoin 160-173 neurotrophic receptor tyrosine kinase 2 Homo sapiens 208-212
32705508-2 2020 HEPC-CB.1 cells" potential to differentiate into endothelial cells was revealed after treating the cells with a mixture of ATRA, cAMP and VEGF, as shown by the reduced expression levels of CD133, CD271 and CD90 antigens, augmentation of CD146 and CD31, and a decrease in cell clonogenicity. Tretinoin 123-127 prominin 1 Homo sapiens 189-194
32705508-2 2020 HEPC-CB.1 cells" potential to differentiate into endothelial cells was revealed after treating the cells with a mixture of ATRA, cAMP and VEGF, as shown by the reduced expression levels of CD133, CD271 and CD90 antigens, augmentation of CD146 and CD31, and a decrease in cell clonogenicity. Tretinoin 123-127 platelet and endothelial cell adhesion molecule 1 Homo sapiens 247-251
32909215-10 2020 Restoration of CRBP-1 expression in H460 cells reduced proliferation and viability in both basal condition and after atRA treatment, likely by down-regulating AKT-related gene level. Tretinoin 117-121 retinol binding protein 1 Homo sapiens 15-21
32497314-1 2020 Fenretinide (4-HPR) is a synthetic derivative of All-Trans-Retinoic Acid (ATRA) characterised by improved therapeutic properties and toxicological profile relative to ATRA. Tretinoin 49-72 haptoglobin-related protein Homo sapiens 15-18
32548665-3 2020 Our previous studies found that the impaired retinoic acid signal decreased ALDH1A2, an essential synthetase of ATRA, in the spinal cord of ALS mice. Tretinoin 45-58 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 76-83
32630207-9 2020 We also provide evidence that ATRA enhances hexokinase 2 expression, and shifts the metabolism of LPS-activated macrophages toward glycolysis, leading to the activation of NLRP3 inflammasome. Tretinoin 30-34 hexokinase 2 Homo sapiens 44-56
32587277-7 2020 A retrospective analysis of NTAL expression in a cohort of patients treated with ATRA and anthracyclines, revealed that NTAL overexpression was associated with a high leukocyte count (P = 0.007) and was independently associated with shorter overall survival (Hazard Ratio: 3.6; 95% Confidence Interval: 1.17-11.28; P = 0.026). Tretinoin 81-85 linker for activation of T cells family member 2 Homo sapiens 120-124
32568233-3 2020 Under the conditions defined here, the 2-day embryoid body formation + 6-day retinoic acid induction protocol permits fast and efficient differentiation from mESCs into neural precursor cells (NPCs), as seen by the formation of well-stacked and neurite-like A2lox and 129 derivatives that are Nestin positive. Tretinoin 77-90 nestin Mus musculus 293-299
32497314-1 2020 Fenretinide (4-HPR) is a synthetic derivative of All-Trans-Retinoic Acid (ATRA) characterised by improved therapeutic properties and toxicological profile relative to ATRA. Tretinoin 74-78 haptoglobin-related protein Homo sapiens 15-18
32849526-3 2020 In the intestine, dendritic cells (DCs) play an important role in inducing Tregs specific to oral antigens, and they efficiently induce Tregs via production of retinoic acid (RA), a vitamin A metabolite, catalyzed by the enzyme retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 160-173 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 228-257
32173553-5 2020 The ERRgamma agonist GSK4716 increased DAT and TH expression, and the ERRgamma inverse agonist GSK5182 attenuated the retinoic acid-induced upregulation of DAT and TH in differentiated SH-SY5Y cells. Tretinoin 118-131 estrogen related receptor gamma Homo sapiens 70-78
32849526-3 2020 In the intestine, dendritic cells (DCs) play an important role in inducing Tregs specific to oral antigens, and they efficiently induce Tregs via production of retinoic acid (RA), a vitamin A metabolite, catalyzed by the enzyme retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 160-173 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 259-265
31987884-3 2020 Within the hyperplastic epidermis of TPA- or ATRA-treated or BCC-bearing murine skin, Wif1 and K10 overlap in Ki67neg suprabasal layers, while basal epidermal layers expressing Ki67, and BCCs expressing Wif1 mRNA, are free of Wif1 protein. Tretinoin 45-49 endothelin receptor type B modifier 1 Mus musculus 95-98
32302545-5 2020 Finally, we find that retinoic acid controls the spatiotemporal dynamics of Hgf/Met signaling to coordinate axon targeting with the developmental progression of the pharyngeal arches and show that experimentally altering the timing of Hgf/Met signaling is sufficient to redirect axon targeting and disrupt the topographic map. Tretinoin 22-35 MET proto-oncogene, receptor tyrosine kinase Danio rerio 80-83
32302545-5 2020 Finally, we find that retinoic acid controls the spatiotemporal dynamics of Hgf/Met signaling to coordinate axon targeting with the developmental progression of the pharyngeal arches and show that experimentally altering the timing of Hgf/Met signaling is sufficient to redirect axon targeting and disrupt the topographic map. Tretinoin 22-35 MET proto-oncogene, receptor tyrosine kinase Danio rerio 239-242
32006898-7 2020 In conclusion, DAC plus ATRA regimen might be effective and well-tolerated for elderly patients partially through modulating miR-34a/MYCN axis. Tretinoin 24-28 microRNA 34a Homo sapiens 125-132
32615991-9 2020 Western blot analysis indicated that protein levels of retinoic acid receptor alpha (RARalpha), MMP2, MMP9, and AT1 were dramatically affected by ATRA treatment. Tretinoin 146-150 matrix metallopeptidase 9 Mus musculus 102-106
32615991-10 2020 CONCLUSIONS: In conclusion, ATRA attenuates the progression of Ang II-induced AAAs, possibly by downregulating MMP2, MMP9, and AT-1 expression. Tretinoin 28-32 matrix metallopeptidase 9 Mus musculus 117-121
32240712-3 2020 In this study, we show that spermatogonial differentiation induced by retinoic acid (RA) was accompanied with increased migration ability and elevated expression of connective tissue growth factor (CTGF), a member of the CCN family. Tretinoin 70-83 cellular communication network factor 2 Mus musculus 165-196
32201329-9 2020 Interestingly, the suppressing effect of As (III) appeared to be partially reversible, and supplementation of all trans retinoic acid (t-RA) doses dependently restored mucin gene expression. Tretinoin 114-133 LOC100508689 Homo sapiens 168-173
32201329-9 2020 Interestingly, the suppressing effect of As (III) appeared to be partially reversible, and supplementation of all trans retinoic acid (t-RA) doses dependently restored mucin gene expression. Tretinoin 135-139 LOC100508689 Homo sapiens 168-173
32240712-3 2020 In this study, we show that spermatogonial differentiation induced by retinoic acid (RA) was accompanied with increased migration ability and elevated expression of connective tissue growth factor (CTGF), a member of the CCN family. Tretinoin 70-83 cellular communication network factor 2 Mus musculus 198-202
32240712-3 2020 In this study, we show that spermatogonial differentiation induced by retinoic acid (RA) was accompanied with increased migration ability and elevated expression of connective tissue growth factor (CTGF), a member of the CCN family. Tretinoin 85-87 cellular communication network factor 2 Mus musculus 165-196
31731254-4 2020 The results showed that 10 nM ATRA sufficiently inhibited cell proliferation, which might be through downregulation of cyclin D1 (P < 0.05) and cyclin-dependent kinase 4 (P < 0.05) and proliferating cell nuclear antigen protein (P < 0.05) abundance. Tretinoin 30-34 proliferating cell nuclear antigen Ovis aries 191-225
32240712-3 2020 In this study, we show that spermatogonial differentiation induced by retinoic acid (RA) was accompanied with increased migration ability and elevated expression of connective tissue growth factor (CTGF), a member of the CCN family. Tretinoin 85-87 cellular communication network factor 2 Mus musculus 198-202
32240712-6 2020 Moreover, depletion of CTGF by neutralizing antibody inhibited the elevated migration ability induced by RA, suggesting both the paracrine and autocrine roles of CTGF in spermatogonial migration associated with differentiation. Tretinoin 105-107 cellular communication network factor 2 Mus musculus 23-27
32240712-6 2020 Moreover, depletion of CTGF by neutralizing antibody inhibited the elevated migration ability induced by RA, suggesting both the paracrine and autocrine roles of CTGF in spermatogonial migration associated with differentiation. Tretinoin 105-107 cellular communication network factor 2 Mus musculus 162-166
32217463-8 2020 After RA treatment, chromatin immunoprecipitation assays using an antibody against NCOR1, revealed that NCOR1 binding to RARbeta promoters was significantly lower in Sirt1-/- mESCs than in Sirt1+/+ mESCs, and luciferase reporter assays showed SIRT1 knockdown decreased RA-induced RARalpha activity. Tretinoin 6-8 nuclear receptor co-repressor 1 Mus musculus 104-109
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 89-94
32217463-8 2020 After RA treatment, chromatin immunoprecipitation assays using an antibody against NCOR1, revealed that NCOR1 binding to RARbeta promoters was significantly lower in Sirt1-/- mESCs than in Sirt1+/+ mESCs, and luciferase reporter assays showed SIRT1 knockdown decreased RA-induced RARalpha activity. Tretinoin 121-123 nuclear receptor co-repressor 1 Mus musculus 83-88
32217463-8 2020 After RA treatment, chromatin immunoprecipitation assays using an antibody against NCOR1, revealed that NCOR1 binding to RARbeta promoters was significantly lower in Sirt1-/- mESCs than in Sirt1+/+ mESCs, and luciferase reporter assays showed SIRT1 knockdown decreased RA-induced RARalpha activity. Tretinoin 121-123 nuclear receptor co-repressor 1 Mus musculus 104-109
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 vav guanine nucleotide exchange factor 1 Homo sapiens 214-217
32256976-8 2020 Roscovitine also enhanced the ATRA-induced nuclear enrichment of other signaling molecules traditionally perceived as cytoplasmic promoters of proliferation, but now known to promote differentiation; in particular: SFKs, Lyn, Fgr; adaptor proteins, c-Cbl, SLP-76; a guanine exchange factor, Vav1; and a transcription factor, IRF-1. Tretinoin 30-34 vav guanine nucleotide exchange factor 1 Homo sapiens 291-295
32032659-4 2020 Roscovitine enhanced ATRA-induced c-Raf interaction with Lyn, Vav, and c-Cbl. Tretinoin 21-25 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 34-39
32258025-0 2020 Inhibition of GSK3 Represses the Expression of Retinoic Acid Synthetic Enzyme ALDH1A2 via Wnt/beta-Catenin Signaling in WiT49 Cells. Tretinoin 47-60 wingless-type MMTV integration site family, member 1 Mus musculus 90-93
32032659-4 2020 Roscovitine enhanced ATRA-induced c-Raf interaction with Lyn, Vav, and c-Cbl. Tretinoin 21-25 vav guanine nucleotide exchange factor 1 Homo sapiens 62-65
32258025-10 2020 Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/beta-catenin signaling in fetal kidney cells, suggesting that Wnt/beta-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development. Tretinoin 302-315 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 27-34
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 79-84
32258025-10 2020 Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/beta-catenin signaling in fetal kidney cells, suggesting that Wnt/beta-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development. Tretinoin 302-315 wingless-type MMTV integration site family, member 1 Mus musculus 79-82
32258025-10 2020 Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/beta-catenin signaling in fetal kidney cells, suggesting that Wnt/beta-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development. Tretinoin 302-315 wingless-type MMTV integration site family, member 1 Mus musculus 145-148
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 92-97
32258025-10 2020 Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/beta-catenin signaling in fetal kidney cells, suggesting that Wnt/beta-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development. Tretinoin 302-315 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 219-226
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 92-97
31697927-7 2020 KLF15 and tight junction protein levels increased with retinoic acid treatment. Tretinoin 55-68 Kruppel like factor 15 Homo sapiens 0-5
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 vav guanine nucleotide exchange factor 1 Homo sapiens 120-124
32428701-9 2020 All-trans retinoic acid (ATRA) protects MSCs from apoptosis by downregulating miR-98-5p, thus providing a potential therapeutic approach for ITP. Tretinoin 0-23 microRNA 98 Mus musculus 78-84
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 annexin A3 Rattus norvegicus 158-161
31830774-8 2020 RESULTS: Rare DNA variants in transcriptional regulators involved in retinoic acid signaling (NCOR2, OMIM *600848 and EP300, OMIM *602700) were found to be associated with immunophenotype. Tretinoin 69-82 nuclear receptor corepressor 2 Homo sapiens 94-99
31732869-2 2020 RA signaling is mediated by nuclear retinoic acid receptors, alpha, beta, and gamma (RARalpha, RARbeta, and RARgamma). Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 95-102
31732869-2 2020 RA signaling is mediated by nuclear retinoic acid receptors, alpha, beta, and gamma (RARalpha, RARbeta, and RARgamma). Tretinoin 36-49 retinoic acid receptor, beta Mus musculus 95-102
32087738-14 2020 Furthermore, we found that retinoic acid increased expression of miR-506-3p and repressed expression of MYCN and PLAGL2. Tretinoin 27-40 PLAG1 like zinc finger 2 Homo sapiens 113-119
31830774-9 2020 CONCLUSION: The expression of TBX1, which seems to confer the major phenotypic features of 22q11.2DS, is regulated via retinoic acid signaling, and alterations in retinoic acid signaling during embryonic development can lead to phenocopies of 22q11.2DS. Tretinoin 119-132 T-box transcription factor 1 Homo sapiens 30-34
31830774-9 2020 CONCLUSION: The expression of TBX1, which seems to confer the major phenotypic features of 22q11.2DS, is regulated via retinoic acid signaling, and alterations in retinoic acid signaling during embryonic development can lead to phenocopies of 22q11.2DS. Tretinoin 163-176 T-box transcription factor 1 Homo sapiens 30-34
32087738-15 2020 CONCLUSIONS: Our findings altogether suggest that the interplay network formed by PLAGL2, MYCN and miR-506-3p is an important mechanism in regulating neuroblastoma cell fate, determining neuroblastoma prognosis, and mediating the therapeutic function of retinoic acid. Tretinoin 254-267 PLAG1 like zinc finger 2 Homo sapiens 82-88
32030959-17 2020 qRT-PCR test showed that the combined use of ATRA and Ad-VEGF also increased the relative mRNA expressions of early-stage osteogenesis-related markers ALP, OPN, and collagen type I ( P<0.05); the relative mRNA expressions of angiogenesis-related markers VEGF, EMCN, and ANGPT1 increased at 7 days ( P<0.05). Tretinoin 45-49 secreted phosphoprotein 1 Mus musculus 156-159
32030959-18 2020 Immunohistochemical staining showed that ATRA combined with Ad-VEGF not only enhanced OPN protein expression, but also increased VEGF protein expression on 7th day. Tretinoin 41-45 secreted phosphoprotein 1 Mus musculus 86-89
32428701-9 2020 All-trans retinoic acid (ATRA) protects MSCs from apoptosis by downregulating miR-98-5p, thus providing a potential therapeutic approach for ITP. Tretinoin 25-29 microRNA 98 Mus musculus 78-84
31913463-3 2020 We show here that retinoic acid signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1.Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into retinoic acid. Tretinoin 18-31 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 218-225
32385093-5 2020 Odor/air stimulates CYP26B1 expression in olfactory sensory neurons mainly located in the dorsomedial OE, which is spatially inverse to ventrolateral constitutive expression of the retinoic acid-synthesizing enzyme (RALDH1) in supporting cells. Tretinoin 181-194 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 216-222
32302545-0 2020 Retinoic Acid Organizes the Zebrafish Vagus Motor Topographic Map via Spatiotemporal Coordination of Hgf/Met Signaling. Tretinoin 0-13 MET proto-oncogene, receptor tyrosine kinase Danio rerio 105-108
31879367-4 2020 In this study, we show that endogenous expression of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) is required for OPC generation and differentiation in the postnatal subcortical white matter. Tretinoin 57-70 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 96-125
32366851-2 2020 Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). Tretinoin 34-47 TANK-binding kinase 1 Mus musculus 167-188
31879367-4 2020 In this study, we show that endogenous expression of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) is required for OPC generation and differentiation in the postnatal subcortical white matter. Tretinoin 57-70 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 127-133
31879367-4 2020 In this study, we show that endogenous expression of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) is required for OPC generation and differentiation in the postnatal subcortical white matter. Tretinoin 72-74 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 96-125
31879367-4 2020 In this study, we show that endogenous expression of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) is required for OPC generation and differentiation in the postnatal subcortical white matter. Tretinoin 72-74 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 127-133
31879367-9 2020 We demonstrate that loss of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) decreased the number and differentiation of OL precursor cells (OPCs), leading to a deficit in OLs. Tretinoin 32-45 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 71-100
31879367-9 2020 We demonstrate that loss of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) decreased the number and differentiation of OL precursor cells (OPCs), leading to a deficit in OLs. Tretinoin 32-45 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 102-108
31879367-9 2020 We demonstrate that loss of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) decreased the number and differentiation of OL precursor cells (OPCs), leading to a deficit in OLs. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 71-100
31879367-9 2020 We demonstrate that loss of the retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) decreased the number and differentiation of OL precursor cells (OPCs), leading to a deficit in OLs. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 102-108
31449909-6 2019 Knockdown of another RA binding partner fatty acid binding protein 5 (Fabp5), did not alter these behaviors. Tretinoin 21-23 fatty acid binding protein 5 Rattus norvegicus 40-68
31586630-5 2019 In Peyer"s patches (PP), ATRA/TGF-beta MPs up-regulated tolerogenic dendritic cells (tolDCs) (CD11c+CD11b-CD103+), while the proportion of mature dendritic cells was not altered. Tretinoin 25-29 transforming growth factor, beta 1 Mus musculus 30-38
31586630-5 2019 In Peyer"s patches (PP), ATRA/TGF-beta MPs up-regulated tolerogenic dendritic cells (tolDCs) (CD11c+CD11b-CD103+), while the proportion of mature dendritic cells was not altered. Tretinoin 25-29 integrin alpha X Mus musculus 94-99
32158187-2 2020 We have shown that bone morphogenetic protein-2 (BMP-2) can only partially antagonize the inhibitive effects of ATRA. Tretinoin 112-116 bone morphogenetic protein 2 Homo sapiens 19-47
32158187-2 2020 We have shown that bone morphogenetic protein-2 (BMP-2) can only partially antagonize the inhibitive effects of ATRA. Tretinoin 112-116 bone morphogenetic protein 2 Homo sapiens 49-54
31682623-4 2019 When XX germ cells at embryonic day (E) 12.5 were cultured with RA, the extracellular-signal-regulated kinase (ERK) 1/2 pathway was predominantly activated. Tretinoin 64-66 mitogen-activated protein kinase 3 Mus musculus 72-119
32366851-2 2020 Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). Tretinoin 34-47 TANK-binding kinase 1 Mus musculus 190-194
31682623-5 2019 MEK1/2 inhibitor (U0126) treatment suppressed the mRNA expressions of RA-induced Stra8 and meiotic marker genes (Rec8, Spo11, Dmc1, and Sycp3) in both XX and XY fetal germ cells. Tretinoin 70-72 mitogen-activated protein kinase kinase 1 Mus musculus 0-6
32158187-11 2020 Conclusion: The antagonist of RARalpha, ER-50891 could significantly attenuate ATRA"s inhibitive effects on BMP 2-induced osteoblastogenesis. Tretinoin 79-83 bone morphogenetic protein 2 Homo sapiens 108-113
31682623-5 2019 MEK1/2 inhibitor (U0126) treatment suppressed the mRNA expressions of RA-induced Stra8 and meiotic marker genes (Rec8, Spo11, Dmc1, and Sycp3) in both XX and XY fetal germ cells. Tretinoin 70-72 REC8 meiotic recombination protein Mus musculus 113-117
31950055-0 2019 All-Trans Retinoic Acid Enhances Bacterial Flagellin-Stimulated Proinflammatory Responses in Human Monocyte THP-1 Cells by Upregulating CD14. Tretinoin 0-23 CD14 molecule Homo sapiens 136-140
31950055-6 2019 To determine the mechanisms underlying the ATRA-enhanced immune response against bacterial flagellin despite the reduced cell surface expression of TLR5 in ATRA-treated THP-1, we examined the cell surface expression of CD14, which has been proposed to be a TLR co-receptor that enhances the response to microbial components. Tretinoin 43-47 CD14 molecule Homo sapiens 219-223
31682623-5 2019 MEK1/2 inhibitor (U0126) treatment suppressed the mRNA expressions of RA-induced Stra8 and meiotic marker genes (Rec8, Spo11, Dmc1, and Sycp3) in both XX and XY fetal germ cells. Tretinoin 70-72 DNA meiotic recombinase 1 Mus musculus 126-130
31682623-7 2019 Taken together, our results suggest the novel concept that the RA functions by stimulating the ERK1/2 pathway and that this activity is critical for Stra8 expression and meiotic progression in fetal germ cells. Tretinoin 63-65 mitogen-activated protein kinase 3 Mus musculus 95-101
32006898-0 2020 Decitabine and all-trans retinoic acid synergistically exhibit cytotoxicity against elderly AML patients via miR-34a/MYCN axis. Tretinoin 15-38 microRNA 34a Homo sapiens 109-116
32006898-6 2020 Meanwhile, we found DAC and ATRA inhibited DNMT1, activated miR-34a via promoter hypomethylation, down-regulated its target MYCN and thus exerted a synergistic antineoplastic effect. Tretinoin 28-32 microRNA 34a Homo sapiens 60-67
32295802-7 2020 Actually, commensal bacteria were shown to control expression of Aldh1a1, which encodes a retinoic acid-producing enzyme and plays an important role in the maintenance of intestinal homeostasis via DNA methylation in the overlapping 5" region of Tmem267 and 3110070M22Rik genes in CoECs. Tretinoin 90-103 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 65-72
31856916-9 2019 Interestingly, RA treatment led to attenuation of H3K27me3 due to cooperate between UTX and Suz12, affecting Hox gene regulation. Tretinoin 15-17 SUZ12 polycomb repressive complex 2 subunit Mus musculus 92-97
32290523-0 2020 All-trans Retinoic Acid-induced Abnormal Hippocampal Expression of Synaptic Genes SynDIG1 and DLG2 is Correlated with Anxiety or Depression-Like Behavior in Mice. Tretinoin 0-23 membrane protein, palmitoylated 2 (MAGUK p55 subfamily member 2) Mus musculus 94-98
31544318-0 2019 All-trans retinoic acid exposure increases connexin 43 expression in cumulus cells and improves embryo development in bovine oocytes. Tretinoin 0-23 gap junction protein alpha 1 Bos taurus 43-54
31544318-4 2019 All-trans retinoic acid (ATRA) has been shown to increase CX43 expression in several different cell types. Tretinoin 0-23 gap junction protein alpha 1 Bos taurus 58-62
31544318-4 2019 All-trans retinoic acid (ATRA) has been shown to increase CX43 expression in several different cell types. Tretinoin 25-29 gap junction protein alpha 1 Bos taurus 58-62
31544318-5 2019 In this study we investigated the effect of ATRA treatment, during maturation, on CX43 expression and localization in cumulus cells and the developmental competence of bovine oocytes. Tretinoin 44-48 gap junction protein alpha 1 Bos taurus 82-86
31544318-6 2019 COCs and granulosa cells exposed to ATRA during maturation had significantly higher CX43 expression and increased gap junctional coupling, respectively. Tretinoin 36-40 gap junction protein alpha 1 Bos taurus 84-88
31544318-8 2019 Data from these studies suggest that not only can CX43 be used as a biomarker for oocyte health, it can also potentially be manipulated using ATRA to increase the number of oocytes achieving developmental competence. Tretinoin 142-146 gap junction protein alpha 1 Bos taurus 50-54
31408612-0 2019 APLNR is involved in ATRA-induced growth inhibition of nasopharyngeal carcinoma and may suppress EMT through PI3K-Akt-mTOR signaling. Tretinoin 21-25 apelin receptor Homo sapiens 0-5
31408612-7 2019 Moreover, ingenuity pathway analysis revealed that an indirect interaction existed between APLNR and retinoic acid (RA) in the cancer regulatory network. Tretinoin 101-114 apelin receptor Homo sapiens 91-96
31408612-7 2019 Moreover, ingenuity pathway analysis revealed that an indirect interaction existed between APLNR and retinoic acid (RA) in the cancer regulatory network. Tretinoin 116-118 apelin receptor Homo sapiens 91-96
31728810-8 2019 In addition, signaling of growth factors including VEGF, PDGF, and IGF1, and retinoic acid signaling were activated in the SATB2 and NRG1 lines, respectively. Tretinoin 77-90 neuregulin 1 Homo sapiens 133-137
32290523-6 2020 In the hippocampus, DLG2 mRNA was significantly decreased by ATRA. Tretinoin 61-65 membrane protein, palmitoylated 2 (MAGUK p55 subfamily member 2) Mus musculus 20-24
32290523-11 2020 To summarize, ATRA administration induced anxiety- and depression-like behavior accompanied by a decreased expression of DLG2 and an increased expression of SynDIG1. Tretinoin 14-18 membrane protein, palmitoylated 2 (MAGUK p55 subfamily member 2) Mus musculus 121-125
31728066-0 2019 Publisher Correction: A new regulatory mechanism for Raf kinase activation, retinoic acid-bound Crabp1. Tretinoin 76-89 zinc fingers and homeoboxes 2 Homo sapiens 53-56
32260461-0 2020 Dysbacteriosis-Derived Lipopolysaccharide Causes Embryonic Osteopenia through Retinoic-Acid-Regulated DLX5 Expression. Tretinoin 78-91 distal-less homeobox 5 Mus musculus 102-106
31728066-0 2019 Publisher Correction: A new regulatory mechanism for Raf kinase activation, retinoic acid-bound Crabp1. Tretinoin 76-89 cellular retinoic acid binding protein 1 Homo sapiens 96-102
31700049-6 2019 Additionally, we reveal that all trans retinoic acid (ATRA) induces VCP expression, creating a positive feedback loop that enhances degradation. Tretinoin 33-52 valosin containing protein Homo sapiens 68-71
31700049-6 2019 Additionally, we reveal that all trans retinoic acid (ATRA) induces VCP expression, creating a positive feedback loop that enhances degradation. Tretinoin 54-58 valosin containing protein Homo sapiens 68-71
31606046-8 2019 H1d knockdown primed ATRA-mediated differentiation of OCI-AML3 and U937 AML cell lines, as assessed on CD11b/CD11c markers, morphological and gene expression analyses. Tretinoin 21-25 integrin subunit alpha X Homo sapiens 109-114
31394504-1 2019 Retinoic acid (RA), an active metabolite of Vitamin A, and Bone Morphogenetic Protein 4 (BMP-4) pathways control the transcription of Proopiomelanocortin (POMC), the precursor of ACTH. Tretinoin 0-13 pro-opiomelanocortin-alpha Mus musculus 134-153
31394504-1 2019 Retinoic acid (RA), an active metabolite of Vitamin A, and Bone Morphogenetic Protein 4 (BMP-4) pathways control the transcription of Proopiomelanocortin (POMC), the precursor of ACTH. Tretinoin 0-13 pro-opiomelanocortin-alpha Mus musculus 155-159
31394504-1 2019 Retinoic acid (RA), an active metabolite of Vitamin A, and Bone Morphogenetic Protein 4 (BMP-4) pathways control the transcription of Proopiomelanocortin (POMC), the precursor of ACTH. Tretinoin 0-13 pro-opiomelanocortin-alpha Mus musculus 179-183
31394504-1 2019 Retinoic acid (RA), an active metabolite of Vitamin A, and Bone Morphogenetic Protein 4 (BMP-4) pathways control the transcription of Proopiomelanocortin (POMC), the precursor of ACTH. Tretinoin 15-17 pro-opiomelanocortin-alpha Mus musculus 134-153
31682623-0 2019 Retinoic acid-stimulated ERK1/2 pathway regulates meiotic initiation in cultured fetal germ cells. Tretinoin 0-13 mitogen-activated protein kinase 3 Mus musculus 25-31
31394504-1 2019 Retinoic acid (RA), an active metabolite of Vitamin A, and Bone Morphogenetic Protein 4 (BMP-4) pathways control the transcription of Proopiomelanocortin (POMC), the precursor of ACTH. Tretinoin 15-17 pro-opiomelanocortin-alpha Mus musculus 155-159
32260461-9 2020 The addition of RA suppressed Dlx5 expression in MC3T3-E1 cells, as was also seen when exposed to LPS. Tretinoin 16-18 distal-less homeobox 5 Mus musculus 30-34
31394504-1 2019 Retinoic acid (RA), an active metabolite of Vitamin A, and Bone Morphogenetic Protein 4 (BMP-4) pathways control the transcription of Proopiomelanocortin (POMC), the precursor of ACTH. Tretinoin 15-17 pro-opiomelanocortin-alpha Mus musculus 179-183
31370073-8 2019 ATRA-treated platelets demonstrated reduced spreading on immobilized fibrinogen or collagen and reduced thrombin-induced clot retraction together with reduced phosphorylation of Syk and PLCgamma2. Tretinoin 0-4 phospholipase C gamma 2 Homo sapiens 186-195
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 MYCN opposite strand Homo sapiens 49-53
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 MYCN opposite strand Homo sapiens 172-176
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 MYCN opposite strand Homo sapiens 49-53
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 MYCN opposite strand Homo sapiens 172-176
31427086-8 2019 Meanwhile, TAp63 knockdown inhibited ATRA-induced repression of NCYM gene expression. Tretinoin 37-41 MYCN opposite strand Homo sapiens 64-68
31607627-4 2020 TLR3 mediated double stranded RNA sensing is critical for the regeneration, activating retinoic acid signaling following wounding. Tretinoin 87-100 toll like receptor 3 Homo sapiens 0-4
31323146-8 2019 ATRA led to inhibition of p-STAT3, p-JAK2, increased the level of p-ERK, and significantly decreased the PD-L1 expression. Tretinoin 0-4 Janus kinase 2 Homo sapiens 37-41
31370073-10 2019 Further, in platelets stimulated with either collagen-related peptide or thrombin, ATRA selectively inhibited phosphorylation of PKCssI (Ser661) and PKCdelta (Thr505), but not PKCalpha or PKCssII phosphorylation (Thr638/641). Tretinoin 83-87 protein kinase C delta Homo sapiens 149-157
32319369-10 2020 The content of MUC1 protein in Tetrandrine group was significantly lower than that in control group and ATRA group (P<0.05). Tretinoin 104-108 mucin 1, cell surface associated Homo sapiens 15-19
31575075-1 2019 DEAD-box helicase 3, X-linked (DDX3X) regulates the retinoic acid-inducible gene I (RIG-I)-like receptor (RLR)-mediated antiviral response, but can also be a host factor contributing to the replication of viruses of significance to human health, such as human immunodeficiency virus type 1 (HIV-1). Tretinoin 52-65 DEAD-box helicase 3 X-linked Homo sapiens 31-36
31300983-2 2019 In RT-PCR study, ATRA- and lipo-ATRA-treated mice samples showed relatively higher TIG3 expression and decreased PPARgamma expression (Band density) than cancer control. Tretinoin 17-21 peroxisome proliferator activated receptor gamma Mus musculus 113-122
31300983-3 2019 Among treatments, lipo-ATRA showed vital effect than free ATRA by enhancing TIG3 and decreasing PPARgamma. Tretinoin 23-27 peroxisome proliferator activated receptor gamma Mus musculus 96-105
31880511-6 2019 We postulate that ATRA can induce the PHB expression by RARalpha in hypoxia/reperfusion related RTEC injury. Tretinoin 18-22 prohibitin 1 Homo sapiens 38-41
32319369-11 2020 CONCLUSION: Tetrandrine and ATRA can synergize to promote the differentiation and maturation of HL-60 cells, and the mechanism may be related with MUC1 expression. Tretinoin 28-32 mucin 1, cell surface associated Homo sapiens 147-151
31500289-6 2019 Here, we demonstrated that inhibition of Cdc42 or Rac not only prevented growth cone turning toward retinoic acid but could also induce a switch in growth cone responsiveness to chemorepulsion or growth cone collapse. Tretinoin 100-113 cell division cycle 42 Homo sapiens 41-46
31880511-0 2019 All-trans retinoic acid regulated prohibitin by retinoic acid receptor alpha in hypoxia-induced renal tubular epithelial cell injury. Tretinoin 0-23 prohibitin 1 Homo sapiens 34-44
31880511-3 2019 The current study investigated whether ATRA regulated PHB is induced by hypoxia/reoxygenation injury in renal tubular epithelial cells (RTEC), using gene interference treatments (knockdown or overexpression of RARalpha). Tretinoin 39-43 prohibitin 1 Homo sapiens 54-57
31500289-9 2019 These data strongly suggest that Cdc42 and Rac are downstream effectors of retinoic acid during growth cone guidance. Tretinoin 75-88 cell division cycle 42 Homo sapiens 33-38
31880511-4 2019 Our results indicate that ATRA can augment the expression of RARalpha and PHB proteins and reduce the expression of TGF-beta1, FN and Col-IV proteins. Tretinoin 26-30 prohibitin 1 Homo sapiens 74-77
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 18-20 interleukin 23, alpha subunit p19 Mus musculus 60-65
31880511-5 2019 PHB expression was reduced in an ATRA treated RARalpha- group, and TGF-beta1, FN and Col-IV were up-regulated compared to the ATRA treated RARalpha+ group. Tretinoin 33-37 prohibitin 1 Homo sapiens 0-3
31880511-5 2019 PHB expression was reduced in an ATRA treated RARalpha- group, and TGF-beta1, FN and Col-IV were up-regulated compared to the ATRA treated RARalpha+ group. Tretinoin 126-130 prohibitin 1 Homo sapiens 0-3
31557800-6 2019 ATRA attenuated kidney injury through the reduction of proteinuria, renal hypertrophy, increase in natriuresis, as well as early markers of damage such as beta2-microglobulin, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL). Tretinoin 0-4 lipocalin 2 Rattus norvegicus 214-256
31557800-6 2019 ATRA attenuated kidney injury through the reduction of proteinuria, renal hypertrophy, increase in natriuresis, as well as early markers of damage such as beta2-microglobulin, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL). Tretinoin 0-4 lipocalin 2 Rattus norvegicus 258-262
31322186-2 2019 The present study aimed to investigate the role of 3-hydroxy-3-methylglutaryl reductase degradation (Hrd1) in the protective effect of ATRA on human skin fibroblasts exposed to UV. Tretinoin 135-139 synoviolin 1 Homo sapiens 101-105
31322186-7 2019 In addition, ATRA could reverse the increase of Hrd1 expression induced by UV radiation in vivo and in vitro. Tretinoin 13-17 synoviolin 1 Homo sapiens 48-52
31322186-9 2019 Notably, overexpression of Hrd1 abolished the protective effect of ATRA on the UV-induced decrease of Nrf2 expression, the production of reactive oxygen species (ROS) and the decrease of cell viability. Tretinoin 67-71 synoviolin 1 Homo sapiens 27-31
31322186-10 2019 In conclusion, the present data demonstrated that ATRA protected skin fibroblasts against UV-induced oxidative damage through inhibition of E3 ligase Hrd1. Tretinoin 50-54 synoviolin 1 Homo sapiens 150-154
31328782-8 2019 Genes involved in post-meiotic development, transition protein 1 (Tnp1) and protamine 1 (Prm1) were upregulated in the presence of RA. Tretinoin 131-133 sperm protamine P1 Sus scrofa 89-93
31852220-6 2020 RA attenuated calcification in a coordinated manner, increasing levels of the calcification inhibitor MGP (matrix Gla protein) while decreasing calcification-promoting TNAP (tissue nonspecific alkaline phosphatase) activity. Tretinoin 0-2 matrix Gla protein Homo sapiens 102-105
30916783-5 2019 In mice, Gata2 is expressed in the undifferentiated ureteric mesenchyme under control of RA signalling. Tretinoin 89-91 GATA binding protein 2 Mus musculus 9-14
31487780-4 2019 All-trans-A14C (ATA14CA) is just a moderate activator of RAR-transactivation in reporter cell lines but can potently activate retinoic acid response element (RARE)-mediated signalling in DR5/RARE-reporter mice and potently increase retinoid-reporter target gene expression in ATA14CA-supplemented mice and treated MM6 cells. Tretinoin 126-139 tumor necrosis factor receptor superfamily, member 10b Mus musculus 187-190
31221621-6 2019 In particular, the concentrations of the ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) and of retinol dehydrogenase 16 (RDH16), which catalyzes the first step in retinoic acid biogenesis, were highly increased. Tretinoin 184-197 retinol dehydrogenase 16 Sus scrofa 116-140
31852220-6 2020 RA attenuated calcification in a coordinated manner, increasing levels of the calcification inhibitor MGP (matrix Gla protein) while decreasing calcification-promoting TNAP (tissue nonspecific alkaline phosphatase) activity. Tretinoin 0-2 matrix Gla protein Homo sapiens 107-125
31221621-6 2019 In particular, the concentrations of the ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) and of retinol dehydrogenase 16 (RDH16), which catalyzes the first step in retinoic acid biogenesis, were highly increased. Tretinoin 184-197 retinol dehydrogenase 16 Sus scrofa 142-147
31646671-8 2020 Also, a significant upregulation was observed in the expression of AKAP3 gene in the RA + P group on days 0 and 4. Tretinoin 85-87 A kinase (PRKA) anchor protein 3 Mus musculus 67-72
31221621-7 2019 Accordingly, elevated levels of retinoic acid, which stimulates the expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PCK1), were measured in the MIDY samples. Tretinoin 32-45 phosphoenolpyruvate carboxykinase 1 Sus scrofa 142-146
31358819-0 2019 A new regulatory mechanism for Raf kinase activation, retinoic acid-bound Crabp1. Tretinoin 54-67 cellular retinoic acid binding protein 1 Homo sapiens 74-80
31358819-3 2019 We recently reported that all-trans retinoic acid (atRA) rapidly (within minutes) activates Erk1/2 to modulate cell cycle progression in stem cells, which is mediated by cellular retinoic acid binding protein 1 (Crabp1). Tretinoin 26-49 cellular retinoic acid binding protein 1 Homo sapiens 170-210
31358819-3 2019 We recently reported that all-trans retinoic acid (atRA) rapidly (within minutes) activates Erk1/2 to modulate cell cycle progression in stem cells, which is mediated by cellular retinoic acid binding protein 1 (Crabp1). Tretinoin 26-49 cellular retinoic acid binding protein 1 Homo sapiens 212-218
31358819-3 2019 We recently reported that all-trans retinoic acid (atRA) rapidly (within minutes) activates Erk1/2 to modulate cell cycle progression in stem cells, which is mediated by cellular retinoic acid binding protein 1 (Crabp1). Tretinoin 51-55 cellular retinoic acid binding protein 1 Homo sapiens 170-210
31358819-3 2019 We recently reported that all-trans retinoic acid (atRA) rapidly (within minutes) activates Erk1/2 to modulate cell cycle progression in stem cells, which is mediated by cellular retinoic acid binding protein 1 (Crabp1). Tretinoin 51-55 cellular retinoic acid binding protein 1 Homo sapiens 212-218
31056772-4 2019 The expression of Adh1 and Aldh1a2 (alcohol dehydrogenase), two enzymes that convert retinol to retinoic acid in this pathway, were decreased at both the gene and protein levels. Tretinoin 96-109 alcohol dehydrogenase 1C (class I), gamma polypeptide Rattus norvegicus 18-22
31056772-4 2019 The expression of Adh1 and Aldh1a2 (alcohol dehydrogenase), two enzymes that convert retinol to retinoic acid in this pathway, were decreased at both the gene and protein levels. Tretinoin 96-109 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 27-34
31358819-7 2019 However, Crabp1 can also compete with Ras for direct interaction with the RBD of Raf, thereby negatively modulating growth factor-stimulated Raf activation, which can be enhanced by atRA binding to Crabp1. Tretinoin 182-186 cellular retinoic acid binding protein 1 Homo sapiens 9-15
31358819-7 2019 However, Crabp1 can also compete with Ras for direct interaction with the RBD of Raf, thereby negatively modulating growth factor-stimulated Raf activation, which can be enhanced by atRA binding to Crabp1. Tretinoin 182-186 cellular retinoic acid binding protein 1 Homo sapiens 198-204
31187490-0 2020 ALDH1A1 in patient-derived bladder cancer spheroids activates retinoic acid signaling leading to TUBB3 overexpression and tumor progression. Tretinoin 62-75 tubulin beta 3 class III Homo sapiens 97-102
31330985-1 2019 Smith-Magenis syndrome (SMS), linked to Retinoic Acid Induced (RAI1) haploinsufficiency, is a unique model of the inversion of circadian melatonin secretion. Tretinoin 40-53 retinoic acid induced 1 Homo sapiens 63-67
31592201-0 2019 Modulation of alphavbeta3 Integrin via Transactivation of beta3 Integrin Gene on Murine Bone Marrow Macrophages by 1,25(OH)2D3, Retinoic Acid and Interleukin-4. Tretinoin 128-141 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 20-25
30986821-0 2019 The protective variant rs7173049 at LOXL1 locus impacts on retinoic acid signaling pathway in pseudoexfoliation syndrome. Tretinoin 59-72 lysyl oxidase like 1 Homo sapiens 36-41
30986821-6 2019 siRNA-mediated downregulation of retinoic acid signaling induces upregulation of LOXL1 and PEX-associated matrix genes in PEX-relevant cell types. Tretinoin 33-46 lysyl oxidase like 1 Homo sapiens 81-86
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 DNA meiotic recombinase 1 Mus musculus 271-275
30859584-4 2019 Western blot analysis showed the protein level of ERK, phosphorylated ERK, cyclin D1 (CCND1), and cyclin-dependent kinase 2 (CDK2) increased after stimulation with RA, and this effect could also be abolished by U0126. Tretinoin 164-166 cyclin D1 Homo sapiens 75-84
30859584-4 2019 Western blot analysis showed the protein level of ERK, phosphorylated ERK, cyclin D1 (CCND1), and cyclin-dependent kinase 2 (CDK2) increased after stimulation with RA, and this effect could also be abolished by U0126. Tretinoin 164-166 cyclin D1 Homo sapiens 86-91
30859584-4 2019 Western blot analysis showed the protein level of ERK, phosphorylated ERK, cyclin D1 (CCND1), and cyclin-dependent kinase 2 (CDK2) increased after stimulation with RA, and this effect could also be abolished by U0126. Tretinoin 164-166 cyclin dependent kinase 2 Homo sapiens 98-123
31273085-1 2019 Retinoic acid (RA), a metabolite of retinol (vitamin A), functions as a ligand for nuclear RA receptors (RARs) that regulate development of chordate animals. Tretinoin 0-13 arginyl-tRNA synthetase 1 Homo sapiens 105-109
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 protein tyrosine phosphatase, non-receptor type 11 Mus musculus 33-37
31273085-1 2019 Retinoic acid (RA), a metabolite of retinol (vitamin A), functions as a ligand for nuclear RA receptors (RARs) that regulate development of chordate animals. Tretinoin 15-17 arginyl-tRNA synthetase 1 Homo sapiens 91-103
31273085-1 2019 Retinoic acid (RA), a metabolite of retinol (vitamin A), functions as a ligand for nuclear RA receptors (RARs) that regulate development of chordate animals. Tretinoin 0-13 arginyl-tRNA synthetase 1 Homo sapiens 91-103
31273085-1 2019 Retinoic acid (RA), a metabolite of retinol (vitamin A), functions as a ligand for nuclear RA receptors (RARs) that regulate development of chordate animals. Tretinoin 15-17 arginyl-tRNA synthetase 1 Homo sapiens 105-109
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 DNA meiotic recombinase 1 Mus musculus 271-275
31661588-8 2020 In addition, RDH16 increases the level of retinoic acid and blocks the de novo synthesis of fatty acid in HCC cells. Tretinoin 42-55 retinol dehydrogenase 16 Homo sapiens 13-18
31215681-4 2019 Treatment with ATRA during the early and late stage of adipogenesis resulted in an increase in the expression level of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12, respectively, whereas expression of Pgc-1alpha, another gene expressed during brown adipogenesis, was unaffected by ATRA. Tretinoin 15-19 cell death inducing DFFA like effector a Homo sapiens 128-133
31215681-11 2019 SIGNIFICANCE OF THE STUDY: Significance of the study treatment with all-trans retinoic acid (ATRA) during the early and late stage of adipogenesis increased the expression of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12. Tretinoin 68-91 cell death inducing DFFA like effector a Homo sapiens 184-189
31215681-11 2019 SIGNIFICANCE OF THE STUDY: Significance of the study treatment with all-trans retinoic acid (ATRA) during the early and late stage of adipogenesis increased the expression of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12. Tretinoin 93-97 cell death inducing DFFA like effector a Homo sapiens 184-189
31076104-3 2019 FAT1 expression was increased during the retinoic acid (RA)-induced differentiation of NTera2 cells. Tretinoin 41-54 FAT atypical cadherin 1 Homo sapiens 0-4
31076104-3 2019 FAT1 expression was increased during the retinoic acid (RA)-induced differentiation of NTera2 cells. Tretinoin 56-58 FAT atypical cadherin 1 Homo sapiens 0-4
31076104-4 2019 Depletion of FAT1 with siRNA decreased the number of neurites produced after RA treatment. Tretinoin 77-79 FAT atypical cadherin 1 Homo sapiens 13-17
31243280-0 2019 Noncoding dsRNA induces retinoic acid synthesis to stimulate hair follicle regeneration via TLR3. Tretinoin 24-37 toll like receptor 3 Homo sapiens 92-96
30788515-1 2019 RDH1 is one of the several enzymes that catalyze the first of the two reactions to convert retinol into all-trans-retinoic acid (atRA). Tretinoin 104-127 retinol dehydrogenase 1 (all trans) Mus musculus 0-4
30788515-1 2019 RDH1 is one of the several enzymes that catalyze the first of the two reactions to convert retinol into all-trans-retinoic acid (atRA). Tretinoin 129-133 retinol dehydrogenase 1 (all trans) Mus musculus 0-4
31239643-14 2019 However, the combination of notopterol and ATRA enhanced the effect of inducing differentiation when compared with using either notopterol or ATRA alone, which can be evidenced by the increased nucleocytoplasmic ratio, NBT positive cells, and expression of CD14. Tretinoin 43-47 CD14 molecule Homo sapiens 257-261
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 19 Homo sapiens 144-149
31143119-6 2019 Our results also demonstrated that ATRA altered the expression of proliferation-related proteins, including CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 in VSMC. Tretinoin 35-39 cyclin-dependent kinase 6 Mus musculus 154-158
30844294-10 2019 Cells treated with ATRA showed decreased expression of PAK1, PAK2, PAK4, and alpha-smooth muscle actin. Tretinoin 19-23 p21 (RAC1) activated kinase 1 Homo sapiens 55-59
30844294-10 2019 Cells treated with ATRA showed decreased expression of PAK1, PAK2, PAK4, and alpha-smooth muscle actin. Tretinoin 19-23 p21 (RAC1) activated kinase 2 Homo sapiens 61-65
30844294-14 2019 NEW & NOTEWORTHY The inhibitory effect of all-trans retinoic acid (ATRA) on cell proliferation, colony formation, and migration/invasion was associated with downregulation of p21-activated kinases (PAKs), and depletion of PAK1 enhanced ATRA sensitivity in MiaPaCa-2 cells. Tretinoin 46-69 p21 (RAC1) activated kinase 1 Homo sapiens 226-230
30844294-14 2019 NEW & NOTEWORTHY The inhibitory effect of all-trans retinoic acid (ATRA) on cell proliferation, colony formation, and migration/invasion was associated with downregulation of p21-activated kinases (PAKs), and depletion of PAK1 enhanced ATRA sensitivity in MiaPaCa-2 cells. Tretinoin 71-75 p21 (RAC1) activated kinase 1 Homo sapiens 226-230
30996344-0 2019 A novel NPM1-RARG-NPM1 chimeric fusion in acute myeloid leukaemia resembling acute promyelocytic leukaemia but resistant to all-trans retinoic acid and arsenic trioxide. Tretinoin 134-147 nucleophosmin 1 Homo sapiens 8-12
30996344-0 2019 A novel NPM1-RARG-NPM1 chimeric fusion in acute myeloid leukaemia resembling acute promyelocytic leukaemia but resistant to all-trans retinoic acid and arsenic trioxide. Tretinoin 134-147 retinoic acid receptor gamma Homo sapiens 13-17
30996344-0 2019 A novel NPM1-RARG-NPM1 chimeric fusion in acute myeloid leukaemia resembling acute promyelocytic leukaemia but resistant to all-trans retinoic acid and arsenic trioxide. Tretinoin 134-147 nucleophosmin 1 Homo sapiens 18-22
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 244-257 nucleophosmin 1 Homo sapiens 16-20
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 244-257 nucleophosmin 1 Homo sapiens 73-77
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 244-257 retinoic acid receptor gamma Homo sapiens 78-82
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 244-257 nucleophosmin 1 Homo sapiens 73-77
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 259-263 nucleophosmin 1 Homo sapiens 16-20
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 259-263 nucleophosmin 1 Homo sapiens 73-77
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 259-263 retinoic acid receptor gamma Homo sapiens 78-82
30996344-5 2019 Here, we report NPM1 as a new partner gene of RARG and identify a unique NPM1-RARG-NPM1 chimeric fusion for the first time in an old male with morphological and immunophenotypical features of hypergranular APL but lacking response to all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) therapy. Tretinoin 259-263 nucleophosmin 1 Homo sapiens 73-77
30339851-7 2019 Ubiquitin protein ligase E3 component N-recognin 5 (Ubr5) and nuclear receptor subfamily 2 group F member 6 (Nr2f6) expression levels decreased in RhoH-deficient T cells, resulting in increased protein levels and DNA binding activity of retinoic acid-related orphan receptor gammat. Tretinoin 237-250 nuclear receptor subfamily 2, group F, member 6 Mus musculus 62-107
31035455-2 2019 In F9 embryonic carcinoma cells, RA can induce differentiation towards somatic lineages via the Ras-extracellular signal-regulated kinase (Ras/Erk) pathway, but the mechanism through which it induces the Erk1/2 phosphorylation is unclear. Tretinoin 33-35 mitogen-activated protein kinase 3 Mus musculus 204-210
31035455-6 2019 In summary, RA can mediate cell differentiation by phosphorylating Erk1/2 via miR-485 and Abhd2. Tretinoin 12-14 mitogen-activated protein kinase 3 Mus musculus 67-73
30986261-3 2019 We have previously described the PTGDR promoter activation mediated by ATRA through response elements (RARE) at position -549T> C. In this study we aimed to analyze the effect of retinoic acid (RA) on the expression of PTGDR, the production of cytokines as well as to evaluate the binding of RA receptors to RA-Response Elements (RARE) sequences. Tretinoin 182-195 prostaglandin D2 receptor Homo sapiens 33-38
30986261-3 2019 We have previously described the PTGDR promoter activation mediated by ATRA through response elements (RARE) at position -549T> C. In this study we aimed to analyze the effect of retinoic acid (RA) on the expression of PTGDR, the production of cytokines as well as to evaluate the binding of RA receptors to RA-Response Elements (RARE) sequences. Tretinoin 182-195 prostaglandin D2 receptor Homo sapiens 222-227
30986261-3 2019 We have previously described the PTGDR promoter activation mediated by ATRA through response elements (RARE) at position -549T> C. In this study we aimed to analyze the effect of retinoic acid (RA) on the expression of PTGDR, the production of cytokines as well as to evaluate the binding of RA receptors to RA-Response Elements (RARE) sequences. Tretinoin 73-75 prostaglandin D2 receptor Homo sapiens 33-38
30986261-3 2019 We have previously described the PTGDR promoter activation mediated by ATRA through response elements (RARE) at position -549T> C. In this study we aimed to analyze the effect of retinoic acid (RA) on the expression of PTGDR, the production of cytokines as well as to evaluate the binding of RA receptors to RA-Response Elements (RARE) sequences. Tretinoin 73-75 prostaglandin D2 receptor Homo sapiens 222-227
30986261-3 2019 We have previously described the PTGDR promoter activation mediated by ATRA through response elements (RARE) at position -549T> C. In this study we aimed to analyze the effect of retinoic acid (RA) on the expression of PTGDR, the production of cytokines as well as to evaluate the binding of RA receptors to RA-Response Elements (RARE) sequences. Tretinoin 103-105 prostaglandin D2 receptor Homo sapiens 33-38
30986261-3 2019 We have previously described the PTGDR promoter activation mediated by ATRA through response elements (RARE) at position -549T> C. In this study we aimed to analyze the effect of retinoic acid (RA) on the expression of PTGDR, the production of cytokines as well as to evaluate the binding of RA receptors to RA-Response Elements (RARE) sequences. Tretinoin 103-105 prostaglandin D2 receptor Homo sapiens 222-227
30986261-10 2019 However, we found that RA up-regulated PTGDR expression through RARalpha mainly in the CTCT variant. Tretinoin 23-25 prostaglandin D2 receptor Homo sapiens 39-44
30986261-11 2019 Experiments on PBMCs from allergic patients carrying the -549T and -549C variant of the PTGDR promoter after ATRA and RAR antagonist administration confirmed the modulation of PTGDR by ATRA. Tretinoin 109-113 prostaglandin D2 receptor Homo sapiens 88-93
30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 prostaglandin D2 receptor Homo sapiens 137-142
30986261-14 2019 We observed genetic differences in the regulation of PTGDR by ATRA that could contribute to the phenotypic differences observed in allergic patients. Tretinoin 62-66 prostaglandin D2 receptor Homo sapiens 53-58
30728260-8 2019 In summary, our study demonstrates that CRABPs serve as an on-off switch that modulates the efficiency of the HCV life cycle and elucidates how HCV evades the antiviral properties of ATRA via the exploitation of CRABP1 functionality.IMPORTANCE ATRA, a biologically active metabolite of vitamin A, exerts pleiotropic biological effects, including the activation of both innate and adaptive immunity, thereby serving as a potent antimicrobial compound against numerous viral pathogens. Tretinoin 183-187 cellular retinoic acid binding protein 1 Homo sapiens 212-218
30728260-8 2019 In summary, our study demonstrates that CRABPs serve as an on-off switch that modulates the efficiency of the HCV life cycle and elucidates how HCV evades the antiviral properties of ATRA via the exploitation of CRABP1 functionality.IMPORTANCE ATRA, a biologically active metabolite of vitamin A, exerts pleiotropic biological effects, including the activation of both innate and adaptive immunity, thereby serving as a potent antimicrobial compound against numerous viral pathogens. Tretinoin 244-248 cellular retinoic acid binding protein 1 Homo sapiens 212-218
30728260-10 2019 Here, we discovered that the hepatocellular response to ATRA creates either a proviral or an antiviral environment depending on its engagement with CRABP1 or -2, respectively. Tretinoin 56-60 cellular retinoic acid binding protein 1 Homo sapiens 148-154
30926808-4 2019 The balance between this distinctive TH program and canonical FoxP3+ TREGS is unaffected by pattern recognition receptor ligation and is modulated by DC expression of retinoic acid. Tretinoin 167-180 forkhead box P3 Homo sapiens 62-67
30837649-0 2019 ALDH1A1 regulates postsynaptic mu-opioid receptor expression in dorsal striatal projection neurons and mitigates dyskinesia through transsynaptic retinoic acid signaling. Tretinoin 146-159 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-7
30837649-5 2019 Furthermore, RA treatment also upregulates striatal MOR1 levels and signaling and alleviates L-DOPA-induced dyskinetic movements in pituitary homeobox 3 (Pitx3)-deficient mice that lack of ALDH1A1-expressing nDA neurons. Tretinoin 13-15 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 189-196
30837649-6 2019 Therefore, our findings demonstrate that ALDH1A1-synthesized RA is required for postsynaptic MOR1 expression in the postnatal and adult dorsal striatum, supporting potential therapeutic benefits of RA supplementation in moderating L-DOPA-induced dyskinesia. Tretinoin 61-63 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 41-48
30837649-6 2019 Therefore, our findings demonstrate that ALDH1A1-synthesized RA is required for postsynaptic MOR1 expression in the postnatal and adult dorsal striatum, supporting potential therapeutic benefits of RA supplementation in moderating L-DOPA-induced dyskinesia. Tretinoin 198-200 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 41-48
30612000-0 2019 Lipid-polymer nanoparticles with CD133 aptamers for targeted delivery of all-trans retinoic acid to osteosarcoma initiating cells. Tretinoin 83-96 prominin 1 Homo sapiens 33-38
30632787-7 2019 Luciferase intensity of RA response element was lower in CHO-K1 cells transfected with Gen1 siRNA than in those transfected with scrambled RNA, and this inhibitory effect could be reversed by ATRA. Tretinoin 192-196 flap endonuclease GEN homolog 1 Cricetulus griseus 87-91
30476341-7 2019 ATRA and MEHP-exposed testes were depleted of DDX4-positive germ cells but not Sertoli cells. Tretinoin 0-4 DEAD-box helicase 4 Rattus norvegicus 46-50
30709353-0 2019 All-trans retinoic acid inhibits lipopolysaccharide-induced inflammatory responses in bovine adipocytes via TGFbeta1/Smad3 signaling pathway. Tretinoin 0-23 transforming growth factor beta 1 Bos taurus 108-116
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 annexin A3 Rattus norvegicus 158-161
31740384-5 2020 We have determined that both the CDK2 depletion and pharmacological inhibitor of CDK2 significantly sensitize three subtypes of AML cells (including two non-APL cells) to ATRA-induced cell differentiation. Tretinoin 171-175 cyclin dependent kinase 2 Homo sapiens 33-37
30531021-0 2019 MGMT is down-regulated independently of promoter DNA methylation in rats with all-trans retinoic acid-induced spina bifida aperta. Tretinoin 88-101 O-6-methylguanine-DNA methyltransferase Rattus norvegicus 0-4
30250298-7 2019 Finally, ATRA replacement suppressed 15-PGDH inhibition-induced tumor progression in KC mice, and ATRA treatment attenuated Aldh1 activity in tumor cells isolated from the pancreas of 15-Pgdh-/- KC mice. Tretinoin 9-13 hydroxyprostaglandin dehydrogenase 15 (NAD) Mus musculus 37-44
31740384-5 2020 We have determined that both the CDK2 depletion and pharmacological inhibitor of CDK2 significantly sensitize three subtypes of AML cells (including two non-APL cells) to ATRA-induced cell differentiation. Tretinoin 171-175 cyclin dependent kinase 2 Homo sapiens 81-85
31740384-8 2020 Thus, our work not only provides relevant experimental evidence for further validating CDK2 as a target for differentiation therapy, but also uncovers the future clinical application of CDK2 inhibitors in ATRA-based differentiation therapeutics for AML. Tretinoin 205-209 cyclin dependent kinase 2 Homo sapiens 87-91
30250298-7 2019 Finally, ATRA replacement suppressed 15-PGDH inhibition-induced tumor progression in KC mice, and ATRA treatment attenuated Aldh1 activity in tumor cells isolated from the pancreas of 15-Pgdh-/- KC mice. Tretinoin 98-102 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 124-129
30250298-7 2019 Finally, ATRA replacement suppressed 15-PGDH inhibition-induced tumor progression in KC mice, and ATRA treatment attenuated Aldh1 activity in tumor cells isolated from the pancreas of 15-Pgdh-/- KC mice. Tretinoin 98-102 hydroxyprostaglandin dehydrogenase 15 (NAD) Mus musculus 184-191
31740384-8 2020 Thus, our work not only provides relevant experimental evidence for further validating CDK2 as a target for differentiation therapy, but also uncovers the future clinical application of CDK2 inhibitors in ATRA-based differentiation therapeutics for AML. Tretinoin 205-209 cyclin dependent kinase 2 Homo sapiens 186-190
31950055-7 2019 The cell surface expression of CD14 was significantly enhanced by ATRA treatment, especially in the presence of flagellin. Tretinoin 66-70 CD14 molecule Homo sapiens 31-35
31112136-5 2019 Intriguingly, myocardial phenotypes in Tie2-cko hearts could be partially rescued by inhibiting in utero RA signaling with pan-retinoic acid receptor antagonist BMS493. Tretinoin 105-107 TEK receptor tyrosine kinase Homo sapiens 39-43
31950055-8 2019 Anti-CD14 antibody treatment prior to ATRA and flagellin treatments completely abolished ATRA-enhanced TNF-alpha and IL-1beta production. Tretinoin 89-93 CD14 molecule Homo sapiens 5-9
30328800-12 2019 Taken together, the microplate, FACS, immunoblot, and immunofluorescence data suggest that retinoic acid or hyperosmotic stress forces dose-dependent differentiation whether LIF is present or not and this is negatively correlated with and possibly compensates for stress-forced diminished ESC population expansion and potency loss. Tretinoin 91-104 acyl-CoA synthetase long-chain family member 1 Mus musculus 32-36
31950055-9 2019 Our results suggest that ATRA enhances flagellin-stimulated proinflammatory responses in human monocyte THP-1 cells by upregulating CD14 in a RAR/RXR-dependent manner. Tretinoin 25-29 CD14 molecule Homo sapiens 132-136
31091225-3 2019 Cyp26-deficient embryos, which have increased retinoic acid (RA) levels, have similar defects in SHF-derived OFT development. Tretinoin 46-59 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-5
31264378-10 2019 Finally, the overexpression of miR-17-5p blocks ATRA-induced differentiation. Tretinoin 48-52 microRNA 17 Homo sapiens 31-40
31091225-3 2019 Cyp26-deficient embryos, which have increased retinoic acid (RA) levels, have similar defects in SHF-derived OFT development. Tretinoin 61-63 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-5
29766641-6 2019 To induce tissue-specific migration, addition of retinoic acid (RA) during Treg expansion induced expression of the gut-homing receptors alpha4beta7-integrin and CCR9. Tretinoin 49-62 C-C motif chemokine receptor 9 Homo sapiens 162-166
29766641-6 2019 To induce tissue-specific migration, addition of retinoic acid (RA) during Treg expansion induced expression of the gut-homing receptors alpha4beta7-integrin and CCR9. Tretinoin 64-66 C-C motif chemokine receptor 9 Homo sapiens 162-166
32195202-8 2019 RA upregulated Stra8 and Piwil2, and downregulated Nanog and Oct-4. Tretinoin 0-2 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 61-66
29543550-9 2019 CONCLUSION: It is indicated that the combination region of Vitamin A acid and fractional laser may lead to low expression of miR-29a, thus the inhibition of downstream Akt activation is loss, Akt activation is enhanced, enhancement of the expression of TGF-beta is induced, leading to proliferation of fibroblasts, and promotion of the collagen proteins" synthesis in skin. Tretinoin 59-73 microRNA 29a Rattus norvegicus 125-132
29543550-10 2019 Therefore miR-29a/Akt/TGF-beta signal pathway may participate in the skin rejuvenation mechanism of action Vitamin A acid and fractional laser. Tretinoin 107-121 microRNA 29a Rattus norvegicus 10-17
30779909-7 2019 Both CD38 and AHR are components of a complex signalsome that enhances retinoic acid-induced differentiation of myeloid progenitor cells to granulocytes. Tretinoin 71-84 aryl hydrocarbon receptor Homo sapiens 14-17
31766690-2 2019 Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. Tretinoin 21-44 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 139-160
31081818-2 2019 In the presence of retinoic acid (RA), the suspension cultured P19 cell line is induced to differentiate into neurons. Tretinoin 19-32 interleukin 23, alpha subunit p19 Mus musculus 63-66
31081818-2 2019 In the presence of retinoic acid (RA), the suspension cultured P19 cell line is induced to differentiate into neurons. Tretinoin 34-36 interleukin 23, alpha subunit p19 Mus musculus 63-66
29926545-0 2019 The Effects of Retinoic Acid and MAPK Inhibitors on Phosphorylation of Smad2/3 Induced by Transforming Growth Factor beta1. Tretinoin 15-28 transforming growth factor, beta 1 Mus musculus 90-122
29926545-2 2019 We investigated the effect of RA and the role of these signaling molecules on the phosphorylation of Smad2/3 (p-Smad2/3) induced by TGF-beta1. Tretinoin 30-32 transforming growth factor, beta 1 Mus musculus 132-141
29926545-7 2019 RESULTS: When A549 cells were pre-stimulated with TGF-beta1 prior to RA treatment, RA completely inhibited the p-Smad2/3. Tretinoin 69-71 transforming growth factor, beta 1 Mus musculus 50-59
29926545-11 2019 In a bleomycin-induced lung injury mouse model, RA decreased the expression of TGF-beta1 and Smad3 at 1 and 3 weeks. Tretinoin 48-50 transforming growth factor, beta 1 Mus musculus 79-88
31766690-2 2019 Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. Tretinoin 21-44 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 162-167
30760627-11 2019 We show that stimulation of RARalpha is required for the differentiation of OPCs and we describe for the first time how oral treatment with a RARbeta agonist (C286, currently being tested in a Phase 1 trial, ISRCTN12424734) leads to the endogenous synthesis of RA through retinaldehyde dehydrogenase 2 (Raldh2) in NG2 cells and controls exosome-associated-RA intracellular levels through a decorin-Ca2+ pathway. Tretinoin 142-144 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 272-301
30760627-11 2019 We show that stimulation of RARalpha is required for the differentiation of OPCs and we describe for the first time how oral treatment with a RARbeta agonist (C286, currently being tested in a Phase 1 trial, ISRCTN12424734) leads to the endogenous synthesis of RA through retinaldehyde dehydrogenase 2 (Raldh2) in NG2 cells and controls exosome-associated-RA intracellular levels through a decorin-Ca2+ pathway. Tretinoin 142-144 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 303-309
31766690-2 2019 Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. Tretinoin 21-44 ataxia telangiectasia mutated Mus musculus 267-270
31766690-2 2019 Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. Tretinoin 46-49 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 139-160
30737277-5 2019 We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum. Tretinoin 148-150 homeobox A1 Homo sapiens 47-58
30737277-5 2019 We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytochrome P450 family 26 subfamily A member 1 (Cyp26a1) transcripts, direct RA target genes, require the expression of the RA-synthesizing enzyme, aldehyde dehydrogenase 1 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires ROL from the serum. Tretinoin 148-150 homeobox A1 Homo sapiens 60-65
29926545-11 2019 In a bleomycin-induced lung injury mouse model, RA decreased the expression of TGF-beta1 and Smad3 at 1 and 3 weeks. Tretinoin 48-50 SMAD family member 3 Mus musculus 93-98
31766690-2 2019 Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. Tretinoin 46-49 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 162-167
30992691-9 2019 Compared with PML-RARA, GTF2I-RARA has a higher affinity to HDAC3 under ATRA treatment. Tretinoin 72-76 histone deacetylase 3 Homo sapiens 60-65
31766690-2 2019 Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. Tretinoin 46-49 ataxia telangiectasia mutated Mus musculus 267-270
30944806-7 2019 The mRNA expression levels of both RAR-beta and RXR-beta were found to be increased in co-treatment (band density of 0.75 and 0.806, respectively) when compared with 9cisRA treatment (0.25 and 0.112) and ATRA treatment (0.01 and 0.081). Tretinoin 204-208 retinoid X receptor beta Homo sapiens 48-56
29926545-12 2019 CONCLUSION: RA had inhibitory effects on the phosphorylation of Smad induced by TGF-beta1 in vitro, and RA also decreased the expression of TGF-beta1 at 1 and 3 weeks in vivo. Tretinoin 12-14 transforming growth factor, beta 1 Mus musculus 80-89
29926545-12 2019 CONCLUSION: RA had inhibitory effects on the phosphorylation of Smad induced by TGF-beta1 in vitro, and RA also decreased the expression of TGF-beta1 at 1 and 3 weeks in vivo. Tretinoin 12-14 transforming growth factor, beta 1 Mus musculus 140-160
30944806-9 2019 We thus conclude that the co-treatment had increased the availability of ATRA, by isomerization of the 9cisRA which then resulted in an increased expression of both RAR-beta and RXR-beta receptors and the target protein RAR-beta which in turn inhibited lung cancer cell growth. Tretinoin 73-77 retinoid X receptor beta Homo sapiens 178-186
31766690-3 2019 In both a human epidermal cell line, HaCaT, and a mouse melanoma B16F10 cell line, we found that tRA could activate SerRS transcription through binding with the SerRS promoter. Tretinoin 97-100 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 116-121
30372846-8 2018 RESULTS AND DISCUSSION: In silico docking, analysis confirms that ATRA interferes with the normal binding of ligands (TNF-alpha, IL6ST) and receptors (TNFR1, IL6) of ERK/JAK-STAT pathways respectively. Tretinoin 66-70 interleukin 6 cytokine family signal transducer Rattus norvegicus 129-134
31766690-3 2019 In both a human epidermal cell line, HaCaT, and a mouse melanoma B16F10 cell line, we found that tRA could activate SerRS transcription through binding with the SerRS promoter. Tretinoin 97-100 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 161-166
31766690-4 2019 However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. Tretinoin 218-221 ataxia telangiectasia mutated Mus musculus 46-49
31766690-4 2019 However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. Tretinoin 218-221 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 65-70
31766690-4 2019 However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. Tretinoin 218-221 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 103-108
30927295-0 2019 Hypothesis: Wound-induced TLR3 activation stimulates endogenous retinoic acid synthesis and signalling during regeneration. Tretinoin 64-77 toll like receptor 3 Homo sapiens 26-30
31766690-5 2019 When combined with ATM inhibitor KU-55933, tRA showed a greatly enhanced efficiency in inhibiting VEGFA expression and a much better protection of mouse skin from photo damage. Tretinoin 43-46 ataxia telangiectasia mutated Mus musculus 19-22
30927295-3 2019 Here, we propose a hypothesis that TLR3 stimulates retinoic acid synthesis and signalling to allow for regeneration, suggesting that common clinical methods of facial rejuvenation in human subjects through damage (such as lasers or dermabrasion), and the use of topical retinoids reflect the same biologic pathway. Tretinoin 51-64 toll like receptor 3 Homo sapiens 35-39
29350420-1 2018 Differentiated embryo chondrocyte 1 (DEC1), a member of basic-helix-loop-helix transcription factor Bhlhe40, also called stimulated by retinoic acid 13, STRA13, plays an important role in the regulation of adipogenesis, tumorigenesis, peripheral circadian output, response to hypoxia, and development of metabolic syndrome. Tretinoin 135-148 centromere protein X Bos taurus 153-159
31766690-7 2019 Taken together, tRA combined with an ATM inhibitor can greatly enhance the anti-angiogenic activity of SerRS under UV irradiation and could be a better strategy in protecting skin from angiogenesis-associated skin damage and melanoma caused by UV radiation. Tretinoin 16-19 ataxia telangiectasia mutated Mus musculus 37-40
31766690-7 2019 Taken together, tRA combined with an ATM inhibitor can greatly enhance the anti-angiogenic activity of SerRS under UV irradiation and could be a better strategy in protecting skin from angiogenesis-associated skin damage and melanoma caused by UV radiation. Tretinoin 16-19 seryl-aminoacyl-tRNA synthetase 2 Mus musculus 103-108
31562240-2 2019 Several enzymes exhibit retinol dehydrogenase activities in vitro; however, their physiological relevance for retinoic acid biosynthesis in vivo remains unclear. Tretinoin 110-123 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 24-45
30888968-3 2019 Cellular retinoic acid binding protein-II (CRABP-II) selectively binds all trans-retinoic acid, the most active retinoid metabolite, contributing to regulate intracytoplasmic retinoid trafficking and keratinocyte differentiation. Tretinoin 75-94 cellular retinoic acid binding protein II Mus musculus 0-41
30888968-3 2019 Cellular retinoic acid binding protein-II (CRABP-II) selectively binds all trans-retinoic acid, the most active retinoid metabolite, contributing to regulate intracytoplasmic retinoid trafficking and keratinocyte differentiation. Tretinoin 75-94 cellular retinoic acid binding protein II Mus musculus 43-51
30612000-7 2019 Using the cytotoxicity assay, colony formation assay, tumorsphere formation assay and flow cytometry, the therapeutic effect of ATRA and ATRA-loaded lipid-polymer nanoparticles conjugated with CD133 aptamers (ATRA-PLNP-CD133) against osteosarcoma initiating cells were investigated. Tretinoin 128-132 prominin 1 Homo sapiens 193-198
30612000-7 2019 Using the cytotoxicity assay, colony formation assay, tumorsphere formation assay and flow cytometry, the therapeutic effect of ATRA and ATRA-loaded lipid-polymer nanoparticles conjugated with CD133 aptamers (ATRA-PLNP-CD133) against osteosarcoma initiating cells were investigated. Tretinoin 137-141 prominin 1 Homo sapiens 193-198
30612000-7 2019 Using the cytotoxicity assay, colony formation assay, tumorsphere formation assay and flow cytometry, the therapeutic effect of ATRA and ATRA-loaded lipid-polymer nanoparticles conjugated with CD133 aptamers (ATRA-PLNP-CD133) against osteosarcoma initiating cells were investigated. Tretinoin 137-141 prominin 1 Homo sapiens 219-224
30612000-9 2019 ATRA-PLNP-CD133, which showed a size of 129.9 nm and a sustained release of ATRA during 144 h, was demonstrated to efficiently and specifically promote the ATRA delivery to osteosarcoma initiating cells, and achieve superior therapeutic efficacy in osteosarcoma compared with ATRA and non-targeted nanoparticles. Tretinoin 0-4 prominin 1 Homo sapiens 10-15
30864551-1 2019 BACKGROUND: All-trans retinoic acid (ATRA) potentiates TGF-beta-dependent regulatory T cells (Treg) induction, while it inhibits pro-inflammatory interleukin-17-producing T helper cells (Th17) differentiation. Tretinoin 22-35 transforming growth factor, beta 1 Mus musculus 55-63
30864551-1 2019 BACKGROUND: All-trans retinoic acid (ATRA) potentiates TGF-beta-dependent regulatory T cells (Treg) induction, while it inhibits pro-inflammatory interleukin-17-producing T helper cells (Th17) differentiation. Tretinoin 37-41 transforming growth factor, beta 1 Mus musculus 55-63
30864551-3 2019 OBJECTIVE: To investigates the effect of ATRA on the regulation of Th17-Treg balance through ERK and p38 signaling pathway. Tretinoin 41-45 mitogen-activated protein kinase 14 Mus musculus 101-104
30864551-5 2019 The effect of ATRA on the phosphorylation of ERK and P38 was evaluated. Tretinoin 14-18 mitogen-activated protein kinase 14 Mus musculus 53-56
30661714-6 2019 Healthy proximal tubules expressed retinaldehyde dehydrogenase 2 (RALDH2), a rate-limiting enzyme in retinoic acid biosynthesis. Tretinoin 101-114 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 66-72
30810639-14 2019 CONCLUSIONS: In summary, RA increased the effect of BMP-2 on osteogenic differentiation of human ASCs. Tretinoin 25-27 bone morphogenetic protein 2 Homo sapiens 52-57
30236456-10 2019 ChIP demonstrated that, after retinoic acid stimulation and aldosterone exposure, MR and PPARgamma concomitantly bind to specific UCP1 promoter motifs. Tretinoin 30-43 peroxisome proliferator activated receptor gamma Mus musculus 89-98
30709353-8 2019 Treatment with ATRA could over-activate TGFbeta1/Smad3 signaling pathway in bovine adipocytes and reversed the over-production of pro-inflammatory cytokines and inhibition of anti-inflammatory cytokines induced by LPS. Tretinoin 15-19 transforming growth factor beta 1 Bos taurus 40-48
30709353-9 2019 Importantly, inhibition of TGFbeta1/Smad3 signaling diminished the effects of ATRA on suppressing the proinflammatory responses induced by LPS. Tretinoin 78-82 transforming growth factor beta 1 Bos taurus 27-35
30709353-10 2019 Furthermore, activation of TGFbeta1/Smad3 signaling further extended the effects of ATRA on suppressing the proinflammatory responses on LPS stimulation. Tretinoin 84-88 transforming growth factor beta 1 Bos taurus 27-35
30709353-11 2019 CONCLUSION: In conclusion, ATRA stimulates TGFbeta1/Smad3 signaling pathway and further suppresses bovine adipocytes inflammatory responses induced by LPS. Tretinoin 27-31 transforming growth factor beta 1 Bos taurus 43-51
30453015-8 2019 Enforced expression of miR-382-5p or specific PTEN inhibitors inhibited ATRA-induced granulocytic differentiation via regulation of the cell cycle regulator cyclinD1. Tretinoin 72-76 cyclin D1 Homo sapiens 157-165
30292490-0 2019 Expression of retinoic acid signaling components ADH7 and ALDH1A1 is reduced in aniridia limbal epithelial cells and a siRNA primary cell based aniridia model. Tretinoin 14-27 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 49-53
30292490-20 2019 These results provide evidence that PAX6 might drive corneal epithelial differentiation by direct or indirect control of retinoic acid signaling processes through ADH7 and ALDH1A1. Tretinoin 121-134 paired box 6 Homo sapiens 36-40
30292490-20 2019 These results provide evidence that PAX6 might drive corneal epithelial differentiation by direct or indirect control of retinoic acid signaling processes through ADH7 and ALDH1A1. Tretinoin 121-134 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 163-167
30678048-3 2019 In this study we focused on the molecular mechanism involving Annexin A8 (ANXA8), a Ca2+ and phospholipid binding protein, which is regulated by all-trans Retinoic Acid (RA), and it is highly expressed in breast DCIS tissue samples relative to atypical ductal hyperplasia, and normal breast tissue. Tretinoin 155-168 annexin A8 Homo sapiens 62-72
30678048-3 2019 In this study we focused on the molecular mechanism involving Annexin A8 (ANXA8), a Ca2+ and phospholipid binding protein, which is regulated by all-trans Retinoic Acid (RA), and it is highly expressed in breast DCIS tissue samples relative to atypical ductal hyperplasia, and normal breast tissue. Tretinoin 155-168 annexin A8 Homo sapiens 74-79
30678048-3 2019 In this study we focused on the molecular mechanism involving Annexin A8 (ANXA8), a Ca2+ and phospholipid binding protein, which is regulated by all-trans Retinoic Acid (RA), and it is highly expressed in breast DCIS tissue samples relative to atypical ductal hyperplasia, and normal breast tissue. Tretinoin 170-172 annexin A8 Homo sapiens 62-72
30678048-3 2019 In this study we focused on the molecular mechanism involving Annexin A8 (ANXA8), a Ca2+ and phospholipid binding protein, which is regulated by all-trans Retinoic Acid (RA), and it is highly expressed in breast DCIS tissue samples relative to atypical ductal hyperplasia, and normal breast tissue. Tretinoin 170-172 annexin A8 Homo sapiens 74-79
30674964-4 2019 We have also found that all-trans retinoic acid (ATRA) treatment increased AGAP2 protein levels in both cell lines whilst curcumin treatment reduced ATRA-mediated AGAP2 increase. Tretinoin 34-47 ArfGAP with GTPase domain, ankyrin repeat and PH domain 2 Homo sapiens 75-80
30674964-4 2019 We have also found that all-trans retinoic acid (ATRA) treatment increased AGAP2 protein levels in both cell lines whilst curcumin treatment reduced ATRA-mediated AGAP2 increase. Tretinoin 49-53 ArfGAP with GTPase domain, ankyrin repeat and PH domain 2 Homo sapiens 75-80
30674964-4 2019 We have also found that all-trans retinoic acid (ATRA) treatment increased AGAP2 protein levels in both cell lines whilst curcumin treatment reduced ATRA-mediated AGAP2 increase. Tretinoin 149-153 ArfGAP with GTPase domain, ankyrin repeat and PH domain 2 Homo sapiens 163-168
30310934-3 2019 We established a chemically defined protocol by application of Activin A, BMP4, and Retinoic acid followed by GDNF, which steered hPSCs to the renal lineage and resulted in populations of SIX2+/CITED1+ metanephric mesenchyme- (MM) and of HOXB7+/GRHL2+ ureteric bud (UB)-like cells already by 6 days. Tretinoin 84-97 SIX homeobox 2 Homo sapiens 188-192
30295852-9 2019 The effect of CREG1 on Ucp1 promoter activity was also stimulated by retinoic acid. Tretinoin 69-82 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 23-27
30814416-11 2019 In the ATRA-experiment, ATRA suppressed the expression of IL-6, TNF-alpha, NO, a disintegrin and metalloprotease with thrombospondin motifs-4 (ADAMTS-4), MMP-3, and MMP-9. Tretinoin 7-11 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 143-151
29926321-5 2019 Furthermore, retinoic acid (RA)-induced neurite outgrowth and expression of neuronal markers are significantly weakened in Bhlhe41-/- cells. Tretinoin 13-26 basic helix-loop-helix family, member e41 Mus musculus 123-130
29926321-5 2019 Furthermore, retinoic acid (RA)-induced neurite outgrowth and expression of neuronal markers are significantly weakened in Bhlhe41-/- cells. Tretinoin 28-30 basic helix-loop-helix family, member e41 Mus musculus 123-130
28125332-4 2019 We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in Syx-/- cells facilitated noggin secretion; and we report unpublished results showing that pharmacological inhibition of RhoA accelerates the neuronal differentiation of human embryonic stem cells. Tretinoin 115-128 noggin Homo sapiens 305-311
30542415-6 2018 In addition, to promote the therapeutic effect of RA in CD133+ lung cancer initiating cells, RA-loaded lipid poly(lactic-co-glycolic acid) (PLGA) nanoparticles with CD133 aptamers (RA-LPNPs-CD133) were developed. Tretinoin 93-95 prominin 1 Homo sapiens 56-61
30542415-6 2018 In addition, to promote the therapeutic effect of RA in CD133+ lung cancer initiating cells, RA-loaded lipid poly(lactic-co-glycolic acid) (PLGA) nanoparticles with CD133 aptamers (RA-LPNPs-CD133) were developed. Tretinoin 93-95 prominin 1 Homo sapiens 165-170
30542415-6 2018 In addition, to promote the therapeutic effect of RA in CD133+ lung cancer initiating cells, RA-loaded lipid poly(lactic-co-glycolic acid) (PLGA) nanoparticles with CD133 aptamers (RA-LPNPs-CD133) were developed. Tretinoin 93-95 prominin 1 Homo sapiens 165-170
30542415-8 2018 RA-LPNPs-CD133 had a size of 129.9 nm, and exhibited sustained release of RA during the 144-h period. Tretinoin 0-2 prominin 1 Homo sapiens 9-14
30542415-9 2018 For the first time, to the best of our knowledge, the present study demonstrated that RA exerted potent activity towards CD133+ lung cancer initiating cells. Tretinoin 86-88 prominin 1 Homo sapiens 121-126
30542415-10 2018 The results also showed that RA-LPNPs-CD133 efficiently and specifically promoted the delivery of RA to CD133+ lung cancer initiating cells, exhibiting superior inhibitory effects against CD133+ lung cancer initiating cells compared with non-targeted nanoparticles and RA. Tretinoin 29-31 prominin 1 Homo sapiens 38-43
30542415-10 2018 The results also showed that RA-LPNPs-CD133 efficiently and specifically promoted the delivery of RA to CD133+ lung cancer initiating cells, exhibiting superior inhibitory effects against CD133+ lung cancer initiating cells compared with non-targeted nanoparticles and RA. Tretinoin 29-31 prominin 1 Homo sapiens 104-109
30542415-10 2018 The results also showed that RA-LPNPs-CD133 efficiently and specifically promoted the delivery of RA to CD133+ lung cancer initiating cells, exhibiting superior inhibitory effects against CD133+ lung cancer initiating cells compared with non-targeted nanoparticles and RA. Tretinoin 29-31 prominin 1 Homo sapiens 104-109
29619741-5 2018 In our recently published study, we have identified a set of miRNAs including miR-145 and miR-29b families differentially expressed in SH-SY5Y cells exposed sequentially with retinoic acid + brain-derived neurotrophic factor (RA+BDNF) for differentiation into mature neurons (Mol Neurobiol (2016) doi: https://doi.org/10.1007/s12035-016-0042-9 ). Tretinoin 175-188 microRNA 29b-1 Homo sapiens 90-97
30016433-8 2018 Furthermore, retinoic acid (RA) signaling is required for Tbx5 activation in Tbx1-positive cells and blocking RA signaling at the time of Tbx5 activation results in atrioventricular septal defects at fetal stages. Tretinoin 13-26 T-box 5 Mus musculus 58-62
30016433-8 2018 Furthermore, retinoic acid (RA) signaling is required for Tbx5 activation in Tbx1-positive cells and blocking RA signaling at the time of Tbx5 activation results in atrioventricular septal defects at fetal stages. Tretinoin 28-30 T-box 5 Mus musculus 58-62
30016433-8 2018 Furthermore, retinoic acid (RA) signaling is required for Tbx5 activation in Tbx1-positive cells and blocking RA signaling at the time of Tbx5 activation results in atrioventricular septal defects at fetal stages. Tretinoin 110-112 T-box 5 Mus musculus 138-142
30420384-0 2018 Retinoic acid-induced CYP51 nuclear translocation promotes meiosis prophase I process and is correlated to the expression of REC8 and STAG3 in mice. Tretinoin 0-13 cytochrome P450, family 51 Mus musculus 22-27
30420384-0 2018 Retinoic acid-induced CYP51 nuclear translocation promotes meiosis prophase I process and is correlated to the expression of REC8 and STAG3 in mice. Tretinoin 0-13 REC8 meiotic recombination protein Mus musculus 125-129
30420384-0 2018 Retinoic acid-induced CYP51 nuclear translocation promotes meiosis prophase I process and is correlated to the expression of REC8 and STAG3 in mice. Tretinoin 0-13 stromal antigen 3 Mus musculus 134-139
30420384-4 2018 Following the addition of retinoic acid (RA) to induce meiosis or the RA receptor pan-antagonist AGN193109 to block meiosis in fetal ovaries, the translocation of CYP51 into the nucleus of oocytes was advanced or delayed, respectively. Tretinoin 26-39 cytochrome P450, family 51 Mus musculus 163-168
30420384-4 2018 Following the addition of retinoic acid (RA) to induce meiosis or the RA receptor pan-antagonist AGN193109 to block meiosis in fetal ovaries, the translocation of CYP51 into the nucleus of oocytes was advanced or delayed, respectively. Tretinoin 41-43 cytochrome P450, family 51 Mus musculus 163-168
30420384-7 2018 To sum up, RA-induced CYP51 nuclear translocation is critical for oocytes meiotic progression, and consequently folliculogenesis, which might act through impacting the expression of meiosis-specific cohesins REC8 and STAG3. Tretinoin 11-13 cytochrome P450, family 51 Mus musculus 22-27
30420384-7 2018 To sum up, RA-induced CYP51 nuclear translocation is critical for oocytes meiotic progression, and consequently folliculogenesis, which might act through impacting the expression of meiosis-specific cohesins REC8 and STAG3. Tretinoin 11-13 REC8 meiotic recombination protein Mus musculus 208-212
30420384-7 2018 To sum up, RA-induced CYP51 nuclear translocation is critical for oocytes meiotic progression, and consequently folliculogenesis, which might act through impacting the expression of meiosis-specific cohesins REC8 and STAG3. Tretinoin 11-13 stromal antigen 3 Mus musculus 217-222
29920752-7 2018 However, additional treatment with pilocarpine significantly suppressed ATRA-induced Nestin expression. Tretinoin 72-76 nestin Mus musculus 85-91
30425691-9 2018 Consistent with this finding, knocking out IRF3 or IRF7, two key downstream regulatory factors in most nucleic acid sensing pathways, resulted in a significant decrease in the adjuvant effect of ATRA/NAFL. Tretinoin 195-199 interferon regulatory factor 3 Homo sapiens 43-47
31596288-11 2019 Specifically, through Smurf promotion of Smad5 ubiquitination, RA could inhibit the BMP4 signal transduction. Tretinoin 63-65 SMAD family member 5 Gallus gallus 41-46
31479736-11 2019 Simultaneously, RA significantly reduced the expression of the WNT genes cMyc, Lef1, Lrp5, Lrp6 and Wnt11 compared to the controls (p < 0.05). Tretinoin 16-18 lymphoid enhancer binding factor 1 Mus musculus 79-83
30300581-5 2018 CD1D transcriptional de-repression by all-trans retinoic acid results in further enhanced cytotoxicity of CAR19-iNKT cells against CD19+ chronic lymphocytic leukemia cells. Tretinoin 48-61 CD19 molecule Homo sapiens 131-135
31479736-11 2019 Simultaneously, RA significantly reduced the expression of the WNT genes cMyc, Lef1, Lrp5, Lrp6 and Wnt11 compared to the controls (p < 0.05). Tretinoin 16-18 low density lipoprotein receptor-related protein 5 Mus musculus 85-89
31613407-2 2019 Our previous work has shown that depletion of RA using the vitamin A deficiency (VAD) model in Wistar rats leads to spatial memory deficits in relation to elevated intrahippocampal basal corticosterone (CORT) levels and increased hippocampal 11beta-Hydroxysteroid Dehydrogenase type 1 (11beta-HSD1) activity. Tretinoin 46-48 cortistatin Rattus norvegicus 203-207
30143559-3 2018 We previously showed that loss of the kidney-enriched zinc finger transcription factor Kruppel-like factor 15 (KLF15) increases susceptibility to proteinuric kidney disease and attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte. Tretinoin 212-225 Kruppel-like factor 15 Mus musculus 87-109
29377254-7 2018 Retinoic acid, an agonist of GnT-V, further increased glycosylated CD147, and activated matrix metalloproteinase-2/-9 (MMP-2 and MMP-9) in the hypertrophied left ventricle of 2K1C rat. Tretinoin 0-13 matrix metallopeptidase 2 Rattus norvegicus 88-117
29377254-7 2018 Retinoic acid, an agonist of GnT-V, further increased glycosylated CD147, and activated matrix metalloproteinase-2/-9 (MMP-2 and MMP-9) in the hypertrophied left ventricle of 2K1C rat. Tretinoin 0-13 matrix metallopeptidase 2 Rattus norvegicus 119-124
29520716-10 2018 RA was also found to rapidly downregulate extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, suggesting a rapid non-genomic action which may be involved in driving the molecular rhythm in ERK1/2 activation in this gland. Tretinoin 0-2 mitogen activated protein kinase 3 Rattus norvegicus 42-89
30143559-3 2018 We previously showed that loss of the kidney-enriched zinc finger transcription factor Kruppel-like factor 15 (KLF15) increases susceptibility to proteinuric kidney disease and attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte. Tretinoin 212-225 Kruppel-like factor 15 Mus musculus 111-116
29520716-10 2018 RA was also found to rapidly downregulate extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, suggesting a rapid non-genomic action which may be involved in driving the molecular rhythm in ERK1/2 activation in this gland. Tretinoin 0-2 mitogen activated protein kinase 3 Rattus norvegicus 202-208
29587617-0 2019 Retinoic Acid Pathway Regulation of Vascular Endothelial Growth Factor in Ovine Amnion. Tretinoin 0-13 vascular endothelial growth factor A Ovis aries 36-70
30415744-12 2018 RESULTS: and Discussion: RA-induced iPSCs exhibited these syncytiotrophoblast-like features and hCG secretion was maintained for at least 28 days after treatment with RA (500 nM) without BMP4. Tretinoin 25-27 hypertrichosis 2 (generalised, congenital) Homo sapiens 96-99
30217263-11 2018 Interestingly, rhein potentiated all-trans retinoic acid (ATRA)-induced macrophage differentiation in NB4 cells by inducing changes in morphology, expression of the differentiation markers CD11b and CD14, ROS production, phagocytic activity, and expression of CCR1 and CCR2. Tretinoin 58-62 C-C motif chemokine receptor 1 Homo sapiens 260-264
30415744-12 2018 RESULTS: and Discussion: RA-induced iPSCs exhibited these syncytiotrophoblast-like features and hCG secretion was maintained for at least 28 days after treatment with RA (500 nM) without BMP4. Tretinoin 167-169 hypertrichosis 2 (generalised, congenital) Homo sapiens 96-99
29587617-4 2019 Further, we explored relationships between RA receptors and VEGF and tested the hypothesis that RA modulates intramembranous absorption (IMA) through induction of amnion VEGF in sheep fetuses subjected to altered IMA rates. Tretinoin 96-98 vascular endothelial growth factor A Ovis aries 170-174
29587617-5 2019 Our study showed that RA receptor isoforms were expressed in sheep amnion, and RA response elements (RAREs) were identified in ovine RARbeta and VEGF gene promoters. Tretinoin 22-24 retinoic acid receptor alpha Ovis aries 133-140
30195874-15 2018 Allicin, ATRA, and allicin/ATRA increased the expression of cyclin D1 mRNA in both CD44+ and CD117+ cells. Tretinoin 9-13 cyclin D1 Homo sapiens 60-69
29587617-5 2019 Our study showed that RA receptor isoforms were expressed in sheep amnion, and RA response elements (RAREs) were identified in ovine RARbeta and VEGF gene promoters. Tretinoin 22-24 vascular endothelial growth factor A Ovis aries 145-149
30195874-15 2018 Allicin, ATRA, and allicin/ATRA increased the expression of cyclin D1 mRNA in both CD44+ and CD117+ cells. Tretinoin 27-31 cyclin D1 Homo sapiens 60-69
32254654-11 2018 Both cell types exhibited more vinculin expression when seeded to RA-loaded PCL scaffolds. Tretinoin 66-68 vinculin Homo sapiens 31-39
29587617-6 2019 In ovine amnion cells, RA treatment upregulated RARbeta messenger RNA (mRNA) and increased VEGF transcript levels. Tretinoin 23-25 retinoic acid receptor alpha Ovis aries 48-55
29587617-6 2019 In ovine amnion cells, RA treatment upregulated RARbeta messenger RNA (mRNA) and increased VEGF transcript levels. Tretinoin 23-25 vascular endothelial growth factor A Ovis aries 91-95
29587617-9 2019 We conclude that an RA pathway is present in ovine fetal membranes and that RA is capable of inducing VEGF. Tretinoin 76-78 vascular endothelial growth factor A Ovis aries 102-106
31447065-0 2019 Characterization of a rarely reported STAT5B/RARA gene fusion in a young adult with newly diagnosed acute promyelocytic leukemia with resistance to ATRA therapy. Tretinoin 148-152 signal transducer and activator of transcription 5B Homo sapiens 38-44
29874129-9 2018 Additionally, transgenic overexpression of Cyp26a1, which catalyzes RA degradation, resulted in breakdown of the BRB. Tretinoin 68-70 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 43-50
29388081-16 2018 Also, retinoic acid transcriptional signaling was shown to be amplified as evidenced by specific increased Rarbeta and decreased Erbb4 mRNA expression in AS mice versus Ctrl mice hippocampi. Tretinoin 6-19 retinoic acid receptor, beta Mus musculus 107-114
31447065-3 2019 Herein, we report a 27-year-old male with newly diagnosed, rapidly progressive APL and a rarely described STAT5B/RARA fusion with known resistance to ATRA therapy. Tretinoin 150-154 signal transducer and activator of transcription 5B Homo sapiens 106-112
31180720-6 2019 In the mechanism, ZIKV nonstructural (NS) 3 and NS2B3 negatively regulate IFN-related retinoic acid-inducible gene I-like receptor signaling pathway by targeting MAVS and MITA, respectively. Tretinoin 86-99 stimulator of interferon response cGAMP interactor 1 Homo sapiens 171-175
29715634-5 2018 The transcription of cyp26a1 (encoding retinoic acid metabolism enzyme) was significantly up-regulated in the 500 ng/L group, which might be a reason causing the teratogenic effect of FBZ. Tretinoin 39-52 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 21-28
30225259-0 2018 All-Trans Retinoic Acid Enhances Matrix Metalloproteinase 2 Expression and Secretion in Human Myeloid Leukemia THP-1 Cells. Tretinoin 10-23 matrix metallopeptidase 2 Homo sapiens 33-59
30225259-4 2018 In this study, we examined the possible modulatory effects of ATRA on MMP-2 expression and secretion in human myeloid leukemia cell line THP-1. Tretinoin 62-66 matrix metallopeptidase 2 Homo sapiens 70-75
30225259-6 2018 MMP-2 expression and secretion started to increase with ATRA concentration as low as 0.1 nM and gradually increased thereafter. Tretinoin 56-60 matrix metallopeptidase 2 Homo sapiens 0-5
30225259-7 2018 Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. Tretinoin 154-158 matrix metallopeptidase 2 Homo sapiens 167-172
30225259-8 2018 ATRA increased intracellular calcium ion levels, and a calcium-channel blocker inhibited ATRA-induced MMP-2 secretion. Tretinoin 0-4 matrix metallopeptidase 2 Homo sapiens 102-107
30225259-8 2018 ATRA increased intracellular calcium ion levels, and a calcium-channel blocker inhibited ATRA-induced MMP-2 secretion. Tretinoin 89-93 matrix metallopeptidase 2 Homo sapiens 102-107
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 22-35 lipocalin 2 Mus musculus 0-11
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 22-35 lipocalin 2 Mus musculus 75-86
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 22-35 lipocalin 2 Mus musculus 88-92
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 206-219 lipocalin 2 Mus musculus 0-11
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 206-219 lipocalin 2 Mus musculus 75-86
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 206-219 lipocalin 2 Mus musculus 88-92
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 221-223 lipocalin 2 Mus musculus 0-11
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 221-223 lipocalin 2 Mus musculus 75-86
30307164-0 2018 Lipocalin 2 regulates retinoic acid-induced activation of beige adipocytes Lipocalin-2 (LCN2) has been previously characterized as an adipokine regulating thermogenic activation of brown adipose tissue and retinoic acid (RA)-induced thermogenesis in mice. Tretinoin 221-223 lipocalin 2 Mus musculus 88-92
30225259-9 2018 Dexamethasone suppressed ATRA-induced MMP-2 secretion. Tretinoin 25-29 matrix metallopeptidase 2 Homo sapiens 38-43
30225259-10 2018 Our results suggest that ATRA enhances MMP-2 expression and secretion in human myeloid leukemia THP-1 cells in a calcium ion dependent manner through RAR/RXR signaling pathways, and this enhanced expression and secretion may be associated with the possible mechanisms of RAS. Tretinoin 25-29 matrix metallopeptidase 2 Homo sapiens 39-44
30307164-1 2018 The objective of this study was to explore the role and mechanism for LCN2 in the recruitment and retinoic acid-induced activation of brown-like or "beige" adipocytes. Tretinoin 98-111 lipocalin 2 Mus musculus 70-74
31235250-11 2019 The gene expression of Aldh1a1, an RA synthesis enzyme, in colonic epithelial cells (CECs) was significantly higher in the puerarin-treated FA mouse colon than in the untreated FA mouse colon. Tretinoin 35-37 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 23-30
30307164-9 2018 Our data suggest a novel LCN2-mediated pathway by which RA and insulin synergistically regulates activation of beige adipocytes via a non-genomic pathway of RA action. Tretinoin 56-58 lipocalin 2 Mus musculus 25-29
30307164-9 2018 Our data suggest a novel LCN2-mediated pathway by which RA and insulin synergistically regulates activation of beige adipocytes via a non-genomic pathway of RA action. Tretinoin 157-159 lipocalin 2 Mus musculus 25-29
29986869-4 2018 In this study, we show that retinoic acid (RA) signaling activity at the site of gland initiation is colocalized with expression of retinol metabolic genes Rdh10 and Aldh1a2 in the underlying SMG mesenchyme. Tretinoin 28-41 small nuclear ribonucleoprotein polypeptide G Homo sapiens 192-195
29945210-5 2018 When being added after 18-24 h of RA-induced F9 cell differentiation, SC1 transitorily activated Nanog and Oct4. Tretinoin 34-36 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 107-111
30030101-9 2018 However, the changes in transporters and enzymes, as well as ameliorative liver histology induced by Rg1 were abrogated by Nrf2 antagonist all-transretinoic acid in vivo and Nrf2 siRNA in vitro. Tretinoin 139-161 protein phosphatase 1, regulatory subunit 3A Mus musculus 101-104
31125456-4 2019 Further, we demonstrate that the expression of CAII and CAIX in these cells is significantly up-regulated by the biologically active metabolites of vitamin A (all-trans retinoic acid) and vitamin D (1alpha,25-dihydroxyvitamin D3 ), respectively. Tretinoin 159-182 carbonic anhydrase 9 Homo sapiens 56-60
30061204-1 2018 BACKGROUND/AIM: N-(4-hydroxyphenyl)retinamide (4-HPR) is a synthetic retinoid, less toxic than the parent all-trans retinoic acid (RA). Tretinoin 116-129 haptoglobin-related protein Homo sapiens 49-52
30061204-1 2018 BACKGROUND/AIM: N-(4-hydroxyphenyl)retinamide (4-HPR) is a synthetic retinoid, less toxic than the parent all-trans retinoic acid (RA). Tretinoin 131-133 haptoglobin-related protein Homo sapiens 49-52
30061204-3 2018 Because 4-HPR can hydrolyze to liberate RA, a potent human teratogen, the unhydrolyzable ketone analog of 4-HPR, 4-hydroxybenzylretinone (4-HBR) has been prepared and has been found to cause apoptosis in tumor cells and shrink carcinogen-induced rat mammary tumors as 4-HPR does. Tretinoin 40-42 haptoglobin-related protein Homo sapiens 10-13
30061204-3 2018 Because 4-HPR can hydrolyze to liberate RA, a potent human teratogen, the unhydrolyzable ketone analog of 4-HPR, 4-hydroxybenzylretinone (4-HBR) has been prepared and has been found to cause apoptosis in tumor cells and shrink carcinogen-induced rat mammary tumors as 4-HPR does. Tretinoin 40-42 haptoglobin-related protein Homo sapiens 108-111
30061204-3 2018 Because 4-HPR can hydrolyze to liberate RA, a potent human teratogen, the unhydrolyzable ketone analog of 4-HPR, 4-hydroxybenzylretinone (4-HBR) has been prepared and has been found to cause apoptosis in tumor cells and shrink carcinogen-induced rat mammary tumors as 4-HPR does. Tretinoin 40-42 haptoglobin-related protein Homo sapiens 108-111
29772445-0 2018 The protective role of all-transretinoic acid (ATRA) against colorectal cancer development is achieved via increasing miR-3666 expression and decreasing E2F7 expression. Tretinoin 27-45 E2F transcription factor 7 Homo sapiens 153-157
29772445-0 2018 The protective role of all-transretinoic acid (ATRA) against colorectal cancer development is achieved via increasing miR-3666 expression and decreasing E2F7 expression. Tretinoin 47-51 E2F transcription factor 7 Homo sapiens 153-157
30030768-2 2018 Most protocols developed so far for directing neural differentiation of P19 cells depend on the use of culture medium supplemented with retinoic acid (RA) and serum, which has an undefined composition. Tretinoin 136-149 interleukin 23, alpha subunit p19 Mus musculus 72-75
30030768-2 2018 Most protocols developed so far for directing neural differentiation of P19 cells depend on the use of culture medium supplemented with retinoic acid (RA) and serum, which has an undefined composition. Tretinoin 151-153 interleukin 23, alpha subunit p19 Mus musculus 72-75
30030768-4 2018 In this study, we achieved neural differentiation of P19 cells in a serum- and RA-free culture medium by employing the knockout serum replacement (KSR) supplement. Tretinoin 79-81 interleukin 23, alpha subunit p19 Mus musculus 53-56
29772445-11 2018 Furthermore, E2F7 was a target gene of miR-3666, and knockdown of E2F7 reversed the combined effects of ATRA and miR-3666 inhibitor on the malignant behaviors of HCT116 cells. Tretinoin 104-108 E2F transcription factor 7 Homo sapiens 13-17
29772445-11 2018 Furthermore, E2F7 was a target gene of miR-3666, and knockdown of E2F7 reversed the combined effects of ATRA and miR-3666 inhibitor on the malignant behaviors of HCT116 cells. Tretinoin 104-108 E2F transcription factor 7 Homo sapiens 66-70
30859584-4 2019 Western blot analysis showed the protein level of ERK, phosphorylated ERK, cyclin D1 (CCND1), and cyclin-dependent kinase 2 (CDK2) increased after stimulation with RA, and this effect could also be abolished by U0126. Tretinoin 164-166 cyclin dependent kinase 2 Homo sapiens 125-129
29772445-14 2018 MiR-3666/E2F7 may play a key role in regulating the inhibitory effects of ATRA on HCT116 cells via suppressing the activation of MAPK/ERK signaling pathway. Tretinoin 74-78 E2F transcription factor 7 Homo sapiens 9-13
29781215-8 2018 Mechanistically, we identified putative Kruppel-like factor 9 (KLF9) binding motifs to be critical in the enhancement of non-canonical RA-induced transactivation of Cyp26A1. Tretinoin 135-137 Kruppel-like factor 9 Mus musculus 40-61
30916783-9 2019 Our study identified GATA2 as a feedback inhibitor of RA signalling important for precise onset of ureteric SMC differentiation, and suggests that in a subset of cases of human congenital ureter dilatations, temporary relief of urine pressure may ameliorate the differentiation status of the SMC coat. Tretinoin 54-56 GATA binding protein 2 Homo sapiens 21-26
29781215-8 2018 Mechanistically, we identified putative Kruppel-like factor 9 (KLF9) binding motifs to be critical in the enhancement of non-canonical RA-induced transactivation of Cyp26A1. Tretinoin 135-137 Kruppel-like factor 9 Mus musculus 63-67
31147716-0 2019 A distal enhancer maintaining Hoxa1 expression orchestrates retinoic acid-induced early ESCs differentiation. Tretinoin 60-73 homeobox A1 Homo sapiens 30-35
29777906-7 2018 Both ATRA and lipo-ATRA treated groups showed detectable RAR-beta expression with relatively lesser density than the normal group. Tretinoin 5-9 retinoic acid receptor, beta Mus musculus 57-65
29777906-14 2018 These results revealed that the lipo-ATRA treatment has efficiently delivered ATRA into target site than free ATRA and in-turn it might have induced the expression of RAR-beta gene or prevented loss of RAR-beta gene in cancer animals. Tretinoin 37-41 retinoic acid receptor, beta Mus musculus 167-175
29777906-14 2018 These results revealed that the lipo-ATRA treatment has efficiently delivered ATRA into target site than free ATRA and in-turn it might have induced the expression of RAR-beta gene or prevented loss of RAR-beta gene in cancer animals. Tretinoin 37-41 retinoic acid receptor, beta Mus musculus 202-210
29777906-14 2018 These results revealed that the lipo-ATRA treatment has efficiently delivered ATRA into target site than free ATRA and in-turn it might have induced the expression of RAR-beta gene or prevented loss of RAR-beta gene in cancer animals. Tretinoin 78-82 retinoic acid receptor, beta Mus musculus 167-175
30089026-1 2018 We designed a study to induce differentiation of Oct4-GFP (expression of Green Fluorescent Protein of oct4) embryonic stem cells (ESCs) by embryoid body (EB) culture system into germ cells (GCs) using retinoic acid (RA) and evaluated the expression level of (Fkbp6, Mov10l1, 4930432K21Rik, and Tex13) in differentiated cells. Tretinoin 201-214 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 49-53
30089026-1 2018 We designed a study to induce differentiation of Oct4-GFP (expression of Green Fluorescent Protein of oct4) embryonic stem cells (ESCs) by embryoid body (EB) culture system into germ cells (GCs) using retinoic acid (RA) and evaluated the expression level of (Fkbp6, Mov10l1, 4930432K21Rik, and Tex13) in differentiated cells. Tretinoin 201-214 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 102-106
30089026-1 2018 We designed a study to induce differentiation of Oct4-GFP (expression of Green Fluorescent Protein of oct4) embryonic stem cells (ESCs) by embryoid body (EB) culture system into germ cells (GCs) using retinoic acid (RA) and evaluated the expression level of (Fkbp6, Mov10l1, 4930432K21Rik, and Tex13) in differentiated cells. Tretinoin 216-218 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 49-53
30089026-1 2018 We designed a study to induce differentiation of Oct4-GFP (expression of Green Fluorescent Protein of oct4) embryonic stem cells (ESCs) by embryoid body (EB) culture system into germ cells (GCs) using retinoic acid (RA) and evaluated the expression level of (Fkbp6, Mov10l1, 4930432K21Rik, and Tex13) in differentiated cells. Tretinoin 216-218 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 102-106
30089026-4 2018 A significant increase occurred in the expression of meiotic markers and specific genes, Fkbp6 (p = 0.00), Mov10l1 (p = 0.01), and Tex13 (p = 0.00) in ESCs treated with RA (+RA) compared with the controls (-RA). Tretinoin 169-171 FK506 binding protein 6 Mus musculus 89-94
33168517-4 2018 The cytotoxic effect of adriamycin was observed in the cells treated with retinoic acid (RA) for enhancing GJ function, in cells treated with oleamide and 18-alpha- glycyrrhizic acid (18-alpha-ga) for inhibiting GJ function, and also in cells transfected with Cx43siRNA for Cx43 knockdown. Tretinoin 89-91 gap junction protein alpha 1 Homo sapiens 260-264
31147716-1 2019 Retinoic acid (RA) induces rapid differentiation of embryonic stem cells (ESCs), partly by activating expression of the transcription factor Hoxa1, which regulates downstream target genes that promote ESCs differentiation. Tretinoin 0-13 homeobox A1 Homo sapiens 141-146
33168517-4 2018 The cytotoxic effect of adriamycin was observed in the cells treated with retinoic acid (RA) for enhancing GJ function, in cells treated with oleamide and 18-alpha- glycyrrhizic acid (18-alpha-ga) for inhibiting GJ function, and also in cells transfected with Cx43siRNA for Cx43 knockdown. Tretinoin 89-91 gap junction protein alpha 1 Homo sapiens 274-278
31147716-1 2019 Retinoic acid (RA) induces rapid differentiation of embryonic stem cells (ESCs), partly by activating expression of the transcription factor Hoxa1, which regulates downstream target genes that promote ESCs differentiation. Tretinoin 15-17 homeobox A1 Homo sapiens 141-146
31147716-2 2019 However, mechanisms of RA-induced Hoxa1 expression and ESCs early differentiation remain largely unknown. Tretinoin 23-25 homeobox A1 Homo sapiens 34-39
31147716-4 2019 Enhancer deletion significantly inhibited expression of RA-induced Hoxa1 and endoderm master control genes such as Gata4 and Gata6. Tretinoin 56-58 homeobox A1 Homo sapiens 67-72
30021172-4 2018 Gene expression analysis demonstrated higher expression of RA-target genes in RA-CFP-dim HSCs, in contrast to the RA-CFP reporter expression, but both RA-CFP-dim and RA-CFP-bright HSCs responded efficiently to RA in vitro. Tretinoin 59-61 complement factor properdin Mus musculus 81-84
29921692-7 2018 However, the response of APL with RARB translocation to retinoids was attenuated compared with that of PML-RARA, an observation in line with the clinical resistance of RARB-positive APL to ATRA. Tretinoin 189-193 retinoic acid receptor, beta Mus musculus 34-38
31147716-5 2019 Transcriptome analysis revealed that RA-induced early ESCs differentiation was blocked in Hoxa1 enhancer knockout cells, suggesting a requirement for the enhancer. Tretinoin 37-39 homeobox A1 Homo sapiens 90-95
31048191-4 2019 It is generally accepted that both CD44 and CD133 are gastric cancer stem cells markers, we hereby developed CD44/CD133-ATRA-PLPN (CD44 and CD133 antibody-conjugated all-trans retinoic acid-loaded poly(lactide-co-glycolide)-lecithin-PEG nanoparticles) to target both CD133+ and CD44+ gastric cancer stem cells. Tretinoin 176-189 prominin 1 Homo sapiens 114-119
29274134-10 2018 Further studies addressing its biology and clinical significance may be especially relevant in the era of IDH inhibitors and recent work showing efficacy of ATRA therapy in NPM1 and IDH1-mutated AML. Tretinoin 157-161 nucleophosmin 1 Homo sapiens 173-177
29447006-7 2018 To understand the molecular mechanisms by which RA regulates epicardial cytoskeletal rearrangement, we used a whole transcriptome profiling approach, which in combination with pull-down and inhibition assays, demonstrated that the Ras homolog gene family, member A (RhoA) pathway is required for the morphologic changes induced by RA in epicardial cells. Tretinoin 48-50 ras homolog family member A Mus musculus 266-270
29447006-8 2018 Collectively, these data demonstrate that RA regulates the cytoskeletal rearrangement of epicardial cells via a signaling cascade that involves the RhoA pathway.-Wang, S., Yu, J., Jones, J. W., Pierzchalski, K., Kane, M. A., Trainor, P. A., Xavier-Neto, J., Moise, A. R. Retinoic acid signaling promotes the cytoskeletal rearrangement of embryonic epicardial cells. Tretinoin 42-44 ras homolog family member A Mus musculus 148-152
29447006-8 2018 Collectively, these data demonstrate that RA regulates the cytoskeletal rearrangement of epicardial cells via a signaling cascade that involves the RhoA pathway.-Wang, S., Yu, J., Jones, J. W., Pierzchalski, K., Kane, M. A., Trainor, P. A., Xavier-Neto, J., Moise, A. R. Retinoic acid signaling promotes the cytoskeletal rearrangement of embryonic epicardial cells. Tretinoin 271-284 ras homolog family member A Mus musculus 148-152
30008902-3 2018 Research into CCR9 and CCL25 has revealed their associated upstream and downstream signaling pathways; CCR9 is regulated by several immunological factors, including NOTCH, interleukin 2, interleukin 4 and retinoic acid. Tretinoin 205-218 C-C motif chemokine receptor 9 Homo sapiens 103-107
31048191-4 2019 It is generally accepted that both CD44 and CD133 are gastric cancer stem cells markers, we hereby developed CD44/CD133-ATRA-PLPN (CD44 and CD133 antibody-conjugated all-trans retinoic acid-loaded poly(lactide-co-glycolide)-lecithin-PEG nanoparticles) to target both CD133+ and CD44+ gastric cancer stem cells. Tretinoin 176-189 prominin 1 Homo sapiens 114-119
31048191-4 2019 It is generally accepted that both CD44 and CD133 are gastric cancer stem cells markers, we hereby developed CD44/CD133-ATRA-PLPN (CD44 and CD133 antibody-conjugated all-trans retinoic acid-loaded poly(lactide-co-glycolide)-lecithin-PEG nanoparticles) to target both CD133+ and CD44+ gastric cancer stem cells. Tretinoin 176-189 prominin 1 Homo sapiens 114-119
30826380-0 2019 Regulation of FOXP3 expression in myeloid cells in response to all-trans-retinoic acid, interleukin 2 and transforming growth factor beta. Tretinoin 63-86 forkhead box P3 Homo sapiens 14-19
29688535-10 2018 The gene expression of both PPARdelta and PPARgamma were increased (P < 0.05) with 1,000 nM of ATRA. Tretinoin 98-102 peroxisome proliferator activated receptor gamma Bos taurus 42-51
29848550-0 2018 Combinatorial knockout of RARalpha, RARbeta, and RARgamma completely abrogates transcriptional responses to retinoic acid in murine embryonic stem cells. Tretinoin 108-121 retinoic acid receptor, beta Mus musculus 36-43
30826380-5 2019 Our experiments revealed that ATRA alone, but also a cocktail of mediators consisting of IL2, TGFbeta and ATRA, upregulate expression of FOXP3 gene in normal and leukemic myeloid cells. Tretinoin 30-34 forkhead box P3 Homo sapiens 137-142
31024166-6 2019 On the other hand, mIDH2 leukaemia display inhibition of LSD1 and a resulting transcriptional signature of all-trans retinoic acid (ATRA) sensitization, in spite of a state of suppressed ATRA signalling due to increased levels of PIN1. Tretinoin 107-130 isocitrate dehydrogenase 2 (NADP+), mitochondrial Mus musculus 19-24
30006626-0 2018 CD200-CD200R imbalance correlates with microglia and pro-inflammatory activation in rat spinal cords exposed to amniotic fluid in retinoic acid-induced spina bifida. Tretinoin 130-143 Cd200 molecule Rattus norvegicus 0-5
31024166-6 2019 On the other hand, mIDH2 leukaemia display inhibition of LSD1 and a resulting transcriptional signature of all-trans retinoic acid (ATRA) sensitization, in spite of a state of suppressed ATRA signalling due to increased levels of PIN1. Tretinoin 132-136 isocitrate dehydrogenase 2 (NADP+), mitochondrial Mus musculus 19-24
29769220-0 2018 Retinoic acid-induced expression of Hnf1b and Fzd4 is required for pancreas development in Xenopus laevis. Tretinoin 0-13 HNF1 homeobox B L homeolog Xenopus laevis 36-41
29769220-0 2018 Retinoic acid-induced expression of Hnf1b and Fzd4 is required for pancreas development in Xenopus laevis. Tretinoin 0-13 frizzled class receptor 4 S homeolog Xenopus laevis 46-50
31024166-6 2019 On the other hand, mIDH2 leukaemia display inhibition of LSD1 and a resulting transcriptional signature of all-trans retinoic acid (ATRA) sensitization, in spite of a state of suppressed ATRA signalling due to increased levels of PIN1. Tretinoin 187-191 isocitrate dehydrogenase 2 (NADP+), mitochondrial Mus musculus 19-24
31143119-6 2019 Our results also demonstrated that ATRA altered the expression of proliferation-related proteins, including CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 in VSMC. Tretinoin 35-39 cyclin D3 Mus musculus 118-126
31143119-6 2019 Our results also demonstrated that ATRA altered the expression of proliferation-related proteins, including CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 in VSMC. Tretinoin 35-39 cyclin A2 Mus musculus 128-136
31218101-5 2019 Therefore, RAF-1-independent MEK/ERK signaling was required for enz-ATRA treatment-induced differentiation via modulation of the protein levels of C/EBPbeta and/or PU.1. Tretinoin 68-72 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 11-16
31218101-5 2019 Therefore, RAF-1-independent MEK/ERK signaling was required for enz-ATRA treatment-induced differentiation via modulation of the protein levels of C/EBPbeta and/or PU.1. Tretinoin 68-72 CCAAT enhancer binding protein beta Homo sapiens 147-156
30992047-3 2019 RESULTS: Here, we show that the H2AK119ub1 E3 ligase CUL4B is required for the activation of retinoic acid (RA)-inducible developmentally critical homeobox (HOX) genes in NT2/D1 embryonal carcinoma cells. Tretinoin 93-106 cullin 4B Homo sapiens 53-58
29891447-5 2018 RESULTS: Compared with the control cells, the hepatocytes treated with ATRA showed a concentration-dependent decrease in AFP expression and increase in the expressions of ALB, CK18, TAT and ApoB. Tretinoin 71-75 albumin Mus musculus 171-174
29891447-5 2018 RESULTS: Compared with the control cells, the hepatocytes treated with ATRA showed a concentration-dependent decrease in AFP expression and increase in the expressions of ALB, CK18, TAT and ApoB. Tretinoin 71-75 keratin 18 Mus musculus 176-180
30992047-3 2019 RESULTS: Here, we show that the H2AK119ub1 E3 ligase CUL4B is required for the activation of retinoic acid (RA)-inducible developmentally critical homeobox (HOX) genes in NT2/D1 embryonal carcinoma cells. Tretinoin 108-110 cullin 4B Homo sapiens 53-58
30992047-4 2019 RA treatment led to attenuation of H2AK119ub1 due to decrease in CUL4B, further affecting HOX gene regulation. Tretinoin 0-2 cullin 4B Homo sapiens 65-70
31157249-0 2019 AMBRA1-mediated autophagy and apoptosis associated with an epithelial-mesenchymal transition in the development of cleft palate induced by all-trans retinoic acid. Tretinoin 149-162 autophagy/beclin 1 regulator 1 Mus musculus 0-6
29910671-0 2018 Inhibition of CRL-NEDD8 pathway as a new approach to enhance ATRA-induced differentiation of acute promyelocytic leukemia cells. Tretinoin 61-65 NEDD8 ubiquitin like modifier Homo sapiens 18-23
29910671-3 2018 In the present study, we found that ATRA could decrease the expression of NEDD8-activating enzyme E1 (NAE1) and inhibit the neddylation of cullin1 and cullin3 in the APL cell line NB4. Tretinoin 36-40 cullin 1 Homo sapiens 139-146
29910671-3 2018 In the present study, we found that ATRA could decrease the expression of NEDD8-activating enzyme E1 (NAE1) and inhibit the neddylation of cullin1 and cullin3 in the APL cell line NB4. Tretinoin 36-40 cullin 3 Homo sapiens 151-158
29326073-5 2018 Overexpression of CFTR mimics the effect of RA on the induction of spermatogonial differentiation or restores the developmental defects induced by the knockdown of RARalpha in spermatogonial cells and Xenopus laevis. Tretinoin 44-46 cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7) Xenopus laevis 18-22
30307485-6 2019 The expression of NKG2D, NKG2DLs, especially Retinoic acid early induced transcript-1e (Rae-1e), perforin and granzyme B was concomitantly up-regulated after MI. Tretinoin 45-58 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 18-23
29407582-5 2018 NM23 expression decreased and EDG2 expression increased during all-trans retinoic acid (ATRA)-induced myeloid differentiation of HL-60, NB4, and THP-1 leukemia cells. Tretinoin 73-86 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 0-4
30601699-6 2019 ATRA administration alleviated DN and downregulated BMP4, phosopho-Smad1, and COL4. Tretinoin 0-4 bone morphogenetic protein 4 Homo sapiens 52-56
29407582-5 2018 NM23 expression decreased and EDG2 expression increased during all-trans retinoic acid (ATRA)-induced myeloid differentiation of HL-60, NB4, and THP-1 leukemia cells. Tretinoin 88-92 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 0-4
30601699-6 2019 ATRA administration alleviated DN and downregulated BMP4, phosopho-Smad1, and COL4. Tretinoin 0-4 SMAD family member 1 Homo sapiens 67-72
30529222-0 2019 Nuclear RXRalpha and RXRbeta receptors exert distinct and opposite effects on RA-mediated neuroblastoma differentiation. Tretinoin 78-80 retinoid X receptor beta Homo sapiens 21-28
29274429-3 2018 Using an established rodent model of RARbeta induced axonal regeneration, we show that neuronal RARbeta activation upregulates the enzymes involved in RA synthesis in a cell specific manner; alcohol dehydrogenase7 (ADH7) in neurons and aldehyde dehydrogenase 2 (Raldh2) in NG2 expressing cells (NG2+ cells). Tretinoin 37-39 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 191-213
29274429-3 2018 Using an established rodent model of RARbeta induced axonal regeneration, we show that neuronal RARbeta activation upregulates the enzymes involved in RA synthesis in a cell specific manner; alcohol dehydrogenase7 (ADH7) in neurons and aldehyde dehydrogenase 2 (Raldh2) in NG2 expressing cells (NG2+ cells). Tretinoin 37-39 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 215-219
30864551-0 2019 All-trans Retinoic Acid Regulates the Balance of Treg-Th17 Cells through ERK and P38 Signaling Pathway. Tretinoin 10-23 mitogen-activated protein kinase 14 Mus musculus 81-84
30810639-0 2019 Retinoic acid increases the effect of bone morphogenetic protein type 2 on osteogenic differentiation of human adipose-derived stem cells. Tretinoin 0-13 bone morphogenetic protein 2 Homo sapiens 38-71
30578278-9 2019 Decreasing retinoic acid synthesis by reducing Raldh2 (also known as Aldh1a2) gene dosage in Hectd1opm/+ heterozygous embryos reveals a genetic interaction. Tretinoin 11-24 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 47-53
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 CD8 antigen, alpha chain Mus musculus 334-342
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 transforming growth factor, beta 1 Mus musculus 439-446
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 CD8 antigen, alpha chain Mus musculus 145-153
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 transforming growth factor, beta 1 Mus musculus 218-225
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 CD8 antigen, alpha chain Mus musculus 334-342
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 transforming growth factor, beta 1 Mus musculus 439-446
30578278-9 2019 Decreasing retinoic acid synthesis by reducing Raldh2 (also known as Aldh1a2) gene dosage in Hectd1opm/+ heterozygous embryos reveals a genetic interaction. Tretinoin 11-24 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 69-76
30338372-5 2019 An in vitro model of Leishmania infection using the murine mphi cell line J774.1 was used to investigate the RA-synthesizing enzymes (RALDH-1 and RALDH-2). Tretinoin 109-111 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 134-141
28436029-14 2018 Collectively, WNT4 may act downstream of BMP2 to mediate the effects of ATRA on the terminal differentiation of antler chondrocytes through targeting RUNX1. Tretinoin 72-76 bone morphogenetic protein 2 Homo sapiens 41-45
28125332-4 2019 We detail several signaling pathways downstream of RhoA that are hindered by the absence of Syx, and obstructed by retinoic acid, resulting in an increase of noggin production; we explain how the lower RhoA activity and, consequently, the sparser peri-junctional stress fibers in Syx-/- cells facilitated noggin secretion; and we report unpublished results showing that pharmacological inhibition of RhoA accelerates the neuronal differentiation of human embryonic stem cells. Tretinoin 115-128 noggin Homo sapiens 158-164
30184259-9 2018 In vitro experiments confirmed that CB1 receptor activation directly inhibits retinoic acid-induced nephrin expression in podocytes and IL-4-induced M2 polarization in macrophages. Tretinoin 78-91 cannabinoid receptor 1 (brain) Mus musculus 36-39
28190238-0 2018 Alpha-Synuclein Suppresses Retinoic Acid-Induced Neuronal Differentiation by Targeting the Glycogen Synthase Kinase-3beta/beta-Catenin Signaling Pathway. Tretinoin 27-40 glycogen synthase kinase 3 beta Homo sapiens 91-121
29339732-0 2018 Glyburide and retinoic acid synergize to promote wound healing by anti-inflammation and RIP140 degradation. Tretinoin 14-27 nuclear receptor interacting protein 1 Mus musculus 88-94
30348891-6 2018 We find that C/EBPbeta is induced by retinoic acid and binds to the methyl-CRE sequence in the Foxp3 TSDR to sustain its expression. Tretinoin 37-50 CCAAT enhancer binding protein beta Homo sapiens 13-22
29339732-3 2018 We previously showed that during an anti-inflammatory response when macrophages were alternatively (M2) polarized, retinoic acid (RA) dramatically activated arginase 1 gene (Arg1), a gene crucial for wound healing. Tretinoin 115-128 arginase, liver Mus musculus 157-167
29339732-3 2018 We previously showed that during an anti-inflammatory response when macrophages were alternatively (M2) polarized, retinoic acid (RA) dramatically activated arginase 1 gene (Arg1), a gene crucial for wound healing. Tretinoin 115-128 arginase, liver Mus musculus 174-178
29339732-3 2018 We previously showed that during an anti-inflammatory response when macrophages were alternatively (M2) polarized, retinoic acid (RA) dramatically activated arginase 1 gene (Arg1), a gene crucial for wound healing. Tretinoin 130-132 arginase, liver Mus musculus 157-167
29339732-3 2018 We previously showed that during an anti-inflammatory response when macrophages were alternatively (M2) polarized, retinoic acid (RA) dramatically activated arginase 1 gene (Arg1), a gene crucial for wound healing. Tretinoin 130-132 arginase, liver Mus musculus 174-178
30348891-6 2018 We find that C/EBPbeta is induced by retinoic acid and binds to the methyl-CRE sequence in the Foxp3 TSDR to sustain its expression. Tretinoin 37-50 forkhead box P3 Homo sapiens 95-100
30497437-5 2018 Administration of ATRA supports the epithelial-like phenotype of DCIS-derived cells cultured under hypoxia and keeps down the number of CD133 positive cells, abrogating almost completely the effects of poor oxygenation. Tretinoin 18-22 prominin 1 Homo sapiens 136-141
29542081-2 2018 Retinoic acid (RA) activates through an RA-response element the transcription of Hox1 in the nerve cord of the ascidian Ciona intestinalis. Tretinoin 0-13 homeobox transcription factor Hox1 Ciona intestinalis 81-85
29542081-2 2018 Retinoic acid (RA) activates through an RA-response element the transcription of Hox1 in the nerve cord of the ascidian Ciona intestinalis. Tretinoin 15-17 homeobox transcription factor Hox1 Ciona intestinalis 81-85
29542081-2 2018 Retinoic acid (RA) activates through an RA-response element the transcription of Hox1 in the nerve cord of the ascidian Ciona intestinalis. Tretinoin 40-42 homeobox transcription factor Hox1 Ciona intestinalis 81-85
29542081-3 2018 We also found a weak RA-independent neural enhancer within the second intron of Hox1. Tretinoin 21-23 BACOIKO006_36 Oikopleura dioica 80-84
29542081-6 2018 We have found that the upstream sequence of the O. dioica Hox1 was able to activate reporter gene expression in the nerve cord of the C. intestinalis embryo, suggesting that an RA-independent regulatory system in the nerve cord might be common in larvaceans and ascidians. Tretinoin 177-179 BACOIKO006_36 Oikopleura dioica 58-62
30497437-6 2018 We also found that the mechanisms triggered by ATRA in non-invasive breast tumor cells cultured under hypoxia is in part mediated by PLC-beta2, responsible to counteract the effects of low oxygen availability on CD133 levels. Tretinoin 47-51 prominin 1 Homo sapiens 212-217
30153436-0 2018 CARM1 (PRMT4) Acts as a Transcriptional Coactivator during Retinoic Acid-Induced Embryonic Stem Cell Differentiation. Tretinoin 59-72 coactivator-associated arginine methyltransferase 1 Mus musculus 0-5
30216786-2 2018 With retinoic acid (RA) induction, a high percentage of cells were found to be arrested at the G0/G1 phase, with decreased levels of cyclinD1, CDK4, phosphorylation status of pRb and E2F1, in addition to an elevated level of p27. Tretinoin 5-18 cyclin D1 Homo sapiens 133-141
30216786-2 2018 With retinoic acid (RA) induction, a high percentage of cells were found to be arrested at the G0/G1 phase, with decreased levels of cyclinD1, CDK4, phosphorylation status of pRb and E2F1, in addition to an elevated level of p27. Tretinoin 5-18 cyclin dependent kinase 4 Homo sapiens 143-147
30216786-2 2018 With retinoic acid (RA) induction, a high percentage of cells were found to be arrested at the G0/G1 phase, with decreased levels of cyclinD1, CDK4, phosphorylation status of pRb and E2F1, in addition to an elevated level of p27. Tretinoin 5-18 RB transcriptional corepressor 1 Homo sapiens 175-178
30153436-0 2018 CARM1 (PRMT4) Acts as a Transcriptional Coactivator during Retinoic Acid-Induced Embryonic Stem Cell Differentiation. Tretinoin 59-72 coactivator-associated arginine methyltransferase 1 Mus musculus 7-12
30153436-5 2018 We address CARM1 function during RA-induced differentiation of murine embryonic stem cells (mESCs) using shRNA lentiviral transduction and CRISPR/Cas9 technology to deplete CARM1 in mESCs. Tretinoin 33-35 coactivator-associated arginine methyltransferase 1 Mus musculus 11-16
29966306-7 2018 Expression of CEBPB induced by ATRA is accompanied by upregulated expression of CEBPE with similar kinetics. Tretinoin 31-35 CCAAT enhancer binding protein beta Homo sapiens 14-19
30153436-7 2018 Furthermore, CARM1 is required for mESCs to differentiate into extraembryonic endoderm in response to RA. Tretinoin 102-104 coactivator-associated arginine methyltransferase 1 Mus musculus 13-18
29945667-1 2018 BACKGROUND: Previous work aimed at understanding the gene regulatory networks (GRNs) governing caudal hindbrain formation identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Tretinoin 152-165 HNF1 homeobox Ba Danio rerio 263-269
30153436-8 2018 We next characterize the epigenetic mechanisms that contribute to RA-induced transcriptional activation of CRABP2 and NR2F1 in mESCs and show for the first time that CARM1 is required for this activation. Tretinoin 66-68 cellular retinoic acid binding protein II Mus musculus 107-113
29945667-1 2018 BACKGROUND: Previous work aimed at understanding the gene regulatory networks (GRNs) governing caudal hindbrain formation identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Tretinoin 167-169 HNF1 homeobox Ba Danio rerio 263-269
30153436-8 2018 We next characterize the epigenetic mechanisms that contribute to RA-induced transcriptional activation of CRABP2 and NR2F1 in mESCs and show for the first time that CARM1 is required for this activation. Tretinoin 66-68 coactivator-associated arginine methyltransferase 1 Mus musculus 166-171
29688244-5 2018 Interestingly, RAREs exist in close proximity with CBSs, and therefore when RA is bound, CTCF cannot bind. Tretinoin 15-17 CCCTC-binding factor Mus musculus 89-93
30153436-9 2018 Collectively, our data demonstrate that CARM1 is required for transcriptional activation of a subset of RA target genes, and we uncover changes in the recruitment of Suz12 and the epigenetic H3K27me3 and H3K27ac marks at gene regulatory regions for CRABP2 and NR2F1 during RA-induced differentiation. Tretinoin 104-106 coactivator-associated arginine methyltransferase 1 Mus musculus 40-45
29634397-7 2018 Results: RA-induced differentiation in the NT2/D1 cells significantly increased the expression of MAP2, NRG1, NRP1, NRP2, NEUROG1 and EN1 genes (genes linked to neural differentiation) compared with undifferentiated NT2/D1 cells. Tretinoin 9-11 neuregulin 1 Homo sapiens 104-108
30322383-2 2018 In addition to nuclear receptors, there are other intracellular RA binding proteins such as cellular retinoic acid binding proteins (CRABP1 and CRABP2) and cytochrome P450 (CYP) enzymes, whose contributions to the RA signaling pathway have not been fully understood. Tretinoin 64-66 cellular retinoic acid binding protein 1 Homo sapiens 133-139
29634397-7 2018 Results: RA-induced differentiation in the NT2/D1 cells significantly increased the expression of MAP2, NRG1, NRP1, NRP2, NEUROG1 and EN1 genes (genes linked to neural differentiation) compared with undifferentiated NT2/D1 cells. Tretinoin 9-11 neuropilin 1 Homo sapiens 110-114
30039749-4 2018 ALDH-activity is also the rate-limiting step in retinoic acid (RA) production, a potent driver of hematopoietic differentiation. Tretinoin 48-61 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 0-4
29423110-0 2018 Potential for subsets of wt-NPM1 primary AML blasts to respond to retinoic acid treatment. Tretinoin 66-79 nucleophosmin 1 Homo sapiens 28-32
29111326-5 2018 Moreover, the expression of C/EBPbeta was increased after ATRA treatment, and the binding of C/EBPbeta in the NEAT1 promoter was also dramatically increased. Tretinoin 58-62 CCAAT enhancer binding protein beta Homo sapiens 28-37
29111326-5 2018 Moreover, the expression of C/EBPbeta was increased after ATRA treatment, and the binding of C/EBPbeta in the NEAT1 promoter was also dramatically increased. Tretinoin 58-62 CCAAT enhancer binding protein beta Homo sapiens 93-102
29111326-6 2018 Finally, knockdown of C/EBPbeta significantly reduced the ATRA-induced upregulation of NEAT1. Tretinoin 58-62 CCAAT enhancer binding protein beta Homo sapiens 22-31
29111326-8 2018 Knockdown of C/EBPbeta impairs ATRA-induced transcriptional activation of NEAT1. Tretinoin 31-35 CCAAT enhancer binding protein beta Homo sapiens 13-22
29111326-9 2018 Our data indicate that C/EBPbeta contributes to ATRA-induced activation of NEAT1 during APL cell differentiation. Tretinoin 48-52 CCAAT enhancer binding protein beta Homo sapiens 23-32
29728589-0 2018 All-trans-retinoic acid activates the pro-invasive Src-YAP-Interleukin 6 axis in triple-negative MDA-MB-231 breast cancer cells while cerivastatin reverses this action. Tretinoin 0-23 Yes1 associated transcriptional regulator Homo sapiens 55-58
29728589-4 2018 We show here that RA activates the pro-invasive axis Src-YAP-Interleukin 6 (Src-YAP-IL6) in triple negative MDA-MB-231 breast cancer cells, yielding to increased invasion of these cells. Tretinoin 18-20 Yes1 associated transcriptional regulator Homo sapiens 57-60
29964319-8 2018 However, the changes in Nrf2 target-genes, as well as ameliorative liver histology induced by Rg1 were abrogated by Nrf2 antagonist all-transretinoic acid in vivo and Nrf2 siRNA in vitro. Tretinoin 136-154 protein phosphatase 1, regulatory subunit 3A Mus musculus 94-97
29728589-4 2018 We show here that RA activates the pro-invasive axis Src-YAP-Interleukin 6 (Src-YAP-IL6) in triple negative MDA-MB-231 breast cancer cells, yielding to increased invasion of these cells. Tretinoin 18-20 Yes1 associated transcriptional regulator Homo sapiens 80-83
29728589-5 2018 On the contrary, RA inhibits the Src-YAP-IL6 axis of triple-negative MDA-MB-468 cells, which results in decreased invasion phenotype. Tretinoin 17-19 Yes1 associated transcriptional regulator Homo sapiens 37-40
29728589-8 2018 Furthermore, interference of YAP nuclear translocation using the statin cerivastatin reverses the upregulation of Interleukin 6 (IL-6) and the pro-invasive effect of RA on MDA-MB-231 breast cancer cells and also decreases invasion and viability of MDA-MB-468 breast cancer cells. Tretinoin 166-168 Yes1 associated transcriptional regulator Homo sapiens 29-32
28978663-6 2017 In contrast, the p73-DAPK2 pathway is essential for ATRA-induced autophagy that is mediated by an interaction of DAPK2 with the key autophagy-related protein (ATG)5. Tretinoin 52-56 tumor protein p73 Homo sapiens 17-20
28978663-7 2017 Lastly, we show that DAPK2 binds and stabilizes the p73 protein; thus, we propose a novel mechanism by which ATO- or ATRA-induced therapy responses initiate a positive p73-DAPK2 feedback loop. Tretinoin 117-121 tumor protein p73 Homo sapiens 52-55
28978663-7 2017 Lastly, we show that DAPK2 binds and stabilizes the p73 protein; thus, we propose a novel mechanism by which ATO- or ATRA-induced therapy responses initiate a positive p73-DAPK2 feedback loop. Tretinoin 117-121 tumor protein p73 Homo sapiens 168-171
29728589-9 2018 These results altogether suggest that RA induces pro-invasive or anti-invasive actions in two triple-negative breast cancer cell lines due to its ability to activate or inhibit the Src-YAP-IL6 axis in different cancer cells. Tretinoin 38-40 Yes1 associated transcriptional regulator Homo sapiens 185-188
30254197-5 2018 RARalpha promotes the development of LCs and langerin+ conventional DCs only in hypo-RA conditions, a function effectively suppressed at systemic RA levels. Tretinoin 0-2 CD207 molecule Homo sapiens 45-53
29377410-5 2018 ALDH-activity generates retinoic acid, a potent driver of hematopoietic differentiation, creating a paradoxical challenge to expand UCB ALDHhi cells while limiting differentiation and retaining pro-angiogenic functions. Tretinoin 24-37 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 0-4
30248940-8 2018 The combined effect of and retinoic acid at a low concentration (10 nM) decreased VDAC1 expression. Tretinoin 27-40 voltage dependent anion channel 1 Homo sapiens 82-87
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 retinol dehydrogenase 5 Rattus norvegicus 95-99
29383137-7 2017 Knockdown of RING1A in an MDS-derived AML cell line facilitated spontaneous and retinoic acid-induced differentiation. Tretinoin 80-93 ring finger protein 1 Homo sapiens 13-19
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 14-27 retinoic acid receptor gamma Homo sapiens 78-82
29263441-7 2018 Treatment of the mDia1/miR-146a double knockout mice with all-trans retinoic acid, which promoted the differentiation of MDSCs and ameliorated the inflammatory bone marrow microenvironment, significantly rescued anemia and ineffective erythropoiesis. Tretinoin 68-81 diaphanous related formin 1 Mus musculus 17-22
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 29-31 retinoic acid receptor gamma Homo sapiens 78-82
29794369-1 2018 Mutations in TBL1X, a component of the nuclear receptor co-repressor (N-CoR) and silencing mediator of retinoic acid and thyroid hormone receptor co-repressor complexes, have recently been implicated in isolated central hypothyroidism (CeH). Tretinoin 103-116 transducin beta like 1 X-linked Homo sapiens 13-18
29398485-7 2018 Rescue experiments indicate that FOXD3-AS1 harbors tumor-suppressive properties by inhibiting the oncogenic roles of PARP1 or CTCF and plays crucial roles in all-trans-retinoic-acid-mediated therapeutic effects on NB. Tretinoin 168-181 prostaglandin D2 receptor Homo sapiens 39-42
29235036-6 2018 Differentiation of SH-SY5Y cells with retinoic acid resulted in increased neurite outgrowth and Alox15 mRNA expression, while co-treatment with the p300 HAT inhibitor C646 and retinoic acid modulated the increases, indicating a role of p300 HAT in differentiation-associated Alox15 upregulation. Tretinoin 38-51 E1A binding protein p300 Homo sapiens 236-244
29109271-7 2017 We found that pachytene spermatocytes, which express an RA-synthesizing enzyme, Aldh1a2, contribute directly and significantly to RA production in testes. Tretinoin 56-58 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 80-87
29109271-7 2017 We found that pachytene spermatocytes, which express an RA-synthesizing enzyme, Aldh1a2, contribute directly and significantly to RA production in testes. Tretinoin 130-132 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 80-87
30158832-2 2018 RA promotes dendritic cells to express CD103 and to produce RA, enhances the differentiation of Foxp3+ inducible regulatory T cells, and induces gut-homing specificity in T cells. Tretinoin 0-2 forkhead box P3 Homo sapiens 96-101
29095919-3 2017 The aldehyde dehydrogenase Raldh1 (Aldh1a1) functions as one of three enzymes that converts the retinol metabolite retinal into RA, and one of many proteins that contribute to RA homeostasis. Tretinoin 128-130 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 27-33
29095919-3 2017 The aldehyde dehydrogenase Raldh1 (Aldh1a1) functions as one of three enzymes that converts the retinol metabolite retinal into RA, and one of many proteins that contribute to RA homeostasis. Tretinoin 128-130 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 35-42
29095919-3 2017 The aldehyde dehydrogenase Raldh1 (Aldh1a1) functions as one of three enzymes that converts the retinol metabolite retinal into RA, and one of many proteins that contribute to RA homeostasis. Tretinoin 176-178 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 27-33
29095919-3 2017 The aldehyde dehydrogenase Raldh1 (Aldh1a1) functions as one of three enzymes that converts the retinol metabolite retinal into RA, and one of many proteins that contribute to RA homeostasis. Tretinoin 176-178 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 35-42
29095919-6 2017 The phenotype observed prompted the conclusion that loss of Raldh1 causes an increase in adipose tissue retinal, and therefore, retinal functions independently of RA to prevent DIO. Tretinoin 163-165 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 60-66
29095919-12 2017 Embryonic fibroblasts from Raldh1-null mice resist differentiating into adipocytes, but retain ability to generate RA. Tretinoin 115-117 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 27-33
29119099-1 2017 Mouse F9 cells differentiate into primitive extraembryonic endoderm (PrE) when treated with retinoic acid (RA), and this is accompanied by an up-regulation of Gata6. Tretinoin 92-105 GATA binding protein 6 Mus musculus 159-164
29119099-1 2017 Mouse F9 cells differentiate into primitive extraembryonic endoderm (PrE) when treated with retinoic acid (RA), and this is accompanied by an up-regulation of Gata6. Tretinoin 107-109 GATA binding protein 6 Mus musculus 159-164
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 zona pellucida sperm-binding protein 2 Bubalus bubalis 300-303
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 spermatid nuclear transition protein 1 Bubalus bubalis 200-206
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 zona pellucida sperm-binding protein 2 Bubalus bubalis 300-303
28973009-5 2017 The TLR9-mediated survival is enhanced by the vitamin A metabolite retinoic acid (RA). Tretinoin 67-80 toll like receptor 9 Homo sapiens 4-8
28973009-5 2017 The TLR9-mediated survival is enhanced by the vitamin A metabolite retinoic acid (RA). Tretinoin 82-84 toll like receptor 9 Homo sapiens 4-8
28961318-4 2017 The HoxA9 expression level was decreased in leukaemia cells with the treatment of all-trans retinoic acid or arsenic trioxide (As2 O3 ). Tretinoin 92-105 homeobox A9 Homo sapiens 4-9
28961318-10 2017 The effect of HoxA9 modulation was correlated with the clinical effect of all-trans retinoic acid and As2 O3 . Tretinoin 84-97 homeobox A9 Homo sapiens 14-19
28836501-5 2017 Both RXRalpha and RXRbeta protein levels decrease was found also by combination ATRA+TBT-Cl/TPT-Cl. Tretinoin 80-84 retinoid X receptor beta Homo sapiens 18-25
28938749-23 2017 WIDER IMPLICATIONS OF THE FINDINGS: The findings that expression of GDNF (a major promoter of spermatogonial stem cell renewal) was not detected in the control juvenile testes, expression of SOHLH1, SOHLH2 and KIT, promoters of spermatogonial differentiation in mice, were not up-regulated in association with the gonadotrophin-induced generation of differentiating spermatogonia, and that robust activation of the retinoic acid signaling pathway was not observed, could not have been predicted. Tretinoin 415-428 glial cell line derived neurotrophic factor Mus musculus 68-72
28959017-5 2017 We demonstrate that Wdr5, Hdac1, and Hdac2 are required for RA signaling in vitro and in vivo. Tretinoin 60-62 WD repeat domain 5 Mus musculus 20-24
29137406-6 2017 In cell lines overexpressing PML-RARA, and in the NB4 t(15;17)-positive cell line, FOXC1 expression was lower than in other non-APL cell lines, and increased following treatment with all-trans retinoic acid (ATRA), due to functional binding of ATRA to the FOXC1 promoter region. Tretinoin 193-206 forkhead box C1 Homo sapiens 83-88
29137406-6 2017 In cell lines overexpressing PML-RARA, and in the NB4 t(15;17)-positive cell line, FOXC1 expression was lower than in other non-APL cell lines, and increased following treatment with all-trans retinoic acid (ATRA), due to functional binding of ATRA to the FOXC1 promoter region. Tretinoin 208-212 forkhead box C1 Homo sapiens 83-88
29137406-6 2017 In cell lines overexpressing PML-RARA, and in the NB4 t(15;17)-positive cell line, FOXC1 expression was lower than in other non-APL cell lines, and increased following treatment with all-trans retinoic acid (ATRA), due to functional binding of ATRA to the FOXC1 promoter region. Tretinoin 244-248 forkhead box C1 Homo sapiens 83-88
28542882-6 2017 Butyrate-treated RA-DCs (Bu-RA-DCs) decreased CD11c, but increased CD103 and alpha4 beta7 expression. Tretinoin 17-19 integrin subunit alpha X Homo sapiens 46-51
28423181-6 2017 This subset expressed Aldh1a2 and Itgb8 genes, which are involved in retinoic acid metabolism and transforming growth factor-beta (TGF-beta) activation, respectively. Tretinoin 69-82 integrin subunit beta 8 Homo sapiens 34-39
28927033-6 2017 After the RA+TMZ treatment of U251 cells, autophagy associated proteins Beclin 1 and LC3B were significantly increased, and the TEM analysis were consistent with autophagy protein levels. Tretinoin 10-12 microtubule associated protein 1 light chain 3 beta Homo sapiens 85-89
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 spermatid nuclear transition protein 1 Bubalus bubalis 200-206
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 zona pellucida sperm-binding protein 2 Bubalus bubalis 300-303
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 spermatid nuclear transition protein 1 Bubalus bubalis 200-206
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 zona pellucida sperm-binding protein 2 Bubalus bubalis 300-303
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 spermatid nuclear transition protein 1 Bubalus bubalis 200-206
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 zona pellucida sperm-binding protein 2 Bubalus bubalis 300-303
28817605-0 2017 All-trans retinoic acid suppresses malignant characteristics of CD133-positive thyroid cancer stem cells and induces apoptosis. Tretinoin 10-23 prominin 1 Homo sapiens 64-69
28817605-8 2017 The effects of all-trans retinoic acid (ATRA) on CD133-positive cells in vivo were explored with Cell Counting Kit-8, colony formation, apoptosis, cell cycle, and ethynyl deoxyuridine assays. Tretinoin 15-38 prominin 1 Homo sapiens 49-54
28817605-8 2017 The effects of all-trans retinoic acid (ATRA) on CD133-positive cells in vivo were explored with Cell Counting Kit-8, colony formation, apoptosis, cell cycle, and ethynyl deoxyuridine assays. Tretinoin 40-44 prominin 1 Homo sapiens 49-54
28817605-11 2017 ATRA inhibited the stem cell characteristics of CD133-positive cells and induced CD133-positive cell differentiation to CD133-negative cells, and promoted CD133-positive cell apoptosis. Tretinoin 0-4 prominin 1 Homo sapiens 48-53
28817605-11 2017 ATRA inhibited the stem cell characteristics of CD133-positive cells and induced CD133-positive cell differentiation to CD133-negative cells, and promoted CD133-positive cell apoptosis. Tretinoin 0-4 prominin 1 Homo sapiens 81-86
28817605-11 2017 ATRA inhibited the stem cell characteristics of CD133-positive cells and induced CD133-positive cell differentiation to CD133-negative cells, and promoted CD133-positive cell apoptosis. Tretinoin 0-4 prominin 1 Homo sapiens 81-86
28817605-11 2017 ATRA inhibited the stem cell characteristics of CD133-positive cells and induced CD133-positive cell differentiation to CD133-negative cells, and promoted CD133-positive cell apoptosis. Tretinoin 0-4 prominin 1 Homo sapiens 81-86
28712951-0 2017 RA-Induced Transcriptional Silencing of Checkpoint Kinase-2 through Promoter Methylation by Dnmt3b Is Required for Neuronal Differentiation of P19 Cells. Tretinoin 0-2 checkpoint kinase 2 Homo sapiens 40-59
28712951-4 2017 Both bisulfite genomic sequence and COBRA analyses showed that the methylation level of Chk2 promoter is progressively increased during RA-induced neuronal differentiation of P19 cells. Tretinoin 39-41 checkpoint kinase 2 Homo sapiens 88-92
28712951-8 2017 Ectopic Chk2 expression also negatively regulated cell cycle arrest and apoptosis following RA treatment, which could also contribute to impaired neuronal differentiation. Tretinoin 92-94 checkpoint kinase 2 Homo sapiens 8-12
28992291-0 2017 Retinoic acid inhibits white adipogenesis by disrupting GADD45A-mediated Zfp423 DNA demethylation. Tretinoin 0-13 growth arrest and DNA damage inducible alpha Homo sapiens 56-63
28992291-4 2017 We found that RA inhibits Zfp423 expression and adipogenesis via blocking DNA demethylation in the promoter of Zfp423, a process mediated by growth arrest and DNA-damage-inducible protein alpha (GADD45A). Tretinoin 14-16 growth arrest and DNA damage inducible alpha Homo sapiens 195-202
28992291-5 2017 RA induces the partnering between retinoic acid receptor (RAR) and tumor suppressor inhibitor of growth protein 1 (ING1), which prevents the formation of GADD45A and ING1 complex necessary for locus-specific Zfp423 DNA demethylation. Tretinoin 0-2 growth arrest and DNA damage inducible alpha Homo sapiens 154-161
28532017-7 2017 Differentiation of P19 cells and expression of beta-tubulin III, Pax-6 and Nestin were improved by incorporating retinoic acid in PLGA-Gelatin freeze-cast scaffolds. Tretinoin 113-126 paired box 6 Homo sapiens 65-70
28750075-5 2017 The induced Foxp3 expression was independent of retinoic acid (RA) signaling but was inhibited by neutralization of TGF-beta. Tretinoin 48-61 forkhead box P3 Homo sapiens 12-17
28750075-5 2017 The induced Foxp3 expression was independent of retinoic acid (RA) signaling but was inhibited by neutralization of TGF-beta. Tretinoin 63-65 forkhead box P3 Homo sapiens 12-17
28696354-7 2017 Furthermore, we observed an increase in the levels of nuclear RARgamma upon ATRA treatment. Tretinoin 76-80 retinoic acid receptor gamma Homo sapiens 62-70
28409399-0 2017 Pro-apoptotic signaling induced by Retinoic acid and dsRNA is under the control of Interferon Regulatory Factor-3 in breast cancer cells. Tretinoin 35-48 interferon regulatory factor 3 Homo sapiens 83-113
28465486-6 2017 Sphk2 overexpression increases the ATRA-induced nuclear RXRalpha export to cytoplasm and then rapidly degrades RXRalpha through the polyubiquitination pathway. Tretinoin 35-39 sphingosine kinase 2 Homo sapiens 0-5
28589680-3 2017 Ciliary neurotrophic factor expression is regulated by many factors such as all-trans retinoic acid (ATRA). Tretinoin 76-99 ciliary neurotrophic factor Mus musculus 0-27
28589680-3 2017 Ciliary neurotrophic factor expression is regulated by many factors such as all-trans retinoic acid (ATRA). Tretinoin 101-105 ciliary neurotrophic factor Mus musculus 0-27
28589680-4 2017 In this study, we found that ATRA increased CNTF expression in mouse retinal pigment epithelial (RPE) cells in a dose- and time-dependent manner, and PKA signaling pathway is necessary for ATRA-induced CNTF upregulation. Tretinoin 29-33 ciliary neurotrophic factor Mus musculus 44-48
28589680-4 2017 In this study, we found that ATRA increased CNTF expression in mouse retinal pigment epithelial (RPE) cells in a dose- and time-dependent manner, and PKA signaling pathway is necessary for ATRA-induced CNTF upregulation. Tretinoin 29-33 ciliary neurotrophic factor Mus musculus 202-206
28589680-5 2017 Furthermore, we showed that ATRA promoted CNTF expression through CREB binding to its promoter region. Tretinoin 28-32 ciliary neurotrophic factor Mus musculus 42-46
28589680-7 2017 In mouse RPE cells cultured with high oxygen, CNTF expression and secretion were decreased, but could be recovered after treatment with ATRA. Tretinoin 136-140 ciliary neurotrophic factor Mus musculus 46-50
28589680-8 2017 In conclusion, our data suggest that ATRA administration upregulates CNTF expression in RPE cells. Tretinoin 37-41 ciliary neurotrophic factor Mus musculus 69-73
28440509-14 2017 Actinomycin D, cyclohexamide and retinoic acid had inhibitory effects on MMP-2, while dexamethasone showed slight stimulatory effect on MMP-2 secretion. Tretinoin 33-46 matrix metallopeptidase 2 Homo sapiens 73-78
28559980-0 2017 All-trans-retinoic acid activates SDF-1/CXCR4/ROCK2 signaling pathway to inhibit chondrogenesis. Tretinoin 0-23 C-X-C motif chemokine ligand 12 Rattus norvegicus 34-39
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 C-X-C motif chemokine ligand 12 Rattus norvegicus 17-22
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 C-X-C motif chemokine ligand 12 Rattus norvegicus 143-148
28559980-5 2017 In contrast, ATRA increases the expression of ROCK2, SDF-1 and CXCR4. Tretinoin 13-17 C-X-C motif chemokine ligand 12 Rattus norvegicus 53-58
28559980-7 2017 In addition, we found that disturbing SDF-1/CXCR4 signaling by AMD3100 decreases ATRA-induced ROCK2 expression. Tretinoin 81-85 C-X-C motif chemokine ligand 12 Rattus norvegicus 38-43
28559980-9 2017 Together, these results show that ATRA activates SDF-1/CXCR4/ROCK2 signaling to inhibit chondrogenesis to lead to CCF by suppressing differentiation through down-regulation of SOX9 and COL2A1 expression in rat embryo hind limb bud mesenchymal cells. Tretinoin 34-38 C-X-C motif chemokine ligand 12 Rattus norvegicus 49-54
28341635-8 2017 Furthermore, we found that depletion of sept7b diminished the expression of retinaldehyde dehydrogenase 2, which catalyzes the synthesis of retinoic acid necessary for heart morphogenesis. Tretinoin 140-153 aldehyde dehydrogenase 1 family, member A2 Danio rerio 76-105
26953980-4 2017 In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced. Tretinoin 105-124 caspase 8 Homo sapiens 177-186
26953980-4 2017 In the present study, 24S-OHC was found to induce apoptosis as determined by caspase-3 activation in all-trans-retinoic acid (atRA)-treated SH-SY5Y cells in which expression of caspase-8 was induced. Tretinoin 126-130 caspase 8 Homo sapiens 177-186
27981737-0 2017 Early induction of pyruvate dehydrogenase kinase 4 by retinoic acids in adipocytes. Tretinoin 54-68 pyruvate dehydrogenase kinase 4 Rattus norvegicus 19-50
27981737-2 2017 Here, we studied the roles of 9-cis RA and all-trans RA on the regulation of pyruvate dehydrogenase kinase 4 (PDK4), an enzyme involved in fatty acid reesterification, which is a crucial metabolic pathway in adipose tissue (AT) lipid homeostasis. Tretinoin 36-38 pyruvate dehydrogenase kinase 4 Rattus norvegicus 77-108
27981737-2 2017 Here, we studied the roles of 9-cis RA and all-trans RA on the regulation of pyruvate dehydrogenase kinase 4 (PDK4), an enzyme involved in fatty acid reesterification, which is a crucial metabolic pathway in adipose tissue (AT) lipid homeostasis. Tretinoin 36-38 pyruvate dehydrogenase kinase 4 Rattus norvegicus 110-114
27981737-2 2017 Here, we studied the roles of 9-cis RA and all-trans RA on the regulation of pyruvate dehydrogenase kinase 4 (PDK4), an enzyme involved in fatty acid reesterification, which is a crucial metabolic pathway in adipose tissue (AT) lipid homeostasis. Tretinoin 53-55 pyruvate dehydrogenase kinase 4 Rattus norvegicus 77-108
27981737-2 2017 Here, we studied the roles of 9-cis RA and all-trans RA on the regulation of pyruvate dehydrogenase kinase 4 (PDK4), an enzyme involved in fatty acid reesterification, which is a crucial metabolic pathway in adipose tissue (AT) lipid homeostasis. Tretinoin 53-55 pyruvate dehydrogenase kinase 4 Rattus norvegicus 110-114
27981737-4 2017 Using site-directed mutagenesis and chomatin immuno-precipitation, we showed that this activation involves two new RA responsive elements in the Pdk4 promoter, RAREa (DR1: -125/-112) and RAREb (DR1: -86/-73), specific to AT. Tretinoin 115-117 pyruvate dehydrogenase kinase 4 Rattus norvegicus 145-149
27981737-5 2017 Furthermore, even though endogeneous Pdk4 gene was upregulated by RA in Fao cells, a rat hepatoma cell line, the induction did not occur through the newly found RAREs. Tretinoin 66-68 pyruvate dehydrogenase kinase 4 Rattus norvegicus 37-41
27981737-6 2017 CONCLUSION: In this study, we showed that adipocyte PDK4 gene is a new target of the vitamin A derived RA and might participate to the reduced fatty acid efflux from the adipocyte, a step that plays an important role in the developement of metabolic diseases. Tretinoin 103-105 pyruvate dehydrogenase kinase 4 Rattus norvegicus 52-56
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 REC8 meiotic recombination protein Mus musculus 256-260
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 REC8 meiotic recombination protein Mus musculus 256-260
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 52-65 interferon regulatory factor 4 Homo sapiens 220-250
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 52-65 CD1c molecule Homo sapiens 317-320
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 67-71 interferon regulatory factor 4 Homo sapiens 220-250
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 67-71 CD1c molecule Homo sapiens 317-320
28380213-0 2017 Retinoic acid protects from experimental cerebral infarction by upregulating GAP-43 expression. Tretinoin 0-13 growth associated protein 43 Rattus norvegicus 77-83
28380213-1 2017 The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. Tretinoin 59-72 growth associated protein 43 Rattus norvegicus 128-156
28380213-1 2017 The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. Tretinoin 59-72 growth associated protein 43 Rattus norvegicus 158-164
28380213-1 2017 The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. Tretinoin 74-76 growth associated protein 43 Rattus norvegicus 128-156
28380213-1 2017 The aim of this study was to investigate whether exogenous retinoic acid (RA) can upregulate the mRNA and protein expression of growth-associated protein 43 (GAP-43), thereby promoting brain functional recovery in a rat distal middle cerebral artery occlusion (MCAO) model of ischemia. Tretinoin 74-76 growth associated protein 43 Rattus norvegicus 158-164
28380213-7 2017 Administration of RA reduced infarction volume, promoted neurological functional recovery and upregulated expression of GAP-43. Tretinoin 18-20 growth associated protein 43 Rattus norvegicus 120-126
28380213-8 2017 Administration of RA can ameliorate neuronal damage and promote nerve regeneration by upregulating the expression of GAP-43 in the perifocal region after distal MCAO. Tretinoin 18-20 growth associated protein 43 Rattus norvegicus 117-123
28228611-9 2017 Potentiation of glucose-stimulated insulin secretion concomitant with enhanced islet cAMP level by all-trans retinoic acid (ATRA) was attenuated upon Gprc5c-KD. Tretinoin 99-122 G protein-coupled receptor, family C, group 5, member C Mus musculus 150-156
28228611-9 2017 Potentiation of glucose-stimulated insulin secretion concomitant with enhanced islet cAMP level by all-trans retinoic acid (ATRA) was attenuated upon Gprc5c-KD. Tretinoin 124-128 G protein-coupled receptor, family C, group 5, member C Mus musculus 150-156
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 5-18 C-C motif chemokine receptor 9 Homo sapiens 72-76
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 20-22 C-C motif chemokine receptor 9 Homo sapiens 72-76
28611979-3 2017 The preferentially expressed antigen of melanoma (PRAME) acts as a dominant repressor of RA signaling by binding to the complex. Tretinoin 51-53 PRAME nuclear receptor transcriptional regulator Homo sapiens 4-48
27605212-0 2017 Activation of G0S2 is coordinated by recruitment of PML/RARalpha and C/EBPepsilon to its promoter during ATRA-induced APL differentiation. Tretinoin 105-109 G0/G1 switch 2 Homo sapiens 14-18
27605212-5 2017 This mode of action is similar to that of a type I nuclear receptor and is highlighted by activation of G0/G1 switch gene 2 (G0S2) during ATRA-induced neutrophil differentiation of leukemia cell lines (NB4 and PR9) and primary human APL cells. Tretinoin 138-142 G0/G1 switch 2 Homo sapiens 104-123
27605212-5 2017 This mode of action is similar to that of a type I nuclear receptor and is highlighted by activation of G0/G1 switch gene 2 (G0S2) during ATRA-induced neutrophil differentiation of leukemia cell lines (NB4 and PR9) and primary human APL cells. Tretinoin 138-142 G0/G1 switch 2 Homo sapiens 125-129
28264498-10 2017 Intriguingly, RA fostered allergic MC degranulation, in a way completely uncoupled from FcepsilonRI expression, but it simultaneously restricted MRGPRX2-triggered histamine release in agreement with the reduced receptor expression. Tretinoin 14-16 Fc epsilon receptor Ia Homo sapiens 88-99
28053092-0 2017 Histone Acetyltransferase p300/CREB-binding Protein-associated Factor (PCAF) Is Required for All-trans-retinoic Acid-induced Granulocytic Differentiation in Leukemia Cells. Tretinoin 103-116 E1A binding protein p300 Homo sapiens 0-30
28053092-0 2017 Histone Acetyltransferase p300/CREB-binding Protein-associated Factor (PCAF) Is Required for All-trans-retinoic Acid-induced Granulocytic Differentiation in Leukemia Cells. Tretinoin 103-116 lysine acetyltransferase 2B Homo sapiens 71-75
28053092-3 2017 Herein, we show that p300/CREB-binding protein-associated factor (PCAF), a histone acetyltransferase (HAT), is a prerequisite for ATRA-induced granulocytic differentiation in leukemia cells. Tretinoin 130-134 E1A binding protein p300 Homo sapiens 21-25
28053092-3 2017 Herein, we show that p300/CREB-binding protein-associated factor (PCAF), a histone acetyltransferase (HAT), is a prerequisite for ATRA-induced granulocytic differentiation in leukemia cells. Tretinoin 130-134 lysine acetyltransferase 2B Homo sapiens 66-70
28053092-4 2017 We found that PCAF expression was markedly increased in leukemia cell lines (NB4 and HL-60) and primary APL cells during ATRA-induced granulocytic differentiation. Tretinoin 121-125 lysine acetyltransferase 2B Homo sapiens 14-18
28053092-5 2017 Consistent with these results, the expression of PCAF was markedly up-regulated in the bone marrow cells of APL patients who received ATRA-containing chemotherapy. Tretinoin 134-138 lysine acetyltransferase 2B Homo sapiens 49-53
28053092-6 2017 The knockdown of PCAF inhibited ATRA-induced granulocytic differentiation in leukemia cell lines and primary APL cells. Tretinoin 32-36 lysine acetyltransferase 2B Homo sapiens 17-21
28053092-8 2017 Acetylome analysis identified the acetylated proteins after ATRA treatment, and we found that histone H3, a known PCAF acetylation substrate, was preferentially acetylated by the ATRA treatment. Tretinoin 179-183 lysine acetyltransferase 2B Homo sapiens 114-118
28053092-10 2017 These results strongly support our hypothesis that PCAF is induced and activated by ATRA, and the subsequent acetylation of PCAF substrates promotes granulocytic differentiation in leukemia cells. Tretinoin 84-88 lysine acetyltransferase 2B Homo sapiens 51-55
28202042-13 2017 Furthermore, loss of HOXC8 in non-tumorigenic mammary epithelial cells expands the cancer stem/progenitor cells pool, increases stem cell self-renewal, prevents differentiation induced by retinoic acid and induces a transformed phenotype. Tretinoin 188-201 homeobox C8 Homo sapiens 21-26
27412076-7 2017 Studies of CV-1 and LNCaP cells transfected with RAR expression vectors and a reporter vector revealed that RARgamma and RARbeta are activated by sub-nM all-trans retinoic acid (EC50-0.3 nM): ~50-fold more is required for activation of RARalpha (EC50-16 nM). Tretinoin 163-176 retinoic acid receptor gamma Homo sapiens 108-116
27999196-3 2017 We firstly found that the deleted in azoospermia-like (DAZL) protein can be detected in 3 d CHIR99021 plus 9 d retinoic acid treated cultures and 12 d CHIR99021 plus retinoic acid co-treated cultures, but not expressed in single CHIR99021 treated cultures, single retinoic acid treated cultures, as well as 3 d retinoic acid plus 9 d CHIR99021 treated cultures. Tretinoin 111-124 deleted in azoospermia like Homo sapiens 55-59
27999196-3 2017 We firstly found that the deleted in azoospermia-like (DAZL) protein can be detected in 3 d CHIR99021 plus 9 d retinoic acid treated cultures and 12 d CHIR99021 plus retinoic acid co-treated cultures, but not expressed in single CHIR99021 treated cultures, single retinoic acid treated cultures, as well as 3 d retinoic acid plus 9 d CHIR99021 treated cultures. Tretinoin 166-179 deleted in azoospermia like Homo sapiens 55-59
27999196-3 2017 We firstly found that the deleted in azoospermia-like (DAZL) protein can be detected in 3 d CHIR99021 plus 9 d retinoic acid treated cultures and 12 d CHIR99021 plus retinoic acid co-treated cultures, but not expressed in single CHIR99021 treated cultures, single retinoic acid treated cultures, as well as 3 d retinoic acid plus 9 d CHIR99021 treated cultures. Tretinoin 166-179 deleted in azoospermia like Homo sapiens 55-59
27999196-3 2017 We firstly found that the deleted in azoospermia-like (DAZL) protein can be detected in 3 d CHIR99021 plus 9 d retinoic acid treated cultures and 12 d CHIR99021 plus retinoic acid co-treated cultures, but not expressed in single CHIR99021 treated cultures, single retinoic acid treated cultures, as well as 3 d retinoic acid plus 9 d CHIR99021 treated cultures. Tretinoin 166-179 deleted in azoospermia like Homo sapiens 55-59
28715808-10 2017 RESULTS: In the present study, ATRA treatment not only increased the TER of the Caco-2 monolayer but also up-regulated the expression levels of RARbeta, TLR4 and ZO-2 in Caco-2 cells. Tretinoin 31-35 tight junction protein 2 Homo sapiens 162-166
28680330-6 2017 CONCLUSIONS: We showed that although ATRA did not increase the frequency of Treg in culture, it significantly increased expression of rarbeta and rxrbeta only in lymphocytes taken from diseased animals and foxp3 expression only in healthy animals. Tretinoin 37-41 forkhead box P3 Rattus norvegicus 206-211
28621427-3 2017 Mining Xenopus embryonic expression databases identified a novel component of the RA metabolic network, ADHFe1. Tretinoin 82-84 alcohol dehydrogenase, iron containing 1 S homeolog Xenopus laevis 104-110
27840957-8 2017 In addition, the expression of HLA-E on the HL-60 cells in the group treated with ATRA plus VPA was not significantly increased. Tretinoin 82-86 major histocompatibility complex, class I, E Homo sapiens 31-36
27840957-9 2017 In conclusion, the combination of VPA and ATRA not only induced the differentiation of HL-60 cells, but also induced enhancement of the sensitivity of HL-60 cells to NK cells by downregulating the expression of HLA-ABC and upregulating the expression of CD54, but not MICA/MICB. Tretinoin 42-46 MHC class I polypeptide-related sequence A Homo sapiens 268-272
27840957-9 2017 In conclusion, the combination of VPA and ATRA not only induced the differentiation of HL-60 cells, but also induced enhancement of the sensitivity of HL-60 cells to NK cells by downregulating the expression of HLA-ABC and upregulating the expression of CD54, but not MICA/MICB. Tretinoin 42-46 MHC class I polypeptide-related sequence B Homo sapiens 273-277
27911779-4 2016 Retinol dehydrogenase 10 (RDH10) and aldehyde dehydrogenase family 1 subfamily A2 (ALDH1A2) mRNAs and proteins and transactivation activity of endogenous RA were found in the stroma of proximal Mullerian ducts and gradually decreased from the proximal to caudal regions in fetal mice. Tretinoin 154-156 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 37-81
27911779-4 2016 Retinol dehydrogenase 10 (RDH10) and aldehyde dehydrogenase family 1 subfamily A2 (ALDH1A2) mRNAs and proteins and transactivation activity of endogenous RA were found in the stroma of proximal Mullerian ducts and gradually decreased from the proximal to caudal regions in fetal mice. Tretinoin 154-156 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 83-90
27671872-0 2016 Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF-A pathways downstream of retinoic acid from the meninges. Tretinoin 103-116 forkhead box C1 Homo sapiens 27-32
27671872-6 2016 We provide evidence that reduced levels of meninges-derived retinoic acid (RA), caused by defects in meninges formation in Foxc1 mutants, is a major contributing factor to the cerebrovascular growth defects in Foxc1 mutants. Tretinoin 60-73 forkhead box C1 Homo sapiens 123-128
27671872-6 2016 We provide evidence that reduced levels of meninges-derived retinoic acid (RA), caused by defects in meninges formation in Foxc1 mutants, is a major contributing factor to the cerebrovascular growth defects in Foxc1 mutants. Tretinoin 60-73 forkhead box C1 Homo sapiens 210-215
27671872-6 2016 We provide evidence that reduced levels of meninges-derived retinoic acid (RA), caused by defects in meninges formation in Foxc1 mutants, is a major contributing factor to the cerebrovascular growth defects in Foxc1 mutants. Tretinoin 75-77 forkhead box C1 Homo sapiens 123-128
27671872-6 2016 We provide evidence that reduced levels of meninges-derived retinoic acid (RA), caused by defects in meninges formation in Foxc1 mutants, is a major contributing factor to the cerebrovascular growth defects in Foxc1 mutants. Tretinoin 75-77 forkhead box C1 Homo sapiens 210-215
27769742-0 2016 All-trans retinoic acid promotes wound healing of primary amniocytes through the induction of LOXL4, a member of the lysyl oxidase family. Tretinoin 0-23 lysyl oxidase like 4 Homo sapiens 94-99
27647308-0 2016 A Novel Combination of Docosahexaenoic Acid, All-Trans Retinoic Acid, and 1, 25-Dihydroxyvitamin D3 Reduces T-Bet Gene Expression, Serum Interferon Gamma, and Clinical Scores but Promotes PPARgamma Gene Expression in Experimental Autoimmune Encephalomyelitis. Tretinoin 45-68 peroxisome proliferator activated receptor gamma Mus musculus 188-197
27647308-9 2016 These findings highlighted that ATRA, D3, and DHA combination modulated PPARgamma and T-bet gene expression and resulted in decrease in Th1 response and lymphocyte invasion into the central nervous system (CNS) and resultant inflammation. Tretinoin 32-36 peroxisome proliferator activated receptor gamma Mus musculus 72-81
27569851-4 2016 The objective was to elucidate gene expression of these RA-metabolizing enzymes (ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1 and CYP26C1) and their protein presence in testes of young, peripubertal and adult dogs. Tretinoin 56-58 aldehyde dehydrogenase 1 family member A1 Canis lupus familiaris 81-88
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 15-17 aldehyde dehydrogenase 1 family member A1 Canis lupus familiaris 40-47
30460049-0 2017 Excessive retinoic acid inhibit mouse embryonic palate mesenchymal cell growth through involvement of Smad signaling. Tretinoin 10-23 SMAD family member 7 Mus musculus 102-106
30460049-13 2017 We demonstrated that RA induced inhibition of MEPM cell growth that could cause cleft palate partly by down-regulation of Smad pathway. Tretinoin 21-23 SMAD family member 7 Mus musculus 122-126
27980750-0 2016 All-trans retinoic acid (ATRA) in non-promyelocytic acute myeloid leukemia (AML): results of combination of ATRA with low-dose Ara-C in three elderly patients with NPM1-mutated AML unfit for intensive chemotherapy and review of the literature. Tretinoin 108-112 nucleophosmin 1 Homo sapiens 164-168
27980750-1 2016 Based upon the clinical behavior of three patients, we suggest that the combination of low-dose Ara-C and all-trans retinoic acid may potentially be effective in some elderly patients, unfit for intensive chemotherapy, affected with NPM1-mutated acute myeloid leukemia without FLT3 mutations, warranting perspective clinical studies in these selected patients. Tretinoin 116-129 nucleophosmin 1 Homo sapiens 233-237
27480083-0 2016 A network including PU.1, Vav1 and miR-142-3p sustains ATRA-induced differentiation of acute promyelocytic leukemia cells - a short report. Tretinoin 55-59 vav guanine nucleotide exchange factor 1 Homo sapiens 26-30
27480083-4 2016 METHODS: ATRA-induced increases in PU.1 and Vav1 expression in APL-derived NB4 cells were counteracted with specific siRNAs, and the expression of miR-142-3p was measured by quantitative real-time PCR (qRT-PCR). Tretinoin 9-13 vav guanine nucleotide exchange factor 1 Homo sapiens 44-48
27480083-9 2016 CONCLUSIONS: Our results suggest the existence of a Vav1/PU.1/miR-142-3p network that supports ATRA-induced differentiation in APL-derived cells. Tretinoin 95-99 vav guanine nucleotide exchange factor 1 Homo sapiens 52-61
27506116-0 2016 Nuclear receptor corepressors Ncor1 and Ncor2 (Smrt) are required for retinoic acid-dependent repression of Fgf8 during somitogenesis. Tretinoin 70-83 nuclear receptor co-repressor 1 Mus musculus 30-35
27506116-2 2016 Here, we show that nuclear receptor corepressors NCOR1 and NCOR2 (SMRT) redundantly mediate the ability of RA to repress Fgf8. Tretinoin 107-109 nuclear receptor co-repressor 1 Mus musculus 49-54
27506116-4 2016 Embryo chromatin immunoprecipitation studies revealed that NCOR1/2 but not coactivators are recruited to the Fgf8 RA response element (RARE) in an RA-dependent manner, whereas coactivators but not NCOR1/2 are recruited RA-dependently to a RARE near Rarb that is activated by RA. Tretinoin 114-116 nuclear receptor co-repressor 1 Mus musculus 59-66
27506116-4 2016 Embryo chromatin immunoprecipitation studies revealed that NCOR1/2 but not coactivators are recruited to the Fgf8 RA response element (RARE) in an RA-dependent manner, whereas coactivators but not NCOR1/2 are recruited RA-dependently to a RARE near Rarb that is activated by RA. Tretinoin 135-137 nuclear receptor co-repressor 1 Mus musculus 59-66
27506116-4 2016 Embryo chromatin immunoprecipitation studies revealed that NCOR1/2 but not coactivators are recruited to the Fgf8 RA response element (RARE) in an RA-dependent manner, whereas coactivators but not NCOR1/2 are recruited RA-dependently to a RARE near Rarb that is activated by RA. Tretinoin 135-137 nuclear receptor co-repressor 1 Mus musculus 59-66
27506116-7 2016 Our studies support a model in which NCOR1/2 mediates direct RA-dependent repression of Fgf8 in caudal progenitors in order to control somitogenesis. Tretinoin 61-63 nuclear receptor co-repressor 1 Mus musculus 37-42
27278254-0 2016 Myeloid cell leukaemia 1 has a vital role in retinoic acid-mediated protection of Toll-like receptor 9-stimulated B cells from spontaneous and DNA damage-induced apoptosis. Tretinoin 45-58 toll like receptor 9 Homo sapiens 82-102
27496193-7 2016 CK14 and p63 messenger RNA (mRNA) expressions in the AA + BMP4 + RA-treated cells were higher than those of the AA + BMP4-treated cells (CK14: 22.4-fold; p63: 84.7-fold). Tretinoin 65-67 bone morphogenetic protein 4 Homo sapiens 58-62
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 0-13 lysine (K)-specific demethylase 5C Mus musculus 73-78
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 0-13 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 0-13 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 0-13 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 0-13 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 15-17 lysine (K)-specific demethylase 5C Mus musculus 73-78
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 15-17 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 15-17 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 15-17 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-5 2016 Retinoic acid (RA)-induced neurite growth was suppressed by the mutation KDM5C (Y751C) , KDM5C (H514A) , and KDM5C (F642L) , but not KDM5C (D87G) or KDM5C (A388P) . Tretinoin 15-17 lysine (K)-specific demethylase 5C Mus musculus 89-94
27421841-6 2016 RNA-seq analysis indicated an upregulation of genes important for neuronal development, such as Ntng2, Enah, Gas1, Slit2, and Dscam, in response to the RA treatment in control Neuro2a cells transfected with GFP or wild-type KDM5C. Tretinoin 152-154 netrin G2 Mus musculus 96-101
27421841-6 2016 RNA-seq analysis indicated an upregulation of genes important for neuronal development, such as Ntng2, Enah, Gas1, Slit2, and Dscam, in response to the RA treatment in control Neuro2a cells transfected with GFP or wild-type KDM5C. Tretinoin 152-154 lysine (K)-specific demethylase 5C Mus musculus 224-229
27441500-3 2016 The CTA PRAME is expressed in various cancers, antagonises retinoic acid signalling and is regulated by DNA methylation and histone acetylation. Tretinoin 59-72 PRAME nuclear receptor transcriptional regulator Homo sapiens 8-13
27441500-11 2016 Surprisingly, knockdown of PRAME in TCam-2 cells did not render the cells sensitive towards retinoic acid, despite the fact that PRAME has been described to antagonise retinoic acid signalling. Tretinoin 168-181 PRAME nuclear receptor transcriptional regulator Homo sapiens 129-134
27595139-5 2016 In the mouse model of allergic eye disease (AED), classical CD11b+ DCs in the ocular mucosa showed increased activity of aldehyde dehydrogenase (ALDH), the enzyme required for retinoic acid synthesis. Tretinoin 176-189 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 121-143
27422020-5 2016 PSCs express many of the same markers as meningeal fibroblasts, including expression of the retinoic acid (RA) synthesis proteins Raldh1 and Raldh2. Tretinoin 92-105 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 130-136
27422020-5 2016 PSCs express many of the same markers as meningeal fibroblasts, including expression of the retinoic acid (RA) synthesis proteins Raldh1 and Raldh2. Tretinoin 107-109 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 130-136
27540526-6 2016 RESULTS: Data showed significant change in nuclear actin incorporation into the promoter regions of NESTIN and PAX6 after RA-induction. Tretinoin 122-124 paired box 6 Homo sapiens 111-115
27214556-9 2016 Together, these findings establish TLX1 as a critical regulator of RA metabolism and provide mechanistic insights into the molecular determinants of human congenital asplenia. Tretinoin 67-69 T cell leukemia homeobox 1 Homo sapiens 35-39
27025872-3 2016 Identification of the aldo-keto reductase enzyme AKR1B10 as highly up-regulated in keloid epidermis suggested that an imbalance of retinoic acid metabolism is likely associated with keloid disease. Tretinoin 131-144 aldo-keto reductase family 1 member B10 Homo sapiens 49-56
27025872-4 2016 Here, we show that AKR1B10 transfection into normal human keratinocytes reproduced the abnormal retinoic acid pathway expression pattern we had identified in keloid epidermis. Tretinoin 96-109 aldo-keto reductase family 1 member B10 Homo sapiens 19-26
27025872-5 2016 Cotransfection of AKR1B10 with a luciferase reporter plasmid showed reduced retinoic acid response element activity, supporting the hypothesis of retinoic acid synthesis deficiency in keloid epidermis. Tretinoin 76-89 aldo-keto reductase family 1 member B10 Homo sapiens 18-25
26577569-5 2016 Despite tolerance development, CD103(+)CD11b(+) DCs, which are the major migratory DC population in the MLNs, and the tolerance-related retinoic acid-generating enzyme RALDH2 were virtually absent from the ILNs. Tretinoin 136-149 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 168-174
28387421-8 2018 Surprisingly, retinoic acid altered the APN/CD13 enzymatic activity only in nLP fibroblasts without modification of APN/CD13 expression. Tretinoin 14-27 alanyl aminopeptidase, membrane Homo sapiens 40-43
28387421-8 2018 Surprisingly, retinoic acid altered the APN/CD13 enzymatic activity only in nLP fibroblasts without modification of APN/CD13 expression. Tretinoin 14-27 alanyl aminopeptidase, membrane Homo sapiens 44-48
28190238-6 2018 In addition, GSK-3beta inactivation and downstream beta-catenin stabilization were associated with RA-induced differentiation, which was attenuated by alpha-SYN. Tretinoin 99-101 glycogen synthase kinase 3 beta Homo sapiens 13-22
29144959-4 2018 Using novel encapsulation techniques and genetic tools, we manipulated retinoic acid-generating enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) in adipocytes that are capable of promoting growth and innervation of white adipose tissue by sympathetic neurons. Tretinoin 71-84 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 103-129
29144959-4 2018 Using novel encapsulation techniques and genetic tools, we manipulated retinoic acid-generating enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) in adipocytes that are capable of promoting growth and innervation of white adipose tissue by sympathetic neurons. Tretinoin 71-84 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 131-138
28945224-3 2018 Here, we suggest a new molecular mechanism of RA resistance by a repressor, named RA resistance factor (RaRF). Tretinoin 46-48 coiled-coil domain containing 137 Homo sapiens 82-102
28945224-3 2018 Here, we suggest a new molecular mechanism of RA resistance by a repressor, named RA resistance factor (RaRF). Tretinoin 46-48 coiled-coil domain containing 137 Homo sapiens 104-108
28945224-6 2018 MCL1 was upregulated by RA treatment upon RaRF depletion, accompanying leukemic myeloblast differentiation, which is negatively regulated by ectopic RaRF expression. Tretinoin 24-26 coiled-coil domain containing 137 Homo sapiens 42-46
28945224-6 2018 MCL1 was upregulated by RA treatment upon RaRF depletion, accompanying leukemic myeloblast differentiation, which is negatively regulated by ectopic RaRF expression. Tretinoin 24-26 coiled-coil domain containing 137 Homo sapiens 149-153
29096166-6 2018 In mammals, RA is principally stored in HSC complexed to cRBP-1 and therefore cRBP-1+ HSC numbers were used as an indicator of fetal RA status. Tretinoin 12-14 retinol binding protein 1 Homo sapiens 57-63
29096166-10 2018 CONCLUSION: Fetal RA stores, reflected in the number of cRBP-1+ HSCs, influence lung growth as well as diaphragm development in human fetuses with CDH. Tretinoin 18-20 retinol binding protein 1 Homo sapiens 56-62
28857442-3 2018 Here, we show that Yes-associated protein (YAP) is a direct target induced by CREB upon retinoic acid (RA)-induced neurite outgrowth stimuli in N2a cells. Tretinoin 88-101 yes-associated protein 1 Mus musculus 19-41
28857442-3 2018 Here, we show that Yes-associated protein (YAP) is a direct target induced by CREB upon retinoic acid (RA)-induced neurite outgrowth stimuli in N2a cells. Tretinoin 88-101 yes-associated protein 1 Mus musculus 43-46
28857442-3 2018 Here, we show that Yes-associated protein (YAP) is a direct target induced by CREB upon retinoic acid (RA)-induced neurite outgrowth stimuli in N2a cells. Tretinoin 103-105 yes-associated protein 1 Mus musculus 19-41
28857442-3 2018 Here, we show that Yes-associated protein (YAP) is a direct target induced by CREB upon retinoic acid (RA)-induced neurite outgrowth stimuli in N2a cells. Tretinoin 103-105 yes-associated protein 1 Mus musculus 43-46
28540746-0 2018 KDM3B shows tumor-suppressive activity and transcriptionally regulates HOXA1 through retinoic acid response elements in acute myeloid leukemia. Tretinoin 85-98 homeobox A1 Homo sapiens 71-76
28919001-8 2018 CONCLUSIONS: Pharmacological suppression of RA synthesis via inhibition of ALDH1A1 may be a potential target for treatment of obesity. Tretinoin 44-46 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 75-82
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 SRY-box transcription factor 9 Homo sapiens 72-76
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 homeobox B5 Homo sapiens 150-155
28981191-12 2017 When platelets were treated with atRA, binding interactions between RARalpha protein and mRNA for MAP1LC3B2, SLAIN2 and ANGPT1 were significantly decreased. Tretinoin 33-37 angiopoietin 1 Homo sapiens 120-126
29096331-0 2017 Nucleostemin silencing induces differentiation and potentiates all-trans-retinoic acid effects in human acute promyelocytic leukemia NB4 cells via autophagy. Tretinoin 67-86 G protein nucleolar 3 Homo sapiens 0-12
29096331-2 2017 In addition, NS silencing promotes the effects of all-trans-retinoic acid (ATRA)-based differentiation therapy in NB4 cells. Tretinoin 50-73 G protein nucleolar 3 Homo sapiens 13-15
29096331-2 2017 In addition, NS silencing promotes the effects of all-trans-retinoic acid (ATRA)-based differentiation therapy in NB4 cells. Tretinoin 75-79 G protein nucleolar 3 Homo sapiens 13-15
29192143-8 2017 Manipulation of the IRF1 transcription factor demonstrates that it is the level of atRA-inducible and epigenetically regulated transcription factors that determine expression of target genes (e.g. CTSS, cathepsin S). Tretinoin 83-87 cathepsin S Homo sapiens 197-201
29184163-0 2017 All-trans retinoic acid enhances cytotoxicity of CIK cells against human lung adenocarcinoma by upregulating MICA and IL-2 secretion. Tretinoin 10-23 MHC class I polypeptide-related sequence A Homo sapiens 109-113
29100091-5 2017 Whole-exome or targeted exome sequencing of 183 unrelated familial and/or severe CAKUT-affected case subjects, including 54 fetuses with BKA, led to the identification of 16 heterozygous variants in GREB1L (growth regulation by estrogen in breast cancer 1-like), a gene reported as a target of retinoic acid signaling. Tretinoin 294-307 growth regulation by estrogen in breast cancer-like Mus musculus 199-205
28885616-0 2017 MyD88 is an essential component of retinoic acid-induced differentiation in human pluripotent embryonal carcinoma cells. Tretinoin 35-48 MYD88 innate immune signal transduction adaptor Homo sapiens 0-5
28885616-1 2017 We have previously reported that myeloid differentiation primary response gene 88 (MyD88) is downregulated during all-trans retinoic acid (RA)-induced differentiation of pluripotent NTera2 human embryonal carcinoma cells (hECCs), whereas its maintained expression is associated with RA differentiation resistance in nullipotent 2102Ep hECCs. Tretinoin 124-137 MYD88 innate immune signal transduction adaptor Homo sapiens 83-88
28885616-1 2017 We have previously reported that myeloid differentiation primary response gene 88 (MyD88) is downregulated during all-trans retinoic acid (RA)-induced differentiation of pluripotent NTera2 human embryonal carcinoma cells (hECCs), whereas its maintained expression is associated with RA differentiation resistance in nullipotent 2102Ep hECCs. Tretinoin 139-141 MYD88 innate immune signal transduction adaptor Homo sapiens 83-88
28885616-1 2017 We have previously reported that myeloid differentiation primary response gene 88 (MyD88) is downregulated during all-trans retinoic acid (RA)-induced differentiation of pluripotent NTera2 human embryonal carcinoma cells (hECCs), whereas its maintained expression is associated with RA differentiation resistance in nullipotent 2102Ep hECCs. Tretinoin 283-285 MYD88 innate immune signal transduction adaptor Homo sapiens 83-88
28885616-3 2017 In this study, we report that loss of MyD88 is essential for RA-facilitated differentiation of hECCs. Tretinoin 61-63 MYD88 innate immune signal transduction adaptor Homo sapiens 38-43
29164236-9 2017 Exposure of cells to various PEX-associated (stress) factors, including TGF-beta1, UV-B light, oxidative stress, mechanical stress, and retinoic acid enhanced LOXL1-a transcript levels (>=1.5-fold; P < 0.05), while partially downregulating LOXL1 levels (<=0.7-fold; P < 0.05). Tretinoin 136-149 lysyl oxidase like 1 Homo sapiens 159-164
29164236-9 2017 Exposure of cells to various PEX-associated (stress) factors, including TGF-beta1, UV-B light, oxidative stress, mechanical stress, and retinoic acid enhanced LOXL1-a transcript levels (>=1.5-fold; P < 0.05), while partially downregulating LOXL1 levels (<=0.7-fold; P < 0.05). Tretinoin 136-149 lysyl oxidase like 1 Homo sapiens 246-251
29073082-5 2017 This transcription factor represses Bco1 gene expression in response to retinoic acid signaling. Tretinoin 72-85 beta-carotene oxygenase 1 Mus musculus 36-40
29073082-8 2017 In the intestine, it increased the expression of retinoic acid-inducible target genes such as Aldh1a2, Dhrs3, and Ccr9 The beta-carotene-inducible disruption of retinoid homeostasis affected gut-homing and differentiation of lymphocytes and displayed morphologically in large lymphoid follicles along the intestine. Tretinoin 49-62 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 94-101
29057906-3 2017 Here we show that RA treatment during EC embryoid body formation is a highly robust protocol for generation of striatal-like GABAergic neurons which display molecular characteristics of striatopallidal medium spiny neurons (MSNs), including expression of functional dopamine D2 receptor. Tretinoin 18-20 dopamine receptor D2 Homo sapiens 266-286
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 spermatid nuclear transition protein 1 Bubalus bubalis 200-206
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 zona pellucida sperm-binding protein 2 Bubalus bubalis 300-303
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 spermatid nuclear transition protein 1 Bubalus bubalis 200-206
28743499-0 2017 All-trans retinoic acid attenuates bleomycin-induced pulmonary fibrosis via downregulating EphA2-EphrinA1 signaling. Tretinoin 0-23 Eph receptor A2 Mus musculus 91-96
28743499-7 2017 However, administration of ATRA attenuated the upregulation of EphA2-EphrinA1 and PI3K-Akt after bleomycin instillation, and decreased pulmonary fibrosis. Tretinoin 27-31 Eph receptor A2 Mus musculus 63-68
28743499-9 2017 Collectively, these data suggest that ATRA attenuates bleomycin-induced pulmonary fibrosis by regulating EphA2-EphrinA1 and PI3K-Akt signaling. Tretinoin 38-42 Eph receptor A2 Mus musculus 105-110
30271852-12 2017 Spontaneous neural differentiation (nestin and Tju1) and retinoic acid-induced endodermal differentiation (Pdx-1 and insulin I) were improved in the EBs produced using the new insert compared to those in EBs produced by suspension culture. Tretinoin 57-70 pancreatic and duodenal homeobox 1 Mus musculus 107-112
28681415-1 2017 BACKGROUND: Retinoic acid is implicated in the induction of the gene encoding Sonic hedgehog (Shh) that specifies anteroposterior positional values and promotes growth of the developing limb bud. Tretinoin 12-25 sonic hedgehog Gallus gallus 78-92
28681415-1 2017 BACKGROUND: Retinoic acid is implicated in the induction of the gene encoding Sonic hedgehog (Shh) that specifies anteroposterior positional values and promotes growth of the developing limb bud. Tretinoin 12-25 sonic hedgehog Gallus gallus 94-97
28681415-4 2017 RESULTS: Retinoic acid up-regulates expression of Hoxd11-13 that encode transcription factors implicated in inducing Shh transcription and that are involved in digit development. Tretinoin 9-22 homeobox D11 Gallus gallus 50-56
28681415-4 2017 RESULTS: Retinoic acid up-regulates expression of Hoxd11-13 that encode transcription factors implicated in inducing Shh transcription and that are involved in digit development. Tretinoin 9-22 sonic hedgehog Gallus gallus 117-120
28681415-5 2017 In our assay, retinoic acid induces Shh transcription and, consequently, a new pattern of digits at a much later stage than anticipated. Tretinoin 14-27 sonic hedgehog Gallus gallus 36-39
28681415-6 2017 Retinoic acid represses many anteriorly expressed genes, including Bmp4, Lhx9, Msx2, and Alx4. Tretinoin 0-13 LIM homeobox 9 Gallus gallus 73-77
28681415-6 2017 Retinoic acid represses many anteriorly expressed genes, including Bmp4, Lhx9, Msx2, and Alx4. Tretinoin 0-13 ALX homeobox 4 Gallus gallus 89-93
28681415-8 2017 We show that transient exposure to retinoic acid can suppress distal development and expedite cells to transcriptionally respond to Shh. Tretinoin 35-48 sonic hedgehog Gallus gallus 132-135
28713967-0 2017 Involvement of Notch2 in all-trans retinoic acid-induced inhibition of mouse embryonic palate mesenchymal cell proliferation. Tretinoin 35-48 notch 2 Mus musculus 15-21
28713967-4 2017 Notch2 was revealed to be upregulated in mouse embryonic palate mesenchymal (MEPM) cells in the atRA-treated group compared with untreated control mice between embryonic day (E)12.5 and E14.5. Tretinoin 96-100 notch 2 Mus musculus 0-6
28713967-5 2017 In addition, atRA was demonstrated to mediate Notch2 expression via the activation of RA receptors (RARs). Tretinoin 13-17 notch 2 Mus musculus 46-52
28713967-7 2017 It was demonstrated that Notch2 silencing partially reversed the atRA-induced inhibition of ERK phosphorylation in MEPM cells. Tretinoin 65-69 notch 2 Mus musculus 25-31
28713967-8 2017 In addition, the atRA-induced cyclin D1 downregulation and p21 upregulation were partially reversed following Notch2 silencing, whereas the atRA-induced inhibition of cellular proliferation was also attenuated. Tretinoin 17-21 notch 2 Mus musculus 110-116
28713967-10 2017 The present findings suggested that during embryonic development, atRA may enhance the expression of Notch2, which may inhibit cellular proliferation, possibly through ERK signaling. Tretinoin 66-70 notch 2 Mus musculus 101-107
28718514-5 2017 Deficient retinoic acid production in aldehyde dehydrogenase 1 A1 (Aldh1a1) knockout adipocytes (KO) inhibits adipogenesis and increases thermogenesis. Tretinoin 10-23 aldehyde dehydrogenase 1 family member A1 Canis lupus familiaris 38-65
28718514-5 2017 Deficient retinoic acid production in aldehyde dehydrogenase 1 A1 (Aldh1a1) knockout adipocytes (KO) inhibits adipogenesis and increases thermogenesis. Tretinoin 10-23 aldehyde dehydrogenase 1 family member A1 Canis lupus familiaris 67-74
28867785-5 2017 RA-treated hiPSC-CMs displayed shorter APs than control hiPSC-CMs and this phenotype became more prominent upon addition of synthetic IK1 through dynamic clamp. Tretinoin 0-2 IKAROS family zinc finger 1 Homo sapiens 134-137
28488074-0 2017 All-trans retinoic acid enhances in vitro mesenchymal stem cells migration by targeting matrix metalloproteinases 2 and 9. Tretinoin 10-23 matrix metallopeptidase 2 Rattus norvegicus 88-121
28488074-1 2017 OBJECTIVES: To investigate the effect of all-trans retinoic acid (ATRA) on caspase 3 activity, matrix metalloproteinase 2 (MMP-2), and MMP-9 expression and activity as well as in vitro rat bone marrow-derived mesenchymal stem cells (MSCs) migration. Tretinoin 66-70 caspase 3 Rattus norvegicus 75-84
28488074-2 2017 RESULTS: The expression of the MMP-2/-9 was at least five times higher in ATRA-treated MSCs (P < 0.001), and MMP-2/-9 activity was enhanced with increasing doses compared to the control MSCs. Tretinoin 74-78 matrix metallopeptidase 2 Rattus norvegicus 31-39
28488074-2 2017 RESULTS: The expression of the MMP-2/-9 was at least five times higher in ATRA-treated MSCs (P < 0.001), and MMP-2/-9 activity was enhanced with increasing doses compared to the control MSCs. Tretinoin 74-78 matrix metallopeptidase 2 Rattus norvegicus 31-36
28488074-5 2017 CONCLUSION: ATRA increases the in vitro migration capacity of the MSCs through stimulating the expression and activity of MMP-2/-9 and inhibiting caspase three enzyme activity. Tretinoin 12-16 matrix metallopeptidase 2 Rattus norvegicus 122-127
28547797-12 2017 Consistently, all-trans-retinoic acid attenuated HV development and increased ocular dre-miR-21 expression. Tretinoin 14-37 suppressor of fused homolog (Drosophila) Danio rerio 85-88
28746369-7 2017 Culturing naive human T cells with IL-2/TGFbeta1 resulted in the generation of 54.2% of Treg cells (CD4+CD25+FOXP3+) whereas the addition of 100 nM atRA increased the yield of Treg cells to 66% (p = 0.0088). Tretinoin 148-152 forkhead box P3 Homo sapiens 109-114
28515123-6 2017 Quantitative genomic and functional analyses revealed that MMP12, a macrophage-secreted elastase, was elevated in IL13-skewed TAM polarization, whereas ATRA treatment downregulated IL13-induced secretion of MMP12. Tretinoin 152-156 matrix metallopeptidase 12 Mus musculus 207-212
28715585-5 2017 Results: AM induction by atRA was confirmed via quantification of retinoic acid receptor beta (RARbeta), a well-established retinoic acid-induced gene. Tretinoin 25-29 retinoic acid receptor, beta Mus musculus 66-93
28715585-5 2017 Results: AM induction by atRA was confirmed via quantification of retinoic acid receptor beta (RARbeta), a well-established retinoic acid-induced gene. Tretinoin 25-29 retinoic acid receptor, beta Mus musculus 95-102
28715585-5 2017 Results: AM induction by atRA was confirmed via quantification of retinoic acid receptor beta (RARbeta), a well-established retinoic acid-induced gene. Tretinoin 66-79 retinoic acid receptor, beta Mus musculus 95-102
27966553-8 2017 Mechanistically, acetate-induced DC expression of Aldh1a2, which converts Vitamin A into its metabolite retinoic acid (RA). Tretinoin 104-117 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 50-57
27966553-8 2017 Mechanistically, acetate-induced DC expression of Aldh1a2, which converts Vitamin A into its metabolite retinoic acid (RA). Tretinoin 119-121 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 50-57
28465486-4 2017 Here we show that SphK2 overexpression contributes to the resistance of all-trans retinoic acid (ATRA) therapy in colon cancer through rapid degradation of cytoplasmic retinoid X receptor alpha (RXRalpha) by lysine 48 (K48)- and lysine 63 (K63)-based polyubiquitination. Tretinoin 82-95 sphingosine kinase 2 Homo sapiens 18-23
28465486-4 2017 Here we show that SphK2 overexpression contributes to the resistance of all-trans retinoic acid (ATRA) therapy in colon cancer through rapid degradation of cytoplasmic retinoid X receptor alpha (RXRalpha) by lysine 48 (K48)- and lysine 63 (K63)-based polyubiquitination. Tretinoin 97-101 sphingosine kinase 2 Homo sapiens 18-23
28465486-5 2017 Human colonic adenocarcinoma HCT-116 cells transfected with SphK2 (HCT-116Sphk2 cells) demonstrate resistance to ATRA therapy as determined by in vitro and in vivo assays. Tretinoin 113-117 sphingosine kinase 2 Homo sapiens 60-65
27419624-0 2017 RARalpha2 and PML-RAR similarities in the control of basal and retinoic acid induced myeloid maturation of acute myeloid leukemia cells. Tretinoin 63-76 PML-RARA regulated adaptor molecule 1 Homo sapiens 14-21
27419624-8 2017 Silencing of PML-RAR and RARalpha2 causes also similar perturbations in the whole genome gene-expression profiles of vehicle and ATRA treated NB4 cells. Tretinoin 129-133 PML-RARA regulated adaptor molecule 1 Homo sapiens 13-20
28584089-3 2017 Within 2 h of retinoic acid treatment, Hoxa1 is rapidly recruited to target sites that are associated with genes involved in regulation of pluripotency, and these genes display early changes in expression. Tretinoin 14-27 homeobox A1 Mus musculus 39-44
28215943-0 2017 All-trans retinoic acid enhances gemcitabine cytotoxicity in human pancreatic cancer cell line AsPC-1 by up-regulating protein expression of deoxycytidine kinase. Tretinoin 0-23 deoxycytidine kinase Homo sapiens 141-161
28479188-6 2017 Treatment with all-trans retinoic acid antagonizes stress-induced activation of dHSCs by restricting protein translation and levels of reactive oxygen species (ROS) and Myc. Tretinoin 25-38 myelocytomatosis oncogene Mus musculus 169-172
28441416-3 2017 Oxidative metabolism of ethanol by alcohol dehydrogenase or cytochrome P450 2E1 has been implicated in some of ethanol"s teratogenic effects, either via production of acetaldehyde or competitive inhibition of retinoic acid synthesis. Tretinoin 209-222 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 35-56
28412739-7 2017 The retinoids, AM80 (tamibarotene) and all-trans retinoic acid, caused dose-dependent growth inhibition, G1 arrest, and CDK2/4/6 down-regulation. Tretinoin 49-62 cyclin dependent kinase 2 Homo sapiens 120-128
28369068-0 2017 All-trans retinoic acid suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and metastasis in esophageal squamous cell carcinoma. Tretinoin 0-23 TEK receptor tyrosine kinase Homo sapiens 52-56
28369068-6 2017 We investigated the effects of ATRA on the expression of angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2) and receptor Tie-2 in EC1 cells in vitro. Tretinoin 31-35 angiopoietin 1 Homo sapiens 57-71
28369068-11 2017 Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Tretinoin 13-17 angiopoietin 1 Homo sapiens 81-86
28369068-11 2017 Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Tretinoin 13-17 angiopoietin 2 Homo sapiens 88-93
28369068-11 2017 Furthermore, ATRA treatment led to a marked decrease of the transcript levels of Ang-1, Ang-2, Tie-2, VEGF, and VEGF receptors, as assessed by real-time RT-PCR. Tretinoin 13-17 TEK receptor tyrosine kinase Homo sapiens 95-100
28369068-12 2017 Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. Tretinoin 74-78 angiopoietin 1 Homo sapiens 35-40
28369068-12 2017 Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. Tretinoin 74-78 angiopoietin 2 Homo sapiens 42-47
28369068-12 2017 Importantly, the protein levels of Ang-1, Ang-2 and Tie-2 were reduced by ATRA treatment. Tretinoin 74-78 TEK receptor tyrosine kinase Homo sapiens 52-57
28369068-14 2017 Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Tretinoin 13-17 platelet and endothelial cell adhesion molecule 1 Homo sapiens 56-60
28369068-14 2017 Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Tretinoin 13-17 angiopoietin 1 Homo sapiens 62-67
28369068-14 2017 Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Tretinoin 13-17 angiopoietin 2 Homo sapiens 69-74
28369068-14 2017 Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Tretinoin 13-17 TEK receptor tyrosine kinase Homo sapiens 79-84
28369068-15 2017 Collectively, our findings demonstrate that ATRA exhibits a dose- and temporal-dependent effect on the metastatic behavior, suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and the progression of xenograft tumors of EC1 cells. Tretinoin 44-48 TEK receptor tyrosine kinase Homo sapiens 152-156
28157617-6 2017 The antiinflammatory effect of ATRA was associated with a reduction in the phosphorylation levels of IkappaB and p65 (~50%, P<.05), two subunits of the NF-kappaB pathway, probably mediated by PGC1alpha, in 3 T3-L1 adipocytes. Tretinoin 31-35 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 195-204
28336971-5 2017 It specifically binds to RARgamma and inhibits all-trans retinoic acid (atRA) stimulation of RARgamma transactivation. Tretinoin 57-70 retinoic acid receptor gamma Homo sapiens 25-33
28336971-5 2017 It specifically binds to RARgamma and inhibits all-trans retinoic acid (atRA) stimulation of RARgamma transactivation. Tretinoin 57-70 retinoic acid receptor gamma Homo sapiens 93-101
28336971-5 2017 It specifically binds to RARgamma and inhibits all-trans retinoic acid (atRA) stimulation of RARgamma transactivation. Tretinoin 72-76 retinoic acid receptor gamma Homo sapiens 25-33
28336971-5 2017 It specifically binds to RARgamma and inhibits all-trans retinoic acid (atRA) stimulation of RARgamma transactivation. Tretinoin 72-76 retinoic acid receptor gamma Homo sapiens 93-101
28256636-7 2017 In mice which have substantially decreased endogenous retinoic acid biosynthesis, Fgf21 expression was increased, whereas acute pharmacological retinoid treatment decreased FGF21 levels. Tretinoin 54-67 fibroblast growth factor 21 Mus musculus 82-87
27648628-5 2017 Furthermore, we showed that Pokemon could repress the transcriptional activity of RARalpha by increasing the recruitment of nuclear receptor co-repressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) to the retinoic acid response element (RARE) element. Tretinoin 187-200 zinc finger and BTB domain containing 7A Homo sapiens 28-35
28112361-13 2017 Actinomycin D, cyclohexamide, retinoic acid and dexamethasone also had inhibitory effects on MMP-2. Tretinoin 30-43 matrix metallopeptidase 2 Homo sapiens 93-98
28442062-4 2017 A novel retinoic acid response element (RARE) positioned at -989 nucleotides upstream of the transcription start site (TSS) was identified, providing a binding site for a dimeric RA receptor (i.e. retinoic acid receptor gamma (RARgamma) and retinoic X receptor). Tretinoin 8-21 retinoic acid receptor gamma Homo sapiens 227-235
28442062-9 2017 We propose that for RA response, an enhanceosome is orchestrated through scaffolding of a CREB-binding protein (CBP)/p300 molecule between RARE and elements in the proximal promoter region, controlling germ-line expression of the c-kit gene. Tretinoin 20-22 E1A binding protein p300 Homo sapiens 117-121
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 150-154 lymphoid enhancer binding factor 1 Homo sapiens 74-78
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 glycogen synthase kinase 3 beta Homo sapiens 93-102
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 glycogen synthase kinase 3 beta Homo sapiens 155-164
28052022-6 2017 By contrast, TbetaRII blocked all-trans retinoic acid-induced differentiation through inhibition of TbetaRII-B. Tretinoin 40-53 transforming growth factor beta receptor 2 Homo sapiens 13-21
28052022-6 2017 By contrast, TbetaRII blocked all-trans retinoic acid-induced differentiation through inhibition of TbetaRII-B. Tretinoin 40-53 transforming growth factor beta receptor 2 Homo sapiens 100-108
28152080-3 2017 We identified the NADPH oxidase (NOX) complexes as candidates for the source of this endogenous ROS, and within this gene family, and over the course of differentiation, Nox1 and Nox 4 show the greatest upregulation induced by RA. Tretinoin 227-229 NADPH oxidase 1 Mus musculus 170-174
28152080-3 2017 We identified the NADPH oxidase (NOX) complexes as candidates for the source of this endogenous ROS, and within this gene family, and over the course of differentiation, Nox1 and Nox 4 show the greatest upregulation induced by RA. Tretinoin 227-229 NADPH oxidase 4 Mus musculus 179-184
28152080-5 2017 Pan-NOX and NOX1-specific inhibitors significantly reduced the ability of RA to induce PrE, and this was recapitulated using a genetic approach to knockdown Nox1 and/or Nox4 transcripts. Tretinoin 74-76 NADPH oxidase 1 Mus musculus 12-16
28152080-5 2017 Pan-NOX and NOX1-specific inhibitors significantly reduced the ability of RA to induce PrE, and this was recapitulated using a genetic approach to knockdown Nox1 and/or Nox4 transcripts. Tretinoin 74-76 NADPH oxidase 1 Mus musculus 157-161
28152080-5 2017 Pan-NOX and NOX1-specific inhibitors significantly reduced the ability of RA to induce PrE, and this was recapitulated using a genetic approach to knockdown Nox1 and/or Nox4 transcripts. Tretinoin 74-76 NADPH oxidase 4 Mus musculus 169-173
28192799-0 2017 Cyp1b1 Regulates Ocular Fissure Closure Through a Retinoic Acid-Independent Pathway. Tretinoin 50-63 cytochrome P450, family 1, subfamily B, polypeptide 1 Danio rerio 0-6
28192799-8 2017 In contrast, cyp1b1 overexpression inhibited cell survival in the ventral ocular fissure and prevented fissure closure via an RA-independent pathway. Tretinoin 126-128 cytochrome P450, family 1, subfamily B, polypeptide 1 Danio rerio 13-19
28192799-11 2017 Conclusions: Cyp1b1 regulation of ocular fissure closure indirectly affects neural crest migration and development through an RA-independent pathway. Tretinoin 126-128 cytochrome P450, family 1, subfamily B, polypeptide 1 Danio rerio 13-19
28125680-8 2017 Finally, cellular assays showed that the phosphorylation of the NTD of RARgamma is differentially regulated by retinoic acid in RARgammaWT and in the S371N, S371E and R387K mutants. Tretinoin 111-124 retinoic acid receptor gamma Homo sapiens 71-79
27840199-8 2017 Retinoic acid (RA) addition and inhibition studies revealed that tbx2a and tbx2b are negatively regulated by RA signaling. Tretinoin 0-13 T-box transcription factor 2b Danio rerio 75-80
27840199-8 2017 Retinoic acid (RA) addition and inhibition studies revealed that tbx2a and tbx2b are negatively regulated by RA signaling. Tretinoin 15-17 T-box transcription factor 2b Danio rerio 75-80
27840199-8 2017 Retinoic acid (RA) addition and inhibition studies revealed that tbx2a and tbx2b are negatively regulated by RA signaling. Tretinoin 109-111 T-box transcription factor 2b Danio rerio 75-80
28049897-2 2017 We found that Tal2 was induced during neural differentiation in P19 cells, which are pluripotent mouse embryonal carcinoma cells that differentiate into the neural lineage upon both exposure to all-trans retinoic acid (atRA) and the formation of cell aggregation. Tretinoin 204-217 T cell acute lymphocytic leukemia 2 Mus musculus 14-18
28049897-2 2017 We found that Tal2 was induced during neural differentiation in P19 cells, which are pluripotent mouse embryonal carcinoma cells that differentiate into the neural lineage upon both exposure to all-trans retinoic acid (atRA) and the formation of cell aggregation. Tretinoin 219-223 T cell acute lymphocytic leukemia 2 Mus musculus 14-18
28049897-3 2017 Tal2 expression during neural differentiation in P19 cells was detected within 3 h after induction with atRA and retinoic acid receptor alpha (RARalpha). Tretinoin 104-108 T cell acute lymphocytic leukemia 2 Mus musculus 0-4
28066180-6 2016 Using RA to induce neuron differentiation in two neuroblastoma cell lines displaying high and low levels of hASH1 expression, we confirmed the link between hASH1 expression and the differentiation defective phenotype, which was reversed by silencing hASH1 or by hypoxic preconditioning. Tretinoin 6-8 achaete-scute family bHLH transcription factor 1 Homo sapiens 156-161
28066180-6 2016 Using RA to induce neuron differentiation in two neuroblastoma cell lines displaying high and low levels of hASH1 expression, we confirmed the link between hASH1 expression and the differentiation defective phenotype, which was reversed by silencing hASH1 or by hypoxic preconditioning. Tretinoin 6-8 achaete-scute family bHLH transcription factor 1 Homo sapiens 156-161
27798106-4 2016 Here, we show that DNA methylation-independent removable CTCF insulator is responsible for retinoic acid (RA)-mediated higher-order chromatin remodeling in the human HOXA gene locus. Tretinoin 91-104 homeobox A cluster Homo sapiens 166-170
27798106-4 2016 Here, we show that DNA methylation-independent removable CTCF insulator is responsible for retinoic acid (RA)-mediated higher-order chromatin remodeling in the human HOXA gene locus. Tretinoin 106-108 homeobox A cluster Homo sapiens 166-170
27989102-9 2016 Furthermore, silencing of either TIG1 or TMEM192 led to alleviation of the upregulation of autophagy induced by all-trans retinoic acid. Tretinoin 122-135 transmembrane protein 192 Homo sapiens 41-48
27989102-11 2016 Our study also suggests that TIG1 and TMEM192 play an important role in the all-trans retinoic acid-mediated upregulation of autophagic activity. Tretinoin 86-99 transmembrane protein 192 Homo sapiens 38-45
27693483-5 2016 VPA elevated expression levels of various developmental regulators, including Cdx1 and Hoxa1, known transcriptional targets of retinoic acid (RA) signaling. Tretinoin 127-140 caudal type homeobox 1 Mus musculus 78-82
27693483-5 2016 VPA elevated expression levels of various developmental regulators, including Cdx1 and Hoxa1, known transcriptional targets of retinoic acid (RA) signaling. Tretinoin 127-140 homeobox A1 Mus musculus 87-92
27693483-5 2016 VPA elevated expression levels of various developmental regulators, including Cdx1 and Hoxa1, known transcriptional targets of retinoic acid (RA) signaling. Tretinoin 142-144 caudal type homeobox 1 Mus musculus 78-82
27693483-5 2016 VPA elevated expression levels of various developmental regulators, including Cdx1 and Hoxa1, known transcriptional targets of retinoic acid (RA) signaling. Tretinoin 142-144 homeobox A1 Mus musculus 87-92
27893754-3 2016 Molecularly, excess RA signaling negatively regulates fibroblast growth factor 8a (fgf8a) expression and positively regulates matrix metalloproteinase 9 (mmp9) expression. Tretinoin 20-22 matrix metallopeptidase 9 Danio rerio 126-152
27893754-3 2016 Molecularly, excess RA signaling negatively regulates fibroblast growth factor 8a (fgf8a) expression and positively regulates matrix metalloproteinase 9 (mmp9) expression. Tretinoin 20-22 matrix metallopeptidase 9 Danio rerio 154-158
27444966-1 2016 Retinoic acid early induced transcript-1 (RAE-1) glycoproteins are ligands of the activating immune receptor NKG2D. Tretinoin 0-13 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 109-114
27299363-7 2016 Retinoic acid can posteriorize and at the same time dorsalize the foregut toward a PDX1-positive pancreatic duodenal cell type whereas active Wnt/beta-catenin signaling synergistically with FGF-2, BMP-4, and RA induces the formation of CDX2-positive posterior endoderm. Tretinoin 0-13 pancreatic and duodenal homeobox 1 Homo sapiens 83-87
27684594-4 2016 Most established reporter systems, both transgenic mice and cell lines, make use of the highly potent RA response element (RARE) upstream of the RAR-beta gene to drive RA-inducible expression of reporter genes, such as beta-galactosidase or luciferase. Tretinoin 102-104 retinoic acid receptor, beta Mus musculus 145-153
27684594-4 2016 Most established reporter systems, both transgenic mice and cell lines, make use of the highly potent RA response element (RARE) upstream of the RAR-beta gene to drive RA-inducible expression of reporter genes, such as beta-galactosidase or luciferase. Tretinoin 123-125 retinoic acid receptor, beta Mus musculus 145-153
26883953-9 2016 Both the acetylation and SUMOylation status of the PXR protein is affected by its ability to associate with the lysine de-acetylating enzyme histone de-acetylase (HDAC)3 in a complex with silencing mediator of retinoic acid and thyroid hormone receptor (SMRT). Tretinoin 210-223 histone deacetylase 3 Homo sapiens 112-169
27307211-4 2016 Here, we show that GPSM3 is induced in the human promyelocytic leukemia NB4 cell line following retinoic acid treatment, which differentiates this cell line into a model of neutrophil physiology (NB4*). Tretinoin 96-109 G protein signaling modulator 3 Homo sapiens 19-24
27416800-3 2016 atRA bound to CRABPs (holo-CRABP) was efficiently metabolized by CYP26B1. Tretinoin 0-4 cellular retinoic acid binding protein 1 Homo sapiens 14-19
27331409-2 2016 Responding to an RA-induced cytosolic signaling machine, c-Raf translocates to the nucleus, providing propulsion for RA-induced differentiation. Tretinoin 17-19 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 57-62
27331409-2 2016 Responding to an RA-induced cytosolic signaling machine, c-Raf translocates to the nucleus, providing propulsion for RA-induced differentiation. Tretinoin 117-119 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 57-62
27085739-6 2016 Silencing NEDD9 in Schwann cells had no effect on basal migratory ability, but completely abrogated RA-induced enhanced migration. Tretinoin 100-102 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 10-15
26980802-1 2016 All-trans-retinoic acid plays a central role in mucosal immunity, where it promotes its synthesis by up-regulating CD103 expression on dendritic cells, induces gut tropic (alpha4beta7(+) and CCR9(+)) T cells, and inhibits Th1/Th17 differentiation. Tretinoin 0-23 C-C motif chemokine receptor 9 Homo sapiens 191-195
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 26-39 C-C motif chemokine receptor 9 Homo sapiens 171-175
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 72-85 C-C motif chemokine receptor 9 Homo sapiens 171-175
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 72-85 C-C motif chemokine receptor 9 Homo sapiens 171-175
27363269-7 2016 The expressions of p-JAK2 and p-STAT3 were down-regulated while the expressions of GRIM-19 and Bax were up-regulated after treated with IFN-beta or ATRA on HepG2 cells, especially the combination of IFN-beta and ATRA. Tretinoin 148-152 Janus kinase 2 Homo sapiens 21-25
27363269-7 2016 The expressions of p-JAK2 and p-STAT3 were down-regulated while the expressions of GRIM-19 and Bax were up-regulated after treated with IFN-beta or ATRA on HepG2 cells, especially the combination of IFN-beta and ATRA. Tretinoin 148-152 interferon beta 1 Homo sapiens 199-207
27364362-7 2016 Function of Cx43 GJ was regulated by Cx43 specific inhibitors, gap26 (300 muM) or enhancer, retinoic acid (10 muM) and two specific siRNAs. Tretinoin 92-105 gap junction protein alpha 1 Homo sapiens 12-16
27151945-11 2016 In enteroids, the stimulation of RA production by SCFA was mimicked by inhibitors of histone deacetylase 3 (HDAC3) but not by HDAC1/2 inhibitors nor by agonists of butyrate receptors G-protein-coupled receptor (GPR)43 or GPR109A, indicating that butyrate stimulates RA production via HDAC3 inhibition. Tretinoin 33-35 histone deacetylase 3 Homo sapiens 85-106
27151945-11 2016 In enteroids, the stimulation of RA production by SCFA was mimicked by inhibitors of histone deacetylase 3 (HDAC3) but not by HDAC1/2 inhibitors nor by agonists of butyrate receptors G-protein-coupled receptor (GPR)43 or GPR109A, indicating that butyrate stimulates RA production via HDAC3 inhibition. Tretinoin 33-35 histone deacetylase 3 Homo sapiens 108-113
27151945-11 2016 In enteroids, the stimulation of RA production by SCFA was mimicked by inhibitors of histone deacetylase 3 (HDAC3) but not by HDAC1/2 inhibitors nor by agonists of butyrate receptors G-protein-coupled receptor (GPR)43 or GPR109A, indicating that butyrate stimulates RA production via HDAC3 inhibition. Tretinoin 33-35 histone deacetylase 3 Homo sapiens 284-289
26915917-0 2016 Differential Regulation of Bcl-xL Gene Expression by Corticosterone, Progesterone, and Retinoic Acid. Tretinoin 87-100 Bcl2-like 1 Rattus norvegicus 27-33
26915917-2 2016 Mechanistically, CT, PG, and RA induce increases of Bcl-xL protein and mRNA, and activate a 3.2 kb bcl-x gene promoter. Tretinoin 29-31 Bcl2-like 1 Rattus norvegicus 52-58
26915917-2 2016 Mechanistically, CT, PG, and RA induce increases of Bcl-xL protein and mRNA, and activate a 3.2 kb bcl-x gene promoter. Tretinoin 29-31 Bcl2-like 1 Rattus norvegicus 99-104
26915917-3 2016 CT and RA, but not PG, induced the activity of a 0.9 kb bcl-x promoter, containing sequences for AP-1 and NF-kB binding. Tretinoin 7-9 Bcl2-like 1 Rattus norvegicus 56-61
26915917-3 2016 CT and RA, but not PG, induced the activity of a 0.9 kb bcl-x promoter, containing sequences for AP-1 and NF-kB binding. Tretinoin 7-9 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 97-101
26991262-0 2016 Liganded retinoic acid X receptor alpha represses connexin 43 through a potential retinoic acid response element in the promoter region. Tretinoin 9-22 gap junction protein alpha 1 Homo sapiens 50-61
26991262-3 2016 METHODS: The activations of retinoic acid response element (RARE) in Cx43 were measured by luciferase transfection assay. Tretinoin 28-41 gap junction protein alpha 1 Homo sapiens 69-73
26991262-10 2016 The RARE-like sequence harbored in the Cx43 promoter region may serve as a functional RARE in the retinoic acid (RA) signaling pathway. Tretinoin 98-111 gap junction protein alpha 1 Homo sapiens 39-43
26991262-10 2016 The RARE-like sequence harbored in the Cx43 promoter region may serve as a functional RARE in the retinoic acid (RA) signaling pathway. Tretinoin 4-6 gap junction protein alpha 1 Homo sapiens 39-43
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 60-79 growth hormone secretagogue receptor Rattus norvegicus 153-158
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 60-79 somatostatin receptor 2 Rattus norvegicus 184-190
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 81-85 growth hormone secretagogue receptor Rattus norvegicus 153-158
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 81-85 somatostatin receptor 2 Rattus norvegicus 184-190
27052215-8 2016 Combination treatment with the RAR-agonist Am80 and RXR-agonist PA024 mimicked the effects of ATRA on Ghrh-r and Ghs-r gene expressions. Tretinoin 94-98 growth hormone secretagogue receptor Rattus norvegicus 113-118
27052215-11 2016 Our results suggest that expressions of Ghrh-r and Ghs-r are regulated by RA through the RAR-RXR receptor complex and that RA enhances the effects of GHRH and ghrelin on GH release from the anterior pituitary gland. Tretinoin 74-76 growth hormone secretagogue receptor Rattus norvegicus 51-56
27052215-11 2016 Our results suggest that expressions of Ghrh-r and Ghs-r are regulated by RA through the RAR-RXR receptor complex and that RA enhances the effects of GHRH and ghrelin on GH release from the anterior pituitary gland. Tretinoin 89-91 growth hormone secretagogue receptor Rattus norvegicus 51-56
27334688-8 2016 Induction of neural differentiation with retinoic acid resulted in downregulation of Sox2 and VRK1 that inversely correlated with the expression of differentiation markers such as N-cadherin, Pax6, mH2A1.2 and mH2A2. Tretinoin 41-54 paired box 6 Homo sapiens 192-196
26873005-0 2016 Erratum to: Phospholipase C-eta2 interacts with nuclear and cytoplasmic LIMK-1 during retinoic acid-stimulated neurite growth. Tretinoin 86-99 LIM domain kinase 1 Homo sapiens 72-78
24141198-2 2016 The mechanism by which Bestatin enhances all-trans retinoic acid (ATRA)-induced cell differentiation of acute promyelocytic leukemia (APL) cells is generally attributed to inhibition of cell surface CD13/aminopeptidase N activity. Tretinoin 51-64 alanyl aminopeptidase, membrane Homo sapiens 199-203
24141198-2 2016 The mechanism by which Bestatin enhances all-trans retinoic acid (ATRA)-induced cell differentiation of acute promyelocytic leukemia (APL) cells is generally attributed to inhibition of cell surface CD13/aminopeptidase N activity. Tretinoin 51-64 alanyl aminopeptidase, membrane Homo sapiens 204-220
24141198-2 2016 The mechanism by which Bestatin enhances all-trans retinoic acid (ATRA)-induced cell differentiation of acute promyelocytic leukemia (APL) cells is generally attributed to inhibition of cell surface CD13/aminopeptidase N activity. Tretinoin 66-70 alanyl aminopeptidase, membrane Homo sapiens 199-203
24141198-2 2016 The mechanism by which Bestatin enhances all-trans retinoic acid (ATRA)-induced cell differentiation of acute promyelocytic leukemia (APL) cells is generally attributed to inhibition of cell surface CD13/aminopeptidase N activity. Tretinoin 66-70 alanyl aminopeptidase, membrane Homo sapiens 204-220
24141198-7 2016 Moreover, CD13 ligation with anti-CD13 antibody WM-15 resulted in phosphorylation of p38 MAPK, reduced the inhibition of Bestatin on the phosphorylation of p38 MAPK, and completely abolished the enhancement of Bestatin on ATRA-inducing differentiation in NB4 cells. Tretinoin 222-226 alanyl aminopeptidase, membrane Homo sapiens 10-14
27101150-0 2016 RAF-1/MEK/ERK pathway regulates ATRA-induced differentiation in acute promyelocytic leukemia cells through C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 32-36 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 0-5
27101150-0 2016 RAF-1/MEK/ERK pathway regulates ATRA-induced differentiation in acute promyelocytic leukemia cells through C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 32-36 CCAAT enhancer binding protein beta Homo sapiens 107-116
27101150-4 2016 In this work, we showed that RAF-1 was activated and the blockade of RAF-1 activation attenuated MEK/ERK activation as well as ATRA-induced differentiation. Tretinoin 127-131 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 29-34
27101150-4 2016 In this work, we showed that RAF-1 was activated and the blockade of RAF-1 activation attenuated MEK/ERK activation as well as ATRA-induced differentiation. Tretinoin 127-131 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 69-74
27101150-5 2016 ATRA-enhanced protein levels of C/EBPbeta, C/EBPepsilon and PU.1, which were required for differentiation in APL cells, were suppressed by the specific inhibitor of MEK. Tretinoin 0-4 CCAAT enhancer binding protein beta Homo sapiens 32-41
27101150-7 2016 Taken together, our study suggested that RAF-1/MEK/ERK cascade was involved in ATRA-induced differentiation in APL cells through enhancing the protein level of C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 79-83 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 41-46
27101150-7 2016 Taken together, our study suggested that RAF-1/MEK/ERK cascade was involved in ATRA-induced differentiation in APL cells through enhancing the protein level of C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 79-83 CCAAT enhancer binding protein beta Homo sapiens 160-169
24141198-7 2016 Moreover, CD13 ligation with anti-CD13 antibody WM-15 resulted in phosphorylation of p38 MAPK, reduced the inhibition of Bestatin on the phosphorylation of p38 MAPK, and completely abolished the enhancement of Bestatin on ATRA-inducing differentiation in NB4 cells. Tretinoin 222-226 alanyl aminopeptidase, membrane Homo sapiens 34-38
29767236-1 2018 N-(4-hydroxyphenyl)retinamide (4-HPR or fenretinide), which is a synthetic analog of all-trans retinoic acid (ATRA), effectively inhibits the growth of several types of tumor cells; however, its molecular mechanism remains unclear. Tretinoin 85-108 haptoglobin-related protein Homo sapiens 33-36
27183470-6 2016 Stimulation of retinoic acid signalling during endothelial-to-haematopoietic transition induced the HOXA cluster and other HSC/definitive haemogenic endothelium genes, and prolonged HSPC maintenance in culture. Tretinoin 15-28 homeobox A cluster Homo sapiens 100-104
27183470-6 2016 Stimulation of retinoic acid signalling during endothelial-to-haematopoietic transition induced the HOXA cluster and other HSC/definitive haemogenic endothelium genes, and prolonged HSPC maintenance in culture. Tretinoin 15-28 proteasome 20S subunit alpha 7 Homo sapiens 182-186
27183470-7 2016 Thus, medial HOXA gene expression induced by retinoic acid signalling marks the establishment of the definitive HSPC fate and controls HSPC identity and function. Tretinoin 45-58 homeobox A cluster Homo sapiens 13-17
27183470-7 2016 Thus, medial HOXA gene expression induced by retinoic acid signalling marks the establishment of the definitive HSPC fate and controls HSPC identity and function. Tretinoin 45-58 proteasome 20S subunit alpha 7 Homo sapiens 112-116
29767236-1 2018 N-(4-hydroxyphenyl)retinamide (4-HPR or fenretinide), which is a synthetic analog of all-trans retinoic acid (ATRA), effectively inhibits the growth of several types of tumor cells; however, its molecular mechanism remains unclear. Tretinoin 110-114 haptoglobin-related protein Homo sapiens 33-36
27183470-7 2016 Thus, medial HOXA gene expression induced by retinoic acid signalling marks the establishment of the definitive HSPC fate and controls HSPC identity and function. Tretinoin 45-58 proteasome 20S subunit alpha 7 Homo sapiens 135-139
27059013-4 2016 Purified recombinant hP450 27C1 bound and desaturated all-trans retinol, retinal, and retinoic acid, as well as 11-cis-retinal. Tretinoin 86-99 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 21-26
29801999-1 2018 All-trans retinoic acid (ATRA) up-regulates, in laboratory animals, the expression of the gut homing markers alpha4beta7 integrin and CCR9 on lymphocytes, increasing their gut tropism. Tretinoin 0-23 C-C motif chemokine receptor 9 Homo sapiens 134-138
26979774-6 2016 KEY FINDINGS: Retinoic acid increased cortisol secretion (149.5+-33.01%, 151.3+-49.45% and 129.3+-8.32% control secretion for 10nM, 100nM and 1muM respectively, p<0.05) and potentiated STAR expression (1.51+-0.22, 1.56+-0.15 and 1.59+-0.14 fold change over baseline, for 10nM, 100nM and 1muM respectively, p<0.05). Tretinoin 14-27 steroidogenic acute regulatory protein Homo sapiens 188-192
26979774-9 2016 SIGNIFICANCE: Retinoic acid stimulates cortisol synthesis and secretion in human adrenals and at the same time markedly blunts ACTH receptor transcription. Tretinoin 14-27 melanocortin 2 receptor Homo sapiens 127-140
26992387-5 2016 Treatment with RA or TO alone, and RA + TO reduced the MWT (46 +- 9, 42 +- 11, 46 +- 8, respectively) and improved the expression of VEGF, VEGFR1, and VEGFR2 compared to CDH (p < 0.05). Tretinoin 15-17 Fms related receptor tyrosine kinase 1 Rattus norvegicus 139-145
26992387-5 2016 Treatment with RA or TO alone, and RA + TO reduced the MWT (46 +- 9, 42 +- 11, 46 +- 8, respectively) and improved the expression of VEGF, VEGFR1, and VEGFR2 compared to CDH (p < 0.05). Tretinoin 35-37 Fms related receptor tyrosine kinase 1 Rattus norvegicus 139-145
27026484-8 2016 On the other hand, GDNF could additionally induce expression of POU5F1, and NANOG as well as other genes which were induced after RA treatment. Tretinoin 130-132 glial cell derived neurotrophic factor Gallus gallus 19-23
29801999-1 2018 All-trans retinoic acid (ATRA) up-regulates, in laboratory animals, the expression of the gut homing markers alpha4beta7 integrin and CCR9 on lymphocytes, increasing their gut tropism. Tretinoin 25-29 C-C motif chemokine receptor 9 Homo sapiens 134-138
29801999-3 2018 The coordinated increase of alpha4beta7 and CCR9 by ATRA was seen in 57% (12/21) of volunteers and only when given together with an oral Vivotif vaccine. Tretinoin 52-56 C-C motif chemokine receptor 9 Homo sapiens 44-48
29657241-6 2018 Aging, hypophysectomy, retinoic acid treatment, and testicular injury induced distinct Fgf2 and Gdnf expression dynamics, suggesting a difference in the expression mechanism of Fgf2 and Gdnf in the testis. Tretinoin 23-36 fibroblast growth factor 2 Mus musculus 87-91
27223470-5 2016 We followed the pattern of expression and regulation of beta-dystrobrevin during the early stages of neuronal differentiation induced by exposure to retinoic acid (RA) under hypoxia as compared with normoxia, and found that beta-dystrobrevin expression is regulated during RA-induced differentiation of NTera-2 cells. Tretinoin 149-162 dystrobrevin beta Homo sapiens 56-73
27223470-5 2016 We followed the pattern of expression and regulation of beta-dystrobrevin during the early stages of neuronal differentiation induced by exposure to retinoic acid (RA) under hypoxia as compared with normoxia, and found that beta-dystrobrevin expression is regulated during RA-induced differentiation of NTera-2 cells. Tretinoin 149-162 dystrobrevin beta Homo sapiens 224-241
27223470-5 2016 We followed the pattern of expression and regulation of beta-dystrobrevin during the early stages of neuronal differentiation induced by exposure to retinoic acid (RA) under hypoxia as compared with normoxia, and found that beta-dystrobrevin expression is regulated during RA-induced differentiation of NTera-2 cells. Tretinoin 164-166 dystrobrevin beta Homo sapiens 56-73
27223470-5 2016 We followed the pattern of expression and regulation of beta-dystrobrevin during the early stages of neuronal differentiation induced by exposure to retinoic acid (RA) under hypoxia as compared with normoxia, and found that beta-dystrobrevin expression is regulated during RA-induced differentiation of NTera-2 cells. Tretinoin 273-275 dystrobrevin beta Homo sapiens 224-241
26936974-3 2016 CYP2W1 converts all-transretinoic acid (atRA) to 4-hydroxyatRA and all-transretinol to 4-OH all-transretinol, and it also oxidizes retinal. Tretinoin 16-38 cytochrome P450 family 2 subfamily W member 1 Homo sapiens 0-6
29657241-6 2018 Aging, hypophysectomy, retinoic acid treatment, and testicular injury induced distinct Fgf2 and Gdnf expression dynamics, suggesting a difference in the expression mechanism of Fgf2 and Gdnf in the testis. Tretinoin 23-36 glial cell line derived neurotrophic factor Mus musculus 96-100
26936974-3 2016 CYP2W1 converts all-transretinoic acid (atRA) to 4-hydroxyatRA and all-transretinol to 4-OH all-transretinol, and it also oxidizes retinal. Tretinoin 40-44 cytochrome P450 family 2 subfamily W member 1 Homo sapiens 0-6
29657241-6 2018 Aging, hypophysectomy, retinoic acid treatment, and testicular injury induced distinct Fgf2 and Gdnf expression dynamics, suggesting a difference in the expression mechanism of Fgf2 and Gdnf in the testis. Tretinoin 23-36 fibroblast growth factor 2 Mus musculus 177-181
29657241-6 2018 Aging, hypophysectomy, retinoic acid treatment, and testicular injury induced distinct Fgf2 and Gdnf expression dynamics, suggesting a difference in the expression mechanism of Fgf2 and Gdnf in the testis. Tretinoin 23-36 glial cell line derived neurotrophic factor Mus musculus 186-190
29731429-3 2018 We performed comprehensive molecular, transcriptomic, and electrophysiologic analyses of retinoic acid (RA)-guided hiPSC atrial-like CMs and demonstrate that RA results in differential expression of genes involved in calcium ion homeostasis that directly interact with an RA receptor, chicken ovalbumin upstream promoter-transcription factor 2 (COUP-TFII). Tretinoin 89-102 nuclear receptor subfamily 2 group F member 2 Gallus gallus 345-354
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 0-13 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 103-124
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 0-13 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 126-129
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 0-13 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 135-161
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 0-13 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 163-167
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 15-17 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 103-124
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 15-17 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 126-129
29731429-3 2018 We performed comprehensive molecular, transcriptomic, and electrophysiologic analyses of retinoic acid (RA)-guided hiPSC atrial-like CMs and demonstrate that RA results in differential expression of genes involved in calcium ion homeostasis that directly interact with an RA receptor, chicken ovalbumin upstream promoter-transcription factor 2 (COUP-TFII). Tretinoin 158-160 nuclear receptor subfamily 2 group F member 2 Gallus gallus 345-354
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 15-17 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 135-161
27022678-1 2016 Retinoic acid (RA) is the active form of vitamin A and is synthesized from retinol by two key enzymes, alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). Tretinoin 15-17 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 163-167
29899874-10 2018 Tz+RA strongly reduced FAK and HER2 expression and induced nuclear FAK translocation. Tretinoin 3-5 protein tyrosine kinase 2 Homo sapiens 23-26
29899874-10 2018 Tz+RA strongly reduced FAK and HER2 expression and induced nuclear FAK translocation. Tretinoin 3-5 protein tyrosine kinase 2 Homo sapiens 67-70
28849722-0 2018 All-trans retinoic acid induces autophagic degradation of ubiquitin-like modifier activating enzyme 3 in acute promyelocytic leukemia cells. Tretinoin 10-23 ubiquitin like modifier activating enzyme 3 Homo sapiens 58-101
26923193-4 2016 We found that the xCyp26c gene, encoding a retinoic acid (RA) degradation enzyme, was upregulated following inhibition of BMP signaling in early neuroectodermal cells. Tretinoin 43-56 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 18-25
26678800-7 2016 Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression. Tretinoin 24-28 superoxide dismutase 2 Homo sapiens 56-61
26678800-7 2016 Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression. Tretinoin 94-98 superoxide dismutase 2 Homo sapiens 56-61
28849722-4 2018 Treating APL cells with ATRA led to the degradation of UBA3, a subunit of neddylation E1. Tretinoin 24-28 ubiquitin like modifier activating enzyme 3 Homo sapiens 55-59
28849722-7 2018 ATRA treatment also led to UBA3 degradation in primary APL cells. Tretinoin 0-4 ubiquitin like modifier activating enzyme 3 Homo sapiens 27-31
29854846-0 2018 All-Trans Retinoic Acid Induces CD4+CD25+FOXP3+ Regulatory T Cells by Increasing FOXP3 Demethylation in Systemic Sclerosis CD4+ T Cells. Tretinoin 10-23 forkhead box P3 Homo sapiens 41-46
26901853-10 2016 ATRA therapy could significantly increase the percentage of Treg cell, IL-10 level and Foxp3 expression. Tretinoin 0-4 forkhead box P3 Homo sapiens 87-92
29854846-0 2018 All-Trans Retinoic Acid Induces CD4+CD25+FOXP3+ Regulatory T Cells by Increasing FOXP3 Demethylation in Systemic Sclerosis CD4+ T Cells. Tretinoin 10-23 forkhead box P3 Homo sapiens 81-86
29854846-5 2018 The addition of all-trans retinoic acid (ATRA) to human naive CD4+ cells could promote the maturation of Tregs and increase the stable expression of Foxp3. Tretinoin 16-39 forkhead box P3 Homo sapiens 149-154
29854846-5 2018 The addition of all-trans retinoic acid (ATRA) to human naive CD4+ cells could promote the maturation of Tregs and increase the stable expression of Foxp3. Tretinoin 41-45 forkhead box P3 Homo sapiens 149-154
29854846-11 2018 Results: The expression of Tregs and FOXP3 in CD4+ T cells from patients with SSc increased in response to ATRA. Tretinoin 107-111 forkhead box P3 Homo sapiens 37-42
26997274-0 2016 NPM and BRG1 Mediate Transcriptional Resistance to Retinoic Acid in Acute Promyelocytic Leukemia. Tretinoin 51-64 nucleophosmin 1 Homo sapiens 0-3
29854846-13 2018 Further studies revealed that stimulation with ATRA increased the expression of FOXP3 in SSc CD4+ T cells by downregulating FOXP3 promoter methylation levels. Tretinoin 47-51 forkhead box P3 Homo sapiens 80-85
26997274-0 2016 NPM and BRG1 Mediate Transcriptional Resistance to Retinoic Acid in Acute Promyelocytic Leukemia. Tretinoin 51-64 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 8-12
29854846-13 2018 Further studies revealed that stimulation with ATRA increased the expression of FOXP3 in SSc CD4+ T cells by downregulating FOXP3 promoter methylation levels. Tretinoin 47-51 forkhead box P3 Homo sapiens 124-129
26997274-4 2016 Surprisingly, RA stimulation in these cells results in enhanced chromatin association of the nucleosome remodeler BRG1. Tretinoin 14-16 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 114-118
29854846-14 2018 Conclusions: ATRA acts as an inducer of Treg response in SSc CD4+ T cells via demethylation of the FOXP3 promoter and activation of FOXP3 expression. Tretinoin 13-17 forkhead box P3 Homo sapiens 99-104
29854846-14 2018 Conclusions: ATRA acts as an inducer of Treg response in SSc CD4+ T cells via demethylation of the FOXP3 promoter and activation of FOXP3 expression. Tretinoin 13-17 forkhead box P3 Homo sapiens 132-137
29689192-7 2018 Lats1/2 mutant cells displayed an arrested developmental trajectory with persistence of epicardial markers and expanded expression of Yap targets Dhrs3, an inhibitor of retinoic acid synthesis, and Dpp4, a protease that modulates extracellular matrix (ECM) composition. Tretinoin 169-182 Yes1 associated transcriptional regulator Homo sapiens 134-137
26827902-11 2016 In epistatic studies, exogenous RA treatment expanded the etv5a domain within the renal progenitor field and RA inhibition blocked etv5a in this populace, indicating that etv5a acts downstream of RA. Tretinoin 32-34 ETS variant transcription factor 5a Danio rerio 58-63
26827902-11 2016 In epistatic studies, exogenous RA treatment expanded the etv5a domain within the renal progenitor field and RA inhibition blocked etv5a in this populace, indicating that etv5a acts downstream of RA. Tretinoin 109-111 ETS variant transcription factor 5a Danio rerio 131-136
26827902-11 2016 In epistatic studies, exogenous RA treatment expanded the etv5a domain within the renal progenitor field and RA inhibition blocked etv5a in this populace, indicating that etv5a acts downstream of RA. Tretinoin 109-111 ETS variant transcription factor 5a Danio rerio 131-136
26827902-12 2016 Additionally, treatment with exogenous RA partially rescued the reduced MCC phenotype after loss of etv5a. Tretinoin 39-41 ETS variant transcription factor 5a Danio rerio 100-105
29500243-0 2018 All-Trans Retinoic Acid Enhances Antibody Production by Inducing the Expression of Thymic Stromal Lymphopoietin Protein. Tretinoin 10-23 thymic stromal lymphopoietin Mus musculus 83-111
26959238-2 2016 The morphogen retinoic acid, together with the Cyp26 enzymes which degrade it, play a central role in this process. Tretinoin 14-27 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 47-52
26959238-3 2016 The cyp26a1 gene expressed in the anterior neural plate thus contributes to the fine modulation of the rostrocaudal retinoic acid gradient. Tretinoin 116-129 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 4-11
29500243-5 2018 In this study, we examined the effects of all-trans retinoic acid (atRA) on TSLP production and Ag-induced Ab production. Tretinoin 52-65 thymic stromal lymphopoietin Mus musculus 76-80
29500243-5 2018 In this study, we examined the effects of all-trans retinoic acid (atRA) on TSLP production and Ag-induced Ab production. Tretinoin 67-71 thymic stromal lymphopoietin Mus musculus 76-80
26935534-0 2016 All trans-retinoic acid analogs promote cancer cell apoptosis through non-genomic Crabp1 mediating ERK1/2 phosphorylation. Tretinoin 4-23 cellular retinoic acid binding protein 1 Homo sapiens 82-88
26935534-6 2016 Re-expressing Crabp1 in Crabp1-negative cancer cells also sensitizes their apoptotic induction by atRA. Tretinoin 98-102 cellular retinoic acid binding protein 1 Homo sapiens 14-20
29500243-6 2018 Application of atRA onto the ear lobes of mice selectively induced TSLP production without inducing apparent inflammation. Tretinoin 15-19 thymic stromal lymphopoietin Mus musculus 67-71
26935534-6 2016 Re-expressing Crabp1 in Crabp1-negative cancer cells also sensitizes their apoptotic induction by atRA. Tretinoin 98-102 cellular retinoic acid binding protein 1 Homo sapiens 24-30
29500243-10 2018 In conclusion, atRA was an effective adjuvant through induction of TSLP production. Tretinoin 15-19 thymic stromal lymphopoietin Mus musculus 67-71
26935534-7 2016 This study reveals a physiological relevance of the non-genomic action of atRA, mediated by Crabp1, in modulating cell cycle progression and apoptosis induction, and provides a new cancer therapeutic strategy whereby compounds specifically targeting Crabp1 can modulate cell cycle and cancer cell apoptosis in a RAR-independent fashion, thereby avoiding atRA"s toxicity caused by its genomic effects. Tretinoin 74-78 cellular retinoic acid binding protein 1 Homo sapiens 92-98
29465800-4 2018 A similar, yet lower, fluctuation was observed for aldh1a2 and rdh10a, the enzymes participating in the two-step RA biosynthesis cascade. Tretinoin 113-115 aldehyde dehydrogenase 1 family, member A2 Danio rerio 51-58
26935534-7 2016 This study reveals a physiological relevance of the non-genomic action of atRA, mediated by Crabp1, in modulating cell cycle progression and apoptosis induction, and provides a new cancer therapeutic strategy whereby compounds specifically targeting Crabp1 can modulate cell cycle and cancer cell apoptosis in a RAR-independent fashion, thereby avoiding atRA"s toxicity caused by its genomic effects. Tretinoin 74-78 cellular retinoic acid binding protein 1 Homo sapiens 250-256
26459180-8 2016 Sorafenib blocks ATRA-induced Mcl-1 increase by reversing p90RSK activation and GSK3beta inactivation, maintains the repressed Bcl-2 level, and enhances ATRA induced apoptosis in non-APL AML cell lines and in primary AML cells. Tretinoin 17-21 glycogen synthase kinase 3 beta Homo sapiens 80-88
29465800-4 2018 A similar, yet lower, fluctuation was observed for aldh1a2 and rdh10a, the enzymes participating in the two-step RA biosynthesis cascade. Tretinoin 113-115 retinol dehydrogenase 10a Danio rerio 63-69
29330921-9 2018 We further show that the expression of Fhl2 is positively regulated by profibrogenic signals including Tgfbeta2, all-trans-retinoic acid, and canonical Wnt signalling molecules and negatively regulated by prochondrogenic factors of the bone morphogenetic protein family. Tretinoin 113-136 four and a half LIM domains 2 Homo sapiens 39-43
25956707-5 2016 We additionally found that short-term treatment of primary osteoblasts with RA causes a rapid induction of specific genes involved in either retinol-dependent signaling (i.e. Rara, Crabp2) or skeletal remodeling (i.e. Twist2, Tnfsf11). Tretinoin 76-78 cellular retinoic acid binding protein II Mus musculus 181-187
25956707-5 2016 We additionally found that short-term treatment of primary osteoblasts with RA causes a rapid induction of specific genes involved in either retinol-dependent signaling (i.e. Rara, Crabp2) or skeletal remodeling (i.e. Twist2, Tnfsf11). Tretinoin 76-78 twist basic helix-loop-helix transcription factor 2 Mus musculus 218-224
29523306-6 2018 Such suppression is in response to a retinoic acid-RARalpha binding initiated pathway and results in the upregulation of gut-homing chemokine receptor CCR9 and downregulation of lymphoid tissue-homing receptor CCR7, which can then guide ILC3 cells to intestine. Tretinoin 37-50 atypical chemokine receptor 2 Homo sapiens 132-155
26661222-6 2016 The increased uptake of phosphorylated human beta-glucuronidase was inhibited by mannose 6-phosphate for the agents (+-)epinephrine and retinoic acid and by L-NG-nitroarginine methyl ester for the agent lipopolysaccharide in neonatal and adult mice. Tretinoin 136-149 glucuronidase beta Homo sapiens 45-63
26661222-7 2016 An in situ brain perfusion study revealed that retinoic acid directly modulated the transport of phosphorylated human beta-glucuronidase across the blood-brain barrier. Tretinoin 47-60 glucuronidase beta Homo sapiens 118-136
29490681-8 2018 Furthermore, OLCs from the RA treated group, expressed significantly more of the meiosis regulatory gene Marf1 and the oocyte marker Oct4. Tretinoin 27-29 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 133-137
26843326-10 2016 Short-term treatment of mice with all-trans retinoic acid resulted in increased PreB lymphopoiesis in BM and an increase in thymic double-negative 4 T cells, inverse to that observed upon Nes cell-specific deletion of Rargamma. Tretinoin 44-57 nestin Mus musculus 188-191
26582233-4 2016 Our data show that RA attenuated BSCB permeability and also attenuated the loss of tight junction molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in brain microvascular endothelial cells. Tretinoin 19-21 catenin delta 1 Homo sapiens 116-120
26892828-0 2016 ALDH1A1 provides a source of meiosis-inducing retinoic acid in mouse fetal ovaries. Tretinoin 46-59 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-7
29490681-9 2018 At the protein level RA treatment was found to increase the expression of the gap junction protein CX43 and the pluripotency marker OCT4. Tretinoin 21-23 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 132-136
26892828-3 2016 Here we show that a third RA-synthesizing enzyme, ALDH1A1, is expressed in fetal ovaries, providing a likely source of RA in the absence of ALDH1A2 and ALDH1A3. Tretinoin 26-28 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 50-57
26892828-3 2016 Here we show that a third RA-synthesizing enzyme, ALDH1A1, is expressed in fetal ovaries, providing a likely source of RA in the absence of ALDH1A2 and ALDH1A3. Tretinoin 119-121 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 50-57
26773000-6 2016 In the hindbrain, RA signaling modulates its own concentration by activating the expression of cyp26a1 and inhibiting the expansion of cdx4. Tretinoin 18-20 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 95-102
26773000-7 2016 Therefore, interactions between Cyp26a1 and Cdx4 modulate RA levels along the AP axis to segregate the posterior neural plate into the hindbrain and spinal cord territories. Tretinoin 58-60 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 32-39
26582233-4 2016 Our data show that RA attenuated BSCB permeability and also attenuated the loss of tight junction molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in brain microvascular endothelial cells. Tretinoin 19-21 occludin Homo sapiens 136-144
26582233-4 2016 Our data show that RA attenuated BSCB permeability and also attenuated the loss of tight junction molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in brain microvascular endothelial cells. Tretinoin 19-21 claudin 5 Homo sapiens 149-157
26747727-7 2016 beta-catenin silencing abolished the stimulatory effect of ATRA on Wnt3A-induced alkaline phosphatase (ALP) activity and reversed its inhibitory effect on Cyp26a1 expression. Tretinoin 59-63 Wnt family member 3A Homo sapiens 67-72
29462197-9 2018 The level of Let-7 in thymic B progenitors was up regulated by in vitro co-culture with IL15, Vitamin-D3, and retinoic acid, thus down-regulating Arid3a to promote B cell differentiation. Tretinoin 110-123 AT rich interactive domain 3A (BRIGHT-like) Mus musculus 146-152
26902400-0 2016 PHOX2A and PHOX2B are differentially regulated during retinoic acid-driven differentiation of SK-N-BE(2)C neuroblastoma cell line. Tretinoin 54-67 paired like homeobox 2A Homo sapiens 0-6
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 CD8 antigen, alpha chain Mus musculus 145-153
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 57-70 paired like homeobox 2A Homo sapiens 174-180
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 57-70 paired like homeobox 2A Homo sapiens 261-267
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 72-76 paired like homeobox 2A Homo sapiens 174-180
26341094-7 2016 Retinoic acid, a morphogen known to interact with BMP-signaling during bone formation, was shown to down-regulate the expression of bmp2, bmp4 and bmp16, although to different extents. Tretinoin 0-13 bone morphogenetic protein 2a Danio rerio 132-136
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 transforming growth factor, beta 1 Mus musculus 218-225
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 72-76 paired like homeobox 2A Homo sapiens 261-267
29330505-5 2018 We also demonstrate that all-trans retinoic acid, a downstream product of the enzymatic activity of SRP-35, mimics the effect of SRP-35 in skeletal muscle, inducing a synergistic effect with insulin on AKTS473 phosphorylation. Tretinoin 35-48 dehydrogenase/reductase (SDR family) member 7C Mus musculus 100-106
26531761-6 2016 Synthetic agonists of the VDR and RARgamma as well as the natural agonist all-trans retinoic acid (ATRA) increased TSLP expression in the skin, while an RXR agonist was not active. Tretinoin 84-97 thymic stromal lymphopoietin Mus musculus 115-119
26531761-6 2016 Synthetic agonists of the VDR and RARgamma as well as the natural agonist all-trans retinoic acid (ATRA) increased TSLP expression in the skin, while an RXR agonist was not active. Tretinoin 99-103 thymic stromal lymphopoietin Mus musculus 115-119
29330505-5 2018 We also demonstrate that all-trans retinoic acid, a downstream product of the enzymatic activity of SRP-35, mimics the effect of SRP-35 in skeletal muscle, inducing a synergistic effect with insulin on AKTS473 phosphorylation. Tretinoin 35-48 dehydrogenase/reductase (SDR family) member 7C Mus musculus 129-135
29324782-2 2018 Previous studies have shown that MAFB is expressed in embryonic and adult mouse testes and is expected to act as the downstream target of retinoic acid (RA) to initiate spermatogenesis. Tretinoin 138-151 v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B (avian) Mus musculus 33-37
26507774-0 2016 All-trans retinoic acid protects against doxorubicin-induced cardiotoxicity by activating the ERK2 signalling pathway. Tretinoin 0-23 mitogen activated protein kinase 1 Rattus norvegicus 94-98
26507774-10 2016 Both a ERK1/2 inhibitor (U0126) and ERK2 siRNA, but not ERK1 siRNA, abolished the protective effect of ATRA against doxorubicin-induced toxicity in H9c2 cells. Tretinoin 103-107 mitogen activated protein kinase 3 Rattus norvegicus 7-13
26507774-10 2016 Both a ERK1/2 inhibitor (U0126) and ERK2 siRNA, but not ERK1 siRNA, abolished the protective effect of ATRA against doxorubicin-induced toxicity in H9c2 cells. Tretinoin 103-107 mitogen activated protein kinase 1 Rattus norvegicus 36-40
26507774-10 2016 Both a ERK1/2 inhibitor (U0126) and ERK2 siRNA, but not ERK1 siRNA, abolished the protective effect of ATRA against doxorubicin-induced toxicity in H9c2 cells. Tretinoin 103-107 mitogen activated protein kinase 3 Rattus norvegicus 7-11
26717879-1 2016 All-trans retinoic acid (ATRA) has been shown to enhance the expression of connexin 43 (Cx43) and the bystander effect (BSE) in suicide gene therapy. Tretinoin 0-23 gap junction protein alpha 1 Homo sapiens 75-86
26717879-1 2016 All-trans retinoic acid (ATRA) has been shown to enhance the expression of connexin 43 (Cx43) and the bystander effect (BSE) in suicide gene therapy. Tretinoin 0-23 gap junction protein alpha 1 Homo sapiens 88-92
26717879-1 2016 All-trans retinoic acid (ATRA) has been shown to enhance the expression of connexin 43 (Cx43) and the bystander effect (BSE) in suicide gene therapy. Tretinoin 25-29 gap junction protein alpha 1 Homo sapiens 75-86
26717879-1 2016 All-trans retinoic acid (ATRA) has been shown to enhance the expression of connexin 43 (Cx43) and the bystander effect (BSE) in suicide gene therapy. Tretinoin 25-29 gap junction protein alpha 1 Homo sapiens 88-92
26694250-7 2016 For instance, PRAME is able to dominantly repress retinoic acid signaling in these cells. Tretinoin 50-63 PRAME nuclear receptor transcriptional regulator Homo sapiens 14-19
29484133-6 2018 Indeed, SCD5 re-established the sensitivity to all-trans retinoic acid in A375M metastatic melanoma, associated with increased levels of Tyrosinase, melanin production and reduced proliferation. Tretinoin 57-70 stearoyl-CoA desaturase 5 Homo sapiens 8-12
26400044-8 2016 To test the significance of phosphorylation of these proteins further, we administered all-trans-retinoic acid (ATRA) to the 3xTg mice, which downregulates Cdk5 and GSK3beta activity. Tretinoin 87-110 glycogen synthase kinase 3 alpha Mus musculus 165-173
26400044-8 2016 To test the significance of phosphorylation of these proteins further, we administered all-trans-retinoic acid (ATRA) to the 3xTg mice, which downregulates Cdk5 and GSK3beta activity. Tretinoin 112-116 glycogen synthase kinase 3 alpha Mus musculus 165-173
26886923-0 2016 Comparative Analysis of Protocols to Induce Human CD4+Foxp3+ Regulatory T Cells by Combinations of IL-2, TGF-beta, Retinoic Acid, Rapamycin and Butyrate. Tretinoin 115-128 forkhead box P3 Homo sapiens 54-59
26747727-0 2016 All-trans retinoic acid modulates Wnt3A-induced osteogenic differentiation of mesenchymal stem cells via activating the PI3K/AKT/GSK3beta signalling pathway. Tretinoin 10-23 Wnt family member 3A Homo sapiens 34-39
26747727-0 2016 All-trans retinoic acid modulates Wnt3A-induced osteogenic differentiation of mesenchymal stem cells via activating the PI3K/AKT/GSK3beta signalling pathway. Tretinoin 10-23 glycogen synthase kinase 3 beta Homo sapiens 129-137
26747727-4 2016 We found that ATRA potentiated the Wnt3A-induced expression of early and late osteogenic markers as well as matrix mineralization and further confirmed the phenomena using foetal limb explant culture and MSC implantation experiments. Tretinoin 14-18 Wnt family member 3A Homo sapiens 35-40
29108781-6 2018 Moreover, ectopic expression of the transcription factor meis3 and/or the receptor ret, partially rescues enteric neuron colonization after RA attenuation. Tretinoin 140-142 myeloid ecotropic viral integration site 3 Danio rerio 57-62
26747727-5 2016 Mechanistically, ATRA cooperated with Wnt3A to induce beta-catenin translocation from cell-cell contacts into the cytosol and nucleus, thereby activating Wnt/beta-catenin signalling. Tretinoin 17-21 Wnt family member 3A Homo sapiens 38-43
26747727-6 2016 Additionally, Wnt3A attenuated ATRA-induced Cyp26a1 expression, inhibiting the degradation of ATRA into its oxidative forms. Tretinoin 31-35 Wnt family member 3A Homo sapiens 14-19
29108781-7 2018 Collectively, our findings suggest that retinoic acid plays a critical temporal role in promoting enteric neural crest chain migration and neuronal survival upstream of Meis3 and RET in vivo. Tretinoin 40-53 myeloid ecotropic viral integration site 3 Danio rerio 169-174
26700766-0 2016 LZTFL1 Upregulated by All-Trans Retinoic Acid during CD4+ T Cell Activation Enhances IL-5 Production. Tretinoin 32-45 interleukin 5 Homo sapiens 85-89
26096167-4 2016 We recently demonstrated that ATRA up-regulated the LMX1B, and down-regulated the transforming growth factor-beta1, collagen IV and fibronectin in a hypoxia/reoxygenation (H-R) injury system in renal tubular epithelial cells (RTEC). Tretinoin 30-34 transforming growth factor beta 1 Felis catus 82-114
26700766-7 2016 Knockdown of LZTFL1 reduced the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overexpression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important regulator of ATRA-induced T cell response. Tretinoin 43-47 interleukin 5 Homo sapiens 66-70
26456050-5 2016 Culture of hMSC with a combination of factors that induce photoreceptor differentiation of hMSC (FGF2, taurine, retinoic acid, and insulin-like growth factor type1; FTRI), markedly upregulated the expression of components of the canonical Wnt signaling pathway, including WNT2B, DKK1, and active beta-CATENIN. Tretinoin 112-125 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 279-283
29085977-0 2018 All-trans-retinoic acid ameliorates doxorubicin-induced cardiotoxicity: in vivo potential involvement of oxidative stress, inflammation, and apoptosis via caspase-3 and p53 down-expression. Tretinoin 0-23 caspase 3 Rattus norvegicus 155-164
26828989-0 2016 All-trans retinoic acid inhibits HOXA7 expression in leukemia cell NB4. Tretinoin 10-23 homeobox A7 Homo sapiens 33-38
26828989-3 2016 The expression level of HOXA7 decreased in the presence of ATRA, which was able to inhibit the proliferation of NB4 cells. Tretinoin 59-63 homeobox A7 Homo sapiens 24-29
29085977-9 2018 Pretreatment with ATRA maintained cardiac function biomarkers, and reduced proinflammatory cytokines, lipid peroxidation, and immunoexpression of caspase 3 and p53. Tretinoin 18-22 caspase 3 Rattus norvegicus 146-155
27830500-4 2016 The major intracellular retinol-binding protein, CRBP1, likely enhances efficient retinoid use by providing a sink to facilitate retinol uptake from sRBP through the plasma membrane or via Stra6, delivering retinol or retinal to select enzymes that generate retinyl esters or retinoic acid, and protecting retinol/retinal from excess catabolism or opportunistic metabolism. Tretinoin 276-289 retinol binding protein 1 Homo sapiens 49-54
29155646-8 2018 DISCUSSION: These results indicate that both DHA and ATRA might help control disease progression in IFN-beta treated RRMS patients with the strongest effects produced by a combination of the two compounds. Tretinoin 53-57 interferon beta 1 Homo sapiens 100-108
27830500-5 2016 Intracellular retinoic acid binding-proteins (CRABP1 and 2, and FABP5) seem to have more diverse functions distinctive to each, such as directing retinoic acid to catabolism, delivering retinoic acid to specific nuclear receptors, and generating non-canonical actions. Tretinoin 14-27 cellular retinoic acid binding protein 1 Homo sapiens 46-58
27830500-5 2016 Intracellular retinoic acid binding-proteins (CRABP1 and 2, and FABP5) seem to have more diverse functions distinctive to each, such as directing retinoic acid to catabolism, delivering retinoic acid to specific nuclear receptors, and generating non-canonical actions. Tretinoin 146-159 cellular retinoic acid binding protein 1 Homo sapiens 46-58
27830500-5 2016 Intracellular retinoic acid binding-proteins (CRABP1 and 2, and FABP5) seem to have more diverse functions distinctive to each, such as directing retinoic acid to catabolism, delivering retinoic acid to specific nuclear receptors, and generating non-canonical actions. Tretinoin 146-159 cellular retinoic acid binding protein 1 Homo sapiens 46-58
27830504-8 2016 The CrabpII gene promoter contains a TATA-box and is rapidly activated by RA through an RA response element. Tretinoin 74-76 cellular retinoic acid binding protein II Mus musculus 4-11
27830504-8 2016 The CrabpII gene promoter contains a TATA-box and is rapidly activated by RA through an RA response element. Tretinoin 88-90 cellular retinoic acid binding protein II Mus musculus 4-11
27830505-1 2016 It has long been established that the transcriptional activity of retinoic acid (RA) is mediated by members of the nuclear receptor family of ligand-activated transcription factors termed RA receptors (RARs). Tretinoin 66-79 arginyl-tRNA synthetase 1 Homo sapiens 188-200
27830505-1 2016 It has long been established that the transcriptional activity of retinoic acid (RA) is mediated by members of the nuclear receptor family of ligand-activated transcription factors termed RA receptors (RARs). Tretinoin 66-79 arginyl-tRNA synthetase 1 Homo sapiens 202-206
27830505-1 2016 It has long been established that the transcriptional activity of retinoic acid (RA) is mediated by members of the nuclear receptor family of ligand-activated transcription factors termed RA receptors (RARs). Tretinoin 81-83 arginyl-tRNA synthetase 1 Homo sapiens 188-200
27830505-1 2016 It has long been established that the transcriptional activity of retinoic acid (RA) is mediated by members of the nuclear receptor family of ligand-activated transcription factors termed RA receptors (RARs). Tretinoin 81-83 arginyl-tRNA synthetase 1 Homo sapiens 202-206
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 arginyl-tRNA synthetase 1 Homo sapiens 24-28
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 arginyl-tRNA synthetase 1 Homo sapiens 173-177
26708897-8 2015 After treatment of ATRA, the proportion of CD71(+) cells detected by the flow cytometry also increased. Tretinoin 19-23 transferrin receptor Homo sapiens 43-47
26582990-1 2015 The cytochrome P450, CYP2C8, metabolizes more than 60 clinically used drugs as well as endogenous substances including retinoic acid and arachidonic acid. Tretinoin 119-132 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 21-27
26333706-14 2015 The levels of Foxp3, TGF-beta, and IL-10 mRNA, as well as the percentage of CD4+CD25+Foxp3+ T cells, were higher in the ATRA group than in theAR group. Tretinoin 120-124 transforming growth factor, beta 1 Mus musculus 21-29
26807202-9 2015 At >1muM concentrations, all trans-retinoic acid and retinol reduced viability more in CRBP-1(+) than in CRBP-1(-) A549 cells. Tretinoin 32-51 retinol binding protein 1 Homo sapiens 90-99
26807202-9 2015 At >1muM concentrations, all trans-retinoic acid and retinol reduced viability more in CRBP-1(+) than in CRBP-1(-) A549 cells. Tretinoin 32-51 retinol binding protein 1 Homo sapiens 90-96
26537191-1 2015 Retinols are metabolized into retinoic acids by alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (Raldh). Tretinoin 30-44 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 71-74
26403865-4 2015 mES exposed to retinoic acid +- 1 mug/L CYN differentiated into neural-like cells confirmed by morphological examination and RT-PCR for Oct4, Brachyury and Nestin. Tretinoin 15-28 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 136-140
26268560-8 2015 In vitro assays showed that Gpat2 expression correlates with DNA demethylation and histone acetylation and that it is up-regulated by retinoic acid. Tretinoin 134-147 glycerol-3-phosphate acyltransferase 2, mitochondrial Mus musculus 28-33
26446715-0 2015 All-trans retinoic acid arrests cell cycle in leukemic bone marrow stromal cells by increasing intercellular communication through connexin 43-mediated gap junction. Tretinoin 10-23 gap junction protein alpha 1 Homo sapiens 131-142
26446715-12 2015 Both Cx43 expression and GJIC function were increased by ATRA treatment. Tretinoin 57-61 gap junction protein alpha 1 Homo sapiens 5-9
27073891-12 2016 CONCLUSION: These data point toward the role of RA signaling together with BATF in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with neoantigen results in impaired mucosal and systemic IgA responses. Tretinoin 48-50 IGAN1 Homo sapiens 94-98
26632609-3 2016 However, it is unclear if the aldehyde dehydrogenase (ALDH) enzymes, which are responsible for RA synthesis, contribute to the regulation of these RA concentration gradients. Tretinoin 95-97 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 30-52
26632609-3 2016 However, it is unclear if the aldehyde dehydrogenase (ALDH) enzymes, which are responsible for RA synthesis, contribute to the regulation of these RA concentration gradients. Tretinoin 95-97 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 54-58
26632609-6 2016 We also show, via treatments with a known ALDH inhibitor, that lowered testicular RA levels result in an increase in blood-testis barrier permeability, meiotic recombination, and meiotic defects. Tretinoin 82-84 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 42-46
27373883-0 2016 Retinoic Acid Modulates PTGDR Promoter Activity. Tretinoin 0-13 prostaglandin D2 receptor Homo sapiens 24-29
27373883-1 2016 BACKGROUND AND OBJECTIVE: Vitamin A has been linked to the development of allergic diseases although its role is not fully understood, Retinoic acid (RA), a metabolite of Vitamin A, has been previously associated with the prostaglandin pathway, and PTGDR, a receptor of PGD2, has been proposed as a candidate gene in allergy and asthma. Tretinoin 135-148 prostaglandin D2 receptor Homo sapiens 249-254
27373883-1 2016 BACKGROUND AND OBJECTIVE: Vitamin A has been linked to the development of allergic diseases although its role is not fully understood, Retinoic acid (RA), a metabolite of Vitamin A, has been previously associated with the prostaglandin pathway, and PTGDR, a receptor of PGD2, has been proposed as a candidate gene in allergy and asthma. Tretinoin 150-152 prostaglandin D2 receptor Homo sapiens 249-254
27373883-2 2016 Considering the role of PTGDR in allergy, the goal of this study was to analyze the effect of RA on the activation of the promoter region of the PTGDR gene. Tretinoin 94-96 prostaglandin D2 receptor Homo sapiens 145-150
26844556-4 2016 AKR1B10 may play a role in the formation and development of carcinomas through multiple mechanisms including detoxification of cytotoxic carbonyls, modulation of retinoic acid level, and regulation of cellular fatty acid synthesis and lipid metabolism. Tretinoin 162-175 aldo-keto reductase family 1 member B10 Homo sapiens 0-7
26372689-0 2016 Retinoic Acid Induces Ubiquitination-Resistant RIP140/LSD1 Complex to Fine-Tune Pax6 Gene in Neuronal Differentiation. Tretinoin 0-13 nuclear receptor interacting protein 1 Homo sapiens 47-53
26372689-0 2016 Retinoic Acid Induces Ubiquitination-Resistant RIP140/LSD1 Complex to Fine-Tune Pax6 Gene in Neuronal Differentiation. Tretinoin 0-13 paired box 6 Homo sapiens 80-84
26372689-2 2016 Here, we identify RIP140 as an immediate retinoic acid (RA)-induced dual-function chaperone for LSD1 (lysine-specific demethylase 1). Tretinoin 41-54 nuclear receptor interacting protein 1 Homo sapiens 18-24
26372689-2 2016 Here, we identify RIP140 as an immediate retinoic acid (RA)-induced dual-function chaperone for LSD1 (lysine-specific demethylase 1). Tretinoin 56-58 nuclear receptor interacting protein 1 Homo sapiens 18-24
26372689-4 2016 In RA-induced neuronal differentiation, the increased RIP140/LSD1 complex is recruited by RA-elevated Pit-1 to specifically reduce H3K4me2 modification on the Pax6 promoter, thereby repressing RA-induction of Pax6. Tretinoin 3-5 nuclear receptor interacting protein 1 Homo sapiens 54-60
26372689-4 2016 In RA-induced neuronal differentiation, the increased RIP140/LSD1 complex is recruited by RA-elevated Pit-1 to specifically reduce H3K4me2 modification on the Pax6 promoter, thereby repressing RA-induction of Pax6. Tretinoin 3-5 paired box 6 Homo sapiens 159-163
26372689-4 2016 In RA-induced neuronal differentiation, the increased RIP140/LSD1 complex is recruited by RA-elevated Pit-1 to specifically reduce H3K4me2 modification on the Pax6 promoter, thereby repressing RA-induction of Pax6. Tretinoin 3-5 paired box 6 Homo sapiens 209-213
26372689-5 2016 This study reveals a new RA-induced gene repressive mechanism that modulates the abundance, enzyme quality, and recruitment of histone modifier LSD1 to neuronal regulator Pax6, which provides a homeostatic control for RA induction of neuronal differentiation. Tretinoin 25-27 paired box 6 Homo sapiens 171-175
26372689-5 2016 This study reveals a new RA-induced gene repressive mechanism that modulates the abundance, enzyme quality, and recruitment of histone modifier LSD1 to neuronal regulator Pax6, which provides a homeostatic control for RA induction of neuronal differentiation. Tretinoin 218-220 paired box 6 Homo sapiens 171-175
26626025-4 2015 Treatment with GSK3beta inhibitors during the initial phase of differentiation in combination with dual SMAD inhibition was sufficient to induce PAX6 (+) and SOX1 (+) neural progenitors within 1 week, and subsequent treatment with retinoic acid (RA) and purmorphamine, which activates sonic hedgehog (SHH) signaling, resulted in the highly efficient induction of HB9(+) and ISL-1(+) motor neurons within 2 weeks. Tretinoin 231-244 glycogen synthase kinase 3 beta Homo sapiens 15-23
26626025-4 2015 Treatment with GSK3beta inhibitors during the initial phase of differentiation in combination with dual SMAD inhibition was sufficient to induce PAX6 (+) and SOX1 (+) neural progenitors within 1 week, and subsequent treatment with retinoic acid (RA) and purmorphamine, which activates sonic hedgehog (SHH) signaling, resulted in the highly efficient induction of HB9(+) and ISL-1(+) motor neurons within 2 weeks. Tretinoin 246-248 glycogen synthase kinase 3 beta Homo sapiens 15-23
26587591-2 2015 We here have described eosinophils in lamina propria (LP) that displayed high aldehyde dehydrogenase (ALDH) activity, a rate-limiting step during all-trans retinoic acid (ATRA) synthesis, and expressed TGF-beta1 mRNA and high levels of ATRA. Tretinoin 156-169 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 78-100
26587591-2 2015 We here have described eosinophils in lamina propria (LP) that displayed high aldehyde dehydrogenase (ALDH) activity, a rate-limiting step during all-trans retinoic acid (ATRA) synthesis, and expressed TGF-beta1 mRNA and high levels of ATRA. Tretinoin 156-169 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 102-106
26587591-2 2015 We here have described eosinophils in lamina propria (LP) that displayed high aldehyde dehydrogenase (ALDH) activity, a rate-limiting step during all-trans retinoic acid (ATRA) synthesis, and expressed TGF-beta1 mRNA and high levels of ATRA. Tretinoin 171-175 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 78-100
26587591-2 2015 We here have described eosinophils in lamina propria (LP) that displayed high aldehyde dehydrogenase (ALDH) activity, a rate-limiting step during all-trans retinoic acid (ATRA) synthesis, and expressed TGF-beta1 mRNA and high levels of ATRA. Tretinoin 171-175 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 102-106
26587591-2 2015 We here have described eosinophils in lamina propria (LP) that displayed high aldehyde dehydrogenase (ALDH) activity, a rate-limiting step during all-trans retinoic acid (ATRA) synthesis, and expressed TGF-beta1 mRNA and high levels of ATRA. Tretinoin 236-240 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 102-106
26581770-4 2015 Subsequent addition of retinoic acid and BMP4 at specific time points and concentrations yielded a high population of neural crest progenitor cells (AP2alpha(+), P75(+)), which further differentiated into nociceptive neurons (TRKA(+), Nav1.7(+), P2X3(+)). Tretinoin 23-36 neurotrophic receptor tyrosine kinase 1 Homo sapiens 226-230
26581770-4 2015 Subsequent addition of retinoic acid and BMP4 at specific time points and concentrations yielded a high population of neural crest progenitor cells (AP2alpha(+), P75(+)), which further differentiated into nociceptive neurons (TRKA(+), Nav1.7(+), P2X3(+)). Tretinoin 23-36 purinergic receptor P2X 3 Homo sapiens 246-250
26324251-4 2015 A total of four different methods with distinct mechanisms were used to change the function and expression of Cx43 channels in human umbilical vein endothelial cells: Cx43 channel inhibitor (oleamide), enhancer (retinoic acid), overexpression of Cx43 by transfection with pcDNA-Cx43 and knock-down of the expression of Cx43 by small interfering RNA against Cx43. Tretinoin 212-225 gap junction protein alpha 1 Homo sapiens 110-114
26044560-8 2015 The retinoic acid amide-treated tumors showed inhibition of JAK2/STAT3 activation and Bcl-XL expression. Tretinoin 4-17 Janus kinase 2 Homo sapiens 60-64
26535632-9 2015 In addition, ATRA was shown to significantly increase the levels of TrkA mRNA expression. Tretinoin 13-17 neurotrophic receptor tyrosine kinase 1 Homo sapiens 68-72
26535632-10 2015 Therefore, we concluded that the elevated expression of the TrkA receptor is associated with ATRA-induced growth arrest and differentiation o neuroblastoma cells. Tretinoin 93-97 neurotrophic receptor tyrosine kinase 1 Homo sapiens 60-64
26240147-10 2015 Furthermore, atRA disrupted LPS-induced nuclear translocation of NFkappaB and its binding to BACE1 promoter as well as promoting the recruitment of the corepressor NCoR. Tretinoin 13-17 nuclear receptor co-repressor 1 Mus musculus 164-168
26335021-5 2015 After treating erythroid myeloid lymphoid (EML) cells with All-trans Retinoic Acid (ATRA), we investigated the expression and regulation of Malat1 during hematopoietic differentiation, the results showed that ATRA significantly down regulates Malat1 expression during the differentiation of EML cells. Tretinoin 69-82 metastasis associated lung adenocarcinoma transcript 1 (non-coding RNA) Mus musculus 243-249
26116175-0 2015 Excessive feedback of Cyp26a1 promotes cell non-autonomous loss of retinoic acid signaling. Tretinoin 67-80 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 22-29
26116175-5 2015 Thus, the sensitivity of cyp26a1 expression to increased RA signaling causes an overcompensation of negative feedback and loss of embryonic RA signaling. Tretinoin 57-59 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 25-32
26116175-6 2015 Additionally, we used blastula transplantation experiments to test if Cyp26a1, despite its cellular localization, can limit RA exposure to neighboring cells. Tretinoin 124-126 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 70-77
26116175-7 2015 We find that enhanced Cyp26a1 expression limits RA signaling in the local environment, thus providing the first direct evidence that Cyp26 enzymes can have cell non-autonomous consequences on RA levels within tissues. Tretinoin 48-50 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 22-29
26116175-7 2015 We find that enhanced Cyp26a1 expression limits RA signaling in the local environment, thus providing the first direct evidence that Cyp26 enzymes can have cell non-autonomous consequences on RA levels within tissues. Tretinoin 48-50 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 22-27
26116175-7 2015 We find that enhanced Cyp26a1 expression limits RA signaling in the local environment, thus providing the first direct evidence that Cyp26 enzymes can have cell non-autonomous consequences on RA levels within tissues. Tretinoin 192-194 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 22-29
26116175-7 2015 We find that enhanced Cyp26a1 expression limits RA signaling in the local environment, thus providing the first direct evidence that Cyp26 enzymes can have cell non-autonomous consequences on RA levels within tissues. Tretinoin 192-194 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 22-27
26116175-8 2015 Therefore, our results provide novel insights into the teratogenic mechanisms of RA signaling and the cellular mechanisms by which Cyp26a1 expression can shape a RA gradient. Tretinoin 162-164 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 131-138
26253402-3 2015 Here, we demonstrate that a retinoic acid (RA)-degrading niche is established by Cyp26a1 in the proximal basal epidermal layer that orchestrates ray-interray organization by spatially restricting osteoblasts. Tretinoin 28-41 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 81-88
26253402-3 2015 Here, we demonstrate that a retinoic acid (RA)-degrading niche is established by Cyp26a1 in the proximal basal epidermal layer that orchestrates ray-interray organization by spatially restricting osteoblasts. Tretinoin 43-45 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 81-88
26552240-0 2015 [Expression of bone morphogenetic protein receptor 2 in cleft mouse embryonic palate induced by retinoic acid]. Tretinoin 96-109 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 15-52
26552240-1 2015 OBJECTIVE: To investigate the effects of all-trans retinoic acid (atRA) on the function of bone morphogenetic protein receptor 2 (BMPR2) expression in embryonic palate. Tretinoin 41-64 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 91-128
26552240-1 2015 OBJECTIVE: To investigate the effects of all-trans retinoic acid (atRA) on the function of bone morphogenetic protein receptor 2 (BMPR2) expression in embryonic palate. Tretinoin 41-64 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 130-135
26552240-1 2015 OBJECTIVE: To investigate the effects of all-trans retinoic acid (atRA) on the function of bone morphogenetic protein receptor 2 (BMPR2) expression in embryonic palate. Tretinoin 66-70 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 91-128
28982536-2 2017 In this study, we performed a comprehensive analysis of Hoxa1 target genes using genome-wide Hoxa1 binding data in mouse ES cells differentiated with retinoic acid (RA) into neural fates in combination with differential gene expression analysis in Hoxa1 gain- and loss-of-function mouse and zebrafish embryos. Tretinoin 150-163 homeobox A1 Mus musculus 56-61
26552240-1 2015 OBJECTIVE: To investigate the effects of all-trans retinoic acid (atRA) on the function of bone morphogenetic protein receptor 2 (BMPR2) expression in embryonic palate. Tretinoin 66-70 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 130-135
26552240-8 2015 Compared with those of the control group, BMPR2 protein and Bmpr2 mRNA decreased in the atRA-treated group (P<0.05). Tretinoin 88-92 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 42-47
26552240-8 2015 Compared with those of the control group, BMPR2 protein and Bmpr2 mRNA decreased in the atRA-treated group (P<0.05). Tretinoin 88-92 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 60-65
28982536-2 2017 In this study, we performed a comprehensive analysis of Hoxa1 target genes using genome-wide Hoxa1 binding data in mouse ES cells differentiated with retinoic acid (RA) into neural fates in combination with differential gene expression analysis in Hoxa1 gain- and loss-of-function mouse and zebrafish embryos. Tretinoin 165-167 homeobox A1 Mus musculus 56-61
26552240-9 2015 CONCLUSION: The treatment of pregnant mice with retinoic acid produces small palatal shelves in their fetuses and down-regulates BMPR2 expressions. Tretinoin 48-61 bone morphogenetic protein receptor, type II (serine/threonine kinase) Mus musculus 129-134
28978663-4 2017 Furthermore, the knocking down of tumor protein p73 (TP73) in NB4 cells resulted in reduced DAPK2 expression associated with decreased cell death and autophagy upon ATO and ATRA treatment, respectively. Tretinoin 173-177 tumor protein p73 Homo sapiens 34-51
28978663-4 2017 Furthermore, the knocking down of tumor protein p73 (TP73) in NB4 cells resulted in reduced DAPK2 expression associated with decreased cell death and autophagy upon ATO and ATRA treatment, respectively. Tretinoin 173-177 tumor protein p73 Homo sapiens 53-57
29344218-14 2017 ATRA treatment decreased the expression of phosphorylated (p-)beta-catenin, p-GSK-3beta, vimentin, and fibronectin, and increased the expression of NIS and E-cadherin, compared with the control. Tretinoin 0-4 glycogen synthase kinase 3 beta Homo sapiens 78-87
26173116-4 2015 Combined treatment of RA and bone morphogenetic protein 4 (BMP-4) increases the pro-apoptotic effect of RA in the RB cells lines WERI-Rb1, Y-79, RB355, RBL-30 and RBL-15, indicating an additive effect. Tretinoin 22-24 bone morphogenetic protein 4 Homo sapiens 59-64
26173116-4 2015 Combined treatment of RA and bone morphogenetic protein 4 (BMP-4) increases the pro-apoptotic effect of RA in the RB cells lines WERI-Rb1, Y-79, RB355, RBL-30 and RBL-15, indicating an additive effect. Tretinoin 104-106 bone morphogenetic protein 4 Homo sapiens 29-57
26173116-4 2015 Combined treatment of RA and bone morphogenetic protein 4 (BMP-4) increases the pro-apoptotic effect of RA in the RB cells lines WERI-Rb1, Y-79, RB355, RBL-30 and RBL-15, indicating an additive effect. Tretinoin 104-106 bone morphogenetic protein 4 Homo sapiens 59-64
26173116-5 2015 We could show that in WERI-Rb1 cells RA/BMP-4 mediated cell death is at least partially caspase-dependent, whereby RA and BMP-4 additively increased (i) Apaf-1 mRNA levels, (ii) caspase-9 cleavage activity and (iii) the number of activated, cleaved caspase-3 positive cells. Tretinoin 37-39 bone morphogenetic protein 4 Homo sapiens 40-45
26173116-5 2015 We could show that in WERI-Rb1 cells RA/BMP-4 mediated cell death is at least partially caspase-dependent, whereby RA and BMP-4 additively increased (i) Apaf-1 mRNA levels, (ii) caspase-9 cleavage activity and (iii) the number of activated, cleaved caspase-3 positive cells. Tretinoin 37-39 bone morphogenetic protein 4 Homo sapiens 122-127
26173116-6 2015 Compared to single application of RA and BMP-4, combined RA/BMP-4 treatment significantly augments mRNA levels of the retinoic acid receptors (RARs) RARalpha and RARss and the retinoic X receptor (RXR) RXRgamma suggesting an interaction in the induction of these RA receptor subtypes in WERI-Rb1 cells. Tretinoin 34-36 bone morphogenetic protein 4 Homo sapiens 60-65
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 10-23 interferon regulatory factor 4 Homo sapiens 41-45
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 10-23 interferon regulatory factor 4 Homo sapiens 71-75
26142905-13 2015 We demonstrate that CRABP1 expression attenuates RA-induced cell growth arrest and inhibits RA signalling in breast cancer cells by sequestering RA in the cytoplasm. Tretinoin 49-51 cellular retinoic acid binding protein 1 Homo sapiens 20-26
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 25-29 interferon regulatory factor 4 Homo sapiens 41-45
26142905-13 2015 We demonstrate that CRABP1 expression attenuates RA-induced cell growth arrest and inhibits RA signalling in breast cancer cells by sequestering RA in the cytoplasm. Tretinoin 49-51 cellular retinoic acid binding protein 1 Homo sapiens 20-26
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 25-29 interferon regulatory factor 4 Homo sapiens 71-75
26142905-17 2015 We propose that these three RA-binding proteins can serve as biomarkers for predicting triple-negative breast cancer response to RA, with elevated levels of either cytoplasmic CRABP1 or FABP5 associated with RA resistance, and elevated levels of nuclear CRABP2 associated with sensitivity to RA. Tretinoin 28-30 cellular retinoic acid binding protein 1 Homo sapiens 176-182
26414475-4 2015 It is important to identify these cryptic and variant translocations because certain variants, including ZBTB16/RARA and STAT5B/RARA, are resistant to treatment with all-trans retinoic acid, arsenic trioxide, and anthracyclines. Tretinoin 176-189 signal transducer and activator of transcription 5B Homo sapiens 121-127
28851699-10 2017 ATRA-treated cGVHD B cells had elevated TLR9 and PAX5, but not BLIMP1 (a gene-expression pattern associated with mature follicular B cells) and also attained increased cytosine guanine dinucleotide responsiveness. Tretinoin 0-4 toll like receptor 9 Homo sapiens 40-44
29166739-1 2017 Objective: To investigate the effect and mechanism of all-trans retinoic acid (ATRA) on leukemic cell line U937 cells with NPM1 mutation. Tretinoin 64-77 nucleophosmin 1 Homo sapiens 123-127
26208884-5 2015 Most interestingly, TLR ligation in the presence of recombinant IL-10 (rIL-10) or retinoic acid (RA) led to ERK1/2 activation independent of MEK1 in BMDMs derived from Mek1(d/d)Sox2(Cre) mice and led to inhibition of STAT4 and decreased IL-12 levels. Tretinoin 82-95 mitogen-activated protein kinase 3 Mus musculus 108-114
26208884-5 2015 Most interestingly, TLR ligation in the presence of recombinant IL-10 (rIL-10) or retinoic acid (RA) led to ERK1/2 activation independent of MEK1 in BMDMs derived from Mek1(d/d)Sox2(Cre) mice and led to inhibition of STAT4 and decreased IL-12 levels. Tretinoin 82-95 mitogen-activated protein kinase kinase 1 Mus musculus 168-172
29166739-1 2017 Objective: To investigate the effect and mechanism of all-trans retinoic acid (ATRA) on leukemic cell line U937 cells with NPM1 mutation. Tretinoin 79-83 nucleophosmin 1 Homo sapiens 123-127
25863234-4 2015 All-trans retinoic acid (atRA) favors Treg expansion and FoxP3 expression in human Tregs. Tretinoin 0-23 forkhead box P3 Homo sapiens 57-62
25863234-4 2015 All-trans retinoic acid (atRA) favors Treg expansion and FoxP3 expression in human Tregs. Tretinoin 25-29 forkhead box P3 Homo sapiens 57-62
25908839-4 2015 Omission of commonly used BMP inhibitors during pancreatic specification prevents precocious endocrine formation while treatment with retinoic acid followed by combined EGF/KGF efficiently generates both PDX1(+) and subsequent PDX1(+)/NKX6.1(+) pancreatic progenitor populations, respectively. Tretinoin 134-147 pancreatic and duodenal homeobox 1 Homo sapiens 204-208
25908839-4 2015 Omission of commonly used BMP inhibitors during pancreatic specification prevents precocious endocrine formation while treatment with retinoic acid followed by combined EGF/KGF efficiently generates both PDX1(+) and subsequent PDX1(+)/NKX6.1(+) pancreatic progenitor populations, respectively. Tretinoin 134-147 pancreatic and duodenal homeobox 1 Homo sapiens 227-231
29166739-6 2017 (3)All the U937 leukemic cells were inhibited under ATRA exposure; the decreased percentages of vector, wild-type and mutant NPM1 cells were 32.7%, 57.9% and 90.9% respectively. Tretinoin 52-56 nucleophosmin 1 Homo sapiens 125-129
25908839-4 2015 Omission of commonly used BMP inhibitors during pancreatic specification prevents precocious endocrine formation while treatment with retinoic acid followed by combined EGF/KGF efficiently generates both PDX1(+) and subsequent PDX1(+)/NKX6.1(+) pancreatic progenitor populations, respectively. Tretinoin 134-147 NK6 homeobox 1 Homo sapiens 235-241
24838400-5 2015 ATRA also induced a remarkable increase in PKCalpha and PKCdelta expression and activity. Tretinoin 0-4 protein kinase C delta Homo sapiens 56-64
24838400-7 2015 Moreover, PKCdelta inhibition also impaired ATRA-induced RARalpha translocation to the nucleus. Tretinoin 44-48 protein kinase C delta Homo sapiens 10-18
29166739-7 2017 (4)p-ERK decreased obviously after ATRA exposure in NPM1 mutated leukemic cells. Tretinoin 35-39 nucleophosmin 1 Homo sapiens 52-56
29166739-8 2017 (5)More mutant NPM1 cells inclined to apoptosis under the exposure of ATRA and cytotoxic drugs than cytotoxic drugs alone, meanwhile more cells apoptosis occurred when ATRA was administrated after cytotoxic drugs exposure. Tretinoin 70-74 nucleophosmin 1 Homo sapiens 15-19
29166739-8 2017 (5)More mutant NPM1 cells inclined to apoptosis under the exposure of ATRA and cytotoxic drugs than cytotoxic drugs alone, meanwhile more cells apoptosis occurred when ATRA was administrated after cytotoxic drugs exposure. Tretinoin 168-172 nucleophosmin 1 Homo sapiens 15-19
29166739-9 2017 Conclusions: ATRA could inhibit cell proliferation and colony formation, blocked the cell cycle in the G(0)/G(1) stage accompanied by the significant reduction of p-ERK in U937 leukemic cells with NPM1 mutation. Tretinoin 13-17 nucleophosmin 1 Homo sapiens 197-201
25991548-0 2015 A Brn2-Zic1 axis specifies the neuronal fate of retinoic-acid-treated embryonic stem cells. Tretinoin 48-61 POU domain, class 3, transcription factor 2 Mus musculus 2-6
29166739-10 2017 Besides, ATRA could synergize with drugs to suppress the leukemic cells survival more effectively when ATRA was administered after the cytotoxic drugs exposure in U937 leukemic cells with NPM1 mutation. Tretinoin 9-13 nucleophosmin 1 Homo sapiens 188-192
25991548-7 2015 Small hairpin RNA (shRNA)-mediated silencing of Zic1 prevented ESCs from differentiating into neuronal precursors, thus defining a hierarchical Brn2-Zic1 axis that is essential to specify neural fate in retinoic-acid-treated ESCs. Tretinoin 203-216 POU domain, class 3, transcription factor 2 Mus musculus 144-148
29166739-10 2017 Besides, ATRA could synergize with drugs to suppress the leukemic cells survival more effectively when ATRA was administered after the cytotoxic drugs exposure in U937 leukemic cells with NPM1 mutation. Tretinoin 103-107 nucleophosmin 1 Homo sapiens 188-192
29021914-4 2017 RA triggered angiogenesis and elicited de novo generation of platelet-derived growth factor receptor alpha positive (PDGFRalpha+) adipose precursor cells via VEGFA/VEGFR2 signaling. Tretinoin 0-2 kinase insert domain protein receptor Mus musculus 164-170
26020124-0 2015 Combination Treatment with All-Trans Retinoic Acid Prevents Cisplatin-Induced Enrichment of CD133+ Tumor-Initiating Cells and Reveals Heterogeneity of Cancer Stem Cell Compartment in Lung Cancer. Tretinoin 37-50 prominin 1 Homo sapiens 92-97
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 109-113 G0/G1 switch 2 Homo sapiens 0-4
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 202-206 G0/G1 switch 2 Homo sapiens 0-4
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 202-206 G0/G1 switch 2 Homo sapiens 169-173
28648614-3 2017 In this study the effects of RA on MMP-2 production in cells of rat uterus were investigated. Tretinoin 29-31 matrix metallopeptidase 2 Rattus norvegicus 35-40
26394147-0 2015 Rdh10a Provides a Conserved Critical Step in the Synthesis of Retinoic Acid during Zebrafish Embryogenesis. Tretinoin 62-75 retinol dehydrogenase 10a Danio rerio 0-6
26394147-3 2015 If the conservation of Rdh10 function in the production of RA extends to teleost embryos has not been investigated. Tretinoin 59-61 retinol dehydrogenase 10b Danio rerio 23-28
26394147-8 2015 Altogether, our results demonstrate that Rdh10a has a conserved requirement in the first step of RA production within vertebrate embryos. Tretinoin 97-99 retinol dehydrogenase 10a Danio rerio 41-47
26368825-3 2015 Here, we found that mouse Raldh2-/- embryos, lacking RA synthesis and displaying a consistent small somite defect, exhibited abnormal expression of key markers of axial stem cell progeny, with decreased Sox2+ and Sox1+ neuroectodermal progeny and increased Tbx6+ presomitic mesodermal progeny. Tretinoin 53-55 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 26-32
26352270-6 2015 Conserved Retinoic Acid Response Elements (RAREs) upstream of human ALDH1A3 and FOXN1 and in mouse Aldh1a3 and Foxn1 genes were revealed using bioinformatic approximation. Tretinoin 10-23 forkhead box N1 Homo sapiens 80-85
26125906-10 2015 WY14643 combined with t-RA can induce the transformation of white adipocytes to brown adipocytes through activation of the p38 MAPK signaling pathway. Tretinoin 22-26 mitogen-activated protein kinase 14 Mus musculus 123-126
26101153-0 2015 Zic1 controls placode progenitor formation non-cell autonomously by regulating retinoic acid production and transport. Tretinoin 79-92 Zic family member 1 Homo sapiens 0-4
28648614-11 2017 CONCLUSION: RA had negative effects on cell proliferation and cell morphology and inhibited MMP-2 expression. Tretinoin 12-14 matrix metallopeptidase 2 Rattus norvegicus 92-97
28679528-5 2017 Mechanistically, alcohol intake increased RA levels in serum and adipose tissue, which was associated with increased expression of aldehyde dehydrogenase family 1 subfamily A1 (Aldh1a1). Tretinoin 42-44 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 131-175
26101153-4 2015 In a screen for genes activated by Zic1, we identify several factors involved in RA metabolism and function. Tretinoin 81-83 Zic family member 1 Homo sapiens 35-39
26101153-6 2015 We propose that RALDH2 and LPGDS induction by Zic1 at the anterior neural plate allows for the localized production and transport of RA, which in turn activates a cranial placode developmental programme in neighbouring cells. Tretinoin 16-18 Zic family member 1 Homo sapiens 46-50
26287494-2 2015 It was previously reported that, in patient-derived HL-60 myeloblastic leukemia cells, retinoic acid (RA)-induced differentiation is driven by a signalsome containing c-Cbl and AhR. Tretinoin 87-100 aryl hydrocarbon receptor Homo sapiens 177-180
26287494-2 2015 It was previously reported that, in patient-derived HL-60 myeloblastic leukemia cells, retinoic acid (RA)-induced differentiation is driven by a signalsome containing c-Cbl and AhR. Tretinoin 102-104 aryl hydrocarbon receptor Homo sapiens 177-180
28679528-5 2017 Mechanistically, alcohol intake increased RA levels in serum and adipose tissue, which was associated with increased expression of aldehyde dehydrogenase family 1 subfamily A1 (Aldh1a1). Tretinoin 42-44 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 177-184
28679652-11 2017 Transient transfection of GapmeR against XLOC_109948 in NPM1-mutated OCI-AML3 cell line treated with Ara-C or ATRA enhances apoptosis suggesting XLOC_109948 plays a role in drug sensitivity. Tretinoin 110-114 nucleophosmin 1 Homo sapiens 56-60
26041820-3 2015 In this study, we report downregulation of the miR-181a/b gene cluster in APL blasts and NB4 leukemia cells upon ATRA treatment as a key event in the drug response. Tretinoin 113-117 microRNA 181a-2 Mus musculus 47-55
25350918-4 2015 Using a retinoic acid deficiency-induced squamous metaplasia model of cultured human nasal epithelial cells (HNECs), we observed a significant increase in the expression of PC5/6A, a PC member, and bone morphogenetic protein-2 (BMP-2), a candidate substrate for PC5/6A. Tretinoin 8-21 proprotein convertase subtilisin/kexin type 5 Homo sapiens 173-179
25350918-4 2015 Using a retinoic acid deficiency-induced squamous metaplasia model of cultured human nasal epithelial cells (HNECs), we observed a significant increase in the expression of PC5/6A, a PC member, and bone morphogenetic protein-2 (BMP-2), a candidate substrate for PC5/6A. Tretinoin 8-21 bone morphogenetic protein 2 Homo sapiens 198-226
25350918-4 2015 Using a retinoic acid deficiency-induced squamous metaplasia model of cultured human nasal epithelial cells (HNECs), we observed a significant increase in the expression of PC5/6A, a PC member, and bone morphogenetic protein-2 (BMP-2), a candidate substrate for PC5/6A. Tretinoin 8-21 bone morphogenetic protein 2 Homo sapiens 228-233
25350918-4 2015 Using a retinoic acid deficiency-induced squamous metaplasia model of cultured human nasal epithelial cells (HNECs), we observed a significant increase in the expression of PC5/6A, a PC member, and bone morphogenetic protein-2 (BMP-2), a candidate substrate for PC5/6A. Tretinoin 8-21 proprotein convertase subtilisin/kexin type 5 Homo sapiens 173-176
28877686-11 2017 Our analyses of primary AML cells during in vivo treatment suggest that ATRA modulates HOX activity (i.e. decreased expression of HOXA3, HOXA4 and HOXA5 and their regulator PBX3), but altered function of DNA methyl transferase 3A (DNMT3A) and G-protein coupled receptor signaling may also contribute to the effect of the overall treatment. Tretinoin 72-76 homeobox A3 Homo sapiens 130-135
25350918-9 2015 Under retinoic acid-sufficient culture conditions for mucociliary differentiation of HNECs, short-term expression of PC5/6A by the adenovirus system and addition of exogenous BMP-2 induced squamous differentiation. Tretinoin 6-19 proprotein convertase subtilisin/kexin type 5 Homo sapiens 117-123
25350918-9 2015 Under retinoic acid-sufficient culture conditions for mucociliary differentiation of HNECs, short-term expression of PC5/6A by the adenovirus system and addition of exogenous BMP-2 induced squamous differentiation. Tretinoin 6-19 bone morphogenetic protein 2 Homo sapiens 175-180
25941627-0 2015 The AhR agonist VAF347 augments retinoic acid-induced differentiation in leukemia cells. Tretinoin 32-45 aryl hydrocarbon receptor Homo sapiens 4-7
25941627-2 2015 We have previously reported that aryl hydrocarbon receptor (AhR) promotes retinoic acid (RA)-induced granulocytic differentiation of lineage bipotent HL-60 myeloblastic leukemia cells. Tretinoin 74-87 aryl hydrocarbon receptor Homo sapiens 33-58
25941627-2 2015 We have previously reported that aryl hydrocarbon receptor (AhR) promotes retinoic acid (RA)-induced granulocytic differentiation of lineage bipotent HL-60 myeloblastic leukemia cells. Tretinoin 74-87 aryl hydrocarbon receptor Homo sapiens 60-63
25941627-2 2015 We have previously reported that aryl hydrocarbon receptor (AhR) promotes retinoic acid (RA)-induced granulocytic differentiation of lineage bipotent HL-60 myeloblastic leukemia cells. Tretinoin 89-91 aryl hydrocarbon receptor Homo sapiens 33-58
25946380-10 2015 ATRA not only influenced the cycle procession but also reduced the expression of cyclin D1. Tretinoin 0-4 cyclin D1 Homo sapiens 81-90
26116962-0 2015 Retinoic acid inhibits tissue factor and HMGB1 via modulation of AMPK activity in TNF-alpha activated endothelial cells and LPS-injected mice. Tretinoin 0-13 high mobility group box 1 Mus musculus 41-46
26116962-8 2015 In addition, RA reduced HMGB1 release in TNF-alpha activated ECs, which was reversed by both LY294001 and siAMPK. Tretinoin 13-15 high mobility group box 1 Mus musculus 24-29
26116962-9 2015 Importantly, administration of RA (1 mg/kg) significantly reduced blood TF activity, circulating HMGB1 and PAI-1 levels and expression of hepatic TF mRNA as well as fibrin deposition in LPS (5 mg/kg)-injected mice. Tretinoin 31-33 high mobility group box 1 Mus musculus 97-102
26116962-10 2015 CONCLUSIONS: Taken together, the activation of PI3K/Akt by RA modulates AMPK activity in ECs and plays a crucial role in the inhibition of coagulatory factors such as TF, PAI-1, and HMGB1 in inflammatory conditions. Tretinoin 59-61 high mobility group box 1 Mus musculus 182-187
25817574-0 2015 GW5074 and PP2 kinase inhibitors implicate nontraditional c-Raf and Lyn function as drivers of retinoic acid-induced maturation. Tretinoin 95-108 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 11-14
25817574-0 2015 GW5074 and PP2 kinase inhibitors implicate nontraditional c-Raf and Lyn function as drivers of retinoic acid-induced maturation. Tretinoin 95-108 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 58-63
25817574-3 2015 In this study GW5074 (a c-Raf inhibitor) and PP2 (a Src-family kinase inhibitor) enhanced RA-induced maturation of t(15;17)-negative myeloblastic leukemia cells and rescued response in RA-resistant cells. Tretinoin 90-92 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 24-29
25817574-3 2015 In this study GW5074 (a c-Raf inhibitor) and PP2 (a Src-family kinase inhibitor) enhanced RA-induced maturation of t(15;17)-negative myeloblastic leukemia cells and rescued response in RA-resistant cells. Tretinoin 90-92 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 45-48
25817574-8 2015 This suggests that an interrelated kinase module involving c-Raf, PI3K, Lyn and perhaps Fgr functions in a nontraditional way during RA-induced maturation or during rescue of RA induction therapy using inhibitor co-treatment in RA-resistant leukemia cells. Tretinoin 133-135 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 59-64
25817574-8 2015 This suggests that an interrelated kinase module involving c-Raf, PI3K, Lyn and perhaps Fgr functions in a nontraditional way during RA-induced maturation or during rescue of RA induction therapy using inhibitor co-treatment in RA-resistant leukemia cells. Tretinoin 175-177 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 59-64
25941627-2 2015 We have previously reported that aryl hydrocarbon receptor (AhR) promotes retinoic acid (RA)-induced granulocytic differentiation of lineage bipotent HL-60 myeloblastic leukemia cells. Tretinoin 89-91 aryl hydrocarbon receptor Homo sapiens 60-63
25941627-8 2015 VAF347 augments RA-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47(phox). Tretinoin 16-18 aryl hydrocarbon receptor Homo sapiens 41-44
25941627-8 2015 VAF347 augments RA-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47(phox). Tretinoin 16-18 vav guanine nucleotide exchange factor 1 Homo sapiens 51-55
28877686-11 2017 Our analyses of primary AML cells during in vivo treatment suggest that ATRA modulates HOX activity (i.e. decreased expression of HOXA3, HOXA4 and HOXA5 and their regulator PBX3), but altered function of DNA methyl transferase 3A (DNMT3A) and G-protein coupled receptor signaling may also contribute to the effect of the overall treatment. Tretinoin 72-76 homeobox A4 Homo sapiens 137-142
28877686-11 2017 Our analyses of primary AML cells during in vivo treatment suggest that ATRA modulates HOX activity (i.e. decreased expression of HOXA3, HOXA4 and HOXA5 and their regulator PBX3), but altered function of DNA methyl transferase 3A (DNMT3A) and G-protein coupled receptor signaling may also contribute to the effect of the overall treatment. Tretinoin 72-76 PBX homeobox 3 Homo sapiens 173-177
25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 MYCN opposite strand Homo sapiens 48-52
28718066-9 2017 In the NTD model, the expression levels of Dvl, RhoA, and p-Jnk were significantly higher in the RA group than in the control group, whereas they were significantly reduced in the RA + taurine group. Tretinoin 97-99 ras homolog family member A Mus musculus 48-52
25959810-8 2015 RESULTS: Retinoic acid acted synergistically with IL-2 and other activating cytokines to induce expression of the gut-homing integrin alpha4beta7 in ILCs, as well as production of IL-5 and IL-13 in ILC2 cells, and IFN-gamma in ILC1 and ILC3 cells. Tretinoin 9-22 interleukin 5 Homo sapiens 180-184
28643469-2 2017 Here, we showed that ATRA could induce the expression of COL9A1 in antler chondrocytes. Tretinoin 21-25 collagen type IX alpha 1 chain Homo sapiens 57-63
26174098-11 2015 Retinoic acid treatment also induced in the proepicardium expression of Hoxb4, a gene which confers to intermediate mesoderm competence to respond to nephrogenic signals. Tretinoin 0-13 homeobox B4 Mus musculus 72-77
25807265-5 2015 The dual-luciferase reporter showed that all-trans retinoic acid (ATRA), a retinoic acid receptor alpha agonist (tamibarotene/Am80), or estradiol (E2) could significantly enhance DAZL transcription. Tretinoin 46-65 deleted in azoospermia like Gallus gallus 180-184
25807265-5 2015 The dual-luciferase reporter showed that all-trans retinoic acid (ATRA), a retinoic acid receptor alpha agonist (tamibarotene/Am80), or estradiol (E2) could significantly enhance DAZL transcription. Tretinoin 67-71 deleted in azoospermia like Gallus gallus 180-184
25807265-6 2015 The in vitro inductive culture of chicken ESCs demonstrated that, with ATRA treatment, DAZL transcription peaked at 6 days and then decreased slowly; whereas, DAZL transcription was continuous and peaked at 10 days with Am80 treatment. Tretinoin 71-75 deleted in azoospermia like Gallus gallus 87-91
25957888-0 2015 All-trans retinoic acid up-regulates the human CD2AP gene expression through Sp1/Sp3 binding sites. Tretinoin 10-23 CD2 associated protein Homo sapiens 47-52
28643469-3 2017 Silencing of cellular retinoic acid binding protein 2 (CRABP2) could impede the ATRA-induced upregulation of COL9A1, whereas overexpression of CRABP2 presented the opposite effect. Tretinoin 80-84 collagen type IX alpha 1 chain Homo sapiens 109-115
25957888-2 2015 It was reported that ATRA could cause an up-regulation of protein expression of CD2AP in nephrotic animals. Tretinoin 21-25 CD2 associated protein Homo sapiens 80-85
25887926-5 2015 Moreover, with the presence of TGF-beta, ATRA upregulated CD4(+)CD25(+)Foxp3(+)Treg cells and suppressed Th17 cells in the blood, spleen and draining lymph nodes of recipient mice, as well as enhanced the Foxp3 expression and inhibited the RORgammat expression in grafts and peripheral blood mononuclear cells (PBMCs). Tretinoin 41-45 transforming growth factor, beta 1 Mus musculus 31-39
28643469-5 2017 In antler chondrocytes, CYP26A1 and CYP26B1 weakened the sensitivity of ATRA to COL9A1. Tretinoin 72-76 collagen type IX alpha 1 chain Homo sapiens 80-86
25957888-5 2015 Chromatin immunoprecipitation assays revealed that ATRA activated the CD2AP transcription through enhancing the DNA-binding activity of Sp1 and Sp3 with the CD2AP promoter. Tretinoin 51-55 CD2 associated protein Homo sapiens 70-75
25957888-5 2015 Chromatin immunoprecipitation assays revealed that ATRA activated the CD2AP transcription through enhancing the DNA-binding activity of Sp1 and Sp3 with the CD2AP promoter. Tretinoin 51-55 CD2 associated protein Homo sapiens 157-162
28758396-10 2017 Instead, expression of LRAT(E14L) led to a rapid increase in cellular levels of retinoic acid upon retinoid supplementation. Tretinoin 80-93 lecithin retinol acyltransferase Homo sapiens 23-27
25957888-6 2015 Taken together, this study provided evidence for the first time showing the stimulating effect of ATRA on CD2AP and new therapeutic strategies for the treatment of nephritic syndrome and other associated diseases of CD2AP deficiency. Tretinoin 98-102 CD2 associated protein Homo sapiens 106-111
26020124-5 2015 Pretreatment with differentiating agent all-trans retinoic acid counteracts cisplatin resistance specifically of the slowly dividing compartment indicating effect on CD133+/CXCR4+ cells. Tretinoin 44-63 prominin 1 Homo sapiens 166-171
26121141-0 2015 Shared Segment Analysis and Next-Generation Sequencing Implicates the Retinoic Acid Signaling Pathway in Total Anomalous Pulmonary Venous Return (TAPVR). Tretinoin 70-83 TAPVR1 Homo sapiens 146-151
25774684-6 2015 Addition of retinoic acid (RA), Noggin and Cyclopamine promoted pancreatic differentiation as indicated by the expression of the early pancreatic progenitor markers ISL1, NGN3 and PDX1. Tretinoin 12-25 pancreatic and duodenal homeobox 1 Homo sapiens 180-184
25774684-6 2015 Addition of retinoic acid (RA), Noggin and Cyclopamine promoted pancreatic differentiation as indicated by the expression of the early pancreatic progenitor markers ISL1, NGN3 and PDX1. Tretinoin 27-29 pancreatic and duodenal homeobox 1 Homo sapiens 180-184
25542995-9 2015 Interestingly, the sim1a expression domain in renal progenitors is responsive to altered levels of RA, suggesting that RA regulates sim1a, directly or indirectly, during nephrogenesis. Tretinoin 99-101 SIM bHLH transcription factor 1a Danio rerio 19-24
26121141-11 2015 These data indicate that genetic variation in the retinoic acid signaling pathway confers, in part, susceptibility to TAPVR. Tretinoin 50-63 TAPVR1 Homo sapiens 118-123
28381549-0 2017 A Dominant Mutation in Nuclear Receptor Interacting Protein 1 Causes Urinary Tract Malformations via Dysregulation of Retinoic Acid Signaling. Tretinoin 118-131 nuclear receptor interacting protein 1 Homo sapiens 23-61
26125906-0 2015 WY14643 combined with all-trans retinoic acid acts via p38 MAPK to induce "browning" of white adipocytes in mice. Tretinoin 32-45 mitogen-activated protein kinase 14 Mus musculus 55-63
26125906-8 2015 WY14643 combined with t-RA was observed to induce UCP1 mRNA expression, protein expression, and phosphory-lation of p38 MAPK (P < 0.05). Tretinoin 22-26 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 50-54
26125906-8 2015 WY14643 combined with t-RA was observed to induce UCP1 mRNA expression, protein expression, and phosphory-lation of p38 MAPK (P < 0.05). Tretinoin 22-26 mitogen-activated protein kinase 14 Mus musculus 116-124
25542995-9 2015 Interestingly, the sim1a expression domain in renal progenitors is responsive to altered levels of RA, suggesting that RA regulates sim1a, directly or indirectly, during nephrogenesis. Tretinoin 119-121 SIM bHLH transcription factor 1a Danio rerio 19-24
25542995-9 2015 Interestingly, the sim1a expression domain in renal progenitors is responsive to altered levels of RA, suggesting that RA regulates sim1a, directly or indirectly, during nephrogenesis. Tretinoin 119-121 SIM bHLH transcription factor 1a Danio rerio 132-137
25542995-10 2015 sim1a deficient embryos treated with exogenous RA formed nephrons that were predominantly composed of PCT segments, but lacked the enlarged PST observed in RA treated wild-types, indicating that RA is not sufficient to rescue the PST in the absence of sim1a expression. Tretinoin 47-49 SIM bHLH transcription factor 1a Danio rerio 0-5
25542995-11 2015 Alternately, when sim1a knockdowns were exposed to the RA inhibitor diethylaminobenzaldehyde (DEAB), the CS was abrogated rather than expanded as seen in DEAB treated wild-types, revealing that CS formation in the absence of sim1a cannot be rescued by RA biosynthesis abrogation. Tretinoin 55-57 SIM bHLH transcription factor 1a Danio rerio 18-23
28381549-7 2017 Notably, we also showed that treatment with retinoic acid enhanced NRIP1 binding to RARalpha RNA in situ hybridization confirmed Nrip1 expression in the developing urogenital system of the mouse. Tretinoin 44-57 nuclear receptor interacting protein 1 Mus musculus 67-72
25542995-11 2015 Alternately, when sim1a knockdowns were exposed to the RA inhibitor diethylaminobenzaldehyde (DEAB), the CS was abrogated rather than expanded as seen in DEAB treated wild-types, revealing that CS formation in the absence of sim1a cannot be rescued by RA biosynthesis abrogation. Tretinoin 252-254 SIM bHLH transcription factor 1a Danio rerio 18-23
25239070-4 2015 Since retinoid is a potential patterning influence on the developing face, we have examined whether retinoic acid (RA) signaling regulated Lhx8, Msx1 and Msx2 transcription through fibroblast growth factor (FGF) signals in the maxillary prominence. Tretinoin 115-117 LIM homeobox 8 Gallus gallus 139-143
28381549-7 2017 Notably, we also showed that treatment with retinoic acid enhanced NRIP1 binding to RARalpha RNA in situ hybridization confirmed Nrip1 expression in the developing urogenital system of the mouse. Tretinoin 44-57 nuclear receptor interacting protein 1 Mus musculus 129-134
25239070-8 2015 The downregulated Lhx8 was rescued by combined treatment with FGF-8b, which indicated a downstream of RA signaling. Tretinoin 102-104 LIM homeobox 8 Gallus gallus 18-22
25964457-4 2015 Increased expression of alpha4beta7 integrin and the chemokine receptor CCR9 following exposure to ATRA can be used to redirect T cells to the gut. Tretinoin 99-103 atypical chemokine receptor 2 Homo sapiens 53-76
28381549-8 2017 In explant cultures of embryonic kidney rudiments, retinoic acid stimulated Nrip1 expression, whereas a pan-RAR antagonist strongly reduced it. Tretinoin 51-64 nuclear receptor interacting protein 1 Homo sapiens 76-81
28992291-8 2017 In summary, RA inhibits white adipogenesis by inducing RAR and ING1 interaction and inhibiting Gadd45a expression, which prevents GADD45A-mediated DNA demethylation. Tretinoin 12-14 growth arrest and DNA damage inducible alpha Homo sapiens 95-102
25878247-5 2015 Assembly of Elongin A into the ubiquitin ligase is strongly induced by genotoxic stress; by transcriptional stresses that lead to accumulation of stalled Pol II; and by other stimuli, including endoplasmic reticulum and nutrient stress and retinoic acid signaling, that activate Elongin A-dependent transcription. Tretinoin 240-253 elongin A Homo sapiens 12-21
28992291-8 2017 In summary, RA inhibits white adipogenesis by inducing RAR and ING1 interaction and inhibiting Gadd45a expression, which prevents GADD45A-mediated DNA demethylation. Tretinoin 12-14 growth arrest and DNA damage inducible alpha Homo sapiens 130-137
28903433-5 2017 A gradually decreased hnRNP A1 expression was detected during granulocytic differentiation in ATRA-induced-NB4 and HL-60 cells and cytokines-induced hematopoietic stem and progenitor cells. Tretinoin 94-98 heterogeneous nuclear ribonucleoprotein A1 Homo sapiens 22-30
25711908-4 2015 The retinoic acid produced by HSCs augmented B-cell survival, plasma cell marker CD138 expression, and immunoglobulin G production. Tretinoin 4-17 syndecan 1 Homo sapiens 81-86
25711908-8 2015 Likewise, targeted deletion of B-cell-intrinsic myeloid differentiation primary response gene 88 signaling, an innate adaptor with involvement in retinoic acid signaling, resulted in reduced infiltration of migratory CD11c(+) dendritic cells and Ly6C(++) monocytes and, hence, reduced liver pathology. Tretinoin 146-159 integrin subunit alpha X Homo sapiens 217-222
25389133-3 2015 atRA signaling was ablated in beta-cells by overexpressing a dominant-negative retinoic acid receptor (RAR)-alpha mutant (RARdn) using an inducible Cre-Lox system under the control of the pancreas duodenal homeobox gene promoter. Tretinoin 0-4 lysyl oxidase Mus musculus 152-155
25443173-10 2015 Accompanying the changes in physiological status were major changes in hypothalamic thyroid hormone (Dio2 and Dio3), retinoic acid (Crabp1 and Stra6) and Wnt/beta-Catenin signalling genes (sFrp2 and Mfrp). Tretinoin 117-130 cellular retinoic acid binding protein 1 Rattus norvegicus 132-138
28666018-7 2017 I3C feeding robustly induced the AhR-target gene CYP4501A1 in the intestine; I3C feeding also induced the aldh1 gene, whose product catalyzes the formation of retinoic acid (RA), an inducer of regulatory T cells. Tretinoin 159-172 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 106-111
25749095-0 2015 Retinoic acid-induced IgG production in TLR-activated human primary B cells involves ULK1-mediated autophagy. Tretinoin 0-13 unc-51 like autophagy activating kinase 1 Homo sapiens 85-89
25749095-2 2015 Thus, RA enhanced autophagy in TLR9- and CD180-stimulated peripheral blood B cells, as revealed by increased levels of the autophagosomal marker LC3B-II, enhanced colocalization between LC3B and the lysosomal marker Lyso-ID, by a larger percentage of cells with more than 5 characteristic LC3B puncta, and by the concomitant reduction in the level of SQSTM1/p62. Tretinoin 6-8 toll like receptor 9 Homo sapiens 31-35
25749095-2 2015 Thus, RA enhanced autophagy in TLR9- and CD180-stimulated peripheral blood B cells, as revealed by increased levels of the autophagosomal marker LC3B-II, enhanced colocalization between LC3B and the lysosomal marker Lyso-ID, by a larger percentage of cells with more than 5 characteristic LC3B puncta, and by the concomitant reduction in the level of SQSTM1/p62. Tretinoin 6-8 microtubule associated protein 1 light chain 3 beta Homo sapiens 145-149
25749095-2 2015 Thus, RA enhanced autophagy in TLR9- and CD180-stimulated peripheral blood B cells, as revealed by increased levels of the autophagosomal marker LC3B-II, enhanced colocalization between LC3B and the lysosomal marker Lyso-ID, by a larger percentage of cells with more than 5 characteristic LC3B puncta, and by the concomitant reduction in the level of SQSTM1/p62. Tretinoin 6-8 microtubule associated protein 1 light chain 3 beta Homo sapiens 186-190
25795919-3 2015 Adjunct of ATRA to chemotherapy was reported to be beneficial for NPM1-mutated AML patients. Tretinoin 11-15 nucleophosmin 1 Homo sapiens 66-70
25795919-5 2015 Here, we explore the mechanisms underlying these observations and show that ATO/ATRA induce proteasome-dependent degradation of NPM1 leukemic protein and apoptosis in NPM1-mutated AML cell lines and primary patients" cells. Tretinoin 80-84 nucleophosmin 1 Homo sapiens 128-132
25795919-8 2015 Strikingly, NPM1 mutant downregulation by ATO/ATRA was shown to potentiate response to the anthracyclin daunorubicin. Tretinoin 46-50 nucleophosmin 1 Homo sapiens 12-16
25795919-9 2015 These findings provide experimental evidence for further exploring ATO/ATRA in preclinical NPM1-mutated AML in vivo models and a rationale for exploiting these compounds in chemotherapeutic regimens in clinics. Tretinoin 71-75 nucleophosmin 1 Homo sapiens 91-95
25800051-0 2015 Retinoic acid and arsenic trioxide trigger degradation of mutated NPM1, resulting in apoptosis of AML cells. Tretinoin 0-13 nucleophosmin 1 Homo sapiens 66-70
28238841-9 2017 RA treatment induced Gck expression only in STZ-VAD rats. Tretinoin 0-2 glucokinase Rattus norvegicus 21-24
25800051-3 2015 Here, we found that RA or arsenic trioxide synergistically induce proteasomal degradation of mutant NPM1 in AML cell lines or primary samples, leading to differentiation and apoptosis. Tretinoin 20-22 nucleophosmin 1 Homo sapiens 100-104
25800051-5 2015 Combined RA/arsenic treatment significantly reduced bone marrow blasts in 3 patients and restored the subnuclear localization of both NPM1 and PML. Tretinoin 9-11 nucleophosmin 1 Homo sapiens 134-138
25800051-6 2015 These findings could explain the proposed benefit of adding RA to chemotherapy in NPM1 mutant AMLs, and warrant a broader clinical evaluation of regimen comprising a RA/arsenic combination. Tretinoin 60-62 nucleophosmin 1 Homo sapiens 82-86
25749095-2 2015 Thus, RA enhanced autophagy in TLR9- and CD180-stimulated peripheral blood B cells, as revealed by increased levels of the autophagosomal marker LC3B-II, enhanced colocalization between LC3B and the lysosomal marker Lyso-ID, by a larger percentage of cells with more than 5 characteristic LC3B puncta, and by the concomitant reduction in the level of SQSTM1/p62. Tretinoin 6-8 microtubule associated protein 1 light chain 3 beta Homo sapiens 186-190
25749095-3 2015 Furthermore, RA induced expression of the autophagy-inducing protein ULK1 at the transcriptional level, in a process that required the retinoic acid receptor RAR. Tretinoin 13-15 unc-51 like autophagy activating kinase 1 Homo sapiens 69-73
28238841-10 2017 Insulin + RA treatment further induced the Cyp26a1 and Gck expressions in STZ-VAD rats. Tretinoin 10-12 glucokinase Rattus norvegicus 55-58
27797397-3 2017 Expression of KLK5 and KLK7 is controlled and upregulated by stimulants such as calcium, 1,25-dihydroxyvitamin D3 [1,25(OH)2 VD3 ] and retinoic acid (RA). Tretinoin 135-148 kallikrein related peptidase 5 Homo sapiens 14-18
24633826-7 2015 Finally, we show that over-expression of SMN is protective for ESCs from retinoic acid-induced differentiation. Tretinoin 73-86 survival motor neuron 1 Mus musculus 41-44
26022051-1 2015 In this issue of Blood, Martelli et al and El Hajj et al independently report that nucleophosmin-1 (NPM1)-mutant leukemia is particularly vulnerable to a novel strategy combining all-trans retinoic acid (ATRA) with arsenic trioxide (ATO). Tretinoin 204-208 nucleophosmin 1 Homo sapiens 83-98
26022051-1 2015 In this issue of Blood, Martelli et al and El Hajj et al independently report that nucleophosmin-1 (NPM1)-mutant leukemia is particularly vulnerable to a novel strategy combining all-trans retinoic acid (ATRA) with arsenic trioxide (ATO). Tretinoin 204-208 nucleophosmin 1 Homo sapiens 100-104
27797397-3 2017 Expression of KLK5 and KLK7 is controlled and upregulated by stimulants such as calcium, 1,25-dihydroxyvitamin D3 [1,25(OH)2 VD3 ] and retinoic acid (RA). Tretinoin 150-152 kallikrein related peptidase 5 Homo sapiens 14-18
25397866-4 2015 Subsequent treatment with retinoic acid highly upregulated PDX1 expression. Tretinoin 26-39 pancreatic and duodenal homeobox 1 Homo sapiens 59-63
28589680-0 2017 All-trans retinoic acid upregulates the expression of ciliary neurotrophic factor in retinal pigment epithelial cells. Tretinoin 10-23 ciliary neurotrophic factor Mus musculus 54-81
25753125-9 2015 The expression patterns of five selected proteins were verified via Western blot, of which we found that Tfrc gene was RA responsive, with a RA responsive element, and could be up regulated by RA in spermatogonial stem cell (SSC) line. Tretinoin 119-121 transferrin receptor Mus musculus 105-109
25753125-9 2015 The expression patterns of five selected proteins were verified via Western blot, of which we found that Tfrc gene was RA responsive, with a RA responsive element, and could be up regulated by RA in spermatogonial stem cell (SSC) line. Tretinoin 141-143 transferrin receptor Mus musculus 105-109
28218902-0 2017 Retinoic acid directs breast cancer cell state changes through regulation of TET2-PKCzeta pathway. Tretinoin 0-13 tet methylcytosine dioxygenase 2 Homo sapiens 77-81
25753125-9 2015 The expression patterns of five selected proteins were verified via Western blot, of which we found that Tfrc gene was RA responsive, with a RA responsive element, and could be up regulated by RA in spermatogonial stem cell (SSC) line. Tretinoin 141-143 transferrin receptor Mus musculus 105-109
26819566-3 2015 Retinal, the precursor of retinoic acid, can be oxidized to retinoic acid by dehydrogenases, including ALDH. Tretinoin 26-39 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 103-107
26819566-3 2015 Retinal, the precursor of retinoic acid, can be oxidized to retinoic acid by dehydrogenases, including ALDH. Tretinoin 60-73 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 103-107
26819566-4 2015 We hypothesized that retinal could potentially be transformed to retinoic acid with higher efficiency by cancer stem cells, due to the higher ALDH activity. Tretinoin 65-78 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 142-146
26819566-7 2015 Our current results demonstrated that retinal preferentially affected the phenotypes of ALDH-high K7M2 cells in contrast to ALDH-low K12 cells, which could be mediated by the more efficient transformation of retinal to retinoic acid by ALDH in K7M2 cells. Tretinoin 219-232 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 88-92
25966166-3 2015 RA distribution is tightly controlled by the RA synthetases ALDH1As and the metabolic enzymes CYP26s. Tretinoin 0-2 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 94-99
28218902-2 2017 This study provides the first evidence showing that all-trans retinoic acid (ATRA) induces the interaction and chromatin recruitment of a novel RARbeta-TET2 complex to epigenetically activate a specific cohort of gene targets, including MiR-200c. Tretinoin 52-75 tet methylcytosine dioxygenase 2 Homo sapiens 152-156
28218902-2 2017 This study provides the first evidence showing that all-trans retinoic acid (ATRA) induces the interaction and chromatin recruitment of a novel RARbeta-TET2 complex to epigenetically activate a specific cohort of gene targets, including MiR-200c. Tretinoin 52-75 microRNA 200c Homo sapiens 237-245
25750174-5 2015 This study demonstrates that gemfibrozil, an agonist of peroxisome proliferator-activated receptor (PPAR) alpha, alone and in conjunction with all-trans-retinoic acid is capable of enhancing TFEB in brain cells. Tretinoin 147-166 transcription factor EB Homo sapiens 191-195
28218902-2 2017 This study provides the first evidence showing that all-trans retinoic acid (ATRA) induces the interaction and chromatin recruitment of a novel RARbeta-TET2 complex to epigenetically activate a specific cohort of gene targets, including MiR-200c. Tretinoin 77-81 tet methylcytosine dioxygenase 2 Homo sapiens 152-156
28218902-2 2017 This study provides the first evidence showing that all-trans retinoic acid (ATRA) induces the interaction and chromatin recruitment of a novel RARbeta-TET2 complex to epigenetically activate a specific cohort of gene targets, including MiR-200c. Tretinoin 77-81 microRNA 200c Homo sapiens 237-245
26401661-4 2015 These 2 ovarian factors, together with retinoic acid (RA) action, promote feminization partially through the repression of the masculinizing activities of SOX9, FGF9 and DMRT1. Tretinoin 39-52 SRY-box transcription factor 9 Homo sapiens 155-159
28218902-4 2017 Our data reveal that pharmacological concentration of ATRA effectively downregulates PKCzeta through activation of miR-200c, leading to a decrease of the stem cell-like populations from non-tumorigenic mammary epithelial cells and non-aggressive breast cancer cells. Tretinoin 54-58 microRNA 200c Homo sapiens 115-123
28218902-5 2017 However, aggressive breast cancer cells that manifest TET2-miR-200c dysregulation sustain a CSC pool highly resistant to ATRA, where inhibition of PKCzeta directs the resistant CSCs to the luminal cell-like state and sensitization to tamoxifen, resulting in abrogation of mammary tumor growth and progression. Tretinoin 121-125 tet methylcytosine dioxygenase 2 Homo sapiens 54-58
25843047-4 2015 Switching to retinoic acid treatment at any point during this process halts colinear HOX activation and transitions the neuromesoderm into SOX2(+)/PAX6(+) neuroectoderm with predictable, discrete HOX gene/protein profiles that can be further differentiated into region-specific cells, e.g., motor neurons. Tretinoin 13-26 paired box 6 Homo sapiens 147-151
29069763-7 2017 Arg1 was also increased via RARbeta after treatment with RA. Tretinoin 28-30 arginase 1 Homo sapiens 0-4
25843049-4 2015 Furthermore, we show that the size of the NKX6-1(+) population is regulated by the duration of treatment with retinoic acid, fibroblast growth factor 10 (FGF10), and inhibitors of bone morphogenetic protein (BMP) and hedgehog signaling pathways. Tretinoin 110-123 NK6 homeobox 1 Homo sapiens 42-48
25725299-5 2015 Using real-time PCR, we then quantified the relative change in expression of cytochrome P450 26a1 (cyp26a1) - a major target gene for RA-induced RAR activation in zebrafish - and found that RA and TPP exposure resulted in a ~5-fold increase and decrease in cyp26a1 expression, respectively, relative to vehicle-exposed embryos. Tretinoin 134-136 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 77-97
25725299-5 2015 Using real-time PCR, we then quantified the relative change in expression of cytochrome P450 26a1 (cyp26a1) - a major target gene for RA-induced RAR activation in zebrafish - and found that RA and TPP exposure resulted in a ~5-fold increase and decrease in cyp26a1 expression, respectively, relative to vehicle-exposed embryos. Tretinoin 134-136 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 99-106
25419806-6 2014 RESULTS: In vitro, all-trans retinoic acid and fully oxidized beta-carotene induced cell-selective, caspase-3-dependent apoptosis in neutrophils, which subsequently enhanced efferocytosis in macrophages. Tretinoin 29-42 caspase 3 Bos taurus 100-109
28257890-8 2017 In addition, overexpression of the long form of Protrudin or the short form of Tau promotes protrusion growth of the retinoic acid-treated, neuronal-differentiated Neuro-2a cells. Tretinoin 117-130 zinc finger, FYVE domain containing 27 Mus musculus 48-57
25477235-4 2014 We found that atRA inhibited MEPM-cell proliferation by downregulating TGF-beta/Smad signaling and that TGF-beta3 treatment was able to antagonize RA signaling. Tretinoin 14-18 transforming growth factor, beta 1 Mus musculus 71-79
25477235-8 2014 Moreover, after deletion of TGIF, both the effects of atRA on TGF-beta-dependent protein expression and the effects of TGF-beta on RA-dependent protein expression were lost. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 62-70
25725299-5 2015 Using real-time PCR, we then quantified the relative change in expression of cytochrome P450 26a1 (cyp26a1) - a major target gene for RA-induced RAR activation in zebrafish - and found that RA and TPP exposure resulted in a ~5-fold increase and decrease in cyp26a1 expression, respectively, relative to vehicle-exposed embryos. Tretinoin 134-136 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 257-264
25631875-6 2015 ATRA treatment was associated with significantly increased Rb expression and decreased HER2 expression in gastric mucosa. Tretinoin 0-4 RB transcriptional corepressor 1 Homo sapiens 59-61
28238096-7 2017 Multivariate analysis showed that serum galectin-3 was an independent unfavorable factor for relapse-free survival in patients with APL treated with all-trans retinoic acid and arsenic trioxide-based frontline therapy. Tretinoin 159-172 galectin 3 Homo sapiens 40-50
25754253-0 2015 All trans retinoic acid (ATRA) mediated modulation of N-methyl D-aspartate receptor (NMDAR) and Kruppel like factor 11 (KLF11) expressions in the mitigation of ethanol induced alterations in the brain. Tretinoin 4-23 Kruppel-like factor 11 Rattus norvegicus 96-118
24689895-0 2014 Sorafenib plus all-trans retinoic acid for AML patients with FLT3-ITD and NPM1 mutations. Tretinoin 25-38 nucleophosmin 1 Homo sapiens 74-78
28363907-0 2017 Retinoic Acid Regulates Immune Responses by Promoting IL-22 and Modulating S100 Proteins in Viral Hepatitis. Tretinoin 0-13 S100 calcium binding protein A1 Mus musculus 75-79
24689895-4 2014 In addition, it is suggested that all-trans retinoic acid (ATRA) used in combination with chemotherapy has shown to improve outcome of patients harbouring NPM1 mutations. Tretinoin 34-57 nucleophosmin 1 Homo sapiens 155-159
24689895-4 2014 In addition, it is suggested that all-trans retinoic acid (ATRA) used in combination with chemotherapy has shown to improve outcome of patients harbouring NPM1 mutations. Tretinoin 59-63 nucleophosmin 1 Homo sapiens 155-159
24689895-5 2014 We report here the clinical course of three patients with refractory or relapsed FLT3-ITD(+) /NPM1(+) AML who achieved significant response upon sorafenib and ATRA combination. Tretinoin 159-163 nucleophosmin 1 Homo sapiens 94-98
25239800-11 2014 Regarding biocompatibility, we found a 76% decrease in macrophage infiltration in the intima layer (P < 0.003) in animals treated with atRA-POC membranes, with a coinciding 53% reduction in VCAM-1 staining (P < 0.001). Tretinoin 138-142 vascular cell adhesion molecule 1 Rattus norvegicus 193-199
25173565-0 2014 RARgamma-C-Fos-PPARgamma2 signaling rather than ROS generation is critical for all-trans retinoic acid-inhibited adipocyte differentiation. Tretinoin 89-102 retinoic acid receptor gamma Homo sapiens 0-8
25173565-11 2014 Inhibition of RARgamma, but not RARalpha, blocked ATRA-induced reduction of PPARgamma2 expression. Tretinoin 50-54 retinoic acid receptor gamma Homo sapiens 14-22
25173565-12 2014 ATRA induced a profound interaction between RARgamma and C-Fos protein, reflected by Co-IP results. Tretinoin 0-4 retinoic acid receptor gamma Homo sapiens 44-52
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 44-48 retinoic acid receptor gamma Homo sapiens 0-8
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 44-48 retinoic acid receptor gamma Homo sapiens 185-193
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 297-301 retinoic acid receptor gamma Homo sapiens 0-8
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 297-301 retinoic acid receptor gamma Homo sapiens 185-193
25236354-0 2014 Knockdown of lecithin retinol acyltransferase increases all-trans retinoic acid levels and restores retinoid sensitivity in malignant melanoma cells. Tretinoin 66-79 lecithin retinol acyltransferase Homo sapiens 13-45
25236354-3 2014 In this study, we show that a stable LRAT knockdown (KD) in the human melanoma cell line SkMel23 leads to significantly increased levels of the substrate ATRol and biologically active ATRA. Tretinoin 184-188 lecithin retinol acyltransferase Homo sapiens 37-41
25236354-5 2014 Furthermore, ATRA-induced gene regulatory mechanisms drive depletion of added ATRol in LRAT KD cells. Tretinoin 13-17 lecithin retinol acyltransferase Homo sapiens 87-91
25004394-7 2014 ATRA administration ameliorates DSS-induced colitis evidenced with decreased TNF level and CD68 expression, while LE135 leads to exacerbation of colitis. Tretinoin 0-4 CD68 antigen Mus musculus 91-95
25175738-7 2014 All-trans RA treatment reduced the gene expression levels of Cyp7a1, Cyp8b1, and Akr1d1, which are involved in bile acid synthesis. Tretinoin 10-12 cytochrome P450, family 8, subfamily b, polypeptide 1 Mus musculus 69-75
25175738-8 2014 All-trans RA also decreased the hepatic mRNA levels of Lrh-1 (Nr5a2) and Hnf4alpha (Nr2a1), which positively regulate the gene expression of Cyp7a1 and Cyp8b1. Tretinoin 10-12 cytochrome P450, family 8, subfamily b, polypeptide 1 Mus musculus 152-158
25175738-9 2014 Moreover, all-trans RA induced the gene expression levels of negative regulators of bile acid synthesis including hepatic Fgfr4, Fxr, and Shp (Nr0b2) as well as ileal Fgf15. Tretinoin 20-22 fibroblast growth factor receptor 4 Mus musculus 122-127
25175738-12 2014 The data suggest that all-trans RA-induced SHP may contribute to the inhibition of CYP7A1 and CYP8B1, which in turn reduces bile acid synthesis and affects lipid absorption in the gastrointestinal tract. Tretinoin 32-34 cytochrome P450, family 8, subfamily b, polypeptide 1 Mus musculus 94-100
25455157-0 2014 Down-regulation of sphingosine kinase 2 (SphK2) increases the effects of all-trans-retinoic acid (ATRA) on colon cancer cells. Tretinoin 73-96 sphingosine kinase 2 Homo sapiens 19-39
25455157-0 2014 Down-regulation of sphingosine kinase 2 (SphK2) increases the effects of all-trans-retinoic acid (ATRA) on colon cancer cells. Tretinoin 73-96 sphingosine kinase 2 Homo sapiens 41-46
25455157-0 2014 Down-regulation of sphingosine kinase 2 (SphK2) increases the effects of all-trans-retinoic acid (ATRA) on colon cancer cells. Tretinoin 98-102 sphingosine kinase 2 Homo sapiens 19-39
25455157-0 2014 Down-regulation of sphingosine kinase 2 (SphK2) increases the effects of all-trans-retinoic acid (ATRA) on colon cancer cells. Tretinoin 98-102 sphingosine kinase 2 Homo sapiens 41-46
25455157-12 2014 Down-regulation of SphK2 resulted in the reverse actions on the S1P-induced antagonistic effects on ATRA. Tretinoin 100-104 sphingosine kinase 2 Homo sapiens 19-24
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 3-23 retinoic acid receptor gamma Homo sapiens 258-286
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 3-23 retinoic acid receptor gamma Homo sapiens 288-297
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 25-29 retinoic acid receptor gamma Homo sapiens 258-286
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 25-29 retinoic acid receptor gamma Homo sapiens 288-297
24694005-3 2014 This study was performed to study the potential signal pathway of ATRA in the expression of matrix metalloproteinases-2 (MMP-2) and matrix metalloproteinases-9 (MMP-9) in injury podocyte. Tretinoin 66-70 matrix metallopeptidase 2 Homo sapiens 92-119
24694005-3 2014 This study was performed to study the potential signal pathway of ATRA in the expression of matrix metalloproteinases-2 (MMP-2) and matrix metalloproteinases-9 (MMP-9) in injury podocyte. Tretinoin 66-70 matrix metallopeptidase 2 Homo sapiens 121-126
24694005-8 2014 Enzymatic activity of MMP-2 and MMP-9 in group AA was significantly enhanced compared to AI group after ATRA-treated 24 h (p < 0.05). Tretinoin 104-108 matrix metallopeptidase 2 Homo sapiens 22-27
24694005-13 2014 In conclusion, ATRA may increase expression of MMP-2 and MMP-9 by the potential signal pathway of RAR-alpha and RAR-gamma in injury podocyte induced by adriamycin, but not RAR-beta. Tretinoin 15-19 matrix metallopeptidase 2 Homo sapiens 47-52
24694005-13 2014 In conclusion, ATRA may increase expression of MMP-2 and MMP-9 by the potential signal pathway of RAR-alpha and RAR-gamma in injury podocyte induced by adriamycin, but not RAR-beta. Tretinoin 15-19 retinoic acid receptor gamma Homo sapiens 112-121
25155613-0 2014 SIRT1-mediated deacetylation of CRABPII regulates cellular retinoic acid signaling and modulates embryonic stem cell differentiation. Tretinoin 59-72 cellular retinoic acid binding protein II Mus musculus 32-39
25155613-4 2014 We show that RA-mediated acetylation of CRABPII at K102 is essential for its nuclear accumulation and subsequent activation of RA signaling. Tretinoin 13-15 cellular retinoic acid binding protein II Mus musculus 40-47
24973045-0 2014 A RARE of hepatic Gck promoter interacts with RARalpha, HNF4alpha and COUP-TFII that affect retinoic acid- and insulin-induced Gck expression. Tretinoin 92-105 glucokinase Rattus norvegicus 18-21
24973045-0 2014 A RARE of hepatic Gck promoter interacts with RARalpha, HNF4alpha and COUP-TFII that affect retinoic acid- and insulin-induced Gck expression. Tretinoin 92-105 glucokinase Rattus norvegicus 127-130
24973045-4 2014 We hypothesized that this is mediated by a retinoic acid responsive element (RARE) in the hepatic Gck promoter. Tretinoin 43-56 glucokinase Rattus norvegicus 98-101
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 0-23 nerve growth factor Rattus norvegicus 95-98
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 25-29 nerve growth factor Rattus norvegicus 74-93
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 25-29 nerve growth factor Rattus norvegicus 95-98
24768685-9 2014 The treatment with vitamin A and ATRA reverted similarly the sensorial disturbances, which was associated with increased contents of NGF and RAR-beta expression. Tretinoin 33-37 nerve growth factor Rattus norvegicus 133-136
25099355-4 2014 atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Tretinoin 0-4 forkhead box P3 Homo sapiens 87-92
25102060-3 2014 Here we report that RA also activates transcription of Rec8, which encodes a component of the cohesin complex that accumulates during meiotic S phase, and which is essential for chromosome synapsis and segregation. Tretinoin 20-22 REC8 meiotic recombination protein Mus musculus 55-59
24953245-0 2014 Src family kinase inhibitor PP2 enhances differentiation of acute promyelocytic leukemia cell line induced by combination of all-trans-retinoic acid and arsenic trioxide. Tretinoin 125-148 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 28-31
24953245-3 2014 We demonstrated SFK (Src family kinase) inhibitor PP2-enhanced APL cell differentiation when combined with either ATRA or ATO with difference in activation of RA-induced genes. Tretinoin 114-118 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 50-53
24686085-5 2014 We observed that Lyn inhibition blocked c-Cbl and p85/p55 PI3K phosphorylation driven by the anti-CD38 agonistic mAb IB4 in ATRA-treated HL-60 cells and untreated CD38+ transfectants. Tretinoin 124-128 membrane protein, palmitoylated Mus musculus 54-57
24046068-1 2014 All-trans retinoic acid (ATRA) and Idarubicin are part of the AIDA protocol employed for the treatment of Acute promyelocytic leaukaemia (APML) and has been associated with marked improvement in the prognosis. Tretinoin 0-23 axin interactor, dorsalization associated Homo sapiens 62-66
24046068-1 2014 All-trans retinoic acid (ATRA) and Idarubicin are part of the AIDA protocol employed for the treatment of Acute promyelocytic leaukaemia (APML) and has been associated with marked improvement in the prognosis. Tretinoin 25-29 axin interactor, dorsalization associated Homo sapiens 62-66
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 SMAD family member 2 Homo sapiens 240-247
24720764-6 2014 High concentrations of RA increased the expression of RARbeta causing an inhibition of the 60% in cell migration and significantly decreased the expression of migration-related proteins [moesin, c-Src and focal adhesion kinase (FAK)]. Tretinoin 23-25 protein tyrosine kinase 2 Homo sapiens 205-226
24563337-8 2014 ATRA treated with C-PC could induce more cell cycle arrests than the single drug used by decrease in cyclin D1 and CDK4 expression. Tretinoin 0-4 cyclin D1 Homo sapiens 101-110
24563337-8 2014 ATRA treated with C-PC could induce more cell cycle arrests than the single drug used by decrease in cyclin D1 and CDK4 expression. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 115-119
24788806-8 2014 Sp1 and the RARalpha/RXRalpha complex bound to GC-rich Sp1-binding sites and an RA response element (RARE) half-site, respectively, near the TATA box in the mouse Aldh1a2 promoter. Tretinoin 12-14 retinoid X receptor alpha Mus musculus 21-29
24788806-8 2014 Sp1 and the RARalpha/RXRalpha complex bound to GC-rich Sp1-binding sites and an RA response element (RARE) half-site, respectively, near the TATA box in the mouse Aldh1a2 promoter. Tretinoin 12-14 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 163-170
24588627-5 2014 Drug-mediated induction of P450 activity or P450 mutants with increased catabolic activity may reduce cellular ATRA levels and FoxO1 expression, thus reducing FoxO-mediated mTORC1 inhibition. Tretinoin 111-115 CREB regulated transcription coactivator 1 Mus musculus 173-179
24503130-13 2014 In vivo, more CD14(+) macrophages from the intestinal mucosa of patients with CD than from controls are capable of generating RA, which might increase the inflammatory phenotype of these cells. Tretinoin 126-128 CD14 molecule Homo sapiens 14-18
24352040-8 2014 Stimulation with flagellin, EGF, and IL-1beta did not alter Spink6 expression, whereas stimulation with tumor necrosis factor-alpha (TNFalpha)/IFNgamma and all-trans retinoic acid resulted in a significant downregulation of Spink6 expression in cultured primary mouse keratinocytes. Tretinoin 166-179 serine peptidase inhibitor, Kazal type 6 Mus musculus 224-230
25151738-5 2014 The mechanism of quercetin enhancing ability of retinoic acid on the induction of RARbeta, activating TPO, using as COX-2 and PDEs inhibitor was approved by biomolecular network and related literatures. Tretinoin 48-61 thyroid peroxidase Rattus norvegicus 102-105
25151738-5 2014 The mechanism of quercetin enhancing ability of retinoic acid on the induction of RARbeta, activating TPO, using as COX-2 and PDEs inhibitor was approved by biomolecular network and related literatures. Tretinoin 48-61 cytochrome c oxidase II, mitochondrial Rattus norvegicus 116-121
24440820-5 2014 We report that the stimulation of CKalpha expression during retinoic acid (RA) induced differentiation depends on a promoter region that contains two CCAAT/Enhancer-binding Protein-beta (C/EBPbeta) sites. Tretinoin 60-73 CCAAT enhancer binding protein beta Homo sapiens 150-185
24440820-5 2014 We report that the stimulation of CKalpha expression during retinoic acid (RA) induced differentiation depends on a promoter region that contains two CCAAT/Enhancer-binding Protein-beta (C/EBPbeta) sites. Tretinoin 60-73 CCAAT enhancer binding protein beta Homo sapiens 187-196
24440820-5 2014 We report that the stimulation of CKalpha expression during retinoic acid (RA) induced differentiation depends on a promoter region that contains two CCAAT/Enhancer-binding Protein-beta (C/EBPbeta) sites. Tretinoin 75-77 CCAAT enhancer binding protein beta Homo sapiens 150-185
24440820-5 2014 We report that the stimulation of CKalpha expression during retinoic acid (RA) induced differentiation depends on a promoter region that contains two CCAAT/Enhancer-binding Protein-beta (C/EBPbeta) sites. Tretinoin 75-77 CCAAT enhancer binding protein beta Homo sapiens 187-196
24440820-6 2014 We demonstrate that during neuronal differentiation of Neuro-2a cells, RA induces Chka expression by a mechanism that involves ERK1/2 activation which triggers C/EBPbeta expression. Tretinoin 71-73 mitogen-activated protein kinase 3 Mus musculus 127-133
24525295-2 2014 In particular, RA signaling is implicated in a rostral expansion of the neural expression domain of 5 Hoxb genes (Hoxb9-Hoxb5) in mice. Tretinoin 15-17 homeobox B9 Mus musculus 115-120
24449765-1 2014 The silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is an established histone deacetylase 3 (HDAC3)-dependent transcriptional corepressor. Tretinoin 26-39 nuclear receptor corepressor 2 Homo sapiens 71-75
24449765-1 2014 The silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is an established histone deacetylase 3 (HDAC3)-dependent transcriptional corepressor. Tretinoin 26-39 histone deacetylase 3 Homo sapiens 95-116
24489122-3 2014 Our previous studies have addressed chromatin-remodeling of the Oct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochromatinization on the proximal promoter region of this gene locus. Tretinoin 83-96 nuclear receptor interacting protein 1 Homo sapiens 160-192
24489122-3 2014 Our previous studies have addressed chromatin-remodeling of the Oct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochromatinization on the proximal promoter region of this gene locus. Tretinoin 83-96 nuclear receptor interacting protein 1 Homo sapiens 194-200
24489122-3 2014 Our previous studies have addressed chromatin-remodeling of the Oct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochromatinization on the proximal promoter region of this gene locus. Tretinoin 98-100 nuclear receptor interacting protein 1 Homo sapiens 160-192
24489122-3 2014 Our previous studies have addressed chromatin-remodeling of the Oct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochromatinization on the proximal promoter region of this gene locus. Tretinoin 98-100 nuclear receptor interacting protein 1 Homo sapiens 194-200
24489122-8 2014 Further, RA induces coordinated chromatin-remodeling of both Nanog and Oct4 gene loci, which requires RA receptor-alpha, RIP140 and Brm. Tretinoin 9-11 nuclear receptor interacting protein 1 Homo sapiens 121-127
24489122-8 2014 Further, RA induces coordinated chromatin-remodeling of both Nanog and Oct4 gene loci, which requires RA receptor-alpha, RIP140 and Brm. Tretinoin 9-11 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2 Homo sapiens 132-135
24489122-9 2014 Finally, in these RA-triggered repressive chromatin-remodeling processes, lysine acetylation of RIP140 is critical for its recruiting Brm. Tretinoin 18-20 nuclear receptor interacting protein 1 Homo sapiens 96-102
24489122-9 2014 Finally, in these RA-triggered repressive chromatin-remodeling processes, lysine acetylation of RIP140 is critical for its recruiting Brm. Tretinoin 18-20 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2 Homo sapiens 134-137
24559867-2 2014 The RAR agonist: all-trans retinoic acid was reported to be an RORbeta inverse agonist, but no information is available regarding ROR activity of its synthetic analogue Am580. Tretinoin 17-40 long intergenic non-protein coding RNA, regulator of reprogramming Homo sapiens 63-66
24603328-6 2014 In vitro, Gal-3 expression and nuclear accumulation accompanied retinoic acid-induced cell differentiation in NB cell lines. Tretinoin 64-77 galectin 3 Homo sapiens 10-15
24374174-3 2014 RA dose-dependently inhibited cell proliferation and mRNA and protein levels of ECM components fibronectin, tenascin C and fibrillin-2. Tretinoin 0-2 fibrillin 2 Homo sapiens 123-134
24374174-4 2014 Zymography revealed that MMP-2 activity was suppressed by RA. Tretinoin 58-60 matrix metallopeptidase 2 Homo sapiens 25-30
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 growth arrest and DNA damage inducible alpha Homo sapiens 178-185
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 cyclin E2 Homo sapiens 187-192
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 interleukin 1 receptor type 2 Homo sapiens 239-244
24588767-7 2014 Further studies indicated that low dose all trans retinoic acid (ATRA) can induce redifferentiation and restoration of miR-1247 in pancreatic cancer cells. Tretinoin 44-63 microRNA 1247 Homo sapiens 119-127
24588767-7 2014 Further studies indicated that low dose all trans retinoic acid (ATRA) can induce redifferentiation and restoration of miR-1247 in pancreatic cancer cells. Tretinoin 65-69 microRNA 1247 Homo sapiens 119-127
24404978-8 2014 RK in the presence of ATRA also increased the levels of mRNAs of osteocalcin, alpha1(I) collagen, and TGF-betas (TGF-beta1, TGF-beta2, and TGF-beta3) compared with ATRA only. Tretinoin 22-26 transforming growth factor, beta 1 Mus musculus 113-122
24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 174-178
24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 214-218
24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 regulatory associated protein of MTOR complex 1 Homo sapiens 226-232
23131047-6 2014 RA treatment upregulated the expressions of VASA and beta1 INTEGRIN and downregulated PIWIL2 and OCT4. Tretinoin 0-2 piwi-like protein 2 Ovis aries 86-92
24253178-2 2014 The retinoic acid analogue, fenretinide (4-hydroxyphenyl retinamide; 4-HPR), induces apoptosis in neuroblastoma cells in vitro and is currently in clinical trials for children with refractory neuroblastoma. Tretinoin 4-17 haptoglobin-related protein Homo sapiens 71-74
24082012-1 2014 It is known that ATRA promotes the development of TGF-beta-induced CD4(+)Foxp3(+) iTregs, which play a vital role in the prevention of autoimmune diseases; however, the role of ATRA in facilitating the differentiation and function of CD8(+)Foxp3(+) iTregs remains elusive. Tretinoin 17-21 forkhead box P3 Homo sapiens 73-78
24082012-1 2014 It is known that ATRA promotes the development of TGF-beta-induced CD4(+)Foxp3(+) iTregs, which play a vital role in the prevention of autoimmune diseases; however, the role of ATRA in facilitating the differentiation and function of CD8(+)Foxp3(+) iTregs remains elusive. Tretinoin 17-21 forkhead box P3 Homo sapiens 240-245
24082012-2 2014 Using a head-to-head comparison, we found that ATRA promoted expression of Foxp3 and development of CD4(+) iTregs, but it did not promote Foxp3 expression on CD8(+) cells. Tretinoin 47-51 forkhead box P3 Homo sapiens 75-80
24082012-7 2014 We have identified the differential role of ATRA in promoting Foxp3(+) Tregs in CD4(+) and CD8(+) cell populations. Tretinoin 44-48 forkhead box P3 Homo sapiens 62-67
24466150-3 2014 Previous reports have suggested that CD11c(Hi) dendritic cells (DCs) of the gastrointestinal tract produce retinaldehyde dehydrogenase (ALDH1A), which metabolizes vitamin A precursors to retinoic acid to support normal mucosal immunity. Tretinoin 187-200 integrin subunit alpha X Homo sapiens 37-42
24466150-8 2014 Moreover, CD11c(Lo/neg) cells from nasal tissue (and a homogeneous respiratory tract epithelial cell line) enhanced IgA production by lipopolysaccharide (LPS)-stimulated splenocyte cultures in the presence of the retinoic acid precursor retinol. Tretinoin 213-226 integrin subunit alpha X Homo sapiens 10-15
24416428-8 2014 C646, a competitive CBP/p300 inhibitor, abolished the upregulation of Ape/Ref-1 induced by ATRA. Tretinoin 91-95 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 70-73
24416428-8 2014 C646, a competitive CBP/p300 inhibitor, abolished the upregulation of Ape/Ref-1 induced by ATRA. Tretinoin 91-95 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 74-79
24416428-10 2014 Hence, our study suggests the existence of a noncanonical mechanism involving p38-MSK-CREB cascade and CBP induction to mediate ATRA-induced Ape/Ref-1 expression and acquired chemoresistance in myeloma cells. Tretinoin 128-132 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 141-144
24416428-10 2014 Hence, our study suggests the existence of a noncanonical mechanism involving p38-MSK-CREB cascade and CBP induction to mediate ATRA-induced Ape/Ref-1 expression and acquired chemoresistance in myeloma cells. Tretinoin 128-132 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 145-150
25754253-0 2015 All trans retinoic acid (ATRA) mediated modulation of N-methyl D-aspartate receptor (NMDAR) and Kruppel like factor 11 (KLF11) expressions in the mitigation of ethanol induced alterations in the brain. Tretinoin 4-23 Kruppel-like factor 11 Rattus norvegicus 120-125
25754253-0 2015 All trans retinoic acid (ATRA) mediated modulation of N-methyl D-aspartate receptor (NMDAR) and Kruppel like factor 11 (KLF11) expressions in the mitigation of ethanol induced alterations in the brain. Tretinoin 25-29 Kruppel-like factor 11 Rattus norvegicus 96-118
25754253-0 2015 All trans retinoic acid (ATRA) mediated modulation of N-methyl D-aspartate receptor (NMDAR) and Kruppel like factor 11 (KLF11) expressions in the mitigation of ethanol induced alterations in the brain. Tretinoin 25-29 Kruppel-like factor 11 Rattus norvegicus 120-125
25754253-17 2015 CONCLUSION: Our results show that ATRA supplementation mitigates the ethanol induced alterations in the brain by reducing oxidative stress in the brain with concurrent suppression of NMDAR and KLF11 expression leading to enhanced catabolism of neurotransmitters. Tretinoin 34-38 Kruppel-like factor 11 Rattus norvegicus 193-198
25878769-0 2015 Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPbeta. Tretinoin 0-13 CCAAT enhancer binding protein beta Homo sapiens 109-118
25027601-2 2015 RA primes dendritic cells (DCs) to express CD103 and produce RA themselves, which induces the gut-homing receptors alpha4beta7 and CCR9 on T cells and amplifies transforming growth factor (TGF)-beta-mediated development of Foxp3(+) regulatory T (Treg) cells. Tretinoin 0-2 C-C motif chemokine receptor 9 Homo sapiens 131-135
25027601-2 2015 RA primes dendritic cells (DCs) to express CD103 and produce RA themselves, which induces the gut-homing receptors alpha4beta7 and CCR9 on T cells and amplifies transforming growth factor (TGF)-beta-mediated development of Foxp3(+) regulatory T (Treg) cells. Tretinoin 0-2 forkhead box P3 Homo sapiens 223-228
25027601-4 2015 We report a novel role of RA in immune regulation by showing that RA-conditioned human DCs did not substantially enhance Foxp3 but induced alpha4beta7(+) CCR9(+) T cells expressing high levels of interleukin (IL)-10, which were functional suppressive Treg cells. Tretinoin 26-28 C-C motif chemokine receptor 9 Homo sapiens 154-158
25027601-7 2015 Experiments with naive CD4(+) T cells stimulated by anti-CD3 and anti-CD28 antibodies in the absence of DCs emphasized that RA induces IL-10 in face of inflammatory mediators. Tretinoin 124-126 CD28 molecule Homo sapiens 70-74
25381698-2 2015 Retinoic acid (RA), a natural metabolite of vitamin A, has been reported to enhance the differentiation of Treg cells in the presence of TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 137-145
25381698-2 2015 Retinoic acid (RA), a natural metabolite of vitamin A, has been reported to enhance the differentiation of Treg cells in the presence of TGF-beta. Tretinoin 15-17 transforming growth factor, beta 1 Mus musculus 137-145
25673193-1 2015 The purpose of this study was to observe the expression of LINGO-1 after cerebral ischemia, investigate the effects of retinoic acid (RA) on the expression of LINGO-1 and GAP-43, and the number of synapses, and to emplore the repressive effect of LINGO-1 on neural regeneration after cerebral ischemia. Tretinoin 134-136 growth associated protein 43 Rattus norvegicus 171-177
25673193-7 2015 The number of Gap-43-positive nerve cells at 7th day after MCAO in sham, CI and RA group was 0, 59.08 +- 1.76 and 76.20 +- 3.12 per high power field, respectively (P<0.05). Tretinoin 80-82 growth associated protein 43 Rattus norvegicus 14-20
25532484-13 2015 Amplified activation of caspase 3/7 was in favor of apoptosis in ATRA treated peripheral nerve fibroblasts. Tretinoin 65-69 caspase 3 Rattus norvegicus 24-33
26451280-4 2015 In addition, retinoic acid inhibited Klf4 and Klf5 expression but not that of Cebpb. Tretinoin 13-26 Kruppel-like factor 5 Mus musculus 46-50
25455455-5 2015 Heat shock protein 27, ribonucleoprotein SmD3, and cofilin-1 were significantly upregulated after treatment with combination of individual retinoic acid isomers. Tretinoin 139-152 small nuclear ribonucleoprotein D3 polypeptide Homo sapiens 41-45
25455455-5 2015 Heat shock protein 27, ribonucleoprotein SmD3, and cofilin-1 were significantly upregulated after treatment with combination of individual retinoic acid isomers. Tretinoin 139-152 cofilin 1 Homo sapiens 51-60
25482166-0 2015 Transcriptional regulation of Tal2 gene by all-trans retinoic acid (atRA) in P19 cells. Tretinoin 53-66 T cell acute lymphocytic leukemia 2 Mus musculus 30-34
25482166-0 2015 Transcriptional regulation of Tal2 gene by all-trans retinoic acid (atRA) in P19 cells. Tretinoin 68-72 T cell acute lymphocytic leukemia 2 Mus musculus 30-34
25482166-2 2015 In a previous study, we demonstrated that the expression of Tal2 gene is induced by the complex of all-trans retinoic acid (atRA) and retinoic acid receptor alpha (RARalpha) in mouse embryonal carcinoma P19 cells. Tretinoin 109-122 T cell acute lymphocytic leukemia 2 Mus musculus 60-64
25482166-2 2015 In a previous study, we demonstrated that the expression of Tal2 gene is induced by the complex of all-trans retinoic acid (atRA) and retinoic acid receptor alpha (RARalpha) in mouse embryonal carcinoma P19 cells. Tretinoin 124-128 T cell acute lymphocytic leukemia 2 Mus musculus 60-64
26500786-6 2015 Thus, we report NRG1 and KITL activate alternative pathways downstream of retinoic acid signaling in the germline that are essential for stem cells to undergo pre-meiotic steps of spermatogenesis in culture. Tretinoin 74-87 neuregulin 1 Homo sapiens 16-20
25537091-5 2015 We have found that cyp26b1, which will catalyze RA, increases dramatically in p19 cells 1 d after RA treatment. Tretinoin 48-50 cytochrome P450 26B1 Bos taurus 19-26
25537091-5 2015 We have found that cyp26b1, which will catalyze RA, increases dramatically in p19 cells 1 d after RA treatment. Tretinoin 98-100 cytochrome P450 26B1 Bos taurus 19-26
25944986-3 2015 Unstimulated Caco2 and HT-29 cells secreted CCL19, CCL21, and CCL22 chemokines, which could attract dendritic cells and macrophages and induced CCR7 receptor up-regulation by retinoic-acid resulting in dendritic cell migration. Tretinoin 175-188 C-C motif chemokine ligand 19 Homo sapiens 44-49
25944986-3 2015 Unstimulated Caco2 and HT-29 cells secreted CCL19, CCL21, and CCL22 chemokines, which could attract dendritic cells and macrophages and induced CCR7 receptor up-regulation by retinoic-acid resulting in dendritic cell migration. Tretinoin 175-188 C-C motif chemokine ligand 21 Homo sapiens 51-56
25944986-3 2015 Unstimulated Caco2 and HT-29 cells secreted CCL19, CCL21, and CCL22 chemokines, which could attract dendritic cells and macrophages and induced CCR7 receptor up-regulation by retinoic-acid resulting in dendritic cell migration. Tretinoin 175-188 C-C motif chemokine ligand 22 Homo sapiens 62-67
25473832-6 2014 RA signalling has opposite roles: it promotes sensory fates, and restricts otx1b expression and the development of non-neural fates. Tretinoin 0-2 orthodenticle homeobox 1 Danio rerio 75-80
25331756-0 2014 The effect of RA on the chick Ebf1-3 genes expression in somites and pharyngeal arches. Tretinoin 14-16 EBF transcription factor 1 Gallus gallus 30-34
25351459-10 2014 Both flow cytometric and antibody-mediated neutralization studies showed that liver NKT cells up-regulate the natural killer group 2, member D (NKG2D) ligand and bind with the NKG2D ligand, retinoic acid early inducible 1 (Rae1), and positively activated HSCs to ameliorate liver fibrosis. Tretinoin 190-203 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 176-181
24506204-2 2014 In the present study, we investigated the potential role of xanthine dehydrogenase (XDH) in retinoic acid biosynthesis in human thyroid glandular cells (HTGC). Tretinoin 92-105 xanthine dehydrogenase Homo sapiens 60-82
24506204-2 2014 In the present study, we investigated the potential role of xanthine dehydrogenase (XDH) in retinoic acid biosynthesis in human thyroid glandular cells (HTGC). Tretinoin 92-105 xanthine dehydrogenase Homo sapiens 84-87
24506204-4 2014 After partial protein purification, the enzyme responsible for retinoic acid biosynthesis was identified and quantified as XDH by immunoassay, by its ability to oxidize xanthine to uric acid and its sensitivity to the inhibitory effect of oxypurinol. Tretinoin 63-76 xanthine dehydrogenase Homo sapiens 123-126
24506204-5 2014 The evidence of XDH-driven formation of retinoic acid in HTGC cultures further corroborates the potential role of XDH in retinoic acid biosynthesis in the epithelia. Tretinoin 40-53 xanthine dehydrogenase Homo sapiens 16-19
24506204-5 2014 The evidence of XDH-driven formation of retinoic acid in HTGC cultures further corroborates the potential role of XDH in retinoic acid biosynthesis in the epithelia. Tretinoin 40-53 xanthine dehydrogenase Homo sapiens 114-117
24506204-5 2014 The evidence of XDH-driven formation of retinoic acid in HTGC cultures further corroborates the potential role of XDH in retinoic acid biosynthesis in the epithelia. Tretinoin 121-134 xanthine dehydrogenase Homo sapiens 16-19
24506204-5 2014 The evidence of XDH-driven formation of retinoic acid in HTGC cultures further corroborates the potential role of XDH in retinoic acid biosynthesis in the epithelia. Tretinoin 121-134 xanthine dehydrogenase Homo sapiens 114-117
25330951-19 2014 CONCLUSION: Increased Lep and Lep-R expression after prenatal administration of ATRA in nitrofen-induced PH suggests that ATRA may have therapeutic potential in attenuating CDH-associated PH by stimulating alveolarization and de novo surfactant production. Tretinoin 122-126 leptin Rattus norvegicus 22-25
25423083-4 2014 Our data indicated that in NTD samples from both human fetuses and retinoic acid (RA)-treated mouse fetuses, the expression level of IGF2/Igf2 was upregulated 6.41-fold and 1.84-fold, respectively, compared to controls. Tretinoin 67-80 fuzzy planar cell polarity protein Homo sapiens 27-30
25423083-4 2014 Our data indicated that in NTD samples from both human fetuses and retinoic acid (RA)-treated mouse fetuses, the expression level of IGF2/Igf2 was upregulated 6.41-fold and 1.84-fold, respectively, compared to controls. Tretinoin 82-84 fuzzy planar cell polarity protein Homo sapiens 27-30
25423083-8 2014 In detail, the upregulation of IGF2/Igf2 is likely controlled by hypermethylation of H19 DMR1 in human NTDs, however, in acute external RA-induced NTD mice it is potentially determined by more open chromatin structure. Tretinoin 136-138 fuzzy planar cell polarity protein Homo sapiens 103-106
24728721-0 2014 In vitro all-trans retinoic acid sensitivity of acute myeloid leukemia blasts with NUP98/RARG fusion gene. Tretinoin 19-32 nucleoporin 98 and 96 precursor Homo sapiens 83-88
24728721-0 2014 In vitro all-trans retinoic acid sensitivity of acute myeloid leukemia blasts with NUP98/RARG fusion gene. Tretinoin 19-32 retinoic acid receptor gamma Homo sapiens 89-93
25161098-0 2014 SPLUNC1 is associated with nasopharyngeal carcinoma prognosis and plays an important role in all-trans-retinoic acid-induced growth inhibition and differentiation in nasopharyngeal cancer cells. Tretinoin 103-116 BPI fold containing family A member 1 Homo sapiens 0-7
25161098-6 2014 A cDNA micro-array analyzed by significant analysis of micro-array (SAM) and ingenuity pathway analysis (IPA) revealed that an indirect interaction existed between SPLUNC1 and retinoic acid (RA) in the cancer regulatory network. Tretinoin 176-189 BPI fold containing family A member 1 Homo sapiens 164-171
25161098-6 2014 A cDNA micro-array analyzed by significant analysis of micro-array (SAM) and ingenuity pathway analysis (IPA) revealed that an indirect interaction existed between SPLUNC1 and retinoic acid (RA) in the cancer regulatory network. Tretinoin 191-193 BPI fold containing family A member 1 Homo sapiens 164-171
25161098-8 2014 The transcriptional activity of the SPLUNC1 promoter was up-regulated significantly by all-trans-retinoic acid (ATRA). Tretinoin 87-110 BPI fold containing family A member 1 Homo sapiens 36-43
25161098-8 2014 The transcriptional activity of the SPLUNC1 promoter was up-regulated significantly by all-trans-retinoic acid (ATRA). Tretinoin 112-116 BPI fold containing family A member 1 Homo sapiens 36-43
25161098-12 2014 Under SPLUNC1 knockdown conditions, differentiation was reversed by ATRA treatment. Tretinoin 68-72 BPI fold containing family A member 1 Homo sapiens 6-13
25164008-5 2014 The breast cancer cell differentiation-inducing agent, all-trans retinoic acid, restored the miR20a-MICA/MICB axis and sensitized BCSC to NK cell-mediated killing, thereby reducing immune escape-associated BCSC metastasis. Tretinoin 65-78 MHC class I polypeptide-related sequence A Homo sapiens 100-104
25164008-5 2014 The breast cancer cell differentiation-inducing agent, all-trans retinoic acid, restored the miR20a-MICA/MICB axis and sensitized BCSC to NK cell-mediated killing, thereby reducing immune escape-associated BCSC metastasis. Tretinoin 65-78 MHC class I polypeptide-related sequence B Homo sapiens 105-109
25239423-6 2014 CD11b and CD11c were negative in all untreated APLs but positive in 76% and 88% of ATRA-treated APLs, respectively. Tretinoin 83-87 integrin subunit alpha X Homo sapiens 10-15
24694005-0 2014 Potential signal pathway of all-trans retinoic acid for MMP-2 and MMP-9 expression in injury podocyte induced by adriamycin. Tretinoin 38-51 matrix metallopeptidase 2 Homo sapiens 56-61
25268355-5 2014 All-trans retinoic acid in vitro induced IL-10 in CD4(+)CD25(high)Foxp3(+) T cells; IL-10 and TGF-beta production in CD4(+)CD25-Foxp3- T cells, and IL-10 in monocytes isolated from healthy children. Tretinoin 10-23 forkhead box P3 Homo sapiens 66-71
25218146-7 2014 To our surprise, the functions of RXRalpha were significantly blocked only in T compared with Wt and P. Namely, the total protein levels of RXRalpha were significantly reduced and the phosphorylation levels of RXRalpha were significantly increased only in T compared with Wt and P. Treatment of H-ras12V transgenic mice at 5-week-old or 5-month-old with atRA had no effect on the prevention of tumorigenesis or cure of developed nodules in liver. Tretinoin 354-358 retinoid X receptor alpha Mus musculus 34-42
24800887-1 2014 Aldo-keto reductase 1B10 (AKR1B10) is an oncogenic carbonyl reductase that eliminates alpha,beta-unsaturated carbonyl compounds/lipid peroxides and mediates retinoic acid signaling. Tretinoin 157-170 aldo-keto reductase family 1 member B10 Homo sapiens 0-24
24800887-1 2014 Aldo-keto reductase 1B10 (AKR1B10) is an oncogenic carbonyl reductase that eliminates alpha,beta-unsaturated carbonyl compounds/lipid peroxides and mediates retinoic acid signaling. Tretinoin 157-170 aldo-keto reductase family 1 member B10 Homo sapiens 26-33
24030488-4 2014 We then performed competitive bone marrow (BM) reconstitution experiments to assess the requirement of alpha4beta7 in the generation of intestinal retinoic acid (RA)-producing CD11c(hi) DC (ALDE(+)DC) and CD64 macrophages. Tretinoin 147-160 integrin alpha X Mus musculus 176-181
24030488-4 2014 We then performed competitive bone marrow (BM) reconstitution experiments to assess the requirement of alpha4beta7 in the generation of intestinal retinoic acid (RA)-producing CD11c(hi) DC (ALDE(+)DC) and CD64 macrophages. Tretinoin 162-164 integrin alpha X Mus musculus 176-181
25031298-0 2014 Effect of all-trans retinoic acid treatment on prohibitin and renin-angiotensin-aldosterone system expression in hypoxia-induced renal tubular epithelial cell injury. Tretinoin 20-33 prohibitin 1 Homo sapiens 47-57
25031298-11 2014 CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. Tretinoin 37-41 prohibitin 1 Homo sapiens 74-78
25031298-11 2014 CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. Tretinoin 37-41 angiotensin converting enzyme 2 Homo sapiens 89-93
24768685-1 2014 All-trans retinoic acid (ATRA) promotes the endogenous expression of both nerve growth factor (NGF) and retinoic acid receptor beta (RAR-beta). Tretinoin 0-23 nerve growth factor Rattus norvegicus 74-93
25200157-0 2014 [Over-expression of prohibitin gene promotes apoptosis in retinoic acid-resistant acute promyelocytic leukemia cell line NB4-R1]. Tretinoin 58-71 prohibitin 1 Homo sapiens 20-30
25200157-1 2014 OBJECTIVE: To construct a eukaryotic expression vector carrying human prohibitin gene and study the effect of prohibitin over-expression on the apoptosis of retinoic acid-resistant acute promyelocytic leukemia NB4-R1 cells. Tretinoin 157-170 prohibitin 1 Homo sapiens 110-120
25099355-7 2014 atRA also increases histone acetylation on Foxp3 gene promoter and CpG demethylation in the region of Foxp3 locus (i.e., Treg-specific demethylated region). Tretinoin 0-4 forkhead box P3 Homo sapiens 43-48
25099355-7 2014 atRA also increases histone acetylation on Foxp3 gene promoter and CpG demethylation in the region of Foxp3 locus (i.e., Treg-specific demethylated region). Tretinoin 0-4 forkhead box P3 Homo sapiens 102-107
25065743-7 2014 In addition, we found that ASXL2 and WTIP are expressed in mouse embryonic epicardial cells, a tissue that is regulated by retinoic acid signaling. Tretinoin 123-136 WT1 interacting protein Mus musculus 37-41
24648413-7 2014 RA increases the expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, Fzd2 and Fzd6), downstream signaling, and Tcf3 expression. Tretinoin 0-2 transcription factor 3 Homo sapiens 140-144
24648413-9 2014 We show that RA signaling increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Tretinoin 13-15 transcription factor 3 Homo sapiens 84-88
24648413-9 2014 We show that RA signaling increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Tretinoin 13-15 Zic family member 5 Homo sapiens 187-191
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 78-80 transcription factor 3 Homo sapiens 13-17
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 78-80 Zic family member 5 Homo sapiens 114-118
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 78-80 Zic family member 5 Homo sapiens 174-178
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 136-138 transcription factor 3 Homo sapiens 13-17
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 136-138 Zic family member 5 Homo sapiens 114-118
24648413-10 2014 Knockdown of Tcf3 increases Lrh-1 transcript levels in mESCs and prevents the RA-associated, fourfold increase in Zic5, indicating that RA requires Tcf3 to effect changes in Zic5 levels. Tretinoin 136-138 Zic family member 5 Homo sapiens 174-178
24648413-11 2014 We demonstrate a novel role for RA in altering the activation of these two Wnt signaling pathways and show that Tcf3 mediates some actions of RA during differentiation. Tretinoin 142-144 transcription factor 3 Homo sapiens 112-116
25072246-5 2014 Since G1 arrest is a hallmark of ATRA-induced NB4 cell differentiation, we observed a decrease in G1 accumulation, as well as decreases in p21WAF1/CIP1 and cyclin D1 inductions, by ATRA in NB4MTOE cells. Tretinoin 33-37 cyclin D1 Homo sapiens 156-165
25072246-5 2014 Since G1 arrest is a hallmark of ATRA-induced NB4 cell differentiation, we observed a decrease in G1 accumulation, as well as decreases in p21WAF1/CIP1 and cyclin D1 inductions, by ATRA in NB4MTOE cells. Tretinoin 181-185 cyclin D1 Homo sapiens 156-165
24833708-3 2014 The current study examines the hepatic binding profile of two RA receptor isoforms, RARA (RARalpha) and RARB (RARbeta), in response to RA treatment in mouse livers. Tretinoin 62-64 retinoic acid receptor, beta Mus musculus 104-108
24833708-3 2014 The current study examines the hepatic binding profile of two RA receptor isoforms, RARA (RARalpha) and RARB (RARbeta), in response to RA treatment in mouse livers. Tretinoin 62-64 retinoic acid receptor, beta Mus musculus 110-117
24833708-7 2014 RA treatment generated 18,821 novel RARB bindings but only 14,798 of RARA bindings, compared with the control group. Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 36-40
24448753-6 2014 In 72 h under treatment with 10 mumol/L all-trans retinoic acid (ATRA), in OV-CDK5 Group, processes of the GFP-positive cells were reduced slightly and little GFP-positive debris was found. Tretinoin 40-63 cyclin-dependent kinase 5 Rattus norvegicus 78-82
24448753-6 2014 In 72 h under treatment with 10 mumol/L all-trans retinoic acid (ATRA), in OV-CDK5 Group, processes of the GFP-positive cells were reduced slightly and little GFP-positive debris was found. Tretinoin 65-69 cyclin-dependent kinase 5 Rattus norvegicus 78-82
24448753-10 2014 Furthermore, CDK5 might antagonize ATRA-induced inhibition against proliferation and differentiation in differentiated neurocytes. Tretinoin 35-39 cyclin-dependent kinase 5 Rattus norvegicus 13-17
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 26-28 vav guanine nucleotide exchange factor 1 Homo sapiens 218-222
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 26-28 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 245-250
24646031-3 2014 In many cases, downregulation of CDK activity by ATRA and vitamin D3 is a result of elevated p21- and p27-bound CDKs. Tretinoin 49-53 cyclin dependent kinase 2 Homo sapiens 112-116
24646031-6 2014 ATRA and vitamin D3 can also downregulate expression of G1 CDKs, especially CDK2 and CDK6. Tretinoin 0-4 cyclin dependent kinase 2 Homo sapiens 59-63
24646031-6 2014 ATRA and vitamin D3 can also downregulate expression of G1 CDKs, especially CDK2 and CDK6. Tretinoin 0-4 cyclin dependent kinase 2 Homo sapiens 76-80
24646031-8 2014 In vitro, not only dephosphorylation of pRb but also elevation of total pRb is required for ATRA and vitamin D3 to suppress growth and trigger their differentiation. Tretinoin 92-96 RB transcriptional corepressor 1 Homo sapiens 40-43
24646031-8 2014 In vitro, not only dephosphorylation of pRb but also elevation of total pRb is required for ATRA and vitamin D3 to suppress growth and trigger their differentiation. Tretinoin 92-96 RB transcriptional corepressor 1 Homo sapiens 72-75
24646031-9 2014 Finally, sharp reduction in c-Myc has been observed in several leukaemia cell lines treated with ATRA, which may regulate expression of CDKs and CKIs. Tretinoin 97-101 cyclin dependent kinase 2 Homo sapiens 136-140
24720764-6 2014 High concentrations of RA increased the expression of RARbeta causing an inhibition of the 60% in cell migration and significantly decreased the expression of migration-related proteins [moesin, c-Src and focal adhesion kinase (FAK)]. Tretinoin 23-25 protein tyrosine kinase 2 Homo sapiens 228-231
24790153-0 2014 All-trans retinoic acid induces arginase-1 and inducible nitric oxide synthase-producing dendritic cells with T cell inhibitory function. Tretinoin 10-23 arginase, liver Mus musculus 32-78
24790153-4 2014 Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Tretinoin 60-64 arginase, liver Mus musculus 0-10
24790153-4 2014 Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Tretinoin 60-64 arginase, liver Mus musculus 12-17
24790153-4 2014 Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Tretinoin 60-64 arginase, liver Mus musculus 89-94
24790153-4 2014 Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Tretinoin 60-64 arginase, liver Mus musculus 89-94
24790153-4 2014 Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Tretinoin 60-64 arginase, liver Mus musculus 89-94
24888826-8 2014 RESULTS: Relative mRNA expression of pulmonary ADRP was significantly increased in Nitrofen+ATRA compared to Nitrofen+Placebo (0.31+-0.02 vs. 0.08+-0.01; P<0.0001). Tretinoin 92-96 perilipin 2 Rattus norvegicus 47-51
24888826-9 2014 ADRP immunoreactivity and oil-red-O-staining were markedly increased in alveolar interstitium of Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 106-110 perilipin 2 Rattus norvegicus 0-4
24038081-6 2014 The Hes6 promoter is specifically activated by the retinoic acid receptor (RAR) in response to its natural agonist ligand, all-trans retinoic acid (atRA), and is repressed by SHP. Tretinoin 123-146 hairy and enhancer of split 6 Mus musculus 4-8
24038081-6 2014 The Hes6 promoter is specifically activated by the retinoic acid receptor (RAR) in response to its natural agonist ligand, all-trans retinoic acid (atRA), and is repressed by SHP. Tretinoin 148-152 hairy and enhancer of split 6 Mus musculus 4-8
24583076-1 2014 BACKGROUND: P19 mouse embryonic carcinoma cells are conventionally induced to differentiate into neural cells by suspension culture in the presence of retinoic acid to form cell aggregates, followed by adhesion culture in a poly-l-lysine-coated dish. Tretinoin 151-164 interleukin 23, alpha subunit p19 Mus musculus 12-15
24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 cyclin D1 Homo sapiens 68-77
24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 103-108
24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 cyclin dependent kinase 2 Homo sapiens 121-125
24361577-5 2014 Tryptophan fluorescence titration reveals that NLaz(L130R) loses its ability to bind ergosterol and the pheromone 7(z)-tricosene but retains retinoic acid binding. Tretinoin 141-154 Neural Lazarillo Drosophila melanogaster 47-51
24440757-0 2014 All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity. Tretinoin 0-23 cathepsin C Homo sapiens 69-73
24440757-0 2014 All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity. Tretinoin 25-29 cathepsin C Homo sapiens 69-73
24440757-12 2014 All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model. Tretinoin 0-23 microRNA 23a Mus musculus 46-53
24440757-12 2014 All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model. Tretinoin 0-23 cathepsin C Mus musculus 76-80
24440757-12 2014 All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model. Tretinoin 0-23 granzyme B Mus musculus 96-106
24440757-12 2014 All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model. Tretinoin 25-29 microRNA 23a Mus musculus 46-53
24440757-12 2014 All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model. Tretinoin 25-29 cathepsin C Mus musculus 76-80
24440757-12 2014 All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model. Tretinoin 25-29 granzyme B Mus musculus 96-106
24449765-1 2014 The silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is an established histone deacetylase 3 (HDAC3)-dependent transcriptional corepressor. Tretinoin 26-39 histone deacetylase 3 Homo sapiens 118-123
24584857-4 2014 In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 96-109 Kruppel like factor 5 Homo sapiens 60-64
24584857-4 2014 In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 111-115 Kruppel like factor 5 Homo sapiens 60-64
24237035-3 2014 All-trans retinoic acid (ATRA) up-regulates expression of alpha4beta7 integrin and CCR9 on lymphocytes in laboratory animals, increasing their gut tropism. Tretinoin 0-23 C-C motif chemokine receptor 9 Homo sapiens 83-87
24237035-3 2014 All-trans retinoic acid (ATRA) up-regulates expression of alpha4beta7 integrin and CCR9 on lymphocytes in laboratory animals, increasing their gut tropism. Tretinoin 25-29 C-C motif chemokine receptor 9 Homo sapiens 83-87
24431331-13 2014 CONCLUSIONS: We conclude that the NAA10 mutation is the cause of LMS in this family, likely through the dysregulation of the retinoic acid signalling pathway. Tretinoin 125-138 N-alpha-acetyltransferase 10, NatA catalytic subunit Homo sapiens 34-39
24548459-8 2014 We found that day 7 MCs differentiated in the presence of RA had an increase in the percent positive and relative expression levels of both maturation (CD80, CD86, and MHCII) and inhibitory (PD-L1 and PD-L2) markers compared to control cells. Tretinoin 58-60 CD80 molecule Homo sapiens 152-156
24548459-8 2014 We found that day 7 MCs differentiated in the presence of RA had an increase in the percent positive and relative expression levels of both maturation (CD80, CD86, and MHCII) and inhibitory (PD-L1 and PD-L2) markers compared to control cells. Tretinoin 58-60 CD86 molecule Homo sapiens 158-162
24548459-10 2014 CONCLUSION: RA induced mature regulatory myeloid cells that were suppressive and had a CD11b+ CD11c-Ly6C low/intermediate monocyte phenotype. Tretinoin 12-14 integrin subunit alpha X Homo sapiens 94-99
25132258-3 2014 Retinoic acid (RA) has been reported to suppress adrenocorticotropic hormone (ACTH) secretion in Cushing"s disease. Tretinoin 0-13 pro-opiomelanocortin-alpha Mus musculus 49-76
25132258-3 2014 Retinoic acid (RA) has been reported to suppress adrenocorticotropic hormone (ACTH) secretion in Cushing"s disease. Tretinoin 0-13 pro-opiomelanocortin-alpha Mus musculus 78-82
25132258-3 2014 Retinoic acid (RA) has been reported to suppress adrenocorticotropic hormone (ACTH) secretion in Cushing"s disease. Tretinoin 15-17 pro-opiomelanocortin-alpha Mus musculus 49-76
25132258-3 2014 Retinoic acid (RA) has been reported to suppress adrenocorticotropic hormone (ACTH) secretion in Cushing"s disease. Tretinoin 15-17 pro-opiomelanocortin-alpha Mus musculus 78-82
24310731-6 2014 However, atRA induced MMP-9 production was via RARalpha activation and retinol and beta-carotene caused MMP-9 production via RARalpha and beta activation. Tretinoin 9-13 matrix metallopeptidase 9 Mus musculus 22-27
24310731-7 2014 These were supported by the observations that the RARalpha and beta agonists/antagonists differentially affected MMP-9 production and that atRA and beta-carotene enhanced RARE-mediated and MMP-9 promoter luciferase activity. Tretinoin 139-143 matrix metallopeptidase 9 Mus musculus 189-194
24310731-8 2014 In parallel, while the MMP-9 induction by atRA was not affected by the MAPKs inhibitors, its induction by retinol and beta-carotene was repressed by the inhibitor targeting ERK1/2. Tretinoin 42-46 matrix metallopeptidase 9 Mus musculus 23-28
24310731-10 2014 Taken together, we provide evidence here for the first time that atRA, retinol, and beta-carotene differentially regulate GM-CSF, IL-16, and MMP-9 production in macrophages, explaining at least in part why these vitamin A-related substances are beneficial for immunity. Tretinoin 65-69 matrix metallopeptidase 9 Mus musculus 141-146
24285836-5 2014 We found that F4/80(+)Ly6C(-)Ly6G(-) mature macrophages (Ms) were up to 30-fold more potent immune suppressors than Gr1(+) cells on a per-cell basis, which we postulate may contribute to the increased metastatic growth observed with ATRA treatment. Tretinoin 233-237 lymphocyte antigen 6 complex, locus G Mus musculus 29-33
24144795-1 2014 CYP2C22 was recently described as a retinoic acid-metabolizing cytochrome P450 enzyme whose transcription is induced by all-trans-retinoic acid (atRA) in hepatoma cells (Qian L, Zolfaghari R, and Ross AC (2010) J Lipid Res 51:1781-1792). Tretinoin 36-49 cytochrome P450, family 2, subfamily c, polypeptide 22 Rattus norvegicus 0-7
24144795-1 2014 CYP2C22 was recently described as a retinoic acid-metabolizing cytochrome P450 enzyme whose transcription is induced by all-trans-retinoic acid (atRA) in hepatoma cells (Qian L, Zolfaghari R, and Ross AC (2010) J Lipid Res 51:1781-1792). Tretinoin 120-143 cytochrome P450, family 2, subfamily c, polypeptide 22 Rattus norvegicus 0-7
24144795-1 2014 CYP2C22 was recently described as a retinoic acid-metabolizing cytochrome P450 enzyme whose transcription is induced by all-trans-retinoic acid (atRA) in hepatoma cells (Qian L, Zolfaghari R, and Ross AC (2010) J Lipid Res 51:1781-1792). Tretinoin 145-149 cytochrome P450, family 2, subfamily c, polypeptide 22 Rattus norvegicus 0-7
24570662-11 2014 Interestingly, RA treatment induces a modulation of RA receptors RARalpha and RARbeta expression in middle-aged mice, a finding which has been correlated with the amplitude of intrahippocampal CORT levels after novelty-induced stress. Tretinoin 15-17 retinoic acid receptor, beta Mus musculus 78-85
24503540-5 2014 We found that ASCs cultured with ATRA or transfected with miRNA let-7e expressed epithelial markers such as cytokeratin-18 and early renal organogenesis markers such as Pax2, Wt1, Wnt4 and megalin. Tretinoin 33-37 LDL receptor related protein 2 Homo sapiens 189-196
25227295-3 2014 The vitamin A (VA) metabolite all-trans retinoic acid (RA) signaling via RA nuclear receptors plays a key role in immune homeostasis in the small bowel, and recent work indicates that RA is required for establishing immune tolerance to dietary antigens in the upper intestinal tract by inducing alpha4beta7(+)CCR9(+) gut-tropic TREG. Tretinoin 40-53 C-C motif chemokine receptor 9 Homo sapiens 309-313
25227295-3 2014 The vitamin A (VA) metabolite all-trans retinoic acid (RA) signaling via RA nuclear receptors plays a key role in immune homeostasis in the small bowel, and recent work indicates that RA is required for establishing immune tolerance to dietary antigens in the upper intestinal tract by inducing alpha4beta7(+)CCR9(+) gut-tropic TREG. Tretinoin 55-57 C-C motif chemokine receptor 9 Homo sapiens 309-313
25140197-3 2014 Addition of subtoxic concentration of all-trans-retinoic acid (ATRA) increases the efficiency of DAC + SAHA combination on viability, apoptosis induction, and ROS generation in HL-60 cells but has no effect in CML-T1 cell line. Tretinoin 38-61 arylacetamide deacetylase Homo sapiens 97-100
25140197-3 2014 Addition of subtoxic concentration of all-trans-retinoic acid (ATRA) increases the efficiency of DAC + SAHA combination on viability, apoptosis induction, and ROS generation in HL-60 cells but has no effect in CML-T1 cell line. Tretinoin 63-67 arylacetamide deacetylase Homo sapiens 97-100
24824789-4 2014 Resistance to ATRA-induced cell cycle arrest at the G1/S phase transition in knockdown cells was accompanied by retained expression of ITGA4 (CD49d) and decreased induction of ITGAX (CD11c). Tretinoin 14-18 integrin subunit alpha X Homo sapiens 176-181
24824789-4 2014 Resistance to ATRA-induced cell cycle arrest at the G1/S phase transition in knockdown cells was accompanied by retained expression of ITGA4 (CD49d) and decreased induction of ITGAX (CD11c). Tretinoin 14-18 integrin subunit alpha X Homo sapiens 183-188
24824789-6 2014 Furthermore, ITGAX was among a small number of genes showing perturbation in transcript levels upon HOTAIRM1 knockdown even without ATRA treatment, suggesting a direct pathway of regulation. Tretinoin 132-136 integrin subunit alpha X Homo sapiens 13-18
24161943-1 2013 Neuron navigator 2 (NAV2) is required for all-trans retinoic acid (atRA) to induce neurite outgrowth in human neuroblastoma cells. Tretinoin 42-65 neuron navigator 2 Homo sapiens 0-18
24161943-1 2013 Neuron navigator 2 (NAV2) is required for all-trans retinoic acid (atRA) to induce neurite outgrowth in human neuroblastoma cells. Tretinoin 42-65 neuron navigator 2 Homo sapiens 20-24
24161943-1 2013 Neuron navigator 2 (NAV2) is required for all-trans retinoic acid (atRA) to induce neurite outgrowth in human neuroblastoma cells. Tretinoin 67-71 neuron navigator 2 Homo sapiens 0-18
24161943-1 2013 Neuron navigator 2 (NAV2) is required for all-trans retinoic acid (atRA) to induce neurite outgrowth in human neuroblastoma cells. Tretinoin 67-71 neuron navigator 2 Homo sapiens 20-24
24085323-11 2013 Actinomycin-D, cyclohexamide, retinoic acid, and dexamethasone inhibited MMP-2 and -9 in chondrosarcoma and fibrosarcoma cells. Tretinoin 30-43 matrix metallopeptidase 2 Homo sapiens 73-85
24045938-0 2013 Dhrs3 protein attenuates retinoic acid signaling and is required for early embryonic patterning. Tretinoin 25-38 dehydrogenase/reductase (SDR family) member 3 L homeolog Xenopus laevis 0-5
24045938-5 2013 We show here that the expression of dhrs3 was induced by atRA treatment and overexpression of Xenopus nodal related 1 (xnr1) in animal cap assay. Tretinoin 57-61 dehydrogenase/reductase (SDR family) member 3 L homeolog Xenopus laevis 36-41
24045938-7 2013 In embryos overexpressing aldh1a2 or retinol dehydrogenase 10 (rdh10) in the presence of their respective substrates, Dhrs3 counteracted the action of Aldh1a2 or Rdh10, indicating that retinoic acid signaling is attenuated. Tretinoin 185-198 retinol dehydrogenase 10 S homeolog Xenopus laevis 37-61
24045938-7 2013 In embryos overexpressing aldh1a2 or retinol dehydrogenase 10 (rdh10) in the presence of their respective substrates, Dhrs3 counteracted the action of Aldh1a2 or Rdh10, indicating that retinoic acid signaling is attenuated. Tretinoin 185-198 retinol dehydrogenase 10 S homeolog Xenopus laevis 63-68
24045938-7 2013 In embryos overexpressing aldh1a2 or retinol dehydrogenase 10 (rdh10) in the presence of their respective substrates, Dhrs3 counteracted the action of Aldh1a2 or Rdh10, indicating that retinoic acid signaling is attenuated. Tretinoin 185-198 dehydrogenase/reductase (SDR family) member 3 L homeolog Xenopus laevis 118-123
24045938-8 2013 Knockdown of Dhrs3 by antisense morpholino oligonucleotides resulted in a phenotype of shortened anteroposterior axis, reduced head structure, and perturbed somitogenesis, which were also found in embryos treated with an excess of atRA. Tretinoin 231-235 dehydrogenase/reductase (SDR family) member 3 L homeolog Xenopus laevis 13-18
24045938-10 2013 Taken together, these studies suggest that dhrs3 participates in atRA metabolism by reducing atRAL levels and is required for proper anteroposterior axis formation, neuroectoderm patterning, and somitogenesis. Tretinoin 65-69 dehydrogenase/reductase (SDR family) member 3 L homeolog Xenopus laevis 43-48
23619336-1 2013 Retinoic acid (RA) regulates many developmental processes through its binding to two types of nuclear receptors, the retinoic acid receptor (RAR), and the retinoid-X receptor (RXR), which preferentially binds to the 9-cis isomer. Tretinoin 0-13 retinoid x receptor, gamma a Danio rerio 155-174
23619336-1 2013 Retinoic acid (RA) regulates many developmental processes through its binding to two types of nuclear receptors, the retinoic acid receptor (RAR), and the retinoid-X receptor (RXR), which preferentially binds to the 9-cis isomer. Tretinoin 0-13 retinoid x receptor, gamma a Danio rerio 176-179
23619336-1 2013 Retinoic acid (RA) regulates many developmental processes through its binding to two types of nuclear receptors, the retinoic acid receptor (RAR), and the retinoid-X receptor (RXR), which preferentially binds to the 9-cis isomer. Tretinoin 15-17 retinoid x receptor, gamma a Danio rerio 155-174
23619336-1 2013 Retinoic acid (RA) regulates many developmental processes through its binding to two types of nuclear receptors, the retinoic acid receptor (RAR), and the retinoid-X receptor (RXR), which preferentially binds to the 9-cis isomer. Tretinoin 15-17 retinoid x receptor, gamma a Danio rerio 176-179
24204796-4 2013 Here we show that ATRA increases ORMDL3 production in vitro via inducing PKA-dependent CREB phosphorylation which in turn binds to the CRE element in promoter region of ORMDL3 and initiates ORMDL3 transcription. Tretinoin 18-22 ORMDL sphingolipid biosynthesis regulator 3 Homo sapiens 169-175
23607934-5 2013 Retinoic acid (RA) induced gut-homing markers (beta7 and CCR9) and a regulatory phenotype and function [decreased human leucocyte antigen D-related (HLA-DR) and increased ILT3 and fluorescein isothiocyanate (FITC-dextran uptake) in MoDC]. Tretinoin 15-17 C-C motif chemokine receptor 9 Homo sapiens 57-61
24040125-4 2013 Experiments showed that zebrafish express aldh1a2, which encodes an RA-synthesizing enzyme, in the gonad rather than in the mesonephros as in mouse. Tretinoin 68-70 aldehyde dehydrogenase 1 family, member A2 Danio rerio 42-49
23806210-4 2013 RA is produced by three different enzymes called retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3) that are all expressed in the developing bowel. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 79-85
23806210-4 2013 RA is produced by three different enzymes called retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3) that are all expressed in the developing bowel. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 87-93
23756134-2 2013 RA directly influences expression of Pdx1, a transcription factor essential for pancreatic development and beta-cell (beta-cell) maturation. Tretinoin 0-2 pancreatic and duodenal homeobox 1 Homo sapiens 37-41
23951127-4 2013 In this study, we examined the skeletal phenotype of mice deficient in retinaldehyde dehydrogenase 1 (Aldh1a1), the enzyme responsible for converting Rald to ATRA in adult animals. Tretinoin 158-162 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 102-109
23824578-3 2013 We show that RA acts early in the neurogenic pathway by inhibiting expression of neural progenitor markers Geminin and Foxd4l1, thereby promoting differentiation. Tretinoin 13-15 forkhead box D4 like 1, gene 1 L homeolog Xenopus laevis 119-126
23824578-6 2013 We hypothesized that RA regulates primary neurogenesis by inducing Erf and Etv3l to antagonize proliferative signals. Tretinoin 21-23 ETS2 repressor factor S homeolog Xenopus laevis 67-70
23777559-9 2013 Our results show that ApoD is necessary and sufficient to allow for RA differentiating activity. Tretinoin 68-70 apolipoprotein D Homo sapiens 22-26
23777559-10 2013 Both human ApoD and Drosophila NLaz successfully deliver RA to immature neurons, driving neurite outgrowth. Tretinoin 57-59 apolipoprotein D Homo sapiens 11-15
23777559-10 2013 Both human ApoD and Drosophila NLaz successfully deliver RA to immature neurons, driving neurite outgrowth. Tretinoin 57-59 Neural Lazarillo Drosophila melanogaster 31-35
23587524-4 2013 ATRA induced upregulation of Pyk2 mRNA, protein and phosphorylation levels and enhanced Pyk2 interaction with paxillin and vinculin. Tretinoin 0-4 vinculin Homo sapiens 123-131
23530929-0 2013 Retinoic acid-elicited RARalpha/RXRalpha signaling attenuates Abeta production by directly inhibiting gamma-secretase-mediated cleavage of amyloid precursor protein. Tretinoin 0-13 retinoid X receptor alpha Mus musculus 32-40
23530929-6 2013 In addition, RA-induced inhibition of gamma-secretase activity was found to be mediated through significant activation of extracellular signal-regulated kinases (ERK1/2). Tretinoin 13-15 mitogen-activated protein kinase 3 Mus musculus 162-168
23530929-9 2013 Finally, we have established that RA inhibits gamma-secretase through nuclear retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-alpha (RXRalpha). Tretinoin 34-36 retinoid X receptor alpha Mus musculus 122-147
23530929-9 2013 Finally, we have established that RA inhibits gamma-secretase through nuclear retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-alpha (RXRalpha). Tretinoin 34-36 retinoid X receptor alpha Mus musculus 149-157
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 25-38 cellular retinoic acid binding protein II Mus musculus 173-181
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 40-42 cellular retinoic acid binding protein II Mus musculus 173-181
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 109-111 cellular retinoic acid binding protein II Mus musculus 173-181
23991366-2 2013 In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARgamma to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. Tretinoin 18-20 cellular retinoic acid binding protein II Mus musculus 51-59
24498316-8 2014 Surprisingly, treatment of Taf4(-/-) MEFs with all-trans retinoic acid (ATRA) restores contact inhibition suppressing 3D growth. Tretinoin 57-70 TATA-box binding protein associated factor 4 Mus musculus 27-31
24498316-8 2014 Surprisingly, treatment of Taf4(-/-) MEFs with all-trans retinoic acid (ATRA) restores contact inhibition suppressing 3D growth. Tretinoin 72-76 TATA-box binding protein associated factor 4 Mus musculus 27-31
24395056-10 2014 The 2-nM retinoic acid exposure also led to alterations of neurobehavior- and optic nerve-related genes, with the transforming growth factor-beta signal transduction inhibitor noggin (nog) and the spinal cord marker homeobox c3a (hox) being underexpressed and the retinal G protein-coupled receptor a (rgr), the photoreceptor cell marker rhodopsin (rho), and the short wave-sensitive cone pigment opsin 1 (opn1sw1) being overexpressed. Tretinoin 9-22 opsin 1 (cone pigments), short-wave-sensitive 1 Danio rerio 406-413
24309293-1 2014 Bone marrow mesenchymal stem cells (MSCs) can be differentiate towards a Schwann cells (SCs) lineage when exposed to pre-inducing reagents beta-mercaptoethanol (BME) and retinoic acid (RA), followed by inducing factors: forskolin (FSK), basic fibroblast growth factor (bFGF), platelet derived growth factor (PDGF), and heregulin (HRG). Tretinoin 185-187 fibroblast growth factor 2 Rattus norvegicus 237-267
24309293-1 2014 Bone marrow mesenchymal stem cells (MSCs) can be differentiate towards a Schwann cells (SCs) lineage when exposed to pre-inducing reagents beta-mercaptoethanol (BME) and retinoic acid (RA), followed by inducing factors: forskolin (FSK), basic fibroblast growth factor (bFGF), platelet derived growth factor (PDGF), and heregulin (HRG). Tretinoin 185-187 fibroblast growth factor 2 Rattus norvegicus 269-273
24269351-5 2014 Changes observed in the expression of factors involved in the retinoid pathway under ATRA, namely an upregulation of CRBP and CRABP2, were also reflected in GCT tissues of different histologies, providing further insight into factors involved in the differentiation of these pluripotent tumors. Tretinoin 85-89 retinol binding protein 1 Homo sapiens 117-121
24416428-2 2014 In this study, we evaluated the effect of ATRA on the expression of apurinic endonuclease/redox factor-1 (Ape/Ref-1) in the U266 and RPMI-8226 myeloma cells to explore the chemoresistance mechanism involved. Tretinoin 42-46 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 106-109
24416428-2 2014 In this study, we evaluated the effect of ATRA on the expression of apurinic endonuclease/redox factor-1 (Ape/Ref-1) in the U266 and RPMI-8226 myeloma cells to explore the chemoresistance mechanism involved. Tretinoin 42-46 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 110-115
24416428-3 2014 ATRA treatment induced upregulation of Ape/Ref-1 via a noncanonical signaling pathway, leading to enhanced pro-survival activity counteracting melphalan (an alkylating agent). Tretinoin 0-4 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 39-42
24416428-3 2014 ATRA treatment induced upregulation of Ape/Ref-1 via a noncanonical signaling pathway, leading to enhanced pro-survival activity counteracting melphalan (an alkylating agent). Tretinoin 0-4 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 43-48
24416428-7 2014 Moreover, ATRA-mediated Ape/Ref-1 upregulation was correlated with histone modification and activation of CBP/p300, an important cofactors for CREB transcriptional activity. Tretinoin 10-14 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 24-27
24416428-7 2014 Moreover, ATRA-mediated Ape/Ref-1 upregulation was correlated with histone modification and activation of CBP/p300, an important cofactors for CREB transcriptional activity. Tretinoin 10-14 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 28-33
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 17-30 chemokine (C-C motif) ligand 25 Mus musculus 195-200
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 32-34 chemokine (C-C motif) ligand 25 Mus musculus 195-200
24398584-5 2014 The results demonstrated that the expression of Stra8, a master gene for germ cell meiosis, and its stimulation by retinoic acid (RA) were reduced after suppression of Notch signaling, and the other meiotic genes, Dazl, Dmc1, and Rec8, were abolished or markedly decreased. Tretinoin 115-128 REC8 meiotic recombination protein Mus musculus 230-234
24398584-5 2014 The results demonstrated that the expression of Stra8, a master gene for germ cell meiosis, and its stimulation by retinoic acid (RA) were reduced after suppression of Notch signaling, and the other meiotic genes, Dazl, Dmc1, and Rec8, were abolished or markedly decreased. Tretinoin 130-132 REC8 meiotic recombination protein Mus musculus 230-234
24430728-9 2014 In addition, TSA, but not GnRH, significantly stimulated gene expression of retinaldehyde dehydrogenase 1 (RALDH1), a retinoic acid (RA) synthesizing enzyme involved in cell differentiation. Tretinoin 118-131 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 76-105
24430728-9 2014 In addition, TSA, but not GnRH, significantly stimulated gene expression of retinaldehyde dehydrogenase 1 (RALDH1), a retinoic acid (RA) synthesizing enzyme involved in cell differentiation. Tretinoin 118-131 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 107-113
24310731-5 2014 AtRA and retinol affected GM-CSF and IL-16 expression mainly through RA receptor beta (RARbeta). Tretinoin 0-4 retinoic acid receptor, beta Mus musculus 87-94
25354450-2 2014 Cdx1 itself is known to be regulated in the primitive streak/tailbud by both retinoic acid (RA) and Wnt3a. Tretinoin 77-90 caudal type homeobox 1 Mus musculus 0-4
24316973-5 2014 T helper cell rerouting in EAE was dependent on IL-4, which enhanced retinoic acid (RA) production by dendritic cells, which further induced expression of gut-homing receptors CCR9 and alpha4beta7 on Bcl11b-deficient CD4+ T cells. Tretinoin 69-82 B cell leukemia/lymphoma 11B Mus musculus 200-206
24314292-0 2013 The retinoic acid receptor-alpha modulators ATRA and Ro415253 reciprocally regulate human IL-5+ Th2 cell proliferation and cytokine expression. Tretinoin 44-48 interleukin 5 Homo sapiens 90-94
24314292-11 2013 ATRA and Ro415253 respectively augmented and inhibited Th2 cell proliferation, and this affect was more pronounced for the IL-5+ vs. IL-5- Th2 subpopulation. Tretinoin 0-4 interleukin 5 Homo sapiens 123-127
24314292-11 2013 ATRA and Ro415253 respectively augmented and inhibited Th2 cell proliferation, and this affect was more pronounced for the IL-5+ vs. IL-5- Th2 subpopulation. Tretinoin 0-4 interleukin 5 Homo sapiens 133-137
24314292-12 2013 ATRA and Ro415253 respectively augmented and inhibited the expression of IL5 in a significant manner, which was not found for IL4 or IL13. Tretinoin 0-4 interleukin 5 Homo sapiens 73-76
24011394-6 2013 In the present study, using antibodies specific to different members of the DPYSL family, DPYSL1, DPYSL2 and DPYSL3, we investigated regulation of their expression and their subcellular distribution during retinoic acid (RA)-induced differentiation in NB cells. Tretinoin 206-219 collapsin response mediator protein 1 Homo sapiens 90-96
24011394-6 2013 In the present study, using antibodies specific to different members of the DPYSL family, DPYSL1, DPYSL2 and DPYSL3, we investigated regulation of their expression and their subcellular distribution during retinoic acid (RA)-induced differentiation in NB cells. Tretinoin 221-223 collapsin response mediator protein 1 Homo sapiens 90-96
24126540-12 2013 The reduced CD138 expression under hypoxic conditions recovered when cells were treated with ATRA, even under hypoxic conditions, along with decreases in the expression of stem cell-specific transcription factor. Tretinoin 93-97 syndecan 1 Homo sapiens 12-17
24029702-8 2013 GCNF is expressed in ES/EC cells and during their differentiation, and has been reported to be required for pluripotency gene repression during retinoic acid (RA)-induced mES cell differentiation. Tretinoin 144-157 nuclear receptor subfamily 6, group A, member 1 Mus musculus 0-4
24029702-8 2013 GCNF is expressed in ES/EC cells and during their differentiation, and has been reported to be required for pluripotency gene repression during retinoic acid (RA)-induced mES cell differentiation. Tretinoin 159-161 nuclear receptor subfamily 6, group A, member 1 Mus musculus 0-4
24052562-7 2013 Furthermore, the heart areas of CTN-exposed embryos demonstrated an elevated levels of aldh1a2 and cspg2 messenger RNA; these 2 cardiac-related genes are known to be involved in retinoic acid (RA) pathway as well as downstream targets of microRNA-138 (miR-138) in zebrafish. Tretinoin 178-191 aldehyde dehydrogenase 1 family, member A2 Danio rerio 87-94
24052562-7 2013 Furthermore, the heart areas of CTN-exposed embryos demonstrated an elevated levels of aldh1a2 and cspg2 messenger RNA; these 2 cardiac-related genes are known to be involved in retinoic acid (RA) pathway as well as downstream targets of microRNA-138 (miR-138) in zebrafish. Tretinoin 193-195 aldehyde dehydrogenase 1 family, member A2 Danio rerio 87-94
24205156-0 2013 Heterodimeric BMP-2/7 antagonizes the inhibition of all-trans retinoic acid and promotes the osteoblastogenesis. Tretinoin 62-75 bone morphogenetic protein 2 Homo sapiens 14-21
24205156-3 2013 We hypothesized that heterodimeric bone morphogenetic protein-2/7 could antagonize all-trans retinoic acid and enhance osteoblastogenesis, with an aim to accelerate and enhance bone regeneration and implant osteointegration. Tretinoin 93-106 bone morphogenetic protein 2 Homo sapiens 35-63
24205156-7 2013 In the presence of ATRA, 50 ng/ml bone morphogenetic protein-2/7 not only completely restored but also significantly enhanced all the osteoblastogenic genes and proteins. Tretinoin 19-23 bone morphogenetic protein 2 Homo sapiens 34-62
24204796-0 2013 All-trans retinoic acid modulates ORMDL3 expression via transcriptional regulation. Tretinoin 10-23 ORMDL sphingolipid biosynthesis regulator 3 Homo sapiens 34-40
24204796-4 2013 Here we show that ATRA increases ORMDL3 production in vitro via inducing PKA-dependent CREB phosphorylation which in turn binds to the CRE element in promoter region of ORMDL3 and initiates ORMDL3 transcription. Tretinoin 18-22 ORMDL sphingolipid biosynthesis regulator 3 Homo sapiens 33-39
24204796-4 2013 Here we show that ATRA increases ORMDL3 production in vitro via inducing PKA-dependent CREB phosphorylation which in turn binds to the CRE element in promoter region of ORMDL3 and initiates ORMDL3 transcription. Tretinoin 18-22 ORMDL sphingolipid biosynthesis regulator 3 Homo sapiens 169-175
23649634-0 2013 HOX antisense lincRNA HOXA-AS2 is an apoptosis repressor in all trans retinoic acid treated NB4 promyelocytic leukemia cells. Tretinoin 64-83 HOXA cluster antisense RNA 2 Homo sapiens 22-30
23649634-4 2013 The increase in death of HOXA-AS2 knockdown cells was accompanied by an elevated TNF-related apoptosis-inducing ligand (TRAIL) levels, but ATRA-induced NB4 cells treated with TRAIL did show an increase in HOXA-AS2 expression. Tretinoin 139-143 HOXA cluster antisense RNA 2 Homo sapiens 205-213
23649634-5 2013 These results demonstrate that ATRA induction of HOXA-AS2 suppresses ATRA-induced apoptosis, possibly through a TRAIL-mediated pathway. Tretinoin 31-35 HOXA cluster antisense RNA 2 Homo sapiens 49-57
23649634-5 2013 These results demonstrate that ATRA induction of HOXA-AS2 suppresses ATRA-induced apoptosis, possibly through a TRAIL-mediated pathway. Tretinoin 69-73 HOXA cluster antisense RNA 2 Homo sapiens 49-57
23649634-6 2013 HOXA-AS2-mediated negative regulation thus contributes to the fine-tuning of apoptosis during ATRA-induced myeloid differentiation in NB4 cells. Tretinoin 94-98 HOXA cluster antisense RNA 2 Homo sapiens 0-8
24006462-0 2013 Retinoic acid improves defective TLR9/RP105-induced immune responses in common variable immunodeficiency-derived B cells. Tretinoin 0-13 toll like receptor 9 Homo sapiens 33-37
24006462-6 2013 This can be explained by impaired RA-mediated isotype switching in TLR9/RP105-stimulated CVID-derived B cells owing to reduced induction of activation-induced deaminase. Tretinoin 34-36 toll like receptor 9 Homo sapiens 67-71
24006462-8 2013 The ability of RA to improve critical immune parameters in CVID-derived B cells stimulated through TLR9 and RP105 support the possibility of combining RA with TLR stimulation for the treatment of CVID. Tretinoin 15-17 toll like receptor 9 Homo sapiens 99-103
24059847-0 2013 Retinoic acid has different effects on UCP1 expression in mouse and human adipocytes. Tretinoin 0-13 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 39-43
24059847-6 2013 ATRA induced UCP1 expression in all mouse white and brown adipocytes, but inhibited or had no effect on UCP1 expression in human adipocyte cell lines and primary human white adipocytes. Tretinoin 0-4 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 13-17
24059847-9 2013 Moreover, the ATRA-mediated induction of UCP1 expression in mouse adipocytes was independent of PPARgamma coactivator-1alpha. Tretinoin 14-18 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 41-45
24059847-11 2013 ATRA induces UCP1 expression in mouse adipocytes through activation of RARs, whereas expression of UCP1 in human adipocytes is not increased by exposure to ATRA. Tretinoin 0-4 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 13-17
24040226-8 2013 RESULTS: Culture of isolated ENS precursors for 3 days with RA decreases expression of the endothelin-3 gene and that of its activation enzyme. Tretinoin 60-62 endothelin 3 Rattus norvegicus 91-103
24032106-1 2013 BACKGROUND: Previous studies have suggested that NPM1 mutations may be a marker for response to all-trans retinoic acid (ATRA) given as an adjunct to intensive chemotherapy in older patients with acute myeloid leukemia (AML). Tretinoin 106-119 nucleophosmin 1 Homo sapiens 49-53
24032106-1 2013 BACKGROUND: Previous studies have suggested that NPM1 mutations may be a marker for response to all-trans retinoic acid (ATRA) given as an adjunct to intensive chemotherapy in older patients with acute myeloid leukemia (AML). Tretinoin 121-125 nucleophosmin 1 Homo sapiens 49-53
23849428-0 2013 Calcium prevents retinoic acid-induced disruption of the spectrin-based cytoskeleton in keratinocytes through the Src/PI3K-p85alpha/AKT/PKCdelta/beta-adducin pathways. Tretinoin 17-30 protein kinase C delta Homo sapiens 136-144
23849428-5 2013 RA also enhanced AKT expression and dramatically induced phosphorylation of AKT((Thr308)), accompanied by phosphorylation of both PKCdelta((Thr505)) and beta-adducin((Ser662)) and upregulated cyclin D2 and down-regulated cyclin B1. Tretinoin 0-2 protein kinase C delta Homo sapiens 130-138
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 protein kinase C delta Homo sapiens 247-255
23765990-2 2013 RA is produced from metabolism of retinol to retinaldehyde by retinol dehydrogenase (RDH), followed by metabolism of retinaldehyde to RA by retinaldehyde dehydrogenase (RALDH). Tretinoin 0-2 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 62-83
23765990-2 2013 RA is produced from metabolism of retinol to retinaldehyde by retinol dehydrogenase (RDH), followed by metabolism of retinaldehyde to RA by retinaldehyde dehydrogenase (RALDH). Tretinoin 0-2 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 85-88
23765990-3 2013 Previous studies on Raldh2-/- and Raldh3-/- mice demonstrated an RA requirement for gamma-aminobutyric acid (GABA)ergic and dopaminergic differentiation in forebrain basal ganglia, but no RA requirement was observed during early forebrain patterning or subsequent forebrain cortical expansion. Tretinoin 65-67 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 20-26
23977218-7 2013 Moreover, our results suggest that hippocampal CRABP-I expression which controls the intracellular availability of retinoic acid (RA), may be an important regulator of neuronal differentiation processes in the aged hippocampus. Tretinoin 115-128 cellular retinoic acid binding protein 1 Rattus norvegicus 47-54
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 11-34 cellular retinoic acid binding protein II Mus musculus 156-162
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 36-40 cellular retinoic acid binding protein II Mus musculus 156-162
23744644-0 2013 Retinoic acid, acting as a highly specific IgA isotype switch factor, cooperates with TGF-beta1 to enhance the overall IgA response. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 86-95
23916085-0 2013 Treatment of CIN with retinoic acid and topical interferon alfa-2b. Tretinoin 22-35 pyridoxal phosphatase Homo sapiens 13-16
28363907-3 2017 RA can promote gammadelta T cells to produce mTORC1-dependent IL-22 in the liver, but inhibits IFN-gamma and IL-17. Tretinoin 0-2 CREB regulated transcription coactivator 1 Mus musculus 45-51
23657628-6 2013 We found that RA significantly enhanced TGF-beta-induced expression of Foxp3 on naive and committed T cells in vitro and that this was blocked by an antagonist of RARalpha (RARi). Tretinoin 14-16 transforming growth factor, beta 1 Mus musculus 40-48
23823803-0 2013 Knockdown of FABP3 impairs cardiac development in Zebrafish through the retinoic acid signaling pathway. Tretinoin 72-85 fatty acid binding protein 3, muscle and heart Danio rerio 13-18
28363907-8 2017 Our study has demonstrated a crucial role for RA in promoting IL-22 production and tempering DC function through downregulating S100 family proteins during viral hepatitis. Tretinoin 46-48 S100 calcium binding protein A1 Mus musculus 128-132
23823803-5 2013 Mechanistically, our data showed that the retinoic acid (RA) catabolizing enzyme Cyp26a1 was upregulated in FABP3-MO zebrafish, as indicated by in situ hybridization and real-time PCR. Tretinoin 42-55 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 81-88
28404891-3 2017 HMGB1 and the pro-inflammatory cytokines IL-1beta and TNF-alpha were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO. Tretinoin 126-130 high mobility group box 1 Homo sapiens 0-5
23823803-5 2013 Mechanistically, our data showed that the retinoic acid (RA) catabolizing enzyme Cyp26a1 was upregulated in FABP3-MO zebrafish, as indicated by in situ hybridization and real-time PCR. Tretinoin 42-55 fatty acid binding protein 3, muscle and heart Danio rerio 108-113
23991366-2 2013 In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARgamma to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. Tretinoin 18-20 delta like non-canonical Notch ligand 1 Mus musculus 151-157
23991366-2 2013 In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARgamma to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. Tretinoin 18-20 SRY (sex determining region Y)-box 9 Mus musculus 159-163
23991366-2 2013 In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARgamma to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. Tretinoin 18-20 Kruppel-like factor 2 (lung) Mus musculus 169-173
28404891-6 2017 Exogenous HMGB1 also enhanced pulmonary infiltration and up-regulated ICAM-1 expression in the ATRA-treated DS mouse. Tretinoin 95-99 high mobility group box 1 Mus musculus 10-15
28404891-6 2017 Exogenous HMGB1 also enhanced pulmonary infiltration and up-regulated ICAM-1 expression in the ATRA-treated DS mouse. Tretinoin 95-99 intercellular adhesion molecule 1 Mus musculus 70-76
28404891-8 2017 Treatment with a HMGB1-neutralizing antibody reduced secretion of TNF-alpha and IL-1beta, arrested the elevation of ICAM-1 and blunted the activation of ERK1/2 in ATRA-induced NB4 cells. Tretinoin 163-167 high mobility group box 1 Homo sapiens 17-22
28404891-9 2017 The HMGB1-neutralizing antibody also decreased ICAM-1 expression and reduced mortality in ATRA-treated DS model mice. Tretinoin 90-94 high mobility group box 1 Mus musculus 4-9
23733880-4 2013 CD103(+) DCs, but not pDCs or lung macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key for the production of retinoic acid, a cofactor for TGF-beta for Foxp3 induction. Tretinoin 154-167 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 78-107
23733880-4 2013 CD103(+) DCs, but not pDCs or lung macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key for the production of retinoic acid, a cofactor for TGF-beta for Foxp3 induction. Tretinoin 154-167 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 109-116
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 23-25 CREB regulated transcription coactivator 1 Mus musculus 231-237
23733880-4 2013 CD103(+) DCs, but not pDCs or lung macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key for the production of retinoic acid, a cofactor for TGF-beta for Foxp3 induction. Tretinoin 154-167 transforming growth factor, beta 1 Mus musculus 184-192
23582512-9 2013 The TGF-beta type II receptor, responsible for binding TGF-beta during neuronal differentiation, was increased 14-fold in NT2 cells treated with RA (P < 0.001). Tretinoin 145-147 transforming growth factor beta receptor 2 Homo sapiens 4-29
28154153-6 2017 Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta. Tretinoin 14-16 retinoic acid receptor, beta Mus musculus 133-140
23636811-5 2013 Finally, we found that RA induced Stra8, Sycp3, Dmc1, and Rec8 transcripts, promoting meiotic entry in culture also in pregonadal 10.5-dpc PGCs of both sexes. Tretinoin 23-25 DNA meiotic recombinase 1 Mus musculus 48-52
23636811-5 2013 Finally, we found that RA induced Stra8, Sycp3, Dmc1, and Rec8 transcripts, promoting meiotic entry in culture also in pregonadal 10.5-dpc PGCs of both sexes. Tretinoin 23-25 REC8 meiotic recombination protein Mus musculus 58-62
23271512-0 2013 All-trans retinoic acid and arsenic trioxide resistance of acute promyelocytic leukemia with the variant STAT5B-RARA fusion gene. Tretinoin 10-23 signal transducer and activator of transcription 5B Homo sapiens 105-111
28154153-6 2017 Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta. Tretinoin 96-98 retinoic acid receptor, beta Mus musculus 133-140
27677346-8 2017 In addition, curcumin and IFN-beta/RA combination inhibited the expression of COX-2 and up-regulated GADD153. Tretinoin 35-37 interferon beta 1 Homo sapiens 26-34
23524428-9 2013 CONCLUSION: Our results indicated that restoration of GJIC via enhanced Cx32 and Cx43 expression might serve as a novel mechanism for the anti-tumor effect of ATRA in OSCC. Tretinoin 159-163 gap junction protein alpha 1 Homo sapiens 81-85
23716670-7 2013 This study provides evidence of an antitumoral mechanism of action upon TLR3 activation and the biological rationale for a combined TLR3 agonist/retinoic acid treatment of prostate and breast cancer. Tretinoin 145-158 toll like receptor 3 Homo sapiens 72-76
23716670-7 2013 This study provides evidence of an antitumoral mechanism of action upon TLR3 activation and the biological rationale for a combined TLR3 agonist/retinoic acid treatment of prostate and breast cancer. Tretinoin 145-158 toll like receptor 3 Homo sapiens 132-136
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 7-20 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 210-214
28098879-14 2017 Actinomycin-D, retinoic acid and dexamethasone also had inhibitory effects on MMP-2. Tretinoin 15-28 matrix metallopeptidase 2 Homo sapiens 78-83
23762260-5 2013 During retinoic acid (RA)-induced differentiation of mouse F9 embryonal carcinoma cells (ECCs), the Akt activation profile as well as its substrate spectrum is strikingly correlated with the down-regulation of Oct4, Klf4 and Nanog, which suggests Akt activation is coupled to the onset of differentiation. Tretinoin 22-24 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 210-214
23711709-0 2013 Identification of target genes of transcription factor CEBPB in acute promyelocytic leukemia cells induced by all-trans retinoic acid. Tretinoin 120-133 CCAAT enhancer binding protein beta Homo sapiens 55-60
28089218-3 2017 unveil a new mechanism that induces the expression of the NKG2D ligand retinoic acid early-inducible (RAE-1) in response to murine cytomegalovirus (MCMV) infection through inhibition of casein kinase 2 (CK2), an activator of the repressor histone deacetylase HDAC3. Tretinoin 71-84 killer cell lectin like receptor K1 Homo sapiens 58-63
23711709-1 2013 OBJECTIVE: To identify target genes of transcription factor CCAAT enhancer-binding protein beta (CEBPB) in acute promyelocytic leukemia cells induced by all-trans retinoic acid. Tretinoin 163-176 CCAAT enhancer binding protein beta Homo sapiens 60-95
23711709-1 2013 OBJECTIVE: To identify target genes of transcription factor CCAAT enhancer-binding protein beta (CEBPB) in acute promyelocytic leukemia cells induced by all-trans retinoic acid. Tretinoin 163-176 CCAAT enhancer binding protein beta Homo sapiens 97-102
23711709-3 2013 Then, 106 potential CEBPB binding fragments from the genome of the all-trans retinoic acid (ATRA)-treated NB4 cells were identified. Tretinoin 77-90 CCAAT enhancer binding protein beta Homo sapiens 20-25
23711709-3 2013 Then, 106 potential CEBPB binding fragments from the genome of the all-trans retinoic acid (ATRA)-treated NB4 cells were identified. Tretinoin 92-96 CCAAT enhancer binding protein beta Homo sapiens 20-25
23801989-6 2013 Furthermore, DCs expressing CD103 in the intestine induce Foxp3(+) T-regs from Foxp3(-) CD4(+) T cells with endogenous TGF-beta and retinoic acid. Tretinoin 132-145 forkhead box P3 Homo sapiens 58-63
23662841-6 2013 These tolerogenic effects were shown to be mediated by the generation of FOXP3(+) regulatory T cells through retinoic acid and the induction of retinaldehyde dehydrogenase enzymes. Tretinoin 109-122 forkhead box P3 Homo sapiens 73-78
28089218-3 2017 unveil a new mechanism that induces the expression of the NKG2D ligand retinoic acid early-inducible (RAE-1) in response to murine cytomegalovirus (MCMV) infection through inhibition of casein kinase 2 (CK2), an activator of the repressor histone deacetylase HDAC3. Tretinoin 71-84 histone deacetylase 3 Homo sapiens 259-264
23553814-3 2013 Here, Aldh1a2 functions as the primary enzyme necessary for RA production which regulates forelimb outgrowth and hindlimb digit separation. Tretinoin 60-62 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 6-13
27862498-8 2017 RESULTS: In ATRA-treated MSCs, expressions of COX-2, HIF-1, CXCR4, CCR2, VEGF, Ang-2 and Ang-4 increased compared to control groups. Tretinoin 12-16 angiopoietin 2 Rattus norvegicus 79-84
23553814-4 2013 Because mice lacking HOXA13 exhibit similar defects in digit separation as Aldh1a2 mutants, we hypothesized that HOXA13 regulates Aldh1a2 to facilitate RA-mediated interdigital programmed cell death (IPCD) and digit separation. Tretinoin 152-154 homeobox A13 Mus musculus 21-27
23553814-4 2013 Because mice lacking HOXA13 exhibit similar defects in digit separation as Aldh1a2 mutants, we hypothesized that HOXA13 regulates Aldh1a2 to facilitate RA-mediated interdigital programmed cell death (IPCD) and digit separation. Tretinoin 152-154 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 75-82
23553814-4 2013 Because mice lacking HOXA13 exhibit similar defects in digit separation as Aldh1a2 mutants, we hypothesized that HOXA13 regulates Aldh1a2 to facilitate RA-mediated interdigital programmed cell death (IPCD) and digit separation. Tretinoin 152-154 homeobox A13 Mus musculus 113-119
23553814-4 2013 Because mice lacking HOXA13 exhibit similar defects in digit separation as Aldh1a2 mutants, we hypothesized that HOXA13 regulates Aldh1a2 to facilitate RA-mediated interdigital programmed cell death (IPCD) and digit separation. Tretinoin 152-154 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 130-137
23553814-8 2013 Finally, decreased RA signaling and IPCD can be partially rescued in the Hoxa13 mutant hindlimb by maternal RA supplementation. Tretinoin 19-21 homeobox A13 Mus musculus 73-79
23553814-8 2013 Finally, decreased RA signaling and IPCD can be partially rescued in the Hoxa13 mutant hindlimb by maternal RA supplementation. Tretinoin 108-110 homeobox A13 Mus musculus 73-79
23553814-9 2013 CONCLUSIONS: Defects in IPCD and digit separation in Hoxa13 mutant mice may be caused in part by reduced levels of RA signaling stemming from a loss in the direct regulation of Aldh1a2. Tretinoin 115-117 homeobox A13 Mus musculus 53-59
23553814-9 2013 CONCLUSIONS: Defects in IPCD and digit separation in Hoxa13 mutant mice may be caused in part by reduced levels of RA signaling stemming from a loss in the direct regulation of Aldh1a2. Tretinoin 115-117 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 177-184
23441061-4 2013 RESULTS: We demonstrate that ski expression is up-regulated in response to retinoic acid in both early Xenopus embryos and in human cell lines. Tretinoin 75-88 SKI proto-oncogene S homeolog Xenopus laevis 29-32
23723417-5 2013 Knockdown analysis revealed that depletion of linc-HOXA1 RNA at its site of transcription increased transcription of the Hoxa1 gene cis to the chromosome and that exposure of cells to retinoic acid can disrupt this interaction. Tretinoin 184-197 Hoxa adjacent long noncoding RNA 1 Mus musculus 46-56
27428727-1 2017 GOALS: To perform an exploratory pilot study of all-trans retinoic acid (ATRA) combined with ursodeoxycholic acid (UDCA) in patients with primary sclerosing cholangitis (PSC). Tretinoin 48-71 PSC Homo sapiens 170-173
23500056-7 2013 We demonstrate that only OVA-encapsulated PLGA NP enhance the induction of FoxP3 in activated T-cells via a TGF-beta and RA dependent mechanism by enhancing retinaldehyde dehydrogenase enzyme (RALDH) expression in CLN-derived DCs that is required for RA production. Tretinoin 121-123 forkhead box P3 Homo sapiens 75-80
23656719-3 2013 We recently reported that AhR promotes retinoic acid (RA)-induced granulocytic differentiation of HL-60 myeloblastic leukemia cells by restricting the nuclear abundance of the stem cell associated transcription factor Oct4. Tretinoin 39-52 aryl hydrocarbon receptor Homo sapiens 26-29
23529927-3 2013 The administration of exogenous RA significantly increased expression of the gut-homing molecules, CCR9 and alpha4beta7, on donor T cells in mesenteric lymph nodes, and augmented the accumulation of proinflammatory CD4(+) and CD8(+) T cells within the gut mucosa, leading to a selective exacerbation of colonic GVHD and increased overall mortality. Tretinoin 32-34 C-C motif chemokine receptor 9 Homo sapiens 99-103
23656719-3 2013 We recently reported that AhR promotes retinoic acid (RA)-induced granulocytic differentiation of HL-60 myeloblastic leukemia cells by restricting the nuclear abundance of the stem cell associated transcription factor Oct4. Tretinoin 54-56 aryl hydrocarbon receptor Homo sapiens 26-29
27428727-1 2017 GOALS: To perform an exploratory pilot study of all-trans retinoic acid (ATRA) combined with ursodeoxycholic acid (UDCA) in patients with primary sclerosing cholangitis (PSC). Tretinoin 73-77 PSC Homo sapiens 170-173
23656719-12 2013 FICZ causes changes in signaling events that are known to drive differentiation, and notably augments the RA-induced sustained activation of the RAF/MEK/ERK axis of the mitogen-activated protein kinase (MAPK) cascade. Tretinoin 106-108 zinc fingers and homeoboxes 2 Homo sapiens 145-148
27428727-4 2017 STUDY: ATRA (45 mg/m/d, divided and given twice daily) was combined with moderate-dose UDCA in patients with PSC who had incomplete response to UDCA monotherapy. Tretinoin 7-11 PSC Homo sapiens 109-112
23656719-14 2013 Moreover, FICZ in combination with RA also increases expression of AhR and even more so of both Cyp1A2 and p47phox, which are known to be transcriptionally regulated by AhR. Tretinoin 35-37 aryl hydrocarbon receptor Homo sapiens 67-70
23656719-14 2013 Moreover, FICZ in combination with RA also increases expression of AhR and even more so of both Cyp1A2 and p47phox, which are known to be transcriptionally regulated by AhR. Tretinoin 35-37 aryl hydrocarbon receptor Homo sapiens 169-172
23532884-3 2013 PRAME is an inhibitor of retinoic acid signaling, which may prove to be an important marker for retinoic acid response. Tretinoin 25-38 PRAME nuclear receptor transcriptional regulator Homo sapiens 0-5
27428727-12 2017 ATRA appears to inhibit bile acid synthesis and reduce markers of inflammation, making it a potential candidate for further study in PSC (NCT 01456468). Tretinoin 0-4 PSC Homo sapiens 133-136
23532884-3 2013 PRAME is an inhibitor of retinoic acid signaling, which may prove to be an important marker for retinoic acid response. Tretinoin 96-109 PRAME nuclear receptor transcriptional regulator Homo sapiens 0-5
27889377-6 2017 MiR-27b-3p mimics recapitulated the RA repression on DTNA expression, C2C12 proliferation and differentiation, while the miR-27b-3p inhibitor circumvented these defects resulting from excess RA. Tretinoin 36-38 microRNA 27b Mus musculus 0-7
23322377-0 2013 Retinoic acid promotes the development of Arg1-expressing dendritic cells for the regulation of T-cell differentiation. Tretinoin 0-13 arginase 1 Homo sapiens 42-46
23322377-4 2013 We report here that optimal expression of Arg1 in DCs requires retinoic acid. Tretinoin 63-76 arginase 1 Homo sapiens 42-46
23322377-5 2013 Induction of Arg1 by retinoic acid is directly mediated by retinoic acid-responsive elements in the 5" noncoding region of the Arg1 gene. Tretinoin 21-34 arginase 1 Homo sapiens 13-17
23322377-5 2013 Induction of Arg1 by retinoic acid is directly mediated by retinoic acid-responsive elements in the 5" noncoding region of the Arg1 gene. Tretinoin 21-34 arginase 1 Homo sapiens 127-131
23580485-0 2013 Retinoic acid promotes apoptosis and differentiation in photoreceptors by activating the P38 MAP kinase pathway. Tretinoin 0-13 mitogen activated protein kinase 14 Rattus norvegicus 89-92
23580485-7 2013 Addition of RA at day 0, but not at day 2, rapidly increased P-p38 levels, but did not affect P-ERK levels. Tretinoin 12-14 mitogen activated protein kinase 14 Rattus norvegicus 63-66
23580485-8 2013 p38 inhibition completely prevented RA-induced apoptosis, and partially decreased differentiation. Tretinoin 36-38 mitogen activated protein kinase 14 Rattus norvegicus 0-3
23322377-5 2013 Induction of Arg1 by retinoic acid is directly mediated by retinoic acid-responsive elements in the 5" noncoding region of the Arg1 gene. Tretinoin 59-72 arginase 1 Homo sapiens 13-17
27889377-8 2017 Therefore, these findings indicated that excess RA inhibited the myoblast proliferation and differentiation by up-regulating miR-27b-3p to target DTNA, which implied a new mechanism in myogenic hypoplasia. Tretinoin 48-50 microRNA 27b Mus musculus 125-132
23322377-5 2013 Induction of Arg1 by retinoic acid is directly mediated by retinoic acid-responsive elements in the 5" noncoding region of the Arg1 gene. Tretinoin 59-72 arginase 1 Homo sapiens 127-131
23322377-6 2013 Arg1, produced by DCs in response to retinoic acid, promotes the generation of FoxP3(+) regulatory T (Treg) cells. Tretinoin 37-50 arginase 1 Homo sapiens 0-4
28111553-6 2016 We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. Tretinoin 167-169 ameloblastin Mus musculus 58-70
23322377-6 2013 Arg1, produced by DCs in response to retinoic acid, promotes the generation of FoxP3(+) regulatory T (Treg) cells. Tretinoin 37-50 forkhead box P3 Homo sapiens 79-84
23322377-8 2013 We found that intestinal CD103(+) DCs that are known to produce retinoic acid highly express Arg1. Tretinoin 64-77 arginase 1 Homo sapiens 93-97
23322377-9 2013 Our results establish retinoic acid as a key signal in expression of Arg1 in DCs. Tretinoin 22-35 arginase 1 Homo sapiens 69-73
23580485-10 2013 CONCLUSIONS: Our results show that RA activation of the p38 intracellular pathway was essential for its early induction of apoptosis and partially responsible for promoting differentiation. Tretinoin 35-37 mitogen activated protein kinase 14 Rattus norvegicus 56-59
28111553-6 2016 We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. Tretinoin 167-169 ameloblastin Mus musculus 72-76
23546556-1 2013 The G0/G1 switch gene 2 (G0S2) is rapidly induced by all-trans-retinoic acid (RA)-treatment of acute promyelocytic leukemia (APL) and other cells. Tretinoin 53-76 G0/G1 switch 2 Homo sapiens 4-23
27306567-0 2017 Retinoic Acid Signaling in P19 Stem Cell Differentiation. Tretinoin 0-13 interleukin 23, alpha subunit p19 Mus musculus 27-30
23546556-1 2013 The G0/G1 switch gene 2 (G0S2) is rapidly induced by all-trans-retinoic acid (RA)-treatment of acute promyelocytic leukemia (APL) and other cells. Tretinoin 53-76 G0/G1 switch 2 Homo sapiens 25-29
23546556-1 2013 The G0/G1 switch gene 2 (G0S2) is rapidly induced by all-trans-retinoic acid (RA)-treatment of acute promyelocytic leukemia (APL) and other cells. Tretinoin 78-80 G0/G1 switch 2 Homo sapiens 4-23
23546556-1 2013 The G0/G1 switch gene 2 (G0S2) is rapidly induced by all-trans-retinoic acid (RA)-treatment of acute promyelocytic leukemia (APL) and other cells. Tretinoin 78-80 G0/G1 switch 2 Homo sapiens 25-29
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 cellular retinoic acid binding protein II Mus musculus 87-93
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 keratin 4 Mus musculus 95-99
23207146-9 2013 PDX-1/Hes-1 interactions on cell proliferation were determined by exposure to All-trans Retinoic Acid (At-RA), an inductor of Hes-1. Tretinoin 88-101 pancreatic and duodenal homeobox 1 Mus musculus 0-5
23207146-9 2013 PDX-1/Hes-1 interactions on cell proliferation were determined by exposure to All-trans Retinoic Acid (At-RA), an inductor of Hes-1. Tretinoin 88-101 hes family bHLH transcription factor 1 Mus musculus 6-11
23207146-9 2013 PDX-1/Hes-1 interactions on cell proliferation were determined by exposure to All-trans Retinoic Acid (At-RA), an inductor of Hes-1. Tretinoin 88-101 hes family bHLH transcription factor 1 Mus musculus 126-131
27306567-5 2017 P19 ES cells can differentiate to endodermal-like, mesodermal-like, and neuronal-like phenotypes in response to specific morphogens including RA and dimethyl sulfoxide (DMSO). Tretinoin 142-144 interleukin 23, alpha subunit p19 Mus musculus 0-3
23349206-6 2013 Concentrations of all-trans-retinoic acid were significantly lower in the livers of Lrat(-/-) mice following PHE, and this was accompanied by diminished expression of known retinoid-responsive genes. Tretinoin 21-41 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 84-88
23518499-8 2013 The regulation of the subcellular content of CDK1 and RARgamma by ATRA is an important process for achieving an effective response in treatment of leukemia. Tretinoin 66-70 retinoic acid receptor gamma Homo sapiens 54-62
27306567-6 2017 At low concentrations, RA directs P19 ES cells to differentiate into cells displaying an endodermal phenotype, whereas at higher concentrations it induces differentiation to neuroectoderm. Tretinoin 23-25 interleukin 23, alpha subunit p19 Mus musculus 34-37
23518499-11 2013 Our study reveals a novel mechanism by which CDK1 and RARgamma coordinate with ATRA to influence cell cycle progression and cellular differentiation. Tretinoin 79-83 retinoic acid receptor gamma Homo sapiens 54-62
27306567-10 2017 In addition to summarizing the reports on gene/protein targets of RA in stem cells, the signaling pathways driven by some of the specific class of proteins in the presence or absence of RA in P19 ES cell differentiation, especially to an endodermal phenotype, are the focus of this review. Tretinoin 186-188 interleukin 23, alpha subunit p19 Mus musculus 192-195
28910567-1 2017 G0/G1 switch gene 2 (G0S2) is a direct retinoic acid target implicated in cancer biology and therapy based on frequent methylation-mediated silencing in diverse solid tumors. Tretinoin 39-52 G0/G1 switch 2 Homo sapiens 0-19
21626648-0 2013 Retinoic acid influences the embryoid body formation in mouse embryonic stem cells by induction of caspase and p38 MAPK/JNK-mediated apoptosis. Tretinoin 0-13 mitogen-activated protein kinase 14 Mus musculus 111-114
23555298-6 2013 Differential analysis found networks mimicking developmental processes (activated all-trans-retinoic acid (ATRA, Z-score = 4.5; P = 6 x 10(-13)) and inhibited aryl-hydrocarbon receptor signaling (AhR, Z-score = -2.3; P = 3 x 10(-7))) with RET. Tretinoin 107-111 aryl hydrocarbon receptor Homo sapiens 159-184
23555298-6 2013 Differential analysis found networks mimicking developmental processes (activated all-trans-retinoic acid (ATRA, Z-score = 4.5; P = 6 x 10(-13)) and inhibited aryl-hydrocarbon receptor signaling (AhR, Z-score = -2.3; P = 3 x 10(-7))) with RET. Tretinoin 107-111 aryl hydrocarbon receptor Homo sapiens 196-199
23264745-0 2013 RARgamma is essential for retinoic acid induced chromatin remodeling and transcriptional activation in embryonic stem cells. Tretinoin 26-39 retinoic acid receptor gamma Homo sapiens 0-8
28910567-1 2017 G0/G1 switch gene 2 (G0S2) is a direct retinoic acid target implicated in cancer biology and therapy based on frequent methylation-mediated silencing in diverse solid tumors. Tretinoin 39-52 G0/G1 switch 2 Homo sapiens 21-25
23201577-6 2013 The enc1l expression in the KV region was specifically regulated by retinoic acid (RA), FGF, and Wnt signaling pathways. Tretinoin 68-81 ectodermal-neural cortex 3 Danio rerio 4-9
29017174-7 2017 RA also reduced citrate synthase, enzymatic mitochondrial complex II, ATP synthase, and enzymes of fatty acid metabolism and was associated with increased enzymes involved in glucose use. Tretinoin 0-2 citrate synthase Rattus norvegicus 16-32
23150428-7 2013 The increase in Cyp26a1 and Rarbeta mRNA during pregnancy indicates increased retinoic acid signaling in the liver during pregnancy. Tretinoin 78-91 retinoic acid receptor, beta Mus musculus 28-35
23150428-8 2013 A putative retinoic acid response element was identified within the Cyp2d40 promoter and the mRNA of Cyp2d40 correlated (P < 0.05) with Cyp26a1 and Rarbeta. Tretinoin 11-24 cytochrome P450, family 2, subfamily d, polypeptide 40 Mus musculus 68-75
23518351-0 2013 The histone demethylase PHF8 governs retinoic acid response in acute promyelocytic leukemia. Tretinoin 37-50 PHD finger protein 8 Homo sapiens 24-28
23518351-2 2013 We identified the histone demethylase PHF8 as a coactivator that is specifically recruited by RARalpha fusions to activate expression of their downstream targets upon ATRA treatment. Tretinoin 167-171 PHD finger protein 8 Homo sapiens 38-42
23518351-4 2013 ATRA sensitivity depends on the enzymatic activity and phosphorylation status of PHF8, which can be pharmacologically manipulated to resurrect ATRA sensitivity to resistant cells. Tretinoin 0-4 PHD finger protein 8 Homo sapiens 81-85
23150428-8 2013 A putative retinoic acid response element was identified within the Cyp2d40 promoter and the mRNA of Cyp2d40 correlated (P < 0.05) with Cyp26a1 and Rarbeta. Tretinoin 11-24 cytochrome P450, family 2, subfamily d, polypeptide 40 Mus musculus 101-108
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 49-51 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 84-91
23150428-8 2013 A putative retinoic acid response element was identified within the Cyp2d40 promoter and the mRNA of Cyp2d40 correlated (P < 0.05) with Cyp26a1 and Rarbeta. Tretinoin 11-24 retinoic acid receptor, beta Mus musculus 151-158
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 49-51 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 93-100
23193184-9 2013 Moreover, FEN induced RA-responsive genes in RALDH1 KO mice, demonstrating that FEN can augment RA signaling when RA synthesis is impaired. Tretinoin 22-24 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 45-51
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 49-51 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 129-135
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 49-51 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 137-143
23370279-2 2013 In this study, we show that RA is able to induce the intrinsic ability of breast cancer cells to recognize double-stranded RNA (dsRNA) through the upregulation of Toll-like receptor 3 (TLR3) expression. Tretinoin 28-30 toll like receptor 3 Homo sapiens 163-183
23370279-2 2013 In this study, we show that RA is able to induce the intrinsic ability of breast cancer cells to recognize double-stranded RNA (dsRNA) through the upregulation of Toll-like receptor 3 (TLR3) expression. Tretinoin 28-30 toll like receptor 3 Homo sapiens 185-189
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 197-199 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 84-91
27840061-2 2017 Loss-of-function studies using gene knockouts of RA-synthesizing enzymes encoded by Aldh1a1, Aldh1a2, and Aldh1a3 (also known as Raldh1, Raldh2, and Raldh3) have provided valuable insight into how RA controls eye morphogenesis including corneal development. Tretinoin 197-199 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 129-135
23885329-5 2013 We demonstrate that although ATRA alone has no effect on the expression or activities of arginase 1, ATRA can dramatically potentiate the induction of arginase 1 by IL-4. Tretinoin 101-105 arginase, liver Mus musculus 151-161
27840061-7 2017 Thus, Aldh1a1,2,3-flox/flox;Rosa26-CreERT2 mice provide a useful model for investigating the mechanistic role of RA signaling in adult corneal maintenance and could provide new insights into therapeutic approaches for controlling corneal repair to prevent vision loss. Tretinoin 113-115 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 6-13
28621427-9 2017 The effects of ADHFe1 manipulation can by rescued by increasing the levels of RA or its biosynthesis. Tretinoin 78-80 alcohol dehydrogenase, iron containing 1 S homeolog Xenopus laevis 15-21
28621427-14 2017 ADHFe1 probably reduces retinaldehyde to retinol thereby restricting the availability of retinaldehyde, the substrate needed by retinaldehyde dehydrogenases to produce RA making it a novel regulator of RA concentrations in the embryo and RA homeostasis. Tretinoin 168-170 alcohol dehydrogenase, iron containing 1 S homeolog Xenopus laevis 0-6
23125214-0 2013 Relaxant effect of all-trans-retinoic acid via NO-sGC-cGMP pathway and calcium-activated potassium channels in rat mesenteric artery. Tretinoin 19-42 guanylate cyclase 1 soluble subunit alpha 1 Rattus norvegicus 50-53
23202364-2 2013 We previously showed that mature heart valves calcify in response to retinoic acid (RA) treatment through downregulation of the SRY transcription factor Sox9. Tretinoin 69-82 SRY (sex determining region Y)-box 9 Mus musculus 153-157
28621427-14 2017 ADHFe1 probably reduces retinaldehyde to retinol thereby restricting the availability of retinaldehyde, the substrate needed by retinaldehyde dehydrogenases to produce RA making it a novel regulator of RA concentrations in the embryo and RA homeostasis. Tretinoin 202-204 alcohol dehydrogenase, iron containing 1 S homeolog Xenopus laevis 0-6
23202364-2 2013 We previously showed that mature heart valves calcify in response to retinoic acid (RA) treatment through downregulation of the SRY transcription factor Sox9. Tretinoin 84-86 SRY (sex determining region Y)-box 9 Mus musculus 153-157
23202364-6 2013 Using a pharmacological approach, we show that RA-mediated Sox9 repression and calcification is regulated by classical RA signaling and requires both RA and retinoid X receptors. Tretinoin 47-49 SRY (sex determining region Y)-box 9 Mus musculus 59-63
28621427-14 2017 ADHFe1 probably reduces retinaldehyde to retinol thereby restricting the availability of retinaldehyde, the substrate needed by retinaldehyde dehydrogenases to produce RA making it a novel regulator of RA concentrations in the embryo and RA homeostasis. Tretinoin 202-204 alcohol dehydrogenase, iron containing 1 S homeolog Xenopus laevis 0-6
22933113-2 2013 We investigated the role of retinoic acid (RA) production by aldehyde dehydrogenase 1 (Aldh1a1, -a2, and -a3), the major RA-producing enzymes, on sex-specific fat depot formation. Tretinoin 28-41 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 87-94
29911777-19 2017 Conclusion: The herbal extract cream is as effective as 0.1% tretinoin cream in the treatment of striae alba. Tretinoin 61-70 afamin Homo sapiens 104-108
22933113-2 2013 We investigated the role of retinoic acid (RA) production by aldehyde dehydrogenase 1 (Aldh1a1, -a2, and -a3), the major RA-producing enzymes, on sex-specific fat depot formation. Tretinoin 43-45 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 87-94
22933113-9 2013 Our data suggest that an HF diet mediates VF formation through a sex-specific autocrine Aldh1 switch, in which Rald-mediated lipolysis in Ucp1-positive visceral adipocytes is replaced by RA-mediated lipid accumulation. Tretinoin 187-189 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 88-93
23014973-8 2013 In view of these findings, RA likely stimulates osteoblast differentiation through the BMP2-Smad-Runx2/Msx2 pathway. Tretinoin 27-29 msh homeobox 2 Mus musculus 103-107
23077214-4 2013 Similarly, RA exposure or genetic loss of RA function via heterozygous mutation of the RA synthetic enzyme Raldh2 induces novel cranial anomalies and enhances cardiovascular phenotypes in LgDel but not other genotypes. Tretinoin 11-13 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 107-113
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 peroxisome proliferator activated receptor gamma Mus musculus 101-149
28798778-6 2017 Stimulation of the Activin/Nodal and BMP signaling cascades and inhibition of the MEK/ERK and PI3K/Act signaling pathways resulted in a significant decrease in the number of Oct4-expressing ES cells and a loss of tumorigenicity, similar to retinoic acid-stimulated EC cells. Tretinoin 240-253 midkine Mus musculus 82-85
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 peroxisome proliferator activated receptor gamma Mus musculus 151-160
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 195-206
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 peroxisome proliferator activated receptor gamma Mus musculus 288-297
23909735-0 2013 Vitamin D transport proteins megalin and disabled-2 are expressed in prostate and colon epithelial cells and are induced and activated by all-trans-retinoic acid. Tretinoin 138-161 LDL receptor related protein 2 Homo sapiens 29-36
23909735-0 2013 Vitamin D transport proteins megalin and disabled-2 are expressed in prostate and colon epithelial cells and are induced and activated by all-trans-retinoic acid. Tretinoin 138-161 DAB adaptor protein 2 Homo sapiens 41-51
23909735-4 2013 Moreover, induction of megalin and Dab2 (protein and mRNA abundance) by all-trans-retinoic acid (RA) enhanced DBP uptake. Tretinoin 72-95 LDL receptor related protein 2 Homo sapiens 23-30
23077214-4 2013 Similarly, RA exposure or genetic loss of RA function via heterozygous mutation of the RA synthetic enzyme Raldh2 induces novel cranial anomalies and enhances cardiovascular phenotypes in LgDel but not other genotypes. Tretinoin 42-44 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 107-113
22982089-3 2013 In this study, we have found that cellular retinoic acid binding protein I (CRABPI) mediates the non-canonical, RAR- and membrane signal-independent activation of ERK1/2 by atRA in various cellular backgrounds. Tretinoin 173-177 cellular retinoic acid binding protein 1 Homo sapiens 34-74
22982089-3 2013 In this study, we have found that cellular retinoic acid binding protein I (CRABPI) mediates the non-canonical, RAR- and membrane signal-independent activation of ERK1/2 by atRA in various cellular backgrounds. Tretinoin 173-177 cellular retinoic acid binding protein 1 Homo sapiens 76-82
23909735-4 2013 Moreover, induction of megalin and Dab2 (protein and mRNA abundance) by all-trans-retinoic acid (RA) enhanced DBP uptake. Tretinoin 72-95 DAB adaptor protein 2 Homo sapiens 35-39
23909735-4 2013 Moreover, induction of megalin and Dab2 (protein and mRNA abundance) by all-trans-retinoic acid (RA) enhanced DBP uptake. Tretinoin 97-99 LDL receptor related protein 2 Homo sapiens 23-30
27919568-0 2016 All-trans retinoic acid suppresses the adhering ability of ARPE-19 cells via mitogen-activated protein kinase and focal adhesion kinase. Tretinoin 10-23 protein tyrosine kinase 2 Homo sapiens 114-135
23909735-4 2013 Moreover, induction of megalin and Dab2 (protein and mRNA abundance) by all-trans-retinoic acid (RA) enhanced DBP uptake. Tretinoin 97-99 DAB adaptor protein 2 Homo sapiens 35-39
23178692-11 2013 The caspase assay demonstrated that the overexpression of GRIM-19 enhanced the cellular sensitivity to interferon(IFN)-beta- and retinoic acid (RA)-induced death in HeLa cells. Tretinoin 144-146 interferon beta 1 Homo sapiens 103-123
23909735-7 2013 Megalin and Dab2 were expressed in prostate and colon epithelial cells, which was markedly enhanced following treatment with RA. Tretinoin 125-127 LDL receptor related protein 2 Homo sapiens 0-7
23909735-7 2013 Megalin and Dab2 were expressed in prostate and colon epithelial cells, which was markedly enhanced following treatment with RA. Tretinoin 125-127 DAB adaptor protein 2 Homo sapiens 12-16
27919568-6 2016 Moreover, ATRA treatment did not affect intracellular F-actin distribution, but remarkably reduced focal adhesion kinase (FAK) expression and its nuclear localization during ARPE-19 cell attachment. Tretinoin 10-14 protein tyrosine kinase 2 Homo sapiens 99-120
27919568-6 2016 Moreover, ATRA treatment did not affect intracellular F-actin distribution, but remarkably reduced focal adhesion kinase (FAK) expression and its nuclear localization during ARPE-19 cell attachment. Tretinoin 10-14 protein tyrosine kinase 2 Homo sapiens 122-125
23554907-0 2013 The Src-family kinase inhibitor PP2 rescues inducible differentiation events in emergent retinoic acid-resistant myeloblastic leukemia cells. Tretinoin 89-102 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 32-35
27919568-7 2016 In conclusion, ATRA suppresses the adhering ability of ARPE-19 cells at least in part through MAPK and FAK pathways. Tretinoin 15-19 protein tyrosine kinase 2 Homo sapiens 103-106
23451132-3 2013 Here, we report that crosstalk between Oct4 and Meis1a, a Pbx-related homeobox protein, is required for neural differentiation of mouse P19 embryonic carcinoma (EC) cells induced by retinoic acid (RA). Tretinoin 182-195 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 39-43
27861498-5 2016 Temporal analyses indicate that RA is required for HSC gene expression prior to dorsal aorta formation, at a time when the predominant RA synthesis enzyme, aldh1a2, is strongly expressed within the paraxial mesoderm and somites. Tretinoin 32-34 aldehyde dehydrogenase 1 family, member A2 Danio rerio 156-163
23451132-3 2013 Here, we report that crosstalk between Oct4 and Meis1a, a Pbx-related homeobox protein, is required for neural differentiation of mouse P19 embryonic carcinoma (EC) cells induced by retinoic acid (RA). Tretinoin 197-199 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 39-43
23451132-4 2013 During neural differentiation, Oct4 expression was transiently enhanced during 6-12 h of RA addition and subsequently disappeared within 48 h. Coinciding with up-regulation of Oct4 expression, the induction of Meis1a expression was initiated and reached a plateau at 48 h, suggesting that transiently induced Oct4 activates Meis1a expression and the up-regulated Meis1a then suppresses Oct4 expression. Tretinoin 89-91 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 31-35
23451132-4 2013 During neural differentiation, Oct4 expression was transiently enhanced during 6-12 h of RA addition and subsequently disappeared within 48 h. Coinciding with up-regulation of Oct4 expression, the induction of Meis1a expression was initiated and reached a plateau at 48 h, suggesting that transiently induced Oct4 activates Meis1a expression and the up-regulated Meis1a then suppresses Oct4 expression. Tretinoin 89-91 Meis homeobox 1 Mus musculus 210-215
23457636-4 2013 In the present study, we show that during retinoic acid (RA)-induced differentiation of human ES cells, expression of STELLA follows that of VASA, a marker of germline differentiation. Tretinoin 42-55 developmental pluripotency associated 3 Homo sapiens 118-124
23505533-3 2013 The aim of this study was to evaluate the gene expression pattern of Irx1 and Irx2 as well as their regulation by important regulators of hindlimb development such as retinoic acid (RA), transforming growth factor beta (TGFbeta) and fibroblast growth factor (FGF) signaling during chick hindlimb development. Tretinoin 167-180 iroquois homeobox 2 Gallus gallus 78-82
27861498-5 2016 Temporal analyses indicate that RA is required for HSC gene expression prior to dorsal aorta formation, at a time when the predominant RA synthesis enzyme, aldh1a2, is strongly expressed within the paraxial mesoderm and somites. Tretinoin 135-137 aldehyde dehydrogenase 1 family, member A2 Danio rerio 156-163
23457636-4 2013 In the present study, we show that during retinoic acid (RA)-induced differentiation of human ES cells, expression of STELLA follows that of VASA, a marker of germline differentiation. Tretinoin 57-59 developmental pluripotency associated 3 Homo sapiens 118-124
27778276-4 2016 Foxp3 expression is increased by the activation of several transcription factors including nuclear factor-kappa B (NF-kappaB), nuclear factor of activated T cells (NFAT), and Smad3 in response to various signals such as TGFbeta, retinoic acid, and rapamycin. Tretinoin 229-242 forkhead box P3 Homo sapiens 0-5
23457636-6 2013 We found that over-expression of STELLA does not interfere with maintenance of the stem cell state of human ES cells, but following retinoic acid induction it leads to up-regulation of germline- and endodermal-associated genes, whereas neural markers PAX6 and NEUROD1 are down-regulated. Tretinoin 132-145 developmental pluripotency associated 3 Homo sapiens 33-39
23071109-9 2012 Interestingly, CYP3A7 and CYP2C8 preferentially formed (4S)-OH-RA from atRA. Tretinoin 71-75 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 26-32
23169621-3 2012 The mouse CMV MHC class I (MHC-I)-like m152/gp40 glycoprotein down-regulates retinoic acid early inducible-1 (RAE1) NKG2D ligands as well as host MHC-I. Tretinoin 77-90 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 116-121
27778276-4 2016 Foxp3 expression is increased by the activation of several transcription factors including nuclear factor-kappa B (NF-kappaB), nuclear factor of activated T cells (NFAT), and Smad3 in response to various signals such as TGFbeta, retinoic acid, and rapamycin. Tretinoin 229-242 SMAD family member 3 Homo sapiens 175-180
23053054-5 2012 The locations of the RA synthetic system (Aldh1a1, Aldh1a2, CRBP1) and catabolizing enzyme (Cyp26a1) were distinctive in the mouse uterus during the peri-implantation period. Tretinoin 21-23 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 42-49
27242163-3 2016 Immunocytochemistry was used to localize different components of RA signaling within sections of the retina and optic tectum, namely, the synthetic enzyme retinaldehyde dehydrogenase (RALDH), the RA binding proteins CRABPI and II, the retinoic acid receptors RARalpha, beta and gamma, and finally the catabolic enzyme CYP26A1. Tretinoin 65-67 cellular retinoic acid binding protein 1 Homo sapiens 216-222
23053054-5 2012 The locations of the RA synthetic system (Aldh1a1, Aldh1a2, CRBP1) and catabolizing enzyme (Cyp26a1) were distinctive in the mouse uterus during the peri-implantation period. Tretinoin 21-23 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 51-58
22998816-3 2012 When treated with neural induction medium containing Noggin/retinoic acid, the encapsulated cells expressed much higher levels of neural progenitor markers SOX1 and PAX6 than those in other treatment conditions. Tretinoin 60-73 paired box 6 Homo sapiens 165-169
27665842-8 2016 Meanwhile, staurosporine also enhanced ATRA-promoted upregulation of the protein level of CCAAT/enhancer-binding protein beta (C/EBPbeta) and C/EBPepsilon in U937 cells. Tretinoin 39-43 CCAAT enhancer binding protein beta Homo sapiens 90-125
23023919-6 2012 In conclusion, downregulation of the PHB gene may inhibit apoptosis of NB4-R1 cells, and it is speculated that this was at least partly due to the downregulation of caspase-3, and PHB may be a novel target for gene therapy for retinoic acid-resistant acute promyelocytic leukemia. Tretinoin 227-240 prohibitin 1 Homo sapiens 37-40
22686587-0 2012 Effect of all-trans retinoic acid (ATRA) on syndecan-1 expression and its chemoprotective effect in benzo(alpha)pyrene-induced lung cancer mice model. Tretinoin 10-33 syndecan 1 Mus musculus 44-54
22686587-0 2012 Effect of all-trans retinoic acid (ATRA) on syndecan-1 expression and its chemoprotective effect in benzo(alpha)pyrene-induced lung cancer mice model. Tretinoin 35-39 syndecan 1 Mus musculus 44-54
22686587-8 2012 Our study for syndecan-1 indicated a chemoprotective effect of ATRA against changes in lung epithelial cell membrane syndecan-1 expression in B(alpha)P-induced lung cancer model. Tretinoin 63-67 syndecan 1 Mus musculus 14-24
23023919-6 2012 In conclusion, downregulation of the PHB gene may inhibit apoptosis of NB4-R1 cells, and it is speculated that this was at least partly due to the downregulation of caspase-3, and PHB may be a novel target for gene therapy for retinoic acid-resistant acute promyelocytic leukemia. Tretinoin 227-240 prohibitin 1 Homo sapiens 180-183
23007396-10 2012 We show specific effects on the Wnt-catenin pathway and on members of the Runx, Fox, and Sox transcription factor families, indicating that RA modulates pathways and factors implicated in hf downgrowth and bending. Tretinoin 140-142 quiescin Q6 sulfhydryl oxidase 1 Mus musculus 89-92
22686587-8 2012 Our study for syndecan-1 indicated a chemoprotective effect of ATRA against changes in lung epithelial cell membrane syndecan-1 expression in B(alpha)P-induced lung cancer model. Tretinoin 63-67 syndecan 1 Mus musculus 117-127
27665842-8 2016 Meanwhile, staurosporine also enhanced ATRA-promoted upregulation of the protein level of CCAAT/enhancer-binding protein beta (C/EBPbeta) and C/EBPepsilon in U937 cells. Tretinoin 39-43 CCAAT enhancer binding protein beta Homo sapiens 127-143
27755557-4 2016 The activation of FGF and Retinoic Acid along with the inhibition of BMP, SHH and TGF-beta led to the generation of 75% NKX6.1+/NGN3+ Endocrine Progenitors. Tretinoin 26-39 NK6 homeobox 1 Homo sapiens 120-126
23155234-0 2012 DNA methylation in ATRA-treated leukemia cell lines lacking a PML-RAR chromosome translocation. Tretinoin 19-23 PML-RARA regulated adaptor molecule 1 Homo sapiens 62-69
23011767-5 2012 We later showed that ATA significantly enhanced the attachment of the retinoic acid differentiated P19 mouse embryonal carcinoma (P19) neurons, with an optimal concentration around 30 mug/mL. Tretinoin 70-83 interleukin 23, alpha subunit p19 Mus musculus 99-102
23011767-5 2012 We later showed that ATA significantly enhanced the attachment of the retinoic acid differentiated P19 mouse embryonal carcinoma (P19) neurons, with an optimal concentration around 30 mug/mL. Tretinoin 70-83 interleukin 23, alpha subunit p19 Mus musculus 130-133
23122963-0 2012 Transcriptional elongation factor elongin A regulates retinoic acid-induced gene expression during neuronal differentiation. Tretinoin 54-67 elongin A Homo sapiens 34-43
27166374-0 2016 Synergistic activation of Arg1 gene by retinoic acid and IL-4 involves chromatin remodeling for transcription initiation and elongation coupling. Tretinoin 39-52 arginase 1 Homo sapiens 26-30
23122963-5 2012 Moreover, we identify Elongin A mutations that selectively inactivate one or the other of the aforementioned activities and show that mutants that retain the elongation stimulatory, but not pol II ubiquitylation, activity of Elongin A rescue neuronal differentiation and support retinoic acid-induced upregulation of a subset of neurogenesis-related genes in Elongin A(-/-) ESCs. Tretinoin 279-292 elongin A Homo sapiens 22-31
23122963-5 2012 Moreover, we identify Elongin A mutations that selectively inactivate one or the other of the aforementioned activities and show that mutants that retain the elongation stimulatory, but not pol II ubiquitylation, activity of Elongin A rescue neuronal differentiation and support retinoic acid-induced upregulation of a subset of neurogenesis-related genes in Elongin A(-/-) ESCs. Tretinoin 279-292 elongin A Homo sapiens 225-234
27166374-4 2016 This involves feed forward regulation of Raldh2, a rate-limiting enzyme for RA biosynthesis, and requires Med25 to coordinate RAR, STAT6 and chromatin remodeler, Brg1 to remodel the +1 nucleosome of Arg1 for transcription initiation. Tretinoin 76-78 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 162-166
23122963-5 2012 Moreover, we identify Elongin A mutations that selectively inactivate one or the other of the aforementioned activities and show that mutants that retain the elongation stimulatory, but not pol II ubiquitylation, activity of Elongin A rescue neuronal differentiation and support retinoic acid-induced upregulation of a subset of neurogenesis-related genes in Elongin A(-/-) ESCs. Tretinoin 279-292 elongin A Homo sapiens 225-234
27166374-4 2016 This involves feed forward regulation of Raldh2, a rate-limiting enzyme for RA biosynthesis, and requires Med25 to coordinate RAR, STAT6 and chromatin remodeler, Brg1 to remodel the +1 nucleosome of Arg1 for transcription initiation. Tretinoin 76-78 arginase 1 Homo sapiens 199-203
22378018-5 2012 We found that ATRA was able to enhance the surface expression of AnxA1 and its receptor (FPR2/ALX) and the release of AnxA1-containing MPs from ATRA-NB4 cells, while the expression of annexin V was not elevated on the latter cells. Tretinoin 14-18 hematopoietic SH2 domain containing Homo sapiens 94-97
27166374-6 2016 This study uncovers synergistic activation of Arg1 by RA and IL-4 in M2 macrophages that involves feed forward regulation of RA synthesis and dual functions of Med25 in nucleosome remodeling and transcription initiation-elongation coupling that underlies robust modulatory activity of RA in innate immunity. Tretinoin 54-56 arginase 1 Homo sapiens 46-50
27166374-6 2016 This study uncovers synergistic activation of Arg1 by RA and IL-4 in M2 macrophages that involves feed forward regulation of RA synthesis and dual functions of Med25 in nucleosome remodeling and transcription initiation-elongation coupling that underlies robust modulatory activity of RA in innate immunity. Tretinoin 125-127 arginase 1 Homo sapiens 46-50
23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 nuclear receptor corepressor 2 Homo sapiens 66-70
27166374-6 2016 This study uncovers synergistic activation of Arg1 by RA and IL-4 in M2 macrophages that involves feed forward regulation of RA synthesis and dual functions of Med25 in nucleosome remodeling and transcription initiation-elongation coupling that underlies robust modulatory activity of RA in innate immunity. Tretinoin 125-127 arginase 1 Homo sapiens 46-50
23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 nuclear receptor corepressor 2 Homo sapiens 87-108
23015261-1 2012 Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), also known as nuclear corepressor 2 (NCOR2) is a transcriptional corepressor for multiple members of the nuclear receptor superfamily of transcription factors, including estrogen receptor-alpha (ERalpha). Tretinoin 22-35 nuclear receptor corepressor 2 Homo sapiens 110-115
22888005-2 2012 In this study, we found that CaMKII induced by Wnt5a remarkably reduced the protein stability of the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT), a co-repressor of Notch signaling, through proteasomal degradation. Tretinoin 123-136 calcium/calmodulin dependent protein kinase II gamma Homo sapiens 29-35
27089940-4 2016 We found that RA had a dramatic suppressive effect on IL-17A and IL-17F production by gammadelta T cells stimulated with IL-1beta and IL-23. Tretinoin 14-16 interleukin 23, alpha subunit p19 Mus musculus 134-139
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 cyclin-dependent kinase inhibitor 1A Rattus norvegicus 73-77
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 cyclin-dependent kinase inhibitor 1A Rattus norvegicus 78-82
22344541-10 2012 CONCLUSION: ATRA inhibited TGF-beta(1)-induced mesangial cell proliferation by up-regulating p21(Waf1/Cip1) mRNA and protein levels, and p27(Kip1) protein level, and down-regulating Skp2 mRNA and protein levels, but it had no significant effect on apoptosis in rat mesangial cells. Tretinoin 12-16 cyclin-dependent kinase inhibitor 1A Rattus norvegicus 97-101
22344541-10 2012 CONCLUSION: ATRA inhibited TGF-beta(1)-induced mesangial cell proliferation by up-regulating p21(Waf1/Cip1) mRNA and protein levels, and p27(Kip1) protein level, and down-regulating Skp2 mRNA and protein levels, but it had no significant effect on apoptosis in rat mesangial cells. Tretinoin 12-16 cyclin-dependent kinase inhibitor 1A Rattus norvegicus 102-106
22945948-9 2012 RBP1, important in retinoic acid metabolism, was found to be hypermethylated in 76 of 79 IDH1 MUT, 3 of 3 IDH2 MUT, and 0 of 116 IDH1/IDH2 WT tumors. Tretinoin 19-32 retinol binding protein 1 Homo sapiens 0-4
22945948-14 2012 Because RBP1 is involved in retinoic acid synthesis, our results suggest that dysregulation of retinoic acid metabolism may contribute to glioma formation along the IDH1/IDH2-mutant pathway. Tretinoin 28-41 retinol binding protein 1 Homo sapiens 8-12
22945948-14 2012 Because RBP1 is involved in retinoic acid synthesis, our results suggest that dysregulation of retinoic acid metabolism may contribute to glioma formation along the IDH1/IDH2-mutant pathway. Tretinoin 95-108 retinol binding protein 1 Homo sapiens 8-12
27595139-5 2016 In the mouse model of allergic eye disease (AED), classical CD11b+ DCs in the ocular mucosa showed increased activity of aldehyde dehydrogenase (ALDH), the enzyme required for retinoic acid synthesis. Tretinoin 176-189 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 145-149
26281901-9 2016 Treatment with retinoic acid, a CCN1 inhibitor, inhibited UV-induced CCN1 promoter activity. Tretinoin 15-28 cyclin A2 Mus musculus 32-36
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 0-23 toll like receptor 3 Homo sapiens 100-120
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 0-23 toll like receptor 3 Homo sapiens 122-126
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 0-23 toll like receptor 3 Homo sapiens 169-173
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 25-29 toll like receptor 3 Homo sapiens 100-120
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 25-29 toll like receptor 3 Homo sapiens 122-126
23335538-5 2012 Contrary to this, RA treatment increased the expression of inhibitory KIR CD158b. Tretinoin 18-20 killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4 Homo sapiens 70-73
26281901-9 2016 Treatment with retinoic acid, a CCN1 inhibitor, inhibited UV-induced CCN1 promoter activity. Tretinoin 15-28 cyclin A2 Mus musculus 69-73
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 25-29 toll like receptor 3 Homo sapiens 169-173
22797253-5 2012 Furthermore, the supernatants of ATRA+polyI:C-activated cultures increased the migration of both human monocyte-derived macrophages and CD1a dendritic cells significantly as compared with the supernatants of cells treated with either ATRA or polyI:C, and this effect occurred in a TLR3-dependent manner. Tretinoin 33-37 CD1a molecule Homo sapiens 136-140
22548301-11 2012 Functional interactions between RA and FGF rather take place at the level of the transcriptional regulation of mkp3, indicating that RA may antagonise FGF signalling at the level of the extracellular signal-regulated kinase (Erk) pathway. Tretinoin 32-34 mitogen-activated protein kinase 1 S homeolog Xenopus laevis 225-228
22797253-5 2012 Furthermore, the supernatants of ATRA+polyI:C-activated cultures increased the migration of both human monocyte-derived macrophages and CD1a dendritic cells significantly as compared with the supernatants of cells treated with either ATRA or polyI:C, and this effect occurred in a TLR3-dependent manner. Tretinoin 33-37 toll like receptor 3 Homo sapiens 281-285
22548301-11 2012 Functional interactions between RA and FGF rather take place at the level of the transcriptional regulation of mkp3, indicating that RA may antagonise FGF signalling at the level of the extracellular signal-regulated kinase (Erk) pathway. Tretinoin 133-135 mitogen-activated protein kinase 1 S homeolog Xenopus laevis 186-223
27256846-0 2016 The BRPF2/BRD1-MOZ complex is involved in retinoic acid-induced differentiation of embryonic stem cells. Tretinoin 42-55 bromodomain containing 1 Mus musculus 10-14
22548301-11 2012 Functional interactions between RA and FGF rather take place at the level of the transcriptional regulation of mkp3, indicating that RA may antagonise FGF signalling at the level of the extracellular signal-regulated kinase (Erk) pathway. Tretinoin 133-135 mitogen-activated protein kinase 1 S homeolog Xenopus laevis 225-228
23103284-0 2012 TLR9-signaling is required for turning retinoic acid into a potent stimulator of RP105 (CD180)-mediated proliferation and IgG synthesis in human memory B cells. Tretinoin 39-52 toll like receptor 9 Homo sapiens 0-4
22797253-6 2012 In conclusion, consecutive treatment with ATRA and polyI:C results in strong, TLR3/MDA5-mediated chemokine and IFN responses in cultured human melanoma cells, which triggers a functional migratory response in professional antigen-presenting cells. Tretinoin 42-46 toll like receptor 3 Homo sapiens 78-82
22580571-8 2012 However, the gene encoding for retinal dehydrogenase (RALDH2), responsible for retinoic acid synthesis, was downregulated in the eyes. Tretinoin 79-92 aldehyde dehydrogenase 1 family, member A2 Danio rerio 54-60
23103284-5 2012 However, co-stimulation with the TLR9-ligand CpG results in turning RA into a potent stimulator of RP105-induced proliferation and IgG synthesis in memory B cells. Tretinoin 68-70 toll like receptor 9 Homo sapiens 33-37
27460990-3 2016 We found that disruption of Syx, a gene encoding a RhoA-specific guanine nucleotide exchange factor, accelerated retinoic acid-induced neural differentiation in murine embryonic stem cells aggregated into embryoid bodies. Tretinoin 113-126 ras homolog family member A Mus musculus 51-55
23135655-0 2012 Adjunctive use of a facial moisturizer SPF 30 containing ceramide precursor improves tolerability of topical tretinoin 0.05%: a randomized, investigator-blinded, split-face study. Tretinoin 109-118 survival motor neuron domain containing 1 Homo sapiens 39-45
22828480-6 2012 Although treatment with l-isoproterenol alone did not affect the expression of Nestin (a specific marker for neural progenitor cells), l-isoproterenol significantly enhanced ATRA-induced Nestin expression. Tretinoin 174-178 nestin Mus musculus 187-193
22828480-8 2012 In addition, the l-isoproterenol treatment significantly enhanced ATRA-induced expression of NeuN (a neuron-specific nuclear protein). Tretinoin 66-70 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 93-97
22828480-8 2012 In addition, the l-isoproterenol treatment significantly enhanced ATRA-induced expression of NeuN (a neuron-specific nuclear protein). Tretinoin 66-70 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 101-132
23135655-1 2012 OBJECTIVES: To assess the benefit of adjunctive use of a SPF 30 moisturizing lotion in reducing local side effects associated with atopical tretinoin cream. Tretinoin 140-149 survival motor neuron domain containing 1 Homo sapiens 57-63
27435798-0 2016 Corrigendum: All trans-retinoic acid analogs promote cancer cell apoptosis through non-genomic Crabp1 mediating ERK1/2 phosphorylation. Tretinoin 17-36 cellular retinoic acid binding protein 1 Homo sapiens 95-101
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 78-91 protein kinase C delta Homo sapiens 166-174
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 93-97 protein kinase C delta Homo sapiens 166-174
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 228-232 protein kinase C delta Homo sapiens 166-174
22658364-3 2012 As a CRABP-II-recognizing moiety, all-trans retinoic acid (ATRA, 3), a physiological ligand of CRABP, was chosen. Tretinoin 44-57 cellular retinoic acid binding protein 1 Homo sapiens 5-10
27130522-0 2016 Retinoic acid induces nuclear FAK translocation and reduces breast cancer cell adhesion through Moesin, FAK, and Paxillin. Tretinoin 0-13 protein tyrosine kinase 2 Homo sapiens 30-33
22658364-3 2012 As a CRABP-II-recognizing moiety, all-trans retinoic acid (ATRA, 3), a physiological ligand of CRABP, was chosen. Tretinoin 59-63 cellular retinoic acid binding protein 1 Homo sapiens 5-10
27130522-0 2016 Retinoic acid induces nuclear FAK translocation and reduces breast cancer cell adhesion through Moesin, FAK, and Paxillin. Tretinoin 0-13 protein tyrosine kinase 2 Homo sapiens 104-107
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 44-57 protein tyrosine kinase 2 Homo sapiens 263-266
23017457-8 2012 However, the phenotype of defected hindbrain in VAD embryos was not as severe as that in the embryos in which aldh1a2, the major gene that is responsible for RA synthesis in zebrafish early development, was knocked down, or the embryos treated with 10 mmol/L DEAB (diethylaminobenzaldehyde, inhibitor of retinal dehydrogenases). Tretinoin 158-160 aldehyde dehydrogenase 1 family, member A2 Danio rerio 110-117
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 59-61 protein tyrosine kinase 2 Homo sapiens 263-266
27130522-4 2016 Here we identify that the administration of 10(-6) M RA (10-20 min) induces the activation of the migration-related proteins Moesin, FAK, and Paxillin in T-47D breast cancer cells. Tretinoin 53-55 protein tyrosine kinase 2 Homo sapiens 133-136
27406002-4 2016 Our data support a model in which RA on the dorsal side of the embryo induces anterior kidney fates while posterior kidney progenitors are protected ventrally by the RA-catabolizing enzyme Cyp26a1. Tretinoin 166-168 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 189-196
22687751-3 2012 Expression of Pod1 and WT1, but not Tbx18 or NFATC1, is activated with all-trans-retinoic acid (RA) treatment of isolated chick EPDCs in culture. Tretinoin 71-94 Wilms tumor 1 Gallus gallus 23-26
22687751-3 2012 Expression of Pod1 and WT1, but not Tbx18 or NFATC1, is activated with all-trans-retinoic acid (RA) treatment of isolated chick EPDCs in culture. Tretinoin 96-98 Wilms tumor 1 Gallus gallus 23-26
22214285-8 2012 Lumbar cells express high levels of Cyp26b1 and low levels of the RA-synthesizing enzyme retinaldehyde dehydrogenase Raldh2, resulting in limited activation of the RA signaling pathway in these cells. Tretinoin 66-68 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 117-123
22214285-8 2012 Lumbar cells express high levels of Cyp26b1 and low levels of the RA-synthesizing enzyme retinaldehyde dehydrogenase Raldh2, resulting in limited activation of the RA signaling pathway in these cells. Tretinoin 164-166 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 117-123
22592974-0 2012 New sources of retinoic acid synthesis revealed by live imaging of an Aldh1a2-GFP reporter fusion protein throughout zebrafish development. Tretinoin 15-28 aldehyde dehydrogenase 1 family, member A2 Danio rerio 70-77
22592974-2 2012 During embryonic patterning, the dynamic expression patterns of the aldh1a2 gene, which encodes a retinaldehyde dehydrogenase, provide the major source of RA, whereas the only other retinaldehyde dehydrogenase in teleosts, aldh1a3, is expressed later and locally restricted. Tretinoin 155-157 aldehyde dehydrogenase 1 family, member A2 Danio rerio 68-75
22592974-3 2012 Aldh1a2-mediated RA synthesis has been shown to also regulate adult cell fates, such as during heart and fin regeneration. Tretinoin 17-19 aldehyde dehydrogenase 1 family, member A2 Danio rerio 0-7
22592974-8 2012 CONCLUSIONS: The novel aldh1a2 reporter line is driven by the complete set of regulatory sequences required for zebrafish development, reports novel sources of RA synthesis, and identifies the source of RA that promotes vertebral ossification. Tretinoin 160-162 aldehyde dehydrogenase 1 family, member A2 Danio rerio 23-30
22592974-8 2012 CONCLUSIONS: The novel aldh1a2 reporter line is driven by the complete set of regulatory sequences required for zebrafish development, reports novel sources of RA synthesis, and identifies the source of RA that promotes vertebral ossification. Tretinoin 203-205 aldehyde dehydrogenase 1 family, member A2 Danio rerio 23-30
27251091-7 2016 Further, retinoic acid downregulated the expression of Cnnm1 in GC1-spg cells. Tretinoin 9-22 cyclin M1 Mus musculus 55-60
22407764-4 2012 Conversely, in SH-SY5Y cells, a paradigm of RA-dependent differentiation, abrogation of BRG1 prevented the response to RA. Tretinoin 44-46 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 88-92
22407764-4 2012 Conversely, in SH-SY5Y cells, a paradigm of RA-dependent differentiation, abrogation of BRG1 prevented the response to RA. Tretinoin 119-121 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 88-92
22407764-5 2012 Further, our data suggest an antagonistic functional connection between BRG1 and MYC, whereby, refractoriness to RA and GC by BRG1 inactivation involves deregulation of MYC activity. Tretinoin 113-115 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 72-76
22407764-5 2012 Further, our data suggest an antagonistic functional connection between BRG1 and MYC, whereby, refractoriness to RA and GC by BRG1 inactivation involves deregulation of MYC activity. Tretinoin 113-115 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Homo sapiens 126-130
22707713-8 2012 LFA-1/ICAM-1-stimulated human and mouse T-cells were refractory to TGF-beta-mediated induction of FOXP3(+) (forkhead box P3) and RORgammat(+) (retinoic acid-related orphan nuclear receptor gammat) Th17 differentiation. Tretinoin 143-156 integrin subunit alpha L Homo sapiens 0-5
22707713-8 2012 LFA-1/ICAM-1-stimulated human and mouse T-cells were refractory to TGF-beta-mediated induction of FOXP3(+) (forkhead box P3) and RORgammat(+) (retinoic acid-related orphan nuclear receptor gammat) Th17 differentiation. Tretinoin 143-156 transforming growth factor, beta 1 Mus musculus 67-75
22614916-5 2012 Upregulated Rap1GAP in NB4 and HL-60 cells promoted cell differentiation induced by ATRA or TPA compared to the empty vector control cells. Tretinoin 96-100 RAP1 GTPase activating protein Homo sapiens 12-19
26868909-6 2016 Finally, we demonstrate that the effect of ATRA on miR-17-92 expression is mediated through its target, transcription factor C/EBPbeta, which interacts with the intronic promoter of the miR-17-92 gene to inhibit transactivation of the cluster. Tretinoin 43-47 CCAAT enhancer binding protein beta Homo sapiens 125-134
22426954-8 2012 The impact of rIL-33 on CD103+ DC induction was the result of indirectly upregulating intestine epithelial cells that produce thymic stromal lymphopoietin and retinoic acid but do not directly act on DCs. Tretinoin 159-172 interleukin 33 Rattus norvegicus 14-20
22056876-3 2012 In addition to these classical genomic effects, we recently demonstrated that RA also induces the rapid activation of the p38MAPK/MSK1 pathway, with characteristic downstream consequences on the phosphorylation of RARs and the expression of their target genes. Tretinoin 78-80 ribosomal protein S6 kinase A5 Homo sapiens 130-134
22472775-4 2012 The tolerogenic features of these subsets are associated with increased production of retinoic acid, which leads to the enhanced induction of Foxp3+ regulatory T cells compared with CD8alpha-beta- pDCs. Tretinoin 86-99 CD8 antigen, alpha chain Mus musculus 182-190
22261335-4 2012 S1P treatment or transient co-transfection with SphK2 expression vector antagonized ATRA-induced RARbeta promoter activity. Tretinoin 84-88 sphingosine kinase 2 Homo sapiens 48-53
22451680-7 2012 Interestingly, GATA-2 was also decreased with ATRA treatment, and experiments using its expression vector and siRNA and chromatin immunoprecipitation assay demonstrated GATA-2 acted as transcription-factor of NCDase gene expression. Tretinoin 46-50 GATA binding protein 2 Homo sapiens 15-21
22451680-7 2012 Interestingly, GATA-2 was also decreased with ATRA treatment, and experiments using its expression vector and siRNA and chromatin immunoprecipitation assay demonstrated GATA-2 acted as transcription-factor of NCDase gene expression. Tretinoin 46-50 GATA binding protein 2 Homo sapiens 169-175
21938722-6 2012 In addition, the targeting of p300 in combination with a differential enrichment of Brm to Brg1 change at the distal promoter region of the gene is induced under RA treatment. Tretinoin 162-164 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Mus musculus 91-95
22352986-10 2012 Finally, we found that RA signals affected the expression of NR1 do not directly through transcriptional regulation. Tretinoin 23-25 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 61-64
22475041-8 2012 In this context, we review the published reports and draw a hypothesis that: (i) The distributions of RARs isoforms are different in different cells; (ii) ATRA activates the different RARs isoforms in different cells; (iii) The roles of different RARs isoforms for regulating the expression of MMP-2 or MMP-9 are different in different cells. Tretinoin 155-159 matrix metallopeptidase 2 Homo sapiens 294-299
21735106-6 2012 We treated hESCs with retinoic acid (RA) and found an enhancement of skeletal myogenesis, and the expression of the myogenic regulatory factors (MRFs) MyoD and myogenin by day 25. Tretinoin 22-35 myogenin Homo sapiens 160-168
22447870-11 2012 RA dose-dependently increased microRNA-328 expression and, in turn, suppressed PAX6 expression. Tretinoin 0-2 paired box 6 Homo sapiens 79-83
22569366-2 2012 Here we use the mammalian Hoxa cluster of developmental genes as a model system to follow changes in DNA modification patterns during retinoic acid-induced differentiation. Tretinoin 134-147 homeobox A cluster Homo sapiens 26-30
22339500-7 2012 Treatment with RA (retinoic acid) triggers NCCIT cell differentiation, reducing NANOG and OCT4 expression and up-regulating several neural markers [i.e. ASCL1 (achaete-scute complex homologue 1), NEUROD1 (neuronal differentiation 1) and PAX6 (paired box 6)]. Tretinoin 19-32 achaete-scute family bHLH transcription factor 1 Homo sapiens 153-158
22339500-7 2012 Treatment with RA (retinoic acid) triggers NCCIT cell differentiation, reducing NANOG and OCT4 expression and up-regulating several neural markers [i.e. ASCL1 (achaete-scute complex homologue 1), NEUROD1 (neuronal differentiation 1) and PAX6 (paired box 6)]. Tretinoin 19-32 achaete-scute family bHLH transcription factor 1 Homo sapiens 160-193
22339500-7 2012 Treatment with RA (retinoic acid) triggers NCCIT cell differentiation, reducing NANOG and OCT4 expression and up-regulating several neural markers [i.e. ASCL1 (achaete-scute complex homologue 1), NEUROD1 (neuronal differentiation 1) and PAX6 (paired box 6)]. Tretinoin 19-32 paired box 6 Homo sapiens 237-241
24130925-7 2012 Matrix metalloproteinase-9 (MMP-9) and MMP-2, well known genes involved in invasion of cancer cells were induced in the ATRA-induced invasion of the SH-SH5Y cells. Tretinoin 120-124 matrix metallopeptidase 2 Homo sapiens 39-44
24130925-8 2012 Treatment of CTM suppressed the MMP-9 and MMP-2 enzyme activities in the ATRA-induced invasion of the SH-SY5Y cells. Tretinoin 73-77 matrix metallopeptidase 2 Homo sapiens 42-47
22387209-5 2012 We documented the expression of gene-encoding enzymes that produce retinoic acid (Raldh2) and enzymes that degrade it (Cyp26a1, Cyp26b1). Tretinoin 67-80 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 82-88
22396202-5 2012 In this study, we show that RA inhibits adipocyte differentiation by activating the CRABP-II/RARgamma path in preadipose cells, thereby upregulating the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2). Tretinoin 28-30 cellular retinoic acid binding protein II Mus musculus 84-92
22396202-5 2012 In this study, we show that RA inhibits adipocyte differentiation by activating the CRABP-II/RARgamma path in preadipose cells, thereby upregulating the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2). Tretinoin 28-30 delta like non-canonical Notch ligand 1 Mus musculus 195-201
22537161-0 2012 Nicotine, IFN-gamma and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades. Tretinoin 24-37 mucin 4, cell surface associated Homo sapiens 60-64
22306363-0 2012 Retinoic acid increases hypoxia-inducible factor-1alpha through intracrine prostaglandin E(2) signaling in human renal proximal tubular cells HK-2. Tretinoin 0-13 hexokinase 2 Homo sapiens 142-146
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 44-48 hexokinase 2 Homo sapiens 28-32
22306363-1 2012 We have previously shown in HK-2 cells that ATRA (all-trans-retinoic acid) up-regulates HIF-1alpha (hypoxia-inducible factor-1alpha) in normoxia, which results in increased production of renal protector VEGF-A (vascular endothelial growth factor-A). Tretinoin 50-73 hexokinase 2 Homo sapiens 28-32
22334445-0 2012 A novel method for retinoic acid administration reveals differential and dose-dependent downregulation of Fgf3 in the developing inner ear and anterior CNS. Tretinoin 19-32 fibroblast growth factor 3 Mus musculus 106-110
22334445-4 2012 We use this delivery system to examine the role of retinoic acid in regulating the expression of the fibroblast growth factor Fgf3, and find that the timing of retinoic acid treatment is critical for its effects on Fgf3 expression. Tretinoin 51-64 fibroblast growth factor 3 Mus musculus 126-130
22334445-4 2012 We use this delivery system to examine the role of retinoic acid in regulating the expression of the fibroblast growth factor Fgf3, and find that the timing of retinoic acid treatment is critical for its effects on Fgf3 expression. Tretinoin 160-173 fibroblast growth factor 3 Mus musculus 126-130
22334445-4 2012 We use this delivery system to examine the role of retinoic acid in regulating the expression of the fibroblast growth factor Fgf3, and find that the timing of retinoic acid treatment is critical for its effects on Fgf3 expression. Tretinoin 160-173 fibroblast growth factor 3 Mus musculus 215-219
22334445-5 2012 Administration of increasing amounts of retinoic acid at 7.75 dpc leads to dose-dependent downregulation of Fgf3 in the otocyst and changes in spatial expression in the hindbrain. Tretinoin 40-53 fibroblast growth factor 3 Mus musculus 108-112
22334445-6 2012 Detailed analysis of the developing inner ear also reveals a lateralisation of Fgf3 expression with increasing retinoic acid dose that is dependent on timing of administration. Tretinoin 111-124 fibroblast growth factor 3 Mus musculus 79-83
22116806-2 2012 The miRNA expression profiles of THY1(+)-enriched undifferentiated spermatogonia were characterized, and members of Mir-17-92 (Mirc1) and its paralog Mir-106b-25 (Mirc3) clusters are significantly downregulated during retinoic acid-induced spermatogonial differentiation, both in vitro and in vivo. Tretinoin 218-231 Mir17 host gene (non-protein coding) Mus musculus 116-125
22116806-3 2012 The repression of microRNA clusters Mir-17-92 (Mirc1) and Mir-106b-25 (Mirc3) by retinoic acid in turn potentially upregulates the expression of Bim, Kit, Socs3, and Stat3. Tretinoin 81-94 Mir17 host gene (non-protein coding) Mus musculus 36-45
22250783-15 2012 ATRA may ease the bleomycin-induced pulmonary fibrosis by inhibiting the expression of IL-6 and TGF-beta, shifting the Treg/Th17 ratio and reducing the secretion of IL-17A. Tretinoin 0-4 transforming growth factor, beta 1 Mus musculus 96-104
22284617-6 2012 Accordingly, such studies were used in selecting the optimal dose for RA using PVC and PIC to islet-1 and oligo-2. Tretinoin 70-72 oligodendrocyte transcription factor 2 Homo sapiens 106-113
22555438-2 2012 Retinoid metabolism is tightly controlled by an enzymatic network in which retinaldehyde dehydrogenases (Aldh1-3) are the rate-limiting enzymes that convert retinaldehyde to retinoic acid. Tretinoin 174-187 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 105-110
22659417-4 2012 In addition, LMP1 suppressed ATRA-mediated activation of Caspase 9, Caspase 3, and PARP but not Caspase 8 in Ad-AH cells, suggesting that LMP1 acts by blocking the activation of intrinsic apoptosis pathway by ATRA. Tretinoin 29-33 collagen type XI alpha 2 chain Homo sapiens 83-87
22573621-0 2012 Retinoic acid-driven Hox1 is required in the epidermis for forming the otic/atrial placodes during ascidian metamorphosis. Tretinoin 0-13 homeobox transcription factor Hox1 Ciona intestinalis 21-25
22573621-1 2012 Retinoic acid (RA)-mediated expression of the homeobox gene Hox1 is a hallmark of the chordate central nervous system (CNS). Tretinoin 0-13 homeobox transcription factor Hox1 Ciona intestinalis 60-64
22573621-1 2012 Retinoic acid (RA)-mediated expression of the homeobox gene Hox1 is a hallmark of the chordate central nervous system (CNS). Tretinoin 15-17 homeobox transcription factor Hox1 Ciona intestinalis 60-64
22573621-5 2012 As previous studies showed that RA directly upregulates Hox1 in the epidermis of Ciona larvae, we also examined the role of RA in ASP formation. Tretinoin 32-34 homeobox transcription factor Hox1 Ciona intestinalis 56-60
22573621-6 2012 We showed that abolishment of RA resulted in loss of the ASP, which could be rescued by forced expression of Hox1 in the epidermis. Tretinoin 30-32 homeobox transcription factor Hox1 Ciona intestinalis 109-113
22619388-7 2012 Exploration of signaling parameters in our models suggests that the ability of Crabp2a to transport RA to Cyp26 enzymes for degradation is a major factor in promoting robustness. Tretinoin 100-102 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 106-111
22182854-0 2012 Src inhibitors, PP2 and dasatinib, increase retinoic acid-induced association of Lyn and c-Raf (S259) and enhance MAPK-dependent differentiation of myeloid leukemia cells. Tretinoin 44-57 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 16-19
22182854-0 2012 Src inhibitors, PP2 and dasatinib, increase retinoic acid-induced association of Lyn and c-Raf (S259) and enhance MAPK-dependent differentiation of myeloid leukemia cells. Tretinoin 44-57 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 89-94
22182854-6 2012 PP2 and dasatinib increased the ATRA-induced expression of Lyn and c-Raf (total and c-RafpS259) and their interaction. Tretinoin 32-36 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 0-3
22182854-6 2012 PP2 and dasatinib increased the ATRA-induced expression of Lyn and c-Raf (total and c-RafpS259) and their interaction. Tretinoin 32-36 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 67-72
22182854-6 2012 PP2 and dasatinib increased the ATRA-induced expression of Lyn and c-Raf (total and c-RafpS259) and their interaction. Tretinoin 32-36 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 84-94
22498432-8 2012 Cell death was not evident in short forelimb, and ATRA inhibited the expression of Ccnb1 and Ccna1, thus retarding chondrocyte maturation. Tretinoin 50-54 cyclin B1 Mus musculus 83-88
22500549-6 2012 The sensitivity of the method is demonstrated using retinoic acid (RA) transfer from various isoforms of cellular RA binding proteins (CRABPs) and RA receptor gamma (RARgamma). Tretinoin 52-65 retinoic acid receptor gamma Homo sapiens 166-174
22500549-6 2012 The sensitivity of the method is demonstrated using retinoic acid (RA) transfer from various isoforms of cellular RA binding proteins (CRABPs) and RA receptor gamma (RARgamma). Tretinoin 67-69 retinoic acid receptor gamma Homo sapiens 147-164
22500549-6 2012 The sensitivity of the method is demonstrated using retinoic acid (RA) transfer from various isoforms of cellular RA binding proteins (CRABPs) and RA receptor gamma (RARgamma). Tretinoin 67-69 retinoic acid receptor gamma Homo sapiens 166-174
22525672-1 2012 F9 embryonic carcinoma (EC) cells undergo extra-embryonic endodermal (ExE) differentiation in response to retinoic acid (RA) treatment, which induces the expression of two isoforms (p96 and p67) of the adaptor protein, Disabled-2 (Dab2). Tretinoin 106-119 DAB adaptor protein 2 Homo sapiens 219-229
22525672-1 2012 F9 embryonic carcinoma (EC) cells undergo extra-embryonic endodermal (ExE) differentiation in response to retinoic acid (RA) treatment, which induces the expression of two isoforms (p96 and p67) of the adaptor protein, Disabled-2 (Dab2). Tretinoin 106-119 DAB adaptor protein 2 Homo sapiens 231-235
22525672-1 2012 F9 embryonic carcinoma (EC) cells undergo extra-embryonic endodermal (ExE) differentiation in response to retinoic acid (RA) treatment, which induces the expression of two isoforms (p96 and p67) of the adaptor protein, Disabled-2 (Dab2). Tretinoin 121-123 DAB adaptor protein 2 Homo sapiens 219-229
22525672-1 2012 F9 embryonic carcinoma (EC) cells undergo extra-embryonic endodermal (ExE) differentiation in response to retinoic acid (RA) treatment, which induces the expression of two isoforms (p96 and p67) of the adaptor protein, Disabled-2 (Dab2). Tretinoin 121-123 DAB adaptor protein 2 Homo sapiens 231-235
22525672-3 2012 During the RA-induced differentiation process, Dab2 expression is induced by the GATA factors in a coherent feed-forward loop; on the other hand, we showed that p96 regulates GATA-4 in a positive feed-back manner in this study. Tretinoin 11-13 DAB adaptor protein 2 Homo sapiens 47-51
22396202-5 2012 In this study, we show that RA inhibits adipocyte differentiation by activating the CRABP-II/RARgamma path in preadipose cells, thereby upregulating the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2). Tretinoin 28-30 SRY (sex determining region Y)-box 9 Mus musculus 203-207
22396202-5 2012 In this study, we show that RA inhibits adipocyte differentiation by activating the CRABP-II/RARgamma path in preadipose cells, thereby upregulating the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2). Tretinoin 28-30 Kruppel-like factor 2 (lung) Mus musculus 213-234
22396202-5 2012 In this study, we show that RA inhibits adipocyte differentiation by activating the CRABP-II/RARgamma path in preadipose cells, thereby upregulating the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2). Tretinoin 28-30 Kruppel-like factor 2 (lung) Mus musculus 236-240
22194415-10 2012 Furthermore, global gene expression analysis of Yap(+/-) livers revealed a role of Yap in regulation of genes involved in bile acid metabolism, retinoic acid metabolism, ion transport, and extracellular matrix proteins. Tretinoin 144-157 yes-associated protein 1 Mus musculus 83-86
22222225-4 2012 Retinoids induced LP CD103(+) DCs to generate ATRA via ALDH1 activity. Tretinoin 46-50 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 55-60
22190473-0 2012 Identification and characterization of a novel retinoic acid response element in zebrafish cyp26a1 promoter. Tretinoin 47-60 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 91-98
22190473-1 2012 Cyp26A1 is a major enzyme that controls retinoic acid (RA) homeostasis by metabolizing RA into bio-inactive metabolites. Tretinoin 40-53 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-7
22190473-1 2012 Cyp26A1 is a major enzyme that controls retinoic acid (RA) homeostasis by metabolizing RA into bio-inactive metabolites. Tretinoin 55-57 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-7
22190473-1 2012 Cyp26A1 is a major enzyme that controls retinoic acid (RA) homeostasis by metabolizing RA into bio-inactive metabolites. Tretinoin 87-89 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-7
22190473-2 2012 Previously, we demonstrated that zebrafish cyp26a1 promoter possesses two conserved RA response elements (RAREs; proximal R1 and distal R2) in response to RA. Tretinoin 84-86 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 43-50
22190473-2 2012 Previously, we demonstrated that zebrafish cyp26a1 promoter possesses two conserved RA response elements (RAREs; proximal R1 and distal R2) in response to RA. Tretinoin 106-108 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 43-50
22190473-8 2012 However, it is expressed in a significantly lower level than the reporter in Tg(cyp26a1:eYFP)nju1/+ in response to exogenous RA. Tretinoin 125-127 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 80-87
22127979-5 2012 We found dynamic patterns of gene expression for the RA-synthesizing enzyme, Raldh2, and for the RA-catabolizing enzyme, Cyp26b1, during GT development. Tretinoin 53-55 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 77-83
22116467-7 2012 Lrat KO mice also exhibited increased levels of retinoic acid-responsive genes, including p21, lower levels of cytochrome P450 enzymes required for DEN bioactivation and higher levels of the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT), both before and after DEN treatment. Tretinoin 48-61 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 0-4
22026435-3 2012 The treatment of MtT/E cells with retinoic acid resulted in a significant increase in GH mRNA and subsequently GH. Tretinoin 34-47 gonadotropin releasing hormone receptor Rattus norvegicus 86-88
22026435-3 2012 The treatment of MtT/E cells with retinoic acid resulted in a significant increase in GH mRNA and subsequently GH. Tretinoin 34-47 gonadotropin releasing hormone receptor Rattus norvegicus 111-113
22026435-4 2012 This stimulatory response to retinoic acid was strongly suppressed by EGF. Tretinoin 29-42 epidermal growth factor like 1 Rattus norvegicus 70-73
22026435-6 2012 The MEK [mitogen-activated protein kinase (MAPK) kinases that activate ERK1 and ERK2] inhibitor, PD98059, clearly inhibited the phosphorylation of Erk1/2 and restored the stimulatory effects of retinoic acid. Tretinoin 194-207 mitogen activated protein kinase 3 Rattus norvegicus 71-75
22026435-6 2012 The MEK [mitogen-activated protein kinase (MAPK) kinases that activate ERK1 and ERK2] inhibitor, PD98059, clearly inhibited the phosphorylation of Erk1/2 and restored the stimulatory effects of retinoic acid. Tretinoin 194-207 mitogen activated protein kinase 1 Rattus norvegicus 80-84
22026435-6 2012 The MEK [mitogen-activated protein kinase (MAPK) kinases that activate ERK1 and ERK2] inhibitor, PD98059, clearly inhibited the phosphorylation of Erk1/2 and restored the stimulatory effects of retinoic acid. Tretinoin 194-207 mitogen activated protein kinase 3 Rattus norvegicus 147-153
21993313-6 2012 Finally, we found an unequivocal increase of HCK expression upon treatment with all-trans retinoic acid. Tretinoin 90-103 HCK proto-oncogene, Src family tyrosine kinase Homo sapiens 45-48
21906262-1 2012 Receptor-interacting protein 140 (RIP140) is a negative transcriptional coregulator of nuclear receptors such as estrogen, retinoic acid or glucocorticoid receptors. Tretinoin 123-136 nuclear receptor interacting protein 1 Mus musculus 0-32
21906262-1 2012 Receptor-interacting protein 140 (RIP140) is a negative transcriptional coregulator of nuclear receptors such as estrogen, retinoic acid or glucocorticoid receptors. Tretinoin 123-136 nuclear receptor interacting protein 1 Mus musculus 34-40
21465477-11 2012 Besides, activities of LRAT and RPE65 may be important for removal of all-trans retinal which is the substrate for retinoic acid production in skin cells. Tretinoin 115-128 lecithin retinol acyltransferase Homo sapiens 23-27
21465477-11 2012 Besides, activities of LRAT and RPE65 may be important for removal of all-trans retinal which is the substrate for retinoic acid production in skin cells. Tretinoin 115-128 retinoid isomerohydrolase RPE65 Homo sapiens 32-37
27367907-3 2016 N-(4-Hydroxyphenyl) retinamide (4-HPR, fenretinide), a synthetic analogue of all-trans retinoic acid, has emerged as a promising and well-tolerated cancer chemopreventive and chemotherapeutic agent for various neoplasms, from breast cancer to neuroblastoma. Tretinoin 87-100 haptoglobin-related protein Homo sapiens 34-37
21504779-1 2012 The vitamin A derivative, retinoic acid (RA), is essential for embryonic development through the activation of cognate nuclear receptors, RARs, which work as ligand dependent regulators of transcription. Tretinoin 26-39 arginyl-tRNA synthetase 1 Homo sapiens 138-142
21504779-1 2012 The vitamin A derivative, retinoic acid (RA), is essential for embryonic development through the activation of cognate nuclear receptors, RARs, which work as ligand dependent regulators of transcription. Tretinoin 41-43 arginyl-tRNA synthetase 1 Homo sapiens 138-142
22197812-10 2012 Additionally, two ER-resident E3 ubiquitin ligases, gp78 and Hrd1, were both upregulated in H9 cells following 5 days of exposure to RA. Tretinoin 133-135 synoviolin 1 Homo sapiens 61-65
28591946-9 2016 The serum levels of TNF-alpha, IFN-gamma and IL-17A were decreased in both ATRA groups; ATRA also can increase the serum level of IL-4. Tretinoin 75-79 interleukin 4 Rattus norvegicus 130-134
22177959-6 2012 In conclusion, atRA at physiological concentrations could reduce AHR-mediated gene transcription via the inhibition of recruitment of ARNT to relevant DNA regions. Tretinoin 15-19 aryl hydrocarbon receptor Homo sapiens 65-68
21515404-2 2012 The first step of RA synthesis is controlled by enzymes of the alcohol dehydrogenase (ADH) and retinol dehydrogenase (RDH) families that catalyze oxidation of retinol to retinaldehyde. Tretinoin 18-20 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 86-89
21515404-2 2012 The first step of RA synthesis is controlled by enzymes of the alcohol dehydrogenase (ADH) and retinol dehydrogenase (RDH) families that catalyze oxidation of retinol to retinaldehyde. Tretinoin 18-20 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 95-116
28591946-10 2016 Compared to CIA model group, the protein expressions of ADAMTS-4, MMP3, MMP1 were decreased in both ATRA groups ( P<0.05). Tretinoin 100-104 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 56-64
21515404-2 2012 The first step of RA synthesis is controlled by enzymes of the alcohol dehydrogenase (ADH) and retinol dehydrogenase (RDH) families that catalyze oxidation of retinol to retinaldehyde. Tretinoin 18-20 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 118-121
27008859-3 2016 We found that Lcn2 is a retinoic acid target gene, and retinoic acid concurrently stimulated UCP1 and Lcn2 expression in adipocytes. Tretinoin 24-37 lipocalin 2 Mus musculus 14-18
21515404-3 2012 The second step of RA synthesis is controlled by members of the aldehyde dehydrogenase (ALDH) family also known as retinaldehyde dehydrogenase (RALDH) that further oxidize retinaldehyde to produce RA. Tretinoin 19-21 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 64-86
21515404-3 2012 The second step of RA synthesis is controlled by members of the aldehyde dehydrogenase (ALDH) family also known as retinaldehyde dehydrogenase (RALDH) that further oxidize retinaldehyde to produce RA. Tretinoin 19-21 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 88-92
21515404-3 2012 The second step of RA synthesis is controlled by members of the aldehyde dehydrogenase (ALDH) family also known as retinaldehyde dehydrogenase (RALDH) that further oxidize retinaldehyde to produce RA. Tretinoin 144-146 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 64-86
21515404-3 2012 The second step of RA synthesis is controlled by members of the aldehyde dehydrogenase (ALDH) family also known as retinaldehyde dehydrogenase (RALDH) that further oxidize retinaldehyde to produce RA. Tretinoin 144-146 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 88-92
21515404-6 2012 ADH knockouts have demonstrated a postnatal role for this enzyme family in clearance of excess retinol to prevent vitamin A toxicity and in generation of RA for postnatal survival during vitamin A deficiency. Tretinoin 154-156 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 0-3
27008859-4 2016 Lcn2 KO mice exhibited a blunted effect of all-trans-retinoic acid (ATRA) on body weight and fat mass, lipid metabolism, and retinoic acid signaling pathway activation in adipose tissue under the high fat diet-induced obese condition. Tretinoin 43-66 lipocalin 2 Mus musculus 0-4
27008859-4 2016 Lcn2 KO mice exhibited a blunted effect of all-trans-retinoic acid (ATRA) on body weight and fat mass, lipid metabolism, and retinoic acid signaling pathway activation in adipose tissue under the high fat diet-induced obese condition. Tretinoin 68-72 lipocalin 2 Mus musculus 0-4
21621639-10 2012 The ratio apo-CRBP1/holo-CRBP1 participates by influencing retinol flux into and out of storage as retinyl esters, thereby modulating substrate to support atRA biosynthesis. Tretinoin 155-159 retinol binding protein 1 Homo sapiens 14-19
27008859-4 2016 Lcn2 KO mice exhibited a blunted effect of all-trans-retinoic acid (ATRA) on body weight and fat mass, lipid metabolism, and retinoic acid signaling pathway activation in adipose tissue under the high fat diet-induced obese condition. Tretinoin 53-66 lipocalin 2 Mus musculus 0-4
21621639-10 2012 The ratio apo-CRBP1/holo-CRBP1 participates by influencing retinol flux into and out of storage as retinyl esters, thereby modulating substrate to support atRA biosynthesis. Tretinoin 155-159 retinol binding protein 1 Homo sapiens 25-30
27008859-5 2016 We further demonstrated that Lcn2 is required for the full action of ATRA on the induction of UCP1 and PGC-1alpha expression in brown adipocytes and the restoration of cold intolerance in Lcn2 KO mice. Tretinoin 69-73 lipocalin 2 Mus musculus 29-33
27008859-5 2016 We further demonstrated that Lcn2 is required for the full action of ATRA on the induction of UCP1 and PGC-1alpha expression in brown adipocytes and the restoration of cold intolerance in Lcn2 KO mice. Tretinoin 69-73 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 94-98
27008859-5 2016 We further demonstrated that Lcn2 is required for the full action of ATRA on the induction of UCP1 and PGC-1alpha expression in brown adipocytes and the restoration of cold intolerance in Lcn2 KO mice. Tretinoin 69-73 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 103-113
27008859-5 2016 We further demonstrated that Lcn2 is required for the full action of ATRA on the induction of UCP1 and PGC-1alpha expression in brown adipocytes and the restoration of cold intolerance in Lcn2 KO mice. Tretinoin 69-73 lipocalin 2 Mus musculus 188-192
23124249-3 2012 ATRA treatment causes neuronal differentiation by inducing tropomyosin-related kinase B (TrkB) expression and increasing the sensitivity to brain-derived neurotrophic factor (BDNF), a TrkB ligand. Tretinoin 0-4 neurotrophic receptor tyrosine kinase 2 Homo sapiens 59-87
27008859-6 2016 Interestingly, we discovered that Lcn2 KO mice have decreased levels of retinoic acid and retinol in adipose tissue. Tretinoin 72-85 lipocalin 2 Mus musculus 34-38
23124249-3 2012 ATRA treatment causes neuronal differentiation by inducing tropomyosin-related kinase B (TrkB) expression and increasing the sensitivity to brain-derived neurotrophic factor (BDNF), a TrkB ligand. Tretinoin 0-4 neurotrophic receptor tyrosine kinase 2 Homo sapiens 89-93
23124249-3 2012 ATRA treatment causes neuronal differentiation by inducing tropomyosin-related kinase B (TrkB) expression and increasing the sensitivity to brain-derived neurotrophic factor (BDNF), a TrkB ligand. Tretinoin 0-4 neurotrophic receptor tyrosine kinase 2 Homo sapiens 184-188
26678800-6 2016 In addition, ATRA-induced stimulation of NF-M at 48 and 72h was enhanced by decreasing SOD activity using siRNA directed at MnSOD. Tretinoin 13-17 superoxide dismutase 2 Homo sapiens 87-90
26678800-6 2016 In addition, ATRA-induced stimulation of NF-M at 48 and 72h was enhanced by decreasing SOD activity using siRNA directed at MnSOD. Tretinoin 13-17 superoxide dismutase 2 Homo sapiens 124-129
26980066-4 2016 We report that the activity of YAP promotes an early neural crest phenotype and migration, and provide the first evidence for an interaction between Hippo/YAP and retinoic acid signaling in this system. Tretinoin 163-176 Yes1 associated transcriptional regulator Homo sapiens 31-34
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 16-29 retinoic acid receptor gamma Homo sapiens 187-191
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 31-33 retinoic acid receptor gamma Homo sapiens 177-185
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 31-33 retinoic acid receptor gamma Homo sapiens 187-191
22562199-6 2012 This anteriorization effect was enhanced when xCOUP-TF-B was co-injected with xCyp26A or xCyp26C, which are known RA metabolizing factors. Tretinoin 114-116 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 89-96
22562199-8 2012 Together, these results suggest that xCOUP-TF and xCyp26 are both regulated by Wnt signaling, and cooperatively function in RA signaling to affect A-P neural patterning. Tretinoin 124-126 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 50-56
26892147-9 2016 A microarray analysis showed that ATRA plus ATO treatment markedly down-regulated the expression of proteinase 3 (PRTN3), which is involved in the differentiation arrest of leukemia cells, compared with treatment with ATRA alone. Tretinoin 34-38 proteinase 3 Homo sapiens 100-112
23275899-7 2012 RESULTS: After wearing -6.00D lens for 15 days, axial length of the lens-induced eye extends and myopia was formed, with RA contents increasing in both the neural retina and RPE/choroid complex. Tretinoin 121-123 ribulose-phosphate 3-epimerase Cavia porcellus 174-177
23275899-8 2012 Comparing with the lens-induced group, myopic degree significantly relieved, and its RA contents in both the neural retina and RPE/choroid complex decreased in the recovering group. Tretinoin 85-87 ribulose-phosphate 3-epimerase Cavia porcellus 127-130
21993314-1 2012 Kruppel-like factor 5 (KLF5) has been implicated as a tumor suppressor in various solid tumors such as breast and prostate, and recent studies have demonstrated a role for this protein in neutrophil differentiation of acute promyelocytic leukemia cells in response to ATRA. Tretinoin 268-272 Kruppel-like factor 5 Mus musculus 0-21
26892147-9 2016 A microarray analysis showed that ATRA plus ATO treatment markedly down-regulated the expression of proteinase 3 (PRTN3), which is involved in the differentiation arrest of leukemia cells, compared with treatment with ATRA alone. Tretinoin 34-38 proteinase 3 Homo sapiens 114-119
21993314-1 2012 Kruppel-like factor 5 (KLF5) has been implicated as a tumor suppressor in various solid tumors such as breast and prostate, and recent studies have demonstrated a role for this protein in neutrophil differentiation of acute promyelocytic leukemia cells in response to ATRA. Tretinoin 268-272 Kruppel-like factor 5 Mus musculus 23-27
26892147-9 2016 A microarray analysis showed that ATRA plus ATO treatment markedly down-regulated the expression of proteinase 3 (PRTN3), which is involved in the differentiation arrest of leukemia cells, compared with treatment with ATRA alone. Tretinoin 218-222 proteinase 3 Homo sapiens 100-112
26892147-9 2016 A microarray analysis showed that ATRA plus ATO treatment markedly down-regulated the expression of proteinase 3 (PRTN3), which is involved in the differentiation arrest of leukemia cells, compared with treatment with ATRA alone. Tretinoin 218-222 proteinase 3 Homo sapiens 114-119
26892147-10 2016 The PRTN3 mRNA level was suppressed by treatment with ATRA alone, and then further suppressed by co-treatment with ATO, accompanied by a concomitant increase in Sp1 protein, which is known to facilitate differentiation. Tretinoin 54-58 proteinase 3 Homo sapiens 4-9
23107969-6 2012 RESULTS: Compared to diseased animals receiving vehicle, ATRA statistically significantly increased the number of glomerular transition cells, defined as cells double-staining for PAX2 and WT-1, in membranous nephropathy at weeks 2, 5 and 16, and in FSGS at weeks 1 and 2. Tretinoin 57-61 WT1 transcription factor Rattus norvegicus 189-193
26967733-0 2016 The Expression of Bone Morphogenetic Protein 2 and Matrix Metalloproteinase 2 through Retinoic Acid Receptor Beta Induced by All-Trans Retinoic Acid in Cultured ARPE-19 Cells. Tretinoin 86-99 bone morphogenetic protein 2 Homo sapiens 18-46
26967733-0 2016 The Expression of Bone Morphogenetic Protein 2 and Matrix Metalloproteinase 2 through Retinoic Acid Receptor Beta Induced by All-Trans Retinoic Acid in Cultured ARPE-19 Cells. Tretinoin 86-99 matrix metallopeptidase 2 Homo sapiens 51-77
22389628-4 2012 In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24. Tretinoin 15-28 E1A binding protein p300 Homo sapiens 34-38
26967733-3 2016 The purpose of this study was to investigate whether retinoic acid affected secretion of bone morphogenetic protein 2 (BMP-2) and matrix metalloproteinase 2 (MMP-2) and to explore the signaling pathway of retinoic acid in cultured acute retinal pigment epithelial 19 (ARPE-19) cells. Tretinoin 53-66 bone morphogenetic protein 2 Homo sapiens 89-117
26967733-3 2016 The purpose of this study was to investigate whether retinoic acid affected secretion of bone morphogenetic protein 2 (BMP-2) and matrix metalloproteinase 2 (MMP-2) and to explore the signaling pathway of retinoic acid in cultured acute retinal pigment epithelial 19 (ARPE-19) cells. Tretinoin 53-66 bone morphogenetic protein 2 Homo sapiens 119-124
26967733-3 2016 The purpose of this study was to investigate whether retinoic acid affected secretion of bone morphogenetic protein 2 (BMP-2) and matrix metalloproteinase 2 (MMP-2) and to explore the signaling pathway of retinoic acid in cultured acute retinal pigment epithelial 19 (ARPE-19) cells. Tretinoin 53-66 matrix metallopeptidase 2 Homo sapiens 130-156
22666498-2 2012 Expression of the gut-specific homing receptors integrin-alpha4beta7 and chemokine receptor CCR9 on T cells is imprinted in gut-associated lymphoid tissues (GALT) under the influence of the vitamin A metabolite retinoic acid. Tretinoin 211-224 atypical chemokine receptor 2 Homo sapiens 18-96
26967733-3 2016 The purpose of this study was to investigate whether retinoic acid affected secretion of bone morphogenetic protein 2 (BMP-2) and matrix metalloproteinase 2 (MMP-2) and to explore the signaling pathway of retinoic acid in cultured acute retinal pigment epithelial 19 (ARPE-19) cells. Tretinoin 53-66 matrix metallopeptidase 2 Homo sapiens 158-163
26967733-3 2016 The purpose of this study was to investigate whether retinoic acid affected secretion of bone morphogenetic protein 2 (BMP-2) and matrix metalloproteinase 2 (MMP-2) and to explore the signaling pathway of retinoic acid in cultured acute retinal pigment epithelial 19 (ARPE-19) cells. Tretinoin 205-218 matrix metallopeptidase 2 Homo sapiens 158-163
26967733-11 2016 CONCLUSION: ATRA induced upregulation of RARbeta in ARPE-19 cells and stimulated these cells to secrete BMP-2 and MMP-2. Tretinoin 12-16 bone morphogenetic protein 2 Homo sapiens 104-109
26967733-11 2016 CONCLUSION: ATRA induced upregulation of RARbeta in ARPE-19 cells and stimulated these cells to secrete BMP-2 and MMP-2. Tretinoin 12-16 matrix metallopeptidase 2 Homo sapiens 114-119
22629307-6 2012 During RA-induced NT2 differentiation, the class III histone deacetylase Sirt1, a putative caspase substrate implicated in the regulation of the proneural bHLH MASH1 gene expression, was cleaved to a ~100 kDa fragment. Tretinoin 7-9 achaete-scute family bHLH transcription factor 1 Homo sapiens 160-165
26442704-3 2016 To address the cellular mechanisms underlying the effects of RA signaling during OFT morphogenesis, we used transient maternal RA supplementation to rescue the early lethality resulting from inactivation of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene. Tretinoin 127-129 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 218-247
22363502-7 2012 However, the RA treatment blocks the increased primitive myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Tretinoin 13-15 aldehyde dehydrogenase 1 family, member A2 Danio rerio 299-306
26271478-0 2016 Retinoic Acid Inhibits Adipogenesis Modulating C/EBPbeta Phosphorylation and Down Regulating Srebf1a Expression. Tretinoin 0-13 CCAAT enhancer binding protein beta Homo sapiens 47-56
21856460-1 2011 Vav1 is a key molecule in the ATRA-induced acquisition of a mature phenotype by tumoral myeloid precursors. Tretinoin 30-34 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
21856460-4 2011 The obtained data demonstrated that, in NB4 cells treated with ATRA, Vav1 is involved in determining the nuclear amount of proteins involved in molecular complexes with DNA and may participate to RNA processing by carrying in the nucleus molecules involved in modulating mRNA production and stability, like hnRNPs and SR proteins. Tretinoin 63-67 vav guanine nucleotide exchange factor 1 Homo sapiens 69-73
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 71-73 aryl hydrocarbon receptor Homo sapiens 29-54
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 71-73 aryl hydrocarbon receptor Homo sapiens 56-59
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 124-126 aryl hydrocarbon receptor Homo sapiens 29-54
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 124-126 aryl hydrocarbon receptor Homo sapiens 56-59
26271478-5 2016 Retinoic acid down regulates the expression of the adipogenic genes, srebf1a, srebf1c, pparg2, and cebpa; however, it did not down regulate the expression of cebpb, but it inhibited C/EBPbeta phosphorylation at Thr188, a critical step for the progression of the adipogenic program. Tretinoin 0-13 CCAAT enhancer binding protein beta Homo sapiens 182-191
25645024-5 2016 CONCLUSION: The SPA-IS exhibited obvious oestrogenic activities on retinoic acid-induced osteoporosis in Kunming mice compared to Mix, IS, and soy protein. Tretinoin 67-80 surfactant associated protein A1 Mus musculus 16-19
21555390-7 2011 RESULTS: In this study, we demonstrate a substantial increase in the expression of the NKG2D ligands retinoic acid early inducible-1 (RAE-1), murine ULBP-like transcript 1 (MULT-1) and histocompatibility-60 (H-60) in mouse kidneys during renal IRI. Tretinoin 101-114 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 87-92
21803488-2 2011 ATRA induced several biomarkers of cellular senescence including irreversible G1 arrest, morphological changes, senescence-associated beta-galactosidase, and heterochromatin foci in HepG2 cells. Tretinoin 0-4 galactosidase beta 1 Homo sapiens 134-152
25645024-6 2016 The results suggest that there is a potential use for SPA-IS in the treatment of osteoporosis induced by intake of retinoic acid. Tretinoin 115-128 surfactant associated protein A1 Mus musculus 54-57
26722220-4 2016 RA attenuated BSCB permeability and decreased the loss of tight junction (TJ) molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in Brain Microvascular Endothelial Cells (BMECs). Tretinoin 0-2 occludin Rattus norvegicus 116-124
21767634-6 2011 Dehydrogenases and a subset of cytochrome p450 genes (cyp26a1, cyp26b1, and cyp26c1) play the major role in providing the retinoic acid and limiting its access. Tretinoin 122-135 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 54-61
26722220-4 2016 RA attenuated BSCB permeability and decreased the loss of tight junction (TJ) molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in Brain Microvascular Endothelial Cells (BMECs). Tretinoin 0-2 claudin 5 Rattus norvegicus 129-137
21435396-2 2012 In cytoplasm, RA binds specifically to cellular retinoic acid binding proteins I (CRABPI), and II. Tretinoin 14-16 cellular retinoic acid binding protein 1 Homo sapiens 39-80
26682679-8 2016 All-trans retinoic acid is known to enhance the expression and activity of choline acetyltransferase in neuronal cell lines. Tretinoin 10-23 choline acetyltransferase Mus musculus 75-100
21435396-2 2012 In cytoplasm, RA binds specifically to cellular retinoic acid binding proteins I (CRABPI), and II. Tretinoin 14-16 cellular retinoic acid binding protein 1 Homo sapiens 82-88
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 16-29 retinoic acid receptor gamma Homo sapiens 177-185
21538808-1 2011 During the early stages of body axis extension, retinoic acid (RA) synthesized in somites by Raldh2 represses caudal fibroblast growth factor (FGF) signaling to limit the tailbud progenitor zone. Tretinoin 48-61 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 93-99
21538808-1 2011 During the early stages of body axis extension, retinoic acid (RA) synthesized in somites by Raldh2 represses caudal fibroblast growth factor (FGF) signaling to limit the tailbud progenitor zone. Tretinoin 63-65 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 93-99
26530921-5 2016 The endogenous miR-124a expression level was detected by miR-124a beacon system during neurogenesis, showing brighter fluorescence intensity in cytoplasmic area of P19 cells after induction of neuronal differentiation by retinoic acid. Tretinoin 221-234 microRNA 124-1 Homo sapiens 15-23
21618588-6 2011 In spite of its lower potency, increased Hoxa1 gene expression was detected 30 min after retinol exposure and increased 40-fold by 2 h. Rdh10 and Aldh1a2/Raldh2, which together convert retinol to atRA in the embryo, were the predominant alcohol and aldehyde dehydrogenases expressed in P19 cells. Tretinoin 196-200 homeobox A1 Mus musculus 41-46
21618588-6 2011 In spite of its lower potency, increased Hoxa1 gene expression was detected 30 min after retinol exposure and increased 40-fold by 2 h. Rdh10 and Aldh1a2/Raldh2, which together convert retinol to atRA in the embryo, were the predominant alcohol and aldehyde dehydrogenases expressed in P19 cells. Tretinoin 196-200 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 146-153
22001116-0 2012 The all-trans retinoic acid (atRA)-regulated gene Calmin (Clmn) regulates cell cycle exit and neurite outgrowth in murine neuroblastoma (Neuro2a) cells. Tretinoin 14-27 calmin Mus musculus 50-56
22001116-0 2012 The all-trans retinoic acid (atRA)-regulated gene Calmin (Clmn) regulates cell cycle exit and neurite outgrowth in murine neuroblastoma (Neuro2a) cells. Tretinoin 29-33 calmin Mus musculus 50-56
21618588-6 2011 In spite of its lower potency, increased Hoxa1 gene expression was detected 30 min after retinol exposure and increased 40-fold by 2 h. Rdh10 and Aldh1a2/Raldh2, which together convert retinol to atRA in the embryo, were the predominant alcohol and aldehyde dehydrogenases expressed in P19 cells. Tretinoin 196-200 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 154-160
26530921-5 2016 The endogenous miR-124a expression level was detected by miR-124a beacon system during neurogenesis, showing brighter fluorescence intensity in cytoplasmic area of P19 cells after induction of neuronal differentiation by retinoic acid. Tretinoin 221-234 microRNA 124-1 Homo sapiens 57-65
26590087-0 2016 Sox6 suppression induces RA-dependent apoptosis mediated by BMP-4 expression during neuronal differentiation in P19 cells. Tretinoin 25-27 SRY-box transcription factor 6 Homo sapiens 0-4
22286811-10 2011 Similarly, ATRA alone or in combination with butyrate induced NCF2 gene expression without any significant influence on the expression of NCOR1 or NCOR2 genes. Tretinoin 11-15 neutrophil cytosolic factor 2 Homo sapiens 62-66
26590087-0 2016 Sox6 suppression induces RA-dependent apoptosis mediated by BMP-4 expression during neuronal differentiation in P19 cells. Tretinoin 25-27 bone morphogenetic protein 4 Homo sapiens 60-65
26590087-1 2016 Sox6 is a transcription factor that induces neuronal differentiation in P19 cells; its suppression not only inhibits neuronal differentiation but also induces retinoic acid (RA)-dependent apoptosis of P19 cells. Tretinoin 159-172 SRY-box transcription factor 6 Homo sapiens 0-4
26590087-1 2016 Sox6 is a transcription factor that induces neuronal differentiation in P19 cells; its suppression not only inhibits neuronal differentiation but also induces retinoic acid (RA)-dependent apoptosis of P19 cells. Tretinoin 174-176 SRY-box transcription factor 6 Homo sapiens 0-4
26590087-4 2016 Sox6 suppression in the presence of RA also induced the expression and secretion of bone morphogenetic protein 4 (BMP-4). Tretinoin 36-38 SRY-box transcription factor 6 Homo sapiens 0-4
26590087-4 2016 Sox6 suppression in the presence of RA also induced the expression and secretion of bone morphogenetic protein 4 (BMP-4). Tretinoin 36-38 bone morphogenetic protein 4 Homo sapiens 84-112
26590087-4 2016 Sox6 suppression in the presence of RA also induced the expression and secretion of bone morphogenetic protein 4 (BMP-4). Tretinoin 36-38 bone morphogenetic protein 4 Homo sapiens 114-119
21478451-10 2011 Expression of caspase 3 (0.4- vs. 1.0-fold) and TNF-alpha (0.4- vs. 1.0-fold) mRNA was downregulated (P < 0.05) in RA-treated blastocysts compared with controls. Tretinoin 118-120 caspase 3 Bos taurus 14-23
26590087-7 2016 Normally, high Sox6 expression leads to RA-mediated neuronal differentiation in P19 cells; however, Sox6 deficiency induces production and secretion of BMP-4, which mediates selective cell death. Tretinoin 40-42 SRY-box transcription factor 6 Homo sapiens 15-19
27830505-4 2016 Consequently, RA signals through RARs in CRABP2-expressing cells, but activates PPARbeta/delta in cells that express a high level of FABP5. Tretinoin 14-16 arginyl-tRNA synthetase 1 Homo sapiens 33-37
27830505-5 2016 RA elicits different and sometimes opposing responses in cells that express different FABP5/CRABP2 ratios because PPARbeta/delta and RARs regulate the expression of distinct sets of genes. Tretinoin 0-2 arginyl-tRNA synthetase 1 Homo sapiens 133-137
26108692-1 2015 We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 67-80 midkine Mus musculus 32-35
21270509-9 2011 CONCLUSIONS: The findings of differential expression of CRABP1 in prolactinomas and of RERG in NFPA compared to normal pituitary suggests that retinoic acid and estrogen receptor, respectively, could be involved in the tumorigenesis of these adenomas subtypes. Tretinoin 143-156 cellular retinoic acid binding protein 1 Homo sapiens 56-62
26108692-1 2015 We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 67-80 mitogen-activated protein kinase 3 Mus musculus 36-42
26108692-1 2015 We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 82-84 midkine Mus musculus 32-35
26108692-1 2015 We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 82-84 mitogen-activated protein kinase 3 Mus musculus 36-42
21273387-13 2011 ATRA reduced both MMP-2 and TIMP-1 activity in BAL fluid of emphysematous lungs. Tretinoin 0-4 matrix metallopeptidase 2 Rattus norvegicus 18-23
26108692-1 2015 We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 131-133 midkine Mus musculus 32-35
26108692-1 2015 We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 131-133 mitogen-activated protein kinase 3 Mus musculus 36-42
26108692-7 2015 In this work, we demonstrate that LiCl, a well-tolerated agent in humans, has antileukemic activity in APL and that it has the potential to restore RA-induced transcriptional activation and differentiation in RA-resistant APL cells in an MEK/ERK-dependent manner. Tretinoin 148-150 midkine Mus musculus 238-241
26618989-4 2015 We find that early embryonic rbp7a expression is negatively regulated by the Nodal/FoxH1-signaling pathway and we show that Nodal/FoxH1 activity has the opposite effect on aldh1a2, which encodes the major enzyme for early embryonic retinoic acid production. Tretinoin 232-245 aldehyde dehydrogenase 1 family, member A2 Danio rerio 172-179
21297158-3 2011 The cascade starts with the RA-induced phosphorylation of a serine residue located in the ligand-binding domain, S(LBD), allowing the recruitment of the cdk7/cyclin H/MAT1 subcomplex of TFIIH through the docking of cyclin H. Tretinoin 28-30 cyclin H Danio rerio 158-166
21297158-3 2011 The cascade starts with the RA-induced phosphorylation of a serine residue located in the ligand-binding domain, S(LBD), allowing the recruitment of the cdk7/cyclin H/MAT1 subcomplex of TFIIH through the docking of cyclin H. Tretinoin 28-30 cyclin H Danio rerio 215-223
26571119-5 2015 ATRA also inhibited the function of PI3K-AKT and enhanced GSK-3beta-dependent degradation of phosphorylated beta-catenin. Tretinoin 0-4 glycogen synthase kinase 3 beta Homo sapiens 58-67
21605549-0 2011 Retinoic acid inhibits BMP4-induced C3H10T1/2 stem cell commitment to adipocyte via downregulating Smad/p38MAPK signaling. Tretinoin 0-13 mitogen-activated protein kinase 14 Mus musculus 104-111
21605549-5 2011 This could be inhibited by RA exposure during the BMP4 treatment stage (commitment stage before adipogenic hormonal inducers were given), as was observed by reductions in key adipogenic genes/transcription factors (C/EBPalpha, PPARgamma, aP2), lipogenic genes (LPL, FAS, GLUT4), and lipid accumulation. Tretinoin 27-29 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 215-225
21605549-5 2011 This could be inhibited by RA exposure during the BMP4 treatment stage (commitment stage before adipogenic hormonal inducers were given), as was observed by reductions in key adipogenic genes/transcription factors (C/EBPalpha, PPARgamma, aP2), lipogenic genes (LPL, FAS, GLUT4), and lipid accumulation. Tretinoin 27-29 peroxisome proliferator activated receptor gamma Mus musculus 227-236
21605549-5 2011 This could be inhibited by RA exposure during the BMP4 treatment stage (commitment stage before adipogenic hormonal inducers were given), as was observed by reductions in key adipogenic genes/transcription factors (C/EBPalpha, PPARgamma, aP2), lipogenic genes (LPL, FAS, GLUT4), and lipid accumulation. Tretinoin 27-29 transcription factor AP-2, alpha Mus musculus 238-241
26427713-7 2015 After 3 wk of treatment with different reagents, the morphology of these spindle-like cells changed to shiny clusters and germ cell-specific markers in mRNA were upregulated in both TCC + retinoic acid (RA) and BMP-4 + RA. Tretinoin 219-221 bone morphogenetic protein 4 Homo sapiens 211-216
21488857-5 2011 Differentiation of HL-60 and NB4 cells towards granulocytes by all trans-retinoic acid (ATRA) resulted in downregulation of LAT2; conversely, it was upregulated during phorbol ester-induced monocytic differentiation of HL-60 cells. Tretinoin 67-86 linker for activation of T cells family member 2 Homo sapiens 124-128
21488857-5 2011 Differentiation of HL-60 and NB4 cells towards granulocytes by all trans-retinoic acid (ATRA) resulted in downregulation of LAT2; conversely, it was upregulated during phorbol ester-induced monocytic differentiation of HL-60 cells. Tretinoin 88-92 linker for activation of T cells family member 2 Homo sapiens 124-128
26427713-8 2015 Induction of HWJMSCs with TCC in the presence of RA resulted in significant upregulation (P <= 0.05) of all germ cell-specific genes (c-Kit 2.6795 +- 0.75, DDX4 4.3188 +- 1.18, Piwil2 4.9962 +- 1.55, Dazl 6.1199 +- 0.78) compared to control and PCC + RA. Tretinoin 49-51 deleted in azoospermia like Homo sapiens 203-207
21488857-6 2011 Forced expression of LAT2 in Kasumi-1 cells resulted in a striking block of ATRA- and phorbol ester-induced differentiation, implicating disturbances of the graded expression of this adaptor molecule in the maturation block of myeloid leukaemia cells. Tretinoin 76-80 linker for activation of T cells family member 2 Homo sapiens 21-25
26427713-8 2015 Induction of HWJMSCs with TCC in the presence of RA resulted in significant upregulation (P <= 0.05) of all germ cell-specific genes (c-Kit 2.6795 +- 0.75, DDX4 4.3188 +- 1.18, Piwil2 4.9962 +- 1.55, Dazl 6.1199 +- 0.78) compared to control and PCC + RA. Tretinoin 49-51 crystallin gamma D Homo sapiens 248-251
26083127-7 2015 Mechanistically, ActA-dependent SMAD3 signaling modulated the expression of members of the retinoic acid (RA) system, including the RA degradation CYP26B1 enzyme and the RA receptors. Tretinoin 91-104 SMAD family member 3 Mus musculus 32-37
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 E1A binding protein p300 Homo sapiens 102-106
26443638-4 2015 Using frog, chick and mice, we analyzed the regulation of Prdm12 and found that its expression in the caudal neural tube is dependent on retinoic acid and Pax6, and that it is restricted to p1 progenitors, due to the repressive action of Dbx1 and Nkx6-1/2 expressed in the adjacent p0 and p2 domains. Tretinoin 137-150 PR domain containing 12 Mus musculus 58-64
21258935-0 2011 Prenatal administration of retinoic acid upregulates connective tissue growth factor in the nitrofen CDH model. Tretinoin 27-40 cellular communication network factor 2 Homo sapiens 53-84
21258935-5 2011 In vitro studies have revealed that RA can induce CTGF gene expression. Tretinoin 36-38 cellular communication network factor 2 Homo sapiens 50-54
21258935-6 2011 We hypothesized that pulmonary gene expression of CTGF is downregulated during the later stages of lung development, and that prenatal administration of RA upregulates CTGF in the nitrofen CDH model. Tretinoin 153-155 cellular communication network factor 2 Homo sapiens 168-172
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 94-107 G0/G1 switch 2 Homo sapiens 0-4
21258935-12 2011 After RA treatment, expression levels of CTGF were significantly upregulated in CDH + RA and control + RA compared to the CDH group. Tretinoin 6-8 cellular communication network factor 2 Homo sapiens 41-45
26276871-0 2015 IRF4 Is a Critical Gene in Retinoic Acid-Mediated Plasma Cell Formation and Is Deregulated in Common Variable Immunodeficiency-Derived B Cells. Tretinoin 27-40 interferon regulatory factor 4 Homo sapiens 0-4
21258935-12 2011 After RA treatment, expression levels of CTGF were significantly upregulated in CDH + RA and control + RA compared to the CDH group. Tretinoin 86-88 cellular communication network factor 2 Homo sapiens 41-45
21258935-12 2011 After RA treatment, expression levels of CTGF were significantly upregulated in CDH + RA and control + RA compared to the CDH group. Tretinoin 86-88 cellular communication network factor 2 Homo sapiens 41-45
21258935-15 2011 Upregulation of CTGF pulmonary gene expression after prenatal RA treatment may promote lung growth by promoting alveologenesis in the nitrofen-induced CDH model. Tretinoin 62-64 cellular communication network factor 2 Homo sapiens 16-20
26276871-1 2015 In the present study, we aimed at identifying the mechanisms whereby the vitamin A metabolite all-trans retinoic acid (RA) promotes the formation of plasma cells upon stimulation of B cells via the innate immunity receptors TLR9 and RP105. Tretinoin 104-117 toll like receptor 9 Homo sapiens 224-228
26276871-1 2015 In the present study, we aimed at identifying the mechanisms whereby the vitamin A metabolite all-trans retinoic acid (RA) promotes the formation of plasma cells upon stimulation of B cells via the innate immunity receptors TLR9 and RP105. Tretinoin 119-121 toll like receptor 9 Homo sapiens 224-228
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 262-275 retinol binding protein 1 Homo sapiens 12-46
26276871-3 2015 By studying the regulatory networks known to drive these reactions, we revealed that RA enhances the expression of the plasma cell-generating transcription factors IFN regulatory factor (IRF)4 and Blimp1, and paradoxically also activation-induced deaminase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells. Tretinoin 85-87 interferon regulatory factor 4 Homo sapiens 187-192
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 262-275 retinol binding protein 1 Homo sapiens 48-53
26276871-3 2015 By studying the regulatory networks known to drive these reactions, we revealed that RA enhances the expression of the plasma cell-generating transcription factors IFN regulatory factor (IRF)4 and Blimp1, and paradoxically also activation-induced deaminase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells. Tretinoin 85-87 activation induced cytidine deaminase Homo sapiens 228-256
26276871-3 2015 By studying the regulatory networks known to drive these reactions, we revealed that RA enhances the expression of the plasma cell-generating transcription factors IFN regulatory factor (IRF)4 and Blimp1, and paradoxically also activation-induced deaminase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells. Tretinoin 85-87 activation induced cytidine deaminase Homo sapiens 258-261
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 45-58 integrin subunit alpha X Homo sapiens 239-244
25640656-0 2015 The role of all-trans retinoic acid in the biology of Foxp3+ regulatory T cells. Tretinoin 22-35 forkhead box P3 Homo sapiens 54-59
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 45-58 integrin subunit alpha X Homo sapiens 271-276
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 60-64 integrin subunit alpha X Homo sapiens 239-244
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 60-64 integrin subunit alpha X Homo sapiens 271-276
25586558-4 2015 IL-21 and retinoic acid (RA) induce IgA(+) B-cell development and IgA production and drives autocrine TGFbeta1 production to initiate IgA CSR. Tretinoin 10-23 transforming growth factor, beta 1 Mus musculus 102-110
21237205-4 2011 Furthermore, when stimulated with flagellin, ATRA-induced THP-1 cells expressed multiple cytokines, including TNF-alpha, IL-1beta, and IL-12p40, and several co-stimulatory molecules, such as CD40, CD80, CD86, and MHC class I and II. Tretinoin 45-49 CD40 molecule Homo sapiens 191-195
21237205-4 2011 Furthermore, when stimulated with flagellin, ATRA-induced THP-1 cells expressed multiple cytokines, including TNF-alpha, IL-1beta, and IL-12p40, and several co-stimulatory molecules, such as CD40, CD80, CD86, and MHC class I and II. Tretinoin 45-49 CD80 molecule Homo sapiens 197-201
26066585-5 2015 In this study, we determined that the injection of RA for 4 consecutive days resulted in increases in zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin) expression, which are crucial components of the BBB structure. Tretinoin 51-53 cadherin 5 Rattus norvegicus 132-161
21237205-4 2011 Furthermore, when stimulated with flagellin, ATRA-induced THP-1 cells expressed multiple cytokines, including TNF-alpha, IL-1beta, and IL-12p40, and several co-stimulatory molecules, such as CD40, CD80, CD86, and MHC class I and II. Tretinoin 45-49 CD86 molecule Homo sapiens 203-207
22116001-2 2012 Retinoic acid (RA) enhances induction of CD4(+) Tregs in the presence of TGFbeta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 73-80
22116001-2 2012 Retinoic acid (RA) enhances induction of CD4(+) Tregs in the presence of TGFbeta. Tretinoin 15-17 transforming growth factor, beta 1 Mus musculus 73-80
22116001-4 2012 We found that in vitro, RA-treated T cells expressed high levels of Foxp3 in the presence of recombinant TGFbeta. Tretinoin 24-26 transforming growth factor, beta 1 Mus musculus 105-112
26066585-5 2015 In this study, we determined that the injection of RA for 4 consecutive days resulted in increases in zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin) expression, which are crucial components of the BBB structure. Tretinoin 51-53 cadherin 5 Rattus norvegicus 163-174
22116001-10 2012 Our data support the hypothesis that RPE cells produce RA, thereby enabling bystander T cells to be converted into Tregs through TGFbeta promotion, which can then participate in the establishment of immune tolerance in the eye. Tretinoin 55-57 transforming growth factor, beta 1 Mus musculus 129-136
26066585-6 2015 We demonstrated that RA pretreatment could alleviate the ischemic stroke-induced enlargement of vascular permeability, which is related to the up-regulated expression of ZO-1 and VE-cadherin proteins in rat models of middle cerebral artery occlusion (MCAO). Tretinoin 21-23 cadherin 5 Rattus norvegicus 179-190
21518431-0 2011 Retinoic acid induces HL-60 cell differentiation via the upregulation of miR-663. Tretinoin 0-13 microRNA 663a Homo sapiens 73-80
26245651-0 2015 Retinoic acid-induced CHD5 upregulation and neuronal differentiation of neuroblastoma. Tretinoin 0-13 chromodomain helicase DNA binding protein 5 Homo sapiens 22-26
21352343-8 2011 RA significantly inhibited the expression of 5-LOX and of TGF-beta1, CTGF, type I and type III collagen. Tretinoin 0-2 cellular communication network factor 2 Homo sapiens 69-73
21352343-10 2011 In vitro, RA reduced 5-LOX expression in scleroderma fibroblasts and downregulated TGF-beta1 and CTGF expression, leading to the inhibition of type I and type III collagen synthesis. Tretinoin 10-12 cellular communication network factor 2 Homo sapiens 97-101
21352343-11 2011 Our results indicate that the clinical effects of RA on scleroderma are, at least in part, attributable to the reduction of 5-LOX expression and the subsequent suppression of TGF-beta1 and CTGF expression that results in the blockade of collagenogenesis. Tretinoin 50-52 cellular communication network factor 2 Homo sapiens 189-193
22396653-4 2012 Using NT2-D1 cells as a model of neuronal differentiation, we furthermore showed that retinoic-acid stimulation led to displacement of PRC1 at REST binding sites, reduced H3K27Me3, and increased gene expression. Tretinoin 86-99 protein regulator of cytokinesis 1 Homo sapiens 135-139
26058854-0 2015 The retinoic acid-metabolizing enzyme CYP26A1 upregulates fascin and promotes the malignant behavior of breast carcinoma cells. Tretinoin 4-17 fascin actin-bundling protein 1 Homo sapiens 58-64
23300837-0 2012 All-trans-retinoic acid modulates ICAM-1 N-glycan composition by influencing GnT-III levels and inhibits cell adhesion and trans-endothelial migration. Tretinoin 0-23 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 77-84
26058854-9 2015 These data suggest that fascin expression is modulated by the intracellular RA status regulated by the expression of CYP26A1 and plays a significant role in the malignant behavior of CYP26A1-expressing breast carcinoma cells. Tretinoin 76-78 fascin actin-bundling protein 1 Homo sapiens 24-30
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 35-58 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 219-226
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 60-64 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 219-226
23300837-5 2012 We noticed that the expression of the mRNA encoding GnT-III, which stops branching, was significantly enhanced following ATRA exposure. Tretinoin 121-125 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 52-59
23300837-10 2012 These data indicate that the alteration of ICAM-1 N-glycan composition by ATRA-induced GnT-III activities hindered cell adhesion and cell migration functions simultaneously, pinpointing a unique regulatory role of specific glycosyltransferases in the biological behaviors of tumor cells and a novel function of ATRA in the modulation of ICAM-1 N-glycan composition. Tretinoin 74-78 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 87-94
21262915-12 2011 Together, our results suggested that therapeutic effects of RA-induced leukemia differentiation depend on AhR and its ability to downregulate the stem cell factor Oct4. Tretinoin 60-62 aryl hydrocarbon receptor Homo sapiens 106-109
21426646-6 2011 After the treatment of 1, 10 and 100 nM/L ATRA for five days, TrkB protein was expressed in SY5Y cells and the TrkB protein level increased with the increasing ATRA concentration. Tretinoin 42-46 neurotrophic receptor tyrosine kinase 2 Homo sapiens 62-66
26035122-5 2015 RESULTS: Retinoic acid treatment reduces the expression of pancreatic stem cell markers CD24, CD44, CD133, and aldehyde dehydrogenase 1 but not c-Met. Tretinoin 9-22 prominin 1 Homo sapiens 100-105
21426646-6 2011 After the treatment of 1, 10 and 100 nM/L ATRA for five days, TrkB protein was expressed in SY5Y cells and the TrkB protein level increased with the increasing ATRA concentration. Tretinoin 42-46 neurotrophic receptor tyrosine kinase 2 Homo sapiens 111-115
21426646-6 2011 After the treatment of 1, 10 and 100 nM/L ATRA for five days, TrkB protein was expressed in SY5Y cells and the TrkB protein level increased with the increasing ATRA concentration. Tretinoin 160-164 neurotrophic receptor tyrosine kinase 2 Homo sapiens 62-66
21426646-6 2011 After the treatment of 1, 10 and 100 nM/L ATRA for five days, TrkB protein was expressed in SY5Y cells and the TrkB protein level increased with the increasing ATRA concentration. Tretinoin 160-164 neurotrophic receptor tyrosine kinase 2 Homo sapiens 111-115
21426646-7 2011 P-TrkB protein was not expressed in SY5Y cells treated only with 10 nM/L ATRA, but it was detectable after the treatment of ATRA along with BDNF. Tretinoin 73-77 neurotrophic receptor tyrosine kinase 2 Homo sapiens 2-6
23300837-10 2012 These data indicate that the alteration of ICAM-1 N-glycan composition by ATRA-induced GnT-III activities hindered cell adhesion and cell migration functions simultaneously, pinpointing a unique regulatory role of specific glycosyltransferases in the biological behaviors of tumor cells and a novel function of ATRA in the modulation of ICAM-1 N-glycan composition. Tretinoin 311-315 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 87-94
26186635-7 2015 The anti-apoptotic effects of ATRA were associated with partial inhibition of reactive oxygen species (ROS) production and significantly less phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, JNK, and ERK. Tretinoin 30-34 mitogen-activated protein kinase 14 Mus musculus 213-216
23028851-5 2012 We hypothesized that the expression of RA production enzymes contributes to the regulation of the hepatic Srebp-1c expression. Tretinoin 39-41 sterol regulatory element binding transcription factor 1 Rattus norvegicus 106-114
23028851-10 2012 INS-1 cells were identified as an ideal tool to study the effects of RA production on the regulation of gene expression because only RA, but not retinal, induced Srebp-1c mRNA expression in them. Tretinoin 69-71 sterol regulatory element binding transcription factor 1 Rattus norvegicus 162-170
21426646-7 2011 P-TrkB protein was not expressed in SY5Y cells treated only with 10 nM/L ATRA, but it was detectable after the treatment of ATRA along with BDNF. Tretinoin 124-128 neurotrophic receptor tyrosine kinase 2 Homo sapiens 2-6
26142905-0 2015 CRABP1 is associated with a poor prognosis in breast cancer: adding to the complexity of breast cancer cell response to retinoic acid. Tretinoin 120-133 cellular retinoic acid binding protein 1 Homo sapiens 0-6
23028851-14 2012 The elevated hepatic expression of Raldh1 in ZF rats may cause the excessive RA production from retinol, and in turn, result in higher Srebp-1c expression. Tretinoin 77-79 sterol regulatory element binding transcription factor 1 Rattus norvegicus 135-143
25934925-5 2015 ATRA inhibited cytokine responses upon restimulation of monocytes, and this effect was exerted through increased expression of SUV39H2, a histone methyltransferase that induces the inhibitory mark H3K9me3. Tretinoin 0-4 SUV39H2 histone lysine methyltransferase Homo sapiens 127-134
21851338-10 2011 Finally, by using lithocholic acid as an AKR1C3 inhibitor and UVI2024 as an RA receptor antagonist, we provide evidence that the pro-proliferative action of AKR1C3 in HL-60 cells involves the RA signalling pathway and that this is in part due to the retinaldehyde reductase activity of AKR1C3. Tretinoin 76-78 aldo-keto reductase family 1 member C3 Homo sapiens 157-163
21851338-10 2011 Finally, by using lithocholic acid as an AKR1C3 inhibitor and UVI2024 as an RA receptor antagonist, we provide evidence that the pro-proliferative action of AKR1C3 in HL-60 cells involves the RA signalling pathway and that this is in part due to the retinaldehyde reductase activity of AKR1C3. Tretinoin 76-78 aldo-keto reductase family 1 member C3 Homo sapiens 157-163
21220692-4 2011 Remarkably, RA itself could directly induce RALDH2 in both DCs and stromal cells in vitro. Tretinoin 12-14 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 44-50
21220692-5 2011 Furthermore, upon provision of a vitamin A-deficient diet, it was found that RA-mediated signaling was strongly reduced within the small intestines, while RALDH2 mRNA and RALDH enzyme activity in lamina propria DCs and MLN-DCs, as well as RALDH2 mRNA expression in MLN stromal cells, were strongly diminished. Tretinoin 77-79 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 239-245
25985851-2 2015 The vitamin A active metabolite, retinoic acid, can re-establish this imbalance through the modulation of gene expression of specific nuclear receptors including Forkhead box P3 (FoxP3). Tretinoin 33-46 forkhead box P3 Homo sapiens 162-177
21998312-5 2011 We show here that RA induces interactions of CRABP-II with the E2 SUMO ligase Ubc9 and triggers SUMOylation of the protein both in vitro and in cultured cells. Tretinoin 18-20 ubiquitin conjugating enzyme E2 I Homo sapiens 78-82
21274875-10 2011 atRA alone or in combination with UDCA greatly repressed CYP7A1 expression in human hepatocytes and significantly inhibited COL1A1, MMP2, and alpha-SMA expression and/or activity in primary human hepatic stellate cells and LX-2 cells. Tretinoin 0-4 matrix metallopeptidase 2 Homo sapiens 132-136
25985851-2 2015 The vitamin A active metabolite, retinoic acid, can re-establish this imbalance through the modulation of gene expression of specific nuclear receptors including Forkhead box P3 (FoxP3). Tretinoin 33-46 forkhead box P3 Homo sapiens 179-184
25304492-9 2015 There are 15 human AKRs of these AKR1B1, AKR1C1-1C3, AKR1D1, and AKR1B10 have been implicated in diabetic complications, steroid hormone dependent malignancies, bile acid deficiency and defects in retinoic acid signaling, respectively. Tretinoin 197-210 aldo-keto reductase family 1 member D1 Homo sapiens 53-59
21069352-0 2011 Prenatal retinoic acid treatment upregulates late gestation lung protein 1 in the nitrofen-induced hypoplastic lung in late gestation. Tretinoin 9-22 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 45-74
21069352-6 2011 In vitro studies have reported that RA is a key modulator of LGL1 during alveologenesis. Tretinoin 36-38 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 61-65
22107957-4 2011 RESULTS: We have examined the expression profile of synemin isoforms in mouse pluripotent ES cells and during their neural differentiation induced by retinoic acid. Tretinoin 150-163 synemin, intermediate filament protein Mus musculus 52-59
21614551-2 2011 To analyze the co-expression patterns of selected TFs with the motor protein prestin of the outer hair cells, we applied an real-time PCR approach combining several kinds of information: (i) expression changes during postnatal development, (ii) expression changes by exposure of organotypic cultures of the organ of Corti to factors which significantly affect prestin expression [thyroid hormone (T4), retinoic acid (RA), butyric acid (BA), increased KCl concentration] and (iii) changes along the apical-basal gradient. Tretinoin 402-415 solute carrier family 26 member 5 Rattus norvegicus 77-84
25304492-9 2015 There are 15 human AKRs of these AKR1B1, AKR1C1-1C3, AKR1D1, and AKR1B10 have been implicated in diabetic complications, steroid hormone dependent malignancies, bile acid deficiency and defects in retinoic acid signaling, respectively. Tretinoin 197-210 aldo-keto reductase family 1 member B10 Homo sapiens 65-72
21069352-7 2011 We hypothesized, that pulmonary gene expression of LGL1 is downregulated in the late stage of lung development, and that prenatal administration of RA upregulates pulmonary LGL1 expression in the nitrofen CDH model. Tretinoin 148-150 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 173-177
25687389-7 2015 RA exposure resulted in up-regulation of the RA metabolizing enzyme genes cyp26a1, cyp26b1 and cyp26c1 in vitro and in vivo. Tretinoin 0-2 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 74-81
21069352-13 2011 After RA treatment, gene expression levels of LGL1 were significantly upregulated in CDH + RA and control + RA compared to CDH group. Tretinoin 6-8 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 46-50
21069352-13 2011 After RA treatment, gene expression levels of LGL1 were significantly upregulated in CDH + RA and control + RA compared to CDH group. Tretinoin 91-93 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 46-50
21069352-13 2011 After RA treatment, gene expression levels of LGL1 were significantly upregulated in CDH + RA and control + RA compared to CDH group. Tretinoin 91-93 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 46-50
21614551-2 2011 To analyze the co-expression patterns of selected TFs with the motor protein prestin of the outer hair cells, we applied an real-time PCR approach combining several kinds of information: (i) expression changes during postnatal development, (ii) expression changes by exposure of organotypic cultures of the organ of Corti to factors which significantly affect prestin expression [thyroid hormone (T4), retinoic acid (RA), butyric acid (BA), increased KCl concentration] and (iii) changes along the apical-basal gradient. Tretinoin 417-419 solute carrier family 26 member 5 Rattus norvegicus 77-84
21069352-16 2011 Upregulation of LGL1 pulmonary gene expression after RA treatment may promote lung growth by stimulating alveologenesis in the nitrofen CDH model. Tretinoin 53-55 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 16-20
25687389-7 2015 RA exposure resulted in up-regulation of the RA metabolizing enzyme genes cyp26a1, cyp26b1 and cyp26c1 in vitro and in vivo. Tretinoin 45-47 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 74-81
21128244-7 2011 When SK-N-SH cells were treated with neural differentiation agents (e.g., retinoic acid and cAMP) in media containing 10% serum, ACY1 was the only aminoacylase whose expression was upregulated. Tretinoin 74-87 aminoacylase 1 Homo sapiens 129-133
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein 2 Mus musculus 39-44
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein 3 Mus musculus 46-51
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein, alpha-crystallin-related, B9 Mus musculus 67-72
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 TNF receptor-associated protein 1 Mus musculus 208-213
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein 2 Mus musculus 39-44
21782811-5 2011 Moreover, we show that this initial step of atRA synthesis occurs predominantly in a membrane-bound cellular compartment, which prevents inhibition by the cytosolic cellular retinol-binding protein (RBP1). Tretinoin 44-48 retinol binding protein 1 Homo sapiens 199-203
21782811-6 2011 These studies reveal that widely expressed cytosolic enzymes with RDH activity play a very limited role in embryonic atRA synthesis under normal dietary conditions. Tretinoin 117-121 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 66-69
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein 3 Mus musculus 46-51
21409183-5 2011 Changes in expression of mRNA for retinaldehyde dehydrogenase II (Raldh2), Crabp1 and Crabp2 genes also occur within the same time window (i.e. 10-11dpc) after RA treatment. Tretinoin 160-162 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 66-72
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein, alpha-crystallin-related, B9 Mus musculus 67-72
21409183-5 2011 Changes in expression of mRNA for retinaldehyde dehydrogenase II (Raldh2), Crabp1 and Crabp2 genes also occur within the same time window (i.e. 10-11dpc) after RA treatment. Tretinoin 160-162 cellular retinoic acid binding protein II Mus musculus 86-92
21612856-0 2011 Retinoic acid-induced Smad3 expression is required for the induction of osteoblastogenesis of mesenchymal stem cells. Tretinoin 0-13 SMAD family member 3 Mus musculus 22-27
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 TNF receptor-associated protein 1 Mus musculus 208-213
25800721-11 2015 Further investigation into the effect of retinoids in vivo revealed that oral administration of 5mg/kg/day ATRA for 10 days protected against bone loss induced by granulocyte colony-stimulating factor (G-CSF) by inhibiting the pro-osteoclastogenic action of G-CSF. Tretinoin 107-111 colony stimulating factor 3 (granulocyte) Mus musculus 163-200
21612856-6 2011 Herein we show that Smad3, whose expression is stimulated by RA, relays the effects of RA on differentiation by initiating the displacement of C/EBPbeta from the Runx2 promoter. Tretinoin 61-63 SMAD family member 3 Mus musculus 20-25
21612856-6 2011 Herein we show that Smad3, whose expression is stimulated by RA, relays the effects of RA on differentiation by initiating the displacement of C/EBPbeta from the Runx2 promoter. Tretinoin 87-89 SMAD family member 3 Mus musculus 20-25
21736279-0 2011 Proliferation of cells and expression of RARs, RXRs and HPV viral E6 and E7 proteins in cervical cancer cell lines after treatment with ATRA. Tretinoin 136-140 arginyl-tRNA synthetase 1 Homo sapiens 41-45
21612856-7 2011 In addition to stimulating Smad3 expression, RA also stimulated the nuclear localization of this factor, such that in the absence of RA, ectopic Smad3 was unable to drive osteoblastogenesis. Tretinoin 45-47 SMAD family member 3 Mus musculus 145-150
25800721-11 2015 Further investigation into the effect of retinoids in vivo revealed that oral administration of 5mg/kg/day ATRA for 10 days protected against bone loss induced by granulocyte colony-stimulating factor (G-CSF) by inhibiting the pro-osteoclastogenic action of G-CSF. Tretinoin 107-111 colony stimulating factor 3 (granulocyte) Mus musculus 202-207
21612856-8 2011 While not sufficient to promote osteoblastogenesis, knockdown of Smad3 using a specific shRNA prevented the RA-mediated stimulation of differentiation and displacement of C/EBPbeta from the Runx2 P1 promoter. Tretinoin 108-110 SMAD family member 3 Mus musculus 65-70
21612856-9 2011 Taken together, these data indicate that Smad3 is an important mediator of RA activity during mesenchymal stem cell differentiation and is necessary for the stimulation of osteoblastogenesis. Tretinoin 75-77 SMAD family member 3 Mus musculus 41-46
22178948-6 2011 RA by itself stimulates UCP-1 mRNA in mouse adipocytes, but not in those from rat. Tretinoin 0-2 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 24-29
25800721-11 2015 Further investigation into the effect of retinoids in vivo revealed that oral administration of 5mg/kg/day ATRA for 10 days protected against bone loss induced by granulocyte colony-stimulating factor (G-CSF) by inhibiting the pro-osteoclastogenic action of G-CSF. Tretinoin 107-111 colony stimulating factor 3 (granulocyte) Mus musculus 258-263
25877907-0 2015 A role for retinoids in human oocyte fertilization: regulation of connexin 43 by retinoic acid in cumulus granulosa cells. Tretinoin 81-94 gap junction protein alpha 1 Homo sapiens 66-77
21278145-9 2011 LRAT deficiency decreased diethylnitrosamine-induced injury and tumour load and increased the expression of the retinoic acid responsive genes Cyp26a1, RARb and p21, suggesting that the lower tumour load of LRAT-deficient mice was a result of increased retinoid signalling and subsequent p21-mediated inhibition of proliferation. Tretinoin 112-125 retinoic acid receptor, beta Mus musculus 152-156
25877907-3 2015 Connexin 43 (C x 43) is the main subunit of gap junction channels in human cumulus granulosa cells (CGC) and is regulated by all-trans retinoic acid (ATRA) in other hormone responsive cell types. Tretinoin 135-148 gap junction protein alpha 1 Homo sapiens 0-11
25877907-3 2015 Connexin 43 (C x 43) is the main subunit of gap junction channels in human cumulus granulosa cells (CGC) and is regulated by all-trans retinoic acid (ATRA) in other hormone responsive cell types. Tretinoin 135-148 gap junction protein alpha 1 Homo sapiens 13-19
25877907-3 2015 Connexin 43 (C x 43) is the main subunit of gap junction channels in human cumulus granulosa cells (CGC) and is regulated by all-trans retinoic acid (ATRA) in other hormone responsive cell types. Tretinoin 150-154 gap junction protein alpha 1 Homo sapiens 0-11
21373967-4 2011 Two variants (145 and 95 kD) of the TrkB protein were dramatically increased by GGA treatment, comparable to the effect of ATRA. Tretinoin 123-127 neurotrophic receptor tyrosine kinase 2 Homo sapiens 36-40
25877907-3 2015 Connexin 43 (C x 43) is the main subunit of gap junction channels in human cumulus granulosa cells (CGC) and is regulated by all-trans retinoic acid (ATRA) in other hormone responsive cell types. Tretinoin 150-154 gap junction protein alpha 1 Homo sapiens 13-19
21373967-7 2011 Time-dependent induction of cell cycle-related genes, such as cyclin D1 and retinoblastoma protein, and amplification of the neural progenitor cell marker, brain lipid binding protein, were suppressed by GGA treatment and were completely abolished by ATRA. Tretinoin 251-255 cyclin D1 Homo sapiens 62-71
25877907-7 2015 ATRA induced a rapid dephosphorylation of C x 43 in CGC and granulosa cell line (KGN) cultures resulting in a >2-fold increase in the expression of the functional non-phosphorylated (P0) species (P < 0.02). Tretinoin 0-4 gap junction protein alpha 1 Homo sapiens 42-48
25877907-8 2015 Similar enhancement of P0 by ATRA was shown in CGC and KGN cultures co-treated with LH or hCG which, by themselves, enhanced the protein levels of C x 43 without altering its phosphorylation profile. Tretinoin 29-33 gap junction protein alpha 1 Homo sapiens 147-153
25877907-11 2015 Regulation of C x 43 by ATRA may serve an important role in folliculogenesis, development of oocyte competency, and successful fertilization by increasing GJIC in CGC. Tretinoin 24-28 gap junction protein alpha 1 Homo sapiens 14-20
21711459-5 2011 Also, BMPs and retinoic acid, which act as apoptosis-promoting factors, induced expression of Smad8 before the onset of cell death, while sonic hedgehog protein, acting as a survival factor, inhibited Smad8 expression in the ANZ. Tretinoin 15-28 SMAD family member 9 Gallus gallus 94-99
21711459-5 2011 Also, BMPs and retinoic acid, which act as apoptosis-promoting factors, induced expression of Smad8 before the onset of cell death, while sonic hedgehog protein, acting as a survival factor, inhibited Smad8 expression in the ANZ. Tretinoin 15-28 SMAD family member 9 Gallus gallus 201-206
26137156-12 2015 However, treatment with high concentrations of ATRA, consisting of 20 and 40 micromol/l ATRA, significantly downregulated the expression levels of MMP-2 in U87 cells. Tretinoin 47-51 matrix metallopeptidase 2 Homo sapiens 147-152
21480163-5 2011 To determine a possible role of the retinoid-mediated signaling pathway in the pathogenesis of ARM, we investigated whether all-trans retinoic acid (ATRA) affected the expression patterns of PCSK5 and GDF11 in ARM-treated mouse embryos. Tretinoin 149-153 growth differentiation factor 11 Mus musculus 201-206
26137156-12 2015 However, treatment with high concentrations of ATRA, consisting of 20 and 40 micromol/l ATRA, significantly downregulated the expression levels of MMP-2 in U87 cells. Tretinoin 88-92 matrix metallopeptidase 2 Homo sapiens 147-152
26137156-13 2015 In contrast to U87 cells, the administration of ATRA treatment to SHG44 glioma cells resulted in a significant and dose-dependent downregulation in MMP-2 mRNA and protein expression (P<0.01). Tretinoin 48-52 matrix metallopeptidase 2 Homo sapiens 148-153
26022051-1 2015 In this issue of Blood, Martelli et al and El Hajj et al independently report that nucleophosmin-1 (NPM1)-mutant leukemia is particularly vulnerable to a novel strategy combining all-trans retinoic acid (ATRA) with arsenic trioxide (ATO). Tretinoin 189-202 nucleophosmin 1 Homo sapiens 83-98
26022051-1 2015 In this issue of Blood, Martelli et al and El Hajj et al independently report that nucleophosmin-1 (NPM1)-mutant leukemia is particularly vulnerable to a novel strategy combining all-trans retinoic acid (ATRA) with arsenic trioxide (ATO). Tretinoin 189-202 nucleophosmin 1 Homo sapiens 100-104
25996952-7 2015 Moreover, treatment of acute promyelocytic cells (APL) with all-trans retinoic acid (ATRA) increased MTSS1 mRNA levels. Tretinoin 70-83 MTSS I-BAR domain containing 1 Homo sapiens 101-106
20853320-3 2011 Upon binding to leukemic cells expressing NKG2D ligands (NKG2DL), including chronic lymphocytic leukemias treated with transretinoic acid, most gammadeltaT (>60%) and half CD8(+) alphabetaT cells (about 50%) received a survival signal, at variance with the majority of NK cells (>80%) that underwent apoptosis by day 5. Tretinoin 119-137 killer cell lectin like receptor K1 Homo sapiens 42-47
25996952-7 2015 Moreover, treatment of acute promyelocytic cells (APL) with all-trans retinoic acid (ATRA) increased MTSS1 mRNA levels. Tretinoin 85-89 MTSS I-BAR domain containing 1 Homo sapiens 101-106
21344672-0 2011 Effects of retinoic acid and butyric acid on the expression of prestin and Gata-3 in organotypic cultures of the organ of corti of newborn rats. Tretinoin 11-24 solute carrier family 26 member 5 Rattus norvegicus 63-70
25727910-6 2015 ERRgamma over-expression enhanced mature DAergic neuronal phenotype with neurite outgrowth as with RA treatment; and RA-induced increase in DAergic phenotype was attenuated by silencing ERRgamma expression. Tretinoin 99-101 estrogen related receptor gamma Homo sapiens 0-8
21344672-3 2011 We studied the effects of the application of retinoic acid, a ligand of a nuclear receptor, and of butyric acid, an inhibitor of histone deacetylase activity, on the expression of mRNA of prestin and Gata-3 in the organotypic culture of the organ of Corti of newborn rats using RT-PCR. Tretinoin 45-58 solute carrier family 26 member 5 Rattus norvegicus 188-195
25727910-6 2015 ERRgamma over-expression enhanced mature DAergic neuronal phenotype with neurite outgrowth as with RA treatment; and RA-induced increase in DAergic phenotype was attenuated by silencing ERRgamma expression. Tretinoin 117-119 estrogen related receptor gamma Homo sapiens 186-194
21610156-3 2011 When provided with exogenous cholesterol substrate, and after treatment with retinoic acid and cAMP, SF-1-ES cells produce progesterone but do not produce other steroids such as cortisol, estradiol, or testosterone. Tretinoin 77-90 splicing factor 1 Mus musculus 101-105
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 estrogen related receptor gamma Homo sapiens 28-59
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 estrogen related receptor gamma Homo sapiens 61-69
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 estrogen related receptor gamma Homo sapiens 118-126
21596042-8 2011 RA-mediated regulation of DC required signaling through the mitogen-activated protein kinase signaling pathway and unexpectedly required MyD88, which is conventionally associated with Toll-like receptor, interleukin-1, and interleukin-18 signaling. Tretinoin 0-2 interleukin 18 Mus musculus 223-237
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 glycogen synthase kinase 3 beta Homo sapiens 345-353
21672091-0 2011 Transcriptional regulation of the CADM1 gene by retinoic acid during the neural differentiation of murine embryonal carcinoma P19 cells. Tretinoin 48-61 interleukin 23, alpha subunit p19 Mus musculus 126-129
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 estrogen related receptor gamma Homo sapiens 118-126
21672091-9 2011 These results suggest that Sp1 plays a critical role in RA-induced CADM1 expression through possible interaction with RARalpha in the neural differentiation of P19. Tretinoin 56-58 interleukin 23, alpha subunit p19 Mus musculus 160-163
26036904-7 2015 Progesterone receptor deficiency leads to progesterone resistance, resulting in decreased retinol uptake and retinoic acid production and altered retinoic acid action. Tretinoin 109-122 progesterone receptor Homo sapiens 0-21
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 14-27 leucine rich repeat and Ig domain containing 1 Homo sapiens 188-195
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 29-31 leucine rich repeat and Ig domain containing 1 Homo sapiens 188-195
21690307-6 2011 Furthermore, we confirm in vivo that RA treatment after a dorsal column overhemisection injury inhibited Lingo-1 expression, specifically through RAR-beta. Tretinoin 37-39 leucine rich repeat and Ig domain containing 1 Homo sapiens 105-112
21605549-8 2011 These data suggest that RA has inhibitory effects on the BMP4 induction of C3H10T1/2 adipocytic commitment via downregulating Smad/p38MAPK signaling. Tretinoin 24-26 mitogen-activated protein kinase 14 Mus musculus 131-138
21555266-8 2011 In contrast, atRA treatment abrogated phosphorylation of Smad2 and Smad3 and inducible expression of Smad7 in ME. Tretinoin 13-17 SMAD family member 2 Homo sapiens 57-62
21555266-8 2011 In contrast, atRA treatment abrogated phosphorylation of Smad2 and Smad3 and inducible expression of Smad7 in ME. Tretinoin 13-17 SMAD family member 3 Homo sapiens 67-72
26036904-7 2015 Progesterone receptor deficiency leads to progesterone resistance, resulting in decreased retinol uptake and retinoic acid production and altered retinoic acid action. Tretinoin 146-159 progesterone receptor Homo sapiens 0-21
25546009-3 2015 Through genetic and chemical approaches, we find that RA signalling is essential, in a highly dose-sensitive manner, for MEF reprogramming. Tretinoin 54-56 E74-like factor 4 (ets domain transcription factor) Mus musculus 121-124
21385575-4 2011 We now show that Hoxb1, Hoxa1, and Hoxa3, as downstream RA targets, are expressed in distinct sub-domains within the SHF. Tretinoin 56-58 homeobox A1 Homo sapiens 24-29
25724646-8 2015 Once the increased retinoic acid level in the foxc1a null embryos was reduced by knocking down aldh1a2, the reduced expression of myod1 was partially rescued by resuming expressions of fgf8a and deltaC in the somites of the mutant embryos. Tretinoin 19-32 aldehyde dehydrogenase 1 family, member A2 Danio rerio 95-102
21385575-4 2011 We now show that Hoxb1, Hoxa1, and Hoxa3, as downstream RA targets, are expressed in distinct sub-domains within the SHF. Tretinoin 56-58 homeobox A3 Homo sapiens 35-40
21573212-6 2011 CONCLUSIONS/SIGNIFICANCE: Proteomic analysis identified only two proteins whose expression was significantly different in treated cells versus control cells: nucleoside diphosphate kinase A (NDKA) and reticulocalbin-1 (RCN1), which were both downregulated after 9 days of ATRA treatment. Tretinoin 272-276 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 158-189
26064333-1 2015 OBJECTIVE: This study was to investigate the effects of all-trans retinoic acid (ATRA) in combination with Genistein on the proliferation, expression of apoptosis related proteins and adhesion molecules (MUC1 and ICAM-1) and invasiveness of A549 cells, aiming to investigate whether combined therapy of ATRA and Genistein is superior to monotherapy in suppressing metastasis of lung cancer cells. Tretinoin 60-79 mucin 1, cell surface associated Homo sapiens 204-208
21573212-6 2011 CONCLUSIONS/SIGNIFICANCE: Proteomic analysis identified only two proteins whose expression was significantly different in treated cells versus control cells: nucleoside diphosphate kinase A (NDKA) and reticulocalbin-1 (RCN1), which were both downregulated after 9 days of ATRA treatment. Tretinoin 272-276 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 191-195
26064333-1 2015 OBJECTIVE: This study was to investigate the effects of all-trans retinoic acid (ATRA) in combination with Genistein on the proliferation, expression of apoptosis related proteins and adhesion molecules (MUC1 and ICAM-1) and invasiveness of A549 cells, aiming to investigate whether combined therapy of ATRA and Genistein is superior to monotherapy in suppressing metastasis of lung cancer cells. Tretinoin 81-85 mucin 1, cell surface associated Homo sapiens 204-208
26064333-5 2015 RESULTS: Combined treatment with ATRA and Genistein was able to reduce the expressions of Bcl-2, MUC1 and ICAM-1 and exerted synergistic effects to inhibit the invasion of A549 cells. Tretinoin 33-37 mucin 1, cell surface associated Homo sapiens 97-101
21469110-4 2011 Addition of TGF-beta and retinoic acid overcame the inhibition of Foxp3 expression observed during high-strength anti-CD3/anti-CD28 stimulation. Tretinoin 25-38 forkhead box P3 Homo sapiens 66-71
26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 mucin 1, cell surface associated Homo sapiens 59-63
26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 cyclin dependent kinase 4 Homo sapiens 146-150
25343668-4 2015 We also found that RA reduced extracellular signal-regulated kinase (ERK) phosphorylation, but increased phosphatase 2A (PP2A) activity in TCR/CD28-stimulated NKT cells. Tretinoin 19-21 CD28 molecule Homo sapiens 143-147
25504116-3 2015 In ESCs, Snai1 does not respond to TGFbeta or BMP4 signaling but it is induced by retinoic acid treatment, which induces the binding, on the Snai1 promoter, of the retinoid receptors RARgamma and RXRalpha, the dissociation of the Polycomb repressor complex 2 which results in the decrease of H3K27me3, and the increase of histone H3K4me3. Tretinoin 82-95 retinoic acid receptor gamma Homo sapiens 183-191
21437295-10 2011 The ensemble of models also correctly predicted Rb and p47phox regulation and the correlation between p21-CDK4-cyclin D formation and G1/0-arrest following exposure to RA. Tretinoin 168-170 cyclin dependent kinase 4 Homo sapiens 106-110
21481001-8 2011 A higher apoptosis rate and caspase-9 in MEPM cells were detected in the ATRA group than in the control or the ATRA+FA group. Tretinoin 73-77 caspase 9 Mus musculus 28-37
21481001-11 2011 Apoptosis and TGFbeta signaling in MEPM cells were involved in folic acid rescued ATRA-induced cleft palate. Tretinoin 82-86 transforming growth factor, beta 1 Mus musculus 14-21
25658587-9 2015 Alcohol dehydrogenase 5 (ADH5) and aldehyde dehydrogenase 1 family member A1 (ALDH1A1) are involved in RA synthesis in the cell. Tretinoin 103-105 aldehyde dehydrogenase 1 family member A1 Gallus gallus 35-76
25658587-9 2015 Alcohol dehydrogenase 5 (ADH5) and aldehyde dehydrogenase 1 family member A1 (ALDH1A1) are involved in RA synthesis in the cell. Tretinoin 103-105 aldehyde dehydrogenase 1 family member A1 Gallus gallus 78-85
25973309-6 2015 Furthermore, ATRA treatment elevated the levels of ROS, enhanced autophagic flux and thereby promoted cytosolic translocation of HMGB1. Tretinoin 13-17 high mobility group box 1 Homo sapiens 129-134
21362455-6 2011 Overexpressed p53 induces marked DUOXA1 expression in P19 cells and intensifies neuronal differentiation in the presence of retinoic acid, which suggests that p53 and DUOXA1 possess a neural differentiation potential. Tretinoin 124-137 interleukin 23, alpha subunit p19 Mus musculus 54-57
25973309-7 2015 HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy. Tretinoin 157-161 high mobility group box 1 Homo sapiens 0-5
25052690-4 2015 Both RA and BMP4 induced OCT4, MVH, DAZL, STELLA, NANOG and C-KIT expression, but RNF17, PIWIL2, STRA8, and SCP3 were only expressed after RA treatment. Tretinoin 5-7 octamer-binding transcription factor 4 Capra hircus 25-29
20926176-9 2011 Induction of ES cells differentiation by retinoic acid (RA) resulted in up-regulation of PrP(C) at Day 20 and nestin at Day 12. Tretinoin 41-54 prion protein Mus musculus 89-95
20926176-9 2011 Induction of ES cells differentiation by retinoic acid (RA) resulted in up-regulation of PrP(C) at Day 20 and nestin at Day 12. Tretinoin 56-58 prion protein Mus musculus 89-95
25052690-4 2015 Both RA and BMP4 induced OCT4, MVH, DAZL, STELLA, NANOG and C-KIT expression, but RNF17, PIWIL2, STRA8, and SCP3 were only expressed after RA treatment. Tretinoin 99-101 bone morphogenetic protein 4 Capra hircus 12-16
26295826-5 2015 RA increased the expression of p110alpha subunit of phosphoinositide 3-kinase (PI3K), Akt and beta1 subunit of Na(+)/K(+)-ATPase. Tretinoin 0-2 ATPase Na+/K+ transporting subunit beta 1 Homo sapiens 94-128
22252490-0 2011 Tgm2/Gh, Gbx1 and TGF-beta are involved in retinoic acid-induced transdifferentiation from epidermis to mucosal epithelium. Tretinoin 43-56 transglutaminase 2 Gallus gallus 0-4
25461845-5 2015 In addition, retinoic acid inducible gene-I (RIG-I) and melanoma differentiation associated gene-5 (MDA5) play key roles in the detection of HTNV infection in HaCaT cells and in the up-regulation of interferon (IFN)-beta expression, which subsequently leads to the production of a large amount of antiviral interferon-stimulated genes (ISGs) and other chemokines used for immune cell recruitment. Tretinoin 13-26 interferon beta 1 Homo sapiens 199-220
22252490-3 2011 Because Gbx1, TG2/Gh (transglutaminase2) and TGF-beta2 are reported individually to be induced by RA in cultures of chick embryonic skin, mouse epidermal cells and human hair follicles respectively, here, we investigated whether cooperative interplay of Gbx1, TG2/Gh and TGF-beta2 is required for the transdifferentiation of epidermal cells to mucosal cells. Tretinoin 98-100 transglutaminase 2 Gallus gallus 22-39
25721651-11 2015 HPLC analysis revealed that the level of inactive retinyl ester increased after ATRol treatment, and levels of the substrate ATRol and biologically active ATRA significantly decreased in LRAT-overexpressing murine melanoma. Tretinoin 155-159 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 187-191
21099229-3 2011 We found that incubation with retinoic acid (RA) and, more potently, with RA in combination with cAMP, induced the expression of the lymphatic competence marker LYVE-1 in the vascular structures of the EBs. Tretinoin 30-43 lymphatic vessel endothelial hyaluronan receptor 1 Mus musculus 161-167
25721651-12 2015 Consistently with this, levels of 4-oxoretinoic acid, an ATRA metabolite and Cyp26a1 product, were also decreased in LRAT-overexpressing cells. Tretinoin 57-61 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 117-121
21099229-3 2011 We found that incubation with retinoic acid (RA) and, more potently, with RA in combination with cAMP, induced the expression of the lymphatic competence marker LYVE-1 in the vascular structures of the EBs. Tretinoin 45-47 lymphatic vessel endothelial hyaluronan receptor 1 Mus musculus 161-167
25721651-14 2015 Thus, our data suggest that LRAT overexpression represents a novel mechanism by which tumor cells can escape high supplementary ATRA levels that mediate tumor-suppressive RAR signaling. Tretinoin 128-132 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 28-32
24846581-1 2014 All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 4-23 retinoic acid receptor gamma Homo sapiens 173-182
21099229-3 2011 We found that incubation with retinoic acid (RA) and, more potently, with RA in combination with cAMP, induced the expression of the lymphatic competence marker LYVE-1 in the vascular structures of the EBs. Tretinoin 74-76 lymphatic vessel endothelial hyaluronan receptor 1 Mus musculus 161-167
21099229-5 2011 RA-cAMP incubation also promoted the development of CD31+/LYVE-1+/Prox1+ cell clusters. Tretinoin 0-2 platelet/endothelial cell adhesion molecule 1 Mus musculus 52-56
24846581-1 2014 All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 25-29 retinoic acid receptor gamma Homo sapiens 173-182
24846581-9 2014 Compared with the injured podocytes, the protein/mRNA expression of RAR-alpha and RAR-gamma was significantly increased after ATRA exposure; however, the expression level of RAR-beta was not significantly different. Tretinoin 126-130 retinoic acid receptor gamma Homo sapiens 82-91
21099229-5 2011 RA-cAMP incubation also promoted the development of CD31+/LYVE-1+/Prox1+ cell clusters. Tretinoin 0-2 lymphatic vessel endothelial hyaluronan receptor 1 Mus musculus 58-64
25330951-0 2014 Prenatal administration of all-trans retinoic acid upregulates leptin signaling in hypoplastic rat lungs with experimental congenital diaphragmatic hernia. Tretinoin 37-50 leptin Rattus norvegicus 63-69
21099229-5 2011 RA-cAMP incubation also promoted the development of CD31+/LYVE-1+/Prox1+ cell clusters. Tretinoin 0-2 prospero homeobox 1 Mus musculus 66-71
21099229-7 2011 Timed exposure of mouse and Xenopus embryos to excess of RA upregulated LYVE-1 and VEGFR-3 on embryonic veins and increased formation of Prox1-positive lymphatic progenitors. Tretinoin 57-59 lymphatic vessel endothelial hyaluronan receptor 1 Mus musculus 72-78
25330951-16 2014 Immunofluorescence analysis demonstrated markedly increased pulmonary SP-B expression in Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 98-102 surfactant protein B Rattus norvegicus 70-74
25330951-17 2014 Relative mRNA expression of Lep and Lep-R was significantly increased in Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 82-86 leptin Rattus norvegicus 28-31
25330951-18 2014 Lep and Lep-R immunoreactivity was markedly increased in interstitial and alveolar epithelial cells of Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 112-116 leptin Rattus norvegicus 0-3
25403085-9 2014 CONCLUSIONS: According to our modeling of metabolic and signalization pathways using differentially expressed genes we have identified a network with major nodes (including Sirt3, Il1b, Cpt1b and Pparg) likely to underlie the observed strain specific response to ATRA. Tretinoin 263-267 carnitine palmitoyltransferase 1B Rattus norvegicus 186-191
21487212-4 2011 Here, we report the levels and subcellular distribution of PREP in human neuroblastoma SH-SY5Y cells in proliferating conditions and under differentiation induced by retinoic acid (RA). Tretinoin 166-179 prolyl endopeptidase Homo sapiens 59-63
21487212-4 2011 Here, we report the levels and subcellular distribution of PREP in human neuroblastoma SH-SY5Y cells in proliferating conditions and under differentiation induced by retinoic acid (RA). Tretinoin 181-183 prolyl endopeptidase Homo sapiens 59-63
25261715-5 2014 Functional studies in mouse organ cultures that faithfully reproduce the initiation of prostate development indicate that one of the roles of retinoic acid signaling in the male is to inhibit the expression of Inhba, which encodes the betaA subunit of Activin, in the UGS mesenchyme. Tretinoin 142-155 inhibin beta-A Mus musculus 210-215
22125642-5 2011 The physiological actions of ATRA are mediated by binding to all three isoforms of the nuclear retinoic acid receptors (RARs): RARalpha, RARbeta, and RARgamma. Tretinoin 29-33 retinoic acid receptor gamma Homo sapiens 150-158
25389900-6 2014 Retinoic acid, the main biologically active form of vitamin A, influences the expression of collagens, laminins, entactin, fibronectin, elastin and proteoglycans, which are the major components of the extracellular matrix. Tretinoin 0-13 nidogen 1 Homo sapiens 113-121
21674001-11 2011 These findings indicate a correlation amongst neural differentiation, aneuploidy, micronuclei formation and survivin downregulation in pluripotent stem cells exposed to RA, providing evidence that somatically generated chromosomal variation accompanies neurogenesis in vitro. Tretinoin 169-171 baculoviral IAP repeat-containing 5 Mus musculus 108-116
25014134-4 2014 In the present study, we have identified several critical genes in lipid homeostasis (Apoa1, Apoa2 and ApoF) that are repressed by RA-treatment in a SHP dependent manner, in vitro and also in vivo with the use of the SHP null mice. Tretinoin 131-133 apolipoprotein A-II Mus musculus 93-98
25014134-4 2014 In the present study, we have identified several critical genes in lipid homeostasis (Apoa1, Apoa2 and ApoF) that are repressed by RA-treatment in a SHP dependent manner, in vitro and also in vivo with the use of the SHP null mice. Tretinoin 131-133 apolipoprotein F Mus musculus 103-107
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 cytochrome P450, family 8, subfamily b, polypeptide 1 Mus musculus 104-110
21179414-0 2010 Characterization of protective human CD4CD25 FOXP3 regulatory T cells generated with IL-2, TGF-beta and retinoic acid. Tretinoin 104-117 forkhead box P3 Homo sapiens 45-50
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 bile acid-Coenzyme A: amino acid N-acyltransferase Mus musculus 124-128
24436055-6 2014 Furthermore, we demonstrated that the binding of the protein complex including RACK1 to the SCN1A promoter motif was decreased in neuron-like differentiation of the NT2 cells induced by retinoic acid and resulted in the upregulation of SCN1A transcription. Tretinoin 186-199 sodium voltage-gated channel alpha subunit 1 Homo sapiens 92-97
20437090-5 2010 In addition, TAM and RAL were able to prevent the RA-dependent decrease of Cx43 immunoreactivity in NTera2/D1 cells, normally observed during neuronal differentiation. Tretinoin 21-23 gap junction protein alpha 1 Homo sapiens 75-79
24436055-6 2014 Furthermore, we demonstrated that the binding of the protein complex including RACK1 to the SCN1A promoter motif was decreased in neuron-like differentiation of the NT2 cells induced by retinoic acid and resulted in the upregulation of SCN1A transcription. Tretinoin 186-199 sodium voltage-gated channel alpha subunit 1 Homo sapiens 236-241
24436055-7 2014 Taken together, this study reports a novel role of RACK1 in regulating SCN1A expression that participates in retinoic acid-induced neuronal differentiation of NT2 cells. Tretinoin 109-122 sodium voltage-gated channel alpha subunit 1 Homo sapiens 71-76
25135475-5 2014 Here, we demonstrate that the HOXA locus is organized by CTCF into chromatin loops and that CTCF depletion causes significantly enhanced activation of HOXA3 to -A7, -A9 to -A11, and -A13 in response to retinoic acid, with the highest effect observed for HOXA9. Tretinoin 202-215 homeobox A cluster Homo sapiens 30-34
20935222-6 2010 RA treatment induced UBE1L, ISG15, and UBP43 expression in RA-sensitive but not RA-resistant APL cells. Tretinoin 0-2 ubiquitin like modifier activating enzyme 7 Homo sapiens 21-26
20935222-6 2010 RA treatment induced UBE1L, ISG15, and UBP43 expression in RA-sensitive but not RA-resistant APL cells. Tretinoin 0-2 ISG15 ubiquitin like modifier Homo sapiens 28-33
25135475-5 2014 Here, we demonstrate that the HOXA locus is organized by CTCF into chromatin loops and that CTCF depletion causes significantly enhanced activation of HOXA3 to -A7, -A9 to -A11, and -A13 in response to retinoic acid, with the highest effect observed for HOXA9. Tretinoin 202-215 homeobox A3 Homo sapiens 151-156
25135475-5 2014 Here, we demonstrate that the HOXA locus is organized by CTCF into chromatin loops and that CTCF depletion causes significantly enhanced activation of HOXA3 to -A7, -A9 to -A11, and -A13 in response to retinoic acid, with the highest effect observed for HOXA9. Tretinoin 202-215 homeobox A9 Homo sapiens 254-259
25257666-5 2014 We identified several FXR-active structural classes including anthracyclines, benzimidazoles, dihydropyridines, pyrethroids, retinoic acids, and vinca alkaloids. Tretinoin 125-139 nuclear receptor subfamily 1 group H member 4 Homo sapiens 22-25
20960542-7 2010 Combining our data with previous reports, we propose a model wherein a sequential code of retinoic acid followed by canonical Wnt signaling are required for activation and maintenance of Pitx2 expression, respectively. Tretinoin 90-103 paired-like homeodomain transcription factor 2 Mus musculus 187-192
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 retinoic acid receptor, beta Mus musculus 73-80
20869113-0 2010 Protective effects of TRH and its analogues against various cytotoxic agents in retinoic acid (RA)-differentiated human neuroblastoma SH-SY5Y cells. Tretinoin 80-93 thyrotropin releasing hormone Homo sapiens 22-25
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 retinoid X receptor alpha Mus musculus 86-111
20869113-0 2010 Protective effects of TRH and its analogues against various cytotoxic agents in retinoic acid (RA)-differentiated human neuroblastoma SH-SY5Y cells. Tretinoin 95-97 thyrotropin releasing hormone Homo sapiens 22-25
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 retinoid X receptor alpha Mus musculus 113-121
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 cyclin-dependent kinase 1 Mus musculus 149-153
20869113-3 2010 We found that TRH and all the tested analogues at concentrations 0.1-50 muM attenuated cell damage induced by MPP(+) (2 mM), 3-nitropropionate (10 mM), hydrogen peroxide (0.5 mM), homocysteine (250 muM) and beta-amyloid (20muM) in retinoic acid differentiated SH-SY5Y cells. Tretinoin 231-244 thyrotropin releasing hormone Homo sapiens 14-17
25087568-5 2014 In addition, RA treatment induced novel binding of RARbeta/RXRalpha to Cdk1, Cdk2, Cyclin D, and Cdk6 genes. Tretinoin 13-15 retinoic acid receptor, beta Mus musculus 51-58
25087568-5 2014 In addition, RA treatment induced novel binding of RARbeta/RXRalpha to Cdk1, Cdk2, Cyclin D, and Cdk6 genes. Tretinoin 13-15 retinoid X receptor alpha Mus musculus 59-67
25087568-5 2014 In addition, RA treatment induced novel binding of RARbeta/RXRalpha to Cdk1, Cdk2, Cyclin D, and Cdk6 genes. Tretinoin 13-15 cyclin-dependent kinase 1 Mus musculus 71-75
25087568-5 2014 In addition, RA treatment induced novel binding of RARbeta/RXRalpha to Cdk1, Cdk2, Cyclin D, and Cdk6 genes. Tretinoin 13-15 cyclin-dependent kinase 6 Mus musculus 97-101
25087568-8 2014 RA signaling was implicated in normal liver regeneration as the mRNA levels of RARbeta, Aldh1a2, Crabp1, and Crbp1 were all induced 1.5 days after PH during the active phase of hepatocyte proliferation. Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 79-86
20632143-9 2010 These results indicate that ATRA within a certain range of concentration could reversibly induce the expression of FR-beta in a dosage- and cell type-dependent manner, and its action in KG-1 cells might be associated with the signal transduction of retinoid receptor RARalpha and RARgamma, rather than RARbeta and RXRs. Tretinoin 28-32 retinoic acid receptor gamma Homo sapiens 280-288
21414315-2 2011 Here we show that cellular retinoic acid binding protein-II (CRABP-II) can be specifically degraded by a novel compound, SNIPER-4, consisting of (--)-N-[(2S,3R)-3-amino-2-hydroxy-4-phenyl-butyryl]-L-leucine methyl ester and all-trans retinoic acid that are ligands for cellular inhibitor of apoptosis protein 1 (cIAP1) and CRABP-II, respectively. Tretinoin 227-247 baculoviral IAP repeat containing 2 Homo sapiens 269-310
21414315-2 2011 Here we show that cellular retinoic acid binding protein-II (CRABP-II) can be specifically degraded by a novel compound, SNIPER-4, consisting of (--)-N-[(2S,3R)-3-amino-2-hydroxy-4-phenyl-butyryl]-L-leucine methyl ester and all-trans retinoic acid that are ligands for cellular inhibitor of apoptosis protein 1 (cIAP1) and CRABP-II, respectively. Tretinoin 227-247 baculoviral IAP repeat containing 2 Homo sapiens 312-317
25087568-8 2014 RA signaling was implicated in normal liver regeneration as the mRNA levels of RARbeta, Aldh1a2, Crabp1, and Crbp1 were all induced 1.5 days after PH during the active phase of hepatocyte proliferation. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 88-95
25087568-9 2014 RA treatment prior to PH resulted in early up-regulation of RARbeta, Aldh1a2, Crabp1, and Crbp1, which was accompanied by an early induction of cell cycle genes. Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 60-67
20944006-2 2010 We report that a subset of bone marrow cells freshly isolated from C57BL/6 mice express the retinoic acid (RA)-synthesizing enzyme aldehyde dehydrogenase family 1, subfamily A2 (ALDH1a2) and are capable of providing RA to DC precursors in the bone marrow microenvironment. Tretinoin 92-105 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 131-176
25087568-9 2014 RA treatment prior to PH resulted in early up-regulation of RARbeta, Aldh1a2, Crabp1, and Crbp1, which was accompanied by an early induction of cell cycle genes. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 69-76
24008270-1 2014 All-trans retinoic acid (ATRA) inhibits matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fibroblasts, skin fibroblasts, bronchoalveolar lavage cells and cancer cells, but activates MMP-9 in neuroblast and leukemia cells. Tretinoin 0-23 matrix metallopeptidase 2 Homo sapiens 40-72
20944006-2 2010 We report that a subset of bone marrow cells freshly isolated from C57BL/6 mice express the retinoic acid (RA)-synthesizing enzyme aldehyde dehydrogenase family 1, subfamily A2 (ALDH1a2) and are capable of providing RA to DC precursors in the bone marrow microenvironment. Tretinoin 107-109 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 131-176
20944006-2 2010 We report that a subset of bone marrow cells freshly isolated from C57BL/6 mice express the retinoic acid (RA)-synthesizing enzyme aldehyde dehydrogenase family 1, subfamily A2 (ALDH1a2) and are capable of providing RA to DC precursors in the bone marrow microenvironment. Tretinoin 107-109 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 178-185
20944006-2 2010 We report that a subset of bone marrow cells freshly isolated from C57BL/6 mice express the retinoic acid (RA)-synthesizing enzyme aldehyde dehydrogenase family 1, subfamily A2 (ALDH1a2) and are capable of providing RA to DC precursors in the bone marrow microenvironment. Tretinoin 216-218 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 131-176
20944006-2 2010 We report that a subset of bone marrow cells freshly isolated from C57BL/6 mice express the retinoic acid (RA)-synthesizing enzyme aldehyde dehydrogenase family 1, subfamily A2 (ALDH1a2) and are capable of providing RA to DC precursors in the bone marrow microenvironment. Tretinoin 216-218 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 178-185
20944006-3 2010 RA induced bone marrow-derived DCs to express CCR9 and ALDH1a2 and conferred upon them mucosal DC functions, including induction of Foxp3(+) regulatory T cells, IgA-secreting B cells, and gut-homing molecules. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 55-62
21497760-1 2011 In vertebrate embryos, retinoic acid (RA) synthesized in the mesoderm by Raldh2 emanates to the hindbrain neuroepithelium, where it induces anteroposterior (AP)-restricted Hox expression patterns and rhombomere segmentation. Tretinoin 23-36 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-79
21497760-1 2011 In vertebrate embryos, retinoic acid (RA) synthesized in the mesoderm by Raldh2 emanates to the hindbrain neuroepithelium, where it induces anteroposterior (AP)-restricted Hox expression patterns and rhombomere segmentation. Tretinoin 38-40 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-79
21497760-3 2011 By analyzing Pbx1/Pbx2 and Hoxa1/Pbx1 null mice, we found that Raldh2 is itself under the transcriptional control of these factors and that the resulting RA-deficient phenotypes can be partially rescued by exogenous RA. Tretinoin 154-156 homeobox A1 Mus musculus 27-32
21497760-3 2011 By analyzing Pbx1/Pbx2 and Hoxa1/Pbx1 null mice, we found that Raldh2 is itself under the transcriptional control of these factors and that the resulting RA-deficient phenotypes can be partially rescued by exogenous RA. Tretinoin 154-156 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 63-69
20944006-5 2010 RA promoted bone marrow-derived DC production of bioactive TGF-beta by inhibiting suppressor of cytokine signaling 3 expression and thereby enhancing STAT3 activation. Tretinoin 0-2 transforming growth factor, beta 1 Mus musculus 59-67
24008270-1 2014 All-trans retinoic acid (ATRA) inhibits matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fibroblasts, skin fibroblasts, bronchoalveolar lavage cells and cancer cells, but activates MMP-9 in neuroblast and leukemia cells. Tretinoin 25-29 matrix metallopeptidase 2 Homo sapiens 40-72
24008270-2 2014 Very little is known regarding whether ATRA can activate or inhibit MMPs in human dental pulp cells (HDPCs). Tretinoin 39-43 matrix metallopeptidase 2 Homo sapiens 68-72
21444662-1 2011 The production of retinoic acid (RA) by dendritic cells (DCs) is critical for the induction of gut-tropic immune responses by driving the expression of intestinal-specific homing receptors, such as alpha4beta7 and CCR9, upon T and B cell activation. Tretinoin 18-31 C-C motif chemokine receptor 9 Homo sapiens 214-218
20944006-7 2010 Furthermore, MyD88 signaling enhanced RA-educated DC ALDH1a2 expression and was required for optimal TGF-beta production. Tretinoin 38-40 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 53-60
21444662-1 2011 The production of retinoic acid (RA) by dendritic cells (DCs) is critical for the induction of gut-tropic immune responses by driving the expression of intestinal-specific homing receptors, such as alpha4beta7 and CCR9, upon T and B cell activation. Tretinoin 33-35 C-C motif chemokine receptor 9 Homo sapiens 214-218
24008270-3 2014 The purpose of this study was to determine the effects of ATRA on the production and secretion of MMP-2 and -9 in HDPCs. Tretinoin 58-62 matrix metallopeptidase 2 Homo sapiens 98-110
24008270-5 2014 ATRA was found to decrease MMP-2 level in a dose-dependent manner. Tretinoin 0-4 matrix metallopeptidase 2 Homo sapiens 27-32
24008270-6 2014 Significant reduction in MMP-2 mRNA expression was also observed in HDPCs treated with 25 micromol L(-1) ATRA. Tretinoin 105-109 matrix metallopeptidase 2 Homo sapiens 25-30
20869773-2 2010 Likewise, it is shown that all-trans retinoic acid (ATRA) can greatly enhance TGF-beta-induced Treg conversion, a phenomenon which has mainly been studied in C57BL/6 mice. Tretinoin 37-50 transforming growth factor, beta 1 Mus musculus 78-86
24008270-8 2014 Taken together, ATRA had an inhibitory effect on MMP-2 expression in HDPCs, which suggests that ATRA could be a candidate as a medicament which could control the inflammation of pulp tissue in vital pulp therapy and regenerative endodontics. Tretinoin 16-20 matrix metallopeptidase 2 Homo sapiens 49-54
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 phosphoserine aminotransferase 1 Homo sapiens 164-168
24008270-8 2014 Taken together, ATRA had an inhibitory effect on MMP-2 expression in HDPCs, which suggests that ATRA could be a candidate as a medicament which could control the inflammation of pulp tissue in vital pulp therapy and regenerative endodontics. Tretinoin 96-100 matrix metallopeptidase 2 Homo sapiens 49-54
21505995-0 2011 Retinoic acid diminished the expression of MMP-2 in hyperoxia-exposed premature rat lung fibroblasts through regulating mitogen-activated protein kinases. Tretinoin 0-13 matrix metallopeptidase 2 Rattus norvegicus 43-48
20869773-2 2010 Likewise, it is shown that all-trans retinoic acid (ATRA) can greatly enhance TGF-beta-induced Treg conversion, a phenomenon which has mainly been studied in C57BL/6 mice. Tretinoin 52-56 transforming growth factor, beta 1 Mus musculus 78-86
20869773-3 2010 Here we show that, although purified naive cells are highly susceptible to Treg generation, total CD4(+) T-cell populations from different mouse strains display significantly different sensitivities to TGF-beta/ATRA-induced Treg conversion. Tretinoin 211-215 transforming growth factor, beta 1 Mus musculus 202-210
24619877-0 2014 Coordinated regulation of retinoic acid signaling pathway by KDM5B and polycomb repressive complex 2. Tretinoin 26-39 lysine demethylase 5B Homo sapiens 61-66
20941745-0 2010 Transcriptional activity analysis of promoter region of human PAX9 gene under dexamethasone, retinoic acid, and ergocalciferol treatment in MCF-7 and MDPC23. Tretinoin 93-106 paired box 9 Homo sapiens 62-66
20941745-5 2010 As results, retinoic acid and dexamethasone showed progressive decrease of PAX9 expression. Tretinoin 12-25 paired box 9 Homo sapiens 75-79
21505995-1 2011 This study examined the effects of retinoic acid (RA), PD98059, SP600125 and SB203580 on the hyperoxia-induced expression and regulation of matrix metalloproteinase-2 (MMP-2) and metalloproteinase-2 (TIMP-2) in premature rat lung fibroblasts (LFs). Tretinoin 35-48 matrix metallopeptidase 2 Rattus norvegicus 140-166
24619877-3 2014 Interestingly, co-occupancy of KDM5B and PRC2 was evidenced at the conserved cis-regulatory DNA element on retinoic acid (RA) responsive genes. Tretinoin 107-120 lysine demethylase 5B Homo sapiens 31-36
20941745-8 2010 In this study, we characterized the transcriptional activity of specific regions of the PAX9 promoter gene and we demonstrated that retinoic acid and ergocalciferol can modulate the transcriptional activity of PAX9 gene. Tretinoin 132-145 paired box 9 Homo sapiens 88-92
24619877-3 2014 Interestingly, co-occupancy of KDM5B and PRC2 was evidenced at the conserved cis-regulatory DNA element on retinoic acid (RA) responsive genes. Tretinoin 122-124 lysine demethylase 5B Homo sapiens 31-36
20941745-8 2010 In this study, we characterized the transcriptional activity of specific regions of the PAX9 promoter gene and we demonstrated that retinoic acid and ergocalciferol can modulate the transcriptional activity of PAX9 gene. Tretinoin 132-145 paired box 9 Homo sapiens 210-214
21344951-6 2011 Surprisingly, eukaryotic initiation factor 5A (Eif5a), a protein which is essential for cell proliferation and differentiation, was significantly down-regulated under RA treatment. Tretinoin 167-169 eukaryotic translation initiation factor 5A Mus musculus 47-52
21344951-7 2011 A time-dependent investigation of Eif5a showed that the RA treatment of stem cells resulted in a significant up-regulation of the Eif5a in the first 48 h followed by a progressive down-regulation thereafter. Tretinoin 56-58 eukaryotic translation initiation factor 5A Mus musculus 34-39
24619877-5 2014 Detailed chromatin immunoprecipitation assays addressed the seemingly paradox by revealing a biphasic effect of KDM5B on RA-induced gene activation through decoupled H3K4me3 demethylation and PRC2-antagonizing activities. Tretinoin 121-123 lysine demethylase 5B Homo sapiens 112-117
21344951-7 2011 A time-dependent investigation of Eif5a showed that the RA treatment of stem cells resulted in a significant up-regulation of the Eif5a in the first 48 h followed by a progressive down-regulation thereafter. Tretinoin 56-58 eukaryotic translation initiation factor 5A Mus musculus 130-135
25053430-6 2014 The co-regulator RERE, the loss of which results in ectopic Fgf8 expression and somite defects, was recruited near the RARb RARE by RA, but was released from the Fgf8 RARE by RA. Tretinoin 124-126 retinoic acid receptor, beta Mus musculus 119-123
21360626-3 2011 Retinoic acid (RA) rapidly downregulates Pml, resulting in the replacement of BRGC with Brm-containing remodeling complex, disassociation of SF1 and Sp1, retaining of TR2, recruitment of receptor-interaction protein 140, G9a and HP1gamma, and sequential insertion of two nucleosomes on CR1 that progressively displays repressive heterochromatin marks. Tretinoin 0-13 chromobox 3 Homo sapiens 229-237
20737513-2 2010 To address this within a physiological context, we used retinaldehyde dehydrogenase-2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Tretinoin 135-148 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 87-93
20737513-2 2010 To address this within a physiological context, we used retinaldehyde dehydrogenase-2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Tretinoin 135-148 Rac family small GTPase 1 Mus musculus 231-235
24821725-6 2014 Importantly, RA treatment differentially mediates the removal of HDACs from the Hoxa1, Cyp26a1, and RARbeta2 genes and promotes the deposition of the H3K27ac mark at these genes. Tretinoin 13-15 homeobox A1 Homo sapiens 80-85
20737513-2 2010 To address this within a physiological context, we used retinaldehyde dehydrogenase-2 (Raldh2) null mouse embryos and demonstrate that retinoic acid (RA) deficiency results in abnormal yolk sac vascular remodeling due to decreased Rac1 activation, increased RhoA activation, and increased focal adhesions. Tretinoin 135-148 ras homolog family member A Mus musculus 258-262
21262915-0 2011 Activation of the aryl hydrocarbon receptor AhR Promotes retinoic acid-induced differentiation of myeloblastic leukemia cells by restricting expression of the stem cell transcription factor Oct4. Tretinoin 57-70 aryl hydrocarbon receptor Homo sapiens 18-43
21262915-0 2011 Activation of the aryl hydrocarbon receptor AhR Promotes retinoic acid-induced differentiation of myeloblastic leukemia cells by restricting expression of the stem cell transcription factor Oct4. Tretinoin 57-70 aryl hydrocarbon receptor Homo sapiens 44-47
21262915-4 2011 RA effects are mediated by RAR/RXR receptors that we show are modified by interactions with the aryl hydrocarbon receptor (AhR), a protein functioning both as a transcription factor and a ligand-dependent adaptor in an ubiquitin ligase complex. Tretinoin 0-2 aryl hydrocarbon receptor Homo sapiens 96-121
21262915-4 2011 RA effects are mediated by RAR/RXR receptors that we show are modified by interactions with the aryl hydrocarbon receptor (AhR), a protein functioning both as a transcription factor and a ligand-dependent adaptor in an ubiquitin ligase complex. Tretinoin 0-2 aryl hydrocarbon receptor Homo sapiens 123-126
24991767-6 2014 As AML cells are blocked in their differentiation, we tested if the expression levels of WIPI-1 and WIPI-2 increase during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of APL. Tretinoin 133-146 WD repeat domain, phosphoinositide interacting 2 Homo sapiens 100-106
21262915-6 2011 Here, we assessed the role of AhR during RA-induced differentiation and a hypothesized convergence at Oct4, a transcription factor believed to maintain stem cell characteristics. Tretinoin 41-43 aryl hydrocarbon receptor Homo sapiens 30-33
21262915-7 2011 RA upregulated AhR and downregulated Oct4 during differentiation of HL-60 promyelocytic leukemia cells. Tretinoin 0-2 aryl hydrocarbon receptor Homo sapiens 15-18
21262915-9 2011 AhR overexpression also increased levels of activated Raf1, which is known to help propel RA-induced differentiation. Tretinoin 90-92 aryl hydrocarbon receptor Homo sapiens 0-3
21262915-9 2011 AhR overexpression also increased levels of activated Raf1, which is known to help propel RA-induced differentiation. Tretinoin 90-92 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 54-58
20222140-7 2010 Specialized CD103(+) intestinal DC can promote the differentiation of Foxp3(+) regulatory T cells via a retinoic acid-dependent process. Tretinoin 104-117 forkhead box P3 Homo sapiens 70-75
20943360-6 2010 The expression of thioredoxin reductase 1 was increased in cells treated with retinoic acid, whereas that of selenoprotein P was decreased in cells exposed to insulin. Tretinoin 78-91 thioredoxin reductase 1 Bos taurus 18-41
24991767-6 2014 As AML cells are blocked in their differentiation, we tested if the expression levels of WIPI-1 and WIPI-2 increase during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of APL. Tretinoin 148-152 WD repeat domain, phosphoinositide interacting 2 Homo sapiens 100-106
24819975-0 2014 Small ubiquitin-related modifier-1 modification regulates all-trans-retinoic acid-induced differentiation via stabilization of retinoic acid receptor alpha. Tretinoin 68-81 small ubiquitin like modifier 1 Homo sapiens 0-34
21487509-7 2010 We demonstrate that RA containing PLGA nanoparticles suppress IL-17 production and ROR-gamma(t) expression in T cells polarized towards the Th17 phenotype in vitro with similar potency to that of free drug. Tretinoin 20-22 long intergenic non-protein coding RNA, regulator of reprogramming Homo sapiens 83-86
21316346-4 2011 In primary hepatocytes, retinal and retinoic acid (RA) synergized with insulin to induce Srebp-1c expression. Tretinoin 36-49 sterol regulatory element binding transcription factor 1 Rattus norvegicus 89-97
21316346-4 2011 In primary hepatocytes, retinal and retinoic acid (RA) synergized with insulin to induce Srebp-1c expression. Tretinoin 51-53 sterol regulatory element binding transcription factor 1 Rattus norvegicus 89-97
24819975-1 2014 Small ubiquitin-related modifier-1 (SUMO-1) modification has been implicated in many important cellular processes, including cell cycle progression, apoptosis, cellular proliferation, and development, but its role in all-trans-retinoic acid (ATRA)-induced differentiation processes of cancer cells remains unclear. Tretinoin 221-240 small ubiquitin like modifier 1 Homo sapiens 0-34
24819975-1 2014 Small ubiquitin-related modifier-1 (SUMO-1) modification has been implicated in many important cellular processes, including cell cycle progression, apoptosis, cellular proliferation, and development, but its role in all-trans-retinoic acid (ATRA)-induced differentiation processes of cancer cells remains unclear. Tretinoin 221-240 small ubiquitin like modifier 1 Homo sapiens 36-42
24819975-1 2014 Small ubiquitin-related modifier-1 (SUMO-1) modification has been implicated in many important cellular processes, including cell cycle progression, apoptosis, cellular proliferation, and development, but its role in all-trans-retinoic acid (ATRA)-induced differentiation processes of cancer cells remains unclear. Tretinoin 242-246 small ubiquitin like modifier 1 Homo sapiens 0-34
24819975-1 2014 Small ubiquitin-related modifier-1 (SUMO-1) modification has been implicated in many important cellular processes, including cell cycle progression, apoptosis, cellular proliferation, and development, but its role in all-trans-retinoic acid (ATRA)-induced differentiation processes of cancer cells remains unclear. Tretinoin 242-246 small ubiquitin like modifier 1 Homo sapiens 36-42
21129252-0 2010 [Expression of ifi56 gene in ATRA-induced APL cell differentiation and construction of ifi56 gene eukaryotic expression plasmid]. Tretinoin 29-33 interferon induced protein with tetratricopeptide repeats 1 Homo sapiens 15-20
21061155-0 2011 Localization of prohibitin in the nuclear matrix and alteration of its expression during differentiation of human neuroblastoma SK-N-SH cells induced by retinoic acid. Tretinoin 153-166 prohibitin 1 Homo sapiens 16-26
24819975-2 2014 Here, we report for the first time that ATRA-induced differentiation of leukemia and osteosarcoma is accompanied by a decrease in the level of SUMO-1 protein. Tretinoin 40-44 small ubiquitin like modifier 1 Homo sapiens 143-149
21061155-2 2011 Results of two-dimensional gel electrophoresis (2-DE), mass spectrometry (MS) identification, and protein immunoblotting all confirm that PHB was present in the components of SK-N-SH nuclear matrix proteins and was down-regulated after RA treatment. Tretinoin 236-238 prohibitin 1 Homo sapiens 138-141
21061155-3 2011 Immunofluorescence microscopy observations show that PHB was localized in the nuclear matrix and its distribution was altered due to RA treatment. Tretinoin 133-135 prohibitin 1 Homo sapiens 53-56
21129252-1 2010 This study was purposed to investigate the expression of ifi56 gene in the ATRA-induced acute promyelocytic leukemia (APL) NB4 cell differentiation and to construct the eukaryotic expression plasmid of ifi56 gene. Tretinoin 75-79 interferon induced protein with tetratricopeptide repeats 1 Homo sapiens 57-62
24819975-3 2014 Our results also demonstrated that depletion or inhibition of SUMO-1 blocks ATRA-induced differentiation, suggesting that SUMO-1 is critical for the differentiation effect of ATRA. Tretinoin 76-80 small ubiquitin like modifier 1 Homo sapiens 62-68
21129252-2 2010 RT-PCR was used to detect the expression of ifi56 in NB4 cells treated with ATRA for different time. Tretinoin 76-80 interferon induced protein with tetratricopeptide repeats 1 Homo sapiens 44-49
21061155-4 2011 Laser confocal microscopy results reveal that PHB colocalized with the expression products of c-myc, c-fos, p53, and Rb, but the colocalization region was altered after RA treatment. Tretinoin 169-171 prohibitin 1 Homo sapiens 46-49
24819975-3 2014 Our results also demonstrated that depletion or inhibition of SUMO-1 blocks ATRA-induced differentiation, suggesting that SUMO-1 is critical for the differentiation effect of ATRA. Tretinoin 76-80 small ubiquitin like modifier 1 Homo sapiens 122-128
21129252-6 2010 The results showed that the ifi56 mRNA was almost undetectable in untreated NB4 cells, but it significantly increased after ATRA treatment for 72 hours. Tretinoin 124-128 interferon induced protein with tetratricopeptide repeats 1 Homo sapiens 28-33
24819975-3 2014 Our results also demonstrated that depletion or inhibition of SUMO-1 blocks ATRA-induced differentiation, suggesting that SUMO-1 is critical for the differentiation effect of ATRA. Tretinoin 175-179 small ubiquitin like modifier 1 Homo sapiens 62-68
24819975-3 2014 Our results also demonstrated that depletion or inhibition of SUMO-1 blocks ATRA-induced differentiation, suggesting that SUMO-1 is critical for the differentiation effect of ATRA. Tretinoin 175-179 small ubiquitin like modifier 1 Homo sapiens 122-128
24819975-8 2014 SUMO-1 modification may thus serve an important role in controlling ATRA-induced cell differentiation in cancers. Tretinoin 68-72 small ubiquitin like modifier 1 Homo sapiens 0-6
21048796-6 2011 Addition of retinoic acid, boosted by the pancreatic endoderm inducer indolactam V (ILV), yielded pancreatic progenitors expressing pancreatic and duodenal homeobox 1 (PDX1), neurogenin 3 (NGN3) and neurogenic differentiation 1 (NEUROD1) markers. Tretinoin 12-25 pancreatic and duodenal homeobox 1 Homo sapiens 168-172
24220301-3 2014 This subset expressed homing receptors for skin and inflammatory sites, and was mainly induced by B220(-)CD8alpha(-)CD11b(+)CD103(-) MLN-DCs in an IL-6- and OX40 ligand-dependent manner, whereas RA inhibited this induction. Tretinoin 195-197 CD8 antigen, alpha chain Mus musculus 105-113
21253593-3 2011 We found that ATRA helped maintain FOXP3 expression during the expansion process, but this effect was transient and serum-dependent. Tretinoin 14-18 forkhead box P3 Homo sapiens 35-40
20691163-2 2010 Ski represses retinoic acid (RA) signaling by interacting with, and stabilizing, key components of the co-repressor complex, namely, HDAC3. Tretinoin 14-27 histone deacetylase 3 Homo sapiens 133-138
24576683-0 2014 Retinoic acid induced repair in the lung of adult hyperoxic mice, reducing transforming growth factor-beta1 (TGF-beta1) mediated abnormal alterations. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 75-107
20691163-2 2010 Ski represses retinoic acid (RA) signaling by interacting with, and stabilizing, key components of the co-repressor complex, namely, HDAC3. Tretinoin 29-31 histone deacetylase 3 Homo sapiens 133-138
21253593-6 2011 Examination of CD45RA+ and CD45RA- Treg subsets revealed that ATRA failed to maintain suppressive activity in either population, but interestingly, Tregs expanded in the presence of both rapamycin and ATRA displayed more suppressive activity and had a more favorable epigenetic status of the FOXP3 gene than Tregs expanded in the presence of rapamycin only. Tretinoin 201-205 forkhead box P3 Homo sapiens 292-297
24576683-0 2014 Retinoic acid induced repair in the lung of adult hyperoxic mice, reducing transforming growth factor-beta1 (TGF-beta1) mediated abnormal alterations. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 109-118
20445074-5 2010 We show that this inductive event is dependent on RA synthesis from aldh1a2 in the ventral posterior pharynx. Tretinoin 50-52 aldehyde dehydrogenase 1 family, member A2 Danio rerio 68-75
24576683-10 2014 This positive effect of retinoic acid resulted from the inhibition of Smad3/TGF-beta1 signaling via reduced Smad4 mRNA and increased Smad7 protein expression. Tretinoin 24-37 SMAD family member 3 Mus musculus 70-75
24576683-10 2014 This positive effect of retinoic acid resulted from the inhibition of Smad3/TGF-beta1 signaling via reduced Smad4 mRNA and increased Smad7 protein expression. Tretinoin 24-37 transforming growth factor, beta 1 Mus musculus 76-85
22167840-3 2011 Factors that regulate expression and activity of MGP include vitamin D, retinoic acid, extracellular calcium ions, cytokines, and some hormones. Tretinoin 72-85 matrix Gla protein Homo sapiens 49-52
24576683-10 2014 This positive effect of retinoic acid resulted from the inhibition of Smad3/TGF-beta1 signaling via reduced Smad4 mRNA and increased Smad7 protein expression. Tretinoin 24-37 SMAD family member 7 Mus musculus 133-138
24576683-11 2014 Retinoic acid also induced alveolarization and restricted Smad3/TGF-beta1 signaling by decreasing Smad4 mRNA in healthy mice. Tretinoin 0-13 SMAD family member 3 Mus musculus 58-63
24576683-11 2014 Retinoic acid also induced alveolarization and restricted Smad3/TGF-beta1 signaling by decreasing Smad4 mRNA in healthy mice. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 64-73
24576683-12 2014 Thus, retinoic acid helped repair Smad3/TGF-beta1-induced lung damage in hyperoxic mice. Tretinoin 6-19 SMAD family member 3 Mus musculus 34-39
22220257-14 2011 Adapting standard AIDA treatment protocols to limited resources by reducing dose-intensity during consolidation, using ATRA in the consolidation phase and alternative anthracyclin (doxorubicin) may be a valid treatment option for APL in developing countries. Tretinoin 119-123 axin interactor, dorsalization associated Homo sapiens 18-22
20534877-4 2010 We have previously shown that all-trans retinoic acid (atRA), a bioactive metabolite of vitamin A, significantly augmented DC MMP-9 mRNA and protein production. Tretinoin 30-53 matrix metallopeptidase 9 Mus musculus 126-131
24576683-12 2014 Thus, retinoic acid helped repair Smad3/TGF-beta1-induced lung damage in hyperoxic mice. Tretinoin 6-19 transforming growth factor, beta 1 Mus musculus 40-49
20534877-4 2010 We have previously shown that all-trans retinoic acid (atRA), a bioactive metabolite of vitamin A, significantly augmented DC MMP-9 mRNA and protein production. Tretinoin 55-59 matrix metallopeptidase 9 Mus musculus 126-131
24677291-0 2014 Retinoic acid induces mouse bone marrow-derived CD15+, Oct4+ and CXCR4+ stem cells into male germ-like cells in a two-dimensional cell culture system. Tretinoin 0-13 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 55-59
20534877-5 2010 We investigated the mechanisms by which atRA increased MMP-9 activity in vitro. Tretinoin 40-44 matrix metallopeptidase 9 Mus musculus 55-60
24677291-1 2014 We have examined the effect of retinoic acid (RA) on differentiation of bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells. Tretinoin 31-44 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 102-106
20534877-8 2010 AtRA-induced Mmp-9 gene expression in DC was blocked by transcriptional inhibition. Tretinoin 0-4 matrix metallopeptidase 9 Mus musculus 13-18
22128244-9 2011 The FRMD7 transcripts showed similar tissue distributions and were upregulated following all trans retinoic acid (ATRA)-induced differentiation of NT2 cells. Tretinoin 99-112 FERM domain containing 7 Homo sapiens 4-9
24677291-1 2014 We have examined the effect of retinoic acid (RA) on differentiation of bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells. Tretinoin 46-48 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 102-106
22128244-9 2011 The FRMD7 transcripts showed similar tissue distributions and were upregulated following all trans retinoic acid (ATRA)-induced differentiation of NT2 cells. Tretinoin 114-118 FERM domain containing 7 Homo sapiens 4-9
20534877-11 2010 Chromatin immunoprecipitation assays indicated RARalpha and histone acetyltransferase p300 recruitment to, and acetylation of, histone H3 at the Mmp-9 promoter was greater after atRA treatment. Tretinoin 178-182 matrix metallopeptidase 9 Mus musculus 145-150
24677291-11 2014 Thus RA can induce differentiation of mouse bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells in vitro. Tretinoin 5-7 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 74-78
22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Tretinoin 34-38 retinoic acid receptor gamma Homo sapiens 140-148
24790153-8 2014 Thus, we conclude that ATRA enhances both Arg-1 and iNOS expression in IFN-gamma-treated DCs, resulting in a tolerogenic phenotype. Tretinoin 23-27 arginase, liver Mus musculus 42-47
24816818-4 2014 We found that the expression of Tal2 gene was induced in P19 cells after addition of atRA in suspension culture. Tretinoin 85-89 T cell acute lymphocytic leukemia 2 Mus musculus 32-36
21931768-0 2011 All-trans retinoic acid promotes TGF-beta-induced Tregs via histone modification but not DNA demethylation on Foxp3 gene locus. Tretinoin 10-23 transforming growth factor, beta 1 Mus musculus 33-41
21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 45-58 transforming growth factor, beta 1 Mus musculus 94-102
21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 60-64 transforming growth factor, beta 1 Mus musculus 94-102
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 CD3 antigen, epsilon polypeptide Mus musculus 99-102
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 transforming growth factor, beta 1 Mus musculus 138-146
21931768-6 2011 atRA did not significantly affect the phosphorylation levels of Smad2/3 and still promoted iTreg differentiation in CD4(+) cells isolated from Smad3 KO and Smad2 conditional KO mice. Tretinoin 0-4 SMAD family member 3 Mus musculus 143-148
20427117-6 2010 Furthermore, inhibition of GSK3beta activity blocked the ability of RA to direct cell differentiation along the neural lineage, suggesting a role for appropriately regulated WNT signalling. Tretinoin 68-70 glycogen synthase kinase 3 beta Homo sapiens 27-35
20061533-5 2010 BCMO1 acts downstream of SR-BI and converts absorbed beta,beta-carotene to the retinoic acid precursor, retinaldehyde. Tretinoin 79-92 beta-carotene oxygenase 1 Mus musculus 0-5
20061533-5 2010 BCMO1 acts downstream of SR-BI and converts absorbed beta,beta-carotene to the retinoic acid precursor, retinaldehyde. Tretinoin 79-92 scavenger receptor class B, member 1 Mus musculus 25-30
24816818-7 2014 These results demonstrate for the first time that atRA induces Tal2 expression in P19 cells, and suggest that TAL2 commits to the acquisition of neural fate in brain development. Tretinoin 50-54 T cell acute lymphocytic leukemia 2 Mus musculus 63-67
24816818-7 2014 These results demonstrate for the first time that atRA induces Tal2 expression in P19 cells, and suggest that TAL2 commits to the acquisition of neural fate in brain development. Tretinoin 50-54 T cell acute lymphocytic leukemia 2 Mus musculus 110-114
24680851-4 2014 The expression of E-cadherin, Occludin and Claudin-1 proteins were up-regulated after treatment with atRA for 6h to 48 h. We concluded that atRA could promote the epithelial barrier function of myopia RPE monolayer possibly by regulating expression of intercellular junction-associated proteins. Tretinoin 101-105 occludin Cavia porcellus 30-38
20428830-2 2010 Previous finding that ligand binding domain (LBD) fragment of RXR alpha specifically inhibits retinoic acid receptor-gamma (RAR gamma) activity led us to investigate the functional role of RXR alpha LBD fragment in radiosensitization by retinoic acid (RA). Tretinoin 94-107 retinoic acid receptor gamma Homo sapiens 124-133
20428830-2 2010 Previous finding that ligand binding domain (LBD) fragment of RXR alpha specifically inhibits retinoic acid receptor-gamma (RAR gamma) activity led us to investigate the functional role of RXR alpha LBD fragment in radiosensitization by retinoic acid (RA). Tretinoin 124-126 retinoic acid receptor gamma Homo sapiens 94-122
20428830-6 2010 Taken together, we hypothesize that the RXR alpha LBD fragment may act as a negative regulator of radiosensitizing effect of RA by restricting the RAR gamma-mediated biological response to RA. Tretinoin 125-127 retinoic acid receptor gamma Homo sapiens 147-156
21931768-7 2011 Conversely, atRA markedly increased ERK1/2 activation, and blockade of ERK1/2 signaling completely abolished the enhanced effects of atRA on Foxp3 expression. Tretinoin 12-16 mitogen-activated protein kinase 3 Mus musculus 36-42
21931768-7 2011 Conversely, atRA markedly increased ERK1/2 activation, and blockade of ERK1/2 signaling completely abolished the enhanced effects of atRA on Foxp3 expression. Tretinoin 133-137 mitogen-activated protein kinase 3 Mus musculus 71-77
24680851-4 2014 The expression of E-cadherin, Occludin and Claudin-1 proteins were up-regulated after treatment with atRA for 6h to 48 h. We concluded that atRA could promote the epithelial barrier function of myopia RPE monolayer possibly by regulating expression of intercellular junction-associated proteins. Tretinoin 140-144 occludin Cavia porcellus 30-38
24410928-0 2014 All-trans-retinoic acid ameliorates the inflammation by inducing transforming growth factor beta 1 and interleukin 10 in mouse epididymitis. Tretinoin 0-23 transforming growth factor, beta 1 Mus musculus 65-98
24410928-7 2014 RESULTS: Our results demonstrate that atRA ameliorates the inflammation in mouse epididymitis by decreasing the expression of the pro-inflammatory cytokines and increasing the expression of anti-inflammatory factors including TGF-beta1 and IL-10. Tretinoin 38-42 transforming growth factor, beta 1 Mus musculus 226-235
20421479-3 2010 In this study, we show that Ag-specific memory Th cells were redifferentiated into Foxp3(+) T cells by TGF-beta when stimulated in the presence of all-trans retinoic acid and rapamycin. Tretinoin 157-170 forkhead box P3 Homo sapiens 83-88
24410928-8 2014 Our results show that the upregulating effect of atRA on TGF-beta1 was mediated by RARalpha, and the enhancing effect of atRA on IL-10 expression was mediated via RARbeta. Tretinoin 49-53 transforming growth factor, beta 1 Mus musculus 57-66
24410928-8 2014 Our results show that the upregulating effect of atRA on TGF-beta1 was mediated by RARalpha, and the enhancing effect of atRA on IL-10 expression was mediated via RARbeta. Tretinoin 121-125 retinoic acid receptor, beta Mus musculus 163-170
21637844-8 2011 Thus the Hoxb1 patterning activity includes the regulation of the cellular response to retinoic acid and the delay of the expression of genes that commit cells to neural differentiation. Tretinoin 87-100 homeobox B1 Mus musculus 9-14
24674590-4 2014 In this study, we established an FGF2 low-dose-dependent embryonic stem cell line from cynomolgus monkeys and then analyzed neural differentiation in cultures supplemented with retinoic acid and FGF2. Tretinoin 177-190 fibroblast growth factor 2 Macaca fascicularis 33-37
20346212-8 2010 RESULTS: The research showed that K1 and FTC-133 cells had cell spacing increases, with an outer edge of smooth, nuclear chromatin condensation after RA combined TSA. Tretinoin 150-152 keratin 1 Homo sapiens 34-48
24674590-5 2014 When only retinoic acid was added to culture, neurons differentiated from FGF2 low-dose-dependent embryonic stem cells. Tretinoin 10-23 fibroblast growth factor 2 Macaca fascicularis 74-78
20346212-14 2010 CONCLUSIONS: Lower concentrations of RA combined with lower concentrations of TSA have both inhibited cell proliferation, decreased toxicity of the drugs, and increased the effect of K1 and FTC-133 cell differentiation. Tretinoin 37-39 keratin 1 Homo sapiens 183-197
21419270-2 2011 Through the RA production, these DCs play a pivotal role in imprinting lymphocytes with gut-homing specificity, and contribute to the development of immune tolerance by enhancing the differentiation of Foxp3(+) regulatory T cells and inhibiting that of inflammatory Th17 cells. Tretinoin 12-14 forkhead box P3 Homo sapiens 202-207
24791595-0 2014 The effect to IL-3Ralpha, downstream PI3k/Akt signaling of all-trans retinoic acid and arsenic trioxide in NB4 cells. Tretinoin 69-82 interleukin 3 receptor subunit alpha Homo sapiens 14-24
21159962-2 2010 Suppression of synaptic activity increases synaptic strength by inducing synthesis of retinoic acid (RA), which activates postsynaptic synthesis of AMPA-type glutamate receptors (AMPARs) in dendrites and promotes synaptic insertion of newly synthesized AMPARs. Tretinoin 86-99 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 179-185
21159962-2 2010 Suppression of synaptic activity increases synaptic strength by inducing synthesis of retinoic acid (RA), which activates postsynaptic synthesis of AMPA-type glutamate receptors (AMPARs) in dendrites and promotes synaptic insertion of newly synthesized AMPARs. Tretinoin 86-99 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 253-259
21159962-2 2010 Suppression of synaptic activity increases synaptic strength by inducing synthesis of retinoic acid (RA), which activates postsynaptic synthesis of AMPA-type glutamate receptors (AMPARs) in dendrites and promotes synaptic insertion of newly synthesized AMPARs. Tretinoin 101-103 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 179-185
21159962-2 2010 Suppression of synaptic activity increases synaptic strength by inducing synthesis of retinoic acid (RA), which activates postsynaptic synthesis of AMPA-type glutamate receptors (AMPARs) in dendrites and promotes synaptic insertion of newly synthesized AMPARs. Tretinoin 101-103 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 253-259
21159962-4 2010 Although activity-dependent RA synthesis is maintained in Fmr1 knock-out neurons, RA-dependent dendritic translation of GluR1-type AMPA receptors is impaired. Tretinoin 82-84 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 120-125
19932628-5 2010 The silencing of PKC-delta prevented the RA-induced inhibition of the secretion and synthesis of IGF-I and cell viability (p<0.05). Tretinoin 41-43 protein kinase C delta Homo sapiens 17-26
19932628-10 2010 These results indicate that the anticancer effects of RA are mediated by inhibition of the secretion and synthesis of IGF-I, and involve a PKC-delta-dependent mechanism, and they provide evidence of an interaction between PKC-delta and reactive oxygen species. Tretinoin 54-56 protein kinase C delta Homo sapiens 139-148
19932628-10 2010 These results indicate that the anticancer effects of RA are mediated by inhibition of the secretion and synthesis of IGF-I, and involve a PKC-delta-dependent mechanism, and they provide evidence of an interaction between PKC-delta and reactive oxygen species. Tretinoin 54-56 protein kinase C delta Homo sapiens 222-231
24608339-4 2014 Immunohistochemistry was performed on the tissue microarray using monoclonal antibodies which we have developed to the retinoic acid metabolising enzymes CYP26A1, CYP26B1, CYP26C1 and lecithin retinol acyl transferase (LRAT) using a semi-quantitative scoring scheme to assess expression. Tretinoin 119-132 lecithin retinol acyltransferase Homo sapiens 184-217
24608339-4 2014 Immunohistochemistry was performed on the tissue microarray using monoclonal antibodies which we have developed to the retinoic acid metabolising enzymes CYP26A1, CYP26B1, CYP26C1 and lecithin retinol acyl transferase (LRAT) using a semi-quantitative scoring scheme to assess expression. Tretinoin 119-132 lecithin retinol acyltransferase Homo sapiens 219-223
20200558-8 2010 Cumulatively, our data suggest a model whereby inhibition of PRKCD decreases TOP2B protein levels, leading to a loss of TOP2B-mediated repressive effects on RA-induced transcription and granulocytic differentiation. Tretinoin 157-159 protein kinase C delta Homo sapiens 61-66
24608339-12 2014 This study has shown that the retinoic acid metabolising enzymes CYP26A1, CYP26B1 and LRAT are significantly overexpressed in colorectal cancer and that CYP26B1 and LRAT are significantly associated with prognosis both in the total cohort and in those tumours which are mismatch repair proficient. Tretinoin 30-43 lecithin retinol acyltransferase Homo sapiens 86-90
20826193-0 2010 Inhibition of the redox function of APE1/Ref-1 in myeloid leukemia cell lines results in a hypersensitive response to retinoic acid-induced differentiation and apoptosis. Tretinoin 118-131 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 36-40
20826193-0 2010 Inhibition of the redox function of APE1/Ref-1 in myeloid leukemia cell lines results in a hypersensitive response to retinoic acid-induced differentiation and apoptosis. Tretinoin 118-131 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 41-46
24608339-12 2014 This study has shown that the retinoic acid metabolising enzymes CYP26A1, CYP26B1 and LRAT are significantly overexpressed in colorectal cancer and that CYP26B1 and LRAT are significantly associated with prognosis both in the total cohort and in those tumours which are mismatch repair proficient. Tretinoin 30-43 lecithin retinol acyltransferase Homo sapiens 165-169
21086135-7 2010 In addition, in cells induced to differentiate by ATRA or VD3, Nitroblue-tetrazolium (NBT) reduction and esterase activity, were blocked either by LY294002, a PI3K inhibitor, or by BIM, a PKC inhibitor, without affecting cell surface markers such as CD11b or CD14. Tretinoin 50-54 CD14 molecule Homo sapiens 259-263
24406248-0 2014 Reactive oxygen species-regulated glycogen synthase kinase-3beta activation contributes to all-trans retinoic acid-induced apoptosis in granulocyte-differentiated HL60 cells. Tretinoin 101-114 glycogen synthase kinase 3 beta Homo sapiens 34-64
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 matrix metallopeptidase 2 Rattus norvegicus 206-211
24406248-5 2014 ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3beta. Tretinoin 0-4 glycogen synthase kinase 3 beta Homo sapiens 165-174
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 360-364
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 matrix metallopeptidase 2 Rattus norvegicus 249-254
20054864-7 2010 The addition of all trans retinoic acid blocked DEAB-mediated expansion of ST-HSCs in culture, suggesting that ALDH1a1 regulates HSC differentiation via augmentation of retinoid signaling. Tretinoin 26-39 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 111-118
24406248-6 2014 Pharmacologically and genetically inhibiting GSK-3beta effectively retarded ATRA-induced Mcl-1 degradation and apoptosis. Tretinoin 76-80 glycogen synthase kinase 3 beta Homo sapiens 45-54
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 17-21 glycogen synthase kinase 3 beta Homo sapiens 185-194
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 172-176 glycogen synthase kinase 3 beta Homo sapiens 185-194
24406248-9 2014 This study indicates that ROS initiate GSK-3beta-dependent apoptosis in granulocyte-differentiated cells after long-term ATRA treatment. Tretinoin 121-125 glycogen synthase kinase 3 beta Homo sapiens 39-48
20167204-5 2010 In animal cap explant assay, we further demonstrated that mkrn2(s)-7 not only inhibits activin and retinoic acid-induced animal cap neuralization and the expression of a pan-neural marker neural cell adhesion molecule, but also induces GSK-3beta expression. Tretinoin 99-112 E3 ubiquitin-protein ligase makorin-2 Xenopus laevis 58-63
21176354-6 2010 The results showed that the expression level of IL-3Ralpha mRNA was obviously down-regulated in NB4 cells treated with ATRA for 24 hours, but during differentiation of ATRA induced NB4 cells, the expression level of IL-3Ralpha mRNA was gradually restored, while the expression levels of GM-CSFRalpha mRNA and hbetac mRNA were gradually up-regulated. Tretinoin 168-172 interleukin 3 receptor subunit alpha Homo sapiens 216-226
20850164-2 2010 We report that the PRRSV nonstructural protein 1alpha (Nsp1alpha) subunit of Nsp1 is a nuclear-cytoplasmic protein distributed to the nucleus and contains a strong suppressive activity for IFN-beta production that is mediated through the retinoic acid-inducible gene I (RIG-I) signaling pathway. Tretinoin 238-251 interferon beta 1 Homo sapiens 189-197
24500985-0 2014 Effects of all-trans retinoic acid on signal pathway of cyclooxygenase-2 and Smad3 in transforming growth factor-beta-stimulated glomerular mesangial cells. Tretinoin 11-34 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 56-72
24500985-3 2014 In this study, the mRNA and protein of Smad3, Smad7, and COX-2 were detected by reverse transcription-polymerase chain reaction and Western blot, respectively, in mesangial cells stimulated by transforming growth factor-beta (TGF-beta) and treated with ATRA at various concentrations and times. Tretinoin 253-257 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 57-62
20142486-3 2010 We show that eve1 is involved in establishing trunk and tail neural ectoderm by two independent mechanisms: First, eve1 posteriorizes neural ectoderm via induction of aldh1a2, which encodes an enzyme that synthesizes retinoic acid; second, eve1 is involved in neural induction in the posterior ectoderm by attenuating BMP expression. Tretinoin 217-230 aldehyde dehydrogenase 1 family, member A2 Danio rerio 167-174
24500985-7 2014 The expression of Smad3, Smad7, and COX-2 mRNA and protein was increased by exogenous TGF-beta, but inhibited by pretreatment of ATRA, in dose and time-dependent manners. Tretinoin 129-133 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 36-41
21076177-5 2010 We showed that the Npm1/Sox2 complex was sustained when cells were induced to differentiate by retinoic acid, while decreased in the other differentiation pathways. Tretinoin 95-108 nucleophosmin 1 Homo sapiens 19-23
19960509-2 2010 In addition to confirming these findings, we further found that ATRA repressed the expression of betaine-homocysteine methyltransferase (BHMT) and cystathionine-beta-synthase (CBS), which are key enzymes that are involved in homocysteine metabolism, increased the level of intracellular homocysteine, and decreased the glutathione (GSH) level in GnT-V-AS/7721 cells. Tretinoin 64-68 betaine--homocysteine S-methyltransferase Homo sapiens 97-135
24500985-13 2014 Therefore, ATRA repressed COX-2, PGE2, and TXA2 via the TGF-beta/Smad-signaling pathway and inhibited mesangial-cell proliferation, which might subsequently prevent renal fibrosis. Tretinoin 11-15 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 26-31
24398626-9 2014 ATRA, an inducer of apoptosis or differentiation, dramatically enhanced FOXO1 expression while it repressed QKI expression. Tretinoin 0-4 QKI, KH domain containing RNA binding Homo sapiens 108-111
19960509-2 2010 In addition to confirming these findings, we further found that ATRA repressed the expression of betaine-homocysteine methyltransferase (BHMT) and cystathionine-beta-synthase (CBS), which are key enzymes that are involved in homocysteine metabolism, increased the level of intracellular homocysteine, and decreased the glutathione (GSH) level in GnT-V-AS/7721 cells. Tretinoin 64-68 betaine--homocysteine S-methyltransferase Homo sapiens 137-141
20692383-5 2010 The purified rLcn12 protein exhibited a high binding affinity for all-trans retinoic acid in fluorescence titration experiments, implying that rLcn12 could be involved in retinoic acid transport in the epididymis. Tretinoin 76-89 lipocalin 12 Rattus norvegicus 13-19
24398626-10 2014 Importantly, the ATRA-induced increase in FOXO1 expression was dependent on QKI-mediated post-transcriptional regulation. Tretinoin 17-21 QKI, KH domain containing RNA binding Homo sapiens 76-79
20692383-5 2010 The purified rLcn12 protein exhibited a high binding affinity for all-trans retinoic acid in fluorescence titration experiments, implying that rLcn12 could be involved in retinoic acid transport in the epididymis. Tretinoin 76-89 lipocalin 12 Rattus norvegicus 143-149
20692383-5 2010 The purified rLcn12 protein exhibited a high binding affinity for all-trans retinoic acid in fluorescence titration experiments, implying that rLcn12 could be involved in retinoic acid transport in the epididymis. Tretinoin 171-184 lipocalin 12 Rattus norvegicus 13-19
20692383-5 2010 The purified rLcn12 protein exhibited a high binding affinity for all-trans retinoic acid in fluorescence titration experiments, implying that rLcn12 could be involved in retinoic acid transport in the epididymis. Tretinoin 171-184 lipocalin 12 Rattus norvegicus 143-149
24384390-7 2014 In contrast, we provide evidence here that lens regeneration in Xenopus actually depends on the attenuation of RA signaling, which is regulated by the RA-degrading enzyme CYP26. Tretinoin 111-113 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 171-176
21061289-6 2010 BMPR-IB and Smad5 mRNA levels increased significantly in cells cultured in OM and declined following treatment with ATRA, whereas the expression of the BMPR-IA mRNA was up-regulated by ATRA. Tretinoin 116-120 SMAD family member 5 Mus musculus 12-17
19824993-1 2010 BACKGROUND: We previously reported that an NAD-dependent in situ retinoic acid supply system, which comprises some isoforms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and provides retinoic acid from retinol via a 2-step oxidation process, exists in the rat esophagus. Tretinoin 65-78 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 159-181
19824993-1 2010 BACKGROUND: We previously reported that an NAD-dependent in situ retinoic acid supply system, which comprises some isoforms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and provides retinoic acid from retinol via a 2-step oxidation process, exists in the rat esophagus. Tretinoin 65-78 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 183-187
19824993-1 2010 BACKGROUND: We previously reported that an NAD-dependent in situ retinoic acid supply system, which comprises some isoforms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and provides retinoic acid from retinol via a 2-step oxidation process, exists in the rat esophagus. Tretinoin 202-215 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 159-181
19824993-1 2010 BACKGROUND: We previously reported that an NAD-dependent in situ retinoic acid supply system, which comprises some isoforms of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) and provides retinoic acid from retinol via a 2-step oxidation process, exists in the rat esophagus. Tretinoin 202-215 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 183-187
24384390-7 2014 In contrast, we provide evidence here that lens regeneration in Xenopus actually depends on the attenuation of RA signaling, which is regulated by the RA-degrading enzyme CYP26. Tretinoin 151-153 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 171-176
24384390-12 2014 Using an inhibitor of CYP26, and separately using exogenous retinoids, as well as RA signaling inhibitors, we demonstrate that CYP26 activity is necessary for lens regeneration to occur. Tretinoin 82-84 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 127-132
20801112-4 2010 We show that diminished expression of Cyp26a1, a retinoic acid inactivating enzyme, and concomitant elevation of retinoic acid activity in the caudal region of Gdf11(-/-) embryos may account for this phenomenon. Tretinoin 113-126 growth differentiation factor 11 Mus musculus 160-165
24330068-0 2014 Nuclear Raf-1 kinase regulates the CXCR5 promoter by associating with NFATc3 to drive retinoic acid-induced leukemic cell differentiation. Tretinoin 86-99 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 8-13
20014094-0 2010 Calmin expression in embryos and the adult brain, and its regulation by all-trans retinoic acid. Tretinoin 82-95 calmin Rattus norvegicus 0-6
24330068-5 2014 The present study shows how the novel localization of Raf-1 to the nucleus results in transcriptional changes that contribute to the differentiation of HL-60 cells induced by RA. Tretinoin 175-177 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 54-59
24330068-6 2014 We find that nuclear pS621 Raf-1 associates with NFATc3 near its cognate binding site in the promoter of CXCR5, a gene that must be up-regulated to drive RA-induced differentiation. Tretinoin 154-156 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 27-32
20014094-5 2010 In vitamin A-deficient embryos, Clmn mRNA is dramatically down-regulated in the neuroepithelium adjacent to the somites, and this expression can be rescued with the addition of atRA. Tretinoin 177-181 calmin Rattus norvegicus 32-36
20719946-10 2010 Moreover, HDAC3, HDAC4, and NCoR act on the gene 50 promoter and are recruited to this promoter in a retinoic acid-responsive manner. Tretinoin 101-114 histone deacetylase 3 Homo sapiens 10-15
24330068-8 2014 Inhibiting the pS621 Raf-1/NFATc3 association with PD98059 inhibits these processes and cripples RA-induced differentiation. Tretinoin 97-99 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 21-26
20034106-2 2010 Here, we report that the RA-generating enzyme retinaldehyde dehydrogenase-2 (Raldh2) is expressed in the interdigital mesenchyme whereas Cyp26b1, controlling RA degradation, is expressed in digits, limiting autopodal RA action to the interdigital zones. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 46-75
24330068-9 2014 In this novel paradigm for Raf-1 and RA function, Raf-1 has a role in driving the nuclear signaling of RA-induced differentiation of leukemic progenitor cells. Tretinoin 37-39 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 50-55
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 glycogen synthase kinase 3 beta Homo sapiens 53-83
20034106-2 2010 Here, we report that the RA-generating enzyme retinaldehyde dehydrogenase-2 (Raldh2) is expressed in the interdigital mesenchyme whereas Cyp26b1, controlling RA degradation, is expressed in digits, limiting autopodal RA action to the interdigital zones. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 77-83
20711222-0 2010 Kruppel-like factor 4 interacts with p300 to activate mitofusin 2 gene expression induced by all-trans retinoic acid in VSMCs. Tretinoin 103-116 E1A binding protein p300 Homo sapiens 37-41
20711222-8 2010 ATRA increased the interaction of KLF4 with p300 by inducing KLF4 phosphorylation via activation of JNK and p38 MAPK signaling. Tretinoin 0-4 E1A binding protein p300 Homo sapiens 44-48
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 glycogen synthase kinase 3 beta Homo sapiens 85-93
20711222-10 2010 CONCLUSION: ATRA induces KLF4 acetylation by p300 and increases the ability of KLF4 to transactivate the mfn-2 promoter in VSMCs. Tretinoin 12-16 E1A binding protein p300 Homo sapiens 45-49
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 glycogen synthase kinase 3 beta Homo sapiens 385-393
24422634-10 2014 Finally, we found genes of the RA pathway (cyp26a1, raraa) the regulation of which by RA is highly robust and can even resist the knockdown of all RARs. Tretinoin 31-33 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 43-50
24422634-11 2014 This suggests that RA-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity. Tretinoin 19-21 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 121-128
19910415-3 2010 When RA was added directly to the activin A-induced hES cells, <20% cells were positive for the pancreatic marker PDX1, whereas the other cells were mainly hepatic cells. Tretinoin 5-7 pancreatic and duodenal homeobox 1 Homo sapiens 117-121
24422634-11 2014 This suggests that RA-responsive genes are differentially sensitive to alterations in the RA pathway and, in particular, cyp26a1 and raraa are under a high pressure to maintain signaling integrity. Tretinoin 90-92 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 121-128
19910415-4 2010 We found that when the activin A-induced hES cells were replated and seeded at low cell densities, the addition of RA induced significant pancreatic differentiation and over 70% of cells in culture expressed PDX1. Tretinoin 115-117 pancreatic and duodenal homeobox 1 Homo sapiens 208-212
20706998-6 2010 For forelimb ectrodactyly, a locus on chromosome 11, Rafar, has linkage to the strain difference, and mRNA localization has shown that specific genes (Fgf8, Dlx3, Bmp4, and Sp8) in the postaxial preAER (prior to formation of the apical ectodermal ridge) of the developing limb bud (the site of the defect) were downregulated hours after atRA administration more in the susceptible C57 than in the SWV strain. Tretinoin 337-341 distal-less homeobox 3 Mus musculus 157-161
24551289-9 2014 Additionally, the caspase-3 activity was also significantly increased in the ATRA-exposed group than control group. Tretinoin 77-81 caspase 3 Rattus norvegicus 18-27
20412539-0 2010 Retinoic acid attenuates acute heart rejection by increasing regulatory T cell and repressing differentiation of Th17 cell in the presence of TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 142-150
19910415-7 2010 We also found that RA inhibited the hepatic differentiation of endodermal cells that were seeded at low cell densities, and this inhibition may have been through the inhibition of Smad1/5/8 activity. Tretinoin 19-21 SMAD family member 1 Homo sapiens 180-187
25118897-5 2014 These findings suggested that JAK2/STAT3, as well as PI3K/Akt, play important roles in mediating the survival and neurite growth response of RA-predifferentiated cells to CNTF. Tretinoin 141-143 Janus kinase 2 Homo sapiens 30-34
19965660-4 2010 The ratio of R1A-RARalpha to RXRalpha proteins affected the retinoic acid response element interaction pattern of R1A-RARalpha/RXRalpha complexes. Tretinoin 60-73 retinoid X receptor alpha Mus musculus 29-37
19965660-4 2010 The ratio of R1A-RARalpha to RXRalpha proteins affected the retinoic acid response element interaction pattern of R1A-RARalpha/RXRalpha complexes. Tretinoin 60-73 retinoid X receptor alpha Mus musculus 127-135
20412539-1 2010 Retinoic acid (RA), in a transforming growth factor beta (TGF-beta)-dependent manner, promotes differentiation of regulatory T cells (Tregs) but inhibits the differentiation of Th17 cells in vitro from naive CD4(+) T cells. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 58-66
20412539-1 2010 Retinoic acid (RA), in a transforming growth factor beta (TGF-beta)-dependent manner, promotes differentiation of regulatory T cells (Tregs) but inhibits the differentiation of Th17 cells in vitro from naive CD4(+) T cells. Tretinoin 15-17 transforming growth factor, beta 1 Mus musculus 58-66
20513361-2 2010 Several P450 enzymes including CYP26A1, CYP2C8, and CYP3A4 have been proposed to be responsible for RA clearance in the liver but their quantitative importance has not been demonstrated. Tretinoin 100-102 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 40-46
20513361-6 2010 CYP2C8, CYP3A4, CYP3A5 and CYP3A7 metabolized RA with unbound K(m) values of 3.4-7.2microM and V(max) values of 2.3-4.9pmol/min/pmol P450, but were less efficient than CYP26A1 in clearing RA. Tretinoin 46-48 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6
20513361-8 2010 HLM incubation data showed that 4-OH RA formation velocity varied from 0.2 to 15.3pmol/min/mg microsomal protein and velocity in HLMs was significantly correlated (p<0.01) to CYP26A1, CYP3A4, and CYP3A5 protein content, but not to CYP2C8. Tretinoin 37-39 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 234-240
20501978-9 2010 We propose other candidates such as STRA6, LRAT, CRBP1, CRBP2 and CRABP1 are directly implicated in retinoic acid metabolism. Tretinoin 100-113 lecithin retinol acyltransferase Homo sapiens 43-47
24190483-9 2014 Doxycycline, epigallocatechin gallate, nutrient mixture (NM), actinomycin-D, cyclohexamide, retinoic acid and dexamethasone inhibited MMP-2 and -9 in U2OS osteosarcoma cells. Tretinoin 92-105 matrix metallopeptidase 2 Homo sapiens 134-146
20501978-9 2010 We propose other candidates such as STRA6, LRAT, CRBP1, CRBP2 and CRABP1 are directly implicated in retinoic acid metabolism. Tretinoin 100-113 retinol binding protein 1 Homo sapiens 49-54
20501978-9 2010 We propose other candidates such as STRA6, LRAT, CRBP1, CRBP2 and CRABP1 are directly implicated in retinoic acid metabolism. Tretinoin 100-113 cellular retinoic acid binding protein 1 Homo sapiens 66-72
21092511-11 2010 In ATRA treated FTC-133 and XTC.UC1 cell lines, MMP2 expression was decreased, but no significant changes in uPA and E-Cadherin expression were observed. Tretinoin 3-7 matrix metallopeptidase 2 Homo sapiens 48-52
23975936-6 2013 Our results uncovered a role of miR-19 family members in controlling RA metabolism through the regulation of CYP26A1 during vertebrate axis formation. Tretinoin 69-71 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 109-116
20506166-0 2010 Localization of nucleophosmin in nuclear matrix and changes in its expression during the differentiation of human neuroblastoma induced by retinoic acid. Tretinoin 139-152 nucleophosmin 1 Homo sapiens 16-29
20506166-3 2010 Results from two-dimensional gel electrophoresis and MALDI-TOF showed that NPM was a component of the nuclear matrix and its expression in SK-N-SH cells post-treated with RA was down-regulated. Tretinoin 171-173 nucleophosmin 1 Homo sapiens 75-78
20506166-4 2010 Immunofluorescent microscopy observations further showed that NPM was localized in the nuclear matrix of SK-N-SH cells, and its expression level and distribution were altered after treatment with RA. Tretinoin 196-198 nucleophosmin 1 Homo sapiens 62-65
20552429-4 2010 This method uses cellular retinoic acid-binding protein I (CRABP-I), a protein that binds RA with high affinity and specificity, as a "read-out" for its ligand. Tretinoin 60-62 cellular retinoic acid binding protein 1 Homo sapiens 17-57
23975936-11 2013 Taken together, these results indicate that the teratogenic effects of RA exposure result, in part, from repression of miR-19 expression and subsequent misregulation of cyp26a1. Tretinoin 71-73 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 169-176
23821302-0 2013 Regulation of URG4/URGCP and PPARalpha gene expressions after retinoic acid treatment in neuroblastoma cells. Tretinoin 62-75 upregulator of cell proliferation Homo sapiens 14-18
20172352-3 2010 It is well known that in the gut, a subset of dendritic cells produces retinoic acid (RA), which together with transforming growth factor (TGF-beta) is able to differentiate naive T cells into Treg. Tretinoin 71-84 transforming growth factor, beta 1 Mus musculus 139-147
20615082-4 2010 ATO augmented ATRA-induced RAF/MEK/ERK axis signaling, expression of CD11b and p47(PHOX), and inducible oxidative metabolism. Tretinoin 14-18 zinc fingers and homeoboxes 2 Homo sapiens 27-30
23821302-0 2013 Regulation of URG4/URGCP and PPARalpha gene expressions after retinoic acid treatment in neuroblastoma cells. Tretinoin 62-75 upregulator of cell proliferation Homo sapiens 19-24
23821302-6 2013 This study aims to detect gene expression patterns of PPARalpha and URG4/URGCP genes in SH-SY5Y NB cell line after RA treatment. Tretinoin 115-117 upregulator of cell proliferation Homo sapiens 68-72
23821302-6 2013 This study aims to detect gene expression patterns of PPARalpha and URG4/URGCP genes in SH-SY5Y NB cell line after RA treatment. Tretinoin 115-117 upregulator of cell proliferation Homo sapiens 73-78
23821302-7 2013 Expressions levels of PPARalpha and URG4/URGCP genes were analyzed after RA treatment for reducing differentiation in SH-SY5Y NB cell line. Tretinoin 73-75 upregulator of cell proliferation Homo sapiens 41-46
19712730-6 2009 The upregulation of Pbx4 was inhibited by an intraperitoneal injection of retinoic acid (RA) (100 microg/g body weight). Tretinoin 74-87 pre-B-cell leukemia transcription factor 4 Gekko japonicus 20-24
23821302-11 2013 PPARalpha gene expression increased in RA-treated groups; URG4/URGCP gene expression decreased in SH-SY5Y cells after RA treatment compared with that in the control cells. Tretinoin 118-120 upregulator of cell proliferation Homo sapiens 58-62
19712730-6 2009 The upregulation of Pbx4 was inhibited by an intraperitoneal injection of retinoic acid (RA) (100 microg/g body weight). Tretinoin 89-91 pre-B-cell leukemia transcription factor 4 Gekko japonicus 20-24
20573951-0 2010 Retinoic acid induces expression of the thyroid hormone transporter, monocarboxylate transporter 8 (Mct8). Tretinoin 0-13 solute carrier family 16 (monocarboxylic acid transporters), member 2 Mus musculus 69-98
23821302-11 2013 PPARalpha gene expression increased in RA-treated groups; URG4/URGCP gene expression decreased in SH-SY5Y cells after RA treatment compared with that in the control cells. Tretinoin 118-120 upregulator of cell proliferation Homo sapiens 63-68
20573951-0 2010 Retinoic acid induces expression of the thyroid hormone transporter, monocarboxylate transporter 8 (Mct8). Tretinoin 0-13 solute carrier family 16 (monocarboxylic acid transporters), member 2 Mus musculus 100-104
19712730-7 2009 These results suggest that gecko Pbx4 is possibly involved in spinal cord regeneration at sites of proximal amputation, and that the expression of Pbx4 in the spinal cord is regulated by retinoic acid in a manner different from that of Pbx1, Pbx2 and Pbx3. Tretinoin 187-200 pre-B-cell leukemia transcription factor 4 Gekko japonicus 147-151
20573951-4 2010 We hypothesized that Mct8 is functionally expressed in F9 cells and induced by RA. Tretinoin 79-81 solute carrier family 16 (monocarboxylic acid transporters), member 2 Mus musculus 21-25
20573951-8 2010 tRA significantly enhanced Mct8 promoter activity through a consensus RA-responsive element located 6.6 kilobases upstream of the coding region. Tretinoin 1-3 solute carrier family 16 (monocarboxylic acid transporters), member 2 Mus musculus 27-31
24294399-8 2013 Expression of cellular retinoic acid Binding Protein, CRABP-1 in whole ovarian cancer tissue sections was higher than in the TMA tissue cores. Tretinoin 23-36 cellular retinoic acid binding protein 1 Homo sapiens 54-61
20735826-0 2010 Nolz1 promotes striatal neurogenesis through the regulation of retinoic acid signaling. Tretinoin 63-76 zinc finger protein 503 Mus musculus 0-5
19830702-3 2009 To further characterize how GSKIP functions in neurons, human neuroblastoma SH-SY5Y cells treated with retinoic acid (RA) to differentiate to neuron-like cells was used as a model. Tretinoin 103-116 GSK3B interacting protein Homo sapiens 28-33
20511343-5 2010 In HBE1 cells, DUOX2 mRNA increased 6-fold after ATRA treatment. Tretinoin 49-53 hemoglobin subunit epsilon 1 Homo sapiens 3-7
23865694-6 2013 Taken together, our data suggest a model whereby part of the immunosuppressive properties of human tolerogenic dendritic cells could be mediated by retinoic acid which, in addition to its known role in favouring T cell differentiation to FoxP3+ regulatory T cells, acts to convert B cells into immunosuppressive cells. Tretinoin 148-161 forkhead box P3 Homo sapiens 238-243
20506167-6 2010 Because CRBP1 plays a dual role in the retina-retinal recycling and generation of retinoic acid-we evaluated both possibilities. Tretinoin 82-95 retinol binding protein 1 Homo sapiens 8-13
20506167-9 2010 The localization of CRBP1 within Muller cells and the RPE and its demonstrated role in modulating the proper folding of nascent outer segment membranes through retinoic acid further elucidates the role of these cells in directly influencing photoreceptor physiology. Tretinoin 160-173 retinol binding protein 1 Homo sapiens 20-25
19666108-0 2009 Down-regulation of miR-17 family expression in response to retinoic acid induced neuronal differentiation. Tretinoin 59-72 microRNA 17 Homo sapiens 19-25
24176856-3 2013 Administration of RA to mice altered cell proliferation and apoptosis in craniofacial tissues by regulating molecules controlling cell cycle and p38 MAPK signaling, respectively. Tretinoin 18-20 mitogen-activated protein kinase 14 Mus musculus 145-148
19801676-5 2009 Comparative analysis revealed raldh2, a rate-limiting enzyme for the synthesis of retinoic acid, as one of the most highly induced genes across the three regeneration platforms. Tretinoin 82-95 aldehyde dehydrogenase 1 family, member A2 Danio rerio 30-36
20809547-8 2010 Furthermore, transcript levels of the enzyme Xcyp26, an enzyme in the retinoic acid signaling pathway, significantly decreased in the intestines of tadpoles exposed to 10 or 35 mg l(-1) atrazine for 48 h. Our results suggest two mechanisms by which atrazine can disrupt tissue morphogenesis: through misregulation of MMPs that are critical in extracellular matrix remodeling throughout development and the disruption of retinoic acid signaling. Tretinoin 70-83 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 45-51
23852377-5 2013 The detection of real-time-PCR showed that the level of GFAP (glial fibrillary acidic protein) mRNA of differentiated GSPCs in the growth factor-free medium containing 1 mumol/L ATRA group was significantly higher than that in the control group, and there was no significant difference in the level of TUBB-3 mRNA between the two groups. Tretinoin 178-182 tubulin beta 3 class III Homo sapiens 302-308
20689834-8 2010 We find that both 9CRA and ATRA effectively induce early osteogenic marker, such as alkaline phosphatase (ALP), and late osteogenic markers, such as osteopontin (OPN) and osteocalcin (OC). Tretinoin 27-31 secreted phosphoprotein 1 Mus musculus 149-160
20689834-8 2010 We find that both 9CRA and ATRA effectively induce early osteogenic marker, such as alkaline phosphatase (ALP), and late osteogenic markers, such as osteopontin (OPN) and osteocalcin (OC). Tretinoin 27-31 secreted phosphoprotein 1 Mus musculus 162-165
20644631-4 2010 Upon stimulation with micromolar concentrations of RA, ESCs significantly downregulated the pluripotency factor OCT-4 but markedly upregulated UP1A, UP1B, UP2, UP3A, and UP3B mRNA levels in comparison to naive ESCs and spontaneously differentiating controls. Tretinoin 51-53 uroplakin 1A Mus musculus 143-147
19443527-4 2009 Previously, it was reported that all-trans-retinoic acid (ATRA) inhibited the production and function of IL-6 and transforming growth factor (TGF)-beta1 in experiments using lung fibroblasts. Tretinoin 33-56 transforming growth factor, beta 1 Mus musculus 114-152
20644631-4 2010 Upon stimulation with micromolar concentrations of RA, ESCs significantly downregulated the pluripotency factor OCT-4 but markedly upregulated UP1A, UP1B, UP2, UP3A, and UP3B mRNA levels in comparison to naive ESCs and spontaneously differentiating controls. Tretinoin 51-53 uroplakin 2 Mus musculus 155-158
23607934-5 2013 Retinoic acid (RA) induced gut-homing markers (beta7 and CCR9) and a regulatory phenotype and function [decreased human leucocyte antigen D-related (HLA-DR) and increased ILT3 and fluorescein isothiocyanate (FITC-dextran uptake) in MoDC]. Tretinoin 0-13 C-C motif chemokine receptor 9 Homo sapiens 57-61
20644631-7 2010 GATA4-/- and GATA6-/- transgenic ESC lines revealed substantial attenuation of RA-mediated UP expression in comparison to wild type controls. Tretinoin 79-81 GATA binding protein 6 Mus musculus 13-18
20644631-8 2010 In addition, EMSA analysis revealed that RA treatment induced formation of transcriptional complexes containing GATA4/6 on both UP1B and UP2 promoter fragments containing putative GATA factor binding sites. Tretinoin 41-43 uroplakin 2 Mus musculus 137-140
19443527-4 2009 Previously, it was reported that all-trans-retinoic acid (ATRA) inhibited the production and function of IL-6 and transforming growth factor (TGF)-beta1 in experiments using lung fibroblasts. Tretinoin 58-62 transforming growth factor, beta 1 Mus musculus 114-152
23966631-0 2013 Human CD1c+ myeloid dendritic cells acquire a high level of retinoic acid-producing capacity in response to vitamin D3. Tretinoin 60-73 CD1c molecule Homo sapiens 6-10
23966631-2 2013 Mouse intestinal CD103+ dendritic cells (DCs) produce a high level of RA by highly expressing retinal dehydrogenase (RALDH)2, an enzyme that converts retinal to RA, and induce gut-homing T cells. Tretinoin 70-72 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 117-124
19676129-8 2009 Finally, HuR was demonstrated to support GJIC after exposure to a genotoxic agent, doxorubicin, or an inducer of differentiation processes, retinoic acid, thus pointing to a crucial role of HuR in the cellular response to stress and in physiological processes modulated by GJIC. Tretinoin 140-153 ELAV like RNA binding protein 1 Rattus norvegicus 9-12
23966631-4 2013 In this study, we show that CD1c+ blood myeloid DCs (mDCs) but not CD141(high) mDCs or plasmacytoid DCs exhibited a high level of RALDH2 mRNA and aldehyde dehydrogenase (ALDH) activity in an RA- and p38-dependent manner when stimulated with 1alpha,25-dihydroxyvitamin D3 (VD3) in the presence of GM-CSF. Tretinoin 130-132 CD1c molecule Homo sapiens 28-32
19676129-8 2009 Finally, HuR was demonstrated to support GJIC after exposure to a genotoxic agent, doxorubicin, or an inducer of differentiation processes, retinoic acid, thus pointing to a crucial role of HuR in the cellular response to stress and in physiological processes modulated by GJIC. Tretinoin 140-153 ELAV like RNA binding protein 1 Rattus norvegicus 190-193
20232320-1 2010 Rex1 (zfp42) was identified by our laboratory because of its reduced expression in F9 teratocarcinoma stem cells after retinoic acid (RA) treatment. Tretinoin 119-132 ZFP42 zinc finger protein Homo sapiens 0-4
20232320-1 2010 Rex1 (zfp42) was identified by our laboratory because of its reduced expression in F9 teratocarcinoma stem cells after retinoic acid (RA) treatment. Tretinoin 119-132 ZFP42 zinc finger protein Homo sapiens 6-11
20147703-0 2010 Liver-specific cytochrome P450 CYP2C22 is a direct target of retinoic acid and a retinoic acid-metabolizing enzyme in rat liver. Tretinoin 61-74 cytochrome P450, family 2, subfamily c, polypeptide 22 Rattus norvegicus 31-38
23966631-9 2013 This study suggests that CD1c+ mDCs are a major human DC subset that produces RA in response to VD3 in the steady state. Tretinoin 78-80 CD1c molecule Homo sapiens 25-29
20147703-0 2010 Liver-specific cytochrome P450 CYP2C22 is a direct target of retinoic acid and a retinoic acid-metabolizing enzyme in rat liver. Tretinoin 81-94 cytochrome P450, family 2, subfamily c, polypeptide 22 Rattus norvegicus 31-38
24040281-9 2013 An increase in H3K27me3 in the promoters of differentiation genes Hoxa1 and Cdx2 in Dicer(-/-)ES cells was coincident with an inability to up-regulate these genes at the same rate as ES upon retinoic acid (RA)-induced differentiation. Tretinoin 206-208 homeobox A1 Mus musculus 66-71
20147703-7 2010 The cDNA-expressed CYP2C22 protein metabolized [3H]at-RA to more polar metabolites. Tretinoin 54-56 cytochrome P450, family 2, subfamily c, polypeptide 22 Rattus norvegicus 19-26
19626646-1 2009 Necdin (NDN), a member of the melanoma-associated antigen (MAGE) family of proteins was first identified in mouse stem cells of embryonal carcinoma origin induced to differentiate by treatment with retinoic acid. Tretinoin 198-211 necdin, MAGE family member Mus musculus 0-6
24040281-9 2013 An increase in H3K27me3 in the promoters of differentiation genes Hoxa1 and Cdx2 in Dicer(-/-)ES cells was coincident with an inability to up-regulate these genes at the same rate as ES upon retinoic acid (RA)-induced differentiation. Tretinoin 206-208 caudal type homeobox 2 Mus musculus 76-80
19626646-1 2009 Necdin (NDN), a member of the melanoma-associated antigen (MAGE) family of proteins was first identified in mouse stem cells of embryonal carcinoma origin induced to differentiate by treatment with retinoic acid. Tretinoin 198-211 necdin, MAGE family member Mus musculus 8-11
23701916-6 2013 Upregulation of MHCII and costimulatory molecule CD86, as well as IL-12 secretion were inhibited by RA treatment. Tretinoin 100-102 CD86 molecule Homo sapiens 49-53
20885005-0 2010 Chronic ethanol exposure changes dopamine D2 receptor splicing during retinoic acid-induced differentiation of human SH-SY5Y cells. Tretinoin 70-83 dopamine receptor D2 Homo sapiens 33-53
23792233-0 2013 Involvement of retinoic acid-induced peroxiredoxin 6 expression in recovery of noise-induced temporary hearing threshold shifts. Tretinoin 15-28 peroxiredoxin 6 Mus musculus 37-52
19752193-6 2009 Correspondingly, IRAK-1(-/-) macrophages exhibit increased expression of ABCA1 mRNA and protein, as well as elevated cholesterol efflux in response to the RAR ligand ATRA. Tretinoin 166-170 interleukin 1 receptor associated kinase 1 Homo sapiens 17-23
23792233-3 2013 Mice fed with ATRA before or after exposure to white noise showed a faster recovery than untreated controls within 1 week, with a concomitant increase of cochlear Prdx 6 expression. Tretinoin 14-18 peroxiredoxin 6 Mus musculus 163-169
23792233-4 2013 Treatment of mouse auditory cells with ATRA induced Prdx 6 expression. Tretinoin 39-43 peroxiredoxin 6 Mus musculus 52-58
23792233-5 2013 A putative retinoic acid (RA)-response element (RARE) was identified in a murine Prdx 6 promoter region. Tretinoin 11-24 peroxiredoxin 6 Mus musculus 81-87
23792233-5 2013 A putative retinoic acid (RA)-response element (RARE) was identified in a murine Prdx 6 promoter region. Tretinoin 26-28 peroxiredoxin 6 Mus musculus 81-87
23792233-8 2013 These findings suggest that ATRA-induced Prdx 6 expression may be associated with rapid recovery from temporary NIHL. Tretinoin 28-32 peroxiredoxin 6 Mus musculus 41-47
20483764-2 2010 In the current study, we demonstrate that naive CD4+CD25-Foxp3- T cells specific for the myelin proteolipid protein (PLP)139-151 peptide can be converted into CD25+Foxp3+ induced Treg cells (iTregs) when stimulated in the presence of TGF-beta, retinoic acid, and IL-2. Tretinoin 244-257 proteolipid protein (myelin) 1 Mus musculus 89-128
23765726-2 2013 Previous studies show that expression of intact MAT1 protein is associated with expansion of human hematopoietic stem cells (HSC), whereas intrinsically programmed or retinoic acid (RA)-induced MAT1 fragmentation accompanies granulocytic differentiation of HSC or leukemic myeloblasts. Tretinoin 167-180 MNAT1 component of CDK activating kinase Homo sapiens 194-198
20563304-8 2010 Adding retinoic acid (10(-6) M) to the culture medium increased the percent of nitric oxide synthase-1 positive cells to 33.9%. Tretinoin 7-20 nitric oxide synthase 1 Homo sapiens 79-102
19690170-10 2009 In acute promyelocytic leukemia (APL) cells, C/EBPbeta activity is known to be required for all-trans-retinoic acid-induced cell differentiation and disease remission. Tretinoin 102-115 CCAAT enhancer binding protein beta Homo sapiens 45-54
19690170-11 2009 We show that all-trans-retinoic acid as well as arsenic trioxide treatment leads to a reduced C/EBPbeta fraction associated with Daxx suggesting a relief of Daxx-dependent C/EBPbeta repression as an important molecular event leading to APL cell differentiation. Tretinoin 13-36 CCAAT enhancer binding protein beta Homo sapiens 94-103
19690170-11 2009 We show that all-trans-retinoic acid as well as arsenic trioxide treatment leads to a reduced C/EBPbeta fraction associated with Daxx suggesting a relief of Daxx-dependent C/EBPbeta repression as an important molecular event leading to APL cell differentiation. Tretinoin 13-36 death domain associated protein Homo sapiens 129-133
19690170-11 2009 We show that all-trans-retinoic acid as well as arsenic trioxide treatment leads to a reduced C/EBPbeta fraction associated with Daxx suggesting a relief of Daxx-dependent C/EBPbeta repression as an important molecular event leading to APL cell differentiation. Tretinoin 13-36 death domain associated protein Homo sapiens 157-161
20563304-9 2010 Combining retinoic acid (10(-6) M) with 8-brom cyclic guanosine monophosphate (10(-5) M), the fluorescence-activated cell sorting analysis demonstrated a further increase of nitric oxide synthase-1 positive cells to 45.4%. Tretinoin 10-23 nitric oxide synthase 1 Homo sapiens 174-197
23765726-2 2013 Previous studies show that expression of intact MAT1 protein is associated with expansion of human hematopoietic stem cells (HSC), whereas intrinsically programmed or retinoic acid (RA)-induced MAT1 fragmentation accompanies granulocytic differentiation of HSC or leukemic myeloblasts. Tretinoin 182-184 MNAT1 component of CDK activating kinase Homo sapiens 194-198
20563304-10 2010 Our current results demonstrate a prodifferentiation potency of nitric oxide synthase-1, stimulated by retinoic acid with and without cyclic guanosine monophosphate. Tretinoin 103-116 nitric oxide synthase 1 Homo sapiens 64-87
19690170-11 2009 We show that all-trans-retinoic acid as well as arsenic trioxide treatment leads to a reduced C/EBPbeta fraction associated with Daxx suggesting a relief of Daxx-dependent C/EBPbeta repression as an important molecular event leading to APL cell differentiation. Tretinoin 13-36 CCAAT enhancer binding protein beta Homo sapiens 172-181
23937294-3 2013 The early vertebrate embryo maintains a balance between retinoic acid synthetic and degradative zones on the basis of reciprocal expression domains of the retinoic acid synthesis gene aldhehyde dehydrogenase 1a2 (aldh1a2) posteriorly and the oxidative gene cytochrome p450 type 26a1 (cyp26a1) in the forebrain, midbrain, and anterior hindbrain. Tretinoin 155-168 aldehyde dehydrogenase 1 family, member A2 Danio rerio 213-220
19625708-4 2009 In leukemia cell lines, PRAME protein expression inhibited granulocytic differentiation only in cell lines that differentiate along this lineage after all-trans retinoic acid (ATRA) exposure. Tretinoin 161-174 PRAME nuclear receptor transcriptional regulator Homo sapiens 24-29
19625708-4 2009 In leukemia cell lines, PRAME protein expression inhibited granulocytic differentiation only in cell lines that differentiate along this lineage after all-trans retinoic acid (ATRA) exposure. Tretinoin 176-180 PRAME nuclear receptor transcriptional regulator Homo sapiens 24-29
19625708-5 2009 Forced PRAME expression in normal hematopoietic progenitors, however, inhibited myeloid differentiation both in the presence and absence of ATRA, and this phenotype was reversed when PRAME was silenced in primary CML progenitors. Tretinoin 140-144 PRAME nuclear receptor transcriptional regulator Homo sapiens 7-12
20566912-6 2010 In addition, we evaluated the effect of 4 physiologically relevant agents, including retinoic acid, interleukin 1beta, phorbol 12-myristate 13-acetate (PMA), and dexamethasone, on the expression of MUC4 and MUC16 in HNPE cells at the gene and protein levels. Tretinoin 85-98 mucin 4, cell surface associated Homo sapiens 198-202
20102671-2 2010 Retinoic acid (RA) plays a central role in the maintenance of cognitive processes via its nuclear receptors (NR), retinoic acid receptor (RAR) and retinoid X receptor (RXR), and the control of target genes, e.g. the synaptic plasticity markers GAP-43/neuromodulin and RC3/neurogranin. Tretinoin 0-13 growth associated protein 43 Rattus norvegicus 244-250
20102671-2 2010 Retinoic acid (RA) plays a central role in the maintenance of cognitive processes via its nuclear receptors (NR), retinoic acid receptor (RAR) and retinoid X receptor (RXR), and the control of target genes, e.g. the synaptic plasticity markers GAP-43/neuromodulin and RC3/neurogranin. Tretinoin 0-13 growth associated protein 43 Rattus norvegicus 251-263
20102671-2 2010 Retinoic acid (RA) plays a central role in the maintenance of cognitive processes via its nuclear receptors (NR), retinoic acid receptor (RAR) and retinoid X receptor (RXR), and the control of target genes, e.g. the synaptic plasticity markers GAP-43/neuromodulin and RC3/neurogranin. Tretinoin 0-13 neurogranin Rattus norvegicus 268-271
25206495-6 2013 Retinoic acid ment caused differential expression of three cell cycle-related genes p57kip2, Cdk5 and Spin, the expression levels of which were downregulated by retinoic acid and upregulated during normal neural tube formation. Tretinoin 0-13 cyclin-dependent kinase inhibitor 1C Rattus norvegicus 84-91
20102671-2 2010 Retinoic acid (RA) plays a central role in the maintenance of cognitive processes via its nuclear receptors (NR), retinoic acid receptor (RAR) and retinoid X receptor (RXR), and the control of target genes, e.g. the synaptic plasticity markers GAP-43/neuromodulin and RC3/neurogranin. Tretinoin 0-13 neurogranin Rattus norvegicus 272-283
20507357-11 2010 ATRA treatment upregulated the expression of Vimentin and Stra13, while it downregulated the expression of Brachyury in MSCs. Tretinoin 0-4 vimentin Rattus norvegicus 45-53
19812318-5 2009 Moreover, retinoic acid-induced differentiation of human SH-SY5Y neuroblastoma cells promoted the accumulation of VCX-A in distinct cytoplasmic foci within neurites that colocalize with staufen1-containing RNA granules, suggesting a role in translational suppression and/or mRNA transport. Tretinoin 10-23 variable charge X-linked 3A Homo sapiens 114-119
19789299-5 2009 ATRA is a highly efficient suppressor of tumor formation in the two-stage mouse skin carcinogenesis model and we have shown that this effect correlates with the suppression of the B-Raf/Mek/Erk signaling pathway. Tretinoin 0-4 midkine Mus musculus 186-189
19789299-10 2009 We hypothesize that ATRA blocks tumor formation, at least in part, by targeting events upstream of Stat3, such as the B-Raf/Mek/Erk pathway, and that in the K5.Stat3C mice, in which Stat3 activity is constitutive, it cannot suppress tumor formation. Tretinoin 20-24 midkine Mus musculus 124-127
25206495-6 2013 Retinoic acid ment caused differential expression of three cell cycle-related genes p57kip2, Cdk5 and Spin, the expression levels of which were downregulated by retinoic acid and upregulated during normal neural tube formation. Tretinoin 0-13 cyclin-dependent kinase 5 Rattus norvegicus 93-97
20507357-11 2010 ATRA treatment upregulated the expression of Vimentin and Stra13, while it downregulated the expression of Brachyury in MSCs. Tretinoin 0-4 centromere protein X Rattus norvegicus 58-64
25206495-6 2013 Retinoic acid ment caused differential expression of three cell cycle-related genes p57kip2, Cdk5 and Spin, the expression levels of which were downregulated by retinoic acid and upregulated during normal neural tube formation. Tretinoin 161-174 cyclin-dependent kinase inhibitor 1C Rattus norvegicus 84-91
19507250-1 2009 Our study explored the drug interaction of all-trans retinoic acid (ATRA) and RAD001 (everolimus), the inhibitor of mammalian target of rapamycin complex 1 (mTORC1), in acute myelogenous leukemia (AML) NB4 and HL60 cells. Tretinoin 53-66 CREB regulated transcription coactivator 1 Mus musculus 157-163
25206495-6 2013 Retinoic acid ment caused differential expression of three cell cycle-related genes p57kip2, Cdk5 and Spin, the expression levels of which were downregulated by retinoic acid and upregulated during normal neural tube formation. Tretinoin 161-174 cyclin-dependent kinase 5 Rattus norvegicus 93-97
19507250-1 2009 Our study explored the drug interaction of all-trans retinoic acid (ATRA) and RAD001 (everolimus), the inhibitor of mammalian target of rapamycin complex 1 (mTORC1), in acute myelogenous leukemia (AML) NB4 and HL60 cells. Tretinoin 68-72 CREB regulated transcription coactivator 1 Mus musculus 157-163
23541806-0 2013 Myocardin-related transcription factor-A is a key regulator in retinoic acid-induced neural-like differentiation of adult bone marrow-derived mesenchymal stem cells. Tretinoin 63-76 myocardin related transcription factor A Homo sapiens 0-40
19507250-3 2009 ATRA (0.1-1 microM) upregulated levels of RTP801, a negative regulator of mTORC1, and inhibited mTORC1 signaling as assessed by measurement of the levels of p-p70S6K and p-4E-BP1 in HL60 and NB4 cells. Tretinoin 0-4 CREB regulated transcription coactivator 1 Mus musculus 74-80
19507250-3 2009 ATRA (0.1-1 microM) upregulated levels of RTP801, a negative regulator of mTORC1, and inhibited mTORC1 signaling as assessed by measurement of the levels of p-p70S6K and p-4E-BP1 in HL60 and NB4 cells. Tretinoin 0-4 CREB regulated transcription coactivator 1 Mus musculus 96-102
20439714-5 2010 To address this, we used transient maternal RA supplementation to overcome early Raldh2(-/-) lethality. Tretinoin 44-46 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 81-87
23541806-5 2013 Of note, myocardin-related transcription factor-A (MRTF-A), a major co-activator of serum response factor (SRF), was significantly activated and its nuclear localization was observed during RA-induced neural-like differentiation. Tretinoin 190-192 myocardin related transcription factor A Homo sapiens 9-49
20400707-6 2010 The Th17 cells, induced in the presence or absence of RA, differentially expressed the trafficking receptors CCR9 and alpha4beta7. Tretinoin 54-56 C-C motif chemokine receptor 9 Homo sapiens 109-113
19633294-0 2009 Repression of Ca2+/calmodulin-dependent protein kinase IV signaling accelerates retinoic acid-induced differentiation of human neuroblastoma cells. Tretinoin 80-93 calcium/calmodulin dependent protein kinase IV Homo sapiens 19-57
19633294-7 2009 RA down-regulates expression of CaMKIV and one of its upstream activators, CaMKK1 (calmodulin-dependent protein kinase kinase 1). Tretinoin 0-2 calcium/calmodulin dependent protein kinase IV Homo sapiens 32-38
19633294-8 2009 This is accompanied by RA-induced suppression of activating phosphorylation of CREB with a time course paralleling that of CaMKIV down-regulation. Tretinoin 23-25 calcium/calmodulin dependent protein kinase IV Homo sapiens 123-129
23541806-5 2013 Of note, myocardin-related transcription factor-A (MRTF-A), a major co-activator of serum response factor (SRF), was significantly activated and its nuclear localization was observed during RA-induced neural-like differentiation. Tretinoin 190-192 myocardin related transcription factor A Homo sapiens 51-57
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 0-2 calcium/calmodulin dependent protein kinase IV Homo sapiens 79-85
20074641-3 2010 In the present study, we used SH-SY5Y neuroblastoma cells to analyse the role of NADPH oxidase in retinoic acid (RA)-induced differentiation, pointing out the involvement of protein kinase C (PKC) delta in the activation of NOX. Tretinoin 98-111 protein kinase C delta Homo sapiens 174-202
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 0-2 calcium/calmodulin dependent protein kinase IV Homo sapiens 222-228
23823803-5 2013 Mechanistically, our data showed that the retinoic acid (RA) catabolizing enzyme Cyp26a1 was upregulated in FABP3-MO zebrafish, as indicated by in situ hybridization and real-time PCR. Tretinoin 57-59 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 81-88
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 0-2 doublecortin Homo sapiens 295-307
20074641-4 2010 Retinoic acid induces neuronal differentiation as revealed by the increased expression of MAP2, the decreased cell doubling rate, and the gain in neuronal morphological features and these events are accompanied by the increased expression level of PKC delta and p67(phox), one of the components of NADPH oxidase. Tretinoin 0-13 protein kinase C delta Homo sapiens 248-257
20074641-6 2010 Moreover, using rottlerin to inhibit PKC delta or transfection experiments to overexpress it, we show that retinoic acid acts through this enzyme to induce MAP2 expression and to increase p67(phox) membrane translocation leading to NADPH oxidase activation. Tretinoin 107-120 protein kinase C delta Homo sapiens 37-46
20074641-7 2010 These findings identify the activation of PKC delta and NADPH oxidase as crucial steps in RA-induced neuroblastoma cell differentiation. Tretinoin 90-92 protein kinase C delta Homo sapiens 42-51
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 252-254 calcium/calmodulin dependent protein kinase IV Homo sapiens 79-85
23823803-5 2013 Mechanistically, our data showed that the retinoic acid (RA) catabolizing enzyme Cyp26a1 was upregulated in FABP3-MO zebrafish, as indicated by in situ hybridization and real-time PCR. Tretinoin 57-59 fatty acid binding protein 3, muscle and heart Danio rerio 108-113
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 252-254 calcium/calmodulin dependent protein kinase IV Homo sapiens 222-228
23823803-6 2013 On the other hand, the expression level of the RA synthesizing enzyme Raldh2 did not significantly change in FABP3-MO injected zebrafish. Tretinoin 47-49 aldehyde dehydrogenase 1 family, member A2 Danio rerio 70-76
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 252-254 calcium/calmodulin dependent protein kinase IV Homo sapiens 79-85
23524428-0 2013 All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions in vitro. Tretinoin 10-23 gap junction protein alpha 1 Homo sapiens 132-136
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 252-254 calcium/calmodulin dependent protein kinase IV Homo sapiens 222-228
19633294-10 2009 RA-induced repression of the CaMKIV signaling pathway may represent an early event in retinoid-dependent neuronal differentiation. Tretinoin 0-2 calcium/calmodulin dependent protein kinase IV Homo sapiens 29-35
20134361-8 2010 RESULTS: Mouse sutures were found to express genes necessary for retinoic acid synthesis, binding, and signal transduction, demonstrated by quantitative real-time polymerase chain reaction (Raldh1, Raldh2, Raldh3, and Rbp4). Tretinoin 65-78 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 190-196
23524428-8 2013 Moreover, ATRA induced upregulation of Cx32 and Cx43 at both the mRNA and protein levels in OSCC cells. Tretinoin 10-14 gap junction protein alpha 1 Homo sapiens 48-52
20134361-8 2010 RESULTS: Mouse sutures were found to express genes necessary for retinoic acid synthesis, binding, and signal transduction, demonstrated by quantitative real-time polymerase chain reaction (Raldh1, Raldh2, Raldh3, and Rbp4). Tretinoin 65-78 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 198-204
23840757-7 2013 ATRA upregulated TRPC3, TRPC4 and TRPC6 expression and enhanced Ca(2+) influx in A549 cells, however, ATRA showed no direct effect on TRPC channels. Tretinoin 0-4 transient receptor potential cation channel subfamily C member 3 Homo sapiens 17-22
20172853-0 2010 All-trans-retinoic acid promotes trafficking of human concentrative nucleoside transporter-3 (hCNT3) to the plasma membrane by a TGF-beta1-mediated mechanism. Tretinoin 0-23 solute carrier family 28 member 3 Homo sapiens 94-99
19556237-8 2009 Examination of gene expression demonstrated that the induction of retinoic acid signaling by cadmium may be mediated by overexpression of Bcmo1. Tretinoin 66-79 beta-carotene oxygenase 1 Mus musculus 138-143
23840757-7 2013 ATRA upregulated TRPC3, TRPC4 and TRPC6 expression and enhanced Ca(2+) influx in A549 cells, however, ATRA showed no direct effect on TRPC channels. Tretinoin 0-4 transient receptor potential cation channel subfamily C member 6 Homo sapiens 34-39
19651648-7 2009 The same result is obtained by the Phox2a(+/-) mutation modifying the number of petrosal chemoafferent neurons, by eliminating acetylcholinesterase and by altering Hox-dependent development of the pons with retinoic acid administration at embryonic day 7.5. Tretinoin 207-220 paired like homeobox 2A Homo sapiens 35-41
23492186-6 2013 We show here for the first time that AMs and AM-conditioned media (AM-CM) from mice and humans induced FoxP3 expression in naive CD4(+) T cells in vitro, an outcome that was reversed in part either by inhibiting retinoic acid (RA) binding to its receptor (RAR), or by blocking transforming growth factor (TGF)-beta1 signaling. Tretinoin 212-225 forkhead box P3 Homo sapiens 103-108
19584707-6 2009 Growth inhibitory concentrations of HCQ and ATRA stimulated purified p300/CBP-associated factor, where CBP is the cAMP-response element binding protein, HAT activity. Tretinoin 44-48 E1A binding protein p300 Homo sapiens 69-73
19388084-8 2009 The protein expression levels of p21, Smad2/3, phospho-Smad2, and phospho-Smad3 were increased, while phospho-Rb was decreased in MEPM after atRA treatment on GD 10. Tretinoin 141-145 SMAD family member 3 Mus musculus 74-79
20179325-0 2010 Transcription factor Smad3 is required for the inhibition of adipogenesis by retinoic acid. Tretinoin 77-90 SMAD family member 3 Homo sapiens 21-26
20179325-4 2010 Retinoic acid (RA) is a potent inhibitor of adipogenesis, and its action appears to block C/EBPbeta transcriptional potential early during differentiation. Tretinoin 0-13 CCAAT enhancer binding protein beta Homo sapiens 90-99
20179325-4 2010 Retinoic acid (RA) is a potent inhibitor of adipogenesis, and its action appears to block C/EBPbeta transcriptional potential early during differentiation. Tretinoin 15-17 CCAAT enhancer binding protein beta Homo sapiens 90-99
20179325-5 2010 Using preadipocytes and mesenchymal stem cell models, we show that RA specifically blocks the occupancy of C/EBPbeta of the Cebpa promoter, thereby abrogating the differentiation process. Tretinoin 67-69 CCAAT enhancer binding protein beta Homo sapiens 107-116
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 4-6 SMAD family member 3 Homo sapiens 27-32
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 4-6 SMAD family member 3 Homo sapiens 89-94
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 4-6 SMAD family member 3 Homo sapiens 89-94
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 4-6 CCAAT enhancer binding protein beta Homo sapiens 234-243
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 4-6 SMAD family member 3 Homo sapiens 89-94
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 345-358 SMAD family member 3 Homo sapiens 27-32
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 345-358 SMAD family member 3 Homo sapiens 89-94
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 345-358 SMAD family member 3 Homo sapiens 89-94
20179325-7 2010 The RA-induced increase in Smad3 expression results in increased cytoplasmic and nuclear Smad3, an important event as ectopic expression of Smad3 in preadipocytes in the absence of RA treatment only modestly inhibits adipogenesis and C/EBPbeta DNA binding, suggesting that Smad3 alone is not sufficient to completely recapitulate the effects of retinoic acid treatment during differentiation. Tretinoin 345-358 SMAD family member 3 Homo sapiens 89-94
19294396-5 2009 In line with a reduced biosynthesis of RA from retinol after exogenous RA, the expression of RDH16 reduced 80% in response to exogenous RA. Tretinoin 39-41 retinol dehydrogenase 16 Homo sapiens 93-98
19294396-5 2009 In line with a reduced biosynthesis of RA from retinol after exogenous RA, the expression of RDH16 reduced 80% in response to exogenous RA. Tretinoin 71-73 retinol dehydrogenase 16 Homo sapiens 93-98
19294396-5 2009 In line with a reduced biosynthesis of RA from retinol after exogenous RA, the expression of RDH16 reduced 80% in response to exogenous RA. Tretinoin 71-73 retinol dehydrogenase 16 Homo sapiens 93-98
23492186-6 2013 We show here for the first time that AMs and AM-conditioned media (AM-CM) from mice and humans induced FoxP3 expression in naive CD4(+) T cells in vitro, an outcome that was reversed in part either by inhibiting retinoic acid (RA) binding to its receptor (RAR), or by blocking transforming growth factor (TGF)-beta1 signaling. Tretinoin 227-229 forkhead box P3 Homo sapiens 103-108
23864846-0 2013 Src Family Kinase Inhibitor PP2 Has Different Effects on All-Trans-Retinoic Acid or Arsenic Trioxide-Induced Differentiation of an Acute Promyelocytic Leukemia Cell Line. Tretinoin 57-80 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 28-31
19618468-3 2009 We report here that the gene encoding a cytosolic class-1 aldehyde dehydrogenase, ALDH1A1, a weak catalyst of RA production, is strongly expressed in a male-specific manner in somatic cells of the developing mouse testis, beginning shortly after Sry expression is first detectable. Tretinoin 110-112 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 82-89
19357873-0 2009 Effect of all-trans retinoic acid on renal expressions of matrix metalloproteinase-2, matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in rats with glomerulosclerosis. Tretinoin 10-33 matrix metallopeptidase 2 Rattus norvegicus 58-84
19357873-3 2009 Therefore, a rat model of GS was established to investigate the effect of all-trans retinoic acid (ATRA) on the renal expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Tretinoin 74-97 matrix metallopeptidase 2 Rattus norvegicus 133-159
19544414-4 2009 Most importantly, GFP expression recapitulated endogenous Olig2 expression when R-Olig2 was induced by sonic hedgehog and retinoic acid, and GFP-positive cells could be purified by fluorescence-activated cell sorting. Tretinoin 122-135 oligodendrocyte transcription factor 2 Homo sapiens 58-63
19544414-4 2009 Most importantly, GFP expression recapitulated endogenous Olig2 expression when R-Olig2 was induced by sonic hedgehog and retinoic acid, and GFP-positive cells could be purified by fluorescence-activated cell sorting. Tretinoin 122-135 oligodendrocyte transcription factor 2 Homo sapiens 82-87
19886770-4 2009 Spermatogenesis can be reinitiated by injection of VAD rats with retinol, the metabolic precursor of retinoic acid, but to date, the functions of retinoic acid in the testis remain elusive. Tretinoin 101-114 potassium channel tetramerization domain containing 1 Rattus norvegicus 51-54
19416972-2 2009 In this study we showed that HAS2 is a primary target of the cAMP activator forskolin and the nuclear hormone all-trans-retinoic acid (RA). Tretinoin 110-133 hyaluronan synthase 2 Homo sapiens 29-33
19416972-2 2009 In this study we showed that HAS2 is a primary target of the cAMP activator forskolin and the nuclear hormone all-trans-retinoic acid (RA). Tretinoin 135-137 hyaluronan synthase 2 Homo sapiens 29-33
19416983-5 2009 The cytoplasmic retention of RARgamma was inhibited by ligand retinoic acid (RA). Tretinoin 62-75 retinoic acid receptor gamma Homo sapiens 29-37
19578722-4 2009 When treated with ATRA for 72 h, the EZH2 and SUZ12 mRNA levels were decreased to 35% and 38% of the control group, respectively. Tretinoin 18-22 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 46-51
19244314-5 2009 These molecules regulate Cdc42 and p38MAPK activities, which increase in a Cdo-dependent manner during neuronal differentiation of C17.2 cells and retinoic acid-treated P19 cells. Tretinoin 147-160 cell division cycle 42 Mus musculus 25-30
19244314-5 2009 These molecules regulate Cdc42 and p38MAPK activities, which increase in a Cdo-dependent manner during neuronal differentiation of C17.2 cells and retinoic acid-treated P19 cells. Tretinoin 147-160 mitogen-activated protein kinase 14 Mus musculus 35-42
19244314-5 2009 These molecules regulate Cdc42 and p38MAPK activities, which increase in a Cdo-dependent manner during neuronal differentiation of C17.2 cells and retinoic acid-treated P19 cells. Tretinoin 147-160 interleukin 23, alpha subunit p19 Mus musculus 169-172
19635392-2 2009 In the present study, we investigated whether CaMKII is involved in activation of ERK and p38 in response to all-trans retinoic acid (ATRA) treatment in PC12 cells. Tretinoin 113-132 mitogen activated protein kinase 14 Rattus norvegicus 90-93
19635392-2 2009 In the present study, we investigated whether CaMKII is involved in activation of ERK and p38 in response to all-trans retinoic acid (ATRA) treatment in PC12 cells. Tretinoin 134-138 mitogen activated protein kinase 14 Rattus norvegicus 90-93
19635392-3 2009 Results showed that ATRA-induced activation of ERK and p38 occurred later than that of CAMKII. Tretinoin 20-24 mitogen activated protein kinase 14 Rattus norvegicus 55-58
19635392-4 2009 Knockdown of CAMKII by siRNA significantly suppressed ATRA-induced activation of ERK and p38. Tretinoin 54-58 mitogen activated protein kinase 14 Rattus norvegicus 89-92
19635392-5 2009 These results demonstrated that activation of ERK and p38 following ATRA exposure is CAMKII-dependent. Tretinoin 68-72 mitogen activated protein kinase 14 Rattus norvegicus 54-57
19528322-6 2009 Strikingly, we were able to show that Zic1 is also required for maintaining early forebrain expression of the retinoic acid (RA)-degrading enzyme cyp26a1. Tretinoin 110-123 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 146-153
19528322-6 2009 Strikingly, we were able to show that Zic1 is also required for maintaining early forebrain expression of the retinoic acid (RA)-degrading enzyme cyp26a1. Tretinoin 125-127 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 146-153
19306865-5 2009 We also provide evidence that Hoxd11 suppresses the expression of Hoxd10 and the retinoic acid synthetic enzyme, retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 81-94 homeobox D11 Gallus gallus 30-36
19439491-8 2009 Ectopic expression of Hoxb4 in anterior non-kidney IM, either by retinoic acid (RA) administration or plasmid-mediated overexpression, resulted in ectopic kidney gene expression. Tretinoin 65-78 homeobox B4 Gallus gallus 22-27
19472184-2 2009 Previous studies have shown that RA activates p38 mitogen-activated protein kinase (MAPK) and steroid receptor coactivator (SRC)-3 in tumor cells in vitro. Tretinoin 33-35 mitogen-activated protein kinase 14 Mus musculus 46-49
19472184-5 2009 Results showed that ATRA treatment rapidly activated p38 MAPK, which in turn resulted in phosphorylation with subsequent degradation of SRC-3. Tretinoin 20-24 mitogen-activated protein kinase 14 Mus musculus 53-61
22666666-8 2009 Conditioned media from SCF, NGF or RA-treated HMC-1 cells, and SCF, NGF, DMSO or RA-treated THP-1 cells enhanced immune complex transport via enhancing the expression of the CD23 in HT29 cells and the release of inflammatory mediator TNF-alpha. Tretinoin 81-83 Fc epsilon receptor II Homo sapiens 174-178
20185795-8 2010 Phenotypic analysis of Raldh2 mutant mice rescued from early cardiac defects by retinoic acid food supply revealed defects of the venous pole and pericardium highly similar to those of Wt1(-/-) mice. Tretinoin 80-93 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 23-29
19932628-4 2010 RA at 10(-8)M and 10(-7)M increased PKC-delta phosphorylation (the ratio of phosphorylated to total PKC-delta) (p<0.05) and decreased the secretion and synthesis of IGF-I (p<0.05) compared to control, with the effects peaking for treatment with 10(-7)M RA for 72h. Tretinoin 0-2 protein kinase C delta Homo sapiens 36-45
19932628-4 2010 RA at 10(-8)M and 10(-7)M increased PKC-delta phosphorylation (the ratio of phosphorylated to total PKC-delta) (p<0.05) and decreased the secretion and synthesis of IGF-I (p<0.05) compared to control, with the effects peaking for treatment with 10(-7)M RA for 72h. Tretinoin 0-2 protein kinase C delta Homo sapiens 100-109
19834471-0 2010 Induction of uncoupling protein-1 in mouse embryonic fibroblast-derived adipocytes by retinoic acid. Tretinoin 86-99 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 13-33
19834471-3 2010 We investigated the capacity of retinoic acid (RA), the carboxylic acid form of vitamin A and a known positive regulator of UCP1 gene transcription in brown adipocytes, to stimulate UCP1 expression in adipocytes differentiated in culture from primary mouse embryonic fibroblasts (MEFs), which are commonly used as white adipocyte model cells. Tretinoin 32-45 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 124-128
19834471-3 2010 We investigated the capacity of retinoic acid (RA), the carboxylic acid form of vitamin A and a known positive regulator of UCP1 gene transcription in brown adipocytes, to stimulate UCP1 expression in adipocytes differentiated in culture from primary mouse embryonic fibroblasts (MEFs), which are commonly used as white adipocyte model cells. Tretinoin 32-45 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 182-186
19834471-3 2010 We investigated the capacity of retinoic acid (RA), the carboxylic acid form of vitamin A and a known positive regulator of UCP1 gene transcription in brown adipocytes, to stimulate UCP1 expression in adipocytes differentiated in culture from primary mouse embryonic fibroblasts (MEFs), which are commonly used as white adipocyte model cells. Tretinoin 47-49 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 182-186
19834471-4 2010 Exposure to all-trans RA (ATRA), but not to rosiglitazone or isoproterenol, potently induced UCP1 expression at both the mRNA and protein level in MEF-derived adipocytes, in a dose-dependent manner. Tretinoin 22-24 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 93-97
19834471-4 2010 Exposure to all-trans RA (ATRA), but not to rosiglitazone or isoproterenol, potently induced UCP1 expression at both the mRNA and protein level in MEF-derived adipocytes, in a dose-dependent manner. Tretinoin 26-30 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 93-97
20057335-0 2010 Modulation of Lgl1 by steroid, retinoic acid, and vitamin D models complex transcriptional regulation during alveolarization. Tretinoin 31-44 cysteine-rich secretory protein LCCL domain containing 2 Rattus norvegicus 14-18
20230754-0 2010 Retinoic acid regulates differentiation of the secondary heart field and TGFbeta-mediated outflow tract septation. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 73-80
20068222-2 2010 Considering that aldehyde dehydrogenase (ALDH) activity controls the production of RA, we used a flow cytometry-based assay to measure ALDH activity at the single-cell level and to perform a comprehensive analysis of the RA-producing DC populations present in lymphoid and nonlymphoid mouse tissues. Tretinoin 83-85 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 17-39
20068222-2 2010 Considering that aldehyde dehydrogenase (ALDH) activity controls the production of RA, we used a flow cytometry-based assay to measure ALDH activity at the single-cell level and to perform a comprehensive analysis of the RA-producing DC populations present in lymphoid and nonlymphoid mouse tissues. Tretinoin 83-85 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 41-45
20056916-8 2010 Furthermore, we show that retinoic acid treatment in mature heart valves is sufficient to promote calcific processes in vitro, which can be attenuated by Sox9 overexpression. Tretinoin 26-39 SRY (sex determining region Y)-box 9 Mus musculus 154-158
20039314-7 2010 Treatment of iPSCs-derived embryoid bodies (EBs) with transforming growth factor beta 1 (TGF-beta1) in the presence of retinoic acid enhanced generation of MSC-like cells. Tretinoin 119-132 transforming growth factor, beta 1 Mus musculus 54-87
20039314-7 2010 Treatment of iPSCs-derived embryoid bodies (EBs) with transforming growth factor beta 1 (TGF-beta1) in the presence of retinoic acid enhanced generation of MSC-like cells. Tretinoin 119-132 transforming growth factor, beta 1 Mus musculus 89-98
20126997-10 2010 Doxycycline, epigallocatechin gallate, a nutrient mixture, actinomycin-D, cyclohexamide, retinoic acid and dexamethasone inhibited MMP-2 in HeLa and SK-OV-3 cell lines and inhibited MMP-9 in DoTc2-4510. Tretinoin 89-102 matrix metallopeptidase 2 Homo sapiens 131-136
20184720-2 2010 Neuron navigator 2 (Nav2) was first identified as an atRA-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, Rainb1), and is required for atRA-mediated neurite outgrowth. Tretinoin 104-117 neuron navigator 2 Homo sapiens 0-18
20184720-2 2010 Neuron navigator 2 (Nav2) was first identified as an atRA-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, Rainb1), and is required for atRA-mediated neurite outgrowth. Tretinoin 104-117 neuron navigator 2 Homo sapiens 20-24
20184720-2 2010 Neuron navigator 2 (Nav2) was first identified as an atRA-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, Rainb1), and is required for atRA-mediated neurite outgrowth. Tretinoin 104-117 neuron navigator 2 Homo sapiens 146-152
20184720-2 2010 Neuron navigator 2 (Nav2) was first identified as an atRA-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, Rainb1), and is required for atRA-mediated neurite outgrowth. Tretinoin 53-57 neuron navigator 2 Homo sapiens 0-18
20184720-2 2010 Neuron navigator 2 (Nav2) was first identified as an atRA-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, Rainb1), and is required for atRA-mediated neurite outgrowth. Tretinoin 53-57 neuron navigator 2 Homo sapiens 20-24
20184720-2 2010 Neuron navigator 2 (Nav2) was first identified as an atRA-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, Rainb1), and is required for atRA-mediated neurite outgrowth. Tretinoin 53-57 neuron navigator 2 Homo sapiens 146-152
20028078-1 2010 Vav1, whose physiological expression is restricted to hematopoietic system, is one of the signaling proteins up-regulated by all-trans retinoic acid (ATRA) in acute promyelocytic leukemia (APL)-derived precursors, in which it promotes the overcoming of the differentiation blockade. Tretinoin 135-148 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
20028078-1 2010 Vav1, whose physiological expression is restricted to hematopoietic system, is one of the signaling proteins up-regulated by all-trans retinoic acid (ATRA) in acute promyelocytic leukemia (APL)-derived precursors, in which it promotes the overcoming of the differentiation blockade. Tretinoin 150-154 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
20028078-3 2010 Here, we have found that phosphorylation of Vav1 Y174, that is known to regulate Vav1 activity in mature neutrophils, is up-regulated by ATRA in NB4 cells. Tretinoin 137-141 vav guanine nucleotide exchange factor 1 Homo sapiens 44-48
20028078-3 2010 Here, we have found that phosphorylation of Vav1 Y174, that is known to regulate Vav1 activity in mature neutrophils, is up-regulated by ATRA in NB4 cells. Tretinoin 137-141 vav guanine nucleotide exchange factor 1 Homo sapiens 81-85
20028078-6 2010 In fact, the overexpression of a mutated form of Vav1, in which Y745 was replaced with a phenylalanine, significantly reduced the ATRA-induced CD11b expression and essentially abrogated the differentiation-related acquisition of the migratory capability. Tretinoin 130-134 vav guanine nucleotide exchange factor 1 Homo sapiens 49-53
20082710-9 2010 Furthermore, our results suggest the interesting possibility that Pax6 regulates anterior-posterior patterning of the hindbrain via activation of Cyp26b1, an enzyme that metabolizes retinoic acid. Tretinoin 182-195 paired box 6 Rattus norvegicus 66-70
19853839-11 2010 On induction of differentiation by retinoic acid, a sequential expression was found in human neuroblastoma, where ANKK1 was expressed first, followed by that of DRD2. Tretinoin 35-48 dopamine receptor D2 Homo sapiens 161-165
20209433-9 2010 In Xenopus, depletion of retinoids from mesoderm by targeted injection of mRNAs for the retinoic acid catabolising enzyme xCYP26 and the cellular retinoic acid binding protein xCRABP blocks 3 Hox gene expression in the overlying neuroectoderm. Tretinoin 88-101 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 122-128
19903244-0 2010 ATRA inhibits ceramide kinase transcription in a human neuroblastoma cell line, SH-SY5Y cells: the role of COUP-TFI. Tretinoin 0-4 ceramide kinase Homo sapiens 14-29
19903244-4 2010 Here, we examined CERK mRNA level during all-trans retinoic acid (ATRA)-induced differentiation of a human neuroblastoma cell line, SH-SY5Y. Tretinoin 51-64 ceramide kinase Homo sapiens 18-22
19903244-4 2010 Here, we examined CERK mRNA level during all-trans retinoic acid (ATRA)-induced differentiation of a human neuroblastoma cell line, SH-SY5Y. Tretinoin 66-70 ceramide kinase Homo sapiens 18-22
19903244-6 2010 Over-expression and small interfering RNA (siRNA) of CERK revealed that CERK is inhibitory against ATRA-induced neuronal differentiation and cell growth arrest. Tretinoin 99-103 ceramide kinase Homo sapiens 53-57
19903244-6 2010 Over-expression and small interfering RNA (siRNA) of CERK revealed that CERK is inhibitory against ATRA-induced neuronal differentiation and cell growth arrest. Tretinoin 99-103 ceramide kinase Homo sapiens 72-76
20110732-0 2010 Kidneys of Alb/TGF-beta1 transgenic mice are deficient in retinoic acid and exogenous retinoic acid shows dose-dependent toxicity. Tretinoin 58-71 albumin Mus musculus 11-14
20110732-0 2010 Kidneys of Alb/TGF-beta1 transgenic mice are deficient in retinoic acid and exogenous retinoic acid shows dose-dependent toxicity. Tretinoin 58-71 transforming growth factor, beta 1 Mus musculus 15-24
20110732-0 2010 Kidneys of Alb/TGF-beta1 transgenic mice are deficient in retinoic acid and exogenous retinoic acid shows dose-dependent toxicity. Tretinoin 86-99 albumin Mus musculus 11-14
20369475-5 2010 RESULTS: Over 21.2% of K562 cells demonstrated features of granulocyte, and the expression of CD13 on cell surface increased significantly at day 5 with ATRA treatment (P < 0.05, compared with control). Tretinoin 153-157 alanyl aminopeptidase, membrane Homo sapiens 94-98
20369475-8 2010 After 5 days of induced cell differentiation, expression levels of MtF and TfR1 mRNA were just 86.5% and 79.2% of that before ATRA treatment. Tretinoin 126-130 transferrin receptor Homo sapiens 75-79
19788910-3 2009 Over-expression of Prickle1 or Prickle2 in C1300 cells induced striking neurite-like process formation in the absence of RA. Tretinoin 121-123 prickle planar cell polarity protein 1 Mus musculus 19-27
19669406-6 2009 Semi-quantitative RT-PCR analysis revealed that ATRA caused a selective inhibition of both the basal and induction levels of C/EBPalpha and PPARgamma, without altering the expression pattern of C/EBPbeta. Tretinoin 48-52 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 125-135
19669406-6 2009 Semi-quantitative RT-PCR analysis revealed that ATRA caused a selective inhibition of both the basal and induction levels of C/EBPalpha and PPARgamma, without altering the expression pattern of C/EBPbeta. Tretinoin 48-52 peroxisome proliferator activated receptor gamma Mus musculus 140-149
19744992-5 2009 ATRA also strongly induced the expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) (an increase of 5- and 50-fold, respectively). Tretinoin 0-4 steroidogenic acute regulatory protein Homo sapiens 45-83
19744992-5 2009 ATRA also strongly induced the expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) (an increase of 5- and 50-fold, respectively). Tretinoin 0-4 steroidogenic acute regulatory protein Homo sapiens 85-89
19903984-2 2009 Targeting p38MAPK using drugs reported to interfere with its phosphorylation, namely statins and all-trans retinoic acid (atRA), might play a role in ameliorating this remodeling. Tretinoin 97-120 mitogen activated protein kinase 14 Rattus norvegicus 10-17
19903984-2 2009 Targeting p38MAPK using drugs reported to interfere with its phosphorylation, namely statins and all-trans retinoic acid (atRA), might play a role in ameliorating this remodeling. Tretinoin 122-126 mitogen activated protein kinase 14 Rattus norvegicus 10-17
19885578-9 2009 Actinomycin-D, cyclohexamide, retinoic acid and dexamethasone inhibited MMP-2 in both cancer cell lines and inhibited MMP-9 in MM. Tretinoin 30-43 matrix metallopeptidase 2 Homo sapiens 72-77
19594026-0 2009 [Effect of Wnt-1 on the process of inducing neural stem cells into neurons by all-trans-retinoic acid in vitro]. Tretinoin 81-101 Wnt family member 1 Rattus norvegicus 11-16
19594026-1 2009 OBJECTIVE: To explore the expression of Wnt-1 during the process of inducing neural stem cells (NSCs) into neurons by using all-trans-retinoic acid (ATRA) in vitro and the effect of Wnt-1 on NSCs differentiation. Tretinoin 124-147 Wnt family member 1 Rattus norvegicus 40-45
19594026-1 2009 OBJECTIVE: To explore the expression of Wnt-1 during the process of inducing neural stem cells (NSCs) into neurons by using all-trans-retinoic acid (ATRA) in vitro and the effect of Wnt-1 on NSCs differentiation. Tretinoin 149-153 Wnt family member 1 Rattus norvegicus 40-45
19594026-10 2009 CONCLUSION: With the induction of ATRA at 1.0 mmicromol/L, Wnt-1 and NSCs differentiation in early stage are positively correlated. Tretinoin 34-38 Wnt family member 1 Rattus norvegicus 59-64
19432991-0 2009 Identification of the B-Raf/Mek/Erk MAP kinase pathway as a target for all-trans retinoic acid during skin cancer promotion. Tretinoin 81-94 midkine Mus musculus 28-31
19118439-4 2009 The Asb-2 (ankyrin repeat SOCS box 2) gene has previously been identified as a transcriptional target in ATRA-treated HL-60 cells. Tretinoin 105-109 ankyrin repeat and SOCS box containing 2 Homo sapiens 4-9
19118439-4 2009 The Asb-2 (ankyrin repeat SOCS box 2) gene has previously been identified as a transcriptional target in ATRA-treated HL-60 cells. Tretinoin 105-109 ankyrin repeat and SOCS box containing 2 Homo sapiens 11-36
23864846-4 2013 In addition, we attempted to determine the difference in retinoic acid-induced gene expression between cells treated with PP2 in combination with ATRA and in combination with ATO. Tretinoin 57-70 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 122-125
19118439-6 2009 To induce granulocytic differentiation, HL-60 cells were treated for 5 d with ATRA and differentiation was confirmed by examining superoxide anion production, nuclear morphology, and changes in the expression of CD11b, CD13, and CD15. Tretinoin 78-82 alanyl aminopeptidase, membrane Homo sapiens 219-223
23864846-5 2013 RESULTS: SFK inhibitor PP2 induced significant enhancement of ATRA- or ATO-induced differentiation of NB4 cells. Tretinoin 62-66 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 23-26
20005394-1 2009 BACKGROUND: Ligands for the natural killer cell-activating receptor NKG2D, such as retinoic acid early inducible (Rae-1), minor histocompatibility antigen H60 (mouse), and major histocompatibility complex class I chain-related (human) may be expressed by tissues in response to stress. Tretinoin 83-96 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 68-73
23864846-12 2013 Intercellular adhesion molecule-1 expression showed a significant increase in cells treated with PP2 in combination with ATRA, whereas cathepsin D expression showed a significant increase in cells treated with PP2 in combination with ATO. Tretinoin 121-125 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 97-100
23864846-13 2013 CONCLUSION: Our data showed that SFK inhibitor PP2 enhanced acute promyelocytic leukemia cell differentiation when combined with either ATRA or ATO with difference in activation of retinoic acid-induced genes. Tretinoin 136-140 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 47-50
19538255-6 2009 Incubation with dibutyryl-cAMP and RA stimulated the expression of the EPC differentiation markers von Willebrand Factor (vWF) and VEGF receptor 2 (VEGFR-2), indicating successful differentiation in the fibrin clot. Tretinoin 35-37 kinase insert domain protein receptor Mus musculus 131-146
23864846-13 2013 CONCLUSION: Our data showed that SFK inhibitor PP2 enhanced acute promyelocytic leukemia cell differentiation when combined with either ATRA or ATO with difference in activation of retinoic acid-induced genes. Tretinoin 181-194 neuropeptide Y receptor Y6 (pseudogene) Homo sapiens 47-50
19538255-6 2009 Incubation with dibutyryl-cAMP and RA stimulated the expression of the EPC differentiation markers von Willebrand Factor (vWF) and VEGF receptor 2 (VEGFR-2), indicating successful differentiation in the fibrin clot. Tretinoin 35-37 kinase insert domain protein receptor Mus musculus 148-155
19151770-0 2009 Effective in vivo induction of NKG2D ligands in acute myeloid leukaemias by all-trans-retinoic acid or sodium valproate. Tretinoin 76-99 killer cell lectin like receptor K1 Homo sapiens 31-36
19841174-2 2009 Expression of gut-homing molecules alpha(4)beta(7) and CCR9 is induced by retinoic acid, a vitamin A metabolite produced by retinal dehydrogenases, which are specifically expressed in dendritic cells as well as stromal cells in mucosa-draining lymph nodes. Tretinoin 74-87 C-C motif chemokine receptor 9 Homo sapiens 55-59
19726747-0 2009 Retinoic acid-induced nNOS expression depends on a novel PI3K/Akt/DAX1 pathway in human TGW-nu-I neuroblastoma cells. Tretinoin 0-13 nitric oxide synthase 1 Homo sapiens 22-26
22996420-6 2013 Exogenous wild-type ELA2 markedly increased THP-1 differentiation, whereas G185R ELA2 was incompetent to promote THP-1 differentiation in response to all-trans retinoic acid (ATRA). Tretinoin 160-173 elastase, neutrophil expressed Homo sapiens 81-85
19726747-5 2009 To investigate regulation of nNOS gene expression by retinoic acid (RA), we used the human neuroblastoma cell line TGW-nu-I as a model system. Tretinoin 53-66 nitric oxide synthase 1 Homo sapiens 29-33
19726747-5 2009 To investigate regulation of nNOS gene expression by retinoic acid (RA), we used the human neuroblastoma cell line TGW-nu-I as a model system. Tretinoin 68-70 nitric oxide synthase 1 Homo sapiens 29-33
19726747-6 2009 We show that RA induces nNOS transcription in a protein synthesis-dependent fashion. Tretinoin 13-15 nitric oxide synthase 1 Homo sapiens 24-28
19151770-3 2009 Herein, we show that in vivo administration of all-trans-retinoic acid (ATRA) or the histone deacetylase inhibitor sodium valproate (VPA) to patients affected with acute myeloid leukaemia (AML) M3 or M1 respectively, leads to the induction of transcription and expression of NKG2D-L at the surface of leukaemic cells. Tretinoin 47-70 killer cell lectin like receptor K1 Homo sapiens 275-280
19151770-3 2009 Herein, we show that in vivo administration of all-trans-retinoic acid (ATRA) or the histone deacetylase inhibitor sodium valproate (VPA) to patients affected with acute myeloid leukaemia (AML) M3 or M1 respectively, leads to the induction of transcription and expression of NKG2D-L at the surface of leukaemic cells. Tretinoin 72-76 killer cell lectin like receptor K1 Homo sapiens 275-280
22996420-6 2013 Exogenous wild-type ELA2 markedly increased THP-1 differentiation, whereas G185R ELA2 was incompetent to promote THP-1 differentiation in response to all-trans retinoic acid (ATRA). Tretinoin 175-179 elastase, neutrophil expressed Homo sapiens 81-85
23508548-11 2013 In addition, we found retinoic acid would decrease the expression of P53 and miR-34c, however, did not change the expression of c-Myc greatly. Tretinoin 22-35 cellular tumor antigen p53 Capra hircus 69-72
19371792-2 2009 For example, regulatory T cells (Tregs) are characterized by expression of FOXP3, which is either induced during thymic development for natural Tregs (nTregs), or in the periphery in the presence of TGF-beta and retinoic acid for induced Tregs (iTreg). Tretinoin 212-225 forkhead box P3 Homo sapiens 75-80
19716814-11 2009 In mouse P19 cells induced by retinoic acid to undergo neural differentiation, overexpression of Xenopus Fz10 leads to an increase in the number of neurons generated while siRNA knockdown of endogenous mouse Fz10 inhibits neurogenesis. Tretinoin 30-43 frizzled class receptor 10 L homeolog Xenopus laevis 105-109
19665003-2 2009 Statins, fibrates, retinoic acid and forskolin activate luciferase gene reporter activity driven by the -334/+3 bp region of the human CAC promoter containing wild-type (but not mutated) PPRE. Tretinoin 19-32 solute carrier family 25 member 20 Homo sapiens 135-138
23528537-0 2013 Retinoic acid-induced HOXA5 expression is co-regulated by HuR and miR-130a. Tretinoin 0-13 microRNA 130a Homo sapiens 66-74
19665003-6 2009 Because CAC is essential for fatty acid beta-oxidation, the above results on the regulation of CAC gene expression provide a novel contribution to the understanding of the hypolipidemic action of statins, fibrates and retinoic acid. Tretinoin 218-231 solute carrier family 25 member 20 Homo sapiens 8-11
19665003-6 2009 Because CAC is essential for fatty acid beta-oxidation, the above results on the regulation of CAC gene expression provide a novel contribution to the understanding of the hypolipidemic action of statins, fibrates and retinoic acid. Tretinoin 218-231 solute carrier family 25 member 20 Homo sapiens 95-98
19814781-4 2009 Thus, the purpose of this study is to examine the molecular mechanisms by which RA enhances skeletal myogenesis and interacts with Wnt and BMP4 signalling during P19 or mouse embryonic stem (ES) cell differentiation. Tretinoin 80-82 interleukin 23, alpha subunit p19 Mus musculus 162-165
19814781-5 2009 RESULTS: Treatment of P19 or mouse ES cells with low levels of RA led to an enhancement of skeletal myogenesis by upregulating the expression of the mesodermal marker, Wnt3a, the skeletal muscle progenitor factors Pax3 and Meox1, and the myogenic regulatory factors (MRFs) MyoD and myogenin. Tretinoin 63-65 interleukin 23, alpha subunit p19 Mus musculus 22-25
19814781-10 2009 Furthermore, RA downregulated BMP4 expression and upregulated the BMP4 inhibitor, Tob1. Tretinoin 13-15 transducer of ErbB-2.1 Mus musculus 82-86
19014918-7 2009 In addition, we demonstrate here that enzymatic activity of AKR1B1 and AKR1B10 lowers all-trans- and 9-cis-retinoic acid-dependent trans-activation in living cells, indicating that both enzymes may contribute to pre-receptor regulation of retinoic acid and retinoid X nuclear receptors. Tretinoin 107-120 aldo-keto reductase family 1 member B10 Homo sapiens 71-78
19014918-7 2009 In addition, we demonstrate here that enzymatic activity of AKR1B1 and AKR1B10 lowers all-trans- and 9-cis-retinoic acid-dependent trans-activation in living cells, indicating that both enzymes may contribute to pre-receptor regulation of retinoic acid and retinoid X nuclear receptors. Tretinoin 239-252 aldo-keto reductase family 1 member B10 Homo sapiens 71-78
19050858-8 2009 These results suggest that RA can reduce ischemia-induced cerebral injury by an anti-inflammatory action, which may be effected via inhibition of C/EBPbeta-mediated COX-2 induction. Tretinoin 27-29 CCAAT enhancer binding protein beta Homo sapiens 146-155
23528537-9 2013 Collectively, these results demonstrate that HuR and miR-130a dynamically regulate HOXA5 gene expression via modulating HOXA5 mRNA turnover and translation, respectively, thereby contributing to RA-induced growth inhibition. Tretinoin 195-197 microRNA 130a Homo sapiens 53-61
23675444-1 2013 The retinoic acid receptor beta2(RARbeta2) is a type of nuclear receptor that is activated by both all-trans retinoic acid and 9-cis retinoic acid, which has been shown to function as a tumor suppressor gene in different types of human tumors. Tretinoin 4-17 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 27-32
19177594-0 2009 NKG2D-retinoic acid early inducible-1 recognition between natural killer cells and Kupffer cells in a novel murine natural killer cell-dependent fulminant hepatitis. Tretinoin 6-19 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 0-5
19509478-11 2009 In ATRA-treated FTC-133 and XTC.UC1 cell lines, MMP-2 expression was decreased, but no significant changes in uPA and E-cadherin expression were observed. Tretinoin 3-7 matrix metallopeptidase 2 Homo sapiens 48-53
19853750-0 2009 Prenatal retinoic acid up-regulates pulmonary gene expression of COUP-TFII, FOG2, and GATA4 in pulmonary hypoplasia. Tretinoin 9-22 zinc finger protein, multitype 2 Rattus norvegicus 76-80
19853750-13 2009 RESULTS: The relative mRNA expression levels of COUP-TFII, FOG2, and GATA4 were significantly increased in CDH + RA lungs compared to control, control + RA, and CDH (P < .05). Tretinoin 113-115 zinc finger protein, multitype 2 Rattus norvegicus 59-63
19853750-14 2009 CONCLUSIONS: Up-regulation of pulmonary gene expression of COUP-TFII, FOG2, and GATA4 after prenatal treatment with retinoic acid in the nitrofen model of CDH suggests that RA may have a therapeutic potential in modulating lung growth. Tretinoin 173-175 zinc finger protein, multitype 2 Rattus norvegicus 70-74
19060179-0 2009 Retinoic acid-mediated down-regulation of ENO1/MBP-1 gene products caused decreased invasiveness of the follicular thyroid carcinoma cell lines. Tretinoin 0-13 proteoglycan 2, pro eosinophil major basic protein Homo sapiens 47-52
23321499-5 2013 Consistently, RA-induced cancer cell cytotoxicity was significantly impaired by Zyxin or PTOV1. Tretinoin 14-16 PTOV1 extended AT-hook containing adaptor protein Homo sapiens 89-94
19060179-9 2009 Both, RA-mediated and specific knock-down of ENO1/MBP-1 resulted in the reduction of MYC oncoprotein, and simultaneously decreased proliferation rates of FTC-133 and FTC-238 cell lines. Tretinoin 6-8 proteoglycan 2, pro eosinophil major basic protein Homo sapiens 50-55
19735730-2 2009 N-CoR (nuclear receptor co-repressor) is the first identified co-repressor that can repress retinoic acid (RA) inducible gene transcription in the absence of RA. Tretinoin 92-105 nuclear receptor corepressor 1 Danio rerio 0-5
19735730-2 2009 N-CoR (nuclear receptor co-repressor) is the first identified co-repressor that can repress retinoic acid (RA) inducible gene transcription in the absence of RA. Tretinoin 92-105 nuclear receptor corepressor 1 Danio rerio 7-36
19735730-2 2009 N-CoR (nuclear receptor co-repressor) is the first identified co-repressor that can repress retinoic acid (RA) inducible gene transcription in the absence of RA. Tretinoin 107-109 nuclear receptor corepressor 1 Danio rerio 0-5
19735730-2 2009 N-CoR (nuclear receptor co-repressor) is the first identified co-repressor that can repress retinoic acid (RA) inducible gene transcription in the absence of RA. Tretinoin 107-109 nuclear receptor corepressor 1 Danio rerio 7-36
19735730-3 2009 Previously, N-CoR was reported to be required for late-stage organogenesis in mouse but whether N-CoR can affect RA-responsive early embryonic patterning is unknown. Tretinoin 113-115 nuclear receptor co-repressor 1 Mus musculus 96-101
19735730-5 2009 Knocking down n-cor elevates endogenous RA signaling in zebrafish embryos and posteriorizes the neural ectoderm. Tretinoin 40-42 nuclear receptor corepressor 1 Danio rerio 14-19
19486889-5 2009 We further demonstrated that HDAC2 directly deacetylated KLF4, and that KLF4 acetylation and binding activity of KLF4 to the SM22alpha promoter were significantly increased in ATRA-treated VSMCs. Tretinoin 176-180 transgelin Homo sapiens 125-134
23444226-1 2013 PURPOSE: In acute myeloid leukemia (AML) without retinoic acid receptor (RAR) rearrangement, the effect of all-trans-retinoic acid (ATRA) is still poorly understood despite an association of NPM1 mutation and ATRA response. Tretinoin 209-213 nucleophosmin 1 Homo sapiens 191-195
19243620-6 2009 BMP4 is additionally able to up-regulate Hoxb4 ventrally, but the effect is restricted to the axial levels at which Hoxb4 is normally expressed, and only in the presence of retinoic acid (RA) or somites, suggesting a role for BMP in rendering the neural tube competent to express Hoxb4 in response to RA or somite signals. Tretinoin 173-186 bone morphogenetic protein 4 Homo sapiens 0-4
23444226-7 2013 In patients with primary AML, repressor activity of high-PRAME levels might be overcome by the addition of ATRA as indicated by better outcome in 2 independent studies (P = 0.029). Tretinoin 107-111 PRAME nuclear receptor transcriptional regulator Homo sapiens 57-62
19230972-0 2009 Inhibition of all-trans retinoic acid-induced granulocytic differentiation of WEHI-3B D+ cells by forced expression of SCL (TAL1) and GATA-1. Tretinoin 24-37 T cell acute lymphocytic leukemia 1 Mus musculus 119-129
19230972-0 2009 Inhibition of all-trans retinoic acid-induced granulocytic differentiation of WEHI-3B D+ cells by forced expression of SCL (TAL1) and GATA-1. Tretinoin 24-37 GATA binding protein 1 Mus musculus 134-140
19097998-4 2009 We show that the ability of P19 cells to undergo the transition from an Oct3/4-positive, undifferentiated status to microtubule-associated protein 2-positive neurons and glial fibrillary acidic protein-positive astrocytes, upon treatment with retinoic acid (RA), requires RA-induced activation of Cdc42 during the neural cell lineage specification phase. Tretinoin 243-256 cell division cycle 42 Mus musculus 297-302
21626648-6 2013 JNK, P-38 and caspase activation were shown in the nature of RA-triggered apoptotic signaling in ES cells. Tretinoin 61-63 mitogen-activated protein kinase 14 Mus musculus 5-9
19097998-6 2009 The constitutively active Cdc42(F28L) mutant was sufficient to up-regulate Hes5 and Pax6 in P19 cells, even in the absence of RA treatment, ultimately promoting their transition to neural progenitor cells. Tretinoin 126-128 cell division cycle 42 Mus musculus 26-31
19230972-2 2009 Transfection of SCL, expressed in D- but absent in D+ cells, into D+ cells, caused resistance to ATRA, while transfection of GATA-1 into D+ cells produced resistance to the combination of ATRA and LiCl. Tretinoin 188-192 GATA binding protein 1 Mus musculus 125-131
21626648-9 2013 The process of EB formation (mimicking the early postimplantation embryo development) is regulated by RA-induced apoptosis through the activation of caspase and P38 MAPK/JNK pathway. Tretinoin 102-104 mitogen-activated protein kinase 14 Mus musculus 161-164
23042455-0 2013 Retinoic acid regulates gap junction intercellular communication in human endometrial stromal cells through modulation of the phosphorylation status of connexin 43. Tretinoin 0-13 gap junction protein alpha 1 Homo sapiens 152-163
19701462-10 2009 More than 33% of HB9+ sMN progenitor cells were observed after differentiation of dissociated neurospheres by all-trans retinoic acid (ATRA) and a Shh agonist for another week on monolayer culture. Tretinoin 110-133 survival of motor neuron 1, telomeric Homo sapiens 22-25
19701462-10 2009 More than 33% of HB9+ sMN progenitor cells were observed after differentiation of dissociated neurospheres by all-trans retinoic acid (ATRA) and a Shh agonist for another week on monolayer culture. Tretinoin 135-139 survival of motor neuron 1, telomeric Homo sapiens 22-25
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 20-33 retinol dehydrogenase 16 Homo sapiens 115-121
18977204-6 2009 Mechanisms of AHR signaling in prostate growth and disease are only beginning to be unraveled and recent studies have revealed its interactions with WNT5A, retinoic acid, fibroblast growth factor 10, and vascular endothelial growth factor signaling pathways. Tretinoin 156-169 aryl hydrocarbon receptor Homo sapiens 14-17
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 20-33 lecithin retinol acyltransferase Homo sapiens 155-159
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 35-37 retinol dehydrogenase 16 Homo sapiens 115-121
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 35-37 lecithin retinol acyltransferase Homo sapiens 155-159
23042455-4 2013 Using primary human endometrial stromal cells (ESCs) and a stable high telomerase-expressing ESC transfectant (T-HESC), we found that retinoic acid (RA) altered the phosphorylation status of Cx43 protein such that there was a decrease in the phosphorylated (P1 and P2) species accompanied by an increase in the non-phosphorylated (P0) form. Tretinoin 134-147 gap junction protein alpha 1 Homo sapiens 191-195
19550115-11 2009 The positive rates of both CD11b and CD14 in HL-60 cells were over 90% after 5-day treatment (2 micromol/L ATRA or 10 micromol/L NSC67657); cell morphology also represented characteristics of differentiation. Tretinoin 107-111 CD14 molecule Homo sapiens 37-41
19298812-0 2009 Retinoic acid induces nuclear accumulation of Raf1 during differentiation of HL-60 cells. Tretinoin 0-13 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 46-50
23042455-4 2013 Using primary human endometrial stromal cells (ESCs) and a stable high telomerase-expressing ESC transfectant (T-HESC), we found that retinoic acid (RA) altered the phosphorylation status of Cx43 protein such that there was a decrease in the phosphorylated (P1 and P2) species accompanied by an increase in the non-phosphorylated (P0) form. Tretinoin 149-151 gap junction protein alpha 1 Homo sapiens 191-195
23042455-5 2013 This process is dependent on protein phosphatase 2A (PP2A) activity since selective PP2A inhibitors prevented the ability of RA to dephosphorylate Cx43. Tretinoin 125-127 gap junction protein alpha 1 Homo sapiens 147-151
19357873-3 2009 Therefore, a rat model of GS was established to investigate the effect of all-trans retinoic acid (ATRA) on the renal expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Tretinoin 74-97 matrix metallopeptidase 2 Rattus norvegicus 161-166
19068090-3 2009 Our study demonstrated that combining ATRA with vaccination not only decreased the number of Gr-1+ CD11b+ ImC, but for the first time also suppressed the function of Gr-1+ CD11b+ ImC with decreased expression of CD80. Tretinoin 38-42 CD80 molecule Homo sapiens 212-216
19357873-3 2009 Therefore, a rat model of GS was established to investigate the effect of all-trans retinoic acid (ATRA) on the renal expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Tretinoin 99-103 matrix metallopeptidase 2 Rattus norvegicus 133-159
23042455-6 2013 Although RA had no effect on total PP2A expression or activity, it significantly increased the intracellular association of Cx43 and PP2A. Tretinoin 9-11 gap junction protein alpha 1 Homo sapiens 124-128
19357873-3 2009 Therefore, a rat model of GS was established to investigate the effect of all-trans retinoic acid (ATRA) on the renal expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Tretinoin 99-103 matrix metallopeptidase 2 Rattus norvegicus 161-166
19357873-15 2009 In conclusion, ATRA may protect renal function and step down the progression of GS by reducing the expression of TIMP-1, enhancing the expression and activity of MMP-2 and MMP-9, and regulating the ratio of MMPs/TIMPs to dynamic balance, so as to reduce the accumulation of ECM. Tretinoin 15-19 matrix metallopeptidase 2 Rattus norvegicus 162-167
23042455-9 2013 Our data indicate that RA stimulates physical association of PP2A with Cx43, resulting in the dephosphorylation of Cx43 and, as a consequence, up-regulation of GJIC in ESCs. Tretinoin 23-25 gap junction protein alpha 1 Homo sapiens 71-75
19357873-15 2009 In conclusion, ATRA may protect renal function and step down the progression of GS by reducing the expression of TIMP-1, enhancing the expression and activity of MMP-2 and MMP-9, and regulating the ratio of MMPs/TIMPs to dynamic balance, so as to reduce the accumulation of ECM. Tretinoin 15-19 matrix metallopeptidase 2 Rattus norvegicus 207-211
19091570-7 2009 There was stable down-regulation of MDM2 and UGB as well as overexpression of SOD2, CSTB, and G3BP when RA-treated SHG-44 was compared with normal SHG-44. Tretinoin 104-106 superoxide dismutase 2 Homo sapiens 78-82
23042455-9 2013 Our data indicate that RA stimulates physical association of PP2A with Cx43, resulting in the dephosphorylation of Cx43 and, as a consequence, up-regulation of GJIC in ESCs. Tretinoin 23-25 gap junction protein alpha 1 Homo sapiens 115-119
23259988-0 2013 Influence of time to complete remission and duration of all-trans retinoic acid therapy on the relapse risk in patients with acute promyelocytic leukemia receiving AIDA protocols. Tretinoin 66-79 axin interactor, dorsalization associated Homo sapiens 164-168
26238624-0 2009 Post-translational modifications of orphan nuclear receptor TR2 - new insights into drug targets for stem cell therapy and the effect of retinoic acid. Tretinoin 137-150 nuclear receptor subfamily 2, group C, member 1 Mus musculus 60-63
19417068-7 2009 FHL2 expression was remarkably up-regulated during retinoic acid-induced differentiation of neuroblastoma cells, during which the expression of Id2 was opposite to that. Tretinoin 51-64 four and a half LIM domains 2 Homo sapiens 0-4
23359509-0 2013 Hepatic stellate cells preferentially induce Foxp3+ regulatory T cells by production of retinoic acid. Tretinoin 88-101 forkhead box P3 Homo sapiens 45-50
19533039-8 2009 Furthermore, differentiating maGS cells from retinoic acid-treated embryoid bodies maintained the androgenetic imprinting pattern of the H19 ICR. Tretinoin 45-58 H19, imprinted maternally expressed transcript Mus musculus 137-140
19385050-3 2009 RA induced N2a cells differentiation into neurite bearing and neuronal specific proteins, microtubule-associated protein 2 (MAP2) and neuronal specific nuclear protein (NeuN), expressing neuronal-like cells. Tretinoin 0-2 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 134-167
19385050-3 2009 RA induced N2a cells differentiation into neurite bearing and neuronal specific proteins, microtubule-associated protein 2 (MAP2) and neuronal specific nuclear protein (NeuN), expressing neuronal-like cells. Tretinoin 0-2 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 169-173
19306865-7 2009 We hypothesize that one of the roles played by Hoxd11 is to modulate Hoxd10 and local retinoic acid levels and thus, perhaps define the caudal boundaries of the LMC and its subtype complement. Tretinoin 86-99 homeobox D11 Gallus gallus 47-53
19236766-5 2009 The results showed that the expression of hoxc4 and hoxc6 genes in the differentiation process increased slightly on day 3, and were up to the most on day 7 (p < 0.05), while became lower on day 12 respectively in normal group, HCMV group and ATRA group. Tretinoin 246-250 homeobox C4 Homo sapiens 42-47
19236766-12 2009 At the same condition, ATRA (6 x 10(-8) mol/L at 60 nmol/ml) can up-regulate hoxc4 and hoxc6 genes expression. Tretinoin 23-27 homeobox C4 Homo sapiens 77-82
22974347-7 2013 Both retinoic acid and GSK 3beta inhibitor upregulated the expression of Pitx2, a homeobox gene involved in the development of the anterior segment of the eye. Tretinoin 5-18 paired-like homeodomain transcription factor 2 Mus musculus 73-78
18992716-0 2009 Retinoic acid modulates retinaldehyde dehydrogenase 1 gene expression through the induction of GADD153-C/EBPbeta interaction. Tretinoin 0-13 CCAAT enhancer binding protein beta Homo sapiens 103-112
18992716-2 2009 RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor alpha (RARalpha) and the CCAAT/enhancer binding protein beta (C/EBPbeta). Tretinoin 0-2 CCAAT enhancer binding protein beta Homo sapiens 142-177
18992716-2 2009 RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor alpha (RARalpha) and the CCAAT/enhancer binding protein beta (C/EBPbeta). Tretinoin 0-2 CCAAT enhancer binding protein beta Homo sapiens 179-188
18992716-5 2009 Here we report that the RARalpha/retinoid X receptor beta (RXRbeta) complex binds to the mouse retinaldehyde dehydrogenase 1 (Raldh1) promoter at a non-consensus RA response element (RARE) with similar affinity to that of the consensus RARE. Tretinoin 24-26 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 95-124
18992716-5 2009 Here we report that the RARalpha/retinoid X receptor beta (RXRbeta) complex binds to the mouse retinaldehyde dehydrogenase 1 (Raldh1) promoter at a non-consensus RA response element (RARE) with similar affinity to that of the consensus RARE. Tretinoin 24-26 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 126-132
19144697-2 2009 The alpha-secretase ADAM10 has been found to be regulated by retinoic acid, the bioreactive metabolite of vitamin A. Tretinoin 61-74 ADAM metallopeptidase domain 10 Homo sapiens 20-26
19332534-6 2009 Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. Tretinoin 110-114 interleukin 6 Sus scrofa 31-34
19332534-6 2009 Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. Tretinoin 110-114 eotaxin Sus scrofa 36-41
18992716-7 2009 Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box. Tretinoin 15-17 CCAAT enhancer binding protein beta Homo sapiens 48-57
23264745-5 2013 Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm"s tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARgamma(-/-) cells. Tretinoin 177-179 retinoic acid receptor gamma Homo sapiens 205-213
18992716-7 2009 Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box. Tretinoin 15-17 CCAAT enhancer binding protein beta Homo sapiens 120-129
19274054-12 2009 Retinoic acid and triiodothyronine increased UCP1 mRNA expression in the BAT(B) adipocytes 1.6- and 2-fold, respectively but, surprisingly, slightly decreased UCP1 mRNA expression in the WAT(B) adipocytes. Tretinoin 0-13 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 45-49
18992716-8 2009 These data support a model in which high RA levels inhibit Raldh1 gene expression by sequestering C/EBPbeta through its interaction to GADD153. Tretinoin 41-43 CCAAT enhancer binding protein beta Homo sapiens 98-107
23264745-7 2013 Mapping of the epigenetic signature of Meis1 revealed that RA induces a rapid increase in the H3K9/K14ac epigenetic mark at the proximal promoter and at two sites downstream of the transcription start site in WT, but not in RARgamma(-/-) cells. Tretinoin 59-61 retinoic acid receptor gamma Homo sapiens 224-232
19274054-12 2009 Retinoic acid and triiodothyronine increased UCP1 mRNA expression in the BAT(B) adipocytes 1.6- and 2-fold, respectively but, surprisingly, slightly decreased UCP1 mRNA expression in the WAT(B) adipocytes. Tretinoin 0-13 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 159-163
23264745-8 2013 Thus, RA-associated increases in H3K9/K14ac epigenetic marks require RARgamma and are associated with increased Meis1 transcript levels, whereas H3K4me3 is present at the Meis1 proximal promoter even in the absence of RARgamma. Tretinoin 6-8 retinoic acid receptor gamma Homo sapiens 69-77
23264745-8 2013 Thus, RA-associated increases in H3K9/K14ac epigenetic marks require RARgamma and are associated with increased Meis1 transcript levels, whereas H3K4me3 is present at the Meis1 proximal promoter even in the absence of RARgamma. Tretinoin 6-8 retinoic acid receptor gamma Homo sapiens 218-226
23264745-9 2013 In contrast, at the Lrat proximal promoter primarily the H3K4me3 mark, and not the H3K9/K14ac mark, increases in response to RA, independently of the presence of RARgamma. Tretinoin 125-127 lecithin retinol acyltransferase Homo sapiens 20-24
22666666-7 2009 Treatment with stem cell factor (SCF), nerve growth factor (NGF), retinoic acid (RA) or dimethyl sulphoxide (DMSO) enhanced CD23 expression in HT29 cells. Tretinoin 66-79 Fc epsilon receptor II Homo sapiens 124-128
22666666-7 2009 Treatment with stem cell factor (SCF), nerve growth factor (NGF), retinoic acid (RA) or dimethyl sulphoxide (DMSO) enhanced CD23 expression in HT29 cells. Tretinoin 81-83 Fc epsilon receptor II Homo sapiens 124-128
23243270-7 2013 Multiplexing mAbs against CD11b and CD11c provided surrogate imaging biomarkers of differentiation therapy in an acute promyelocytic leukemia model treated with all-trans retinoic acid combined with the histone-deacetylase inhibitor valproic acid. Tretinoin 171-184 integrin subunit alpha X Homo sapiens 36-41
22666666-8 2009 Conditioned media from SCF, NGF or RA-treated HMC-1 cells, and SCF, NGF, DMSO or RA-treated THP-1 cells enhanced immune complex transport via enhancing the expression of the CD23 in HT29 cells and the release of inflammatory mediator TNF-alpha. Tretinoin 35-37 Fc epsilon receptor II Homo sapiens 174-178
19476657-11 2009 CONCLUSION: These results indicate that Tbx1 expression in the POM regulates cochlear outgrowth potentially via control of local retinoic acid activity. Tretinoin 129-142 T-box transcription factor 1 Homo sapiens 40-44
19173746-0 2009 The retinoic acid binding protein CRABP2 is increased in murine models of degenerative joint disease. Tretinoin 4-17 cellular retinoic acid binding protein II Mus musculus 34-40
19059939-7 2009 In Cox regression analysis, a significant interaction between the genotype mutant NPM1 without FLT3-ITD and treatment with all-trans retinoic acid was identified, in that the beneficial effect of all-trans retinoic acid on relapse-free and overall survival was restricted to this subgroup of patients. Tretinoin 133-146 nucleophosmin 1 Homo sapiens 82-86
19432991-8 2009 The counter-regulated genes have been clustered into functional categories and bioinformatic analysis has identified the B-Raf/Mek/Erk branch of the MAP kinase pathway as one containing several genes whose upregulation by TPA is blocked by ATRA. Tretinoin 240-244 midkine Mus musculus 127-130
23302037-0 2013 Identification of a retinoic acid-responsive neural enhancer in the Ciona intestinalis Hox1 gene. Tretinoin 20-33 homeobox transcription factor Hox1 Ciona intestinalis 87-91
19059939-7 2009 In Cox regression analysis, a significant interaction between the genotype mutant NPM1 without FLT3-ITD and treatment with all-trans retinoic acid was identified, in that the beneficial effect of all-trans retinoic acid on relapse-free and overall survival was restricted to this subgroup of patients. Tretinoin 206-219 nucleophosmin 1 Homo sapiens 82-86
19059939-9 2009 CONCLUSIONS: In elderly patients with acute myeloid leukemia, NPM1 mutations are associated with achievement of complete remission, and the genotype "mutant NPM1 without FLT3-ITD" appears to be a predictive marker for response to all-trans retinoic acid given as an adjunct to intensive chemotherapy (ClinicalTrials.gov Identifier: NCT00151242). Tretinoin 240-253 nucleophosmin 1 Homo sapiens 157-161
19217924-1 2009 Midkine is a 13-kDa retinoic acid-induced heparin-binding growth factor involved in various biological phenomena such as cell migration, neurogenesis, and tissue repair. Tretinoin 20-33 midkine Mus musculus 0-7
23302037-2 2013 We identified a nerve cord enhancer in the second intron of Ci-Hox1, and demonstrated that retinoic acid (RA) plays a major role in activating this enhancer. Tretinoin 91-104 homeobox transcription factor Hox1 Ciona intestinalis 60-67
23302037-2 2013 We identified a nerve cord enhancer in the second intron of Ci-Hox1, and demonstrated that retinoic acid (RA) plays a major role in activating this enhancer. Tretinoin 106-108 homeobox transcription factor Hox1 Ciona intestinalis 60-67
18792915-0 2009 p38-MAPK- and caspase-3-mediated superoxide-induced apoptosis of rat hepatic stellate cells: reversal by retinoic acid. Tretinoin 105-118 mitogen activated protein kinase 14 Rattus norvegicus 0-3
23526672-2 2013 Recent findings describe a new step for the induction of oral tolerance, consisting in the homing of FOXP3+ regulatory T cells to the small bowel and the local acquisition of full immunosuppressive capacities, a process in which retinoic acid-producing dendritic cells might play a crucial role. Tretinoin 229-242 forkhead box P3 Homo sapiens 101-106
18792915-0 2009 p38-MAPK- and caspase-3-mediated superoxide-induced apoptosis of rat hepatic stellate cells: reversal by retinoic acid. Tretinoin 105-118 caspase 3 Rattus norvegicus 14-23
19636436-0 2009 Studies on Multifunctional Effect of All-Trans Retinoic Acid (ATRA) on Matrix Metalloproteinase-2 (MMP-2) and Its Regulatory Molecules in Human Breast Cancer Cells (MCF-7). Tretinoin 62-66 matrix metallopeptidase 2 Homo sapiens 71-97
19275242-2 2009 P19 mouse embryonic carcinoma cells can differentiate into neural cells by the addition of retinoic acid (RA) or by overexpression of the Wnt1 gene, with both processes dependent on cell aggregation. Tretinoin 91-104 interleukin 23, alpha subunit p19 Mus musculus 0-3
19275242-2 2009 P19 mouse embryonic carcinoma cells can differentiate into neural cells by the addition of retinoic acid (RA) or by overexpression of the Wnt1 gene, with both processes dependent on cell aggregation. Tretinoin 106-108 interleukin 23, alpha subunit p19 Mus musculus 0-3
19275242-9 2009 Silencing of NDRG1 reduced the size of cell aggregates and the expression of N-cadherin, and it also impaired the RA-induced P19 cell neural differentiation. Tretinoin 114-116 N-myc downstream regulated gene 1 Mus musculus 13-18
19275242-9 2009 Silencing of NDRG1 reduced the size of cell aggregates and the expression of N-cadherin, and it also impaired the RA-induced P19 cell neural differentiation. Tretinoin 114-116 interleukin 23, alpha subunit p19 Mus musculus 125-128
19636436-0 2009 Studies on Multifunctional Effect of All-Trans Retinoic Acid (ATRA) on Matrix Metalloproteinase-2 (MMP-2) and Its Regulatory Molecules in Human Breast Cancer Cells (MCF-7). Tretinoin 62-66 matrix metallopeptidase 2 Homo sapiens 99-104
23178912-9 2013 Since RA treatment increased cytoplasmic reactive oxygen species (ROS) levels in these cells, an IRE/IRP independent, ROS-mediated mechanism may account for dysregulation of iron-related genes. Tretinoin 6-8 Wnt family member 2 Homo sapiens 101-104
19636436-3 2009 We studied the effect of ATRA on MMP-2 in MCF-7, human breast cancer cells, and the probable signaling pathways which are affected by ATRA on regulating pro-MMP-2 activity and expression. Tretinoin 134-138 matrix metallopeptidase 2 Homo sapiens 157-162
19636436-7 2009 Gelatin zymography showed that ATRA caused a dose-dependent inhibition of pro-MMP-2 activity. Tretinoin 31-35 matrix metallopeptidase 2 Homo sapiens 78-83
19636436-8 2009 ATRA treatment downregulates the expression of MT1-MMP, EMMPRIN, FAK, NF-kB, and p-ERK. Tretinoin 0-4 matrix metallopeptidase 14 Homo sapiens 47-54
19636436-8 2009 ATRA treatment downregulates the expression of MT1-MMP, EMMPRIN, FAK, NF-kB, and p-ERK. Tretinoin 0-4 protein tyrosine kinase 2 Homo sapiens 65-68
19252500-5 2009 Retinoic acid acted on DCs to induce suppressor of cytokine signaling-3 expression, which suppressed activation of p38 mitogen-activated protein kinase and proinflammatory cytokines. Tretinoin 0-13 suppressor of cytokine signaling 3 Homo sapiens 37-71
19144990-6 2009 Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes. Tretinoin 45-47 homeobox A1 Homo sapiens 70-75
19144990-6 2009 Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes. Tretinoin 45-47 homeobox A4 Homo sapiens 80-85
19636436-9 2009 However, expression of E-cadherin, RAR, and CRABP increased upon ATRA treatment. Tretinoin 65-69 cellular retinoic acid binding protein 1 Homo sapiens 44-49
23237802-1 2013 We previously showed that all-trans retinoic acid (atRA) decreased nitric oxide (NO) production through Akt-mediated decreased phosphorylation of endothelial NO synthase at serine 1179 (eNOS-Ser(1179)) in bovine aortic endothelial cells (BAEC). Tretinoin 26-49 AKT serine/threonine kinase 1 Bos taurus 104-107
19636436-12 2009 The experimental findings clearly showed the inhibition of MMP-2 activity upon ATRA treatment. Tretinoin 79-83 matrix metallopeptidase 2 Homo sapiens 59-64
19636436-13 2009 This inhibitory effect of ATRA on MMP-2 activity in human breast cancer cells (MCF-7) may result due to its inhibitory effect on MT1-MMP, EMMPRIN, and upregulation of TIMP-2. Tretinoin 26-30 matrix metallopeptidase 2 Homo sapiens 34-39
19636436-13 2009 This inhibitory effect of ATRA on MMP-2 activity in human breast cancer cells (MCF-7) may result due to its inhibitory effect on MT1-MMP, EMMPRIN, and upregulation of TIMP-2. Tretinoin 26-30 matrix metallopeptidase 14 Homo sapiens 129-136
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 10-23 retinol dehydrogenase 16 Homo sapiens 91-96
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 10-23 lecithin retinol acyltransferase Homo sapiens 110-114
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 25-27 retinol dehydrogenase 16 Homo sapiens 91-96
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 25-27 lecithin retinol acyltransferase Homo sapiens 110-114
19171200-4 2009 RA (1 microM) induced CYP26A1, CYP26B1, CYP2S1, CRABPII and LRAT mRNA. Tretinoin 0-2 lecithin retinol acyltransferase Homo sapiens 60-64
19050858-7 2009 Moreover, cerebral ischemic induction of cyclooxygenase-2 (COX-2) and CCAAT/enhancer binding protein beta (C/EBPbeta), which binds to the COX-2 promoter, was also inhibited by RA. Tretinoin 176-178 CCAAT enhancer binding protein beta Homo sapiens 70-105
19050858-7 2009 Moreover, cerebral ischemic induction of cyclooxygenase-2 (COX-2) and CCAAT/enhancer binding protein beta (C/EBPbeta), which binds to the COX-2 promoter, was also inhibited by RA. Tretinoin 176-178 CCAAT enhancer binding protein beta Homo sapiens 107-116
19636436-14 2009 This study is focused on the effect of ATRA on MMP, MMP-integrin-E-cadherin interrelationship, and also the effect of the drug on different signaling molecules which may involve in the progression of malignant tumor development. Tretinoin 39-43 matrix metallopeptidase 2 Homo sapiens 47-50
18845239-8 2008 Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA. Tretinoin 82-86 mitogen-activated protein kinase kinase 1 Mus musculus 14-18
18845239-8 2008 Inhibition of MEK1/ERK mitogen-activated protein kinases significantly suppressed atRA-induced NRF2 activation and ARE-regulated gene expression, reducing cell resistance against toxic concentrations of RA. Tretinoin 84-86 mitogen-activated protein kinase kinase 1 Mus musculus 14-18
23237802-1 2013 We previously showed that all-trans retinoic acid (atRA) decreased nitric oxide (NO) production through Akt-mediated decreased phosphorylation of endothelial NO synthase at serine 1179 (eNOS-Ser(1179)) in bovine aortic endothelial cells (BAEC). Tretinoin 51-55 AKT serine/threonine kinase 1 Bos taurus 104-107
19178302-0 2009 Transcription factor TBX1 overexpression induces downregulation of proteins involved in retinoic acid metabolism: a comparative proteomic analysis. Tretinoin 88-101 T-box transcription factor 1 Homo sapiens 21-25
19178302-4 2009 The most interesting observation is that overexpression of TBX1 results in down-regulation of two proteins involved in retinoic acid metabolism. Tretinoin 119-132 T-box transcription factor 1 Homo sapiens 59-63
23392891-2 2013 However, whether the hormone calcitriol (1,25-dihydroxyvitamin D(3)) and retinoic acid regulate the expression of the TauT gene is unknown. Tretinoin 73-86 solute carrier family 6 member 6 Homo sapiens 118-122
19061903-3 2009 Calcium imaging experiments revealed that P2Y-induced calcium mobilization is diminished in mouse neuroblastoma Neuro 2a cells stably transfected with BM88 (N2A-BM88 cells) as compared with N2A cells or N2A cells differentiated with retinoic acid. Tretinoin 233-246 cell cycle exit and neuronal differentiation 1 Mus musculus 151-155
19035346-1 2008 Cyp26A1 is a major enzyme that controls retinoic acid (RA) homeostasis by metabolizing RA into bio-inactive metabolites. Tretinoin 40-53 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-7
19035346-1 2008 Cyp26A1 is a major enzyme that controls retinoic acid (RA) homeostasis by metabolizing RA into bio-inactive metabolites. Tretinoin 55-57 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-7
19035346-1 2008 Cyp26A1 is a major enzyme that controls retinoic acid (RA) homeostasis by metabolizing RA into bio-inactive metabolites. Tretinoin 87-89 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-7
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 98-111 solute carrier family 6 member 6 Homo sapiens 47-51
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 113-115 solute carrier family 6 member 6 Homo sapiens 47-51
19006694-0 2008 Retinoic acid enhances Foxp3 induction indirectly by relieving inhibition from CD4+CD44hi Cells. Tretinoin 0-13 forkhead box P3 Homo sapiens 23-28
19204112-0 2009 Contrasting roles for all-trans retinoic acid in TGF-beta-mediated induction of Foxp3 and Il10 genes in developing regulatory T cells. Tretinoin 32-45 transforming growth factor, beta 1 Mus musculus 49-57
24592121-0 2013 Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells. Tretinoin 61-74 upregulator of cell proliferation Homo sapiens 14-18
24592121-0 2013 Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells. Tretinoin 61-74 upregulator of cell proliferation Homo sapiens 19-24
24592121-0 2013 Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells. Tretinoin 61-74 cyclin D1 Homo sapiens 26-35
24592121-6 2013 In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. Tretinoin 30-32 upregulator of cell proliferation Homo sapiens 46-50
24592121-6 2013 In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. Tretinoin 30-32 upregulator of cell proliferation Homo sapiens 51-56
24592121-6 2013 In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. Tretinoin 30-32 cyclin D1 Homo sapiens 58-63
18653720-9 2008 BPA animals showed that the Hoxa10 reduction was accompanied by an increased stromal expression of the silencing mediator for retinoic acid and thyroid hormone receptor. Tretinoin 126-139 homeobox A10 Rattus norvegicus 28-34
19168680-3 2009 We show that, in addition to posterior mesendoderm, primitive streak and node cells transiently express the RA-synthesizing enzyme Raldh2 prior to the headfold stage. Tretinoin 108-110 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 131-137
24592121-13 2013 Our preliminary results suggest that RA may induce cell proliferation and escape apoptosis using a novel pathway by the URG4/URGCP gene. Tretinoin 37-39 upregulator of cell proliferation Homo sapiens 120-124
24592121-13 2013 Our preliminary results suggest that RA may induce cell proliferation and escape apoptosis using a novel pathway by the URG4/URGCP gene. Tretinoin 37-39 upregulator of cell proliferation Homo sapiens 125-130
18615582-0 2008 S10 phosphorylation of p27 mediates atRA induced growth arrest in ovarian carcinoma cell lines. Tretinoin 36-40 ribosomal protein S10 Homo sapiens 0-3
23409080-0 2013 Knock-down of PRAME increases retinoic acid signaling and cytotoxic drug sensitivity of Hodgkin lymphoma cells. Tretinoin 30-43 PRAME nuclear receptor transcriptional regulator Homo sapiens 14-19
18615582-2 2008 We report here that phosphorylation at S10 residue is an important event in mediating p27 role in atRA induced growth arrest. Tretinoin 98-102 ribosomal protein S10 Homo sapiens 39-42
18778953-3 2009 First, RA enhances the induction of Foxp3(+) T regulatory cells by DCs. Tretinoin 7-9 forkhead box P3 Homo sapiens 36-41
18809338-2 2009 Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. Tretinoin 28-30 forkhead box P3 Homo sapiens 274-279
23409080-7 2013 After knock-down of PRAME using vector based RNA interference we observed increased sensitivity for cisplatin, etoposide and retinoic acid. Tretinoin 125-138 PRAME nuclear receptor transcriptional regulator Homo sapiens 20-25
18615582-3 2008 atRA treatment of atRA sensitive CAOV3 cells increases the levels of S10 phospho-p27 in both nuclear and cytoplasmic cell compartments. Tretinoin 0-4 ribosomal protein S10 Homo sapiens 69-72
23409080-10 2013 Our data suggest that PRAME inhibits retinoic acid signaling in HL cells and that the knock-down of PRAME might be an interesting option for the development of new therapy strategies for patients with chemo-resistant HL. Tretinoin 37-50 PRAME nuclear receptor transcriptional regulator Homo sapiens 22-27
18941112-3 2009 We identified several miRNAs transcriptionally repressed by the APL-associated PML-RAR oncogene which are released after treatment with all-trans retinoic acid. Tretinoin 146-159 PML-RARA regulated adaptor molecule 1 Homo sapiens 79-86
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 0-13 cellular retinoic acid binding protein II Mus musculus 230-238
18622580-5 2008 We show forced expression of EWS-FLI1 causes absence of retinoic acid-induced neural morphology, and decreases expression of neural-specific proteins MAPT and NCAM. Tretinoin 56-69 EWS RNA binding protein 1 Homo sapiens 29-32
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 15-17 cellular retinoic acid binding protein II Mus musculus 230-238
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 cellular retinoic acid binding protein II Mus musculus 106-114
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 cyclin dependent kinase 2 Homo sapiens 82-86
23105114-6 2012 The switch in RA signaling is accomplished by a transient up-regulation of RARbeta concomitantly with a transient increase in the CRABP-II/FABP5 ratio at early stages of differentiation. Tretinoin 14-16 retinoic acid receptor, beta Mus musculus 75-82
19078967-2 2009 Here, we highlighted a novel paradigm in which the transcription of RARalpha target genes is controlled by phosphorylation cascades initiated by the rapid RA activation of the p38MAPK/MSK1 pathway. Tretinoin 68-70 ribosomal protein S6 kinase A5 Homo sapiens 184-188
19078967-6 2009 Cancer cells characterized by a deregulated p38MAPK/MSK1 pathway, do not respond to RA, outlining the essential contribution of the RA-triggered phosphorylation cascade in RA signalling. Tretinoin 132-134 ribosomal protein S6 kinase A5 Homo sapiens 52-56
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 cyclin dependent kinase 4 Homo sapiens 91-95
23105114-6 2012 The switch in RA signaling is accomplished by a transient up-regulation of RARbeta concomitantly with a transient increase in the CRABP-II/FABP5 ratio at early stages of differentiation. Tretinoin 14-16 cellular retinoic acid binding protein II Mus musculus 130-138
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 cyclin dependent kinase 2 Homo sapiens 82-86
22344541-0 2012 All-trans retinoic acid inhibits mesangial cell proliferation by up-regulating p21Waf1/Cip1 and p27Kip1 and down-regulating Skp2. Tretinoin 10-23 cyclin-dependent kinase inhibitor 1A Rattus norvegicus 87-91
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 cyclin dependent kinase 4 Homo sapiens 91-95
23064179-3 2012 Using an integrative approach based on several bioinformatics resources together with experimental validations, we indeed found that retinoic acid positively regulates miR-210 and miR-23a/24-2 expressions and is counteracted by estrogen. Tretinoin 133-146 microRNA 210 Homo sapiens 168-175
20429413-11 2009 For example, retinoic acid, produced by the dendritic cells and epithelial cells in the intestine, works together with TGF-beta1 and promotes generation of small intestine-homing FOXP3 T-cells by upregulating the expression ofFOXP3 and gut homing receptors. Tretinoin 13-26 forkhead box P3 Homo sapiens 179-184
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 86-99 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 17-46
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 86-99 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 48-54
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 101-103 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 17-46
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 101-103 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 48-54
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 173-175 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 17-46
19075394-5 2009 Here we identify retinaldehyde dehydrogenase 2 (Raldh2), the rate-limiting enzyme for retinoic acid (RA) synthesis in the limb, as a direct Hoxd13 target and show decreased RA production in limbs from Spdh/Spdh mice. Tretinoin 173-175 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 48-54
18838553-1 2008 Silencing mediator for retinoic acid and thyroid hormone receptor (SMRT) is a transcriptional corepressor that participates in diverse signaling pathways and human diseases. Tretinoin 23-36 nuclear receptor corepressor 2 Homo sapiens 67-71
23021139-2 2012 Retinaldehyde dehydrogenase 2 (Raldh2, a gene critical for the generation of retinoic acid) is expressed in the mouse duodenum during the temporal window when duodenal atresias form. Tretinoin 77-90 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 0-29
18846337-12 2008 ATRA treatment increased the protein levels of MMP2 and MMP13. Tretinoin 0-4 matrix metallopeptidase 2 Rattus norvegicus 47-51
18663367-10 2009 Besides the biogenesis of lysosome-related organelles complex 1 and dystrophin-associated protein complex, several molecules in the DTNBP1 network likely provide insight into the role of DTNBP1 in biological systems: retinoic acid, beta-estradiol, calmodulin and tumour necrosis factor. Tretinoin 217-230 dystrobrevin binding protein 1 Homo sapiens 132-138
23021139-2 2012 Retinaldehyde dehydrogenase 2 (Raldh2, a gene critical for the generation of retinoic acid) is expressed in the mouse duodenum during the temporal window when duodenal atresias form. Tretinoin 77-90 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 31-37
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 matrix metallopeptidase 2 Rattus norvegicus 175-179
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 matrix metallopeptidase 2 Rattus norvegicus 219-223
19816090-7 2009 With retinoic-acid-induced differentiation of retinoblastoma cells, TrkA expression significantly increased whereas TrkB significantly decreased. Tretinoin 5-18 neurotrophic receptor tyrosine kinase 1 Homo sapiens 68-72
19816090-7 2009 With retinoic-acid-induced differentiation of retinoblastoma cells, TrkA expression significantly increased whereas TrkB significantly decreased. Tretinoin 5-18 neurotrophic receptor tyrosine kinase 2 Homo sapiens 116-120
22681667-4 2012 In this study, we show that functionally suppressive, alloantigen-specific CD8(+) Foxp3(+) T cells can be induced and significantly expanded by stimulating naive CD8(+) T cells with donor dendritic cells in the presence of IL-2, TGF-beta1 and retinoic acid. Tretinoin 243-256 forkhead box P3 Homo sapiens 82-87
18641199-0 2008 Retinoic acid decreases adherence of murine myeloid dendritic cells and increases production of matrix metalloproteinase-9. Tretinoin 0-13 matrix metallopeptidase 9 Mus musculus 96-122
22801367-2 2012 Using chromatin immunoprecipitation with microarray technology (ChIP-chip) analysis, we found that the H3K9-me2 target gene JAK2 was an important factor during differentiation of the HL-60 promyelocytic leukemia cell line by all-trans-retinoic acid (ATRA) treatment. Tretinoin 225-248 Janus kinase 2 Homo sapiens 124-128
18641199-8 2008 These data suggest that atRA is essential to augment MMP-9 expression in myeloid DC and can alter their surface expression of adhesion molecules. Tretinoin 24-28 matrix metallopeptidase 9 Mus musculus 53-58
18950872-7 2008 The expression of the pharmacodynamic mRNA markers of IFN-beta effect showed differences in time profiles for the Good Responder and Partial Responders to IFN-beta therapy and the Jak-STAT, TNFRSF10B, IL6, TGFbeta, retinoic acid and CDC42 pathways were differentially modulated. Tretinoin 215-228 interferon beta 1 Homo sapiens 54-62
18927084-0 2008 Retinoic acid leads to cytoskeletal rearrangement through AMPK-Rac1 and stimulates glucose uptake through AMPK-p38 MAPK in skeletal muscle cells. Tretinoin 0-13 Rac family small GTPase 1 Mus musculus 63-67
22801367-2 2012 Using chromatin immunoprecipitation with microarray technology (ChIP-chip) analysis, we found that the H3K9-me2 target gene JAK2 was an important factor during differentiation of the HL-60 promyelocytic leukemia cell line by all-trans-retinoic acid (ATRA) treatment. Tretinoin 250-254 Janus kinase 2 Homo sapiens 124-128
18927084-0 2008 Retinoic acid leads to cytoskeletal rearrangement through AMPK-Rac1 and stimulates glucose uptake through AMPK-p38 MAPK in skeletal muscle cells. Tretinoin 0-13 mitogen-activated protein kinase 14 Mus musculus 111-119
18927084-3 2008 RA induced Rac1-GTP formation and phosphorylation of its downstream target, p21-activated kinase (PAK), whereas the inhibition of AMPK blocked RA-induced Rac1 activation. Tretinoin 0-2 Rac family small GTPase 1 Mus musculus 11-15
18665267-4 2008 Here we show that the retinoic acid (RA) synthesizing enzyme Raldh1 is expressed in developing mouse and human pancreas at stages when beta-cells are generated. Tretinoin 22-35 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 61-67
18927084-3 2008 RA induced Rac1-GTP formation and phosphorylation of its downstream target, p21-activated kinase (PAK), whereas the inhibition of AMPK blocked RA-induced Rac1 activation. Tretinoin 143-145 Rac family small GTPase 1 Mus musculus 154-158
22801367-3 2012 Here, we report that the H3K9 methyltransferase G9a negatively regulated JAK2 transcription in histone methyltransferase activity and in a YY1-dependent manner during ATRA-mediated leukemia cell differentiation. Tretinoin 167-171 Janus kinase 2 Homo sapiens 73-77
18927084-7 2008 Finally, the inhibition of AMPK and p38 MAPK blocked retinoic acid-induced glucose uptake. Tretinoin 53-66 mitogen-activated protein kinase 14 Mus musculus 36-44
18927084-8 2008 In summary, our results suggest that retinoic acid may have cytoskeletal roles in skeletal muscle cells via stimulation of the AMPK-Rac1-PAK-cofillin pathway and may also have beneficial roles in glucose metabolism via stimulation of the AMPK-p38 MAPK pathway. Tretinoin 37-50 Rac family small GTPase 1 Mus musculus 132-136
22801424-5 2012 Knockdown of HNK-1ST restored the glycosylation of alpha-DG and the migration of RA-treated S91 cells, indicating that HNK-1ST functions through glycans on alpha-DG. Tretinoin 81-83 carbohydrate sulfotransferase 10 Mus musculus 13-20
18927084-8 2008 In summary, our results suggest that retinoic acid may have cytoskeletal roles in skeletal muscle cells via stimulation of the AMPK-Rac1-PAK-cofillin pathway and may also have beneficial roles in glucose metabolism via stimulation of the AMPK-p38 MAPK pathway. Tretinoin 37-50 mitogen-activated protein kinase 14 Mus musculus 243-251
18467351-7 2008 Experimental examples demonstrating the issue include the stimulatory effects of serum on the expression of retinoic acid-inducible genes (e.g. GPRC5A) leading to the potentially erroneous conclusion that such genes are overexpressed in cancer cells. Tretinoin 108-121 G protein-coupled receptor class C group 5 member A Bos taurus 144-150
22801424-5 2012 Knockdown of HNK-1ST restored the glycosylation of alpha-DG and the migration of RA-treated S91 cells, indicating that HNK-1ST functions through glycans on alpha-DG. Tretinoin 81-83 carbohydrate sulfotransferase 10 Mus musculus 119-126
18805411-3 2008 We show that cellular RA-binding proteins CRABP1 and CRABP2 and the fatty acid-binding protein FABP5 are dynamically expressed during skin development and in adult tissue. Tretinoin 22-24 cellular retinoic acid binding protein 1 Homo sapiens 42-48
22270475-3 2012 Our results show that the expression of mouse liver, bone, and kidney ALP (mL/B/K-ALP) induced by ATRA in C3H10T 1/2 cells was related to the retinoic acid nuclear receptors, RARalpha and RARbeta, which are not involved in the MAPK pathway. Tretinoin 98-102 retinoic acid receptor, beta Mus musculus 188-195
19075782-8 2008 On the other hand, retinoic acid induces a subset of FoxP3+ regulatory T cells which is important for maintaining immune tolerance in the gut. Tretinoin 19-32 forkhead box P3 Homo sapiens 53-58
18989765-13 2008 Furthermore, ATRA suppressed the expression of LPS-stimulated c-Raf, MKK1/2 and ERK expression of THP-1 cells. Tretinoin 13-17 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 62-67
18989765-14 2008 In conclusion, ATRA suppressed Th2- and Th1-related chemokines expression in THP-1 cells, at least in part via the c-Raf-MKK1/2-ERK/MAPK pathway. Tretinoin 15-19 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 115-120
18989765-14 2008 In conclusion, ATRA suppressed Th2- and Th1-related chemokines expression in THP-1 cells, at least in part via the c-Raf-MKK1/2-ERK/MAPK pathway. Tretinoin 15-19 mitogen-activated protein kinase kinase 2 Homo sapiens 121-127
18399539-3 2008 The activity of RALDHs is known to be crucial for RA synthesis; however, recently a retinol dehydrogenase (RDH10) has been shown to represent a new limiting factor in this synthesis. Tretinoin 16-18 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 84-105
21633925-3 2012 In the present study, we show that retinoic acid enhances the cytostatic and apoptogenic properties of the novel adamantyl retinoid ST1926 in a panel of neuroblastoma cells with different p53 status and caspase 8 expression, resulting in synergistic effects as assessed by Combination Index and Isobologram analysis. Tretinoin 35-48 caspase 8 Homo sapiens 203-212
18427164-6 2008 The vitamin A metabolite retinoic acid is involved in this process via TGF-beta dependent induction of Foxp3. Tretinoin 25-38 forkhead box P3 Homo sapiens 103-108
18495959-6 2008 RA generated by RALDH2 in basophils modulates IL-3-induced gene expression in an autocrine manner, providing positive (CD25) as well as negative (granzyme B) regulation. Tretinoin 0-2 interleukin 2 receptor subunit alpha Homo sapiens 119-123
22521346-6 2012 An assay of hepatocyte cell lines of differing AFP expression showed that cytoplasmic AFP is able to block ATRA-induced nuclear translocation of RAR and expression of the Fn14 gene. Tretinoin 107-111 TNF receptor superfamily member 12A Homo sapiens 171-175
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 63-76 neuron navigator 2 Homo sapiens 0-18
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 63-76 neuron navigator 2 Homo sapiens 20-24
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 78-82 neuron navigator 2 Homo sapiens 0-18
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 78-82 neuron navigator 2 Homo sapiens 20-24
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 78-82 neuron navigator 2 Homo sapiens 172-178
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 130-143 neuron navigator 2 Homo sapiens 0-18
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 130-143 neuron navigator 2 Homo sapiens 20-24
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 130-143 neuron navigator 2 Homo sapiens 172-178
18396173-3 2008 Our previous study suggested that RDH12 protects cells against toxic levels of retinaldehyde and retinoic acid [S.A. Lee, O.V. Tretinoin 97-110 retinol dehydrogenase 12 Homo sapiens 34-39
18396173-5 2008 Popov, N.Y. Kedishvili, Overproduction of bioactive retinoic acid in cells expressing disease-associated mutants of retinol dehydrogenase 12, J. Biol. Tretinoin 52-65 retinol dehydrogenase 12 Homo sapiens 116-140
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 219-223 neuron navigator 2 Homo sapiens 0-18
22681644-7 2012 A second RA synthesizing enzyme, RALDH2 was also present in tanycytes lining the third ventricle. Tretinoin 9-11 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 33-39
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 219-223 neuron navigator 2 Homo sapiens 20-24
18726912-1 2008 Neuron navigator 2 (Nav2) was first identified as an all-trans retinoic acid (atRA)-responsive gene in human neuroblastoma cells (retinoic acid-induced in neuroblastoma 1, RAINB1) that extend neurites after exposure to atRA. Tretinoin 219-223 neuron navigator 2 Homo sapiens 172-178
18614847-4 2008 The differences were found in the gene expression of importin alpha3 and exportin 6 between the cells after treatments with DVD and ATRA. Tretinoin 132-136 karyopherin subunit alpha 3 Homo sapiens 53-68
22705300-0 2012 Acidic leucine-rich nuclear phosphoprotein 32 family member B (ANP32B) contributes to retinoic acid-induced differentiation of leukemic cells. Tretinoin 86-99 acidic nuclear phosphoprotein 32 family member B Homo sapiens 0-61
18082256-2 2008 The ALDH1A1 gene, whose product participates in retinoic acid synthesis, was previously identified as a TLX1-responsive gene. Tretinoin 48-61 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 4-11
18212744-8 2008 Thus, retinoic acid downregulates Rae1, hence facilitating APC(Cdh1)-mediated Skp2 degradation leading to the arrest of cell cycle progression and neuroblastoma differentiation. Tretinoin 6-19 S-phase kinase associated protein 2 Homo sapiens 78-82
18684862-4 2008 We found that the formation of yolk sac hemogenic endothelium and its hematopoietic potential were significantly impaired in the absence of retinoic acid (RA) signaling, and could be restored in RA-deficient (Raldh2(-/-)) embryos by provision of exogenous RA in utero. Tretinoin 140-153 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 209-215
18684862-4 2008 We found that the formation of yolk sac hemogenic endothelium and its hematopoietic potential were significantly impaired in the absence of retinoic acid (RA) signaling, and could be restored in RA-deficient (Raldh2(-/-)) embryos by provision of exogenous RA in utero. Tretinoin 195-197 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 209-215
22705300-0 2012 Acidic leucine-rich nuclear phosphoprotein 32 family member B (ANP32B) contributes to retinoic acid-induced differentiation of leukemic cells. Tretinoin 86-99 acidic nuclear phosphoprotein 32 family member B Homo sapiens 63-69
18838813-2 2008 In the present study, ATRA and retinol inhibited melanin synthesis in melanoma cells stimulated by alpha-melanocyte stimulating hormone (alpha-MSH) or 3-isobutyl-1-methylxanthine (IBMX). Tretinoin 22-26 pro-opiomelanocortin-alpha Mus musculus 99-135
18838813-2 2008 In the present study, ATRA and retinol inhibited melanin synthesis in melanoma cells stimulated by alpha-melanocyte stimulating hormone (alpha-MSH) or 3-isobutyl-1-methylxanthine (IBMX). Tretinoin 22-26 pro-opiomelanocortin-alpha Mus musculus 137-146
22705300-3 2012 In this work, we provided the first demonstration that ANP32B expression was down-regulated during differentiation induction of leukemic cells by all-trans retinoic acid (ATRA). Tretinoin 156-169 acidic nuclear phosphoprotein 32 family member B Homo sapiens 55-61
22705300-3 2012 In this work, we provided the first demonstration that ANP32B expression was down-regulated during differentiation induction of leukemic cells by all-trans retinoic acid (ATRA). Tretinoin 171-175 acidic nuclear phosphoprotein 32 family member B Homo sapiens 55-61
18443282-8 2008 Importantly, during striatal neurogenesis, endogenous levels of retinoic acid were spatiotemporally regulated such that transduction of high levels of retinoic acid through RARbeta selectively expanded the population of late-born striosomal progenitors, which evolved into a highly elaborate compartment in the rostral striatum. Tretinoin 64-77 retinoic acid receptor, beta Mus musculus 173-180
18443282-8 2008 Importantly, during striatal neurogenesis, endogenous levels of retinoic acid were spatiotemporally regulated such that transduction of high levels of retinoic acid through RARbeta selectively expanded the population of late-born striosomal progenitors, which evolved into a highly elaborate compartment in the rostral striatum. Tretinoin 151-164 retinoic acid receptor, beta Mus musculus 173-180
18512762-0 2008 Hoxa1 is required for the retinoic acid-induced differentiation of embryonic stem cells into neurons. Tretinoin 26-39 homeobox A1 Homo sapiens 0-5
22705300-4 2012 Knockdown of ANP32B expression by specific shRNA enhanced ATRA-induced leukemic cell differentiation, while ectopic expression of ANP32B attenuated it, indicating an inhibitory role of ANP32B against leukemic cell differentiation. Tretinoin 58-62 acidic nuclear phosphoprotein 32 family member B Homo sapiens 13-19
22180426-2 2012 We have recently shown that all-trans-retinoic acid is capable of inducing hCNT3 trafficking to plasma membrane in the MEC1 cell line. Tretinoin 28-51 solute carrier family 28 member 3 Homo sapiens 75-80
18590718-6 2008 Embryo culture experiments showed that Retinoic Acid (RA), Sonic hedgehog (Shh) and Fibroblast Growth Factor signals act in concert on this enhancer to control the spatial and temporal induction of Neurog2. Tretinoin 39-52 neurogenin 2 Mus musculus 198-205
18590718-6 2008 Embryo culture experiments showed that Retinoic Acid (RA), Sonic hedgehog (Shh) and Fibroblast Growth Factor signals act in concert on this enhancer to control the spatial and temporal induction of Neurog2. Tretinoin 54-56 neurogenin 2 Mus musculus 198-205
18590718-7 2008 We further demonstrated by transgenesis that two RA response elements and a Gli binding site within the Neurog2-798 element are absolutely required for its activity, strongly suggesting that the regulation of Neurog2 early expression by RA and Shh signals is direct. Tretinoin 49-51 neurogenin 2 Mus musculus 209-216
18343808-5 2008 RA and retinol also regulate expression of ADH1, cellular retinol binding protein 1 and cellular RA binding protein 2 in fibroid and myometrial cells. Tretinoin 0-2 retinol binding protein 1 Homo sapiens 49-83
18590718-7 2008 We further demonstrated by transgenesis that two RA response elements and a Gli binding site within the Neurog2-798 element are absolutely required for its activity, strongly suggesting that the regulation of Neurog2 early expression by RA and Shh signals is direct. Tretinoin 237-239 neurogenin 2 Mus musculus 104-111
22180426-3 2012 We, therefore, evaluated the effect of all-trans-retinoic acid on hCNT3 in primary chronic lymphocytic leukemia cells as a suitable mechanism to improve fludarabine-based therapy of chronic lymphocytic leukemia. Tretinoin 39-62 solute carrier family 28 member 3 Homo sapiens 66-71
18590718-7 2008 We further demonstrated by transgenesis that two RA response elements and a Gli binding site within the Neurog2-798 element are absolutely required for its activity, strongly suggesting that the regulation of Neurog2 early expression by RA and Shh signals is direct. Tretinoin 237-239 neurogenin 2 Mus musculus 209-216
22180426-7 2012 The effect of all-trans-retinoic acid on hCNT3 subcellular localization was analyzed by confocal microscopy and its effect on fludarabine-induced apoptosis was evaluated by flow cytometry analysis using annexin V staining. Tretinoin 14-37 solute carrier family 28 member 3 Homo sapiens 41-46
18280257-0 2008 All-trans-retinoic acid induces manganese superoxide dismutase in human neuroblastoma through NF-kappaB. Tretinoin 0-23 superoxide dismutase 2 Homo sapiens 32-62
22180426-10 2012 Treatment of the fludarabine-resistant subset of chronic lymphocytic leukemia cells with all-trans-retinoic acid induced increased fludarabine transport via hCNT3 which was associated with a significant increase in fludarabine sensitivity. Tretinoin 89-112 solute carrier family 28 member 3 Homo sapiens 157-162
22180426-11 2012 CONCLUSIONS: Improvement of ex vivo fludarabine sensitivity in chronic lymphocytic leukemia cells is associated with increased hCNT3 activity after all-trans-retinoic acid treatment. Tretinoin 158-171 solute carrier family 28 member 3 Homo sapiens 127-132
18495327-7 2008 RESULTS: Remarkably, overexpression of FLRF significantly attenuated erythroid and myeloid differentiation of EML cells in response to cytokines erythropoietin (EPO) and interleukin-3 (IL-3), and retinoic acid (RA), and resulted in significant and constitutive decrease of steady-state levels of IL-3, EPO, and RA receptor-alpha (RARalpha) in EML and BaF3 cells. Tretinoin 196-209 ring finger protein 41 Mus musculus 39-43
22493483-9 2012 Also, KLF15 binding to the promoter regions of nephrin and podocin was increased in RA-treated podocytes. Tretinoin 84-86 Kruppel-like factor 15 Mus musculus 6-11
18495327-7 2008 RESULTS: Remarkably, overexpression of FLRF significantly attenuated erythroid and myeloid differentiation of EML cells in response to cytokines erythropoietin (EPO) and interleukin-3 (IL-3), and retinoic acid (RA), and resulted in significant and constitutive decrease of steady-state levels of IL-3, EPO, and RA receptor-alpha (RARalpha) in EML and BaF3 cells. Tretinoin 211-213 ring finger protein 41 Mus musculus 39-43
18511453-4 2008 Here, we show that treatment of VSMCs with ATRA resulted in significant inhibition of proliferation and migration of VSMCs, as well as up-regulation of KLF4 and the VSMC differentiation marker genes SM22alpha and SM alpha-actin (alpha-SMA). Tretinoin 43-47 transgelin Homo sapiens 199-208
18511453-7 2008 Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22alpha and alpha-SMA expression and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration. Tretinoin 110-114 transgelin Homo sapiens 123-132
18412219-0 2008 Retinoic acid-induced inner ear teratogenesis caused by defective Fgf3/Fgf10-dependent Dlx5 signaling. Tretinoin 0-13 fibroblast growth factor 3 Mus musculus 66-70
18412219-0 2008 Retinoic acid-induced inner ear teratogenesis caused by defective Fgf3/Fgf10-dependent Dlx5 signaling. Tretinoin 0-13 distal-less homeobox 5 Mus musculus 87-91
22496486-7 2012 Interestingly, PKCdelta was involved in ATRA-induced increased NSMase2 transcription. Tretinoin 40-44 protein kinase C delta Homo sapiens 15-23
18412219-4 2008 METHODS: This study investigates the role of Dlx5 in the epithelial-mesenchymal interactions that guide otic capsule chondrogenesis, as well as the effect of excess in utero RA exposure on Dlx5 expression in the developing mouse inner ear. Tretinoin 174-176 distal-less homeobox 5 Mus musculus 189-193
18412219-7 2008 Downregulation in Dlx5 ensues as a consequence of in utero RA exposure in association with inner ear dysmorphogenesis. Tretinoin 59-61 distal-less homeobox 5 Mus musculus 18-22
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 93-95 fibroblast growth factor 3 Mus musculus 28-32
18642942-0 2008 Vav1 modulates protein expression during ATRA-induced maturation of APL-derived promyelocytes: a proteomic-based analysis. Tretinoin 41-45 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
18642942-2 2008 At variance, down-modulation of Vav1 prevents ATRA-induced maturation, and in particular, the inhibition of its tyrosine phosphorylation prevents the neutrophil differentiation-related changes of cell morphology. Tretinoin 46-50 vav guanine nucleotide exchange factor 1 Homo sapiens 32-36
18642942-4 2008 By means of a proteomic approach, here we have investigated a possible role for Vav1 in modulating protein expression during ATRA treatment of tumoral promyelocytes. Tretinoin 125-129 vav guanine nucleotide exchange factor 1 Homo sapiens 80-84
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 190-192 fibroblast growth factor 3 Mus musculus 127-131
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 190-192 distal-less homeobox 5 Mus musculus 171-175
22496486-8 2012 ATRA-induced PKCdelta phosphorylation and then activated PKCdelta phosphorylated Sp1. Tretinoin 0-4 protein kinase C delta Homo sapiens 13-21
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 190-192 fibroblast growth factor 3 Mus musculus 127-131
22496486-8 2012 ATRA-induced PKCdelta phosphorylation and then activated PKCdelta phosphorylated Sp1. Tretinoin 0-4 protein kinase C delta Homo sapiens 57-65
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 190-192 distal-less homeobox 5 Mus musculus 171-175
18602376-0 2008 The effects of retinoic acid on the expression of neurogranin after experimental cerebral ischemia. Tretinoin 15-28 neurogranin Rattus norvegicus 50-61
21492869-5 2012 Accordingly, we hypothesized that Fgfr2IIIb-/- mouse embryos would exhibit disruptions in expression of Raldh2, the gene for the enzyme that regulates the final step in the conversion of vitamin A to the active form RA, during duodenal atresia formation. Tretinoin 216-218 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 104-110
18602376-8 2008 The RA group showed an increase in NG protein or mRNA expression, compared with the vehicle group. Tretinoin 4-6 neurogranin Rattus norvegicus 35-37
17960384-0 2008 Combination of all-trans retinoic acid and interferon-gamma upregulated p27(kip1) and down regulated CDK2 to cause cell cycle arrest leading to differentiation and apoptosis in human glioblastoma LN18 (PTEN-proficient) and U87MG (PTEN-deficient) cells. Tretinoin 25-38 cyclin dependent kinase 2 Homo sapiens 101-105
18412219-10 2008 CONCLUSIONS: Disruption in an Fgf3, -10/Dlx5 signaling cascade is operant in molecular mechanisms of inner ear teratogenesis by excess RA. Tretinoin 135-137 fibroblast growth factor 3 Mus musculus 30-34
18412219-10 2008 CONCLUSIONS: Disruption in an Fgf3, -10/Dlx5 signaling cascade is operant in molecular mechanisms of inner ear teratogenesis by excess RA. Tretinoin 135-137 distal-less homeobox 5 Mus musculus 40-44
22182854-11 2012 This is the first evidence suggesting SFK inhibitors enhance ATRA-induced differentiation through a possible feedback loop involving KSR1-scaffolded c-Raf and ERK complexed with Lyn and CK2. Tretinoin 61-65 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 149-154
18024835-9 2008 The interferon-gamma, retinoic acid, and transforming growth factor-beta signaling pathways regulate MUC4 expression in a partially interdependent manner. Tretinoin 22-35 mucin 4, cell surface associated Homo sapiens 101-105
18636162-10 2008 G0S2 protein was rapidly induced in cultured NB4-S1 human APL cells and in APL transgenic mice treated with RA. Tretinoin 108-110 G0/G1 switch 2 Homo sapiens 0-4
22362749-3 2012 In the present study we demonstrate that the regulation of the hTGP gene depends mainly on retinoic acid (RA). Tretinoin 91-104 transglutaminase 4 Homo sapiens 63-67
17943189-5 2008 Using a selective agonist, we demonstrated that the effect of ATRA was predominantly mediated by retinoic acid receptor subtype gamma (RARgamma). Tretinoin 62-66 retinoic acid receptor gamma Homo sapiens 97-144
22362749-3 2012 In the present study we demonstrate that the regulation of the hTGP gene depends mainly on retinoic acid (RA). Tretinoin 106-108 transglutaminase 4 Homo sapiens 63-67
18502750-6 2008 Targeted small interfering RNA-mediated silencing of endogenous RDH10 or RoDH4 expression in human cells results in a significant decrease in retinoic acid production from retinol, identifying both human enzymes as physiologically relevant retinol dehydrogenases. Tretinoin 142-155 retinol dehydrogenase 16 Homo sapiens 73-78
22457346-3 2012 Cdx genes are known as integrators of posteriorizing signals from Wnt, retinoic acid, and FGF pathways. Tretinoin 71-84 caudal type homeobox 1 Mus musculus 0-3
18596964-4 2008 The ability of PP-DC to promote anti-CD40 dependent IgA was partially dependent on retinoic acid (RA) and transforming growth factor (TGF)-beta, whilst BAFF and APRIL signaling were not required. Tretinoin 83-96 CD40 antigen Mus musculus 37-41
18093970-7 2008 Moreover, in the case of excessive maternal dietary vitamin A intake, LRAT acts together with Cyp26A1, one of the enzymes that catalyze the degradation of retinoic acid, and possibly with STRA6, the recently identified cell surface receptor for retinol-RBP, in maintaining adequate levels of retinoids in embryonic and extraembryonic tissues. Tretinoin 155-168 lecithin retinol acyltransferase Homo sapiens 70-74
22405964-4 2012 Retinoic acid synthesis enzyme, RALDH2, and retinoic acid receptor gamma (RARgamma) are expressed in complementary and partially overlapping regions of the orofacial prominences that fate mapping revealed contribute to the upper lip and primary palate. Tretinoin 0-13 retinoic acid receptor gamma S homeolog Xenopus laevis 74-82
18287057-2 2008 The retinaldehyde dehydrogenase 2 (RALDH2) enzyme catalyzes the second oxidative step in RA biosynthesis and its loss of function creates a severe embryonic RA deficiency. Tretinoin 35-37 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 4-33
18489899-3 2008 All-trans-retinoic acid activates UCP1 within cells, whereas beta-carotene only does so after metabolism. Tretinoin 0-23 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 34-38
22405964-6 2012 To further understand how retinoic acid regulates upper lip and palate morphogenesis we searched for genes downregulated in response to RARgamma inhibition in orofacial tissue, and uncovered homeobox genes lhx8 and msx2. Tretinoin 26-39 retinoic acid receptor gamma S homeolog Xenopus laevis 136-144
22162152-2 2012 Tissue-specific RA signaling requires precise spatial and temporal synthesis of RA from retinal by retinaldehyde dehydrogenases (Raldh) and the conversion of retinol to retinal by retinol dehydrogenases (Rdh) of the short-chain dehydrogenase/reducatase gene family (SDR). Tretinoin 16-18 caveolae associated protein 2 Homo sapiens 266-269
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 132-151 LDL receptor related protein 2 Homo sapiens 54-61
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 132-151 DAB adaptor protein 2 Homo sapiens 76-80
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 153-155 LDL receptor related protein 2 Homo sapiens 54-61
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 153-155 DAB adaptor protein 2 Homo sapiens 76-80
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 201-203 LDL receptor related protein 2 Homo sapiens 54-61
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 201-203 DAB adaptor protein 2 Homo sapiens 76-80
18006504-6 2008 Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. Tretinoin 26-28 zinc fingers and homeoboxes 2 Homo sapiens 187-190
18230156-0 2008 Retinoic acid reduces human neuroblastoma cell migration and invasiveness: effects on DCX, LIS1, neurofilaments-68 and vimentin expression. Tretinoin 0-13 doublecortin Homo sapiens 86-89
18230156-3 2008 The mechanism of action of retinoic acid is still unclear, and the development of resistance to this differentiating agent is a great therapy problem.Doublecortin, a microtubule-associated protein involved in neuronal migration, has recently been proposed as a molecular marker for the detection of minimal residual disease in human neuroblastoma. Tretinoin 27-40 doublecortin Homo sapiens 150-162
18230156-9 2008 Treatment with retinoic acid reduces cell migration and invasiveness, down regulates doublecortin and lissencephaly-1 expression and up regulates neurofilament-68 expression. Tretinoin 15-28 doublecortin Homo sapiens 85-97
18230156-10 2008 However, some cells that escape from retinoic acid action maintain migration capability and invasiveness and express doublecortin. Tretinoin 37-50 doublecortin Homo sapiens 117-129
18443043-5 2008 CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. Tretinoin 160-162 lysine acetyltransferase 2B Homo sapiens 31-57
18443043-5 2008 CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. Tretinoin 160-162 lysine acetyltransferase 2B Homo sapiens 59-63
22916501-9 2012 Combination of ATRA and MNM induced MSCs into neural-like cells which expressed neuronal specific markers, Nestin, NSE, MAP-2, and Tau. Tretinoin 15-19 nestin Rattus norvegicus 107-113
18230156-11 2008 CONCLUSION: a) Doublecortin is expressed in human neuroblastoma cells that show high motility and invasiveness;b) Retinoic acid treatment reduces migration and invasiveness of the more aggressive cell components of SK-N-SH cells;c) The cells that after retinoic acid exposure show migration and invasive capability may be identified on the basis of doublecortin expression. Tretinoin 114-127 doublecortin Homo sapiens 15-27
22537161-4 2012 Smoking is strongly correlated with pancreatic cancer and in the present study; we elucidate the molecular mechanisms by which nicotine as well as agents like retinoic acid (RA) and interferon-gamma (IFN-gamma) induce the expression of MUC4 in pancreatic cancer cell lines CD18, CAPAN2, AsPC1 and BxPC3. Tretinoin 159-172 mucin 4, cell surface associated Homo sapiens 236-240
18230156-11 2008 CONCLUSION: a) Doublecortin is expressed in human neuroblastoma cells that show high motility and invasiveness;b) Retinoic acid treatment reduces migration and invasiveness of the more aggressive cell components of SK-N-SH cells;c) The cells that after retinoic acid exposure show migration and invasive capability may be identified on the basis of doublecortin expression. Tretinoin 114-127 doublecortin Homo sapiens 349-361
18230156-11 2008 CONCLUSION: a) Doublecortin is expressed in human neuroblastoma cells that show high motility and invasiveness;b) Retinoic acid treatment reduces migration and invasiveness of the more aggressive cell components of SK-N-SH cells;c) The cells that after retinoic acid exposure show migration and invasive capability may be identified on the basis of doublecortin expression. Tretinoin 253-266 doublecortin Homo sapiens 15-27
18342014-0 2008 Retinoic acid induces caspase-8 transcription via phospho-CREB and increases apoptotic responses to death stimuli in neuroblastoma cells. Tretinoin 0-13 caspase 8 Homo sapiens 22-31
18342014-3 2008 Here we show that four different retinoic acid (RA) derivatives also increase caspase-8 protein expression in neuroblastoma, medulloblastoma and small cell lung carcinoma cell lines. Tretinoin 33-46 caspase 8 Homo sapiens 78-87
18342014-3 2008 Here we show that four different retinoic acid (RA) derivatives also increase caspase-8 protein expression in neuroblastoma, medulloblastoma and small cell lung carcinoma cell lines. Tretinoin 48-50 caspase 8 Homo sapiens 78-87
22537161-4 2012 Smoking is strongly correlated with pancreatic cancer and in the present study; we elucidate the molecular mechanisms by which nicotine as well as agents like retinoic acid (RA) and interferon-gamma (IFN-gamma) induce the expression of MUC4 in pancreatic cancer cell lines CD18, CAPAN2, AsPC1 and BxPC3. Tretinoin 174-176 mucin 4, cell surface associated Homo sapiens 236-240
22529810-9 2012 AKR1B10 and AKR1C3, through their retinaldehyde reductase activity, trigger a decrease in the RA biosynthesis flow, resulting in RA deprivation and consequently lower differentiation, with an increased cancer risk in target tissues. Tretinoin 94-96 aldo-keto reductase family 1 member B10 Homo sapiens 0-7
18498088-5 2008 Here, we demonstrate that Raldh2(-/-) mouse embryos lacking retinoic acid signaling exhibit a posterior expansion of the cardiac Fgf8 expression domain as well as an expansion of Isl1 expression into mesoderm lying posterior to the cardiac field. Tretinoin 60-73 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 26-32
18354491-7 2008 Pretreatment of NB4 cells with indomethacin significantly impaired ATRA/As(2)O(3)-induced differentiation, as assessed by cell morphology, nitroblue tetrazolium test or CD11c expression. Tretinoin 67-71 integrin subunit alpha X Homo sapiens 169-174
18212744-1 2008 In neuroblastoma cells, retinoic acid induces cell cycle arrest and differentiation through degradation of the F-box protein, Skp2, and stabilization of cyclin-dependent kinase inhibitor, p27. Tretinoin 24-37 S-phase kinase associated protein 2 Homo sapiens 126-130
18212744-2 2008 However, the mechanism responsible for retinoic acid-mediated Skp2 destabilization is unknown. Tretinoin 39-52 S-phase kinase associated protein 2 Homo sapiens 62-66
18212744-4 2008 We found that retinoic acid induced the nuclear accumulation of Cdh1 that paralleled Skp2 destabilization and p27 accumulation. Tretinoin 14-27 S-phase kinase associated protein 2 Homo sapiens 85-89
17637747-0 2008 Retinoic acid induces TGFbeta-dependent autocrine fibroblast growth. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 22-29
17986385-3 2008 Western blot analysis showed that exposure to retinoic acid resulted in significantly increased levels of ADAM10 and TACE, suggesting that regulation of alpha-secretases causes the effects on APP processing. Tretinoin 46-59 ADAM metallopeptidase domain 10 Homo sapiens 106-112
22529810-9 2012 AKR1B10 and AKR1C3, through their retinaldehyde reductase activity, trigger a decrease in the RA biosynthesis flow, resulting in RA deprivation and consequently lower differentiation, with an increased cancer risk in target tissues. Tretinoin 94-96 aldo-keto reductase family 1 member C3 Homo sapiens 12-18
22374841-6 2012 Furthermore, disease-stabilizing therapy altered the serum-cytokine profile, but the correlations between HSP70/HSP90/IL-1ra/HGF were maintained only when ATRA + valproic acid were combined with theophyllin but not when combined with cytarabine. Tretinoin 155-159 hepatocyte growth factor Homo sapiens 125-128
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 40-63 matrix metallopeptidase 2 Homo sapiens 86-91
18439490-1 2008 OBJECTIVE: The retinoic acid receptors (RARs) alpha, beta2, and gamma regulate specific subsets of target genes during all-trans retinoic acid (RA) induced differentiation of F9 teratocarcinoma stem cells. Tretinoin 15-28 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 53-58
18439490-1 2008 OBJECTIVE: The retinoic acid receptors (RARs) alpha, beta2, and gamma regulate specific subsets of target genes during all-trans retinoic acid (RA) induced differentiation of F9 teratocarcinoma stem cells. Tretinoin 40-42 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 53-58
18439490-6 2008 Treatment with a RARgamma selective agonist plus a retinoid X receptor agonist (LGD1069) increased Tie1 mRNA levels by 11- +/- 2.5-fold 48 hours after RA addition in F9 WT, but not in F9 RARgamma-/- cells, by quantitative reverse transcription polymerase chain reaction. Tretinoin 17-19 retinoic acid receptor gamma Homo sapiens 187-195
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 40-63 matrix metallopeptidase 14 Homo sapiens 103-109
18058943-7 2008 Retinoic acid-treated P19 cells activated GTPases, Rac1, and Cdc42. Tretinoin 0-13 cell division cycle 42 Homo sapiens 61-66
22309941-9 2012 In conclusion, bFGF suppresses RA-induced entry of germ cells into meiosis to ensure embryonic ovarian germ cells to maintain at undifferentiated status and accelerate germ cell proliferation by binding with FGFR1 involving PKC activation in the chicken. Tretinoin 31-33 fibroblast growth factor 2 Gallus gallus 15-19
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 65-69 matrix metallopeptidase 2 Homo sapiens 86-91
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 65-69 matrix metallopeptidase 14 Homo sapiens 103-109
19068145-0 2008 All-trans retinoic acid suppresses interleukin-6 expression in interleukin-1-stimulated synovial fibroblasts by inhibition of ERK1/2 pathway independently of RAR activation. Tretinoin 10-23 mitogen activated protein kinase 3 Rattus norvegicus 126-132
19068145-6 2008 The effect of ATRA on upstream MAPK (p38 MAPK, c-Jun N-terminal kinase [JNK], and extracellularly regulated kinase 1/2 [ERK1/2]) was assessed by Western blot, and the contribution of the ERK1/2 pathway to the activation of pro-inflammatory transcription factors was studied by TransAm assays. Tretinoin 14-18 mitogen activated protein kinase 14 Rattus norvegicus 37-40
18308702-1 2008 Cytochrome P450 1B1 (CYP1B1) is a heme-containing monooxygenase that metabolizes various polycyclic aromatic hydrocarbons and aryl amines, as well as retinoic acid and steroid hormones. Tretinoin 150-163 cytochrome P450, family 1, subfamily B, polypeptide 1 Danio rerio 0-19
18308702-1 2008 Cytochrome P450 1B1 (CYP1B1) is a heme-containing monooxygenase that metabolizes various polycyclic aromatic hydrocarbons and aryl amines, as well as retinoic acid and steroid hormones. Tretinoin 150-163 cytochrome P450, family 1, subfamily B, polypeptide 1 Danio rerio 21-27
22019713-5 2012 In mouse embryonal carcinoma P19 cells endowed to differentiate into neuronal and astroglial lineages, a transient increase was seen in both mRNA and corresponding protein for TfR1 in association with neuronal marker expression during culture with all-trans retinoic acid (ATRA). Tretinoin 258-271 transferrin receptor Mus musculus 176-180
19099751-0 2008 [Retinoic acid diminished the expression of lung tissue matrix metalloproteinase-2 and matrix metalloproteinase-9 in hyperoxia-exposed premature rats through regulating mitogen-activated protein kinases]. Tretinoin 1-14 matrix metallopeptidase 2 Rattus norvegicus 56-113
19068145-10 2008 ATRA also reduced the phosphorylation of ERK1/2, but not of p38 MAPK or of JNK. Tretinoin 0-4 mitogen activated protein kinase 3 Rattus norvegicus 41-47
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 26-30 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 52-71
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 26-30 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 73-77
19099751-12 2008 The pups treated with RA in the hyperoxic environment expressed significantly lower mRNA levels of MMP-2 and MMP-9 than the hyperoxic control pups on each experimental day (P < 0.05 for all). Tretinoin 22-24 matrix metallopeptidase 2 Rattus norvegicus 99-104
22019713-5 2012 In mouse embryonal carcinoma P19 cells endowed to differentiate into neuronal and astroglial lineages, a transient increase was seen in both mRNA and corresponding protein for TfR1 in association with neuronal marker expression during culture with all-trans retinoic acid (ATRA). Tretinoin 273-277 transferrin receptor Mus musculus 176-180
19099751-13 2008 The levels of active MMP-2 and pro/active MMP-9 decreased to a different degree after RA treatment in hyperoxia exposure rat pups. Tretinoin 86-88 matrix metallopeptidase 2 Rattus norvegicus 21-26
19099751-14 2008 In addition, RA treatment led to a decrease of p-JNK1/2 and p-38 (P < 0.01 for all) protein levels and a further elevation of p-ERK1/2 compared with hyperoxia-exposed group. Tretinoin 13-15 mitogen activated protein kinase 3 Rattus norvegicus 131-137
19099751-16 2008 RA could have a protective effect on hyperoxia induced lung injury by decreasing active levels of JNK and p38, which subsequently reduce the expression and activation of MMP-2 and MMP-9. Tretinoin 0-2 mitogen activated protein kinase 14 Rattus norvegicus 106-109
19099751-16 2008 RA could have a protective effect on hyperoxia induced lung injury by decreasing active levels of JNK and p38, which subsequently reduce the expression and activation of MMP-2 and MMP-9. Tretinoin 0-2 matrix metallopeptidase 2 Rattus norvegicus 170-175
18280804-3 2008 We now demonstrate that treatment of acute promyelocytic leukemia (APL)-derived NB4 cells with ATRA results in dissociation of the translational repressor 4E-BP1 from the eukaryotic initiation factor eIF4E, and subsequent formation of eIF4G-eIF4E complexes. Tretinoin 95-99 eukaryotic translation initiation factor 4E Homo sapiens 200-205
18280804-3 2008 We now demonstrate that treatment of acute promyelocytic leukemia (APL)-derived NB4 cells with ATRA results in dissociation of the translational repressor 4E-BP1 from the eukaryotic initiation factor eIF4E, and subsequent formation of eIF4G-eIF4E complexes. Tretinoin 95-99 eukaryotic translation initiation factor 4E Homo sapiens 241-246
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 26-30 mitogen activated protein kinase kinase 1 Rattus norvegicus 135-139
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 26-30 mitogen activated protein kinase kinase 1 Rattus norvegicus 141-208
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 Sp7 transcription factor Homo sapiens 99-106
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 solute carrier family 2 member 4 Homo sapiens 307-312
18280257-4 2008 Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro. Tretinoin 105-128 superoxide dismutase 2 Homo sapiens 157-187
18280257-4 2008 Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro. Tretinoin 105-128 superoxide dismutase 2 Homo sapiens 189-194
22019713-6 2012 In neuronal Neuro2A cells cultured with ATRA, moreover, neurite was elongated together with increased expression of both mRNA and protein for TfR1. Tretinoin 40-44 transferrin receptor Mus musculus 142-146
18280257-4 2008 Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro. Tretinoin 130-134 superoxide dismutase 2 Homo sapiens 157-187
18280257-4 2008 Using the SK-N-SH human neuroblastoma cell line we investigated the effects of the differentiation agent all-trans-retinoic acid (ATRA) on the expression of manganese superoxide dismutase (MnSOD), an enzyme previously shown to enhance differentiation in vitro. Tretinoin 130-134 superoxide dismutase 2 Homo sapiens 189-194
22449228-12 2012 Our results suggest that CRBP-1 plays a role in ventricular remodeling after MI allegedly through its RA binding activity. Tretinoin 102-104 retinol binding protein 1 Homo sapiens 25-31
18280257-5 2008 Manganese superoxide dismutase mRNA, protein, and activity levels increased in a time-dependent manner upon treatment with ATRA. Tretinoin 123-127 superoxide dismutase 2 Homo sapiens 0-30
18280257-6 2008 Nuclear levels of the NF-kappaB proteins p50 and p65 increased within 24 h of ATRA administration. Tretinoin 78-82 RELA proto-oncogene, NF-kB subunit Homo sapiens 49-52
18280257-8 2008 Furthermore an increase in DNA binding to a NF-kappaB element occurred within a 342-bp enhancer (I2E) of the SOD2 gene with 10 microM ATRA treatment. Tretinoin 134-138 superoxide dismutase 2 Homo sapiens 109-113
18280257-10 2008 This study identifies SOD2 as a retinoid-responsive gene and demonstrates activation of the NF-kappaB pathway in response to ATRA treatment of SK-N-SH cells. Tretinoin 125-129 superoxide dismutase 2 Homo sapiens 22-26
17943186-5 2008 These effects were consistent with the findings that all-trans RA upregulated heparin-binding epidermal growth factor-like growth factor mRNA expression and increased the phosphorylation of EGFR and extracellular signal-regulated kinase 1/2 (ERK1/2). Tretinoin 63-65 mitogen activated protein kinase 3 Rattus norvegicus 199-240
17943186-5 2008 These effects were consistent with the findings that all-trans RA upregulated heparin-binding epidermal growth factor-like growth factor mRNA expression and increased the phosphorylation of EGFR and extracellular signal-regulated kinase 1/2 (ERK1/2). Tretinoin 63-65 mitogen activated protein kinase 3 Rattus norvegicus 242-248
18956319-8 2008 We also assessed the effects of retinoic acid (RA) on xCyp26c expression. Tretinoin 32-45 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 54-61
18956319-8 2008 We also assessed the effects of retinoic acid (RA) on xCyp26c expression. Tretinoin 47-49 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 54-61
18956319-9 2008 Embryos treated with 10(-7) M RA showed an anterior shift in the spatial expression of xCyp26c, reflecting a posteriorization effect. Tretinoin 30-32 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 87-94
17943186-6 2008 Interestingly, the activation of EGFR and ERK1/2 was seen already 30 minutes after all-trans RA treatment, suggesting that the activation of this signaling pathway is a primary response to all-trans RA. Tretinoin 93-95 mitogen activated protein kinase 3 Rattus norvegicus 42-48
22541086-8 2012 The expression of HOXA9 protein in ATRA group at day 1- day 3 was higher than that in control group (P < 0.05). Tretinoin 35-39 homeobox A9 Homo sapiens 18-23
18060600-10 2008 Interestingly, a p38 MAP kinase inhibitor that partially blocks RA-induced apoptosis did not inhibit the activity of RA + SAHA. Tretinoin 64-66 mitogen-activated protein kinase 14 Mus musculus 17-20
19088887-2 2008 Our results suggest that the cytostatic effects of RA could be mediated by the activation of endogenous CBR3 gene in oral squamous cell carcinomas (OSCCs), and the expression is a potential marker for oral malignancy. Tretinoin 51-53 carbonyl reductase 3 Homo sapiens 104-108
18413804-4 2008 RA treatment is known to repress PML/RARalpha and augment ubiquitin-activating enzyme-E1-like (UBE1L) protein expression in NB4-S1 APL cells. Tretinoin 0-2 ubiquitin like modifier activating enzyme 7 Homo sapiens 58-93
18413804-4 2008 RA treatment is known to repress PML/RARalpha and augment ubiquitin-activating enzyme-E1-like (UBE1L) protein expression in NB4-S1 APL cells. Tretinoin 0-2 ubiquitin like modifier activating enzyme 7 Homo sapiens 95-100
18413804-5 2008 We previously reported RA-induced UBE1L and the IFN-stimulated gene, 15-kDa protein ISG15ylation in APL cells. Tretinoin 23-25 ubiquitin like modifier activating enzyme 7 Homo sapiens 34-39
18413804-5 2008 We previously reported RA-induced UBE1L and the IFN-stimulated gene, 15-kDa protein ISG15ylation in APL cells. Tretinoin 23-25 ISG15 ubiquitin like modifier Homo sapiens 84-89
22541086-12 2012 The mechanisms of treatment of leukemia by ATRA and As2O3 may be associated with the regulation of the HOXA9 mRNA or protein expression. Tretinoin 43-47 homeobox A9 Homo sapiens 103-108
17925390-6 2007 Disease-associated mutants of RDH12, T49M and I51N, exhibit significant residual activity in vitro, but are unable to control retinoic acid levels in the cells because of their dramatically reduced affinity for NADPH and much lower protein expression levels. Tretinoin 126-139 retinol dehydrogenase 12 Mus musculus 30-35
22291023-2 2012 Here, we report that a novel member of the short chain dehydrogenase/reductase superfamily, frog sdr16c5, acts as a highly active retinol dehydrogenase (rdhe2) that promotes retinoic acid biosynthesis when expressed in mammalian cells. Tretinoin 174-187 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 130-151
17925390-7 2007 These results suggest that RDH12 acts as a regulator of retinoic acid biosynthesis and protects photoreceptors against overproduction of retinoic acid from all-trans-retinaldehyde, which diffuses into the inner segments of photoreceptors from illuminated rhodopsin. Tretinoin 56-69 retinol dehydrogenase 12 Mus musculus 27-32
17925390-7 2007 These results suggest that RDH12 acts as a regulator of retinoic acid biosynthesis and protects photoreceptors against overproduction of retinoic acid from all-trans-retinaldehyde, which diffuses into the inner segments of photoreceptors from illuminated rhodopsin. Tretinoin 137-150 retinol dehydrogenase 12 Mus musculus 27-32
22419909-10 2012 AKR1B10 catalyzes the reduction of retinal to retinol, and thus lessens the formation of retinoic acid, with potential pro-differentiating actions. Tretinoin 89-102 aldo-keto reductase family 1 member B10 Homo sapiens 0-7
18345250-2 2007 Both retinoids and rexinoids are either natural or synthetic compounds related to retinoic acids that act through interaction with two basic types of nuclear receptors belonging to the nuclear receptor superfamily: All-trans retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 82-96 retinoic acid receptor gamma Homo sapiens 273-281
18345250-2 2007 Both retinoids and rexinoids are either natural or synthetic compounds related to retinoic acids that act through interaction with two basic types of nuclear receptors belonging to the nuclear receptor superfamily: All-trans retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 82-96 retinoid X receptor beta Homo sapiens 319-326
18237746-1 2008 Rex1 (Zfp42), first identified as a gene that is transcriptionally repressed by retinoic acid (RA), encodes a zinc finger transcription factor expressed at high levels in F9 teratocarcinoma stem cells, embryonic stem cells, and other stem cells. Tretinoin 80-93 ZFP42 zinc finger protein Homo sapiens 0-4
18237746-1 2008 Rex1 (Zfp42), first identified as a gene that is transcriptionally repressed by retinoic acid (RA), encodes a zinc finger transcription factor expressed at high levels in F9 teratocarcinoma stem cells, embryonic stem cells, and other stem cells. Tretinoin 80-93 ZFP42 zinc finger protein Homo sapiens 6-11
18237746-1 2008 Rex1 (Zfp42), first identified as a gene that is transcriptionally repressed by retinoic acid (RA), encodes a zinc finger transcription factor expressed at high levels in F9 teratocarcinoma stem cells, embryonic stem cells, and other stem cells. Tretinoin 95-97 ZFP42 zinc finger protein Homo sapiens 0-4
18237746-1 2008 Rex1 (Zfp42), first identified as a gene that is transcriptionally repressed by retinoic acid (RA), encodes a zinc finger transcription factor expressed at high levels in F9 teratocarcinoma stem cells, embryonic stem cells, and other stem cells. Tretinoin 95-97 ZFP42 zinc finger protein Homo sapiens 6-11
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 growth arrest and DNA-damage-inducible 45 beta Mus musculus 137-147
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 epithelial membrane protein 1 Mus musculus 185-189
18052984-9 2007 Based on these results we propose that TIS7 inhibits CRABP II expression during axonal regeneration, thereby modulating retinoic acid signalling. Tretinoin 120-133 cellular retinoic acid binding protein II Mus musculus 53-61
22227495-1 2012 The DHRS4 gene encodes an NADP(H)-dependent retinol dehydrogenase/reductase (NRDR) and plays an important role in regulating the synthesis of retinoic acid. Tretinoin 142-155 dehydrogenase/reductase 4 Homo sapiens 4-9
17686814-6 2007 RESULTS: ATRA unexpectedly exacerbated renal injury in TSLP tg mice with increased glomerular extracellular matrix, mesangial cell activation, glomerular cell proliferation, glomerular macrophage influx and immune complex deposition. Tretinoin 9-13 thymic stromal lymphopoietin Mus musculus 55-59
18202528-4 2008 The oxidation of retinal to RA is catalyzed by the retinaldehyde dehydrogenases (RALDHs), including RALDH1, RALDH2 and RALDH3. Tretinoin 28-30 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 108-114
18202528-4 2008 The oxidation of retinal to RA is catalyzed by the retinaldehyde dehydrogenases (RALDHs), including RALDH1, RALDH2 and RALDH3. Tretinoin 28-30 aldehyde dehydrogenase 1 family, member A3 Rattus norvegicus 119-125
18286198-2 2008 Retinoic acid (RA)-treatment of neuroblastoma (NB) cells implicates activation of Ret and TrkB RTKs as critical step to induce cell differentiation. Tretinoin 0-13 neurotrophic receptor tyrosine kinase 2 Homo sapiens 90-94
22227495-1 2012 The DHRS4 gene encodes an NADP(H)-dependent retinol dehydrogenase/reductase (NRDR) and plays an important role in regulating the synthesis of retinoic acid. Tretinoin 142-155 dehydrogenase/reductase 4 Homo sapiens 26-75
18286198-2 2008 Retinoic acid (RA)-treatment of neuroblastoma (NB) cells implicates activation of Ret and TrkB RTKs as critical step to induce cell differentiation. Tretinoin 15-17 neurotrophic receptor tyrosine kinase 2 Homo sapiens 90-94
17956315-1 2007 A region of the rat FAS (fatty acid synthase) promoter has been defined as being responsible for RA (retinoic acid) responsiveness. Tretinoin 101-114 fatty acid synthase Rattus norvegicus 25-44
18156191-9 2008 The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Tretinoin 76-78 renin Rattus norvegicus 212-217
17956315-3 2007 Our results are consistent with SREBP-1c (sterol-regulatory-element-binding protein 1c) binding in this region, thus bringing about the RA responsiveness of the rat FAS proximal promoter. Tretinoin 136-138 sterol regulatory element binding transcription factor 1 Rattus norvegicus 32-40
17956315-3 2007 Our results are consistent with SREBP-1c (sterol-regulatory-element-binding protein 1c) binding in this region, thus bringing about the RA responsiveness of the rat FAS proximal promoter. Tretinoin 136-138 sterol regulatory element binding transcription factor 1 Rattus norvegicus 42-86
17956315-3 2007 Our results are consistent with SREBP-1c (sterol-regulatory-element-binding protein 1c) binding in this region, thus bringing about the RA responsiveness of the rat FAS proximal promoter. Tretinoin 136-138 fatty acid synthase Rattus norvegicus 165-168
18156191-11 2008 These results demonstrate that RA has a significant inhibitory effect on pressure overload-induced cardiac remodeling, through inhibition of the expression of renin-angiotensin system components. Tretinoin 31-33 renin Rattus norvegicus 159-164
17951529-0 2008 Retinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathway. Tretinoin 0-13 forkhead box P3 Homo sapiens 54-59
22227495-1 2012 The DHRS4 gene encodes an NADP(H)-dependent retinol dehydrogenase/reductase (NRDR) and plays an important role in regulating the synthesis of retinoic acid. Tretinoin 142-155 dehydrogenase/reductase 4 Homo sapiens 77-81
17951529-3 2008 Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Tretinoin 28-41 forkhead box P3 Homo sapiens 163-168
17951529-3 2008 Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Tretinoin 43-47 forkhead box P3 Homo sapiens 163-168
22200593-0 2012 Specification of GnRH-1 neurons by antagonistic FGF and retinoic acid signaling. Tretinoin 56-69 gonadotropin releasing hormone 1 Homo sapiens 17-23
17951529-4 2008 Conversely, inhibition of retinoic acid signaling constrains transforming growth factor beta (TGF-beta1) induction of FoxP3. Tretinoin 26-39 forkhead box P3 Homo sapiens 118-123
17951529-5 2008 The effect of ATRA is mediated independently of IL-2, signal transducer and activator of transcription 5 (Stat5) and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. Tretinoin 14-18 forkhead box P3 Homo sapiens 176-181
18049370-7 2007 Maternal retinoic acid treatment significantly increased PDGF-A and -B mRNA expression in control and oligohydramnios-exposed rats compared with all rats and oligohydramnios-exposed rats of maternal vehicle-treated dams, respectively. Tretinoin 9-22 platelet derived growth factor subunit A Rattus norvegicus 57-70
22157753-9 2012 Overexpression of p38beta or Rac1 significantly enhanced (1.9- and 3.9-fold, respectively), the tRA-stimulated NIS expression in MCF-7 cells. Tretinoin 96-99 mitogen-activated protein kinase 11 Homo sapiens 18-25
17680017-0 2007 Safety and efficacy of combining ATRA with G-CSF in HSPC mobilization; a pilot study in multiple myeloma and non-Hodgkin"s lymphoma patients. Tretinoin 33-37 proteasome 20S subunit alpha 7 Homo sapiens 52-56
18199582-5 2008 Subsequently, RA suppresses expression of the nuclear receptors Ad4BP/SF-1 and estrogen receptor alpha in the right ovarian primordium. Tretinoin 14-16 estrogen receptor 1 Gallus gallus 79-102
18941534-4 2008 Here, we investigated the effects of vitamin A deficiency (VAD) on neurogenesis and memory and the ability of retinoic acid (RA) treatment to prevent VAD-induced impairments. Tretinoin 110-123 potassium channel tetramerization domain containing 1 Rattus norvegicus 150-153
22116818-9 2012 Next, FACS-sorted VEGFR2+ cells expressed highest and lowest levels of SMC- and fibroblast-specific markers, respectively, at days 7-14 after retinoic acid (RA) as compared with VEGFR2+/PDGFRalpha+ cells. Tretinoin 142-155 acyl-CoA synthetase long-chain family member 1 Mus musculus 6-10
18941534-4 2008 Here, we investigated the effects of vitamin A deficiency (VAD) on neurogenesis and memory and the ability of retinoic acid (RA) treatment to prevent VAD-induced impairments. Tretinoin 125-127 potassium channel tetramerization domain containing 1 Rattus norvegicus 150-153
17728141-3 2007 Following ASK1 over-expression and ATRA treatment in AHPs, a larger number of cells differentiated into neurons and the MASH1 promoter became activated. Tretinoin 35-39 achaete-scute family bHLH transcription factor 1 Homo sapiens 120-125
22116818-9 2012 Next, FACS-sorted VEGFR2+ cells expressed highest and lowest levels of SMC- and fibroblast-specific markers, respectively, at days 7-14 after retinoic acid (RA) as compared with VEGFR2+/PDGFRalpha+ cells. Tretinoin 142-155 kinase insert domain protein receptor Mus musculus 18-24
17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MAX dimerization protein 1 Homo sapiens 69-73
17916804-4 2008 We show herein that microRNA (miR)-134 levels are maximally elevated at day 4 after retinoic acid-induced differentiation or day 2 after N2B27-induced differentiation of mouse embryonic stem cells (mESCs), but this change is not observed during embryoid body differentiation. Tretinoin 84-97 microRNA 134 Mus musculus 20-38
22116818-9 2012 Next, FACS-sorted VEGFR2+ cells expressed highest and lowest levels of SMC- and fibroblast-specific markers, respectively, at days 7-14 after retinoic acid (RA) as compared with VEGFR2+/PDGFRalpha+ cells. Tretinoin 157-159 acyl-CoA synthetase long-chain family member 1 Mus musculus 6-10
22116818-9 2012 Next, FACS-sorted VEGFR2+ cells expressed highest and lowest levels of SMC- and fibroblast-specific markers, respectively, at days 7-14 after retinoic acid (RA) as compared with VEGFR2+/PDGFRalpha+ cells. Tretinoin 157-159 kinase insert domain protein receptor Mus musculus 18-24
22116818-11 2012 Notably, RA was required to more fully differentiate SMC from VEGFR2+ cells and completely blocked differentiation of cardiomyocytes from VEGFR2+/PDGFRalpha+ cells. Tretinoin 9-11 kinase insert domain protein receptor Mus musculus 62-68
18055984-6 2007 In addition, CD54 and CD18 knock-out mice were injected with NB4 cells and concomitantly treated with ATRA. Tretinoin 102-106 intercellular adhesion molecule 1 Mus musculus 13-17
22116818-11 2012 Notably, RA was required to more fully differentiate SMC from VEGFR2+ cells and completely blocked differentiation of cardiomyocytes from VEGFR2+/PDGFRalpha+ cells. Tretinoin 9-11 kinase insert domain protein receptor Mus musculus 138-144
22209845-5 2012 For stage II induction, the addition of retinoic acid (R) in the continuous presence of A4L during days 6-8 was most effective to induce nephrogenic intermediate mesodermal markers, such as Pax2 and Lim1. Tretinoin 40-53 LIM homeobox protein 1 Mus musculus 199-203
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 64-77 PRAME like, X-linked 1 Mus musculus 241-285
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 64-77 PRAME like, X-linked 1 Mus musculus 287-292
17873879-4 2007 These macrophages induced, by a mechanism dependent on IL-10, retinoic acid and exogenous transforming growth factor-beta, the differentiation of Foxp3+ regulatory T cells. Tretinoin 62-75 forkhead box P3 Homo sapiens 146-151
17953490-7 2007 Loss of cdx function caused abrogation of distal segments, a posterior shift in the position of the pronephros, and alterations in the expression boundaries of raldh2 and cyp26a1, which encode enzymes that synthesize and degrade RA, respectively. Tretinoin 229-231 aldehyde dehydrogenase 1 family, member A2 Danio rerio 160-166
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 79-81 PRAME like, X-linked 1 Mus musculus 241-285
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 79-81 PRAME like, X-linked 1 Mus musculus 287-292
21855651-5 2012 An exciting, recent publication in regeneration research shows that ALDH1a2 (RALDH2), which is the rate-limiting enzyme in the production of RA from retinaldehyde, is highly induced shortly after amputation in the regenerating heart, adult fin, and larval fin in zebrafish. Tretinoin 77-79 aldehyde dehydrogenase 1 family, member A2 Danio rerio 68-75
17726077-2 2007 Moreover, protein C inhibitor (PCI), which specifically binds retinoic acid, was found to be increased in myocardial infarction survivors who are also insulin resistant. Tretinoin 62-75 serpin family A member 5 Homo sapiens 10-29
17953490-7 2007 Loss of cdx function caused abrogation of distal segments, a posterior shift in the position of the pronephros, and alterations in the expression boundaries of raldh2 and cyp26a1, which encode enzymes that synthesize and degrade RA, respectively. Tretinoin 229-231 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 171-178
17628022-4 2007 This contrasts with our recent findings about the P/D transition in normal primitive hematopoietic cells, where MAT1 degradation proceeds intrinsically together with granulocytic development, in accord with dynamic expression of aldehyde dehydrogenases (ALDHs) 1A1 and 1B1, which catalyze RA synthesis. Tretinoin 289-291 MNAT1 component of CDK activating kinase Homo sapiens 112-116
18031199-2 2007 Experimental evidence has suggested that RA, which is produced in paraxial mesoderm posterior to the hindbrain by aldehyde dehydrogenase 1a2 (aldh1a2/raldh2), forms a posterior-to-anterior gradient across the hindbrain field, and provides the positional information that specifies the locations and fates of rhombomeres. Tretinoin 41-43 aldehyde dehydrogenase 1 family, member A2 Danio rerio 142-149
18031199-2 2007 Experimental evidence has suggested that RA, which is produced in paraxial mesoderm posterior to the hindbrain by aldehyde dehydrogenase 1a2 (aldh1a2/raldh2), forms a posterior-to-anterior gradient across the hindbrain field, and provides the positional information that specifies the locations and fates of rhombomeres. Tretinoin 41-43 aldehyde dehydrogenase 1 family, member A2 Danio rerio 150-156
22973984-2 2012 P19 mouse embryonal carcinoma cells can differentiate into neurons when cultured in aggregates and induced with RA (retinoic acid). Tretinoin 112-114 interleukin 23, alpha subunit p19 Mus musculus 0-3
18031199-6 2007 We also show that expression of Cyp26a1, the major RA-degrading enzyme during gastrulation, is under complex feedback and feedforward control by RA and Fgf signaling. Tretinoin 51-53 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 32-39
17880687-0 2007 Selective repression of retinoic acid target genes by RIP140 during induced tumor cell differentiation of pluripotent human embryonal carcinoma cells. Tretinoin 24-37 nuclear receptor interacting protein 1 Homo sapiens 54-60
17880687-4 2007 RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). Tretinoin 84-97 nuclear receptor interacting protein 1 Homo sapiens 0-6
17880687-4 2007 RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). Tretinoin 84-97 nuclear receptor interacting protein 1 Homo sapiens 20-25
17666047-7 2007 Based on our results, it appears likely that RA-induces reelin expression through a critical Sp1 site that resides adjacent to the Pax6 site within this multisite enhancer region. Tretinoin 45-47 paired box 6 Homo sapiens 131-135
17880687-4 2007 RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). Tretinoin 99-101 nuclear receptor interacting protein 1 Homo sapiens 0-6
22973984-2 2012 P19 mouse embryonal carcinoma cells can differentiate into neurons when cultured in aggregates and induced with RA (retinoic acid). Tretinoin 116-129 interleukin 23, alpha subunit p19 Mus musculus 0-3
17880687-4 2007 RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). Tretinoin 99-101 nuclear receptor interacting protein 1 Homo sapiens 20-25
17646388-3 2007 In the present study, we further demonstrated that this nonclassical signaling of RA on the activation of CREB plays a critical role in regulating the expression of airway epithelial cell differentiation markers, the MUC2, MUC5AC, and MUC5B genes. Tretinoin 82-84 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 235-240
17646388-4 2007 We found that RA rapidly activates the protein kinase Calpha isozyme and transmits the activation signal to CREB via the Raf/MEK/extracellular signal-regulated kinase/p90 ribosomal S6 kinase (RSK) pathway. Tretinoin 14-16 zinc fingers and homeoboxes 2 Homo sapiens 121-124
22973984-5 2012 P27KIP1 was up-regulated during the differentiation process of both P19/ADAM23KD cells without RA induction, and P19 cells with RA induction. Tretinoin 128-130 interleukin 23, alpha subunit p19 Mus musculus 113-116
17646388-8 2007 Taken together, our findings demonstrate that CREB activation via this nonclassical RA signaling pathway may play an important role in regulating the expression of mucin genes and mediating the early biological effects of RA during normal mucous differentiation in NHTBE cells. Tretinoin 84-86 LOC100508689 Homo sapiens 164-169
17880687-5 2007 We had previously shown that RIP140 limits RA induced tumor cell differentiation of embryonal carcinoma; the pluriopotent stem cells of testicular germ cell tumors. Tretinoin 43-45 nuclear receptor interacting protein 1 Homo sapiens 29-35
22973984-7 2012 The findings indicate that ADAM23 suppresses neuronal differentiation through its disintegrin domain, and Adam23 KD up-regulates P27KIP1 in P19/ADAM23KD cells, one reason that P19/ADAM23KD cells can differentiate into neurons without RA induction. Tretinoin 234-236 interleukin 23, alpha subunit p19 Mus musculus 140-143
17880687-13 2007 We also demonstrated that RIP140 silencing sensitizes embryonal carcinoma cells to low doses of RA. Tretinoin 96-98 nuclear receptor interacting protein 1 Homo sapiens 26-32
22973984-7 2012 The findings indicate that ADAM23 suppresses neuronal differentiation through its disintegrin domain, and Adam23 KD up-regulates P27KIP1 in P19/ADAM23KD cells, one reason that P19/ADAM23KD cells can differentiate into neurons without RA induction. Tretinoin 234-236 interleukin 23, alpha subunit p19 Mus musculus 176-179
17785809-4 2007 Retinoic acid can promote TGF-beta1-dependent generation of FoxP3+ regulatory T cells but decrease the TGF-beta1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 26-35
17785809-4 2007 Retinoic acid can promote TGF-beta1-dependent generation of FoxP3+ regulatory T cells but decrease the TGF-beta1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 103-112
22029601-7 2012 The effects of RA on the expression of MUC1, -4, and -16 were analyzed by immunohistochemistry, quantitative real-time PCR and Western blot analysis. Tretinoin 15-17 mucin 1, cell surface associated Homo sapiens 39-43
17611083-4 2007 RA treatment for 24 h transiently increased invasion and expression of MMP9 in SH-SY5Y, LA-N-5 and MMP2 in SMS-KCNR cells. Tretinoin 0-2 matrix metallopeptidase 2 Homo sapiens 99-103
17786207-7 2007 METHODOLOGY/PRINCIPAL FINDINGS: We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. Tretinoin 82-84 sphingomyelin phosphodiesterase 2 Homo sapiens 250-274
17786207-7 2007 METHODOLOGY/PRINCIPAL FINDINGS: We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. Tretinoin 82-84 sphingomyelin phosphodiesterase 2 Homo sapiens 276-282
18082674-0 2007 Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4. Tretinoin 0-13 CD40 antigen Mus musculus 96-100
22029601-12 2012 In addition, MUC1, -4, and -16 expressions were highly associated with RA concentrations. Tretinoin 71-73 mucin 1, cell surface associated Homo sapiens 13-17
22029601-14 2012 Also, our results suggested modulating effect of RA on differentiation and mucin expression in corneal epithelium. Tretinoin 49-51 LOC100508689 Homo sapiens 75-80
18082674-4 2007 Overall, RA can promote B-cell maturation at the population level by increasing the number of sIgG1 and CD138 expressing cells, which may be related to the potentiation of humoral immunity in vivo. Tretinoin 9-11 syndecan 1 Mus musculus 104-109
17908044-6 2007 Retinoic acid (RA) was identified as an inducer of human ADAM10 promoter activity. Tretinoin 0-13 ADAM metallopeptidase domain 10 Homo sapiens 57-63
22099177-3 2012 Data revealed an elevation in expression level of PPARgamma when neural precursors (NPs) are formed upon retinoic acid treatment. Tretinoin 105-118 peroxisome proliferator activated receptor gamma Mus musculus 50-59
17908044-6 2007 Retinoic acid (RA) was identified as an inducer of human ADAM10 promoter activity. Tretinoin 15-17 ADAM metallopeptidase domain 10 Homo sapiens 57-63
17908044-7 2007 In human neuroblastoma cell lines RA treatment upregulated the expression of both the alpha-secretase ADAM10 and its substrates APP and the related APP-like-protein 2 (APLP2), and led to an enhanced secretion of their extracellular domains. Tretinoin 34-36 ADAM metallopeptidase domain 10 Homo sapiens 102-108
17453147-12 2007 In conclusion, we have provided evidence for the first time that RA may induce cell cycle arrest in vitro in DAOY MB cells via inhibition of CyclinD1 or C-myc. Tretinoin 65-67 cyclin D1 Homo sapiens 141-149
17908044-7 2007 In human neuroblastoma cell lines RA treatment upregulated the expression of both the alpha-secretase ADAM10 and its substrates APP and the related APP-like-protein 2 (APLP2), and led to an enhanced secretion of their extracellular domains. Tretinoin 34-36 amyloid beta precursor like protein 2 Homo sapiens 148-166
22099177-7 2012 Here, we have demonstrated the stage dependent role of PPARgamma modulation on neural differentiation of mESCs by retinoic acid treatment for the first time. Tretinoin 114-127 peroxisome proliferator activated receptor gamma Mus musculus 55-64
17908044-7 2007 In human neuroblastoma cell lines RA treatment upregulated the expression of both the alpha-secretase ADAM10 and its substrates APP and the related APP-like-protein 2 (APLP2), and led to an enhanced secretion of their extracellular domains. Tretinoin 34-36 amyloid beta precursor like protein 2 Homo sapiens 168-173
17690467-5 2007 Furthermore, five mammalian GP-PDEs were virtually identified, and very recent studies indicate that retinoic acid-induced expression of GDE2 plays essential roles in neuronal differentiation and neurite outgrowth. Tretinoin 101-114 glycerophosphodiester phosphodiesterase domain containing 5 Homo sapiens 137-141
22129829-0 2012 The Osr1 and Osr2 genes act in the pronephric anlage downstream of retinoic acid signaling and upstream of Wnt2b to maintain pectoral fin development. Tretinoin 67-80 odd-skipped related transciption factor 2 Danio rerio 13-17
17622165-0 2007 A differential phosphoproteomic analysis of retinoic acid-treated P19 cells. Tretinoin 44-57 interleukin 23, alpha subunit p19 Mus musculus 66-69
17923756-6 2007 In particular, sequential treatment with 1 microM ATRA or 13-cis RA and 4-HPR markedly inhibited H1703 cell growth; these cells exhibited no basal RAR beta expression and were refractory to 4-HPR. Tretinoin 50-54 haptoglobin-related protein Homo sapiens 192-195
23118506-4 2012 S100A10 is constitutively expressed in many cells and is also induced by many diverse factors and physiological stimuli including dexamethasone, epidermal growth factor, transforming growth factor-alpha, interferon-gamma, nerve growth factor, keratinocyte growth factor, retinoic acid, and thrombin. Tretinoin 271-284 S100 calcium binding protein A10 (calpactin) Mus musculus 0-7
18095569-0 2007 [Translocation of p38 MAPK induced by retinoic acid in H9c2 cells]. Tretinoin 38-51 mitogen activated protein kinase 14 Rattus norvegicus 18-21
17699721-1 2007 We have recently reported that PML-RAR-induced misfolding of the N-CoR protein could be reversed by retinoic acid (RA), a therapeutic agent that promotes differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 100-113 PML-RARA regulated adaptor molecule 1 Homo sapiens 31-38
23259068-0 2012 PKCdelta Regulates Translation Initiation through PKR and eIF2alpha in Response to Retinoic Acid in Acute Myeloid Leukemia Cells. Tretinoin 83-96 protein kinase C delta Homo sapiens 0-8
17592014-5 2007 Ahd2 is involved in the synthesis of retinoic acid (RA), which has a crucial role in neuronal patterning, differentiation and survival in the brain. Tretinoin 37-50 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-4
18095569-1 2007 OBJECTIVE: To study the distribution of p38 MAPK and translocation of p38 induced by all-trans retinoic acid (atRA) in cardiomyocytes. Tretinoin 85-108 mitogen activated protein kinase 14 Rattus norvegicus 40-43
18095569-1 2007 OBJECTIVE: To study the distribution of p38 MAPK and translocation of p38 induced by all-trans retinoic acid (atRA) in cardiomyocytes. Tretinoin 85-108 mitogen activated protein kinase 14 Rattus norvegicus 70-73
18095569-1 2007 OBJECTIVE: To study the distribution of p38 MAPK and translocation of p38 induced by all-trans retinoic acid (atRA) in cardiomyocytes. Tretinoin 110-114 mitogen activated protein kinase 14 Rattus norvegicus 40-43
18095569-1 2007 OBJECTIVE: To study the distribution of p38 MAPK and translocation of p38 induced by all-trans retinoic acid (atRA) in cardiomyocytes. Tretinoin 110-114 mitogen activated protein kinase 14 Rattus norvegicus 70-73
17592014-5 2007 Ahd2 is involved in the synthesis of retinoic acid (RA), which has a crucial role in neuronal patterning, differentiation and survival in the brain. Tretinoin 52-54 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-4
18095569-6 2007 Thus, the statistical analysis of these data showed the effects of atRA or SB202 190 on p38 translocation. Tretinoin 67-71 mitogen activated protein kinase 14 Rattus norvegicus 88-91
18095569-7 2007 RESULTS: p38 was located more in the cytoplasm without stimulation, while in the cells with atRA treatment for 5 min and 30 min, p38 labeled with green fluorescence in the cytoplasm decreased. Tretinoin 92-96 mitogen activated protein kinase 14 Rattus norvegicus 9-12
23259068-3 2012 ATRA and ATO induce Ser-51 phosphorylation (inactivation) of eIF2alpha, through the induction of protein kinase C delta (PKCdelta) and PKR, but not other eIF2alpha kinases, such as GCN2 and PERK in APL (NB4) and AML cells (HL60, U937, and THP-1). Tretinoin 0-4 protein kinase C delta Homo sapiens 121-129
22218901-2 2012 Overexpression of Prickle1 or Prickle2 in C1300 cells induced striking neurite-like process formation without RA. Tretinoin 110-112 prickle planar cell polarity protein 1 Mus musculus 18-26
18095569-7 2007 RESULTS: p38 was located more in the cytoplasm without stimulation, while in the cells with atRA treatment for 5 min and 30 min, p38 labeled with green fluorescence in the cytoplasm decreased. Tretinoin 92-96 mitogen activated protein kinase 14 Rattus norvegicus 129-132
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 81-102
18095569-9 2007 As the specific inhibitor of p38, SB202190 could obviously inhibited the nuclear translocation of p38 induced by atRA (P < 0.01). Tretinoin 113-117 mitogen activated protein kinase 14 Rattus norvegicus 29-32
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 119-144
22876133-7 2012 RESULTS: The promoter LEP503-mediated HSV-tk was specifically expressed in HLECs, and ATRA dose-dependently strengthened the bystander effect following LEP503-mediated HSV-tk/GCV gene therapy against lens cells by upregulating the expression of the gap junction protein Cx43. Tretinoin 86-90 gap junction protein alpha 1 Homo sapiens 270-274
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 146-153
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 cellular retinoic acid binding protein II Mus musculus 193-199
17718197-4 2007 Furthermore, using semi-quantitative and real-time quantitative RT-PCR as well as western blot methods, high expression of insulin-like growth factor binding protein-2 (IGFBP-2) in A549 cells treated with CSE was found at both transcriptional and protein levels, and concomitant with the restoration of cell growth after treatment with tretinoin or NAC, down regulation of IGFBP-2 was observed. Tretinoin 336-345 insulin like growth factor binding protein 2 Homo sapiens 169-176
18095569-9 2007 As the specific inhibitor of p38, SB202190 could obviously inhibited the nuclear translocation of p38 induced by atRA (P < 0.01). Tretinoin 113-117 mitogen activated protein kinase 14 Rattus norvegicus 98-101
18095569-11 2007 CONCLUSION: atRA could induce the nuclear translocation of p38 in cardiomyocytes. Tretinoin 12-16 mitogen activated protein kinase 14 Rattus norvegicus 59-62
21952554-15 2012 PGP 9.5 protein levels were decreased in nitrofen-exposed lungs, but they normalized when RA was added. Tretinoin 90-92 ubiquitin C-terminal hydrolase L1 Rattus norvegicus 0-7
17620361-0 2007 A functionally specialized population of mucosal CD103+ DCs induces Foxp3+ regulatory T cells via a TGF-beta and retinoic acid-dependent mechanism. Tretinoin 113-126 forkhead box P3 Homo sapiens 68-73
17620362-0 2007 Small intestine lamina propria dendritic cells promote de novo generation of Foxp3 T reg cells via retinoic acid. Tretinoin 99-112 forkhead box P3 Homo sapiens 77-82
17568621-0 2007 Activation of p38/MEF2C pathway by all-trans retinoic acid in cardiac myoblasts. Tretinoin 45-58 mitogen activated protein kinase 14 Rattus norvegicus 14-17
17568621-4 2007 Here, our results, obtained from Western blot and protein kinase assays, showed that the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and MEF2C was induced by atRA in H9c2 myocardial cells. Tretinoin 177-181 mitogen activated protein kinase 14 Rattus norvegicus 108-144
23285066-8 2012 Overexpression of transcription factor Nanog was possibly achieved through a RA-induced non-genomic c-Src/Stat3/Nanog signaling pathway mediated by the subcellular c-Src mRNA localization for the maintenance of pluripotency in tNSCs. Tretinoin 77-79 Nanog homeobox Rattus norvegicus 39-44
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 patched 1 Rattus norvegicus 335-339
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 GLI family zinc finger 1 Rattus norvegicus 358-362
17620363-1 2007 We demonstrate that all-trans retinoic acid (RA) induces FoxP3(+) adaptive T regulatory cells (A-Tregs) to acquire a gut-homing phenotype (alpha 4 beta 7(+) CC chemokine receptor 9(+)) and the capacity to home to the lamina propria of the small intestine. Tretinoin 30-43 forkhead box P3 Homo sapiens 57-62
17620363-1 2007 We demonstrate that all-trans retinoic acid (RA) induces FoxP3(+) adaptive T regulatory cells (A-Tregs) to acquire a gut-homing phenotype (alpha 4 beta 7(+) CC chemokine receptor 9(+)) and the capacity to home to the lamina propria of the small intestine. Tretinoin 45-47 forkhead box P3 Homo sapiens 57-62
17620363-4 2007 In the presence of RA, A-Treg generation occurs even in the presence of high levels of co-stimulation, with RA attenuating co-stimulation from interfering from FoxP3 induction. Tretinoin 108-110 forkhead box P3 Homo sapiens 160-165
23285066-8 2012 Overexpression of transcription factor Nanog was possibly achieved through a RA-induced non-genomic c-Src/Stat3/Nanog signaling pathway mediated by the subcellular c-Src mRNA localization for the maintenance of pluripotency in tNSCs. Tretinoin 77-79 Nanog homeobox Rattus norvegicus 112-117
23077538-9 2012 A similar correlation between the increase of miR-223/Ago2 association and the resistance of miR-223 against RNaseA was observed during all trans retinoic acid (ATRA)-induced cell differentiation of promyelocytic HL60 cells. Tretinoin 146-159 microRNA 223 Homo sapiens 46-53
17335046-5 2007 RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Tretinoin 53-55 distal-less homeobox 3 Mus musculus 205-209
17335046-5 2007 RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Tretinoin 53-55 transformation related protein 63 Mus musculus 238-241
17332158-4 2007 Here, we show differential regulation of MMPs in cultured chondrocytes from chickens and turkeys; retinoic acid (RA) elevated MMP-2 activity in both species, but only in chicken did it induce MMP-9 activity. Tretinoin 98-111 matrix metallopeptidase 2 Gallus gallus 41-45
23077538-9 2012 A similar correlation between the increase of miR-223/Ago2 association and the resistance of miR-223 against RNaseA was observed during all trans retinoic acid (ATRA)-induced cell differentiation of promyelocytic HL60 cells. Tretinoin 146-159 microRNA 223 Homo sapiens 93-100
17318222-3 2007 In the present study, we conditionally suppressed L3/Lhx8 function during retinoic acid-induced neural differentiation of a murine embryonic stem (ES) cell line using an L3/Lhx8-targeted small interfering RNA (siRNA) produced by an H1.2 promoter-driven vector. Tretinoin 74-87 LIM homeobox protein 8 Mus musculus 53-57
23077538-9 2012 A similar correlation between the increase of miR-223/Ago2 association and the resistance of miR-223 against RNaseA was observed during all trans retinoic acid (ATRA)-induced cell differentiation of promyelocytic HL60 cells. Tretinoin 161-165 microRNA 223 Homo sapiens 46-53
23077538-9 2012 A similar correlation between the increase of miR-223/Ago2 association and the resistance of miR-223 against RNaseA was observed during all trans retinoic acid (ATRA)-induced cell differentiation of promyelocytic HL60 cells. Tretinoin 161-165 microRNA 223 Homo sapiens 93-100
22745828-5 2012 We also observed that SCD5 expression markedly accelerated the rate of cell proliferation and suppressed the induction of neurite outgrowth, a typical marker of neuronal differentiation, by retinoic acid indicating that the desaturase plays a key role in the mechanisms of cell division and differentiation. Tretinoin 190-203 stearoyl-CoA desaturase 5 Homo sapiens 22-26
17537796-4 2007 Wnt and RA are believed to impact on Cdx1 through an atypical RA-response element (RARE) and Lef/Tcf-response elements (LRE), respectively, in the proximal promoter. Tretinoin 8-10 caudal type homeobox 1 Mus musculus 37-41
17537796-7 2007 Mutation of the LRE also greatly reduced induction of Cdx1 by RA, demonstrating a requirement for Wnt signaling in the regulation of this gene by retinoids. Tretinoin 62-64 caudal type homeobox 1 Mus musculus 54-58
22319578-14 2012 These data demonstrate that RDH10 plays a critical role in mediating the rate limiting RDH step of Vitamin A metabolism and functions as a nodal point in feedback regulation of RA synthesis. Tretinoin 177-179 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 28-31
22079120-2 2012 Small intestine (SI) CD103(+) DCs have an enhanced capacity to generate the vitamin A metabolite, retinoic acid, a property that underlies their ability to induce the gut homing receptors CC chemokine receptor 9 and alpha4beta7 on responding T and B cells, and enhance forkhead box P3(+) T regulatory and IgA plasma cell differentiation in vitro. Tretinoin 98-111 forkhead box P3 Homo sapiens 269-284
22147914-0 2011 Cullin 3 mediates SRC-3 ubiquitination and degradation to control the retinoic acid response. Tretinoin 70-83 cullin 3 Homo sapiens 0-8
17329364-0 2007 RALDH-independent generation of retinoic acid during vertebrate embryogenesis by CYP1B1. Tretinoin 32-45 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 81-87
17329364-4 2007 Here we describe the identification, expression, biochemistry and functional analysis of CYP1B1, a member of the cytochrome p450 family of mono-oxygenases, and provide evidence that it contributes to RA synthesis during embryonic patterning. Tretinoin 200-202 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 89-95
17329364-5 2007 We present in vitro biochemical data demonstrating that this enzyme can generate both all-trans-retinal (t-RAL) and all-trans-retinoic acid (t-RA) from the precursor all-trans-retinol (t-ROH), but unlike the CYP26s, CYP1B1 cannot degrade t-RA. Tretinoin 116-139 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 216-222
22147914-4 2011 Here, by using an RNAi E3-ubiquitin ligase entry screen, we identified CUL-3 and RBX1 as components of the E3 ubiquitin ligase involved in the RA-induced ubiquitination and subsequent degradation of SRC-3. Tretinoin 143-145 cullin 3 Homo sapiens 71-76
17329364-7 2007 Concordant with its sites of expression and biochemistry, data are presented demonstrating that CYP1B1 is capable of eliciting responses that are consistent with the production of RA. Tretinoin 180-182 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 96-102
22147914-5 2011 We also show that the RA-induced ubiquitination of SRC-3 depends on its prior phosphorylation at serine 860 that promotes binding of the CUL-3-based E3 ligase in the nucleus. Tretinoin 22-24 cullin 3 Homo sapiens 137-142
17329364-8 2007 Taken together, we propose that these data provide strong support for CYP1B1 being one of the RALDH-independent components by which embryos direct RA-mediated patterning. Tretinoin 94-96 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 70-76
22069189-6 2011 In the search for genes that were affected in Pitx3-deficient mdDA neurons and restored upon embryonic RA treatment, we provide evidence that Delta-like 1, D2R (Drd2) and Th are regulated by Pitx3 and RA signaling, which influences the mdDA terminal differentiated phenotype. Tretinoin 103-105 dopamine receptor D2 Homo sapiens 156-159
22069189-6 2011 In the search for genes that were affected in Pitx3-deficient mdDA neurons and restored upon embryonic RA treatment, we provide evidence that Delta-like 1, D2R (Drd2) and Th are regulated by Pitx3 and RA signaling, which influences the mdDA terminal differentiated phenotype. Tretinoin 103-105 dopamine receptor D2 Homo sapiens 161-165
21838537-0 2011 miR-15a/16-1 enhances retinoic acid-mediated differentiation of leukemic cells and is up-regulated by retinoic acid. Tretinoin 22-35 microRNA 15a Homo sapiens 0-7
17272500-5 2007 We used Q(2)ChIP to monitor changes in histone H3 modifications on the 5" regulatory regions of the developmentally regulated genes OCT4, NANOG, LMNA, and PAX6 in the context of retinoic-acid-mediated human embryonal carcinoma cell differentiation. Tretinoin 178-191 paired box 6 Homo sapiens 155-159
21838537-0 2011 miR-15a/16-1 enhances retinoic acid-mediated differentiation of leukemic cells and is up-regulated by retinoic acid. Tretinoin 102-115 microRNA 15a Homo sapiens 0-7
21838537-2 2011 In this study, we found that the expression level of miR-15a/16-1 was up-regulated by all-trans retinoic acid (ATRA) treatment in NB4, HL-60 and U937 cell lines and primary leukemic cells. Tretinoin 96-109 microRNA 15a Homo sapiens 53-60
21838537-2 2011 In this study, we found that the expression level of miR-15a/16-1 was up-regulated by all-trans retinoic acid (ATRA) treatment in NB4, HL-60 and U937 cell lines and primary leukemic cells. Tretinoin 111-115 microRNA 15a Homo sapiens 53-60
21838537-3 2011 Overexpression of miR-15a/16-1 could not directly drive cells to undergo differentiation but enhanced ATRA-induced differentiation in NB4 and U937 cells. Tretinoin 102-106 microRNA 15a Homo sapiens 18-25
17196583-8 2007 In contrast, fibin expression was abolished in retinoic acid signaling-inhibited or wnt2b-knockdown presumptive fin bud regions. Tretinoin 47-60 fin bud initiation factor b Danio rerio 13-18
17196583-9 2007 These results indicate that fibin is a secreted signal essential for pectoral fin bud initiation in that it potentially acts downstream of retinoic acid and wnt signaling and is essential for tbx5 expression. Tretinoin 139-152 fin bud initiation factor b Danio rerio 28-33
21839859-0 2011 CD4+ Foxp3+ regulatory T cells induced by TGF-beta, IL-2 and all-trans retinoic acid attenuate obliterative bronchiolitis in rat trachea transplantation. Tretinoin 71-84 forkhead box P3 Rattus norvegicus 5-10
17491551-1 2007 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RARalpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as ligand-activated, DNA-binding, transacting, transcription-modulating proteins involved in a general molecular mechanism responsible for transcriptional responses in target genes. Tretinoin 57-70 retinoic acid receptor gamma Homo sapiens 190-198
21839859-4 2011 We show that the combination of TGF-beta, Interleukin (IL)-2, and all-trans retinoic acid (atRA) could induce naive rat CD4(+)CD25(-) T cells to differentiate into CD4(+)CD25(+)Foxp3(+) T cells in vitro, and they acquired suppressive function. Tretinoin 76-89 forkhead box P3 Rattus norvegicus 177-182
17491551-1 2007 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RARalpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as ligand-activated, DNA-binding, transacting, transcription-modulating proteins involved in a general molecular mechanism responsible for transcriptional responses in target genes. Tretinoin 57-70 retinoid X receptor beta Homo sapiens 236-243
21839859-4 2011 We show that the combination of TGF-beta, Interleukin (IL)-2, and all-trans retinoic acid (atRA) could induce naive rat CD4(+)CD25(-) T cells to differentiate into CD4(+)CD25(+)Foxp3(+) T cells in vitro, and they acquired suppressive function. Tretinoin 91-95 forkhead box P3 Rattus norvegicus 177-182
22173253-11 2011 The data suggests that genotypes of the ACE gene are linked to certain haplotypes, which could influence IgAN patients" response to ACEI/ATRA therapy. Tretinoin 137-141 IGAN1 Homo sapiens 105-109
17184907-3 2007 Several peptides including D22, PGC1alpha, SRC3-2, PRIP/RAP250 and SRC1-4 also formed a complex with RXRbeta LBD in the presence of all-trans retinoic acid (at-RA) and the fatty acids, phytanic acid (PA) and docosahexaenoic acid (DHA). Tretinoin 142-155 retinoid X receptor beta Homo sapiens 101-108
21988834-3 2011 Using an RA-inducible differentiation model, we defined the temporal changes in the genome-wide binding patterns of RARgamma and RXRalpha and correlated them with transcription regulation. Tretinoin 9-11 retinoic acid receptor gamma Homo sapiens 116-124
17223708-7 2007 The RXR ligand, 9-cis-RA, generates a second SRC-1 site and increases the affinity by improving the entropic component of binding. Tretinoin 16-24 nuclear receptor coactivator 1 Homo sapiens 45-50
17098223-10 2007 Strikingly, expression of the RA-degrading enzyme cyp26a1 in the tailbud was controlled by Su(H) activity, and morpholino knockdown of cyp26a1 alone caused asymmetric cyclic dlc expression, suggesting that excess RA in the tailbud may contribute to the cyclic asymmetries. Tretinoin 30-32 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 50-57
21872643-4 2011 All-trans retinoic acid (ATRA) has been shown to up-regulate the expression of Connexin43 and GJIC. Tretinoin 0-23 gap junction protein alpha 1 Homo sapiens 79-89
17098223-10 2007 Strikingly, expression of the RA-degrading enzyme cyp26a1 in the tailbud was controlled by Su(H) activity, and morpholino knockdown of cyp26a1 alone caused asymmetric cyclic dlc expression, suggesting that excess RA in the tailbud may contribute to the cyclic asymmetries. Tretinoin 30-32 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 135-142
17098223-10 2007 Strikingly, expression of the RA-degrading enzyme cyp26a1 in the tailbud was controlled by Su(H) activity, and morpholino knockdown of cyp26a1 alone caused asymmetric cyclic dlc expression, suggesting that excess RA in the tailbud may contribute to the cyclic asymmetries. Tretinoin 30-32 deltaC Danio rerio 174-177
17098223-10 2007 Strikingly, expression of the RA-degrading enzyme cyp26a1 in the tailbud was controlled by Su(H) activity, and morpholino knockdown of cyp26a1 alone caused asymmetric cyclic dlc expression, suggesting that excess RA in the tailbud may contribute to the cyclic asymmetries. Tretinoin 213-215 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 50-57
21872643-4 2011 All-trans retinoic acid (ATRA) has been shown to up-regulate the expression of Connexin43 and GJIC. Tretinoin 25-29 gap junction protein alpha 1 Homo sapiens 79-89
21872643-6 2011 We found that the expression of Connexin43 in Daoy cells was significantly increased when cells were exposed to 3mumol/l of ATRA (P<0.05). Tretinoin 124-128 gap junction protein alpha 1 Homo sapiens 32-42
22040956-1 2011 This study was purposed to investigate the effect of aminopeptidase N/CD13 on bestatin enhancing all-trans-retinoic acid (ATRA)-inducing differentiation in NB4 cells. Tretinoin 97-120 alanyl aminopeptidase, membrane Homo sapiens 53-69
17259349-0 2007 Programmed cell death-4 tumor suppressor protein contributes to retinoic acid-induced terminal granulocytic differentiation of human myeloid leukemia cells. Tretinoin 64-77 programmed cell death 4 Homo sapiens 0-23
17259349-3 2007 Expression of PDCD4 was markedly up-regulated during all-trans retinoic acid (ATRA)-induced granulocytic differentiation in NB4 and HL60 AML cell lines and in primary human promyelocytic leukemia (AML-M3) and CD34(+) hematopoietic progenitor cells but not in differentiation-resistant NB4.R1 and HL60R cells. Tretinoin 63-76 programmed cell death 4 Homo sapiens 14-19
22040956-1 2011 This study was purposed to investigate the effect of aminopeptidase N/CD13 on bestatin enhancing all-trans-retinoic acid (ATRA)-inducing differentiation in NB4 cells. Tretinoin 97-120 alanyl aminopeptidase, membrane Homo sapiens 70-74
17259349-3 2007 Expression of PDCD4 was markedly up-regulated during all-trans retinoic acid (ATRA)-induced granulocytic differentiation in NB4 and HL60 AML cell lines and in primary human promyelocytic leukemia (AML-M3) and CD34(+) hematopoietic progenitor cells but not in differentiation-resistant NB4.R1 and HL60R cells. Tretinoin 78-82 programmed cell death 4 Homo sapiens 14-19
22040956-1 2011 This study was purposed to investigate the effect of aminopeptidase N/CD13 on bestatin enhancing all-trans-retinoic acid (ATRA)-inducing differentiation in NB4 cells. Tretinoin 122-126 alanyl aminopeptidase, membrane Homo sapiens 53-69
17259349-9 2007 In conclusion, our data suggest that PDCD4 expression contributes to ATRA-induced granulocytic but not monocytic/macrophagic differentiation. Tretinoin 69-73 programmed cell death 4 Homo sapiens 37-42
22040956-1 2011 This study was purposed to investigate the effect of aminopeptidase N/CD13 on bestatin enhancing all-trans-retinoic acid (ATRA)-inducing differentiation in NB4 cells. Tretinoin 122-126 alanyl aminopeptidase, membrane Homo sapiens 70-74
17259349-10 2007 The PI3K/Akt/mTOR pathway constitutively represses PDCD4 expression in AML, and ATRA induces PDCD4 through inhibition of this pathway. Tretinoin 80-84 programmed cell death 4 Homo sapiens 93-98
22040956-9 2011 It is concluded that aminopeptidase N/CD13 inhibitor bestatin may enhance the differentiation-inducing activity of ATRA through inhibiting the phosphorylation of P38 MAPK in NB4 cells mediated by the cell surface APN/CD13. Tretinoin 115-119 alanyl aminopeptidase, membrane Homo sapiens 21-37
22040956-9 2011 It is concluded that aminopeptidase N/CD13 inhibitor bestatin may enhance the differentiation-inducing activity of ATRA through inhibiting the phosphorylation of P38 MAPK in NB4 cells mediated by the cell surface APN/CD13. Tretinoin 115-119 alanyl aminopeptidase, membrane Homo sapiens 38-42
22040956-9 2011 It is concluded that aminopeptidase N/CD13 inhibitor bestatin may enhance the differentiation-inducing activity of ATRA through inhibiting the phosphorylation of P38 MAPK in NB4 cells mediated by the cell surface APN/CD13. Tretinoin 115-119 alanyl aminopeptidase, membrane Homo sapiens 213-216
17389641-6 2007 RA induces the recruitment of histone acetyl transferase-containing/GRIP1/p300/CBP-associated factor (PCAF) complex to the TR2 promoter in undifferentiated cells, whereas it triggers recruitment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in differentiated cells. Tretinoin 0-2 lysine acetyltransferase 2B Homo sapiens 74-100
22040956-9 2011 It is concluded that aminopeptidase N/CD13 inhibitor bestatin may enhance the differentiation-inducing activity of ATRA through inhibiting the phosphorylation of P38 MAPK in NB4 cells mediated by the cell surface APN/CD13. Tretinoin 115-119 alanyl aminopeptidase, membrane Homo sapiens 217-221
17389641-6 2007 RA induces the recruitment of histone acetyl transferase-containing/GRIP1/p300/CBP-associated factor (PCAF) complex to the TR2 promoter in undifferentiated cells, whereas it triggers recruitment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in differentiated cells. Tretinoin 0-2 lysine acetyltransferase 2B Homo sapiens 102-106
21719597-7 2011 Knockdown of NPM1 also sensitized OCI-AML3 to all-trans retinoic acid (ATRA) and cytarabine. Tretinoin 46-69 nucleophosmin 1 Homo sapiens 13-17
17389641-6 2007 RA induces the recruitment of histone acetyl transferase-containing/GRIP1/p300/CBP-associated factor (PCAF) complex to the TR2 promoter in undifferentiated cells, whereas it triggers recruitment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in differentiated cells. Tretinoin 0-2 nuclear receptor interacting protein 1 Homo sapiens 269-275
17601378-9 2007 ACEI/ATRA therapy was found to be effective in retarding disease progression in IgAN with years to ESRF significantly extended in patients at all levels of renal function, including patients whose outcome were ESRF. Tretinoin 5-9 IGAN1 Homo sapiens 80-84
17307735-2 2007 We screened the first 2250 bp of the HAS2 promoter for transcription factor response elements (REs) in silico and found 1 cluster of 2 retinoic acid (RA) REs, 3 discrete NF-kappaB factors, and 12 Sp1 REs. Tretinoin 135-148 hyaluronan synthase 2 Homo sapiens 37-41
17307735-2 2007 We screened the first 2250 bp of the HAS2 promoter for transcription factor response elements (REs) in silico and found 1 cluster of 2 retinoic acid (RA) REs, 3 discrete NF-kappaB factors, and 12 Sp1 REs. Tretinoin 150-152 hyaluronan synthase 2 Homo sapiens 37-41
21719597-7 2011 Knockdown of NPM1 also sensitized OCI-AML3 to all-trans retinoic acid (ATRA) and cytarabine. Tretinoin 71-75 nucleophosmin 1 Homo sapiens 13-17
17159378-2 2007 COX-2 increased through a transcriptional mechanism independent of retinoic acid receptors (RAR) and retinoid X receptors (RXR) and dependent on extracellular regulated kinase-1/2 (ERK1/2), that became phosphorylated 5 min after ATRA addition. Tretinoin 229-233 cytochrome c oxidase II, mitochondrial Rattus norvegicus 0-5
21719597-8 2011 Inhibition of NPM1 oligomerization by NSC348884 induced apoptosis and sensitized OCI-AML3 and primary AML cells expressing NPM1c+ to ATRA. Tretinoin 133-137 nucleophosmin 1 Homo sapiens 14-18
17164434-1 2007 Retinoic acid (RA) is a signaling molecule in the morphogenesis of the mammary gland, modulating the expression of matrix metalloproteinases (MMPs). Tretinoin 0-13 matrix metallopeptidase 2 Rattus norvegicus 142-146
17159378-2 2007 COX-2 increased through a transcriptional mechanism independent of retinoic acid receptors (RAR) and retinoid X receptors (RXR) and dependent on extracellular regulated kinase-1/2 (ERK1/2), that became phosphorylated 5 min after ATRA addition. Tretinoin 229-233 mitogen activated protein kinase 3 Rattus norvegicus 181-187
21719597-10 2011 Thus, attenuating levels or oligomerization of NPM1 selectively induces apoptosis and sensitizes NPM1c+ expressing AML cells to treatment with ATRA and cytarabine. Tretinoin 143-147 nucleophosmin 1 Homo sapiens 47-51
21843507-3 2011 These effects were mediated by retinoic acid receptor beta2 whose promoter was also hypomethylated in the presence of ATRA. Tretinoin 118-122 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 54-59
21741961-5 2011 Moreover, both the FGF and retinoic acid (RA) signaling pathways, which are critical components of the hierarchy controlling craniofacial patterning, regulate this domain of vgll2a expression. Tretinoin 27-40 vestigial-like family member 2a Danio rerio 174-180
17073778-1 2006 P450 (cytochrome P450) enzymes have major roles in the biosynthesis of endogenous factors such as steroids and eicosanoids, in the termination of the action of endogenous factors such as retinoic acid, in the metabolism of most drugs and xenobiotics and in the generation of toxic and carcinogenic products. Tretinoin 187-200 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 0-4
17426693-4 2007 Further, all-trans retinoic acid (RA) was used to promote pancreatic differentiation, as indicated by the expression of the early pancreatic transcription factors pdx1 and hlxb9. Tretinoin 9-32 pancreatic and duodenal homeobox 1 Homo sapiens 163-167
17426693-4 2007 Further, all-trans retinoic acid (RA) was used to promote pancreatic differentiation, as indicated by the expression of the early pancreatic transcription factors pdx1 and hlxb9. Tretinoin 34-36 pancreatic and duodenal homeobox 1 Homo sapiens 163-167
21741961-5 2011 Moreover, both the FGF and retinoic acid (RA) signaling pathways, which are critical components of the hierarchy controlling craniofacial patterning, regulate this domain of vgll2a expression. Tretinoin 42-44 vestigial-like family member 2a Danio rerio 174-180
17073778-1 2006 P450 (cytochrome P450) enzymes have major roles in the biosynthesis of endogenous factors such as steroids and eicosanoids, in the termination of the action of endogenous factors such as retinoic acid, in the metabolism of most drugs and xenobiotics and in the generation of toxic and carcinogenic products. Tretinoin 187-200 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 17-21
17318229-3 2007 Among potential interactors, we found that activating protein transcription factor 2 (AP2)alpha forms a complex with NPM during retinoic-acid-induced cell differentiation. Tretinoin 128-141 nucleophosmin 1 Homo sapiens 117-120
21512846-3 2011 DISCUSSION: Disorders in the retinoic acid (Raldh) and hedgehog (Hh) signaling pathways, which appear to play a role in the development of DAP, have been implicated in other diseases of the pancreas such as pancreatic ductal adenocarcinoma (PDA) and nonalcoholic chronic calcific pancreatitis (NCCP). Tretinoin 29-42 death associated protein Homo sapiens 139-142
17318229-4 2007 We show that this complex is recruited to the promoters of certain retinoic-acid-responsive genes, including NPM itself. Tretinoin 67-80 nucleophosmin 1 Homo sapiens 109-112
17056112-7 2007 Growth-inhibitory and proapoptotic activity of DAC was significantly higher in Kasumi-1 than in KG-1a cells, and sensitization of cells to a cooperating effect of All-trans retinoic acid and of the histone deacetylase (HDAC) inhibitor Trichostatin A was observed. Tretinoin 173-186 arylacetamide deacetylase Homo sapiens 47-50
17177861-0 2006 Rescue of morphogenetic defects and of retinoic acid signaling in retinaldehyde dehydrogenase 2 (Raldh2) mouse mutants by chimerism with wild-type cells. Tretinoin 39-52 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 66-95
17177861-0 2006 Rescue of morphogenetic defects and of retinoic acid signaling in retinaldehyde dehydrogenase 2 (Raldh2) mouse mutants by chimerism with wild-type cells. Tretinoin 39-52 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 97-103
17177861-3 2006 Retinaldehyde dehydrogenase 2 (RALDH2) is the main RA-synthesizing enzyme acting during development. Tretinoin 31-33 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 0-29
17244623-3 2007 The conversion of retinol into its active form, retinoic acid, requires retinol dehydrogenase enzymes. Tretinoin 48-61 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 72-93
21816673-2 2011 These cells originate in the lamina propria (LP) and migrate to the mesenteric lymph nodes (MLNs), where they drive the differentiation of gut-homing FoxP3(+) regulatory T cells by producing retinoic acid from dietary vitamin A. Tretinoin 191-204 forkhead box P3 Homo sapiens 150-155
17183585-12 2007 The branchial arch malformations resulting from fetal RA exposure are caused at least partially by loss of PDGF-C and subsequent misregulations of the expressions of MMP-2, MMP-14, and TIMP-2. Tretinoin 54-56 tissue inhibitor of metalloproteinase 2 Mus musculus 185-191
17047027-5 2006 Expression of the RA synthesizing enzyme Raldh2 was also up-regulated and altered Hoxb1 expression indicated that RA levels are raised in R115866-treated embryos as reported for Tbx1 null mice. Tretinoin 18-20 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 41-47
21383690-4 2011 RA treatment rapidly induced morphology changes, induced growth arrest at G1/G0 to S transition, decreased cyclin D1 expression and increased p27 expression. Tretinoin 0-2 cyclin D1 Homo sapiens 107-116
17184764-1 2007 We have previously shown that retinoic acid (RA) synthesized by the retinaldehyde dehydrogenase 2 (RALDH2) is required in forebrain development. Tretinoin 30-43 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 68-97
17184764-1 2007 We have previously shown that retinoic acid (RA) synthesized by the retinaldehyde dehydrogenase 2 (RALDH2) is required in forebrain development. Tretinoin 30-43 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 99-105
21383690-5 2011 Immunofluorescence and western blot analysis indicated that RA induced the expression of lineage-specific differentiation markers Tuj1 and GFAP and reduced the expression of neural stem cell markers such as CD133, Msi-1, nestin and Sox-2. Tretinoin 60-62 prominin 1 Homo sapiens 207-212
17170094-13 2007 Moreover, ATRA-induced secretion of hepatocyte growth factor as well as angiopoietin-2 in the coculture. Tretinoin 10-14 hepatocyte growth factor Homo sapiens 36-60
17170094-13 2007 Moreover, ATRA-induced secretion of hepatocyte growth factor as well as angiopoietin-2 in the coculture. Tretinoin 10-14 angiopoietin 2 Homo sapiens 72-86
16985168-6 2006 CYP2C18, 2C19, 2C9, 2W1, 3A4, and 4B1 are up-regulated by cellular differentiation; mRNA levels for these CYP genes were inhibited in differentiating keratinocytes exposed to retinoic acid and aryl hydrocarbon receptor (AhR) ligands. Tretinoin 175-188 cytochrome P450 family 2 subfamily C member 18 Homo sapiens 0-7
16985168-6 2006 CYP2C18, 2C19, 2C9, 2W1, 3A4, and 4B1 are up-regulated by cellular differentiation; mRNA levels for these CYP genes were inhibited in differentiating keratinocytes exposed to retinoic acid and aryl hydrocarbon receptor (AhR) ligands. Tretinoin 175-188 aryl hydrocarbon receptor Homo sapiens 193-218
17170094-14 2007 Taken together, ATRA may have induced angiogenesis via RAR mainly by stimulation of HUVEC proliferation and enhancement of endogenous VEGF signaling and in part by induction of hepatocyte growth factor and angiopoietin-2 production. Tretinoin 16-20 hepatocyte growth factor Homo sapiens 177-201
21383690-5 2011 Immunofluorescence and western blot analysis indicated that RA induced the expression of lineage-specific differentiation markers Tuj1 and GFAP and reduced the expression of neural stem cell markers such as CD133, Msi-1, nestin and Sox-2. Tretinoin 60-62 musashi RNA binding protein 1 Homo sapiens 214-219
17170094-14 2007 Taken together, ATRA may have induced angiogenesis via RAR mainly by stimulation of HUVEC proliferation and enhancement of endogenous VEGF signaling and in part by induction of hepatocyte growth factor and angiopoietin-2 production. Tretinoin 16-20 angiopoietin 2 Homo sapiens 206-220
16985168-6 2006 CYP2C18, 2C19, 2C9, 2W1, 3A4, and 4B1 are up-regulated by cellular differentiation; mRNA levels for these CYP genes were inhibited in differentiating keratinocytes exposed to retinoic acid and aryl hydrocarbon receptor (AhR) ligands. Tretinoin 175-188 aryl hydrocarbon receptor Homo sapiens 220-223
21685476-0 2011 Retinoic acid enhances TRAIL-induced apoptosis in cancer cells by upregulating TRAIL receptor 1 expression. Tretinoin 0-13 TNF receptor superfamily member 10a Homo sapiens 79-95
17318068-3 2007 METHODS: We tested the potential of the retinoic acid receptor alpha (RARalpha) specific agonist VTP195183, and the pan-RAR agonist all-trans retinoic acid (ATRA), to enhance G-CSF-mediated mobilization of HSPC, in two mouse strains. Tretinoin 132-155 colony stimulating factor 3 (granulocyte) Mus musculus 175-180
21685476-4 2011 All-trans retinoic acid (ATRA) upregulated TRAIL-R1 expression in human cancer cells at the transcriptional level. Tretinoin 0-23 TNF receptor superfamily member 10a Homo sapiens 43-51
17318068-3 2007 METHODS: We tested the potential of the retinoic acid receptor alpha (RARalpha) specific agonist VTP195183, and the pan-RAR agonist all-trans retinoic acid (ATRA), to enhance G-CSF-mediated mobilization of HSPC, in two mouse strains. Tretinoin 157-161 colony stimulating factor 3 (granulocyte) Mus musculus 175-180
21685476-4 2011 All-trans retinoic acid (ATRA) upregulated TRAIL-R1 expression in human cancer cells at the transcriptional level. Tretinoin 25-29 TNF receptor superfamily member 10a Homo sapiens 43-51
17318068-5 2007 In contrast, ATRA had only a marginal effect on G-CSF-induced mobilization. Tretinoin 13-17 colony stimulating factor 3 (granulocyte) Mus musculus 48-53
21685476-5 2011 The ability of ATRA to activate TRAIL-R1 expression was inhibited by retinoic acid receptor (RAR) antagonists or siRNAs, but augmented by several RAR agonists. Tretinoin 15-19 TNF receptor superfamily member 10a Homo sapiens 32-40
21685476-8 2011 Consistent with this observation, RAR binding to DR-11, but not to Pal-17, was detected by chromatin immunoprecipitation assay in ATRA-treated cells, arguing that DR-11 was responsible for ATRA-mediated activation of the TRAIL-R1 gene. Tretinoin 130-134 TNF receptor superfamily member 10a Homo sapiens 221-229
21685476-9 2011 ATRA augmented TRAIL-induced apoptosis of cancer cells, and this activity was attenuated by a blockade to upregulation of TRAIL-R1 expression. Tretinoin 0-4 TNF receptor superfamily member 10a Homo sapiens 122-130
16901972-4 2006 This compound is also more potent than the natural ligand to transrepress the activation of the retinoic acid receptor beta2 promoter by retinoic acid and the response of the collagenase promoter to 4alpha-12-O-tetradecanoylphorbol 13-acetate. Tretinoin 96-109 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 119-124
21480163-12 2011 CONCLUSION: ATRA treatment affected the caudal development in mouse embryos, resulting in anorectal, sacral, and spinal malformations, and inhibited PCSK5 and GDF11 expression in the hindgut region. Tretinoin 12-16 growth differentiation factor 11 Mus musculus 159-164
17203214-2 2007 This study explores D-type cyclins as molecular targets in GCTs because all-trans-retinoic acid (RA)-mediated differentiation of the human embryonal carcinoma (EC) cell line NT2/D1 is associated with G1 cell cycle arrest and proteasomal degradation of cyclin D1. Tretinoin 72-95 cyclin D1 Homo sapiens 252-261
17203214-2 2007 This study explores D-type cyclins as molecular targets in GCTs because all-trans-retinoic acid (RA)-mediated differentiation of the human embryonal carcinoma (EC) cell line NT2/D1 is associated with G1 cell cycle arrest and proteasomal degradation of cyclin D1. Tretinoin 97-99 cyclin D1 Homo sapiens 252-261
16983661-7 2006 We also show that this pH(i) pathway is involved in the process of retinoic acid-induced OPC differentiation. Tretinoin 67-80 glucose-6-phosphate isomerase Homo sapiens 23-25
21480163-14 2011 This study offers a new insight into the pathogenesis of ARM in mice as affected by the interaction between ATRA and PCSK5/GDF11. Tretinoin 108-112 growth differentiation factor 11 Mus musculus 123-128
17098734-3 2007 During embryogenesis, lratb is expressed in mostly non-overlapping domains opposite to retinal dehydrogenase 2 (raldh2), the key enzyme for retinoic acid synthesis. Tretinoin 140-153 lecithin retinol acyltransferase b, tandem duplicate 1 Danio rerio 22-27
21393419-0 2011 All-trans retinoic acid and a novel synthetic retinoid tamibarotene (Am80) differentially regulate CD38 expression in human leukemia HL-60 cells: possible involvement of protein kinase C-delta. Tretinoin 0-23 protein kinase C delta Homo sapiens 170-192
17098734-3 2007 During embryogenesis, lratb is expressed in mostly non-overlapping domains opposite to retinal dehydrogenase 2 (raldh2), the key enzyme for retinoic acid synthesis. Tretinoin 140-153 aldehyde dehydrogenase 1 family, member A2 Danio rerio 87-110
17098734-3 2007 During embryogenesis, lratb is expressed in mostly non-overlapping domains opposite to retinal dehydrogenase 2 (raldh2), the key enzyme for retinoic acid synthesis. Tretinoin 140-153 aldehyde dehydrogenase 1 family, member A2 Danio rerio 112-118
17098734-4 2007 Blocking retinyl ester formation by a targeted knock down of Lratb results in significantly increased retinoic acid levels, which lead to severe embryonic patterning defects. Tretinoin 102-115 lecithin retinol acyltransferase b, tandem duplicate 1 Danio rerio 61-66
17098734-5 2007 Thus, we provide evidence that a balanced competition between Lratb and Raldh2 for yolk vitamin A defines embryonic compartments either for retinyl ester or retinoic acid synthesis. Tretinoin 157-170 lecithin retinol acyltransferase b, tandem duplicate 1 Danio rerio 62-67
17079450-2 2006 Here, we show for the first time that RA, via the RA receptor alpha (RARalpha), epigenetically regulates in a concerted fashion the transcription of two RA-responsive genes, the RA receptor beta2 (RARbeta2) and the cellular retinol-binding protein 1 (CRBP1). Tretinoin 38-40 retinol binding protein 1 Homo sapiens 215-249
17079450-2 2006 Here, we show for the first time that RA, via the RA receptor alpha (RARalpha), epigenetically regulates in a concerted fashion the transcription of two RA-responsive genes, the RA receptor beta2 (RARbeta2) and the cellular retinol-binding protein 1 (CRBP1). Tretinoin 38-40 retinol binding protein 1 Homo sapiens 251-256
17098734-5 2007 Thus, we provide evidence that a balanced competition between Lratb and Raldh2 for yolk vitamin A defines embryonic compartments either for retinyl ester or retinoic acid synthesis. Tretinoin 157-170 aldehyde dehydrogenase 1 family, member A2 Danio rerio 72-78
21393419-2 2011 ATRA induces CD38 antigen during HL-60 cell differentiation, which interacts with CD31 antigen on the vascular EC surface and may induce disadvantages in the therapy. Tretinoin 0-4 platelet and endothelial cell adhesion molecule 1 Homo sapiens 82-86
17079450-3 2006 Specifically, an impaired RA signal through RARalpha in human breast epithelial cells triggers a repressive epigenetic domino effect, involving first RARbeta2 and second CRBP1. Tretinoin 26-28 retinol binding protein 1 Homo sapiens 170-175
21393419-8 2011 Moreover, ATRA, but not tamibarotene, induced PKCdelta expression without affecting its mRNA stability. Tretinoin 10-14 protein kinase C delta Homo sapiens 46-54
17079450-4 2006 The phenotype acquired by breast epithelial cells clearly implies that the resistance to RA-mediated growth inhibition precedes the acquisition of morphological epithelial transformation, thus supporting the occurrence of sequential transcriptional silencing of first RARbeta2 and second CRBP1. Tretinoin 89-91 retinol binding protein 1 Homo sapiens 288-293
23326066-13 2011 CONCLUSION: Our findings suggest that retinoic acid therapy may induce radioiodine uptake and reduce serum thyroglobulin levels in some patients with DTC, but whether this results in clinically significant response can only be ascertained on long-term follow-up. Tretinoin 38-51 thyroglobulin Homo sapiens 107-120
16875885-4 2007 As the migration of NCCs is controlled by the HOX code and by an anteroposterior retinoic acid (RA) gradient, we analyzed the expression of CYP26, a key enzyme in RA metabolism, following FON exposure. Tretinoin 163-165 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 140-145
21470678-5 2011 Accordingly, we observed a strong induction of KLF5/6 upon ATRA-treatment in NB4 and HT93 APL but not in ATRA-resistant NB4-R cells. Tretinoin 59-63 Kruppel like factor 5 Homo sapiens 47-51
16979371-7 2007 Truncated H2A proteins in THP-1 cells were transiently increased in amount by short-term treatment with phorbol 12-myristate 13-acetate or all-trans-retinoic acid, both of which induce macrophage-like differentiation. Tretinoin 139-162 H2A clustered histone 18 Homo sapiens 10-13
16979153-3 2006 Pronephros formation in Xenopus embryo is severely impaired when RA signalling is inhibited either through expression of a dominant-negative RA receptor, or by expressing the RA-catabolizing enzyme XCyp26 or through treatment with chemical inhibitors. Tretinoin 65-67 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 198-204
16979153-8 2006 Raldh2 knockout mouse embryos fail to initiate the expression of early kidney-specific genes, suggesting that implication of RA signalling in the early steps of kidney formation is evolutionary conserved in vertebrates. Tretinoin 125-127 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 0-6
21491086-0 2011 Rab15 expression correlates with retinoic acid-induced differentiation of neuroblastoma cells. Tretinoin 33-46 RAB15, member RAS oncogene family Homo sapiens 0-5
17032197-2 2006 Recently, we have demonstrated that MUC4 expression in pancreatic tumor cells is regulated by interferon-gamma (IFNgamma) and by retinoic acid via transforming growth factor beta 2 (TGFbeta-2). Tretinoin 129-142 mucin 4, cell surface associated Homo sapiens 36-40
16935935-4 2006 We previously found that ATRA-induced cell differentiation accompanies ubiquitination-proteolysis of menage a trois 1 (MAT1), an assembly factor and targeting subunit of cyclin-dependent kinase (CDK)-activating kinase (CAK) that regulates G1 exit. Tretinoin 25-29 MNAT1 component of CDK activating kinase Homo sapiens 101-117
16764927-0 2007 beta2 Integrins are characteristically absent in acute promyelocytic leukemia and rapidly upregulated in vivo upon differentiation with all-trans retinoic acid. Tretinoin 146-159 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 0-5
21491086-10 2011 RA induced neuronal differentiation of neuroblastoma BE(2)-C cells and specifically up-regulated Rab15CN expression. Tretinoin 0-2 RAB15, member RAS oncogene family Homo sapiens 97-102
17337883-7 2007 Furthermore, BMP-4 mediates the antiproliferative action of retinoic acid in these cells. Tretinoin 60-73 bone morphogenetic protein 4 Homo sapiens 13-18
16935935-4 2006 We previously found that ATRA-induced cell differentiation accompanies ubiquitination-proteolysis of menage a trois 1 (MAT1), an assembly factor and targeting subunit of cyclin-dependent kinase (CDK)-activating kinase (CAK) that regulates G1 exit. Tretinoin 25-29 MNAT1 component of CDK activating kinase Homo sapiens 119-123
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 MNAT1 component of CDK activating kinase Homo sapiens 70-74
21491086-13 2011 These results suggest that Rab15 expression correlates with RA-induced differentiation of neuroblastoma cells. Tretinoin 60-62 RAB15, member RAS oncogene family Homo sapiens 27-32
16935935-8 2006 Both MAT1 degradation and PML/RARalpha hypophosphorylation occur in ATRA-induced G1-arresting cells undergoing differentiation but not in the synchronized G1 cells that do not differentiate. Tretinoin 68-72 MNAT1 component of CDK activating kinase Homo sapiens 5-9
21708033-1 2011 INTRODUCTION: CD25(+) FOXP3(+) CD4(+) regulatory T cells (Tregs) are induced by transforming growth factor beta (TGFbeta) and further expanded by retinoic acid (RA). Tretinoin 146-159 interleukin 2 receptor subunit alpha Homo sapiens 14-18
21708033-1 2011 INTRODUCTION: CD25(+) FOXP3(+) CD4(+) regulatory T cells (Tregs) are induced by transforming growth factor beta (TGFbeta) and further expanded by retinoic acid (RA). Tretinoin 146-159 forkhead box P3 Homo sapiens 22-27
17028196-4 2006 Further, CtBP1 suppresses the expression of intestinal retinol dehydrogenases, which are required for retinoic acid production and intestinal differentiation. Tretinoin 102-115 C-terminal binding protein 1 Homo sapiens 9-14
21708033-1 2011 INTRODUCTION: CD25(+) FOXP3(+) CD4(+) regulatory T cells (Tregs) are induced by transforming growth factor beta (TGFbeta) and further expanded by retinoic acid (RA). Tretinoin 161-163 interleukin 2 receptor subunit alpha Homo sapiens 14-18
17028196-6 2006 The relationship between APC and CtBP1 is conserved between humans and zebrafish and provides a mechanistic model explaining APC control of intestinal retinoic acid biosynthesis. Tretinoin 151-164 APC regulator of WNT signaling pathway Homo sapiens 25-28
17028196-6 2006 The relationship between APC and CtBP1 is conserved between humans and zebrafish and provides a mechanistic model explaining APC control of intestinal retinoic acid biosynthesis. Tretinoin 151-164 C-terminal binding protein 1 Homo sapiens 33-38
16619265-8 2006 Further studies revealed that pretreatment with 10 microM BQ-123, a selective endothelin-1 receptor (ETAR) antagonist, for 2 h can significantly counteract the inhibition of 5 microM atRA treatment for 2 h of dHAND mRNA and protein expression. Tretinoin 183-187 endothelin receptor type A Rattus norvegicus 78-99
17028196-6 2006 The relationship between APC and CtBP1 is conserved between humans and zebrafish and provides a mechanistic model explaining APC control of intestinal retinoic acid biosynthesis. Tretinoin 151-164 APC regulator of WNT signaling pathway Homo sapiens 125-128
21708033-1 2011 INTRODUCTION: CD25(+) FOXP3(+) CD4(+) regulatory T cells (Tregs) are induced by transforming growth factor beta (TGFbeta) and further expanded by retinoic acid (RA). Tretinoin 161-163 forkhead box P3 Homo sapiens 22-27
21594970-3 2011 The expression of some genes (Shh, Ptch-1, Gsc, and Msx2) controlled by retinoic acid is downregulated in rat embryos exposed at the phylotypic stage to the triazole triadimefon (FON). Tretinoin 72-85 patched 1 Rattus norvegicus 35-41
17130476-0 2006 Hyperglycemia inhibits retinoic acid-induced activation of Rac1, prevents differentiation of cortical neurons, and causes oxidative stress in a rat model of diabetic pregnancy. Tretinoin 23-36 Rac family small GTPase 1 Rattus norvegicus 59-63
16724269-3 2006 Exposure of SN56 cholinergic neuroblastoma cells to dibutyryl cAMP and retinoic acid for 3 days caused their morphologic differentiation along with the increase in choline acetyltransferase activity, acetylcholine content and release, calcium content, and the expression of p75 neurotrophin receptors. Tretinoin 71-84 choline acetyltransferase Mus musculus 164-189
21504781-3 2011 A human neuronal hybridoma cell line (A1 cell) was treated with CysC in both undifferentiated and retinoic acid (RA)-induced differentiated conditions, which decreased overall process length in both conditions. Tretinoin 98-111 cystatin C Homo sapiens 64-68
16712891-8 2006 Importantly, atRA-induced DNA fragmentation and capase-3 activation were prevented by pretreatment with the JNK inhibitor (SP600125) and the p38 MAPK inhibitor (SB202190), but not by pretreatment with MEK inhibitor (U0126). Tretinoin 13-17 mitogen-activated protein kinase 14 Mus musculus 141-149
16712891-8 2006 Importantly, atRA-induced DNA fragmentation and capase-3 activation were prevented by pretreatment with the JNK inhibitor (SP600125) and the p38 MAPK inhibitor (SB202190), but not by pretreatment with MEK inhibitor (U0126). Tretinoin 13-17 midkine Mus musculus 201-204
17024248-3 2006 Smith-Magenis syndrome is associated with a 3.7-Mb deletion in 17p11.2, and its clinical presentation is caused by retinoic acid inducible 1 (RAI1) haploinsufficiency. Tretinoin 115-128 retinoic acid induced 1 Mus musculus 142-146
21504781-3 2011 A human neuronal hybridoma cell line (A1 cell) was treated with CysC in both undifferentiated and retinoic acid (RA)-induced differentiated conditions, which decreased overall process length in both conditions. Tretinoin 113-115 cystatin C Homo sapiens 64-68
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 58-71 gap junction protein alpha 1 Homo sapiens 176-187
21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 49-62 forkhead box P3 Homo sapiens 122-127
21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 64-66 forkhead box P3 Homo sapiens 122-127
21514413-6 2011 Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. Tretinoin 21-23 retinol binding protein 1 Homo sapiens 84-89
16919229-3 2006 We describe a fluorescence-based method for quantitating RA that takes advantage of the high affinity and selectivity of the intracellular lipid-binding protein termed CRABP-I and CRABP-II and that uses them as RA sensors. Tretinoin 57-59 cellular retinoic acid binding protein 1 Homo sapiens 168-175
16845368-4 2006 By contrast, in retinoic-acid-induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of Hoxb1, at the 3" boundary of the HoxB domain. Tretinoin 16-29 homeobox B1 Mus musculus 198-203
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 277-279 retinol binding protein 1 Homo sapiens 12-46
16904661-5 2006 Shox expression is inhibited distally by signals from the apical ectodermal ridge, both Fgfs and Bmps, and proximally by retinoic acid signaling. Tretinoin 121-134 short stature homeobox Gallus gallus 0-4
17069899-6 2006 In addition, the transcriptional activity of hST8Sia III induced by RA in U-87MG cells was strongly inhibited by SP600125, c-Jun N-terminal Kinase (JNK) inhibitor, as determined by RT-PCR and luciferase assay of hST8Sia III promoter containing the -1194 to -816 regions. Tretinoin 68-70 Oncogene OVC (ovarian adenocarcinoma oncogene) Homo sapiens 45-49
16971787-7 2006 These results strongly suggest that ledgerline is essential for mesodermal RA activity and differentiation of the presomitic mesoderm during Xenopus somitogenesis. Tretinoin 75-77 ripply transcriptional repressor 2 L homeolog Xenopus laevis 36-46
21382444-1 2011 BACKGROUND: Cellular retinol binding-protein I (CRBPI) and cellular retinol binding-protein II (CRBPII) serve as intracellular retinoid chaperones that bind retinol and retinal with high affinity and facilitate substrate delivery to select enzymes that catalyze retinoic acid (RA) and retinyl ester biosynthesis. Tretinoin 277-279 retinol binding protein 1 Homo sapiens 48-53
21354561-8 2011 In part of the leiomyoma cells, ATRA induced a relative increase of Bax (proapoptotic) as well as a relative decrease of phosphorylated glycogen synthase kinase 3beta (proapoptotic). Tretinoin 32-36 glycogen synthase kinase 3 beta Homo sapiens 136-166
21481001-0 2011 Folic acid rescue of ATRA-induced cleft palate by restoring the TGF-beta signal and inhibiting apoptosis. Tretinoin 21-25 transforming growth factor, beta 1 Mus musculus 64-72
16766008-6 2006 In addition, CAPE enhanced ATRA-induced cell cycle arrest at the G1 phase by decreasing the association of cdk2-cyclin E complex. Tretinoin 27-31 cyclin dependent kinase 2 Homo sapiens 107-111
21481001-2 2011 To gain more insight into the molecular pathways affected by FA, TGF-beta signaling and apoptosis in mouse embryonic palatal mesenchymal (MEPM) cells of all-trans retinoic acid (ATRA)-induced cleft palate in organ culture were tested. Tretinoin 163-176 transforming growth factor, beta 1 Mus musculus 65-73
16854221-13 2006 MCF-7 treatment with all-trans retinoic acid enhanced HEX expression and induced a diffuse nuclear localization. Tretinoin 31-44 hematopoietically expressed homeobox Homo sapiens 54-57
21481001-2 2011 To gain more insight into the molecular pathways affected by FA, TGF-beta signaling and apoptosis in mouse embryonic palatal mesenchymal (MEPM) cells of all-trans retinoic acid (ATRA)-induced cleft palate in organ culture were tested. Tretinoin 178-182 transforming growth factor, beta 1 Mus musculus 65-73
21436255-2 2011 The aldehyde dehydrogenase-1 (Aldh1) family of enzymes (Aldh1a1, a2, and a3) catalyzes RA production from retinaldehyde and thereby controls concentrations of this transcriptionally active metabolite. Tretinoin 87-89 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 4-28
21436255-2 2011 The aldehyde dehydrogenase-1 (Aldh1) family of enzymes (Aldh1a1, a2, and a3) catalyzes RA production from retinaldehyde and thereby controls concentrations of this transcriptionally active metabolite. Tretinoin 87-89 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 30-35
16794265-4 2006 We further show that despite a high expression of the NKG2D ligand retinoic acid early inducible-1 by mouse ESCs, they remain resistant to natural killer cell lysis. Tretinoin 67-80 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 54-59
16818722-4 2006 Consistent with this, antagonism of retinoid signaling phenocopies BMP4 action, whereas RA inhibits the chondrogenic stimulatory activity of BMP4. Tretinoin 88-90 bone morphogenetic protein 4 Homo sapiens 141-145
21436255-2 2011 The aldehyde dehydrogenase-1 (Aldh1) family of enzymes (Aldh1a1, a2, and a3) catalyzes RA production from retinaldehyde and thereby controls concentrations of this transcriptionally active metabolite. Tretinoin 87-89 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 56-63
21436255-4 2011 We hypothesized that Aldh1 enzymes produce endogenous RA and regulate adipogenesis and fat formation in a fat depot-specific manner. Tretinoin 54-56 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 21-26
21436255-5 2011 We demonstrate that adipogenesis in vitro is accompanied by RA production generated primarily by Aldh1a1. Tretinoin 60-62 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 97-104
21436255-10 2011 This loss of RA-producing enzymes was accompanied by 70% decreased expression of ZFP423, PPARgamma, and Fabp4 in visceral fat of Aldh1a1(-/-) vs. wild-type mice and by the predominant loss of visceral fat. Tretinoin 13-15 peroxisome proliferator activated receptor gamma Mus musculus 89-98
21436255-10 2011 This loss of RA-producing enzymes was accompanied by 70% decreased expression of ZFP423, PPARgamma, and Fabp4 in visceral fat of Aldh1a1(-/-) vs. wild-type mice and by the predominant loss of visceral fat. Tretinoin 13-15 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 129-136
16889372-2 2006 When treated with retinoic acid, P19 cells can be differentiated along a neural cell lineage in culture. Tretinoin 18-31 interleukin 23, alpha subunit p19 Mus musculus 33-36
21436255-11 2011 Subcutaneous fat of Aldh1a1(-/-) mice expressed Aldh1a3 for RA production that was sufficient to maintain expression of ZFP423 and PPARgamma and sc fat mass. Tretinoin 60-62 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 20-27
21436255-11 2011 Subcutaneous fat of Aldh1a1(-/-) mice expressed Aldh1a3 for RA production that was sufficient to maintain expression of ZFP423 and PPARgamma and sc fat mass. Tretinoin 60-62 peroxisome proliferator activated receptor gamma Mus musculus 131-140
21436255-12 2011 Our data suggest a paradigm for regulation of fat depots through the concerted action of Aldh1 enzymes that establish RA-dependent tandem regulation of transcription factors ZFP423 and PPARgamma in a depot-specific manner. Tretinoin 118-120 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 89-94
21436255-12 2011 Our data suggest a paradigm for regulation of fat depots through the concerted action of Aldh1 enzymes that establish RA-dependent tandem regulation of transcription factors ZFP423 and PPARgamma in a depot-specific manner. Tretinoin 118-120 peroxisome proliferator activated receptor gamma Mus musculus 185-194
21156171-9 2011 Another is Vav1, which also showed only basal expression after ATRA treatment in CD38 Delta11-20 expressing cells. Tretinoin 63-67 vav guanine nucleotide exchange factor 1 Homo sapiens 11-15
16819395-8 2006 FXR activity requires heterodimerization with the 9-cis retinoid receptor (RXR alpha), and when bound by bile acids and retinoic acid, the complex effectively activates the transcription of BSEP. Tretinoin 120-133 nuclear receptor subfamily 1 group H member 4 Homo sapiens 0-3
16455818-4 2006 The metabolites of all-trans RA produced by Cyp26D1 were the same as that produced by Cyp26A1, which are mainly 4-hydroxy-all-trans-RA and 4-oxo-all-trans-RA. Tretinoin 29-31 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 86-93
21397850-2 2011 Here, we show that within 3 hr of ventricular injury, the entire endocardium undergoes morphological changes and induces expression of the retinoic acid (RA)-synthesizing enzyme raldh2. Tretinoin 139-152 aldehyde dehydrogenase 1 family, member A2 Danio rerio 178-184
16455818-4 2006 The metabolites of all-trans RA produced by Cyp26D1 were the same as that produced by Cyp26A1, which are mainly 4-hydroxy-all-trans-RA and 4-oxo-all-trans-RA. Tretinoin 132-134 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 86-93
16455818-6 2006 These alterations were similar to those caused by the overexpression of cyp26a1 in zebrafish embryos and to that which resulted from treating embryos with 1 microm 4-diethylamino-benzaldehyde (retinal dehydrogenase inhibitor), implying that cyp26d1 can antagonize RA activity in vivo. Tretinoin 264-266 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 72-79
21397850-2 2011 Here, we show that within 3 hr of ventricular injury, the entire endocardium undergoes morphological changes and induces expression of the retinoic acid (RA)-synthesizing enzyme raldh2. Tretinoin 154-156 aldehyde dehydrogenase 1 family, member A2 Danio rerio 178-184
21187285-10 2011 Furthermore, the RhoA expression level was significantly decreased by serum withdrawal or retinoic acid in control cells, although this decrease was not observed in PLCdelta3KD cells. Tretinoin 90-103 ras homolog family member A Mus musculus 17-21
20717697-0 2011 The promoting effect of retinoic acid on proliferation of chicken primordial germ cells by increased expression of cadherin and catenins. Tretinoin 24-37 cadherin Gallus gallus 115-123
21426646-2 2011 METHODS: TrkB protein expression in SY5Y cells before and after all-trans-retinoicacid (ATRA) treatment was detected by Western blot. Tretinoin 64-86 neurotrophic receptor tyrosine kinase 2 Homo sapiens 9-13
21426646-2 2011 METHODS: TrkB protein expression in SY5Y cells before and after all-trans-retinoicacid (ATRA) treatment was detected by Western blot. Tretinoin 88-92 neurotrophic receptor tyrosine kinase 2 Homo sapiens 9-13
21426646-3 2011 P-TrkB protein expression in SY5Y cells before and after the treatment of ATRA along with BDNF was also detected by Western blot. Tretinoin 74-78 neurotrophic receptor tyrosine kinase 2 Homo sapiens 2-6
21138835-7 2011 siRNA knockdown indicates that Rdh10, Rdh2 (mRdh1), and Raldh1, -2, and -3 contribute to atRA production. Tretinoin 89-93 retinol dehydrogenase 1 (all trans) Mus musculus 44-49
20971141-9 2011 The cancer relapse model was successfully established by xenografting breast cancer stem cells into NOD/SCID mice, and the formation and growth of the xenografted tumors were significantly inhibited by all-trans retinoic acid stealth liposomes. Tretinoin 212-225 protein kinase, DNA activated, catalytic polypeptide Mus musculus 104-108
21111795-7 2011 Another structural N-PAH variant, 1,7-phenanthroline, downregulated ATRA-mediated response at most of tested ATRA concentrations and exposure times. Tretinoin 68-72 phenylalanine hydroxylase Homo sapiens 21-24
21054342-1 2011 BACKGROUND AND PURPOSE: Fenretinide (4-HPR) is a retinoic acid analogue, currently used in clinical trials in oncology. Tretinoin 49-62 haptoglobin-related protein Homo sapiens 39-42
21228001-9 2011 We show that RA downregulates the Hh signaling components ptc1 and smo in endodermal explants, indicating a possible molecular mechanism for blocking axial mesoderm-derived Hh ligands from the prepancreatic endoderm during the specification stage. Tretinoin 13-15 patched 2 Danio rerio 58-62
21427903-5 2011 RESULTS: (1) Gene-chip analysis showed that in RA-induced cleft palate group wnt8a and fgf9 were down-regulated, wnt3 and fgf10 were up-regulated in conversely. Tretinoin 47-49 wingless-type MMTV integration site family, member 8A Mus musculus 77-82
21427903-5 2011 RESULTS: (1) Gene-chip analysis showed that in RA-induced cleft palate group wnt8a and fgf9 were down-regulated, wnt3 and fgf10 were up-regulated in conversely. Tretinoin 47-49 wingless-type MMTV integration site family, member 3 Mus musculus 113-117
20857416-4 2011 Addition of RA causes removal of H2A.Z and Suz12 from RARgamma target genes when the genes are transcriptionally activated. Tretinoin 12-14 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 43-48
16889531-4 2006 Interestingly, vitamin D and RA demonstrated a consistent, dose-dependent enhancement of osteogenesis and upregulated osteoblast specific markers including osteopontin and osteocalcin. Tretinoin 29-31 secreted phosphoprotein 1 Mus musculus 156-167
16636064-5 2006 EBBP undergoes serine threonine phosphorylation and enhanced protein stability after RA treatment. Tretinoin 85-87 tripartite motif containing 16 Homo sapiens 0-4
16636064-6 2006 Following RA treatment, we also observed increased nuclear EBBP levels in aggregates with the promyelocytic leukemia protein at promyelocytic leukemia nuclear bodies. Tretinoin 10-12 tripartite motif containing 16 Homo sapiens 59-63
16688769-8 2006 Some of these effects, such as that on neuron navigator 2 (NAV2), may be direct, whereas others may be secondary to other atRA-induced changes in the cell. Tretinoin 122-126 neuron navigator 2 Homo sapiens 39-57
16688769-8 2006 Some of these effects, such as that on neuron navigator 2 (NAV2), may be direct, whereas others may be secondary to other atRA-induced changes in the cell. Tretinoin 122-126 neuron navigator 2 Homo sapiens 59-63
16574167-7 2006 Decreases in CyclinB2 and BIRC5 mRNA induced by FK506 or retinoic acid, both of which exert potentiation of NGF-induced neurite outgrowth effects but with different mechanisms, also correlated with their neurite outgrowth activities. Tretinoin 57-70 cyclin B2 Homo sapiens 13-21
16477621-2 2006 This study was undertaken to investigate the expression of CB1 and CB2 cannabinoid receptors in neurons that develop from retinoic acid (RA)-primed mouse P19 embryonal carcinoma cells. Tretinoin 122-135 cannabinoid receptor 1 (brain) Mus musculus 59-62
16477621-2 2006 This study was undertaken to investigate the expression of CB1 and CB2 cannabinoid receptors in neurons that develop from retinoic acid (RA)-primed mouse P19 embryonal carcinoma cells. Tretinoin 122-135 interleukin 23, alpha subunit p19 Mus musculus 154-157
16477621-2 2006 This study was undertaken to investigate the expression of CB1 and CB2 cannabinoid receptors in neurons that develop from retinoic acid (RA)-primed mouse P19 embryonal carcinoma cells. Tretinoin 137-139 cannabinoid receptor 1 (brain) Mus musculus 59-62
16477621-2 2006 This study was undertaken to investigate the expression of CB1 and CB2 cannabinoid receptors in neurons that develop from retinoic acid (RA)-primed mouse P19 embryonal carcinoma cells. Tretinoin 137-139 interleukin 23, alpha subunit p19 Mus musculus 154-157
16477621-3 2006 Both undifferentiated P19 cells and RA-treated P19 neurons were positive, by using reverse transcription-polymerase chain reaction (RT-PCR), for CB1 (but not CB2) mRNA. Tretinoin 36-38 interleukin 23, alpha subunit p19 Mus musculus 47-50
16477621-3 2006 Both undifferentiated P19 cells and RA-treated P19 neurons were positive, by using reverse transcription-polymerase chain reaction (RT-PCR), for CB1 (but not CB2) mRNA. Tretinoin 36-38 cannabinoid receptor 1 (brain) Mus musculus 145-148
16581781-0 2006 GA-binding protein and p300 are essential components of a retinoic acid-induced enhanceosome in myeloid cells. Tretinoin 58-71 E1A binding protein p300 Homo sapiens 23-27
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 integrin subunit alpha X Homo sapiens 209-214
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 RB transcriptional corepressor 1 Homo sapiens 256-259
16549780-7 2006 Conversely, silencing of ENH by RNA interference prevents cytoplasmic relocation of Id2 in neuroblastoma cells differentiated with retinoic acid. Tretinoin 131-144 PDZ and LIM domain 5 Homo sapiens 25-28
16257998-8 2006 These effects of ATRA were inhibited by rottlerin, which suggests ATRA abolished irradiation-induced stimulation through a PKCdelta-dependent pathway. Tretinoin 17-21 protein kinase C delta Homo sapiens 123-131
16257998-8 2006 These effects of ATRA were inhibited by rottlerin, which suggests ATRA abolished irradiation-induced stimulation through a PKCdelta-dependent pathway. Tretinoin 66-70 protein kinase C delta Homo sapiens 123-131
16757381-8 2006 The p300/CBP may enhance acetylation of histones bound to the hPDK4 promoter and cooperate with Sp1 and CBF to stimulate transcription of the hPDK4 gene in response to RA and TSA. Tretinoin 168-170 E1A binding protein p300 Homo sapiens 4-8
17042689-6 2006 The redifferentiating effect of RA was evaluated by serum thyroglobulin (Tg) monitoring during RA treatment and qualitative analysis of iodine uptake on the post-therapeutic whole body scan. Tretinoin 32-34 thyroglobulin Homo sapiens 58-71
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 139-152 checkpoint kinase 2 Homo sapiens 169-173
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 154-158 checkpoint kinase 2 Homo sapiens 169-173
16938888-4 2006 In contrast, treatment of apc mutants with all-trans retinoic acid rescued retinal differentiation defects but had no apparent effect on the lens. Tretinoin 53-66 APC regulator of WNT signaling pathway Homo sapiens 26-29
16938888-6 2006 Morpholino knockdown of Rdh5 phenocopied the apc mutant retinal differentiation defects and was rescued by treatment with exogenous all-trans retinoic acid. Tretinoin 142-155 retinol dehydrogenase 5 Homo sapiens 24-28
16938888-8 2006 These findings support a model wherein Apc serves a dual role in regulating Wnt and retinoic acid signaling within the eye and suggest retinoic acid deficiency as an explanation for APC mutation-associated retinal defects such as congenital hypertrophy/hyperplasia of the retinal pigmented epithelium. Tretinoin 84-97 APC regulator of WNT signaling pathway Homo sapiens 39-42
17225872-10 2006 RA treatment increased RARA gene expression in both cell populations but upregulated GABRB3 mRNA expression only in N-SP cells. Tretinoin 0-2 gamma-aminobutyric acid type A receptor subunit beta3 Homo sapiens 85-91
16918696-7 2006 In contrast, ATRA-induced expression of PU.1, C/EBPalpha, C/EBPbeta and IRF-1 was unaffected. Tretinoin 13-17 CCAAT enhancer binding protein beta Homo sapiens 58-67
16737695-7 2006 Immunoprecipitation and Western blot analyses showed that LIF induces tyrosine phosphorylation of JAK1, TYK2 and STAT3 in 30 min and treatment with 15d-PGJ2 or ATRA results in a dose-dependent decrease in LIF-induced phosphorylation of JAK1 and STAT3 in D3-ES cells. Tretinoin 160-164 Janus kinase 1 Mus musculus 98-102
16494909-0 2006 Expression of the helix-loop-helix protein inhibitor of DNA binding-1 (ID-1) is activated by all-trans retinoic acid in normal human keratinocytes. Tretinoin 93-116 inhibitor of DNA binding 1, HLH protein Homo sapiens 43-69
16494909-0 2006 Expression of the helix-loop-helix protein inhibitor of DNA binding-1 (ID-1) is activated by all-trans retinoic acid in normal human keratinocytes. Tretinoin 93-116 inhibitor of DNA binding 1, HLH protein Homo sapiens 71-75
16494909-6 2006 We examined the effect of all-trans retinoic acid on expression of ID-1, -2, -3, and -4 in normal human keratinocytes and found that exposure of these cells to all-trans retinoic acid causes an increase in both ID-1 and ID-3 gene expression. Tretinoin 36-49 inhibitor of DNA binding 1, HLH protein Homo sapiens 67-87
16608438-4 2006 ChIP (chromatin immunoprecipitation) assays revealed that in vivo binding of C/EBPalpha to the region markedly decreases upon incubation with ATRA, whereas ATRA treatment marginally increases the recruitment of C/EBPbeta. Tretinoin 156-160 CCAAT enhancer binding protein beta Homo sapiens 211-220
16226872-2 2006 Here, we show that HL-60/FAK cells are highly resistant to all-trans retinoic acid (ATRA)-induced differentiation, whereas original HL-60 or HL-60/Vect cells are sensitive. Tretinoin 69-82 protein tyrosine kinase 2 Homo sapiens 25-28
16226872-2 2006 Here, we show that HL-60/FAK cells are highly resistant to all-trans retinoic acid (ATRA)-induced differentiation, whereas original HL-60 or HL-60/Vect cells are sensitive. Tretinoin 84-88 protein tyrosine kinase 2 Homo sapiens 25-28
16226872-3 2006 Treatment with ATRA at 1 muM for 5 days markedly inhibited the proliferation and increased the expression of differentiation markers (CD38, CD11b) in HL-60/Vect cells, but showed no such effect in HL-60/FAK cells. Tretinoin 15-19 protein tyrosine kinase 2 Homo sapiens 203-206
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 150-154 protein tyrosine kinase 2 Homo sapiens 197-200
16226872-4 2006 Electrophoretic mobility shift assay (EMSA) using an oligonucleotide for the c/EBP consensus binding sequence showed that c/EBPalpha was activated in ATRA-treated HL-60/Vect cells but not in HL-60/FAK cells, indicating that c/EBPalpha activation by ATRA was impaired in HL-60/FAK cells. Tretinoin 150-154 protein tyrosine kinase 2 Homo sapiens 276-279
16226872-5 2006 In addition, the association of retinoblastoma protein (pRb) and c/EBPalpha after treatment with ATRA was seen in HL-60/Vect cells but not in HL-60/FAK cells. Tretinoin 97-101 RB transcriptional corepressor 1 Homo sapiens 56-59
16226872-7 2006 Finally, the introduction of FAK siRNA into HL-60/FAK cells resulted in the recovery of sensitivity to ATRA-induced differentiation, confirming that the inhibition of HL-60/FAK differentiation resulted from both the induction of pRb hyperphosphorylation and the inhibition of association of pRb and c/EBPalpha. Tretinoin 103-107 protein tyrosine kinase 2 Homo sapiens 29-32
16226872-7 2006 Finally, the introduction of FAK siRNA into HL-60/FAK cells resulted in the recovery of sensitivity to ATRA-induced differentiation, confirming that the inhibition of HL-60/FAK differentiation resulted from both the induction of pRb hyperphosphorylation and the inhibition of association of pRb and c/EBPalpha. Tretinoin 103-107 protein tyrosine kinase 2 Homo sapiens 50-53
16226872-7 2006 Finally, the introduction of FAK siRNA into HL-60/FAK cells resulted in the recovery of sensitivity to ATRA-induced differentiation, confirming that the inhibition of HL-60/FAK differentiation resulted from both the induction of pRb hyperphosphorylation and the inhibition of association of pRb and c/EBPalpha. Tretinoin 103-107 protein tyrosine kinase 2 Homo sapiens 50-53
16226872-7 2006 Finally, the introduction of FAK siRNA into HL-60/FAK cells resulted in the recovery of sensitivity to ATRA-induced differentiation, confirming that the inhibition of HL-60/FAK differentiation resulted from both the induction of pRb hyperphosphorylation and the inhibition of association of pRb and c/EBPalpha. Tretinoin 103-107 RB transcriptional corepressor 1 Homo sapiens 229-232
16226872-7 2006 Finally, the introduction of FAK siRNA into HL-60/FAK cells resulted in the recovery of sensitivity to ATRA-induced differentiation, confirming that the inhibition of HL-60/FAK differentiation resulted from both the induction of pRb hyperphosphorylation and the inhibition of association of pRb and c/EBPalpha. Tretinoin 103-107 RB transcriptional corepressor 1 Homo sapiens 291-294
16774994-2 2006 Mutants in aldh1a2 (raldh2), an embryonically expressed gene encoding a retinoic acid (RA)-synthesizing enzyme, have been used to show that limb development and patterning of the limb bud are crucially dependent on RA signaling. Tretinoin 72-85 aldehyde dehydrogenase 1 family, member A2 Danio rerio 11-18
16774994-2 2006 Mutants in aldh1a2 (raldh2), an embryonically expressed gene encoding a retinoic acid (RA)-synthesizing enzyme, have been used to show that limb development and patterning of the limb bud are crucially dependent on RA signaling. Tretinoin 72-85 aldehyde dehydrogenase 1 family, member A2 Danio rerio 20-26
16774994-2 2006 Mutants in aldh1a2 (raldh2), an embryonically expressed gene encoding a retinoic acid (RA)-synthesizing enzyme, have been used to show that limb development and patterning of the limb bud are crucially dependent on RA signaling. Tretinoin 87-89 aldehyde dehydrogenase 1 family, member A2 Danio rerio 11-18
16774994-2 2006 Mutants in aldh1a2 (raldh2), an embryonically expressed gene encoding a retinoic acid (RA)-synthesizing enzyme, have been used to show that limb development and patterning of the limb bud are crucially dependent on RA signaling. Tretinoin 87-89 aldehyde dehydrogenase 1 family, member A2 Danio rerio 20-26
16774994-2 2006 Mutants in aldh1a2 (raldh2), an embryonically expressed gene encoding a retinoic acid (RA)-synthesizing enzyme, have been used to show that limb development and patterning of the limb bud are crucially dependent on RA signaling. Tretinoin 215-217 aldehyde dehydrogenase 1 family, member A2 Danio rerio 11-18
16774994-2 2006 Mutants in aldh1a2 (raldh2), an embryonically expressed gene encoding a retinoic acid (RA)-synthesizing enzyme, have been used to show that limb development and patterning of the limb bud are crucially dependent on RA signaling. Tretinoin 215-217 aldehyde dehydrogenase 1 family, member A2 Danio rerio 20-26
17044982-6 2006 METHODS: The expression of TrkB protein was detected with Western-blot after the treatment with different concentrations of all trans-retinoic acid (ATRA). Tretinoin 128-147 neurotrophic receptor tyrosine kinase 2 Homo sapiens 27-31
17044982-6 2006 METHODS: The expression of TrkB protein was detected with Western-blot after the treatment with different concentrations of all trans-retinoic acid (ATRA). Tretinoin 149-153 neurotrophic receptor tyrosine kinase 2 Homo sapiens 27-31
17044982-11 2006 The level of TrkB protein was increased with adding of ATRA at different concentrations. Tretinoin 55-59 neurotrophic receptor tyrosine kinase 2 Homo sapiens 13-17
16765349-7 2006 Data presented here suggest a novel RA-signaling, by which RA-induced p21 induction and complex formation with cyclin E/CDK2 diverts CDK2 function from normally driving proliferation to alternatively promoting apoptosis. Tretinoin 36-38 cyclin dependent kinase 2 Homo sapiens 120-124
16765349-7 2006 Data presented here suggest a novel RA-signaling, by which RA-induced p21 induction and complex formation with cyclin E/CDK2 diverts CDK2 function from normally driving proliferation to alternatively promoting apoptosis. Tretinoin 36-38 cyclin dependent kinase 2 Homo sapiens 133-137
16671996-7 2006 Treatment with retinoic acid (RA), an inducer of TG2 expression, significantly decreased EGF-induced DNA synthesis in both PPH and PVH. Tretinoin 15-28 transglutaminase 2 Rattus norvegicus 49-52
16671996-7 2006 Treatment with retinoic acid (RA), an inducer of TG2 expression, significantly decreased EGF-induced DNA synthesis in both PPH and PVH. Tretinoin 15-28 epidermal growth factor like 1 Rattus norvegicus 89-92
16751185-4 2006 Thus, the ligand that possibly binds and activates RXRalpha heterodimerized with PPARbeta(delta) cannot be a retinoic acid, as it would also bind RARgamma and relieve the RARgamma-mediated repression, thereby yielding abnormal LGs. Tretinoin 109-122 retinoid X receptor alpha Mus musculus 51-59
16423341-3 2006 Early in cardiogenesis, retinoic acid alters the expression of key genes in the lateral plate mesoderm including Nkx2.5 and HAND1, indicating that early patterning of the lateral plate mesoderm is, in part, controlled by retinoic acid. Tretinoin 24-37 heart and neural crest derivatives expressed 1 L homeolog Xenopus laevis 124-129
16427040-8 2006 Similar analysis of wild type foregut shows that endogenous RAR alpha activity is required to maintain overall RA signaling, and to refine the RAR beta effects in the lung field. Tretinoin 60-62 retinoic acid receptor, beta Mus musculus 143-151
16496350-8 2006 The conditional allele described herein is a genetic tool for studying tissue-specific, RALDH2-dependent functions of retinoic acid during development and in adult life. Tretinoin 118-131 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 88-94
20857416-4 2011 Addition of RA causes removal of H2A.Z and Suz12 from RARgamma target genes when the genes are transcriptionally activated. Tretinoin 12-14 retinoic acid receptor gamma Homo sapiens 54-62
16813970-6 2006 Proteins involved in mediating the cellular responses to RA include the cellular retinoic acid binding proteins CRABP-I and CRABP-II and the nuclear retinoic acid receptors RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 57-59 cellular retinoic acid binding protein II Mus musculus 124-132
16813970-6 2006 Proteins involved in mediating the cellular responses to RA include the cellular retinoic acid binding proteins CRABP-I and CRABP-II and the nuclear retinoic acid receptors RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 57-59 retinoic acid receptor, beta Mus musculus 184-192
21206085-4 2011 Mechanistic studies revealed that A20 regulated DC production of retinoic acid and proinflammatory cytokines, inhibiting the expression of gut-homing receptors on T and B cells. Tretinoin 65-78 tumor necrosis factor, alpha-induced protein 3 Mus musculus 34-37
16501610-3 2006 In the NB4 cell line, which was derived from an APL patient and expresses PML:RARalpha, we observed a retinoic acid-dependent change in the modification of specific proteins by SUMO-1. Tretinoin 102-115 small ubiquitin like modifier 1 Homo sapiens 177-183
16522742-1 2006 Farnesoid X receptor (FXR), the receptor for bile acids, including chenodeoxycholic acid (CDCA), is a member of the nuclear receptor superfamily, which also includes the receptors for retinoic acid, vitamin D (D3), thyroid hormone, thiazolidinedione and 22(R)-hydroxycholesterol. Tretinoin 184-197 nuclear receptor subfamily 1 group H member 4 Homo sapiens 22-25
21425084-3 2011 By use of beta-galactosidase chemiluminescence, we show that a mouse Cdx1/lacZ reporter expressed in P19 EC cells responds to RA by the combined activities of an intron retinoic acid response element (RARE) and an upstream RARE. Tretinoin 126-128 caudal type homeobox 1 Mus musculus 69-73
16489341-2 2006 The location of somite segmentation depends on opposing signalling gradients of retinoic acid (generated by retinaldehyde dehydrogenase-2; Raldh2) anteriorly and fibroblast growth factor (FGF; generated by Fgf8) posteriorly. Tretinoin 80-93 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 108-137
16489341-2 2006 The location of somite segmentation depends on opposing signalling gradients of retinoic acid (generated by retinaldehyde dehydrogenase-2; Raldh2) anteriorly and fibroblast growth factor (FGF; generated by Fgf8) posteriorly. Tretinoin 80-93 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 139-145
16489341-6 2006 The late stages of somitogenesis were rescued in Raldh2(-/-) mouse embryos when the maternal diet was supplemented with retinoic acid until only the 6-somite stage, demonstrating that retinoic acid is only needed during node stages. Tretinoin 184-197 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 49-55
16489341-7 2006 A retinoic-acid-reporter transgene marking the action of maternal retinoic acid in rescued Raldh2(-/-) embryos revealed that the targets of retinoic-acid signalling during somitogenesis are the node ectoderm and the posterior neural plate, not the presomitic mesoderm. Tretinoin 2-15 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 91-97
16489341-7 2006 A retinoic-acid-reporter transgene marking the action of maternal retinoic acid in rescued Raldh2(-/-) embryos revealed that the targets of retinoic-acid signalling during somitogenesis are the node ectoderm and the posterior neural plate, not the presomitic mesoderm. Tretinoin 66-79 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 91-97
16538685-10 2006 These findings support the hypothesis that RA is synthesized in the postnatal OE (catalyzed by RALDH 1) and underlying LP (differentially catalyzed by RALDH 1 and RALDH 2) at sites that could influence the development, maturation, targeting, and/or turnover of olfactory receptor neurons throughout the olfactory organ. Tretinoin 43-45 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 163-170
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 199-212 ISG15 ubiquitin like modifier Homo sapiens 34-39
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 199-212 ISG15 ubiquitin like modifier Homo sapiens 52-57
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 199-212 ISG15 ubiquitin like modifier Homo sapiens 52-57
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 199-212 ISG15 ubiquitin like modifier Homo sapiens 52-57
16647867-3 2006 It was recently demonstrated that ISG15 expression, ISG15 conjugation, and several enzymes involved in ISG15 modification are upregulated in an acute promyelocytic cell line following treatment with retinoic acid, suggesting a possible retinoic acid induced IFN-independent ISG15 modification pathway. Tretinoin 236-249 ISG15 ubiquitin like modifier Homo sapiens 34-39
16647867-4 2006 In this study, we examined a possible link between IFN signaling and retinoic acid-induced ISG15 conjugation. Tretinoin 69-82 ISG15 ubiquitin like modifier Homo sapiens 91-96
16647867-7 2006 Blockade of the type I IFN receptor with a neutralizing antibody blocked retinoic acid induced ISG15 expression and ISG15 conjugation. Tretinoin 73-86 ISG15 ubiquitin like modifier Homo sapiens 95-100
16647867-7 2006 Blockade of the type I IFN receptor with a neutralizing antibody blocked retinoic acid induced ISG15 expression and ISG15 conjugation. Tretinoin 73-86 ISG15 ubiquitin like modifier Homo sapiens 116-121
16489341-7 2006 A retinoic-acid-reporter transgene marking the action of maternal retinoic acid in rescued Raldh2(-/-) embryos revealed that the targets of retinoic-acid signalling during somitogenesis are the node ectoderm and the posterior neural plate, not the presomitic mesoderm. Tretinoin 140-153 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 91-97
21425084-3 2011 By use of beta-galactosidase chemiluminescence, we show that a mouse Cdx1/lacZ reporter expressed in P19 EC cells responds to RA by the combined activities of an intron retinoic acid response element (RARE) and an upstream RARE. Tretinoin 169-182 caudal type homeobox 1 Mus musculus 69-73
21695257-0 2011 Leucine-rich repeat kinase 2 modulates retinoic acid-induced neuronal differentiation of murine embryonic stem cells. Tretinoin 39-52 leucine-rich repeat kinase 2 Mus musculus 0-28
16274701-4 2006 Similarly, the increase of Akt activation, as well as PTEN inactivation, was accompanied both by a decrease of CKIepsilon expression induced by all-trans retinoic acid and by the addition of a specific inhibitor for CKIepsilon in HL-60 cells. Tretinoin 154-167 TPTEP2-CSNK1E readthrough Homo sapiens 111-121
16424397-4 2006 We found that p38 mitogen-activated protein kinase (p38MAPK) activity peaked spontaneously, between day 3 and day 5, during ES cell differentiation and that RA completely inhibited this peak of activity. Tretinoin 157-159 mitogen-activated protein kinase 14 Mus musculus 52-59
16638120-9 2006 In NB4 cells undergoing retinoic acid mediated differentiation, the level of endogenous hARD1 and NATH protein decreases while the level of hARD2 protein is stable. Tretinoin 24-37 N-alpha-acetyltransferase 10, NatA catalytic subunit Homo sapiens 88-93
21695257-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: In the present study, differential gene expression profiling revealed a faster silencing of pluripotency-associated genes, like Nanog, Oct4, and Lin28, during retinoic acid-induced neuronal differentiation of LRRK2-deficient mouse embryonic stem cells compared to wildtype cultures. Tretinoin 191-204 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 167-171
21695257-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: In the present study, differential gene expression profiling revealed a faster silencing of pluripotency-associated genes, like Nanog, Oct4, and Lin28, during retinoic acid-induced neuronal differentiation of LRRK2-deficient mouse embryonic stem cells compared to wildtype cultures. Tretinoin 191-204 leucine-rich repeat kinase 2 Mus musculus 241-246
21159819-2 2010 We show that exogenous retinoic acid (RA), which dramatically truncates the embryo, represses expression of the zebrafish brachyury ortholog no tail (ntl), causing a failure to sustain the loop. Tretinoin 23-36 T-box transcription factor Tb Danio rerio 122-131
16707846-3 2006 A dramatic increase of TG2 expression and activation is induced by retinoic acid (RA). Tretinoin 67-80 transglutaminase 2 Rattus norvegicus 23-26
16707846-3 2006 A dramatic increase of TG2 expression and activation is induced by retinoic acid (RA). Tretinoin 82-84 transglutaminase 2 Rattus norvegicus 23-26
16707846-4 2006 Here we show the effect of the RA-induced overexpression of TG2 on liver regeneration after PH. Tretinoin 31-33 transglutaminase 2 Rattus norvegicus 60-63
16707846-9 2006 The treatment of RA greatly increased TG2 activity at 1 day after PH. Tretinoin 17-19 transglutaminase 2 Rattus norvegicus 38-41
16406622-0 2006 Inhibition of benzo(a)pyrene-induced cell cycle progression by all-trans retinoic acid partly through cyclin D1/E2F-1 pathway in human embryo lung fibroblasts. Tretinoin 73-86 cyclin D1 Homo sapiens 102-111
16406622-5 2006 There were almost no changes of CDK4 and E2F-4 expression by treatment with B(a)P. As expected, pretreatment with ATRA could efficiently decrease B(a)P-induced overexpression of cyclin D1 and E2F-1. Tretinoin 114-118 cyclin D1 Homo sapiens 178-187
21159819-2 2010 We show that exogenous retinoic acid (RA), which dramatically truncates the embryo, represses expression of the zebrafish brachyury ortholog no tail (ntl), causing a failure to sustain the loop. Tretinoin 38-40 T-box transcription factor Tb Danio rerio 122-131
16406622-8 2006 Pretreatment with ATRA, cells expressing antisense cyclinD1 or antisense CDK4 showed a lesser decrease of B(a)P-induced overexpression of E2F-1 compared with similarly treated HELF. Tretinoin 18-22 cyclin D1 Homo sapiens 51-59
16406622-8 2006 Pretreatment with ATRA, cells expressing antisense cyclinD1 or antisense CDK4 showed a lesser decrease of B(a)P-induced overexpression of E2F-1 compared with similarly treated HELF. Tretinoin 18-22 cyclin dependent kinase 4 Homo sapiens 73-77
16406622-10 2006 It was suggested that ATRA could block B(a)P-induced cell cycle promotion partly through the cyclin D1/E2F-1 pathway in HELF. Tretinoin 22-26 cyclin D1 Homo sapiens 93-102
20846163-4 2010 We reported recently that two substances (ATRA and thalidomide) have preventive effects on pulmonary fibrosis by inhibiting IL-6-dependent proliferation and TGF-beta1-dependent transdifferentiation of lung fibroblasts. Tretinoin 42-46 transforming growth factor, beta 1 Mus musculus 157-166
16439309-0 2006 Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Tretinoin 94-107 colony stimulating factor 1 receptor Homo sapiens 60-65
16439309-12 2006 This is the first indication to our knowledge that RA induces the expression of an adapter molecule to facilitate induced differentiation via co-operation between c-FMS and SLP-76. Tretinoin 51-53 colony stimulating factor 1 receptor Homo sapiens 163-168
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 162-175 nucleophosmin 1 Homo sapiens 68-71
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 177-181 nucleophosmin 1 Homo sapiens 68-71
21042705-3 2010 As CRBP1 regulates intracellular retinoic acid (vitamin A) homeostasis, which is involved in morphogenesis, and cellular proliferation and differentiation, the loss of CRBP1 could cause tumorigenesis in BC. Tretinoin 33-46 retinol binding protein 1 Homo sapiens 3-8
16452093-3 2006 To identify how RA signals to pancreatic progenitors in the endoderm, we have developed a novel cell transplantation technique, using the ability of the SOX32 transcription factor to confer endodermal identity, to selectively target reagents to (or exclude them from) the endodermal germ layer of the zebrafish. Tretinoin 16-18 SRY-box transcription factor 32 Danio rerio 153-158
16410076-0 2006 All-trans retinoic acid inhibited chondrogenesis of mouse embryonic palate mesenchymal cells by down-regulation of TGF-beta/Smad signaling. Tretinoin 10-23 SMAD family member 7 Mus musculus 124-128
16410076-8 2006 Further study showed that atRA inhibited phosphorylation of Smad2 and Smad3 and increased Smad7 expression. Tretinoin 26-30 SMAD family member 3 Mus musculus 70-75
16472598-8 2006 Expression of retinoic acid early inducible 1, the NKG2D ligand, was undetectable on quiescent hepatic stellate cells, whereas high levels were found on activated hepatic stellate cells, which correlated with the resistance and susceptibility of quiescent hepatic stellate cells and activated hepatic stellate cells to natural killer cell lysis, respectively. Tretinoin 14-27 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 51-56
16472598-11 2006 CONCLUSIONS: Our findings suggest that natural killer cells kill activated hepatic stellate cells via retinoic acid early inducible 1/NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent mechanisms, thereby ameliorating liver fibrosis. Tretinoin 102-115 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 134-139
16410076-8 2006 Further study showed that atRA inhibited phosphorylation of Smad2 and Smad3 and increased Smad7 expression. Tretinoin 26-30 SMAD family member 7 Mus musculus 90-95
21176354-4 2010 In order to investigate the role of IL-3 receptor system (IL-3Ralpha, GM-CSFRalpha and hbetac) in myeloid differentiation, the expression level of IL-3 receptor system gene in all-trans retinoic acid (ATRA)-induced NB4 cell differentiation was detected by quantitative real time RT-PCR. Tretinoin 201-205 colony stimulating factor 2 receptor subunit alpha Homo sapiens 70-82
16410076-9 2006 Activation of the Smad pathways by transfection with Smad7deltaC mutant or constitutively active TbetaRII retroviral vector abolished atRA-induced inhibition of chondrogenesis as indicated by Alcian blue staining, indicating that Smad signaling is essential for this response. Tretinoin 134-138 SMAD family member 7 Mus musculus 18-22
16410076-9 2006 Activation of the Smad pathways by transfection with Smad7deltaC mutant or constitutively active TbetaRII retroviral vector abolished atRA-induced inhibition of chondrogenesis as indicated by Alcian blue staining, indicating that Smad signaling is essential for this response. Tretinoin 134-138 SMAD family member 7 Mus musculus 53-58
16410076-9 2006 Activation of the Smad pathways by transfection with Smad7deltaC mutant or constitutively active TbetaRII retroviral vector abolished atRA-induced inhibition of chondrogenesis as indicated by Alcian blue staining, indicating that Smad signaling is essential for this response. Tretinoin 134-138 SMAD family member 7 Mus musculus 53-57
21176354-6 2010 The results showed that the expression level of IL-3Ralpha mRNA was obviously down-regulated in NB4 cells treated with ATRA for 24 hours, but during differentiation of ATRA induced NB4 cells, the expression level of IL-3Ralpha mRNA was gradually restored, while the expression levels of GM-CSFRalpha mRNA and hbetac mRNA were gradually up-regulated. Tretinoin 119-123 interleukin 3 receptor subunit alpha Homo sapiens 48-58
16470614-5 2006 Further studies revealed that the cellular role of qkI is to regulate visceral endoderm function, including the local synthesis of retinoic acid (RA) and the subsequent control of endothelial cell proliferation, matrix production, and visceral endoderm survival. Tretinoin 131-144 QKI, KH domain containing RNA binding Homo sapiens 51-54
21176354-6 2010 The results showed that the expression level of IL-3Ralpha mRNA was obviously down-regulated in NB4 cells treated with ATRA for 24 hours, but during differentiation of ATRA induced NB4 cells, the expression level of IL-3Ralpha mRNA was gradually restored, while the expression levels of GM-CSFRalpha mRNA and hbetac mRNA were gradually up-regulated. Tretinoin 119-123 interleukin 3 receptor subunit alpha Homo sapiens 216-226
16470614-5 2006 Further studies revealed that the cellular role of qkI is to regulate visceral endoderm function, including the local synthesis of retinoic acid (RA) and the subsequent control of endothelial cell proliferation, matrix production, and visceral endoderm survival. Tretinoin 146-148 QKI, KH domain containing RNA binding Homo sapiens 51-54
21176354-6 2010 The results showed that the expression level of IL-3Ralpha mRNA was obviously down-regulated in NB4 cells treated with ATRA for 24 hours, but during differentiation of ATRA induced NB4 cells, the expression level of IL-3Ralpha mRNA was gradually restored, while the expression levels of GM-CSFRalpha mRNA and hbetac mRNA were gradually up-regulated. Tretinoin 119-123 colony stimulating factor 2 receptor subunit alpha Homo sapiens 287-299
16428452-7 2006 Interaction between TGIF and RXRalpha is reduced by the addition of retinoic acid, consistent with a role for TGIF as an RXRalpha transcriptional corepressor. Tretinoin 68-81 retinoid X receptor alpha Mus musculus 29-37
21176354-6 2010 The results showed that the expression level of IL-3Ralpha mRNA was obviously down-regulated in NB4 cells treated with ATRA for 24 hours, but during differentiation of ATRA induced NB4 cells, the expression level of IL-3Ralpha mRNA was gradually restored, while the expression levels of GM-CSFRalpha mRNA and hbetac mRNA were gradually up-regulated. Tretinoin 168-172 interleukin 3 receptor subunit alpha Homo sapiens 48-58
16402912-4 2006 Together, their results demonstrate that (a) RXR/RAR heterodimers in which RXR is either transcriptionally active or silent are involved in the transduction of the RA signal during prenatal development, (b) specific RXRalpha/RAR heterodimers are required at many distinct stages during early embryogenesis and organogenesis, (c) the physiological role of RA and its receptors cannot be extrapolated from teratogenesis studies using retinoids in excess. Tretinoin 49-51 retinoid X receptor alpha Mus musculus 216-224
16291826-3 2006 atRA-induced apoptosis is associated with activation of the initiator caspase-9 and the effector caspase-3, but not of the effector caspase-8. Tretinoin 0-4 caspase 9 Mus musculus 70-79
21152098-0 2010 Identification of retinoic acid in a high content screen for agents that overcome the anti-myogenic effect of TGF-beta-1. Tretinoin 18-31 transforming growth factor, beta 1 Mus musculus 110-120
16316642-8 2006 We propose that, in the developing embryo, localised synthesis of RA by Raldh2 in the anterior psm and in somites activates fgf8 expression which in turn induces the expression of myogenic genes and fast muscle differentiation. Tretinoin 66-68 aldehyde dehydrogenase 1 family, member A2 Danio rerio 72-78
16850740-13 2006 Western blotting showed that the amounts of JNK, p38 and ERK proteins in hyperoxia-exposure or RA-treated lung tissues were same as those in untreated lung tissues (P>0.05), whereas activation of these MAPKs was markedly altered by hyperoxia and RA. Tretinoin 95-97 mitogen activated protein kinase 14 Rattus norvegicus 49-52
16368932-0 2006 Retinaldehyde dehydrogenase 2 (RALDH2)-mediated retinoic acid synthesis regulates early mouse embryonic forebrain development by controlling FGF and sonic hedgehog signaling. Tretinoin 48-61 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 0-29
21152098-7 2010 Only all-trans retinoic acid and 9-cis retinoic acid allowed a maximal level of C2C12 cell differentiation in the presence of TGF-beta1; the angiotensin-converting enzyme inhibitor captopril and 10 nM estrogen provided partial rescue. Tretinoin 15-28 transforming growth factor, beta 1 Mus musculus 126-135
16368932-0 2006 Retinaldehyde dehydrogenase 2 (RALDH2)-mediated retinoic acid synthesis regulates early mouse embryonic forebrain development by controlling FGF and sonic hedgehog signaling. Tretinoin 48-61 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 31-37
21152098-8 2010 Vitamin D was a potent inhibitor of retinoic acid-induced myogenesis in the presence of TGF-beta1. Tretinoin 36-49 transforming growth factor, beta 1 Mus musculus 88-97
16368932-2 2006 We show that the retinaldehyde dehydrogenase 2 (RALDH2) enzyme is responsible for RA synthesis in the mouse craniofacial region and forebrain between the 8- and 15-somite stages. Tretinoin 48-50 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 17-46
21152098-10 2010 CONCLUSIONS/SIGNIFICANCE: Retinoic acid alleviated the anti-myogenic effect of TGF-beta1 by a Smad3-independent mechanism. Tretinoin 26-39 transforming growth factor, beta 1 Mus musculus 79-88
16159706-2 2006 At the embryonic level, Cyp enzymes are involved also in the catabolism of the retinoic acid. Tretinoin 79-92 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 24-27
21152098-10 2010 CONCLUSIONS/SIGNIFICANCE: Retinoic acid alleviated the anti-myogenic effect of TGF-beta1 by a Smad3-independent mechanism. Tretinoin 26-39 SMAD family member 3 Mus musculus 94-99
20702525-10 2010 CONCLUSIONS: In endometrial stromal cells, progesterone receptor up-regulates expression of STRA6 and CRABP2, which control retinol uptake and growth-suppressor actions of RA. Tretinoin 94-96 progesterone receptor Homo sapiens 43-64
16275619-4 2005 RA enhanced the immunoglobulin synthesis by tonsillar B cells in anti-CD40 plus IL-10-mediated culture system. Tretinoin 0-2 CD40 molecule Homo sapiens 70-74
16403262-1 2005 The retinoid N-4-hydroxyphenyl retinamide (4-HPR also known as fenretinide), a synthetic derivative of all trans retinoic acid (ATRA), has shown as an efficient chemopreventive, chemotherapeutic agent and a potent inducer of apoptosis in various cancer cell types in vitro, including leukemic cells. Tretinoin 107-126 haptoglobin-related protein Homo sapiens 45-48
16809920-4 2006 Moreover, BMP-4 mediates the antiproliferative action of retinoic acid in these cells. Tretinoin 57-70 bone morphogenetic protein 4 Homo sapiens 10-15
20709030-10 2010 Our in vitro results suggested that Abeta42 oligomer-induced miR-106b leads to impairment in TGF-beta signaling through TbetaR II, concomitant with retinoic acid-induced neurodegeneration in SH-SY5Y cells. Tretinoin 148-161 transforming growth factor alpha Homo sapiens 93-101
16403262-1 2005 The retinoid N-4-hydroxyphenyl retinamide (4-HPR also known as fenretinide), a synthetic derivative of all trans retinoic acid (ATRA), has shown as an efficient chemopreventive, chemotherapeutic agent and a potent inducer of apoptosis in various cancer cell types in vitro, including leukemic cells. Tretinoin 128-132 haptoglobin-related protein Homo sapiens 45-48
17090972-3 2006 In MtT/S cells, triiodothyronine (T3), all-trans retinoic acid (RA) and 9-cis retinoic acid (9cRA) stimulated GH promoter activity but dexamethasone (DEX) did not. Tretinoin 39-62 gonadotropin releasing hormone receptor Rattus norvegicus 110-112
16197938-7 2005 An enzyme involved in RA synthesis, RALDH2, was immunocytochemically localized to retinal progenitor cells and the retinal pigmented epithelium (RPE), suggesting the presence of RA in the vicinity of developing photoreceptors. Tretinoin 22-24 aldehyde dehydrogenase 1 family, member A2 Danio rerio 36-42
20709030-10 2010 Our in vitro results suggested that Abeta42 oligomer-induced miR-106b leads to impairment in TGF-beta signaling through TbetaR II, concomitant with retinoic acid-induced neurodegeneration in SH-SY5Y cells. Tretinoin 148-161 transforming growth factor beta receptor 2 Homo sapiens 120-129
20841484-10 2010 We conclude that functionally important, miRNA-mediated DNA demethylation changes contribute to the process of ATRA-induced differentiation resulting in the activation of NOS1, a critical determinant of neural cell differentiation. Tretinoin 111-115 nitric oxide synthase 1 Homo sapiens 171-175
16207763-1 2005 Using genetic approaches in the mouse, we show that the primary target tissue of retinoic acid (RA) action during eye morphogenesis is not the retina nor the corneal ectoderm, which both express RA-synthesizing retinaldehyde dehydrogenases (RALDH1 and RALDH3), but the neural crest cell-derived periocular mesenchyme (POM), which is devoid of RALDH. Tretinoin 81-94 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 241-247
16207763-1 2005 Using genetic approaches in the mouse, we show that the primary target tissue of retinoic acid (RA) action during eye morphogenesis is not the retina nor the corneal ectoderm, which both express RA-synthesizing retinaldehyde dehydrogenases (RALDH1 and RALDH3), but the neural crest cell-derived periocular mesenchyme (POM), which is devoid of RALDH. Tretinoin 96-98 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 241-247
16207763-2 2005 In POM, the effects of the paracrine RA signal are mediated by the nuclear RA receptors heterodimers RXRalpha/RARbeta and RXRalpha/RARgamma. Tretinoin 37-39 retinoid X receptor alpha Mus musculus 101-109
16207763-2 2005 In POM, the effects of the paracrine RA signal are mediated by the nuclear RA receptors heterodimers RXRalpha/RARbeta and RXRalpha/RARgamma. Tretinoin 37-39 retinoic acid receptor, beta Mus musculus 110-117
16207763-2 2005 In POM, the effects of the paracrine RA signal are mediated by the nuclear RA receptors heterodimers RXRalpha/RARbeta and RXRalpha/RARgamma. Tretinoin 37-39 retinoid X receptor alpha Mus musculus 122-130
16898870-13 2006 beta-Carotene-induced changes in RARbeta isoform gene expression levels were not predictive for the number of lung tumors but were indicative of intact beta-carotene metabolism and persistent sensitivity to retinoic acid in the mice. Tretinoin 207-220 retinoic acid receptor, beta Mus musculus 33-40
16050810-12 2005 CBP and PCAF occupancy of the proximal ERK1 promoter was dramatically decreased by RA treatment. Tretinoin 83-85 lysine acetyltransferase 2B Homo sapiens 8-12
16134180-1 2005 BACKGROUND: Hypermethylation of CpG islands has been associated with silencing of various tumor suppressor genes, and the retinoid acid receptor beta (RARbeta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) genes have been associated with retinoic acid signaling. Tretinoin 274-287 retinol binding protein 1 Homo sapiens 197-202
20525643-10 2010 Conversely, blockage of dopamine biosynthesis and loss of TH activity decreased AMHC1 and Tbx5 expression, whereas exposure to retinoic acid (RA) induced TH expression in parallel to that of AMHC1 and Tbx5. Tretinoin 127-140 tyrosine hydroxylase Gallus gallus 154-156
16316409-8 2005 As CRABPI was elevated far more than any other genes, we observed that the retinoids, all-trans retinoic acid and 9-cis retinoic acid, that bind CRABPI, promoted nitroblue tetrazolium-associated functional cell differentiation in p75NTR PC-3 cells, but not in neo control PC-3 cells. Tretinoin 96-109 cellular retinoic acid binding protein 1 Homo sapiens 3-9
16325577-3 2005 The two factors compete for binding to the miR-223 promoter: NFI-A maintains miR-223 at low levels, whereas its replacement by C/EBPalpha, following retinoic acid (RA)-induced differentiation, upregulates miR-223 expression. Tretinoin 149-162 microRNA 223 Homo sapiens 43-50
16325577-3 2005 The two factors compete for binding to the miR-223 promoter: NFI-A maintains miR-223 at low levels, whereas its replacement by C/EBPalpha, following retinoic acid (RA)-induced differentiation, upregulates miR-223 expression. Tretinoin 164-166 microRNA 223 Homo sapiens 43-50
20525643-10 2010 Conversely, blockage of dopamine biosynthesis and loss of TH activity decreased AMHC1 and Tbx5 expression, whereas exposure to retinoic acid (RA) induced TH expression in parallel to that of AMHC1 and Tbx5. Tretinoin 127-140 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 191-196
20525643-10 2010 Conversely, blockage of dopamine biosynthesis and loss of TH activity decreased AMHC1 and Tbx5 expression, whereas exposure to retinoic acid (RA) induced TH expression in parallel to that of AMHC1 and Tbx5. Tretinoin 142-144 tyrosine hydroxylase Gallus gallus 154-156
16266505-1 2005 OBJECTIVE: To investigate the reverse effect of all-trans retinoic acid (ATRA) on Benzo (a) pyrene (B (a) P)-induced cyclin D1, CDK4, E2F-1 and E2F-4 expression and cell cycle progression in human embryo lung fibroblast (HELF). Tretinoin 73-77 E2F transcription factor 1 L homeolog Xenopus laevis 134-149
20525643-10 2010 Conversely, blockage of dopamine biosynthesis and loss of TH activity decreased AMHC1 and Tbx5 expression, whereas exposure to retinoic acid (RA) induced TH expression in parallel to that of AMHC1 and Tbx5. Tretinoin 142-144 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 191-196
16266505-4 2005 CONCLUSION: ATRA could block B (a) P-induced cell cycle promotion through cyclin D1/E2F-1 pathway in HELF. Tretinoin 12-16 E2F transcription factor 1 L homeolog Xenopus laevis 84-89
16150056-3 2005 Here, we demonstrate that RA also affects the processing of APLP2 and APP, as shown by increased shedding of both sAPLP2 and sAPPalpha, as well as elevated levels of the APP intracellular domains (AICDs). Tretinoin 26-28 amyloid beta precursor like protein 2 Homo sapiens 60-65
20525643-11 2010 Concordantly, inhibition of endogenous RA synthesis decreased TH expression as well as that of AMHC1 and Tbx5. Tretinoin 39-41 tyrosine hydroxylase Gallus gallus 62-64
16150056-4 2005 Brain-derived neurotrophic factor (BDNF) has been reported to induce APP promoter activity and RA induces expression of the tyrosine kinase receptor B (TrkB) in neuroblastoma cells. Tretinoin 95-97 neurotrophic receptor tyrosine kinase 2 Homo sapiens 124-150
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 forkhead box P3 Homo sapiens 148-153
16150056-4 2005 Brain-derived neurotrophic factor (BDNF) has been reported to induce APP promoter activity and RA induces expression of the tyrosine kinase receptor B (TrkB) in neuroblastoma cells. Tretinoin 95-97 neurotrophic receptor tyrosine kinase 2 Homo sapiens 152-156
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 interleukin 27 Homo sapiens 218-223
16150056-5 2005 We show that the increase in shedding of both APLP2 and APP in response to RA is not mediated through the TrkB receptor. Tretinoin 75-77 amyloid beta precursor like protein 2 Homo sapiens 46-51
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 SMAD family member 3 Homo sapiens 334-339
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 forkhead box P3 Homo sapiens 148-153
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 interleukin 27 Homo sapiens 218-223
20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 SMAD family member 3 Homo sapiens 334-339
16162334-3 2005 We analyzed the in vitro differentiation of mouse embryonic stem cells deficient of GATA factors and conclude that GATA-4 is required for ES cells to perceive a cell positioning (cell aggregation) signal and GATA-6 is required to sense morphogenic (retinoic acid) signal. Tretinoin 249-262 glutaminyl-tRNA synthase (glutamine-hydrolyzing)-like 1 Mus musculus 84-88
20619784-7 2010 Therefore, by using lentiviral vector-based short hairpin RNA targeting RHAMM, the study further reveals that knockdown of RHAMM obviously inhibits the ciliary differentiation of RECs on collagen with RA and on HYAFF with/without RA. Tretinoin 201-203 hyaluronan mediated motility receptor Homo sapiens 123-128
16142318-1 2005 The P19 mouse embryonal carcinoma cell line was used as a model for a study of apoptosis accompanying differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 129-152 interleukin 23, alpha subunit p19 Mus musculus 4-7
16102743-6 2005 We show that early zebrafish rhombomere-specification genes, including vhnf1 in r5-r6 and hoxd4a in r7, initiate expression sequentially in the hindbrain, each adjacent to the source of RA synthesis in paraxial mesoderm. Tretinoin 186-188 HNF1 homeobox Ba Danio rerio 71-76
20619784-8 2010 In addition to demonstrating that hyaluronan-based biomaterials partially "replace" RA in the ciliary differentiation of RECs, which is regulated by RHAMM, this study establishes that RHAMM regulates the ciliary differentiation-promoting effect of RA on RECs. Tretinoin 248-250 hyaluronan mediated motility receptor Homo sapiens 184-189
16142318-1 2005 The P19 mouse embryonal carcinoma cell line was used as a model for a study of apoptosis accompanying differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 154-158 interleukin 23, alpha subunit p19 Mus musculus 4-7
20557428-6 2010 The anti-inflammatory activity of RA engaged RA and retinoid X receptors and correlated with a decreased expression of the lipopolysaccharides co-receptor CD14. Tretinoin 34-36 CD14 antigen Mus musculus 155-159
16166633-0 2005 Orphan nuclear receptor GCNF is required for the repression of pluripotency genes during retinoic acid-induced embryonic stem cell differentiation. Tretinoin 89-102 nuclear receptor subfamily 6, group A, member 1 Mus musculus 24-28
16166633-6 2005 Loss of repression of ES cell marker genes Oct4, Nanog, Sox2, FGF4, and Stella was observed upon treatment of GCNF-/- ES cells with retinoic acid. Tretinoin 132-145 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 43-47
16102743-6 2005 We show that early zebrafish rhombomere-specification genes, including vhnf1 in r5-r6 and hoxd4a in r7, initiate expression sequentially in the hindbrain, each adjacent to the source of RA synthesis in paraxial mesoderm. Tretinoin 186-188 homeobox D4a Danio rerio 90-96
16102743-7 2005 By knocking down RA signaling, we show that progressively more posterior rhombomeres require increasingly higher levels of RA signaling, and vhnf1 and hoxd4a expression are particularly RA-dependent. Tretinoin 17-19 HNF1 homeobox Ba Danio rerio 141-146
16102743-7 2005 By knocking down RA signaling, we show that progressively more posterior rhombomeres require increasingly higher levels of RA signaling, and vhnf1 and hoxd4a expression are particularly RA-dependent. Tretinoin 17-19 homeobox D4a Danio rerio 151-157
16102743-8 2005 RA synthesis is required just at the time of initiation, but not for maintenance, of vhnf1 and hoxd4a expression. Tretinoin 0-2 homeobox D4a Danio rerio 95-101
16102743-9 2005 Furthermore, a premature RA increase causes premature activation of vhnf1 and hoxd4a expression. Tretinoin 25-27 HNF1 homeobox Ba Danio rerio 68-73
16102743-9 2005 Furthermore, a premature RA increase causes premature activation of vhnf1 and hoxd4a expression. Tretinoin 25-27 homeobox D4a Danio rerio 78-84
20735826-8 2010 Retinoic acid (RA) is one of the most important morphogens involved in striatal neurogenesis, and regulates Nolz1 expression in different systems. Tretinoin 0-13 zinc finger protein 503 Mus musculus 108-113
20735826-8 2010 Retinoic acid (RA) is one of the most important morphogens involved in striatal neurogenesis, and regulates Nolz1 expression in different systems. Tretinoin 15-17 zinc finger protein 503 Mus musculus 108-113
20735826-12 2010 These findings suggest that Nolz1 might act downstream of Gsx2 to regulate RA-induced neurogenesis. Tretinoin 75-77 zinc finger protein 503 Mus musculus 28-33
15860641-1 2005 Alcohol dehydrogenase (ADH) participates in the formation of retinoic acid from retinol in various organs including the gastric mucosa. Tretinoin 61-74 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 23-26
16109390-5 2005 Mice absent in the three proteins CRBP I, CRABP I, and CRABP II (CI/CAI/CAII-/-) displayed significantly lower hepatic retinyl ester, retinol, and all-trans-retinoic acid levels compared to wildtype mice, whereas the liver concentrations of 9-cis-4-oxo-13,14-dihydro-retinoic acid was considerably higher. Tretinoin 151-170 cellular retinoic acid binding protein II Mus musculus 55-63
20735826-15 2010 This RA signaling is essential for Nolz1-induced neurogenesis, which is impaired in a RA-free environment or in the presence of a RAR inverse agonist. Tretinoin 5-7 zinc finger protein 503 Mus musculus 35-40
15860641-0 2005 Retinoic acid formation from retinol in the human gastric mucosa: role of class IV alcohol dehydrogenase and its relevance to morphological changes. Tretinoin 0-13 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 74-104
15860641-3 2005 In this study, we identified the ADH isoforms responsible for the retinoic acid formation among various ADH isoforms and examined associations among the ADH activities, the retinoic acid formation level, and morphological changes in the human gastric mucosa. Tretinoin 66-79 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 33-36
15860641-3 2005 In this study, we identified the ADH isoforms responsible for the retinoic acid formation among various ADH isoforms and examined associations among the ADH activities, the retinoic acid formation level, and morphological changes in the human gastric mucosa. Tretinoin 66-79 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 104-107
20735826-18 2010 CONCLUSIONS: Nolz1 promotes RA signaling in the LGE, contributing to the striatal neurogenesis during development. Tretinoin 28-30 zinc finger protein 503 Mus musculus 13-18
15860641-3 2005 In this study, we identified the ADH isoforms responsible for the retinoic acid formation among various ADH isoforms and examined associations among the ADH activities, the retinoic acid formation level, and morphological changes in the human gastric mucosa. Tretinoin 66-79 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 104-107
15860641-7 2005 Among activities of the three ADH isoforms, class IV ADH activity was solely associated with the ATRA formation level. Tretinoin 97-101 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 30-33
20547768-0 2010 Vitamin A metabolite, all-trans-retinoic acid, mediates alternative splicing of protein kinase C deltaVIII (PKCdeltaVIII) isoform via splicing factor SC35. Tretinoin 22-45 protein kinase C delta Homo sapiens 80-154
16128742-2 2005 Retinoic acid receptor-beta (RAR-beta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) have been linked to retinoic acid signaling. Tretinoin 141-154 retinol binding protein 1 Homo sapiens 40-74
16128742-2 2005 Retinoic acid receptor-beta (RAR-beta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) have been linked to retinoic acid signaling. Tretinoin 141-154 retinol binding protein 1 Homo sapiens 76-81
15967793-7 2005 Further, we have found that although APC mutants are deficient in rdh1l expression, they harbor increased expression of raldh2 suggesting the control of RA production by APC is via retinol dehydrogenase activity. Tretinoin 153-155 aldehyde dehydrogenase 1 family, member A2 Danio rerio 120-126
16350840-5 2005 In this study, we show that RA suppresses the cell growth, cartilage nodule formation, accumulation of proteoglycan, alkaline phosphatase (ALPase) activity and mineralization and that RA dose dependently upregulates the levels of type X collagen and matrix metalloproteinase-13 (MMP-13) mRNA which are marker proteins of hypertrophic chondrocytes, in ATDC5 cells. Tretinoin 28-30 matrix metallopeptidase 13 Mus musculus 279-285
16350840-5 2005 In this study, we show that RA suppresses the cell growth, cartilage nodule formation, accumulation of proteoglycan, alkaline phosphatase (ALPase) activity and mineralization and that RA dose dependently upregulates the levels of type X collagen and matrix metalloproteinase-13 (MMP-13) mRNA which are marker proteins of hypertrophic chondrocytes, in ATDC5 cells. Tretinoin 184-186 matrix metallopeptidase 13 Mus musculus 279-285
20547768-4 2010 RA regulates the splicing and expression of PKCdeltaVIII via utilization of a downstream 5" splice site of exon 10 on PKCdelta pre-mRNA. Tretinoin 0-2 protein kinase C delta Homo sapiens 44-52
16096774-4 2005 Recent studies in vitro show that retinoic acid (RA) downregulates the release of MCP-1 and TGF-beta1 by tumor cells. Tretinoin 34-47 transforming growth factor, beta 1 Mus musculus 92-101
15950969-3 2005 Previously, we described a system of retinoic acid (RA) synthesis in the cycling rat uterus consisting of cellular retinol binding protein (Crbp), epithelial retinol dehydrogenase (eRoldh), retinal dehydrogenase 2 (Aldh1a2), and cellular retinoic acid binding protein type II (Crabp2). Tretinoin 52-54 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 215-222
16096774-4 2005 Recent studies in vitro show that retinoic acid (RA) downregulates the release of MCP-1 and TGF-beta1 by tumor cells. Tretinoin 49-51 transforming growth factor, beta 1 Mus musculus 92-101
20547768-10 2010 Mutation of the SC35 binding site in the PKCdelta minigene abolished RA-mediated utilization of 5" splice splice II. Tretinoin 69-71 serine and arginine rich splicing factor 2 Homo sapiens 16-20
20547768-10 2010 Mutation of the SC35 binding site in the PKCdelta minigene abolished RA-mediated utilization of 5" splice splice II. Tretinoin 69-71 protein kinase C delta Homo sapiens 41-49
20716331-10 2010 In serum-containing medium, the expression percentages of CD133 and GFAP in the differentiated BTSCs were (2.29% +/- 0.27%) and (75.60% +/- 4.03%) respectively in the ATRA group, and (7.05% +/- 0.49%) and (12.51% +/- 0.77%) respectively in the control group. Tretinoin 167-171 prominin 1 Homo sapiens 58-63
15950488-0 2005 Retinoic acid negatively regulates GDNF and neurturin receptor expression and responsiveness in embryonic chicken sympathetic neurons. Tretinoin 0-13 glial cell derived neurotrophic factor Gallus gallus 35-39
15950488-4 2005 RA caused a dose-dependent decrease in the survival response to both GDNF and neurturin. Tretinoin 0-2 glial cell derived neurotrophic factor Gallus gallus 69-73
15817812-9 2005 Finally, the activity of FXR was mapped to a retinoic acid response element (RARE) site containing an imbedded farnesoid X response element (FXRE) on the human ICAM-1 promoter and FXR and retinoid X receptor were demonstrated to bind to this site. Tretinoin 45-58 nuclear receptor subfamily 1 group H member 4 Homo sapiens 25-28
15817812-9 2005 Finally, the activity of FXR was mapped to a retinoic acid response element (RARE) site containing an imbedded farnesoid X response element (FXRE) on the human ICAM-1 promoter and FXR and retinoid X receptor were demonstrated to bind to this site. Tretinoin 45-58 nuclear receptor subfamily 1 group H member 4 Homo sapiens 141-144
15950488-5 2005 Transcripts for the ligand-specifying receptors for GDNF and neurturin, GFRalpha-1 and GFRalpha-2, as well as the common signal transducing receptor Ret were all down-regulated by RA treatment in a dose-dependent manner. Tretinoin 180-182 glial cell derived neurotrophic factor Gallus gallus 52-56
20716331-11 2010 The differentiation rate of BTSCs in the ATRA group was significantly higher than that in the control group (P < 0.05), but there was still CD133 expressed in the ATRA group. Tretinoin 166-170 prominin 1 Homo sapiens 143-148
15950488-8 2005 These findings implicate RA in regulating the actions of members of the GDNF family on developing sympathetic neurons. Tretinoin 25-27 glial cell derived neurotrophic factor Gallus gallus 72-76
20673043-1 2010 PURPOSE: To examine the effect of all-trans retinoic acid (ATRA) treatment on connexin 43 (Cx43) expression, gap junction intercellular communication (GJIC), and cellular differentiation in primary canine lens epithelial cells (LEC). Tretinoin 59-63 gap junction protein alpha 1 Canis lupus familiaris 78-89
15928487-8 2005 Gut dendritic cells and retinoic acid induce the expression of alpha4beta7 and CCR9 on T cells for their homing to the gut. Tretinoin 24-37 C-C motif chemokine receptor 9 Homo sapiens 79-83
16019559-6 2005 We also examined the expression of hoxC4 in bone marrow cells from APL patients and found that the hoxC4 expression was reproducibly induced during an ATRA treatment. Tretinoin 151-155 homeobox C4 Homo sapiens 35-40
16019559-6 2005 We also examined the expression of hoxC4 in bone marrow cells from APL patients and found that the hoxC4 expression was reproducibly induced during an ATRA treatment. Tretinoin 151-155 homeobox C4 Homo sapiens 99-104
16019559-8 2005 The NB4 cells expressing HoxC4 showed differentiated phenotypes including a CD14 expression, which strongly suggests that upregulated hoxC4 is functionally involved in NB4 cell differentiation in response to ATRA. Tretinoin 208-212 homeobox C4 Homo sapiens 25-30
16019559-8 2005 The NB4 cells expressing HoxC4 showed differentiated phenotypes including a CD14 expression, which strongly suggests that upregulated hoxC4 is functionally involved in NB4 cell differentiation in response to ATRA. Tretinoin 208-212 CD14 molecule Homo sapiens 76-80
16019559-8 2005 The NB4 cells expressing HoxC4 showed differentiated phenotypes including a CD14 expression, which strongly suggests that upregulated hoxC4 is functionally involved in NB4 cell differentiation in response to ATRA. Tretinoin 208-212 homeobox C4 Homo sapiens 134-139
20673043-1 2010 PURPOSE: To examine the effect of all-trans retinoic acid (ATRA) treatment on connexin 43 (Cx43) expression, gap junction intercellular communication (GJIC), and cellular differentiation in primary canine lens epithelial cells (LEC). Tretinoin 59-63 gap junction protein alpha 1 Canis lupus familiaris 91-95
20673043-4 2010 RESULTS: Treatment with ATRA at non-cytotoxic concentrations significantly increased Cx43 protein, mRNA and GJIC in primary canine LEC. Tretinoin 24-28 gap junction protein alpha 1 Canis lupus familiaris 85-89
20673043-6 2010 Inhibition of GJIC via pre-treatment with a synthetic inhibitor, 18-alpha glycyrrethinic acid (AGA), reduced ATRA-induced increases in Cx43 and GJIC and partially blocked ATRA-induced beta crystallin protein. Tretinoin 109-113 gap junction protein alpha 1 Canis lupus familiaris 135-139
15882811-5 2005 We also analyzed FSCN1 expression profile during NT2 neuronal differentiation induced by retinoic acid (RA), showing that FSCN1 was up-regulated during neurogenesis. Tretinoin 89-102 fascin actin-bundling protein 1 Homo sapiens 17-22
15811935-0 2005 Up-regulation of gap junctional intercellular communication and connexin43 expression by retinoic acid in human endometrial stromal cells. Tretinoin 89-102 gap junction protein alpha 1 Homo sapiens 64-74
15882811-5 2005 We also analyzed FSCN1 expression profile during NT2 neuronal differentiation induced by retinoic acid (RA), showing that FSCN1 was up-regulated during neurogenesis. Tretinoin 89-102 fascin actin-bundling protein 1 Homo sapiens 122-127
20673043-7 2010 CONCLUSIONS: Treatment with ATRA significantly increased Cx43 expression and GJIC in canine LEC, and these effects were associated with increased LEC differentiation. Tretinoin 28-32 gap junction protein alpha 1 Canis lupus familiaris 57-61
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 132-145 integrin subunit alpha X Homo sapiens 18-23
20338915-0 2010 Retinoic acid represses CYP7A1 expression in human hepatocytes and HepG2 cells by FXR/RXR-dependent and independent mechanisms. Tretinoin 0-13 nuclear receptor subfamily 1 group H member 4 Homo sapiens 82-85
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 132-145 CD14 molecule Homo sapiens 29-33
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 fibroblast growth factor 19 Homo sapiens 140-167
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 fibroblast growth factor 19 Homo sapiens 169-174
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 147-149 CD14 molecule Homo sapiens 29-33
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 nuclear receptor subfamily 0 group B member 2 Homo sapiens 207-210
15882811-5 2005 We also analyzed FSCN1 expression profile during NT2 neuronal differentiation induced by retinoic acid (RA), showing that FSCN1 was up-regulated during neurogenesis. Tretinoin 104-106 fascin actin-bundling protein 1 Homo sapiens 122-127
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 nuclear receptor subfamily 1 group H member 4 Homo sapiens 277-280
20338915-7 2010 Knocking down of FXR or RXRalpha by small interference RNA (siRNA) in human hepatocytes increased CYP7A1 basal expression, but the repressive effect of atRA persisted, suggesting there are also FXR/RXR-independent mechanisms mediating atRA repression of CYP7A1 expression. Tretinoin 152-156 nuclear receptor subfamily 1 group H member 4 Homo sapiens 17-20
20034809-1 2010 Clinical trials have revealed that N-(4-hydroxyphenyl) retinamide (4HPR; fenretinide), a synthetic retinoic acid derivative, is a highly active and promising therapeutic and chemopreventive agent. Tretinoin 99-112 haptoglobin-related protein Homo sapiens 68-71
15872003-1 2005 Retinoic acid (RA) generated by Raldh2 in paraxial mesoderm is required for specification of the posterior hindbrain, including restriction of Hoxb1 expression to presumptive rhombomere 4 (r4). Tretinoin 0-13 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 32-38
15872003-1 2005 Retinoic acid (RA) generated by Raldh2 in paraxial mesoderm is required for specification of the posterior hindbrain, including restriction of Hoxb1 expression to presumptive rhombomere 4 (r4). Tretinoin 0-13 homeobox B1 Mus musculus 143-148
15872003-1 2005 Retinoic acid (RA) generated by Raldh2 in paraxial mesoderm is required for specification of the posterior hindbrain, including restriction of Hoxb1 expression to presumptive rhombomere 4 (r4). Tretinoin 15-17 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 32-38
15872003-1 2005 Retinoic acid (RA) generated by Raldh2 in paraxial mesoderm is required for specification of the posterior hindbrain, including restriction of Hoxb1 expression to presumptive rhombomere 4 (r4). Tretinoin 15-17 homeobox B1 Mus musculus 143-148
15872003-6 2005 Analysis of Raldh2-/- and vHnf1-/- embryos supports a direct role for RA in Hoxb1 induction up to r4 and repression in r3/r5, as well as an indirect role for RA in Hoxb1 repression posterior to r4 via RA induction of vHnf1 up to the r4/r5 boundary. Tretinoin 70-72 homeobox B1 Mus musculus 76-81
15891578-3 2005 Here, we show that retinoic acid-induced neurite outgrowth in MN9D dopaminergic neuronal cells was accompanied by activation of c-Jun N-terminal kinase but not p38. Tretinoin 19-32 mitogen-activated protein kinase 14 Mus musculus 160-163
20577838-5 2010 These data suggested that miR-146a might influence proliferation of APL cells through TGF-beta1/Smad signal transduction pathway during ATRA induction. Tretinoin 136-140 SMAD family member 4 Homo sapiens 96-100
15809060-7 2005 However, the RA-mediated induction of C/EBPbeta in cells expressing the DeltaC-C mutant was comparable to that of control cells. Tretinoin 13-15 CCAAT enhancer binding protein beta Homo sapiens 38-47
16158929-6 2005 The sensitivity of leukemia cells to 4-HPR could be modulated, either by increasing intracellular glutathione contents using all-trans retinoic acid (ATRA), or by decreasing it using DL-buthionine-S,R-sulfoximine (BSO). Tretinoin 125-148 haptoglobin-related protein Homo sapiens 39-42
15907702-1 2005 Binding of all-trans Retinoic Acid (RA) to Cellular Retinoic Acid Binding Protein I (CRABP I) does not result in significant changes of the protein tertiary structure, even though the binding site is inaccessible in a static apo-protein conformation. Tretinoin 21-34 cellular retinoic acid binding protein 1 Homo sapiens 43-83
15907702-1 2005 Binding of all-trans Retinoic Acid (RA) to Cellular Retinoic Acid Binding Protein I (CRABP I) does not result in significant changes of the protein tertiary structure, even though the binding site is inaccessible in a static apo-protein conformation. Tretinoin 21-34 cellular retinoic acid binding protein 1 Homo sapiens 85-92
15907702-1 2005 Binding of all-trans Retinoic Acid (RA) to Cellular Retinoic Acid Binding Protein I (CRABP I) does not result in significant changes of the protein tertiary structure, even though the binding site is inaccessible in a static apo-protein conformation. Tretinoin 36-38 cellular retinoic acid binding protein 1 Homo sapiens 43-83
15907702-1 2005 Binding of all-trans Retinoic Acid (RA) to Cellular Retinoic Acid Binding Protein I (CRABP I) does not result in significant changes of the protein tertiary structure, even though the binding site is inaccessible in a static apo-protein conformation. Tretinoin 36-38 cellular retinoic acid binding protein 1 Homo sapiens 85-92
15907702-3 2005 In this work, RA binding to CRABP I is studied in dilute solutions (low micro-molar range), where no dimer and/or oligomer formation occurs. Tretinoin 14-16 cellular retinoic acid binding protein 1 Homo sapiens 28-35
16158929-6 2005 The sensitivity of leukemia cells to 4-HPR could be modulated, either by increasing intracellular glutathione contents using all-trans retinoic acid (ATRA), or by decreasing it using DL-buthionine-S,R-sulfoximine (BSO). Tretinoin 150-154 haptoglobin-related protein Homo sapiens 39-42
20075418-0 2010 Retinoic acid modulates the subcellular localization of small ubiquitin-related modifier-2/3 (SUMO-2/3) in the testis. Tretinoin 0-13 small ubiquitin-like modifier 2 Rattus norvegicus 56-92
15814302-0 2005 Regulation of the human tissue-nonspecific alkaline phosphatase gene expression by all-trans-retinoic acid in SaOS-2 osteosarcoma cell line. Tretinoin 86-106 alkaline phosphatase, biomineralization associated Homo sapiens 24-63
15878332-3 2005 We have previously demonstrated that the amount and the tyrosine phosphorylation of Vav are up-regulated in both whole cells and nuclei of tumoral promyelocytes induced to granulocytic maturation by ATRA and that tyrosine-phosphorylated Vav does not display any ATRA-induced GEF activity but contributes to the regulation of PI 3-K activity. Tretinoin 199-203 vav guanine nucleotide exchange factor 1 Homo sapiens 84-87
15878332-3 2005 We have previously demonstrated that the amount and the tyrosine phosphorylation of Vav are up-regulated in both whole cells and nuclei of tumoral promyelocytes induced to granulocytic maturation by ATRA and that tyrosine-phosphorylated Vav does not display any ATRA-induced GEF activity but contributes to the regulation of PI 3-K activity. Tretinoin 262-266 vav guanine nucleotide exchange factor 1 Homo sapiens 84-87
15878332-4 2005 In this study, we report that Vav accumulates in nuclei of ATRA-treated APL-derived cells and that the down-modulation of Vav prevents differentiation of tumoral promyelocytes, indicating that it is a key molecule in ATRA-dependent myeloid maturation. Tretinoin 59-63 vav guanine nucleotide exchange factor 1 Homo sapiens 30-33
15878332-6 2005 Consistent with an effect of Vav on the transcriptional machinery, array profiling shows that the inhibition of the Syk-dependent tyrosine phosphorylation of Vav reduces the number of ATRA-induced genes. Tretinoin 184-188 vav guanine nucleotide exchange factor 1 Homo sapiens 29-32
15870295-3 2005 In embryonic carcinoma cells, endogenous Hes1 expression was repressed by retinoic acid in concord with enhanced p27(Kip1) expression and cell cycle arrest. Tretinoin 74-87 hes family bHLH transcription factor 1 Homo sapiens 41-45
20075418-0 2010 Retinoic acid modulates the subcellular localization of small ubiquitin-related modifier-2/3 (SUMO-2/3) in the testis. Tretinoin 0-13 small ubiquitin-like modifier 2 Rattus norvegicus 94-102
15878332-6 2005 Consistent with an effect of Vav on the transcriptional machinery, array profiling shows that the inhibition of the Syk-dependent tyrosine phosphorylation of Vav reduces the number of ATRA-induced genes. Tretinoin 184-188 vav guanine nucleotide exchange factor 1 Homo sapiens 158-161
20075418-7 2010 These results suggest that retinoic acid might have a role in controlling the subcellular localization of SUMO-2/3. Tretinoin 27-40 small ubiquitin-like modifier 2 Rattus norvegicus 106-114
15814302-2 2005 The aim of the present study was therefore to clarify the mechanism by which retinoic acid modulates expression of TNSALP. Tretinoin 77-90 alkaline phosphatase, biomineralization associated Homo sapiens 115-121
15814302-3 2005 After culturing SaOS-2 human osteoblastic osteosarcoma cells in the presence or absence of 10(-6) M all-trans-retinoic acid, real-time RT-PCR confirmed that retinoic acid up-regulates expression of TNSALP mRNA. Tretinoin 100-123 alkaline phosphatase, biomineralization associated Homo sapiens 198-204
20361354-6 2010 CsA (0, 1, 5 10, 15 ug/ml) down-regulated BDNF and TrkB gene expression through cultured SH-SY5Y cells, as did all-trans retinoic acid (ATRA), and there was no effect on cell viability. Tretinoin 121-134 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 0-3
15814302-7 2005 It thus appears that retinoic acid regulates the expression of human TNSALP via a retinoic acid response element in the genes promoter region. Tretinoin 21-34 alkaline phosphatase, biomineralization associated Homo sapiens 69-75
15814302-7 2005 It thus appears that retinoic acid regulates the expression of human TNSALP via a retinoic acid response element in the genes promoter region. Tretinoin 82-95 alkaline phosphatase, biomineralization associated Homo sapiens 69-75
15722554-3 2005 Disruption of the Hoxa1 gene, the most 3" member of the Hoxa cluster and a retinoic acid (RA) direct target gene, results in abnormal ossification of the skull, hindbrain, and inner ear deficiencies, and neonatal death. Tretinoin 75-88 homeobox A1 Homo sapiens 18-23
15722554-3 2005 Disruption of the Hoxa1 gene, the most 3" member of the Hoxa cluster and a retinoic acid (RA) direct target gene, results in abnormal ossification of the skull, hindbrain, and inner ear deficiencies, and neonatal death. Tretinoin 90-92 homeobox A1 Homo sapiens 18-23
15867264-6 2005 RESULTS: We identified aberrant expression of several components of the retinoic acid (RA) signaling pathway (RARalpha, MUC4, Id-1, MMP9, uPAR, HB-EGF, HOXB6, and HOXB2), many of which are known to be aberrantly expressed in pancreatic cancer and PanIN. Tretinoin 87-89 mucin 4, cell surface associated Homo sapiens 120-124
20410309-0 2010 Transcriptional regulation of cannabinoid receptor-1 expression in the liver by retinoic acid acting via retinoic acid receptor-gamma. Tretinoin 80-93 cannabinoid receptor 1 (brain) Mus musculus 30-52
15824860-13 2005 Tests with Noggin showed that RA induction of CTGF expression was negatively influenced by BMP signaling, whereas induction of collagen X expression was BMP-dependent. Tretinoin 30-32 noggin Gallus gallus 11-17
15849313-0 2005 The repressor DREAM acts as a transcriptional activator on Vitamin D and retinoic acid response elements. Tretinoin 73-86 potassium voltage-gated channel interacting protein 3 Homo sapiens 14-19
20410309-7 2010 The endocannabinoid 2-arachidonoylglycerol (2-AG) also increased hepatic CB(1)R expression, which was mediated indirectly via RA, because it was absent in hepatocytes from mice lacking retinaldehyde dehydrogenase 1, the enzyme catalyzing the generation of RA from retinaldehyde. Tretinoin 126-128 cannabinoid receptor 1 (brain) Mus musculus 73-79
20410309-7 2010 The endocannabinoid 2-arachidonoylglycerol (2-AG) also increased hepatic CB(1)R expression, which was mediated indirectly via RA, because it was absent in hepatocytes from mice lacking retinaldehyde dehydrogenase 1, the enzyme catalyzing the generation of RA from retinaldehyde. Tretinoin 256-258 cannabinoid receptor 1 (brain) Mus musculus 73-79
15849313-3 2005 In this work, we find that DREAM stimulates basal and ligand-dependent activation of promoters containing vitamin D and retinoic acid response elements (VDREs and RAREs), consisting of direct repeats of the sequence AGT/GTCA spaced by 3 or 5 nt, respectively. Tretinoin 120-133 potassium voltage-gated channel interacting protein 3 Homo sapiens 27-32
15790515-2 2005 We have shown previously that retinoic acids, the Vitamin A derivatives, promote both apoptosis of neglected thymocytes and the activation-induced cell death of peripheral T-cells via ligating the nuclear retinoid receptor (RAR) gamma. Tretinoin 30-44 retinoic acid receptor gamma Homo sapiens 205-234
20484817-4 2010 Here, we present evidence that endogenous RA acts as a major regulatory signal integrating Wnt and Tgfbeta pathways in the control of Fgf10 expression during induction of the mouse primordial lung. Tretinoin 42-44 transforming growth factor, beta 1 Mus musculus 99-106
15677473-3 2005 Cdx members are themselves targets of signaling molecules that are also implicated in axial patterning, including retinoic acid (RA) and certain members of Wnt and fibroblast growth factor families. Tretinoin 129-131 caudal type homeobox 1 Mus musculus 0-3
15677473-3 2005 Cdx members are themselves targets of signaling molecules that are also implicated in axial patterning, including retinoic acid (RA) and certain members of Wnt and fibroblast growth factor families. Tretinoin 114-127 caudal type homeobox 1 Mus musculus 0-3
19937743-9 2010 Thus, the specific defects in spermiogenesis in RARalpha-deficient testes may correlate with a disrupted cyclic expression of RA-responsive structural components, including vimentin, a downregulation of connexin-40 in spermatogenic cells, and delayed assembly of ZO-1 into Sertoli cell tight junctions. Tretinoin 48-50 gap junction protein, alpha 5 Mus musculus 203-214
20620545-7 2010 The CsA+ATRA group showed a marked reduction in PCNA- and CD68-positive cells: namely, 33.96 +/- 8.65% versus 60.17 +/- 17.74% (P < .01) and 17.63 +/- 4.24% versus 32.13 +/- 9.26 (P < .01), respectively. Tretinoin 8-12 Cd68 molecule Rattus norvegicus 58-62
15799023-0 2005 Transforming growth factor-beta1 signaling participates in the physiological and pathological regulation of mouse inner ear development by all-trans retinoic acid. Tretinoin 149-162 transforming growth factor, beta 1 Mus musculus 0-32
15799023-9 2005 CONCLUSIONS: Our findings support a role for TGFbeta in the physiological and pathological effects of RA on inner ear development. Tretinoin 102-104 transforming growth factor, beta 1 Mus musculus 45-52
15677473-4 2005 In this regard, we have previously shown that, in the mouse, Cdx1 is directly regulated by RA at the late primitive streak stage (embryonic day (E) 7.5) through a RA response element in the proximal Cdx1 promoter. Tretinoin 91-93 caudal type homeobox 1 Mus musculus 61-65
20620545-8 2010 RT-PCR analysis showed that relative PDGF-A mRNA content in the CsA+ATRA group was significantly decreased compared with the CsA group (0.46 +/- 0.08 vs 0.94 +/- 0.11; P < .01). Tretinoin 68-72 platelet derived growth factor subunit A Rattus norvegicus 37-43
15677473-4 2005 In this regard, we have previously shown that, in the mouse, Cdx1 is directly regulated by RA at the late primitive streak stage (embryonic day (E) 7.5) through a RA response element in the proximal Cdx1 promoter. Tretinoin 91-93 caudal type homeobox 1 Mus musculus 199-203
15677473-4 2005 In this regard, we have previously shown that, in the mouse, Cdx1 is directly regulated by RA at the late primitive streak stage (embryonic day (E) 7.5) through a RA response element in the proximal Cdx1 promoter. Tretinoin 163-165 caudal type homeobox 1 Mus musculus 61-65
15677473-4 2005 In this regard, we have previously shown that, in the mouse, Cdx1 is directly regulated by RA at the late primitive streak stage (embryonic day (E) 7.5) through a RA response element in the proximal Cdx1 promoter. Tretinoin 163-165 caudal type homeobox 1 Mus musculus 199-203
15690164-8 2005 Comparison of changes in transcript expression between BMP-2-induced epithelial versus all-trans-retinoic acid (ATRA)-induced neural differentiation revealed potential candidates for regulation of BMP-2 signaling and suppression of neural fate by BMP-2. Tretinoin 91-110 bone morphogenetic protein 2 Homo sapiens 197-202
20025061-4 2010 Upon differentiation into neuronal cells in the presence of retinoic acid and BDNF, all three types of BRINP-mRNA were induced with a similar time course peaking at day three of treatment. Tretinoin 60-73 bone morphogenic protein/retinoic acid inducible neural specific 1 Mus musculus 103-108
15690164-8 2005 Comparison of changes in transcript expression between BMP-2-induced epithelial versus all-trans-retinoic acid (ATRA)-induced neural differentiation revealed potential candidates for regulation of BMP-2 signaling and suppression of neural fate by BMP-2. Tretinoin 91-110 bone morphogenetic protein 2 Homo sapiens 197-202
15690164-8 2005 Comparison of changes in transcript expression between BMP-2-induced epithelial versus all-trans-retinoic acid (ATRA)-induced neural differentiation revealed potential candidates for regulation of BMP-2 signaling and suppression of neural fate by BMP-2. Tretinoin 112-116 bone morphogenetic protein 2 Homo sapiens 197-202
15690164-8 2005 Comparison of changes in transcript expression between BMP-2-induced epithelial versus all-trans-retinoic acid (ATRA)-induced neural differentiation revealed potential candidates for regulation of BMP-2 signaling and suppression of neural fate by BMP-2. Tretinoin 112-116 bone morphogenetic protein 2 Homo sapiens 197-202
15735731-0 2005 Retinoic acid stabilizes p27Kip1 in EBV-immortalized lymphoblastoid B cell lines through enhanced proteasome-dependent degradation of the p45Skp2 and Cks1 proteins. Tretinoin 0-13 S-phase kinase associated protein 2 Homo sapiens 138-145
15735731-3 2005 Furthermore, we demonstrate that RA downregulates the expression of the p45Skp2 and Cks1 proteins, two essential components of the SCF(Skp2) ubiquitin ligase complex that target p27Kip1 for degradation. Tretinoin 33-35 S-phase kinase associated protein 2 Homo sapiens 72-79
20231276-5 2010 Retinoid receptors (RARgamma, RXRalpha), coactivators (pCIP (NCOA3, SRC3)), and p300 and RNA polymerase II are recruited only to the RARbeta(2) RA response element (RARE) in Balb/c3T3, whereas these proteins are recruited to RAREs of all three genes by RA in F9 cells. Tretinoin 20-22 retinoic acid receptor, beta Mus musculus 133-140
15735731-3 2005 Furthermore, we demonstrate that RA downregulates the expression of the p45Skp2 and Cks1 proteins, two essential components of the SCF(Skp2) ubiquitin ligase complex that target p27Kip1 for degradation. Tretinoin 33-35 S-phase kinase associated protein 2 Homo sapiens 75-79
15735731-5 2005 Moreover, overexpression of p45Skp2 in DG75 cells prevents p27Kip1 protein accumulation and promotes resistance to the antiproliferative effects of RA. Tretinoin 148-150 S-phase kinase associated protein 2 Homo sapiens 28-35
15735731-9 2005 These results indicate that downregulation of p45Skp2 is a key element underlying RA-induced p27Kip1 stabilization in B cells, resulting in an impaired targeting of the protein to the ubiquitin-proteasome pathway and probably contributing to the nuclear accumulation of p27Kip1. Tretinoin 82-84 S-phase kinase associated protein 2 Homo sapiens 46-53
15777839-4 2005 Cholera toxin-induced activation of cAMP responsive element (CRE)-binding protein (CREB) was enhanced by pretreating cells with ATRA for 24 h. In contrast, HGF production induced by epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) was potently inhibited by ATRA. Tretinoin 279-283 hepatocyte growth factor Homo sapiens 156-159
15777839-5 2005 These modulatory effects of ATRA were different from the effects of transforming growth factor-beta1 (TGF-beta) and dexamethasone, both of which inhibited HGF production induced by all of the four inducers. Tretinoin 28-32 hepatocyte growth factor Homo sapiens 155-158
20154154-7 2010 Phytanic acid, all-trans retinoic acid, and 9-cis retinoic acid were the best activators of PPARgamma expression, and the combination of 9-cis and all-trans retinoic acid was the best activator of PGC-1alpha expression (P < 0.05). Tretinoin 15-38 peroxisome proliferator activated receptor gamma Bos taurus 92-101
15777839-7 2005 Both 9-cis-retinoic acid (9-cis-RA) and 13-cis-retinoic acid (13-cis-RA), which are stereo-isomers of ATRA, showed a modulatory effect on HGF induction similar to that of ATRA. Tretinoin 102-106 hepatocyte growth factor Homo sapiens 138-141
15777839-7 2005 Both 9-cis-retinoic acid (9-cis-RA) and 13-cis-retinoic acid (13-cis-RA), which are stereo-isomers of ATRA, showed a modulatory effect on HGF induction similar to that of ATRA. Tretinoin 171-175 hepatocyte growth factor Homo sapiens 138-141
15777839-8 2005 These results suggest that ATRA augments the induction of HGF production caused by increased intracellular cAMP. Tretinoin 27-31 hepatocyte growth factor Homo sapiens 58-61
15739227-0 2005 Retinoic acid generated by Raldh2 in mesoderm is required for mouse dorsal endodermal pancreas development. Tretinoin 0-13 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 27-33
15739227-2 2005 We have analyzed mouse embryos carrying a null mutation of the gene encoding retinaldehyde dehydrogenase 2 (Raldh2), which controls RA synthesis. Tretinoin 132-134 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 77-106
15739227-2 2005 We have analyzed mouse embryos carrying a null mutation of the gene encoding retinaldehyde dehydrogenase 2 (Raldh2), which controls RA synthesis. Tretinoin 132-134 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 108-114
15739227-6 2005 Comparison of wild-type and Raldh2-/- embryos carrying an RA-reporter transgene demonstrates that RA activity is normally present throughout the endoderm except in the ventral-most region but is totally missing in endoderm of Raldh2-/- embryos. Tretinoin 58-60 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 28-34
15739227-6 2005 Comparison of wild-type and Raldh2-/- embryos carrying an RA-reporter transgene demonstrates that RA activity is normally present throughout the endoderm except in the ventral-most region but is totally missing in endoderm of Raldh2-/- embryos. Tretinoin 98-100 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 28-34
15739227-7 2005 Thus, Raldh2 expressed in adjacent splanchnic lateral plate mesoderm provides an RA signal to dorsal endoderm. Tretinoin 81-83 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 6-12
15739227-8 2005 Dorsal Pdx1 expression is rescued in Raldh2-/- embryos by low-dose maternal administration of RA, which preferentially restores RA-reporter expression in the dorsal endoderm. Tretinoin 94-96 pancreatic and duodenal homeobox 1 Mus musculus 7-11
15739227-8 2005 Dorsal Pdx1 expression is rescued in Raldh2-/- embryos by low-dose maternal administration of RA, which preferentially restores RA-reporter expression in the dorsal endoderm. Tretinoin 94-96 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 37-43
15739227-9 2005 Our findings demonstrate a specific role for RA in mouse embryos as a mesodermally synthesized signal needed for dorsal endodermal expression of Pdx1 during development of the dorsal pancreatic lineage. Tretinoin 45-47 pancreatic and duodenal homeobox 1 Mus musculus 145-149
15632153-2 2005 We have previously demonstrated that all-trans-retinoic acid (RA) induction of RIP140 constitutes a rate-limiting step in the regulation of retinoid receptor signaling. Tretinoin 37-60 nuclear receptor interacting protein 1 Homo sapiens 79-85
15632153-2 2005 We have previously demonstrated that all-trans-retinoic acid (RA) induction of RIP140 constitutes a rate-limiting step in the regulation of retinoid receptor signaling. Tretinoin 62-64 nuclear receptor interacting protein 1 Homo sapiens 79-85
20154154-7 2010 Phytanic acid, all-trans retinoic acid, and 9-cis retinoic acid were the best activators of PPARgamma expression, and the combination of 9-cis and all-trans retinoic acid was the best activator of PGC-1alpha expression (P < 0.05). Tretinoin 25-38 peroxisome proliferator activated receptor gamma Bos taurus 92-101
15632153-11 2005 Together these data implicate a regulatory role for RIP140 in mediating anti-estrogenic effects of RA in estrogen-dependent breast cancer cells and suggest that acute regulation of coregulator expression may be a general mechanism to integrate diverse hormone signals. Tretinoin 99-101 nuclear receptor interacting protein 1 Homo sapiens 52-58
20172853-5 2010 Here, we report that all-trans-retinoic acid (ATRA), currently used in the treatment of acute promyelocytic leukemia (APL), increases hCNT3-related activity through a mechanism that involves trafficking of pre-existing hCNT3 proteins to the plasma membrane. Tretinoin 21-44 solute carrier family 28 member 3 Homo sapiens 134-139
20172853-5 2010 Here, we report that all-trans-retinoic acid (ATRA), currently used in the treatment of acute promyelocytic leukemia (APL), increases hCNT3-related activity through a mechanism that involves trafficking of pre-existing hCNT3 proteins to the plasma membrane. Tretinoin 21-44 solute carrier family 28 member 3 Homo sapiens 219-224
15773917-4 2005 Synaptic activity, acting via the nuclear Ca(2+)-dependent activation of CaM kinase IV, triggers the disruption of subnuclear domains containing class II histone deacetylases (HDACs) and silencing mediator of retinoic acid and thyroid hormone receptors (SMRT), a broad-specificity co-repressor which represses nuclear hormone receptors and CBF1. Tretinoin 209-222 calcium/calmodulin dependent protein kinase IV Homo sapiens 73-86
20172853-5 2010 Here, we report that all-trans-retinoic acid (ATRA), currently used in the treatment of acute promyelocytic leukemia (APL), increases hCNT3-related activity through a mechanism that involves trafficking of pre-existing hCNT3 proteins to the plasma membrane. Tretinoin 46-50 solute carrier family 28 member 3 Homo sapiens 134-139
20172853-5 2010 Here, we report that all-trans-retinoic acid (ATRA), currently used in the treatment of acute promyelocytic leukemia (APL), increases hCNT3-related activity through a mechanism that involves trafficking of pre-existing hCNT3 proteins to the plasma membrane. Tretinoin 46-50 solute carrier family 28 member 3 Homo sapiens 219-224
15715961-0 2005 CDK2/4 regulate retinoic acid-induced G1 arrest in hepatocellular carcinoma cells. Tretinoin 16-29 cyclin dependent kinase 2 Homo sapiens 0-4
19322650-0 2010 SOX9 mediates the retinoic acid-induced HES-1 gene expression in human breast cancer cells. Tretinoin 18-31 SRY-box transcription factor 9 Homo sapiens 0-4
15715961-4 2005 Our findings suggested that the growth inhibition of RA in HCC cells differed according to G(1) phase delay by CDK2 or 4, finally induction of apoptosis. Tretinoin 53-55 cyclin dependent kinase 2 Homo sapiens 111-115
15715961-6 2005 RA treatment caused cell cycle arrest at G(1) and decreased the expressions and activities of CDK2 or CDK4 in RA-sensitive HepG2 and SNU354 cells. Tretinoin 0-2 cyclin dependent kinase 2 Homo sapiens 94-98
15715961-6 2005 RA treatment caused cell cycle arrest at G(1) and decreased the expressions and activities of CDK2 or CDK4 in RA-sensitive HepG2 and SNU354 cells. Tretinoin 0-2 cyclin dependent kinase 4 Homo sapiens 102-106
15800190-7 2005 Chromatin immunoprecipitation assay demonstrated RA induced replacement of the c-Myc/Max complex with the Max/Mad1 complex on the E box located within nucleosome N1, coinciding with reduced Sp1 binding to GC boxes located within nucleosome N2 and recruitment of chromatin remodeling factor Brahma-related gene 1 (BRG-1) to this promoter. Tretinoin 49-51 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Mus musculus 313-318
15800190-9 2005 It is concluded that RA induces KOR gene suppression, as early neuronal differentiation marker, by inducing substitution of c-Myc/Max with Max/Mad on the E box and by BRG-1 involved nucleosome recruitment and chromatin condensation, thereby abolishing Sp1 binding. Tretinoin 21-23 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Mus musculus 167-172
15715961-7 2005 On the other hand, RA-resistant Hep3B and SNU449 cells progressed into the S/G(2)+M phase and showed increased CDK2 and CDK4 expression and activity. Tretinoin 19-21 cyclin dependent kinase 2 Homo sapiens 111-115
15715961-7 2005 On the other hand, RA-resistant Hep3B and SNU449 cells progressed into the S/G(2)+M phase and showed increased CDK2 and CDK4 expression and activity. Tretinoin 19-21 cyclin dependent kinase 4 Homo sapiens 120-124
15637062-1 2005 The promyelocytic leukemia RARalpha target gene encoding an adaptor molecule-1 (PRAM-1) is involved in a signaling pathway induced by retinoic acid in acute promyelocytic leukemia (APL) cells. Tretinoin 134-147 PML-RARA regulated adaptor molecule 1 Homo sapiens 80-86
15883744-0 2005 Retinoic acid inhibits CD40 plus IL-4 mediated IgE production through alterations of sCD23, sCD54 and IL-6 production. Tretinoin 0-13 CD40 molecule Homo sapiens 23-27
15883744-1 2005 BACKGROUND: All-trans retinoic acid (ATRA) inhibits IgE synthesis from anti-CD40 plus IL-4 stimulated human B lymphocytes. Tretinoin 12-35 CD40 molecule Homo sapiens 76-80
15883744-1 2005 BACKGROUND: All-trans retinoic acid (ATRA) inhibits IgE synthesis from anti-CD40 plus IL-4 stimulated human B lymphocytes. Tretinoin 37-41 CD40 molecule Homo sapiens 76-80
15715961-8 2005 Since the inhibition of CDK2 or 4 activities resulted in sensitization of HCC cells to RA, the combination of RA and compounds of inhibiting CDKs such as UCN01 and flavopiridol might be a useful targeted therapy strategy for HCC. Tretinoin 87-89 cyclin dependent kinase 2 Homo sapiens 24-28
19322650-0 2010 SOX9 mediates the retinoic acid-induced HES-1 gene expression in human breast cancer cells. Tretinoin 18-31 hes family bHLH transcription factor 1 Homo sapiens 40-45
15883744-7 2005 RESULTS: ATRA induced a dose-dependent increase of percent CD23 (3.4 fold) or CD54 (1.6 fold) positive B cells. Tretinoin 9-13 Fc epsilon receptor II Homo sapiens 59-63
15883744-12 2005 CONCLUSIONS: ATRA interferes through several pathways with the anti-CD40 plus IL-4 mediated B cell activation, namely IL-6, CD23 and CD54. Tretinoin 13-17 CD40 molecule Homo sapiens 68-72
19322650-1 2010 We have previously shown that the anti-proliferative effect of retinoic acid in human breast cancer cell line MCF-7 is dependent on HES-1 expression. Tretinoin 63-76 hes family bHLH transcription factor 1 Homo sapiens 132-137
15883744-12 2005 CONCLUSIONS: ATRA interferes through several pathways with the anti-CD40 plus IL-4 mediated B cell activation, namely IL-6, CD23 and CD54. Tretinoin 13-17 Fc epsilon receptor II Homo sapiens 124-128
19322650-2 2010 Here we show that retinoic acid induces HES-1 expression via upregulation of transcription factor SOX9. Tretinoin 18-31 hes family bHLH transcription factor 1 Homo sapiens 40-45
15728448-4 2005 Treatment of primary human monocytes with ATRA led to the down-regulation of TLR2 as well as its coreceptor CD14, but not TLR1 or TLR4. Tretinoin 42-46 CD14 molecule Homo sapiens 108-112
19322650-2 2010 Here we show that retinoic acid induces HES-1 expression via upregulation of transcription factor SOX9. Tretinoin 18-31 SRY-box transcription factor 9 Homo sapiens 98-102
15728448-7 2005 These data indicate that ATRA exerts an anti-inflammatory effect on monocytes via two pathways, one specifically affecting TLR2/1 and CD14 expression and one independent of TLR expression. Tretinoin 25-29 CD14 molecule Homo sapiens 134-138
15471950-6 2005 RA treatment of leukemia cells also resulted in an mTOR-mediated phosphorylation of the 4E-BP1 repressor of mRNA translation, to induce its deactivation and dissociation from the eukaryotic initiation factor-4E (eIF-4E) complex. Tretinoin 0-2 eukaryotic translation initiation factor 4E Homo sapiens 179-210
19322650-3 2010 By expressing a dominant negative form of SOX9, disrupting endogenous SOX9 activity, the retinoic acid-induced HES-1 mRNA expression was inhibited. Tretinoin 89-102 SRY-box transcription factor 9 Homo sapiens 42-46
15471950-6 2005 RA treatment of leukemia cells also resulted in an mTOR-mediated phosphorylation of the 4E-BP1 repressor of mRNA translation, to induce its deactivation and dissociation from the eukaryotic initiation factor-4E (eIF-4E) complex. Tretinoin 0-2 eukaryotic translation initiation factor 4E Homo sapiens 212-218
19322650-3 2010 By expressing a dominant negative form of SOX9, disrupting endogenous SOX9 activity, the retinoic acid-induced HES-1 mRNA expression was inhibited. Tretinoin 89-102 SRY-box transcription factor 9 Homo sapiens 70-74
19322650-3 2010 By expressing a dominant negative form of SOX9, disrupting endogenous SOX9 activity, the retinoic acid-induced HES-1 mRNA expression was inhibited. Tretinoin 89-102 hes family bHLH transcription factor 1 Homo sapiens 111-116
19322650-5 2010 By performing chromatin immunoprecipitation, we showed that SOX9 binding to the HES-1 enhancer was induced by retinoic acid in vivo. Tretinoin 110-123 SRY-box transcription factor 9 Homo sapiens 60-64
15591223-0 2005 Modulation of clusterin isoforms is associated with all-trans retinoic acid-induced proliferative arrest and apoptosis of intimal smooth muscle cells. Tretinoin 62-75 clusterin Homo sapiens 14-23
19322650-5 2010 By performing chromatin immunoprecipitation, we showed that SOX9 binding to the HES-1 enhancer was induced by retinoic acid in vivo. Tretinoin 110-123 hes family bHLH transcription factor 1 Homo sapiens 80-85
19322650-7 2010 The enhancer responded to retinoic acid; furthermore, the expression of a dominant negative SOX9 abolished this response. Tretinoin 26-39 SRY-box transcription factor 9 Homo sapiens 92-96
20122913-0 2010 Retinoic acid signaling in perioptic mesenchyme represses Wnt signaling via induction of Pitx2 and Dkk2. Tretinoin 0-13 paired-like homeodomain transcription factor 2 Mus musculus 89-94
15645120-4 2005 Injection of SB or ATRA near SCC25-derived tumors in nude mice resulted in inhibition of growth and elevation of differentiation of the tumor accompanied by marked keratinization and increased expression of keratin 13 and decreased expression of COX-2. Tretinoin 19-23 keratin 13 Mus musculus 207-217
15645120-4 2005 Injection of SB or ATRA near SCC25-derived tumors in nude mice resulted in inhibition of growth and elevation of differentiation of the tumor accompanied by marked keratinization and increased expression of keratin 13 and decreased expression of COX-2. Tretinoin 19-23 cytochrome c oxidase II, mitochondrial Mus musculus 246-251
15680360-0 2005 Retinoic acid-metabolizing enzyme Cyp26a1 is essential for determining territories of hindbrain and spinal cord in zebrafish. Tretinoin 0-13 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 34-41
15680360-2 2005 Here we characterize a mutant of the zebrafish named giraffe (gir) in which the gene for the RA-degrading enzyme Cyp26a1 is mutated. Tretinoin 93-95 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 113-120
15680360-5 2005 The cyp26a1 expression in the rostral spinal cord was strongly upregulated in the gir mutant, suggesting a strong feedback control of its expression by RA signaling. Tretinoin 152-154 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 4-11
15680360-8 2005 We propose a model in which Cyp26a1 attenuates RA signaling in the prospective rostral spinal cord to limit the expression of hox genes and to determine the hindbrain-spinal cord boundary. Tretinoin 47-49 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 28-35
15725579-3 2005 As retinoic acid (RA) has been used in the treatment of psoriasis and a mechanism for its beneficial effects is not understood, we investigated the effects of RA on SOD mRNA and protein expression levels in human normal and psoriatic fibroblasts. Tretinoin 159-161 superoxide dismutase 2 Homo sapiens 165-168
15725579-5 2005 However, in contrast to normal fibroblasts, exposure of psoriatic fibroblasts to 1 microM RA down-regulated Mn-SOD mRNA, and also decreased Mn-SOD activity by approximately 80% with no change in Mn-SOD protein levels. Tretinoin 90-92 superoxide dismutase 2 Homo sapiens 108-114
15591223-12 2005 All-trans retinoic acid-induced proliferative arrest showed association with s-CLU reduction and n-CLU overexpression with apoptosis, supporting a different biological role of these isoforms. Tretinoin 10-23 clusterin Homo sapiens 99-102
15607726-6 2005 Concurrently, atRA also decreased the expressions of vascular endothelial growth factor (VEGF) and its receptor KDR/Flk-1, and Akt phosphorylation. Tretinoin 14-18 kinase insert domain receptor Bos taurus 112-115
19778331-4 2010 MATERIAL AND METHODS: In the present study, the alteration of expression of tight junction constituent proteins and keratin peptides in immortalized oral mucosal epithelial cells (GE1) induced by 1 microm retinoic acid was analyzed by immunofluorescence, electron microscopy and reverse transcription-polymerase chain reaction (RT-PCR). Tretinoin 205-218 enhancer of mRNA decapping 4 Homo sapiens 180-183
15607726-6 2005 Concurrently, atRA also decreased the expressions of vascular endothelial growth factor (VEGF) and its receptor KDR/Flk-1, and Akt phosphorylation. Tretinoin 14-18 kinase insert domain receptor Bos taurus 116-121
15607726-6 2005 Concurrently, atRA also decreased the expressions of vascular endothelial growth factor (VEGF) and its receptor KDR/Flk-1, and Akt phosphorylation. Tretinoin 14-18 AKT serine/threonine kinase 1 Bos taurus 127-130
15607726-10 2005 Thus, atRA decreases eNOS-Ser(1179) phosphorylation through a mechanism that depends on VEGF-KDR/Flk-1-mediated Akt phosphorylation but is independent of RARE, leading to reduction in NO production. Tretinoin 6-10 kinase insert domain receptor Bos taurus 93-96
20054531-7 2010 In particular, Fgf and retinoic acid signalling are dysregulated in Tbx1 mutants. Tretinoin 23-36 T-box transcription factor 1 Homo sapiens 68-72
15607726-10 2005 Thus, atRA decreases eNOS-Ser(1179) phosphorylation through a mechanism that depends on VEGF-KDR/Flk-1-mediated Akt phosphorylation but is independent of RARE, leading to reduction in NO production. Tretinoin 6-10 kinase insert domain receptor Bos taurus 97-102
15607726-10 2005 Thus, atRA decreases eNOS-Ser(1179) phosphorylation through a mechanism that depends on VEGF-KDR/Flk-1-mediated Akt phosphorylation but is independent of RARE, leading to reduction in NO production. Tretinoin 6-10 AKT serine/threonine kinase 1 Bos taurus 112-115
15695403-0 2005 Retinoic acid inhibits the proliferative response induced by CD40 activation and interleukin-4 in mantle cell lymphoma. Tretinoin 0-13 CD40 molecule Homo sapiens 61-65
15585742-0 2005 Retinoic acid induces Pdx1-positive endoderm in differentiating mouse embryonic stem cells. Tretinoin 0-13 pancreatic and duodenal homeobox 1 Mus musculus 22-26
15585742-3 2005 By monitoring GFP expression during the course of ES cell differentiation, we have shown that retinoic acid (RA) can regulate the commitment of ES cells to form Pdx1(+) pancreatic endoderm. Tretinoin 94-107 pancreatic and duodenal homeobox 1 Mus musculus 161-165
15585742-3 2005 By monitoring GFP expression during the course of ES cell differentiation, we have shown that retinoic acid (RA) can regulate the commitment of ES cells to form Pdx1(+) pancreatic endoderm. Tretinoin 109-111 pancreatic and duodenal homeobox 1 Mus musculus 161-165
15585742-4 2005 RA was most effective at inducing Pdx1 expression when added to cultures at day 4 of ES differentiation, a period corresponding to the end of gastrulation in the embryo. Tretinoin 0-2 pancreatic and duodenal homeobox 1 Mus musculus 34-38
15695403-2 2005 Here, we show that retinoic acid (RA) isomers significantly inhibit the proliferation of both primary MCL cultures (n = 7) and established cell lines (Granta 519 and SP-53) as shown by [(3)H]thymidine uptake and carboxyfluorescein diacetate succinimidyl ester labeling coupled with cyclin D1 staining. Tretinoin 19-32 cyclin D1 Homo sapiens 282-291
20212135-2 2010 We now describe an experimental system in which the pluripotency genes Sox2 and Oct4 are repressed in retinoic acid-treated ES cells but are reprogrammed up to 100% within 24 h by injection of nuclei into the germinal vesicle (GV) of growing Xenopus oocytes. Tretinoin 102-115 POU class 5 homeobox 3, gene 1 L homeolog Xenopus laevis 80-84
15695403-2 2005 Here, we show that retinoic acid (RA) isomers significantly inhibit the proliferation of both primary MCL cultures (n = 7) and established cell lines (Granta 519 and SP-53) as shown by [(3)H]thymidine uptake and carboxyfluorescein diacetate succinimidyl ester labeling coupled with cyclin D1 staining. Tretinoin 34-36 cyclin D1 Homo sapiens 282-291
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 8-10 cyclin D1 Homo sapiens 42-77
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 8-10 RB transcriptional corepressor 1 Homo sapiens 174-177
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 210-212 cyclin D1 Homo sapiens 42-77
15695403-7 2005 Notably, RA isomers, and particularly 9-cis-RA, also inhibited the growth-promoting effect induced in primary MCL cells by CD40 activation alone or in combination with interleukin-4. Tretinoin 9-11 CD40 molecule Homo sapiens 123-127
15634700-3 2005 We have analysed the murine retinoic acid receptor beta gene (Rarb) and show that it is induced prior to segmentation, by retinoic-acid (RA) signalling from the mesoderm. Tretinoin 122-135 retinoic acid receptor, beta Mus musculus 28-55
15634700-3 2005 We have analysed the murine retinoic acid receptor beta gene (Rarb) and show that it is induced prior to segmentation, by retinoic-acid (RA) signalling from the mesoderm. Tretinoin 122-135 retinoic acid receptor, beta Mus musculus 62-66
20197465-1 2010 Retinoic acid receptors (RAR; alpha, beta, and gamma), members of the nuclear receptor superfamily, mediate the pleiotropic effects of the vitamin A metabolite retinoic acid (RA) and derivatives (retinoids) in normal and cancer cells. Tretinoin 160-173 retinoic acid receptor gamma Homo sapiens 25-28
15634700-3 2005 We have analysed the murine retinoic acid receptor beta gene (Rarb) and show that it is induced prior to segmentation, by retinoic-acid (RA) signalling from the mesoderm. Tretinoin 137-139 retinoic acid receptor, beta Mus musculus 28-55
15634700-3 2005 We have analysed the murine retinoic acid receptor beta gene (Rarb) and show that it is induced prior to segmentation, by retinoic-acid (RA) signalling from the mesoderm. Tretinoin 137-139 retinoic acid receptor, beta Mus musculus 62-66
19263240-7 2010 Moreover, exposure of the reprogrammed cells to all trans-retinoic acid (RA) medium elicited the generation of neuronal class IIIbeta-tubulin-positive, neuron-specific enolase (NSE)-positive, nestin-positive, and neurofilament light chain (NF-L)-positive neural-like cells. Tretinoin 52-71 enolase 2, gamma neuronal Mus musculus 152-175
15750294-6 2005 Furthermore, RA may promote cytoplasmic maturation of bovine oocytes via its modulatory effects on the gene expression of gonadotrophin receptors, midkine, cyclooxygenase-2, and nitric oxide synthase in cumulus-granulosa cells. Tretinoin 13-15 midkine Bos taurus 147-154
15652522-5 2005 RA increased the release of TSP-1 and PEDF, but not that of VEGF, from human RPE cells in vitro. Tretinoin 0-2 serpin family F member 1 Homo sapiens 38-42
15717686-3 2005 The protein and message expressions of p67phox, the gene for the dose-limiting component of phagocyte NADPH oxidase, were significantly enhanced by the coexistence of DHEA and ATRA. Tretinoin 176-180 neutrophil cytosolic factor 2 Homo sapiens 39-46
15717686-5 2005 Moreover, the ATRA-induced increment of CCAAT/enhancer-binding protein beta (C/EBPbeta) and the reciprocal reduction in C/EBPUalpha expression were also potentiated by DHEA. Tretinoin 14-18 CCAAT enhancer binding protein beta Homo sapiens 40-75
15717686-5 2005 Moreover, the ATRA-induced increment of CCAAT/enhancer-binding protein beta (C/EBPbeta) and the reciprocal reduction in C/EBPUalpha expression were also potentiated by DHEA. Tretinoin 14-18 CCAAT enhancer binding protein beta Homo sapiens 77-86
15607369-6 2005 RA treatment induced cleavage of caspase-8 and PARP in NB4. Tretinoin 0-2 caspase 8 Homo sapiens 33-42
19263240-7 2010 Moreover, exposure of the reprogrammed cells to all trans-retinoic acid (RA) medium elicited the generation of neuronal class IIIbeta-tubulin-positive, neuron-specific enolase (NSE)-positive, nestin-positive, and neurofilament light chain (NF-L)-positive neural-like cells. Tretinoin 52-71 enolase 2, gamma neuronal Mus musculus 177-180
19263240-7 2010 Moreover, exposure of the reprogrammed cells to all trans-retinoic acid (RA) medium elicited the generation of neuronal class IIIbeta-tubulin-positive, neuron-specific enolase (NSE)-positive, nestin-positive, and neurofilament light chain (NF-L)-positive neural-like cells. Tretinoin 73-75 enolase 2, gamma neuronal Mus musculus 152-175
15567562-3 2005 RT-PCR assays showed that NT2 cells express mRNAs of several neural bHLH genes such as Hes1, Ngn1, Mash1, NeuroD, Math1 and Pax6, just in the early days of RA exposure. Tretinoin 156-158 hes family bHLH transcription factor 1 Homo sapiens 87-91
19263240-7 2010 Moreover, exposure of the reprogrammed cells to all trans-retinoic acid (RA) medium elicited the generation of neuronal class IIIbeta-tubulin-positive, neuron-specific enolase (NSE)-positive, nestin-positive, and neurofilament light chain (NF-L)-positive neural-like cells. Tretinoin 73-75 enolase 2, gamma neuronal Mus musculus 177-180
19960509-7 2010 These results demonstrate that ATRA intensifies ER stress and induces apoptosis in GnT-V-AS/7721 cells by disturbing homocysteine metabolism through the down-regulation of CBS and BHMT, depleting the cellular GSH and, in turn, altering the cellular redox status. Tretinoin 31-35 betaine--homocysteine S-methyltransferase Homo sapiens 180-184
15596294-0 2005 Expression profiles of Id1 and p16 proteins in all-trans-retinoic acid-induced apoptosis and cell cycle re-distribution in melanoma. Tretinoin 57-70 inhibitor of DNA binding 1, HLH protein Homo sapiens 23-26
20035057-10 2010 Activation of RXRalpha by retinoic acids increased the cyclin E1 promoter activity indicating retinoic acid-mediated signaling positively controls cyclin E1 gene expression. Tretinoin 26-40 retinoid X receptor alpha Mus musculus 14-22
15389522-6 2005 Retinoic acid treatment markedly increased expression of osteopontin up to 48 h after stimulation. Tretinoin 0-13 secreted phosphoprotein 1 Rattus norvegicus 57-68
20035057-10 2010 Activation of RXRalpha by retinoic acids increased the cyclin E1 promoter activity indicating retinoic acid-mediated signaling positively controls cyclin E1 gene expression. Tretinoin 26-39 retinoid X receptor alpha Mus musculus 14-22
15389595-0 2005 Regulation of proliferation and migration in retinoic acid treated C3H10T1/2 cells by TGF-beta isoforms. Tretinoin 45-58 transforming growth factor, beta 1 Mus musculus 86-94
16400881-4 2005 Treatment of ras-transformed cells with interferon-alpha with or without retinoic acid results in their persistent reversion to a non-transformed state that is dependent on the restoration of LO expression. Tretinoin 73-86 lysyl oxidase Mus musculus 192-194
15389595-8 2005 C3H10T1/2 cells treated with all-trans-retinoic acid (ATRA) and expressing relatively higher levels of osteoblastic gene markers such as alkaline phosphatase and collagen type I, lower levels of chondrocytic gene markers collagen type II and aggrecan, and unchanged levels of the adipose marker adipsin did not demonstrate significant chemokinesis or chemotaxis in response to TGF-beta1 or -beta3 at concentrations ranging from 10(-12) to 10(-9) g/ml. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 377-396
20081195-1 2010 Comparative studies of the tetrapod raldh2 (aldh1a2) gene, which encodes a retinoic acid (RA) synthesis enzyme, have led to the identification of a dorsal spinal cord enhancer. Tretinoin 75-88 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 36-42
20081195-1 2010 Comparative studies of the tetrapod raldh2 (aldh1a2) gene, which encodes a retinoic acid (RA) synthesis enzyme, have led to the identification of a dorsal spinal cord enhancer. Tretinoin 75-88 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 44-51
15934296-7 2005 The NSE positive cells" ratio in the cells induced with ATRA and ACM was higher than that of the cells induced by ATRA at different time points of differentiation, and finally reached up to 73.5% among the total differentiated population. Tretinoin 56-60 enolase 2, gamma neuronal Mus musculus 4-7
15591039-0 2005 Mucin biosynthesis: upregulation of core 2 beta 1,6 N-acetylglucosaminyltransferase by retinoic acid and Th2 cytokines in a human airway epithelial cell line. Tretinoin 87-100 LOC100508689 Homo sapiens 0-5
15591039-0 2005 Mucin biosynthesis: upregulation of core 2 beta 1,6 N-acetylglucosaminyltransferase by retinoic acid and Th2 cytokines in a human airway epithelial cell line. Tretinoin 87-100 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 36-83
20081195-1 2010 Comparative studies of the tetrapod raldh2 (aldh1a2) gene, which encodes a retinoic acid (RA) synthesis enzyme, have led to the identification of a dorsal spinal cord enhancer. Tretinoin 90-92 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 36-42
20081195-1 2010 Comparative studies of the tetrapod raldh2 (aldh1a2) gene, which encodes a retinoic acid (RA) synthesis enzyme, have led to the identification of a dorsal spinal cord enhancer. Tretinoin 90-92 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 44-51
20110328-2 2010 We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinol-binding-protein-deficient (Rbp4(-/-)) mice. Tretinoin 24-37 glial cell line derived neurotrophic factor Mus musculus 58-62
15591039-3 2005 Here, we report the upregulation of core 2 beta1,6 N-acetylglucosaminyltransferase (C2GnT) activity both by all-trans retinoic acid (RA) and by IL-4 and IL-13 in the H292 airway epithelial cell line. Tretinoin 118-131 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 36-82
15591039-3 2005 Here, we report the upregulation of core 2 beta1,6 N-acetylglucosaminyltransferase (C2GnT) activity both by all-trans retinoic acid (RA) and by IL-4 and IL-13 in the H292 airway epithelial cell line. Tretinoin 118-131 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 84-89
15589822-0 2004 c-Myc-mediated expression of nucleophosmin/B23 decreases during retinoic acid-induced differentiation of human leukemia HL-60 cells. Tretinoin 64-77 nucleophosmin 1 Homo sapiens 29-42
15589822-0 2004 c-Myc-mediated expression of nucleophosmin/B23 decreases during retinoic acid-induced differentiation of human leukemia HL-60 cells. Tretinoin 64-77 nucleophosmin 1 Homo sapiens 43-46
15589822-1 2004 The retinoic acid-induced differentiation of human leukemia HL-60 cells towards mature granulocytic cells was accompanied by the decline in the protein levels of c-myc, nucleophosmin/B23 and its promoter activity. Tretinoin 4-17 nucleophosmin 1 Homo sapiens 169-182
15589822-1 2004 The retinoic acid-induced differentiation of human leukemia HL-60 cells towards mature granulocytic cells was accompanied by the decline in the protein levels of c-myc, nucleophosmin/B23 and its promoter activity. Tretinoin 4-17 nucleophosmin 1 Homo sapiens 183-186
15591039-3 2005 Here, we report the upregulation of core 2 beta1,6 N-acetylglucosaminyltransferase (C2GnT) activity both by all-trans retinoic acid (RA) and by IL-4 and IL-13 in the H292 airway epithelial cell line. Tretinoin 133-135 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 36-82
15591039-3 2005 Here, we report the upregulation of core 2 beta1,6 N-acetylglucosaminyltransferase (C2GnT) activity both by all-trans retinoic acid (RA) and by IL-4 and IL-13 in the H292 airway epithelial cell line. Tretinoin 133-135 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 84-89
20110328-2 2010 We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinol-binding-protein-deficient (Rbp4(-/-)) mice. Tretinoin 39-41 glial cell line derived neurotrophic factor Mus musculus 58-62
15591039-6 2005 Enhancement of the M isoform of C2GnT by RA was abolished by an inhibitor of RA receptor alpha, implicating RA receptor alpha in the effect of RA. Tretinoin 41-43 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 32-37
15604289-7 2004 More importantly, they also lysed autologous B-CLL cells when transcription and expression of MIC-A or up-regulation of ULBP3 were achieved either by activation or by exposure to trans-retinoic acid. Tretinoin 179-198 MHC class I polypeptide-related sequence A Homo sapiens 94-99
20155467-10 2010 After treatment with 10 mumol/L ATRA for 48 h, the Caspase3 and Caspase8 were significantly activated as compared with the control group (P<0.05). Tretinoin 32-36 caspase 3 Rattus norvegicus 51-59
15581350-5 2004 Mutation of arginine 241 had marked effects on the hydroxylation of anionic substrates of CYP2C8 such as retinoic acid and fluvastatin. Tretinoin 105-118 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 90-96
15581350-9 2004 The S114F and F205A mutants were the best catalysts for retinoic acid and paclitaxel (or fluvastatin) hydroxylation, respectively, with k(cat)/K(m) values 5 and 2.1 (or 2.4) times higher, respectively, than those found for CYP2C8. Tretinoin 56-69 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 223-229
15591039-6 2005 Enhancement of the M isoform of C2GnT by RA was abolished by an inhibitor of RA receptor alpha, implicating RA receptor alpha in the effect of RA. Tretinoin 77-79 glucosaminyl (N-acetyl) transferase 1 Homo sapiens 32-37
15492006-7 2004 Expression of the dominant negative p115RhoGEF was able to inhibit activation of both RhoA and JNK1 in response to either retinoic acid or the expression of a constitutively activated mutant of G alpha(13). Tretinoin 122-135 ras homolog family member A Mus musculus 86-90
20021200-5 2010 The purified enzyme was catalytically active towards aminopyrine, all-trans-retinoic acid, and particularly arachidonic acid forming 20-HETE, 19-HETE, and 18-HETE (about 86% of the total) and 14,15-, 11,12-, 8,9-, and 5,6-EETs (cis-epoxyeicosatrienoic acids; about 14% of total), with a regioselectivity similar to that shown by the mammalian CYP2J2s. Tretinoin 66-89 cytochrome P450 family 2 subfamily J member 2 Homo sapiens 343-349
15492006-8 2004 Expression of the dominant negative mutants of RhoA as well as those of either Cdc42 or Rac1, but not Ras, attenuated G alpha(13)-stimulated as well as retinoic acid-stimulated activation of all three of these small molecular weight GTPases, suggesting complex interrelationships among the three GTPases in this pathway. Tretinoin 152-165 ras homolog family member A Mus musculus 47-51
15492006-8 2004 Expression of the dominant negative mutants of RhoA as well as those of either Cdc42 or Rac1, but not Ras, attenuated G alpha(13)-stimulated as well as retinoic acid-stimulated activation of all three of these small molecular weight GTPases, suggesting complex interrelationships among the three GTPases in this pathway. Tretinoin 152-165 cell division cycle 42 Mus musculus 79-84
15492006-8 2004 Expression of the dominant negative mutants of RhoA as well as those of either Cdc42 or Rac1, but not Ras, attenuated G alpha(13)-stimulated as well as retinoic acid-stimulated activation of all three of these small molecular weight GTPases, suggesting complex interrelationships among the three GTPases in this pathway. Tretinoin 152-165 Rac family small GTPase 1 Mus musculus 88-92
15492006-9 2004 The formation of primitive endoderm in response to retinoic acid also could be blocked by expression of dominant negative mutants of RhoA, Cdc42, or Rac1. Tretinoin 51-64 ras homolog family member A Mus musculus 133-137
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 protein kinase C delta Homo sapiens 81-90
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 protein kinase C delta Homo sapiens 36-45
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 protein kinase C delta Homo sapiens 81-90
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 protein kinase C delta Homo sapiens 81-90
15492006-9 2004 The formation of primitive endoderm in response to retinoic acid also could be blocked by expression of dominant negative mutants of RhoA, Cdc42, or Rac1. Tretinoin 51-64 cell division cycle 42 Mus musculus 139-144
15492006-9 2004 The formation of primitive endoderm in response to retinoic acid also could be blocked by expression of dominant negative mutants of RhoA, Cdc42, or Rac1. Tretinoin 51-64 Rac family small GTPase 1 Mus musculus 149-153
20460768-9 2010 To gain insight into the mechanism of the SOD up-regulation by atRA, the activity of p38 mitogenactivated protein kinase (p38MAKP) and Akt was measured. Tretinoin 63-67 mitogen activated protein kinase 14 Rattus norvegicus 85-88
15489901-8 2004 Three out of eight genes including WBSCR5 were regulated during ATRA-induced monocytic differentiation of U-937 cells, however, none of them antagonistically, upon both ATRA treatment and AML1/ETO induction. Tretinoin 64-68 linker for activation of T cells family member 2 Homo sapiens 35-41
15489901-8 2004 Three out of eight genes including WBSCR5 were regulated during ATRA-induced monocytic differentiation of U-937 cells, however, none of them antagonistically, upon both ATRA treatment and AML1/ETO induction. Tretinoin 169-173 linker for activation of T cells family member 2 Homo sapiens 35-41
15597402-9 2004 In addition to these inhibitors of CYP5, CYP17, and CYP19, liarozole, known to be a potent inhibitor of CYP26 (retinoic acid-4-hydroxylase) and ATRA (all-trans-retinoic acid) metabolism, was able to reduce tumor cell adhesion to 51% of the initial rate. Tretinoin 144-148 cytochrome P450 family 17 subfamily A member 1 Homo sapiens 41-46
15358764-9 2004 Treatment of either APC or zRDHB morphant embryos with retinoic acid rescued the defective phenotypes. Tretinoin 55-68 retinol dehydrogenase 1 Danio rerio 27-32
15597402-9 2004 In addition to these inhibitors of CYP5, CYP17, and CYP19, liarozole, known to be a potent inhibitor of CYP26 (retinoic acid-4-hydroxylase) and ATRA (all-trans-retinoic acid) metabolism, was able to reduce tumor cell adhesion to 51% of the initial rate. Tretinoin 150-173 cytochrome P450 family 17 subfamily A member 1 Homo sapiens 41-46
20040494-5 2010 Conversely, we find that RA-receptor signaling in ureteric bud cells depends mainly on RA generated in nearby stromal cells by retinaldehyde dehydrogenase 2, an enzyme required for most fetal RA synthesis. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 127-156
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 26-30 protein kinase C delta Homo sapiens 103-124
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 26-30 protein kinase C delta Homo sapiens 126-134
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 26-30 protein kinase C delta Homo sapiens 145-153
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 26-30 protein kinase C delta Homo sapiens 145-153
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 205-209 protein kinase C delta Homo sapiens 145-153
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 205-209 protein kinase C delta Homo sapiens 145-153
15581624-7 2004 Moreover, ATRA inhibited proliferation of several human colon cancer cell lines with high levels of KLF5 expression but not those with low levels of KLF5 expression. Tretinoin 10-14 Kruppel like factor 5 Homo sapiens 100-104
20040494-5 2010 Conversely, we find that RA-receptor signaling in ureteric bud cells depends mainly on RA generated in nearby stromal cells by retinaldehyde dehydrogenase 2, an enzyme required for most fetal RA synthesis. Tretinoin 87-89 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 127-156
15610140-6 2004 Treatment with RA had only a slight effect on the mRNA expression of the tight junction-associated proteins occludin, ZO-1, claudin-1, -3, and -4, but enhanced the expression of claudin-2, which was recently suggested to form a paracellular ion channel. Tretinoin 15-17 occludin Homo sapiens 108-116
19747912-0 2010 Vav1 and PU.1 are recruited to the CD11b promoter in APL-derived promyelocytes: role of Vav1 in modulating PU.1-containing complexes during ATRA-induced differentiation. Tretinoin 140-144 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
15467735-1 2004 We have previously shown that expression of the transcription factor HES-1 is required for the growth-inhibitory effect of all-trans retinoic acid on MCF-7 cells. Tretinoin 133-146 hes family bHLH transcription factor 1 Homo sapiens 69-74
15467735-8 2004 In addition, we found that two important downstream target genes of estrogen and heregulin-beta1 that are regulated through E2F-1, cyclin E and NPAT, were both regulated in a similar fashion by all-trans retinoic acid, and these effects were antagonized by dominant-negative HES-1. Tretinoin 204-217 hes family bHLH transcription factor 1 Homo sapiens 275-280
15762294-0 2004 DNA rearrangement activity during retinoic acid-induced neural differentiation of P19 mouse embryonal carcinoma cells. Tretinoin 34-47 interleukin 23, alpha subunit p19 Mus musculus 82-85
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 RELA proto-oncogene, NF-kB subunit Homo sapiens 33-37
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 RELA proto-oncogene, NF-kB subunit Homo sapiens 39-42
19747912-1 2010 Vav1 plays an important role in the all-trans retinoic acid (ATRA)-induced completion of the differentiation program of acute promyelocytic leukemia (APL)-derived cells, in which it strengthens the drug effects and is involved in the regulation of maturation-related proteins, such as the CD11b surface antigen. Tretinoin 46-59 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
15610518-6 2004 ATRA increased the expression of RelA (p65), RelB, nuclear factor (NF)-kappaB2 (p52), and NF-kappaB1 (p50), and elevated the DNA-binding activity of p65 and phosphorylation of inhibitor kappaB (IkappaB) alpha. Tretinoin 0-4 RELA proto-oncogene, NF-kB subunit Homo sapiens 149-152
19747912-1 2010 Vav1 plays an important role in the all-trans retinoic acid (ATRA)-induced completion of the differentiation program of acute promyelocytic leukemia (APL)-derived cells, in which it strengthens the drug effects and is involved in the regulation of maturation-related proteins, such as the CD11b surface antigen. Tretinoin 61-65 vav guanine nucleotide exchange factor 1 Homo sapiens 0-4
15527762-0 2004 Suppression of Sox6 in P19 cells leads to failure of neuronal differentiation by retinoic acid and induces retinoic acid-dependent apoptosis. Tretinoin 81-94 SRY-box transcription factor 6 Homo sapiens 15-19
19747912-6 2010 The reported data suggest that the ATRA-induced increase of Vav1 expression and tyrosine phosphorylation may be involved in recruiting PU.1 to its consensus sequence on the CD11b promoter and, ultimately, in regulating CD11b expression during the late stages of neutrophil differentiation of APL-derived promyelocytes. Tretinoin 35-39 vav guanine nucleotide exchange factor 1 Homo sapiens 60-64
15527762-0 2004 Suppression of Sox6 in P19 cells leads to failure of neuronal differentiation by retinoic acid and induces retinoic acid-dependent apoptosis. Tretinoin 107-120 SRY-box transcription factor 6 Homo sapiens 15-19
20036862-6 2010 Reduction in the levels of miR-124 mediated by locked nucleic acids resulted in the accumulation of Hes-1 and hindered the retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 123-136 hes family bHLH transcription factor 1 Mus musculus 100-105
15527762-6 2004 Further, Sox6 suppression caused RA-dependent apoptosis by P19[anti-Sox6] cells: RA-treated P19[anti-Sox6] cells showed chromatin condensation, DNA fragmentation, and an increase in caspase-3-like activity. Tretinoin 33-35 SRY-box transcription factor 6 Homo sapiens 9-13
15527762-6 2004 Further, Sox6 suppression caused RA-dependent apoptosis by P19[anti-Sox6] cells: RA-treated P19[anti-Sox6] cells showed chromatin condensation, DNA fragmentation, and an increase in caspase-3-like activity. Tretinoin 33-35 SRY-box transcription factor 6 Homo sapiens 68-72
15527762-6 2004 Further, Sox6 suppression caused RA-dependent apoptosis by P19[anti-Sox6] cells: RA-treated P19[anti-Sox6] cells showed chromatin condensation, DNA fragmentation, and an increase in caspase-3-like activity. Tretinoin 33-35 SRY-box transcription factor 6 Homo sapiens 68-72
15527762-6 2004 Further, Sox6 suppression caused RA-dependent apoptosis by P19[anti-Sox6] cells: RA-treated P19[anti-Sox6] cells showed chromatin condensation, DNA fragmentation, and an increase in caspase-3-like activity. Tretinoin 81-83 SRY-box transcription factor 6 Homo sapiens 9-13
15527762-6 2004 Further, Sox6 suppression caused RA-dependent apoptosis by P19[anti-Sox6] cells: RA-treated P19[anti-Sox6] cells showed chromatin condensation, DNA fragmentation, and an increase in caspase-3-like activity. Tretinoin 81-83 SRY-box transcription factor 6 Homo sapiens 68-72
15527762-6 2004 Further, Sox6 suppression caused RA-dependent apoptosis by P19[anti-Sox6] cells: RA-treated P19[anti-Sox6] cells showed chromatin condensation, DNA fragmentation, and an increase in caspase-3-like activity. Tretinoin 81-83 SRY-box transcription factor 6 Homo sapiens 68-72
15520223-7 2004 UBE1L expression was also induced after prolonged RA-treatment of immortalized HBE cells. Tretinoin 50-52 ubiquitin like modifier activating enzyme 7 Homo sapiens 0-5
15380350-1 2004 Exogenous expression of the transcription factor Scl (Tal1) in WEHI-3B D+ myelomonocytic leukemia cells interferes with their capacity to respond to all-trans retinoic acid (ATRA) induced differentiation; combination of ATRA with LiCl, however, circumvents the inhibition of differentiation produced by Scl. Tretinoin 159-172 T cell acute lymphocytic leukemia 1 Mus musculus 49-58
15380350-1 2004 Exogenous expression of the transcription factor Scl (Tal1) in WEHI-3B D+ myelomonocytic leukemia cells interferes with their capacity to respond to all-trans retinoic acid (ATRA) induced differentiation; combination of ATRA with LiCl, however, circumvents the inhibition of differentiation produced by Scl. Tretinoin 174-178 T cell acute lymphocytic leukemia 1 Mus musculus 49-58
20036862-7 2010 Thus, our results indicate that miR-124 regulates the expression of Hes-1 at the post-transcriptional level and is involved in the retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 131-144 hes family bHLH transcription factor 1 Mus musculus 68-73
15380350-1 2004 Exogenous expression of the transcription factor Scl (Tal1) in WEHI-3B D+ myelomonocytic leukemia cells interferes with their capacity to respond to all-trans retinoic acid (ATRA) induced differentiation; combination of ATRA with LiCl, however, circumvents the inhibition of differentiation produced by Scl. Tretinoin 220-224 T cell acute lymphocytic leukemia 1 Mus musculus 49-58
15345685-3 2004 Recent studies demonstrate that retinoic acid (RA)-induced human HL60 cell proliferation/differentiation (P/D) transition is accompanied by MAT1 degradation and decreased CAK phosphorylation of retinoic acid receptor alpha (RARa). Tretinoin 32-45 MNAT1 component of CDK activating kinase Homo sapiens 140-144
15345685-3 2004 Recent studies demonstrate that retinoic acid (RA)-induced human HL60 cell proliferation/differentiation (P/D) transition is accompanied by MAT1 degradation and decreased CAK phosphorylation of retinoic acid receptor alpha (RARa). Tretinoin 47-49 MNAT1 component of CDK activating kinase Homo sapiens 140-144
15345685-5 2004 We find that RA induces ubiquitination-proteolysis of MAT1 and that ubiquitin-proteasome targets CAK-free MAT1 only. Tretinoin 13-15 MNAT1 component of CDK activating kinase Homo sapiens 54-58
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 27-29 MNAT1 component of CDK activating kinase Homo sapiens 38-42
20336520-4 2010 The neuroepithelial cells are then specified to OLIG2-expressing motoneuron progenitors in the presence of retinoic acid (RA) and sonic hedgehog (SHH) in the following 2 weeks. Tretinoin 107-120 oligodendrocyte transcription factor 2 Homo sapiens 48-53
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 27-29 MNAT1 component of CDK activating kinase Homo sapiens 171-175
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 93-95 MNAT1 component of CDK activating kinase Homo sapiens 38-42
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 93-95 MNAT1 component of CDK activating kinase Homo sapiens 171-175
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 93-95 MNAT1 component of CDK activating kinase Homo sapiens 38-42
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 93-95 MNAT1 component of CDK activating kinase Homo sapiens 171-175
15508108-7 2004 The mechanisms by which alcohol causes HCC are incompletely understood, but may include chromosomal loss, oxidative stress, a decreased retinoic acid level in the liver, altered DNA methylation, and genetic susceptibility. Tretinoin 136-149 HCC Homo sapiens 39-42
15206905-6 2004 The present study has revealed a novel RA-response element in Col11a2 that does not interact directly with the promoter, but instead requires the D/E enhancer to mediate transcriptional activation. Tretinoin 39-41 collagen type XI alpha 2 chain Homo sapiens 62-69
15366004-1 2004 Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. Tretinoin 138-151 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 41-47
15366004-1 2004 Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. Tretinoin 138-151 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 49-55
15366004-1 2004 Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. Tretinoin 153-155 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 41-47
15366004-1 2004 Three retinaldehyde dehydrogenase genes (Raldh1, Raldh2, and Raldh3) expressed in unique spatiotemporal patterns may control synthesis of retinoic acid (RA) needed for retina development. Tretinoin 153-155 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 49-55
15366004-2 2004 However, previous studies indicate that retina formation still proceeds normally in Raldh1-/- mouse embryos lacking RA synthesis in the dorsal neural retina at the optic cup stage. Tretinoin 116-118 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 84-90
15366004-3 2004 Here, we demonstrate that Raldh2-/- embryos lacking RA synthesis in the optic vesicle exhibit a failure in retina invagination needed to develop an optic cup. Tretinoin 52-54 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 26-32
15366004-6 2004 Maternal RA administration at the optic vesicle stage rescues optic cup formation in Raldh2-/- and Raldh1-/-:Raldh2-/- embryos, demonstrating that Raldh1 is not required during rescue of optic cup development. Tretinoin 9-11 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 85-91
15366004-6 2004 Maternal RA administration at the optic vesicle stage rescues optic cup formation in Raldh2-/- and Raldh1-/-:Raldh2-/- embryos, demonstrating that Raldh1 is not required during rescue of optic cup development. Tretinoin 9-11 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 99-105
15366004-6 2004 Maternal RA administration at the optic vesicle stage rescues optic cup formation in Raldh2-/- and Raldh1-/-:Raldh2-/- embryos, demonstrating that Raldh1 is not required during rescue of optic cup development. Tretinoin 9-11 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 109-115
15366004-6 2004 Maternal RA administration at the optic vesicle stage rescues optic cup formation in Raldh2-/- and Raldh1-/-:Raldh2-/- embryos, demonstrating that Raldh1 is not required during rescue of optic cup development. Tretinoin 9-11 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 147-153
15366004-8 2004 Thus, RA signaling initiates in the optic vesicle in response to Raldh2 but can be maintained during optic cup formation by a gene other than Raldh1, most likely Raldh3. Tretinoin 6-8 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 65-71
15646024-2 2004 RA was previously shown to down-regulate the steady state levels of retinoic acid receptor alpha (RARalpha) and retinoid X receptor alpha (RXRalpha) in primary brown adipocytes differentiated in culture. Tretinoin 0-2 retinoid X receptor alpha Mus musculus 112-137
15646024-2 2004 RA was previously shown to down-regulate the steady state levels of retinoic acid receptor alpha (RARalpha) and retinoid X receptor alpha (RXRalpha) in primary brown adipocytes differentiated in culture. Tretinoin 0-2 retinoid X receptor alpha Mus musculus 139-147
15646024-6 2004 RESULTS: ATRA-treatment resulted in a reduction of the specific RARalpha and especially RXRalpha content in BAT that paralleled the induction of UCP1 appearance in the tissue. Tretinoin 9-13 retinoid X receptor alpha Mus musculus 88-96
15646024-6 2004 RESULTS: ATRA-treatment resulted in a reduction of the specific RARalpha and especially RXRalpha content in BAT that paralleled the induction of UCP1 appearance in the tissue. Tretinoin 9-13 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 145-149
15367666-2 2004 GRIM-19 was originally identified as a nuclear protein with apoptotic nature in interferon (IFN)- and all-trans-retinoic acid (RA)-induced tumor cells. Tretinoin 102-125 NADH:ubiquinone oxidoreductase subunit A13 Mus musculus 0-7
15367666-2 2004 GRIM-19 was originally identified as a nuclear protein with apoptotic nature in interferon (IFN)- and all-trans-retinoic acid (RA)-induced tumor cells. Tretinoin 127-129 NADH:ubiquinone oxidoreductase subunit A13 Mus musculus 0-7
15356197-3 2004 ES cells were exposed to retinoic acid (RA) and sonic hedgehog agonist (Hh-Ag1.3) to stimulate differentiation into MNs marked by expression of eGFP and the cholinergic transmitter synthetic enzyme choline acetyltransferase. Tretinoin 25-38 choline acetyltransferase Mus musculus 198-223
15356197-3 2004 ES cells were exposed to retinoic acid (RA) and sonic hedgehog agonist (Hh-Ag1.3) to stimulate differentiation into MNs marked by expression of eGFP and the cholinergic transmitter synthetic enzyme choline acetyltransferase. Tretinoin 40-42 choline acetyltransferase Mus musculus 198-223
15383631-0 2004 ERbeta sensitizes breast cancer cells to retinoic acid: evidence of transcriptional crosstalk. Tretinoin 41-54 estrogen receptor 2 Homo sapiens 0-6
15383631-5 2004 A significant retinoic acid (RA)-mediated growth inhibition was observed in the transduced ERbeta-positive cells as shown by proliferation assays. Tretinoin 14-27 estrogen receptor 2 Homo sapiens 91-97
15383631-5 2004 A significant retinoic acid (RA)-mediated growth inhibition was observed in the transduced ERbeta-positive cells as shown by proliferation assays. Tretinoin 29-31 estrogen receptor 2 Homo sapiens 91-97
15317450-3 2004 The transcriptional antagonism of the 3"-n-butyl analogue was demonstrated by its blockade of retinoic acid receptor (RAR) beta expression induced by the RXRalpha/peroxisome proliferator-activated receptor (PPAR) gamma heterodimer complexed with an RXRalpha agonist plus the PPARgamma agonist ciglitazone and the inhibition of 9-cis-RA-induced coactivator SRC-1a recruitment to RXRalpha. Tretinoin 327-335 retinoic acid receptor gamma Homo sapiens 118-121
15238362-0 2004 LEDGF regulation of alcohol and aldehyde dehydrogenases in lens epithelial cells: stimulation of retinoic acid production and protection from ethanol toxicity. Tretinoin 97-110 PC4 and SFRS1 interacting protein 1 Homo sapiens 0-5
15238362-9 2004 Cells overexpressing LEDGF typically exhibited elevated RA levels and survived well during ethanol stress. Tretinoin 56-58 PC4 and SFRS1 interacting protein 1 Homo sapiens 21-26
15238362-10 2004 The present findings indicate that LEDGF is one of the transcriptional activators of these genes that facilitates cellular protection against ethanol stress and plays a role in RA production. Tretinoin 177-179 PC4 and SFRS1 interacting protein 1 Homo sapiens 35-40
15262888-9 2004 Neurons induced by beta-catenin overexpression either alone or in association with RA express the caudal neuronal marker Hoxc4. Tretinoin 83-85 homeobox C4 Homo sapiens 121-126
15254248-9 2004 In addition, inhibition by RA of GATA-2-dependent hematopoietic colony formation in an embryonic stem cell model of hematopoietic differentiation provided biological evidence for functional cross talk between RA and GATA-2-dependent pathways. Tretinoin 27-29 GATA binding protein 2 Homo sapiens 33-39
15254248-9 2004 In addition, inhibition by RA of GATA-2-dependent hematopoietic colony formation in an embryonic stem cell model of hematopoietic differentiation provided biological evidence for functional cross talk between RA and GATA-2-dependent pathways. Tretinoin 27-29 GATA binding protein 2 Homo sapiens 216-222
15254248-9 2004 In addition, inhibition by RA of GATA-2-dependent hematopoietic colony formation in an embryonic stem cell model of hematopoietic differentiation provided biological evidence for functional cross talk between RA and GATA-2-dependent pathways. Tretinoin 209-211 GATA binding protein 2 Homo sapiens 33-39
15281009-1 2004 The aim of this study was to confirm if catabolism of all-trans retinoic acid (RA) is enhanced by type I cellular retinoic acid binding protein (CRABP-I) expression and to investigate the effect of this enhanced catabolism on cell proliferation of the head and neck squamous cell carcinoma (HNSCC) cell line, AMC-HN-7. Tretinoin 64-77 cellular retinoic acid binding protein 1 Homo sapiens 145-152
15281009-1 2004 The aim of this study was to confirm if catabolism of all-trans retinoic acid (RA) is enhanced by type I cellular retinoic acid binding protein (CRABP-I) expression and to investigate the effect of this enhanced catabolism on cell proliferation of the head and neck squamous cell carcinoma (HNSCC) cell line, AMC-HN-7. Tretinoin 114-127 cellular retinoic acid binding protein 1 Homo sapiens 145-152
15271423-0 2004 Ornithine decarboxylase, polyamines and CD11b expression in HL-60 cells during differentiation induced by retinoic acid. Tretinoin 106-119 ornithine decarboxylase 1 Homo sapiens 0-23
15271423-4 2004 ODC activity and PUT levels are correlated with mieloid cell differentiation induced by retinoic acid treatment. Tretinoin 88-101 ornithine decarboxylase 1 Homo sapiens 0-3
15271423-5 2004 Only the ODC/PUT ratio is connected with retinoic acid treated HL-60 cells. Tretinoin 41-54 ornithine decarboxylase 1 Homo sapiens 9-12
15271423-10 2004 Our data show that retinoic acid treatment modifies ODC activity and the turnover of PA. Tretinoin 19-32 ornithine decarboxylase 1 Homo sapiens 52-55
15194426-7 2004 Overall, RA increased the functionality of pRb as an inhibitor of cell cycle progression. Tretinoin 9-11 RB transcriptional corepressor 1 Homo sapiens 43-46
15239098-8 2004 SHP repressed the activity of the ASBT promoter and reduced activation by retinoic acid. Tretinoin 74-87 nuclear receptor subfamily 0 group B member 2 Homo sapiens 0-3
20110732-0 2010 Kidneys of Alb/TGF-beta1 transgenic mice are deficient in retinoic acid and exogenous retinoic acid shows dose-dependent toxicity. Tretinoin 86-99 transforming growth factor, beta 1 Mus musculus 15-24
20042001-2 2010 Carrier proteins that move the RA from the cytosol into the nucleus are the fatty acid-binding protein 5 (FABP5), activating PPARdelta, and the cellular retinoic acid-binding protein II (CRABPII), activating RAR. Tretinoin 31-33 cellular retinoic acid binding protein II Mus musculus 144-185
20042001-2 2010 Carrier proteins that move the RA from the cytosol into the nucleus are the fatty acid-binding protein 5 (FABP5), activating PPARdelta, and the cellular retinoic acid-binding protein II (CRABPII), activating RAR. Tretinoin 31-33 cellular retinoic acid binding protein II Mus musculus 187-194
15485630-2 2004 Here, we show that the vitamin A (retinol) metabolite, retinoic acid, enhances the expression of alpha4beta7 and CCR9 on T cells upon activation and imprints them with the gut tropism. Tretinoin 55-68 C-C motif chemokine receptor 9 Homo sapiens 113-117
20013305-5 2010 By UV-visible and circular dichroism spectroscopy studies, we studied for the first time the structural stability and all-trans-retinoic acid binding capability of the CYP2C8 variants. Tretinoin 122-141 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 168-174
15375546-7 2004 All-trans retinoic acid (atRA), 9-cis retinoic acid (9cRA), and 4-(hydroxyphenyl) retinamide (4-HPR) induced RARbeta2 protein expression exclusively in the benign MCF10A cells and the former two retinoids, mRNA expression in MCF10A and MCF10AT cells, but not in malignant, MCF10CA1a cells, suggesting that the loss of inducible RARbeta expression is associated with the progression and malignant transformation of MCF10A cells. Tretinoin 0-23 haptoglobin-related protein Homo sapiens 96-99
20011517-5 2009 Genetic mapping revealed a mutation resulting in a glycine to arginine change in the catalytic domain of the aldh1a2 gene, which is required for the production of retinoic acid from vitamin A. Tretinoin 163-176 aldehyde dehydrogenase 1 family, member A2 Danio rerio 109-116
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 0-13 transglutaminase 1 Homo sapiens 40-45
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 0-13 transglutaminase 1 Homo sapiens 115-120
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 15-17 transglutaminase 1 Homo sapiens 40-45
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 15-17 transglutaminase 1 Homo sapiens 115-120
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 104-106 transglutaminase 1 Homo sapiens 40-45
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 104-106 transglutaminase 1 Homo sapiens 115-120
15272014-4 2004 Here we investigate whether EGF also antagonized RA-induced TGase expression in breast cancer cells. Tretinoin 49-51 transglutaminase 1 Homo sapiens 60-65
19651168-0 2009 TRPV1 expression and activity during retinoic acid-induced neuronal differentiation. Tretinoin 37-50 transient receptor potential cation channel subfamily V member 1 Homo sapiens 0-5
15467907-6 2004 Moreover, following treatment with retinoic acid, CD133(+) cells exhibited neural morphology associated with the expression of beta-III-tubulin. Tretinoin 35-48 prominin 1 Homo sapiens 50-55
19651168-4 2009 We show that RA highly up-regulated the total and cell surface TRPV1 protein expression but the TRPV1 mRNA level was unaffected. Tretinoin 13-15 transient receptor potential cation channel subfamily V member 1 Homo sapiens 63-68
19651168-7 2009 The results show that TRPV1 protein expression increases during RA-induced differentiation in vitro, which generates an altered intracellular Ca(2+) homeostasis. Tretinoin 64-66 transient receptor potential cation channel subfamily V member 1 Homo sapiens 22-27
19782671-0 2009 Epidermal expression of Hox1 is directly activated by retinoic acid in the Ciona intestinalis embryo. Tretinoin 54-67 homeobox transcription factor Hox1 Ciona intestinalis 24-28
15331636-4 2004 In a neuronal NO synthase (nNOS) overexpressing neuroblastoma cell line exposed to the differentiative action of retinoic acid, NO slowed down proliferation and accelerated differentiation towards a neuronal phenotype. Tretinoin 113-126 nitric oxide synthase 1 Homo sapiens 27-31
19782671-10 2009 These results indicate that retinoic acid directly activates the epidermal enhancer of Ci-Hox1. Tretinoin 28-41 homeobox transcription factor Hox1 Ciona intestinalis 87-94
19737349-15 2009 RA was shown to induce Alb-GLuc activity and late hepatocyte markers. Tretinoin 0-2 albumin Mus musculus 23-26
15313187-3 2004 ATRA dose-dependently down-regulated protein levels of OPG in MG-63 cells, with a maximum (-56%) observed at a dose of 10(-6)M. This effect was confirmed with quantitative real-time PCR, where OPG mRNA was decreased after 4h (-68%) in primary cultures and after 8h (-87%) in MG-63 cells. Tretinoin 0-4 TNF receptor superfamily member 11b Homo sapiens 55-58
15313187-3 2004 ATRA dose-dependently down-regulated protein levels of OPG in MG-63 cells, with a maximum (-56%) observed at a dose of 10(-6)M. This effect was confirmed with quantitative real-time PCR, where OPG mRNA was decreased after 4h (-68%) in primary cultures and after 8h (-87%) in MG-63 cells. Tretinoin 0-4 TNF receptor superfamily member 11b Homo sapiens 193-196
15281068-3 2004 Murine P19 embryonal stem cells differentiate to neurons upon aggregation in the presence of retinoic acid, and we previously showed that RhoA and Cdc42 RhoGTPases are sequentially up-regulated during neuroinduction, suggesting a role at this very early developmental stage. Tretinoin 93-106 ras homolog family member A Mus musculus 138-142
15281068-3 2004 Murine P19 embryonal stem cells differentiate to neurons upon aggregation in the presence of retinoic acid, and we previously showed that RhoA and Cdc42 RhoGTPases are sequentially up-regulated during neuroinduction, suggesting a role at this very early developmental stage. Tretinoin 93-106 cell division cycle 42 Mus musculus 147-152
19737349-15 2009 RA was shown to induce Alb-GLuc activity and late hepatocyte markers. Tretinoin 0-2 glucosidase, beta, acid Mus musculus 27-31
15316117-8 2004 In vivo, the OT/OTR system in the fetal heart was sensitive to the actions of retinoic acid (RA), recognized as a major cardiac morphogen. Tretinoin 78-91 oxytocin receptor Rattus norvegicus 16-19
15316117-8 2004 In vivo, the OT/OTR system in the fetal heart was sensitive to the actions of retinoic acid (RA), recognized as a major cardiac morphogen. Tretinoin 93-95 oxytocin receptor Rattus norvegicus 16-19
19862326-0 2009 Retinoic acid mediates long-paced oscillations in retinoid receptor activity: evidence for a potential role for RIP140. Tretinoin 0-13 nuclear receptor interacting protein 1 Homo sapiens 112-118
15234273-4 2004 In the presence of RA, the coactivators SRC-1 and GRIP-1 formed complexes with RAR beta and RXR alpha which are bound to an oligonucleotide specifying a RARE site in the promoter. Tretinoin 19-21 nuclear receptor coactivator 1 Homo sapiens 40-45
15234273-5 2004 In conclusion, this study shows that in the presence of retinoic acid, the coactivators SRC-1 and GRIP-1 augment, while the corepressor N-CoR abolishes, the suppressive effects of RAR beta and RXR alpha on alpha 2(I) collagen promoter activity. Tretinoin 56-69 nuclear receptor coactivator 1 Homo sapiens 88-93
15262180-0 2004 Possible involvement of p44/p42 MAP kinase in retinoic acid-stimulated vascular endothelial growth factor release in aortic smooth muscle cells. Tretinoin 46-59 interferon induced protein 44 Homo sapiens 24-27
15262180-6 2004 Retinoic acid induced the phosphorylation of p44/p42 mitogen-activated protein (MAP) kinase but not p38 MAP kinase or stress-activated protein kinase/c-Jun N-terminal kinase among the MAP kinase superfamily. Tretinoin 0-13 interferon induced protein 44 Homo sapiens 45-48
15262180-8 2004 The retinoic acid-stimulated release of VEGF was significantly reduced by PD98059 and U0126, specific MEK inhibitors, which attenuated the retinoic acid-induced phosphorylation of p44/p42 MAP kinase. Tretinoin 4-17 interferon induced protein 44 Homo sapiens 180-183
15262180-8 2004 The retinoic acid-stimulated release of VEGF was significantly reduced by PD98059 and U0126, specific MEK inhibitors, which attenuated the retinoic acid-induced phosphorylation of p44/p42 MAP kinase. Tretinoin 139-152 interferon induced protein 44 Homo sapiens 180-183
19862326-4 2009 Previously, we showed that RIP140 is inducible by all-trans retinoic acid (RA) and mediates limiting, negative-feedback regulation of retinoid signaling. Tretinoin 60-73 nuclear receptor interacting protein 1 Homo sapiens 27-33
19862326-4 2009 Previously, we showed that RIP140 is inducible by all-trans retinoic acid (RA) and mediates limiting, negative-feedback regulation of retinoid signaling. Tretinoin 75-77 nuclear receptor interacting protein 1 Homo sapiens 27-33
19693777-4 2009 In these latter two cell lines, as opposed to HMEC cells, we observe a residual ability of XDH to produce retinoic acid from retinaldehyde and the inability to use retinol, as a consequence of a deficit in CRBP. Tretinoin 106-119 xanthine dehydrogenase Homo sapiens 91-94
15245423-3 2004 Retinal dehydrogenases (Aldh1a1, 2, and 3, formerly Raldh 1, 2, and 3) are the enzymes responsible for the last step in retinoic acid synthesis. Tretinoin 120-133 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 24-41
15245423-3 2004 Retinal dehydrogenases (Aldh1a1, 2, and 3, formerly Raldh 1, 2, and 3) are the enzymes responsible for the last step in retinoic acid synthesis. Tretinoin 120-133 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 52-69
19625708-2 2009 PRAME is a tumor-associated antigen and has been described as a corepressor of retinoic acid signaling in solid tumor cells, but its function in hematopoietic cells is unknown. Tretinoin 79-92 PRAME nuclear receptor transcriptional regulator Homo sapiens 0-5
15328373-8 2004 Mad1-expression, however, neither enforced spontaneous differentiation nor enhanced differentiation induced by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, retinoic acid (RA), or vitamin D3 but rather led to delayed RA-stimulated differentiation. Tretinoin 227-229 MAX dimerization protein 1 Homo sapiens 0-4
19614676-7 2009 Conversely, treatment with retinoic acid, an inducer of TG2, significantly decreased EGF-induced EGFR dimerization and its phosphorylation with a significant increase in TG2 expression and its catalysed products, isopeptide bonds, in both subpopulations. Tretinoin 27-40 transglutaminase 2 Rattus norvegicus 56-59
15328373-9 2004 Mad1-expressing cells were further found to be reduced in cell size in all phases of the cells cycle and particularly in response to RA-induced differentiation. Tretinoin 133-135 MAX dimerization protein 1 Homo sapiens 0-4
15218101-0 2004 The specific binding of retinoic acid to RPE65 and approaches to the treatment of macular degeneration. Tretinoin 24-37 retinoid isomerohydrolase RPE65 Homo sapiens 41-46
19614676-7 2009 Conversely, treatment with retinoic acid, an inducer of TG2, significantly decreased EGF-induced EGFR dimerization and its phosphorylation with a significant increase in TG2 expression and its catalysed products, isopeptide bonds, in both subpopulations. Tretinoin 27-40 transglutaminase 2 Rattus norvegicus 170-173
15218101-6 2004 A retinoic acid analog that binds weakly to RPE65 is not inhibitory. Tretinoin 2-15 retinoid isomerohydrolase RPE65 Homo sapiens 44-49
19619546-2 2009 In the epithelial cell membrane, we show that manipulation of tgase2 function by monodansylcadaverine or retinoic acid (RA) alters the activity of a membrane-bound protein kinase, nucleoside diphosphate kinase (NDPK, nm23-H1/H2) that is known to control G-protein function. Tretinoin 105-118 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 217-227
15196955-2 2004 The main biosynthetic enzyme responsible for RA signaling in the hindbrain and spinal cord is Raldh2. Tretinoin 45-47 aldehyde dehydrogenase 1 family, member A2 Danio rerio 94-100
19619546-2 2009 In the epithelial cell membrane, we show that manipulation of tgase2 function by monodansylcadaverine or retinoic acid (RA) alters the activity of a membrane-bound protein kinase, nucleoside diphosphate kinase (NDPK, nm23-H1/H2) that is known to control G-protein function. Tretinoin 120-122 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 217-227
19665987-2 2009 Nuclear run-on assays demonstrated transcriptional regulation of the Lrat gene in vivo by all-trans-retinoic acid (RA) and other retinoids. Tretinoin 94-113 lecithin retinol acyltransferase Homo sapiens 69-73
15161940-7 2004 These results suggest that RA acts through the activation of RARbeta, to induce a rapid, non-genomic increase in the frequency of spontaneous transmitter release at developing neuromuscular synapses. Tretinoin 27-29 retinoic acid receptor beta L homeolog Xenopus laevis 61-68
15242250-4 2004 All-trans retinoic acid, taxol and okadiac acid induce downregulation or inactivation of nucleolin, which destabilizes bcl-2 mRNA and triggers apoptosis. Tretinoin 10-23 nucleolin Homo sapiens 89-98
15241564-10 2004 In neuroblastoma cells incubated with ATRA, a concentration-dependent increase in the expression of COX-2 protein was observed. Tretinoin 38-42 cytochrome c oxidase II, mitochondrial Rattus norvegicus 100-105
15241564-12 2004 An increase in COX-2 expression in the lumbar spinal cord was also observed in animals treated with ATRA. Tretinoin 100-104 cytochrome c oxidase II, mitochondrial Rattus norvegicus 15-20
19665987-2 2009 Nuclear run-on assays demonstrated transcriptional regulation of the Lrat gene in vivo by all-trans-retinoic acid (RA) and other retinoids. Tretinoin 115-117 lecithin retinol acyltransferase Homo sapiens 69-73
15693634-9 2004 In our study, RA treatment with brain-derived growth factor and TGFalpha in neuron differentiation medium induced not only neuronal differentiation but also pluripotential differentiation. Tretinoin 14-16 transforming growth factor alpha Homo sapiens 64-72
19860663-5 2009 Mucosal dendritic cells (DCs) regulate the expression of the gut homing receptors alpha(4)beta(7) integrin and the chemokine receptor CCR9 on activated effector and regulatory lymphocytes in a retinoic acid-dependent manner. Tretinoin 193-206 atypical chemokine receptor 2 Homo sapiens 115-138
15209417-3 2004 A defined pattern of PS1 expression was observed during differentiation with both RA and the phorbol ester TPA. Tretinoin 82-84 presenilin 1 Homo sapiens 21-24
15143193-3 2004 We have previously shown that retinoic acid plays a key role in early stages of Cdx1 expression at embryonic day 7.5 (E7.5), while both Wnt3a signaling and an autoregulatory loop, dependent on Cdx1 itself, are involved in later stages of expression (E8.5 to E9.5). Tretinoin 30-43 caudal type homeobox 1 Homo sapiens 80-84
15143193-3 2004 We have previously shown that retinoic acid plays a key role in early stages of Cdx1 expression at embryonic day 7.5 (E7.5), while both Wnt3a signaling and an autoregulatory loop, dependent on Cdx1 itself, are involved in later stages of expression (E8.5 to E9.5). Tretinoin 30-43 caudal type homeobox 1 Homo sapiens 193-197
15133197-1 2004 Retinoic acid and its amide derivative, N-(4-hydroxyphenyl)retinamide (4-HPR), have been proposed as chemopreventative and chemotherapeutic agents. Tretinoin 0-13 haptoglobin-related protein Homo sapiens 73-76
15133197-5 2004 Transcription assays in COS-1 cells indicated that the N-acylated derivatives (2A-5A) and 4-HPR (1A) were much weaker ligands for all three subtypes of retinoic acid receptor (RAR) than all-trans retinoic acid (ATRA), although they showed some selectivity for RARbeta and RARgamma. Tretinoin 152-165 haptoglobin-related protein Homo sapiens 92-95
15133197-5 2004 Transcription assays in COS-1 cells indicated that the N-acylated derivatives (2A-5A) and 4-HPR (1A) were much weaker ligands for all three subtypes of retinoic acid receptor (RAR) than all-trans retinoic acid (ATRA), although they showed some selectivity for RARbeta and RARgamma. Tretinoin 211-215 haptoglobin-related protein Homo sapiens 92-95
15209417-4 2004 Full-length PS1 was shown to increase dramatically within 5-24 h of RA treatment. Tretinoin 68-70 presenilin 1 Homo sapiens 12-15
19539783-2 2009 At early somite stages, Wnt/beta-catenin and FGF signaling domains exist both anterior and posterior to the developing trunk, whereas RA signaling occurs in between in the trunk under the control of the RA-synthesizing enzyme retinaldehyde dehydrogenase-2 (Raldh2). Tretinoin 203-205 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 226-255
15209417-6 2004 The intracellular distribution pattern of PS1 was markedly altered following RA treatment. Tretinoin 77-79 presenilin 1 Homo sapiens 42-45
15209417-9 2004 Increases in PS1 expression upon treatment with RA and TPA were blocked by treatment with cycloheximide, indicating a role of de-novo protein synthesis in this effect. Tretinoin 48-50 presenilin 1 Homo sapiens 13-16
15051476-0 2004 Retinoic acid and dexamethasone regulate the expression of PEDF in retinal and endothelial cells. Tretinoin 0-13 serpin family F member 1 Homo sapiens 59-63
15051476-4 2004 Mouse Muller glial cells and rat C6 glioma cells showed at least a 2.5 fold increase in PEDF RNA levels after ATRA treatment, as measured by quantitative PCR. Tretinoin 110-114 serpin family F member 1 Rattus norvegicus 88-92
19539783-3 2009 Previous studies demonstrated that vitamin A deficient quail embryos and Raldh2(-/-) mouse embryos lacking RA synthesis exhibit ectopic expression of Fgf8 and Wnt8a in the developing trunk. Tretinoin 107-109 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-79
15051476-11 2004 This study clearly indicates an interaction between PEDF and ATRA. Tretinoin 61-65 serpin family F member 1 Homo sapiens 52-56
19539783-5 2009 Following loss of RA signaling, the caudal expression domains of Fgf8, Wnt8a, and Wnt3a expand anteriorly into the trunk, but no change is observed in caudal expression of Fgf4 or Fgf17 plus caudal expression of Fgf18 and Cdx1 is reduced. Tretinoin 18-20 wingless-type MMTV integration site family, member 8A Mus musculus 71-76
19539783-5 2009 Following loss of RA signaling, the caudal expression domains of Fgf8, Wnt8a, and Wnt3a expand anteriorly into the trunk, but no change is observed in caudal expression of Fgf4 or Fgf17 plus caudal expression of Fgf18 and Cdx1 is reduced. Tretinoin 18-20 caudal type homeobox 1 Mus musculus 222-226
15152096-5 2004 Retinoic acid bound equally well to wild type and P85V-CRABP I, confirming the functional integrity of this mutation. Tretinoin 0-13 retinol binding protein 1 Homo sapiens 55-62
19671662-6 2009 Subsequent treatment with retinoic acid and taurine induces photoreceptors that express recoverin, rhodopsin and genes involved in phototransduction. Tretinoin 26-39 recoverin Homo sapiens 88-97
15093729-0 2004 T-box binding protein type two (TBX2) is an immediate early gene target in retinoic-acid-treated B16 murine melanoma cells. Tretinoin 75-88 T-box 2 Mus musculus 32-36
15093729-4 2004 Increased TBX2 mRNA is seen within 2 h after addition of retinoic acid to B16 cells. Tretinoin 57-70 T-box 2 Mus musculus 10-14
15093729-6 2004 We identified a degenerate retinoic acid response element (RARE) between -186 and -163 in the promoter region of the tbx2 gene. Tretinoin 27-40 T-box 2 Mus musculus 117-121
15095411-0 2004 Retinoic acid regulates the expression of PBX1, PBX2, and PBX3 in P19 cells both transcriptionally and post-translationally. Tretinoin 0-13 pre B cell leukemia homeobox 2 Mus musculus 48-52
15095411-3 2004 In this report, we demonstrate that PBX1a, PBX1b, PBX2, and PBX3 mRNAs and PBX1/2/3 proteins are induced during endodermal and neuronal differentiation of P19 cells in a RAR-dependent subtype-unspecific manner following RA treatment. Tretinoin 170-172 pre B cell leukemia homeobox 2 Mus musculus 50-54
19569129-0 2009 ICAT as a potential enhancer of monocytic differentiation: implications from the comparative proteome analysis of the HL60 cell line stimulated by all-trans retinoic acid and NSC67657. Tretinoin 157-170 catenin beta interacting protein 1 Homo sapiens 0-4
14976209-6 2004 RA treatment of APL and other RA-responsive leukemic cells induced expression of UBE1L and ISG15 as well as intracellular ISG15 conjugates. Tretinoin 0-2 autophagy related 7 Homo sapiens 81-86
14976209-6 2004 RA treatment of APL and other RA-responsive leukemic cells induced expression of UBE1L and ISG15 as well as intracellular ISG15 conjugates. Tretinoin 0-2 ISG15 ubiquitin like modifier Homo sapiens 91-96
14976209-6 2004 RA treatment of APL and other RA-responsive leukemic cells induced expression of UBE1L and ISG15 as well as intracellular ISG15 conjugates. Tretinoin 0-2 ISG15 ubiquitin like modifier Homo sapiens 122-127
15046780-6 2004 We demonstrate that retinoic acid already affects in the early stage of germ layer formation, which was demonstrated by a change of Oct-4 and Brachyury gene expression. Tretinoin 20-33 T-box transcription factor 1 Homo sapiens 142-151
15155579-2 2004 We reveal programmed changes in chromatin structure and nuclear organization upon induction of Hoxb expression by retinoic acid. Tretinoin 114-127 homeobox B cluster Homo sapiens 95-99
14709332-2 2004 We have previously demonstrated that tyrosine-phosphorylated Vav, also located inside the nucleus of myeloid cells, is up-regulated during maturation of promyelocytic precursors induced by all-trans-retinoic acid (ATRA). Tretinoin 189-212 vav guanine nucleotide exchange factor 1 Homo sapiens 61-64
19519663-3 2009 We show that cells of the vomeronasal nerve express the retinoic acid (RA) synthesizing enzyme retinal dehydrogenase 2. Tretinoin 56-69 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 95-118
14709332-2 2004 We have previously demonstrated that tyrosine-phosphorylated Vav, also located inside the nucleus of myeloid cells, is up-regulated during maturation of promyelocytic precursors induced by all-trans-retinoic acid (ATRA). Tretinoin 214-218 vav guanine nucleotide exchange factor 1 Homo sapiens 61-64
14709332-4 2004 These ATRA-induced events are independent on the guanine nucleotide exchange activity of Vav. Tretinoin 6-10 vav guanine nucleotide exchange factor 1 Homo sapiens 89-92
14709332-6 2004 The Vav/p85 interaction is essential for the ATRA-induced PI 3-K activity and for association of PI 3-K with actin, particularly in the nucleus. Tretinoin 45-49 vav guanine nucleotide exchange factor 1 Homo sapiens 4-7
14709332-6 2004 The Vav/p85 interaction is essential for the ATRA-induced PI 3-K activity and for association of PI 3-K with actin, particularly in the nucleus. Tretinoin 45-49 peptidase inhibitor 3 Homo sapiens 58-62
15291358-1 2004 N-(4-hydroxyphenyl) retinamide (Fenretinide, 4-HPR) inhibits cell growth by inducing apoptosis in numerous tumor cell types including all-trans-retinoic acid (ATRA)-resistant tumor cells. Tretinoin 137-157 haptoglobin-related protein Homo sapiens 47-50
15291358-1 2004 N-(4-hydroxyphenyl) retinamide (Fenretinide, 4-HPR) inhibits cell growth by inducing apoptosis in numerous tumor cell types including all-trans-retinoic acid (ATRA)-resistant tumor cells. Tretinoin 159-163 haptoglobin-related protein Homo sapiens 47-50
15291358-4 2004 We treated HL-60 and ATRA-resistant HL-60 (HL-60R) cells that express mutated RARalpha and very low levels of RARbeta, RARgamma and RXRalpha with 4-HPR (2 microM) for 3 days. Tretinoin 21-25 retinoic acid receptor gamma Homo sapiens 119-127
15291358-4 2004 We treated HL-60 and ATRA-resistant HL-60 (HL-60R) cells that express mutated RARalpha and very low levels of RARbeta, RARgamma and RXRalpha with 4-HPR (2 microM) for 3 days. Tretinoin 21-25 haptoglobin-related protein Homo sapiens 148-151
19519663-3 2009 We show that cells of the vomeronasal nerve express the retinoic acid (RA) synthesizing enzyme retinal dehydrogenase 2. Tretinoin 71-73 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 95-118
19477923-0 2009 Induction of HoxB transcription by retinoic acid requires actin polymerization. Tretinoin 35-48 homeobox B cluster Homo sapiens 13-17
15073138-8 2004 Transfection experiments in BEAS-2B cells indicated that RA treatment repressed expression of wild-type cyclin D1 and cyclin E, but ALLN inhibited this degradation. Tretinoin 57-59 cyclin D1 Homo sapiens 104-113
19477923-1 2009 We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. Tretinoin 53-66 homeobox B cluster Homo sapiens 80-84
17216084-9 2004 Factors regulating mucin gene expression include retinoic acid, serum, and dexamethasone. Tretinoin 49-62 LOC100508689 Homo sapiens 19-24
15233552-6 2004 Three parameters for assessment of RA effects were established: a) reduction of serum thyroglobulin levels; b) increment of the post-therapeutic dose radioiodine uptake; c) tumor size regression after therapy. Tretinoin 35-37 thyroglobulin Homo sapiens 86-99
19477923-1 2009 We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. Tretinoin 53-66 homeobox B cluster Homo sapiens 125-129
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 tubulin beta 3 class III Homo sapiens 216-232
14743441-7 2004 In addition, RA-treated CD133+ cells expressed cell type-specific markers for oligodendrocytes including myelin basic protein (MBP) as shown by RT-PCR, proteolipid protein (PLP) by Western blot analysis, and cyclic nucleotide phosphodiesterase (CNPase) by immunostaining. Tretinoin 13-15 myelin basic protein Homo sapiens 105-125
19477923-1 2009 We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. Tretinoin 68-70 homeobox B cluster Homo sapiens 80-84
19477923-1 2009 We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. Tretinoin 68-70 homeobox B cluster Homo sapiens 125-129
19477923-2 2009 RA induction of the HoxB genes can be prevented by the inhibition of actin polymerization. Tretinoin 0-2 homeobox B cluster Homo sapiens 20-24
14977075-6 2004 We also determined the effect of RA on the mRNA expressions of the cornifin-alpha and mucin genes as indicators of squamous and mucous differentiation, respectively. Tretinoin 33-35 small proline rich protein 1A Homo sapiens 67-81
19477923-4 2009 RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. Tretinoin 0-2 non-POU domain containing octamer binding Homo sapiens 185-191
14977075-6 2004 We also determined the effect of RA on the mRNA expressions of the cornifin-alpha and mucin genes as indicators of squamous and mucous differentiation, respectively. Tretinoin 33-35 LOC100508689 Homo sapiens 86-91
14991612-11 2004 Natural RA also induced the expression of FasL in phytohemagglutinin-activated peripheral murine T cells. Tretinoin 8-10 Fas ligand (TNF superfamily, member 6) Mus musculus 42-46
14977075-9 2004 In addition, the expression of cornifin-alpha mRNA was suppressed, and the expressions of mucin gene 5AC (MUC5AC) and MUC5B mRNA increased progressively with RA treatment. Tretinoin 158-160 small proline rich protein 1A Homo sapiens 31-45
19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 41-43 collagen type XI alpha 2 chain Homo sapiens 117-121
14977075-9 2004 In addition, the expression of cornifin-alpha mRNA was suppressed, and the expressions of mucin gene 5AC (MUC5AC) and MUC5B mRNA increased progressively with RA treatment. Tretinoin 158-160 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 118-123
15587392-7 2004 ATRA inhibited the mRNA expression of CDK6, CDK4, cyclinD3 and cyclinD1. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 44-48
15587392-7 2004 ATRA inhibited the mRNA expression of CDK6, CDK4, cyclinD3 and cyclinD1. Tretinoin 0-4 cyclin D1 Homo sapiens 63-71
15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 64-68
15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin dependent kinase 2 Homo sapiens 70-74
14991612-12 2004 It is proposed that therapeutically administered RA might induce apoptosis in Fas-sensitive cells via induction of FasL expression in activated Tcells. Tretinoin 49-51 Fas ligand (TNF superfamily, member 6) Mus musculus 115-119
14978018-11 2004 Furthermore, a blocking anti-IL-2 receptor antibody completely abrogated the anti-apoptotic effect of atRA. Tretinoin 102-106 interleukin 2 receptor subunit beta Homo sapiens 29-42
14749706-7 2004 The gene expression levels of CXC chemokines (MIP-2 and KC) and ICAM-1 were increased in the lung and heart by the ATRA administration. Tretinoin 115-119 intercellular adhesion molecule 1 Mus musculus 64-70
19954601-1 2009 OBJECTIVE: To explore the characteristics of CpG islands methylation at promoter region of HOX A gene cluster in leukemia cells before and after all-trans retinoic acid (ATRA) treatment. Tretinoin 155-168 homeobox A cluster Homo sapiens 91-96
19954601-1 2009 OBJECTIVE: To explore the characteristics of CpG islands methylation at promoter region of HOX A gene cluster in leukemia cells before and after all-trans retinoic acid (ATRA) treatment. Tretinoin 170-174 homeobox A cluster Homo sapiens 91-96
14607780-7 2004 On the basis of microarray data analysis, we hypothesize that Dex-induced inhibition of septation is associated with a block in angiogenesis due to downregulation of the kinase domain receptor (KDR), also known as VEGF receptor-2 and fetal liver kinase, and that the downregulation of KDR is prevented by treatment with RA. Tretinoin 320-322 kinase insert domain protein receptor Mus musculus 170-192
15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin D1 Homo sapiens 76-84
19954601-11 2009 Methylation levels of HOX A4, A6 and A10 in HL-60 cells and of HOX A6 in K562 cells were reduced by ATRA treatment. Tretinoin 100-104 homeobox A6 Homo sapiens 63-69
14607780-7 2004 On the basis of microarray data analysis, we hypothesize that Dex-induced inhibition of septation is associated with a block in angiogenesis due to downregulation of the kinase domain receptor (KDR), also known as VEGF receptor-2 and fetal liver kinase, and that the downregulation of KDR is prevented by treatment with RA. Tretinoin 320-322 kinase insert domain protein receptor Mus musculus 194-197
19516907-13 2009 We further show that the RA pathway acts synergistically with FGF4 in endoderm patterning rather than mediating FGF4 activity. Tretinoin 25-27 fibroblast growth factor 4 Gallus gallus 62-66
19472184-9 2009 Treatment of the fetal cortical neurons with ATRA significantly increased the expression of HOXd3, a retinoid-target gene. Tretinoin 45-49 homeobox D3 Mus musculus 92-97
14581485-7 2004 Importantly, we demonstrate that circadian gene expression of the serum protein insulin-like growth factor-binding protein 1 and of the NKG2D receptor ligand retinoic acid early transcript was suppressed in Stra13-/- mice. Tretinoin 158-171 centromere protein X Mus musculus 207-213
19472184-11 2009 Results suggest that ATRA activates the p38 MAPK signal pathway with resultant degradation of SRC-3, and that p38 MAPK is involved in the regulation of RARalpha-mediated signaling in developing neurons. Tretinoin 21-25 mitogen-activated protein kinase 14 Mus musculus 40-43
14666262-0 2003 Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid. Tretinoin 102-115 heterochromatin, Chr 11 Mus musculus 7-11
19472184-11 2009 Results suggest that ATRA activates the p38 MAPK signal pathway with resultant degradation of SRC-3, and that p38 MAPK is involved in the regulation of RARalpha-mediated signaling in developing neurons. Tretinoin 21-25 mitogen-activated protein kinase 14 Mus musculus 40-48
14666262-1 2003 The objective of the present study was to determine the effects of retinoic acid on the growth of the mouse mammary cells HC11 and HC11ras, which are a model for in vitro breast cancer progression. Tretinoin 67-80 heterochromatin, Chr 11 Mus musculus 122-126
19156866-6 2009 Interestingly, the antiapoptotic effects of atRA were inhibited by DDAH2 small RNA interference. Tretinoin 44-48 dimethylarginine dimethylaminohydrolase 2 Rattus norvegicus 67-72
15641697-2 2004 The Cx43 expression was detected by flowcytometry, Western blot, and immunofluorescence in two ovarian tumor cell lines OVCAR3, CaOV3 before and after RA treatment. Tretinoin 151-153 gap junction protein alpha 1 Homo sapiens 4-8
15641697-6 2004 The expression of Cx43 in both cell lines could be induced by RA. Tretinoin 62-64 gap junction protein alpha 1 Homo sapiens 18-22
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 protein regulator of cytokinesis 1 Homo sapiens 103-107
14704332-4 2004 In vitamin A-deficient liver, both LRAT mRNA and activity are significantly down-regulated as well as rapidly induced after the administration of vitamin A or its principal hormonal metabolite, retinoic acid (RA). Tretinoin 194-207 lecithin retinol acyltransferase Homo sapiens 35-39
14635200-0 2003 Runx2/Cbfa1 stimulation by retinoic acid is potentiated by BMP2 signaling through interaction with Smad1 on the collagen X promoter in chondrocytes. Tretinoin 27-40 runt related transcription factor 2 Gallus gallus 0-5
14668795-8 2003 Such a combination therapy might hold promise in clinic to avoid side effects of ATRA whose administration can indiscriminately activate all RARs. Tretinoin 81-85 arginyl-tRNA synthetase 1 Homo sapiens 141-145
14623241-3 2003 Here, we find that correct patterning of Hgf expression in forelimb buds is dependent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proximally. Tretinoin 89-102 hepatocyte growth factor Homo sapiens 41-44
14623241-3 2003 Here, we find that correct patterning of Hgf expression in forelimb buds is dependent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proximally. Tretinoin 104-106 hepatocyte growth factor Homo sapiens 41-44
14713576-0 2003 CRABP I expression and the mediation of the sensitivity of human tumour cells to retinoic acid and irradiation. Tretinoin 81-94 cellular retinoic acid binding protein 1 Homo sapiens 0-7
14713576-1 2003 PURPOSE: To examine the role cytoplasmic retinoic acid binding protein type 1 (CRABP I) and retinoic acid receptor beta 2 (RAR-beta 2) in mediating radiosensitization of human tumour cells in vitro by retinoic acid. Tretinoin 41-54 cellular retinoic acid binding protein 1 Homo sapiens 79-86
14713576-5 2003 The retinoic acid-sensitive cell line HTB35 was transfected for inducible CRABP I overexpression to test the role of this protein in modulating the sensitivity to retinoic acid and radiation as well as in regulating RAR-beta 2 and cyclin D1 expression. Tretinoin 4-17 cellular retinoic acid binding protein 1 Homo sapiens 74-81
14713576-5 2003 The retinoic acid-sensitive cell line HTB35 was transfected for inducible CRABP I overexpression to test the role of this protein in modulating the sensitivity to retinoic acid and radiation as well as in regulating RAR-beta 2 and cyclin D1 expression. Tretinoin 4-17 cyclin D1 Homo sapiens 231-240
14506269-4 2003 Previously we have shown that the ligand-dependent corepressor, RIP140, is a direct transcriptional target of all-trans retinoic acid (RA). Tretinoin 120-133 nuclear receptor interacting protein 1 Homo sapiens 64-70
14506269-4 2003 Previously we have shown that the ligand-dependent corepressor, RIP140, is a direct transcriptional target of all-trans retinoic acid (RA). Tretinoin 135-137 nuclear receptor interacting protein 1 Homo sapiens 64-70
14506269-5 2003 Here we demonstrate that RA induction of RIP140 constitutes a rate-limiting step in the regulation of retinoic acid receptor signaling. Tretinoin 25-27 nuclear receptor interacting protein 1 Homo sapiens 41-47
14506269-7 2003 The data suggest that RA induction of RIP140 constitutes a functional negative feedback loop that limits activation of retinoid receptors in the continued presence of RA and that acutely regulated expression of coregulators may be a general regulatory mechanism in hormonal signaling. Tretinoin 22-24 nuclear receptor interacting protein 1 Homo sapiens 38-44
14506269-7 2003 The data suggest that RA induction of RIP140 constitutes a functional negative feedback loop that limits activation of retinoid receptors in the continued presence of RA and that acutely regulated expression of coregulators may be a general regulatory mechanism in hormonal signaling. Tretinoin 167-169 nuclear receptor interacting protein 1 Homo sapiens 38-44
14502603-4 2003 Gene expression of MK was enhanced by 9-cis-RA, but not by 1% ethanol (vehicle). Tretinoin 38-46 midkine Bos taurus 19-21
14508522-6 2003 Cotreatment of U937/NPM-RARalpha cells with all-trans retinoic acid (atRA) abrogated the induction of apoptosis by TG. Tretinoin 54-67 nucleophosmin 1 Homo sapiens 20-23
12851412-5 2003 Serum RA levels following a 50 mg/kg dose of retinol were reduced 72% in Raldh1-/- mice and 82% in Adh1-/- mice. Tretinoin 6-8 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 73-79
12930397-7 2003 ATRA-DCs exhibited DC morphology, had a phenotype of immature DCs, with the expression of CD1a, and upregulation of adhesion and co-stimulatory molecules. Tretinoin 0-4 CD1a molecule Homo sapiens 90-94
14565857-6 2003 IFN-alpha2 expression was retained in mature neurons after SV[HIVLTR]IFN-transduced NT2 precursor cells were induced to differentiate using retinoic acid. Tretinoin 140-153 interferon alpha 2 Homo sapiens 0-10
12906928-12 2003 We hypothesise that inhibition of AP-1 signalling may be involved in the mediation of biological effects of ATRA on PSCs. Tretinoin 108-112 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 34-38
12910240-0 2003 Down-regulation of RPE65 protein expression and promoter activity by retinoic acid. Tretinoin 69-82 retinoid isomerohydrolase RPE65 Homo sapiens 19-24
12907615-8 2003 Remarkably, in both mouse models, administration of exogenous RA had no additional beneficial effect, indicating that endogenous levels of RA are sufficient for maximal tumor suppression on CRABP-II overexpression. Tretinoin 139-141 cellular retinoic acid binding protein II Mus musculus 190-198
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 E1A binding protein p300 Homo sapiens 187-191
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 nuclear receptor coactivator 1 Homo sapiens 239-269
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 nuclear receptor coactivator 1 Homo sapiens 271-276
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 nuclear receptor coactivator 1 Homo sapiens 278-283
12812792-6 2003 Stimulation of activin, BMP, or retinoic acid signaling is sufficient to induce Pdx1 expression in endoderm anterior to the pancreas. Tretinoin 32-45 pancreatic and duodenal homeobox 1 Gallus gallus 80-84
14649730-3 2003 Exposure of retinoic acid (RA)-differentiated SH-SY5Y cells to MPP+ (1 mM, 72 h) also resulted in a decrease in RMB3 expression and an increase in GADD153 expression. Tretinoin 27-29 M-phase phosphoprotein 6 Homo sapiens 63-66
14592467-5 2003 Analysis of plasma from 4-HPR- and atRA-treated VAD animals revealed the presence of atRA whereas it was not detected in plasma from animals given 4-HBR. Tretinoin 85-89 haptoglobin-related protein Homo sapiens 26-29
14592467-6 2003 To determine whether hydrolysis to atRA is necessary for apoptosis induced by 4-HPR in MCF-7 breast cancer cells, morphological and biochemical assays for apoptosis were performed. Tretinoin 35-39 haptoglobin-related protein Homo sapiens 80-83
14592467-8 2003 Apoptosis was not induced even at high concentrations of atRA, showing that 4-HPR and 4-HBR act in cells via a distinct signaling pathway. Tretinoin 57-61 haptoglobin-related protein Homo sapiens 78-81
14592978-0 2003 C/EBPbeta: a major PML-RARA-responsive gene in retinoic acid-induced differentiation of APL cells. Tretinoin 47-60 CCAAT enhancer binding protein beta Homo sapiens 0-9
14592978-2 2003 Here we report that upon treatment with ATRA, t(15;17) cells (NB4) reveal a very rapid increase in protein level and binding activity of C/EBPbeta, a C/EBP family member, which was not observed in an ATRA-resistant NB4 cell line. Tretinoin 40-44 CCAAT enhancer binding protein beta Homo sapiens 137-146
14592978-2 2003 Here we report that upon treatment with ATRA, t(15;17) cells (NB4) reveal a very rapid increase in protein level and binding activity of C/EBPbeta, a C/EBP family member, which was not observed in an ATRA-resistant NB4 cell line. Tretinoin 40-44 CCAAT enhancer binding protein beta Homo sapiens 137-142
14592978-2 2003 Here we report that upon treatment with ATRA, t(15;17) cells (NB4) reveal a very rapid increase in protein level and binding activity of C/EBPbeta, a C/EBP family member, which was not observed in an ATRA-resistant NB4 cell line. Tretinoin 200-204 CCAAT enhancer binding protein beta Homo sapiens 137-146
14592978-2 2003 Here we report that upon treatment with ATRA, t(15;17) cells (NB4) reveal a very rapid increase in protein level and binding activity of C/EBPbeta, a C/EBP family member, which was not observed in an ATRA-resistant NB4 cell line. Tretinoin 200-204 CCAAT enhancer binding protein beta Homo sapiens 137-142
14592978-3 2003 We further provide evidence that ATRA mediates a direct increase of C/EBPbeta, only in PML-RARA (promyelocytic leukemia-retinoic acid receptor alpha)-expressing cells. Tretinoin 33-37 CCAAT enhancer binding protein beta Homo sapiens 68-77
14592978-5 2003 These results suggest that PML-RARA mediates ATRA-induced C/EBPbeta expression. Tretinoin 45-49 CCAAT enhancer binding protein beta Homo sapiens 58-67
14592978-7 2003 We show that not only does C/EBPbeta induce granulocytic differentiation of non-APL myeloid cell lines independent of addition of ATRA or other cytokines, but also that C/EBPbeta induction is required during ATRA-induced differentiation of APL cells. Tretinoin 208-212 CCAAT enhancer binding protein beta Homo sapiens 27-36
14592978-7 2003 We show that not only does C/EBPbeta induce granulocytic differentiation of non-APL myeloid cell lines independent of addition of ATRA or other cytokines, but also that C/EBPbeta induction is required during ATRA-induced differentiation of APL cells. Tretinoin 208-212 CCAAT enhancer binding protein beta Homo sapiens 169-178
14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 0-23 cyclin D1 Homo sapiens 110-119
14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 0-23 cyclin dependent kinase 2 Homo sapiens 124-128
14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 25-29 cyclin D1 Homo sapiens 110-119
14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 25-29 cyclin dependent kinase 2 Homo sapiens 124-128
14646600-4 2003 Effect of the ATRA treatment was demonstrated by the concomitant induction of cd14 and il1beta genes in four patients. Tretinoin 14-18 CD14 molecule Homo sapiens 78-82
12915404-8 2003 Obligate CDK4 phosphorylation sites seemed most important to the stability of the protein and are among the candidate sites that are dephosphorylated by PP2A following ATRA treatment. Tretinoin 168-172 cyclin dependent kinase 4 Homo sapiens 9-13
14508522-6 2003 Cotreatment of U937/NPM-RARalpha cells with all-trans retinoic acid (atRA) abrogated the induction of apoptosis by TG. Tretinoin 69-73 nucleophosmin 1 Homo sapiens 20-23
12929139-5 2003 Differentiation by cAMP and retinoic acid caused an increase of choline acetyltransferase activity and decrease of acetyl-CoA levels in both cell lines. Tretinoin 28-41 choline acetyltransferase Mus musculus 64-89
12912909-4 2003 We find that hydroxynonenal and structurally related compounds (such as trans-retinoic acid, trans-retinal and other 2-alkenals) specifically induce uncoupling of mitochondria through the uncoupling proteins UCP1, UCP2 and UCP3 and the adenine nucleotide translocase (ANT). Tretinoin 72-91 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 208-212
12912909-4 2003 We find that hydroxynonenal and structurally related compounds (such as trans-retinoic acid, trans-retinal and other 2-alkenals) specifically induce uncoupling of mitochondria through the uncoupling proteins UCP1, UCP2 and UCP3 and the adenine nucleotide translocase (ANT). Tretinoin 72-91 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 223-227
14632301-7 2003 RESULTS: Normalized RA-induced Hoxb1 expression demonstrated that only some reference genes accurately quantitated the expected 1.5- to 2-fold increase in Hoxb1 expression. Tretinoin 20-22 homeo box B1 Rattus norvegicus 31-36
14632301-7 2003 RESULTS: Normalized RA-induced Hoxb1 expression demonstrated that only some reference genes accurately quantitated the expected 1.5- to 2-fold increase in Hoxb1 expression. Tretinoin 20-22 homeo box B1 Rattus norvegicus 155-160
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 E1A binding protein p300 Homo sapiens 187-191
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 nuclear receptor coactivator 1 Homo sapiens 239-269
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 nuclear receptor coactivator 1 Homo sapiens 271-276
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 nuclear receptor coactivator 1 Homo sapiens 278-283
12887690-0 2003 Regulation of expression of sulfoglucuronyl carbohydrate (HNK-1), Amphoterin and RAGE in retinoic acid-differentiated P19 embryonal carcinoma cells. Tretinoin 89-102 high mobility group box 1 Homo sapiens 66-76
12887690-10 2003 RA also upregulated the synthesis of Amphoterin and RAGE in P19 cells. Tretinoin 0-2 high mobility group box 1 Homo sapiens 37-47
12880980-4 2003 The cytotoxic retinoid 4-HPR achieved multi-log cell kills in neuroblastoma cell lines resistant to ATRA and 13-cis-RA, and a pediatric phase I trial has shown it to be well tolerated. Tretinoin 100-104 haptoglobin-related protein Homo sapiens 25-28
12836159-0 2003 Presenilin 1 mediates retinoic acid-induced differentiation of SH-SY5Y cells through facilitation of Wnt signaling. Tretinoin 22-35 presenilin 1 Homo sapiens 0-12
12836159-3 2003 We demonstrate that SH-SY5Y cells stably expressing D385A mutant presenilin 1 failed to differentiate in response to retinoic acid treatment. Tretinoin 117-130 presenilin 1 Homo sapiens 65-77
12836159-4 2003 Retinoic acid caused an increase in nuclear beta-catenin levels in SH-SY5Y cells, which was followed by an increase in cyclin D1 protein levels. Tretinoin 0-13 cyclin D1 Homo sapiens 119-128
12801520-9 2003 Retinoic acid, which alone failed to affect VEGF synthesis, markedly enhanced the VEGF synthesis stimulated by TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 111-119
12801520-10 2003 Retinoic acid enhanced the TGF-beta-increased levels of VEGF mRNA. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 27-35
12801520-11 2003 The amplifications by retinoic acid of TGF-beta-increased VEGF synthesis and levels of VEGF mRNA were reduced by PD98059 or SB203580. Tretinoin 22-35 transforming growth factor, beta 1 Mus musculus 39-47
12844391-4 2003 Thus, the effects of vitamin A depletion and subsequent administration with RA and/or T3 on the expression of RA nuclear receptors (RAR, RXR), T3 nuclear receptor (TR) and on RC3 in the brain were examined. Tretinoin 76-78 neurogranin Rattus norvegicus 175-178
14508119-5 2003 Unlike other NKG2D ligands, Letal mRNA expression progressively decreased after treatment of tumor cells with retinoic acid. Tretinoin 110-123 killer cell lectin like receptor K1 Homo sapiens 13-18
14508119-5 2003 Unlike other NKG2D ligands, Letal mRNA expression progressively decreased after treatment of tumor cells with retinoic acid. Tretinoin 110-123 retinoic acid early transcript 1E Homo sapiens 28-33
12756180-3 2003 Grafting of somites or retinoic acid-loaded beads beneath the rostral hindbrain induced the formation of somatic motoneurones in rhombomere 4 only, and Hox genes normally expressed more caudally (Hoxa3, Hoxd4) were induced in this region. Tretinoin 23-36 homeobox A3 Homo sapiens 196-201
12813000-0 2003 Prevention of cultured rat stellate cell transformation and endothelin-B receptor upregulation by retinoic acid. Tretinoin 98-111 endothelin receptor type B Rattus norvegicus 60-81
12813000-8 2003 Retinoic acid also prevented upregulation of ETB receptors without affecting ET-1 or ETA expression. Tretinoin 0-13 endothelin receptor type B Rattus norvegicus 45-48
12813000-13 2003 4 These results showing prevention of HSC activation and negative regulation of ETB receptor expression in them by retinoic acid may have important pathophysiologic implications. Tretinoin 115-128 endothelin receptor type B Rattus norvegicus 80-83
12702665-1 2003 Targeted inactivation of the mouse retinaldehyde dehydrogenase 2 (RALDH2/ALDH1a2), the enzyme responsible for early embryonic retinoic acid synthesis, is embryonic lethal because of defects in early heart morphogenesis. Tretinoin 126-139 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 35-64
12702665-1 2003 Targeted inactivation of the mouse retinaldehyde dehydrogenase 2 (RALDH2/ALDH1a2), the enzyme responsible for early embryonic retinoic acid synthesis, is embryonic lethal because of defects in early heart morphogenesis. Tretinoin 126-139 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 66-72
12702665-1 2003 Targeted inactivation of the mouse retinaldehyde dehydrogenase 2 (RALDH2/ALDH1a2), the enzyme responsible for early embryonic retinoic acid synthesis, is embryonic lethal because of defects in early heart morphogenesis. Tretinoin 126-139 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-80
12746314-0 2003 Retinoic acid stimulates chondrocyte differentiation and enhances bone morphogenetic protein effects through induction of Smad1 and Smad5. Tretinoin 0-13 SMAD family member 5 Gallus gallus 132-137
12746314-7 2003 RA did not increase the expression of the type IA BMP receptor but did markedly up-regulate the expression of Smad1 and Smad5 proteins, important participants in the BMP pathway. Tretinoin 0-2 SMAD family member 1 Homo sapiens 110-115
12808116-0 2003 Expression of trkB in human neuroblastoma in relation to MYCN expression and retinoic acid treatment. Tretinoin 77-90 neurotrophic receptor tyrosine kinase 2 Homo sapiens 14-18
12808116-5 2003 trkB expression and BDNF responsiveness in neuroblastoma cells can be induced by all-trans-retinoic acid (RA). Tretinoin 81-104 neurotrophic receptor tyrosine kinase 2 Homo sapiens 0-4
12808116-5 2003 trkB expression and BDNF responsiveness in neuroblastoma cells can be induced by all-trans-retinoic acid (RA). Tretinoin 106-108 neurotrophic receptor tyrosine kinase 2 Homo sapiens 0-4
12866655-7 2003 An increased expression of PLC-beta3 and PKC-alpha and -beta2 was also evidentiated at the longer time points explored, when the effects of ATRA in preservation of the differentiated morphology were maximal. Tretinoin 140-144 phospholipase C beta 3 Homo sapiens 27-36
12866655-7 2003 An increased expression of PLC-beta3 and PKC-alpha and -beta2 was also evidentiated at the longer time points explored, when the effects of ATRA in preservation of the differentiated morphology were maximal. Tretinoin 140-144 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 56-61
12834868-2 2003 Treatment with retinoic acid (RA) increases Rarb expression and reduces explant bud formation through a signaling mechanism involving RARbeta. Tretinoin 15-28 retinoic acid receptor, beta Mus musculus 44-48
12870655-0 2003 Transcript profiling of cytochrome P450 genes in HL-60 human leukemic cells: upregulation of CYP1B1 by all-trans-retinoic acid. Tretinoin 103-126 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 93-99
12870655-5 2003 ATRA treatment (0.1-40 microM for 3 days) increased CYP1B1 mRNA levels by up to 3 fold, as determined by a quantitative real-time PCR method. Tretinoin 0-4 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 52-58
12480939-1 2003 MCF-7 and ZR-75 breast cancer cells infected with an adenovirus constitutively expressing high levels of cyclin D1 demonstrated widespread mitochondrial translocation of Bax and cytochrome c release that was approximately doubled after the addition of all-trans retinoic acid (RA) or Bcl-2 antisense oligonucleotide. Tretinoin 262-275 cyclin D1 Homo sapiens 105-114
12955881-5 2003 In fetal cells, however, the induction of apoptosis and differentiation by RA was obtained via inhibition of cyclin D1-cdk4 activity, as result of an increased binding to the p16 inhibitor. Tretinoin 75-77 cyclin D1 Homo sapiens 109-118
12955881-5 2003 In fetal cells, however, the induction of apoptosis and differentiation by RA was obtained via inhibition of cyclin D1-cdk4 activity, as result of an increased binding to the p16 inhibitor. Tretinoin 75-77 cyclin dependent kinase 4 Homo sapiens 119-123
19416885-3 2009 Here we show that the RA-degrading Cyp26 enzymes play a critical role in defining the normal anterior limit of the pancreatic field. Tretinoin 22-24 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 35-40
12844477-6 2003 Indinavir leads to altered retinoic acid signaling most likely by an activation of the RAR/RXR heterodimer, perhaps by displacing all-trans-retinoic acid from CRABP. Tretinoin 27-40 cellular retinoic acid binding protein 1 Homo sapiens 159-164
12569559-0 2003 Expression and role of MICA and MICB in human hepatocellular carcinomas and their regulation by retinoic acid. Tretinoin 96-109 MHC class I polypeptide-related sequence A Homo sapiens 23-27
12569559-0 2003 Expression and role of MICA and MICB in human hepatocellular carcinomas and their regulation by retinoic acid. Tretinoin 96-109 MHC class I polypeptide-related sequence B Homo sapiens 32-36
19416885-5 2009 The cyp26a1 gene is expressed in the anterior trunk endoderm at developmental stages when RA is signaling to specify pancreas, and analysis of cyp26a1/giraffe (gir) mutant zebrafish embryos confirms that cyp26a1 plays the primary role in setting the anterior limit of the pancreas. Tretinoin 90-92 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 4-11
12569559-7 2003 Of interest is the finding that retinoic acid upregulated expression of MICA/B in Huh7 and HepG2 cells. Tretinoin 32-45 MHC class I polypeptide-related sequence A Homo sapiens 72-76
12606540-8 2003 In addition, ATRA induced multiple features of hypertrophic differentiation (including type X collagen, alkaline phosphatase, and MMP-13), and these effects required TG2. Tretinoin 13-17 matrix metallopeptidase 13 Mus musculus 130-136
19416885-7 2009 We used cell transplantation to determine that Cyp26a1 functions directly in endoderm to modulate RA signaling and limit the pancreatic field. Tretinoin 98-100 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 47-54
14613334-3 2003 The aim of this study was to define the action of RA in the presence of decreased levels of TGF-beta1, as are found in growth factor-reduced Matrigel (GFRM), on the proportion of insulin cells. Tretinoin 50-52 transforming growth factor beta 1 Gallus gallus 92-101
12569559-11 2003 Furthermore, retinoic acid can function as a modulator of MICA/B expression and thereby further activate NK cells. Tretinoin 13-26 MHC class I polypeptide-related sequence A Homo sapiens 58-62
19147277-8 2009 The effect of EBBP on retinoid-responsive transcription appeared to be limited to genes with the retinoic acid response element (betaRARE) regulatory sequence, such as CYP26A1. Tretinoin 97-110 tripartite motif containing 16 Homo sapiens 14-18
12666199-0 2003 Differential expression of decorin and biglycan genes during palatogenesis in normal and retinoic acid-treated mice. Tretinoin 89-102 decorin Mus musculus 27-34
12714583-3 2003 Indeed, ATRA treatment induced the expression of CCAAT/enhancer-binding protein beta (C/EBPbeta), a CRE-dependent transcription factor important in monocytic differentiation, and the inhibition of CRE-enhancer activity by the expression of a dominant-negative CRE-binding protein (dn-CREB) abolished the induction of C/EBPbeta. Tretinoin 8-12 CCAAT enhancer binding protein beta Homo sapiens 49-84
12714583-3 2003 Indeed, ATRA treatment induced the expression of CCAAT/enhancer-binding protein beta (C/EBPbeta), a CRE-dependent transcription factor important in monocytic differentiation, and the inhibition of CRE-enhancer activity by the expression of a dominant-negative CRE-binding protein (dn-CREB) abolished the induction of C/EBPbeta. Tretinoin 8-12 CCAAT enhancer binding protein beta Homo sapiens 86-95
12714583-3 2003 Indeed, ATRA treatment induced the expression of CCAAT/enhancer-binding protein beta (C/EBPbeta), a CRE-dependent transcription factor important in monocytic differentiation, and the inhibition of CRE-enhancer activity by the expression of a dominant-negative CRE-binding protein (dn-CREB) abolished the induction of C/EBPbeta. Tretinoin 8-12 CCAAT enhancer binding protein beta Homo sapiens 317-326
12666199-10 2003 In the retinoic acid-treated mice, the area of the decorin gene expression expanded to the core region of the palate primordium where little signal was observed in control mice. Tretinoin 7-20 decorin Mus musculus 51-58
12666199-13 2003 Up-regulation of decorin gene expression in the retinoic acid-treated mice might influence the pathogenesis of cleft palate. Tretinoin 48-61 decorin Mus musculus 17-24
19173678-13 2009 Furthermore, an intravenous injection of RA rapidly raised hepatic Gck expression in rats fed with a VAS control diet. Tretinoin 41-43 glucokinase Rattus norvegicus 67-70
19371709-0 2009 Retinoic acid can directly promote TGF-beta-mediated Foxp3(+) Treg cell conversion of naive T cells. Tretinoin 0-13 forkhead box P3 Homo sapiens 53-58
12660332-10 2003 In conclusion, active metabolites of vitamin A, especially ATRA produced by RALDH2 play relevant roles during the repairing process of injured podocytes. Tretinoin 59-63 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 76-82
19341452-5 2009 We found that the fluorescence signal from Oct-4-targeting molecular beacons provides a clear discrimination between undifferentiated and retinoic acid-induced differentiated cells. Tretinoin 138-151 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 43-48
12616482-0 2003 All-trans retinoic acid down-regulates expression and function of beta2 integrins by human monocytes: opposite effects on monocytic cell lines. Tretinoin 10-23 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 66-71
19190084-2 2009 The expression of aldehyde dehydrogenase (ALDH) 1A in these DCs is essential for the RA production. Tretinoin 85-87 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 18-40
12616482-3 2003 As evidenced by flow cytometry, ATRA (at 1 microM) clearly and donor-independently suppressed the expression of all integrin chains investigated (CD11a, CD11b, CD11c, and CD18), most strikingly of CD11a. Tretinoin 32-36 integrin subunit alpha L Homo sapiens 146-151
12616482-3 2003 As evidenced by flow cytometry, ATRA (at 1 microM) clearly and donor-independently suppressed the expression of all integrin chains investigated (CD11a, CD11b, CD11c, and CD18), most strikingly of CD11a. Tretinoin 32-36 integrin subunit alpha X Homo sapiens 160-165
12616482-3 2003 As evidenced by flow cytometry, ATRA (at 1 microM) clearly and donor-independently suppressed the expression of all integrin chains investigated (CD11a, CD11b, CD11c, and CD18), most strikingly of CD11a. Tretinoin 32-36 integrin subunit alpha L Homo sapiens 197-202
19190084-2 2009 The expression of aldehyde dehydrogenase (ALDH) 1A in these DCs is essential for the RA production. Tretinoin 85-87 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 42-46
19273910-0 2009 Upregulation of SOX9 inhibits the growth of human and mouse melanomas and restores their sensitivity to retinoic acid. Tretinoin 104-117 SRY-box transcription factor 9 Homo sapiens 16-20
12609598-7 2003 Finally, HMGB1 subcellular localization changes during retinoic acid induced differentiation of P19 neuroblastoma cells. Tretinoin 55-68 high mobility group box 1 Mus musculus 9-14
18831967-2 2009 The final step in the conversion of retinol to retinoic acid is carried out by three retinaldehyde dehydrogenases encoded by Raldh1 (Aldh1a1), Raldh2 (Aldh1a2), and Raldh3 (Aldh1a3). Tretinoin 47-60 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 125-131
18831967-2 2009 The final step in the conversion of retinol to retinoic acid is carried out by three retinaldehyde dehydrogenases encoded by Raldh1 (Aldh1a1), Raldh2 (Aldh1a2), and Raldh3 (Aldh1a3). Tretinoin 47-60 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 133-140
18831967-2 2009 The final step in the conversion of retinol to retinoic acid is carried out by three retinaldehyde dehydrogenases encoded by Raldh1 (Aldh1a1), Raldh2 (Aldh1a2), and Raldh3 (Aldh1a3). Tretinoin 47-60 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 143-149
12601020-9 2003 The cell-cycle-arrest stage correlated with the observed microarray results in which the RA treatment downregulated critical genes such as cyclins (cyclin E, cyclin D3) and cyclin-dependent kinases (CDK5, CDK10). Tretinoin 89-91 cyclin dependent kinase 10 Homo sapiens 205-210
18831967-2 2009 The final step in the conversion of retinol to retinoic acid is carried out by three retinaldehyde dehydrogenases encoded by Raldh1 (Aldh1a1), Raldh2 (Aldh1a2), and Raldh3 (Aldh1a3). Tretinoin 47-60 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 151-158
18831967-5 2009 During optic cup formation Raldh2 is first expressed transiently in perioptic mesenchyme, then later Raldh1 and Raldh3 expression begins in the dorsal and ventral retina, respectively, and these sources of retinoic acid are maintained in the fetus. Tretinoin 206-219 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 27-33
19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 nuclear receptor corepressor 2 Homo sapiens 457-461
12594048-2 2003 RDH1 is the most efficient known mouse short-chain dehydrogenase that catalyzes dehydrogenation of all-trans-retinol, and contributes to a reconstituted path of all-trans-retinoic acid biosynthesis, when coexpressed in reporter cells with any one of three retinal dehydrogenases. Tretinoin 165-184 retinol dehydrogenase 1 (all trans) Mus musculus 0-4
12684871-1 2003 Cellular retinoic acid binding proteins, types I and II (CRABP I and II), are cytosolic proteins that exhibit a binding preference for all-trans retinoic acid. Tretinoin 9-22 cellular retinoic acid binding protein 1 Rattus norvegicus 57-71
12684871-1 2003 Cellular retinoic acid binding proteins, types I and II (CRABP I and II), are cytosolic proteins that exhibit a binding preference for all-trans retinoic acid. Tretinoin 145-158 cellular retinoic acid binding protein 1 Rattus norvegicus 57-71
19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 nuclear receptor corepressor 2 Homo sapiens 457-461
12547725-5 2003 Specifically, inhibition of retinal dehydrogenase-2 (RALDH2), a key enzyme necessary for the production of retinoic acid and that is expressed in the developing diaphragm, was assayed by measuring retinoic acid production in cytosolic extracts from an oligodendrocyte cell line. Tretinoin 107-120 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 28-51
12547725-5 2003 Specifically, inhibition of retinal dehydrogenase-2 (RALDH2), a key enzyme necessary for the production of retinoic acid and that is expressed in the developing diaphragm, was assayed by measuring retinoic acid production in cytosolic extracts from an oligodendrocyte cell line. Tretinoin 107-120 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 53-59
18652909-5 2009 Retinoic acid (RA) treatment increased this LRAT promoter-luciferase activity in PrEC cells, but not in PC-3 cells. Tretinoin 0-13 lecithin retinol acyltransferase Homo sapiens 44-48
12547725-5 2003 Specifically, inhibition of retinal dehydrogenase-2 (RALDH2), a key enzyme necessary for the production of retinoic acid and that is expressed in the developing diaphragm, was assayed by measuring retinoic acid production in cytosolic extracts from an oligodendrocyte cell line. Tretinoin 197-210 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 28-51
12547725-5 2003 Specifically, inhibition of retinal dehydrogenase-2 (RALDH2), a key enzyme necessary for the production of retinoic acid and that is expressed in the developing diaphragm, was assayed by measuring retinoic acid production in cytosolic extracts from an oligodendrocyte cell line. Tretinoin 197-210 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 53-59
12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 S-phase kinase associated protein 2 Homo sapiens 149-153
12487626-4 2003 We show that, in P19 embryonal carcinoma cells, GCs potentiate RA-induced expression of the murine Hoxb -1 gene through an autoregulatory element, b1-ARE, recognized by the Pbx1 and HOXB1 homoeodomain proteins. Tretinoin 63-65 homeobox B1 Mus musculus 99-106
12487626-4 2003 We show that, in P19 embryonal carcinoma cells, GCs potentiate RA-induced expression of the murine Hoxb -1 gene through an autoregulatory element, b1-ARE, recognized by the Pbx1 and HOXB1 homoeodomain proteins. Tretinoin 63-65 homeobox B1 Mus musculus 182-187
12623064-1 2003 The cellular retinoic acid (RA) binding proteins I and II (CRABPI and CRABPII), intracellular proteins which bind retinoic acid with high affinity, are involved in the actions of RA, though their exact roles are not fully understood. Tretinoin 13-26 cellular retinoic acid binding protein II Mus musculus 70-77
12700651-10 2003 However, RA also decreases Skp2 levels thus impairing the ability of p27 to be ubiquitinated. Tretinoin 9-11 S-phase kinase associated protein 2 Homo sapiens 27-31
12623064-1 2003 The cellular retinoic acid (RA) binding proteins I and II (CRABPI and CRABPII), intracellular proteins which bind retinoic acid with high affinity, are involved in the actions of RA, though their exact roles are not fully understood. Tretinoin 28-30 cellular retinoic acid binding protein II Mus musculus 70-77
18652909-5 2009 Retinoic acid (RA) treatment increased this LRAT promoter-luciferase activity in PrEC cells, but not in PC-3 cells. Tretinoin 15-17 lecithin retinol acyltransferase Homo sapiens 44-48
12623064-1 2003 The cellular retinoic acid (RA) binding proteins I and II (CRABPI and CRABPII), intracellular proteins which bind retinoic acid with high affinity, are involved in the actions of RA, though their exact roles are not fully understood. Tretinoin 114-127 cellular retinoic acid binding protein II Mus musculus 70-77
19039095-1 2009 Regulation of hairy and enhancer of split homologue-1 (HES-1) by estradiol and all-trans retinoic acid affects proliferation of human breast cancer cells. Tretinoin 89-102 hes family bHLH transcription factor 1 Homo sapiens 55-60
12579317-1 2003 The human retinoic acid receptor beta (RARbeta) has three isoforms (beta1, beta2, and beta4), which play important, distinct roles in mediating the effects of retinoic acid on cell growth and apoptosis. Tretinoin 10-23 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 75-80
12494454-0 2003 Retinoic acid-induced AP-1 transcriptional activity regulates B16 mouse melanoma growth inhibition and differentiation. Tretinoin 0-13 jun proto-oncogene Mus musculus 22-26
19039095-3 2009 In the distal 5" promoter of the HES-1 gene, we found a retinoic acid response element and in the distal 3" region, an estrogen receptor alpha(ER)alpha binding site. Tretinoin 56-69 hes family bHLH transcription factor 1 Homo sapiens 33-38
12494454-4 2003 Treatment of these clones with phorbol dibutyrate increased AP-1 activity which peaked at 2-4 h and returned to baseline level by 24 h. In contrast, RA treatment resulted in a slow increase in AP-1 activity that reached a maximum level at 48 h and was maintained for the duration of the treatment. Tretinoin 149-151 jun proto-oncogene Mus musculus 60-64
12554770-5 2003 These differing transcriptional properties appear to reflect the differing abilities of the three RAR isotypes to interact with the SMRT (silencing mediator of retinoic acid and thyroid hormone receptor) corepressor protein: RARalpha binds to SMRT strongly both in vitro and in vivo, whereas RARbeta and RARgamma interact only weakly with SMRT. Tretinoin 160-173 nuclear receptor corepressor 2 Homo sapiens 132-136
12554770-5 2003 These differing transcriptional properties appear to reflect the differing abilities of the three RAR isotypes to interact with the SMRT (silencing mediator of retinoic acid and thyroid hormone receptor) corepressor protein: RARalpha binds to SMRT strongly both in vitro and in vivo, whereas RARbeta and RARgamma interact only weakly with SMRT. Tretinoin 160-173 nuclear receptor corepressor 2 Homo sapiens 243-247
12494454-4 2003 Treatment of these clones with phorbol dibutyrate increased AP-1 activity which peaked at 2-4 h and returned to baseline level by 24 h. In contrast, RA treatment resulted in a slow increase in AP-1 activity that reached a maximum level at 48 h and was maintained for the duration of the treatment. Tretinoin 149-151 jun proto-oncogene Mus musculus 193-197
12554770-5 2003 These differing transcriptional properties appear to reflect the differing abilities of the three RAR isotypes to interact with the SMRT (silencing mediator of retinoic acid and thyroid hormone receptor) corepressor protein: RARalpha binds to SMRT strongly both in vitro and in vivo, whereas RARbeta and RARgamma interact only weakly with SMRT. Tretinoin 160-173 nuclear receptor corepressor 2 Homo sapiens 243-247
18986761-2 2009 Hypoxia and retinoic acid (RA) may also induce interleukin-2 (IL-2) receptor expression, and thus we evaluated if RA and IL-2 receptor-targeted therapy are indicated in hypoxic HCCs. Tretinoin 27-29 interleukin 2 receptor subunit beta Homo sapiens 62-76
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 nuclear receptor corepressor 2 Homo sapiens 82-86
12494454-9 2003 The ability of RA to induce RARbeta and PKCalpha expression was retained in A-fos clones, suggesting that A-fos was not interfering with RAR transcription activation functions. Tretinoin 15-17 retinoic acid receptor, beta Mus musculus 28-35
12494454-10 2003 We tested whether the RA-induced AP-1 activity might be mediated by the ERK1/2 MAPK pathway. Tretinoin 22-24 jun proto-oncogene Mus musculus 33-37
12494454-10 2003 We tested whether the RA-induced AP-1 activity might be mediated by the ERK1/2 MAPK pathway. Tretinoin 22-24 mitogen-activated protein kinase 3 Mus musculus 72-78
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 nuclear receptor corepressor 2 Homo sapiens 124-128
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 nuclear receptor corepressor 2 Homo sapiens 82-86
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 nuclear receptor corepressor 2 Homo sapiens 124-128
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 254-258 nuclear receptor corepressor 2 Homo sapiens 82-86
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 254-258 nuclear receptor corepressor 2 Homo sapiens 124-128
12494454-13 2003 Our observations suggest that AP-1 transcriptional activity induced by RA likely plays an important role in the biological changes mediated by this retinoid in B16 melanoma cells. Tretinoin 71-73 jun proto-oncogene Mus musculus 30-34
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 75-88 glial fibrillary acidic protein Gallus gallus 260-291
12604205-6 2003 As for the second step of RA synthesis, a null mutation of RALDH2 is embryonic lethal, eliminating most mesodermal RA synthesis, whereas loss of RALDH1 eliminates RA synthesis only in the embryonic dorsal retina with no obvious effect on development. Tretinoin 26-28 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 59-65
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 75-88 glial fibrillary acidic protein Gallus gallus 293-297
12534290-10 2003 The results of this study suggest that the human retinol-active SDRs are not functionally equivalent and that, in contrast to RoDH-like 3alpha-HSD, RoDH-4 can access the bound form of retinol for retinoic acid production and is regulated by the apo-/holo-CRBP ratio. Tretinoin 196-209 retinol dehydrogenase 16 Homo sapiens 148-154
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 75-88 glial fibrillary acidic protein Gallus gallus 367-371
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 26-39 retinoic acid receptor gamma Homo sapiens 109-117
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 26-39 retinoid X receptor beta Homo sapiens 155-162
12393416-0 2003 Levels of phospho-Smad2/3 are sensors of the interplay between effects of TGF-beta and retinoic acid on monocytic and granulocytic differentiation of HL-60 cells. Tretinoin 87-100 SMAD family member 2 Homo sapiens 18-23
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 168-187 glial fibrillary acidic protein Gallus gallus 260-291
12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 57-80 SMAD family member 2 Homo sapiens 199-204
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 41-43 retinoic acid receptor gamma Homo sapiens 109-117
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 41-43 retinoid X receptor beta Homo sapiens 155-162
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 168-187 glial fibrillary acidic protein Gallus gallus 293-297
12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 82-86 SMAD family member 2 Homo sapiens 199-204
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 168-187 glial fibrillary acidic protein Gallus gallus 367-371
12393416-6 2003 Addition of the inhibitor-of-protein serine/threonine phosphatases, okadaic acid, blocks the ATRA-mediated reduction in TGF-beta-induced phospho-Smad2 and shifts the differentiation toward monocytic end points. Tretinoin 93-97 SMAD family member 2 Homo sapiens 145-150
12401808-8 2003 The results of our studies suggest a novel mechanism of RA signaling, which involves activation of TGase and transamidation of RhoA. Tretinoin 56-58 transglutaminase 1 Homo sapiens 99-104
12401808-9 2003 RA-induced activation of TGase is proposed to induce multiple signaling pathways that regulate neuronal differentiation. Tretinoin 0-2 transglutaminase 1 Homo sapiens 25-30
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 174-187 glial fibrillary acidic protein Gallus gallus 260-291
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 174-187 glial fibrillary acidic protein Gallus gallus 293-297
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 174-187 glial fibrillary acidic protein Gallus gallus 367-371
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 174-187 glial fibrillary acidic protein Gallus gallus 260-291
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 174-187 glial fibrillary acidic protein Gallus gallus 293-297
14515147-1 2003 In the retinoic acid-differentiated neuroblastoma SH-SY5Y cells, IL-1 induced binding activity of NFkappaB and up-regulated the expression and activity of MnSOD. Tretinoin 7-20 superoxide dismutase 2 Homo sapiens 155-160
18948137-4 2009 To demonstrate the utility of this approach, we examined the effect of the retinoic acid signaling pathway on cells in these slices, showing that addition of exogenous trans-retinoic acid to slice cultures promotes expression of a marker of mature astrocytes, glial fibrillary acidic protein (GFAP), while the inhibition of endogenous retinoic acid synthesis reduces GFAP expression; the results suggest a role for retinoic acid in modulating glial differentiation. Tretinoin 174-187 glial fibrillary acidic protein Gallus gallus 367-371
19216755-7 2009 CRBP-1 is a key regulator of All-trans retinoic acid (ATRA) through ATRA metabolism and nuclear localization. Tretinoin 29-52 retinol binding protein 1 Homo sapiens 0-6
14529416-2 2003 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RAR alpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 57-70 retinoic acid receptor gamma Homo sapiens 191-199
19216755-7 2009 CRBP-1 is a key regulator of All-trans retinoic acid (ATRA) through ATRA metabolism and nuclear localization. Tretinoin 54-58 retinol binding protein 1 Homo sapiens 0-6
14529416-2 2003 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RAR alpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 57-70 retinoid X receptor beta Homo sapiens 237-244
19216755-7 2009 CRBP-1 is a key regulator of All-trans retinoic acid (ATRA) through ATRA metabolism and nuclear localization. Tretinoin 68-72 retinol binding protein 1 Homo sapiens 0-6
19216755-16 2009 CONCLUSION: Collectively our data provides evidence that Chmp1A mediates the growth inhibitory activity of ATRA in human pancreatic cancer cells via regulation of CRBP-1. Tretinoin 107-111 retinol binding protein 1 Homo sapiens 163-169
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 195-218 xanthine dehydrogenase Homo sapiens 38-60
12514310-5 2003 In one of these genes, T-box binding protein-2 (Tbx-2), an RA response element, was identified in the promoter region that mediates the RA responsiveness of this gene. Tretinoin 59-61 T-box 2 Mus musculus 23-46
12514310-5 2003 In one of these genes, T-box binding protein-2 (Tbx-2), an RA response element, was identified in the promoter region that mediates the RA responsiveness of this gene. Tretinoin 59-61 T-box 2 Mus musculus 48-53
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 195-218 xanthine dehydrogenase Homo sapiens 62-65
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 195-218 retinol binding protein 1 Homo sapiens 139-143
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 195-218 retinol binding protein 1 Homo sapiens 150-154
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 185-189 xanthine dehydrogenase Homo sapiens 38-60
12517593-2 2003 A promising oral retinoid, 4-hydroxyphenylretinamide (4-HPR) induced apoptosis through non-retinoic acid-mediated pathways and is being studied in National Cancer Institute phase II trials in several organ sites. Tretinoin 91-104 haptoglobin-related protein Homo sapiens 56-59
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 185-189 xanthine dehydrogenase Homo sapiens 62-65
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 185-189 retinol binding protein 1 Homo sapiens 139-143
12505482-3 2003 Here we asked whether Runx2 expression and function are affected by retinoic acid (RA) and parathyroid hormone-related peptide (PTHrP), which represent an important stimulator and inhibitor of chondrocyte maturation, respectively. Tretinoin 68-81 runt related transcription factor 2 Gallus gallus 22-27
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 185-189 retinol binding protein 1 Homo sapiens 150-154
12505482-3 2003 Here we asked whether Runx2 expression and function are affected by retinoic acid (RA) and parathyroid hormone-related peptide (PTHrP), which represent an important stimulator and inhibitor of chondrocyte maturation, respectively. Tretinoin 83-85 runt related transcription factor 2 Gallus gallus 22-27
19250215-3 2009 Since both XDH and CRBP are required for the biosynthesis of t-RA, we have inspected their bioavailability in both estrogen-responsive and nonresponsive human mammary epithelial cancer cells. Tretinoin 61-65 xanthine dehydrogenase Homo sapiens 11-14
19250215-3 2009 Since both XDH and CRBP are required for the biosynthesis of t-RA, we have inspected their bioavailability in both estrogen-responsive and nonresponsive human mammary epithelial cancer cells. Tretinoin 61-65 retinol binding protein 1 Homo sapiens 19-23
19252374-5 2009 For example, all-trans retinoic acid (ATRA) inhibits Th17 differentiation and instead promotes the upregulation of Foxp3, a key transcription factor in regulatory T cells. Tretinoin 13-36 forkhead box P3 Homo sapiens 115-120
14535836-9 2003 Forty-eight hours after 6 Gy irradiation, late apoptotic cells were found in the group of ATRA pretreated cells, as determined by APO2.7 positivity. Tretinoin 90-94 TNF receptor superfamily member 10a Homo sapiens 130-134
19252374-5 2009 For example, all-trans retinoic acid (ATRA) inhibits Th17 differentiation and instead promotes the upregulation of Foxp3, a key transcription factor in regulatory T cells. Tretinoin 38-42 forkhead box P3 Homo sapiens 115-120
26238624-5 2009 Specific PTMs of TR2 could differentially regulate its biological activity mediated by multiple signaling pathways including one elicited by the nongenomic action of retinoic acid. Tretinoin 166-179 nuclear receptor subfamily 2, group C, member 1 Mus musculus 17-20
19255510-1 2009 We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-beta/Smad signaling. Tretinoin 26-30 transforming growth factor, beta 1 Mus musculus 109-117
12453892-4 2002 Furthermore, we show that RA treatment potentiates ATF-2-dependent transactivation by inducing specific phosphorylation of ATF-2 by p38beta kinase. Tretinoin 26-28 mitogen-activated protein kinase 11 Homo sapiens 132-139
12453892-5 2002 ATF-2 activation by RA blocked the inhibitory intramolecular interaction of ATF-2 amino and carboxyl terminal domains in a p38beta kinase-dependent manner. Tretinoin 20-22 mitogen-activated protein kinase 11 Homo sapiens 123-130
12453892-7 2002 Taken together, the data suggest that RA activates the p38beta kinase pathway leading to phosphorylation and activation of ATF-2, thereby enhancing PEPCK gene transcription and glucose production. Tretinoin 38-40 mitogen-activated protein kinase 11 Homo sapiens 55-62
12429992-6 2002 WNT3A, WNT8A, WNT8B, WNT10B and WNT11 are down-regulated in NT2 cells after ATRA treatment, while WNT2, WNT7B and WNT14B are up-regulated. Tretinoin 76-80 Wnt family member 3A Homo sapiens 0-5
19255510-1 2009 We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-beta/Smad signaling. Tretinoin 32-55 transforming growth factor, beta 1 Mus musculus 109-117
12429992-6 2002 WNT3A, WNT8A, WNT8B, WNT10B and WNT11 are down-regulated in NT2 cells after ATRA treatment, while WNT2, WNT7B and WNT14B are up-regulated. Tretinoin 76-80 Wnt family member 8B Homo sapiens 14-19
12429992-7 2002 FZD4 and FZD10 are up-regulated in NT2 cells after ATRA treatment. Tretinoin 51-55 frizzled class receptor 4 Homo sapiens 0-4
19255510-1 2009 We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-beta/Smad signaling. Tretinoin 57-61 transforming growth factor, beta 1 Mus musculus 109-117
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 transforming growth factor, beta 1 Mus musculus 97-105
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 311-315 transforming growth factor, beta 1 Mus musculus 97-105
19255510-9 2009 Furthermore, we demonstrated that the effects of atRA on TGF-beta-dependent gene activation and of TGF-beta on RA-dependent gene activation are mediated by TGIF with siRNA to downregulate TGIF. Tretinoin 49-53 transforming growth factor, beta 1 Mus musculus 57-65
12775111-7 2002 When VA-deficient rats received a single injection of retinoic acid (2 mg/rat), tissue IGF-I and IGF-IR gene expression did not change after 4 or 8 h, while the expression of IGF-II, IGFBP-4, and IGFBP-6 mRNAs in some tissues increased rapidly. Tretinoin 54-67 insulin-like growth factor 1 receptor Rattus norvegicus 97-103
19247936-1 2009 During limb development, expression of the TALE homeobox transcription factor Meis1 is activated by retinoic acid in the proximal-most limb bud regions, which give rise to the upper forelimb and hindlimb. Tretinoin 100-113 Meis homeobox 1 Mus musculus 78-83
12775111-7 2002 When VA-deficient rats received a single injection of retinoic acid (2 mg/rat), tissue IGF-I and IGF-IR gene expression did not change after 4 or 8 h, while the expression of IGF-II, IGFBP-4, and IGFBP-6 mRNAs in some tissues increased rapidly. Tretinoin 54-67 insulin-like growth factor binding protein 4 Rattus norvegicus 183-190
12443882-2 2002 We found that bestatin, an inhibitor of CD13/aminopeptidase N, enhanced the sensitivity of APL NB4 cells to ATRA at concentrations of 0.1-1000ng/ml. Tretinoin 108-112 alanyl aminopeptidase, membrane Homo sapiens 40-44
12443882-2 2002 We found that bestatin, an inhibitor of CD13/aminopeptidase N, enhanced the sensitivity of APL NB4 cells to ATRA at concentrations of 0.1-1000ng/ml. Tretinoin 108-112 alanyl aminopeptidase, membrane Homo sapiens 45-61
12443882-3 2002 A structurally different aminopeptidase N inhibitor, actinonin, also increased the effect of ATRA on differentiation, but an inactive stereoisomer of bestatin, (2R,3S)-AHPA-(R)-Leu, did not. Tretinoin 93-97 alanyl aminopeptidase, membrane Homo sapiens 25-41
12443882-5 2002 Masking of the cell-surface CD13 by anti-CD13 antibody WM15 blocked the synergistic effect of bestatin and ATRA on differentiation. Tretinoin 107-111 alanyl aminopeptidase, membrane Homo sapiens 28-32
12443882-5 2002 Masking of the cell-surface CD13 by anti-CD13 antibody WM15 blocked the synergistic effect of bestatin and ATRA on differentiation. Tretinoin 107-111 alanyl aminopeptidase, membrane Homo sapiens 41-45
19636436-0 2009 Studies on Multifunctional Effect of All-Trans Retinoic Acid (ATRA) on Matrix Metalloproteinase-2 (MMP-2) and Its Regulatory Molecules in Human Breast Cancer Cells (MCF-7). Tretinoin 47-60 matrix metallopeptidase 2 Homo sapiens 71-97
12443882-6 2002 Thus bestatin, an immunomodulator clinically used for nonlymphocytic leukemia, synergistically increased the ATRA-induced differentiation of NB4 cells by inhibiting CD13/aminopeptidase N on the cell-surface. Tretinoin 109-113 alanyl aminopeptidase, membrane Homo sapiens 165-169
12443882-6 2002 Thus bestatin, an immunomodulator clinically used for nonlymphocytic leukemia, synergistically increased the ATRA-induced differentiation of NB4 cells by inhibiting CD13/aminopeptidase N on the cell-surface. Tretinoin 109-113 alanyl aminopeptidase, membrane Homo sapiens 170-186
19636436-0 2009 Studies on Multifunctional Effect of All-Trans Retinoic Acid (ATRA) on Matrix Metalloproteinase-2 (MMP-2) and Its Regulatory Molecules in Human Breast Cancer Cells (MCF-7). Tretinoin 47-60 matrix metallopeptidase 2 Homo sapiens 99-104
19834476-3 2009 In the following 10 d, these neuroepithelial cells are specified to OLIG2-expressing progenitors in the presence of retinoic acid (RA) and sonic hedgehog (SHH). Tretinoin 116-129 oligodendrocyte transcription factor 2 Homo sapiens 68-73
12513708-2 2002 The results showed that 1.0 and 10.0 micro mol/L RA increased the expression of ICAM-1 and the adhesive rate of U CBMNC to BMSC, however, RA did not induced the increase of expression of VCAM-1. Tretinoin 49-51 intercellular adhesion molecule 1 Mus musculus 80-86
12513708-4 2002 It is concluded that RA up-regulated ICAM-1 expression of BMSC and increased the adhesion of UCBMNC to BMSC in vitro. Tretinoin 21-23 intercellular adhesion molecule 1 Mus musculus 37-43
19834476-3 2009 In the following 10 d, these neuroepithelial cells are specified to OLIG2-expressing progenitors in the presence of retinoic acid (RA) and sonic hedgehog (SHH). Tretinoin 131-133 oligodendrocyte transcription factor 2 Homo sapiens 68-73
12381680-6 2002 In [35S]-GTPgammaS exchange assays, membranes from cells cultured with retinoic acid (4-6 days) were the most responsive to activation by MIP-1alpha and MPIF-1. Tretinoin 71-84 C-C motif chemokine receptor 1 Homo sapiens 138-148
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 61-63 CD14 molecule Homo sapiens 124-128
12404122-5 2002 Luciferase assays of promoter activity indicate that B-myb-dependent transactivation is enhanced in LAN-5 cells treated with retinoic acid (RA) for 24 h. The enhancement is independent from cyclin A but is suppressed by a degradation-resistant mutant form of cyclin D1. Tretinoin 125-138 cyclin D1 Homo sapiens 259-268
12404122-5 2002 Luciferase assays of promoter activity indicate that B-myb-dependent transactivation is enhanced in LAN-5 cells treated with retinoic acid (RA) for 24 h. The enhancement is independent from cyclin A but is suppressed by a degradation-resistant mutant form of cyclin D1. Tretinoin 140-142 cyclin D1 Homo sapiens 259-268
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 184-186 CD14 molecule Homo sapiens 124-128
12404122-6 2002 The importance of cyclin D1 in controlling B-myb activity is further suggested by co-immunoprecipitation experiments, showing that the amount of cyclin D1 co-immunoprecipitated with B-myb decreased after RA treatment. Tretinoin 204-206 cyclin D1 Homo sapiens 18-27
12404122-6 2002 The importance of cyclin D1 in controlling B-myb activity is further suggested by co-immunoprecipitation experiments, showing that the amount of cyclin D1 co-immunoprecipitated with B-myb decreased after RA treatment. Tretinoin 204-206 cyclin D1 Homo sapiens 145-154
19277121-0 2009 FGF4 and retinoic acid direct differentiation of hESCs into PDX1-expressing foregut endoderm in a time- and concentration-dependent manner. Tretinoin 9-22 pancreatic and duodenal homeobox 1 Homo sapiens 60-64
12353219-3 2002 In the mature dorsal spinal cord, expression of a direct repeat 5 RA response element (DR5-RARE) transgene is seen in interneurons in laminae I and II, as well as in ependymal cells around the central canal. Tretinoin 66-68 tumor necrosis factor receptor superfamily, member 10b Mus musculus 87-95
18976680-11 2009 The results show that the two RA-related molecules (TGF-beta1 and CRABPI) are altered by FON exposure in vitro. Tretinoin 30-32 cellular retinoic acid binding protein 1 Rattus norvegicus 66-72
12356739-3 2002 In addition, antisense oligonucleotide treatment of embryonic mouse lung explants suggests that Rcd1 also plays a role in retinoic acid-controlled lung development. Tretinoin 122-135 CCR4-NOT transcription complex, subunit 9 Mus musculus 96-100
19087254-12 2008 This consequently reduced all-trans retinoic acid (RA)-induced differentiation, validated by CRABP1 knock down, which led to recovery of the cellular response to RA treatment and cellular sprouting under physiological RA concentrations. Tretinoin 26-49 cellular retinoic acid binding protein 1 Homo sapiens 93-99
12445277-5 2002 More recently, it has become clear that a stimulatory receptor expressed by NK cells, T cells and macrophages (NKG2D) recognizes ligands (MHC class I chain related [MIC], H6O, retinoic acid early inducible [Rae1] and UL16 binding proteins [ULBP]) that are up-regulated on tumor cells and virally infected cells but are not expressed well by normal cells. Tretinoin 176-189 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 111-116
19087254-12 2008 This consequently reduced all-trans retinoic acid (RA)-induced differentiation, validated by CRABP1 knock down, which led to recovery of the cellular response to RA treatment and cellular sprouting under physiological RA concentrations. Tretinoin 51-53 cellular retinoic acid binding protein 1 Homo sapiens 93-99
12124800-3 2002 In our study, we show that 4-HPR inhibits growth on a broad panel of lung cancer cell lines (12/12 small cell lung cancer and 9/12 nonsmall cell lung cancer cell lines), including cell lines unresponsive to all-trans-retinoic acid (ATRA). Tretinoin 211-230 haptoglobin-related protein Homo sapiens 29-32
12124800-3 2002 In our study, we show that 4-HPR inhibits growth on a broad panel of lung cancer cell lines (12/12 small cell lung cancer and 9/12 nonsmall cell lung cancer cell lines), including cell lines unresponsive to all-trans-retinoic acid (ATRA). Tretinoin 232-236 haptoglobin-related protein Homo sapiens 29-32
12514132-3 2003 A retinoic acid response element (RARE) was identified downstream of Hoxb5 and shown to be essential for expression of Hoxb5 and Hoxb8 reporter transgenes in the anterior neural tube. Tretinoin 2-15 homeobox B8 Mus musculus 129-134
18799729-3 2008 Retinoic acid induces expression of ankyrin repeat-containing protein with a suppressor of cytokine signaling box 2 (ASB2) in acute promyelocytic leukemia cells, and ASB2 expression inhibits growth and promotes commitment, recapitulating an early step critical for differentiation. Tretinoin 0-13 ankyrin repeat and SOCS box containing 2 Homo sapiens 117-121
12524175-4 2003 The expression of Trip15/CSN2 mRNA was induced at an early stage of neuronal differentiation in the retinoic acid (RA)-treated P19 cells, but not in the triiodothyronine (T3)-primed cardiac muscular cell differentiation. Tretinoin 100-113 casein beta Rattus norvegicus 25-29
12080040-0 2002 The anti-estrogenic effect of all-trans-retinoic acid on the breast cancer cell line MCF-7 is dependent on HES-1 expression. Tretinoin 30-53 hes family bHLH transcription factor 1 Homo sapiens 107-112
18799729-6 2008 Knockdown of endogenous ASB2 in leukemia cells delays retinoic acid-induced differentiation and filamin degradation; conversely, ASB2 expression in leukemia cells induces filamin degradation. Tretinoin 54-67 ankyrin repeat and SOCS box containing 2 Homo sapiens 24-28
12524175-4 2003 The expression of Trip15/CSN2 mRNA was induced at an early stage of neuronal differentiation in the retinoic acid (RA)-treated P19 cells, but not in the triiodothyronine (T3)-primed cardiac muscular cell differentiation. Tretinoin 115-117 casein beta Rattus norvegicus 25-29
12524175-6 2003 Enforced expression of sense rat Trip15/CSN2 mRNA caused the downregulation of Oct-3/4 mRNA expression and was sufficient to convert P19 cells into neurons, but not glial cells, only after the aggregation without RA. Tretinoin 213-215 casein beta Rattus norvegicus 40-44
12139968-0 2002 The silencing mediator of retinoic acid and thyroid hormone receptors can interact with the aryl hydrocarbon (Ah) receptor but fails to repress Ah receptor-dependent gene expression. Tretinoin 26-39 aryl hydrocarbon receptor Homo sapiens 92-122
12524175-7 2003 In the presence of RA, exogenous expression of the sense mRNA caused the intense and rapid induction of neurogenic Brn-2 and Mash-1 mRNA expressions accompanying the strong downregulation of Oct-3/4 mRNA expression, and stimulated both neuronal and glial cell differentiations of P19 cells. Tretinoin 19-21 POU class 3 homeobox 2 Rattus norvegicus 115-120
19029830-2 2008 RA exerts its biological functions primarily through binding to and activating nuclear RA receptors (RARs, which include the RAR alpha, beta and gamma isotypes RARA, RARB and RARC). Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 166-170
12401808-3 2003 Here we report that RA-induced neuronal differentiation of SH-SY5Y cells is coupled with increased expression/activation of TGase and in vivo transamidation and activation of RhoA. Tretinoin 20-22 transglutaminase 1 Homo sapiens 124-129
12052862-4 2002 AP1 transrepression by retinoic acid was concomitant to glycogen synthase kinase 3 activation, negative regulation of junD hyperphosphorylation, and to decreased RNA polymerase II recruitment. Tretinoin 23-36 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-3
18767146-7 2008 Differential expression of the retinoic acid target genes, RARB, CRABP1, and CRABP2, indicated that deletion of TBL1XR1 compromised the function of SMRT/N-CoR in the appropriate control of gene expression. Tretinoin 31-44 nuclear receptor corepressor 2 Homo sapiens 148-152
12502496-7 2003 Furthermore, we demonstrate that atRA upregulates the PDX-1 expression. Tretinoin 33-37 pancreatic and duodenal homeobox 1 Homo sapiens 54-59
12502496-8 2003 Taken together, our data suggest that atRA-mediated mesenchymal/epithelial interactions play an important role in determining the cell fate of epithelial cells via regulation of the PDX-1 gene, leading to the proper formation of the endocrine versus exocrine component during pancreatic organogenesis. Tretinoin 38-42 pancreatic and duodenal homeobox 1 Homo sapiens 182-187
18775481-3 2008 v-erbA belongs to a superfamily of transcription factors called nuclear receptors, which includes the retinoic acid receptors (RARs) responsible for mediating the effects of retinoic acid. Tretinoin 102-115 thyroid hormone receptor alpha Mus musculus 2-6
12485405-4 2003 PCR analysis of total mRNA from RA-treated cells showed a biphasic early induction of CRBP-I, CRABP-II, and RARgamma2 genes. Tretinoin 32-34 retinol binding protein 1 Homo sapiens 86-92
12050134-6 2002 Raldh2 synthesises retinoic acid (RA) from its immediate precursor retinal. Tretinoin 19-32 aldehyde dehydrogenase 1 family, member A2 Danio rerio 0-6
12054477-4 2002 Mutation of the retinoic acid response element (RARE) at -879 to -874 (site 1) enhanced promoter activity and diminished but did not eliminate the suppression by RARbeta and RXRalpha. Tretinoin 16-29 retinoic acid receptor, beta Mus musculus 162-169
12054477-6 2002 Mutation of the AP-2-binding site enhanced promoter activity that was inhibited by retinoic acid. Tretinoin 83-96 transcription factor AP-2, alpha Mus musculus 16-20
12485405-8 2003 These data suggest that the RA-specific induction of CRBP-I and CRABP-II could be an early event in the process leading to neuronal differentiation of NT2 cells. Tretinoin 28-30 retinol binding protein 1 Homo sapiens 53-59
18775481-5 2008 In order to study the effect of v-erbA on RA-responsive genes, we used microarray analysis to identify genes differentially expressed in murine hepatocytes in culture (AML12 cells) stably transfected with v-erbA and exposed to RA for 3 h or 24 h. We have identified RA-responsive genes that are affected by v-erbA, as well as genes that are regulated by v-erbA alone. Tretinoin 42-44 thyroid hormone receptor alpha Mus musculus 34-38
12514310-5 2003 In one of these genes, T-box binding protein-2 (Tbx-2), an RA response element, was identified in the promoter region that mediates the RA responsiveness of this gene. Tretinoin 136-138 T-box 2 Mus musculus 23-46
12514310-5 2003 In one of these genes, T-box binding protein-2 (Tbx-2), an RA response element, was identified in the promoter region that mediates the RA responsiveness of this gene. Tretinoin 136-138 T-box 2 Mus musculus 48-53
12054477-7 2002 This study shows that the suppressive effect of retinoic acid on the promoter is maximal with a combination of RARbeta and RXRalpha and occurs at more than one RARE site. Tretinoin 48-61 retinoic acid receptor, beta Mus musculus 111-118
12054477-7 2002 This study shows that the suppressive effect of retinoic acid on the promoter is maximal with a combination of RARbeta and RXRalpha and occurs at more than one RARE site. Tretinoin 48-61 retinoid X receptor alpha Mus musculus 123-131
18775481-6 2008 We have found that v-erbA can affect gene expression in the presence of RA and at the level of basal transcription. Tretinoin 72-74 thyroid hormone receptor alpha Mus musculus 21-25
19006694-2 2008 Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. Tretinoin 0-13 forkhead box P3 Homo sapiens 60-65
11906819-0 2002 Prenylcysteine carboxymethyltransferase type III activity is decreased in retinoic acid-treated SH-SY5Y neuroblastoma cells. Tretinoin 74-87 isoprenylcysteine carboxyl methyltransferase Homo sapiens 0-39
19006694-2 2008 Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. Tretinoin 15-17 forkhead box P3 Homo sapiens 60-65
11906819-2 2002 In this paper, we report on modulation of pcCMT activity in retinoic acid (RA)-treated SH-SY5Y neuroblastoma cells using N-acetyl-S-farnesyl-L-cysteine (AFC) as artificial methyl acceptor. Tretinoin 60-73 isoprenylcysteine carboxyl methyltransferase Homo sapiens 42-47
11906819-2 2002 In this paper, we report on modulation of pcCMT activity in retinoic acid (RA)-treated SH-SY5Y neuroblastoma cells using N-acetyl-S-farnesyl-L-cysteine (AFC) as artificial methyl acceptor. Tretinoin 75-77 isoprenylcysteine carboxyl methyltransferase Homo sapiens 42-47
12529666-3 2003 c-fms was constitutively and constantly expressed in all cases sensitive in vivo to all-trans retinoic acid (ATRA) and its expression was further potentiated following in vitro induction with ATRA. Tretinoin 94-107 colony stimulating factor 1 receptor Homo sapiens 0-5
12529666-3 2003 c-fms was constitutively and constantly expressed in all cases sensitive in vivo to all-trans retinoic acid (ATRA) and its expression was further potentiated following in vitro induction with ATRA. Tretinoin 109-113 colony stimulating factor 1 receptor Homo sapiens 0-5
12529666-3 2003 c-fms was constitutively and constantly expressed in all cases sensitive in vivo to all-trans retinoic acid (ATRA) and its expression was further potentiated following in vitro induction with ATRA. Tretinoin 192-196 colony stimulating factor 1 receptor Homo sapiens 0-5
12529666-9 2003 Finally, low c-fms expression was observed in an APL relapsing patient resistant to ATRA, as well as in an APL case with t(11;17), PLZF/RAR alpha+. Tretinoin 84-88 colony stimulating factor 1 receptor Homo sapiens 13-18
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 89-98
11953746-6 2002 We show that Cyp26a1(-/-) mice are phenotypically rescued by heterozygous disruption of Aldh1a2 (also known as Raldh2), which encodes a retinaldehyde dehydrogenase responsible for the synthesis of retinoic acid during early embryonic development. Tretinoin 197-210 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 88-95
11953746-6 2002 We show that Cyp26a1(-/-) mice are phenotypically rescued by heterozygous disruption of Aldh1a2 (also known as Raldh2), which encodes a retinaldehyde dehydrogenase responsible for the synthesis of retinoic acid during early embryonic development. Tretinoin 197-210 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 111-117
11953746-10 2002 We provide genetic evidence that ALDH1A2 and CYP26A1 activities concurrently establish local embryonic retinoic acid levels that must be finely tuned to allow posterior organ development and to prevent spina bifida. Tretinoin 103-116 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 33-40
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 89-97
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 354-363
18806776-5 2008 miR-134, miR-296 and miR-470, upregulated on retinoic-acid-induced differentiation of mouse embryonic stem cells, target the CDS of each transcription factor in various combinations, leading to transcriptional and morphological changes characteristic of differentiating mouse embryonic stem cells, and resulting in a new phenotype. Tretinoin 45-58 microRNA 134 Homo sapiens 0-7
12128097-0 2002 Expression of c-Myc and other apoptosis-related genes in Swiss Webster mouse fetuses after maternal exposure to all trans-retinoic acid. Tretinoin 116-135 myelocytomatosis oncogene Mus musculus 16-19
12128097-3 2002 Reverse transcriptase-polymerase chain reaction and ribonuclease protection assay revealed decreased c-myc expression at 48 h followed by an increase at 72 h in fetuses from RA-treated dams. Tretinoin 174-176 myelocytomatosis oncogene Mus musculus 103-106
12128097-4 2002 Increased c-Myc protein was detected at 72 h in the RA-treated group. Tretinoin 52-54 myelocytomatosis oncogene Mus musculus 12-15
12128097-5 2002 In utero RA-treatment resulted in decreased expression of max, mad, caspases, bax, and bad genes at 48 h. Terminal uridinetriphosphate nick end-labeling (TUNEL) analysis revealed increased apoptosis at 24-48 h, followed by decreased apoptosis 72 h after in utero RA-exposure, which correlated with the decreased expression of pro-apoptotic genes noted at 48 h. Further investigations are needed to understand the role of Myc family genes during RA-mediated teratogenesis. Tretinoin 9-11 myelocytomatosis oncogene Mus musculus 421-424
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 21-23 neurotrophic receptor tyrosine kinase 2 Homo sapiens 50-54
18847503-15 2008 Pathway analysis suggests that CDC2, CHEK1, CDC45L and MCM6 are key players in mediating the biological activity of RA in B16 melanoma cells. Tretinoin 116-118 cyclin-dependent kinase 1 Mus musculus 31-35
14510471-5 2003 In this study, we further investigate that the expression of Hes1 is regulated by miR-23 during the retinoic acid (RA)-induced neural differentiation of NT2 cells. Tretinoin 100-113 hes family bHLH transcription factor 1 Homo sapiens 61-65
14510471-5 2003 In this study, we further investigate that the expression of Hes1 is regulated by miR-23 during the retinoic acid (RA)-induced neural differentiation of NT2 cells. Tretinoin 115-117 hes family bHLH transcription factor 1 Homo sapiens 61-65
14510502-3 2003 Previously we showed that JDP2 inhibits the retinoic acid (RA) dependent transcription by recruiting a histone deacetylase 3 (HDAC3) complex to the promoter region of the target genes. Tretinoin 44-57 histone deacetylase 3 Homo sapiens 103-124
14510502-3 2003 Previously we showed that JDP2 inhibits the retinoic acid (RA) dependent transcription by recruiting a histone deacetylase 3 (HDAC3) complex to the promoter region of the target genes. Tretinoin 44-57 histone deacetylase 3 Homo sapiens 126-131
14510502-3 2003 Previously we showed that JDP2 inhibits the retinoic acid (RA) dependent transcription by recruiting a histone deacetylase 3 (HDAC3) complex to the promoter region of the target genes. Tretinoin 59-61 histone deacetylase 3 Homo sapiens 103-124
14510502-3 2003 Previously we showed that JDP2 inhibits the retinoic acid (RA) dependent transcription by recruiting a histone deacetylase 3 (HDAC3) complex to the promoter region of the target genes. Tretinoin 59-61 histone deacetylase 3 Homo sapiens 126-131
11832495-5 2002 Reproducible alterations in gene expression that occurred in response to retinoic acid, Wnt-1, or retinoic acid plus Wnt-1 relative to untreated cells were identified. Tretinoin 73-86 wingless-type MMTV integration site family, member 1 Mus musculus 117-122
11836246-1 2002 The ability of class I alcohol dehydrogenase (ADH1) and class IV alcohol dehydrogenase (ADH4) to metabolize retinol to retinoic acid is supported by genetic studies in mice carrying Adh1 or Adh4 gene disruptions. Tretinoin 119-132 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 23-44
11959987-0 2002 Stimulation of retinoic acid production and growth by ubiquitously expressed alcohol dehydrogenase Adh3. Tretinoin 15-28 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 99-103
11959987-5 2002 Adh3 null mutant mice exhibit reduced RA generation in vivo, growth deficiency that can be rescued by retinol supplementation, and completely penetrant postnatal lethality during vitamin A deficiency. Tretinoin 38-40 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 0-4
12679006-11 2003 CONCLUSION: ATRA combined with As(2)O(3) in de novo APL treatment can yield a high CR rate without intolerable side effects. Tretinoin 12-16 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 83-85
18280134-3 2008 All-transretinoic acid (RA), an active metabolite of vitamin A, regulates the activity of several metabolic enzymes related to OAT, including ornithine decarboxylase and arginase, which may influence the function of OAT through effects on substrate (ornithine) availability. Tretinoin 0-22 ornithine aminotransferase Homo sapiens 127-130
12388538-3 2002 4-HPR, a synthetic derivative of retinoic acid that induces ceramide in tumor cell lines, has been shown to have antiangiogenic effects, but the molecular mechanism of these is largely unknown. Tretinoin 33-46 haptoglobin-related protein Homo sapiens 2-5
18280134-3 2008 All-transretinoic acid (RA), an active metabolite of vitamin A, regulates the activity of several metabolic enzymes related to OAT, including ornithine decarboxylase and arginase, which may influence the function of OAT through effects on substrate (ornithine) availability. Tretinoin 0-22 ornithine decarboxylase 1 Homo sapiens 142-165
18280134-3 2008 All-transretinoic acid (RA), an active metabolite of vitamin A, regulates the activity of several metabolic enzymes related to OAT, including ornithine decarboxylase and arginase, which may influence the function of OAT through effects on substrate (ornithine) availability. Tretinoin 0-22 ornithine aminotransferase Homo sapiens 216-219
18987612-3 2008 For this reason, the modification of retinoic acid (RA) induced neuronal differentiation of mouse embryonal carcinoma cells P19 by selected ROS scavengers and flavoprotein inhibitor was evaluated. Tretinoin 37-50 interleukin 23, alpha subunit p19 Mus musculus 124-127
12213824-4 2002 The switch to CAK hypophosphorylation of RARalpha is accompanied by decreased MAT1 expression and MAT1 fragmentation that occurs in the differentiating cells through the all-trans-retinoic acid (ATRA)-mediated proteasome degradation pathway. Tretinoin 170-193 MNAT1 component of CDK activating kinase Homo sapiens 98-102
12213824-4 2002 The switch to CAK hypophosphorylation of RARalpha is accompanied by decreased MAT1 expression and MAT1 fragmentation that occurs in the differentiating cells through the all-trans-retinoic acid (ATRA)-mediated proteasome degradation pathway. Tretinoin 195-199 MNAT1 component of CDK activating kinase Homo sapiens 78-82
12213824-4 2002 The switch to CAK hypophosphorylation of RARalpha is accompanied by decreased MAT1 expression and MAT1 fragmentation that occurs in the differentiating cells through the all-trans-retinoic acid (ATRA)-mediated proteasome degradation pathway. Tretinoin 195-199 MNAT1 component of CDK activating kinase Homo sapiens 98-102
18987612-3 2008 For this reason, the modification of retinoic acid (RA) induced neuronal differentiation of mouse embryonal carcinoma cells P19 by selected ROS scavengers and flavoprotein inhibitor was evaluated. Tretinoin 52-54 interleukin 23, alpha subunit p19 Mus musculus 124-127
18987612-7 2008 The RA-induced neuronal differentiation was determined based on changes in the expression of protein markers characteristic for undifferentiated (Oct-4) and neuron-like cell differentiated cells (N-cadherin and III-beta tubulin). Tretinoin 4-6 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 146-151
12445205-4 2002 Here we show that retinoic acid, at concentrations inhibiting terminal differentiation of keratinocytes, strongly suppressed caspase-14 mRNA and protein expression by keratinocytes in monolayer culture and in a three-dimensional in vitro model of differentiating human epidermis (skin equivalent). Tretinoin 18-31 caspase 14 Homo sapiens 125-135
18585997-1 2008 We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Tretinoin 91-104 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 25-30
12537770-1 2002 In vitro, cells derived from Ewing sarcoma (ES) with the characteristic somatic rearrangement between the genes EWS and FLII can be induced to differentiate toward a neuronal phenotype by exposure to agents such as dibutyryl cyclic AMP (db cAMP) or retinoic acid. Tretinoin 249-262 EWS RNA binding protein 1 Homo sapiens 112-115
18585997-1 2008 We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Tretinoin 91-104 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 39-43
18585997-1 2008 We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Tretinoin 91-104 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 44-49
18585997-1 2008 We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Tretinoin 106-110 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 25-30
12397630-0 2002 PBX, MEIS, and IGF-I are potential mediators of retinoic acid-induced proximodistal limb reduction defects. Tretinoin 48-61 Ultrabithorax Drosophila melanogaster 0-3
12397630-0 2002 PBX, MEIS, and IGF-I are potential mediators of retinoic acid-induced proximodistal limb reduction defects. Tretinoin 48-61 insulin-like growth factor 1 Mus musculus 15-20
18585997-1 2008 We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Tretinoin 106-110 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 39-43
12397630-7 2002 In addition to the two PBX1 isoforms, the mRNA level of the other two subtypes (PBX2 and PBX3) and the level of PBX1/2/3 protein were also found to be elevated in limb buds after RA treatment. Tretinoin 179-181 pre B cell leukemia homeobox 2 Mus musculus 80-84
18585997-1 2008 We previously identified NEDD9 (RAINB2/HEF1/Cas-L) as a new downstream target of all-trans retinoic acid (atRA) and its receptors in the human neuroblastoma cell line, SH-SY5Y [R.A. Merrill, A.W.-M. See, M.L. Tretinoin 106-110 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 44-49
12397630-10 2002 CONCLUSIONS: Because both PBX and MEIS (and their orthologs) are believed to be involved in the control of proximodistal axis formation in mouse and fly limbs and IGFs in the development of limbs, we suggest that increases in PBX, MEIS and IGF-1 mRNA levels may contribute to proximodistal limb reduction defects caused by teratogenic doses of RA. Tretinoin 344-346 Ultrabithorax Drosophila melanogaster 26-29
12383199-2 2002 While RA (10(-8) m) alone did not alter STAT-1 activation or expression in THP-1 cells, RA enhanced or prolonged STAT-1 activation (tyrosine 701 phosphorylation) and gene expression (mRNA and protein) induced by either IFN-beta or IFN-gamma. Tretinoin 88-90 interferon beta 1 Homo sapiens 219-227
18585997-11 2008 We now provide functional evidence that NEDD9 is directly regulated by atRA through a complex retinoic acid response element (RARE) located in the NEDD9 proximal promoter and consisting of four conserved half-sites separated by 1, 5, and 1 intervening base pairs. Tretinoin 94-107 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 40-45
18585997-11 2008 We now provide functional evidence that NEDD9 is directly regulated by atRA through a complex retinoic acid response element (RARE) located in the NEDD9 proximal promoter and consisting of four conserved half-sites separated by 1, 5, and 1 intervening base pairs. Tretinoin 94-107 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 147-152
18437159-6 2008 In addition, we have demonstrated that some genes, similarly regulated by both inhibitors (upregulated as Bcl2, Id2, Cd24a or downregulated as Nodal), are bona fide p38alpha targets involved in neurogenesis and found a correlation with their expression profiles and the onset of neuronal differentiation triggered upon retinoic acid treatment. Tretinoin 319-332 inhibitor of DNA binding 2 Mus musculus 112-115
12183385-11 2002 Thus, cyp26 has an important role in linking the Fgf, Wnt and RA signals to regulate AP patterning of the neural ectoderm in the late blastula to gastrula embryo in zebrafish. Tretinoin 62-64 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 6-11
18437159-6 2008 In addition, we have demonstrated that some genes, similarly regulated by both inhibitors (upregulated as Bcl2, Id2, Cd24a or downregulated as Nodal), are bona fide p38alpha targets involved in neurogenesis and found a correlation with their expression profiles and the onset of neuronal differentiation triggered upon retinoic acid treatment. Tretinoin 319-332 mitogen-activated protein kinase 14 Mus musculus 165-173
18298548-10 2008 Retinoic acid influenced NKR expression consistent with an imprinting of the NKR expression profile in intestine-associated lymphoid tissues. Tretinoin 0-13 tachykinin receptor 3 Mus musculus 25-28
12154074-2 2002 Here, we examined TIF1beta distribution in the nucleus of mouse embryonic carcinoma F9 cells during retinoic-acid-induced primitive endodermal differentiation. Tretinoin 100-113 tripartite motif-containing 28 Mus musculus 18-26
12070176-9 2002 For RAR gamma the EC(50) values were: ATRA (2 nM), 5,6-epoxy-RA (4 nM), 18-OH-RA (14 nM), 13-cis-RA (36 nM), 9-cis-RA (58 nM), 4-oxo-RA (89 nM), and 4-OH-RA (94 nM). Tretinoin 38-42 retinoic acid receptor gamma Homo sapiens 4-13
12070176-9 2002 For RAR gamma the EC(50) values were: ATRA (2 nM), 5,6-epoxy-RA (4 nM), 18-OH-RA (14 nM), 13-cis-RA (36 nM), 9-cis-RA (58 nM), 4-oxo-RA (89 nM), and 4-OH-RA (94 nM). Tretinoin 109-117 retinoic acid receptor gamma Homo sapiens 4-13
18298548-10 2008 Retinoic acid influenced NKR expression consistent with an imprinting of the NKR expression profile in intestine-associated lymphoid tissues. Tretinoin 0-13 tachykinin receptor 3 Mus musculus 77-80
18552205-7 2008 Cell-cycle arrest in HL-60 cells involved reduction in expression levels of p21, cyclins D and E, while Rb1 exhibited reduction in protein levels without changes in mRNA levels over the time course of ATRA treatment. Tretinoin 201-205 RB transcriptional corepressor 1 Homo sapiens 104-107
12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 36-38 RELA proto-oncogene, NF-kB subunit Homo sapiens 293-296
12223147-5 2002 RESULTS: Transfection of RAR-beta gene and treatment with ligand ATRA could increase the expression of RAR-beta protein for at least 144h and inhibit the proliferation and the expression of alpha-SMA and desmin in PDGF-activated HSC. Tretinoin 65-69 desmin Rattus norvegicus 204-210
18546281-6 2008 The differentiating factor retinoic acid induced a heterogeneous response pattern of OMP expression and axon elongation. Tretinoin 27-40 olfactory marker protein Mus musculus 85-88
12000751-9 2002 The down-regulation of PKC also inhibited the binding of RAR to a retinoic acid response element and the retinoic acid induction of RAR beta expression. Tretinoin 105-118 retinoic acid receptor, beta Mus musculus 132-140
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 68-70 achaete-scute family bHLH transcription factor 1 Homo sapiens 130-135
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 68-70 achaete-scute family bHLH transcription factor 1 Homo sapiens 137-143
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 177-179 achaete-scute family bHLH transcription factor 1 Homo sapiens 130-135
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 177-179 achaete-scute family bHLH transcription factor 1 Homo sapiens 137-143
18684916-0 2008 Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression. Tretinoin 0-13 forkhead box P3 Homo sapiens 24-29
12000762-6 2002 RA also reduces the activity of an AP-1 and TCF-sensitive cyclin D1 reporter in SKBR3 cells in a manner that is independent of the TCF site. Tretinoin 0-2 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-39
12000762-6 2002 RA also reduces the activity of an AP-1 and TCF-sensitive cyclin D1 reporter in SKBR3 cells in a manner that is independent of the TCF site. Tretinoin 0-2 cyclin D1 Homo sapiens 58-67
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 57-59 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-230
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 171-173 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-230
12052888-4 2002 Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. Tretinoin 239-241 E1A binding protein p300 Homo sapiens 211-215
18684916-0 2008 Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression. Tretinoin 0-13 SMAD family member 3 Homo sapiens 118-123
18408763-2 2008 RARalpha heterodimerizes with the retinoid X receptor-alpha (RXRalpha) and transcriptionally regulates myeloid differentiation in response to ATRA (all-trans retinoic acid). Tretinoin 142-146 retinoid X receptor alpha Mus musculus 34-59
12218287-5 2002 All-trans-retinoic acid, dithranol and the p38 mitogen-activated protein (MAP) kinase inhibitor SB220025 displayed a strong inhibitory effect on SKALP expression while cyclosporin A, dexamethasone, the vitamin D(3) derivative calcipotriol and the p38 MAP kinase inhibitor SB203580 showed only moderate inhibition. Tretinoin 0-23 peptidase inhibitor 3 Homo sapiens 145-150
18408763-2 2008 RARalpha heterodimerizes with the retinoid X receptor-alpha (RXRalpha) and transcriptionally regulates myeloid differentiation in response to ATRA (all-trans retinoic acid). Tretinoin 142-146 retinoid X receptor alpha Mus musculus 61-69
18408763-2 2008 RARalpha heterodimerizes with the retinoid X receptor-alpha (RXRalpha) and transcriptionally regulates myeloid differentiation in response to ATRA (all-trans retinoic acid). Tretinoin 148-171 retinoid X receptor alpha Mus musculus 34-59
11971897-3 2002 Whereas a number of retinoids, including retinol, 14-hydroxyretroretinol, anhydroretinol (AR), and retinoic acid bound the c-Raf cysteine-rich domain (CRD) with equal affinity in vitro as well as in vivo, they displayed different, even opposing, effects on UV-mediated kinase activation; retinol and 14-hydroxyretroretinol augmented responses, whereas retinoic acid and AR were inhibitory. Tretinoin 99-112 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 123-128
11971897-3 2002 Whereas a number of retinoids, including retinol, 14-hydroxyretroretinol, anhydroretinol (AR), and retinoic acid bound the c-Raf cysteine-rich domain (CRD) with equal affinity in vitro as well as in vivo, they displayed different, even opposing, effects on UV-mediated kinase activation; retinol and 14-hydroxyretroretinol augmented responses, whereas retinoic acid and AR were inhibitory. Tretinoin 352-365 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 123-128
18408763-2 2008 RARalpha heterodimerizes with the retinoid X receptor-alpha (RXRalpha) and transcriptionally regulates myeloid differentiation in response to ATRA (all-trans retinoic acid). Tretinoin 148-171 retinoid X receptor alpha Mus musculus 61-69
11960985-0 2002 Retinol/ethanol drug interaction during acute alcohol intoxication in mice involves inhibition of retinol metabolism to retinoic acid by alcohol dehydrogenase. Tretinoin 120-133 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 137-158
18636162-4 2008 Reverse transcription (RT)-polymerase chain reaction (PCR) and heteronuclear PCR assays performed +/- treatment with the protein synthesis inhibitor cycloheximide (CHX) revealed G0S2 induction within 3 h of RA-treatment. Tretinoin 207-209 G0/G1 switch 2 Homo sapiens 178-182
11960985-3 2002 A reduction in RA synthesis may also be involved as ethanol competitively inhibits retinol oxidation catalyzed by alcohol dehydrogenase (ADH) in vitro. Tretinoin 15-17 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 114-135
11960985-3 2002 A reduction in RA synthesis may also be involved as ethanol competitively inhibits retinol oxidation catalyzed by alcohol dehydrogenase (ADH) in vitro. Tretinoin 15-17 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 137-140
18495661-1 2008 All-trans-retinoic acid stimulates dendritic growth in hippocampal neurons within minutes by activating mitogen-activated protein kinase and mTOR and increasing dendritic translation of calcium calmodulin-dependent protein kinase II alpha and the alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate receptor subunit GluR1. Tretinoin 0-23 calcium/calmodulin dependent protein kinase II alpha Homo sapiens 186-238
12042033-6 2002 We previously reported that induction of MUC2, MUC5AC, and MUC5B gene expressions by retinoic acid is mediated by the retinoic acid receptor (RARalpha), and inhibited by the specific RARalpha antagonist Ro 41-5253. Tretinoin 85-98 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 59-64
18628953-8 2008 RA rapidly induced the expression of Sox-9 and ER81, which in turn form a complex on the VE-cadherin promoter and are required to mediate the transcriptional regulation of VE-cadherin by RA. Tretinoin 0-2 SRY-box transcription factor 9 Homo sapiens 37-42
18478160-0 2008 Expression of the retinoic acid-metabolizing enzymes RALDH2 and CYP26b1 during mouse postnatal testis development. Tretinoin 18-31 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 53-59
11907032-4 2002 Upon culture in a differentiation medium containing fetal calf serum (1%) and retinoic acid (10 nm), cells transfected with the calreticulin gene were highly susceptible to apoptosis compared with controls. Tretinoin 78-91 calreticulin Rattus norvegicus 128-140
19035179-6 2008 Western blot displayed that ATRA could decrease the expression of cyclin A, up-regulate the expression of p21 and p27, and down-regulate the expression of p27 related proteins Skp2. Tretinoin 28-32 S-phase kinase associated protein 2 Homo sapiens 176-180
11964310-6 2002 Functional experiments showed that this interaction has the capacity to render GATA-dependent transcription responsive to treatment with a combination of all-trans retinoic acid and the histone deacetylase inhibitor trichostatin A (TSA). Tretinoin 164-177 GATA binding protein 2 Homo sapiens 79-83
18512787-7 2008 TS-4/TS-5 Delta-cat cartilage explants released aggrecan in response to retinoic acid. Tretinoin 72-85 Trichinella spiralis resistance 4 Mus musculus 0-4
11980644-6 2002 Treatment with RA stimulated an interaction between RA receptor-alpha and CBP/p300; a corresponding decrease in the interaction between CBP/p300 and c-Jun was observed. Tretinoin 15-17 E1A binding protein p300 Homo sapiens 78-82
12027900-3 2002 Following an acute dose of retinol (50 mg.kg(-1)), metabolism of retinol to retinoic acid in liver was reduced 10-fold in Adh1 mutants and 3.8-fold in Adh3 mutants, but was not significantly reduced in Adh4 mutants. Tretinoin 76-89 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 151-155
18420480-3 2008 Interestingly, our previous work has also shown Fibroblast Growth Factor-2 (FGF-2) to strongly inhibit this osteogenic differentiation, even in the presence of retinoic acid. Tretinoin 160-173 fibroblast growth factor 2 Mus musculus 48-74
11956596-0 2002 Expression and regulation of WNT8A and WNT8B mRNAs in human tumor cell lines: up-regulation of WNT8B mRNA by beta-estradiol in MCF-7 cells, and down-regulation of WNT8A and WNT8B mRNAs by retinoic acid in NT2 cells. Tretinoin 188-201 Wnt family member 8B Homo sapiens 39-44
11956596-9 2002 Because NT2 cells differentiate into neuronal cells after all-trans retinoic-acid treatment, effects of all-trans retinoic acid on mRNA expression of WNT8A and WNT8B were next investigated. Tretinoin 114-127 Wnt family member 8B Homo sapiens 160-165
18420480-3 2008 Interestingly, our previous work has also shown Fibroblast Growth Factor-2 (FGF-2) to strongly inhibit this osteogenic differentiation, even in the presence of retinoic acid. Tretinoin 160-173 fibroblast growth factor 2 Mus musculus 76-81
11956596-10 2002 WNT8A and WNT8B mRNAs were down-regulated together in NT2 cells after all-trans retinoic-acid treatment. Tretinoin 80-93 Wnt family member 8B Homo sapiens 10-15
18420480-4 2008 In this report, we investigated the molecular mechanisms underlying FGF-2 mediated osteogenic inhibition, demonstrating that addition of exogenous FGF-2 to mASCs antagonizes upregulation of BMPR-IB gene expression in response to retinoic acid. Tretinoin 229-242 fibroblast growth factor 2 Mus musculus 68-73
18420480-4 2008 In this report, we investigated the molecular mechanisms underlying FGF-2 mediated osteogenic inhibition, demonstrating that addition of exogenous FGF-2 to mASCs antagonizes upregulation of BMPR-IB gene expression in response to retinoic acid. Tretinoin 229-242 fibroblast growth factor 2 Mus musculus 147-152
12068955-1 2002 Since it is known that a 307 bp fragment of the position specific regulatory element of human HOXA-7 contains two (DR3 and DR5) retinoic acid response elements (RAREs) at its 3" end, we constructed several deletion constructs containing different numbers of RAREs and examined their effects in vitro and in vivo. Tretinoin 128-141 homeobox A7 Homo sapiens 94-100
18420480-7 2008 Collectively, our data therefore indicate that FGF-2 antagonizes the response of mASCs to retinoic acid and also suggest that threshold levels of BMPR-IB may play a crucial role both in counteracting the inhibitory role of FGF-2 and in promoting osteogenic differentiation of ASCs in the absence of retinoic acid. Tretinoin 90-103 fibroblast growth factor 2 Mus musculus 47-52
17994277-0 2008 Indomethacin and retinoic acid modify mouse intestinal inflammation and fibrosis: a role for SPARC. Tretinoin 17-30 secreted acidic cysteine rich glycoprotein Mus musculus 93-98
12479267-0 2002 Retinoic acid-induced growth arrest and differentiation: retinoic acid up-regulates CD32 (Fc gammaRII) expression, the ectopic expression of which retards the cell cycle. Tretinoin 0-13 Fc gamma receptor IIa Homo sapiens 84-88
12479267-0 2002 Retinoic acid-induced growth arrest and differentiation: retinoic acid up-regulates CD32 (Fc gammaRII) expression, the ectopic expression of which retards the cell cycle. Tretinoin 57-70 Fc gamma receptor IIa Homo sapiens 84-88
12479267-12 2002 The known retinoic acid-induced sustained activation of various mitogen-activated protein kinase signaling molecules, including extracellular signal-regulated kinase 2, src-like kinases, and adapter molecules, may in part reflect induced expression of Fc gammaRIIA, which is known to activate a similar ensemble of signaling molecules through its ITAM domain. Tretinoin 10-23 Fc gamma receptor IIa Homo sapiens 252-264
12479267-13 2002 The data suggest that retinoic acid induces increased Fc gammaRIIA expression, which is of functional consequence in eliciting growth arrest and differentiation. Tretinoin 22-35 Fc gamma receptor IIa Homo sapiens 54-66
11832495-8 2002 Administration of retinoic acid to mice bearing tumors driven by activation of the Wnt-1/beta-catenin pathway resulted in increased expression of stra6 in the tumors but not in normal tissue. Tretinoin 18-31 wingless-type MMTV integration site family, member 1 Mus musculus 83-88
11967490-0 2002 Expression of a retinol dehydrogenase (hRoDH-4), a member of the retinol/steroid dehydrogenase family implicated in retinoic acid biosynthesis, in normal and neoplastic endometria. Tretinoin 116-129 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 16-37
11967490-0 2002 Expression of a retinol dehydrogenase (hRoDH-4), a member of the retinol/steroid dehydrogenase family implicated in retinoic acid biosynthesis, in normal and neoplastic endometria. Tretinoin 116-129 retinol dehydrogenase 16 Homo sapiens 39-46
11967490-2 2002 The goal of this study was to determine whether hRoDH-4, an enzyme that can catalyze the first and rate-limiting step in retinoic acid biosynthesis, is expressed in normal endometrium and, if so, whether its expression is altered in endometrial cancer. Tretinoin 121-134 retinol dehydrogenase 16 Homo sapiens 48-55
12207051-9 2002 Significant increase observed in interferon gamma inducing factor (IGIF/IL-18) mRNA expression in all-trans-retinoic acid-treated cells on day 14 and 17 did not translate to increased INF gamma expression. Tretinoin 108-121 interleukin 18 Mus musculus 72-77
12207051-11 2002 The function of TNF alpha, IGIF/IL-18 and MIF in all-trans-retinoic acid-treated cells during ES differentiation and apoptosis is still speculatory. Tretinoin 59-72 interleukin 18 Mus musculus 27-31
12207051-11 2002 The function of TNF alpha, IGIF/IL-18 and MIF in all-trans-retinoic acid-treated cells during ES differentiation and apoptosis is still speculatory. Tretinoin 59-72 interleukin 18 Mus musculus 32-37
12207052-7 2002 Furthermore, a pronounced induction of midkine by retinoic acid was observed in neonatal lungs. Tretinoin 50-63 midkine Mus musculus 39-46
11891284-2 2002 Microarray analyses previously revealed induction of UBE1L (ubiquitin-activating enzyme E1-like) after RA treatment of NB4 APL cells. Tretinoin 103-105 ubiquitin like modifier activating enzyme 7 Homo sapiens 53-58
11891284-2 2002 Microarray analyses previously revealed induction of UBE1L (ubiquitin-activating enzyme E1-like) after RA treatment of NB4 APL cells. Tretinoin 103-105 ubiquitin like modifier activating enzyme 7 Homo sapiens 60-95
11891284-3 2002 We report here that this occurs within 3 h in RA-sensitive but not RA-resistant APL cells, implicating UBE1L as a direct retinoid target. Tretinoin 46-48 ubiquitin like modifier activating enzyme 7 Homo sapiens 103-108
11891284-4 2002 A 1.3-kb fragment of the UBE1L promoter was capable of mediating transcriptional response to RA in a retinoid receptor-selective manner. Tretinoin 93-95 ubiquitin like modifier activating enzyme 7 Homo sapiens 25-30
11872252-4 2002 These results suggest that RA disrupts the differentiation of cardiac neural crest cells into ganglionic cells destined to contribute to the parasympathetic innervation of the heart, by regulating the expression of Phox2a and Phox2b. Tretinoin 27-29 paired-like homeobox 2b Rattus norvegicus 226-232
12058867-8 2002 The present study suggests a regulatory interference by 1alpha25(OH)2D3 for RA inhibition of TNF-alpha-induced AP-1 activity in osteoblasts. Tretinoin 76-78 jun proto-oncogene Mus musculus 111-115
11869806-7 2002 Western analysis indicates that RA activates a 45-kDa protein corresponding to the size of the fos B protein. Tretinoin 32-34 FosB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 95-100
11909638-7 2002 Retinoic acid, a vitamin A (retinol) metabolite, which alone had little effect on the HSP27 level, markedly enhanced the HSP27 accumulation stimulated by TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 154-162
11909638-8 2002 Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 27-35
11909638-9 2002 The amplification of TGF-beta-stimulated HSP27 accumulation by retinoic acid was reduced by PD98059 or SB203580. Tretinoin 63-76 transforming growth factor, beta 1 Mus musculus 21-29
11842302-0 2002 Retinoic acid modulates IL-5 receptor expression and selectively inhibits eosinophil-basophil differentiation of hemopoietic progenitor cells. Tretinoin 0-13 interleukin 5 Homo sapiens 24-28
11842302-8 2002 Most importantly, these effects of ATRA (10(-8) to 10(-6) mol/L) on CD34(+) cells were associated with a dose-dependent inhibition of IL-5Ralpha but no change in GM-CSF receptor expression, as detected with flow cytometry. Tretinoin 35-39 interleukin 5 receptor subunit alpha Homo sapiens 134-144
11821953-5 2002 The inhibitory effect of RAR-beta on COX-2 expression was further enhanced in the presence of RA, which was blocked by an RAR antagonist. Tretinoin 25-27 cytochrome c oxidase II, mitochondrial Mus musculus 37-42
11821953-7 2002 Furthermore, RA blocked bile acid-induced COX-2 expression and prostaglandin E(2) production only in the RAR-beta positive cells. Tretinoin 13-15 cytochrome c oxidase II, mitochondrial Mus musculus 42-47
11821953-7 2002 Furthermore, RA blocked bile acid-induced COX-2 expression and prostaglandin E(2) production only in the RAR-beta positive cells. Tretinoin 13-15 retinoic acid receptor, beta Mus musculus 105-113
11682484-3 2002 Here we have identified the human ankyrin repeat-containing protein with a suppressor of cytokine signaling box-2 (ASB-2) cDNA, as a novel RA-induced gene in APL cells. Tretinoin 139-141 ankyrin repeat and SOCS box containing 2 Homo sapiens 115-120
11682484-4 2002 PML-RARalpha strongly enhanced RA-induced ASB-2 mRNA expression. Tretinoin 4-6 ankyrin repeat and SOCS box containing 2 Homo sapiens 42-47
11682484-5 2002 In myeloid leukemia cells, ASB-2 expression induced growth inhibition and chromatin condensation recapitulating early events critical to RA-induced differentiation of APL cells. Tretinoin 137-139 ankyrin repeat and SOCS box containing 2 Homo sapiens 27-32
12064575-0 2002 Modulation of c-myc, max, and mad gene expression during neural differentiation of embryonic stem cells by all-trans-retinoic acid. Tretinoin 107-130 myelocytomatosis oncogene Mus musculus 16-19
12064575-2 2002 Temporal expression of c-Myc during all-trans-retinoic acid (RA)-mediated neural differentiation in murine embryonic stem cell (ES) was investigated. Tretinoin 61-63 myelocytomatosis oncogene Mus musculus 25-28
12064575-4 2002 In RA-treated cells, increase in c-myc mRNA was detected by reverse transcriptase polymerase chain reaction on days 11 and 14 of differentiation compared with the vehicle-treated controls. Tretinoin 3-5 myelocytomatosis oncogene Mus musculus 35-38
12244570-0 2002 Discovery of sonic hedgehog expression in postnatal growth plate chondrocytes: differential regulation of sonic and Indian hedgehog by retinoic acid. Tretinoin 135-148 sonic hedgehog Gallus gallus 13-27
12244570-9 2002 We find that RA strongly suppresses Ihh, but enhances expression of Shh in this system. Tretinoin 13-15 sonic hedgehog Gallus gallus 68-71
11744377-1 2002 Three retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3), which catalyze the oxidation of retinaldehyde into retinoic acid, have been shown to be differentially expressed during early embryogenesis. Tretinoin 115-128 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 36-42
11744377-1 2002 Three retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3), which catalyze the oxidation of retinaldehyde into retinoic acid, have been shown to be differentially expressed during early embryogenesis. Tretinoin 115-128 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 44-50
11744378-8 2002 In addition, Cyp26B1 was expressed at specific levels of the differentiating upper and lower thoracic spinal cord, adjacent to the cervical and lumbar regions that express the RA-synthesizing enzyme RALDH-2. Tretinoin 176-178 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 199-206
11731283-4 2002 We followed by competitive PCR the expression of DAP complex components during retinoic acid (RA)-induced neuronal differentiation of P19 cells. Tretinoin 79-92 death associated protein Homo sapiens 49-52
11731283-4 2002 We followed by competitive PCR the expression of DAP complex components during retinoic acid (RA)-induced neuronal differentiation of P19 cells. Tretinoin 94-96 death associated protein Homo sapiens 49-52
11577091-10 2001 Thus, Dab2 is one of the principal genes induced by retinoic acid involved in cell growth suppression, and expression of Dab2 alone is sufficient for uncoupling of MAPK activation and c-Fos expression. Tretinoin 52-65 DAB adaptor protein 2 Homo sapiens 6-10
11577091-11 2001 Resistance to retinoic acid regulation in PA-1 cells likely results from defects in retinoic acid up-regulation of Dab2 expression. Tretinoin 14-27 DAB adaptor protein 2 Homo sapiens 115-119
11684028-2 2001 The distribution of the enzyme retinaldehyde dehydrogenase-2 (RALDH 2), which is involved in the synthesis of retinoic acid, was studied using immunocytochemical techniques in: (1) the developing orodental region of rats aged between 15 days in utero and 6 months; and (2) in archival human autopsy material consisting of abdominal skin and mucosa from various regions of the mouth. Tretinoin 110-123 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 31-60
11684028-2 2001 The distribution of the enzyme retinaldehyde dehydrogenase-2 (RALDH 2), which is involved in the synthesis of retinoic acid, was studied using immunocytochemical techniques in: (1) the developing orodental region of rats aged between 15 days in utero and 6 months; and (2) in archival human autopsy material consisting of abdominal skin and mucosa from various regions of the mouth. Tretinoin 110-123 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 62-69
11766909-3 2001 Expression of the LRAT mRNA is induced by retinoic acid (RA), or by dietary vitamin A, and is downregulated upon vitamin A depletion. Tretinoin 42-55 lecithin retinol acyltransferase Homo sapiens 18-22
11753686-6 2001 These studies demonstrated that both atRA and BMS453 induce Rb hypophosphorylation and decrease CDK2 kinase activity. Tretinoin 37-41 cyclin dependent kinase 2 Homo sapiens 96-100
11562362-2 2001 This work reports cDNA cloning, enzymatic characterization, function in a reconstituted path of all-trans-retinoic acid biosynthesis in cell culture, and mRNA expression patterns in adult tissues and embryos of a mouse retinol dehydrogenase, RDH1. Tretinoin 100-119 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 219-240
11562362-8 2001 Cells cotransfected with RDH1 and any one of three retinal dehydrogenase isozymes synthesize all-trans-retinoic acid from retinol, demonstrating that RDH1contributes to a path of all-trans-retinoic acid biosynthesis in intact cells. Tretinoin 93-116 retinol dehydrogenase 1 (all trans) Mus musculus 25-29
11562362-8 2001 Cells cotransfected with RDH1 and any one of three retinal dehydrogenase isozymes synthesize all-trans-retinoic acid from retinol, demonstrating that RDH1contributes to a path of all-trans-retinoic acid biosynthesis in intact cells. Tretinoin 93-116 retinol dehydrogenase 1 (all trans) Mus musculus 150-154
12034496-1 2002 Members of the cellular retinoic acid (CRABP) and retinol binding (CRBP) proteins family are involved in the metabolic pathways of retinoic acid (RA) and retinal respectively. Tretinoin 24-37 cellular retinoic acid binding protein 1 Homo sapiens 39-44
11562362-8 2001 Cells cotransfected with RDH1 and any one of three retinal dehydrogenase isozymes synthesize all-trans-retinoic acid from retinol, demonstrating that RDH1contributes to a path of all-trans-retinoic acid biosynthesis in intact cells. Tretinoin 97-116 retinol dehydrogenase 1 (all trans) Mus musculus 25-29
18569334-0 2008 Xanthine dehydrogenase processes retinol to retinoic acid in human mammary epithelial cells. Tretinoin 44-57 xanthine dehydrogenase Homo sapiens 0-22
11562362-8 2001 Cells cotransfected with RDH1 and any one of three retinal dehydrogenase isozymes synthesize all-trans-retinoic acid from retinol, demonstrating that RDH1contributes to a path of all-trans-retinoic acid biosynthesis in intact cells. Tretinoin 97-116 retinol dehydrogenase 1 (all trans) Mus musculus 150-154
11562362-9 2001 These characteristics are consistent with RDH1 functioning in a path of all-trans-retinoic acid biosynthesis starting early during embryogenesis. Tretinoin 82-95 retinol dehydrogenase 1 (all trans) Mus musculus 42-46
12034496-1 2002 Members of the cellular retinoic acid (CRABP) and retinol binding (CRBP) proteins family are involved in the metabolic pathways of retinoic acid (RA) and retinal respectively. Tretinoin 24-37 retinol binding protein 1 Homo sapiens 67-71
12034496-1 2002 Members of the cellular retinoic acid (CRABP) and retinol binding (CRBP) proteins family are involved in the metabolic pathways of retinoic acid (RA) and retinal respectively. Tretinoin 131-144 cellular retinoic acid binding protein 1 Homo sapiens 39-44
12034496-1 2002 Members of the cellular retinoic acid (CRABP) and retinol binding (CRBP) proteins family are involved in the metabolic pathways of retinoic acid (RA) and retinal respectively. Tretinoin 131-144 retinol binding protein 1 Homo sapiens 67-71
11929748-2 2002 Initially described in a patient with all-trans retinoic acid (ATRA)-unresponsive disease, STAT5b-RARalpha resulted from an interstitial deletion on chromosome 17. Tretinoin 48-61 signal transducer and activator of transcription 5B Homo sapiens 91-97
11929748-4 2002 STAT5b-RARalpha bound to retinoic acid response elements (RAREs) both as a homodimer and as a heterodimer with RXRalpha and inhibited wild-type RARalpha/RXRalpha transactivation. Tretinoin 25-38 signal transducer and activator of transcription 5B Homo sapiens 0-6
11929749-5 2002 Oligomerization of this domain in the Stat5-RARalpha fusion protein leads to stable binding of the corepressor SMRT independent of all-trans retinoic acid (ATRA) stimulation and is accompanied by an impaired response to differentiation signals in hematopoietic cells. Tretinoin 156-160 nuclear receptor corepressor 2 Homo sapiens 111-115
11687288-3 2001 In this study, we found that neural differentiation of multipotent mouse P19 embryonal carcinoma cells by retinoic acid led to the appearance of Scrt together with neuron-specific class III beta-tubulin (Tuj1), following the earlier elaboration of Mash1. Tretinoin 106-119 scratch family zinc finger 1 Mus musculus 145-149
11959987-7 2002 Unlike the second step, the first step of RA synthesis is not tissue-restricted because it is catalyzed by ADH3, a ubiquitous enzyme having an ancient origin. Tretinoin 42-44 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 107-111
18569334-6 2008 is capable to oxidize all-trans-retinol bound to CRBP (holo-CRBP) to all-trans-retinaldehyde and then to all-trans-retinoic acid. Tretinoin 105-128 retinol binding protein 1 Homo sapiens 49-53
11880314-8 2002 Interestingly, we observed that RA abrogated TNF-alpha-induced growth arrest and that this effect was associated with a dramatic decrease in IGFBP-2 expression. Tretinoin 32-34 insulin like growth factor binding protein 2 Homo sapiens 141-148
11722589-8 2001 Therefore, our present data, together with the fact that PCI is abundantly expressed in tissues requiring retinoic acid for differentiation processes (e.g. the male reproductive tract, epithelia in various organs), suggest an additional biological role for PCI as a retinoic acid-binding and/or delivering serpin. Tretinoin 266-279 serpin family A member 5 Homo sapiens 57-60
11722589-8 2001 Therefore, our present data, together with the fact that PCI is abundantly expressed in tissues requiring retinoic acid for differentiation processes (e.g. the male reproductive tract, epithelia in various organs), suggest an additional biological role for PCI as a retinoic acid-binding and/or delivering serpin. Tretinoin 266-279 serpin family A member 5 Homo sapiens 257-260
11880314-9 2002 These results suggest a protective role of RA from TNF-alpha antiproliferative action, through mechanisms involving modulation of IGFBP-2 production. Tretinoin 43-45 insulin like growth factor binding protein 2 Homo sapiens 130-137
18569334-6 2008 is capable to oxidize all-trans-retinol bound to CRBP (holo-CRBP) to all-trans-retinaldehyde and then to all-trans-retinoic acid. Tretinoin 105-128 retinol binding protein 1 Homo sapiens 60-64
12207051-0 2002 Expression of selected apoptosis related genes, MIF, IGIF and TNF alpha, during retinoic acid-induced neural differentiation in murine embryonic stem cells. Tretinoin 80-93 interleukin 18 Mus musculus 53-57
18569334-7 2008 To get further knowledge regarding this process we have evaluated the biosynthetic pathway of retinoic acid in a human mammary epithelial cell line (HMEC) in which xanthine dehydrogenase (E.C. Tretinoin 94-107 xanthine dehydrogenase Homo sapiens 164-186
12207051-9 2002 Significant increase observed in interferon gamma inducing factor (IGIF/IL-18) mRNA expression in all-trans-retinoic acid-treated cells on day 14 and 17 did not translate to increased INF gamma expression. Tretinoin 108-121 interleukin 18 Mus musculus 67-71
18686604-5 2008 RESULTS: Necl1 expression increased after retinoic acid (RA) induction in SH-SY5Y and P19 cells. Tretinoin 42-55 cell adhesion molecule 3 Homo sapiens 9-14
11904524-9 2002 Because PAI-1 inhibits the production of fibrinolytic protein plasmin that facilitates SMC migration, induction of the PAI-1 gene expression by atRA may at least partly account for the role of atRA as an important inhibitor of neointima formation. Tretinoin 193-197 plasminogen Homo sapiens 62-69
11522775-6 2001 The new complex I subunit (B16.6) is the bovine homolog of GRIM-19, the product of a cell death regulatory gene induced by interferon-beta and retinoic acid, thus providing a new link between the mitochondrion and its electron-transport chain and apoptotic cell death. Tretinoin 143-156 NADH:ubiquinone oxidoreductase subunit A13 Bos taurus 59-66
19031736-0 2008 [Expression level changes of inhibitor of differentiation 1 during ATRA-induced acute promyelocytic leukemia cells differentiation]. Tretinoin 67-71 inhibitor of DNA binding 1, HLH protein Homo sapiens 29-59
11588034-6 2001 The addition of all-trans retinoic acid also enhanced this granulocytic differentiation of the cultured C/EBPalpha(-/-) cells, indicating that the activated retinoic acid receptors can enhance granulocytic differentiation through a molecular pathway that is independent of C/EBPalpha. Tretinoin 26-39 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 104-114
11588034-6 2001 The addition of all-trans retinoic acid also enhanced this granulocytic differentiation of the cultured C/EBPalpha(-/-) cells, indicating that the activated retinoic acid receptors can enhance granulocytic differentiation through a molecular pathway that is independent of C/EBPalpha. Tretinoin 26-39 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 273-283
12153175-2 2002 Intracellular retinoid signaling induced by endogenous or exogenous RA is regulated by retinoid binding proteins such as CRBPI, CRABPI and CRABPII and there are data suggesting that the expression of these proteins can influence the sensitivity to the growth inhibitory effects of ATRA. Tretinoin 68-70 retinol binding protein 1 Homo sapiens 121-126
12153175-2 2002 Intracellular retinoid signaling induced by endogenous or exogenous RA is regulated by retinoid binding proteins such as CRBPI, CRABPI and CRABPII and there are data suggesting that the expression of these proteins can influence the sensitivity to the growth inhibitory effects of ATRA. Tretinoin 68-70 retinol binding protein 1 Homo sapiens 128-134
12153175-2 2002 Intracellular retinoid signaling induced by endogenous or exogenous RA is regulated by retinoid binding proteins such as CRBPI, CRABPI and CRABPII and there are data suggesting that the expression of these proteins can influence the sensitivity to the growth inhibitory effects of ATRA. Tretinoin 281-285 retinol binding protein 1 Homo sapiens 121-126
12153175-3 2002 In this study, we investigated the basal and ATRA-induced expression of CRBPI and CRABPI and II in leukemic cell lines and in cells from patients with acute myeloid leukemia (AML). Tretinoin 45-49 retinol binding protein 1 Homo sapiens 72-77
12153175-3 2002 In this study, we investigated the basal and ATRA-induced expression of CRBPI and CRABPI and II in leukemic cell lines and in cells from patients with acute myeloid leukemia (AML). Tretinoin 45-49 retinol binding protein 1 Homo sapiens 82-88
12165291-3 2002 We investigated patients with APL receiving all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)) treatment, contributing to the downregulation of the expression of annexin II on APL cells, and decreasing the generation of plasmin by tissue plasminogen activator (t-PA). Tretinoin 44-67 plasminogen Homo sapiens 232-239
11562472-6 2001 In contrast, when RMA cells were transfected with the retinoic acid early inducible gene-1 gamma or delta (RAE-1), ligands for the activating receptor NKG2D, the tumors were rejected. Tretinoin 54-67 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 151-156
12165291-3 2002 We investigated patients with APL receiving all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)) treatment, contributing to the downregulation of the expression of annexin II on APL cells, and decreasing the generation of plasmin by tissue plasminogen activator (t-PA). Tretinoin 69-73 plasminogen Homo sapiens 232-239
19031736-1 2008 OBJECTIVE: To study the role of inhibitor of differentiation 1 (ID1) in ATRA-induced acute promyelocytic leukemia (APL) cells differentiation. Tretinoin 72-76 inhibitor of DNA binding 1, HLH protein Homo sapiens 32-62
11788590-5 2002 Interleukin 6 and interleukin 11, known to activate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at least partially mediated through interactions between STAT3 and retinoid nuclear receptor enhanceosome proteins in pulmonary epithelial cells. Tretinoin 118-131 surfactant protein B Homo sapiens 90-94
11669453-4 2001 Forskolin, but not TGF-beta1, abrogated RA-induced expression of a reporter construct containing 900 base pair (bp) of the RAR-beta gene promoter, transfected into MEPM cells, suggesting that this portion of the promoter contains the forskolin-responsive, but not the TGF-beta-responsive, element. Tretinoin 40-42 retinoic acid receptor, beta Mus musculus 123-131
11669453-5 2001 Thus, a putative TGF-beta Inhibitory Element (TIE) adjacent to the retinoic acid response element (RARE) in the RAR-beta promoter is either non-functional, or requires promoter/enhancer elements not present in the promoter construct used in these experiments. Tretinoin 67-80 transforming growth factor, beta 1 Mus musculus 17-25
19031736-1 2008 OBJECTIVE: To study the role of inhibitor of differentiation 1 (ID1) in ATRA-induced acute promyelocytic leukemia (APL) cells differentiation. Tretinoin 72-76 inhibitor of DNA binding 1, HLH protein Homo sapiens 64-67
11669453-5 2001 Thus, a putative TGF-beta Inhibitory Element (TIE) adjacent to the retinoic acid response element (RARE) in the RAR-beta promoter is either non-functional, or requires promoter/enhancer elements not present in the promoter construct used in these experiments. Tretinoin 67-80 retinoic acid receptor, beta Mus musculus 112-120
19031736-5 2008 ID1 expression level reached the peak at 2 h in bone marrow cells from APL patents treated with ATRA, and its level detected 3 times in one of the patient was (311.1 +/- 48.7) fold of control. Tretinoin 96-100 inhibitor of DNA binding 1, HLH protein Homo sapiens 0-3
19031736-7 2008 CONCLUSION: ID1 may be involved in ATRA-induced granulocytic differentiation as an ATRA-targeted gene. Tretinoin 35-39 inhibitor of DNA binding 1, HLH protein Homo sapiens 12-15
12133451-6 2002 Moreover, the dephosphorylation rate of PRB was increased by the treatment with EPA or/and RA. Tretinoin 91-93 RB transcriptional corepressor 1 Homo sapiens 40-43
18400747-7 2008 Retinoic acid has also been shown to suppress loss of Foxp3 induced by TGF-beta1. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 71-80
12133451-7 2002 CONCLUSION: The changes of RB expression and PRB phosphorylation may be one of the mechanisms of the synergistic effects of EPA and RA on the HL-60 cell proliferation and differentiation. Tretinoin 132-134 RB transcriptional corepressor 1 Homo sapiens 45-48
11904404-0 2002 A mammalian homolog of unc-53 is regulated by all-trans retinoic acid in neuroblastoma cells and embryos. Tretinoin 56-69 Adapter protein unc-53;Calponin-homology (CH) domain-containing protein Caenorhabditis elegans 23-29
11904404-3 2002 By using the human neuroblastoma cell line, SH-SY5Y, we have identified an atRA-responsive gene (RAINB1: retinoic acid inducible in neuroblastoma cells) that is induced within 4 h after exposure of SH-SY5Y cells to atRA. Tretinoin 105-118 neuron navigator 2 Homo sapiens 97-103
11527412-1 2001 Expression of the DCC (deleted in colorectal cancer) protein is strongly induced during the neural differentiation of mouse P19 embryonal carcinoma (EC) cells that occurs when these cells are treated with retinoic acid (RA). Tretinoin 205-218 deleted in colorectal carcinoma Mus musculus 18-21
11527412-1 2001 Expression of the DCC (deleted in colorectal cancer) protein is strongly induced during the neural differentiation of mouse P19 embryonal carcinoma (EC) cells that occurs when these cells are treated with retinoic acid (RA). Tretinoin 205-218 deleted in colorectal carcinoma Mus musculus 23-51
11527412-1 2001 Expression of the DCC (deleted in colorectal cancer) protein is strongly induced during the neural differentiation of mouse P19 embryonal carcinoma (EC) cells that occurs when these cells are treated with retinoic acid (RA). Tretinoin 220-222 deleted in colorectal carcinoma Mus musculus 18-21
11527412-1 2001 Expression of the DCC (deleted in colorectal cancer) protein is strongly induced during the neural differentiation of mouse P19 embryonal carcinoma (EC) cells that occurs when these cells are treated with retinoic acid (RA). Tretinoin 220-222 deleted in colorectal carcinoma Mus musculus 23-51
11904404-3 2002 By using the human neuroblastoma cell line, SH-SY5Y, we have identified an atRA-responsive gene (RAINB1: retinoic acid inducible in neuroblastoma cells) that is induced within 4 h after exposure of SH-SY5Y cells to atRA. Tretinoin 75-79 neuron navigator 2 Homo sapiens 97-103
18400747-8 2008 Retinoic acid in the presence of TGF-beta1 reduced STAT6 binding to the Foxp3 promoter and enhanced histone acetylation, thereby reverting the effect of IL-4. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 33-42
11870076-12 2002 Expression of mRNA for RXR alpha, RXR beta, RALDH2, and PPAR gamma suggests that the early embryo may be competent to synthesize retinoic acid and regulate gene expression during preattachment development in vitro. Tretinoin 129-142 peroxisome proliferator activated receptor gamma Bos taurus 56-66
11506860-3 2001 Western blotting showed that protein expression of RhoA, RhoB and Cdc42 RhoGTPases dramatically increased, in a programmed manner, during neuronal differentiation of P19 mouse embryonal carcinoma cells with retinoic acid. Tretinoin 207-220 ras homolog family member A Mus musculus 51-55
18400747-8 2008 Retinoic acid in the presence of TGF-beta1 reduced STAT6 binding to the Foxp3 promoter and enhanced histone acetylation, thereby reverting the effect of IL-4. Tretinoin 0-13 signal transducer and activator of transcription 6 Mus musculus 51-56
11506860-3 2001 Western blotting showed that protein expression of RhoA, RhoB and Cdc42 RhoGTPases dramatically increased, in a programmed manner, during neuronal differentiation of P19 mouse embryonal carcinoma cells with retinoic acid. Tretinoin 207-220 ras homolog family member B Mus musculus 57-61
18453568-6 2008 Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Tretinoin 58-71 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 164-193
11506860-3 2001 Western blotting showed that protein expression of RhoA, RhoB and Cdc42 RhoGTPases dramatically increased, in a programmed manner, during neuronal differentiation of P19 mouse embryonal carcinoma cells with retinoic acid. Tretinoin 207-220 cell division cycle 42 Mus musculus 66-71
11478838-3 2001 Immunoblotting analyses and capillary zone electrophoresis demonstrated that following RA treatment: lamins A/C and B1, and vimentin decreased to negligible amounts; LAP2 beta, lamin B2 and emerin remained essentially unchanged; lamin B receptor (LBR) increased markedly; histone subtypes H1.4 and 1.5 exhibited dephosphorylation. Tretinoin 87-89 lamin B2 Homo sapiens 177-185
11478839-13 2001 These data support the hypothesis that RA and BMP4 together induce the p27 protein leading to Rb activation and ultimately apoptosis. Tretinoin 39-41 RB transcriptional corepressor 1 Homo sapiens 94-96
11479234-10 2001 These results suggest that an RXR-selective retinoic acid decreases SCCHN proliferation in part by interfering with TGF-alpha/EGFR autocrine signaling. Tretinoin 44-57 transforming growth factor alpha Homo sapiens 116-125
11788904-4 2002 WNT3 and WNT3A mRNAs were co-expressed in an embryonal carcinoma cell line NT2, which is reported to differentiate into postmitotic CNS neurons by treatment with retinoic acid for two weeks. Tretinoin 162-175 Wnt family member 3A Homo sapiens 9-14
11788904-5 2002 Expression level of WNT3 mRNA in NT2 cells was not changed during 72 h after retinoic acid treatment, while expression of WNT3A mRNA was down-regulated in NT2 cells by retinoic acid. Tretinoin 168-181 Wnt family member 3A Homo sapiens 122-127
11788904-8 2002 WNT3A, down-regulated by retinoic acid in NT2 cells, might play key roles in the maintenance of NT2 cells in the undifferentiated proliferation stage through activation of the beta-catenin - TCF signaling pathway. Tretinoin 25-38 Wnt family member 3A Homo sapiens 0-5
12055350-7 2002 The essentiality of the retinoid receptors in mediating the activity of atRA is exemplified by the many compound null mutant embryos that now recapitulate both the original vitamin A-deficiency syndrome and exhibit a host of new defects, many of which can also be observed in the VAD-atRA-supported rat embryo model and in retinaldehyde dehydrogenase type 2 (RALDH2) mutant mice. Tretinoin 72-76 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 323-357
12055350-7 2002 The essentiality of the retinoid receptors in mediating the activity of atRA is exemplified by the many compound null mutant embryos that now recapitulate both the original vitamin A-deficiency syndrome and exhibit a host of new defects, many of which can also be observed in the VAD-atRA-supported rat embryo model and in retinaldehyde dehydrogenase type 2 (RALDH2) mutant mice. Tretinoin 72-76 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 359-365
11683493-3 2001 This motivates the question of whether RA also activated RAF as part of a typical RAF/MEK/MAPK cascade. Tretinoin 39-41 zinc fingers and homeoboxes 2 Homo sapiens 57-60
11683493-3 2001 This motivates the question of whether RA also activated RAF as part of a typical RAF/MEK/MAPK cascade. Tretinoin 39-41 zinc fingers and homeoboxes 2 Homo sapiens 82-85
18453568-6 2008 Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Tretinoin 73-75 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 164-193
11683493-4 2001 Retinoic acid is shown here to also increase the phosphorylation of RAF, but in an unusual way. Tretinoin 0-13 zinc fingers and homeoboxes 2 Homo sapiens 68-71
18453568-6 2008 Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Tretinoin 257-259 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 164-193
11683493-10 2001 RA-induced MEK-dependent RAF phosphorylation is not due to changes in the amount of cellular MEK. Tretinoin 0-2 zinc fingers and homeoboxes 2 Homo sapiens 25-28
11876525-4 2002 Both URA liposomes and retinoic acid decreased markers of keratinocyte differentiation (keratin 1, keratin 10 and involucrin) in cultured NHEK. Tretinoin 23-36 keratin 1 Homo sapiens 88-97
11683493-13 2001 In summary, RA induces a MEK-dependent prolonged RAF activation, whose slow onset occurs after ERK2 activation but still well before cell cycle arrest and cell differentiation. Tretinoin 12-14 zinc fingers and homeoboxes 2 Homo sapiens 49-52
18367164-7 2008 We further propose a model placing PITX2 as an essential integration node between retinoic acid and canonical Wnt signaling during eye development. Tretinoin 82-95 paired-like homeodomain transcription factor 2 Mus musculus 35-40
11872149-2 2002 Following the reports that two members of the superfamily of aldehyde dehydrogenase (ALDH) enzymes, ALDH1A1 and ALDH1A2, were capable of catalyzing the oxidation of all-trans retinal to all-trans retinoic acid with submicromolar Km values, we initiated an investigation of the ability of 4-(N,N-dipropylamino)benzaldehyde (DPAB) to inhibit the oxidation of retinal by purified mouse and human ALDH1A1. Tretinoin 186-209 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 61-83
11872149-2 2002 Following the reports that two members of the superfamily of aldehyde dehydrogenase (ALDH) enzymes, ALDH1A1 and ALDH1A2, were capable of catalyzing the oxidation of all-trans retinal to all-trans retinoic acid with submicromolar Km values, we initiated an investigation of the ability of 4-(N,N-dipropylamino)benzaldehyde (DPAB) to inhibit the oxidation of retinal by purified mouse and human ALDH1A1. Tretinoin 186-209 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 85-89
11472854-0 2001 Specific expression of the retinoic acid-synthesizing enzyme RALDH2 during mouse inner ear development. Tretinoin 27-40 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 61-67
17612537-5 2008 Effects of dihydrotestosterone (DHT), insulin, and all-trans retinoic acid (ATRA) on COMT messenger RNA expression were investigated by using COMTP1 promoter-luciferase reporter and Northern blot. Tretinoin 51-74 catechol-O-methyltransferase Homo sapiens 85-89
11472854-2 2001 Here, we report that the retinaldehyde dehydrogenase 2 (Raldh2) gene, whose product is involved in the enzymatic generation of retinoic acid (RA), exhibits a restricted expression pattern during mouse inner ear ontogenesis. Tretinoin 127-140 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 25-54
11472854-2 2001 Here, we report that the retinaldehyde dehydrogenase 2 (Raldh2) gene, whose product is involved in the enzymatic generation of retinoic acid (RA), exhibits a restricted expression pattern during mouse inner ear ontogenesis. Tretinoin 127-140 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 56-62
11472854-2 2001 Here, we report that the retinaldehyde dehydrogenase 2 (Raldh2) gene, whose product is involved in the enzymatic generation of retinoic acid (RA), exhibits a restricted expression pattern during mouse inner ear ontogenesis. Tretinoin 142-144 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 25-54
11472854-2 2001 Here, we report that the retinaldehyde dehydrogenase 2 (Raldh2) gene, whose product is involved in the enzymatic generation of retinoic acid (RA), exhibits a restricted expression pattern during mouse inner ear ontogenesis. Tretinoin 142-144 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 56-62
11872149-2 2002 Following the reports that two members of the superfamily of aldehyde dehydrogenase (ALDH) enzymes, ALDH1A1 and ALDH1A2, were capable of catalyzing the oxidation of all-trans retinal to all-trans retinoic acid with submicromolar Km values, we initiated an investigation of the ability of 4-(N,N-dipropylamino)benzaldehyde (DPAB) to inhibit the oxidation of retinal by purified mouse and human ALDH1A1. Tretinoin 186-209 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 100-107
11872149-2 2002 Following the reports that two members of the superfamily of aldehyde dehydrogenase (ALDH) enzymes, ALDH1A1 and ALDH1A2, were capable of catalyzing the oxidation of all-trans retinal to all-trans retinoic acid with submicromolar Km values, we initiated an investigation of the ability of 4-(N,N-dipropylamino)benzaldehyde (DPAB) to inhibit the oxidation of retinal by purified mouse and human ALDH1A1. Tretinoin 186-209 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 112-119
11872149-7 2002 CONCLUSION: Although ALDH1A1 may be the major catalytic activity for retinal oxidation in some retinoid-dependent mouse and Xenopus embryonic tissues and in adult human and mouse hematopoietic stem cells, another catalytic activity appears to synthesize the retinoic acid ligand necessary to stimulate the differentiation of HL-60 cells to end stage granulocytes. Tretinoin 258-271 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 21-28
11879576-6 2002 We hypothesize that the loss of CRBP1 and RBP expression disrupts retinol metabolism and retinoic acid production, which may facilitate the occurrence of genetic damage leading to the malignant transformation of the ovarian surface epithelium, the cells from which ovarian cancer arises. Tretinoin 89-102 retinol binding protein 1 Homo sapiens 32-37
11437413-3 2001 BHY cells expressed all of retinoid nuclear receptors (RARalpha, beta, gamma, and RXRalpha) and cytoplasmic retinoic acid binding proteins (CRABP1 and CRABP2). Tretinoin 108-121 cellular retinoic acid binding protein 1 Homo sapiens 140-146
17612537-5 2008 Effects of dihydrotestosterone (DHT), insulin, and all-trans retinoic acid (ATRA) on COMT messenger RNA expression were investigated by using COMTP1 promoter-luciferase reporter and Northern blot. Tretinoin 76-80 catechol-O-methyltransferase Homo sapiens 85-89
17612537-10 2008 Dihydrotestosterone, insulin, and ATRA all induced a dose-dependent increase in COMTP1-luciferase transactivation, as well as up-regulated COMT messenger RNA expression in granulosa cells. Tretinoin 34-38 catechol-O-methyltransferase Homo sapiens 80-84
17612537-11 2008 CONCLUSION(S): Catechol O-methyltransferase expression in granulosa cells was up-regulated by insulin, DHT, and ATRA. Tretinoin 112-116 catechol-O-methyltransferase Homo sapiens 15-43
11493562-3 2001 A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud. Tretinoin 139-152 receptor for activated C kinase 1 Gallus gallus 16-21
11779708-2 2002 Retinoic acid (RA, active metabolite) exacerbates liver fibrosis that is not accompanied by hepatic necroinflammation, in which RA acts directly on hepatic stellate cells (HSCs); RA enhances plasminogen activator/plasmin levels and thereby induces proteolytic activation of latent transforming growth factor-beta (TGF-beta), a strong fibrogenic cytokine, resulting in enhanced collagen production. Tretinoin 0-13 plasminogen Homo sapiens 191-198
18183617-0 2008 Retinoic acid enhances prostaglandin E2 production through increased expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in rat brain microglia. Tretinoin 0-13 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 83-99
12397600-9 2002 On the other hand, okadaic acid (310 nM) and all trans-retinoic acid (1 micro M) significantly increased (3)H-MPP(+) uptake and inhibited ecto-ALP activity. Tretinoin 49-68 tripartite motif containing 33 Homo sapiens 138-142
11734301-13 2002 However, P-gp/MDR1 expression augmented by ATRA, which was observed in monocytic AML, was recognized as a functional molecule of mature monocyte/macrophage, because CD34 expression decreased and CD13 expression increased by ATRA. Tretinoin 43-47 alanyl aminopeptidase, membrane Homo sapiens 195-199
11720243-6 2001 PRL (20 ng/mL) stimulated its expression, reaching maximal levels within 12 h. Expression of XIAP was also evaluated in Nb2-SFJCD1 cells subsequent to treatment with differentiating agents (sodium butyrate [2 mM, 72 h], all trans-retinoic acid [10 microM, 72 h], or 1,25-dihydroxycholecalciferol [100 nM, 24 h]). Tretinoin 224-243 X-linked inhibitor of apoptosis Rattus norvegicus 93-97
18183617-5 2008 Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. Tretinoin 15-38 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 87-92
18183617-5 2008 Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. Tretinoin 15-38 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 118-123
11510982-6 2001 These studies lead to the conclusion that most RA-induced events (e.g. primitive and visceral differentiation, growth arrest, apoptosis and activation of expression of a number of genes) are transduced by RARgamma/RXRalpha heterodimers, whereas some other events (e.g. parietal differentiation) are mediated by RARalpha/RXRalpha. Tretinoin 47-49 retinoid X receptor alpha Mus musculus 214-222
18183617-5 2008 Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. Tretinoin 40-44 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 87-92
11510982-6 2001 These studies lead to the conclusion that most RA-induced events (e.g. primitive and visceral differentiation, growth arrest, apoptosis and activation of expression of a number of genes) are transduced by RARgamma/RXRalpha heterodimers, whereas some other events (e.g. parietal differentiation) are mediated by RARalpha/RXRalpha. Tretinoin 47-49 retinoid X receptor alpha Mus musculus 320-328
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 E1A binding protein p300 Homo sapiens 134-138
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 E1A binding protein p300 Homo sapiens 134-138
11369141-8 2001 Moreover, the proteolytic cleavage of alpha5beta1 integrin and focal adhesion kinase (FAK) proteins is linked to the early phase of the ATRA-induced apoptotic process. Tretinoin 136-140 protein tyrosine kinase 2 Homo sapiens 63-84
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 E1A binding protein p300 Homo sapiens 134-138
18183617-5 2008 Interestingly, all-trans retinoic acid (ATRA) suppressed the expression of early-phase COX-2 but augmented late-phase COX-2 and inhibited iNOS in the whole time sequence. Tretinoin 40-44 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 118-123
11748248-6 2001 RA treatment of chondrocytic cells also induces the production of MT1-MMP, a membrane-bound metalloproteinase essential for skeletal formation, which participates in a proteolytic cascade with collagenase-3. Tretinoin 0-2 matrix metallopeptidase 14 Homo sapiens 66-73
11369141-8 2001 Moreover, the proteolytic cleavage of alpha5beta1 integrin and focal adhesion kinase (FAK) proteins is linked to the early phase of the ATRA-induced apoptotic process. Tretinoin 136-140 protein tyrosine kinase 2 Homo sapiens 86-89
11369141-9 2001 Furthermore, ATRA-induced detachment, death, and cleavage of alpha5beta1 integrin and FAK were drastically suppressed by plating cells onto Matrigel-coated plates. Tretinoin 13-17 protein tyrosine kinase 2 Homo sapiens 86-89
11369141-10 2001 These findings provide evidence that abrogation of cell adhesion, through proteolysis of alpha5beta1 integrin and FAK, is closely linked to ATRA-induced apoptosis in Hep3B cells. Tretinoin 140-144 protein tyrosine kinase 2 Homo sapiens 114-117
18183617-8 2008 The results collectively suggest that ATRA modulates microglial responses to inflammatory stimulators, particularly at the late phase, via enhancement of COX-2 expression and PGE(2) production. Tretinoin 38-42 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 154-159
11595732-0 2001 Retinoic acid-mediated growth arrest requires ubiquitylation and degradation of the F-box protein Skp2. Tretinoin 0-13 S-phase kinase associated protein 2 Homo sapiens 98-102
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 47-70 interleukin 5 Homo sapiens 127-131
11595732-2 2001 We show here that the decrease in D-type cyclin levels observed following ATRA treatment correlates with an increase in the rate of cyclin D1 ubiquitylation in both T-47D and MCF-7 breast cancer cell lines. Tretinoin 74-78 cyclin D1 Homo sapiens 132-141
11301322-0 2001 PRAM-1 is a novel adaptor protein regulated by retinoic acid (RA) and promyelocytic leukemia (PML)-RA receptor alpha in acute promyelocytic leukemia cells. Tretinoin 47-60 PML-RARA regulated adaptor molecule 1 Homo sapiens 0-6
11301322-4 2001 By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARalpha target gene encoding an Adaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. Tretinoin 87-100 PML-RARA regulated adaptor molecule 1 Homo sapiens 115-121
11301322-6 2001 In U937 myeloid precursor cells, PRAM-1 expression is inhibited by expression of PML-RARalpha in the absence of ligand and de novo superinduced by retinoic acid. Tretinoin 147-160 PML-RARA regulated adaptor molecule 1 Homo sapiens 33-39
11595732-5 2001 Furthermore, we demonstrate that ATRA promotes the ubiquitylation of Skp2, an F-box protein that targets p27 for degradation. Tretinoin 33-37 S-phase kinase associated protein 2 Homo sapiens 69-73
18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 72-76 interleukin 5 Homo sapiens 127-131
11595732-8 2001 We found that the mechanism of ATRA-induced ubiquitylation of cyclin D1 and Skp2 is independent of CUL-1 expression and that ATRA can rescue cyclin D1 degradation in the uterine cell line SK-UT-1, where D-type cyclins are stabilized due to a specific defect in proteolysis. Tretinoin 31-35 cyclin D1 Homo sapiens 62-71
11595732-8 2001 We found that the mechanism of ATRA-induced ubiquitylation of cyclin D1 and Skp2 is independent of CUL-1 expression and that ATRA can rescue cyclin D1 degradation in the uterine cell line SK-UT-1, where D-type cyclins are stabilized due to a specific defect in proteolysis. Tretinoin 31-35 S-phase kinase associated protein 2 Homo sapiens 76-80
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 10-23 surfactant protein B Homo sapiens 113-117
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 10-23 surfactant protein B Homo sapiens 184-188
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 10-23 surfactant protein B Homo sapiens 190-195
11595732-8 2001 We found that the mechanism of ATRA-induced ubiquitylation of cyclin D1 and Skp2 is independent of CUL-1 expression and that ATRA can rescue cyclin D1 degradation in the uterine cell line SK-UT-1, where D-type cyclins are stabilized due to a specific defect in proteolysis. Tretinoin 31-35 cullin 1 Homo sapiens 99-104
11595732-8 2001 We found that the mechanism of ATRA-induced ubiquitylation of cyclin D1 and Skp2 is independent of CUL-1 expression and that ATRA can rescue cyclin D1 degradation in the uterine cell line SK-UT-1, where D-type cyclins are stabilized due to a specific defect in proteolysis. Tretinoin 31-35 cyclin D1 Homo sapiens 141-150
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 145-158 surfactant protein B Homo sapiens 113-117
11595732-8 2001 We found that the mechanism of ATRA-induced ubiquitylation of cyclin D1 and Skp2 is independent of CUL-1 expression and that ATRA can rescue cyclin D1 degradation in the uterine cell line SK-UT-1, where D-type cyclins are stabilized due to a specific defect in proteolysis. Tretinoin 125-129 cyclin D1 Homo sapiens 141-150
18008394-3 2008 To investigate the role of TG2 and ODC activities in regenerating liver, we used retinoic acid (RA), an inducer of TG2 and a suppressor of ODC. Tretinoin 81-94 transglutaminase 2 Rattus norvegicus 115-118
11595732-9 2001 These data suggest that ATRA induces a novel pathway of ubiquitylation and that the degradation of the F-box protein Skp2 is the mechanism underlying p27 accumulation and cyclin E-cdk2 inactivation following ATRA treatment. Tretinoin 24-28 S-phase kinase associated protein 2 Homo sapiens 117-121
11595732-9 2001 These data suggest that ATRA induces a novel pathway of ubiquitylation and that the degradation of the F-box protein Skp2 is the mechanism underlying p27 accumulation and cyclin E-cdk2 inactivation following ATRA treatment. Tretinoin 208-212 S-phase kinase associated protein 2 Homo sapiens 117-121
11753676-6 2001 Also, RA treatment increased expression of the cdk inhibitor p27 and decreased activity of cdk 2, cdk 4 and cdk 6. Tretinoin 6-8 cyclin dependent kinase 2 Homo sapiens 91-96
11753676-6 2001 Also, RA treatment increased expression of the cdk inhibitor p27 and decreased activity of cdk 2, cdk 4 and cdk 6. Tretinoin 6-8 cyclin dependent kinase 4 Homo sapiens 98-103
11429697-0 2001 Ectopic expression of cyclin D1 amplifies a retinoic acid-induced mitochondrial death pathway in breast cancer cells. Tretinoin 44-57 cyclin D1 Homo sapiens 22-31
11429697-1 2001 All-trans retinoic acid inhibits growth associated with downregulation of cyclin D1 and can cause low level apoptosis in estrogen receptor positive breast cancer cell lines. Tretinoin 10-23 cyclin D1 Homo sapiens 74-83
11429697-3 2001 Constitutive expression of cyclin D1 in estrogen receptor positive MCF-7 and ZR-75 breast cancer cells (MCF-7(cycD1) and ZR-75(cycD1)) Increased the fraction of cells in S phase and reduced the G1 accumulation following retinoic acid treatment compared with control cells. Tretinoin 220-233 cyclin D1 Homo sapiens 27-36
11429697-9 2001 Accordingly, coexpression of Bcl-2 and cyclin D1 rendered the cells resistant to retinoic acid-induced apoptosis. Tretinoin 81-94 cyclin D1 Homo sapiens 39-48
11429697-10 2001 We conclude that constitutive expression of cyclin D1 sensitizes ER-positive breast cancer cells to a retinoic acid-induced mitochondrial death pathway involving Bax activation, cytochrome c release and caspase-9 cleavage. Tretinoin 102-115 cyclin D1 Homo sapiens 44-53
11340568-7 2001 We found that RAR-gamma mRNA expression was strongly correlated with RA-induced growth inhibition (p = 0.016, R = 0.92) and RA turnover (p = 0.041, R = 0.86). Tretinoin 69-71 retinoic acid receptor gamma Homo sapiens 14-23
11713095-4 2001 Regardless of the airway tissue sources, MUC5B message was regulated by all-trans-retinoic acid (RA) and culture conditions in both primary and passage-1 cultures of TBE cells. Tretinoin 76-95 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 41-46
18008394-3 2008 To investigate the role of TG2 and ODC activities in regenerating liver, we used retinoic acid (RA), an inducer of TG2 and a suppressor of ODC. Tretinoin 96-98 transglutaminase 2 Rattus norvegicus 115-118
11340568-10 2001 These findings suggest that in HNSCC cell lines RAR-gamma is the most important retinoid receptor for regulation of RA turnover rate and RA-induced growth inhibition. Tretinoin 116-118 retinoic acid receptor gamma Homo sapiens 48-57
17941088-6 2008 RA inhibited stretch- and Ang II-induced intracellular reactive oxygen species (ROS) generation and upregulated the SOD2 level. Tretinoin 0-2 superoxide dismutase 2 Homo sapiens 116-120
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 neuropilin 1 Homo sapiens 189-193
11350930-0 2001 Role of transglutaminase II in retinoic acid-induced activation of RhoA-associated kinase-2. Tretinoin 31-44 transglutaminase 1 Homo sapiens 8-27
11350930-0 2001 Role of transglutaminase II in retinoic acid-induced activation of RhoA-associated kinase-2. Tretinoin 31-44 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 67-91
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 necdin, MAGE family member Homo sapiens 202-205
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 0-13 transglutaminase 1 Homo sapiens 100-105
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 0-13 transglutaminase 1 Homo sapiens 125-130
11713095-4 2001 Regardless of the airway tissue sources, MUC5B message was regulated by all-trans-retinoic acid (RA) and culture conditions in both primary and passage-1 cultures of TBE cells. Tretinoin 97-99 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 41-46
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 SMAD family member 3 Homo sapiens 242-247
11713105-3 2001 Since cytokines can induce matrix metalloproteinase (MMP) production in fibroblasts and neutrophil elastase (NE) can activate MMPs, we hypothesized that retinoic acid could attenuate collagen degradation by modifying MMP production and activation. Tretinoin 153-166 elastase, neutrophil expressed Homo sapiens 88-107
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 0-13 transglutaminase 1 Homo sapiens 272-277
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 15-17 transglutaminase 1 Homo sapiens 100-105
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 15-17 transglutaminase 1 Homo sapiens 125-130
11713105-3 2001 Since cytokines can induce matrix metalloproteinase (MMP) production in fibroblasts and neutrophil elastase (NE) can activate MMPs, we hypothesized that retinoic acid could attenuate collagen degradation by modifying MMP production and activation. Tretinoin 153-166 elastase, neutrophil expressed Homo sapiens 109-111
11350930-2 2001 Retinoic acid (RA), which is known to have a role in cell differentiation, is a potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which is inhibited by monodansylcadaverine (MDC; an inhibitor of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity). Tretinoin 15-17 transglutaminase 1 Homo sapiens 272-277
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 neuropilin 1 Homo sapiens 249-253
18261720-6 2008 Both Tr-mespb and Xl-mespb are directly upregulated by RA, through a complex, distal element. Tretinoin 55-57 mesoderm posterior ba Danio rerio 8-13
11747085-7 2001 When supernumerary digits were induced at the anterior limb margin by retinoic acid treatment, their development was also preceded by vascular regression; interestingly, cotreatment with VEGF inhibited supernumerary digit development as well. Tretinoin 70-83 vascular endothelial growth factor A Gallus gallus 187-191
18261720-6 2008 Both Tr-mespb and Xl-mespb are directly upregulated by RA, through a complex, distal element. Tretinoin 55-57 mesoderm posterior homolog B L homeolog Xenopus laevis 21-26
11278635-1 2001 Receptor-interacting protein 140 (RIP140) interacts with retinoic acid receptor and retinoid X receptor in a ligand-dependent manner and suppresses retinoic acid (RA) induction of its target genes. Tretinoin 57-70 nuclear receptor interacting protein 1 Homo sapiens 0-32
11278635-1 2001 Receptor-interacting protein 140 (RIP140) interacts with retinoic acid receptor and retinoid X receptor in a ligand-dependent manner and suppresses retinoic acid (RA) induction of its target genes. Tretinoin 57-70 nuclear receptor interacting protein 1 Homo sapiens 34-40
11278635-1 2001 Receptor-interacting protein 140 (RIP140) interacts with retinoic acid receptor and retinoid X receptor in a ligand-dependent manner and suppresses retinoic acid (RA) induction of its target genes. Tretinoin 163-165 nuclear receptor interacting protein 1 Homo sapiens 0-32
11278635-1 2001 Receptor-interacting protein 140 (RIP140) interacts with retinoic acid receptor and retinoid X receptor in a ligand-dependent manner and suppresses retinoic acid (RA) induction of its target genes. Tretinoin 163-165 nuclear receptor interacting protein 1 Homo sapiens 34-40
11278635-4 2001 RA induces coimmunoprecipitation of histone deacetylase 3 with retinoic acid receptor/retinoid X receptor in the presence of wild type RIP140, but not in the presence of the C-terminal motif-deleted RIP140. Tretinoin 0-2 nuclear receptor interacting protein 1 Homo sapiens 135-141
11722649-7 2001 RA + PIC-treated rats had significantly higher levels of interleukin (IL)-10, IL-12, and signal transducer and activator of transcription-1 (STAT-1) mRNA (P < 0.05), and STAT-1 protein (P < 0.02). Tretinoin 0-2 signal transducer and activator of transcription 1 Rattus norvegicus 89-139
11722649-7 2001 RA + PIC-treated rats had significantly higher levels of interleukin (IL)-10, IL-12, and signal transducer and activator of transcription-1 (STAT-1) mRNA (P < 0.05), and STAT-1 protein (P < 0.02). Tretinoin 0-2 signal transducer and activator of transcription 1 Rattus norvegicus 141-147
11278635-4 2001 RA induces coimmunoprecipitation of histone deacetylase 3 with retinoic acid receptor/retinoid X receptor in the presence of wild type RIP140, but not in the presence of the C-terminal motif-deleted RIP140. Tretinoin 0-2 nuclear receptor interacting protein 1 Homo sapiens 199-205
11278635-5 2001 A decrease in histone acetylation on the promoter region that carries a RA response element is associated with the expression of wild type RIP140, but not with expression of the mutant RIP140, in a dose-dependent manner. Tretinoin 72-74 nuclear receptor interacting protein 1 Homo sapiens 139-145
18331719-6 2008 The Aldh1a family is required for retinoic acid (RA) synthesis, and, in Foxh1 mutants, expression of Aldh1a1, -2, and -3 and activation of a RA-responsive transgenic reporter is abolished in anterior structures. Tretinoin 34-47 forkhead box H1 Homo sapiens 72-77
11377978-1 2001 The 11-cis retinol dehydrogenase (11-cis-RoDH) enzyme catalyzes the oxidation of cis-retinols to their respective retinals, a rate limiting step in the formation of retinoic acids. Tretinoin 165-179 retinol dehydrogenase 5 Homo sapiens 4-32
11722649-7 2001 RA + PIC-treated rats had significantly higher levels of interleukin (IL)-10, IL-12, and signal transducer and activator of transcription-1 (STAT-1) mRNA (P < 0.05), and STAT-1 protein (P < 0.02). Tretinoin 0-2 signal transducer and activator of transcription 1 Rattus norvegicus 173-179
18331719-6 2008 The Aldh1a family is required for retinoic acid (RA) synthesis, and, in Foxh1 mutants, expression of Aldh1a1, -2, and -3 and activation of a RA-responsive transgenic reporter is abolished in anterior structures. Tretinoin 141-143 forkhead box H1 Homo sapiens 72-77
11704871-4 2001 Ectopic CRBP-mediated inhibition of anchorage-independent cell survival and colony formation in the absence of significantly altered responses to either retinol or retinoic acid was also documented in T47D human breast cancer cells. Tretinoin 164-177 retinol binding protein 1 Homo sapiens 8-12
18331719-7 2008 Integrated mapping of a developmental transcription factor network thus reveals a key role for Foxh1 in patterning and initiating RA signaling in the forebrain. Tretinoin 130-132 forkhead box H1 Homo sapiens 95-100
11602619-9 2001 The antiproliferative action and the inhibition of ACTH and corticosterone produced by retinoic acid were confirmed in vivo in experimental ACTH-secreting tumors in nude mice. Tretinoin 87-100 pro-opiomelanocortin-alpha Mus musculus 51-55
11602619-9 2001 The antiproliferative action and the inhibition of ACTH and corticosterone produced by retinoic acid were confirmed in vivo in experimental ACTH-secreting tumors in nude mice. Tretinoin 87-100 pro-opiomelanocortin-alpha Mus musculus 140-144
11376562-5 2001 In vivo administration of ATRA or FK228 alone partly inhibited the growth of established tumors of NB4 subcutaneously transplanted in NOD / Shi-scid / scid mice, and the combination was synergistically effective. Tretinoin 26-30 atrophin 1 Homo sapiens 134-137
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 114-127 aldehyde dehydrogenase 1 family, member A2 Danio rerio 134-140
11331248-0 2001 Requirement of tyrosine-phosphorylated Vav for morphological differentiation of all-trans-retinoic acid-treated HL-60 cells. Tretinoin 84-103 vav guanine nucleotide exchange factor 1 Homo sapiens 39-42
11438548-4 2001 In attempting to discover the underlying biochemical activities that might account for these cellular effects, we found that monodansylcadaverine (MDC), which binds to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and in fact caused RA to become an apoptotic factor, suggesting that the ability of RA to protect against apoptosis is linked to the expression of active TGase. Tretinoin 253-255 transglutaminase 1 Homo sapiens 234-239
11438548-4 2001 In attempting to discover the underlying biochemical activities that might account for these cellular effects, we found that monodansylcadaverine (MDC), which binds to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and in fact caused RA to become an apoptotic factor, suggesting that the ability of RA to protect against apoptosis is linked to the expression of active TGase. Tretinoin 305-307 transglutaminase 1 Homo sapiens 234-239
11438548-4 2001 In attempting to discover the underlying biochemical activities that might account for these cellular effects, we found that monodansylcadaverine (MDC), which binds to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and in fact caused RA to become an apoptotic factor, suggesting that the ability of RA to protect against apoptosis is linked to the expression of active TGase. Tretinoin 305-307 transglutaminase 1 Homo sapiens 234-239
11675954-4 2001 Pretreatment with ATRA dose-dependently inhibited DNA synthesis induced by basic fibroblast growth factor. Tretinoin 18-22 fibroblast growth factor 2 Rattus norvegicus 75-105
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 129-131 aldehyde dehydrogenase 1 family, member A2 Danio rerio 134-140
18312642-4 2008 Following induction of differentiation using retinoic acid treatment, we observed a 16-fold increase in doublecortin mRNA expression, as well as strong induction of doublecortin polypeptide expression. Tretinoin 45-58 doublecortin Homo sapiens 104-116
11528388-3 2001 Here we show that a single maternal administration of a low dose of the vitamin A metabolite retinoic acid is sufficient to compensate the requirement for Hoxa1 function. Tretinoin 93-106 homeobox A1 Mus musculus 155-160
11769669-1 2001 OBJECTIVE: To explore the relationship of connexin 43(Cx43) and bystander effect in ovarian tumor cells in herpes simplex virus thymidine kinase/ganciclovir (HSV-TK/GCV) gene therapy in vitro, and to investigate the effection of all-trans retinoic acid (RA) on expression of Cx43 and bystander effect. Tretinoin 239-252 gap junction protein alpha 1 Homo sapiens 42-53
11245568-2 2001 To block endogenous RA synthesis, we have disrupted the gene encoding RALDH2, the first retinaldehyde dehydrogenase whose expression has been detected during early mouse post-implantation development. Tretinoin 20-22 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 70-76
11248329-2 2001 For each clone, we found a significant correlation between the reduction in 3[H]-thymidine incorporation and the reduction in CD25 expression (r=0.701, P<0.05) following treatment with 10(-5) M ATRA for 48 h. Agarose gel electrophoresis revealed DNA fragmentation of the cell lines treated with ATRA, indicative of apoptosis. Tretinoin 197-201 interleukin 2 receptor subunit alpha Homo sapiens 126-130
11248329-2 2001 For each clone, we found a significant correlation between the reduction in 3[H]-thymidine incorporation and the reduction in CD25 expression (r=0.701, P<0.05) following treatment with 10(-5) M ATRA for 48 h. Agarose gel electrophoresis revealed DNA fragmentation of the cell lines treated with ATRA, indicative of apoptosis. Tretinoin 298-302 interleukin 2 receptor subunit alpha Homo sapiens 126-130
18312642-4 2008 Following induction of differentiation using retinoic acid treatment, we observed a 16-fold increase in doublecortin mRNA expression, as well as strong induction of doublecortin polypeptide expression. Tretinoin 45-58 doublecortin Homo sapiens 165-177
18312642-6 2008 Moreover, stable transfection in NTERA-2 cells of reporter constructs encoding fluorescent or luminescent genes under the control of the doublecortin promoter allowed us to directly detect induction of neuronal differentiation in cell culture, such as following retinoic acid treatment or mouse Ngn2 transient overexpression. Tretinoin 262-275 doublecortin Homo sapiens 137-149
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 zinc fingers and homeoboxes 2 Homo sapiens 82-85
11783369-0 2001 [Phosphorylation of gap junction gene connexin 43 protein and dissociated calcium in HeLa cell line by all-trans-retinoic acid]. Tretinoin 103-126 gap junction protein alpha 1 Homo sapiens 38-49
11470752-9 2001 In contrast, RA supplementation in ethanol-fed rats raised hepatic RA concentration to normal levels and almost completely abolished the ethanol-enhanced c-Jun, cyclin D and AP-1 DNA-binding activities. Tretinoin 13-15 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 174-178
11683493-0 2001 Retinoic acid causes MEK-dependent RAF phosphorylation through RARalpha plus RXR activation in HL-60 cells. Tretinoin 0-13 zinc fingers and homeoboxes 2 Homo sapiens 35-38
11783369-1 2001 OBJECTIVE: To investigate the regulation effect on signal transduction pathway of gap junction gene connexin (Cx)43 in human cervical carcinoma cell line HeLa by all-trans-retinoic acid(ATRA). Tretinoin 162-185 gap junction protein alpha 1 Homo sapiens 82-115
18006504-2 2008 In this study, RA is found to cause MAPK activation with sustained association of RAF to MEK or ERK, leading to a MAPK-dependent accumulation of p21(Waf1/Cip1) and binding to CDK2 blocking G(1)/S transition. Tretinoin 15-17 cyclin dependent kinase 2 Homo sapiens 175-179
11783369-1 2001 OBJECTIVE: To investigate the regulation effect on signal transduction pathway of gap junction gene connexin (Cx)43 in human cervical carcinoma cell line HeLa by all-trans-retinoic acid(ATRA). Tretinoin 186-190 gap junction protein alpha 1 Homo sapiens 82-115
18269766-6 2008 It appears that this effect is mediated through p38 MAPK, because RA decreased p38 phosphorylation, and a selective inhibitor of p38 MAPK (SB203580) also inhibited the phosphorylation of ATF-2. Tretinoin 66-68 mitogen-activated protein kinase 14 Mus musculus 48-56
18269766-6 2008 It appears that this effect is mediated through p38 MAPK, because RA decreased p38 phosphorylation, and a selective inhibitor of p38 MAPK (SB203580) also inhibited the phosphorylation of ATF-2. Tretinoin 66-68 mitogen-activated protein kinase 14 Mus musculus 48-51
11467847-0 2001 Transcriptional activation of the nuclear receptor corepressor RIP140 by retinoic acid: a potential negative-feedback regulatory mechanism. Tretinoin 73-86 nuclear receptor interacting protein 1 Homo sapiens 63-69
11246122-3 2001 Mucous differentiation and expression of MUC2, MUC5AC, MUC5B and MUC7, but not MUCi, MUC4, and MUC8 mucin genes, were shown to be retinoic acid- (RA) or retinol-dependent. Tretinoin 130-143 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 55-60
11467847-1 2001 Through the use of microarray analysis it was discovered that the nuclear receptor coregulator, receptor interacting protein 140 (RIP140), was induced early during all-trans retinoic acid (RA)-induced differentiation of human embryonal carcinoma cells. Tretinoin 174-187 nuclear receptor interacting protein 1 Homo sapiens 96-128
18156191-0 2008 All-trans retinoic acid prevents development of cardiac remodeling in aortic banded rats by inhibiting the renin-angiotensin system. Tretinoin 10-23 renin Rattus norvegicus 107-112
11467847-1 2001 Through the use of microarray analysis it was discovered that the nuclear receptor coregulator, receptor interacting protein 140 (RIP140), was induced early during all-trans retinoic acid (RA)-induced differentiation of human embryonal carcinoma cells. Tretinoin 174-187 nuclear receptor interacting protein 1 Homo sapiens 130-136
11467847-1 2001 Through the use of microarray analysis it was discovered that the nuclear receptor coregulator, receptor interacting protein 140 (RIP140), was induced early during all-trans retinoic acid (RA)-induced differentiation of human embryonal carcinoma cells. Tretinoin 189-191 nuclear receptor interacting protein 1 Homo sapiens 96-128
11246122-3 2001 Mucous differentiation and expression of MUC2, MUC5AC, MUC5B and MUC7, but not MUCi, MUC4, and MUC8 mucin genes, were shown to be retinoic acid- (RA) or retinol-dependent. Tretinoin 130-143 mucin 7, secreted Homo sapiens 65-69
11246122-3 2001 Mucous differentiation and expression of MUC2, MUC5AC, MUC5B and MUC7, but not MUCi, MUC4, and MUC8 mucin genes, were shown to be retinoic acid- (RA) or retinol-dependent. Tretinoin 146-148 mucin 7, secreted Homo sapiens 65-69
11246122-5 2001 Our studies also showed that other important bioregulators such as thyroid hormone (T3) and epidermal growth factor (EGF) modulate basal expression of mucin genes, interacting with RA in a concentration-dependent manner. Tretinoin 181-183 LOC100508689 Homo sapiens 151-156
11467847-1 2001 Through the use of microarray analysis it was discovered that the nuclear receptor coregulator, receptor interacting protein 140 (RIP140), was induced early during all-trans retinoic acid (RA)-induced differentiation of human embryonal carcinoma cells. Tretinoin 189-191 nuclear receptor interacting protein 1 Homo sapiens 130-136
11467847-2 2001 A rapid, fourfold induction of RIP140 mRNA was detected within 3 h of RA treatment in human embryonal carcinoma and MCF-7 human breast cancer cells. Tretinoin 70-72 nuclear receptor interacting protein 1 Homo sapiens 31-37
18156191-7 2008 RA restored the ratio of Bcl-2 to Bax, inhibited cleavage of caspase-3 and -9, and prevented the decreases in the levels of SOD-1 and SOD-2. Tretinoin 0-2 caspase 3 Rattus norvegicus 61-77
11467847-3 2001 RIP140 protein levels were induced within 6 h of RA treatment. Tretinoin 49-51 nuclear receptor interacting protein 1 Homo sapiens 0-6
11467847-8 2001 These data are consistent with a model by which RA induction of RIP140 supplies a negative feedback signal toward ligand-activated retinoid receptors. Tretinoin 48-50 nuclear receptor interacting protein 1 Homo sapiens 64-70
11437442-12 2001 Conversely, treatment of wild-type embryos with retinoic acid greatly expands the periotic domains of expression of fgf3, fgf8, and pax8 and leads to formation of supernumerary and ectopic otic vesicles. Tretinoin 48-61 fibroblast growth factor 3 Danio rerio 116-120
11230116-7 2001 In conclusion, RA can stimulate endothelial cell proliferation and differentiation in vitro via enhanced RARalpha-dependent FGF-2 production, and it can also induce angiogenesis in vivo. Tretinoin 15-17 fibroblast growth factor 2 Mus musculus 124-129
18156191-8 2008 Pressure overload-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by RA, via upregulation of mitogen-activated protein kinase phosphatase (MKP)-1 and MKP-2. Tretinoin 83-85 mitogen activated protein kinase 3 Rattus norvegicus 45-51
18156191-8 2008 Pressure overload-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by RA, via upregulation of mitogen-activated protein kinase phosphatase (MKP)-1 and MKP-2. Tretinoin 83-85 mitogen activated protein kinase 14 Rattus norvegicus 62-65
18156191-8 2008 Pressure overload-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by RA, via upregulation of mitogen-activated protein kinase phosphatase (MKP)-1 and MKP-2. Tretinoin 83-85 dual specificity phosphatase 4 Rattus norvegicus 164-169
17561254-3 2008 For HL60 cells, ATRA induced major increases in descending order of CD38, CD11b, CD45RO, CD11c, CD54 and CD36 with repression of CD117 and CD44. Tretinoin 16-20 integrin subunit alpha X Homo sapiens 89-94
11368409-0 2001 Suppression of pRB expression in normal human mammary epithelial cells is associated with resistance to all-trans-retinoic acid but not N-(4-hydroxylphenyl)-retinamide. Tretinoin 107-127 RB transcriptional corepressor 1 Homo sapiens 15-18
11368409-2 2001 We observe that G(1/0)-phase arrest induced by all-trans-retinoic acid (ATRA) in normal human mammary epithelial cells (HMECs) is temporally associated with a significant decrease in the levels of hyperphosphorylated retinoblastoma protein (pRB). Tretinoin 47-70 RB transcriptional corepressor 1 Homo sapiens 241-244
11368409-2 2001 We observe that G(1/0)-phase arrest induced by all-trans-retinoic acid (ATRA) in normal human mammary epithelial cells (HMECs) is temporally associated with a significant decrease in the levels of hyperphosphorylated retinoblastoma protein (pRB). Tretinoin 72-76 RB transcriptional corepressor 1 Homo sapiens 241-244
11368409-3 2001 Suppression of pRB protein expression in HMECs by retroviral-mediated expression of the E7 protein of the human papillomavirus strain 16 (HPV-16) was associated with resistance to ATRA-mediated growth arrest but not to the synthetic retinoid N-(4-hydroxyphenyl) retinamide (4-HPR or fenretinide). Tretinoin 180-184 RB transcriptional corepressor 1 Homo sapiens 15-18
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 integrin subunit alpha X Homo sapiens 67-72
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 integrin subunit alpha L Homo sapiens 80-85
11224525-2 2001 The natural ligands for murine NKG2D are distant major histocompatibility complex homologs, retinoic acid early transcript (Rae1) and H-60 minor histocompatibility antigen. Tretinoin 92-105 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 31-36
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 syndecan 1 Homo sapiens 106-111
17561254-6 2008 Approximately half of the antigens up-regulated by ATRA on NB4 cells were adhesion molecules, including CD11a, CD11b, CD11c, CD54, CD66c and CD138, consistent with the increased adhesiveness of leukaemia cells observed for APL patients treated with ATRA. Tretinoin 51-55 integrin subunit alpha L Homo sapiens 104-109
17561254-6 2008 Approximately half of the antigens up-regulated by ATRA on NB4 cells were adhesion molecules, including CD11a, CD11b, CD11c, CD54, CD66c and CD138, consistent with the increased adhesiveness of leukaemia cells observed for APL patients treated with ATRA. Tretinoin 51-55 integrin subunit alpha X Homo sapiens 118-123
17561254-6 2008 Approximately half of the antigens up-regulated by ATRA on NB4 cells were adhesion molecules, including CD11a, CD11b, CD11c, CD54, CD66c and CD138, consistent with the increased adhesiveness of leukaemia cells observed for APL patients treated with ATRA. Tretinoin 51-55 syndecan 1 Homo sapiens 141-146
17561254-8 2008 For NB4 cells, ATRA induced some remarkable increases in CD antigens not seen for HL60: CD14 (16.6-fold), CD32 (27.8), CD53 (20.5), CD65 (139), CD66c (79.7), CD126 (15.1), and CD138 (57.6). Tretinoin 15-19 CD14 molecule Homo sapiens 88-92
11092879-7 2001 It is proposed that in an RA-induced P19 differentiation model, RA elevates Ik-1 expression, which recruits histone deacetylase to intron 1 of the KOR gene and silences KOR gene promoters. Tretinoin 26-28 interleukin 23, alpha subunit p19 Mus musculus 37-40
17561254-8 2008 For NB4 cells, ATRA induced some remarkable increases in CD antigens not seen for HL60: CD14 (16.6-fold), CD32 (27.8), CD53 (20.5), CD65 (139), CD66c (79.7), CD126 (15.1), and CD138 (57.6). Tretinoin 15-19 Fc gamma receptor IIa Homo sapiens 106-110
17561254-8 2008 For NB4 cells, ATRA induced some remarkable increases in CD antigens not seen for HL60: CD14 (16.6-fold), CD32 (27.8), CD53 (20.5), CD65 (139), CD66c (79.7), CD126 (15.1), and CD138 (57.6). Tretinoin 15-19 syndecan 1 Homo sapiens 176-181
18289471-4 2008 Expression of TrkB was induced with nM all trans-retinoid acid (ATRA). Tretinoin 64-68 neurotrophic receptor tyrosine kinase 2 Homo sapiens 14-18
11171071-1 2001 We reported previously that the expression of the gene encoding MUC5AC mucin in human airway epithelial cells is controlled by retinoic acid via the retinoic acid receptor (RAR)-alpha and that 3,3",5-tri-iodothyronine (T(3)) inhibits the expression of MUC5AC. Tretinoin 127-140 LOC100508689 Homo sapiens 71-76
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 cellular retinoic acid binding protein 1 Homo sapiens 186-193
17637747-4 2008 T-RA rapidly and potently induces expression of connective tissue growth factor (CTGF) via a conserved DR2 type response element in its proximal promoter leading to serum-free autocrine growth. Tretinoin 0-4 cellular communication network factor 2 Mus musculus 48-79
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 cellular retinoic acid binding protein 1 Homo sapiens 186-193
17637747-4 2008 T-RA rapidly and potently induces expression of connective tissue growth factor (CTGF) via a conserved DR2 type response element in its proximal promoter leading to serum-free autocrine growth. Tretinoin 0-4 cellular communication network factor 2 Mus musculus 81-85
11212249-0 2001 Increased retinoic acid responsiveness in lung carcinoma cells that are nonresponsive despite the presence of endogenous retinoic acid receptor (RAR) beta by expression of exogenous retinoid receptors retinoid X receptor alpha, RAR alpha, and RAR gamma. Tretinoin 10-23 retinoic acid receptor gamma Homo sapiens 243-252
17991421-6 2008 In addition, we revealed that co-repressor SMRT co-localized with PML-RARalpha, resulting in the immobilization of SMRT while ATRA treatment eliminated their association and reversed the immobile effect of SMRT. Tretinoin 126-130 nuclear receptor corepressor 2 Homo sapiens 43-47
11205873-14 2001 The treatment of retinoic acid induced expression of mucin and CFTR, whereas it inhibited expression of cornifin. Tretinoin 17-30 LOC100508689 Homo sapiens 53-58
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 238-242 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 52-71
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 238-242 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 73-77
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 238-242 mitogen activated protein kinase kinase 1 Rattus norvegicus 135-139
19068145-12 2008 CONCLUSIONS: Among RAR and RXR agonists, only ATRA inhibited IL-1-induced IL-6 expression in rat synovial fibroblasts by inhibiting ERK1/2 pathway and subsequent activation of AP-1 and NF-IL-6 independently of RAR. Tretinoin 46-50 mitogen activated protein kinase 3 Rattus norvegicus 132-138
19068145-12 2008 CONCLUSIONS: Among RAR and RXR agonists, only ATRA inhibited IL-1-induced IL-6 expression in rat synovial fibroblasts by inhibiting ERK1/2 pathway and subsequent activation of AP-1 and NF-IL-6 independently of RAR. Tretinoin 46-50 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 176-180
18347417-0 2008 The effectiveness of retinoic acid treatment in bladder cancer: impact on recurrence, survival and TGFalpha and VEGF as end-point biomarkers. Tretinoin 21-34 transforming growth factor alpha Homo sapiens 99-107
17727842-6 2008 ATRA treatment (10 microM) resulted in a 59.9+/-9.8% increase (p<0.05) in the BrdU labeling index in K10/FLAG-CRABPI TG(+) mice vs. TG(-) mice. Tretinoin 0-4 keratin 10 Mus musculus 104-107
17712061-4 2008 atRA (10 nM) increased ERK1/2 phosphorylation within 10 min. Tretinoin 0-4 mitogen-activated protein kinase 3 Mus musculus 23-29
17712061-11 2008 atRA specifically increased dendritic translation and surface expression of the alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate receptor (AMPAR) subunit 1 (GluR1), without affecting GluR2. Tretinoin 0-4 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 163-168
18956319-11 2008 Moreover, injection of xCyp26c mRNA into animal poles caused head defects, and exogenous expression of xCyp26c rescued the posteriorizing effect of RA treatment. Tretinoin 148-150 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 103-110
18956319-12 2008 Taken together, these results implicated a role for xCyp26c in anterior patterning via RA signaling. Tretinoin 87-89 cytochrome P450 family 26 subfamily C member 1 L homeolog Xenopus laevis 52-59
18097013-2 2008 Total CD19+ B lineage cells increased substantially in the marrow and spleens of all-trans retinoic acid (ATRA)-treated C57BL6 mice, while lymphoid progenitors were reduced. Tretinoin 91-104 CD19 antigen Mus musculus 6-10
18097013-2 2008 Total CD19+ B lineage cells increased substantially in the marrow and spleens of all-trans retinoic acid (ATRA)-treated C57BL6 mice, while lymphoid progenitors were reduced. Tretinoin 106-110 CD19 antigen Mus musculus 6-10
19012162-0 2008 Effects of retinoic acid on the expressions of Vangl1 and vangl2 in mouse fetuses. Tretinoin 11-24 VANGL planar cell polarity 1 Mus musculus 47-53
19012162-1 2008 This study reports the effects of retinoic acid on the spatiotemporal expressions of Vangl1 and Vangl2 in mouse fetuses. Tretinoin 34-47 VANGL planar cell polarity 1 Mus musculus 85-91
19012162-8 2008 In conclusion, Vangl1 and Vangl2 transcript downregulation might be implicated in the occurrence of mouse NTDs induced by retinoic acid. Tretinoin 122-135 VANGL planar cell polarity 1 Mus musculus 15-21
18773862-6 2008 Consistent with the inhibition effect and G1 arrest, ATRA and SB, alone or in combination, induced the expression of G1 phase markers cyclin-dependent kinase (CDK) 6, p21, and p27; inhibited the expression of S-G2 phase proteins CDK2; and decreased Rb phosphorylation. Tretinoin 53-57 cyclin dependent kinase 2 Homo sapiens 229-233
18773862-7 2008 Cyclin D1 expression was increased in the SB- and ATRA + SB-treated groups, but inhibited in the ATRA-treated group. Tretinoin 50-54 cyclin D1 Homo sapiens 0-9
18773862-7 2008 Cyclin D1 expression was increased in the SB- and ATRA + SB-treated groups, but inhibited in the ATRA-treated group. Tretinoin 97-101 cyclin D1 Homo sapiens 0-9
18773862-9 2008 These results indicate that the growth inhibition and G1 arrest of oral squamous carcinoma cells in response to ATRA and/or SB correlates with the induction of G1 phase cell cycle regulatory proteins CDK6, p21, and p27 and the inhibition of S-G2 phase cell cycle regulatory protein CDK2. Tretinoin 112-116 cyclin dependent kinase 2 Homo sapiens 282-286
18079182-8 2007 Upon retinoic acid-induced transcriptional activation of HoxA2 in a cell model of neuronal differentiation, PRMT6 recruitment and H3 R2 methylation are diminished and H3 K4 trimethylation increases at the gene. Tretinoin 5-18 homeobox A2 Homo sapiens 57-62
17925390-0 2007 Overproduction of bioactive retinoic acid in cells expressing disease-associated mutants of retinol dehydrogenase 12. Tretinoin 28-41 retinol dehydrogenase 12 Mus musculus 92-116
11526081-3 2001 First, we show that aldehyde dehydrogenase 6, which synthesizes the ligand, retinoic acid, is localized to the ventral epithelium of the presumptive frontonasal process of chick embryos. Tretinoin 76-89 aldehyde dehydrogenase 1 family member A3 Gallus gallus 20-44
17925390-4 2007 Here we demonstrate that, although bi-directional in vitro, in living cells, RDH12 acts exclusively as a retinaldehyde reductase, shifting the retinoid homeostasis toward the increased levels of retinol and decreased levels of bioactive retinoic acid. Tretinoin 237-250 retinol dehydrogenase 12 Mus musculus 77-82
17925390-5 2007 The retinaldehyde reductase activity of RDH12 protects the cells from retinaldehyde-induced cell death, especially at high retinaldehyde concentrations, and this protective effect correlates with the lower levels of retinoic acid in RDH12-expressing cells. Tretinoin 216-229 retinol dehydrogenase 12 Mus musculus 40-45
17925390-5 2007 The retinaldehyde reductase activity of RDH12 protects the cells from retinaldehyde-induced cell death, especially at high retinaldehyde concentrations, and this protective effect correlates with the lower levels of retinoic acid in RDH12-expressing cells. Tretinoin 216-229 retinol dehydrogenase 12 Mus musculus 233-238
11304536-1 2001 The silencing mediator for retinoic acid and thyroid hormone receptors (SMRT) mediates transcriptional repression by recruiting histone deacetylases (HDACs) to the DNA-bound nuclear receptor complex. Tretinoin 27-40 nuclear receptor corepressor 2 Homo sapiens 72-76
18075836-0 2007 Retinol and retinoic acid increase MMP-2 activity by different pathways in cultured Sertoli cells. Tretinoin 12-25 matrix metallopeptidase 2 Homo sapiens 35-40
11394872-0 2001 Photoaffinity labeling of human IRBP with all-trans-retinoic acid. Tretinoin 42-65 retinol binding protein 3 Homo sapiens 32-36
11394872-3 2001 Here we asked (i) whether each repeat of IRBP possesses the capability of photo-crosslinking all-trans-retinoic acid (RA), (ii) within Repeat 1 whether a single retinoic acid-binding domain exists, and (iii) whether protease and CNBr digestion of Repeat 1 bound RA indicate the exact location of the binding site. Tretinoin 96-116 retinol binding protein 3 Homo sapiens 41-45
11394872-3 2001 Here we asked (i) whether each repeat of IRBP possesses the capability of photo-crosslinking all-trans-retinoic acid (RA), (ii) within Repeat 1 whether a single retinoic acid-binding domain exists, and (iii) whether protease and CNBr digestion of Repeat 1 bound RA indicate the exact location of the binding site. Tretinoin 118-120 retinol binding protein 3 Homo sapiens 41-45
11394872-3 2001 Here we asked (i) whether each repeat of IRBP possesses the capability of photo-crosslinking all-trans-retinoic acid (RA), (ii) within Repeat 1 whether a single retinoic acid-binding domain exists, and (iii) whether protease and CNBr digestion of Repeat 1 bound RA indicate the exact location of the binding site. Tretinoin 103-116 retinol binding protein 3 Homo sapiens 41-45
11394872-4 2001 3H-RA cross-linked to all four repeats, consistent with the current model of multiple binding sites in IRBP. Tretinoin 3-5 retinol binding protein 3 Homo sapiens 103-107
18075836-5 2007 We found that retinol (7 microM) and retinoic acid (1 nM) induced MMP-2 activity in Sertoli cells. Tretinoin 37-50 matrix metallopeptidase 2 Homo sapiens 66-71
17910947-3 2007 Phenotype-based screening of differentiating SH-SY5Y cells following retinoic acid (RA) stimulation indicated that twinfilin-2 is a protein that is involved in neurite outgrowth, as confirmed by morphological analysis of twinfilin-2-overexpressing cells. Tretinoin 69-82 twinfilin actin binding protein 2 Homo sapiens 115-126
11432447-0 2001 Effect of retinoic acid on glucokinase activity and gene expression in neonatal and adult cultured hepatocytes. Tretinoin 10-23 glucokinase Rattus norvegicus 27-38
11432447-1 2001 It has been shown that all-trans retinoic acid induces prematurely hepatic glucokinase mRNA in ten days-old neonatal rat hepatocytes, however, this effect could be related to the capacity of the retinoid to promote a more differentiated state of the hepatocyte. Tretinoin 33-46 glucokinase Rattus norvegicus 75-86
17910947-3 2007 Phenotype-based screening of differentiating SH-SY5Y cells following retinoic acid (RA) stimulation indicated that twinfilin-2 is a protein that is involved in neurite outgrowth, as confirmed by morphological analysis of twinfilin-2-overexpressing cells. Tretinoin 84-86 twinfilin actin binding protein 2 Homo sapiens 115-126
11432447-2 2001 In this report we demonstrate that physiological concentrations of all-trans retinoic acid stimulate glucokinase activity in both mature fully differentiated hepatocytes and at the onset of the induction of the enzyme in 15 to 17 days-old neonatal hepatocytes. Tretinoin 77-90 glucokinase Rattus norvegicus 101-112
11432447-5 2001 Using the branched DNA assay, a sensitive signal amplification technique, we detected relative increases in glucokinase mRNA levels of about 70% at 3 and 24 h after the treatment with 10(-6) M all-trans retinoic acid, in both neonatal and adult hepatocytes. Tretinoin 203-216 glucokinase Rattus norvegicus 108-119
17875646-7 2007 We also demonstrated that RA-mediated displacement of the polycomb group protein SUZ12 from a RARE was inhibited in the absence of RARgamma. Tretinoin 26-28 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 81-86
11432447-6 2001 These data show that retinoic acid exerts a stimulatory effect on hepatic glucokinase independent of the hepatocyte stage of maturity and suggest a physiological role of retinoic acid on glucose metabolism. Tretinoin 21-34 glucokinase Rattus norvegicus 74-85
11432447-6 2001 These data show that retinoic acid exerts a stimulatory effect on hepatic glucokinase independent of the hepatocyte stage of maturity and suggest a physiological role of retinoic acid on glucose metabolism. Tretinoin 170-183 glucokinase Rattus norvegicus 74-85
11432447-7 2001 The action of retinoic acid on hepatic glucokinase might explain previous observations on the relationship between vitamin A status and liver glycogen synthesis. Tretinoin 14-27 glucokinase Rattus norvegicus 39-50
17875646-7 2007 We also demonstrated that RA-mediated displacement of the polycomb group protein SUZ12 from a RARE was inhibited in the absence of RARgamma. Tretinoin 26-28 retinoic acid receptor gamma Homo sapiens 131-139
17971411-8 2007 Retinoic-acid-induced differentiation resulted in more consistent patterns of replication and upregulation of Polg, Polg2 and Tfam, whereas siRNA knockdown demonstrated that steady-state expression of POLG is essential for maintaining pluripotency. Tretinoin 0-13 polymerase (DNA directed), gamma 2, accessory subunit Mus musculus 116-121
11254472-3 2001 In differentiated T37i cells, UCP1 mRNA levels increased 10- to 20-fold after retinoic acid or beta-adrenergic treatment. Tretinoin 78-91 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 30-34
11254472-5 2001 Aldosterone treatment induced a drastic decrease in isoproterenol- and retinoic acid-stimulated UCP1 mRNA levels in a time- and dose-dependent manner (IC(50) approximately 1 nM aldosterone). Tretinoin 71-84 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 96-100
17971411-8 2007 Retinoic-acid-induced differentiation resulted in more consistent patterns of replication and upregulation of Polg, Polg2 and Tfam, whereas siRNA knockdown demonstrated that steady-state expression of POLG is essential for maintaining pluripotency. Tretinoin 0-13 transcription factor A, mitochondrial Mus musculus 126-130
11230985-12 2001 Finally, protein expression and activity of the matrix metalloproteinases MMP-2 and MMP-9 were inhibited significantly by atRA. Tretinoin 122-126 matrix metallopeptidase 2 Homo sapiens 74-79
17956315-0 2007 Retinoic acid-mediated transcription and maturation of SREBP-1c regulates fatty acid synthase via cis-elements responsible for nutritional regulation. Tretinoin 0-13 sterol regulatory element binding transcription factor 1 Rattus norvegicus 55-63
17956315-0 2007 Retinoic acid-mediated transcription and maturation of SREBP-1c regulates fatty acid synthase via cis-elements responsible for nutritional regulation. Tretinoin 0-13 fatty acid synthase Rattus norvegicus 74-93
17956315-1 2007 A region of the rat FAS (fatty acid synthase) promoter has been defined as being responsible for RA (retinoic acid) responsiveness. Tretinoin 97-99 fatty acid synthase Rattus norvegicus 20-23
17956315-1 2007 A region of the rat FAS (fatty acid synthase) promoter has been defined as being responsible for RA (retinoic acid) responsiveness. Tretinoin 97-99 fatty acid synthase Rattus norvegicus 25-44
11223164-0 2001 Agonists of the retinoic acid- and retinoid X-receptors inhibit hepatocyte growth factor secretion and expression in U87 human astrocytoma cells. Tretinoin 16-29 hepatocyte growth factor Homo sapiens 64-88
17956315-1 2007 A region of the rat FAS (fatty acid synthase) promoter has been defined as being responsible for RA (retinoic acid) responsiveness. Tretinoin 101-114 fatty acid synthase Rattus norvegicus 20-23
11234892-8 2001 A 24-h exposure to ATRA increased the expression of RAR alpha, RAR beta, RAR gamma, and RXR alpha in 46%, 77%, 30%, and 38% of the samples, respectively. Tretinoin 19-23 retinoic acid receptor gamma Homo sapiens 73-82
11234892-13 2001 We conclude that RAR alpha, RAR beta, RAR gamma, and RXR alpha are expressed in non-M3 AML blast cells and that ATRA-induced expression of RAR beta may be a marker for retinoid sensitivity. Tretinoin 112-116 retinoic acid receptor gamma Homo sapiens 38-47
17656649-0 2007 Chemokine stromal cell-derived factor-1 induction by C/EBPbeta activation is associated with all-trans-retinoic acid-induced leukemic cell differentiation. Tretinoin 93-116 C-X-C motif chemokine ligand 12 Homo sapiens 10-39
11161715-4 2001 We show that RA induces the TJ structure and expression of several TJ-associated molecules, such as ZO-1, occludin, claudin-6, and claudin-7, as well as a barrier function in the genetically engineered cell line F9:rtTA:Cre-ER(T) L32T2, which allows sophisticated genetic manipulations simply by addition of ligands (H. Chiba et al., 2000, Exp. Tretinoin 13-15 claudin 6 Mus musculus 116-125
11161715-8 2001 We also compared the RA-induced expression of TJ components and barrier function in RXRalpha(-/-)-RARgamma(-/-) F9 cells with those in wild-type cells and show that the retinoid signals for transduction of these events are mediated by specific RXR-RAR pairs. Tretinoin 21-23 retinoid X receptor alpha Mus musculus 84-92
11306068-1 2001 Biochemical studies indicate that alcohol dehydrogenase (ADH) metabolizes retinol to retinal, and that aldehyde dehydrogenase (ALDH) metabolizes retinal to retinoic acid, a molecule essential for growth and development. Tretinoin 156-169 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 103-125
11306068-1 2001 Biochemical studies indicate that alcohol dehydrogenase (ADH) metabolizes retinol to retinal, and that aldehyde dehydrogenase (ALDH) metabolizes retinal to retinoic acid, a molecule essential for growth and development. Tretinoin 156-169 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 127-131
11306068-2 2001 Summarized herein are several genetic studies supporting in vivo functions for ADH and ALDH in retinoic acid synthesis. Tretinoin 95-108 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 87-91
11306068-9 2001 Injection of mRNAs for either mouse Raldh1 or Raldh2 stimulated retinoic acid synthesis in frog embryos at the blastula stage when retinoic acid is normally undetectable. Tretinoin 64-77 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 36-42
11306068-9 2001 Injection of mRNAs for either mouse Raldh1 or Raldh2 stimulated retinoic acid synthesis in frog embryos at the blastula stage when retinoic acid is normally undetectable. Tretinoin 64-77 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 46-52
11133659-3 2001 Three proteins involved in 1) serum transport of retinol (retinol binding protein [RBP]), 2) cellular transport and metabolism of retinol (cellular RBP [CRBP] I), and 3) retinoic acid (cellular retinoic acid binding protein [CRABP] I), respectively, have been located by immunohistochemistry during gestation in the porcine placenta. Tretinoin 170-183 cellular retinoic acid binding protein 1 Homo sapiens 185-223
11306068-9 2001 Injection of mRNAs for either mouse Raldh1 or Raldh2 stimulated retinoic acid synthesis in frog embryos at the blastula stage when retinoic acid is normally undetectable. Tretinoin 131-144 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 36-42
11269738-0 2001 Upregulation of gap junctional intercellular communication and connexin 43 expression by cyclic-AMP and all-trans-retinoic acid is associated with glutathione depletion and chemosensitivity in neuroblastoma cells. Tretinoin 104-127 gap junction protein alpha 1 Homo sapiens 63-74
11306068-9 2001 Injection of mRNAs for either mouse Raldh1 or Raldh2 stimulated retinoic acid synthesis in frog embryos at the blastula stage when retinoic acid is normally undetectable. Tretinoin 131-144 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 46-52
11269738-4 2001 METHODS: We examined the effect of dibutyryl-cyclic AMP (db-cAMP) and all-trans-retinoic acid (tRA) on Cx43 and GJIC, glutathione (GSH) and gamma-glutamyl-cysteine-synthetase (gamma-GCS) levels, and glutathione S-transferase (GST) activity. Tretinoin 70-93 gap junction protein alpha 1 Homo sapiens 103-107
17656649-0 2007 Chemokine stromal cell-derived factor-1 induction by C/EBPbeta activation is associated with all-trans-retinoic acid-induced leukemic cell differentiation. Tretinoin 93-116 CCAAT enhancer binding protein beta Homo sapiens 53-62
11914476-6 2001 Since retinoic acid inhibits the secretion of parathyroid hormone and CRABP I is thought to play a key role in regulating the amount of retinoic acid available to interact with specific nuclear receptors, these data may suggest impaired transport of retinoic acid to cell nuclei, thus contributing to the development of hyperparathyroidism. Tretinoin 6-19 cellular retinoic acid binding protein 1 Homo sapiens 70-77
11306068-12 2001 Overall, these studies provide genetic evidence that Adh1, Adh4, Raldh1, and Raldh2 encode retinoid dehydrogenases involved in retinoic acid synthesis in vivo. Tretinoin 127-140 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 65-71
11306068-12 2001 Overall, these studies provide genetic evidence that Adh1, Adh4, Raldh1, and Raldh2 encode retinoid dehydrogenases involved in retinoic acid synthesis in vivo. Tretinoin 127-140 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 77-83
11914476-6 2001 Since retinoic acid inhibits the secretion of parathyroid hormone and CRABP I is thought to play a key role in regulating the amount of retinoic acid available to interact with specific nuclear receptors, these data may suggest impaired transport of retinoic acid to cell nuclei, thus contributing to the development of hyperparathyroidism. Tretinoin 136-149 cellular retinoic acid binding protein 1 Homo sapiens 70-77
17656649-3 2007 Here, we suggest a novel mechanism by which all-trans-retinoic acid (ATRA) induces the expression of SDF-1 during the differentiation of promyelomonocytic leukemic U937 cells. Tretinoin 44-67 C-X-C motif chemokine ligand 12 Homo sapiens 101-106
11914476-6 2001 Since retinoic acid inhibits the secretion of parathyroid hormone and CRABP I is thought to play a key role in regulating the amount of retinoic acid available to interact with specific nuclear receptors, these data may suggest impaired transport of retinoic acid to cell nuclei, thus contributing to the development of hyperparathyroidism. Tretinoin 136-149 cellular retinoic acid binding protein 1 Homo sapiens 70-77
17656649-3 2007 Here, we suggest a novel mechanism by which all-trans-retinoic acid (ATRA) induces the expression of SDF-1 during the differentiation of promyelomonocytic leukemic U937 cells. Tretinoin 69-73 C-X-C motif chemokine ligand 12 Homo sapiens 101-106
11208727-2 2001 The decrease of RA by ethanol treatment has been proposed to be a cytochrome P450 enzyme (CYP)-dependent process. Tretinoin 16-18 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 66-88
17656649-7 2007 Indeed, silencing the expression of SDF-1 inhibits ATRA-induced granulocyte differentiation significantly. Tretinoin 51-55 C-X-C motif chemokine ligand 12 Homo sapiens 36-41
11208727-2 2001 The decrease of RA by ethanol treatment has been proposed to be a cytochrome P450 enzyme (CYP)-dependent process. Tretinoin 16-18 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 90-93
11208727-3 2001 However, the role of the major ethanol-induced CYP, CYP2E1, in the metabolism of RA has not been defined. Tretinoin 81-83 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 47-50
29350863-0 2007 Chemokine stromal cell-derived factor-1 induction by C/EBPbeta activation is associated with all-trans-retinoic acid-induced leukemic cell differentiation. Tretinoin 93-116 C-X-C motif chemokine ligand 12 Homo sapiens 10-39
11208727-8 2001 The enhancement of RA catabolism by ethanol was inhibited by both CYP2E1 antibody and specific inhibitors (allyl sulfide and chlormethiazole) in a dose-dependent fashion, whereas the metabolism of RA into polar metabolites was abolished completely by nonspecific CYP inhibitors (disulfiram and liarozole). Tretinoin 19-21 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 66-69
11306982-9 2001 ATRA may be of therapeutic benefit in allergic inflammatory disorders in which eosinophil differentiation and membrane-bound IL-5R are upregulated. Tretinoin 0-4 interleukin 5 receptor subunit alpha Homo sapiens 125-130
10995752-0 2000 Feedback inhibition of the retinaldehyde dehydrogenase gene ALDH1 by retinoic acid through retinoic acid receptor alpha and CCAAT/enhancer-binding protein beta. Tretinoin 69-82 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 60-65
11161790-5 2000 Furthermore, EVI9 was down-regulated during myeloid differentiation of HL60 cells induced by all-trans-retinoic acid, whereas the expression remained during monocytic differentiation induced by phorbol 12-myristate 13-acetate. Tretinoin 93-116 BAF chromatin remodeling complex subunit BCL11A Homo sapiens 13-17
29350863-0 2007 Chemokine stromal cell-derived factor-1 induction by C/EBPbeta activation is associated with all-trans-retinoic acid-induced leukemic cell differentiation. Tretinoin 93-116 CCAAT enhancer binding protein beta Homo sapiens 53-62
11078493-3 2000 RESULTS: Prostate tumors in mice treated with 4-HPR contained high levels of 4-HPR and of all-trans-retinoic acid (RA) and reduced levels of retinol (ROH). Tretinoin 90-113 haptoglobin-related protein Homo sapiens 48-51
11108612-8 2001 In contrast, a drastic increase of ST8SiaIV was specifically induced by RA-treatment of SH-SY5Y cells. Tretinoin 72-74 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 Homo sapiens 35-43
29350863-3 2007 Here, we suggest a novel mechanism by which all-trans-retinoic acid (ATRA) induces the expression of SDF-1 during the differentiation of promyelomonocytic leukemic U937 cells. Tretinoin 44-67 C-X-C motif chemokine ligand 12 Homo sapiens 101-106
29350863-3 2007 Here, we suggest a novel mechanism by which all-trans-retinoic acid (ATRA) induces the expression of SDF-1 during the differentiation of promyelomonocytic leukemic U937 cells. Tretinoin 69-73 C-X-C motif chemokine ligand 12 Homo sapiens 101-106
11464865-0 2001 Downregulation of hASH1 is associated with the retinoic acid-induced differentiation of human neuroblastoma cell lines. Tretinoin 47-60 achaete-scute family bHLH transcription factor 1 Homo sapiens 18-23
11060034-7 2000 Retinoic acid, but not dimethylsulfoxide, permitted activation of the mesodermal marker gene T(Bra), which was also activated when SRF was expressed in SRF(-/-) ES cells. Tretinoin 0-13 serum response factor Mus musculus 131-134
11060034-7 2000 Retinoic acid, but not dimethylsulfoxide, permitted activation of the mesodermal marker gene T(Bra), which was also activated when SRF was expressed in SRF(-/-) ES cells. Tretinoin 0-13 serum response factor Mus musculus 152-155
29350863-7 2007 Indeed, silencing the expression of SDF-1 inhibits ATRA-induced granulocyte differentiation significantly. Tretinoin 51-55 C-X-C motif chemokine ligand 12 Homo sapiens 36-41
17988991-0 2007 Successful all-trans retinoic acid treatment of acute promyelocytic leukemia in a patient with NPM/RAR fusion. Tretinoin 21-34 nucleophosmin 1 Homo sapiens 95-98
11044606-4 2000 Since this molecule showed enzymatic activity to produce RA from retinaldehyde, we designated it retinaldehyde dehydrogenase 3 (RALDH-3). Tretinoin 57-59 aldehyde dehydrogenase 1 family member A3 Gallus gallus 97-126
11044606-4 2000 Since this molecule showed enzymatic activity to produce RA from retinaldehyde, we designated it retinaldehyde dehydrogenase 3 (RALDH-3). Tretinoin 57-59 aldehyde dehydrogenase 1 family member A3 Gallus gallus 128-135
11266607-3 2001 Photoaffinity labeling of purified CRABPs with [(3)H]atRA was light- and concentration-dependent, saturable, and protected by several retinoids in a concentration-dependent manner, indicating that binding occurred in the CRABP atRA-binding site. Tretinoin 53-57 cellular retinoic acid binding protein 1 Homo sapiens 35-40
11266607-10 2001 Therefore, photoaffinity labeling with [(3)H]atRA can be used to identify new ligands for CRABP and retinoid nuclear receptors and also provide information concerning the identity of amino acid(s) localized in the atRA-binding site of these proteins. Tretinoin 45-49 cellular retinoic acid binding protein 1 Homo sapiens 90-95
17988991-2 2007 Most APL patients have a t(15;17) translocation that generates the PML-RAR fusion gene, and such patients respond well to treatment with all-trans retinoic acid (ATRA). Tretinoin 147-160 PML-RARA regulated adaptor molecule 1 Homo sapiens 67-74
17988991-2 2007 Most APL patients have a t(15;17) translocation that generates the PML-RAR fusion gene, and such patients respond well to treatment with all-trans retinoic acid (ATRA). Tretinoin 162-166 PML-RARA regulated adaptor molecule 1 Homo sapiens 67-74
10938282-11 2000 In conclusion, induction of MUC4 expression in pancreatic carcinoma by RA is mediated through the RAR-alpha signaling pathway, and TGF-beta2 may serve as an interim mediator of this regulated expression. Tretinoin 71-73 mucin 4, cell surface associated Homo sapiens 28-32
11115359-0 2000 A newly characterized human endometrial adenocarcinoma cell line (CAC-1) differentiates in response to retinoic acid treatment. Tretinoin 103-116 transmembrane protein 54 Homo sapiens 66-71
17988991-6 2007 These findings suggest that ATRA can be used to treat APL patients with NPM/RAR as well as APL with PML/RAR. Tretinoin 28-32 nucleophosmin 1 Homo sapiens 72-75
11115359-7 2000 CAC-1 cells exhibited a similar response because they also organized actin filaments and enlarged in response to retinoic acid treatment. Tretinoin 113-126 transmembrane protein 54 Homo sapiens 0-5
18779873-7 2007 However, the Ex2 IRES is only active in response to retinoic acid induced neural differentiation, a state which correlates with the synthesis of the ITAF polypyrimidine tract binding protein (PTB1). Tretinoin 52-65 polypyrimidine tract binding protein 1 Mus musculus 192-196
11115359-9 2000 A slight lag in cell growth was observed when CAC-1 cells were treated with 1 microM 13-cis or all-trans retinoic acid during a 12-day growth curve. Tretinoin 105-118 transmembrane protein 54 Homo sapiens 46-51
11115359-12 2000 In contrast, MARCKS increased in the membrane in response to retinoic acid treatment. Tretinoin 61-74 myristoylated alanine rich protein kinase C substrate Homo sapiens 13-19
11027136-0 2000 Direct photoaffinity labeling of cellular retinoic acid-binding protein I (CRABP-I) with all-trans-retinoic acid: identification of amino acids in the ligand binding site. Tretinoin 92-112 cellular retinoic acid binding protein 1 Homo sapiens 33-73
17663992-0 2007 Retinoid regulated association of transcriptional co-regulators and the polycomb group protein SUZ12 with the retinoic acid response elements of Hoxa1, RARbeta(2), and Cyp26A1 in F9 embryonal carcinoma cells. Tretinoin 110-123 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 95-100
11027136-0 2000 Direct photoaffinity labeling of cellular retinoic acid-binding protein I (CRABP-I) with all-trans-retinoic acid: identification of amino acids in the ligand binding site. Tretinoin 92-112 cellular retinoic acid binding protein 1 Homo sapiens 75-82
11027136-1 2000 Cellular retinoic acid-binding proteins I and II (CRABP-I and -II, respectively) are transport proteins for all-trans-retinoic acid (RA), an active metabolite of vitamin A (retinol), and have been reported to be directly involved in the metabolism of RA. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 50-65
11027136-1 2000 Cellular retinoic acid-binding proteins I and II (CRABP-I and -II, respectively) are transport proteins for all-trans-retinoic acid (RA), an active metabolite of vitamin A (retinol), and have been reported to be directly involved in the metabolism of RA. Tretinoin 112-131 cellular retinoic acid binding protein 1 Homo sapiens 50-65
11027641-2 2000 Two isomers of RA, 9-cis- and all-trans-RA, suppressed markedly the effect of PB on CYP2B1/2 expression, while ASE had no suppressive effect. Tretinoin 40-42 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 84-90
11161966-1 2000 Previous work has shown that neuroblastoma cells secrete IGFBP-2, -4 and -6 and that expression of these proteins is regulated by retinoic acid (at-RA) which promotes differentiation in these cells. Tretinoin 130-143 insulin like growth factor binding protein 2 Homo sapiens 57-75
11108736-8 2000 LRAT mRNA was rapidly induced by retinoic acid (RA) in liver of vitamin A-deficient mice and rats (P < 0.01). Tretinoin 33-46 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 0-4
17663992-0 2007 Retinoid regulated association of transcriptional co-regulators and the polycomb group protein SUZ12 with the retinoic acid response elements of Hoxa1, RARbeta(2), and Cyp26A1 in F9 embryonal carcinoma cells. Tretinoin 110-123 homeobox A1 Homo sapiens 145-150
10979975-6 2000 These findings suggested that the prevention of RARalpha protein loss by G-CSF or LiCl in ATRA-treated cells functioned to extend the differentiation response to the retinoid and was responsible, at least in part, for the observed synergism. Tretinoin 90-94 colony stimulating factor 3 (granulocyte) Mus musculus 73-78
11115082-2 2000 We therefore studied the relationship between the response of patients with IgA nephritis (IgAN) to ACEI/ATRA therapy by decreasing proteinuria and its effect on the selectivity index (SI) in these patients. Tretinoin 105-109 IGAN1 Homo sapiens 91-95
17663992-7 2007 Conversely, SUZ12 was found associated with all RAREs studied and these associations were attenuated by treatment with RA. Tretinoin 48-50 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 12-17
11115082-22 2000 CONCLUSION: Our data suggest that ACEI/ATRA therapy may be beneficial in patients with IgAN with renal impairment and nonselective proteinuria, as such patients may respond to therapy with improvement in protein selectivity, decrease in proteinuria, and improvement in renal function. Tretinoin 39-43 IGAN1 Homo sapiens 87-91
17663992-8 2007 Upon RA removal, SUZ12 re-associated with RAREs. Tretinoin 5-7 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 17-22
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 forkhead box P3 Homo sapiens 176-199
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 forkhead box P3 Homo sapiens 201-206
11150643-0 2000 Retinoic acid down-regulates VPAC(1) receptors and TGF-beta 3 but up-regulates TGF-beta 2 in lung cancer cells. Tretinoin 0-13 transforming growth factor beta 3 Homo sapiens 51-61
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 forkhead box P3 Homo sapiens 176-199
11150643-9 2000 These results suggest that RA may inhibit lung cancer growth by down-regulating VPAC(1) receptor and TGF-beta 3 mRNA but up-regulating TGF-beta 2 mRNA. Tretinoin 27-29 transforming growth factor beta 3 Homo sapiens 101-111
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 forkhead box P3 Homo sapiens 201-206
10938282-0 2000 Retinoic acid-dependent transforming growth factor-beta 2-mediated induction of MUC4 mucin expression in human pancreatic tumor cells follows retinoic acid receptor-alpha signaling pathway. Tretinoin 0-13 mucin 4, cell surface associated Homo sapiens 80-84
17525233-6 2007 In contrast, direct RA-responsive genes that are rapidly induced, such as Hoxa1, showed a loss of EZH2 binding and K27me3 after only a few hours of RA treatment. Tretinoin 20-22 homeobox A1 Mus musculus 74-79
10938282-0 2000 Retinoic acid-dependent transforming growth factor-beta 2-mediated induction of MUC4 mucin expression in human pancreatic tumor cells follows retinoic acid receptor-alpha signaling pathway. Tretinoin 0-13 LOC100508689 Homo sapiens 85-90
10938282-6 2000 Among several serum constituents, all-trans-retinoic acid (RA) induced the expression of MUC4 transcripts in a concentration- and time-dependent manner. Tretinoin 34-57 mucin 4, cell surface associated Homo sapiens 89-93
10938282-6 2000 Among several serum constituents, all-trans-retinoic acid (RA) induced the expression of MUC4 transcripts in a concentration- and time-dependent manner. Tretinoin 59-61 mucin 4, cell surface associated Homo sapiens 89-93
10938282-8 2000 The antagonist of the retinoic acid receptor (RAR)-alpha (Ro41-5253) abrogated the expression of MUC4 and TGF-beta2 induced by RA. Tretinoin 46-48 mucin 4, cell surface associated Homo sapiens 97-101
10944482-0 2000 Retinoic acid and polyriboinosinic acid act synergistically to enhance the antibody response to tetanus toxoid during vitamin A deficiency: possible involvement of interleukin-2 receptor-beta, signal transducer and activator of transcription-1, and interferon regulatory factor-1. Tretinoin 0-13 interferon regulatory factor 1 Rattus norvegicus 249-279
10978779-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human chronic myelogenous leukemia K562 cells. Tretinoin 31-44 neurotrophic receptor tyrosine kinase 1 Homo sapiens 76-80
10978779-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human chronic myelogenous leukemia K562 cells. Tretinoin 46-48 neurotrophic receptor tyrosine kinase 1 Homo sapiens 76-80
10953040-2 2000 In HTBE cells, retinoic acid (RA) inhibits squamous differentiation and induces mucous cell differentiation as indicated by the suppression of transglutaminase I and increased expression of the mucin gene MUC2. Tretinoin 15-28 LOC100508689 Homo sapiens 194-199
10953040-2 2000 In HTBE cells, retinoic acid (RA) inhibits squamous differentiation and induces mucous cell differentiation as indicated by the suppression of transglutaminase I and increased expression of the mucin gene MUC2. Tretinoin 30-32 LOC100508689 Homo sapiens 194-199
11042692-3 2000 In combination treatment RA potentiates IFN-beta effect in SCC ME-180 but not in SiHa cell line, partially resistant to RA antiproliferative action. Tretinoin 25-27 interferon beta 1 Homo sapiens 40-48
10933889-4 2000 Here we have examined the role of the hydroxyl group of RARgamma Ser(289) and its homologous amino acid residues in RARalpha (Ser(287)) and RARbeta (Ser(280)) alone and in conjunction with their respective RARgamma Arg(278) homologs for RA binding and RA-dependent transactivation activity. Tretinoin 116-118 retinoic acid receptor gamma Homo sapiens 56-64
11027641-0 2000 Suppression of the expression of the CYP2B1/2 gene by retinoic acids. Tretinoin 54-68 cytochrome P450, family 2, subfamily b, polypeptide 12 Rattus norvegicus 37-45
11027641-1 2000 The effects of 5alpha-androsten-3alpha-ol (ASE), and retinoic acids (RAs) and their precursors on the phenobarbital (PB)-mediated induction of CYP2B1 and 2B2 were examined in cultured rat hepatocytes. Tretinoin 69-72 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 143-157
11027641-2 2000 Two isomers of RA, 9-cis- and all-trans-RA, suppressed markedly the effect of PB on CYP2B1/2 expression, while ASE had no suppressive effect. Tretinoin 15-17 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 84-90
17525233-6 2007 In contrast, direct RA-responsive genes that are rapidly induced, such as Hoxa1, showed a loss of EZH2 binding and K27me3 after only a few hours of RA treatment. Tretinoin 148-150 homeobox A1 Mus musculus 74-79
10862743-6 2000 We show that this phenotype likely results from RA interfering with the establishment of a distal signaling center, altering levels and distribution of Fgf10 and Bmp4, genes that are essential for distal lung formation. Tretinoin 48-50 bone morphogenetic protein 4 Homo sapiens 162-166
10861789-6 2000 In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Tretinoin 13-15 nerve growth factor Rattus norvegicus 38-41
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 40-53 nuclear receptor coactivator 2 Homo sapiens 25-29
10861789-6 2000 In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Tretinoin 116-118 nerve growth factor Rattus norvegicus 38-41
10861789-6 2000 In addition, RA-enhanced 2.6-fold the NGF secretion from cultured rat cortical astrocytes and conditioned medium of RA-treated astrocytes reduced the percentage of apoptotic chick neurons after a 24 hr-incubation with staurosporine in the same manner as the external addition of RA and NGF. Tretinoin 116-118 nerve growth factor Rattus norvegicus 38-41
11010814-4 2000 The exogenous expression of dominant-negative MEK1 efficiently abrogated RA-mediated induction of the cytokeratins EndoA and EndoC in the F9 cells. Tretinoin 73-75 mitogen-activated protein kinase kinase 1 Mus musculus 46-50
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 40-53 CCAAT enhancer binding protein beta Homo sapiens 90-99
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 55-57 nuclear receptor coactivator 2 Homo sapiens 25-29
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 55-57 CCAAT enhancer binding protein beta Homo sapiens 90-99
11054542-19 2000 Retinoic acid compounds and the phorbol ester, PMA were found to stimulate BMP-2 and, to a lesser degree, BMP-4. Tretinoin 0-13 bone morphogenetic protein 2 Homo sapiens 75-80
11054542-19 2000 Retinoic acid compounds and the phorbol ester, PMA were found to stimulate BMP-2 and, to a lesser degree, BMP-4. Tretinoin 0-13 bone morphogenetic protein 4 Homo sapiens 106-111
10894171-0 2000 Retinoic acid early inducible genes define a ligand family for the activating NKG2D receptor in mice. Tretinoin 0-13 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 78-83
17634193-0 2007 Inhibition of Tgf beta signaling by endogenous retinoic acid is essential for primary lung bud induction. Tretinoin 47-60 transforming growth factor, beta 1 Mus musculus 14-22
10894171-3 2000 Expression of the NKG2D ligands is low or absent on normal, adult tissues; however, they are constitutively expressed on some tumors and upregulated by retinoic acid. Tretinoin 152-165 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 18-23
10929206-1 2000 Exposure of aggregated murine P19 embryonal carcinoma cells to dimethylsulfoxide (DMSO) induces mesoderm and both embryonic cardiac and skeletal muscle differentiation, while retinoic acid (RA) is an inducer of neuroectodermal differentiation. Tretinoin 175-188 interleukin 23, alpha subunit p19 Mus musculus 30-33
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 12-25 LOC100508689 Homo sapiens 67-72
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 12-25 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 140-146
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 27-29 LOC100508689 Homo sapiens 67-72
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 27-29 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 140-146
10929206-1 2000 Exposure of aggregated murine P19 embryonal carcinoma cells to dimethylsulfoxide (DMSO) induces mesoderm and both embryonic cardiac and skeletal muscle differentiation, while retinoic acid (RA) is an inducer of neuroectodermal differentiation. Tretinoin 190-192 interleukin 23, alpha subunit p19 Mus musculus 30-33
10929206-2 2000 P19 cells constitutively express the retinoic acid receptor alpha (RAR alpha) and RAR gamma mRNAs while RAR beta expression is induced by RA through a consensus RA-response element in the RAR beta promoter. Tretinoin 67-69 interleukin 23, alpha subunit p19 Mus musculus 0-3
10929206-2 2000 P19 cells constitutively express the retinoic acid receptor alpha (RAR alpha) and RAR gamma mRNAs while RAR beta expression is induced by RA through a consensus RA-response element in the RAR beta promoter. Tretinoin 82-84 interleukin 23, alpha subunit p19 Mus musculus 0-3
17634193-6 2007 RA rescue of the lung phenotype was associated with low levels of Smad2 phosphorylation and downregulation of Tgfbeta targets in Raldh2-null foreguts. Tretinoin 0-2 transforming growth factor, beta 1 Mus musculus 110-117
10929206-3 2000 In the present study we show that the RAR beta transcript is strongly expressed in both P19 cells and in a RA-nonresponsive derivative of P19 cells, called RAC65, during DMSO-induced mesoderm and muscle differentiation. Tretinoin 38-40 interleukin 23, alpha subunit p19 Mus musculus 88-91
10929206-3 2000 In the present study we show that the RAR beta transcript is strongly expressed in both P19 cells and in a RA-nonresponsive derivative of P19 cells, called RAC65, during DMSO-induced mesoderm and muscle differentiation. Tretinoin 38-40 interleukin 23, alpha subunit p19 Mus musculus 138-141
11000524-4 2000 We also found that retinoic acid regulates the matrix metalloproteinase 2 activity and invasion. Tretinoin 19-32 matrix metallopeptidase 2 Homo sapiens 47-73
11030153-8 2000 We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Tretinoin 98-102 cyclin dependent kinase 4 Homo sapiens 54-58
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 0-2 interleukin 23, alpha subunit p19 Mus musculus 16-19
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 85-93
17634193-6 2007 RA rescue of the lung phenotype was associated with low levels of Smad2 phosphorylation and downregulation of Tgfbeta targets in Raldh2-null foreguts. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 129-135
11030619-3 2000 Unexpectedly, N-CoR and a specific deacetylase were also required for transcriptional activation of one class of retinoic acid response element. Tretinoin 113-126 nuclear receptor co-repressor 1 Mus musculus 14-19
17634193-9 2007 Our data support a novel mechanism of RA-Tgfbeta-Fgf10 interactions in the developing foregut, in which endogenous RA controls Tgfbeta activity in the prospective lung field to allow local expression of Fgf10 and induction of lung buds. Tretinoin 38-40 transforming growth factor, beta 1 Mus musculus 41-48
17634193-9 2007 Our data support a novel mechanism of RA-Tgfbeta-Fgf10 interactions in the developing foregut, in which endogenous RA controls Tgfbeta activity in the prospective lung field to allow local expression of Fgf10 and induction of lung buds. Tretinoin 38-40 transforming growth factor, beta 1 Mus musculus 127-134
17538947-5 2007 This result has pointed the way toward the detailed study of Raf/Mek/Erk pathway signaling in skin cancer development and its potential as a target pathway for chemoprevention by ATRA and other chemopreventive drugs. Tretinoin 179-183 midkine Mus musculus 65-68
10974645-0 2000 Opposite effects of feeding a vitamin A-deficient diet and retinoic acid treatment on brown adipose tissue uncoupling protein 1 (UCP1), UCP2 and leptin expression. Tretinoin 59-72 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 107-127
10974645-0 2000 Opposite effects of feeding a vitamin A-deficient diet and retinoic acid treatment on brown adipose tissue uncoupling protein 1 (UCP1), UCP2 and leptin expression. Tretinoin 59-72 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 129-133
10737769-3 2000 Here, we report that Stra13 expression is closely associated with cell growth arrest induced by several triggers such as retinoic acid and trichostatin A (TSA; a specific histone deacetylase inhibitor) as well as by serum starvation. Tretinoin 121-134 centromere protein X Mus musculus 21-27
17420285-8 2007 UBE2D3 is physically associated with cyclin D1 and mediates ATRA-induced cyclin D1 degradation. Tretinoin 60-64 cyclin D1 Homo sapiens 37-46
10773887-0 2000 The Ets1 proto-oncogene is upregulated by retinoic acid: characterization of a functional retinoic acid response element in the Ets1 promoter. Tretinoin 42-55 E26 avian leukemia oncogene 1, 5' domain Mus musculus 4-8
10773887-0 2000 The Ets1 proto-oncogene is upregulated by retinoic acid: characterization of a functional retinoic acid response element in the Ets1 promoter. Tretinoin 90-103 E26 avian leukemia oncogene 1, 5' domain Mus musculus 4-8
10942599-1 2000 The homeobox gene Hoxa-1 is transcriptionally regulated by retinoic acid (RA) and encodes a transcription factor which has been shown to play important roles in cell differentiation and embryogenesis. Tretinoin 59-72 homeobox A1 Homo sapiens 18-24
10942599-1 2000 The homeobox gene Hoxa-1 is transcriptionally regulated by retinoic acid (RA) and encodes a transcription factor which has been shown to play important roles in cell differentiation and embryogenesis. Tretinoin 74-76 homeobox A1 Homo sapiens 18-24
10773887-0 2000 The Ets1 proto-oncogene is upregulated by retinoic acid: characterization of a functional retinoic acid response element in the Ets1 promoter. Tretinoin 90-103 E26 avian leukemia oncogene 1, 5' domain Mus musculus 128-132
17420285-8 2007 UBE2D3 is physically associated with cyclin D1 and mediates ATRA-induced cyclin D1 degradation. Tretinoin 60-64 cyclin D1 Homo sapiens 73-82
10773887-5 2000 Here, we demonstrate that RA treatment increases the expression of Ets1 mRNA, but not that of Ets2, Elk1 or Fli1 in MC3T3-E1 cells. Tretinoin 26-28 E26 avian leukemia oncogene 1, 5' domain Mus musculus 67-71
17420285-9 2007 Knocking down UBE2D3 by RNA interference (RNAi) leads to blockage of ATRA-induced cyclin D1 degradation and cell-cycle arrest. Tretinoin 69-73 cyclin D1 Homo sapiens 82-91
19262136-4 2007 A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation. Tretinoin 24-37 forkhead box P3 Homo sapiens 185-190
10773887-9 2000 Furthermore, RA induces transcription of Ets1 promoter-reporter constructs containing this RARE half site. Tretinoin 13-15 E26 avian leukemia oncogene 1, 5' domain Mus musculus 41-45
10926763-4 2000 In this paper, we show that in the absence of M33, the window of Hoxd4 retinoic acid (RA) responsiveness is opened earlier and that Hoxd11 gene expression is activated earlier in development This indicates that M33 antagonizes the RA pathway and has a function in the establishment of the early temporal sequence of activation of Hox genes. Tretinoin 231-233 homeobox D11 Mus musculus 132-138
10933889-0 2000 Role of Ser(289) in RARgamma and its homologous amino acid residue of RARalpha and RARbeta in the binding of retinoic acid. Tretinoin 109-122 retinoic acid receptor gamma Homo sapiens 20-28
10933889-3 2000 We have previously demonstrated the importance for RA binding and RA-dependent transactivation of Arg(276) in RARalpha and Arg(278) in RARgamma; however, in RARbeta Arg(269) functions in conjunction with Lys(220). Tretinoin 66-68 retinoic acid receptor gamma Homo sapiens 135-143
10733907-4 2000 Cellular caspase 3 activity, another marker of apoptosis, was increased by RA (10 microM) (P < 0.05), but not by 50 microm C2-ceramide. Tretinoin 75-77 caspase 3 Rattus norvegicus 9-18
19262136-4 2007 A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation. Tretinoin 39-41 forkhead box P3 Homo sapiens 185-190
10733907-6 2000 These results suggest that fat cell loss by apoptosis can be regulated, in part, by RA (10 microM) which increases caspase 3 activity and decreases Bcl-2 expression in rat S-V cells. Tretinoin 84-86 caspase 3 Rattus norvegicus 115-124
17522161-12 2007 Thus, excess RA expands otic competence, whereas the loss of RA impairs the expression of fgf3 and wnt8b in the hindbrain, compromising the induction and maintenance of otic fate. Tretinoin 61-63 fibroblast growth factor 3 Danio rerio 90-94
10910773-2 2000 Knock out of all RARgamma isoforms (RARgamma(-/-) line) drastically impairs primitive and subsequent parietal endodermal differentiation and affects the induction of many endogenous RA-responsive genes. Tretinoin 17-19 retinoic acid receptor gamma Homo sapiens 36-44
10725232-7 2000 Alterations in the endodermal expression pattern of Hoxa1, Hoxb1, Pax1, Pax9, Fgf3 and Fgf8 in response to the antagonist-induced block in RA signal transduction demonstrate for the first time that RA signaling is indispensable for the specification of the pharyngeal endoderm and suggest that this signaling is necessary to provide a permissive environment locally for the migration of NCC and mesodermal cells. Tretinoin 139-141 homeobox A1 Homo sapiens 52-57
10725232-7 2000 Alterations in the endodermal expression pattern of Hoxa1, Hoxb1, Pax1, Pax9, Fgf3 and Fgf8 in response to the antagonist-induced block in RA signal transduction demonstrate for the first time that RA signaling is indispensable for the specification of the pharyngeal endoderm and suggest that this signaling is necessary to provide a permissive environment locally for the migration of NCC and mesodermal cells. Tretinoin 139-141 paired box 1 Homo sapiens 66-70
10725232-7 2000 Alterations in the endodermal expression pattern of Hoxa1, Hoxb1, Pax1, Pax9, Fgf3 and Fgf8 in response to the antagonist-induced block in RA signal transduction demonstrate for the first time that RA signaling is indispensable for the specification of the pharyngeal endoderm and suggest that this signaling is necessary to provide a permissive environment locally for the migration of NCC and mesodermal cells. Tretinoin 139-141 paired box 9 Homo sapiens 72-76
10725232-7 2000 Alterations in the endodermal expression pattern of Hoxa1, Hoxb1, Pax1, Pax9, Fgf3 and Fgf8 in response to the antagonist-induced block in RA signal transduction demonstrate for the first time that RA signaling is indispensable for the specification of the pharyngeal endoderm and suggest that this signaling is necessary to provide a permissive environment locally for the migration of NCC and mesodermal cells. Tretinoin 139-141 fibroblast growth factor 3 Homo sapiens 78-82
10953340-4 2000 To address the above issues, three dosages (5, 8 and 10 mumol/L) of RA were used to treat Med-3 cells and their effects on the target cells were evaluated by multiple approaches. Tretinoin 68-70 mediator complex subunit 27 Homo sapiens 90-95
17718197-4 2007 Furthermore, using semi-quantitative and real-time quantitative RT-PCR as well as western blot methods, high expression of insulin-like growth factor binding protein-2 (IGFBP-2) in A549 cells treated with CSE was found at both transcriptional and protein levels, and concomitant with the restoration of cell growth after treatment with tretinoin or NAC, down regulation of IGFBP-2 was observed. Tretinoin 336-345 insulin like growth factor binding protein 2 Homo sapiens 123-167
10807954-0 2000 Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis. Tretinoin 101-114 nuclear receptor subfamily 2, group C, member 1 Mus musculus 54-60
17475621-8 2007 Furthermore, treatment of NB4 cells with all-trans-retinoic acid, which promotes PML-RARalpha degradation, resulted in increased activation of GILZ. Tretinoin 41-64 TSC22 domain family member 3 Homo sapiens 143-147
10807954-0 2000 Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis. Tretinoin 101-114 interleukin 23, alpha subunit p19 Mus musculus 123-126
10807954-7 2000 In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. Tretinoin 104-106 interleukin 23, alpha subunit p19 Mus musculus 3-6
10807954-7 2000 In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. Tretinoin 104-106 nuclear receptor subfamily 2, group C, member 1 Mus musculus 34-40
10807954-8 2000 The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. Tretinoin 28-30 nuclear receptor subfamily 2, group C, member 1 Mus musculus 18-24
10807954-8 2000 The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. Tretinoin 28-30 nuclear receptor subfamily 2, group C, member 1 Mus musculus 18-21
10798446-7 2000 The expression of ZAN75 was transiently increased at both the mRNA and the protein levels when P19 cells were treated with retinoic acid to induce neuronal differentiation. Tretinoin 123-136 interleukin 23, alpha subunit p19 Mus musculus 95-98
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 colony stimulating factor 1 receptor Homo sapiens 144-148
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 colony stimulating factor 1 receptor Homo sapiens 144-148
10852350-13 2000 Ectopic expression of cFMS and differential sensitivity to ERK2 inhibition thus reveal that retinoic acid-induced HL-60 cell differentiation and G1/0 arrest are differentially dependent on ERK2 and can be uncoupled. Tretinoin 92-105 colony stimulating factor 1 receptor Homo sapiens 22-26
10852350-14 2000 A significant unanticipated finding was that retinoic acid caused a MEK-dependent increase in the amount of phosphorylated RAF. Tretinoin 45-58 zinc fingers and homeoboxes 2 Homo sapiens 123-126
17521827-0 2007 Retinoic acids acting through retinoid receptors protect hippocampal neurons from oxygen-glucose deprivation-mediated cell death by inhibition of c-jun-N-terminal kinase and p38 mitogen-activated protein kinase. Tretinoin 0-14 mitogen activated protein kinase 14 Rattus norvegicus 174-177
10983416-7 2000 Level of keratin-1 (K1) mRNA was increased by 11-cis-retinoic acid and 13-cis-retinoic acid, but suppressed by 9,13-di-cis-retinoic acids while all-trans-retinoic acid and 9-cis-retinoic acid had no effect. Tretinoin 148-167 keratin 1 Homo sapiens 9-18
10983416-7 2000 Level of keratin-1 (K1) mRNA was increased by 11-cis-retinoic acid and 13-cis-retinoic acid, but suppressed by 9,13-di-cis-retinoic acids while all-trans-retinoic acid and 9-cis-retinoic acid had no effect. Tretinoin 148-167 keratin 1 Homo sapiens 20-22
17679169-9 2007 ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both the cell lines. Tretinoin 0-4 thyroglobulin Homo sapiens 95-97
10772242-8 2000 HAS2 and HAS3 mRNAs were also expressed by bovine chondrocytes isolated from either the superficial or deep zone of articular cartilage, and by human chondrocytes cultured either in the absence or presence of IL-1 and retinoic acid. Tretinoin 218-231 hyaluronan synthase 3 Bos taurus 9-13
17451432-8 2007 Treatment of cells with the RARalpha/RXRalpha ligands, all-trans retinoic acid and 9-cis-retinoic acid, reduced and increased GnRH II gene expression in TE671 and JEG-3 cells, respectively. Tretinoin 65-78 gonadotropin releasing hormone 2 Homo sapiens 126-133
10684855-7 2000 Upon retinoic acid treatment, which induces disease remission in APL, Daxx relocalizes to the PML NBs. Tretinoin 5-18 death domain associated protein Homo sapiens 70-74
17451684-8 2007 Following RA induction, quantitative RT-PCR analysis demonstrated downregulation of nestin, PAX-6, thy1.1, and PKCalpha, and upregulation of rhodopsin, glial fibrillary acidic protein (GFAP), and CrX. Tretinoin 10-12 nestin Rattus norvegicus 84-90
17451684-8 2007 Following RA induction, quantitative RT-PCR analysis demonstrated downregulation of nestin, PAX-6, thy1.1, and PKCalpha, and upregulation of rhodopsin, glial fibrillary acidic protein (GFAP), and CrX. Tretinoin 10-12 paired box 6 Rattus norvegicus 92-97
10664247-0 2000 Effects of all-trans retinoic acid and epidermal growth factor on the expression of nm23-H1 in human hepatocarcinoma cells. Tretinoin 21-34 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 84-91
10664247-1 2000 The effects of all-trans retinoic acid (ATRA) and epidermal growth factor (EGF) on the expression of nm23-H1, a metastasis suppressor gene, were studied in a human 7721 hepatocarcinoma cell line. Tretinoin 15-38 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 101-108
10664247-1 2000 The effects of all-trans retinoic acid (ATRA) and epidermal growth factor (EGF) on the expression of nm23-H1, a metastasis suppressor gene, were studied in a human 7721 hepatocarcinoma cell line. Tretinoin 40-44 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 101-108
10664247-7 2000 These results reveal that the metastasis-preventing effect of ATRA may partly result from the up-regulation of nm23-H1, and the metastasis-promoting effects of EGF and c-erbB-2/neu were probably mediated in part by the down-regulation of nm23-H1. Tretinoin 62-66 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 111-118
17325034-3 2007 CSK overexpression inhibited RA-mediated neurite outgrowth, a result which correlated with the inhibition of the SFK c-SRC. Tretinoin 29-31 C-terminal Src kinase Homo sapiens 0-3
17325034-11 2007 We have elucidated a nongenomic extranuclear signal mediated by the RAR-SRC interaction that is negatively regulated by CSK and is required for RA-induced neuronal differentiation. Tretinoin 68-70 C-terminal Src kinase Homo sapiens 120-123
17244680-2 2007 Here, we show that AML1/ETO, the most common translocation fusion product in acute myeloid leukemia (AML), counteracts the activity of retinoic acid (RA), a transcriptional regulator of myelopoiesis. Tretinoin 135-148 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 24-27
10617585-3 2000 Previous studies supported the role of retinoic acids (RA) and their receptors (RARs) in SP-B gene transcription. Tretinoin 55-57 surfactant protein B Homo sapiens 89-93
10617585-8 2000 Importantly, RA stimulation of the hSP-B promoter depends on tissue-specific thyroid transcription factor (TTF-1) DNA-binding sites. Tretinoin 13-15 surfactant protein B Homo sapiens 35-40
17244680-2 2007 Here, we show that AML1/ETO, the most common translocation fusion product in acute myeloid leukemia (AML), counteracts the activity of retinoic acid (RA), a transcriptional regulator of myelopoiesis. Tretinoin 150-152 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 24-27
10617585-8 2000 Importantly, RA stimulation of the hSP-B promoter depends on tissue-specific thyroid transcription factor (TTF-1) DNA-binding sites. Tretinoin 13-15 transcription termination factor 1 Homo sapiens 107-112
17244680-5 2007 The link among AML1/ETO, heterochromatic RARbeta2 repression, RA resistance, and myeloid differentiation block is indicated by the ability of either siRNA-AML1/ETO or the DNA methylation inhibitor 5-azacytidine to revert these epigenetic alterations and to restore RA differentiation response in AML1/ETO blasts. Tretinoin 62-64 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 160-163
10642314-3 2000 Because the renin-angiotensin system is one of the crucial components of atherosclerosis, we examined the effects of atRA on the expression of angiotensin II type 1 receptor (AT(1)-R) in vascular smooth muscle cells. Tretinoin 117-121 angiotensin II receptor, type 1a Rattus norvegicus 143-182
17244680-5 2007 The link among AML1/ETO, heterochromatic RARbeta2 repression, RA resistance, and myeloid differentiation block is indicated by the ability of either siRNA-AML1/ETO or the DNA methylation inhibitor 5-azacytidine to revert these epigenetic alterations and to restore RA differentiation response in AML1/ETO blasts. Tretinoin 62-64 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 160-163
10649440-9 2000 The dephosphorylating properties of ecto-ALP are induced by RA, suggesting a specific function in differentiating P19 teratocarcinoma and HL-60 myeloblastic leukemia cells. Tretinoin 60-62 tripartite motif containing 33 Homo sapiens 36-40
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 16-29 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 138-142
10714240-2 2000 The biological action of retinoic acid and synthetic analogs, referred to as retinoids, is mediated by RAR alpha, RAR beta, or RAR gamma and/or by RXR alpha, RXR beta, or RXR gamma, all being nuclear receptors. Tretinoin 25-38 retinoic acid receptor gamma Homo sapiens 127-136
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 31-33 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 138-142
10714240-2 2000 The biological action of retinoic acid and synthetic analogs, referred to as retinoids, is mediated by RAR alpha, RAR beta, or RAR gamma and/or by RXR alpha, RXR beta, or RXR gamma, all being nuclear receptors. Tretinoin 25-38 retinoid X receptor beta Homo sapiens 158-166
17463084-3 2007 The present work reports that TLR3 signaling by polyinosinic-polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8alphaalpha intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. Tretinoin 146-159 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 192-197
17463084-3 2007 The present work reports that TLR3 signaling by polyinosinic-polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8alphaalpha intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. Tretinoin 146-159 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 213-218
10585260-3 1999 Cyclin D1 and D3 mRNA levels decreased during complete differentiation induced by all-trans-retinoic acid and dibutyryl cAMP, while the levels of cyclin D2 and the cyclin-dependent kinase (Cdk) inhibitor p27 mRNAs increased. Tretinoin 82-105 cyclin D1 Homo sapiens 0-9
17317001-4 2007 Retinoic acid induced marked increase in p47phox expression and in catalytic activity of PKC delta: the upregulation of a pathway involving NADPH oxidase and PKC delta is likely to be responsible for neuronal susceptibility to AGE. Tretinoin 0-13 protein kinase C delta Homo sapiens 89-98
10570055-1 1999 N-(4-Hydroxyphenyl)retinamide (4-HPR), a retinoic acid analog, induces apoptosis in several cell types. Tretinoin 41-54 haptoglobin-related protein Homo sapiens 33-36
17317001-4 2007 Retinoic acid induced marked increase in p47phox expression and in catalytic activity of PKC delta: the upregulation of a pathway involving NADPH oxidase and PKC delta is likely to be responsible for neuronal susceptibility to AGE. Tretinoin 0-13 protein kinase C delta Homo sapiens 158-167
17600477-9 2007 ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both cell lines. Tretinoin 0-4 thyroglobulin Homo sapiens 95-97
10605367-4 1999 OCT, calcitriol and ATRA significantly increased the: ALP activity from 1.58 +/- 0.14 mumol/min/mg protein (mean +/- SD; control) to 2.50 +/- 0.09 (P < 0.0001), 2.30 +/- 0.14 (P < 0.0001) and 2.00 +/- 0.14 (P = 0.0008), respectively; GLA-OC production from 0.71 +/- 0.01 ng/ml (control) to 2.87 +/- 0.01 (P < 0.0001), 2.87 +/- 0.11 (P < 0.0001) and 1.36 +/- 0.06 (P < 0.0001), respectively; and PIP production from 433.91 +/- 23.29 ng/ml (control) to 536.54 +/- 15.46 (P = 0.0002), 497.06 +/- 1.99 (P = 0.0028) and 481.66 +/- 0.01 (P = 0.0104), respectively. Tretinoin 20-24 alkaline phosphatase, biomineralization associated Canis lupus familiaris 54-57
10508860-8 1999 PS1 suppressed c-jun-associated apoptosis by retinoic acid in F9 embryonic carcinoma cells, whereas this suppression of apoptosis is attenuated by mutation in PS1. Tretinoin 45-58 presenilin 1 Homo sapiens 0-3
17207476-1 2007 Retinoic acid (RA) synthesized by Raldh3 in the frontonasal surface ectoderm of chick embryos has been suggested to function in early forebrain patterning by regulating Fgf8, Shh, and Meis2 expression. Tretinoin 0-13 sonic hedgehog Gallus gallus 175-178
17207476-1 2007 Retinoic acid (RA) synthesized by Raldh3 in the frontonasal surface ectoderm of chick embryos has been suggested to function in early forebrain patterning by regulating Fgf8, Shh, and Meis2 expression. Tretinoin 0-13 Meis homeobox 2 Gallus gallus 184-189
17336257-5 2007 Long-term event-free survival (EFS) has been excellent in first remission (CR1) cytogenetically favorable groups, particularly with post-transplant treatment for acute promyelocytic leukemia (APL) patients with all-trans retinoic acid (ATRA; EFS 88%). Tretinoin 221-234 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 75-78
10516147-6 1999 PAF-R expression by human colon epithelial cells was upregulated by stimulation with retinoic acid but not by stimulation with PAF, proinflammatory agonists (tumor necrosis factor-alpha, interleukin-1, interferon-gamma), or transforming growth factor-alpha. Tretinoin 85-98 platelet activating factor receptor Homo sapiens 0-5
17336257-5 2007 Long-term event-free survival (EFS) has been excellent in first remission (CR1) cytogenetically favorable groups, particularly with post-transplant treatment for acute promyelocytic leukemia (APL) patients with all-trans retinoic acid (ATRA; EFS 88%). Tretinoin 236-240 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 75-78
16826196-3 2007 Here, we demonstrate that mitochondrial respiratory chain (MRC) plays an essential role in the IFN-beta/RA-induced cancer cell death. Tretinoin 104-106 interferon beta 1 Homo sapiens 95-103
10530919-0 1999 Tissue-non-specific alkaline phosphatase mRNA expression and alkaline phosphatase activity following application of retinoic acid in cultured human dental pulp cells. Tretinoin 116-129 alkaline phosphatase, biomineralization associated Homo sapiens 0-40
10530919-1 1999 Retinoic acid is a potent inducer of tissue-non-specific alkaline phosphatase (TNSALP) expression in various osteoblastic and fibroblastic cells, and may be involved in morphogenesis, cellular growth and differentiation. Tretinoin 0-13 alkaline phosphatase, biomineralization associated Homo sapiens 37-77
10530919-1 1999 Retinoic acid is a potent inducer of tissue-non-specific alkaline phosphatase (TNSALP) expression in various osteoblastic and fibroblastic cells, and may be involved in morphogenesis, cellular growth and differentiation. Tretinoin 0-13 alkaline phosphatase, biomineralization associated Homo sapiens 79-85
10530919-7 1999 RT-PCR showed that retinoic acid enhanced the expression of bone-type TNSALP mRNA in pulp cells. Tretinoin 19-32 alkaline phosphatase, biomineralization associated Homo sapiens 70-76
10530919-9 1999 These findings suggest that the high alkaline phosphatase activity of retinoic acid-treated dental pulp cells is associated with increased transcription of the bone-type mRNA of the TNSALP gene and not with liver-type. Tretinoin 70-83 alkaline phosphatase, biomineralization associated Homo sapiens 182-188
17113230-3 2007 We generated WldS or Nmnat1-overexpressing Neuro2A cell lines, in which neuronal differentiation including neurite elongation can be induced by retinoic acid. Tretinoin 144-157 wallerian degeneration Mus musculus 13-17
10484078-0 1999 Participation of CYP2C8 in retinoic acid 4-hydroxylation in human hepatic microsomes. Tretinoin 27-40 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 17-23
10484078-7 1999 Inhibition of microsomal ATRA 4-hydroxylation was elicited by chemicals that interact with CYP2C8 (paclitaxel and diclofenac), but not those that interact with CYP2C9 (sulfaphenazole, tolbutamide, and torasemide). Tretinoin 25-29 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 91-97
10484078-11 1999 Individual variation in CYP2C8 and 3A4 expression may influence ATRA pharmacokinetics and drug interactions during therapy. Tretinoin 64-68 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 24-30
17107666-6 2007 Our results demonstrated that ATRA suppressed NF-kappaB activity and prevented IkappaBalpha degradation in a dose-dependent way, inhibited IFN-gamma production and gene expression of granzyme B and NKp46. Tretinoin 30-34 natural cytotoxicity triggering receptor 1 Homo sapiens 198-203
17217039-10 2007 The activation of both pathways of transcriptional regulation by the myeloid lineage-specific transcription factor C/EBPalpha (CCAAT/enhancer-binding protein-alpha), and posttranscriptional regulation by miR-223 appears essential for granulocytic differentiation and clinical response of acute promyelocytic leukemia (APL) blasts to all-trans retinoic acid (ATRA). Tretinoin 343-356 microRNA 223 Homo sapiens 204-211
10520028-8 1999 Untreated NB-4 cells used alpha4 integrin to arrest on endothelium, but beta2 integrin dependent arrest was induced by ATRA. Tretinoin 119-123 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 72-77
10520028-9 1999 With the acquisition of beta2 integrin function, ATRA-treated cells acquired the ability to transmigrate through activated endothelium. Tretinoin 49-53 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 24-29
10520028-10 1999 Thus, ATRA dramatically altered the adhesion phenotype on NB-4 cells: ATRA induced rolling largely attributable to E-selectin, abrogated alpha4 integrin dependent rolling, and promoted acquisition of beta2 integrin dependent firm adherence and transmigration. Tretinoin 6-10 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 200-205
10959555-0 2000 Regulation of LFA-3 (CD58) by dexamethasone and retinoic acids in vitro. Tretinoin 48-62 CD58 molecule Homo sapiens 14-19
10959555-0 2000 Regulation of LFA-3 (CD58) by dexamethasone and retinoic acids in vitro. Tretinoin 48-62 CD58 molecule Homo sapiens 21-25
10959555-7 2000 RESULTS: ATRA and 13RA were found to have a more pronounced inhibitory effect on LFA-3 expression than did DEX, the U937 cells being the most sensitive and the KB cells the least affected. Tretinoin 9-13 CD58 molecule Homo sapiens 81-86
17217039-10 2007 The activation of both pathways of transcriptional regulation by the myeloid lineage-specific transcription factor C/EBPalpha (CCAAT/enhancer-binding protein-alpha), and posttranscriptional regulation by miR-223 appears essential for granulocytic differentiation and clinical response of acute promyelocytic leukemia (APL) blasts to all-trans retinoic acid (ATRA). Tretinoin 358-362 microRNA 223 Homo sapiens 204-211
10477294-3 1999 We show that retinoic acid expands the N-tubulin, X-ngnr-1, X-MyT1, X-&Dgr;-1 and Gli3 domains and inhibits the expression of Zic2 and sonic hedgehog in the neural ectoderm, whereas a retinoid antagonist produces opposite changes. Tretinoin 13-26 myelin transcription factor 1 S homeolog Xenopus laevis 60-66
10477294-3 1999 We show that retinoic acid expands the N-tubulin, X-ngnr-1, X-MyT1, X-&Dgr;-1 and Gli3 domains and inhibits the expression of Zic2 and sonic hedgehog in the neural ectoderm, whereas a retinoid antagonist produces opposite changes. Tretinoin 13-26 GLI family zinc finger 3 L homeolog Xenopus laevis 86-90
17570033-11 2007 However, in strict contrast, when ES cell are on a differentiation pathway through exposure to retinoic acid or the removal of LIF, altering cAMP levels can rescue the self-renewal process promoting Oct4 expression. Tretinoin 95-108 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 199-203
10501184-2 1999 RA treatment of SH-SY5Y cells induces the appearance of functional Trk B and Trk C receptors. Tretinoin 0-2 neurotrophic receptor tyrosine kinase 2 Homo sapiens 67-72
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 neurotrophic receptor tyrosine kinase 1 Homo sapiens 199-202
10706449-8 1999 The levels of CDK2 activity were inhibited approximately 60% in ATRA-treated cells, suggesting that the increased p21 levels were sufficient to inhibit CDK activity and cause RB hypophosphorylation. Tretinoin 64-68 cyclin dependent kinase 2 Homo sapiens 14-17
10926209-4 2000 One such gene, gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), is essential for tumor cell death induced by interferon-beta (IFN-beta) and retinoic acid (RA). Tretinoin 179-181 interferon beta 1 Homo sapiens 133-148
10926209-4 2000 One such gene, gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), is essential for tumor cell death induced by interferon-beta (IFN-beta) and retinoic acid (RA). Tretinoin 179-181 interferon beta 1 Homo sapiens 150-158
17368311-1 2007 Data from a variety of animal and cell culture model systems have demonstrated an interaction between the aryl hydrocarbon receptor (AhR)- and retinoic acid (RA)-signaling pathways. Tretinoin 143-156 aryl hydrocarbon receptor Homo sapiens 106-131
10906479-2 2000 RALDH1 (also called E1, AHD2 or ALDH1) is expressed in the dorsal retina, and RALDH2 (V2, ALDH11) generates most RA in the embryonic trunk. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 24-28
10852968-4 2000 During retinoic acid-induced neurogenesis of these cells, a dominant negative form of MEF2 enhances apoptosis but does not affect cell division. Tretinoin 7-20 myocyte enhancer factor 2A Homo sapiens 86-90
10499631-4 1999 Previous work exploring the growth-inhibitory activity of ATRA in human malignancies has implicated several mechanisms that can arrest cells in the G1 phase of the cell cycle, including activation of p21Waf1 and inhibition of cyclin D1 expression. Tretinoin 58-62 cyclin D1 Homo sapiens 226-235
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 83-96 RB transcriptional corepressor 1 Homo sapiens 106-109
10442642-7 1999 Moreover, induction of differentiation of mouse F9 line by retinoic acid leads to the inhibition of both POMp100 and TLS/POMp75 activities. Tretinoin 59-72 fused in sarcoma Mus musculus 117-120
17368311-1 2007 Data from a variety of animal and cell culture model systems have demonstrated an interaction between the aryl hydrocarbon receptor (AhR)- and retinoic acid (RA)-signaling pathways. Tretinoin 143-156 aryl hydrocarbon receptor Homo sapiens 133-136
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 290-303 retinoic acid receptor gamma Homo sapiens 82-90
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 retinoic acid receptor gamma Homo sapiens 82-90
17368311-1 2007 Data from a variety of animal and cell culture model systems have demonstrated an interaction between the aryl hydrocarbon receptor (AhR)- and retinoic acid (RA)-signaling pathways. Tretinoin 158-160 aryl hydrocarbon receptor Homo sapiens 106-131
17368311-1 2007 Data from a variety of animal and cell culture model systems have demonstrated an interaction between the aryl hydrocarbon receptor (AhR)- and retinoic acid (RA)-signaling pathways. Tretinoin 158-160 aryl hydrocarbon receptor Homo sapiens 133-136
17368311-3 2007 In addition, activation of the AhR pathway alters the function of nuclear hormone-signaling pathways, including the estrogen, thyroid, and RA pathways. Tretinoin 139-141 aryl hydrocarbon receptor Homo sapiens 31-34
10855573-0 2000 Secretory differentiation of serially passaged normal human nasal epithelial cells by retinoic acid: expression of mucin and lysozyme. Tretinoin 86-99 LOC100508689 Homo sapiens 115-120
10416619-4 1999 Similarly, cytokeratin 1 mRNA level was more suppressed in ATRA-treated LNSbeta clones than it was in LNSX cells. Tretinoin 59-63 keratin 1 Homo sapiens 11-24
10855573-4 2000 The cells became squamous and mucin secretion decreased when retinoic acid was deleted from the culture media. Tretinoin 61-74 LOC100508689 Homo sapiens 30-35
17368311-4 2007 Activation of the AhR pathway through exposure to environmental compounds results in significant changes in RA synthesis, catabolism, transport, and excretion. Tretinoin 108-110 aryl hydrocarbon receptor Homo sapiens 18-21
17001699-6 2006 In both retinoid sensitive and resistant cells, expression of full-length beta 2 and beta 4 isoforms results in elevated sensitivity to retinoic acid treatment and caspase-independent cell death. Tretinoin 136-149 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 74-80
10820202-5 2000 Treatment of SN56 cells with retinoic acid (RA; 1 microM) for 48 h increased ChAT mRNA (+126%), protein (+88%), and activity (+215%) and increased nNOS mRNA (+98%), protein (+400%), and activity (+15%). Tretinoin 29-42 nitric oxide synthase 1, neuronal Mus musculus 147-151
10820202-5 2000 Treatment of SN56 cells with retinoic acid (RA; 1 microM) for 48 h increased ChAT mRNA (+126%), protein (+88%), and activity (+215%) and increased nNOS mRNA (+98%), protein (+400%), and activity (+15%). Tretinoin 44-46 nitric oxide synthase 1, neuronal Mus musculus 147-151
10820202-7 2000 Treatment with dexamethasone, which largely blocked the RA-mediated increase in nNOS expression, or inhibition of nNOS activity with methylthiocitrulline strongly potentiated the apoptotic response to SNAP in RA-treated SN56 cells. Tretinoin 56-58 nitric oxide synthase 1, neuronal Mus musculus 80-84
10394471-5 1999 Furthermore, there are at least two mouse mutations--in the Pax-6 and Gli-3 genes--that cause peripheral malformations and specifically disrupt neural crest mediated, RA-dependent induction and differentiation in the forebrain. Tretinoin 167-169 GLI-Kruppel family member GLI3 Mus musculus 70-75
10408388-2 1999 This study analyses the ability of all-trans retinoic acid (RA) to alter both sICAM and mICAM-1 expression in C8161 and Hs294T human melanoma cell lines and investigates the involvement of ICAM-1 in the interaction between tumour and lymphokine-activated killer (LAK) cells using the Cr-51 release assay. Tretinoin 45-58 intercellular adhesion molecule 1 Mus musculus 88-95
17132853-3 2006 The physiological effects of retinoic acids (RAs) are mediated by members of two families of nuclear receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), which are encoded by three distinct human genes, RXRalpha, RXRbeta, and RXRgamma. Tretinoin 29-43 retinoid X receptor beta Homo sapiens 243-250
10408388-2 1999 This study analyses the ability of all-trans retinoic acid (RA) to alter both sICAM and mICAM-1 expression in C8161 and Hs294T human melanoma cell lines and investigates the involvement of ICAM-1 in the interaction between tumour and lymphokine-activated killer (LAK) cells using the Cr-51 release assay. Tretinoin 60-62 intercellular adhesion molecule 1 Mus musculus 88-95
10408388-3 1999 Our data showed that 4-day pretreatment of the tumour cells with 10(-7) M RA and 10(-6) M RA induced an increase in lysis of both cell lines and also increased mICAM-1 expression without having any effect on sICAM-1 levels. Tretinoin 74-76 intercellular adhesion molecule 1 Mus musculus 160-167
10408388-3 1999 Our data showed that 4-day pretreatment of the tumour cells with 10(-7) M RA and 10(-6) M RA induced an increase in lysis of both cell lines and also increased mICAM-1 expression without having any effect on sICAM-1 levels. Tretinoin 90-92 intercellular adhesion molecule 1 Mus musculus 160-167
10417615-11 1999 Additionally, protein C inhibitor could contribute to the regulation of retinoid supply in the epidermis, as we have shown recently that retinoic acid binds specifically to protein C inhibitor. Tretinoin 137-150 serpin family A member 5 Homo sapiens 14-33
10797533-7 2000 In addition, we found that the expression of the vesicular monoamine transporter 2 (VMAT2) and the vesicular acetylcholine transporter (VAChT) was increased in those cells treated with retinoic acid. Tretinoin 185-198 solute carrier family 18 member A2 Homo sapiens 49-82
10797533-7 2000 In addition, we found that the expression of the vesicular monoamine transporter 2 (VMAT2) and the vesicular acetylcholine transporter (VAChT) was increased in those cells treated with retinoic acid. Tretinoin 185-198 solute carrier family 18 member A2 Homo sapiens 84-89
10799277-6 2000 The putative porcine RNA helicase induced by virus (RHIV -1) showed 84% amino acid similarity to human retinoic acid-induced gene (RIG-I). Tretinoin 103-116 DExD/H-box helicase 58 Sus scrofa 52-59
10751444-4 2000 In the present study, we further examined the effects of BMP2 and RA on the regulation of the responsiveness of SCG neurons to GDNF family members. Tretinoin 66-68 glial cell derived neurotrophic factor Rattus norvegicus 127-131
10751444-5 2000 Consequently, we found that RA alone induced the responsiveness of SCG neurons specifically to GDNF by upregulating the ligand-specifying receptor for GDNF (GFRalpha-1) at both the mRNA and protein levels. Tretinoin 28-30 glial cell derived neurotrophic factor Rattus norvegicus 95-99
10406468-0 1999 Identification of a retinoic acid-inducible element in the murine PTH/PTHrP (parathyroid hormone/parathyroid hormone-related peptide) receptor gene. Tretinoin 20-33 parathyroid hormone Mus musculus 66-69
16893893-7 2006 Conversely, BM88 gene silencing using RNA interference experiments resulted in acceleration of cell proliferation accompanied by impairment of retinoic acid-induced neuronal differentiation of Neuro 2a cells. Tretinoin 143-156 cell cycle exit and neuronal differentiation 1 Mus musculus 12-16
10406468-4 1999 The data show that RA-induced expression of the PTH/ PTHrP-receptor gene is mediated by the downstream P2 promoter. Tretinoin 19-21 parathyroid hormone Mus musculus 48-51
10751444-5 2000 Consequently, we found that RA alone induced the responsiveness of SCG neurons specifically to GDNF by upregulating the ligand-specifying receptor for GDNF (GFRalpha-1) at both the mRNA and protein levels. Tretinoin 28-30 glial cell derived neurotrophic factor Rattus norvegicus 151-155
10751444-7 2000 Although the upregulation of signal-transducing receptor Ret by the RA treatment was rather small, this treatment significantly increased the efficacy of tyrosine phosphorylation of Ret by GDNF. Tretinoin 68-70 glial cell derived neurotrophic factor Rattus norvegicus 189-193
10751444-8 2000 Experiments using synthetic retinoids suggested that RA acts through alpha-type of nuclear retinoic acid receptor to exert the induction of GDNF responsiveness. Tretinoin 53-55 glial cell derived neurotrophic factor Rattus norvegicus 140-144
10751444-9 2000 On the other hand, BMP2, which had no significant effect by itself on the GDNF responsiveness, promoted the action of RA to upregulate GFRalpha-1 and enhance the GDNF responsiveness. Tretinoin 118-120 bone morphogenetic protein 2 Rattus norvegicus 19-23
10751444-9 2000 On the other hand, BMP2, which had no significant effect by itself on the GDNF responsiveness, promoted the action of RA to upregulate GFRalpha-1 and enhance the GDNF responsiveness. Tretinoin 118-120 glial cell derived neurotrophic factor Rattus norvegicus 162-166
10393239-1 1999 The regulation of the rat fatty acid synthase gene by mediators such as diet, hormones, cAMP, sterols or retinoic acid is controlled by three NF-Y binding sites. Tretinoin 105-118 fatty acid synthase Rattus norvegicus 26-45
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 73-77 gap junction protein alpha 1 Homo sapiens 176-187
10361124-10 1999 These results suggest that (1) RA induces RARs mainly via RARalpha and that (2) RAR/RXR physically and functionally interact with Sp1, resulting in a potentiation of uPA transcription. Tretinoin 31-33 arginyl-tRNA synthetase 1 Homo sapiens 42-46
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 73-77 gap junction protein alpha 1 Homo sapiens 189-194
10358022-2 1999 Targeting of mouse alcohol dehydrogenase genes Adh1, Adh3, and Adh4 resulted in null mutant mice that all developed and reproduced apparently normally but differed markedly in clearance of ethanol and formaldehyde plus metabolism of retinol to the signaling molecule retinoic acid. Tretinoin 267-280 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 53-57
10753524-0 2000 Identification of endogenous retinoids, enzymes, binding proteins, and receptors during early postimplantation development in mouse: important role of retinal dehydrogenase type 2 in synthesis of all-trans-retinoic acid. Tretinoin 196-219 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 151-179
10753524-7 2000 We also detected retinal dehydrogenase type 2 (RALDH2), an enzyme capable of oxidising the final step in the all-trans-retinoic acid synthesis. Tretinoin 109-132 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 17-45
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 108-121 gap junction protein alpha 1 Homo sapiens 176-187
10753524-7 2000 We also detected retinal dehydrogenase type 2 (RALDH2), an enzyme capable of oxidising the final step in the all-trans-retinoic acid synthesis. Tretinoin 109-132 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 47-53
10753524-11 2000 Therefore, our results suggest that RALDH2 is a key regulator in initiating retinoic acid synthesis sometime between the mid-primitive streak stage and the late allantoic bud stage in mouse embryos. Tretinoin 76-89 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 36-42
16959971-3 2006 In addition, we have investigated the effect of all-trans retinoic acid (ATRA) on the expression of several retinoic acid response genes including cyclooxygenase-2 (COX-2) and connexin-43 (Cx-43). Tretinoin 108-121 gap junction protein alpha 1 Homo sapiens 189-194
16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 174-178 gap junction protein alpha 1 Homo sapiens 38-43
10753864-0 2000 SOX9 enhances aggrecan gene promoter/enhancer activity and is up-regulated by retinoic acid in a cartilage-derived cell line, TC6. Tretinoin 78-91 SRY (sex determining region Y)-box 9 Mus musculus 0-4
10753864-11 2000 Among these, retinoic acid (RA) specifically enhanced Sox9 mRNA expression in TC6 cells. Tretinoin 13-26 SRY (sex determining region Y)-box 9 Mus musculus 54-58
10411240-2 1999 The rationale behind is that certain carotenoids have provitamin A activity in mammals, and that one of the active forms of vitamin A, (retinoic acid) is known to behave as a transcriptional activator of the key gene for brown fat thermogenesis, the one encoding the uncoupling protein thermogenin (UCP1). Tretinoin 136-149 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 286-297
10411240-2 1999 The rationale behind is that certain carotenoids have provitamin A activity in mammals, and that one of the active forms of vitamin A, (retinoic acid) is known to behave as a transcriptional activator of the key gene for brown fat thermogenesis, the one encoding the uncoupling protein thermogenin (UCP1). Tretinoin 136-149 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 299-303
10753864-11 2000 Among these, retinoic acid (RA) specifically enhanced Sox9 mRNA expression in TC6 cells. Tretinoin 28-30 SRY (sex determining region Y)-box 9 Mus musculus 54-58
16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 174-178 retinol binding protein 1 Homo sapiens 45-51
10753864-12 2000 The basal levels of Sox9 expression and its enhancement by RA were observed similarly at both permissive (33 degrees C) and nonpermissive (39 degrees C) temperatures. Tretinoin 59-61 SRY (sex determining region Y)-box 9 Mus musculus 20-24
10228945-5 1999 TRAB-11 cells synthesize fibroblast growth factor-2 (FGF-2), which has potent autocrine mitogenic effects on these cells and acts synergistically with RA. Tretinoin 1-3 fibroblast growth factor 2 Rattus norvegicus 53-58
10753864-13 2000 Furthermore, RA treatment enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence in TC6 cells. Tretinoin 13-15 quiescin Q6 sulfhydryl oxidase 1 Mus musculus 107-110
18221089-7 2006 discovered TRA-418 (a benzene-condensed heterocyclic derivative) having a TP receptor antagonistic activity and a prostaglandin I(2) receptor agonistic activity. Tretinoin 11-14 thromboxane A2 receptor Homo sapiens 74-85
10745031-8 2000 Electrophoretic mobility shift assay (EMSA) demonstrated that ATRA enhanced DNA-NF-kappaB complex formation, especially with the p65 subunit. Tretinoin 62-66 RELA proto-oncogene, NF-kB subunit Homo sapiens 129-132
10715587-11 2000 In this study, P19 cells were driven to the neuronal pathway with retinoic acid. Tretinoin 66-79 interleukin 23, alpha subunit p19 Mus musculus 15-18
10329442-3 1999 Here we demonstrate that the expression of the human MMP-2 gene is enhanced by a synergistic action of retinoic acid (RA) and dibutyryl cyclic AMP (Bt2cAMP). Tretinoin 103-116 matrix metallopeptidase 2 Homo sapiens 53-58
18221089-7 2006 discovered TRA-418 (a benzene-condensed heterocyclic derivative) having a TP receptor antagonistic activity and a prostaglandin I(2) receptor agonistic activity. Tretinoin 11-14 prostaglandin I2 receptor Homo sapiens 114-141
16788101-5 2006 In this study, we assess the potential for cooperativity between increased C/EBP activity and ATRA therapy. Tretinoin 94-98 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 75-80
10344761-4 1999 RA inhibited the growth of five of seven cell lines and also the constitutive expression of the squamous differentiation markers cytokeratin 1 and transglutaminase I in all cell lines. Tretinoin 0-2 keratin 1 Homo sapiens 129-142
10716749-0 2000 Treatment with all-trans-retinoic acid decreases levels of endogenous TGF-beta(1) in the mesenchyme of the developing mouse inner ear. Tretinoin 15-38 transforming growth factor, beta 1 Mus musculus 70-81
10716749-2 2000 METHODS: In this study, we examine the effects of atRA exposure on the endogenous expression of transforming growth factor-beta(1) (TGF-beta(1)), a signaling molecule that mediates the epithelial-mesenchymal interactions that guide the development of the capsule of the inner ear. Tretinoin 50-54 transforming growth factor, beta 1 Mus musculus 96-130
10716749-2 2000 METHODS: In this study, we examine the effects of atRA exposure on the endogenous expression of transforming growth factor-beta(1) (TGF-beta(1)), a signaling molecule that mediates the epithelial-mesenchymal interactions that guide the development of the capsule of the inner ear. Tretinoin 50-54 transforming growth factor, beta 1 Mus musculus 132-143
10716749-4 2000 Consistent with these in vivo findings, high-density cultures of E10.5 periotic mesenchyme plus otic epithelium, treated with doses of atRA that suppress chondrogenesis, showed significantly decreased levels of TGF-beta(1), as compared with TGF-beta(1) levels in untreated control cultures. Tretinoin 135-139 transforming growth factor, beta 1 Mus musculus 211-222
10716749-4 2000 Consistent with these in vivo findings, high-density cultures of E10.5 periotic mesenchyme plus otic epithelium, treated with doses of atRA that suppress chondrogenesis, showed significantly decreased levels of TGF-beta(1), as compared with TGF-beta(1) levels in untreated control cultures. Tretinoin 135-139 transforming growth factor, beta 1 Mus musculus 241-252
10320792-6 1999 During the differentiation of mouse carcinoma cells P19 to neuron-like cells by retinoic acid, Bdm1 mRNA was up-regulated almost parallel to neurofilament mRNA. Tretinoin 80-93 interleukin 23, alpha subunit p19 Mus musculus 52-55
10320792-6 1999 During the differentiation of mouse carcinoma cells P19 to neuron-like cells by retinoic acid, Bdm1 mRNA was up-regulated almost parallel to neurofilament mRNA. Tretinoin 80-93 NDRG family member 4 Rattus norvegicus 95-99
17026715-5 2006 Western blot analysis showed a dramatic increase in ERK 1/2 phosphorylation (p-ERK 1/2) 1-5 days after RA induction, which was attenuated in the presence of the p-ERK 1/2-specific inhibitor UO126. Tretinoin 103-105 mitogen-activated protein kinase 3 Mus musculus 52-59
10432011-6 1999 Results show that 1 microM and 10 microM 4-HPR caused 31% and 96% inhibition of growth, while all-trains retinoic acid (ATRA) produced similar effects at 10 and 100 microM, making 4-HPR ten times more effective than ATRA. Tretinoin 105-118 haptoglobin-related protein Homo sapiens 182-185
10691970-6 2000 TNAP activity was induced only by retinoic acid and IAP activity was induced only by dexamethasone. Tretinoin 34-47 TNAP Homo sapiens 0-4
10432011-6 1999 Results show that 1 microM and 10 microM 4-HPR caused 31% and 96% inhibition of growth, while all-trains retinoic acid (ATRA) produced similar effects at 10 and 100 microM, making 4-HPR ten times more effective than ATRA. Tretinoin 120-124 haptoglobin-related protein Homo sapiens 182-185
17026715-5 2006 Western blot analysis showed a dramatic increase in ERK 1/2 phosphorylation (p-ERK 1/2) 1-5 days after RA induction, which was attenuated in the presence of the p-ERK 1/2-specific inhibitor UO126. Tretinoin 103-105 mitogen-activated protein kinase 3 Mus musculus 79-86
10702810-10 2000 During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis. Tretinoin 7-11 superoxide dismutase 2 Homo sapiens 22-27
10702810-10 2000 During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis. Tretinoin 166-170 superoxide dismutase 2 Homo sapiens 22-27
10702810-10 2000 During ATRA exposure, MnSOD was induced in the sensitive cell line, but not until after 72 h. Buthionine sulfoximine significantly increased the inhibitory effect of ATRA on colony formation in both cell lines, but only marginally enhanced the effect of ATRA on the induction of apoptosis. Tretinoin 166-170 superoxide dismutase 2 Homo sapiens 22-27
10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 3 Homo sapiens 186-194
17026715-5 2006 Western blot analysis showed a dramatic increase in ERK 1/2 phosphorylation (p-ERK 1/2) 1-5 days after RA induction, which was attenuated in the presence of the p-ERK 1/2-specific inhibitor UO126. Tretinoin 103-105 mitogen-activated protein kinase 3 Mus musculus 52-57
17003410-10 2006 Defects in Ski-/- mice closely resemble those described in animals lacking several of the retinoic acid receptor genes, or in animals exposed to excess retinoic acid during gestation. Tretinoin 90-103 ski sarcoma viral oncogene homolog (avian) Mus musculus 11-14
10215635-5 1999 The IL-2-mediated c-myc overexpression and CYP down-regulation were prevented by 1) genistein (a tyrosine kinase inhibitor that blocks the initial transduction of the IL-2R signal), 2) retinoic acid, butyric acid, or dimethyl sulfoxide (three agents that block c-myc transcription), or 3) an antisense c-myc oligonucleotide (which may cause rapid degradation of the c-myc transcript). Tretinoin 185-198 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 18-23
10704832-3 2000 Co-injecting synthetic mRNA encoding retinoic acid receptor alpha (NR1B1) and retinoid X receptor beta (NR2B2) results in an increase in the number of primary neurons and this is further enhanced by the addition of retinoic acid indicating that elevated retinoid signalling promotes an increase in the number of cells undergoing primary neurogenesis. Tretinoin 37-50 retinoic acid receptor alpha L homeolog Xenopus laevis 67-72
10737720-6 2000 Retinoic acid induced neuronal differentiation and a reduction of proliferation of P19 cells; the differentiated cells produced significantly more MMP-2 than untreated cells. Tretinoin 0-13 matrix metallopeptidase 2 Homo sapiens 147-152
16619265-8 2006 Further studies revealed that pretreatment with 10 microM BQ-123, a selective endothelin-1 receptor (ETAR) antagonist, for 2 h can significantly counteract the inhibition of 5 microM atRA treatment for 2 h of dHAND mRNA and protein expression. Tretinoin 183-187 endothelin receptor type A Rattus norvegicus 101-105
10191271-0 1999 Molecular analysis of two closely related mouse aldehyde dehydrogenase genes: identification of a role for Aldh1, but not Aldh-pb, in the biosynthesis of retinoic acid. Tretinoin 154-167 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 107-112
10191271-2 1999 As the first step towards studying the regulation of ALDH1 and its physiological role in the biosynthesis of retinoic acid, mouse ALDH1 cDNA and genomic clones have been characterized. Tretinoin 109-122 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 53-58
16806149-2 2006 Here we show that mouse embryos deficient for the RA-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2), if rescued from early lethality by maternal RA supplementation between E7.5 and E8.5, lack active RA signaling in the foregut region. Tretinoin 50-52 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-102
10094816-4 1999 In addition, RA had no effect on the levels of Bcl-XL; Bcl-XS; cyclins A, B, D1, D3, or E; or Rb1 expression but markedly down-modulated Cdk2 kinase activity and reduced Cdk4 expression. Tretinoin 13-15 cyclin dependent kinase 2 Homo sapiens 137-141
10100988-15 1999 When RA-deficient cultures were treated on Day 7 with 10(-6) M RA, intracellular LZ levels did not substantially decrease until 3 d later, coinciding with a marked increase in mucin secretion. Tretinoin 5-7 LOC100508689 Homo sapiens 176-181
10100990-9 1999 Northern blot analysis showed a similar increase for MUC4 and demonstrated that induction of MUC4 and MUC5B expression depended on retinoic acid. Tretinoin 131-144 mucin 4, cell surface associated Homo sapiens 93-97
10100990-9 1999 Northern blot analysis showed a similar increase for MUC4 and demonstrated that induction of MUC4 and MUC5B expression depended on retinoic acid. Tretinoin 131-144 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 102-107
10645966-8 2000 ELISA assays revealed that retinoic acid treated myocyte cultures contained significantly more hLAMP-1 and fibronectin than either normal or DMSO controls. Tretinoin 27-40 lysosomal associated membrane protein 1 Homo sapiens 95-102
10639592-1 2000 Retinoic acid (RA) can promote human medulloblastoma cells Med-3 toward differentiation but is not sufficient to induce cell death, suggesting its limited effect on medulloblastomas. Tretinoin 0-13 mediator complex subunit 27 Homo sapiens 59-64
10639592-1 2000 Retinoic acid (RA) can promote human medulloblastoma cells Med-3 toward differentiation but is not sufficient to induce cell death, suggesting its limited effect on medulloblastomas. Tretinoin 15-17 mediator complex subunit 27 Homo sapiens 59-64
16806149-2 2006 Here we show that mouse embryos deficient for the RA-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2), if rescued from early lethality by maternal RA supplementation between E7.5 and E8.5, lack active RA signaling in the foregut region. Tretinoin 50-52 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 104-110
10639592-5 2000 Anti-Fas antibody was used to incubate the Med-3 cells pretreated by 10 microM/l RA or 1.0 microg/ml CP. Tretinoin 81-83 mediator complex subunit 27 Homo sapiens 43-48
10639592-12 2000 Our data thus suggest that RA can enhance the chemosensitivity of human medulloblastoma Med-3 cells presumably via modulating the Fas expression pattern. Tretinoin 27-29 mediator complex subunit 27 Homo sapiens 88-93
16806149-2 2006 Here we show that mouse embryos deficient for the RA-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2), if rescued from early lethality by maternal RA supplementation between E7.5 and E8.5, lack active RA signaling in the foregut region. Tretinoin 104-106 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-102
10085234-5 1999 Expression of Hex was increased in F9 cells during differentiation into visceral endoderm cells by treatment with retinoic acid. Tretinoin 114-127 hematopoietically expressed homeobox Rattus norvegicus 14-17
16806149-2 2006 Here we show that mouse embryos deficient for the RA-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2), if rescued from early lethality by maternal RA supplementation between E7.5 and E8.5, lack active RA signaling in the foregut region. Tretinoin 104-106 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-102
16847436-11 2006 The expression of COX-2 enzyme, but not COX-1, was significantly higher in animals treated with ATRA. Tretinoin 96-100 cytochrome c oxidase II, mitochondrial Rattus norvegicus 18-23
10210322-9 1999 Moreover, RA induced apoptosis of CD34+ cells and CD34+CD71+ cells stimulated with erythropoietin. Tretinoin 10-12 transferrin receptor Homo sapiens 55-59
10202931-3 1999 Ultraviolet irradiation caused a near-total loss of retinoic acid induction of two RAR/RXR target genes, cellular retinoic acid binding protein-II and RA 4-hydroxylase, but did not affect 1,25-dihydroxyvitamin D3 induction of the vitamin D receptor/RXR-regulated gene vitamin D 24-hydroxylase. Tretinoin 52-65 retinoic acid receptor gamma Homo sapiens 83-86
10720163-6 2000 Other agents which act via the nuclear receptor pathway, all-trans and 9-cis retinoic acid, also induce expression of growth hormone mRNA. Tretinoin 77-90 gonadotropin releasing hormone receptor Rattus norvegicus 118-132
10629053-2 2000 Expression of RARbeta is highly induced by retinoic acid (RA) through a RA response element (betaRARE) that is activated by heterodimers of RARs and retinoid X receptors (RXRs). Tretinoin 43-56 arginyl-tRNA synthetase 1 Homo sapiens 140-144
10629053-2 2000 Expression of RARbeta is highly induced by retinoic acid (RA) through a RA response element (betaRARE) that is activated by heterodimers of RARs and retinoid X receptors (RXRs). Tretinoin 14-16 arginyl-tRNA synthetase 1 Homo sapiens 140-144
10629053-2 2000 Expression of RARbeta is highly induced by retinoic acid (RA) through a RA response element (betaRARE) that is activated by heterodimers of RARs and retinoid X receptors (RXRs). Tretinoin 58-60 arginyl-tRNA synthetase 1 Homo sapiens 140-144
10617585-0 2000 Retinoic acid stimulation of the human surfactant protein B promoter is thyroid transcription factor 1 site-dependent. Tretinoin 0-13 surfactant protein B Homo sapiens 39-59
16847438-15 2006 The sensitization-like effect induced by ATRA was mediated by RARs and associated with a modulation of COX-2 and interleukin-1 activities. Tretinoin 41-45 cytochrome c oxidase II, mitochondrial Rattus norvegicus 103-108
10617585-3 2000 Previous studies supported the role of retinoic acids (RA) and their receptors (RARs) in SP-B gene transcription. Tretinoin 39-53 surfactant protein B Homo sapiens 89-93
10070102-7 1999 The mutant retained DNA binding activity in the presence of retinoid X receptor-gamma to an RA response element in the hSP-B promoter. Tretinoin 92-94 surfactant protein B Homo sapiens 119-124
16839543-7 2006 We found that addition of exogenous retinoic acid (RA) rescued mbp expression in neckless mutant embryos, which lack endogenous RA synthesis. Tretinoin 36-49 myelin basic protein a Danio rerio 63-66
10024510-0 1999 Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells. Tretinoin 73-86 LOC100508689 Homo sapiens 48-53
10066345-9 1999 Therefore, RA inhibition of Smu-Sgamma1 switch rearrangement was regulated at the level of germline Cgamma1 transcription. Tretinoin 11-13 T cell receptor gamma, constant 1 Mus musculus 100-107
9935210-6 1999 Here, we show that a synthetic retinoid, CD-271, that activates selectively the RAR gamma subtype in a given context, shows increased anti-proliferative activity against certain carcinoma cells over all-trans-retinoic acid (tRA). Tretinoin 203-222 retinoic acid receptor gamma Homo sapiens 80-89
9935210-6 1999 Here, we show that a synthetic retinoid, CD-271, that activates selectively the RAR gamma subtype in a given context, shows increased anti-proliferative activity against certain carcinoma cells over all-trans-retinoic acid (tRA). Tretinoin 224-227 retinoic acid receptor gamma Homo sapiens 80-89
9880584-4 1999 Expression of antisense PS1 resulted in a failure of the clones to differentiate into neurons after retinoic acid induction, whereas cells transfected with antisense PS2 differentiated normally. Tretinoin 100-113 presenilin 1 Homo sapiens 24-27
9880584-5 1999 Concomitantly, antisense PS1 clones were associated with increased apoptosis both under basal conditions and during the early period of neuronal differentiation after retinoic acid treatment. Tretinoin 167-180 presenilin 1 Homo sapiens 25-28
10079512-6 1999 We used the mouse P19 embryonal carcinoma cell line, which differentiates into neurons and astrocytes upon retinoic acid (RA) induction. Tretinoin 107-120 interleukin 23, alpha subunit p19 Mus musculus 18-21
10025664-0 1999 Identification of a cis-acting element in the rat alpha-fetoprotein gene and its specific binding proteins in F9 cells during retinoic acid-induced differentiation. Tretinoin 126-139 alpha-fetoprotein Rattus norvegicus 50-67
10025664-2 1999 Following retinoic acid (RA) treatment, alpha-fetoprotein (AFP), a differentiation marker, is expressed and secreted. Tretinoin 10-23 alpha-fetoprotein Rattus norvegicus 40-57
10025664-2 1999 Following retinoic acid (RA) treatment, alpha-fetoprotein (AFP), a differentiation marker, is expressed and secreted. Tretinoin 10-23 alpha-fetoprotein Rattus norvegicus 59-62
10025664-2 1999 Following retinoic acid (RA) treatment, alpha-fetoprotein (AFP), a differentiation marker, is expressed and secreted. Tretinoin 25-27 alpha-fetoprotein Rattus norvegicus 40-57
10025664-2 1999 Following retinoic acid (RA) treatment, alpha-fetoprotein (AFP), a differentiation marker, is expressed and secreted. Tretinoin 25-27 alpha-fetoprotein Rattus norvegicus 59-62
10426553-1 1999 P19 embryonal carcinoma cells are pluripotential and able to differentiate into a variety of cell types, including neurons, glia and fibroblast-like cells, upon retinoic acid treatment and cellular aggregation. Tretinoin 161-174 interleukin 23, alpha subunit p19 Mus musculus 0-3
10780452-2 1999 In this report, we examined levels of p300 protein and the related protein, CREB binding protein (CBP), during the retinoic acid (RA)-induced differentiation of F9 cell. Tretinoin 115-128 E1A binding protein p300 Homo sapiens 38-42
10780452-2 1999 In this report, we examined levels of p300 protein and the related protein, CREB binding protein (CBP), during the retinoic acid (RA)-induced differentiation of F9 cell. Tretinoin 130-132 E1A binding protein p300 Homo sapiens 38-42
10780452-3 1999 As a result, the level of p300 protein began to decrease at 36 h after treatment with RA dramatically, however, the level of CBP protein did not alter. Tretinoin 86-88 E1A binding protein p300 Homo sapiens 26-30
10780480-2 1999 In this study, we investigated functions of p300 and CBP during the retinoic acid (RA) induced F9 cell differentiation using hammerhead ribozymes. Tretinoin 68-81 E1A binding protein p300 Homo sapiens 44-48
10780480-2 1999 In this study, we investigated functions of p300 and CBP during the retinoic acid (RA) induced F9 cell differentiation using hammerhead ribozymes. Tretinoin 83-85 E1A binding protein p300 Homo sapiens 44-48
10506831-6 1999 Similarly, CRBP and/or other retinoid-binding proteins function in the synthesis of retinal esters, the reduction of retinal generated from intestinal beta-carotene metabolism, and retinoic acid metabolism. Tretinoin 181-194 retinol binding protein 1 Homo sapiens 11-15
10023853-0 1999 Complement receptor type 1 gene regulation: retinoic acid and cytosine arabinoside increase CR1 expression. Tretinoin 44-57 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 0-26
10023853-0 1999 Complement receptor type 1 gene regulation: retinoic acid and cytosine arabinoside increase CR1 expression. Tretinoin 44-57 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 92-95
9885947-0 1998 Upregulation of ecto-5"-nucleotidase in human neuroblastoma SH-SY5Y cells on differentiation by retinoic acid or phorbolester. Tretinoin 96-109 5'-nucleotidase ecto Homo sapiens 16-36
9865735-4 1998 Consistent with this finding, the RA binding activity of CRABP in APL cells from three pretreatment cases (range, 27.2-53.2 fmol/mg protein) was similar to that of NB4 cells (22.6 +/- 5.4 fmol/mg protein). Tretinoin 34-36 cellular retinoic acid binding protein 1 Homo sapiens 57-62
9858140-1 1998 Recognition that cellular retinoic acid binding protein (CRABP)-I and CRABP-II are found in different cell types has provided additional support for the presumably divergent roles of these two proteins in mediating retinoic acid (RA) effects in human skin. Tretinoin 26-39 cellular retinoic acid binding protein 1 Homo sapiens 57-65
9858140-1 1998 Recognition that cellular retinoic acid binding protein (CRABP)-I and CRABP-II are found in different cell types has provided additional support for the presumably divergent roles of these two proteins in mediating retinoic acid (RA) effects in human skin. Tretinoin 215-228 cellular retinoic acid binding protein 1 Homo sapiens 57-65
9858140-5 1998 We report that CRABP-I is expressed in isolated melanocytes at the mRNA level, although under these circumstances the protein has minimal RA-binding activity, and that keratinocytic and dermal influences are required for CRABP-I activity in melanocytes. Tretinoin 16-18 cellular retinoic acid binding protein 1 Homo sapiens 221-228
10349632-2 1998 Following treatment of embryo-like aggregates with retinoic acid (RA), Pax-6, a protein expressed by ventral central nervous system (CNS) progenitors is induced. Tretinoin 51-64 paired box 6 Homo sapiens 71-76
10349632-2 1998 Following treatment of embryo-like aggregates with retinoic acid (RA), Pax-6, a protein expressed by ventral central nervous system (CNS) progenitors is induced. Tretinoin 66-68 paired box 6 Homo sapiens 71-76
9862446-4 1998 HAKR e is dramatically and transiently up-regulated in HL60 cells within 24 h of exposure to ATRA, further supporting the proposition that a member(s) of this family of enzymes play(s) a role in controlling cell growth and/or differentiation. Tretinoin 93-97 aldo-keto reductase family 1 member C3 Homo sapiens 0-6
10022762-3 1998 Preadipocytes from cervical BAT of foetal or newborn rabbits differentiated in a chemically-defined medium and expressed low levels of uncoupled protein-1 (UCP1) mRNA, greatly increased by beta3-adrenergic or retinoic acid stimulations. Tretinoin 209-222 mitochondrial brown fat uncoupling protein 1 Oryctolagus cuniculus 156-160
9811861-1 1998 Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Tretinoin 27-40 insulin-like growth factor 2 receptor Mus musculus 119-128
9811861-1 1998 Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Tretinoin 27-40 insulin-like growth factor 2 receptor Mus musculus 166-175
9811861-1 1998 Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Tretinoin 42-44 insulin-like growth factor 2 receptor Mus musculus 119-128
9811861-1 1998 Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Tretinoin 42-44 insulin-like growth factor 2 receptor Mus musculus 166-175
9811861-1 1998 Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Tretinoin 198-200 insulin-like growth factor 2 receptor Mus musculus 119-128
9811861-1 1998 Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Tretinoin 198-200 insulin-like growth factor 2 receptor Mus musculus 166-175
9811861-5 1998 Furthermore, the RA-induced translocation of cathepsin B was not observed in M6P/IGF2R-deficient P388D1 cells but occurred in stably transfected P388D1 cells expressing the receptor, suggesting that the effect of RA might be the result of direct interaction with M6P/IGF2R, rather than the result of binding to the nuclear receptors. Tretinoin 17-19 insulin-like growth factor 2 receptor Mus musculus 263-272
10630309-4 2000 Phorbol 12-myristate 13-acetate and all-trans-retinoic acid, which induce differentiation in U-937 cells, up-regulated CD11b (MAC1 alpha-integrin) and CD82 and down-regulated CD71 (transferrin receptor) in a time- and dose-dependent manner. Tretinoin 36-59 transferrin receptor Homo sapiens 175-179
10630309-4 2000 Phorbol 12-myristate 13-acetate and all-trans-retinoic acid, which induce differentiation in U-937 cells, up-regulated CD11b (MAC1 alpha-integrin) and CD82 and down-regulated CD71 (transferrin receptor) in a time- and dose-dependent manner. Tretinoin 36-59 transferrin receptor Homo sapiens 181-201
10672899-0 2000 Molecular cloning of a novel retinoic acid-responsive gene, HA1R-62, which is also up-regulated in Hoxa-1-overexpressing cells. Tretinoin 29-42 homeobox A1 Mus musculus 99-105
10649440-0 2000 Ecto-alkaline phosphatase activity identified at physiological pH range on intact P19 and HL-60 cells is induced by retinoic acid. Tretinoin 116-129 tripartite motif containing 33 Homo sapiens 0-4
10649440-6 2000 Retinoic acid (RA), which promotes the differentiation of P19 and HL-60 cells, induced levamisole-sensitive ecto-phosphohydrolase activity at pH 7.4. Tretinoin 0-13 tripartite motif containing 33 Homo sapiens 108-112
10649440-6 2000 Retinoic acid (RA), which promotes the differentiation of P19 and HL-60 cells, induced levamisole-sensitive ecto-phosphohydrolase activity at pH 7.4. Tretinoin 15-17 tripartite motif containing 33 Homo sapiens 108-112
10649440-7 2000 After its autophosphorylation by ecto-kinase activity, a 98-kDa membrane protein in P19 cells was found to be sensitive to ecto-ALP, and protein dephosphorylation increased after incubation of cells with RA for 24 h and 48 h. Orthovanadate, an inhibitor of all phosphatase activities, blocked the levamisole-sensitive dephosphorylation of the membrane phosphoproteins, while (R)-(-)-epinephrine reversed the effect by complexation of the inhibitor. Tretinoin 204-206 tripartite motif containing 33 Homo sapiens 33-37
10649440-7 2000 After its autophosphorylation by ecto-kinase activity, a 98-kDa membrane protein in P19 cells was found to be sensitive to ecto-ALP, and protein dephosphorylation increased after incubation of cells with RA for 24 h and 48 h. Orthovanadate, an inhibitor of all phosphatase activities, blocked the levamisole-sensitive dephosphorylation of the membrane phosphoproteins, while (R)-(-)-epinephrine reversed the effect by complexation of the inhibitor. Tretinoin 204-206 tripartite motif containing 33 Homo sapiens 123-127
10791768-8 2000 Appearance of both IGFBP-3 and lactoferrin in conditioned media of primary cultures of bovine mammary cells was stimulated by all trans retinoic acid (atRA). Tretinoin 136-149 insulin like growth factor binding protein 3 Bos taurus 19-26
10791768-8 2000 Appearance of both IGFBP-3 and lactoferrin in conditioned media of primary cultures of bovine mammary cells was stimulated by all trans retinoic acid (atRA). Tretinoin 151-155 insulin like growth factor binding protein 3 Bos taurus 19-26
10791768-9 2000 Furthermore, atRA was necessary for the entry of exogenously added lactoferrin into the mammary cell nucleus, while IGFBP-3 entry into the nuclei of atRA treated cells required the presence of lactoferrin. Tretinoin 149-153 insulin like growth factor binding protein 3 Bos taurus 116-123
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 188-201 nuclear receptor corepressor 2 Homo sapiens 126-130
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 nuclear receptor corepressor 2 Homo sapiens 126-130
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 nuclear receptor corepressor 2 Homo sapiens 220-224
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 nuclear receptor corepressor 2 Homo sapiens 252-256
10637480-3 2000 We demonstrate that SMRT association, as with PML-RARalpha, can be released from NPM-RARalpha at pharmacological concentration of ATRA (10-6 M). Tretinoin 130-134 nuclear receptor corepressor 2 Homo sapiens 20-24
10581176-7 1999 On the other hand, in P19 mouse embryonal carcinoma cells, TIP120A expression was elevated upon retinoic acid treatment, which induces differentiation. Tretinoin 96-109 cullin associated and neddylation dissociated 1 Homo sapiens 59-66
10581176-9 1999 The level of TIP120A was also elevated in such stem-like cells as F9 and HL60 after each differentiation procedure, retinoic acid and DMSO, respectively. Tretinoin 116-129 cullin associated and neddylation dissociated 1 Homo sapiens 13-20
10590479-7 1999 Moreover, removal of the apical ectodermal ridge or retinoic-acid treatment of distal cells, which results in a change in the pattern of sorting-out, inhibits the accumulation of N-cadherin proteins, suggesting that the distribution of these proteins is related to the positional identity that gives rise to the different shape and number of cartilage elements along the proximodistal axis. Tretinoin 52-65 cadherin 2 Gallus gallus 179-189
10531331-7 1999 By using different retinoic acid reporter systems, it is demonstrated that RIP140 strongly suppresses retinoic acid induction of reporter activities, but coactivator SRC-1 enhances it. Tretinoin 19-32 nuclear receptor interacting protein 1 Homo sapiens 75-81
10531331-7 1999 By using different retinoic acid reporter systems, it is demonstrated that RIP140 strongly suppresses retinoic acid induction of reporter activities, but coactivator SRC-1 enhances it. Tretinoin 102-115 nuclear receptor interacting protein 1 Homo sapiens 75-81
10523855-2 1999 We previously reported that all-trans retinoic acid (RA) triggers terminal differentiation in the human embryonal carcinoma cell line NTERA-2 clone D1 (NT2/D1), through an RARgamma dependent pathway. Tretinoin 38-51 retinoic acid receptor gamma Homo sapiens 172-180
10523855-2 1999 We previously reported that all-trans retinoic acid (RA) triggers terminal differentiation in the human embryonal carcinoma cell line NTERA-2 clone D1 (NT2/D1), through an RARgamma dependent pathway. Tretinoin 53-55 retinoic acid receptor gamma Homo sapiens 172-180
10687528-0 1999 Effect of retinoic acid on osteopontin expression in rat clonal dental pulp cells. Tretinoin 10-23 secreted phosphoprotein 1 Rattus norvegicus 27-38
10687528-2 1999 An immunoprecipitation assay clarified that retinoic acid caused an increase in phosphorylated osteopontin synthesis that was dose-dependent, and marked increases were observed at retinoic acid concentrations of 10(-6) to 10(-5) M (1.7-fold). Tretinoin 44-57 secreted phosphoprotein 1 Rattus norvegicus 95-106
10687528-2 1999 An immunoprecipitation assay clarified that retinoic acid caused an increase in phosphorylated osteopontin synthesis that was dose-dependent, and marked increases were observed at retinoic acid concentrations of 10(-6) to 10(-5) M (1.7-fold). Tretinoin 180-193 secreted phosphoprotein 1 Rattus norvegicus 95-106
10687528-4 1999 Because osteopontin has an important role in the mineralization process, these results suggest that retinoic acid regulates mineralization, which takes place in the pulp cavity, including reparative dentin formation. Tretinoin 100-113 secreted phosphoprotein 1 Rattus norvegicus 8-19
10706449-6 1999 ATRA decreased the level of phosphorylation of the RB protein at doses > 5 x 10(-9) M and also induced a five fold increase in p21WAF1, while levels of p27KIP1 and CDK2 were unchanged. Tretinoin 0-4 cyclin dependent kinase 2 Homo sapiens 167-171
10706449-8 1999 The levels of CDK2 activity were inhibited approximately 60% in ATRA-treated cells, suggesting that the increased p21 levels were sufficient to inhibit CDK activity and cause RB hypophosphorylation. Tretinoin 64-68 cyclin dependent kinase 2 Homo sapiens 14-18
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 89-102 cellular retinoic acid binding protein 1 Homo sapiens 240-246
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 104-106 cellular retinoic acid binding protein 1 Homo sapiens 240-246
10569185-1 1999 We have mutated the type I cellular retinoic acid binding protein (CRABP-I), individually at the Arg131 (into Ala) and the Tyr133 (into Phe) residues which have been predicted to make direct contact with retinoic acid (RA) based upon previous structural studies. Tretinoin 36-49 cellular retinoic acid binding protein 1 Homo sapiens 67-74
10569185-4 1999 By using an RA-inducible reporter, it is found that the wild type CRABP-I exerts biphasic effects on RA induction of the reporter. Tretinoin 12-14 cellular retinoic acid binding protein 1 Homo sapiens 66-73
10479456-4 1999 4-Hydroxy- and 18-hydroxy-RA are products of the hydroxylation of RA by a novel cytochrome P450 (CYP)-type of enzyme, CYP26, expression of which is rapidly induced by RA. Tretinoin 26-28 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 118-123
10479456-4 1999 4-Hydroxy- and 18-hydroxy-RA are products of the hydroxylation of RA by a novel cytochrome P450 (CYP)-type of enzyme, CYP26, expression of which is rapidly induced by RA. Tretinoin 66-68 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 118-123
10462505-2 1999 Expression of the rae28/mph1 gene is induced during retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 52-65 polyhomeotic homolog 1 Homo sapiens 18-23
10462505-2 1999 Expression of the rae28/mph1 gene is induced during retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 52-65 TTK protein kinase Homo sapiens 24-28
10462505-2 1999 Expression of the rae28/mph1 gene is induced during retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 67-69 polyhomeotic homolog 1 Homo sapiens 18-23
10462505-2 1999 Expression of the rae28/mph1 gene is induced during retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 67-69 TTK protein kinase Homo sapiens 24-28
10447003-8 1999 These findings provide the first evidence that t-RA activates degradation of CDK-4 through the ubiquitin-proteasome pathway, a novel mechanism by which t-RA causes HBE cells to exit the cell cycle, and blockade of these signaling events may contribute to the development of retinoid resistance in NSCLC cells. Tretinoin 47-51 cyclin dependent kinase 4 Homo sapiens 77-82
10447003-8 1999 These findings provide the first evidence that t-RA activates degradation of CDK-4 through the ubiquitin-proteasome pathway, a novel mechanism by which t-RA causes HBE cells to exit the cell cycle, and blockade of these signaling events may contribute to the development of retinoid resistance in NSCLC cells. Tretinoin 152-156 cyclin dependent kinase 4 Homo sapiens 77-82
10448131-3 1999 All-trans-N-(4-hydroxyphenyl)retinamide (4HPR or fenretinide) is a synthetic retinoid that is reported to have fewer side-effects compared to naturally occurring retinoids such as all-trans retinoic acid (ATRA) and 9-cis retinoic acid. Tretinoin 180-203 haptoglobin-related protein Homo sapiens 42-45
10448131-3 1999 All-trans-N-(4-hydroxyphenyl)retinamide (4HPR or fenretinide) is a synthetic retinoid that is reported to have fewer side-effects compared to naturally occurring retinoids such as all-trans retinoic acid (ATRA) and 9-cis retinoic acid. Tretinoin 205-209 haptoglobin-related protein Homo sapiens 42-45
10470859-10 1999 USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. Tretinoin 78-91 insulin-like growth factor 2 receptor Mus musculus 105-114
10470859-10 1999 USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. Tretinoin 78-91 insulin-like growth factor 2 receptor Mus musculus 159-168
10470859-10 1999 USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. Tretinoin 93-95 insulin-like growth factor 2 receptor Mus musculus 105-114
10470859-10 1999 USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. Tretinoin 93-95 insulin-like growth factor 2 receptor Mus musculus 159-168
10470859-10 1999 USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. Tretinoin 211-213 insulin-like growth factor 2 receptor Mus musculus 105-114
10470859-10 1999 USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. Tretinoin 211-213 insulin-like growth factor 2 receptor Mus musculus 159-168
10470859-12 1999 RA and those retinoids capable of binding to the M6P/IGF2R induced a remarkable morphological change with characteristics of round shape and reduced spreading, apoptosis, and growth inhibition in stably transfected mouse P388D1 cells overexpressing the M6P/IGF2R but not in the M6P/IGF2R-deficient P388D1 cells. Tretinoin 0-2 insulin-like growth factor 2 receptor Mus musculus 49-58
10470859-12 1999 RA and those retinoids capable of binding to the M6P/IGF2R induced a remarkable morphological change with characteristics of round shape and reduced spreading, apoptosis, and growth inhibition in stably transfected mouse P388D1 cells overexpressing the M6P/IGF2R but not in the M6P/IGF2R-deficient P388D1 cells. Tretinoin 0-2 insulin-like growth factor 2 receptor Mus musculus 253-262
10419526-0 1999 Retinoic acid promotes ubiquitination and proteolysis of cyclin D1 during induced tumor cell differentiation. Tretinoin 0-13 cyclin D1 Homo sapiens 57-66
10419526-3 1999 In response to all-trans-retinoic acid (RA) treatment, the human embryonal carcinoma cell line NT2/D1 exhibits a progressive decline in cyclin D1 expression beginning when the cells are committed to differentiate, but before onset of terminal neuronal differentiation. Tretinoin 15-38 cyclin D1 Homo sapiens 136-145
10419526-3 1999 In response to all-trans-retinoic acid (RA) treatment, the human embryonal carcinoma cell line NT2/D1 exhibits a progressive decline in cyclin D1 expression beginning when the cells are committed to differentiate, but before onset of terminal neuronal differentiation. Tretinoin 40-42 cyclin D1 Homo sapiens 136-145
10419526-6 1999 Notably, stable transfection of retinoic acid receptor gamma restores RA-mediated growth suppression and differentiation to NT2/D1-R1 cells and restores the decline of cyclin D1. Tretinoin 70-72 retinoic acid receptor gamma Homo sapiens 32-60
10419526-7 1999 The proteasome inhibitor LLnL blocks this RA-mediated decline in cyclin D1. Tretinoin 42-44 cyclin D1 Homo sapiens 65-74
10419526-8 1999 RA treatment markedly accelerates ubiquitination of wild-type cyclin D1, but not a cyclin D1 (T286A) mutant. Tretinoin 0-2 cyclin D1 Homo sapiens 62-71
9811861-6 1998 These observations not only support the idea that M6P/IGF2R mediates an RA-response pathway but also indicate a role for RA in control of intracellular trafficking of lysosomal enzymes. Tretinoin 72-74 insulin-like growth factor 2 receptor Mus musculus 50-59
9811866-7 1998 The range of phenotypes observed in the chimeras displays a significant overlap with those caused by teratogenic levels of retinoic acid, strongly suggesting that AP-2 is an important component of the mechanism of action of this morphogen. Tretinoin 123-136 transcription factor AP-2, alpha Mus musculus 163-167
9879709-0 1998 Expression of two even-skipped genes eve1 and evx2 during zebrafish fin morphogenesis and their regulation by retinoic acid. Tretinoin 110-123 even-skipped homeobox 2 Danio rerio 46-50
9879709-6 1998 Exposure of the regenerates to retinoic acid (RA) modifies the boundaries of eve1 and evx2 expression: the signal is down-regulated in the ray region and up-regulated in the interray region. Tretinoin 31-44 even-skipped homeobox 2 Danio rerio 86-90
9879709-6 1998 Exposure of the regenerates to retinoic acid (RA) modifies the boundaries of eve1 and evx2 expression: the signal is down-regulated in the ray region and up-regulated in the interray region. Tretinoin 46-48 even-skipped homeobox 2 Danio rerio 86-90
9795362-0 1998 Retinoic acid stimulates IGF binding protein (IGFBP)-6 and depresses IGFBP-2 and IGFBP-4 in SK-N-SH human neuroblastoma cells. Tretinoin 0-13 insulin like growth factor binding protein 2 Homo sapiens 69-76
9795362-5 1998 Analysis of transcriptional activity of the IGFBP-2, -4 and -6 genes in isolated nuclei (run-on experiments) showed that RA increased the transcriptional activity of the IGFBP-6 gene, reduced that of the IGFBP-4 gene and had no effect on that of the IGFBP-2 gene. Tretinoin 121-123 insulin like growth factor binding protein 2 Homo sapiens 44-62
9795362-5 1998 Analysis of transcriptional activity of the IGFBP-2, -4 and -6 genes in isolated nuclei (run-on experiments) showed that RA increased the transcriptional activity of the IGFBP-6 gene, reduced that of the IGFBP-4 gene and had no effect on that of the IGFBP-2 gene. Tretinoin 121-123 insulin like growth factor binding protein 2 Homo sapiens 44-51
9795362-6 1998 Northern blot analysis following treatment with actinomycin D showed that RA increased the stability of IGFBP-6 mRNA by a factor of 2.6, decreased that of IGFBP-2 mRNA by a factor of 2.3 and failed to affect IGFBP-4 mRNA. Tretinoin 74-76 insulin like growth factor binding protein 2 Homo sapiens 155-162
9795362-10 1998 With RA-induced differentiation, IGFBP-6 is strongly stimulated, whereas IGFBP-2 and IGFBP-4 are severely depressed, which would suggest that each IGFBP plays a specific role. Tretinoin 5-7 insulin like growth factor binding protein 2 Homo sapiens 73-80
9799805-10 1998 HNF-3 was required for both basal transcriptional activity and stimulation of the rat CYP7A promoter activity by retinoic acid. Tretinoin 113-126 forkhead box E3 Rattus norvegicus 0-5
9788609-1 1998 TCF17, the human homologue of the rat zinc finger gene Kid1, is highly expressed in neurons derived from the retinoic acid-treated human embryonal carcinoma (EC) cell line, NTERA-2. Tretinoin 109-122 zinc finger protein 354A Rattus norvegicus 55-59
10419526-9 1999 Transient expression of cyclin D1 (T286A) in NT2/D1 cells blocks RA-mediated transcriptional decline of a differentiation-sensitive reporter plasmid and represses induction of immunophenotypic neuronal markers. Tretinoin 65-67 cyclin D1 Homo sapiens 24-33
10419526-10 1999 Taken together, these findings strongly implicate RA-mediated degradation of cyclin D1 as a means of coupling induced differentiation and cell cycle control of human embryonal carcinoma cells. Tretinoin 50-52 cyclin D1 Homo sapiens 77-86
10393558-0 1999 Characterization of an inverted repeat with a zero spacer (IR0)-type retinoic acid response element from the mouse nuclear orphan receptor TR2-11 gene. Tretinoin 69-82 nuclear receptor subfamily 2, group C, member 1 Mus musculus 139-145
9826179-2 1998 The choroid plexus, which expresses the RA-synthesizing retinaldehyde dehydrogenase RALDH-2, is likely to represent a diffusion source of RA for the closely apposed cerebellum, regulating its development. Tretinoin 40-42 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 84-91
16839543-7 2006 We found that addition of exogenous retinoic acid (RA) rescued mbp expression in neckless mutant embryos, which lack endogenous RA synthesis. Tretinoin 51-53 myelin basic protein a Danio rerio 63-66
9826179-4 1998 A technique that characterizes RA-binding proteins according to their isoelectric point showed both CRABP I and CRABP II to be present in the cerebellum and P19 cells, and only CRABP II to be present in the choroid plexus. Tretinoin 31-33 cellular retinoic acid binding protein II Mus musculus 112-120
16920920-2 2006 In this study, we show that an active metabolite of vitamin A, all-trans retinoic acid (RA), potently stimulates T cell proliferation by modulating IL-2-mediated signaling downstream of IL-2R and independent of the induction of IL-2. Tretinoin 73-86 interleukin 2 receptor subunit alpha Homo sapiens 186-191
10512201-3 1999 Retinoic acid induced differentiation of embryonal carcinoma cells is also accompanied by a decrease in Oct-4 expression. Tretinoin 0-13 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 104-109
16712891-7 2006 In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase (p38), as well as an early but transient activation of extracellular signal-regulated kinase (ERK). Tretinoin 13-17 mitogen-activated protein kinase 14 Mus musculus 106-109
10512201-8 1999 The initial repression of Oct-4 by retinoic acid coincides with the disappearance of the first factor (named UCF for undifferentiated cellular factor) and the appearance of a transiently induced factor (TRIF) which forms a larger complex with DR0 in electrophoretic mobility shift assays. Tretinoin 35-48 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 26-31
9742213-0 1998 Chondrocyte-mediated catabolism of aggrecan: aggrecanase-dependent cleavage induced by interleukin-1 or retinoic acid can be inhibited by glucosamine. Tretinoin 104-117 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 45-56
16712891-7 2006 In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase (p38), as well as an early but transient activation of extracellular signal-regulated kinase (ERK). Tretinoin 13-17 mitogen-activated protein kinase 14 Mus musculus 118-121
9742213-9 1998 Inhibition was apparently not due to cytotoxicity or interference with IL-1 signalling, since biosynthetic activity was not inhibited and inhibition of the aggrecanase response was also obtained when RA was used as the catabolic stimulator. Tretinoin 200-202 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 156-167
16565789-9 2006 Cell treatment with lycopene and atRA inhibited IGF-I-stimulated cell cycle progression from G1 to S phase and decreased retinoblastoma protein (pRb) phosphorylation. Tretinoin 33-37 RB transcriptional corepressor 1 Homo sapiens 145-148
10385401-0 1999 Effect of retinoic acid on glucokinase activity and gene expression and on insulin secretion in primary cultures of pancreatic islets. Tretinoin 10-23 glucokinase Rattus norvegicus 27-38
10385401-2 1999 Previously we reported that retinoic acid increases glucokinase activity and messenger RNA (mRNA) levels in the insulinoma cell line RIN-m5F; however, we could not rule out the possibility that the effect of retinoic acid on RIN-m5F glucokinase was inherent to the cell line or related to its differentiating capacity. Tretinoin 28-41 glucokinase Rattus norvegicus 52-63
10385401-2 1999 Previously we reported that retinoic acid increases glucokinase activity and messenger RNA (mRNA) levels in the insulinoma cell line RIN-m5F; however, we could not rule out the possibility that the effect of retinoic acid on RIN-m5F glucokinase was inherent to the cell line or related to its differentiating capacity. Tretinoin 28-41 glucokinase Rattus norvegicus 233-244
10385401-5 1999 Using the branched DNA (bDNA) assay, a sensitive signal amplification technique, we detected relative increases in glucokinase mRNA levels of 51.8+/-13.3% and 62.8+/-16.1% at 12 and 24 h, respectively, in adult islets treated with] 10(-6) M retinoic acid. Tretinoin 241-254 glucokinase Rattus norvegicus 115-126
10385401-7 1999 In transfected fetal islets, retinoic acid increased the activity of the -1000 kb rat glucokinase promoter by 51.3%. Tretinoin 29-42 glucokinase Rattus norvegicus 86-97
10385401-10 1999 These data show that retinoic acid increases pancreatic glucokinase in cultured islets and that the mechanism may involve a stimulatory effect on the glucokinase promoter. Tretinoin 21-34 glucokinase Rattus norvegicus 56-67
9751509-11 1998 Similar to ATRA, 9-cis-RA transiently induced the messenger RNA expression of the nuclear RA receptor RAR beta, suggesting a role for this receptor in the effects of retinoids on the differentiation and proliferation of A spermatogonia. Tretinoin 11-15 retinoic acid receptor, beta Mus musculus 102-110
16565789-12 2006 Our results showed that ectopic expression of cyclin D1 can overcome cell cycle inhibition caused by lycopene and atRA. Tretinoin 114-118 cyclin D1 Homo sapiens 46-55
16494909-6 2006 We examined the effect of all-trans retinoic acid on expression of ID-1, -2, -3, and -4 in normal human keratinocytes and found that exposure of these cells to all-trans retinoic acid causes an increase in both ID-1 and ID-3 gene expression. Tretinoin 36-49 inhibitor of DNA binding 1, HLH protein Homo sapiens 211-224
9758708-1 1998 The AP2alpha gene encodes a transcription factor containing a basic, helix-span-helix DNA-binding/dimerization domain, which is developmentally regulated and retinoic acid inducible. Tretinoin 158-171 transcription factor AP-2, alpha Mus musculus 4-12
10347207-4 1999 ATRA induces TRKB expression, and exogenous BDNF stimulates both autophosphorylation of TRKB and induction of the immediate early gene, FOS, in these cells. Tretinoin 0-4 neurotrophic receptor tyrosine kinase 2 Homo sapiens 13-17
10347207-6 1999 Because the time course of TRKB induction closely parallels phenotypic differentiation of these cells, it seems probable that ATRA induces differentiation of NB1643 cells by establishing an autocrine loop involving BDNF and TRKB. Tretinoin 126-130 neurotrophic receptor tyrosine kinase 2 Homo sapiens 27-31
10347207-6 1999 Because the time course of TRKB induction closely parallels phenotypic differentiation of these cells, it seems probable that ATRA induces differentiation of NB1643 cells by establishing an autocrine loop involving BDNF and TRKB. Tretinoin 126-130 neurotrophic receptor tyrosine kinase 2 Homo sapiens 224-228
9731743-0 1998 Differential expression and biological activity of retinoic acid-induced TGFbeta isoforms in embryonic palate mesenchymal cells. Tretinoin 51-64 transforming growth factor, beta 1 Mus musculus 73-80
9731743-1 1998 The effect of retinoic acid (RA) on TGF-beta mRNA expression and protein production in murine embryonic palate mesenchymal (MEPM) cells was examined by Northern blotting and TGF-beta bioassay in association with TGF-beta isoform-specific neutralizing antibodies. Tretinoin 14-27 transforming growth factor, beta 1 Mus musculus 36-44
9731743-1 1998 The effect of retinoic acid (RA) on TGF-beta mRNA expression and protein production in murine embryonic palate mesenchymal (MEPM) cells was examined by Northern blotting and TGF-beta bioassay in association with TGF-beta isoform-specific neutralizing antibodies. Tretinoin 29-31 transforming growth factor, beta 1 Mus musculus 36-44
9731743-9 1998 Coincubation of heat-activated CM from RA-treated MEPM cells with pan-specific or TGF-beta2 or beta3-specific neutralizing antibodies partially relieved the inhibitory effect on 3H-thymidine incorporation, suggesting that this proliferative response was due to RA-induced TGF-beta. Tretinoin 39-41 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 95-100
10421061-8 1999 RA indeed downregulated the transcript levels of all HaCaT desmosomal cadherins, except dsg2. Tretinoin 0-2 desmoglein 2 Homo sapiens 88-92
9731743-9 1998 Coincubation of heat-activated CM from RA-treated MEPM cells with pan-specific or TGF-beta2 or beta3-specific neutralizing antibodies partially relieved the inhibitory effect on 3H-thymidine incorporation, suggesting that this proliferative response was due to RA-induced TGF-beta. Tretinoin 39-41 transforming growth factor, beta 1 Mus musculus 82-90
16494909-6 2006 We examined the effect of all-trans retinoic acid on expression of ID-1, -2, -3, and -4 in normal human keratinocytes and found that exposure of these cells to all-trans retinoic acid causes an increase in both ID-1 and ID-3 gene expression. Tretinoin 170-183 inhibitor of DNA binding 1, HLH protein Homo sapiens 67-87
9842508-2 1998 Since retinoic acid (RA) has been shown as a potent inducer of TNSALP expression in various osteoblastic and fibroblastic cells, we investigated the effects of RA on the level of ALP activity and expression of TNSALP mRNAs in HPDL cells. Tretinoin 6-19 alkaline phosphatase, biomineralization associated Homo sapiens 63-69
16494909-6 2006 We examined the effect of all-trans retinoic acid on expression of ID-1, -2, -3, and -4 in normal human keratinocytes and found that exposure of these cells to all-trans retinoic acid causes an increase in both ID-1 and ID-3 gene expression. Tretinoin 170-183 inhibitor of DNA binding 1, HLH protein Homo sapiens 211-224
9842508-2 1998 Since retinoic acid (RA) has been shown as a potent inducer of TNSALP expression in various osteoblastic and fibroblastic cells, we investigated the effects of RA on the level of ALP activity and expression of TNSALP mRNAs in HPDL cells. Tretinoin 21-23 alkaline phosphatase, biomineralization associated Homo sapiens 63-69
16699180-9 2006 Our findings support a sequence of events in which mutations in APC result in impaired retinoic acid biosynthesis, elevated levels of C/EBP-beta, up-regulation of COX-2, increased prostaglandin E(2) accumulation, and activation of Wnt target genes. Tretinoin 87-100 APC regulator of WNT signaling pathway Homo sapiens 64-67
9733106-2 1998 Alcohol dehydrogenases ADH1 (class I ADH) and ADH4 (class IV ADH) function as retinol dehydrogenases in the oxidation of retinol, a necessary step in the synthesis of retinoic acid from vitamin A. Tretinoin 167-180 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 58-64
10533485-5 1999 ATRA increased the expression of connexin 43 mRNA and protein without affecting Cx 43 phosphorylation and prevented inadequate Cx 43 localisation caused by TPA/KBrO3 or DMN. Tretinoin 0-4 gap junction protein alpha 1 Canis lupus familiaris 127-132
10533485-7 1999 These data suggest that ATRA enhanced GJIC by upregulating Cx 43 expression and that ATRA might be useful for prevention of renal cell carcinoma. Tretinoin 24-28 gap junction protein alpha 1 Canis lupus familiaris 59-64
16684888-0 2006 All-trans retinoic acid-induced expression of bactericidal/permeability-increasing protein (BPI) in human myeloid cells correlates to binding of C/EBPbeta and C/EBPepsilon to the BPI promoter. Tretinoin 10-23 CCAAT enhancer binding protein beta Homo sapiens 145-154
10228945-5 1999 TRAB-11 cells synthesize fibroblast growth factor-2 (FGF-2), which has potent autocrine mitogenic effects on these cells and acts synergistically with RA. Tretinoin 1-3 fibroblast growth factor 2 Rattus norvegicus 25-51
10328955-0 1999 Dysregulated expression of cyclin D1 in normal human mammary epithelial cells inhibits all-trans-retinoic acid-mediated G0/G1-phase arrest and differentiation in vitro. Tretinoin 87-110 cyclin D1 Homo sapiens 27-36
10328955-2 1999 We investigated whether retroviral-mediated expression of cyclin D1 might affect all-trans-retinoic acid (ATRA)-mediated growth inhibition and differentiation of normal cultured human mammary epithelial cells (HMECs). Tretinoin 84-104 cyclin D1 Homo sapiens 58-67
10328955-2 1999 We investigated whether retroviral-mediated expression of cyclin D1 might affect all-trans-retinoic acid (ATRA)-mediated growth inhibition and differentiation of normal cultured human mammary epithelial cells (HMECs). Tretinoin 106-110 cyclin D1 Homo sapiens 58-67
10328955-6 1999 Dysregulated expression of cyclin D1 in HMECs results in inhibition of G0/G1-phase arrest mediated by ATRA. Tretinoin 102-106 cyclin D1 Homo sapiens 27-36
9731565-7 1998 To investigate the molecular mechanism of the effects of RA, we evaluated the expression of two proteins, c-myc and p53, which are known to be involved in both cell differentiation and apoptosis. Tretinoin 57-59 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 106-111
9731565-9 1998 On the contrary, a dose-dependent reduction in c-myc levels was found, suggesting that RA action may be mediated by modulation of this oncogene. Tretinoin 87-89 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 47-52
9699512-8 1998 The RAR alpha-specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXR alpha in mediating the biological effects of retinoids on JEG-3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. Tretinoin 4-6 glycoprotein hormones, alpha polypeptide Homo sapiens 46-49
9716179-10 1998 RXR-gamma expression produced significant reduction in levels of RA-responsive genes including the cyclin-dependent kinase inhibitors p21Cip1/WAF1 and p27Kip1, resulting in increased cdc2 and cdk2 kinase activity and RB phosphorylation. Tretinoin 65-67 cyclin dependent kinase 2 Homo sapiens 192-196
16684888-9 2006 Here, we show that induction of NB4 cells with ATRA correlates to direct binding of C/EBPbeta and C/EBPepsilon to the proximal BPI promoter, as determined by electrophoretic mobility shift analysis and chromatin immunoprecipitation. Tretinoin 47-51 CCAAT enhancer binding protein beta Homo sapiens 84-93
10224151-1 1999 All-trans-retinoic acid (RA), an active metabolite of vitamin A, induces the gene expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) and suppresses leptin gene expression in white adipose tissue (WAT) when given as an acute dose. Tretinoin 0-23 leptin Rattus norvegicus 169-175
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 37-50 neurotrophic receptor tyrosine kinase 1 Homo sapiens 170-173
10340464-7 1999 In RA-treated regenerates, overall gelatinase activities increased, especially the MMP-2-like gelatinase activity which increased markedly. Tretinoin 3-5 matrix metallopeptidase 2 Homo sapiens 83-88
9683534-4 1998 We used a neuroblastoma differentiation model, the retinoic acid-induced neuronal differentiation of SMS-KCNR cells, to study the regulation of the ENC-1 gene during neural crest cell differentiation. Tretinoin 51-64 ectodermal-neural cortex 1 Homo sapiens 148-153
9699718-1 1998 Embryonic mouse upper-lip skin explants treated with 16.7 microM all-trans retinoic acid (tRA) give rise to a glandular metaplasia of hair vibrissa follicles; however, at this concentration, tRA can activate not only the three retinoic acid receptors (RARalpha, beta, and gamma), but also the retinoid X receptors (RXRalpha, beta, and gamma) as a consequence of its isomerization to 9-cis retinoic acid. Tretinoin 75-88 retinoid X receptor alpha Mus musculus 315-323
10340464-8 1999 These results suggest that MMP-2-like and MMP-9-like gelatinases play a role in ECM remodeling during regeneration, and that gelatinases are involved in the excessive dedifferentiation after RA treatment. Tretinoin 191-193 matrix metallopeptidase 2 Homo sapiens 27-32
9699718-1 1998 Embryonic mouse upper-lip skin explants treated with 16.7 microM all-trans retinoic acid (tRA) give rise to a glandular metaplasia of hair vibrissa follicles; however, at this concentration, tRA can activate not only the three retinoic acid receptors (RARalpha, beta, and gamma), but also the retinoid X receptors (RXRalpha, beta, and gamma) as a consequence of its isomerization to 9-cis retinoic acid. Tretinoin 90-93 retinoid X receptor alpha Mus musculus 315-323
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 52-54 neurotrophic receptor tyrosine kinase 1 Homo sapiens 170-173
17147245-0 2006 [Experimental study of the enhancement effect of aminopeptidase N inhibitor ubenimex on the differentiation induction activity of all-trans-retinoic acid in acute promyelocytic leukemia cells and its mechanism]. Tretinoin 130-153 alanyl aminopeptidase, membrane Homo sapiens 49-65
9711991-0 1998 The induction of P450-mediated oxidation of all-trans retinoic acid by retinoids in head and neck squamous cell carcinoma cell lines. Tretinoin 54-67 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 17-21
9711991-1 1998 All-trans retinoic acid (RA) can be catabolized into polar metabolites by cytochrome P450 (P450) in several tissues including the skin. Tretinoin 0-23 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 85-89
9711991-1 1998 All-trans retinoic acid (RA) can be catabolized into polar metabolites by cytochrome P450 (P450) in several tissues including the skin. Tretinoin 0-23 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 91-95
10205176-3 1999 PSU1 interacts in a ligand-dependent manner with the LBD of several NRs, including retinoic acid (RARalpha), retinoid X (RXRalpha), thyroid hormone (TRalpha), vitamin D3 (VDR) and oestrogen (ERalpha) receptors. Tretinoin 83-96 decapping enzyme complex catalytic subunit Saccharomyces cerevisiae S288C 0-4
10094816-4 1999 In addition, RA had no effect on the levels of Bcl-XL; Bcl-XS; cyclins A, B, D1, D3, or E; or Rb1 expression but markedly down-modulated Cdk2 kinase activity and reduced Cdk4 expression. Tretinoin 13-15 cyclin dependent kinase 4 Homo sapiens 170-174
10094816-6 1999 Olomoucine, a potent p34(cdc2) and Cdk2 inhibitor, effectively blocked RA-mediated p34(cdc2) kinase activation and prevented RA-induced apoptosis. Tretinoin 71-73 cyclin dependent kinase 2 Homo sapiens 35-39
10095099-10 1999 Moreover, we showed that endogenous AP-2 induced by retinoic acid also activated transcription via box-II in P19 cells. Tretinoin 52-65 transcription factor AP-2, alpha Mus musculus 36-40
17147245-1 2006 OBJECTIVE: To investigate the effect of aminopeptidase N inhibitor ubenimex on differentiation induction of all-trans-retinoic acid (ATRA) in acute promyelocytic leukemia (APL) cells and its mechanism. Tretinoin 108-131 alanyl aminopeptidase, membrane Homo sapiens 40-56
17147245-1 2006 OBJECTIVE: To investigate the effect of aminopeptidase N inhibitor ubenimex on differentiation induction of all-trans-retinoic acid (ATRA) in acute promyelocytic leukemia (APL) cells and its mechanism. Tretinoin 133-137 alanyl aminopeptidase, membrane Homo sapiens 40-56
16712844-0 2006 CYP4A11 is repressed by retinoic acid in human liver cells. Tretinoin 24-37 cytochrome P450 family 4 subfamily A member 11 Homo sapiens 0-7
10195743-2 1999 The production of human chorionic gonadotropin (hCG), a trophoectoderm-specific hormone, begins 7 days after retinoic acid (RR1) treatment and peaks on day 12-13. Tretinoin 109-122 chorionic gonadotropin subunit beta 5 Homo sapiens 24-52
9711991-1 1998 All-trans retinoic acid (RA) can be catabolized into polar metabolites by cytochrome P450 (P450) in several tissues including the skin. Tretinoin 25-27 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 85-89
9711991-1 1998 All-trans retinoic acid (RA) can be catabolized into polar metabolites by cytochrome P450 (P450) in several tissues including the skin. Tretinoin 25-27 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 91-95
9711991-2 1998 We examined eight different squamous cell carcinoma (SCC) cell lines to determine their capacity to induce P450-mediated oxidation of RA. Tretinoin 134-136 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 107-111
16712844-3 2006 Treatment of HepaRG cells with all-trans-retinoic acid resulted in a strong decrease in CYP4A11 gene expression and apoprotein content and, furthermore, was associated with a 50% decrease in the microsomal lauric acid hydroxylation activity. Tretinoin 31-54 cytochrome P450 family 4 subfamily A member 11 Homo sapiens 88-95
10094499-6 1999 The expression of TIF1alpha, TIF1beta and SUG1 did not change in response to retinoic acid; however, SMRT was induced in both neuroblastoma cell lines, but particularly by all-trans retinoic acid in SH S EP cells. Tretinoin 182-195 nuclear receptor corepressor 2 Homo sapiens 101-105
9655929-4 1998 mMcl1/EAT increases dramatically with exposure to retinoic acid in murine embryonal carcinoma cell lines (F9 and PCC3) as well as embryonic stem cells, both of which are models of early embryogenesis. Tretinoin 50-63 myeloid cell leukemia sequence 1 Mus musculus 0-9
16556707-3 2006 When the HSC(LSK) cells were cultured in vitro in neuronal differentiation medium supplemented with retinoic acid, 50% of the cells expressed the neural progenitor marker nestin and no cells had become postmitotic. Tretinoin 100-113 lymphocyte protein tyrosine kinase Mus musculus 13-16
10050872-4 1999 Recently, the all-trans-retinoic acid (RA)-induced proteolysis of cyclin D1 that leads to the arrest of cells in G1 phase of the cell cycle was described in human bronchial epithelial cells and is a promising candidate for such a mechanism. Tretinoin 14-37 cyclin D1 Homo sapiens 66-75
10050872-4 1999 Recently, the all-trans-retinoic acid (RA)-induced proteolysis of cyclin D1 that leads to the arrest of cells in G1 phase of the cell cycle was described in human bronchial epithelial cells and is a promising candidate for such a mechanism. Tretinoin 39-41 cyclin D1 Homo sapiens 66-75
10224351-5 1999 Both retinoic acid and corticosteroids were able to downregulate IL-3- and IL-5-induced expression of IL-5R on cord-blood-derived as well as HL-60 cloned Eo-B progenitors. Tretinoin 5-18 interleukin 5 receptor subunit alpha Homo sapiens 102-107
16611695-4 2006 Here, we report Raldh1, Raldh2 and Raldh3 single, double and triple null mice exhibiting progressively less or no RA synthesis in the eye. Tretinoin 114-116 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 16-22
16611695-7 2006 At early stages, Raldh2 expressed in mesenchyme and Raldh3 expressed in the retinal pigmented epithelium generate RA that delivers an essential signal to the neural retina required for morphogenetic movements that lead to ventral invagination of the optic cup. Tretinoin 114-116 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 17-23
16611695-8 2006 At later stages, Raldh1 expressed in dorsal neural retina and Raldh3 expressed in ventral neural retina (plus weaker expression of each in lens/corneal ectoderm) generates RA that travels to surrounding mesenchyme, where it is needed to limit the anterior invasion of perioptic mesenchyme during the formation of corneal mesenchyme and eyelids. Tretinoin 172-174 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 17-23
9920669-2 1999 In dissociated cultures of sympathetic neuroblasts, retinoic acid inhibited the developmental increase in trkA mRNA expression and the developmental decrease in trkC mRNA expression that normally occurs in these cells but did not affect p75 mRNA expression. Tretinoin 52-65 neurotrophic tyrosine kinase, receptor, type 3 Mus musculus 161-165
9618139-0 1998 Transcriptional and posttranscriptional regulation of osteopontin gene expression in preosteoblasts by retinoic acid. Tretinoin 103-116 secreted phosphoprotein 1 Rattus norvegicus 54-65
16636307-9 2006 With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. Tretinoin 53-57 CD2-associated protein Rattus norvegicus 110-115
9618139-1 1998 This study examines the relative importance of transcriptional and posttranscriptional actions of retinoic acid (RA) in the regulation of osteopontin gene expression in a rat clonal preosteoblastic cell line, UMR 201. Tretinoin 98-111 secreted phosphoprotein 1 Rattus norvegicus 138-149
11601206-0 1999 [Study of the role of cyclin-dependent kinases (CDKs) in retinoic acid (RA) inducing HL-60 cell differentiation]. Tretinoin 57-70 cyclin dependent kinase 2 Homo sapiens 48-52
11601206-0 1999 [Study of the role of cyclin-dependent kinases (CDKs) in retinoic acid (RA) inducing HL-60 cell differentiation]. Tretinoin 72-74 cyclin dependent kinase 2 Homo sapiens 48-52
16636307-10 2006 After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. Tretinoin 182-186 CD2-associated protein Rattus norvegicus 140-145
11601206-3 1999 Meanwhile, histone H1 kinase assay was used to observe the changes of CDK2 activities in HL-60 cells treatment with ATRA and AE. Tretinoin 116-120 cyclin dependent kinase 2 Homo sapiens 70-74
11601206-6 1999 The activities of cyclin E/CDK2 and the amounts of cyclin D1/CDK4 complexes were decreased in ATRA- or AE-treated HL-60 cells. Tretinoin 94-98 cyclin dependent kinase 2 Homo sapiens 27-31
9618139-1 1998 This study examines the relative importance of transcriptional and posttranscriptional actions of retinoic acid (RA) in the regulation of osteopontin gene expression in a rat clonal preosteoblastic cell line, UMR 201. Tretinoin 113-115 secreted phosphoprotein 1 Rattus norvegicus 138-149
9618139-2 1998 Nuclear run-on analysis demonstrated constitutive expression of the osteopontin gene which was increased by threefold after 4 hr treatment with 1 microM RA, returning to a basal level by 24 hr. Tretinoin 153-155 secreted phosphoprotein 1 Rattus norvegicus 68-79
9618139-3 1998 However, Northern blot analysis, performed concurrently, showed that RA progressively increased the steady-state osteopontin mRNA level beginning 2 hr before any increase in gene transcription and peaking at 24 hr. Tretinoin 69-71 secreted phosphoprotein 1 Rattus norvegicus 113-124
11601206-6 1999 The activities of cyclin E/CDK2 and the amounts of cyclin D1/CDK4 complexes were decreased in ATRA- or AE-treated HL-60 cells. Tretinoin 94-98 cyclin D1 Homo sapiens 51-60
16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Tretinoin 88-92 CD2-associated protein Rattus norvegicus 207-212
11601206-6 1999 The activities of cyclin E/CDK2 and the amounts of cyclin D1/CDK4 complexes were decreased in ATRA- or AE-treated HL-60 cells. Tretinoin 94-98 cyclin dependent kinase 4 Homo sapiens 61-65
9618139-7 1998 However, RA resulted in a time-dependent accumulation of mature osteopontin mRNA in all cellular subfractions, suggesting that the proficiency of nuclear processing of primary mRNA transcripts was greatly enhanced by RA. Tretinoin 9-11 secreted phosphoprotein 1 Rattus norvegicus 64-75
11601206-7 1999 CONCLUSION: The effects of RA on the proliferation and differentiation of HL-60 cells may be associated with significant decreases in the activities of CDKs. Tretinoin 27-29 cyclin dependent kinase 2 Homo sapiens 152-156
16242776-6 2006 Upregulation of c-FLIP(L) protein, an inhibitor of apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), correspond with inhibition of ATRA-induced (autocrine TRAIL-mediated) caspase-8 activation and apoptosis. Tretinoin 167-171 caspase 8 Homo sapiens 207-216
16352814-4 2006 ATRA-induced activation was mediated by a region in the PU.1 promoter to which CEBPB and OCT-1 binding were induced. Tretinoin 0-4 CCAAT enhancer binding protein beta Homo sapiens 79-84
9927199-5 1999 Overexpression of c-raf in E2.5 explants increased the proliferative response to low serum and IGF-I and blocked differentiation induced by retinoic acid. Tretinoin 140-153 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 18-23
9927199-7 1999 Consistent with these results, the expression of a dominant negative c-Raf mutant potentiated retinoic acid action and decreased the rate of cell proliferation. Tretinoin 94-107 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 69-74
9773502-2 1998 The present study was conducted to elucidate correlation of mRNA expression of CaBP-D28k and vitamin D3 receptor (VDR) in the kidney and cerebellum of the developing chick by Northern blot analysis, localization of CaBP-D28k mRNA within the cerebellum by in situ hybridization, and effect of retinoic acid in ovo on CaBP-D28k mRNA levels. Tretinoin 292-305 vitamin D (1,25- dihydroxyvitamin D3) receptor Gallus gallus 114-117
16569592-6 2006 HP1 and MNEI levels inversely correlate in a number of normal and leukemia myeloid cells and show strikingly opposite coordinated changes during differentiation of U937 cell line induced by retinoic acid. Tretinoin 190-203 serpin family B member 1 Homo sapiens 8-12
9888458-0 1999 Retinoic acid modulates prolactin receptor expression and prolactin-induced STAT-5 activation in breast cancer cells in vitro. Tretinoin 0-13 prolactin receptor Homo sapiens 24-42
9888458-6 1999 Pretreatment with retinoic acid also reduced the prolactin-/prolactin receptor-dependent signal transduction and activation of transcription 5 (STAT-5) activation in T47D cells. Tretinoin 18-31 prolactin receptor Homo sapiens 60-78
9785384-0 1998 Potentiation of retinoic acid-induced differentiation of HL-60 cells by prostaglandin EP2 receptor. Tretinoin 16-29 prostaglandin E receptor 2 Homo sapiens 86-89
9785384-7 1998 These results demonstrate that the EP2 receptor enhances the RA-induced differentiation of HL-60 cells via stimulation of adenylate cyclase. Tretinoin 61-63 prostaglandin E receptor 2 Homo sapiens 35-38
16581781-9 2006 A dominant negative p300 construct disrupts enhanceosome formation and reduces the RA responsiveness of CD18. Tretinoin 83-85 E1A binding protein p300 Homo sapiens 20-24
9612277-6 1998 In addition, epimorphin mRNA studied by Northern blot was also the highest in one ileal clone, in which it was selectively upregulated by all-trans retinoic acid (RA) treatment. Tretinoin 148-161 syntaxin 2 Rattus norvegicus 13-23
10402668-1 1999 Adh4, a member of the mouse alcohol dehydrogenase (ADH) gene family, encodes an enzyme that functions in vitro as a retinol dehydrogenase in the conversion of retinol to retinoic acid, an important developmental signaling molecule. Tretinoin 170-183 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 51-54
10402668-1 1999 Adh4, a member of the mouse alcohol dehydrogenase (ADH) gene family, encodes an enzyme that functions in vitro as a retinol dehydrogenase in the conversion of retinol to retinoic acid, an important developmental signaling molecule. Tretinoin 170-183 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 116-137
9612277-6 1998 In addition, epimorphin mRNA studied by Northern blot was also the highest in one ileal clone, in which it was selectively upregulated by all-trans retinoic acid (RA) treatment. Tretinoin 163-165 syntaxin 2 Rattus norvegicus 13-23
16581781-11 2006 This is the first description of an RA-induced enhanceosome and demonstrates that GABP and p300 are essential components of CD18 RA responsiveness in myeloid cells. Tretinoin 36-38 E1A binding protein p300 Homo sapiens 91-95
9659296-9 1998 However, retinoic acid (10(-6) M) stimulated both IGFBP-2 and IGFBP-6 protein and mRNA levels, but it decreased IGFBP-3 mRNA levels relative to controls. Tretinoin 9-22 insulin like growth factor binding protein 3 Bos taurus 112-119
16581781-11 2006 This is the first description of an RA-induced enhanceosome and demonstrates that GABP and p300 are essential components of CD18 RA responsiveness in myeloid cells. Tretinoin 129-131 E1A binding protein p300 Homo sapiens 91-95
10570467-2 1999 Various forms of mammalian aldehyde dehydrogenase (ALDH) have been shown to oxidize the vitamin A precursor retinal to RA in vitro. Tretinoin 119-121 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 51-55
16222702-6 2006 Stimulation of HEXIM1 is not restricted to hematopoietic cells, as induction of phenotypic differentiation of neuroblastoma cells by retinoic acid results in up-regulation of HEXIM1. Tretinoin 133-146 hexamethylene bis-acetamide inducible 1 Mus musculus 15-21
10570467-3 1999 Here we show that injection of Xenopus embryos with mRNAs for either mouse Aldh1 or mouse Raldh2 stimulates RA synthesis at low and high levels, respectively, while injection of human ALDH3 mRNA is unable to stimulate any detectable level of RA synthesis. Tretinoin 108-110 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 75-80
10570467-3 1999 Here we show that injection of Xenopus embryos with mRNAs for either mouse Aldh1 or mouse Raldh2 stimulates RA synthesis at low and high levels, respectively, while injection of human ALDH3 mRNA is unable to stimulate any detectable level of RA synthesis. Tretinoin 108-110 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 90-96
10570467-4 1999 This provides evidence that some members of the ALDH gene family can indeed perform RA synthesis in vivo. Tretinoin 84-86 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 48-52
10570467-9 1999 As previous findings indicate that embryonic RA is more abundant in trunk rather than cranial tissues, our findings suggest that Raldh2 and Aldh1 control distinct retinoid signaling pathways by stimulating high and low RA biosynthetic activities, respectively, in various trunk and cranial tissues. Tretinoin 45-47 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 129-135
10570467-9 1999 As previous findings indicate that embryonic RA is more abundant in trunk rather than cranial tissues, our findings suggest that Raldh2 and Aldh1 control distinct retinoid signaling pathways by stimulating high and low RA biosynthetic activities, respectively, in various trunk and cranial tissues. Tretinoin 45-47 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 140-145
9528758-2 1998 Prior analysis identified an octamer motif in the Rex-1 promoter which is required for promoter activity in undifferentiated F9 cells and is involved in retinoic acid (RA)-associated reduction in expression. Tretinoin 153-166 ZFP42 zinc finger protein Homo sapiens 50-55
9528758-2 1998 Prior analysis identified an octamer motif in the Rex-1 promoter which is required for promoter activity in undifferentiated F9 cells and is involved in retinoic acid (RA)-associated reduction in expression. Tretinoin 168-170 ZFP42 zinc finger protein Homo sapiens 50-55
16222702-6 2006 Stimulation of HEXIM1 is not restricted to hematopoietic cells, as induction of phenotypic differentiation of neuroblastoma cells by retinoic acid results in up-regulation of HEXIM1. Tretinoin 133-146 hexamethylene bis-acetamide inducible 1 Mus musculus 175-181
9535729-0 1998 Long-term exposure to retinoic acid induces the expression of IRK1 channels in HERG channel-endowed neuroblastoma cells. Tretinoin 22-35 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 62-66
10208011-8 1999 Excess RA causes abnormalities of many systems; altered susceptibility to RA excess in mice lacking RAR gamma or RXR alpha suggests that the teratogenic signal is transduced through different receptors compared with physiological RA function in the same tissue. Tretinoin 74-76 retinoid X receptor alpha Mus musculus 113-122
9535729-3 1998 After 10-20 days exposure to Retinoic Acid (RA), SH-SY5Y cells showed, in addition to HERG currents, a novel current characterized by inward rectification, dependence on the extracellular K+ concentration, and blockade by Cs+ and Ba2+, the main features of the IRK1 current. Tretinoin 29-42 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 261-265
16439309-0 2006 Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Tretinoin 0-13 colony stimulating factor 1 receptor Homo sapiens 60-65
9535729-3 1998 After 10-20 days exposure to Retinoic Acid (RA), SH-SY5Y cells showed, in addition to HERG currents, a novel current characterized by inward rectification, dependence on the extracellular K+ concentration, and blockade by Cs+ and Ba2+, the main features of the IRK1 current. Tretinoin 44-46 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 261-265
9535729-5 1998 RT-PCR experiments confirmed that a transcript of the IRK1 (Kir 2.1) gene actually appears in SH-SY5Y cells treated for 10-20 days with RA. Tretinoin 136-138 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 54-58
9535729-5 1998 RT-PCR experiments confirmed that a transcript of the IRK1 (Kir 2.1) gene actually appears in SH-SY5Y cells treated for 10-20 days with RA. Tretinoin 136-138 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 60-67
9535729-6 1998 On the whole, data here presented demonstrate that RA-induced neuronal differentiation of neuroblastoma cells is accompanied by the switch from a HERG-driven to a IRK1-driven control of Vrest, similarly to what happens in normal differentiating neurons; however, in tumor cells, this switch does not imply the abolition of HERG channel expression. Tretinoin 51-53 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 163-167
9535737-4 1998 After 25 days of RA treatment, a significant proportion of cells differentiated into neurons in NT2 cells expressing wt PS1 (27.7% of total cells), which was comparable to that in untransfected cells, whereas very few cells differentiated into neurons in NT2 cells expressing M146V mutant PS1 (2.6% of total cells). Tretinoin 17-19 presenilin 1 Homo sapiens 120-123
9535737-4 1998 After 25 days of RA treatment, a significant proportion of cells differentiated into neurons in NT2 cells expressing wt PS1 (27.7% of total cells), which was comparable to that in untransfected cells, whereas very few cells differentiated into neurons in NT2 cells expressing M146V mutant PS1 (2.6% of total cells). Tretinoin 17-19 presenilin 1 Homo sapiens 289-292
10208011-8 1999 Excess RA causes abnormalities of many systems; altered susceptibility to RA excess in mice lacking RAR gamma or RXR alpha suggests that the teratogenic signal is transduced through different receptors compared with physiological RA function in the same tissue. Tretinoin 74-76 retinoid X receptor alpha Mus musculus 113-122
10578478-1 1999 N-(4 hydroxyphenyl)retinamide (4-HPR), a synthetic derivative of all-trans-retinoic acid, induces DNA synthesis arrest and apoptosis in human breast cancer cells in a dose- and time-dependent manner. Tretinoin 65-88 haptoglobin-related protein Homo sapiens 33-36
16291826-4 2006 A broad caspase inhibitor (z-VAD-fmk), caspase-9 inhibitor z-LEHD-fmk and caspase-3 inhibitor (z-DEVD-fmk) blocked atRA-induced DNA fragmentation and sub-G1 fraction, but not caspase-8 inhibitor z-IETD-fmk. Tretinoin 115-119 caspase 9 Mus musculus 39-48
9534887-5 1998 In the presence of retinoic acid and 1,25-dihydroxyvitamin D3 SKALP expression was inhibited, whereas supplementation with ascorbic acid and a-tocopherol had no effect. Tretinoin 19-32 peptidase inhibitor 3 Homo sapiens 62-67
9505268-6 1998 In addition, RA inhibited several features of DEX-induced accelerated maturation, such as: 1) the increased levels of SP-A, SP-B, and CC10 mRNAs; 2) the attenuation of mesenchymal tissue; and 3) the mature distribution of cells expressing SP-C mRNA. Tretinoin 13-15 surfactant protein B Rattus norvegicus 124-128
16291826-5 2006 We further showed that atRA dose-dependently promoted mRNA expression of retinoic acid receptor beta (RAR-beta) and gamma. Tretinoin 23-27 retinoic acid receptor, beta Mus musculus 73-100
9852056-0 1998 Arg278, but not Lys229 or Lys236, plays an important role in the binding of retinoic acid by retinoic acid receptor gamma. Tretinoin 76-89 retinoic acid receptor gamma Homo sapiens 93-121
16291826-5 2006 We further showed that atRA dose-dependently promoted mRNA expression of retinoic acid receptor beta (RAR-beta) and gamma. Tretinoin 23-27 retinoic acid receptor, beta Mus musculus 102-110
9852056-5 1998 Like RARalpha but dissimilar to RARbeta, Arg278 in RARgamma alone was found to play an important role in RA binding and RA-dependent transactivation. Tretinoin 5-7 retinoic acid receptor gamma Homo sapiens 51-59
17017122-0 2006 PKCdelta alternatively spliced isoforms modulate cellular apoptosis in retinoic acid-induced differentiation of human NT2 cells and mouse embryonic stem cells. Tretinoin 71-84 protein kinase C delta Homo sapiens 0-8
9488639-8 1998 However, eosinophil-derived neurotoxin and eosinophil cationic protein were not detected or were only detected at a low level in the lysates of the HML cells treated with RA. Tretinoin 171-173 ribonuclease A family member 2 Homo sapiens 9-38
17017122-8 2006 Our results indicate that RA regulates the expression of PKCdelta alternative splicing variants in NT2 cells. Tretinoin 26-28 protein kinase C delta Homo sapiens 57-65
9526050-0 1998 Retinoic acid regulates gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 0-13 retinoic acid induced 1 Mus musculus 128-131
9834237-2 1998 The resulting PML-RAR protein induces a block in the differentiation of the myeloid progenitor cells, which can be released by retinoic acid (RA) in vitro and in vivo. Tretinoin 127-140 PML-RARA regulated adaptor molecule 1 Homo sapiens 14-21
9526050-11 1998 We also showed that GT1-1 cells as well as the hypothalamic tissues express mRNA for multiple subtypes of retinoid receptors, and that reporter plasmids with three copies of the strong retinoic acid response element (RARE) were activated by 80 folds upon treatment with RA in GT1-1 cells, suggesting that retinoid receptors in GT1-1 cells are functional. Tretinoin 185-198 retinoic acid induced 1 Mus musculus 276-279
16837774-7 2006 The results show an increased uptake of atROH in intimal SMCs compared to medial SMCs as well as increased expression of the retinoid-metabolizing enzymes retinol dehydrogenase-5 and retinal dehydrogenase-1 and, in conjunction with this gene expression, increased production of all-trans retinoic acid (atRA). Tretinoin 288-301 retinol dehydrogenase 5 Homo sapiens 155-178
9526050-11 1998 We also showed that GT1-1 cells as well as the hypothalamic tissues express mRNA for multiple subtypes of retinoid receptors, and that reporter plasmids with three copies of the strong retinoic acid response element (RARE) were activated by 80 folds upon treatment with RA in GT1-1 cells, suggesting that retinoid receptors in GT1-1 cells are functional. Tretinoin 185-198 retinoic acid induced 1 Mus musculus 276-279
9526050-11 1998 We also showed that GT1-1 cells as well as the hypothalamic tissues express mRNA for multiple subtypes of retinoid receptors, and that reporter plasmids with three copies of the strong retinoic acid response element (RARE) were activated by 80 folds upon treatment with RA in GT1-1 cells, suggesting that retinoid receptors in GT1-1 cells are functional. Tretinoin 217-219 retinoic acid induced 1 Mus musculus 276-279
9526050-11 1998 We also showed that GT1-1 cells as well as the hypothalamic tissues express mRNA for multiple subtypes of retinoid receptors, and that reporter plasmids with three copies of the strong retinoic acid response element (RARE) were activated by 80 folds upon treatment with RA in GT1-1 cells, suggesting that retinoid receptors in GT1-1 cells are functional. Tretinoin 217-219 retinoic acid induced 1 Mus musculus 276-279
16837774-7 2006 The results show an increased uptake of atROH in intimal SMCs compared to medial SMCs as well as increased expression of the retinoid-metabolizing enzymes retinol dehydrogenase-5 and retinal dehydrogenase-1 and, in conjunction with this gene expression, increased production of all-trans retinoic acid (atRA). Tretinoin 303-307 retinol dehydrogenase 5 Homo sapiens 155-178
9874511-4 1998 Northern analysis showed modulation of the expression of BMP-2 and BMP-4 mRNAs in two human osteosarcoma cell lines, MG63 and Saos-2, by prostaglandin E2 (PGE2), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interferon-alpha (IFN-alpha), retinoic acid and 1,25(OH)2 vitamin D3. Tretinoin 244-257 bone morphogenetic protein 2 Homo sapiens 57-62
9874511-4 1998 Northern analysis showed modulation of the expression of BMP-2 and BMP-4 mRNAs in two human osteosarcoma cell lines, MG63 and Saos-2, by prostaglandin E2 (PGE2), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interferon-alpha (IFN-alpha), retinoic acid and 1,25(OH)2 vitamin D3. Tretinoin 244-257 bone morphogenetic protein 4 Homo sapiens 67-72
17047365-6 2006 We found a common upregulation of ADAM10, APP, and APP-like protein 2 during differentiation of neuronal cells by retinoic acid, and increased alpha-secretase cleavage of the two substrates. Tretinoin 114-127 ADAM metallopeptidase domain 10 Homo sapiens 34-40
9874511-8 1998 IL-6 completely abolished detectable expression of BMP-2 mRNA, which was also greatly reduced by IL-1beta, retinoic acid and 1,25(OH)2 vitamin D3. Tretinoin 107-120 bone morphogenetic protein 2 Homo sapiens 51-56
9889406-4 1998 The two cell lines differ in their sensitivity to the anti-proliferative effects of the different agents and their combination: i) both cell lines were more responsive to IFN-beta than to IFN-alpha2b; ii) combined treatment with RA increases the growth inhibitory effect of the single agents in ME180, but not in SiHa; iii) the antiproliferative effect correlates with the induction of apoptosis. Tretinoin 229-231 interferon beta 1 Homo sapiens 171-179
9541123-4 1998 Similarly, an increase in gp330/megalin mRNA expression was seen in JEG-3 cells cultured with vitamin D and retinoids, as well as when F9 cells were differentiated by incubation with retinoic acid and cAMP. Tretinoin 183-196 LDL receptor related protein 2 Homo sapiens 26-31
9541123-4 1998 Similarly, an increase in gp330/megalin mRNA expression was seen in JEG-3 cells cultured with vitamin D and retinoids, as well as when F9 cells were differentiated by incubation with retinoic acid and cAMP. Tretinoin 183-196 LDL receptor related protein 2 Homo sapiens 32-39
9541123-7 1998 At 41 degrees C, gp330/megalin mRNA expression was significantly increased compared with cells incubated at 34 degrees C. CONCLUSION: The results indicate a correlation between exposure to retinoic acid or vitamin D or induction of cell differentiation (by retinoic acid/cAMP in F9 cells or inhibition of SV40 transcription in IRPTCs) and an increase in gp330/megalin protein and mRNA expression. Tretinoin 189-202 LDL receptor related protein 2 Homo sapiens 17-22
9541123-7 1998 At 41 degrees C, gp330/megalin mRNA expression was significantly increased compared with cells incubated at 34 degrees C. CONCLUSION: The results indicate a correlation between exposure to retinoic acid or vitamin D or induction of cell differentiation (by retinoic acid/cAMP in F9 cells or inhibition of SV40 transcription in IRPTCs) and an increase in gp330/megalin protein and mRNA expression. Tretinoin 189-202 LDL receptor related protein 2 Homo sapiens 23-30
9541123-7 1998 At 41 degrees C, gp330/megalin mRNA expression was significantly increased compared with cells incubated at 34 degrees C. CONCLUSION: The results indicate a correlation between exposure to retinoic acid or vitamin D or induction of cell differentiation (by retinoic acid/cAMP in F9 cells or inhibition of SV40 transcription in IRPTCs) and an increase in gp330/megalin protein and mRNA expression. Tretinoin 189-202 LDL receptor related protein 2 Homo sapiens 354-359
9541123-7 1998 At 41 degrees C, gp330/megalin mRNA expression was significantly increased compared with cells incubated at 34 degrees C. CONCLUSION: The results indicate a correlation between exposure to retinoic acid or vitamin D or induction of cell differentiation (by retinoic acid/cAMP in F9 cells or inhibition of SV40 transcription in IRPTCs) and an increase in gp330/megalin protein and mRNA expression. Tretinoin 189-202 LDL receptor related protein 2 Homo sapiens 360-367
9541123-7 1998 At 41 degrees C, gp330/megalin mRNA expression was significantly increased compared with cells incubated at 34 degrees C. CONCLUSION: The results indicate a correlation between exposure to retinoic acid or vitamin D or induction of cell differentiation (by retinoic acid/cAMP in F9 cells or inhibition of SV40 transcription in IRPTCs) and an increase in gp330/megalin protein and mRNA expression. Tretinoin 257-270 LDL receptor related protein 2 Homo sapiens 17-22
9458362-0 1998 Retinoic acid suppresses insulin-induced cell growth and cyclin D1 gene expression in human breast cancer cells. Tretinoin 0-13 cyclin D1 Homo sapiens 57-66
9819390-8 1998 This result suggests that expression of Aldh1 protein is negatively regulated by Hox11 and that abnormal expression of Aldh1 in Hox11 null mice may cause loss of splenic precursor cells by aberrant retinoic acid metabolism. Tretinoin 198-211 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 119-124
16051641-7 2005 The retinoic acid-induced TrkB expression in parental SH-SY5Y cells was also associated with enhanced cell invasiveness. Tretinoin 4-17 neurotrophic receptor tyrosine kinase 2 Homo sapiens 26-30
9811468-1 1998 Functional nerve growth factor (NGF) responsiveness was investigated in human neuroblastoma (NB) cell lines in vitro and retinoic acid (RA) was found to transcriptionally enhance expression of the trkA, but not the trkB gene in GOTO cells, while the reverse was found in HTLA230 NB cells. Tretinoin 121-134 neurotrophic receptor tyrosine kinase 1 Homo sapiens 197-201
9811468-1 1998 Functional nerve growth factor (NGF) responsiveness was investigated in human neuroblastoma (NB) cell lines in vitro and retinoic acid (RA) was found to transcriptionally enhance expression of the trkA, but not the trkB gene in GOTO cells, while the reverse was found in HTLA230 NB cells. Tretinoin 136-138 neurotrophic receptor tyrosine kinase 1 Homo sapiens 197-201
9458362-1 1998 We examined the effects of all-trans retinoic acid (RA) on the insulin-induced cell growth, cell cycle progression and cyclin D1 gene expression in breast cancer cells. Tretinoin 52-54 cyclin D1 Homo sapiens 119-128
9458362-3 1998 The RA antagonism of insulin growth effect was associated with an inhibition of cell cycle progression and a suppression of insulin-induced cyclin D1 mRNA. Tretinoin 4-6 cyclin D1 Homo sapiens 140-149
9458362-4 1998 The effect of RA on cyclin D1 mRNA was dose-dependent and was observed within 5 h of treatment when insulin response was maximal. Tretinoin 14-16 cyclin D1 Homo sapiens 20-29
9478048-0 1998 Alcohol dehydrogenase as a critical mediator of retinoic acid synthesis from vitamin A in the mouse embryo. Tretinoin 48-61 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 0-21
9478048-6 1998 The spatiotemporal expression patterns of ADH-IV and two forms of ALDH match the spatiotemporal detection of retinoic acid during mouse embryogenesis, i.e., no detection at 6.5 d of embryogenesis (E6.5), followed by detection at E7.5 in the primitive streak, and then detection in numerous tissues later in development. Tretinoin 109-122 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 42-45
9478048-6 1998 The spatiotemporal expression patterns of ADH-IV and two forms of ALDH match the spatiotemporal detection of retinoic acid during mouse embryogenesis, i.e., no detection at 6.5 d of embryogenesis (E6.5), followed by detection at E7.5 in the primitive streak, and then detection in numerous tissues later in development. Tretinoin 109-122 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 66-70
9478048-7 1998 This suggests that certain forms of ADH and ALDH may cooperate to upregulated retinoic acid synthesis during development. Tretinoin 78-91 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 36-39
9811468-1 1998 Functional nerve growth factor (NGF) responsiveness was investigated in human neuroblastoma (NB) cell lines in vitro and retinoic acid (RA) was found to transcriptionally enhance expression of the trkA, but not the trkB gene in GOTO cells, while the reverse was found in HTLA230 NB cells. Tretinoin 136-138 neurotrophic receptor tyrosine kinase 2 Homo sapiens 215-219
16251210-6 2005 RA signaling was found to play a role in regulating the expression of EphB2, EphB3 and ephrin B2, three molecules whose graded expression in the retina along the DV axis is important for establishing the correct retinotectal map. Tretinoin 0-2 EPH receptor B3 Gallus gallus 77-82
9753672-11 1998 Amputations of caudal fins immediately after the first branching point of the lepidotrichia, and global administration of all-trans-retinoic acid, two procedures known to cause fusion of adjacent rays, result in a transient decrease in the expression of shh, ptc1 and bmp2. Tretinoin 122-145 bone morphogenetic protein 2a Danio rerio 268-272
9478048-7 1998 This suggests that certain forms of ADH and ALDH may cooperate to upregulated retinoic acid synthesis during development. Tretinoin 78-91 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 44-48
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 141-154 retinoid X receptor alpha Mus musculus 75-84
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 178-191 retinoid X receptor alpha Mus musculus 75-84
9442090-7 1998 These experiments, as well as others using synthetic receptor subtype-specific retinoids, suggest that the RAR gamma and RXR alpha receptors mediate the effects of retinoic acid on the expression of the P450RAI gene. Tretinoin 164-177 retinoid X receptor alpha Mus musculus 121-130
9772283-3 1998 We have previously demonstrated that both all-trans retinoic acid (ATRA) and interferon a (IFNa) can inhibit proliferation of human PNET cells and that ATRA can up-regulate IFNa receptor expression in vitro. Tretinoin 152-156 interferon alpha 2 Homo sapiens 173-177
16448226-2 2005 Removal of LIF, reduced levels of fetal calf serum (FCS), and addition of retinoic acid all induced embryonic stem cell differentiation as measured by reduced Oct 4 expression. Tretinoin 74-87 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 159-164
9839358-7 1998 The interactions between RA and TGF-beta s were very complex. Tretinoin 25-27 transforming growth factor, beta 1 Mus musculus 32-40
9839358-10 1998 Differential regulation was evident, because RA treatment resulted in an increase in TGF-beta 1 mRNA steady levels followed by a decrease in the intracellular and extracellular forms of TGF-beta 1 protein. Tretinoin 45-47 transforming growth factor, beta 1 Mus musculus 85-95
9839358-10 1998 Differential regulation was evident, because RA treatment resulted in an increase in TGF-beta 1 mRNA steady levels followed by a decrease in the intracellular and extracellular forms of TGF-beta 1 protein. Tretinoin 45-47 transforming growth factor, beta 1 Mus musculus 186-196
9839358-12 1998 The increases in mRNA steady-state levels for TGF-beta 2 and TGF-beta 3, as for TGF-beta 1, were rapid and transient in nature, again arguing for direct mediation by RA. Tretinoin 166-168 transforming growth factor, beta 1 Mus musculus 80-90
9473674-6 1998 Treatment of SCG neurons with retinoic acid (RA) promoted the effect of BMP2 on the induction of trkC mRNA levels. Tretinoin 30-43 bone morphogenetic protein 2 Rattus norvegicus 72-76
9473674-6 1998 Treatment of SCG neurons with retinoic acid (RA) promoted the effect of BMP2 on the induction of trkC mRNA levels. Tretinoin 45-47 bone morphogenetic protein 2 Rattus norvegicus 72-76
9473674-7 1998 BMP2 treatment, on the other hand, promoted the effect of RA on the suppressions of trkA mRNA levels and the NGF-dependent survival of the SCG neurons. Tretinoin 58-60 bone morphogenetic protein 2 Rattus norvegicus 0-4
16316409-8 2005 As CRABPI was elevated far more than any other genes, we observed that the retinoids, all-trans retinoic acid and 9-cis retinoic acid, that bind CRABPI, promoted nitroblue tetrazolium-associated functional cell differentiation in p75NTR PC-3 cells, but not in neo control PC-3 cells. Tretinoin 96-109 cellular retinoic acid binding protein 1 Homo sapiens 145-151
9791009-5 1998 All-trans (ATRA) and 9-cis retinoic acid (9cRA) reduce c-erbB-1 protein to 50-100%, c-erbB-2 to 20-30%, and c-erbB-3 to 10-50% of control, depending on the concentration, respectively, without influencing the tyrosine phosphorylation status. Tretinoin 11-15 erb-b2 receptor tyrosine kinase 3 Homo sapiens 108-116
9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 cyclin dependent kinase 2 Homo sapiens 146-150
9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 cyclin dependent kinase 2 Homo sapiens 152-156
9693177-8 1998 Inversely, treatment with retinoic acid, which inhibits cell differentiation, increased the level of MMP-2. Tretinoin 26-39 matrix metallopeptidase 2 Homo sapiens 101-106
16142401-6 2005 RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. Tretinoin 97-101 retinoic acid receptor gamma Homo sapiens 14-23
9397150-7 1998 A similar pattern was observed for TGase protein, but, RA, which, by itself, reduced INV, markedly enhanced the ability of 1,25(OH)2D3 to raise INV levels, possibly by inhibiting 1,25(OH)2D3-stimulated TGase activity and cross-linking of soluble INV into the insoluble cornified envelope (CE). Tretinoin 55-57 transglutaminase 1 Homo sapiens 202-207
9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 cyclin dependent kinase 4 Homo sapiens 158-162
9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 RB transcriptional corepressor 1 Homo sapiens 222-225
9778049-5 1998 In addition, RA-treated LCLs showed a marked up-regulation of the CDK inhibitor (CKI) p27Kip-1 at the protein but not mRNA level, which correlated with a progressive increase of p27Kip-1 in CDK2 complexes (more than 2.5-fold) and with a reduction in the active phosphorylated form of CDK2. Tretinoin 13-15 cyclin dependent kinase 2 Homo sapiens 190-194
16166633-6 2005 Loss of repression of ES cell marker genes Oct4, Nanog, Sox2, FGF4, and Stella was observed upon treatment of GCNF-/- ES cells with retinoic acid. Tretinoin 132-145 nuclear receptor subfamily 6, group A, member 1 Mus musculus 110-114
9778049-5 1998 In addition, RA-treated LCLs showed a marked up-regulation of the CDK inhibitor (CKI) p27Kip-1 at the protein but not mRNA level, which correlated with a progressive increase of p27Kip-1 in CDK2 complexes (more than 2.5-fold) and with a reduction in the active phosphorylated form of CDK2. Tretinoin 13-15 cyclin dependent kinase 2 Homo sapiens 284-288
9778049-6 1998 p27Kip-1 may also contribute to the inhibition of CDK4 kinase activity, as the amount of CDK4-associated p27Kip-1 was increased by 50% after RA exposure. Tretinoin 141-143 cyclin dependent kinase 4 Homo sapiens 50-54
9778049-6 1998 p27Kip-1 may also contribute to the inhibition of CDK4 kinase activity, as the amount of CDK4-associated p27Kip-1 was increased by 50% after RA exposure. Tretinoin 141-143 cyclin dependent kinase 4 Homo sapiens 89-93
9508341-0 1998 Topical tretinoin replenishes CD1a-positive epidermal Langerhans cells in chronically photodamaged human skin. Tretinoin 8-17 CD1a molecule Homo sapiens 30-34
9778049-9 1998 Overall, these results demonstrate that RA treatment of EBV-immortalized B lymphocytes is associated with multiple effects on G1 regulatory proteins, including p27Kip1 up-regulation, decreased levels of cyclins D2, D3 and A, and inhibition of CDK2, CDK4 and CDK6 activity, which ultimately result in reduced pRb phosphorylation and G0/G1 growth arrest. Tretinoin 40-42 cyclin dependent kinase 2 Homo sapiens 243-247
9778049-9 1998 Overall, these results demonstrate that RA treatment of EBV-immortalized B lymphocytes is associated with multiple effects on G1 regulatory proteins, including p27Kip1 up-regulation, decreased levels of cyclins D2, D3 and A, and inhibition of CDK2, CDK4 and CDK6 activity, which ultimately result in reduced pRb phosphorylation and G0/G1 growth arrest. Tretinoin 40-42 cyclin dependent kinase 4 Homo sapiens 249-253
9778049-9 1998 Overall, these results demonstrate that RA treatment of EBV-immortalized B lymphocytes is associated with multiple effects on G1 regulatory proteins, including p27Kip1 up-regulation, decreased levels of cyclins D2, D3 and A, and inhibition of CDK2, CDK4 and CDK6 activity, which ultimately result in reduced pRb phosphorylation and G0/G1 growth arrest. Tretinoin 40-42 RB transcriptional corepressor 1 Homo sapiens 308-311
9417809-4 1997 Transient transfection analyses using deletion mutants lacking both the 11-bp core NRE and both the NRE and an adjacent putative retinoic acid response element (RARE) motif illustrated that the NRE element is a functional suppressor of CD25 transcription in B cells. Tretinoin 129-142 interleukin 2 receptor subunit alpha Homo sapiens 236-240
16166633-10 2005 These findings establish a central role for GCNF in the repression of pluripotency gene expression during retinoic acid-induced ES cell differentiation. Tretinoin 106-119 nuclear receptor subfamily 6, group A, member 1 Mus musculus 44-48
9447831-7 1997 Addition of ATRA induced the progressive expression and accumulation of p22phox, p91phox, p47phox and p67phox. Tretinoin 12-16 neutrophil cytosolic factor 2 Homo sapiens 102-109
16277846-2 2005 By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively. Tretinoin 111-115 alanyl aminopeptidase, membrane Homo sapiens 29-33
9892899-10 1998 Immunohistochemically, both RA and SDS were shown to reduce epidermal staining for desmoplakin, desmoglein 1, plakophilin 1 and desmocollin 3 equally compared with vehicle-treated skin (P < 0.001). Tretinoin 28-30 desmocollin 3 Homo sapiens 128-141
16277846-2 2005 By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively. Tretinoin 111-115 CD14 molecule Homo sapiens 35-39
16007204-0 2005 Synergistic induction of the MUC4 mucin gene by interferon-gamma and retinoic acid in human pancreatic tumour cells involves a reprogramming of signalling pathways. Tretinoin 69-82 mucin 4, cell surface associated Homo sapiens 29-33
10100049-11 1998 These findings indicate that the induction of RAR beta mRNA in the fetal palate correlates well with the tissue concentration of all-trans RA after RA treatment, and RAR beta may be one of the most influential candidate molecules for RA-induced teratogenesis. Tretinoin 139-141 retinoic acid receptor, beta Mus musculus 46-54
9789841-0 1998 Influence of retinoic acid and of cyclic AMP on the expression of choline acetyltransferase and of vesicular acetylcholine transporter in NG108-15 cells. Tretinoin 13-26 choline acetyltransferase Mus musculus 66-91
9348290-2 1997 RXRalpha-/-/ RARalpha-/- cells were resistant to retinoic acid treatment for the induction of primitive and parietal endodermal differentiation, as well as for antiproliferative and apoptotic responses, whereas they could differentiate into visceral endodermlike cells, as previously observed for RXRalpha-/- cells. Tretinoin 49-62 retinoid X receptor alpha Mus musculus 0-8
9395064-4 1997 The results demonstrated that among several PTP genes expressed in P19 cells, a cytosolic Src homology region 2 domain-containing PTP, SHP-1, is expressed highly in undifferentiated P19 cells, but is reduced to an undetectable level at day 3 after replating in the presence of RA. Tretinoin 277-279 protein tyrosine phosphatase, non-receptor type 6 Mus musculus 135-140
9395064-6 1997 When ectopic SHP-1 was constitutively expressed, P19 cells continued to proliferate and failed to differentiate upon stimulation with RA. Tretinoin 134-136 protein tyrosine phosphatase, non-receptor type 6 Mus musculus 13-18
9334271-3 1997 Accordingly, Hoxb-8 expression is rapidly induced by retinoic acid (RA) treatment in the anterior of the forelimb in a spatial and temporal manner that is consistent with the induction of Shh and formation of the ZPA. Tretinoin 68-70 sonic hedgehog Gallus gallus 188-191
9334271-4 1997 Furthermore, inhibition of RA synthesis in the flank downregulates the expression of endogenous Hoxb-8 and results in the loss of Shh expression. Tretinoin 27-29 sonic hedgehog Gallus gallus 130-133
9789841-1 1998 Treatment of the cholinergic cell line NG108-15 with retinoic acid or cAMP results in an increase of choline acetyltransferase activity (ChAT) whereas none of these agents influences the amount of the vesicular acetylcholine transporter (VAChT) as judged from vesamicol binding and immunoblot studies. Tretinoin 53-66 choline acetyltransferase Mus musculus 101-126
9716600-0 1998 Retinoic acid inhibits CD40 + interleukin-4-mediated IgE production in vitro. Tretinoin 0-13 CD40 molecule Homo sapiens 23-27
16007204-0 2005 Synergistic induction of the MUC4 mucin gene by interferon-gamma and retinoic acid in human pancreatic tumour cells involves a reprogramming of signalling pathways. Tretinoin 69-82 LOC100508689 Homo sapiens 34-39
9716600-2 1998 Anti-CD40 + IL-4-mediated proliferation of PBMC and B cells was inhibited by RA in a dose-dependent manner, with maximal inhibition of 62% +/- 5% in PBMC and 55% +/- 4.4% in B cells by all-trans RA, and 58% +/- 6.7% and 51% +/- 4.7%, respectively by 13-cis RA. Tretinoin 77-79 CD40 molecule Homo sapiens 5-9
9716600-2 1998 Anti-CD40 + IL-4-mediated proliferation of PBMC and B cells was inhibited by RA in a dose-dependent manner, with maximal inhibition of 62% +/- 5% in PBMC and 55% +/- 4.4% in B cells by all-trans RA, and 58% +/- 6.7% and 51% +/- 4.7%, respectively by 13-cis RA. Tretinoin 195-197 CD40 molecule Homo sapiens 5-9
9395333-3 1997 NCNF is exclusively expressed in the neuronal derivatives of PCC7-Mz1 cells, with the expression beginning within hours of exposure to retinoic acid. Tretinoin 135-148 nuclear receptor subfamily 6, group A, member 1 Mus musculus 0-4
16007204-2 2005 Our recent studies have shown that interferon-gamma (IFNgamma) and retinoic acid (RA) are important regulators of MUC4 in pancreatic tumour cells. Tretinoin 67-80 mucin 4, cell surface associated Homo sapiens 114-118
9716600-10 1998 Taken together, this study shows that RA inhibits IgE production of anti-CD40 + IL-4-stimulated B cells in vitro. Tretinoin 38-40 CD40 molecule Homo sapiens 73-77
16007204-2 2005 Our recent studies have shown that interferon-gamma (IFNgamma) and retinoic acid (RA) are important regulators of MUC4 in pancreatic tumour cells. Tretinoin 82-84 mucin 4, cell surface associated Homo sapiens 114-118
15972296-7 2005 Finally, we identified vitamin A acid (RA) as an inducer of human ADAM10 promoter activity. Tretinoin 23-37 ADAM metallopeptidase domain 10 Homo sapiens 66-72
9737723-1 1998 The nuclear receptors for thyroid hormone (TRs) and retinoic acid (RARs and RXRs) cooperate with the pituitary-specific transcription factor GHF-1 to activate the rat growth hormone (GH) gene. Tretinoin 52-65 gonadotropin releasing hormone receptor Rattus norvegicus 167-181
9737723-1 1998 The nuclear receptors for thyroid hormone (TRs) and retinoic acid (RARs and RXRs) cooperate with the pituitary-specific transcription factor GHF-1 to activate the rat growth hormone (GH) gene. Tretinoin 52-65 gonadotropin releasing hormone receptor Rattus norvegicus 141-143
9699509-4 1998 RA increased the numbers of high- and low-affinity binding sites for 125I-TGF-beta1 2.1-fold and 1.5-fold, respectively, without alteration of their Kd values. Tretinoin 0-2 transforming growth factor beta 1 Bos taurus 74-83
9699509-8 1998 Pretreatment of BAECs with either RA or retinol lowered the concentration of TGF-beta1 required to suppress PA levels, to enhance PAI-1 levels, and to inhibit cell proliferation. Tretinoin 34-36 transforming growth factor beta 1 Bos taurus 77-86
9699509-8 1998 Pretreatment of BAECs with either RA or retinol lowered the concentration of TGF-beta1 required to suppress PA levels, to enhance PAI-1 levels, and to inhibit cell proliferation. Tretinoin 34-36 serpin family E member 1 Bos taurus 130-135
9699512-5 1998 We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all-trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RAR alpha and RXR alpha. Tretinoin 109-111 glycoprotein hormones, alpha polypeptide Homo sapiens 54-57
9550098-6 1997 Since these enzymes (EROD, CYP 1A1/2 and PROD, CYP2B1) activate polycyclic hydrocarbons, aromatic amines and aliphatic halogenated hydrocarbons to their ultimate mutagenic or carcinogenic forms, and are effective in producing reactive oxygen species such as superoxide, hydroxyl radical and hydrogen peroxide, the new compound, BITN, appears to have a greater anticarcinogenic and antioxidant potential than RA and BHT. Tretinoin 408-410 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 47-53
9366521-3 1997 RA-induced cell cycle arrest is also associated with induction of p27Kip1 expression, inhibition of cdk2-associated kinase activity and alteration of the phosphorylation state of the pRB-family proteins. Tretinoin 0-2 cyclin dependent kinase 2 Homo sapiens 100-104
9357979-0 1997 Distinct patterns of all-trans retinoic acid dependent expression of HOXB and HOXC homeogenes in human embryonal and small-cell lung carcinoma cell lines. Tretinoin 31-44 homeobox B cluster Homo sapiens 69-73
9357979-1 1997 The expression patterns of the class I homeogenes HOXB and HOXC clusters in the presence of retinoic acid (RA) were studied in two human small-cell lung cancer (SCLC) cell lines and compared to that of NT2/D1 embryonal carcinoma cells. Tretinoin 92-105 homeobox B cluster Homo sapiens 50-54
9357979-1 1997 The expression patterns of the class I homeogenes HOXB and HOXC clusters in the presence of retinoic acid (RA) were studied in two human small-cell lung cancer (SCLC) cell lines and compared to that of NT2/D1 embryonal carcinoma cells. Tretinoin 107-109 homeobox B cluster Homo sapiens 50-54
9370300-6 1997 Expression of st-ob in C3H10T1/2 cells was increased by transforming growth factor-beta1 (TGF-beta1), retinoic acid and dexamethasone as well as BMP-2. Tretinoin 102-115 solute carrier family 26 (sulfate transporter), member 2 Mus musculus 14-19
9891902-9 1998 Tretinoin very potently stimulated IL-5 release, and inhibited IFN gamma release by SEB-stimulated human PBMCs. Tretinoin 0-9 interleukin 5 Homo sapiens 35-39
9891902-9 1998 Tretinoin very potently stimulated IL-5 release, and inhibited IFN gamma release by SEB-stimulated human PBMCs. Tretinoin 0-9 SET binding protein 1 Homo sapiens 84-87
15933212-2 2005 CYP2C8 is an important member of the CYP2C subfamily, which metabolizes both endogenous compounds (i.e., arachidonic acids and retinoic acid) and xenobiotics (e.g., paclitaxel). Tretinoin 127-140 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6
9806360-9 1998 Overexpression of cyclin D3 blocks the RA-induced growth arrest of F9 cells, indicating that the downregulation of this gene following RA treatment may constitute a necessary step in the cascade of events leading to growth inhibition by RA. Tretinoin 39-41 cyclin D3 Mus musculus 18-27
9390004-8 1997 It was concluded that RA had a suppressive effect on CRABP-I gene expression in embryos and P19 cells and the effect could be mediated through RAR beta, RAR gamma or RXR alpha. Tretinoin 22-24 retinoic acid receptor, beta Mus musculus 143-151
9390004-8 1997 It was concluded that RA had a suppressive effect on CRABP-I gene expression in embryos and P19 cells and the effect could be mediated through RAR beta, RAR gamma or RXR alpha. Tretinoin 22-24 retinoid X receptor alpha Mus musculus 166-175
9305907-0 1997 Galpha12 and Galpha13 mediate differentiation of P19 mouse embryonal carcinoma cells in response to retinoic acid. Tretinoin 100-113 interleukin 23, alpha subunit p19 Mus musculus 49-52
9806360-9 1998 Overexpression of cyclin D3 blocks the RA-induced growth arrest of F9 cells, indicating that the downregulation of this gene following RA treatment may constitute a necessary step in the cascade of events leading to growth inhibition by RA. Tretinoin 135-137 cyclin D3 Mus musculus 18-27
16086018-4 2005 Additionally, bone marrow from C57BL/6 mice transgenic for retinoic acid early inducible 1epsilon was rejected by syngeneic mice but was accepted after treatment with antibody to NKG2D. Tretinoin 59-72 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 179-184
9806360-9 1998 Overexpression of cyclin D3 blocks the RA-induced growth arrest of F9 cells, indicating that the downregulation of this gene following RA treatment may constitute a necessary step in the cascade of events leading to growth inhibition by RA. Tretinoin 135-137 cyclin D3 Mus musculus 18-27
9305907-2 1997 At low concentrations, retinoic acid stimulates P19 embryonal cells to differentiate to cells displaying an endodermal phenotype, whereas at higher concentrations it stimulates differentiation to neuroectoderm. Tretinoin 23-36 interleukin 23, alpha subunit p19 Mus musculus 48-51
16026781-0 2005 Dorsal pancreas agenesis in retinoic acid-deficient Raldh2 mutant mice. Tretinoin 28-41 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 52-58
9294605-1 1997 To investigate whether MAZ (Myc-associated zinc finger protein) affects the expression of the c-myc gene during the retinoic acid-induced (RA-induced) neuroectodermal differentiation of P19 embryonal carcinoma (EC) cells, we introduced a CAT reporter construct, human c-myc promoter/CAT (pMyc2CAT), and a mutant CAT derivative that lacked an ME1a1 site (pMyc1CAT) into P19EC cells to monitor the promoter activity of the c-myc gene. Tretinoin 116-129 MYC associated zinc finger protein Homo sapiens 23-26
9677409-13 1998 RoDH-4 can potentially contribute to the biosynthesis of two powerful modulators of gene expression: retinoic acid from retinol and dihydrotestosterone from 3alpha-androstane-diol. Tretinoin 101-114 retinol dehydrogenase 16 Homo sapiens 0-6
16026781-12 2005 Maternal supplementation of RA rescues early dorsal pancreas development and restores endodermal Pdx 1 and mesenchymal Isl 1 expression as well as endocrine cell differentiation. Tretinoin 28-30 pancreatic and duodenal homeobox 1 Mus musculus 97-102
22358769-5 1997 Following retinoic acid treatment, RAd35 infected cell lines ND7/23, NG108 and NTera2, showed beta-galactosidase expression in up to 90% of the cells. Tretinoin 10-23 galactosidase beta 1 Homo sapiens 94-112
16026781-14 2005 We conclude that RA synthesized in the mesenchyme is specifically required for the normal development of the dorsal pancreatic endoderm at a stage preceding Pdx 1 function. Tretinoin 17-19 pancreatic and duodenal homeobox 1 Mus musculus 157-162
9579574-4 1998 Electrophoretic mobility shift and super-shift assays using a DR2 ("direct repeat" 2) RA response element demonstrated DNA-binding of RARalpha, RARgamma, RXRalpha and RXRbeta in nuclear extracts of FTC-133 and anaplastic HTh74 cells. Tretinoin 86-88 retinoic acid receptor gamma Homo sapiens 144-152
9579574-4 1998 Electrophoretic mobility shift and super-shift assays using a DR2 ("direct repeat" 2) RA response element demonstrated DNA-binding of RARalpha, RARgamma, RXRalpha and RXRbeta in nuclear extracts of FTC-133 and anaplastic HTh74 cells. Tretinoin 86-88 retinoid X receptor beta Homo sapiens 167-174
9260897-2 1997 RA did not affect cyclins D1, A, and E and cyclin-dependent kinase 2 (CDK2) expression, but significantly reduced cyclin D3 and CDK4 expression after 24 h. RA also inhibited cyclin B1 and CDC2 expression, possibly responsible for the reduction of the proportion of cells in G2 + M and S phases. Tretinoin 0-2 cyclin dependent kinase 4 Homo sapiens 128-132
9259311-0 1997 CDK2 is a target for retinoic acid-mediated growth inhibition in MCF-7 human breast cancer cells. Tretinoin 21-34 cyclin dependent kinase 2 Homo sapiens 0-4
15977162-7 2005 Simultaneous treatment of embryos with retinoic acid and puromycin revealed a few direct targets, including genes encoding Ci-Hox1, Ci-Cyp26, and an Rnf126-like ring finger protein. Tretinoin 39-52 homeobox transcription factor Hox1 Ciona intestinalis 123-130
9259311-3 1997 Flow cytometry analysis of MCF-7 cells treated with RA revealed a decrease in the percentage of cells in S phase by 48 h, which was maximal by 72 h. Phosphorylation of the retinoblastoma protein (pRb) was partially reduced in RA-treated cells accompanied by a decrease in the level of retinoblastoma protein. Tretinoin 52-54 RB transcriptional corepressor 1 Homo sapiens 196-199
9259311-3 1997 Flow cytometry analysis of MCF-7 cells treated with RA revealed a decrease in the percentage of cells in S phase by 48 h, which was maximal by 72 h. Phosphorylation of the retinoblastoma protein (pRb) was partially reduced in RA-treated cells accompanied by a decrease in the level of retinoblastoma protein. Tretinoin 226-228 RB transcriptional corepressor 1 Homo sapiens 196-199
9259311-6 1997 While cdk4 activity was similar in control and RA-treated cells, cdk2 activity began to decrease within 48 h of exposure to RA and was profoundly reduced after 72 h. This reduced activity was associated with decreased phosphorylation of cdk2. Tretinoin 47-49 cyclin dependent kinase 4 Homo sapiens 6-10
9259311-6 1997 While cdk4 activity was similar in control and RA-treated cells, cdk2 activity began to decrease within 48 h of exposure to RA and was profoundly reduced after 72 h. This reduced activity was associated with decreased phosphorylation of cdk2. Tretinoin 47-49 cyclin dependent kinase 2 Homo sapiens 65-69
9259311-6 1997 While cdk4 activity was similar in control and RA-treated cells, cdk2 activity began to decrease within 48 h of exposure to RA and was profoundly reduced after 72 h. This reduced activity was associated with decreased phosphorylation of cdk2. Tretinoin 47-49 cyclin dependent kinase 2 Homo sapiens 237-241
9259311-6 1997 While cdk4 activity was similar in control and RA-treated cells, cdk2 activity began to decrease within 48 h of exposure to RA and was profoundly reduced after 72 h. This reduced activity was associated with decreased phosphorylation of cdk2. Tretinoin 124-126 cyclin dependent kinase 2 Homo sapiens 65-69
9259311-8 1997 However, assays of cdk2 from pooled lysates from RA-treated and control cells showed that RA-treated cells contain a cdk2-inhibitory activity. Tretinoin 49-51 cyclin dependent kinase 2 Homo sapiens 19-23
9560322-0 1998 Synergistic transcriptional activation of the mouse urokinase plasminogen activator (uPA) gene and of its enhancer activator protein 1 (AP1) site by cAMP and retinoic acid. Tretinoin 158-171 jun proto-oncogene Mus musculus 115-134
9560322-0 1998 Synergistic transcriptional activation of the mouse urokinase plasminogen activator (uPA) gene and of its enhancer activator protein 1 (AP1) site by cAMP and retinoic acid. Tretinoin 158-171 jun proto-oncogene Mus musculus 136-139
9659286-0 1998 Differential effects of retinoic acid on uncoupling protein-1 and leptin gene expression. Tretinoin 24-37 leptin Rattus norvegicus 66-72
15914525-15 2005 CONCLUSIONS: Differential responses to retinol and retinoids in normal and PCOS theca suggest that altered retinoic acid synthesis and action may be involved in augmented CYP17 gene expression and androgen production in PCOS. Tretinoin 107-120 cytochrome P450 family 17 subfamily A member 1 Homo sapiens 171-176
9575874-2 1998 We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line. Tretinoin 49-68 surfactant protein A1 Homo sapiens 77-81
9575874-2 1998 We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line. Tretinoin 49-68 surfactant protein B Homo sapiens 86-90
9575874-2 1998 We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line. Tretinoin 70-72 surfactant protein A1 Homo sapiens 77-81
9575874-2 1998 We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line. Tretinoin 70-72 surfactant protein B Homo sapiens 86-90
9575874-5 1998 RA alone and the combination of cortisol and RA both significantly increased SP-B mRNA levels. Tretinoin 0-2 surfactant protein B Homo sapiens 77-81
9575874-10 1998 We conclude that RA has no effect on SP-A gene expression and increases SP-B mRNA levels by an effect on SP-B mRNA stability and not on the rate of SP-B gene transcription. Tretinoin 17-19 surfactant protein B Homo sapiens 72-76
9352625-3 1997 Retinoic acid (RA-, 1 microM)-treatment and aggregation for 4 days induced and greatly increased MASH-1, neuroD and NSCL-2 mRNA in P19 cells. Tretinoin 0-13 neurogenic differentiation 1 Mus musculus 105-111
9352625-3 1997 Retinoic acid (RA-, 1 microM)-treatment and aggregation for 4 days induced and greatly increased MASH-1, neuroD and NSCL-2 mRNA in P19 cells. Tretinoin 0-13 nescient helix loop helix 2 Mus musculus 116-122
9228041-6 1997 CYP26 is highly homologous to a Zebrafish gene, CYPRA1, which has been proposed to participate in the degradation of RA, but is minimally homologous to other mammalian cytochrome P450 proteins. Tretinoin 51-53 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 0-5
9575874-10 1998 We conclude that RA has no effect on SP-A gene expression and increases SP-B mRNA levels by an effect on SP-B mRNA stability and not on the rate of SP-B gene transcription. Tretinoin 17-19 surfactant protein B Homo sapiens 105-109
9575874-10 1998 We conclude that RA has no effect on SP-A gene expression and increases SP-B mRNA levels by an effect on SP-B mRNA stability and not on the rate of SP-B gene transcription. Tretinoin 17-19 surfactant protein B Homo sapiens 105-109
16024653-2 2005 We reported previously that all-trans-retinoic acid chemo-prevented carcinogenic transformation of human bronchial epithelial (HBE) cells through proteasomal degradation of cyclin D1. Tretinoin 28-51 cyclin D1 Homo sapiens 173-182
16024653-5 2005 Retinoic acid decreased cyclin D1 and cyclin D3 protein expression. Tretinoin 0-13 cyclin D1 Homo sapiens 24-33
16024653-9 2005 Lithium chloride and SB216763, both glycogen synthase kinase 3 (GSK3) inhibitors, inhibited retinoic acid repression of cyclin D1, but not cyclin D3 proteins. Tretinoin 92-105 cyclin D1 Homo sapiens 120-129
16024653-11 2005 Expression of cyclin D1 and cyclin D3 was deregulated in retinoic acid-resistant HBE cells, directly implicating these species in retinoic acid response. Tretinoin 57-70 cyclin D1 Homo sapiens 14-23
9582431-5 1998 However, at later ages, when in vivo levels of Brn3b mRNA are high, FGF2, TGFbeta1 and retinoic acid all up-regulate Brn3b mRNA expression in cultured trigeminal neurons. Tretinoin 87-100 POU domain, class 4, transcription factor 2 Mus musculus 117-122
9582431-7 1998 Similarly, Brn3b may mediate some of the effects that FGF2, TGFbeta1 and retinoic acid have on neurons. Tretinoin 73-86 POU domain, class 4, transcription factor 2 Mus musculus 11-16
9224784-2 1997 UGT1.1 glucuronidation activity was 91 +/- 18 pmol/mg x min for atRA and 113 +/- 19 pmol/mg x min for 5,6-epoxy-atRA. Tretinoin 64-68 UDP glucuronosyltransferase family 1 member A1 Rattus norvegicus 0-6
9224784-4 1997 SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells. Tretinoin 109-113 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 38-41
9224784-4 1997 SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells. Tretinoin 181-185 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 38-41
9224784-5 1997 Liver microsomes from Gunn rats, which lack UGT1.1, had significant activity toward atRA (111 +/- 28 pmol/mg x min). Tretinoin 84-88 UDP glucuronosyltransferase family 1 member A1 Rattus norvegicus 44-50
9514867-7 1998 Treatment of activated stellate cells with either 1 microM retionic acid or 10 microM retinol acetate resulted in the inhibition of leptin mRNA expression. Tretinoin 59-72 leptin Rattus norvegicus 132-138
16024653-11 2005 Expression of cyclin D1 and cyclin D3 was deregulated in retinoic acid-resistant HBE cells, directly implicating these species in retinoic acid response. Tretinoin 130-143 cyclin D1 Homo sapiens 14-23
16024653-15 2005 Thus, retinoic acid repressed cyclin D1 and cyclin D3 through distinct mechanisms. Tretinoin 6-19 cyclin D1 Homo sapiens 30-39
15811935-3 2005 OBJECTIVE: In this study, we investigated the ability of the retinoid, all-trans-retinoic acid (RA), to regulate Cx43 expression in human endometrial stromal cells. Tretinoin 71-94 gap junction protein alpha 1 Homo sapiens 113-117
9211986-7 1997 Connexin43 mRNA was expressed at high levels in NT2/D1 cells before RA treatment, but it decreased significantly during RA induction. Tretinoin 68-70 gap junction protein alpha 1 Homo sapiens 0-10
9625433-3 1998 There is clinical evidence that both IFN-alpha2a-all-trans retinoic acid (ATRA) and IFN-alpha2a-cisplatin have significant activities on growth of malignant cells, cell differentiation or programmed cell death in solid tumors. Tretinoin 52-72 interferon alpha 2 Homo sapiens 37-47
15811935-3 2005 OBJECTIVE: In this study, we investigated the ability of the retinoid, all-trans-retinoic acid (RA), to regulate Cx43 expression in human endometrial stromal cells. Tretinoin 96-98 gap junction protein alpha 1 Homo sapiens 113-117
9625433-3 1998 There is clinical evidence that both IFN-alpha2a-all-trans retinoic acid (ATRA) and IFN-alpha2a-cisplatin have significant activities on growth of malignant cells, cell differentiation or programmed cell death in solid tumors. Tretinoin 74-78 interferon alpha 2 Homo sapiens 37-47
9211986-12 1997 However, we detected connexin43 immunoreactivity in NT2/D1 cells with a decreasing pattern upon RA induction. Tretinoin 96-98 gap junction protein alpha 1 Homo sapiens 21-31
9256344-7 1997 Treatment of Gata4 -/- embryoid bodies with retinoic acid induces expression of another GATA-binding protein, GATA-6, in both visceral and parietal endoderm cells. Tretinoin 44-57 GATA binding protein 6 Mus musculus 110-116
9625433-8 1998 We observed a potentiation after pretreatment with ATRA followed by IFN-alpha2a and ATRA or after pretreatment with IFN-alpha2a followed by IFN-alpha2a and cisplatin. Tretinoin 51-55 interferon alpha 2 Homo sapiens 68-78
15811935-4 2005 DESIGN: Primary endometrial stromal cells obtained from patients undegoing surgery for infertility workup were treated in vitro with RA and control compounds for different time periods, up to 48 h. Cx43 mRNA and protein levels, protein phosphorylation, and gap junctional intercellular communication (GJIC) were analyzed. Tretinoin 133-135 gap junction protein alpha 1 Homo sapiens 198-202
15811935-5 2005 RESULTS: Treatment of the cells with RA showed a dose-dependent increase in Cx43 expression at both the mRNA and protein levels. Tretinoin 37-39 gap junction protein alpha 1 Homo sapiens 76-80
15811935-6 2005 In addition, RA induced a relative decrease in the phosphorylated species of Cx43 while causing a corresponding increase in the nonphosphorylated form. Tretinoin 13-15 gap junction protein alpha 1 Homo sapiens 77-81
15811935-8 2005 Augmentation of GJIC and alterations of Cx43 expression were observed over the same range of RA concentrations. Tretinoin 93-95 gap junction protein alpha 1 Homo sapiens 40-44
9506453-0 1998 Retinoic acid receptor-gamma in human epidermis preferentially traps all-trans retinoic acid as its ligand rather than 9-cis retinoic acid. Tretinoin 79-92 retinoic acid receptor gamma Homo sapiens 0-28
15872003-7 2005 Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. Tretinoin 75-77 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 26-32
9207247-2 1997 When HL-60 cells undergo terminal myeloid differentiation in the presence of ATRA, the beta2 isoform appeared inside nuclei and was up-regulated until 72 hours of ATRA treatment. Tretinoin 77-81 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 87-92
9207247-2 1997 When HL-60 cells undergo terminal myeloid differentiation in the presence of ATRA, the beta2 isoform appeared inside nuclei and was up-regulated until 72 hours of ATRA treatment. Tretinoin 163-167 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 87-92
15872003-7 2005 Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. Tretinoin 130-132 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 26-32
15872003-7 2005 Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. Tretinoin 130-132 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 26-32
9484783-0 1998 Down-regulation of nucleophosmin/B23 during retinoic acid-induced differentiation of human promyelocytic leukemia HL-60 cells. Tretinoin 44-57 nucleophosmin 1 Homo sapiens 19-32
15744343-0 2005 ID1 and ID2 are retinoic acid responsive genes and induce a G0/G1 accumulation in acute promyelocytic leukemia cells. Tretinoin 16-29 inhibitor of DNA binding 1, HLH protein Homo sapiens 0-3
9484783-0 1998 Down-regulation of nucleophosmin/B23 during retinoic acid-induced differentiation of human promyelocytic leukemia HL-60 cells. Tretinoin 44-57 nucleophosmin 1 Homo sapiens 33-36
9484783-6 1998 The decrease in nucleophosmin/B23 mRNA expression in HL-60 cells subsequent to retinoic acid treatment can thus be attributed to cellular differentiation rather than the growth arrest induced by RA. Tretinoin 79-92 nucleophosmin 1 Homo sapiens 16-29
9484783-6 1998 The decrease in nucleophosmin/B23 mRNA expression in HL-60 cells subsequent to retinoic acid treatment can thus be attributed to cellular differentiation rather than the growth arrest induced by RA. Tretinoin 79-92 nucleophosmin 1 Homo sapiens 30-33
9473310-0 1998 Human MDR1 and mouse mdr1a P-glycoprotein alter the cellular retention and disposition of erythromycin, but not of retinoic acid or benzo(a)pyrene. Tretinoin 115-128 ATP-binding cassette, sub-family B (MDR/TAP), member 1A Mus musculus 21-26
9436983-0 1998 p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells. Tretinoin 66-79 E1A binding protein p300 Homo sapiens 0-4
9191094-2 1997 In catecholaminergic cells, the expression of TH-mRNA is up-regulated by forskolin (FK) and is suppressed by retinoic acid (RA). Tretinoin 109-122 tyrosine hydroxylase Rattus norvegicus 46-48
9191094-2 1997 In catecholaminergic cells, the expression of TH-mRNA is up-regulated by forskolin (FK) and is suppressed by retinoic acid (RA). Tretinoin 124-126 tyrosine hydroxylase Rattus norvegicus 46-48
9191094-5 1997 The results indicate that a cAMP response element (CRE) mediates constitutive transcription of the TH gene, as well as responsiveness to FK and RA. Tretinoin 144-146 tyrosine hydroxylase Rattus norvegicus 99-101
9185997-7 1997 Expression of cyclin D1, cyclin-dependent kinase 4, and cyclin E proteins, however, decreased in association with RA-mediated G1 arrest. Tretinoin 114-116 cyclin D1 Homo sapiens 14-23
9185997-7 1997 Expression of cyclin D1, cyclin-dependent kinase 4, and cyclin E proteins, however, decreased in association with RA-mediated G1 arrest. Tretinoin 114-116 cyclin dependent kinase 4 Homo sapiens 25-50
9220339-5 1997 RA, both, in the all-trans and in the 9-cis configuration resulted in a significant acceleration of cardiomyocyte differentiation and a transient increase of beta-galactosidase activity. Tretinoin 0-2 galactosidase beta 1 Homo sapiens 158-176
9220339-6 1997 To test whether this acceleration of cardiac differentiation and RA-induced increase of the MLC-2v promotor/beta-galactosidase activity reflects an increase of cardiac- and ventricle-specific gene expression, a semi-quantitative RT-PCR analysis was performed for alpha-cardiac myosin heavy chain (alpha-MHC) and MLC-2v genes. Tretinoin 65-67 galactosidase beta 1 Homo sapiens 108-126
15744343-4 2005 ATRA induced a rapid increase in ID1 and ID2, both in the APL cell line NB4 as well as in primary patient cells. Tretinoin 0-4 inhibitor of DNA binding 1, HLH protein Homo sapiens 33-36
9458794-0 1998 Retinoic acid and dexamethasone affect RAR-beta and surfactant protein C mRNA in the MLE lung cell line. Tretinoin 0-13 retinoic acid receptor, beta Mus musculus 39-47
9458794-7 1998 Despite Dex, RA increased both RAR-beta and SP-C mRNA. Tretinoin 13-15 retinoic acid receptor, beta Mus musculus 31-39
15744343-7 2005 The simultaneous upregulation of ID1 and ID2, and the downregulation of E2A suggest a role for bHLH proteins in the induction of differentiation of APL cells following ATRA treatment. Tretinoin 168-172 inhibitor of DNA binding 1, HLH protein Homo sapiens 33-36
15744343-7 2005 The simultaneous upregulation of ID1 and ID2, and the downregulation of E2A suggest a role for bHLH proteins in the induction of differentiation of APL cells following ATRA treatment. Tretinoin 168-172 transcription factor 3 Homo sapiens 72-75
9159159-0 1997 Blocking activator protein-1 activity, but not activating retinoic acid response element, is required for the antitumor promotion effect of retinoic acid. Tretinoin 140-153 jun proto-oncogene Mus musculus 9-28
15744343-10 2005 These results indicate that ID1 and ID2 are important retinoic acid responsive genes in APL, and suggest that the inhibition of specific bHLH transcription factor complexes may play a role in the therapeutic effect of ATRA in APL. Tretinoin 218-222 inhibitor of DNA binding 1, HLH protein Homo sapiens 28-31
9159159-5 1997 The results showed that the SR11302, an AP-1 inhibition-specific retinoid, and other AP-1 inhibitors such as trans-retinoic acid and fluocinolone acetonide, markedly inhibit both 12-O-tetradecanoylphorbol-13-acetate-induced papilloma formation and AP-1 activation in 7,12-dimethyl benz(a)anthracene-initiated mouse skin (P < 0.05). Tretinoin 109-128 jun proto-oncogene Mus musculus 85-89
9159159-5 1997 The results showed that the SR11302, an AP-1 inhibition-specific retinoid, and other AP-1 inhibitors such as trans-retinoic acid and fluocinolone acetonide, markedly inhibit both 12-O-tetradecanoylphorbol-13-acetate-induced papilloma formation and AP-1 activation in 7,12-dimethyl benz(a)anthracene-initiated mouse skin (P < 0.05). Tretinoin 109-128 jun proto-oncogene Mus musculus 85-89
9600389-3 1998 In this study we investigated whether the well-known retinoic acid-induced differentiation of ES cells into neurons (identified by immunostaining for neuron-specific enolase and synaptophysin) was accompanied by cells expressing astroglial (GFAP), oligodendroglial (O4), and microglial (5C6, galectin-3) markers. Tretinoin 53-66 enolase 2, gamma neuronal Mus musculus 150-173
15708448-0 2005 Differential effect of retinoic acid and triiodothyronine on the age-related hypo-expression of neurogranin in rat. Tretinoin 23-36 neurogranin Rattus norvegicus 96-107
9407317-3 1998 To study the potential involvement of MMPs in retinoic acid (RA) regulation of skeletal development, we studied the effect of all-trans-RA on MMPs levels in mineralizing chicken epiphyseal chondrocyte primary cultures. Tretinoin 136-138 matrix metallopeptidase 2 Gallus gallus 142-146
9407317-6 1998 Time-course studies indicated that RA elevated MMP-2 activity levels in the cultures within 16 h. This increase was inhibited by cycloheximide and was enhanced by forskolin. Tretinoin 35-37 matrix metallopeptidase 2 Gallus gallus 47-52
9407317-7 1998 The increase in MMP-2 activity induced by RA was accompanied by an increase in MMP-2 mRNA levels and was abolished by treatment with cycloheximide. Tretinoin 42-44 matrix metallopeptidase 2 Gallus gallus 16-21
9153406-4 1997 Analyses of the distribution of limiting amounts of [3H]-all-trans-retinoic acid between cytoplasmic retinoic acid binding proteins, CRABP-I and CRABP-II, and the purified heterocomplexes indicate that all-trans-retinoic acid binds with comparable affinity to CRABP-I and the heterocomplexes, but with approximately 10-fold less affinity to CRABP-II. Tretinoin 61-80 cellular retinoic acid binding protein 1 Homo sapiens 145-152
9407317-7 1998 The increase in MMP-2 activity induced by RA was accompanied by an increase in MMP-2 mRNA levels and was abolished by treatment with cycloheximide. Tretinoin 42-44 matrix metallopeptidase 2 Gallus gallus 79-84
15777796-2 2005 Retinoic acid (RA) stimulates these events, including upregulation of expression and activity of alkaline phosphatase (APase), expression of annexins II, V, and VI proteins, which bind to membranes and form Ca(2+) channels, expression of osteocalcin and runx2, another mineralization-related protein and terminal differentiation-related transcription factor, and ultimately mineralization. Tretinoin 0-13 runt related transcription factor 2 Gallus gallus 254-259
9169003-3 1997 We investigated the expression of the co-repressor (SMRT) and co-activator (Trip 1) for retinoid and thyroid-hormone receptors in several neuroectodermal tumour cell lines, and its modulation by all-trans-retinoic acid, as well as by synthetic agonists, for RAR alpha, RAR beta, RAR gamma and RXR. Tretinoin 199-218 nuclear receptor corepressor 2 Homo sapiens 52-56
15721283-5 2005 Both RA isoforms also reduced IFN-gamma-induced activation of signal transducers and activators of transcription (STAT)1, STAT3, Janus kinase (JAK)1, and JAK2. Tretinoin 5-7 signal transducer and activator of transcription 1 Rattus norvegicus 114-120
9130512-0 1997 Retinoic acid-induced modulation of IL-2 mRNA production and IL-2 receptor expression on T cells. Tretinoin 0-13 interleukin 2 receptor subunit beta Homo sapiens 61-74
9180290-1 1997 All-trans retinoic acid (ATRA) has recently been shown to synergize with the inhibitory effect of interferon alpha (IFN alpha) on the growth of malignant cells isolated from solid tumors. Tretinoin 0-23 interferon alpha 17 Homo sapiens 116-125
9180290-2 1997 We investigated whether ATRA could potentiate the inhibitory effects of IFN alpha on the proliferation of leukemic progenitors in chronic myeloid leukemia (CML). Tretinoin 24-28 interferon alpha 17 Homo sapiens 72-81
9180290-6 1997 Addition of ATRA to IFN alpha dramatically potentiated the inhibitory effects of INF alpha on CFU-GM growth. Tretinoin 12-16 interferon alpha 17 Homo sapiens 20-29
9412494-8 1998 These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Tretinoin 56-69 thyroid hormone receptor alpha Mus musculus 18-22
9405093-4 1997 We previously showed that HoxD1 was induced as an immediate early response to retinoic acid in naive ectoderm (animal caps). Tretinoin 78-91 homeobox D1 S homeolog Xenopus laevis 26-31
9351827-0 1997 Phosphorylation of activation functions AF-1 and AF-2 of RAR alpha and RAR gamma is indispensable for differentiation of F9 cells upon retinoic acid and cAMP treatment. Tretinoin 135-148 retinoic acid receptor gamma Homo sapiens 71-80
15721283-5 2005 Both RA isoforms also reduced IFN-gamma-induced activation of signal transducers and activators of transcription (STAT)1, STAT3, Janus kinase (JAK)1, and JAK2. Tretinoin 5-7 Janus kinase 1 Rattus norvegicus 129-148
15721283-11 2005 SOCS3 may be at least one of the mechanisms that mediate the anti-inflammatory roles of RA. Tretinoin 88-90 suppressor of cytokine signaling 3 Rattus norvegicus 0-5
9174119-3 1997 The IC50 plots of DDRA for inhibition of [3H]RA binding to CRABP I and II and to RAR alpha, beta and gamma illustrate that this retinoid binds with the same affinity as RA to these proteins. Tretinoin 20-22 cellular retinoic acid binding protein 1 Homo sapiens 59-73
9345016-6 1997 RNA expression of myeloblastin and transglutaminase, genes regulated by RA-induced differentiation in NB4 cells, was unchanged by RA treatment. Tretinoin 72-74 proteinase 3 Homo sapiens 18-30
15908778-10 2005 TGase was induced between 3-5-fold the control level and its inhibition partially reversed the antiproliferative effect of atRA. Tretinoin 123-127 transglutaminase 1 Homo sapiens 0-5
9174119-3 1997 The IC50 plots of DDRA for inhibition of [3H]RA binding to CRABP I and II and to RAR alpha, beta and gamma illustrate that this retinoid binds with the same affinity as RA to these proteins. Tretinoin 45-47 cellular retinoic acid binding protein 1 Homo sapiens 59-73
15777839-3 2005 ATRA alone did not induce HGF production, but it significantly enhanced HGF production induced by the cAMP-elevating agent cholera toxin or the membrane-permeable cAMP analog 8-bromo-cAMP. Tretinoin 0-4 hepatocyte growth factor Homo sapiens 72-75
9367652-5 1997 Flies grown on media capable of activating the opsin gene"s transcription and which contain alternate transcription activators including retinoic acid yielded extracts containing significant amounts of Retinoid and Fatty Acid Binding Glycoprotein. Tretinoin 137-150 apolipophorin Drosophila melanogaster 202-246
9367652-10 1997 Although the synthesis of Retinoid and Fatty Acid Binding Glycoprotein does not require chromophore precursors as does that of opsin, the control of Retinoid and Fatty Acid Binding Glycoprotein and opsin transcription by retinoids including retinoic acid might very well be the same. Tretinoin 241-254 apolipophorin Drosophila melanogaster 26-70
9367652-10 1997 Although the synthesis of Retinoid and Fatty Acid Binding Glycoprotein does not require chromophore precursors as does that of opsin, the control of Retinoid and Fatty Acid Binding Glycoprotein and opsin transcription by retinoids including retinoic acid might very well be the same. Tretinoin 241-254 apolipophorin Drosophila melanogaster 149-193
9077482-4 1997 In contrast, SR11237 did not synergize with but antagonized an RAR-selective ligand activation of a retinoic acid-responsive element (DR5) via endogenous RAR-RXR. Tretinoin 100-113 tumor necrosis factor receptor superfamily, member 10b Mus musculus 134-137
15713534-2 2005 The silencing mediator of retinoic acid and thyroid hormone (SMRT) and other members of the corepressor complex are enriched in spherical intranuclear foci, and repress estrogen receptor alpha (ERalpha)-dependent transcriptional activity. Tretinoin 26-39 nuclear receptor corepressor 2 Homo sapiens 61-65
9175086-0 1997 Induction of TrkA receptor by retinoic acid in leukaemia cell lines. Tretinoin 30-43 neurotrophic receptor tyrosine kinase 1 Homo sapiens 13-17
9363862-1 1997 PURPOSE: To determine the maximum-tolerated dose (MTD) of all-trans-retinoic acid (ATRA) administered on an intermittent oral schedule with interferon-alpha2a (IFN-alpha2a) in children with refractory cancer, and whether the marked reduction in plasma ATRA concentrations observed with chronic daily oral dosing could be circumvented with an intermittent dosing schedule. Tretinoin 58-81 interferon alpha 2 Homo sapiens 140-158
15664402-6 2005 CONCLUSIONS: Chronic atRA treatment activates gene and protein expression of APJ and apelin and reduces blood pressure in SHR, suggesting that atRA may regulate the balance between apelin-APJ and angiotensin II-AT(1) signaling and have potential clinical value in the prevention and treatment of human hypertension. Tretinoin 21-25 apelin receptor Homo sapiens 77-80
9363862-1 1997 PURPOSE: To determine the maximum-tolerated dose (MTD) of all-trans-retinoic acid (ATRA) administered on an intermittent oral schedule with interferon-alpha2a (IFN-alpha2a) in children with refractory cancer, and whether the marked reduction in plasma ATRA concentrations observed with chronic daily oral dosing could be circumvented with an intermittent dosing schedule. Tretinoin 83-87 interferon alpha 2 Homo sapiens 140-158
9342364-0 1997 Posttranslational regulation of cyclin D1 by retinoic acid: a chemoprevention mechanism. Tretinoin 45-58 cyclin D1 Homo sapiens 32-41
9342364-5 1997 Exogenous cyclin D1 protein also declined after RA treatment of transfected, immortalized human bronchial epithelial cells, suggesting that posttranslational mechanisms were active in this regulation of cyclin D1 expression. Tretinoin 48-50 cyclin D1 Homo sapiens 10-19
9175086-1 1997 To explore the potential involvement of neurotrophins in the actions of retinoic acid (RA) on leukaemia differentiation, we examined the ability of RA to regulate the expression of neurotrophins and Trk receptors in several leukaemia cell lines. Tretinoin 148-150 neurotrophic receptor tyrosine kinase 1 Homo sapiens 199-202
15664402-6 2005 CONCLUSIONS: Chronic atRA treatment activates gene and protein expression of APJ and apelin and reduces blood pressure in SHR, suggesting that atRA may regulate the balance between apelin-APJ and angiotensin II-AT(1) signaling and have potential clinical value in the prevention and treatment of human hypertension. Tretinoin 21-25 apelin receptor Homo sapiens 188-191
9071982-9 1997 The biological activities of TR2-11 and TR2-11-t on a direct repeat 5-type retinoic acid (RA) response element (RARE)-containing reporter gene was examined in Cos cells. Tretinoin 90-92 nuclear receptor subfamily 2, group C, member 1 Mus musculus 29-32
15699255-9 2005 Gene array analysis showed that retinoic acid induces the expression of GADD45A, a known cell growth suppressor. Tretinoin 32-45 growth arrest and DNA damage inducible alpha Homo sapiens 72-79
9071982-10 1997 TR2-11 repressed RA induction of this reporter whereas TR2-11-t enhanced RA induction of the same reporter, and the opposite biological effects of these isoforms were dose-dependent. Tretinoin 17-19 nuclear receptor subfamily 2, group C, member 1 Mus musculus 0-3
9106168-0 1997 Restricted expression and retinoic acid-induced downregulation of the retinaldehyde dehydrogenase type 2 (RALDH-2) gene during mouse development. Tretinoin 26-39 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 70-104
9106168-0 1997 Restricted expression and retinoic acid-induced downregulation of the retinaldehyde dehydrogenase type 2 (RALDH-2) gene during mouse development. Tretinoin 26-39 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 106-113
9106168-1 1997 Retinaldehyde dehydrogenase type 2 (RALDH-2) was identified as a major retinoic acid generating enzyme in the early embryo. Tretinoin 71-84 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 0-34
9106168-1 1997 Retinaldehyde dehydrogenase type 2 (RALDH-2) was identified as a major retinoic acid generating enzyme in the early embryo. Tretinoin 71-84 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 36-43
9106168-2 1997 Here we report the expression domains of the RALDH-2 gene during mouse embryogenesis, which are likely to indicate regions of endogenous retinoic acid (RA) synthesis. Tretinoin 137-150 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 45-52
9315656-3 1997 We have investigated here the function of SNF2beta-BRG1 in the RA receptor-retinoid X receptor-mediated transduction of the retinoid signal in F9 embryonal carcinoma (EC) cells which differentiate into endodermal-like cells upon RA treatment. Tretinoin 63-65 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 Mus musculus 42-55
9305908-0 1997 c-Jun amino-terminal kinase is regulated by Galpha12/Galpha13 and obligate for differentiation of P19 embryonal carcinoma cells by retinoic acid. Tretinoin 131-144 jun proto-oncogene Mus musculus 0-5
9305908-1 1997 Retinoic acid induces P19 mouse embryonal carcinoma cells to differentiate to endoderm and increases expression of the heterotrimeric G-protein subunits Galpha12 and Galpha13. Tretinoin 0-13 interleukin 23, alpha subunit p19 Mus musculus 22-25
9305908-2 1997 Retinoic acid was found to induce differentiation and sustained activation of c-Jun amino-terminal kinase, but not of ERK1,2 or of p38 mitogen-activated protein kinases. Tretinoin 0-13 jun proto-oncogene Mus musculus 78-83
9305908-4 1997 Expression of the dominant negative form of c-Jun amino-terminal kinase 1 blocked both the activation of c-Jun amino-terminal kinase and the induction of endodermal differentiation in the presence of retinoic acid. Tretinoin 200-213 jun proto-oncogene Mus musculus 44-49
9305908-5 1997 These data implicate c-Jun amino-terminal kinase as a downstream element of activation of Galpha12 or Galpha13 obligate for retinoic acid-induced differentiation. Tretinoin 124-137 jun proto-oncogene Mus musculus 21-26
9106168-8 1997 Administration of a teratogenic dose of RA at embryonic day 8.5 results in downregulation of RALDH-2 transcript levels in caudal regions of the embryo, and may reflect a mechanism of negative feedback regulation of RA synthesis. Tretinoin 40-42 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 93-100
15725648-0 2005 The administration of retinoic acid down-regulates cAMP-responsive element modulator (CREM) mRNA in vitamin A-deficient testes. Tretinoin 22-35 cAMP responsive element modulator Rattus norvegicus 51-84
8999919-4 1997 We previously identified a 3" enhancer called the RAIDR5, which contained a DR5 retinoic acid response element (RARE) and was responsible for the retinoic acid (RA)-associated expression of the murine Hoxa-1 gene in teratocarcinoma cells. Tretinoin 80-93 homeobox A1 Mus musculus 201-207
8999919-4 1997 We previously identified a 3" enhancer called the RAIDR5, which contained a DR5 retinoic acid response element (RARE) and was responsible for the retinoic acid (RA)-associated expression of the murine Hoxa-1 gene in teratocarcinoma cells. Tretinoin 146-159 homeobox A1 Mus musculus 201-207
8999919-4 1997 We previously identified a 3" enhancer called the RAIDR5, which contained a DR5 retinoic acid response element (RARE) and was responsible for the retinoic acid (RA)-associated expression of the murine Hoxa-1 gene in teratocarcinoma cells. Tretinoin 50-52 homeobox A1 Mus musculus 201-207
9331505-1 1997 Serum-free culture conditions for retinoic acid-induced neural differentiation of mouse P19 embryonal carcinoma cells were determined for future ex vivo retroviral gene transfer and brain transplantation studies. Tretinoin 34-47 interleukin 23, alpha subunit p19 Mus musculus 88-91
8999919-6 1997 This enhancer, the Hoxb-1 RAIDR5, regulates the RA responsiveness of the Hoxb-1 gene and is different in location and sequence from the RA-regulated 3" Hoxb-1 enhancers previously described. Tretinoin 26-28 homeobox B1 Mus musculus 19-25
9261178-11 1997 Furthermore, we demonstrated, using mouse P19 embryonal carcinoma cells, that this 371-base pair sequence is likely to be sufficient to confer the transcriptional activation of the ERK2 promoter during the retinoic acid-induced differentiation of P19 cells. Tretinoin 206-219 interleukin 23, alpha subunit p19 Mus musculus 42-45
8999919-6 1997 This enhancer, the Hoxb-1 RAIDR5, regulates the RA responsiveness of the Hoxb-1 gene and is different in location and sequence from the RA-regulated 3" Hoxb-1 enhancers previously described. Tretinoin 26-28 homeobox B1 Mus musculus 73-79
15725648-3 2005 In this study, we found that administration of all-trans retinoic acid (ATRA) or retinol to VAD rats down-regulates the testicular mRNA levels of the cAMP responsive element modulator (CREM), an essential transcription factor for spermatogenesis. Tretinoin 47-70 cAMP responsive element modulator Rattus norvegicus 150-183
8999919-6 1997 This enhancer, the Hoxb-1 RAIDR5, regulates the RA responsiveness of the Hoxb-1 gene and is different in location and sequence from the RA-regulated 3" Hoxb-1 enhancers previously described. Tretinoin 26-28 homeobox B1 Mus musculus 73-79
9261178-11 1997 Furthermore, we demonstrated, using mouse P19 embryonal carcinoma cells, that this 371-base pair sequence is likely to be sufficient to confer the transcriptional activation of the ERK2 promoter during the retinoic acid-induced differentiation of P19 cells. Tretinoin 206-219 interleukin 23, alpha subunit p19 Mus musculus 247-250
15725648-3 2005 In this study, we found that administration of all-trans retinoic acid (ATRA) or retinol to VAD rats down-regulates the testicular mRNA levels of the cAMP responsive element modulator (CREM), an essential transcription factor for spermatogenesis. Tretinoin 72-76 cAMP responsive element modulator Rattus norvegicus 150-183
15725579-5 2005 However, in contrast to normal fibroblasts, exposure of psoriatic fibroblasts to 1 microM RA down-regulated Mn-SOD mRNA, and also decreased Mn-SOD activity by approximately 80% with no change in Mn-SOD protein levels. Tretinoin 90-92 superoxide dismutase 2 Homo sapiens 140-146
9066685-4 1997 Western blot analysis showed that the expression of both NM23 and MTS1 proteins was reduced in human lung cancer CH27 cells by retinoic acid treatment, but the ratio of NM23: MTS1 increased in a dose-dependent manner. Tretinoin 127-140 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 57-61
15725579-5 2005 However, in contrast to normal fibroblasts, exposure of psoriatic fibroblasts to 1 microM RA down-regulated Mn-SOD mRNA, and also decreased Mn-SOD activity by approximately 80% with no change in Mn-SOD protein levels. Tretinoin 90-92 superoxide dismutase 2 Homo sapiens 140-146
9066685-4 1997 Western blot analysis showed that the expression of both NM23 and MTS1 proteins was reduced in human lung cancer CH27 cells by retinoic acid treatment, but the ratio of NM23: MTS1 increased in a dose-dependent manner. Tretinoin 127-140 malignant transformation suppression-1 Homo sapiens 66-70
9268495-2 1997 As a cell line model for studying this phenomenon, we tested the effects of retinoic acid (RA) on the expression of IL-2Ralpha and IL-2Rbeta in Hut78 cells, a mature T-cell line derived from a Sezary T-cell leukemia. Tretinoin 76-89 interleukin 2 receptor subunit alpha Homo sapiens 116-126
9268495-2 1997 As a cell line model for studying this phenomenon, we tested the effects of retinoic acid (RA) on the expression of IL-2Ralpha and IL-2Rbeta in Hut78 cells, a mature T-cell line derived from a Sezary T-cell leukemia. Tretinoin 76-89 interleukin 2 receptor subunit beta Homo sapiens 131-140
9268495-2 1997 As a cell line model for studying this phenomenon, we tested the effects of retinoic acid (RA) on the expression of IL-2Ralpha and IL-2Rbeta in Hut78 cells, a mature T-cell line derived from a Sezary T-cell leukemia. Tretinoin 91-93 interleukin 2 receptor subunit alpha Homo sapiens 116-126
9268495-2 1997 As a cell line model for studying this phenomenon, we tested the effects of retinoic acid (RA) on the expression of IL-2Ralpha and IL-2Rbeta in Hut78 cells, a mature T-cell line derived from a Sezary T-cell leukemia. Tretinoin 91-93 interleukin 2 receptor subunit beta Homo sapiens 131-140
9268495-4 1997 RA-induced upregulation of IL-2Rbeta was found to be transcriptionally mediated in a protein-synthesis-independent fashion; however, activation of the IL-2Rbeta promoter could not be demonstrated in transient transfection experiments utilizing reporter gene constructs containing all currently known regulatory elements of the IL-2Rbeta promoter. Tretinoin 0-2 interleukin 2 receptor subunit beta Homo sapiens 27-36
9268495-4 1997 RA-induced upregulation of IL-2Rbeta was found to be transcriptionally mediated in a protein-synthesis-independent fashion; however, activation of the IL-2Rbeta promoter could not be demonstrated in transient transfection experiments utilizing reporter gene constructs containing all currently known regulatory elements of the IL-2Rbeta promoter. Tretinoin 0-2 interleukin 2 receptor subunit beta Homo sapiens 151-160
9551182-5 1997 To investigate the relationships between the spatial distribution of retinoid signalling and the regulation of retinoid target genes, we studied the downregulation by retinoic acid of two genes expressed in anterior regions of the embryo, goosecoid and otx1. Tretinoin 167-180 orthodenticle homeobox 1 Danio rerio 253-257
15725579-8 2005 These results indicate that RA can serve as a regulatory agent to down-regulate the steady-state levels of both Mn-SOD and Cu,Zn-SOD in psoriatic cells. Tretinoin 28-30 superoxide dismutase 2 Homo sapiens 112-118
9103677-15 1997 Further characterisation of NPM and PLZF at the structural and functional level will determine whether PML and other proteins disrupted in APL associated translocations play an active or purely permissive role in leukaemogenesis and will help dissect the events leading to transformation from those causing blockade of myeloid differentiation and mediating the response to ATRA. Tretinoin 373-377 nucleophosmin 1 Homo sapiens 28-31
9268495-4 1997 RA-induced upregulation of IL-2Rbeta was found to be transcriptionally mediated in a protein-synthesis-independent fashion; however, activation of the IL-2Rbeta promoter could not be demonstrated in transient transfection experiments utilizing reporter gene constructs containing all currently known regulatory elements of the IL-2Rbeta promoter. Tretinoin 0-2 interleukin 2 receptor subunit beta Homo sapiens 151-160
9268495-5 1997 Enhancement of IL-2Ralpha/beta by RA was accompanied by upregulation of the expression of CD38, CD69, CD45RO, and HLA-DR, surface molecules known to be associated with T-cell activation. Tretinoin 34-36 interleukin 2 receptor subunit alpha Homo sapiens 15-25
9268495-5 1997 Enhancement of IL-2Ralpha/beta by RA was accompanied by upregulation of the expression of CD38, CD69, CD45RO, and HLA-DR, surface molecules known to be associated with T-cell activation. Tretinoin 34-36 CD69 molecule Homo sapiens 96-100
15652703-0 2005 Requirement of mesodermal retinoic acid generated by Raldh2 for posterior neural transformation. Tretinoin 26-39 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 53-59
9268495-7 1997 Taken together, our findings demonstrate the ability of RA to upregulate IL-2R expression and enhance the activation state of Hut78 cells. Tretinoin 56-58 interleukin 2 receptor subunit alpha Homo sapiens 73-78
9202972-0 1997 Regulation of ceruloplasmin by retinoic acid in the developing rat. Tretinoin 31-44 ceruloplasmin Rattus norvegicus 14-27
15652703-2 2005 We have tested this hypothesis in retinaldehyde dehydrogenase-2 (Raldh2) null mutant mice lacking RA synthesis in the somitic mesoderm. Tretinoin 98-100 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 34-63
15652703-2 2005 We have tested this hypothesis in retinaldehyde dehydrogenase-2 (Raldh2) null mutant mice lacking RA synthesis in the somitic mesoderm. Tretinoin 98-100 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 65-71
15652703-4 2005 Spinal cord differentiation in Raldh2(-/-) embryos was rescued by maternal RA administration, and during the rescue RA was found to act directly in the neuroectoderm but not the somitic mesoderm. Tretinoin 75-77 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 31-37
9272954-5 1997 Comparative analysis of the retinoid responses of Hoxd4, Hoxa4 and Hoxb4 reveals that, while they can be rapidly induced by RA, there is a window of competence for this response, which is different to that of more 3" Hox genes. Tretinoin 124-126 homeobox A4 Homo sapiens 57-62
15652703-5 2005 RA generated by Raldh2 in the somitic mesoderm was found to normally travel as a signal throughout the mesoderm and neuroectoderm of the trunk and into tailbud neuroectoderm, but not into tailbud mesoderm. Tretinoin 0-2 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 16-22
9392437-1 1997 The human mineralocorticoid receptor (MR) is a member of the steroid-thyroid hormone receptor superfamily, which includes receptors for retinoic acid, vitamin D, and other steroids, such as the glucocorticoids (which bind the glucocorticoid receptor, GR). Tretinoin 136-149 nuclear receptor subfamily 3 group C member 2 Homo sapiens 10-36
9392437-1 1997 The human mineralocorticoid receptor (MR) is a member of the steroid-thyroid hormone receptor superfamily, which includes receptors for retinoic acid, vitamin D, and other steroids, such as the glucocorticoids (which bind the glucocorticoid receptor, GR). Tretinoin 136-149 nuclear receptor subfamily 3 group C member 2 Homo sapiens 38-40
15652703-7 2005 Our findings demonstrate that RA synthesized in the somitic mesoderm is necessary for posterior neural transformation in the mouse and that Raldh2 provides the only source of RA for posterior development. Tretinoin 175-177 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 140-146
15895831-0 2005 Tra2alpha promotes RA induced neural differentiation of P19 cells. Tretinoin 19-21 transformer 2 alpha Mus musculus 0-9
12219215-0 1997 Regulatory Effect of All-trans Retinoic Acid (ATRA) on the Activities of N-acetylglucosaminyl Transferase (GnT) III, IV in HL-60 Cells. Tretinoin 21-44 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 107-115
12219215-0 1997 Regulatory Effect of All-trans Retinoic Acid (ATRA) on the Activities of N-acetylglucosaminyl Transferase (GnT) III, IV in HL-60 Cells. Tretinoin 46-50 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 107-115
12219215-1 1997 The regulatory effect of all-trans retinoic acid (ATRA) on the activities of N-acetylglucosaminyl transferase (GnT) III and IV in HL-60 Cells were studied. Tretinoin 25-48 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 111-119
12219215-1 1997 The regulatory effect of all-trans retinoic acid (ATRA) on the activities of N-acetylglucosaminyl transferase (GnT) III and IV in HL-60 Cells were studied. Tretinoin 50-54 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 111-119
12219215-2 1997 It was found that the activities of GnT-III and GnT-IV were significantly decreased by 0.1 &mgr;M ATRA, but not further decreased with the increase in concentration of ATRA to 1.0 or 10 &mgr;M. The activities of both GnT-III and GnT-IV in the untreated control cells were variable during the incubation of cells, showing a peak level at 24 h and 48 h in the un-synchronized culture and the synchronized culture respectively. Tretinoin 102-106 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 36-43
12219215-2 1997 It was found that the activities of GnT-III and GnT-IV were significantly decreased by 0.1 &mgr;M ATRA, but not further decreased with the increase in concentration of ATRA to 1.0 or 10 &mgr;M. The activities of both GnT-III and GnT-IV in the untreated control cells were variable during the incubation of cells, showing a peak level at 24 h and 48 h in the un-synchronized culture and the synchronized culture respectively. Tretinoin 102-106 alpha-1,3-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase B Homo sapiens 48-54
12219215-2 1997 It was found that the activities of GnT-III and GnT-IV were significantly decreased by 0.1 &mgr;M ATRA, but not further decreased with the increase in concentration of ATRA to 1.0 or 10 &mgr;M. The activities of both GnT-III and GnT-IV in the untreated control cells were variable during the incubation of cells, showing a peak level at 24 h and 48 h in the un-synchronized culture and the synchronized culture respectively. Tretinoin 172-176 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 36-43
12219215-2 1997 It was found that the activities of GnT-III and GnT-IV were significantly decreased by 0.1 &mgr;M ATRA, but not further decreased with the increase in concentration of ATRA to 1.0 or 10 &mgr;M. The activities of both GnT-III and GnT-IV in the untreated control cells were variable during the incubation of cells, showing a peak level at 24 h and 48 h in the un-synchronized culture and the synchronized culture respectively. Tretinoin 172-176 alpha-1,3-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase B Homo sapiens 48-54
12219215-3 1997 After the treatment with ATRA, the peak value was still at 24h in un-synchronized culture, and the activities of GnT-III and GnT-IV were gradually decreased only after 24 h of incubation both in un- synchronized and synchronized culture of HL-60 cells. Tretinoin 25-29 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 113-120
27747415-11 1997 By analogy, we propose that local overexpression of Xlcpl1 reflects precisely the situation of exogenous application of retinoic acid. Tretinoin 120-133 prostaglandin D2 synthase L homeolog Xenopus laevis 52-58
9233783-4 1997 We report that 9-cis retinoic acid (9-cis RA) and all trans retinoic acid (tRA) inhibited the cyclin D1 and D3 expression levels of human MCF-7, ZR-75 and T-47D breast carcinoma cells in vitro. Tretinoin 21-34 cyclin D1 Homo sapiens 94-103
9233783-4 1997 We report that 9-cis retinoic acid (9-cis RA) and all trans retinoic acid (tRA) inhibited the cyclin D1 and D3 expression levels of human MCF-7, ZR-75 and T-47D breast carcinoma cells in vitro. Tretinoin 75-78 cyclin D1 Homo sapiens 94-103
9202249-0 1997 Retinoic acid and alcohol/retinol dehydrogenase in the mouse adrenal gland: a potential endocrine source of retinoic acid during development. Tretinoin 108-121 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 26-47
9202249-1 1997 Retinoid signaling requires the conversion of retinol to retinoic acid by a two-step process, the first of which can be catalyzed in vitro by class I and class IV alcohol dehydrogenases (ADH). Tretinoin 57-70 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 187-190
12219215-3 1997 After the treatment with ATRA, the peak value was still at 24h in un-synchronized culture, and the activities of GnT-III and GnT-IV were gradually decreased only after 24 h of incubation both in un- synchronized and synchronized culture of HL-60 cells. Tretinoin 25-29 alpha-1,3-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase B Homo sapiens 125-131
15895831-3 2005 In P19 carcinoma cells, Tra2alpha is transiently up-regulated upon retinoic acid (RA) treatment. Tretinoin 67-80 transformer 2 alpha Mus musculus 24-33
9207922-1 1997 Apoptotic cell death was observed during aggregate culture of the mouse embryonal carcinoma cell line P19 exposed to all-trans retinoic acid (tRA). Tretinoin 127-140 interleukin 23, alpha subunit p19 Mus musculus 102-105
15895831-3 2005 In P19 carcinoma cells, Tra2alpha is transiently up-regulated upon retinoic acid (RA) treatment. Tretinoin 82-84 transformer 2 alpha Mus musculus 24-33
9207922-1 1997 Apoptotic cell death was observed during aggregate culture of the mouse embryonal carcinoma cell line P19 exposed to all-trans retinoic acid (tRA). Tretinoin 142-145 interleukin 23, alpha subunit p19 Mus musculus 102-105
15895831-4 2005 Although over-expression of Tra2alpha protein alone does not elicit P19 differentiation, under these conditions the response of P19 cells to RA is significantly increased. Tretinoin 141-143 transformer 2 alpha Mus musculus 28-37
15895831-5 2005 The results suggest that Tra2alpha proteins may act as a mediator in the signal pathway associated with RA-induced differentiation in P19 cells. Tretinoin 104-106 transformer 2 alpha Mus musculus 25-34
9199334-4 1997 We found that stable expression of SF-1 is sufficient to alter ES cell morphology, permit cyclic AMP (cAMP) and retinoic acid-induced expression of the endogenous side chain cleavage enzyme gene, and consequently, promote steroidogenesis. Tretinoin 112-125 splicing factor 1 Mus musculus 35-39
8977246-4 1996 In the promyelocytic cell line HL-60, GRK6 protein levels and activity rose twofold to fourfold over the course of treatment with agents that induce differentiation toward either the myeloid (dimethyl sulfoxide and retinoic acid) or monocytic [1alpha,25(OH)2-vitamin D3] lineage, whereas betaARK protein levels and activity were only slightly altered. Tretinoin 215-228 G protein-coupled receptor kinase 6 Homo sapiens 38-42
15596294-3 2005 In this study, we used a model system of matched primary and metastatic melanoma cells to investigate whether expression of Id1 and p16 proteins were involved in atRA-induced apoptosis and cell cycle re-distribution. Tretinoin 162-166 inhibitor of DNA binding 1, HLH protein Homo sapiens 124-127
15596294-7 2005 Expression level of Id1 protein was decreased and the p16 was increased in a dose- and time-dependent (P<0.05) manner after treatment with atRA. Tretinoin 142-146 inhibitor of DNA binding 1, HLH protein Homo sapiens 20-23
15596294-9 2005 These data suggested that the alterations of Id1 and/or p16 proteins were involved in atRA-induced apoptosis and cell cycle re-distribution in melanoma. Tretinoin 86-90 inhibitor of DNA binding 1, HLH protein Homo sapiens 45-48
8903394-12 1996 Upregulation of uPA synthesis by retinoic acid may have implications in matrix remodeling in sites of stellate cell activation in which high concentrations of retinoids may be achieved. Tretinoin 33-46 plasminogen activator, urokinase Rattus norvegicus 16-19
9188458-8 1997 Analysis of alternative splicing of agrin mRNA revealed that NGF elicited a specific increase in agriny4 and agrinz8 mRNAs that did not occur in the presence of epidermal growth factor, insulin, dexamethasone, or retinoic acid. Tretinoin 213-226 nerve growth factor Rattus norvegicus 61-64
9191474-5 1997 Removal of RA from the media caused a drastic decrease in mucin secretion and a decrease in expression of the mucin genes MUC2 and MUC5AC.LZ and SLPI secretions were increased in these cultures. Tretinoin 11-13 LOC100508689 Homo sapiens 58-63
15550691-8 2005 Enhanced expression of tTG, induced by retinoic acid, increased inward remodeling of porcine coronary arteries kept in organ culture for 3 days. Tretinoin 39-52 transglutaminase 2 Rattus norvegicus 23-26
9191474-5 1997 Removal of RA from the media caused a drastic decrease in mucin secretion and a decrease in expression of the mucin genes MUC2 and MUC5AC.LZ and SLPI secretions were increased in these cultures. Tretinoin 11-13 LOC100508689 Homo sapiens 110-115
9158000-0 1997 Increasing c-FMS (CSF-1 receptor) expression decreases retinoic acid concentration needed to cause cell differentiation and retinoblastoma protein hypophosphorylation. Tretinoin 55-68 colony stimulating factor 1 receptor Homo sapiens 11-16
9158000-0 1997 Increasing c-FMS (CSF-1 receptor) expression decreases retinoic acid concentration needed to cause cell differentiation and retinoblastoma protein hypophosphorylation. Tretinoin 55-68 colony stimulating factor 1 receptor Homo sapiens 18-32
9158000-1 1997 Increasing the expression of c-FMS (colony-stimulating factor 1 receptor) by introduction of a transgene reduced the concentration of retinoic acid or 1,25-dihydroxy vitamin D3 needed to cause myeloid or monocytic cell differentiation and hypophosphorylation of the retinoblastoma tumor suppressor protein (RB) typically associated with cell cycle G0 arrest and differentiation of HL-60 human myelo-monoblastic precursor cells. Tretinoin 134-147 colony stimulating factor 1 receptor Homo sapiens 29-34
9158000-1 1997 Increasing the expression of c-FMS (colony-stimulating factor 1 receptor) by introduction of a transgene reduced the concentration of retinoic acid or 1,25-dihydroxy vitamin D3 needed to cause myeloid or monocytic cell differentiation and hypophosphorylation of the retinoblastoma tumor suppressor protein (RB) typically associated with cell cycle G0 arrest and differentiation of HL-60 human myelo-monoblastic precursor cells. Tretinoin 134-147 colony stimulating factor 1 receptor Homo sapiens 36-72
9158000-9 1997 A 10-fold higher retinoic acid concentration, 10(-1) M, induced significant differentiation of both intermediate and high c-FMS-expressing cells. Tretinoin 17-30 colony stimulating factor 1 receptor Homo sapiens 122-127
9158000-11 1997 The highest retinoic acid concentration, 10(-6) M, elicited differentiation, hypophosphorylation of RB, and G0 arrest in low, intermediate, and high c-FMS-expressing cells. Tretinoin 12-25 colony stimulating factor 1 receptor Homo sapiens 149-154
8908199-1 1996 Treatment of synovial fibroblasts with retinoic acid (RA) decreases their expression of collagenase (matrix metalloproteinase-1 or MMP-1), an enzyme that degrades interstitial collagens and contributes to the pathology of rheumatoid arthritis. Tretinoin 39-52 interstitial collagenase Oryctolagus cuniculus 101-127
8908199-1 1996 Treatment of synovial fibroblasts with retinoic acid (RA) decreases their expression of collagenase (matrix metalloproteinase-1 or MMP-1), an enzyme that degrades interstitial collagens and contributes to the pathology of rheumatoid arthritis. Tretinoin 39-52 interstitial collagenase Oryctolagus cuniculus 131-136
8908199-1 1996 Treatment of synovial fibroblasts with retinoic acid (RA) decreases their expression of collagenase (matrix metalloproteinase-1 or MMP-1), an enzyme that degrades interstitial collagens and contributes to the pathology of rheumatoid arthritis. Tretinoin 54-56 interstitial collagenase Oryctolagus cuniculus 101-127
8908199-1 1996 Treatment of synovial fibroblasts with retinoic acid (RA) decreases their expression of collagenase (matrix metalloproteinase-1 or MMP-1), an enzyme that degrades interstitial collagens and contributes to the pathology of rheumatoid arthritis. Tretinoin 54-56 interstitial collagenase Oryctolagus cuniculus 131-136
8908199-2 1996 This inhibition results, at least in part, from RA-induced decreases in the mRNA for the transactivators Fos and Jun (with concominant increases in RAR mRNA) and by sequestration of Fos/Jun by RARs/RXRs. Tretinoin 48-50 proto-oncogene c-Fos Oryctolagus cuniculus 105-108
8908199-2 1996 This inhibition results, at least in part, from RA-induced decreases in the mRNA for the transactivators Fos and Jun (with concominant increases in RAR mRNA) and by sequestration of Fos/Jun by RARs/RXRs. Tretinoin 48-50 proto-oncogene c-Fos Oryctolagus cuniculus 182-185
8900141-4 1996 Consistent with their involvement in activation of neuronal gene expression, members of the MEF2 family are expressed in P19 embryonal carcinoma cells that have been induced to form neurons following treatment with retinoic acid. Tretinoin 215-228 myocyte enhancer factor 2A Homo sapiens 92-96
8878554-5 1996 Treatment of two acute promyelocytic leukemia patients with ATRA induced maximal 2.7- and 3.2-fold increases in serum Lp(a) concentrations, respectively. Tretinoin 60-64 lipoprotein(a) Homo sapiens 118-123
9158000-12 1997 As the concentration of retinoic acid increased, cell differentiation, hypophosphorylation of RB, and G0 arrest were progressively elicited within this ensemble of cells with different c-FMS expression levels. Tretinoin 24-37 colony stimulating factor 1 receptor Homo sapiens 185-190
9158000-13 1997 Thus, for example, at the lowest concentration of retinoic acid, expression of high enough c-FMS still allowed differentiation. Tretinoin 50-63 colony stimulating factor 1 receptor Homo sapiens 91-96
9130512-7 1997 CONCLUSION: These studies suggest that RA can augment IL-2 mRNA production by T cells with a possible paracrine effect on IL-2R-alpha expression. Tretinoin 39-41 interleukin 2 receptor subunit alpha Homo sapiens 122-133
15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 99-103 nucleolin Homo sapiens 67-76
9180290-6 1997 Addition of ATRA to IFN alpha dramatically potentiated the inhibitory effects of INF alpha on CFU-GM growth. Tretinoin 12-16 interferon alpha 17 Homo sapiens 81-90
9180290-9 1997 RT-PCR analysis of the colonies resulting from the action of the combination IFN alpha plus ATRA showed the presence of an increased number of BCR-ABL-negative colonies relatively to what was observed with IFN alpha alone. Tretinoin 92-96 interferon alpha 17 Homo sapiens 206-215
8806687-9 1996 However, following all trans retinoic acid treatment of NB4 cells a significant relocalisation of PIC1 and PML is observed. Tretinoin 29-42 small ubiquitin like modifier 1 Homo sapiens 98-102
15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 99-103 VPS52 subunit of GARP complex Homo sapiens 236-241
9128293-2 1997 We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants. Tretinoin 97-120 surfactant protein A1 Homo sapiens 61-65
15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 279-283 nucleolin Homo sapiens 67-76
9128293-2 1997 We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants. Tretinoin 122-124 surfactant protein B Homo sapiens 30-34
9128293-2 1997 We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants. Tretinoin 122-124 surfactant protein A1 Homo sapiens 61-65
15492114-6 2005 However, when recombinant nucleolin was added to extracts of ATRA-treated cells, the rate of bcl-2 mRNA decay was similar to the rate in extracts of untreated cells. Tretinoin 61-65 nucleolin Homo sapiens 26-35
9128293-7 1997 Human fetal lung explants were treated with 9-cis-RA for 6 d. 9-cis-RA did not significantly increase SP-B mRNA levels, significantly inhibited SP-A mRNA levels at all concentrations tested, and significantly inhibited SP-C mRNA levels at 10(-6) M in the human fetal lung explants. Tretinoin 62-70 surfactant protein A1 Homo sapiens 144-148
8892527-0 1996 Expression patterns of class I and class IV alcohol dehydrogenase genes in developing epithelia suggest a role for alcohol dehydrogenase in local retinoic acid synthesis. Tretinoin 146-159 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 44-65
8892527-0 1996 Expression patterns of class I and class IV alcohol dehydrogenase genes in developing epithelia suggest a role for alcohol dehydrogenase in local retinoic acid synthesis. Tretinoin 146-159 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 115-136
8892527-5 1996 To explore whether any ADH isozymes are linked to retinoic acid synthesis, herein we have examined the expression patterns of all known classes of ADH in mouse embryonic and adult tissues, and also measured retinoic acid levels. Tretinoin 50-63 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 23-26
15492114-7 2005 These results provide evidence that ATRA-induced apoptosis is a consequence of cellular differentiation, which leads to nucleolin down-regulation and bcl-2 mRNA instability. Tretinoin 36-40 nucleolin Homo sapiens 120-129
8892527-9 1996 We detected significant retinoic acid levels in the fetal kidney, fetal/adult intestine and adrenal gland, as well as the adult liver, lung, testis, epididymis, and uterus--all sites of class I and/or class IV ADH gene expression. Tretinoin 24-37 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 207-213
8892527-10 1996 These findings indicate that the expression patterns of class I ADH and class IV ADH, but not class III ADH, are consistent with a function in local retinoic acid synthesis needed for the development and maintenance of many specialized epithelial tissues. Tretinoin 149-162 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 64-67
9111003-6 1997 Furthermore, in transient transfection experiments, the activity of the stromelysin-3 promoter was induced by retinoic acid through endogenous receptors acting on a DR1 retinoic acid-responsive element. Tretinoin 110-123 down-regulator of transcription 1 Homo sapiens 165-168
8892527-10 1996 These findings indicate that the expression patterns of class I ADH and class IV ADH, but not class III ADH, are consistent with a function in local retinoic acid synthesis needed for the development and maintenance of many specialized epithelial tissues. Tretinoin 149-162 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 78-84
15533322-4 2004 The use of retinoic acid greatly increased the number of differentiated cells, and the most effective concentration was 10(-6) M. NeuN immunohistochemistry was positive in 9.6+/-1.7% of morphologically differentiated neuron-like cells. Tretinoin 11-24 RNA binding protein, fox-1 homolog (C. elegans) 3 Mus musculus 130-134
8892527-10 1996 These findings indicate that the expression patterns of class I ADH and class IV ADH, but not class III ADH, are consistent with a function in local retinoic acid synthesis needed for the development and maintenance of many specialized epithelial tissues. Tretinoin 149-162 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 81-84
9109417-0 1997 Retinoic acid modulates retinoid X receptor alpha and retinoic acid receptor alpha levels of cultured brown adipocytes. Tretinoin 0-13 retinoic acid receptor RXR-alpha Cricetulus griseus 24-49
15516986-0 2004 Retinoic acid mediates degradation of IRS-1 by the ubiquitin-proteasome pathway, via a PKC-dependant mechanism. Tretinoin 0-13 protein kinase C delta Homo sapiens 87-90
8706017-9 1996 p145TrkB expression is induced by 1 nM retinoic acid. Tretinoin 39-52 neurotrophic receptor tyrosine kinase 2 Homo sapiens 4-8
15516986-7 2004 Two PKC inhibitors, but not a MAPK inhibitor, blocked the RA-induced degradation and serine phosphorylation of IRS-1. Tretinoin 58-60 protein kinase C delta Homo sapiens 4-7
15516986-8 2004 We demonstrate that RA activates PKC-delta in the sensitive, but not in the resistant cells, with a time course that is consistent with the RA-induced decrease of IRS-1. Tretinoin 20-22 protein kinase C delta Homo sapiens 33-42
9101090-4 1997 Treatment of HL-60 cells with retinoic acid/DMSO (granulocytic) or phorbol 12-myristate 13-acetate (monocytic) results in apoptosis and in down-regulation of APE expression at both the RNA and protein levels. Tretinoin 30-43 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 158-161
15516986-8 2004 We demonstrate that RA activates PKC-delta in the sensitive, but not in the resistant cells, with a time course that is consistent with the RA-induced decrease of IRS-1. Tretinoin 140-142 protein kinase C delta Homo sapiens 33-42
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 protein kinase C delta Homo sapiens 36-45
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 protein kinase C delta Homo sapiens 81-90
9075714-3 1997 Only the expression of RAR beta messenger RNA was transiently induced within 24 h after ATRA injection. Tretinoin 88-92 retinoic acid receptor, beta Mus musculus 23-31
8877453-10 1996 Expression of the HoxA genes is altered coordinately in response to retinoic acid in a manner consistent with the transformation of a distal blastema to a proximal blastema. Tretinoin 68-81 homeobox A cluster Homo sapiens 18-22
9075714-4 1997 ATRA-induced RAR beta expression was also found in purified Sertoli cells, suggesting that these cells mediate at least part of the effect of retinoids on germ cells. Tretinoin 0-4 retinoic acid receptor, beta Mus musculus 13-21
15358764-5 2004 To examine the relationship between APC and retinoic acid biosynthesis in normal enterocytes, we have identified two novel zebrafish retinol dehydrogenases, termed zRDHA and zRDHB, that show strong expression within the gut of developing zebrafish embryos. Tretinoin 44-57 retinol dehydrogenase 1 Danio rerio 174-179
9075714-7 1997 Upon administration of ATRA, messenger RNA expression of RXR alpha and -beta did not change significantly. Tretinoin 23-27 retinoid X receptor alpha Mus musculus 57-66
15358764-6 2004 Morpholino knockdown of either APC or zRDHB in zebrafish embryos resulted in defects in structures known to require retinoic acid. Tretinoin 116-129 retinol dehydrogenase 1 Danio rerio 38-43
8703946-5 1996 All-trans-retinoic acid (RA) treatment of Jun-deficient, mouse F9, teratocarcinoma cells causes the induction of c-jun expression. Tretinoin 25-27 jun proto-oncogene Mus musculus 113-118
15650242-9 2004 The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression. Tretinoin 4-17 haptoglobin-related protein Homo sapiens 28-31
8713132-2 1996 A significant percentage of the RA-treated cells also displayed differentiation towards neutrophils, as assayed by changes in nitroblue tetrazolium reduction (NBT) and alpha-naphthyl-acetate esterase (ANAE) activities, whereas the 4-HPR treated cells remained essentially undifferentiated. Tretinoin 32-34 haptoglobin-related protein Homo sapiens 233-236
8755604-11 1996 The reductions in AcCho content caused by Abeta 1-42 could be prevented by a cotreatment with all-trans-retinoic acid (10 nM), a compound previously shown to increase choline acetyltransferase mRNA expression in SN56 cells. Tretinoin 94-117 choline acetyltransferase Mus musculus 167-192
9168437-1 1997 We demonstrate that N-(4-hydroxyphenyl)-all-trans-retinamide (4-HPR), a synthetic retinoic acid (RA) derivative, is a potent and selective inducer of apoptosis in malignant T lymphoid cells, but has little effect on normal lymphoid cells of the thymus or spleen. Tretinoin 82-95 haptoglobin-related protein Homo sapiens 64-67
9122176-0 1997 Identification of a novel negative retinoic acid responsive element in the promoter of the human matrix Gla protein gene. Tretinoin 35-48 matrix Gla protein Homo sapiens 97-115
9122176-2 1997 Expression of the MGP gene is regulated by various growth factors, steroid hormones, and the vitamin A metabolite retinoic acid (RA). Tretinoin 114-127 matrix Gla protein Homo sapiens 18-21
9122176-2 1997 Expression of the MGP gene is regulated by various growth factors, steroid hormones, and the vitamin A metabolite retinoic acid (RA). Tretinoin 129-131 matrix Gla protein Homo sapiens 18-21
9122176-9 1997 Our results indicate that RA-mediated repression of the hMGP gene is due to binding of liganded RAR/RXR to a novel negative RA response element. Tretinoin 26-28 matrix Gla protein Homo sapiens 56-60
8759021-1 1996 HOX A genes are induced in a temporal fashion after retinoic acid (RA) treatment in non-N-ras-transformed PA-1 human teratcarcinoma cells. Tretinoin 52-65 homeobox A cluster Homo sapiens 0-5
8759021-1 1996 HOX A genes are induced in a temporal fashion after retinoic acid (RA) treatment in non-N-ras-transformed PA-1 human teratcarcinoma cells. Tretinoin 67-69 homeobox A cluster Homo sapiens 0-5
9122176-9 1997 Our results indicate that RA-mediated repression of the hMGP gene is due to binding of liganded RAR/RXR to a novel negative RA response element. Tretinoin 96-98 matrix Gla protein Homo sapiens 56-60
15650242-9 2004 The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression. Tretinoin 4-17 caspase 8 Homo sapiens 143-152
15650242-9 2004 The retinoic acid analogue 4HPR, IFN-gamma, and the demethylating agent 5-aza-cytidine activate this promoter in NB cells that lack endogenous caspase-8, indicating that this element may regulate both constitutive and inducible CASP8 expression. Tretinoin 4-17 caspase 8 Homo sapiens 228-233
15308560-0 2004 Protein kinase Cdelta mediates retinoic acid and phorbol myristate acetate-induced phospholipid scramblase 1 gene expression: its role in leukemic cell differentiation. Tretinoin 31-44 protein kinase C delta Homo sapiens 0-21
9125196-7 1997 We found that 4-hydroxyphenylretinamide (4-HPR) inhibited the catabolism of RA. Tretinoin 76-78 haptoglobin-related protein Homo sapiens 43-46
9125196-11 1997 These results suggest some retinoid analogs, including 4-HPR, may have clinical utility because of their ability to increase the biological half-life of RA. Tretinoin 153-155 haptoglobin-related protein Homo sapiens 57-60
8663150-3 1996 In this report, we demonstrate that RA-induced CD38 protein from human myeloid (HL-60) leukemia cells coimmunoprecipitates with another protein of molecular mass approximately190 kDa (p190). Tretinoin 36-38 contactin associated protein 1 Homo sapiens 184-188
15477383-6 2004 In conclusion, chronic atRA treatment increases gene and protein expressions of ACE2, resulting in the reduction of blood pressure and the attenuation of myocardial damage in SHR, which suggests that atRA may be an attractive candidate for the potential prevention and treatment of human essential hypertension. Tretinoin 23-27 angiotensin converting enzyme 2 Homo sapiens 80-84
8841765-3 1996 The retinol-binding proteins CRBP I and CRBP II appear to play an essential role in retinyl ester hydrolysis and formation and in retinoic acid formation. Tretinoin 130-143 retinol binding protein 1 Homo sapiens 29-35
8663081-6 1996 Induction of LRAT by retinoic acid reduced conversion of retinol to retinoic acid by 50%. Tretinoin 21-34 lecithin retinol acyltransferase Homo sapiens 13-17
9056251-2 1997 PP2A activity of HL-60 cells for phosphorylated myelin basic protein showed a sharp and transient increase after 18-h treatment with 1 microM retinoic acid, which corresponded to G1/S boundary of the cell cycle. Tretinoin 142-155 myelin basic protein Homo sapiens 48-68
8663081-6 1996 Induction of LRAT by retinoic acid reduced conversion of retinol to retinoic acid by 50%. Tretinoin 68-81 lecithin retinol acyltransferase Homo sapiens 13-17
15477383-6 2004 In conclusion, chronic atRA treatment increases gene and protein expressions of ACE2, resulting in the reduction of blood pressure and the attenuation of myocardial damage in SHR, which suggests that atRA may be an attractive candidate for the potential prevention and treatment of human essential hypertension. Tretinoin 200-204 angiotensin converting enzyme 2 Homo sapiens 80-84
8663081-7 1996 This reduction in retinoic acid synthesis resulted from sequestration of retinol as retinyl esters, since inhibition of LRAT restored retinoic acid synthesis to control levels. Tretinoin 18-31 lecithin retinol acyltransferase Homo sapiens 120-124
8663081-7 1996 This reduction in retinoic acid synthesis resulted from sequestration of retinol as retinyl esters, since inhibition of LRAT restored retinoic acid synthesis to control levels. Tretinoin 134-147 lecithin retinol acyltransferase Homo sapiens 120-124
9121125-4 1997 Expression of HB5 and HF2 antigens was down-regulated during cellular differentiation of G3 cells by retinoic acid or N,N"-hexamethylene-bis-acetamide treatment, whereas that of HE11 antigen was up-regulated with cellular differentiation by retinoic acid. Tretinoin 101-114 keratin 85 Homo sapiens 14-17
9121125-4 1997 Expression of HB5 and HF2 antigens was down-regulated during cellular differentiation of G3 cells by retinoic acid or N,N"-hexamethylene-bis-acetamide treatment, whereas that of HE11 antigen was up-regulated with cellular differentiation by retinoic acid. Tretinoin 241-254 keratin 85 Homo sapiens 14-17
8663081-9 1996 Regulation of LRAT activity by retinoic acid provides a novel mechanism through which retinoic acid can regulate its own level by controlling availability of retinol for conversion to retinoic acid. Tretinoin 31-44 lecithin retinol acyltransferase Homo sapiens 14-18
15302897-7 2004 One CpG island was aberrantly methylated in NB4 cells, but became hyperacetylated and was induced following ATRA treatment and was associated with the HoxA1 gene, suggesting it may be a target gene of ATRA in APL. Tretinoin 108-112 homeobox A1 Homo sapiens 151-156
8663081-9 1996 Regulation of LRAT activity by retinoic acid provides a novel mechanism through which retinoic acid can regulate its own level by controlling availability of retinol for conversion to retinoic acid. Tretinoin 86-99 lecithin retinol acyltransferase Homo sapiens 14-18
8663081-9 1996 Regulation of LRAT activity by retinoic acid provides a novel mechanism through which retinoic acid can regulate its own level by controlling availability of retinol for conversion to retinoic acid. Tretinoin 86-99 lecithin retinol acyltransferase Homo sapiens 14-18
9070313-0 1997 Retinoic acid induces the expression of germ-line C alpha transcript mainly by a TGF-beta-independent mechanism. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 81-89
9070313-8 1997 These results suggest that the major induction pathway of I alpha C alpha was not mediated by active TGF-beta and that RA at physiological concentrations may be involved in IgA isotype switching in vivo in a TGF-beta-independent manner. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 208-216
9051263-1 1997 The mouse EC cell line P19, differentiating in vitro into neural cell types under the influence of retinoic acid, represents a well established model system for neurogenesis. Tretinoin 99-112 interleukin 23, alpha subunit p19 Mus musculus 23-26
8660922-1 1996 A 2.8-kb cDNA encoding a new transcription factor (AP-2.2) has been cloned from mouse P19 embryonal carcinoma cells, in which the corresponding mRNA begins to accumulate 30 min after retinoic acid (RA) addition. Tretinoin 183-196 interleukin 23, alpha subunit p19 Mus musculus 86-89
8660922-1 1996 A 2.8-kb cDNA encoding a new transcription factor (AP-2.2) has been cloned from mouse P19 embryonal carcinoma cells, in which the corresponding mRNA begins to accumulate 30 min after retinoic acid (RA) addition. Tretinoin 198-200 interleukin 23, alpha subunit p19 Mus musculus 86-89
15371543-6 2004 CREB is a major target of extracellular signal regulated kinase ERK1/2 signaling in neuronal cells, and we demonstrate here that RA induces an early stimulation of ERK1/2, which is required both for CREB phosphorylation and transcriptional activity. Tretinoin 129-131 mitogen activated protein kinase 3 Rattus norvegicus 64-70
8639786-3 1996 We investigated how LFA-1/ICAM-1-mediated adhesion and aggregation are regulated in HL-60 cells induced to differentiate into neutrophils by retinoic acid (RA). Tretinoin 141-154 integrin subunit alpha L Homo sapiens 20-25
8639786-3 1996 We investigated how LFA-1/ICAM-1-mediated adhesion and aggregation are regulated in HL-60 cells induced to differentiate into neutrophils by retinoic acid (RA). Tretinoin 156-158 integrin subunit alpha L Homo sapiens 20-25
8639786-9 1996 The HL-60 cells transfected with the active form of Ras (Val12) exhibited LFA-1/ICAM-1-dependent aggregation by RA stimulation without change in the avidity of LFA-1. Tretinoin 112-114 integrin subunit alpha L Homo sapiens 74-79
9071982-9 1997 The biological activities of TR2-11 and TR2-11-t on a direct repeat 5-type retinoic acid (RA) response element (RARE)-containing reporter gene was examined in Cos cells. Tretinoin 75-88 nuclear receptor subfamily 2, group C, member 1 Mus musculus 29-35
9071982-9 1997 The biological activities of TR2-11 and TR2-11-t on a direct repeat 5-type retinoic acid (RA) response element (RARE)-containing reporter gene was examined in Cos cells. Tretinoin 75-88 nuclear receptor subfamily 2, group C, member 1 Mus musculus 29-32
9071982-9 1997 The biological activities of TR2-11 and TR2-11-t on a direct repeat 5-type retinoic acid (RA) response element (RARE)-containing reporter gene was examined in Cos cells. Tretinoin 90-92 nuclear receptor subfamily 2, group C, member 1 Mus musculus 29-35
15371543-6 2004 CREB is a major target of extracellular signal regulated kinase ERK1/2 signaling in neuronal cells, and we demonstrate here that RA induces an early stimulation of ERK1/2, which is required both for CREB phosphorylation and transcriptional activity. Tretinoin 129-131 mitogen activated protein kinase 3 Rattus norvegicus 164-170
15376324-0 2004 Crk-associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all-trans retinoic acid. Tretinoin 139-152 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 46-51
9015314-2 1997 There are three types of nuclear receptors for all-trans retinoic acid in mammals, RAR alpha, RAR beta, and RAR gamma, which transduce the retinoic acid signal by inducing or repressing the transcription of target genes (Leid, M., P. Kastner, and P. Chambon. Tretinoin 57-70 retinoic acid receptor, beta Mus musculus 94-102
9002638-3 1997 Here we have examined mouse testis and epididymis for the presence of endogenous retinoic acid and for the expression of genes encoding class I and class IV alcohol dehydrogenases (ADH), both of which catalyze retinol oxidation, the rate-limiting step in the conversion of retinol to retinoic acid. Tretinoin 284-297 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 181-184
8666241-0 1996 An apparent autocrine mechanism amplifies the dexamethasone- and retinoic acid-induced expression of mouse lipocalin-encoding gene 24p3. Tretinoin 65-78 lipocalin 2 Mus musculus 131-135
15376324-2 2004 In the human neuroblastoma cell line, SH-SY5Y, atRA rapidly induces (within 4 hr) the expression of the Crk-associated substrate (Cas) family member, neural precursor cell-expressed, developmentally down-regulated gene 9 (NEDD9) also called the human enhancer of filamentation (HEF1). Tretinoin 47-51 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 150-220
15376324-2 2004 In the human neuroblastoma cell line, SH-SY5Y, atRA rapidly induces (within 4 hr) the expression of the Crk-associated substrate (Cas) family member, neural precursor cell-expressed, developmentally down-regulated gene 9 (NEDD9) also called the human enhancer of filamentation (HEF1). Tretinoin 47-51 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 222-227
8631848-5 1996 Pretreatment of cells with retinoic acid (RA) for 16 h followed by IFN-beta, but not the converse, induced cytotoxic effects in the cells. Tretinoin 27-40 interferon beta 1 Homo sapiens 67-75
9067636-3 1997 Treatment with retinoic acid (RA, 1 microM) or 1,250(OH)2-vitamin D3 (1,25-D3, 10 nM) increased the expression of the monocytic surface antigens CD11b plus CD11c, and CD11b, CD11c, CD14 plus CD18, respectively. Tretinoin 15-28 integrin subunit alpha X Homo sapiens 156-161
8631848-5 1996 Pretreatment of cells with retinoic acid (RA) for 16 h followed by IFN-beta, but not the converse, induced cytotoxic effects in the cells. Tretinoin 42-44 interferon beta 1 Homo sapiens 67-75
15376324-2 2004 In the human neuroblastoma cell line, SH-SY5Y, atRA rapidly induces (within 4 hr) the expression of the Crk-associated substrate (Cas) family member, neural precursor cell-expressed, developmentally down-regulated gene 9 (NEDD9) also called the human enhancer of filamentation (HEF1). Tretinoin 47-51 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 278-282
8732669-5 1996 RA-induced differentiation to primitive endoderm led to a transition from PKC beta to PKC alpha expression. Tretinoin 0-2 protein kinase C beta Homo sapiens 74-82
9067636-3 1997 Treatment with retinoic acid (RA, 1 microM) or 1,250(OH)2-vitamin D3 (1,25-D3, 10 nM) increased the expression of the monocytic surface antigens CD11b plus CD11c, and CD11b, CD11c, CD14 plus CD18, respectively. Tretinoin 15-28 integrin subunit alpha X Homo sapiens 174-179
9067636-3 1997 Treatment with retinoic acid (RA, 1 microM) or 1,250(OH)2-vitamin D3 (1,25-D3, 10 nM) increased the expression of the monocytic surface antigens CD11b plus CD11c, and CD11b, CD11c, CD14 plus CD18, respectively. Tretinoin 15-28 CD14 molecule Homo sapiens 181-185
15376324-6 2004 A putative retinoic acid response element in the 5" region of the NEDD9 promoter binds specifically to a RXR/RAR heterodimer and forms a higher molecular weight complex upon addition of a retinoic acid receptor-specific antibody. Tretinoin 11-24 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 66-71
8732669-8 1996 The PKC beta to PKC alpha transition was specific for parietal endoderm; aggregation of RA-treated F9 cells induced visceral endoderm differentiation with elevated expression of PKC beta. Tretinoin 88-90 protein kinase C beta Homo sapiens 178-186
15492863-9 2004 DGAT expression was similar in lean and obese rats and was reduced by treatment with ATRA in obese rats. Tretinoin 85-89 diacylglycerol O-acyltransferase 1 Rattus norvegicus 0-4
8817533-0 1996 Induction of trk receptors by retinoic acid in a human embryonal carcinoma cell line. Tretinoin 30-43 neurotrophic receptor tyrosine kinase 1 Homo sapiens 13-16
8817533-4 1996 Our study demonstrated that the expression of mRNAs for three human trk receptors was significantly induced after treatment with retinoic acid. Tretinoin 129-142 neurotrophic receptor tyrosine kinase 1 Homo sapiens 68-71
8943263-0 1996 Retinoic acid-induced expression of apolipoprotein D and concomitant growth arrest in human breast cancer cells are mediated through a retinoic acid receptor RARalpha-dependent signaling pathway. Tretinoin 0-13 apolipoprotein D Homo sapiens 36-52
8943263-1 1996 Apolipoprotein D (apoD) is a human plasma protein, belonging to the lipocalin superfamily, that is produced by a specific subtype of highly differentiated breast carcinomas and that is strongly up-regulated by retinoic acid (RA) in breast cancer cells. Tretinoin 210-223 apolipoprotein D Homo sapiens 0-16
8943263-1 1996 Apolipoprotein D (apoD) is a human plasma protein, belonging to the lipocalin superfamily, that is produced by a specific subtype of highly differentiated breast carcinomas and that is strongly up-regulated by retinoic acid (RA) in breast cancer cells. Tretinoin 210-223 apolipoprotein D Homo sapiens 18-22
8943263-1 1996 Apolipoprotein D (apoD) is a human plasma protein, belonging to the lipocalin superfamily, that is produced by a specific subtype of highly differentiated breast carcinomas and that is strongly up-regulated by retinoic acid (RA) in breast cancer cells. Tretinoin 225-227 apolipoprotein D Homo sapiens 0-16
8943263-1 1996 Apolipoprotein D (apoD) is a human plasma protein, belonging to the lipocalin superfamily, that is produced by a specific subtype of highly differentiated breast carcinomas and that is strongly up-regulated by retinoic acid (RA) in breast cancer cells. Tretinoin 225-227 apolipoprotein D Homo sapiens 18-22
8959336-13 1996 Activin and bFGF appeared to exert differential actions on RA-induced neuronal differentiation. Tretinoin 59-61 fibroblast growth factor 2 Mus musculus 12-16
15646024-0 2004 Retinoic acid administration and vitamin A status modulate retinoid X receptor alpha and retinoic acid receptor alpha levels in mouse brown adipose tissue. Tretinoin 0-13 retinoid X receptor alpha Mus musculus 59-84
8726400-3 1996 In vitro treatment with ATRA dramatically modifies the adhesion phenotype of APL blast cells, promoting a consistently striking up-regulation of CD11b, CD11c, CD15, CD65, CD54, and CD38. Tretinoin 24-28 integrin subunit alpha X Homo sapiens 152-157
15646024-1 2004 BACKGROUND/AIMS: Retinoic acid (RA), the carboxylic acid form of vitamin A, through the activation of cognate receptors, stimulates the transcription of the gene encoding uncoupling protein 1 (UCP1), which is critical to brown adipose tissue (BAT) thermogenesis. Tretinoin 17-30 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 171-191
15646024-1 2004 BACKGROUND/AIMS: Retinoic acid (RA), the carboxylic acid form of vitamin A, through the activation of cognate receptors, stimulates the transcription of the gene encoding uncoupling protein 1 (UCP1), which is critical to brown adipose tissue (BAT) thermogenesis. Tretinoin 17-30 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 193-197
15646024-1 2004 BACKGROUND/AIMS: Retinoic acid (RA), the carboxylic acid form of vitamin A, through the activation of cognate receptors, stimulates the transcription of the gene encoding uncoupling protein 1 (UCP1), which is critical to brown adipose tissue (BAT) thermogenesis. Tretinoin 32-34 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 171-191
15646024-1 2004 BACKGROUND/AIMS: Retinoic acid (RA), the carboxylic acid form of vitamin A, through the activation of cognate receptors, stimulates the transcription of the gene encoding uncoupling protein 1 (UCP1), which is critical to brown adipose tissue (BAT) thermogenesis. Tretinoin 32-34 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 193-197
8758274-1 1996 OBJECTIVES: To determine if the sera of patients with acute promyelocytic leukemia (APL) and all-trans retinoic acid (ATRA) inhibit the formation of colony-forming-unit of megakaryocyte (CFU-Meg). Tretinoin 93-116 protein tyrosine phosphatase non-receptor type 4 Homo sapiens 191-194
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 261-274 prolyl 4-hydroxylase subunit beta Homo sapiens 17-44
8758274-1 1996 OBJECTIVES: To determine if the sera of patients with acute promyelocytic leukemia (APL) and all-trans retinoic acid (ATRA) inhibit the formation of colony-forming-unit of megakaryocyte (CFU-Meg). Tretinoin 118-122 protein tyrosine phosphatase non-receptor type 4 Homo sapiens 191-194
8758274-8 1996 ATRA could stimulate the growth of CFU-Meg. Tretinoin 0-4 protein tyrosine phosphatase non-receptor type 4 Homo sapiens 39-42
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 261-274 prolyl 4-hydroxylase subunit beta Homo sapiens 46-49
8758274-10 1996 ATRA stimulates the growth of CFU-Meg. Tretinoin 0-4 protein tyrosine phosphatase non-receptor type 4 Homo sapiens 34-37
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 261-274 prolyl 4-hydroxylase subunit beta Homo sapiens 105-108
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 276-278 prolyl 4-hydroxylase subunit beta Homo sapiens 17-44
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 276-278 prolyl 4-hydroxylase subunit beta Homo sapiens 46-49
15353226-4 2004 We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. Tretinoin 276-278 prolyl 4-hydroxylase subunit beta Homo sapiens 105-108
8636104-0 1996 Murine laminin B1 gene regulation during the retinoic acid- and dibutyryl cyclic AMP-induced differentiation of embryonic F9 teratocarcinoma stem cells. Tretinoin 45-58 laminin B1 Mus musculus 7-17
8636104-2 1996 Laminin B1 is induced in this differentiation process, but is not transcriptionally activated until 24-48 h after RA addition and is not maximally induced until approximately 72 h. Cyclic AMP analogs enhance this transcriptional activation. Tretinoin 114-116 laminin B1 Mus musculus 0-10
15328022-0 2004 Retinoic acid selectively regulates Fgf10 expression and maintains cell identity in the prospective lung field of the developing foregut. Tretinoin 0-13 fibroblast growth factor 10 Rattus norvegicus 36-41
8710207-1 1996 P19 embryonal carcinoma cells differentiate into neuroectodermal derivates upon aggregation and treatment with retinoic acid (RA). Tretinoin 111-124 interleukin 23, alpha subunit p19 Mus musculus 0-3
8710207-1 1996 P19 embryonal carcinoma cells differentiate into neuroectodermal derivates upon aggregation and treatment with retinoic acid (RA). Tretinoin 126-128 interleukin 23, alpha subunit p19 Mus musculus 0-3
8710207-2 1996 Such RA-induced P19 cells, concomitant with neuronal differentiation, produce the neuropeptide head activator (HA) and release HA into the culture medium. Tretinoin 5-7 interleukin 23, alpha subunit p19 Mus musculus 16-19
15328022-2 2004 Here, we provide novel evidence that a major role for RA is to selectively maintain mesodermal proliferation and induce fibroblast growth factor 10 (Fgf10) expression in the foregut region where the lung forms. Tretinoin 54-56 fibroblast growth factor 10 Rattus norvegicus 120-147
15328022-2 2004 Here, we provide novel evidence that a major role for RA is to selectively maintain mesodermal proliferation and induce fibroblast growth factor 10 (Fgf10) expression in the foregut region where the lung forms. Tretinoin 54-56 fibroblast growth factor 10 Rattus norvegicus 149-154
15313187-6 2004 Thus, the RANKL/OPG ratio was markedly increased, suggesting a potential mechanism of ATRA-induced bone resorption. Tretinoin 86-90 TNF receptor superfamily member 11b Homo sapiens 16-19
8593698-1 1996 Use of retinoic acid and antisense against the central nervous system-specific POU transcription factor Brn-2. Tretinoin 7-20 POU domain, class 3, transcription factor 2 Mus musculus 104-109
15331408-7 2004 Moreover, retinoic acid repressed the vitamin D3-induced caspase-14 expression level. Tretinoin 10-23 caspase 14 Homo sapiens 57-67
8593698-5 1996 Under chemical induction of high concentrations of retinoic acid (1 micromol/L), P19 cells showed optimum differentiation into SMCs. Tretinoin 51-64 interleukin 23, alpha subunit p19 Mus musculus 81-84
9238678-9 1996 With RA treatment, RAR-alpha and RAR-gamma mRNA concentrations were approximately 70 and 25% respectively of those in cells decidualized in the absence of RA. Tretinoin 5-7 retinoic acid receptor gamma Homo sapiens 33-42
15331408-8 2004 In addition, the use of organotypic skin cultures demonstrated that 1alpha,25-dihydroxycholecalciferol enhanced epidermal differentiation and caspase-14 activation, whereas retinoic acid completely blocked caspase-14 processing. Tretinoin 173-186 caspase 14 Homo sapiens 206-216
15342476-0 2004 vhnf1 integrates global RA patterning and local FGF signals to direct posterior hindbrain development in zebrafish. Tretinoin 24-26 HNF1 homeobox Ba Danio rerio 0-5
8608243-9 1996 However, in the presence of PML-RAR, the synthetic retinoid is a much better transactivator of retinoic acid-responsive element-containing promoters than the natural retinoid, whereas, in the presence of RAR alpha, AM580 and ATRA have similar activity. Tretinoin 95-108 PML-RARA regulated adaptor molecule 1 Homo sapiens 28-35
15342476-6 2004 We show that RA induces val expression via activation of vhnf1 expression in the hindbrain. Tretinoin 13-15 HNF1 homeobox Ba Danio rerio 57-62
8611633-0 1996 Synergistic and selective stimulation of gelatinase B production in macrophages by lipopolysaccharide, trans-retinoic acid and CGP 41251, a protein kinase C regulator. Tretinoin 103-122 matrix metallopeptidase 9 Mus musculus 41-53
15262180-9 2004 These results strongly suggest that retinoic acid stimulates the release of VEGF in a p44/p42 MAP kinase-dependent manner in aortic smooth muscle cells. Tretinoin 36-49 interferon induced protein 44 Homo sapiens 86-89
8611633-7 1996 The stimulatory effect of CGP 41251 on gelatinase B production in RAW 264.7 was: (a) inhibited by calphostin C (as is the LPS-induced response), indicating a PKC-dependence; (b) inhibited by dexamethasone (as opposed to the LPS-induced response); and (c) enhanced by addition of trans-retinoic acid (RA). Tretinoin 279-298 matrix metallopeptidase 9 Mus musculus 39-51
8611633-7 1996 The stimulatory effect of CGP 41251 on gelatinase B production in RAW 264.7 was: (a) inhibited by calphostin C (as is the LPS-induced response), indicating a PKC-dependence; (b) inhibited by dexamethasone (as opposed to the LPS-induced response); and (c) enhanced by addition of trans-retinoic acid (RA). Tretinoin 66-68 matrix metallopeptidase 9 Mus musculus 39-51
8611633-8 1996 In fact, RA can induce gelatinase B production, either alone or in synergy with LPS and/or CGP 41251, since the combination of the three agents gives the highest gelatinase B response, at both the protein and the mRNA levels. Tretinoin 9-11 matrix metallopeptidase 9 Mus musculus 23-35
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 ankyrin repeat and BTB domain containing 3 Homo sapiens 194-200
8611633-8 1996 In fact, RA can induce gelatinase B production, either alone or in synergy with LPS and/or CGP 41251, since the combination of the three agents gives the highest gelatinase B response, at both the protein and the mRNA levels. Tretinoin 9-11 matrix metallopeptidase 9 Mus musculus 162-174
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 cyclin and CBS domain divalent metal cation transport mediator 2 Homo sapiens 210-219
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 240-245
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 74-78 tenascin R Homo sapiens 258-268
8562957-8 1996 In transcriptional assays using a retinoic acid response element reporter construct, both NPM-RAR fusion proteins act as retinoic acid-dependent transcriptional activators. Tretinoin 34-47 nucleophosmin 1 Homo sapiens 90-93
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 80-93 neural precursor cell expressed, developmentally down-regulated 9 Homo sapiens 240-245
8562957-8 1996 In transcriptional assays using a retinoic acid response element reporter construct, both NPM-RAR fusion proteins act as retinoic acid-dependent transcriptional activators. Tretinoin 121-134 nucleophosmin 1 Homo sapiens 90-93
8780165-5 1996 Clinically achievable doses of RA rapidly caused large- and small-vessel endothelial cells to become refractory to stimulation of migration either by tumor-conditioned media or purified angiogenic factors (a-fibroblast growth factor (aFGF), bFGF, vascular endothelial GF, platelet-derived GF, TGF beta-1, and IL-8). Tretinoin 31-33 fibroblast growth factor 2 Rattus norvegicus 241-245
15318809-4 2004 We report here the identification of 14 genes that are rapidly induced by atRA (retinoic acid induced in neuroblastoma or RAINB), eight of which were previously not known to be atRA responsive (BTBD11, calmin, cyclin M2, ephrin B2, HOXD10, NEDD9, RAINB6 and tenascin R). Tretinoin 80-93 tenascin R Homo sapiens 258-268
15280446-6 2004 In vitro, these metastasis-associated NDPK-A aberrations abrogated retinoic acid-induced neuronal differentiation while increasing cloning efficiency, cell survival, and colony formation of NB69 derivatives. Tretinoin 67-80 NME/NM23 nucleoside diphosphate kinase 1 Homo sapiens 38-44
8574972-0 1996 Retinoic acid normalizes the increased gene transcription rate of TGF-alpha and EGFR in head and neck cancer cell lines. Tretinoin 0-13 transforming growth factor alpha Homo sapiens 66-75
8574972-4 1996 In this report, we examined the hypothesis that the action of RA on the mucosa of the upper aerodigestive tract is mediated via downregulation of steady-state TGF-alpha and/or EGFR mRNA levels. Tretinoin 62-64 transforming growth factor alpha Homo sapiens 159-168
8574972-6 1996 Nuclear run-on analysis indicated that the RA-mediated reduction of TGF-alpha and EGFR steady-state mRNA levels was a result of decreased gene transcription. Tretinoin 43-45 transforming growth factor alpha Homo sapiens 68-77
8574972-7 1996 These results suggest that the clinical effects of RA in SCCHN patients may be due to a downmodulation of TGF-alpha and EGFR mRNA production. Tretinoin 51-53 transforming growth factor alpha Homo sapiens 106-115
15175265-3 2004 We found that although the enzyme required for RA production during early embryogenesis, retinaldehyde dehydrogenase-2 (Raldh2), was expressed in the visceral endoderm, RA receptors alpha1 and alpha2 were expressed in endothelial cells in the mesoderm, indicating that they are direct targets of RA. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 89-118
8868305-3 1996 The expression of LHRH mRNA and LHRH protein level was correlated with neuronal differentiation induced by retinoic acid (RA). Tretinoin 107-120 gonadotropin releasing hormone 1 Homo sapiens 18-22
8868305-3 1996 The expression of LHRH mRNA and LHRH protein level was correlated with neuronal differentiation induced by retinoic acid (RA). Tretinoin 107-120 gonadotropin releasing hormone 1 Homo sapiens 32-36
15175265-3 2004 We found that although the enzyme required for RA production during early embryogenesis, retinaldehyde dehydrogenase-2 (Raldh2), was expressed in the visceral endoderm, RA receptors alpha1 and alpha2 were expressed in endothelial cells in the mesoderm, indicating that they are direct targets of RA. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 120-126
8868305-3 1996 The expression of LHRH mRNA and LHRH protein level was correlated with neuronal differentiation induced by retinoic acid (RA). Tretinoin 122-124 gonadotropin releasing hormone 1 Homo sapiens 18-22
8868305-3 1996 The expression of LHRH mRNA and LHRH protein level was correlated with neuronal differentiation induced by retinoic acid (RA). Tretinoin 122-124 gonadotropin releasing hormone 1 Homo sapiens 32-36
15175265-3 2004 We found that although the enzyme required for RA production during early embryogenesis, retinaldehyde dehydrogenase-2 (Raldh2), was expressed in the visceral endoderm, RA receptors alpha1 and alpha2 were expressed in endothelial cells in the mesoderm, indicating that they are direct targets of RA. Tretinoin 169-171 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 120-126
8868305-5 1996 These results suggest that RA affects the expression of LHRH mRNA and the level of LHRH protein in SK-N-SH cells. Tretinoin 27-29 gonadotropin releasing hormone 1 Homo sapiens 56-60
8868305-5 1996 These results suggest that RA affects the expression of LHRH mRNA and the level of LHRH protein in SK-N-SH cells. Tretinoin 27-29 gonadotropin releasing hormone 1 Homo sapiens 83-87
15175265-5 2004 Exogenous provision of RA or Fn to Raldh2(-/-) explants in whole mouse embryo culture restored vascular remodeling, visceral endoderm survival, as well as integrin alpha5 expression and its downstream signaling that controls endothelial growth. Tretinoin 23-25 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 35-41
8868305-7 1996 The ability of RA to induce changes in LHRH at the mRNA and at the peptide levels will allow further study of RA regulation of LHRH at the neuronal level. Tretinoin 15-17 gonadotropin releasing hormone 1 Homo sapiens 39-43
15161698-7 2004 We examined the effect of retinoic acid and ROL on LRAT mRNA expression in five human bladder cancer cell lines. Tretinoin 26-39 lecithin retinol acyltransferase Homo sapiens 51-55
8868305-7 1996 The ability of RA to induce changes in LHRH at the mRNA and at the peptide levels will allow further study of RA regulation of LHRH at the neuronal level. Tretinoin 15-17 gonadotropin releasing hormone 1 Homo sapiens 127-131
8868305-7 1996 The ability of RA to induce changes in LHRH at the mRNA and at the peptide levels will allow further study of RA regulation of LHRH at the neuronal level. Tretinoin 110-112 gonadotropin releasing hormone 1 Homo sapiens 39-43
8868305-7 1996 The ability of RA to induce changes in LHRH at the mRNA and at the peptide levels will allow further study of RA regulation of LHRH at the neuronal level. Tretinoin 110-112 gonadotropin releasing hormone 1 Homo sapiens 127-131
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 0-13 RB transcriptional corepressor 1 Homo sapiens 188-191
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 0-13 RB transcriptional corepressor 1 Homo sapiens 231-234
8570633-0 1996 Tissue-specific response of the human platelet-activating factor receptor gene to retinoic acid and thyroid hormone by alternative promoter usage. Tretinoin 82-95 platelet activating factor receptor Homo sapiens 38-73
8570633-1 1996 We have studied the effects of retinoic acid (RA) and thyroid hormone (3,3",5-triiodothyronine; T3) on platelet-activating factor receptor (PAFR) gene expression in intact rats and the ability of two human PAFR gene promoters (PAFR promoters 1 and 2) to generate two transcripts (PAFR transcripts 1 and 2). Tretinoin 31-44 platelet-activating factor receptor Rattus norvegicus 103-138
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 15-17 RB transcriptional corepressor 1 Homo sapiens 188-191
8570633-1 1996 We have studied the effects of retinoic acid (RA) and thyroid hormone (3,3",5-triiodothyronine; T3) on platelet-activating factor receptor (PAFR) gene expression in intact rats and the ability of two human PAFR gene promoters (PAFR promoters 1 and 2) to generate two transcripts (PAFR transcripts 1 and 2). Tretinoin 31-44 platelet-activating factor receptor Rattus norvegicus 140-144
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 15-17 RB transcriptional corepressor 1 Homo sapiens 231-234
8557705-6 1996 To assess promoter activity, the 5"-flanking sequence (844 base pairs) of the necdin gene was fused to the LacZ reporter gene and transiently transfected into retinoic acid-treated P19 embryonal carcinoma cells. Tretinoin 159-172 necdin, MAGE family member Mus musculus 78-84
8788034-6 1996 RA-induced reduction in Cdk2 activity was modest and occurred after %S phase declined, while Cdk4 activity was reduced, coincident with cell cycle changes. Tretinoin 0-2 cyclin dependent kinase 2 Homo sapiens 24-28
15126328-6 2004 Manipulation of MAT1 abundance shows that MAT1 reduction mimics RA-induced hypophosphorylation of pRb/RXRalpha, proliferation inhibition, and neurite outgrowth, whereas MAT1 overexpression resists these RA actions. Tretinoin 64-66 MNAT1 component of CDK activating kinase Homo sapiens 16-20
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 97-110 bone morphogenetic protein 2 Homo sapiens 33-38
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 97-110 bone morphogenetic protein 4 Homo sapiens 43-48
15126328-6 2004 Manipulation of MAT1 abundance shows that MAT1 reduction mimics RA-induced hypophosphorylation of pRb/RXRalpha, proliferation inhibition, and neurite outgrowth, whereas MAT1 overexpression resists these RA actions. Tretinoin 64-66 MNAT1 component of CDK activating kinase Homo sapiens 42-46
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 97-110 bone morphogenetic protein 2 Homo sapiens 166-171
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 97-110 bone morphogenetic protein 4 Homo sapiens 210-215
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 112-114 bone morphogenetic protein 2 Homo sapiens 33-38
15126328-6 2004 Manipulation of MAT1 abundance shows that MAT1 reduction mimics RA-induced hypophosphorylation of pRb/RXRalpha, proliferation inhibition, and neurite outgrowth, whereas MAT1 overexpression resists these RA actions. Tretinoin 64-66 RB transcriptional corepressor 1 Homo sapiens 98-101
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 112-114 bone morphogenetic protein 4 Homo sapiens 43-48
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 112-114 bone morphogenetic protein 2 Homo sapiens 166-171
15126328-6 2004 Manipulation of MAT1 abundance shows that MAT1 reduction mimics RA-induced hypophosphorylation of pRb/RXRalpha, proliferation inhibition, and neurite outgrowth, whereas MAT1 overexpression resists these RA actions. Tretinoin 64-66 MNAT1 component of CDK activating kinase Homo sapiens 42-46
8788040-2 1996 The bone morphogenetic proteins, Bmp-2 and Bmp-4, are candidates for such growth factors because retinoic acid (RA) treatment of F9 embryonal carcinoma cells induced Bmp-2 mRNA, while simultaneously repressing Bmp-4 levels. Tretinoin 112-114 bone morphogenetic protein 4 Homo sapiens 210-215
15040006-9 2004 We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Tretinoin 28-32 cyclin dependent kinase 4 Homo sapiens 133-158
15040006-9 2004 We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Tretinoin 28-32 cyclin dependent kinase 4 Homo sapiens 160-164
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 139-143 cyclin dependent kinase 4 Homo sapiens 173-177
8835849-3 1996 Retinoic acid (RA) acted synergistically with type I collagen at each concentration to induce a much greater increase in OP mRNA than in cells on plastic. Tretinoin 0-13 secreted phosphoprotein 1 Rattus norvegicus 121-123
8835849-3 1996 Retinoic acid (RA) acted synergistically with type I collagen at each concentration to induce a much greater increase in OP mRNA than in cells on plastic. Tretinoin 15-17 secreted phosphoprotein 1 Rattus norvegicus 121-123
15189689-12 2004 When RA was added to the medium and the culture was continued for nine days, the percent of immature DC (CD1a + HLA-DR+) was much higher than that of the control (absence of RA) (58.93 +/- 4.70 vs. 45.80 +/- 7.88, t = 6.575, P < 0.001); whereas, mature DC (CD83 + HLA-DR+) percentage was markedly lower than that of the control (17.25 +/- 8.49 vs. 27.92 +/- 13.94, t = 4.435, P = 0.002). Tretinoin 5-7 CD1a molecule Homo sapiens 105-109
8835849-4 1996 In addition, RA increased the phosphorylation of secreted OP. Tretinoin 13-15 secreted phosphoprotein 1 Rattus norvegicus 58-60
9004232-4 1996 Soluble factors such as retinoic acid and the products of the Noggin and Sonic hedgehog genes induce changes in families of transcription factors such as the Hox, Sox, Pax and Pou gene products and these alter the expression of banks of downstream genes thereby controlling the developmental fate of those cells. Tretinoin 24-37 noggin Homo sapiens 62-68
15113415-7 2004 In some cells CRBP reexpression was potentiated by co-treatment with retinoic acid, an inducer of CRBP, and trichostatin A, a histone deacetylase inhibitor. Tretinoin 69-82 retinol binding protein 1 Homo sapiens 14-18
8960371-7 1996 RAR beta 2 promoter activation by calcitriol was blocked by inhibitors of protein kinase C indicating that calcitriol elicits its effect via protein kinase C. Therefore, calcitriol induces differentiation of F9 mouse embryonal carcinoma cells at least in part by a pathway different from the classical one operative with retinoic acids. Tretinoin 321-335 retinoic acid receptor, beta Mus musculus 0-8
8936593-1 1996 Rev-erb beta is a member of the nuclear receptor superfamily, which includes a group of transcription factors involved in the response to steroids, vitamin D, retinoic acids, and other lipophilic molecules. Tretinoin 159-173 nuclear receptor subfamily 1 group D member 2 Homo sapiens 0-12
8964570-7 1996 Within the cell, two cellular retinoic acid-binding proteins (CRABP-I and -II) and a ROL-binding protein (CRBP-I) regulate the levels of free RA and ROL. Tretinoin 30-43 retinol binding protein 1 Homo sapiens 62-77
21544324-10 1996 Treatment with retinoic acid increased RAR-alpha level in C4I, HT-3, and CaSki; RAR-beta in HT-3; and RAR-gamma in HT-3 and C4I cells. Tretinoin 15-28 retinoic acid receptor, beta Mus musculus 80-88
15113415-7 2004 In some cells CRBP reexpression was potentiated by co-treatment with retinoic acid, an inducer of CRBP, and trichostatin A, a histone deacetylase inhibitor. Tretinoin 69-82 retinol binding protein 1 Homo sapiens 98-102
15093674-3 2004 All-trans retinoic acid (t-RA) and all-trans retinol significantly inhibited a LPS-induced PGE(2) production as assessed by enzyme-linked immunosorbant assay (ELISA) and COX-2 protein expression as assessed by Western blot assay in mouse peritoneal macrophages, after knocking out the COX-1 activity by aspirin. Tretinoin 0-23 cytochrome c oxidase II, mitochondrial Mus musculus 170-175
8524311-0 1996 Vitamin D interferes with transactivation of the growth hormone gene by thyroid hormone and retinoic acid. Tretinoin 92-105 gonadotropin releasing hormone receptor Rattus norvegicus 49-63
8524311-2 1996 Incubation of pituitary GH4C1 cells with nanomolar concentrations of vitamin D markedly reduces the response of the rat growth hormone mRNA to thyroid hormone triiodothyronine (T3) and RA. Tretinoin 185-187 gonadotropin releasing hormone receptor Rattus norvegicus 120-134
8824230-1 1996 Mouse P19 embryonal carcinoma cells in aggregation culture in the presence of 10(-6) M retinoic acid followed by monolayer culture differentiate into nerve and glial cells. Tretinoin 87-100 interleukin 23, alpha subunit p19 Mus musculus 6-9
15093674-3 2004 All-trans retinoic acid (t-RA) and all-trans retinol significantly inhibited a LPS-induced PGE(2) production as assessed by enzyme-linked immunosorbant assay (ELISA) and COX-2 protein expression as assessed by Western blot assay in mouse peritoneal macrophages, after knocking out the COX-1 activity by aspirin. Tretinoin 25-29 cytochrome c oxidase II, mitochondrial Mus musculus 170-175
14976428-4 2004 We proposed that C/EBPbeta is an ATRA-dependent PML/RARA target gene and that its activation is critical during ATRA-induced differentiation of APL cells. Tretinoin 33-37 CCAAT enhancer binding protein beta Homo sapiens 17-26
8895514-7 1996 Lastly, the pluripotent embryonal cancer cell line Tera-2 expressed IPW at the same level before and after differentiation induced by retinoic acid, suggesting that this gene functions in a "housekeeping" capacity throughout cell growth. Tretinoin 134-147 imprinted in Prader-Willi syndrome Homo sapiens 68-71
15110044-10 2004 Conversely, raldh2 expression is reduced with RA treatment. Tretinoin 46-48 aldehyde dehydrogenase 1 family, member A2 Danio rerio 12-18
8912806-0 1996 Regulation of cornifin alpha expression in the vaginal and uterine epithelium by estrogen and retinoic acid. Tretinoin 94-107 small proline rich protein 1A Homo sapiens 14-28
7497526-10 1995 These findings suggest that RA induces IgA production by (IL-5 + LPS)-stimulated B-cells in TGF-beta-independent and TGF-beta-dependent manners. Tretinoin 28-30 transforming growth factor, beta 1 Mus musculus 92-100
7497526-10 1995 These findings suggest that RA induces IgA production by (IL-5 + LPS)-stimulated B-cells in TGF-beta-independent and TGF-beta-dependent manners. Tretinoin 28-30 transforming growth factor, beta 1 Mus musculus 117-125
7588278-11 1995 RA also induced osteopontin gene expression in concert with vitamin D in normal rats. Tretinoin 0-2 secreted phosphoprotein 1 Rattus norvegicus 16-27
8912806-1 1996 In this study, we analyze the regulation of the squamous-specific gene, cornifin alpha, by estrogen and retinoic acid in vaginal and uterine epithelial cells. Tretinoin 104-117 small proline rich protein 1A Homo sapiens 72-86
15110044-11 2004 Tests of the raldh2 promoter in cell transfections proved that RA directly represses its activity. Tretinoin 63-65 aldehyde dehydrogenase 1 family, member A2 Danio rerio 13-19
8614415-5 1995 The fusion protein PML-RAR which is not localized in nuclear bodies, also enhanced the transactivating activity of PR, but this effect was totally suppressed by the administration of retinoic acid. Tretinoin 183-196 PML-RARA regulated adaptor molecule 1 Homo sapiens 19-26
8614415-5 1995 The fusion protein PML-RAR which is not localized in nuclear bodies, also enhanced the transactivating activity of PR, but this effect was totally suppressed by the administration of retinoic acid. Tretinoin 183-196 progesterone receptor Homo sapiens 115-117
15024057-3 2004 Exposure to retinoic acid (RA), a differentiation agent in many cell types, causes an upregulation of neurotrophin receptor TrkB and the cyclin kinase inhibitor p21(Cip1) at a transcriptional level. Tretinoin 12-25 neurotrophic receptor tyrosine kinase 2 Homo sapiens 124-128
8931868-3 1996 We have also previously identified a skin-specific gene (RIS-1/psoriasin) which is rapidly induced in human skin treated with RA. Tretinoin 126-128 transmembrane protein 158 Homo sapiens 57-62
15024057-3 2004 Exposure to retinoic acid (RA), a differentiation agent in many cell types, causes an upregulation of neurotrophin receptor TrkB and the cyclin kinase inhibitor p21(Cip1) at a transcriptional level. Tretinoin 27-29 neurotrophic receptor tyrosine kinase 2 Homo sapiens 124-128
8931868-6 1996 Relative to VH-treated skin, RA induced RIS-1 mRNA levels within 6 h, which further increased to 6.4-fold by 24 h (n = 4). Tretinoin 29-31 transmembrane protein 158 Homo sapiens 40-45
15024057-5 2004 As reported for other E-box-regulated promoters, ectopic expression of E47 and E12 basic helix-loop-helix (bHLH) proteins enhances RA-dependent expression of TrkB and p21(Cip1), whereas the inhibitory HLH Id2 exerts opposite effects. Tretinoin 131-133 transcription factor 3 Homo sapiens 71-74
8931868-10 1996 RA-induced skin erythema was not obvious until 24 to 48 h. We conclude, therefore, that induction of RIS-1 and CRABP II mRNA levels by topical RA in human skin are early, coordinated molecular events which precede the clinical cutaneous erythematous response to RA. Tretinoin 0-2 transmembrane protein 158 Homo sapiens 101-106
7492559-1 1995 Cellular retinoic acid binding protein-I (CRABP-I) and cellular retinoic acid binding protein-II (CRABP-II) are highly homologous, 15 kDa proteins which bind all-trans-retinoic acid. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 42-49
15024057-5 2004 As reported for other E-box-regulated promoters, ectopic expression of E47 and E12 basic helix-loop-helix (bHLH) proteins enhances RA-dependent expression of TrkB and p21(Cip1), whereas the inhibitory HLH Id2 exerts opposite effects. Tretinoin 131-133 epididymal sperm binding protein 1 Homo sapiens 79-82
7492559-3 1995 To obtain structural information which could aid the design of more selective ligands, isotope-directed NMR methods were employed to observe the CRABP-bound conformation of 13C-labeled retinoic acid and to identify its contact points with neighboring amino acids. Tretinoin 185-198 cellular retinoic acid binding protein 1 Homo sapiens 145-150
15024057-5 2004 As reported for other E-box-regulated promoters, ectopic expression of E47 and E12 basic helix-loop-helix (bHLH) proteins enhances RA-dependent expression of TrkB and p21(Cip1), whereas the inhibitory HLH Id2 exerts opposite effects. Tretinoin 131-133 neurotrophic receptor tyrosine kinase 2 Homo sapiens 158-162
7492559-10 1995 The pattern of intermolecular NOESY cross-peaks between 13C-labeled protons in the ring portion of retinoic acid and protein protons were different between CRABP-I and CRABP-II. Tretinoin 99-112 cellular retinoic acid binding protein 1 Homo sapiens 156-163
8947829-0 1996 Identification of an interleukin-1 beta converting enzyme-like activity that increases upon treatment of P19 cells with retinoic acid as the proteasome. Tretinoin 120-133 caspase 1 Mus musculus 21-57
8947829-2 1996 The interleukin-1 beta converting enzyme (ICE)-like Ac-YVAD-MCA hydrolytic activity was increased about 6-fold by treatment with retinoic acid. Tretinoin 129-142 caspase 1 Mus musculus 4-40
8947829-2 1996 The interleukin-1 beta converting enzyme (ICE)-like Ac-YVAD-MCA hydrolytic activity was increased about 6-fold by treatment with retinoic acid. Tretinoin 129-142 caspase 1 Mus musculus 42-45
8947829-6 1996 Enzymatic purification, Western blot analysis, and an immunoabsorption study demonstrated that the ICE-like activity in P19 cells is caused by the proteasome, and is stimulated during retinoic acid-induced differentiation. Tretinoin 184-197 caspase 1 Mus musculus 99-102
7556459-1 1995 We have previously shown that both transforming growth factor-beta (TGF-beta) and retinoic acid (RA) regulate the expression of cellular retinoic acid binding proteins (CRABP) I and II and TGF-beta 3 mRNAs in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Tretinoin 137-150 transforming growth factor, beta 1 Mus musculus 68-76
7556459-3 1995 Northern blot hybridization revealed that RA induced the expression of RAR-beta mRNA, there being little or no detectable expression in untreated MEPM cells. Tretinoin 42-44 retinoic acid receptor, beta Mus musculus 71-79
14676196-5 2004 CYP2C8 is one of the principal hepatic drug-metabolizing enzymes that oxidizes therapeutic drugs such as taxol and cerivastatin and endobiotics such as retinoic acid and arachidonic acid. Tretinoin 152-165 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6
7556459-4 1995 Induction by 3.3 microM RA was abrogated by simultaneous treatment with TGF-beta 1 (5 ng/ml). Tretinoin 24-26 transforming growth factor, beta 1 Mus musculus 72-82
8666391-8 1995 NET transcripts are detected in human NTera-2 teratocarcinoma cells after retinoic acid-induced neuronal differentiation. Tretinoin 74-87 EPH receptor B1 Homo sapiens 0-3
8952316-1 1996 We observed the effects of the retinoic acid (13-cis retinoic acid; 13-cis RA, and all-trans retinoic acid; ATRA) for the cell growth and the expression of CD 25 on peripheral blood mononuclear cells (PBMC) from 17 patients with adult T cell leukemia (ATL). Tretinoin 31-44 interleukin 2 receptor subunit alpha Homo sapiens 156-161
8952316-1 1996 We observed the effects of the retinoic acid (13-cis retinoic acid; 13-cis RA, and all-trans retinoic acid; ATRA) for the cell growth and the expression of CD 25 on peripheral blood mononuclear cells (PBMC) from 17 patients with adult T cell leukemia (ATL). Tretinoin 53-66 interleukin 2 receptor subunit alpha Homo sapiens 156-161
8952316-1 1996 We observed the effects of the retinoic acid (13-cis retinoic acid; 13-cis RA, and all-trans retinoic acid; ATRA) for the cell growth and the expression of CD 25 on peripheral blood mononuclear cells (PBMC) from 17 patients with adult T cell leukemia (ATL). Tretinoin 108-112 interleukin 2 receptor subunit alpha Homo sapiens 156-161
14988021-6 2004 These P19[Sox6] had acquired both characteristics of the wild-type P19 induced by RA. Tretinoin 82-84 SRY-box transcription factor 6 Homo sapiens 10-14
8703017-9 1996 Two isoforms (B56beta and B56delta) are highly expressed in adult brain; here we show that mRNA for these isoforms increases severalfold when neuroblastoma cell lines are induced to differentiate by retinoic acid treatment. Tretinoin 199-212 protein phosphatase 2 regulatory subunit B'beta Homo sapiens 14-21
7654186-1 1995 Functional retinoic acid response elements (RAREs) have been described wherein the direct repeats are separated by 1, 2 or 5 bp (termed DR1, DR2 and DR5 respectively). Tretinoin 11-24 down-regulator of transcription 1 Homo sapiens 136-139
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 30-43 down-regulator of transcription 1 Homo sapiens 91-94
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 74-76 down-regulator of transcription 1 Homo sapiens 91-94
7556191-7 1995 Exposure of HUVEC to 1 microM retinoic acid or the retinobenzoic acid, Ch55, led to the induction of the two RAR-beta mRNAs, RXR-alpha mRNA and CRBP-I mRNA, whereas the expression of the other receptor and CRABP-I transcripts did not change appreciably. Tretinoin 30-43 retinol binding protein 1 Homo sapiens 144-150
9387266-6 1996 Retinoic acid significantly inhibited monolayer growth of the breast carcinoma cells expressing RAR beta, while it had no effect on the growth of the control cells. Tretinoin 0-13 retinoic acid receptor, beta Mus musculus 96-104
7556191-7 1995 Exposure of HUVEC to 1 microM retinoic acid or the retinobenzoic acid, Ch55, led to the induction of the two RAR-beta mRNAs, RXR-alpha mRNA and CRBP-I mRNA, whereas the expression of the other receptor and CRABP-I transcripts did not change appreciably. Tretinoin 30-43 cellular retinoic acid binding protein 1 Homo sapiens 206-213
14743441-7 2004 In addition, RA-treated CD133+ cells expressed cell type-specific markers for oligodendrocytes including myelin basic protein (MBP) as shown by RT-PCR, proteolipid protein (PLP) by Western blot analysis, and cyclic nucleotide phosphodiesterase (CNPase) by immunostaining. Tretinoin 13-15 myelin basic protein Homo sapiens 127-130
14603524-5 2004 We demonstrate that RA-induced differentiation of CCE ES cells is associated with (1) downregulation of the LIF receptor (LIFR); (2) decreased tyrosine phosphorylation of signal transducer and activator of transcription 3 protein (Stat3); and (3) increased activation of extracellular regulated kinase (Erk1/2). Tretinoin 20-22 mitogen-activated protein kinase 3 Mus musculus 303-309
21552848-6 1995 Inhibition of AP-1 activity by retinoic acid or fluocinolone acetonide inhibited expression of tumor phenotype as measured by AI growth. Tretinoin 31-44 jun proto-oncogene Mus musculus 14-18
8760369-0 1996 In vitro and in vivo induction of brown adipocyte uncoupling protein (thermogenin) by retinoic acid. Tretinoin 86-99 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 70-81
8760369-1 1996 The effects of retinoic acid (RA) isomers (all-trans-RA and 9-cis-RA) on the appearance of uncoupling protein (UCP; thermogenin), the only unequivocal molecular marker of the brown adipocyte differentiated phenotype, have been investigated in primary cultures of brown adipocytes, in the brown adipocyte cell line HIB 1B and directly in intact mice. Tretinoin 15-28 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 111-114
8760369-1 1996 The effects of retinoic acid (RA) isomers (all-trans-RA and 9-cis-RA) on the appearance of uncoupling protein (UCP; thermogenin), the only unequivocal molecular marker of the brown adipocyte differentiated phenotype, have been investigated in primary cultures of brown adipocytes, in the brown adipocyte cell line HIB 1B and directly in intact mice. Tretinoin 15-28 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 116-127
14707044-2 2004 Primary rejection of class I-deficient RMA-S lymphoma cells expressing the NKG2D ligand, retinoic acid early inducible-1beta, was critically dependent upon NK cell perforin and occurred independently of T cells. Tretinoin 89-102 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 75-80
8760369-1 1996 The effects of retinoic acid (RA) isomers (all-trans-RA and 9-cis-RA) on the appearance of uncoupling protein (UCP; thermogenin), the only unequivocal molecular marker of the brown adipocyte differentiated phenotype, have been investigated in primary cultures of brown adipocytes, in the brown adipocyte cell line HIB 1B and directly in intact mice. Tretinoin 30-32 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 111-114
8760369-1 1996 The effects of retinoic acid (RA) isomers (all-trans-RA and 9-cis-RA) on the appearance of uncoupling protein (UCP; thermogenin), the only unequivocal molecular marker of the brown adipocyte differentiated phenotype, have been investigated in primary cultures of brown adipocytes, in the brown adipocyte cell line HIB 1B and directly in intact mice. Tretinoin 30-32 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 116-127
8760369-3 1996 The two RA isomers displayed similar effectiveness as UCP inducers, their effect being comparable with that triggered by noradrenaline, so far considered to be the main modulator of UCP gene expression. Tretinoin 8-10 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 182-185
8808829-32 1996 All trans retinoic acid (RA) could suppress the secretion of MMPs in SAOV cells in time and concentration dependent manners. Tretinoin 4-23 matrix metallopeptidase 2 Homo sapiens 61-65
8808829-32 1996 All trans retinoic acid (RA) could suppress the secretion of MMPs in SAOV cells in time and concentration dependent manners. Tretinoin 25-27 matrix metallopeptidase 2 Homo sapiens 61-65
7638202-7 1995 We hypothesize that retinoic acid provides a critical signal mediated through the RXR alpha pathway that is required to allow progression of development of the ventricular region of the heart from its early atrial-like form to the thick-walled adult ventricle. Tretinoin 20-33 retinoid X receptor alpha Mus musculus 82-91
7615548-6 1995 After 48 h of treatment with retinoic acid, Complex I is replaced by a faster migrating Complex II, which can be supershifted by anti-RAR beta and anti-RXR alpha antibodies. Tretinoin 29-42 retinoic acid receptor, beta Mus musculus 134-142
7615548-6 1995 After 48 h of treatment with retinoic acid, Complex I is replaced by a faster migrating Complex II, which can be supershifted by anti-RAR beta and anti-RXR alpha antibodies. Tretinoin 29-42 retinoid X receptor alpha Mus musculus 152-161
8703946-5 1996 All-trans-retinoic acid (RA) treatment of Jun-deficient, mouse F9, teratocarcinoma cells causes the induction of c-jun expression. Tretinoin 0-23 jun proto-oncogene Mus musculus 113-118
14707044-3 2004 NKG2D-triggered NK cell rejection of RMA-S-retinoic acid early inducible-1beta tumor primed a secondary tumor-specific T cell response mediated by both CD4+ and CD8+ T cells in the effector phase. Tretinoin 43-56 killer cell lectin-like receptor subfamily K, member 1 Mus musculus 0-5
8702428-3 1996 In this study, we examined the effect of RA on expression of IL-1 beta and IL-ra in phorbol-myristate-acetate (PMA)-activated human monocytes. Tretinoin 41-43 interleukin 7 receptor Homo sapiens 75-80
7622051-9 1995 In PA-1 human teratocarcinoma cells HOX A1 is the earliest HOX A gene to be expressed after treatment with RA. Tretinoin 107-109 homeobox A1 Homo sapiens 36-42
7622051-9 1995 In PA-1 human teratocarcinoma cells HOX A1 is the earliest HOX A gene to be expressed after treatment with RA. Tretinoin 107-109 homeobox A cluster Homo sapiens 36-41
14717701-8 2004 Whole mount in situ hybridization of zebrafish embryos revealed rbp1 mRNA expression in the developing zebrafish central nervous system at specific sites that are known to have abundant retinoic acid distribution and significant retinoic acid action. Tretinoin 186-199 retinol binding protein 1a, cellular Danio rerio 64-68
7476016-0 1995 Cloning of a retinoic acid-induced gene, GT1, in the embryonal carcinoma cell line P19: neuron-specific expression in the mouse brain. Tretinoin 13-26 retinoic acid induced 1 Mus musculus 41-44
7476016-0 1995 Cloning of a retinoic acid-induced gene, GT1, in the embryonal carcinoma cell line P19: neuron-specific expression in the mouse brain. Tretinoin 13-26 interleukin 23, alpha subunit p19 Mus musculus 83-86
8663198-10 1996 These data support a function for RalDH(II) in the pathway of retinoic acid biogenesis. Tretinoin 62-75 aldehyde dehydrogenase 1 family, member A2 Rattus norvegicus 34-43
14983400-2 2004 In the present work, we have investigated whether hepatic IGFBP-4 expression is regulated by retinoic acid (RA), which acts via nuclear receptors belonging to the steroid/thyroid hormone receptor superfamily. Tretinoin 93-106 insulin-like growth factor binding protein 4 Rattus norvegicus 58-65
8800419-0 1996 Expression of Fgf-3 in relation to hindbrain segmentation, otic pit position and pharyngeal arch morphology in normal and retinoic acid-exposed mouse embryos. Tretinoin 122-135 fibroblast growth factor 3 Mus musculus 14-19
8800419-6 1996 Fgf-3 is a good marker for the epithelium of pharyngeal arches 2 and 3, and our in situ hybridization results confirm the dual identity of the apparently fused first and second arches in some retinoic acid-exposed embryos, and the fusion of the first arch with the maxillary region in others. Tretinoin 192-205 fibroblast growth factor 3 Mus musculus 0-5
7476016-1 1995 Mouse P19 embryonal carcinoma cells can be reproducibly differentiated into neurons and glial cells upon treatment with high concentrations of retinoic acid (RA). Tretinoin 143-156 interleukin 23, alpha subunit p19 Mus musculus 6-9
7476016-1 1995 Mouse P19 embryonal carcinoma cells can be reproducibly differentiated into neurons and glial cells upon treatment with high concentrations of retinoic acid (RA). Tretinoin 158-160 interleukin 23, alpha subunit p19 Mus musculus 6-9
14983400-2 2004 In the present work, we have investigated whether hepatic IGFBP-4 expression is regulated by retinoic acid (RA), which acts via nuclear receptors belonging to the steroid/thyroid hormone receptor superfamily. Tretinoin 108-110 insulin-like growth factor binding protein 4 Rattus norvegicus 58-65
7578983-8 1995 Like PA and PB, other differentiation inducers such as all-trans-retinoic acid, dimethyl sulfoxide, and 5-aza-2"-deoxycytidine, all induced TGF-alpha expression in the melanoma cells. Tretinoin 55-78 transforming growth factor alpha Homo sapiens 140-149
14983400-7 2004 AtRA and thyroid hormone act synergistically in increasing hepatic IGFBP-4 expression. Tretinoin 0-4 insulin-like growth factor binding protein 4 Rattus norvegicus 67-74
8774361-3 1996 Surprisingly, treatment of HL-60 cells with 10 nM all-trans retinoic acid (RA) for 7 days (HL-60-R7) resulted in a marked increase in MLC stimulation although the cells lacked detectable MHC class II antigen expression at the initiation of the MLC. Tretinoin 60-73 major histocompatibility complex, class II, DR beta 6 (pseudogene) Homo sapiens 187-207
14691162-8 2004 To determine whether RA-associated MUC4 mRNA induction is a direct or indirect effect, HCjE cells were treated with RA and the protein synthesis inhibitor cycloheximide (1.0 microg/mL) for 12 hours. Tretinoin 21-23 mucin 4, cell surface associated Homo sapiens 35-39
8843397-6 1996 Differential effects of RA on the expression of GATA-1 and GATA-2 suggest that RA has a direct action on haematopoietic differentiation, rather than on the formation of haematopoietic mesoderm. Tretinoin 24-26 GATA binding protein 1 L homeolog Xenopus laevis 48-54
8843397-6 1996 Differential effects of RA on the expression of GATA-1 and GATA-2 suggest that RA has a direct action on haematopoietic differentiation, rather than on the formation of haematopoietic mesoderm. Tretinoin 79-81 GATA binding protein 1 L homeolog Xenopus laevis 48-54
7628539-9 1995 In previous studies, we have demonstrated that retinoic acid induces the expression of RAR beta and RAR gamma in human dermal fibroblasts. Tretinoin 47-60 retinoic acid receptor gamma Homo sapiens 100-109
14691162-13 2004 Treatment with RA upregulated the expression of both MUC4 and -16 mRNA and protein, but MUC1 was unaffected. Tretinoin 15-17 mucin 4, cell surface associated Homo sapiens 53-57
8819158-2 1996 It was found that this lipocalin, termed Xlcpl1, binds retinal at a nanomolar concentration, retinoic acid in the micromolar range, but does not show binding to retinol. Tretinoin 93-106 prostaglandin D2 synthase L homeolog Xenopus laevis 23-32
8819158-2 1996 It was found that this lipocalin, termed Xlcpl1, binds retinal at a nanomolar concentration, retinoic acid in the micromolar range, but does not show binding to retinol. Tretinoin 93-106 prostaglandin D2 synthase L homeolog Xenopus laevis 41-47
14691162-15 2004 CONCLUSIONS: The membrane-associated mucins of the ocular surface epithelia, MUC1, -4, and -16, are differentially regulated by serum and RA in the telomerase-immortalized human conjunctival epithelial cell line. Tretinoin 138-140 mucin 1, cell surface associated Homo sapiens 17-94
15315332-8 2004 RA could elevate significantly the expression levels of PDGF-A mRNA and protein (P<0.01), but not affect the expression levels of PDGF-B mRNA and protein markedly (P>0.05). Tretinoin 0-2 platelet derived growth factor subunit A Rattus norvegicus 56-62
8674422-1 1996 Excess all-trans retinoic acid (RA) causes severe craniofacial malformations in vertebrate embryos: pharyngeal arches are fused or absent, and a rostrad expansion of Hoxb-1 expression in the hindbrain shows that anterior rhombomeres are homeotically respecified to a more posterior identity. Tretinoin 17-30 homeobox B1 Mus musculus 166-172
15315332-10 2004 RA can stimulate lung development through increasing the expression levels of PDGF-A mRNA and protein. Tretinoin 0-2 platelet derived growth factor subunit A Rattus norvegicus 78-84
8674422-1 1996 Excess all-trans retinoic acid (RA) causes severe craniofacial malformations in vertebrate embryos: pharyngeal arches are fused or absent, and a rostrad expansion of Hoxb-1 expression in the hindbrain shows that anterior rhombomeres are homeotically respecified to a more posterior identity. Tretinoin 32-34 homeobox B1 Mus musculus 166-172
15641681-8 2004 It was indicated that retinoic acid could increase beta-catenin level of the whole cell protein and decrease nuclear beta-catenin, downregulating beta-cat/TCF signaling activity and reducing target gene cyclinD1 protein level. Tretinoin 22-35 cyclin D1 Homo sapiens 203-211
8655603-12 1996 However, RA significantly reduced IGFBP-3 levels in conditioned media and eliminated IGFBP-3 associated with the plasma membrane. Tretinoin 9-11 insulin like growth factor binding protein 3 Bos taurus 34-41
8655603-12 1996 However, RA significantly reduced IGFBP-3 levels in conditioned media and eliminated IGFBP-3 associated with the plasma membrane. Tretinoin 9-11 insulin like growth factor binding protein 3 Bos taurus 85-92
15111235-4 2004 The kinetics of [3H]DA uptake and [3H]MPP+ uptake to DAT in RA/TPA differentiated cells were similar to that of rat and mouse caudate-putamen synaptosomes. Tretinoin 60-62 solute carrier family 6 member 3 Rattus norvegicus 53-56
8655603-13 1996 Thus, RA is a potent but transient inhibitor of bovine mammary epithelial cell proliferation, and this growth inhibition is correlated with increased IGFBP-2 accumulation and inhibition of IGF-I stimulated IGFBP-3 protein secretion. Tretinoin 6-8 insulin like growth factor binding protein 3 Bos taurus 206-213
15207330-2 2004 We showed that the LAMB1 gene, which encodes the laminin beta1 subunit, is transcriptionally activated by retinoic acid in embryonic stem cells. Tretinoin 106-119 laminin B1 Mus musculus 19-24
8635515-2 1996 RA activity is thought to be mediated by nuclear RA receptors (RARs), transcription factors whose activity is dependent on RA. Tretinoin 49-51 arginyl-tRNA synthetase 1 Homo sapiens 63-67
8635515-7 1996 We conclude that dominant negative mutants of RAR alpha act by heterodimerizing with RXRs or RARs and binding to RA response elements on DNA, thereby preventing binding of the normal receptors to those sites. Tretinoin 46-48 arginyl-tRNA synthetase 1 Homo sapiens 93-97
15013071-5 2004 Expression of Hox-b1 and Krox20 (markers of specific rhombomeres) was altered after FLUCO and RA exposure. Tretinoin 94-96 homeo box B1 Rattus norvegicus 14-20
8739045-0 1996 Retinoic acid enhances expression of bone morphogenetic protein-2 in human adenocarcinoma cell line (HSG-S8). Tretinoin 0-13 bone morphogenetic protein 2 Homo sapiens 37-65
8739045-1 1996 Expression of bone morphogenetic protein (BMP)-2 mRNA was stimulated by retinoic acid in human adenocarcinoma cell line, HSG-S8, in a dose-dependent manner. Tretinoin 72-85 bone morphogenetic protein 2 Homo sapiens 14-48
8739045-2 1996 Northern blot analysis demonstrated that retinoic acid most strongly increased the level of BMP-2 mRNA 6 h after the treatment and the stimulatory effect was maintained at 48 h. The mature peptides of 16 and 18 kDa molecular masses of BMP-2 were also increased in the conditioned medium by the treatment of retinoic acid on western blotting. Tretinoin 41-54 bone morphogenetic protein 2 Homo sapiens 92-97
8739045-2 1996 Northern blot analysis demonstrated that retinoic acid most strongly increased the level of BMP-2 mRNA 6 h after the treatment and the stimulatory effect was maintained at 48 h. The mature peptides of 16 and 18 kDa molecular masses of BMP-2 were also increased in the conditioned medium by the treatment of retinoic acid on western blotting. Tretinoin 41-54 bone morphogenetic protein 2 Homo sapiens 235-240
14623241-8 2003 Our studies suggest that RA signaling provides proximodistal information for limb buds that counterbalances Bmp signaling, which in turn helps mediate proximodistal and anteroposterior patterning of Hgf expression to correctly direct migration of Met-expressing myogenic precursor cells. Tretinoin 25-27 hepatocyte growth factor Homo sapiens 199-202
8739045-2 1996 Northern blot analysis demonstrated that retinoic acid most strongly increased the level of BMP-2 mRNA 6 h after the treatment and the stimulatory effect was maintained at 48 h. The mature peptides of 16 and 18 kDa molecular masses of BMP-2 were also increased in the conditioned medium by the treatment of retinoic acid on western blotting. Tretinoin 307-320 bone morphogenetic protein 2 Homo sapiens 235-240
8739045-4 1996 1 alpha, 25(OH)2D3, like retinoic acid, clearly increased the mRNA level of BMP-2, whereas dibuthryl cyclic AMP remarkably diminished it, and bromodeoxyuridine had no effect on the expression of BMP-2 mRNA. Tretinoin 25-38 bone morphogenetic protein 2 Homo sapiens 76-81
14713576-6 2003 RESULTS: The basal CRABP I level clearly correlated with the clonogenic survival of tumour cells and normal fibroblasts after treatment with retinoic acid and ionizing irradiation (IR). Tretinoin 141-154 cellular retinoic acid binding protein 1 Homo sapiens 19-26
8614642-1 1996 Transcription of the murine laminin gamma 1 gene is activated during retinoic acid/cAMP induced differentiation of F9 embryonal carcinoma cells. Tretinoin 69-82 laminin, gamma 1 Mus musculus 28-43
14713576-7 2003 Cells expressing high basal CRABP I were more resistant to combined retinoic acid radiation treatment than cells with low basal expression. Tretinoin 68-81 cellular retinoic acid binding protein 1 Homo sapiens 28-35
14713576-8 2003 Overexpression of CRABP I in retinoic acid-sensitive HTB35 cells induced a retinoic acid-insensitive phenotype resistant to combined treatment with retinoic acid and radiation. Tretinoin 29-42 cellular retinoic acid binding protein 1 Homo sapiens 18-25
14713576-10 2003 CRABP I overexpression resulted in stimulated cyclin D1 expression indicating the dependency of this cell cycle control protein on retinoic acid metabolism. Tretinoin 131-144 cellular retinoic acid binding protein 1 Homo sapiens 0-7
14713576-11 2003 CONCLUSION: CRABP I plays an important role not only in mediating the retinoid effects, but also in modulating the radiation sensitivity of tumour cells after combined retinoic acid radiation treatment. Tretinoin 168-181 cellular retinoic acid binding protein 1 Homo sapiens 12-19
18406732-5 1996 In addition, regulatory studies of the TRH gene by T(3) should be relevant to other hormone receptor interactions with DNA sequences in general, as glucocorticoids, mineralocorticoids, sex steroids, vitamin D, and retinoic acid are ligands for homologous receptor proteins in the nuclear receptor superfamily. Tretinoin 214-227 thyrotropin releasing hormone Homo sapiens 39-42
14585314-10 2003 Recent studies proved that the control occurs by different expressions of retinoid receptors as well as by time-dependent changes of the vitamin-A-metabolism respectively via cellular vitamin-A-binding proteins (CRBP: cytoplasmatic retinol binding protein; CRABP: cytoplasmatic retinoic acid binding protein). Tretinoin 278-291 cellular retinoic acid binding protein 1 Homo sapiens 257-262
8634442-2 1996 In the present study, we show that t-RA treatment dramatically induced type II transglutaminase (type II TGase) expression in cells carrying the t(15;17) translocation and expressing the PML-RARalpha product such as the APL-derived NB4 cell line and fresh leukemic cells from APL patients. Tretinoin 35-39 transglutaminase 1 Homo sapiens 105-110
14649730-3 2003 Exposure of retinoic acid (RA)-differentiated SH-SY5Y cells to MPP+ (1 mM, 72 h) also resulted in a decrease in RMB3 expression and an increase in GADD153 expression. Tretinoin 12-25 M-phase phosphoprotein 6 Homo sapiens 63-66
14597230-5 2003 We observed that retinoic acid (RA)-induced neuronal differentiation of human SH-SY5Y cells resulted in increased expression of APP, APLP1 and APLP2. Tretinoin 17-30 amyloid beta precursor like protein 2 Homo sapiens 143-148
8631256-6 1996 In addition, r4 gene expression is also partially altered by RA; within 6 hours of r4 exposure to RA, ectopic expression of Krox-20 is seen in r4 and Hoxb-1 expression is lost while Hoxa-2 expression continues normally. Tretinoin 98-100 homeobox A2 Homo sapiens 182-188
9183635-5 1996 RXR alpha and RXR beta were cloned from HSG cells, and these RXRs, together with RAR, seemed to play a physiological role in RA signaling in vivo. Tretinoin 81-83 retinoid X receptor beta Homo sapiens 14-22
14597230-5 2003 We observed that retinoic acid (RA)-induced neuronal differentiation of human SH-SY5Y cells resulted in increased expression of APP, APLP1 and APLP2. Tretinoin 32-34 amyloid beta precursor like protein 2 Homo sapiens 143-148
14708597-8 2003 The constitutive expression of MMP-19 was upregulated with phorbol myristate acetate and downregulated with retinoic acid and dexamethasone. Tretinoin 108-121 matrix metallopeptidase 19 Homo sapiens 31-37
8852383-2 1996 RNAase protection and western blot analysis revealed that E14-ES cells up regulate RPTP alpha expression upon neuronal differentiation with retinoic acid. Tretinoin 140-153 protein tyrosine phosphatase receptor type A Homo sapiens 83-93
8852383-3 1996 Overexpression of RPTP alpha, by stable DNA transfection, and subsequent differentiation with retinoic acid, resulted in a temporally enhanced expression of the neuronal markers GAP-43 and NF-164. Tretinoin 94-107 protein tyrosine phosphatase receptor type A Homo sapiens 18-28
14561924-4 2003 AT-RA was a better differentiating agent in inducing the highest expression of the neurotrophic factor receptor TrkA. Tretinoin 3-5 neurotrophic receptor tyrosine kinase 1 Homo sapiens 112-116
8621736-9 1996 The inhibition of CD-RAP mRNA expression by RA in vitro was time- and dose-dependent and was tested over concentrations from 10(-8) to 10(-6) M. Southern blot analysis of genomic DNA indicated that CD-RAP was encoded by a single copy gene and that no other genes were closely related. Tretinoin 21-23 melanoma-derived growth regulatory protein Bos taurus 198-204
14519946-1 2003 4-(N-Hydroxyphenyl)retinamide (also known as 4-HPR or fenretinide), a synthetic amide of all-trans retinoic acid (RA), has been implicated as a promising anticancer agent associated with reducing the toxicity related to RA. Tretinoin 89-112 haptoglobin-related protein Homo sapiens 47-50
8591987-0 1996 Retinoic acid inhibits hydrocortisone-stimulated expression of phenol sulfotransferase in bovine bronchial epithelial cells. Tretinoin 0-13 sulfotransferase 1A1 Bos taurus 63-86
8591987-8 1996 Varied concentrations of RA had a general repressive effect on HC-stimulated PST expression, with no change in the half-maximal HC stimulatory concentration of 12.5 nM. Tretinoin 25-27 sulfotransferase 1A1 Bos taurus 77-80
14511111-4 2003 After retinoic acid (RA) treatment and in the absence of doxycycline, neuronal progenitor cells in the p19 clone were found to extend their processes towards the neighboring colony to form network-like connections, as revealed by neuron-specific microtubule-associated protein 2 staining and laser scanning confocal microscopy. Tretinoin 6-19 interleukin 23, alpha subunit p19 Mus musculus 103-106
14511111-4 2003 After retinoic acid (RA) treatment and in the absence of doxycycline, neuronal progenitor cells in the p19 clone were found to extend their processes towards the neighboring colony to form network-like connections, as revealed by neuron-specific microtubule-associated protein 2 staining and laser scanning confocal microscopy. Tretinoin 21-23 interleukin 23, alpha subunit p19 Mus musculus 103-106
8789718-9 1996 Displacement of 1,8-ANS from CRBP by all-trans-retinal and all-trans-retinoic acid yielded Ki values of 1.7 and 5.3 microM, respectively. Tretinoin 59-82 retinol binding protein 1 Homo sapiens 29-33
12851412-0 2003 Genetic evidence that retinaldehyde dehydrogenase Raldh1 (Aldh1a1) functions downstream of alcohol dehydrogenase Adh1 in metabolism of retinol to retinoic acid. Tretinoin 146-159 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 50-56
12851412-0 2003 Genetic evidence that retinaldehyde dehydrogenase Raldh1 (Aldh1a1) functions downstream of alcohol dehydrogenase Adh1 in metabolism of retinol to retinoic acid. Tretinoin 146-159 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 58-65
12941622-4 2003 At all sites, expression of additional RA signaling molecules (RARalpha, RARbeta, RXR, CRABP1) depends on M/E interactions. Tretinoin 39-41 cellular retinoic acid binding protein 1 Homo sapiens 87-93
8881287-5 1996 The fusion protein PML-RAR, which is not localized in nuclear bodies, also enhanced the transactivating activity of PR but this effect was totally suppressed by the administration of retinoic acid. Tretinoin 183-196 progesterone receptor Homo sapiens 116-118
8881287-7 1996 This mechanism may also play a role in the oncogenic properties of PML-RAR and in their suppression by the retinoic acid. Tretinoin 107-120 PML-RARA regulated adaptor molecule 1 Homo sapiens 67-74
12941622-6 2003 Expression of Fgf8, shh, and Bmp4, all of which are thought to influence RA signaling, is also regulated by M/E interactions independent of RA at all sites. Tretinoin 73-75 bone morphogenetic protein 4 Homo sapiens 29-33
12956703-2 2003 We suggest that the transcriptional activator retinoic acid (RA), takes part in gene regulation after peripheral nerve injury and that RA signalling is activated via the cellular retinoic acid binding protein (CRABP)-II and cellular retinol binding protein (CRBP)-I. Tretinoin 46-59 retinol binding protein 1 Homo sapiens 258-265
9018378-10 1996 Based on its kinetic properties, it is suggested that the ALDH1 enzyme may be the primary enzyme for oxidizing retinal to retinoic acid in bovine kidney. Tretinoin 122-135 aldehyde dehydrogenase 1 family member A1 Bos taurus 58-63
8792611-4 1996 HoxD gene expression domains in the distal handplate were narrowed by 5 hr after maternal retinoic acid administration on day 11. Tretinoin 90-103 homeobox D cluster Mus musculus 0-4
8792611-5 1996 Following retinoic acid treatment on both day 11 and day 12, the normal downregulation of Hoxd-11 and Hoxd-13 in the digital mesenchymal condensations was retarded. Tretinoin 10-23 homeobox D11 Mus musculus 90-97
8792611-7 1996 We suggest (1) that the apical ectodermal ridge is the most functionally significant of these sites, (2) that raised retinoic acid levels in the ridge result in altered gene expression and/or altered cell proliferation within this epithelium, (3) that both altered HoxD gene expression domains and altered skeletal pattern formation are secondary to this effect. Tretinoin 117-130 homeobox D cluster Mus musculus 265-269
8792611-8 1996 There was a good correlation between the effects of retinoic acid on Hoxd-11 and Hoxd-13 expression and delay of skeletal differentiation, suggesting that this may be a direct effect. Tretinoin 52-65 homeobox D11 Mus musculus 69-76
7549784-2 1995 These cells could be induced to differentiate in vitro into neuronal-like cells upon incubation with retinoic acid, an event that was accompanied by an enhancement in levels of neuron-specific acetylcholinesterase. Tretinoin 101-114 acetylcholinesterase Mus musculus 193-213
7655081-6 1995 Application of retinoic acid or a polarizing region graft to the anterior of ta3 limb buds changed digit morphology but did not induce digit duplications or digits with any characteristic a-p pattern. Tretinoin 15-28 TALPID3 Gallus gallus 77-80
8570187-5 1995 RA induces RAR-gamma 2 > RAR gamma 1 in BZR-T33 cells but expression at the total cellular RNA level of RAR alpha and RXR alpha is not augmented by RA-treatment. Tretinoin 0-2 retinoic acid receptor gamma Homo sapiens 28-37
12956703-2 2003 We suggest that the transcriptional activator retinoic acid (RA), takes part in gene regulation after peripheral nerve injury and that RA signalling is activated via the cellular retinoic acid binding protein (CRABP)-II and cellular retinol binding protein (CRBP)-I. Tretinoin 61-63 retinol binding protein 1 Homo sapiens 258-265
12956703-2 2003 We suggest that the transcriptional activator retinoic acid (RA), takes part in gene regulation after peripheral nerve injury and that RA signalling is activated via the cellular retinoic acid binding protein (CRABP)-II and cellular retinol binding protein (CRBP)-I. Tretinoin 135-137 retinol binding protein 1 Homo sapiens 258-265
12956703-6 2003 Sciatic nerve crush as well as transection resulted in a more than 10-fold up-regulation of CRBP-I, which is thought to facilitate the synthesis of RA. Tretinoin 148-150 retinol binding protein 1 Homo sapiens 92-98
7610998-0 1995 [Beneficial effect of a retinoic acid responsive gene product, midkine, on constant light-induced retinal damage in albino mice]. Tretinoin 24-37 midkine Mus musculus 63-70
12805378-4 2003 In this report, we provide evidence that a member of the protein kinase C (PKC) family of proteins, PKC delta, is activated during RA treatment of the NB-4 and HL-60 acute myeloid leukemia cell lines as well as the MCF-7 breast cancer cell line. Tretinoin 131-133 protein kinase C delta Homo sapiens 75-78
7742011-4 1995 We found that retinoic acid interferes, in a dose-dependent fashion, with the expression of epithelial genes that are found in distal segments of the fetal lung (surfactant-associated proteins SP-A, SP-B, and SP-C). Tretinoin 14-27 surfactant protein B Homo sapiens 199-203
8575300-0 1995 Mouse embryos lacking RXR alpha are resistant to retinoic-acid-induced limb defects. Tretinoin 49-62 retinoid X receptor alpha Mus musculus 22-31
8575300-5 1995 We now describe resistance to limb malformations normally induced by teratogenic RA exposure in the RXR alpha-/- background. Tretinoin 81-83 retinoid X receptor alpha Mus musculus 100-109
8575300-6 1995 RA treatments that cause limb defects in 100% of wild-type embryos fail to elicit malformations in RXR alpha homozygotes, implicating RXR alpha as a component in the teratogenic process in the limbs. Tretinoin 0-2 retinoid X receptor alpha Mus musculus 134-143
8575300-11 1995 These observations indicate that transcriptional processes which are inappropriately regulated in the mouse limb by exogenous RA require RXR alpha for their execution, and that specific teratogenic processes, as well as specific normal developmental processes under vitamin A control, occur through individual members of the RXR and RAR families. Tretinoin 126-128 retinoid X receptor alpha Mus musculus 137-146
8614415-7 1995 This mechanism may also play a role in the oncogenic properties of PML-RAR and in their suppression by retinoic acid. Tretinoin 103-116 PML-RARA regulated adaptor molecule 1 Homo sapiens 67-74
12805378-4 2003 In this report, we provide evidence that a member of the protein kinase C (PKC) family of proteins, PKC delta, is activated during RA treatment of the NB-4 and HL-60 acute myeloid leukemia cell lines as well as the MCF-7 breast cancer cell line. Tretinoin 131-133 protein kinase C delta Homo sapiens 100-109
7698992-0 1995 Midkine (MK), a heparin-binding growth/differentiation factor, is regulated by retinoic acid and epithelial-mesenchymal interactions in the developing mouse tooth, and affects cell proliferation and morphogenesis. Tretinoin 79-92 midkine Mus musculus 0-7
12805378-5 2003 Such RA-dependent phosphorylation was also observed in primary acute promyelocytic leukemia cells and resulted in activation of the kinase domain of PKC delta. Tretinoin 5-7 protein kinase C delta Homo sapiens 149-158
7698992-0 1995 Midkine (MK), a heparin-binding growth/differentiation factor, is regulated by retinoic acid and epithelial-mesenchymal interactions in the developing mouse tooth, and affects cell proliferation and morphogenesis. Tretinoin 79-92 midkine Mus musculus 9-11
12805378-6 2003 In studies aimed at understanding the functional relevance of PKC delta in the induction of RA responses, we found that pharmacological inhibition of PKC delta (but not of other PKC isoforms) diminished RA-dependent gene transcription via RAREs. Tretinoin 92-94 protein kinase C delta Homo sapiens 62-71
12805378-6 2003 In studies aimed at understanding the functional relevance of PKC delta in the induction of RA responses, we found that pharmacological inhibition of PKC delta (but not of other PKC isoforms) diminished RA-dependent gene transcription via RAREs. Tretinoin 92-94 protein kinase C delta Homo sapiens 150-159
7488013-0 1995 Retinoic acid induces three newly cloned HOXA1 transcripts in MCF7 breast cancer cells. Tretinoin 0-13 homeobox A1 Homo sapiens 41-46
12805378-6 2003 In studies aimed at understanding the functional relevance of PKC delta in the induction of RA responses, we found that pharmacological inhibition of PKC delta (but not of other PKC isoforms) diminished RA-dependent gene transcription via RAREs. Tretinoin 92-94 protein kinase C delta Homo sapiens 62-65
7488013-5 1995 Moreover, we demonstrate that all three HOXA1 transcripts are induced by retinoic acid in MCF7 cells. Tretinoin 73-86 homeobox A1 Homo sapiens 40-45
7698992-7 1995 The expression of MK gene and protein in the mandibular arch mesenchyme from the tooth region were stimulated by local application of retinoic acid in beads. Tretinoin 134-147 midkine Mus musculus 18-20
12805378-8 2003 Gel shift assays and chromatin immunoprecipitation studies demonstrated that PKC delta associated with retinoic acid receptor-alpha and was present in an RA-inducible protein complex that bound to RAREs. Tretinoin 154-156 protein kinase C delta Homo sapiens 77-86
12805378-10 2003 Altogether, our data provide strong evidence that PKC delta is activated in an RA-dependent manner and plays a critical role in the generation of the biological effects of RA in malignant cells. Tretinoin 79-81 protein kinase C delta Homo sapiens 50-59
12805378-10 2003 Altogether, our data provide strong evidence that PKC delta is activated in an RA-dependent manner and plays a critical role in the generation of the biological effects of RA in malignant cells. Tretinoin 172-174 protein kinase C delta Homo sapiens 50-59
7786847-1 1995 An enzyme of bovine retina that catalyzes oxidation of retinaldehyde to retinoic acid was purified to homogeneity and a monoclonal antibody (mAb H-4) was generated. Tretinoin 72-85 abhydrolase domain containing 4 Mus musculus 141-148
7586155-2 1995 N-(4-hydroxyphenyl) retinamide (4-HPR), a derivative of all-trans-retinoic acid (RA) is currently in clinical trials as a chemopreventive agent for breast cancer. Tretinoin 56-79 haptoglobin-related protein Homo sapiens 34-37
7586155-2 1995 N-(4-hydroxyphenyl) retinamide (4-HPR), a derivative of all-trans-retinoic acid (RA) is currently in clinical trials as a chemopreventive agent for breast cancer. Tretinoin 81-83 haptoglobin-related protein Homo sapiens 34-37
7539613-0 1995 9-cis-retinoic acid is more effective than all-trans-retinoic acid in upregulating expression of the alpha-fetoprotein gene. Tretinoin 43-66 alpha-fetoprotein Rattus norvegicus 101-118
12930800-4 2003 This study shows that a rich source of RA lies around the hindbrain from the RA synthetic enzyme retinaldehyde dehydrogenase-2 (RALDH2) present in the surrounding meninges and mesenchyme by embryonic day 13. Tretinoin 39-41 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 97-126
7539613-1 1995 In McA-RH 8994 rat hepatoma cells, all-trans-retinoic acid (t-RA) induces expression of the alpha-fetoprotein (AFP) and albumin genes and results in a phenotype similar to differentiated fetal hepatocytes. Tretinoin 35-58 alpha-fetoprotein Rattus norvegicus 92-109
7539613-1 1995 In McA-RH 8994 rat hepatoma cells, all-trans-retinoic acid (t-RA) induces expression of the alpha-fetoprotein (AFP) and albumin genes and results in a phenotype similar to differentiated fetal hepatocytes. Tretinoin 35-58 alpha-fetoprotein Rattus norvegicus 111-114
12930800-4 2003 This study shows that a rich source of RA lies around the hindbrain from the RA synthetic enzyme retinaldehyde dehydrogenase-2 (RALDH2) present in the surrounding meninges and mesenchyme by embryonic day 13. Tretinoin 39-41 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 128-134
7539613-1 1995 In McA-RH 8994 rat hepatoma cells, all-trans-retinoic acid (t-RA) induces expression of the alpha-fetoprotein (AFP) and albumin genes and results in a phenotype similar to differentiated fetal hepatocytes. Tretinoin 60-64 alpha-fetoprotein Rattus norvegicus 92-109
7539613-1 1995 In McA-RH 8994 rat hepatoma cells, all-trans-retinoic acid (t-RA) induces expression of the alpha-fetoprotein (AFP) and albumin genes and results in a phenotype similar to differentiated fetal hepatocytes. Tretinoin 60-64 alpha-fetoprotein Rattus norvegicus 111-114
7641199-1 1995 Synergistic inhibition of hematopoietic tumor growth can be observed in vitro when the iron chelator deferoxamine (DFO) is used in combination with an IgG mAb against the anti-transferrin receptor antibody (ATRA). Tretinoin 207-211 immunoglobulin heavy variable V1-62 Mus musculus 151-154
7539613-2 1995 The present study elucidated the mechanism involved in AFP gene regulation mediated by retinoic acid. Tretinoin 87-100 alpha-fetoprotein Rattus norvegicus 55-58
12929933-7 2003 Because the basal expression level of gelatinase B was almost undetectable, we induced its expression by different culturing conditions, the most dramatic induction achieved by treatment with retinoic acid, which is known as an inducer of vascular invasion in the epiphyseal plates. Tretinoin 192-205 matrix metallopeptidase 9 Mus musculus 38-50
7539613-5 1995 Northern blots and transfection assays using the 7.3 kb full-length regulatory region of the AFP gene demonstrated that c-RA was more effective than t-RA in regulating expression of the AFP gene. Tretinoin 149-153 alpha-fetoprotein Rattus norvegicus 93-96
7539613-5 1995 Northern blots and transfection assays using the 7.3 kb full-length regulatory region of the AFP gene demonstrated that c-RA was more effective than t-RA in regulating expression of the AFP gene. Tretinoin 149-153 alpha-fetoprotein Rattus norvegicus 186-189
7539613-7 1995 In contrast, t-RA at a concentration of 10(-7) M exerted no significant effect; 10(-6) to 10(-5) M t-RA was needed to affect AFP gene expression. Tretinoin 99-103 alpha-fetoprotein Rattus norvegicus 125-128
8690713-0 1995 Induction of CD40 in promyelocytic HL60 cells cultured with retinoic acid and/or various cytokines. Tretinoin 60-73 CD40 molecule Homo sapiens 13-17
8690713-3 1995 We show here that CD40 protein is induced in promyelocytic HL60 cells, when cultured with retinoic acid, a vitamin that converts them to granulocyte-like cells. Tretinoin 90-103 CD40 molecule Homo sapiens 18-22
7669674-2 1995 We studied the effect of interferon-alpha 2a (IFN) on ATRA pharmacokinetics in two patients with acute promyelocytic leukaemia (APL) in complete remission maintained by alternating 15 d of IFN and 15 d of ATRA. Tretinoin 54-58 interferon alpha 2 Homo sapiens 25-44
7823950-0 1995 Targeted disruption of retinoic acid receptor alpha (RAR alpha) and RAR gamma results in receptor-specific alterations in retinoic acid-mediated differentiation and retinoic acid metabolism. Tretinoin 122-135 retinoic acid receptor gamma Homo sapiens 68-77
12873812-3 2003 METHODS: Rat hepatocytes were cultured with or without diverse substances for 72 h and EGF for the last 48 h. RESULTS: EGF increased c-myc mRNA and protein, and decreased CYP mRNAs and proteins; both effects were prevented by two agents blocking c-myc transcription (retinoic acid and DMSO) and two antisense c-myc oligomers. Tretinoin 267-280 epidermal growth factor like 1 Rattus norvegicus 119-122
7823950-5 1995 The absence of RAR gamma is associated with a loss of the RA-inducible expression of the Hoxa-1 (formerly Hox-1.6), Hoxa-3 (formerly Hox-1.5), laminin B1, collagen IV (alpha 1), GATA-4, and BMP-2 genes. Tretinoin 15-17 homeobox A3 Homo sapiens 116-122
7649373-9 1995 We also report the sequence and expression pattern in mouse embryos and adult tissues of one of these novel RA-inducible genes, Stra1, and show that it corresponds to the mouse ligand for the Cek5 receptor protein-tyrosine kinase. Tretinoin 108-110 Eph receptor B2 Mus musculus 192-196
8619960-2 1995 Since one of the RA receptors--RAR-beta 2, is specifically induced in the limb bud cells upon treatment of embryos with teratogenic doses of RA, we investigated if this receptor played a role in teratogenesis by regulating the process of chondrogenesis. Tretinoin 17-19 retinoic acid receptor, beta Mus musculus 31-39
8619960-6 1995 Our results further strengthen the argument that RA-dependent elevation in RAR-beta 2 levels plays a unique role in RA-induced teratogenesis. Tretinoin 49-51 retinoic acid receptor, beta Mus musculus 75-83
8777434-5 1995 All trans-retinoic acid (RA) abolished the transformation of the 43C line and TPA-treated RELcJ1 cells, suggesting that RA could decrease AP1 activity in these cells despite c-fos or c-jun overexpression. Tretinoin 4-23 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 138-141
12801520-12 2003 The combination of PD98059 and SB203580 almost completely suppressed the enhancement by retinoic acid of VEGF synthesis induced by TGF-beta. Tretinoin 88-101 transforming growth factor, beta 1 Mus musculus 131-139
8777434-5 1995 All trans-retinoic acid (RA) abolished the transformation of the 43C line and TPA-treated RELcJ1 cells, suggesting that RA could decrease AP1 activity in these cells despite c-fos or c-jun overexpression. Tretinoin 25-27 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 138-141
8777434-5 1995 All trans-retinoic acid (RA) abolished the transformation of the 43C line and TPA-treated RELcJ1 cells, suggesting that RA could decrease AP1 activity in these cells despite c-fos or c-jun overexpression. Tretinoin 120-122 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 138-141
7851655-7 1995 Retinoic acid strongly induced HoxA1 and HoxD1 throughout the ectoderm and mesendoderm of gastrula stages, while in older embryos retinoids induced ectopic expression of these genes in more limited regions. Tretinoin 0-13 homeobox D1 S homeolog Xenopus laevis 41-46
7547509-0 1995 Regulation of cathepsin D gene expression in HL-60 cells by retinoic acid and calcitriol. Tretinoin 60-73 cathepsin D Homo sapiens 14-25
7547509-3 1995 Treatment with either retinoic acid or calcitriol enhances the steady-state levels of ctsd mRNA in a dose-dependent manner. Tretinoin 22-35 cathepsin D Homo sapiens 86-90
7547509-5 1995 Pretreatment with retinoic acid enhances the response of the ctsd gene to prostaglandin E2. Tretinoin 18-31 cathepsin D Homo sapiens 61-65
7851655-11 1995 Overexpression of thyroid hormone receptor (c-erbA) prevented induction of HoxD1 by retinoic acid in animal caps. Tretinoin 84-97 thyroid hormone receptor alpha L homeolog Xenopus laevis 44-50
12801520-13 2003 Taken together, our results strongly suggest that both p44/p42 MAP kinase and p38 MAP kinase take part in TGF-beta-stimulated VEGF synthesis in osteoblasts, and that retinoic acid upregulates the VEGF synthesis. Tretinoin 166-179 transforming growth factor, beta 1 Mus musculus 106-114
7851655-11 1995 Overexpression of thyroid hormone receptor (c-erbA) prevented induction of HoxD1 by retinoic acid in animal caps. Tretinoin 84-97 homeobox D1 S homeolog Xenopus laevis 75-80
12808103-0 2003 Targeted disruption of Aldh1a1 (Raldh1) provides evidence for a complex mechanism of retinoic acid synthesis in the developing retina. Tretinoin 85-98 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 23-30
7527821-5 1995 All-trans-retinoic acid (tRA) inhibited the proliferation of MBP-specific LNC in vitro. Tretinoin 0-23 myelin basic protein Homo sapiens 61-64
7527821-5 1995 All-trans-retinoic acid (tRA) inhibited the proliferation of MBP-specific LNC in vitro. Tretinoin 25-28 myelin basic protein Homo sapiens 61-64
8528505-11 1995 Inhibition of endogenous CRABP expression renders MEPM cells less responsive to RA with respect to induction of TGF-beta 3, RAR-beta, and tenascin gene expression. Tretinoin 26-28 retinoic acid receptor, beta Mus musculus 124-132
8528505-11 1995 Inhibition of endogenous CRABP expression renders MEPM cells less responsive to RA with respect to induction of TGF-beta 3, RAR-beta, and tenascin gene expression. Tretinoin 26-28 tenascin C Mus musculus 138-146
12808103-0 2003 Targeted disruption of Aldh1a1 (Raldh1) provides evidence for a complex mechanism of retinoic acid synthesis in the developing retina. Tretinoin 85-98 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 32-38
12808103-1 2003 Genetic studies have shown that retinoic acid (RA) signaling is required for mouse retina development, controlled in part by an RA-generating aldehyde dehydrogenase encoded by Aldh1a2 (Raldh2) expressed transiently in the optic vesicles. Tretinoin 32-45 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 176-183
7642751-7 1995 In isolated microglia, mRNA(IL-3) was increased upon treatment with LPS, PHA, with the cytokines IL-1 or TNF-alpha, with retinoic acid, dbcAMP or the phorbol ester TPA. Tretinoin 121-134 interleukin 3 Rattus norvegicus 28-32
12808103-1 2003 Genetic studies have shown that retinoic acid (RA) signaling is required for mouse retina development, controlled in part by an RA-generating aldehyde dehydrogenase encoded by Aldh1a2 (Raldh2) expressed transiently in the optic vesicles. Tretinoin 32-45 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 185-191
7746099-0 1995 Retinoic acid induces osteoclast-like cell formation by directly acting on hemopoietic blast cells and stimulates osteopontin mRNA expression in isolated osteoclasts. Tretinoin 0-13 secreted phosphoprotein 1 Mus musculus 114-125
12808103-1 2003 Genetic studies have shown that retinoic acid (RA) signaling is required for mouse retina development, controlled in part by an RA-generating aldehyde dehydrogenase encoded by Aldh1a2 (Raldh2) expressed transiently in the optic vesicles. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 176-183
12808103-1 2003 Genetic studies have shown that retinoic acid (RA) signaling is required for mouse retina development, controlled in part by an RA-generating aldehyde dehydrogenase encoded by Aldh1a2 (Raldh2) expressed transiently in the optic vesicles. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 185-191
12808103-7 2003 We observed that RA synthesis in liver of Raldh1(-/-) mice was greatly reduced, thus showing that Raldh1 indeed participates in RA synthesis in vivo. Tretinoin 17-19 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 42-48
12808103-7 2003 We observed that RA synthesis in liver of Raldh1(-/-) mice was greatly reduced, thus showing that Raldh1 indeed participates in RA synthesis in vivo. Tretinoin 17-19 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 98-104
7790895-4 1995 These data and the presence of putative retinoic acid response elements in the 5" region of the murine choline acetyltransferase gene indicate that retinoids stimulate choline acetyltransferase transcription in murine cholinergic neurons. Tretinoin 40-53 choline acetyltransferase Mus musculus 103-128
12808103-7 2003 We observed that RA synthesis in liver of Raldh1(-/-) mice was greatly reduced, thus showing that Raldh1 indeed participates in RA synthesis in vivo. Tretinoin 128-130 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 98-104
7790895-4 1995 These data and the presence of putative retinoic acid response elements in the 5" region of the murine choline acetyltransferase gene indicate that retinoids stimulate choline acetyltransferase transcription in murine cholinergic neurons. Tretinoin 40-53 choline acetyltransferase Mus musculus 168-193
7526151-1 1994 The differentiation of both embryonal carcinoma (EC) and embryonic stem (ES) cells can be triggered in culture by exposure to retinoic acid and results in the transcriptional induction of both the endogenous mouse keratin 18 (mK18) intermediate filament gene and an experimentally introduced human keratin 18 (K18) gene as well as a variety of other markers characteristic of extraembryonic endoderm. Tretinoin 126-139 keratin 18 Mus musculus 214-224
7780141-12 1995 Overall, our results indicate that RA downmodulates both the p60 and p80 form of the TNF receptor on cells of myeloid origin, which correlates with the cellular response. Tretinoin 35-37 Rho guanine nucleotide exchange factor 5 Homo sapiens 61-64
7526151-1 1994 The differentiation of both embryonal carcinoma (EC) and embryonic stem (ES) cells can be triggered in culture by exposure to retinoic acid and results in the transcriptional induction of both the endogenous mouse keratin 18 (mK18) intermediate filament gene and an experimentally introduced human keratin 18 (K18) gene as well as a variety of other markers characteristic of extraembryonic endoderm. Tretinoin 126-139 keratin 18 Mus musculus 226-230
12808103-8 2003 Our findings suggest that RA signaling may be necessary only during early stages of retina development and that if RA synthesis is needed in dorsal retina, it is catalyzed by multiple enzymes, including Raldh1. Tretinoin 115-117 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 203-209
7780141-12 1995 Overall, our results indicate that RA downmodulates both the p60 and p80 form of the TNF receptor on cells of myeloid origin, which correlates with the cellular response. Tretinoin 35-37 coilin Homo sapiens 69-72
12808467-0 2003 Hes1 is a target of microRNA-23 during retinoic-acid-induced neuronal differentiation of NT2 cells. Tretinoin 39-52 hes family bHLH transcription factor 1 Homo sapiens 0-4
9816026-6 1995 These results suggest that 4-HPR may be a member of a class of retinoids that are active because they displace RA from extracellular and intracellular sites or because they inhibit RA catabolism. Tretinoin 111-113 haptoglobin-related protein Homo sapiens 29-32
9816026-6 1995 These results suggest that 4-HPR may be a member of a class of retinoids that are active because they displace RA from extracellular and intracellular sites or because they inhibit RA catabolism. Tretinoin 181-183 haptoglobin-related protein Homo sapiens 29-32
7961875-10 1994 In addition, both HL-60 and HL-60/R-CP cells underwent cell differentiation in response to 12-O-tetradecanoylphorbol-13-acetate, retinoic acid, and dimethyl sulfoxide, resulting in proliferation arrest as well as a remarkable decrease in the c-myc mRNA levels. Tretinoin 129-142 opsin 1, long wave sensitive Homo sapiens 28-38
7956917-0 1994 9-cis retinoic acid regulation of rat growth hormone gene expression: potential roles of multiple nuclear hormone receptors. Tretinoin 6-19 gonadotropin releasing hormone receptor Rattus norvegicus 38-52
7626495-1 1995 The two cellular retinoic acid binding proteins, CRABP I and CRABP II, belong to a family of small cytosolic lipid binding proteins and are highly conserved during evolution. Tretinoin 17-30 cellular retinoic acid binding protein 1 Homo sapiens 49-56
12808467-7 2003 Thus, our results indicate that miR-23 regulates the expression of Hes1 at the post-transcriptional level, and participates in retinoic-acid-induced neuronal differentiation of NT2 cells. Tretinoin 127-140 hes family bHLH transcription factor 1 Homo sapiens 67-71
7626495-5 1995 It has been proposed that CRABP I sequesters retinoic acid in the cytoplasm and prevents nuclear uptake of retinoic acid. Tretinoin 45-58 cellular retinoic acid binding protein 1 Homo sapiens 26-33
7626495-5 1995 It has been proposed that CRABP I sequesters retinoic acid in the cytoplasm and prevents nuclear uptake of retinoic acid. Tretinoin 107-120 cellular retinoic acid binding protein 1 Homo sapiens 26-33
7935425-6 1994 In contrast, the RXR-specific ligand induced rat growth hormone mRNA in GH3 pituitary cells, indicating that the effects of RA on growth hormone gene expression at least in part involve ligand binding to endogenous RXRs in vivo. Tretinoin 124-126 gonadotropin releasing hormone receptor Rattus norvegicus 49-63
12828686-5 2003 Strong RA-induced upregulation of Hox-1 and Cyp26 was observed, as is the case in vertebrates. Tretinoin 7-9 homeobox transcription factor Hox1 Ciona intestinalis 34-39
7935425-6 1994 In contrast, the RXR-specific ligand induced rat growth hormone mRNA in GH3 pituitary cells, indicating that the effects of RA on growth hormone gene expression at least in part involve ligand binding to endogenous RXRs in vivo. Tretinoin 124-126 gonadotropin releasing hormone receptor Rattus norvegicus 130-144
7626495-9 1995 A regulated nuclear uptake of CRABP I implies a role for this protein in the intracellular transport of retinoic acid. Tretinoin 104-117 cellular retinoic acid binding protein 1 Homo sapiens 30-37
7742011-4 1995 We found that retinoic acid interferes, in a dose-dependent fashion, with the expression of epithelial genes that are found in distal segments of the fetal lung (surfactant-associated proteins SP-A, SP-B, and SP-C). Tretinoin 14-27 surfactant protein A1 Homo sapiens 193-197
12799071-0 2003 Expression of Raldh2, Cyp26 and Hox-1 in normal and retinoic acid-treated Ciona intestinalis embryos. Tretinoin 52-65 homeobox transcription factor Hox1 Ciona intestinalis 32-37
7720661-0 1995 Cell-type specific interactions between retinoic acid and thyroid hormone in the regulation of expression of the gene encoding ornithine aminotransferase. Tretinoin 40-53 ornithine aminotransferase Rattus norvegicus 127-153
7720661-1 1995 The purposes of this study were to determine whether expression of the gene encoding ornithine aminotransferase (OAT) in the rat liver and kidney is regulated by retinoic acid (RA) and to characterize further the role of thyroid hormone in regulating the expression of this gene. Tretinoin 162-175 ornithine aminotransferase Rattus norvegicus 85-111
7720661-1 1995 The purposes of this study were to determine whether expression of the gene encoding ornithine aminotransferase (OAT) in the rat liver and kidney is regulated by retinoic acid (RA) and to characterize further the role of thyroid hormone in regulating the expression of this gene. Tretinoin 177-179 ornithine aminotransferase Rattus norvegicus 85-111
7803267-9 1994 In APL cases ATRA generated an asynchronous phenotype (CD15+, CDw65+, CD11b+, CD11a-), undetectable on normally maturing myeloid cells, but consistent with the concept that incomplete differentiation, in terms of surface molecule expression, can be sufficient to obtain therapeutic results. Tretinoin 13-17 integrin subunit alpha L Homo sapiens 78-83
7958425-3 1994 During retinoic acid (RA)-mediated differentiation of P19 embryonal carcinoma cells into neuroectodermal cell types that include immunohistochemically defined neurons and astrocytes, we observed a strong induction of AP-2 transcripts and protein. Tretinoin 7-20 transcription factor AP-2, alpha Mus musculus 217-221
7958425-3 1994 During retinoic acid (RA)-mediated differentiation of P19 embryonal carcinoma cells into neuroectodermal cell types that include immunohistochemically defined neurons and astrocytes, we observed a strong induction of AP-2 transcripts and protein. Tretinoin 22-24 transcription factor AP-2, alpha Mus musculus 217-221
7958425-10 1994 Our results indicate that AP-2 may play a role as a retinoic acid-sensitive regulator during differentiation of neurons and glia from an embryonic neural precursor. Tretinoin 52-65 transcription factor AP-2, alpha Mus musculus 26-30
12834868-2 2003 Treatment with retinoic acid (RA) increases Rarb expression and reduces explant bud formation through a signaling mechanism involving RARbeta. Tretinoin 15-28 retinoic acid receptor, beta Mus musculus 134-141
7730337-7 1995 The expression of a Ng/RC3-luciferase fusion construct (-1508/+256) in transfected 293 cells was stimulated by phorbol 12-myristate 13-acetate (PMA), but not by cAMP, arachidonic acid, vitamin D, retinoic acid, or thyroxines T3 and T4. Tretinoin 196-209 neurogranin Homo sapiens 23-26
12834868-2 2003 Treatment with retinoic acid (RA) increases Rarb expression and reduces explant bud formation through a signaling mechanism involving RARbeta. Tretinoin 30-32 retinoic acid receptor, beta Mus musculus 44-48
12834868-2 2003 Treatment with retinoic acid (RA) increases Rarb expression and reduces explant bud formation through a signaling mechanism involving RARbeta. Tretinoin 30-32 retinoic acid receptor, beta Mus musculus 134-141
7731708-4 1995 Using NTera2/clone D1 (NT2/D1) human embryonal carcinoma cells as a model, we report that the RA induced terminal differentiation of these cells into a neuronal phenotype is characterized by an increase in expression of RAR alpha, RAR beta, RAR gamma, and a slight induction of RXR alpha. Tretinoin 94-96 retinoic acid receptor gamma Homo sapiens 241-250
12834868-7 2003 We therefore discuss an interbud/proximal tubule signaling niche involving feedback between Rarb expression and Raldh1-mediated synthesis of RA. Tretinoin 141-143 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 112-118
7731708-7 1995 Over-expression of these receptors in the derived RA resistant subclone NT2/D1-R1 showed phenotypic changes characteristic of RA response in RAR gamma transfectants. Tretinoin 50-52 retinoic acid receptor gamma Homo sapiens 141-150
7731708-7 1995 Over-expression of these receptors in the derived RA resistant subclone NT2/D1-R1 showed phenotypic changes characteristic of RA response in RAR gamma transfectants. Tretinoin 126-128 retinoic acid receptor gamma Homo sapiens 141-150
7854351-13 1994 Treatment of AtT-20 cells with all-trans retinoic acid gave different kinetics for GR and c-jun mRNA regulation than obtained with TA; however, the GR and c-jun mRNA levels were still coordinately regulated after retinoic acid treatment. Tretinoin 41-54 jun proto-oncogene Mus musculus 90-95
7854351-13 1994 Treatment of AtT-20 cells with all-trans retinoic acid gave different kinetics for GR and c-jun mRNA regulation than obtained with TA; however, the GR and c-jun mRNA levels were still coordinately regulated after retinoic acid treatment. Tretinoin 41-54 jun proto-oncogene Mus musculus 155-160
7537465-0 1995 Glucocorticoid stimulation of fatty-acid synthase gene transcription in fetal lung: antagonism by retinoic acid. Tretinoin 98-111 fatty acid synthase Rattus norvegicus 30-49
12773567-8 2003 All-trans-retinoic acid induced reorganization of the PML nuclear body (NB) and reappearance of the IR-induced TopBP1 foci. Tretinoin 0-23 DNA topoisomerase II binding protein 1 Homo sapiens 111-117
7537465-8 1995 Retinoic acid antagonized the stimulatory effects of dexamethasone on FAS activity, mRNA content as measured by Northern analysis, mass as measured by Western blotting, and rate of transcription. Tretinoin 0-13 fatty acid synthase Rattus norvegicus 70-73
7537465-9 1995 The effect of retinoic acid was dependent on concentration in the relatively narrow range of 5 x 10(-6) to 5 x 10(-4) M. These data show that glucocorticoids stimulate transcription of the FAS gene in late gestation fetal rat lung, that normal transcription of the FAS gene is dependent on ongoing protein synthesis, and that glucocorticoid stimulation of FAS gene expression is antagonized by retinoic acid. Tretinoin 14-27 fatty acid synthase Rattus norvegicus 189-192
7537465-9 1995 The effect of retinoic acid was dependent on concentration in the relatively narrow range of 5 x 10(-6) to 5 x 10(-4) M. These data show that glucocorticoids stimulate transcription of the FAS gene in late gestation fetal rat lung, that normal transcription of the FAS gene is dependent on ongoing protein synthesis, and that glucocorticoid stimulation of FAS gene expression is antagonized by retinoic acid. Tretinoin 14-27 fatty acid synthase Rattus norvegicus 265-268
7537465-9 1995 The effect of retinoic acid was dependent on concentration in the relatively narrow range of 5 x 10(-6) to 5 x 10(-4) M. These data show that glucocorticoids stimulate transcription of the FAS gene in late gestation fetal rat lung, that normal transcription of the FAS gene is dependent on ongoing protein synthesis, and that glucocorticoid stimulation of FAS gene expression is antagonized by retinoic acid. Tretinoin 14-27 fatty acid synthase Rattus norvegicus 265-268
7537465-9 1995 The effect of retinoic acid was dependent on concentration in the relatively narrow range of 5 x 10(-6) to 5 x 10(-4) M. These data show that glucocorticoids stimulate transcription of the FAS gene in late gestation fetal rat lung, that normal transcription of the FAS gene is dependent on ongoing protein synthesis, and that glucocorticoid stimulation of FAS gene expression is antagonized by retinoic acid. Tretinoin 394-407 fatty acid synthase Rattus norvegicus 189-192
8090764-1 1994 The cellular retinoic acid binding proteins I and II (CRABPI and CRABPII) bind retinoic acid with high affinity, exhibit distinct patterns of expression during embryonic development, and are thought to play important roles in the RA signaling pathway. Tretinoin 13-26 cellular retinoic acid binding protein II Mus musculus 65-72
8090764-1 1994 The cellular retinoic acid binding proteins I and II (CRABPI and CRABPII) bind retinoic acid with high affinity, exhibit distinct patterns of expression during embryonic development, and are thought to play important roles in the RA signaling pathway. Tretinoin 79-92 cellular retinoic acid binding protein II Mus musculus 65-72
8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tretinoin 13-15 jun proto-oncogene Mus musculus 26-45
8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tretinoin 13-15 jun proto-oncogene Mus musculus 213-232
8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tretinoin 170-172 jun proto-oncogene Mus musculus 26-45
8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tretinoin 170-172 jun proto-oncogene Mus musculus 213-232
7537232-6 1995 BMP 4 and FGF 2 can also maintain Msx-1 expression in limb mesenchyme as well as retinoic acid which is usually associated with polarizing activity in the early limb. Tretinoin 81-94 fibroblast growth factor 2 Mus musculus 10-15
12668623-0 2003 Retinoic acid-induced developmental defects are mediated by RARbeta/RXR heterodimers in the pharyngeal endoderm. Tretinoin 0-13 retinoic acid receptor, beta Mus musculus 60-67
7706775-5 1995 Increasing RA concentrations altered the in vivo-like terminal differentiation of oral keratinocytes by disruption of organized stratification, inhibition of filaggrin/profilaggrin and K1 expression, and stimulation of K13 and K19 expression. Tretinoin 11-13 keratin 19 Homo sapiens 227-230
7536865-5 1995 In U-937 cells, showing constitutive TGF-alpha expression, RA but not vitamin D3 or PMA, caused marked increase in TGF-alpha mRNA (approximately 5-fold) and protein (approximately 3-fold) levels. Tretinoin 59-61 transforming growth factor alpha Homo sapiens 37-46
7536865-5 1995 In U-937 cells, showing constitutive TGF-alpha expression, RA but not vitamin D3 or PMA, caused marked increase in TGF-alpha mRNA (approximately 5-fold) and protein (approximately 3-fold) levels. Tretinoin 59-61 transforming growth factor alpha Homo sapiens 115-124
21559589-0 1994 Expression of a retinoic Acid-inducible mitochondrial nd5 gene is regulated by cell-density in bovine papillomavirus DNA-transformed mouse c127 cells but not in revertant cells. Tretinoin 16-29 NADH dehydrogenase 5, mitochondrial Mus musculus 54-57
12668623-1 2003 Fusion and hypoplasia of the first two branchial arches, a defect typically observed in retinoic acid (RA) embryopathy, is generated in cultured mouse embryos upon treatment with BMS453, a synthetic compound that exhibits retinoic acid receptor beta (RARbeta) agonistic properties in transfected cells. Tretinoin 88-101 retinoic acid receptor, beta Mus musculus 222-249
12668623-1 2003 Fusion and hypoplasia of the first two branchial arches, a defect typically observed in retinoic acid (RA) embryopathy, is generated in cultured mouse embryos upon treatment with BMS453, a synthetic compound that exhibits retinoic acid receptor beta (RARbeta) agonistic properties in transfected cells. Tretinoin 103-105 retinoic acid receptor, beta Mus musculus 222-249
7914950-0 1994 Modulation of CD13 expression during retinoic acid-induced differentiation of HL60 cells. Tretinoin 37-50 alanyl aminopeptidase, membrane Homo sapiens 14-18
12668623-1 2003 Fusion and hypoplasia of the first two branchial arches, a defect typically observed in retinoic acid (RA) embryopathy, is generated in cultured mouse embryos upon treatment with BMS453, a synthetic compound that exhibits retinoic acid receptor beta (RARbeta) agonistic properties in transfected cells. Tretinoin 103-105 retinoic acid receptor, beta Mus musculus 251-258
7914950-2 1994 In this study we have used the myeloid leukaemic cell line HL60, and its ability to differentiate when induced by all-trans-retinoic acid (ATRA), to study the regulation of CD13 molecules, and its associated aminopeptidase-N enzyme activity during the myeloid differentiation pathway. Tretinoin 114-137 alanyl aminopeptidase, membrane Homo sapiens 173-177
7914950-2 1994 In this study we have used the myeloid leukaemic cell line HL60, and its ability to differentiate when induced by all-trans-retinoic acid (ATRA), to study the regulation of CD13 molecules, and its associated aminopeptidase-N enzyme activity during the myeloid differentiation pathway. Tretinoin 139-143 alanyl aminopeptidase, membrane Homo sapiens 173-177
7914950-4 1994 Our results show that CD13 expression, and its enzyme activity, is downregulated during differentiation of HL60 induced by ATRA, but not when using GM-CSF. Tretinoin 123-127 alanyl aminopeptidase, membrane Homo sapiens 22-26
7890733-1 1995 In this study, we show that all-trans-retinoic acid (RA) is a potent inducer of tissue transglutaminase (TGase II) and apoptosis in the rat tracheobronchial epithelial cell line SPOC-1. Tretinoin 28-51 transglutaminase 2 Rattus norvegicus 105-113
8013374-7 1994 However, VLDLR and low density lipoprotein receptor-related protein were increased in the presence of retinoic acid, whereas the induction of lipoprotein lipase and hormone-sensitive lipase mRNAs was inhibited. Tretinoin 102-115 very low density lipoprotein receptor Mus musculus 9-14
7876191-2 1995 Class IV ADH has been found to be the most active as a retinol dehydrogenase, thus it may participate in retinoic acid synthesis. Tretinoin 105-118 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 9-12
12742548-10 2003 In vitro studies with a bovine primary mammary epithelial cell culture showed that all-trans-retinoic acid stimulates the appearance of bovine IGFBP-3 and bLf in the conditioned media and that [125I]rhIGFBP-3 could be utilized to detect conditioned media bLf. Tretinoin 83-106 insulin like growth factor binding protein 3 Bos taurus 143-150
7720575-1 1995 The cytoplasmic retinoic acid (RA)-binding protein CRABP-II is expressed widely throughout early morphogenesis in mouse embryo, but its expression becomes more restricted as organogenesis progresses. Tretinoin 16-29 cellular retinoic acid binding protein II Mus musculus 51-59
7720575-1 1995 The cytoplasmic retinoic acid (RA)-binding protein CRABP-II is expressed widely throughout early morphogenesis in mouse embryo, but its expression becomes more restricted as organogenesis progresses. Tretinoin 31-33 cellular retinoic acid binding protein II Mus musculus 51-59
7720576-0 1995 Genesis and prevention of spinal neural tube defects in the curly tail mutant mouse: involvement of retinoic acid and its nuclear receptors RAR-beta and RAR-gamma. Tretinoin 100-113 retinoic acid receptor, beta Mus musculus 140-148
7720576-1 1995 A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Tretinoin 15-34 retinoic acid receptor, beta Mus musculus 146-154
8058062-1 1994 It has previously been reported that retinaldehyde can be converted to retinoic acid by cytosolic aldehyde dehydrogenase (AHD-2) in liver extracts [Biochem. Tretinoin 71-84 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 122-127
7720576-1 1995 A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Tretinoin 21-34 retinoic acid receptor, beta Mus musculus 146-154
12782274-6 2003 The cdx-A/lacZ expression pattern requires an intron enhancer that includes two functional control elements: a DR2-type retinoic acid response element and a Tcf/beta-catenin binding motif. Tretinoin 120-133 caudal type homeobox 1 Mus musculus 4-7
7533818-1 1995 Retinoic acid (RA) and 1,25-(OH)2-vitamin D3 (1,25-D3) induced U937 cell maturation into distinct monocytic phenotypes, as demonstrated by up-regulation of CD23 by RA and CD14 by 1,25-D3. Tretinoin 0-13 Fc epsilon receptor II Homo sapiens 156-160
7533818-1 1995 Retinoic acid (RA) and 1,25-(OH)2-vitamin D3 (1,25-D3) induced U937 cell maturation into distinct monocytic phenotypes, as demonstrated by up-regulation of CD23 by RA and CD14 by 1,25-D3. Tretinoin 0-13 CD14 molecule Homo sapiens 171-175
7533818-1 1995 Retinoic acid (RA) and 1,25-(OH)2-vitamin D3 (1,25-D3) induced U937 cell maturation into distinct monocytic phenotypes, as demonstrated by up-regulation of CD23 by RA and CD14 by 1,25-D3. Tretinoin 15-17 Fc epsilon receptor II Homo sapiens 156-160
7533818-1 1995 Retinoic acid (RA) and 1,25-(OH)2-vitamin D3 (1,25-D3) induced U937 cell maturation into distinct monocytic phenotypes, as demonstrated by up-regulation of CD23 by RA and CD14 by 1,25-D3. Tretinoin 15-17 CD14 molecule Homo sapiens 171-175
7911240-0 1994 Inhibition of retinoic acid-induced activation of 3" human HOXB genes by antisense oligonucleotides affects sequential activation of genes located upstream in the four HOX clusters. Tretinoin 14-27 homeobox B cluster Homo sapiens 59-63
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 37-50 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 216-222
7954877-6 1994 Either retinoic acid (RA) or transforming growth factor-beta 1 (TGF-beta 1) induced the Cx43 expression of SV-HFO cells, as revealed by Northern blot analysis and immunocytochemistry. Tretinoin 7-20 gap junction protein alpha 1 Homo sapiens 88-92
7954877-6 1994 Either retinoic acid (RA) or transforming growth factor-beta 1 (TGF-beta 1) induced the Cx43 expression of SV-HFO cells, as revealed by Northern blot analysis and immunocytochemistry. Tretinoin 22-24 gap junction protein alpha 1 Homo sapiens 88-92
8078100-4 1994 In parallel with the neuronal differentiation following retinoic acid treatment, drebrin E was accumulated, accompanying filamentous (F) actin, in the submembranous cortical cytoplasm. Tretinoin 56-69 drebrin 1 Homo sapiens 81-90
7850796-7 1995 Moreover, RA treatment blocked the proliferative effect of oncostatin M and tumor necrosis factor alpha, two major KS autocrine growth factors. Tretinoin 10-12 oncostatin M Homo sapiens 59-103
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 52-54 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 216-222
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 31-44 retinoic acid receptor gamma Homo sapiens 243-252
12594185-5 2003 PGE2, forskolin, and retinoic acid induced a time-dependent up-regulation of Stra13 mRNA and protein expression in podocytes. Tretinoin 21-34 basic helix-loop-helix family member e40 Homo sapiens 77-83
7698301-3 1995 This study shows that all trans retinoic acid significantly enhances this activity by increasing production of tumour necrosis factor and gamma interferon, which results in enhanced expression of the p55 part of the interleukin 2 receptor. Tretinoin 32-45 interleukin 2 receptor subunit alpha Homo sapiens 200-203
7935490-0 1994 Thyroid hormone receptor-alpha inhibits retinoic acid-responsive gene expression and modulates retinoic acid-stimulated neural differentiation in mouse embryonic stem cells. Tretinoin 40-53 thyroid hormone receptor alpha Mus musculus 0-30
7935490-0 1994 Thyroid hormone receptor-alpha inhibits retinoic acid-responsive gene expression and modulates retinoic acid-stimulated neural differentiation in mouse embryonic stem cells. Tretinoin 95-108 thyroid hormone receptor alpha Mus musculus 0-30
7935490-4 1994 Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. Tretinoin 68-70 thyroid hormone receptor alpha Mus musculus 13-22
7935490-4 1994 Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. Tretinoin 68-70 retinoic acid receptor, beta Mus musculus 129-137
7935490-4 1994 Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. Tretinoin 68-70 thyroid hormone receptor alpha Mus musculus 188-197
7935490-4 1994 Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. Tretinoin 108-110 thyroid hormone receptor alpha Mus musculus 13-22
7935490-4 1994 Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. Tretinoin 108-110 retinoic acid receptor, beta Mus musculus 129-137
7935490-4 1994 Loss of both T3R alpha alleles resulted in an increase in basal and RA-induced expression of the endogenous RA-responsive genes, RAR beta and alkaline phosphatase, which demonstrates that T3R alpha has an inhibitory effect on the RA response. Tretinoin 108-110 thyroid hormone receptor alpha Mus musculus 188-197
7935490-6 1994 Cotransfection experiments were used to demonstrate that inhibition of the RA response could be mediated by T3R alpha 1. Tretinoin 75-77 thyroid hormone receptor alpha Mus musculus 108-117
7935490-7 1994 The addition of T3R alpha 1, but not the T3R alpha variant c-erbA alpha 2, to T3R alpha-null ES cells restored the inhibitory effect on RA-induced gene expression. Tretinoin 136-138 thyroid hormone receptor alpha Mus musculus 16-25
7829878-5 1995 Increasing RA concentrations altered the in vivo-like terminal differentiation of oral keratinocytes by disruption of organized stratification, inhibition of filaggrin/profilaggrin and K1 expression, and stimulation of K13 and K19 expression. Tretinoin 11-13 keratin 19 Homo sapiens 227-230
12594186-6 2003 Furthermore, we found that administration of 10(-7) M retinoic acid (RA) to embryoid bodies increased the percentage of MLC2v(-)ANP(+) cells; this also increased the expression of atrial-specific genes in the Nkx2.5/GFP(+) fraction, in a time- and dose-dependent fashion. Tretinoin 54-67 NK2 homeobox 5 Mus musculus 209-215
12632092-4 2003 Since ABCA1 is highly regulated by liver X receptor (LXR) we also analysed the mRNA and protein expressions of LXR-alpha and LXR-beta in the THP-1 cells after treatment with atRA. Tretinoin 174-178 nuclear receptor subfamily 1 group H member 3 Homo sapiens 111-120
7836350-3 1995 Differentiation of HL-60 cells by all-trans-retinoic acid (tRA) is directly mediated by down-regulation of the serine protease myeloblastin (mbn). Tretinoin 34-57 proteinase 3 Homo sapiens 127-139
7836350-3 1995 Differentiation of HL-60 cells by all-trans-retinoic acid (tRA) is directly mediated by down-regulation of the serine protease myeloblastin (mbn). Tretinoin 59-62 proteinase 3 Homo sapiens 127-139
8185572-1 1994 The pluripotent mouse embryonal carcinoma cell line P19 provides an excellent model system to study the mechanisms by which retinoic acid (RA) exerts its biological effects. Tretinoin 124-137 interleukin 23, alpha subunit p19 Mus musculus 52-55
8185572-1 1994 The pluripotent mouse embryonal carcinoma cell line P19 provides an excellent model system to study the mechanisms by which retinoic acid (RA) exerts its biological effects. Tretinoin 139-141 interleukin 23, alpha subunit p19 Mus musculus 52-55
8185572-2 1994 When aggregated and exposed to low concentrations of RA, P19 cells differentiate into neuron- and glial-like cells. Tretinoin 53-55 interleukin 23, alpha subunit p19 Mus musculus 57-60
12632092-6 2003 In conclusion, our results show that LXR-alpha and ABCA1 are simultaneously induced by atRA. Tretinoin 87-91 nuclear receptor subfamily 1 group H member 3 Homo sapiens 37-46
12676320-8 2003 The effect of xEmGCNF knockdown on hindbrain patterning is similar to conditions of reduced RA signaling, which may be caused by a reduction of RAR gamma expression specifically in the presumptive hindbrain. Tretinoin 92-94 retinoic acid receptor gamma S homeolog Xenopus laevis 144-153
8200851-7 1994 For the samples in group C, exposure to 10(-7) M RA for 1 day clearly increased GMR, but did not affect GR. Tretinoin 49-51 colony stimulating factor 2 receptor subunit alpha Homo sapiens 80-83
8200851-8 1994 This finding supports the hypothesis that the increase of GMR is one of the causes of the stimulative effects of RA on cells cultured with GM-CSF in group C. Tretinoin 113-115 colony stimulating factor 2 receptor subunit alpha Homo sapiens 58-61
12522100-6 2003 Although Nif3l1 was mainly detected in the cytoplasm, the translocation of Nif3l1 into the nuclei was observed in retinoic acid-primed neural differentiation of P19 cells and enhanced by the enforced expression of Trip15/CSN2. Tretinoin 114-127 COP9 signalosome subunit 2 Homo sapiens 214-220
28305623-7 1994 The wild-type RARgamma increases the severity of retinoic acid-mediated defects. Tretinoin 49-62 retinoic acid receptor gamma S homeolog Xenopus laevis 14-22
8018908-0 1994 All-trans retinoic acid induced hypercalcemia in a patient with acute promyelocytic leukemia: its relation to increased PTH-rP. Tretinoin 10-23 parathyroid hormone like hormone Homo sapiens 120-126
12537979-2 2003 N-(4-Hydroxyphenyl)-all-trans-retinamide (fenretinide, 4-HPR) is a synthetic ATRA derivative with chemopreventive and cytotoxic activity against various cancer cell lines including myeloid leukemia. Tretinoin 77-81 haptoglobin-related protein Homo sapiens 57-60
8157276-1 1994 In this study, we demonstrated that retinoic acid (RA) up-regulated interleukin-2 receptor-alpha (IL-2R alpha) expression on two human B-cell lines, IE8.6 and SKW6.4. Tretinoin 36-49 interleukin 2 receptor subunit alpha Homo sapiens 68-96
8157276-1 1994 In this study, we demonstrated that retinoic acid (RA) up-regulated interleukin-2 receptor-alpha (IL-2R alpha) expression on two human B-cell lines, IE8.6 and SKW6.4. Tretinoin 36-49 interleukin 2 receptor subunit alpha Homo sapiens 98-109
8157276-1 1994 In this study, we demonstrated that retinoic acid (RA) up-regulated interleukin-2 receptor-alpha (IL-2R alpha) expression on two human B-cell lines, IE8.6 and SKW6.4. Tretinoin 51-53 interleukin 2 receptor subunit alpha Homo sapiens 68-96
8157276-1 1994 In this study, we demonstrated that retinoic acid (RA) up-regulated interleukin-2 receptor-alpha (IL-2R alpha) expression on two human B-cell lines, IE8.6 and SKW6.4. Tretinoin 51-53 interleukin 2 receptor subunit alpha Homo sapiens 98-109
8157276-9 1994 Taken together, our results suggested that RA-induced activation of the IL-2R alpha promoter was through changes in the function of a NRE present between bases -400 and -368. Tretinoin 43-45 interleukin 2 receptor subunit alpha Homo sapiens 72-83
8157276-10 1994 This 31-base pair element may interact with an adjacent RA-responsive regulatory site as well as being responsible for down-regulation of basal IL-2R alpha expression under certain conditions. Tretinoin 56-58 interleukin 2 receptor subunit alpha Homo sapiens 144-155
7512149-4 1994 The effect was directly related to the drug concentration in the range from 10(-9) to 10(-5) M. Combined exposure of the cells to dexamethasone and retinoic acid featured an additive effect on PLP gene expression, whereas MAG gene expression was depressed below detectability level. Tretinoin 148-161 proteolipid protein 1 Rattus norvegicus 193-196
8289793-0 1994 Characterization of a negative retinoic acid response element in the murine Oct4 promoter. Tretinoin 31-44 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 76-80
8289793-1 1994 Expression of Oct4 in embryonic stem cells is controlled by a distal upstream stem cell-specific enhancer that is deactivated during retinoic acid (RA)-induced differentiation by an indirect mechanism not involving binding of RA receptors (H. Okazawa, K. Okamoto, F. Ishino, T. Ishino-Kaneko, S. Takeda, Y. Toyoda, M. Muramatsu, and H. Hamada, EMBO J. Tretinoin 133-146 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 14-18
8289793-1 1994 Expression of Oct4 in embryonic stem cells is controlled by a distal upstream stem cell-specific enhancer that is deactivated during retinoic acid (RA)-induced differentiation by an indirect mechanism not involving binding of RA receptors (H. Okazawa, K. Okamoto, F. Ishino, T. Ishino-Kaneko, S. Takeda, Y. Toyoda, M. Muramatsu, and H. Hamada, EMBO J. Tretinoin 148-150 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 14-18
8288641-10 1994 While recent studies have shown that HL-525 cells are deficient in PKC beta, the present results demonstrate that PKC beta expression is up-regulated in the HL-525 variant by treatment with retinoic acid. Tretinoin 190-203 protein kinase C beta Homo sapiens 114-122
8288641-11 1994 The results also demonstrate that retinoic acid-treated HL-525 cells respond to TPA with activation of Raf-1 and MAP kinase, as well as induction of monocytic differentiation. Tretinoin 34-47 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 103-108
27315712-0 1994 5,6-Epoxidation of All-trans-retinoic Acid with Soybean Lipoxygenase-2 and -3. Tretinoin 19-42 seed linoleate 9S-lipoxygenase-2 Glycine max 56-77
27315712-1 1994 Cooxidation activity of highly purified soybean lipoxygenase-2 and -3 was investigated with all-trans-retinoic acid as a co-substrate. Tretinoin 92-115 seed linoleate 9S-lipoxygenase-2 Glycine max 48-69
27315712-2 1994 Both the isoenzymes rapidly degraded retinoic acid in the presence of linoleic acid, but lipoxygenase-2 had more cooxidation activity than lipoxygenase-3. Tretinoin 37-50 seed linoleate 9S-lipoxygenase-2 Glycine max 89-103
27315712-2 1994 Both the isoenzymes rapidly degraded retinoic acid in the presence of linoleic acid, but lipoxygenase-2 had more cooxidation activity than lipoxygenase-3. Tretinoin 37-50 seed linoleate 9S-lipoxygenase-3 Glycine max 139-153
8265348-0 1993 Identification of positive and negative regulatory elements involved in the retinoic acid/cAMP induction of Fgf-3 transcription in F9 cells. Tretinoin 76-89 fibroblast growth factor 3 Mus musculus 108-113
8227157-9 1993 In contrast, RA treatment induced osteopontin (OP) mRNA expression more strongly in cells plated on collagen compared with plastic within 24 hr and this was maintained for 72 hr. Tretinoin 13-15 secreted phosphoprotein 1 Rattus norvegicus 34-45
8227157-9 1993 In contrast, RA treatment induced osteopontin (OP) mRNA expression more strongly in cells plated on collagen compared with plastic within 24 hr and this was maintained for 72 hr. Tretinoin 13-15 secreted phosphoprotein 1 Rattus norvegicus 47-49
8402688-10 1993 Conversely, stimulation of this I-type clone with retinoic acid resulted in an accumulation of N-type cells (which are thought to represent embryonic precursors of sympathetic neurons), decreased vimentin and beta-2-microglobulin, increased neurofilament-M, and a marked elevation in p26-Bcl-2. Tretinoin 50-63 transmembrane p24 trafficking protein 3 Homo sapiens 284-287
8105479-0 1993 Loss of retinoic acid receptor gamma function in F9 cells by gene disruption results in aberrant Hoxa-1 expression and differentiation upon retinoic acid treatment. Tretinoin 8-21 homeobox A1 Homo sapiens 97-103
8105479-5 1993 In contrast, transcripts encoding Hoxb-1 (Hox-2.9) and cellular RA binding protein II (CRABPII) are activated by RA for a longer period of time in the RAR gamma-/- lines compared to the wild-type F9 line. Tretinoin 64-66 retinoic acid receptor gamma Homo sapiens 151-160
8269032-5 1993 Relative to conditioned medium from cells grown in the absence of RA, conditioned medium from epidermal cells treated with RA contained increased concentrations of functionally active TGF alpha as determined by radioimmunoassays and radioreceptor assays. Tretinoin 123-125 transforming growth factor alpha Homo sapiens 184-193
8269032-6 1993 In addition, we found a marked reduction in the ability of TGF alpha to bind epidermal cells treated with RA. Tretinoin 106-108 transforming growth factor alpha Homo sapiens 59-68
8269032-7 1993 Decreased TGF alpha binding capacity is thought to be due to the ability of RA to stimulate TGF alpha, thereby resulting in EGF receptor binding and internalization. Tretinoin 76-78 transforming growth factor alpha Homo sapiens 10-19
8269032-7 1993 Decreased TGF alpha binding capacity is thought to be due to the ability of RA to stimulate TGF alpha, thereby resulting in EGF receptor binding and internalization. Tretinoin 76-78 transforming growth factor alpha Homo sapiens 92-101
8269032-8 1993 These results lead us to speculate that RA is capable of stimulating the secretion of TGF alpha by epidermal cells in vivo. Tretinoin 40-42 transforming growth factor alpha Homo sapiens 86-95
8269032-9 1993 TGF alpha may then act in an autocrine manner to mediate the hyperplastic response of the epidermis to topical RA treatment. Tretinoin 111-113 transforming growth factor alpha Homo sapiens 0-9
8162338-1 1993 Mammalian cell cytoplasm contains at least two proteins which bind retinoic acid (RA): CRABP I and CRABP II. Tretinoin 67-80 cellular retinoic acid binding protein 1 Homo sapiens 87-94
8162338-1 1993 Mammalian cell cytoplasm contains at least two proteins which bind retinoic acid (RA): CRABP I and CRABP II. Tretinoin 82-84 cellular retinoic acid binding protein 1 Homo sapiens 87-94
8413217-0 1993 Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers. Tretinoin 0-13 RELA proto-oncogene, NF-kB subunit Homo sapiens 149-152
8413217-4 1993 Region I binding activity was not present in undifferentiated NT2 cells, but binding of an NF-kappa B heterodimer, p50-p65, was induced following RA treatment. Tretinoin 146-148 RELA proto-oncogene, NF-kB subunit Homo sapiens 119-122
8413217-6 1993 Region II binding activity was present in undifferentiated cells at low levels but was greatly augmented by RA treatment because of activation of a nuclear hormone receptor heterodimer composed of the retinoid X receptor (RXR beta) and the RA receptor (RAR beta). Tretinoin 108-110 retinoid X receptor beta Homo sapiens 222-230
8413217-7 1993 The RXR beta-RAR beta heterodimer also bound RA responsive elements present in other genes which are likely to be involved in RA triggering of EC cell differentiation. Tretinoin 13-15 retinoid X receptor beta Homo sapiens 4-12
8410463-6 1993 Individually, RA and calcitriol induced mRNA expression for ALP, matrix-gla protein (MGP), and osteopontin (OP). Tretinoin 14-16 secreted phosphoprotein 1 Rattus norvegicus 95-106
8410463-6 1993 Individually, RA and calcitriol induced mRNA expression for ALP, matrix-gla protein (MGP), and osteopontin (OP). Tretinoin 14-16 secreted phosphoprotein 1 Rattus norvegicus 108-110
8410463-8 1993 The combination of RA and calcitriol had a synergistic effect on ALP, OP, and especially MGP mRNA expression but significantly reduced the expression of pro-alpha 1(I) collagen mRNA. Tretinoin 19-21 secreted phosphoprotein 1 Rattus norvegicus 70-72
8410463-10 1993 The addition of AA to RA resulted in a decrease in the steady state level of OP, whereas its cotreatment with calcitriol caused a decrease in pro-alpha 1(I) collagen and ALP mRNA. Tretinoin 22-24 secreted phosphoprotein 1 Rattus norvegicus 77-79
8393814-5 1993 The acidic dehydrogenase accounts for most of the retinoic acid synthesis in the retina during embryonic and early postnatal stages; during later postnatal stages it disappears and in the adult retina all retinoic acid synthesis is mediated by AHD-2. Tretinoin 205-218 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 244-249
8388815-4 1993 In this paper we demonstrate that met/HGF/SFR mRNA, protein, and its ligand are expressed at a low level in undifferentiated P19 cells and that their expression is increased as P19 cells are induced to differentiate into neuroectodermal derivatives following treatment with retinoic acid (RA) and into mesodermal derivatives following treatment with dimethyl sulfoxide (DMSO). Tretinoin 274-287 interleukin 23, alpha subunit p19 Mus musculus 177-180
8162329-9 1993 Pretreatment of cultures with retinoic acid (10(-5)-10(-7) M) significantly inhibited the induction of ODC by EGF. Tretinoin 30-43 ornithine decarboxylase 1 Homo sapiens 103-106
8162329-10 1993 Retinoic acid decreased the steady-state levels of ODC mRNA. Tretinoin 0-13 ornithine decarboxylase 1 Homo sapiens 51-54
8641047-8 1995 Constitutive expression of RAR gamma 2.2 following neurulation appears to be depressed by treatment with retinoic acid, but domains of highest expression, namely, the head and tail, remain relatively unaffected, as do patterns of expression prior to late neurulation. Tretinoin 105-118 retinoic acid receptor gamma S homeolog Xenopus laevis 27-36
8641047-10 1995 Using microinjection techniques, we show that changes of RAR-gamma 2.1 expression in presumptive head structures occur as an early and local consequence of retinoic acid administration. Tretinoin 156-169 retinoic acid receptor gamma S homeolog Xenopus laevis 57-70
8641047-11 1995 Since RAR-gamma 2.1 expression is inhibited by retinoic acid, we tested to see if other treatments that perturb axis formation had any effect. Tretinoin 47-60 retinoic acid receptor gamma S homeolog Xenopus laevis 6-19
7813633-4 1995 The effects of LPA are compared with all-trans-retinoic acid (RA), a structurally unrelated lipid that has previously been shown to induce both TGF alpha and TGF beta and have pronounced effects on keratinocyte proliferation and differentiation. Tretinoin 62-64 transforming growth factor alpha Homo sapiens 144-153
7813633-5 1995 Treatment of cultured human keratinocytes with LPA or RA induced the production of TGF alpha by four- to eightfold. Tretinoin 54-56 transforming growth factor alpha Homo sapiens 83-92
7538894-4 1995 Retinoic acid reduced the response to IL-6 of alpha-2-macroglobulin but enhanced that of alpha-1-acid glycoprotein and especially of C3 complement. Tretinoin 0-13 alpha-2-macroglobulin Rattus norvegicus 46-67
7531260-8 1995 Moreover, was observed a rapid simultaneous correction of low fibrinogen levels and plasmin activation markers in APL patients undergoing ATRA therapy (before day 5), but a more prolonged persistence of DIC markers (until day 14). Tretinoin 138-142 plasminogen Homo sapiens 84-91
7531260-11 1995 In vivo differentiation ATRA therapy induces a rapid decrease in the plasmin activation and a normalization of fibrinogen level, while DIC may in vivo persist for several weeks. Tretinoin 24-28 plasminogen Homo sapiens 69-76
7488392-3 1995 CRABP-II mRNA was significantly induced (3- to 4.5-fold) by a single dose of RA at 6 and 16 h after RA treatment, with a return to control levels at 48 h. CRABP-II message was not significantly elevated by 3 or 4 consecutive days of RA treatment, when assessed 24 h after the last treatment. Tretinoin 77-79 cellular retinoic acid binding protein II Mus musculus 0-8
7488392-3 1995 CRABP-II mRNA was significantly induced (3- to 4.5-fold) by a single dose of RA at 6 and 16 h after RA treatment, with a return to control levels at 48 h. CRABP-II message was not significantly elevated by 3 or 4 consecutive days of RA treatment, when assessed 24 h after the last treatment. Tretinoin 77-79 cellular retinoic acid binding protein II Mus musculus 0-8
7488392-6 1995 By this protein assay method, increases in CRABP-II were detected 24 and 48 h after a single application of RA, as well as after 3 and 4 days of RA treatment. Tretinoin 108-110 cellular retinoic acid binding protein II Mus musculus 43-51
7805865-1 1994 A new 8.2 kDa differentiation factor has been purified to homogeneity from the cultural media of human myelogenous HL-60 leukemia cells induced by retinoic acid. Tretinoin 147-160 ribosomal protein S21 Homo sapiens 6-36
7898304-7 1994 Retinoic acid and dexamethasone, respectively, increased activity of the RC3 promoter in neuroblastoma cells when a deletion construct containing the retinoic acid and the glucocorticoid responsive elements was cotransfected with retinoic acid receptor or glucocorticoid receptor expression vectors. Tretinoin 0-13 neurogranin Homo sapiens 73-76
7898304-7 1994 Retinoic acid and dexamethasone, respectively, increased activity of the RC3 promoter in neuroblastoma cells when a deletion construct containing the retinoic acid and the glucocorticoid responsive elements was cotransfected with retinoic acid receptor or glucocorticoid receptor expression vectors. Tretinoin 150-163 neurogranin Homo sapiens 73-76
7961858-1 1994 Transcriptional regulation of the progesterone receptor gene involves induction by estrogens and down-regulation by progestins, retinoic acid, and AP-1 proteins. Tretinoin 128-141 progesterone receptor Homo sapiens 34-55
7931322-0 1994 Phorbol ester- and retinoic acid-induced regulation of the protein kinase C substrate MARCKS in immortalized hippocampal cells. Tretinoin 19-32 myristoylated alanine rich protein kinase C substrate Homo sapiens 86-92
7931322-1 1994 The expression of MARCKS, a major protein kinase C (PKC) substrate, was examined in the immortalized hippocampal cell line HN33, following differentiation using phorbol esters or retinoic acid. Tretinoin 179-192 myristoylated alanine rich protein kinase C substrate Homo sapiens 18-24
7931322-7 1994 MARCKS protein expression was also down-regulated in a dose-dependent manner on exposure of HN33 cells to retinoic acid. Tretinoin 106-119 myristoylated alanine rich protein kinase C substrate Homo sapiens 0-6
7931322-8 1994 In cells exposed to 10 microM retinoic acid, the MARCKS protein level was reduced in the membrane fraction within 4 h. Reduction of MARCKS protein levels was maximal (> 90%) by 12 h with no evidence for any alteration in PKC activity. Tretinoin 30-43 myristoylated alanine rich protein kinase C substrate Homo sapiens 49-55
7931322-8 1994 In cells exposed to 10 microM retinoic acid, the MARCKS protein level was reduced in the membrane fraction within 4 h. Reduction of MARCKS protein levels was maximal (> 90%) by 12 h with no evidence for any alteration in PKC activity. Tretinoin 30-43 myristoylated alanine rich protein kinase C substrate Homo sapiens 132-138
7931322-9 1994 Reduced levels of MARCKS protein were also observed in the soluble fraction of retinoic acid-exposed cells, but to a significantly lesser extent. Tretinoin 79-92 myristoylated alanine rich protein kinase C substrate Homo sapiens 18-24
7682243-8 1993 Furthermore, the VitD3- and the PMA-induced CD14 expression was inhibited as a temporal consequence of the RA-induced differentiation. Tretinoin 107-109 CD14 molecule Homo sapiens 44-48
8384988-5 1993 Furthermore, while AtT-20 and F9 cells both expressed multiple RAR beta isoforms, including RAR beta 2, which was profoundly induced by RA in F9 cells, none of these was highly regulated by RA in AtT-20 cells. Tretinoin 63-65 retinoic acid receptor, beta Mus musculus 92-100
8384988-5 1993 Furthermore, while AtT-20 and F9 cells both expressed multiple RAR beta isoforms, including RAR beta 2, which was profoundly induced by RA in F9 cells, none of these was highly regulated by RA in AtT-20 cells. Tretinoin 92-94 retinoic acid receptor, beta Mus musculus 63-71
12393450-6 2003 PML-RARalpha inhibits expression of C/EBPepsilon, whereas all-trans retinoic acid (tRA), a differentiating agent to which APL is particularly susceptible, induces C/EBPepsilon expression. Tretinoin 68-81 CCAAT/enhancer binding protein (C/EBP), epsilon Mus musculus 163-175
8319825-0 1993 Differential regulation of matrix Gla protein (MGP) gene expression by retinoic acid and estrogen in human breast carcinoma cells. Tretinoin 71-84 matrix Gla protein Homo sapiens 27-45
8319825-0 1993 Differential regulation of matrix Gla protein (MGP) gene expression by retinoic acid and estrogen in human breast carcinoma cells. Tretinoin 71-84 matrix Gla protein Homo sapiens 47-50
8319825-1 1993 Expression of matrix Gla protein (MGP) gene and its regulation by retinoic acid (RA) and estrogen was investigated in eight human breast cancer cell lines. Tretinoin 66-79 matrix Gla protein Homo sapiens 14-32
7923112-6 1994 Decreased expression of the N-myc oncogene in neuroblastoma cell lines SH-SY5Y and BE(2)-C, following treatment with retinoic acid, was paralleled by down-regulation of MRP gene expression, contrasting with increased expression of the MDR1 gene. Tretinoin 117-130 ATP binding cassette subfamily C member 3 Homo sapiens 169-172
7889981-1 1994 Expression of an activated raf transgene accelerated the terminal myeloid differentiation of HL-60 human promyelocytic leukemia cells induced by retinoic acid. Tretinoin 145-158 zinc fingers and homeoboxes 2 Homo sapiens 27-30
12393450-6 2003 PML-RARalpha inhibits expression of C/EBPepsilon, whereas all-trans retinoic acid (tRA), a differentiating agent to which APL is particularly susceptible, induces C/EBPepsilon expression. Tretinoin 83-86 CCAAT/enhancer binding protein (C/EBP), epsilon Mus musculus 163-175
7934172-4 1994 In all cases, incubation with ATRA induces either an increase in the number of affinity of GM-CSF R (n = 212.7 +/- 116.2 sites/cell, Kd = 43.2 +/- 22.5 pM). Tretinoin 30-34 colony stimulating factor 2 receptor subunit alpha Homo sapiens 91-99
12559492-1 2003 In a differential display screening for genes regulated by retinoic acid in the developing chick limb bud, we have isolated a novel gene, termed rigf, retinoic-acid induced growth factor, that encodes a protein belonging to the vascular endothelial growth factor (VEGF) family. Tretinoin 59-72 vascular endothelial growth factor A Gallus gallus 228-262
7815961-5 1994 Given that the intracellular abundance of thymosins beta-4 and beta-10 is related to cell division and differentiation and that anticancer/morphogenic agents such as retinoic acid (RA) and cyclic AMP modulate expression of their respective genes, it is possible that these G-actin sequestering proteins play significant roles in apoptosis perhaps mediated via DNase I. Tretinoin 181-183 tubulin beta 3 class III Homo sapiens 52-70
8319825-1 1993 Expression of matrix Gla protein (MGP) gene and its regulation by retinoic acid (RA) and estrogen was investigated in eight human breast cancer cell lines. Tretinoin 66-79 matrix Gla protein Homo sapiens 34-37
8319825-1 1993 Expression of matrix Gla protein (MGP) gene and its regulation by retinoic acid (RA) and estrogen was investigated in eight human breast cancer cell lines. Tretinoin 81-83 matrix Gla protein Homo sapiens 14-32
8319825-1 1993 Expression of matrix Gla protein (MGP) gene and its regulation by retinoic acid (RA) and estrogen was investigated in eight human breast cancer cell lines. Tretinoin 81-83 matrix Gla protein Homo sapiens 34-37
8319825-2 1993 The promoter region of the MGP gene contains a consensus retinoic acid response element (RARE) and the MGP gene expression has been shown to be strongly induced by RA in other systems. Tretinoin 57-70 matrix Gla protein Homo sapiens 27-30
8319825-2 1993 The promoter region of the MGP gene contains a consensus retinoic acid response element (RARE) and the MGP gene expression has been shown to be strongly induced by RA in other systems. Tretinoin 89-91 matrix Gla protein Homo sapiens 27-30
8319825-3 1993 Our results suggest that RA negatively regulates MGP mRNA expression in human breast cancer cells that have high levels of estrogen receptors (ER), i.e. MCF-7, ZR-75 and BT474 and positively regulates its expression in cells with either no ERs, i.e. MDA-MB-468 or very low levels of ERs, i.e. T47D. Tretinoin 25-27 matrix Gla protein Homo sapiens 49-52
8319825-4 1993 This indicates that ER levels may affect RA modulation of MGP gene expression in human breast cancer cells. Tretinoin 41-43 matrix Gla protein Homo sapiens 58-61
8319825-5 1993 The inhibitory effect of RA on MGP gene expression was abolished in RRO-I, the RA-resistant MCF-7 subline. Tretinoin 25-27 matrix Gla protein Homo sapiens 31-34
7914354-0 1994 A conserved retinoic acid response element required for early expression of the homeobox gene Hoxb-1. Tretinoin 12-25 homeobox B1 Mus musculus 94-100
7914354-4 1994 We have now identified two enhancers, 3" of the mouse Hoxb-1 gene, which together reconstruct the early endogenous expression pattern and mediate the early ectopic response to retinoic acid. Tretinoin 176-189 homeobox B1 Mus musculus 54-60
7914354-8 1994 Therefore, this RARE is not only involved in the ectopic response to retinoic acid, but is also essential for establishing aspects of the early Hoxb-1 expression pattern. Tretinoin 69-82 homeobox B1 Mus musculus 144-150
8319825-5 1993 The inhibitory effect of RA on MGP gene expression was abolished in RRO-I, the RA-resistant MCF-7 subline. Tretinoin 79-81 matrix Gla protein Homo sapiens 31-34
8319825-6 1993 We also demonstrate for the first time that estrogen strongly induces MGP gene expression in ER-positive cells and that estrogen-mediated induction of MGP is blocked by RA even in otherwise RA-resistant cells. Tretinoin 169-171 matrix Gla protein Homo sapiens 151-154
12559492-1 2003 In a differential display screening for genes regulated by retinoic acid in the developing chick limb bud, we have isolated a novel gene, termed rigf, retinoic-acid induced growth factor, that encodes a protein belonging to the vascular endothelial growth factor (VEGF) family. Tretinoin 59-72 vascular endothelial growth factor A Gallus gallus 264-268
12559492-1 2003 In a differential display screening for genes regulated by retinoic acid in the developing chick limb bud, we have isolated a novel gene, termed rigf, retinoic-acid induced growth factor, that encodes a protein belonging to the vascular endothelial growth factor (VEGF) family. Tretinoin 151-164 vascular endothelial growth factor A Gallus gallus 228-262
8387121-3 1993 CRBP (I) functions in cellular uptake of retinol from the plasma, solubilizes and renders retinol nontoxic in the aqueous system, and presents retinol to the appropriate enzymes to biosynthesize retinoic acid (an active form of retinoids) or retinyl esters (a storage form). Tretinoin 195-208 retinol binding protein 1 Homo sapiens 0-4
7527270-0 1994 Expression and down-regulation by retinoic acid of IGF binding protein-2 and -4 in medium from human neuroblastoma cells. Tretinoin 34-47 insulin like growth factor binding protein 2 Homo sapiens 51-79
7527270-3 1994 We investigated, by Western ligand blotting (WLB), the presence of IGFBPs and their possible modulation by retinoic acid (RA), IGF-I, IGF-II and truncated Des(1-3)IGF-I in conditioned medium (CM) of the human neuroblastoma SK-N-BE(2) cell line. Tretinoin 107-120 insulin like growth factor binding protein 2 Homo sapiens 67-73
7527270-3 1994 We investigated, by Western ligand blotting (WLB), the presence of IGFBPs and their possible modulation by retinoic acid (RA), IGF-I, IGF-II and truncated Des(1-3)IGF-I in conditioned medium (CM) of the human neuroblastoma SK-N-BE(2) cell line. Tretinoin 122-124 insulin like growth factor binding protein 2 Homo sapiens 67-73
8387121-5 1993 CRBP (III) is recognized as one of oncofetal proteins and binds both retinol and retinoic acid, the function of which still remains unclear. Tretinoin 81-94 retinol binding protein 1 Homo sapiens 0-4
8387121-6 1993 CRABP (I), previously recognized as a transport protein of retinoic acid to the nucleus, is now assumed to sequester retinoic acid from retinoic acid receptor(s) in the tissue where retinoic acid levels are required to be low. Tretinoin 59-72 cellular retinoic acid binding protein 1 Homo sapiens 0-5
7527270-8 1994 These findings suggest that IGFBPs have a role in RA-induced differentiation in human neuroblastoma cells. Tretinoin 50-52 insulin like growth factor binding protein 2 Homo sapiens 28-34
12559492-1 2003 In a differential display screening for genes regulated by retinoic acid in the developing chick limb bud, we have isolated a novel gene, termed rigf, retinoic-acid induced growth factor, that encodes a protein belonging to the vascular endothelial growth factor (VEGF) family. Tretinoin 151-164 vascular endothelial growth factor A Gallus gallus 264-268
7979182-0 1994 Retinoblastoma protein in non-small cell lung carcinoma, cells arrested for growth by retinoic acid. Tretinoin 86-99 RB transcriptional corepressor 1 Homo sapiens 0-14
8387121-6 1993 CRABP (I), previously recognized as a transport protein of retinoic acid to the nucleus, is now assumed to sequester retinoic acid from retinoic acid receptor(s) in the tissue where retinoic acid levels are required to be low. Tretinoin 117-130 cellular retinoic acid binding protein 1 Homo sapiens 0-5
8387121-6 1993 CRABP (I), previously recognized as a transport protein of retinoic acid to the nucleus, is now assumed to sequester retinoic acid from retinoic acid receptor(s) in the tissue where retinoic acid levels are required to be low. Tretinoin 117-130 cellular retinoic acid binding protein 1 Homo sapiens 0-5
12409287-2 2003 Using cDNA microarray, we identified a clone, DD4, that contains the cDNA of a novel gene, spurt (secretory protein in upper respiratory tracts) that was significantly induced by all-trans-retinoic acid in primary cultured human tracheobroncheal epithelia. Tretinoin 179-202 BPI fold containing family A member 1 Homo sapiens 91-96
8387121-7 1993 CRABP (I) also functions in the catabolism of retinoic acid to modulate its concentration in the cell. Tretinoin 46-59 cellular retinoic acid binding protein 1 Homo sapiens 0-5
8384845-2 1993 A partial induction by retinoic acid was obtained with the -181 bp of the rat GH promoter, and sequences up to -209 were required for a full response. Tretinoin 23-36 gonadotropin releasing hormone receptor Rattus norvegicus 78-80
7947389-8 1994 Furthermore, the expression of c-jun led to an enhancement of the induction of the differentiation of WEHI-3B D+ cells by retinoic acid, suggesting an involvement of c-jun in the retinoic acid signal transduction pathway. Tretinoin 179-192 jun proto-oncogene Mus musculus 31-36
7947389-8 1994 Furthermore, the expression of c-jun led to an enhancement of the induction of the differentiation of WEHI-3B D+ cells by retinoic acid, suggesting an involvement of c-jun in the retinoic acid signal transduction pathway. Tretinoin 179-192 jun proto-oncogene Mus musculus 166-171
8463554-0 1993 Retinoic acid inhibits human thyroid peroxidase and thyroglobulin gene expression in cultured human thyrocytes. Tretinoin 0-13 thyroglobulin Homo sapiens 52-65
12414803-0 2003 Rosiglitazone and retinoic acid induce uncoupling protein-1 (UCP-1) in a p38 mitogen-activated protein kinase-dependent manner in fetal primary brown adipocytes. Tretinoin 18-31 mitogen activated protein kinase 14 Rattus norvegicus 73-109
8463554-1 1993 The effect of retinoic acid (RA) on thyroid peroxidase (TPO) and thyroglobulin (Tg) gene expression was investigated in cultured human thyrocytes. Tretinoin 14-27 thyroglobulin Homo sapiens 80-82
8463554-1 1993 The effect of retinoic acid (RA) on thyroid peroxidase (TPO) and thyroglobulin (Tg) gene expression was investigated in cultured human thyrocytes. Tretinoin 29-31 thyroglobulin Homo sapiens 65-78
8463554-5 1993 Furthermore, RA inhibited forskolin and 8-Bromo-cyclic-AMP-induced TPO and Tg gene expression, suggesting a distal action site for these cAMP mediated gene expressions. Tretinoin 13-15 thyroglobulin Homo sapiens 75-77
8463554-9 1993 RA also inhibited TSH-induced Tg secretion in a dose dependent manner. Tretinoin 0-2 thyroglobulin Homo sapiens 30-32
8463554-11 1993 In conclusion, RA inhibits the synthesis of TPO and Tg via the suppression of thyroid-specific gene expression although the exact site of RA action on these genes in human thyroids remains to be further elucidated. Tretinoin 15-17 thyroglobulin Homo sapiens 52-54
8463554-12 1993 These results suggest that RA may play a regulatory role in Tg and TPO gene expression, subsequently resulting in the suppression of thyroid hormone synthesis. Tretinoin 27-29 thyroglobulin Homo sapiens 60-62
7525384-0 1994 Identification of a retinoic acid response element upstream of the rat alpha-fetoprotein gene. Tretinoin 20-33 alpha-fetoprotein Rattus norvegicus 71-88
7525384-8 1994 Furthermore, responsiveness of AFP-RARE1 to RA was independent of orientation. Tretinoin 35-37 alpha-fetoprotein Rattus norvegicus 31-34
7525384-9 1994 These studies present a novel target for RA action by identifying a RARE in the AFP gene. Tretinoin 41-43 alpha-fetoprotein Rattus norvegicus 80-83
12532155-0 2003 Up-regulation of muscle uncoupling protein 3 gene expression in mice following high fat diet, dietary vitamin A supplementation and acute retinoic acid-treatment. Tretinoin 138-151 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 24-44
8058062-11 1994 When the AHD-M1 and AHD-2 cDNAs were inserted into the expression vector pSG5 and transfected into cultured COS cells, 3-5-fold and 100-fold increases, respectively, in the conversion of [3H]retinaldehyde to [3H]retinoic acid could be detected by high performance liquid chromatographic assay. Tretinoin 212-225 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 20-25
21607448-1 1994 Fenretinide (4-HPR), a synthetic amide derivative of retinoic acid, has proven effective in preventing chemically induced mammary carcinoma in rodents. Tretinoin 53-66 haptoglobin-related protein Homo sapiens 15-18
8022710-6 1994 Androgen-induced levels of both prostate-specific antigen (PSA) and human glandular kallikrein-1 (hKLK2) mRNAs were significantly repressed by RA in a dose- and time-dependent manner. Tretinoin 143-145 kallikrein 1 Homo sapiens 74-96
8472843-2 1993 We have investigated whether retinoic acid (RA), whose receptors (RARs) share a high degree of homology with the thyroid hormone receptors (TRs), can regulate this gene in a manner similar to T3, as has been shown for the growth hormone (GH) gene. Tretinoin 29-42 gonadotropin releasing hormone receptor Rattus norvegicus 222-236
8472843-2 1993 We have investigated whether retinoic acid (RA), whose receptors (RARs) share a high degree of homology with the thyroid hormone receptors (TRs), can regulate this gene in a manner similar to T3, as has been shown for the growth hormone (GH) gene. Tretinoin 29-42 gonadotropin releasing hormone receptor Rattus norvegicus 238-240
8472843-2 1993 We have investigated whether retinoic acid (RA), whose receptors (RARs) share a high degree of homology with the thyroid hormone receptors (TRs), can regulate this gene in a manner similar to T3, as has been shown for the growth hormone (GH) gene. Tretinoin 44-46 gonadotropin releasing hormone receptor Rattus norvegicus 222-236
8472843-2 1993 We have investigated whether retinoic acid (RA), whose receptors (RARs) share a high degree of homology with the thyroid hormone receptors (TRs), can regulate this gene in a manner similar to T3, as has been shown for the growth hormone (GH) gene. Tretinoin 44-46 gonadotropin releasing hormone receptor Rattus norvegicus 238-240
8472843-4 1993 We observed a 73% decrease in TR beta-2 mRNA levels after incubation with T3 and a two-fold increase in TR beta-2 mRNA levels after incubation with RA alone. Tretinoin 148-150 thyroid hormone receptor beta Rattus norvegicus 104-111
7955315-2 1994 cDNA cloning and expression revealed that HB-GAM is a novel secretory protein that is homologous with the retinoic acid-inducible MK protein. Tretinoin 106-119 pleiotrophin Rattus norvegicus 42-48
7748347-1 1993 We previously proposed an hypothesis that fetal alcohol syndrome is caused by an ethanol-induced inhibition of retinoic acid synthesis catalyzed by alcohol dehydrogenase (ADH). Tretinoin 111-124 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 148-169
7935490-9 1994 Our results demonstrate that the early expression of unliganded T3R alpha functions to modulate the RA response and RA-stimulated neural differentiation. Tretinoin 100-102 thyroid hormone receptor alpha Mus musculus 64-73
7748347-1 1993 We previously proposed an hypothesis that fetal alcohol syndrome is caused by an ethanol-induced inhibition of retinoic acid synthesis catalyzed by alcohol dehydrogenase (ADH). Tretinoin 111-124 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 171-174
7935490-9 1994 Our results demonstrate that the early expression of unliganded T3R alpha functions to modulate the RA response and RA-stimulated neural differentiation. Tretinoin 116-118 thyroid hormone receptor alpha Mus musculus 64-73
12532155-1 2003 OBJECTIVE: To analyse the impact of vitamin A supplementation of both a normal fat (NF) diet and a high fat (HF) diet and of acute retinoic acid (RA)-treatment on the expression of uncoupling protein 3 (UCP3) in mice. Tretinoin 131-144 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 181-201
7748347-3 1993 Retinoic acid is derived from retinol (vitamin A alcohol) via oxidation by retinol dehydrogenases that are members of the ADH family of isozymes, many of which also use ethanol as a substrate. Tretinoin 0-13 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 122-125
7936086-0 1994 Trans retinoic acid inhibits in vivo tumour growth of C6 glioma in rats: effect negatively influenced by nerve growth factor. Tretinoin 0-19 nerve growth factor Rattus norvegicus 105-124
7748347-7 1993 Thus, embryonic ADH can presumably be induced by retinoic acid, further strengthening the argument that ADH plays a role in embryonic retinoic acid synthesis and fetal alcohol syndrome. Tretinoin 49-62 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 16-19
12532155-1 2003 OBJECTIVE: To analyse the impact of vitamin A supplementation of both a normal fat (NF) diet and a high fat (HF) diet and of acute retinoic acid (RA)-treatment on the expression of uncoupling protein 3 (UCP3) in mice. Tretinoin 146-148 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 181-201
7748347-7 1993 Thus, embryonic ADH can presumably be induced by retinoic acid, further strengthening the argument that ADH plays a role in embryonic retinoic acid synthesis and fetal alcohol syndrome. Tretinoin 134-147 aldo-keto reductase family 1, member A1 (aldehyde reductase) Mus musculus 16-19
12532155-1 2003 OBJECTIVE: To analyse the impact of vitamin A supplementation of both a normal fat (NF) diet and a high fat (HF) diet and of acute retinoic acid (RA)-treatment on the expression of uncoupling protein 3 (UCP3) in mice. Tretinoin 146-148 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 203-207
12532155-5 2003 The effect of acute RA-treatment (100 mg/kg/day, 4 days) on UCP3 mRNA levels in skeletal muscle and BAT of NMRI mice was also assessed. Tretinoin 20-22 uncoupling protein 3 (mitochondrial, proton carrier) Mus musculus 60-64
8144640-11 1994 Reduced metabolism of CRABP-bound C4-derivatized retinoids suggests pathways of retinoic acid metabolism besides the one initiated by C4-hydroxylation. Tretinoin 80-93 cellular retinoic acid binding protein 1 Homo sapiens 22-27
12514092-6 2003 Results suggest that diminished RXRbeta expression might be related to prostate cancer progression and because the responsiveness to retinoic acid treatments depends on the expression of different receptors, it is important to study their expression before therapy. Tretinoin 133-146 retinoid X receptor beta Homo sapiens 32-39
8144640-13 1994 Ketoconazole inhibited the metabolism by testis microsomes of free and CRABP-bound retinoic acid with IC50 values of 2 and 0.7 microM, respectively, denoting catalysis by cytochrome P-450. Tretinoin 83-96 cellular retinoic acid binding protein 1 Homo sapiens 71-76
8144640-14 1994 These results indicate that cloistering retinoic acid in CRABP, while permitting metabolism, may operate throughout CRABP-expressing tissues as a mechanism of controlling the concentrations of free retinoic acid. Tretinoin 40-53 cellular retinoic acid binding protein 1 Homo sapiens 57-62
8144640-14 1994 These results indicate that cloistering retinoic acid in CRABP, while permitting metabolism, may operate throughout CRABP-expressing tissues as a mechanism of controlling the concentrations of free retinoic acid. Tretinoin 40-53 cellular retinoic acid binding protein 1 Homo sapiens 116-121
8144640-14 1994 These results indicate that cloistering retinoic acid in CRABP, while permitting metabolism, may operate throughout CRABP-expressing tissues as a mechanism of controlling the concentrations of free retinoic acid. Tretinoin 198-211 cellular retinoic acid binding protein 1 Homo sapiens 57-62
8144640-14 1994 These results indicate that cloistering retinoic acid in CRABP, while permitting metabolism, may operate throughout CRABP-expressing tissues as a mechanism of controlling the concentrations of free retinoic acid. Tretinoin 198-211 cellular retinoic acid binding protein 1 Homo sapiens 116-121
8381386-1 1993 The murine retinoid X receptor beta (mRXR beta) is a nuclear hormone receptor that activates transcription of murine major histocompatibility complex (MHC) class I genes in response to retinoic acid. Tretinoin 185-198 retinoid X receptor beta Homo sapiens 11-35
12925606-9 2003 Retinoic acid rapidly and dramatically stimulated accumulation of BMP-2 and BMP-6 messenger RNAs. Tretinoin 0-13 bone morphogenetic protein 6 Gallus gallus 76-81
8007703-1 1993 Fenretinide (4-HPR), a synthetic derivative of retinoic acid, has proven effective at inhibiting in vitro breast cancer cell growth and preventing the progression of chemically induced mammary carcinoma in rodents. Tretinoin 47-60 haptoglobin-related protein Homo sapiens 15-18
1282809-3 1992 Undifferentiated P19 cells are completely devoid of lamins A and C. We show that undifferentiated P19 cells contain low, but detectable steady-state levels of RNAs for lamins A and C that begin to increase by 24 h of retinoic acid-induced differentiation. Tretinoin 217-230 interleukin 23, alpha subunit p19 Mus musculus 98-101
1361214-4 1992 Here we follow the changes induced by retinoic acid to hindbrain segmentation and the branchial arches using transgenic mice which contain lacZ reporter genes that reveal the endogenous segment-restricted expression of the Hox-B1 (Hox-2.9), Hox-B2(Hox-2.8) and Krox-20 genes. Tretinoin 38-51 homeobox B1 Mus musculus 223-229
7514032-0 1994 Antagonistic effects of retinoic acid and triiodothyronine in the expression of corticoid-binding globulin (CBG) by cultured fetal hepatocytes. Tretinoin 24-37 serpin family A member 6 Rattus norvegicus 80-106
7514032-0 1994 Antagonistic effects of retinoic acid and triiodothyronine in the expression of corticoid-binding globulin (CBG) by cultured fetal hepatocytes. Tretinoin 24-37 serpin family A member 6 Rattus norvegicus 108-111
7514032-1 1994 Cultures of rat fetal hepatocytes were used to investigate the effects and interplay of triiodothyronine (T3) and retinoic acid (RA) in the regulation of gene expression of CBG, compared to that of alpha-fetoprotein (AFP). Tretinoin 114-127 serpin family A member 6 Rattus norvegicus 173-176
7514032-1 1994 Cultures of rat fetal hepatocytes were used to investigate the effects and interplay of triiodothyronine (T3) and retinoic acid (RA) in the regulation of gene expression of CBG, compared to that of alpha-fetoprotein (AFP). Tretinoin 129-131 serpin family A member 6 Rattus norvegicus 173-176
7514032-5 1994 Culturing of hepatocytes in the presence of T3 resulted in dose-dependent stimulations of both medium CBG and cell mRNA levels, with an EC50 concentration of about 10(-9) M. In sharp contrast, RA caused a reduction in CBG biosynthesis (IC50 = 1.7 x 10(-7) M) and, in addition, antagonized the stimulatory influence of T3. Tretinoin 193-195 serpin family A member 6 Rattus norvegicus 218-221
7514032-7 1994 We conclude that thyroid hormones and RA directly act on hepatocytes to specifically regulate the expression of CBG in an antagonistic way. Tretinoin 38-40 serpin family A member 6 Rattus norvegicus 112-115
1431107-11 1992 RA at 0.01 to 1 microM significantly inhibited the induction of thymocyte apoptosis by co-immobilized mAb to CD3 and LFA-1 molecules. Tretinoin 0-2 integrin subunit alpha L Homo sapiens 117-122
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 163-176 neurotrophic receptor tyrosine kinase 2 Homo sapiens 50-54
12760771-2 2003 METHODS: Immunocytochemistry and flow cytometry (FCM) were used to analyze the expression of Cx43 protein in Tca8113 cells after treated with ATRA; The bystander effect of HSV-TK/GCV system on tongue carcinoma cells before and after treatment with ATRA was detected by MTT assays. Tretinoin 142-146 gap junction protein alpha 1 Homo sapiens 93-97
1328234-0 1992 The level of CRABP-I expression influences the amounts and types of all-trans-retinoic acid metabolites in F9 teratocarcinoma stem cells. Tretinoin 78-91 cellular retinoic acid binding protein 1 Homo sapiens 13-20
8134128-6 1994 In contrast to these two genes the expression of mad was induced upon differentiation in the three cell lines by TPA, retinoic acid, vitamin D3, dimethyl sulfoxide, and interferon-gamma and remained elevated for at least 3 days. Tretinoin 118-131 MAX dimerization protein 1 Homo sapiens 49-52
12760771-4 2003 RESULTS: After treated by ATRA (10(-7) mol/L - 10(-5) mol/L), the expression of Cx43 protein was up-regulated in Tca8113 cells and the positive rate of Cx43 protein increased from 5.17% (before treatment) to 30.53% (10(-5) mol/L ATRA). Tretinoin 26-30 gap junction protein alpha 1 Homo sapiens 80-84
12760771-4 2003 RESULTS: After treated by ATRA (10(-7) mol/L - 10(-5) mol/L), the expression of Cx43 protein was up-regulated in Tca8113 cells and the positive rate of Cx43 protein increased from 5.17% (before treatment) to 30.53% (10(-5) mol/L ATRA). Tretinoin 26-30 gap junction protein alpha 1 Homo sapiens 152-156
8135739-4 1994 Northern-blot analysis and receptor-binding studies demonstrate that bradykinin also inhibits the retinoic acid-induced increase in EGF receptor levels in these cells. Tretinoin 98-111 epidermal growth factor like 1 Rattus norvegicus 132-135
1328234-3 1992 We have previously shown that overexpression of the CRABP-I protein in stably transfected F9 stem cell lines results in a lower sensitivity to a given external concentration of retinoic acid relative to that of untransfected F9 cells; in contrast, reduced CRABP-I expression in CRABP-I cDNA anti-sense transfected lines is associated with increased sensitivity of these lines to retinoic acid. Tretinoin 177-190 cellular retinoic acid binding protein 1 Homo sapiens 52-59
1328234-3 1992 We have previously shown that overexpression of the CRABP-I protein in stably transfected F9 stem cell lines results in a lower sensitivity to a given external concentration of retinoic acid relative to that of untransfected F9 cells; in contrast, reduced CRABP-I expression in CRABP-I cDNA anti-sense transfected lines is associated with increased sensitivity of these lines to retinoic acid. Tretinoin 379-392 cellular retinoic acid binding protein 1 Homo sapiens 52-59
1328234-4 1992 These three types of cell lines were cultured in the presence of 50 nM [3H]retinoic acid, and the metabolism of retinoic acid was followed over the next 24 h. The results demonstrate that CRABP-I has the ability to alter both the levels and types of RA metabolites produced in the cytoplasm of differentiating embryonic stem cells. Tretinoin 75-88 cellular retinoic acid binding protein 1 Homo sapiens 188-195
8125154-6 1994 Treatment of chondrocytes with retinoic acid for the first 3 days of culture, prior to use in attachment assays, resulted in a decrease in the attachment to collagen but not to fibronectin or MGP. Tretinoin 31-44 matrix Gla protein Homo sapiens 192-195
8125154-7 1994 Seven days of retinoic acid treatment resulted in decreased attachment to fibronectin, MGP, and collagen. Tretinoin 14-27 matrix Gla protein Homo sapiens 87-90
1328234-4 1992 These three types of cell lines were cultured in the presence of 50 nM [3H]retinoic acid, and the metabolism of retinoic acid was followed over the next 24 h. The results demonstrate that CRABP-I has the ability to alter both the levels and types of RA metabolites produced in the cytoplasm of differentiating embryonic stem cells. Tretinoin 112-125 cellular retinoic acid binding protein 1 Homo sapiens 188-195
12760771-4 2003 RESULTS: After treated by ATRA (10(-7) mol/L - 10(-5) mol/L), the expression of Cx43 protein was up-regulated in Tca8113 cells and the positive rate of Cx43 protein increased from 5.17% (before treatment) to 30.53% (10(-5) mol/L ATRA). Tretinoin 229-233 gap junction protein alpha 1 Homo sapiens 80-84
1328234-5 1992 Moreover, the level of CRABP-I determines the rate of RA metabolism to 4-oxo-RA such that the higher the CRABP-I level, the faster the metabolism of [3H]retinoic acid. Tretinoin 149-166 cellular retinoic acid binding protein 1 Homo sapiens 23-30
1328234-5 1992 Moreover, the level of CRABP-I determines the rate of RA metabolism to 4-oxo-RA such that the higher the CRABP-I level, the faster the metabolism of [3H]retinoic acid. Tretinoin 149-166 cellular retinoic acid binding protein 1 Homo sapiens 105-112
8067288-14 1994 Recent data suggest a role for the RAR-beta in mediating the effect of retinoic acid on PKC induction. Tretinoin 71-84 retinoic acid receptor, beta Mus musculus 35-43
12760771-4 2003 RESULTS: After treated by ATRA (10(-7) mol/L - 10(-5) mol/L), the expression of Cx43 protein was up-regulated in Tca8113 cells and the positive rate of Cx43 protein increased from 5.17% (before treatment) to 30.53% (10(-5) mol/L ATRA). Tretinoin 229-233 gap junction protein alpha 1 Homo sapiens 152-156
8067288-17 1994 When B16 cells were transfected with and overexpressed RAR-beta, they also expressed more PKC-alpha mRNA and protein, and the induction of PKC by retinoic acid was not blocked by protein synthesis inhibitors. Tretinoin 146-159 retinoic acid receptor, beta Mus musculus 55-63
8032159-2 1994 However, mammalian ADH has also been shown to function in vitro as a retinol dehydrogenase in the conversion of retinol (vitamin A alcohol) to retinoic acid, a hormone which regulates gene expression at the transcriptional level. Tretinoin 143-156 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 69-90
1327537-0 1992 All-trans and 9-cis retinoic acid induction of CRABPII transcription is mediated by RAR-RXR heterodimers bound to DR1 and DR2 repeated motifs. Tretinoin 20-33 down-regulator of transcription 1 Homo sapiens 114-117
12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 233-246 SMAD family member 1 Homo sapiens 116-121
12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 233-246 SMAD family member 4 Homo sapiens 126-131
12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 248-250 SMAD family member 1 Homo sapiens 116-121
1356818-0 1992 Regulation of transglutaminase 1 gene expression by 12-O-tetradecanoylphorbol-13-acetate, dexamethasone, and retinoic acid in cultured human keratinocytes. Tretinoin 109-122 transglutaminase 1 Homo sapiens 14-32
12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 248-250 SMAD family member 4 Homo sapiens 126-131
1356818-9 1992 Moreover, 1 microM of retinoic acid completely inhibited the induction of TG1 mRNA by both TPA and dexamethasone. Tretinoin 22-35 transglutaminase 1 Homo sapiens 74-77
7514938-6 1994 The determination of the keratin pattern expressed by cells grown on gel revealed an expression of keratin 13, already considered as a specific marker of squamous metaplasia, that diminished with retinoic acid treatment. Tretinoin 196-209 keratin, type I cytoskeletal 13 Oryctolagus cuniculus 99-109
7815831-0 1994 In vitro all-trans retinoic acid (ATRA) sensitivity and cellular retinoic acid binding protein (CRABP) levels in relapse leukemic cells after remission induction by ATRA in acute promyelocytic leukemia. Tretinoin 165-169 cellular retinoic acid binding protein 1 Homo sapiens 56-94
12454286-0 2002 Retinaldehyde dehydrogenase 2 (RALDH2)- independent patterns of retinoic acid synthesis in the mouse embryo. Tretinoin 64-77 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 0-29
7815831-0 1994 In vitro all-trans retinoic acid (ATRA) sensitivity and cellular retinoic acid binding protein (CRABP) levels in relapse leukemic cells after remission induction by ATRA in acute promyelocytic leukemia. Tretinoin 165-169 cellular retinoic acid binding protein 1 Homo sapiens 96-101
7815831-6 1994 We have demonstrated that AML3 patients" cells (from four patients) at relapse show high levels of CRABP, a cytosolic retinoic acid binding protein and this protein was not detected prior to ATRA therapy. Tretinoin 191-195 cellular retinoic acid binding protein 1 Homo sapiens 99-104
7815831-9 1994 This induced ATRA hypercatabolytic state should be monitored during consolidation therapy and at relapse by evaluating CRABP and RA metabolite levels, in order to detect ATRA resistance in patients with AML3. Tretinoin 13-17 cellular retinoic acid binding protein 1 Homo sapiens 119-124
1464411-0 1992 Comparative effects of thyroxine and/or retinoic acid treatment in vivo on growth hormone synthesis and release by pituitaries from thyroidectomized rats. Tretinoin 40-53 gonadotropin releasing hormone receptor Rattus norvegicus 75-89
1464411-1 1992 Thyroid hormones and retinoic acid (RA) coregulate growth hormone (GH) synthesis and release from cultured pituitary tumor cells by interacting with nuclear receptors that activate GH gene transcription. Tretinoin 21-34 gonadotropin releasing hormone receptor Rattus norvegicus 51-65
7715611-0 1994 A retinoic acid-inducible skin-specific gene (RIS-1/psoriasin): molecular cloning and analysis of gene expression in human skin in vivo and cultured skin cells in vitro. Tretinoin 2-15 transmembrane protein 158 Homo sapiens 46-51
1464411-1 1992 Thyroid hormones and retinoic acid (RA) coregulate growth hormone (GH) synthesis and release from cultured pituitary tumor cells by interacting with nuclear receptors that activate GH gene transcription. Tretinoin 21-34 gonadotropin releasing hormone receptor Rattus norvegicus 67-69
7715611-1 1994 A retinoic acid (RA) inducible skin-specific gene transcript (RIS-1) was isolated by differential hybridization screening of a RA-treated human skin cDNA library. Tretinoin 2-15 transmembrane protein 158 Homo sapiens 62-67
1464411-1 1992 Thyroid hormones and retinoic acid (RA) coregulate growth hormone (GH) synthesis and release from cultured pituitary tumor cells by interacting with nuclear receptors that activate GH gene transcription. Tretinoin 21-34 gonadotropin releasing hormone receptor Rattus norvegicus 181-183
7715611-1 1994 A retinoic acid (RA) inducible skin-specific gene transcript (RIS-1) was isolated by differential hybridization screening of a RA-treated human skin cDNA library. Tretinoin 17-19 transmembrane protein 158 Homo sapiens 62-67
1464411-1 1992 Thyroid hormones and retinoic acid (RA) coregulate growth hormone (GH) synthesis and release from cultured pituitary tumor cells by interacting with nuclear receptors that activate GH gene transcription. Tretinoin 36-38 gonadotropin releasing hormone receptor Rattus norvegicus 51-65
7715611-1 1994 A retinoic acid (RA) inducible skin-specific gene transcript (RIS-1) was isolated by differential hybridization screening of a RA-treated human skin cDNA library. Tretinoin 127-129 transmembrane protein 158 Homo sapiens 62-67
12454286-0 2002 Retinaldehyde dehydrogenase 2 (RALDH2)- independent patterns of retinoic acid synthesis in the mouse embryo. Tretinoin 64-77 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 31-37
7715611-3 1994 RIS-1 cDNA corresponded to a 0.6 kb transcript that was barely detectable in normal adult human skin but was significantly induced by 8 h in RA-treated compared to vehicle-treated skin (range 1.1-3.6 fold). Tretinoin 141-143 transmembrane protein 158 Homo sapiens 0-5
1464411-1 1992 Thyroid hormones and retinoic acid (RA) coregulate growth hormone (GH) synthesis and release from cultured pituitary tumor cells by interacting with nuclear receptors that activate GH gene transcription. Tretinoin 36-38 gonadotropin releasing hormone receptor Rattus norvegicus 67-69
7715611-5 1994 HPLC analysis of the RA content of 0.1% RA-treated skin in vivo revealed significant levels at 6 h (18.8-120.6 ng RA/g wet weight tissue; approximately 240 nM), immediately preceding the time point at which the increased RIS-1 mRNA level was first seen. Tretinoin 40-42 transmembrane protein 158 Homo sapiens 221-226
1328400-9 1992 Dermal fibroblasts, in contrast, exhibited a dose-dependent increased expression of Cx43 at concentrations up to 10(-7) M retinoic acid and proportionately increased their junctional communication over this dose range. Tretinoin 122-135 gap junction protein alpha 1 Homo sapiens 84-88
8264603-4 1994 DBD- was transfected into P19 murine embryonal carcinoma (EC) cells, in which reporters containing the RA-responsive elements (RAREs) were activated by RA through the activity of endogenous RXR-RA receptor (RAR) heterodimers. Tretinoin 103-105 retinoic acid receptor, beta Mus musculus 127-130
12454286-1 2002 Knockout of the murine retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) gene leads to early morphogenetic defects and embryonic lethality. Tretinoin 23-36 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 62-91
8264603-10 1994 By genomic footprinting, we show that RA treatment induces in vivo occupancy of the RARE in the endogenous RAR beta gene in control P19 cells but that this occupancy is not observed with the DBD- cells. Tretinoin 38-40 retinoic acid receptor, beta Mus musculus 107-115
12454286-1 2002 Knockout of the murine retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) gene leads to early morphogenetic defects and embryonic lethality. Tretinoin 23-36 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 93-99
1355099-0 1992 Short-term retinoic acid treatment increases in vivo, but decreases in vitro, epidermal transglutaminase-K enzyme activity and immunoreactivity. Tretinoin 11-24 transglutaminase 1 Homo sapiens 88-106
12454286-1 2002 Knockout of the murine retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) gene leads to early morphogenetic defects and embryonic lethality. Tretinoin 38-40 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 62-91
1355099-3 1992 We have investigated whether the hyperproliferative state induced by short-term application of topical retinoic acid is similarly characterized by an increase in transglutaminase-K enzyme activity and immunoreactivity. Tretinoin 103-116 transglutaminase 1 Homo sapiens 162-180
1355099-4 1992 Retinoic acid (0.1% cream) or vehicle were applied to human skin and occluded for 4 d. Skin biopsies were obtained for measurement of transglutaminase-K and transglutaminase-C activity and immunoreactivity. Tretinoin 0-13 transglutaminase 1 Homo sapiens 134-152
12454286-1 2002 Knockout of the murine retinoic acid (RA)-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2) gene leads to early morphogenetic defects and embryonic lethality. Tretinoin 38-40 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 93-99
1355099-6 1992 Transglutaminase-K activity was increased 2.8 times in retinoic acid compared to vehicle-treated skin (p less than 0.005, n = 12) whereas there was no significant difference in transglutaminase-C activity. Tretinoin 55-68 transglutaminase 1 Homo sapiens 0-18
1355099-8 1992 In vehicle-treated skin, transglutaminase-K immunoreactivity was limited to a narrow, substratum corneal band, but was considerably expanded in a diffuse suprabasal pattern in retinoic acid-treated epidermis. Tretinoin 176-189 transglutaminase 1 Homo sapiens 25-43
8167409-5 1993 We have also identified native Wnt proteins in retinoic acid-treated P19 embryonal carcinoma cells, and they exhibit the same biochemical characteristics as the recombinant proteins. Tretinoin 47-60 wingless-type MMTV integration site family, member 1 Mus musculus 31-34
12454286-3 2002 To this end, the early defects of Raldh2(-/-) embryos were rescued through maternal dietary RA supplementation under conditions that do not interfere with the activity of the reporter transgene in WT embryos. Tretinoin 92-94 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 34-40
1355099-9 1992 In contrast, transglutaminase-K immunostaining was decreased and its enzymatic activity reduced sixfold in retinoic acid-treated keratinocytes (p less than 0.01, n = 4). Tretinoin 107-120 transglutaminase 1 Homo sapiens 13-31
1355099-10 1992 These results demonstrate that retinoic acid treatment in vivo, in contrast to in vitro, leads to not only increased transglutaminase-K protein expression but also increased enzymatic activity in the absence of detectable increases in mRNA levels. Tretinoin 31-44 transglutaminase 1 Homo sapiens 117-135
12454286-8 2002 These data suggest the existence of additional RA-generating activities in the differentiating forebrain, hindbrain, and spinal cord, which, along with RALDH1 and RALDH3, may account for the development of Raldh2(-/-) mutants once these have been rescued for early lethality. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 152-158
12454286-8 2002 These data suggest the existence of additional RA-generating activities in the differentiating forebrain, hindbrain, and spinal cord, which, along with RALDH1 and RALDH3, may account for the development of Raldh2(-/-) mutants once these have been rescued for early lethality. Tretinoin 47-49 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 206-212
8404668-4 1993 We report here that retinoic acid (RA) reduces the level of Myf5 message in both mouse C2 and rat L6 cell lines, probably at the transcriptional level, because Myf5 mRNA stability is not affected by RA. Tretinoin 20-33 myogenic factor 5 Rattus norvegicus 160-164
12492429-10 2002 These data suggest that SK-N-SH cells differentiated by brief treatment with RA may represent an unlimited source of neuron-like cells suitable for studying molecular events associated with activation of human NR1/NR2B receptors. Tretinoin 77-79 glutamate ionotropic receptor NMDA type subunit 2B Homo sapiens 214-218
8404668-4 1993 We report here that retinoic acid (RA) reduces the level of Myf5 message in both mouse C2 and rat L6 cell lines, probably at the transcriptional level, because Myf5 mRNA stability is not affected by RA. Tretinoin 35-37 myogenic factor 5 Rattus norvegicus 160-164
8404668-7 1993 As 9-cis RA is about 10 times more efficient than all-trans RA in repressing Myf5, whereas TTNPB, which preferentially activates RA receptors, is far less potent, our data provide evidence for an important role of ligand-bound retinoid X-receptors in the mediation of this inhibition. Tretinoin 9-11 myogenic factor 5 Rattus norvegicus 77-81
8404668-7 1993 As 9-cis RA is about 10 times more efficient than all-trans RA in repressing Myf5, whereas TTNPB, which preferentially activates RA receptors, is far less potent, our data provide evidence for an important role of ligand-bound retinoid X-receptors in the mediation of this inhibition. Tretinoin 60-62 myogenic factor 5 Rattus norvegicus 77-81
1360810-0 1992 Identification of a retinoic acid responsive enhancer 3" of the murine homeobox gene Hox-1.6. Tretinoin 20-33 homeobox A1 Mus musculus 85-92
1360810-2 1992 Using the teratocarcinoma cell line F9 as a model system, we have studied the RA-response of the murine homeobox gene Hox-1.6. Tretinoin 78-80 homeobox A1 Mus musculus 118-125
1360810-3 1992 RA treatment of F9 cells causes the appearance of a DNAse I hypersensitive site 3" of Hox-1.6, approximately 5 kb downstream of the Hox-1.6 promoter, and this site has been shown to reflect the presence of an RA-responsive enhancer 3" of the gene. Tretinoin 0-2 homeobox A1 Mus musculus 86-93
1360810-3 1992 RA treatment of F9 cells causes the appearance of a DNAse I hypersensitive site 3" of Hox-1.6, approximately 5 kb downstream of the Hox-1.6 promoter, and this site has been shown to reflect the presence of an RA-responsive enhancer 3" of the gene. Tretinoin 0-2 homeobox A1 Mus musculus 132-139
1360810-4 1992 The RA-responsiveness of the enhancer is controlled by a retinoic acid responsive element (RARE) identical to the RARE of the retinoic acid receptor (RAR) beta gene; however, other sequences also influence the activity of the enhancer, suggesting the presence of binding sites for novel proteins which regulate Hox-1.6 expression. Tretinoin 4-6 homeobox A1 Mus musculus 311-318
1360810-4 1992 The RA-responsiveness of the enhancer is controlled by a retinoic acid responsive element (RARE) identical to the RARE of the retinoic acid receptor (RAR) beta gene; however, other sequences also influence the activity of the enhancer, suggesting the presence of binding sites for novel proteins which regulate Hox-1.6 expression. Tretinoin 57-70 homeobox A1 Mus musculus 311-318
1360810-6 1992 Our results support the idea that RA is an endogenous vertebrate morphogen; identification of the RA-responsive enhancer downstream of Hox-1.6 demonstrates that RA directly controls the transcription of at least one member of a gene family that determines tissue identity in the vertebrate embryo. Tretinoin 98-100 homeobox A1 Mus musculus 135-142
1319834-4 1992 Addition of retinoic acid resulted in a greater than 70% inhibition of estradiol-induced TGF-alpha synthesis and secretion in MCF-7 cells. Tretinoin 12-25 transforming growth factor alpha Homo sapiens 89-98
1319834-5 1992 The increase in TGF-alpha mRNA expression by estradiol was also inhibited by exposure of the cells to retinoic acid. Tretinoin 102-115 transforming growth factor alpha Homo sapiens 16-25
1319834-6 1992 Pretreatment of the cells with retinoic acid for 24 or 72 h caused more than 50 and 90% inhibition, respectively, of the estradiol-enhanced expression of TGF-alpha mRNA. Tretinoin 31-44 transforming growth factor alpha Homo sapiens 154-163
1319834-12 1992 These results indicate that retinoic acid can inhibit estradiol-induced TGF-alpha and pS2 mRNA expression in MCF-7 cells. Tretinoin 28-41 transforming growth factor alpha Homo sapiens 72-81
8246923-8 1993 In the presence of GH, the induction of P4502C7 mRNA appeared additive to the effect of retinol at all concentrations used and to all-trans retinoic acid at concentrations up to 1 microM. Tretinoin 140-153 gonadotropin releasing hormone receptor Rattus norvegicus 19-21
8246923-13 1993 We conclude that both GH and retinoids can induce P4502C7 mRNA in rat liver hepatocytes, retinoic acid being the dominant inducer. Tretinoin 89-102 gonadotropin releasing hormone receptor Rattus norvegicus 22-24
7691597-4 1993 By contrast, retinoic acid treatment leads to neuronal differentiation of P19 cells, ectopically expressing functional RPTP alpha, as illustrated by their ability to generate action potentials. Tretinoin 13-26 protein tyrosine phosphatase receptor type A Homo sapiens 119-129
12486767-2 2002 Furthermore, retinoic acid (RA) induces RARbeta expression, a molecular event associated with neural tube closure, but treatment with RA at the appropriate gestation time causes failure of neural tube closure. Tretinoin 13-26 retinoic acid receptor, beta Mus musculus 40-47
8228520-14 1993 Osteopontin mRNA was increased by the treatment with 1 alpha,25(OH)2D3 or retinoic acid. Tretinoin 74-87 secreted phosphoprotein 1 Mus musculus 0-11
1633816-3 1992 The synthesis of Opn by bone cells is regulated by glucocorticoids and growth factors, which promote bone formation, and by the osteotropic hormone calcitriol (1,25-dihydroxycholecalciferol) and retinoic acid, which mediate bone resorption, indicating a bifunctional role for this protein in bone remodelling. Tretinoin 195-208 secreted phosphoprotein 1 Mus musculus 17-20
12486767-2 2002 Furthermore, retinoic acid (RA) induces RARbeta expression, a molecular event associated with neural tube closure, but treatment with RA at the appropriate gestation time causes failure of neural tube closure. Tretinoin 28-30 retinoic acid receptor, beta Mus musculus 40-47
1334737-1 1992 Many of the biological effects of retinoic acid are mediated by its nuclear receptors (RAR-alpha, RAR-beta, and RAR-gamma), and each of these three receptors exist in multiple isoforms. Tretinoin 34-47 retinoic acid receptor, beta Mus musculus 98-106
12421932-5 2002 The presence of atRA led to elevated levels of cyclin D3, -E, and -A, decreased levels of p27(Kip1), increased activity of cyclin-dependent kinase 2, and enhanced phosphorylation of the retinoblastoma protein (pRB). Tretinoin 16-20 cyclin dependent kinase 2 Homo sapiens 123-148
12421932-5 2002 The presence of atRA led to elevated levels of cyclin D3, -E, and -A, decreased levels of p27(Kip1), increased activity of cyclin-dependent kinase 2, and enhanced phosphorylation of the retinoblastoma protein (pRB). Tretinoin 16-20 RB transcriptional corepressor 1 Homo sapiens 210-213
1358593-7 1992 4 hours after retinoic acid administration on day 8 + 5 hours, Hox-1.8, Hox-1.9, and Hox-4.5 transcripts were not detected in their usual posterior expression domains, whereas transcripts of the anterior Hox-1.5 gene remained unaffected. Tretinoin 14-27 homeobox A10 Homo sapiens 63-70
8408867-1 1993 Effects of trans and cis isomers of retinol and retinoic acid on IgM secretion by bovine peripheral blood mononuclear leukocytes were evaluated in vitro. Tretinoin 48-61 IgM Bos taurus 65-68
8408867-9 1993 These results indicate that retinol and retinoic acid modulate polyclonal IgM secretion by cultures of bovine mononuclear leukocytes stimulated by mitogen. Tretinoin 40-53 IgM Bos taurus 74-77
12421932-9 2002 rIL-2 was able to substitute for the effects of atRA on the cell cycle machinery and on DNA synthesis, and blocking the IL-2R markedly inhibited atRA-induced cell proliferation and pRB phosphorylation. Tretinoin 145-149 interleukin 2 receptor subunit alpha Homo sapiens 120-125
7684042-12 1993 The addition of RA also blocked IGF-I stimulation of IGFBP-2 and IGFBP-5 levels. Tretinoin 16-18 insulin like growth factor binding protein 2 Homo sapiens 53-60
1379951-0 1992 The effects of retinoic acid on the expression of alpha-fetoprotein and albumin genes in rat hepatoma cell lines. Tretinoin 15-28 alpha-fetoprotein Rattus norvegicus 50-67
12421932-9 2002 rIL-2 was able to substitute for the effects of atRA on the cell cycle machinery and on DNA synthesis, and blocking the IL-2R markedly inhibited atRA-induced cell proliferation and pRB phosphorylation. Tretinoin 145-149 RB transcriptional corepressor 1 Homo sapiens 181-184
12421932-11 2002 Furthermore, a RAR-selective antagonist completely suppressed T cell proliferation and pRB phosphorylation induced by atRA. Tretinoin 118-122 RB transcriptional corepressor 1 Homo sapiens 87-90
1379951-3 1992 In the present study, we demonstrated that retinoic acid, whose receptors belong to the steroid/thyroid hormone receptor gene family, also enhanced the expression of alpha-fetoprotein and albumin gene in McA-RH 8994 cells, but had no effect on alpha-fetoprotein gene expression in McA-RH 7777 cells. Tretinoin 43-56 alpha-fetoprotein Rattus norvegicus 166-183
1379951-3 1992 In the present study, we demonstrated that retinoic acid, whose receptors belong to the steroid/thyroid hormone receptor gene family, also enhanced the expression of alpha-fetoprotein and albumin gene in McA-RH 8994 cells, but had no effect on alpha-fetoprotein gene expression in McA-RH 7777 cells. Tretinoin 43-56 alpha-fetoprotein Rattus norvegicus 244-261
1379951-5 1992 Actinomycin D inhibited the retinoic acid mediated increase in alpha-fetoprotein and albumin mRNA expression. Tretinoin 28-41 alpha-fetoprotein Rattus norvegicus 63-80
7682243-0 1993 Functional antagonism between vitamin D3 and retinoic acid in the regulation of CD14 and CD23 expression during monocytic differentiation of U-937 cells. Tretinoin 45-58 CD14 molecule Homo sapiens 80-84
7682243-0 1993 Functional antagonism between vitamin D3 and retinoic acid in the regulation of CD14 and CD23 expression during monocytic differentiation of U-937 cells. Tretinoin 45-58 Fc epsilon receptor II Homo sapiens 89-93
7682243-7 1993 In contrast, U-937 cells induced by RA strongly increased their expression of CD23 mRNA and protein, whereas they completely lacked detectable CD14 cell surface or mRNA expression. Tretinoin 36-38 Fc epsilon receptor II Homo sapiens 78-82
1425331-1 1992 An aldehyde dehydrogenase present at high levels in the dorsal retina of the embryonic and adult mouse was identified as the isoform AHD-2 known to oxidize retinaldehyde to retinoic acid. Tretinoin 173-186 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 133-138
12553043-3 2002 ATRA significantly and dose-dependently inhibited matrigel membrane invasion of the cells by 53%, inhibited MMP-2 activity by 71%, MMP-9(80%), alpha-(59%) and beta-(65%) catenin expression at 10 microM (p < 0.01). Tretinoin 0-4 matrix metallopeptidase 2 Rattus norvegicus 108-113
1378916-2 1992 In an effort to increase the therapeutic efficacy of RA, we have measured the capacity of granulocyte colony-stimulating factor (G-CSF) to enhance the differentiation inducing activity of RA in WEHI-3B D+ monomyelocytic leukemia cells. Tretinoin 53-55 colony stimulating factor 3 (granulocyte) Mus musculus 90-127
1378916-2 1992 In an effort to increase the therapeutic efficacy of RA, we have measured the capacity of granulocyte colony-stimulating factor (G-CSF) to enhance the differentiation inducing activity of RA in WEHI-3B D+ monomyelocytic leukemia cells. Tretinoin 53-55 colony stimulating factor 3 (granulocyte) Mus musculus 129-134
8453763-1 1993 Pleiotrophin (PTN) is a newly identified heparin-binding growth factor which is closely related to the retinoic acid-inducible MK protein. Tretinoin 103-116 pleiotrophin Rattus norvegicus 0-12
8453763-1 1993 Pleiotrophin (PTN) is a newly identified heparin-binding growth factor which is closely related to the retinoic acid-inducible MK protein. Tretinoin 103-116 pleiotrophin Rattus norvegicus 14-17
1378916-2 1992 In an effort to increase the therapeutic efficacy of RA, we have measured the capacity of granulocyte colony-stimulating factor (G-CSF) to enhance the differentiation inducing activity of RA in WEHI-3B D+ monomyelocytic leukemia cells. Tretinoin 188-190 colony stimulating factor 3 (granulocyte) Mus musculus 90-127
12417027-1 2002 Fenretinide, N-(4-hydroxyphenyl)retinamide (4-HPR), is a synthetic amide of all-trans-retinoic acid (RA), which inhibits cell growth, induces apoptosis, and is an antioxidant, and cancer chemopreventive and antiproliferative agent. Tretinoin 76-99 haptoglobin-related protein Homo sapiens 46-49
1630583-6 1992 However, further studies carried out in freely-moving rats showed the typical GH secretory pattern usually found in male rats of the control group, while retinoic acid-deficient rats displayed a highly variable GH secretory pattern with GH peaks of much lower amplitude. Tretinoin 154-167 gonadotropin releasing hormone receptor Rattus norvegicus 211-213
8449605-7 1993 The expression of myc-specific mRNA and protein in aberrant crypt foci significantly decreased with both levels of all-trans retinoic acid. Tretinoin 125-138 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 18-21
8449605-9 1993 The most important findings of this investigation are that intervention with all-trans retinoic acid in the pre-malignant stage of colon carcinogenesis is effective in decreasing the number and growth of aberrant crypt foci and altering the expression of the c-myc and c-fos genes. Tretinoin 87-100 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 259-264
8445950-0 1993 All-trans retinoic acid induces monocyte growth factor receptor (c-fms) gene expression in HL-60 leukemia cells. Tretinoin 10-23 colony stimulating factor 1 receptor Homo sapiens 65-70
8445950-3 1993 However, our results demonstrate that ATRA (0.1-10 microM) induces expression of the c-fms (monocyte colony-stimulating factor receptor) gene in HL-60 cells. Tretinoin 38-42 colony stimulating factor 1 receptor Homo sapiens 85-90
8445950-6 1993 The results also demonstrate that ATRA-induced c-fms expression is potentiated by exposure to tumor necrosis factor alpha (TNF alpha) or dibutyryl cyclic adenosine monophosphate (cAMP). Tretinoin 34-38 colony stimulating factor 1 receptor Homo sapiens 47-52
8445950-7 1993 The induction of c-fms transcripts by ATRA is associated with induction of M-CSF-binding ability, suggesting cell surface expression of the monocyte growth factor receptor. Tretinoin 38-42 colony stimulating factor 1 receptor Homo sapiens 17-22
1630583-6 1992 However, further studies carried out in freely-moving rats showed the typical GH secretory pattern usually found in male rats of the control group, while retinoic acid-deficient rats displayed a highly variable GH secretory pattern with GH peaks of much lower amplitude. Tretinoin 154-167 gonadotropin releasing hormone receptor Rattus norvegicus 211-213
12417027-1 2002 Fenretinide, N-(4-hydroxyphenyl)retinamide (4-HPR), is a synthetic amide of all-trans-retinoic acid (RA), which inhibits cell growth, induces apoptosis, and is an antioxidant, and cancer chemopreventive and antiproliferative agent. Tretinoin 101-103 haptoglobin-related protein Homo sapiens 46-49
12372612-2 2002 A significant increase in the activity of immunoprecipitated PI3K-C2beta was observed in the nuclei and nuclear envelopes isolated from all-trans-retinoic acid (ATRA)-differentiated cells which was inhibited by the presence of PI3K inhibitor LY 294002. Tretinoin 136-159 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta Homo sapiens 61-72
1535214-5 1992 All-trans retinoic acid and 13-cis retinoic acid had a greater ability to induce IL-1 production than the two aromatic retinoids, etretinate and acitretin. Tretinoin 0-23 interleukin 1 complex Mus musculus 81-85
1384809-6 1992 Retinoic acid increases the steady state level of transcripts from Hox genes with the greatest effect on Hox 2.7, the most anterior of the genes studied. Tretinoin 0-13 homeobox B3 S homeolog Xenopus laevis 105-112
8381481-0 1993 Biosynthesis and metabolism of retinoic acid: roles of CRBP and CRABP in retinoic acid: roles of CRBP and CRABP in retinoic acid homeostasis. Tretinoin 31-44 retinol binding protein 1 Homo sapiens 55-59
8381481-0 1993 Biosynthesis and metabolism of retinoic acid: roles of CRBP and CRABP in retinoic acid: roles of CRBP and CRABP in retinoic acid homeostasis. Tretinoin 31-44 cellular retinoic acid binding protein 1 Homo sapiens 64-69
8381481-0 1993 Biosynthesis and metabolism of retinoic acid: roles of CRBP and CRABP in retinoic acid: roles of CRBP and CRABP in retinoic acid homeostasis. Tretinoin 31-44 cellular retinoic acid binding protein 1 Homo sapiens 106-111
8381481-5 1993 A cytosolic retinal dehydrogenase has been purified that produces retinoic acid from retinal generated by microsomes in the presence of CRBP and from the complex CRBP-retinal itself. Tretinoin 66-79 retinol binding protein 1 Homo sapiens 136-140
8381481-5 1993 A cytosolic retinal dehydrogenase has been purified that produces retinoic acid from retinal generated by microsomes in the presence of CRBP and from the complex CRBP-retinal itself. Tretinoin 66-79 retinol binding protein 1 Homo sapiens 162-166
8381481-6 1993 Thus, CRBP(type I) seems to channel retinoids through the reactions of retinoic acid synthesis via a series of protein-protein interactions. Tretinoin 71-84 retinol binding protein 1 Homo sapiens 6-10
8381482-4 1993 Teratogenic doses of RA increase the level of RAR-beta 2 mRNA, RAR-alpha 2 mRNA, CRBP-I mRNA and CRABP-II mRNA in mouse conceptuses and embryos. Tretinoin 21-23 cellular retinoic acid binding protein II Mus musculus 97-105
1568462-0 1992 Schedule-dependent sphinganine potentiation of retinoic acid-induced differentiation, cell growth inhibition, and nucleophosmin translocation in a human leukemia cell line (HL-60). Tretinoin 47-60 nucleophosmin 1 Homo sapiens 114-127
1568462-1 1992 Induction of differentiation, inhibition of cell growth, and localization of nucleophosmin in HL-60 cells under the treatment of retinoic acid (RA) were studied. Tretinoin 129-142 nucleophosmin 1 Homo sapiens 77-90
1568462-1 1992 Induction of differentiation, inhibition of cell growth, and localization of nucleophosmin in HL-60 cells under the treatment of retinoic acid (RA) were studied. Tretinoin 144-146 nucleophosmin 1 Homo sapiens 77-90
1568462-3 1992 The addition of RA in the culture system resulted in time- and dose-dependent induction of differentiation, cell growth inhibition, and nucleophosmin translocation from nucleoli to nucleoplasm. Tretinoin 16-18 nucleophosmin 1 Homo sapiens 136-149
1568462-7 1992 Differentiation, translocation of nucleophosmin, and inhibition of cell growth occurred with lesser doses of RA or in shorter incubation times in the presence of sphinganine. Tretinoin 109-111 nucleophosmin 1 Homo sapiens 34-47
1568462-11 1992 Nucleophosmin translocation as observed by immunofluorescence may be a simple and rapid method for assessing inhibition of cellular growth in response to differentiation inducers such as RA in cancer chemotherapy. Tretinoin 187-189 nucleophosmin 1 Homo sapiens 0-13
8385738-2 1993 Retinoic acid (10(-6) M) reduces the incidence of myoblast and adipocyte formation and induces or increases alkaline phosphatase expression and responsiveness to PTH, two indicators of the osteoblastic phenotype. Tretinoin 0-13 parathyroid hormone Mus musculus 162-165
8385738-3 1993 Because transforming growth factor-beta (TGF beta) superfamily members, including the different TGF beta isoforms and the bone morphogenetic proteins (BMPs), are thought to play a role in regulating bone and cartilage formation, and because exogenous TGF beta and BMP-2 have already been found to modulate osteoblastic differentiation of C26 and 10T1/2 cells, we evaluated the endogenous expression of these factors in both cell lines cultured in the presence or absence of retinoic acid. Tretinoin 474-487 transforming growth factor, beta 1 Mus musculus 41-49
8385738-3 1993 Because transforming growth factor-beta (TGF beta) superfamily members, including the different TGF beta isoforms and the bone morphogenetic proteins (BMPs), are thought to play a role in regulating bone and cartilage formation, and because exogenous TGF beta and BMP-2 have already been found to modulate osteoblastic differentiation of C26 and 10T1/2 cells, we evaluated the endogenous expression of these factors in both cell lines cultured in the presence or absence of retinoic acid. Tretinoin 474-487 transforming growth factor, beta 1 Mus musculus 96-104
8385738-3 1993 Because transforming growth factor-beta (TGF beta) superfamily members, including the different TGF beta isoforms and the bone morphogenetic proteins (BMPs), are thought to play a role in regulating bone and cartilage formation, and because exogenous TGF beta and BMP-2 have already been found to modulate osteoblastic differentiation of C26 and 10T1/2 cells, we evaluated the endogenous expression of these factors in both cell lines cultured in the presence or absence of retinoic acid. Tretinoin 474-487 transforming growth factor, beta 1 Mus musculus 96-104
12372612-2 2002 A significant increase in the activity of immunoprecipitated PI3K-C2beta was observed in the nuclei and nuclear envelopes isolated from all-trans-retinoic acid (ATRA)-differentiated cells which was inhibited by the presence of PI3K inhibitor LY 294002. Tretinoin 161-165 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta Homo sapiens 61-72
12392597-5 2002 RESULTS: We have determined that RA inhibits cyclin H and cdk7 expression thereby decreasing levels of phosphorylated RARalpha in human cancer cell lines. Tretinoin 33-35 cyclin H Homo sapiens 45-53
8099268-7 1993 Retinoic acid skin treatment brings about RAR beta expression in the dermis, leading to the formation of glomerular glands. Tretinoin 0-13 retinoic acid receptor, beta Mus musculus 42-50
1373617-2 1992 The PTN gene is developmentally regulated and is closely related to the MK and RI-HB genes, both of which are developmentally regulated and induced by retinoic acid. Tretinoin 151-164 pleiotrophin Mus musculus 4-7
1550338-3 1992 We found that RA treatment of B16 cells resulted in an increase in PKC alpha mRNA beginning at 4-8 h and reached a maximum of 10- to 12-fold over control levels by 48 h. There was also a small amount of PKC gamma mRNA, present only in 48-h RA-treated cells, but no PKC beta mRNA was detected. Tretinoin 14-16 protein kinase C, beta Mus musculus 265-273
12242694-7 2002 Inhibition of RAR function in HMECs by DNRAR suppressed expression of CBP/p300 and expression of RARbeta2 in MCF-7 cells promoted induction of CBP/p300 when cells were treated with 1.0 microM all-trans-retinoic acid (ATRA). Tretinoin 192-215 E1A binding protein p300 Homo sapiens 74-78
7683225-1 1993 The retinoic acid-stimulated mouse-transformed epidermal cell line Pam 212 generated soluble mediators (RA-Pam sup) which showed mast cell-proliferating activity and induced mast cell-like colonies from bone marrow cells. Tretinoin 4-17 peptidylglycine alpha-amidating monooxygenase Mus musculus 67-70
12161154-1 2002 Retinoic acid analogues such as N-(4-hydroxyphenyl)retinamide (4-HPR) are effective chemopreventatives and chemotherapeutics for numerous types of cancer. Tretinoin 0-13 haptoglobin-related protein Homo sapiens 65-68
7683225-1 1993 The retinoic acid-stimulated mouse-transformed epidermal cell line Pam 212 generated soluble mediators (RA-Pam sup) which showed mast cell-proliferating activity and induced mast cell-like colonies from bone marrow cells. Tretinoin 4-17 peptidylglycine alpha-amidating monooxygenase Mus musculus 107-110
8456086-4 1993 RA had no effect on cell proliferation in JAR spheroids, but 10(-5) M RA treatment induced a fivefold increase in secretion of human chorionic gonadotrophin (hCG), a known marker of conversion of cytotrophoblast to syncytiotrophoblast-like cells. Tretinoin 70-72 chorionic gonadotropin subunit beta 5 Homo sapiens 133-162
1314168-0 1992 H-2RIIBP (RXR beta) heterodimerization provides a mechanism for combinatorial diversity in the regulation of retinoic acid and thyroid hormone responsive genes. Tretinoin 109-122 retinoid X receptor beta Homo sapiens 0-8
1314168-0 1992 H-2RIIBP (RXR beta) heterodimerization provides a mechanism for combinatorial diversity in the regulation of retinoic acid and thyroid hormone responsive genes. Tretinoin 109-122 retinoid X receptor beta Homo sapiens 10-18
1314168-1 1992 H-2RIIBP (RXR beta) is a member of the nuclear hormone receptor superfamily that activates transcription of MHC class I genes in response to retinoic acid (RA). Tretinoin 141-154 retinoid X receptor beta Homo sapiens 0-8
1314168-1 1992 H-2RIIBP (RXR beta) is a member of the nuclear hormone receptor superfamily that activates transcription of MHC class I genes in response to retinoic acid (RA). Tretinoin 141-154 retinoid X receptor beta Homo sapiens 10-18
1314168-1 1992 H-2RIIBP (RXR beta) is a member of the nuclear hormone receptor superfamily that activates transcription of MHC class I genes in response to retinoic acid (RA). Tretinoin 156-158 retinoid X receptor beta Homo sapiens 0-8
1314168-1 1992 H-2RIIBP (RXR beta) is a member of the nuclear hormone receptor superfamily that activates transcription of MHC class I genes in response to retinoic acid (RA). Tretinoin 156-158 retinoid X receptor beta Homo sapiens 10-18
12230954-12 2002 In addition, ATRA induced ICAM-1 protein expression in vivo and in vitro. Tretinoin 13-17 intercellular adhesion molecule 1 Mus musculus 26-32
1372572-0 1992 Induction of avascular yolk sac due to reduction of basic fibroblast growth factor by retinoic acid in mice. Tretinoin 86-99 fibroblast growth factor 2 Mus musculus 52-82
1372572-11 1992 Retinoic acid does not affect the angiogenic capacity of the VYS mesenchyme but destroys lysosomes, which release hydrolytic enzymes, leading to degradation of AAT in the endodermal cells and then digestion of endocytosed bFGF. Tretinoin 0-13 serine (or cysteine) preptidase inhibitor, clade A, member 1B Mus musculus 160-163
1372572-11 1992 Retinoic acid does not affect the angiogenic capacity of the VYS mesenchyme but destroys lysosomes, which release hydrolytic enzymes, leading to degradation of AAT in the endodermal cells and then digestion of endocytosed bFGF. Tretinoin 0-13 fibroblast growth factor 2 Mus musculus 222-226
1374482-1 1992 The effect of retinoic acid (RA) on the expression of myelin-specific genes, i.e., proteolipid protein (PLP) and myelin-associated glycoprotein (MAG) in rat glioma C6 cells, was analyzed by Northern blot hybridization. Tretinoin 14-27 proteolipid protein 1 Rattus norvegicus 104-107
1374482-1 1992 The effect of retinoic acid (RA) on the expression of myelin-specific genes, i.e., proteolipid protein (PLP) and myelin-associated glycoprotein (MAG) in rat glioma C6 cells, was analyzed by Northern blot hybridization. Tretinoin 29-31 proteolipid protein 1 Rattus norvegicus 104-107
1374482-2 1992 RA-treatment increased the steady-state level of the PLP-specific messages within one day after RA administration and the upregulation reached a maximum on the third day. Tretinoin 0-2 proteolipid protein 1 Rattus norvegicus 53-56
1374482-2 1992 RA-treatment increased the steady-state level of the PLP-specific messages within one day after RA administration and the upregulation reached a maximum on the third day. Tretinoin 96-98 proteolipid protein 1 Rattus norvegicus 53-56
1374482-4 1992 The expression of the PLP gene was directly related to the RA concentration increasing to approximately 44-fold over the control (untreated cells) level at 10(-6) M RA. Tretinoin 59-61 proteolipid protein 1 Rattus norvegicus 22-25
7687781-5 1993 In post-confluent cultures, retinoic acid prevented the appearance of keratin 1, which accompanied the development of a squamous phenotype by cells maintained under these conditions. Tretinoin 28-41 keratin 1 Homo sapiens 70-79
1467987-0 1992 Chronological expression of microtubule-associated proteins (MAPs) in EC cell P19 after neuronal induction by retinoic acid. Tretinoin 110-123 interleukin 23, alpha subunit p19 Mus musculus 78-81
1467987-1 1992 Pluripotent murine embryonal carcinoma (EC) P19 cells are induced at a high rate into neural cells using retinoic acid and serum-free medium. Tretinoin 105-118 interleukin 23, alpha subunit p19 Mus musculus 44-47
1360646-2 1992 We found that the mouse embryonal carcinoma cell line P19 expresses Hox-2.5 during differentiation by the treatment with retinoic acid (RA). Tretinoin 121-134 interleukin 23, alpha subunit p19 Mus musculus 54-57
1360646-2 1992 We found that the mouse embryonal carcinoma cell line P19 expresses Hox-2.5 during differentiation by the treatment with retinoic acid (RA). Tretinoin 121-134 homeobox B9 Mus musculus 68-75
1542003-5 1992 The ability of pure hCRBP(II) to bind all-trans-retinol, retinal and retinoic acid was examined by competitive binding assay and compared with the binding specificity of pure human cellular retinol-binding protein (hCRBP). Tretinoin 69-82 retinol binding protein 1 Homo sapiens 20-25
12213675-8 2002 RESULTS: We found that RA increased the expression of both trkA and p75 NGF receptors in NCI-N-592 and GLC8 cell lines and prevented the loss of both NGF production and NGF receptor expression occurring when NGF treatment was discontinued. Tretinoin 23-25 neurotrophic receptor tyrosine kinase 1 Homo sapiens 59-63
12063257-1 2002 The morphogen retinoic acid promotes the formation of primitive endoderm in mouse F9 teratocarcinoma cells as does the stimulation of the Frizzled-1 pathway. Tretinoin 14-27 frizzled class receptor 1 Mus musculus 138-148
1509209-1 1992 Induction of the murine laminin B1 gene in F9 cells occurs 24-48 hours after the retinoic acid (RA) addition. Tretinoin 81-94 laminin B1 Mus musculus 24-34
1509209-1 1992 Induction of the murine laminin B1 gene in F9 cells occurs 24-48 hours after the retinoic acid (RA) addition. Tretinoin 96-98 laminin B1 Mus musculus 24-34
1332041-5 1992 Electrophoretic mobility shift analyses demonstrated that protein extracts from RAR gamma-producing insect cells or larvae are capable of retinoic acid responsive element binding. Tretinoin 138-151 retinoic acid receptor gamma Homo sapiens 80-89
1363087-5 1992 The Hox-2.9 and Hox-2.8 genes were induced anteriorly in the neurectoderm in response to RA on day 7 but not at later stages. Tretinoin 89-91 homeobox B1 Mus musculus 4-11
1363087-6 1992 Expression of Hox-2.6 and Hox-2.1 was ectopically induced anteriorly in neurectoderm in response to RA on day 8. Tretinoin 100-102 homeobox B4 Mus musculus 14-21
1363087-12 1992 The ectopic anterior expression of Hox-2.8 and Hox-2.9 induced by RA on day 7 was persistent to day 8, as was the altered expression of Krox-20. Tretinoin 66-68 homeobox B1 Mus musculus 47-54
12063257-2 2002 We investigated whether the beta-catenin/Lef-Tcf-sensitive transcriptional pathway activated by Frizzled-1 plays a role in the retinoic acid-induced pathway to primitive endoderm formation. Tretinoin 127-140 frizzled class receptor 1 Mus musculus 96-106
1325442-0 1992 Retinoic acid regulates both expression of the nerve growth factor receptor and sensitivity to nerve growth factor. Tretinoin 0-13 nerve growth factor receptor Rattus norvegicus 47-75
12032153-3 2002 Knock-out of the retinoic X receptor alpha (RXRalpha) gene abolishes endodermal differentiation and the induction of several endogenous RA-responsive genes. Tretinoin 136-138 retinoid X receptor alpha Mus musculus 44-52
1325442-1 1992 In PC12 cells, retinoic acid (RA) stimulates the expression of p75NGFR, a component of the nerve growth factor (NGF) receptor, as indicated by a rapid increase in p75NGFR mRNA, an increase in the binding of 125I-labeled NGF to p75NGFR, and an increase in the binding of NGF to low affinity sites. Tretinoin 15-28 nerve growth factor receptor Rattus norvegicus 91-125
1325442-1 1992 In PC12 cells, retinoic acid (RA) stimulates the expression of p75NGFR, a component of the nerve growth factor (NGF) receptor, as indicated by a rapid increase in p75NGFR mRNA, an increase in the binding of 125I-labeled NGF to p75NGFR, and an increase in the binding of NGF to low affinity sites. Tretinoin 30-32 nerve growth factor receptor Rattus norvegicus 91-125
1322331-0 1992 Retinoic acid and dexamethasone interact to regulate S14 gene transcription in 3T3-F442A adipocytes. Tretinoin 0-13 thyroid hormone responsive Homo sapiens 53-56
1322331-1 1992 We have examined the effects of retinoic acid (RA) on S14 gene expression in 3T3-F442A preadipocytes and adipocytes. Tretinoin 32-45 thyroid hormone responsive Homo sapiens 54-57
12032153-4 2002 RXRalpha null cells are also drastically impaired in their antiproliferative response to RA. Tretinoin 89-91 retinoid X receptor alpha Mus musculus 0-8
12075005-3 2002 In the present study, we have determined the subcellular localization of SMN during retinoic-acid-induced neuronal differentiation of mouse embryonal teratocarcinoma P19 cells as well as in skeletal muscle during the critical period of neuromuscular maturation. Tretinoin 84-97 survival motor neuron 1 Mus musculus 73-76
1550961-2 1992 We observed that the level of endogenous BMP-2 mRNA increased an average of 11-fold on differentiation of F9 embryonal carcinoma cells into parietal endoderm after treatment with retinoic acid (RA) and cAMP, whereas the message for the closely related BMP-4 decreased 12-fold after this treatment. Tretinoin 194-196 bone morphogenetic protein 2 Homo sapiens 41-46
1550961-4 1992 BMP-2 addition altered the growth and morphology of RA-treated but not untreated cells. Tretinoin 52-54 bone morphogenetic protein 2 Homo sapiens 0-5
1550961-7 1992 The observations suggest that RA, which is known to affect bone morphogenesis, may regulate the osteoinductive proteins, BMP-2 and -4. Tretinoin 30-32 bone morphogenetic protein 2 Homo sapiens 121-133
1736309-0 1992 Retinoic acid-dependent transactivation of major histocompatibility complex class I promoters by the nuclear hormone receptor H-2RIIBP in undifferentiated embryonal carcinoma cells. Tretinoin 0-13 retinoid X receptor beta Homo sapiens 126-134
1339296-1 1992 Expression of the laminin B1 gene is known to be induced late during the differentiation of F9 cells by retinoic acid (RA) and dibutyryl cAMP. Tretinoin 104-117 laminin B1 Mus musculus 18-28
1339296-1 1992 Expression of the laminin B1 gene is known to be induced late during the differentiation of F9 cells by retinoic acid (RA) and dibutyryl cAMP. Tretinoin 119-121 laminin B1 Mus musculus 18-28
1321136-13 1992 Since ADH production in rat liver is known to be repressed by thyroid hormone, these findings suggest that human ADH production may also be subject to thyroid hormone repression and that the mechanism involves an interference with retinoic acid induction. Tretinoin 231-244 alcohol dehydrogenase 1C (class I), gamma polypeptide Rattus norvegicus 6-9
1736309-4 1992 Transfection of the expression plasmid led to production of H-2RIIBP transcripts and enhanced MHC class I promoter activity in cells that were treated with retinoic acid but not yet differentiated. Tretinoin 156-169 retinoid X receptor beta Homo sapiens 60-68
1736309-9 1992 As observed in other cell lines, N-Tera2 cells that had undergone differentiation failed to elicit transactivation, suggesting that H-2RIIBP acts in concert with a cofactor expressed in undifferentiated N-Tera2 cells that requires retinoic acid for its function. Tretinoin 231-244 retinoid X receptor beta Homo sapiens 132-140
1354431-4 1992 Neuroblastoma cell lines induced to differentiate in vitro by retinoic acid showed a decline of the activities of DNA polymerase alpha, DNA polymerase delta/epsilon, uracil-DNA glycosylase and thymidine kinase similar to that observed during in vivo differentiation. Tretinoin 62-75 DNA polymerase alpha 1, catalytic subunit Homo sapiens 114-134
12063559-12 2002 Western blot analysis revealed that ATRA induced an increase in RARbeta expression and a decrease in RARgamma expression, while 9cisRA down-regulated RXRalpha expression. Tretinoin 36-40 retinoic acid receptor gamma Homo sapiens 101-109
1354431-4 1992 Neuroblastoma cell lines induced to differentiate in vitro by retinoic acid showed a decline of the activities of DNA polymerase alpha, DNA polymerase delta/epsilon, uracil-DNA glycosylase and thymidine kinase similar to that observed during in vivo differentiation. Tretinoin 62-75 DNA polymerase delta 1, catalytic subunit Homo sapiens 136-156
12052862-4 2002 AP1 transrepression by retinoic acid was concomitant to glycogen synthase kinase 3 activation, negative regulation of junD hyperphosphorylation, and to decreased RNA polymerase II recruitment. Tretinoin 23-36 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122
12052874-1 2002 Early in vitro cell culture studies suggested that testicular orphan nuclear receptor 2 (TR2), a member of the nuclear receptor superfamily, may play important roles in the control of several pathways including retinoic acids, vitamin D, thyroid hormones, and ciliary neurotrophic factor. Tretinoin 211-225 nuclear receptor subfamily 2, group C, member 1 Mus musculus 51-87
1370462-9 1992 Retinoic acid treatment of endothelial cells results in down-regulation of GATA-2 expression as well as down-regulation of PPET-1 gene expression. Tretinoin 0-13 GATA binding protein 2 Homo sapiens 75-81
12052874-1 2002 Early in vitro cell culture studies suggested that testicular orphan nuclear receptor 2 (TR2), a member of the nuclear receptor superfamily, may play important roles in the control of several pathways including retinoic acids, vitamin D, thyroid hormones, and ciliary neurotrophic factor. Tretinoin 211-225 nuclear receptor subfamily 2, group C, member 1 Mus musculus 89-92
1525036-4 1992 To characterize further the mechanism of mesoderm induction, the effect of RA exposure on the transcriptional properties of the muscle actin gene has been investigated. Tretinoin 75-77 actin alpha 4 S homeolog Xenopus laevis 128-140
12052888-0 2002 JDP2, a repressor of AP-1, recruits a histone deacetylase 3 complex to inhibit the retinoic acid-induced differentiation of F9 cells. Tretinoin 83-96 histone deacetylase 3 Homo sapiens 38-59
1525036-5 1992 Interestingly, prior exposure of embryos to RA appears to inhibit accumulation, rather than initial activation, of the mesoderm-specific muscle actin transcript. Tretinoin 44-46 actin alpha 4 S homeolog Xenopus laevis 137-149
12052888-4 2002 Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. Tretinoin 239-241 histone deacetylase 3 Homo sapiens 68-73
1324421-6 1992 RXR alpha complexes with RAR alpha, RAR beta, and RAR gamma bound selectively to retinoic acid responsive elements from the human RAR beta 2 gene (hRAR beta 2), the gene of the rat cellular retinol binding protein I and the human apolipoprotein A1 gene. Tretinoin 81-94 retinoic acid receptor gamma Homo sapiens 50-59
1334741-7 1992 The cellular transport and biological activity of retinoids may be mediated by their specific cytoplasmic binding proteins cellular retinol binding protein (CRBP) and the cellular retinoic acid binding protein (CRABP) which may function as shuttles targetting RA to nucleosol fraction and/or as regulator of cellular concentration of RA. Tretinoin 212-214 cellular retinoic acid binding protein 1 Homo sapiens 171-209
12049641-6 2002 The expression of SLC7A4 can be induced in NT2 teratocarcinoma cells by treatment with retinoic acid. Tretinoin 87-100 solute carrier family 7 member 4 Homo sapiens 18-24
1346761-2 1992 HOX3D is developmentally regulated during embryogenesis and is activated by retinoic acid (RA) in cultured embryonal carcinoma (EC) cells. Tretinoin 76-89 homeobox C5 Homo sapiens 0-5
1346761-2 1992 HOX3D is developmentally regulated during embryogenesis and is activated by retinoic acid (RA) in cultured embryonal carcinoma (EC) cells. Tretinoin 91-93 homeobox C5 Homo sapiens 0-5
1597470-2 1992 The cDNA for the developmentally regulated, neurite outgrowth-promoting protein HB-GAM (heparin-binding growth-associated molecule) was recently cloned and shown to encode a novel lysine-rich sequence that is homologous with retinoic acid-induced sequences suggested to function in cell differentiation (Merenmies, J., and Rauvala, H. (1990) J. Biol. Tretinoin 225-238 pleiotrophin Rattus norvegicus 80-86
1597470-2 1992 The cDNA for the developmentally regulated, neurite outgrowth-promoting protein HB-GAM (heparin-binding growth-associated molecule) was recently cloned and shown to encode a novel lysine-rich sequence that is homologous with retinoic acid-induced sequences suggested to function in cell differentiation (Merenmies, J., and Rauvala, H. (1990) J. Biol. Tretinoin 225-238 pleiotrophin Rattus norvegicus 88-130
12012012-7 2002 Our results indicate that ATRA-pretreatment modified the CDDP-induced regulation of CDK2 activity by the CDK inhibitors p21 and p27. Tretinoin 26-30 cyclin dependent kinase 2 Homo sapiens 84-88
1630583-1 1992 Retinoic acid has recently been shown to increase growth hormone (GH)-gene transcription rate and GH synthesis in vitro. Tretinoin 0-13 gonadotropin releasing hormone receptor Rattus norvegicus 50-64
1630583-1 1992 Retinoic acid has recently been shown to increase growth hormone (GH)-gene transcription rate and GH synthesis in vitro. Tretinoin 0-13 gonadotropin releasing hormone receptor Rattus norvegicus 66-68
12012012-7 2002 Our results indicate that ATRA-pretreatment modified the CDDP-induced regulation of CDK2 activity by the CDK inhibitors p21 and p27. Tretinoin 26-30 cyclin dependent kinase 2 Homo sapiens 84-87
1630583-1 1992 Retinoic acid has recently been shown to increase growth hormone (GH)-gene transcription rate and GH synthesis in vitro. Tretinoin 0-13 gonadotropin releasing hormone receptor Rattus norvegicus 98-100
1630583-2 1992 To investigate the role retinoic acid plays in the neuroregulation of GH secretion we have studied GH responses to growth hormone-releasing hormone (GHRH) in retinoic acid-deficient rats. Tretinoin 24-37 gonadotropin releasing hormone receptor Rattus norvegicus 70-72
1727694-1 1992 The objective of this study was to investigate the possible regulation of the vitamin K-dependent matrix Gla (gamma-carboxyglutamic acid) protein (MGP) by retinoic acid, a regulation suggested by the recent observation that the human MGP promoter has a perfect direct repeat which is nearly identical to the retinoic acid-responsive element in the retinoic acid receptor-beta gene. Tretinoin 155-168 matrix Gla protein Homo sapiens 147-150
12012012-8 2002 Taken together, our findings suggest that ATRA potentiates the apoptosis induced by CDDP in ovarian carcinoma cells and that this action is sustained by modulation of the activity of CDK2/cyclin A. Tretinoin 42-46 cyclin dependent kinase 2 Homo sapiens 183-187
1727694-1 1992 The objective of this study was to investigate the possible regulation of the vitamin K-dependent matrix Gla (gamma-carboxyglutamic acid) protein (MGP) by retinoic acid, a regulation suggested by the recent observation that the human MGP promoter has a perfect direct repeat which is nearly identical to the retinoic acid-responsive element in the retinoic acid receptor-beta gene. Tretinoin 155-168 matrix Gla protein Homo sapiens 234-237
1727694-1 1992 The objective of this study was to investigate the possible regulation of the vitamin K-dependent matrix Gla (gamma-carboxyglutamic acid) protein (MGP) by retinoic acid, a regulation suggested by the recent observation that the human MGP promoter has a perfect direct repeat which is nearly identical to the retinoic acid-responsive element in the retinoic acid receptor-beta gene. Tretinoin 308-321 matrix Gla protein Homo sapiens 147-150
1727694-1 1992 The objective of this study was to investigate the possible regulation of the vitamin K-dependent matrix Gla (gamma-carboxyglutamic acid) protein (MGP) by retinoic acid, a regulation suggested by the recent observation that the human MGP promoter has a perfect direct repeat which is nearly identical to the retinoic acid-responsive element in the retinoic acid receptor-beta gene. Tretinoin 308-321 matrix Gla protein Homo sapiens 234-237
1567193-1 1992 Hepatic cytosol from normal deermice having cytosolic alcohol dehydrogenase (ADH+) also displays retinol dehydrogenase activity and converts retinol to retinoic acid, whereas cytosol from ADH- deermice lacks these enzyme activities and does not produce retinoic acid. Tretinoin 152-165 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 77-80
1567193-1 1992 Hepatic cytosol from normal deermice having cytosolic alcohol dehydrogenase (ADH+) also displays retinol dehydrogenase activity and converts retinol to retinoic acid, whereas cytosol from ADH- deermice lacks these enzyme activities and does not produce retinoic acid. Tretinoin 253-266 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 77-80
1727694-2 1992 We report that retinoic acid strongly increases MGP mRNA levels in all human cells tested, including osteoblasts, articular cartilage chondrocytes, and fibroblasts. Tretinoin 15-28 matrix Gla protein Homo sapiens 48-51
12042460-8 2002 beta-apo-14"-CA and atRA inhibited the expression of E2F1 protein in MCF-7 and Hs578T cells. Tretinoin 20-24 E2F transcription factor 1 L homeolog Xenopus laevis 53-57
1727694-3 1992 In osteoblastic cells, MGP mRNA levels are increased by 25-fold at 1 microM retinoic acid and achieve half-maximal levels at 0.1 microM hormone. Tretinoin 76-89 matrix Gla protein Homo sapiens 23-26
1727694-5 1992 The present results suggest that part of the known actions of retinoic acid on skin, bone, cartilage, and other tissues in the human may be mediated by the stimulation of MGP synthesis and the consequent effect of increased MGP secretion on nearby target cells. Tretinoin 62-75 matrix Gla protein Homo sapiens 171-174
1727694-5 1992 The present results suggest that part of the known actions of retinoic acid on skin, bone, cartilage, and other tissues in the human may be mediated by the stimulation of MGP synthesis and the consequent effect of increased MGP secretion on nearby target cells. Tretinoin 62-75 matrix Gla protein Homo sapiens 224-227
1567193-3 1992 However, when cytosol from ADH- animals is added to the microsomes, retinoic acid is produced. Tretinoin 68-81 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 27-30
1567193-5 1992 Microsomal retinol dehydrogenase also catalyzes the reduction of retinal to retinol, thereby explaining the decrease in retinoic acid production from retinol in liver cytosol of ADH+ deermice when microsomes are added. Tretinoin 120-133 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 11-32
1638993-5 1992 Exposure of early neural plate stage embryos to retinoic acid caused reduced expression of TGF beta 1 and TGF beta 2 proteins but had no effect on TGF beta 3. Tretinoin 48-61 transforming growth factor, beta 1 Mus musculus 91-101
1638993-8 1992 The down-regulation of intracellular TGF beta 1 was observed up to 48 hours after initial exposure to retinoic acid while some down-regulation of TGF beta 2 was still seen up to 60 hours after initial exposure. Tretinoin 102-115 transforming growth factor, beta 1 Mus musculus 37-47
12032336-10 2002 In these cases, the aberrant V-type PML-RAR(alpha) protein displayed increased affinity to the nuclear corepressor protein SMRT, providing further evidence that RA exerts the therapeutic effect on APL through modulation of the RAR-corepressor interaction. Tretinoin 40-42 nuclear receptor corepressor 2 Homo sapiens 123-127
1315322-4 1992 Antiporter protein synthesis increased by seven-fold during RA-induced granulocytic differentiation of HL60 cells as measured by immunoprecipitation of 35S-methionine-labeled proteins with the RP1-c28 Na+/H+ antiporter antibody. Tretinoin 60-62 RP1 axonemal microtubule associated Homo sapiens 193-196
1353003-1 1992 Expression of the murine homeobox gene Hox 1.6 rapidly increases in F9 teratocarcinoma cells when these cells are induced with retinoic acid to differentiate into primitive and parietal endoderm. Tretinoin 127-140 homeobox A1 Mus musculus 39-46
1728634-0 1992 Differential modulation of transforming growth factor-beta 1 expression and mucin deposition by retinoic acid and sodium lauryl sulfate in human skin. Tretinoin 96-109 LOC100508689 Homo sapiens 76-81
1728634-6 1992 In contrast, mucin deposition, which is induced by transforming growth factor-beta, was elevated in retinoic acid-treated but not sodium lauryl sulfate-treated skin. Tretinoin 100-113 LOC100508689 Homo sapiens 13-18
1728634-9 1992 These data demonstrate disassociation of modulation of transforming growth factor-beta 1 expression and mucin deposition by retinoic acid and sodium lauryl sulfate in human skin in vivo. Tretinoin 124-137 LOC100508689 Homo sapiens 104-109
1728634-10 1992 Whereas alterations in transforming growth factor-beta 1 expression were observed in both retinoic acid- and sodium lauryl sulfate-treated skin, accumulation of mucin was specific to retinoic acid-treated skin. Tretinoin 183-196 LOC100508689 Homo sapiens 161-166
1314862-3 1992 In an attempt to identify other potential regulators of RA responsiveness, we have used RNA blot hybridization to study the expression of the cellular retinoic acid binding proteins (CRABP) CRABP-I and CRABP-II, the RAR-gamma isoforms RAR-gamma 1 and RAR-gamma 2, and the low-affinity RAR homologue RXR in normal, RA-treated, and psoriatic human epidermis. Tretinoin 56-58 cellular retinoic acid binding protein 1 Homo sapiens 190-197
1313739-12 1992 However, the mRNA loss was transient, and recovery of RAR alpha and RAR gamma mRNA levels was noted 12-24 h after retinoic acid treatment. Tretinoin 114-127 retinoic acid receptor gamma Homo sapiens 68-77
1313739-14 1992 The previously reported ability of retinoic acid to down-regulate PR mRNA and the present demonstration that progestins down-regulate RAR alpha and RAR gamma mRNA suggest that mutual regulation may be a mechanism through which PR and the RARs interact in human breast cancer cells. Tretinoin 35-48 retinoic acid receptor gamma Homo sapiens 148-157
1662118-3 1991 This protein, termed RXR beta, forms heterodimers with RAR, preferentially increasing its DNA binding and transcriptional activity on promoters containing retinoic acid, but not thyroid hormone or vitamin D, response elements. Tretinoin 155-168 retinoid X receptor beta Homo sapiens 21-29
11983289-3 2002 We report a significant transcriptional upregulation of all three synapsins (synapsin I, 2.1-fold; synapsin II, 2.6-fold; and synapsin III, 5.5-fold) by retinoic acid-induced differentiation of NTera-2cl.D1 cells, a human paradigm for neuronal differentiation. Tretinoin 153-166 synapsin III Homo sapiens 126-138
1725165-2 1991 Retinoic acid (RA) is known to modulate stratified squamous epithelial differentiation, including expression of the basal cell keratin K19 and the suprabasal keratins K1/K10 and K4/K13. Tretinoin 0-13 keratin 19 Homo sapiens 135-138
1725165-2 1991 Retinoic acid (RA) is known to modulate stratified squamous epithelial differentiation, including expression of the basal cell keratin K19 and the suprabasal keratins K1/K10 and K4/K13. Tretinoin 0-13 keratin 1 Homo sapiens 167-173
1725165-2 1991 Retinoic acid (RA) is known to modulate stratified squamous epithelial differentiation, including expression of the basal cell keratin K19 and the suprabasal keratins K1/K10 and K4/K13. Tretinoin 15-17 keratin 19 Homo sapiens 135-138
1725165-2 1991 Retinoic acid (RA) is known to modulate stratified squamous epithelial differentiation, including expression of the basal cell keratin K19 and the suprabasal keratins K1/K10 and K4/K13. Tretinoin 15-17 keratin 1 Homo sapiens 167-173
1545142-0 1992 Regulation of ornithine decarboxylase gene expression, polyamine levels, and DNA synthetic rates by all-trans-retinoic acid in cultured human keratinocytes. Tretinoin 100-123 ornithine decarboxylase 1 Homo sapiens 14-37
1545142-1 1992 Regulation of ornithine decarboxylase (ODC) gene expression and cell growth by all-trans-retinoic acid in the presence and absence of exogenous putrescine were examined in normal keratinocyte cultures maintained in serum-free medium containing 0.15 mM Ca++. Tretinoin 82-102 ornithine decarboxylase 1 Homo sapiens 39-42
1545142-4 1992 Northern blot analysis of total RNA isolated from breast reduction keratinocytes treated with retinoic acid up to 24 h showed a time-dependent suppression of ODC mRNA levels that was unaffected by putrescine. Tretinoin 94-107 ornithine decarboxylase 1 Homo sapiens 158-161
1545145-3 1992 Immunochemical methods have shown an increase in TGF-beta 1 and, to a lesser extent, of TGF-beta 2 in the epidermis following retinoic acid treatment. Tretinoin 126-139 transforming growth factor, beta 1 Mus musculus 49-59
1545145-5 1992 This study suggests that TGF-beta may mediate the effect of retinoic acids on dermal repair through the stimulation of collagen gene expression. Tretinoin 60-74 transforming growth factor, beta 1 Mus musculus 25-33
1725165-5 1991 Exposure to 10(-6) M RA increases the levels of RAR beta and K19 mRNA; conversely, complete removal of RA from the medium results in reduced levels of these messages. Tretinoin 21-23 keratin 19 Homo sapiens 61-64
12223961-1 2002 The active metabolite of vitamin A (retinoic acid, RA) acts through the nuclear receptors RARalpha, beta and gamma and RXRalpha, beta and gamma. Tretinoin 36-49 retinoid X receptor alpha Mus musculus 119-127
1961035-3 1991 Some blast cells were stimulated by RA in the presence of rGM-CSF and rIL-3 and inhibited when cultured with RA and rG-CSF. Tretinoin 36-38 interleukin 3 Rattus norvegicus 70-75
1961035-7 1991 Colony formation was stimulated by RA in the presence of rGM-CSF or rIL-3 but inhibited by RA with rG-CSF. Tretinoin 35-37 interleukin 3 Rattus norvegicus 68-73
1737772-5 1992 Remarkably, however, RA completely inhibited the down-regulation of TR beta 2 mRNA by T3. Tretinoin 21-23 thyroid hormone receptor beta Rattus norvegicus 68-75
11959834-0 2002 Novel retinoic acid generating activities in the neural tube and heart identified by conditional rescue of Raldh2 null mutant mice. Tretinoin 6-19 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 107-113
11959834-2 2002 The RA biosynthetic enzyme RALDH2 catalyzes much, but not all, RA production in mouse embryos, as revealed here with Raldh2 null mutants carrying an RA-responsive transgene. Tretinoin 4-6 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 27-33
1370674-7 1992 The result that RA induced expression of keratins K6, K16, and K17, as commonly expressed in hyperproliferative epidermis, is consistent with the notion that retinoids increase epidermal cell proliferation in the basal and/or lower spinous layers. Tretinoin 16-18 keratin 16 Homo sapiens 54-57
1918012-1 1991 Retinoic acid (RA) treatment of T-47D human breast cancer cells results in a rapid decrease in the concentration of progesterone receptor (PR) mRNA which causes a slow loss of cellular PR protein (Clarke, C. L., Roman, S. D., Graham, J., Koga, M., Sutherland, R. L. (1990) J. Biol. Tretinoin 0-13 progesterone receptor Homo sapiens 116-137
1918012-1 1991 Retinoic acid (RA) treatment of T-47D human breast cancer cells results in a rapid decrease in the concentration of progesterone receptor (PR) mRNA which causes a slow loss of cellular PR protein (Clarke, C. L., Roman, S. D., Graham, J., Koga, M., Sutherland, R. L. (1990) J. Biol. Tretinoin 0-13 progesterone receptor Homo sapiens 139-141
11959834-2 2002 The RA biosynthetic enzyme RALDH2 catalyzes much, but not all, RA production in mouse embryos, as revealed here with Raldh2 null mutants carrying an RA-responsive transgene. Tretinoin 4-6 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 117-123
1918012-1 1991 Retinoic acid (RA) treatment of T-47D human breast cancer cells results in a rapid decrease in the concentration of progesterone receptor (PR) mRNA which causes a slow loss of cellular PR protein (Clarke, C. L., Roman, S. D., Graham, J., Koga, M., Sutherland, R. L. (1990) J. Biol. Tretinoin 0-13 progesterone receptor Homo sapiens 185-187
1918012-1 1991 Retinoic acid (RA) treatment of T-47D human breast cancer cells results in a rapid decrease in the concentration of progesterone receptor (PR) mRNA which causes a slow loss of cellular PR protein (Clarke, C. L., Roman, S. D., Graham, J., Koga, M., Sutherland, R. L. (1990) J. Biol. Tretinoin 15-17 progesterone receptor Homo sapiens 116-137
1635177-12 1992 Dryness of mouth and lips, irritation around eyes and the elevations of GOT, GPT and triglyceride level were seen as the side effects of ATRA, however they were tolerable. Tretinoin 137-141 glutamic--pyruvic transaminase Homo sapiens 77-80
1918012-1 1991 Retinoic acid (RA) treatment of T-47D human breast cancer cells results in a rapid decrease in the concentration of progesterone receptor (PR) mRNA which causes a slow loss of cellular PR protein (Clarke, C. L., Roman, S. D., Graham, J., Koga, M., Sutherland, R. L. (1990) J. Biol. Tretinoin 15-17 progesterone receptor Homo sapiens 139-141
11959834-2 2002 The RA biosynthetic enzyme RALDH2 catalyzes much, but not all, RA production in mouse embryos, as revealed here with Raldh2 null mutants carrying an RA-responsive transgene. Tretinoin 27-29 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 117-123
1918012-1 1991 Retinoic acid (RA) treatment of T-47D human breast cancer cells results in a rapid decrease in the concentration of progesterone receptor (PR) mRNA which causes a slow loss of cellular PR protein (Clarke, C. L., Roman, S. D., Graham, J., Koga, M., Sutherland, R. L. (1990) J. Biol. Tretinoin 15-17 progesterone receptor Homo sapiens 185-187
1918012-11 1991 The diminished progestin responsiveness of RA-pretreated cells was confirmed in separate experiments which showed that the progestin inducibility of TGF-alpha mRNA was also decreased in cells treated with ORG 2058 following pretreatment with RA for 24 h. These data demonstrate that RA decreases PR mRNA concentrations by direct transcriptional inhibition, leading to decreased cellular PR concentrations. Tretinoin 43-45 transforming growth factor alpha Homo sapiens 149-158
1918012-11 1991 The diminished progestin responsiveness of RA-pretreated cells was confirmed in separate experiments which showed that the progestin inducibility of TGF-alpha mRNA was also decreased in cells treated with ORG 2058 following pretreatment with RA for 24 h. These data demonstrate that RA decreases PR mRNA concentrations by direct transcriptional inhibition, leading to decreased cellular PR concentrations. Tretinoin 43-45 progesterone receptor Homo sapiens 296-298
1918012-11 1991 The diminished progestin responsiveness of RA-pretreated cells was confirmed in separate experiments which showed that the progestin inducibility of TGF-alpha mRNA was also decreased in cells treated with ORG 2058 following pretreatment with RA for 24 h. These data demonstrate that RA decreases PR mRNA concentrations by direct transcriptional inhibition, leading to decreased cellular PR concentrations. Tretinoin 43-45 progesterone receptor Homo sapiens 387-389
1918012-11 1991 The diminished progestin responsiveness of RA-pretreated cells was confirmed in separate experiments which showed that the progestin inducibility of TGF-alpha mRNA was also decreased in cells treated with ORG 2058 following pretreatment with RA for 24 h. These data demonstrate that RA decreases PR mRNA concentrations by direct transcriptional inhibition, leading to decreased cellular PR concentrations. Tretinoin 242-244 transforming growth factor alpha Homo sapiens 149-158
1918012-11 1991 The diminished progestin responsiveness of RA-pretreated cells was confirmed in separate experiments which showed that the progestin inducibility of TGF-alpha mRNA was also decreased in cells treated with ORG 2058 following pretreatment with RA for 24 h. These data demonstrate that RA decreases PR mRNA concentrations by direct transcriptional inhibition, leading to decreased cellular PR concentrations. Tretinoin 242-244 transforming growth factor alpha Homo sapiens 149-158
1576967-7 1992 In retinoic-acid-treated P19 cells, MASH1 protein expression precedes and then overlaps expression of neuronal markers. Tretinoin 3-16 achaete-scute family bHLH transcription factor 1 Homo sapiens 36-41
11959834-2 2002 The RA biosynthetic enzyme RALDH2 catalyzes much, but not all, RA production in mouse embryos, as revealed here with Raldh2 null mutants carrying an RA-responsive transgene. Tretinoin 27-29 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 117-123
1918012-12 1991 The decreased levels of PR result in impaired responsiveness to progestins and this suggests that RA derived from dietary vitamin A may have a role in modulating cellular sensitivity to progestins. Tretinoin 98-100 progesterone receptor Homo sapiens 24-26
11959834-3 2002 Targeted disruption of Raldh2 arrests development at midgestation and eliminates all RA synthesis except that associated with Raldh3 expression in the surface ectoderm of the eye field. Tretinoin 85-87 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 23-29
1292933-1 1992 The major cytosolic aldehyde dehydrogenase isozyme (ALDH1) exhibits strong activity for oxidation of retinal to retinoic acid, while the major mitochondrial ALDH2 and the stomach cytosolic ALDH3 have no such activity. Tretinoin 112-125 aldehyde dehydrogenase 3 family member A1 Homo sapiens 189-194
11959834-4 2002 Conditional rescue of Raldh2(-/-) embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Tretinoin 62-64 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 22-28
1915273-0 1991 Effects of retinoic acid excess on expression of Hox-2.9 and Krox-20 and on morphological segmentation in the hindbrain of mouse embryos. Tretinoin 11-24 homeobox B1 Mus musculus 49-56
11959834-4 2002 Conditional rescue of Raldh2(-/-) embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Tretinoin 62-64 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 189-195
1656191-1 1991 Biological effects of retinoic acid (RA) are mediated through its binding to three closely related nuclear receptors (RAR alpha, RAR beta, and RAR gamma) belonging to the steroid-thyroid nuclear receptor family. Tretinoin 22-35 retinoic acid receptor gamma Homo sapiens 143-152
1450664-0 1992 Regulation of E2F/cyclin A-containing complex upon retinoic acid-induced differentiation of teratocarcinoma cells. Tretinoin 51-64 cyclin A2 Mus musculus 18-26
11959834-4 2002 Conditional rescue of Raldh2(-/-) embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Tretinoin 166-168 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 22-28
1315557-1 1992 From a series of naphthalene and benzoic acid derivatives we have identified synthetic retinoic acid analogues exhibiting high selectivity for the nuclear retinoic acid receptors RAR alpha (Am 580), RAR beta (CD 2019) and RAR gamma (CD 437) as well as ligands sharing high affinities for all RAR subtypes (CD 367). Tretinoin 87-100 retinoic acid receptor gamma Homo sapiens 222-231
1656191-1 1991 Biological effects of retinoic acid (RA) are mediated through its binding to three closely related nuclear receptors (RAR alpha, RAR beta, and RAR gamma) belonging to the steroid-thyroid nuclear receptor family. Tretinoin 37-39 retinoic acid receptor gamma Homo sapiens 143-152
11959834-4 2002 Conditional rescue of Raldh2(-/-) embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Tretinoin 166-168 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 189-195
11959834-5 2002 Unexpectedly, conditionally rescued Raldh2(-/-) embryos also possess novel sites of RA synthesis in the neural tube and heart that do not correspond to expression of Raldh1-3. Tretinoin 84-86 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 36-42
1662118-0 1991 RXR beta: a coregulator that enhances binding of retinoic acid, thyroid hormone, and vitamin D receptors to their cognate response elements. Tretinoin 49-62 retinoid X receptor beta Homo sapiens 0-8
1685814-0 1991 HOX gene activation by retinoic acid. Tretinoin 23-36 tinman Drosophila melanogaster 0-3
11959834-9 2002 These novel RA-generating activities in the neural tube and heart fill gaps in our knowledge of how RA is generated spatiotemporally and may, along with Raldh1 and Raldh3, contribute to rescue of Raldh2(-/-) embryos by producing RA locally. Tretinoin 12-14 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 153-159
1685814-2 1991 Recent data obtained from embryonal carcinoma cells induced to differentiate by retinoic acid cast some light on the molecular mechanisms underlying the collinear expression of the Hox genes. Tretinoin 80-93 tinman Drosophila melanogaster 181-184
1656958-4 1991 In response to retinoic acid, the three hybrid receptors ER-RAR alpha, ER-RAR beta and ER-RAR gamma exhibited the same induction profile as the corresponding wild type receptors RAR alpha, RAR beta, and RAR gamma. Tretinoin 15-28 retinoic acid receptor gamma Homo sapiens 90-99
1656958-4 1991 In response to retinoic acid, the three hybrid receptors ER-RAR alpha, ER-RAR beta and ER-RAR gamma exhibited the same induction profile as the corresponding wild type receptors RAR alpha, RAR beta, and RAR gamma. Tretinoin 15-28 retinoic acid receptor gamma Homo sapiens 203-212
1939157-8 1991 Recent studies have shown that MGP is strongly induced by retinoic acid in fibroblasts, chondrocytes, and osteoblasts, a response which suggests that MGP mediates an action of retinoic acid on an aspect of cell growth or differentiation. Tretinoin 58-71 matrix Gla protein Homo sapiens 31-34
1939157-8 1991 Recent studies have shown that MGP is strongly induced by retinoic acid in fibroblasts, chondrocytes, and osteoblasts, a response which suggests that MGP mediates an action of retinoic acid on an aspect of cell growth or differentiation. Tretinoin 58-71 matrix Gla protein Homo sapiens 150-153
11959834-9 2002 These novel RA-generating activities in the neural tube and heart fill gaps in our knowledge of how RA is generated spatiotemporally and may, along with Raldh1 and Raldh3, contribute to rescue of Raldh2(-/-) embryos by producing RA locally. Tretinoin 12-14 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 196-202
1939157-8 1991 Recent studies have shown that MGP is strongly induced by retinoic acid in fibroblasts, chondrocytes, and osteoblasts, a response which suggests that MGP mediates an action of retinoic acid on an aspect of cell growth or differentiation. Tretinoin 176-189 matrix Gla protein Homo sapiens 31-34
11959834-9 2002 These novel RA-generating activities in the neural tube and heart fill gaps in our knowledge of how RA is generated spatiotemporally and may, along with Raldh1 and Raldh3, contribute to rescue of Raldh2(-/-) embryos by producing RA locally. Tretinoin 100-102 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 196-202
1678362-0 1991 Retinoic acid perturbs the expression of Xhox.lab genes and alters mesodermal determination in Xenopus laevis. Tretinoin 0-13 homeobox D1 S homeolog Xenopus laevis 41-49
11959834-9 2002 These novel RA-generating activities in the neural tube and heart fill gaps in our knowledge of how RA is generated spatiotemporally and may, along with Raldh1 and Raldh3, contribute to rescue of Raldh2(-/-) embryos by producing RA locally. Tretinoin 100-102 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 196-202
11994141-0 2002 Topical retinoic acid alters the expression of cellular retinoic acid-binding protein-I and cellular retinoic acid-binding protein-II in non-lesional but not lesional psoriatic skin. Tretinoin 8-21 cellular retinoic acid binding protein 1 Homo sapiens 47-133
1649387-3 1991 Transcription of RAR beta is rapidly upregulated through a retinoic acid-responsive element (here referred to as the beta RARE) in its promoter. Tretinoin 59-72 retinoic acid receptor, beta Mus musculus 17-25
1668276-0 1991 Developmental analysis of the retinoic acid-inducible RAR-beta 2 promoter in transgenic animals. Tretinoin 30-43 retinoic acid receptor, beta Mus musculus 54-62
1668276-2 1991 There are three known types of nuclear receptors for RA in mammals, RAR-alpha, RAR-beta and RAR-gamma, which transduce the RA signal by inducing or repressing the transcription of target genes. Tretinoin 53-55 retinoic acid receptor, beta Mus musculus 79-87
1668276-6 1991 Analysis of the lacZ expression pattern in embryos from mothers treated with teratogenic doses of RA, indicated that mRAR-beta 2 promoter is selectively induced in a manner suggesting that overexpression of the mRAR-beta 2 isoform is involved in RA-generated malformations. Tretinoin 98-100 retinoic acid receptor, beta Mus musculus 117-126
1668276-6 1991 Analysis of the lacZ expression pattern in embryos from mothers treated with teratogenic doses of RA, indicated that mRAR-beta 2 promoter is selectively induced in a manner suggesting that overexpression of the mRAR-beta 2 isoform is involved in RA-generated malformations. Tretinoin 98-100 retinoic acid receptor, beta Mus musculus 211-220
1661245-5 1991 Response elements for retinoic acid have so far been identified for the rat growth hormone and phosphoenolpyruvate carboxykinase, the mouse complement H and laminin B1, the human and mouse retinoic acid receptor beta, the human osteocalcin, and the human alcohol dehydrogenase genes. Tretinoin 22-35 gonadotropin releasing hormone receptor Rattus norvegicus 76-90
1877746-3 1991 Retinol dehydrogenase is an enzyme needed to convert vitamin A (retinol) to retinoic acid, a molecule that specifies embryonic pattern formation by controlling gene expression. Tretinoin 76-89 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 0-21
1661245-5 1991 Response elements for retinoic acid have so far been identified for the rat growth hormone and phosphoenolpyruvate carboxykinase, the mouse complement H and laminin B1, the human and mouse retinoic acid receptor beta, the human osteocalcin, and the human alcohol dehydrogenase genes. Tretinoin 22-35 laminin B1 Mus musculus 157-167
11891985-0 2002 Analysis of two distinct retinoic acid response elements in the homeobox gene Hoxb1 in transgenic mice. Tretinoin 25-38 homeobox B1 Mus musculus 78-83
1661245-5 1991 Response elements for retinoic acid have so far been identified for the rat growth hormone and phosphoenolpyruvate carboxykinase, the mouse complement H and laminin B1, the human and mouse retinoic acid receptor beta, the human osteocalcin, and the human alcohol dehydrogenase genes. Tretinoin 22-35 retinoic acid receptor, beta Mus musculus 189-216
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
1711202-3 1991 Our studies revealed that the epidermal keratins, K5, K6, K14, and K16, their mRNAs, and their transcripts were diminished relative to actin as a consequence of retinoic acid (RA) treatment. Tretinoin 161-174 keratin 16 Homo sapiens 67-70
1711202-3 1991 Our studies revealed that the epidermal keratins, K5, K6, K14, and K16, their mRNAs, and their transcripts were diminished relative to actin as a consequence of retinoic acid (RA) treatment. Tretinoin 176-178 keratin 16 Homo sapiens 67-70
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
11891985-5 2002 We demonstrate that the DR(5) RARE is required for the regulation of Hoxb-1 transgene region-specific expression in the gut and extraembryonic tissues, as well as for the RA-induced anteriorization of Hoxb-1 transgene expression in the gut. Tretinoin 30-32 homeobox B1 Mus musculus 69-75
1653241-7 1991 These data indicate a direct role for CRABP in retinoic acid metabolism and suggest a mechanism for discriminating metabolically between all-trans- and 13-cis-retinoids. Tretinoin 47-60 cellular retinoic acid binding protein 1 Homo sapiens 38-43
1851295-0 1991 Transcriptional control of c-jun by retinoic acid. Tretinoin 36-49 jun proto-oncogene Mus musculus 27-32
11891985-5 2002 We demonstrate that the DR(5) RARE is required for the regulation of Hoxb-1 transgene region-specific expression in the gut and extraembryonic tissues, as well as for the RA-induced anteriorization of Hoxb-1 transgene expression in the gut. Tretinoin 30-32 homeobox B1 Mus musculus 201-207
1851295-2 1991 Retinoic acid (RA) induced differentiation causes a strong increase in the levels of c-jun mRNA. Tretinoin 0-13 jun proto-oncogene Mus musculus 85-90
1851295-2 1991 Retinoic acid (RA) induced differentiation causes a strong increase in the levels of c-jun mRNA. Tretinoin 15-17 jun proto-oncogene Mus musculus 85-90
1713123-6 1991 The expression of keratin 19 message, which is RA inducible in normal keratinocytes, was also abnormal in many of the SCC cell lines. Tretinoin 47-49 keratin 19 Homo sapiens 18-28
11739380-4 2002 In this study we have investigated a possible role of RAGE and amphoterin in the retinoic acid-induced differentiation of neuroblastoma cells. Tretinoin 81-94 high mobility group box 1 Homo sapiens 63-73
1649749-3 1991 Treatment with retinoic acid decreased GAG synthesis in cultured chondrocytes and the number of PTH receptors, measured by binding of [125I]-[Nle8,18,Tyr34]bovine PTH-(1-34) amide to the cells. Tretinoin 15-28 parathyroid hormone Oryctolagus cuniculus 163-166
1649749-6 1991 When chondrocytes that had been treated with retinoic acid were cultured in the absence of retinoic acid for 3 days, both their GAG synthesis and their number of PTH receptors were restored. Tretinoin 45-58 parathyroid hormone Oryctolagus cuniculus 162-165
1649749-6 1991 When chondrocytes that had been treated with retinoic acid were cultured in the absence of retinoic acid for 3 days, both their GAG synthesis and their number of PTH receptors were restored. Tretinoin 91-104 parathyroid hormone Oryctolagus cuniculus 162-165
1649749-10 1991 In addition, the PTH-stimulated cAMP level in chondrocytes pretreated with retinoic acid, epidermal growth factor, and fibroblast growth factor was lower than that in control cells. Tretinoin 75-88 parathyroid hormone Oryctolagus cuniculus 17-20
1851295-4 1991 Our results show that RA treatment causes a strong enhancement in c-jun promoter activity, an effect probably mediated by the RA-receptor beta (RAR beta). Tretinoin 22-24 jun proto-oncogene Mus musculus 66-71
1851295-4 1991 Our results show that RA treatment causes a strong enhancement in c-jun promoter activity, an effect probably mediated by the RA-receptor beta (RAR beta). Tretinoin 22-24 retinoic acid receptor, beta Mus musculus 144-152
1647813-2 1991 In certain embryonal carcinoma cell lines, multiple int-2 transcripts accumulate when the cells are induced to differentiate with retinoic acid and dibutyryl cyclic AMP. Tretinoin 130-143 fibroblast growth factor 3 Mus musculus 52-57
12058867-0 2002 1Alpha25(OH)2D3 interferes with retinoic acid-induced inhibition of c-fos gene expression for AP-1 formation in osteoblastic cells. Tretinoin 32-45 jun proto-oncogene Mus musculus 94-98
1899405-2 1991 In this study, basic FGF was found to stimulate hyaluronan synthesis and production of hyaluronan-dependent pericellular coats by mesodermal cells from the chick embryo limb; acidic FGF, platelet-derived growth factor, epidermal growth factor, and retinoic acid either had a much smaller effect than basic FGF or an inhibitory effect. Tretinoin 248-261 fibroblast growth factor 2 Gallus gallus 21-24
1653151-11 1991 The data presented here indicate that fetal CRABP appears to play a role in differential accumulation of retinoic acid in certain structures of the developing hamster. Tretinoin 105-118 cellular retinoic acid binding protein 1 Homo sapiens 44-49
12058867-1 2002 Our previous studies demonstrated retinoic acid (RA) inhibition of activation protein-1 (AP-1) formation in TNF-alpha-treated osteoblastic MC3T3-E1 cells via c-fos suppression. Tretinoin 34-47 jun proto-oncogene Mus musculus 89-93
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 32-34 epidermal growth factor like 1 Rattus norvegicus 146-149
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 41-54 cellular retinoic acid binding protein 1 Homo sapiens 219-224
12058867-1 2002 Our previous studies demonstrated retinoic acid (RA) inhibition of activation protein-1 (AP-1) formation in TNF-alpha-treated osteoblastic MC3T3-E1 cells via c-fos suppression. Tretinoin 49-51 jun proto-oncogene Mus musculus 89-93
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 41-54 retinol binding protein 1 Homo sapiens 240-244
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 204-217 cellular retinoic acid binding protein 1 Homo sapiens 219-224
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 32-34 epidermal growth factor like 1 Rattus norvegicus 146-149
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 205-207 epidermal growth factor like 1 Rattus norvegicus 146-149
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 205-207 epidermal growth factor like 1 Rattus norvegicus 146-149
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 204-217 retinol binding protein 1 Homo sapiens 240-244
12058867-6 2002 1alpha25(OH)2D3 interfered with RA inhibition of the TPA-response element binding activity of AP-1 in the cytokine-treated cells. Tretinoin 32-34 jun proto-oncogene Mus musculus 94-98
2257974-4 1990 After formation of parietal endoderm-like cells by addition of retinoic acid (RA) to BRL-CM, the 1.8-kb transcript of TGF beta 1 and PDGF-A expression were reduced, IGF II mRNA and a single TGF beta 3 transcript of 3.8 kb were induced while PDGF-B and TGF beta 4 remained virtually unchanged. Tretinoin 63-76 platelet derived growth factor subunit A Rattus norvegicus 133-139
1935685-2 1991 It was characterized as a cytosolic isoform with basic isoelectric point and preference for aliphatic substrates, features that resemble those of the isoform AHD-2 which is known to oxidize retinaldehyde to retinoic acid. Tretinoin 207-220 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 158-163
11802792-5 2002 To investigate the role of ERK activation, co-treatment of RA with PD98059, a specific inhibitor of the ERK signalling pathway, prevented both adipocyte formation and expression of the adipogenic markers, adipocyte lipid-binding protein and peroxisome-proliferator-activated receptor gamma. Tretinoin 59-61 peroxisome proliferator activated receptor gamma Mus musculus 241-289
2250167-4 1990 The aim of the present study was to determine if RA administered under similar conditions would affect the penetrance or expression of the Axd mutation or survival of Axd homozygotes. Tretinoin 49-51 axial defects Mus musculus 167-170
1711471-0 1991 Aberrant in vitro expression of keratin K13 induced by Ca2+ and vitamin A acid in mouse epidermal cell lines. Tretinoin 64-78 keratin 13 Mus musculus 40-43
12142036-0 2002 Retinoic acid promotes the development of Th2-like human myelin basic protein-reactive T cells. Tretinoin 0-13 myelin basic protein Homo sapiens 57-77
1645738-3 1991 In A126-1B2 cells, RA also induced the expression of other markers of differentiation including acetylcholinesterase and the mRNAs for neurofilament (NF-M) and GAP-43 as effectively as nerve growth factor (NGF). Tretinoin 19-21 growth associated protein 43 Rattus norvegicus 160-166
2087681-12 1990 RA exposure altered the expression of TFG-alpha, TGF-beta 1, and TGF-beta 2, but significant effects on EGF were not found. Tretinoin 0-2 transforming growth factor, beta 1 Mus musculus 49-59
2122968-2 1990 Recently, we showed that a parathyroid hormone-related protein (PTHrP), by activating adenylate cyclase, can substitute for exogenous cAMP in promoting retinoic acid-induced differentiation of F9 cells. Tretinoin 152-165 parathyroid hormone like hormone Homo sapiens 27-62
2122968-2 1990 Recently, we showed that a parathyroid hormone-related protein (PTHrP), by activating adenylate cyclase, can substitute for exogenous cAMP in promoting retinoic acid-induced differentiation of F9 cells. Tretinoin 152-165 parathyroid hormone like hormone Homo sapiens 64-69
2122968-8 1990 In the presence of retinoic acid, exogenous human PTHrP-(1-34)-amide (20 nM) produced a further 2-fold increase in Gs alpha mRNA. Tretinoin 19-32 parathyroid hormone like hormone Homo sapiens 50-55
11825567-1 2002 Induced by retinoic acid and implicated in playing a role in development, rodent RAE-1 proteins are ligands for the activating immunoreceptor NKG2D, widely expressed on natural killer cells, T cells, and macrophages. Tretinoin 11-24 killer cell lectin like receptor K1 Homo sapiens 142-147
1366990-2 1990 We determined that TGF-beta activity increases approximately 25-100% when the mouse EC cell line, F9, is induced to differentiate with retinoic acid (RA). Tretinoin 135-148 transforming growth factor, beta 1 Mus musculus 19-27
1850696-0 1991 The late retinoic acid induction of laminin B1 gene transcription involves RAR binding to the responsive element. Tretinoin 9-22 laminin B1 Mus musculus 36-46
1850696-1 1991 Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Tretinoin 64-77 laminin B1 Mus musculus 28-38
1850696-1 1991 Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Tretinoin 64-77 laminin B1 Mus musculus 40-43
1850696-1 1991 Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Tretinoin 79-81 laminin B1 Mus musculus 28-38
1850696-1 1991 Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Tretinoin 79-81 laminin B1 Mus musculus 40-43
1366990-2 1990 We determined that TGF-beta activity increases approximately 25-100% when the mouse EC cell line, F9, is induced to differentiate with retinoic acid (RA). Tretinoin 150-152 transforming growth factor, beta 1 Mus musculus 19-27
1850696-1 1991 Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Tretinoin 116-118 laminin B1 Mus musculus 28-38
11827792-0 2002 Temporal expression of CD44 during embryonic chick limb development and modulation of its expression with retinoic acid. Tretinoin 106-119 CD44 molecule (Indian blood group) Gallus gallus 23-27
1850696-1 1991 Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Tretinoin 116-118 laminin B1 Mus musculus 40-43
1850696-2 1991 Here we have shown by gel retardation assay that all three retinoic acid receptors (RARs) alpha, beta and gamma expressed in Cos cells can bind directly to the previously characterized retinoic acid response element (RARE) of the LB1 promoter, albeit with a weaker affinity than to the RAR-beta gene RARE. Tretinoin 59-72 laminin B1 Mus musculus 230-233
1850696-5 1991 Analyses of LB1 RARE mutants provide a strong correlation between RA-inducibility in vivo and efficiency of RAR binding in vitro. Tretinoin 16-18 laminin B1 Mus musculus 12-15
16788631-5 1990 The cytosolic retinoic acid-binding protein (CRABP), which is differentially expressed during squamous differentiation of human epidermal keratinocytes, may control the effective concentration of retinoic acid in the cell and therefore regulate indirectly gene expression. Tretinoin 14-27 cellular retinoic acid binding protein 1 Homo sapiens 45-50
11827792-12 2002 Tibial chondrocytes were cultured in the presence or absence of retinoic acid for 36 or 72 h. By RT-PCR, expression of aggrecan and the CD44 mRNA by chick chondrocytes was decreased after retinoic acid treatment, while GAPDH expression showed no change. Tretinoin 64-77 CD44 molecule (Indian blood group) Gallus gallus 136-140
1849102-0 1991 Retinoic acid-induced glandular metaplasia in mouse skin is linked to the dermal expression of retinoic acid receptor beta mRNA. Tretinoin 0-13 retinoic acid receptor, beta Mus musculus 95-122
2232701-10 1990 In contrast, acute exposure to retinoic acid in the absence or presence of EGF caused a greater than 2-fold increase in the amount of type I-homotrimers synthesized but substantially decreased the amount of type I-heterotrimers produced. Tretinoin 31-44 epidermal growth factor like 1 Rattus norvegicus 75-78
11827792-12 2002 Tibial chondrocytes were cultured in the presence or absence of retinoic acid for 36 or 72 h. By RT-PCR, expression of aggrecan and the CD44 mRNA by chick chondrocytes was decreased after retinoic acid treatment, while GAPDH expression showed no change. Tretinoin 188-201 CD44 molecule (Indian blood group) Gallus gallus 136-140
1650576-7 1991 These results clearly show that RAR alpha and RAR gamma 1 can transactivate the RAR beta gene; that RAR beta can stimulate its own expression and that resistance to RA in RAC65 cells is probably due to the altered RAR alpha transcript present in these cells. Tretinoin 32-34 retinoic acid receptor, beta Mus musculus 80-88
11795432-6 2001 RA triggered G1 arrest at least partly through proteasome-dependent degradation of cyclin D1. Tretinoin 0-2 cyclin D1 Homo sapiens 83-92
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 235-248 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 138-159
11795432-8 2001 To confirm that a specific proteolysis pathway was induced by RA-treatment, a degradation assay was established using in vitro translated cyclin D1 and cellular extracts from RA-treated or untreated human bronchial epithelial cells. Tretinoin 62-64 cyclin D1 Homo sapiens 138-147
1711402-1 1991 Retinoic acid promotes the neuronal survival properties of the class 1 heparin-binding growth factor (HBGF-1) on 8-day-old chick ciliary and sensory neurones. Tretinoin 0-13 fibroblast growth factor 1 Gallus gallus 102-108
11795432-9 2001 Incubation of RA-treated but not the control cellular extracts with in vitro translated cyclin D1 led to cyclin degradation. Tretinoin 14-16 cyclin D1 Homo sapiens 88-97
11784046-8 2001 Cdx1 has recently been demonstrated to be a direct RA target, suggesting an indirect means by which retinoid signaling may impact vertebral patterning. Tretinoin 51-53 caudal type homeobox 1 Mus musculus 0-4
1841512-5 1991 Irreversible induction of neural development was achieved if cell-aggregation and retinonic acid acted simultaneously, and for a period longer than 48 h. Retinoic acid, on the other hand, was found to be toxic on non-aggregated PCC-7 cells. Tretinoin 154-167 crystallin gamma D Homo sapiens 228-231
2178220-6 1990 RAR beta mRNA, which was undetectable in untreated cells, was detected after 24 h of treatment with a RA concentration as low as 10(-9) M, and its level increased with up to 10(-6) M RA. Tretinoin 102-104 retinoic acid receptor, beta Mus musculus 0-8
2178220-9 1990 Several retinoids and related synthetic compounds, including 13-cis RA, TTNPB, Ch55, Am80, and the trifluoromethyl nonyloxyphenyl analog of RA, also induced RAR beta mRNA, whereas a 24-h treatment with 10(-6) M retinol, TTNP (a decarboxylated analog of TTNPB), or the phenyl analog of RA failed to induce RAR beta mRNA. Tretinoin 68-70 retinoic acid receptor, beta Mus musculus 157-165
2178220-11 1990 However, S91-C154, a RA-resistant mutant subclone derived from S91-C2 cells, showed mRNA levels of RAR alpha and RAR gamma and induction of RAR beta by RA similar to those detected in the sensitive S91-C2 cells. Tretinoin 21-23 retinoic acid receptor, beta Mus musculus 140-148
11784046-9 2001 To further investigate this relationship, a complete allelic series of Cdx1-RARgamma mutants was generated and the skeletal phenotype assessed either following normal gestation or after administration of RA. Tretinoin 76-78 caudal type homeobox 1 Mus musculus 71-75
2006470-2 1991 The purposes of these studies were (1) to observe the effects of retinoic acid on the frequency of exencephaly in SELH/Bc embryos; (2) to compare the SELH/Bc response with those of normal strains and of other neural tube mutants; and (3) to compare, between SELH/Bc and a normal strain (SWV/Bc), the effects of retinoic acid on morphology of the closing anterior neural tube. Tretinoin 65-78 selenoprotein H Mus musculus 114-118
11784046-10 2001 Synergistic interactions between these null alleles were observed in compound mutants, and the full effects of exogenous RA on vertebral morphogenesis required Cdx1. Tretinoin 121-123 caudal type homeobox 1 Mus musculus 160-164
2006470-3 1991 SELH/Bc was more liable to retinoic acid-induced exencephaly than were normal strains. Tretinoin 27-40 selenoprotein H Mus musculus 0-4
11784046-11 2001 These findings are consistent with a role for RA upstream of Cdx1 as regards axial patterning. Tretinoin 46-48 caudal type homeobox 1 Mus musculus 61-65
2006470-4 1991 After maternal treatment with 5 mg/kg retinoic acid on day 8.5 of gestation, 53% of SELH/Bc embryos had exencephaly, compared with 22% in ICR/Bc and 14% in SWV/Bc. Tretinoin 38-51 selenoprotein H Mus musculus 84-88
2006470-9 1991 The study comparing the morphology of anterior neural tube closure in SELH/Bc and normal SWV/Bc embryos showed that retinoic acid delays the elevation of the mesencephalic neural folds. Tretinoin 116-129 selenoprotein H Mus musculus 70-74
11784046-12 2001 However, exogenous RA attenuated several defects inherent to Cdx1 null mutants. Tretinoin 19-21 caudal type homeobox 1 Mus musculus 61-65
2166951-5 1990 The up-regulation of the gene encoding CRABP-II by its ligand suggests that CRABP-II might be involved in a feedback regulatory role in the mechanism of action of retinoic acid on cellular differentiation. Tretinoin 163-176 cellular retinoic acid binding protein II Mus musculus 39-47
2250167-4 1990 The aim of the present study was to determine if RA administered under similar conditions would affect the penetrance or expression of the Axd mutation or survival of Axd homozygotes. Tretinoin 49-51 axial defects Mus musculus 139-142
2166951-5 1990 The up-regulation of the gene encoding CRABP-II by its ligand suggests that CRABP-II might be involved in a feedback regulatory role in the mechanism of action of retinoic acid on cellular differentiation. Tretinoin 163-176 cellular retinoic acid binding protein II Mus musculus 76-84
11712082-7 2001 Retinoic acid (10 microM) induced a transient up-regulation of WNT2 in NT2 cells. Tretinoin 0-13 Wnt family member 2 Homo sapiens 63-67
1982997-9 1990 Examination of immediate-early transcription factor expression during the MDI regimen revealed that RA mediated an elevated, prolonged expression of c-Jun mRNA accompanied by diminished expression of c-Fos and Jun-B mRNAs. Tretinoin 100-102 jun proto-oncogene Mus musculus 149-154
11733135-5 2001 Specifically, the minimal SMN promoter is four times more active in undifferentiated embryonal carcinoma P19 cells compared to cells treated with retinoic acid (RA) to initiate neuronal differentiation. Tretinoin 146-159 survival of motor neuron 1, telomeric Homo sapiens 26-29
2373707-0 1990 Progesterone receptor regulation by retinoic acid in the human breast cancer cell line T-47D. Tretinoin 36-49 progesterone receptor Homo sapiens 0-21
2373707-1 1990 Data are presented which document the first known effect of retinoic acid on progesterone receptor (PR) gene expression. Tretinoin 60-73 progesterone receptor Homo sapiens 77-98
2373707-1 1990 Data are presented which document the first known effect of retinoic acid on progesterone receptor (PR) gene expression. Tretinoin 60-73 progesterone receptor Homo sapiens 100-102
2373707-2 1990 Treatment of T-47D human breast cancer cells with retinoic acid for 48 h resulted in a marked concentration-dependent decrease in the level of PR mRNA and immunoreactive protein which was similar to the known effect of progestins on these parameters. Tretinoin 50-63 progesterone receptor Homo sapiens 143-145
2373707-3 1990 Retinoic acid, however, did not bind to PR, nor did it cause the previously demonstrated increase in PR molecular weight observed after progestin exposure. Tretinoin 0-13 progesterone receptor Homo sapiens 101-103
2172028-4 1990 Both 13-cis-retinoic acid and 3,4-didehydro-all trans-retinoic acid also induced expression of RAR-beta but were only effective at concentrations 100-fold greater than all trans-retinoic acid. Tretinoin 48-67 retinoic acid receptor, beta Mus musculus 95-103
11733135-5 2001 Specifically, the minimal SMN promoter is four times more active in undifferentiated embryonal carcinoma P19 cells compared to cells treated with retinoic acid (RA) to initiate neuronal differentiation. Tretinoin 161-163 survival of motor neuron 1, telomeric Homo sapiens 26-29
2110809-0 1990 Plasminogen activator activity of normal and retinoic acid-treated post-implantation embryos. Tretinoin 45-58 plasminogen Mus musculus 0-11
2373707-4 1990 When T-47D cells were treated with retinoic acid for 6 h rather than 48 h, no reduction in the level of PR protein was noted at any retinoic acid concentration whereas the effects of retinoic acid on PR mRNA at 6 and 48 h were the same. Tretinoin 35-48 progesterone receptor Homo sapiens 200-202
2373707-5 1990 Examination of the time course of the effects of retinoic acid revealed a rapid decrease in PR mRNA levels detectable 1 h after and maximal 6 h after treatment of T-47D cells with retinoic acid. Tretinoin 49-62 progesterone receptor Homo sapiens 92-94
2373707-5 1990 Examination of the time course of the effects of retinoic acid revealed a rapid decrease in PR mRNA levels detectable 1 h after and maximal 6 h after treatment of T-47D cells with retinoic acid. Tretinoin 180-193 progesterone receptor Homo sapiens 92-94
2373707-7 1990 As expected, the PR protein concentration was unaffected for at least 6 h but was maximally decreased 24-48 h after retinoic acid treatment. Tretinoin 116-129 progesterone receptor Homo sapiens 17-19
2373707-8 1990 In summary, retinoic acid treatment of T-47D cells caused a decrease in the cellular PR concentration by decreasing levels of receptor mRNA and protein, suggesting that retinoic acid is capable of modulating sensitivity to progestins in human breast cancer cells. Tretinoin 12-25 progesterone receptor Homo sapiens 85-87
2373707-8 1990 In summary, retinoic acid treatment of T-47D cells caused a decrease in the cellular PR concentration by decreasing levels of receptor mRNA and protein, suggesting that retinoic acid is capable of modulating sensitivity to progestins in human breast cancer cells. Tretinoin 169-182 progesterone receptor Homo sapiens 85-87
11733135-8 2001 Most notably, AhR, HNF-3 and N-Oct3 have already been shown to respond to RA treatment of EC cells, while E47, HNF-3, MAZ, N-Oct3 and Pit-1a have been implicated in embryonic, muscle or neural development. Tretinoin 74-76 aryl hydrocarbon receptor Homo sapiens 14-17
11698455-3 2001 In retinoic acid-differentiated HL-60 cells, cross-linking of FcgammaRs resulted in a marked increase in the tyrosine phosphorylation of FcgammaRIIa, p58(lyn), and p120(c-cbl), which was inhibited by a specific inhibitor of Src family protein tyrosine kinases. Tretinoin 3-16 catenin delta 1 Homo sapiens 164-168
1967595-7 1990 RA treatment (I microM, 6 days) decreased TGase activity by more than 50% in 3 (UMSCC-10A, -22B and 1483) of the 7 cell lines, and the effect on UMSCC-22B was dose-dependent. Tretinoin 0-2 coagulation factor XIII B chain Homo sapiens 42-47
1967595-8 1990 Type II TGase (soluble, tissue type) activity was detected in 3 cell lines, and after RA treatment its activity increased in HNSCC 1483 and 183 cells and decreased in UMSCC-19. Tretinoin 86-88 coagulation factor XIII B chain Homo sapiens 8-13
2295835-3 1990 Treatment of cells for 24 h resulted in a dose-dependent decrease in ODC mRNA levels, with an estimated IC50 of approximately 1 X 10(-8) M for all-trans- and 13-cis-retinoic acid, while Ro15-0778 was somewhat less effective (IC50 approximately 1-5 X 10(-7) M). Tretinoin 164-178 ornithine decarboxylase 1 Homo sapiens 69-72
2164349-2 1990 RA inhibition of cell invasive potential was accompanied by a significant increase in specific high affinity cellular retinoic acid binding protein (CRABP) level. Tretinoin 0-2 cellular retinoic acid binding protein 1 Homo sapiens 109-147
2164349-2 1990 RA inhibition of cell invasive potential was accompanied by a significant increase in specific high affinity cellular retinoic acid binding protein (CRABP) level. Tretinoin 0-2 cellular retinoic acid binding protein 1 Homo sapiens 149-154
2108933-5 1990 These effects of RA and NMF were preceded by a marked enhancement of c-raf expression which became evident 6 and 12 hr after exposure to RA and NMF, respectively, and which persisted throughout the observation period of 5 days. Tretinoin 17-19 Raf-1 proto-oncogene, serine/threonine kinase Rattus norvegicus 69-74
2295835-4 1990 The suppression of ODC mRNA levels by retinoids was detectable at approximately 3 h of incubation, with essentially a maximal inhibition at 12 h. Reduced ODC mRNA levels noted after 24 h of incubation with 5 X 10(-7) M all-trans-retinoic acid were accompanied by a reduction in ODC enzyme activity. Tretinoin 219-242 ornithine decarboxylase 1 Homo sapiens 19-22
2295835-7 1990 These findings suggest that suppression of ODC gene expression is not a direct effect of all-trans-retinoic acid, but depends on ongoing protein synthesis. Tretinoin 92-112 ornithine decarboxylase 1 Homo sapiens 43-46
11592949-0 2001 Effects of all-trans retinoic acid on renin-angiotensin system in rats with experimental nephritis. Tretinoin 11-34 renin Rattus norvegicus 38-43
2156569-1 1990 Two different species of cellular retinoic acid binding proteins, CRABP-I and CRABP-II, have been found in neonatal rat pups (Bailey, J. S. and Siu, C.-H. (1988) J. Biol. Tretinoin 34-47 cellular retinoic acid binding protein 1 Rattus norvegicus 66-73
11714638-5 2001 Specific expression of MT5-MMP was observed in the neurons but not in the glial cells when embryonal mouse carcinoma P19 cells were differentiated in vitro by retinoic acid treatment. Tretinoin 159-172 matrix metallopeptidase 24 Mus musculus 23-30
2110861-3 1990 RA treatment dramatically increased the incorporation of the labeled monosaccharides into one glycoprotein of Mr 160,000 (gp160), which has been previously implicated in the growth-inhibitory effect of RA on these cells. Tretinoin 0-2 leucyl/cystinyl aminopeptidase Mus musculus 122-127
2126321-0 1990 Inhibition of the activity of human leukocyte elastase by lipids particularly oleic acid and retinoic acid. Tretinoin 93-106 elastase, neutrophil expressed Homo sapiens 36-54
2126321-5 1990 In vivo studies of an emphysema model in mice indicated that intrapulmonary instillation of oleic or retinoic acid reduced lung injury caused by human leukocyte elastase. Tretinoin 101-114 elastase, neutrophil expressed Homo sapiens 151-169
32796005-10 2020 Forced expression of SHANK2 in neuroblastoma cells resulted in significant growth inhibition (P=2.6x10-2 to 3.4x10-5) and accelerated neuronal differentiation following treatment with all-trans retinoic acid (P=3.1x10-13 to 2.4x10-30). Tretinoin 194-207 SH3 and multiple ankyrin repeat domains 2 Homo sapiens 21-27
31308194-12 2019 Here we show that exposure to valproic acid (VPA) downregulates TrkB expression and functional activity in retinoic acid-differentiated human neuroblastoma cell lines and primary mouse cortical neurons. Tretinoin 107-120 neurotrophic receptor tyrosine kinase 2 Homo sapiens 64-68
11722589-0 2001 Binding of retinoic acid by the inhibitory serpin protein C inhibitor. Tretinoin 11-24 serpin family A member 5 Homo sapiens 50-69
11722589-6 2001 Intact and protease-cleaved PCI bound retinoic acid equally well, and retinoic acid did not influence inhibition of tissue kallikrein by PCI. Tretinoin 38-51 serpin family A member 5 Homo sapiens 28-31
2152965-3 1990 In the presence of RA, cyclic AMP analogs also greatly reduced the RAR alpha and RAR gamma mRNA levels, even though cyclic AMP analogs alone did not alter these mRNA levels. Tretinoin 19-21 retinoic acid receptor gamma Homo sapiens 81-90
11722589-7 2001 Gel filtration confirmed binding of retinoic acid to PCI in purified systems and suggested that PCI may also function as a retinoic acid-binding protein in seminal plasma. Tretinoin 36-49 serpin family A member 5 Homo sapiens 53-56
30309678-5 2018 mRNA expression of Oct4 and Dazl were downregulated in embryonic stem cells by the retinoic acid group, whereas Mvh transcription was reduced by retinoic acid and estrogen group in these cells compared to the control group. Tretinoin 83-96 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 19-23
2320376-0 1990 Retinoic acid causes a decline in TGF-alpha expression, cloning efficiency, and tumorigenicity in a human embryonal cancer cell line. Tretinoin 0-13 transforming growth factor alpha Homo sapiens 34-43
11722589-7 2001 Gel filtration confirmed binding of retinoic acid to PCI in purified systems and suggested that PCI may also function as a retinoic acid-binding protein in seminal plasma. Tretinoin 36-49 serpin family A member 5 Homo sapiens 96-99
2320376-8 1990 We conclude that TGF-alpha expression inversely correlates with the state of RA-induced differentiation of this human teratocarcinoma cell and that TGF-alpha and EGF proteins are stimulatory growth factors in NT2/D1 cells under these culture conditions. Tretinoin 77-79 transforming growth factor alpha Homo sapiens 17-26
26701854-1 2016 BACKGROUND & AIMS: All-trans Retinoic acid (RA) regulates hepatic lipid and bile acid homeostasis. Tretinoin 33-46 glucosidase beta 2 Mus musculus 80-89
11722589-8 2001 Therefore, our present data, together with the fact that PCI is abundantly expressed in tissues requiring retinoic acid for differentiation processes (e.g. the male reproductive tract, epithelia in various organs), suggest an additional biological role for PCI as a retinoic acid-binding and/or delivering serpin. Tretinoin 106-119 serpin family A member 5 Homo sapiens 57-60
26701854-1 2016 BACKGROUND & AIMS: All-trans Retinoic acid (RA) regulates hepatic lipid and bile acid homeostasis. Tretinoin 48-50 glucosidase beta 2 Mus musculus 80-89
12031254-7 2001 LRAT induction was dependent upon retinoic acid, while that of ARAT was dependent upon the overall induction of the fat storing phenotype. Tretinoin 34-47 lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) Mus musculus 0-4
34525250-2 2022 In a previous study, we identified a heterozygous truncating variant in nuclear receptor-interacting protein 1 (NRIP1) as CAKUT causing via dysregulation of retinoic acid signaling. Tretinoin 157-170 nuclear receptor interacting protein 1 Homo sapiens 72-110
34525250-2 2022 In a previous study, we identified a heterozygous truncating variant in nuclear receptor-interacting protein 1 (NRIP1) as CAKUT causing via dysregulation of retinoic acid signaling. Tretinoin 157-170 nuclear receptor interacting protein 1 Homo sapiens 112-117
11483862-1 2001 4-HPR (fenretinide) is a synthetic analog of retinoic acid (RA) whose potential as a chemopreventative agent has gained support from in vitro and animal experiments and in limited clinical trials. Tretinoin 45-58 haptoglobin-related protein Homo sapiens 2-5
34936504-10 2022 Dual-luciferase reporter assay and electrophoretic mobility shift assay showed that NR1D1 inhibited Atg5 transcription by binding to two putative retinoic acid-related orphan receptor response elements within the promoter. Tretinoin 146-159 autophagy related 5 Mus musculus 100-104
11483862-1 2001 4-HPR (fenretinide) is a synthetic analog of retinoic acid (RA) whose potential as a chemopreventative agent has gained support from in vitro and animal experiments and in limited clinical trials. Tretinoin 60-62 haptoglobin-related protein Homo sapiens 2-5
34954205-9 2022 Using our cell model, with Ca2+ supplementation and PAX6 knockdown with siRNA treatment against PAX6, we provide evidence that haploinsufficiency of the master regulatory gene PAX6 contributes to differentiation defect in the corneal epithelium through alterations of RA signalling. Tretinoin 268-270 paired box 6 Homo sapiens 176-180
34632533-0 2022 Protective effects of all-trans retinoic acid against gastric premalignant lesions by repressing exosomal LncHOXA10-pyruvate carboxylase axis. Tretinoin 22-45 homeobox A10 Homo sapiens 106-115
34632533-9 2022 ATRA also ameliorated the deterioration of GPL and prevented the malignant progression of GPL by reducing exosomal LncHOXA10 and PC expression. Tretinoin 0-4 homeobox A10 Homo sapiens 115-124
11566180-5 2001 In this study, we screened the specific genes expressed in the course of differentiation of HL-60 cells, and demonstrated that ASB-2, one of the ASB proteins, was rapidly induced by all-trans retinoic acid (ATRA). Tretinoin 192-205 ankyrin repeat and SOCS box containing 2 Homo sapiens 127-132
34632533-10 2022 CONCLUSIONS: Collectively, the LncHOXA10-PC axis participated in the early stage of GC tumorigenesis, and ATRA might be useful to prevent GPL from developing into GC because it targets this axis. Tretinoin 106-110 homeobox A10 Homo sapiens 31-40
34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin 38-51 retinoic acid receptor gamma Homo sapiens 134-137
34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin 53-55 retinoic acid receptor gamma Homo sapiens 134-137
34537259-8 2021 The expression levels of retinoic acid inducible gene I (RIG-I), melanoma differentiation-associated gene-5(MDA5), Toll-like receptor3(TLR3) and interferon regulatory Factor 3(IRF3), as well as IFNalpha and IFNbeta, were increased in parallel with MxA upregulation. Tretinoin 25-38 MX dynamin like GTPase 1 Homo sapiens 248-251
11566180-5 2001 In this study, we screened the specific genes expressed in the course of differentiation of HL-60 cells, and demonstrated that ASB-2, one of the ASB proteins, was rapidly induced by all-trans retinoic acid (ATRA). Tretinoin 192-205 5'-aminolevulinate synthase 2 Homo sapiens 127-130
11566180-5 2001 In this study, we screened the specific genes expressed in the course of differentiation of HL-60 cells, and demonstrated that ASB-2, one of the ASB proteins, was rapidly induced by all-trans retinoic acid (ATRA). Tretinoin 207-211 ankyrin repeat and SOCS box containing 2 Homo sapiens 127-132
11566180-5 2001 In this study, we screened the specific genes expressed in the course of differentiation of HL-60 cells, and demonstrated that ASB-2, one of the ASB proteins, was rapidly induced by all-trans retinoic acid (ATRA). Tretinoin 207-211 5'-aminolevulinate synthase 2 Homo sapiens 127-130
34723340-2 2021 Here, we report enhancer architecture-dependent multilayered transcriptional regulation at the Halr1-Hoxa1 locus that orchestrates retinoic acid (RA) signaling-induced early lineage differentiation of ESCs. Tretinoin 131-144 homeobox A1 Homo sapiens 101-106
34811400-8 2021 Finally, ATAC-seq data unveiled the role of the RAR-direct targets Hnf1ba and Gata6 in opening chromatin at many regulatory loci upon RA treatment. Tretinoin 134-136 HNF1 homeobox Ba Danio rerio 67-73
34811400-8 2021 Finally, ATAC-seq data unveiled the role of the RAR-direct targets Hnf1ba and Gata6 in opening chromatin at many regulatory loci upon RA treatment. Tretinoin 134-136 GATA binding protein 6 Mus musculus 78-83
34723340-2 2021 Here, we report enhancer architecture-dependent multilayered transcriptional regulation at the Halr1-Hoxa1 locus that orchestrates retinoic acid (RA) signaling-induced early lineage differentiation of ESCs. Tretinoin 146-148 homeobox A1 Homo sapiens 101-106
11438548-5 2001 Furthermore, it was determined that expression of exogenous TGase in cells exhibited enhanced GTP binding and transamidation activities and mimicked the survival advantage imparted by RA. Tretinoin 184-186 transglutaminase 1 Homo sapiens 60-65
34723340-4 2021 Chromosome conformation capture-based screens indicate that RA signaling promotes enhancer interactions essential for Hoxa1 and Halr1 expression and mesendoderm differentiation of ESCs. Tretinoin 60-62 homeobox A1 Homo sapiens 118-123
34723340-5 2021 Furthermore, the results also show that HOXA1 promotes expression of Halr1 through binding to enhancer; conversely, loss of Halr1 enhances interaction between Hoxa1 chromatin and four distal enhancers but weakens interaction with chromatin inside the HoxA cluster, leading to RA signaling-induced Hoxa1 overactivation and enhanced endoderm differentiation. Tretinoin 276-278 homeobox A1 Homo sapiens 40-45
34723340-5 2021 Furthermore, the results also show that HOXA1 promotes expression of Halr1 through binding to enhancer; conversely, loss of Halr1 enhances interaction between Hoxa1 chromatin and four distal enhancers but weakens interaction with chromatin inside the HoxA cluster, leading to RA signaling-induced Hoxa1 overactivation and enhanced endoderm differentiation. Tretinoin 276-278 homeobox A1 Homo sapiens 159-164
34723340-5 2021 Furthermore, the results also show that HOXA1 promotes expression of Halr1 through binding to enhancer; conversely, loss of Halr1 enhances interaction between Hoxa1 chromatin and four distal enhancers but weakens interaction with chromatin inside the HoxA cluster, leading to RA signaling-induced Hoxa1 overactivation and enhanced endoderm differentiation. Tretinoin 276-278 homeobox A cluster Homo sapiens 251-255
34723340-5 2021 Furthermore, the results also show that HOXA1 promotes expression of Halr1 through binding to enhancer; conversely, loss of Halr1 enhances interaction between Hoxa1 chromatin and four distal enhancers but weakens interaction with chromatin inside the HoxA cluster, leading to RA signaling-induced Hoxa1 overactivation and enhanced endoderm differentiation. Tretinoin 276-278 homeobox A1 Homo sapiens 297-302
34775955-11 2021 Furthermore, our results revealed that CRBP-1 could increase the intracellular levels of retinoic acid, which induced the activation of RARs/RXRs leading to the transcriptional expression of WIF1, a secreted antagonist of the Wnt/beta-catenin signaling pathway, by physically interacting with the region on WIF1 promoter. Tretinoin 89-102 retinol binding protein 1 Homo sapiens 39-45
11574166-10 2001 We found that IP(3)R3 gene expression was repressed in retinoic acid-treated and neural differentiated P19 mouse embryonic carcinoma cells. Tretinoin 55-68 inositol 1,4,5-triphosphate receptor 3 Mus musculus 14-21
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 4-8 retinoic acid receptor gamma Homo sapiens 74-83
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 137-141 retinoic acid receptor gamma Homo sapiens 74-83
34543639-0 2021 Regulation of inflammation and COX-2 gene expression in benzo (a) pyrene induced lung carcinogenesis in mice by all trans retinoic acid (ATRA). Tretinoin 116-135 cytochrome c oxidase II, mitochondrial Mus musculus 31-36
34543639-0 2021 Regulation of inflammation and COX-2 gene expression in benzo (a) pyrene induced lung carcinogenesis in mice by all trans retinoic acid (ATRA). Tretinoin 137-141 cytochrome c oxidase II, mitochondrial Mus musculus 31-36
34543639-12 2021 SIGNIFICANCE: The ATRA has decreased the inflammatory condition with downregulation of COX-2 gene expression and thereby prevented carcinogenesis during early stage of B(a)P induced cancer development. Tretinoin 18-22 cytochrome c oxidase II, mitochondrial Mus musculus 87-92
11520943-3 2001 The present study shows that atRA can also potentiate the survival and neurite outgrowth-promoting activities of NT-3. Tretinoin 29-33 neurotrophin 3 Gallus gallus 113-117
34147602-6 2021 Via chip-qPCR and RT-qPCR, genes involved in lipid metabolism and cell proliferation were target genes of RARalpha/RXRalpha in small intestinal organoids treated with RA and lipid micelles. Tretinoin 167-169 retinoid X receptor alpha Mus musculus 115-123
34643182-3 2021 Here using Xenopus and mouse embryos, we establish molecular links between Tbx5 and retinoic acid (RA)-signaling in the mesoderm and between RA signaling and sonic hedgehog expression in the endoderm to unveil a conserved RA-Hedgehog-Wnt signaling cascade coordinating cardiopulmonary development. Tretinoin 84-97 T-box 5 Mus musculus 75-79
11520943-5 2001 atRA also enhanced neurite outgrowth of the NT-3-treated cells; however, the neurites appeared thicker and less branched than cells treated with atRA in combination with NGF. Tretinoin 0-4 neurotrophin 3 Gallus gallus 44-48
34643182-3 2021 Here using Xenopus and mouse embryos, we establish molecular links between Tbx5 and retinoic acid (RA)-signaling in the mesoderm and between RA signaling and sonic hedgehog expression in the endoderm to unveil a conserved RA-Hedgehog-Wnt signaling cascade coordinating cardiopulmonary development. Tretinoin 99-101 T-box 5 Mus musculus 75-79
34643182-3 2021 Here using Xenopus and mouse embryos, we establish molecular links between Tbx5 and retinoic acid (RA)-signaling in the mesoderm and between RA signaling and sonic hedgehog expression in the endoderm to unveil a conserved RA-Hedgehog-Wnt signaling cascade coordinating cardiopulmonary development. Tretinoin 141-143 wingless-type MMTV integration site family, member 2 Mus musculus 234-237
11520943-7 2001 The atRA-induced increase in trkA mRNA may play a role in the enhanced survival of neurons cultured in the presence of either NGF or NT-3, as both neurotrophins have been shown to signal through this receptor. Tretinoin 4-8 neurotrophin 3 Gallus gallus 133-137
34643182-3 2021 Here using Xenopus and mouse embryos, we establish molecular links between Tbx5 and retinoic acid (RA)-signaling in the mesoderm and between RA signaling and sonic hedgehog expression in the endoderm to unveil a conserved RA-Hedgehog-Wnt signaling cascade coordinating cardiopulmonary development. Tretinoin 222-224 wingless-type MMTV integration site family, member 2 Mus musculus 234-237
34643182-5 2021 Tbx5 promotes posterior second heart field identity in a positive feedback loop with RA, antagonizing a Fgf8-Cyp regulatory module to restrict FGF activity to the anterior. Tretinoin 85-87 T-box 5 Mus musculus 0-4
34687254-6 2022 Alcohol intake led to increases in hepatic centrilobular levels of ALDH1A1, a rate-limiting enzyme in RA synthesis, and co-localization of ALDH1A1 with the alcohol-metabolizing enzyme CYP2E1, and 4-HNE, a marker of oxidative stress; expression of these targets was abrogated in mice co-treated with AC261 and alcohol. Tretinoin 102-104 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 67-74
34643182-5 2021 Tbx5 promotes posterior second heart field identity in a positive feedback loop with RA, antagonizing a Fgf8-Cyp regulatory module to restrict FGF activity to the anterior. Tretinoin 85-87 peptidyl-prolyl isomerase G (cyclophilin G) Mus musculus 109-112
11520943-9 2001 Thus, during development, atRA may play a role in fine-tuning embryonic responsiveness to both NT-3 and NGF. Tretinoin 26-30 neurotrophin 3 Gallus gallus 95-99
34643182-6 2021 We find that Tbx5/Aldh1a2-dependent RA signaling directly activates shh transcription in the adjacent foregut endoderm through a conserved MACS1 enhancer. Tretinoin 36-38 T-box 5 Mus musculus 13-17
11699639-0 2001 Phase-independent inhibition by retinoic acid of mineralization correlated with loss of tetranectin expression in a human osteoblastic cell line. Tretinoin 32-45 C-type lectin domain family 3 member B Homo sapiens 88-99
34643182-6 2021 We find that Tbx5/Aldh1a2-dependent RA signaling directly activates shh transcription in the adjacent foregut endoderm through a conserved MACS1 enhancer. Tretinoin 36-38 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 18-25
34599305-6 2021 Genetic deletions in mice revealed that retinoic acid signalling through the retinoic acid receptors RXRG and RARB, as well as CYP26B1-dependent catabolism, are involved in proper molecular patterning of prefrontal and motor areas, development of PFC-mediodorsal thalamus connectivity, intra-PFC dendritic spinogenesis and expression of the layer 4 marker RORB. Tretinoin 40-53 retinoic acid receptor, beta Mus musculus 110-114
34599305-6 2021 Genetic deletions in mice revealed that retinoic acid signalling through the retinoic acid receptors RXRG and RARB, as well as CYP26B1-dependent catabolism, are involved in proper molecular patterning of prefrontal and motor areas, development of PFC-mediodorsal thalamus connectivity, intra-PFC dendritic spinogenesis and expression of the layer 4 marker RORB. Tretinoin 40-53 RAR-related orphan receptor beta Mus musculus 356-360
34660779-4 2021 Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels. Tretinoin 23-27 caspase 8 Homo sapiens 110-119
34696339-2 2021 NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). Tretinoin 110-123 tripartite motif containing 25 Homo sapiens 229-235
34733553-13 2021 ACE2 expression slightly increased in CRL-127 post RA-treatment. Tretinoin 51-53 angiotensin converting enzyme 2 Homo sapiens 0-4
11699639-2 2001 In this study, we show that this inhibitory effect on alkaline phosphatase activity depends on the stage of cell differentiation; however, expression of tetranectin, which is a recently reported bone matrix protein, was completely inhibited by treatment with retinoic acid, irrespective of the stage of cell differentiation. Tretinoin 259-272 C-type lectin domain family 3 member B Homo sapiens 153-164
34417575-0 2021 All-trans retinoic acid impairs glucose-stimulated insulin secretion by activating the RXR/SREBP-1c/UCP2 pathway. Tretinoin 0-23 sterol regulatory element binding transcription factor 1 Rattus norvegicus 91-99
11699639-4 2001 To our knowledge, this is the first report that retinoic acid downregulates the tetranectin expression in human osteoblastic cells independent of the stage of cell differentiation, and is correlated with inhibition of mineralization. Tretinoin 48-61 C-type lectin domain family 3 member B Homo sapiens 80-91
34417575-5 2021 Importantly, ATRA impaired glucose-stimulated insulin secretion (GSIS) and increased the expression of sterol regulatory element-binding protein 1c (SREBP-1c) and uncoupling protein 2 (UCP2) in the rat pancreas. Tretinoin 13-17 sterol regulatory element binding transcription factor 1 Rattus norvegicus 103-147
11481496-7 2001 Inhibition of DNA synthesis by RA is significantly more rapid in SH-F than in SH-N. SH-F, which expresses basal amounts of p16(INK4A), responds to RA with elevation of p18(INK4C), marked down-regulation of cyclin D1, and swift inhibition of cyclin D-dependent kinases (cdks). Tretinoin 31-33 cyclin D1 Homo sapiens 206-215
34417575-5 2021 Importantly, ATRA impaired glucose-stimulated insulin secretion (GSIS) and increased the expression of sterol regulatory element-binding protein 1c (SREBP-1c) and uncoupling protein 2 (UCP2) in the rat pancreas. Tretinoin 13-17 sterol regulatory element binding transcription factor 1 Rattus norvegicus 149-157
34282811-7 2021 LP22A3 induced TGF-beta secretion from the IECs of the small intestine with retinoic acid production probably through TLR2, resulting in an increase in CD103+ DCs and the Foxp3+ Treg population. Tretinoin 76-89 toll-like receptor 2 Mus musculus 118-122
11451739-7 2001 tRA-induced apoptosis associated with an increased ratio of bax to bcl-2 by bax overexpression and cleavage of caspase-3. Tretinoin 0-3 caspase 3 Rattus norvegicus 111-120
34349281-2 2021 This protocol first induces definitive endoderm by treatment with Activin A and CHIR99021, then generates PDX1+/NKX6-1+ pancreatic progenitors through the timed application of keratinocyte growth factor, SANT1, TPPB, LDN193189 and retinoic acid. Tretinoin 231-244 pancreatic and duodenal homeobox 1 Homo sapiens 106-110
34381436-4 2021 After maternal ATRA administration, Hoxa1-/- neonatal piglets had significantly higher diversity and species richness, higher relative abundances of two bacterial phyla (Bacteroidetes and Proteobacteria), and lower relative abundances of phylum Firmicutes and genus Lactobacillus in the jejunum than non-Hoxa1-/- neonatal piglets. Tretinoin 15-19 homeobox A1 Sus scrofa 36-41
34381436-5 2021 Hoxa1-/- neonatal piglets delivered by sows with maternal ATRA administration had lower diversity and species richness and higher relative abundance of phylum Firmicutes in the jejunum than Hoxa1-/- neonatal piglets born by sows with no maternal ATRA administration. Tretinoin 58-62 homeobox A1 Sus scrofa 0-5
34381436-6 2021 Non-Hoxa1-/- neonatal piglets delivered by sows with maternal ATRA administration had higher diversity and species richness and significantly lower relative abundances of phyla Firmicutes and Actinobacteria and genus Lactobacillus in the ileum than non-Hoxa1-/- neonatal piglets born by sows with no maternal ATRA administration. Tretinoin 62-66 homeobox A1 Sus scrofa 4-9
34381436-9 2021 Hoxa1 mutation resulted in bacterial dysbiosis of the small intestine of Hoaxa1-/- neonatal piglets, and maternal ATRA administration restored the bacterial dysbiosis of Hoxa1-/- neonatal piglets and altered the bacterial composition of the small intestine of non-Hoxa1-/- neonatal piglets. Tretinoin 114-118 homeobox A1 Sus scrofa 170-175
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 145-158 surfactant protein B Homo sapiens 184-188
34381436-9 2021 Hoxa1 mutation resulted in bacterial dysbiosis of the small intestine of Hoaxa1-/- neonatal piglets, and maternal ATRA administration restored the bacterial dysbiosis of Hoxa1-/- neonatal piglets and altered the bacterial composition of the small intestine of non-Hoxa1-/- neonatal piglets. Tretinoin 114-118 homeobox A1 Sus scrofa 264-269
34452533-7 2021 Further, we showed the anti-SARS-CoV-2 effect of ATRA on the currently circulating variants of concern (VOC); alpha, beta, gamma, and delta. Tretinoin 49-53 beta, gamma, and delta None 117-139
11274148-3 2001 Clustered retinoic acid-responsive element and TTF-1 binding sites were identified in the enhancer region of the SP-B gene and were required for retinoic acid stimulation of the human SP-B (hSP-B) promoter. Tretinoin 145-158 surfactant protein B Homo sapiens 190-195
11274148-9 2001 RAR DBD greatly enhanced TTF-1 homeodomain DNA binding activity to a hSP-B enhancer oligonucleotide, in which retinoic acid-responsive element and TTF-1 DNA binding sites overlap. Tretinoin 110-123 surfactant protein B Homo sapiens 69-74
34381436-0 2021 Administration of All-Trans Retinoic Acid to Pregnant Sows Alters Gut Bacterial Community of Neonatal Piglets With Different Hoxa1 Genotypes. Tretinoin 18-41 homeobox A1 Sus scrofa 125-130
34381436-1 2021 Administration of all-trans retinoic acid (ATRA) to pregnant sows improves developmental defects of Hoxa1-/- fetal pigs, and this study aimed to explore the influence of maternal ATRA administration during pregnancy on gut microbiota of neonatal piglets. Tretinoin 18-41 homeobox A1 Sus scrofa 100-105
34381436-1 2021 Administration of all-trans retinoic acid (ATRA) to pregnant sows improves developmental defects of Hoxa1-/- fetal pigs, and this study aimed to explore the influence of maternal ATRA administration during pregnancy on gut microbiota of neonatal piglets. Tretinoin 43-47 homeobox A1 Sus scrofa 100-105
34335757-0 2021 All-Trans Retinoic Acid Enhances Chemosensitivity to 5-FU by Targeting miR-378c/E2F7 Axis in Colorectal Cancer. Tretinoin 10-23 microRNA 378c Homo sapiens 71-79
34335757-0 2021 All-Trans Retinoic Acid Enhances Chemosensitivity to 5-FU by Targeting miR-378c/E2F7 Axis in Colorectal Cancer. Tretinoin 10-23 E2F transcription factor 7 Homo sapiens 80-84
34335757-7 2021 Additionally, treatment of 5-FU combined with ATRA could increase miR-378c expression, whereas it decreased the expression of E2F7. Tretinoin 46-50 microRNA 378c Homo sapiens 66-74
11274148-10 2001 Chromatin immunoprecipitation assay demonstrated that retinoic acid treatment of H441 cells greatly stimulated both RAR and TTF-1 DNA binding to the hSP-B enhancer region in H441 cells. Tretinoin 54-67 surfactant protein B Homo sapiens 149-154
34335757-7 2021 Additionally, treatment of 5-FU combined with ATRA could increase miR-378c expression, whereas it decreased the expression of E2F7. Tretinoin 46-50 E2F transcription factor 7 Homo sapiens 126-130
34335757-9 2021 Furthermore, miR-378c inhibitor or vector with E2F7 partially counteracted the effects of 5-FU combined with ATRA on viability, migration, invasion, and apoptosis of HCT116 cells. Tretinoin 109-113 microRNA 378c Homo sapiens 13-21
34335757-9 2021 Furthermore, miR-378c inhibitor or vector with E2F7 partially counteracted the effects of 5-FU combined with ATRA on viability, migration, invasion, and apoptosis of HCT116 cells. Tretinoin 109-113 E2F transcription factor 7 Homo sapiens 47-51
34178974-5 2021 Notably, we found that excessive atRA upregulated the expression of miR-124-3p, but not of miR-27a-3p and miR-27b-3p, in both in vivo and in vitro. Tretinoin 33-37 microRNA 124a-3 Mus musculus 68-78
34178974-6 2021 Importantly, treatment with a specific inhibitor for miR-124-3p restored decreased cell proliferation through the normalization of target gene expression in atRA-treated MEPM cells and atRA-exposed mouse embryos, resulting in the rescue of CP in mice. Tretinoin 157-161 microRNA 124a-3 Mus musculus 53-63
34178974-6 2021 Importantly, treatment with a specific inhibitor for miR-124-3p restored decreased cell proliferation through the normalization of target gene expression in atRA-treated MEPM cells and atRA-exposed mouse embryos, resulting in the rescue of CP in mice. Tretinoin 185-189 microRNA 124a-3 Mus musculus 53-63
34178974-7 2021 Taken together, our results indicate that atRA causes CP through the induction of miR-124-3p in mice. Tretinoin 42-46 microRNA 124a-3 Mus musculus 82-92
11397002-7 2001 The reduction in PECAM-1 transcripts in retinoic acid-induced differentiation of F9 teratocarcinoma cells, a model of epiblast-to-primitive endoderm differentiation, confirmed the epiblast-specific expression of PECAM-1. Tretinoin 40-53 platelet/endothelial cell adhesion molecule 1 Mus musculus 17-24
34085926-5 2021 Mechanistically, Rela deletion suppresses expression of Aldh1a1, an enzyme required for retinoic acid synthesis from vitamin A. Tretinoin 88-101 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 56-63
34236140-0 2021 All-trans retinoic acid induces leukemia resistance to NK cell cytotoxicity by down-regulating B7-H6 expression via c-Myc signaling. Tretinoin 3-23 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 95-100
34236140-3 2021 In this study, we investigated the regulation of B7-H6 by all-trans retinoic acid (atRA), a terminal differentiation inducer of tumor cells that is extensively used for clinical leukemia therapy. Tretinoin 61-81 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 49-54
11397002-7 2001 The reduction in PECAM-1 transcripts in retinoic acid-induced differentiation of F9 teratocarcinoma cells, a model of epiblast-to-primitive endoderm differentiation, confirmed the epiblast-specific expression of PECAM-1. Tretinoin 40-53 platelet/endothelial cell adhesion molecule 1 Mus musculus 212-219
34236140-3 2021 In this study, we investigated the regulation of B7-H6 by all-trans retinoic acid (atRA), a terminal differentiation inducer of tumor cells that is extensively used for clinical leukemia therapy. Tretinoin 83-87 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 49-54
34236140-5 2021 We evaluated the effect of atRA treatment on the expression of B7-H6 using real-time PCR, flow cytometry and western blotting. Tretinoin 27-31 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 63-68
11278854-9 2001 We found that mutation of the SOX/OCT site and targeted inactivation of Hoxa1 both impair the response of the b1-ARE to retinoic acid in transgenic mice. Tretinoin 120-133 quiescin Q6 sulfhydryl oxidase 1 Mus musculus 30-33
34236140-6 2021 We used CRISPR/Cas9 to knockdown B7-H6 expression and siRNA to knockdown c-Myc in U-937 cells to evaluate the role of B7-H6 and c-Myc in atRA-induced tumor resistance against NK cells. Tretinoin 137-141 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 118-123
34236140-9 2021 atRA treatment induced U-937 resistance to NK cell cytotoxicity by reducing B7-H6 expression, and showed no effect on NK cytotoxicity against B7-H6 knockdown U-937 cells. Tretinoin 0-4 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 76-81
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 C-C motif chemokine receptor 9 Homo sapiens 119-123
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 forkhead box P3 Homo sapiens 130-135
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 forkhead box P3 Homo sapiens 250-255
34236140-11 2021 On the other hand, atRA treatment reduced c-Myc expression, which in turn inhibited the transcription of B7-H6 on leukemia cells. Tretinoin 19-23 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 105-110
34236140-12 2021 CONCLUSION: atRA treatment promotes tumor cell resistance against NK cell-mediated lysis by down-regulating B7-H6 expression via the c-Myc signaling pathway, suggesting that more attention needs to be paid to the immunological adverse effects in the clinical use of atRA treatment. Tretinoin 12-16 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 108-113
11278854-9 2001 We found that mutation of the SOX/OCT site and targeted inactivation of Hoxa1 both impair the response of the b1-ARE to retinoic acid in transgenic mice. Tretinoin 120-133 plexin A2 Mus musculus 34-37
34236140-12 2021 CONCLUSION: atRA treatment promotes tumor cell resistance against NK cell-mediated lysis by down-regulating B7-H6 expression via the c-Myc signaling pathway, suggesting that more attention needs to be paid to the immunological adverse effects in the clinical use of atRA treatment. Tretinoin 266-270 natural killer cell cytotoxicity receptor 3 ligand 1 Homo sapiens 108-113
35550944-7 2022 Retinoic acid mainly regulates 3" HOX/Hox paralogs but may also modify the expression of downstream HOX/Hox genes, including HOXA/Hoxa10. Tretinoin 0-13 homeobox A cluster Homo sapiens 125-129
35550944-7 2022 Retinoic acid mainly regulates 3" HOX/Hox paralogs but may also modify the expression of downstream HOX/Hox genes, including HOXA/Hoxa10. Tretinoin 0-13 homeobox A10 Sus scrofa 130-136
35562751-6 2022 In this study, we investigated whether retinoic acid regulates the expression of deubiquitinating enzymes ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in cerebral ischemic injury. Tretinoin 39-52 ubiquitin C-terminal hydrolase L1 Rattus norvegicus 106-145
35562751-16 2022 CONCLUSIONS: These findings suggest that retinoic acid regulates ubiquitin- and proteasome-related proteins including ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in a brain ischemia model. Tretinoin 41-54 ubiquitin C-terminal hydrolase L1 Rattus norvegicus 118-157
35608517-5 2022 Results obtained with talarozole, a specific CYP26A1 inhibitor, and ketoconazole, a generalist inhibitor of cytochrome-P450 enzymes, revealed that CYP26A1 is mainly responsible for retinoic acid catabolism in ZFL but not PLHC-1 cells. Tretinoin 181-194 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 45-52
35562751-16 2022 CONCLUSIONS: These findings suggest that retinoic acid regulates ubiquitin- and proteasome-related proteins including ubiquitin carboxy-terminal hydrolase L1, ubiquitin thioesterase OTUB1, and proteasome subunit alpha types 1 and 3 in a brain ischemia model. Tretinoin 41-54 proteasome 20S subunit alpha 1 Rattus norvegicus 193-231
35608517-5 2022 Results obtained with talarozole, a specific CYP26A1 inhibitor, and ketoconazole, a generalist inhibitor of cytochrome-P450 enzymes, revealed that CYP26A1 is mainly responsible for retinoic acid catabolism in ZFL but not PLHC-1 cells. Tretinoin 181-194 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 147-154
11278854-9 2001 We found that mutation of the SOX/OCT site and targeted inactivation of Hoxa1 both impair the response of the b1-ARE to retinoic acid in transgenic mice. Tretinoin 120-133 homeobox A1 Mus musculus 72-77
35545255-6 2022 In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner. Tretinoin 37-41 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 125-131
11278854-10 2001 Our results show that Hoxa1 is the primary mediator of the response of b1-ARE to retinoic acid in vivo and that this function is dependent on the binding of SOX/OCT heterodimers to the b1-ARE. Tretinoin 81-94 homeobox A1 Mus musculus 22-27
11278854-10 2001 Our results show that Hoxa1 is the primary mediator of the response of b1-ARE to retinoic acid in vivo and that this function is dependent on the binding of SOX/OCT heterodimers to the b1-ARE. Tretinoin 81-94 quiescin Q6 sulfhydryl oxidase 1 Mus musculus 157-160
11278854-10 2001 Our results show that Hoxa1 is the primary mediator of the response of b1-ARE to retinoic acid in vivo and that this function is dependent on the binding of SOX/OCT heterodimers to the b1-ARE. Tretinoin 81-94 plexin A2 Mus musculus 161-164
35077967-6 2022 Of these, (10)-gingerol, angelicin, corticosterone, eupatilin, etofenprox, oxadixyl, and tretinoin were identified as novel AhR agonists. Tretinoin 89-98 aryl hydrocarbon receptor Homo sapiens 124-127
11394905-3 2001 Culturing retinoic acid treated ES cells in the presence of the osteogenic supplements ascorbic acid and beta-glycerophosphate resulted in the expression of several osteoblast marker genes, osteocalcin, alkaline phosphatase, and osteopontin. Tretinoin 10-23 secreted phosphoprotein 1 Mus musculus 229-240
35420127-5 2022 We have previously reported that a miR-124-3p inhibitor can also partially rescue the CP phenotype in atRA-induced CP mouse model. Tretinoin 102-106 microRNA 124a-3 Mus musculus 35-45
35420127-6 2022 In this study, we found that a cocktail of miR-124-3p and miR-340-5p inhibitors rescued atRA-induced CP with almost complete penetrance. Tretinoin 88-92 microRNA 124a-3 Mus musculus 43-53
35526247-4 2022 This study was conducted to determine whether HMGB1 polymorphisms (rs1360485, rs2249825 and rs1060348) are associated with the incidence of differentiation syndrome in acute promyelocytic leukemia patients treated with all-trans retinoic acid and arsenic trioxide. Tretinoin 219-242 high mobility group box 1 Homo sapiens 46-51
35523143-4 2022 Ablating PDGFRalpha in the LTBR stromal lineage demonstrates that PDGFRalpha has a major impact on the lineage fate and function, inducing a transcriptomic switch from prostemness genes, such as Rspo3 and Grem1, to prodifferentiation factors, including BMPs, retinoic acid, and laminins, and on spatial organization within the crypt-villus and repair responses. Tretinoin 259-272 lymphotoxin B receptor Mus musculus 27-31
11558869-8 2001 Five out of 6 patients with KRT10 mutations benefited from treatment with oral acitretin (5-25mg/day) or topical tretinoin/tazarotene, but none of the patients with KRT1 mutations derived any benefit. Tretinoin 113-122 keratin 1 Homo sapiens 28-32
35565206-5 2022 The cancer cell-CAF interaction in the CIPCO promoted epithelial-mesenchymal transition of cancer cells, which was reversed by CAF inhibition using all-trans retinoic acid. Tretinoin 158-171 lysine acetyltransferase 2B Homo sapiens 16-19
35565206-5 2022 The cancer cell-CAF interaction in the CIPCO promoted epithelial-mesenchymal transition of cancer cells, which was reversed by CAF inhibition using all-trans retinoic acid. Tretinoin 158-171 lysine acetyltransferase 2B Homo sapiens 127-130
35248720-0 2022 Aberrant epigenetic regulation of RARbeta by TET2 is involved in cutaneous squamous cell carcinoma resistance to retinoic acid. Tretinoin 113-126 tet methylcytosine dioxygenase 2 Homo sapiens 45-49
35248720-11 2022 We upregulated TET2 could reverse promoter hypermethylation and showed a significantly increased expression of RARbeta, which enhanced the sensitivity of tumor cells to retinoic acid treatment. Tretinoin 169-182 tet methylcytosine dioxygenase 2 Homo sapiens 15-19
35248720-13 2022 While reversing the hypermethylation of the RARbeta promoter by recovering the TET2 could enhance tumor cells to be sensitive to retinoic acid. Tretinoin 129-142 tet methylcytosine dioxygenase 2 Homo sapiens 79-83
34982407-5 2022 Two piRNAs, DQ582359 and DQ596268, were increasingly upregulated during the RA-induced differentiation and involved in regulating the expression of neuronal markers, MAP2 and TUBB3. Tretinoin 76-78 tubulin beta 3 class III Homo sapiens 175-180
35086406-8 2022 By immunofluorescence, we verified the positive expression of HSD17B3, GDNF, ACRV-1, and TRIM-36, indicating their differentiation using RA in vitro, reinforcing the possibility of EB in male germ cell differentiation. Tretinoin 137-139 glial cell derived neurotrophic factor Rattus norvegicus 71-75
35086406-8 2022 By immunofluorescence, we verified the positive expression of HSD17B3, GDNF, ACRV-1, and TRIM-36, indicating their differentiation using RA in vitro, reinforcing the possibility of EB in male germ cell differentiation. Tretinoin 137-139 acrosomal vesicle protein 1 Rattus norvegicus 77-83
35086406-8 2022 By immunofluorescence, we verified the positive expression of HSD17B3, GDNF, ACRV-1, and TRIM-36, indicating their differentiation using RA in vitro, reinforcing the possibility of EB in male germ cell differentiation. Tretinoin 137-139 tripartite motif-containing 36 Rattus norvegicus 89-96
35173714-7 2022 ATRA also significantly reversed the reduction of ZO-1 and Occludin protein levels induced by TGEV infection and maintained epithelial barrier integrity. Tretinoin 0-4 occludin Homo sapiens 59-67
35173714-8 2022 Moreover, ATRA treatment significantly prevented the upregulation of IkBalpha and NF-kappaB p65 phosphorylation levels and the nuclear translocation of NF-kB p65 induced by TGEV. Tretinoin 10-14 RELA proto-oncogene, NF-kB subunit Homo sapiens 92-95
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 toll like receptor 3 Homo sapiens 97-101
35154092-8 2022 Here we show that select novel rexinoids act as ATRA mimics, as they cause increased CCR9 and alpha4beta7 expression and enhanced migration to the CCR9 ligand, CCL25 in vitro, even in the absence of ATRA. Tretinoin 48-52 C-C motif chemokine receptor 9 Homo sapiens 85-89
34411225-6 2022 Similar to ATRA, BMS961, a selective RARgamma agonist, could also (re)sensitize MM cells to Cfz in vitro, and both ATRA and BMS961 significantly enhanced the therapeutic effects of Cfz in established MM in vivo. Tretinoin 115-119 retinoic acid receptor gamma Homo sapiens 37-45
35152350-4 2022 Overexpression of UBC9 in Kasumi-1 attenuated myeloid differentiation induced by all-trans retinoic acid, G-CSF, and GM-CSF (AGGM), which was judged by suppression of CD11b. Tretinoin 81-104 ubiquitin conjugating enzyme E2 I Homo sapiens 18-22
35565751-1 2022 Cellular retinoic acid binding proteins (CRABP1 and CRABP2) bind all-trans-retinoic acid (atRA), the active metabolite of vitamin A, with high affinity. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 41-47
35565751-1 2022 Cellular retinoic acid binding proteins (CRABP1 and CRABP2) bind all-trans-retinoic acid (atRA), the active metabolite of vitamin A, with high affinity. Tretinoin 65-88 cellular retinoic acid binding protein 1 Homo sapiens 41-47
35565751-1 2022 Cellular retinoic acid binding proteins (CRABP1 and CRABP2) bind all-trans-retinoic acid (atRA), the active metabolite of vitamin A, with high affinity. Tretinoin 90-94 cellular retinoic acid binding protein 1 Homo sapiens 41-47
35565751-2 2022 CRABP1 and CRABP2 have been shown to interact with the atRA-clearing cytochrome P450 enzymes CYP26B1 and CYP26C1 and with nuclear retinoic acid receptors (RARs). Tretinoin 130-143 cellular retinoic acid binding protein 1 Homo sapiens 0-6
35565751-3 2022 We hypothesized that CRABP1 and CRABP2 also alter atRA metabolism and clearance by CYP26A1, the third key atRA-metabolizing enzyme in the CYP26 family. Tretinoin 50-54 cellular retinoic acid binding protein 1 Homo sapiens 21-27
35565751-6 2022 In comparison, the apparent kcat value was about 30% lower (0.71 +- 0.07 min-1 for holo-CRABP1 and 0.75 +- 0.09 min-1 for holo-CRABP2) in the presence of CRABPs than with free atRA (1.07 +- 0.08 min-1). Tretinoin 176-180 cellular retinoic acid binding protein 1 Homo sapiens 88-94
35493071-9 2022 Rbp7 overexpression significantly increased expression of Raldh1, responsible for RA production, and up-regulation of Lrat and Cyp26a1, involved in retinol storage and RA catabolism, respectively, in 3T3-L1 adipocytes. Tretinoin 82-84 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 58-64
35406141-0 2022 CRABP1 in Non-Canonical Activities of Retinoic Acid in Health and Diseases. Tretinoin 38-51 cellular retinoic acid binding protein 1 Homo sapiens 0-6
35406141-1 2022 In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. Tretinoin 143-156 cellular retinoic acid binding protein 1 Homo sapiens 48-88
35406141-1 2022 In this review, we discuss the emerging role of Cellular Retinoic Acid Binding Protein 1 (CRABP1) as a mediator of non-canonical activities of retinoic acid (RA) and relevance to human diseases. Tretinoin 143-156 cellular retinoic acid binding protein 1 Homo sapiens 90-96
35409392-10 2022 When ALDH1A3 was up regulated by retinoic acid treatment in OMECS, Pax-6 expression was down regulated, suggesting a decrease in regenerative capacity when ALDH enzymes are up regulated. Tretinoin 33-46 paired box 6 Homo sapiens 67-72
35406069-2 2022 Acting through the retinoic acid receptors RARalpha, RARbeta, and RARgamma, all-trans-retinoic acid, an active metabolite of VA, is a potent regulator of numerous biological pathways, including embryonic and somatic cellular differentiation, immune functions, and energy metabolism. Tretinoin 76-99 retinoic acid receptor gamma Homo sapiens 66-74
35402250-8 2022 The positive effects of tretinoin could be extended to ICT antibodies targeting OX40, GITR and CTLA4 monotherapy in multiple cancer models. Tretinoin 24-33 tumor necrosis factor receptor superfamily, member 4 Mus musculus 80-84
35225106-8 2022 Consistently, in the GPL rat model, we observed a similar disorder; however, ATRA supplementation significantly not only corrected the disorder by increasing Rdh10, Aldh1a1 and decreasing Cyp26b1, but also reduced claudin-18 (P < 0.05). Tretinoin 77-81 claudin 18 Rattus norvegicus 214-224
35063128-4 2022 In the absence of the RA-synthesizing enzyme Aldh1a2, a sensitive RA reporter revealed a hitherto unidentified residual RA signaling that specified neural fate. Tretinoin 66-68 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 45-52
35063128-4 2022 In the absence of the RA-synthesizing enzyme Aldh1a2, a sensitive RA reporter revealed a hitherto unidentified residual RA signaling that specified neural fate. Tretinoin 120-122 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 45-52
35197751-6 2022 ATRA also supported ADMSCs by a significant down-regulation of caspase-3, il-6 and TGFbeta1, and a significant up-regulation of HIF1, VEGF and CD31 compared to group of cisplatin which reversed the cisplatin effect. Tretinoin 0-4 caspase 3 Rattus norvegicus 63-72
35204719-4 2022 We employed all-trans-retinoic acid (ATRA) and 2-(3-ethylureido)-6-methylpyridine (UDP-4) to induce neural differentiation of human MSC from the dental apical papilla (SCAP). Tretinoin 12-35 SREBF chaperone Homo sapiens 168-172
35204719-12 2022 Our findings indicate that SCAP can be differentiated into neural-like cells after treatment with ATRA or UDP-4 by exhibiting a disparate pattern of differentiation. Tretinoin 98-102 SREBF chaperone Homo sapiens 27-31
35154092-2 2022 All-trans-retinoic acid (ATRA) promotes T cell migration to mucosal surfaces by inducing transcription of the mucosal-homing receptors CCR9 and alpha4beta7 via binding to retinoic acid receptors (RARs), which heterodimerize with retinoid X receptors (RXRs) to function. Tretinoin 0-23 C-C motif chemokine receptor 9 Homo sapiens 135-139
35154092-2 2022 All-trans-retinoic acid (ATRA) promotes T cell migration to mucosal surfaces by inducing transcription of the mucosal-homing receptors CCR9 and alpha4beta7 via binding to retinoic acid receptors (RARs), which heterodimerize with retinoid X receptors (RXRs) to function. Tretinoin 25-29 C-C motif chemokine receptor 9 Homo sapiens 135-139
34673934-6 2022 Mechanistically, we showed that NUP98-JADE2 could impair all-trans retinoic acid (ATRA)-mediated transcriptional control and myeloid differentiation. Tretinoin 67-80 nucleoporin 98 and 96 precursor Homo sapiens 32-37
34673934-6 2022 Mechanistically, we showed that NUP98-JADE2 could impair all-trans retinoic acid (ATRA)-mediated transcriptional control and myeloid differentiation. Tretinoin 82-86 nucleoporin 98 and 96 precursor Homo sapiens 32-37
34673934-7 2022 Intriguingly, NUP98-JADE2 was found to alter the subcellular distribution of wild-type JADE2, whose down-regulation similarly led to attenuated ATRA-induced responses and myeloid activation, suggesting that NUP98-JADE2 may mediate JADE2 inhibition. Tretinoin 144-148 nucleoporin 98 and 96 precursor Homo sapiens 14-19
34673934-7 2022 Intriguingly, NUP98-JADE2 was found to alter the subcellular distribution of wild-type JADE2, whose down-regulation similarly led to attenuated ATRA-induced responses and myeloid activation, suggesting that NUP98-JADE2 may mediate JADE2 inhibition. Tretinoin 144-148 nucleoporin 98 and 96 precursor Homo sapiens 207-212
34999109-0 2022 CD14 is induced by Retinoic Acid and required for dsRNA-induced regeneration. Tretinoin 19-32 CD14 molecule Homo sapiens 0-4
11331070-3 2001 Incubation of these cells with 10(-6) M RA induced a rapid breakdown of both RARalpha and RARgamma in spite of the accumulation of their mRNAs. Tretinoin 40-42 retinoic acid receptor gamma Homo sapiens 90-98
11378441-4 2001 Compared with wild type fibroblasts, low activities of RA synthesis were determined on HPLC in mouse fibroblasts lacking XP group A (XPA) gene and UV-induced XPA deficient cancer cells. Tretinoin 55-57 xeroderma pigmentosum, complementation group A Mus musculus 121-131
11378441-4 2001 Compared with wild type fibroblasts, low activities of RA synthesis were determined on HPLC in mouse fibroblasts lacking XP group A (XPA) gene and UV-induced XPA deficient cancer cells. Tretinoin 55-57 xeroderma pigmentosum, complementation group A Mus musculus 133-136
11378441-4 2001 Compared with wild type fibroblasts, low activities of RA synthesis were determined on HPLC in mouse fibroblasts lacking XP group A (XPA) gene and UV-induced XPA deficient cancer cells. Tretinoin 55-57 xeroderma pigmentosum, complementation group A Mus musculus 158-161
11378441-6 2001 Finally, pre-treatment of RA isoforms significantly protected the XPA deficient fibroblasts from UV-induced death. Tretinoin 26-28 xeroderma pigmentosum, complementation group A Mus musculus 66-69
11404087-6 2001 Expression analysis in swirl and chordino mutants as well as in retinoic acid treated embryos indicate that noz1 is activated by BMP antagonists and neural posteriorizing signals. Tretinoin 64-77 zinc finger protein 703 Danio rerio 108-112
11331971-6 2001 In addition retinoic acid increased the production of hLAMP-1 and fibronectin but not transferrin, confirming our earlier report. Tretinoin 12-25 lysosomal associated membrane protein 1 Homo sapiens 54-61
11348869-5 2001 TTNPB, atRA, and AGN4204 inhibited the mitogenic induction of cyclin D1, whereas 9cRA had no effect. Tretinoin 7-11 cyclin D1 Homo sapiens 62-71
11491531-7 2001 Moreover, NKG2D stably interacted with surface molecules encoded by three newly identified cDNA sequences (N2DL-1, -2, and -3), which are identical to the human ULBP proteins and may represent homologs of the mouse retinoic acid-early inducible family of NKG2D ligands. Tretinoin 215-228 killer cell lectin like receptor K1 Homo sapiens 10-15
11491531-7 2001 Moreover, NKG2D stably interacted with surface molecules encoded by three newly identified cDNA sequences (N2DL-1, -2, and -3), which are identical to the human ULBP proteins and may represent homologs of the mouse retinoic acid-early inducible family of NKG2D ligands. Tretinoin 215-228 UL16 binding protein 1 Homo sapiens 107-125
11335108-0 2001 cis-acting DNA regulatory elements, including the retinoic acid response element, are required for tissue specific laminin B1 promoter/lacZ expression in transgenic mice. Tretinoin 50-63 laminin B1 Mus musculus 115-125
11335108-7 2001 Mutation of the retinoic acid response element (RARE) in the context of the 3.9LAMB1betagal transgene results in loss of LAMB1 transgene expression in all tissues. Tretinoin 16-29 laminin B1 Mus musculus 79-84
11335108-7 2001 Mutation of the retinoic acid response element (RARE) in the context of the 3.9LAMB1betagal transgene results in loss of LAMB1 transgene expression in all tissues. Tretinoin 16-29 laminin B1 Mus musculus 121-126
11290610-0 2001 Myeloblastin is an Myb target gene: mechanisms of regulation in myeloid leukemia cells growth-arrested by retinoic acid. Tretinoin 106-119 proteinase 3 Homo sapiens 0-12
11290610-8 2001 Inhibition of myeloblastin expression in leukemia cells growth-arrested by retinoic acid is demonstrated to depend on Myb down-regulation. Tretinoin 75-88 proteinase 3 Homo sapiens 14-26
11290610-10 2001 Altogether, the data offer a clue as to how a myeloid-specific transcriptional machinery can be accessible to regulation by retinoic acid and point to myeloblastin as a novel target of Myb. Tretinoin 124-137 proteinase 3 Homo sapiens 151-163
11290610-11 2001 This link between Myb and myeloblastin suggests a previously nonidentified Myb pathway through which growth arrest is induced by retinoic acid in myeloid leukemia cells. Tretinoin 129-142 proteinase 3 Homo sapiens 26-38
11401397-9 2001 These data demonstrate that the JNK signaling pathway and c-Jun activation are critical for cardiac neural crest outgrowth and are potential targets for the action of RA. Tretinoin 167-169 jun proto-oncogene Mus musculus 58-63
11599126-7 2001 Treatment with dibutyryl cyclic AMP (cAMP) induces expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, and treatment with retinoic acid (RA) induces expression of myelin proteolipid protein (PLP), a marker of oligodendrocytes, respectively. Tretinoin 148-161 proteolipid protein 1 Rattus norvegicus 189-215
11599126-7 2001 Treatment with dibutyryl cyclic AMP (cAMP) induces expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, and treatment with retinoic acid (RA) induces expression of myelin proteolipid protein (PLP), a marker of oligodendrocytes, respectively. Tretinoin 148-161 proteolipid protein 1 Rattus norvegicus 217-220
11599126-7 2001 Treatment with dibutyryl cyclic AMP (cAMP) induces expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, and treatment with retinoic acid (RA) induces expression of myelin proteolipid protein (PLP), a marker of oligodendrocytes, respectively. Tretinoin 163-165 proteolipid protein 1 Rattus norvegicus 189-215
11599126-7 2001 Treatment with dibutyryl cyclic AMP (cAMP) induces expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, and treatment with retinoic acid (RA) induces expression of myelin proteolipid protein (PLP), a marker of oligodendrocytes, respectively. Tretinoin 163-165 proteolipid protein 1 Rattus norvegicus 217-220
11599126-9 2001 Heat treatment after the initiation of differentiation by cAMP or RA accelerated the expression of GFAP or PLP mRNAs. Tretinoin 66-68 proteolipid protein 1 Rattus norvegicus 107-110
11274759-7 2001 RESULTS: Treatment with ATRA also resulted in an increase in the proportion of 5T33 cells expressing the CD54 adhesion molecule, which is known to be highly expressed on mature myeloma cells. Tretinoin 24-28 intercellular adhesion molecule 1 Mus musculus 105-109
11238746-7 2001 Retinoic acid receptors (RAR) in partnership with retinoid X receptor (RXR)alpha appear to be the important retinoid receptor transcription factors regulating vitamin A function at the gene level during development via the physiologic ligand all-trans-retinoic acid. Tretinoin 245-265 retinoid X receptor alpha Mus musculus 71-80
11231062-2 2001 We have previously reported on a RA degrading enzyme, XCYP26, which appears to be critical for the anteroposterior patterning of the central nervous system (EMBO J. Tretinoin 33-35 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 54-60
11179956-0 2001 Structure-function relationships in UCP1, UCP2 and chimeras: EPR analysis and retinoic acid activation of UCP2. Tretinoin 78-91 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 36-40
11179956-0 2001 Structure-function relationships in UCP1, UCP2 and chimeras: EPR analysis and retinoic acid activation of UCP2. Tretinoin 78-91 uncoupling protein 2 Homo sapiens 106-110
11179956-5 2001 Our results confirm the observations reported for recombinant yeast that retinoic acid, but not fatty acids known to activate UCP1, activates proton transport by UCP2 and that this activation is insensitive to nucleotide inhibition. Tretinoin 73-86 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 126-130
11179956-5 2001 Our results confirm the observations reported for recombinant yeast that retinoic acid, but not fatty acids known to activate UCP1, activates proton transport by UCP2 and that this activation is insensitive to nucleotide inhibition. Tretinoin 73-86 uncoupling protein 2 Homo sapiens 162-166
11179956-9 2001 In the other chimeric construct U2U1, hUCP2 (amino acids 1-210) and mUCP1 (amino acids 199-307), retinoic acid still acted as an activator, but no inhibition was observed with GTP. Tretinoin 97-110 uncoupling protein 2 Homo sapiens 38-43
11179956-9 2001 In the other chimeric construct U2U1, hUCP2 (amino acids 1-210) and mUCP1 (amino acids 199-307), retinoic acid still acted as an activator, but no inhibition was observed with GTP. Tretinoin 97-110 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 68-73
11212271-6 2001 ATRA and its metabolites could induce NB4 cells differentiation with similar activity, as evaluated by cell morphology, by the nitroblue tetrazolium reduction test (82-88% at 120 h) or by the expression of the maturation specific cell surface marker CD11c. Tretinoin 0-4 integrin subunit alpha X Homo sapiens 250-255
11212271-9 2001 The ATRA metabolites were found to exert their differentiation effects via the RAR alpha nuclear receptors, because the RAR alpha-specific antagonist BMS614 blocked metabolite-induced CD11c expression in NB4 cells. Tretinoin 4-8 integrin subunit alpha X Homo sapiens 184-189
11285139-0 2001 Coordinate regulation of RARgamma2, TBP, and TAFII135 by targeted proteolysis during retinoic acid-induced differentiation of F9 embryonal carcinoma cells. Tretinoin 85-98 TATA-box binding protein associated factor 4 Mus musculus 45-53
11196162-5 2001 Accordingly, we show that AML1/ETO, the commonest AML-associated fusion protein, is an HDAC-dependent repressor of RA signaling. Tretinoin 115-117 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 31-34
11455572-0 2001 Transcriptional suppression of Sox9 expression in chondrocytes by retinoic acid. Tretinoin 66-79 SRY (sex determining region Y)-box 9 Mus musculus 31-35
11162450-1 2000 Retinyl ester concentration is regulated by retinoic acid (RA) through an autoregulatory loop, which acts on lecithin:retinol acyltransferase (LRAT). Tretinoin 44-57 lecithin retinol acyltransferase Homo sapiens 109-141
11162450-1 2000 Retinyl ester concentration is regulated by retinoic acid (RA) through an autoregulatory loop, which acts on lecithin:retinol acyltransferase (LRAT). Tretinoin 44-57 lecithin retinol acyltransferase Homo sapiens 143-147
11162450-1 2000 Retinyl ester concentration is regulated by retinoic acid (RA) through an autoregulatory loop, which acts on lecithin:retinol acyltransferase (LRAT). Tretinoin 59-61 lecithin retinol acyltransferase Homo sapiens 109-141
11162450-1 2000 Retinyl ester concentration is regulated by retinoic acid (RA) through an autoregulatory loop, which acts on lecithin:retinol acyltransferase (LRAT). Tretinoin 59-61 lecithin retinol acyltransferase Homo sapiens 143-147
11175361-5 2000 In addition, the expression of Ets1 can be induced in MC3T3-E1 and fetal rat calvaria cells by retinoic acid (RA) which is known to exert profound effects on skeletal growth and development, bone turnover, and induce specific cellular responses in bone cells. Tretinoin 95-108 E26 avian leukemia oncogene 1, 5' domain Mus musculus 31-35
10995752-1 2000 Aldehyde dehydrogenase 1 (ALDH1) plays a major role in the biosynthesis of retinoic acid (RA), a hormone required for several essential life processes. Tretinoin 75-88 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-24
10995752-1 2000 Aldehyde dehydrogenase 1 (ALDH1) plays a major role in the biosynthesis of retinoic acid (RA), a hormone required for several essential life processes. Tretinoin 75-88 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 26-31
10995752-1 2000 Aldehyde dehydrogenase 1 (ALDH1) plays a major role in the biosynthesis of retinoic acid (RA), a hormone required for several essential life processes. Tretinoin 90-92 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-24
10995752-1 2000 Aldehyde dehydrogenase 1 (ALDH1) plays a major role in the biosynthesis of retinoic acid (RA), a hormone required for several essential life processes. Tretinoin 90-92 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 26-31
10995752-2 2000 Recent evidence, using the aryl hydrocarbon receptor-null mouse, suggests that elevated hepatic RA down-regulates ALDH1 in a unique feedback pathway to control RA biosynthesis. Tretinoin 96-98 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 114-119
10995752-2 2000 Recent evidence, using the aryl hydrocarbon receptor-null mouse, suggests that elevated hepatic RA down-regulates ALDH1 in a unique feedback pathway to control RA biosynthesis. Tretinoin 160-162 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 114-119
10995752-3 2000 To determine the mechanism of suppression of the ALDH1 gene by RA, transactivation studies were carried out in Hepa-1 mouse hepatoma cells. Tretinoin 63-65 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 49-54
10995752-5 2000 Retinoic acid receptor alpha (RARalpha) transactivates the ALDH1 gene promoter through a complex with an RA response-like element (RARE) located at -91/-75 bp, which bound to the RARalpha/retinoid X receptor beta heterodimer. Tretinoin 30-32 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 59-64
10995752-8 2000 These data support a model in which the RARalpha and C/EBPbeta activate the ALDH1 gene promoter through the RARE and C/EBP response elements, and in Hepa-1 cells, high levels of RA inhibit this activation by decreasing cellular levels of C/EBPbeta. Tretinoin 40-42 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 76-81
11098153-0 2000 A novel cis-acting element regulates HES-1 gene expression in P19 embryonal carcinoma cells treated with retinoic acid. Tretinoin 105-118 hes family bHLH transcription factor 1 Homo sapiens 37-42
11098153-7 2000 These results indicate that ARX transduces signals that up-regulate HES-1 gene expression in response to RA-treatment. Tretinoin 105-107 hes family bHLH transcription factor 1 Homo sapiens 68-73
11093772-1 2000 Cytochrome P450 (P450)-dependent metabolism of all-trans-retinoic acid (atRA) is important for the expression of its biological activity. Tretinoin 47-70 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 0-22
11093772-1 2000 Cytochrome P450 (P450)-dependent metabolism of all-trans-retinoic acid (atRA) is important for the expression of its biological activity. Tretinoin 72-76 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 0-22
11072095-8 2000 Retinoids induced RARgamma mRNA, which paralleled the increase in the transactivation of strong retinoic acid response element (RARE) reporter construct. Tretinoin 96-109 retinoic acid receptor gamma Homo sapiens 18-26
11024001-6 2000 Deletion and point-mutation analysis of the hUCP-3 promoter led us to identify a direct-repeat element with one base-pair spacing (DR1) at position -71/-59 responsible for the induction by RA of the activity of the promoter. Tretinoin 189-191 down-regulator of transcription 1 Homo sapiens 131-134
11054668-0 2000 Over-expression of nucleophosmin/B23 decreases the susceptibility of human leukemia HL-60 cells to retinoic acid-induced differentiation and apoptosis. Tretinoin 99-112 nucleophosmin 1 Homo sapiens 19-32
11054668-0 2000 Over-expression of nucleophosmin/B23 decreases the susceptibility of human leukemia HL-60 cells to retinoic acid-induced differentiation and apoptosis. Tretinoin 99-112 nucleophosmin 1 Homo sapiens 33-36
11027136-1 2000 Cellular retinoic acid-binding proteins I and II (CRABP-I and -II, respectively) are transport proteins for all-trans-retinoic acid (RA), an active metabolite of vitamin A (retinol), and have been reported to be directly involved in the metabolism of RA. Tretinoin 133-135 cellular retinoic acid binding protein 1 Homo sapiens 50-65
11027136-3 2000 Photoaffinity labeling of CRABP-I with [(3)H]RA was light- and concentration-dependent and was protected by unlabeled RA and various retinoids, indicating that the labeling was directed to the RA-binding site. Tretinoin 45-47 cellular retinoic acid binding protein 1 Homo sapiens 26-33
11027136-3 2000 Photoaffinity labeling of CRABP-I with [(3)H]RA was light- and concentration-dependent and was protected by unlabeled RA and various retinoids, indicating that the labeling was directed to the RA-binding site. Tretinoin 45-47 cellular retinoic acid binding protein 1 Homo sapiens 26-33
11007958-3 2000 At the molecular level, PML protein has been shown to be a coactivator of nuclear hormone receptors, whereas its oncogenic counterpart PML-retinoic acid receptor alpha, which promotes POD disaggregation, has been found to activate activator protein-1 transcription in a retinoic acid-dependent manner. Tretinoin 139-152 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 231-250
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 127-140 down-regulator of transcription 1 Homo sapiens 122-125
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 142-144 down-regulator of transcription 1 Homo sapiens 122-125
11063125-3 2000 We report that RA enhances p27 expression, which results in increased association with cyclin E/cyclin-dependent kinase 2 complexes and suppression of their activity; however, antisense clones, which have greatly reduced RA-dependent p27 inducibility (NT2-p27AS), continue to synthesize DNA and are unable to differentiate properly in response to RA as determined by lack of neurite outgrowth and by the failure to modify surface antigens. Tretinoin 15-17 cyclin dependent kinase 2 Homo sapiens 96-121
11002347-5 2000 In addition, brief treatments of fin regenerates with retinoic acid or the synthetic Fgfr1 inhibitor SU5402 down-regulate epidermal lef1, similar to their effects on shh. Tretinoin 54-67 lymphoid enhancer-binding factor 1 Danio rerio 132-136
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 50-74
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 76-81
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 87-116
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 25-27 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 118-124
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 188-190 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 50-74
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 188-190 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 76-81
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 188-190 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 87-116
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 188-190 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 118-124
11025231-1 2000 The enzymes that generate retinoic acid during development have been identified as members of the aldehyde dehydrogenase (ALDH) family. Tretinoin 26-39 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 98-120
11025231-1 2000 The enzymes that generate retinoic acid during development have been identified as members of the aldehyde dehydrogenase (ALDH) family. Tretinoin 26-39 aldehyde dehydrogenase family 3, subfamily A1 Mus musculus 122-126
11030153-7 2000 These results suggest that complex regulation of CDKs play a key role in G1 arrest of ML-1 after treatment with ATRA and GM-CSF. Tretinoin 112-116 cyclin dependent kinase 2 Homo sapiens 49-53
11030153-8 2000 We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Tretinoin 98-102 cyclin dependent kinase 2 Homo sapiens 35-39
10999756-2 2000 13-cis-Retinoic acid (13-cis-RA) was comparable to all-trans-retinoic acid (RA) in inducing transglutaminase II (TGase II) in cultured human cells. Tretinoin 29-31 transglutaminase 2 Rattus norvegicus 113-121
10938104-7 2000 Functional experiments further demonstrated that this interaction has the capacity to render GATA-dependent transcription inducible by retinoic acid, raising the possibility that GATA target genes may be involved in the molecular pathogenesis of APL. Tretinoin 135-148 GATA binding protein 2 Homo sapiens 93-97
10938104-7 2000 Functional experiments further demonstrated that this interaction has the capacity to render GATA-dependent transcription inducible by retinoic acid, raising the possibility that GATA target genes may be involved in the molecular pathogenesis of APL. Tretinoin 135-148 GATA binding protein 2 Homo sapiens 179-183
10976925-2 2000 We recently reported the identification of a RA-inducible cytochrome P450 [P450RAI(CYP26)], in zebrafish, mouse, and human, which was shown to be responsible for RA catabolism. Tretinoin 45-47 cytochrome P450, family 26, subfamily A, polypeptide 1 Danio rerio 75-88
10874126-4 2000 Using inhibition studies and correlation analysis, we also concluded that CYP2C8 was the major all-trans-retinoic acid 4-hydroxylating cytochrome P450 in human liver microsomes, though CYP3A4 and, to a lesser extent CYP2C9, also made a contribution. Tretinoin 95-118 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 74-80
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin dependent kinase 2 Homo sapiens 155-159
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin dependent kinase 2 Homo sapiens 206-210
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin dependent kinase 4 Homo sapiens 255-259
11095078-6 2000 Marked cyclical changes of alcohol dehydrogenase 4 activity in the stratum germinativum of the vaginal epithelium strongly support the assumption that this isoenzyme is responsible for retinoic acid synthesis, and that it is essential for the changes accompanying keratinization and mucification. Tretinoin 185-198 alcohol dehydrogenase 4 (class II), pi polypeptide Rattus norvegicus 27-50
10852718-5 2000 We also measured binding of FA to a retinoic acid (CRABP-I) and a retinol (CRBP-II) binding protein and we have extended to 19 different FA our characterization of the FA-ADIFAB and FA-rat intestinal FABP interactions. Tretinoin 36-49 cellular retinoic acid binding protein 1 Rattus norvegicus 51-58
10820192-4 2000 Retinoic acid-mediated differentiation of NT2 precursor cells to the neuronal phenotype resulted in five- to 15-fold increases in the expression of PLC-beta1, PLC-beta4, and Galpha(q/11) (the prime G protein activator of these isozymes). Tretinoin 0-13 phospholipase C beta 1 Homo sapiens 148-157
10820202-0 2000 Retinoic acid-mediated enhancement of the cholinergic/neuronal nitric oxide synthase phenotype of the medial septal SN56 clone: establishment of a nitric oxide-sensitive proapoptotic state. Tretinoin 0-13 nitric oxide synthase 1, neuronal Mus musculus 54-84
10799323-0 2000 Differential regulation of the carbonic anhydrase II gene expression by hormonal nuclear receptors in monocytic cells: identification of the retinoic acid response element. Tretinoin 141-154 carbonic anhydrase 2 Gallus gallus 31-52
10799323-6 2000 Our results demonstrate the first retinoic acid response element in the CAII promoter and show that according to cell type, different nuclear receptors of the VDR subfamily can regulate the CAII gene. Tretinoin 34-47 carbonic anhydrase 2 Gallus gallus 72-76
10799323-6 2000 Our results demonstrate the first retinoic acid response element in the CAII promoter and show that according to cell type, different nuclear receptors of the VDR subfamily can regulate the CAII gene. Tretinoin 34-47 vitamin D (1,25- dihydroxyvitamin D3) receptor Gallus gallus 159-162
10799323-6 2000 Our results demonstrate the first retinoic acid response element in the CAII promoter and show that according to cell type, different nuclear receptors of the VDR subfamily can regulate the CAII gene. Tretinoin 34-47 carbonic anhydrase 2 Gallus gallus 190-194
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 0-2 retinoic acid receptor, beta Mus musculus 111-119
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 54-56 interleukin 23, alpha subunit p19 Mus musculus 16-19
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 54-56 retinoic acid receptor, beta Mus musculus 85-93
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 54-56 retinoic acid receptor, beta Mus musculus 111-119
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 54-56 interleukin 23, alpha subunit p19 Mus musculus 16-19
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 54-56 retinoic acid receptor, beta Mus musculus 85-93
10929206-8 2000 RA treatment of P19 cells stably transfected with the RA-responsive element from the RAR beta gene showed that RAR beta 2 mRNA expression during DMSO differentiation was associated with increased sensitivity to RA. Tretinoin 54-56 retinoic acid receptor, beta Mus musculus 111-119
10929206-9 2000 Together these data show that RAR beta 2 is expressed spontaneously in an apparently RA-independent manner in differentiating mesoderm and mesoderm derivatives, resulting in increased sensitivity to RA in these cells. Tretinoin 85-87 retinoic acid receptor, beta Mus musculus 30-38
10762643-8 2000 Overxpression of inhibitory polypeptides that block signals generated from Ras and Cdc42 was found to reverse the retinoic acid activation-dependent induction of GST expression in PC12 cells. Tretinoin 114-127 cell division cycle 42 Rattus norvegicus 83-88
10760565-2 2000 We had found that gal-1 expression is increased in F9 murine embryonal carcinoma cells concurrently with induction of differentiation by all-trans retinoic acid (RA). Tretinoin 147-160 lectin, galactose binding, soluble 1 Mus musculus 18-23
10760565-2 2000 We had found that gal-1 expression is increased in F9 murine embryonal carcinoma cells concurrently with induction of differentiation by all-trans retinoic acid (RA). Tretinoin 162-164 lectin, galactose binding, soluble 1 Mus musculus 18-23
10760565-6 2000 The results indicate that the induction of gal-1 by RA is regulated at least partially at the level of transcription. Tretinoin 52-54 lectin, galactose binding, soluble 1 Mus musculus 43-48
10777532-1 2000 Silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is known to interact with Sin3 and recruit the histone deacetylases (HDACs) that lead to hypoacetylation of histones and transrepression of target transcription factors. Tretinoin 22-35 nuclear receptor corepressor 2 Homo sapiens 67-71
10751444-0 2000 Regulation of glial cell line-derived neurotrophic factor responsiveness in developing rat sympathetic neurons by retinoic acid and bone morphogenetic protein-2. Tretinoin 114-127 glial cell derived neurotrophic factor Rattus norvegicus 14-57
10753851-5 2000 The NPM-RAR fusion proteins bind to retinoic acid response element sequences as either homodimers or as heterodimers with RXR. Tretinoin 36-49 nucleophosmin 1 Homo sapiens 4-7
10753851-9 2000 Both NPM-RAR and PML-RAR interact with the co-repressor protein SMRTe in a manner that is less sensitive than RARalpha to dissociation by retinoic acid. Tretinoin 138-151 nucleophosmin 1 Homo sapiens 5-8
10753851-9 2000 Both NPM-RAR and PML-RAR interact with the co-repressor protein SMRTe in a manner that is less sensitive than RARalpha to dissociation by retinoic acid. Tretinoin 138-151 PML-RARA regulated adaptor molecule 1 Homo sapiens 17-24
10753851-9 2000 Both NPM-RAR and PML-RAR interact with the co-repressor protein SMRTe in a manner that is less sensitive than RARalpha to dissociation by retinoic acid. Tretinoin 138-151 nuclear receptor corepressor 2 Homo sapiens 64-69
10786691-3 2000 The actions of retinoic acid in skin keratinocytes are mediated primarily by nuclear retinoic acid receptor gamma (RARgamma) and retinoid X receptor alpha (RXRalpha). Tretinoin 15-28 retinoic acid receptor gamma Homo sapiens 85-113
10786691-3 2000 The actions of retinoic acid in skin keratinocytes are mediated primarily by nuclear retinoic acid receptor gamma (RARgamma) and retinoid X receptor alpha (RXRalpha). Tretinoin 15-28 retinoic acid receptor gamma Homo sapiens 115-123
10729205-8 2000 This study shows that retinoic acid depresses alpha(2)(I) collagen gene expression but that this effect is less pronounced when the expression of this collagen is enhanced by acetaldehyde, which also decreases RARbeta message and protein. Tretinoin 22-35 retinoic acid receptor, beta Mus musculus 210-217
10885580-4 2000 Undifferentiated HL-60 cells highly expressed RPS3a/nbl whereas all-trans retinoic acid -induced differentiated cells exhibited markedly reduced levels, suggesting that apoptosis-resistance of differentiated cells could be due to low RPS3a/nbl expression. Tretinoin 74-87 ribosomal protein S3A Homo sapiens 234-239
10877072-8 2000 Treatment with retinoic acid caused a 3-fold increase of the trkA expression in neuroblastoma cell lines. Tretinoin 15-28 neurotrophic receptor tyrosine kinase 1 Homo sapiens 61-65
10852350-0 2000 Retinoic acid increases amount of phosphorylated RAF; ectopic expression of cFMS reveals that retinoic acid-induced differentiation is more strongly dependent on ERK2 signaling than induced GO arrest is. Tretinoin 0-13 zinc fingers and homeoboxes 2 Homo sapiens 49-52
10852350-0 2000 Retinoic acid increases amount of phosphorylated RAF; ectopic expression of cFMS reveals that retinoic acid-induced differentiation is more strongly dependent on ERK2 signaling than induced GO arrest is. Tretinoin 94-107 zinc fingers and homeoboxes 2 Homo sapiens 49-52
10852350-0 2000 Retinoic acid increases amount of phosphorylated RAF; ectopic expression of cFMS reveals that retinoic acid-induced differentiation is more strongly dependent on ERK2 signaling than induced GO arrest is. Tretinoin 94-107 colony stimulating factor 1 receptor Homo sapiens 76-80
10852350-2 2000 It has also been shown that ectopic expression of cFMS, a platelet-derived growth factor (PDGF)-family transmembrane tyrosine kinase receptor, enhances retinoic acid-induced differentiation and G1/0 arrest. Tretinoin 152-165 colony stimulating factor 1 receptor Homo sapiens 50-54
10852350-4 2000 The present data show that the ectopic expression of cFMS results in the differential loss of sensitivity of retinoic acid-induced differentiation or G1/0 arrest to inhibition of ERK2 activation. Tretinoin 109-122 colony stimulating factor 1 receptor Homo sapiens 53-57
10852350-8 2000 This differential sensitivity to PD98059 and uncoupling of retinoic acid-induced differentiation and G1/0 arrest in cFMS transfectants is associated with changes in mitogen-activated protein kinase signaling molecules. Tretinoin 59-72 colony stimulating factor 1 receptor Homo sapiens 116-120
10852350-10 2000 Retinoic acid increased the amount of activated ERK2 and phosphorylated RAF in both cell lines. Tretinoin 0-13 zinc fingers and homeoboxes 2 Homo sapiens 72-75
10852350-11 2000 But PD98059 eliminated detectable ERK2 activation, as well as inhibited RAF phosphorylation, in untreated and retinoic acid-treated wild-type HL-60 and cFMS transfectants, consistent with MEK or ERK feedback-regulation of RAF, in all four cases. Tretinoin 110-123 zinc fingers and homeoboxes 2 Homo sapiens 72-75
10852350-11 2000 But PD98059 eliminated detectable ERK2 activation, as well as inhibited RAF phosphorylation, in untreated and retinoic acid-treated wild-type HL-60 and cFMS transfectants, consistent with MEK or ERK feedback-regulation of RAF, in all four cases. Tretinoin 110-123 colony stimulating factor 1 receptor Homo sapiens 152-156
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 colony stimulating factor 1 receptor Homo sapiens 25-29
10852350-12 2000 Since PD98059 blocks the cFMS-conferred enhancement of the retinoic acid-induced differentiation, but not growth arrest, the data indicate that cFMS-enhanced differentiation acts primarily through MEK and ERK2, but cFMS-enhanced G1/0 arrest allied with RB hypophosphorylation depends on another cFMS signal route, which by itself can effect G1/0 arrest without activated ERK2. Tretinoin 59-72 colony stimulating factor 1 receptor Homo sapiens 144-148
10768863-1 2000 Reverse transcription-PCR and Northern and Western blot analyses indicate that mRNA and protein encoded by the Brachyury gene are expressed by the pluripotent human embryonal carcinoma cell line NTERA2 and are only modestly down-regulated during retinoic acid-induced differentiation. Tretinoin 246-259 T-box transcription factor 1 Homo sapiens 111-120
10681376-11 2000 CYP1A1 and CYP1B1 SUPERSOMES both exhibited exceptionally high activities, and in extrahepatic tissues, these isoforms could play important roles in biosynthesis of all-trans-retinoic acid from t-ROH. Tretinoin 165-188 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 11-17
10698945-0 2000 Structure of the RXR-RAR DNA-binding complex on the retinoic acid response element DR1. Tretinoin 52-65 down-regulator of transcription 1 Homo sapiens 83-86
10698945-2 2000 We describe the 1.70 A resolution structure of the ternary complex of RXR and RAR DNA-binding regions in complex with the retinoic acid response element DR1. Tretinoin 122-135 down-regulator of transcription 1 Homo sapiens 153-156
10691970-8 2000 Interestingly, TNAP was found to be the only isozyme activity superinduced when the cells were costimulated with retinoic acid and dexamethasone. Tretinoin 113-126 TNAP Homo sapiens 15-19
10691970-12 2000 Furthermore, in the presence of retinoic acid, RU486 behaved as an agonist, and conferred superinduction of TNAP gene expression in the same way as dexamethasone. Tretinoin 32-45 TNAP Homo sapiens 108-112
10691970-14 2000 In addition, retinoic acid plays an essential role in the superinduction of TNAP gene expression by enabling dexamethasone to exert its agonist activity, which otherwise has no effect. Tretinoin 13-26 TNAP Homo sapiens 76-80
10712606-5 2000 We searched for a suitable cell line expressing the MT-3 gene to be used for determination of MT-3 promoter tissue specificity, and showed that MT-3 expression is activated during neuroectodermal differentiation of P19 cells induced by retinoic acid to levels similar to those found in whole brain. Tretinoin 236-249 interleukin 23, alpha subunit p19 Mus musculus 215-218
10699467-10 2000 The decrease in GnT-V and the corresponding increase in GnT-III activities were also found after the cells were treated with all-trans retinoic acid (ATRA), and the mechanism of this might be different from that in the cell cycle. Tretinoin 135-148 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 56-63
10699467-10 2000 The decrease in GnT-V and the corresponding increase in GnT-III activities were also found after the cells were treated with all-trans retinoic acid (ATRA), and the mechanism of this might be different from that in the cell cycle. Tretinoin 150-154 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 56-63
10645966-4 2000 In this study we have tested the effect of retinoic acid on cardiac mesenchyme formation in vitro and then tested retinoic acid treated myocyte cultures for changes in the expression of hLAMP-1, fibronectin and transferrin members of the particulate matrix that is required for mesenchyme formation. Tretinoin 114-127 lysosomal associated membrane protein 1 Homo sapiens 186-193
10676652-8 2000 In agreement with the recent identification of nuclear receptors for bile acids, our data suggest that functional interactions between nuclear bile acid signaling pathways, PKC, and nuclear receptors for retinoic acid and vitamin D3 are involved in the down-regulation of the myeloblastin gene and the induction of cell differentiation in human leukemic cells. Tretinoin 204-217 proteinase 3 Homo sapiens 276-288
10704061-0 2000 The influence of retinoic acid and retinoic acid derivatives on beta2 integrins and L-selectin expression in HL-60 cells in vitro. Tretinoin 17-30 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 64-69
10704061-0 2000 The influence of retinoic acid and retinoic acid derivatives on beta2 integrins and L-selectin expression in HL-60 cells in vitro. Tretinoin 35-48 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 64-69
10784405-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human myeloid leukemia KG-1 cells. Tretinoin 31-44 neurotrophic receptor tyrosine kinase 1 Homo sapiens 76-80
10784405-1 2000 We have recently reported that retinoic acid (RA) induced the expression of trkA, the high affinity receptor for nerve growth factor (NGF), in human myeloid leukemia KG-1 cells. Tretinoin 46-48 neurotrophic receptor tyrosine kinase 1 Homo sapiens 76-80
10784405-3 2000 Interestingly, RA in combination with NaBut or PMA synergistically induced cellular differentiation as well as the expression of trkA in KG-1 cells. Tretinoin 15-17 neurotrophic receptor tyrosine kinase 1 Homo sapiens 129-133
10784405-4 2000 Furthermore, activation of the induced trkA receptor by exogenous NGF potentiated the differentiating effects of RA and NaBut. Tretinoin 113-115 neurotrophic receptor tyrosine kinase 1 Homo sapiens 39-43
10644979-4 2000 Our findings demonstrate that the retinoic acid-dependent growth arrest of LAN-5 neuroblastoma cell line is associated to a very large accumulation (>tenfold) of p27Kip1 protein, a cyclin-dependent kinase inhibitor; the protein binds and inhibits cyclin-dependent kinase 2, 4 and 6 activities, thus hampering pRb and p107 phosphorylation. Tretinoin 34-47 cyclin dependent kinase 2 Homo sapiens 250-275
10644979-4 2000 Our findings demonstrate that the retinoic acid-dependent growth arrest of LAN-5 neuroblastoma cell line is associated to a very large accumulation (>tenfold) of p27Kip1 protein, a cyclin-dependent kinase inhibitor; the protein binds and inhibits cyclin-dependent kinase 2, 4 and 6 activities, thus hampering pRb and p107 phosphorylation. Tretinoin 34-47 RB transcriptional corepressor 1 Homo sapiens 312-315
10644979-4 2000 Our findings demonstrate that the retinoic acid-dependent growth arrest of LAN-5 neuroblastoma cell line is associated to a very large accumulation (>tenfold) of p27Kip1 protein, a cyclin-dependent kinase inhibitor; the protein binds and inhibits cyclin-dependent kinase 2, 4 and 6 activities, thus hampering pRb and p107 phosphorylation. Tretinoin 34-47 RB transcriptional corepressor like 1 Homo sapiens 320-324
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 41-54 retinoid X receptor alpha Mus musculus 301-309
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 56-58 retinoid X receptor alpha Mus musculus 301-309
11237167-5 2000 And, RA inhibited PPARgamma2 expression more effectively and caused concomitantly a greater inhibition of adipocyte differentiation. Tretinoin 5-7 peroxisome proliferator activated receptor gamma Mus musculus 18-28
10654602-1 2000 Targeted disruption of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene precludes embryonic retinoic acid (RA) synthesis, leading to midgestational lethality (Niederreither, K., Subbarayan, V., Dolle, P. and Chambon, P. (1999). Tretinoin 98-111 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 34-63
10654602-1 2000 Targeted disruption of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene precludes embryonic retinoic acid (RA) synthesis, leading to midgestational lethality (Niederreither, K., Subbarayan, V., Dolle, P. and Chambon, P. (1999). Tretinoin 98-111 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 65-71
10654602-1 2000 Targeted disruption of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene precludes embryonic retinoic acid (RA) synthesis, leading to midgestational lethality (Niederreither, K., Subbarayan, V., Dolle, P. and Chambon, P. (1999). Tretinoin 113-115 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 34-63
10654602-1 2000 Targeted disruption of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene precludes embryonic retinoic acid (RA) synthesis, leading to midgestational lethality (Niederreither, K., Subbarayan, V., Dolle, P. and Chambon, P. (1999). Tretinoin 113-115 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 65-71
11178239-2 2000 The mouse Gcnf gene is expressed in the placenta and the developing nervous system and germ cells, and responds to retinoic acid. Tretinoin 115-128 nuclear receptor subfamily 6, group A, member 1 Mus musculus 10-14
10634639-6 2000 Adenosine deaminase-resistant analogs such as fludarabine (FLU) and cladribine (CdA) also induced the differentiation of human myelomonocytic leukemia cells, and these analogs synergistically enhanced the differentiation induced by all-trans retinoic acid (ATRA) or VD3. Tretinoin 236-255 cytidine deaminase Homo sapiens 80-83
10634639-6 2000 Adenosine deaminase-resistant analogs such as fludarabine (FLU) and cladribine (CdA) also induced the differentiation of human myelomonocytic leukemia cells, and these analogs synergistically enhanced the differentiation induced by all-trans retinoic acid (ATRA) or VD3. Tretinoin 257-261 cytidine deaminase Homo sapiens 80-83
11776585-1 2000 OBJECTIVE: To elucidate the chemosensitivity of retinoic acid (RA)-differentiated medulloblastoma Med-3 cells to conventional anti-cancer drug and to determine the potential genetic factor(s) mediating this sensitivity. Tretinoin 48-61 mediator complex subunit 27 Homo sapiens 98-103
11776585-1 2000 OBJECTIVE: To elucidate the chemosensitivity of retinoic acid (RA)-differentiated medulloblastoma Med-3 cells to conventional anti-cancer drug and to determine the potential genetic factor(s) mediating this sensitivity. Tretinoin 63-65 mediator complex subunit 27 Homo sapiens 98-103
11776585-2 2000 METHODS: Ten mumol/L RA, 5 micrograms/ml cisplatin (DDP) and their combination with one half concentration of each were used respectively to treat human medulloblastoma cell line Med-3 in vitro. Tretinoin 21-23 mediator complex subunit 27 Homo sapiens 179-184
11776585-9 2000 CONCLUSION: RA could enhance the apoptotic susceptibility of Med-3 cells to DDP presumably through modulating the Fas expression pattern. Tretinoin 12-14 mediator complex subunit 27 Homo sapiens 61-66
10554038-0 1999 Effect of all-trans-retinoic acid on c-fms proto-oncogene [colony-stimulating factor 1 (CSF-1) receptor] expression and CSF-1-induced invasion and anchorage-independent growth of human breast carcinoma cells. Tretinoin 10-33 colony stimulating factor 1 receptor Homo sapiens 37-42
10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 41-54 colony stimulating factor 1 receptor Homo sapiens 166-171
10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 56-58 colony stimulating factor 1 receptor Homo sapiens 166-171
10529422-12 1999 These data, which indicate that retinoic acid signaling through RARalpha and/or RARbeta is essential for the specification of rhombomere identities and for the control of caudal hindbrain segmentation by restricting the expression domains of kreisler and of Krox-20, also strongly suggest that this signaling plays a crucial role in the posteriorization of the hindbrain neurectoderm. Tretinoin 32-45 retinoic acid receptor, beta Mus musculus 80-87
10477294-5 1999 Thus, retinoic acid and hedgehog signaling have opposite effects on the prepattern genes Gli3 and Zic2 and on other genes acting downstream in the neurogenesis cascade. Tretinoin 6-19 GLI family zinc finger 3 L homeolog Xenopus laevis 89-93
10573135-5 1999 These results suggest that hypophosphorylation of pRB and repression of cyclin D3 and cdc25A are induced synergistically by treatment with ATRA plus GM-CSF in ML-1 cells. Tretinoin 139-143 RB transcriptional corepressor 1 Homo sapiens 50-53
10610030-0 1999 The role of RXR-alpha in retinoic acid-induced cleft palate as assessed with the RXR-alpha knockout mouse. Tretinoin 25-38 retinoid X receptor alpha Mus musculus 12-21
10610030-2 1999 RXR-alpha has been previously shown to mediate the teratogenic effects of RA in the limb. Tretinoin 74-76 retinoid X receptor alpha Mus musculus 0-9
10610030-4 1999 Treatment of RXR-alpha knockout mice with a teratogenic dose of RA on gestation day 11 or 12 induces cleft palate at a lower frequency than that seen in wild-type animals. Tretinoin 64-66 retinoid X receptor alpha Mus musculus 13-22
10460195-3 1999 Thus, high expression of human CRBP(I) [hCRBP(I)] in transgenic mice might be expected to increase the production of retinoic acid in tissues, thereby inducing a phenotype resembling vitamin A toxicity. Tretinoin 117-130 retinol binding protein 1 Homo sapiens 31-38
10460195-3 1999 Thus, high expression of human CRBP(I) [hCRBP(I)] in transgenic mice might be expected to increase the production of retinoic acid in tissues, thereby inducing a phenotype resembling vitamin A toxicity. Tretinoin 117-130 retinol binding protein 1 Homo sapiens 40-48
10579191-0 1999 [Analysis of expression of ets-1 and fli-1 proto-oncogenes in murine embryonic stem cells, induced to differentiation by retinoic acid]. Tretinoin 121-134 E26 avian leukemia oncogene 1, 5' domain Mus musculus 27-32
2481663-5 1989 G-CSF significantly enhanced the RA-induced granulocytic differentiation of APL cells in vitro. Tretinoin 33-35 colony stimulating factor 3 Homo sapiens 0-5
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 cellular retinoic acid binding protein 1 Homo sapiens 185-192
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 cellular retinoic acid binding protein 1 Homo sapiens 185-192
2783693-1 1989 In normal rat kidney fibroblasts, retinoic acid increases the level of epidermal growth factor (EGF) binding and synergizes with EGF and transforming growth factor-beta to stimulate anchorage-independent growth. Tretinoin 34-47 epidermal growth factor Rattus norvegicus 96-99
2479696-8 1989 These results suggest that retinoic acid may have complex, as yet undefined, RAR-mediated regulatory functions in both dermis and epidermis. Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 77-80
10446126-6 1999 The rate constant for movement of RA from CRABP-II, but not from CRABP-I, to RAR strongly depended on the concentration of the acceptor. Tretinoin 34-36 cellular retinoic acid binding protein 1 Homo sapiens 42-49
2783693-1 1989 In normal rat kidney fibroblasts, retinoic acid increases the level of epidermal growth factor (EGF) binding and synergizes with EGF and transforming growth factor-beta to stimulate anchorage-independent growth. Tretinoin 34-47 epidermal growth factor Rattus norvegicus 129-132
10438723-0 1999 Retinoic acid prevents phosphorylation of pRB in normal human B lymphocytes: regulation of cyclin E, cyclin A, and p21(Cip1). Tretinoin 0-13 RB transcriptional corepressor 1 Homo sapiens 42-45
10438723-3 1999 When retinoic acid was administered to B cells stimulated into mid to late G1 by anti-IgM antibodies (anti-mu) and Staphylococcus aureus crude cell suspension (SAC), the phosphorylation of pRB required for S-phase entry was prevented in a time- and dose-dependent manner. Tretinoin 5-18 RB transcriptional corepressor 1 Homo sapiens 189-192
10438723-4 1999 Thus, 2-hour treatment with retinoic acid at the optimal concentration of 1 micromol/L prevented phosphorylation of pRB, and effects were noted at concentrations as low as 10 nmol/L. Tretinoin 28-41 RB transcriptional corepressor 1 Homo sapiens 116-119
2558044-8 1989 It is hypothesized that the RAR vectors are interfering with endogenous RAR(s) in a dominant-negative manner to inhibit retinoic acid-induced differentiation of F9 EC cells. Tretinoin 120-133 retinoic acid receptor alpha Homo sapiens 28-31
10438723-5 1999 Based on our results, we suggest that the rapid effect of retinoic acid on pRB phosphorylation is due primarily to the reduced expression of cyclin E and cyclin A in late G1. Tretinoin 58-71 RB transcriptional corepressor 1 Homo sapiens 75-78
2558044-8 1989 It is hypothesized that the RAR vectors are interfering with endogenous RAR(s) in a dominant-negative manner to inhibit retinoic acid-induced differentiation of F9 EC cells. Tretinoin 120-133 retinoic acid receptor alpha Homo sapiens 72-75
2912547-8 1989 Furthermore, the autophosphorylation of either RA-treated or untreated EGF receptors occurred on similar amino acid residues. Tretinoin 47-49 epidermal growth factor Homo sapiens 71-74
2912547-9 1989 These results demonstrate that RA exhibits a heterogeneous growth-inhibitory activity against human glioma cells and suggest that the effects of RA may be mediated, at least in part, by modulation of EGF receptor phosphotyrosine kinase activity. Tretinoin 31-33 epidermal growth factor Homo sapiens 200-203
2912547-9 1989 These results demonstrate that RA exhibits a heterogeneous growth-inhibitory activity against human glioma cells and suggest that the effects of RA may be mediated, at least in part, by modulation of EGF receptor phosphotyrosine kinase activity. Tretinoin 145-147 epidermal growth factor Homo sapiens 200-203
2472150-10 1989 Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells. Tretinoin 131-144 NRAS proto-oncogene, GTPase Rattus norvegicus 73-78
10438723-8 1999 Thus, retinoic acid induced a rapid, but transient increased binding of p21(Cip1) to CDK2. Tretinoin 6-19 cyclin dependent kinase 2 Homo sapiens 85-89
3142527-3 1988 Recombinant IL-1 (10-100 U/ml) could stimulate cartilage resorption, although the maximum degree of tissue breakdown rarely reached the levels obtained when cartilage was treated with crude mononuclear-cell conditioned medium or all-trans retinoic acid (1 microM) over a similar time course. Tretinoin 239-252 interleukin 1 alpha Homo sapiens 12-16
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 4-17 RB transcriptional corepressor 1 Homo sapiens 106-109
10470859-12 1999 RA and those retinoids capable of binding to the M6P/IGF2R induced a remarkable morphological change with characteristics of round shape and reduced spreading, apoptosis, and growth inhibition in stably transfected mouse P388D1 cells overexpressing the M6P/IGF2R but not in the M6P/IGF2R-deficient P388D1 cells. Tretinoin 0-2 insulin-like growth factor 2 receptor Mus musculus 253-262
2465548-8 1989 Although constitutive levels of IL-1 biological activity and protein are significant in these cultures, IL-1 levels increase when either PMA or retinoic acid alone are added to cultures. Tretinoin 144-157 interleukin 1 alpha Homo sapiens 104-108
2465548-9 1989 IL-1 does not increase when PMA and retinoic acid are added simultaneously to cultures; nor is it induced when extracellular Ca2+ concentrations are raised to 2 mM. Tretinoin 36-49 interleukin 1 alpha Homo sapiens 0-4
10470859-15 1999 Furthermore, overexpression of the M6P/IGF2R in a RA-resistant cancer cell line (HL-60R) that lacked functional RARs gave the cells a susceptibility to RA-induced apoptosis. Tretinoin 50-52 insulin-like growth factor 2 receptor Mus musculus 35-44
2459072-0 1988 Retinoic-acid-induced modulation of c-myc not dependent on its continued presence: possible role in pre-commitment for HL-60 cells. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-41
2459072-7 1988 Thus, retinoic acid induced a change in HL-60 c-myc RNA levels which was sustained regardless of the continued presence or absence of RA. Tretinoin 6-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-51
10432387-13 1999 TGF-beta1 levels in mesangial cells stimulated with LPS/IFN-gamma in presence of ATRA or 13-cis-RA were also reduced indicating that TGF-beta1 did not mediate the suppressive effect of retinoids on iNOS. Tretinoin 81-85 transforming growth factor, beta 1 Mus musculus 0-9
2480694-2 1989 Expression of N-myc gene product was reduced in neuroblastoma cell line SK-N-DZ differentiated by retinoic acid as compared with untreated cells. Tretinoin 98-111 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 14-19
3262523-3 1988 Retinol and each retinoid were capable of stimulating fibroblast growth alone (0-86%), while 13-cis and all-trans-retinoic acid were the most potent in potentiating the EGF promotion of fibroblast growth. Tretinoin 104-127 epidermal growth factor Homo sapiens 169-172
10407146-1 1999 Some members of the human alcohol dehydrogenase (ADH) family possess retinol dehydrogenase activity and may thus function in production of the active nuclear receptor ligand retinoic acid. Tretinoin 174-187 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 69-90
3262523-5 1988 While EGF and FGF stimulated fibroblast growth to the same degree (2.3-fold), only growth stimulated by EGF was potentiated by retinoic acid. Tretinoin 127-140 epidermal growth factor Homo sapiens 104-107
3262523-6 1988 Since retinoic acid might enhance the EGF stimulation of cell growth by increasing either EGF receptor number or binding affinity, the binding of 125I-labeled EGF was carried out in the presence of retinoic acid and the data were subjected to a Scatchard-type analysis. Tretinoin 6-19 epidermal growth factor Homo sapiens 38-41
3262523-6 1988 Since retinoic acid might enhance the EGF stimulation of cell growth by increasing either EGF receptor number or binding affinity, the binding of 125I-labeled EGF was carried out in the presence of retinoic acid and the data were subjected to a Scatchard-type analysis. Tretinoin 6-19 epidermal growth factor Homo sapiens 90-93
3262523-6 1988 Since retinoic acid might enhance the EGF stimulation of cell growth by increasing either EGF receptor number or binding affinity, the binding of 125I-labeled EGF was carried out in the presence of retinoic acid and the data were subjected to a Scatchard-type analysis. Tretinoin 6-19 epidermal growth factor Homo sapiens 90-93
2590998-1 1989 The relationship between plasminogen activator (PA)/plasminogen activator inhibitor (PAI) activity and morphological differentiation was investigated in human neuroblastoma (NB) cells treated with retinoic acid (RA). Tretinoin 197-210 serpin family E member 1 Homo sapiens 85-88
2590998-1 1989 The relationship between plasminogen activator (PA)/plasminogen activator inhibitor (PAI) activity and morphological differentiation was investigated in human neuroblastoma (NB) cells treated with retinoic acid (RA). Tretinoin 212-214 serpin family E member 1 Homo sapiens 85-88
10381520-13 1999 ATRA was further shown to upregulate p21(WAF1) expression and cause dephosphorylation of the retinoblastoma protein (pRB) in both OPM-2 and C5 cells. Tretinoin 0-4 RB transcriptional corepressor 1 Homo sapiens 117-120
2837484-3 1988 Two retinoic acid-binding peaks were resolved at the DEAE-cellulose step, with CRABP-I in the major peak and CRABP-II in the minor peak. Tretinoin 4-17 cellular retinoic acid binding protein 2 Rattus norvegicus 109-117
2837484-7 1988 The dissociation constant for CRABP-II of retinoic acid was estimated to be 65 nM by fluorescence titration. Tretinoin 42-55 cellular retinoic acid binding protein 2 Rattus norvegicus 30-38
2849937-4 1988 CRABP II was a novel cellular retinoic acid binding protein, in which the amino acids at 6 positions of the NH2 terminal sequence are different from those in CRABP I. Tretinoin 30-43 cellular retinoic acid binding protein 2 Gallus gallus 0-8
10381520-15 1999 Thus, the growth inhibitory activity of ATRA is not mediated through cellular IL-6Ralpha downregulation and is likely to result from a direct upregulation of p21(WAF1) and consequent dephosphorylation of pRB. Tretinoin 40-44 RB transcriptional corepressor 1 Homo sapiens 204-207
10358083-6 1999 The GATA binding site mediates the retinoic acid/dibutyryl cyclic AMP stimulation of transcription and correlates with the binding of Gata-4 which is induced by retinoic acid in differentiating F9 cells. Tretinoin 35-48 glutaminyl-tRNA synthase (glutamine-hydrolyzing)-like 1 Mus musculus 4-8
2905127-0 1988 Induction of gamma-glutamyl transpeptidase activity by all-trans retinoic acid in cultured rat liver epithelial cells. Tretinoin 55-78 gamma-glutamyltransferase 1 Rattus norvegicus 13-42
2905127-1 1988 The induction of activity of gamma-glutamyl transpeptidase (GGT) by all-trans retinoic acid in a chemically transformed rat liver epithelial cell line has been investigated. Tretinoin 68-91 gamma-glutamyltransferase 1 Rattus norvegicus 29-58
2905127-1 1988 The induction of activity of gamma-glutamyl transpeptidase (GGT) by all-trans retinoic acid in a chemically transformed rat liver epithelial cell line has been investigated. Tretinoin 68-91 gamma-glutamyltransferase 1 Rattus norvegicus 60-63
2905127-2 1988 Retinoic acid increased the level of the GGT mRNA and this enhancement was progressive, depending on the duration of exposure and on the concentration of retinoic acid in the culture medium. Tretinoin 0-13 gamma-glutamyltransferase 1 Rattus norvegicus 41-44
2905127-2 1988 Retinoic acid increased the level of the GGT mRNA and this enhancement was progressive, depending on the duration of exposure and on the concentration of retinoic acid in the culture medium. Tretinoin 154-167 gamma-glutamyltransferase 1 Rattus norvegicus 41-44
2905127-3 1988 When retinoic acid was removed from cultures which had been exposed to it for 4 days, the induced GGT activity remained unchanged. Tretinoin 5-18 gamma-glutamyltransferase 1 Rattus norvegicus 98-101
3294336-7 1988 We also show that expression of Leu-17 (CD38), a surface marker that is re-expressed in the late pre-plasma stage of B cell development, was increased by RA from less than 20% to greater than 90% of the total cell population, with a concomitant 4-10-fold augmentation in the mean fluorescence intensity. Tretinoin 154-156 CD38 molecule Homo sapiens 40-44
2458292-8 1988 In the course of differentiation of OTF9-63 cells induced by retinoic acid, the epitope disappeared with the onset of morphological differentiation. Tretinoin 61-74 POU domain, class 3, transcription factor 4 Mus musculus 36-40
10358083-6 1999 The GATA binding site mediates the retinoic acid/dibutyryl cyclic AMP stimulation of transcription and correlates with the binding of Gata-4 which is induced by retinoic acid in differentiating F9 cells. Tretinoin 161-174 glutaminyl-tRNA synthase (glutamine-hydrolyzing)-like 1 Mus musculus 4-8
3180083-0 1988 Changes in c-myc, c-fms, and N-ras proto-oncogene expression associated with retinoic acid-induced monocytic differentiation of human leukemia HL60/MRI cells. Tretinoin 77-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 11-16
10331979-3 1999 SMyHC3-HAP transgene expression overlapped synthesis and endogenous response to retinoic acid (RA) in the heart, as determined by antibodies directed against a key RA synthetic enzyme and by staining of RAREhsplacZ transgenic animals. Tretinoin 80-93 reticulon 3 Homo sapiens 7-10
3191561-7 1988 A special stimulating effect of retinoic acid on ODC, contemporary with early deficiency, was observed in the liver; this effect was not observed at a later stage in normally fed rats. Tretinoin 32-45 ornithine decarboxylase 1 Rattus norvegicus 49-52
2447102-3 1987 When retinoic acid is added to the medium at 1 X 10(-8) to 1 X 10(-6) M, keratin synthesis is increased, vimentin synthesis is decreased, and the cells assume an epithelioid morphology. Tretinoin 5-18 vimentin Homo sapiens 105-113
2840075-2 1987 As F9 cells can be induced to differentiate into parietal endoderm-like cells by the addition of retinoic acid and dibutyryl cAMP, we examined levels of the c-myb transcript under this experimental condition and found that the c-myb transcript was decreased significantly. Tretinoin 97-110 myeloblastosis oncogene Mus musculus 227-232
10331979-3 1999 SMyHC3-HAP transgene expression overlapped synthesis and endogenous response to retinoic acid (RA) in the heart, as determined by antibodies directed against a key RA synthetic enzyme and by staining of RAREhsplacZ transgenic animals. Tretinoin 95-97 reticulon 3 Homo sapiens 7-10
10332029-5 1999 Overexpression of PQBP-1 in P19 embryonic carcinoma cells suppresses their growth rate and enhances their susceptibility to various stresses including serum deprivation, retinoic acid treatment and UV irradiation. Tretinoin 170-183 polyglutamine binding protein 1 Rattus norvegicus 18-24
2885743-2 1987 CAD regulation was studied in the human promyelocyte leukemic line HL-60 as it differentiated into monocytic or granulocytic lineages after induction by 12-O-tetradecanoylphorbol-13-acetate or trans-retinoic acid and dibutyryl cyclic AMP, respectively. Tretinoin 193-212 aconitate decarboxylase 1 Homo sapiens 0-3
3100942-0 1987 Synergistic effect of retinoic acid and calcium ionophore A23187 on differentiation, c-myc expression, and membrane tyrosine kinase activity in human promyelocytic leukemia cell line HL-60. Tretinoin 22-35 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-90
3100942-8 1987 Significantly greater reduction in c-myc mRNA levels was also observed 24 hr after treatment with RA and A23187 in comparison to that observed with either agent alone. Tretinoin 98-100 MYC proto-oncogene, bHLH transcription factor Homo sapiens 35-40
3100942-9 1987 These results suggest that a Ca2+-mediated process sensitizes cells to the differentiating effect of RA and that this effect is associated with a significant reduction of c-myc expression and the induction of membrane tyrosine kinase activity in this cell line. Tretinoin 101-103 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176
3499133-0 1987 Effects of retinoic acid on receptors for epidermal growth factor in mouse palatal mesenchymal cells in vitro. Tretinoin 11-24 epidermal growth factor Mus musculus 42-65
3499133-1 1987 Retinoic acid (RA), one of the inducers of cleft palate in vivo, specifically increased the 125I-epidermal growth factor (EGF) binding capacity of embryonic palatal mesenchymal cells; the increase was completely inhibited by actinomycin D, suggesting that transcription is required for this change. Tretinoin 0-13 epidermal growth factor Mus musculus 92-120
3499133-1 1987 Retinoic acid (RA), one of the inducers of cleft palate in vivo, specifically increased the 125I-epidermal growth factor (EGF) binding capacity of embryonic palatal mesenchymal cells; the increase was completely inhibited by actinomycin D, suggesting that transcription is required for this change. Tretinoin 0-13 epidermal growth factor Mus musculus 122-125
3499133-1 1987 Retinoic acid (RA), one of the inducers of cleft palate in vivo, specifically increased the 125I-epidermal growth factor (EGF) binding capacity of embryonic palatal mesenchymal cells; the increase was completely inhibited by actinomycin D, suggesting that transcription is required for this change. Tretinoin 15-17 epidermal growth factor Mus musculus 92-120
3499133-1 1987 Retinoic acid (RA), one of the inducers of cleft palate in vivo, specifically increased the 125I-epidermal growth factor (EGF) binding capacity of embryonic palatal mesenchymal cells; the increase was completely inhibited by actinomycin D, suggesting that transcription is required for this change. Tretinoin 15-17 epidermal growth factor Mus musculus 122-125
3499133-2 1987 When the increase in EGF receptors was related to the stimulation of DNA synthesis by EGF in the presence of various concentrations of RA, the maximum stimulation of [3H]-thymidine by EGF was at 10(-9) M RA, but the maximum increase in the number of EGF receptors was at 10(-6) M RA. Tretinoin 135-137 epidermal growth factor Mus musculus 21-24
3499133-2 1987 When the increase in EGF receptors was related to the stimulation of DNA synthesis by EGF in the presence of various concentrations of RA, the maximum stimulation of [3H]-thymidine by EGF was at 10(-9) M RA, but the maximum increase in the number of EGF receptors was at 10(-6) M RA. Tretinoin 135-137 epidermal growth factor Mus musculus 86-89
3499133-2 1987 When the increase in EGF receptors was related to the stimulation of DNA synthesis by EGF in the presence of various concentrations of RA, the maximum stimulation of [3H]-thymidine by EGF was at 10(-9) M RA, but the maximum increase in the number of EGF receptors was at 10(-6) M RA. Tretinoin 135-137 epidermal growth factor Mus musculus 86-89
3499133-2 1987 When the increase in EGF receptors was related to the stimulation of DNA synthesis by EGF in the presence of various concentrations of RA, the maximum stimulation of [3H]-thymidine by EGF was at 10(-9) M RA, but the maximum increase in the number of EGF receptors was at 10(-6) M RA. Tretinoin 135-137 epidermal growth factor Mus musculus 86-89
3567383-2 1987 Retinol deficient rats fed with retinoic acid (all-trans) show a mucosal ODC induction, but no morphological lesion. Tretinoin 32-45 ornithine decarboxylase 1 Rattus norvegicus 73-76
3021829-4 1986 In several tumor cells, including human promyelocytic leukemia, human and murine neuroblastoma, and murine teratocarcinoma, retinoic acid induces terminal differentiation, accompanied by suppression of the expression of either the c-myc or the N-myc gene. Tretinoin 124-137 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 244-249
3021829-5 1986 Many studies have indicated that retinoic acid can markedly increase the number of cellular receptors for epidermal growth factor, which is partially encoded by another oncogene, erb-B. Tretinoin 33-46 epidermal growth factor Homo sapiens 106-129
3747550-5 1986 Oral administration of all trans-retinoic acid also inhibited the ornithine decarboxylase activity induced by cellotape stripping. Tretinoin 27-46 ornithine decarboxylase 1 Rattus norvegicus 66-89
3460694-1 1986 The dynamics in levels of HL-60 (a human promyelocytic leukemia cell line) c-myc RNA due to retinoic acid-induced myeloid differentiation were measured. Tretinoin 92-105 MYC proto-oncogene, bHLH transcription factor Homo sapiens 75-80
3460694-8 1986 Since c-myc encodes a putative nuclear matrix protein, the results suggest a regulatory role for increased c-myc expression in mediating the nuclear structural change characteristic of precommitment early in the retinoic acid-induced process of HL-60 terminal myeloid differentiation. Tretinoin 212-225 MYC proto-oncogene, bHLH transcription factor Homo sapiens 107-112
3011479-6 1986 By contrast, other derivatives of P19, isolated from retinoic acid (RA)-treated aggregates and resembling neuroectodermal or endodermal cell types respond only to EGF; PDGF neither binds nor induces phosphorylation and a mitogenic response in these cells. Tretinoin 53-66 interleukin 23 subunit alpha Homo sapiens 34-37
3011479-6 1986 By contrast, other derivatives of P19, isolated from retinoic acid (RA)-treated aggregates and resembling neuroectodermal or endodermal cell types respond only to EGF; PDGF neither binds nor induces phosphorylation and a mitogenic response in these cells. Tretinoin 68-70 interleukin 23 subunit alpha Homo sapiens 34-37
2851444-4 1988 Although stimulation of tyrosinase activity with RA enhanced the cytotoxicity of 4-OHA, no similar enhancement occurred with alpha-MSH. Tretinoin 49-51 tyrosinase Mus musculus 24-34
2846152-10 1988 The Kelly cell line with amplified N-myc genome, which correlates with clinical progression of neuroblastoma, was also sensitive to RA plus herb-A. Tretinoin 132-134 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-40
2900242-2 1988 Retinoic acid acts as an acute and specific inducer of tissue transglutaminase in mouse resident peritoneal macrophages. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 55-78
2900242-3 1988 We have isolated cDNA clones for this enzyme and used them to demonstrate that this induction is due to the accumulation of tissue transglutaminase mRNA that occurs within minutes of exposure of macrophages to retinoic acid. Tretinoin 210-223 transglutaminase 2, C polypeptide Mus musculus 124-147
2900242-4 1988 The retinoic acid-induced increase in tissue transglutaminase mRNA is independent of concurrent protein synthesis and is due to an increased transcription of the tissue transglutaminase gene. Tretinoin 4-17 transglutaminase 2, C polypeptide Mus musculus 38-61
2900242-4 1988 The retinoic acid-induced increase in tissue transglutaminase mRNA is independent of concurrent protein synthesis and is due to an increased transcription of the tissue transglutaminase gene. Tretinoin 4-17 transglutaminase 2, C polypeptide Mus musculus 162-185
2456573-7 1988 The results of nuclear run-off experiments with uninduced and induced F9 cell nuclei indicate that there is a substantial increase in the rate of Hox-1.3 transcription upon induction of F9 cells with retinoic acid. Tretinoin 200-213 homeobox A5 Mus musculus 146-153
3164710-2 1988 In the present report, Northern analysis indicates that addition of the maturational agent N,N-dimethylformamide (DMF) (1.0%) to proliferating HCT 116 and MOSER cells resulted in a repression of c-myc proto-oncogene expression; retinoic acid (1.0 microM) was less effective in this regard. Tretinoin 228-241 MYC proto-oncogene, bHLH transcription factor Homo sapiens 195-200
2454667-0 1988 The new basement membrane antigen recognized by the monoclonal antibody GB3 is a large size glycoprotein: modulation of its expression by retinoic acid. Tretinoin 138-151 alpha 1,4-galactosyltransferase (P blood group) Homo sapiens 72-75
2896607-0 1988 Posttranscriptional regulation of the expression of CAD gene during differentiation of F9 teratocarcinoma cells by induction with retinoic acid and dibutyryl cyclic AMP. Tretinoin 130-143 aconitate decarboxylase 1 Homo sapiens 52-55
3380093-0 1988 Regulation of c-myb expression in human neuroblastoma cells during retinoic acid-induced differentiation. Tretinoin 67-80 MYB proto-oncogene, transcription factor Homo sapiens 14-19
3380093-2 1988 Since the level of c-myb expression declined during fetal development, we studied the regulation of its expression in human neuroblastoma cell lines induced to differentiate by retinoic acid. Tretinoin 177-190 MYB proto-oncogene, transcription factor Homo sapiens 19-24
2470302-1 1988 Keratinocytes in culture produce detectable amounts of IL-1 alpha mRNA constitutively and can be stimulated to express increased amounts of IL-1 alpha mRNA by cycloheximide, PMA, and retinoic acid. Tretinoin 183-196 interleukin 1 alpha Homo sapiens 55-65
2470302-1 1988 Keratinocytes in culture produce detectable amounts of IL-1 alpha mRNA constitutively and can be stimulated to express increased amounts of IL-1 alpha mRNA by cycloheximide, PMA, and retinoic acid. Tretinoin 183-196 interleukin 1 alpha Homo sapiens 140-150
2898410-1 1988 We have studied the expression of nine homeobox genes from Hox 1, Hox 2, Hox 3 and Hox 5 clusters in human embryonal carcinoma (EC) cell lines analyzed as both stem cells and after exposure to the differentiation-inducing agents retinoic acid (RA), hexamethylenebisacetamide (HMBA) and bromodeoxyuridine (BUdR). Tretinoin 229-242 homeobox A5 Homo sapiens 59-64
3060804-4 1988 Following retinoic acid addition, N-myc expression declines but then returns to initial levels as the cells undergo endodermal differentiation. Tretinoin 10-23 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 34-39
3040236-0 1987 Differential responsiveness of normal and simian virus 40-transformed BALB/c 3T3 cells to retinoic acid: rapid enhancement of epidermal growth factor receptor binding in a simian virus 40-3T3 variant. Tretinoin 90-103 epidermal growth factor receptor Mus musculus 126-158
3600188-7 1987 There was, however, a significant decrease in the activity of ornithine decarboxylase early during the treatment with RA, and an increase in the levels of fibronectin secreted into the media by the RA-treated cell. Tretinoin 118-120 ornithine decarboxylase 1 Rattus norvegicus 62-85
3600188-7 1987 There was, however, a significant decrease in the activity of ornithine decarboxylase early during the treatment with RA, and an increase in the levels of fibronectin secreted into the media by the RA-treated cell. Tretinoin 198-200 fibronectin 1 Rattus norvegicus 155-166
3606573-2 1987 Treatment of these cells with dimethyl sulphoxide, 1 alpha,25-dihydroxycholecalciferol or retinoic acid caused progressive increases in P47 content. Tretinoin 90-103 pleckstrin Homo sapiens 136-139
3606573-3 1987 Retinoic acid (1 microM) elicited the largest response, a 4-fold increase in P47 protein after 7 days that was accompanied by an increase in translatable P47 mRNA. Tretinoin 0-13 pleckstrin Homo sapiens 77-80
3606573-3 1987 Retinoic acid (1 microM) elicited the largest response, a 4-fold increase in P47 protein after 7 days that was accompanied by an increase in translatable P47 mRNA. Tretinoin 0-13 pleckstrin Homo sapiens 154-157
3606573-4 1987 The induction of P47 by retinoic acid preceded cessation of cell proliferation and development of the capacity to reduce Nitro Blue Tetrazolium, indicating that its expression is an early event in the myeloid differentiation of HL-60 cells. Tretinoin 24-37 pleckstrin Homo sapiens 17-20
3566738-2 1987 The ecto-kinase reaction of the HLF-cells was cAMP-independent, showed an apparent Km for ATP of 6.99 +/- 0.35 (microM) and was substantially inhibited by TPA and RA. Tretinoin 163-165 HLF transcription factor, PAR bZIP family member Homo sapiens 32-35
3566738-7 1987 The drop in ecto-kinase activity of HLF-cells in situ caused by TPA, RA and the diacylglycerols was accompanied by an increase in total basal-(Mg++-dependent) protein kinase activity present in extracts of treated cells. Tretinoin 69-71 HLF transcription factor, PAR bZIP family member Homo sapiens 36-39
3325885-6 1987 In contrast, when the cells were exposed to retinoic acid, which results in a maturation along an alternative pathway, the inhibition of N-myc and c-myc expression was similar. Tretinoin 44-57 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 137-142
3325885-6 1987 In contrast, when the cells were exposed to retinoic acid, which results in a maturation along an alternative pathway, the inhibition of N-myc and c-myc expression was similar. Tretinoin 44-57 MYC proto-oncogene, bHLH transcription factor Homo sapiens 147-152
3467175-7 1986 The expression of the vimentin gene was also increased when HL60 cells were induced to differentiate by phorbol esters; it decreased when differentiation was induced by retinoic acid. Tretinoin 169-182 vimentin Homo sapiens 22-30
3019756-1 1986 The mechanism of the in vitro inhibition of Ca2+-, phosphatidylserine-dependent protein kinase C (PK-C)2 by the purified holo (ligand-saturated) forms of cellular retinol-binding protein (cRBP) and cellular retinoic acid-binding protein (cRABP) was studied. Tretinoin 207-220 retinol binding protein 1, cellular Mus musculus 154-186
3512042-5 1986 Studies on the biosynthesis of MAP2 indicated that RA induced a 2-3-fold increase in MAP2 synthesis in 24 h; however, this effect was transient, with the synthesis of MAP2 in RA-treated cells returning to control level by 72 h. Although biosynthetic studies suggested the synthesis of species at 250-300 kdalton, the major molecular weight form in the neuroblastoma cells was 230 kdalton. Tretinoin 51-53 microtubule-associated protein 2 Rattus norvegicus 31-35
3512042-5 1986 Studies on the biosynthesis of MAP2 indicated that RA induced a 2-3-fold increase in MAP2 synthesis in 24 h; however, this effect was transient, with the synthesis of MAP2 in RA-treated cells returning to control level by 72 h. Although biosynthetic studies suggested the synthesis of species at 250-300 kdalton, the major molecular weight form in the neuroblastoma cells was 230 kdalton. Tretinoin 51-53 microtubule-associated protein 2 Rattus norvegicus 85-89
3512042-5 1986 Studies on the biosynthesis of MAP2 indicated that RA induced a 2-3-fold increase in MAP2 synthesis in 24 h; however, this effect was transient, with the synthesis of MAP2 in RA-treated cells returning to control level by 72 h. Although biosynthetic studies suggested the synthesis of species at 250-300 kdalton, the major molecular weight form in the neuroblastoma cells was 230 kdalton. Tretinoin 51-53 microtubule-associated protein 2 Rattus norvegicus 85-89
3785153-0 1986 c-myc regulation during retinoic acid-induced differentiation of F9 cells is posttranscriptional and associated with growth arrest. Tretinoin 24-37 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
3785153-1 1986 We have shown that c-myc mRNA levels decrease more than 20-fold when F9 teratocarcinoma stem cells are induced to arrest growth and terminally differentiate to parietal endoderm after exposure to retinoic acid and cyclic AMP (Campisi et al., Cell 36:241-247, 1984). Tretinoin 196-209 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24
3785153-2 1986 Here, we demonstrate that although growth arrest and full expression of the differentiated phenotype required about 3 days, c-myc mRNA declined abruptly between 8 and 16 h after the addition of retinoic acid and cyclic AMP. Tretinoin 194-207 MYC proto-oncogene, bHLH transcription factor Homo sapiens 124-129
3785153-5 1986 Thus, decreased c-myc mRNA is a consequence of very early posttranscriptional regulation directed by retinoic acid. Tretinoin 101-114 MYC proto-oncogene, bHLH transcription factor Homo sapiens 16-21
3663577-2 1986 Formation of retinyl esters catalyzed by acyl-CoA:retinol acyltransferase (ARAT; retinol fatty-acyltransferase; EC 2.3.1.76) from intestinal mucosa has been studied in vitro in the presence of all-trans-retinoic acid. Tretinoin 193-216 diacylglycerol O-acyltransferase 2 Homo sapiens 41-73
3663577-2 1986 Formation of retinyl esters catalyzed by acyl-CoA:retinol acyltransferase (ARAT; retinol fatty-acyltransferase; EC 2.3.1.76) from intestinal mucosa has been studied in vitro in the presence of all-trans-retinoic acid. Tretinoin 193-216 diacylglycerol O-acyltransferase 2 Homo sapiens 75-79
3663577-7 1986 All-trans-retinoic acid inhibited ARAT both from rat and human intestinal mucosa. Tretinoin 0-23 diacylglycerol O-acyltransferase 2 Rattus norvegicus 34-38
3663577-12 1986 The inhibition of ARAT by retinoic acid may be of importance for normal retinol absorption in patients receiving retinoid therapy. Tretinoin 26-39 diacylglycerol O-acyltransferase 2 Homo sapiens 18-22
2983883-12 1985 In contrast to 1 alpha,25(OH)2D3, retinoic acid inhibited melanin synthesis and tyrosinase activity of B16 melanoma cells dose and time dependently. Tretinoin 34-47 tyrosinase Mus musculus 80-90
3855502-0 1985 Decreased expression of N-myc precedes retinoic acid-induced morphological differentiation of human neuroblastoma. Tretinoin 39-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 24-29
3916193-4 1985 The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene. Tretinoin 143-156 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 229-234
6085562-7 1984 The number of vimentin-positive cells could be increased by retinoic acid treatment of NTera-2 cells or by seeding the 2102Ep cells at low cell density. Tretinoin 60-73 vimentin Homo sapiens 14-22
6205395-6 1984 Treatment of epidermal cells with arotinoid Ro 13-6298, a potent synthetic analog of retinoic acid, increased the abundance of mRNA for keratin 13 by 25-fold and for keratin 19 by greater than 40-fold but had no effect on the abundance of mRNA for keratins 5 and 6. Tretinoin 85-98 keratin 13 Homo sapiens 136-146
6188622-7 1983 RA treatment finally led to the appearance and co-expression of keratin fibrils in many of the vimentin-containing F9 cells. Tretinoin 0-2 vimentin Homo sapiens 95-103
6812947-0 1982 Stimulation of fibronectin production by retinoic acid in mouse skin tumors. Tretinoin 41-54 fibronectin 1 Mus musculus 15-26
6174520-3 1982 Embryonal carcinoma cells induced to differentiate by exposure to retinoic acid synthesized increased amounts of Endo A approximately 48 h after exposure to the inducer. Tretinoin 66-79 keratin 8 Mus musculus 113-119
6968676-3 1980 However, when EGF was added in combination with trans-retinoic acid, cell growth was increased 159 to 214%. Tretinoin 48-67 epidermal growth factor Homo sapiens 14-17
6968676-5 1980 These results indicate that, under certain conditions, a presumed inhibitor of fibroblast growth (retinoic acid) can potentiate the mitogenic action of a hormone, namely, epidermal growth factor. Tretinoin 98-111 epidermal growth factor Homo sapiens 171-194
883229-4 1977 In the testes of rats receiving retinoic acid a reduced activity of the acid phosphatase and a rise of beta-galactosidase, as compared to their activity in controls was also demonstrable. Tretinoin 32-45 galactosidase, beta 1 Rattus norvegicus 103-121
33241484-9 2021 Compared to OCT4A which is sharply down-regulated in retinoic acid induced differentiation of NT2 cell line, the expression of OCT4B5 remains at low level in differentiated state. Tretinoin 53-66 POU class 5 homeobox 1 Homo sapiens 12-17
34015278-11 2021 Treatment with free ATRA and the selected formulations led to a significant amelioration of DN by reducing of creatinine, urea, TNF-alpha, ICAM-1, GM-CSF, VEGF levels as well as elevating AMPK and LKB1 levels. Tretinoin 20-24 vascular endothelial growth factor A Rattus norvegicus 155-159
34015278-11 2021 Treatment with free ATRA and the selected formulations led to a significant amelioration of DN by reducing of creatinine, urea, TNF-alpha, ICAM-1, GM-CSF, VEGF levels as well as elevating AMPK and LKB1 levels. Tretinoin 20-24 serine/threonine kinase 11 Rattus norvegicus 197-201
33835049-1 2021 Initiation of spermatogonial differentiation in the mouse testis begins with the response to retinoic acid (RA) characterized by activation of KIT and STRA8 expression. Tretinoin 93-106 KIT proto-oncogene receptor tyrosine kinase Mus musculus 143-146
33835049-1 2021 Initiation of spermatogonial differentiation in the mouse testis begins with the response to retinoic acid (RA) characterized by activation of KIT and STRA8 expression. Tretinoin 93-106 stimulated by retinoic acid gene 8 Mus musculus 151-156
33835049-1 2021 Initiation of spermatogonial differentiation in the mouse testis begins with the response to retinoic acid (RA) characterized by activation of KIT and STRA8 expression. Tretinoin 108-110 KIT proto-oncogene receptor tyrosine kinase Mus musculus 143-146
33835049-1 2021 Initiation of spermatogonial differentiation in the mouse testis begins with the response to retinoic acid (RA) characterized by activation of KIT and STRA8 expression. Tretinoin 108-110 stimulated by retinoic acid gene 8 Mus musculus 151-156
33835049-7 2021 Following acute RA treatment (2-4hr), significantly more Dppa3+ late progenitors induced KIT, including at the midpoint of the cycle (stages VI-IX), than Dppa3- late progenitors. Tretinoin 16-18 KIT proto-oncogene receptor tyrosine kinase Mus musculus 89-92
33128583-7 2021 Although CD1d expression was low on glioblastoma stem-like cells, retinoic acid, which is the most common differentiating agent, upregulated CD1d expression in these cells and induced iNKT cell-mediated cytotoxicity. Tretinoin 66-79 CD1d molecule Homo sapiens 141-145
33878891-9 2021 Conclusion: The authors propose that HDAC7 controls the uptake of all-trans-retinoic acid, thus influencing RXRA activity and IGF1 signaling. Tretinoin 66-89 histone deacetylase 7 Homo sapiens 37-42
33933435-2 2021 Here, a series of amphiphilic retinoyl-bPEI conjugates (RP-1, RP-2 and RP-3) has been synthesized by allowing the reaction between bPEI (1.8 kDa) and a bioactive and hydrophobic vitamin A metabolite, all-trans-retinoic acid (ATRA), in varying amounts. Tretinoin 200-223 microtubule associated protein RP/EB family member 3 Homo sapiens 71-75
33933435-2 2021 Here, a series of amphiphilic retinoyl-bPEI conjugates (RP-1, RP-2 and RP-3) has been synthesized by allowing the reaction between bPEI (1.8 kDa) and a bioactive and hydrophobic vitamin A metabolite, all-trans-retinoic acid (ATRA), in varying amounts. Tretinoin 225-229 microtubule associated protein RP/EB family member 3 Homo sapiens 71-75
33933435-5 2021 RP-3/pDNA complex, with the highest content of retinoic acid, exhibited the best transfection efficiency. Tretinoin 47-60 microtubule associated protein RP/EB family member 3 Homo sapiens 0-4
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 erb-b2 receptor tyrosine kinase 4 Mus musculus 100-105
33987177-0 2021 Bhlhe40/Sirt1 Axis-Regulated Mitophagy Is Implicated in All-Trans Retinoic Acid-Induced Spina Bifida Aperta. Tretinoin 66-79 basic helix-loop-helix family, member e40 Rattus norvegicus 0-7
33987177-10 2021 Collectively, our results for the first time demonstrate that Bhlhe40/Sirt1 axis regulated mitophagy is implicated in ATRA-induced SBA. Tretinoin 118-122 basic helix-loop-helix family, member e40 Rattus norvegicus 62-69
33901013-2 2021 Previous studies have primarily focused on the retinoic acid signaling pathway and how it is interfered with by promyelocytic leukemia/retinoic acid receptor-alpha (PML/RARalpha) fusion protein. Tretinoin 47-60 retinoic acid receptor alpha Homo sapiens 135-163
33901013-2 2021 Previous studies have primarily focused on the retinoic acid signaling pathway and how it is interfered with by promyelocytic leukemia/retinoic acid receptor-alpha (PML/RARalpha) fusion protein. Tretinoin 47-60 PML nuclear body scaffold Homo sapiens 165-168
33901013-2 2021 Previous studies have primarily focused on the retinoic acid signaling pathway and how it is interfered with by promyelocytic leukemia/retinoic acid receptor-alpha (PML/RARalpha) fusion protein. Tretinoin 47-60 retinoic acid receptor alpha Homo sapiens 169-177
33901013-6 2021 Consistently, mutation of the C/EBP sites or deletion of retinoic acid responsive elements (RAREs) and RARE half motifs abrogated the PML/RARalpha-mediated repression. Tretinoin 57-70 PML nuclear body scaffold Homo sapiens 134-137
33901013-6 2021 Consistently, mutation of the C/EBP sites or deletion of retinoic acid responsive elements (RAREs) and RARE half motifs abrogated the PML/RARalpha-mediated repression. Tretinoin 57-70 retinoic acid receptor alpha Homo sapiens 138-146
33901013-8 2021 Finally, simultaneous knockdown of C/EBPalpha and C/EBPbeta reduces ATRA-induced upregulation of C/EBPepsilon and dramatically impaired NEAT1 activation and APL cell differentiation. Tretinoin 68-72 CCAAT enhancer binding protein epsilon Homo sapiens 97-109
33891336-10 2021 In addition, the expression of TXNDC5, RhoGDI, and RSU1 increased, while that of Vimentin decreased, in skin explants upon treatment with one of the anti-aging compounds, retinoic acid. Tretinoin 171-184 thioredoxin domain containing 5 Homo sapiens 31-37
33891336-10 2021 In addition, the expression of TXNDC5, RhoGDI, and RSU1 increased, while that of Vimentin decreased, in skin explants upon treatment with one of the anti-aging compounds, retinoic acid. Tretinoin 171-184 Rho GDP dissociation inhibitor alpha Homo sapiens 39-45
33891336-10 2021 In addition, the expression of TXNDC5, RhoGDI, and RSU1 increased, while that of Vimentin decreased, in skin explants upon treatment with one of the anti-aging compounds, retinoic acid. Tretinoin 171-184 Ras suppressor protein 1 Homo sapiens 51-55
33891336-10 2021 In addition, the expression of TXNDC5, RhoGDI, and RSU1 increased, while that of Vimentin decreased, in skin explants upon treatment with one of the anti-aging compounds, retinoic acid. Tretinoin 171-184 vimentin Homo sapiens 81-89
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin dependent kinase 2 Bos taurus 220-224
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin-dependent kinase 4 Bos taurus 226-230
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin dependent kinase 6 Bos taurus 232-236
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 164-177 retinoic acid receptor alpha Homo sapiens 193-196
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 164-177 aldehyde dehydrogenase 1 family member A3 Homo sapiens 238-245
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 179-181 retinoic acid receptor alpha Homo sapiens 193-196
33472949-3 2021 Here we found that experimental YAP activation in 5FU-sensitive and 5FU-resistant HT29 CRC cells enhanced nuclear YAP localization and the transcript levels of the retinoic acid (RA) receptors RARalpha/gamma and RAR target genes CYP26A1, ALDH1A3 and LGR5 through RA Response Elements (RAREs). Tretinoin 179-181 aldehyde dehydrogenase 1 family member A3 Homo sapiens 238-245
32854112-5 2021 All-trans retinoic acid and arsenic trioxide, two widely used drugs in APL therapy, exert synergistic effects on controlling super-enhancer-associated PML/RARalpha-regulated targets in APL cells. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 151-154
32854112-5 2021 All-trans retinoic acid and arsenic trioxide, two widely used drugs in APL therapy, exert synergistic effects on controlling super-enhancer-associated PML/RARalpha-regulated targets in APL cells. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 155-163
33451981-7 2021 The expression of CD1d on CLL cells is upregulated by all-trans retinoic acid, and sensitizes the malignant cells to bispecific VHH-induced lysis. Tretinoin 64-77 CD1d molecule Homo sapiens 18-22
33355213-2 2021 atRA is predominantly synthesized from retinaldehyde by aldehyde dehydrogenase 1A1 (ALDH1A1) but aldehyde oxidase (AOX) may also contribute to atRA biosynthesis. Tretinoin 0-4 aldehyde dehydrogenase 1 family member A1 Homo sapiens 56-82
33355213-2 2021 atRA is predominantly synthesized from retinaldehyde by aldehyde dehydrogenase 1A1 (ALDH1A1) but aldehyde oxidase (AOX) may also contribute to atRA biosynthesis. Tretinoin 0-4 aldehyde dehydrogenase 1 family member A1 Homo sapiens 84-91
33355213-7 2021 The two enzymes were identified as AOX and ALDH1A1 based on inhibition of atRA formation by AOX inhibitor hydralazine (20-50% inhibition) and ALDH1A1 inhibitor WIN18,446 (50-80% inhibition). Tretinoin 74-78 aldehyde dehydrogenase 1 family member A1 Homo sapiens 43-50
33355213-9 2021 The formation velocity of atRA in the presence of NAD+ correlated significantly with the expression of ALDH1A1 and AOX protein. Tretinoin 26-30 aldehyde dehydrogenase 1 family member A1 Homo sapiens 103-110
33355213-10 2021 Taken together the data show that both AOX and ALDH1A1 contribute to atRA biosynthesis in the human liver with ALDH1A1 being the high affinity low capacity enzyme and AOX the low affinity high capacity enzyme. Tretinoin 69-73 aldehyde dehydrogenase 1 family member A1 Homo sapiens 47-54
33355213-10 2021 Taken together the data show that both AOX and ALDH1A1 contribute to atRA biosynthesis in the human liver with ALDH1A1 being the high affinity low capacity enzyme and AOX the low affinity high capacity enzyme. Tretinoin 69-73 aldehyde dehydrogenase 1 family member A1 Homo sapiens 111-118
33411644-6 2021 Intrathecal RA application in the absence of reduced respiratory neural activity elicited an increase in phrenic inspiratory output, which was prevented by pre-treatment with an RARa inhibitor. Tretinoin 12-14 retinoic acid receptor, alpha Rattus norvegicus 178-182
33655333-3 2021 The aim of the present study was to investigate the expression pattern and function of Notch1 (N1) in all-trans retinoic acid (atRA)-induced NTDs and NSC differentiation. Tretinoin 121-134 notch 1 Mus musculus 87-93
33655333-3 2021 The aim of the present study was to investigate the expression pattern and function of Notch1 (N1) in all-trans retinoic acid (atRA)-induced NTDs and NSC differentiation. Tretinoin 136-140 notch 1 Mus musculus 87-93
33655333-12 2021 Western blotting results demonstrated that there were significantly, synchronous decreased expression levels of N1 and PS1, but increased expression levels of NF, GFAP and GALC in NSCs treated with atRA compared with those observed in the controls (P<0.05). Tretinoin 198-202 presenilin 1 Mus musculus 119-122
33655333-12 2021 Western blotting results demonstrated that there were significantly, synchronous decreased expression levels of N1 and PS1, but increased expression levels of NF, GFAP and GALC in NSCs treated with atRA compared with those observed in the controls (P<0.05). Tretinoin 198-202 glial fibrillary acidic protein Mus musculus 163-167
33655333-12 2021 Western blotting results demonstrated that there were significantly, synchronous decreased expression levels of N1 and PS1, but increased expression levels of NF, GFAP and GALC in NSCs treated with atRA compared with those observed in the controls (P<0.05). Tretinoin 198-202 galactosylceramidase Mus musculus 172-176
33605051-8 2021 Remarkably, the cleavage site on the RNA helicases MDA5 and LGP2, two relevant immune sensors of the retinoic acid-inducible gene-I (RIG-I)-like receptors family, resembles the L target site of Gemin5 and Daxx, and similar cleavage sites have been reported in ISG15 and TBK1, two proteins involved in type I interferon response and signaling pathway, respectively. Tretinoin 101-114 interferon induced with helicase C domain 1 Homo sapiens 51-55
33605051-8 2021 Remarkably, the cleavage site on the RNA helicases MDA5 and LGP2, two relevant immune sensors of the retinoic acid-inducible gene-I (RIG-I)-like receptors family, resembles the L target site of Gemin5 and Daxx, and similar cleavage sites have been reported in ISG15 and TBK1, two proteins involved in type I interferon response and signaling pathway, respectively. Tretinoin 101-114 DExH-box helicase 58 Homo sapiens 60-64
33605051-8 2021 Remarkably, the cleavage site on the RNA helicases MDA5 and LGP2, two relevant immune sensors of the retinoic acid-inducible gene-I (RIG-I)-like receptors family, resembles the L target site of Gemin5 and Daxx, and similar cleavage sites have been reported in ISG15 and TBK1, two proteins involved in type I interferon response and signaling pathway, respectively. Tretinoin 101-114 TANK binding kinase 1 Homo sapiens 270-274
33044585-12 2021 Meanwhile, ATRA could reduce the interaction between KLF5 and RARalpha, thereby inhibiting the function of cis-elements of KLF5. Tretinoin 11-15 retinoic acid receptor alpha Homo sapiens 62-70
33074481-7 2021 Taken together, our study reveals a novel role for SIK in the regulation of ATRA-mediated AML differentiation, implicating the combination of ATRA and SIK inhibition as a promising approach for future differentiation therapy. Tretinoin 76-80 salt inducible kinase 1 Homo sapiens 51-54
33074481-7 2021 Taken together, our study reveals a novel role for SIK in the regulation of ATRA-mediated AML differentiation, implicating the combination of ATRA and SIK inhibition as a promising approach for future differentiation therapy. Tretinoin 142-146 salt inducible kinase 1 Homo sapiens 51-54
33400349-6 2021 However, the spermatogonia from STRA8 knockout mice displayed a muted RA response such that there were more transcripts typical of undifferentiated cells and fewer transcripts typical of differentiating cells following RA action. Tretinoin 70-72 stimulated by retinoic acid gene 8 Mus musculus 32-37
33446666-0 2021 The demethylase inhibitor GSK-J4 limits inflammatory colitis by promoting de novo synthesis of retinoic acid in dendritic cells. Tretinoin 95-108 methyl-CpG binding domain protein 2 Homo sapiens 4-15
33473264-4 2021 Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 (CPSF6)-RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine. Tretinoin 150-154 cleavage and polyadenylation specific factor 6 Homo sapiens 60-106
33473264-4 2021 Here, we present an AML patient resembling APL with a novel cleavage and polyadenylation specific factor 6 (CPSF6)-RARG fusion, showing resistance to ATRA and poor response to chemotherapy with homoharringtonine and cytarabine. Tretinoin 150-154 cleavage and polyadenylation specific factor 6 Homo sapiens 108-113
33490645-7 2021 Immunoblotting also revealed that ATRA plus urolithin A-treatment up-regulated protein levels of p22-phox (to ~160%) and gp91-phox (to ~170%) although ATRA plus ellagic acid-treatment down-regulated protein levels of p22-phox (to ~70%) and gp91-phox (to ~60%). Tretinoin 34-38 cytochrome b-245 alpha chain Homo sapiens 97-105
33490645-7 2021 Immunoblotting also revealed that ATRA plus urolithin A-treatment up-regulated protein levels of p22-phox (to ~160%) and gp91-phox (to ~170%) although ATRA plus ellagic acid-treatment down-regulated protein levels of p22-phox (to ~70%) and gp91-phox (to ~60%). Tretinoin 34-38 cytochrome b-245 alpha chain Homo sapiens 217-225
33241870-3 2021 The protein ankyrin repeat domain 17 (Ankrd17), a positive regulator of inflammatory responses via the retinoic acid-inducible gene-I (RIG-I)-like receptor (RLR) signaling pathway, was identified as a specific PA-X binding partner that preferred PA-X to the PA protein. Tretinoin 103-116 DExH-box helicase 58 Homo sapiens 157-160
33375774-7 2022 Furthermore, the cytotoxic potential of CD38 CAR-NK cells was augmented by pre-treatment of the AML cells with all-trans retinoic acid which drove enhanced CD38 expression offering a rational combination therapy. Tretinoin 121-134 CD38 molecule Homo sapiens 40-44
33375774-7 2022 Furthermore, the cytotoxic potential of CD38 CAR-NK cells was augmented by pre-treatment of the AML cells with all-trans retinoic acid which drove enhanced CD38 expression offering a rational combination therapy. Tretinoin 121-134 CD38 molecule Homo sapiens 156-160
33241756-3 2021 In this study, we induced differentiation of four AML cell lines by all-trans retinoic acid (ATRA) and found HOTAIR was significantly upregulated in the process. Tretinoin 78-91 HOX transcript antisense RNA Homo sapiens 109-115
33241756-4 2021 Chromatin immunoprecipitation (ChIP) assays indicated that C/EBPbeta upregulated HOTAIR during ATRA induced differentiation in HL-60 cells. Tretinoin 95-99 HOX transcript antisense RNA Homo sapiens 81-87
33241756-5 2021 By gain- and loss-of-function analysis, we then observed that HOTAIR expression was positively correlated with ATRA-induced differentiation and negatively regulated G1 phase arrest in HL-60 cells. Tretinoin 111-115 HOX transcript antisense RNA Homo sapiens 62-68
33241756-6 2021 In addition, we found that HOTAIR promoted ATRA-induced differentiation via the regulation of the cell cycle regulator p21 via miR-17-5p. Tretinoin 43-47 HOX transcript antisense RNA Homo sapiens 27-33
33241756-6 2021 In addition, we found that HOTAIR promoted ATRA-induced differentiation via the regulation of the cell cycle regulator p21 via miR-17-5p. Tretinoin 43-47 H3 histone pseudogene 16 Homo sapiens 119-122
32865619-9 2020 RESULTS: Our findings suggest that high PKCalpha levels improve the differentiation response to ATRA in a RAR signaling-dependent manner. Tretinoin 96-100 retinoic acid receptor alpha Homo sapiens 106-109
32865619-10 2020 Moreover, RARbeta expression appears to be critical to induce ATRA sensitization, throughout AP1 trans-repression. Tretinoin 62-66 retinoic acid receptor alpha Homo sapiens 10-17
32865844-11 2020 The expression of GATA3 and IL-4 genes was significantly increased in the ATRA-, calcitriol-, and combination-treated mice when compared with the control group (p < 0.05). Tretinoin 74-78 GATA binding protein 3 Mus musculus 18-23
32865844-11 2020 The expression of GATA3 and IL-4 genes was significantly increased in the ATRA-, calcitriol-, and combination-treated mice when compared with the control group (p < 0.05). Tretinoin 74-78 interleukin 4 Mus musculus 28-32
33058427-6 2020 Whole transcriptome analysis shows significant alterations in gene expression profiles associated with transforming growth factor-beta (TGF-beta) and retinoic acid (RA) signalling pathways because of Tgif1 loss. Tretinoin 150-163 TGFB-induced factor homeobox 1 Mus musculus 200-205
32715478-8 2020 We propose that WT1 maintains retinoic acid signalling in the cortical stroma, which in turn, assures proper levels and dynamics of Ret expression in the ureteric bud tips, and thus, normal ramification of the ureteric tree. Tretinoin 30-43 WT1 transcription factor Mus musculus 16-19
33120864-5 2020 In a retrospective analysis using a cohort of patients treated with all-trans retinoic acid (ATRA) and anthracyclines, high SLIT2 expression was correlated with reduced leukocyte count (p = 0.024), and independently associated with improved overall survival (hazard ratio: 0.94; 95% confidence interval: 0.92-0.97; p < 0.001). Tretinoin 78-91 slit guidance ligand 2 Homo sapiens 124-129
33120864-5 2020 In a retrospective analysis using a cohort of patients treated with all-trans retinoic acid (ATRA) and anthracyclines, high SLIT2 expression was correlated with reduced leukocyte count (p = 0.024), and independently associated with improved overall survival (hazard ratio: 0.94; 95% confidence interval: 0.92-0.97; p < 0.001). Tretinoin 93-97 slit guidance ligand 2 Homo sapiens 124-129
33096610-11 2020 Further, regulation of its expression appeared to be dependent on a variety of factors, including exposure to all-trans retinoic acid (ATRA), a potent and highly specific inducer of CD38 expression in human promyelocytic leukemia cells that are now approved for in vivo use. Tretinoin 110-133 CD38 molecule Homo sapiens 182-186
33096610-11 2020 Further, regulation of its expression appeared to be dependent on a variety of factors, including exposure to all-trans retinoic acid (ATRA), a potent and highly specific inducer of CD38 expression in human promyelocytic leukemia cells that are now approved for in vivo use. Tretinoin 135-139 CD38 molecule Homo sapiens 182-186
33190441-6 2020 ATRA acted on the ERS-related PERK/eif2alpha signaling pathway and continued to increase the ERS of FLT3-ITD cells, resulting in an upregulation of apoptotic gene CHOP expression. Tretinoin 0-4 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 30-34
33190441-9 2020 Conclusions: ATRA further raises the ERS level of FLT3-ITD cells continuously by activating the ERS-related PERK/eif2alpha signal pathway and induces FLT3-ITD protein autophagy degradation through ERAA pathway, which induces apoptosis of FLT3-ITD-mutated leukemia cells. Tretinoin 13-17 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 108-112
32959699-0 2021 All-Trans Retinoic Acid Rescues the Tumor Suppressive Role of RAR-beta by Inhibiting LncHOXA10 Expression in Gastric Tumorigenesis. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 62-70
32959699-8 2021 Subsequently, mechanistic investigations revealed that LncHOXA10 can repress RAR-beta expression and that all-trans retinoic acid (ATRA) can rescue the expression of RAR-beta. Tretinoin 106-129 retinoic acid receptor alpha Homo sapiens 166-174
32959699-8 2021 Subsequently, mechanistic investigations revealed that LncHOXA10 can repress RAR-beta expression and that all-trans retinoic acid (ATRA) can rescue the expression of RAR-beta. Tretinoin 131-135 retinoic acid receptor alpha Homo sapiens 166-174
32955735-5 2021 Moreover, in SH-SY5Y cells differentiated into neurons by exposure to retinoic acid (10 microM), overexpression of GSK3beta and tau provokes an imbalance in cholinergic activity with a decrease in the neurotransmitter acetylcholine in the cell (45 +- 10%). Tretinoin 70-83 microtubule associated protein tau Homo sapiens 128-131
32485245-10 2020 Therefore, GA, the active metabolite of GL, as a novel AKR1B10 inhibitor, could promote retinoic acid synthesis. Tretinoin 88-101 aldo-keto reductase family 1, member B10 (aldose reductase) Mus musculus 55-62
32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 49-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3
32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 49-72 MYC proto-oncogene, bHLH transcription factor Homo sapiens 20-23
32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 49-72 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 25-29
32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 74-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-3
32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 74-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 20-23
32927768-7 2020 Myc proto-oncogene (MYC)/NMYC activity inhibitor all-trans retinoic acid (ATRA) significantly reduced the number of tumor spheres for both and the volume of BKZ-2 spheres. Tretinoin 74-78 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 25-29
32916897-0 2020 Enhanced Antiproliferative Effect of Combined Treatment with Calcitriol and All-Trans Retinoic Acid in Relation to Vitamin D Receptor and Retinoic Acid Receptor alpha Expression in Osteosarcoma Cell Lines. Tretinoin 86-99 retinoic acid receptor alpha Homo sapiens 138-166
32916897-8 2020 According to our results, the endogenous levels of RARalpha and VDR could be used as a predictor of possible synergy between ATRA and calcitriol in osteosarcoma cells. Tretinoin 125-129 retinoic acid receptor alpha Homo sapiens 51-59
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 56-84
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 86-90
32851975-1 2020 Retinoic Acid-Related Orphan Receptor Beta (RORbeta) is a transcription factor (TF) and marker of layer 4 (L4) neurons, which are distinctive both in transcriptional identity and the ability to form aggregates such as barrels in rodent somatosensory cortex. Tretinoin 0-13 RAR-related orphan receptor alpha Mus musculus 44-51
32823855-4 2020 In this review, we mostly focus on emerging RA-regulated epigenetic mechanisms involving RA receptor alpha (RARA) and Annexin A8 (ANXA8), which is a member of the Annexin family, as well as ANXA8 regulatory microRNAs (miRNAs). Tretinoin 44-46 retinoic acid receptor alpha Homo sapiens 108-112
32823855-5 2020 The first cancer showing ANXA8 upregulation was reported in acute promyelocytic leukemia (APL), which induces the differentiation arrest of promyelocytes due to defective RA signaling caused by RARA fusion genes as the PML-RARA gene. Tretinoin 171-173 PML nuclear body scaffold Homo sapiens 219-222
32929351-11 2020 Indeed, the PPAR activator not only enhanced the anti-APL effects of arsenic/ATRA by suppressing TRIB3 expression but also reduced therapy-induced dyslipidemia in APL patients. Tretinoin 77-81 peroxisome proliferator activated receptor alpha Homo sapiens 12-16
32929351-12 2020 Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment. Tretinoin 189-193 retinoic acid receptor alpha Homo sapiens 58-66
32323584-2 2020 The cases of increased PML-RARa transcripts received induction treatment mainly based on ATRA and ATO. Tretinoin 89-93 PML nuclear body scaffold Homo sapiens 23-26
32323584-2 2020 The cases of increased PML-RARa transcripts received induction treatment mainly based on ATRA and ATO. Tretinoin 89-93 retinoic acid receptor alpha Homo sapiens 27-31
32171039-8 2020 Interestingly, the data suggest that all-trans retinoic acid (ATRA)-induced ADAM17-mediated MerTK cleavage plays a critical role in regulating the levels of MerTK receptor on macrophages and that this pathway is impaired in NASH fibrosis. Tretinoin 37-60 MER proto-oncogene, tyrosine kinase Homo sapiens 92-97
32171039-8 2020 Interestingly, the data suggest that all-trans retinoic acid (ATRA)-induced ADAM17-mediated MerTK cleavage plays a critical role in regulating the levels of MerTK receptor on macrophages and that this pathway is impaired in NASH fibrosis. Tretinoin 37-60 MER proto-oncogene, tyrosine kinase Homo sapiens 157-162
32556644-8 2020 We then evaluated the effect of all-trans retinoic acid (ATRA), which is a retinoic acid receptor (RAR)alpha, RARbeta and RARgamma agonist, on the differentiation from the hiPSC-derived foregut. Tretinoin 32-55 retinoic acid receptor alpha Homo sapiens 110-117
32556644-8 2020 We then evaluated the effect of all-trans retinoic acid (ATRA), which is a retinoic acid receptor (RAR)alpha, RARbeta and RARgamma agonist, on the differentiation from the hiPSC-derived foregut. Tretinoin 57-61 retinoic acid receptor alpha Homo sapiens 110-117
31924349-0 2020 Corrigendum to "All-trans retinoic acid prevents epidural fibrosis through NF-kB signaling pathway in post-laminectomy rats" [Neuropharmacology 79 (2014) 275-281]. Tretinoin 16-39 nuclear factor kappa B subunit 1 Rattus norvegicus 75-80
32240058-0 2020 MYCN Silencing by RNA Interference Induces Neurogenesis and Suppresses Proliferation in Models of Neuroblastoma with Resistance to Retinoic Acid. Tretinoin 131-144 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-4
32240058-9 2020 Our result suggests that gene therapy using RNAi targeting MYCN can be a novel therapy toward MYCN-amplified NB that have complete or partial resistance toward RA. Tretinoin 160-162 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 59-63
32240058-9 2020 Our result suggests that gene therapy using RNAi targeting MYCN can be a novel therapy toward MYCN-amplified NB that have complete or partial resistance toward RA. Tretinoin 160-162 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 94-98
32695508-4 2020 ALDH1 has a role in early stem cell differentiation through its function in the oxidation of retinol to retinoic acid, proposed to be a strong candidate for breast cancer stem cells. Tretinoin 104-117 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-5
32630207-5 2020 Here, we showed that ATRA prolongs the expression of IL-6 and IL-1beta following a 2-, 6-, 12-, and 24-h LPS (100ng/mL) activation in human monocyte-derived macrophages. Tretinoin 21-25 interleukin 1 alpha Homo sapiens 62-70
32304991-2 2020 Although up-regulated retinoic acid signal responds further to maintain HSC activation, the underlying molecular mechanisms are largely unknown. Tretinoin 22-35 fucosyltransferase 1 (H blood group) Homo sapiens 72-75
32304991-4 2020 We found that lncRNA-H19 upregulation could enhance retinoic acid signals to induce HSC activation, whereas lncRNA-H19 knockdown completely disturbed retinoic acid signals. Tretinoin 52-65 fucosyltransferase 1 (H blood group) Homo sapiens 84-87
32304991-5 2020 Moreover, the activation of retinoic acid signals impaired the lncRNA-H19 knockdown mediated HSC inactivation. Tretinoin 28-41 fucosyltransferase 1 (H blood group) Homo sapiens 93-96
32304991-6 2020 Interestingly, we also found that enhanced retinoic acid signals by lncRNA-H19 was associated with a coordinate increase in retinol metabolism during HSC activation. Tretinoin 43-56 fucosyltransferase 1 (H blood group) Homo sapiens 150-153
32304991-12 2020 Overall, these results provided novel implications to reveal the molecular mechanism of increased retinoic acid signals during HSC activation, and identify lncRNA-H19/ADH3 pathway as a potential target for the treatment of liver fibrosis. Tretinoin 98-111 fucosyltransferase 1 (H blood group) Homo sapiens 127-130
32295917-2 2020 Both cellular and viral RNA cleavage products of RNase L bind pattern recognition receptors (PRR) like Retinoic acid-inducible I (Rig-I) and or melanoma differentiation-associated protein 5 (MDA5) to further amplify interferon (IFN) production and antiviral response. Tretinoin 103-116 ribonuclease L Homo sapiens 49-56
32295917-2 2020 Both cellular and viral RNA cleavage products of RNase L bind pattern recognition receptors (PRR) like Retinoic acid-inducible I (Rig-I) and or melanoma differentiation-associated protein 5 (MDA5) to further amplify interferon (IFN) production and antiviral response. Tretinoin 103-116 interferon induced with helicase C domain 1 Homo sapiens 191-195
32527063-3 2020 Retinoic acid (RA)/sonic hedgehog (Shh)-induced embryonic stem cells differentiation into motor neurons are employed to study up-regulation of Crabp1 by Shh. Tretinoin 0-13 sonic hedgehog signaling molecule Homo sapiens 35-38
32527063-3 2020 Retinoic acid (RA)/sonic hedgehog (Shh)-induced embryonic stem cells differentiation into motor neurons are employed to study up-regulation of Crabp1 by Shh. Tretinoin 0-13 sonic hedgehog signaling molecule Homo sapiens 153-156
31480153-8 2020 Conclusion: ATRA promotes the synthesis of casein by regulating JAK2/STAT5 pathway and downstream mTOR signaling pathway, and it improves the fatty acid composition of MAC-T cells by regulating SREBP1-related genes. Tretinoin 12-16 Janus kinase 2 Bos taurus 64-68
31480153-8 2020 Conclusion: ATRA promotes the synthesis of casein by regulating JAK2/STAT5 pathway and downstream mTOR signaling pathway, and it improves the fatty acid composition of MAC-T cells by regulating SREBP1-related genes. Tretinoin 12-16 signal transducer and activator of transcription 5A Homo sapiens 69-74
32124141-3 2020 RESULTS: The results show that the expression of Fra-1 is higher in all-trans retinoic acid-treated cervical cancer. Tretinoin 78-91 FOS like 1, AP-1 transcription factor subunit Homo sapiens 49-54
32124141-4 2020 Flow cytometry and kit detection show that all-trans retinoic acid can enhance the ability of Fra-1 to lose the mitochondrial membrane potential, inhibit the glucose consumption and the production of lactic acid as well as ATP. Tretinoin 53-66 FOS like 1, AP-1 transcription factor subunit Homo sapiens 94-99
32124141-5 2020 CCK8 and colony formation assays indicate that all-trans retinoic acid enhances the ability of Fra-1 to inhibit cell proliferation. Tretinoin 47-70 FOS like 1, AP-1 transcription factor subunit Homo sapiens 95-100
32124141-7 2020 CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 77-90 FOS like 1, AP-1 transcription factor subunit Homo sapiens 114-119
32124141-7 2020 CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 77-90 H3 histone pseudogene 16 Homo sapiens 236-239
32125053-4 2020 Here, we show that RXRalpha collaborated with myocardin-related transcription factor-A (MRTF-A) to strongly promote the RA-induced process as evidenced by the increase in NF-H expression and NF-H promoter transcription activity. Tretinoin 120-122 neurofilament heavy chain Homo sapiens 171-175
32125053-4 2020 Here, we show that RXRalpha collaborated with myocardin-related transcription factor-A (MRTF-A) to strongly promote the RA-induced process as evidenced by the increase in NF-H expression and NF-H promoter transcription activity. Tretinoin 120-122 neurofilament heavy chain Homo sapiens 191-195
32239597-0 2020 Complex context-relationships between DNA methylation and accessibility, histone marks, and hTERT gene expression in acute promyelocytic leukemia cells: perspectives for all-trans retinoic acid (ATRA) in cancer therapy. Tretinoin 180-193 telomerase reverse transcriptase Homo sapiens 92-97
32239597-0 2020 Complex context-relationships between DNA methylation and accessibility, histone marks, and hTERT gene expression in acute promyelocytic leukemia cells: perspectives for all-trans retinoic acid (ATRA) in cancer therapy. Tretinoin 195-199 telomerase reverse transcriptase Homo sapiens 92-97
3011686-6 1986 On the other hand, an inhibitor of ODC, DFMO, the protein kinase inhibitors, the calmodulin inhibitor and retinoic acid suppressed TPA-induced HTLV-I p19 expression but did not suppress multinucleated cell formation. Tretinoin 106-119 interleukin 23 subunit alpha Homo sapiens 150-153
3520340-3 1986 When the human promyelocytic leukaemia cell line HL60 is treated with retinoic acid, the cells differentiate into granulocytes, and there is a reduction in steady state c-myc RNA of more than 10-fold. Tretinoin 70-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 169-174
3512256-0 1986 Retinoic acid enhances cell responses to epidermal growth factor in mouse mammary gland in culture. Tretinoin 0-13 epidermal growth factor Mus musculus 41-64
3512256-2 1986 Addition of retinoic acid alone at 10 micrograms/ml to the medium had no significant effect on DNA synthesis, but addition of EGF with retinoic acid enhanced the EGF-stimulated DNA synthesis. Tretinoin 135-148 epidermal growth factor Mus musculus 126-129
3512256-2 1986 Addition of retinoic acid alone at 10 micrograms/ml to the medium had no significant effect on DNA synthesis, but addition of EGF with retinoic acid enhanced the EGF-stimulated DNA synthesis. Tretinoin 135-148 epidermal growth factor Mus musculus 162-165
3512256-3 1986 Furthermore, pretreatment of mammary explants with retinoic acid enhanced the effect of EGF plus retinoic acid on cell growth. Tretinoin 51-64 epidermal growth factor Mus musculus 88-91
3512256-7 1986 Measurement of specific binding of [125I]EGF to mouse mammary glands in culture demonstrated that pretreatment of the explants with retinoic acid slightly, but significantly, enhanced the specific binding of EGF to its cellular receptors. Tretinoin 132-145 epidermal growth factor Mus musculus 41-44
3512256-7 1986 Measurement of specific binding of [125I]EGF to mouse mammary glands in culture demonstrated that pretreatment of the explants with retinoic acid slightly, but significantly, enhanced the specific binding of EGF to its cellular receptors. Tretinoin 132-145 epidermal growth factor Mus musculus 208-211
2867089-0 1986 Cyclic AMP potentiates the retinoic acid-induced expression of tissue transglutaminase in peritoneal macrophages. Tretinoin 27-40 transglutaminase 2, C polypeptide Mus musculus 63-86
2994850-0 1985 Effect of retinoic acid on growth and morphological differentiation of mouse NB2a neuroblastoma cells in culture. Tretinoin 10-23 contactin 5 Mus musculus 77-80
3977910-0 1985 Retinoic acid treatment of human neuroblastoma cells is associated with decreased N-myc expression. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 82-87
3977910-2 1985 We report here that N-myc mRNA content is markedly decreased in cells of a neuroblastoma cell line (LA-N-5) following differentiation induced with retinoic acid. Tretinoin 147-160 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 20-25
3977910-3 1985 Exposure of the cells to retinoic acid induced morphologic changes consistent with neuronal differentiation, and led to a 75% decrease in expression of N-myc mRNA. Tretinoin 25-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 152-157
3967339-5 1985 The vitamin A derivative retinoic acid (RA) antagonized the TPA-caused FN-release in promotable clones. Tretinoin 25-38 fibronectin 1 Mus musculus 71-73
3967339-5 1985 The vitamin A derivative retinoic acid (RA) antagonized the TPA-caused FN-release in promotable clones. Tretinoin 40-42 fibronectin 1 Mus musculus 71-73
3896697-7 1985 The possibility was tested that RA directly or indirectly influences the production of IL-2 and thereby stimulates the induction of T killer cells. Tretinoin 32-34 interleukin 2 Mus musculus 87-91
3896697-8 1985 Results indeed show that RA-injected mice display an increased capacity to produce IL-2 upon stimulation of their splenocytes in a mixed lymphocyte reaction. Tretinoin 25-27 interleukin 2 Mus musculus 83-87
3896697-9 1985 It appears therefore that RA has an effect on T cells that are destined to produce IL-2 upon antigenic challenge. Tretinoin 26-28 interleukin 2 Mus musculus 83-87
6149218-0 1984 Retinoic acid-induced expression of tissue transglutaminase in mouse peritoneal macrophages. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 36-59
6149218-5 1984 Our studies suggest that retinoic acid and serum retinol-binding protein can directly regulate macrophage gene expression and specifically induce the synthesis of tissue transglutaminase. Tretinoin 25-38 transglutaminase 2, C polypeptide Mus musculus 163-186
6733848-1 1984 We have studied the effects of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and its in vivo and in vitro antagonist retinoic acid (RA) on the synthesis and release of a major extracellular glycoprotein, fibronectin (FN), in human lung fibroblasts (HLF). Tretinoin 148-150 HLF transcription factor, PAR bZIP family member Homo sapiens 265-268
6424665-1 1984 A decrease in the expression of the myc proto-oncogene of HL-60 cells has been reported as an accompaniment of myeloid differentiation induced by either dimethylsulfoxide or retinoic acid. Tretinoin 174-187 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-39
6607129-9 1984 In addition, the differentiative response of TH2.52 to TPA was completely blocked by retinoic acid (RA). Tretinoin 85-98 heart and neural crest derivatives expressed 2 Mus musculus 45-48
6607129-9 1984 In addition, the differentiative response of TH2.52 to TPA was completely blocked by retinoic acid (RA). Tretinoin 100-102 heart and neural crest derivatives expressed 2 Mus musculus 45-48
6427413-5 1984 MCCA was additive in its ability to induce differentiation of HL-60 with retinoic acid, another compound that induces differentiation at pharmacologic concentrations. Tretinoin 73-86 methylcrotonyl-CoA carboxylase subunit 1 Homo sapiens 0-4
6190140-5 1983 The synthesis of PS beta G in the secondary placental cells and human fibroblasts was induced by sodium butyrate and 5-bromo-2"-deoxyuridine (BrdUrd) but was not affected by agents that increase intracellular cAMP concentrations and retinoic acid. Tretinoin 233-246 protein S (beta) pseudogene Homo sapiens 17-24
6288114-0 1982 Effect of retinoic acid and 12-O-tetradecanoyl phorbol-13-acetate on the binding of epidermal growth factor to its cellular receptors. Tretinoin 10-23 epidermal growth factor Mus musculus 84-107
32397071-10 2020 The mRNA levels of IL-6, IL-1beta, TNF-alpha, and autophagy-related genes were detected after adding niacin, shRNA, compound C, trans retinoic acid, 3-methyladenine to BMECs. Tretinoin 134-147 tumor necrosis factor Bos taurus 35-44
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 141-160 interleukin 13 Sus scrofa 37-41
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 162-166 interleukin 13 Sus scrofa 37-41
32431691-4 2020 ATRA also increased IL-4 induced phosphorylation of signal transducer and activator of transcription 6 (STAT6) and mRNA expression of the chloride channel, calcium activated, family member 1 (CLCA1), important for mucus formation, and chemokine (C-C motif) ligand 26 (CCL26), a potent eosinophil chemoattractant. Tretinoin 0-4 signal transducer and activator of transcription 6 Homo sapiens 52-102
32431691-4 2020 ATRA also increased IL-4 induced phosphorylation of signal transducer and activator of transcription 6 (STAT6) and mRNA expression of the chloride channel, calcium activated, family member 1 (CLCA1), important for mucus formation, and chemokine (C-C motif) ligand 26 (CCL26), a potent eosinophil chemoattractant. Tretinoin 0-4 signal transducer and activator of transcription 6 Homo sapiens 104-109
32431691-5 2020 We extended these findings to human Mphi THP-1 cells and showed that ATRA synergistically increased IL-4-induced CCL2, CCL13, and CCL26 mRNA and protein levels. Tretinoin 69-73 C-C motif chemokine ligand 2 Homo sapiens 113-117
6811129-1 1982 Retinoic acid is a weak promotor of skin tumorigenesis in Charles River CD-1 mice. Tretinoin 0-13 CD1 antigen complex Mus musculus 72-76
10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 3 Homo sapiens 25-33
32380366-9 2020 Nevertheless, patients that required additional tests for diagnosis (PML immunofluorescence or molecular) started on ATRA later (28.5 versus 5.3 h; P < 0.0001), and had more thrombo-haemorrhagic complications (P = 0.04). Tretinoin 117-121 PML nuclear body scaffold Homo sapiens 69-72
10191271-11 1999 Injection of ALDH1, but not ALDH-PB, mRNA stimulated retinoic acid synthesis in Xenopus embryos at the blastula stage. Tretinoin 53-66 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 13-17
31858119-6 2020 Butyrate upregulated the production of transforming growth factor beta1 and all-trans retinoic acid by CD103+CD11b+ dendritic cells, both of which are critical for T-cell-independent IgA CSR. Tretinoin 86-99 integrin subunit alpha E Homo sapiens 103-108
10191271-12 1999 Thus our results indicate that Aldh1 can function in retinoic acid synthesis under physiological conditions, but that the closely related Aldh-pb does not share this property. Tretinoin 53-66 aldehyde dehydrogenase 3 family, member A1 Rattus norvegicus 31-35
10209249-2 1999 Immunohistochemistry was used to localise the cellular retinoid binding-proteins for retinol (CRBP I) and retinoic acid (CRABP I) in the embryonic and adult olfactory system. Tretinoin 106-119 retinol binding protein 1 Homo sapiens 121-128
31964534-2 2020 Early studies from model animal mice suggested that the retinoic acid (RA) response signal protein STRA8 (stimulated by retinoic acid gene 8) and the meiosis-specific chromosomal behavior marker protein SCP3 (Synaptonemal Complex Protein 3) were two crucial molecular markers during meiosis. Tretinoin 56-69 stimulated by retinoic acid gene 8 Mus musculus 99-104
31964534-2 2020 Early studies from model animal mice suggested that the retinoic acid (RA) response signal protein STRA8 (stimulated by retinoic acid gene 8) and the meiosis-specific chromosomal behavior marker protein SCP3 (Synaptonemal Complex Protein 3) were two crucial molecular markers during meiosis. Tretinoin 56-69 stimulated by retinoic acid gene 8 Mus musculus 106-140
10374844-6 1999 In contrast, the RARgamma agonist CD437 inhibited cell growth up to 90-99% in both retinoic acid sensitive and resistant gastric cancer cells at a concentration of 1 microM. Tretinoin 83-96 retinoic acid receptor gamma Homo sapiens 17-25
32970979-0 2020 Retinoic Acid-Loaded Poly(lactic-co-glycolic acid) Nanoparticle Formulation of ApoB-100-Derived Peptide 210 Attenuates Atherosclerosis. Tretinoin 0-13 apolipoprotein B Mus musculus 79-87
10192400-3 1999 Here we show that production of RA by the retinaldehyde dehydrogenase-2 (Raldh2) enzyme is required for mouse embryo survival and early morphogenesis. Tretinoin 32-34 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 42-71
32255397-2 2020 Materials & methods: All-trans retinoic acid (ATRA)-poly(lactide-co-glycolide acid) (PLGA)-poly(ethylene glycol) (PEG)-programmed death-ligand 1 (PD-L1) nanomedicines were fabricated by loading ATRA into PLGA-PEG nanocarriers and modification using an anti-PD-L1 antibody. Tretinoin 46-50 CD274 molecule Homo sapiens 146-151
32255397-2 2020 Materials & methods: All-trans retinoic acid (ATRA)-poly(lactide-co-glycolide acid) (PLGA)-poly(ethylene glycol) (PEG)-programmed death-ligand 1 (PD-L1) nanomedicines were fabricated by loading ATRA into PLGA-PEG nanocarriers and modification using an anti-PD-L1 antibody. Tretinoin 46-50 CD274 molecule Homo sapiens 257-262
10192400-3 1999 Here we show that production of RA by the retinaldehyde dehydrogenase-2 (Raldh2) enzyme is required for mouse embryo survival and early morphogenesis. Tretinoin 32-34 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 73-79
10024510-1 1999 To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). Tretinoin 84-97 LOC100508689 Homo sapiens 110-115
10024510-1 1999 To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). Tretinoin 99-101 LOC100508689 Homo sapiens 110-115
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 125-127 integrin subunit alpha E Homo sapiens 193-198
10024510-1 1999 To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). Tretinoin 99-101 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 139-144
32256976-8 2020 Roscovitine also enhanced the ATRA-induced nuclear enrichment of other signaling molecules traditionally perceived as cytoplasmic promoters of proliferation, but now known to promote differentiation; in particular: SFKs, Lyn, Fgr; adaptor proteins, c-Cbl, SLP-76; a guanine exchange factor, Vav1; and a transcription factor, IRF-1. Tretinoin 30-34 Cbl proto-oncogene Homo sapiens 249-254
10102471-8 1999 However, in HL-525 cells either pretreated by retinoic acid that reinduces PKCbeta gene expression or transfected with PKCbeta cDNA, PMA significantly activated PAI-1 synthesis and adhesion of cells. Tretinoin 46-59 protein kinase C beta Homo sapiens 75-82
32256561-4 2020 Whereas Abeta 1-42 needs transcription and translation for DSB production, RA protects against Abeta 1-42-induced DSBs at the posttranslational level through both the RARalpha/beta/gamma and PPARbeta/delta receptors as demonstrated by using specific antagonists. Tretinoin 75-77 retinoic acid receptor alpha Homo sapiens 167-205
32256561-7 2020 Overall, this study shows that RA can not only repair Abeta 1-42-induced DSBs but also prevent them via the RARalpha/beta/gamma and PPARbeta/delta receptors. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 108-146
10219964-2 1999 Effects of arachidonic acid, prostaglandins, retinol, retinoic acid and cholecalciferol on xenobiotic oxidations catalysed by 12 recombinant human cytochrome P450 (P450 or CYP) enzymes and by human liver microsomes have been investigated. Tretinoin 54-67 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 147-175
32168763-6 2020 The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1beta and TNF-alpha 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. Tretinoin 216-220 C-C motif chemokine ligand 2 Homo sapiens 136-141
32168763-6 2020 The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1beta and TNF-alpha 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. Tretinoin 216-220 interleukin 1 alpha Homo sapiens 143-151
10026291-1 1999 Microsomal enzymes that catalyze the first step in the biosynthesis of retinoic acid from retinal, retinol dehydrogenases (RDHs), access retinol bound to cellular retinol-binding protein (CRBP). Tretinoin 71-84 retinol binding protein 1 Homo sapiens 154-186
31879364-6 2020 Furthermore, shRNA-mediated genetic or all-trans retinoic acid-mediated pharmaceutical inhibition of Pin1 in multiple human gastric cancer cells potently suppresses the EMT, cell migration and invasion, and lung metastasis. Tretinoin 39-62 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 101-105
32093330-7 2020 Direct activation of the RAR pathway by application of the physiological RAR agonist retinoic acid (RA) further enhanced the hypertrophic phenotype. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 25-28
32093330-7 2020 Direct activation of the RAR pathway by application of the physiological RAR agonist retinoic acid (RA) further enhanced the hypertrophic phenotype. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 73-76
10026291-1 1999 Microsomal enzymes that catalyze the first step in the biosynthesis of retinoic acid from retinal, retinol dehydrogenases (RDHs), access retinol bound to cellular retinol-binding protein (CRBP). Tretinoin 71-84 retinol binding protein 1 Homo sapiens 188-192
9920855-1 1999 The synthetic retinoid 6-[3-adamantyl-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437), which was originally developed as an retinoic acid receptor (RAR)-gamma agonist, induces rapid apoptosis in all-trans retinoic acid (ATRA)-sensitive and ATRA-resistant clones of the NB4 cell line, a widely used experimental model of acute promyelocytic leukemia (APL). Tretinoin 131-144 retinoic acid receptor gamma Homo sapiens 155-158
32027669-6 2020 Use in situ hybridization to resolve effects on mRNA distributions of Aldh1a2 and Cyp26a1 (RA homeostasis); Hoxb1 and Pax6 (RA targets). Tretinoin 91-93 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 82-89
32027669-14 2020 In DKO embryos, RA-dependent Cyp26a1 is lost but Hoxb1 is sustained with Cyp1b1 at multiple sites. Tretinoin 16-18 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 29-36
9920855-1 1999 The synthetic retinoid 6-[3-adamantyl-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437), which was originally developed as an retinoic acid receptor (RAR)-gamma agonist, induces rapid apoptosis in all-trans retinoic acid (ATRA)-sensitive and ATRA-resistant clones of the NB4 cell line, a widely used experimental model of acute promyelocytic leukemia (APL). Tretinoin 227-231 retinoic acid receptor gamma Homo sapiens 155-158
9920855-1 1999 The synthetic retinoid 6-[3-adamantyl-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437), which was originally developed as an retinoic acid receptor (RAR)-gamma agonist, induces rapid apoptosis in all-trans retinoic acid (ATRA)-sensitive and ATRA-resistant clones of the NB4 cell line, a widely used experimental model of acute promyelocytic leukemia (APL). Tretinoin 247-251 retinoic acid receptor gamma Homo sapiens 155-158
9920792-5 1999 A tight correlation between the induction of tissue TGase, the inhibition of cell growth, and apoptosis was evident in all eight RA-sensitive cell lines. Tretinoin 129-131 transglutaminase 1 Homo sapiens 52-57
31666191-14 2020 These results indicated that TG2 expression was upregulated through ATRA-mediated RARgamma and that extracellular TG2 induced myotube hypertrophy by activating mTOR signaling-mediated protein synthesis through GPR56, independent of transglutaminase activity. Tretinoin 68-72 transglutaminase 2, C polypeptide Mus musculus 29-32
9989277-13 1999 Consistent with increased substrate-driven retinoic acid synthesis in SCC, the expression of transglutaminase 1 was suppressed to a greater extent in the SCCs than in NHK, when cells were exposed to equivalent medium concentrations of retinol. Tretinoin 43-56 transglutaminase 1 Homo sapiens 93-111
32089684-0 2020 All-Trans Retinoic Acid Inhibits Bone Marrow Mesenchymal Stem Cell Commitment to Adipocytes via Upregulating FRA1 Signaling. Tretinoin 10-23 FOS like 1, AP-1 transcription factor subunit Homo sapiens 109-113
32089684-4 2020 The expression level of FRA1 (FOS like 1, AP-1 transcription factor subunit) in atRA-treated BMSCs increased, suggesting that atRA-mediated inhibition of BMSCs adipogenesis involves FRA1. Tretinoin 80-84 FOS like 1, AP-1 transcription factor subunit Homo sapiens 24-28
32089684-4 2020 The expression level of FRA1 (FOS like 1, AP-1 transcription factor subunit) in atRA-treated BMSCs increased, suggesting that atRA-mediated inhibition of BMSCs adipogenesis involves FRA1. Tretinoin 80-84 FOS like 1, AP-1 transcription factor subunit Homo sapiens 182-186
32089684-4 2020 The expression level of FRA1 (FOS like 1, AP-1 transcription factor subunit) in atRA-treated BMSCs increased, suggesting that atRA-mediated inhibition of BMSCs adipogenesis involves FRA1. Tretinoin 126-130 FOS like 1, AP-1 transcription factor subunit Homo sapiens 24-28
32089684-4 2020 The expression level of FRA1 (FOS like 1, AP-1 transcription factor subunit) in atRA-treated BMSCs increased, suggesting that atRA-mediated inhibition of BMSCs adipogenesis involves FRA1. Tretinoin 126-130 FOS like 1, AP-1 transcription factor subunit Homo sapiens 182-186
32089684-11 2020 The results supported the conclusion that atRA inhibits BMSC adipogenesis partially through the RARG-FRA1-PPARG2 or the CEBPA axis or both. Tretinoin 42-46 FOS like 1, AP-1 transcription factor subunit Homo sapiens 101-105
9989277-14 1999 The data demonstrate a central role of LRAT in regulating retinoic acid synthesis via its capacity to modulate cellular levels of substrate retinol. Tretinoin 58-71 lecithin retinol acyltransferase Homo sapiens 39-43
9870916-7 1999 Within 12 h after the start of RA treatment, cornifin alpha expression decreased, signaling the beginning of a change in cellular phenotype. Tretinoin 31-33 small proline rich protein 1A Homo sapiens 45-59
32010697-4 2019 We have recently shown that retinoic acid (RA) significantly enhances Zscan4 cell population. Tretinoin 28-41 zinc finger and SCAN domain containing 4 Homo sapiens 70-76
32010697-4 2019 We have recently shown that retinoic acid (RA) significantly enhances Zscan4 cell population. Tretinoin 43-45 zinc finger and SCAN domain containing 4 Homo sapiens 70-76
32010697-6 2019 Here we found that RA is decisive for ESCs to 2C-like cell transition, and reconstructed the gene network surrounding Zscan4. Tretinoin 19-21 zinc finger and SCAN domain containing 4 Homo sapiens 118-124
9870916-8 1999 At 24 h after addition of RA to the cultures, a significant number of mucous cells appeared, and at 72 h mucin was secreted in measurable amounts. Tretinoin 26-28 LOC100508689 Homo sapiens 105-110
10473269-4 1999 As the NT2/D1 teratocarcinoma cell line is treated with retinoic acid to induce differentiation to hNT cells, presenilin-1 messenger RNA expression is dramatically increased. Tretinoin 56-69 presenilin 1 Homo sapiens 110-122
31813960-7 2020 Transcript and protein analyses indicate an enhanced production of retinol and reduced conversion the retinoic acids (unchanged LRAT, Pnpla2/ATGL and Pnpla3 up, Cyp26a1 down) in L-G6pc-/- mice. Tretinoin 102-116 patatin-like phospholipase domain containing 2 Mus musculus 134-140
9831819-6 1999 RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. Tretinoin 0-2 spermidine/spermine N1-acetyltransferase 1 Bos taurus 172-212
31706164-1 2020 Hepatitis B virus (HBV) X protein (HBx) has been reported to counteract the innate immune responses through interfering with the pattern recognition receptors signaling activated by retinoic acid-inducible gene-I (RIG-I)-mitochondrial antiviral signaling protein (MAVS). Tretinoin 182-195 X protein Hepatitis B virus 35-38
31706164-1 2020 Hepatitis B virus (HBV) X protein (HBx) has been reported to counteract the innate immune responses through interfering with the pattern recognition receptors signaling activated by retinoic acid-inducible gene-I (RIG-I)-mitochondrial antiviral signaling protein (MAVS). Tretinoin 182-195 mitochondrial antiviral signaling protein Homo sapiens 264-268
9831819-6 1999 RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. Tretinoin 0-2 spermidine/spermine N1-acetyltransferase 1 Bos taurus 214-217
6984014-6 1982 SENCAR cells have a greater binding capacity for epidermal growth factor than BALB/c cells; however, the increased binding in response to retinoic acid and the rapid decrease after exposure to phorbol esters are similar in the two strains. Tretinoin 138-151 epidermal growth factor Mus musculus 49-72
9831819-7 1999 The putrescine content was significantly increased in RA-treated RPE cells up until 24 h, while spermidine, spermine and N1-acetylspermidine contents were significantly increased until 16 h. Our findings suggest that RA treatment increases the intracellular polyamine concentration of RPE cells via activation of ODC, SAMDC and SAT and that this results in the promotion of RPE cell growth until the cells reach full confluency. Tretinoin 217-219 spermidine/spermine N1-acetyltransferase 1 Bos taurus 328-331
31518508-4 2020 RA treatment attenuated cardiac injury as evidenced by decreased heart mass and left ventricular mass, mRNA expressions of ANP and BNP, and cardiac fibrosis compared with that in GDM mice. Tretinoin 0-2 natriuretic peptide type A Mus musculus 123-126
9857192-3 1998 In Xenopus embryos, XCYP26 can rescue developmental defects induced by application of exogenous RA, suggesting that the enzymatic modifications introduced inhibit RA signalling activities in vivo. Tretinoin 96-98 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 20-26
31518508-4 2020 RA treatment attenuated cardiac injury as evidenced by decreased heart mass and left ventricular mass, mRNA expressions of ANP and BNP, and cardiac fibrosis compared with that in GDM mice. Tretinoin 0-2 natriuretic peptide type B Mus musculus 131-134
31518508-5 2020 The protective effect of RA on GDM cardiomyopathy was related to the decreased MDA content and ROS generation, the increased GSH-Px and SOD content as well as the reduced TNF-alpha and IL-1beta content and inhibition of NF-kappaB signaling. Tretinoin 25-27 interleukin 1 alpha Mus musculus 185-193
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 vascular endothelial growth factor A Rattus norvegicus 233-237
6260817-7 1981 In high-passage (p28) cells, as well as in low-passage cells (less than p10) treated with tyrosinase inhibitor phenylthiocarbamate, melanin synthesis was suppressed in the absence and presence of RA, yet the ability of RA to inhibit cell proliferation was not compromised. Tretinoin 196-198 tyrosinase Mus musculus 90-100
6260817-7 1981 In high-passage (p28) cells, as well as in low-passage cells (less than p10) treated with tyrosinase inhibitor phenylthiocarbamate, melanin synthesis was suppressed in the absence and presence of RA, yet the ability of RA to inhibit cell proliferation was not compromised. Tretinoin 219-221 tyrosinase Mus musculus 90-100
9857192-3 1998 In Xenopus embryos, XCYP26 can rescue developmental defects induced by application of exogenous RA, suggesting that the enzymatic modifications introduced inhibit RA signalling activities in vivo. Tretinoin 163-165 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 20-26
33960560-0 2021 Retinoic acid induces NELFA-mediated 2C-like state of mouse embryonic stem cells associates with epigenetic modifications and metabolic processes in chemically defined media. Tretinoin 0-13 negative elongation factor complex member A, Whsc2 Mus musculus 22-27
31905996-4 2019 Since we demonstrated how high doses of ascorbate (ASC) preferentially kill leukemic blast cells from APL patients, we aimed to define the underlying mechanism and found that promyelocytic leukemia/retinoic acid receptor alpha (PML/RARa) inhibits NRF2 function, impedes its transfer to the nucleus and enhances its degradation in the cytoplasm. Tretinoin 198-211 PML nuclear body scaffold Homo sapiens 228-236
9857192-4 1998 Alterations in the expression pattern of a number of different molecular markers for neural development induced upon ectopic expression of XCYP26 reflect a primary function of RA signalling in hindbrain development. Tretinoin 176-178 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 139-145
33960560-7 2021 RESULTS: Retinoic acid drives a NELFA (negative elongation factor A)-mediated 2C-like state in mouse ESCs, characterized with 2C-specific transcriptional networks and the ability to contribute trophectoderm (TE) when injected into developing embryos. Tretinoin 9-22 negative elongation factor complex member A, Whsc2 Mus musculus 32-37
33960560-7 2021 RESULTS: Retinoic acid drives a NELFA (negative elongation factor A)-mediated 2C-like state in mouse ESCs, characterized with 2C-specific transcriptional networks and the ability to contribute trophectoderm (TE) when injected into developing embryos. Tretinoin 9-22 negative elongation factor complex member A, Whsc2 Mus musculus 39-67
9857192-6 1998 The expression pattern of XCYP26 during gastrulation appears to define areas within the prospective neural plate that develop in response to different concentrations of RA. Tretinoin 169-171 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 26-32
9857192-7 1998 Taken together, these observations appear to reflect an important regulatory function of XCYP26 for RA signalling; XCYP26-mediated modification of RA modulates its signalling activity and helps to establish boundaries of differentially responsive and non-responsive territories. Tretinoin 100-102 cytochrome P450 family 26 subfamily A member 1 S homeolog Xenopus laevis 89-95
9869297-3 1998 We have previously identified an retinoic acid (RA)-inducible enhancer (RAIDR5) located approximately 6.5 kb 3" of the coding region of the murine Hoxb1 gene. Tretinoin 33-46 homeobox B1 Mus musculus 147-152
33475861-9 2021 Additionally, EYA3 gene expression was deregulated in vitro by retinoic acid exposure. Tretinoin 63-76 EYA transcriptional coactivator and phosphatase 3 Danio rerio 14-18
31867329-0 2019 Targeting Pin1 by All-Trans Retinoic Acid (ATRA) Overcomes Tamoxifen Resistance in Breast Cancer via Multifactorial Mechanisms. Tretinoin 22-41 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 10-14
31867329-4 2019 Here, we explore the mechanism and effect of targeting Pin1 using its chemical inhibitor all-trans retinoic acid (ATRA) in the treatment of tamoxifen-resistant breast cancer. Tretinoin 89-112 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 55-59
9869297-3 1998 We have previously identified an retinoic acid (RA)-inducible enhancer (RAIDR5) located approximately 6.5 kb 3" of the coding region of the murine Hoxb1 gene. Tretinoin 48-50 homeobox B1 Mus musculus 147-152
9869297-4 1998 This 3" enhancer contains three sequences that are highly conserved in similar RA-inducible enhancers identified in the murine and human Hoxa1 genes and in the chicken Hoxb1 gene. Tretinoin 79-81 homeobox A1 Homo sapiens 137-142
34047175-0 2021 A Pin1/PML/P53 axis activated by retinoic acid in NPM-1c-acute myeloid leukemia. Tretinoin 33-46 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 2-6
9869297-5 1998 One element, a DR5 RA response element, contributes to the RA inducibility of a Hoxb1 reporter gene construct in F9 cells. Tretinoin 19-21 homeobox B1 Mus musculus 80-85
34047175-0 2021 A Pin1/PML/P53 axis activated by retinoic acid in NPM-1c-acute myeloid leukemia. Tretinoin 33-46 PML nuclear body scaffold Homo sapiens 7-10
34047175-4 2021 Here, we demonstrate that PML is required to initiate RA-driven NPM-1c degradation, P53 activation and cell death. Tretinoin 54-56 PML nuclear body scaffold Homo sapiens 26-29
34047175-5 2021 Mechanistically, RA enhances PML basal expression through inhibition of activated Pin1, prior to NPM-1c degradation. Tretinoin 17-19 PML nuclear body scaffold Homo sapiens 29-32
34047175-5 2021 Mechanistically, RA enhances PML basal expression through inhibition of activated Pin1, prior to NPM-1c degradation. Tretinoin 17-19 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 82-86
31805753-3 2019 All-trans retinoic acid (ATRA) is the principal endogenous ligand for the retinoic acid receptor alpha (RARA) and is produced by the enzymatic oxidation of dietary vitamin A, whose deficiency is associated with several pathological conditions. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 74-102
31805753-3 2019 All-trans retinoic acid (ATRA) is the principal endogenous ligand for the retinoic acid receptor alpha (RARA) and is produced by the enzymatic oxidation of dietary vitamin A, whose deficiency is associated with several pathological conditions. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 104-108
31805753-3 2019 All-trans retinoic acid (ATRA) is the principal endogenous ligand for the retinoic acid receptor alpha (RARA) and is produced by the enzymatic oxidation of dietary vitamin A, whose deficiency is associated with several pathological conditions. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 74-102
31805753-3 2019 All-trans retinoic acid (ATRA) is the principal endogenous ligand for the retinoic acid receptor alpha (RARA) and is produced by the enzymatic oxidation of dietary vitamin A, whose deficiency is associated with several pathological conditions. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 104-108
34001245-12 2021 RESULTS: ATRA enhanced BMP9-induced ALP, RUNX2 expressions, ALP activities, and matrix mineralization in mouse embryonic fibroblasts as well as C3H10T1/2 and C2C12 cells, while a high concentration of DEX attenuated these markers. Tretinoin 9-13 runt related transcription factor 2 Mus musculus 41-46
9869297-5 1998 One element, a DR5 RA response element, contributes to the RA inducibility of a Hoxb1 reporter gene construct in F9 cells. Tretinoin 59-61 homeobox B1 Mus musculus 80-85
9869297-10 1998 A single Hoxb1 CE1 binding complex is also detected by gel shift assays in nuclear extracts prepared from both stem and RA-treated F9 cells. Tretinoin 120-122 homeobox B1 Mus musculus 9-14
11367680-5 1998 However, immunostaining data showed that beta-catenin was translocalized into nuclei after retinoic acid induced P19 cell aggregates were trypsinized and cultured in serum free N2 medium for 2 and 4 d. In this period, transcription of En-2, a downstream target gene of Wnt signal, increased evidently. Tretinoin 91-104 interleukin 23, alpha subunit p19 Mus musculus 113-116
33989617-7 2021 Additionally, upregulated transcriptions of spermatogenic differentiation marker C-KIT and meiotic marker SYCP3 were detected in these cells after retinoic acid-induced differentiation. Tretinoin 147-160 synaptonemal complex protein 3 Bos taurus 106-111
31372995-5 2019 In mesenteric lymph nodes, retinoic acid (RA) released by CD103+ dendritic cells downregulated lamin A/C in CD4+ T-cells, enhancing Treg differentiation. Tretinoin 27-40 lamin A Mus musculus 95-104
31372995-5 2019 In mesenteric lymph nodes, retinoic acid (RA) released by CD103+ dendritic cells downregulated lamin A/C in CD4+ T-cells, enhancing Treg differentiation. Tretinoin 42-44 lamin A Mus musculus 95-104
9865605-4 1998 RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. Tretinoin 0-2 lectin, galactose binding, soluble 1 Mus musculus 68-78
31894006-0 2019 [All-trans retinoic acid promotes differentiation of human leukemia cells by degrading NLS-RARalpha]. Tretinoin 11-24 retinoic acid receptor alpha Homo sapiens 91-99
31894006-1 2019 Objective To investigate the effect of all-trans retinoic acid (ATRA) on cell differentiation in nuclear localization signal-retinoic acid receptor-alpha (NLS-RARalpha)-overexpressing leukemia cells. Tretinoin 64-68 retinoic acid receptor alpha Homo sapiens 125-153
31894006-7 2019 NLS-RARalpha could be degraded by ATRA in a concentration- and time-dependent manner; ATRA promoted cell differentiation in both negative control cells and NLS-RARalpha-overexpressing cells. Tretinoin 34-38 retinoic acid receptor alpha Homo sapiens 4-12
33964145-0 2021 Retinoic acid stimulates transcription of the rat SHARP-2 gene via multiple pathways. Tretinoin 0-13 basic helix-loop-helix family, member e40 Rattus norvegicus 50-57
33964145-3 2021 RA rapidly and temporarily induced the SHARP-2 mRNA expression in hepatic H4IIE cells. Tretinoin 0-2 basic helix-loop-helix family, member e40 Rattus norvegicus 39-46
33964145-7 2021 The RA-induction of SHARP-2 mRNA level was mainly inhibited by LY294002, staurosporine, and actinomycin D, respectively. Tretinoin 4-6 basic helix-loop-helix family, member e40 Rattus norvegicus 20-27
33964145-8 2021 Finally, whether RA acts on the transcriptional regulatory region of the SHARP-2 gene was analyzed using luciferase reporter gene assay. Tretinoin 17-19 basic helix-loop-helix family, member e40 Rattus norvegicus 73-80
33964145-9 2021 At least two RA-responsive regions were mapped at the nucleotide sequences between -3,700 and -1,600 of the SHARP-2 gene. Tretinoin 13-15 basic helix-loop-helix family, member e40 Rattus norvegicus 108-115
31894006-7 2019 NLS-RARalpha could be degraded by ATRA in a concentration- and time-dependent manner; ATRA promoted cell differentiation in both negative control cells and NLS-RARalpha-overexpressing cells. Tretinoin 34-38 retinoic acid receptor alpha Homo sapiens 160-168
31894006-7 2019 NLS-RARalpha could be degraded by ATRA in a concentration- and time-dependent manner; ATRA promoted cell differentiation in both negative control cells and NLS-RARalpha-overexpressing cells. Tretinoin 86-90 retinoic acid receptor alpha Homo sapiens 160-168
33964145-11 2021 Thus, we conclude that RA stimulated transcription of the SHARP-2 gene via multiple pathways. Tretinoin 23-25 basic helix-loop-helix family, member e40 Rattus norvegicus 58-65
9865605-4 1998 RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. Tretinoin 0-2 lysosomal-associated membrane protein 3 Mus musculus 169-173
9865605-4 1998 RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. Tretinoin 0-2 lectin, galactose binding, soluble 1 Mus musculus 299-309
9865605-4 1998 RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. Tretinoin 0-2 lysosomal-associated membrane protein 3 Mus musculus 324-328
33743351-4 2021 We showed that lack of p53 has no effect on cell pluripotency but significantly hinders the differentiation process induced by retinoic acid. Tretinoin 127-140 transformation related protein 53, pseudogene Mus musculus 23-26
33743351-6 2021 However, under retinoic acid-induced differentiation, the accumulation of autophagosomes and lysosomes is impaired in p53 KO mESCs, indicating a critical role of p53 in the regulation of autophagy upon differentiation. Tretinoin 15-28 transformation related protein 53, pseudogene Mus musculus 118-121
33743351-6 2021 However, under retinoic acid-induced differentiation, the accumulation of autophagosomes and lysosomes is impaired in p53 KO mESCs, indicating a critical role of p53 in the regulation of autophagy upon differentiation. Tretinoin 15-28 transformation related protein 53, pseudogene Mus musculus 162-165
31768440-1 2019 Objective: To identify an agonist of RXRalpha and RARalpha with reduced undesired profiles of all-trans retinoic acid for differentiation-inducing therapy of acute promyelocytic leukemia (APL), such as its susceptibility to P450 enzyme, induction of P450 enzyme, increased sequestration by cellular retinoic acid binding protein and increased expression of P-glycoprotein, a virtual screening was performed. Tretinoin 94-117 retinoic acid receptor alpha Homo sapiens 50-58
31768440-1 2019 Objective: To identify an agonist of RXRalpha and RARalpha with reduced undesired profiles of all-trans retinoic acid for differentiation-inducing therapy of acute promyelocytic leukemia (APL), such as its susceptibility to P450 enzyme, induction of P450 enzyme, increased sequestration by cellular retinoic acid binding protein and increased expression of P-glycoprotein, a virtual screening was performed. Tretinoin 104-117 retinoic acid receptor alpha Homo sapiens 50-58
9798948-6 1998 A similar result was obtained with retinoic acid-differentiated SH-SY5Y cells, which endogenously express both the ORL1 receptor and Gz. Tretinoin 35-48 opioid related nociceptin receptor 1 Homo sapiens 115-119
31694721-1 2019 BACKGROUND: Increasing evidence shows that stimulated by retinoic acid 6 (STRA6) participates in regulating multiple cancers. Tretinoin 57-70 signaling receptor and transporter of retinol STRA6 Homo sapiens 74-79
31682623-3 2019 In this study, using a germ cell culture system, we investigated (1) whether RA treatment activates any mitogen-activated protein kinase (MAPK) pathways in fetal germ cells at the time of sex differentiation, and (2) if this is the case, whether the corresponding RA-stimulated signaling pathway regulates Stra8 expression in fetal germ cells and their entry into meiosis. Tretinoin 77-79 stimulated by retinoic acid gene 8 Mus musculus 306-311
33957999-2 2021 More than 95% of patients with this disease belong to typical APL, which express PML-RARA and are sensitive to differentiation induction therapy containing all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), and they exhibit an excellent clinical outcome. Tretinoin 181-185 PML nuclear body scaffold Homo sapiens 81-84
33957999-2 2021 More than 95% of patients with this disease belong to typical APL, which express PML-RARA and are sensitive to differentiation induction therapy containing all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), and they exhibit an excellent clinical outcome. Tretinoin 181-185 retinoic acid receptor alpha Homo sapiens 85-89
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 retinoic acid receptor alpha Homo sapiens 22-26
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 retinoic acid receptor alpha Homo sapiens 33-37
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 retinoic acid receptor alpha Homo sapiens 33-37
33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 retinoic acid receptor alpha Homo sapiens 33-37
33957999-10 2021 If ATRA-sensitive RARA rearrangement was identified, ATRA could be added back for re-induction of differentiation. Tretinoin 3-7 retinoic acid receptor alpha Homo sapiens 18-22
33957999-10 2021 If ATRA-sensitive RARA rearrangement was identified, ATRA could be added back for re-induction of differentiation. Tretinoin 53-57 retinoic acid receptor alpha Homo sapiens 18-22
31682623-5 2019 MEK1/2 inhibitor (U0126) treatment suppressed the mRNA expressions of RA-induced Stra8 and meiotic marker genes (Rec8, Spo11, Dmc1, and Sycp3) in both XX and XY fetal germ cells. Tretinoin 70-72 stimulated by retinoic acid gene 8 Mus musculus 81-86
31682623-5 2019 MEK1/2 inhibitor (U0126) treatment suppressed the mRNA expressions of RA-induced Stra8 and meiotic marker genes (Rec8, Spo11, Dmc1, and Sycp3) in both XX and XY fetal germ cells. Tretinoin 70-72 synaptonemal complex protein 3 Mus musculus 136-141
31682623-7 2019 Taken together, our results suggest the novel concept that the RA functions by stimulating the ERK1/2 pathway and that this activity is critical for Stra8 expression and meiotic progression in fetal germ cells. Tretinoin 63-65 stimulated by retinoic acid gene 8 Mus musculus 149-154
9820587-0 1998 Modulation of UVA-induced lipid peroxidation and suppression of UVB-induced ornithine decarboxylase response by all-trans-retinoic acid in human skin fibroblasts in vitro. Tretinoin 112-135 ornithine decarboxylase 1 Homo sapiens 76-99
31365169-0 2019 ARID1A-SIN3A drives retinoic acid-induced neuroblastoma differentiation by transcriptional repression of TERT. Tretinoin 20-33 AT-rich interaction domain 1A Homo sapiens 0-6
31365169-0 2019 ARID1A-SIN3A drives retinoic acid-induced neuroblastoma differentiation by transcriptional repression of TERT. Tretinoin 20-33 SIN3 transcription regulator family member A Homo sapiens 7-12
31365169-0 2019 ARID1A-SIN3A drives retinoic acid-induced neuroblastoma differentiation by transcriptional repression of TERT. Tretinoin 20-33 telomerase reverse transcriptase Homo sapiens 105-109
33959758-0 2021 Roles of Stra8 and Tcerg1l in retinoic acid induced spermatogonial differentiation in mouse. Tretinoin 30-43 stimulated by retinoic acid gene 8 Mus musculus 9-14
33724958-6 2021 Pertinently, a pan-CYP26 inhibitor, talarozole, abrogates the impact of phenylephrine on ATRA decline and hypertrophy in neonatal rat ventricular myocytes. Tretinoin 89-93 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 19-24
9820587-10 1998 with 50 mJ/cm2 UVB, ODC activity peaked in vehicle treated cells at a 7.4+/-0.2-fold increase compared to sham irradiated control cells, and was reduced to a 4.9+/-0.2-fold increase by 3 microM atRA. Tretinoin 194-198 ornithine decarboxylase 1 Homo sapiens 20-23
31880511-0 2019 All-trans retinoic acid regulated prohibitin by retinoic acid receptor alpha in hypoxia-induced renal tubular epithelial cell injury. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 48-76
9820587-11 1998 Treatment with 10 microM atRA further decreased ODC activity (3.7+/-1.0-fold increase) and this delayed activity peak occurred at 36 h p.i. Tretinoin 25-29 ornithine decarboxylase 1 Homo sapiens 48-51
31880511-4 2019 Our results indicate that ATRA can augment the expression of RARalpha and PHB proteins and reduce the expression of TGF-beta1, FN and Col-IV proteins. Tretinoin 26-30 retinoic acid receptor alpha Homo sapiens 61-69
31880511-5 2019 PHB expression was reduced in an ATRA treated RARalpha- group, and TGF-beta1, FN and Col-IV were up-regulated compared to the ATRA treated RARalpha+ group. Tretinoin 33-37 retinoic acid receptor alpha Homo sapiens 46-54
31557800-6 2019 ATRA attenuated kidney injury through the reduction of proteinuria, renal hypertrophy, increase in natriuresis, as well as early markers of damage such as beta2-microglobulin, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL). Tretinoin 0-4 hepatitis A virus cellular receptor 1 Rattus norvegicus 202-207
31557800-10 2019 ATRA administration restored the expression of RAR-alpha and inhibited direct interactions of JNK/RAR-alpha. Tretinoin 0-4 retinoic acid receptor, alpha Rattus norvegicus 47-56
33482354-0 2021 Differential expression patterns of the two paralogous Rec8 from Nile tilapia and their responsiveness to retinoic acid signaling. Tretinoin 106-119 meiotic recombination protein REC8 homolog Oreochromis niloticus 55-59
33482354-2 2021 Interestingly, two paralogous rec8 genes happen to exist in the stra8 (stimulated by retinoic acid gene 8)-absent fishes but not in stra8-existing fishes. Tretinoin 85-98 meiotic recombination protein REC8 homolog Oreochromis niloticus 30-34
33482354-5 2021 Here we characterized the two paralogous rec8 genes in Nile tilapia (Onrec8a and Onrec8b), and investigated their expression patterns and responsiveness to RA signaling by treatment of ex vivo testicular culture and promoter luciferase reporter assay. Tretinoin 156-158 meiotic recombination protein REC8 homolog Oreochromis niloticus 41-45
31557800-10 2019 ATRA administration restored the expression of RAR-alpha and inhibited direct interactions of JNK/RAR-alpha. Tretinoin 0-4 mitogen-activated protein kinase 8 Rattus norvegicus 94-97
9748586-9 1998 To further study the control of Ptx2 gene expression, we used an in vitro model for neural differentiation by treating mouse embryonic stem cells with retinoic acid. Tretinoin 151-164 paired-like homeodomain transcription factor 2 Mus musculus 32-36
31557800-10 2019 ATRA administration restored the expression of RAR-alpha and inhibited direct interactions of JNK/RAR-alpha. Tretinoin 0-4 retinoic acid receptor, alpha Rattus norvegicus 98-107
31527569-0 2019 Retinoic Acid Promotes Retinoic Acid Signaling by Suppression of Pitx1 In Tendon Cells: A Possible Mechanism of a Clubfoot-Like Phenotype Induced by Retinoic Acid. Tretinoin 23-36 paired like homeodomain 1 Homo sapiens 65-70
33555349-8 2021 As a proof-of-principle that these fusions can generate altered gene products, we characterized a ZNF451-BAG2 fusion, producing a truncated BAG2-protein which inhibited retinoic acid induced differentiation. Tretinoin 169-182 zinc finger protein 451 Homo sapiens 98-104
33555349-8 2021 As a proof-of-principle that these fusions can generate altered gene products, we characterized a ZNF451-BAG2 fusion, producing a truncated BAG2-protein which inhibited retinoic acid induced differentiation. Tretinoin 169-182 BAG cochaperone 2 Homo sapiens 105-109
33555349-8 2021 As a proof-of-principle that these fusions can generate altered gene products, we characterized a ZNF451-BAG2 fusion, producing a truncated BAG2-protein which inhibited retinoic acid induced differentiation. Tretinoin 169-182 BAG cochaperone 2 Homo sapiens 140-144
31527569-0 2019 Retinoic Acid Promotes Retinoic Acid Signaling by Suppression of Pitx1 In Tendon Cells: A Possible Mechanism of a Clubfoot-Like Phenotype Induced by Retinoic Acid. Tretinoin 23-36 paired like homeodomain 1 Homo sapiens 65-70
31527569-13 2019 In the presence of retinoic acid, the expression of Pitx1 was inhibited in tendon cells. Tretinoin 19-32 paired like homeodomain 1 Homo sapiens 52-57
9731743-11 1998 These data demonstrate a role for RA and RA-induced TGF-beta in the regulation of palate cell proliferation and GAG synthesis and suggest a role for TGF-beta in retinoid-induced cleft palate. Tretinoin 41-43 transforming growth factor, beta 1 Mus musculus 52-60
9773980-6 1998 In addition, the NCoR interaction domains interact much more strongly with the TR than those present in the silencing mediator of retinoic acid and TRs (SMRT). Tretinoin 130-143 nuclear receptor corepressor 2 Homo sapiens 153-157
31238067-8 2019 Cell culture experiments confirm that RA inhibits CaMKII phosphorylation, which requires Crabp1. Tretinoin 38-40 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 50-56
31238067-10 2019 Together, these data demonstrate that RA bound Crabp1 plays a protective role in beta-adrenergic stimulated cardiac remodeling, which is partially attributed to its dampening CaMKII activation. Tretinoin 38-40 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 175-181
33855282-4 2021 MSCl cells promote the differentiation of CTLA-4 expressing DCs via the production of all-trans retinoic acid (ATRA) functioning as a ligand of RARalpha, a key nuclear receptor in DC development. Tretinoin 86-109 retinoic acid receptor alpha Homo sapiens 144-152
33855282-4 2021 MSCl cells promote the differentiation of CTLA-4 expressing DCs via the production of all-trans retinoic acid (ATRA) functioning as a ligand of RARalpha, a key nuclear receptor in DC development. Tretinoin 111-115 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 42-48
33855282-4 2021 MSCl cells promote the differentiation of CTLA-4 expressing DCs via the production of all-trans retinoic acid (ATRA) functioning as a ligand of RARalpha, a key nuclear receptor in DC development. Tretinoin 111-115 retinoic acid receptor alpha Homo sapiens 144-152
9846167-5 1998 Retinoic acid (RA), which has also been shown to promote osteoblastic differentiation, synergized with type I collagen to cause super-induction of OP mRNA. Tretinoin 0-13 secreted phosphoprotein 1 Rattus norvegicus 147-149
33383158-5 2021 However, when H9c2s are differentiated to a more cardiac-like phenotype via treatment with retinoic acid (RA) in low serum media, loss of Delta psim induces robust, and reversible, cleavage of L-OPA1 and subsequent OMA1 degradation. Tretinoin 91-104 OMA1 zinc metallopeptidase Homo sapiens 215-219
33383158-5 2021 However, when H9c2s are differentiated to a more cardiac-like phenotype via treatment with retinoic acid (RA) in low serum media, loss of Delta psim induces robust, and reversible, cleavage of L-OPA1 and subsequent OMA1 degradation. Tretinoin 106-108 OMA1 zinc metallopeptidase Homo sapiens 215-219
9846167-5 1998 Retinoic acid (RA), which has also been shown to promote osteoblastic differentiation, synergized with type I collagen to cause super-induction of OP mRNA. Tretinoin 15-17 secreted phosphoprotein 1 Rattus norvegicus 147-149
9700083-3 1998 In the present work, the mechanism by which retinoic acid (RA) regulates surfactant protein (SP) B expression was assessed in vitro. Tretinoin 44-57 surfactant protein B Homo sapiens 73-98
32943753-6 2021 Retinoic acid receptor-alpha is the key mediator of the renal protective effects of retinoic acid, and repair of the endogenous retinoic acid pathway offers another potential therapeutic strategy for glomerular disease. Tretinoin 84-97 retinoic acid receptor alpha Homo sapiens 0-28
33627760-0 2021 All-trans-retinoic acid ameliorates atherosclerosis, promotes perivascular adipose tissue browning, and increases adiponectin production in Apo-E mice. Tretinoin 0-23 adiponectin, C1Q and collagen domain containing Mus musculus 114-125
33627760-7 2021 AtRa administration ameliorated atherosclerosis, induced PVAT browning, and increased adiponectin production in PVAT in Apo-E mice. Tretinoin 0-4 adiponectin, C1Q and collagen domain containing Mus musculus 86-97
33627760-11 2021 Besides, atRA increased the synthesis of adiponectin in PVAT and augmented NO level in the aorta in ApoE mice. Tretinoin 9-13 adiponectin, C1Q and collagen domain containing Mus musculus 41-52
9700083-3 1998 In the present work, the mechanism by which retinoic acid (RA) regulates surfactant protein (SP) B expression was assessed in vitro. Tretinoin 59-61 surfactant protein B Homo sapiens 73-98
33747646-4 2021 These medications inhibit two vital enzymes of cytochrome P-450, CYP2C9 and CYP3A4, potentiating the effects of ATRA on calcium metabolism. Tretinoin 112-116 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 65-71
9700083-7 1998 An RA responsive element mediating RA stimulation of the human SP-B promoter was identified. Tretinoin 3-5 surfactant protein B Homo sapiens 63-67
9700083-7 1998 An RA responsive element mediating RA stimulation of the human SP-B promoter was identified. Tretinoin 35-37 surfactant protein B Homo sapiens 63-67
9671595-0 1998 A conserved retinoic acid responsive element in the murine Hoxb-1 gene is required for expression in the developing gut. Tretinoin 12-25 homeobox B1 Mus musculus 59-65
32905596-0 2021 Retinoic acid-responsive CD8 effector T-cells are selectively increased in IL-23-rich tissue in gastrointestinal GvHD. Tretinoin 0-13 interleukin 23 subunit alpha Homo sapiens 75-80
32905596-6 2021 Using a targeted candidate protein approach we predicted the phenotype of RA-responsive T-cells in the context of increased microenvironmental IL-23. Tretinoin 74-76 interleukin 23 subunit alpha Homo sapiens 143-148
9671595-2 1998 We previously identified a conserved retinoic acid (RA)-inducible enhancer, named the RAIDR5, which contains a DR5 RARE; this RAIDR5 enhancer is located 3" of the Hoxb-1-coding region in both the mouse and chick. Tretinoin 37-50 tumor necrosis factor receptor superfamily, member 10b Mus musculus 89-92
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 0-13 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 15-22
9671595-2 1998 We previously identified a conserved retinoic acid (RA)-inducible enhancer, named the RAIDR5, which contains a DR5 RARE; this RAIDR5 enhancer is located 3" of the Hoxb-1-coding region in both the mouse and chick. Tretinoin 37-50 homeobox B1 Mus musculus 163-169
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 151-164 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 15-22
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 187-200 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 15-22
9671595-2 1998 We previously identified a conserved retinoic acid (RA)-inducible enhancer, named the RAIDR5, which contains a DR5 RARE; this RAIDR5 enhancer is located 3" of the Hoxb-1-coding region in both the mouse and chick. Tretinoin 52-54 tumor necrosis factor receptor superfamily, member 10b Mus musculus 89-92
9671595-2 1998 We previously identified a conserved retinoic acid (RA)-inducible enhancer, named the RAIDR5, which contains a DR5 RARE; this RAIDR5 enhancer is located 3" of the Hoxb-1-coding region in both the mouse and chick. Tretinoin 52-54 homeobox B1 Mus musculus 163-169
33074481-0 2021 Salt-inducible kinase inhibition sensitizes human acute myeloid leukemia cells to all-trans retinoic acid-induced differentiation. Tretinoin 92-105 salt inducible kinase 1 Homo sapiens 0-21
9671595-3 1998 In the F9 murine teratocarcinoma cell line, this DR5 RARE is required for the RA response of the Hoxb-1 gene, suggesting a functional role of the DR5 RARE in Hoxb-1 gene expression during embryogenesis. Tretinoin 53-55 tumor necrosis factor receptor superfamily, member 10b Mus musculus 49-52
33074481-3 2021 Here, we show that the combination of ATRA with salt-inducible kinase (SIK) inhibition significantly enhances ATRA-mediated AML differentiation. Tretinoin 110-114 salt inducible kinase 1 Homo sapiens 48-69
33074481-3 2021 Here, we show that the combination of ATRA with salt-inducible kinase (SIK) inhibition significantly enhances ATRA-mediated AML differentiation. Tretinoin 110-114 salt inducible kinase 1 Homo sapiens 71-74
9671595-3 1998 In the F9 murine teratocarcinoma cell line, this DR5 RARE is required for the RA response of the Hoxb-1 gene, suggesting a functional role of the DR5 RARE in Hoxb-1 gene expression during embryogenesis. Tretinoin 53-55 homeobox B1 Mus musculus 97-103
33074481-4 2021 SIK inhibition augmented the ability of ATRA to induce growth inhibition and G1 cell cycle arrest of AML cells. Tretinoin 40-44 salt inducible kinase 1 Homo sapiens 0-3
9671595-3 1998 In the F9 murine teratocarcinoma cell line, this DR5 RARE is required for the RA response of the Hoxb-1 gene, suggesting a functional role of the DR5 RARE in Hoxb-1 gene expression during embryogenesis. Tretinoin 53-55 tumor necrosis factor receptor superfamily, member 10b Mus musculus 146-149
9671595-3 1998 In the F9 murine teratocarcinoma cell line, this DR5 RARE is required for the RA response of the Hoxb-1 gene, suggesting a functional role of the DR5 RARE in Hoxb-1 gene expression during embryogenesis. Tretinoin 53-55 homeobox B1 Mus musculus 158-164
9711991-4 1998 It was found that the enhanced catabolism brought on by P450 induction was blocked when RA was added to AMC-HN-6 along with actinomycin D or cyclohexamide. Tretinoin 88-90 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 56-60
33495566-0 2021 PRMT3 interacts with ALDH1A1 and regulates gene-expression by inhibiting retinoic acid signaling. Tretinoin 73-86 aldehyde dehydrogenase 1 family member A1 Homo sapiens 21-28
33495566-4 2021 ALDH1A1 regulates variety of cellular processes by catalyzing the conversion of retinaldehyde to retinoic acid. Tretinoin 97-110 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7
33495566-6 2021 PRMT3 inhibits the enzymatic activity of ALDH1A1 and negatively regulates the expression of retinoic acid responsive genes in a methyltransferase activity independent manner. Tretinoin 92-105 aldehyde dehydrogenase 1 family member A1 Homo sapiens 41-48
9711991-6 1998 P450-mediated oxidation was detectable within 4 hours of RA treatment, and RA catabolism reached its maximum 16 hours after treatment. Tretinoin 57-59 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 0-4
33495541-12 2021 Thus, ATRA induced ATG7 and autophagy participated in its cytotoxicity on HCC cells and AFP interfere with the induction of ATG7 and autophagy through forming complex with RAR. Tretinoin 6-10 retinoic acid receptor alpha Homo sapiens 172-175
9657734-0 1998 Mutations in the E-domain of RAR portion of the PML/RAR chimeric gene may confer clinical resistance to all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 114-127 PML-RARA regulated adaptor molecule 1 Homo sapiens 48-55
9679985-6 1998 In contrast to RA (which activates RA receptors (RARs) and retinoid X receptors in HL-60 cells with its metabolite retinoids), a retinoid that selectively binds RAR-gamma, which is not expressed in HL-60 cells, was relatively ineffective in causing ERK2 activation. Tretinoin 15-17 retinoic acid receptor gamma Homo sapiens 161-170
33452727-0 2021 Effect of retinoic acid signaling on Ripply3 expression and pharyngeal arch morphogenesis in mouse embryos. Tretinoin 10-23 ripply transcriptional repressor 3 Mus musculus 37-44
33452727-9 2021 CONCLUSION: Spatio-temporal regulation of Ripply3 expression by RA signaling is indispensable for the posterior PA development in mouse. Tretinoin 64-66 ripply transcriptional repressor 3 Mus musculus 42-49
9688937-9 1998 These results together with the known stimulatory effect of TGF-beta1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-beta1 pathway. Tretinoin 112-114 insulin like growth factor binding protein 2 Homo sapiens 73-80
33177108-5 2021 Reduced ADH1-mediated retinol metabolism was associated with attenuated RA signaling and accumulated MDSCs in CRC tumors. Tretinoin 72-74 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 8-12
9706393-3 1998 Expression of Brn-2 is activated when P19 embryonal carcinoma cells are induced to differentiate into neural cells with retinoic acid (RA). Tretinoin 120-133 POU domain, class 3, transcription factor 2 Mus musculus 14-19
33177108-9 2021 Our results indicated that the defect in ADH1-mediated RA synthesis could provide a possible mechanism that fosters the generation of PMN-MDSCs in CRC and that restoring RA signaling in the TME could serve as a promising therapeutic strategy to abrogate the generation of PMN-MDSCs. Tretinoin 55-57 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 41-45
33177108-9 2021 Our results indicated that the defect in ADH1-mediated RA synthesis could provide a possible mechanism that fosters the generation of PMN-MDSCs in CRC and that restoring RA signaling in the TME could serve as a promising therapeutic strategy to abrogate the generation of PMN-MDSCs. Tretinoin 170-172 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 41-45
32771670-10 2020 While treatment with all-trans retinoic acid (ATRA), epidermal growth factor (EGF), and basic fibroblast growth factor (FGF) significantly induced NeuN expression in the differentiated NPCs (P < 0.01), the addition of ox-LDL significantly inhibited the NeuN expression (P < 0.05). Tretinoin 21-44 epidermal growth factor Mus musculus 78-81
9706393-3 1998 Expression of Brn-2 is activated when P19 embryonal carcinoma cells are induced to differentiate into neural cells with retinoic acid (RA). Tretinoin 135-137 POU domain, class 3, transcription factor 2 Mus musculus 14-19
32729137-0 2020 All-trans-retinoic acid shifts Th1 towards Th2 cell differentiation by targeting NFAT1 signalling to ameliorate immune-mediated aplastic anaemia. Tretinoin 0-23 nuclear factor of activated T cells 2 Homo sapiens 81-86
9662427-4 1998 Incubation with RA did not alter NGFI-A mRNA levels, but significantly reduced the NGFI-B and c-fos response to NGF and serum. Tretinoin 16-18 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 83-89
33105029-3 2020 In adult rodents, inhibition of Cyp26a1 and Cyp26b1 increases atRA concentrations and signaling. Tretinoin 62-66 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 32-39
9626505-1 1998 In a retinoic acid (RA) gene trap screen of mouse embryonic stem (ES) cells, a novel gene, named Aquarius (Aqr), was identified and characterized. Tretinoin 5-18 aquarius Mus musculus 97-105
33105029-11 2020 Postnatal knockout of Cyp26b1 resulted in increased atRA concentrations in the skin while the postnatal knockout of both Cyp26a1 and Cyp26b1 resulted in increased atRA concentrations in the liver, serum, skin, spleen, and intestines. Tretinoin 163-167 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 121-128
32536235-6 2020 Further studies revealed that ATO/ATRA may suppress the Expression of FLT3-ITD by promoting the UBE2L6-mediated ubiquitination pathway and decreasing the expression of C-MYC. Tretinoin 34-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 168-173
9626505-1 1998 In a retinoic acid (RA) gene trap screen of mouse embryonic stem (ES) cells, a novel gene, named Aquarius (Aqr), was identified and characterized. Tretinoin 5-18 aquarius Mus musculus 107-110
9626505-1 1998 In a retinoic acid (RA) gene trap screen of mouse embryonic stem (ES) cells, a novel gene, named Aquarius (Aqr), was identified and characterized. Tretinoin 20-22 aquarius Mus musculus 97-105
32992291-3 2020 Previously studies by our group and others have confirmed that PDCoV nucleocapsid (N) protein performs an important role in antagonizing retinoic acid-induced gene I-like receptor (RLR) activation. Tretinoin 137-150 DExH-box helicase 58 Homo sapiens 164-185
9626505-1 1998 In a retinoic acid (RA) gene trap screen of mouse embryonic stem (ES) cells, a novel gene, named Aquarius (Aqr), was identified and characterized. Tretinoin 20-22 aquarius Mus musculus 107-110
9626505-3 1998 Aqr transcripts are strongly induced in response to RA in vitro. Tretinoin 52-54 aquarius Mus musculus 0-3
9607768-0 1998 Distinct roles of the co-activators p300 and CBP in retinoic-acid-induced F9-cell differentiation. Tretinoin 52-65 E1A binding protein p300 Homo sapiens 36-40
9607768-6 1998 F9 cells expressing a p300-specific ribozyme became resistant to retinoic-acid-induced differentiation, whereas cells expressing a CBP-specific ribozyme were unaffected. Tretinoin 65-78 E1A binding protein p300 Homo sapiens 22-26
33113163-7 2021 The expression of both EGR3 and RELN were decreased during neuronal differentiation induced by retinoic acid (RA) in SH-SY5Y cells, and EGR3 overexpression reduced neurite outgrowth which could be partially reversed by the knockdown of RELN. Tretinoin 95-108 early growth response 3 Homo sapiens 23-27
33113163-7 2021 The expression of both EGR3 and RELN were decreased during neuronal differentiation induced by retinoic acid (RA) in SH-SY5Y cells, and EGR3 overexpression reduced neurite outgrowth which could be partially reversed by the knockdown of RELN. Tretinoin 110-112 early growth response 3 Homo sapiens 23-27
9607768-7 1998 Similarly, retinoic-acid-induced transcriptional upregulation of the cell-cycle inhibitor p21Cip1 required normal levels of p300, but not CBP, whereas the reverse was true for p27Kip1. Tretinoin 11-24 E1A binding protein p300 Homo sapiens 124-128
33081033-0 2020 Retinoic Acid Sensitivity of Triple-Negative Breast Cancer Cells Characterized by Constitutive Activation of the notch1 Pathway: The Role of Rarbeta. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 141-148
33081033-7 2020 ATRA inhibits the growth of HCC-1599, MB-157 and MDA-MB-157 cells via RARalpha, which up-regulates several retinoid target-genes, including RARbeta. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 70-78
9605760-6 1998 Although GDNF alone induced a rather weak differentiation independent of the disease stages, the enhancement of neurite outgrowth induced by treatment with both GDNF and all-trans-retinoic acid was significantly correlated with younger age (less than 1 year; P = 0.0039), non-stage 4 diseases (P = 0.0023), a single copy of N-myc (P = 0.027), and high levels of TRK-A expression (P = 0.0062). Tretinoin 174-193 neurotrophic receptor tyrosine kinase 1 Homo sapiens 362-367
33081033-7 2020 ATRA inhibits the growth of HCC-1599, MB-157 and MDA-MB-157 cells via RARalpha, which up-regulates several retinoid target-genes, including RARbeta. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 140-147
33081033-8 2020 RARbeta is a key determinant of ATRA anti-proliferative activity, as its silencing suppresses the effects exerted by the retinoid. Tretinoin 32-36 retinoic acid receptor alpha Homo sapiens 0-7
9566959-10 1998 Both in vivo and in vitro experiments demonstrate that NRP/B can be phosphorylated and can bind to the functionally active hypophosphorylated form of the p110(RB) during neuronal differentiation of SH-SY5Y neuroblastoma cells induced by retinoic acid. Tretinoin 237-250 ectodermal-neural cortex 1 Homo sapiens 55-60
32781074-4 2020 MAIN METHODS: Expression of eEF1A2 and PRDX1 in SH-SY5Y cells at various durations of retinoic acid (RA) induction was detected using qRT-PCR, Western blotting and immunofluorescence. Tretinoin 86-99 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 28-34
32781074-4 2020 MAIN METHODS: Expression of eEF1A2 and PRDX1 in SH-SY5Y cells at various durations of retinoic acid (RA) induction was detected using qRT-PCR, Western blotting and immunofluorescence. Tretinoin 86-99 peroxiredoxin 1 Homo sapiens 39-44
32329577-8 2020 RESULTS: NOX4, as a novel target of miR-322, was upregulated in ATRA-induced mouse model of NTDs. Tretinoin 64-68 microRNA 322 Mus musculus 36-43
31283017-9 2019 mRNAs of genes involved in retinoic acid (RA) synthesis (Stra6 and Rdh10) were also increased by EtOH, AcH, and 4-HNE treatment. Tretinoin 27-40 signaling receptor and transporter of retinol STRA6 Homo sapiens 57-62
31283017-9 2019 mRNAs of genes involved in retinoic acid (RA) synthesis (Stra6 and Rdh10) were also increased by EtOH, AcH, and 4-HNE treatment. Tretinoin 42-44 signaling receptor and transporter of retinol STRA6 Homo sapiens 57-62
9673404-7 1998 In contrast, the synthetic RAR-gamma selective agonists CD437 and CD2325 induced a concentration- and time-dependent antiproliferative effect, which was similar or even more pronounced than ATRA. Tretinoin 190-194 retinoic acid receptor gamma Homo sapiens 27-36
31262872-3 2019 We recently found that combination of all-trans retinoic acid (ATRA) with the beta1-integrin-activating peptide TNIIIA2 attenuated cancer-associated properties of neuroblastoma cells through N-Myc degradation. Tretinoin 38-61 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 191-196
31262872-3 2019 We recently found that combination of all-trans retinoic acid (ATRA) with the beta1-integrin-activating peptide TNIIIA2 attenuated cancer-associated properties of neuroblastoma cells through N-Myc degradation. Tretinoin 63-67 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 191-196
31676951-8 2020 Furthermore, CYP26A1 a retinoic acid receptor-specific target was revealed as a new player mediating the suppressive effect of fish oil-supplemented diet on SCD1 and ELOVL6 hepatic gene expression. Tretinoin 23-36 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 13-20
9617542-5 1998 The most marked inhibition was observed on day 10 of culture, and the most effective concentration of RA was 10(-6) M. Melanin synthesis was increased on day 10, and the most effective concentration of RA was also 10(-6) M. TGF-beta 1 also inhibited RPE cell proliferation and increased melanin synthesis. Tretinoin 102-104 transforming growth factor beta 1 Gallus gallus 224-234
31063220-0 2019 Chemerin partly mediates tumor-inhibitory effect of all-trans retinoic acid via CMKLR1-dependent natural killer cell recruitment. Tretinoin 62-75 chemokine-like receptor 1 Mus musculus 80-86
31063220-7 2019 Moreover, atRA treatment significantly enhanced tumor-infiltrating NK cells, which was completely abrogated in Rarres2-/- mice and Cmklr1-/- mice, suggesting a dependency of NK cell recruitment on the chemerin-CMKLR1 axis in melanoma. Tretinoin 10-14 chemokine-like receptor 1 Mus musculus 131-137
31063220-7 2019 Moreover, atRA treatment significantly enhanced tumor-infiltrating NK cells, which was completely abrogated in Rarres2-/- mice and Cmklr1-/- mice, suggesting a dependency of NK cell recruitment on the chemerin-CMKLR1 axis in melanoma. Tretinoin 10-14 chemokine-like receptor 1 Mus musculus 210-216
32973801-0 2020 Role for Retinoic Acid-Related Orphan Receptor Alpha (RORalpha) Expressing Macrophages in Diet-Induced Obesity. Tretinoin 9-22 RAR-related orphan receptor alpha Mus musculus 54-62
9617542-5 1998 The most marked inhibition was observed on day 10 of culture, and the most effective concentration of RA was 10(-6) M. Melanin synthesis was increased on day 10, and the most effective concentration of RA was also 10(-6) M. TGF-beta 1 also inhibited RPE cell proliferation and increased melanin synthesis. Tretinoin 202-204 transforming growth factor beta 1 Gallus gallus 224-234
32705508-2 2020 HEPC-CB.1 cells" potential to differentiate into endothelial cells was revealed after treating the cells with a mixture of ATRA, cAMP and VEGF, as shown by the reduced expression levels of CD133, CD271 and CD90 antigens, augmentation of CD146 and CD31, and a decrease in cell clonogenicity. Tretinoin 123-127 nerve growth factor receptor Homo sapiens 196-201
31063220-8 2019 Despite comparable melanoma growth detected in wild-type mice and Cmklr1-/- mice, lack of CMKLR1 partially abrogated the melanoma-inhibitory effect of atRA. Tretinoin 151-155 chemokine-like receptor 1 Mus musculus 90-96
31063220-10 2019 Collectively, our study suggests that down-regulation of chemerin could be a strategy used by cancers such as melanoma to impair anti-tumor NK cell immunity and identifies a new anti-tumor mechanism of atRA by up-regulating chemerin to enhance CMKLR1-dependent NK cell recruitment. Tretinoin 202-206 chemokine-like receptor 1 Mus musculus 244-250
32705508-2 2020 HEPC-CB.1 cells" potential to differentiate into endothelial cells was revealed after treating the cells with a mixture of ATRA, cAMP and VEGF, as shown by the reduced expression levels of CD133, CD271 and CD90 antigens, augmentation of CD146 and CD31, and a decrease in cell clonogenicity. Tretinoin 123-127 Thy-1 cell surface antigen Homo sapiens 206-210
9635256-0 1998 Expression of nitric oxide synthase isoforms in normal human tracheobronchial epithelial cells in vitro: dependence on retinoic acid and the state of differentiation. Tretinoin 119-132 nitric oxide synthase 1 Homo sapiens 14-35
32193285-6 2020 In vitro growth of HR-proficient breast, prostate, and pancreatic cancer cells was modestly repressed by Olaparib or Pin1 inhibition using all-trans retinoic acid (ATRA), while combination treatment resulted in near-complete block of cell proliferation. Tretinoin 149-162 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 117-121
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 18 Homo sapiens 133-138
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 5 Homo sapiens 208-212
9635256-1 1998 The retinoic acid (RA) and differentiation dependence of constitutive expression of the nitric oxide synthase (NOS) isoforms, iNOS, eNOS, and bNOS, was examined by reverse transcriptase polymerase chain recitation (RT-PCR) in cultured, normal, human, tracheobronchial epithelial (NHTBE) cells. Tretinoin 4-17 nitric oxide synthase 1 Homo sapiens 88-109
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 10 Homo sapiens 214-219
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 13 Homo sapiens 221-226
32193285-6 2020 In vitro growth of HR-proficient breast, prostate, and pancreatic cancer cells was modestly repressed by Olaparib or Pin1 inhibition using all-trans retinoic acid (ATRA), while combination treatment resulted in near-complete block of cell proliferation. Tretinoin 164-168 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 117-121
32193285-8 2020 Together our study reveals that Pin1 inhibition with widely used ATRA acts as an effective HR disrupter that sensitizes BRCA1-proficient tumors to PARP inhibition. Tretinoin 65-69 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 32-36
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 14 Homo sapiens 232-237
9635256-1 1998 The retinoic acid (RA) and differentiation dependence of constitutive expression of the nitric oxide synthase (NOS) isoforms, iNOS, eNOS, and bNOS, was examined by reverse transcriptase polymerase chain recitation (RT-PCR) in cultured, normal, human, tracheobronchial epithelial (NHTBE) cells. Tretinoin 19-21 nitric oxide synthase 1 Homo sapiens 88-109
32663289-0 2020 Retinoic Acid Potentiates Orbital Tissues for Inflammation Through NF-kappaB and MCP-1. Tretinoin 0-13 C-C motif chemokine ligand 2 Homo sapiens 81-86
31186810-0 2019 lncRNAs combine and crosstalk with NSPc1 in ATRA-induced differentiation of U87 glioma cells. Tretinoin 44-48 polycomb group ring finger 1 Homo sapiens 35-40
9635256-11 1998 eNOS expression was depressed by 10(-8) M RA, while bNOS mRNA levels were slightly reduced by 10(-6) M RA. Tretinoin 103-105 nitric oxide synthase 1 Homo sapiens 52-56
9635256-15 1998 bNOS expression was only marginally affected by the RA or differentiation status. Tretinoin 52-54 nitric oxide synthase 1 Homo sapiens 0-4
9537245-8 1998 Because up-regulated expression of TGF-beta1 suppresses papilloma formation, these studies suggest a mechanism whereby RA can prevent papilloma eruption via a TGF-beta intermediate, but papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 35-44
30876657-8 2019 Results of PML IF influenced decision to start ATRA in 25 (36%) APL patients and led to its termination in six non-APL patients. Tretinoin 47-51 PML nuclear body scaffold Homo sapiens 11-14
32488128-10 2021 Similarly, in patients without clozapine treatment, mRNA expression of RA-inducible targets CYP26A and STRA6, as well as at-RA/retinol ratio, were significantly reduced. Tretinoin 71-73 signaling receptor and transporter of retinol STRA6 Homo sapiens 103-108
9537245-8 1998 Because up-regulated expression of TGF-beta1 suppresses papilloma formation, these studies suggest a mechanism whereby RA can prevent papilloma eruption via a TGF-beta intermediate, but papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 35-43
9537245-8 1998 Because up-regulated expression of TGF-beta1 suppresses papilloma formation, these studies suggest a mechanism whereby RA can prevent papilloma eruption via a TGF-beta intermediate, but papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 159-167
31135261-1 2019 Transcriptional activation by PML-RARalpha, an acute promyelocytic leukemia-related oncofusion protein, requires pharmacological concentrations of all-trans retinoic acid (ATRA). Tretinoin 157-170 PML nuclear body scaffold Homo sapiens 30-33
31135261-1 2019 Transcriptional activation by PML-RARalpha, an acute promyelocytic leukemia-related oncofusion protein, requires pharmacological concentrations of all-trans retinoic acid (ATRA). Tretinoin 157-170 retinoic acid receptor alpha Homo sapiens 34-42
9502726-6 1998 The in vitro differentiation with retinoic acid and cAMP led to a 5- to 10-fold induction of flk-1, von Willebrand Factor (vWF), TM, GATA-4 and GATA-6. Tretinoin 34-47 kinase insert domain protein receptor Mus musculus 93-98
31135261-1 2019 Transcriptional activation by PML-RARalpha, an acute promyelocytic leukemia-related oncofusion protein, requires pharmacological concentrations of all-trans retinoic acid (ATRA). Tretinoin 172-176 PML nuclear body scaffold Homo sapiens 30-33
31135261-1 2019 Transcriptional activation by PML-RARalpha, an acute promyelocytic leukemia-related oncofusion protein, requires pharmacological concentrations of all-trans retinoic acid (ATRA). Tretinoin 172-176 retinoic acid receptor alpha Homo sapiens 34-42
31135261-4 2019 Luciferase reporter assays showed that PML-RARalpha induced significant transcription at pharmacological doses (1 muM) of ATRA; however, this was submaximal and equivalent to the level of transcription driven by intact RARalpha at physiological doses (1 nM) of ATRA. Tretinoin 122-126 PML nuclear body scaffold Homo sapiens 39-42
31135261-4 2019 Luciferase reporter assays showed that PML-RARalpha induced significant transcription at pharmacological doses (1 muM) of ATRA; however, this was submaximal and equivalent to the level of transcription driven by intact RARalpha at physiological doses (1 nM) of ATRA. Tretinoin 122-126 retinoic acid receptor alpha Homo sapiens 43-51
32455804-2 2020 Resistance to all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) has been suggested in PLZF/RARalpha and other variant APLs. Tretinoin 14-37 retinoic acid receptor alpha Homo sapiens 99-107
32455804-2 2020 Resistance to all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) has been suggested in PLZF/RARalpha and other variant APLs. Tretinoin 39-43 retinoic acid receptor alpha Homo sapiens 99-107
9502726-6 1998 The in vitro differentiation with retinoic acid and cAMP led to a 5- to 10-fold induction of flk-1, von Willebrand Factor (vWF), TM, GATA-4 and GATA-6. Tretinoin 34-47 GATA binding protein 6 Mus musculus 144-150
32205185-9 2020 In vitro, too high and too low of an RA intervention resulted in decreased proliferation, while an appropriate RA concentration (1-5 micromol/L) significantly promoted proliferation, S phase cells and high beta-catenin pathway expression. Tretinoin 111-113 catenin beta 1 Rattus norvegicus 206-218
31135261-4 2019 Luciferase reporter assays showed that PML-RARalpha induced significant transcription at pharmacological doses (1 muM) of ATRA; however, this was submaximal and equivalent to the level of transcription driven by intact RARalpha at physiological doses (1 nM) of ATRA. Tretinoin 261-265 PML nuclear body scaffold Homo sapiens 39-42
31135261-4 2019 Luciferase reporter assays showed that PML-RARalpha induced significant transcription at pharmacological doses (1 muM) of ATRA; however, this was submaximal and equivalent to the level of transcription driven by intact RARalpha at physiological doses (1 nM) of ATRA. Tretinoin 261-265 retinoic acid receptor alpha Homo sapiens 43-51
31135261-7 2019 These results suggest that PML-RARalpha initiates ATRA-induced transcription through its interaction with MED1. Tretinoin 50-54 retinoic acid receptor alpha Homo sapiens 31-39
9563832-8 1998 Northern analysis demonstrates a concentration dependent induction of GCNF mRNA by retinoic acid. Tretinoin 83-96 nuclear receptor subfamily 6, group A, member 1 Mus musculus 70-74
31143119-9 2019 In addition, ATRA dose-dependently reduced the phosphorylation levels of mTOR and mTOR target proteins p70 S6 kinase (p70S6K) and 4E-binding protein 1 (4EBP1) in A7r5 and HASMC. Tretinoin 13-17 mechanistic target of rapamycin kinase Mus musculus 73-77
31143119-9 2019 In addition, ATRA dose-dependently reduced the phosphorylation levels of mTOR and mTOR target proteins p70 S6 kinase (p70S6K) and 4E-binding protein 1 (4EBP1) in A7r5 and HASMC. Tretinoin 13-17 mechanistic target of rapamycin kinase Mus musculus 82-86
31143119-9 2019 In addition, ATRA dose-dependently reduced the phosphorylation levels of mTOR and mTOR target proteins p70 S6 kinase (p70S6K) and 4E-binding protein 1 (4EBP1) in A7r5 and HASMC. Tretinoin 13-17 eukaryotic translation initiation factor 4E binding protein 1 Mus musculus 130-150
31143119-9 2019 In addition, ATRA dose-dependently reduced the phosphorylation levels of mTOR and mTOR target proteins p70 S6 kinase (p70S6K) and 4E-binding protein 1 (4EBP1) in A7r5 and HASMC. Tretinoin 13-17 eukaryotic translation initiation factor 4E binding protein 1 Mus musculus 152-157
31143119-14 2019 These data demonstrated that ATRA might inhibit neointimal hyperplasia and suppress VSMC proliferation and migration by direct activation of AMPK and inhibition of mTOR signaling. Tretinoin 29-33 mechanistic target of rapamycin kinase Mus musculus 164-168
30844294-10 2019 Cells treated with ATRA showed decreased expression of PAK1, PAK2, PAK4, and alpha-smooth muscle actin. Tretinoin 19-23 p21 (RAC1) activated kinase 4 Homo sapiens 67-71
32006898-6 2020 Meanwhile, we found DAC and ATRA inhibited DNMT1, activated miR-34a via promoter hypomethylation, down-regulated its target MYCN and thus exerted a synergistic antineoplastic effect. Tretinoin 28-32 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 124-128
32006898-7 2020 In conclusion, DAC plus ATRA regimen might be effective and well-tolerated for elderly patients partially through modulating miR-34a/MYCN axis. Tretinoin 24-28 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 133-137
32036017-1 2020 The promyelocytic leukemia-retinoic acid receptor alpha (PML/RARalpha) is hypothesized to play a vital role in the pathogenesis of acute promyelocytic leukemia (APL). Tretinoin 27-40 PML nuclear body scaffold Homo sapiens 57-60
32036017-1 2020 The promyelocytic leukemia-retinoic acid receptor alpha (PML/RARalpha) is hypothesized to play a vital role in the pathogenesis of acute promyelocytic leukemia (APL). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 61-69
9506453-4 1998 Recombinant RAR-gamma preferentially binds t-RA over 9c-RA in cell-free assays containing mixtures of the two retinoic acid isomers. Tretinoin 110-123 retinoic acid receptor gamma Homo sapiens 12-21
32293355-3 2020 All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. Tretinoin 0-23 aldehyde dehydrogenase 1 family member A1 Homo sapiens 124-131
9478951-7 1998 In contrast, increased concentration of AP-2, stimulated by retinoic acid, led to decreased transcription of the CD-RAP promoter, an effect that was abolished by mutation of the AP-2 binding site. Tretinoin 60-73 transcription factor AP-2, alpha Mus musculus 40-44
32293355-3 2020 All-trans retinoic acid (ATRA) has been shown to be a potential targeted therapy against CSCs due to its ability to inhibit ALDH1A1 activity. Tretinoin 25-29 aldehyde dehydrogenase 1 family member A1 Homo sapiens 124-131
32293355-7 2020 Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay, RESULTS: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Tretinoin 64-68 aldehyde dehydrogenase 1 family member A1 Homo sapiens 72-79
32293355-7 2020 Using DEAB as the positive control, direct inhibitory effect of ATRA on ALDH1A1 activity was determined by ALDEFLUOR assay, RESULTS: GSCs showed higher expression of ALDH1A1 and CD44 and IC50 values for gefitinib than their respective parental cells, suggesting that gefitinib can lead to propagation of CSC-enriched gefitinib-resistant cells. Tretinoin 64-68 aldehyde dehydrogenase 1 family member A1 Homo sapiens 166-173
30894405-2 2019 Retinoic acid (RA) can promote peripheral conversion of naive T cells into Foxp3+ Treg cells. Tretinoin 0-13 forkhead box P3 Mus musculus 75-80
31035455-0 2019 Retinoic Acid Induces Differentiation of Mouse F9 Embryonic Carcinoma Cell by Modulating the miR-485 Targeting of Abhd2. Tretinoin 0-13 microRNA 485 Mus musculus 93-100
31035455-4 2019 RA up-regulates miR-485 and concurrently down-regulates Abhd2. Tretinoin 0-2 microRNA 485 Mus musculus 16-23
31035455-6 2019 In summary, RA can mediate cell differentiation by phosphorylating Erk1/2 via miR-485 and Abhd2. Tretinoin 12-14 microRNA 485 Mus musculus 78-85
30986261-10 2019 However, we found that RA up-regulated PTGDR expression through RARalpha mainly in the CTCT variant. Tretinoin 23-25 retinoic acid receptor alpha Homo sapiens 64-72
30992691-14 2019 Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed. Tretinoin 35-39 retinoic acid receptor alpha Homo sapiens 55-59
30992691-14 2019 Using the combination of MG132 and ATRA to treat GTF2I-RARA-HL60 cells, a synergistic effect leading to GTF2I-RARA-HL60 cell differentiation was confirmed. Tretinoin 35-39 retinoic acid receptor alpha Homo sapiens 110-114
31731254-4 2020 The results showed that 10 nM ATRA sufficiently inhibited cell proliferation, which might be through downregulation of cyclin D1 (P < 0.05) and cyclin-dependent kinase 4 (P < 0.05) and proliferating cell nuclear antigen protein (P < 0.05) abundance. Tretinoin 30-34 G1/S-specific cyclin-D1 Ovis aries 119-128
31731254-5 2020 Moreover, compared with control cells, both 10 nM and 100 nM ATRA promoted myotube formation and increased fusion index (P < 0.05), which was associated with elevated myogenin mRNA content (P < 0.05). Tretinoin 61-65 myogenin Ovis aries 170-178
9478951-7 1998 In contrast, increased concentration of AP-2, stimulated by retinoic acid, led to decreased transcription of the CD-RAP promoter, an effect that was abolished by mutation of the AP-2 binding site. Tretinoin 60-73 transcription factor AP-2, alpha Mus musculus 178-182
31731254-6 2020 As expected, both myogenin (P < 0.01) and myosin heavy chain (P < 0.05) protein levels were increased by ATRA. Tretinoin 111-115 myogenin Ovis aries 18-26
9485034-5 1998 After retinoic acid-induced differentiation, only the PSA-positive, neuron-like cell type gave clear signals for ST8SiaII and ST8SiaIV in in situ hybridization, whereas both signals were drastically reduced in the weakly PSA-positive substrate adherent phenotype. Tretinoin 6-19 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 Homo sapiens 126-134
31731254-7 2020 Interestingly, ATRA treatment increased H3K4me3 and decreased H3K27me3 enrichment in the myogenin promoter region (P < 0.05). Tretinoin 15-19 myogenin Ovis aries 89-97
32061868-0 2020 Melatonin inhibits apoptosis in mouse Leydig cells via the retinoic acid-related orphan nuclear receptor alpha/p53 pathway. Tretinoin 59-72 transformation related protein 53, pseudogene Mus musculus 111-114
30532072-11 2019 Conversely, S100A3 knockdown in PML-RARalpha+ APL and PML-RARalpha- AML cells reduces the amounts of RARalpha/PML-RARalpha and increases basal and ATRA-induced differentiation. Tretinoin 147-151 retinoic acid receptor alpha Homo sapiens 58-66
30532072-12 2019 In this cellular context, opposite effects on RARalpha/PML-RARalpha levels and ATRA-induced differentiation are observed upon S100A3 overexpression. Tretinoin 79-83 S100 calcium binding protein A3 Homo sapiens 126-132
30532072-13 2019 Our results provide new insights into the molecular mechanisms controlling RARalpha activity and have practical implications, as S100A3 represents a novel target for rational drug combinations aimed at potentiating the activity of ATRA. Tretinoin 231-235 retinoic acid receptor alpha Homo sapiens 75-83
30532072-13 2019 Our results provide new insights into the molecular mechanisms controlling RARalpha activity and have practical implications, as S100A3 represents a novel target for rational drug combinations aimed at potentiating the activity of ATRA. Tretinoin 231-235 S100 calcium binding protein A3 Homo sapiens 129-135
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 76-89 PML nuclear body scaffold Homo sapiens 35-38
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 76-89 retinoic acid receptor alpha Homo sapiens 39-43
32061868-3 2020 In this study, we investigated the mechanism through which melatonin inhibits apoptosis in mouse Leydig cells by activating the retinoic acid-related orphan nuclear receptor (ROR) alpha/p53 signaling pathway. Tretinoin 128-141 RAR-related orphan receptor alpha Mus musculus 174-185
32061868-3 2020 In this study, we investigated the mechanism through which melatonin inhibits apoptosis in mouse Leydig cells by activating the retinoic acid-related orphan nuclear receptor (ROR) alpha/p53 signaling pathway. Tretinoin 128-141 transformation related protein 53, pseudogene Mus musculus 186-189
32217463-3 2020 We employed Sirt1+/+ and Sirt1-/- mouse embryonic stem cells (mESCs) to evaluate the role of SIRT1 during the early stage mESC differentiation to adipocytes in response to retinoic acid (RA) treatment. Tretinoin 172-185 sirtuin 1 Mus musculus 93-98
32217463-3 2020 We employed Sirt1+/+ and Sirt1-/- mouse embryonic stem cells (mESCs) to evaluate the role of SIRT1 during the early stage mESC differentiation to adipocytes in response to retinoic acid (RA) treatment. Tretinoin 187-189 sirtuin 1 Mus musculus 93-98
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 76-89 heat shock protein 90 alpha family class A member 1 Homo sapiens 110-115
9486851-4 1998 Constitutive expression of PKCalpha or inhibition of PKCbeta expression in F9 stem cells enhanced RA induced differentiation, both by increasing total expression and accelerating RA-induced expression of laminins A, B1, B2, and type IV collagen. Tretinoin 98-100 protein kinase C beta Homo sapiens 53-60
30554401-1 2019 Retinoic acid-induced 14 is a developmentally regulated gene induced by retinoic acid and is closely associated with NIK/NF-kappaB signaling. Tretinoin 0-13 mitogen-activated protein kinase kinase kinase 14 Homo sapiens 117-120
30632787-3 2019 Gen1 mutant mice showed CAKUT phenotypes similar to those observed in retinoic acid (RA)-deficient models. Tretinoin 85-87 GEN1, Holliday junction 5' flap endonuclease Mus musculus 0-4
32217463-8 2020 After RA treatment, chromatin immunoprecipitation assays using an antibody against NCOR1, revealed that NCOR1 binding to RARbeta promoters was significantly lower in Sirt1-/- mESCs than in Sirt1+/+ mESCs, and luciferase reporter assays showed SIRT1 knockdown decreased RA-induced RARalpha activity. Tretinoin 121-123 sirtuin 1 Mus musculus 166-171
32296441-5 2020 We show that Dectin-1 expression is enhanced by the vitamin A metabolite retinoic acid and our data suggests that Dectin-1 triggering might provide a switch to induce a rapid production of pro-inflammatory cytokines. Tretinoin 73-86 C-type lectin domain containing 7A Homo sapiens 13-21
9486851-4 1998 Constitutive expression of PKCalpha or inhibition of PKCbeta expression in F9 stem cells enhanced RA induced differentiation, both by increasing total expression and accelerating RA-induced expression of laminins A, B1, B2, and type IV collagen. Tretinoin 179-181 protein kinase C beta Homo sapiens 53-60
32296441-5 2020 We show that Dectin-1 expression is enhanced by the vitamin A metabolite retinoic acid and our data suggests that Dectin-1 triggering might provide a switch to induce a rapid production of pro-inflammatory cytokines. Tretinoin 73-86 C-type lectin domain containing 7A Homo sapiens 114-122
9519778-5 1998 As interferons (IFNs) and dexamethasone can be used together with RA in the treatment of patients with APL, we have now studied the effects of RA together with IFNs and dexamethasone on the plasminogen activation cascade of these cells, including measurement of plasmin generation and uPA receptor (uPAR), using enzyme immunoassays, fluorescence-activated cell sorter analysis and RNA extraction with Northern blotting. Tretinoin 143-145 plasminogen Homo sapiens 190-197
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen Homo sapiens 27-34
30813330-8 2019 It is predicted that retinoic acid serves as a transcription factor in the GPAT2 promoter. Tretinoin 21-34 glycerol-3-phosphate acyltransferase 2, mitochondrial Homo sapiens 75-80
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen Homo sapiens 105-112
32209731-4 2020 Herein, we observed dramatically decreased Alphabeta deposition in the brains of amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice (APP/PS1) treated intranasally with 9-cis RA for 4 weeks compared to that in the brains of vehicle-treated mice. Tretinoin 201-203 presenilin 1 Mus musculus 117-129
32209731-4 2020 Herein, we observed dramatically decreased Alphabeta deposition in the brains of amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice (APP/PS1) treated intranasally with 9-cis RA for 4 weeks compared to that in the brains of vehicle-treated mice. Tretinoin 201-203 presenilin 1 Mus musculus 131-134
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen Homo sapiens 105-112
32209731-4 2020 Herein, we observed dramatically decreased Alphabeta deposition in the brains of amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice (APP/PS1) treated intranasally with 9-cis RA for 4 weeks compared to that in the brains of vehicle-treated mice. Tretinoin 201-203 amyloid beta (A4) precursor protein Mus musculus 160-167
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 192-194 plasminogen Homo sapiens 27-34
32209731-5 2020 Importantly, intranasal delivery of 9-cis RA suppressed Alphabeta-associated astrocyte activation and neuroinflammation and ultimately restored synaptic deficits in APP/PS1 transgenic mice. Tretinoin 42-44 amyloid beta (A4) precursor protein Mus musculus 165-172
30572725-1 2019 INTRODUCTION: The outcome of acute promyelocytic leukemia (APL) has drastically improved following the identification of the PML-RARA oncogene as a key player in the pathogenesis of APL, and the subsequent introduction of all-trans retinoic acid (ATRA) as a therapeutic agent. Tretinoin 247-251 PML nuclear body scaffold Homo sapiens 125-128
32266229-8 2020 atRA release from scaffolds led to an increase in mucociliary gene expression at high scaffold loading doses, with augmented MUC5AC and FOXJ1 detected by RT-PCR. Tretinoin 0-4 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 125-131
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 192-194 plasminogen Homo sapiens 27-34
32258025-0 2020 Inhibition of GSK3 Represses the Expression of Retinoic Acid Synthetic Enzyme ALDH1A2 via Wnt/beta-Catenin Signaling in WiT49 Cells. Tretinoin 47-60 catenin beta 1 Homo sapiens 94-106
29948941-3 2019 ALDH1A1 is also a major regulator of retinoic acid (RA) signaling, which is critical for normal brain homeostasis. Tretinoin 37-50 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7
29948941-3 2019 ALDH1A1 is also a major regulator of retinoic acid (RA) signaling, which is critical for normal brain homeostasis. Tretinoin 52-54 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7
9448745-0 1998 Identification of a retinoic acid response domain involved in the activation of the beta 1-adrenergic receptor gene by retinoic acid in F9 teratocarcinoma cells. Tretinoin 20-33 adrenoceptor beta 1 Homo sapiens 84-110
30250298-5 2019 Moreover, we demonstrated that pharmacological inhibition of 15-PGDH enhanced CYP26A1 expression, leading to depletion of all-trans retinoic acid (ATRA) and expansion of the ALDH1-positive subset in both human PDAC cells and tumor cells of KrasLSL-G12D/+; Ptf1aCre/+ (KC) mice. Tretinoin 147-151 15-hydroxyprostaglandin dehydrogenase Homo sapiens 61-68
30328800-12 2019 Taken together, the microplate, FACS, immunoblot, and immunofluorescence data suggest that retinoic acid or hyperosmotic stress forces dose-dependent differentiation whether LIF is present or not and this is negatively correlated with and possibly compensates for stress-forced diminished ESC population expansion and potency loss. Tretinoin 91-104 leukemia inhibitory factor Mus musculus 174-177
32258025-10 2020 Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/beta-catenin signaling in fetal kidney cells, suggesting that Wnt/beta-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development. Tretinoin 302-315 catenin beta 1 Rattus norvegicus 83-95
32258025-10 2020 Our work demonstrates that ALDH1A2 expression can be directly repressed by the Wnt/beta-catenin signaling in fetal kidney cells, suggesting that Wnt/beta-catenin may play a role in maintaining the expression pattern of ALDH1A2 in the fetal kidney, thus controlling the availability and localization of retinoic acid and regulating aspects of kidney development. Tretinoin 302-315 catenin beta 1 Rattus norvegicus 149-161
32179842-0 2020 Serum lipids, retinoic acid and phenol red differentially regulate expression of keratins K1, K10 and K2 in cultured keratinocytes. Tretinoin 14-27 keratin 10 Homo sapiens 94-97
30621740-4 2019 METHODS: In this study we determined the effects of ATRA treatment (1-5 muM) on annexin A2 and S100A10 expression, plasmin activation, and the ability of ATRA to inhibit serous ovarian cancer cell survival, motility and invasion in vitro. Tretinoin 52-56 annexin A2 Homo sapiens 80-90
9448745-0 1998 Identification of a retinoic acid response domain involved in the activation of the beta 1-adrenergic receptor gene by retinoic acid in F9 teratocarcinoma cells. Tretinoin 119-132 adrenoceptor beta 1 Homo sapiens 84-110
30621740-10 2019 In OAW28 cells, reduced cell survival following ATRA treatment was associated with a reduction of S100A10 mRNA and protein levels, S100A10 and annexin A2 membrane localization, plasmin generation, motility and invasion. Tretinoin 48-52 annexin A2 Homo sapiens 143-153
32179842-6 2020 The effect was reversed for K1 and K10 by adding all-trans retinoic acid (ATRA) but increased for K2 in the absence of PR. Tretinoin 49-72 keratin 10 Homo sapiens 35-38
32179842-6 2020 The effect was reversed for K1 and K10 by adding all-trans retinoic acid (ATRA) but increased for K2 in the absence of PR. Tretinoin 74-78 keratin 10 Homo sapiens 35-38
9448745-1 1998 The density of beta 1-adrenergic receptors (beta 1-AR) is up-regulated upon differentiation of embryonic F9 teratocarcinoma cells by retinoic acid (RA) to the primitive endodermal phenotype. Tretinoin 133-146 adrenoceptor beta 1 Homo sapiens 15-42
9448745-1 1998 The density of beta 1-adrenergic receptors (beta 1-AR) is up-regulated upon differentiation of embryonic F9 teratocarcinoma cells by retinoic acid (RA) to the primitive endodermal phenotype. Tretinoin 133-146 adrenoceptor beta 1 Homo sapiens 44-53
32007421-9 2020 Cardioprotective potential of rosuvastatin and retinoic acid could be attributed to their influence on the redox pathways, immunomodulation, membrane stability, Nrf2 preservation, iNOS and Bax expression levels. Tretinoin 47-60 BCL2 associated X, apoptosis regulator Rattus norvegicus 189-192
9448745-1 1998 The density of beta 1-adrenergic receptors (beta 1-AR) is up-regulated upon differentiation of embryonic F9 teratocarcinoma cells by retinoic acid (RA) to the primitive endodermal phenotype. Tretinoin 148-150 adrenoceptor beta 1 Homo sapiens 15-42
32087738-7 2020 We examined the effect of retinoic acid, the differentiation agent used in neuroblastoma therapy, on miR-506-3p, PLAGL2 and MYCN expressions by quantitative PCR and Western blots. Tretinoin 26-39 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 124-128
30448346-5 2019 The expression of ACTL6A was gradually decreased during granulocytic differentiation in all-trans retinoic acid-treated NB4 and HL-60 cells, and phorbol myristate acetate-treated HL-60 cells. Tretinoin 98-111 actin like 6A Homo sapiens 18-24
9448745-1 1998 The density of beta 1-adrenergic receptors (beta 1-AR) is up-regulated upon differentiation of embryonic F9 teratocarcinoma cells by retinoic acid (RA) to the primitive endodermal phenotype. Tretinoin 148-150 adrenoceptor beta 1 Homo sapiens 44-53
32087738-14 2020 Furthermore, we found that retinoic acid increased expression of miR-506-3p and repressed expression of MYCN and PLAGL2. Tretinoin 27-40 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 104-108
9448745-7 1998 Therefore, transcriptional activation of the beta 1-AR gene by thyroid hormone or RA involves a single binding site in the promoter. Tretinoin 82-84 adrenoceptor beta 1 Homo sapiens 45-54
32087738-15 2020 CONCLUSIONS: Our findings altogether suggest that the interplay network formed by PLAGL2, MYCN and miR-506-3p is an important mechanism in regulating neuroblastoma cell fate, determining neuroblastoma prognosis, and mediating the therapeutic function of retinoic acid. Tretinoin 254-267 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 90-94
9457077-11 1998 By super-shift assays using specific anti-RAR and -RXR antibodies, RA treatment decreased the amount of RXR alpha while increasing the amount RAR beta bound to retinoic acid response element-DR1 (direct repeat with spacer of one nucleotide), indicating the levels of RAR/RXR heterodimer, RXR/RXR homodimer, or RAR/RAR homodimers were altered upon RA treatment of Hep3B cells. Tretinoin 42-44 down-regulator of transcription 1 Homo sapiens 191-194
32195202-8 2019 RA upregulated Stra8 and Piwil2, and downregulated Nanog and Oct-4. Tretinoin 0-2 stimulated by retinoic acid gene 8 Mus musculus 15-20
31899223-9 2020 At the same time, All-trans retinoic acid (ATRA), which has the properties of pro-differentiation and inhibition of invasion and metastasis, upregulated the expression of PD-L1 and E-cadherin. Tretinoin 18-41 CD274 molecule Homo sapiens 171-176
9438427-4 1998 We have previously identified a 10 bp element, called CE2, which is located approximately 3 kilobases 3" of the Hoxa1 coding region in the RAIDR5 enhancer, and which binds to an approximately 170 kd protein in retinoic acid treated P19 embryonal carcinoma cells. Tretinoin 210-223 homeobox A1 Mus musculus 112-117
31899223-9 2020 At the same time, All-trans retinoic acid (ATRA), which has the properties of pro-differentiation and inhibition of invasion and metastasis, upregulated the expression of PD-L1 and E-cadherin. Tretinoin 43-47 CD274 molecule Homo sapiens 171-176
31899223-10 2020 SIGNIFICANCE: These findings not only identify PD-L1 may have a positive role for the treatment of GC, but also implicate that ATRA combined PD-L1 antibody drugs may enhance anti-tumor Immunity in GC. Tretinoin 127-131 CD274 molecule Homo sapiens 47-52
30622531-10 2018 In MoDCs generated in the presence of retinoic acid, which express increased CD103, intracellular CD103 significantly redistributed toward the E-cadherin-coated glass surface. Tretinoin 38-51 integrin subunit alpha E Homo sapiens 77-82
30622531-10 2018 In MoDCs generated in the presence of retinoic acid, which express increased CD103, intracellular CD103 significantly redistributed toward the E-cadherin-coated glass surface. Tretinoin 38-51 integrin subunit alpha E Homo sapiens 98-103
31875385-6 2020 Moreover, CyN was qualified for imaging dynamic change of AChE activity in PC12 cells with retinoic acid or hypoxia stimulation. Tretinoin 91-104 acetylcholinesterase Rattus norvegicus 58-62
9570344-0 1998 Counteraction of retinoic acid and 1,25-dihydroxyvitamin D3 on up-regulation of adipocyte differentiation with PPARgamma ligand, an antidiabetic thiazolidinedione, in 3T3-L1 cells. Tretinoin 17-30 peroxisome proliferator activated receptor gamma Mus musculus 111-120
32158187-0 2020 The Antagonist of Retinoic Acid Receptor alpha, ER-50891 Antagonizes the Inhibitive Effect of All-Trans Retinoic Acid and Rescues Bone Morphogenetic Protein 2-Induced Osteoblastogenic Differentiation. Tretinoin 94-117 retinoic acid receptor alpha Homo sapiens 18-46
32158187-11 2020 Conclusion: The antagonist of RARalpha, ER-50891 could significantly attenuate ATRA"s inhibitive effects on BMP 2-induced osteoblastogenesis. Tretinoin 79-83 retinoic acid receptor alpha Homo sapiens 30-38
30157453-2 2018 In this study, we used a retinoic acid (RA)-induced differentiation model of NTERA-2/clone D1 (NT2) cells to explore the functional significance of PPARalpha in neuronal differentiation. Tretinoin 25-38 peroxisome proliferator activated receptor alpha Homo sapiens 148-157
31898934-4 2020 Mechanistically the increased level of RA sensitizes McSCs to differentiation signal KIT-ligand by increasing its c-Kit receptor protein level in vivo. Tretinoin 39-41 kit ligand Mus musculus 85-95
9570344-1 1998 Retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25 (OH)2 D3) inhibited adipocyte differentiation of 3T3-L1 preadipocytes in the presence of thiazolidinedione, a specific ligand for peroxisome proliferator-activated receptory (PPARgamma). Tretinoin 0-13 peroxisome proliferator activated receptor gamma Mus musculus 229-238
30522558-7 2018 At the same time, RA could arrest the cell cycle of CSCs and reduce the expression of Sox-2, Oct-4 in CSCs of melanoma, thereby induced the differentiation of CSCs and increased its sensitivity to paclitaxel. Tretinoin 18-20 POU class 5 homeobox 1 Homo sapiens 93-98
9570344-1 1998 Retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25 (OH)2 D3) inhibited adipocyte differentiation of 3T3-L1 preadipocytes in the presence of thiazolidinedione, a specific ligand for peroxisome proliferator-activated receptory (PPARgamma). Tretinoin 15-17 peroxisome proliferator activated receptor gamma Mus musculus 229-238
10612460-4 1998 In cell line GCT 27X-1, treatment with BMP-2 reduces proliferation, induces morphological changes similar to obtained following treatment with retinoic acid, and causes a decrease in the expression of transcripts for the stem cell markers CD30 and Oct-4. Tretinoin 143-156 bone morphogenetic protein 2 Homo sapiens 39-44
30547071-2 2018 Neurite outgrowth was observed within 24 h in DMEM supplemented with reduced serum and retinoic acid (GpIV). Tretinoin 87-100 CD36 molecule Mus musculus 102-106
29377254-7 2018 Retinoic acid, an agonist of GnT-V, further increased glycosylated CD147, and activated matrix metalloproteinase-2/-9 (MMP-2 and MMP-9) in the hypertrophied left ventricle of 2K1C rat. Tretinoin 0-13 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Rattus norvegicus 29-34
32348995-12 2020 At last, we detected stimulated by retinoic acid gene 6 homolog (STRA6), a cell surface receptor formerly known as a gene preventing podocytes from over-proliferative lesion induced by HIV infection and was up-regulated by retinoic acid, expressed at a much higher level in SRNS kidneys. Tretinoin 35-48 signaling receptor and transporter of retinol STRA6 Homo sapiens 65-70
9425271-9 1997 These results show that RA but not DMSO induces the expression of GM3, GD3, GT1b and GQ1b synthases, and particularly GD3 synthase mRNA, in the ganglioside biosynthetic pathway during the neural differentiation of embryonic carcinoma P19 cells. Tretinoin 24-26 interleukin 23, alpha subunit p19 Mus musculus 234-237
31726045-2 2020 Retinoic acid receptor alpha (RARalpha), as an important nuclear RA receptor, is activated upon RA binding and facilitates the transcription of target genes related to differentiation, which ultimately initiates cell differentiation. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 0-28
29520716-7 2018 The RA-responsive gene Cyp26a1 was found to change between day and night, suggesting diurnal changes in RA activity. Tretinoin 4-6 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 23-30
29520716-7 2018 The RA-responsive gene Cyp26a1 was found to change between day and night, suggesting diurnal changes in RA activity. Tretinoin 104-106 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 23-30
29520716-9 2018 Long-term RA treatment in vitro upregulated Aanat transcription, while short-term treatment had no effect. Tretinoin 10-12 aralkylamine N-acetyltransferase Rattus norvegicus 44-49
9503603-0 1997 Retinoic acid mediates Pax6 expression during in vitro differentiation of embryonic stem cells. Tretinoin 0-13 paired box 6 Homo sapiens 23-27
31654721-1 2020 The fusion oncogene, promyelocytic leukemia (PML)-retinoic acid receptor-alpha (RARalpha), is crucial for acute promyelocytic leukemia (APL) pathogenesis. Tretinoin 50-63 PML nuclear body scaffold Homo sapiens 45-48
30289902-8 2018 In deletion PML-RARA-transduced cells, the CD11b expression levels and NBT reducing ability were significantly decreased compared with control cells and the formation of PML nuclear bodies was rarely observed after RA treatment. Tretinoin 16-18 PML nuclear body scaffold Homo sapiens 12-15
31654721-1 2020 The fusion oncogene, promyelocytic leukemia (PML)-retinoic acid receptor-alpha (RARalpha), is crucial for acute promyelocytic leukemia (APL) pathogenesis. Tretinoin 50-63 retinoic acid receptor alpha Homo sapiens 80-88
30289902-8 2018 In deletion PML-RARA-transduced cells, the CD11b expression levels and NBT reducing ability were significantly decreased compared with control cells and the formation of PML nuclear bodies was rarely observed after RA treatment. Tretinoin 16-18 PML nuclear body scaffold Homo sapiens 170-173
9503603-8 1997 Addition of RA resulted in the appearance of Pax6-expressing cells in a concentration-dependent manner, with a peak at 100 nM RA. Tretinoin 12-14 paired box 6 Homo sapiens 45-49
9503603-8 1997 Addition of RA resulted in the appearance of Pax6-expressing cells in a concentration-dependent manner, with a peak at 100 nM RA. Tretinoin 126-128 paired box 6 Homo sapiens 45-49
31914680-0 2020 Zebrafish prmt7 negatively regulates antiviral responses by suppressing the retinoic acid-inducible gene-I-like receptor signaling. Tretinoin 76-89 protein arginine methyltransferase 7 Danio rerio 10-15
9398056-6 1997 RA stimulated the association of t-PA with the external cell membrane surface, which could be inhibited by heparin sulphate but not by mannose sugars or chelators of divalent cations, consistent with a role for amphoterin. Tretinoin 0-2 high mobility group box 1 Homo sapiens 211-221
30121453-10 2018 Additionally, ATRA reduces the expression of immunosuppressive genes including PD-L1, IL-10, and indoleamine 2,3-dioxygenase by MDSCs. Tretinoin 14-18 CD274 molecule Homo sapiens 79-84
9295294-5 1997 mCAR1, like hCAR, binds as a heterodimer with the retinoid X receptor to the retinoic acid response element from the promoter of the retinoic acid receptor beta2 isoform. Tretinoin 77-90 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 156-161
30241502-8 2018 The RA-dependent mode of action for minocycline appears to be predominantly mediated through RAR-signaling. Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 93-96
33132350-1 2020 Aldehyde dehydrogenase 1A1 (ALDH1A1) in intestinal epithelial cells (IECs) plays a critical role in regulating immune responses through the production of retinoic acid (RA). Tretinoin 154-167 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-26
33132350-1 2020 Aldehyde dehydrogenase 1A1 (ALDH1A1) in intestinal epithelial cells (IECs) plays a critical role in regulating immune responses through the production of retinoic acid (RA). Tretinoin 154-167 aldehyde dehydrogenase 1 family member A1 Homo sapiens 28-35
33132350-1 2020 Aldehyde dehydrogenase 1A1 (ALDH1A1) in intestinal epithelial cells (IECs) plays a critical role in regulating immune responses through the production of retinoic acid (RA). Tretinoin 169-171 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-26
33132350-1 2020 Aldehyde dehydrogenase 1A1 (ALDH1A1) in intestinal epithelial cells (IECs) plays a critical role in regulating immune responses through the production of retinoic acid (RA). Tretinoin 169-171 aldehyde dehydrogenase 1 family member A1 Homo sapiens 28-35
9337080-9 1997 The presence of 9-cis RA or ATRA appeared to contribute to the further increase of CD14 in these cells. Tretinoin 28-32 CD14 molecule Homo sapiens 83-87
32175266-9 2020 It was found that the use of retinoic acid led to the highest expression of C-kit, SSEA4, VASA genes and lower expression of Oct4. Tretinoin 29-42 POU class 5 homeobox 1 Homo sapiens 125-129
30012853-2 2018 We observed that tumors treated with PD-1/PD-L1 blocking antibodies develop resistance through the upregulation of CD38, which is induced by all-trans retinoic acid and IFNbeta in the tumor microenvironment. Tretinoin 151-164 CD274 molecule Homo sapiens 42-47
30012853-2 2018 We observed that tumors treated with PD-1/PD-L1 blocking antibodies develop resistance through the upregulation of CD38, which is induced by all-trans retinoic acid and IFNbeta in the tumor microenvironment. Tretinoin 151-164 CD38 molecule Homo sapiens 115-119
9284045-1 1997 We report the cDNA cloning of Stra13, a novel retinoic acid (RA)-inducible gene from P19 embryonal carcinoma cells that encodes a basic helix-loop-helix (bHLH) protein that shows the highest sequence similarities to the Drosophila Hairy and Enhancer of split and mouse Hes proteins. Tretinoin 46-59 centromere protein X Mus musculus 30-36
29350080-0 2018 IRF2BP2-RARA t(1;17)(q42.3;q21.2) APL blasts differentiate in response to all-trans retinoic acid. Tretinoin 84-97 retinoic acid receptor alpha Homo sapiens 8-12
29781215-0 2018 Serine Threonine Kinase Receptor-Associated Protein Deficiency Impairs Mouse Embryonic Stem Cells Lineage Commitment Through CYP26A1-Mediated Retinoic Acid Homeostasis. Tretinoin 142-155 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 125-132
29781215-6 2018 Signature gene expression analyses revealed that Strap deletion attenuated intracellular RA signaling in embryoid bodies (EBs), and exogenous RA significantly rescued this deficiency. Tretinoin 89-91 serine/threonine kinase receptor associated protein Mus musculus 49-54
29781215-7 2018 Moreover, loss of Strap selectively induced Cyp26A1 expression in mouse EBs, suggesting a potential role of STRAP in RA signaling. Tretinoin 110-112 serine/threonine kinase receptor associated protein Mus musculus 18-23
32359645-3 2020 The (patho)physiological functions of RAR-RXR heterodimers rely on a dynamic sequence of protein-protein interactions, many of which being modulated by natural (retinoic acid) or synthetic ligands. Tretinoin 161-174 retinoic acid receptor alpha Homo sapiens 38-41
29781215-7 2018 Moreover, loss of Strap selectively induced Cyp26A1 expression in mouse EBs, suggesting a potential role of STRAP in RA signaling. Tretinoin 110-112 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 44-51
9284045-1 1997 We report the cDNA cloning of Stra13, a novel retinoic acid (RA)-inducible gene from P19 embryonal carcinoma cells that encodes a basic helix-loop-helix (bHLH) protein that shows the highest sequence similarities to the Drosophila Hairy and Enhancer of split and mouse Hes proteins. Tretinoin 61-63 centromere protein X Mus musculus 30-36
29781215-8 2018 Mechanistically, we identified putative Kruppel-like factor 9 (KLF9) binding motifs to be critical in the enhancement of non-canonical RA-induced transactivation of Cyp26A1. Tretinoin 135-137 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 165-172
31619506-10 2020 The AP-2gamma gene signature predicts outcome of patients with HER2+ breast cancer and pathway analysis predicts that subsets of patients will respond to drugs that target the MAPK or retinoic acid pathways. Tretinoin 184-197 transcription factor AP-2 gamma Homo sapiens 4-13
9242707-7 1997 (ii) Aggrecanase activity was specifically induced by exposing chondrocytes to retinoic acid. Tretinoin 79-92 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 5-16
31501521-0 2020 Targeting the TR4 nuclear receptor-mediated lncTASR/AXL signaling with tretinoin increases the sunitinib sensitivity to better suppress the RCC progression. Tretinoin 71-80 AXL receptor tyrosine kinase Homo sapiens 52-55
30159139-10 2018 Conclusions: All-trans retinoic acid inhibits BMP2/7-induced osteoclastogenesis, and resorption activity possibly via RANKL-RANK pathway. Tretinoin 23-36 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 118-123
9259311-8 1997 However, assays of cdk2 from pooled lysates from RA-treated and control cells showed that RA-treated cells contain a cdk2-inhibitory activity. Tretinoin 90-92 cyclin dependent kinase 2 Homo sapiens 19-23
29274134-10 2018 Further studies addressing its biology and clinical significance may be especially relevant in the era of IDH inhibitors and recent work showing efficacy of ATRA therapy in NPM1 and IDH1-mutated AML. Tretinoin 157-161 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 182-186
9259311-8 1997 However, assays of cdk2 from pooled lysates from RA-treated and control cells showed that RA-treated cells contain a cdk2-inhibitory activity. Tretinoin 90-92 cyclin dependent kinase 2 Homo sapiens 117-121
33029554-4 2020 We demonstrate discrete, zonal expression of the RA-inducible protein Stra8 within mEBs in response to release of RA from polymer microparticles, corresponding directly to the defined 3D positioning of the microparticles using HOTs. Tretinoin 49-51 stimulated by retinoic acid gene 8 Mus musculus 70-75
33029554-4 2020 We demonstrate discrete, zonal expression of the RA-inducible protein Stra8 within mEBs in response to release of RA from polymer microparticles, corresponding directly to the defined 3D positioning of the microparticles using HOTs. Tretinoin 114-116 stimulated by retinoic acid gene 8 Mus musculus 70-75
29947893-2 2018 HDAC8 inhibition synergizes with retinoic acid treatment to induce neuroblast maturation in vitro and to inhibit neuroblastoma xenograft growth in vivo. Tretinoin 33-46 histone deacetylase 8 Homo sapiens 0-5
9259311-9 1997 Our results show that RA inhibits cell cycle progression of MCF-7 cells by inhibiting cdk2 mRNA and protein production and by decreasing cdk2 activity. Tretinoin 22-24 cyclin dependent kinase 2 Homo sapiens 86-90
29940355-7 2018 In summary, our data illustrate a previously unrecognized pathway in which SETD1A contributes to RA-induced TM expression in vascular endothelial cells by modulating the activity and expression of KLF4. Tretinoin 97-99 thrombomodulin Homo sapiens 108-110
9259311-9 1997 Our results show that RA inhibits cell cycle progression of MCF-7 cells by inhibiting cdk2 mRNA and protein production and by decreasing cdk2 activity. Tretinoin 22-24 cyclin dependent kinase 2 Homo sapiens 137-141
32147608-3 2020 The patient was diagnosed with acute promyelocytic leukemia (APL) with PML-RARA and was treated using all-trans retinoic acid (ATRA). Tretinoin 102-125 retinoic acid receptor alpha Homo sapiens 75-79
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, ionotropic, kainate 1 Mus musculus 364-370
31950055-5 2019 The cell surface expression of toll-like receptor 5 (TLR5), which is the receptor for bacterial flagellin, was significantly reduced by ATRA in a concentration- and time-dependent manner. Tretinoin 136-140 toll like receptor 5 Homo sapiens 31-51
31950055-5 2019 The cell surface expression of toll-like receptor 5 (TLR5), which is the receptor for bacterial flagellin, was significantly reduced by ATRA in a concentration- and time-dependent manner. Tretinoin 136-140 toll like receptor 5 Homo sapiens 53-57
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, ionotropic, AMPA2 (alpha 2) Mus musculus 380-386
31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tretinoin 71-84 lysine methyltransferase 2A Homo sapiens 283-286
31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tretinoin 86-88 lysine methyltransferase 2A Homo sapiens 283-286
29936250-10 2018 Fluorescence-activated cell sorting (FACS) analysis demonstrated a marked increase in systemic CD34+/Flk-1+ EPCs in ATRA-treated rat. Tretinoin 116-120 kinase insert domain receptor Rattus norvegicus 101-106
9218485-11 1997 Retinoic acid, an inducer of myogenesis, inhibited syndecan-1 expression and abolished the effect of the growth factors. Tretinoin 0-13 syndecan 1 Homo sapiens 51-61
29936250-11 2018 The expression of ANG2 and VEGF was increased in diabetic flap tissues under ATRA administration. Tretinoin 77-81 vascular endothelial growth factor A Rattus norvegicus 27-31
29926353-0 2018 Correction to: All-Trans Retinoic Acid Ameliorates the Early Experimental Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting the Loss of the Blood-Brain Barrier via the JNK/P38MAPK Signaling Pathway. Tretinoin 25-38 mitogen-activated protein kinase 8 Rattus norvegicus 177-180
31834935-6 2019 Our data provide a proof of concept that low amounts of drugs that generate ER and oxidative stresses combined with RA could be an effective targeted therapy to hit AML cells characterized by MLL fusion proteins and FLT3-ITD mutation. Tretinoin 116-118 lysine methyltransferase 2A Homo sapiens 192-195
31856916-9 2019 Interestingly, RA treatment led to attenuation of H3K27me3 due to cooperate between UTX and Suz12, affecting Hox gene regulation. Tretinoin 15-17 lysine (K)-specific demethylase 6A Mus musculus 84-87
9218485-12 1997 These results indicate that syndecan-1 expression is down-regulated during myogenesis and that growth factors and retinoic acid modulate syndecan-1 expression by a mechanism that is independent of myogenin. Tretinoin 114-127 syndecan 1 Homo sapiens 137-147
30008902-3 2018 Research into CCR9 and CCL25 has revealed their associated upstream and downstream signaling pathways; CCR9 is regulated by several immunological factors, including NOTCH, interleukin 2, interleukin 4 and retinoic acid. Tretinoin 205-218 C-C motif chemokine ligand 25 Homo sapiens 23-28
31810919-0 2019 All-trans Retinoic Acid Overcomes Acquired Resistance to PLX4032 via Inhibition of PIN1 in Melanoma Cells. Tretinoin 0-23 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 83-87
9242489-5 1997 In this study we show that disruption of the type IIB activin receptor (ActRIIB) by gene targeting results in altered expression of multiple Hox genes and abnormal patterning of the vertebrae, similar to but severer than retinoic acid (RA)-induced anterior transformation. Tretinoin 221-234 activin receptor IIB Mus musculus 72-79
31810919-6 2019 Importantly, PLX4032, when used in combination with ATRA, an inhibitor of PIN1, reduced EGFR expression, and consequently reduced cell viability and anchorage-independent growth of A375R cells compared to PLX4032 alone. Tretinoin 52-56 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 74-78
29899137-5 2018 Additionally, blocking RA signaling in Leydig cells resulted in increased permeability of the blood-testis barrier, decreased levels of the steroidogenic enzyme cytochrome P450 17a1 and decreased testosterone levels. Tretinoin 23-25 cytochrome P450, family 17, subfamily a, polypeptide 1 Mus musculus 161-181
9221897-6 1997 Estrogen, thyroid hormone and retinoic acid all showed a minimal degree of promoter stimulation when the rat galanin-gene promoter was co-transfected with the appropriate hormone receptors in Neuro 2A cells, while co-transfection of the nuclear orphan receptor ELP1 was able to stimulate transcription of a galanin promoter-driven reporter-gene construct (-374 bp) by 35-fold. Tretinoin 30-43 erythrocyte membrane protein band 4.1 Mus musculus 261-265
29620249-4 2018 Here we have shown that retinoic acid (RA) leads to PGC differentiation, and SCF can improve the efficiency of induction. Tretinoin 24-37 progastricsin Gallus gallus 52-55
31694317-1 2019 The three subtypes (alpha, beta, and gamma) of the retinoic acid receptor (RAR) are ligand-dependent transcription factors that mediate retinoic acid signaling by forming heterodimers with the retinoid X receptor (RXR). Tretinoin 51-64 retinoic acid receptor alpha Homo sapiens 75-78
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 28-41 stimulated by retinoic acid gene 8 Mus musculus 140-174
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 28-41 stimulated by retinoic acid gene 8 Mus musculus 176-181
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 43-45 stimulated by retinoic acid gene 8 Mus musculus 140-174
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 43-45 stimulated by retinoic acid gene 8 Mus musculus 176-181
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 293-295 stimulated by retinoic acid gene 8 Mus musculus 140-174
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 293-295 stimulated by retinoic acid gene 8 Mus musculus 176-181
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 293-295 stimulated by retinoic acid gene 8 Mus musculus 140-174
31682623-1 2019 In murine fetal germ cells, retinoic acid (RA) is an extrinsic cue for meiotic initiation that stimulates transcriptional activation of the Stimulated by retinoic acid gene 8 (Stra8), which is required for entry of germ cells into meiotic prophase I. Canonically, the biological activities of RA are mediated by nuclear RA receptors. Tretinoin 293-295 stimulated by retinoic acid gene 8 Mus musculus 176-181
9220022-0 1997 Effects of triiodothyronine and retinoic acid on glucokinase gene expression in neonatal rat hepatocytes. Tretinoin 32-45 glucokinase Rattus norvegicus 49-60
31328592-4 2019 In the present study, we identified the retinoic acid-induced gene I (RIG-I) like receptors (RLRs)/mitochondrial antiviral signaling (MAVS) pathway as a target of SWCNT-induced oxidative stress in small airway epithelial cells (SAEC) that contribute to significantly enhanced influenza viral titers. Tretinoin 40-53 mitochondrial antiviral signaling protein Homo sapiens 134-138
9268491-6 1997 However, when these cells were induced by retinoic acid to differentiate, Ca2+-dependent PC-PLC and gamma-GT activities decreased significantly, together with alpha-fetoprotein expression. Tretinoin 42-55 alpha-fetoprotein Rattus norvegicus 159-176
9139890-10 1997 For this reason and because of a possible low toxicity, as compared with retinoic acid, we speculate that these RAR-gamma selective binding retinoids might be of clinical importance. Tretinoin 73-86 retinoic acid receptor gamma Homo sapiens 112-121
20607477-5 1997 In addition, BMP4 inhibits retinoic acid (RA)-induced neural differentiation of P19 cells and induces keratin expression. Tretinoin 27-40 bone morphogenetic protein 4 Homo sapiens 13-17
20607477-5 1997 In addition, BMP4 inhibits retinoic acid (RA)-induced neural differentiation of P19 cells and induces keratin expression. Tretinoin 42-44 bone morphogenetic protein 4 Homo sapiens 13-17
9166904-1 1997 Cytosolic aldehyde dehydrogenase, ALDH1, participates in the oxidation of different aldehydes including that of all-trans retinal to retinoic acid. Tretinoin 133-146 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 34-39
9097017-0 1997 Class IV alcohol/retinol dehydrogenase localization in epidermal basal layer: potential site of retinoic acid synthesis during skin development. Tretinoin 96-109 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 17-38
9097017-8 1997 This apparent down-regulation of class IV ADH expression during keratinocyte terminal differentiation provides evidence that the basal layer of the epidermis may be the primary site of local retinoic acid synthesis needed for retinoid signaling in the skin. Tretinoin 191-204 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 39-45
9097025-9 1997 Thus, ADH-IV and ALDH-1, two metabolic enzymes able to convert retinol to retinoic acid, are both initially expressed in primitive streak mesoderm at E7.5 when retinoic acid is first detectable. Tretinoin 74-87 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 17-23
9097025-9 1997 Thus, ADH-IV and ALDH-1, two metabolic enzymes able to convert retinol to retinoic acid, are both initially expressed in primitive streak mesoderm at E7.5 when retinoic acid is first detectable. Tretinoin 160-173 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 17-23
9130647-10 1997 In contrast, all-trans retinoic acid (0.1 microM, 7 days), which induces differentiation into the granulocytic phenotype, led to an up-regulation of IL-8RB in AML-193 cells and to an expression of IL-8RB and C5aR in HL-60 cells. Tretinoin 23-36 C-X-C motif chemokine receptor 2 Homo sapiens 149-155
9130647-10 1997 In contrast, all-trans retinoic acid (0.1 microM, 7 days), which induces differentiation into the granulocytic phenotype, led to an up-regulation of IL-8RB in AML-193 cells and to an expression of IL-8RB and C5aR in HL-60 cells. Tretinoin 23-36 C-X-C motif chemokine receptor 2 Homo sapiens 197-203
9126489-1 1997 Class IV alcohol dehydrogenase (ADH) has been shown to function in vitro as a retinol dehydrogenase catalyzing the synthesis of retinoic acid, a pleiotropic gene regulator. Tretinoin 128-141 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 32-35
9126489-1 1997 Class IV alcohol dehydrogenase (ADH) has been shown to function in vitro as a retinol dehydrogenase catalyzing the synthesis of retinoic acid, a pleiotropic gene regulator. Tretinoin 128-141 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 78-99
9084412-3 1997 In the present study, we examined the effects of retinoic acid (RA), a classic morphogen, on apoptosis in PC12 cells after serum deprivation and NGF-mediated rescue. Tretinoin 49-62 nerve growth factor Rattus norvegicus 145-148
9084412-9 1997 RA also decreased thymidine incorporation and proliferation in NGF-treated PC12 cells. Tretinoin 0-2 nerve growth factor Rattus norvegicus 63-66
9209395-4 1997 Because patients with APL can be induced into remission with high dose RA therapy, we propose that PML-RAR is a new class of dominant negative oncogene that disrupts a structure that includes at least five other proteins. Tretinoin 71-73 PML-RARA regulated adaptor molecule 1 Homo sapiens 99-106
9126603-9 1997 Scatchard analysis of 3H-labeled all-trans retinoic acid binding to purified human RAR gamma revealed a single, high-affinity binding site with a Kd of approximately 2 nM. Tretinoin 43-56 retinoic acid receptor gamma Homo sapiens 83-92
9126603-10 1997 Binding of the pure RAR gamma to a DR5-type retinoic acid response element was also studied. Tretinoin 44-57 retinoic acid receptor gamma Homo sapiens 20-29
9050783-7 1997 However, in Pax6(Sey-Neu)/ Pax6(Sey-Neu) embryos, retinoic acid (RA) is not produced by the frontonasal mesenchyme, which normally provides local retinoid signals to the placode and forebrain. Tretinoin 50-63 paired box 6 Homo sapiens 12-16
9050783-7 1997 However, in Pax6(Sey-Neu)/ Pax6(Sey-Neu) embryos, retinoic acid (RA) is not produced by the frontonasal mesenchyme, which normally provides local retinoid signals to the placode and forebrain. Tretinoin 50-63 paired box 6 Homo sapiens 27-31
9067580-0 1997 Inhibition of proliferation and CD25 down-regulation by retinoic acid in human adult T cell leukemia cells. Tretinoin 56-69 interleukin 2 receptor subunit alpha Homo sapiens 32-36
9067580-2 1997 Incubation of these cells for 48 h with either 13-cis retinoid acid (13-cis RA) or all-trans retinoic acid (ATRA) resulted in marked inhibition of cell growth, determined by 3H-thymidine incorporation, and in down-regulation of CD25 expression, determined by flow cytometry. Tretinoin 93-106 interleukin 2 receptor subunit alpha Homo sapiens 228-232
9067580-2 1997 Incubation of these cells for 48 h with either 13-cis retinoid acid (13-cis RA) or all-trans retinoic acid (ATRA) resulted in marked inhibition of cell growth, determined by 3H-thymidine incorporation, and in down-regulation of CD25 expression, determined by flow cytometry. Tretinoin 108-112 interleukin 2 receptor subunit alpha Homo sapiens 228-232
9032283-0 1997 Retinoic acid blocks adipogenesis by inhibiting C/EBPbeta-mediated transcription. Tretinoin 0-13 CCAAT enhancer binding protein beta Homo sapiens 48-57
9073458-6 1997 RA treatment predictably altered the expression of these proteins in a manner consistent with subsequent heart laterality: RA treatments which randomize heart loop direction also equalized or reversed the left/right JB3 and hLAMP-1 distribution prior to heart tube fusion. Tretinoin 0-2 lysosomal associated membrane protein 1 Homo sapiens 224-231
9003003-7 1997 Conversely, with 2 microM retinoic acid, the mitogenic effect of PLG, IGFBP-2 proteolysis, and tissue-type PLG activator mRNAs were increased. Tretinoin 26-39 plasminogen Homo sapiens 65-68
9003003-7 1997 Conversely, with 2 microM retinoic acid, the mitogenic effect of PLG, IGFBP-2 proteolysis, and tissue-type PLG activator mRNAs were increased. Tretinoin 26-39 insulin like growth factor binding protein 2 Homo sapiens 70-77
9003003-7 1997 Conversely, with 2 microM retinoic acid, the mitogenic effect of PLG, IGFBP-2 proteolysis, and tissue-type PLG activator mRNAs were increased. Tretinoin 26-39 plasminogen Homo sapiens 107-110
9001218-3 1997 In limited proteolysis analyses, both RXR and RAR in the heterodimer bound their respective ligands and underwent a conformational change in the presence of a retinoic acid-responsive element. Tretinoin 159-172 retinoid x receptor, gamma a Danio rerio 38-41
8999826-2 1997 It has been suggested that electrostatic interactions are critical for binding of retinoic acid by cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 82-95 cellular retinoic acid binding protein 1 Homo sapiens 140-147
8999826-3 1997 However, the roles of two conserved arginine residues (Arg-111 and Arg-131 in CRABP-I; Arg-111 and Arg-132 in CRABP-II) that interact with the carboxyl group of retinoic acid have not been evaluated. Tretinoin 161-174 cellular retinoic acid binding protein 1 Homo sapiens 78-85
9121703-0 1997 Increased gene expression of beta-amyloid precursor protein and its homologues APLP1 and APLP2 in human neuroblastoma cells in response to retinoic acid. Tretinoin 139-152 amyloid beta precursor like protein 2 Homo sapiens 89-94
9121703-3 1997 In this paper we show that APLP1 and APLP2 mRNA expression is upregulated during RA-induced differentiation of human SH-SY5Y neuroblastoma cells. Tretinoin 81-83 amyloid beta precursor like protein 2 Homo sapiens 37-42
9121703-5 1997 RA induced a 2- to 3-fold increase in the gene expression of both APLP2 and APP, whereas the increase in APLP1 mRNA expression was significantly higher. Tretinoin 0-2 amyloid beta precursor like protein 2 Homo sapiens 66-71
29752384-6 2018 Analysis of evx1 null mutants reveals that evx1 is acting upstream of pthlha and downstream of or in parallel with hoxa13a Calcineurin activity, potentially through the inhibition of retinoic acid signaling, regulates evx1, pthlha and hoxa13a expression during joint formation. Tretinoin 183-196 even-skipped homeobox 1 Homo sapiens 12-16
9049046-0 1997 Retinoic acids and dexamethasone alter cell-surface density of beta 2-integrins and ICAM-1 on human leukemic (HMC-1) mast cells. Tretinoin 0-14 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 63-69
29752384-6 2018 Analysis of evx1 null mutants reveals that evx1 is acting upstream of pthlha and downstream of or in parallel with hoxa13a Calcineurin activity, potentially through the inhibition of retinoic acid signaling, regulates evx1, pthlha and hoxa13a expression during joint formation. Tretinoin 183-196 even-skipped homeobox 1 Homo sapiens 43-47
29752384-6 2018 Analysis of evx1 null mutants reveals that evx1 is acting upstream of pthlha and downstream of or in parallel with hoxa13a Calcineurin activity, potentially through the inhibition of retinoic acid signaling, regulates evx1, pthlha and hoxa13a expression during joint formation. Tretinoin 183-196 even-skipped homeobox 1 Homo sapiens 43-47
9053316-6 1997 Interestingly, we also find that the Hoxa-1 expression response to RA treatment is not entirely controlled by the RARE, suggesting the existence of other retinoid-induced factors mediating the Hoxa-1 response to RA and/or the presence of additional RAREs. Tretinoin 67-69 homeobox A1 Mus musculus 37-43
29928370-0 2018 Retinoic acid-metabolizing enzyme cytochrome P450 26A1 promotes skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene. Tretinoin 0-13 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 34-54
29928370-1 2018 Elevated expression of the retinoic acid-metabolizing enzyme cytochrome P450 26A1 (CYP26A1) has been demonstrated to have an oncogenic function in carcinogenesis. Tretinoin 27-40 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 61-81
29928370-1 2018 Elevated expression of the retinoic acid-metabolizing enzyme cytochrome P450 26A1 (CYP26A1) has been demonstrated to have an oncogenic function in carcinogenesis. Tretinoin 27-40 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 83-90
9053316-6 1997 Interestingly, we also find that the Hoxa-1 expression response to RA treatment is not entirely controlled by the RARE, suggesting the existence of other retinoid-induced factors mediating the Hoxa-1 response to RA and/or the presence of additional RAREs. Tretinoin 67-69 homeobox A1 Mus musculus 193-199
29795382-1 2018 Retinoic acid (RA) and arsenic target the t(15;17)(q24;q21) PML/RARA driver of acute promyelocytic leukemia (APL), their combination now curing over 95% patients. Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 60-63
29795382-1 2018 Retinoic acid (RA) and arsenic target the t(15;17)(q24;q21) PML/RARA driver of acute promyelocytic leukemia (APL), their combination now curing over 95% patients. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 64-68
29795382-1 2018 Retinoic acid (RA) and arsenic target the t(15;17)(q24;q21) PML/RARA driver of acute promyelocytic leukemia (APL), their combination now curing over 95% patients. Tretinoin 15-17 PML nuclear body scaffold Homo sapiens 60-63
29795382-1 2018 Retinoic acid (RA) and arsenic target the t(15;17)(q24;q21) PML/RARA driver of acute promyelocytic leukemia (APL), their combination now curing over 95% patients. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 64-68
29795382-6 2018 Accordingly, clonogenic activity of PML/RARA-immortalized progenitors ex vivo is only transiently affected by RA, but selectively abrogated by arsenic. Tretinoin 40-42 PML nuclear body scaffold Homo sapiens 36-39
9053323-12 1997 Fourth, we show that otx2-GR is sufficient to overcome the inhibitory effects of retinoic acid on cement gland formation, indicating that this effect is caused by failure to express otx2. Tretinoin 81-94 orthodenticle homeobox 2 L homeolog Xenopus laevis 21-25
29891447-5 2018 RESULTS: Compared with the control cells, the hepatocytes treated with ATRA showed a concentration-dependent decrease in AFP expression and increase in the expressions of ALB, CK18, TAT and ApoB. Tretinoin 71-75 apolipoprotein B Mus musculus 190-194
29891447-8 2018 ATRA treatment resulted in significantly increased the expressions of autophagy-related markers LC3-II, Beclin-1, RAB7 and P62 and also an increased ratio of LC3-II/LC3-I(P<0.05). Tretinoin 0-4 beclin 1, autophagy related Mus musculus 104-112
9053323-13 1997 Corroboratively, we show that otx2 autoactivation is prevented by retinoic acid. Tretinoin 66-79 orthodenticle homeobox 2 L homeolog Xenopus laevis 30-34
9285932-0 1997 Retinoic acid regulation of the VIP and PACAP autocrine ligand and receptor system in human neuroblastoma cell lines. Tretinoin 0-13 adenylate cyclase activating polypeptide 1 Homo sapiens 40-45
9285932-8 1997 The studies indicate that several components of the VIP/PACAP autocrine system are regulated in neuroblastoma cell lines during RA differentiation. Tretinoin 128-130 adenylate cyclase activating polypeptide 1 Homo sapiens 56-61
8980110-9 1996 In Raji cells, PLCgamma2 mRNA is expressed at low levels with a half life greater than 4 h. After treatment with serum, TPA, retinoic acid, or with 5-azacytidine increased levels of PLCgamma2 mRNA were induced in B-cells. Tretinoin 125-138 phospholipase C gamma 2 Homo sapiens 15-24
29596829-5 2018 Recent studies suggest that pharmacological concentrations of the APL therapeutic drugs, all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), affect post-mitotic nuclear import of the APL-associated oncoprotein PML/RARA. Tretinoin 89-112 PML nuclear body scaffold Homo sapiens 217-220
29596829-5 2018 Recent studies suggest that pharmacological concentrations of the APL therapeutic drugs, all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), affect post-mitotic nuclear import of the APL-associated oncoprotein PML/RARA. Tretinoin 89-112 retinoic acid receptor alpha Homo sapiens 221-225
29596829-5 2018 Recent studies suggest that pharmacological concentrations of the APL therapeutic drugs, all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), affect post-mitotic nuclear import of the APL-associated oncoprotein PML/RARA. Tretinoin 114-118 PML nuclear body scaffold Homo sapiens 217-220
8980110-9 1996 In Raji cells, PLCgamma2 mRNA is expressed at low levels with a half life greater than 4 h. After treatment with serum, TPA, retinoic acid, or with 5-azacytidine increased levels of PLCgamma2 mRNA were induced in B-cells. Tretinoin 125-138 phospholipase C gamma 2 Homo sapiens 182-191
9025717-0 1996 Post-transcriptional induction of beta 1-adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors. Tretinoin 64-77 adrenoceptor beta 1 Homo sapiens 34-60
29650589-1 2018 Zebrafish mutants with increased retinoic acid (RA) signaling due to the loss of the RA-inactivating enzyme Cyp26b1 develop a hyper-mineralized spine with gradually fusing vertebral body precursors (centra). Tretinoin 33-46 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 108-115
29650589-1 2018 Zebrafish mutants with increased retinoic acid (RA) signaling due to the loss of the RA-inactivating enzyme Cyp26b1 develop a hyper-mineralized spine with gradually fusing vertebral body precursors (centra). Tretinoin 48-50 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 108-115
29650589-1 2018 Zebrafish mutants with increased retinoic acid (RA) signaling due to the loss of the RA-inactivating enzyme Cyp26b1 develop a hyper-mineralized spine with gradually fusing vertebral body precursors (centra). Tretinoin 85-87 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 108-115
9025717-6 1996 The beta 1-AR mRNA concentrations were, however, altered by retinoic acid (RA) treatment. Tretinoin 60-73 adrenoceptor beta 1 Homo sapiens 4-13
29488619-12 2018 ATRA is able to ameliorate high-fat-induced AS in rabbits, which is mediated through the activation of eNOS and downregulating CAV-1 expression. Tretinoin 0-4 caveolin-1 Oryctolagus cuniculus 127-132
9025717-7 1996 Retinoic acid caused a rapid up-regulation of beta 1-AR mRNA levels that was blocked by cycloheximide. Tretinoin 0-13 adrenoceptor beta 1 Homo sapiens 46-55
8940255-0 1996 FMS (CSF-1 receptor) prolongs cell cycle and promotes retinoic acid-induced hypophosphorylation of retinoblastoma protein, G1 arrest, and cell differentiation. Tretinoin 54-67 colony stimulating factor 1 receptor Homo sapiens 5-19
29910671-3 2018 In the present study, we found that ATRA could decrease the expression of NEDD8-activating enzyme E1 (NAE1) and inhibit the neddylation of cullin1 and cullin3 in the APL cell line NB4. Tretinoin 36-40 NEDD8 activating enzyme E1 subunit 1 Homo sapiens 74-100
29910671-3 2018 In the present study, we found that ATRA could decrease the expression of NEDD8-activating enzyme E1 (NAE1) and inhibit the neddylation of cullin1 and cullin3 in the APL cell line NB4. Tretinoin 36-40 NEDD8 activating enzyme E1 subunit 1 Homo sapiens 102-106
29596381-9 2018 Our results demonstrate for the first time: (1) the therapeutic value of resveratrol by itself or in combination with RA in the management of ATCs, (2) the capacity of resveratrol to overcome RA resistance in ATC cells by reprogramming CRABP2/RAR- and fatty acid-binding protein 5 (FABP5)/PPAR-beta/delta-mediated RA signaling, and (3) the redifferentiating potential of resveratrol in ATC cells. Tretinoin 192-194 retinoic acid receptor alpha Homo sapiens 243-246
8950195-0 1996 Retinoic acid affects the expression rate of the differentiation-related genes aryl hydrocarbon receptor, ARNT and keratin 4 in proliferative keratinocytes only. Tretinoin 0-13 aryl hydrocarbon receptor Homo sapiens 79-104
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 forkhead box P3 Mus musculus 158-163
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 embryonic ectoderm development Mus musculus 168-171
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 embryonic ectoderm development Mus musculus 264-267
28436029-14 2018 Collectively, WNT4 may act downstream of BMP2 to mediate the effects of ATRA on the terminal differentiation of antler chondrocytes through targeting RUNX1. Tretinoin 72-76 RUNX family transcription factor 1 Homo sapiens 150-155
28190238-0 2018 Alpha-Synuclein Suppresses Retinoic Acid-Induced Neuronal Differentiation by Targeting the Glycogen Synthase Kinase-3beta/beta-Catenin Signaling Pathway. Tretinoin 27-40 synuclein alpha Homo sapiens 0-15
28190238-0 2018 Alpha-Synuclein Suppresses Retinoic Acid-Induced Neuronal Differentiation by Targeting the Glycogen Synthase Kinase-3beta/beta-Catenin Signaling Pathway. Tretinoin 27-40 catenin beta 1 Homo sapiens 122-134
8950195-6 1996 When keratinocytes were continuously treated with 1 microM retinoic acid (RA), the upregulation of AhR- and ARNT-mRNA levels was inhibited as was keratin 4-expression, a marker of HaCaT-keratinocyte differentiation. Tretinoin 59-72 aryl hydrocarbon receptor Homo sapiens 99-102
31640715-0 2019 Upregulation of FNDC5 gene expression in C2C12 cells after single and combined treatments of resveratrol and ATRA. Tretinoin 109-113 fibronectin type III domain containing 5 Mus musculus 16-21
8950195-6 1996 When keratinocytes were continuously treated with 1 microM retinoic acid (RA), the upregulation of AhR- and ARNT-mRNA levels was inhibited as was keratin 4-expression, a marker of HaCaT-keratinocyte differentiation. Tretinoin 74-76 aryl hydrocarbon receptor Homo sapiens 99-102
31640715-4 2019 In the present study, the effects of single and combined treatments of Res and ATRA on fibronectin type III domain containing 5 (FNDC5) gene expression was explored. Tretinoin 79-83 fibronectin type III domain containing 5 Mus musculus 87-127
8950195-9 1996 Our data suggest that the regulation of AhR-, ARNT- and keratin 4-expression by RA is indirect and mediated by a yet to be identified factor. Tretinoin 80-82 aryl hydrocarbon receptor Homo sapiens 40-43
31640715-4 2019 In the present study, the effects of single and combined treatments of Res and ATRA on fibronectin type III domain containing 5 (FNDC5) gene expression was explored. Tretinoin 79-83 fibronectin type III domain containing 5 Mus musculus 129-134
31640715-10 2019 RESULTS: The FNDC5 gene expression in C2C12 myotubes of alone-treated with 1 muM, 25 muM Res and 10 muM ATRA did not change compared to vehicle group. Tretinoin 104-108 fibronectin type III domain containing 5 Mus musculus 13-18
29337667-6 2018 In this revised view, ISL1 is antagonized by retinoic acid signaling via a novel player, MEIS2. Tretinoin 45-58 Meis homeobox 2 Homo sapiens 89-94
29337667-7 2018 Conversely, ISL1 competes with the retinoic acid pathway for prospective cardiomyocyte fate, which converges on the atrial specifier NR2F1. Tretinoin 35-48 ISL LIM homeobox 1 Homo sapiens 12-16
31640715-12 2019 CONCLUSION: This is the first evidence that Res and ATRA can regulate FNDC5 gene expression in C2C12 myotubes. Tretinoin 52-56 fibronectin type III domain containing 5 Mus musculus 70-75
8944731-5 1996 In contrast, maximal stimulation of SP-C (6x) was noted at 10(-5) M retinoic acid and that of SP-B (2x) at 10(-7) to 10(-5) M retinoic acid. Tretinoin 126-139 surfactant protein B Rattus norvegicus 94-98
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 44-48
8945636-3 1996 alpha-Fetoprotein (AFP), a hepatocyte differentiation, maturation, and carcinogenesis marker, is transcriptionally upregulated by RA in McA-RH8994 hepatoma cells. Tretinoin 130-132 alpha-fetoprotein Rattus norvegicus 0-17
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 0-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 167-171
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 44-48
31427086-7 2019 All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions. Tretinoin 25-29 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 167-171
29183727-5 2018 On the other hand, immunoblot analysis revealed that co-treatment with RA and resveratrol caused remarkable accumulation of protein levels of gp91-phox (to 4-fold), p22-phox (to 5-fold) and p47-phox (to 4-fold) compared with those of the RA-treatment alone. Tretinoin 71-73 cytochrome b-245 alpha chain Homo sapiens 165-173
8945636-3 1996 alpha-Fetoprotein (AFP), a hepatocyte differentiation, maturation, and carcinogenesis marker, is transcriptionally upregulated by RA in McA-RH8994 hepatoma cells. Tretinoin 130-132 alpha-fetoprotein Rattus norvegicus 19-22
8945636-10 1996 CAT assays demonstrated that overexpression of RXRalpha conferred the best RA response, consistent with our previous observation that 9-cis-RA is more potent than all-trans-RA for inducing the expression of the AFP gene. Tretinoin 75-77 alpha-fetoprotein Rattus norvegicus 211-214
30114705-9 2018 RESULTS: MAT improved the sensitivity of NB4-LR1cells to ATRA treatment, which was consistent with the expression of PML-RARalpha fusion protein. Tretinoin 57-61 PML nuclear body scaffold Homo sapiens 117-120
8903394-10 1996 Treatment of cultured HSCs with retinoic acid (1 micromol/L) increased uPA secretion 2.6-fold but did not alter PAI-1. Tretinoin 32-45 plasminogen activator, urokinase Rattus norvegicus 71-74
30114705-9 2018 RESULTS: MAT improved the sensitivity of NB4-LR1cells to ATRA treatment, which was consistent with the expression of PML-RARalpha fusion protein. Tretinoin 57-61 retinoic acid receptor alpha Homo sapiens 121-129
30423583-0 2018 Novel Zinc Finger Transcription Factor ZFP580 Facilitates All-Trans Retinoic Acid -Induced Vascular Smooth Muscle Cells Differentiation by Raralpha-Mediated PI3K/Akt and ERK Signaling. Tretinoin 68-81 retinoic acid receptor, alpha Rattus norvegicus 139-147
31292998-6 2019 In patients relapsing after ATRA/ATO, the PML gene was a preferential mutation target. Tretinoin 28-32 PML nuclear body scaffold Homo sapiens 42-45
30423583-12 2018 In contrast, silencing of the RARalpha gene or inhibiting RARalpha with its antagonist Ro41-5253 abrogated the ATRA-induced ZFP580 expression. Tretinoin 111-115 retinoic acid receptor, alpha Rattus norvegicus 30-38
30423583-12 2018 In contrast, silencing of the RARalpha gene or inhibiting RARalpha with its antagonist Ro41-5253 abrogated the ATRA-induced ZFP580 expression. Tretinoin 111-115 retinoic acid receptor, alpha Rattus norvegicus 58-66
30423583-13 2018 Furthermore, ATRA binding to RARalpha induced ZFP580 expression via the PI3K/Akt and ERK pathways. Tretinoin 13-17 retinoic acid receptor, alpha Rattus norvegicus 29-37
30423583-17 2018 CONCLUSION: The novel zinc finger transcription factor ZFP580 facilitates ATRA-induced VSMC differentiation by the RARalpha-mediated PI3K/Akt and ERK signaling pathways. Tretinoin 74-78 retinoic acid receptor, alpha Rattus norvegicus 115-123
30939964-0 2019 Retinoic acid worsens ATG10-dependent autophagy impairment in TBK1-mutant hiPSC-derived motoneurons through SQSTM1/p62 accumulation. Tretinoin 0-13 TANK binding kinase 1 Homo sapiens 62-66
8910304-3 1996 In the absence of RA treatment, the transglutaminase immunoreactivity elutes from a gel filtration column with an apparent size of approximately 600 kDa (designated TGa), whereas following RA treatment, a second peak of transglutaminase immunoreactivity (designated TGb) is detected with an apparent size of approximately 150 kDa. Tretinoin 189-191 pro-platelet basic protein Homo sapiens 266-269
31416840-4 2019 In this study, INCENP was highly expressed by NB cells and its expression decreased following retinoic acid-induced NB differentiation. Tretinoin 94-107 inner centromere protein Homo sapiens 15-21
30216786-2 2018 With retinoic acid (RA) induction, a high percentage of cells were found to be arrested at the G0/G1 phase, with decreased levels of cyclinD1, CDK4, phosphorylation status of pRb and E2F1, in addition to an elevated level of p27. Tretinoin 5-18 E2F transcription factor 1 Homo sapiens 183-187
29321952-3 2018 One of its interactors is retinoic acid receptor (RAR), which is activated by retinoic acid and controls many target genes and physiological process. Tretinoin 26-39 retinoic acid receptor alpha Homo sapiens 50-53
8910304-7 1996 In addition, the TGb fraction shows a markedly enhanced ability (relative to TGa) to associate with membranes from control (non-RA-treated) cells. Tretinoin 128-130 pro-platelet basic protein Homo sapiens 17-20
8930166-2 1996 The following agents inhibited phorbol 12-myristate 13-acetate-stimulated O2- generation significantly in the all-trans retinoic acid-treated HL-60 cells (expressed as percentage of control, P < .05): 1) PKC inhibitors: staurosporine (100 nM, 3 +/- 1%); Ro 31-8220 (1 microM, 3 +/- 2%); sphingosine (100 microM, 15 +/- 7%); 2) PSP 1 and 2a inhibitors, okadaic acid (10 microM, 35 +/- 1%); calyculin A (10 microM, 73 +/- 1%); 3) MAPK inhibitor: SB-203580 (100 microM, 62 +/- 1%); 4) PTP inhibitors: phenylarsine oxide (1 microM, 12 +/- 9%); diamide (1 mM, 21 +/- 11%); and 5) secretory phospholipase A2 inhibitors: manoalide (1 microM, 24 +/- 10%); scalaradial (1 microM, 11 +/- 4%). Tretinoin 120-133 protein tyrosine phosphatase receptor type U Homo sapiens 485-488
29200759-7 2017 In cultured keratinocytes, the RA combination significantly decreased cell viability, but increased cytotoxicity and extracellular interleukin 1 alpha release with corresponding doses of HQ. Tretinoin 31-33 interleukin 1 alpha Homo sapiens 131-150
31343737-0 2019 Syndromic chorioretinal coloboma associated with heterozygous de novo RARA mutation affecting an amino acid critical for retinoic acid interaction. Tretinoin 121-134 retinoic acid receptor alpha Homo sapiens 70-74
31343737-1 2019 Retinoid acid receptors (RAR) are transcription factors that bind retinoic acid (RA), a metabolite of vitamin A. Tretinoin 66-79 retinoic acid receptor alpha Homo sapiens 25-28
31343737-9 2019 We propose that RARA p.Arg276Trp causes the disease by affecting RA interaction with the RARA receptor. Tretinoin 16-18 retinoic acid receptor alpha Homo sapiens 89-93
31419710-0 2019 Retinoic acid modulates IL-4, IL-10 and MCP-1 pathways in immune mediated hepatitis and interrupts CD4+ T cells infiltration. Tretinoin 0-13 interleukin 4 Mus musculus 24-28
31419710-7 2019 KEY FINDINGS: Injection of RA before ConA significantly (p < 0.001) decreased ALT, AST and LDH levels compared to their levels in ConA group. Tretinoin 27-29 glutamic pyruvic transaminase, soluble Mus musculus 81-84
31419710-7 2019 KEY FINDINGS: Injection of RA before ConA significantly (p < 0.001) decreased ALT, AST and LDH levels compared to their levels in ConA group. Tretinoin 27-29 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 86-89
29042055-0 2017 Mechanism underlying the suppressor activity of retinoic acid on IL4-induced IgE synthesis and its physiological implication. Tretinoin 48-61 interleukin 4 Mus musculus 65-68
8805369-7 1996 The application of a bead soaked in RA can rescue Shh expression. Tretinoin 36-38 sonic hedgehog Gallus gallus 50-53
28978663-6 2017 In contrast, the p73-DAPK2 pathway is essential for ATRA-induced autophagy that is mediated by an interaction of DAPK2 with the key autophagy-related protein (ATG)5. Tretinoin 52-56 death associated protein kinase 2 Homo sapiens 21-26
28978663-6 2017 In contrast, the p73-DAPK2 pathway is essential for ATRA-induced autophagy that is mediated by an interaction of DAPK2 with the key autophagy-related protein (ATG)5. Tretinoin 52-56 death associated protein kinase 2 Homo sapiens 113-118
28978663-7 2017 Lastly, we show that DAPK2 binds and stabilizes the p73 protein; thus, we propose a novel mechanism by which ATO- or ATRA-induced therapy responses initiate a positive p73-DAPK2 feedback loop. Tretinoin 117-121 death associated protein kinase 2 Homo sapiens 21-26
28978663-7 2017 Lastly, we show that DAPK2 binds and stabilizes the p73 protein; thus, we propose a novel mechanism by which ATO- or ATRA-induced therapy responses initiate a positive p73-DAPK2 feedback loop. Tretinoin 117-121 death associated protein kinase 2 Homo sapiens 172-177
29055789-0 2017 In vitro studies on the role of recombinant human soluble thrombomodulin in the context of retinoic acid mediated APL differentiation syndrome. Tretinoin 91-104 thrombomodulin Homo sapiens 58-72
31419710-10 2019 A significant decrease in the measured cytokines TNF-alpha and IL-4 was observed in ConA + RA group in addition to a decrease in MCP-1 level. Tretinoin 91-93 interleukin 4 Mus musculus 63-67
31419710-12 2019 SIGNIFICANCE: RA can protect against ConA-induced hepatitis through: interrupting early inflammatory response as neutrophils, monocytes and CD4+ T cells infiltration, modulating IL-4 level and subsequent production of TNF-alpha and NF-kappab activation, mitigating second inflammatory responses through increasing IL-10 liver production. Tretinoin 14-16 interleukin 4 Mus musculus 178-182
31323146-8 2019 ATRA led to inhibition of p-STAT3, p-JAK2, increased the level of p-ERK, and significantly decreased the PD-L1 expression. Tretinoin 0-4 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 66-71
31323146-8 2019 ATRA led to inhibition of p-STAT3, p-JAK2, increased the level of p-ERK, and significantly decreased the PD-L1 expression. Tretinoin 0-4 CD274 molecule Homo sapiens 105-110
31323146-10 2019 The effect of ATRA on cell growth inhibition, apoptosis induction, and PD-L1 expression decrease was significantly (P < .05) enhanced after the STAT3 signaling blockade. Tretinoin 14-18 CD274 molecule Homo sapiens 71-76
31323146-11 2019 CONCLUSION: These findings suggested that ATRA-induced anti-tumor effects and downregulated PD-L1 expression via STAT3 signaling inhibition in both OSCC and oral dysplasia. Tretinoin 42-46 CD274 molecule Homo sapiens 92-97
31880511-5 2019 PHB expression was reduced in an ATRA treated RARalpha- group, and TGF-beta1, FN and Col-IV were up-regulated compared to the ATRA treated RARalpha+ group. Tretinoin 126-130 retinoic acid receptor alpha Homo sapiens 139-147
31880511-6 2019 We postulate that ATRA can induce the PHB expression by RARalpha in hypoxia/reperfusion related RTEC injury. Tretinoin 18-22 retinoic acid receptor alpha Homo sapiens 56-64
29109271-6 2017 We measured RA concentrations and found that they changed periodically, as also reflected in the expression patterns of an RA-responsive gene, STRA8; RA levels were low before the four transitions, increased when the transitions occurred, and remained elevated thereafter. Tretinoin 123-125 stimulated by retinoic acid gene 8 Mus musculus 143-148
29068287-2 2017 In this study, we found that the oncogenic hepatitis B virus (HBV) X protein (HBx) of HBV, derived from both overexpression and 1.2-mer replicon systems, suppresses ATRA-induced apoptosis in p53-positive human hepatocytes. Tretinoin 165-169 X protein Hepatitis B virus 78-81
29068287-3 2017 For this effect, HBx upregulated both protein and enzyme activity levels of DNA methyltransferase 1, 3a and 3b, in the presence of ATRA and thereby inhibited p14 expression via promoter hypermethylation, resulting in inactivation of the p14-mouse double minute 2 pathway and subsequent downregulation of p53 levels. Tretinoin 131-135 X protein Hepatitis B virus 17-20
29068287-4 2017 As a result, HBx was able to impair the potential of ATRA to activate apoptosis-related molecules, including Bax, p53-upregulated modulator of apoptosis, caspase-9, caspase-3 and poly (ADP-ribose) polymerase. Tretinoin 53-57 X protein Hepatitis B virus 13-16
29068287-5 2017 In conclusion, the present study provides a new oncogenic action mechanism of HBx, namely by suppressing the anticancer potential of ATRA to induce p53-dependent apoptosis in HBV-infected hepatocytes. Tretinoin 133-137 X protein Hepatitis B virus 78-81
8805369-9 1996 Again, RA can rescue the expression of Shh in these limb buds. Tretinoin 7-9 sonic hedgehog Gallus gallus 39-42
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 DNA mismatch repair protein Mlh1 Bubalus bubalis 194-198
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 PRM2 Bubalus bubalis 211-215
32648650-6 2019 Results indicate beta-catenin translocalization and activation of TCF/LEF responsive transcription in response to MNP and magnetic fields, which result in dopaminergic marker expression when synergistically combined with differentiation factors retinoic acid and the phorbol ester phorbol 12-myristate 13-acetate. Tretinoin 245-258 catenin beta 1 Homo sapiens 17-29
8805369-11 1996 The expression of Shh and Fgf-4 remains dependent upon the continued synthesis of RA within the limb bud. Tretinoin 82-84 sonic hedgehog Gallus gallus 18-21
8805369-11 1996 The expression of Shh and Fgf-4 remains dependent upon the continued synthesis of RA within the limb bud. Tretinoin 82-84 fibroblast growth factor 4 Gallus gallus 26-31
31026381-8 2019 These results not only provide the first evidence for a critical role of Pin1 in the tumorigenesis of gastric cancer but also suggest that targeting Pin1 using ATRA or other inhibitors offers an effective new therapeutic approach for treating advanced gastric cancer. Tretinoin 160-164 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 149-153
8751982-0 1996 A limited role for retinoic acid and retinoic acid receptors RAR alpha and RAR beta in regulating keratin 19 expression and keratinization in oral and epidermal keratinocytes. Tretinoin 19-32 keratin 19 Homo sapiens 98-108
31221621-6 2019 In particular, the concentrations of the ketogenic enzyme 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) and of retinol dehydrogenase 16 (RDH16), which catalyzes the first step in retinoic acid biogenesis, were highly increased. Tretinoin 184-197 hydroxymethylglutaryl-CoA synthase, mitochondrial Sus scrofa 101-107
28780376-0 2017 Retinoic acid induction of CD1d expression primes chronic lymphocytic leukemia B cells for killing by CD8+ invariant natural killer T cells. Tretinoin 0-13 CD1d molecule Homo sapiens 27-31
8751982-8 1996 Overexpression of either receptor enhanced the RA inducibility of K19 in conventional culture, in that the proportion of the transductants becoming K19+ in response to RA was markedly increased compared with controls. Tretinoin 47-49 keratin 19 Homo sapiens 66-69
8751982-8 1996 Overexpression of either receptor enhanced the RA inducibility of K19 in conventional culture, in that the proportion of the transductants becoming K19+ in response to RA was markedly increased compared with controls. Tretinoin 168-170 keratin 19 Homo sapiens 66-69
8751982-8 1996 Overexpression of either receptor enhanced the RA inducibility of K19 in conventional culture, in that the proportion of the transductants becoming K19+ in response to RA was markedly increased compared with controls. Tretinoin 168-170 keratin 19 Homo sapiens 148-151
28959017-5 2017 We demonstrate that Wdr5, Hdac1, and Hdac2 are required for RA signaling in vitro and in vivo. Tretinoin 60-62 histone deacetylase 1 Mus musculus 26-31
31167781-2 2019 We hypothesized that loss of Cyp26a1 activity via inducible knockout in juvenile or adult mice would result in decreased atRA clearance and increased tissue atRA concentrations and atRA-related adverse effects. Tretinoin 121-125 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 29-36
8887314-6 1996 The potential role of a CRABP I-controlled nuclear import of retinoic acid is discussed. Tretinoin 61-74 cellular retinoic acid binding protein 1 Rattus norvegicus 24-31
31167781-2 2019 We hypothesized that loss of Cyp26a1 activity via inducible knockout in juvenile or adult mice would result in decreased atRA clearance and increased tissue atRA concentrations and atRA-related adverse effects. Tretinoin 157-161 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 29-36
31167781-2 2019 We hypothesized that loss of Cyp26a1 activity via inducible knockout in juvenile or adult mice would result in decreased atRA clearance and increased tissue atRA concentrations and atRA-related adverse effects. Tretinoin 157-161 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 29-36
31167781-9 2019 In addition, the Cyp26a1 knockout decreased clearance of exogenous atRA by 70% and increased atRA half-life 6-fold. Tretinoin 67-71 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 17-24
31215681-4 2019 Treatment with ATRA during the early and late stage of adipogenesis resulted in an increase in the expression level of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12, respectively, whereas expression of Pgc-1alpha, another gene expressed during brown adipogenesis, was unaffected by ATRA. Tretinoin 15-19 uncoupling protein 1 Homo sapiens 119-123
31215681-11 2019 SIGNIFICANCE OF THE STUDY: Significance of the study treatment with all-trans retinoic acid (ATRA) during the early and late stage of adipogenesis increased the expression of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12. Tretinoin 68-91 uncoupling protein 1 Homo sapiens 175-179
31215681-11 2019 SIGNIFICANCE OF THE STUDY: Significance of the study treatment with all-trans retinoic acid (ATRA) during the early and late stage of adipogenesis increased the expression of Ucp1 and Cidea, genes highly expressed in brown adipocytes, on day 8 and day 12. Tretinoin 93-97 uncoupling protein 1 Homo sapiens 175-179
31243280-4 2019 Here we show that self-noncoding dsRNA activates the anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice. Tretinoin 121-134 toll-like receptor 3 Mus musculus 73-93
31243280-4 2019 Here we show that self-noncoding dsRNA activates the anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice. Tretinoin 121-134 toll-like receptor 3 Mus musculus 95-99
28542882-5 2017 The results showed that RA-induced DCs (RA-DCs) showed mucosal DC properties, including expression of CD103 and gut homing receptor alpha4 beta7 , low proinflammatory cytokine secretion and low priming capability to antigen-specific CD4+ T cells. Tretinoin 24-26 integrin subunit alpha E Homo sapiens 102-107
28542882-5 2017 The results showed that RA-induced DCs (RA-DCs) showed mucosal DC properties, including expression of CD103 and gut homing receptor alpha4 beta7 , low proinflammatory cytokine secretion and low priming capability to antigen-specific CD4+ T cells. Tretinoin 40-42 integrin subunit alpha E Homo sapiens 102-107
28542882-6 2017 Butyrate-treated RA-DCs (Bu-RA-DCs) decreased CD11c, but increased CD103 and alpha4 beta7 expression. Tretinoin 17-19 integrin subunit alpha E Homo sapiens 67-72
28677722-2 2017 Enzymes that catalyze the oxidation of retinol to generate atRA, including aldehyde dehydrogenase 1 family (ALDH1)A1, ALDH1A2 and ALDH1A3, exhibit complex expression patterns at different stages of renal development. Tretinoin 59-63 aldehyde dehydrogenase 1 family member A1 Homo sapiens 108-113
28677722-2 2017 Enzymes that catalyze the oxidation of retinol to generate atRA, including aldehyde dehydrogenase 1 family (ALDH1)A1, ALDH1A2 and ALDH1A3, exhibit complex expression patterns at different stages of renal development. Tretinoin 59-63 aldehyde dehydrogenase 1 family member A3 Homo sapiens 130-137
28677722-4 2017 In this study, we provide in vitro evidence to demonstrate that Wilms" tumor 1 (WT1) negatively regulates the expression of the atRA synthetic enzymes, ALDH1A1, ALDH1A2 and ALDH1A3, in the 293 cell line, leading to significant blockage of atRA production. Tretinoin 128-132 aldehyde dehydrogenase 1 family member A1 Homo sapiens 152-159
28677722-4 2017 In this study, we provide in vitro evidence to demonstrate that Wilms" tumor 1 (WT1) negatively regulates the expression of the atRA synthetic enzymes, ALDH1A1, ALDH1A2 and ALDH1A3, in the 293 cell line, leading to significant blockage of atRA production. Tretinoin 128-132 aldehyde dehydrogenase 1 family member A3 Homo sapiens 173-180
28656276-7 2017 Further investigations indicated that with ATRA-induced expression of RIG-I, levels of phosphorylated (p)AKT-Thr308 and pForkhead Box (FOX) O3A-Thr32 were decreased, the expression levels of cell cycle arrest protein p27 and the apoptotic protein, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), directly transcribed by FOXO3A were increased. Tretinoin 43-47 interferon alpha inducible protein 27 Homo sapiens 217-220
28656276-8 2017 By contrast, following the knockdown of ATRA-induced expression of RIG-I, the levels of pAKT-Thr308 and pFOXO3A-Thr32 were increased, and the protein expression levels of p27 and TRAIL were decreased. Tretinoin 40-44 interferon alpha inducible protein 27 Homo sapiens 171-174
31243280-4 2019 Here we show that self-noncoding dsRNA activates the anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice. Tretinoin 136-138 toll-like receptor 3 Mus musculus 73-93
31243280-4 2019 Here we show that self-noncoding dsRNA activates the anti-viral receptor toll like receptor 3 (TLR3) to induce intrinsic retinoic acid (RA) synthesis in a pattern that predicts new hair follicle formation after wounding in mice. Tretinoin 136-138 toll-like receptor 3 Mus musculus 95-99
8887323-0 1996 A new mouse member of the Wnt gene family, mWnt-8, is expressed during early embryogenesis and is ectopically induced by retinoic acid. Tretinoin 121-134 Wnt family member 8A Gallus gallus 26-29
8887323-0 1996 A new mouse member of the Wnt gene family, mWnt-8, is expressed during early embryogenesis and is ectopically induced by retinoic acid. Tretinoin 121-134 wingless-type MMTV integration site family, member 8A Mus musculus 43-49
8887323-1 1996 We have identified a novel mouse Wnt genc using a cDNA differential screening procedure for retinoic-acid-induced transcripts in P19 embryonal carcinoma cells. Tretinoin 92-105 Wnt family member 8A Gallus gallus 33-36
8887323-3 1996 The expression of the mWnt-8 gene, which is rapidly induced by retinoic acid in P19 and embryonic stem cells, appears to be restricted to early stages of mouse embryogenesis. Tretinoin 63-76 wingless-type MMTV integration site family, member 8A Mus musculus 22-28
31234811-11 2019 Analysis of conserved SDH-loss master regulators in human tumors and MEFs implicated ZNF423, a known modulator of retinoic acid response in neuroblastoma. Tretinoin 114-127 zinc finger protein 423 Homo sapiens 85-91
28689802-1 2017 Retinoic acid functions through two classes of receptors, i.e., the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). Tretinoin 0-13 retinoic acid receptor alpha Xenopus tropicalis 68-90
28689802-1 2017 Retinoic acid functions through two classes of receptors, i.e., the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). Tretinoin 0-13 retinoic acid receptor alpha Xenopus tropicalis 92-95
8913320-4 1996 9-cis RA, a high-affinity ligand for RXR, greatly enhanced D3-induced CD14 expression in U937 cells, while RA alone did not induce CD14 expression. Tretinoin 6-8 CD14 molecule Homo sapiens 70-74
8760042-2 1996 In normal cells, trans-retinoic acid (RA) and 2.0 mM Ca2+ significantly stimulated PTHRP mRNA expression and secretion and led to a significant reduction in the rate of proliferation. Tretinoin 17-36 parathyroid hormone like hormone Homo sapiens 83-88
28783931-1 2017 Objective: Retinal dehydrogenase 1 (RALDH1) is a cytosolic enzyme which acts both as a source of retinoic acid (RA) and as a detoxification enzyme. Tretinoin 97-110 aldehyde dehydrogenase 1 family member A1 Homo sapiens 11-34
28783931-1 2017 Objective: Retinal dehydrogenase 1 (RALDH1) is a cytosolic enzyme which acts both as a source of retinoic acid (RA) and as a detoxification enzyme. Tretinoin 97-110 aldehyde dehydrogenase 1 family member A1 Homo sapiens 36-42
28783931-1 2017 Objective: Retinal dehydrogenase 1 (RALDH1) is a cytosolic enzyme which acts both as a source of retinoic acid (RA) and as a detoxification enzyme. Tretinoin 36-38 aldehyde dehydrogenase 1 family member A1 Homo sapiens 11-34
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 DNA mismatch repair protein Mlh1 Bubalus bubalis 194-198
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 PRM2 Bubalus bubalis 211-215
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 DNA mismatch repair protein Mlh1 Bubalus bubalis 194-198
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 PRM2 Bubalus bubalis 211-215
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 DNA mismatch repair protein Mlh1 Bubalus bubalis 194-198
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 PRM2 Bubalus bubalis 211-215
31133469-4 2019 To prevent degradation and possible mucosa irritation, RA was encapsulated in solid lipid nanoparticles (RA-SLN). Tretinoin 55-57 sarcolipin Mus musculus 108-111
31133469-4 2019 To prevent degradation and possible mucosa irritation, RA was encapsulated in solid lipid nanoparticles (RA-SLN). Tretinoin 105-107 sarcolipin Mus musculus 108-111
31133469-7 2019 No histological sign of irritation or inflammation was produced in the nasal mucosa after RA-SLN administration. Tretinoin 90-92 sarcolipin Mus musculus 93-96
30556162-1 2019 This study demonstrates that adipose-derived stem cells from debrided skin (dsASCs) of burn patients can be isolated in sufficient quantities and differentiated into cytokeratin-expressing cells by treating them with all-trans retinoic acid (ATRA) and the peroxisome proliferator-activated receptor-alpha (PPARalpha) specific activator fenofibrate. Tretinoin 242-246 peroxisome proliferator activated receptor alpha Homo sapiens 256-304
30556162-1 2019 This study demonstrates that adipose-derived stem cells from debrided skin (dsASCs) of burn patients can be isolated in sufficient quantities and differentiated into cytokeratin-expressing cells by treating them with all-trans retinoic acid (ATRA) and the peroxisome proliferator-activated receptor-alpha (PPARalpha) specific activator fenofibrate. Tretinoin 242-246 peroxisome proliferator activated receptor alpha Homo sapiens 306-315
31141879-10 2019 Retinoic acid-induced activation of retinoic acid receptor response element (RARE)-tk-luciferase is dependent on exogenous expression of retinoic acid receptor alpha (RARa)/RXRa heterodimer in MDA-MB 231 but not in MCF7 and KAIMRC1 cell lines. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 137-165
31141879-10 2019 Retinoic acid-induced activation of retinoic acid receptor response element (RARE)-tk-luciferase is dependent on exogenous expression of retinoic acid receptor alpha (RARa)/RXRa heterodimer in MDA-MB 231 but not in MCF7 and KAIMRC1 cell lines. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 167-171
31091225-0 2019 HDAC1-mediated repression of the retinoic acid-responsive gene ripply3 promotes second heart field development. Tretinoin 33-46 histone deacetylase 1 Danio rerio 0-5
8760042-2 1996 In normal cells, trans-retinoic acid (RA) and 2.0 mM Ca2+ significantly stimulated PTHRP mRNA expression and secretion and led to a significant reduction in the rate of proliferation. Tretinoin 38-40 parathyroid hormone like hormone Homo sapiens 83-88
31091225-8 2019 Our study highlights that transcriptional repression via the epigenetic regulator Hdac1 facilitates OFT development through directly preventing expression of the RA-responsive gene ripply3 within SHF progenitors. Tretinoin 162-164 histone deacetylase 1 Danio rerio 82-87
8801166-4 1996 This has prompted us to hypothesize that ethanol-induced defects observed in fetal alcohol syndrome involve ethanol inhibition of ADH-catalyzed RA synthesis. Tretinoin 144-146 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 130-133
28827763-0 2017 Peroxiredoxin1, a novel regulator of pronephros development, influences retinoic acid and Wnt signaling by controlling ROS levels. Tretinoin 72-85 peroxiredoxin 1 Homo sapiens 0-14
30779909-7 2019 Both CD38 and AHR are components of a complex signalsome that enhances retinoic acid-induced differentiation of myeloid progenitor cells to granulocytes. Tretinoin 71-84 CD38 molecule Homo sapiens 5-9
8801166-8 1996 Thus, the observed ethanol-induced reduction in RA may be caused by ethanol inhibition of retinol oxidation catalyzed by class IV ADH. Tretinoin 48-50 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 127-133
8687453-5 1996 The data suggest a role for AP-2 as an intermediate factor in the pathway of RA action in keratinocyte differentiation, explaining both the downregulation of K4 and AhR transcript levels in proliferative keratinocytes and the loss of RA effects in already differentiated cells. Tretinoin 77-79 aryl hydrocarbon receptor Homo sapiens 165-168
31083206-1 2019 RATIONALE: The vast majority of acute promyelocytic leukemia (APL) is characterized with a specific chromosomal translocation t (15, 17) (q22, q21), which fuses PML-RARalpha leading to a good response to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 208-227 retinoic acid receptor alpha Homo sapiens 165-173
28394339-0 2017 NSPc1 promotes cancer stem cell self-renewal by repressing the synthesis of all-trans retinoic acid via targeting RDH16 in malignant glioma. Tretinoin 86-99 polycomb group ring finger 1 Homo sapiens 0-5
28394339-7 2017 Finally, we showed that ATRA partly reversed the NSPc1-induced stemness enhancement in SLCs, through mechanisms correlated with an ATRA-dependent decrease in the expression of NSPc1. Tretinoin 24-28 polycomb group ring finger 1 Homo sapiens 49-54
28394339-7 2017 Finally, we showed that ATRA partly reversed the NSPc1-induced stemness enhancement in SLCs, through mechanisms correlated with an ATRA-dependent decrease in the expression of NSPc1. Tretinoin 24-28 polycomb group ring finger 1 Homo sapiens 176-181
28394339-8 2017 Thus, our results demonstrate that NSPc1 promotes cancer stem cell self-renewal by repressing the synthesis of ATRA via targeting RDH16 and may provide novel targets for glioma treatment in the future. Tretinoin 111-115 polycomb group ring finger 1 Homo sapiens 35-40
28712951-0 2017 RA-Induced Transcriptional Silencing of Checkpoint Kinase-2 through Promoter Methylation by Dnmt3b Is Required for Neuronal Differentiation of P19 Cells. Tretinoin 0-2 DNA methyltransferase 3 beta Homo sapiens 92-98
31083206-1 2019 RATIONALE: The vast majority of acute promyelocytic leukemia (APL) is characterized with a specific chromosomal translocation t (15, 17) (q22, q21), which fuses PML-RARalpha leading to a good response to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 229-233 retinoic acid receptor alpha Homo sapiens 165-173
31015532-6 2019 Finally, we found that retinoic acid (RA) signaling affects the irx2a expression domain in renal progenitors, positioning irx2a downstream of RA. Tretinoin 23-36 iroquois homeobox 2a Danio rerio 64-69
28712951-1 2017 In a previous study, we identified several novel targets of Dnmt3b using a chromatin library from retinoic acid (RA)-treated P19 cells. Tretinoin 98-111 DNA methyltransferase 3 beta Homo sapiens 60-66
28712951-1 2017 In a previous study, we identified several novel targets of Dnmt3b using a chromatin library from retinoic acid (RA)-treated P19 cells. Tretinoin 113-115 DNA methyltransferase 3 beta Homo sapiens 60-66
31015532-6 2019 Finally, we found that retinoic acid (RA) signaling affects the irx2a expression domain in renal progenitors, positioning irx2a downstream of RA. Tretinoin 23-36 iroquois homeobox 2a Danio rerio 122-127
8687458-6 1996 mRNAs encoding the neural genes Wnt-1, MASH1, the light and medium isoforms of neurofilaments, and the neurotransmitter-synthesizing enzyme glutamic acid decarboxylase are all strongly upregulated by retinoic acid treatment; expression of these genes occurs in a temporal pattern resembling that in the developing brain. Tretinoin 200-213 wingless-type MMTV integration site family, member 1 Mus musculus 32-37
31015532-6 2019 Finally, we found that retinoic acid (RA) signaling affects the irx2a expression domain in renal progenitors, positioning irx2a downstream of RA. Tretinoin 38-40 iroquois homeobox 2a Danio rerio 64-69
31015532-6 2019 Finally, we found that retinoic acid (RA) signaling affects the irx2a expression domain in renal progenitors, positioning irx2a downstream of RA. Tretinoin 38-40 iroquois homeobox 2a Danio rerio 122-127
31015532-6 2019 Finally, we found that retinoic acid (RA) signaling affects the irx2a expression domain in renal progenitors, positioning irx2a downstream of RA. Tretinoin 142-144 iroquois homeobox 2a Danio rerio 64-69
28568315-11 2017 The retinoate biosynthesis pathway was also enriched due to the differential expression of the genes AKR1C3, ALDH8A1, RDH8, RDH13 and SDR9C7. Tretinoin 4-13 aldehyde dehydrogenase 8 family member A1 Bos taurus 109-116
28568315-11 2017 The retinoate biosynthesis pathway was also enriched due to the differential expression of the genes AKR1C3, ALDH8A1, RDH8, RDH13 and SDR9C7. Tretinoin 4-13 retinol dehydrogenase 13 Bos taurus 124-129
8650243-6 1996 Interestingly, only RARgamma can mediate the retinoic acid-induced differentiation of wild-type F9 cells, whereas the differentiation of P19 cells can be mediated by either RARalpha or RARgamma. Tretinoin 45-58 retinoic acid receptor gamma Homo sapiens 20-28
29044428-5 2017 We therefore examined aspects of the retinoic acid/STRA8/CYP26B1 pathway during gonadal development in the tammar wallaby, a marsupial, to understand whether retinoic acid stimulation of STRA8 and CYP26B1 degradation of retinoic acid was conserved between widely divergent mammals. Tretinoin 158-171 stimulated by retinoic acid gene 8 Mus musculus 187-192
29044428-7 2017 Exposure of pre-meiotic tammar ovaries to exogenous retinoic acid in vitro upregulated STRA8 expression compared to controls. Tretinoin 52-65 stimulated by retinoic acid gene 8 Mus musculus 87-92
31015532-7 2019 In sum, this work reveals new roles for irx2a during nephrogenesis, identifying irx2a as a crucial connection between RA signaling, segmentation, and the control of etv5a mediated MCC formation. Tretinoin 118-120 iroquois homeobox 2a Danio rerio 80-85
30760627-0 2019 Regulation of Myelination by Exosome Associated Retinoic Acid Release from NG2-Positive Cells. Tretinoin 48-61 chondroitin sulfate proteoglycan 4 Rattus norvegicus 75-78
30760627-5 2019 Decorin promoted the activation of RARalpha in NG2+ cells by increasing the availability of the endogenous ligand RA. Tretinoin 35-37 chondroitin sulfate proteoglycan 4 Rattus norvegicus 47-50
30760627-6 2019 NG2+ cells synthesize RA, which is released in association with exosomes. Tretinoin 22-24 chondroitin sulfate proteoglycan 4 Rattus norvegicus 0-3
30760627-10 2019 Pharmacological and knock-down experiments show that the retinoic acid (RA) signaling promotes differentiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA receptor-beta (RARbeta) and RARalpha in NG2+ cells. Tretinoin 57-70 retinoic acid receptor, alpha Rattus norvegicus 222-229
30760627-10 2019 Pharmacological and knock-down experiments show that the retinoic acid (RA) signaling promotes differentiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA receptor-beta (RARbeta) and RARalpha in NG2+ cells. Tretinoin 57-70 retinoic acid receptor, alpha Rattus norvegicus 235-243
30760627-10 2019 Pharmacological and knock-down experiments show that the retinoic acid (RA) signaling promotes differentiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA receptor-beta (RARbeta) and RARalpha in NG2+ cells. Tretinoin 57-70 chondroitin sulfate proteoglycan 4 Rattus norvegicus 247-250
9816270-1 1996 The differentiation and growth suppressive effects of retinoic acid are mediated through retinoic acid nuclear receptors (RARs and RXRs), which are ligand-activated transcription factors. Tretinoin 54-67 arginyl-tRNA synthetase 1 Homo sapiens 122-126
30760627-10 2019 Pharmacological and knock-down experiments show that the retinoic acid (RA) signaling promotes differentiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA receptor-beta (RARbeta) and RARalpha in NG2+ cells. Tretinoin 72-74 retinoic acid receptor, alpha Rattus norvegicus 222-229
30760627-10 2019 Pharmacological and knock-down experiments show that the retinoic acid (RA) signaling promotes differentiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA receptor-beta (RARbeta) and RARalpha in NG2+ cells. Tretinoin 72-74 retinoic acid receptor, alpha Rattus norvegicus 235-243
30760627-10 2019 Pharmacological and knock-down experiments show that the retinoic acid (RA) signaling promotes differentiation of oligodendrocyte precursor cells (OPCs) and remyelination in a cross talk between neuronal RA receptor-beta (RARbeta) and RARalpha in NG2+ cells. Tretinoin 72-74 chondroitin sulfate proteoglycan 4 Rattus norvegicus 247-250
30760627-11 2019 We show that stimulation of RARalpha is required for the differentiation of OPCs and we describe for the first time how oral treatment with a RARbeta agonist (C286, currently being tested in a Phase 1 trial, ISRCTN12424734) leads to the endogenous synthesis of RA through retinaldehyde dehydrogenase 2 (Raldh2) in NG2 cells and controls exosome-associated-RA intracellular levels through a decorin-Ca2+ pathway. Tretinoin 142-144 chondroitin sulfate proteoglycan 4 Rattus norvegicus 314-317
28106276-6 2017 Immunofluorescent staining revealed that the mutagenized ESCs (RA (Retinoic Acid) with C1EIS Knock out) expressed lower levels of integrin alpha6 and integrin beta1 compared to wild type cells. Tretinoin 63-65 integrin subunit beta 1 Gallus gallus 150-164
28106276-6 2017 Immunofluorescent staining revealed that the mutagenized ESCs (RA (Retinoic Acid) with C1EIS Knock out) expressed lower levels of integrin alpha6 and integrin beta1 compared to wild type cells. Tretinoin 67-80 integrin subunit beta 1 Gallus gallus 150-164
8738758-3 1996 In this study we use Northern blot analysis, double-label immunocytochemistry, and single cell RNA analysis using polymerase chain reaction to show that RA-treated P19 cells with neuronal-like morphology also express neuronal nicotinic acetylcholine receptor (nAChR) subunits alpha 3, alpha 4, and beta 2. Tretinoin 153-155 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 298-304
28087980-11 2017 During HCC differentiation induced by ATRA, the mean value of GPC3 expression treated with ATRA was much lower than the ones in placebo. Tretinoin 38-42 glypican 3 Homo sapiens 62-66
28087980-11 2017 During HCC differentiation induced by ATRA, the mean value of GPC3 expression treated with ATRA was much lower than the ones in placebo. Tretinoin 91-95 glypican 3 Homo sapiens 62-66
28992291-0 2017 Retinoic acid inhibits white adipogenesis by disrupting GADD45A-mediated Zfp423 DNA demethylation. Tretinoin 0-13 zinc finger protein 423 Homo sapiens 73-79
31285641-6 2019 The possible role of Wnt-Fzd interactions in developmental toxicity due to selected teratogens were also investigated using molecular docking studies which showed that Retinoic Acid possessed the maximum binding affinity with binding energy of for hWnt5b-hFzd8 complex while VPA was observed to have lowest binding affinity towards all the studied hWnt5b-hFzd complexes. Tretinoin 168-181 Wnt family member 5B Homo sapiens 21-24
31285641-6 2019 The possible role of Wnt-Fzd interactions in developmental toxicity due to selected teratogens were also investigated using molecular docking studies which showed that Retinoic Acid possessed the maximum binding affinity with binding energy of for hWnt5b-hFzd8 complex while VPA was observed to have lowest binding affinity towards all the studied hWnt5b-hFzd complexes. Tretinoin 168-181 Wnt family member 5B Homo sapiens 248-254
31285641-6 2019 The possible role of Wnt-Fzd interactions in developmental toxicity due to selected teratogens were also investigated using molecular docking studies which showed that Retinoic Acid possessed the maximum binding affinity with binding energy of for hWnt5b-hFzd8 complex while VPA was observed to have lowest binding affinity towards all the studied hWnt5b-hFzd complexes. Tretinoin 168-181 Wnt family member 5B Homo sapiens 348-354
30992691-0 2019 RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance. Tretinoin 24-28 ring finger protein 8 Homo sapiens 0-4
28992291-4 2017 We found that RA inhibits Zfp423 expression and adipogenesis via blocking DNA demethylation in the promoter of Zfp423, a process mediated by growth arrest and DNA-damage-inducible protein alpha (GADD45A). Tretinoin 14-16 zinc finger protein 423 Homo sapiens 26-32
28992291-4 2017 We found that RA inhibits Zfp423 expression and adipogenesis via blocking DNA demethylation in the promoter of Zfp423, a process mediated by growth arrest and DNA-damage-inducible protein alpha (GADD45A). Tretinoin 14-16 zinc finger protein 423 Homo sapiens 111-117
28992291-5 2017 RA induces the partnering between retinoic acid receptor (RAR) and tumor suppressor inhibitor of growth protein 1 (ING1), which prevents the formation of GADD45A and ING1 complex necessary for locus-specific Zfp423 DNA demethylation. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 34-56
30992691-0 2019 RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance. Tretinoin 24-28 retinoic acid receptor alpha Homo sapiens 91-95
30992691-0 2019 RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance. Tretinoin 187-191 ring finger protein 8 Homo sapiens 0-4
28992291-5 2017 RA induces the partnering between retinoic acid receptor (RAR) and tumor suppressor inhibitor of growth protein 1 (ING1), which prevents the formation of GADD45A and ING1 complex necessary for locus-specific Zfp423 DNA demethylation. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 58-61
8752654-0 1996 CD23-mediated nitric oxide synthase pathway induction in human keratinocytes is inhibited by retinoic acid derivatives. Tretinoin 93-106 Fc epsilon receptor II Homo sapiens 0-4
28992291-5 2017 RA induces the partnering between retinoic acid receptor (RAR) and tumor suppressor inhibitor of growth protein 1 (ING1), which prevents the formation of GADD45A and ING1 complex necessary for locus-specific Zfp423 DNA demethylation. Tretinoin 0-2 inhibitor of growth family member 1 Homo sapiens 115-119
28992291-5 2017 RA induces the partnering between retinoic acid receptor (RAR) and tumor suppressor inhibitor of growth protein 1 (ING1), which prevents the formation of GADD45A and ING1 complex necessary for locus-specific Zfp423 DNA demethylation. Tretinoin 0-2 inhibitor of growth family member 1 Homo sapiens 166-170
30992691-7 2019 Flow cytometry and Wright-Giemsa staining were used to study the effect of MG132 and ATRA on the GTF2I-RARA-transfected HL60 cell model. Tretinoin 85-89 retinoic acid receptor alpha Homo sapiens 103-107
30992691-9 2019 Compared with PML-RARA, GTF2I-RARA has a higher affinity to HDAC3 under ATRA treatment. Tretinoin 72-76 PML nuclear body scaffold Homo sapiens 14-17
30992691-9 2019 Compared with PML-RARA, GTF2I-RARA has a higher affinity to HDAC3 under ATRA treatment. Tretinoin 72-76 retinoic acid receptor alpha Homo sapiens 18-22
28992291-5 2017 RA induces the partnering between retinoic acid receptor (RAR) and tumor suppressor inhibitor of growth protein 1 (ING1), which prevents the formation of GADD45A and ING1 complex necessary for locus-specific Zfp423 DNA demethylation. Tretinoin 0-2 zinc finger protein 423 Homo sapiens 208-214
8635515-2 1996 RA activity is thought to be mediated by nuclear RA receptors (RARs), transcription factors whose activity is dependent on RA. Tretinoin 0-2 arginyl-tRNA synthetase 1 Homo sapiens 49-61
30532072-2 2019 The pharmacological activity of ATRA is mediated by the ligand-activated RAR and RXR transcription factors. Tretinoin 32-36 retinoic acid receptor alpha Homo sapiens 73-76
8635515-2 1996 RA activity is thought to be mediated by nuclear RA receptors (RARs), transcription factors whose activity is dependent on RA. Tretinoin 0-2 arginyl-tRNA synthetase 1 Homo sapiens 63-67
30532072-11 2019 Conversely, S100A3 knockdown in PML-RARalpha+ APL and PML-RARalpha- AML cells reduces the amounts of RARalpha/PML-RARalpha and increases basal and ATRA-induced differentiation. Tretinoin 147-151 S100 calcium binding protein A3 Homo sapiens 12-18
30532072-11 2019 Conversely, S100A3 knockdown in PML-RARalpha+ APL and PML-RARalpha- AML cells reduces the amounts of RARalpha/PML-RARalpha and increases basal and ATRA-induced differentiation. Tretinoin 147-151 retinoic acid receptor alpha Homo sapiens 36-44
28715412-2 2017 Using the developing murine tongue as a model, we uncovered unknown relationships between Sonic hedgehog (SHH) and retinoic acid (RA) signaling. Tretinoin 115-128 sonic hedgehog Mus musculus 90-104
8635871-2 1996 Retinoic acid (RA) treatment of NT2D1 cells leads to a neuronal differentiation program and to concomitant loss of CRIPTO mRNA expression. Tretinoin 0-13 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 115-121
28715412-2 2017 Using the developing murine tongue as a model, we uncovered unknown relationships between Sonic hedgehog (SHH) and retinoic acid (RA) signaling. Tretinoin 115-128 sonic hedgehog Mus musculus 106-109
28715412-2 2017 Using the developing murine tongue as a model, we uncovered unknown relationships between Sonic hedgehog (SHH) and retinoic acid (RA) signaling. Tretinoin 130-132 sonic hedgehog Mus musculus 90-104
28715412-3 2017 Genetic loss of SHH signaling leads to enhanced RA activity subsequent to loss of SHH-dependent expression of Cyp26a1 and Cyp26c1. Tretinoin 48-50 sonic hedgehog Mus musculus 16-19
30532072-11 2019 Conversely, S100A3 knockdown in PML-RARalpha+ APL and PML-RARalpha- AML cells reduces the amounts of RARalpha/PML-RARalpha and increases basal and ATRA-induced differentiation. Tretinoin 147-151 retinoic acid receptor alpha Homo sapiens 58-66
30532072-11 2019 Conversely, S100A3 knockdown in PML-RARalpha+ APL and PML-RARalpha- AML cells reduces the amounts of RARalpha/PML-RARalpha and increases basal and ATRA-induced differentiation. Tretinoin 147-151 retinoic acid receptor alpha Homo sapiens 58-66
28291070-8 2019 CONCLUSION: Acute promyelocytic leukemia treated with ATRA may result in upregulation of vascular endothelial growth factor in retinal tissues. Tretinoin 54-58 PML nuclear body scaffold Homo sapiens 18-40
28715412-7 2017 We show that RA promotes, whereas SHH, acting strictly within the lingual epithelium, inhibits taste placode and lingual gland formation by thwarting RA activity. Tretinoin 150-152 sonic hedgehog Mus musculus 34-37
8635871-2 1996 Retinoic acid (RA) treatment of NT2D1 cells leads to a neuronal differentiation program and to concomitant loss of CRIPTO mRNA expression. Tretinoin 15-17 teratocarcinoma-derived growth factor 1 pseudogene 3 Homo sapiens 115-121
33429696-7 2017 Immunofluorescence studies and RT-PCR revealed that the atRA-loaded biomaterials increased the expression of two epithelial markers of mucociliary differentiation, MUC5AC and beta-tubulin IV, via upregulation of MUC5AC and FOXJ1 genes, both in epithelial monoculture and in a 3D scaffold coculture system with lung fibroblasts. Tretinoin 56-60 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 164-170
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 91-95 PML nuclear body scaffold Homo sapiens 35-38
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 39-43
33429696-7 2017 Immunofluorescence studies and RT-PCR revealed that the atRA-loaded biomaterials increased the expression of two epithelial markers of mucociliary differentiation, MUC5AC and beta-tubulin IV, via upregulation of MUC5AC and FOXJ1 genes, both in epithelial monoculture and in a 3D scaffold coculture system with lung fibroblasts. Tretinoin 56-60 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 212-218
30536958-6 2019 We show that in vitro treatment of PML/RARA expressing cells with all-trans retinoic acid (ATRA) up-regulates HSP90 expression and stabilizes AKT. Tretinoin 91-95 heat shock protein 90 alpha family class A member 1 Homo sapiens 110-115
8967521-12 1996 Treatment with RA resulted in a rapid (24 h) downregulation of PGHS-1 mRNA expression. Tretinoin 15-17 prostaglandin-endoperoxide synthase 1 Rattus norvegicus 63-69
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 93-97 heat shock protein 90 alpha family class A member 1 Homo sapiens 151-156
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 174-178 heat shock protein 90 alpha family class A member 1 Homo sapiens 16-21
30536958-7 2019 Addition of the HSP90-inhibitor 17-(allylamino)-17-demethoxygeldanamycin in combination with ATRA, blocks upregulation of AKT protein, indicating that HSP90 is necessary for ATRA action on AKT. Tretinoin 174-178 heat shock protein 90 alpha family class A member 1 Homo sapiens 151-156
28584011-5 2017 All-trans retinoic acid also increased regulatory T cells and prevented the hypertension, endothelial dysfunction, and glomerular injury in genetically modified mice that phenocopy calcineurin inhibitor-treated mice (FKBP12-Tie2 knockout). Tretinoin 10-23 FK506 binding protein 1a Mus musculus 217-223
28712407-1 2017 Objective To study the expression patterns of promyelocytic leukemia (PML) protein at different stages of acute promyelocytic leukemia (APL) and investigate the effects that the arsenical, all-trans retinoic acid (ATRA) and chemotherapeutic drugs on PML protein expression patterns. Tretinoin 214-218 PML nuclear body scaffold Homo sapiens 70-73
30718413-4 2019 DGAT1 acyltransferase activity sequesters retinol in ester form, preventing synthesis of retinoic acid, a cofactor for Treg generation. Tretinoin 89-102 diacylglycerol O-acyltransferase 1 Homo sapiens 0-5
8967521-13 1996 However, the cPLA2 and PGHS-2 genes were expressed in squamous cultures only after 3 days of RA treatment coincident with redifferentiation of the culture to a mucociliary phenotype. Tretinoin 93-95 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 23-29
28712407-5 2017 Compared with control group without medication, the PML protein expression of APL cells in initial onset cases had larger fluorescent signals in the ATRA group, As2O3 group and As4S4 group, whereas there were no significant changes in the arabinoside cytosine group and the homoharringtonine group. Tretinoin 149-153 PML nuclear body scaffold Homo sapiens 52-55
9019248-10 1996 Furthermore, exogenous 9-cis RA produces a qualitative alteration in the multiple-site expression pattern of the hlx-1 gene within the rostral CNS, while treatment with all-trans RA leads only to a weakened expression signal. Tretinoin 29-31 H2.0-like homeo box 1 (Drosophila) Danio rerio 113-118
8621625-2 1996 Some members of the alcohol dehydrogenase (ADH) family catalyze retinol oxidation, the rate-limiting step in RA synthesis. Tretinoin 109-111 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Mus musculus 43-46
28583171-4 2017 METHODS: Retinoic acid-treated P19 and SH-SY5Y cells and nerve growth factor-stimulated PC12 cells, allowed to differentiate for 6 days, were exposed to MeHg, okadaic acid and acrylamide for 48 h. Cell survival and neurite outgrowth were assessed with the calcein-AM assay and fluorescence detection of antibodies against the cytoskeletal neuron-specific protein betaIII-tubulin, respectively. Tretinoin 9-22 interleukin 23 subunit alpha Homo sapiens 31-34
28601081-3 2017 We demonstrated decrease in OCT4 and NANOG mRNA and protein levels following exposure to retinoic acid. Tretinoin 89-102 POU class 5 homeobox 1 Homo sapiens 28-32
30721228-3 2019 Here, we identify that retinoic acid (RA) signaling directly promotes the expression of the transcription factor Nr2f1a within the anterior lateral plate mesoderm. Tretinoin 23-36 nuclear receptor subfamily 2, group F, member 1a Danio rerio 113-119
30721228-3 2019 Here, we identify that retinoic acid (RA) signaling directly promotes the expression of the transcription factor Nr2f1a within the anterior lateral plate mesoderm. Tretinoin 38-40 nuclear receptor subfamily 2, group F, member 1a Danio rerio 113-119
8735598-2 1996 In these cells, RA potentiated the hCG secretion increase induced by EGF. Tretinoin 16-18 chorionic gonadotropin subunit beta 5 Homo sapiens 35-38
30236456-10 2019 ChIP demonstrated that, after retinoic acid stimulation and aldosterone exposure, MR and PPARgamma concomitantly bind to specific UCP1 promoter motifs. Tretinoin 30-43 nuclear receptor subfamily 3, group C, member 2 Mus musculus 82-84
28559980-0 2017 All-trans-retinoic acid activates SDF-1/CXCR4/ROCK2 signaling pathway to inhibit chondrogenesis. Tretinoin 0-23 Rho-associated coiled-coil containing protein kinase 2 Rattus norvegicus 46-51
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 Rho-associated coiled-coil containing protein kinase 2 Rattus norvegicus 133-138
28559980-4 2017 We found that ATRA dose-dependently inhibits proliferation and expression of chondrogenic transcription factors (SOX9 and COL2A1) in rEHBMCs. Tretinoin 14-18 collagen type II alpha 1 chain Rattus norvegicus 122-128
28559980-5 2017 In contrast, ATRA increases the expression of ROCK2, SDF-1 and CXCR4. Tretinoin 13-17 Rho-associated coiled-coil containing protein kinase 2 Rattus norvegicus 46-51
28559980-7 2017 In addition, we found that disturbing SDF-1/CXCR4 signaling by AMD3100 decreases ATRA-induced ROCK2 expression. Tretinoin 81-85 Rho-associated coiled-coil containing protein kinase 2 Rattus norvegicus 94-99
28559980-8 2017 In vivo studies we also confirm that SOX9 expression of early-stage cartilage progenitors in the proliferative zone and COL2A1 expression in prehypertrophic chondrocytes are decreased in ATRA-treated rat embryo hind limb. Tretinoin 187-191 collagen type II alpha 1 chain Rattus norvegicus 120-126
28559980-9 2017 Together, these results show that ATRA activates SDF-1/CXCR4/ROCK2 signaling to inhibit chondrogenesis to lead to CCF by suppressing differentiation through down-regulation of SOX9 and COL2A1 expression in rat embryo hind limb bud mesenchymal cells. Tretinoin 34-38 Rho-associated coiled-coil containing protein kinase 2 Rattus norvegicus 61-66
30453015-0 2019 miR-382-5p modulates the ATRA-induced differentiation of acute promyelocytic leukemia by targeting tumor suppressor PTEN. Tretinoin 25-29 microRNA 382 Homo sapiens 0-7
30453015-0 2019 miR-382-5p modulates the ATRA-induced differentiation of acute promyelocytic leukemia by targeting tumor suppressor PTEN. Tretinoin 25-29 phosphatase and tensin homolog Homo sapiens 116-120
30453015-4 2019 In the present study, we found that miR-382-5p expression was elevated with ATRA-induced differentiation of APL. Tretinoin 76-80 microRNA 382 Homo sapiens 36-43
30453015-8 2019 Enforced expression of miR-382-5p or specific PTEN inhibitors inhibited ATRA-induced granulocytic differentiation via regulation of the cell cycle regulator cyclinD1. Tretinoin 72-76 microRNA 382 Homo sapiens 23-30
30453015-8 2019 Enforced expression of miR-382-5p or specific PTEN inhibitors inhibited ATRA-induced granulocytic differentiation via regulation of the cell cycle regulator cyclinD1. Tretinoin 72-76 phosphatase and tensin homolog Homo sapiens 46-50
8735598-5 1996 In parallel, we demonstrated that the choriocarcinoma cells JEG 3, which respond to RA by an increase in hCG secretion, express constitutively high levels of RXR alpha protein. Tretinoin 84-86 chorionic gonadotropin subunit beta 5 Homo sapiens 105-108
30292490-0 2019 Expression of retinoic acid signaling components ADH7 and ALDH1A1 is reduced in aniridia limbal epithelial cells and a siRNA primary cell based aniridia model. Tretinoin 14-27 aldehyde dehydrogenase 1 family member A1 Homo sapiens 58-65
28492552-1 2017 All-trans retinoic acid (ATRA) and/or arsenic trioxide (ATO) administration leads to granulocytic maturation and/or apoptosis of acute promyelocytic leukemia (APL) cells mainly by targeting promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha). Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 243-246
8735598-6 1996 Furthermore, RXR alpha-transfected trophoblastic cells also become RA responsive for hCG secretion. Tretinoin 67-69 chorionic gonadotropin subunit beta 5 Homo sapiens 85-88
28492552-1 2017 All-trans retinoic acid (ATRA) and/or arsenic trioxide (ATO) administration leads to granulocytic maturation and/or apoptosis of acute promyelocytic leukemia (APL) cells mainly by targeting promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 247-255
28492552-1 2017 All-trans retinoic acid (ATRA) and/or arsenic trioxide (ATO) administration leads to granulocytic maturation and/or apoptosis of acute promyelocytic leukemia (APL) cells mainly by targeting promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha). Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 243-246
30292490-20 2019 These results provide evidence that PAX6 might drive corneal epithelial differentiation by direct or indirect control of retinoic acid signaling processes through ADH7 and ALDH1A1. Tretinoin 121-134 aldehyde dehydrogenase 1 family member A1 Homo sapiens 172-179
8735598-7 1996 All these data suggest that RXR alpha expression is modulated by EGF, and may be involved in the effect of RA on hCG secretion. Tretinoin 107-109 chorionic gonadotropin subunit beta 5 Homo sapiens 113-116
28492552-1 2017 All-trans retinoic acid (ATRA) and/or arsenic trioxide (ATO) administration leads to granulocytic maturation and/or apoptosis of acute promyelocytic leukemia (APL) cells mainly by targeting promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 247-255
28492552-2 2017 Yet, ~10-15% of APL patients are not cured by ATRA- and ATO-based therapies, and a potential failure of ATRA and ATO in completely reversing PML/RARalpha-driven oncogenic alterations has not been comprehensively examined. Tretinoin 104-108 PML nuclear body scaffold Homo sapiens 141-144
8641674-2 1996 The PP2A activity determined with myelin basic protein (MBP) as a substrate showed a sharp transient increase at 18 h of incubation of the cells with retinoic acid, whereas during incubation without retinoic acid, the activity remained at the initial level. Tretinoin 150-163 myelin basic protein Homo sapiens 34-54
28492552-2 2017 Yet, ~10-15% of APL patients are not cured by ATRA- and ATO-based therapies, and a potential failure of ATRA and ATO in completely reversing PML/RARalpha-driven oncogenic alterations has not been comprehensively examined. Tretinoin 104-108 retinoic acid receptor alpha Homo sapiens 145-153
28492552-5 2017 Irf8, whose expression increased along with spontaneous differentiation of the APL progenitors in vivo, represented such a PML/RARalpha-dysregulated gene that was refractory to ATRA/ATO signaling. Tretinoin 177-181 interferon regulatory factor 8 Homo sapiens 0-4
30055117-6 2019 Using a comprehensive set of biophysical methods combined with cellular and molecular biology, we have elucidated the biomechanical mechanism by which all trans-retinoic acid promotes HSC deactivation via RAR-beta-dependent transcriptional downregulation of myosin light chain 2 expression. Tretinoin 155-174 fucosyltransferase 1 (H blood group) Homo sapiens 184-187
28492552-5 2017 Irf8, whose expression increased along with spontaneous differentiation of the APL progenitors in vivo, represented such a PML/RARalpha-dysregulated gene that was refractory to ATRA/ATO signaling. Tretinoin 177-181 retinoic acid receptor alpha Homo sapiens 127-135
8641674-2 1996 The PP2A activity determined with myelin basic protein (MBP) as a substrate showed a sharp transient increase at 18 h of incubation of the cells with retinoic acid, whereas during incubation without retinoic acid, the activity remained at the initial level. Tretinoin 150-163 myelin basic protein Homo sapiens 56-59
30055117-6 2019 Using a comprehensive set of biophysical methods combined with cellular and molecular biology, we have elucidated the biomechanical mechanism by which all trans-retinoic acid promotes HSC deactivation via RAR-beta-dependent transcriptional downregulation of myosin light chain 2 expression. Tretinoin 155-174 retinoic acid receptor alpha Homo sapiens 205-213
30055117-6 2019 Using a comprehensive set of biophysical methods combined with cellular and molecular biology, we have elucidated the biomechanical mechanism by which all trans-retinoic acid promotes HSC deactivation via RAR-beta-dependent transcriptional downregulation of myosin light chain 2 expression. Tretinoin 155-174 myosin light chain 2 Homo sapiens 258-278
8603926-1 1996 We report here that all trans-retinoic acid (RA), a classical morphogen, induces apoptosis during the neural differentiation of the embryonic stem cell line P19. Tretinoin 24-43 interleukin 23, alpha subunit p19 Mus musculus 157-160
30535439-7 2019 Furthermore, the intranasal EPO-exerted neuroprotection was almost abolished when the specific Nrf2 antagonist ATRA was administered intraperitoneally prior to intranasal EPO treatment. Tretinoin 111-115 erythropoietin Mus musculus 28-31
27244887-10 2017 In regard to clinical relevance, inhibition of Oct4 by all-trans retinoic acid (ATRA) synergistically increased sensitivity to cisplatin in bladder cancer cells. Tretinoin 55-78 POU class 5 homeobox 1 Homo sapiens 47-51
27244887-10 2017 In regard to clinical relevance, inhibition of Oct4 by all-trans retinoic acid (ATRA) synergistically increased sensitivity to cisplatin in bladder cancer cells. Tretinoin 80-84 POU class 5 homeobox 1 Homo sapiens 47-51
28404959-9 2017 Furthermore, all-trans retinoic acid (ATRA), a known anticancer drug that inhibits and ultimately induces degradation of active Pin1 in cancer cells, also potently sensitized HCC cells to sorafenib-induced cell death at least in part through a caspase-dependent manner. Tretinoin 13-36 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 128-132
30733805-6 2019 Much emphasis has been placed on the ALDH1A1 and ALDH1A3 members of the ALDH1 family of cytosolic enzymes required for RA biosynthesis. Tretinoin 119-121 aldehyde dehydrogenase 1 family member A1 Homo sapiens 37-44
8603926-1 1996 We report here that all trans-retinoic acid (RA), a classical morphogen, induces apoptosis during the neural differentiation of the embryonic stem cell line P19. Tretinoin 45-47 interleukin 23, alpha subunit p19 Mus musculus 157-160
30733805-6 2019 Much emphasis has been placed on the ALDH1A1 and ALDH1A3 members of the ALDH1 family of cytosolic enzymes required for RA biosynthesis. Tretinoin 119-121 aldehyde dehydrogenase 1 family member A3 Homo sapiens 49-56
28404959-9 2017 Furthermore, all-trans retinoic acid (ATRA), a known anticancer drug that inhibits and ultimately induces degradation of active Pin1 in cancer cells, also potently sensitized HCC cells to sorafenib-induced cell death at least in part through a caspase-dependent manner. Tretinoin 38-42 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 128-132
8639464-1 1996 Retinoic acid (RA) regulation of human cathepsin D (cath D) gene expression was investigated in this study. Tretinoin 0-13 cathepsin D Homo sapiens 39-50
28375930-2 2017 The effects of RA are mediated by the RA receptor (RAR), and RARalpha/RARbeta especially acts as a tumor suppressor. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 38-49
8639464-1 1996 Retinoic acid (RA) regulation of human cathepsin D (cath D) gene expression was investigated in this study. Tretinoin 0-13 cathepsin D Homo sapiens 52-58
28375930-2 2017 The effects of RA are mediated by the RA receptor (RAR), and RARalpha/RARbeta especially acts as a tumor suppressor. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 51-54
30591532-4 2019 The gut-tropic T cells induced by retinoic acid secrete the exosomes that upregulate integrin alpha4beta7 binding to the MAdCAM-1 expressed on high endothelial venules in the gut. Tretinoin 34-47 mucosal vascular addressin cell adhesion molecule 1 Homo sapiens 121-129
8639464-1 1996 Retinoic acid (RA) regulation of human cathepsin D (cath D) gene expression was investigated in this study. Tretinoin 15-17 cathepsin D Homo sapiens 39-50
30621740-3 2019 The aim of this study was to investigate the potential utility of all-trans retinoid acid (ATRA), an inhibitor of the annexin A2-S100A10 signalling pathway, as a new therapeutic against serous ovarian cancer. Tretinoin 91-95 annexin A2 Homo sapiens 118-128
28375930-8 2017 RARalpha and RARbeta knockdown dose dependently reduced the inhibition of migration by ATRA, but the effect was more pronounced with RARbeta knockdown than with RARalpha knockdown. Tretinoin 87-91 retinoic acid receptor alpha Homo sapiens 0-8
28375930-8 2017 RARalpha and RARbeta knockdown dose dependently reduced the inhibition of migration by ATRA, but the effect was more pronounced with RARbeta knockdown than with RARalpha knockdown. Tretinoin 87-91 retinoic acid receptor alpha Homo sapiens 161-169
8639464-1 1996 Retinoic acid (RA) regulation of human cathepsin D (cath D) gene expression was investigated in this study. Tretinoin 15-17 cathepsin D Homo sapiens 52-58
8639464-2 1996 RA enhanced cath D mRNA levels in a concentration-dependent manner in MCF-7 human breast carcinoma cells. Tretinoin 0-2 cathepsin D Homo sapiens 12-18
8929985-3 1996 Both n-NOS activity and its mRNA level were also increased in the human neuroblastoma cell line, TGW, following trans-retinoic acid (RA)-induced neuronal differentiation. Tretinoin 112-131 nitric oxide synthase 1 Homo sapiens 5-10
28087652-0 2017 Differential regulation of CD103 (alphaE integrin) expression in human dendritic cells by retinoic acid and Toll-like receptor ligands. Tretinoin 90-103 integrin subunit alpha E Homo sapiens 27-32
28087652-3 2017 Here, we show that retinoic acid (RA) treatment of human monocyte-derived DCs (MoDCs) increased the ability of the DCs to synthesize RA and induced MoDC expression of CD103 and beta7 at the mRNA and protein level. Tretinoin 19-32 integrin subunit alpha E Homo sapiens 167-172
28087652-3 2017 Here, we show that retinoic acid (RA) treatment of human monocyte-derived DCs (MoDCs) increased the ability of the DCs to synthesize RA and induced MoDC expression of CD103 and beta7 at the mRNA and protein level. Tretinoin 34-36 integrin subunit alpha E Homo sapiens 167-172
28087652-6 2017 Conversely, when RA-treated MoDCs were stimulated with live Helicobacter pylori, commensal bacteria, LPS, or a TLR2 agonist, the RA-induced up-regulation of CD103 and beta7 integrin expression was completely abrogated. Tretinoin 17-19 integrin subunit alpha E Homo sapiens 157-162
30631055-8 2019 In addition, we show that KDM6B functions downstream of the retinoic acid-HOXC9 axis in inducing neuroblastoma cell differentiation: KDM6B expression is upregulated by retinoic acid via HOXC9, and KDM6B is required for HOXC9-induced neuroblastoma cell differentiation. Tretinoin 60-73 homeobox C9 Homo sapiens 74-79
28087652-6 2017 Conversely, when RA-treated MoDCs were stimulated with live Helicobacter pylori, commensal bacteria, LPS, or a TLR2 agonist, the RA-induced up-regulation of CD103 and beta7 integrin expression was completely abrogated. Tretinoin 129-131 integrin subunit alpha E Homo sapiens 157-162
8929985-3 1996 Both n-NOS activity and its mRNA level were also increased in the human neuroblastoma cell line, TGW, following trans-retinoic acid (RA)-induced neuronal differentiation. Tretinoin 133-135 nitric oxide synthase 1 Homo sapiens 5-10
28087652-9 2017 In summary, our data demonstrate that RA, bacterial products, and the tissue environment all contribute to the regulation of CD103 on human DCs and that DC induction of mucosal homing in T cells is RA dependent but not CD103 dependent. Tretinoin 38-40 integrin subunit alpha E Homo sapiens 125-130
30310934-3 2019 We established a chemically defined protocol by application of Activin A, BMP4, and Retinoic acid followed by GDNF, which steered hPSCs to the renal lineage and resulted in populations of SIX2+/CITED1+ metanephric mesenchyme- (MM) and of HOXB7+/GRHL2+ ureteric bud (UB)-like cells already by 6 days. Tretinoin 84-97 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 1 Homo sapiens 194-200
8558234-3 1996 Within 2-3 weeks after induction by retinoic acid, subsets of P19 and ES cells formed excitatory synapses, mediated by glutamate receptors, or inhibitory synapses, mediated by receptors for GABA or glycine. Tretinoin 36-49 interleukin 23, alpha subunit p19 Mus musculus 62-65
30566883-0 2018 Commensals Suppress Intestinal Epithelial Cell Retinoic Acid Synthesis to Regulate Interleukin-22 Activity and Prevent Microbial Dysbiosis. Tretinoin 47-60 interleukin 22 Mus musculus 83-97
26953980-9 2017 Esterification of 24S-OHC followed by lipid droplet (LD) formation due to acyl-CoA:cholesterol acyltransferase 1 (ACAT1) are key events in 24S-OHC-induced cell death in atRA-treated SH-SY5Y cells as demonstrated by inhibition of cell death by ACAT1 inhibitor. Tretinoin 169-173 acetyl-CoA acetyltransferase 1 Homo sapiens 74-112
26953980-9 2017 Esterification of 24S-OHC followed by lipid droplet (LD) formation due to acyl-CoA:cholesterol acyltransferase 1 (ACAT1) are key events in 24S-OHC-induced cell death in atRA-treated SH-SY5Y cells as demonstrated by inhibition of cell death by ACAT1 inhibitor. Tretinoin 169-173 acetyl-CoA acetyltransferase 1 Homo sapiens 114-119
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 PR domain containing 14 Mus musculus 218-224
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 synaptonemal complex protein 3 Mus musculus 240-244
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 stimulated by retinoic acid gene 8 Mus musculus 246-251
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 PR domain containing 14 Mus musculus 218-224
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 synaptonemal complex protein 3 Mus musculus 240-244
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 stimulated by retinoic acid gene 8 Mus musculus 246-251
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 52-65 retinoic acid receptor alpha Homo sapiens 207-215
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 52-65 integrin subunit alpha E Homo sapiens 361-366
30541574-0 2018 Stemness marker ALDH1A1 promotes tumor angiogenesis via retinoic acid/HIF-1alpha/VEGF signalling in MCF-7 breast cancer cells. Tretinoin 56-69 aldehyde dehydrogenase 1 family member A1 Homo sapiens 16-23
30541574-15 2018 CONCLUSION: In breast tumors, ALDH1A1 expression primes a permissive microenvironment by promoting tumor angiogenesis via retinoic acid dependent mechanism. Tretinoin 122-135 aldehyde dehydrogenase 1 family member A1 Homo sapiens 30-37
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 67-71 retinoic acid receptor alpha Homo sapiens 207-215
8652408-6 1996 Xgbx-2 expression is induced by retinoic acid (RA) in animal caps, and RA treatment of whole embryos expands and enhances Xgbx-2 expression in the ectoderm. Tretinoin 32-45 gastrulation brain homeobox 2, gene 1 S homeolog Xenopus laevis 0-6
28458670-5 2017 Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RARalpha and interferon regulatory factor 4, and concomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. Tretinoin 67-71 integrin subunit alpha E Homo sapiens 361-366
28458670-8 2017 These results altogether demonstrate that selected commensal bacterial strains are able to drive strong effector immune responses by moDCs, while in the presence of ATRA, they support the development of both tolerogenic and inflammatory moDC in a RARalpha-dependent manner. Tretinoin 165-169 retinoic acid receptor alpha Homo sapiens 247-255
30409702-1 2018 The retinaldehyde dehydrogenase (RALDH) enzymes, RALDH1, RALDH2, and RALDH3, catalyze the irreversible oxidation of retinaldehyde to all-trans-retinoic acid (ATRA). Tretinoin 137-156 aldehyde dehydrogenase 1 family member A3 Homo sapiens 69-75
30409702-1 2018 The retinaldehyde dehydrogenase (RALDH) enzymes, RALDH1, RALDH2, and RALDH3, catalyze the irreversible oxidation of retinaldehyde to all-trans-retinoic acid (ATRA). Tretinoin 158-162 aldehyde dehydrogenase 1 family member A1 Homo sapiens 49-55
30409702-1 2018 The retinaldehyde dehydrogenase (RALDH) enzymes, RALDH1, RALDH2, and RALDH3, catalyze the irreversible oxidation of retinaldehyde to all-trans-retinoic acid (ATRA). Tretinoin 158-162 aldehyde dehydrogenase 1 family member A3 Homo sapiens 69-75
8652408-6 1996 Xgbx-2 expression is induced by retinoic acid (RA) in animal caps, and RA treatment of whole embryos expands and enhances Xgbx-2 expression in the ectoderm. Tretinoin 47-49 gastrulation brain homeobox 2, gene 1 S homeolog Xenopus laevis 0-6
27841975-9 2017 Exogenous 9-cis-RA enhanced the differentiation of OPCs into mature oligodendrocytes by activating RXR-gamma. Tretinoin 10-18 retinoid X receptor gamma Rattus norvegicus 99-108
8652408-6 1996 Xgbx-2 expression is induced by retinoic acid (RA) in animal caps, and RA treatment of whole embryos expands and enhances Xgbx-2 expression in the ectoderm. Tretinoin 71-73 gastrulation brain homeobox 2, gene 1 S homeolog Xenopus laevis 122-128
28350049-0 2017 Activation of the CRABPII/RAR pathway by curcumin induces retinoic acid mediated apoptosis in retinoic acid resistant breast cancer cells. Tretinoin 58-71 retinoic acid receptor alpha Homo sapiens 26-29
30396492-2 2018 Hence, RetSat is speculated to be involved in a rapid unusual conversion of alpha-ESA to conjugated linoleic acid (CLA), giving a less priority to its usual substrate all trans retinol, which would subsequently be converted into "all trans retinoic acid" (atRA). Tretinoin 234-253 retinol saturase Homo sapiens 7-13
30396492-2 2018 Hence, RetSat is speculated to be involved in a rapid unusual conversion of alpha-ESA to conjugated linoleic acid (CLA), giving a less priority to its usual substrate all trans retinol, which would subsequently be converted into "all trans retinoic acid" (atRA). Tretinoin 256-260 retinol saturase Homo sapiens 7-13
28350049-0 2017 Activation of the CRABPII/RAR pathway by curcumin induces retinoic acid mediated apoptosis in retinoic acid resistant breast cancer cells. Tretinoin 94-107 retinoic acid receptor alpha Homo sapiens 26-29
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 79-92 retinoic acid receptor gamma Homo sapiens 133-161
28350049-7 2017 Co-treatment of the cells with curcumin and RA results in increased apoptosis as demonstrated by elevated cleavage of poly(ADP-ribose) polymerase and cleaved caspase-9. Tretinoin 44-46 caspase 9 Homo sapiens 158-167
28350049-9 2017 These findings provide mechanistic insights into sensitizing TNBC cells to RA-mediated cell death by curcumin-induced upregulation of the CRABPII/RAR pathway. Tretinoin 75-77 retinoic acid receptor alpha Homo sapiens 146-149
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 79-92 retinoic acid receptor gamma Homo sapiens 163-172
29619741-5 2018 In our recently published study, we have identified a set of miRNAs including miR-145 and miR-29b families differentially expressed in SH-SY5Y cells exposed sequentially with retinoic acid + brain-derived neurotrophic factor (RA+BDNF) for differentiation into mature neurons (Mol Neurobiol (2016) doi: https://doi.org/10.1007/s12035-016-0042-9 ). Tretinoin 175-188 microRNA 145 Homo sapiens 78-85
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 94-96 retinoic acid receptor gamma Homo sapiens 133-161
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 94-96 retinoic acid receptor gamma Homo sapiens 163-172
28065858-2 2017 In this study, we investigated the regulation of TG2 activity by the PAC1 receptor in retinoic acid-induced differentiating N2a neuroblastoma cells. Tretinoin 86-99 transglutaminase 2, C polypeptide Mus musculus 49-52
8615638-8 1996 These results suggest that two factors may be responsible for synergistic action of RA and IFN-alpha: the inhibition of the CRABP II expression and an IFN-alpha/RA mediated upregulation of RAR-gamma. Tretinoin 84-86 retinoic acid receptor gamma Homo sapiens 189-198
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 5-18 integrin subunit alpha 4 Homo sapiens 82-97
30235988-1 2018 BACKGROUND: Thyroid hormone receptors (TRs) are tightly regulated by the corepressors nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptors. Tretinoin 148-161 nuclear receptor corepressor 1 Homo sapiens 116-120
8960364-4 1996 Oct-4 gene expression is also down-regulated when murine embryonic stem cells or embryonal carcinoma cells are induced to differentiate in the presence of retinoic acid. Tretinoin 155-168 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 0-5
30016433-8 2018 Furthermore, retinoic acid (RA) signaling is required for Tbx5 activation in Tbx1-positive cells and blocking RA signaling at the time of Tbx5 activation results in atrioventricular septal defects at fetal stages. Tretinoin 13-26 T-box 1 Mus musculus 77-81
30016433-8 2018 Furthermore, retinoic acid (RA) signaling is required for Tbx5 activation in Tbx1-positive cells and blocking RA signaling at the time of Tbx5 activation results in atrioventricular septal defects at fetal stages. Tretinoin 28-30 T-box 1 Mus musculus 77-81
28321213-5 2017 Upon retinoic acid (RA) exposure, CD161+ T cells were more enriched for CCR9+ and integrin alpha4+beta7+ cells than CD161- T cells. Tretinoin 20-22 integrin subunit alpha 4 Homo sapiens 82-97
8960364-7 1996 This antibody has been used to measure Oct-4 protein levels during retinoic acid induced differentiation of F9 embryonal carcinoma cells, It was observed that Oct-4 protein was abundant in undifferentiated F9 cells but decreased to levels below detection as the cells differentiated, consistent with changes in levels of expression in early embryos. Tretinoin 67-80 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 39-44
28063140-3 2017 We used real-time quantitative PCR to determine whether PML/RARalpha affects the expression of S100A9 in NB4 and PR9 cells upon ATRA treatment. Tretinoin 128-132 PML nuclear body scaffold Homo sapiens 56-59
8960364-7 1996 This antibody has been used to measure Oct-4 protein levels during retinoic acid induced differentiation of F9 embryonal carcinoma cells, It was observed that Oct-4 protein was abundant in undifferentiated F9 cells but decreased to levels below detection as the cells differentiated, consistent with changes in levels of expression in early embryos. Tretinoin 67-80 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 159-164
28063140-3 2017 We used real-time quantitative PCR to determine whether PML/RARalpha affects the expression of S100A9 in NB4 and PR9 cells upon ATRA treatment. Tretinoin 128-132 retinoic acid receptor alpha Homo sapiens 60-68
8522994-7 1996 RA also caused a transient increase in level of tyrosine hydroxylase (TH) mRNA (twofold after 16 h), which returned to basal levels and then decreased relative to basal levels at 48 h. The effect of NGF on the expression of these genes was identical to that produced by RA. Tretinoin 0-2 tyrosine hydroxylase Rattus norvegicus 48-68
28063140-7 2017 In addition, PU.1 could bind to the promoter of S100A9, especially when treated with ATRA in NB4 cells, and promote its activity. Tretinoin 85-89 Spi-1 proto-oncogene Homo sapiens 13-17
28063140-9 2017 Collectively, our data indicated that PML/RARalpha and PU.1 were necessary for the ATRA-induced expression of S100A9 in APL cells. Tretinoin 83-87 PML nuclear body scaffold Homo sapiens 38-41
28063140-9 2017 Collectively, our data indicated that PML/RARalpha and PU.1 were necessary for the ATRA-induced expression of S100A9 in APL cells. Tretinoin 83-87 retinoic acid receptor alpha Homo sapiens 42-50
28063140-9 2017 Collectively, our data indicated that PML/RARalpha and PU.1 were necessary for the ATRA-induced expression of S100A9 in APL cells. Tretinoin 83-87 Spi-1 proto-oncogene Homo sapiens 55-59
27605212-0 2017 Activation of G0S2 is coordinated by recruitment of PML/RARalpha and C/EBPepsilon to its promoter during ATRA-induced APL differentiation. Tretinoin 105-109 PML nuclear body scaffold Homo sapiens 52-55
27605212-0 2017 Activation of G0S2 is coordinated by recruitment of PML/RARalpha and C/EBPepsilon to its promoter during ATRA-induced APL differentiation. Tretinoin 105-109 CCAAT enhancer binding protein epsilon Homo sapiens 69-81
27605212-1 2017 All-trans retinoic acid (ATRA) binds the promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) fusion protein and is an effective oncogene-targeted therapy for acute promyelocytic leukemia (APL). Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 94-97
27605212-1 2017 All-trans retinoic acid (ATRA) binds the promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) fusion protein and is an effective oncogene-targeted therapy for acute promyelocytic leukemia (APL). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 98-106
27605212-1 2017 All-trans retinoic acid (ATRA) binds the promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) fusion protein and is an effective oncogene-targeted therapy for acute promyelocytic leukemia (APL). Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 94-97
30359286-10 2018 As expected, inhibiting UCHL1 by knockdown or LDN57444 could significantly inhibit RA-induced neural differentiation of NB tumor cells, characterized by decreased neurite outgrowth and neural differentiation markers. Tretinoin 83-85 ubiquitin C-terminal hydrolase L1 Homo sapiens 24-29
30359286-11 2018 This effect of UCHL1 was associated with positively regulating RA-induced AKT and ERK1/2 signaling activation. Tretinoin 63-65 ubiquitin C-terminal hydrolase L1 Homo sapiens 15-20
30359286-12 2018 What"s more, knockdown of UCHL1 conferred resistance to RA-induced growth arrest. Tretinoin 56-58 ubiquitin C-terminal hydrolase L1 Homo sapiens 26-31
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 40-53 retinoic acid receptor alpha Homo sapiens 145-167
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 40-53 retinoic acid receptor alpha Homo sapiens 169-172
30300581-5 2018 CD1D transcriptional de-repression by all-trans retinoic acid results in further enhanced cytotoxicity of CAR19-iNKT cells against CD19+ chronic lymphocytic leukemia cells. Tretinoin 48-61 CD1d molecule Homo sapiens 0-4
30289902-0 2018 Identification of the novel deletion-type PML-RARA mutation associated with the retinoic acid resistance in acute promyelocytic leukemia. Tretinoin 80-93 PML nuclear body scaffold Homo sapiens 42-45
27605212-1 2017 All-trans retinoic acid (ATRA) binds the promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) fusion protein and is an effective oncogene-targeted therapy for acute promyelocytic leukemia (APL). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 98-106
27605212-2 2017 However, the molecular basis of PML/RARalpha-mediated transcriptional control during ATRA-induced differentiation is unclear. Tretinoin 85-89 PML nuclear body scaffold Homo sapiens 32-35
27605212-2 2017 However, the molecular basis of PML/RARalpha-mediated transcriptional control during ATRA-induced differentiation is unclear. Tretinoin 85-89 retinoic acid receptor alpha Homo sapiens 36-44
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 236-240 PML nuclear body scaffold Homo sapiens 165-168
30289902-0 2018 Identification of the novel deletion-type PML-RARA mutation associated with the retinoic acid resistance in acute promyelocytic leukemia. Tretinoin 80-93 retinoic acid receptor alpha Homo sapiens 46-50
30289902-6 2018 To clarify the biological significance of the identified PML-RARA mutations, we analyzed the ATRA-induced differentiation and PML nuclear body formation in mutant PML-RARA-transduced HL-60 cells. Tretinoin 93-97 PML nuclear body scaffold Homo sapiens 57-60
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 236-240 retinoic acid receptor alpha Homo sapiens 169-177
30289902-6 2018 To clarify the biological significance of the identified PML-RARA mutations, we analyzed the ATRA-induced differentiation and PML nuclear body formation in mutant PML-RARA-transduced HL-60 cells. Tretinoin 93-97 retinoic acid receptor alpha Homo sapiens 61-65
8522994-7 1996 RA also caused a transient increase in level of tyrosine hydroxylase (TH) mRNA (twofold after 16 h), which returned to basal levels and then decreased relative to basal levels at 48 h. The effect of NGF on the expression of these genes was identical to that produced by RA. Tretinoin 0-2 tyrosine hydroxylase Rattus norvegicus 70-72
30289902-7 2018 At molecular relapse, the p.K227_T233del deletion and the p.R217S point-mutation in the RARA region of PML-RARA were identified, and their frequencies increased after re-induction therapy with another type of retinoiec acid (RA), tamibarotene. Tretinoin 88-90 PML nuclear body scaffold Homo sapiens 103-106
30289902-7 2018 At molecular relapse, the p.K227_T233del deletion and the p.R217S point-mutation in the RARA region of PML-RARA were identified, and their frequencies increased after re-induction therapy with another type of retinoiec acid (RA), tamibarotene. Tretinoin 88-90 retinoic acid receptor alpha Homo sapiens 107-111
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 236-240 PML nuclear body scaffold Homo sapiens 187-190
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 236-240 retinoic acid receptor alpha Homo sapiens 191-199
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 303-307 PML nuclear body scaffold Homo sapiens 165-168
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 303-307 retinoic acid receptor alpha Homo sapiens 169-177
8522994-7 1996 RA also caused a transient increase in level of tyrosine hydroxylase (TH) mRNA (twofold after 16 h), which returned to basal levels and then decreased relative to basal levels at 48 h. The effect of NGF on the expression of these genes was identical to that produced by RA. Tretinoin 0-2 nerve growth factor Rattus norvegicus 199-202
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 303-307 PML nuclear body scaffold Homo sapiens 187-190
27605212-4 2017 Here, we performed a series of chromatin immunoprecipitation (ChIP)-quantitative PCR (qPCR) experiments, demonstrating that there is an additional mode of action of PML/RARalpha, wherein PML/RARalpha does not bind DNA in the absence of ATRA but binds DNA and activates adjacent genes in the presence of ATRA. Tretinoin 303-307 retinoic acid receptor alpha Homo sapiens 191-199
27605212-5 2017 This mode of action is similar to that of a type I nuclear receptor and is highlighted by activation of G0/G1 switch gene 2 (G0S2) during ATRA-induced neutrophil differentiation of leukemia cell lines (NB4 and PR9) and primary human APL cells. Tretinoin 138-142 Picrotoxin-resistant Drosophila melanogaster 210-213
30209067-4 2018 Retinoic acid treatment also decreased c-myb gene expression in human leukemia cells. Tretinoin 0-13 MYB proto-oncogene, transcription factor Homo sapiens 39-44
30209067-6 2018 Retinoic acid agonists inhibited tumor growth in vivo in ACC patient-derived xenograft models and decreased MYB binding at translocated enhancers, thereby potentially diminishing the MYB positive feedback loop driving ACC. Tretinoin 0-13 MYB proto-oncogene, transcription factor Homo sapiens 108-111
30209067-6 2018 Retinoic acid agonists inhibited tumor growth in vivo in ACC patient-derived xenograft models and decreased MYB binding at translocated enhancers, thereby potentially diminishing the MYB positive feedback loop driving ACC. Tretinoin 0-13 MYB proto-oncogene, transcription factor Homo sapiens 183-186
8522994-7 1996 RA also caused a transient increase in level of tyrosine hydroxylase (TH) mRNA (twofold after 16 h), which returned to basal levels and then decreased relative to basal levels at 48 h. The effect of NGF on the expression of these genes was identical to that produced by RA. Tretinoin 270-272 tyrosine hydroxylase Rattus norvegicus 48-68
8950833-7 1996 Pentoxifylline (40 mumol/L), retinoic acid (0.01 mmol/L) and cyclosporin A (0.08 mumol/L) inhibited TF expression when added concurrently with LPS or TNF, but not when added 4 h after stimulation. Tretinoin 29-42 LOC101909187 Bos taurus 100-102
29981365-4 2018 All-trans retinoic acid (ATRA), the biologically active metabolite of vitamin A/RA, has been shown to have pleiotropic effects on hematopoietic cells, enhancing HSC self-renewal while also increasing differentiation of more mature progenitors. Tretinoin 0-23 fucosyltransferase 1 (H blood group) Homo sapiens 161-164
29981365-4 2018 All-trans retinoic acid (ATRA), the biologically active metabolite of vitamin A/RA, has been shown to have pleiotropic effects on hematopoietic cells, enhancing HSC self-renewal while also increasing differentiation of more mature progenitors. Tretinoin 25-29 fucosyltransferase 1 (H blood group) Homo sapiens 161-164
28220862-4 2017 A highly proliferative and plastic LNGFR(+)THY-1(+) subset of iMCs was subsequently programmed using retinoic acid and DP cell activating culture medium to acquire DP properties. Tretinoin 101-114 Thy-1 cell surface antigen Homo sapiens 43-48
8950833-9 1996 In contrast, exposure to LPS or TNF for 6 h induced marked expression of TF mRNA, which was inhibited by treatment with pentoxifylline, retinoic acid and cyclosporin A. Tretinoin 136-149 LOC101909187 Bos taurus 73-75
28230720-5 2017 RA signaling appears to be essential for expression of genes involved in developmental hematopoiesis, regulating the endothelial/blood cells balance in the yolk sac, promoting the hemogenic program in the aorta-gonad-mesonephros area and stimulating eryrthropoiesis in fetal liver by activating the expression of erythropoietin. Tretinoin 0-2 erythropoietin Mus musculus 313-327
8950833-12 1996 The concentrations of pentoxifylline and retinoic acid necessary for inhibition of TF expression in vitro may not be achievable in vivo owing to their toxic effects. Tretinoin 41-54 LOC101909187 Bos taurus 83-85
28053092-2 2017 We previously reported that the inhibition of the NAD-dependent histone deacetylase (HDAC) SIRT2 induces granulocytic differentiation in leukemia cells, suggesting the involvement of protein acetylation in ATRA-induced leukemia cell differentiation. Tretinoin 206-210 sirtuin 2 Homo sapiens 91-96
7588287-0 1995 Retinoic acid induces expression of the transcription factor GHF-1/Pit-1 in pituitary prolactin- and growth hormone-producing cell lines. Tretinoin 0-13 gonadotropin releasing hormone receptor Rattus norvegicus 101-115
29388081-16 2018 Also, retinoic acid transcriptional signaling was shown to be amplified as evidenced by specific increased Rarbeta and decreased Erbb4 mRNA expression in AS mice versus Ctrl mice hippocampi. Tretinoin 6-19 erb-b2 receptor tyrosine kinase 4 Mus musculus 129-134
8524212-0 1995 Synergistic activation of retinoic acid (RA)-responsive genes and induction of embryonal carcinoma cell differentiation by an RA receptor alpha (RAR alpha)-, RAR beta-, or RAR gamma-selective ligand in combination with a retinoid X receptor-specific ligand. Tretinoin 26-39 retinoic acid receptor gamma Homo sapiens 172-181
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 174-187 retinoic acid receptor gamma Homo sapiens 94-103
28187790-5 2017 We altered MYCN expression levels in a MYCN-inducible neuroblastoma cell line to facilitate or block retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 101-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 39-43
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 65-67 retinoic acid receptor gamma Homo sapiens 94-103
28187790-11 2017 Co-targeting of the retinoic acid and TGF-beta pathways, through RA and kartogenin (KGN; a TGF-beta signalling activating small molecule) combination treatment, induced the loss of viability of MYCN-amplified retinoid-resistant neuroblastoma cells. Tretinoin 20-33 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 194-198
28536942-5 2018 It was down-regulated in multiple acute myeloid leukemia (AML) cell lines and bone marrow cells of AML patients and up-regulated after all-trans retinoic acid (ATRA)-mediated granulocytic differentiation in AML cell lines and acute promyelocytic leukemia (APL; AML-M3, FAB classification) cells. Tretinoin 145-158 FA complementation group B Homo sapiens 269-272
7589553-5 1995 Overexpression of NSCL1 in F9 cells blocks the downregulation of Id2 gene expression during retinoic acid induced differentiation. Tretinoin 92-105 inhibitor of DNA binding 2 Mus musculus 65-68
28536942-5 2018 It was down-regulated in multiple acute myeloid leukemia (AML) cell lines and bone marrow cells of AML patients and up-regulated after all-trans retinoic acid (ATRA)-mediated granulocytic differentiation in AML cell lines and acute promyelocytic leukemia (APL; AML-M3, FAB classification) cells. Tretinoin 160-164 FA complementation group B Homo sapiens 269-272
30166332-0 2018 Correction: RDH10-mediated retinol metabolism and RARalpha-mediated retinoic acid signaling are required for submandibular salivary gland initiation (doi: 10.1242/dev.164822). Tretinoin 68-81 retinoic acid receptor alpha Homo sapiens 50-58
30166520-11 2018 Second, all-trans retinoic acid (ATRA) suppressed ALDH1 expression, inhibiting NRF2 activation, which led to the attenuation of CSC-like properties in ALDH-H cells but not in ALDH-L cells. Tretinoin 8-31 aldehyde dehydrogenase 1 family member A1 Homo sapiens 50-55
30166520-11 2018 Second, all-trans retinoic acid (ATRA) suppressed ALDH1 expression, inhibiting NRF2 activation, which led to the attenuation of CSC-like properties in ALDH-H cells but not in ALDH-L cells. Tretinoin 33-37 aldehyde dehydrogenase 1 family member A1 Homo sapiens 50-55
27412076-7 2017 Studies of CV-1 and LNCaP cells transfected with RAR expression vectors and a reporter vector revealed that RARgamma and RARbeta are activated by sub-nM all-trans retinoic acid (EC50-0.3 nM): ~50-fold more is required for activation of RARalpha (EC50-16 nM). Tretinoin 163-176 retinoic acid receptor alpha Homo sapiens 49-52
27412076-7 2017 Studies of CV-1 and LNCaP cells transfected with RAR expression vectors and a reporter vector revealed that RARgamma and RARbeta are activated by sub-nM all-trans retinoic acid (EC50-0.3 nM): ~50-fold more is required for activation of RARalpha (EC50-16 nM). Tretinoin 163-176 retinoic acid receptor alpha Homo sapiens 236-244
27740626-5 2017 We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. Tretinoin 80-93 PML nuclear body scaffold Homo sapiens 125-128
27740626-5 2017 We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. Tretinoin 80-93 retinoic acid receptor alpha Homo sapiens 129-133
30225259-7 2018 Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 12-34
30225259-7 2018 Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 36-39
30225259-7 2018 Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 111-114
27740626-5 2017 We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. Tretinoin 95-99 PML nuclear body scaffold Homo sapiens 125-128
27740626-5 2017 We further revealed that the downregulation of HOTAIRM1 could inhibit all-trans retinoic acid (ATRA) -induced degradation of PML-RARA in APL cells and repress the process of differentiation from promyelocytic to granulocytic cells. Tretinoin 95-99 retinoic acid receptor alpha Homo sapiens 129-133
7564522-1 1995 We studied tissue transglutaminase (TGase) expression in human myelomonocytic leukemia cells treated by combinations of all-trans retinoic acid (RA) and 1,25 dihydroxyvitamin D3 (VD). Tretinoin 145-147 transglutaminase 1 Homo sapiens 36-41
8563020-18 1995 Exogenous RA can activate a more widespread response resulting in ectopic transgene and RAR beta expression in the thoracic and sacral cord. Tretinoin 10-12 retinoic acid receptor, beta Mus musculus 88-96
27884045-6 2017 Moreover, we demonstrate that inhibition of RA signaling represses cell proliferation and expression of FGF10 signaling targets, and upregulates expression of basal epithelial keratins Krt5 and Krt14. Tretinoin 44-46 keratin 5 Homo sapiens 185-189
27884045-6 2017 Moreover, we demonstrate that inhibition of RA signaling represses cell proliferation and expression of FGF10 signaling targets, and upregulates expression of basal epithelial keratins Krt5 and Krt14. Tretinoin 44-46 keratin 14 Homo sapiens 194-199
27884045-7 2017 Importantly, we show that the stem cell gene Kit is regulated inversely from Krt5/Krt14 by RA signaling. Tretinoin 91-93 keratin 5 Homo sapiens 77-81
27884045-7 2017 Importantly, we show that the stem cell gene Kit is regulated inversely from Krt5/Krt14 by RA signaling. Tretinoin 91-93 keratin 14 Homo sapiens 82-87
30093655-2 2018 ATRA inhibits leukemia, breast, and liver cancer by targeting isomerase Pin1, a master regulator of oncogenic signaling networks. Tretinoin 0-4 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 72-76
30093655-6 2018 ATO and ATRA, at clinically safe doses, cooperatively ablate Pin1 to block numerous cancer-driving pathways and inhibit the growth of triple-negative breast cancer cells and tumor-initiating cells in cell and animal models including patient-derived orthotopic xenografts, like Pin1 knockout, which is substantiated by comprehensive protein and microRNA analyses. Tretinoin 8-12 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 61-65
30093655-6 2018 ATO and ATRA, at clinically safe doses, cooperatively ablate Pin1 to block numerous cancer-driving pathways and inhibit the growth of triple-negative breast cancer cells and tumor-initiating cells in cell and animal models including patient-derived orthotopic xenografts, like Pin1 knockout, which is substantiated by comprehensive protein and microRNA analyses. Tretinoin 8-12 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 277-281
30093655-7 2018 Thus, synergistic targeting of Pin1 by ATO and ATRA offers an attractive approach to combating breast and other cancers. Tretinoin 47-51 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 31-35
28111553-6 2016 We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. Tretinoin 167-169 enamelin Mus musculus 41-49
29945210-0 2018 SC1 inhibits the differentiation of F9 embryonic carcinoma cells induced by retinoic acid. Tretinoin 76-89 spinal cord QTL 1 Mus musculus 0-3
28111553-6 2016 We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. Tretinoin 167-169 enamelin Mus musculus 51-55
7581951-5 1995 Short-term (24 h) exposure to RA at 10(-8) mol/l, which is a physiological concentration, decreased and increased the levels of ALP and osteopontin mRNA on day 6, respectively. Tretinoin 30-32 secreted phosphoprotein 1 Rattus norvegicus 136-147
29945210-3 2018 SC1 can noticeably change the morphology of retinoic acid (RA)-induced F9 embryonic carcinoma cells (F9 cells). Tretinoin 44-57 spinal cord QTL 1 Mus musculus 0-3
29945210-3 2018 SC1 can noticeably change the morphology of retinoic acid (RA)-induced F9 embryonic carcinoma cells (F9 cells). Tretinoin 59-61 spinal cord QTL 1 Mus musculus 0-3
29945210-5 2018 When being added after 18-24 h of RA-induced F9 cell differentiation, SC1 transitorily activated Nanog and Oct4. Tretinoin 34-36 spinal cord QTL 1 Mus musculus 70-73
7581951-8 1995 At a high concentration (10(-6) mol/l), RA increased the level of osteopontin mRNA on day 6 and decreased the levels of ALP and osteocalcin mRNA irrespective of culture period. Tretinoin 40-42 secreted phosphoprotein 1 Rattus norvegicus 66-77
29945211-6 2018 Moreover, exposure to beta-CYP and 3-PBA at 100 muM inhibited all-trans retinoic acid (ATRA)-induced mRNA expressions of the granulocytic differentiation-related genes, CD11b and CSF-3R. Tretinoin 72-85 peptidylprolyl isomerase G Homo sapiens 27-30
29772445-0 2018 The protective role of all-transretinoic acid (ATRA) against colorectal cancer development is achieved via increasing miR-3666 expression and decreasing E2F7 expression. Tretinoin 27-45 microRNA 3666 Homo sapiens 118-126
29772445-0 2018 The protective role of all-transretinoic acid (ATRA) against colorectal cancer development is achieved via increasing miR-3666 expression and decreasing E2F7 expression. Tretinoin 47-51 microRNA 3666 Homo sapiens 118-126
29772445-2 2018 This study aimed to investigate whether miR-3666 was involved in inhibitory effects of all-transretinoic acid (ATRA) on the development of colorectal cancer (CRC). Tretinoin 87-109 microRNA 3666 Homo sapiens 40-48
29772445-2 2018 This study aimed to investigate whether miR-3666 was involved in inhibitory effects of all-transretinoic acid (ATRA) on the development of colorectal cancer (CRC). Tretinoin 111-115 microRNA 3666 Homo sapiens 40-48
28715808-0 2017 Retinoic Acid Facilitates Toll-Like Receptor 4 Expression to Improve Intestinal Barrier Function through Retinoic Acid Receptor Beta. Tretinoin 0-13 toll like receptor 4 Homo sapiens 26-46
28715808-10 2017 RESULTS: In the present study, ATRA treatment not only increased the TER of the Caco-2 monolayer but also up-regulated the expression levels of RARbeta, TLR4 and ZO-2 in Caco-2 cells. Tretinoin 31-35 toll like receptor 4 Homo sapiens 153-157
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 retinoic acid receptor, alpha Rattus norvegicus 30-38
28680330-3 2017 Gene expression of the foxp3, raralpha, rarbeta, rxrbeta, and ppar beta/delta and protein expression of the Raralpha, Rarbeta, and Rxrbeta in cells after stimulation with ATRA were also investigated. Tretinoin 171-175 retinoic acid receptor, alpha Rattus norvegicus 108-116
28680330-7 2017 Moreover, after ATRA stimulation, the frequency of Treg-produced IL-10 tended to be lower in diseased animals than in the healthy group. Tretinoin 16-20 interleukin 10 Rattus norvegicus 65-70
29772445-10 2018 Moreover, ATRA increased miR-3666 expression, and effects of ATRA on the malignant behaviors of HCT116 cells were achieved by positive regulating miR-3666 expression. Tretinoin 10-14 microRNA 3666 Homo sapiens 25-33
29772445-10 2018 Moreover, ATRA increased miR-3666 expression, and effects of ATRA on the malignant behaviors of HCT116 cells were achieved by positive regulating miR-3666 expression. Tretinoin 10-14 microRNA 3666 Homo sapiens 146-154
7657606-6 1995 However, a specific cis-acting retinoic acid responsive element of the DR1 type was identified in the proximal region (-385) of the ST3 gene promoter. Tretinoin 31-44 down-regulator of transcription 1 Homo sapiens 71-74
29772445-10 2018 Moreover, ATRA increased miR-3666 expression, and effects of ATRA on the malignant behaviors of HCT116 cells were achieved by positive regulating miR-3666 expression. Tretinoin 61-65 microRNA 3666 Homo sapiens 146-154
29772445-11 2018 Furthermore, E2F7 was a target gene of miR-3666, and knockdown of E2F7 reversed the combined effects of ATRA and miR-3666 inhibitor on the malignant behaviors of HCT116 cells. Tretinoin 104-108 microRNA 3666 Homo sapiens 39-47
29772445-12 2018 Besides, ATRA inhibited the activation of MAPK/ERK signaling pathway, which was reversed by inhibition of miR-3666. Tretinoin 9-13 microRNA 3666 Homo sapiens 106-114
29772445-14 2018 MiR-3666/E2F7 may play a key role in regulating the inhibitory effects of ATRA on HCT116 cells via suppressing the activation of MAPK/ERK signaling pathway. Tretinoin 74-78 microRNA 3666 Homo sapiens 0-8
29521230-9 2017 Moreover, when treated with exogenous RA, endogenous fhl1A expression in skeletal muscles was robust. Tretinoin 38-40 four and a half LIM domains 1a Danio rerio 53-58
29521230-12 2017 The role of fhl1A in skeletal myogenesis is regulated by RA signaling. Tretinoin 57-59 four and a half LIM domains 1a Danio rerio 12-17
8585424-2 1995 We hypothesize that the expression of this more osteoblastic phenotype subsequent to RA exposure is the result of the treated cell"s extracellular matrix (ECM) becoming a repository and active source of putative osteoinductive growth factors including, specifically, select members of the TGF-beta superfamily. Tretinoin 85-87 transforming growth factor, beta 1 Mus musculus 289-297
30695510-2 2017 All-trans retinoic acid (ATRA) is a representa- tive molecular-targeted drug and is directed against PML-RARA. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 101-104
30089026-4 2018 A significant increase occurred in the expression of meiotic markers and specific genes, Fkbp6 (p = 0.00), Mov10l1 (p = 0.01), and Tex13 (p = 0.00) in ESCs treated with RA (+RA) compared with the controls (-RA). Tretinoin 169-171 Mov10 like RISC complex RNA helicase 1 Mus musculus 107-114
30089026-6 2018 The expression levels of 4930432K21Rik, Mvh, Stra8, and Scp3 in the +RA group was higher than that of the -RA group. Tretinoin 69-71 stimulated by retinoic acid gene 8 Mus musculus 45-50
30089026-6 2018 The expression levels of 4930432K21Rik, Mvh, Stra8, and Scp3 in the +RA group was higher than that of the -RA group. Tretinoin 69-71 synaptonemal complex protein 3 Mus musculus 56-60
30695510-2 2017 All-trans retinoic acid (ATRA) is a representa- tive molecular-targeted drug and is directed against PML-RARA. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 105-109
7628451-1 1995 Transcription of the c-jun gene is up-regulated by either retinoic acid (RA) or adenovirus E1A during the differentiation of F9 cells. Tretinoin 58-71 jun proto-oncogene Mus musculus 21-26
30695510-2 2017 All-trans retinoic acid (ATRA) is a representa- tive molecular-targeted drug and is directed against PML-RARA. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 101-104
30695510-2 2017 All-trans retinoic acid (ATRA) is a representa- tive molecular-targeted drug and is directed against PML-RARA. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 105-109
7619051-2 1995 Pretreatment of keratinocytes with all-trans-retinoic retinoic acid inhibited the EGF induction of ODC activity. Tretinoin 54-67 ornithine decarboxylase 1 Homo sapiens 99-102
27978814-16 2016 The analysis revealed eight patterns of the gene expression responses to ATRA, indicating the induction of the BMP, WNT, Notch, FGF and NTRK-receptor signaling pathways involved in cell differentiation, as well as the repression of the cell-cycle related genes. Tretinoin 73-77 bone morphogenetic protein 1 Homo sapiens 111-114
30026570-3 2018 Moreover, PML/RARA is specifically targeted by All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), two agents that synergistically act to induce degradation of the oncoprotein. Tretinoin 47-70 PML nuclear body scaffold Homo sapiens 10-13
30026570-3 2018 Moreover, PML/RARA is specifically targeted by All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), two agents that synergistically act to induce degradation of the oncoprotein. Tretinoin 47-70 retinoic acid receptor alpha Homo sapiens 14-18
30026570-3 2018 Moreover, PML/RARA is specifically targeted by All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), two agents that synergistically act to induce degradation of the oncoprotein. Tretinoin 72-76 PML nuclear body scaffold Homo sapiens 10-13
7547504-9 1995 In contrast, the osteoinductive effect of matrix from retinoic acid-treated cells was blocked with both vgr-1 and TGF-beta 1 antibodies, suggesting that TGF-beta 1 may act prior to vgr-1 during osteoblastic differentiation. Tretinoin 54-67 transforming growth factor, beta 1 Mus musculus 114-124
30026570-3 2018 Moreover, PML/RARA is specifically targeted by All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), two agents that synergistically act to induce degradation of the oncoprotein. Tretinoin 72-76 retinoic acid receptor alpha Homo sapiens 14-18
29447006-5 2018 In vivo treatment with an inhibitor of RA synthesis delayed the migration of epicardial-derived precursor cells (EPDCs) into the myocardium; the opposite was seen in the case of dehydrogenase/reductase superfamily (DHRS)3-deficient embryos, a mouse model of RA excess. Tretinoin 258-260 dehydrogenase/reductase (SDR family) member 3 Mus musculus 215-221
27977740-5 2016 Studies to identify the factor(s) in MP responsible for promoting IL-4-induced M2 skewing suggests that all-trans retinoic acid (ATRA), TGFbeta and prostaglandin E2 (PGE2) all play a role. Tretinoin 114-127 interleukin 4 Mus musculus 66-70
27977740-5 2016 Studies to identify the factor(s) in MP responsible for promoting IL-4-induced M2 skewing suggests that all-trans retinoic acid (ATRA), TGFbeta and prostaglandin E2 (PGE2) all play a role. Tretinoin 129-133 interleukin 4 Mus musculus 66-70
27569851-4 2016 The objective was to elucidate gene expression of these RA-metabolizing enzymes (ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1 and CYP26C1) and their protein presence in testes of young, peripubertal and adult dogs. Tretinoin 56-58 aldehyde dehydrogenase 1 family member A2 Canis lupus familiaris 90-97
27569851-4 2016 The objective was to elucidate gene expression of these RA-metabolizing enzymes (ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1 and CYP26C1) and their protein presence in testes of young, peripubertal and adult dogs. Tretinoin 56-58 ALDH1A3 Canis lupus familiaris 99-106
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 15-17 aldehyde dehydrogenase 1 family member A2 Canis lupus familiaris 49-56
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 15-17 ALDH1A3 Canis lupus familiaris 61-68
27569851-6 2016 Based on detailed analyses of mRNA expression patterns, ALDH1A2 was regarded as a primary RA-synthesizing enzyme and CYP26B1 as a critical RA-hydrolysing enzyme; presumably, these genes have vital roles in maintaining RA homeostasis, which is imperative to spermatogenesis and other testicular functions in post-natal canine testis. Tretinoin 90-92 aldehyde dehydrogenase 1 family member A2 Canis lupus familiaris 56-63
27569851-6 2016 Based on detailed analyses of mRNA expression patterns, ALDH1A2 was regarded as a primary RA-synthesizing enzyme and CYP26B1 as a critical RA-hydrolysing enzyme; presumably, these genes have vital roles in maintaining RA homeostasis, which is imperative to spermatogenesis and other testicular functions in post-natal canine testis. Tretinoin 139-141 aldehyde dehydrogenase 1 family member A2 Canis lupus familiaris 56-63
29720480-5 2018 The expression of USP22 in CICs is markedly reduced upon FBS/retinoic acid-induced differentiation. Tretinoin 61-74 ubiquitin specific peptidase 22 Homo sapiens 18-23
7547504-9 1995 In contrast, the osteoinductive effect of matrix from retinoic acid-treated cells was blocked with both vgr-1 and TGF-beta 1 antibodies, suggesting that TGF-beta 1 may act prior to vgr-1 during osteoblastic differentiation. Tretinoin 54-67 transforming growth factor, beta 1 Mus musculus 153-163
27569851-6 2016 Based on detailed analyses of mRNA expression patterns, ALDH1A2 was regarded as a primary RA-synthesizing enzyme and CYP26B1 as a critical RA-hydrolysing enzyme; presumably, these genes have vital roles in maintaining RA homeostasis, which is imperative to spermatogenesis and other testicular functions in post-natal canine testis. Tretinoin 139-141 aldehyde dehydrogenase 1 family member A2 Canis lupus familiaris 56-63
7615982-1 1995 We examined the regulation of cellular retinol-binding protein (CRBP) mRNA and protein expression in human skin in vivo by all-trans retinoic acid and all-trans retinol. Tretinoin 133-146 retinol binding protein 1 Homo sapiens 64-68
27480083-0 2016 A network including PU.1, Vav1 and miR-142-3p sustains ATRA-induced differentiation of acute promyelocytic leukemia cells - a short report. Tretinoin 55-59 Spi-1 proto-oncogene Homo sapiens 20-24
27480083-4 2016 METHODS: ATRA-induced increases in PU.1 and Vav1 expression in APL-derived NB4 cells were counteracted with specific siRNAs, and the expression of miR-142-3p was measured by quantitative real-time PCR (qRT-PCR). Tretinoin 9-13 Spi-1 proto-oncogene Homo sapiens 35-39
27506116-0 2016 Nuclear receptor corepressors Ncor1 and Ncor2 (Smrt) are required for retinoic acid-dependent repression of Fgf8 during somitogenesis. Tretinoin 70-83 nuclear receptor co-repressor 2 Mus musculus 40-45
27506116-0 2016 Nuclear receptor corepressors Ncor1 and Ncor2 (Smrt) are required for retinoic acid-dependent repression of Fgf8 during somitogenesis. Tretinoin 70-83 nuclear receptor co-repressor 2 Mus musculus 47-51
27506116-2 2016 Here, we show that nuclear receptor corepressors NCOR1 and NCOR2 (SMRT) redundantly mediate the ability of RA to repress Fgf8. Tretinoin 107-109 nuclear receptor co-repressor 2 Mus musculus 59-64
29966306-7 2018 Expression of CEBPB induced by ATRA is accompanied by upregulated expression of CEBPE with similar kinetics. Tretinoin 31-35 CCAAT enhancer binding protein epsilon Homo sapiens 80-85
7615982-2 1995 Treatment of human skin for 24 h with all-trans retinoic acid (0.1%) or all-trans retinol (1.6%) induced CRBP mRNA 5.5-fold (p < 0.01, n = 10) and 5.7-fold (p < 0.01, n = 5), respectively, compared with skin treated with vehicle or sodium lauryl sulfate (used as an irritant control). Tretinoin 48-61 retinol binding protein 1 Homo sapiens 105-109
27506116-2 2016 Here, we show that nuclear receptor corepressors NCOR1 and NCOR2 (SMRT) redundantly mediate the ability of RA to repress Fgf8. Tretinoin 107-109 nuclear receptor co-repressor 2 Mus musculus 66-70
7615982-3 1995 In vitro translation of poly A+ RNA from all-trans retinoic acid, all-trans retinol, sodium lauryl sulfate, and vehicle-treated human skin demonstrated that the observed increased CRBP mRNA in all-trans retinoic acid- and all-trans retinol-treated skin was able to direct increased (2.3-2.9-fold) CRBP protein synthesis. Tretinoin 51-64 retinol binding protein 1 Homo sapiens 180-184
27354299-0 2016 Targeting leiomyomas with all-trans-retinoic acid at phosphoinositide 3-kinase pathway suppression: Effective roles of beta-catenin and of signaling interactions. Tretinoin 26-49 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 53-78
27354299-0 2016 Targeting leiomyomas with all-trans-retinoic acid at phosphoinositide 3-kinase pathway suppression: Effective roles of beta-catenin and of signaling interactions. Tretinoin 26-49 catenin beta 1 Homo sapiens 119-131
29356312-3 2018 METHODS: Bile duct-ligated (BDL) rats and Mdr2(Abcb4)-/- mice were treated with all-trans retinoic acid (atRA), a potent inhibitor of bile acid synthesis, 5 mg/kg/d by gavage, or Cenicriviroc (CVC), a known antagonist of CCR2 and CCR5, 50 mg/kg/d alone or in combination for 14 days and 1 month respectively. Tretinoin 105-109 ATP binding cassette subfamily B member 4 Rattus norvegicus 42-46
7615982-4 1995 Riboprobe in situ hybridization revealed that CRBP mRNA was uniformly elevated throughout the epidermis and in dermal cells after all-trans retinoic acid treatment of human skin. Tretinoin 140-153 retinol binding protein 1 Homo sapiens 46-50
29356312-3 2018 METHODS: Bile duct-ligated (BDL) rats and Mdr2(Abcb4)-/- mice were treated with all-trans retinoic acid (atRA), a potent inhibitor of bile acid synthesis, 5 mg/kg/d by gavage, or Cenicriviroc (CVC), a known antagonist of CCR2 and CCR5, 50 mg/kg/d alone or in combination for 14 days and 1 month respectively. Tretinoin 105-109 ATP binding cassette subfamily B member 4 Rattus norvegicus 47-52
27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 44-67 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 97-122
27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 69-73 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 97-122
27564600-0 2016 All-Trans Retinoic Acid Inhibits Human Colorectal Cancer Cells RKO Migration via Downregulating Myosin Light Chain Kinase Expression through MAPK Signaling Pathway. Tretinoin 10-23 myosin light chain kinase Homo sapiens 96-121
27564600-4 2016 ATRA inhibited the expression and activation of myosin light chain kinase (MLCK) in RKO cells, while the expression level of MLC phosphatase (MLCP) had no change in RKO cells treated with or without ATRA. Tretinoin 0-4 myosin light chain kinase Homo sapiens 48-73
29802528-0 2018 All-Trans Retinoic Acid Ameliorates the Early Experimental Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting the Loss of the Blood-Brain Barrier via the JNK/P38MAPK Signaling Pathway. Tretinoin 10-23 mitogen-activated protein kinase 8 Rattus norvegicus 162-165
27564600-4 2016 ATRA inhibited the expression and activation of myosin light chain kinase (MLCK) in RKO cells, while the expression level of MLC phosphatase (MLCP) had no change in RKO cells treated with or without ATRA. Tretinoin 0-4 myosin light chain kinase Homo sapiens 75-79
29802528-6 2018 ATRA treatment also reduced the p-P38 and p-JNK protein level. Tretinoin 0-4 mitogen-activated protein kinase 8 Rattus norvegicus 44-47
7615982-5 1995 Western analysis revealed that CRBP protein was elevated 3.2-fold (p < 0.01, n = 6) and 3.0-fold (p < 0.01, n = 6) after all-trans retinoic acid treatment of human skin in vivo for 24 and 96 h, respectively, compared with vehicle- and sodium lauryl sulfate-treated skin. Tretinoin 137-150 retinol binding protein 1 Homo sapiens 31-35
29802528-8 2018 SP600125 and SB203580, which is the JNK/P38 pathway inhibitors has the same protective effect as ATRA. Tretinoin 97-101 mitogen-activated protein kinase 8 Rattus norvegicus 36-39
27564600-13 2016 In conclusion, ATRA inhibits RKO migration by reducing MLCK expression via extracellular signal-regulated kinase 1/Mitogen-activated protein kinase (ERK1/MAPK) signaling pathway. Tretinoin 15-19 myosin light chain kinase Homo sapiens 55-59
29802528-9 2018 These results indicated that ATRA may inhibit the JNK/P38 MAPK pathway to alleviate BBB disruption and improve CIR outcomes. Tretinoin 29-33 mitogen-activated protein kinase 8 Rattus norvegicus 50-53
7615982-6 1995 In addition, functional CRBP levels measured by [3H]all-trans retinol binding were elevated 1.9-fold (p < 0.01, n = 6) and 3.5-fold (p < 0.01, n = 6) at 24 and 94 h, respectively, after all-trans retinoic acid treatment, compared with vehicle- or sodium lauryl sulfate-treated skin. Tretinoin 202-215 retinol binding protein 1 Homo sapiens 24-28
7615982-8 1995 Monoclonal antibodies to nuclear retinoid receptors demonstrated that predominantly retinoic acid receptor-alpha/retinoid X receptor-alpha heterodimers bound to the CRBP retinoic acid response element. Tretinoin 84-97 retinol binding protein 1 Homo sapiens 165-169
7615982-9 1995 These data demonstrate that CRBP expression in human skin in vivo is regulated by exogenous all-trans retinoic acid and all-trans retinol. Tretinoin 102-115 retinol binding protein 1 Homo sapiens 28-32
27488031-8 2016 When RA was given together with 2-aminoethoxydiphenylborane (2-APB), a blocker of IP3R-dependent ER Ca2+ release and SOCE, with xestospongin C, a selective IP3R- receptor antagonist, or with 3,5-bis (trifluoromethyl)pyrazole (BTP-2), a specific SOCE blocker, the stimulatory effect of RA on cell proliferation was abolished. Tretinoin 5-7 inositol 1,4,5-trisphosphate receptor 1 Mus musculus 82-86
7626500-6 1995 Considerable data favor a model pathway of RA biosynthesis and metabolism consisting of enzymes that recognize CRBP (apo and holo) and holo-CRABP as substrates and/or affecters of activity. Tretinoin 43-45 retinol binding protein 1 Homo sapiens 111-115
27488031-8 2016 When RA was given together with 2-aminoethoxydiphenylborane (2-APB), a blocker of IP3R-dependent ER Ca2+ release and SOCE, with xestospongin C, a selective IP3R- receptor antagonist, or with 3,5-bis (trifluoromethyl)pyrazole (BTP-2), a specific SOCE blocker, the stimulatory effect of RA on cell proliferation was abolished. Tretinoin 5-7 inositol 1,4,5-trisphosphate receptor 1 Mus musculus 156-160
29848638-4 2018 The SOX30 protein was predominantly expressed in spermatids, while its transcription was regulated by retinoic acid and by MYBL1 before and during meiosis. Tretinoin 102-115 SRY (sex determining region Y)-box 30 Mus musculus 4-9
7626500-6 1995 Considerable data favor a model pathway of RA biosynthesis and metabolism consisting of enzymes that recognize CRBP (apo and holo) and holo-CRABP as substrates and/or affecters of activity. Tretinoin 43-45 cellular retinoic acid binding protein 1 Homo sapiens 140-145
29596829-5 2018 Recent studies suggest that pharmacological concentrations of the APL therapeutic drugs, all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), affect post-mitotic nuclear import of the APL-associated oncoprotein PML/RARA. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 221-225
7626500-11 1995 Retinal generated in microsomes from holo-CRBP by RDH supports cytosolic RA synthesis by an NAD-dependent retinal dehydrogenase (RalDH). Tretinoin 73-75 retinol binding protein 1 Homo sapiens 42-46
7626500-11 1995 Retinal generated in microsomes from holo-CRBP by RDH supports cytosolic RA synthesis by an NAD-dependent retinal dehydrogenase (RalDH). Tretinoin 73-75 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 50-53
27278254-4 2016 RA-mediated survival involved up-regulation of the anti-apoptotic protein myeloid cell leukemia 1 (MCL1) at the transcriptional level, and knock down of MCL1 by small interfering RNA partially reversed the effects of RA. Tretinoin 0-2 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 74-97
7626500-13 1995 CRABP is also important to modulating the steady-state concentrations of RA, through sequestering RA and facilitating its metabolism, because the complex CRABP/RA acts as a low Km substrate. Tretinoin 1-3 cellular retinoic acid binding protein 1 Homo sapiens 154-159
27278254-4 2016 RA-mediated survival involved up-regulation of the anti-apoptotic protein myeloid cell leukemia 1 (MCL1) at the transcriptional level, and knock down of MCL1 by small interfering RNA partially reversed the effects of RA. Tretinoin 0-2 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 99-103
27278254-4 2016 RA-mediated survival involved up-regulation of the anti-apoptotic protein myeloid cell leukemia 1 (MCL1) at the transcriptional level, and knock down of MCL1 by small interfering RNA partially reversed the effects of RA. Tretinoin 217-219 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 99-103
28521962-6 2018 All-trans retinoic acid and arsenic trioxide treatment has been implemented for promyelocytic leukemia to target the PML-RARalpha fusion protein. Tretinoin 10-23 PML nuclear body scaffold Homo sapiens 117-120
27278254-4 2016 RA-mediated survival involved up-regulation of the anti-apoptotic protein myeloid cell leukemia 1 (MCL1) at the transcriptional level, and knock down of MCL1 by small interfering RNA partially reversed the effects of RA. Tretinoin 217-219 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 153-157
7626500-13 1995 CRABP is also important to modulating the steady-state concentrations of RA, through sequestering RA and facilitating its metabolism, because the complex CRABP/RA acts as a low Km substrate. Tretinoin 73-75 cellular retinoic acid binding protein 1 Homo sapiens 0-5
29620445-6 2018 RA induction led to slender spindles and tadpole-like changes of cell morphology, and the expression of germ cell-specific markers (Oct4, Piwil2, Itgb1, SSEA-1, and Stra8) presented significant upregulation in the RA treatment group according to the polymerase chain reaction and immunofluorescence results. Tretinoin 0-2 POU class 5 homeobox 1 Homo sapiens 132-136
7626500-13 1995 CRABP is also important to modulating the steady-state concentrations of RA, through sequestering RA and facilitating its metabolism, because the complex CRABP/RA acts as a low Km substrate. Tretinoin 73-75 cellular retinoic acid binding protein 1 Homo sapiens 154-159
27496193-7 2016 CK14 and p63 messenger RNA (mRNA) expressions in the AA + BMP4 + RA-treated cells were higher than those of the AA + BMP4-treated cells (CK14: 22.4-fold; p63: 84.7-fold). Tretinoin 65-67 keratin 14 Homo sapiens 0-4
7738026-1 1995 Humans possess five classes of alcohol dehydrogenase (ADH), including forms able to oxidize ethanol or formaldehyde as part of a defense mechanism, as well as forms acting as retinol dehydrogenases in the synthesis of the regulatory ligand retinoic acid. Tretinoin 240-253 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 54-57
27496193-7 2016 CK14 and p63 messenger RNA (mRNA) expressions in the AA + BMP4 + RA-treated cells were higher than those of the AA + BMP4-treated cells (CK14: 22.4-fold; p63: 84.7-fold). Tretinoin 65-67 tumor protein p63 Homo sapiens 9-12
27496193-7 2016 CK14 and p63 messenger RNA (mRNA) expressions in the AA + BMP4 + RA-treated cells were higher than those of the AA + BMP4-treated cells (CK14: 22.4-fold; p63: 84.7-fold). Tretinoin 65-67 tumor protein p63 Homo sapiens 154-157
28959333-1 2016 BACKGROUND: Promyelocytic leukemia protein (PML) is a tumor suppressor protein that is involved in myeloid cell differentiation in response to retinoic acid (RA). Tretinoin 143-156 PML nuclear body scaffold Homo sapiens 12-42
28959333-1 2016 BACKGROUND: Promyelocytic leukemia protein (PML) is a tumor suppressor protein that is involved in myeloid cell differentiation in response to retinoic acid (RA). Tretinoin 143-156 PML nuclear body scaffold Homo sapiens 44-47
28959333-1 2016 BACKGROUND: Promyelocytic leukemia protein (PML) is a tumor suppressor protein that is involved in myeloid cell differentiation in response to retinoic acid (RA). Tretinoin 158-160 PML nuclear body scaffold Homo sapiens 12-42
29516351-5 2018 ATRA significantly decreased the nuclear to cytoplasmic ratio of SIRT1 and SIRT2.1, while sirtinol inhibited that of SIRT1, and TSA increased that of SIRT1 and SIRT2.1 during early differentiation. Tretinoin 0-4 sirtuin 2 Homo sapiens 75-80
28959333-1 2016 BACKGROUND: Promyelocytic leukemia protein (PML) is a tumor suppressor protein that is involved in myeloid cell differentiation in response to retinoic acid (RA). Tretinoin 158-160 PML nuclear body scaffold Homo sapiens 44-47
7721890-5 1995 BAECs constitutively synthesized and secreted MK and its production was enhanced 2-fold with 1 microM retinoic acid or 10 microM retinol. Tretinoin 102-115 midkine Bos taurus 46-48
29263441-7 2018 Treatment of the mDia1/miR-146a double knockout mice with all-trans retinoic acid, which promoted the differentiation of MDSCs and ameliorated the inflammatory bone marrow microenvironment, significantly rescued anemia and ineffective erythropoiesis. Tretinoin 68-81 microRNA 146 Mus musculus 23-31
7785896-6 1995 Expression of OPN mRNA is upregulated by growth and differentiation factors (PDGF, EGF, TGF-beta and BMP-7/OP-1) and by mechanical stress, which promote bone formation, as well as by osteotropic hormones (retinoic acid and vitamin D3), which can promote bone resorption and remodelling. Tretinoin 205-218 secreted phosphoprotein 1 Rattus norvegicus 14-17
29743862-4 2018 Histone acetylation in the regulatory region of CYP1A1 was enhanced by treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or all-trans retinoic acid (at-RA). Tretinoin 142-155 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 48-54
26513600-0 2016 Amniotic fluid levels of phospholipase A2 in fetal rats with retinoic acid induced myelomeningocele: the potential "second hit" in neurologic damage. Tretinoin 61-74 phospholipase A2 group IB Rattus norvegicus 25-41
27421841-6 2016 RNA-seq analysis indicated an upregulation of genes important for neuronal development, such as Ntng2, Enah, Gas1, Slit2, and Dscam, in response to the RA treatment in control Neuro2a cells transfected with GFP or wild-type KDM5C. Tretinoin 152-154 DS cell adhesion molecule Mus musculus 126-131
29743862-8 2018 In conclusion, the present data improve our knowledge on retinoic acid-dependent effects on CYP1A1 expression and demonstrate unexpected mixture effects by cross-talk of the different receptors. Tretinoin 57-70 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 92-98
7542037-4 1995 In contrast, retinoic acid induces the expression of TrkA, the high-affinity receptor for nerve growth factor, and of a non-catalytic form of TrkB, in non-neural subsets of differentiated cells. Tretinoin 13-26 neurotrophic receptor tyrosine kinase 1 Homo sapiens 53-57
29541688-0 2016 Retinoic acid enhances progesterone production via the cAMP/PKA signaling pathway in immature rat granulosa cells. Tretinoin 0-13 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 60-63
29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. Tretinoin 96-100 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 35-51
29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. Tretinoin 96-100 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-56
29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. Tretinoin 96-100 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 168-171
29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. Tretinoin 118-122 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 35-51
29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. Tretinoin 118-122 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 53-56
29541688-7 2016 In addition, H-89, an inhibitor of protein kinase A (PKA), abolished the stimulatory effects of atRA, indicating that atRA enhanced progesterone synthesis through cAMP/PKA signaling. Tretinoin 118-122 protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus 168-171
7542037-4 1995 In contrast, retinoic acid induces the expression of TrkA, the high-affinity receptor for nerve growth factor, and of a non-catalytic form of TrkB, in non-neural subsets of differentiated cells. Tretinoin 13-26 neurotrophic receptor tyrosine kinase 2 Homo sapiens 142-146
7733941-0 1995 The differentiation-related upregulation of aryl hydrocarbon receptor transcript levels is suppressed by retinoic acid. Tretinoin 105-118 aryl hydrocarbon receptor Homo sapiens 44-69
27531765-1 2016 OBJECTIVE: To explore effect of all-trans retinoic acid(ATRA) on annexin II expression in NB4 cells and to analyze the luciferase activity of annexinII promoter in condition of ATRA-induced treatment. Tretinoin 177-181 annexin A2 Homo sapiens 65-75
27531765-2 2016 METHODS: NB4 cells were cultured in vitro, the transcriptional or translational expression levels of Annexin II in NB4 cells treated with 1 micromol/L ATRA at different time points were detected by RT-PCR or Western blot respectively. Tretinoin 151-155 annexin A2 Homo sapiens 101-111
27531765-4 2016 RESULTS: The transcriptional expression of Annexin II was down-regulated after 48 h. The translation expression of Annexin II was slowly weakened after 24 h, and it was seriously reduced after 48 h. Further, Luciferase activity of AnnexinII promoter in NB4 cells treated with 1 micromol/L ATRA was down-regulated, and showed a decreased tendency at indicated time points. Tretinoin 289-293 annexin A2 Homo sapiens 43-53
27531765-4 2016 RESULTS: The transcriptional expression of Annexin II was down-regulated after 48 h. The translation expression of Annexin II was slowly weakened after 24 h, and it was seriously reduced after 48 h. Further, Luciferase activity of AnnexinII promoter in NB4 cells treated with 1 micromol/L ATRA was down-regulated, and showed a decreased tendency at indicated time points. Tretinoin 289-293 annexin A2 Homo sapiens 115-125
7733941-2 1995 Herein we report on the relative levels of Ah-receptor-mRNA and TCDD-induced cytochrome P450 1A1 (Cyp1A1)-mRNA and their modulation by retinoic acid in the human keratinocyte cell line HaCaT. Tretinoin 135-148 aryl hydrocarbon receptor Homo sapiens 43-54
7733941-8 1995 These results indicate that the expression of the AhR is dependent on the state of differentiation of keratinocytes and seems to be affected by retinoic acid. Tretinoin 144-157 aryl hydrocarbon receptor Homo sapiens 50-53
27468685-2 2016 All-trans-retinoic acid (RA) treatment induces PML-RARalpha degradation, restores PML-NB functions, and causes terminal cell differentiation of APL blasts. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 47-50
27468685-2 2016 All-trans-retinoic acid (RA) treatment induces PML-RARalpha degradation, restores PML-NB functions, and causes terminal cell differentiation of APL blasts. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 82-85
7726866-2 1995 In chloramphenicol acetyl transferase (CAT) assay with retinoic acid response element-beta, GGA and 4,5-didehydro GGA were both positive, but 2,3-dihydro GGA was negative, even though these GGA derivatives have been reported to be all potent ligands for cellular retinoic-acid-binding protein(CRABP). Tretinoin 55-68 cellular retinoic acid binding protein 1 Homo sapiens 293-298
27468685-2 2016 All-trans-retinoic acid (RA) treatment induces PML-RARalpha degradation, restores PML-NB functions, and causes terminal cell differentiation of APL blasts. Tretinoin 25-27 PML nuclear body scaffold Homo sapiens 47-50
27468685-2 2016 All-trans-retinoic acid (RA) treatment induces PML-RARalpha degradation, restores PML-NB functions, and causes terminal cell differentiation of APL blasts. Tretinoin 25-27 PML nuclear body scaffold Homo sapiens 82-85
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 151-170 latent transforming growth factor beta binding protein 1 Homo sapiens 269-275
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 172-176 latent transforming growth factor beta binding protein 1 Homo sapiens 86-92
27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 172-176 latent transforming growth factor beta binding protein 1 Homo sapiens 269-275
7743939-6 1995 The third enhancer is essential for the most extensive expression domain of Hoxa-1 and contains a retinoic acid response element. Tretinoin 98-111 homeobox A1 Mus musculus 76-82
26860546-6 2016 RA was found to increase retinoic acid receptor-alpha (RAR-alpha) protein expression in the hippocampus, suggesting an activation of RA-induced signaling mechanisms. Tretinoin 0-2 retinoic acid receptor, alpha Rattus norvegicus 25-53
26860546-6 2016 RA was found to increase retinoic acid receptor-alpha (RAR-alpha) protein expression in the hippocampus, suggesting an activation of RA-induced signaling mechanisms. Tretinoin 0-2 retinoic acid receptor, alpha Rattus norvegicus 55-64
7619212-0 1995 Retinoic acid induces activin receptor IIB mRNA in F9 embryonal carcinoma cells. Tretinoin 0-13 activin receptor IIB Mus musculus 22-42
26860546-6 2016 RA was found to increase retinoic acid receptor-alpha (RAR-alpha) protein expression in the hippocampus, suggesting an activation of RA-induced signaling mechanisms. Tretinoin 55-57 retinoic acid receptor, alpha Rattus norvegicus 25-53
27214556-0 2016 Transcription factor TLX1 controls retinoic acid signaling to ensure spleen development. Tretinoin 35-48 T cell leukemia, homeobox 1 Mus musculus 21-25
7891690-7 1995 DNA-binding analysis revealed that RAR gamma Bm382 is able to form a heterodimer with the retinoid X receptor and bind to the different types of retinoic acid response elements with almost the same efficiency as normal RAR. Tretinoin 145-158 retinoic acid receptor gamma Homo sapiens 35-44
27214556-4 2016 Herein, we have shown that TLX1-dependent regulation of retinoic acid (RA) metabolism is critical for spleen organogenesis. Tretinoin 56-69 T cell leukemia, homeobox 1 Mus musculus 27-31
27214556-4 2016 Herein, we have shown that TLX1-dependent regulation of retinoic acid (RA) metabolism is critical for spleen organogenesis. Tretinoin 71-73 T cell leukemia, homeobox 1 Mus musculus 27-31
27214556-5 2016 In a murine model, loss of Tlx1 during formation of the splenic anlage increased RA signaling by regulating several genes involved in RA metabolism. Tretinoin 81-83 T cell leukemia, homeobox 1 Mus musculus 27-31
27214556-5 2016 In a murine model, loss of Tlx1 during formation of the splenic anlage increased RA signaling by regulating several genes involved in RA metabolism. Tretinoin 134-136 T cell leukemia, homeobox 1 Mus musculus 27-31
7758830-6 1995 In myoblast cells, retinoic acid increased the content of GLUT4 mRNA in a dose and time dependent manner, an effect that was partially attenuated by insulin. Tretinoin 19-32 solute carrier family 2 member 4 Homo sapiens 58-63
7758830-7 1995 In myocytes retinoic acid increased GLUT4 mRNA levels to 2.3 times basal. Tretinoin 12-25 solute carrier family 2 member 4 Homo sapiens 36-41
27214556-7 2016 Pharmacological inhibition of RA signaling in Tlx1-deficient animals partially rescued the spleen defect. Tretinoin 30-32 T cell leukemia, homeobox 1 Mus musculus 46-50
7758830-9 1995 The results suggest a role for retinoic acid in regulation of expression of the GLUT 4 gene in muscle cells. Tretinoin 31-44 solute carrier family 2 member 4 Homo sapiens 80-86
27437091-5 2016 Treatment of RA-stimulated differentiating SH-SY5Y cells with 0.3 to 3 mug/mL propolis resulted in decreased level of transglutaminase and 43-kDa growth-associated protein (GAP-43) in a dose-dependent manner. Tretinoin 13-15 growth associated protein 43 Homo sapiens 173-179
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 10-23 retinoic acid receptor gamma Homo sapiens 243-252
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 60-79 growth hormone releasing hormone receptor Rattus norvegicus 142-148
27052215-7 2016 Quantitative real-time PCR revealed that treatment with all-trans retinoic acid (ATRA; 10(-6) M) for 24 h increased gene expression levels of Ghrh-r and Ghs-r; however, expressions of Sst-r2 and Sst-r5 were unchanged. Tretinoin 81-85 growth hormone releasing hormone receptor Rattus norvegicus 142-148
27052215-8 2016 Combination treatment with the RAR-agonist Am80 and RXR-agonist PA024 mimicked the effects of ATRA on Ghrh-r and Ghs-r gene expressions. Tretinoin 94-98 growth hormone releasing hormone receptor Rattus norvegicus 102-108
7531436-6 1995 Both interleukin-1 and retinoic acid treatment caused an increase in aggrecan catabolism resulting in an increased release to the medium of specific aggrecan degradation products containing the BC-3 neoepitope generated by the action of "aggrecanase". Tretinoin 23-36 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 237-249
27052215-11 2016 Our results suggest that expressions of Ghrh-r and Ghs-r are regulated by RA through the RAR-RXR receptor complex and that RA enhances the effects of GHRH and ghrelin on GH release from the anterior pituitary gland. Tretinoin 74-76 growth hormone releasing hormone receptor Rattus norvegicus 40-46
27052215-11 2016 Our results suggest that expressions of Ghrh-r and Ghs-r are regulated by RA through the RAR-RXR receptor complex and that RA enhances the effects of GHRH and ghrelin on GH release from the anterior pituitary gland. Tretinoin 89-91 growth hormone releasing hormone receptor Rattus norvegicus 40-46
27320915-5 2016 Finally, RA regulates the competence of the endoderm to activate the Nkx2-1+ respiratory program in response to these mesodermal WNT and BMP signals. Tretinoin 9-11 bone morphogenetic protein 1 Homo sapiens 137-140
7532115-3 1995 Our results indicate that the differentiation markers cytokeratins K5 and K16 and transglutaminase type 1 are suppressed by all-trans-retinoic acid (RA). Tretinoin 124-147 keratin 16 Homo sapiens 74-77
7532115-3 1995 Our results indicate that the differentiation markers cytokeratins K5 and K16 and transglutaminase type 1 are suppressed by all-trans-retinoic acid (RA). Tretinoin 149-151 keratin 16 Homo sapiens 74-77
7832751-0 1995 Effect of retinoic acid on protein synthesis by foetal bovine chondrocytes in high-density culture: down-regulation of the glucose-regulated protein, GRP-78, and type II collagen. Tretinoin 10-23 heat shock protein family A (Hsp70) member 5 Bos taurus 150-156
27334688-8 2016 Induction of neural differentiation with retinoic acid resulted in downregulation of Sox2 and VRK1 that inversely correlated with the expression of differentiation markers such as N-cadherin, Pax6, mH2A1.2 and mH2A2. Tretinoin 41-54 macroH2A.2 histone Mus musculus 210-215
27055905-2 2016 We hypothesized that retinoic acid-related orphan nuclear receptor gamma (RORgamma) and its downstream effector, interleukin (IL)-17A, upregulate VEGF and hence are important treatment targets for neovascular retinopathies. Tretinoin 21-34 vascular endothelial growth factor A Rattus norvegicus 146-150
7851378-5 1995 However, when coincubated with activin A, retinoic acid specifically induced the synthesis of thromboxane-A-synthase-specific mRNA and induced an increase in enzyme activity with a synergistic effect on cyclooxygenase-1 protein and mRNA. Tretinoin 42-55 thromboxane A synthase 1, platelet Mus musculus 94-116
27182202-10 2016 Augmented downregulation of c-Myc protein expression was observed in the combination treatment with ATRA, VD3 and dasatinib compared to treatment with each reagent alone in HL-60 cells. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33
7756127-3 1995 This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA. Tretinoin 140-142 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 55-58
27146823-6 2016 The induction of HOTAIRM1 by ATRA was dependent on PU.1, and ectopic expression of PU.1 significantly up-regulated HOTAIRM1. Tretinoin 29-33 Spi-1 proto-oncogene Homo sapiens 83-87
7756127-3 1995 This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA. Tretinoin 210-212 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 55-58
8564566-0 1995 [Effect of translocation t(15;17) on the gene expression regulation of myeloblastin during all trans retinoic acid induced myeloid differentiation in human leukemic cells]. Tretinoin 101-114 proteinase 3 Homo sapiens 71-83
27013100-3 2016 Previously, we reported that nSMase2 is induced by all-trans retinoic acid (ATRA) in MCF7 cells and implicated nSMase2 in ATRA-induced growth arrest. Tretinoin 51-74 sphingomyelin phosphodiesterase 3 Homo sapiens 29-36
27013100-3 2016 Previously, we reported that nSMase2 is induced by all-trans retinoic acid (ATRA) in MCF7 cells and implicated nSMase2 in ATRA-induced growth arrest. Tretinoin 76-80 sphingomyelin phosphodiesterase 3 Homo sapiens 29-36
7586754-5 1995 Exogenous retinoic acid, a teratogen that is known to affect the formation of the midbrain-hindbrain boundary, has a profound affect on both wnt1 and pax2 expression at gastrulation. Tretinoin 10-23 wingless-type MMTV integration site family, member 1 Danio rerio 141-145
27013100-3 2016 Previously, we reported that nSMase2 is induced by all-trans retinoic acid (ATRA) in MCF7 cells and implicated nSMase2 in ATRA-induced growth arrest. Tretinoin 122-126 sphingomyelin phosphodiesterase 3 Homo sapiens 29-36
27013100-3 2016 Previously, we reported that nSMase2 is induced by all-trans retinoic acid (ATRA) in MCF7 cells and implicated nSMase2 in ATRA-induced growth arrest. Tretinoin 122-126 sphingomyelin phosphodiesterase 3 Homo sapiens 111-118
26582233-4 2016 Our data show that RA attenuated BSCB permeability and also attenuated the loss of tight junction molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in brain microvascular endothelial cells. Tretinoin 19-21 catenin beta 1 Homo sapiens 122-134
27050967-6 2016 Meanwhile, ATRA was shown to decrease the levels of IFN-gamma and increase the levels of IL-4 as well as the IFN-gamma/IL-4 ratio in STZ-treated animals (P < 0.05). Tretinoin 11-15 interleukin 4 Mus musculus 89-93
27050967-6 2016 Meanwhile, ATRA was shown to decrease the levels of IFN-gamma and increase the levels of IL-4 as well as the IFN-gamma/IL-4 ratio in STZ-treated animals (P < 0.05). Tretinoin 11-15 interleukin 4 Mus musculus 119-123
27050967-8 2016 This study demonstrated that ATRA effectively prevents the progression of T1DM in a murine model of the disease by reducing IFN-gamma levels and increasing IL-4 levels. Tretinoin 29-33 interleukin 4 Mus musculus 156-160
27081671-8 2016 Overexpression of StAR in mouse RAW 264.7 macrophages increased the effects of both all-trans retinoic acid (atRA) and 9-cis RA on cholesterol efflux, suggesting StAR enhances the efficacy of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) ligands. Tretinoin 94-107 steroidogenic acute regulatory protein Mus musculus 18-22
27081671-8 2016 Overexpression of StAR in mouse RAW 264.7 macrophages increased the effects of both all-trans retinoic acid (atRA) and 9-cis RA on cholesterol efflux, suggesting StAR enhances the efficacy of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) ligands. Tretinoin 109-113 steroidogenic acute regulatory protein Mus musculus 18-22
29242118-2 2018 In this study, we investigated the regulation of TG2 transamidase activity by NGF in retinoic acid-induced differentiating mouse N2a and human SH-SY5Y neuroblastoma cells. Tretinoin 85-98 transglutaminase 2, C polypeptide Mus musculus 49-52
8688195-1 1995 The three retinoic acid receptors (RAR alpha, RAR beta and RAR gamma) are known to modulate the transcription of target genes through interaction of the individual receptors with their naturally occurring ligand, retinoic acid (RA). Tretinoin 10-23 retinoic acid receptor, beta Mus musculus 46-54
29217200-6 2018 We further mapped how RA modulates the response to Wnt and BMP in a temporal specific manner. Tretinoin 22-24 bone morphogenetic protein 1 Homo sapiens 59-62
7798614-0 1994 Retinoic acid upregulates human Langerhans cell antigen presentation and surface expression of HLA-DR and CD11c, a beta 2 integrin critically involved in T-cell activation. Tretinoin 0-13 integrin subunit alpha X Homo sapiens 106-111
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 18-20 integrin subunit beta 1 Gallus gallus 228-242
27113312-6 2016 As the ATRA concentration enhanced and action time prolonged, the survival rate of RPE cells was reduced, but the expressions of HGF and MMP-2 increased, so did the secretion of HGF. Tretinoin 7-11 72 kDa type IV collagenase Oryctolagus cuniculus 137-142
26902198-4 2016 Additionally, ATRA effectively upregulated the protein level of NIS, and reversed EMT phenotype in alcohol treated cells, with absence in epithelial expression of E-cadherin and cytokeratin 18, as well as abnormal expression of Vimentin, urinary plasminogen activator (uPA), uPAR and Fibronectin.Compared with alcohol-treated group, both in vitro proliferation and invasion potential of ATRA treated cells markedly decreased (all P<0.05), and iodine uptake in vitro increased about 3.5-folds (P=0.007). Tretinoin 14-18 keratin 18 Homo sapiens 178-192
26902198-4 2016 Additionally, ATRA effectively upregulated the protein level of NIS, and reversed EMT phenotype in alcohol treated cells, with absence in epithelial expression of E-cadherin and cytokeratin 18, as well as abnormal expression of Vimentin, urinary plasminogen activator (uPA), uPAR and Fibronectin.Compared with alcohol-treated group, both in vitro proliferation and invasion potential of ATRA treated cells markedly decreased (all P<0.05), and iodine uptake in vitro increased about 3.5-folds (P=0.007). Tretinoin 14-18 vimentin Homo sapiens 228-236
7798615-1 1994 The cellular retinoic acid-binding proteins (CRABP I and II) are thought to mediate the effects of retinoic acid on target cells. Tretinoin 13-26 cellular retinoic acid binding protein 1 Homo sapiens 45-59
26902198-4 2016 Additionally, ATRA effectively upregulated the protein level of NIS, and reversed EMT phenotype in alcohol treated cells, with absence in epithelial expression of E-cadherin and cytokeratin 18, as well as abnormal expression of Vimentin, urinary plasminogen activator (uPA), uPAR and Fibronectin.Compared with alcohol-treated group, both in vitro proliferation and invasion potential of ATRA treated cells markedly decreased (all P<0.05), and iodine uptake in vitro increased about 3.5-folds (P=0.007). Tretinoin 14-18 plasminogen activator, urokinase receptor Homo sapiens 275-279
26902198-6 2016 CONCLUSIONS: ATRA can increase functional expression of NIS via downregulating transcriptional activity of beta-catenin and promote isotope sensitivity to radio-iodine in human undifferentiated thyroid cancer. Tretinoin 13-17 catenin beta 1 Homo sapiens 107-119
28815778-4 2018 In Retinoic acid (RA) induced in vitro differentiation assays, the expression of germ cell marker genes, cvh, c-kit, integrin alpha6 and integrin beta1, was observed to upregulate while activating JNK signaling significantly. Tretinoin 3-16 KIT proto-oncogene, receptor tyrosine kinase Gallus gallus 110-115
28815778-4 2018 In Retinoic acid (RA) induced in vitro differentiation assays, the expression of germ cell marker genes, cvh, c-kit, integrin alpha6 and integrin beta1, was observed to upregulate while activating JNK signaling significantly. Tretinoin 3-16 integrin subunit beta 1 Gallus gallus 137-151
28815778-4 2018 In Retinoic acid (RA) induced in vitro differentiation assays, the expression of germ cell marker genes, cvh, c-kit, integrin alpha6 and integrin beta1, was observed to upregulate while activating JNK signaling significantly. Tretinoin 18-20 KIT proto-oncogene, receptor tyrosine kinase Gallus gallus 110-115
26747727-5 2016 Mechanistically, ATRA cooperated with Wnt3A to induce beta-catenin translocation from cell-cell contacts into the cytosol and nucleus, thereby activating Wnt/beta-catenin signalling. Tretinoin 17-21 catenin beta 1 Homo sapiens 54-66
28815778-4 2018 In Retinoic acid (RA) induced in vitro differentiation assays, the expression of germ cell marker genes, cvh, c-kit, integrin alpha6 and integrin beta1, was observed to upregulate while activating JNK signaling significantly. Tretinoin 18-20 integrin subunit beta 1 Gallus gallus 137-151
26747727-5 2016 Mechanistically, ATRA cooperated with Wnt3A to induce beta-catenin translocation from cell-cell contacts into the cytosol and nucleus, thereby activating Wnt/beta-catenin signalling. Tretinoin 17-21 catenin beta 1 Homo sapiens 158-170
7798615-1 1994 The cellular retinoic acid-binding proteins (CRABP I and II) are thought to mediate the effects of retinoic acid on target cells. Tretinoin 99-112 cellular retinoic acid binding protein 1 Homo sapiens 45-59
26747727-7 2016 beta-catenin silencing abolished the stimulatory effect of ATRA on Wnt3A-induced alkaline phosphatase (ALP) activity and reversed its inhibitory effect on Cyp26a1 expression. Tretinoin 59-63 catenin beta 1 Homo sapiens 0-12
28190238-5 2018 Our results indicate that overexpression of wild-type or mutant A53T alpha-SYN attenuated the RA-induced upregulation of tyrosine hydroxylase and dopamine transporter as well as neurite outgrowth in SH-SY5Y cells. Tretinoin 94-96 synuclein alpha Homo sapiens 69-78
7961696-4 1994 When the cells were treated with retinoic acid either alone or in the presence of cAMP for 120 h, PKC alpha mRNA and protein levels increased, whereas those of PKC beta and PKC gamma became undetectable. Tretinoin 33-46 protein kinase C beta Homo sapiens 160-168
28190238-6 2018 In addition, GSK-3beta inactivation and downstream beta-catenin stabilization were associated with RA-induced differentiation, which was attenuated by alpha-SYN. Tretinoin 99-101 catenin beta 1 Homo sapiens 51-63
28190238-6 2018 In addition, GSK-3beta inactivation and downstream beta-catenin stabilization were associated with RA-induced differentiation, which was attenuated by alpha-SYN. Tretinoin 99-101 synuclein alpha Homo sapiens 151-160
28190238-7 2018 Moreover, protein phosphatase 2A was positively regulated by alpha-SYN and was implicated in the alpha-SYN-mediated interference with RA signaling. Tretinoin 134-136 synuclein alpha Homo sapiens 61-70
28190238-7 2018 Moreover, protein phosphatase 2A was positively regulated by alpha-SYN and was implicated in the alpha-SYN-mediated interference with RA signaling. Tretinoin 134-136 synuclein alpha Homo sapiens 97-106
28945224-6 2018 MCL1 was upregulated by RA treatment upon RaRF depletion, accompanying leukemic myeloblast differentiation, which is negatively regulated by ectopic RaRF expression. Tretinoin 24-26 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 0-4
26840068-0 2016 Retinoic Acid Specifically Enhances Embryonic Stem Cell Metastate Marked by Zscan4. Tretinoin 0-13 zinc finger and SCAN domain containing 4 Homo sapiens 76-82
26840068-4 2016 Here, we report that in ESC cultures treated with retinoic acid (RA), Zscan4 ESCs metastate is strongly enhanced. Tretinoin 50-63 zinc finger and SCAN domain containing 4 Homo sapiens 70-76
26840068-4 2016 Here, we report that in ESC cultures treated with retinoic acid (RA), Zscan4 ESCs metastate is strongly enhanced. Tretinoin 65-67 zinc finger and SCAN domain containing 4 Homo sapiens 70-76
26840068-6 2016 Remarkably, Zscan4 metastate induced by RA lacks canonical pluripotency genes Oct3/4 and Nanog but retained both self-renewal and pluripotency capabilities. Tretinoin 40-42 zinc finger and SCAN domain containing 4 Homo sapiens 12-18
26840068-6 2016 Remarkably, Zscan4 metastate induced by RA lacks canonical pluripotency genes Oct3/4 and Nanog but retained both self-renewal and pluripotency capabilities. Tretinoin 40-42 POU class 5 homeobox 1 Homo sapiens 78-84
26700766-0 2016 LZTFL1 Upregulated by All-Trans Retinoic Acid during CD4+ T Cell Activation Enhances IL-5 Production. Tretinoin 32-45 leucine zipper transcription factor like 1 Homo sapiens 0-6
26700766-3 2016 Leucine zipper transcription factor-like 1 (LZTFL1) was upregulated by ATRA in a dose- and time-dependent manner. Tretinoin 71-75 leucine zipper transcription factor like 1 Homo sapiens 0-42
29337667-6 2018 In this revised view, ISL1 is antagonized by retinoic acid signaling via a novel player, MEIS2. Tretinoin 45-58 ISL LIM homeobox 1 Homo sapiens 22-26
7525098-0 1994 Retinoic acid-induced normal and tumor-associated aberrant expression of the murine keratin K13 gene does not involve a promotor sequence with striking homology to a natural retinoic acid responsive element. Tretinoin 0-13 keratin 13 Mus musculus 92-95
29170140-0 2018 A novel controlled release formulation of the Pin1 inhibitor ATRA to improve liver cancer therapy by simultaneously blocking multiple cancer pathways. Tretinoin 61-65 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 46-50
26700766-3 2016 Leucine zipper transcription factor-like 1 (LZTFL1) was upregulated by ATRA in a dose- and time-dependent manner. Tretinoin 71-75 leucine zipper transcription factor like 1 Homo sapiens 44-50
26700766-7 2016 Knockdown of LZTFL1 reduced the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overexpression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important regulator of ATRA-induced T cell response. Tretinoin 43-47 leucine zipper transcription factor like 1 Homo sapiens 13-19
26700766-7 2016 Knockdown of LZTFL1 reduced the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overexpression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important regulator of ATRA-induced T cell response. Tretinoin 213-217 leucine zipper transcription factor like 1 Homo sapiens 112-118
26700766-7 2016 Knockdown of LZTFL1 reduced the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overexpression of LZTFL1 enhanced the TCR-mediated NFAT signaling, suggesting that LZTFL1 is an important regulator of ATRA-induced T cell response. Tretinoin 213-217 leucine zipper transcription factor like 1 Homo sapiens 112-118
29170140-2 2018 The identification of all-trans retinoic acid (ATRA) as a potent Pin1 inhibitor provides a promising candidate for HCC targeted therapy because Pin1 is overexpressed in most HCC and activates numerous cancer-driving pathways. Tretinoin 22-45 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 65-69
29170140-2 2018 The identification of all-trans retinoic acid (ATRA) as a potent Pin1 inhibitor provides a promising candidate for HCC targeted therapy because Pin1 is overexpressed in most HCC and activates numerous cancer-driving pathways. Tretinoin 22-45 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 144-148
7525098-3 1994 As in cultured primary keratinocytes from normal internal stratified epithelia, the in vitro expression of K13 in transformed epidermal cell lines can be induced either by Ca2+ or by retinoic acid (RA). Tretinoin 183-196 keratin 13 Mus musculus 107-110
29170140-2 2018 The identification of all-trans retinoic acid (ATRA) as a potent Pin1 inhibitor provides a promising candidate for HCC targeted therapy because Pin1 is overexpressed in most HCC and activates numerous cancer-driving pathways. Tretinoin 47-51 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 65-69
29170140-2 2018 The identification of all-trans retinoic acid (ATRA) as a potent Pin1 inhibitor provides a promising candidate for HCC targeted therapy because Pin1 is overexpressed in most HCC and activates numerous cancer-driving pathways. Tretinoin 47-51 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 144-148
7525098-3 1994 As in cultured primary keratinocytes from normal internal stratified epithelia, the in vitro expression of K13 in transformed epidermal cell lines can be induced either by Ca2+ or by retinoic acid (RA). Tretinoin 198-200 keratin 13 Mus musculus 107-110
29170140-9 2018 Indeed, Pin1 knock-down abolished ATRA inhibitory effects on HCC cells and ATRA-PLLA did not inhibit normal liver cells, as expected because ATRA selectively inhibits active Pin1 in cancer cells. Tretinoin 34-38 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 8-12
27803451-3 2016 GDF3 and OCT4 was highly expressed in undifferentiated NCCIT cells and then significantly decreased upon retinoic acid-induced differentiation in a time-dependent manner. Tretinoin 105-118 growth differentiation factor 3 Homo sapiens 0-4
27803451-3 2016 GDF3 and OCT4 was highly expressed in undifferentiated NCCIT cells and then significantly decreased upon retinoic acid-induced differentiation in a time-dependent manner. Tretinoin 105-118 POU class 5 homeobox 1 Homo sapiens 9-13
7525098-4 1994 We have found that the promoter of the K13 gene contains a sequence element GGTTCA(N)5TGTTCT, in the following referred to as K13-RARE, that is highly related to the natural retinoic acid responsive element (RARE) of the retinoic acid receptor beta 2 gene. Tretinoin 174-187 keratin 13 Mus musculus 39-42
7525098-4 1994 We have found that the promoter of the K13 gene contains a sequence element GGTTCA(N)5TGTTCT, in the following referred to as K13-RARE, that is highly related to the natural retinoic acid responsive element (RARE) of the retinoic acid receptor beta 2 gene. Tretinoin 174-187 keratin 13 Mus musculus 126-134
7720566-0 1994 Relationship between retinoic acid and sonic hedgehog, two polarizing signals in the chick wing bud. Tretinoin 21-34 sonic hedgehog Gallus gallus 39-53
26188161-7 2015 Conversely, in the mouse model, the observed decrease in Dio3 expression could be explained by increased levels of inhibitory histone modifications in the Dio3 promoter region, suggesting that overactive RA signaling may ectopically derepress TH signaling. Tretinoin 204-206 deiodinase, iodothyronine type III Mus musculus 57-61
26188161-7 2015 Conversely, in the mouse model, the observed decrease in Dio3 expression could be explained by increased levels of inhibitory histone modifications in the Dio3 promoter region, suggesting that overactive RA signaling may ectopically derepress TH signaling. Tretinoin 204-206 deiodinase, iodothyronine type III Mus musculus 155-159
29587291-7 2018 Circulating irisin levels were increased by 5-fold in ATRA-treated mice, linked to increased Fndc5 transcription in liver and adipose tissues, rather than skeletal muscle. Tretinoin 54-58 fibronectin type III domain containing 5 Mus musculus 93-98
29587291-8 2018 Immunohistochemistry analysis of FNDC5 suggested that ATRA treatment enhances the release of FNDC5/irisin from skeletal muscle and the liver and its accumulation in interscapular brown and inguinal white adipose depots. Tretinoin 54-58 fibronectin type III domain containing 5 Mus musculus 33-38
29587291-8 2018 Immunohistochemistry analysis of FNDC5 suggested that ATRA treatment enhances the release of FNDC5/irisin from skeletal muscle and the liver and its accumulation in interscapular brown and inguinal white adipose depots. Tretinoin 54-58 fibronectin type III domain containing 5 Mus musculus 93-98
7867896-0 1994 Retinoic acid prevents downregulation of ras recision gene/lysyl oxidase early in adipocyte differentiation. Tretinoin 0-13 lysyl oxidase Mus musculus 41-53
29984664-5 2018 METHODS: Real-time RT-PCR was used to examine the expression of genes families involved in xenobiotic metabolism, such as CYP1 (CYP1A1, CYP1B1), CYP2 (CYP2E1, CYP2D6), CYP3 (CYP3A4); and of a family involved in the catabolism of the all-trans-retinoic acid (ATRA), CYP26 (CYP26A1, CYP26B1). Tretinoin 233-256 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 122-126
29984664-5 2018 METHODS: Real-time RT-PCR was used to examine the expression of genes families involved in xenobiotic metabolism, such as CYP1 (CYP1A1, CYP1B1), CYP2 (CYP2E1, CYP2D6), CYP3 (CYP3A4); and of a family involved in the catabolism of the all-trans-retinoic acid (ATRA), CYP26 (CYP26A1, CYP26B1). Tretinoin 233-256 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 128-134
29984664-5 2018 METHODS: Real-time RT-PCR was used to examine the expression of genes families involved in xenobiotic metabolism, such as CYP1 (CYP1A1, CYP1B1), CYP2 (CYP2E1, CYP2D6), CYP3 (CYP3A4); and of a family involved in the catabolism of the all-trans-retinoic acid (ATRA), CYP26 (CYP26A1, CYP26B1). Tretinoin 258-262 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 122-126
29984664-5 2018 METHODS: Real-time RT-PCR was used to examine the expression of genes families involved in xenobiotic metabolism, such as CYP1 (CYP1A1, CYP1B1), CYP2 (CYP2E1, CYP2D6), CYP3 (CYP3A4); and of a family involved in the catabolism of the all-trans-retinoic acid (ATRA), CYP26 (CYP26A1, CYP26B1). Tretinoin 258-262 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 128-134
26635706-8 2015 Recently FOXP2 was found to regulate genes involved in retinoic acid (RA) signaling and to modify the cellular response to RA, a key regulator of brain development. Tretinoin 55-68 forkhead box P2 Homo sapiens 9-14
26635706-8 2015 Recently FOXP2 was found to regulate genes involved in retinoic acid (RA) signaling and to modify the cellular response to RA, a key regulator of brain development. Tretinoin 70-72 forkhead box P2 Homo sapiens 9-14
26635706-8 2015 Recently FOXP2 was found to regulate genes involved in retinoic acid (RA) signaling and to modify the cellular response to RA, a key regulator of brain development. Tretinoin 123-125 forkhead box P2 Homo sapiens 9-14
7867896-0 1994 Retinoic acid prevents downregulation of ras recision gene/lysyl oxidase early in adipocyte differentiation. Tretinoin 0-13 lysyl oxidase Mus musculus 59-72
7867896-8 1994 RA completely blocked the differ-entiation-related reduction in rrg/lysyl oxidase gene expression, although RA had no independent stimulatory effect on rrg/lysyl oxidase expression in cells not exposed to differentiating conditions. Tretinoin 0-2 lysyl oxidase Mus musculus 68-81
29224413-9 2018 Interestingly, the combination of GSK-J4 and all-trans retinoic acid (ATRA) significantly increased PML-RARalpha-positive cell apoptosis compared with ATRA treatment alone. Tretinoin 45-68 PML nuclear body scaffold Homo sapiens 100-103
7867896-9 1994 Thus, differential display has been successfully used to identify rrg/lysyl oxidase as an early marker for adipose conversion that is responsive to RA. Tretinoin 148-150 lysyl oxidase Mus musculus 70-83
29224413-9 2018 Interestingly, the combination of GSK-J4 and all-trans retinoic acid (ATRA) significantly increased PML-RARalpha-positive cell apoptosis compared with ATRA treatment alone. Tretinoin 45-68 retinoic acid receptor alpha Homo sapiens 104-112
26592976-2 2015 Here we show that these biological compounds also regulate gene expression and that they do so by controlling the transcriptional activities of the retinoic acid (RA)-activated nuclear receptors RAR and PPARbeta/delta. Tretinoin 148-161 retinoic acid receptor alpha Homo sapiens 195-198
26592976-2 2015 Here we show that these biological compounds also regulate gene expression and that they do so by controlling the transcriptional activities of the retinoic acid (RA)-activated nuclear receptors RAR and PPARbeta/delta. Tretinoin 163-165 retinoic acid receptor alpha Homo sapiens 195-198
29224413-9 2018 Interestingly, the combination of GSK-J4 and all-trans retinoic acid (ATRA) significantly increased PML-RARalpha-positive cell apoptosis compared with ATRA treatment alone. Tretinoin 70-74 PML nuclear body scaffold Homo sapiens 100-103
7958449-6 1994 This RA effect is particularly interesting since under conditions of RA excess, RAR beta 2 promoter activity and transcript accumulation are induced in regions of developing embryos in which malformations subsequently appear, such as the craniofacial region, the hindbrain, and the limbs. Tretinoin 5-7 retinoic acid receptor, beta Mus musculus 80-88
29224413-9 2018 Interestingly, the combination of GSK-J4 and all-trans retinoic acid (ATRA) significantly increased PML-RARalpha-positive cell apoptosis compared with ATRA treatment alone. Tretinoin 70-74 retinoic acid receptor alpha Homo sapiens 104-112
7958449-6 1994 This RA effect is particularly interesting since under conditions of RA excess, RAR beta 2 promoter activity and transcript accumulation are induced in regions of developing embryos in which malformations subsequently appear, such as the craniofacial region, the hindbrain, and the limbs. Tretinoin 69-71 retinoic acid receptor, beta Mus musculus 80-88
7958450-4 1994 Oct-4 protein is present in both embryonic stem cells and embryonal carcinoma cells, but is down-regulated following differentiation of these cells by culture in the absence of leukemia inhibitory factor or in the presence of retinoic acid, respectively. Tretinoin 226-239 POU domain, class 5, transcription factor 1, related sequence 1 Mus musculus 0-5
26181105-6 2015 ECS activation and RA exposure increased lipid abundance and the expression of lipoprotein lipase. Tretinoin 19-21 lipoprotein lipase Danio rerio 79-97
7958454-8 1994 Similarly to the parental cell line, addition of RA to P19 cells overexpressing Wnt-1 induced the neuroectodermal pathway, but expression of cell type-specific markers such as MASH-1, HNK-1, and GAP-43 was diminished and the morphology of neuronal processes, stained with an antibody to neurofilament, was abnormal. Tretinoin 49-51 achaete-scute family bHLH transcription factor 1 Homo sapiens 176-182
28833556-2 2018 This hypothesis predicts that isotretinoin (13-cis retinoic acid), the prodrug of all-trans retinoic acid (ATRA), exaggerates neural crest cell (NCC) apoptosis via upregulation of the pro-apoptotic transcription factor p53, the guardian of the genome. Tretinoin 51-64 tumor protein p53 Danio rerio 219-222
28833556-2 2018 This hypothesis predicts that isotretinoin (13-cis retinoic acid), the prodrug of all-trans retinoic acid (ATRA), exaggerates neural crest cell (NCC) apoptosis via upregulation of the pro-apoptotic transcription factor p53, the guardian of the genome. Tretinoin 107-111 tumor protein p53 Danio rerio 219-222
7868977-6 1994 Treatment of vitamin A-deficient rats with a single dose of retinoic acid (20 micrograms, 20 h before tissues were collected) reduced the hepatic apoA-I mRNA/beta-actin ratio by about 40%, while further reduction (about 60-65%) was observed after two treatments with retinoic acid. Tretinoin 60-73 actin, beta Rattus norvegicus 158-168
28540746-0 2018 KDM3B shows tumor-suppressive activity and transcriptionally regulates HOXA1 through retinoic acid response elements in acute myeloid leukemia. Tretinoin 85-98 lysine demethylase 3B Homo sapiens 0-5
28540746-6 2018 We further showed KDM3B binding at retinoic acid response elements (RARE) but not at the promoter region of HOXA1 gene. Tretinoin 35-48 lysine demethylase 3B Homo sapiens 18-23
26249743-8 2015 Hox gene activity, under the influence of retinoic acid signalling, is directly linked with the initiation of Tbx5 gene expression in the region along the antero-posterior axis of the body that will form wings/forelimbs and determines antero-posterior polarity of the buds. Tretinoin 42-55 T-box 5 Gallus gallus 110-114
25975191-6 2015 Importantly, all-trans retinoic acid (ATRA) increased CD38 expression levels but also reduced expression of the complement-inhibitory proteins CD55 and CD59 in both cell lines and primary MM samples. Tretinoin 13-36 CD38 molecule Homo sapiens 54-58
25975191-6 2015 Importantly, all-trans retinoic acid (ATRA) increased CD38 expression levels but also reduced expression of the complement-inhibitory proteins CD55 and CD59 in both cell lines and primary MM samples. Tretinoin 38-42 CD38 molecule Homo sapiens 54-58
29973452-2 2018 The advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) as molecular targeted therapies directed against PML-RARalpha has been a major breakthrough in APL treatment. Tretinoin 14-37 PML nuclear body scaffold Homo sapiens 121-124
7929425-0 1994 Apolipoprotein D gene induction by retinoic acid is concomitant with growth arrest and cell differentiation in human breast cancer cells. Tretinoin 35-48 apolipoprotein D Homo sapiens 0-16
29973452-2 2018 The advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) as molecular targeted therapies directed against PML-RARalpha has been a major breakthrough in APL treatment. Tretinoin 14-37 retinoic acid receptor alpha Homo sapiens 125-133
29973452-2 2018 The advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) as molecular targeted therapies directed against PML-RARalpha has been a major breakthrough in APL treatment. Tretinoin 39-43 PML nuclear body scaffold Homo sapiens 121-124
29973452-2 2018 The advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) as molecular targeted therapies directed against PML-RARalpha has been a major breakthrough in APL treatment. Tretinoin 39-43 retinoic acid receptor alpha Homo sapiens 125-133
26305673-9 2015 In conclusion, ALDH1 expression in tumor-associated stromal cells indicates reduced BrCa progression, possibly via RA secretion. Tretinoin 115-117 aldehyde dehydrogenase 1 family member A1 Homo sapiens 15-20
26378784-7 2015 In the presence of Dazl, RA induces at least two pathways: one Stra8-independent, and one Stra8-dependent. Tretinoin 25-27 stimulated by retinoic acid gene 8 Mus musculus 90-95
7929425-1 1994 We have examined the regulation by retinoic acid of the gene encoding apolipoprotein D (apoD), a human plasma protein belonging to the superfamily of the lipocalins that is produced by a specific subtype of highly differentiated breast carcinomas. Tretinoin 35-48 apolipoprotein D Homo sapiens 70-86
26116234-5 2015 In addition, treatment of the GT1-7 cells with RA dose-dependently inhibited the expression of GnRH mRNA. Tretinoin 47-49 gonadotropin releasing hormone 1 Mus musculus 95-99
29234114-0 2017 Probing the requirement for CD38 in retinoic acid-induced HL-60 cell differentiation with a small molecule dimerizer and genetic knockout. Tretinoin 36-49 CD38 molecule Homo sapiens 28-32
29234114-4 2017 In all-trans retinoic acid (RA)-induced differentiation of acute promyelocytic leukaemia and HL-60 cells, CD38 is one of the earliest and most prominently upregulated proteins known. Tretinoin 13-26 CD38 molecule Homo sapiens 106-110
7929425-1 1994 We have examined the regulation by retinoic acid of the gene encoding apolipoprotein D (apoD), a human plasma protein belonging to the superfamily of the lipocalins that is produced by a specific subtype of highly differentiated breast carcinomas. Tretinoin 35-48 apolipoprotein D Homo sapiens 88-92
29234114-4 2017 In all-trans retinoic acid (RA)-induced differentiation of acute promyelocytic leukaemia and HL-60 cells, CD38 is one of the earliest and most prominently upregulated proteins known. Tretinoin 28-30 CD38 molecule Homo sapiens 106-110
26240147-0 2015 All-trans-retinoic acid reduces BACE1 expression under inflammatory conditions via modulation of nuclear factor kappaB (NFkappaB) signaling. Tretinoin 0-23 beta-site APP cleaving enzyme 1 Mus musculus 32-37
26240147-4 2015 Previous studies have suggested that there is therapeutic potential for retinoic acid in treating neurodegeneration based on decreased Abeta. Tretinoin 72-85 amyloid beta (A4) precursor protein Mus musculus 135-140
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 Meis homeobox 2 Homo sapiens 139-144
7929425-2 1994 Northern blot analysis revealed that all-trans-retinoic acid (RA) strongly induced the accumulation of apoD mRNA in T-47D and ZR-75-1 estrogen receptor-positive human breast cancer cells in a time- and dose-dependent manner, while no inductive effect was observed in estrogen receptor-negative cell lines, including MDA-MB-231 and MDA-MB-435. Tretinoin 37-60 apolipoprotein D Homo sapiens 103-107
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 fibroblast growth factor receptor 2 Homo sapiens 220-225
26240147-7 2015 We found that administration of all-trans-retinoic acid (atRA) down-regulated the expression of BACE1 in the brains of Tg2576 mice and in mice fed a high fat diet. Tretinoin 32-55 beta-site APP cleaving enzyme 1 Mus musculus 96-101
26240147-7 2015 We found that administration of all-trans-retinoic acid (atRA) down-regulated the expression of BACE1 in the brains of Tg2576 mice and in mice fed a high fat diet. Tretinoin 57-61 beta-site APP cleaving enzyme 1 Mus musculus 96-101
26240147-8 2015 Moreover, in LPS-treated mice and cultured neurons, BACE1 expression was repressed by the addition of atRA, correlating with the anti-inflammatory efficacy of atRA. Tretinoin 102-106 beta-site APP cleaving enzyme 1 Mus musculus 52-57
7929425-2 1994 Northern blot analysis revealed that all-trans-retinoic acid (RA) strongly induced the accumulation of apoD mRNA in T-47D and ZR-75-1 estrogen receptor-positive human breast cancer cells in a time- and dose-dependent manner, while no inductive effect was observed in estrogen receptor-negative cell lines, including MDA-MB-231 and MDA-MB-435. Tretinoin 62-64 apolipoprotein D Homo sapiens 103-107
26240147-8 2015 Moreover, in LPS-treated mice and cultured neurons, BACE1 expression was repressed by the addition of atRA, correlating with the anti-inflammatory efficacy of atRA. Tretinoin 159-163 beta-site APP cleaving enzyme 1 Mus musculus 52-57
26240147-9 2015 Mutations of the NFkappaB binding site in BACE1 promoter abolished the suppressive effect of atRA. Tretinoin 93-97 beta-site APP cleaving enzyme 1 Mus musculus 42-47
26240147-10 2015 Furthermore, atRA disrupted LPS-induced nuclear translocation of NFkappaB and its binding to BACE1 promoter as well as promoting the recruitment of the corepressor NCoR. Tretinoin 13-17 beta-site APP cleaving enzyme 1 Mus musculus 93-98
26240147-11 2015 Our findings indicate that atRA represses BACE1 gene expression under inflammatory conditions via the modulation of NFkappaB signaling. Tretinoin 27-31 beta-site APP cleaving enzyme 1 Mus musculus 42-47
28732729-6 2017 We superimposed the structure of retinoic acid bound to human ALDH1A3 onto the BcALDH structure and speculated a model of the substrate all-trans-retinal bound to BcALDH. Tretinoin 33-46 aldehyde dehydrogenase 1 family member A3 Homo sapiens 62-69
7929425-3 1994 The effect of RA on apoD expression by T-47D cells was at least 12-fold more potent than the effect of the steroids dihydrotestosterone and dexamethasone, which had been previously described as hormonal up-regulators of apoD expression in these cells. Tretinoin 14-16 apolipoprotein D Homo sapiens 20-24
7929425-3 1994 The effect of RA on apoD expression by T-47D cells was at least 12-fold more potent than the effect of the steroids dihydrotestosterone and dexamethasone, which had been previously described as hormonal up-regulators of apoD expression in these cells. Tretinoin 14-16 apolipoprotein D Homo sapiens 220-224
7929425-4 1994 A time course study demonstrated that the induction of apoD mRNA reached a level of 15-fold over the untreated control cells after 48 h of incubation in the presence of a 10(-7) M concentration of RA. Tretinoin 197-199 apolipoprotein D Homo sapiens 55-59
28981191-3 2017 All-trans retinoic acid (atRA) releases RARalpha from its target mRNA. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 40-48
28981191-3 2017 All-trans retinoic acid (atRA) releases RARalpha from its target mRNA. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 40-48
26313912-1 2015 All-trans retinoic acid (ATRA), a pan-retinoic acid receptor (RAR) agonist, is, along with other retinoids, a promising therapeutic agent for the treatment of a variety of solid tumors. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 34-60
7929425-8 1994 By contrast, treatment of the T-47D cells with RA produced an increase of approximately 8-fold in the rate of transcription of the apoD gene. Tretinoin 47-49 apolipoprotein D Homo sapiens 131-135
26313912-1 2015 All-trans retinoic acid (ATRA), a pan-retinoic acid receptor (RAR) agonist, is, along with other retinoids, a promising therapeutic agent for the treatment of a variety of solid tumors. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 62-65
26313912-1 2015 All-trans retinoic acid (ATRA), a pan-retinoic acid receptor (RAR) agonist, is, along with other retinoids, a promising therapeutic agent for the treatment of a variety of solid tumors. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 34-60
28981191-7 2017 Methods Isolated human platelets were treated with the pan-RAR agonist all-trans-retinoic acid (atRA). Tretinoin 71-94 retinoic acid receptor alpha Homo sapiens 59-62
28981191-7 2017 Methods Isolated human platelets were treated with the pan-RAR agonist all-trans-retinoic acid (atRA). Tretinoin 96-100 retinoic acid receptor alpha Homo sapiens 59-62
7929425-9 1994 Furthermore, treatment of the T-47D cells with RA induced the synthesis and secretion to the culture medium of apoD. Tretinoin 47-49 apolipoprotein D Homo sapiens 111-115
28981191-12 2017 When platelets were treated with atRA, binding interactions between RARalpha protein and mRNA for MAP1LC3B2, SLAIN2 and ANGPT1 were significantly decreased. Tretinoin 33-37 retinoic acid receptor alpha Homo sapiens 68-76
26313912-1 2015 All-trans retinoic acid (ATRA), a pan-retinoic acid receptor (RAR) agonist, is, along with other retinoids, a promising therapeutic agent for the treatment of a variety of solid tumors. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 62-65
26313912-9 2015 In summary, our findings demonstrate that ATRA-induced autophagy is mediated by RARalpha in breast cancer cells. Tretinoin 42-46 retinoic acid receptor alpha Homo sapiens 80-88
28981191-12 2017 When platelets were treated with atRA, binding interactions between RARalpha protein and mRNA for MAP1LC3B2, SLAIN2 and ANGPT1 were significantly decreased. Tretinoin 33-37 microtubule associated protein 1 light chain 3 beta 2 Homo sapiens 98-107
7945330-2 1994 Upon differentiation with retinoic acid (RA), transcription of the Rex-1 gene decreases rapidly. Tretinoin 26-39 ZFP42 zinc finger protein Homo sapiens 67-72
26235895-5 2015 Treatment with BIO, a GSK3s inhibitor, significantly increased disease remission by enhancing renal progenitor sensitivity to the differentiation effect of endogenous retinoic acid. Tretinoin 167-180 glycogen synthase kinase 3 beta Mus musculus 22-26
28923486-4 2017 In this study we tested the requirement of multiple signaling pathways, such as Wnt, Bmp Fgf, and Retinoic Acid for aLLp and pLLp induction. Tretinoin 98-111 plasmolipin Danio rerio 125-129
7945330-2 1994 Upon differentiation with retinoic acid (RA), transcription of the Rex-1 gene decreases rapidly. Tretinoin 41-43 ZFP42 zinc finger protein Homo sapiens 67-72
28923486-5 2017 We determined that aLLp specification requires Fgf signaling, whilst pLLp specification requires retinoic acid which inhibits Fgf signaling. Tretinoin 97-110 plasmolipin Danio rerio 69-73
7916164-0 1994 Role of a conserved retinoic acid response element in rhombomere restriction of Hoxb-1. Tretinoin 20-33 homeobox B1 Mus musculus 80-86
29972949-8 2017 Moreover, atRA decreased the levels of p-Smad2 and Smad4 in embryonic palate mesenchymal cells, whereas the expression of Smad7 was significantly increased at GD14 and GD15. Tretinoin 10-14 SMAD family member 4 Mus musculus 51-56
26238290-11 2015 Treatment of N2a cells with RA induced marked differentiation and neurite outgrowth accompanied by significantly increased Omi and decreased E2F1 levels, which were suppressed by pretreatment with the specific Omi inhibitor UCF-101. Tretinoin 28-30 E2F transcription factor 1 Mus musculus 141-145
8093047-1 1994 An ecto-enzyme of NAD glycohydrolase induced by retinoic acid in human leukemic HL-60 cells is attributed to the molecule of leukocyte cell surface antigen CD38 (Kontani, K., et al. Tretinoin 48-61 tripartite motif containing 33 Homo sapiens 3-7
26059631-6 2015 Finally, miR-125b-2 overexpression was found to impair all-trans-retinoic acid-induced neuron development in embryoid bodies. Tretinoin 65-78 microRNA 125b-2 Mus musculus 9-19
26186544-3 2015 Here we show that three groups of diterpenoids emerged: 1) GGA, 2,3-dihydro GGA and 9-cis retinoic acid induce cell death and XBP1 splicing; 2) all-trans retinoic acid induces XBP1 splicing but little cell death; and 3) phytanic acid, phytenic acid and geranylgeraniol induce neither cell death nor XBP1 splicing. Tretinoin 90-103 X-box binding protein 1 Homo sapiens 126-130
26186544-3 2015 Here we show that three groups of diterpenoids emerged: 1) GGA, 2,3-dihydro GGA and 9-cis retinoic acid induce cell death and XBP1 splicing; 2) all-trans retinoic acid induces XBP1 splicing but little cell death; and 3) phytanic acid, phytenic acid and geranylgeraniol induce neither cell death nor XBP1 splicing. Tretinoin 90-103 X-box binding protein 1 Homo sapiens 176-180
28374919-13 2017 The results revealed that ATRA reversed arsenic-induced free radical generation, activated the anti-oxidant defence system, and subsequently repressed p53-dependent apoptosis through inhibition of the MAPK signaling components. Tretinoin 26-30 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 151-154
28667519-0 2017 Retinoic acid ameliorates high-fat diet-induced liver steatosis through sirt1. Tretinoin 0-13 sirtuin 1 Mus musculus 72-77
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 89-102 glutamic pyruvic transaminase, soluble Mus musculus 269-289
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 89-102 glutamic pyruvic transaminase, soluble Mus musculus 291-294
26186544-3 2015 Here we show that three groups of diterpenoids emerged: 1) GGA, 2,3-dihydro GGA and 9-cis retinoic acid induce cell death and XBP1 splicing; 2) all-trans retinoic acid induces XBP1 splicing but little cell death; and 3) phytanic acid, phytenic acid and geranylgeraniol induce neither cell death nor XBP1 splicing. Tretinoin 90-103 X-box binding protein 1 Homo sapiens 176-180
26173116-5 2015 We could show that in WERI-Rb1 cells RA/BMP-4 mediated cell death is at least partially caspase-dependent, whereby RA and BMP-4 additively increased (i) Apaf-1 mRNA levels, (ii) caspase-9 cleavage activity and (iii) the number of activated, cleaved caspase-3 positive cells. Tretinoin 37-39 caspase 9 Homo sapiens 178-187
26173116-6 2015 Compared to single application of RA and BMP-4, combined RA/BMP-4 treatment significantly augments mRNA levels of the retinoic acid receptors (RARs) RARalpha and RARss and the retinoic X receptor (RXR) RXRgamma suggesting an interaction in the induction of these RA receptor subtypes in WERI-Rb1 cells. Tretinoin 34-36 retinoic acid receptor alpha Homo sapiens 149-157
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 89-102 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 300-326
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 89-102 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 328-331
7519122-5 1994 Interestingly, retinoic acid (RA) treatment suppresses the differentiation blockade induced by high level PML-RAR alpha protein; indeed, Zn(2+)-treated MTPR9 cells incubated with RA plus D3 exhibited significant terminal monocytic maturation, comparable to that of cells treated with D3 alone or combined with RA in absence of Zn2+. Tretinoin 15-28 PML-RARA regulated adaptor molecule 1 Homo sapiens 106-113
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 104-106 glutamic pyruvic transaminase, soluble Mus musculus 269-289
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 104-106 glutamic pyruvic transaminase, soluble Mus musculus 291-294
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 104-106 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 300-326
28667519-1 2017 In this study, treatment of C57BL/6J (wild type, WT) mice fed a high-fat diet (HFD) with retinoic acid (RA) decreased body weight and subcutaneous and visceral fat content, reversed the apparent hepatosteatosis, and reduced hepatic intracellular triglyceride and serum alanine transaminase (ALT) and aspartate aminotransferase (AST) concentrations. Tretinoin 104-106 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 328-331
28667519-3 2017 However, these RA-induced effects in WT mice fed a HFD were alleviated in liver specific Sirtuin 1 (Sirt1) deficient (LKO) mice fed a HFD. Tretinoin 15-17 sirtuin 1 Mus musculus 89-98
25986924-5 2015 Importantly, ectopic Plzf expression in F9 cells suppressed retinoic acid (RA)-induced Stra8 activation, a gene required for meiosis initiation. Tretinoin 60-73 stimulated by retinoic acid gene 8 Mus musculus 87-92
25986924-5 2015 Importantly, ectopic Plzf expression in F9 cells suppressed retinoic acid (RA)-induced Stra8 activation, a gene required for meiosis initiation. Tretinoin 75-77 stimulated by retinoic acid gene 8 Mus musculus 87-92
28667519-3 2017 However, these RA-induced effects in WT mice fed a HFD were alleviated in liver specific Sirtuin 1 (Sirt1) deficient (LKO) mice fed a HFD. Tretinoin 15-17 sirtuin 1 Mus musculus 100-105
28667519-5 2017 The mechanism studies indicated that RA indeed increased the expression of hepatic Sirt1 and superoxide dismutase 2 (Sod2), and inhibited the expression of sterol regulatory element binding protein 1c (Srebp-1c) in WT mice in vivo and in vitro. Tretinoin 37-39 sirtuin 1 Mus musculus 83-88
7519122-5 1994 Interestingly, retinoic acid (RA) treatment suppresses the differentiation blockade induced by high level PML-RAR alpha protein; indeed, Zn(2+)-treated MTPR9 cells incubated with RA plus D3 exhibited significant terminal monocytic maturation, comparable to that of cells treated with D3 alone or combined with RA in absence of Zn2+. Tretinoin 30-32 PML-RARA regulated adaptor molecule 1 Homo sapiens 106-113
28667519-5 2017 The mechanism studies indicated that RA indeed increased the expression of hepatic Sirt1 and superoxide dismutase 2 (Sod2), and inhibited the expression of sterol regulatory element binding protein 1c (Srebp-1c) in WT mice in vivo and in vitro. Tretinoin 37-39 sterol regulatory element binding transcription factor 1 Mus musculus 156-200
28667519-5 2017 The mechanism studies indicated that RA indeed increased the expression of hepatic Sirt1 and superoxide dismutase 2 (Sod2), and inhibited the expression of sterol regulatory element binding protein 1c (Srebp-1c) in WT mice in vivo and in vitro. Tretinoin 37-39 sterol regulatory element binding transcription factor 1 Mus musculus 202-210
7915087-1 1994 Spontaneous and all-trans-retinoic acid (RA)-induced differentiation of normal human monocytes and of leukemic THP-1 monocytes into macrophages resulted in a progressive loss of adenosine 3",5"-cyclic monophosphate production induced by histamine via typical H2 receptors (H2R). Tretinoin 16-39 histamine receptor H2 Homo sapiens 259-271
28667519-8 2017 In summary, RA protected against HFD-induced hepatosteatosis by decreasing Srebp-1c expression and improving antioxidant capacity through a Sirt1-mediated mechanism. Tretinoin 12-14 sterol regulatory element binding transcription factor 1 Mus musculus 75-83
28667519-8 2017 In summary, RA protected against HFD-induced hepatosteatosis by decreasing Srebp-1c expression and improving antioxidant capacity through a Sirt1-mediated mechanism. Tretinoin 12-14 sirtuin 1 Mus musculus 140-145
29073082-8 2017 In the intestine, it increased the expression of retinoic acid-inducible target genes such as Aldh1a2, Dhrs3, and Ccr9 The beta-carotene-inducible disruption of retinoid homeostasis affected gut-homing and differentiation of lymphocytes and displayed morphologically in large lymphoid follicles along the intestine. Tretinoin 49-62 dehydrogenase/reductase (SDR family) member 3 Mus musculus 103-108
7915087-1 1994 Spontaneous and all-trans-retinoic acid (RA)-induced differentiation of normal human monocytes and of leukemic THP-1 monocytes into macrophages resulted in a progressive loss of adenosine 3",5"-cyclic monophosphate production induced by histamine via typical H2 receptors (H2R). Tretinoin 16-39 histamine receptor H2 Homo sapiens 273-276
7915087-1 1994 Spontaneous and all-trans-retinoic acid (RA)-induced differentiation of normal human monocytes and of leukemic THP-1 monocytes into macrophages resulted in a progressive loss of adenosine 3",5"-cyclic monophosphate production induced by histamine via typical H2 receptors (H2R). Tretinoin 41-43 histamine receptor H2 Homo sapiens 259-271
28927789-2 2017 The human high-risk neuroblastoma cell line, SK-N-AS (non-amplified N-myc) is derived from stromal cells and it is resistant to treatment with retinoic acid (1, RA), which is a chemotherapeutic agent used to induce neuronal cellular differentiation of neuroblastomas. Tretinoin 143-156 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 68-73
7915087-1 1994 Spontaneous and all-trans-retinoic acid (RA)-induced differentiation of normal human monocytes and of leukemic THP-1 monocytes into macrophages resulted in a progressive loss of adenosine 3",5"-cyclic monophosphate production induced by histamine via typical H2 receptors (H2R). Tretinoin 41-43 histamine receptor H2 Homo sapiens 273-276
7915087-2 1994 In THP-1 cells and in HL-60 human acute myelocytic leukemia cells, RA treatment increased the abundance of the 4.5-kb messenger RNA of the H2R gene fourfold, suggesting transcriptional control by a RA response element. Tretinoin 67-69 histamine receptor H2 Homo sapiens 139-142
7915087-2 1994 In THP-1 cells and in HL-60 human acute myelocytic leukemia cells, RA treatment increased the abundance of the 4.5-kb messenger RNA of the H2R gene fourfold, suggesting transcriptional control by a RA response element. Tretinoin 198-200 histamine receptor H2 Homo sapiens 139-142
28743391-8 2017 Furthermore, VA or ATRA treatment effectively reversed the ISO-induced altered expression of Npr1 and PKG-I genes, proto-oncogenes, and hypertrophic markers genes. Tretinoin 19-23 natriuretic peptide receptor 1 Rattus norvegicus 93-97
28743391-8 2017 Furthermore, VA or ATRA treatment effectively reversed the ISO-induced altered expression of Npr1 and PKG-I genes, proto-oncogenes, and hypertrophic markers genes. Tretinoin 19-23 protein kinase cGMP-dependent 1 Rattus norvegicus 102-107
7520101-6 1994 Furthermore, in several patients examined, APL cells induced by ATRA with G-CSF showed an increased activity of chemotaxis and CD11a expression. Tretinoin 64-68 integrin subunit alpha L Homo sapiens 127-132
8028004-6 1994 In addition, we have found that the distribution of these HLA-DRA mRNA binding proteins is different in different cell types; in particular, their pattern of expression in Ntera-2, a human teratocarcinoma cell line, is distinct from that observed in Raji, a human B-lymphoma cell line, and is modulated by growth in retinoic acid. Tretinoin 316-329 major histocompatibility complex, class II, DR alpha Homo sapiens 58-65
28802580-0 2017 Suppressive role of OGT-mediated O-GlcNAcylation of BAP1 in retinoic acid signaling. Tretinoin 60-73 O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase) Mus musculus 20-23
28802580-6 2017 OGT promoted the BAP1-induced repression of retinoic acid (RA)-induced RA receptor (RAR) activation. Tretinoin 44-57 O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase) Mus musculus 0-3
28802580-6 2017 OGT promoted the BAP1-induced repression of retinoic acid (RA)-induced RA receptor (RAR) activation. Tretinoin 59-61 O-linked N-acetylglucosamine (GlcNAc) transferase (UDP-N-acetylglucosamine:polypeptide-N-acetylglucosaminyl transferase) Mus musculus 0-3
7947389-8 1994 Furthermore, the expression of c-jun led to an enhancement of the induction of the differentiation of WEHI-3B D+ cells by retinoic acid, suggesting an involvement of c-jun in the retinoic acid signal transduction pathway. Tretinoin 122-135 jun proto-oncogene Mus musculus 31-36
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 DNA mismatch repair protein Mlh1 Bubalus bubalis 194-198
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 PRM2 Bubalus bubalis 211-215
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 DNA mismatch repair protein Mlh1 Bubalus bubalis 194-198
7947389-8 1994 Furthermore, the expression of c-jun led to an enhancement of the induction of the differentiation of WEHI-3B D+ cells by retinoic acid, suggesting an involvement of c-jun in the retinoic acid signal transduction pathway. Tretinoin 122-135 jun proto-oncogene Mus musculus 166-171
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 PRM2 Bubalus bubalis 211-215
28743499-0 2017 All-trans retinoic acid attenuates bleomycin-induced pulmonary fibrosis via downregulating EphA2-EphrinA1 signaling. Tretinoin 0-23 ephrin A1 Mus musculus 97-105
7981625-1 1994 Normal rat kidney fibroblasts, density-arrested in the presence of epidermal growth factor (EGF), can be restimulated to proliferate in a synchronous way and acquire a transformed phenotype following treatment with additional growth factors like retinoic acid (RA) and transforming growth factor (TGF)-beta. Tretinoin 246-259 epidermal growth factor like 1 Rattus norvegicus 67-90
28743499-7 2017 However, administration of ATRA attenuated the upregulation of EphA2-EphrinA1 and PI3K-Akt after bleomycin instillation, and decreased pulmonary fibrosis. Tretinoin 27-31 ephrin A1 Mus musculus 69-77
28743499-9 2017 Collectively, these data suggest that ATRA attenuates bleomycin-induced pulmonary fibrosis by regulating EphA2-EphrinA1 and PI3K-Akt signaling. Tretinoin 38-42 ephrin A1 Mus musculus 111-119
30271852-12 2017 Spontaneous neural differentiation (nestin and Tju1) and retinoic acid-induced endodermal differentiation (Pdx-1 and insulin I) were improved in the EBs produced using the new insert compared to those in EBs produced by suspension culture. Tretinoin 57-70 insulin I Mus musculus 117-126
7981625-1 1994 Normal rat kidney fibroblasts, density-arrested in the presence of epidermal growth factor (EGF), can be restimulated to proliferate in a synchronous way and acquire a transformed phenotype following treatment with additional growth factors like retinoic acid (RA) and transforming growth factor (TGF)-beta. Tretinoin 246-259 epidermal growth factor like 1 Rattus norvegicus 92-95
7981625-1 1994 Normal rat kidney fibroblasts, density-arrested in the presence of epidermal growth factor (EGF), can be restimulated to proliferate in a synchronous way and acquire a transformed phenotype following treatment with additional growth factors like retinoic acid (RA) and transforming growth factor (TGF)-beta. Tretinoin 261-263 epidermal growth factor like 1 Rattus norvegicus 67-90
7981625-1 1994 Normal rat kidney fibroblasts, density-arrested in the presence of epidermal growth factor (EGF), can be restimulated to proliferate in a synchronous way and acquire a transformed phenotype following treatment with additional growth factors like retinoic acid (RA) and transforming growth factor (TGF)-beta. Tretinoin 261-263 epidermal growth factor like 1 Rattus norvegicus 92-95
17180006-6 1994 In this study we isolated RA-resistant 15N cell lines and analyzed their growth properties and changes in cell cycle related (cdc2, cdk2, cyclins A, B, D and E) and early response (fos and jun) gene expression to evaluate the role IGF2 may play in mediating RA resistance. Tretinoin 26-28 cyclin dependent kinase 2 Homo sapiens 132-136
28500502-3 2017 On the other hand, retinoic acid (RA) can bind to E-FABP and is stored abundantly in the GP cartilage. Tretinoin 19-32 fatty acid binding protein 5, epidermal Mus musculus 50-56
28500502-3 2017 On the other hand, retinoic acid (RA) can bind to E-FABP and is stored abundantly in the GP cartilage. Tretinoin 34-36 fatty acid binding protein 5, epidermal Mus musculus 50-56
8026630-9 1994 Surprisingly, the altered malformation patterns induced by retinoic acid in lgl mutants were nearly identical to those from earlier, pre-emergence exposure. Tretinoin 59-72 legless Mus musculus 76-79
28696319-9 2017 A small-molecule inhibitor of HIF2alpha activity diminishes the tumor response to AZA+RA treatment, indicating that the increase in HIF2alpha levels is a key component in tumor response to AZA+RA. Tretinoin 86-88 endothelial PAS domain protein 1 Homo sapiens 30-39
28696319-9 2017 A small-molecule inhibitor of HIF2alpha activity diminishes the tumor response to AZA+RA treatment, indicating that the increase in HIF2alpha levels is a key component in tumor response to AZA+RA. Tretinoin 86-88 endothelial PAS domain protein 1 Homo sapiens 132-141
28696319-9 2017 A small-molecule inhibitor of HIF2alpha activity diminishes the tumor response to AZA+RA treatment, indicating that the increase in HIF2alpha levels is a key component in tumor response to AZA+RA. Tretinoin 193-195 endothelial PAS domain protein 1 Homo sapiens 30-39
7947324-7 1994 During RA mediated differentiation of P19 cells, RXR alpha expression was induced while RXR beta expression was not modulated and RXR gamma expression was down regulated. Tretinoin 7-9 retinoid X receptor alpha Mus musculus 49-58
28696319-9 2017 A small-molecule inhibitor of HIF2alpha activity diminishes the tumor response to AZA+RA treatment, indicating that the increase in HIF2alpha levels is a key component in tumor response to AZA+RA. Tretinoin 193-195 endothelial PAS domain protein 1 Homo sapiens 132-141
7911974-7 1994 Finally, T cells stimulated by a low dosage of PHA in the presence of 1 microM retinoic acid show a marked increase of both HOXB expression, particularly B2, and cell proliferation. Tretinoin 79-92 homeobox B cluster Homo sapiens 124-128
28544237-2 2017 Computational and experimental evidence supports an asymmetric atom-transfer radical addition (ATRA) mechanism in which the stereodetermining step involves outer-sphere bromine abstraction from a [(bisphosphine)RhII BrCl] complex by a benzylic radical intermediate. Tretinoin 95-99 Rh blood group D antigen Homo sapiens 211-215
7974255-7 1994 RA, which binds to all 3 RARs with similar affinity, produced a 50% inhibition (IC50) of cartilage formation at 4 x 10(-10) M. We also tested Ch55, which also binds to all 3 RARs, but with higher affinity than RA. Tretinoin 0-2 arginyl-tRNA synthetase 1 Homo sapiens 25-29
28515123-4 2017 ATRA suppressed IL13- or IL4-induced M2-type macrophages, and then inhibited migration of osteosarcoma cells as promoted by M2-type macrophages in vitro ATRA reduced the number of pulmonary metastatic nodes of osteosarcoma and decreased expression of M2-type macrophages in metastatic nodes both in intravenous injection and orthotopic transplantation models. Tretinoin 0-4 interleukin 4 Mus musculus 25-28
7974255-7 1994 RA, which binds to all 3 RARs with similar affinity, produced a 50% inhibition (IC50) of cartilage formation at 4 x 10(-10) M. We also tested Ch55, which also binds to all 3 RARs, but with higher affinity than RA. Tretinoin 0-2 arginyl-tRNA synthetase 1 Homo sapiens 174-178
7974255-9 1994 9-cis RA, which binds to the 3 RARs with affinities similar to RA and also binds to the 3 RXRs, was less active (IC50 8 x 10(-9) M), suggesting that RXR binding interferes with the inhibitory effect of ligand-activated RARs. Tretinoin 6-8 arginyl-tRNA synthetase 1 Homo sapiens 31-35
7974255-9 1994 9-cis RA, which binds to the 3 RARs with affinities similar to RA and also binds to the 3 RXRs, was less active (IC50 8 x 10(-9) M), suggesting that RXR binding interferes with the inhibitory effect of ligand-activated RARs. Tretinoin 6-8 arginyl-tRNA synthetase 1 Homo sapiens 219-223
28477983-6 2017 Furthermore, roscovitine counter-acted the effect of RA on GR sensitive target proteins such as BDNF or tissue-transglutaminase. Tretinoin 53-55 brain derived neurotrophic factor Mus musculus 96-100
8061571-0 1994 Steroid hormones and retinoic acid interact in the regulation of calcitonin and calcitonin gene-related peptide secretion and messenger ribonucleic acid levels in CA-77 C cells. Tretinoin 21-34 calcitonin-related polypeptide alpha Rattus norvegicus 65-75
28477983-6 2017 Furthermore, roscovitine counter-acted the effect of RA on GR sensitive target proteins such as BDNF or tissue-transglutaminase. Tretinoin 53-55 transglutaminase 2, C polypeptide Mus musculus 104-127
8061571-0 1994 Steroid hormones and retinoic acid interact in the regulation of calcitonin and calcitonin gene-related peptide secretion and messenger ribonucleic acid levels in CA-77 C cells. Tretinoin 21-34 calcitonin-related polypeptide alpha Rattus norvegicus 80-111
8061571-1 1994 Northern hybridizations were used to evaluate the modulated action of retinoic acid (R.A.) in presence of dexamethasone (Dex) and/or calcitriol (1,25-(OH)2D3) on calcitonin (CT) and calcitonin gene-related peptide (CGRP) mRNA steady state levels in the murine CA-77 C cell line. Tretinoin 70-83 calcitonin-related polypeptide alpha Rattus norvegicus 162-172
8207983-0 1994 In vitro all-trans retinoic acid (ATRA) sensitivity and cellular retinoic acid binding protein (CRABP) levels in relapse leukemic cells after remission induction by ATRA in acute promyelocytic leukemia. Tretinoin 165-169 cellular retinoic acid binding protein 1 Homo sapiens 56-94
27922552-0 2017 Novel Use of All-Trans-Retinoic Acid in A Model of Lipopolysaccharide-Immunosuppression to Decrease the Generation of Myeloid-Derived Suppressor Cells by Reducing the Proliferation of CD34+ Precursor Cells. Tretinoin 13-36 CD34 antigen Mus musculus 184-188
27922552-4 2017 We found that ATRA administration in vivo and in vitro decreased the number of CD34+ precursor cells that were increased in IS mice. Tretinoin 14-18 CD34 antigen Mus musculus 79-83
8207983-0 1994 In vitro all-trans retinoic acid (ATRA) sensitivity and cellular retinoic acid binding protein (CRABP) levels in relapse leukemic cells after remission induction by ATRA in acute promyelocytic leukemia. Tretinoin 165-169 cellular retinoic acid binding protein 1 Homo sapiens 96-101
8207983-6 1994 We have demonstrated that AML3 patients" cells (from four patients) at relapse show high levels of CRABP, a cytosolic retinoic acid binding protein and this protein was not detected prior to ATRA therapy. Tretinoin 191-195 cellular retinoic acid binding protein 1 Homo sapiens 99-104
28595619-8 2017 RESULTS: IFN-gamma and a multiple cytokine cocktail (MC) consisting of IFN-gamma, TGFbeta and retinoic acid upregulated the expression of immunomodulatory factor PD-L1 and IDO activity. Tretinoin 94-107 indoleamine 2,3-dioxygenase 1 Mus musculus 172-175
8207983-9 1994 This induced ATRA hypercatabolytic state should be monitored during consolidation therapy and at relapse by evaluating CRABP and RA metabolite levels, in order to detect ATRA resistance in patients with AML3. Tretinoin 13-17 cellular retinoic acid binding protein 1 Homo sapiens 119-124
28559980-9 2017 Together, these results show that ATRA activates SDF-1/CXCR4/ROCK2 signaling to inhibit chondrogenesis to lead to CCF by suppressing differentiation through down-regulation of SOX9 and COL2A1 expression in rat embryo hind limb bud mesenchymal cells. Tretinoin 34-38 collagen type II alpha 1 chain Rattus norvegicus 185-191
8185324-9 1994 Binding studies demonstrated that CRABP-I and CRABP-II possess two classes of RA-binding sites: one class of high-affinity binding sites with a constant of dissociation (Kd) of 1.5 nM for CRABP-I and 4.7 nM for CRABP-II and one class of low-affinity binding sites with a Kd of 69 nM for CRABP-I and 101 nM for CRABP-II. Tretinoin 35-37 cellular retinoic acid binding protein 1 Homo sapiens 188-201
28063149-11 2017 Further, low availability of RA in cell milieu is known to decrease the expression of Nrf2, a transcription factor necessary for the expression of several antioxidants and antioxidant enzymes. Tretinoin 29-31 nfe2 like bZIP transcription factor 2a Danio rerio 86-90
8144640-2 1994 This report extends our observation that cellular retinoic acid-binding protein type I (CRABP) serves as substrate for retinoic acid metabolism by testis microsomes. Tretinoin 50-63 cellular retinoic acid binding protein 1 Homo sapiens 88-93
8144640-3 1994 Retinoic acid bound to excess CRABP was metabolized at 70% of the unbound retinoic acid rate with testis microsomes and at the same rates as unbound retinoic acid with kidney and lung microsomes. Tretinoin 0-13 cellular retinoic acid binding protein 1 Homo sapiens 30-35
27880037-3 2017 EPO is a direct target of RA, and the retinoid pathway is altered in the nitrofen-induced congenital diaphragmatic hernia (CDH) model. Tretinoin 26-28 erythropoietin Rattus norvegicus 0-3
8144640-3 1994 Retinoic acid bound to excess CRABP was metabolized at 70% of the unbound retinoic acid rate with testis microsomes and at the same rates as unbound retinoic acid with kidney and lung microsomes. Tretinoin 74-87 cellular retinoic acid binding protein 1 Homo sapiens 30-35
8144640-3 1994 Retinoic acid bound to excess CRABP was metabolized at 70% of the unbound retinoic acid rate with testis microsomes and at the same rates as unbound retinoic acid with kidney and lung microsomes. Tretinoin 149-162 cellular retinoic acid binding protein 1 Homo sapiens 30-35
8144640-7 1994 Retinoids bound to CRABP, isolated from a testis microsomal incubation, consisted of 50% retinoic acid, 32% P1 and 17% P2, suggesting that CRABP may bind retinoic acid metabolites in vivo. Tretinoin 89-102 cellular retinoic acid binding protein 1 Homo sapiens 19-24
28441416-3 2017 Oxidative metabolism of ethanol by alcohol dehydrogenase or cytochrome P450 2E1 has been implicated in some of ethanol"s teratogenic effects, either via production of acetaldehyde or competitive inhibition of retinoic acid synthesis. Tretinoin 209-222 cytochrome P450, family 2, subfamily e, polypeptide 1 Mus musculus 60-79
8144640-7 1994 Retinoids bound to CRABP, isolated from a testis microsomal incubation, consisted of 50% retinoic acid, 32% P1 and 17% P2, suggesting that CRABP may bind retinoic acid metabolites in vivo. Tretinoin 89-102 cellular retinoic acid binding protein 1 Homo sapiens 139-144
8144640-7 1994 Retinoids bound to CRABP, isolated from a testis microsomal incubation, consisted of 50% retinoic acid, 32% P1 and 17% P2, suggesting that CRABP may bind retinoic acid metabolites in vivo. Tretinoin 154-167 cellular retinoic acid binding protein 1 Homo sapiens 19-24
8144640-7 1994 Retinoids bound to CRABP, isolated from a testis microsomal incubation, consisted of 50% retinoic acid, 32% P1 and 17% P2, suggesting that CRABP may bind retinoic acid metabolites in vivo. Tretinoin 154-167 cellular retinoic acid binding protein 1 Homo sapiens 139-144
7600964-7 1994 The expression domain of AMHC1 can be expanded anteriorly within the heart tube by treating embryos with retinoic acid as the heart primordia fuse. Tretinoin 105-118 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 25-30
28426756-2 2017 These findings have also been described in humans, mice and zebrafish with loss-of-function mutations in the enzyme CYP26B1 that degrades retinoic acid (RA), the active metabolite of vitamin A, indicating that these effects are indeed caused by too high levels of vitamin A and that evolutionary conserved mechanisms are involved. Tretinoin 138-151 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 116-123
28426756-2 2017 These findings have also been described in humans, mice and zebrafish with loss-of-function mutations in the enzyme CYP26B1 that degrades retinoic acid (RA), the active metabolite of vitamin A, indicating that these effects are indeed caused by too high levels of vitamin A and that evolutionary conserved mechanisms are involved. Tretinoin 153-155 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 116-123
25907597-3 2015 The amphiphilic ATRA-PEG conjugates were synthesized by esterification reaction between all trans-retinoic acid and mPEGs (mPEG500, mPEG1000, mPEG2000, and mPEG5000). Tretinoin 92-111 progestagen associated endometrial protein Homo sapiens 21-24
25907597-7 2015 With PEG chain length ranging from 500 to 5000, ATRA-PEG nanomicelles exhibited a bell shape of chemical stability in different pH buffers, intestinal homogenate and plasma. Tretinoin 48-52 progestagen associated endometrial protein Homo sapiens 5-8
25907597-7 2015 With PEG chain length ranging from 500 to 5000, ATRA-PEG nanomicelles exhibited a bell shape of chemical stability in different pH buffers, intestinal homogenate and plasma. Tretinoin 48-52 progestagen associated endometrial protein Homo sapiens 53-56
25907597-11 2015 Our results indicated that PEG1000 chain length of ATRA-PEG prodrug nanomicelles has the optimal oral bioavailability probably due to improved stability and balanced mucus penetration capability and cell binding, and that the PEG chain length on a surface of nanoparticles cannot exceed a key threshold with the purpose of enhancement in oral bioavailability. Tretinoin 51-55 progestagen associated endometrial protein Homo sapiens 27-30
25907597-11 2015 Our results indicated that PEG1000 chain length of ATRA-PEG prodrug nanomicelles has the optimal oral bioavailability probably due to improved stability and balanced mucus penetration capability and cell binding, and that the PEG chain length on a surface of nanoparticles cannot exceed a key threshold with the purpose of enhancement in oral bioavailability. Tretinoin 51-55 progestagen associated endometrial protein Homo sapiens 56-59
28484611-6 2017 Correlating with these effects, key RA-responsive regulatory regions in the Hoxb cluster displayed opposite enrichment of activating or repressing histone marks in rostral and caudal NSPCs. Tretinoin 36-38 homeobox B cluster Mus musculus 76-80
28484611-7 2017 Finally, RA was able to strengthen Hoxb chromatin activation in caudal NSPCs, but was ineffective on the repressed Hoxb chromatin of rostral NSPCs. Tretinoin 9-11 homeobox B cluster Mus musculus 35-39
28369068-8 2017 ATRA treatment caused 29.5% and 40.3% reduction of the growth of EC1 cells after 24 hours and 48 hours, relative to the control. Tretinoin 0-4 Susceptibility to lysis by alloreactive natural killer cells Homo sapiens 65-68
25867809-10 2015 Altered genes in PTC suggested a loss of T4 responsiveness and dysregulation of retinoic acid metabolism, highlighting the putative activation of EZH2 and histone deacetylases (predicted in silico). Tretinoin 80-93 coiled-coil domain containing 6 Homo sapiens 17-20
7600964-8 1994 Embryos treated with retinoic acid prior to the initiation of fusion of the heart primordia express AMHC1 throughout the entire heart-forming region and fusion of the heart primordia is inhibited. Tretinoin 21-34 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 100-105
28369068-14 2017 Importantly, ATRA treatment decreased the expression of CD31, Ang-1, Ang-2 and Tie-2 in subcutaneous tumors of EC1 cells. Tretinoin 13-17 Susceptibility to lysis by alloreactive natural killer cells Homo sapiens 111-114
28369068-15 2017 Collectively, our findings demonstrate that ATRA exhibits a dose- and temporal-dependent effect on the metastatic behavior, suppresses the angiopoietin-Tie2 pathway and inhibits angiogenesis and the progression of xenograft tumors of EC1 cells. Tretinoin 44-48 Susceptibility to lysis by alloreactive natural killer cells Homo sapiens 234-237
8139911-1 1994 The polymorphic nature of sequences which act as retinoic acid response elements (RAREs and RXREs) in transactivation assays in mammalian cells, suggests that elements consisting of a direct repetition of a half site motif, separated by 1 to 5 base pairs (DR1 to DR5), are targets for retinoic acid (RA) signalling. Tretinoin 82-84 down-regulator of transcription 1 Homo sapiens 256-259
28087565-4 2017 Here, we find that Cyp26a1, which encodes a key enzyme for catabolic inactivation of RA required for tight control of local RA concentrations, is significantly downregulated in embryos of diabetic mice. Tretinoin 85-87 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 19-26
28087565-4 2017 Here, we find that Cyp26a1, which encodes a key enzyme for catabolic inactivation of RA required for tight control of local RA concentrations, is significantly downregulated in embryos of diabetic mice. Tretinoin 124-126 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 19-26
25847073-4 2015 In vitro expression of VNUT decreases neuritogenesis in N2a cells differentiated by retinoic acid treatment, whereas silencing of VNUT expression increases the number and length of neurites in these cells. Tretinoin 84-97 solute carrier family 17, member 9 Mus musculus 23-27
8120040-9 1994 These findings indicate that at least one human ADH isozyme may exist in the correct tissues to act as an embryonic retinol dehydrogenase catalyzing the synthesis of retinoic acid. Tretinoin 166-179 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 116-137
25902548-3 2015 We first found that, in mice lacking the retinoic acid (RA) target gene Stimulated by retinoic acid gene 8 (Stra8), undifferentiated spermatogonia accumulated in unusually high numbers as early as 10 d after birth, whereas differentiating spermatogonia were depleted. Tretinoin 41-54 stimulated by retinoic acid gene 8 Mus musculus 72-106
25902548-3 2015 We first found that, in mice lacking the retinoic acid (RA) target gene Stimulated by retinoic acid gene 8 (Stra8), undifferentiated spermatogonia accumulated in unusually high numbers as early as 10 d after birth, whereas differentiating spermatogonia were depleted. Tretinoin 41-54 stimulated by retinoic acid gene 8 Mus musculus 108-113
25902548-3 2015 We first found that, in mice lacking the retinoic acid (RA) target gene Stimulated by retinoic acid gene 8 (Stra8), undifferentiated spermatogonia accumulated in unusually high numbers as early as 10 d after birth, whereas differentiating spermatogonia were depleted. Tretinoin 56-58 stimulated by retinoic acid gene 8 Mus musculus 72-106
25902548-3 2015 We first found that, in mice lacking the retinoic acid (RA) target gene Stimulated by retinoic acid gene 8 (Stra8), undifferentiated spermatogonia accumulated in unusually high numbers as early as 10 d after birth, whereas differentiating spermatogonia were depleted. Tretinoin 56-58 stimulated by retinoic acid gene 8 Mus musculus 108-113
28157617-6 2017 The antiinflammatory effect of ATRA was associated with a reduction in the phosphorylation levels of IkappaB and p65 (~50%, P<.05), two subunits of the NF-kappaB pathway, probably mediated by PGC1alpha, in 3 T3-L1 adipocytes. Tretinoin 31-35 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 113-116
8125162-3 1994 Recently, three nuclear receptors specific for retinoic acid (RAR alpha, RAR beta, and RAR gamma) have been cloned and all are members of a large multigene family of ligand-inducible transcription enhancer factors. Tretinoin 47-60 retinoic acid receptor gamma Homo sapiens 87-96
28179426-5 2017 Lin28a-S200D-expressing cells, but not Lin28a-S200A-expressing or control P19 embryonic carcinoma cells, displayed impaired inhibition of let-7 miRNA and resulted in decreased cyclin D1, whereas Lin28a-S200A knock-in cells expressed less let-7 miRNA, proliferated faster, and exhibited differentiation defect upon retinoic acid induction. Tretinoin 314-327 lin-28 homolog A Mus musculus 0-6
8125162-6 1994 When treated with 1 microM RA, the messenger RNAs for both RAR beta and RAR gamma are induced. Tretinoin 27-29 retinoic acid receptor gamma Homo sapiens 72-81
8011555-0 1994 RAR beta isoforms: distinct transcriptional control by retinoic acid and specific spatial patterns of promoter activity during mouse embryonic development. Tretinoin 55-68 retinoic acid receptor, beta Mus musculus 0-8
27236567-5 2017 Here, we show that in vitro adenosine, adenosine, and retinoic acid or adenosine, TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes. Tretinoin 54-67 transglutaminase 2, C polypeptide Mus musculus 149-152
27236567-5 2017 Here, we show that in vitro adenosine, adenosine, and retinoic acid or adenosine, TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes. Tretinoin 95-109 transglutaminase 2, C polypeptide Mus musculus 149-152
25934412-0 2015 MicroRNA-10a is reduced in breast cancer and regulated in part through retinoic acid. Tretinoin 71-84 microRNA 10a Homo sapiens 0-12
25934412-7 2015 The in vitro effects of all-trans Retinoic acid (ATRA) and L-Thyroxine (T4) both individually and in combination, on miR-10a expression was investigated in breast cancer cell lines, T47D and SK-BR-3. Tretinoin 34-47 microRNA 10a Homo sapiens 117-124
25934412-7 2015 The in vitro effects of all-trans Retinoic acid (ATRA) and L-Thyroxine (T4) both individually and in combination, on miR-10a expression was investigated in breast cancer cell lines, T47D and SK-BR-3. Tretinoin 49-53 microRNA 10a Homo sapiens 117-124
25934412-11 2015 In vitro stimulation assays revealed miR-10a expression was increased in both T47D and SK-BR-3 cells following addition of ATRA (2 fold (0.7)). Tretinoin 123-127 microRNA 10a Homo sapiens 37-44
25934412-13 2015 CONCLUSION: The data presented supports a potential tumour suppressor role for miR-10a in breast cancer, and highlights retinoic acid as a positive regulator of the microRNA. Tretinoin 120-133 microRNA 10a Homo sapiens 79-86
27648628-5 2017 Furthermore, we showed that Pokemon could repress the transcriptional activity of RARalpha by increasing the recruitment of nuclear receptor co-repressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) to the retinoic acid response element (RARE) element. Tretinoin 187-200 retinoic acid receptor alpha Homo sapiens 82-90
28442062-0 2017 Retinoic acid triggers c-kit gene expression in spermatogonial stem cells through an enhanceosome constituted between transcription factor binding sites for retinoic acid response element (RARE), spleen focus forming virus proviral integration oncogene (SPFI1) (PU.1) and E26 transformation-specific (ETS). Tretinoin 0-13 Spi-1 proto-oncogene Homo sapiens 262-266
25572300-3 2015 Increased expression of Fndc5 has been reported upon retinoic acid treatment during neural differentiation and its knockdown decreased neural differentiation and neurite outgrowth. Tretinoin 53-66 fibronectin type III domain containing 5 Mus musculus 24-29
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 128-148 catenin beta 1 Homo sapiens 101-113
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 38-40 retinoic acid receptor, beta Mus musculus 55-63
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 150-154 catenin beta 1 Homo sapiens 60-72
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 38-40 retinoic acid receptor, beta Mus musculus 191-199
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 150-154 POU class 5 homeobox 1 Homo sapiens 80-84
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 150-154 catenin beta 1 Homo sapiens 101-113
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 55-57 retinoic acid receptor, beta Mus musculus 191-199
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 retinoic acid receptor alpha Homo sapiens 0-8
28122350-8 2017 RARalpha-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3beta leading to laryngeal cancer differentiation through GSK-3beta-involved Wnt/beta-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation. Tretinoin 269-273 catenin beta 1 Homo sapiens 178-190
25759405-1 2015 The majority of patients with acute promyelocytic leukaemia (APL) carry the hallmark t(15;17)(q22;q21) translocation, involving the promyelocytic leukaemia/retinoic acid receptor-alpha (PML/RARalpha) fusion gene, and by sensitivity of blast cells to all-trans retinoic acid (ATRA) and/or arsenic trioxide therapy. Tretinoin 275-279 PML nuclear body scaffold Homo sapiens 186-189
8011555-4 1994 In contrast, the mechanism by which RA up-regulates RAR beta 1/beta 3 transcripts has not yet been elucidated. Tretinoin 36-38 retinoic acid receptor, beta Mus musculus 52-60
8011555-4 1994 In contrast, the mechanism by which RA up-regulates RAR beta 1/beta 3 transcripts has not yet been elucidated. Tretinoin 36-38 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 63-69
8011556-1 1994 We have previously shown that oral treatment of pregnant mice with all-trans retinoic acid (RA) at doses which cause 100% fetal dysmorphogenesis results in a rapid elevation in the mRNA of one specific isoform of the RA receptor-beta, RAR-beta 2, in susceptible embryonic regions. Tretinoin 71-90 retinoic acid receptor, beta Mus musculus 235-243
25849135-3 2015 By using mechanism-based screening, here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the first example of targeted therapy in cancer, but whose drug target remains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to the substrate phosphate- and proline-binding pockets in the Pin1 active site. Tretinoin 64-77 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 271-275
25849135-3 2015 By using mechanism-based screening, here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the first example of targeted therapy in cancer, but whose drug target remains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to the substrate phosphate- and proline-binding pockets in the Pin1 active site. Tretinoin 64-77 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 387-391
25849135-3 2015 By using mechanism-based screening, here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the first example of targeted therapy in cancer, but whose drug target remains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to the substrate phosphate- and proline-binding pockets in the Pin1 active site. Tretinoin 79-83 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 271-275
28129653-2 2017 All-trans retinoic acid (ATRA) and arsenic trioxide cure most patients by directly targeting PML-RARalpha. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 93-96
28129653-2 2017 All-trans retinoic acid (ATRA) and arsenic trioxide cure most patients by directly targeting PML-RARalpha. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 97-105
8011556-1 1994 We have previously shown that oral treatment of pregnant mice with all-trans retinoic acid (RA) at doses which cause 100% fetal dysmorphogenesis results in a rapid elevation in the mRNA of one specific isoform of the RA receptor-beta, RAR-beta 2, in susceptible embryonic regions. Tretinoin 92-94 retinoic acid receptor, beta Mus musculus 235-243
28129653-2 2017 All-trans retinoic acid (ATRA) and arsenic trioxide cure most patients by directly targeting PML-RARalpha. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 93-96
25849135-3 2015 By using mechanism-based screening, here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the first example of targeted therapy in cancer, but whose drug target remains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to the substrate phosphate- and proline-binding pockets in the Pin1 active site. Tretinoin 79-83 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 387-391
25849135-4 2015 ATRA-induced Pin1 ablation degrades the protein encoded by the fusion oncogene PML-RARA and treats APL in APL cell and animal models as well as in human patients. Tretinoin 0-4 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 13-17
25849135-4 2015 ATRA-induced Pin1 ablation degrades the protein encoded by the fusion oncogene PML-RARA and treats APL in APL cell and animal models as well as in human patients. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 79-82
25849135-4 2015 ATRA-induced Pin1 ablation degrades the protein encoded by the fusion oncogene PML-RARA and treats APL in APL cell and animal models as well as in human patients. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 83-87
25849135-5 2015 ATRA-induced Pin1 ablation also potently inhibits triple-negative breast cancer cell growth in human cells and in animal models by acting on many Pin1 substrate oncogenes and tumor suppressors. Tretinoin 0-4 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 13-17
25849135-5 2015 ATRA-induced Pin1 ablation also potently inhibits triple-negative breast cancer cell growth in human cells and in animal models by acting on many Pin1 substrate oncogenes and tumor suppressors. Tretinoin 0-4 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 146-150
28129653-2 2017 All-trans retinoic acid (ATRA) and arsenic trioxide cure most patients by directly targeting PML-RARalpha. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 97-105
28187790-0 2017 Retinoic acid and TGF-beta signalling cooperate to overcome MYCN-induced retinoid resistance. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 60-64
28187790-5 2017 We altered MYCN expression levels in a MYCN-inducible neuroblastoma cell line to facilitate or block retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 101-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 11-15
25849135-6 2015 Thus, ATRA simultaneously blocks multiple Pin1-regulated cancer-driving pathways, an attractive property for treating aggressive and drug-resistant tumors. Tretinoin 6-10 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 42-46
8127183-4 1994 A cohort of MTS was treated with the chemopreventive agent retinoic acid (RA) to determine its effect on tumor cells. Tretinoin 59-72 MLRL Homo sapiens 12-15
25896049-3 2015 To further define whether retinoic acid receptor alpha (RARalpha) mediated the induction of apelin by ATRA, endogenous RARalpha was down regulated by transfection of siRNA against RARalpha (si-RARalpha) or RARalpha was over-expressed by infection of the adenovirus vector pAd-GFP-RARalpha in the VSMCs. Tretinoin 102-106 retinoic acid receptor alpha Homo sapiens 56-64
28179876-0 2017 Talking Convergence: Growing Evidence Links FOXP2 and Retinoic Acid in Shaping Speech-Related Motor Circuitry. Tretinoin 54-67 forkhead box P2 Homo sapiens 44-49
8127183-4 1994 A cohort of MTS was treated with the chemopreventive agent retinoic acid (RA) to determine its effect on tumor cells. Tretinoin 74-76 MLRL Homo sapiens 12-15
8127183-6 1994 Spectroscopic scans demonstrated consistently that RA-treated MTS exhibit a decrease in the peak associated with reduced nicotinamide-adenine dinucleotide (NADH) and an increase in the peaks associated with flavins, tryptophan, and cytokeratins when compared to controls. Tretinoin 51-53 MLRL Homo sapiens 62-65
8108126-3 1994 To identify which retinoic acid receptor (RAR) is directly linked to RA response in these cells, nine RA resistant subclones were derived and characterized. Tretinoin 69-71 retinoic acid receptor gamma Homo sapiens 42-45
27729412-5 2017 A decrease of adiponectin expression in addition to an up-regulation of aldehyde dehydrogenase A1 (ALDH1A1), retinoid signaling, and retinoic acid response element signaling was selectively observed in WAT of mice fed a normal-vitamin A, high-fat diet. Tretinoin 133-146 adiponectin, C1Q and collagen domain containing Mus musculus 14-25
28408791-0 2017 All-Trans Retinoic Acid Modulates TLR4/NF-kappaB Signaling Pathway Targeting TNF-alpha and Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer. Tretinoin 10-23 toll like receptor 4 Homo sapiens 34-38
28408791-9 2017 Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF-kappaB signaling pathway targeting NOS2 and TNF-alpha expression. Tretinoin 39-43 toll like receptor 4 Homo sapiens 66-70
25843403-5 2015 Moreover, RA-induced AMPAR trafficking utilized the Q-SNARE syntaxin-4, whereas LTP utilized syntaxin-3; both additionally required the Q-SNARE SNAP-47 and the R-SNARE synatobrevin-2. Tretinoin 10-12 YKT6 v-SNARE homolog Homo sapiens 160-167
25941627-8 2015 VAF347 augments RA-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47(phox). Tretinoin 16-18 Cbl proto-oncogene Homo sapiens 61-66
25941627-8 2015 VAF347 augments RA-induced expression of AhR, Lyn, Vav1, and c-Cbl as well as p47(phox). Tretinoin 16-18 pleckstrin Homo sapiens 78-81
8108126-10 1994 The dose dependent co-transfection of an expressed RAR gamma cDNA with this reporter more efficiently repressed its transcriptional activity in the presence of RA than transfection of the reporter without expressed RAR gamma. Tretinoin 51-53 retinoic acid receptor gamma Homo sapiens 215-224
8061932-4 1994 We have analyzed the effects of topical application of triamcinolone acetonide (TA) on the retinoic acid-induced altered expression of CRABP I and II in normal human skin, at the protein and mRNA levels. Tretinoin 91-104 cellular retinoic acid binding protein 1 Homo sapiens 135-142
25742746-0 2015 All-trans retinoic acid downregulates ALDH1-mediated stemness and inhibits tumour formation in ovarian cancer cells. Tretinoin 10-23 aldehyde dehydrogenase 1 family member A1 Homo sapiens 38-43
25742746-2 2015 Here, we investigated the ALDH1-regulated function and its underlying signalling and tested whether all-trans retinoic acid (ATRA) can suppress ALDH1-regulated tumour behaviour in ovarian cancer cells. Tretinoin 110-123 aldehyde dehydrogenase 1 family member A1 Homo sapiens 144-149
25742746-2 2015 Here, we investigated the ALDH1-regulated function and its underlying signalling and tested whether all-trans retinoic acid (ATRA) can suppress ALDH1-regulated tumour behaviour in ovarian cancer cells. Tretinoin 125-129 aldehyde dehydrogenase 1 family member A1 Homo sapiens 144-149
25742746-8 2015 We conclude that ATRA downregulates ALDH1/FoxM1/Notch1 signalling and suppresses tumour formation in ovarian cancer cells. Tretinoin 17-21 aldehyde dehydrogenase 1 family member A1 Homo sapiens 36-41
27166558-4 2017 A major subset of oral cDCs with the CD103-CD11b+ phenotype showed retinoic acid (RA)-producing activity and converted naive CD4+ T cells to Foxp3+ Treg cells in a transforming growth factor-beta- and RA-dependent manner in vitro. Tretinoin 67-80 integrin subunit alpha E Homo sapiens 37-42
27166558-4 2017 A major subset of oral cDCs with the CD103-CD11b+ phenotype showed retinoic acid (RA)-producing activity and converted naive CD4+ T cells to Foxp3+ Treg cells in a transforming growth factor-beta- and RA-dependent manner in vitro. Tretinoin 82-84 integrin subunit alpha E Homo sapiens 37-42
27166558-4 2017 A major subset of oral cDCs with the CD103-CD11b+ phenotype showed retinoic acid (RA)-producing activity and converted naive CD4+ T cells to Foxp3+ Treg cells in a transforming growth factor-beta- and RA-dependent manner in vitro. Tretinoin 201-203 integrin subunit alpha E Homo sapiens 37-42
27166558-5 2017 In the ManLNs, migratory CD103-CD11b+ cDCs also showed RA-producing activity. Tretinoin 55-57 integrin subunit alpha E Homo sapiens 25-30
28090317-0 2016 All-trans retinoic acid enhances cytotoxic effect of T cells with an anti-CD38 chimeric antigen receptor in acute myeloid leukemia. Tretinoin 10-23 CD38 molecule Homo sapiens 74-78
28090317-5 2016 Intriguingly, 10 nM all-trans retinoic acid (ATRA) augmented CD38 expression in KG1, U937 and HL60 cells and primary leukemic cells from AML patients. Tretinoin 30-43 CD38 molecule Homo sapiens 61-65
28090317-5 2016 Intriguingly, 10 nM all-trans retinoic acid (ATRA) augmented CD38 expression in KG1, U937 and HL60 cells and primary leukemic cells from AML patients. Tretinoin 45-49 CD38 molecule Homo sapiens 61-65
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 132-134 apoptotic chromatin condensation inducer 1 Homo sapiens 5-11
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 132-134 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 132-134 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
28090317-6 2016 Moreover, the withdrawal of ATRA from the medium decreased CD38 expression in AML cells. Tretinoin 28-32 CD38 molecule Homo sapiens 59-63
8061932-6 1994 In contrast, CRABP I protein was decreased by topical retinoic acid, and the down modulating effect of retinoic acid was counteracted by triamcinolone acetonide. Tretinoin 54-67 cellular retinoic acid binding protein 1 Homo sapiens 13-20
28090317-7 2016 Killing effects of anti-CD38-CAR T cells against AML lines and AML cells were limited without ATRA, whereas CD38-specific T cells enhanced cytotoxicity on AML cells by ATRA in association with enhanced CD38 expression. Tretinoin 168-172 CD38 molecule Homo sapiens 108-112
28090317-7 2016 Killing effects of anti-CD38-CAR T cells against AML lines and AML cells were limited without ATRA, whereas CD38-specific T cells enhanced cytotoxicity on AML cells by ATRA in association with enhanced CD38 expression. Tretinoin 168-172 CD38 molecule Homo sapiens 108-112
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 132-134 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 199-201 apoptotic chromatin condensation inducer 1 Homo sapiens 5-11
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 199-201 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 199-201 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
8286746-4 1994 Whereas treatment of HL-525 cells with ATRA or TPA alone had no effect on features of monocytic differentiation, these agents in combination resulted in cellular adhesion, nonspecific esterase staining, and induction of the c-fms (monocyte growth factor receptor) gene. Tretinoin 39-43 colony stimulating factor 1 receptor Homo sapiens 224-229
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 199-201 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
25205379-4 2015 RA treatment further enhances the splicing of the weak 5" splice site by Acinus in a dose- and time-dependent manner, suggesting a RA-dependent activity in addition to a RA-independent activity of Acinus. Tretinoin 0-2 apoptotic chromatin condensation inducer 1 Homo sapiens 73-79
8286746-6 1994 Exposure of HL-525 cells to ATRA for 3 days resulted in induction of PKC beta transcripts, whereas there was little change in PKC alpha mRNA levels. Tretinoin 28-32 protein kinase C beta Homo sapiens 69-77
25205379-4 2015 RA treatment further enhances the splicing of the weak 5" splice site by Acinus in a dose- and time-dependent manner, suggesting a RA-dependent activity in addition to a RA-independent activity of Acinus. Tretinoin 0-2 apoptotic chromatin condensation inducer 1 Homo sapiens 197-203
25205379-4 2015 RA treatment further enhances the splicing of the weak 5" splice site by Acinus in a dose- and time-dependent manner, suggesting a RA-dependent activity in addition to a RA-independent activity of Acinus. Tretinoin 131-133 apoptotic chromatin condensation inducer 1 Homo sapiens 73-79
27732960-3 2016 Based on the known interaction of redox-active selenium compounds with thiolate ligands of zinc, we herein have investigated the abrogatory effects of selenite alone or in combination with all-trans retinoic acid on PML/RARalpha and the possible effects on differentiation in these cells. Tretinoin 199-212 PML nuclear body scaffold Homo sapiens 216-219
8286746-7 1994 ATRA treatment was also associated with an increase in PKC activity and an induction of cytosolic PKC beta protein levels. Tretinoin 0-4 protein kinase C beta Homo sapiens 98-106
25205379-4 2015 RA treatment further enhances the splicing of the weak 5" splice site by Acinus in a dose- and time-dependent manner, suggesting a RA-dependent activity in addition to a RA-independent activity of Acinus. Tretinoin 131-133 apoptotic chromatin condensation inducer 1 Homo sapiens 73-79
25205379-7 2015 The RRM domain is necessary for the RA-dependent splicing activity of Acinus and the RA-independent splicing activity of Acinus is repressed by RNPS1. Tretinoin 36-38 apoptotic chromatin condensation inducer 1 Homo sapiens 70-76
8276858-7 1994 This suggests that the J6 gene is likely to be transactivated by the GATA-2, GATA-3, or related transcription factor, which is activated by retinoic acid during F9 cell differentiation. Tretinoin 140-153 GATA binding protein 2 Homo sapiens 69-75
25793304-13 2015 Taken together, these results suggest that RALDH1 and 2 may play a role in the regulation of postnatal ocular growth in humans through the synthesis of atRA. Tretinoin 152-156 aldehyde dehydrogenase 1 family member A1 Homo sapiens 43-55
27592281-2 2016 In addition to being a CSC marker, ALDH1A3 regulates gene expression via retinoic acid (RA) signaling and plays a key role in the progression and chemotherapy resistance of cancer. Tretinoin 73-86 aldehyde dehydrogenase 1 family member A3 Homo sapiens 35-42
27592281-2 2016 In addition to being a CSC marker, ALDH1A3 regulates gene expression via retinoic acid (RA) signaling and plays a key role in the progression and chemotherapy resistance of cancer. Tretinoin 88-90 aldehyde dehydrogenase 1 family member A3 Homo sapiens 35-42
27041581-3 2016 We demonstrated that TGF-beta1 stimulation upregulated CD147 expression and mediated the dedifferentiation of HCC cells, whereas all-trans-retinoic acid induced the downregulation of CD147 and promoted differentiation in HCC cells. Tretinoin 133-152 basigin (Ok blood group) Homo sapiens 183-188
25887926-5 2015 Moreover, with the presence of TGF-beta, ATRA upregulated CD4(+)CD25(+)Foxp3(+)Treg cells and suppressed Th17 cells in the blood, spleen and draining lymph nodes of recipient mice, as well as enhanced the Foxp3 expression and inhibited the RORgammat expression in grafts and peripheral blood mononuclear cells (PBMCs). Tretinoin 41-45 forkhead box P3 Mus musculus 71-76
25887926-5 2015 Moreover, with the presence of TGF-beta, ATRA upregulated CD4(+)CD25(+)Foxp3(+)Treg cells and suppressed Th17 cells in the blood, spleen and draining lymph nodes of recipient mice, as well as enhanced the Foxp3 expression and inhibited the RORgammat expression in grafts and peripheral blood mononuclear cells (PBMCs). Tretinoin 41-45 forkhead box P3 Mus musculus 205-210
27157614-3 2016 In this paper, we investigated cellular and molecular consequences of loss of HOXA5 in breast cancer, and the role played by retinoic acid in HOXA5 function. Tretinoin 125-138 homeobox A5 Homo sapiens 142-147
7535512-8 1994 Bidimensional gel electrophoresis showed that cytokeratins 1, 2, 10 and 11 disappeared only in the tretinoin group (60 p. 100 of the cases). Tretinoin 99-108 keratin 1 Homo sapiens 46-74
27157614-9 2016 Retinoic acid is a known upstream regulator of HOXA5 expression. Tretinoin 0-13 homeobox A5 Homo sapiens 47-52
27724856-2 2016 The subfamily of aldehyde dehydrogenases 1 (ALDH1) isoenzymes, which comprises ALDH1A1, ALDH1A2, and ALDH1A3, is involved in the synthesis of retinoic acid, and has been identified as functional stem cell markers in diverse cancers. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A1 Homo sapiens 17-42
25573434-6 2015 Knockdown of NIF-1 expression attenuated both neurite outgrowth in cultured cortical neurons and retinoic acid (RA)-treated Neuro-2a neuroblastoma cells. Tretinoin 97-110 zinc finger protein 335 Mus musculus 13-18
25573434-6 2015 Knockdown of NIF-1 expression attenuated both neurite outgrowth in cultured cortical neurons and retinoic acid (RA)-treated Neuro-2a neuroblastoma cells. Tretinoin 112-114 zinc finger protein 335 Mus musculus 13-18
25774684-6 2015 Addition of retinoic acid (RA), Noggin and Cyclopamine promoted pancreatic differentiation as indicated by the expression of the early pancreatic progenitor markers ISL1, NGN3 and PDX1. Tretinoin 12-25 ISL LIM homeobox 1 Homo sapiens 165-169
25774684-6 2015 Addition of retinoic acid (RA), Noggin and Cyclopamine promoted pancreatic differentiation as indicated by the expression of the early pancreatic progenitor markers ISL1, NGN3 and PDX1. Tretinoin 12-25 neurogenin 3 Homo sapiens 171-175
25774684-6 2015 Addition of retinoic acid (RA), Noggin and Cyclopamine promoted pancreatic differentiation as indicated by the expression of the early pancreatic progenitor markers ISL1, NGN3 and PDX1. Tretinoin 27-29 ISL LIM homeobox 1 Homo sapiens 165-169
25774684-6 2015 Addition of retinoic acid (RA), Noggin and Cyclopamine promoted pancreatic differentiation as indicated by the expression of the early pancreatic progenitor markers ISL1, NGN3 and PDX1. Tretinoin 27-29 neurogenin 3 Homo sapiens 171-175
27724856-2 2016 The subfamily of aldehyde dehydrogenases 1 (ALDH1) isoenzymes, which comprises ALDH1A1, ALDH1A2, and ALDH1A3, is involved in the synthesis of retinoic acid, and has been identified as functional stem cell markers in diverse cancers. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A1 Homo sapiens 44-49
27724856-2 2016 The subfamily of aldehyde dehydrogenases 1 (ALDH1) isoenzymes, which comprises ALDH1A1, ALDH1A2, and ALDH1A3, is involved in the synthesis of retinoic acid, and has been identified as functional stem cell markers in diverse cancers. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A1 Homo sapiens 79-86
27724856-2 2016 The subfamily of aldehyde dehydrogenases 1 (ALDH1) isoenzymes, which comprises ALDH1A1, ALDH1A2, and ALDH1A3, is involved in the synthesis of retinoic acid, and has been identified as functional stem cell markers in diverse cancers. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A3 Homo sapiens 101-108
7535512-11 1994 Bidimensional electrophoresis demonstrated that cytokeratins 1, 2, 10 and 11 disappeared in 43 p. 100 of the patients treated with tretinoin. Tretinoin 131-140 keratin 1 Homo sapiens 48-76
8143931-0 1994 All-trans-retinoic acid and hexamethylene bisacetamide (HMBA) regulate TGF-alpha and Hst-1/kFGF expression in differentiation sensitive but not in resistant human teratocarcinomas. Tretinoin 0-23 transforming growth factor alpha Homo sapiens 71-80
25652838-5 2015 Heterozygous adult zebrafish heterozygous for the cyp26b1 mutant that encodes an enzyme able to degrade RA possess an extra tooth in the ventral row. Tretinoin 104-106 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 50-57
7991046-0 1994 Retinoic acid enhances the number of epidermal growth factor receptors in rat glomerular epithelial cells in vitro. Tretinoin 0-13 epidermal growth factor like 1 Rattus norvegicus 37-60
27602766-1 2016 The expression of the retinoic acid-induced G (Rig-G) gene, an all trans retinoic acid (ATRA)-inducible gene, was observed in multiple cancer cells, including lung cancer cells. Tretinoin 22-35 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 47-52
27602766-1 2016 The expression of the retinoic acid-induced G (Rig-G) gene, an all trans retinoic acid (ATRA)-inducible gene, was observed in multiple cancer cells, including lung cancer cells. Tretinoin 73-86 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 47-52
27602766-1 2016 The expression of the retinoic acid-induced G (Rig-G) gene, an all trans retinoic acid (ATRA)-inducible gene, was observed in multiple cancer cells, including lung cancer cells. Tretinoin 88-92 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 47-52
25576519-4 2015 Here we show that retinoic acids induce the expression of Nur77, and retinoid-induced apoptosis is completely dependent on Nur77, as retinoids were unable to induce apoptosis in Nur77 null thymocytes. Tretinoin 18-32 nuclear receptor subfamily 4, group A, member 1 Mus musculus 58-63
7991046-2 1994 We report here that retinoic acid enhances the proliferative effect of EGF on glomerular epithelial cells (GEC) in vitro and also increases EGF binding to GEC. Tretinoin 20-33 epidermal growth factor like 1 Rattus norvegicus 71-74
7991046-2 1994 We report here that retinoic acid enhances the proliferative effect of EGF on glomerular epithelial cells (GEC) in vitro and also increases EGF binding to GEC. Tretinoin 20-33 epidermal growth factor like 1 Rattus norvegicus 140-143
25435432-6 2015 Activated NF-kappaB enhanced the degree of ATRA-induced differentiation of HL-60 cells to macrophages, rather than granulocytes, as assessed by morphologic examination and expressions of differentiation markers such as CD11b, CD38, CD68, MMP9 and Btg2. Tretinoin 43-47 CD38 molecule Homo sapiens 226-230
25435432-6 2015 Activated NF-kappaB enhanced the degree of ATRA-induced differentiation of HL-60 cells to macrophages, rather than granulocytes, as assessed by morphologic examination and expressions of differentiation markers such as CD11b, CD38, CD68, MMP9 and Btg2. Tretinoin 43-47 BTG anti-proliferation factor 2 Homo sapiens 247-251
7991046-4 1994 Moreover, the stimulating effect of EGF was synergistically increased by retinoic acid at 5 micrograms/ml. Tretinoin 73-86 epidermal growth factor like 1 Rattus norvegicus 36-39
26883918-8 2016 The retinoic acid induced bovine mGSCs were positive for Stra8, SCP3, DZAL, EMA1 and VASA, and resembled spermatid cells morphologically. Tretinoin 4-17 synaptonemal complex protein 3 Bos taurus 64-68
7991046-5 1994 125I-EGF binding to cultured GEC was increased approximately 3-fold after addition of retinoic acid to cultures for 48 h. Analysis of 125I-EGF binding revealed 8.1 x 10(4) receptors per control (untreated) cell, while retinoic acid-treated cells demonstrated an increase to 14.3 x 10(4) receptors per cell with no detectable change in receptor affinity. Tretinoin 86-99 epidermal growth factor like 1 Rattus norvegicus 5-8
25588842-6 2015 Finally, we show that disruption of RA results both in an inhibition of intracellular Ca(2+) signaling and of TRPP2 incorporation into the plasma membrane of kidney field cells. Tretinoin 36-38 polycystin 2, transient receptor potential cation channel L homeolog Xenopus laevis 110-115
27617494-0 2016 Thwarting PTEN Expression by siRNA Augments HL-60 Cell Differentiation to Neutrophil-Like Cells by DMSO and ATRA. Tretinoin 108-112 phosphatase and tensin homolog Homo sapiens 10-14
7991046-5 1994 125I-EGF binding to cultured GEC was increased approximately 3-fold after addition of retinoic acid to cultures for 48 h. Analysis of 125I-EGF binding revealed 8.1 x 10(4) receptors per control (untreated) cell, while retinoic acid-treated cells demonstrated an increase to 14.3 x 10(4) receptors per cell with no detectable change in receptor affinity. Tretinoin 218-231 epidermal growth factor like 1 Rattus norvegicus 5-8
27617494-6 2016 Our results show that PTEN siRNA increases HL-60 cell differentiation in the presence of DMSO and ATRA. Tretinoin 98-102 phosphatase and tensin homolog Homo sapiens 22-26
7972206-2 1994 Clinical response to retinoic acid was noted only in the two children with tumors coexpressing trk protooncogene mRNA, encoding an essential part of the nerve growth factor (NGF) high affinity receptor, and low affinity NGF receptor gene (LNGFR) mRNA. Tretinoin 21-34 neurotrophic receptor tyrosine kinase 1 Homo sapiens 95-98
25497839-5 2015 To differentiate which isoform of FNDC5 is involved in the process of human neural differentiation, we have used hESCs as an in vitro model for neural differentiation by retinoic acid (RA) induction. Tretinoin 170-183 fibronectin type III domain containing 5 Homo sapiens 34-39
7972206-6 1994 Analysis of trk and LNGFR mRNA may be useful to predict clinical response to retinoic acid in these children. Tretinoin 77-90 neurotrophic receptor tyrosine kinase 1 Homo sapiens 12-15
8247529-12 1993 This finding demonstrates that TGF-alpha can inhibit the anti-tumorigenic effects of RA in human TCs. Tretinoin 85-87 transforming growth factor alpha Homo sapiens 31-40
25544292-0 2015 An alternative retinoic acid-responsive Stra6 promoter regulated in response to retinol deficiency. Tretinoin 15-28 stimulated by retinoic acid gene 6 Mus musculus 40-45
25544292-5 2015 We employed CRISPR-Cas9 genome editing to show that the endogenous RARE is required for RA-induced transcription of both Stra6 isoforms. Tretinoin 67-69 stimulated by retinoic acid gene 6 Mus musculus 121-126
27133819-0 2016 PML-RARalpha kinetics and impact of FLT3-ITD mutations in newly diagnosed acute promyelocytic leukaemia treated with ATRA and ATO or ATRA and chemotherapy. Tretinoin 117-121 PML nuclear body scaffold Homo sapiens 0-3
27133819-0 2016 PML-RARalpha kinetics and impact of FLT3-ITD mutations in newly diagnosed acute promyelocytic leukaemia treated with ATRA and ATO or ATRA and chemotherapy. Tretinoin 117-121 retinoic acid receptor alpha Homo sapiens 4-12
27133819-0 2016 PML-RARalpha kinetics and impact of FLT3-ITD mutations in newly diagnosed acute promyelocytic leukaemia treated with ATRA and ATO or ATRA and chemotherapy. Tretinoin 133-137 PML nuclear body scaffold Homo sapiens 0-3
27133819-0 2016 PML-RARalpha kinetics and impact of FLT3-ITD mutations in newly diagnosed acute promyelocytic leukaemia treated with ATRA and ATO or ATRA and chemotherapy. Tretinoin 133-137 retinoic acid receptor alpha Homo sapiens 4-12
25544292-6 2015 We further demonstrate that in ES cells, 1) both RARgamma and RXRalpha are present at the Stra6 RARE; 2) RA increases co-activator p300 (KAT3B) binding and histone H3 Lys-27 acetylation at both promoters; 3) RA decreases Suz12 levels and histone H3 Lys-27 trimethylation epigenetic marks at both promoters; and 4) these epigenetic changes are diminished in the absence of RARgamma. Tretinoin 49-51 stimulated by retinoic acid gene 6 Mus musculus 90-95
25544292-6 2015 We further demonstrate that in ES cells, 1) both RARgamma and RXRalpha are present at the Stra6 RARE; 2) RA increases co-activator p300 (KAT3B) binding and histone H3 Lys-27 acetylation at both promoters; 3) RA decreases Suz12 levels and histone H3 Lys-27 trimethylation epigenetic marks at both promoters; and 4) these epigenetic changes are diminished in the absence of RARgamma. Tretinoin 49-51 retinoic acid response element 2 Mus musculus 96-103
26991532-4 2016 ALDH1A3 participates in various physiological processes in human cells by oxidizing all-trans-retinal to retinoic acid. Tretinoin 105-118 aldehyde dehydrogenase 1 family member A3 Homo sapiens 0-7
8240270-3 1993 Using HeLa cells, we now show that treatment with 0.5 microM RA for 24 h suppresses endogenous ODC mRNA levels and the expression of a transfected ODC/chloramphenicol acetyltransferase plasmid (Kpn-ODCCAT), containing sequences from -1450 to +810 of the human ODC gene. Tretinoin 61-63 ornithine decarboxylase 1 Homo sapiens 95-98
27443528-11 2016 ATRA treatment led to downregulation of the ALDH1A1, P-gp and BCRP proteins. Tretinoin 0-4 aldehyde dehydrogenase 1 family member A1 Homo sapiens 44-51
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 118-140
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 142-145
8240270-3 1993 Using HeLa cells, we now show that treatment with 0.5 microM RA for 24 h suppresses endogenous ODC mRNA levels and the expression of a transfected ODC/chloramphenicol acetyltransferase plasmid (Kpn-ODCCAT), containing sequences from -1450 to +810 of the human ODC gene. Tretinoin 61-63 ornithine decarboxylase 1 Homo sapiens 147-150
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 118-140
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 142-145
8240270-3 1993 Using HeLa cells, we now show that treatment with 0.5 microM RA for 24 h suppresses endogenous ODC mRNA levels and the expression of a transfected ODC/chloramphenicol acetyltransferase plasmid (Kpn-ODCCAT), containing sequences from -1450 to +810 of the human ODC gene. Tretinoin 61-63 ornithine decarboxylase 1 Homo sapiens 147-150
7910550-0 1993 v-erbA and citral reduce the teratogenic effects of all-trans retinoic acid and retinol, respectively, in Xenopus embryogenesis. Tretinoin 62-75 thyroid hormone receptor alpha L homeolog Xenopus laevis 2-6
25120220-7 2015 When the 5.2 kb construct is modified (eight point mutations) to eliminate responsiveness of the RARE to all-trans retinoic acid (atRA) [Nedd9(mutRARE)-lacZ], virtually all beta-galactosidase (beta-gal, lacZ) expression is lost. Tretinoin 115-128 galactosidase, beta 1 Mus musculus 173-191
25120220-7 2015 When the 5.2 kb construct is modified (eight point mutations) to eliminate responsiveness of the RARE to all-trans retinoic acid (atRA) [Nedd9(mutRARE)-lacZ], virtually all beta-galactosidase (beta-gal, lacZ) expression is lost. Tretinoin 115-128 galactosidase, beta 1 Mus musculus 173-181
25120220-7 2015 When the 5.2 kb construct is modified (eight point mutations) to eliminate responsiveness of the RARE to all-trans retinoic acid (atRA) [Nedd9(mutRARE)-lacZ], virtually all beta-galactosidase (beta-gal, lacZ) expression is lost. Tretinoin 130-134 galactosidase, beta 1 Mus musculus 173-191
25120220-7 2015 When the 5.2 kb construct is modified (eight point mutations) to eliminate responsiveness of the RARE to all-trans retinoic acid (atRA) [Nedd9(mutRARE)-lacZ], virtually all beta-galactosidase (beta-gal, lacZ) expression is lost. Tretinoin 130-134 galactosidase, beta 1 Mus musculus 173-181
26776160-0 2016 The E3 ubiquitin protein ligase MDM2 dictates all-trans retinoic acid-induced osteoblastic differentiation of osteosarcoma cells by modulating the degradation of RARalpha. Tretinoin 56-69 retinoic acid receptor alpha Homo sapiens 162-170
26776160-1 2016 Retinoic acid receptor alpha (RARalpha) has a critical role in the differentiation process of osteosarcoma cells induced by all-trans retinoic acid (ATRA). Tretinoin 124-147 retinoic acid receptor alpha Homo sapiens 0-28
26776160-1 2016 Retinoic acid receptor alpha (RARalpha) has a critical role in the differentiation process of osteosarcoma cells induced by all-trans retinoic acid (ATRA). Tretinoin 124-147 retinoic acid receptor alpha Homo sapiens 30-38
26776160-1 2016 Retinoic acid receptor alpha (RARalpha) has a critical role in the differentiation process of osteosarcoma cells induced by all-trans retinoic acid (ATRA). Tretinoin 149-153 retinoic acid receptor alpha Homo sapiens 0-28
26776160-1 2016 Retinoic acid receptor alpha (RARalpha) has a critical role in the differentiation process of osteosarcoma cells induced by all-trans retinoic acid (ATRA). Tretinoin 149-153 retinoic acid receptor alpha Homo sapiens 30-38
26776160-8 2016 Therefore, our study indicates that MDM2 serves as an E3 ubiquitin ligase to regulate the degradation of RARalpha and suggests that MDM2 is a novel therapeutic target for ATRA-based differentiation therapeutic approaches in osteosarcoma. Tretinoin 171-175 retinoic acid receptor alpha Homo sapiens 105-113
7910550-4 1993 The feasibility of this approach was demonstrated by the ability of citral treatment and v-erbA mRNA injection to reduce the teratogenic effects of exogenous retinol and retinoic acid, respectively, in early Xenopus development. Tretinoin 170-183 thyroid hormone receptor alpha L homeolog Xenopus laevis 91-95
27402696-5 2016 This suggests that in Treg, ATRA-induced upregulation of CCR9 and alpha4beta7 is dependent on activation of a mTOR signaling pathway. Tretinoin 28-32 mechanistic target of rapamycin kinase Mus musculus 110-114
25636082-3 2015 NR2F1-dependent dormancy is recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C and retinoic acid across various cancer types. Tretinoin 105-118 nuclear receptor subfamily 2, group F, member 1 Mus musculus 0-5
8404646-6 1993 Retinoic acid reduced SP-A protein levels in a concentration-dependent manner [analysis of variance (ANOVA), P < 0.01]. Tretinoin 0-13 surfactant protein A1 Homo sapiens 22-26
26660958-0 2016 All Trans-Retinoic Acid Mediates MED28/HMG Box-Containing Protein 1 (HBP1)/beta-Catenin Signaling in Human Colorectal Cancer Cells. Tretinoin 4-23 mediator complex subunit 28 Homo sapiens 33-38
8404646-10 1993 Retinoic acid reduced SP-A mRNA levels in a concentration-dependent manner (ANOVA, P < 0.02) and reduced SP-C mRNA levels at 3 microM. Tretinoin 0-13 surfactant protein A1 Homo sapiens 22-26
26660958-0 2016 All Trans-Retinoic Acid Mediates MED28/HMG Box-Containing Protein 1 (HBP1)/beta-Catenin Signaling in Human Colorectal Cancer Cells. Tretinoin 4-23 HMG-box transcription factor 1 Homo sapiens 39-67
26660958-0 2016 All Trans-Retinoic Acid Mediates MED28/HMG Box-Containing Protein 1 (HBP1)/beta-Catenin Signaling in Human Colorectal Cancer Cells. Tretinoin 4-23 HMG-box transcription factor 1 Homo sapiens 69-73
25609642-4 2015 Like ESCs, we found that mouse iPSCs treated with retinoic acid and a smoothened agonist differentiated into motoneurons expressing the LIM homeodomain protein Lhx3. Tretinoin 50-63 LIM homeobox protein 3 Mus musculus 160-164
26660958-0 2016 All Trans-Retinoic Acid Mediates MED28/HMG Box-Containing Protein 1 (HBP1)/beta-Catenin Signaling in Human Colorectal Cancer Cells. Tretinoin 4-23 catenin beta 1 Homo sapiens 75-87
8404646-11 1993 In contrast, retinoic acid increased SP-B mRNA levels in a concentration-dependent manner (ANOVA, P < 0.03). Tretinoin 13-26 surfactant protein B Homo sapiens 37-41
26660958-6 2016 In the current study we investigated the effect of ATRA on MED28 and Wnt/beta-catenin signaling in colorectal cancer. Tretinoin 51-55 mediator complex subunit 28 Homo sapiens 59-64
7521344-2 1993 We have used T47D cells to investigate the regulation of IGFBPs by IGF-I and retinoic acid (RA), agents that affect cell proliferation and have been shown to regulate IGFBP levels in other cell types. Tretinoin 77-90 insulin like growth factor binding protein 2 Homo sapiens 57-63
26660958-11 2016 Taken together, ATRA can reverse the suppressive effect of MED28 on HBP1 and E-cadherin and inactivate the Wnt/beta-catenin pathway in colorectal cancer, suggesting a protective effect of ATRA against colorectal cancer. Tretinoin 16-20 mediator complex subunit 28 Homo sapiens 59-64
26660958-11 2016 Taken together, ATRA can reverse the suppressive effect of MED28 on HBP1 and E-cadherin and inactivate the Wnt/beta-catenin pathway in colorectal cancer, suggesting a protective effect of ATRA against colorectal cancer. Tretinoin 16-20 HMG-box transcription factor 1 Homo sapiens 68-72
26660958-11 2016 Taken together, ATRA can reverse the suppressive effect of MED28 on HBP1 and E-cadherin and inactivate the Wnt/beta-catenin pathway in colorectal cancer, suggesting a protective effect of ATRA against colorectal cancer. Tretinoin 16-20 catenin beta 1 Homo sapiens 111-123
25514379-3 2015 All-trans-retinoic acid (ATRA) induces the proteasomal degradation of PML-RARalpha and granulocytic differentiation. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 70-73
25514379-3 2015 All-trans-retinoic acid (ATRA) induces the proteasomal degradation of PML-RARalpha and granulocytic differentiation. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 74-82
25514379-3 2015 All-trans-retinoic acid (ATRA) induces the proteasomal degradation of PML-RARalpha and granulocytic differentiation. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 70-73
25514379-3 2015 All-trans-retinoic acid (ATRA) induces the proteasomal degradation of PML-RARalpha and granulocytic differentiation. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 74-82
27531765-1 2016 OBJECTIVE: To explore effect of all-trans retinoic acid(ATRA) on annexin II expression in NB4 cells and to analyze the luciferase activity of annexinII promoter in condition of ATRA-induced treatment. Tretinoin 56-60 annexin A2 Homo sapiens 65-75
7521344-2 1993 We have used T47D cells to investigate the regulation of IGFBPs by IGF-I and retinoic acid (RA), agents that affect cell proliferation and have been shown to regulate IGFBP levels in other cell types. Tretinoin 92-94 insulin like growth factor binding protein 2 Homo sapiens 57-63
27499693-0 2016 NLS-RARalpha Inhibits the Effects of All-trans Retinoic Acid on NB4 Cells by Interacting with P38alpha MAPK. Tretinoin 47-60 retinoic acid receptor alpha Homo sapiens 4-12
27499693-5 2016 We also found that NLS-RARalpha could inhibit differentiation while accelerate proliferation of NB4 cells via downregulating the expression of p-p38alpha protein in the presence of ATRA. Tretinoin 181-185 retinoic acid receptor alpha Homo sapiens 23-31
27499693-7 2016 Finally, application of PD169316, an inhibitor of p38alpha protein, suggested that recruitment p38alpha-combinded NLS-RARalpha by ATRA eventually caused activation of p38alpha protein. Tretinoin 130-134 retinoic acid receptor alpha Homo sapiens 118-126
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 56-69 retinoic acid receptor alpha Homo sapiens 86-94
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 56-69 PML nuclear body scaffold Homo sapiens 97-100
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 56-69 retinoic acid receptor alpha Homo sapiens 101-109
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 190-194 PML nuclear body scaffold Homo sapiens 47-50
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 190-194 retinoic acid receptor alpha Homo sapiens 56-84
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 190-194 retinoic acid receptor alpha Homo sapiens 86-94
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 190-194 PML nuclear body scaffold Homo sapiens 97-100
27499693-8 2016 In summary, our study demonstrated that ATRA cound promote differentiation while inhibit proliferation of APL NB4 cells via activating p38alpha protein after recruiting p38alpha-combinded NLS-RARalpha, while NLS-RARalpha could inhibit the effects of ATRA in the process. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 192-200
27499693-8 2016 In summary, our study demonstrated that ATRA cound promote differentiation while inhibit proliferation of APL NB4 cells via activating p38alpha protein after recruiting p38alpha-combinded NLS-RARalpha, while NLS-RARalpha could inhibit the effects of ATRA in the process. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 212-220
25973309-2 2015 As a fusion protein of promyelocytic leukemia (PML) and retinoic acid receptor-alpha (RARalpha), PML-RARalpha oncoprotein is degraded through the differentiation of all-trans retinoic acid (ATRA)-induced cells. Tretinoin 190-194 retinoic acid receptor alpha Homo sapiens 101-109
8231238-10 1993 Retinoic acid and DMSO induced differentiation in HL-60 cells, and as this process progressed, p145 levels gradually fell until they approached isotype antibody control levels at 9 and 6 days, respectively. Tretinoin 0-13 POM121 transmembrane nucleoporin Homo sapiens 95-99
25398881-0 2015 Heat shock 70-kDa protein 5 (Hspa5) is essential for pronephros formation by mediating retinoic acid signaling. Tretinoin 87-100 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 0-27
25398881-0 2015 Heat shock 70-kDa protein 5 (Hspa5) is essential for pronephros formation by mediating retinoic acid signaling. Tretinoin 87-100 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 29-34
27048541-8 2016 When LPEAT1/MBOAT1 was knocked down with small interfering RNA (siRNA), outgrowth of neurites and expression of neuronal markers decreased in ATRA-treated P19C6 cells. Tretinoin 142-146 membrane bound O-acyltransferase domain containing 1 Mus musculus 5-11
27048541-8 2016 When LPEAT1/MBOAT1 was knocked down with small interfering RNA (siRNA), outgrowth of neurites and expression of neuronal markers decreased in ATRA-treated P19C6 cells. Tretinoin 142-146 membrane bound O-acyltransferase domain containing 1 Mus musculus 12-18
26980802-1 2016 All-trans-retinoic acid plays a central role in mucosal immunity, where it promotes its synthesis by up-regulating CD103 expression on dendritic cells, induces gut tropic (alpha4beta7(+) and CCR9(+)) T cells, and inhibits Th1/Th17 differentiation. Tretinoin 0-23 integrin subunit alpha E Homo sapiens 115-120
25398881-8 2015 Depletion of Hspa5 in animal caps, however, blocked the induction of pronephros as well as reduced the expression of retinoic acid (RA)-responsive genes, suggesting that knockdown of Hspa5 attenuated RA signaling. Tretinoin 117-130 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 13-18
25398881-8 2015 Depletion of Hspa5 in animal caps, however, blocked the induction of pronephros as well as reduced the expression of retinoic acid (RA)-responsive genes, suggesting that knockdown of Hspa5 attenuated RA signaling. Tretinoin 132-134 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 13-18
28591946-10 2016 Compared to CIA model group, the protein expressions of ADAMTS-4, MMP3, MMP1 were decreased in both ATRA groups ( P<0.05). Tretinoin 100-104 matrix metallopeptidase 1 Rattus norvegicus 72-76
8413259-7 1993 In vivo footprinting was also performed with F9 embryonal carcinoma cells, in which expression of the beta 2-m and MHC class I genes is induced at a low level only upon stimulation with retinoic acid (RA). Tretinoin 186-199 beta-2 microglobulin Mus musculus 102-110
27362937-7 2016 The paradigm of these proteins is the RA receptor alpha (RARalpha), which was phosphorylated in MCF7 cells but not in BT474 cells after RA addition. Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 57-65
25398881-8 2015 Depletion of Hspa5 in animal caps, however, blocked the induction of pronephros as well as reduced the expression of retinoic acid (RA)-responsive genes, suggesting that knockdown of Hspa5 attenuated RA signaling. Tretinoin 132-134 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 183-188
25398881-8 2015 Depletion of Hspa5 in animal caps, however, blocked the induction of pronephros as well as reduced the expression of retinoic acid (RA)-responsive genes, suggesting that knockdown of Hspa5 attenuated RA signaling. Tretinoin 200-202 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 13-18
25398881-8 2015 Depletion of Hspa5 in animal caps, however, blocked the induction of pronephros as well as reduced the expression of retinoic acid (RA)-responsive genes, suggesting that knockdown of Hspa5 attenuated RA signaling. Tretinoin 200-202 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 183-188
25398881-12 2015 This study shows that Hspa5, a key regulator of the unfolded protein response, plays an essential role in pronephros formation, which is mediated in part through RA signaling during early embryonic development. Tretinoin 162-164 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 22-27
8413259-7 1993 In vivo footprinting was also performed with F9 embryonal carcinoma cells, in which expression of the beta 2-m and MHC class I genes is induced at a low level only upon stimulation with retinoic acid (RA). Tretinoin 201-203 beta-2 microglobulin Mus musculus 102-110
26583087-5 2015 We also demonstrate that the presence of IL-2 during the in vitro generation of iTreg cells confers resistance to Th17 conversion but that IL-2 and retinoic acid (RA) cooperate to maintain Foxp3 expression following stimulation under Th17-polarizing conditions. Tretinoin 148-161 forkhead box P3 Mus musculus 189-194
27129260-4 2016 We document that overexpression of EVI1 abrogates retinoic acid-induced maturation of EML cells into committed myeloid cells, a process that can be documented by the down-regulation of stem cell antigen-1 and acquisition of responsiveness to granulocyte-macrophage colony-stimulating factor. Tretinoin 50-63 colony stimulating factor 2 Homo sapiens 242-290
8413259-8 1993 No in vivo protection was detected before and after RA treatment of F9 cells, indicating that RA induction of beta 2-m (and MHC class I) expression occurs without detectable in vivo factor occupancy, whereas EL4 T lymphocytes expressing beta 2-m at a high level exhibited strong protection similar to that in spleen. Tretinoin 94-96 beta-2 microglobulin Mus musculus 110-118
8402696-4 1993 Nondifferentiated HL-60 cells and HL-60 cells grown in the presence of 1.24 microM retinoic acid expressed only trace amounts of hL-31. Tretinoin 83-96 galectin 3 Homo sapiens 129-134
27244900-0 2016 Retinoic acid treated human dendritic cells induce T regulatory cells via the expression of CD141 and GARP which is impaired with age. Tretinoin 0-13 thrombomodulin Homo sapiens 92-97
27244900-6 2016 Examinations of the underlying mechanisms indicated that RA exposure led to the upregulation of CD141 and GARP on DCs which rendered the DCs tolerogenic. Tretinoin 57-59 thrombomodulin Homo sapiens 96-101
25208926-7 2015 Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal). Tretinoin 58-60 TNF receptor superfamily member 10b Homo sapiens 121-130
8274453-9 1993 Retinoic acid-treated, but not untreated, cells lost expression of vimentin and fibronectin, gained the ability to incorporate acetylated low density lipoprotein, and expressed Factor VIII-related antigen. Tretinoin 0-13 coagulation factor VIII Mus musculus 177-188
25208926-7 2015 Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal). Tretinoin 58-60 TNF receptor superfamily member 10b Homo sapiens 175-184
25208926-7 2015 Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal). Tretinoin 58-60 TNF receptor superfamily member 10b Homo sapiens 198-206
25052690-0 2015 Ectopic expression of DAZL gene in goat bone marrow-derived mesenchymal stem cells enhances the trans-differentiation to putative germ cells compared to the exogenous treatment of retinoic acid or bone morphogenetic protein 4 signalling molecules. Tretinoin 180-193 LOC102184271 Capra hircus 22-26
26957434-8 2016 However, transglutaminase 2 (TG2) induction, an adverse effect of ATRA, was much weaker in bexarotene treated primary GBM cells. Tretinoin 66-70 transglutaminase 2, C polypeptide Mus musculus 9-27
26957434-8 2016 However, transglutaminase 2 (TG2) induction, an adverse effect of ATRA, was much weaker in bexarotene treated primary GBM cells. Tretinoin 66-70 transglutaminase 2, C polypeptide Mus musculus 29-32
26915917-3 2016 CT and RA, but not PG, induced the activity of a 0.9 kb bcl-x promoter, containing sequences for AP-1 and NF-kB binding. Tretinoin 7-9 nuclear factor kappa B subunit 1 Rattus norvegicus 106-111
26915917-4 2016 RA, but not CT or PG, induced NF-kB activation. Tretinoin 0-2 nuclear factor kappa B subunit 1 Rattus norvegicus 30-35
8413210-1 1993 We have investigated the mechanism underlying repression of calcitonin/calcitonin gene-related peptide (CT/CGRP) gene expression by retinoic acid. Tretinoin 132-145 calcitonin-related polypeptide alpha Rattus norvegicus 107-111
27101150-0 2016 RAF-1/MEK/ERK pathway regulates ATRA-induced differentiation in acute promyelocytic leukemia cells through C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 32-36 CCAAT enhancer binding protein epsilon Homo sapiens 118-130
27101150-0 2016 RAF-1/MEK/ERK pathway regulates ATRA-induced differentiation in acute promyelocytic leukemia cells through C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 32-36 Spi-1 proto-oncogene Homo sapiens 135-139
26862315-2 2015 The discovery of all-trans retinoic acid (ATRA), which acts directly on promyelocytic locus-retinoic acid receptor alpha (PML-RARalpha) gene product, brought a revolution to the therapy of this disorder. Tretinoin 17-40 retinoic acid receptor alpha Homo sapiens 92-120
26862315-2 2015 The discovery of all-trans retinoic acid (ATRA), which acts directly on promyelocytic locus-retinoic acid receptor alpha (PML-RARalpha) gene product, brought a revolution to the therapy of this disorder. Tretinoin 17-40 PML nuclear body scaffold Homo sapiens 122-125
26862315-2 2015 The discovery of all-trans retinoic acid (ATRA), which acts directly on promyelocytic locus-retinoic acid receptor alpha (PML-RARalpha) gene product, brought a revolution to the therapy of this disorder. Tretinoin 17-40 retinoic acid receptor alpha Homo sapiens 126-134
26862315-2 2015 The discovery of all-trans retinoic acid (ATRA), which acts directly on promyelocytic locus-retinoic acid receptor alpha (PML-RARalpha) gene product, brought a revolution to the therapy of this disorder. Tretinoin 42-46 retinoic acid receptor alpha Homo sapiens 92-120
26862315-2 2015 The discovery of all-trans retinoic acid (ATRA), which acts directly on promyelocytic locus-retinoic acid receptor alpha (PML-RARalpha) gene product, brought a revolution to the therapy of this disorder. Tretinoin 42-46 PML nuclear body scaffold Homo sapiens 122-125
27101150-5 2016 ATRA-enhanced protein levels of C/EBPbeta, C/EBPepsilon and PU.1, which were required for differentiation in APL cells, were suppressed by the specific inhibitor of MEK. Tretinoin 0-4 CCAAT enhancer binding protein epsilon Homo sapiens 43-55
27101150-5 2016 ATRA-enhanced protein levels of C/EBPbeta, C/EBPepsilon and PU.1, which were required for differentiation in APL cells, were suppressed by the specific inhibitor of MEK. Tretinoin 0-4 Spi-1 proto-oncogene Homo sapiens 60-64
27101150-7 2016 Taken together, our study suggested that RAF-1/MEK/ERK cascade was involved in ATRA-induced differentiation in APL cells through enhancing the protein level of C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 79-83 CCAAT enhancer binding protein epsilon Homo sapiens 171-183
26862315-2 2015 The discovery of all-trans retinoic acid (ATRA), which acts directly on promyelocytic locus-retinoic acid receptor alpha (PML-RARalpha) gene product, brought a revolution to the therapy of this disorder. Tretinoin 42-46 retinoic acid receptor alpha Homo sapiens 126-134
27101150-7 2016 Taken together, our study suggested that RAF-1/MEK/ERK cascade was involved in ATRA-induced differentiation in APL cells through enhancing the protein level of C/EBPbeta, C/EBPepsilon and PU.1. Tretinoin 79-83 Spi-1 proto-oncogene Homo sapiens 188-192
27183470-6 2016 Stimulation of retinoic acid signalling during endothelial-to-haematopoietic transition induced the HOXA cluster and other HSC/definitive haemogenic endothelium genes, and prolonged HSPC maintenance in culture. Tretinoin 15-28 fucosyltransferase 1 (H blood group) Homo sapiens 123-126
26992387-5 2016 Treatment with RA or TO alone, and RA + TO reduced the MWT (46 +- 9, 42 +- 11, 46 +- 8, respectively) and improved the expression of VEGF, VEGFR1, and VEGFR2 compared to CDH (p < 0.05). Tretinoin 15-17 kinase insert domain receptor Rattus norvegicus 151-157
25446031-5 2015 Here, we determined a requirement for RA in the expression of KIT, a receptor tyrosine kinase essential for spermatogonial differentiation. Tretinoin 38-40 KIT proto-oncogene receptor tyrosine kinase Mus musculus 62-65
8413210-2 1993 Retinoic acid treatment of the CA77 thyroid C-cell line decreased CT/CGRP promoter activity two- to threefold, which correlates well with the decrease in calcitonin and CGRP mRNA levels. Tretinoin 0-13 calcitonin-related polypeptide alpha Rattus norvegicus 69-73
26992387-5 2016 Treatment with RA or TO alone, and RA + TO reduced the MWT (46 +- 9, 42 +- 11, 46 +- 8, respectively) and improved the expression of VEGF, VEGFR1, and VEGFR2 compared to CDH (p < 0.05). Tretinoin 35-37 kinase insert domain receptor Rattus norvegicus 151-157
8413210-2 1993 Retinoic acid treatment of the CA77 thyroid C-cell line decreased CT/CGRP promoter activity two- to threefold, which correlates well with the decrease in calcitonin and CGRP mRNA levels. Tretinoin 0-13 calcitonin-related polypeptide alpha Rattus norvegicus 169-173
25446031-6 2015 We found that RA signaling utilized the PI3K/AKT/mTOR signaling pathway to induce the efficient translation of mRNAs for Kit, which are present but not translated in undifferentiated spermatogonia. Tretinoin 14-16 mechanistic target of rapamycin kinase Mus musculus 49-53
25446031-6 2015 We found that RA signaling utilized the PI3K/AKT/mTOR signaling pathway to induce the efficient translation of mRNAs for Kit, which are present but not translated in undifferentiated spermatogonia. Tretinoin 14-16 KIT proto-oncogene receptor tyrosine kinase Mus musculus 121-124
8370078-9 1993 TGF-beta activity in the culture medium was also determined, finding that RA rapidly stimulates secretion of biologically active TGF-beta, the elevation being evident after 1 day of culture. Tretinoin 74-76 transforming growth factor, beta 1 Mus musculus 0-8
25311225-1 2015 The vitamin A metabolite retinoic acid (RA) has been reported to suppress Th1 responses and enhance Th2 responses. Tretinoin 25-38 heart and neural crest derivatives expressed 2 Mus musculus 100-103
25311225-1 2015 The vitamin A metabolite retinoic acid (RA) has been reported to suppress Th1 responses and enhance Th2 responses. Tretinoin 40-42 heart and neural crest derivatives expressed 2 Mus musculus 100-103
27026484-7 2016 Expression analysis of specific genes after 7days of RA treatment, as examined by RT-PCR, proved positive for some germ cell markers such as CVH, STRA8, PLZF and some genes involved in spermatogonial stem cell maintenance like BCL6b and c-KIT. Tretinoin 53-55 KIT proto-oncogene, receptor tyrosine kinase Gallus gallus 237-242
27146823-6 2016 The induction of HOTAIRM1 by ATRA was dependent on PU.1, and ectopic expression of PU.1 significantly up-regulated HOTAIRM1. Tretinoin 29-33 Spi-1 proto-oncogene Homo sapiens 51-55
27130680-2 2016 However, previous studies show that RA treatment of cells cultured in the presence of a leukemia inhibitory factor (LIF) also result in the upregulation of a gene called Zscan4, whose transient expression is a marker for undifferentiated ESCs. Tretinoin 36-38 leukemia inhibitory factor Mus musculus 88-114
27130680-2 2016 However, previous studies show that RA treatment of cells cultured in the presence of a leukemia inhibitory factor (LIF) also result in the upregulation of a gene called Zscan4, whose transient expression is a marker for undifferentiated ESCs. Tretinoin 36-38 leukemia inhibitory factor Mus musculus 116-119
8370078-9 1993 TGF-beta activity in the culture medium was also determined, finding that RA rapidly stimulates secretion of biologically active TGF-beta, the elevation being evident after 1 day of culture. Tretinoin 74-76 transforming growth factor, beta 1 Mus musculus 129-137
7505782-0 1993 Retinoic acid mediates post-transcriptional regulation of keratin 19 mRNA levels. Tretinoin 0-13 keratin 19 Homo sapiens 58-68
27008339-4 2016 All-trans retinoic acid (ATRA) induces CD38 expression, and we reasoned that this hydrophobic molecule might be absorbed by PDMS. Tretinoin 0-23 CD38 molecule Homo sapiens 39-43
27008339-4 2016 All-trans retinoic acid (ATRA) induces CD38 expression, and we reasoned that this hydrophobic molecule might be absorbed by PDMS. Tretinoin 25-29 CD38 molecule Homo sapiens 39-43
27008339-5 2016 Through a series of experiments we demonstrated that ATRA-mediated CD38 expression was attenuated when cultures were maintained on PDMS. Tretinoin 53-57 CD38 molecule Homo sapiens 67-71
25855932-9 2015 ATRA/As2O3 up-regulate the expression of HOXB8 mRNA/protein, and treatment of leukemia with ATRA/As2O3 may regulate HOX gene expression. Tretinoin 92-96 homeobox B8 Homo sapiens 41-46
7505782-2 1993 Retinoic acid (RA) is known to modulate expression of the basal cell keratins K19 and K5. Tretinoin 0-13 keratin 19 Homo sapiens 78-81
27008339-11 2016 We demonstrate here that ATRA is absorbed by PDMS in a time-dependent manner and results in the concomitant reduced expression of CD38 on the cell surface of CB-derived CD34(+) cells. Tretinoin 25-29 CD38 molecule Homo sapiens 130-134
26637766-2 2015 Acute promyelocytic leukemia (APL) is characterized commonly by a fusion between the PML gene and the RARA gene, genes targetable by arsenic (ATO) and retinoic acid (ATRA), respectively. Tretinoin 151-164 PML nuclear body scaffold Homo sapiens 85-88
7505782-2 1993 Retinoic acid (RA) is known to modulate expression of the basal cell keratins K19 and K5. Tretinoin 15-17 keratin 19 Homo sapiens 78-81
26637766-2 2015 Acute promyelocytic leukemia (APL) is characterized commonly by a fusion between the PML gene and the RARA gene, genes targetable by arsenic (ATO) and retinoic acid (ATRA), respectively. Tretinoin 151-164 retinoic acid receptor alpha Homo sapiens 102-106
7505782-4 1993 We have found that K19 mRNA levels increase over time in cultured keratinocytes exposed to elevated concentrations of RA. Tretinoin 118-120 keratin 19 Homo sapiens 19-22
26637766-2 2015 Acute promyelocytic leukemia (APL) is characterized commonly by a fusion between the PML gene and the RARA gene, genes targetable by arsenic (ATO) and retinoic acid (ATRA), respectively. Tretinoin 166-170 PML nuclear body scaffold Homo sapiens 85-88
26637766-2 2015 Acute promyelocytic leukemia (APL) is characterized commonly by a fusion between the PML gene and the RARA gene, genes targetable by arsenic (ATO) and retinoic acid (ATRA), respectively. Tretinoin 166-170 retinoic acid receptor alpha Homo sapiens 102-106
7505782-8 1993 These results suggest that an RA-dependent post-transcriptional mechanism modulates K19 intermediate filament expression in stratified squamous epithelia. Tretinoin 30-32 keratin 19 Homo sapiens 84-87
27080036-9 2016 Porcine T-cells expressed beta7 integrin and CCR9 receptors and migrated to CCL25 by a mechanism that was dependent of activation by RA-pretreated DCs, rather than direct activation by RA. Tretinoin 133-135 C-C motif chemokine ligand 25 Homo sapiens 76-81
8363564-7 1993 In contrast, when HL-60 cells were treated with retinoic acid, a granulocytic differentiation inducer, no enhanced AP-1 binding activity was observed, and only a weak increase in jun D mRNA level was detected. Tretinoin 48-61 JunD proto-oncogene, AP-1 transcription factor subunit Homo sapiens 179-184
26903503-1 2016 We have previously shown that, in human and zebrafish, hypomorphic mutations of the gene encoding the retinoic acid (RA)-metabolizing enzyme Cyp26b1 result in coronal craniosynostosis, caused by an RA-induced premature transitioning of suture osteoblasts to preosteocytes, inducing ectopic mineralization of the suture"s osteoid matrix. Tretinoin 102-115 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 141-148
26903503-1 2016 We have previously shown that, in human and zebrafish, hypomorphic mutations of the gene encoding the retinoic acid (RA)-metabolizing enzyme Cyp26b1 result in coronal craniosynostosis, caused by an RA-induced premature transitioning of suture osteoblasts to preosteocytes, inducing ectopic mineralization of the suture"s osteoid matrix. Tretinoin 117-119 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 141-148
26903503-1 2016 We have previously shown that, in human and zebrafish, hypomorphic mutations of the gene encoding the retinoic acid (RA)-metabolizing enzyme Cyp26b1 result in coronal craniosynostosis, caused by an RA-induced premature transitioning of suture osteoblasts to preosteocytes, inducing ectopic mineralization of the suture"s osteoid matrix. Tretinoin 198-200 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 141-148
25248321-0 2015 All-trans-retinoic acid and CD38 ligation differentially regulate CD1d expression and alpha-galactosylceramide-induced immune responses. Tretinoin 0-23 CD1d molecule Homo sapiens 66-70
25248321-3 2015 All-trans-retinoic acid (RA) and CD38, which is itself a target of RA, both independently regulate the differentiation of antigen presenting cells. Tretinoin 67-69 CD38 molecule Homo sapiens 33-37
25248321-5 2015 Whereas a physiological concentration (20 nM) of RA alone rapidly and markedly increased CD1d protein in THP-1 cells, there was a marked synergy between RA and ligation of CD38 with antibody to CD38. Tretinoin 49-51 CD1d molecule Homo sapiens 89-93
25248321-5 2015 Whereas a physiological concentration (20 nM) of RA alone rapidly and markedly increased CD1d protein in THP-1 cells, there was a marked synergy between RA and ligation of CD38 with antibody to CD38. Tretinoin 49-51 CD38 molecule Homo sapiens 172-176
25248321-5 2015 Whereas a physiological concentration (20 nM) of RA alone rapidly and markedly increased CD1d protein in THP-1 cells, there was a marked synergy between RA and ligation of CD38 with antibody to CD38. Tretinoin 49-51 CD38 molecule Homo sapiens 194-198
8344913-7 1993 Treatment of preadipocytes with retinoic acid inhibited adipocyte differentiation and also prevented Rev-Erb induction. Tretinoin 32-45 nuclear receptor subfamily 1, group D, member 2 Mus musculus 101-108
25403801-6 2015 RESULTS: Increased mineralized nodule formation, ALP activity, osteocalcin, and osteopontin expression levels were detected in LPS + atRA-treated BMSCs after osteogenic induction, when compared with LPS-treated cells. Tretinoin 133-137 secreted phosphoprotein 1 Homo sapiens 80-91
26873617-6 2016 One of those retinoic acid synthesis genes is ALDH1A3 and biallelic mutations in that gene have been recently found to lead to MA phenotype in patients. Tretinoin 13-26 aldehyde dehydrogenase 1 family member A3 Homo sapiens 46-53
8377224-0 1993 Retinoic acid responsive gene product, midkine, has neurotrophic functions for mouse spinal cord and dorsal root ganglion neurons in culture. Tretinoin 0-13 midkine Mus musculus 39-46
26671998-1 2016 Type 2 cannabinoid receptor (CB2) has been proposed to play a pivotal role in meiotic entry of male germ cells, similar to retinoic acid (RA). Tretinoin 123-136 cannabinoid receptor 2 Homo sapiens 29-32
26672737-0 2016 Antenatal retinoic acid administration increases trophoblastic retinol-binding protein dependent retinol transport in the nitrofen model of congenital diaphragmatic hernia. Tretinoin 10-23 retinol binding protein 4 Rattus norvegicus 63-86
26401661-4 2015 These 2 ovarian factors, together with retinoic acid (RA) action, promote feminization partially through the repression of the masculinizing activities of SOX9, FGF9 and DMRT1. Tretinoin 39-52 doublesex and mab-3 related transcription factor 1 Homo sapiens 170-175
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 141-154 NIMA related kinase 2 Homo sapiens 18-22
26672737-4 2016 We hypothesized that maternal administration of RA can increase trophoblastic RBP-dependent retinol transport in a nitrofen model of CDH. Tretinoin 48-50 retinol binding protein 4 Rattus norvegicus 78-81
26672737-11 2016 RESULTS: Markedly increased trophoblastic RBP immunoreactivity was observed in CDH+RA compared to CDH. Tretinoin 83-85 retinol binding protein 4 Rattus norvegicus 42-45
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 141-154 aldehyde dehydrogenase 1 family member A1 Homo sapiens 54-61
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 245-249 NIMA related kinase 2 Homo sapiens 18-22
26672737-14 2016 CONCLUSION: Increased trophoblastic RBP expression and retinol transport after antenatal administration of RA suggest that retinol-triggered RSP activation may attenuate CDH-associated PH by elevating serum and pulmonary retinol levels. Tretinoin 107-109 retinol binding protein 4 Rattus norvegicus 36-39
8394722-0 1993 Induction of TrkB by retinoic acid mediates biologic responsiveness to BDNF and differentiation of human neuroblastoma cells. Tretinoin 21-34 neurotrophic receptor tyrosine kinase 2 Homo sapiens 13-17
26997274-2 2016 From a retinoic acid (RA)-sensitive acute promyelocytic leukemia (APL) cell line, we derived an RA-resistant clone characterized by a block in transcription initiation, despite maintaining wild-type PML/RARA expression. Tretinoin 96-98 PML nuclear body scaffold Homo sapiens 199-202
26997274-2 2016 From a retinoic acid (RA)-sensitive acute promyelocytic leukemia (APL) cell line, we derived an RA-resistant clone characterized by a block in transcription initiation, despite maintaining wild-type PML/RARA expression. Tretinoin 96-98 retinoic acid receptor alpha Homo sapiens 203-207
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 245-249 aldehyde dehydrogenase 1 family member A1 Homo sapiens 54-61
25477235-8 2014 Moreover, after deletion of TGIF, both the effects of atRA on TGF-beta-dependent protein expression and the effects of TGF-beta on RA-dependent protein expression were lost. Tretinoin 54-58 TGFB-induced factor homeobox 1 Mus musculus 28-32
8394722-3 1993 In this study, we show that RA treatment of neuroblastoma cells induces the expression of TrkB, the receptor for the neurotrophins BDNF, NT-3, and NT-4/5. Tretinoin 28-30 neurotrophic receptor tyrosine kinase 2 Homo sapiens 90-94
8394722-4 1993 BDNF addition to RA-treated SH-SY5Y neuroblastoma cells stimulated the tyrosine phosphorylation of TrkB and neuronal differentiation. Tretinoin 17-19 neurotrophic receptor tyrosine kinase 2 Homo sapiens 99-103
25568859-5 2014 HSC are not only the major storage site for dietary vitamin A (Vit A) (retinol, retinoic acid), which is essential for proper function of the immune system. Tretinoin 80-93 fucosyltransferase 1 (H blood group) Homo sapiens 0-3
25649943-6 2014 Additionally, exogenous induction of the dominant-negative (dn) type of JunD canceled ATRA-induced upregulation of TUBB4a, and the dn type of ATF2 suppressed even the basal activity. Tretinoin 86-90 jun D proto-oncogene Mus musculus 72-76
27023064-7 2016 Moreover, cell exposure to all-trans-Retinoic acid (ATRA, 3 muM) reduces the binding of Nrf2 to the ARE sequences, decreases HO-1 induction and lowers GSH level increasing the efficacy of bortezomib. Tretinoin 27-50 heme oxygenase 1 Homo sapiens 125-129
27023064-7 2016 Moreover, cell exposure to all-trans-Retinoic acid (ATRA, 3 muM) reduces the binding of Nrf2 to the ARE sequences, decreases HO-1 induction and lowers GSH level increasing the efficacy of bortezomib. Tretinoin 52-56 heme oxygenase 1 Homo sapiens 125-129
26985947-0 2016 Effect of retinoic acid on aquaporin 3 expression in keratinocytes. Tretinoin 10-23 aquaporin 3 (Gill blood group) Homo sapiens 27-38
26985947-7 2016 Retinoic acid can increase AQP3 expression in HaCaT cells, with significant effects observed with 0.010 mg/mL isotretinoin treatment for 12 h. The side effects, namely skin and mucosa dryness caused by retinoic acid might be related to its effects on AQP3 expression. Tretinoin 0-13 aquaporin 3 (Gill blood group) Homo sapiens 27-31
25649943-6 2014 Additionally, exogenous induction of the dominant-negative (dn) type of JunD canceled ATRA-induced upregulation of TUBB4a, and the dn type of ATF2 suppressed even the basal activity. Tretinoin 86-90 tubulin, beta 4A class IVA Mus musculus 115-121
26985947-7 2016 Retinoic acid can increase AQP3 expression in HaCaT cells, with significant effects observed with 0.010 mg/mL isotretinoin treatment for 12 h. The side effects, namely skin and mucosa dryness caused by retinoic acid might be related to its effects on AQP3 expression. Tretinoin 0-13 aquaporin 3 (Gill blood group) Homo sapiens 251-255
8394722-5 1993 RA treatment of KCNR neuroblastoma cells, which constitutively express BDNF mRNA, resulted in the expression of TrkB and differentiation in the absence of added BDNF. Tretinoin 0-2 neurotrophic receptor tyrosine kinase 2 Homo sapiens 112-116
26935534-7 2016 This study reveals a physiological relevance of the non-genomic action of atRA, mediated by Crabp1, in modulating cell cycle progression and apoptosis induction, and provides a new cancer therapeutic strategy whereby compounds specifically targeting Crabp1 can modulate cell cycle and cancer cell apoptosis in a RAR-independent fashion, thereby avoiding atRA"s toxicity caused by its genomic effects. Tretinoin 74-78 retinoic acid receptor alpha Homo sapiens 312-315
8394722-6 1993 Finally, in 15N neuroblastoma cells, which express BDNF mRNA but do not differentiate in response to RA, RA induced only a truncated form of TrkB. Tretinoin 105-107 neurotrophic receptor tyrosine kinase 2 Homo sapiens 141-145
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 152-165 retinoid X receptor beta Homo sapiens 0-24
26728337-2 2016 PML and RARA mutations have been shown to directly respond to arsenic trioxide (ATO) and all-trans retinoic (ATRA). Tretinoin 109-113 PML nuclear body scaffold Homo sapiens 0-3
26728337-2 2016 PML and RARA mutations have been shown to directly respond to arsenic trioxide (ATO) and all-trans retinoic (ATRA). Tretinoin 109-113 retinoic acid receptor alpha Homo sapiens 8-12
26459180-0 2016 Sorafenib Inhibition of Mcl-1 Accelerates ATRA-Induced Apoptosis in Differentiation-Responsive AML Cells. Tretinoin 42-46 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 24-29
26459180-2 2016 We aim to improve ATRA therapy of AML by enhancing apoptosis through repression of the antiapoptotic proteins Bcl-2 and Mcl-1. Tretinoin 18-22 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 120-125
25251699-8 2014 We further confirmed direct retinoic acid regulation of the F11r gene, a new RA target, using tissue culture models. Tretinoin 28-41 F11 receptor Mus musculus 60-64
25192658-4 2014 Following treatment with ATRA, CHOP expression was increased and dimerized with LIP more preferentially than LAP to rescue function of LAP. Tretinoin 25-29 LAP Homo sapiens 109-112
25192658-4 2014 Following treatment with ATRA, CHOP expression was increased and dimerized with LIP more preferentially than LAP to rescue function of LAP. Tretinoin 25-29 LAP Homo sapiens 135-138
25192658-9 2014 We conclude that oroxylin A possessed abilities of inhibiting the ATRA-induced IL-6 production via modulation of LAP/LIP/CHOP in leukemia cell lines, which could providing a therapeutic strategy for RAS. Tretinoin 66-70 LAP Homo sapiens 113-116
25173565-10 2014 In the presence of ATRA, retinoic acid receptor (RAR) alpha/gamma expression was increased. Tretinoin 19-23 retinoic acid receptor alpha Homo sapiens 49-52
26459180-5 2016 RESULTS: In differentiation-responsive AML cells, ATRA treatment induces long-lasting repression of Bcl-2 while first upmodulating and then reducing the Mcl-1 level. Tretinoin 50-54 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 153-158
26459180-8 2016 Sorafenib blocks ATRA-induced Mcl-1 increase by reversing p90RSK activation and GSK3beta inactivation, maintains the repressed Bcl-2 level, and enhances ATRA induced apoptosis in non-APL AML cell lines and in primary AML cells. Tretinoin 17-21 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 30-35
26459180-8 2016 Sorafenib blocks ATRA-induced Mcl-1 increase by reversing p90RSK activation and GSK3beta inactivation, maintains the repressed Bcl-2 level, and enhances ATRA induced apoptosis in non-APL AML cell lines and in primary AML cells. Tretinoin 17-21 ribosomal protein S6 kinase A1 Homo sapiens 58-64
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 152-165 retinoid X receptor beta Homo sapiens 26-30
26459180-10 2016 ATRA and sorafenib can be developed as a novel drug combination therapy for AML patients because this drug combination augments apoptosis by inhibiting Bcl-2 and Mcl-1. Tretinoin 0-4 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 162-167
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 167-169 retinoid X receptor beta Homo sapiens 0-24
25956707-5 2016 We additionally found that short-term treatment of primary osteoblasts with RA causes a rapid induction of specific genes involved in either retinol-dependent signaling (i.e. Rara, Crabp2) or skeletal remodeling (i.e. Twist2, Tnfsf11). Tretinoin 76-78 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 226-233
24916380-7 2014 In summary, deleterious mutations in RDH11, an important enzyme for vision-related and systemic retinoic acid metabolism, cause a new syndrome with RP. Tretinoin 96-109 retinol dehydrogenase 11 Homo sapiens 37-42
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 167-169 retinoid X receptor beta Homo sapiens 26-30
8104620-6 1993 To date 6 Homeobox genes (HoxC6, HoxC8, HoxD1, HoxD4, HoxD8, and HoxD9) have been identified in the cDNA library prepared from LA-N-5 cells treated with retinoic acid. Tretinoin 153-166 homeobox C8 Homo sapiens 33-38
25201493-3 2014 The present study investigated the effects of ATRA on the expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1alpha (HIF-1alpha) in various glioma cell lines under normoxia and hypoxia. Tretinoin 46-50 vascular endothelial growth factor A Rattus norvegicus 72-106
25201493-3 2014 The present study investigated the effects of ATRA on the expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1alpha (HIF-1alpha) in various glioma cell lines under normoxia and hypoxia. Tretinoin 46-50 vascular endothelial growth factor A Rattus norvegicus 108-112
25201493-9 2014 Following ATRA treatment, the expression of VEGF and HIF-1alpha was found to vary among the different concentration groups. Tretinoin 10-14 vascular endothelial growth factor A Rattus norvegicus 44-48
26578346-8 2016 RESULTS: Four weeks of retinoic acid and retinol treatments both increased epidermal thickness, and upregulated genes for collagen type 1 (COL1A1), and collagen type 3 (COL3A1) with corresponding increases in procollagen I and procollagen III protein expression. Tretinoin 23-36 collagen type III alpha 1 chain Homo sapiens 169-175
26902198-0 2016 [All-trans retinoic acid improves iodine uptake of thyroid cancer cells via repressing transcriptional activity of beta-catenin]. Tretinoin 1-24 catenin beta 1 Homo sapiens 115-127
26902198-1 2016 OBJECTIVE: To determine whether all-trans retinoic acid (ATRA) could improve iodine uptake via repressing transcriptional activity of beta-catenin in thyroid cancer cells. Tretinoin 32-55 catenin beta 1 Homo sapiens 134-146
26902198-1 2016 OBJECTIVE: To determine whether all-trans retinoic acid (ATRA) could improve iodine uptake via repressing transcriptional activity of beta-catenin in thyroid cancer cells. Tretinoin 57-61 catenin beta 1 Homo sapiens 134-146
26902198-2 2016 METHODS: Three kinds of treatment models were firstly established with alcohol, ATRA, and transfection of beta-catenin shRNA in undifferentiated human thyroid cancer cell line-SW1736.Then the expressions of sodium iodide symporter (NIS), beta-catenin and its regulating factors, epithelial-mensechymal transition (EMT)-phenotype, invasion and metastasis associated proteins were further measured in above three cell models.After that, the influence of ATRA on the functional expression of NIS, iodine uptake potency, tumor growth curve and treatment effect inducing by radioactive iodine was comparatively analyzed in vitro and in vivo trials. Tretinoin 452-456 catenin beta 1 Homo sapiens 106-118
25201493-10 2014 In the glioma cells in the lower concentration groups (5 and 10 micromol/l ATRA), a significant increase in VEGF and HIF-1alpha expression was observed. Tretinoin 75-79 vascular endothelial growth factor A Rattus norvegicus 108-112
25201493-11 2014 Conversely, a significant decrease in VEGF and HIF-1alpha expression was found in the glioma cells in the high ATRA concentration group (40 micromol/l), compared with that in the cells in the control group. Tretinoin 111-115 vascular endothelial growth factor A Rattus norvegicus 38-42
8103115-4 1993 Concomitantly, RA reduced the specific activities of two catecholamine synthetic enzymes, tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) and the level of norepinephrine (NE). Tretinoin 15-17 tyrosine hydroxylase Rattus norvegicus 90-110
25531381-5 2014 PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src. Tretinoin 285-289 phosphatase and tensin homolog Homo sapiens 88-92
25175738-7 2014 All-trans RA treatment reduced the gene expression levels of Cyp7a1, Cyp8b1, and Akr1d1, which are involved in bile acid synthesis. Tretinoin 10-12 aldo-keto reductase family 1, member D1 Mus musculus 81-87
25175738-8 2014 All-trans RA also decreased the hepatic mRNA levels of Lrh-1 (Nr5a2) and Hnf4alpha (Nr2a1), which positively regulate the gene expression of Cyp7a1 and Cyp8b1. Tretinoin 10-12 nuclear receptor subfamily 5, group A, member 2 Mus musculus 55-60
25175738-8 2014 All-trans RA also decreased the hepatic mRNA levels of Lrh-1 (Nr5a2) and Hnf4alpha (Nr2a1), which positively regulate the gene expression of Cyp7a1 and Cyp8b1. Tretinoin 10-12 nuclear receptor subfamily 5, group A, member 2 Mus musculus 62-67
25175738-9 2014 Moreover, all-trans RA induced the gene expression levels of negative regulators of bile acid synthesis including hepatic Fgfr4, Fxr, and Shp (Nr0b2) as well as ileal Fgf15. Tretinoin 20-22 fibroblast growth factor 15 Mus musculus 167-172
28219859-8 2016 CONCLUSION: ATRA can reduce the production of TNF-alpha and IL-17A and increase the production of IL-10 to alleviate the inflammation in rats with CIA. Tretinoin 12-16 interleukin 17A Rattus norvegicus 60-66
28219859-8 2016 CONCLUSION: ATRA can reduce the production of TNF-alpha and IL-17A and increase the production of IL-10 to alleviate the inflammation in rats with CIA. Tretinoin 12-16 interleukin 10 Rattus norvegicus 98-103
8103115-4 1993 Concomitantly, RA reduced the specific activities of two catecholamine synthetic enzymes, tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) and the level of norepinephrine (NE). Tretinoin 15-17 tyrosine hydroxylase Rattus norvegicus 112-114
26892828-1 2016 Substantial evidence exists that during fetal ovarian development in mammals, retinoic acid (RA) induces germ cells to express the pre-meiotic marker Stra8 and enter meiosis, and that these effects are prevented in the fetal testis by the RA-degrading P450 enzyme CYP26B1. Tretinoin 78-91 stimulated by retinoic acid gene 8 Mus musculus 150-155
26892828-1 2016 Substantial evidence exists that during fetal ovarian development in mammals, retinoic acid (RA) induces germ cells to express the pre-meiotic marker Stra8 and enter meiosis, and that these effects are prevented in the fetal testis by the RA-degrading P450 enzyme CYP26B1. Tretinoin 93-95 stimulated by retinoic acid gene 8 Mus musculus 150-155
8251184-1 1993 Nuclear retinoic acid receptors RAR alpha, RAR beta and RAR gamma are transcription factors that bind all-trans retinoic acid as their ligand and mediate its action by activating particular set of genes that contain retinoic acid responsive elements in their promoter-enhancers. Tretinoin 8-21 retinoic acid receptor, beta Mus musculus 43-51
26830006-5 2016 We found that just like natural ligand RA, a RAR-selective ligand is an effective enhancer in the commitment of skeletal muscle lineage at the early stage of myogenic differentiation. Tretinoin 39-41 retinoic acid receptor alpha Homo sapiens 45-48
25143356-8 2014 Rbp1(-/-) mice showed reduced endometrial ATRA concentrations compared with wild type, associated with loss of tissue organization and hypercellularity. Tretinoin 42-46 retinol binding protein 1, cellular Mus musculus 0-4
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 3-23 retinoic acid receptor alpha Homo sapiens 173-201
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 3-23 retinoic acid receptor alpha Homo sapiens 203-212
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 173-201
24694005-1 2014 All-trans-retinoic acid (ATRA) can regulate some specific genes expression in various tissue and cells via nuclear retinoic acid receptors (RARs), including three subtypes: retinoic acid receptor-alpha (RAR-alpha), retinoic acid receptor-beta (RAR-beta) and retinoic acid receptor-gamma (RAR-gamma). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 203-212
24694005-13 2014 In conclusion, ATRA may increase expression of MMP-2 and MMP-9 by the potential signal pathway of RAR-alpha and RAR-gamma in injury podocyte induced by adriamycin, but not RAR-beta. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 98-107
26830006-7 2016 Also similar to natural ligand RA, the RAR-selective ligand enhances myogenic differentiation through beta-catenin signaling pathway while inhibiting cardiac differentiation. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 39-42
26830006-7 2016 Also similar to natural ligand RA, the RAR-selective ligand enhances myogenic differentiation through beta-catenin signaling pathway while inhibiting cardiac differentiation. Tretinoin 31-33 catenin beta 1 Homo sapiens 102-114
8251184-1 1993 Nuclear retinoic acid receptors RAR alpha, RAR beta and RAR gamma are transcription factors that bind all-trans retinoic acid as their ligand and mediate its action by activating particular set of genes that contain retinoic acid responsive elements in their promoter-enhancers. Tretinoin 112-125 retinoic acid receptor, beta Mus musculus 43-51
8507200-0 1993 Midkine is a mediator of retinoic acid induced neuronal differentiation of embryonal carcinoma cells. Tretinoin 25-38 midkine Mus musculus 0-7
26341094-3 2016 In this work, insights on BMP16 were provided through the comparative analysis of structural and functional data for zebrafish BMP2a, BMP2b, BMP4 and BMP16 genes and proteins, determined from three-dimensional models, patterns of gene expression during development and in adult tissues, regulation by retinoic acid and capacity to activate BMP-signaling pathway. Tretinoin 301-314 bone morphogenetic protein 16 Danio rerio 26-31
26341094-7 2016 Retinoic acid, a morphogen known to interact with BMP-signaling during bone formation, was shown to down-regulate the expression of bmp2, bmp4 and bmp16, although to different extents. Tretinoin 0-13 bone morphogenetic protein 16 Danio rerio 147-152
27089249-3 2016 In classic APL harboring PML-RARalpha transcripts, more than 90% of patients can achieve complete remission when treated with ATRA combined with arsenic trioxide chemotherapy. Tretinoin 126-130 retinoic acid receptor alpha Homo sapiens 29-37
25071154-3 2014 Here, we show that UTX interacts with the retinoic acid receptor alpha (RARalpha) and that this interaction is essential for proper differentiation of leukemic U937 cells in response to retinoic acid. Tretinoin 42-55 retinoic acid receptor alpha Homo sapiens 72-80
25309332-0 2014 FOXP2 drives neuronal differentiation by interacting with retinoic acid signaling pathways. Tretinoin 58-71 forkhead box P2 Homo sapiens 0-5
25309332-5 2014 We identified a network of FOXP2 regulated genes related to retinoic acid signaling and neuronal differentiation. Tretinoin 60-73 forkhead box P2 Homo sapiens 27-32
25309332-7 2014 Crucially, cells expressing FOXP2 displayed increased sensitivity to retinoic acid exposure. Tretinoin 69-82 forkhead box P2 Homo sapiens 28-33
8507200-3 1993 Synthesis and release of MK in the EC cells treated with retinoic acid were shown by Western blot analysis, and rabbit anti-MK antibody attenuated the action of retinoic acid to induce the neuronal differentiation. Tretinoin 57-70 midkine Mus musculus 25-27
25309332-8 2014 This suggests a mechanism by which FOXP2 may be able to increase the cellular differentiation response to environmental retinoic acid cues for specific subsets of neurons in the brain. Tretinoin 120-133 forkhead box P2 Homo sapiens 35-40
8507200-3 1993 Synthesis and release of MK in the EC cells treated with retinoic acid were shown by Western blot analysis, and rabbit anti-MK antibody attenuated the action of retinoic acid to induce the neuronal differentiation. Tretinoin 161-174 midkine Mus musculus 124-126
25155613-0 2014 SIRT1-mediated deacetylation of CRABPII regulates cellular retinoic acid signaling and modulates embryonic stem cell differentiation. Tretinoin 59-72 sirtuin 1 Mus musculus 0-5
26373900-2 2016 The disorder is caused by mutations in STRA6, an important regulator of vitamin A and retinoic acid metabolism. Tretinoin 86-99 signaling receptor and transporter of retinol STRA6 Homo sapiens 39-44
8507200-4 1993 These results indicate that MK is one of the mediators of retinoic acid action to induce the neuronal differentiation in EC cells. Tretinoin 58-71 midkine Mus musculus 28-30
8103274-1 1993 The induction of epidermal ornithine decarboxylase (ODC) can be partially blocked by corticosteroids, retinoic acid or active vitamin D3. Tretinoin 102-115 ornithine decarboxylase 1 Homo sapiens 27-50
24800886-9 2014 Combined treatment with belinostat and RA dose dependently accelerated and reinforced granulocytic differentiation, accompanied by changes in the expression of CD11b, C/EBPalpha (CCAAT/enhancer binding protein-alpha), and C/EBPepsilon. Tretinoin 39-41 CCAAT enhancer binding protein epsilon Homo sapiens 222-234
8103274-1 1993 The induction of epidermal ornithine decarboxylase (ODC) can be partially blocked by corticosteroids, retinoic acid or active vitamin D3. Tretinoin 102-115 ornithine decarboxylase 1 Homo sapiens 52-55
26096167-4 2016 We recently demonstrated that ATRA up-regulated the LMX1B, and down-regulated the transforming growth factor-beta1, collagen IV and fibronectin in a hypoxia/reoxygenation (H-R) injury system in renal tubular epithelial cells (RTEC). Tretinoin 30-34 LIM homeobox transcription factor 1 beta Felis catus 52-57
8387038-7 1993 The differential effects between these two hormone are likely to be related to the ability of RA-activated endogenous retinoic acid receptors (RARs) to induce C2 myoblasts growth-arrest and to extinguish AP1 activity (thought to act as an inhibitor of myogenesis) whereas T3-activated endogenous thyroid hormones receptors (THRs) are relatively inefficient. Tretinoin 94-96 jun proto-oncogene Mus musculus 204-207
26456050-5 2016 Culture of hMSC with a combination of factors that induce photoreceptor differentiation of hMSC (FGF2, taurine, retinoic acid, and insulin-like growth factor type1; FTRI), markedly upregulated the expression of components of the canonical Wnt signaling pathway, including WNT2B, DKK1, and active beta-CATENIN. Tretinoin 112-125 musculin Homo sapiens 11-15
26456050-5 2016 Culture of hMSC with a combination of factors that induce photoreceptor differentiation of hMSC (FGF2, taurine, retinoic acid, and insulin-like growth factor type1; FTRI), markedly upregulated the expression of components of the canonical Wnt signaling pathway, including WNT2B, DKK1, and active beta-CATENIN. Tretinoin 112-125 musculin Homo sapiens 91-95
25126713-3 2014 Retinoic acid (RA) decreases the levels of epidermal melanin by suppressing the expression of melanogenic enzymes including tyrosinase, which is the rate-limiting enzyme in melanin synthesis. Tretinoin 0-13 tyrosinase Mus musculus 124-134
25126713-3 2014 Retinoic acid (RA) decreases the levels of epidermal melanin by suppressing the expression of melanogenic enzymes including tyrosinase, which is the rate-limiting enzyme in melanin synthesis. Tretinoin 15-17 tyrosinase Mus musculus 124-134
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 glutamic-oxaloacetic transaminase 2 Homo sapiens 184-210
25136779-0 2014 All-trans-retinoid acid (ATRA) suppresses chondrogenesis of rat primary hind limb bud mesenchymal cells by downregulating p63 and cartilage-specific molecules. Tretinoin 25-29 tumor protein p63 Homo sapiens 122-125
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 48-50 retinoic acid receptor, beta Mus musculus 17-44
25136779-12 2014 Western blotting assays additionally showed that ATRA dose-dependently reduced the expression of Sox9, Col2al and p63 (P<0.05 in all vs. controls). Tretinoin 49-53 tumor protein p63 Homo sapiens 114-117
25136779-13 2014 Together, our results suggest that ATRA suppresses chondrogenesis by modulating the expression of Sox9, Col2al and p63 in primary hind limb bud mesenchymal cells. Tretinoin 35-39 tumor protein p63 Homo sapiens 115-118
26417682-4 2015 Here, we report that DPF2, a plant homeodomain (PHD) finger protein, is upregulated during H9 cell differentiation induced by retinoic acid. Tretinoin 126-139 double PHD fingers 2 Homo sapiens 21-25
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 83-85 retinoic acid receptor, beta Mus musculus 17-44
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 83-85 retinoic acid receptor, beta Mus musculus 17-44
8096385-1 1993 Exposure of midgastrulation mouse embryos to retinoic acid induced anteriorized expression of the Hoxa-1 (Hox-1.6) and Hoxb-1 (Hox-2.9) genes. Tretinoin 45-58 homeobox A1 Mus musculus 98-104
26476360-5 2015 Additionally, expression of BAX and SHC1 were lower in both non-encapsulated tretinoin (TTN) and TTN-LNC-treated groups. Tretinoin 77-86 BCL2 associated X, apoptosis regulator Bos taurus 28-31
25249571-6 2014 Treatment of RA-stimulated differentiating SH-SY5Y cells with 1 to 3 mumol/L cadmium resulted in decreased level of cross-reactivities with 43-kDa growth-associated protein (GAP-43) in a dose-dependent manner. Tretinoin 13-15 growth associated protein 43 Homo sapiens 174-180
24973045-0 2014 A RARE of hepatic Gck promoter interacts with RARalpha, HNF4alpha and COUP-TFII that affect retinoic acid- and insulin-induced Gck expression. Tretinoin 92-105 retinoic acid receptor, alpha Rattus norvegicus 46-54
24973045-0 2014 A RARE of hepatic Gck promoter interacts with RARalpha, HNF4alpha and COUP-TFII that affect retinoic acid- and insulin-induced Gck expression. Tretinoin 92-105 hepatocyte nuclear factor 4, alpha Rattus norvegicus 56-65
24973045-0 2014 A RARE of hepatic Gck promoter interacts with RARalpha, HNF4alpha and COUP-TFII that affect retinoic acid- and insulin-induced Gck expression. Tretinoin 92-105 nuclear receptor subfamily 2, group F, member 2 Rattus norvegicus 70-79
26708897-9 2015 Benzidine staining showed that ATRA could induce hemoglobin production in K562 cells with TBLR1-RARalpha fusion gene expression. Tretinoin 31-35 retinoic acid receptor alpha Homo sapiens 96-104
8096385-1 1993 Exposure of midgastrulation mouse embryos to retinoic acid induced anteriorized expression of the Hoxa-1 (Hox-1.6) and Hoxb-1 (Hox-2.9) genes. Tretinoin 45-58 homeobox A1 Mus musculus 106-113
8096385-1 1993 Exposure of midgastrulation mouse embryos to retinoic acid induced anteriorized expression of the Hoxa-1 (Hox-1.6) and Hoxb-1 (Hox-2.9) genes. Tretinoin 45-58 homeobox B1 Mus musculus 119-125
8096385-1 1993 Exposure of midgastrulation mouse embryos to retinoic acid induced anteriorized expression of the Hoxa-1 (Hox-1.6) and Hoxb-1 (Hox-2.9) genes. Tretinoin 45-58 homeobox B1 Mus musculus 127-134
25008916-5 2014 gp120 from multiple HIV-1 subtypes bound to RA-activated PBMCs from three donors in a CD4-dependent manner, but little or no alpha4beta7 binding was detected. Tretinoin 44-46 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 0-5
8382035-4 1993 In binding studies the equilibrium dissociation constant, Kd, of retinoic acid (RA) for E. coli-derived CRABP-I and CRABP-II was 6.8 and 39 nM, respectively. Tretinoin 65-78 cellular retinoic acid binding protein 1 Homo sapiens 104-111
26600489-0 2015 Effect of all-trans retinoic acids (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in the lung tissues of rats with pulmonary arterial hypertension (PAH). Tretinoin 10-34 actin gamma 2, smooth muscle Rattus norvegicus 63-88
8382035-4 1993 In binding studies the equilibrium dissociation constant, Kd, of retinoic acid (RA) for E. coli-derived CRABP-I and CRABP-II was 6.8 and 39 nM, respectively. Tretinoin 80-82 cellular retinoic acid binding protein 1 Homo sapiens 104-111
26600489-0 2015 Effect of all-trans retinoic acids (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in the lung tissues of rats with pulmonary arterial hypertension (PAH). Tretinoin 10-34 actin gamma 2, smooth muscle Rattus norvegicus 90-99
26600489-0 2015 Effect of all-trans retinoic acids (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in the lung tissues of rats with pulmonary arterial hypertension (PAH). Tretinoin 36-40 actin gamma 2, smooth muscle Rattus norvegicus 63-88
24803390-1 2014 Transcription factor Foxa1 plays a critical role during neural differentiation and is induced immediately after retinoic acid (RA)-initiated differentiation of pluripotent P19 embryonal carcinoma cells, correlated with the downregulated expression of pluripotency-related genes such as Nanog. Tretinoin 112-125 forkhead box A1 Homo sapiens 21-26
24803390-1 2014 Transcription factor Foxa1 plays a critical role during neural differentiation and is induced immediately after retinoic acid (RA)-initiated differentiation of pluripotent P19 embryonal carcinoma cells, correlated with the downregulated expression of pluripotency-related genes such as Nanog. Tretinoin 127-129 forkhead box A1 Homo sapiens 21-26
26600489-0 2015 Effect of all-trans retinoic acids (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in the lung tissues of rats with pulmonary arterial hypertension (PAH). Tretinoin 36-40 actin gamma 2, smooth muscle Rattus norvegicus 90-99
8382035-6 1993 RA competed with the binding of CD 367 to CRABP-I and CRABP-II with IC50 values of 20.0 and 90.0 nM, respectively. Tretinoin 0-2 cellular retinoic acid binding protein 1 Homo sapiens 42-49
26600489-1 2015 The effect of all-trans retinoic acid (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Tretinoin 14-37 actin gamma 2, smooth muscle Rattus norvegicus 66-91
26600489-1 2015 The effect of all-trans retinoic acid (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Tretinoin 14-37 actin gamma 2, smooth muscle Rattus norvegicus 93-102
8382035-10 1993 The observed difference in affinity for RA supports the idea that CRABP-I, which is constitutively expressed, and CRABP-II, which is induced by RA, have different functions in the cell. Tretinoin 40-42 cellular retinoic acid binding protein 1 Homo sapiens 66-73
26600489-1 2015 The effect of all-trans retinoic acid (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Tretinoin 39-43 actin gamma 2, smooth muscle Rattus norvegicus 66-91
26600489-1 2015 The effect of all-trans retinoic acid (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Tretinoin 39-43 actin gamma 2, smooth muscle Rattus norvegicus 93-102
26600489-1 2015 The effect of all-trans retinoic acid (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Tretinoin 203-207 actin gamma 2, smooth muscle Rattus norvegicus 66-91
26600489-1 2015 The effect of all-trans retinoic acid (ATRA) on the expression of alpha-smooth muscle actin (alpha-SMA) in rats with pulmonary arterial hypertension (PAH) was studied, and the mechanism of the effect of ATRA on PAH was proposed. Tretinoin 203-207 actin gamma 2, smooth muscle Rattus norvegicus 93-102
26600489-11 2015 ATRA inhibited the alpha-SMA mRNA and protein expressionin the lung tissues of rats with MCT-induced PAH, and could be used to treat PAH. Tretinoin 0-4 actin gamma 2, smooth muscle Rattus norvegicus 19-28
25116125-6 2014 Celastrol"s effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. Tretinoin 32-36 mitogen-activated protein kinase kinase 1 Homo sapiens 73-77
8382159-1 1993 The levels of the mRNA corresponding to the intracellular binding proteins for retinoic acid and retinol (CRABP1 and CRBP1, respectively) were studied in primary cultures of somatic and germ cells of the rat seminiferous tubules. Tretinoin 79-92 cellular retinoic acid binding protein 1 Rattus norvegicus 106-112
25102060-2 2014 In mice, retinoic acid (RA), the extrinsic signal for meiotic initiation, activates transcription of Stra8, which is required for meiotic DNA replication and the subsequent processes of meiotic prophase. Tretinoin 9-22 stimulated by retinoic acid gene 8 Mus musculus 101-106
25102060-2 2014 In mice, retinoic acid (RA), the extrinsic signal for meiotic initiation, activates transcription of Stra8, which is required for meiotic DNA replication and the subsequent processes of meiotic prophase. Tretinoin 24-26 stimulated by retinoic acid gene 8 Mus musculus 101-106
8436299-0 1993 An everted repeat mediates retinoic acid induction of the gamma F-crystallin gene: evidence of a direct role for retinoids in lens development. Tretinoin 27-40 crystallin, gamma F Mus musculus 58-76
24994461-9 2014 Taken together, these results indicate that RA induces IgA isotype switching mainly through RARalpha in human B cells. Tretinoin 44-46 retinoic acid receptor alpha Homo sapiens 92-100
24953245-10 2014 Annexin-V-fluorescein staining revealed that a combination of ATRA and ATO and combination of the three agents did not induce apoptosis in NB4 cells. Tretinoin 62-66 annexin A5 Homo sapiens 0-9
26545364-6 2015 We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. Tretinoin 78-91 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-40
26545364-6 2015 We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. Tretinoin 78-91 Pvt1 oncogene Homo sapiens 45-49
26545364-6 2015 We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. Tretinoin 93-97 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-40
26545364-6 2015 We then observed significantly lower MYC and PVT1 expression during all-trans retinoic acid (ATRA)-induced differentiation and cell cycle arrest in the APL cell line. Tretinoin 93-97 Pvt1 oncogene Homo sapiens 45-49
25072246-0 2014 A PU.1 suppressive target gene, metallothionein 1G, inhibits retinoic acid-induced NB4 cell differentiation. Tretinoin 61-74 metallothionein 1G Homo sapiens 32-50
8436299-3 1993 We have identified a novel type of RA response element (RARE) within the lens-specific mouse gamma F-crystallin promoter, consisting of two (A/G)GGTCA motifs in an everted arrangement spaced by 8 nucleotides. Tretinoin 35-37 crystallin, gamma F Mus musculus 93-111
24686085-1 2014 The leukocyte antigen CD38 is expressed after all-trans retinoic acid (ATRA) treatment in HL-60 myelogenous leukemia cells and promotes induced myeloid differentiation when overexpressed. Tretinoin 56-69 CD38 molecule Homo sapiens 22-26
24686085-1 2014 The leukocyte antigen CD38 is expressed after all-trans retinoic acid (ATRA) treatment in HL-60 myelogenous leukemia cells and promotes induced myeloid differentiation when overexpressed. Tretinoin 71-75 CD38 molecule Homo sapiens 22-26
8386111-6 1993 While in the dependent lines and Hs578T RA activated RA responsive element-dependent transcriptional activity, this response was very low in MDA-MB231, MDA-MB468, and BT20, suggesting that the RA resistance of these latter three ER-negative lines is due to underexpression of functional RARs. Tretinoin 40-42 arginyl-tRNA synthetase 1 Homo sapiens 287-291
24686085-5 2014 We observed that Lyn inhibition blocked c-Cbl and p85/p55 PI3K phosphorylation driven by the anti-CD38 agonistic mAb IB4 in ATRA-treated HL-60 cells and untreated CD38+ transfectants. Tretinoin 124-128 Casitas B-lineage lymphoma Mus musculus 40-45
24686085-5 2014 We observed that Lyn inhibition blocked c-Cbl and p85/p55 PI3K phosphorylation driven by the anti-CD38 agonistic mAb IB4 in ATRA-treated HL-60 cells and untreated CD38+ transfectants. Tretinoin 124-128 CD38 molecule Homo sapiens 163-167
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 77-81 Cbl proto-oncogene Homo sapiens 118-123
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 77-81 CD38 molecule Homo sapiens 274-278
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 105-109 Cbl proto-oncogene Homo sapiens 118-123
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 105-109 CD38 molecule Homo sapiens 274-278
26333706-14 2015 The levels of Foxp3, TGF-beta, and IL-10 mRNA, as well as the percentage of CD4+CD25+Foxp3+ T cells, were higher in the ATRA group than in theAR group. Tretinoin 120-124 forkhead box P3 Mus musculus 14-19
26333706-14 2015 The levels of Foxp3, TGF-beta, and IL-10 mRNA, as well as the percentage of CD4+CD25+Foxp3+ T cells, were higher in the ATRA group than in theAR group. Tretinoin 120-124 forkhead box P3 Mus musculus 85-90
26248086-10 2015 Genes in a pathway regulated by retinoic acid-regulated nuclear protein made the largest contribution to this gene set (P < .0001); the transcription factor MYC regulated at least 30% of genes within the signature (P < .0001). Tretinoin 32-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 160-163
24686085-11 2014 Therefore, Lyn kinase activity is important for CD38-associated signaling that may drive ATRA-induced differentiation. Tretinoin 89-93 CD38 molecule Homo sapiens 48-52
8472843-5 1993 In the presence of RA, the T3 effect on TR beta-2 mRNA levels was blunted with mRNA levels decreasing by only 20%. Tretinoin 19-21 thyroid hormone receptor beta Rattus norvegicus 40-47
24592821-2 2014 However, in the majority of patients given all-trans retinoic acid (ATRA)/anthracycline-based induction therapy, PML-RARalpha transcript remains even when haematologic complete remission is achieved. Tretinoin 43-66 retinoic acid receptor alpha Homo sapiens 117-125
24592821-2 2014 However, in the majority of patients given all-trans retinoic acid (ATRA)/anthracycline-based induction therapy, PML-RARalpha transcript remains even when haematologic complete remission is achieved. Tretinoin 68-72 PML nuclear body scaffold Homo sapiens 113-116
25899567-5 2015 Antagonism of RA receptors reduced production of resistin-like molecule alpha by DCs responding to IL-4, while addition of exogenous RA enhanced production of this marker of alternative activation. Tretinoin 14-16 interleukin 4 Mus musculus 99-103
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 14-16 interleukin 4 Mus musculus 93-97
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 14-16 heart and neural crest derivatives expressed 2 Mus musculus 227-230
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 154-156 heart and neural crest derivatives expressed 2 Mus musculus 227-230
24592821-2 2014 However, in the majority of patients given all-trans retinoic acid (ATRA)/anthracycline-based induction therapy, PML-RARalpha transcript remains even when haematologic complete remission is achieved. Tretinoin 68-72 retinoic acid receptor alpha Homo sapiens 117-125
8422465-0 1993 Regulation of myeloblastin messenger RNA expression in myeloid leukemia cells treated with all-trans retinoic acid. Tretinoin 101-114 proteinase 3 Homo sapiens 14-26
25161869-9 2014 Finally, we analyzed the effect of retinoic acid (RA), a potent stimulator of keratinocyte proliferation, on AQP3 and AQP9 mRNA expression in differentiated NHEK. Tretinoin 35-48 aquaporin 3 (Gill blood group) Homo sapiens 109-113
25161869-9 2014 Finally, we analyzed the effect of retinoic acid (RA), a potent stimulator of keratinocyte proliferation, on AQP3 and AQP9 mRNA expression in differentiated NHEK. Tretinoin 50-52 aquaporin 3 (Gill blood group) Homo sapiens 109-113
26483874-5 2015 RAR bind to all-trans-retinoic acid (ATRA) to induce the transcription of genes responsible for cellular differentiation. Tretinoin 12-35 retinoic acid receptor alpha Homo sapiens 0-3
26483874-5 2015 RAR bind to all-trans-retinoic acid (ATRA) to induce the transcription of genes responsible for cellular differentiation. Tretinoin 37-41 retinoic acid receptor alpha Homo sapiens 0-3
8422465-5 1993 Here we have investigated the regulation of mbn messenger RNA (mRNA) expression in two human leukemia cell lines, HL-60 and NB4, treated with all-trans retinoic acid. Tretinoin 152-165 proteinase 3 Homo sapiens 44-47
24720386-3 2014 The resulting fusion proteins retain domains of the RARA protein allowing binding to retinoic acid response elements (RARE) and dimerization with the retinoid X receptor protein (RXRA). Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 52-56
24720386-7 2014 RARA fusion proteins behave as potent transcriptional repressors of retinoic acid signalling, inducing a differentiation blockage at the promyelocyte stage which can be overcome with therapeutic doses of ATRA or arsenic trioxide. Tretinoin 68-81 retinoic acid receptor alpha Homo sapiens 0-4
8422465-9 1993 Our results show that in HL-60 cells, all-trans retinoic acid rapidly decreased transcription of mbn. Tretinoin 48-61 proteinase 3 Homo sapiens 97-100
24720386-7 2014 RARA fusion proteins behave as potent transcriptional repressors of retinoic acid signalling, inducing a differentiation blockage at the promyelocyte stage which can be overcome with therapeutic doses of ATRA or arsenic trioxide. Tretinoin 204-208 retinoic acid receptor alpha Homo sapiens 0-4
8385449-5 1993 In this article I propose that the amount of RA reaching the nucleus in different embryonic tissues is modulated by a mechanism involving three cytoplasmic binding proteins for retinol (CRBP I) and retinoic acid (CRABP I and II). Tretinoin 45-47 retinol binding protein 1 Homo sapiens 186-192
26414475-4 2015 It is important to identify these cryptic and variant translocations because certain variants, including ZBTB16/RARA and STAT5B/RARA, are resistant to treatment with all-trans retinoic acid, arsenic trioxide, and anthracyclines. Tretinoin 176-189 retinoic acid receptor alpha Homo sapiens 112-116
26414475-4 2015 It is important to identify these cryptic and variant translocations because certain variants, including ZBTB16/RARA and STAT5B/RARA, are resistant to treatment with all-trans retinoic acid, arsenic trioxide, and anthracyclines. Tretinoin 176-189 retinoic acid receptor alpha Homo sapiens 128-132
24733397-1 2014 The retinoic acid-inducible dehydrogenase reductase 3 (DHRS3) is thought to function as a retinaldehyde reductase that controls the levels of all-trans-retinaldehyde, the immediate precursor for bioactive all-trans-retinoic acid. Tretinoin 205-228 dehydrogenase/reductase (SDR family) member 3 Mus musculus 28-53
8385449-5 1993 In this article I propose that the amount of RA reaching the nucleus in different embryonic tissues is modulated by a mechanism involving three cytoplasmic binding proteins for retinol (CRBP I) and retinoic acid (CRABP I and II). Tretinoin 45-47 retinol binding protein 1 Homo sapiens 213-227
24733397-1 2014 The retinoic acid-inducible dehydrogenase reductase 3 (DHRS3) is thought to function as a retinaldehyde reductase that controls the levels of all-trans-retinaldehyde, the immediate precursor for bioactive all-trans-retinoic acid. Tretinoin 205-228 dehydrogenase/reductase (SDR family) member 3 Mus musculus 55-60
8385449-5 1993 In this article I propose that the amount of RA reaching the nucleus in different embryonic tissues is modulated by a mechanism involving three cytoplasmic binding proteins for retinol (CRBP I) and retinoic acid (CRABP I and II). Tretinoin 198-211 retinol binding protein 1 Homo sapiens 213-227
24733397-4 2014 The RDH10-activated DHRS3 acts as a robust high affinity all-trans-retinaldehyde-specific reductase that effectively converts retinaldehyde back to retinol, decreasing the rate of retinoic acid biosynthesis. Tretinoin 180-193 dehydrogenase/reductase (SDR family) member 3 Mus musculus 20-25
27148563-4 2015 Analysis of the sequencing data permitted characterization of both chromosomal breakpoints and revealed two additional alterations, a small deletion in RARA exon 9 and a RARA R276W substitution, that have been linked to resistance to all-trans retinoic acid. Tretinoin 244-257 retinoic acid receptor alpha Homo sapiens 152-156
27148563-4 2015 Analysis of the sequencing data permitted characterization of both chromosomal breakpoints and revealed two additional alterations, a small deletion in RARA exon 9 and a RARA R276W substitution, that have been linked to resistance to all-trans retinoic acid. Tretinoin 244-257 retinoic acid receptor alpha Homo sapiens 170-174
24733397-6 2014 At E13.5, DHRS3-null embryos have ~4-fold lower levels of retinol and retinyl esters, but only slightly elevated levels of retinoic acid. Tretinoin 123-136 dehydrogenase/reductase (SDR family) member 3 Mus musculus 10-15
7678784-1 1993 It was previously demonstrated that retinoic acid (RA) can enhance the functional responses of human T lymphocytes by increasing surface IL-2R alpha chain protein expression on proliferating T blasts, resulting in augmented IL-2-dependent growth. Tretinoin 36-49 interleukin 2 receptor subunit alpha Homo sapiens 137-148
24657437-0 2014 MicroRNA-432 contributes to dopamine cocktail and retinoic acid induced differentiation of human neuroblastoma cells by targeting NESTIN and RCOR1 genes. Tretinoin 50-63 REST corepressor 1 Homo sapiens 141-146
25753094-4 2015 The functional inhibition of gap junctions using either siRNA or pharmacological inhibition eliminated the miR-124-3p-mediated antiproliferation, whereas the enhancement of gap junctions with retinoic acid treatment augmented this miR-124-3p-mediated antiproliferation. Tretinoin 192-205 microRNA 124-3 Homo sapiens 231-241
7678784-1 1993 It was previously demonstrated that retinoic acid (RA) can enhance the functional responses of human T lymphocytes by increasing surface IL-2R alpha chain protein expression on proliferating T blasts, resulting in augmented IL-2-dependent growth. Tretinoin 51-53 interleukin 2 receptor subunit alpha Homo sapiens 137-148
24788806-0 2014 Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 121-124
24788806-3 2014 Granulocyte-macrophage colony-stimulating factor (GM-CSF) potently induces RALDH2 expression in DCs in an RA-dependent manner, and RA alone weakly induces the expression. Tretinoin 75-77 colony stimulating factor 2 Homo sapiens 0-48
7678784-2 1993 In the present study, we used IL-2-maintained lymphoblasts generated from human thymocytes to show that RA enhancement of IL-2R alpha is accompanied by an increase in steady-state levels of IL-2R alpha mRNA. Tretinoin 104-106 interleukin 2 receptor subunit alpha Homo sapiens 122-133
24788806-3 2014 Granulocyte-macrophage colony-stimulating factor (GM-CSF) potently induces RALDH2 expression in DCs in an RA-dependent manner, and RA alone weakly induces the expression. Tretinoin 75-77 colony stimulating factor 2 Homo sapiens 50-56
24788806-3 2014 Granulocyte-macrophage colony-stimulating factor (GM-CSF) potently induces RALDH2 expression in DCs in an RA-dependent manner, and RA alone weakly induces the expression. Tretinoin 106-108 colony stimulating factor 2 Homo sapiens 0-48
25975191-0 2015 Upregulation of CD38 expression on multiple myeloma cells by all-trans retinoic acid improves the efficacy of daratumumab. Tretinoin 71-84 CD38 molecule Homo sapiens 16-20
24838400-7 2015 Moreover, PKCdelta inhibition also impaired ATRA-induced RARalpha translocation to the nucleus. Tretinoin 44-48 retinoic acid receptor alpha Homo sapiens 57-65
24788806-3 2014 Granulocyte-macrophage colony-stimulating factor (GM-CSF) potently induces RALDH2 expression in DCs in an RA-dependent manner, and RA alone weakly induces the expression. Tretinoin 106-108 colony stimulating factor 2 Homo sapiens 50-56
7678784-2 1993 In the present study, we used IL-2-maintained lymphoblasts generated from human thymocytes to show that RA enhancement of IL-2R alpha is accompanied by an increase in steady-state levels of IL-2R alpha mRNA. Tretinoin 104-106 interleukin 2 receptor subunit alpha Homo sapiens 190-201
24788806-10 2014 In the presence of RA, ectopic expression of RARalpha/RXRalpha and Sp1 synergistically enhanced Aldh1a2 promoter-reporter activity. Tretinoin 19-21 retinoic acid receptor alpha Homo sapiens 45-53
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 109-113 patatin like phospholipase domain containing 2 Homo sapiens 146-150
7678784-5 1993 This contention was supported by the demonstrated ability of RA to activate the IL-2R alpha promoter in a chloramphenicol acetyltransferase plasmid construct that was transfected into the blast cells. Tretinoin 61-63 interleukin 2 receptor subunit alpha Homo sapiens 80-91
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 202-206 patatin like phospholipase domain containing 2 Homo sapiens 146-150
7678784-6 1993 In addition to inducing IL-2R alpha expression, RA also increased the surface expression and mRNA levels of IL-2R beta, the 75-kDa component of the IL-2 receptor that mediates IL-2 signal transduction. Tretinoin 48-50 interleukin 2 receptor subunit alpha Homo sapiens 24-35
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 53-66 stimulated by retinoic acid gene 8 Mus musculus 173-178
7678784-6 1993 In addition to inducing IL-2R alpha expression, RA also increased the surface expression and mRNA levels of IL-2R beta, the 75-kDa component of the IL-2 receptor that mediates IL-2 signal transduction. Tretinoin 48-50 interleukin 2 receptor subunit beta Homo sapiens 108-118
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 68-70 stimulated by retinoic acid gene 8 Mus musculus 173-178
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 162-164 stimulated by retinoic acid gene 8 Mus musculus 173-178
24525073-6 2014 Data from evaluation of DNA content and Annexin V binding assay by flow cytometry showed that TTN-LNC induced apoptosis and cell cycle arrest at the G1-phase while TTN did not. Tretinoin 94-97 annexin A5 Homo sapiens 40-49
26378784-5 2015 We characterized the regulation of these genes by 1) retinoic acid (RA), which induces meiosis, 2) Dazl, which is required for germ cell competence to respond to RA, and 3) Stra8, a downstream target of RA required for the chromosomal program of meiotic prophase. Tretinoin 162-164 stimulated by retinoic acid gene 8 Mus musculus 173-178
7678784-7 1993 These new findings showing regulation by RA of both IL-2R alpha and IL-2R beta suggest multiple pathways by which this retinoid can modulate functional IL-2 receptors. Tretinoin 41-43 interleukin 2 receptor subunit alpha Homo sapiens 52-63
26378784-7 2015 In the presence of Dazl, RA induces at least two pathways: one Stra8-independent, and one Stra8-dependent. Tretinoin 25-27 stimulated by retinoic acid gene 8 Mus musculus 63-68
7678784-7 1993 These new findings showing regulation by RA of both IL-2R alpha and IL-2R beta suggest multiple pathways by which this retinoid can modulate functional IL-2 receptors. Tretinoin 41-43 interleukin 2 receptor subunit beta Homo sapiens 68-78
26352270-6 2015 Conserved Retinoic Acid Response Elements (RAREs) upstream of human ALDH1A3 and FOXN1 and in mouse Aldh1a3 and Foxn1 genes were revealed using bioinformatic approximation. Tretinoin 10-23 aldehyde dehydrogenase 1 family member A3 Homo sapiens 68-75
24582848-9 2014 Reports depict that retinoic acid isomers enhance, the expression of genes linked with cholesterol efflux e.g. apoe, abca-1 and abcg-1 proteins in astrocytes. Tretinoin 20-33 ATP binding cassette subfamily G member 1 Mus musculus 128-134
1281109-5 1992 Retinoic acid suppressed the synthesis of peripherin, an intermediate filament protein predominantly found in peripheral nerve cells, but a high level of simple keratins, normally found in simple epithelial cells, was present in retinoic acid-treated PC12 cells. Tretinoin 0-13 peripherin Rattus norvegicus 42-52
25112011-5 2014 In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. Tretinoin 13-15 POU class 5 homeobox 1 Homo sapiens 132-136
26253409-7 2015 Stump osteoblasts manage to contribute to the blastema by upregulating expression of the RA-degrading enzyme cyp26b1. Tretinoin 89-91 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 109-116
26253409-10 2015 In turn, cyp26b1(+) fibroblast-derived blastema cells in the more proximal regenerate serve as a sink to reduce RA levels, thereby allowing differentiation of neighboring preosteoblasts. Tretinoin 112-114 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 9-16
1332684-9 1992 Gel-retardation analysis demonstrated that RAR-gamma 1 specifically bound the RA response element of the mouse RAR-beta gene. Tretinoin 43-45 retinoic acid receptor, beta Mus musculus 111-119
26038242-4 2015 RESULTS: LNCaP and PC3 parent cells were capable of responding to stem cell differentiation morphogen retinoic acid (RA), suggesting the presence of inherent stem-like properties. Tretinoin 102-115 chromobox 8 Homo sapiens 19-22
26038242-4 2015 RESULTS: LNCaP and PC3 parent cells were capable of responding to stem cell differentiation morphogen retinoic acid (RA), suggesting the presence of inherent stem-like properties. Tretinoin 117-119 chromobox 8 Homo sapiens 19-22
24660829-8 2014 Using this fluorescent probe, we revealed that CD38 is predominately on the plasma membrane of Raji and retinoic acid (RA)-treated HL-60 cells. Tretinoin 104-117 CD38 molecule Homo sapiens 47-51
24660829-8 2014 Using this fluorescent probe, we revealed that CD38 is predominately on the plasma membrane of Raji and retinoic acid (RA)-treated HL-60 cells. Tretinoin 119-121 CD38 molecule Homo sapiens 47-51
1480182-5 1992 Vgr-2 is expressed in F9 teratocarcinoma cells, and its RNA levels are down-regulated within 24 h after differentiation with retinoic acid. Tretinoin 125-138 growth differentiation factor 3 Mus musculus 0-5
24440820-6 2014 We demonstrate that during neuronal differentiation of Neuro-2a cells, RA induces Chka expression by a mechanism that involves ERK1/2 activation which triggers C/EBPbeta expression. Tretinoin 71-73 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 160-169
24655379-8 2014 When differentiation was induced by all-trans retinoic acid, CEACAM6 expression strongly correlated with luminal-like differentiation. Tretinoin 46-59 CEA cell adhesion molecule 6 Homo sapiens 61-68
26359103-9 2015 The levels of nestin, MAP2 and GFAP proteins in the ATRA group were significantly higher than those in both the brain slice co-culture group and the brain tissue homogenate supernatant group, but there was no significant difference between the brain slice co-culture group and the brain tissue homogenate supernatant group. Tretinoin 52-56 glial fibrillary acidic protein Mus musculus 31-35
1332671-6 1992 We show that CRABP-I and -II have similar M(r) values (15,000), but differ in their dissociation constant towards retinoic acid (Kd of 16.6 nM and 50 nM respectively), in pI (4.86 and 5.13) and in their relative mobilities (RF) on PAGE under nondenaturating conditions (RF values 0.65 and 0.44). Tretinoin 114-127 cellular retinoic acid binding protein 1 Homo sapiens 13-28
26201974-9 2015 Moreover, treatment with 9-cis-RA significantly increased the protein expression levels of ABCA1 and ABCG1 in J774A.1 macrophages in a dose-dependent manner. Tretinoin 30-33 ATP binding cassette subfamily G member 1 Mus musculus 101-106
24374552-0 2014 Aldehyde dehydrogenase 1 activity in the developing human pancreas modulates retinoic acid signalling in mediating islet differentiation and survival. Tretinoin 77-90 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-24
24374552-1 2014 AIMS/HYPOTHESIS: Aldehyde dehydrogenase 1 (ALDH1), a human stem-cell marker, is an enzyme responsible for converting retinaldehydes to retinoic acids (RAs) to modulate cell differentiation. Tretinoin 135-149 aldehyde dehydrogenase 1 family member A1 Homo sapiens 17-41
24374552-1 2014 AIMS/HYPOTHESIS: Aldehyde dehydrogenase 1 (ALDH1), a human stem-cell marker, is an enzyme responsible for converting retinaldehydes to retinoic acids (RAs) to modulate cell differentiation. Tretinoin 135-149 aldehyde dehydrogenase 1 family member A1 Homo sapiens 43-48
1332671-17 1992 The sharp increases in CRABP-II levels are associated with an alteration in the differentiation programme, as well as with cell response to retinoic acid overload, whereas CRABP-I might be a marker for terminal differentiation. Tretinoin 140-153 cellular retinoic acid binding protein 1 Homo sapiens 23-30
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 0-13 insulin like growth factor binding protein 2 Homo sapiens 231-237
24525295-0 2014 Long-range regulation by shared retinoic acid response elements modulates dynamic expression of posterior Hoxb genes in CNS development. Tretinoin 32-45 homeobox B cluster Mus musculus 106-110
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 0-13 insulin like growth factor binding protein 2 Homo sapiens 319-325
26296154-0 2015 Retinoic Acid Signaling Regulates Differential Expression of the Tandemly-Duplicated Long Wavelength-Sensitive Cone Opsin Genes in Zebrafish. Tretinoin 0-13 parapinopsin b Danio rerio 116-121
26296154-2 2015 Here we elucidate the role of RA in differential regulation of the tandemly-duplicated long wavelength-sensitive (LWS) cone opsin genes. Tretinoin 30-32 parapinopsin b Danio rerio 124-129
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 15-17 insulin like growth factor binding protein 2 Homo sapiens 231-237
26296154-9 2015 The RA signaling reporter line, RARE:YFP indicated that increased RA signaling in cones was associated with this opsin switch, and experimental reduction of RA signaling in larvae at the normal time of onset of LWS1 expression significantly inhibited LWS1 expression. Tretinoin 4-6 parapinopsin b Danio rerio 113-118
26296154-9 2015 The RA signaling reporter line, RARE:YFP indicated that increased RA signaling in cones was associated with this opsin switch, and experimental reduction of RA signaling in larvae at the normal time of onset of LWS1 expression significantly inhibited LWS1 expression. Tretinoin 4-6 opsin 1 (cone pigments), long-wave-sensitive, 1 Danio rerio 251-255
26296154-9 2015 The RA signaling reporter line, RARE:YFP indicated that increased RA signaling in cones was associated with this opsin switch, and experimental reduction of RA signaling in larvae at the normal time of onset of LWS1 expression significantly inhibited LWS1 expression. Tretinoin 32-34 parapinopsin b Danio rerio 113-118
26296154-10 2015 A role for endogenous RA signaling in regulating differential expression of the LWS genes in postmitotic cones was further supported by the presence of an RA signaling domain in ventral retina of juvenile zebrafish that coincided with a ventral zone of LWS1 expression. Tretinoin 22-24 opsin 1 (cone pigments), long-wave-sensitive, 1 Danio rerio 253-257
26287494-2 2015 It was previously reported that, in patient-derived HL-60 myeloblastic leukemia cells, retinoic acid (RA)-induced differentiation is driven by a signalsome containing c-Cbl and AhR. Tretinoin 87-100 Cbl proto-oncogene Homo sapiens 167-172
26287494-2 2015 It was previously reported that, in patient-derived HL-60 myeloblastic leukemia cells, retinoic acid (RA)-induced differentiation is driven by a signalsome containing c-Cbl and AhR. Tretinoin 102-104 Cbl proto-oncogene Homo sapiens 167-172
26287494-3 2015 FICZ enhances RA-induced differentiation, assessed by expression of the membrane differentiation markers CD38 and CD11b, cell cycle arrest and the functional differentiation marker, inducible oxidative metabolism. Tretinoin 14-16 CD38 molecule Homo sapiens 105-109
1382963-1 1992 Retinoic acid (RA) blocks insulin-like growth factor-I (IGF-I) stimulation of proliferation in the MCF-7 breast carcinoma cell line, and this is associated with the appearance of 42- to 46-kilodalton (kDa) IGF-binding proteins(s) (IGFBPs) in the conditioned medium (CM), in addition to the approximately 34- and 27-kDa IGFBPs present in the CM of unstimulated cells. Tretinoin 15-17 insulin like growth factor binding protein 2 Homo sapiens 319-325
26290227-1 2015 UNLABELLED: The derivation of somatic motoneurons (MNs) from ES cells (ESCs) after exposure to sonic hedgehog (SHH) and retinoic acid (RA) is one of the best defined, directed differentiation strategies to specify fate in pluripotent lineages. Tretinoin 135-137 sonic hedgehog signaling molecule Homo sapiens 95-109
1464411-1 1992 Thyroid hormones and retinoic acid (RA) coregulate growth hormone (GH) synthesis and release from cultured pituitary tumor cells by interacting with nuclear receptors that activate GH gene transcription. Tretinoin 36-38 gonadotropin releasing hormone receptor Rattus norvegicus 181-183
26290227-1 2015 UNLABELLED: The derivation of somatic motoneurons (MNs) from ES cells (ESCs) after exposure to sonic hedgehog (SHH) and retinoic acid (RA) is one of the best defined, directed differentiation strategies to specify fate in pluripotent lineages. Tretinoin 135-137 sonic hedgehog signaling molecule Homo sapiens 111-114
26290227-9 2015 Our data demonstrate that RA-mediated suppression of GLI3 is sufficient to generate MNs in an SHH-independent manner and that temporal changes in exposure to patterning factors such as RA affect chromatin state and competency of hESC-derived lineages to adopt specific neuronal fates. Tretinoin 26-28 sonic hedgehog signaling molecule Homo sapiens 94-97
26290227-13 2015 We show that early exposure to retinoic acid modulates the chromatin state of cells to be permissive for motoneuron generation and directly suppresses the induction of GLI3, a negative regulator of SHH signaling. Tretinoin 31-44 sonic hedgehog signaling molecule Homo sapiens 198-201
26290227-14 2015 Therefore, our data point to a novel mechanism by which retinoic acid exposure can bypass the requirement for extrinsic SHH treatment during motoneuron induction. Tretinoin 56-69 sonic hedgehog signaling molecule Homo sapiens 120-123
24525295-2 2014 In particular, RA signaling is implicated in a rostral expansion of the neural expression domain of 5 Hoxb genes (Hoxb9-Hoxb5) in mice. Tretinoin 15-17 homeobox B cluster Mus musculus 103-107
24525295-2 2014 In particular, RA signaling is implicated in a rostral expansion of the neural expression domain of 5 Hoxb genes (Hoxb9-Hoxb5) in mice. Tretinoin 15-17 homeobox B5 Mus musculus 121-126
24525295-3 2014 However, underlying mechanisms for this gene regulation have remained elusive due to the lack of RA responsive element (RARE) in the 5 half of the HoxB cluster. Tretinoin 97-99 homeobox B cluster Mus musculus 148-152
26238290-12 2015 Knockdown of Omi in N2a cells suppressed RA-induced neurite outgrowth, which was partially restored by knockdown of E2F1. Tretinoin 41-43 E2F transcription factor 1 Mus musculus 116-120
24525295-8 2014 Knock-out of endogenous DE-RARE lead to significantly reduced expression of multiple Hoxb genes and attenuated Hox gene response to exogenous RA treatment in utero. Tretinoin 27-29 homeobox B cluster Mus musculus 85-89
1464411-3 1992 Therefore we compared the effects of in vivo replacement therapy with thyroxine (T4) and/or retinoic acid (RA) on GH synthesis and release in pituitaries from hypothyroid rats. Tretinoin 92-105 gonadotropin releasing hormone receptor Rattus norvegicus 114-116
26116962-9 2015 Importantly, administration of RA (1 mg/kg) significantly reduced blood TF activity, circulating HMGB1 and PAI-1 levels and expression of hepatic TF mRNA as well as fibrin deposition in LPS (5 mg/kg)-injected mice. Tretinoin 31-33 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 107-112
26116962-10 2015 CONCLUSIONS: Taken together, the activation of PI3K/Akt by RA modulates AMPK activity in ECs and plays a crucial role in the inhibition of coagulatory factors such as TF, PAI-1, and HMGB1 in inflammatory conditions. Tretinoin 59-61 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 171-176
24489122-3 2014 Our previous studies have addressed chromatin-remodeling of the Oct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochromatinization on the proximal promoter region of this gene locus. Tretinoin 83-96 POU class 5 homeobox 1 Homo sapiens 64-68
24489122-3 2014 Our previous studies have addressed chromatin-remodeling of the Oct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves receptor-interacting protein 140 (RIP140) for heterochromatinization on the proximal promoter region of this gene locus. Tretinoin 98-100 POU class 5 homeobox 1 Homo sapiens 64-68
1464411-3 1992 Therefore we compared the effects of in vivo replacement therapy with thyroxine (T4) and/or retinoic acid (RA) on GH synthesis and release in pituitaries from hypothyroid rats. Tretinoin 107-109 gonadotropin releasing hormone receptor Rattus norvegicus 114-116
24489122-5 2014 The current study examines RA repression of the Nanog gene and compares the results with RA repression of the Oct4 gene on the chromatin level. Tretinoin 89-91 POU class 5 homeobox 1 Homo sapiens 110-114
1464411-12 1992 RA treatment had no effect on GH synthesis or absolute release, but like T4 it decreased the fractional release of newly synthesized GH. Tretinoin 0-2 gonadotropin releasing hormone receptor Rattus norvegicus 133-135
24489122-8 2014 Further, RA induces coordinated chromatin-remodeling of both Nanog and Oct4 gene loci, which requires RA receptor-alpha, RIP140 and Brm. Tretinoin 9-11 POU class 5 homeobox 1 Homo sapiens 71-75
26096456-20 2015 This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up-regulation of RARalpha and RARgamma. Tretinoin 145-147 retinoic acid receptor, alpha Rattus norvegicus 173-181
1333403-6 1992 Interestingly, the expression of the three genes, RAR-beta, CRABP II and CRBP I, is induced by retinoic acid, which suggests a link between the synthesis of RA from retinol and the control of expression of subsets of RA-responsive genes. Tretinoin 95-108 retinoic acid receptor, beta Mus musculus 50-58
25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 42-46
25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 POU class 5 homeobox 1 Homo sapiens 58-62
25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 POU class 5 homeobox 1 Homo sapiens 114-118
24559867-2 2014 The RAR agonist: all-trans retinoic acid was reported to be an RORbeta inverse agonist, but no information is available regarding ROR activity of its synthetic analogue Am580. Tretinoin 17-40 retinoic acid receptor alpha Homo sapiens 4-7
24594504-2 2014 We focus on the characterization of the aldehyde dehydrogenase-1 family of enzymes (ALDH1A1, ALDH1A2, ALDH1A3) that catalyze conversion of retinaldehyde to retinoic acid. Tretinoin 156-169 aldehyde dehydrogenase 1 family member A1 Homo sapiens 84-91
1333403-6 1992 Interestingly, the expression of the three genes, RAR-beta, CRABP II and CRBP I, is induced by retinoic acid, which suggests a link between the synthesis of RA from retinol and the control of expression of subsets of RA-responsive genes. Tretinoin 95-108 cellular retinoic acid binding protein II Mus musculus 60-68
24594504-2 2014 We focus on the characterization of the aldehyde dehydrogenase-1 family of enzymes (ALDH1A1, ALDH1A2, ALDH1A3) that catalyze conversion of retinaldehyde to retinoic acid. Tretinoin 156-169 aldehyde dehydrogenase 1 family member A3 Homo sapiens 102-109
24594504-4 2014 Although estrogen does not directly influence expression of Aldh1a1, it has the ability to suppress Aldh1a2 and Aldh1a3, thereby establishing a female-specific mechanism for retinoic acid generation in target tissues. Tretinoin 174-187 aldehyde dehydrogenase 1 family member A3 Homo sapiens 112-119
25959810-10 2015 In contrast, RA completely inhibited the IL-2-induced expression of cutaneous lymphocyte antigen (CLA) in ILCs. Tretinoin 13-15 selectin P ligand Homo sapiens 98-101
1378478-1 1992 We have previously shown that cellular retinoic acid-binding protein II (CRABP-II), but not cellular retinoic acid-binding protein I (CRABP-I), mRNA expression is markedly induced in human skin by topical retinoic acid. Tretinoin 39-52 cellular retinoic acid binding protein 1 Homo sapiens 73-80
25888236-0 2015 Cellular and molecular determinants of all-trans retinoic acid sensitivity in breast cancer: Luminal phenotype and RARalpha expression. Tretinoin 49-62 retinoic acid receptor alpha Homo sapiens 115-123
25888236-9 2015 RARalpha over-expression sensitizes retinoid-resistant MDA-MB453 cells to ATRA anti-proliferative action. Tretinoin 74-78 retinoic acid receptor alpha Homo sapiens 0-8
25888236-11 2015 All this is paralleled by similar effects on ATRA-dependent inhibition of cell motility, indicating that RARalpha may mediate also ATRA anti-metastatic effects. Tretinoin 45-49 retinoic acid receptor alpha Homo sapiens 105-113
24907012-6 2014 More recently, arsenic trioxide (ATO) has been shown to contribute degradation of the PML-RARalpha oncoprotein through bonding the PML moiety and has shown excellent synergism with ATRA in clinical trials. Tretinoin 181-185 PML nuclear body scaffold Homo sapiens 86-89
24907012-6 2014 More recently, arsenic trioxide (ATO) has been shown to contribute degradation of the PML-RARalpha oncoprotein through bonding the PML moiety and has shown excellent synergism with ATRA in clinical trials. Tretinoin 181-185 PML nuclear body scaffold Homo sapiens 131-134
1321791-1 1992 Two highly conserved forms of cellular retinoic acid binding protein (CRABP-I and CRABP-II) have been described, and one, CRABP-II, is highly expressed in human skin. Tretinoin 39-52 cellular retinoic acid binding protein 1 Homo sapiens 70-77
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 147-152
24404978-8 2014 RK in the presence of ATRA also increased the levels of mRNAs of osteocalcin, alpha1(I) collagen, and TGF-betas (TGF-beta1, TGF-beta2, and TGF-beta3) compared with ATRA only. Tretinoin 22-26 transforming growth factor, beta 3 Mus musculus 139-148
24421389-1 2014 To investigate the mechanisms by which elevated retinol-binding protein 4 (RBP4) causes insulin resistance, we studied the role of the high-affinity receptor for RBP4, STRA6 (stimulated by retinoic acid), in insulin resistance and obesity. Tretinoin 189-202 stimulated by retinoic acid gene 6 Mus musculus 168-173
24123714-2 2014 Many studies suggested that all-trans retinoic acid can be used to treat atherosclerosis through retinoic acid receptor (RAR)-mediated upregulation of CYP27A1 expression. Tretinoin 38-51 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 151-158
24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 synuclein alpha Homo sapiens 123-127
24269733-2 2014 The loss of viability in retinoic acid-differentiated SH-SY5Y human neuroblastoma cells inducibly overexpressing wild-type ASYN was associated with the reduced activation of AMPK and its activator LKB1, as well as AMPK target Raptor. Tretinoin 25-38 serine/threonine kinase 11 Homo sapiens 197-201
24333507-2 2014 In the present study, we found that DNMT3B is rapidly down-regulated in human ES cells during retinoic acid (RA)-induced differentiation compared with DNMT3A2, which is also highly expressed in ES cells. Tretinoin 94-107 DNA methyltransferase 3 beta Homo sapiens 36-42
24333507-2 2014 In the present study, we found that DNMT3B is rapidly down-regulated in human ES cells during retinoic acid (RA)-induced differentiation compared with DNMT3A2, which is also highly expressed in ES cells. Tretinoin 109-111 DNA methyltransferase 3 beta Homo sapiens 36-42
24333507-5 2014 Upon retinoic acid-induced differentiation, we found that depletion of DNMT3B leads to a decrease in expression of the surface antigen A2B5 and of neural tube-associated genes PAX7 and BRN3A. Tretinoin 5-18 DNA methyltransferase 3 beta Homo sapiens 71-77
24333507-5 2014 Upon retinoic acid-induced differentiation, we found that depletion of DNMT3B leads to a decrease in expression of the surface antigen A2B5 and of neural tube-associated genes PAX7 and BRN3A. Tretinoin 5-18 POU class 4 homeobox 1 Homo sapiens 185-190
24412926-5 2014 Upon RA-induced PML-RARA degradation, normal Pml elicits NB reformation and induces a Trp53 response exhibiting features of senescence but not apoptosis, ultimately abrogating APL-initiating activity. Tretinoin 5-7 transformation related protein 53 Mus musculus 86-91
24352370-4 2014 It has been demonstrated that prenatal administration of retinoic acid (RA) suppresses decidual RARalpha expression. Tretinoin 57-70 retinoic acid receptor, alpha Rattus norvegicus 96-104
24352370-4 2014 It has been demonstrated that prenatal administration of retinoic acid (RA) suppresses decidual RARalpha expression. Tretinoin 72-74 retinoic acid receptor, alpha Rattus norvegicus 96-104
24352370-7 2014 We therefore hypothesized that nitrofen decreases trophoblastic IGF2 expression and prenatal administration of RA increases it through decidual RARalpha in the nitrofen-induced CDH model. Tretinoin 111-113 retinoic acid receptor, alpha Rattus norvegicus 144-152
24352371-0 2014 Abnormal neural crest innervation in Sox10-Venus mice with all-trans retinoic acid-induced anorectal malformations. Tretinoin 69-82 SRY (sex determining region Y)-box 10 Mus musculus 37-42
24475288-3 2014 Using the human embryonal carcinoma cell line NTera2/D1, we confirmed that exposure to the differentiating agent retinoic acid produced a reduction in pluripotency markers NANOG and POU5F1 (Oct3/4) and an acute concentration-dependent increase in resistance to both cisplatin and paclitaxel that reached as high as 18-fold for cisplatin and 61-fold for paclitaxel within four days. Tretinoin 113-126 POU class 5 homeobox 1 Homo sapiens 182-188
24475288-3 2014 Using the human embryonal carcinoma cell line NTera2/D1, we confirmed that exposure to the differentiating agent retinoic acid produced a reduction in pluripotency markers NANOG and POU5F1 (Oct3/4) and an acute concentration-dependent increase in resistance to both cisplatin and paclitaxel that reached as high as 18-fold for cisplatin and 61-fold for paclitaxel within four days. Tretinoin 113-126 POU class 5 homeobox 1 Homo sapiens 190-196
24608861-0 2014 E2F1 impairs all-trans retinoic acid-induced osteogenic differentiation of osteosarcoma via promoting ubiquitination-mediated degradation of RARalpha. Tretinoin 23-36 E2F transcription factor 1 Homo sapiens 0-4
24608861-0 2014 E2F1 impairs all-trans retinoic acid-induced osteogenic differentiation of osteosarcoma via promoting ubiquitination-mediated degradation of RARalpha. Tretinoin 23-36 retinoic acid receptor alpha Homo sapiens 141-149
24608861-2 2014 In this study, we identified E2F1 as a novel regulator involved in ATRA-induced osteogenic differentiation of osteosarcoma cells. Tretinoin 67-71 E2F transcription factor 1 Homo sapiens 29-33
24608861-3 2014 We observed that osteosarcoma cells are coupled with individual differences in the expression levels of E2F1 in patients, and E2F1 impairs ATRA-induced differentiation of osteosarcoma cells. Tretinoin 139-143 E2F transcription factor 1 Homo sapiens 104-108
24608861-3 2014 We observed that osteosarcoma cells are coupled with individual differences in the expression levels of E2F1 in patients, and E2F1 impairs ATRA-induced differentiation of osteosarcoma cells. Tretinoin 139-143 E2F transcription factor 1 Homo sapiens 126-130
24608861-4 2014 Moreover, remarkable anti-proliferative and differentiation-inducing effects of ATRA treatment are only observed in E2F1 low to negative expressed primary osteosarcoma cultures. Tretinoin 80-84 E2F transcription factor 1 Homo sapiens 116-120
24608861-5 2014 These results strongly suggested that E2F1 may serve as a potent indicator for the effectiveness of ATRA treatment in osteosarcoma. Tretinoin 100-104 E2F transcription factor 1 Homo sapiens 38-42
24608861-6 2014 Interestingly, E2F1 is found to downregulate retinoic acid receptor alpha (RARalpha), a key factor determines the effectiveness of ATRA. Tretinoin 131-135 E2F transcription factor 1 Homo sapiens 15-19
24608861-6 2014 Interestingly, E2F1 is found to downregulate retinoic acid receptor alpha (RARalpha), a key factor determines the effectiveness of ATRA. Tretinoin 131-135 retinoic acid receptor alpha Homo sapiens 45-73
24608861-6 2014 Interestingly, E2F1 is found to downregulate retinoic acid receptor alpha (RARalpha), a key factor determines the effectiveness of ATRA. Tretinoin 131-135 retinoic acid receptor alpha Homo sapiens 75-83
23904188-9 2014 Retinoic acid interferes i21 Flt1 expression by downregulating Notch-3 and upregulating miR-200 expression. Tretinoin 0-13 notch receptor 3 Homo sapiens 63-70
24285836-5 2014 We found that F4/80(+)Ly6C(-)Ly6G(-) mature macrophages (Ms) were up to 30-fold more potent immune suppressors than Gr1(+) cells on a per-cell basis, which we postulate may contribute to the increased metastatic growth observed with ATRA treatment. Tretinoin 233-237 lymphocyte antigen 6 complex, locus C1 Mus musculus 14-26
24038216-3 2014 DAPK2 levels were restored in APL patients undergoing ATRA therapy. Tretinoin 54-58 death associated protein kinase 2 Homo sapiens 0-5
24824789-4 2014 Resistance to ATRA-induced cell cycle arrest at the G1/S phase transition in knockdown cells was accompanied by retained expression of ITGA4 (CD49d) and decreased induction of ITGAX (CD11c). Tretinoin 14-18 integrin subunit alpha 4 Homo sapiens 135-140
24824789-4 2014 Resistance to ATRA-induced cell cycle arrest at the G1/S phase transition in knockdown cells was accompanied by retained expression of ITGA4 (CD49d) and decreased induction of ITGAX (CD11c). Tretinoin 14-18 integrin subunit alpha 4 Homo sapiens 142-147
25509416-5 2014 As induction of neuronal differentiation in the studied MSCs using differentiation medium containing B27 and N2 supplements, 5-azacytidine, retinoic acid, IBMX and dbcAMF caused changes in the cells morphology, the increased expression of beta-III-tubulin, and the appearance of neuronal markers GFAP, NF-H, NeuN and MAP2. Tretinoin 140-153 neurofilament heavy chain Homo sapiens 302-306
24346134-9 2013 Additional in vitro studies confirmed that RA abolished GR-mediated glucocorticoid-induced suppression of CRH expression, indicating a negative cross-talk between RAR-alpha and GR signaling pathways. Tretinoin 43-45 retinoic acid receptor, alpha Rattus norvegicus 163-172
24005908-0 2013 The retinaldehyde reductase DHRS3 is essential for preventing the formation of excess retinoic acid during embryonic development. Tretinoin 86-99 dehydrogenase/reductase (SDR family) member 3 Mus musculus 28-33
24005908-4 2013 Lack of DHRS3 leads to a 40% increase in the levels of ATRA and a 60% and 55% decrease in the levels of retinol and retinyl esters, respectively, in Dhrs3(-/-) embryos compared to wild-type littermates. Tretinoin 55-59 dehydrogenase/reductase (SDR family) member 3 Mus musculus 8-13
23816303-2 2013 Previously, we showed that all-trans-retinoic acid (RA) increases the expression of CD1d and the magnitude of CD1d-mediated antibody production in vivo. Tretinoin 27-50 CD1d molecule Homo sapiens 84-88
23816303-2 2013 Previously, we showed that all-trans-retinoic acid (RA) increases the expression of CD1d and the magnitude of CD1d-mediated antibody production in vivo. Tretinoin 27-50 CD1d molecule Homo sapiens 110-114
23816303-2 2013 Previously, we showed that all-trans-retinoic acid (RA) increases the expression of CD1d and the magnitude of CD1d-mediated antibody production in vivo. Tretinoin 52-54 CD1d molecule Homo sapiens 84-88
23816303-2 2013 Previously, we showed that all-trans-retinoic acid (RA) increases the expression of CD1d and the magnitude of CD1d-mediated antibody production in vivo. Tretinoin 52-54 CD1d molecule Homo sapiens 110-114
23821302-11 2013 PPARalpha gene expression increased in RA-treated groups; URG4/URGCP gene expression decreased in SH-SY5Y cells after RA treatment compared with that in the control cells. Tretinoin 39-41 peroxisome proliferator activated receptor alpha Homo sapiens 0-9
24045938-2 2013 During early embryonic development, atRA is synthesized from all-trans-retinal (atRAL) in an irreversible reaction mainly catalyzed by retinal dehydrogenase 2 (aldh1a2), whereas atRAL is converted from all-trans-retinol via reversible oxidation by retinol dehydrogenases, members of the short-chain dehydrogenase/reductase family. Tretinoin 36-40 aldehyde dehydrogenase 1 family member A2 S homeolog Xenopus laevis 135-158
24490497-0 2013 [Effect of recombinant adenovirus carrying NLS-RARalpha gene on the proliferation of HL-60 cell and the differentiation of HL-60 cells induced by ATRA and relevant mechanism]. Tretinoin 146-150 retinoic acid receptor alpha Homo sapiens 47-55
24490497-1 2013 OBJECTIVE: To explore the effect and mechanism of recombined adenovirus carrying NLS-RARalpha gene on proliferation of HL-60 cells and the differentiation of HL-60 cells induced by ATRA. Tretinoin 181-185 retinoic acid receptor alpha Homo sapiens 85-93
24096236-3 2013 We isolated a retinoic acid receptor (RAR)-like cDNA (TcRAR) in the rock shell, Thais clavigera, and examined the transcriptional activity of the TcRAR protein by using all-trans retinoic acid (ATRA). Tretinoin 14-27 retinoic acid receptor alpha Homo sapiens 38-41
24096236-3 2013 We isolated a retinoic acid receptor (RAR)-like cDNA (TcRAR) in the rock shell, Thais clavigera, and examined the transcriptional activity of the TcRAR protein by using all-trans retinoic acid (ATRA). Tretinoin 194-198 retinoic acid receptor alpha Homo sapiens 38-41
22374508-11 2013 CONCLUSION: These in-vivo and in-vitro results show that to achieve maximum effects of RA on tumor progression both the LEP and MEP cell compartments have to be present, suggesting that the interaction between the LEP and MEP cells is crucial to full activation of the RARs. Tretinoin 87-89 leptin Mus musculus 120-123
22374508-11 2013 CONCLUSION: These in-vivo and in-vitro results show that to achieve maximum effects of RA on tumor progression both the LEP and MEP cell compartments have to be present, suggesting that the interaction between the LEP and MEP cells is crucial to full activation of the RARs. Tretinoin 87-89 leptin Mus musculus 214-217
23607934-5 2013 Retinoic acid (RA) induced gut-homing markers (beta7 and CCR9) and a regulatory phenotype and function [decreased human leucocyte antigen D-related (HLA-DR) and increased ILT3 and fluorescein isothiocyanate (FITC-dextran uptake) in MoDC]. Tretinoin 15-17 leukocyte immunoglobulin like receptor B4 Homo sapiens 171-175
24227948-4 2013 Many genes involved in hepatic retinoid physiology, including CRBP-I, were altered and the tissue levels of retinol and all-trans retinoic acid (ATRA) were elevated in the liver of HBx Tg mice compared to those of wild type (WT) control mice. Tretinoin 130-143 X protein Hepatitis B virus 181-184
24227948-4 2013 Many genes involved in hepatic retinoid physiology, including CRBP-I, were altered and the tissue levels of retinol and all-trans retinoic acid (ATRA) were elevated in the liver of HBx Tg mice compared to those of wild type (WT) control mice. Tretinoin 145-149 X protein Hepatitis B virus 181-184
23960232-3 2013 We found that IL-4 and retinoic acid (RA) cotreatment of GM-CSF-differentiated IDCs synergistically induced the expression of aldehyde dehydrogenase family 1, subfamily A2, a rate-limiting enzyme for RA synthesis in DCs. Tretinoin 23-36 colony stimulating factor 2 Homo sapiens 57-63
23960232-3 2013 We found that IL-4 and retinoic acid (RA) cotreatment of GM-CSF-differentiated IDCs synergistically induced the expression of aldehyde dehydrogenase family 1, subfamily A2, a rate-limiting enzyme for RA synthesis in DCs. Tretinoin 38-40 colony stimulating factor 2 Homo sapiens 57-63
23960232-3 2013 We found that IL-4 and retinoic acid (RA) cotreatment of GM-CSF-differentiated IDCs synergistically induced the expression of aldehyde dehydrogenase family 1, subfamily A2, a rate-limiting enzyme for RA synthesis in DCs. Tretinoin 200-202 colony stimulating factor 2 Homo sapiens 57-63
23960232-4 2013 IL-4 plus RA-treated IDCs upregulated CD103 expression and markedly reduced the production of proinflammatory cytokines upon activation. Tretinoin 10-12 integrin subunit alpha E Homo sapiens 38-43
23861398-0 2013 beta-Transducin repeat-containing protein 1 (beta-TrCP1)-mediated silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) protein degradation promotes tumor necrosis factor alpha (TNFalpha)-induced inflammatory gene expression. Tretinoin 88-101 beta-transducin repeat containing E3 ubiquitin protein ligase Homo sapiens 0-43
23861398-0 2013 beta-Transducin repeat-containing protein 1 (beta-TrCP1)-mediated silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) protein degradation promotes tumor necrosis factor alpha (TNFalpha)-induced inflammatory gene expression. Tretinoin 88-101 beta-transducin repeat containing E3 ubiquitin protein ligase Homo sapiens 45-55
23839944-4 2013 We show that the contribution of STRA6 to retinol uptake by tissues in vivo is small and that, with the exception of the eye, ablation of Stra6 has only a modest effect on retinoid homeostasis and does not impair physiological functions that critically depend on retinoic acid in the embryo or in the adult. Tretinoin 263-276 stimulated by retinoic acid gene 6 Mus musculus 138-143
25976705-6 2015 Our results indicated that the expression of CD24, enhanced by a combination of retinoic acid (RA), noggin and fibroblast growth factor 8 (FGF8) under serum-free conditions promoted neural precursor differentiation. Tretinoin 80-93 CD24a antigen Mus musculus 45-49
25976705-6 2015 Our results indicated that the expression of CD24, enhanced by a combination of retinoic acid (RA), noggin and fibroblast growth factor 8 (FGF8) under serum-free conditions promoted neural precursor differentiation. Tretinoin 95-97 CD24a antigen Mus musculus 45-49
25827071-3 2015 For this effect, ATRA activated p14 expression via promoter hypomethylation, resulting in ubiquitin-dependent degradation of mouse double minute 2 (MDM2) and subsequent stabilization of p53. Tretinoin 17-21 transformed mouse 3T3 cell double minute 2 Mus musculus 148-152
25827071-3 2015 For this effect, ATRA activated p14 expression via promoter hypomethylation, resulting in ubiquitin-dependent degradation of mouse double minute 2 (MDM2) and subsequent stabilization of p53. Tretinoin 17-21 transformation related protein 53, pseudogene Mus musculus 186-189
26121141-10 2015 Additional sequence analysis also uncovered deleterious variants in genes associated with retinoic acid signaling, including NODAL and retinol dehydrogenase 10. Tretinoin 90-103 nodal growth differentiation factor Homo sapiens 125-130
26121149-4 2015 The results show that RA-induced H9c2 differentiation increased the expression of genes encoding for cardiac sarcomeric proteins such as troponin T, or calcium transporters and associated machinery, including SERCA2, ryanodine receptor and phospholamban as well as genes associated with mitochondrial energy production including respiratory chain complexes subunits, mitochondrial creatine kinase, carnitine palmitoyltransferase I and uncoupling proteins. Tretinoin 22-24 ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2 Rattus norvegicus 209-215
25869623-7 2015 Our previous study has revealed that RA induces Fndc5 expression during neural differentiation process. Tretinoin 37-39 fibronectin type III domain containing 5 Homo sapiens 48-53
25869623-12 2015 This led us to conclude that RA enhances Fndc5 expression through a non-genomic pathway via the ERK signaling pathway. Tretinoin 29-31 fibronectin type III domain containing 5 Homo sapiens 41-46
25724388-5 2015 atRA levels increased with the low activity of CYP2E1 and decreased with high CYP26 activity in the UChB dorsal prostate. Tretinoin 0-4 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 78-83
25795919-2 2015 Oncoprotein targeting can be a successful strategy to treat AML, as proved in acute promyelocytic leukemia by treatment with all-trans retinoic acid (ATRA) plus arsenic trioxide (ATO), which degrade the promyelocytic leukemia (PML)-retinoic acid receptor fusion protein. Tretinoin 125-148 PML nuclear body scaffold Homo sapiens 227-230
25795919-2 2015 Oncoprotein targeting can be a successful strategy to treat AML, as proved in acute promyelocytic leukemia by treatment with all-trans retinoic acid (ATRA) plus arsenic trioxide (ATO), which degrade the promyelocytic leukemia (PML)-retinoic acid receptor fusion protein. Tretinoin 150-154 PML nuclear body scaffold Homo sapiens 227-230
25800051-5 2015 Combined RA/arsenic treatment significantly reduced bone marrow blasts in 3 patients and restored the subnuclear localization of both NPM1 and PML. Tretinoin 9-11 PML nuclear body scaffold Homo sapiens 143-146
25887778-6 2015 In addition, we demonstrated that treatment of AML with all-trans retinoic acid (ATRA) enhanced FRbeta expression, resulting in improved immune recognition by m909 CAR T cells. Tretinoin 56-79 folate receptor beta Homo sapiens 96-102
25887778-6 2015 In addition, we demonstrated that treatment of AML with all-trans retinoic acid (ATRA) enhanced FRbeta expression, resulting in improved immune recognition by m909 CAR T cells. Tretinoin 81-85 folate receptor beta Homo sapiens 96-102
25887778-9 2015 Our results indicate that FRbeta is a promising target for CAR T-cell therapy of AML, which may be augmented by combination with ATRA. Tretinoin 129-133 folate receptor beta Homo sapiens 26-32
24992177-2 2015 It is now becoming apparent that signaling through vitamin A metabolites, such as all-trans retinoic acid (ATRA), is indispensable for spermatogenesis and disruption of retinoic acid receptor-alpha (RARalpha) function may result in male sterility and aberrant spermatogenesis. Tretinoin 92-105 retinoic acid receptor alpha Homo sapiens 199-207
24992177-2 2015 It is now becoming apparent that signaling through vitamin A metabolites, such as all-trans retinoic acid (ATRA), is indispensable for spermatogenesis and disruption of retinoic acid receptor-alpha (RARalpha) function may result in male sterility and aberrant spermatogenesis. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 169-197
24992177-2 2015 It is now becoming apparent that signaling through vitamin A metabolites, such as all-trans retinoic acid (ATRA), is indispensable for spermatogenesis and disruption of retinoic acid receptor-alpha (RARalpha) function may result in male sterility and aberrant spermatogenesis. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 199-207
25683251-5 2015 Cell viability assays in six HCC cell lines, HepG2, PLC/PRF/5, HuH6, HLE, HLF, and Hep3B, revealed that 5 and 10 muM ATRA, concentrations that do not exert cytotoxic effects, enhanced the cytotoxicity of sorafenib, being much more effective than NIK-333 and Am80. Tretinoin 117-121 heparan sulfate proteoglycan 2 Homo sapiens 52-55
25391663-12 2015 RAI14, thought to play a role in porcine adipocyte differentiation and with links to retinoic acid metabolism, has an unusual expression profile. Tretinoin 85-98 retinoic acid induced 14 Bos taurus 0-5
25834349-0 2015 Retinoic Acid promotes interleukin-4 plasmid-dimethylsulfoxide topical transdermal delivery for treatment of psoriasis. Tretinoin 0-13 interleukin 4 Mus musculus 23-36
25834349-4 2015 OBJECTIVE: We investigated whether RA could improve anti-psoriasis efficiency using IL-4 expression plasmid pORF-mIL-4 (pIL-4) via transdermal delivery system in K14-vascular endothelial growth (K14-VEGF) factor transgenic mice. Tretinoin 35-37 interleukin 4 Mus musculus 84-88
25614514-12 2015 CONCLUSIONS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, likely in part by attenuating the production of MMP-1 and MMP-3 and by stimulating the production of TIMP-1. Tretinoin 13-17 matrix metallopeptidase 1 Homo sapiens 136-141
25805962-14 2015 These results suggest G-CSF activates STAT5 through the JAK pathway in combination with ATRA, resulting in myeloid differentiation in HT93A cells. Tretinoin 88-92 colony stimulating factor 3 Homo sapiens 22-27
25343668-0 2015 Retinoic acid modulates interferon-gamma production by hepatic natural killer T cells via phosphatase 2A and the extracellular signal-regulated kinase pathway. Tretinoin 0-13 protein phosphatase 2 phosphatase activator Homo sapiens 90-104
25343668-4 2015 We also found that RA reduced extracellular signal-regulated kinase (ERK) phosphorylation, but increased phosphatase 2A (PP2A) activity in TCR/CD28-stimulated NKT cells. Tretinoin 19-21 protein phosphatase 2 phosphatase activator Homo sapiens 105-119
25027601-2 2015 RA primes dendritic cells (DCs) to express CD103 and produce RA themselves, which induces the gut-homing receptors alpha4beta7 and CCR9 on T cells and amplifies transforming growth factor (TGF)-beta-mediated development of Foxp3(+) regulatory T (Treg) cells. Tretinoin 0-2 integrin subunit alpha E Homo sapiens 43-48
25642823-0 2015 IL-1 signaling modulates activation of STAT transcription factors to antagonize retinoic acid signaling and control the TH17 cell-iTreg cell balance. Tretinoin 80-93 interleukin 1 alpha Homo sapiens 0-4
25695609-0 2015 Selective inhibition of HDAC8 decreases neuroblastoma growth in vitro and in vivo and enhances retinoic acid-mediated differentiation. Tretinoin 95-108 histone deacetylase 8 Mus musculus 24-29
25695609-9 2015 Upon combination with retinoic acid, differentiation was significantly enhanced, as demonstrated by elongated neurofilament-positive neurites and upregulation of NTRK1. Tretinoin 22-35 neurotrophic tyrosine kinase, receptor, type 1 Mus musculus 162-167
25692052-11 2015 Similar to APL with chromosomal translocations other than classical t(15;17) which result in the typical PML-RARA fusion, our patient responded promptly to an ATRA-containing regimen and remains in complete remission. Tretinoin 159-163 PML nuclear body scaffold Homo sapiens 105-108
25692052-11 2015 Similar to APL with chromosomal translocations other than classical t(15;17) which result in the typical PML-RARA fusion, our patient responded promptly to an ATRA-containing regimen and remains in complete remission. Tretinoin 159-163 retinoic acid receptor alpha Homo sapiens 109-113
26500786-3 2015 Here, we analyzed EGF superfamily receptor and ligand diversity in rat testis cells, and delineated germline-intrinsic signaling via an ERBB3 co-transducer, ERBB2, as essential for retinoic acid-induced syncytial growth by differentiating spermatogonia. Tretinoin 181-194 erb-b2 receptor tyrosine kinase 3 Rattus norvegicus 136-141
25855932-0 2015 ATRA and As2O3 regulate differentiation of human hematopoietic stem cells into granulocyte progenitor via alteration of HoxB8 expression. Tretinoin 0-4 homeobox B8 Homo sapiens 120-125
25855932-1 2015 OBJECTIVE: This study aimed to investigate the effect of all-trans retinoic acid (ATRA) and/or arsenic trioxide (As2O3) on homeobox B8 (HOXB8) mRNA and protein expressions during the differentiation and proliferation of hematopoietic stem cells (HSCs) to colony forming unit-granulocyte (CFU-G) in order to explore the pathogenesis of leukemia mediated by HOXB8 at mRNA and protein level. Tretinoin 57-80 homeobox B8 Homo sapiens 123-134
25855932-1 2015 OBJECTIVE: This study aimed to investigate the effect of all-trans retinoic acid (ATRA) and/or arsenic trioxide (As2O3) on homeobox B8 (HOXB8) mRNA and protein expressions during the differentiation and proliferation of hematopoietic stem cells (HSCs) to colony forming unit-granulocyte (CFU-G) in order to explore the pathogenesis of leukemia mediated by HOXB8 at mRNA and protein level. Tretinoin 57-80 homeobox B8 Homo sapiens 136-141
25855932-1 2015 OBJECTIVE: This study aimed to investigate the effect of all-trans retinoic acid (ATRA) and/or arsenic trioxide (As2O3) on homeobox B8 (HOXB8) mRNA and protein expressions during the differentiation and proliferation of hematopoietic stem cells (HSCs) to colony forming unit-granulocyte (CFU-G) in order to explore the pathogenesis of leukemia mediated by HOXB8 at mRNA and protein level. Tretinoin 57-80 homeobox B8 Homo sapiens 356-361
25855932-1 2015 OBJECTIVE: This study aimed to investigate the effect of all-trans retinoic acid (ATRA) and/or arsenic trioxide (As2O3) on homeobox B8 (HOXB8) mRNA and protein expressions during the differentiation and proliferation of hematopoietic stem cells (HSCs) to colony forming unit-granulocyte (CFU-G) in order to explore the pathogenesis of leukemia mediated by HOXB8 at mRNA and protein level. Tretinoin 82-86 homeobox B8 Homo sapiens 123-134
25855932-1 2015 OBJECTIVE: This study aimed to investigate the effect of all-trans retinoic acid (ATRA) and/or arsenic trioxide (As2O3) on homeobox B8 (HOXB8) mRNA and protein expressions during the differentiation and proliferation of hematopoietic stem cells (HSCs) to colony forming unit-granulocyte (CFU-G) in order to explore the pathogenesis of leukemia mediated by HOXB8 at mRNA and protein level. Tretinoin 82-86 homeobox B8 Homo sapiens 136-141
25855932-1 2015 OBJECTIVE: This study aimed to investigate the effect of all-trans retinoic acid (ATRA) and/or arsenic trioxide (As2O3) on homeobox B8 (HOXB8) mRNA and protein expressions during the differentiation and proliferation of hematopoietic stem cells (HSCs) to colony forming unit-granulocyte (CFU-G) in order to explore the pathogenesis of leukemia mediated by HOXB8 at mRNA and protein level. Tretinoin 82-86 homeobox B8 Homo sapiens 356-361
25855932-5 2015 RESULTS: HOXB8 mRNA/protein expression was detected in control, ATRA, As2O3 and ATRA +As2O3 groups on days 3, 7, and 12 of culture. Tretinoin 64-68 homeobox B8 Homo sapiens 9-14
25855932-5 2015 RESULTS: HOXB8 mRNA/protein expression was detected in control, ATRA, As2O3 and ATRA +As2O3 groups on days 3, 7, and 12 of culture. Tretinoin 80-84 homeobox B8 Homo sapiens 9-14
25855932-7 2015 HOXB8 mRNA/protein expression in ATRA, As2O3 and ATRA+As2O3 was upregulated compared with control group (p < 0.05). Tretinoin 33-37 homeobox B8 Homo sapiens 0-5
25855932-9 2015 ATRA/As2O3 up-regulate the expression of HOXB8 mRNA/protein, and treatment of leukemia with ATRA/As2O3 may regulate HOX gene expression. Tretinoin 0-4 homeobox B8 Homo sapiens 41-46
25537091-6 2015 Bmp3, egr3, and stra8 are stimulated after 1 d of RA treatment and then recover to normal after 3 d of RA treatment. Tretinoin 50-52 bone morphogenetic protein 3 Bos taurus 0-4
25537091-6 2015 Bmp3, egr3, and stra8 are stimulated after 1 d of RA treatment and then recover to normal after 3 d of RA treatment. Tretinoin 103-105 bone morphogenetic protein 3 Bos taurus 0-4
25944986-5 2015 In the presence of ATRA the supernatants of these cells induced CD103 expression on monocyte-derived dendritic cells and when conditioned by ATRA and cocultured with CD4(+) T-lymphocytes they reduced the proportion of Th17 T-cells. Tretinoin 19-23 integrin subunit alpha E Homo sapiens 64-69
25104850-10 2014 Moreover, neuroblastoma cell differentiation, induced by all-trans retinoic acid or NGF-NTRK1-signaling, activated p19-INK4d expression. Tretinoin 67-80 cyclin dependent kinase inhibitor 2D Homo sapiens 115-118
25104850-10 2014 Moreover, neuroblastoma cell differentiation, induced by all-trans retinoic acid or NGF-NTRK1-signaling, activated p19-INK4d expression. Tretinoin 67-80 cyclin dependent kinase inhibitor 2D Homo sapiens 119-124
25040912-9 2014 Overexpression and knockdown of miR-302b significantly influenced ATRA-mediated cytotoxicity. Tretinoin 66-70 microRNA 302b Homo sapiens 32-40
25040912-15 2014 The E2F3 repression, a novel target gene of miR-302b, was involved in ATRA-induced glioblastoma cell cytotoxicity. Tretinoin 70-74 microRNA 302b Homo sapiens 44-52
25330951-19 2014 CONCLUSION: Increased Lep and Lep-R expression after prenatal administration of ATRA in nitrofen-induced PH suggests that ATRA may have therapeutic potential in attenuating CDH-associated PH by stimulating alveolarization and de novo surfactant production. Tretinoin 122-126 leptin receptor Rattus norvegicus 30-35
25450689-2 2014 Although it is appreciated that isomers of retinoic acid activate the retinoic acid receptor (RAR) and retinoid X receptor (RXR) family of nuclear receptors to elicit cellular changes, the molecular details of retinoic acid action remain poorly defined in immune processes. Tretinoin 43-56 retinoic acid receptor alpha Homo sapiens 70-92
25450689-2 2014 Although it is appreciated that isomers of retinoic acid activate the retinoic acid receptor (RAR) and retinoid X receptor (RXR) family of nuclear receptors to elicit cellular changes, the molecular details of retinoic acid action remain poorly defined in immune processes. Tretinoin 43-56 retinoic acid receptor alpha Homo sapiens 94-97
25450689-2 2014 Although it is appreciated that isomers of retinoic acid activate the retinoic acid receptor (RAR) and retinoid X receptor (RXR) family of nuclear receptors to elicit cellular changes, the molecular details of retinoic acid action remain poorly defined in immune processes. Tretinoin 70-83 retinoic acid receptor alpha Homo sapiens 94-97
25423083-4 2014 Our data indicated that in NTD samples from both human fetuses and retinoic acid (RA)-treated mouse fetuses, the expression level of IGF2/Igf2 was upregulated 6.41-fold and 1.84-fold, respectively, compared to controls. Tretinoin 67-80 insulin-like growth factor 2 Mus musculus 133-137
25423083-4 2014 Our data indicated that in NTD samples from both human fetuses and retinoic acid (RA)-treated mouse fetuses, the expression level of IGF2/Igf2 was upregulated 6.41-fold and 1.84-fold, respectively, compared to controls. Tretinoin 67-80 insulin-like growth factor 2 Mus musculus 138-142
25423083-4 2014 Our data indicated that in NTD samples from both human fetuses and retinoic acid (RA)-treated mouse fetuses, the expression level of IGF2/Igf2 was upregulated 6.41-fold and 1.84-fold, respectively, compared to controls. Tretinoin 82-84 insulin-like growth factor 2 Mus musculus 133-137
25423083-4 2014 Our data indicated that in NTD samples from both human fetuses and retinoic acid (RA)-treated mouse fetuses, the expression level of IGF2/Igf2 was upregulated 6.41-fold and 1.84-fold, respectively, compared to controls. Tretinoin 82-84 insulin-like growth factor 2 Mus musculus 138-142
25423083-8 2014 In detail, the upregulation of IGF2/Igf2 is likely controlled by hypermethylation of H19 DMR1 in human NTDs, however, in acute external RA-induced NTD mice it is potentially determined by more open chromatin structure. Tretinoin 136-138 insulin like growth factor 2 Homo sapiens 31-35
25423083-8 2014 In detail, the upregulation of IGF2/Igf2 is likely controlled by hypermethylation of H19 DMR1 in human NTDs, however, in acute external RA-induced NTD mice it is potentially determined by more open chromatin structure. Tretinoin 136-138 insulin like growth factor 2 Homo sapiens 36-40
25277705-10 2014 Silencing of retinoic acid-inducible gene-1 (RIG-I) expression in A549 cells had a greater impact on RSV-inducible cytokines than melanoma differentiation-associated protein 5 (MDA5) and laboratory of genetics and physiology 2 (LGP2), and Trif expression. Tretinoin 13-26 toll-like receptor adaptor molecule 1 Mus musculus 239-243
25088254-2 2014 All-trans retinoic acid (atRA) treatment is the standard drug treatment for APL yielding cure rates > 80% by activating transcription and proteasomal degradation of retinoic acid receptor, alpha (RARalpha). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 168-197
25088254-2 2014 All-trans retinoic acid (atRA) treatment is the standard drug treatment for APL yielding cure rates > 80% by activating transcription and proteasomal degradation of retinoic acid receptor, alpha (RARalpha). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 199-207
25088254-2 2014 All-trans retinoic acid (atRA) treatment is the standard drug treatment for APL yielding cure rates > 80% by activating transcription and proteasomal degradation of retinoic acid receptor, alpha (RARalpha). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 168-197
25088254-2 2014 All-trans retinoic acid (atRA) treatment is the standard drug treatment for APL yielding cure rates > 80% by activating transcription and proteasomal degradation of retinoic acid receptor, alpha (RARalpha). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 199-207
28250390-4 2014 Long-term (5 Day) retinoic acid treatment functioned as a radiosensitizer and was associated with downregulation of ATM protein levels. Tretinoin 18-31 ATM serine/threonine kinase Homo sapiens 116-119
25691937-1 2014 OBJECTIVES: Recent evidence have proposed that Tretinoin produced in the gut preferentially promote differentiation of FoxP3+Treg cells but inhibits Th17 lymphocytes, and this may be the main immunomdulatory mechanism of Tretinoin in vivo. Tretinoin 47-56 forkhead box P3 Mus musculus 119-124
25691937-13 2014 CONCLUSION: The in vivo immunomudlatoty effects of Tretinoin may be partly due to immune deviation from pro-inflammatory cytokine interleukin-17 to anti-inflammatory cytokine interleukin-10, but not absolutely depend on the expansion of FoxP3(+)Treg cells. Tretinoin 51-60 forkhead box P3 Mus musculus 237-242
25031298-11 2014 CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. Tretinoin 37-41 prohibitin 2 Homo sapiens 80-84
25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 293-306 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 56-61
25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 293-306 H3 histone pseudogene 16 Homo sapiens 149-152
25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 293-306 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 218-223
25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 308-312 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 56-61
25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 308-312 H3 histone pseudogene 16 Homo sapiens 149-152
25564054-4 2014 RESULTS: Western blot showed that the overexpression of RIG-G protein significantly upregulated p21 protein level in the NB4 cells, and the level of p21 protein largely increased along with the induction of endogenous RIG-G protein during the differentiation of NB4 cells treated by all-trans retinoic acid (ATRA). Tretinoin 308-312 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 218-223
25065743-0 2014 WTIP interacts with ASXL2 and blocks ASXL2-mediated activation of retinoic acid signaling. Tretinoin 66-79 ASXL transcriptional regulator 2 Homo sapiens 37-42
25065743-7 2014 In addition, we found that ASXL2 and WTIP are expressed in mouse embryonic epicardial cells, a tissue that is regulated by retinoic acid signaling. Tretinoin 123-136 ASXL transcriptional regulator 2 Mus musculus 27-32
25065743-8 2014 Together, these results implicate ASXL2 and WTIP in regulation of retinoic acid signaling during heart development. Tretinoin 66-79 ASXL transcriptional regulator 2 Homo sapiens 34-39
24603314-13 2014 9-cis-RA antagonized Ang II-induced LKB1/AMPK and p70S6K activation changes in vitro. Tretinoin 0-8 serine/threonine kinase 11 Rattus norvegicus 36-40
24603314-13 2014 9-cis-RA antagonized Ang II-induced LKB1/AMPK and p70S6K activation changes in vitro. Tretinoin 0-8 ribosomal protein S6 kinase B1 Rattus norvegicus 50-56
24796963-0 2014 Prognostic impact of KMT2E transcript levels on outcome of patients with acute promyelocytic leukaemia treated with all-trans retinoic acid and anthracycline-based chemotherapy: an International Consortium on Acute Promyelocytic Leukaemia study. Tretinoin 126-139 lysine methyltransferase 2E (inactive) Homo sapiens 21-26
24796963-2 2014 Its close relationship with retinoic acid-induced granulopoiesis suggests that the deregulated expression of KMT2E might lead acute promyelocytic leukaemia (APL) blasts to become less susceptible to the conventional treatment protocols. Tretinoin 28-41 lysine methyltransferase 2E (inactive) Homo sapiens 109-114
24796963-3 2014 Here, we assessed the impact of KMT2E expression on the prognosis of 121 APL patients treated with ATRA and anthracycline-based chemotherapy. Tretinoin 99-103 lysine methyltransferase 2E (inactive) Homo sapiens 32-37
24648413-7 2014 RA increases the expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, Fzd2 and Fzd6), downstream signaling, and Tcf3 expression. Tretinoin 0-2 frizzled class receptor 2 Homo sapiens 98-102
24648413-8 2014 RA reduces the phosphorylated beta-catenin levels by fourfold, although total beta-catenin levels do not change. Tretinoin 0-2 catenin beta 1 Homo sapiens 30-42
24648413-9 2014 We show that RA signaling increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Tretinoin 13-15 transcription factor 7 Homo sapiens 56-60
24648413-9 2014 We show that RA signaling increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Tretinoin 13-15 cellular communication network factor 1 Homo sapiens 180-185
25072246-3 2014 Real-time PCR analyses demonstrated that the inductions of CD11b and CD11c and reductions in myeloperoxidase and c-myc by ATRA were significantly attenuated in NB4MTOE cells. Tretinoin 122-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 113-118
24993014-6 2014 Transcriptional profiles and functional pathway analyses further demonstrated that 7 genes (FEN1, RFC5, EXO1, XRCC5, PARP1, POLR2F, and GTF2H3) that were relatively up-regulated in HL-60[R] cells and repressed in cells with ATRA-induced differentiation were related to mismatch repair in eukaryotes, DNA double-strand break repair, and nucleotide excision repair pathways. Tretinoin 224-228 flap structure-specific endonuclease 1 Homo sapiens 92-96
1419902-4 1992 Although other examples of overlapping, opposite-strand eukaryotic genes exist, N-myc and N-cym are unique in that they appear to be coregulated in tumor cell lines under basal growth conditions and in response to the differentiating agent retinoic acid. Tretinoin 240-253 MYCN opposite strand Homo sapiens 90-95
24706335-8 2014 Upon treating with retinoic acid, FNDC5 expression was upregulated during embryoid body formation and decreased slowly at final stage of neural differentiation when neurospheres emerged. Tretinoin 19-32 fibronectin type III domain containing 5 Mus musculus 34-39
24592821-2 2014 However, in the majority of patients given all-trans retinoic acid (ATRA)/anthracycline-based induction therapy, PML-RARalpha transcript remains even when haematologic complete remission is achieved. Tretinoin 43-66 PML nuclear body scaffold Homo sapiens 113-116
1534272-6 1992 In contrast, cells exposed to RA contained larger amounts of alpha-actinin, vinculin, talin, lipocortin I, and lipocortin II, as determined with their respective antibodies followed by flow cytometric analysis as described above. Tretinoin 30-32 vinculin Homo sapiens 76-84
24967705-5 2014 ATRA induced robust expression of CD38, a cell surface marker and cellular NADase. Tretinoin 0-4 CD38 molecule Homo sapiens 34-38
1534272-8 1992 Treatment of HL-60/S4 with RA led to increases in vinculin, talin, lipocortin I, and lipocortin II. Tretinoin 27-29 vinculin Homo sapiens 50-58
24959884-0 2014 Nuclear MEK1 sequesters PPARgamma and bisects MEK1/ERK signaling: a non-canonical pathway of retinoic acid inhibition of adipocyte differentiation. Tretinoin 93-106 mitogen-activated protein kinase kinase 1 Homo sapiens 8-12
1534272-9 1992 An RA-resistant clone, designated HL-60/R3, constitutively expressed larger amounts of alpha-actinin, vinculin, lipocortin I, and lipocortin II than parental HL-60 cells. Tretinoin 3-5 vinculin Homo sapiens 102-110
24959884-0 2014 Nuclear MEK1 sequesters PPARgamma and bisects MEK1/ERK signaling: a non-canonical pathway of retinoic acid inhibition of adipocyte differentiation. Tretinoin 93-106 mitogen-activated protein kinase kinase 1 Homo sapiens 46-50
1375906-5 1992 In this study we find that retinoic acid (RA), a naturally occurring morphogen, that has been shown to be indispensable in the development of the chick limb bud, stimulates an increase in IGF-II messenger RNA (mRNA) in the Lan-1-15N neuroblastoma cell line. Tretinoin 27-40 IGFII Gallus gallus 188-194
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 26-28 CD38 molecule Homo sapiens 104-108
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 26-28 Cbl proto-oncogene Homo sapiens 224-229
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 91-93 CD38 molecule Homo sapiens 104-108
24922062-5 2014 Two sequentially emergent RA-resistant HL-60 cell lines, R38+ and R38-, distinguishable by RA-inducible CD38 expression, do not arrest in G1/G0 and fail to upregulate CD11b and the myeloid-associated signaling factors Vav1, c-Cbl, Lyn, Fgr, and c-Raf after RA treatment. Tretinoin 91-93 CD38 molecule Homo sapiens 104-108
24646031-3 2014 In many cases, downregulation of CDK activity by ATRA and vitamin D3 is a result of elevated p21- and p27-bound CDKs. Tretinoin 49-53 H3 histone pseudogene 16 Homo sapiens 93-96
1375906-5 1992 In this study we find that retinoic acid (RA), a naturally occurring morphogen, that has been shown to be indispensable in the development of the chick limb bud, stimulates an increase in IGF-II messenger RNA (mRNA) in the Lan-1-15N neuroblastoma cell line. Tretinoin 42-44 IGFII Gallus gallus 188-194
24646031-3 2014 In many cases, downregulation of CDK activity by ATRA and vitamin D3 is a result of elevated p21- and p27-bound CDKs. Tretinoin 49-53 interferon alpha inducible protein 27 Homo sapiens 102-105
1375906-6 1992 This increase in IGF-II is coincident with RA mediated inhibition of DNA synthesis. Tretinoin 43-45 IGFII Gallus gallus 17-23
24646031-9 2014 Finally, sharp reduction in c-Myc has been observed in several leukaemia cell lines treated with ATRA, which may regulate expression of CDKs and CKIs. Tretinoin 97-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 28-33
1378916-2 1992 In an effort to increase the therapeutic efficacy of RA, we have measured the capacity of granulocyte colony-stimulating factor (G-CSF) to enhance the differentiation inducing activity of RA in WEHI-3B D+ monomyelocytic leukemia cells. Tretinoin 188-190 colony stimulating factor 3 (granulocyte) Mus musculus 129-134
1378916-4 1992 In the presence of 50 ng/ml of G-CSF, which produced only 12% differentiation when used alone, 0.5 microM RA induced the same degree of cellular differentiation as the optimum concentration of RA (i.e. 7 microM) employed alone. Tretinoin 106-108 colony stimulating factor 3 (granulocyte) Mus musculus 31-36
1378916-4 1992 In the presence of 50 ng/ml of G-CSF, which produced only 12% differentiation when used alone, 0.5 microM RA induced the same degree of cellular differentiation as the optimum concentration of RA (i.e. 7 microM) employed alone. Tretinoin 193-195 colony stimulating factor 3 (granulocyte) Mus musculus 31-36
24637061-2 2014 Previous studies indicated that in acute promyelocytic leukemia (APL), a subtype of acute myelogenous leukemia (AML) bearing the leukemia promoting PML/RARalpha fusion protein, let-7c expression seems to be controlled by the host gene promoter, in which canonical Retinoic Acid Responsive Elements (RAREs) are bound by PML/RARalpha in an all transretinoic acid (ATRA)-sensitive manner. Tretinoin 264-277 microRNA let-7c Homo sapiens 177-183
1537314-0 1992 Regulation of glucokinase and proinsulin gene expression and insulin secretion in RIN-m5F cells by dexamethasone, retinoic acid, and thyroid hormone. Tretinoin 114-127 glucokinase Rattus norvegicus 14-25
24637061-2 2014 Previous studies indicated that in acute promyelocytic leukemia (APL), a subtype of acute myelogenous leukemia (AML) bearing the leukemia promoting PML/RARalpha fusion protein, let-7c expression seems to be controlled by the host gene promoter, in which canonical Retinoic Acid Responsive Elements (RAREs) are bound by PML/RARalpha in an all transretinoic acid (ATRA)-sensitive manner. Tretinoin 342-360 microRNA let-7c Homo sapiens 177-183
24637061-2 2014 Previous studies indicated that in acute promyelocytic leukemia (APL), a subtype of acute myelogenous leukemia (AML) bearing the leukemia promoting PML/RARalpha fusion protein, let-7c expression seems to be controlled by the host gene promoter, in which canonical Retinoic Acid Responsive Elements (RAREs) are bound by PML/RARalpha in an all transretinoic acid (ATRA)-sensitive manner. Tretinoin 362-366 microRNA let-7c Homo sapiens 177-183
24637061-6 2014 It was demonstrated that ATRA treatment leads to let-7c upregulation inducing a more open chromatin conformation of the host gene promoter, with an enrichment of epigenetic marks that correlate with a more active transcriptional state. Tretinoin 25-29 microRNA let-7c Homo sapiens 49-55
1537314-1 1992 In RIN-5mF cells, treatment with either dexamethasone or retinoic acid resulted in increased glucokinase activity. Tretinoin 57-70 glucokinase Rattus norvegicus 93-104
23770850-3 2014 We report here the regulatory mechanism of the repression of PU.1-dependent activation of PSMBs by PML/RARalpha in the pathogenesis of acute promyelocytic leukemia (APL) and the unidentified function of all-trans retinoic acid (ATRA) as an immunomodulator in the treatment of APL. Tretinoin 213-226 Spi-1 proto-oncogene Homo sapiens 61-65
23770850-3 2014 We report here the regulatory mechanism of the repression of PU.1-dependent activation of PSMBs by PML/RARalpha in the pathogenesis of acute promyelocytic leukemia (APL) and the unidentified function of all-trans retinoic acid (ATRA) as an immunomodulator in the treatment of APL. Tretinoin 228-232 Spi-1 proto-oncogene Homo sapiens 61-65
23770850-3 2014 We report here the regulatory mechanism of the repression of PU.1-dependent activation of PSMBs by PML/RARalpha in the pathogenesis of acute promyelocytic leukemia (APL) and the unidentified function of all-trans retinoic acid (ATRA) as an immunomodulator in the treatment of APL. Tretinoin 228-232 PML nuclear body scaffold Homo sapiens 99-102
23770850-3 2014 We report here the regulatory mechanism of the repression of PU.1-dependent activation of PSMBs by PML/RARalpha in the pathogenesis of acute promyelocytic leukemia (APL) and the unidentified function of all-trans retinoic acid (ATRA) as an immunomodulator in the treatment of APL. Tretinoin 228-232 retinoic acid receptor alpha Homo sapiens 103-111
1537314-2 1992 Treatment with dexamethasone (50 and 500 nM) increased glucokinase activity 140% and 260%, respectively, whereas treatment with retinoic acid (100 and 1000 nM) increased glucokinase activity by 50% and 80%, respectively. Tretinoin 128-141 glucokinase Rattus norvegicus 170-181
23770850-9 2014 Collectively, our data demonstrate that PML/RARalpha suppresses PU.1-dependent activation of the immunosubunits, which may facilitate the escape of APL cells from immune surveillance in leukemia development, and ATRA treatment is able to reactivate their expression, which would promote more efficient T-cell-mediated recognition in the treatment. Tretinoin 212-216 PML nuclear body scaffold Homo sapiens 40-43
23770850-9 2014 Collectively, our data demonstrate that PML/RARalpha suppresses PU.1-dependent activation of the immunosubunits, which may facilitate the escape of APL cells from immune surveillance in leukemia development, and ATRA treatment is able to reactivate their expression, which would promote more efficient T-cell-mediated recognition in the treatment. Tretinoin 212-216 retinoic acid receptor alpha Homo sapiens 44-52
23770850-9 2014 Collectively, our data demonstrate that PML/RARalpha suppresses PU.1-dependent activation of the immunosubunits, which may facilitate the escape of APL cells from immune surveillance in leukemia development, and ATRA treatment is able to reactivate their expression, which would promote more efficient T-cell-mediated recognition in the treatment. Tretinoin 212-216 Spi-1 proto-oncogene Homo sapiens 64-68
23903816-3 2013 The neuronal differentiation triggered by exposure to retinoic acid (RA) was characterized in the control culture by mRNA expression analysis of neuronal specific markers such as MAP2, NF-200, Tubulin betaIII, MAPT-tau, synaptophysin as well as excitatory (NMDA, AMPA) and inhibitory (GABA) receptors. Tretinoin 54-67 microtubule associated protein tau Homo sapiens 210-214
1537314-14 1992 We conclude that the glucokinase and proinsulin genes respond in parallel to dexamethasone and retinoic acid (both increased) and to T3 (both decreased). Tretinoin 95-108 glucokinase Rattus norvegicus 21-32
1312497-5 1992 We extend those findings to show that 9-cis RA is also "retinoid X" for mouse RXR alpha, beta, and gamma. Tretinoin 44-46 retinoid X receptor alpha Mus musculus 78-87
23562609-7 2013 During SIRPalpha induction, levels of these 3 miRNAs were all reduced, and their downregulation by retinoic acid or phorbol 12-myristate 13-acetate occurred through suppression of the c-Myc signaling pathway. Tretinoin 99-112 MYC proto-oncogene, bHLH transcription factor Homo sapiens 184-189
23587524-0 2013 Retinoic acid induces adhesion and migration in NB4 cells through Pyk2 signaling. Tretinoin 0-13 protein tyrosine kinase 2 beta Homo sapiens 66-70
23587524-4 2013 ATRA induced upregulation of Pyk2 mRNA, protein and phosphorylation levels and enhanced Pyk2 interaction with paxillin and vinculin. Tretinoin 0-4 protein tyrosine kinase 2 beta Homo sapiens 29-33
23587524-4 2013 ATRA induced upregulation of Pyk2 mRNA, protein and phosphorylation levels and enhanced Pyk2 interaction with paxillin and vinculin. Tretinoin 0-4 protein tyrosine kinase 2 beta Homo sapiens 88-92
24845860-4 2014 In vitro experiments showed that RA is necessary and sufficient to induce the development of distal-like hair cell phenotypes and promotes expression of the actin-crosslinking proteins, Espin and Fscn2. Tretinoin 33-35 espin Gallus gallus 186-191
24810481-11 2014 Serum FOLR1 concentrations may be influenced by the steroid retinoic acid (vitamin A) but do not appear to be associated with folate nutritional status. Tretinoin 60-73 folate receptor alpha Homo sapiens 6-11
23587524-4 2013 ATRA induced upregulation of Pyk2 mRNA, protein and phosphorylation levels and enhanced Pyk2 interaction with paxillin and vinculin. Tretinoin 0-4 paxillin Homo sapiens 110-118
1311919-5 1992 EGF receptors on chondrocytes were increased by treatment with retinoic acid and interleukin-1 beta, which inhibited proteoglycan synthesis. Tretinoin 63-76 pro-epidermal growth factor Oryctolagus cuniculus 0-3
23587524-5 2013 Pyk2 inhibition resulted in a reduction of NB4 cell adhesion and migration following ATRA treatment. Tretinoin 85-89 protein tyrosine kinase 2 beta Homo sapiens 0-4
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 25-38 fatty acid binding protein 5, epidermal Mus musculus 213-218
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 40-42 fatty acid binding protein 5, epidermal Mus musculus 213-218
24711541-7 2014 As a consequence, inhibiting HIF-1alpha in APL mouse models delays leukemia progression and exquisitely synergizes with ATRA to eliminate leukemia-initiating cells (LICs). Tretinoin 120-124 hypoxia inducible factor 1, alpha subunit Mus musculus 29-39
24522204-8 2014 Activation of nuclear AKT during ATRA-mediated differentiation results in the phosphorylation of several proteins, including PHB2, which may serve to coordinate nuclear-mitochondrial events during differentiation. Tretinoin 33-37 prohibitin 2 Homo sapiens 125-129
1737056-13 1992 These results show that changes in ferritin and transferrin receptor caused by treatment with retinoic acid are similar to those induced by excess iron, and suggest that changes in these proteins during cell differentiation are due to redistribution of intracellular iron into the regulatory pool(s), rather than to iron-independent mechanisms. Tretinoin 94-107 transferrin receptor Homo sapiens 48-68
24569880-1 2014 Retinoic acid (RA) plays key roles in cell differentiation and growth arrest by activating nuclear RA receptors (RARs) (alpha, beta and gamma), which are ligand-dependent transcription factors. Tretinoin 0-13 arginyl-tRNA synthetase Mus musculus 99-111
23957476-6 2013 With this cellular assay, we identified potent selective ALDH1A1 inhibitors to explore the role of retinoic acid production in various preclinical disease models. Tretinoin 99-112 aldehyde dehydrogenase 1 family member A1 Homo sapiens 57-64
1624215-4 1992 In non-immunized animals retinoic acid stimulated the production of IL-1 but not of IL-2. Tretinoin 25-38 interleukin 1 complex Mus musculus 68-72
23627671-0 2013 The short isoform of the long-type PML-RARA fusion gene in acute promyelocytic leukaemia lacks sensitivity to all-trans-retinoic acid. Tretinoin 110-133 PML nuclear body scaffold Homo sapiens 35-38
23627671-0 2013 The short isoform of the long-type PML-RARA fusion gene in acute promyelocytic leukaemia lacks sensitivity to all-trans-retinoic acid. Tretinoin 110-133 retinoic acid receptor alpha Homo sapiens 39-43
23657628-6 2013 We found that RA significantly enhanced TGF-beta-induced expression of Foxp3 on naive and committed T cells in vitro and that this was blocked by an antagonist of RARalpha (RARi). Tretinoin 14-16 forkhead box P3 Mus musculus 71-76
24569880-1 2014 Retinoic acid (RA) plays key roles in cell differentiation and growth arrest by activating nuclear RA receptors (RARs) (alpha, beta and gamma), which are ligand-dependent transcription factors. Tretinoin 0-13 arginyl-tRNA synthetase Mus musculus 113-117
24569880-1 2014 Retinoic acid (RA) plays key roles in cell differentiation and growth arrest by activating nuclear RA receptors (RARs) (alpha, beta and gamma), which are ligand-dependent transcription factors. Tretinoin 15-17 arginyl-tRNA synthetase Mus musculus 99-111
24569880-1 2014 Retinoic acid (RA) plays key roles in cell differentiation and growth arrest by activating nuclear RA receptors (RARs) (alpha, beta and gamma), which are ligand-dependent transcription factors. Tretinoin 15-17 arginyl-tRNA synthetase Mus musculus 113-117
25112011-5 2014 In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. Tretinoin 13-15 POU class 5 homeobox 1 Homo sapiens 154-158
25112011-5 2014 In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. Tretinoin 13-15 POU class 5 homeobox 1 Homo sapiens 227-231
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 Spi-1 proto-oncogene Homo sapiens 128-132
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 lysine methyltransferase 2A Homo sapiens 136-139
1550961-2 1992 We observed that the level of endogenous BMP-2 mRNA increased an average of 11-fold on differentiation of F9 embryonal carcinoma cells into parietal endoderm after treatment with retinoic acid (RA) and cAMP, whereas the message for the closely related BMP-4 decreased 12-fold after this treatment. Tretinoin 179-192 bone morphogenetic protein 2 Homo sapiens 41-46
24769646-4 2014 Combining ATRA with cytarabine had a synergistic antileukemic effect in MLL-AF9-positive cells in vitro. Tretinoin 10-14 lysine methyltransferase 2A Homo sapiens 72-75
23438903-10 2013 We also showed the expression of fhlA in the heart to be increased by retinoic acid (RA) and decreased by the RA synthase inhibitor DEAB. Tretinoin 70-83 four and a half LIM domains 1a Danio rerio 33-37
23438903-10 2013 We also showed the expression of fhlA in the heart to be increased by retinoic acid (RA) and decreased by the RA synthase inhibitor DEAB. Tretinoin 85-87 four and a half LIM domains 1a Danio rerio 33-37
24769646-5 2014 The level of dimethyl histone H3 lysine 4 (H3K4me2) in the RARalpha gene-promoter region, PU.1 upstream regulatory region (URE) and RUNX1+24/+25 intronic enhancer was higher in MLL-AF9-positive cells than in MLL-AF4-positive cells, and inhibiting lysine-specific demethylase 1, which acts as a histone demethylase inhibitor, reactivated ATRA sensitivity in MLL-AF4-positive cells. Tretinoin 337-341 retinoic acid receptor alpha Homo sapiens 59-67
1538719-0 1992 Role of isozymes of rabbit microsomal cytochrome P-450 in the metabolism of retinoic acid, retinol, and retinal. Tretinoin 76-89 cytochrome P-450 Oryctolagus cuniculus 38-54
24769646-5 2014 The level of dimethyl histone H3 lysine 4 (H3K4me2) in the RARalpha gene-promoter region, PU.1 upstream regulatory region (URE) and RUNX1+24/+25 intronic enhancer was higher in MLL-AF9-positive cells than in MLL-AF4-positive cells, and inhibiting lysine-specific demethylase 1, which acts as a histone demethylase inhibitor, reactivated ATRA sensitivity in MLL-AF4-positive cells. Tretinoin 337-341 Spi-1 proto-oncogene Homo sapiens 90-94
24769646-5 2014 The level of dimethyl histone H3 lysine 4 (H3K4me2) in the RARalpha gene-promoter region, PU.1 upstream regulatory region (URE) and RUNX1+24/+25 intronic enhancer was higher in MLL-AF9-positive cells than in MLL-AF4-positive cells, and inhibiting lysine-specific demethylase 1, which acts as a histone demethylase inhibitor, reactivated ATRA sensitivity in MLL-AF4-positive cells. Tretinoin 337-341 RUNX family transcription factor 1 Homo sapiens 132-137
23727579-3 2013 The cardiac differentiation of H9c2 cells cultured in media containing 1% fetal bovine serum and all-trans retinoic acid was confirmed by enhanced expression of cardiac troponin T (cTnT), the appearance of multinucleated cells, and cell cycle arrest at G0/G1 phase. Tretinoin 107-120 troponin T2, cardiac type Rattus norvegicus 161-179
23727579-3 2013 The cardiac differentiation of H9c2 cells cultured in media containing 1% fetal bovine serum and all-trans retinoic acid was confirmed by enhanced expression of cardiac troponin T (cTnT), the appearance of multinucleated cells, and cell cycle arrest at G0/G1 phase. Tretinoin 107-120 troponin T2, cardiac type Rattus norvegicus 181-185
23636811-2 2013 Similarly, we found that the same low RA concentration up-regulated or induced stimulation by retinoic acid 8 (Stra8) in such cells, both at mRNA and protein level. Tretinoin 38-40 stimulated by retinoic acid gene 8 Mus musculus 111-116
24566867-3 2014 In acute promyelocytic leukemia (APL), repression by the PML-RARalpha oncofusion protein is mediated by an HDAC-containing complex that can be dissociated by pharmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the expense of side effects and recurrence. Tretinoin 191-204 PML nuclear body scaffold Homo sapiens 57-60
24566867-3 2014 In acute promyelocytic leukemia (APL), repression by the PML-RARalpha oncofusion protein is mediated by an HDAC-containing complex that can be dissociated by pharmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the expense of side effects and recurrence. Tretinoin 191-204 retinoic acid receptor alpha Homo sapiens 61-69
23636811-5 2013 Finally, we found that RA induced Stra8, Sycp3, Dmc1, and Rec8 transcripts, promoting meiotic entry in culture also in pregonadal 10.5-dpc PGCs of both sexes. Tretinoin 23-25 stimulated by retinoic acid gene 8 Mus musculus 34-39
1569964-7 1992 While retinoic acid treatment decreased both calcitonin and CGRP mRNA levels, the combination of dexamethasone and retinoic acid still yielded the increase in calcitonin relative to CGRP mRNA. Tretinoin 6-19 calcitonin-related polypeptide alpha Rattus norvegicus 60-64
23636811-5 2013 Finally, we found that RA induced Stra8, Sycp3, Dmc1, and Rec8 transcripts, promoting meiotic entry in culture also in pregonadal 10.5-dpc PGCs of both sexes. Tretinoin 23-25 synaptonemal complex protein 3 Mus musculus 41-46
24566867-3 2014 In acute promyelocytic leukemia (APL), repression by the PML-RARalpha oncofusion protein is mediated by an HDAC-containing complex that can be dissociated by pharmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the expense of side effects and recurrence. Tretinoin 206-210 PML nuclear body scaffold Homo sapiens 57-60
24566867-3 2014 In acute promyelocytic leukemia (APL), repression by the PML-RARalpha oncofusion protein is mediated by an HDAC-containing complex that can be dissociated by pharmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the expense of side effects and recurrence. Tretinoin 206-210 retinoic acid receptor alpha Homo sapiens 61-69
24566867-4 2014 We hypothesized that the context-specific close physical proximity of a retinoid and HDACi-binding protein in the repressive PML-RARalpha-HDAC complex may permit selective targeting by a hybrid molecule of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS-275, yielding MC2392. Tretinoin 206-210 PML nuclear body scaffold Homo sapiens 125-128
24566867-4 2014 We hypothesized that the context-specific close physical proximity of a retinoid and HDACi-binding protein in the repressive PML-RARalpha-HDAC complex may permit selective targeting by a hybrid molecule of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS-275, yielding MC2392. Tretinoin 206-210 retinoic acid receptor alpha Homo sapiens 129-137
24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 H3 histone pseudogene 16 Homo sapiens 198-201
24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 interferon alpha inducible protein 27 Homo sapiens 206-209
24440757-0 2014 All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity. Tretinoin 0-23 granzyme B Homo sapiens 89-99
24440757-0 2014 All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity. Tretinoin 25-29 granzyme B Homo sapiens 89-99
23785470-2 2013 However, little is known about the epigenetic mechanism by which RA induces Stra8 expression. Tretinoin 65-67 stimulated by retinoic acid gene 8 Mus musculus 76-81
23785470-3 2013 Utilizing a chromatin immunoprecipitation assay (ChIP), we showed that RA increases histone acetylation at the Stra8 promoter in murine embryonic stem cells (ESCs), a model for germ cell differentiation. Tretinoin 71-73 stimulated by retinoic acid gene 8 Mus musculus 111-116
23508548-3 2013 Recent studies demonstrated that Boule and stimulated by retinoic acid 8 (Stra8) played important roles in initiation meiosis in male germ cells. Tretinoin 57-70 protein boule-like Capra hircus 33-38
1569964-7 1992 While retinoic acid treatment decreased both calcitonin and CGRP mRNA levels, the combination of dexamethasone and retinoic acid still yielded the increase in calcitonin relative to CGRP mRNA. Tretinoin 115-128 calcitonin-related polypeptide alpha Rattus norvegicus 182-186
24492652-0 2014 All-trans-retinoic acid improves cholestasis in alpha-naphthylisothiocyanate-treated rats and Mdr2-/- mice. Tretinoin 0-23 ATP binding cassette subfamily B member 4 Rattus norvegicus 94-98
1733233-6 1992 Other differentiating agents, dimethyl sulfoxide, retinoic acid, and dexamethasone, also increased levels of MRP-8 and MRP-14 mRNA. Tretinoin 50-63 S100 calcium binding protein A8 Homo sapiens 109-114
24492652-8 2014 atRA alone or in combination with UDCA significantly reduced plasma levels of alkaline phosphatase and bile salts in 12-week-old Mdr2(-/-) mice. Tretinoin 0-4 ATP binding cassette subfamily B member 4 Rattus norvegicus 129-133
24548459-8 2014 We found that day 7 MCs differentiated in the presence of RA had an increase in the percent positive and relative expression levels of both maturation (CD80, CD86, and MHCII) and inhibitory (PD-L1 and PD-L2) markers compared to control cells. Tretinoin 58-60 CD274 molecule Homo sapiens 191-196
23441061-0 2013 Expression of Ski can act as a negative feedback mechanism on retinoic acid signaling. Tretinoin 62-75 SKI proto-oncogene Homo sapiens 14-17
1576967-3 1992 MASH1 and MASH2 display complementary patterns of expression during the retinoic-acid-induced neuronal differentiation of P19 cells. Tretinoin 72-85 achaete-scute family bHLH transcription factor 1 Homo sapiens 0-5
24360906-9 2014 In addition, they may modulate the transcriptional output of multiple signaling pathways involved in neural crest development (Wnt, Retinoic Acid) through the induction of key pathway regulators (Axin2 and Cyp26c1). Tretinoin 132-145 axin 2 Homo sapiens 196-201
23670176-3 2013 Genetic mutations resulting in amino acid substitution in the retinoic acid receptor alpha (RARalpha) ligand binding domain (LBD) and the PML-B2 domain of PML-RARalpha, respectively, have been reported as molecular mechanisms underlying resistance to ATRA and As2O3. Tretinoin 251-255 retinoic acid receptor alpha Homo sapiens 62-90
1576967-4 1992 MASH1 mRNA is undetectable in undifferentiated P19 cells but is induced to high levels by retinoic acid coincident with neuronal differentiation. Tretinoin 90-103 achaete-scute family bHLH transcription factor 1 Homo sapiens 0-5
23670176-3 2013 Genetic mutations resulting in amino acid substitution in the retinoic acid receptor alpha (RARalpha) ligand binding domain (LBD) and the PML-B2 domain of PML-RARalpha, respectively, have been reported as molecular mechanisms underlying resistance to ATRA and As2O3. Tretinoin 251-255 retinoic acid receptor alpha Homo sapiens 92-100
23670176-3 2013 Genetic mutations resulting in amino acid substitution in the retinoic acid receptor alpha (RARalpha) ligand binding domain (LBD) and the PML-B2 domain of PML-RARalpha, respectively, have been reported as molecular mechanisms underlying resistance to ATRA and As2O3. Tretinoin 251-255 PML nuclear body scaffold Homo sapiens 138-141
1939209-0 1991 Induction of expression of the alpha v beta 1 and alpha v beta 3 integrin heterodimers during retinoic acid-induced neuronal differentiation of murine embryonal carcinoma cells. Tretinoin 94-107 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 58-64
23670176-3 2013 Genetic mutations resulting in amino acid substitution in the retinoic acid receptor alpha (RARalpha) ligand binding domain (LBD) and the PML-B2 domain of PML-RARalpha, respectively, have been reported as molecular mechanisms underlying resistance to ATRA and As2O3. Tretinoin 251-255 PML nuclear body scaffold Homo sapiens 155-158
23670176-3 2013 Genetic mutations resulting in amino acid substitution in the retinoic acid receptor alpha (RARalpha) ligand binding domain (LBD) and the PML-B2 domain of PML-RARalpha, respectively, have been reported as molecular mechanisms underlying resistance to ATRA and As2O3. Tretinoin 251-255 retinoic acid receptor alpha Homo sapiens 159-167
24503540-5 2014 We found that ASCs cultured with ATRA or transfected with miRNA let-7e expressed epithelial markers such as cytokeratin-18 and early renal organogenesis markers such as Pax2, Wt1, Wnt4 and megalin. Tretinoin 33-37 keratin 18 Homo sapiens 108-122
23228968-8 2013 In the ATRA-treated AE cells, gene expression analyses revealed functional networks involving SERPINE1 and bone morphogenetic protein 2; AKT phosphorylation was upregulated. Tretinoin 7-11 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 94-102
1939209-9 1991 The 90-kDa polypeptide, also induced by retinoic acid, was identified as beta 3, whereas the identity of the uninduced 96-kDa polypeptide remains unclear as yet. Tretinoin 40-53 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 73-79
23656719-3 2013 We recently reported that AhR promotes retinoic acid (RA)-induced granulocytic differentiation of HL-60 myeloblastic leukemia cells by restricting the nuclear abundance of the stem cell associated transcription factor Oct4. Tretinoin 39-52 POU class 5 homeobox 1 Homo sapiens 218-222
23656719-3 2013 We recently reported that AhR promotes retinoic acid (RA)-induced granulocytic differentiation of HL-60 myeloblastic leukemia cells by restricting the nuclear abundance of the stem cell associated transcription factor Oct4. Tretinoin 54-56 POU class 5 homeobox 1 Homo sapiens 218-222
23656719-14 2013 Moreover, FICZ in combination with RA also increases expression of AhR and even more so of both Cyp1A2 and p47phox, which are known to be transcriptionally regulated by AhR. Tretinoin 35-37 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 96-102
24395056-10 2014 The 2-nM retinoic acid exposure also led to alterations of neurobehavior- and optic nerve-related genes, with the transforming growth factor-beta signal transduction inhibitor noggin (nog) and the spinal cord marker homeobox c3a (hox) being underexpressed and the retinal G protein-coupled receptor a (rgr), the photoreceptor cell marker rhodopsin (rho), and the short wave-sensitive cone pigment opsin 1 (opn1sw1) being overexpressed. Tretinoin 9-22 rhodopsin Danio rerio 338-347
24300824-0 2014 All-trans retinoic acid modulates bone morphogenic protein 9-induced osteogenesis and adipogenesis of preadipocytes through BMP/Smad and Wnt/beta-catenin signaling pathways. Tretinoin 10-23 bone morphogenetic protein 1 Homo sapiens 124-127
24300824-0 2014 All-trans retinoic acid modulates bone morphogenic protein 9-induced osteogenesis and adipogenesis of preadipocytes through BMP/Smad and Wnt/beta-catenin signaling pathways. Tretinoin 10-23 catenin beta 1 Homo sapiens 141-153
24309293-1 2014 Bone marrow mesenchymal stem cells (MSCs) can be differentiate towards a Schwann cells (SCs) lineage when exposed to pre-inducing reagents beta-mercaptoethanol (BME) and retinoic acid (RA), followed by inducing factors: forskolin (FSK), basic fibroblast growth factor (bFGF), platelet derived growth factor (PDGF), and heregulin (HRG). Tretinoin 185-187 myotrophin Rattus norvegicus 254-267
1939209-13 1991 These data demonstrate that retinoic acid strongly induces the expression of the integrin heterodimer alpha v beta 1 and also, to a smaller extent, the expression of alpha v beta 3. Tretinoin 28-41 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 166-180
1658797-2 1991 This promoter contains a retinoic acid response element (RARE) that closely resembles the RARE that is present in the RAR-beta 2 promoter. Tretinoin 25-38 retinoic acid receptor, beta Mus musculus 118-126
25520935-5 2014 Also, the common cell cycle inhibiting protein, p27, and the new cell cycle regulator, Cdk5, are involved in retinoic acid"s effects. Tretinoin 109-122 interferon alpha inducible protein 27 Homo sapiens 48-51
25520935-5 2014 Also, the common cell cycle inhibiting protein, p27, and the new cell cycle regulator, Cdk5, are involved in retinoic acid"s effects. Tretinoin 109-122 cyclin dependent kinase 5 Homo sapiens 87-91
23634885-13 2013 Retinoic acid (RA) increased transcription of all Hoxb genes in differentiating ES cells within 24 h, but thereafter transcription remained the same, increased progressively or fell progressively in a locus-specific manner. Tretinoin 0-13 homeobox B cluster Mus musculus 50-54
23634885-13 2013 Retinoic acid (RA) increased transcription of all Hoxb genes in differentiating ES cells within 24 h, but thereafter transcription remained the same, increased progressively or fell progressively in a locus-specific manner. Tretinoin 15-17 homeobox B cluster Mus musculus 50-54
1939157-8 1991 Recent studies have shown that MGP is strongly induced by retinoic acid in fibroblasts, chondrocytes, and osteoblasts, a response which suggests that MGP mediates an action of retinoic acid on an aspect of cell growth or differentiation. Tretinoin 176-189 matrix Gla protein Homo sapiens 150-153
1661245-6 1991 The retinoic acid response element (RARE) for the rat growth hormone gene is also a thyroid hormone response element (TRE), and the AP-1 binding site of the human osteocalcin promoter is also a vitamin D response element (VDRE) and a RARE. Tretinoin 4-17 gonadotropin releasing hormone receptor Rattus norvegicus 54-68
23614737-5 2013 The authors demonstrated that ALDH1A1 substrate 9-cis retinal and its corresponding product 9-cis retinoic acid potently induced the accumulation of MITF mRNA, tyrosinase mRNA and melanin. Tretinoin 98-111 aldehyde dehydrogenase 1 family member A1 Homo sapiens 30-37
23614737-5 2013 The authors demonstrated that ALDH1A1 substrate 9-cis retinal and its corresponding product 9-cis retinoic acid potently induced the accumulation of MITF mRNA, tyrosinase mRNA and melanin. Tretinoin 98-111 melanocyte inducing transcription factor Homo sapiens 149-153
24206578-3 2014 We assessed the clinical significance of CD56 antigen in 239 APL patients prospectively treated with all-trans retinoic acid and chemotherapy according to the Japan Adult Leukemia Study Group APL97 protocol. Tretinoin 101-124 neural cell adhesion molecule 1 Homo sapiens 41-45
24398584-5 2014 The results demonstrated that the expression of Stra8, a master gene for germ cell meiosis, and its stimulation by retinoic acid (RA) were reduced after suppression of Notch signaling, and the other meiotic genes, Dazl, Dmc1, and Rec8, were abolished or markedly decreased. Tretinoin 115-128 stimulated by retinoic acid gene 8 Mus musculus 48-53
24398584-5 2014 The results demonstrated that the expression of Stra8, a master gene for germ cell meiosis, and its stimulation by retinoic acid (RA) were reduced after suppression of Notch signaling, and the other meiotic genes, Dazl, Dmc1, and Rec8, were abolished or markedly decreased. Tretinoin 130-132 stimulated by retinoic acid gene 8 Mus musculus 48-53
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 13-26 interferon alpha inducible protein 27 Homo sapiens 203-206
1655814-5 1991 Contrary to expectation, we find that retinoic acid persists for longer (t 1/2 3 d) in cultures than retinol (t 1/2 1 d). Tretinoin 38-51 interleukin 1 receptor like 1 Homo sapiens 73-82
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 13-26 cyclin dependent kinase inhibitor 1B Homo sapiens 207-211
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 28-30 interferon alpha inducible protein 27 Homo sapiens 203-206
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 28-30 cyclin dependent kinase inhibitor 1B Homo sapiens 207-211
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 retinol binding protein 1, cellular Mus musculus 81-85
23638129-5 2013 ATRA and the RARgamma agonist further increased retinoid target gene expression (Rbp1, Crabp2, Krt4, Cyp26a1, Cyp26b1) and the chemokines Ccl17 and Ccl22. Tretinoin 0-4 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 101-108
24316973-5 2014 T helper cell rerouting in EAE was dependent on IL-4, which enhanced retinoic acid (RA) production by dendritic cells, which further induced expression of gut-homing receptors CCR9 and alpha4beta7 on Bcl11b-deficient CD4+ T cells. Tretinoin 69-82 interleukin 4 Mus musculus 48-52
24316973-5 2014 T helper cell rerouting in EAE was dependent on IL-4, which enhanced retinoic acid (RA) production by dendritic cells, which further induced expression of gut-homing receptors CCR9 and alpha4beta7 on Bcl11b-deficient CD4+ T cells. Tretinoin 84-86 interleukin 4 Mus musculus 48-52
25030439-3 2014 Several authors have described the induction of P-gp expression/activity in malignant cell lines after treatment with all-trans retinoic acid (AtRA; ligand of retinoic acid nuclear receptors, RARs). Tretinoin 122-141 arginyl-tRNA synthetase Mus musculus 192-196
25030439-3 2014 Several authors have described the induction of P-gp expression/activity in malignant cell lines after treatment with all-trans retinoic acid (AtRA; ligand of retinoic acid nuclear receptors, RARs). Tretinoin 143-147 arginyl-tRNA synthetase Mus musculus 192-196
23518499-5 2013 We showed that CDK1 function is required for all-trans retinoic acid (ATRA) to achieve the optimal effect in U-937 human leukemic cells. Tretinoin 45-68 cyclin dependent kinase 1 Homo sapiens 15-19
23518499-5 2013 We showed that CDK1 function is required for all-trans retinoic acid (ATRA) to achieve the optimal effect in U-937 human leukemic cells. Tretinoin 70-74 cyclin dependent kinase 1 Homo sapiens 15-19
23518499-6 2013 CDK1 modulates the levels of P27(kip) and AKT phosphorylation in response to ATRA treatment. Tretinoin 77-81 cyclin dependent kinase 1 Homo sapiens 0-4
23518499-6 2013 CDK1 modulates the levels of P27(kip) and AKT phosphorylation in response to ATRA treatment. Tretinoin 77-81 interferon alpha inducible protein 27 Homo sapiens 29-37
23518499-8 2013 The regulation of the subcellular content of CDK1 and RARgamma by ATRA is an important process for achieving an effective response in treatment of leukemia. Tretinoin 66-70 cyclin dependent kinase 1 Homo sapiens 45-49
23518499-10 2013 In addition, expression of wee1 kinase and Cdc25A/C phosphatases also coincide with CDK1 expression and its subcellular localization in response to ATRA treatment. Tretinoin 148-152 cyclin dependent kinase 1 Homo sapiens 84-88
25030439-4 2014 An isomer of AtRA also exists, 9-cis retinoic acid, which is a ligand of both RARs and nuclear retinoid X receptors (RXRs). Tretinoin 13-17 arginyl-tRNA synthetase Mus musculus 78-82
24314292-0 2013 The retinoic acid receptor-alpha modulators ATRA and Ro415253 reciprocally regulate human IL-5+ Th2 cell proliferation and cytokine expression. Tretinoin 44-48 retinoic acid receptor alpha Homo sapiens 4-32
23518499-11 2013 Our study reveals a novel mechanism by which CDK1 and RARgamma coordinate with ATRA to influence cell cycle progression and cellular differentiation. Tretinoin 79-83 cyclin dependent kinase 1 Homo sapiens 45-49
1917145-6 1991 Administration of RA also caused a significant increase in the proportion of myc p110-negative lesions to the total pre-neoplastic lesions observed. Tretinoin 18-20 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 77-80
24080087-2 2013 We provide evidence that the retinoic acid-producing enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) is an oncogene suppressor in specific splenic IgG1(+)/CD19(-) and IgG1(+)/CD19(+) B cell populations. Tretinoin 29-42 aldehyde dehydrogenase 1 family member A1 Homo sapiens 60-86
24080087-2 2013 We provide evidence that the retinoic acid-producing enzyme aldehyde dehydrogenase 1a1 (Aldh1a1) is an oncogene suppressor in specific splenic IgG1(+)/CD19(-) and IgG1(+)/CD19(+) B cell populations. Tretinoin 29-42 aldehyde dehydrogenase 1 family member A1 Homo sapiens 88-95
24005908-5 2013 Furthermore, accumulation of excess ATRA is accompanied by a compensatory 30-50% reduction in the expression of ATRA synthetic genes and a 120% increase in the expression of the ATRA catabolic enzyme Cyp26a1 in Dhrs3(-/-) embryos vs. controls. Tretinoin 36-40 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 200-207
23565812-3 2013 All-trans-retinoic acid (ATRA) causes some neuroblastoma (NB) cell lines to undergo differentiation and leads to a significant decrease in the oncogenic transcription factor MYCN. Tretinoin 0-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 174-178
24005908-5 2013 Furthermore, accumulation of excess ATRA is accompanied by a compensatory 30-50% reduction in the expression of ATRA synthetic genes and a 120% increase in the expression of the ATRA catabolic enzyme Cyp26a1 in Dhrs3(-/-) embryos vs. controls. Tretinoin 36-40 dehydrogenase/reductase (SDR family) member 3 Mus musculus 211-216
23565812-3 2013 All-trans-retinoic acid (ATRA) causes some neuroblastoma (NB) cell lines to undergo differentiation and leads to a significant decrease in the oncogenic transcription factor MYCN. Tretinoin 25-29 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 174-178
1917145-8 1991 These findings indicate that RA inhibits hepatocarcinogenesis and suggest that this effect may be related to its influence in reducing the expression of myc gene proteins and its subsequent inhibition of cell proliferation in pre-neoplastic lesions. Tretinoin 29-31 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 153-156
24052562-7 2013 Furthermore, the heart areas of CTN-exposed embryos demonstrated an elevated levels of aldh1a2 and cspg2 messenger RNA; these 2 cardiac-related genes are known to be involved in retinoic acid (RA) pathway as well as downstream targets of microRNA-138 (miR-138) in zebrafish. Tretinoin 178-191 versican a Danio rerio 99-104
1654334-1 1991 Retinoic acid-induced expression of CRABP-II but not CRABP-I in adult human skin in vivo and in skin fibroblasts in vitro. Tretinoin 0-13 cellular retinoic acid binding protein 1 Homo sapiens 36-43
24052562-7 2013 Furthermore, the heart areas of CTN-exposed embryos demonstrated an elevated levels of aldh1a2 and cspg2 messenger RNA; these 2 cardiac-related genes are known to be involved in retinoic acid (RA) pathway as well as downstream targets of microRNA-138 (miR-138) in zebrafish. Tretinoin 193-195 versican a Danio rerio 99-104
23379615-2 2013 Here we show that RARalpha signalling is down-regulated by amyloid beta (Abeta), which inhibits the synthesis of the endogenous ligand, retinoic acid (RA). Tretinoin 136-149 amyloid beta (A4) precursor protein Mus musculus 73-78
1654334-6 1991 External application of 0.1% retinoic acid cream in vivo for 16 h resulted in a 16-fold induction of CRABP-II transcripts, while CRABP-I mRNA remained undetectable. Tretinoin 29-42 cellular retinoic acid binding protein 1 Homo sapiens 101-108
23379615-2 2013 Here we show that RARalpha signalling is down-regulated by amyloid beta (Abeta), which inhibits the synthesis of the endogenous ligand, retinoic acid (RA). Tretinoin 18-20 amyloid beta (A4) precursor protein Mus musculus 73-78
1654334-7 1991 Expression of CRABP-II, but not CRABP-I mRNA, was also markedly increased (greater than 15-fold) by retinoic acid treatment of fibroblasts cultured from human skin, whereas no significant induction of CRABP-II mRNA was observed in human lung fibroblasts. Tretinoin 100-113 cellular retinoic acid binding protein 1 Homo sapiens 14-21
23871845-7 2013 In addition, analysis of retinoic acid-responsive genes, such as Cyp26a1 in these embryos suggests that bC cleavage results in the production of retinoic acid which then can be used by the embryo. Tretinoin 25-38 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 65-72
23871845-7 2013 In addition, analysis of retinoic acid-responsive genes, such as Cyp26a1 in these embryos suggests that bC cleavage results in the production of retinoic acid which then can be used by the embryo. Tretinoin 145-158 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 65-72
1653241-1 1991 Characterization and evidence that holo-CRABP is a substrate in retinoic acid metabolism. Tretinoin 64-77 cellular retinoic acid binding protein 1 Homo sapiens 40-45
24150763-8 2013 RA also promoted the expression of keratocyte-characteristic proteoglycans, such as keratocan, lumican, and decorin, and increased the amounts of collagen type-I in culture while significantly reducing the expression of matrix metalloproteases 1, 3, and 9. Tretinoin 0-2 matrix metallopeptidase 1 Homo sapiens 220-255
23361361-0 2013 Comparative SRY incorporation on the regulatory regions of pluripotency/differentiation genes in human embryonic carcinoma cells after retinoic acid induction. Tretinoin 135-148 sex determining region Y Homo sapiens 12-15
1653241-2 1991 Cellular retinoic acid binding protein (CRABP) has been expressed efficiently in Escherichia coli from the cDNA of bovine adrenal CRABP and characterized, especially with respect to affinity for endogenous retinoids and a role for it in retinoic acid metabolism. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 40-45
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 high mobility group AT-hook 2 Rattus norvegicus 218-247
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 high mobility group AT-hook 2 Rattus norvegicus 249-254
23590952-1 2013 BACKGROUND: All-trans retinoic acid (ATRA) induces in vitro angiogenesis and vascular endothelial growth factor (VEGF) secretion. Tretinoin 12-35 vascular endothelial growth factor A Rattus norvegicus 77-111
1653241-2 1991 Cellular retinoic acid binding protein (CRABP) has been expressed efficiently in Escherichia coli from the cDNA of bovine adrenal CRABP and characterized, especially with respect to affinity for endogenous retinoids and a role for it in retinoic acid metabolism. Tretinoin 9-22 cellular retinoic acid binding protein 1 Homo sapiens 130-135
23590952-1 2013 BACKGROUND: All-trans retinoic acid (ATRA) induces in vitro angiogenesis and vascular endothelial growth factor (VEGF) secretion. Tretinoin 12-35 vascular endothelial growth factor A Rattus norvegicus 113-117
23590952-1 2013 BACKGROUND: All-trans retinoic acid (ATRA) induces in vitro angiogenesis and vascular endothelial growth factor (VEGF) secretion. Tretinoin 37-41 vascular endothelial growth factor A Rattus norvegicus 77-111
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 31-44 cellular retinoic acid binding protein 1 Homo sapiens 5-10
23590952-1 2013 BACKGROUND: All-trans retinoic acid (ATRA) induces in vitro angiogenesis and vascular endothelial growth factor (VEGF) secretion. Tretinoin 37-41 vascular endothelial growth factor A Rattus norvegicus 113-117
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 5-10
24204656-3 2013 Here we demonstrate that Sirt2 is up-regulated during RA (retinoic acid)-induced and embryoid body (EB) differentiation of mouse ESCs. Tretinoin 54-56 sirtuin 2 Mus musculus 25-30
24204656-3 2013 Here we demonstrate that Sirt2 is up-regulated during RA (retinoic acid)-induced and embryoid body (EB) differentiation of mouse ESCs. Tretinoin 58-71 sirtuin 2 Mus musculus 25-30
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23531410-5 2013 Numerous genes belonging to specific signaling pathways (the Hedgehog, Notch, Wnt, FGF, TGFbeta/BMP, and retinoic acid pathways), and/or to the homeobox gene superfamily, were also uncovered when a less stringent fold change threshold was used. Tretinoin 105-118 bone morphogenetic protein 1 Homo sapiens 96-99
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23518351-2 2013 We identified the histone demethylase PHF8 as a coactivator that is specifically recruited by RARalpha fusions to activate expression of their downstream targets upon ATRA treatment. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 94-102
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 5-10
23995757-5 2013 Ectopic AKAP95 stimulates expression of a chromosomal reporter gene in synergy with MLL1 or MLL2, whereas AKAP95 depletion impairs retinoic acid-mediated gene induction in embryonic stem cells. Tretinoin 131-144 A-kinase anchoring protein 8 Homo sapiens 106-112
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23337719-11 2013 CONCLUSIONS: Simvastatin interacts with the RA system, inducing the expression of the key protein regulating the uptake of retinol (STRA6) and the expression of apoptosis-promoting CRABP2. Tretinoin 44-46 signaling receptor and transporter of retinol STRA6 Homo sapiens 132-137
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 33-46 fucosyltransferase 1 (H blood group) Homo sapiens 134-137
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 33-46 fucosyltransferase 1 (H blood group) Homo sapiens 298-301
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 48-50 fucosyltransferase 1 (H blood group) Homo sapiens 134-137
23267795-14 2013 CONCLUSION: The protective effects of atRA against hypoxia-induced injury might be involved in suppression of VEGF expression via stimulating Scpep1 distinct pathways and inhibiting the NFkappaB pathway. Tretinoin 38-42 vascular endothelial growth factor A Rattus norvegicus 110-114
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 48-50 fucosyltransferase 1 (H blood group) Homo sapiens 298-301
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 5-10
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 0-13 arginyl-tRNA synthetase Mus musculus 137-149
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 0-13 arginyl-tRNA synthetase Mus musculus 151-155
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 15-17 arginyl-tRNA synthetase Mus musculus 137-149
23885329-3 2013 In this report, we focus on the combinatorial effects of IL-4 with all-trans retinoic acid (ATRA) and lipopolysaccharide (LPS). Tretinoin 67-90 interleukin 4 Mus musculus 57-61
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23885329-3 2013 In this report, we focus on the combinatorial effects of IL-4 with all-trans retinoic acid (ATRA) and lipopolysaccharide (LPS). Tretinoin 92-96 interleukin 4 Mus musculus 57-61
24059847-3 2013 Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPARdelta). Tretinoin 15-17 arginyl-tRNA synthetase Mus musculus 151-155
24059847-11 2013 ATRA induces UCP1 expression in mouse adipocytes through activation of RARs, whereas expression of UCP1 in human adipocytes is not increased by exposure to ATRA. Tretinoin 0-4 arginyl-tRNA synthetase Mus musculus 71-75
23885329-5 2013 We demonstrate that although ATRA alone has no effect on the expression or activities of arginase 1, ATRA can dramatically potentiate the induction of arginase 1 by IL-4. Tretinoin 101-105 interleukin 4 Mus musculus 165-169
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 5-10
23087051-6 2013 Our results showed that alveolar hypoplasia caused by caloric restriction can be reversed with refeeding, and that retinoic acid prevents the alveolar hypoplasia coincident with the increased expression of elastin and retinoic acid receptor-alpha and decreased transforming growth factor-beta activity in developing rat lungs. Tretinoin 115-128 retinoic acid receptor, alpha Rattus norvegicus 218-246
24028740-4 2013 RESULTS: In this study, we evaluated the stability of various references during retinoic acid-induced (2 microM) differentiation of hES cells. Tretinoin 80-93 ribosome binding protein 1 Homo sapiens 132-135
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23202364-2 2013 We previously showed that mature heart valves calcify in response to retinoic acid (RA) treatment through downregulation of the SRY transcription factor Sox9. Tretinoin 69-82 sex determining region of Chr Y Mus musculus 128-131
23202364-2 2013 We previously showed that mature heart valves calcify in response to retinoic acid (RA) treatment through downregulation of the SRY transcription factor Sox9. Tretinoin 84-86 sex determining region of Chr Y Mus musculus 128-131
24023268-0 2013 Aromatase activity induction in human adipose fibroblasts by retinoic acids via retinoic acid receptor alpha. Tretinoin 61-75 retinoic acid receptor alpha Homo sapiens 80-108
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23849428-5 2013 RA also enhanced AKT expression and dramatically induced phosphorylation of AKT((Thr308)), accompanied by phosphorylation of both PKCdelta((Thr505)) and beta-adducin((Ser662)) and upregulated cyclin D2 and down-regulated cyclin B1. Tretinoin 0-2 cyclin B1 Homo sapiens 221-230
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 cyclin B1 Homo sapiens 102-111
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 5-10
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23526782-3 2013 In this study, we observed that the mRNA levels and protein expression of Rnf10 increase significantly upon the retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 112-125 cyclin dependent kinase inhibitor 2D Homo sapiens 162-165
23032629-11 2013 In neu3a gene-transfected neuroblastoma cells, the enzyme was found to positively regulate retinoic acid-induced differentiation with the elongation of axon length. Tretinoin 91-104 sialidase-3 Oryzias latipes 3-8
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 5-10
23904167-6 2013 However, Vdelta2T cell activation with HDMAPP and exposure to retinoic acid (signaling via retinoic acid receptor alpha) increased alpha4beta7 expression and enhanced binding to mucosal addressin cell adhesion molecule-1 in vitro while simultaneously suppressing cutaneous leukocyte Ag, thereby generating a committed gut-tropic phenotype. Tretinoin 62-75 retinoic acid receptor alpha Homo sapiens 91-119
1653241-6 1991 Holo-CRABP was a substrate for retinoic acid catabolism in rat testes microsomes by three criteria: 1) the rate of retinoic acid metabolism with CRABP in excess of retinoic acid exceeded the rate supported by the free retinoic acid; 2) increasing the apo-CRABP did not decrease the rate as predicted if free retinoic acid were the only substrate; and 3) holo-CRABP had a lower Michaelis constant (1.8 nM) for retinoic acid elimination than did free retinoic acid (49 nM). Tretinoin 115-128 cellular retinoic acid binding protein 1 Homo sapiens 145-150
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 11-34 fatty acid binding protein 5, epidermal Mus musculus 112-117
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 36-40 fatty acid binding protein 5, epidermal Mus musculus 112-117
22718360-8 2013 The RA effects on IKK and IkappaBalpha were blocked by okadaic acid or silencing the expression of PP2Ac-subunit, indicating that the inhibitory effect of RA on NF-kappaB is regulated through activation of PP2A and subsequent dephosphorylation of IKK/IkappaBalpha. Tretinoin 4-6 NFKB inhibitor alpha Rattus norvegicus 26-38
22718360-8 2013 The RA effects on IKK and IkappaBalpha were blocked by okadaic acid or silencing the expression of PP2Ac-subunit, indicating that the inhibitory effect of RA on NF-kappaB is regulated through activation of PP2A and subsequent dephosphorylation of IKK/IkappaBalpha. Tretinoin 4-6 NFKB inhibitor alpha Rattus norvegicus 251-263
1888336-10 1991 AHD-2 and AHD-7, catalyzed the oxidation of retinaldehyde to retinoic acid. Tretinoin 61-74 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 0-5
23221399-0 2013 MicroRNA 146 (Mir146) modulates spermatogonial differentiation by retinoic acid in mice. Tretinoin 66-79 microRNA 146 Mus musculus 14-20
23221399-3 2013 In this study, we discovered microRNA 146 (Mir146) to be highly regulated during spermatogonial differentiation, a process dependent on retinoic acid (RA) signaling. Tretinoin 136-149 microRNA 146 Mus musculus 43-49
23221399-3 2013 In this study, we discovered microRNA 146 (Mir146) to be highly regulated during spermatogonial differentiation, a process dependent on retinoic acid (RA) signaling. Tretinoin 151-153 microRNA 146 Mus musculus 43-49
23221399-9 2013 When undifferentiated spermatogonia were exposed to RA, Mir146 was downregulated along with a marker for undifferentiated germ cells, zinc finger and BTB domain containing 16 (Zbtb16; Plzf); Kit was upregulated. Tretinoin 52-54 microRNA 146 Mus musculus 56-62
23221399-12 2013 We conclude that Mir146 modulates the effects of RA on spermatogonial differentiation. Tretinoin 49-51 microRNA 146 Mus musculus 17-23
23889243-5 2013 Furthermore, Culicoides-specific CD4(+) CD25(high) regulatory cells were expanded or induced from CD4(+) CD25(-) cells in vitro in the presence of a combination of rIL-2 and rTGF-beta1 (rIL-2/rTGF-beta1) or of retinoic acid and rapamycin (RetA/Rapa). Tretinoin 210-223 CD4 molecule Equus caballus 33-36
22964640-4 2013 In particular, PML/RARalpha-positive blasts from APL patients display lower levels of miRNA let-7c, a member of the let-7 family, than normal promyelocytes and its expression increases after ATRA treatment. Tretinoin 191-195 PML nuclear body scaffold Homo sapiens 15-18
22964640-4 2013 In particular, PML/RARalpha-positive blasts from APL patients display lower levels of miRNA let-7c, a member of the let-7 family, than normal promyelocytes and its expression increases after ATRA treatment. Tretinoin 191-195 retinoic acid receptor alpha Homo sapiens 19-27
1886422-0 1991 Retinoic acid inhibits the expression of cytidine deaminase linked to the differentiation of the human leukemic cell line HL-60. Tretinoin 0-13 cytidine deaminase Homo sapiens 41-59
22964640-4 2013 In particular, PML/RARalpha-positive blasts from APL patients display lower levels of miRNA let-7c, a member of the let-7 family, than normal promyelocytes and its expression increases after ATRA treatment. Tretinoin 191-195 microRNA let-7c Homo sapiens 92-98
23850490-0 2013 Retracted: Histone H2B ubquitination regulates retinoic acid signaling through the cooperation of ASXL1 and BAP1. Tretinoin 47-60 H2B clustered histone 21 Homo sapiens 19-22
23850490-7 2013 Both ASXL1 and BAP1 were downregulated during RA-induced P19 cell differentiation with concomitant increase of ubiquitinated H2B, leading to activation of Hox genes. Tretinoin 46-48 H2B clustered histone 21 Homo sapiens 125-128
23850490-8 2013 Our data demonstrate the critical role of ASXL1 cooperation with BAP1 in cell differentiation through the regulation of RA signaling associated with H2B ubiquitination. Tretinoin 120-122 H2B clustered histone 21 Homo sapiens 149-152
21997537-4 2013 Besides TGF-beta, the TG2 promoter contains retinoic acid response elements as well. Tretinoin 44-57 transglutaminase 2, C polypeptide Mus musculus 22-25
21997537-5 2013 Here we show that in vitro retinoic acids, or TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes, and the apoptotic signal contributes to the TG2 induction. Tretinoin 27-41 transglutaminase 2, C polypeptide Mus musculus 113-116
21997537-5 2013 Here we show that in vitro retinoic acids, or TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes, and the apoptotic signal contributes to the TG2 induction. Tretinoin 27-41 transglutaminase 2, C polypeptide Mus musculus 198-201
21997537-5 2013 Here we show that in vitro retinoic acids, or TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes, and the apoptotic signal contributes to the TG2 induction. Tretinoin 59-73 transglutaminase 2, C polypeptide Mus musculus 113-116
21997537-5 2013 Here we show that in vitro retinoic acids, or TGF-beta and retinoic acids together can significantly enhance the TG2 mRNA expression in dying thymocytes, and the apoptotic signal contributes to the TG2 induction. Tretinoin 59-73 transglutaminase 2, C polypeptide Mus musculus 198-201
21997537-6 2013 Inhibition of retinoic acid synthesis either by alcohol or retinaldehyde dehydrogenases significantly attenuates the in vivo induction of TG2 following apoptosis induction indicating that retinoids indeed might contribute in vivo to the apoptosis-related TG2 expression. Tretinoin 14-27 transglutaminase 2, C polypeptide Mus musculus 138-141
21997537-6 2013 Inhibition of retinoic acid synthesis either by alcohol or retinaldehyde dehydrogenases significantly attenuates the in vivo induction of TG2 following apoptosis induction indicating that retinoids indeed might contribute in vivo to the apoptosis-related TG2 expression. Tretinoin 14-27 transglutaminase 2, C polypeptide Mus musculus 255-258
1886422-1 1991 The activity of cytidine deaminase markedly increases during the differentiation of HL-60 cells induced by dimethylsulfoxide or 1,25-dihydroxy vitamin D3, but does not increase when the inducer is retinoic acid. Tretinoin 197-210 cytidine deaminase Homo sapiens 16-34
23752611-6 2013 Moreover, p38alpha in CD103(+) DCs was required for optimal expression of retinaldehyde dehydrogenase, a key enzyme for retinoic acid synthesis, which in turn imprinted gut-homing receptors on responding T cells. Tretinoin 120-133 integrin subunit alpha E Homo sapiens 22-27
24648886-8 2013 Sox17, GATA6 and HNF4alpha were expressed after exposure a combination of oncostatin M, epidermal growth factor, retinoic acid, dexamethasone and ITS (OERDITS). Tretinoin 113-126 SRY-box transcription factor 17 Homo sapiens 0-5
1886422-2 1991 Here it is demonstrated that retinoic acid inhibits the increase in cytidine deaminase activity elicited by the other two inducers. Tretinoin 29-42 cytidine deaminase Homo sapiens 68-86
23733880-4 2013 CD103(+) DCs, but not pDCs or lung macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key for the production of retinoic acid, a cofactor for TGF-beta for Foxp3 induction. Tretinoin 154-167 forkhead box P3 Mus musculus 197-202
1886422-4 1991 These data indicate that retinoic acid negatively regulates the expression of cytidine deaminase in HL-60 cells, and suggest that this effect is mediated by a protein, the synthesis of which should be controlled by the nuclear receptor of retinoic acid. Tretinoin 25-38 cytidine deaminase Homo sapiens 78-96
23509752-6 2013 mRNA expression of Stra8, Odf2, Act, and Prm1 was upregulated in iPS cells by retinoic acid or testosterone induction, whereas Oct-4 transcription was reduced in these cells compared to the controls. Tretinoin 78-91 stimulated by retinoic acid gene 8 Mus musculus 19-24
1886422-4 1991 These data indicate that retinoic acid negatively regulates the expression of cytidine deaminase in HL-60 cells, and suggest that this effect is mediated by a protein, the synthesis of which should be controlled by the nuclear receptor of retinoic acid. Tretinoin 239-252 cytidine deaminase Homo sapiens 78-96
23271512-0 2013 All-trans retinoic acid and arsenic trioxide resistance of acute promyelocytic leukemia with the variant STAT5B-RARA fusion gene. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 112-116
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 0-13 alcohol dehydrogenase 7 (class IV), mu or sigma polypeptide Homo sapiens 138-159
23856557-4 2013 In P19 cells, Prdm12 is induced by Retinoic acid (RA). Tretinoin 35-48 interleukin 23 subunit alpha Homo sapiens 3-6
1846802-1 1991 The ecdysone-responsive DNA sequence of the Drosophila hsp27 gene promoter contains four direct and inverted repeats reminiscent of those that compose the vertebrate palindromic estrogen response element (ERE) and the thyroid hormone/retinoic acid response element (TRE/RRE). Tretinoin 234-247 Heat shock protein 27 Drosophila melanogaster 55-60
23856557-4 2013 In P19 cells, Prdm12 is induced by Retinoic acid (RA). Tretinoin 50-52 interleukin 23 subunit alpha Homo sapiens 3-6
23236537-1 2013 ALDH1A1 metabolizes a variety of endogenous and exogenous aldehyde, and also oxidizes retinol to synthesize retinoic acid and modulate cell differentiation. Tretinoin 108-121 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7
23801989-6 2013 Furthermore, DCs expressing CD103 in the intestine induce Foxp3(+) T-regs from Foxp3(-) CD4(+) T cells with endogenous TGF-beta and retinoic acid. Tretinoin 132-145 integrin subunit alpha E Homo sapiens 28-33
23587393-8 2013 Expression of alphaS1-casein, alphaS2-casein, and beta-casein was increased 12.9-fold, 11.9-fold, and 19.3-fold, respectively, following treatment with RA and PRL combined compared with the control group. Tretinoin 152-154 casein alpha s1 Bos taurus 14-28
1702702-1 1991 Retinoic acid (RA), an active metabolite of vitamin A, is an important mediator of cellular differentiation and has been shown to stimulate human CG (hCG) secretion by JEG-3 choriocarcinoma cells in vitro. Tretinoin 0-13 glycoprotein hormones, alpha polypeptide Homo sapiens 146-148
1702702-1 1991 Retinoic acid (RA), an active metabolite of vitamin A, is an important mediator of cellular differentiation and has been shown to stimulate human CG (hCG) secretion by JEG-3 choriocarcinoma cells in vitro. Tretinoin 0-13 glycoprotein hormones, alpha polypeptide Homo sapiens 150-153
23131127-14 2013 Moreover, we found special interest in the literature to retinoic acid-related genes (e.g. FABP5/CRABP2) that might indicate abnormalities in post-partum tissue repair mechanisms. Tretinoin 57-70 cellular retinoic acid binding protein 2 Bos taurus 97-103
23554907-2 2013 Using HL60 model human myeloid leukemia cells, where all-trans retinoic acid (RA) induces granulocytic differentiation, we developed two emergent RA-resistant HL60 cell lines which are characterized by loss of RA-inducible G1/G0 arrest, CD11b expression, inducible oxidative metabolism and p47(phox) expression. Tretinoin 146-148 pleckstrin Homo sapiens 290-293
23554907-2 2013 Using HL60 model human myeloid leukemia cells, where all-trans retinoic acid (RA) induces granulocytic differentiation, we developed two emergent RA-resistant HL60 cell lines which are characterized by loss of RA-inducible G1/G0 arrest, CD11b expression, inducible oxidative metabolism and p47(phox) expression. Tretinoin 146-148 pleckstrin Homo sapiens 290-293
1702702-1 1991 Retinoic acid (RA), an active metabolite of vitamin A, is an important mediator of cellular differentiation and has been shown to stimulate human CG (hCG) secretion by JEG-3 choriocarcinoma cells in vitro. Tretinoin 15-17 glycoprotein hormones, alpha polypeptide Homo sapiens 146-148
1702702-1 1991 Retinoic acid (RA), an active metabolite of vitamin A, is an important mediator of cellular differentiation and has been shown to stimulate human CG (hCG) secretion by JEG-3 choriocarcinoma cells in vitro. Tretinoin 15-17 glycoprotein hormones, alpha polypeptide Homo sapiens 150-153
1702702-3 1991 RA stimulated hCG and hCG-alpha secretion in a dose-dependent fashion by each of the three cell lines. Tretinoin 0-2 glycoprotein hormones, alpha polypeptide Homo sapiens 14-17
23362116-0 2013 CrbpI regulates mammary retinoic acid homeostasis and the mammary microenvironment. Tretinoin 24-37 retinol binding protein 1, cellular Mus musculus 0-5
1702702-5 1991 Cycloheximide (1 microM) abolished the effect of RA on hCG and hCG-alpha secretion in the BeWo cell line. Tretinoin 49-51 glycoprotein hormones, alpha polypeptide Homo sapiens 55-58
23362116-2 2013 CrbpI delivers vitamin A to enzymes for metabolism into an active metabolite, all-trans retinoic acid (atRA), where atRA is essential to cell proliferation, apoptosis, differentiation, and migration. Tretinoin 78-101 retinol binding protein 1, cellular Mus musculus 0-5
23362116-2 2013 CrbpI delivers vitamin A to enzymes for metabolism into an active metabolite, all-trans retinoic acid (atRA), where atRA is essential to cell proliferation, apoptosis, differentiation, and migration. Tretinoin 103-107 retinol binding protein 1, cellular Mus musculus 0-5
23505533-3 2013 The aim of this study was to evaluate the gene expression pattern of Irx1 and Irx2 as well as their regulation by important regulators of hindlimb development such as retinoic acid (RA), transforming growth factor beta (TGFbeta) and fibroblast growth factor (FGF) signaling during chick hindlimb development. Tretinoin 167-180 iroquois homeobox 1 Gallus gallus 69-73
1702702-10 1991 RA in physiologic concentrations stimulates hCG and hCG-alpha secretion by three choriocarcinoma cell lines in vitro. Tretinoin 0-2 glycoprotein hormones, alpha polypeptide Homo sapiens 44-47
23362116-2 2013 CrbpI delivers vitamin A to enzymes for metabolism into an active metabolite, all-trans retinoic acid (atRA), where atRA is essential to cell proliferation, apoptosis, differentiation, and migration. Tretinoin 116-120 retinol binding protein 1, cellular Mus musculus 0-5
23362116-4 2013 Rbp1(-/-) mouse mammary tissue has disrupted retinoid homeostasis that results in 40% depleted endogenous atRA. Tretinoin 106-110 retinol binding protein 1, cellular Mus musculus 0-4
2176152-0 1990 Negative regulation of the rat stromelysin gene promoter by retinoic acid is mediated by an AP1 binding site. Tretinoin 60-73 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-95
23362116-7 2013 Mammary subcellular fractions isolated from Rbp1(-/-) mice have altered retinol dehydrogenase/reductase (Rdh) enzyme activity that results in 24-42% less atRA production. Tretinoin 154-158 retinol binding protein 1, cellular Mus musculus 44-48
23460868-0 2013 beta-catenin is essential for efficient in vitro premyogenic mesoderm formation but can be partially compensated by retinoic acid signalling. Tretinoin 116-129 catenin beta 1 Homo sapiens 0-12
23135993-6 2013 One hundred fifty three protein spots with significantly different intensities were identified by MS. We detected alterations in the abundance of several proteins assigned to retinoic acid metabolism (e.g. retinal-binding protein 5) and the actin-cytoskeleton (e.g. vinculin and gelsolin). Tretinoin 175-188 gelsolin Gallus gallus 279-287
23799583-6 2013 TBX1 interacts with several signaling pathways, including fibroblast growth factor, retinoic acid, CTNNB1 (formerly known as beta-catenin), and bone morphogenetic protein (BMP), and may regulate pathways by both DNA-binding and non-binding activity. Tretinoin 84-97 T-box 1 Mus musculus 0-4
2176152-6 1990 We show also that RA represses the transcriptional activity of a reporter gene containing a TPA responding AP1 binding site driving the HSV tk promoter. Tretinoin 18-20 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 107-110
23322377-8 2013 We found that intestinal CD103(+) DCs that are known to produce retinoic acid highly express Arg1. Tretinoin 64-77 integrin subunit alpha E Homo sapiens 25-30
2170395-11 1990 The marked potentiation of short-term stimulation of tPA secretion in the differentiated state may be best explained by the retinoic acid-induced increase in expression of beta-adrenergic receptors coupled with a decline in Gi alpha 2 levels. Tretinoin 124-137 plasminogen activator, tissue Mus musculus 53-56
23174944-0 2012 Genetic modifier to chromatin may contribute to 22q11 deletion/VCF/DiGeorge syndrome variability: MOZ gene may also exacerbate effects of retinoic acid in genetic disorder. Tretinoin 138-151 DiGeorge syndrome chromosome region Homo sapiens 63-66
23174944-0 2012 Genetic modifier to chromatin may contribute to 22q11 deletion/VCF/DiGeorge syndrome variability: MOZ gene may also exacerbate effects of retinoic acid in genetic disorder. Tretinoin 138-151 lysine acetyltransferase 6A Homo sapiens 98-101
23053054-5 2012 The locations of the RA synthetic system (Aldh1a1, Aldh1a2, CRBP1) and catabolizing enzyme (Cyp26a1) were distinctive in the mouse uterus during the peri-implantation period. Tretinoin 21-23 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 92-99
23053054-9 2012 Taken together, these results suggest that the accumulation of RA in the stroma during mouse embryo implantation has an inhibitory effect on the expression of the three implantation-essential genes, LIF, HB-EGF and CSF-1. Tretinoin 63-65 leukemia inhibitory factor Mus musculus 199-202
23053054-9 2012 Taken together, these results suggest that the accumulation of RA in the stroma during mouse embryo implantation has an inhibitory effect on the expression of the three implantation-essential genes, LIF, HB-EGF and CSF-1. Tretinoin 63-65 heparin-binding EGF-like growth factor Mus musculus 204-210
23385081-5 2013 Conversely, activated microglia showed increased protein expression of RA-degrading cytochromes CYP26A1, CYP26B1, CYP3A4 and CYP2C. Tretinoin 71-73 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 96-103
23385081-5 2013 Conversely, activated microglia showed increased protein expression of RA-degrading cytochromes CYP26A1, CYP26B1, CYP3A4 and CYP2C. Tretinoin 71-73 cytochrome P450, family 2, subfamily c, polypeptide 29 Mus musculus 125-130
1966833-5 1990 A candidate gene involved in the regulation of endogenous RA concentrations is the gene encoding cellular RA binding protein (CRABP). Tretinoin 58-60 cellular retinoic acid binding protein 1 Homo sapiens 126-131
23352986-1 2013 All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 179-182
23352986-1 2013 All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 179-182
23352986-3 2013 Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5 muM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). Tretinoin 79-83 solute carrier organic anion transporter family member 2B1 Homo sapiens 185-234
23352986-3 2013 Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5 muM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). Tretinoin 79-83 solute carrier organic anion transporter family member 1B1 Homo sapiens 236-243
23352986-6 2013 atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARalpha and RXRalpha through siRNA transfection in HepaRG cells. Tretinoin 0-4 solute carrier organic anion transporter family member 2B1 Homo sapiens 29-36
23053054-10 2012 Therefore, the expression of Cyp26a1 in luminal and glandular epithelium might block the adverse effect of RA in order to promote successful embryo implantation. Tretinoin 107-109 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 29-36
23063977-0 2012 All-trans retinoic acid combined with 5-Aza-2"-deoxycitidine induces C/EBPalpha expression and growth inhibition in MLL-AF9-positive leukemic cells. Tretinoin 0-23 lysine methyltransferase 2A Homo sapiens 116-119
23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 43-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 222-227
23063977-1 2012 The present study tested whether all-trans retinoic acid (ATRA) and 5-Aza-2"-deoxycitidine (5-Aza) affect AML cell differentiation and growth in vitro by acting on the CCAAT/enhancer binding protein alpha (C/EBPalpha) and c-Myc axis. Tretinoin 58-62 MYC proto-oncogene, bHLH transcription factor Homo sapiens 222-227
23063977-3 2012 These findings indicate that MLL-AF9-expressing cells are more sensitive to ATRA and 5-Aza, indicating that different MLL fusion proteins possess different epigenetic properties associated with retinoic acid pathway inactivation. Tretinoin 76-80 lysine methyltransferase 2A Homo sapiens 29-32
23063977-3 2012 These findings indicate that MLL-AF9-expressing cells are more sensitive to ATRA and 5-Aza, indicating that different MLL fusion proteins possess different epigenetic properties associated with retinoic acid pathway inactivation. Tretinoin 76-80 lysine methyltransferase 2A Homo sapiens 118-121
23063977-3 2012 These findings indicate that MLL-AF9-expressing cells are more sensitive to ATRA and 5-Aza, indicating that different MLL fusion proteins possess different epigenetic properties associated with retinoic acid pathway inactivation. Tretinoin 194-207 lysine methyltransferase 2A Homo sapiens 29-32
23063977-3 2012 These findings indicate that MLL-AF9-expressing cells are more sensitive to ATRA and 5-Aza, indicating that different MLL fusion proteins possess different epigenetic properties associated with retinoic acid pathway inactivation. Tretinoin 194-207 lysine methyltransferase 2A Homo sapiens 118-121
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 112-115
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 116-120
23352986-6 2013 atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARalpha and RXRalpha through siRNA transfection in HepaRG cells. Tretinoin 0-4 solute carrier organic anion transporter family member 1B1 Homo sapiens 38-45
23352986-6 2013 atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARalpha and RXRalpha through siRNA transfection in HepaRG cells. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 146-154
23264745-5 2013 Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm"s tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARgamma(-/-) cells. Tretinoin 177-179 PBX homeobox 1 Homo sapiens 42-46
23264745-5 2013 Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm"s tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARgamma(-/-) cells. Tretinoin 177-179 PBX homeobox 1 Homo sapiens 48-78
1975088-0 1990 Sequential activation of HOX2 homeobox genes by retinoic acid in human embryonal carcinoma cells. Tretinoin 48-61 homeobox B cluster Homo sapiens 25-29
23312594-5 2013 ALDH1A3 is a key enzyme in the formation of a retinoic acid gradient along the dorso-ventral axis during early eye development. Tretinoin 46-59 aldehyde dehydrogenase 1 family member A3 Homo sapiens 0-7
23312594-6 2013 Transitory expression of mutant ALDH1A3 open reading frames showed that both missense mutations reduce the accumulation of the enzyme, potentially leading to altered retinoic acid synthesis. Tretinoin 166-179 aldehyde dehydrogenase 1 family member A3 Homo sapiens 32-39
23150428-7 2013 The increase in Cyp26a1 and Rarbeta mRNA during pregnancy indicates increased retinoic acid signaling in the liver during pregnancy. Tretinoin 78-91 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 16-23
22940758-0 2012 Granulocyte colony-stimulating factor potentiates differentiation induction by all-trans retinoic acid and arsenic trioxide and enhances arsenic uptake in the acute promyelocytic leukemia cell line HT93A. Tretinoin 101-114 colony stimulating factor 3 Homo sapiens 0-37
22940758-5 2012 G-CSF promoted differentiation-inducing activities of both ATO and ATRA. Tretinoin 67-71 colony stimulating factor 3 Homo sapiens 0-5
22940758-12 2012 G-CSF not only promotes differentiation-inducing activities of both ATRA and ATO, but also makes APL cells vulnerable to increased arsenic uptake. Tretinoin 68-72 colony stimulating factor 3 Homo sapiens 0-5
23150428-8 2013 A putative retinoic acid response element was identified within the Cyp2d40 promoter and the mRNA of Cyp2d40 correlated (P < 0.05) with Cyp26a1 and Rarbeta. Tretinoin 11-24 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 139-146
1975088-4 1990 We now show that the nine genes of the HOX2 cluster are differentially activated in NT2/D1 cells exposed to retinoic acid concentrations ranging from 10(-8) to 10(-5) M. Genes located in the 3" half of the cluster are induced at peak levels by 10(-8) M retinoic acid, whereas a concentration of 10(-6) to 10(-5) M is required to fully activate 5" genes. Tretinoin 108-121 homeobox B cluster Homo sapiens 39-43
22341854-4 2012 We have shown here that the tumour suppressor TIS21 negatively regulated c-Myc expression during all-trans-retinoic acid (ATRA)-induced differentiation that accelerated differentiation and reduced proliferation of acute promyelocytic leukaemia (APL) HL-60 cells. Tretinoin 100-120 BTG anti-proliferation factor 2 Homo sapiens 46-51
22341854-4 2012 We have shown here that the tumour suppressor TIS21 negatively regulated c-Myc expression during all-trans-retinoic acid (ATRA)-induced differentiation that accelerated differentiation and reduced proliferation of acute promyelocytic leukaemia (APL) HL-60 cells. Tretinoin 100-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 73-78
1975088-4 1990 We now show that the nine genes of the HOX2 cluster are differentially activated in NT2/D1 cells exposed to retinoic acid concentrations ranging from 10(-8) to 10(-5) M. Genes located in the 3" half of the cluster are induced at peak levels by 10(-8) M retinoic acid, whereas a concentration of 10(-6) to 10(-5) M is required to fully activate 5" genes. Tretinoin 253-266 homeobox B cluster Homo sapiens 39-43
22341854-4 2012 We have shown here that the tumour suppressor TIS21 negatively regulated c-Myc expression during all-trans-retinoic acid (ATRA)-induced differentiation that accelerated differentiation and reduced proliferation of acute promyelocytic leukaemia (APL) HL-60 cells. Tretinoin 122-126 BTG anti-proliferation factor 2 Homo sapiens 46-51
22341854-4 2012 We have shown here that the tumour suppressor TIS21 negatively regulated c-Myc expression during all-trans-retinoic acid (ATRA)-induced differentiation that accelerated differentiation and reduced proliferation of acute promyelocytic leukaemia (APL) HL-60 cells. Tretinoin 122-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 73-78
23243061-0 2013 Bortezomib sensitizes human acute myeloid leukemia cells to all-trans-retinoic acid-induced differentiation by modifying the RARalpha/STAT1 axis. Tretinoin 70-83 retinoic acid receptor alpha Homo sapiens 125-133
23243061-1 2013 All-trans-retinoic acid (ATRA) has held great promise for differentiation-based therapy but reportedly downregulates retinoic acid receptor-alpha (RARalpha) in a proteasome-dependent manner, which leads to decreased acute myeloid leukemia (AML) cell differentiation efficiency. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 117-145
22341854-5 2012 TIS21 downregulated c-Myc mRNA and additionally decreased c-Myc protein stability by increasing its phosphorylation at S(62) and T(58) residues via activation of Erk1/2 and inhibition of PI3K/Akt along with the subsequent activation of GSK-3beta in response to ATRA treatment. Tretinoin 261-265 BTG anti-proliferation factor 2 Homo sapiens 0-5
23243061-1 2013 All-trans-retinoic acid (ATRA) has held great promise for differentiation-based therapy but reportedly downregulates retinoic acid receptor-alpha (RARalpha) in a proteasome-dependent manner, which leads to decreased acute myeloid leukemia (AML) cell differentiation efficiency. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 147-155
1975088-5 1990 At both high and low retinoic acid concentrations, HOX2 genes are sequentially activated in embryonal carcinoma cells in the 3" to 5" direction. Tretinoin 21-34 homeobox B cluster Homo sapiens 51-55
23243061-1 2013 All-trans-retinoic acid (ATRA) has held great promise for differentiation-based therapy but reportedly downregulates retinoic acid receptor-alpha (RARalpha) in a proteasome-dependent manner, which leads to decreased acute myeloid leukemia (AML) cell differentiation efficiency. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 117-145
2166951-4 1990 We also show that CRABP-II mRNA levels are induced by at least 50-fold upon treatment of F9 teratocarcinoma cells with retinoic acid. Tretinoin 119-132 cellular retinoic acid binding protein II Mus musculus 18-26
23159843-2 2013 Rapid detection of the PML-RARA fusion gene provides the molecular basis for a highly effective therapy with all-trans retinoic acid. Tretinoin 119-132 PML nuclear body scaffold Homo sapiens 23-26
23159843-2 2013 Rapid detection of the PML-RARA fusion gene provides the molecular basis for a highly effective therapy with all-trans retinoic acid. Tretinoin 119-132 retinoic acid receptor alpha Homo sapiens 27-31
22531980-7 2012 ATRA treatment significantly up-regulated leptin receptor (LEPR) expression in the livers of NAFLD mice. Tretinoin 0-4 leptin receptor Mus musculus 42-57
22531980-7 2012 ATRA treatment significantly up-regulated leptin receptor (LEPR) expression in the livers of NAFLD mice. Tretinoin 0-4 leptin receptor Mus musculus 59-63
22531980-8 2012 In agreement with these observations, in vitro experiments showed that in the presence of leptin, ATRA directly induced LEPR gene expression through RARalpha, resulting in enhancement of STAT3 and insulin-induced insulin receptor substrate 1 phosphorylation. Tretinoin 98-102 leptin receptor Mus musculus 120-124
2163611-8 1990 Using PAGE/radiobinding assay, we demonstrated that retinoic acid formed from retinol was bound in differentiating keratinocytes to endogenous cellular retinoic acid-binding protein (CRABP). Tretinoin 52-65 cellular retinoic acid binding protein 1 Homo sapiens 143-181
22963770-2 2012 GDF3 expression was affected by shRNA-mediated downregulation and by exogenous overexpression of NANOG specifically, as well as by retinoic acid-mediated differentiation. Tretinoin 131-144 growth differentiation factor 3 Homo sapiens 0-4
23014973-8 2013 In view of these findings, RA likely stimulates osteoblast differentiation through the BMP2-Smad-Runx2/Msx2 pathway. Tretinoin 27-29 runt related transcription factor 2 Mus musculus 97-102
23014973-9 2013 In contrast, RA markedly inhibited BMP2-induced adipocyte differentiation, suppressing expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), CCAAT/enhancer-binding protein (C/EBP)alpha and C/EBPdelta, and inhibiting adipogenic function of C/EBPbeta, C/EBPdelta, and PPARgamma. Tretinoin 13-15 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 261-270
2163611-8 1990 Using PAGE/radiobinding assay, we demonstrated that retinoic acid formed from retinol was bound in differentiating keratinocytes to endogenous cellular retinoic acid-binding protein (CRABP). Tretinoin 52-65 cellular retinoic acid binding protein 1 Homo sapiens 183-188
23533658-9 2013 Finally, we show that impedance profiles of substance-induced NT2 cells and those triggered to differentiate by depletion of the stem cell factor OCT4 are very similar, suggesting that reduction of OCT4 levels has a dominant function for differentiation induced by nucleoside drugs and retinoic acid. Tretinoin 286-299 POU class 5 homeobox 1 Homo sapiens 198-202
22815530-7 2012 Consistent with an established antagonistic relationship between AP1 expression and retinoic acid receptor activity, increased differentiation was seen in the DNMT3B7-expressing neuroblastoma cells following treatment with all-trans retinoic acid (ATRA) compared to controls. Tretinoin 248-252 DNA methyltransferase 3 beta Homo sapiens 159-165
2142376-8 1990 Preincubation of cells with IL-1, retinoic acid, transforming growth factor beta (TGF-beta), or phorbol ester caused a reduction in apparent receptor numbers per cell, while preincubation with epidermal growth factor (EGF), dexamethasone, or parathyroid hormone (PTH) increased receptor numbers per cell. Tretinoin 34-47 parathyroid hormone Mus musculus 242-261
22826214-5 2012 Treatment with 1 muM retinoic acid for 24 hr inhibited feather-bud formation and induced the transdifferentiation of the epidermis to a mucosal epithelium with a concomitant increase in Gbx1 mRNA expression in the epithelium. Tretinoin 21-34 gastrulation brain homeobox 1 Gallus gallus 186-190
22826214-7 2012 CONCLUSIONS: These results indicate that Gbx1 was involved in the feather-bud formation and was one of target genes of retinoic acid and that other signals in addition to Gbx1 were required for epidermal mucous transdifferentiation. Tretinoin 119-132 gastrulation brain homeobox 1 Gallus gallus 41-45
23460868-5 2013 The loss of beta-catenin resulted in a reduction of skeletal myogenesis in the absence of RA as early as premyogenic mesoderm, with the loss of Pax3/7, Eya2, Six1, Meox1, Gli2, Foxc1/2, and Sox7 transcript levels. Tretinoin 90-92 catenin beta 1 Homo sapiens 12-24
23460868-10 2013 RA can at least partially compensate for the loss of beta-catenin in the expression of many myogenic precursor genes, but not for myoblast gene expression or overall myogenesis. Tretinoin 0-2 catenin beta 1 Homo sapiens 53-65
23155234-1 2012 A deficient retinoic acid signaling has been suggested to be an important cause of the clinical inefficacy of all-trans retinoic acid (ATRA) therapy in non-promyelocytic (non-PML) forms of acute myeloid leukemia (AML). Tretinoin 12-25 PML nuclear body scaffold Homo sapiens 175-178
2142376-8 1990 Preincubation of cells with IL-1, retinoic acid, transforming growth factor beta (TGF-beta), or phorbol ester caused a reduction in apparent receptor numbers per cell, while preincubation with epidermal growth factor (EGF), dexamethasone, or parathyroid hormone (PTH) increased receptor numbers per cell. Tretinoin 34-47 parathyroid hormone Mus musculus 263-266
2158037-5 1990 Three growth factors were markedly down-regulated following RA treatment: Hst-1/kFGF and TGF-alpha expression became undetectable by Northern analysis and bFGF expression was substantially reduced. Tretinoin 60-62 transforming growth factor alpha Homo sapiens 89-98
2110861-3 1990 RA treatment dramatically increased the incorporation of the labeled monosaccharides into one glycoprotein of Mr 160,000 (gp160), which has been previously implicated in the growth-inhibitory effect of RA on these cells. Tretinoin 202-204 leucyl/cystinyl aminopeptidase Mus musculus 122-127
22845560-8 2012 This work provides novel experimental evidence of the beneficial role of the DNMT inhibitor RG108 in combinations with RA and HDACIs in the effective differentiation of human PML based on epigenetics. Tretinoin 119-121 PML nuclear body scaffold Homo sapiens 175-178
22766505-0 2012 PI3K/AKT and ERK regulate retinoic acid-induced neuroblastoma cellular differentiation. Tretinoin 26-39 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 0-8
22766505-6 2012 The protein levels of cyclin-dependent kinase inhibitors, p21 and p27(Kip), which inhibit cell proliferation by blocking cell cycle progression at G1/S phase, increased after RA treatment. Tretinoin 175-177 H3 histone pseudogene 16 Homo sapiens 58-61
2110861-4 1990 Following RA treatment, cell-surface sialic acid residues on gp160 were also more intensely labeled by NaIO4 oxidation and subsequent NaB[3H]4 reduction than were those on gp160 of untreated cells. Tretinoin 10-12 leucyl/cystinyl aminopeptidase Mus musculus 61-66
22548360-4 2012 The results show that RA significantly promoted PGC proliferation in a dose- and time-dependent manner, confirmed by BrdU (bromodeoxyuridine) incorporation and cell cycle analysis. Tretinoin 22-24 progastricsin Gallus gallus 48-51
1980557-5 1990 These effects were preceded by a uniform enhancement of c-raf mRNA expression, which became evident 6 h after exposure to RA, NaBut and FCS-depleted media. Tretinoin 122-124 Raf-1 proto-oncogene, serine/threonine kinase Rattus norvegicus 56-61
22696440-5 2012 Interestingly, Foxp3(+) regulatory T cells were markedly increased and IL-17-producing CD4(+) T cells (Th17 cells) were decreased in the spleens of ATRA-treated mice. Tretinoin 148-152 forkhead box P3 Mus musculus 15-20
22378018-5 2012 We found that ATRA was able to enhance the surface expression of AnxA1 and its receptor (FPR2/ALX) and the release of AnxA1-containing MPs from ATRA-NB4 cells, while the expression of annexin V was not elevated on the latter cells. Tretinoin 14-18 formyl peptide receptor 2 Homo sapiens 89-93
22378018-5 2012 We found that ATRA was able to enhance the surface expression of AnxA1 and its receptor (FPR2/ALX) and the release of AnxA1-containing MPs from ATRA-NB4 cells, while the expression of annexin V was not elevated on the latter cells. Tretinoin 14-18 annexin A5 Homo sapiens 184-193
23000165-2 2012 LRH-1 and OCT4 are co-expressed in undifferentiated NCCIT cells and decreased during retinoic acid-induced differentiation. Tretinoin 85-98 POU class 5 homeobox 1 Homo sapiens 10-14
22621815-0 2012 Prenatal retinoic acid improves lung vascularization and VEGF expression in CDH rat. Tretinoin 9-22 vascular endothelial growth factor A Rattus norvegicus 57-61
1980557-6 1990 C-raf mRNA expression persisted at an elevated level throughout the observation period of 5 days after exposure to RA or NaBut, whereas the increased expression of c-raf mRNA observed after FCS-depletion declined near to the basal level after only 24 h. Furthermore, a transient c-fos mRNA expression was observed 15 and 30 min after exposure to RA-supplemented and FCS-depleted medium but not after exposure to NaBut. Tretinoin 115-117 Raf-1 proto-oncogene, serine/threonine kinase Rattus norvegicus 0-5
22621815-9 2012 ATRA recovered expression of VEGF and receptors, which were reduced in CDH. Tretinoin 0-4 vascular endothelial growth factor A Rattus norvegicus 29-33
1980557-8 1990 Since all our experiments with RA, NaBut and FCS-depletion resulted in an early peak of c-raf mRNA expression, it is suggested that this early peak may be sufficient to trigger events crucial for differentiation and proliferation of BA-HAN-1C tumor cells. Tretinoin 31-33 Raf-1 proto-oncogene, serine/threonine kinase Rattus norvegicus 88-93
22902413-3 2012 Conditional disruption of RA signaling in CD8(+) T cells using a dominant negative retinoic acid receptor alpha (dnRARalpha) established that RA signaling is required for tumor-specific CD8(+) T-cell expansion/accumulation and protective antitumor immunity. Tretinoin 26-28 retinoic acid receptor alpha Homo sapiens 83-111
7527354-0 1994 Differential effects of topical retinoic acid application on keratin K1 and filaggrin expression in mouse epidermis. Tretinoin 32-45 filaggrin Mus musculus 76-85
22982681-2 2012 RA responses are mediated by transcriptional activation by the retinoic acid receptor (RAR) and retinoid X receptor (RXR) in cooperation with various types of coregulators at RA-responsive gene promoters. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 87-90
22982681-6 2012 Finally, depletion of CAC1 increases RA-induced neuronal differentiation of P19 cells, a response accompanied by significant upregulation of the neuronal marker nestin. Tretinoin 37-39 CDK2 associated cullin domain 1 Homo sapiens 22-26
22675213-4 2012 We further show that Bmp signalling acts in parallel with retinoic acid signalling, possibly by inhibiting the known limb-inducing gene wnt2ba. Tretinoin 58-71 wingless-type MMTV integration site family, member 2Ba Danio rerio 136-142
22407764-5 2012 Further, our data suggest an antagonistic functional connection between BRG1 and MYC, whereby, refractoriness to RA and GC by BRG1 inactivation involves deregulation of MYC activity. Tretinoin 113-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 81-84
22407764-5 2012 Further, our data suggest an antagonistic functional connection between BRG1 and MYC, whereby, refractoriness to RA and GC by BRG1 inactivation involves deregulation of MYC activity. Tretinoin 113-115 MYC proto-oncogene, bHLH transcription factor Homo sapiens 169-172
22945948-14 2012 Because RBP1 is involved in retinoic acid synthesis, our results suggest that dysregulation of retinoic acid metabolism may contribute to glioma formation along the IDH1/IDH2-mutant pathway. Tretinoin 95-108 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 165-169
7527354-1 1994 Retinoic acid (RA) modulates epidermal homeostasis and affects differentiation-associated proteins such as keratin K1 and filaggrin. Tretinoin 0-13 filaggrin Mus musculus 122-131
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 0-23 interferon induced with helicase C domain 1 Homo sapiens 132-136
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 0-23 interferon induced with helicase C domain 1 Homo sapiens 178-182
22585464-2 2012 Although RA promotes natural killer T (NKT) cell activation in vitro by increasing CD1d expression on antigen-presenting cells (APCs), the direct effects of RA on NKT-cell responses in vivo are not known. Tretinoin 9-11 CD1d molecule Homo sapiens 83-87
22585464-8 2012 The regulatory effect of RA on NKT cells was mediated by RAR-alpha, and RA reduced the phosphorylation of MAPK. Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 57-66
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 25-29 interferon induced with helicase C domain 1 Homo sapiens 132-136
7527354-1 1994 Retinoic acid (RA) modulates epidermal homeostasis and affects differentiation-associated proteins such as keratin K1 and filaggrin. Tretinoin 15-17 filaggrin Mus musculus 122-131
22797253-2 2012 All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. Tretinoin 25-29 interferon induced with helicase C domain 1 Homo sapiens 178-182
34365653-0 2022 The bile acid-activated retinoic acid response in dendritic cells is involved in food allergen sensitization. Tretinoin 24-37 glucosidase beta 2 Mus musculus 4-13
22797253-6 2012 In conclusion, consecutive treatment with ATRA and polyI:C results in strong, TLR3/MDA5-mediated chemokine and IFN responses in cultured human melanoma cells, which triggers a functional migratory response in professional antigen-presenting cells. Tretinoin 42-46 interferon induced with helicase C domain 1 Homo sapiens 83-87
22921202-4 2012 Importantly, DiGeorge syndrome-like anomalies are present in mice with homozygous mutation of Moz and in heterozygous Moz mutants when combined with Tbx1 haploinsufficiency or oversupply of retinoic acid. Tretinoin 190-203 K(lysine) acetyltransferase 6A Mus musculus 118-121
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 78-91 C-C motif chemokine ligand 3 Homo sapiens 127-131
22533963-3 2012 In retinoic acid-treated human SH-SY5Y neuroblastoma cells and mouse primary cortical neurons, long-term exposure to IFNs curtailed BDNF-induced activation of phosphatidylinositol 3-kinase, phospholipase Cgamma and extracellular-regulated kinases 1 and 2 signaling. Tretinoin 3-16 brain derived neurotrophic factor Mus musculus 132-136
22659417-4 2012 In addition, LMP1 suppressed ATRA-mediated activation of Caspase 9, Caspase 3, and PARP but not Caspase 8 in Ad-AH cells, suggesting that LMP1 acts by blocking the activation of intrinsic apoptosis pathway by ATRA. Tretinoin 29-33 caspase 9 Homo sapiens 57-66
22496486-0 2012 Transcriptional regulation of neutral sphingomyelinase 2 in all-trans retinoic acid-treated human breast cancer cell line, MCF-7. Tretinoin 70-83 sphingomyelin phosphodiesterase 3 Homo sapiens 30-56
22496486-2 2012 Increased NSMase activity, NSMase2 mRNA and protein were observed in ATRA-treated MCF-7 but not in ATRA-treated MDA-MB-231. Tretinoin 69-73 sphingomyelin phosphodiesterase 3 Homo sapiens 27-34
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 78-91 C-C motif chemokine ligand 4 Homo sapiens 136-140
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 93-97 C-C motif chemokine ligand 3 Homo sapiens 127-131
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 93-97 C-C motif chemokine ligand 4 Homo sapiens 136-140
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 228-232 C-C motif chemokine ligand 3 Homo sapiens 127-131
22356114-8 2012 We also demonstrate that the potent enhancing effects of statins on all-trans retinoic acid (ATRA)-induced gene expression for CCL3 and CCL4 requires the function of PKCdelta, suggesting a mechanism by which statins may promote ATRA-induced antileukemic responses. Tretinoin 228-232 C-C motif chemokine ligand 4 Homo sapiens 136-140
34921867-6 2022 KEY FINDINGS: We report that the progression of APL and the attenuation of APL sensitivity to ATRA are positively associated with Skp2. Tretinoin 94-98 S-phase kinase associated protein 2 Homo sapiens 130-134
23071480-7 2012 The variant APL with t(11;17)(q23;q21) cases that are associated with the ZBTB16/RARA fusion gene have been reported as being resistant to all-trans-retinoic acid (ATRA). Tretinoin 142-162 retinoic acid receptor alpha Homo sapiens 81-85
23071480-7 2012 The variant APL with t(11;17)(q23;q21) cases that are associated with the ZBTB16/RARA fusion gene have been reported as being resistant to all-trans-retinoic acid (ATRA). Tretinoin 164-168 retinoic acid receptor alpha Homo sapiens 81-85
22653585-7 2012 After 21 days of induction by retinoic acid, expression of neural markers (neuroD1 and synaptophysin) was higher in induced cell clones than in induced parental cells. Tretinoin 30-43 neuronal differentiation 1 Homo sapiens 76-83
22248258-7 2012 A low level of Lin28 was expressed in EBs treated with atRA for 2 days or 5 days. Tretinoin 55-59 lin-28 homolog A Mus musculus 15-20
22687751-0 2012 Pod1/Tcf21 is regulated by retinoic acid signaling and inhibits differentiation of epicardium-derived cells into smooth muscle in the developing heart. Tretinoin 27-40 transcription factor 21 Mus musculus 5-10
34921867-8 2022 Coupled with ATRA or GSK3beta inhibitor treatment, genetic or pharmacological inhibition of Skp2 strikingly induces JunB expression by accelerating the degradation of PML-RARalpha, which contributes to the eradication of APL. Tretinoin 13-17 S-phase kinase associated protein 2 Homo sapiens 92-96
34944824-5 2021 Somewhat unexpectedly, TGFbeta treatment resulted in an increase in intracellular levels of retinoic acid (RA) that in turn resulted in increased levels of extracellular matrix (ECM) proteins including fibronectin (FN) and collagen (COL1). Tretinoin 92-105 transforming growth factor alpha Homo sapiens 23-30
22739370-0 2012 Oral vitamin A and retinoic acid supplementation stimulates antibody production and splenic Stra6 expression in tetanus toxoid-immunized mice. Tretinoin 19-32 stimulated by retinoic acid gene 6 Mus musculus 92-97
34784434-9 2021 These data suggest that RA metabolism is decreased in asthmatic lung and that enhancing RAR signaling using ATRA or RARgamma agonists may mitigate airway remodeling associated with asthma. Tretinoin 24-26 retinoic acid receptor gamma Homo sapiens 88-91
22739370-10 2012 In conclusion, retinoid treatments that included VA, RA, VA and RA combined, and the combination of retinoid and PIC stimulated the expression of Stra6 in spleen, which potentially could increase the local uptake of retinol. Tretinoin 53-55 stimulated by retinoic acid gene 6 Mus musculus 146-151
22696440-6 2012 In vitro treatment with ATRA induced the expression of Foxp3 and repressed the IL-17 expression in the CD4(+) T cells in mice. Tretinoin 24-28 forkhead box P3 Mus musculus 55-60
34784434-9 2021 These data suggest that RA metabolism is decreased in asthmatic lung and that enhancing RAR signaling using ATRA or RARgamma agonists may mitigate airway remodeling associated with asthma. Tretinoin 24-26 retinoic acid receptor gamma Homo sapiens 116-124
22696440-7 2012 ATRA suppressed the production of total IgG and IgG2a in splenocytes that were stimulated by LPS. Tretinoin 0-4 immunoglobulin heavy variable V1-9 Mus musculus 48-53
34784434-9 2021 These data suggest that RA metabolism is decreased in asthmatic lung and that enhancing RAR signaling using ATRA or RARgamma agonists may mitigate airway remodeling associated with asthma. Tretinoin 108-112 retinoic acid receptor gamma Homo sapiens 88-91
34829934-8 2021 While ATO + ATRA had significant biological activity in NPM1c IMS-M2 cell line, those cells were resistant to BETi. Tretinoin 12-16 nucleophosmin 1 Homo sapiens 56-60
22056876-6 2012 This rapid RA-induced formation of RARalpha/Galphaq complexes in lipid rafts is required for the activation of p38MAPK that occurs in response to RA. Tretinoin 11-13 retinoic acid receptor alpha Homo sapiens 35-43
22056876-6 2012 This rapid RA-induced formation of RARalpha/Galphaq complexes in lipid rafts is required for the activation of p38MAPK that occurs in response to RA. Tretinoin 11-13 G protein subunit alpha q Homo sapiens 44-51
22056876-6 2012 This rapid RA-induced formation of RARalpha/Galphaq complexes in lipid rafts is required for the activation of p38MAPK that occurs in response to RA. Tretinoin 35-37 G protein subunit alpha q Homo sapiens 44-51
34829934-10 2021 ATO + ATRA downregulated a NPM1c specific HOX gene signature while anti-leukemic effects of BETi appear HOX gene independent. Tretinoin 6-10 nucleophosmin 1 Homo sapiens 27-31
34831243-5 2021 We show that primary liver cells sense RNA through retinoic acid-inducible gene I (RIG-I) like receptor (RLR) and Toll-like receptor 3 (TLR3) pathways. Tretinoin 51-64 toll like receptor 3 Homo sapiens 114-134
22568433-6 2012 Retinoic acid-induced differentiation of human precursor NT2 cells into dopaminergic cells increased expression of TH, NURR1, D2 R and SRY. Tretinoin 0-13 sex determining region Y Homo sapiens 135-138
34831243-5 2021 We show that primary liver cells sense RNA through retinoic acid-inducible gene I (RIG-I) like receptor (RLR) and Toll-like receptor 3 (TLR3) pathways. Tretinoin 51-64 toll like receptor 3 Homo sapiens 136-140
22472775-4 2012 The tolerogenic features of these subsets are associated with increased production of retinoic acid, which leads to the enhanced induction of Foxp3+ regulatory T cells compared with CD8alpha-beta- pDCs. Tretinoin 86-99 forkhead box P3 Mus musculus 142-147
22451680-0 2012 Role of down-regulated neutral ceramidase during all-trans retinoic acid-induced neuronal differentiation in SH-SY5Y neuroblastoma cells. Tretinoin 59-72 N-acylsphingosine amidohydrolase 2 Homo sapiens 23-41
22451680-4 2012 In this study, we observed that ATRA-induced cellular ceramide accumulation, cell-growth arrest and differentiation accompanied with down-regulation of NCDase in SH-SY5Y cells, without a decrease in sphingosine or sphingosine 1-phosphate. Tretinoin 32-36 N-acylsphingosine amidohydrolase 2 Homo sapiens 152-158
34957453-5 2021 Retinoic acid receptor (RAR) antagonist also tested to identify the effect of ATRA on PPARgamma -RAR related gene expression in IM cells. Tretinoin 78-82 peroxisome proliferator activated receptor gamma Bos taurus 86-95
22451680-7 2012 Interestingly, GATA-2 was also decreased with ATRA treatment, and experiments using its expression vector and siRNA and chromatin immunoprecipitation assay demonstrated GATA-2 acted as transcription-factor of NCDase gene expression. Tretinoin 46-50 N-acylsphingosine amidohydrolase 2 Homo sapiens 209-215
22451680-8 2012 By establishing stable transfectants with decreased NCDase expression and activity, we clarified the significance of NCDase down-regulation for ATRA-induced neuronal differentiation. Tretinoin 144-148 N-acylsphingosine amidohydrolase 2 Homo sapiens 52-58
22451680-8 2012 By establishing stable transfectants with decreased NCDase expression and activity, we clarified the significance of NCDase down-regulation for ATRA-induced neuronal differentiation. Tretinoin 144-148 N-acylsphingosine amidohydrolase 2 Homo sapiens 117-123
22451137-4 2012 In a secondary pathway, BCO2 cleaves beta-carotene into retinoic acid, the most potent form of vitamin A. Tretinoin 56-69 beta-carotene oxygenase 2 Bos taurus 24-28
34957453-6 2021 The addition of ATRA to bovine IM decreased (p < 0.05) expression of PPARgamma. Tretinoin 16-20 peroxisome proliferator activated receptor gamma Bos taurus 69-78
21735106-7 2012 Furthermore, we found that RA treatment expanded the muscle progenitor pool, which occurred as a distinct Pax3(+ve) population prior to MRF expression. Tretinoin 27-29 myelin regulatory factor Homo sapiens 136-139
34957453-7 2021 The expression of PPARgamma was also tended to be downregulated (p < 0.1) in high levels (10 muM) of ATRA treatment in SC cells. Tretinoin 101-105 peroxisome proliferator activated receptor gamma Bos taurus 18-27
22339500-7 2012 Treatment with RA (retinoic acid) triggers NCCIT cell differentiation, reducing NANOG and OCT4 expression and up-regulating several neural markers [i.e. ASCL1 (achaete-scute complex homologue 1), NEUROD1 (neuronal differentiation 1) and PAX6 (paired box 6)]. Tretinoin 19-32 POU class 5 homeobox 1 Homo sapiens 90-94
22339500-7 2012 Treatment with RA (retinoic acid) triggers NCCIT cell differentiation, reducing NANOG and OCT4 expression and up-regulating several neural markers [i.e. ASCL1 (achaete-scute complex homologue 1), NEUROD1 (neuronal differentiation 1) and PAX6 (paired box 6)]. Tretinoin 19-32 neuronal differentiation 1 Homo sapiens 196-203
34957453-10 2021 Increasing levels of ATRA may block adipogenic differentiation via transcriptional regulation of PPARgamma. Tretinoin 21-25 peroxisome proliferator activated receptor gamma Bos taurus 97-106
34390859-1 2021 OBJECTIVE: The nuclear receptor corepressor 1 (NCOR1) and the silencing mediator of retinoic acid and thyroid hormone (SMRT, also known as NCOR2) play critical and specific roles in nuclear receptor action. Tretinoin 84-97 nuclear receptor co-repressor 1 Mus musculus 15-45
22969967-10 2012 Together, IFN-gamma augments the proliferation inhibition effect of ATRA on NB4 and NB4-R1 cells through enhancing the expression of PML protein. Tretinoin 68-72 PML nuclear body scaffold Homo sapiens 133-136
34390859-1 2021 OBJECTIVE: The nuclear receptor corepressor 1 (NCOR1) and the silencing mediator of retinoic acid and thyroid hormone (SMRT, also known as NCOR2) play critical and specific roles in nuclear receptor action. Tretinoin 84-97 nuclear receptor co-repressor 1 Mus musculus 47-52
34623260-5 2021 Ablation of RA signaling through deletion of the Aldh1a1/a2/a3 genes encoding RA-synthesizing enzymes leads to increased cardiomyocyte apoptosis in adults subjected to MI. Tretinoin 12-14 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 49-56
22307745-8 2012 This may in part be due to differences in the expression of Fas ligand, which we found to be upregulated by retinoic acid, but not dehydroretinoic acid. Tretinoin 108-121 Fas ligand Homo sapiens 60-70
34623260-5 2021 Ablation of RA signaling through deletion of the Aldh1a1/a2/a3 genes encoding RA-synthesizing enzymes leads to increased cardiomyocyte apoptosis in adults subjected to MI. Tretinoin 78-80 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 49-56
22544395-0 2012 TGF-beta and retinoic acid induce the microRNA miR-10a, which targets Bcl-6 and constrains the plasticity of helper T cells. Tretinoin 13-26 microRNA 10a Homo sapiens 47-54
22544395-4 2012 Here we report that naturally occurring regulatory T cells (T(reg) cells) had high expression of the microRNA miR-10a and that miR-10a was induced by retinoic acid and transforming growth factor-beta (TGF-beta) in inducible T(reg) cells. Tretinoin 150-163 microRNA 10a Homo sapiens 127-134
34480899-9 2021 The kcat/Km value for holo-CRABP-1, however, decreased ~65-fold in comparison with reactions with free all-trans retinoic acid. Tretinoin 113-126 cellular retinoic acid binding protein 1 Homo sapiens 27-34
22537161-0 2012 Nicotine, IFN-gamma and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades. Tretinoin 24-37 E2F transcription factor 1 Homo sapiens 95-99
22306363-2 2012 Here we investigated the role of COXs (cyclooxygenases) in these effects and we found that, i) ATRA increased the expression of COX-1 and COX-2 mRNA and protein and the intracellular levels (but not the extracellular ones) of PGE(2). Tretinoin 95-99 mitochondrially encoded cytochrome c oxidase I Homo sapiens 128-133
22306363-5 2012 These results indicated that COX activity is critical for ATRA-induced HIF-1alpha up-regulation and suggested that intracellular PGE(2) could mediate the effects of ATRA; ii) Treatment with PGE(2) analog 16,16-dimethyl-PGE(2) resulted in up-regulation of HIF-1alpha and antagonists of EP1-4 receptors inhibited 16,16-dimethyl-PGE(2)- and ATRA-induced HIF-1alpha up-regulation. Tretinoin 58-62 prostaglandin E receptor 1 Homo sapiens 285-290
34087410-0 2021 Calcitriol and Retinoic acid antagonize each other to suppress the production of IL-9 by Th9 cells. Tretinoin 15-28 interleukin 9 Homo sapiens 81-85
22248690-0 2012 Regulation of neurogenesis and gliogenesis of retinoic acid-induced P19 embryonal carcinoma cells by P2X2 and P2X7 receptors studied by RNA interference. Tretinoin 46-59 purinergic receptor P2X 2 Homo sapiens 101-105
22248690-3 2012 Wild-type P19 embryonal carcinoma cells or cells stably expressing shRNAs targeting P2X2 or P2X7 receptor expression were induced to differentiate into neurons and glial cells in the presence of retinoic acid. Tretinoin 195-208 purinergic receptor P2X 2 Homo sapiens 84-88
34087410-6 2021 While the recruitment of PU.1 was significantly impaired to the Il9 gene in the presence of calcitriol or retinoic acid in Th9 cells, addition of both vitamins together increased the recruitment of PU.1 to the Il9 gene. Tretinoin 106-119 interleukin 9 Homo sapiens 64-67
34087410-7 2021 Calcitriol and retinoic acid together impaired the recruitment of HDAC1 to the Il9 gene without impacting Gcn5 recruitment. Tretinoin 15-28 interleukin 9 Homo sapiens 79-82
34087410-8 2021 Importantly, retinoic acid negated the effect of calcitriol and impaired the binding of VDR on the Il9 gene by dampened VDR-RXR formation. Tretinoin 13-26 interleukin 9 Homo sapiens 99-102
22167418-6 2012 ATRA-loaded NLC had an average size of less than 200 nm (141.80 to 172.95 nm) with a narrow PDI and negative zeta potential that was within an acceptable range for intravenous injection. Tretinoin 0-4 peptidyl arginine deiminase 1 Homo sapiens 92-95
34572134-9 2021 We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Tretinoin 55-68 matrix metallopeptidase 2 Homo sapiens 116-121
22134223-9 2012 Also in the MLNs are CD103+ dendritic cells, which drive the differentiation of Foxp3+ T cells in the presence of TGF-beta and retinoic acid produced from dietary vitamin A. Tretinoin 127-140 forkhead box P3 Mus musculus 80-85
34572134-9 2021 We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Tretinoin 70-72 matrix metallopeptidase 2 Homo sapiens 116-121
34536327-0 2022 Anterior patterning genes induced by Zic1 are sensitive to retinoic acid and its metabolite, 4-oxo-RA. Tretinoin 59-72 Zic family member 1 S homeolog Xenopus laevis 37-41
22275070-0 2012 Identification of putative retinoic acid target genes downstream of mesenchymal Tbx1 during inner ear development. Tretinoin 27-40 T-box 1 Mus musculus 80-84
22275070-3 2012 We have previously reported that mesodermal Tbx1 loss of function mutants (Mest-KO) have reduced expression of retinoic acid (RA) metabolic genes, Cyp26a1 and Cyp26c1, in the POM, consistent with other studies showing an increase in mesodermal RA reporter expression in Tbx1-/- embryos. Tretinoin 111-124 T-box 1 Mus musculus 44-48
22275070-3 2012 We have previously reported that mesodermal Tbx1 loss of function mutants (Mest-KO) have reduced expression of retinoic acid (RA) metabolic genes, Cyp26a1 and Cyp26c1, in the POM, consistent with other studies showing an increase in mesodermal RA reporter expression in Tbx1-/- embryos. Tretinoin 126-128 T-box 1 Mus musculus 44-48
22275070-3 2012 We have previously reported that mesodermal Tbx1 loss of function mutants (Mest-KO) have reduced expression of retinoic acid (RA) metabolic genes, Cyp26a1 and Cyp26c1, in the POM, consistent with other studies showing an increase in mesodermal RA reporter expression in Tbx1-/- embryos. Tretinoin 244-246 T-box 1 Mus musculus 44-48
34536327-4 2022 RESULTS: In this study, we have analyzed a number of Zic1 targets for their expression during PPR patterning, as well as their regulation by retinoic acid (RA) and one of its major metabolites, 4-oxo-RA. Tretinoin 141-154 Zic family member 1 S homeolog Xenopus laevis 53-57
22284617-6 2012 Accordingly, such studies were used in selecting the optimal dose for RA using PVC and PIC to islet-1 and oligo-2. Tretinoin 70-72 ISL LIM homeobox 1 Homo sapiens 94-101
34536327-4 2022 RESULTS: In this study, we have analyzed a number of Zic1 targets for their expression during PPR patterning, as well as their regulation by retinoic acid (RA) and one of its major metabolites, 4-oxo-RA. Tretinoin 156-158 Zic family member 1 S homeolog Xenopus laevis 53-57
34292881-4 2021 Reduction in RA signaling activity severely affects the ability of the uterus to achieve receptive status and decidualize, partially through dampening follistatin expression and downstream activin B/BMP2 signaling. Tretinoin 13-15 bone morphogenetic protein 2 Homo sapiens 199-203
22293198-0 2012 Retinoic acid regulates germ cell differentiation in mouse embryonic stem cells through a Smad-dependent pathway. Tretinoin 0-13 SMAD family member 1 Mus musculus 90-94
22293198-4 2012 In this study, we determined if RA induced ESC differentiation to the germ lineage through modulation of the (bone morphogenetic protein) BMP/Smad pathway activity. Tretinoin 32-34 SMAD family member 1 Mus musculus 142-146
22293198-5 2012 In a monolayer culture, RA significantly induced both the expression of the early germ-specific genes, Stra8, Dazl and Mvh, and prolonged activation of Smad1/5 (for at least 24h). Tretinoin 24-26 stimulated by retinoic acid gene 8 Mus musculus 103-108
22293198-5 2012 In a monolayer culture, RA significantly induced both the expression of the early germ-specific genes, Stra8, Dazl and Mvh, and prolonged activation of Smad1/5 (for at least 24h). Tretinoin 24-26 SMAD family member 1 Mus musculus 152-159
22293198-7 2012 Moreover, RA-induced germ-specific gene expression was significantly increased by treatment with the potential activator of Smad1/5, SB431542. Tretinoin 10-12 SMAD family member 1 Mus musculus 124-131
22438569-5 2012 Additionally, we discovered that genes expressed in pre-meiotic embryonic female and adult male germ cells, including cyclin D1 (Ccnd1) and stimulated by retinoic acid 8 (Stra8), were prematurely expressed in teratoma-susceptible germ cells and, in rare instances, induced entry into meiosis. Tretinoin 154-167 stimulated by retinoic acid gene 8 Mus musculus 171-176
22293198-8 2012 Furthermore, the biochemical manipulation of Smad1/5 expression through shRNA knockdown significantly reduced RA-mediated up-regulation of germ-specific gene expression. Tretinoin 110-112 SMAD family member 1 Mus musculus 45-52
34417575-7 2021 Srebp-1c or Ucp2 silencing attenuated GSIS impairment by reversing the ATRA-induced increase in UCP2 expression and decrease in ATP content. Tretinoin 71-75 sterol regulatory element binding transcription factor 1 Rattus norvegicus 0-8
22293198-9 2012 Our results clearly demonstrate that the Smad1/5 pathway is specifically required at an early stage of germ cell differentiation, corresponding to the RA-dependent commitment of ESCs. Tretinoin 151-153 SMAD family member 1 Mus musculus 41-48
22258322-2 2012 Our recent in vitro studies suggest that all-trans retinoic acid induces podocyte differentiation by activating the retinoic acid receptor-alpha (RARalpha)/cAMP/PKA/CREB pathway. Tretinoin 51-64 retinoic acid receptor alpha Homo sapiens 116-144
22258322-2 2012 Our recent in vitro studies suggest that all-trans retinoic acid induces podocyte differentiation by activating the retinoic acid receptor-alpha (RARalpha)/cAMP/PKA/CREB pathway. Tretinoin 51-64 retinoic acid receptor alpha Homo sapiens 146-154
34417575-8 2021 ATRA and the retinoid X receptor (RXR) agonists 9-cis RA and LG100268 induced the gene expression of Srebp-1c, which was almost completely abolished by the RXR antagonist HX531. Tretinoin 0-4 sterol regulatory element binding transcription factor 1 Rattus norvegicus 101-109
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 76-80 sterol regulatory element binding transcription factor 1 Rattus norvegicus 321-329
22101194-4 2012 In this protocol, P19 EC cells are induced in Minimum Essential Medium alpha supplemented with all-trans retinoic acid (RA) and 2.5% serum, and cultured as a monolayer. Tretinoin 105-118 interleukin 23 subunit alpha Homo sapiens 18-21
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 258-262 sterol regulatory element binding transcription factor 1 Rattus norvegicus 321-329
22101194-4 2012 In this protocol, P19 EC cells are induced in Minimum Essential Medium alpha supplemented with all-trans retinoic acid (RA) and 2.5% serum, and cultured as a monolayer. Tretinoin 120-122 interleukin 23 subunit alpha Homo sapiens 18-21
22101194-8 2012 Furthermore, RA-induced P19 EC cells progressively acquired functional neuronal traits and after approximately 3 weeks in culture revealed mature neurophysiological properties, characteristics of CNS neurons. Tretinoin 13-15 interleukin 23 subunit alpha Homo sapiens 24-27
22107969-3 2012 Consistent with this result, suppression of UTF1 expression in P19 cells by RNA interference enhanced retinoic acid (RA)-induced neuronal differentiation. Tretinoin 102-115 interleukin 23 subunit alpha Homo sapiens 63-66
22107969-3 2012 Consistent with this result, suppression of UTF1 expression in P19 cells by RNA interference enhanced retinoic acid (RA)-induced neuronal differentiation. Tretinoin 117-119 interleukin 23 subunit alpha Homo sapiens 63-66
22393026-4 2012 Rhox10 is highly transcribed in spermatogonia in vivo and is upregulated in response to the differentiation-inducing agent retinoic acid in vitro. Tretinoin 123-136 reproductive homeobox 10 Mus musculus 0-6
22278040-9 2012 Interestingly, however, knockdown of Nr2f2 augmented the induction of renin expression caused by retinoic acid. Tretinoin 97-110 nuclear receptor subfamily 2, group F, member 2 Mus musculus 37-42
22107969-5 2012 Interestingly, the growth rates of UTF1-deficient P19 cells did not differ from that of parental cells in adherent cultures, but were increased in embryoid bodies during RA-induced differentiation. Tretinoin 170-172 interleukin 23 subunit alpha Homo sapiens 50-53
34417575-9 2021 RXRalpha-LBD luciferase reporter plasmid experiments also demonstrated that ATRA concentration-dependently activated RXRalpha, the EC50 of which was 1.37 muM, which was lower than the ATRA concentration in the pancreas of GK rats treated with a high dose of ATRA (approximately 3 muM), inferring that ATRA can upregulate Srebp-1c expression in the pancreas by activating RXR. Tretinoin 301-305 sterol regulatory element binding transcription factor 1 Rattus norvegicus 321-329
34417575-10 2021 In conclusion, ATRA impaired GSIS partly by activating the RXR/SREBP-1c/UCP2 pathway, thus worsening diabetic symptoms. Tretinoin 15-19 sterol regulatory element binding transcription factor 1 Rattus norvegicus 63-71
22532966-7 2012 We found that melatonin in combination with all-trans retinoic acid and somatostatin potentiated the effects of melatonin alone on MCF-7 cell viability and growth inhibition; this phenomenon was associated with altered conductance through Ca2+ and voltage-activated K+ (BK) channels, and with substantial impairments of Notch-1 and epidermal growth factor (EGF)-mediated signaling. Tretinoin 54-67 epidermal growth factor Homo sapiens 332-355
34122632-5 2021 Knocking down the expression of SphK1 or SphK2 in K562 cells by small interfering RNA enhanced the inhibitory effects of ATRA and induced the expression of CYP26A1. Tretinoin 121-125 sphingosine kinase 2 Homo sapiens 41-46
22532966-7 2012 We found that melatonin in combination with all-trans retinoic acid and somatostatin potentiated the effects of melatonin alone on MCF-7 cell viability and growth inhibition; this phenomenon was associated with altered conductance through Ca2+ and voltage-activated K+ (BK) channels, and with substantial impairments of Notch-1 and epidermal growth factor (EGF)-mediated signaling. Tretinoin 54-67 epidermal growth factor Homo sapiens 357-360
22353356-3 2012 All-trans retinoic acid (ATRA), an RAR ligand, increased ABCG1 protein levels and apoA-I/HDL-mediated cholesterol efflux from the macrophages. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 35-38
22131125-4 2012 This mirrors a corresponding change in transcripts and protein levels of ALDH1A3, an enzyme involved in retinoic acid synthesis and the most highly expressed ALDH gene in normal human mammary tissue. Tretinoin 104-117 aldehyde dehydrogenase 1 family member A3 Homo sapiens 73-80
34122632-6 2021 Crude asterosaponins, which abrogated the expression of SphK2, also enhanced the effects of ATRA on K562 cells. Tretinoin 92-96 sphingosine kinase 2 Homo sapiens 56-61
22353356-5 2012 The stimulatory effects of ATRA on ABCG1 expression were completely abolished in the presence of RAR/RXR antagonists but were only partially canceled in the presence of an LXR antagonist. Tretinoin 27-31 retinoic acid receptor alpha Homo sapiens 97-100
34307338-11 2021 Moreover, elevated RA signaling resulted in a reduction in Dlx5 and Dlx6 expression in cranial neural crest cells (CNCCs), which disturbed their interactions with branchiomeric mesoderm cells. Tretinoin 19-21 distal-less homeobox 5 Mus musculus 59-63
22116806-3 2012 The repression of microRNA clusters Mir-17-92 (Mirc1) and Mir-106b-25 (Mirc3) by retinoic acid in turn potentially upregulates the expression of Bim, Kit, Socs3, and Stat3. Tretinoin 81-94 KIT proto-oncogene receptor tyrosine kinase Mus musculus 150-153
22116806-3 2012 The repression of microRNA clusters Mir-17-92 (Mirc1) and Mir-106b-25 (Mirc3) by retinoic acid in turn potentially upregulates the expression of Bim, Kit, Socs3, and Stat3. Tretinoin 81-94 suppressor of cytokine signaling 3 Mus musculus 155-160
22406747-0 2012 Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia. Tretinoin 59-82 methyl-CpG binding domain protein 2 Homo sapiens 31-42
22180614-4 2012 At the molecular level, Sle1a.1 corresponds to an increased expression of a novel splice isoform of Pbx1, Pbx1-d. Pbx1-d overexpression is sufficient to induce an activated/inflammatory phenotype in Jurkat T cells and to decrease their apoptotic response to retinoic acid. Tretinoin 258-271 PBX homeobox 1 Homo sapiens 100-104
22180614-4 2012 At the molecular level, Sle1a.1 corresponds to an increased expression of a novel splice isoform of Pbx1, Pbx1-d. Pbx1-d overexpression is sufficient to induce an activated/inflammatory phenotype in Jurkat T cells and to decrease their apoptotic response to retinoic acid. Tretinoin 258-271 PBX homeobox 1 Homo sapiens 106-110
22180614-4 2012 At the molecular level, Sle1a.1 corresponds to an increased expression of a novel splice isoform of Pbx1, Pbx1-d. Pbx1-d overexpression is sufficient to induce an activated/inflammatory phenotype in Jurkat T cells and to decrease their apoptotic response to retinoic acid. Tretinoin 258-271 PBX homeobox 1 Homo sapiens 106-110
22197812-9 2012 XBP-1 was downregulated immediately after RA treatment in H9 cells, but its downregulation was much slower in HEK293 cells. Tretinoin 42-44 X-box binding protein 1 Homo sapiens 0-5
22197812-12 2012 In H9 cells treated with RA for 29 days, GRP78/Bip, XBP-1 and Bcl2 were all upregulated. Tretinoin 25-27 X-box binding protein 1 Homo sapiens 52-57
22406747-1 2012 Acute promyelocytic leukemia (APL), a cytogenetically distinct subtype of acute myeloid leukemia (AML), characterized by the t(15;17)-associated PML-RARA fusion, has been successfully treated with therapy utilizing all-trans-retinoic acid (ATRA) to differentiate leukemic blasts. Tretinoin 215-238 PML nuclear body scaffold Homo sapiens 145-148
22406747-1 2012 Acute promyelocytic leukemia (APL), a cytogenetically distinct subtype of acute myeloid leukemia (AML), characterized by the t(15;17)-associated PML-RARA fusion, has been successfully treated with therapy utilizing all-trans-retinoic acid (ATRA) to differentiate leukemic blasts. Tretinoin 240-244 PML nuclear body scaffold Homo sapiens 145-148
34307338-11 2021 Moreover, elevated RA signaling resulted in a reduction in Dlx5 and Dlx6 expression in cranial neural crest cells (CNCCs), which disturbed their interactions with branchiomeric mesoderm cells. Tretinoin 19-21 distal-less homeobox 6 Mus musculus 68-72
22177959-0 2012 All-trans retinoic acid inhibits the recruitment of ARNT to DNA, resulting in the decrease of CYP1A1 mRNA expression in HepG2 cells. Tretinoin 10-23 aryl hydrocarbon receptor nuclear translocator Homo sapiens 52-56
22177959-0 2012 All-trans retinoic acid inhibits the recruitment of ARNT to DNA, resulting in the decrease of CYP1A1 mRNA expression in HepG2 cells. Tretinoin 10-23 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 94-100
22177959-4 2012 Treatment with atRA significantly reduced transactivation and expression of CYP1A1 mRNA to less than half of its control value, and this inhibitory effect was mediated by RARalpha. Tretinoin 15-19 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 76-82
22177959-4 2012 Treatment with atRA significantly reduced transactivation and expression of CYP1A1 mRNA to less than half of its control value, and this inhibitory effect was mediated by RARalpha. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 171-179
22177959-5 2012 The result of chromatin immunoprecipitation assay indicated that treatment with atRA at 1-100 nM drastically inhibited the recruitment of ARNT to DNA regions containing xenobiotic responsive elements. Tretinoin 80-84 aryl hydrocarbon receptor nuclear translocator Homo sapiens 138-142
22177959-6 2012 In conclusion, atRA at physiological concentrations could reduce AHR-mediated gene transcription via the inhibition of recruitment of ARNT to relevant DNA regions. Tretinoin 15-19 aryl hydrocarbon receptor nuclear translocator Homo sapiens 134-138
22222225-1 2012 Dendritic cells (DCs) use all-trans retinoic acid (ATRA) to promote characteristic intestinal responses, including Foxp3(+) Treg conversion, lymphocyte gut homing molecule expression, and IgA production. Tretinoin 26-49 forkhead box P3 Mus musculus 115-120
22222225-1 2012 Dendritic cells (DCs) use all-trans retinoic acid (ATRA) to promote characteristic intestinal responses, including Foxp3(+) Treg conversion, lymphocyte gut homing molecule expression, and IgA production. Tretinoin 51-55 forkhead box P3 Mus musculus 115-120
34307338-12 2021 Altogether, we discovered that embryonic craniofacial muscle defects caused by excessive RA signaling were associated with the downregulation of Pitx2, Tbx1, MyoD1, and Dlx5/6, and reduced survival of cranial myogenic precursor cells. Tretinoin 89-91 paired-like homeodomain transcription factor 2 Mus musculus 145-150
21801466-0 2012 Comparative effects of retinoic acid, vitamin D and resveratrol alone and in combination with adenosine analogues on methylation and expression of phosphatase and tensin homologue tumour suppressor gene in breast cancer cells. Tretinoin 23-36 phosphatase and tensin homolog Homo sapiens 147-179
21801466-3 2012 The present results showed that in non-invasive MCF-7 cells, ATRA, vitamin D3 and resveratrol possess high efficacy in the reduction of PTEN promoter methylation. Tretinoin 61-65 phosphatase and tensin homolog Homo sapiens 136-140
22182411-3 2012 Retinoic acid (RA), which acts as a ligand to nuclear receptors including RARalpha, plays crucial roles in development, differentiation, cell cycles and apoptosis. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 74-82
34307338-12 2021 Altogether, we discovered that embryonic craniofacial muscle defects caused by excessive RA signaling were associated with the downregulation of Pitx2, Tbx1, MyoD1, and Dlx5/6, and reduced survival of cranial myogenic precursor cells. Tretinoin 89-91 distal-less homeobox 5 Mus musculus 169-175
22182411-3 2012 Retinoic acid (RA), which acts as a ligand to nuclear receptors including RARalpha, plays crucial roles in development, differentiation, cell cycles and apoptosis. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 74-82
34207434-6 2021 Investigating the response to all trans-retinoic acid (ATRA) revealed its sequestering of the prominin-1 stem cell marker. Tretinoin 34-53 prominin 1 Homo sapiens 94-104
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 133-155
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 157-161
22125055-7 2012 Immunofluorescence detection showed that E-cadherin expression was not detectable in the control group, whereas the positive expression rates of E-cadherin in the I/R, ATRA, EGF, BMP-7 and the combined group were 6 75% +- 2 13%, 16 40% +- 2 69%, 18 25% +- 3 50%, 16 06% +- 2 00% and 30 26% +- 5 16%, respectively. Tretinoin 168-172 cadherin 1 Rattus norvegicus 145-155
21365646-7 2012 Both ATRA administration and AFP knockdown were each able to promote greater binding of RAR to its response element with consequent elevation of the proportion of apoptotic cells. Tretinoin 5-9 retinoic acid receptor alpha Homo sapiens 88-91
23304206-0 2012 Retinoic Acid Induces Apoptosis of Prostate Cancer DU145 Cells through Cdk5 Overactivation. Tretinoin 0-13 cyclin dependent kinase 5 Homo sapiens 71-75
34207434-6 2021 Investigating the response to all trans-retinoic acid (ATRA) revealed its sequestering of the prominin-1 stem cell marker. Tretinoin 55-59 prominin 1 Homo sapiens 94-104
23304206-5 2012 Subsequently, RA-triggered DU145 apoptosis detected by sub-G1 phase accumulation and Annexin V staining could also be blocked by CP treatment. Tretinoin 14-16 annexin A5 Homo sapiens 85-94
34074333-3 2021 As a nuclear receptor transcriptional regulator, PRAME has been extensively studied in cancer biology and is believed to play a role in cancer cell proliferation by suppressing retinoic acid (RA) signaling. Tretinoin 177-190 PRAME like, X-linked 1 Mus musculus 49-54
23304206-6 2012 Furthermore, RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown. Tretinoin 13-15 cyclin dependent kinase 5 Homo sapiens 61-65
23304206-6 2012 Furthermore, RA-triggered caspase 3 activation and following Cdk5 over-activation were destroyed by treatments of both CP and Cdk5 knockdown. Tretinoin 13-15 cyclin dependent kinase 5 Homo sapiens 126-130
23304206-7 2012 In conclusion, we report a new mechanism in which RA could cause apoptosis of androgen-independent prostate cancer cells through p35 cleavage and Cdk5 over-activation. Tretinoin 50-52 cyclin dependent kinase 5 Homo sapiens 146-150
20686816-1 2012 Unlike its cytotoxicity in p53-functional cell lines, Nutlin-1, the small-molecule inhibitor of murine double minute (MDM2), significantly enhanced the differentiation-inducing activity of all-trans retinoic acid (ATRA) in HL60 and NB4 cells (p53-nonfunctional) but not in U937 cells (p53 wild-type). Tretinoin 199-212 transformed mouse 3T3 cell double minute 2 Mus musculus 118-122
22135230-2 2012 We previously found that retinoic acid receptor alpha (RARalpha), a transcription factor activated by retinoic acid (RA), mediates both granulocytic and osteoblastic differentiation. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 55-63
34074333-3 2021 As a nuclear receptor transcriptional regulator, PRAME has been extensively studied in cancer biology and is believed to play a role in cancer cell proliferation by suppressing retinoic acid (RA) signaling. Tretinoin 192-194 PRAME like, X-linked 1 Mus musculus 49-54
22135230-2 2012 We previously found that retinoic acid receptor alpha (RARalpha), a transcription factor activated by retinoic acid (RA), mediates both granulocytic and osteoblastic differentiation. Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 25-53
22135230-4 2012 In this article, we report that, by suppressing CAK phosphorylation of RARalpha, RA induces FGF8f to mediate osteosarcoma U2OS cell differentiation in an autocrine manner. Tretinoin 71-73 fibroblast growth factor 8 Homo sapiens 92-96
22505807-8 2012 AtRA also inhibited the expression of P-selectin and fibrinogen binding on platelets and deposition on the intima of the aorta. Tretinoin 0-4 P-selectin Oryctolagus cuniculus 38-48
34113673-11 2021 Moreover, RA treatment repressed the expression of OCT4 and NANOG in these cells. Tretinoin 10-12 homeobox protein NANOG Bos taurus 60-65
22629307-2 2012 In view of the emerging role of caspases in murine stem cell/neural precursor differentiation, caspases activity was evaluated during RA differentiation. Tretinoin 134-136 caspase 2 Homo sapiens 95-103
22629307-5 2012 The RA-induced expression of neuronal markers, i.e. neural cell adhesion molecule (NCAM), microtubule associated protein-2 (MAP2) and tyrosine hydroxylase (TH) mRNAs and proteins, was decreased in si-Casp9, but markedly increased in si-Casp2 cells. Tretinoin 4-6 neural cell adhesion molecule 1 Homo sapiens 52-81
22629307-5 2012 The RA-induced expression of neuronal markers, i.e. neural cell adhesion molecule (NCAM), microtubule associated protein-2 (MAP2) and tyrosine hydroxylase (TH) mRNAs and proteins, was decreased in si-Casp9, but markedly increased in si-Casp2 cells. Tretinoin 4-6 neural cell adhesion molecule 1 Homo sapiens 83-87
22629307-5 2012 The RA-induced expression of neuronal markers, i.e. neural cell adhesion molecule (NCAM), microtubule associated protein-2 (MAP2) and tyrosine hydroxylase (TH) mRNAs and proteins, was decreased in si-Casp9, but markedly increased in si-Casp2 cells. Tretinoin 4-6 caspase 9 Homo sapiens 200-205
22391160-2 2012 This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 54-77 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 176-205
22391160-2 2012 This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. Tretinoin 79-83 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 176-205
22108894-4 2012 MP2 complete basis set (CBS) extrapolations single energy calculations are also carried out for both the experimental conformations and QM optimized geometries of RA in the gas as well as solution phase. Tretinoin 163-165 tryptase pseudogene 1 Homo sapiens 0-3
22629307-9 2012 Thus, caspase-2 and -9 may perform opposite functions during RA-induced NT2 neuronal differentiation. Tretinoin 61-63 caspase 2 Homo sapiens 6-22
34434004-0 2021 Neuregulin-1, in a Conducive Milieu with Wnt/BMP/Retinoic Acid, Prolongs the Epicardial-Mediated Cardiac Regeneration Capacity of Neonatal Heart Explants. Tretinoin 49-62 neuregulin 1 Homo sapiens 0-12
22629307-10 2012 While caspase-9 activation is relevant for proper neuronal differentiation, likely through the fine tuning of Sirt1 function, caspase-2 activation appears to hinder the RA-induced neuronal differentiation of NT2 cells. Tretinoin 169-171 caspase 2 Homo sapiens 126-135
22490698-1 2012 OBJECTIVE: To explore the relationship between interferon (IFN) alpha and all-trans retinoic acid (ATRA)-induced signaling pathways in the expression of retinoic acid-induced gene G (RIG-G). Tretinoin 84-97 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 153-181
22490698-1 2012 OBJECTIVE: To explore the relationship between interferon (IFN) alpha and all-trans retinoic acid (ATRA)-induced signaling pathways in the expression of retinoic acid-induced gene G (RIG-G). Tretinoin 84-97 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 183-188
22490698-1 2012 OBJECTIVE: To explore the relationship between interferon (IFN) alpha and all-trans retinoic acid (ATRA)-induced signaling pathways in the expression of retinoic acid-induced gene G (RIG-G). Tretinoin 99-103 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 153-181
22490698-1 2012 OBJECTIVE: To explore the relationship between interferon (IFN) alpha and all-trans retinoic acid (ATRA)-induced signaling pathways in the expression of retinoic acid-induced gene G (RIG-G). Tretinoin 99-103 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 183-188
22363502-3 2012 RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. Tretinoin 0-2 LIM domain only 2 (rhombotin-like 1) Danio rerio 86-90
22363502-3 2012 RA treatment significantly reduces expressions of anterior hemangioblast markers scl, lmo2, gata2 and etsrp in the rostral end of ALPM (anterior lateral plate mesoderm) of the embryos. Tretinoin 0-2 ETS1-related protein Danio rerio 102-107
35628438-0 2022 The Cytoskeletal Protein Zyxin Inhibits Retinoic Acid Signaling by Destabilizing the Maternal mRNA of the RXRgamma Nuclear Receptor. Tretinoin 40-53 zyxin S homeolog Xenopus laevis 25-30
22363502-6 2012 Overexpressions of scl and lmo2 partially rescue the block of primitive myelopoiesis in the embryos treated with 250 nM RA during 10-11 hpf, suggesting RA acts upstream of scl to control primitive myelopoiesis. Tretinoin 120-122 LIM domain only 2 (rhombotin-like 1) Danio rerio 27-31
22864348-4 2012 ATRA treatment significantly upregulated hepatic leptin receptor (LEPR) expression. Tretinoin 0-4 leptin receptor Mus musculus 49-64
22125274-0 2012 A zebrafish model of axenfeld-rieger syndrome reveals that pitx2 regulation by retinoic acid is essential for ocular and craniofacial development. Tretinoin 79-92 paired-like homeodomain 2 Danio rerio 59-64
21439680-5 2012 RESULTS: In all treatments, stem cells were first exposed to retinoic acid, which was sufficient to induce Brn3a-positive patterning in 8-day differentiated embryoid bodies. Tretinoin 61-74 POU domain, class 4, transcription factor 1 Mus musculus 107-112
22864348-4 2012 ATRA treatment significantly upregulated hepatic leptin receptor (LEPR) expression. Tretinoin 0-4 leptin receptor Mus musculus 66-70
35628438-6 2022 As a result, Zyxin appears to play an essential role in the regulation of the retinoic acid signal pathway during early embryonic development. Tretinoin 78-91 zyxin S homeolog Xenopus laevis 13-18
22864348-8 2012 In in vitro experiments, ATRA significantly enhanced insulin-induced IRS1 tyrosine phosphorylation solely in the presence of leptin. Tretinoin 25-29 insulin receptor substrate 1 Mus musculus 69-73
35532157-4 2022 We employed all-trans retinoic acid (ATRA) as an inducer of profilin expression and showed that profilin induces autophagy through mTOR inhibition, autophagy-activating kinase ULK1 upregulation, and AMPK stabilization as well as its activation. Tretinoin 12-35 unc-51 like autophagy activating kinase 1 Homo sapiens 176-180
21740303-8 2011 Interestingly, expression of aryl hydrocarbon receptor (AhR), which is RA-induced and known to down-regulate Oct4 and drive RA-induced differentiation, also enhances IRF-1 expression. Tretinoin 71-73 POU class 5 homeobox 1 Homo sapiens 109-113
21555390-7 2011 RESULTS: In this study, we demonstrate a substantial increase in the expression of the NKG2D ligands retinoic acid early inducible-1 (RAE-1), murine ULBP-like transcript 1 (MULT-1) and histocompatibility-60 (H-60) in mouse kidneys during renal IRI. Tretinoin 101-114 histocompatibility 60a Mus musculus 185-206
21555390-7 2011 RESULTS: In this study, we demonstrate a substantial increase in the expression of the NKG2D ligands retinoic acid early inducible-1 (RAE-1), murine ULBP-like transcript 1 (MULT-1) and histocompatibility-60 (H-60) in mouse kidneys during renal IRI. Tretinoin 101-114 histocompatibility 60a Mus musculus 208-212
21803488-0 2011 All-trans retinoic acid induces cellular senescence via upregulation of p16, p21, and p27. Tretinoin 10-23 H3 histone pseudogene 16 Homo sapiens 77-80
21803488-3 2011 ATRA also upregulated levels of p16, p21, and p27 which lead to activation of Rb and subsequent inactivation of E2F1. Tretinoin 0-4 H3 histone pseudogene 16 Homo sapiens 37-40
21803488-3 2011 ATRA also upregulated levels of p16, p21, and p27 which lead to activation of Rb and subsequent inactivation of E2F1. Tretinoin 0-4 E2F transcription factor 1 Homo sapiens 112-116
21992189-0 2012 Modulation of Wnt and Hedgehog signaling pathways is linked to retinoic acid-induced amelioration of chronic allograft dysfunction. Tretinoin 63-76 Wnt family member 2 Rattus norvegicus 14-17
22901127-10 2012 Patients whose tumors exhibited low levels of RARa expression had significantly lower overall survival compared with patients who had higher expression levels of this receptor (p<0.001, HR=0.42, 95.0% CI 0.24-0.73), and patients undergoing ATRA treatment had significantly longer median survival times (p=0.007, HR=0.41, 95.0% CI 0.21-0.80). Tretinoin 243-247 retinoic acid receptor alpha Homo sapiens 46-50
22848226-2 2012 Retinoic acid is a critical ligand in the differentiation pathway of multiple tissues, mediated through binding to an RAR. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 118-121
35532157-4 2022 We employed all-trans retinoic acid (ATRA) as an inducer of profilin expression and showed that profilin induces autophagy through mTOR inhibition, autophagy-activating kinase ULK1 upregulation, and AMPK stabilization as well as its activation. Tretinoin 37-41 unc-51 like autophagy activating kinase 1 Homo sapiens 176-180
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 16-29 retinoic acid receptor alpha Homo sapiens 133-155
35532157-4 2022 We employed all-trans retinoic acid (ATRA) as an inducer of profilin expression and showed that profilin induces autophagy through mTOR inhibition, autophagy-activating kinase ULK1 upregulation, and AMPK stabilization as well as its activation. Tretinoin 37-41 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 199-203
22045663-2 2012 Its metabolite, retinoic acid (RA), acts in a hormone-like manner through binding to and activating three nuclear receptor isotypes, RA receptor (RAR)alpha (RARA), RARbeta, and RARgamma (RARG). Tretinoin 16-29 retinoic acid receptor alpha Homo sapiens 157-161
35491689-9 2022 The computational screening results suggested Retinoic acid and Torularhodin as potential drug candidates for the stimulation of BMP-4. Tretinoin 46-59 bone morphogenetic protein 4 Homo sapiens 129-134
22116001-4 2012 We found that in vitro, RA-treated T cells expressed high levels of Foxp3 in the presence of recombinant TGFbeta. Tretinoin 24-26 forkhead box P3 Mus musculus 68-73
21790894-6 2011 The introduction of drugs such as all-trans retinoic acid (ATRA) that promote progenitor differentiation by directly inhibiting the PML-RARalpha fusion protein has changed the treatment paradigm for APL and markedly improved patient survival. Tretinoin 34-57 PML nuclear body scaffold Homo sapiens 132-135
21790894-6 2011 The introduction of drugs such as all-trans retinoic acid (ATRA) that promote progenitor differentiation by directly inhibiting the PML-RARalpha fusion protein has changed the treatment paradigm for APL and markedly improved patient survival. Tretinoin 34-57 retinoic acid receptor alpha Homo sapiens 136-144
21790894-6 2011 The introduction of drugs such as all-trans retinoic acid (ATRA) that promote progenitor differentiation by directly inhibiting the PML-RARalpha fusion protein has changed the treatment paradigm for APL and markedly improved patient survival. Tretinoin 59-63 PML nuclear body scaffold Homo sapiens 132-135
21790894-6 2011 The introduction of drugs such as all-trans retinoic acid (ATRA) that promote progenitor differentiation by directly inhibiting the PML-RARalpha fusion protein has changed the treatment paradigm for APL and markedly improved patient survival. Tretinoin 59-63 retinoic acid receptor alpha Homo sapiens 136-144
23185633-7 2012 In vitro treatment with PPARgamma agonists and ATRA also induced modest increase in the expression of neuronal beta-III tubulin and astrocyte-specific GFAP in NSCs in 3-7 days. Tretinoin 47-51 glial fibrillary acidic protein Mus musculus 151-155
35147911-0 2022 All-Trans Retinoic Acid-Preconditioned Mesenchymal Stem Cells Improve Motor Function and Alleviate Tissue Damage After Spinal Cord Injury by Inhibition of HMGB1/NF-kappaB/NLRP3 Pathway Through Autophagy Activation. Tretinoin 0-23 high mobility group box 1 Homo sapiens 155-160
35456995-7 2022 Additionally, retinoic acid represses miR-133a, while it increases Raldh2, Tbx5 and AMHC1. Tretinoin 14-27 myosin, heavy chain 7, cardiac muscle, beta Gallus gallus 84-89
23049808-6 2012 METHODOLOGY/PRINCIPAL FINDINGS: Knock-down of Lamin A/C (LMNA-KD) in neuroblastoma cells blocked retinoic acid-induced differentiation, preventing neurites outgrowth and the expression of neural markers. Tretinoin 97-110 lamin A/C Homo sapiens 46-55
23049808-6 2012 METHODOLOGY/PRINCIPAL FINDINGS: Knock-down of Lamin A/C (LMNA-KD) in neuroblastoma cells blocked retinoic acid-induced differentiation, preventing neurites outgrowth and the expression of neural markers. Tretinoin 97-110 lamin A/C Homo sapiens 57-61
21908575-7 2011 RESULTS: The expression of NLRR3 mRNA was upregulated during differentiation of NBL cells induced by retinoic acid, accompanied with reduced expression of MYCN, suggesting that NLRR3 expression was inversely correlated with MYCN in differentiation. Tretinoin 101-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 224-228
21767634-6 2011 Dehydrogenases and a subset of cytochrome p450 genes (cyp26a1, cyp26b1, and cyp26c1) play the major role in providing the retinoic acid and limiting its access. Tretinoin 122-135 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 63-70
21767634-6 2011 Dehydrogenases and a subset of cytochrome p450 genes (cyp26a1, cyp26b1, and cyp26c1) play the major role in providing the retinoic acid and limiting its access. Tretinoin 122-135 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 76-83
22558462-5 2012 Combined stimulation with BMP4 and all-trans Retinoic Acid (RA) inhibited self-renewal and resulted in 90% of cells expressing Desmin and Nestin. Tretinoin 35-58 desmin Mus musculus 127-133
35397003-8 2022 To test the functional significance of these findings, we ectopically expressed wild-type alpha-synuclein in retinoic acid-differentiated dopaminergic SH-SY5Y cells which resulted in decreased levels of NMNAT3 protein plus a neurite pathology which could be rescued by FK866, an inhibitor of nicotinamide phosphoribosyltransferase that acts as a key enzyme in the regulation of NAD+ synthesis. Tretinoin 109-122 nicotinamide nucleotide adenylyltransferase 3 Homo sapiens 203-209
22927819-6 2012 Finally, in vivo derived AAMphi have an enhanced capacity to induce Foxp3 expression in CD4+ cells through an RA dependent mechanism, especially in combination with TGF-beta. Tretinoin 110-112 forkhead box P3 Mus musculus 68-73
22020439-10 2011 Phospho-MYC synergizes with retinoic acid to eliminate circulating leukaemic cells and to decrease the level of tumour invasion. Tretinoin 28-41 MYC proto-oncogene, bHLH transcription factor Homo sapiens 8-11
35318262-6 2022 ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on GADD34 mRNA via p-38 MAPK, resulting in the instability of GADD34 mRNA. Tretinoin 0-4 mitogen-activated protein kinase 14 Mus musculus 116-125
21704588-0 2011 Retinoic acid-induced pancreatic stellate cell quiescence reduces paracrine Wnt-beta-catenin signaling to slow tumor progression. Tretinoin 0-13 catenin beta 1 Homo sapiens 80-92
21848810-6 2011 Retinoic acid promotes differentiation and alpha-synuclein oligomer formation in neuroblastoma cells, while addition of a proteasomal inhibitor induces neurite outgrowth and toxicity to certain wild-type and truncated alpha-synuclein clones. Tretinoin 0-13 synuclein alpha Homo sapiens 43-58
23049403-4 2012 The immunofluorescence staining technique using the anti-PML antibody may be used to provide a rapid diagnosis and to immediately start therapy using all-trans retinoic acid. Tretinoin 160-173 PML nuclear body scaffold Homo sapiens 57-60
22079989-6 2011 Consistent with this finding, retinoic acid-inducible gene I- and TBK1-induced phosphorylation of IFN regulatory factor 3 was significantly diminished when MIP-T3 was overexpressed. Tretinoin 30-43 TANK binding kinase 1 Homo sapiens 66-70
21998312-2 2011 In the nucleus, CRABP-II directly binds to the nuclear receptor RAR to form a complex through which RA is "channeled" from the binding protein to the receptor. Tretinoin 17-19 retinoic acid receptor alpha Homo sapiens 64-67
21998312-10 2011 Hence, SUMOylation of K102 in response to RA binding is critical for dissociation of CRABP-II from ER and, consequently, for mobilization of the protein to nucleus and for its cooperation with RAR. Tretinoin 42-44 retinoic acid receptor alpha Homo sapiens 193-196
35237315-9 2022 RA also enhanced the expression of BARD1 and of the 90 kDa BRCA1 isoform. Tretinoin 0-2 BRCA1 associated RING domain 1 Mus musculus 35-40
21715325-8 2011 Stimulation of Rankl mRNA by ATRA was competitively inhibited by the RARalpha antagonist GR110. Tretinoin 29-33 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 15-20
21715325-12 2011 The data suggest that ATRA enhances periosteal bone resorption by increasing the RANKL/OPG ratio via RARalpha receptors, a response that can be inhibited by monomeric GR. Tretinoin 22-26 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 81-86
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 glutamate-cysteine ligase catalytic subunit Homo sapiens 298-302
21554333-6 2011 We also performed rescue experiments using administration of exogenous RA and microinjection of cholesterol, which augments Shh signaling. Tretinoin 71-73 sonic hedgehog signaling molecule Homo sapiens 124-127
22384442-3 2011 The present study was conducted to determine the relationship between retinoic acid (RA) and RA-mediated expression of Irf-1 and the mouse oocyte maturation. Tretinoin 70-83 interferon regulatory factor 1 Mus musculus 119-124
22384442-3 2011 The present study was conducted to determine the relationship between retinoic acid (RA) and RA-mediated expression of Irf-1 and the mouse oocyte maturation. Tretinoin 85-87 interferon regulatory factor 1 Mus musculus 119-124
22384442-3 2011 The present study was conducted to determine the relationship between retinoic acid (RA) and RA-mediated expression of Irf-1 and the mouse oocyte maturation. Tretinoin 93-95 interferon regulatory factor 1 Mus musculus 119-124
22384442-9 2011 With 100 nM RA treatment, lowest level of Irf-1 mRNA and cumulus cell"s apoptosis was found. Tretinoin 12-14 interferon regulatory factor 1 Mus musculus 42-47
35197751-0 2022 Impact of preconditioning stem cells with all-trans retinoic acid signaling pathway on cisplatin-induced nephrotoxicity by down-regulation of TGFbeta1, IL-6, and caspase-3 and up-regulation of HIF1alpha and VEGF. Tretinoin 52-65 caspase 3 Rattus norvegicus 162-171
35154092-9 2022 Conversely, other rexinoids act synergistically with ATRA, as culturing cells with suboptimal doses of both compounds resulted in CCR9 expression and migration to CCL25. Tretinoin 53-57 C-C motif chemokine receptor 9 Homo sapiens 130-134
21667021-9 2011 RARbeta5 suppression by siRNA in BCA-2 cells increased their susceptibility to atRA. Tretinoin 79-83 ring finger protein 115 Homo sapiens 33-38
35205034-8 2022 RA-treatment also reduced the expression of TRPV1 and TRPA1, and minor electrophysiological responses to their agonists were found in untreated cells. Tretinoin 0-2 transient receptor potential cation channel subfamily V member 1 Homo sapiens 44-49
21478451-3 2011 Retinoic acid inhibits TNF-alpha production in various cell lines. Tretinoin 0-13 tumor necrosis factor Bos taurus 23-32
21478451-10 2011 Expression of caspase 3 (0.4- vs. 1.0-fold) and TNF-alpha (0.4- vs. 1.0-fold) mRNA was downregulated (P < 0.05) in RA-treated blastocysts compared with controls. Tretinoin 118-120 tumor necrosis factor Bos taurus 48-57
21964460-8 2011 Concomitant up regulation of ERalpha, VEGF, cyclin D1, CDK4 and Ki-67 was also observed to be more prominent for ATRA-treated rats as compared to the rats that were allowed to recover naturally for 56 days. Tretinoin 113-117 estrogen receptor 1 Rattus norvegicus 29-36
21964460-8 2011 Concomitant up regulation of ERalpha, VEGF, cyclin D1, CDK4 and Ki-67 was also observed to be more prominent for ATRA-treated rats as compared to the rats that were allowed to recover naturally for 56 days. Tretinoin 113-117 vascular endothelial growth factor A Rattus norvegicus 38-42
21964460-10 2011 Since structural and functional maintenance of the pubertal uterus is under the influence of estradiol, ATRA consequently up regulated the estrogen receptor and resumed cellular proliferation, possibly by an antioxidant therapeutic approach against arsenic toxicity. Tretinoin 104-108 estrogen receptor 1 Rattus norvegicus 139-156
21478451-11 2011 Moreover, 9-cis RA rescued (P < 0.001) development rates (24.5 +- 11.1 vs. 15.6 +- 9.0%), increased total cell number (124.6 +- 36.5 vs. 106.9 +- 31.1), and reduced apoptosis (5.8 +- 2.0 vs. 8.1 +- 3.1%) in blastocysts exposed to TNF-alpha (TNF group). Tretinoin 16-18 tumor necrosis factor Bos taurus 233-242
21478451-11 2011 Moreover, 9-cis RA rescued (P < 0.001) development rates (24.5 +- 11.1 vs. 15.6 +- 9.0%), increased total cell number (124.6 +- 36.5 vs. 106.9 +- 31.1), and reduced apoptosis (5.8 +- 2.0 vs. 8.1 +- 3.1%) in blastocysts exposed to TNF-alpha (TNF group). Tretinoin 16-18 tumor necrosis factor Bos taurus 233-236
35205034-8 2022 RA-treatment also reduced the expression of TRPV1 and TRPA1, and minor electrophysiological responses to their agonists were found in untreated cells. Tretinoin 0-2 transient receptor potential cation channel subfamily A member 1 Homo sapiens 54-59
21478451-13 2011 In conclusion, the present study suggests that 9-cis RA exerts its beneficial roles on oocyte developmental competence and embryo quality by attenuating oocyte TNF-alpha mRNA expression. Tretinoin 53-55 tumor necrosis factor Bos taurus 160-169
35159132-3 2022 Retinol is first converted to retinaldehyde by retinol dehydrogenase 10 (RDH10) and then to RA by all three retinaldehyde dehydrogenases (ALDH1A1, ALDH1A2, and ALDH1A3). Tretinoin 92-94 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 138-145
21816185-5 2011 Suppression of retinoic acid-inducible gene-I (RIG-I) expression using siRNA significantly reduced IFN-lambda1 production in RSV-infected hTERT-NECs, while suppression of melanoma differentiation-associated gene 5 (MDA5) expression did not. Tretinoin 15-28 telomerase reverse transcriptase Homo sapiens 138-143
21523764-0 2011 Retinoic acid induces REST degradation and neuronal differentiation by modulating the expression of SCF(beta-TRCP) in neuroblastoma cells. Tretinoin 0-13 beta-transducin repeat containing E3 ubiquitin protein ligase Homo sapiens 104-113
21523764-12 2011 CONCLUSIONS: The current results indicated that elevated transcription of REST compounded by its impaired degradation by SCF(beta-TRCP) may contribute to the failure of these tumors to differentiate in response to retinoic acid. Tretinoin 214-227 beta-transducin repeat containing E3 ubiquitin protein ligase Homo sapiens 125-134
22514573-10 2011 Although the addition of ATRA alone or in combination with IL-12 resulted in decreases in CD62L expression on day 3, they showed a dose-dependent effect on the restoration of CD62L expression on day 5. Tretinoin 25-29 selectin L Homo sapiens 90-95
22514573-10 2011 Although the addition of ATRA alone or in combination with IL-12 resulted in decreases in CD62L expression on day 3, they showed a dose-dependent effect on the restoration of CD62L expression on day 5. Tretinoin 25-29 selectin L Homo sapiens 175-180
21867633-2 2011 RT-PCR was performed to detect the expression change of BHLHB2 before and after the induction of PML-RARalpha in PR9 cells, and its expression level after the treatment of ATRA in PR9 and APL patient derived NB4 cells. Tretinoin 172-176 Picrotoxin-resistant Drosophila melanogaster 180-183
35159132-3 2022 Retinol is first converted to retinaldehyde by retinol dehydrogenase 10 (RDH10) and then to RA by all three retinaldehyde dehydrogenases (ALDH1A1, ALDH1A2, and ALDH1A3). Tretinoin 92-94 aldehyde dehydrogenase family 1, subfamily A2 Mus musculus 147-154
35159132-7 2022 Binding of RA to RARs regulates recruitment of transcriptional coregulators such as nuclear receptor coactivator (NCOA) or nuclear receptor corepressor (NCOR), which in turn control binding of the generic coactivator p300 or the generic corepressor PRC2. Tretinoin 11-13 nuclear receptor co-repressor 1 Mus musculus 153-157
21684744-0 2011 A transcription factor hijacking to regulate RARalpha by using a chimeric molecule of retinoic acid and a DNA alkylator. Tretinoin 86-99 retinoic acid receptor alpha Homo sapiens 45-53
21959331-1 2011 BACKGROUND: CYP26a1, which functioned mainly as a retinoic acid (RA) catabolic enzyme, has been shown to be oncogenic and to support cell survival in many breast carcinoma cells. Tretinoin 50-63 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 12-19
35051272-5 2022 We found that pressure activates RA signaling through the mechanosensor Yap. Tretinoin 33-35 yes-associated protein 1 Mus musculus 72-75
21903586-6 2011 Interestingly, we found that this novel pathway including CDX2, miR-125b, and CBFbeta was mediated by undergoing all-trans-retinoic acid induction. Tretinoin 113-136 core-binding factor subunit beta Homo sapiens 78-85
22093791-0 2011 [Effects of simvastatin plus all-trans retinoic acid on WT1/hDMP1 gene expression profiles of human promyelocytic leukemia cell line NB4]. Tretinoin 39-52 dentin matrix acidic phosphoprotein 1 Homo sapiens 60-65
2555051-5 1989 Retinoic acid incubation caused a reproducible decrease in c-myc expression in variant SCLC cells, but was not noted to increase L-dopa decarboxylase, an enzyme which biochemically distinguishes classic from variant SCLC cell lines. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 59-64
21536668-0 2011 Neutral sphingomyelinase-2 mediates growth arrest by retinoic acid through modulation of ribosomal S6 kinase. Tretinoin 53-66 sphingomyelin phosphodiesterase 3 Homo sapiens 0-26
21536668-4 2011 Notably, induction of nSMase2 was the primary effect of ATRA on the sphingolipid network and was both time- and dose-dependent. Tretinoin 56-60 sphingomyelin phosphodiesterase 3 Homo sapiens 22-29
21536668-8 2011 In contrast, ATRA suppressed phosphorylation of ribosomal S6 kinase (S6K) and its downstream targets S6 and eIF4B. Tretinoin 13-17 ribosomal protein S6 kinase B1 Homo sapiens 69-72
21536668-8 2011 In contrast, ATRA suppressed phosphorylation of ribosomal S6 kinase (S6K) and its downstream targets S6 and eIF4B. Tretinoin 13-17 eukaryotic translation initiation factor 4B Homo sapiens 108-113
21536668-13 2011 Taken together, these results implicate nSMase2 as a major component of ATRA-induced growth arrest of MCF-7 cells and identify S6K as a novel downstream target of nSMase2. Tretinoin 72-76 sphingomyelin phosphodiesterase 3 Homo sapiens 40-47
21605549-0 2011 Retinoic acid inhibits BMP4-induced C3H10T1/2 stem cell commitment to adipocyte via downregulating Smad/p38MAPK signaling. Tretinoin 0-13 SMAD family member 1 Mus musculus 99-103
20812861-0 2011 Retinoic acid induces autophagosome maturation through redistribution of the cation-independent mannose-6-phosphate receptor. Tretinoin 0-13 insulin like growth factor 2 receptor Homo sapiens 77-124
20812861-5 2011 RA did not affect the levels of upstream regulators of autophagy, such as Beclin-1, phospho-mTOR, and phospho-Akt1, but induced redistribution of both endogenous cation-independent mannose-6-phosphate receptor CIMPR and transiently transfected GFP and RFP full-length CIMPR fusion proteins from the trans-Golgi region to acidified AUT structures. Tretinoin 0-2 insulin like growth factor 2 receptor Homo sapiens 162-209
20812861-5 2011 RA did not affect the levels of upstream regulators of autophagy, such as Beclin-1, phospho-mTOR, and phospho-Akt1, but induced redistribution of both endogenous cation-independent mannose-6-phosphate receptor CIMPR and transiently transfected GFP and RFP full-length CIMPR fusion proteins from the trans-Golgi region to acidified AUT structures. Tretinoin 0-2 insulin like growth factor 2 receptor Homo sapiens 210-215
20812861-5 2011 RA did not affect the levels of upstream regulators of autophagy, such as Beclin-1, phospho-mTOR, and phospho-Akt1, but induced redistribution of both endogenous cation-independent mannose-6-phosphate receptor CIMPR and transiently transfected GFP and RFP full-length CIMPR fusion proteins from the trans-Golgi region to acidified AUT structures. Tretinoin 0-2 insulin like growth factor 2 receptor Homo sapiens 268-273
21209416-4 2011 After culturing either whole testes or germ cells isolated from mice at 2 days postpartum (dpp) with WIN 18,446 or with WIN 18,446 plus ROL, Stra8 expression was suppressed, demonstrating that WIN 18,446 inhibited the conversion of ROL to RA in both systems. Tretinoin 239-241 stimulated by retinoic acid gene 8 Mus musculus 141-146
21471156-5 2011 In particular, retinoic acid (RA) target genes were upregulated proximally, while the expression of the RA-inactivating Cyp26b1 enzyme was downregulated distally, pointing to increased RA activity in Shh-deficient mouse limb buds. Tretinoin 15-28 sonic hedgehog Mus musculus 200-203
21471156-5 2011 In particular, retinoic acid (RA) target genes were upregulated proximally, while the expression of the RA-inactivating Cyp26b1 enzyme was downregulated distally, pointing to increased RA activity in Shh-deficient mouse limb buds. Tretinoin 30-32 sonic hedgehog Mus musculus 200-203
21471156-5 2011 In particular, retinoic acid (RA) target genes were upregulated proximally, while the expression of the RA-inactivating Cyp26b1 enzyme was downregulated distally, pointing to increased RA activity in Shh-deficient mouse limb buds. Tretinoin 104-106 sonic hedgehog Mus musculus 200-203
21471156-5 2011 In particular, retinoic acid (RA) target genes were upregulated proximally, while the expression of the RA-inactivating Cyp26b1 enzyme was downregulated distally, pointing to increased RA activity in Shh-deficient mouse limb buds. Tretinoin 104-106 sonic hedgehog Mus musculus 200-203
21471156-11 2011 In summary, SHH promotes distal progression of limb development by enhancing CYP26B1-mediated RA clearance as part of a signalling network linking the SHH/GREM1/AER-FGF feedback loop to the newly identified AER-FGF/CYP26B1/RA module. Tretinoin 94-96 sonic hedgehog Mus musculus 12-15
22977519-12 2011 In conclusion, the combination of RSG and ATRA reduced the expression of COX-2, MMP-7 and TIMP-1, caused cell cycle arrest at the G1 phase and induced apoptosis, which resulted in the inhibition of cell proliferation in the HCT-15 human colorectal cancer cell line. Tretinoin 42-46 matrix metallopeptidase 7 Homo sapiens 80-85
21237205-0 2011 All-trans retinoic acid induces TLR-5 expression and cell differentiation and promotes flagellin-mediated cell functions in human THP-1 cells. Tretinoin 10-23 toll like receptor 5 Homo sapiens 32-37
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 45-58 toll like receptor 5 Homo sapiens 93-98
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 60-64 toll like receptor 5 Homo sapiens 93-98
21518431-3 2011 RESULTS: Six microRNAs were upregulated by ATRA treatment, miR-663, miR-494, miR-145, miR-22, miR-363* and miR-223; and three microRNAs were downregulated, miR-10a, miR-181 and miR-612. Tretinoin 43-47 microRNA 145 Homo sapiens 77-84
21187718-2 2011 A hallmark of all-trans retinoic acid (ATRA) responses in APL is PML-RARalpha degradation which promotes cell differentiation. Tretinoin 24-37 PML nuclear body scaffold Homo sapiens 65-68
21187718-2 2011 A hallmark of all-trans retinoic acid (ATRA) responses in APL is PML-RARalpha degradation which promotes cell differentiation. Tretinoin 24-37 retinoic acid receptor alpha Homo sapiens 69-77
21187718-2 2011 A hallmark of all-trans retinoic acid (ATRA) responses in APL is PML-RARalpha degradation which promotes cell differentiation. Tretinoin 39-43 PML nuclear body scaffold Homo sapiens 65-68
21187718-2 2011 A hallmark of all-trans retinoic acid (ATRA) responses in APL is PML-RARalpha degradation which promotes cell differentiation. Tretinoin 39-43 retinoic acid receptor alpha Homo sapiens 69-77
21187718-7 2011 Furthermore, knockdown of p62/SQSTM1 inhibited ATRA-induced PML-RARalpha degradation and myeloid cell differentiation. Tretinoin 47-51 PML nuclear body scaffold Homo sapiens 60-63
21187718-7 2011 Furthermore, knockdown of p62/SQSTM1 inhibited ATRA-induced PML-RARalpha degradation and myeloid cell differentiation. Tretinoin 47-51 retinoic acid receptor alpha Homo sapiens 64-72
21262915-11 2011 Consistent with the hypothesized importance of Oct4 downregulation for differentiation, parental cells rendered resistant to RA by biweekly high RA exposure displayed elevated Oct4 levels that failed to be downregulated. Tretinoin 145-147 POU class 5 homeobox 1 Homo sapiens 176-180
21262915-12 2011 Together, our results suggested that therapeutic effects of RA-induced leukemia differentiation depend on AhR and its ability to downregulate the stem cell factor Oct4. Tretinoin 60-62 POU class 5 homeobox 1 Homo sapiens 163-167
20952403-0 2011 Chromatin and DNA methylation dynamics during retinoic acid-induced RET gene transcriptional activation in neuroblastoma cells. Tretinoin 46-59 ret proto-oncogene Homo sapiens 68-71
20952403-1 2011 Although it is well known that RET gene is strongly activated by retinoic acid (RA) in neuroblastoma cells, the mechanisms underlying such activation are still poorly understood. Tretinoin 65-78 ret proto-oncogene Homo sapiens 31-34
20952403-1 2011 Although it is well known that RET gene is strongly activated by retinoic acid (RA) in neuroblastoma cells, the mechanisms underlying such activation are still poorly understood. Tretinoin 80-82 ret proto-oncogene Homo sapiens 31-34
20354914-12 2011 In conclusion, RAR, RXR and VDR are expressed in human fetal PPCs and PPC proliferation can be promoted by calcitriol, atRA or both together, data valuable for elucidating mechanisms underlying islet development and for developing clinical islet transplantation. Tretinoin 119-123 retinoic acid receptor alpha Homo sapiens 15-18
21426648-10 2011 The CTGF mRNA and protein expression were up-regulated in the hyperoxia groups with and without RA treatment 7 and 14 days after exposure compared with the air control group. Tretinoin 96-98 cellular communication network factor 2 Rattus norvegicus 4-8
21426648-11 2011 Significantly decreased CTGF mRNA and protein expression were noted in the RA-treated hyperoxia group compared with the untreated hyperoxia group 14 days after exposure. Tretinoin 75-77 cellular communication network factor 2 Rattus norvegicus 24-28
21426648-13 2011 RA may provide protections against the lung injury possibly through down-regulating CTGF expression. Tretinoin 0-2 cellular communication network factor 2 Rattus norvegicus 84-88
21131350-2 2011 Wild-type RARalpha is a transcription factor that binds to the SMRT/NCoR family of corepressors in the absence of hormone but releases from corepressor and binds coactivators in response to retinoic acid. Tretinoin 190-203 retinoic acid receptor alpha Homo sapiens 10-18
21148082-0 2011 Clinical significance of CD56 expression in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline-based regimens. Tretinoin 110-123 neural cell adhesion molecule 1 Homo sapiens 25-29
21131358-0 2011 Induction of miR-21 by retinoic acid in estrogen receptor-positive breast carcinoma cells: biological correlates and molecular targets. Tretinoin 23-36 microRNA 21 Homo sapiens 13-19
21131358-3 2011 We found that pro-oncogenic miR-21 is selectively induced by ATRA in ERalpha(+) cells. Tretinoin 61-65 microRNA 21 Homo sapiens 28-34
21131358-4 2011 Induction of miR-21 counteracts the anti-proliferative action of ATRA but has the potentially beneficial effect of reducing cell motility. Tretinoin 65-69 microRNA 21 Homo sapiens 13-19
21326615-4 2011 METHODOLOGY/PRINCIPAL FINDINGS: RARE-hsp68-lacZ transgenic mice were employed as a reporter for endogenous retinoic acid activity that was determined by X-gal assay and immunostaining of the reporter gene product, beta-galactosidase. Tretinoin 107-120 galactosidase, beta 1 Mus musculus 214-232
21047566-6 2011 Of these proteins, FABP7 is a marker of NS cells, CRMP2 is involved in axon guidance, and CRABP1 is thought to regulate retinoic acid access to its nuclear receptors. Tretinoin 120-133 fatty acid-binding protein, brain Macaca fascicularis 19-24
21338350-9 2011 In addition, retinoic acid can activate ICD directly or through a Bmp-mediated mechanism. Tretinoin 13-26 bone morphogenetic protein 1 Homo sapiens 66-69
21224842-1 2011 Sex-specific initiation of meiosis in the fetal ovary has been suggested to require retinoic acid (RA) for induction of Stra8, with expression of the RA-degrading enzyme Cyp26b1 in fetal testis delaying meiosis until postnatal development. Tretinoin 84-97 stimulated by retinoic acid gene 8 Mus musculus 120-125
21224842-1 2011 Sex-specific initiation of meiosis in the fetal ovary has been suggested to require retinoic acid (RA) for induction of Stra8, with expression of the RA-degrading enzyme Cyp26b1 in fetal testis delaying meiosis until postnatal development. Tretinoin 99-101 stimulated by retinoic acid gene 8 Mus musculus 120-125
21045116-7 2011 Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naive rats, evidenced by increased CYP26A1 gene expression and increased conversion of [(3)H]RA to polar metabolites. Tretinoin 57-59 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 10-17
21045116-7 2011 Moreover, CYP26A1 increased more rapidly in the liver of RA-primed rats than naive rats, evidenced by increased CYP26A1 gene expression and increased conversion of [(3)H]RA to polar metabolites. Tretinoin 57-59 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 112-119
21045116-9 2011 Overall, whether RA is produced endogenously from retinol or administered exogenously, changes in retinoid homeostatic gene expression simultaneously favor both retinol esterification and RA oxidation, with CYP26A1 exhibiting the greatest dynamic change. Tretinoin 17-19 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 207-214
21206504-0 2011 Amelioration of glomerulosclerosis with all-trans retinoic acid is linked to decreased plasminogen activator inhibitor-1 and alpha-smooth muscle actin. Tretinoin 50-63 actin gamma 2, smooth muscle Rattus norvegicus 125-150
21736279-2 2011 The effects of ATRA on the proliferation of cells and gene regulation are mediated by retinoid receptors (RAR and RXR), which belong to the nuclear receptor superfamily of ligand- inducible transcription factors. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 106-109
21736279-6 2011 The overexpression of RAR alpha in HeLa cells after the administration of 10(-7) mM ATRA was also observed 72 hours, and the decrease of CaSki by 60-90%. Tretinoin 84-88 retinoic acid receptor alpha Homo sapiens 22-31
21212668-12 2011 The combination of RA treatment with IGF-I or IRS-1 small interfering RNA resulted in an additive decrease in cell viability. Tretinoin 19-21 insulin receptor substrate 1 Homo sapiens 46-51
21138976-0 2011 Retinoic acid stimulates myocardial expansion by induction of hepatic erythropoietin which activates epicardial Igf2. Tretinoin 0-13 erythropoietin Mus musculus 70-84
21138976-0 2011 Retinoic acid stimulates myocardial expansion by induction of hepatic erythropoietin which activates epicardial Igf2. Tretinoin 0-13 insulin-like growth factor 2 Mus musculus 112-116
22252490-0 2011 Tgm2/Gh, Gbx1 and TGF-beta are involved in retinoic acid-induced transdifferentiation from epidermis to mucosal epithelium. Tretinoin 43-56 gastrulation brain homeobox 1 Gallus gallus 9-13
22252490-3 2011 Because Gbx1, TG2/Gh (transglutaminase2) and TGF-beta2 are reported individually to be induced by RA in cultures of chick embryonic skin, mouse epidermal cells and human hair follicles respectively, here, we investigated whether cooperative interplay of Gbx1, TG2/Gh and TGF-beta2 is required for the transdifferentiation of epidermal cells to mucosal cells. Tretinoin 98-100 gastrulation brain homeobox 1 Gallus gallus 8-12
22252490-3 2011 Because Gbx1, TG2/Gh (transglutaminase2) and TGF-beta2 are reported individually to be induced by RA in cultures of chick embryonic skin, mouse epidermal cells and human hair follicles respectively, here, we investigated whether cooperative interplay of Gbx1, TG2/Gh and TGF-beta2 is required for the transdifferentiation of epidermal cells to mucosal cells. Tretinoin 98-100 transforming growth factor beta 2 Gallus gallus 45-54
22252490-4 2011 We have shown that expression of Gbx1, TG2/Gh and TGF-beta proteins were all upregulated in RA-induced transdifferentiated skin and that the former two were expressed in the epidermis, while TGF-beta was expressed in the dermis. Tretinoin 92-94 gastrulation brain homeobox 1 Gallus gallus 33-37
22252490-8 2011 This study showed that coexpression of TG/2 and Gbx1 in the epidermis was required for esophagus-like mucosal transdifferentiation, and that increase in TGF-beta2 expression by RA in the dermis was essential to induce transdifferentiation through epithelial-mesenchymal interaction. Tretinoin 177-179 transforming growth factor beta 2 Gallus gallus 153-162
20705791-2 2011 As retinoic acid is essential for spermatogenesis, we hypothesized that WIN 18,446 might inhibit retinoic acid biosynthesis from retinol (vitamin A) within the testes by inhibiting the enzyme aldehyde dehydrogenase 1a2 (ALDH1a2). Tretinoin 3-16 retinal dehydrogenase 2 Oryctolagus cuniculus 192-218
20705791-2 2011 As retinoic acid is essential for spermatogenesis, we hypothesized that WIN 18,446 might inhibit retinoic acid biosynthesis from retinol (vitamin A) within the testes by inhibiting the enzyme aldehyde dehydrogenase 1a2 (ALDH1a2). Tretinoin 97-110 retinal dehydrogenase 2 Oryctolagus cuniculus 192-218
20705791-8 2011 These findings demonstrate that bisdichloroacetyldiamines such as WIN 18,446 reversibly suppress spermatogenesis via inhibition of testicular retinoic acid biosynthesis by ALDH1a2. Tretinoin 142-155 retinal dehydrogenase 2 Oryctolagus cuniculus 172-179
20941602-5 2011 We present a detailed protocol demonstrating that polyclonal activation of conventional CD4(+) T cells in the presence of IL-2, TGFbeta, and all trans retinoic acid induces >90% conversion of these T cells to Foxp3-expressing iTregs as well as promotes a three- to fourfold increase in proliferation following a 4-day incubation period in vitro. Tretinoin 151-164 forkhead box P3 Mus musculus 212-217
22125642-5 2011 The physiological actions of ATRA are mediated by binding to all three isoforms of the nuclear retinoic acid receptors (RARs): RARalpha, RARbeta, and RARgamma. Tretinoin 29-33 retinoic acid receptor alpha Homo sapiens 127-135
21674038-5 2011 Expression of the three RA-synthesising enzymes, ALDH1A1, 2 and 3 in the fetal ovary and testis was equal to or greater than that in the mesonephros at 8-9 weeks gestation, indicating an intrinsic capacity within the gonad to synthesise RA. Tretinoin 237-239 aldehyde dehydrogenase 1 family member A1 Homo sapiens 49-56
21280163-3 2011 Retinoic acid treatment inhibited beta-catenin/Tcf activity in NTERA-2 cells but not in 2102Ep cells. Tretinoin 0-13 catenin beta 1 Homo sapiens 34-46
21280163-6 2011 Retinoic acid treatment of NTERA-2 cells induced the expression of Wnt-4 and Wnt-11, both of which were able to inhibit beta-catenin/Tcf activity. Tretinoin 0-13 catenin beta 1 Homo sapiens 120-132
21057085-8 2010 Moreover, trichostatin A and retinoic acid enhanced the generation of iTregs synergistically with PPARalpha and PPARgamma agonists. Tretinoin 29-42 peroxisome proliferator activated receptor alpha Homo sapiens 98-107
20935222-2 2010 APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is generated in APL by chromosomal translocation. Tretinoin 24-47 PML nuclear body scaffold Homo sapiens 122-149
20935222-2 2010 APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is generated in APL by chromosomal translocation. Tretinoin 24-47 PML nuclear body scaffold Homo sapiens 151-154
20935222-2 2010 APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is generated in APL by chromosomal translocation. Tretinoin 24-47 retinoic acid receptor alpha Homo sapiens 156-164
20935222-2 2010 APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is generated in APL by chromosomal translocation. Tretinoin 49-51 PML nuclear body scaffold Homo sapiens 122-149
20935222-2 2010 APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is generated in APL by chromosomal translocation. Tretinoin 49-51 PML nuclear body scaffold Homo sapiens 151-154
20935222-2 2010 APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is generated in APL by chromosomal translocation. Tretinoin 49-51 retinoic acid receptor alpha Homo sapiens 156-164
20659790-6 2010 Furthermore, the mRNA expression of corticotropin release factor (CRF) and retinoic acid receptor-alpha (RAR-alpha) in the hypothalamus was both markedly increased in ATRA-treated rats compared with vehicle. Tretinoin 167-171 retinoic acid receptor, alpha Rattus norvegicus 75-103
20659790-6 2010 Furthermore, the mRNA expression of corticotropin release factor (CRF) and retinoic acid receptor-alpha (RAR-alpha) in the hypothalamus was both markedly increased in ATRA-treated rats compared with vehicle. Tretinoin 167-171 retinoic acid receptor, alpha Rattus norvegicus 105-114
20940140-0 2010 Retinoic acid metabolizing enzyme CYP26A1 is implicated in rat embryo implantation. Tretinoin 0-13 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 34-41
20940140-1 2010 BACKGROUND: The retinoic acid metabolizing enzyme Cyp26a1 plays a pivotal role in vertebrate embryo development. Tretinoin 16-29 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 50-57
20632143-9 2010 These results indicate that ATRA within a certain range of concentration could reversibly induce the expression of FR-beta in a dosage- and cell type-dependent manner, and its action in KG-1 cells might be associated with the signal transduction of retinoid receptor RARalpha and RARgamma, rather than RARbeta and RXRs. Tretinoin 28-32 folate receptor beta Homo sapiens 115-122
20944006-3 2010 RA induced bone marrow-derived DCs to express CCR9 and ALDH1a2 and conferred upon them mucosal DC functions, including induction of Foxp3(+) regulatory T cells, IgA-secreting B cells, and gut-homing molecules. Tretinoin 0-2 forkhead box P3 Mus musculus 132-137
20650878-6 2010 Additionally, beta-galactosidase activity in premeiotic germ cells colocalized with STRA8 protein and was induced in germ cells with exogenous RA treatment. Tretinoin 86-88 galactosidase, beta 1 Mus musculus 14-32
21180254-0 2010 Effects of retinoic acid and hydrogen peroxide on sterol regulatory element-binding protein-1a activation during adipogenic differentiation of 3T3-L1 cells. Tretinoin 11-24 sterol regulatory element binding transcription factor 1 Mus musculus 50-93
21180254-1 2010 Both retinoic acid (RA) and oxidative stress (H2O2) increased transcription and cleavage of membrane-bound sterol regulatory element-binding protein (SREBP)-1, leading to enhanced transcription of fatty acid synthase (FAS) in hepatoma cells. Tretinoin 5-18 sterol regulatory element binding transcription factor 1 Mus musculus 107-158
21180254-1 2010 Both retinoic acid (RA) and oxidative stress (H2O2) increased transcription and cleavage of membrane-bound sterol regulatory element-binding protein (SREBP)-1, leading to enhanced transcription of fatty acid synthase (FAS) in hepatoma cells. Tretinoin 20-22 sterol regulatory element binding transcription factor 1 Mus musculus 107-158
21180254-2 2010 On the other hand, RA and H2O2 decreased and increased lipogenesis in adipocytes, respectively, although roles of SREBP-1 activation in these effects remain to be elucidated. Tretinoin 19-21 sterol regulatory element binding transcription factor 1 Mus musculus 114-121
21180254-4 2010 RA (1 microM) treatment suppressed expression of SREBP-1a and FAS genes and lipid accumulation. Tretinoin 0-2 sterol regulatory element binding transcription factor 1 Mus musculus 49-57
21180254-6 2010 Increased cleavage of SREBP-1a by H2O2 was also observed even in the presence of RA. Tretinoin 81-83 sterol regulatory element binding transcription factor 1 Mus musculus 22-30
21180254-7 2010 These results suggest that H2O2, enhances a cleavage of SREBP-1a precursor protein, which independently occurs with the RA suppression of SREBP-1a gene expression, and that RA itself has no role in the SREBP-1a activation in adipocytes. Tretinoin 120-122 sterol regulatory element binding transcription factor 1 Mus musculus 56-64
21180254-7 2010 These results suggest that H2O2, enhances a cleavage of SREBP-1a precursor protein, which independently occurs with the RA suppression of SREBP-1a gene expression, and that RA itself has no role in the SREBP-1a activation in adipocytes. Tretinoin 120-122 sterol regulatory element binding transcription factor 1 Mus musculus 138-146
21180254-7 2010 These results suggest that H2O2, enhances a cleavage of SREBP-1a precursor protein, which independently occurs with the RA suppression of SREBP-1a gene expression, and that RA itself has no role in the SREBP-1a activation in adipocytes. Tretinoin 120-122 sterol regulatory element binding transcription factor 1 Mus musculus 138-146
20736163-0 2010 A novel cytoplasmic adaptor for retinoic acid receptor (RAR) and thyroid receptor functions as a Derepressor of RAR in the absence of retinoic acid. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 56-59
20736163-0 2010 A novel cytoplasmic adaptor for retinoic acid receptor (RAR) and thyroid receptor functions as a Derepressor of RAR in the absence of retinoic acid. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 112-115
20736163-1 2010 In most mammalian cells, the retinoic acid receptor (RAR) is nuclear rather than cytoplasmic, regardless of its cognate ligand, retinoic acid (RA). Tretinoin 29-42 retinoic acid receptor alpha Homo sapiens 53-56
20736163-1 2010 In most mammalian cells, the retinoic acid receptor (RAR) is nuclear rather than cytoplasmic, regardless of its cognate ligand, retinoic acid (RA). Tretinoin 53-55 retinoic acid receptor alpha Homo sapiens 29-51
20629094-7 2010 A set of 447 primary target genes of TFAP2C was identified, which included ESR1 (ERalpha), FREM2, RET, FOXA1, WWOX, GREB1, MYC, and members of the retinoic acid response pathway. Tretinoin 147-160 transcription factor AP-2 gamma Homo sapiens 37-43
20877641-5 2010 Results showed that palladin expression was rapidly induced in an A404 cell line upon retinoic acid (RA) induced differentiation. Tretinoin 86-99 palladin, cytoskeletal associated protein Mus musculus 20-28
20877641-5 2010 Results showed that palladin expression was rapidly induced in an A404 cell line upon retinoic acid (RA) induced differentiation. Tretinoin 101-103 palladin, cytoskeletal associated protein Mus musculus 20-28
20846364-0 2010 Hif1alpha down-regulation is associated with transposition of great arteries in mice treated with a retinoic acid antagonist. Tretinoin 100-113 hypoxia inducible factor 1, alpha subunit Mus musculus 0-9
20846364-13 2010 CONCLUSIONS: We propose that Hif1alpha down-regulation in response to blocking retinoic acid binding may contribute to the development of cardiac defects in mouse newborns. Tretinoin 79-92 hypoxia inducible factor 1, alpha subunit Mus musculus 29-38
20846364-15 2010 To the best of our knowledge, this is the first report that links retinoic acid metabolism to Hif1alpha regulation and the development of D-TGA. Tretinoin 66-79 hypoxia inducible factor 1, alpha subunit Mus musculus 94-103
20844755-8 2010 We also found that RA inhibits cell cycle progression in the presence of proliferating signals such as epidermal growth factor (EGF) combined with basic fibroblast growth factor (bFGF). Tretinoin 19-21 epidermal growth factor Homo sapiens 128-131
20691163-2 2010 Ski represses retinoic acid (RA) signaling by interacting with, and stabilizing, key components of the co-repressor complex, namely, HDAC3. Tretinoin 14-27 SKI proto-oncogene Homo sapiens 0-3
20691163-2 2010 Ski represses retinoic acid (RA) signaling by interacting with, and stabilizing, key components of the co-repressor complex, namely, HDAC3. Tretinoin 29-31 SKI proto-oncogene Homo sapiens 0-3
20600628-9 2010 RA is able to induce proliferation through non-classical and redox-dependent mechanisms accompanied by increased levels of FABP5 mRNA. Tretinoin 0-2 fatty acid binding protein 5, epidermal Mus musculus 123-128
20679534-2 2010 All-trans retinoic acid (atRA), the active derivative of vitamin A, has been demonstrated to promote Foxp3(+) Treg differentiation and suppress Th17 development. Tretinoin 0-23 forkhead box P3 Mus musculus 101-106
20679534-2 2010 All-trans retinoic acid (atRA), the active derivative of vitamin A, has been demonstrated to promote Foxp3(+) Treg differentiation and suppress Th17 development. Tretinoin 25-29 forkhead box P3 Mus musculus 101-106
20679534-4 2010 We found that nTregs treated with atRA were resistant to Th17 and other Th cell conversion and maintained Foxp3 expression and suppressive activity in the presence of IL-6 in vitro. Tretinoin 34-38 forkhead box P3 Mus musculus 106-111
19916800-1 2010 Transcription factor FoxA1 plays a critical role during embryonic development and is activated during retinoic acid (RA)-induced neural differentiation of pluripotent P19 embryonal carcinoma cells at the early stage, which is marked by decreased expression of Nanog and increased expression of neural stem cell marker Nestin. Tretinoin 102-115 forkhead box A1 Homo sapiens 21-26
19916800-1 2010 Transcription factor FoxA1 plays a critical role during embryonic development and is activated during retinoic acid (RA)-induced neural differentiation of pluripotent P19 embryonal carcinoma cells at the early stage, which is marked by decreased expression of Nanog and increased expression of neural stem cell marker Nestin. Tretinoin 117-119 forkhead box A1 Homo sapiens 21-26
19916800-6 2010 During RA-induced P19 cell differentiation, elevated levels of FoxA1 increase the population of neurons, evidenced by stimulated expression of neuron-specific Neurofilament-1 and Tubulin betaIII. Tretinoin 7-9 forkhead box A1 Homo sapiens 63-68
20538039-1 2010 Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. Tretinoin 39-52 enolase 1 Homo sapiens 111-115
20538039-1 2010 Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. Tretinoin 39-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149
20538039-1 2010 Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. Tretinoin 54-56 enolase 1 Homo sapiens 111-115
20538039-1 2010 Our previous studies demonstrated that retinoic acid (RA)-induced reduction of both, the key glycolytic enzyme ENO1 and proliferation-promoting c-Myc, resulted in decreased vitality and invasiveness of the follicular thyroid carcinoma cell lines FTC-133 and FTC-238. Tretinoin 54-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149
20525991-3 2010 We demonstrate that during retinoic acid (RA)-induced differentiation of Neuro-2a cells, PtdCho synthesis was promoted by an ordered and sequential activation of choline kinase alpha (CK(alpha)) and choline cytidylyltransferase alpha (CCT(alpha)). Tretinoin 27-40 phosphate cytidylyltransferase 1, choline, alpha isoform Mus musculus 235-245
20525991-3 2010 We demonstrate that during retinoic acid (RA)-induced differentiation of Neuro-2a cells, PtdCho synthesis was promoted by an ordered and sequential activation of choline kinase alpha (CK(alpha)) and choline cytidylyltransferase alpha (CCT(alpha)). Tretinoin 42-44 phosphate cytidylyltransferase 1, choline, alpha isoform Mus musculus 235-245
20525991-4 2010 Early after RA stimulation, the increase in PtdCho synthesis is mainly governed by the biochemical activation of CCT(alpha). Tretinoin 12-14 phosphate cytidylyltransferase 1, choline, alpha isoform Mus musculus 113-123
20477760-7 2010 We demonstrate that WRNp localizes to the Oct4 promoter during retinoic acid-induced differentiation of human pluripotent cells and associates with the de novo methyltransferase Dnmt3b in the chromatin of differentiating pluripotent cells. Tretinoin 63-76 POU class 5 homeobox 1 Homo sapiens 42-46
20477760-9 2010 The lack of DNA methylation was associated with continued, albeit greatly reduced, Oct4 expression in WRN-deficient, retinoic acid-treated cells, which resulted in attenuated differentiation. Tretinoin 117-130 POU class 5 homeobox 1 Homo sapiens 83-87
20659317-0 2010 Effects of ATRA combined with citrus and ginger-derived compounds in human SCC xenografts. Tretinoin 11-15 serpin family B member 3 Homo sapiens 75-78
20507312-9 2010 At ATRA concentrations that induced apoptosis, expression levels of retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-gamma (RXRgamma) were increased. Tretinoin 3-7 retinoic acid receptor alpha Homo sapiens 68-96
20507312-9 2010 At ATRA concentrations that induced apoptosis, expression levels of retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-gamma (RXRgamma) were increased. Tretinoin 3-7 retinoic acid receptor alpha Homo sapiens 98-106
20432234-1 2010 Intestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naive CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). Tretinoin 160-173 forkhead box P3 Mus musculus 54-59
20432234-1 2010 Intestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naive CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). Tretinoin 175-177 forkhead box P3 Mus musculus 54-59
20061533-3 2010 Retinoic acid via retinoic acid receptors induced expression of the intestinal transcription factor ISX. Tretinoin 0-13 intestine specific homeobox Mus musculus 100-103
20455087-3 2010 Both retinoic acid (RA) and arsenic trioxide directly target PML/RARA-mediated transcriptional repression and protein stability, inducing rapid differentiation of the promyelocytes and clinical remission in most APL patients. Tretinoin 5-18 PML nuclear body scaffold Homo sapiens 61-64
20455087-3 2010 Both retinoic acid (RA) and arsenic trioxide directly target PML/RARA-mediated transcriptional repression and protein stability, inducing rapid differentiation of the promyelocytes and clinical remission in most APL patients. Tretinoin 5-18 retinoic acid receptor alpha Homo sapiens 65-69
20455087-3 2010 Both retinoic acid (RA) and arsenic trioxide directly target PML/RARA-mediated transcriptional repression and protein stability, inducing rapid differentiation of the promyelocytes and clinical remission in most APL patients. Tretinoin 20-22 PML nuclear body scaffold Homo sapiens 61-64
20455087-3 2010 Both retinoic acid (RA) and arsenic trioxide directly target PML/RARA-mediated transcriptional repression and protein stability, inducing rapid differentiation of the promyelocytes and clinical remission in most APL patients. Tretinoin 20-22 retinoic acid receptor alpha Homo sapiens 65-69
21120193-2 2010 The variant APL with t(11;17)(q23;q12); ZBTB16-RARA subgroup has been reported to have leukemic cells with regular nuclei, many granules, absence of Auer rods, an increased number of Pelgeroid neutrophils, strong myeloperoxidase (MPO) activity, and all-trans-retinoic-acid (ATRA) resistance. Tretinoin 253-272 retinoic acid receptor alpha Homo sapiens 47-51
21120193-2 2010 The variant APL with t(11;17)(q23;q12); ZBTB16-RARA subgroup has been reported to have leukemic cells with regular nuclei, many granules, absence of Auer rods, an increased number of Pelgeroid neutrophils, strong myeloperoxidase (MPO) activity, and all-trans-retinoic-acid (ATRA) resistance. Tretinoin 274-278 retinoic acid receptor alpha Homo sapiens 47-51
20100636-8 2010 Finally, RARA may be the key to unlocking the problem of resistance to all-trans retinoic acid (ATRA) in breast cancer sufferers; this treatment has previously been demonstrated to induce remission in over 80% of patients with acute promyelocytic leukaemia (APML). Tretinoin 81-94 retinoic acid receptor alpha Homo sapiens 9-13
20100636-8 2010 Finally, RARA may be the key to unlocking the problem of resistance to all-trans retinoic acid (ATRA) in breast cancer sufferers; this treatment has previously been demonstrated to induce remission in over 80% of patients with acute promyelocytic leukaemia (APML). Tretinoin 96-100 retinoic acid receptor alpha Homo sapiens 9-13
20096012-0 2010 Epigallocatechin-3-gallate induces cell death in acute myeloid leukaemia cells and supports all-trans retinoic acid-induced neutrophil differentiation via death-associated protein kinase 2. Tretinoin 102-115 death associated protein kinase 2 Homo sapiens 155-188
20096012-6 2010 Moreover, combined ATRA and EGCG treatment resulted in cooperative DAPK2 induction and potentiated differentiation. Tretinoin 19-23 death associated protein kinase 2 Homo sapiens 67-72
20200558-6 2010 Co-treatment with a pharmacologic inhibitor of PRKCD and RA resulted in the induction of an RA responsive reporter construct, as well as the endogenous RA target genes, CEBPE, CYP26A1 and RIG-I. Tretinoin 57-59 CCAAT enhancer binding protein epsilon Homo sapiens 169-174
21384111-7 2011 These results suggest that RA blocks in vitro RANKL-mediated osteoclastogenesis by decreasing NFATc1 function. Tretinoin 27-29 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 46-51
22055260-10 2011 Two muM retinoic acid reduced MMP-1 but did not significantly affect skin structure. Tretinoin 8-21 matrix metallopeptidase 1 Homo sapiens 30-35
21801775-0 2011 Retinoic acid-induced upregulation of the metalloendopeptidase nardilysin is accelerated by co-expression of the brain-specific protein p42(IP4) (centaurin alpha 1; ADAP1) in neuroblastoma cells. Tretinoin 0-13 ArfGAP with dual PH domains 1 Homo sapiens 146-163
21801775-0 2011 Retinoic acid-induced upregulation of the metalloendopeptidase nardilysin is accelerated by co-expression of the brain-specific protein p42(IP4) (centaurin alpha 1; ADAP1) in neuroblastoma cells. Tretinoin 0-13 ArfGAP with dual PH domains 1 Homo sapiens 165-170
21479819-12 2011 LPS induced a state of adiponectin resistance in dendritic cells that was reversed by treatment with PPARgamma agonist and retinoic acid. Tretinoin 123-136 adiponectin, C1Q and collagen domain containing Mus musculus 23-34
21737465-2 2011 RET displays both E2 and retinoic acid (RA)-dependent transcriptional modulation in E2-responsive breast cancers. Tretinoin 25-38 ret proto-oncogene Homo sapiens 0-3
21737465-2 2011 RET displays both E2 and retinoic acid (RA)-dependent transcriptional modulation in E2-responsive breast cancers. Tretinoin 40-42 ret proto-oncogene Homo sapiens 0-3
22040992-2 2011 As a subtype of acute myeloid leukemia, acute promyelocytic leukemia (APL) represents the target of therapy due to the good response of the oncogenic protein PML-RARalpha to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 184-197 PML nuclear body scaffold Homo sapiens 158-161
22040992-2 2011 As a subtype of acute myeloid leukemia, acute promyelocytic leukemia (APL) represents the target of therapy due to the good response of the oncogenic protein PML-RARalpha to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 184-197 retinoic acid receptor alpha Homo sapiens 162-170
22040992-2 2011 As a subtype of acute myeloid leukemia, acute promyelocytic leukemia (APL) represents the target of therapy due to the good response of the oncogenic protein PML-RARalpha to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 199-203 PML nuclear body scaffold Homo sapiens 158-161
22040992-2 2011 As a subtype of acute myeloid leukemia, acute promyelocytic leukemia (APL) represents the target of therapy due to the good response of the oncogenic protein PML-RARalpha to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 199-203 retinoic acid receptor alpha Homo sapiens 162-170
21865574-3 2011 ATRA (20 mg/kg PO) was administered for 15 days in groups C and E. We evaluated neuropathy and nerve regeneration-related morphologic changes in sciatic nerve, the concentration of nerve growth factor (NGF), and retinoic acid receptor (RAR)-alpha and RAR-beta expression. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 212-246
21612856-4 2011 In particular, RA treatment stimulates the expression of the osteoblast master regulator, runt-related transcription factor 2 (Runx2), whose expression is necessary for the formation of bone. Tretinoin 15-17 runt related transcription factor 2 Mus musculus 90-125
21612856-4 2011 In particular, RA treatment stimulates the expression of the osteoblast master regulator, runt-related transcription factor 2 (Runx2), whose expression is necessary for the formation of bone. Tretinoin 15-17 runt related transcription factor 2 Mus musculus 127-132
21612856-5 2011 We have shown previously in mesenchymal stem cells that RA acts to stimulate osteoblastogenesis by interfering with the actions of the bzip transcription factor CCAAT/Enhancer Binding Protein beta (C/EBPbeta), where it binds to a negative regulatory element within the Runx2 promoter and inhibits its expression. Tretinoin 56-58 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 161-196
21612856-5 2011 We have shown previously in mesenchymal stem cells that RA acts to stimulate osteoblastogenesis by interfering with the actions of the bzip transcription factor CCAAT/Enhancer Binding Protein beta (C/EBPbeta), where it binds to a negative regulatory element within the Runx2 promoter and inhibits its expression. Tretinoin 56-58 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 198-207
21612856-5 2011 We have shown previously in mesenchymal stem cells that RA acts to stimulate osteoblastogenesis by interfering with the actions of the bzip transcription factor CCAAT/Enhancer Binding Protein beta (C/EBPbeta), where it binds to a negative regulatory element within the Runx2 promoter and inhibits its expression. Tretinoin 56-58 runt related transcription factor 2 Mus musculus 269-274
21612856-6 2011 Herein we show that Smad3, whose expression is stimulated by RA, relays the effects of RA on differentiation by initiating the displacement of C/EBPbeta from the Runx2 promoter. Tretinoin 61-63 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 143-152
21612856-6 2011 Herein we show that Smad3, whose expression is stimulated by RA, relays the effects of RA on differentiation by initiating the displacement of C/EBPbeta from the Runx2 promoter. Tretinoin 61-63 runt related transcription factor 2 Mus musculus 162-167
21612856-6 2011 Herein we show that Smad3, whose expression is stimulated by RA, relays the effects of RA on differentiation by initiating the displacement of C/EBPbeta from the Runx2 promoter. Tretinoin 87-89 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 143-152
21612856-6 2011 Herein we show that Smad3, whose expression is stimulated by RA, relays the effects of RA on differentiation by initiating the displacement of C/EBPbeta from the Runx2 promoter. Tretinoin 87-89 runt related transcription factor 2 Mus musculus 162-167
21612856-8 2011 While not sufficient to promote osteoblastogenesis, knockdown of Smad3 using a specific shRNA prevented the RA-mediated stimulation of differentiation and displacement of C/EBPbeta from the Runx2 P1 promoter. Tretinoin 108-110 runt related transcription factor 2 Mus musculus 190-195
21278145-9 2011 LRAT deficiency decreased diethylnitrosamine-induced injury and tumour load and increased the expression of the retinoic acid responsive genes Cyp26a1, RARb and p21, suggesting that the lower tumour load of LRAT-deficient mice was a result of increased retinoid signalling and subsequent p21-mediated inhibition of proliferation. Tretinoin 112-125 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 143-150
21628419-3 2011 We hypothesized that retinoic acid may affect cholesterol homeostasis in rat astrocytes, which regulate cholesterol distribution in the brain, through the up-regulation of cholesterol transporters ATP binding cassette (Abc)a1 and Abcg1. Tretinoin 21-34 ATP binding cassette subfamily G member 1 Rattus norvegicus 230-235
21715427-2 2011 In murine embryonic ovaries and juvenile testes, retinoic acid (RA) induces meiosis via the stimulated by retinoic acid gene 8 (Stra8), but its molecular pathway requires elucidation. Tretinoin 49-62 stimulated by retinoic acid gene 8 Mus musculus 92-126
21715427-2 2011 In murine embryonic ovaries and juvenile testes, retinoic acid (RA) induces meiosis via the stimulated by retinoic acid gene 8 (Stra8), but its molecular pathway requires elucidation. Tretinoin 49-62 stimulated by retinoic acid gene 8 Mus musculus 128-133
21715427-2 2011 In murine embryonic ovaries and juvenile testes, retinoic acid (RA) induces meiosis via the stimulated by retinoic acid gene 8 (Stra8), but its molecular pathway requires elucidation. Tretinoin 64-66 stimulated by retinoic acid gene 8 Mus musculus 92-126
21715427-2 2011 In murine embryonic ovaries and juvenile testes, retinoic acid (RA) induces meiosis via the stimulated by retinoic acid gene 8 (Stra8), but its molecular pathway requires elucidation. Tretinoin 64-66 stimulated by retinoic acid gene 8 Mus musculus 128-133
21480163-5 2011 To determine a possible role of the retinoid-mediated signaling pathway in the pathogenesis of ARM, we investigated whether all-trans retinoic acid (ATRA) affected the expression patterns of PCSK5 and GDF11 in ARM-treated mouse embryos. Tretinoin 134-147 proprotein convertase subtilisin/kexin type 5 Mus musculus 191-196
21480163-5 2011 To determine a possible role of the retinoid-mediated signaling pathway in the pathogenesis of ARM, we investigated whether all-trans retinoic acid (ATRA) affected the expression patterns of PCSK5 and GDF11 in ARM-treated mouse embryos. Tretinoin 149-153 proprotein convertase subtilisin/kexin type 5 Mus musculus 191-196
21480163-12 2011 CONCLUSION: ATRA treatment affected the caudal development in mouse embryos, resulting in anorectal, sacral, and spinal malformations, and inhibited PCSK5 and GDF11 expression in the hindgut region. Tretinoin 12-16 proprotein convertase subtilisin/kexin type 5 Mus musculus 149-154
21659316-2 2011 RA mediates induction of 17 beta-hydroxysteroid dehydrogenase type 2 mRNA, catalyzing the conversion of estradiol to estrone, in endometrium but not endometriosis because of a defect in endometriotic stromal cells. Tretinoin 0-2 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 25-68
21184786-10 2011 At the molecular level, SRC-3 interacts with retinoic receptor alpha (RARalpha) to activate COUP-TFII expression under all-trans retinoic acid (ARTA) treatment. Tretinoin 129-142 nuclear receptor coactivator 3 Homo sapiens 24-29
21184786-10 2011 At the molecular level, SRC-3 interacts with retinoic receptor alpha (RARalpha) to activate COUP-TFII expression under all-trans retinoic acid (ARTA) treatment. Tretinoin 129-142 retinoic acid receptor alpha Homo sapiens 70-78
21184786-10 2011 At the molecular level, SRC-3 interacts with retinoic receptor alpha (RARalpha) to activate COUP-TFII expression under all-trans retinoic acid (ARTA) treatment. Tretinoin 144-148 nuclear receptor coactivator 3 Homo sapiens 24-29
21184786-10 2011 At the molecular level, SRC-3 interacts with retinoic receptor alpha (RARalpha) to activate COUP-TFII expression under all-trans retinoic acid (ARTA) treatment. Tretinoin 144-148 retinoic acid receptor alpha Homo sapiens 70-78
21488975-6 2011 In skin equivalent cultures, all-trans retinoic acid (RA), the major bioactive form of vitamin A in skin, significantly increased type I procollagen and reduced collagenase (matrix metalloproteinases-1, MMP-1). Tretinoin 39-52 matrix metallopeptidase 1 Homo sapiens 130-201
21488975-6 2011 In skin equivalent cultures, all-trans retinoic acid (RA), the major bioactive form of vitamin A in skin, significantly increased type I procollagen and reduced collagenase (matrix metalloproteinases-1, MMP-1). Tretinoin 39-52 matrix metallopeptidase 1 Homo sapiens 203-208
21488975-6 2011 In skin equivalent cultures, all-trans retinoic acid (RA), the major bioactive form of vitamin A in skin, significantly increased type I procollagen and reduced collagenase (matrix metalloproteinases-1, MMP-1). Tretinoin 54-56 matrix metallopeptidase 1 Homo sapiens 130-201
21488975-6 2011 In skin equivalent cultures, all-trans retinoic acid (RA), the major bioactive form of vitamin A in skin, significantly increased type I procollagen and reduced collagenase (matrix metalloproteinases-1, MMP-1). Tretinoin 54-56 matrix metallopeptidase 1 Homo sapiens 203-208
21488975-8 2011 Importantly, RA significantly reduced CCN1 expression in skin equivalent cultures. Tretinoin 13-15 cellular communication network factor 1 Homo sapiens 38-42
21672091-7 2011 Sp1BS-1 and adjacent Sp1-binding sites (Sp1BS-2 and Sp1BS-3) showed enhanced transcriptional activity by RA. Tretinoin 105-107 trans-acting transcription factor 1 Mus musculus 40-47
21672091-7 2011 Sp1BS-1 and adjacent Sp1-binding sites (Sp1BS-2 and Sp1BS-3) showed enhanced transcriptional activity by RA. Tretinoin 105-107 trans-acting transcription factor 1 Mus musculus 52-59
21493725-3 2011 Here, we report that DGL-alpha and DGL-beta may contribute to all-trans-retinoic acid (RA)-induced neurite outgrowth in neuroblastoma Neuro-2a cells through distinct mechanisms. Tretinoin 65-85 diacylglycerol lipase, alpha Mus musculus 21-30
21493725-3 2011 Here, we report that DGL-alpha and DGL-beta may contribute to all-trans-retinoic acid (RA)-induced neurite outgrowth in neuroblastoma Neuro-2a cells through distinct mechanisms. Tretinoin 65-85 diacylglycerol lipase, beta Mus musculus 35-43
21493725-3 2011 Here, we report that DGL-alpha and DGL-beta may contribute to all-trans-retinoic acid (RA)-induced neurite outgrowth in neuroblastoma Neuro-2a cells through distinct mechanisms. Tretinoin 87-89 diacylglycerol lipase, alpha Mus musculus 21-30
21493725-3 2011 Here, we report that DGL-alpha and DGL-beta may contribute to all-trans-retinoic acid (RA)-induced neurite outgrowth in neuroblastoma Neuro-2a cells through distinct mechanisms. Tretinoin 87-89 diacylglycerol lipase, beta Mus musculus 35-43
21493725-4 2011 RA-induced differentiation of Neuro-2a cells was associated with elevations of cellular 2-AG levels and DGL activity, which were accompanied by temporally separated transcription of DGL-alpha and DGL-beta mRNA. Tretinoin 0-2 diacylglycerol lipase, alpha Mus musculus 182-191
21493725-4 2011 RA-induced differentiation of Neuro-2a cells was associated with elevations of cellular 2-AG levels and DGL activity, which were accompanied by temporally separated transcription of DGL-alpha and DGL-beta mRNA. Tretinoin 0-2 diacylglycerol lipase, beta Mus musculus 196-204
21493725-7 2011 After RA-induced differentiation, both DGL-alpha- and DGL-beta-green fluorescent protein were distributed also in neurites but in distinguishable patterns. Tretinoin 6-8 diacylglycerol lipase, alpha Mus musculus 39-48
21493725-7 2011 After RA-induced differentiation, both DGL-alpha- and DGL-beta-green fluorescent protein were distributed also in neurites but in distinguishable patterns. Tretinoin 6-8 diacylglycerol lipase, beta Mus musculus 54-62
21422471-6 2011 All-trans retinoic acid, which targets PML-RARalpha for degradation through its RARalpha moiety, synergizes with arsenic in eliminating leukemia-initiating cells. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 39-42
21422471-6 2011 All-trans retinoic acid, which targets PML-RARalpha for degradation through its RARalpha moiety, synergizes with arsenic in eliminating leukemia-initiating cells. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 43-51
21422471-6 2011 All-trans retinoic acid, which targets PML-RARalpha for degradation through its RARalpha moiety, synergizes with arsenic in eliminating leukemia-initiating cells. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 80-88
21507931-5 2011 HOXC9 expression is upregulated by retinoic acid (RA), and knockdown of HOXC9 expression confers resistance to RA-induced growth arrest and differentiation. Tretinoin 35-48 homeobox C9 Homo sapiens 0-5
21507931-5 2011 HOXC9 expression is upregulated by retinoic acid (RA), and knockdown of HOXC9 expression confers resistance to RA-induced growth arrest and differentiation. Tretinoin 50-52 homeobox C9 Homo sapiens 0-5
21507931-5 2011 HOXC9 expression is upregulated by retinoic acid (RA), and knockdown of HOXC9 expression confers resistance to RA-induced growth arrest and differentiation. Tretinoin 111-113 homeobox C9 Homo sapiens 72-77
21507931-7 2011 These findings identified HOXC9 as a key regulator of neuroblastoma differentiation and suggested a therapeutic strategy for RA-resistant neuroblastomas through epigenetic activation of HOXC9 expression. Tretinoin 125-127 homeobox C9 Homo sapiens 26-31
21507931-7 2011 These findings identified HOXC9 as a key regulator of neuroblastoma differentiation and suggested a therapeutic strategy for RA-resistant neuroblastomas through epigenetic activation of HOXC9 expression. Tretinoin 125-127 homeobox C9 Homo sapiens 186-191
21605549-8 2011 These data suggest that RA has inhibitory effects on the BMP4 induction of C3H10T1/2 adipocytic commitment via downregulating Smad/p38MAPK signaling. Tretinoin 24-26 SMAD family member 1 Mus musculus 126-130
21557943-6 2011 Finally, we have shown that all-trans retinoic acid (ATRA), a known inducer of CD38 transcription, can rescue low CD38 expressing LBC lines derived from ASD subjects and restore normal levels of transcription of this ectoenzyme providing "proof of principle" in a peripheral model that retinoids are potential therapeutic agents in ASD. Tretinoin 38-51 CD38 molecule Homo sapiens 79-83
21557943-6 2011 Finally, we have shown that all-trans retinoic acid (ATRA), a known inducer of CD38 transcription, can rescue low CD38 expressing LBC lines derived from ASD subjects and restore normal levels of transcription of this ectoenzyme providing "proof of principle" in a peripheral model that retinoids are potential therapeutic agents in ASD. Tretinoin 38-51 CD38 molecule Homo sapiens 114-118
21557943-6 2011 Finally, we have shown that all-trans retinoic acid (ATRA), a known inducer of CD38 transcription, can rescue low CD38 expressing LBC lines derived from ASD subjects and restore normal levels of transcription of this ectoenzyme providing "proof of principle" in a peripheral model that retinoids are potential therapeutic agents in ASD. Tretinoin 53-57 CD38 molecule Homo sapiens 79-83
21557943-6 2011 Finally, we have shown that all-trans retinoic acid (ATRA), a known inducer of CD38 transcription, can rescue low CD38 expressing LBC lines derived from ASD subjects and restore normal levels of transcription of this ectoenzyme providing "proof of principle" in a peripheral model that retinoids are potential therapeutic agents in ASD. Tretinoin 53-57 CD38 molecule Homo sapiens 114-118
21498506-2 2011 We show here that Amer1 directly interacts with the armadillo repeats of beta-catenin via a domain consisting of repeated arginine-glutamic acid-alanine (REA) motifs, and that Amer1 assembles the beta-catenin destruction complex at the plasma membrane by recruiting beta-catenin, adenomatous polyposis coli, and Axin/Conductin. Tretinoin 154-157 APC membrane recruitment protein 1 Homo sapiens 18-23
21498506-2 2011 We show here that Amer1 directly interacts with the armadillo repeats of beta-catenin via a domain consisting of repeated arginine-glutamic acid-alanine (REA) motifs, and that Amer1 assembles the beta-catenin destruction complex at the plasma membrane by recruiting beta-catenin, adenomatous polyposis coli, and Axin/Conductin. Tretinoin 154-157 catenin beta 1 Homo sapiens 73-85
21498506-2 2011 We show here that Amer1 directly interacts with the armadillo repeats of beta-catenin via a domain consisting of repeated arginine-glutamic acid-alanine (REA) motifs, and that Amer1 assembles the beta-catenin destruction complex at the plasma membrane by recruiting beta-catenin, adenomatous polyposis coli, and Axin/Conductin. Tretinoin 154-157 APC membrane recruitment protein 1 Homo sapiens 176-181
21325480-0 2011 Hepatitis B virus X protein overcomes all-trans retinoic acid-induced cellular senescence by downregulating levels of p16 and p21 via DNA methylation. Tretinoin 48-61 H3 histone pseudogene 16 Homo sapiens 126-129
21325480-2 2011 Here, it was shown that HBx overcomes cellular senescence provoked by all-trans retinoic acid (ATRA) in HepG2 cells, as demonstrated by the impaired induction of irreversible G(1) arrest and senescence-associated beta-galactosidase activity by ATRA in the presence of HBx. Tretinoin 80-93 X protein Hepatitis B virus 24-27
21325480-2 2011 Here, it was shown that HBx overcomes cellular senescence provoked by all-trans retinoic acid (ATRA) in HepG2 cells, as demonstrated by the impaired induction of irreversible G(1) arrest and senescence-associated beta-galactosidase activity by ATRA in the presence of HBx. Tretinoin 95-99 X protein Hepatitis B virus 24-27
21325480-2 2011 Here, it was shown that HBx overcomes cellular senescence provoked by all-trans retinoic acid (ATRA) in HepG2 cells, as demonstrated by the impaired induction of irreversible G(1) arrest and senescence-associated beta-galactosidase activity by ATRA in the presence of HBx. Tretinoin 244-248 X protein Hepatitis B virus 24-27
21325480-4 2011 In addition, HBx suppressed ATRA-mediated induction of p16 and p21 in HepG2 cells via promoter hypermethylation, resulting in inactivation of retinoblastoma protein. Tretinoin 28-32 X protein Hepatitis B virus 13-16
21325480-4 2011 In addition, HBx suppressed ATRA-mediated induction of p16 and p21 in HepG2 cells via promoter hypermethylation, resulting in inactivation of retinoblastoma protein. Tretinoin 28-32 H3 histone pseudogene 16 Homo sapiens 63-66
21325480-5 2011 Furthermore, the ability of HBx to overcome ATRA-induced cellular senescence almost completely disappeared when the levels of p16 and p21 in the HBx-expressing cells became similar to those in the control cells by complementation in the former by exogenous expression, knockdown of their expression in the latter using specific small interfering RNA or treatment with a DNA methylation inhibitor, 5-Aza-2"-deoxycytidine. Tretinoin 44-48 X protein Hepatitis B virus 28-31
21325480-5 2011 Furthermore, the ability of HBx to overcome ATRA-induced cellular senescence almost completely disappeared when the levels of p16 and p21 in the HBx-expressing cells became similar to those in the control cells by complementation in the former by exogenous expression, knockdown of their expression in the latter using specific small interfering RNA or treatment with a DNA methylation inhibitor, 5-Aza-2"-deoxycytidine. Tretinoin 44-48 H3 histone pseudogene 16 Homo sapiens 134-137
21385575-4 2011 We now show that Hoxb1, Hoxa1, and Hoxa3, as downstream RA targets, are expressed in distinct sub-domains within the SHF. Tretinoin 56-58 homeobox B1 Homo sapiens 17-22
21360789-1 2011 Retinoic acid (RA) is purported to be required for expression of genes controlling proximodistal (Meis2) or anteroposterior (Shh) limb patterning. Tretinoin 0-13 sonic hedgehog Mus musculus 125-128
21360789-1 2011 Retinoic acid (RA) is purported to be required for expression of genes controlling proximodistal (Meis2) or anteroposterior (Shh) limb patterning. Tretinoin 15-17 sonic hedgehog Mus musculus 125-128
21509893-2 2011 An RA signal leads to transcription of tbx5 in forelimb precursors which is necessary and sufficient for limb development. Tretinoin 3-5 T-box transcription factor 5a Danio rerio 39-43
21509893-5 2011 Specifically, an early gastrula stage RA signal triggers the process that leads to determination of tbx5-expressing limb precursors, while a later somitogenesis stage RA signal maintains these precursors. Tretinoin 38-40 T-box transcription factor 5a Danio rerio 100-104
20740690-5 2011 In the results of immunocytochemistry, rMDSC treated with RA showed abundant positive cells against the neuronal markers neuronal-specific enolase (NSE) and tubulin-betaIII (Tuj1). Tretinoin 58-60 enolase 2 Rattus norvegicus 121-146
20740690-5 2011 In the results of immunocytochemistry, rMDSC treated with RA showed abundant positive cells against the neuronal markers neuronal-specific enolase (NSE) and tubulin-betaIII (Tuj1). Tretinoin 58-60 enolase 2 Rattus norvegicus 148-151
21339756-3 2011 The knockdown of beta-catenin, using a short hairpin RNA (shRNA) lentiviral approach, accelerates all-trans retinoic acid-induced differentiation and impairs the proliferation of HL60 leukemic cell line. Tretinoin 108-121 catenin beta 1 Homo sapiens 17-29
21729599-4 2011 The apoptosis rate of cells treated with different concentration of MAT combined with 1 micromol/L ATRA was tested by flow cytometry with Annexin V/PI staining. Tretinoin 99-103 annexin A5 Homo sapiens 138-147
21362455-6 2011 Overexpressed p53 induces marked DUOXA1 expression in P19 cells and intensifies neuronal differentiation in the presence of retinoic acid, which suggests that p53 and DUOXA1 possess a neural differentiation potential. Tretinoin 124-137 transformation related protein 53, pseudogene Mus musculus 14-17
21362455-6 2011 Overexpressed p53 induces marked DUOXA1 expression in P19 cells and intensifies neuronal differentiation in the presence of retinoic acid, which suggests that p53 and DUOXA1 possess a neural differentiation potential. Tretinoin 124-137 transformation related protein 53, pseudogene Mus musculus 159-162
21497760-3 2011 By analyzing Pbx1/Pbx2 and Hoxa1/Pbx1 null mice, we found that Raldh2 is itself under the transcriptional control of these factors and that the resulting RA-deficient phenotypes can be partially rescued by exogenous RA. Tretinoin 154-156 pre B cell leukemia homeobox 1 Mus musculus 13-17
21497760-3 2011 By analyzing Pbx1/Pbx2 and Hoxa1/Pbx1 null mice, we found that Raldh2 is itself under the transcriptional control of these factors and that the resulting RA-deficient phenotypes can be partially rescued by exogenous RA. Tretinoin 154-156 pre B cell leukemia homeobox 1 Mus musculus 33-37
21091440-0 2011 Retinoic acid induces myoblasts transdifferentiation into premeiotic Stra8-positive cells. Tretinoin 0-13 stimulated by retinoic acid gene 8 Mus musculus 69-74
21091440-6 2011 Flow cytometry results indicated that up to 20% of RA-induced C2C12 cells were Stra8-positive. Tretinoin 51-53 stimulated by retinoic acid gene 8 Mus musculus 79-84
20857408-0 2011 PP2A interaction with Rb2/p130 mediates translocation of Rb2/p130 into the nucleus in all-trans retinoic acid-treated ovarian carcinoma cells. Tretinoin 96-109 protein phosphatase 2 phosphatase activator Homo sapiens 0-4
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 protein phosphatase 2 phosphatase activator Homo sapiens 34-38
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 protein phosphatase 2 phosphatase activator Homo sapiens 127-131
22254103-5 2011 The activity of the catabolic CYP26 enzymes in determining what tissues have access to RA has emerged as a key regulatory mechanism, and helps to explain why exogenous RA can rescue many vitamin A deficiency defects. Tretinoin 87-89 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 30-35
22254103-5 2011 The activity of the catabolic CYP26 enzymes in determining what tissues have access to RA has emerged as a key regulatory mechanism, and helps to explain why exogenous RA can rescue many vitamin A deficiency defects. Tretinoin 168-170 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 30-35
21532733-3 2011 Neurospheres generated from the lateral ganglionic eminence (LGE), where Raldh3 is highly expressed, produce endogenous RA, which is required for differentiation to GABAergic neurons. Tretinoin 120-122 aldehyde dehydrogenase 1 family member A3 Homo sapiens 73-79
21360626-0 2011 Promyelocytic leukemia protein in retinoic acid-induced chromatin remodeling of Oct4 gene promoter. Tretinoin 34-47 PML nuclear body scaffold Homo sapiens 0-30
21360626-0 2011 Promyelocytic leukemia protein in retinoic acid-induced chromatin remodeling of Oct4 gene promoter. Tretinoin 34-47 POU class 5 homeobox 1 Homo sapiens 80-84
21360626-3 2011 Retinoic acid (RA) rapidly downregulates Pml, resulting in the replacement of BRGC with Brm-containing remodeling complex, disassociation of SF1 and Sp1, retaining of TR2, recruitment of receptor-interaction protein 140, G9a and HP1gamma, and sequential insertion of two nucleosomes on CR1 that progressively displays repressive heterochromatin marks. Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 41-44
21360626-3 2011 Retinoic acid (RA) rapidly downregulates Pml, resulting in the replacement of BRGC with Brm-containing remodeling complex, disassociation of SF1 and Sp1, retaining of TR2, recruitment of receptor-interaction protein 140, G9a and HP1gamma, and sequential insertion of two nucleosomes on CR1 that progressively displays repressive heterochromatin marks. Tretinoin 0-13 nuclear receptor subfamily 2 group C member 1 Homo sapiens 167-170
21419664-0 2011 Essential role for retinoic acid in the promotion of CD4(+) T cell effector responses via retinoic acid receptor alpha. Tretinoin 19-32 retinoic acid receptor alpha Homo sapiens 90-118
21262915-0 2011 Activation of the aryl hydrocarbon receptor AhR Promotes retinoic acid-induced differentiation of myeloblastic leukemia cells by restricting expression of the stem cell transcription factor Oct4. Tretinoin 57-70 POU class 5 homeobox 1 Homo sapiens 190-194
21262915-7 2011 RA upregulated AhR and downregulated Oct4 during differentiation of HL-60 promyelocytic leukemia cells. Tretinoin 0-2 POU class 5 homeobox 1 Homo sapiens 37-41
21262915-11 2011 Consistent with the hypothesized importance of Oct4 downregulation for differentiation, parental cells rendered resistant to RA by biweekly high RA exposure displayed elevated Oct4 levels that failed to be downregulated. Tretinoin 145-147 POU class 5 homeobox 1 Homo sapiens 47-51
21048796-6 2011 Addition of retinoic acid, boosted by the pancreatic endoderm inducer indolactam V (ILV), yielded pancreatic progenitors expressing pancreatic and duodenal homeobox 1 (PDX1), neurogenin 3 (NGN3) and neurogenic differentiation 1 (NEUROD1) markers. Tretinoin 12-25 neurogenin 3 Homo sapiens 175-187
21048796-6 2011 Addition of retinoic acid, boosted by the pancreatic endoderm inducer indolactam V (ILV), yielded pancreatic progenitors expressing pancreatic and duodenal homeobox 1 (PDX1), neurogenin 3 (NGN3) and neurogenic differentiation 1 (NEUROD1) markers. Tretinoin 12-25 neurogenin 3 Homo sapiens 189-193
21048796-6 2011 Addition of retinoic acid, boosted by the pancreatic endoderm inducer indolactam V (ILV), yielded pancreatic progenitors expressing pancreatic and duodenal homeobox 1 (PDX1), neurogenin 3 (NGN3) and neurogenic differentiation 1 (NEUROD1) markers. Tretinoin 12-25 neuronal differentiation 1 Homo sapiens 199-227
21048796-6 2011 Addition of retinoic acid, boosted by the pancreatic endoderm inducer indolactam V (ILV), yielded pancreatic progenitors expressing pancreatic and duodenal homeobox 1 (PDX1), neurogenin 3 (NGN3) and neurogenic differentiation 1 (NEUROD1) markers. Tretinoin 12-25 neuronal differentiation 1 Homo sapiens 229-236
21148082-2 2011 We investigated the clinical significance of CD56 expression in a large series of patients with APL treated with all-trans retinoic acid and anthracycline-based regimens. Tretinoin 123-136 neural cell adhesion molecule 1 Homo sapiens 45-49
21148082-9 2011 In summary, CD56 expression is associated with the coexpression of immaturity-associated and T-cell antigens and is an independent adverse prognostic factor for relapse in patients with APL treated with all-trans-retinoic acid plus idarubicin-derived regimens. Tretinoin 203-226 neural cell adhesion molecule 1 Homo sapiens 12-16
22184527-4 2011 In the acute promyelocytic leukemia cell line NB4 however, sumoylated p42 remains persistently bound to the LF promoter following ATRA-induction. Tretinoin 130-134 cyclin dependent kinase 20 Homo sapiens 70-73
21206504-10 2011 Treatment with atRA significantly reduced the expressions of PAI-1 and alpha-SMA. Tretinoin 15-19 actin gamma 2, smooth muscle Rattus norvegicus 71-80
20826732-3 2011 Recent studies have revealed the importance of retinoic acid and one of its target genes, Stra8, in meiotic initiation in both sexes. Tretinoin 47-60 stimulated by retinoic acid gene 8 Mus musculus 90-95
21207215-3 2011 With the differentiation of cells, enhanced expression of IL-3Rbeta was also observed in all-trans-retinoic acid (ATRA)-induced NB4 cells. Tretinoin 93-112 colony stimulating factor 2 receptor subunit beta Homo sapiens 58-67
21207215-3 2011 With the differentiation of cells, enhanced expression of IL-3Rbeta was also observed in all-trans-retinoic acid (ATRA)-induced NB4 cells. Tretinoin 114-118 colony stimulating factor 2 receptor subunit beta Homo sapiens 58-67
21207215-4 2011 To unravel the role of IL-3Rbeta upregulation in NB4 cells induced with ATRA, we knocked down IL-3Rbeta expression by RNA interference (RNAi). Tretinoin 72-76 colony stimulating factor 2 receptor subunit beta Homo sapiens 23-32
21207215-5 2011 Knockdown of IL-3Rbeta resulted in decreased proliferation in NB4 cells induced with or without ATRA, observed by cell growth curves, colony formation assays and cell cycle analysis. Tretinoin 96-100 colony stimulating factor 2 receptor subunit beta Homo sapiens 13-22
21207215-10 2011 Together, these results suggest that abnormalities of IL-3Rbeta expression were observed in APL; knockdown of IL-3Rbeta inhibited the proliferation of NB4 cells with or without ATRA, but no effect was detected in the cellular differentiation. Tretinoin 177-181 colony stimulating factor 2 receptor subunit beta Homo sapiens 110-119
20945414-5 2011 Further studies demonstrated that the synergistic differentiating effects of ATRA and proteasome inhibitors might be associated with the protection of retinoic acid receptor alpha (RARalpha) from degradation by the ubiquitin-proteasome pathway (UPP). Tretinoin 77-81 retinoic acid receptor alpha Homo sapiens 151-179
20945414-5 2011 Further studies demonstrated that the synergistic differentiating effects of ATRA and proteasome inhibitors might be associated with the protection of retinoic acid receptor alpha (RARalpha) from degradation by the ubiquitin-proteasome pathway (UPP). Tretinoin 77-81 retinoic acid receptor alpha Homo sapiens 181-189
22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Tretinoin 34-38 retinoic acid receptor alpha Homo sapiens 121-129
22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Tretinoin 34-38 H3 histone pseudogene 16 Homo sapiens 160-163
21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 45-58 forkhead box P3 Mus musculus 117-122
21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 60-64 forkhead box P3 Mus musculus 117-122
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 CD28 antigen Mus musculus 103-107
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 forkhead box P3 Mus musculus 166-171
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 forkhead box P3 Mus musculus 213-218
21931768-7 2011 Conversely, atRA markedly increased ERK1/2 activation, and blockade of ERK1/2 signaling completely abolished the enhanced effects of atRA on Foxp3 expression. Tretinoin 133-137 forkhead box P3 Mus musculus 141-146
21419270-6 2011 RA itself is essential for the GM-CSF-induced RALDH2 expression. Tretinoin 0-2 colony stimulating factor 2 Homo sapiens 31-37
20739655-3 2010 Pharicin B also enhances ATRA-dependent the transcriptional activity of RAR-alpha protein in the promyelocytic leukemia-RARalpha-positive APL cell line NB4 cells. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 72-81
20601236-7 2010 In the presence of the soluble factors retinoic acid and bone morphogenetic protein-4 the ESCs differentiated towards the ectodermal lineage on the ECM microarray with differential ECM effects. Tretinoin 39-52 multimerin 1 Homo sapiens 148-151
20601236-7 2010 In the presence of the soluble factors retinoic acid and bone morphogenetic protein-4 the ESCs differentiated towards the ectodermal lineage on the ECM microarray with differential ECM effects. Tretinoin 39-52 multimerin 1 Homo sapiens 181-184
20826193-2 2010 RA induces cell differentiation through retinoic acid receptor (RAR) transcription factors. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 40-62
20826193-2 2010 RA induces cell differentiation through retinoic acid receptor (RAR) transcription factors. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 64-67
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 cellular communication network factor 2 Rattus norvegicus 200-204
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 TIMP metallopeptidase inhibitor 2 Rattus norvegicus 221-227
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 mitogen-activated protein kinase 8 Rattus norvegicus 352-355
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 cellular communication network factor 2 Rattus norvegicus 243-247
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 TIMP metallopeptidase inhibitor 2 Rattus norvegicus 264-270
20661648-0 2010 C/EBPepsilon participates in all-trans retinoic acid induction of PI3Kgamma in U937 cells via an intronic matrix attachment region sequence. Tretinoin 39-52 CCAAT enhancer binding protein epsilon Homo sapiens 0-12
20661648-0 2010 C/EBPepsilon participates in all-trans retinoic acid induction of PI3Kgamma in U937 cells via an intronic matrix attachment region sequence. Tretinoin 39-52 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 66-75
20661648-1 2010 ATRA (all-trans retinoic acid) regulates gene expression by binding as a ligand to its specific receptors like C/EBPepsilon which is directly induced. Tretinoin 0-4 CCAAT enhancer binding protein epsilon Homo sapiens 111-123
20661648-1 2010 ATRA (all-trans retinoic acid) regulates gene expression by binding as a ligand to its specific receptors like C/EBPepsilon which is directly induced. Tretinoin 6-29 CCAAT enhancer binding protein epsilon Homo sapiens 111-123
20661648-2 2010 In the U937 cell line, PI3Kgamma is selectively induced over other PI3Ks by ATRA, although the mechanism is still unclear. Tretinoin 76-80 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 23-32
20661648-3 2010 Here, we show that C/EBPepsilon and PI3Kgamma are induced in U937 cells by ATRA both in levels of mRNA and protein. Tretinoin 75-79 CCAAT enhancer binding protein epsilon Homo sapiens 19-31
20661648-3 2010 Here, we show that C/EBPepsilon and PI3Kgamma are induced in U937 cells by ATRA both in levels of mRNA and protein. Tretinoin 75-79 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 36-45
21152046-3 2010 To address the question of the effect of rexinoid antagonists on RAR/RXR function, we solved the crystal structure of the heterodimer formed by the ligand binding domain (LBD) of the RARalpha bound to its natural agonist ligand (all-trans retinoic acid, atRA) and RXRalpha bound to a rexinoid antagonist (LG100754). Tretinoin 239-252 retinoic acid receptor alpha Homo sapiens 183-191
21152046-3 2010 To address the question of the effect of rexinoid antagonists on RAR/RXR function, we solved the crystal structure of the heterodimer formed by the ligand binding domain (LBD) of the RARalpha bound to its natural agonist ligand (all-trans retinoic acid, atRA) and RXRalpha bound to a rexinoid antagonist (LG100754). Tretinoin 254-258 retinoic acid receptor alpha Homo sapiens 183-191
20801112-4 2010 We show that diminished expression of Cyp26a1, a retinoic acid inactivating enzyme, and concomitant elevation of retinoic acid activity in the caudal region of Gdf11(-/-) embryos may account for this phenomenon. Tretinoin 49-62 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 38-45
20719946-9 2010 Retinoic acid, a known ligand for the NCoR complex, derepresses gene 50 expression and enhances MHV68 lytic replication. Tretinoin 0-13 nuclear receptor corepressor 1 Homo sapiens 38-42
20719946-10 2010 Moreover, HDAC3, HDAC4, and NCoR act on the gene 50 promoter and are recruited to this promoter in a retinoic acid-responsive manner. Tretinoin 101-114 histone deacetylase 4 Homo sapiens 17-22
20719946-10 2010 Moreover, HDAC3, HDAC4, and NCoR act on the gene 50 promoter and are recruited to this promoter in a retinoic acid-responsive manner. Tretinoin 101-114 nuclear receptor corepressor 1 Homo sapiens 28-32
20949013-11 2010 Furthermore, RA treatment suppressed the expression of the transcription factor nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and increased the expression of interferon regulatory factor-8 (IRF-8) in osteoclast progenitors via RARs. Tretinoin 13-15 interferon regulatory factor 8 Homo sapiens 171-201
20949013-11 2010 Furthermore, RA treatment suppressed the expression of the transcription factor nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and increased the expression of interferon regulatory factor-8 (IRF-8) in osteoclast progenitors via RARs. Tretinoin 13-15 interferon regulatory factor 8 Homo sapiens 203-208
20547764-2 2010 ZFP423 is a known interactor of SMAD1-SMAD4 and of Collier/Olf-1/EBF proteins, and acts as a modifier of retinoic acid-induced differentiation. Tretinoin 105-118 zinc finger protein 423 L homeolog Xenopus laevis 0-6
20547764-2 2010 ZFP423 is a known interactor of SMAD1-SMAD4 and of Collier/Olf-1/EBF proteins, and acts as a modifier of retinoic acid-induced differentiation. Tretinoin 105-118 SMAD family member 1 S homeolog Xenopus laevis 32-37
20547764-2 2010 ZFP423 is a known interactor of SMAD1-SMAD4 and of Collier/Olf-1/EBF proteins, and acts as a modifier of retinoic acid-induced differentiation. Tretinoin 105-118 SMAD family member 4, gene 1 L homeolog Xenopus laevis 38-43
20574048-1 2010 Treatment of acute promyelocytic leukemia (APL) with all-trans retinoic acid and/or arsenic trioxide represents a paradigm in targeted cancer therapy because these drugs cause clinical remission by affecting the stability of the fusion oncoprotein promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARA). Tretinoin 63-76 PML nuclear body scaffold Homo sapiens 272-275
20574048-1 2010 Treatment of acute promyelocytic leukemia (APL) with all-trans retinoic acid and/or arsenic trioxide represents a paradigm in targeted cancer therapy because these drugs cause clinical remission by affecting the stability of the fusion oncoprotein promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARA). Tretinoin 63-76 retinoic acid receptor alpha Homo sapiens 277-305
20574048-1 2010 Treatment of acute promyelocytic leukemia (APL) with all-trans retinoic acid and/or arsenic trioxide represents a paradigm in targeted cancer therapy because these drugs cause clinical remission by affecting the stability of the fusion oncoprotein promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARA). Tretinoin 63-76 retinoic acid receptor alpha Homo sapiens 307-311
20574048-4 2010 We found that both all-trans retinoic acid and arsenic trioxide induce autophagy via the mammalian target of rapamycin pathway in APL cells and that autophagic degradation contributes significantly both to the basal turnover as well as the therapy-induced proteolysis of PML/RARA. Tretinoin 29-42 PML nuclear body scaffold Homo sapiens 271-274
20574048-4 2010 We found that both all-trans retinoic acid and arsenic trioxide induce autophagy via the mammalian target of rapamycin pathway in APL cells and that autophagic degradation contributes significantly both to the basal turnover as well as the therapy-induced proteolysis of PML/RARA. Tretinoin 29-42 retinoic acid receptor alpha Homo sapiens 275-279
20709019-2 2010 The formation of the most active retinoid, all-trans-retinoic acid (RA) by oxidation of retinal is catalyzed by aldehyde dehydrogenases (ALDH), of which ALDH1A3 has been shown to be most efficient. Tretinoin 43-66 aldehyde dehydrogenase 1 family member A3 Homo sapiens 137-141
20709019-2 2010 The formation of the most active retinoid, all-trans-retinoic acid (RA) by oxidation of retinal is catalyzed by aldehyde dehydrogenases (ALDH), of which ALDH1A3 has been shown to be most efficient. Tretinoin 43-66 aldehyde dehydrogenase 1 family member A3 Homo sapiens 153-160
20709019-2 2010 The formation of the most active retinoid, all-trans-retinoic acid (RA) by oxidation of retinal is catalyzed by aldehyde dehydrogenases (ALDH), of which ALDH1A3 has been shown to be most efficient. Tretinoin 68-70 aldehyde dehydrogenase 1 family member A3 Homo sapiens 137-141
20709019-2 2010 The formation of the most active retinoid, all-trans-retinoic acid (RA) by oxidation of retinal is catalyzed by aldehyde dehydrogenases (ALDH), of which ALDH1A3 has been shown to be most efficient. Tretinoin 68-70 aldehyde dehydrogenase 1 family member A3 Homo sapiens 153-160
20709019-5 2010 Among a panel of ALDH genes, only ALDH1A3 was upregulated by RA in primary keratinocytes. Tretinoin 61-63 aldehyde dehydrogenase 1 family member A3 Homo sapiens 17-21
20709019-5 2010 Among a panel of ALDH genes, only ALDH1A3 was upregulated by RA in primary keratinocytes. Tretinoin 61-63 aldehyde dehydrogenase 1 family member A3 Homo sapiens 34-41
20709019-6 2010 RA increased the expression of ALDH1A3 also in organotypic human skin cultures and in an epidermal explant in vitro whereas no upregulation was detected in dermal fibroblasts and HeLa cells. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A3 Homo sapiens 31-38
20709019-7 2010 Our results indicate that the regulation of the retinoic acid metabolism in the epidermis involves transcriptional activation of ALDH1A3, possibly representing a positive feedback loop, which enhances the effect of exogenous RA. Tretinoin 48-61 aldehyde dehydrogenase 1 family member A3 Homo sapiens 129-136
20709019-7 2010 Our results indicate that the regulation of the retinoic acid metabolism in the epidermis involves transcriptional activation of ALDH1A3, possibly representing a positive feedback loop, which enhances the effect of exogenous RA. Tretinoin 225-227 aldehyde dehydrogenase 1 family member A3 Homo sapiens 129-136
20828405-7 2010 RESULTS: Our Gene Set Enrichment Analysis results identify Wnt and retinoic acid signaling as likely downstream targets of tbx16 in the developing zebrafish intermediate mesoderm, the site of primitive red blood cell formation. Tretinoin 67-80 T-box transcription factor 16 Danio rerio 123-128
20828405-8 2010 In addition, such results identify retinoic acid signaling as a downstream target of tbx16 in the developing zebrafish posterior somites. Tretinoin 35-48 T-box transcription factor 16 Danio rerio 85-90
20564173-3 2010 Moreover, ELF-MF- and ATRA-treated cells showed more differentiated morphological traits (a higher neurite number/cell, an increased neurite length), together with a significant increase of mRNA levels of p21(WAF1/CIP1) and cdk5 genes, both involved in neuronal differentiation. Tretinoin 22-26 cyclin dependent kinase 5 Homo sapiens 224-228
20615082-0 2010 Arsenic trioxide cooperates with all trans retinoic acid to enhance mitogen-activated protein kinase activation and differentiation in PML-RARalpha negative human myeloblastic leukemia cells. Tretinoin 43-56 PML nuclear body scaffold Homo sapiens 135-138
20615082-0 2010 Arsenic trioxide cooperates with all trans retinoic acid to enhance mitogen-activated protein kinase activation and differentiation in PML-RARalpha negative human myeloblastic leukemia cells. Tretinoin 43-56 retinoic acid receptor alpha Homo sapiens 139-147
20615082-1 2010 Arsenic trioxide (ATO) synergistically promotes all trans retinoic acid (ATRA)-induced differentiation of PML-RARalpha negative HL-60 myeloblastic leukemia cells. Tretinoin 58-71 PML nuclear body scaffold Homo sapiens 106-109
20615082-1 2010 Arsenic trioxide (ATO) synergistically promotes all trans retinoic acid (ATRA)-induced differentiation of PML-RARalpha negative HL-60 myeloblastic leukemia cells. Tretinoin 58-71 retinoic acid receptor alpha Homo sapiens 110-118
20615082-1 2010 Arsenic trioxide (ATO) synergistically promotes all trans retinoic acid (ATRA)-induced differentiation of PML-RARalpha negative HL-60 myeloblastic leukemia cells. Tretinoin 73-77 PML nuclear body scaffold Homo sapiens 106-109
20615082-1 2010 Arsenic trioxide (ATO) synergistically promotes all trans retinoic acid (ATRA)-induced differentiation of PML-RARalpha negative HL-60 myeloblastic leukemia cells. Tretinoin 73-77 retinoic acid receptor alpha Homo sapiens 110-118
20727175-0 2010 Retinoic acid accelerates downregulation of the Xist repressor, Oct4, and increases the likelihood of Xist activation when Tsix is deficient. Tretinoin 0-13 X inactive specific transcript Homo sapiens 48-52
20727175-0 2010 Retinoic acid accelerates downregulation of the Xist repressor, Oct4, and increases the likelihood of Xist activation when Tsix is deficient. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 64-68
20727175-0 2010 Retinoic acid accelerates downregulation of the Xist repressor, Oct4, and increases the likelihood of Xist activation when Tsix is deficient. Tretinoin 0-13 X inactive specific transcript Homo sapiens 102-106
20727175-7 2010 RESULTS: We compared suspension and cell-adhesion cultures in the presence or absence of RA and find that RA significantly impacts Xist expression in Tsix-mutant male cells. Tretinoin 106-108 X inactive specific transcript Homo sapiens 131-135
20727175-8 2010 Whereas the standard embryoid body method infrequently leads to ectopic Xist expression, adding RA generates a significant number of Xist-positive male cells. Tretinoin 96-98 X inactive specific transcript Homo sapiens 133-137
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 27-29 X inactive specific transcript Homo sapiens 33-37
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 27-29 POU class 5 homeobox 1 Homo sapiens 70-74
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 27-29 X inactive specific transcript Homo sapiens 134-138
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 41-43 X inactive specific transcript Homo sapiens 33-37
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 41-43 POU class 5 homeobox 1 Homo sapiens 70-74
20727175-11 2010 We attribute the effect of RA on Xist to RA"s repressive influence on Oct4, a pluripotency factor recently shown to regulate Tsix and Xist. Tretinoin 41-43 X inactive specific transcript Homo sapiens 134-138
20727175-15 2010 CONCLUSIONS: We conclude that RA treatment leads to premature downregulation of Oct4 and partial derepression of Xist irrespective of X-chromosome counting. Tretinoin 30-32 POU class 5 homeobox 1 Homo sapiens 80-84
20727175-15 2010 CONCLUSIONS: We conclude that RA treatment leads to premature downregulation of Oct4 and partial derepression of Xist irrespective of X-chromosome counting. Tretinoin 30-32 X inactive specific transcript Homo sapiens 113-117
20727175-16 2010 RA-induced Xist clusters in male cells do not result in global or stable silencing, and excess cell death is not observed. Tretinoin 0-2 X inactive specific transcript Homo sapiens 11-15
20493835-0 2010 Beneficial effect of all-trans retinoic acid (ATRA) on glomerulosclerosis rats via the down-regulation of the expression of alpha-smooth muscle actin: a comparative study between ATRA and benazepril. Tretinoin 21-44 actin gamma 2, smooth muscle Rattus norvegicus 124-149
20493835-0 2010 Beneficial effect of all-trans retinoic acid (ATRA) on glomerulosclerosis rats via the down-regulation of the expression of alpha-smooth muscle actin: a comparative study between ATRA and benazepril. Tretinoin 46-50 actin gamma 2, smooth muscle Rattus norvegicus 124-149
20493835-0 2010 Beneficial effect of all-trans retinoic acid (ATRA) on glomerulosclerosis rats via the down-regulation of the expression of alpha-smooth muscle actin: a comparative study between ATRA and benazepril. Tretinoin 179-183 actin gamma 2, smooth muscle Rattus norvegicus 124-149
20723292-7 2010 The c-myc expression of HL-60 cells in ATRA + hucMSC group was lower than that in ATRA group (p < 0.05). Tretinoin 39-43 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9
20723292-7 2010 The c-myc expression of HL-60 cells in ATRA + hucMSC group was lower than that in ATRA group (p < 0.05). Tretinoin 82-86 MYC proto-oncogene, bHLH transcription factor Homo sapiens 4-9
20689834-8 2010 We find that both 9CRA and ATRA effectively induce early osteogenic marker, such as alkaline phosphatase (ALP), and late osteogenic markers, such as osteopontin (OPN) and osteocalcin (OC). Tretinoin 27-31 bone gamma-carboxyglutamate protein 2 Mus musculus 171-182
20689834-8 2010 We find that both 9CRA and ATRA effectively induce early osteogenic marker, such as alkaline phosphatase (ALP), and late osteogenic markers, such as osteopontin (OPN) and osteocalcin (OC). Tretinoin 27-31 bone gamma-carboxyglutamate protein 2 Mus musculus 184-186
20661723-2 2010 In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Tretinoin 117-130 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 65-90
20661723-2 2010 In this study, we examined the regulation of Nanog expression by phosphoinositide-3-kinase (PI3K)/Akt pathway during retinoic acid (RA)-induced differentiation of F9 embryonic carcinoma cells. Tretinoin 132-134 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 65-90
20661723-5 2010 RA treatment of F9 cells also led to a transient and parallel increase in both Akt and glycogen synthase kinase 3beta phosphorylations. Tretinoin 0-2 glycogen synthase kinase 3 beta Mus musculus 87-117
20456496-5 2010 Addition of ATRA to the medium for 48 h caused a dose-dependent increase in KRT4/KRT13 and a down-regulation of KRT2 mRNA. Tretinoin 12-16 keratin 13 Homo sapiens 81-86
20117194-3 2010 The present study detected expression of sHsps, Hsp40 and Hsp60 in normal and abnormal development of embryonic forelimbs in all-trans retinoic acid (atRA)-induced phocomelic, oligodactylic and atRA-induced abnormal limb bud development models in mice ex vivo. Tretinoin 135-148 heat shock protein 1 (chaperonin) Mus musculus 58-63
20117194-3 2010 The present study detected expression of sHsps, Hsp40 and Hsp60 in normal and abnormal development of embryonic forelimbs in all-trans retinoic acid (atRA)-induced phocomelic, oligodactylic and atRA-induced abnormal limb bud development models in mice ex vivo. Tretinoin 150-154 DnaJ heat shock protein family (Hsp40) member B1 Mus musculus 48-53
20117194-3 2010 The present study detected expression of sHsps, Hsp40 and Hsp60 in normal and abnormal development of embryonic forelimbs in all-trans retinoic acid (atRA)-induced phocomelic, oligodactylic and atRA-induced abnormal limb bud development models in mice ex vivo. Tretinoin 150-154 heat shock protein 1 (chaperonin) Mus musculus 58-63
20170512-0 2010 Upstream molecular signaling pathways of p27(Kip1) expression: effects of 4-hydroxytamoxifen, dexamethasone, and retinoic acids. Tretinoin 113-127 cyclin dependent kinase inhibitor 1B Homo sapiens 45-49
20170512-6 2010 1) The evidence indicated that 4-hydroxytamoxifen, dexamethasone, and various retinoic acids up-regulated expression of p27 in both estrogen receptor-positive and negative human breast cancer cells in vitro. Tretinoin 78-92 interferon alpha inducible protein 27 Homo sapiens 120-123
20170512-11 2010 Retinoic acids up-regulated expression of p27 without using either 4E-BP1 or RTKs/PI3K/Akt/AMPK/mTOR protein kinase signaling pathways. Tretinoin 0-14 interferon alpha inducible protein 27 Homo sapiens 42-45
20170512-13 2010 Retinoic acids also up-regulated translation initiation of p27, but without using any of these pathways. Tretinoin 0-14 interferon alpha inducible protein 27 Homo sapiens 59-62
20034106-0 2010 Retinoic acid controls expression of tissue remodeling genes Hmgn1 and Fgf18 at the digit-interdigit junction. Tretinoin 0-13 high mobility group nucleosomal binding domain 1 Mus musculus 61-66
20102612-0 2010 Retinoic acid protects human breast cancer cells against etoposide-induced apoptosis by NF-kappaB-dependent but cIAP2-independent mechanisms. Tretinoin 0-13 baculoviral IAP repeat containing 3 Homo sapiens 112-117
19550295-0 2010 Effect of cytotoxic agents and retinoic acid on Myc-N protein expression in neuroblastoma. Tretinoin 31-44 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 48-53
19550295-13 2010 Myc-N expression was negative in retinoic acid combined with vincristine group. Tretinoin 33-46 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-5
19550295-14 2010 CONCLUSIONS: Myc-N expression is reduced with cytotoxic agents and retinoic acid in neuroblastoma although Myc-N amplification remains the same. Tretinoin 67-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 13-16
20501978-9 2010 We propose other candidates such as STRA6, LRAT, CRBP1, CRBP2 and CRABP1 are directly implicated in retinoic acid metabolism. Tretinoin 100-113 signaling receptor and transporter of retinol STRA6 Homo sapiens 36-41
19797313-8 2010 Cyp26a1, encoding an enzyme involved in the degradation of retinoic acid, is shown to be up-regulated in mutant podocytes. Tretinoin 59-72 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
20563989-1 2010 Two new components of the retinoic acid (RA) synthetic pathway, the cell surface receptor for retinol, Stra6, and the enzyme converting retinol into retinal, Rdh10, have recently been described. Tretinoin 26-39 stimulated by retinoic acid 6 Gallus gallus 103-108
20563989-1 2010 Two new components of the retinoic acid (RA) synthetic pathway, the cell surface receptor for retinol, Stra6, and the enzyme converting retinol into retinal, Rdh10, have recently been described. Tretinoin 41-43 stimulated by retinoic acid 6 Gallus gallus 103-108
19860856-6 2010 Retinoid synthetic enzymes and the retinol transport protein Stra6 were located in the cells lining the third ventricle allowing synthesis of RA from retinol present in the CNS to act via RA receptors and retinoid X receptors in the hypothalamus. Tretinoin 142-144 signaling receptor and transporter of retinol STRA6 Homo sapiens 61-66
19841617-5 2010 Although suppression of angiogenesis by atRA was partially rescued by the simultaneous addition of angiopoietin-1, suppression of angiogenesis by ACR was not rescued under the same condition at all. Tretinoin 40-44 angiopoietin 1 Gallus gallus 99-113
19907998-3 2010 Here we describe a robust strategy for generating cytokeratin 14+ (K14+)/p63+ keratinocyte progenitors from hES cells through stage-specific application of retinoic acid (RA) and bone morphogenetic protein-4 (BMP4). Tretinoin 156-169 keratin 14 Homo sapiens 50-64
19907998-3 2010 Here we describe a robust strategy for generating cytokeratin 14+ (K14+)/p63+ keratinocyte progenitors from hES cells through stage-specific application of retinoic acid (RA) and bone morphogenetic protein-4 (BMP4). Tretinoin 171-173 keratin 14 Homo sapiens 50-64
19907998-4 2010 Induction of undifferentiated hES cells with RA stimulates expression of epithelial genes such as K18 and p63. Tretinoin 45-47 ribosome binding protein 1 Homo sapiens 30-33
19907998-4 2010 Induction of undifferentiated hES cells with RA stimulates expression of epithelial genes such as K18 and p63. Tretinoin 45-47 tumor protein p63 Homo sapiens 106-109
20224284-7 2010 RESULTS: The outcome of our investigations indicates that a heterodimeric retinoid receptor mediates the activation of the ADAM10 promoter by all-trans-retinoic acid. Tretinoin 142-165 a disintegrin and metallopeptidase domain 10 Mus musculus 123-129
19819227-4 2009 Wnt3a or leukemia inhibitory factor (LIF) inhibited the RA-induced differentiation in F9 cells. Tretinoin 56-58 wingless-type MMTV integration site family, member 3A Mus musculus 0-5
19819227-4 2009 Wnt3a or leukemia inhibitory factor (LIF) inhibited the RA-induced differentiation in F9 cells. Tretinoin 56-58 leukemia inhibitory factor Mus musculus 9-35
19819227-4 2009 Wnt3a or leukemia inhibitory factor (LIF) inhibited the RA-induced differentiation in F9 cells. Tretinoin 56-58 leukemia inhibitory factor Mus musculus 37-40
19819227-6 2009 RA evoked ZO-1alpha+ signals at cell-to-cell contacts in F9 cells in a Wnt3a sensitive manner. Tretinoin 0-2 wingless-type MMTV integration site family, member 3A Mus musculus 71-76
19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 29-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 61-65
19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 29-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92
19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 29-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92
19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 54-58 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 61-65
19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 54-58 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92
19766596-7 2009 Intriguingly, in response to all-trans-retinoic acid (ATRA), MYCN was down-regulated in MYCN-amplified SK-N-BE neuroblastoma cells, and the recruitment of MYCN protein onto its own intron 1 region was reduced in association with an induction of neuronal differentiation. Tretinoin 54-58 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 88-92
20044602-2 2009 MATERIALS AND METHODS: The effects of prolonged all-trans retinoic acid (ATRA) exposure on hTERT regulation in estrogen receptor-negative SK-BR-3 breast cancer cells were examined. Tretinoin 58-71 telomerase reverse transcriptase Homo sapiens 91-96
20044602-2 2009 MATERIALS AND METHODS: The effects of prolonged all-trans retinoic acid (ATRA) exposure on hTERT regulation in estrogen receptor-negative SK-BR-3 breast cancer cells were examined. Tretinoin 73-77 telomerase reverse transcriptase Homo sapiens 91-96
20044602-5 2009 The effect of ATRA on the decrease of telomerase activity was found to be associated with a rapid decrease in histone H3-lysine 9 acetylation (H3-K9-Ac) of the hTERT promoter. Tretinoin 14-18 telomerase reverse transcriptase Homo sapiens 160-165
19932006-5 2010 In in vitro cultured Peyer"s patches, all-trans retinoic acid promoted DC maturation, upregulated RAR-alpha mRNA, reduced IL-12 and IFN-gamma, but increased IL-10 gene expression; these effects of all-trans retinoic acid were reversed when cultured with Ro 41-5253 (a specific antagonist of RAR-alpha). Tretinoin 48-61 retinoic acid receptor, alpha Rattus norvegicus 98-107
19932006-5 2010 In in vitro cultured Peyer"s patches, all-trans retinoic acid promoted DC maturation, upregulated RAR-alpha mRNA, reduced IL-12 and IFN-gamma, but increased IL-10 gene expression; these effects of all-trans retinoic acid were reversed when cultured with Ro 41-5253 (a specific antagonist of RAR-alpha). Tretinoin 48-61 interleukin 12B Rattus norvegicus 122-127
19932006-5 2010 In in vitro cultured Peyer"s patches, all-trans retinoic acid promoted DC maturation, upregulated RAR-alpha mRNA, reduced IL-12 and IFN-gamma, but increased IL-10 gene expression; these effects of all-trans retinoic acid were reversed when cultured with Ro 41-5253 (a specific antagonist of RAR-alpha). Tretinoin 48-61 interferon gamma Rattus norvegicus 132-141
19932006-5 2010 In in vitro cultured Peyer"s patches, all-trans retinoic acid promoted DC maturation, upregulated RAR-alpha mRNA, reduced IL-12 and IFN-gamma, but increased IL-10 gene expression; these effects of all-trans retinoic acid were reversed when cultured with Ro 41-5253 (a specific antagonist of RAR-alpha). Tretinoin 48-61 interleukin 10 Rattus norvegicus 157-162
19932006-5 2010 In in vitro cultured Peyer"s patches, all-trans retinoic acid promoted DC maturation, upregulated RAR-alpha mRNA, reduced IL-12 and IFN-gamma, but increased IL-10 gene expression; these effects of all-trans retinoic acid were reversed when cultured with Ro 41-5253 (a specific antagonist of RAR-alpha). Tretinoin 48-61 retinoic acid receptor, alpha Rattus norvegicus 291-300
20483764-2 2010 In the current study, we demonstrate that naive CD4+CD25-Foxp3- T cells specific for the myelin proteolipid protein (PLP)139-151 peptide can be converted into CD25+Foxp3+ induced Treg cells (iTregs) when stimulated in the presence of TGF-beta, retinoic acid, and IL-2. Tretinoin 244-257 forkhead box P3 Mus musculus 57-62
20483764-2 2010 In the current study, we demonstrate that naive CD4+CD25-Foxp3- T cells specific for the myelin proteolipid protein (PLP)139-151 peptide can be converted into CD25+Foxp3+ induced Treg cells (iTregs) when stimulated in the presence of TGF-beta, retinoic acid, and IL-2. Tretinoin 244-257 forkhead box P3 Mus musculus 164-169
20193324-11 2009 The expression of p27(Kip1) and p21(Waf1) in myeloma cells was up-regulated by RGZ and this change was more apparent when RGZ was used in combination with ATRA. Tretinoin 155-159 interferon alpha inducible protein 27 Homo sapiens 18-21
20193324-11 2009 The expression of p27(Kip1) and p21(Waf1) in myeloma cells was up-regulated by RGZ and this change was more apparent when RGZ was used in combination with ATRA. Tretinoin 155-159 cyclin dependent kinase inhibitor 1B Homo sapiens 22-26
2554072-1 1989 Retinoic acid receptor (RAR)-alpha mRNA expression was studied in a variety of myeloid leukemia cells with variable responsiveness to the induction of terminal differentiation by retinoic acid (RA). Tretinoin 179-192 retinoic acid receptor alpha Homo sapiens 24-34
19749800-5 2009 Patients successfully treated with all-trans-retinoic acid (ATRA) and chemotherapy showed downregulation of miR-181b and upregulation of miR-15b, -16, -107, -223, -342 and let-7c. Tretinoin 35-58 microRNA let-7c Homo sapiens 172-178
19749800-5 2009 Patients successfully treated with all-trans-retinoic acid (ATRA) and chemotherapy showed downregulation of miR-181b and upregulation of miR-15b, -16, -107, -223, -342 and let-7c. Tretinoin 60-64 microRNA let-7c Homo sapiens 172-178
19749800-8 2009 In addition, we observed, in response to ATRA, the release of PML/RARalpha paralleled by their transcriptional activation, together with their host genes, EVL and C21orf34alpha. Tretinoin 41-45 PML nuclear body scaffold Homo sapiens 62-65
19749800-8 2009 In addition, we observed, in response to ATRA, the release of PML/RARalpha paralleled by their transcriptional activation, together with their host genes, EVL and C21orf34alpha. Tretinoin 41-45 retinoic acid receptor alpha Homo sapiens 66-74
19749800-8 2009 In addition, we observed, in response to ATRA, the release of PML/RARalpha paralleled by their transcriptional activation, together with their host genes, EVL and C21orf34alpha. Tretinoin 41-45 Enah/Vasp-like Homo sapiens 155-158
20233719-5 2010 The neuronal differentiation in nip1-overexpressing P19 cells was achieved in a retinoic acid-independent manner and was corroborated by an increase in the expression of the neuronal basic helix-loop-helix transcription factors and neural-lineage cell markers. Tretinoin 80-93 BCL2 interacting protein 1 Homo sapiens 32-36
19965837-7 2010 RESULTS: ATRA synergised with TGF-beta to induce Foxp3(+) T regulatory cells (Treg) and reciprocally inhibited development of IL-17-producing T helper cells (Th17) induced by TGF-beta and IL-6. Tretinoin 9-13 forkhead box P3 Mus musculus 49-54
20505363-7 2010 Differentiation by retinoic acid decreases Tpt1-Npm1 complex levels. Tretinoin 19-32 tumor protein, translationally-controlled 1 Mus musculus 43-47
20505363-7 2010 Differentiation by retinoic acid decreases Tpt1-Npm1 complex levels. Tretinoin 19-32 nucleophosmin 1 Mus musculus 48-52
20507360-3 2010 Here we report that a dinucleotide repeat in the cis-element of Snail2 (previously known as Slug) gene plays a role in repression by all-trans retinoic acid. Tretinoin 143-156 snail family zinc finger 2 L homeolog Xenopus laevis 64-70
20507360-3 2010 Here we report that a dinucleotide repeat in the cis-element of Snail2 (previously known as Slug) gene plays a role in repression by all-trans retinoic acid. Tretinoin 143-156 snail family zinc finger 2 L homeolog Xenopus laevis 92-96
20507360-4 2010 We analyzed the cis-acting regulatory regions of the Xenopus Snail2 gene, whose expression is repressed by all-trans retinoic acid. Tretinoin 117-130 snail family zinc finger 2 L homeolog Xenopus laevis 61-67
19702568-2 2009 All-trans retinoic acid (ATRA) and arsenic trioxide, which are the major molecularly targeted therapies in APL, affect or degrade the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 134-137
19702568-2 2009 All-trans retinoic acid (ATRA) and arsenic trioxide, which are the major molecularly targeted therapies in APL, affect or degrade the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 138-142
19702568-2 2009 All-trans retinoic acid (ATRA) and arsenic trioxide, which are the major molecularly targeted therapies in APL, affect or degrade the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 134-137
19538480-6 2010 Gene reporter assays confirmed that the RA-induced t-PA gene expression occurred through interactions of retinoid receptors (RARs and RXRs) with a DR5 response element located at -7 kb from the transcription site. Tretinoin 40-42 TNF receptor superfamily member 10b Homo sapiens 147-150
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 retinoic acid receptor alpha Homo sapiens 119-128
19702568-2 2009 All-trans retinoic acid (ATRA) and arsenic trioxide, which are the major molecularly targeted therapies in APL, affect or degrade the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 138-142
2554331-9 1989 First, all of the tissues that are known to be teratogenic targets of retinoic acid and retinol also express CRABP and CRBP transcripts. Tretinoin 70-83 retinol binding protein 1, cellular Mus musculus 119-123
19752193-6 2009 Correspondingly, IRAK-1(-/-) macrophages exhibit increased expression of ABCA1 mRNA and protein, as well as elevated cholesterol efflux in response to the RAR ligand ATRA. Tretinoin 166-170 retinoic acid receptor alpha Homo sapiens 155-158
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 TNF receptor superfamily member 10b Homo sapiens 145-148
2481498-5 1989 Additionally, H-ALBP saturably bound retinoic acid as determined by the quenching of intrinsic tryptophan fluorescence. Tretinoin 37-50 fatty acid binding protein 4 Homo sapiens 16-20
19879845-7 2009 Lastly, in utero RA treatment rescued the cortical phenotype in Foxc1 mutants. Tretinoin 17-19 forkhead box C1 Mus musculus 64-69
2788413-0 1989 EGF-induced PGE2 release is synergistically enhanced in retinoic acid treated fetal rat lung cells. Tretinoin 56-69 epidermal growth factor Rattus norvegicus 0-3
19789299-5 2009 ATRA is a highly efficient suppressor of tumor formation in the two-stage mouse skin carcinogenesis model and we have shown that this effect correlates with the suppression of the B-Raf/Mek/Erk signaling pathway. Tretinoin 0-4 Braf transforming gene Mus musculus 180-185
19789299-10 2009 We hypothesize that ATRA blocks tumor formation, at least in part, by targeting events upstream of Stat3, such as the B-Raf/Mek/Erk pathway, and that in the K5.Stat3C mice, in which Stat3 activity is constitutive, it cannot suppress tumor formation. Tretinoin 20-24 Braf transforming gene Mus musculus 118-123
19632226-1 2009 BACKGROUND & AIMS: Retinoic acid plays a positive role in induction of FoxP3(+) regulatory T cells. Tretinoin 23-36 forkhead box P3 Mus musculus 75-80
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 TNF receptor superfamily member 10b Homo sapiens 224-227
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 119-121 TNF receptor superfamily member 10b Homo sapiens 145-148
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 119-121 TNF receptor superfamily member 10b Homo sapiens 224-227
19507250-3 2009 ATRA (0.1-1 microM) upregulated levels of RTP801, a negative regulator of mTORC1, and inhibited mTORC1 signaling as assessed by measurement of the levels of p-p70S6K and p-4E-BP1 in HL60 and NB4 cells. Tretinoin 0-4 ribosomal protein S6 kinase B1 Homo sapiens 159-165
19507250-4 2009 ATRA (0.1-1 microM) in combination with RAD001 (10 nM) strikingly downregulated the levels of p-70S6K and p-4E-BP1 without affecting the total amount of these proteins. Tretinoin 0-4 ribosomal protein S6 kinase B1 Homo sapiens 94-101
19507250-5 2009 Notably, RAD001 (10 nM) significantly augmented ATRA-induced expression of CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) and p27(kip1) and downregulated levels of c-Myc in these cells. Tretinoin 48-52 CCAAT enhancer binding protein epsilon Homo sapiens 75-113
19507250-5 2009 Notably, RAD001 (10 nM) significantly augmented ATRA-induced expression of CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) and p27(kip1) and downregulated levels of c-Myc in these cells. Tretinoin 48-52 CCAAT enhancer binding protein epsilon Homo sapiens 115-127
20536349-1 2010 The binding of all-trans retinoic acid (ATRA) to retinoid receptor-alpha (RAR-alpha) relieves transcriptional repression induced by the promyelocytic leukemia-retinoic acid receptor (PML-RAR) oncoprotein. Tretinoin 15-38 retinoic acid receptor alpha Homo sapiens 74-83
20536349-1 2010 The binding of all-trans retinoic acid (ATRA) to retinoid receptor-alpha (RAR-alpha) relieves transcriptional repression induced by the promyelocytic leukemia-retinoic acid receptor (PML-RAR) oncoprotein. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 74-83
19507250-5 2009 Notably, RAD001 (10 nM) significantly augmented ATRA-induced expression of CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) and p27(kip1) and downregulated levels of c-Myc in these cells. Tretinoin 48-52 cyclin dependent kinase inhibitor 1B Homo sapiens 137-141
2788413-1 1989 Retinoic acid has been shown to induce a 2.5-fold increase in 125I-EGF binding capacity through increased EGF receptor synthesis in a fetal rat lung (FRL) cell line (1). Tretinoin 0-13 epidermal growth factor Rattus norvegicus 67-70
19507250-5 2009 Notably, RAD001 (10 nM) significantly augmented ATRA-induced expression of CCAAT/enhancer-binding protein epsilon (C/EBPepsilon) and p27(kip1) and downregulated levels of c-Myc in these cells. Tretinoin 48-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176
20561408-0 2010 [The effect of ATRA-induced leukemic cell differentiation on Brd7 gene expression in leukemia cell lines]. Tretinoin 15-19 bromodomain containing 7 Homo sapiens 61-65
2788413-1 1989 Retinoic acid has been shown to induce a 2.5-fold increase in 125I-EGF binding capacity through increased EGF receptor synthesis in a fetal rat lung (FRL) cell line (1). Tretinoin 0-13 epidermal growth factor Rattus norvegicus 106-109
2788413-4 1989 Retinoic acid and EGF dose-response curves demonstrate that the effect on PGE2 secretion correlates with the retinoic acid induced increase in EGF receptors. Tretinoin 0-13 epidermal growth factor Rattus norvegicus 143-146
2788413-4 1989 Retinoic acid and EGF dose-response curves demonstrate that the effect on PGE2 secretion correlates with the retinoic acid induced increase in EGF receptors. Tretinoin 109-122 epidermal growth factor Rattus norvegicus 18-21
2788413-4 1989 Retinoic acid and EGF dose-response curves demonstrate that the effect on PGE2 secretion correlates with the retinoic acid induced increase in EGF receptors. Tretinoin 109-122 epidermal growth factor Rattus norvegicus 143-146
19285840-8 2009 As a protein is rapidly responsive to all-trans retinoic acid (ATRA), a classical clinical differentiation-inducing drug for AML, HIF-1alpha also plays a role in ATRA-induced differentiation of leukemic cells. Tretinoin 42-61 hypoxia inducible factor 1, alpha subunit Mus musculus 130-140
2502111-0 1989 Retinoic acid blockade of imidazole-induced tyrosinase expression in B16 melanoma cultures: similar effects of the active retinoid and triiodothyronine. Tretinoin 0-13 tyrosinase Mus musculus 44-54
19285840-8 2009 As a protein is rapidly responsive to all-trans retinoic acid (ATRA), a classical clinical differentiation-inducing drug for AML, HIF-1alpha also plays a role in ATRA-induced differentiation of leukemic cells. Tretinoin 63-67 hypoxia inducible factor 1, alpha subunit Mus musculus 130-140
19285840-8 2009 As a protein is rapidly responsive to all-trans retinoic acid (ATRA), a classical clinical differentiation-inducing drug for AML, HIF-1alpha also plays a role in ATRA-induced differentiation of leukemic cells. Tretinoin 162-166 hypoxia inducible factor 1, alpha subunit Mus musculus 130-140
19633294-5 2009 This is evidenced by RA-dependent induction of the cell cycle inhibitor p21/Cip1 (Cdk-interacting protein 1) and cell cycle arrest, induction of the neuroblastic marker doublecortin and of the neuron-specific intermediate filament protein, peripherin, and by RA-stimulated extension of neuritic processes. Tretinoin 21-23 peripherin Homo sapiens 240-250
20305693-7 2010 Both meta-analysis of available mRNA and CGH profiling data and our experimental study revealed three major pathogenetic pathways: (1) cell cycle, (2) retinoic acid signalling (including lipopolysaccharide/Toll like receptor 4 pathway), (3) complement system and antigen presentation. Tretinoin 151-164 toll like receptor 4 Homo sapiens 206-226
20348100-4 2010 Forkhead family member Foxa1 is activated by retinoic acid treatment of embryonic stem cells, binds its DNA consensus site within the short interspersed transposable/medium reiterated sequence 1 elements, and displaces linker histone H1 from silent Afp chromatin. Tretinoin 45-58 forkhead box A1 Homo sapiens 23-28
19635790-0 2009 c-Cbl tyrosine kinase-binding domain mutant G306E abolishes the interaction of c-Cbl with CD38 and fails to promote retinoic acid-induced cell differentiation and G0 arrest. Tretinoin 116-129 Cbl proto-oncogene Homo sapiens 0-5
19635790-4 2009 Unlike wild-type (WT) c-Cbl, the G306E mutant c-Cbl fails to propel RA-induced differentiation, and disrupts the normal association with CD38. Tretinoin 68-70 Cbl proto-oncogene Homo sapiens 46-51
2502111-1 1989 The effect of retinoic acid on the induction of tyrosinase (EC 1:14.18.1) by imidazole was determined in cultured B16/C3 melanoma cells. Tretinoin 14-27 tyrosinase Mus musculus 48-58
19635790-12 2009 Without the G306E mutation the c-Cbl unites CD38 with the signaling complex and delivers a MAPK signal that drives RA-induced differentiation. Tretinoin 115-117 Cbl proto-oncogene Homo sapiens 31-36
20112286-0 2010 Retinoic acid-metabolizing enzyme cytochrome P450 26a1 (cyp26a1) is essential for implantation: functional study of its role in early pregnancy. Tretinoin 0-13 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 34-54
20112286-0 2010 Retinoic acid-metabolizing enzyme cytochrome P450 26a1 (cyp26a1) is essential for implantation: functional study of its role in early pregnancy. Tretinoin 0-13 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 56-63
19635790-12 2009 Without the G306E mutation the c-Cbl unites CD38 with the signaling complex and delivers a MAPK signal that drives RA-induced differentiation. Tretinoin 115-117 CD38 molecule Homo sapiens 44-48
20112286-3 2010 Cytochrome P450 26A1 (cyp26a1), a retinoic acid (RA)-metabolizing enzyme, is involved in VA metabolism. Tretinoin 34-47 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-20
19635790-13 2009 The results demonstrate the importance of the Gly306 residue in the ability of c-Cbl to propel RA-induced differentiation. Tretinoin 95-97 Cbl proto-oncogene Homo sapiens 79-84
2613755-2 1989 Both control cells grown to subconfluence and cells treated with 10(-6) M-retinoic acid adhered and spread rapidly on fibronectin (greater than 75% following 1 h of incubation) but adhered poorly to type I collagen (less than 15%). Tretinoin 74-87 fibronectin 1 Mus musculus 118-129
19409899-3 2009 Furthermore, although administration of atRA and 9cRA into the rat uterus at 13.5days postcoitum robustly induced mRNA expression of cellular retinol binding protein II, the gene for which is targeted by RAR and/or RXR, in the placenta, neither RA affected the expression of placental steroidogenic enzymes, and both had little effect on progesterone and androgen levels in the placenta and embryo, suggesting that placental steroidogenesis is not regulated by RAs in rats. Tretinoin 40-44 retinol binding protein 2 Rattus norvegicus 133-168
20112286-3 2010 Cytochrome P450 26A1 (cyp26a1), a retinoic acid (RA)-metabolizing enzyme, is involved in VA metabolism. Tretinoin 34-47 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 22-29
20112286-3 2010 Cytochrome P450 26A1 (cyp26a1), a retinoic acid (RA)-metabolizing enzyme, is involved in VA metabolism. Tretinoin 49-51 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-20
20112286-3 2010 Cytochrome P450 26A1 (cyp26a1), a retinoic acid (RA)-metabolizing enzyme, is involved in VA metabolism. Tretinoin 49-51 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 22-29
20134361-10 2010 Addition of retinoic acid enhanced the osteogenic differentiation of suture-derived mesenchymal cells in vitro, including up-regulation of alkaline phosphatase activity and Runx2 expression. Tretinoin 12-25 runt related transcription factor 2 Mus musculus 173-178
20346917-6 2010 On the other hand, immunoblot analysis revealed that co-treatment with RA and curcumin caused remarkable accumulation of protein levels of p47-phox (to 7-fold) and p67-phox (to 4-fold) compared with those of the RA-treatment alone. Tretinoin 71-73 pleckstrin Homo sapiens 139-142
2565341-3 1989 Several years ago, we found that retinoic acid caused an accumulation of the enzyme tissue transglutaminase in murine peritoneal macrophages and in human promyelocytic leukemia (HL-60) cells. Tretinoin 33-46 transglutaminase 2, C polypeptide Mus musculus 84-107
20116096-8 2010 This responsive region in PSG3 maps within a 130 bp promoter sequence, which overlaps the transcription start site and requires a functional Retinoic Acid Responsive Element (RARE) and a GA-binding protein (GABP) consensus site for basal and differentiation-dependent promoter activity, respectively. Tretinoin 141-154 pregnancy specific beta-1-glycoprotein 3 Homo sapiens 26-30
19556237-9 2009 Furthermore, cadmium inhibited the expression of Cyp26a1 and Cyp26b1, which are involved in retinoic acid degradation. Tretinoin 92-105 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 49-56
19594405-6 2009 CYP1A2 and CYP3A4 appear to be the major P450 enzymes catalyzing the oxidation of all-trans-retinol to all-trans-retinoic acid in human liver, and CYP3A4 is one of the vitamin D3 25-hydroxylases. Tretinoin 103-126 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 0-6
2917804-4 1989 Decreased N-myc expression and increased c-src expression were observed during neuronal differentiation by retinoic acid, polyprenoic acid (E5166) and dibutyryl cyclic AMP, whereas the expression of N-myc and c-src genes was considerably reduced during schwannian differentiation by bromodeoxyuridine, demonstrating that the expression of N-myc and c-src genes was regulated independently in the bipolar differentiation processes of NB cells. Tretinoin 107-120 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 10-15
19156541-6 2009 In retinoic acid-differentiated SH-SY5Y neuronal cells where ObRb was induced, leptin increased the expression of Cdk5, p35, and p25 kinases. Tretinoin 3-16 leptin Homo sapiens 79-85
19156541-6 2009 In retinoic acid-differentiated SH-SY5Y neuronal cells where ObRb was induced, leptin increased the expression of Cdk5, p35, and p25 kinases. Tretinoin 3-16 cyclin dependent kinase 5 Homo sapiens 114-118
20130111-4 2010 GRp58 interacted with RARA in the presence of all-trans retinoic acid (ATRA) ligand and, as a complex, it was translocated from the cytoplasm to the nucleus and, then with time, GRp58 dissociated from RARA and was found in the cytoplasm. Tretinoin 56-69 protein disulfide isomerase associated 3 Mus musculus 0-5
20130111-4 2010 GRp58 interacted with RARA in the presence of all-trans retinoic acid (ATRA) ligand and, as a complex, it was translocated from the cytoplasm to the nucleus and, then with time, GRp58 dissociated from RARA and was found in the cytoplasm. Tretinoin 71-75 protein disulfide isomerase associated 3 Mus musculus 0-5
20130111-6 2010 Moreover, treatment with sulfhydryl-modifying agents that oxidize SH-groups of cysteine residues to disulfide bonds abolished ATRA-mediated RARA nuclear localization, suggesting that the thiol oxidoreductase activity of GRp58 may be required for RARA nuclear import. Tretinoin 126-130 protein disulfide isomerase associated 3 Mus musculus 220-225
2764454-3 1989 Pre-treatment of TPH1 cells with retinoic acid induced the cells to differentiate into unreplicating macrophage-like cells. Tretinoin 33-46 tryptophan hydroxylase 1 Homo sapiens 17-21
20117817-3 2010 RARalpha agonistic activity was commonly detected in the surface water samples collected along two rivers at different periods, with maximum all-trans retinoic acid (atRA) equivalents of 47.6 ng-atRA/L and 23.5 ng-atRA/L being observed in Lake Biwa-Yodo River and Ina River, respectively. Tretinoin 151-164 retinoic acid receptor alpha Homo sapiens 0-8
20117817-3 2010 RARalpha agonistic activity was commonly detected in the surface water samples collected along two rivers at different periods, with maximum all-trans retinoic acid (atRA) equivalents of 47.6 ng-atRA/L and 23.5 ng-atRA/L being observed in Lake Biwa-Yodo River and Ina River, respectively. Tretinoin 166-170 retinoic acid receptor alpha Homo sapiens 0-8
19661293-4 2009 Effects of all-trans retinoic acid (AT-RA) on the growth, protein expression of RAR-alpha, beta and gamma, and RARE transcriptional activation were determined. Tretinoin 11-34 retinoic acid receptor alpha Homo sapiens 80-89
19294396-6 2009 The mRNA expression of RA-regulated genes (KRT2, KRT4, CRABPII and HBEGF) was altered within 24 h after RA exposure. Tretinoin 23-25 heparin binding EGF like growth factor Homo sapiens 67-72
2550293-1 1989 We have examined the regulation of plasma membrane proteolipid (PM-PLP) synthesis and steady-state levels in mouse NB2a/d1 neuroblastoma cells during differentiation with dibutyryl cyclic AMP (dbcAMP) and retinoic acid (RA), agents which have been previously shown to induce the elaboration of exclusively axonal or dendritic neurites, respectively. Tretinoin 205-218 plasma membrane proteolipid Mus musculus 35-62
19602592-9 2009 Sustained expression of CBX7 in EC cells confers a growth advantage and resistance to retinoic acid-induced differentiation. Tretinoin 86-99 chromobox 7 Homo sapiens 24-28
19917671-2 2010 Retinoic acid receptor alpha (RARalpha) is a transcription factor activated by RA, and its serine 77 (RARalphaS77) is the main residue phosphorylated by the cyclin-dependent kinase (CDK)-activating kinase (CAK) complex. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 0-28
19917671-7 2010 These studies demonstrate, for the first time, that RA couples G(1) arrest to transcriptional control of cancer cell differentiation by suppressing CAK phosphorylation of RARalpha to release transcriptional repression.-Wang, A., Alimova, I. N., Luo, P. Jong, A., Triche, T. J., Wu, L. Loss of CAK phosphorylation of RARalpha mediates transcriptional control of retinoid-induced cancer cell differentiation. Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 171-179
19917671-7 2010 These studies demonstrate, for the first time, that RA couples G(1) arrest to transcriptional control of cancer cell differentiation by suppressing CAK phosphorylation of RARalpha to release transcriptional repression.-Wang, A., Alimova, I. N., Luo, P. Jong, A., Triche, T. J., Wu, L. Loss of CAK phosphorylation of RARalpha mediates transcriptional control of retinoid-induced cancer cell differentiation. Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 316-324
19618468-3 2009 We report here that the gene encoding a cytosolic class-1 aldehyde dehydrogenase, ALDH1A1, a weak catalyst of RA production, is strongly expressed in a male-specific manner in somatic cells of the developing mouse testis, beginning shortly after Sry expression is first detectable. Tretinoin 110-112 sex determining region of Chr Y Mus musculus 246-249
20118278-8 2010 Increasing the abundance of alpha4 integrin relative to beta1 integrin is critical to retinoic acid-mediated expression of alpha4beta7 integrin during T cell activation. Tretinoin 86-99 hemoglobin, beta adult major chain Mus musculus 56-61
2696709-4 1989 GM-CSF showed a profound stimulatory effect on the proliferation of myeloid progenitors from the child bone marrow and restored colony numbers in the retinoic acid-, dimethylsulphoxide- and actinomycin-D-inhibited cultures. Tretinoin 150-163 colony stimulating factor 2 Homo sapiens 0-6
20019757-1 2010 The intracellular retinoic acid-inducible gene I-like receptors (RLRs) sense viral ribonucleic acid and signal through the mitochondrial protein mitochondrial antiviral signalling (MAVS) to trigger the production of type I interferons and proinflammatory cytokines. Tretinoin 18-31 mitochondrial antiviral signaling protein Homo sapiens 181-185
19483654-5 2009 Vaccination concomitantly with application of all-trans-retinoic acid and anti-CD25 treatment significantly increased the survival time and rate of IL-1alpha/beta(comp), but even of IL-1alpha(-/-)beta(comp) IL-1RI(comp) tumor-bearing mice. Tretinoin 46-69 interleukin 1 alpha Mus musculus 148-157
19483654-5 2009 Vaccination concomitantly with application of all-trans-retinoic acid and anti-CD25 treatment significantly increased the survival time and rate of IL-1alpha/beta(comp), but even of IL-1alpha(-/-)beta(comp) IL-1RI(comp) tumor-bearing mice. Tretinoin 46-69 interleukin 1 alpha Mus musculus 182-191
3136932-3 1988 When RA was added to resting thymocyte cultures in the presence of recombinant interleukin-2 (rIL-2), blastogenesis was increased two- to fourfold. Tretinoin 5-7 interleukin 2 Rattus norvegicus 94-99
19715998-3 2009 The aim of this study was to establish if RA synergizing with TGF-beta induced antigen specific CD4(+) CD25(high) Foxp3(+) Treg portraying gut homing receptors. Tretinoin 42-44 forkhead box P3 Mus musculus 114-119
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 44-57 X protein Hepatitis B virus 13-16
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 44-57 H3 histone pseudogene 16 Homo sapiens 131-134
3136932-5 1988 Instead, RA markedly potentiated the growth rate of long-term rIL-2-dependent thymocyte blasts and, correspondingly, increased the Tac expression on these proliferating cells. Tretinoin 9-11 interleukin 2 Rattus norvegicus 62-67
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 44-57 E2F transcription factor 1 Homo sapiens 171-175
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 59-61 X protein Hepatitis B virus 13-16
2896607-2 1988 Steady-state levels of CAD mRNA decreased by 7-fold in F9 cells following 120 h of retinoic acid and dibutyryl cyclic AMP induction as compared to levels in uninduced cells. Tretinoin 83-96 aconitate decarboxylase 1 Homo sapiens 23-26
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 59-61 H3 histone pseudogene 16 Homo sapiens 131-134
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 59-61 E2F transcription factor 1 Homo sapiens 171-175
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 195-197 X protein Hepatitis B virus 13-16
27265273-9 2009 Based on in vitro and clinical observations, several mechanisms, including induction of accelerated metabolism of ATRA, decreased bioavailability and plasma drug levels, point mutations in the ATRA-binding domain of promyelocytic leukemia (PML)-retinoic acid receptor-alpha (RARalpha) and other molecular events have been proposed to explain ATRA resistance. Tretinoin 193-197 retinoic acid receptor alpha Homo sapiens 275-283
19828754-3 2010 In addition, HBx abolished the potential of retinoic acid (RA) to downregulate levels of G(1)-checkpoint regulators including p16, p21 and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 195-197 E2F transcription factor 1 Homo sapiens 171-175
2891434-1 1988 Retinoic acid (RA) induces tissue transglutaminase (TGASE) and inhibits terminal differentiation induced either by calcium ion or by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in primary mouse epidermal cells in culture. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 27-50
20137113-0 2010 [Regulation mechanism for rig-g gene expression induced by all-trans retinoic acid]. Tretinoin 69-82 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 26-31
20137113-1 2010 To investigate the molecular mechanisms of all-trans retinoic acid (ATRA)-induced rig-g gene expression and to better understand the signal transduction of ATRA during acute promyelocytic leukemia (APL) cell differentiation, the luciferase reporter assay, co-immunoprecipitation and chromatin immunoprecipitation were used to clarify the basic transcriptional factors, which directly initiated the expression of rig-g gene. Tretinoin 53-66 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 82-87
20137113-1 2010 To investigate the molecular mechanisms of all-trans retinoic acid (ATRA)-induced rig-g gene expression and to better understand the signal transduction of ATRA during acute promyelocytic leukemia (APL) cell differentiation, the luciferase reporter assay, co-immunoprecipitation and chromatin immunoprecipitation were used to clarify the basic transcriptional factors, which directly initiated the expression of rig-g gene. Tretinoin 53-66 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 412-417
20137113-1 2010 To investigate the molecular mechanisms of all-trans retinoic acid (ATRA)-induced rig-g gene expression and to better understand the signal transduction of ATRA during acute promyelocytic leukemia (APL) cell differentiation, the luciferase reporter assay, co-immunoprecipitation and chromatin immunoprecipitation were used to clarify the basic transcriptional factors, which directly initiated the expression of rig-g gene. Tretinoin 68-72 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 82-87
20137113-1 2010 To investigate the molecular mechanisms of all-trans retinoic acid (ATRA)-induced rig-g gene expression and to better understand the signal transduction of ATRA during acute promyelocytic leukemia (APL) cell differentiation, the luciferase reporter assay, co-immunoprecipitation and chromatin immunoprecipitation were used to clarify the basic transcriptional factors, which directly initiated the expression of rig-g gene. Tretinoin 68-72 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 412-417
19329942-1 2009 Aldehyde dehydrogenase 1 (ALDH1), a detoxifying enzyme responsible for the oxidation of intracellular aldehydes, was shown to have a function in the early differentiation of stem cells, through its function in oxidizing retinol to retinoic acid. Tretinoin 231-244 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-24
19329942-1 2009 Aldehyde dehydrogenase 1 (ALDH1), a detoxifying enzyme responsible for the oxidation of intracellular aldehydes, was shown to have a function in the early differentiation of stem cells, through its function in oxidizing retinol to retinoic acid. Tretinoin 231-244 aldehyde dehydrogenase 1 family member A1 Homo sapiens 26-31
19428697-0 2009 Neurotrophin-3 improves retinoic acid-induced neural differentiation of skin-derived precursors through a p75NTR-dependent signaling pathway. Tretinoin 24-37 nerve growth factor receptor Homo sapiens 106-112
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 29-42 neuronal differentiation 1 Homo sapiens 142-148
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 29-42 H3 histone pseudogene 16 Homo sapiens 183-186
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 29-42 nerve growth factor receptor Homo sapiens 214-239
19892780-5 2010 Furthermore, we show that FRMD7 expression is up-regulated upon retinoic acid (RA)-induced differentiation of mouse neuroblastoma NEURO2A cells, suggesting FRMD7 may play a role in this process. Tretinoin 64-77 FERM domain containing 7 Mus musculus 26-31
19892780-5 2010 Furthermore, we show that FRMD7 expression is up-regulated upon retinoic acid (RA)-induced differentiation of mouse neuroblastoma NEURO2A cells, suggesting FRMD7 may play a role in this process. Tretinoin 64-77 FERM domain containing 7 Mus musculus 156-161
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 29-42 nerve growth factor receptor Homo sapiens 241-247
2891434-1 1988 Retinoic acid (RA) induces tissue transglutaminase (TGASE) and inhibits terminal differentiation induced either by calcium ion or by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in primary mouse epidermal cells in culture. Tretinoin 15-17 transglutaminase 2, C polypeptide Mus musculus 27-50
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 44-46 neuronal differentiation 1 Homo sapiens 142-148
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 44-46 H3 histone pseudogene 16 Homo sapiens 183-186
19892780-5 2010 Furthermore, we show that FRMD7 expression is up-regulated upon retinoic acid (RA)-induced differentiation of mouse neuroblastoma NEURO2A cells, suggesting FRMD7 may play a role in this process. Tretinoin 79-81 FERM domain containing 7 Mus musculus 26-31
19892780-5 2010 Furthermore, we show that FRMD7 expression is up-regulated upon retinoic acid (RA)-induced differentiation of mouse neuroblastoma NEURO2A cells, suggesting FRMD7 may play a role in this process. Tretinoin 79-81 FERM domain containing 7 Mus musculus 156-161
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 44-46 nerve growth factor receptor Homo sapiens 214-239
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 44-46 nerve growth factor receptor Homo sapiens 241-247
2451772-2 1988 The phosphorylation of 22 kD, pI 6.0 and 5.8 proteins (pp22) in HL-60 cells or myeloid leukemic cells from patients, was enhanced by treatment with granuloid inducers such as retinoic acid, dimethyl sulfoxide or G-CSF, in common with prostaglandin E2 and theophylline, or dibutyryl c-AMP, which increased intracellular c-AMP. Tretinoin 175-188 colony stimulating factor 3 Homo sapiens 212-217
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 198-200 nerve growth factor receptor Homo sapiens 214-239
19428697-2 2009 This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD and cell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) up-regulation and apoptosis of SKPs. Tretinoin 198-200 nerve growth factor receptor Homo sapiens 241-247
19428697-5 2009 The results indicate that NT-3 improves the neural differentiation of SKPs induced by RA through a p75NTR-dependent signaling pathway. Tretinoin 86-88 nerve growth factor receptor Homo sapiens 99-105
19432991-0 2009 Identification of the B-Raf/Mek/Erk MAP kinase pathway as a target for all-trans retinoic acid during skin cancer promotion. Tretinoin 81-94 Braf transforming gene Mus musculus 22-27
19853839-11 2010 On induction of differentiation by retinoic acid, a sequential expression was found in human neuroblastoma, where ANKK1 was expressed first, followed by that of DRD2. Tretinoin 35-48 ankyrin repeat and kinase domain containing 1 Homo sapiens 114-119
19787411-5 2010 In subconfluent cells co-treated with EGF (100 ng/mL) and increasing concentrations of RA (10(-8) M-10(-5) M RA), thymidine incorporation was significantly greater at all concentrations than RA alone, with greatest increases observed at 10(-7) (422% of control) and 10(-6) (470% of control) M RA. Tretinoin 109-111 epidermal growth factor Rattus norvegicus 38-41
3691670-2 1987 Both retinoic acid-treated and control cells attached efficiently to fibronectin or gelatin substrates without any significant difference. Tretinoin 5-18 fibronectin 1 Mus musculus 69-80
19787411-5 2010 In subconfluent cells co-treated with EGF (100 ng/mL) and increasing concentrations of RA (10(-8) M-10(-5) M RA), thymidine incorporation was significantly greater at all concentrations than RA alone, with greatest increases observed at 10(-7) (422% of control) and 10(-6) (470% of control) M RA. Tretinoin 109-111 epidermal growth factor Rattus norvegicus 38-41
19787411-5 2010 In subconfluent cells co-treated with EGF (100 ng/mL) and increasing concentrations of RA (10(-8) M-10(-5) M RA), thymidine incorporation was significantly greater at all concentrations than RA alone, with greatest increases observed at 10(-7) (422% of control) and 10(-6) (470% of control) M RA. Tretinoin 109-111 epidermal growth factor Rattus norvegicus 38-41
20979027-6 2010 In addition, we identified Crabp2 (cellular retinoic acid binding protein 2) as an indirect target that potentially links the activities of Wnt and retinoic acid during antero-posterior patterning. Tretinoin 44-57 cellular retinoic acid binding protein 2 L homeolog Xenopus laevis 27-33
19903244-9 2010 The electrophoresis mobility shift assay revealed that ATRA produced two retarded bands, which were erased by antibody against chicken ovalbumin upstream promoter transcription factor I (COUP-TFI), RARalpha, and RXRalpha, respectively. Tretinoin 55-59 retinoic acid receptor alpha Gallus gallus 198-206
19131575-7 2009 Mechanism dissection suggests that TR2 and TR4 may affect the Oct-3/4 gene by binding to a direct repeat-1 element located in its promoter region, which is influenced by retinoic acid. Tretinoin 170-183 nuclear receptor subfamily 2 group C member 1 Homo sapiens 35-38
19131575-7 2009 Mechanism dissection suggests that TR2 and TR4 may affect the Oct-3/4 gene by binding to a direct repeat-1 element located in its promoter region, which is influenced by retinoic acid. Tretinoin 170-183 POU class 5 homeobox 1 Homo sapiens 62-69
19118439-11 2009 Increased expression of multiple components of the Cul5-containing E3 ubiquitin ligase complex with ATRA treatment of HL-60 cells indicates that this complex may play an important role in granulocytic differentiation. Tretinoin 100-104 cullin 5 Homo sapiens 51-55
2821315-6 1987 The TPA-induced as well as the RA- and cAMP-induced decreases in the RNAs hybridizable to pFT27 were regulated at the transcriptional level, whereas similar decreases in the RNAs hybridizable to pFT43 and pFT60 were regulated at the post-transcriptional level. Tretinoin 31-33 transmembrane protein 165 Mus musculus 90-95
19058293-3 2009 The current study investigated all-trans-retinoic acid (ATRA)-induced alteration of Smad expression in the developing neural tubes of mice. Tretinoin 31-54 SMAD family member 1 Mus musculus 84-88
19058293-3 2009 The current study investigated all-trans-retinoic acid (ATRA)-induced alteration of Smad expression in the developing neural tubes of mice. Tretinoin 56-60 SMAD family member 1 Mus musculus 84-88
19058293-6 2009 Results showed that ATRA treatment significantly increased expression of both p-Smad1 and total Smad1, while Smad6 was decreased in neural tissues of ATRA-exposed embryos in utero from E8 to E11, a critical period for neural tube formation. Tretinoin 20-24 SMAD family member 1 Mus musculus 80-85
19058293-6 2009 Results showed that ATRA treatment significantly increased expression of both p-Smad1 and total Smad1, while Smad6 was decreased in neural tissues of ATRA-exposed embryos in utero from E8 to E11, a critical period for neural tube formation. Tretinoin 20-24 SMAD family member 1 Mus musculus 96-101
19058293-7 2009 Data suggest that disruption of Smad signaling may be involved in ATRA-induced neural tube defects. Tretinoin 66-70 SMAD family member 1 Mus musculus 32-36
19538255-6 2009 Incubation with dibutyryl-cAMP and RA stimulated the expression of the EPC differentiation markers von Willebrand Factor (vWF) and VEGF receptor 2 (VEGFR-2), indicating successful differentiation in the fibrin clot. Tretinoin 35-37 Von Willebrand factor Mus musculus 122-125
19538255-7 2009 EPC differentiation induced by dibutyryl-cAMP and RA was confirmed in 2-D chamber slide cultures by positive vWF immunostaining, which was absent in BM controls. Tretinoin 50-52 Von Willebrand factor Mus musculus 109-112
19913583-6 2010 In contrast, PMA activated hMOR gene transcription when REST expression was knocked down by an antisense strategy or by retinoic acid-induced cell differentiation. Tretinoin 120-133 opioid receptor mu 1 Homo sapiens 27-31
19836325-7 2010 However, during differentiation with retinoic acid, a GLI-responsive luciferase assay and target genes PTCH1 and GLI1 expression reveal that the SHH signaling pathway is highly activated. Tretinoin 37-50 sonic hedgehog signaling molecule Homo sapiens 145-148
3327864-1 1987 The quantity of c-myc mRNA was measured during the retinoic-acid-induced differentiation of the pluripotent human teratoma cell line, Tera-2 cl. Tretinoin 51-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 16-21
19808863-15 2010 P19 cells metabolized RA to polar retinoids. Tretinoin 22-24 interleukin 23 subunit alpha Homo sapiens 0-3
19966493-5 2009 Gene expression levels of Toll-like receptor (TLR)1, TLR2, TLR4, TLR6 and dectin-1 in HL-60 cells were additionally affected by retinoic acid or DMSO and by co-culturing with S. cerevisiae or C. albicans. Tretinoin 128-141 toll like receptor 4 Homo sapiens 59-63
19151778-5 2009 Moreover, we showed that enforced expression of miR-342 in APL cells stimulated ATRA-induced differentiation. Tretinoin 80-84 microRNA 342 Homo sapiens 48-55
19351818-1 2009 Retinoic acid-induced gene G (RIG-G), a gene originally identified in all-trans retinoic acid-treated NB4 acute promyelocytic leukemia cells, is also induced by IFNalpha in various hematopoietic and solid tumor cells. Tretinoin 80-93 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 0-28
19351818-1 2009 Retinoic acid-induced gene G (RIG-G), a gene originally identified in all-trans retinoic acid-treated NB4 acute promyelocytic leukemia cells, is also induced by IFNalpha in various hematopoietic and solid tumor cells. Tretinoin 80-93 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 30-35
19966493-5 2009 Gene expression levels of Toll-like receptor (TLR)1, TLR2, TLR4, TLR6 and dectin-1 in HL-60 cells were additionally affected by retinoic acid or DMSO and by co-culturing with S. cerevisiae or C. albicans. Tretinoin 128-141 C-type lectin domain containing 7A Homo sapiens 74-82
2444656-5 1987 The differentiating capacity of retinoic acid was enhanced by all the IFNs-alpha tested, and by rIFN-beta, but not rIFN-gamma. Tretinoin 32-45 interferon beta 1 Rattus norvegicus 96-105
20078939-0 2009 [Role of Ezh2 in the all-trans retinoic acid induced P19 neural differentiation]. Tretinoin 31-44 interleukin 23 subunit alpha Homo sapiens 53-56
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 161-174 zinc finger protein 423 Homo sapiens 114-120
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 176-178 zinc finger protein 423 Homo sapiens 77-83
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 176-178 zinc finger protein 423 Homo sapiens 99-104
3793729-6 1987 The increase was paralleled by an increase in fibronectin mRNA, also reversed by exogenous retinoic acid. Tretinoin 91-104 fibronectin 1 Rattus norvegicus 46-57
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 176-178 zinc finger protein 423 Homo sapiens 106-109
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 176-178 zinc finger protein 423 Homo sapiens 114-120
19345331-4 2009 Downregulation of ZNF423 expression by RNA interference in neuroblastoma cells results in a growth advantage and resistance to RA-induced differentiation, whereas overexpression of ZNF423 leads to growth inhibition and enhanced differentiation. Tretinoin 127-129 zinc finger protein 423 Homo sapiens 18-24
18778286-0 2009 Retinoic acid inhibits in vivo interleukin-2 gene expression and T-cell activation in mice. Tretinoin 0-13 interleukin 2 Mus musculus 31-44
18778286-6 2009 Accordingly, after 7 hr, IL-2 gene expression was on average 55% lower in the atRA-treated mice compared with the control mice. Tretinoin 78-82 interleukin 2 Mus musculus 25-29
18778286-8 2009 Importantly, the atRA-mediated inhibition of IL-2 gene expression was accompanied by decreased DNA synthesis in murine T cells, suggesting a physiological relevance of the reduced IL-2 gene expression observed in transgenic reporter mice. Tretinoin 17-21 interleukin 2 Mus musculus 45-49
18778286-8 2009 Importantly, the atRA-mediated inhibition of IL-2 gene expression was accompanied by decreased DNA synthesis in murine T cells, suggesting a physiological relevance of the reduced IL-2 gene expression observed in transgenic reporter mice. Tretinoin 17-21 interleukin 2 Mus musculus 180-184
19922872-4 2009 H3K9 hypoacetylation, Hox gene repression, and the homeotic transformation caused by lack of Moz are all reversed by treatment with retinoic acid (RA). Tretinoin 132-145 K(lysine) acetyltransferase 6A Mus musculus 93-96
19922872-4 2009 H3K9 hypoacetylation, Hox gene repression, and the homeotic transformation caused by lack of Moz are all reversed by treatment with retinoic acid (RA). Tretinoin 147-149 K(lysine) acetyltransferase 6A Mus musculus 93-96
19839007-2 2009 It has been shown recently that intestinal mucosal DC are able to induce Foxp3(+) Treg through production of TGF-beta plus retinoic acid (RA). Tretinoin 123-136 forkhead box P3 Mus musculus 73-78
19839007-2 2009 It has been shown recently that intestinal mucosal DC are able to induce Foxp3(+) Treg through production of TGF-beta plus retinoic acid (RA). Tretinoin 138-140 forkhead box P3 Mus musculus 73-78
19808868-4 2009 RA targets the RARA moiety of the fusion, whereas arsenic targets its PML part. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 15-19
2895720-1 1987 A 2.4 kb RNA encoded by the murine Hox 1.1 (m6) homeobox gene is induced when F9 stem cells are differentiated with retinoic acid and dibutyryl cyclic AMP. Tretinoin 116-129 homeobox A7 Mus musculus 35-42
19814781-4 2009 Thus, the purpose of this study is to examine the molecular mechanisms by which RA enhances skeletal myogenesis and interacts with Wnt and BMP4 signalling during P19 or mouse embryonic stem (ES) cell differentiation. Tretinoin 80-82 wingless-type MMTV integration site family, member 3A Mus musculus 131-134
19814781-5 2009 RESULTS: Treatment of P19 or mouse ES cells with low levels of RA led to an enhancement of skeletal myogenesis by upregulating the expression of the mesodermal marker, Wnt3a, the skeletal muscle progenitor factors Pax3 and Meox1, and the myogenic regulatory factors (MRFs) MyoD and myogenin. Tretinoin 63-65 wingless-type MMTV integration site family, member 3A Mus musculus 168-173
19814781-5 2009 RESULTS: Treatment of P19 or mouse ES cells with low levels of RA led to an enhancement of skeletal myogenesis by upregulating the expression of the mesodermal marker, Wnt3a, the skeletal muscle progenitor factors Pax3 and Meox1, and the myogenic regulatory factors (MRFs) MyoD and myogenin. Tretinoin 63-65 myogenic differentiation 1 Mus musculus 273-277
19814781-5 2009 RESULTS: Treatment of P19 or mouse ES cells with low levels of RA led to an enhancement of skeletal myogenesis by upregulating the expression of the mesodermal marker, Wnt3a, the skeletal muscle progenitor factors Pax3 and Meox1, and the myogenic regulatory factors (MRFs) MyoD and myogenin. Tretinoin 63-65 myogenin Mus musculus 282-290
19814781-12 2009 CONCLUSION: RA can enhance skeletal myogenesis in stem cells at the muscle specification/progenitor stage by activating RARs bound directly to mesoderm and skeletal muscle progenitor genes, activating beta-catenin function and inhibiting bone morphogenetic protein (BMP) signalling. Tretinoin 12-14 arginyl-tRNA synthetase Mus musculus 120-124
19167408-7 2009 KEY FINDINGS: The cells treated with all-trans retinoic acid (ATRA) became well differentiated and had a gradually attenuated cell proliferation and migration, accompanied by a significant decrease in type II VLDLR expression. Tretinoin 62-66 very low density lipoprotein receptor Homo sapiens 209-214
19060179-0 2009 Retinoic acid-mediated down-regulation of ENO1/MBP-1 gene products caused decreased invasiveness of the follicular thyroid carcinoma cell lines. Tretinoin 0-13 enolase 1 Homo sapiens 42-46
19060179-8 2009 RA caused the dephosphorylation of ENO1-A1. Tretinoin 0-2 enolase 1 Homo sapiens 35-39
19060179-9 2009 Both, RA-mediated and specific knock-down of ENO1/MBP-1 resulted in the reduction of MYC oncoprotein, and simultaneously decreased proliferation rates of FTC-133 and FTC-238 cell lines. Tretinoin 6-8 enolase 1 Homo sapiens 45-49
3805126-8 1987 Addition of retinoic acid also stimulated RBP secretion by retinol-deficient hepatocytes. Tretinoin 12-25 retinol binding protein 4 Rattus norvegicus 42-45
19060179-9 2009 Both, RA-mediated and specific knock-down of ENO1/MBP-1 resulted in the reduction of MYC oncoprotein, and simultaneously decreased proliferation rates of FTC-133 and FTC-238 cell lines. Tretinoin 6-8 MYC proto-oncogene, bHLH transcription factor Homo sapiens 85-88
19060179-10 2009 In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies. Tretinoin 16-18 enolase 1 Homo sapiens 51-55
19060179-10 2009 In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies. Tretinoin 16-18 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-77
19060179-10 2009 In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies. Tretinoin 173-175 enolase 1 Homo sapiens 51-55
19060179-10 2009 In summary, the RA-mediated down-regulation of the ENO1 gene products and MYC oncoprotein provides a novel molecular mechanism facilitating the anti-proliferative effect of RA in human thyroid carcinoma cells and suggests new pathways for supportive RA therapies. Tretinoin 173-175 MYC proto-oncogene, bHLH transcription factor Homo sapiens 74-77
19546303-3 2009 All-trans-retinoic acid (ATRA) did not stimulate osteoclastogenesis in BMCs, but inhibited hormone and RANKL-induced gene expression and formation of osteoclasts. Tretinoin 0-23 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 103-108
19546303-3 2009 All-trans-retinoic acid (ATRA) did not stimulate osteoclastogenesis in BMCs, but inhibited hormone and RANKL-induced gene expression and formation of osteoclasts. Tretinoin 25-29 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 103-108
19546303-4 2009 In BMMs, spleen cells, and RAW264.7 cells, osteoclast differentiation and formation stimulated by M-CSF/RANKL were inhibited (IC(50) = 0.3 nM) by ATRA. Tretinoin 146-150 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 104-109
19853750-0 2009 Prenatal retinoic acid up-regulates pulmonary gene expression of COUP-TFII, FOG2, and GATA4 in pulmonary hypoplasia. Tretinoin 9-22 nuclear receptor subfamily 2, group F, member 2 Rattus norvegicus 65-74
19853750-13 2009 RESULTS: The relative mRNA expression levels of COUP-TFII, FOG2, and GATA4 were significantly increased in CDH + RA lungs compared to control, control + RA, and CDH (P < .05). Tretinoin 113-115 nuclear receptor subfamily 2, group F, member 2 Rattus norvegicus 48-57
19853750-13 2009 RESULTS: The relative mRNA expression levels of COUP-TFII, FOG2, and GATA4 were significantly increased in CDH + RA lungs compared to control, control + RA, and CDH (P < .05). Tretinoin 153-155 nuclear receptor subfamily 2, group F, member 2 Rattus norvegicus 48-57
19853750-14 2009 CONCLUSIONS: Up-regulation of pulmonary gene expression of COUP-TFII, FOG2, and GATA4 after prenatal treatment with retinoic acid in the nitrofen model of CDH suggests that RA may have a therapeutic potential in modulating lung growth. Tretinoin 116-129 nuclear receptor subfamily 2, group F, member 2 Rattus norvegicus 59-68
19853750-14 2009 CONCLUSIONS: Up-regulation of pulmonary gene expression of COUP-TFII, FOG2, and GATA4 after prenatal treatment with retinoic acid in the nitrofen model of CDH suggests that RA may have a therapeutic potential in modulating lung growth. Tretinoin 173-175 nuclear receptor subfamily 2, group F, member 2 Rattus norvegicus 59-68
19701462-10 2009 More than 33% of HB9+ sMN progenitor cells were observed after differentiation of dissociated neurospheres by all-trans retinoic acid (ATRA) and a Shh agonist for another week on monolayer culture. Tretinoin 110-133 motor neuron and pancreas homeobox 1 Homo sapiens 17-20
19701462-10 2009 More than 33% of HB9+ sMN progenitor cells were observed after differentiation of dissociated neurospheres by all-trans retinoic acid (ATRA) and a Shh agonist for another week on monolayer culture. Tretinoin 135-139 motor neuron and pancreas homeobox 1 Homo sapiens 17-20
19243620-6 2009 BMP4 is additionally able to up-regulate Hoxb4 ventrally, but the effect is restricted to the axial levels at which Hoxb4 is normally expressed, and only in the presence of retinoic acid (RA) or somites, suggesting a role for BMP in rendering the neural tube competent to express Hoxb4 in response to RA or somite signals. Tretinoin 173-186 bone morphogenetic protein 1 Homo sapiens 0-3
19100254-6 2009 We further show that fibroblast growth factor (FGF) signalling, induces the expression of the retinoic acid degrading enzyme cytochrome P450 (cyp) 26a1, and that one of its products, 4-oxo-RA, mimics the action of the RARalpha agonist in the differentiation of the NPCs into cholinergic neurons. Tretinoin 94-107 retinoic acid receptor alpha Homo sapiens 218-226
19115248-2 2009 The combined action of tamoxifen/all-trans retinoic acid was advantageous in MCF-7 cells, reducing cell proliferation, Bcl-2 and c-Myc protein levels and increasing E-Cadherin protein levels and Gap junctional Intercellular Communication. Tretinoin 43-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 129-134
19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 MYC proto-oncogene, bHLH transcription factor Homo sapiens 146-151
19115248-6 2009 We showed that the anti-tumoral effect of tamoxifen/all-trans retinoic acid is beneficial in MCF-7 breast cancer cells grown in a bradykinin-pro-mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2-bradykinin receptor inhibition. Tretinoin 62-75 bradykinin receptor B2 Homo sapiens 240-262
19701462-12 2009 These HB9+ cells differentiated into electrophysiologically functional cells and formed synapses with myotubes during a few weeks after ATRA/SAG treatment. Tretinoin 136-140 motor neuron and pancreas homeobox 1 Homo sapiens 6-9
2876993-0 1986 Pertussis toxin inhibits retinoic acid-induced expression of tissue transglutaminase in macrophages. Tretinoin 25-38 transglutaminase 2, C polypeptide Mus musculus 61-84
19506080-8 2009 During retinoic acid-induced differentiation, Neu4 expression was down-regulated in Neuro2a cells. Tretinoin 7-20 sialidase 4 Mus musculus 46-50
19357873-12 2009 ATRA and benazepril also significantly down-regulated Col-IV, FN expression and TIMP-1 expression (protein and mRNA) (P < 0.05). Tretinoin 0-4 fibronectin 1 Rattus norvegicus 62-64
19155306-0 2009 Inhibition of the peptidyl-prolyl-isomerase Pin1 enhances the responses of acute myeloid leukemia cells to retinoic acid via stabilization of RARalpha and PML-RARalpha. Tretinoin 107-120 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 44-48
19155306-0 2009 Inhibition of the peptidyl-prolyl-isomerase Pin1 enhances the responses of acute myeloid leukemia cells to retinoic acid via stabilization of RARalpha and PML-RARalpha. Tretinoin 107-120 retinoic acid receptor alpha Homo sapiens 142-150
19155306-0 2009 Inhibition of the peptidyl-prolyl-isomerase Pin1 enhances the responses of acute myeloid leukemia cells to retinoic acid via stabilization of RARalpha and PML-RARalpha. Tretinoin 107-120 PML nuclear body scaffold Homo sapiens 155-158
19155306-0 2009 Inhibition of the peptidyl-prolyl-isomerase Pin1 enhances the responses of acute myeloid leukemia cells to retinoic acid via stabilization of RARalpha and PML-RARalpha. Tretinoin 107-120 retinoic acid receptor alpha Homo sapiens 159-167
19155306-8 2009 Suppression of Pin1 by a specific short hairpin RNA in HL-60 or NB4 cells stabilizes RARalpha and PML-RARalpha, resulting in increased sensitivity to the cytodifferentiating and antiproliferative activities of all-trans retinoic acid. Tretinoin 220-233 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 15-19
2876993-1 1986 Retinoic acid rapidly induces the accumulation of a specific enzyme, tissue transglutaminase (EC 2.3.2.13), in mouse macrophages. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 69-92
19464179-1 2009 Retinoic acid (RA) is thought to be a key signaling molecule involved in limb bud patterning along the proximodistal or anteroposterior axes functioning through induction of Meis2 and Shh, respectively. Tretinoin 0-13 sonic hedgehog Mus musculus 184-187
2876993-2 1986 We have used the induction of tissue transglutaminase to study the regulation of gene expression by retinoic acid. Tretinoin 100-113 transglutaminase 2, C polypeptide Mus musculus 30-53
19464179-1 2009 Retinoic acid (RA) is thought to be a key signaling molecule involved in limb bud patterning along the proximodistal or anteroposterior axes functioning through induction of Meis2 and Shh, respectively. Tretinoin 15-17 sonic hedgehog Mus musculus 184-187
2876993-3 1986 In this study we report that pertussis toxin can inhibit retinoic acid-induced expression of tissue transglutaminase in mouse resident peritoneal macrophages. Tretinoin 57-70 transglutaminase 2, C polypeptide Mus musculus 93-116
3017743-0 1986 Action of retinoic acid on the diacylglycerol-induced ornithine decarboxylase activity, reduction in EGF binding and protein kinase C activation in rat tracheal epithelial 2C5 cells. Tretinoin 10-23 ornithine decarboxylase 1 Rattus norvegicus 54-77
19524524-3 2009 Here, we report that extrinsic signal retinoic acid (RA) and intrinsic transcription factor Neurogenin2 (Ngn2) collaboratively trigger transcriptionally active chromatin in spinal motor neuron genes during development. Tretinoin 38-51 neurogenin 2 Homo sapiens 105-109
19524524-5 2009 RA then facilitates the recruitment of a histone acetyltransferase CBP to the Ngn2/RAR-complex, markedly inducing histone H3/H4-acetylation. Tretinoin 0-2 neurogenin 2 Homo sapiens 78-82
19524524-5 2009 RA then facilitates the recruitment of a histone acetyltransferase CBP to the Ngn2/RAR-complex, markedly inducing histone H3/H4-acetylation. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 83-86
18803283-3 2009 The purpose of this study is to examine whether RA reduces ischemic brain injury through a BMP7 mechanism. Tretinoin 48-50 bone morphogenetic protein 7 Rattus norvegicus 91-95
19246282-5 2009 CONCLUSION: Retinoic acid can reduce the expression of MMP-1 and increase the expression of TIMP-1 in cultured human fibroblasts, suggesting its therapeutic potential for heat shock-induced skin aging. Tretinoin 12-25 matrix metallopeptidase 1 Homo sapiens 55-60
19236766-5 2009 The results showed that the expression of hoxc4 and hoxc6 genes in the differentiation process increased slightly on day 3, and were up to the most on day 7 (p < 0.05), while became lower on day 12 respectively in normal group, HCMV group and ATRA group. Tretinoin 246-250 homeobox C6 Homo sapiens 52-57
19236766-12 2009 At the same condition, ATRA (6 x 10(-8) mol/L at 60 nmol/ml) can up-regulate hoxc4 and hoxc6 genes expression. Tretinoin 23-27 homeobox C6 Homo sapiens 87-92
18992716-0 2009 Retinoic acid modulates retinaldehyde dehydrogenase 1 gene expression through the induction of GADD153-C/EBPbeta interaction. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A1 Homo sapiens 24-53
18992716-1 2009 Mammalian class I aldehyde dehydrogenase (ALDH) plays an important role in the biosynthesis of the hormone retinoic acid (RA), which modulates gene expression and cell differentiation. Tretinoin 107-120 aldehyde dehydrogenase 1 family member A1 Homo sapiens 42-46
18992716-1 2009 Mammalian class I aldehyde dehydrogenase (ALDH) plays an important role in the biosynthesis of the hormone retinoic acid (RA), which modulates gene expression and cell differentiation. Tretinoin 122-124 aldehyde dehydrogenase 1 family member A1 Homo sapiens 42-46
19282871-3 2009 The use of multidimensional protein identification technology (MudPIT) to identify changes in phosphoprotein levels in rat neural precursor cells treated with cytokines or retinoic acid showed that phosphorylation of the catalytic subunit of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K p110alpha) and dephosphorylation of the inositol phosphatase synaptojanin-1 were common to the gliogenic stimuli. Tretinoin 172-185 synaptojanin 1 Rattus norvegicus 356-370
3017743-0 1986 Action of retinoic acid on the diacylglycerol-induced ornithine decarboxylase activity, reduction in EGF binding and protein kinase C activation in rat tracheal epithelial 2C5 cells. Tretinoin 10-23 epidermal growth factor Rattus norvegicus 101-104
19332534-6 2009 Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. Tretinoin 110-114 interleukin 13 Sus scrofa 19-23
18992716-2 2009 RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor alpha (RARalpha) and the CCAAT/enhancer binding protein beta (C/EBPbeta). Tretinoin 0-2 aldehyde dehydrogenase 1 family member A1 Homo sapiens 46-51
18992716-2 2009 RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor alpha (RARalpha) and the CCAAT/enhancer binding protein beta (C/EBPbeta). Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 94-122
18992716-2 2009 RA has been shown to mediate control of human ALDH1 gene expression through modulation of the retinoic acid receptor alpha (RARalpha) and the CCAAT/enhancer binding protein beta (C/EBPbeta). Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 124-132
19432991-8 2009 The counter-regulated genes have been clustered into functional categories and bioinformatic analysis has identified the B-Raf/Mek/Erk branch of the MAP kinase pathway as one containing several genes whose upregulation by TPA is blocked by ATRA. Tretinoin 240-244 Braf transforming gene Mus musculus 121-126
3017743-5 1986 These results are consistent with the concept that RA does not act at the level of protein kinase C and inhibits ODC induction during a stage following protein kinase C activation. Tretinoin 51-53 ornithine decarboxylase 1 Rattus norvegicus 113-116
18992716-5 2009 Here we report that the RARalpha/retinoid X receptor beta (RXRbeta) complex binds to the mouse retinaldehyde dehydrogenase 1 (Raldh1) promoter at a non-consensus RA response element (RARE) with similar affinity to that of the consensus RARE. Tretinoin 24-26 retinoid X receptor beta Mus musculus 59-66
18992716-7 2009 Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box. Tretinoin 15-17 aldehyde dehydrogenase 1 family member A1 Homo sapiens 149-155
3747550-3 1986 Topical application of all trans-retinoic acid (25 nmol/cm2) immediately after the tape stripping of the skin significantly inhibited the induction of ornithine decarboxylase activity at all time points measured. Tretinoin 27-46 ornithine decarboxylase 1 Rattus norvegicus 151-174
18992716-8 2009 These data support a model in which high RA levels inhibit Raldh1 gene expression by sequestering C/EBPbeta through its interaction to GADD153. Tretinoin 41-43 aldehyde dehydrogenase 1 family member A1 Homo sapiens 59-65
19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 0-30
19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 32-40
3747550-4 1986 The inhibition by all trans-retinoic acid of ornithine decarboxylase induced by cellotape stripping was dose dependent as was found to be the case for arotinoid, retinol, Ro-10-1670, motretinid, 13-cis-retinoic acid, etretinate, and vitamin A. Tretinoin 22-41 ornithine decarboxylase 1 Rattus norvegicus 45-68
19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 149-157
19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 149-157
19753331-3 2009 In the current work, we have demonstrated a constitutive production of B2 receptor mRNA in the human promonocyte U937 cells and its two-fold augmentation after cell differentiation with retinoic acid and phorbol ester. Tretinoin 186-199 bradykinin receptor B2 Homo sapiens 71-82
19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 185-187 glycogen synthase kinase 3 beta Mus musculus 0-30
19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 185-187 glycogen synthase kinase 3 beta Mus musculus 32-40
3700483-4 1986 The level of N-myc mRNA decreased by 85% when PCC7 EC cells were induced by retinoic acid and cAMP treatment to form nerve-like cells. Tretinoin 76-89 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 13-18
19504631-6 2009 RESULT: RA up-regulated the mRNA expression of Mtap2 and Nefm, especially Mtap2 increased by 1.27 times, which was consistent with the morphological alteration. Tretinoin 8-10 neurofilament, medium polypeptide Mus musculus 57-61
19581203-7 2009 The lowest fraction of PCNA positive cells was also observed after the simultaneous addition ATRA (10(-5) M) and tamoxifen (10 microM) (30.75%+/-0.95, p<0.01, compared to the tamoxifen group). Tretinoin 93-97 proliferating cell nuclear antigen Homo sapiens 23-27
19636436-8 2009 ATRA treatment downregulates the expression of MT1-MMP, EMMPRIN, FAK, NF-kB, and p-ERK. Tretinoin 0-4 basigin (Ok blood group) Homo sapiens 56-63
19636436-8 2009 ATRA treatment downregulates the expression of MT1-MMP, EMMPRIN, FAK, NF-kB, and p-ERK. Tretinoin 0-4 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 81-86
19636436-13 2009 This inhibitory effect of ATRA on MMP-2 activity in human breast cancer cells (MCF-7) may result due to its inhibitory effect on MT1-MMP, EMMPRIN, and upregulation of TIMP-2. Tretinoin 26-30 basigin (Ok blood group) Homo sapiens 138-145
19429397-2 2009 In the present study the impact of a teratogenic pulse of fluconazole on the gene expression of cytochrome P450 (CYP) 26 isoforms, which plays a central role in maintaining proper retinoic acid levels by mediating its degradation, was investigated. Tretinoin 180-193 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 96-120
2871126-2 1986 Addition of retinoic acid to mouse resident peritoneal macrophages increased the level of tissue transglutaminase mRNA within 30-60 min. Tretinoin 12-25 transglutaminase 2, C polypeptide Mus musculus 90-113
19167408-7 2009 KEY FINDINGS: The cells treated with all-trans retinoic acid (ATRA) became well differentiated and had a gradually attenuated cell proliferation and migration, accompanied by a significant decrease in type II VLDLR expression. Tretinoin 37-60 very low density lipoprotein receptor Homo sapiens 209-214
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 10-23 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 145-151
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 25-27 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 145-151
19171200-4 2009 RA (1 microM) induced CYP26A1, CYP26B1, CYP2S1, CRABPII and LRAT mRNA. Tretinoin 0-2 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 40-46
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 24-47 nuclear receptor subfamily 2 group C member 1 Homo sapiens 280-283
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 49-53 nuclear receptor subfamily 2 group C member 1 Homo sapiens 151-154
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 49-53 PML nuclear body scaffold Homo sapiens 214-217
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 49-53 nuclear receptor subfamily 2 group C member 1 Homo sapiens 280-283
19204783-15 2009 2001) and this interaction is enhanced by the atRA-stimulated phosphorylation of TR2 at Thr-210 (Gupta et al. Tretinoin 46-50 nuclear receptor subfamily 2 group C member 1 Homo sapiens 81-84
3161611-9 1985 Also present was a prominent PL-Ca-dependent pp19 which remained unchanged following treatment with DMSO, RA, and 1,25(OH)2D3, but which diminished markedly in TPA-treated cells. Tretinoin 106-108 stathmin 1 Homo sapiens 45-49
19489262-0 2009 [Immunofluorescence examination of CK-13 expression in cell line KB differentiated by all-trans retinoic acid or As2 O3]. Tretinoin 96-109 keratin 13 Homo sapiens 35-40
19187242-1 2009 The retinoid-inducible serine carboxypeptidase 1 (Scpep1; formerly RISC) is a lysosomal matrix protein that was initially identified in a screen for genes induced by retinoic acid. Tretinoin 166-179 serine carboxypeptidase 1 Mus musculus 50-56
19187242-1 2009 The retinoid-inducible serine carboxypeptidase 1 (Scpep1; formerly RISC) is a lysosomal matrix protein that was initially identified in a screen for genes induced by retinoic acid. Tretinoin 166-179 serine carboxypeptidase 1 Mus musculus 67-71
4053079-3 1985 Studies with TPA and retinoic acid have shown that the first stage of neoplastic transformation of RTE cells cannot be enhanced by TPA but is inhibited by retinoic acid. Tretinoin 155-168 plasminogen activator, tissue type Rattus norvegicus 13-16
19642359-6 2009 Both Annexin II and u-PAR were highly expressed on APL cells, which declined after treatment with ATRA and/or ATO, but remained higher than those on normal bone marrow mononuclear cells. Tretinoin 98-102 annexin A2 Homo sapiens 5-15
19642359-6 2009 Both Annexin II and u-PAR were highly expressed on APL cells, which declined after treatment with ATRA and/or ATO, but remained higher than those on normal bone marrow mononuclear cells. Tretinoin 98-102 plasminogen activator, urokinase receptor Homo sapiens 20-25
19073915-3 2008 We have recently reported that RA mediates a type of homeostatic synaptic plasticity through activation of dendritic protein synthesis, a process that requires dendritically localized RARalpha and is independent of transcriptional regulation. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 184-192
19642359-8 2009 ATRA and ATO therapy induces down-regulation of Annexin II and u-PAR expression, which may be contribute, at least in part, to the relief of the hemorrhagic complications in APL. Tretinoin 0-4 annexin A2 Homo sapiens 48-58
19642359-8 2009 ATRA and ATO therapy induces down-regulation of Annexin II and u-PAR expression, which may be contribute, at least in part, to the relief of the hemorrhagic complications in APL. Tretinoin 0-4 plasminogen activator, urokinase receptor Homo sapiens 63-68
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 0-13 lysine methyltransferase 2A Homo sapiens 91-94
3916193-3 1985 In particular, it is shown that retinoic acid inhibits the proliferative effects of transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) on fibroblasts that have been transfected with the c-myc oncogene. Tretinoin 32-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 220-225
19011747-4 2008 ADH1 and ADH2 are the major MDR enzymes in liver retinol detoxification, while ADH3 (less active) and ADH4 (most active) participate in RA generation in tissues. Tretinoin 136-138 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 0-4
19011747-4 2008 ADH1 and ADH2 are the major MDR enzymes in liver retinol detoxification, while ADH3 (less active) and ADH4 (most active) participate in RA generation in tissues. Tretinoin 136-138 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 79-83
19764350-0 2009 The role of Cdk5 in retinoic acid-induced apoptosis of cervical cancer cell line. Tretinoin 20-33 cyclin dependent kinase 5 Homo sapiens 12-16
19764350-7 2009 Here, we report that RA treatment decreased the growth of human cervical cancer cell line, HeLa, and Cdk5 contributed to this effect. Tretinoin 21-23 cyclin dependent kinase 5 Homo sapiens 101-105
19764350-9 2009 We further identified that RA-induced growth inhibition was partly correlated to Cdk5 activity-related apoptosis by detecting cell cycle distribution of sub G1 phase and the signals of Annexin V staining. Tretinoin 27-29 cyclin dependent kinase 5 Homo sapiens 81-85
3916193-4 1985 The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene. Tretinoin 15-28 MYC proto-oncogene, bHLH transcription factor Homo sapiens 198-203
19764350-9 2009 We further identified that RA-induced growth inhibition was partly correlated to Cdk5 activity-related apoptosis by detecting cell cycle distribution of sub G1 phase and the signals of Annexin V staining. Tretinoin 27-29 annexin A5 Homo sapiens 185-194
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 cyclin dependent kinase 5 Homo sapiens 45-49
18987198-2 2008 The aim of the present study was to evaluate the therapeutic effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the neuropathology and deficits of spatial learning and memory in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice, a well established AD mouse model. Tretinoin 71-94 amyloid beta (A4) precursor protein Mus musculus 207-232
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 cyclin dependent kinase 5 Homo sapiens 237-241
3916193-4 1985 The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene. Tretinoin 15-28 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 229-234
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 cyclin dependent kinase 5 Homo sapiens 237-241
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 277-279 cyclin dependent kinase 5 Homo sapiens 45-49
18987198-2 2008 The aim of the present study was to evaluate the therapeutic effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the neuropathology and deficits of spatial learning and memory in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice, a well established AD mouse model. Tretinoin 71-94 presenilin 1 Mus musculus 243-255
18987198-2 2008 The aim of the present study was to evaluate the therapeutic effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the neuropathology and deficits of spatial learning and memory in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice, a well established AD mouse model. Tretinoin 71-94 presenilin 1 Mus musculus 257-260
18987198-2 2008 The aim of the present study was to evaluate the therapeutic effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the neuropathology and deficits of spatial learning and memory in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice, a well established AD mouse model. Tretinoin 96-100 amyloid beta (A4) precursor protein Mus musculus 207-232
3916193-4 1985 The ability of retinoic acid to induce differentiation in several types of human and murine tumor cells also is associated with the ability of retinoic acid to suppress the expression of either the c-myc oncogene, or the related N-myc gene. Tretinoin 143-156 MYC proto-oncogene, bHLH transcription factor Homo sapiens 198-203
18987198-2 2008 The aim of the present study was to evaluate the therapeutic effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the neuropathology and deficits of spatial learning and memory in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice, a well established AD mouse model. Tretinoin 96-100 presenilin 1 Mus musculus 243-255
18987198-2 2008 The aim of the present study was to evaluate the therapeutic effect of all-trans retinoic acid (ATRA), an active metabolite of vitamin A, on the neuropathology and deficits of spatial learning and memory in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic mice, a well established AD mouse model. Tretinoin 96-100 presenilin 1 Mus musculus 257-260
6322972-0 1984 Retinoic acid-induced changes in epidermal growth factor binding and in biological responses mediated by phorbol ester tumor promoter. Tretinoin 0-13 epidermal growth factor Mus musculus 33-56
18771528-2 2008 Recently, many synthetic retinoids have been developed and among them, a novel synthetic retinoid, Am80 (Tamibarotene) is an RARalpha- and RARbeta-specific retinoid expected to overcome ATRA resistance. Tretinoin 186-190 retinoic acid receptor alpha Homo sapiens 125-133
19135033-6 2009 In addition, we demonstrate that the RA-mediated activation of Galanin promoter activity and Brn-3a N-terminal transcriptional activity are both blocked by pan-MEK inhibitors, and show that the expression of a constitutively-active mutant of MEK1, but not MEK5, is sufficient to increase Brn-3a activity. Tretinoin 37-39 mitogen-activated protein kinase kinase 1 Homo sapiens 242-246
19135033-6 2009 In addition, we demonstrate that the RA-mediated activation of Galanin promoter activity and Brn-3a N-terminal transcriptional activity are both blocked by pan-MEK inhibitors, and show that the expression of a constitutively-active mutant of MEK1, but not MEK5, is sufficient to increase Brn-3a activity. Tretinoin 37-39 POU class 4 homeobox 1 Homo sapiens 288-294
19135033-7 2009 These results reveal an important role for the ERK1/2 pathway in Brn-3a regulation during RA-mediated neuronal differentiation and define the neuropeptide Galanin as a novel target of this transcription factor. Tretinoin 90-92 POU class 4 homeobox 1 Homo sapiens 65-71
19204112-0 2009 Contrasting roles for all-trans retinoic acid in TGF-beta-mediated induction of Foxp3 and Il10 genes in developing regulatory T cells. Tretinoin 32-45 forkhead box P3 Mus musculus 80-85
18637026-6 2008 The differentiation-inhibitory effect of RA was mimicked by conditioned medium from RA-treated ESCs and was accompanied with up-regulated expression of leukemia inhibitory factor (LIF), Wnt3a, Wnt5a, and Wnt6. Tretinoin 41-43 leukemia inhibitory factor Mus musculus 152-178
18637026-6 2008 The differentiation-inhibitory effect of RA was mimicked by conditioned medium from RA-treated ESCs and was accompanied with up-regulated expression of leukemia inhibitory factor (LIF), Wnt3a, Wnt5a, and Wnt6. Tretinoin 41-43 leukemia inhibitory factor Mus musculus 180-183
6322972-1 1984 We investigated the ability of retinoic acid (RA) to alter the binding of epidermal growth factor (EGF) to Rat-1 and Swiss mouse 3T3 cells, the EGF-related induction of ornithine decarboxylase (ODC) activity and DNA synthesis. Tretinoin 31-44 epidermal growth factor Mus musculus 144-147
18637026-6 2008 The differentiation-inhibitory effect of RA was mimicked by conditioned medium from RA-treated ESCs and was accompanied with up-regulated expression of leukemia inhibitory factor (LIF), Wnt3a, Wnt5a, and Wnt6. Tretinoin 41-43 wingless-type MMTV integration site family, member 3A Mus musculus 186-191
19176369-2 2009 ATRA-induced phosphorylation of the Akt kinase and ribosomal S6 protein in APL cells was sensitive to class I PI3K, and p110beta or p110delta inhibitors, and to the mammalian target of rapamycin (mTOR) inhibitor rapamycin. Tretinoin 0-4 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 132-141
18637026-7 2008 Such RA-induced prevention of ESC differentiation was attenuated by a neutralizing antibody against LIF or by a specific Wnt antagonist Fz8-Fc and was totally reversed in the presence of both of them. Tretinoin 5-7 leukemia inhibitory factor Mus musculus 100-103
6603411-2 1983 Retinoic acid increased the production of HCG and PS beta G but inhibited the production of HCG alpha in these cells. Tretinoin 0-13 protein S (beta) pseudogene Homo sapiens 50-57
18637026-7 2008 Such RA-induced prevention of ESC differentiation was attenuated by a neutralizing antibody against LIF or by a specific Wnt antagonist Fz8-Fc and was totally reversed in the presence of both of them. Tretinoin 5-7 wingless-type MMTV integration site family, member 3A Mus musculus 121-124
18637026-8 2008 Furthermore, knock-down of beta-catenin, a component of the Wnt signaling pathway, by small interfering RNA counteracted the effect of RA. Tretinoin 135-137 wingless-type MMTV integration site family, member 3A Mus musculus 60-63
18637026-10 2008 These findings reveal a novel role of RA in ESC self-renewal and provide new insight into the regulatory mechanism of differentiation-dependent self-renewal of ESCs, in which Wnt proteins and LIF induced by RA have the synergistic action. Tretinoin 38-40 wingless-type MMTV integration site family, member 3A Mus musculus 175-178
18637026-10 2008 These findings reveal a novel role of RA in ESC self-renewal and provide new insight into the regulatory mechanism of differentiation-dependent self-renewal of ESCs, in which Wnt proteins and LIF induced by RA have the synergistic action. Tretinoin 38-40 leukemia inhibitory factor Mus musculus 192-195
18637026-10 2008 These findings reveal a novel role of RA in ESC self-renewal and provide new insight into the regulatory mechanism of differentiation-dependent self-renewal of ESCs, in which Wnt proteins and LIF induced by RA have the synergistic action. Tretinoin 207-209 wingless-type MMTV integration site family, member 3A Mus musculus 175-178
18637026-10 2008 These findings reveal a novel role of RA in ESC self-renewal and provide new insight into the regulatory mechanism of differentiation-dependent self-renewal of ESCs, in which Wnt proteins and LIF induced by RA have the synergistic action. Tretinoin 207-209 leukemia inhibitory factor Mus musculus 192-195
19176369-4 2009 Class I PI3K inhibition could also reverse ATRA-induced protection of these cells against doxorubicin and arsenic trioxide, correlating with impaired induction of the antiapoptotic MCL-1 protein. Tretinoin 43-47 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 181-186
19176369-6 2009 In summary, class I PI3K signaling, mediated by p110beta and p110delta, plays an important role in basal and ATRA-induced cell survival mechanisms in APL. Tretinoin 109-113 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 61-70
19168680-7 2009 We demonstrate that RA signalling is required at late gastrulation stages for mesodermal and neural progenitors to respond to the Shh signal. Tretinoin 20-22 sonic hedgehog Mus musculus 130-133
19168680-8 2009 Whole-embryo culture experiments indicate that the proper response of cells to Shh requires two RA-dependent mechanisms: (1) a balanced antagonism between Fgf and RA signals, and (2) a RA-mediated repression of Gli2 expression. Tretinoin 96-98 sonic hedgehog Mus musculus 79-82
6603411-3 1983 Passage of SPA255-26 placental cells in medium containing retinoic acid induced a stable altered phenotype characterized by elevated levels of HCG and PS beta G and a reduced level of HCG alpha. Tretinoin 58-71 protein S (beta) pseudogene Homo sapiens 151-158
6603411-4 1983 The retinoic acid induced phenotypic changes in these placental cells were reversible; removal of retinoic acid immediately decreased the production of HCG and PS beta G while increasing the production of HCG alpha. Tretinoin 4-17 protein S (beta) pseudogene Homo sapiens 160-167
6603411-4 1983 The retinoic acid induced phenotypic changes in these placental cells were reversible; removal of retinoic acid immediately decreased the production of HCG and PS beta G while increasing the production of HCG alpha. Tretinoin 98-111 protein S (beta) pseudogene Homo sapiens 160-167
19010342-10 2009 Chemical and immuno-inhibition metabolism studies suggested that Cyp26a1, Cyp2b, and Cyp3a, but not Cyp1a1 proteins were involved in atRA metabolism. Tretinoin 133-137 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 65-72
18949372-3 2008 Retinoic acid (RA), a molecule able to induce differentiation and to decrease MYCN expression, is used in the therapy of neuroblastomas. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 78-82
18949372-3 2008 Retinoic acid (RA), a molecule able to induce differentiation and to decrease MYCN expression, is used in the therapy of neuroblastomas. Tretinoin 15-17 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 78-82
6603411-7 1983 Our data suggest that retinoic acid may be needed to maintain a balanced production of HCG, HCG alpha, and PS beta G in placental cells in vitro. Tretinoin 22-35 protein S (beta) pseudogene Homo sapiens 107-114
18957893-3 2008 Retinoic acid-elicited differentiation promoted assembly of alpha-syn aggregates after TetOff induction in 3D5 cells. Tretinoin 0-13 synuclein alpha Homo sapiens 60-69
19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 62-85 colony stimulating factor 3 Homo sapiens 51-56
19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 62-85 colony stimulating factor 3 Homo sapiens 244-249
6667418-1 1983 We report here than skin fibroblasts (SF) from patients with hereditary adenomatosis of the colon and rectum (ACR) and its Gardner syndrome (GS) variant are abnormally resistant to retinoic acid (RA). Tretinoin 181-194 acrosin Homo sapiens 110-113
19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 87-91 colony stimulating factor 3 Homo sapiens 51-56
19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 87-91 colony stimulating factor 3 Homo sapiens 244-249
19537526-7 2009 Coadministration of 100 microg/kg x 5 injection of G-CSF with all-trans-retinoic acid (ATRA; 3 mg/ kg/d) for 3 weeks from 2 weeks after PPE instillation significantly inhibited the increase in Lm by 36% (p < 0.01), whereas administration of G-CSF or ATRA alone did not produce significant improvement. Tretinoin 253-257 colony stimulating factor 3 Homo sapiens 51-56
19671997-12 2009 These results strongly suggest that RALDH1 mRNA expression is suppressed by 17beta-estradiol through ERalpha, and that estrogen regulates the expression of RALDH1 and production of RA in the anterior pituitary gland. Tretinoin 36-38 estrogen receptor 1 Rattus norvegicus 101-108
18713813-5 2008 Altogether, these findings support the conclusion that RXRB heterodimerized with a RA-liganded RARA transduces signals required in SC for spermatid release. Tretinoin 83-85 retinoid X receptor beta Mus musculus 55-59
18957211-3 2008 demonstrate that synthesis of retinoic acid offsets chronic network inactivity by increasing synaptic strength through upregulation of GluR1 receptors. Tretinoin 30-43 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 135-140
6667418-1 1983 We report here than skin fibroblasts (SF) from patients with hereditary adenomatosis of the colon and rectum (ACR) and its Gardner syndrome (GS) variant are abnormally resistant to retinoic acid (RA). Tretinoin 196-198 acrosin Homo sapiens 110-113
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 H3 histone pseudogene 16 Homo sapiens 120-123
20067883-5 2009 The aim of the study was to determine the effects of vitamin A family compounds (retinol, beta-carotene, lycopene, all-trans -, 9-cis - and 13-cis retinoic acid) on the growth and proliferation of CRL-11731 endometrioid ovary cancer cell line and on docetaxel and estradiol activity in this culture. Tretinoin 147-160 interleukin 31 receptor A Homo sapiens 197-200
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 E2F transcription factor 1 Homo sapiens 161-165
6667418-4 1983 ACR cells were abnormally resistant to RA at all concentrations tested. Tretinoin 39-41 acrosin Homo sapiens 0-3
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 H3 histone pseudogene 16 Homo sapiens 120-123
6667418-5 1983 Although more resistant to RA-induced cytotoxicity, ACR cells showed morphological changes on exposure to RA similar to those seen in normal cells. Tretinoin 106-108 acrosin Homo sapiens 52-55
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 E2F transcription factor 1 Homo sapiens 161-165
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 185-187 E2F transcription factor 1 Homo sapiens 161-165
6959135-3 1982 Retinoic acid, a derivative of vitamin A, inhibited in a dose-dependent manner both the increase in OrnDCase activity and the release of FN induced by TPA. Tretinoin 0-13 fibronectin 1 Mus musculus 137-139
18840692-3 2008 We have previously shown that all-trans retinoic acid (RA) mediates activity blockade-induced synaptic scaling by activating dendritic GluR1 synthesis and that this process requires RARalpha, a member of the nuclear RA receptor family. Tretinoin 40-53 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 135-140
18840692-3 2008 We have previously shown that all-trans retinoic acid (RA) mediates activity blockade-induced synaptic scaling by activating dendritic GluR1 synthesis and that this process requires RARalpha, a member of the nuclear RA receptor family. Tretinoin 40-53 retinoic acid receptor alpha Homo sapiens 182-190
18840692-3 2008 We have previously shown that all-trans retinoic acid (RA) mediates activity blockade-induced synaptic scaling by activating dendritic GluR1 synthesis and that this process requires RARalpha, a member of the nuclear RA receptor family. Tretinoin 55-57 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 135-140
19273155-4 2009 The treatment of APL patients with all-transretinoic acid (ATRA) and arsenic trioxide which target the PML-RARA oncoprotein results in clinical remission, associated with blast cell differentiation and reformation of the PML NBs, thus linking NB integrity with disease status. Tretinoin 35-57 PML nuclear body scaffold Homo sapiens 103-106
19273155-4 2009 The treatment of APL patients with all-transretinoic acid (ATRA) and arsenic trioxide which target the PML-RARA oncoprotein results in clinical remission, associated with blast cell differentiation and reformation of the PML NBs, thus linking NB integrity with disease status. Tretinoin 35-57 retinoic acid receptor alpha Homo sapiens 107-111
19273155-4 2009 The treatment of APL patients with all-transretinoic acid (ATRA) and arsenic trioxide which target the PML-RARA oncoprotein results in clinical remission, associated with blast cell differentiation and reformation of the PML NBs, thus linking NB integrity with disease status. Tretinoin 35-57 PML nuclear body scaffold Homo sapiens 221-224
19273155-4 2009 The treatment of APL patients with all-transretinoic acid (ATRA) and arsenic trioxide which target the PML-RARA oncoprotein results in clinical remission, associated with blast cell differentiation and reformation of the PML NBs, thus linking NB integrity with disease status. Tretinoin 59-63 PML nuclear body scaffold Homo sapiens 103-106
19273155-4 2009 The treatment of APL patients with all-transretinoic acid (ATRA) and arsenic trioxide which target the PML-RARA oncoprotein results in clinical remission, associated with blast cell differentiation and reformation of the PML NBs, thus linking NB integrity with disease status. Tretinoin 59-63 retinoic acid receptor alpha Homo sapiens 107-111
19273155-4 2009 The treatment of APL patients with all-transretinoic acid (ATRA) and arsenic trioxide which target the PML-RARA oncoprotein results in clinical remission, associated with blast cell differentiation and reformation of the PML NBs, thus linking NB integrity with disease status. Tretinoin 59-63 PML nuclear body scaffold Homo sapiens 221-224
19173001-3 2009 In previous studies we demonstrated that either genetic mutations, or loss, of retinoic acid receptor alpha (RARalpha), can impair the integration of the retinoic acid (RA) signal at the chromatin of RA-responsive genes downstream of RARalpha, and can lead to aberrant repressive chromatin states marked by epigenetic modifications. Tretinoin 79-92 retinoic acid receptor alpha Homo sapiens 109-117
19173001-3 2009 In previous studies we demonstrated that either genetic mutations, or loss, of retinoic acid receptor alpha (RARalpha), can impair the integration of the retinoic acid (RA) signal at the chromatin of RA-responsive genes downstream of RARalpha, and can lead to aberrant repressive chromatin states marked by epigenetic modifications. Tretinoin 79-92 retinoic acid receptor alpha Homo sapiens 234-242
18840692-3 2008 We have previously shown that all-trans retinoic acid (RA) mediates activity blockade-induced synaptic scaling by activating dendritic GluR1 synthesis and that this process requires RARalpha, a member of the nuclear RA receptor family. Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 182-190
18840692-5 2008 Here, we show that activity blockade or RA treatment in neurons enhances the concentration of RARalpha in the dendritic RNA granules and activates local GluR1 synthesis in these RNA granules. Tretinoin 40-42 retinoic acid receptor alpha Homo sapiens 94-102
18840692-5 2008 Here, we show that activity blockade or RA treatment in neurons enhances the concentration of RARalpha in the dendritic RNA granules and activates local GluR1 synthesis in these RNA granules. Tretinoin 40-42 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 153-158
18840692-7 2008 Taken together, our results provide a direct link between dendritically localized RARalpha and local GluR1 synthesis in RNA granules during RA-mediated synaptic signaling in homeostatic synaptic plasticity. Tretinoin 82-84 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 101-106
19173001-3 2009 In previous studies we demonstrated that either genetic mutations, or loss, of retinoic acid receptor alpha (RARalpha), can impair the integration of the retinoic acid (RA) signal at the chromatin of RA-responsive genes downstream of RARalpha, and can lead to aberrant repressive chromatin states marked by epigenetic modifications. Tretinoin 109-111 retinoic acid receptor alpha Homo sapiens 79-107
19173001-3 2009 In previous studies we demonstrated that either genetic mutations, or loss, of retinoic acid receptor alpha (RARalpha), can impair the integration of the retinoic acid (RA) signal at the chromatin of RA-responsive genes downstream of RARalpha, and can lead to aberrant repressive chromatin states marked by epigenetic modifications. Tretinoin 109-111 retinoic acid receptor alpha Homo sapiens 234-242
19173001-5 2009 METHODOLOGY/PRINCIPAL FINDINGS: To hamper the availability of RA at RARalpha in untransformed human mammary epithelial cells, we targeted the cellular RA-binding protein 2 (CRABP2), which transports RA from the cytoplasm onto the nuclear RARs. Tretinoin 62-64 retinoic acid receptor alpha Homo sapiens 68-76
6959135-6 1982 Moreover, addition of retinoic acid to the enucleated cells inhibited the phorbol ester-induced release of FN in a dose-dependent manner. Tretinoin 22-35 fibronectin 1 Mus musculus 107-109
6813141-1 1982 The activity of phospholipase A2 was tested both in rat skin and human psoriatic skin before and after systemic treatment with a retinoic acid derivative: RO 10-9359. Tretinoin 129-142 phospholipase A2 group IB Rattus norvegicus 16-32
18930031-6 2008 During retinoic acid-induced neuronal differentiation, Cyclin D2 protein but not mRNA expression is strongly increased, concurrent with the down-regulation of miR-302b and Oct4. Tretinoin 7-20 microRNA 302b Homo sapiens 159-167
18930031-6 2008 During retinoic acid-induced neuronal differentiation, Cyclin D2 protein but not mRNA expression is strongly increased, concurrent with the down-regulation of miR-302b and Oct4. Tretinoin 7-20 POU class 5 homeobox 1 Homo sapiens 172-176
18692045-8 2008 To a lesser degree they also diminished retinoic acid-induced earlier markers of cell differentiation, namely CD38 and CD11b. Tretinoin 40-53 CD38 molecule Homo sapiens 110-114
7201471-4 1982 Endo A and Endo B messenger RNA can be detected in F9.22 cells 48 to 72 h after exposure to retinoic acid, which is coincident with the expression of Endo A and Endo B proteins. Tretinoin 92-105 keratin 8 Mus musculus 0-6
18813784-12 2008 TGFbeta and retinoic acid downregulated the expression of p63 in immortalized nasopharyngeal epithelial cells and may play a role in regulating differentiation in squamous epithelial cells with potential applications in prevention and treatment of nasopharyngeal carcinoma. Tretinoin 12-25 tumor protein p63 Homo sapiens 58-61
18846337-14 2008 In comparison with group A, the mRNA levels of TGF-beta1 and CTGF in ATRA-treated CBDL groups were significantly decreased (P<0.05). Tretinoin 69-73 cellular communication network factor 2 Rattus norvegicus 61-65
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 cellular communication network factor 2 Rattus norvegicus 124-128
18805411-8 2008 Our findings demonstrate that there is dynamic regulation of RA signalling in different regions of the skin and provide evidence for interactions between the RA, beta-catenin and Notch pathways. Tretinoin 61-63 catenin beta 1 Homo sapiens 162-174
18989765-13 2008 Furthermore, ATRA suppressed the expression of LPS-stimulated c-Raf, MKK1/2 and ERK expression of THP-1 cells. Tretinoin 13-17 mitogen-activated protein kinase kinase 1 Homo sapiens 69-75
7201471-4 1982 Endo A and Endo B messenger RNA can be detected in F9.22 cells 48 to 72 h after exposure to retinoic acid, which is coincident with the expression of Endo A and Endo B proteins. Tretinoin 92-105 keratin 8 Mus musculus 150-156
18799012-8 2008 Previous studies have shown that, in the mouse embryo, female-specific induction of STRA8 and meiosis are triggered by retinoic acid. Tretinoin 119-132 stimulated by retinoic acid gene 8 Mus musculus 84-89
233127-4 1979 This letter describes the binding characteristics and numbers of the EGF receptors on EC and END cells and shows that exogenous retinoic acid increases the numbers of EGF receptors on END cells. Tretinoin 128-141 epidermal growth factor Mus musculus 69-72
19175987-0 2008 [In vitro study of the effects of CDA-II combined with cAMP on apoptosis induction in retinoic acid resistant acute promyelocytic leukemia cells]. Tretinoin 86-99 SEC23 homolog B, COPII coat complex component Homo sapiens 34-40
19175987-1 2008 OBJECTIVE: To investigate the effects of CDA-II alone or combined with cAMP on the retinoic acid (RA)-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 83-96 SEC23 homolog B, COPII coat complex component Homo sapiens 41-47
19175987-1 2008 OBJECTIVE: To investigate the effects of CDA-II alone or combined with cAMP on the retinoic acid (RA)-resistant acute promyelocytic leukemia (APL) cells. Tretinoin 98-100 SEC23 homolog B, COPII coat complex component Homo sapiens 41-47
18682553-0 2008 Retinoic acid-stimulated sequential phosphorylation, PML recruitment, and SUMOylation of nuclear receptor TR2 to suppress Oct4 expression. Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 53-56
18682553-0 2008 Retinoic acid-stimulated sequential phosphorylation, PML recruitment, and SUMOylation of nuclear receptor TR2 to suppress Oct4 expression. Tretinoin 0-13 nuclear receptor subfamily 2 group C member 1 Homo sapiens 106-109
18682553-0 2008 Retinoic acid-stimulated sequential phosphorylation, PML recruitment, and SUMOylation of nuclear receptor TR2 to suppress Oct4 expression. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 122-126
18642056-5 2008 C-myc was down regulated by treatment with ATRA, alpha-TS and their combination to 22%, 48.5%, and 52%, respectively. Tretinoin 43-47 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
18801339-4 2008 Specifically, phosphorylation of tau at amino acid residues Ser(202), Ser(396) and Ser(404) was monitored in retinoic acid induced, human cell lines: SH-SY5Y and NTera-2. Tretinoin 109-122 microtubule associated protein tau Homo sapiens 33-36
18495959-0 2008 Human basophils activated by mast cell-derived IL-3 express retinaldehyde dehydrogenase-II and produce the immunoregulatory mediator retinoic acid. Tretinoin 133-146 interleukin 3 Homo sapiens 47-51
233127-4 1979 This letter describes the binding characteristics and numbers of the EGF receptors on EC and END cells and shows that exogenous retinoic acid increases the numbers of EGF receptors on END cells. Tretinoin 128-141 epidermal growth factor Mus musculus 167-170
18495959-6 2008 RA generated by RALDH2 in basophils modulates IL-3-induced gene expression in an autocrine manner, providing positive (CD25) as well as negative (granzyme B) regulation. Tretinoin 0-2 interleukin 3 Homo sapiens 46-50
18495959-6 2008 RA generated by RALDH2 in basophils modulates IL-3-induced gene expression in an autocrine manner, providing positive (CD25) as well as negative (granzyme B) regulation. Tretinoin 0-2 granzyme B Homo sapiens 146-156
18539269-1 2008 Retinoic acid (RA) is known to be required at various levels of eye patterning via Retinoic Acid Receptors (RAR); however the molecular and cellular mechanisms triggered by these nuclear receptors are still obscure. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 108-111
18495959-8 2008 Furthermore, RA derived from IL-3-activated basophils provides a novel mechanism of Th2 polarization. Tretinoin 13-15 interleukin 3 Homo sapiens 29-33
33757404-0 2021 Retinoic acid abrogates LPS-induced inflammatory response via negative regulation of NF-kappa B/miR-21 signaling. Tretinoin 0-13 microRNA 21 Homo sapiens 96-102
18406560-6 2008 The distribution of RA was experimentally changed either by ectopic expression of Cyp26A1, or by applications of RA. Tretinoin 20-22 cytochrome P450 family 26 subfamily A member 1 Gallus gallus 82-89
18406560-8 2008 The results show that in the chick retina the compartmentalized expression of RA metabolizing enzymes requires the spatially restricted expression of the transcription factors cVax/Vax2 and Tbx5. Tretinoin 78-80 T-box 5 Gallus gallus 190-194
18636178-6 2008 In this study, we observed that while atRA upregulates AQP3 expression in cultured human skin keratinocytes (HaCaT cells), nicotinamide attenuates the effect of atRA in a concentration-dependent manner. Tretinoin 38-42 aquaporin 3 (Gill blood group) Homo sapiens 55-59
18974118-0 2008 c-Cbl interacts with CD38 and promotes retinoic acid-induced differentiation and G0 arrest of human myeloblastic leukemia cells. Tretinoin 39-52 Cbl proto-oncogene Homo sapiens 0-5
18636178-8 2008 PD153035, an EGFR inhibitor, and U0126, an ERK inhibitor, inhibit atRA-induced upregulation of AQP3. Tretinoin 66-70 aquaporin 3 (Gill blood group) Homo sapiens 95-99
33757404-8 2021 RA shifted the polarization away from the M1 state by negative regulation of IKKalpha/beta, p65, and miR-21. Tretinoin 0-2 microRNA 21 Homo sapiens 101-107
18636178-9 2008 Nicotinamide also inhibits atRA-induced activation of EGFR/ERK signal transduction and decreases water permeability by downregulating AQP3 expression. Tretinoin 27-31 aquaporin 3 (Gill blood group) Homo sapiens 134-138
18974118-4 2008 Stable transfectants ectopically expressing c-Cbl underwent myeloid differentiation faster than wild-type (wt) cells when treated with RA. Tretinoin 135-137 Cbl proto-oncogene Homo sapiens 44-49
18974118-5 2008 In contrast, c-Cbl knockdown stable transfectants differentiated slower than wt cells when treated with RA. Tretinoin 104-106 Cbl proto-oncogene Homo sapiens 13-18
18636178-10 2008 Collectively, our results indicate that the effect of atRA on AQP3 expression is at least partly mediated by EGFR/ERK signaling in cultured human skin keratinocytes. Tretinoin 54-58 aquaporin 3 (Gill blood group) Homo sapiens 62-66
18974118-6 2008 Cells ectopically expressing c-Cbl had enhanced CD38 expression when treated with RA, and cells ectopically expressing CD38 had enhanced c-Cbl expression, even without with RA, suggesting an interaction between c-Cbl and CD38. Tretinoin 82-84 Cbl proto-oncogene Homo sapiens 29-34
18636178-11 2008 Nicotinamide attenuates atRA-induced AQP3 expression through inhibition of EGFR/ERK signal transduction and eventually decreases water permeability and water loss. Tretinoin 24-28 aquaporin 3 (Gill blood group) Homo sapiens 37-41
33757404-9 2021 RA hindered the phosphorylation of IKKalpha/beta, translocation of p65 into the nucleus, and the subsequent upregulation of miR-21. Tretinoin 0-2 microRNA 21 Homo sapiens 124-130
18974118-6 2008 Cells ectopically expressing c-Cbl had enhanced CD38 expression when treated with RA, and cells ectopically expressing CD38 had enhanced c-Cbl expression, even without with RA, suggesting an interaction between c-Cbl and CD38. Tretinoin 173-175 CD38 molecule Homo sapiens 119-123
18974118-6 2008 Cells ectopically expressing c-Cbl had enhanced CD38 expression when treated with RA, and cells ectopically expressing CD38 had enhanced c-Cbl expression, even without with RA, suggesting an interaction between c-Cbl and CD38. Tretinoin 173-175 CD38 molecule Homo sapiens 119-123
18641199-5 2008 Replacement of the RARalpha antagonist with atRA on d 8 of the culture period decreased DC surface expression of the adhesion molecule CD11a (P < 0.0001) but not the gene expression. Tretinoin 44-48 integrin alpha L Mus musculus 135-140
18974118-8 2008 RA causes the gradual down-regulation and eventual loss of c-Cbl expression, resulting in loss of the Cbl-CD38 interaction, suggesting that c-Cbl plays a relatively early role in promoting RA-induced differentiation. Tretinoin 0-2 Cbl proto-oncogene Homo sapiens 59-64
33757404-11 2021 CONCLUSION: miR-21 is involved in the LPS-induced pro-inflammatory profile of macrophages and that RA negatively regulates the inflammatory response by targeting NF-kB/miR-21 signaling. Tretinoin 99-101 microRNA 21 Homo sapiens 168-174
18974118-8 2008 RA causes the gradual down-regulation and eventual loss of c-Cbl expression, resulting in loss of the Cbl-CD38 interaction, suggesting that c-Cbl plays a relatively early role in promoting RA-induced differentiation. Tretinoin 0-2 Cbl proto-oncogene Homo sapiens 61-64
18974118-8 2008 RA causes the gradual down-regulation and eventual loss of c-Cbl expression, resulting in loss of the Cbl-CD38 interaction, suggesting that c-Cbl plays a relatively early role in promoting RA-induced differentiation. Tretinoin 0-2 CD38 molecule Homo sapiens 106-110
18974118-8 2008 RA causes the gradual down-regulation and eventual loss of c-Cbl expression, resulting in loss of the Cbl-CD38 interaction, suggesting that c-Cbl plays a relatively early role in promoting RA-induced differentiation. Tretinoin 0-2 Cbl proto-oncogene Homo sapiens 140-145
18491231-6 2008 ATRA and ATO-induced expression of DAP5/p97 was associated with inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Tretinoin 0-4 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 82-111
33757404-12 2021 Our data exposes RA"s potential as a pharmacological agent to manipulate miR-21 and counteract hyper-inflammatory response. Tretinoin 17-19 microRNA 21 Homo sapiens 73-79
18322276-0 2008 Expression of stimulated by retinoic acid gene 8 (Stra8) in spermatogenic cells induced by retinoic acid: an in vivo study in vitamin A-sufficient postnatal murine testes. Tretinoin 28-41 stimulated by retinoic acid gene 8 Mus musculus 50-55
18927155-4 2008 stocksteif encodes cyp26b1, a cytochrome P450 member that metabolizes RA. Tretinoin 70-72 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 19-26
34048060-8 2021 Moreover, pharmacological inhibition of PIN1 via all-trans retinoic acid (ATRA), an FDA-approved drug, impairs the growth of both cultured and xenografted ICC cells. Tretinoin 49-72 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 40-44
18927155-6 2008 Cyp26b1 is expressed within osteoblast cells, demonstrating that RA levels within these cells need to be tightly controlled. Tretinoin 65-67 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 0-7
18927157-0 2008 Restriction of retinoic acid activity by Cyp26b1 is required for proper timing and patterning of osteogenesis during zebrafish development. Tretinoin 15-28 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 41-48
18927157-6 2008 cyp26b1 mutants and RA-treated wild-type fish display a reduction in midline cartilage and the hyperossification of facial and axial bones, leading to fusions of vertebral primordia, a defect not previously described in the context of RA signaling. Tretinoin 235-237 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 0-7
18322276-10 2008 In the vitamin A-sufficient adult testes, RA but not retinol acetate stimulated Stra8 mRNA expression. Tretinoin 42-44 stimulated by retinoic acid gene 8 Mus musculus 80-85
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 58-77 aldehyde dehydrogenase 1 family member A1 Homo sapiens 115-121
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 79-83 aldehyde dehydrogenase 1 family member A1 Homo sapiens 115-121
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 184-188 aldehyde dehydrogenase 1 family member A1 Homo sapiens 115-121
34048060-8 2021 Moreover, pharmacological inhibition of PIN1 via all-trans retinoic acid (ATRA), an FDA-approved drug, impairs the growth of both cultured and xenografted ICC cells. Tretinoin 74-78 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 40-44
18508800-0 2008 Expression of the nuclear oncogene Ski in patients with acute myeloid leukemia treated with all-trans retinoic acid. Tretinoin 102-115 SKI proto-oncogene Homo sapiens 35-38
18838394-2 2008 We demonstrated that hypoxia-inducible factor (HIF) represses the SREBP-1c gene by inducing Stimulated with retinoic acid (Stra)13/Differentiated embryo chondrocyte 1(DEC1) and its isoform, DEC2. Tretinoin 108-121 sterol regulatory element binding transcription factor 1 Homo sapiens 66-74
34031932-2 2021 Retinoic acid-inducible gene (RIG)-I-like receptors (RLR), including melanoma differentiation-associated protein 5 (MDA5) and RIG-I, recognize the double-strand (ds) virus RNA and induce the production of Type I interferon (Type I IFN) as well as pro-inflammatory cytokines like Interleukin (IL)-6. Tretinoin 0-13 DExH-box helicase 58 Homo sapiens 53-56
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 40-53 retinoic acid receptor alpha Homo sapiens 80-83
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 55-59 retinoic acid receptor alpha Homo sapiens 80-83
18850042-2 2008 Protein phosphatase 2A (PP2A) has been demonstrated to take part in the differentiation and apoptosis of malignant hematological cells induced by commonly used medicines, such as all-transretinoic acid (ATRA), interferon, arsenic sulfide, etc. Tretinoin 179-201 protein phosphatase 2 phosphatase activator Homo sapiens 24-28
18850042-2 2008 Protein phosphatase 2A (PP2A) has been demonstrated to take part in the differentiation and apoptosis of malignant hematological cells induced by commonly used medicines, such as all-transretinoic acid (ATRA), interferon, arsenic sulfide, etc. Tretinoin 203-207 protein phosphatase 2 phosphatase activator Homo sapiens 24-28
34031932-2 2021 Retinoic acid-inducible gene (RIG)-I-like receptors (RLR), including melanoma differentiation-associated protein 5 (MDA5) and RIG-I, recognize the double-strand (ds) virus RNA and induce the production of Type I interferon (Type I IFN) as well as pro-inflammatory cytokines like Interleukin (IL)-6. Tretinoin 0-13 interferon induced with helicase C domain 1 Homo sapiens 69-114
18715948-10 2008 Finally, we find that retinoic acid signalling activates both Irx1 and Irx3 genes in the pronephros. Tretinoin 22-35 iroquois homeobox 1 L homeolog Xenopus laevis 62-66
34031932-2 2021 Retinoic acid-inducible gene (RIG)-I-like receptors (RLR), including melanoma differentiation-associated protein 5 (MDA5) and RIG-I, recognize the double-strand (ds) virus RNA and induce the production of Type I interferon (Type I IFN) as well as pro-inflammatory cytokines like Interleukin (IL)-6. Tretinoin 0-13 interferon induced with helicase C domain 1 Homo sapiens 116-120
18590718-6 2008 Embryo culture experiments showed that Retinoic Acid (RA), Sonic hedgehog (Shh) and Fibroblast Growth Factor signals act in concert on this enhancer to control the spatial and temporal induction of Neurog2. Tretinoin 39-52 sonic hedgehog Mus musculus 75-78
18367126-1 2008 OBJECTIVES: All-trans retinoic acid (ATRA) has been shown to inhibit the growth of many malignancies by altering gap junctional intercellular communication (GJIC) and the expression of connexin (Cx) 43. Tretinoin 12-35 LOC100128922 Homo sapiens 185-193
18367126-1 2008 OBJECTIVES: All-trans retinoic acid (ATRA) has been shown to inhibit the growth of many malignancies by altering gap junctional intercellular communication (GJIC) and the expression of connexin (Cx) 43. Tretinoin 37-41 LOC100128922 Homo sapiens 185-193
18590718-7 2008 We further demonstrated by transgenesis that two RA response elements and a Gli binding site within the Neurog2-798 element are absolutely required for its activity, strongly suggesting that the regulation of Neurog2 early expression by RA and Shh signals is direct. Tretinoin 49-51 sonic hedgehog Mus musculus 244-247
33744437-4 2021 Disulfiram also inhibits ALDH1a1, another member of the aldehyde dehydrogenases that catalyzes the oxidation of retinal into retinoic acid. Tretinoin 125-138 aldehyde dehydrogenase 1 family member A1 Homo sapiens 25-32
18789152-0 2008 Enhancement of docetaxel-induced cytotoxicity and apoptosis by all-trans retinoic acid (ATRA) through downregulation of survivin (BIRC5), MCL-1 and LTbeta-R in hormone- and drug resistant prostate cancer cell line, DU-145. Tretinoin 67-86 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 138-143
18789152-0 2008 Enhancement of docetaxel-induced cytotoxicity and apoptosis by all-trans retinoic acid (ATRA) through downregulation of survivin (BIRC5), MCL-1 and LTbeta-R in hormone- and drug resistant prostate cancer cell line, DU-145. Tretinoin 67-86 lymphotoxin beta receptor Homo sapiens 148-156
18789152-0 2008 Enhancement of docetaxel-induced cytotoxicity and apoptosis by all-trans retinoic acid (ATRA) through downregulation of survivin (BIRC5), MCL-1 and LTbeta-R in hormone- and drug resistant prostate cancer cell line, DU-145. Tretinoin 88-92 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 138-143
18789152-0 2008 Enhancement of docetaxel-induced cytotoxicity and apoptosis by all-trans retinoic acid (ATRA) through downregulation of survivin (BIRC5), MCL-1 and LTbeta-R in hormone- and drug resistant prostate cancer cell line, DU-145. Tretinoin 88-92 lymphotoxin beta receptor Homo sapiens 148-156
18789152-11 2008 We have found out that docetaxel-ATRA combination significantly downregulates survivin (BIRC5), myeloid cell leukemia-1 (MCL-1) and lymphotoxin beta-receptor (LTbetaR) genes, which all three have pivotal roles in regulation of apoptosis and cell cycle progression. Tretinoin 33-37 lymphotoxin beta receptor Homo sapiens 132-157
18789152-11 2008 We have found out that docetaxel-ATRA combination significantly downregulates survivin (BIRC5), myeloid cell leukemia-1 (MCL-1) and lymphotoxin beta-receptor (LTbetaR) genes, which all three have pivotal roles in regulation of apoptosis and cell cycle progression. Tretinoin 33-37 lymphotoxin beta receptor Homo sapiens 159-166
18492826-2 2008 Glyceroneogenesis and cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C), which is the key enzyme in this pathway, are both regulated by a series of hormones and nutrients, among which all-trans retinoic acid (all-trans RA) is a transcriptional inducer of the PEPCK-C gene (Pck1). Tretinoin 198-211 phosphoenolpyruvate carboxykinase 1 Homo sapiens 67-74
18492826-4 2008 Three RXR-binding elements [retinoic acid response element (RARE)1/PCK1, RARE2, and RARE3/PCK2] were previously located in the promoter of Pck1. Tretinoin 28-41 phosphoenolpyruvate carboxykinase 1 Homo sapiens 139-143
19035249-15 2008 After the ATRA treatment, cells were stained strongly positive, strongly positive and moderately positive by NSE, vimentin and GFAP antibodies, respectively. Tretinoin 10-14 vimentin Homo sapiens 114-122
18495924-0 2008 Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR. Tretinoin 11-24 retinoic acid receptor alpha Homo sapiens 108-111
18495924-0 2008 Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR. Tretinoin 71-84 retinoic acid receptor alpha Homo sapiens 108-111
18718172-0 2008 All-trans retinoic acid inhibits the increases in fibronectin and PAI-1 induced by TGF-beta1 and Ang II in rat mesangial cells. Tretinoin 10-23 fibronectin 1 Rattus norvegicus 50-61
33950345-0 2021 All-Trans Retinoic Acid Attenuates Blue Light-Induced Apoptosis of Retinal Photoreceptors by Upregulating MKP-1 Expression. Tretinoin 0-23 dual specificity phosphatase 1 Rattus norvegicus 106-111
18718172-6 2008 atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA didn"t affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction. Tretinoin 0-4 fibronectin 1 Rattus norvegicus 38-49
18177425-0 2008 Overexpression of COUP-TF1 in murine embryonic stem cells reduces retinoic acid-associated growth arrest and increases extraembryonic endoderm gene expression. Tretinoin 66-79 nuclear receptor subfamily 2, group F, member 1 Mus musculus 18-26
18177425-7 2008 We also showed that COUP-TF1 overexpression enhanced RA-induced extraembryonic endoderm gene expression. Tretinoin 53-55 nuclear receptor subfamily 2, group F, member 1 Mus musculus 20-28
18291094-0 2008 Interleukin-1beta mediates LPS-induced inhibition of apoptosis in retinoic acid-differentiated HL-60 cells. Tretinoin 66-79 interferon regulatory factor 6 Homo sapiens 27-30
18393306-2 2008 This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Tretinoin 20-43 sonic hedgehog Mus musculus 204-207
18393306-2 2008 This report reveals all-trans-retinoic acid (RA) to be a powerful inducer of mouse prostatic budding that is associated with reciprocal changes in expression of two regulators of budding: sonic hedgehog (Shh) and bone morphogenetic protein 4 (Bmp4). Tretinoin 45-47 sonic hedgehog Mus musculus 204-207
18682553-6 2008 To normally proliferating P19 stem cell culture, exposure to a physiological concentration of atRA triggers a rapid nongenomic signaling cascade to suppress Oct4 gene and regulate cell proliferation. Tretinoin 94-98 cyclin dependent kinase inhibitor 2D Homo sapiens 26-29
33721419-8 2021 Indeed, retinoic acid levels were reduced owing to increased degradation following the elevation of Cyp26b1 in Sox30-null testes. Tretinoin 8-21 SRY (sex determining region Y)-box 30 Mus musculus 111-116
18682553-6 2008 To normally proliferating P19 stem cell culture, exposure to a physiological concentration of atRA triggers a rapid nongenomic signaling cascade to suppress Oct4 gene and regulate cell proliferation. Tretinoin 94-98 POU class 5 homeobox 1 Homo sapiens 157-161
17960384-0 2008 Combination of all-trans retinoic acid and interferon-gamma upregulated p27(kip1) and down regulated CDK2 to cause cell cycle arrest leading to differentiation and apoptosis in human glioblastoma LN18 (PTEN-proficient) and U87MG (PTEN-deficient) cells. Tretinoin 25-38 cyclin dependent kinase inhibitor 1B Homo sapiens 72-81
18343808-5 2008 RA and retinol also regulate expression of ADH1, cellular retinol binding protein 1 and cellular RA binding protein 2 in fibroid and myometrial cells. Tretinoin 0-2 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 43-47
18270252-12 2008 CONCLUSIONS: In endometrial epithelial cells, RA stimulates formation of a multimeric complex comprised of RARalpha/RXRalpha tethered to transcription factors SP1 and SP3 on the HSD17B2 promoter. Tretinoin 46-48 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 178-185
18270252-13 2008 Assembly of this transcriptional complex is necessary for RA induction of HSD17B2 expression and may be an important mechanism for local estradiol inactivation in the endometrium. Tretinoin 58-60 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 74-81
17960384-0 2008 Combination of all-trans retinoic acid and interferon-gamma upregulated p27(kip1) and down regulated CDK2 to cause cell cycle arrest leading to differentiation and apoptosis in human glioblastoma LN18 (PTEN-proficient) and U87MG (PTEN-deficient) cells. Tretinoin 25-38 phosphatase and tensin homolog Homo sapiens 202-206
17960384-10 2008 The variation in induction of apoptosis by ATRA alone might be attributed to difference in PTEN expression in the two cell lines. Tretinoin 43-47 phosphatase and tensin homolog Homo sapiens 91-95
17960384-11 2008 Compared with control cells, IFN-gamma alone and ATRA plus IFN-gamma increased PTEN expression in LN18 cells while there was no PTEN expression or induction in U87MG cells after treatments with ATRA alone and ATRA plus IFN-gamma. Tretinoin 49-53 phosphatase and tensin homolog Homo sapiens 79-83
17960384-15 2008 Thus, our study indicated that the growth of both PTEN-proficient and PTEN-deficient glioblastoma cells could effectively be controlled by treatment with the combination of ATRA and IFN-gamma. Tretinoin 173-177 phosphatase and tensin homolog Homo sapiens 50-54
18217212-0 2008 ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of beta-catenin via up-regulation of Axin. Tretinoin 0-4 catenin beta 1 Homo sapiens 94-106
18217212-1 2008 Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/beta-catenin signaling pathway in some tumor cell lines. Tretinoin 0-13 catenin beta 1 Homo sapiens 127-139
18636178-0 2008 Nicotinamide attenuates aquaporin 3 overexpression induced by retinoic acid through inhibition of EGFR/ERK in cultured human skin keratinocytes. Tretinoin 62-75 aquaporin 3 (Gill blood group) Homo sapiens 24-35
33515676-5 2021 The microarray analysis revealed a reduction in the retinoic acid signals which was accompanied by a downstream reduction in the expression of voltage-gated Na+ channels (SCN5A). Tretinoin 52-65 sodium voltage-gated channel alpha subunit 5 Homo sapiens 171-176
18636178-4 2008 Our previous studies showed that atRA upregulates aquaporin 3 (AQP3) in cultured human skin keratinocytes and fibroblasts. Tretinoin 33-37 aquaporin 3 (Gill blood group) Homo sapiens 50-61
18636178-4 2008 Our previous studies showed that atRA upregulates aquaporin 3 (AQP3) in cultured human skin keratinocytes and fibroblasts. Tretinoin 33-37 aquaporin 3 (Gill blood group) Homo sapiens 63-67
18458045-11 2008 Furthermore, RA increased PGIS transcriptional activity in transient transfection assays, an effect that was prevented by an RAR antagonist. Tretinoin 13-15 retinoic acid receptor alpha Homo sapiens 125-128
18500686-9 2008 The expression pattern of GSTP1 and four other genes, ABCG2 (xenobiotic transport), CRABP2 (retinoic acid signaling), GATA3 (lineage-specific transcription), and SLPI (immune response), was confirmed by immunohistochemistry. Tretinoin 92-105 glutathione S-transferase pi 1 Homo sapiens 26-31
18217212-1 2008 Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/beta-catenin signaling pathway in some tumor cell lines. Tretinoin 15-17 catenin beta 1 Homo sapiens 127-139
18217212-2 2008 However, the definite mechanism of RA trans-repression of the Wnt/beta-catenin signaling pathway has not been elucidated clearly. Tretinoin 35-37 catenin beta 1 Homo sapiens 66-78
18217212-3 2008 In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of beta-catenin. Tretinoin 28-51 catenin beta 1 Homo sapiens 205-217
18217212-3 2008 In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of beta-catenin. Tretinoin 53-57 catenin beta 1 Homo sapiens 205-217
18416830-4 2008 The RAR-alpha-selective agonist, AM580 recapitulated all of the T cell activation and type 2 cytokine-inducing effects of ATRA and 9-cis-RA, while the RAR-alpha-selective antagonist, RO 41-5253, inhibited these effects. Tretinoin 122-126 retinoic acid receptor alpha Homo sapiens 4-13
18416830-4 2008 The RAR-alpha-selective agonist, AM580 recapitulated all of the T cell activation and type 2 cytokine-inducing effects of ATRA and 9-cis-RA, while the RAR-alpha-selective antagonist, RO 41-5253, inhibited these effects. Tretinoin 131-139 retinoic acid receptor alpha Homo sapiens 4-13
18358086-7 2008 In arterial duct VSMC, RA stimulated PCNA expression, but such stimulation could be suppressed by CD2366, an antagonist of nuclear retinoid receptor activation. Tretinoin 23-25 proliferating cell nuclear antigen Homo sapiens 37-41
33493612-0 2021 LncRNA Meg3-mediated regulation of the Smad pathway in atRA-induced cleft palate. Tretinoin 55-59 maternally expressed 3 Mus musculus 7-11
17943179-2 2008 It is oxidized by CYP26A1 to 4-oxoretinoic acid, considered as an inactive catabolite of retinoic acid. Tretinoin 34-47 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 18-25
18471880-4 2008 In addition, the helicases retinoic acid induced protein I (RIG-I)/melanoma differentiation associated gene 5 (MDA5) binds cytoplasmic dsRNA generated during viral replication. Tretinoin 27-40 interferon induced with helicase C domain 1 Homo sapiens 111-115
19031739-1 2008 OBJECTIVE: To study the changes in expression and activity of protein phosphatases type 2A (PP2A ) during differentiation of NB4 and NB4-MR2 cells induced by all-trans retinoic acid (ATRA), and evaluate the role of PP2A in MR2 resistance to ATRA. Tretinoin 168-181 protein phosphatase 2 phosphatase activator Homo sapiens 92-96
19031739-1 2008 OBJECTIVE: To study the changes in expression and activity of protein phosphatases type 2A (PP2A ) during differentiation of NB4 and NB4-MR2 cells induced by all-trans retinoic acid (ATRA), and evaluate the role of PP2A in MR2 resistance to ATRA. Tretinoin 183-187 protein phosphatase 2 phosphatase activator Homo sapiens 92-96
19031739-1 2008 OBJECTIVE: To study the changes in expression and activity of protein phosphatases type 2A (PP2A ) during differentiation of NB4 and NB4-MR2 cells induced by all-trans retinoic acid (ATRA), and evaluate the role of PP2A in MR2 resistance to ATRA. Tretinoin 241-245 protein phosphatase 2 phosphatase activator Homo sapiens 92-96
19031739-7 2008 2) Phosphatase assay showed a decrease in PP2A phosphatase activity [(534 +/- 43) pmol x min(-1) x microg protein(-1)] in NB4 after ATRA treatment, accompanied with that activity [(959 +/- 83) pmol x min(-1) x microg protein(-1)] in untreated NB4 cells. Tretinoin 132-136 protein phosphatase 2 phosphatase activator Homo sapiens 42-46
18250153-5 2008 Our data demonstrate that Acinus-S" can specifically repress ligand-independent and ligand-dependent expression of a DR5 RA response element(RARE)-dependent reporter gene and several endogenous RAR-regulated genes in a dose-dependent and gene-specific manner. Tretinoin 121-123 retinoic acid receptor alpha Homo sapiens 141-144
18413804-11 2008 These findings confirmed that RA triggers PML/RARalpha degradation through different domains and distinct mechanisms. Tretinoin 30-32 PML nuclear body scaffold Homo sapiens 42-45
19031739-10 2008 3) Western blot analysis showed that the level of PP2A catalytic subunit (PP2A/C) was decreased during the course of ATRA-induced NB4 cell differentiation, whereas expressions of every subunits of PP2A in MR2 cells were somewhat unaltered. Tretinoin 117-121 protein phosphatase 2 catalytic subunit alpha Homo sapiens 50-72
18413804-11 2008 These findings confirmed that RA triggers PML/RARalpha degradation through different domains and distinct mechanisms. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 46-54
33493612-3 2021 Herein, we found that atRA treatment (100 mg/kg) promoted Meg3 upregulation in MEPM cells, and that such upregulation was linked to the suppression of MEPM cell proliferation in the context of secondary palate fusion on gestational day (GD) 13 and 14. Tretinoin 22-26 maternally expressed 3 Mus musculus 58-62
19031739-10 2008 3) Western blot analysis showed that the level of PP2A catalytic subunit (PP2A/C) was decreased during the course of ATRA-induced NB4 cell differentiation, whereas expressions of every subunits of PP2A in MR2 cells were somewhat unaltered. Tretinoin 117-121 protein phosphatase 2 catalytic subunit alpha Homo sapiens 74-80
19031739-10 2008 3) Western blot analysis showed that the level of PP2A catalytic subunit (PP2A/C) was decreased during the course of ATRA-induced NB4 cell differentiation, whereas expressions of every subunits of PP2A in MR2 cells were somewhat unaltered. Tretinoin 117-121 protein phosphatase 2 phosphatase activator Homo sapiens 50-54
17922036-4 2008 Dab2 levels induced during retinoic acid-induced differentiation of F9, or during transforming growth factor-beta-induced epithelial-mesenchymal transdifferentiation of mouse mammary epithelial cells result in the stabilization of Axin and concomitant inhibition of beta-catenin signaling. Tretinoin 27-40 coagulation factor IX Mus musculus 68-113
33493612-4 2021 Moreover, the demethylation of specific CpG sites within the lncRNA Meg3 promoter was detected in atRA-treated MEPM cells, likely explaining the observed upregulation of this lncRNA. Tretinoin 98-102 maternally expressed 3 Mus musculus 68-72
18064629-0 2008 All-trans retinoic acid attenuates ultraviolet radiation-induced down-regulation of aquaporin-3 and water permeability in human keratinocytes. Tretinoin 10-23 aquaporin 3 (Gill blood group) Homo sapiens 84-95
33493612-5 2021 Smad signaling was also suppressed by atRA treatment in these cells, and RNA immunoprecipitation analyses revealed that Smad2 can directly interact with Meg3 in MEPM cells following atRA treatment. Tretinoin 182-186 maternally expressed 3 Mus musculus 153-157
18270252-0 2008 Retinoic acid (RA) regulates 17beta-hydroxysteroid dehydrogenase type 2 expression in endometrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. Tretinoin 0-13 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 29-71
33493612-6 2021 Therefore, we propose a model wherein Meg3 is involved in the suppression of MEPM cell proliferation, functioning at least in part via interacting with the Smad2 protein and thereby suppressing Smad signaling in the context of atRA-induced cleft palate. Tretinoin 227-231 maternally expressed 3 Mus musculus 38-42
18270252-0 2008 Retinoic acid (RA) regulates 17beta-hydroxysteroid dehydrogenase type 2 expression in endometrium: interaction of RA receptors with specificity protein (SP) 1/SP3 for estradiol metabolism. Tretinoin 15-17 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 29-71
18270252-2 2008 Retinoic acid (RA) induces HSD17B2 expression, but the underlying mechanism is not known. Tretinoin 0-13 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 27-34
18032419-0 2008 Expression of stimulated by retinoic acid gene 8 (Stra8) and maturation of murine gonocytes and spermatogonia induced by retinoic acid in vitro. Tretinoin 28-41 stimulated by retinoic acid gene 8 Mus musculus 50-55
18032419-4 2008 The expression of Stimulated by retinoic acid gene 8 (Stra8), which is required for spermatogenesis, is directly related to the availability of retinoic acid (RA). Tretinoin 32-45 stimulated by retinoic acid gene 8 Mus musculus 54-59
18270252-2 2008 Retinoic acid (RA) induces HSD17B2 expression, but the underlying mechanism is not known. Tretinoin 15-17 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 27-34
33909480-3 2021 In this study, we tried to investigate the effects of tretinoin-loaded solid lipid core nanocapsules (TTN-SLN) added to freezing/thawing and handling media (in three experimental groups) on sperm motility (total/progressive), viability, DNA fragmentation, and extracellular reactive oxygen species (ROS) levels. Tretinoin 54-63 sarcolipin Mus musculus 106-109
18270252-5 2008 RESULTS: RA induced HSD17B2 mRNA levels in a dose- and time-dependent manner in endometrial cells. Tretinoin 9-11 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 20-27
18270252-6 2008 The RA antagonist ANG11273 abolished RA-induced HSD17B2 expression. Tretinoin 4-6 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 48-55
18270252-7 2008 Small interfering RNA ablation of RA receptor (RAR)alpha or retinoid X receptor (RXR)alpha completely blocked RA-induced HSD17B2 gene expression. Tretinoin 34-36 retinoic acid receptor alpha Homo sapiens 47-56
18270252-7 2008 Small interfering RNA ablation of RA receptor (RAR)alpha or retinoid X receptor (RXR)alpha completely blocked RA-induced HSD17B2 gene expression. Tretinoin 34-36 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 121-128
18270252-8 2008 Analysis of serial deletion and site-directed mutants of the HSD17B2 promoter fused to a reporter gene indicated that RA induction requires a cis-regulatory sequence that binds the specificity protein (SP) class of transcription factors. Tretinoin 118-120 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 61-68
18270252-11 2008 Finally, immunoprecipitationimmunoblotting demonstrated RA-induced interactions between RARalpha/RXRalpha and SP1/SP3 in intact endometrial cells. Tretinoin 56-58 retinoic acid receptor alpha Homo sapiens 88-96
18032419-4 2008 The expression of Stimulated by retinoic acid gene 8 (Stra8), which is required for spermatogenesis, is directly related to the availability of retinoic acid (RA). Tretinoin 159-161 stimulated by retinoic acid gene 8 Mus musculus 18-52
18032419-4 2008 The expression of Stimulated by retinoic acid gene 8 (Stra8), which is required for spermatogenesis, is directly related to the availability of retinoic acid (RA). Tretinoin 159-161 stimulated by retinoic acid gene 8 Mus musculus 54-59
18070204-8 2008 RESULTS: In agreement with previous studies, the patch-test study revealed that RA produced significant fibrillin-1 deposition in the papillary dermis (P<0.01) but had little effect on procollagen I or matrix metalloproteinase-1 expression. Tretinoin 80-82 fibrillin 1 Homo sapiens 104-115
18070204-8 2008 RESULTS: In agreement with previous studies, the patch-test study revealed that RA produced significant fibrillin-1 deposition in the papillary dermis (P<0.01) but had little effect on procollagen I or matrix metalloproteinase-1 expression. Tretinoin 80-82 matrix metallopeptidase 1 Homo sapiens 205-231
18270252-12 2008 CONCLUSIONS: In endometrial epithelial cells, RA stimulates formation of a multimeric complex comprised of RARalpha/RXRalpha tethered to transcription factors SP1 and SP3 on the HSD17B2 promoter. Tretinoin 46-48 retinoic acid receptor alpha Homo sapiens 107-115
33909480-7 2021 Briefly, our results indicate that SLN can deliver the lowest concentrations of tretinoin in a controlled release mechanism into the intracellular space of sperm. Tretinoin 80-89 sarcolipin Mus musculus 35-38
18280804-3 2008 We now demonstrate that treatment of acute promyelocytic leukemia (APL)-derived NB4 cells with ATRA results in dissociation of the translational repressor 4E-BP1 from the eukaryotic initiation factor eIF4E, and subsequent formation of eIF4G-eIF4E complexes. Tretinoin 95-99 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 155-161
18280804-4 2008 We also show that siRNA-mediated inhibition of 4E-BP1 expression enhances ATRA-dependent upregulation of p21(Waf1/Cip1), a protein that plays a key role in the induction of retinoid-dependent responses. Tretinoin 74-78 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 47-53
33997692-4 2021 We show that in NB4 (APL/AML-M3) cells, ATRA activates canonical myeloid lineage factors-including SPI1, CEBPE, and STAT1-to direct near-normal differentiation toward mature granulocytes. Tretinoin 40-44 Spi-1 proto-oncogene Homo sapiens 99-103
18280804-6 2008 Moreover, generation of ATRA- or cis-retinoic acid (cis-RA)-antiproliferative responses is enhanced in 4E-BP1 knockout cells. Tretinoin 24-28 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 103-109
17376583-4 2008 Treatment with ATRA alone also induced cell cycle arrest and moderate increase in p21 expression but joint treatment of ATRA and TSA/VPA did not further enhance cell cycle arrest as compared with TSA/VPA treatment alone. Tretinoin 15-19 H3 histone pseudogene 16 Homo sapiens 82-85
17943186-3 2008 All-trans RA treatment of organotypic REK cultures (10 days) increased the synthesis of hyaluronan, the expression of hyaluronan synthases Has2 and Has3, and the CD44 receptor, with hyperplasia of the epidermis. Tretinoin 10-12 CD44 molecule (Indian blood group) Rattus norvegicus 162-166
18437907-0 2008 Retinoic acid down-regulates bone morphogenetic protein 7 expression in rat with cleft palate. Tretinoin 0-13 bone morphogenetic protein 7 Rattus norvegicus 29-57
18437907-1 2008 OBJECTIVE: To evaluate the effects of retinoic acid (RA) on expression of bone morphogenetic protein 7 (BMP-7) in rat fetus with cleft palate, and the effects of RA on proliferation and apoptosis of osteoblasts. Tretinoin 38-51 bone morphogenetic protein 7 Rattus norvegicus 74-102
18437907-1 2008 OBJECTIVE: To evaluate the effects of retinoic acid (RA) on expression of bone morphogenetic protein 7 (BMP-7) in rat fetus with cleft palate, and the effects of RA on proliferation and apoptosis of osteoblasts. Tretinoin 38-51 bone morphogenetic protein 7 Rattus norvegicus 104-109
18437907-1 2008 OBJECTIVE: To evaluate the effects of retinoic acid (RA) on expression of bone morphogenetic protein 7 (BMP-7) in rat fetus with cleft palate, and the effects of RA on proliferation and apoptosis of osteoblasts. Tretinoin 53-55 bone morphogenetic protein 7 Rattus norvegicus 74-102
18437907-1 2008 OBJECTIVE: To evaluate the effects of retinoic acid (RA) on expression of bone morphogenetic protein 7 (BMP-7) in rat fetus with cleft palate, and the effects of RA on proliferation and apoptosis of osteoblasts. Tretinoin 53-55 bone morphogenetic protein 7 Rattus norvegicus 104-109
17943189-0 2008 Retinoic acid increases aquaporin 3 expression in normal human skin. Tretinoin 0-13 aquaporin 3 (Gill blood group) Homo sapiens 24-35
17943189-1 2008 We have investigated the effects of all-trans retinoic acid (ATRA) on aquaporin 3 (AQP3) expression and function both in vitro and ex vivo. Tretinoin 46-59 aquaporin 3 (Gill blood group) Homo sapiens 70-81
17943189-1 2008 We have investigated the effects of all-trans retinoic acid (ATRA) on aquaporin 3 (AQP3) expression and function both in vitro and ex vivo. Tretinoin 46-59 aquaporin 3 (Gill blood group) Homo sapiens 83-87
17943189-1 2008 We have investigated the effects of all-trans retinoic acid (ATRA) on aquaporin 3 (AQP3) expression and function both in vitro and ex vivo. Tretinoin 61-65 aquaporin 3 (Gill blood group) Homo sapiens 70-81
18413804-2 2008 RA treatment can confer PML/RARalpha degradation, overcoming dominant-negative effects of this oncogenic protein. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 24-27
18413804-2 2008 RA treatment can confer PML/RARalpha degradation, overcoming dominant-negative effects of this oncogenic protein. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 28-36
18413804-4 2008 RA treatment is known to repress PML/RARalpha and augment ubiquitin-activating enzyme-E1-like (UBE1L) protein expression in NB4-S1 APL cells. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 33-36
18413804-4 2008 RA treatment is known to repress PML/RARalpha and augment ubiquitin-activating enzyme-E1-like (UBE1L) protein expression in NB4-S1 APL cells. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 37-45
17943189-1 2008 We have investigated the effects of all-trans retinoic acid (ATRA) on aquaporin 3 (AQP3) expression and function both in vitro and ex vivo. Tretinoin 61-65 aquaporin 3 (Gill blood group) Homo sapiens 83-87
17943189-2 2008 ATRA treatment provoked a rapid accumulation of AQP3 transcripts in cultured normal human epidermal keratinocytes (NHEK). Tretinoin 0-4 aquaporin 3 (Gill blood group) Homo sapiens 48-52
33997692-4 2021 We show that in NB4 (APL/AML-M3) cells, ATRA activates canonical myeloid lineage factors-including SPI1, CEBPE, and STAT1-to direct near-normal differentiation toward mature granulocytes. Tretinoin 40-44 CCAAT enhancer binding protein epsilon Homo sapiens 105-110
17943189-6 2008 Incubation of NHEK in ATRA for 24, 48, and 72 hours stimulated glycerol influx, suggesting that the increase in AQP3 gene and protein expression was followed by an enhancement of biological activity. Tretinoin 22-26 aquaporin 3 (Gill blood group) Homo sapiens 112-116
17943189-7 2008 Topical application of ATRA for 24 hours on skin explants induced significant epidermal expression of AQP3 and strong immunoreactivity in the epidermal basal layers. Tretinoin 23-27 aquaporin 3 (Gill blood group) Homo sapiens 102-106
33508625-4 2021 Regulation of FNDC5/irisin expression in hPDL cells, hDPCs and hOBs were evaluated after administration of different concentrations of irisin and all-trans retinoic acid (ATRA). Tretinoin 146-169 fibronectin type III domain containing 5 Rattus norvegicus 14-19
18288394-0 2008 Up-regulation of the BTG2 gene in TPA- or RA-treated HL-60 cell lines. Tretinoin 42-44 BTG anti-proliferation factor 2 Homo sapiens 21-25
18288394-5 2008 Our data show that the expression of the BTG2 gene was increased in 32 nM TPA-treated and 1 microM RA-treated HL-60 cells, but the expression of the BTG1 and BTG3 genes was not increased. Tretinoin 99-101 BTG anti-proliferation factor 2 Homo sapiens 41-45
18288394-6 2008 The expression of BTG2 in TPA- or RA-treated HL-60 cells was also increased even in the presence of cyclohexamide, which is an inhibitor of translation, implying that the increased expression of BTG2 mRNA did not require the new synthesis of another protein. Tretinoin 34-36 BTG anti-proliferation factor 2 Homo sapiens 18-22
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 homeobox A5 Mus musculus 146-151
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 159-166
18288394-6 2008 The expression of BTG2 in TPA- or RA-treated HL-60 cells was also increased even in the presence of cyclohexamide, which is an inhibitor of translation, implying that the increased expression of BTG2 mRNA did not require the new synthesis of another protein. Tretinoin 34-36 BTG anti-proliferation factor 2 Homo sapiens 195-199
18256537-4 2008 As expected, using organ cultures, we observed that addition of RA in 11.5 days post-conception (dpc) testes induced Stra8 expression and meiosis. Tretinoin 64-66 stimulated by retinoic acid gene 8 Mus musculus 117-122
33481153-11 2021 KEGG pathway analysis showed that most of the enriched signaling pathways were involved in lipid metabolism, including the PPAR signaling pathway associated with retinoic acid (RA)-mediated nuclear receptors. Tretinoin 162-175 peroxisome proliferator activated receptor alpha Rattus norvegicus 123-127
18256537-5 2008 Surprisingly, in 13.5 dpc testes although RA induced Stra8 expression it did not promote meiosis. Tretinoin 42-44 stimulated by retinoic acid gene 8 Mus musculus 53-58
18315501-4 2008 Using the well-established retinoic acid induction protocol we found that all Wnt genes except Wnt8b are expressed as ES cells differentiate into neurons, many of them in dynamic patterns. Tretinoin 27-40 wingless-type MMTV integration site family, member 8B Mus musculus 78-81
18207650-7 2008 Compared with untreated cells, ATRA-treated C6 cells express less Slc1a3 mRNA, for the transporter GLAST, but significantly higher levels of Slc1a2 mRNA, for the transporter GLT-1, although no expression of either protein is detected with Western blot in both untreated and ATRA-treated cells. Tretinoin 31-35 solute carrier family 1 member 3 Rattus norvegicus 66-72
18207650-7 2008 Compared with untreated cells, ATRA-treated C6 cells express less Slc1a3 mRNA, for the transporter GLAST, but significantly higher levels of Slc1a2 mRNA, for the transporter GLT-1, although no expression of either protein is detected with Western blot in both untreated and ATRA-treated cells. Tretinoin 31-35 solute carrier family 1 member 3 Rattus norvegicus 99-104
18025157-2 2008 At physiological concentrations of retinoic acid, PML-RARalpha silences RARalpha target genes, blocking differentiation of the cells. Tretinoin 35-48 retinoic acid receptor alpha Homo sapiens 54-62
18288394-7 2008 Notably, the up-regulation of BTG2 in TPA- or RA-treated HL-60 cells was observed prior to the increased expression of p21. Tretinoin 46-48 BTG anti-proliferation factor 2 Homo sapiens 30-34
18288394-9 2008 Thus, the up-regulation of BTG2 genes may be involved in the differentiation process of HL-60 cells after TPA or RA treatment. Tretinoin 113-115 BTG anti-proliferation factor 2 Homo sapiens 27-31
33481153-11 2021 KEGG pathway analysis showed that most of the enriched signaling pathways were involved in lipid metabolism, including the PPAR signaling pathway associated with retinoic acid (RA)-mediated nuclear receptors. Tretinoin 177-179 peroxisome proliferator activated receptor alpha Rattus norvegicus 123-127
18286198-2 2008 Retinoic acid (RA)-treatment of neuroblastoma (NB) cells implicates activation of Ret and TrkB RTKs as critical step to induce cell differentiation. Tretinoin 15-17 ret proto-oncogene Homo sapiens 0-3
18025157-2 2008 At physiological concentrations of retinoic acid, PML-RARalpha silences RARalpha target genes, blocking differentiation of the cells. Tretinoin 35-48 retinoic acid receptor alpha Homo sapiens 72-80
33550205-0 2021 Exploitation of the vitamin A/retinoic acid axis depletes ALDH1-positive cancer stem cells and re-sensitises resistant non-small cell lung cancer cells to cisplatin. Tretinoin 30-43 aldehyde dehydrogenase 1 family member A1 Homo sapiens 58-63
17706770-0 2008 Role of Myc in differentiation and apoptosis in HL60 cells after exposure to arsenic trioxide or all-trans retinoic acid. Tretinoin 97-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 8-11
17706770-4 2008 Characterization of expression and activity of c-Myc and its target genes hTERT (human telomerase reverse transcriptase) and CAD (carbamoyltransferase-dihydroorotase) revealed marked down-regulation in response to ATRA, but not As2O3. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52
17706770-4 2008 Characterization of expression and activity of c-Myc and its target genes hTERT (human telomerase reverse transcriptase) and CAD (carbamoyltransferase-dihydroorotase) revealed marked down-regulation in response to ATRA, but not As2O3. Tretinoin 214-218 telomerase reverse transcriptase Homo sapiens 74-79
17993618-1 2008 The retinoic acid receptor (RAR) alpha gene (RARA) encodes 2 major isoforms and mediates positive effects of all-trans retinoic acid (ATRA) on myelomonocytic differentiation. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 28-31
17993618-1 2008 The retinoic acid receptor (RAR) alpha gene (RARA) encodes 2 major isoforms and mediates positive effects of all-trans retinoic acid (ATRA) on myelomonocytic differentiation. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 45-49
17993618-1 2008 The retinoic acid receptor (RAR) alpha gene (RARA) encodes 2 major isoforms and mediates positive effects of all-trans retinoic acid (ATRA) on myelomonocytic differentiation. Tretinoin 134-138 retinoic acid receptor alpha Homo sapiens 28-31
17993618-1 2008 The retinoic acid receptor (RAR) alpha gene (RARA) encodes 2 major isoforms and mediates positive effects of all-trans retinoic acid (ATRA) on myelomonocytic differentiation. Tretinoin 134-138 retinoic acid receptor alpha Homo sapiens 45-49
17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 110-114
17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 cyclin dependent kinase 1 Homo sapiens 215-219
18053799-6 2008 In the myeloid cells, but not in the epithelial cells, we observed that the leukotriene C(4) synthase promoter activity was stimulated by 12-O-tetradecanoylphorbol-13-acetate and all-trans-retinoic acid. Tretinoin 179-202 leukotriene C4 synthase Homo sapiens 76-101
33855282-4 2021 MSCl cells promote the differentiation of CTLA-4 expressing DCs via the production of all-trans retinoic acid (ATRA) functioning as a ligand of RARalpha, a key nuclear receptor in DC development. Tretinoin 86-109 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 42-48
17951529-0 2008 Retinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathway. Tretinoin 0-13 signal transducer and activator of transcription 5A Homo sapiens 88-94
17420990-2 2008 In evaluating the mechanisms by which retinoic acid (RA) or nerve growth factor (NGF) decrease cell number in MYCN amplified NB cells, we have identified a number of proteins whose expression either decreases (E2F, CDC2, CDK6, cyclin dependent kinase activity) or increases (p27) in association with a decrease in MYCN expression. Tretinoin 38-51 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 314-318
17951529-3 2008 Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Tretinoin 28-41 retinoic acid receptor alpha Homo sapiens 75-103
33574039-3 2021 In particular, there has been considerable debate regarding whether retinoic acid is required, in vivo, to initiate Stra8 expression in the mouse fetal ovary. Tretinoin 68-81 stimulated by retinoic acid gene 8 Mus musculus 116-121
17951529-3 2008 Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Tretinoin 28-41 retinoic acid receptor alpha Homo sapiens 105-113
17951529-3 2008 Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Tretinoin 43-47 retinoic acid receptor alpha Homo sapiens 75-103
17951529-3 2008 Here we show that all-trans retinoic acid (ATRA) and other agonists of the retinoic acid receptor alpha (RARalpha) inhibit the formation of Th17 cells and promote FoxP3 expression. Tretinoin 43-47 retinoic acid receptor alpha Homo sapiens 105-113
17951529-5 2008 The effect of ATRA is mediated independently of IL-2, signal transducer and activator of transcription 5 (Stat5) and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. Tretinoin 14-18 signal transducer and activator of transcription 5A Homo sapiens 54-104
17951529-5 2008 The effect of ATRA is mediated independently of IL-2, signal transducer and activator of transcription 5 (Stat5) and Stat3, representing a novel mechanism for the induction of FoxP3 in CD4 T cells. Tretinoin 14-18 signal transducer and activator of transcription 5A Homo sapiens 106-111
17951529-6 2008 As previous studies have shown that vitamin A derivatives are protective in animal models of autoimmune disease, the current data suggest a previously unrecognized role for RARalpha in the regulation of CD4(+) T-cell differentiation and provide a mechanism for the anti-inflammatory effects of retinoic acid. Tretinoin 294-307 retinoic acid receptor alpha Homo sapiens 173-181
18066588-3 2008 HSP27, which showed peculiar variability in different NB cell preparations, responded to all trans-retinoic acid treatment in NB cells but not in ES cells at gene and protein expression levels. Tretinoin 93-112 heat shock protein family B (small) member 1 Homo sapiens 0-5
18365622-0 2008 [Pro-apoptotic effect of retinoic acid on chondrocyte through regulation on gene expression of IGF-2]. Tretinoin 25-38 insulin-like growth factor II Oryctolagus cuniculus 95-100
18365622-1 2008 OBJECTIVE: To investigate the effect of retinoic acid (RA) on cell apoptosis and gene regulation of IGF-2 in chondrocyte. Tretinoin 40-53 insulin-like growth factor II Oryctolagus cuniculus 100-105
18365622-1 2008 OBJECTIVE: To investigate the effect of retinoic acid (RA) on cell apoptosis and gene regulation of IGF-2 in chondrocyte. Tretinoin 55-57 insulin-like growth factor II Oryctolagus cuniculus 100-105
18230156-0 2008 Retinoic acid reduces human neuroblastoma cell migration and invasiveness: effects on DCX, LIS1, neurofilaments-68 and vimentin expression. Tretinoin 0-13 vimentin Homo sapiens 119-127
18230156-3 2008 The mechanism of action of retinoic acid is still unclear, and the development of resistance to this differentiating agent is a great therapy problem.Doublecortin, a microtubule-associated protein involved in neuronal migration, has recently been proposed as a molecular marker for the detection of minimal residual disease in human neuroblastoma. Tretinoin 27-40 regulator of microtubule dynamics 1 Homo sapiens 166-196
17387511-9 2008 We propose to take a retinoic acid chemoprevention into account in children with proven biallelic PMS2 mismatch repair mutations being at highest risk concerning the development of a malignancy. Tretinoin 21-34 PMS1 homolog 2, mismatch repair system component Homo sapiens 98-102
33684176-3 2021 Upon viral RNA recognition, retinoic acid-inducible gene-I-like receptors (RLRs) physically interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type-I interferon (IFN-I) production. Tretinoin 28-41 mitochondrial antiviral signaling protein Homo sapiens 110-151
17573914-2 2008 Therefore, we have studied the differences in the level of chromatin condensation in pluripotent and all-trans retinoic acid-differentiated hES cells. Tretinoin 111-124 ribosome binding protein 1 Homo sapiens 140-143
17997979-4 2008 The retinoic acid derivative also reverses an early liver fibrosis, as assayed by liver contents of hydroxyproline, alpha-smooth muscle actin (alpha-SMA), and collagen 1A2, in an early liver fibrosis model we established previously where an inducible expression vector containing a TGF-beta gene was hydrodynamically transferred into a testing animal. Tretinoin 4-17 actin gamma 2, smooth muscle Rattus norvegicus 116-141
17997979-4 2008 The retinoic acid derivative also reverses an early liver fibrosis, as assayed by liver contents of hydroxyproline, alpha-smooth muscle actin (alpha-SMA), and collagen 1A2, in an early liver fibrosis model we established previously where an inducible expression vector containing a TGF-beta gene was hydrodynamically transferred into a testing animal. Tretinoin 4-17 actin gamma 2, smooth muscle Rattus norvegicus 143-152
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 40-63 matrix metallopeptidase 1 Homo sapiens 79-84
18536179-12 2008 The aim of this study was to examine if all-trans-retinoic acid (ATRA) effects MMP-1, MMP-2, MMP-3 and MMP-14 gene expression in fibroblasts cultured in vitro. Tretinoin 65-69 matrix metallopeptidase 1 Homo sapiens 79-84
18974614-3 2008 In this study, the effects of all-trans retinoic acid (atRA), 9-cis RA, and the RAR agonist TTNPB, on UGT2B7 and UGT2B15 mRNA expression in Caco-2 cells have been examined. Tretinoin 40-53 UDP glucuronosyltransferase family 2 member B15 Homo sapiens 113-120
19068145-6 2008 The effect of ATRA on upstream MAPK (p38 MAPK, c-Jun N-terminal kinase [JNK], and extracellularly regulated kinase 1/2 [ERK1/2]) was assessed by Western blot, and the contribution of the ERK1/2 pathway to the activation of pro-inflammatory transcription factors was studied by TransAm assays. Tretinoin 14-18 mitogen-activated protein kinase 8 Rattus norvegicus 72-75
18974614-3 2008 In this study, the effects of all-trans retinoic acid (atRA), 9-cis RA, and the RAR agonist TTNPB, on UGT2B7 and UGT2B15 mRNA expression in Caco-2 cells have been examined. Tretinoin 55-59 UDP glucuronosyltransferase family 2 member B15 Homo sapiens 113-120
33684176-3 2021 Upon viral RNA recognition, retinoic acid-inducible gene-I-like receptors (RLRs) physically interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type-I interferon (IFN-I) production. Tretinoin 28-41 mitochondrial antiviral signaling protein Homo sapiens 153-157
18974614-5 2008 However, no inhibition was observed when two other UGTs, UGT2B15 or -1A6, were exposed to atRA, 9-cis RA, or TTNPB, demonstrating that the inhibitory effect of retinoids might be specific for the UGT2B7 isoform. Tretinoin 90-94 UDP glucuronosyltransferase family 2 member B15 Homo sapiens 57-72
19088398-2 2008 All-trans retinoic acid (RA) induced expression of osteoblast-specific mRNAs encoding Cbfa1/Runx2, osterix, alkaline phosphatase, osteopontin, parathyroid hormone receptor, and osteocalcin in the DFAT cells, but did not induce the expression of adipocyte-specific mRNAs encoding PPARgamma2, C/EBPalpha, and GLUT4. Tretinoin 10-23 secreted phosphoprotein 1 Homo sapiens 130-141
33684176-3 2021 Upon viral RNA recognition, retinoic acid-inducible gene-I-like receptors (RLRs) physically interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type-I interferon (IFN-I) production. Tretinoin 28-41 TANK binding kinase 1 Homo sapiens 172-193
33684176-3 2021 Upon viral RNA recognition, retinoic acid-inducible gene-I-like receptors (RLRs) physically interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type-I interferon (IFN-I) production. Tretinoin 28-41 TANK binding kinase 1 Homo sapiens 195-199
33631212-4 2021 The homeodomain transcription factor ISX controls the activity of the vitamin A-forming enzyme BCO1 in intestinal enterocytes in response to increasing concentration of the vitamin A metabolite retinoic acid. Tretinoin 194-207 intestine specific homeobox Mus musculus 37-40
18444141-1 2008 Retinol utilizes a retinoid X receptor (RXR)-mediated degradation pathway to decrease beta-catenin protein in all-trans retinoic acid (ATRA)-resistant human colon cancer cells. Tretinoin 120-133 catenin beta 1 Homo sapiens 86-98
18444141-1 2008 Retinol utilizes a retinoid X receptor (RXR)-mediated degradation pathway to decrease beta-catenin protein in all-trans retinoic acid (ATRA)-resistant human colon cancer cells. Tretinoin 135-139 catenin beta 1 Homo sapiens 86-98
17925390-7 2007 These results suggest that RDH12 acts as a regulator of retinoic acid biosynthesis and protects photoreceptors against overproduction of retinoic acid from all-trans-retinaldehyde, which diffuses into the inner segments of photoreceptors from illuminated rhodopsin. Tretinoin 137-150 rhodopsin Mus musculus 255-264
18345250-2 2007 Both retinoids and rexinoids are either natural or synthetic compounds related to retinoic acids that act through interaction with two basic types of nuclear receptors belonging to the nuclear receptor superfamily: All-trans retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 82-96 retinoic acid receptor alpha Homo sapiens 250-258
18075297-4 2007 All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 49-60
18075297-4 2007 All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 62-65
18075297-4 2007 All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 49-60
18001002-8 2008 In addition, intravenous injection of ATRA-lipoplexes inhibited the activation of NFkappaB in liver, and subsequently suppressed the serum levels of tumor necrosis factor-alpha (TNF-alpha) and alanine aminotransferase (ALT) compared with lipoplexes. Tretinoin 38-42 glutamic pyruvic transaminase, soluble Mus musculus 193-217
18001002-8 2008 In addition, intravenous injection of ATRA-lipoplexes inhibited the activation of NFkappaB in liver, and subsequently suppressed the serum levels of tumor necrosis factor-alpha (TNF-alpha) and alanine aminotransferase (ALT) compared with lipoplexes. Tretinoin 38-42 glutamic pyruvic transaminase, soluble Mus musculus 219-222
18791934-3 2008 Evidence was obtained that this interaction depends on histone deactylase one (HDAC1) inhibition by butyrate and retinoic acid receptor alpha (RARalpha) activation by ATRA. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 113-141
18791934-3 2008 Evidence was obtained that this interaction depends on histone deactylase one (HDAC1) inhibition by butyrate and retinoic acid receptor alpha (RARalpha) activation by ATRA. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 143-151
18055984-2 2007 As(2)O(3), Phenylbutyrate (PB) and G-CSF are known to potentiate ATRA effects. Tretinoin 65-69 colony stimulating factor 3 Homo sapiens 35-40
18075297-4 2007 All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 62-65
18075297-4 2007 All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA. Tretinoin 199-203 retinoic acid receptor alpha Homo sapiens 49-60
18075297-4 2007 All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA. Tretinoin 199-203 retinoic acid receptor alpha Homo sapiens 62-65
33570783-0 2021 Retinol Binding Protein 1 Affects Xenopus Anterior Neural Development via All-trans Retinoic Acid Signalling. Tretinoin 84-97 retinol binding protein 1 S homeolog Xenopus laevis 0-25
18052984-9 2007 Based on these results we propose that TIS7 inhibits CRABP II expression during axonal regeneration, thereby modulating retinoic acid signalling. Tretinoin 120-133 interferon-related developmental regulator 1 Mus musculus 39-43
17653734-1 2007 It has been reported that heparin-binding epidermal-growth-factor-like growth factor (HB-EGF) plays an important role in regulating keratinocyte growth after retinoic acid treatment. Tretinoin 158-171 heparin binding EGF like growth factor Homo sapiens 26-84
17653734-1 2007 It has been reported that heparin-binding epidermal-growth-factor-like growth factor (HB-EGF) plays an important role in regulating keratinocyte growth after retinoic acid treatment. Tretinoin 158-171 heparin binding EGF like growth factor Homo sapiens 86-92
17646388-3 2007 In the present study, we further demonstrated that this nonclassical signaling of RA on the activation of CREB plays a critical role in regulating the expression of airway epithelial cell differentiation markers, the MUC2, MUC5AC, and MUC5B genes. Tretinoin 82-84 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 223-229
33659900-2 2021 In protocol 1, we use retinoic acid (RA) to induce pain, itch, and heat mediating dI4/dI6 interneurons, and in protocol 2, RA with bone morphogenetic protein 4 (RA+BMP4) is used to induce proprioceptive dI1s and mechanosensory dI3s in hPSC cultures. Tretinoin 22-35 l(2)39DEf Drosophila melanogaster 82-85
17628022-1 2007 Little is known about the mechanisms by which retinoic acid receptor alpha (RAR alpha) mediates the effects of retinoic acid (RA) to coordinate granulocytic proliferation/differentiation (P/D) transition. Tretinoin 46-59 retinoic acid receptor alpha Homo sapiens 76-85
17628022-1 2007 Little is known about the mechanisms by which retinoic acid receptor alpha (RAR alpha) mediates the effects of retinoic acid (RA) to coordinate granulocytic proliferation/differentiation (P/D) transition. Tretinoin 76-78 retinoic acid receptor alpha Homo sapiens 46-74
17628022-3 2007 We previously found that in myeloid leukemia cells, the lack of RA-induced RAR alpha-CAK dissociation and MAT1 degradation suppresses cell differentiation by inhibiting CAK-dependent G(1) exit and sustaining CAK hyperphosphorylation of RAR alpha. Tretinoin 64-66 retinoic acid receptor alpha Homo sapiens 75-84
17931360-3 2007 The treatment of rat astrocytes with retinoic acid and dibutyryl cAMP, which induce apolipoprotein E (apoE) synthesis and HDL-like lipoprotein formation, stimulated extracellular S1P accumulation in the presence of its precursor sphingosine. Tretinoin 37-50 sphingosine-1-phosphate receptor 1 Mus musculus 179-182
17694433-3 2007 We found that all-trans retinoic acid (ATRA) or 13-cis retinoic acid (13-CRA) induced astrocytic differentiation with down regulation of telomerase activity in rat glioblastoma C6 cells and enhanced sensitivity of the cells to interferon-gamma (IFN-gamma) or taxol (TXL) for apoptosis. Tretinoin 14-37 interferon gamma Rattus norvegicus 227-243
17694433-3 2007 We found that all-trans retinoic acid (ATRA) or 13-cis retinoic acid (13-CRA) induced astrocytic differentiation with down regulation of telomerase activity in rat glioblastoma C6 cells and enhanced sensitivity of the cells to interferon-gamma (IFN-gamma) or taxol (TXL) for apoptosis. Tretinoin 14-37 interferon gamma Rattus norvegicus 245-254
17694433-3 2007 We found that all-trans retinoic acid (ATRA) or 13-cis retinoic acid (13-CRA) induced astrocytic differentiation with down regulation of telomerase activity in rat glioblastoma C6 cells and enhanced sensitivity of the cells to interferon-gamma (IFN-gamma) or taxol (TXL) for apoptosis. Tretinoin 39-43 interferon gamma Rattus norvegicus 227-243
17694433-3 2007 We found that all-trans retinoic acid (ATRA) or 13-cis retinoic acid (13-CRA) induced astrocytic differentiation with down regulation of telomerase activity in rat glioblastoma C6 cells and enhanced sensitivity of the cells to interferon-gamma (IFN-gamma) or taxol (TXL) for apoptosis. Tretinoin 39-43 interferon gamma Rattus norvegicus 245-254
33659900-2 2021 In protocol 1, we use retinoic acid (RA) to induce pain, itch, and heat mediating dI4/dI6 interneurons, and in protocol 2, RA with bone morphogenetic protein 4 (RA+BMP4) is used to induce proprioceptive dI1s and mechanosensory dI3s in hPSC cultures. Tretinoin 37-39 l(2)39DEf Drosophila melanogaster 82-85
17928865-4 2007 Analysis of a series of markers in SMRT-gene-deleted mice revealed the functional requirement of SMRT in the actions of both retinoic-acid-dependent and Notch-dependent forebrain development. Tretinoin 125-138 nuclear receptor co-repressor 2 Mus musculus 35-39
17928865-4 2007 Analysis of a series of markers in SMRT-gene-deleted mice revealed the functional requirement of SMRT in the actions of both retinoic-acid-dependent and Notch-dependent forebrain development. Tretinoin 125-138 nuclear receptor co-repressor 2 Mus musculus 97-101
17693386-5 2007 A retinoic acid response element-containing luciferase assay indicated that HSCs became responsive to retinoids only after activation in vitro and that this response was mediated by, at least in part, RARalpha subtype. Tretinoin 2-15 retinoic acid receptor, alpha Rattus norvegicus 201-209
17693386-7 2007 All-trans retinoic acid treatment strongly lowered the cytosolic RARalpha protein levels. Tretinoin 10-23 retinoic acid receptor, alpha Rattus norvegicus 65-73
17785809-2 2007 We found that the major vitamin A metabolite all-trans-retinoic acid induces histone acetylation at the FoxP3 gene promoter and expression of the FoxP3 protein in CD4+ T cells. Tretinoin 45-68 forkhead box P3 Mus musculus 104-109
17785809-2 2007 We found that the major vitamin A metabolite all-trans-retinoic acid induces histone acetylation at the FoxP3 gene promoter and expression of the FoxP3 protein in CD4+ T cells. Tretinoin 45-68 forkhead box P3 Mus musculus 146-151
17785809-4 2007 Retinoic acid can promote TGF-beta1-dependent generation of FoxP3+ regulatory T cells but decrease the TGF-beta1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Tretinoin 0-13 forkhead box P3 Mus musculus 60-65
33321629-5 2021 It was reported that FRbeta could be selectively augmented by all-trans retinoic acid (ATRA). Tretinoin 62-85 rabaptin, RAB GTPase binding effector protein 2 Homo sapiens 21-27
17538076-3 2007 The aim of this study was to investigate the effects of potential regulatory factors including progesterone, estradiol, and retinoic acid (RA) onHSD17B2 expression in primary human placental endothelial cells in culture.HSD17B2 mRNA expression was not regulated by progesterone, the progesterone agonist R5020, or estradiol treatment. Tretinoin 124-137 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 145-152
17538076-3 2007 The aim of this study was to investigate the effects of potential regulatory factors including progesterone, estradiol, and retinoic acid (RA) onHSD17B2 expression in primary human placental endothelial cells in culture.HSD17B2 mRNA expression was not regulated by progesterone, the progesterone agonist R5020, or estradiol treatment. Tretinoin 139-141 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 145-152
17916406-4 2007 Our results demonstrate that the only RA isomers detected in RALDH1-expressing or non-expressing cells corresponded to the same steric conformation as the supplied retinoids, indicating a lack of measurable 9-cis/all-trans retinoid-isomerizing activity. Tretinoin 38-40 aldehyde dehydrogenase 1 family member A1 Homo sapiens 61-67
17916406-5 2007 Finally, HeLa cells transfected with RALDH1 derivatives that were retinal isomer-selective in vitro produced only the corresponding RA isomers, establishing these enzymes as useful tools to assess the respective roles of the two RA isomers in vivo. Tretinoin 132-134 aldehyde dehydrogenase 1 family member A1 Homo sapiens 37-43
33321629-5 2021 It was reported that FRbeta could be selectively augmented by all-trans retinoic acid (ATRA). Tretinoin 87-91 rabaptin, RAB GTPase binding effector protein 2 Homo sapiens 21-27
17676605-13 2007 The rescue of ethanol-induced cell death by RA and similar changes in Shh transcription further suggest that RA contributes to ethanol-induced limb dysmorphology. Tretinoin 109-111 sonic hedgehog Mus musculus 70-73
33017025-10 2021 Tretinoin exhibited a significant concentration-dependent cytotoxic effect in CH22, sacral chordoma-derived cell lines but to a much lesser extent in UM-Chor1, a cell line derived from skull base chordoma. Tretinoin 0-9 CHDM Homo sapiens 91-99
17804711-9 2007 Knockdown of HOXA5 expression partially abrogates retinoid-induced apoptosis and promotes cell survival upon RA treatment. Tretinoin 109-111 homeobox A5 Homo sapiens 13-18
17896343-3 2007 METHODS: To investigate this hypothesis, cell lines including P19 and F9 were differentiated with retinoic acid into neuronal and endodermal derivatives respectively. Tretinoin 98-111 interleukin 23 subunit alpha Homo sapiens 62-65
17909034-0 2007 Insulin receptor substrate-1 is an important mediator of ovarian cancer cell growth suppression by all-trans retinoic acid. Tretinoin 109-122 insulin receptor substrate 1 Homo sapiens 0-28
17909034-4 2007 Our studies revealed that insulin receptor substrate-1 (IRS-1) protein levels decrease in CA-OV3 cells on ATRA treatment, whereas no differences in IRS-1 levels were seen in the ATRA-resistant SK-OV3 cells. Tretinoin 106-110 insulin receptor substrate 1 Homo sapiens 26-54
17909034-4 2007 Our studies revealed that insulin receptor substrate-1 (IRS-1) protein levels decrease in CA-OV3 cells on ATRA treatment, whereas no differences in IRS-1 levels were seen in the ATRA-resistant SK-OV3 cells. Tretinoin 106-110 insulin receptor substrate 1 Homo sapiens 56-61
18082674-0 2007 Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4. Tretinoin 0-13 interleukin 4 Mus musculus 105-109
17909034-5 2007 Moreover, CA-OV3 clones overexpressing IRS-1 were growth inhibited less by ATRA, whereas SK-OV3 clones in which levels of IRS-1 were reduced by expression of antisense IRS-1 became sensitive to growth inhibition by ATRA treatment. Tretinoin 75-79 insulin receptor substrate 1 Homo sapiens 39-44
33017025-10 2021 Tretinoin exhibited a significant concentration-dependent cytotoxic effect in CH22, sacral chordoma-derived cell lines but to a much lesser extent in UM-Chor1, a cell line derived from skull base chordoma. Tretinoin 0-9 CHDM Homo sapiens 196-204
33441739-6 2021 Furthermore, we revealed the SV region-specific expression of Cyp26a1, which encodes an RA-degrading enzyme, and demonstrated that the increased RA levels in the SV region disrupt its pool of Aundiff by inducing their differentiation. Tretinoin 88-90 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 62-69
17595318-0 2007 Rapid, nongenomic actions of retinoic acid on phosphatidylinositol-3-kinase signaling pathway mediated by the retinoic acid receptor. Tretinoin 29-42 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 46-75
17595318-0 2007 Rapid, nongenomic actions of retinoic acid on phosphatidylinositol-3-kinase signaling pathway mediated by the retinoic acid receptor. Tretinoin 29-42 retinoic acid receptor alpha Homo sapiens 110-132
17595318-1 2007 Retinoic acid (RA) treatment of SH-SY5Y neuroblastoma cells results in activation of phosphatidylinositol-3-kinase (PI3K) signaling pathway, and this activation is required for RA-induced differentiation. Tretinoin 0-13 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 85-114
17595318-1 2007 Retinoic acid (RA) treatment of SH-SY5Y neuroblastoma cells results in activation of phosphatidylinositol-3-kinase (PI3K) signaling pathway, and this activation is required for RA-induced differentiation. Tretinoin 15-17 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 85-114
17595318-1 2007 Retinoic acid (RA) treatment of SH-SY5Y neuroblastoma cells results in activation of phosphatidylinositol-3-kinase (PI3K) signaling pathway, and this activation is required for RA-induced differentiation. Tretinoin 177-179 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 85-114
17453147-12 2007 In conclusion, we have provided evidence for the first time that RA may induce cell cycle arrest in vitro in DAOY MB cells via inhibition of CyclinD1 or C-myc. Tretinoin 65-67 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158
17579210-6 2007 Ectopic expression of C/EBPbeta in C3H10T1/2 cells causes a reduction in Runx2 expression concomitant with a decrease in osteogenic potential during all-trans retinoic acid (ATRA)-induced differentiation. Tretinoin 159-172 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 22-31
17579210-6 2007 Ectopic expression of C/EBPbeta in C3H10T1/2 cells causes a reduction in Runx2 expression concomitant with a decrease in osteogenic potential during all-trans retinoic acid (ATRA)-induced differentiation. Tretinoin 174-178 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 22-31
33441739-6 2021 Furthermore, we revealed the SV region-specific expression of Cyp26a1, which encodes an RA-degrading enzyme, and demonstrated that the increased RA levels in the SV region disrupt its pool of Aundiff by inducing their differentiation. Tretinoin 145-147 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 62-69
17579210-8 2007 ATRA, the effects of which are mediated by retinoic acid receptor alpha and gamma in C3H10T1/2 cells, stimulates the dissociation of C/EBPbeta from this element and promotes Runx2 expression. Tretinoin 0-4 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 133-142
17579210-8 2007 ATRA, the effects of which are mediated by retinoic acid receptor alpha and gamma in C3H10T1/2 cells, stimulates the dissociation of C/EBPbeta from this element and promotes Runx2 expression. Tretinoin 0-4 runt related transcription factor 2 Mus musculus 174-179
17671166-4 2007 The addition of retinoic acid (RA) induced large-scale chromatin decondensation in cells expressing RARalpha; however, cells expressing X-RARalpha, especially PML-RARalpha, demonstrated insensitive response to this effect of all-trans retinoic acid (ATRA). Tretinoin 16-29 retinoic acid receptor alpha Homo sapiens 100-108
17671166-4 2007 The addition of retinoic acid (RA) induced large-scale chromatin decondensation in cells expressing RARalpha; however, cells expressing X-RARalpha, especially PML-RARalpha, demonstrated insensitive response to this effect of all-trans retinoic acid (ATRA). Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 100-108
33158927-7 2020 Development of the caudal PP2 and more posterior PPs is affected by impaired retinoic acid signaling or pax1a/b dysfunction, suggesting that the rostral front of posterior PA development corresponds to the caudal PP2. Tretinoin 77-90 parapinopsin b Danio rerio 26-29
17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 59-64
17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 109-114
17938259-0 2007 Combined IFN-gamma and retinoic acid treatment targets the N-Myc/Max/Mad1 network resulting in repression of N-Myc target genes in MYCN-amplified neuroblastoma cells. Tretinoin 23-36 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 131-135
17628022-3 2007 We previously found that in myeloid leukemia cells, the lack of RA-induced RAR alpha-CAK dissociation and MAT1 degradation suppresses cell differentiation by inhibiting CAK-dependent G(1) exit and sustaining CAK hyperphosphorylation of RAR alpha. Tretinoin 64-66 retinoic acid receptor alpha Homo sapiens 236-245
17628022-4 2007 This contrasts with our recent findings about the P/D transition in normal primitive hematopoietic cells, where MAT1 degradation proceeds intrinsically together with granulocytic development, in accord with dynamic expression of aldehyde dehydrogenases (ALDHs) 1A1 and 1B1, which catalyze RA synthesis. Tretinoin 289-291 aldehyde dehydrogenase 1 family member A1 Homo sapiens 229-272
17708654-3 2007 Upregulation of FR-beta may also be selectively induced in AML cells by treatment with all-trans-retinoic acid (ATRA). Tretinoin 87-110 folate receptor beta Homo sapiens 16-23
17708654-3 2007 Upregulation of FR-beta may also be selectively induced in AML cells by treatment with all-trans-retinoic acid (ATRA). Tretinoin 112-116 folate receptor beta Homo sapiens 16-23
17708654-7 2007 In MV4-11 cells, the binding and cytotoxicity of FR-targeted liposomal DOX based on this formulation was also enhanced by ATRA-induced FR-beta upregulation. Tretinoin 122-126 folate receptor beta Homo sapiens 135-142
32424865-10 2020 Mechanistically, RA could activate the AKT/GSK3beta/beta-catenin pathway during the process of iPSCs osteogenesis. Tretinoin 17-19 catenin beta 1 Homo sapiens 52-64
17628018-5 2007 ESC engineered to overexpress Zfp206 were found to be resistant to differentiation induced by retinoic acid. Tretinoin 94-107 zinc finger and SCAN domain containing 10 Mus musculus 30-36
17628018-6 2007 In addition, ESC with knocked-down expression of Zfp206 were more sensitive to differentiation by retinoic acid treatment. Tretinoin 98-111 zinc finger and SCAN domain containing 10 Mus musculus 49-55
17786207-3 2007 In the course of one of our studies we observed that disruption of RA-receptor alpha, RARalpha, abrogates the RA-mediated growth-inhibitory effects and unmasks the growth-promoting face of RA (Ren et al., Mol. Tretinoin 67-69 retinoic acid receptor alpha Homo sapiens 86-94
17786207-7 2007 METHODOLOGY/PRINCIPAL FINDINGS: We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. Tretinoin 82-84 retinoic acid receptor alpha Homo sapiens 130-138
17786207-7 2007 METHODOLOGY/PRINCIPAL FINDINGS: We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. Tretinoin 82-84 retinoic acid receptor alpha Homo sapiens 130-138
17786207-7 2007 METHODOLOGY/PRINCIPAL FINDINGS: We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. Tretinoin 82-84 sphingosine kinase 1 Homo sapiens 363-383
17786207-7 2007 METHODOLOGY/PRINCIPAL FINDINGS: We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. Tretinoin 82-84 sphingosine kinase 1 Homo sapiens 385-388
17786207-9 2007 By combining genetic, pharmacological and biochemical approaches, we mechanistically demonstrated that RA-induced growth is, at least in part, due to non-RAR-mediated activation of the SK1-S1P signaling. Tretinoin 103-105 retinoic acid receptor alpha Homo sapiens 154-157
17786207-9 2007 By combining genetic, pharmacological and biochemical approaches, we mechanistically demonstrated that RA-induced growth is, at least in part, due to non-RAR-mediated activation of the SK1-S1P signaling. Tretinoin 103-105 sphingosine kinase 1 Homo sapiens 185-188
17825229-0 2007 [Effects of arsenic trioxide and ATRA on PLZF-RARalpha-positive U937 leukemic cells]. Tretinoin 33-37 retinoic acid receptor alpha Homo sapiens 46-54
17825229-1 2007 AIM: To investigate effects of arsenic trioxide (As(2)O(3)) and alltrans retinoic acid (ATRA) on PLZF-RARalpha-positive cells. Tretinoin 73-86 retinoic acid receptor alpha Homo sapiens 102-110
17825229-1 2007 AIM: To investigate effects of arsenic trioxide (As(2)O(3)) and alltrans retinoic acid (ATRA) on PLZF-RARalpha-positive cells. Tretinoin 88-92 retinoic acid receptor alpha Homo sapiens 102-110
17805463-9 2007 Dishevelled1/2/3 mRNA was significantly down-regulated at 4 and 18 h and up-regulated at 42 h in the fetus after RA treatment, except for an up-regulation of Dishevelled3 at 66 h. The Dishevelled2 mRNA and its protein matched each other. Tretinoin 113-115 dishevelled segment polarity protein 2 Mus musculus 184-196
33273838-2 2020 Recent studies have analyzed the impact of the two adipokines, RBP4 (retinol binding protein 4) and STRA6 (stimulated by retinoic acid 6) in pediatric obese subjects with contradictory results. Tretinoin 121-134 signaling receptor and transporter of retinol STRA6 Homo sapiens 100-105
17494859-0 2007 MN1 overexpression induces acute myeloid leukemia in mice and predicts ATRA resistance in patients with AML. Tretinoin 71-75 meningioma 1 Mus musculus 0-3
17923756-9 2007 Moreover, sequential treatments with ATRA or 13-cis RA followed by 4-HPR were found to have synergistic growth-inhibitory effects and to regulate RAR expression. Tretinoin 37-41 retinoic acid receptor alpha Homo sapiens 146-149
17923756-9 2007 Moreover, sequential treatments with ATRA or 13-cis RA followed by 4-HPR were found to have synergistic growth-inhibitory effects and to regulate RAR expression. Tretinoin 39-41 retinoic acid receptor alpha Homo sapiens 146-149
17699721-1 2007 We have recently reported that PML-RAR-induced misfolding of the N-CoR protein could be reversed by retinoic acid (RA), a therapeutic agent that promotes differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 100-113 nuclear receptor corepressor 1 Homo sapiens 65-70
17699721-1 2007 We have recently reported that PML-RAR-induced misfolding of the N-CoR protein could be reversed by retinoic acid (RA), a therapeutic agent that promotes differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 35-37 nuclear receptor corepressor 1 Homo sapiens 65-70
17662308-2 2007 In vitro, hNT neurons express tyrosine hydroxylase (TH), depending on the length of time they are exposed to retinoic acid. Tretinoin 109-122 neurotrimin Homo sapiens 10-13
32603414-8 2020 Lastly, we evaluate the impact of exposure to all-trans retinoic acid (ATRA) on wild type NK and CD38KO NK cells function and highlight potential benefit and drawbacks of combining ATRA with DARA in patients with MM. Tretinoin 46-69 CD38 molecule Homo sapiens 97-101
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 retinol binding protein 1, cellular Mus musculus 40-72
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 retinol binding protein 1, cellular Mus musculus 74-78
17363914-2 2007 One RA biosynthesis pathway consists of cellular retinol-binding protein (Crbp), retinol dehydrogenase (Dhrs9/eRoldh), retinal dehydrogenase 1-3 (Aldh1a1-3), and cellular RA-binding protein 2 (Crabp2). Tretinoin 4-6 dehydrogenase/reductase (SDR family) member 9 Mus musculus 104-109
17333391-2 2007 P19 cells could differentiate into neuroectodermal cell lineage after cell aggregates have been induced by retinoic acid (RA). Tretinoin 107-120 interleukin 23 subunit alpha Homo sapiens 0-3
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 41-54 retinoic acid receptor alpha Homo sapiens 66-88
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 41-54 retinoic acid receptor alpha Homo sapiens 90-93
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 56-58 retinoic acid receptor alpha Homo sapiens 66-88
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 56-58 retinoic acid receptor alpha Homo sapiens 90-93
17784840-0 2007 Neurospheres derived from human embryoid bodies treated with retinoic Acid show an increase in nestin and ngn2 expression that correlates with the proportion of tyrosine hydroxylase-positive cells. Tretinoin 61-74 neurogenin 2 Homo sapiens 106-110
17784840-8 2007 Neurospheres derived from RA-treated EBs contained many nestin-positive cells within regions that expressed Ngn2. Tretinoin 26-28 neurogenin 2 Homo sapiens 108-112
17333391-2 2007 P19 cells could differentiate into neuroectodermal cell lineage after cell aggregates have been induced by retinoic acid (RA). Tretinoin 122-124 interleukin 23 subunit alpha Homo sapiens 0-3
32603414-8 2020 Lastly, we evaluate the impact of exposure to all-trans retinoic acid (ATRA) on wild type NK and CD38KO NK cells function and highlight potential benefit and drawbacks of combining ATRA with DARA in patients with MM. Tretinoin 71-75 CD38 molecule Homo sapiens 97-101
32868073-6 2020 However, massive cell death was observed after retinoic acid treatment, suggesting a role of Ulk1-induced p53 activation in the elimination of defective pluripotent cells prior to differentiation. Tretinoin 47-60 transformation related protein 53, pseudogene Mus musculus 106-109
17486130-2 2007 As intracellular metabolism of ATRA by CYP26 may result in clinical resistance to 13cisRA, an increase in efficacy may be achieved through modulation of this metabolic pathway. Tretinoin 31-35 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 39-44
17486130-4 2007 In neuroblastoma cells, which showed a high level of CYP26 induction in response to ATRA, R116010 selectively inhibited ATRA metabolism. Tretinoin 84-88 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 53-58
17486130-5 2007 In addition, siRNA-mediated knockdown of CYP26 selectively increased ATRA levels and the expression of retinoid-responsive marker genes was potentiated by R116010. Tretinoin 69-73 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 41-46
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 cadherin 1 Rattus norvegicus 183-193
17822036-3 2007 The gene Stra 8 (Stimulated by Retinoic Acid) was one of the gene in this group. Tretinoin 31-44 stimulated by retinoic acid gene 8 Mus musculus 9-15
17478430-11 2007 Retinoic acid, which induces teratogenic effects similarly to ethanol, also caused up-regulation of ABCA1 and ABCG1. Tretinoin 0-13 ATP binding cassette subfamily G member 1 Rattus norvegicus 110-115
17332158-4 2007 Here, we show differential regulation of MMPs in cultured chondrocytes from chickens and turkeys; retinoic acid (RA) elevated MMP-2 activity in both species, but only in chicken did it induce MMP-9 activity. Tretinoin 98-111 matrix metallopeptidase 9 Gallus gallus 192-197
32865844-0 2020 The effect of calcitriol and all-trans retinoic acid on T-bet, IFN-gamma, GATA3 and IL-4 genes expression in experimental autoimmune encephalomyelitis. Tretinoin 29-52 interleukin 4 Mus musculus 84-88
17475621-8 2007 Furthermore, treatment of NB4 cells with all-trans-retinoic acid, which promotes PML-RARalpha degradation, resulted in increased activation of GILZ. Tretinoin 41-64 PML nuclear body scaffold Homo sapiens 81-84
17475621-8 2007 Furthermore, treatment of NB4 cells with all-trans-retinoic acid, which promotes PML-RARalpha degradation, resulted in increased activation of GILZ. Tretinoin 41-64 retinoic acid receptor alpha Homo sapiens 85-93
32920510-9 2020 4-amino-2-trifluoromethyl-phenyl retinate (ATPR) is the derivative of all-trans retinoic acid (ATRA), which was able to reduce both MLCK expression and activity in FaDu cells. Tretinoin 70-93 myosin light chain kinase Homo sapiens 132-136
17551590-5 2007 We provide evidence showing that RA acts on the signalling epithelium of the 1(st) PA, gradually reducing the expression of endothelin-1 and Fgf8. Tretinoin 33-35 fibroblast growth factor 8 Homo sapiens 141-145
17335046-6 2007 Furthermore, although RA caused comparable reductions of Shh expression between the strains in the 12 h after administration, some Shh downstream genes were differentially expressed (e.g., Gli1, Ptc, and Hoxd13), whereas others were not (e.g., Fgf4, Bmp4, and Gremlin). Tretinoin 22-24 sonic hedgehog Mus musculus 57-60
17600781-5 2007 RA may control somitogenesis through its ability to repress posterior ectodermal expression of fibroblast growth factor-8 (Fgf8) for a short period of time during the late primitive streak stage when the somitogenesis clock initiates. Tretinoin 0-2 fibroblast growth factor 8 Homo sapiens 95-121
17600781-5 2007 RA may control somitogenesis through its ability to repress posterior ectodermal expression of fibroblast growth factor-8 (Fgf8) for a short period of time during the late primitive streak stage when the somitogenesis clock initiates. Tretinoin 0-2 fibroblast growth factor 8 Homo sapiens 123-127
17600781-6 2007 During this tight temporal window, RA is required to limit Fgf8 expression to the most posterior ectoderm (epiblast), thus preventing ectopic Fgf8 expression in more anterior ectoderm including the node ectoderm and neuroectoderm. Tretinoin 35-37 fibroblast growth factor 8 Homo sapiens 59-63
17600781-6 2007 During this tight temporal window, RA is required to limit Fgf8 expression to the most posterior ectoderm (epiblast), thus preventing ectopic Fgf8 expression in more anterior ectoderm including the node ectoderm and neuroectoderm. Tretinoin 35-37 fibroblast growth factor 8 Homo sapiens 142-146
32920510-9 2020 4-amino-2-trifluoromethyl-phenyl retinate (ATPR) is the derivative of all-trans retinoic acid (ATRA), which was able to reduce both MLCK expression and activity in FaDu cells. Tretinoin 95-99 myosin light chain kinase Homo sapiens 132-136
17507413-7 2007 Furthermore, although FGF inhibition of neuronal differentiation involves repression of the RA-responsive gene, retinoic acid receptor beta (RARbeta), Wnt signals are weaker repressors of neuron production and do not interfere with RA signal transduction. Tretinoin 92-94 retinoic acid receptor beta Gallus gallus 112-139
17526768-1 2007 Previous gene array data from our laboratory identified the retinoic acid (RA) biosynthesis enzyme aldehyde dehydrogenase 1A3 (ALDH1A3) as a putative androgen-responsive gene in human prostate cancer epithelial (LNCaP) cells. Tretinoin 60-73 aldehyde dehydrogenase 1 family member A3 Homo sapiens 99-125
17507413-7 2007 Furthermore, although FGF inhibition of neuronal differentiation involves repression of the RA-responsive gene, retinoic acid receptor beta (RARbeta), Wnt signals are weaker repressors of neuron production and do not interfere with RA signal transduction. Tretinoin 92-94 retinoic acid receptor beta Gallus gallus 141-148
17526768-1 2007 Previous gene array data from our laboratory identified the retinoic acid (RA) biosynthesis enzyme aldehyde dehydrogenase 1A3 (ALDH1A3) as a putative androgen-responsive gene in human prostate cancer epithelial (LNCaP) cells. Tretinoin 60-73 aldehyde dehydrogenase 1 family member A3 Homo sapiens 127-134
32737889-0 2020 P38 MAPK Signaling Mediates Retinoic Acid-Induced CD103 Expression in Human Dendritic Cells. Tretinoin 28-41 integrin subunit alpha E Homo sapiens 50-55
17526768-1 2007 Previous gene array data from our laboratory identified the retinoic acid (RA) biosynthesis enzyme aldehyde dehydrogenase 1A3 (ALDH1A3) as a putative androgen-responsive gene in human prostate cancer epithelial (LNCaP) cells. Tretinoin 75-77 aldehyde dehydrogenase 1 family member A3 Homo sapiens 99-125
17526768-1 2007 Previous gene array data from our laboratory identified the retinoic acid (RA) biosynthesis enzyme aldehyde dehydrogenase 1A3 (ALDH1A3) as a putative androgen-responsive gene in human prostate cancer epithelial (LNCaP) cells. Tretinoin 75-77 aldehyde dehydrogenase 1 family member A3 Homo sapiens 127-134
17526768-9 2007 Taken together, these data suggest that (i) the RA biosynthesis enzyme ALDH1A3 is androgen responsive and (ii) DHT up-regulation of ALDH1A3 can increase the oxidation of retinal to RA and indirectly affect RA bioactivity and metabolism. Tretinoin 48-50 aldehyde dehydrogenase 1 family member A3 Homo sapiens 71-78
17526768-9 2007 Taken together, these data suggest that (i) the RA biosynthesis enzyme ALDH1A3 is androgen responsive and (ii) DHT up-regulation of ALDH1A3 can increase the oxidation of retinal to RA and indirectly affect RA bioactivity and metabolism. Tretinoin 181-183 aldehyde dehydrogenase 1 family member A3 Homo sapiens 71-78
17526768-9 2007 Taken together, these data suggest that (i) the RA biosynthesis enzyme ALDH1A3 is androgen responsive and (ii) DHT up-regulation of ALDH1A3 can increase the oxidation of retinal to RA and indirectly affect RA bioactivity and metabolism. Tretinoin 181-183 aldehyde dehydrogenase 1 family member A3 Homo sapiens 132-139
17526768-9 2007 Taken together, these data suggest that (i) the RA biosynthesis enzyme ALDH1A3 is androgen responsive and (ii) DHT up-regulation of ALDH1A3 can increase the oxidation of retinal to RA and indirectly affect RA bioactivity and metabolism. Tretinoin 181-183 aldehyde dehydrogenase 1 family member A3 Homo sapiens 71-78
17526768-9 2007 Taken together, these data suggest that (i) the RA biosynthesis enzyme ALDH1A3 is androgen responsive and (ii) DHT up-regulation of ALDH1A3 can increase the oxidation of retinal to RA and indirectly affect RA bioactivity and metabolism. Tretinoin 181-183 aldehyde dehydrogenase 1 family member A3 Homo sapiens 132-139
17426037-6 2007 Furthermore, ATM-negative cells failed to differentiate into neuronal-like cells when exposed to retinoic acid; instead, they underwent cell death. Tretinoin 97-110 ATM serine/threonine kinase Homo sapiens 13-16
17426037-9 2007 The results demonstrate that ATM is required for the retinoic acid-induced differentiation of SH-SY5Y cells through the ATM dependent-phosphorylation of serine 133 of CREB. Tretinoin 53-66 ATM serine/threonine kinase Homo sapiens 29-32
17426037-9 2007 The results demonstrate that ATM is required for the retinoic acid-induced differentiation of SH-SY5Y cells through the ATM dependent-phosphorylation of serine 133 of CREB. Tretinoin 53-66 ATM serine/threonine kinase Homo sapiens 120-123
17426037-10 2007 These results therefore define a novel mechanism for activation of the activity of ATM kinase by RA, and implicate ATM in the regulation of CREB function during RA-induced differentiation. Tretinoin 97-99 ATM serine/threonine kinase Homo sapiens 83-86
17499973-3 2007 It has been suggested that vitamin A (VA) and its physiologic active metabolite retinoic acid influence longitudinal growth by promoting the differentiation of pituitary cells toward GH-secreting cells and by stimulating secretion of GH. Tretinoin 80-93 growth hormone Mus musculus 183-185
17499973-3 2007 It has been suggested that vitamin A (VA) and its physiologic active metabolite retinoic acid influence longitudinal growth by promoting the differentiation of pituitary cells toward GH-secreting cells and by stimulating secretion of GH. Tretinoin 80-93 growth hormone Mus musculus 234-236
17426037-10 2007 These results therefore define a novel mechanism for activation of the activity of ATM kinase by RA, and implicate ATM in the regulation of CREB function during RA-induced differentiation. Tretinoin 161-163 ATM serine/threonine kinase Homo sapiens 115-118
32737889-3 2020 In this study, we analyzed the cell type specificity and the molecular mechanisms involved in RA-induced CD103 expression. Tretinoin 94-96 integrin subunit alpha E Homo sapiens 105-110
32737889-4 2020 We show that RA treatment caused a significant upregulation of CD103 in differentiated monocyte-derived DCs and blood DCs, but not in differentiated monocyte-derived macrophages or T cells. Tretinoin 13-15 integrin subunit alpha E Homo sapiens 63-68
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 71-84 GRDX Homo sapiens 25-28
17512397-1 2007 Retinoic acid-the active metabolite of vitamin A-influences biological processes by activating the retinoic acid receptor (RAR). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 99-121
32737889-5 2020 DC treatment with an RARalpha agonist lead to a similar increase in CD103 expression as RA treatment, while RARA gene silencing with siRNA blocked RA-induced upregulation of CD103, pointing to a major role of RARalpha in the regulation of CD103 expression. Tretinoin 21-23 integrin subunit alpha E Homo sapiens 68-73
17512397-1 2007 Retinoic acid-the active metabolite of vitamin A-influences biological processes by activating the retinoic acid receptor (RAR). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 123-126
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 86-88 GRDX Homo sapiens 25-28
32737889-6 2020 To elucidate RA-induced signaling downstream of RARalpha, we used Western blot analysis of RA-treated DCs and showed a significant increase of p38 MAPK phosphorylation. Tretinoin 13-15 retinoic acid receptor alpha Homo sapiens 48-56
17512397-4 2007 Remarkably, retinoic acid signaling through RAR or PPARbeta/delta-which depends on cytoplasmic retinoic acid transporters-commits the cell to opposite fates, apoptosis or survival, respectively. Tretinoin 12-25 retinoic acid receptor alpha Homo sapiens 44-47
32737889-7 2020 In addition, DCs cultured with RA and a p38 MAPK inhibitor had a significantly reduced expression of CD103 compared with DCs cultured with RA only, indicating that p38 MAPK is involved in CD103 regulation. Tretinoin 31-33 integrin subunit alpha E Homo sapiens 101-106
32737889-7 2020 In addition, DCs cultured with RA and a p38 MAPK inhibitor had a significantly reduced expression of CD103 compared with DCs cultured with RA only, indicating that p38 MAPK is involved in CD103 regulation. Tretinoin 31-33 integrin subunit alpha E Homo sapiens 188-193
32737889-7 2020 In addition, DCs cultured with RA and a p38 MAPK inhibitor had a significantly reduced expression of CD103 compared with DCs cultured with RA only, indicating that p38 MAPK is involved in CD103 regulation. Tretinoin 139-141 integrin subunit alpha E Homo sapiens 101-106
17209053-3 2007 RA enhanced the CpG-mediated proliferation of CD27(+) memory B cells, and the proliferative response was accompanied by increased immunoglobulin (Ig) secretion indicative of plasma-cell formation. Tretinoin 0-2 CD27 molecule Homo sapiens 46-50
32737889-7 2020 In addition, DCs cultured with RA and a p38 MAPK inhibitor had a significantly reduced expression of CD103 compared with DCs cultured with RA only, indicating that p38 MAPK is involved in CD103 regulation. Tretinoin 139-141 integrin subunit alpha E Homo sapiens 188-193
17209053-7 2007 Hence, we propose that RA can strengthen humoral immunity by promoting CpG-mediated stimulation of CD27(+) B cells via activation of p38MAPK resulting in increased proliferation and differentiation to Ig-secreting plasma cells. Tretinoin 23-25 CD27 molecule Homo sapiens 99-103
17290005-2 2007 Pharmacological NR ligands serve as important therapeutic agents; for example, all-trans retinoic acid, an activating ligand for retinoic acid receptor alpha (RARalpha), is used to treat leukemia. Tretinoin 89-102 retinoic acid receptor alpha Homo sapiens 129-157
17290005-2 2007 Pharmacological NR ligands serve as important therapeutic agents; for example, all-trans retinoic acid, an activating ligand for retinoic acid receptor alpha (RARalpha), is used to treat leukemia. Tretinoin 89-102 retinoic acid receptor alpha Homo sapiens 159-167
32737889-8 2020 In summary, these findings suggest that the RA-induced expression of CD103 is specific to DCs, is mediated primarily through RARalpha and involves p38 MAPK signaling. Tretinoin 44-46 integrin subunit alpha E Homo sapiens 69-74
32737889-8 2020 In summary, these findings suggest that the RA-induced expression of CD103 is specific to DCs, is mediated primarily through RARalpha and involves p38 MAPK signaling. Tretinoin 44-46 retinoic acid receptor alpha Homo sapiens 125-133
33080103-4 2020 However, HRH1-mediated signalling was critical for the activation of the differentiation process induced by several agents including all-trans retinoic acid, establishing a role for HRH1 in myeloid differentiation. Tretinoin 133-156 histamine receptor H1 Homo sapiens 9-13
17314394-7 2007 Retinoic acid-mediated differentiation of reprogrammed cells elicits OCT4 promoter remethylation and transcriptional repression. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 69-73
17463084-3 2007 The present work reports that TLR3 signaling by polyinosinic-polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8alphaalpha intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. Tretinoin 146-159 toll-like receptor 3 Mus musculus 308-312
17289015-7 2007 Each of these subtypes was detected in differentiated trophoblast stem cell cultures and can be differentially regulated; treatment with retinoic acid induces Pl1/Plf+ TGCs preferentially. Tretinoin 137-150 prolactin family 2, subfamily c, member 2 Mus musculus 163-166
17426693-4 2007 Further, all-trans retinoic acid (RA) was used to promote pancreatic differentiation, as indicated by the expression of the early pancreatic transcription factors pdx1 and hlxb9. Tretinoin 9-32 motor neuron and pancreas homeobox 1 Homo sapiens 172-177
17426693-4 2007 Further, all-trans retinoic acid (RA) was used to promote pancreatic differentiation, as indicated by the expression of the early pancreatic transcription factors pdx1 and hlxb9. Tretinoin 34-36 motor neuron and pancreas homeobox 1 Homo sapiens 172-177
17483060-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand (all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 82-105 retinoic acid receptor alpha Homo sapiens 70-73
17483060-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand (all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 82-105 phosphatase and tensin homolog Homo sapiens 127-131
17387344-7 2007 Similar to ATRA, they also induced apoptosis via activation of caspase 9. Tretinoin 11-15 caspase 9 Homo sapiens 63-72
32372724-6 2020 By using an established cell model for studying neurogenesis, NTera2/D1 (NT2) cells, we found that a particular PIWI homolog, PIWIL4 was increasingly upregulated throughout the course of all-trans retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 197-210 piwi like RNA-mediated gene silencing 4 Homo sapiens 126-132
17483060-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand (all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 70-73
17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 H3 histone pseudogene 16 Homo sapiens 345-348
16920192-6 2007 RA also upregulated the expression of CD38, an ectoenzyme responsible for the generation of the calcium messenger cyclic ADP-ribose. Tretinoin 0-2 CD38 molecule Homo sapiens 38-42
32372724-6 2020 By using an established cell model for studying neurogenesis, NTera2/D1 (NT2) cells, we found that a particular PIWI homolog, PIWIL4 was increasingly upregulated throughout the course of all-trans retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 212-214 piwi like RNA-mediated gene silencing 4 Homo sapiens 126-132
32372724-7 2020 During this process, PIWIL4 knockdown led to partial recovery of embryonic stem cell markers, while suppressing RA-induced expression of neuronal markers. Tretinoin 112-114 piwi like RNA-mediated gene silencing 4 Homo sapiens 21-27
17351639-5 2007 Furthermore, we show that IKK1-deficient cells display impaired retinoic acid-induced gene transcription, and that IKK1 is recruited to the promoters of retinoic acid-regulated genes, suggesting that one mechanism by which IKK1 controls epidermal-barrier formation is by regulating the expression of retinoic acid receptor target genes in keratinocytes. Tretinoin 64-77 conserved helix-loop-helix ubiquitous kinase Mus musculus 26-30
32372724-9 2020 Furthermore, co-immunoprecipitation revealed an RA-induced interaction between PIWIL4 and the H3K27me3 demethylase UTX. Tretinoin 48-50 piwi like RNA-mediated gene silencing 4 Homo sapiens 79-85
33120845-13 2020 LESSONS: APL patients with STAT5B-RARa is not only resistant to ATRA, but also to conventional combination chemotherapy such as daunorubicin and cytarabine/idarubicin and cytarabine or other regimens. Tretinoin 64-68 retinoic acid receptor alpha Homo sapiens 34-38
33082341-6 2020 GATA6 expression contributes to the therapeutic effect of retinoic acid, the main treatment for acne. Tretinoin 58-71 GATA binding protein 6 Homo sapiens 0-5
17431108-0 2007 The RET oncogene is a critical component of transcriptional programs associated with retinoic acid-induced differentiation in neuroblastoma. Tretinoin 85-98 ret proto-oncogene Homo sapiens 4-7
17431108-6 2007 RET, a receptor tyrosine kinase involved with differentiation, was consistently up-regulated throughout the time course of RA treatment in the majority of neuroblastic tumor cell lines. Tretinoin 123-125 ret proto-oncogene Homo sapiens 0-3
33054971-5 2020 Remarkably, an exon 4 GATA6 missense variant, highly associated with extra-cardiac malformations, caused ectopic pioneer activities, profoundly diminishing GATA4, FOXA1/2 and PDX1 expression and increasing normal retinoic acid signaling that promotes diaphragm development. Tretinoin 213-226 GATA binding protein 6 Homo sapiens 22-27
17493354-0 2007 [Effects of arsenic trioxide or retinoic acid on mRNA and protein expression of tissue factor and thrombomodulin and procoagulant activity in NB4 cells]. Tretinoin 32-45 coagulation factor III, tissue factor Homo sapiens 80-93
17493354-0 2007 [Effects of arsenic trioxide or retinoic acid on mRNA and protein expression of tissue factor and thrombomodulin and procoagulant activity in NB4 cells]. Tretinoin 32-45 thrombomodulin Homo sapiens 98-112
17493354-1 2007 To investigate the effect of arsenic trioxide (As(2)O(3)) or all-trans retinoic acid (ATRA) on the mRNA and protein expression of tissue factor (TF) and thrombomodulin (TM) and procoagulant activity (PCA) in NB4 cells. Tretinoin 71-84 coagulation factor III, tissue factor Homo sapiens 130-143
17493354-1 2007 To investigate the effect of arsenic trioxide (As(2)O(3)) or all-trans retinoic acid (ATRA) on the mRNA and protein expression of tissue factor (TF) and thrombomodulin (TM) and procoagulant activity (PCA) in NB4 cells. Tretinoin 71-84 coagulation factor III, tissue factor Homo sapiens 145-147
17493354-1 2007 To investigate the effect of arsenic trioxide (As(2)O(3)) or all-trans retinoic acid (ATRA) on the mRNA and protein expression of tissue factor (TF) and thrombomodulin (TM) and procoagulant activity (PCA) in NB4 cells. Tretinoin 71-84 thrombomodulin Homo sapiens 153-167
17493354-1 2007 To investigate the effect of arsenic trioxide (As(2)O(3)) or all-trans retinoic acid (ATRA) on the mRNA and protein expression of tissue factor (TF) and thrombomodulin (TM) and procoagulant activity (PCA) in NB4 cells. Tretinoin 86-90 coagulation factor III, tissue factor Homo sapiens 130-143
17493354-1 2007 To investigate the effect of arsenic trioxide (As(2)O(3)) or all-trans retinoic acid (ATRA) on the mRNA and protein expression of tissue factor (TF) and thrombomodulin (TM) and procoagulant activity (PCA) in NB4 cells. Tretinoin 86-90 coagulation factor III, tissue factor Homo sapiens 145-147
33024217-5 2020 We sought to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the expression of FABP5 acts as a novel positive regulator of ST2 expression in alveolar ECs to generate retinoic acid (RA) and supports the synthesis of RA from type II alveolar ECs to suppress excessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation. Tretinoin 200-213 fatty acid binding protein 5, epidermal Mus musculus 113-118
17493354-1 2007 To investigate the effect of arsenic trioxide (As(2)O(3)) or all-trans retinoic acid (ATRA) on the mRNA and protein expression of tissue factor (TF) and thrombomodulin (TM) and procoagulant activity (PCA) in NB4 cells. Tretinoin 86-90 thrombomodulin Homo sapiens 153-167
17493354-3 2007 The results showed that 1 micromol/L As(2)O(3) and 1 micromol/L ATRA both gradually downregulated the expression of TF antigen and mRNA on NB4 cells, a human promyelocytic leukemia cell line, in time-dependent manner, as compared with control. Tretinoin 64-68 coagulation factor III, tissue factor Homo sapiens 116-118
17244623-7 2007 Furthermore, BZLF1 expression in AGS cells is sufficient to activate DHRS9 gene expression and increases the ability of retinol to induce the RA-responsive gene, CYP26A1. Tretinoin 142-144 protein Zta Human gammaherpesvirus 4 13-18
32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 lysine methyltransferase 2A Homo sapiens 26-29
17291686-3 2007 Here we investigated the effects of all-trans-retinoic acid (ATRA) and MIAs, i.e. colchicine, nocodazole and taxol on the regulation of retinoic acid receptor (RAR) genes in primary cultures of rat hepatocytes. Tretinoin 36-59 retinoic acid receptor alpha Homo sapiens 160-163
17291686-3 2007 Here we investigated the effects of all-trans-retinoic acid (ATRA) and MIAs, i.e. colchicine, nocodazole and taxol on the regulation of retinoic acid receptor (RAR) genes in primary cultures of rat hepatocytes. Tretinoin 61-65 retinoic acid receptor alpha Homo sapiens 160-163
32680845-8 2020 Finally, we described that administration of retinoic acid to IR-Rph nephrocytes rescued some altered aspects as the filtration and molecular uptake as well as the maintenance of cell fate. Tretinoin 45-58 Rabphilin Drosophila melanogaster 65-68
17126317-0 2007 Rescue of cytochrome P450 oxidoreductase (Por) mouse mutants reveals functions in vasculogenesis, brain and limb patterning linked to retinoic acid homeostasis. Tretinoin 134-147 cytochrome p450 oxidoreductase Mus musculus 42-45
17126317-2 2007 Knockout mouse Por(-/-) mutants, which are early embryonic (E9.5) lethal, have been found to have overall elevated retinoic acid (RA) levels, leading to the idea that POR early developmental function is mainly linked to the activity of the CYP26 RA-metabolizing enzymes (Otto et al., Mol. Tretinoin 115-128 cytochrome p450 oxidoreductase Mus musculus 15-18
17126317-2 2007 Knockout mouse Por(-/-) mutants, which are early embryonic (E9.5) lethal, have been found to have overall elevated retinoic acid (RA) levels, leading to the idea that POR early developmental function is mainly linked to the activity of the CYP26 RA-metabolizing enzymes (Otto et al., Mol. Tretinoin 115-128 cytochrome p450 oxidoreductase Mus musculus 167-170
17126317-2 2007 Knockout mouse Por(-/-) mutants, which are early embryonic (E9.5) lethal, have been found to have overall elevated retinoic acid (RA) levels, leading to the idea that POR early developmental function is mainly linked to the activity of the CYP26 RA-metabolizing enzymes (Otto et al., Mol. Tretinoin 130-132 cytochrome p450 oxidoreductase Mus musculus 15-18
17126317-2 2007 Knockout mouse Por(-/-) mutants, which are early embryonic (E9.5) lethal, have been found to have overall elevated retinoic acid (RA) levels, leading to the idea that POR early developmental function is mainly linked to the activity of the CYP26 RA-metabolizing enzymes (Otto et al., Mol. Tretinoin 130-132 cytochrome p450 oxidoreductase Mus musculus 167-170
17126317-2 2007 Knockout mouse Por(-/-) mutants, which are early embryonic (E9.5) lethal, have been found to have overall elevated retinoic acid (RA) levels, leading to the idea that POR early developmental function is mainly linked to the activity of the CYP26 RA-metabolizing enzymes (Otto et al., Mol. Tretinoin 246-248 cytochrome p450 oxidoreductase Mus musculus 167-170
17126317-6 2007 By crossing Por mutants with a RA-reporter lacZ transgene, we show that Por(-/-) embryos exhibit both elevated and ectopic RA signaling activity e.g. in cephalic and caudal tissues. Tretinoin 31-33 cytochrome p450 oxidoreductase Mus musculus 72-75
17126317-12 2007 Thus, POR function is indispensable for the proper regulation of RA levels and tissue distribution not only during early embryonic development but also in later morphogenesis and molecular patterning of the brain, abdominal/caudal region and limbs. Tretinoin 65-67 cytochrome p450 oxidoreductase Mus musculus 6-9
32932813-9 2020 In addition, flow cytometry analysis revealed that RA improved estimates of various viral reservoir assays by eliciting broad CD4 T-cell activation as demonstrated by elevated CD25 and CD38 but reduced CD69 and PD-1 expressing cells. Tretinoin 51-53 interleukin 2 receptor subunit alpha Sus scrofa 176-180
17211890-0 2007 The oxidizing enzyme CYP26a1 tightly regulates the availability of retinoic acid in the gastrulating mouse embryo to ensure proper head development and vasculogenesis. Tretinoin 67-80 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 21-28
17211890-5 2007 This might result from RA catabolism mediated by the CYP26A1 oxidizing enzyme, which is transiently expressed in anteriormost embryonic tissues; however, previous analysis of Cyp26a1(-/-) mouse mutants did not clearly support this hypothesis. Tretinoin 23-25 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 53-60
17211890-5 2007 This might result from RA catabolism mediated by the CYP26A1 oxidizing enzyme, which is transiently expressed in anteriormost embryonic tissues; however, previous analysis of Cyp26a1(-/-) mouse mutants did not clearly support this hypothesis. Tretinoin 23-25 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 175-182
17211890-6 2007 Here we show that Cyp26a1(-/-) null mutants undergo head truncations when exposed to maternally-derived RA, at doses that do not affect wild-type head development. Tretinoin 104-106 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 18-25
17211890-7 2007 These anomalies are linked to a widespread ectopic RA signaling activity in rostral head tissues of CYP26A1-deficient embryos. Tretinoin 51-53 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 100-107
17211890-8 2007 Thus, CYP26A1 is required in the anterior region of the gastrulating mouse embryo to prevent teratological effects that may result from RA signaling. Tretinoin 136-138 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 6-13
32899900-4 2020 In retinoic acid (RA)-differentiated SH-SY5Y cells challenged with alpha-synuclein (alpha-syn) plus rotenone (Rot), glutamate significantly improved cell viability by increasing ATP levels, reducing oxidative damage and cytosolic and mitochondrial Ca2+ overload. Tretinoin 3-16 synuclein alpha Homo sapiens 67-82
17170094-11 2007 Transcription activity of human VEGF gene promoter in NHDFs was stimulated by ATRA, which was augmented by RAR overexpression. Tretinoin 78-82 retinoic acid receptor alpha Homo sapiens 107-110
17170094-14 2007 Taken together, ATRA may have induced angiogenesis via RAR mainly by stimulation of HUVEC proliferation and enhancement of endogenous VEGF signaling and in part by induction of hepatocyte growth factor and angiopoietin-2 production. Tretinoin 16-20 retinoic acid receptor alpha Homo sapiens 55-58
32899900-4 2020 In retinoic acid (RA)-differentiated SH-SY5Y cells challenged with alpha-synuclein (alpha-syn) plus rotenone (Rot), glutamate significantly improved cell viability by increasing ATP levels, reducing oxidative damage and cytosolic and mitochondrial Ca2+ overload. Tretinoin 3-16 synuclein alpha Homo sapiens 67-76
32899900-4 2020 In retinoic acid (RA)-differentiated SH-SY5Y cells challenged with alpha-synuclein (alpha-syn) plus rotenone (Rot), glutamate significantly improved cell viability by increasing ATP levels, reducing oxidative damage and cytosolic and mitochondrial Ca2+ overload. Tretinoin 18-20 synuclein alpha Homo sapiens 67-82
17312396-5 2007 Treatment of glioma cell lines with a combination of retinoic acid and low-dose okadaic acid decreases the corepressor effect of N-CoR and has a striking synergistic effect on growth inhibition. Tretinoin 53-66 nuclear receptor corepressor 1 Homo sapiens 129-134
32899900-4 2020 In retinoic acid (RA)-differentiated SH-SY5Y cells challenged with alpha-synuclein (alpha-syn) plus rotenone (Rot), glutamate significantly improved cell viability by increasing ATP levels, reducing oxidative damage and cytosolic and mitochondrial Ca2+ overload. Tretinoin 18-20 synuclein alpha Homo sapiens 67-76
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 239-252 neuronal differentiation 1 Homo sapiens 191-198
17239557-6 2007 It is presumed that these cells release RA in a paracrine fashion in the region of the wound; however, the RALDH2/NG2-immunoreactive cells expressed the retinoid receptors RARalpha, RARbeta, RXRalpha and RXRbeta, suggesting that RA also serves an autocrine function. Tretinoin 107-109 retinoic acid receptor alpha Homo sapiens 172-180
17161435-4 2007 Expressions of all three genes (SLIM1, SM alpha-actin and CNN-1) were simultaneously elevated in the cells treated with 9-cis retinoic acid (RA). Tretinoin 141-143 calponin 1 Rattus norvegicus 58-63
33088261-8 2020 At the biochemical level, changes in Willin/FRMD6 expression inversely affected the activity of the extracellular signal-regulated kinases (ERK) pathway and downstream transcriptional factor NeuroD1, which seems to prime SH-SY5Y cells for retinoic acid (RA)-induced neuronal differentiation. Tretinoin 254-256 neuronal differentiation 1 Homo sapiens 191-198
32741018-0 2020 Novel evidence for retinoic acid-induced G (Rig-G) as a tumor suppressor by activating p53 signaling pathway in lung cancer. Tretinoin 19-32 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 44-49
17113559-6 2007 Tau/P19 cells underwent drastic apoptosis during neural differentiation induced by retinoic acid (RA). Tretinoin 98-100 microtubule associated protein tau Homo sapiens 0-3
17113559-9 2007 The apoptosis induced by RA was inhibited by the treatment of glycogen synthase kinase 3 (GSK3) inhibitor in tau/P19 cells. Tretinoin 25-27 microtubule associated protein tau Homo sapiens 109-112
17113559-10 2007 We propose that translocation of tau into nucleus affects RA signaling in apoptosis via GSK3 in the cells. Tretinoin 58-60 microtubule associated protein tau Homo sapiens 33-36
32597569-1 2020 BACKGROUND: Syndromic microphthalmia-9 (MCOPS9) is a rare autosomal recessive disorder caused by mutations in STRA6, an important regulator of vitamin A and retinoic acid metabolism. Tretinoin 157-170 signaling receptor and transporter of retinol STRA6 Homo sapiens 40-46
17573627-0 2007 Tin mesoporphyrin in conjunction with retinoic acid reverses the retinoic acid induced enhancement of phospholipase A(2) activity in vivo in rats. Tretinoin 38-51 phospholipase A2 group IB Rattus norvegicus 102-120
17573627-0 2007 Tin mesoporphyrin in conjunction with retinoic acid reverses the retinoic acid induced enhancement of phospholipase A(2) activity in vivo in rats. Tretinoin 65-78 phospholipase A2 group IB Rattus norvegicus 102-120
17573627-2 2007 The effect of one of its natural derivatives, Retinoic Acid, was therefore studied on membrane stability, by inversely correlating this stability with Phospholipase A(2) activity. Tretinoin 46-59 phospholipase A2 group IB Rattus norvegicus 151-168
17573627-6 2007 However when Retinoic Acid and Tin-mesoporphyrin (50 micromol/kgbw) were co-administered, hepatic Phospholipase A(2) activity was inhibited. Tretinoin 13-26 phospholipase A2 group IB Rattus norvegicus 98-115
32597569-1 2020 BACKGROUND: Syndromic microphthalmia-9 (MCOPS9) is a rare autosomal recessive disorder caused by mutations in STRA6, an important regulator of vitamin A and retinoic acid metabolism. Tretinoin 157-170 signaling receptor and transporter of retinol STRA6 Homo sapiens 110-115
32520724-5 2020 Doses as low as 0.01microM reduced transcript levels of the retinoic acid response genes Stra8 and Rarbeta without affecting germ cell number. Tretinoin 60-73 stimulated by retinoic acid gene 8 Mus musculus 89-94
17011172-2 2007 RA suppresses the expression of alpha2(I) collagen by means of the activities of specific nuclear receptors RARalpha, RXRbeta and their coregulators. Tretinoin 0-2 retinoid X receptor beta Mus musculus 118-125
17069763-0 2006 Bidirectional CLOCK/BMAL1-dependent circadian gene regulation by retinoic acid in vitro. Tretinoin 65-78 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 20-25
32882760-8 2020 A RAF-1/MEK/ERK pathway was founded to be associated with AG-221 and ATRA-induced differentiation in IDH2-mutant AML cells. Tretinoin 69-73 A-Raf proto-oncogene, serine/threonine kinase Homo sapiens 0-7
17069763-4 2006 We found that retinoic acids (RAs) significantly up-regulate mPer1 expression in an E-box-dependent manner. Tretinoin 14-28 period circadian clock 1 Mus musculus 61-66
17069763-4 2006 We found that retinoic acids (RAs) significantly up-regulate mPer1 expression in an E-box-dependent manner. Tretinoin 30-33 period circadian clock 1 Mus musculus 61-66
32882760-9 2020 IDH-associated changes in histone methylation markers decreased after AG-221 and ATRA combination treatment. Tretinoin 81-85 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 0-3
32562756-6 2020 We define a novel pathway in which the CND is remodeled by ROBO2 and retinoic acid rescued the ureter anomalies in the Robo2-/-embryo. Tretinoin 69-82 roundabout guidance receptor 2 Homo sapiens 119-124
16873554-4 2006 All-trans retinoic acid (ATRA) increased pgrn mRNA levels in myelomonocytic cells (CD34(+) progenitors; monoblastic U-937; monocytic THP-1; progranulocytic HL-60; macrophage RAW 264.7) but not in nonmyeloid cells tested. Tretinoin 10-23 CD34 antigen Mus musculus 83-87
16873554-4 2006 All-trans retinoic acid (ATRA) increased pgrn mRNA levels in myelomonocytic cells (CD34(+) progenitors; monoblastic U-937; monocytic THP-1; progranulocytic HL-60; macrophage RAW 264.7) but not in nonmyeloid cells tested. Tretinoin 25-29 CD34 antigen Mus musculus 83-87
17428999-7 2007 Supplementation with retinoic acid or valproic acid induces differentiation of these cells primarily into Crx (cone rod homeobox)-positive and rhodopsin-positive photoreceptors. Tretinoin 21-34 cone-rod homeobox Homo sapiens 106-109
32171039-8 2020 Interestingly, the data suggest that all-trans retinoic acid (ATRA)-induced ADAM17-mediated MerTK cleavage plays a critical role in regulating the levels of MerTK receptor on macrophages and that this pathway is impaired in NASH fibrosis. Tretinoin 62-66 MER proto-oncogene, tyrosine kinase Homo sapiens 92-97
17428999-7 2007 Supplementation with retinoic acid or valproic acid induces differentiation of these cells primarily into Crx (cone rod homeobox)-positive and rhodopsin-positive photoreceptors. Tretinoin 21-34 cone-rod homeobox Homo sapiens 111-128
17110582-4 2006 However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Tretinoin 9-11 interleukin 5 Mus musculus 77-81
32171039-8 2020 Interestingly, the data suggest that all-trans retinoic acid (ATRA)-induced ADAM17-mediated MerTK cleavage plays a critical role in regulating the levels of MerTK receptor on macrophages and that this pathway is impaired in NASH fibrosis. Tretinoin 62-66 MER proto-oncogene, tyrosine kinase Homo sapiens 157-162
17306764-0 2007 Retinoic acid activates human inducible nitric oxide synthase gene through binding of RARalpha/RXRalpha heterodimer to a novel retinoic acid response element in the promoter. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 86-94
32475642-3 2020 Here, we demonstrate that one of the cleavage products of PML-RARalpha, NLS-RARalpha, can block cell differentiation by repressing the expression of the target genes within the retinoic acid signalling pathway. Tretinoin 177-190 retinoic acid receptor alpha Homo sapiens 62-70
17306764-0 2007 Retinoic acid activates human inducible nitric oxide synthase gene through binding of RARalpha/RXRalpha heterodimer to a novel retinoic acid response element in the promoter. Tretinoin 127-140 retinoic acid receptor alpha Homo sapiens 86-94
17407572-13 2007 Lastly, estrogen affects retinoic acid (RA) synthesis and mobilization by regulating expression of CRABP2 and ALDH1A1. Tretinoin 25-38 aldehyde dehydrogenase 1 family member A1 Homo sapiens 110-117
17407572-13 2007 Lastly, estrogen affects retinoic acid (RA) synthesis and mobilization by regulating expression of CRABP2 and ALDH1A1. Tretinoin 40-42 aldehyde dehydrogenase 1 family member A1 Homo sapiens 110-117
17001604-5 2006 Transient cotransfection assay revealed that PML-RARalpha is a potent activator of OP18 promoter and this transcriptional activation is retinoic acid sensitive. Tretinoin 136-149 PML nuclear body scaffold Homo sapiens 45-48
17001604-5 2006 Transient cotransfection assay revealed that PML-RARalpha is a potent activator of OP18 promoter and this transcriptional activation is retinoic acid sensitive. Tretinoin 136-149 retinoic acid receptor alpha Homo sapiens 49-57
17001604-5 2006 Transient cotransfection assay revealed that PML-RARalpha is a potent activator of OP18 promoter and this transcriptional activation is retinoic acid sensitive. Tretinoin 136-149 stathmin 1 Homo sapiens 83-87
16982809-0 2006 PPARgamma controls CD1d expression by turning on retinoic acid synthesis in developing human dendritic cells. Tretinoin 49-62 CD1d molecule Homo sapiens 19-23
16982809-7 2006 The retinoic acid-induced elevated expression of CD1d is coupled to enhanced iNKT cell activation. Tretinoin 4-17 CD1d molecule Homo sapiens 49-53
17329364-2 2007 Molecular analyses have previously identified the major RA-synthesising (RALDH1-3) and RA-degrading (CYP26A-C1) enzymes as well as other components involved in RA processing (e.g. CRABP). Tretinoin 56-58 aldehyde dehydrogenase 1 family member A1 Homo sapiens 73-79
32475642-6 2020 When treated with all-trans retinoic acid (ATRA), NLS-RARalpha exhibits diminished transcriptional activity compared to RARalpha. Tretinoin 18-41 retinoic acid receptor alpha Homo sapiens 54-62
32475642-6 2020 When treated with all-trans retinoic acid (ATRA), NLS-RARalpha exhibits diminished transcriptional activity compared to RARalpha. Tretinoin 18-41 retinoic acid receptor alpha Homo sapiens 120-128
16957513-8 2006 Most importantly, ATRA could induce SW480 cells to differentiate, increase the expression of Fas and decrease the expression of FasL. Tretinoin 18-22 Fas ligand Homo sapiens 128-132
29349704-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand(all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 81-104 retinoic acid receptor alpha Homo sapiens 70-73
32475642-6 2020 When treated with all-trans retinoic acid (ATRA), NLS-RARalpha exhibits diminished transcriptional activity compared to RARalpha. Tretinoin 43-47 retinoic acid receptor alpha Homo sapiens 54-62
29349704-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand(all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 81-104 phosphatase and tensin homolog Homo sapiens 126-130
32475642-8 2020 Together, these results indicate that NLS-RARalpha blocks cell differentiation by inhibiting the retinoic acid signalling pathway. Tretinoin 97-110 retinoic acid receptor alpha Homo sapiens 42-50
29349704-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand(all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 106-110 retinoic acid receptor alpha Homo sapiens 70-73
29349704-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand(all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 106-110 phosphatase and tensin homolog Homo sapiens 126-130
32434928-0 2020 The transcriptional corepressor CBFA2T3 inhibits all-trans-retinoic acid-induced myeloid gene expression and differentiation in acute myeloid leukemia. Tretinoin 49-72 CBFA2/RUNX1 partner transcriptional co-repressor 3 Homo sapiens 32-39
17272500-5 2007 We used Q(2)ChIP to monitor changes in histone H3 modifications on the 5" regulatory regions of the developmentally regulated genes OCT4, NANOG, LMNA, and PAX6 in the context of retinoic-acid-mediated human embryonal carcinoma cell differentiation. Tretinoin 178-191 POU class 5 homeobox 1 Homo sapiens 132-136
17272500-5 2007 We used Q(2)ChIP to monitor changes in histone H3 modifications on the 5" regulatory regions of the developmentally regulated genes OCT4, NANOG, LMNA, and PAX6 in the context of retinoic-acid-mediated human embryonal carcinoma cell differentiation. Tretinoin 178-191 lamin A/C Homo sapiens 145-149
16854989-6 2006 DNaseI footprinting and electrophoretic mobility shift assays (EMSA) using bovine retinal nuclear extract demonstrate that RA response elements (RAREs) identified within the Nrl promoter bind to RA receptors. Tretinoin 123-125 neural retina leucine zipper Bos taurus 174-177
16757478-2 2006 In this study, we identified components of the Hoxd4 P1 promoter directing expression in neurally differentiating retinoic acid-treated P19 cells. Tretinoin 114-127 homeobox D4 Homo sapiens 47-52
16757478-3 2006 We mapped three nucleosomes that are subsequently remodeled into an open chromatin state upon retinoic acid-induced Hoxd4 transcription. Tretinoin 94-107 homeobox D4 Homo sapiens 116-121
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 139-152 PML nuclear body scaffold Homo sapiens 0-3
32434928-4 2020 Here, we show that CBFA2T3 represses retinoic acid receptor (RAR) target gene expression and inhibits all-trans-retinoic acid (ATRA)-induced myeloid differentiation of AML cells. Tretinoin 102-125 CBFA2/RUNX1 partner transcriptional co-repressor 3 Homo sapiens 19-26
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 139-152 PML nuclear body scaffold Homo sapiens 112-115
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 139-152 retinoic acid receptor alpha Homo sapiens 116-124
32434928-4 2020 Here, we show that CBFA2T3 represses retinoic acid receptor (RAR) target gene expression and inhibits all-trans-retinoic acid (ATRA)-induced myeloid differentiation of AML cells. Tretinoin 127-131 CBFA2/RUNX1 partner transcriptional co-repressor 3 Homo sapiens 19-26
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 154-158 PML nuclear body scaffold Homo sapiens 0-3
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 4-12
16740359-0 2007 Retinoic acid attenuates promyelocytic leukemia protein-induced cell death in breast cancer cells by activation of the ubiquitin-proteasome pathway. Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 25-55
16740359-5 2007 We concluded that PML and all-trans-retinoic acid cause cell death by different pathways: PML activates ERK1/2, p38 MAPK, and p21; arrests the cell cycle; and later causes cell death; and all-trans-retinoic acid activates proteasome function, caspase cleavage, and apoptosis. Tretinoin 26-49 PML nuclear body scaffold Homo sapiens 90-93
16740359-5 2007 We concluded that PML and all-trans-retinoic acid cause cell death by different pathways: PML activates ERK1/2, p38 MAPK, and p21; arrests the cell cycle; and later causes cell death; and all-trans-retinoic acid activates proteasome function, caspase cleavage, and apoptosis. Tretinoin 26-49 H3 histone pseudogene 16 Homo sapiens 126-129
16740359-5 2007 We concluded that PML and all-trans-retinoic acid cause cell death by different pathways: PML activates ERK1/2, p38 MAPK, and p21; arrests the cell cycle; and later causes cell death; and all-trans-retinoic acid activates proteasome function, caspase cleavage, and apoptosis. Tretinoin 188-211 PML nuclear body scaffold Homo sapiens 18-21
16740359-6 2007 The combined use of all-trans-retinoic acid and PML gene therapy may not be the best treatment for patients with cancer, because the ubiquitinylation of PML and its subsequent proteasome-dependent degradation by retinoic acids occur before overexpressed PML exhibits tumor-suppressive activity. Tretinoin 20-43 PML nuclear body scaffold Homo sapiens 153-156
16740359-6 2007 The combined use of all-trans-retinoic acid and PML gene therapy may not be the best treatment for patients with cancer, because the ubiquitinylation of PML and its subsequent proteasome-dependent degradation by retinoic acids occur before overexpressed PML exhibits tumor-suppressive activity. Tretinoin 20-43 PML nuclear body scaffold Homo sapiens 153-156
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 154-158 PML nuclear body scaffold Homo sapiens 112-115
16835227-7 2006 PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 116-124
16894348-12 2006 CONCLUSIONS AND IMPLICATIONS: These results highlight the relevance of RAR-independent mechanisms to the biological effects of ATRA. Tretinoin 127-131 retinoic acid receptor alpha Homo sapiens 71-74
16740359-6 2007 The combined use of all-trans-retinoic acid and PML gene therapy may not be the best treatment for patients with cancer, because the ubiquitinylation of PML and its subsequent proteasome-dependent degradation by retinoic acids occur before overexpressed PML exhibits tumor-suppressive activity. Tretinoin 212-226 PML nuclear body scaffold Homo sapiens 48-51
16740359-6 2007 The combined use of all-trans-retinoic acid and PML gene therapy may not be the best treatment for patients with cancer, because the ubiquitinylation of PML and its subsequent proteasome-dependent degradation by retinoic acids occur before overexpressed PML exhibits tumor-suppressive activity. Tretinoin 212-226 PML nuclear body scaffold Homo sapiens 153-156
16925845-0 2006 Prevention of retinoic acid-induced early craniofacial abnormalities by folinic acid and expression of endothelin-1/dHAND in the branchial arches in mouse. Tretinoin 14-27 endothelin 1 Mus musculus 103-115
32434928-6 2020 CRISPR/Cas9-mediated abrogation of CBFA2T3 resulted in spontaneous and ATRA-induced activation of myeloid-specific genes in a manner correlated with myeloid differentiation. Tretinoin 71-75 CBFA2/RUNX1 partner transcriptional co-repressor 3 Homo sapiens 35-42
16740359-6 2007 The combined use of all-trans-retinoic acid and PML gene therapy may not be the best treatment for patients with cancer, because the ubiquitinylation of PML and its subsequent proteasome-dependent degradation by retinoic acids occur before overexpressed PML exhibits tumor-suppressive activity. Tretinoin 212-226 PML nuclear body scaffold Homo sapiens 153-156
17291686-7 2007 The effects of ATRA were reversed by proteasome inhibitor MG-132, implying ligand-dependent RARalpha degradation. Tretinoin 15-19 retinoic acid receptor, alpha Rattus norvegicus 92-100
32434928-10 2020 To our knowledge, this is the first study to show that CBFA2T3 down-regulation is both necessary and sufficient for enhancing ATRA-induced myeloid gene expression and differentiation of AML cells. Tretinoin 126-130 CBFA2/RUNX1 partner transcriptional co-repressor 3 Homo sapiens 55-62
32434928-11 2020 Our findings suggest that CBFA2T3 can serve as a potential target for enhancing AML responsiveness to ATRA differentiation therapies. Tretinoin 102-106 CBFA2/RUNX1 partner transcriptional co-repressor 3 Homo sapiens 26-33
17491551-1 2007 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RARalpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as ligand-activated, DNA-binding, transacting, transcription-modulating proteins involved in a general molecular mechanism responsible for transcriptional responses in target genes. Tretinoin 57-70 retinoic acid receptor alpha Homo sapiens 168-176
17225872-8 2006 In N-SP and CLP-SP fibroblasts, RA decreased GAG and FN secretion and increased TGF-beta3 mRNA expression but reduced the number of TGF-beta receptors. Tretinoin 32-34 calmodulin like 3 Homo sapiens 12-15
17225872-11 2006 These results show that CLP-SP fibroblasts compared with N-SP fibroblasts exhibit an abnormal phenotype in vitro and respond differently to RA treatment, and suggest that altered crosstalk between RA, GABAergic, and TGF-beta signaling systems could be involved in human cleft palate fibroblast phenotype. Tretinoin 140-142 calmodulin like 3 Homo sapiens 24-27
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 Cbl proto-oncogene Homo sapiens 196-201
17225872-11 2006 These results show that CLP-SP fibroblasts compared with N-SP fibroblasts exhibit an abnormal phenotype in vitro and respond differently to RA treatment, and suggest that altered crosstalk between RA, GABAergic, and TGF-beta signaling systems could be involved in human cleft palate fibroblast phenotype. Tretinoin 197-199 calmodulin like 3 Homo sapiens 24-27
17170094-0 2007 All-trans retinoic acid induces in vitro angiogenesis via retinoic acid receptor: possible involvement of paracrine effects of endogenous vascular endothelial growth factor signaling. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 58-80
32032659-4 2020 Roscovitine enhanced ATRA-induced c-Raf interaction with Lyn, Vav, and c-Cbl. Tretinoin 21-25 Cbl proto-oncogene Homo sapiens 71-76
32902409-0 2020 CD44 and vimentin, markers involved with epithelial-mesenchymal transition: A proteomic analysis of sequential proteins extraction of triple-negative breast cancer cells after treatment with all-trans retinoic acid. Tretinoin 191-214 vimentin Homo sapiens 9-17
17170094-1 2007 A natural retinoid all-trans retinoic acid (ATRA) regulates a variety of important cellular functions via retinoic acid receptor (RAR). Tretinoin 23-42 retinoic acid receptor alpha Homo sapiens 106-128
17170094-1 2007 A natural retinoid all-trans retinoic acid (ATRA) regulates a variety of important cellular functions via retinoic acid receptor (RAR). Tretinoin 23-42 retinoic acid receptor alpha Homo sapiens 130-133
17170094-1 2007 A natural retinoid all-trans retinoic acid (ATRA) regulates a variety of important cellular functions via retinoic acid receptor (RAR). Tretinoin 44-48 retinoic acid receptor alpha Homo sapiens 106-128
17170094-1 2007 A natural retinoid all-trans retinoic acid (ATRA) regulates a variety of important cellular functions via retinoic acid receptor (RAR). Tretinoin 44-48 retinoic acid receptor alpha Homo sapiens 130-133
16989981-3 2006 Retinoic acid produces similar terata and is known to act in part by increasing the expression of Hoxa1. Tretinoin 0-13 homeobox A1 Rattus norvegicus 98-103
16918696-6 2006 We demonstrate that ATRA-induced upregulation of Stat2, ICSBP/IRF8 and C/EBPepsilon, key transcription factors linked to myelomonocytic differentiation, is selectively impaired in cells expressing mutant Stat1. Tretinoin 20-24 interferon regulatory factor 8 Homo sapiens 56-61
16918696-6 2006 We demonstrate that ATRA-induced upregulation of Stat2, ICSBP/IRF8 and C/EBPepsilon, key transcription factors linked to myelomonocytic differentiation, is selectively impaired in cells expressing mutant Stat1. Tretinoin 20-24 interferon regulatory factor 8 Homo sapiens 62-66
32902409-7 2020 We have found that all-trans retinoic acid results in significantly reduced levels of vimentin and CD44 in both the cytoplasmic and membrane fractions. Tretinoin 29-42 vimentin Homo sapiens 86-94
16918696-6 2006 We demonstrate that ATRA-induced upregulation of Stat2, ICSBP/IRF8 and C/EBPepsilon, key transcription factors linked to myelomonocytic differentiation, is selectively impaired in cells expressing mutant Stat1. Tretinoin 20-24 CCAAT enhancer binding protein epsilon Homo sapiens 71-83
31903789-5 2020 Here, we demonstrate that in cultured neuroblastoma tumour cells, RAMBAs enhance RA action as seen by morphological differentiation, AKT signalling and suppression of MYCN protein. Tretinoin 66-68 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 167-171
16918696-7 2006 In contrast, ATRA-induced expression of PU.1, C/EBPalpha, C/EBPbeta and IRF-1 was unaffected. Tretinoin 13-17 Spi-1 proto-oncogene Homo sapiens 40-44
16918696-8 2006 Taken together, our data suggest that ATRA-induced regulation of Stat2, ICSBP and C/EBPepsilon is dependent on active Stat1, and that a failure to correctly regulate these transcription factors is associated with the inhibition of monocytic differentiation. Tretinoin 38-42 interferon regulatory factor 8 Homo sapiens 72-77
16918696-8 2006 Taken together, our data suggest that ATRA-induced regulation of Stat2, ICSBP and C/EBPepsilon is dependent on active Stat1, and that a failure to correctly regulate these transcription factors is associated with the inhibition of monocytic differentiation. Tretinoin 38-42 CCAAT enhancer binding protein epsilon Homo sapiens 82-94
32676119-9 2020 Activation of RA signal in vitro inhibited ALP activities and mineralization of human DPSCs and decreased the mRNA expression of ALP, osteocalcin, osteopontin, and a transcription factor, osterix. Tretinoin 14-16 secreted phosphoprotein 1 Homo sapiens 147-158
17278423-1 2006 OBJECTIVES: To study the fibrinolytic activity and the expression of uPAR and Annexin II in leukemic cell lines and their alterations on all-trans retinoic acid ( ATRA) treatment. Tretinoin 147-160 plasminogen activator, urokinase receptor Homo sapiens 69-73
17278423-1 2006 OBJECTIVES: To study the fibrinolytic activity and the expression of uPAR and Annexin II in leukemic cell lines and their alterations on all-trans retinoic acid ( ATRA) treatment. Tretinoin 147-160 annexin A2 Homo sapiens 78-88
17278423-1 2006 OBJECTIVES: To study the fibrinolytic activity and the expression of uPAR and Annexin II in leukemic cell lines and their alterations on all-trans retinoic acid ( ATRA) treatment. Tretinoin 163-167 plasminogen activator, urokinase receptor Homo sapiens 69-73
17278423-1 2006 OBJECTIVES: To study the fibrinolytic activity and the expression of uPAR and Annexin II in leukemic cell lines and their alterations on all-trans retinoic acid ( ATRA) treatment. Tretinoin 163-167 annexin A2 Homo sapiens 78-88
16568081-5 2006 ATRA-mediated apoptosis in CHP134 and NB-39-nu cells was associated with a significant activation of caspase-9 and caspase-3 as well as cytoplasmic release of cytochrome c from mitochondria in a p53-independent manner. Tretinoin 0-4 caspase 9 Homo sapiens 101-110
32445470-0 2020 Nkx2.1 downregulation is involved in brain abnormality induced by excess retinoic acid. Tretinoin 73-86 NK2 homeobox 1 Mus musculus 0-6
32124141-0 2020 All-trans retinoic acid enhances the effect of Fra-1 to inhibit cell proliferation and metabolism in cervical cancer. Tretinoin 0-23 FOS like 1, AP-1 transcription factor subunit Homo sapiens 47-52
16790478-8 2006 We propose a model in which RA signaling from the somitic mesoderm leads to activation of wnt2b expression in the intermediate mesoderm, which then signals to the LPM to trigger tbx5 expression. Tretinoin 28-30 wingless-type MMTV integration site family, member 2Ba Danio rerio 90-95
16790478-8 2006 We propose a model in which RA signaling from the somitic mesoderm leads to activation of wnt2b expression in the intermediate mesoderm, which then signals to the LPM to trigger tbx5 expression. Tretinoin 28-30 T-box transcription factor 5a Danio rerio 178-182
32124141-1 2020 OBJECTIVES: This study on all-trans retinoic acid was designed to explore its effect on the ability of Fra-1 to cervical cancer cell development. Tretinoin 36-49 FOS like 1, AP-1 transcription factor subunit Homo sapiens 103-108
32124141-2 2020 The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 32-45 FOS like 1, AP-1 transcription factor subunit Homo sapiens 69-74
16737695-7 2006 Immunoprecipitation and Western blot analyses showed that LIF induces tyrosine phosphorylation of JAK1, TYK2 and STAT3 in 30 min and treatment with 15d-PGJ2 or ATRA results in a dose-dependent decrease in LIF-induced phosphorylation of JAK1 and STAT3 in D3-ES cells. Tretinoin 160-164 leukemia inhibitory factor Mus musculus 58-61
32124141-2 2020 The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 32-45 H3 histone pseudogene 16 Homo sapiens 304-307
32492981-8 2020 By multivariate analysis, overexpression of CD56 in blast was an independent unfavorable prognostic factor for relapse-free survival (RFS) (p = 0.006) together with more than 10.0 x 109/L WBC counts (p = 0.001) and the ATRA arm in maintenance (p = 0.028). Tretinoin 219-223 neural cell adhesion molecule 1 Homo sapiens 44-48
16872382-8 2006 The actions of all-trans-retinoic acid on dendritic cells were mediated through retinoic acid receptor alpha. Tretinoin 19-38 retinoic acid receptor alpha Homo sapiens 80-108
32492981-11 2020 CD56 is continuously an independent unfavorable prognostic factor for RFS in APL patients treated with ATRA and chemotherapy followed by ATRA or tamibarotene maintenance therapy. Tretinoin 103-107 neural cell adhesion molecule 1 Homo sapiens 0-4
16857736-6 2006 The effects of DEAB on HSC differentiation could be reversed by the coadministration of the retinoic acid receptor agonist, all-trans-retinoic acid, suggesting that the ability of ALDH to generate retinoic acids is important in determining HSC fate. Tretinoin 124-147 fucosyltransferase 1 (H blood group) Homo sapiens 23-26
32492981-11 2020 CD56 is continuously an independent unfavorable prognostic factor for RFS in APL patients treated with ATRA and chemotherapy followed by ATRA or tamibarotene maintenance therapy. Tretinoin 137-141 neural cell adhesion molecule 1 Homo sapiens 0-4
16857736-6 2006 The effects of DEAB on HSC differentiation could be reversed by the coadministration of the retinoic acid receptor agonist, all-trans-retinoic acid, suggesting that the ability of ALDH to generate retinoic acids is important in determining HSC fate. Tretinoin 124-147 fucosyltransferase 1 (H blood group) Homo sapiens 240-243
16857736-6 2006 The effects of DEAB on HSC differentiation could be reversed by the coadministration of the retinoic acid receptor agonist, all-trans-retinoic acid, suggesting that the ability of ALDH to generate retinoic acids is important in determining HSC fate. Tretinoin 197-211 fucosyltransferase 1 (H blood group) Homo sapiens 23-26
16857736-6 2006 The effects of DEAB on HSC differentiation could be reversed by the coadministration of the retinoic acid receptor agonist, all-trans-retinoic acid, suggesting that the ability of ALDH to generate retinoic acids is important in determining HSC fate. Tretinoin 197-211 fucosyltransferase 1 (H blood group) Homo sapiens 240-243
16226872-3 2006 Treatment with ATRA at 1 muM for 5 days markedly inhibited the proliferation and increased the expression of differentiation markers (CD38, CD11b) in HL-60/Vect cells, but showed no such effect in HL-60/FAK cells. Tretinoin 15-19 CD38 molecule Homo sapiens 134-138
32240539-7 2020 The interaction of retinoic acid and heat shock 70-kDa protein may play a pivotal role in intramuscular fat deposition as a consequence of vitamin A supplementation by impairing de novo fatty acid synthesis as a result of a possible decrease in insulin sensitivity in the skeletal muscle. Tretinoin 19-32 insulin Bos taurus 245-252
16782888-0 2006 Btg2 enhances retinoic acid-induced differentiation by modulating histone H4 methylation and acetylation. Tretinoin 14-27 BTG anti-proliferation factor 2 Homo sapiens 0-4
16782888-4 2006 We show here that retinoic acid treatment of hematopoietic cells induces the expression of BTG2. Tretinoin 18-31 BTG anti-proliferation factor 2 Homo sapiens 91-95
32494737-2 2020 All-trans retinoic acid (ATRA) signaling is considered the key pathway that promotes Stra8 (stimulated by retinoic acid 8) expression and, in turn, meiosis entry. Tretinoin 0-23 stimulated by retinoic acid gene 8 Mus musculus 85-90
16782888-10 2006 Overall, our data show that BTG2 contributes to retinoic acid activity by favoring differentiation through a gene-specific modification of histone H4 arginine methylation and acetylation levels. Tretinoin 48-61 BTG anti-proliferation factor 2 Homo sapiens 28-32
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 101-114 H3 histone pseudogene 16 Homo sapiens 23-26
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 101-114 retinoic acid receptor alpha Homo sapiens 131-139
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 101-114 retinoic acid receptor alpha Homo sapiens 165-173
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 131-133 H3 histone pseudogene 16 Homo sapiens 23-26
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 131-133 retinoic acid receptor alpha Homo sapiens 101-129
32494737-2 2020 All-trans retinoic acid (ATRA) signaling is considered the key pathway that promotes Stra8 (stimulated by retinoic acid 8) expression and, in turn, meiosis entry. Tretinoin 25-29 stimulated by retinoic acid gene 8 Mus musculus 85-90
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 131-133 retinoic acid receptor alpha Homo sapiens 165-173
32381997-12 2020 Further bioinformatics analysis of GSE74146 suggested FGFR2 mainly participated in regulating degradation and organization of the extracellular matrix and signaling of retinoic acid. Tretinoin 168-181 fibroblast growth factor receptor 2 Homo sapiens 54-59
16765349-2 2006 Yet the role of p21 upregulation by RA in lymphoma cells remains unknown. Tretinoin 36-38 H3 histone pseudogene 16 Homo sapiens 16-19
16765349-4 2006 Upregulated p21 by RA accompanies caspase-3 activation and precedes the occurrence of apoptosis. Tretinoin 19-21 H3 histone pseudogene 16 Homo sapiens 12-15
16765349-7 2006 Data presented here suggest a novel RA-signaling, by which RA-induced p21 induction and complex formation with cyclin E/CDK2 diverts CDK2 function from normally driving proliferation to alternatively promoting apoptosis. Tretinoin 36-38 H3 histone pseudogene 16 Homo sapiens 70-73
16800735-3 2006 In this study, we analyzed the promoter region of hK10 using a website software (TRANSFAC 3.0), which predicted three possible retinoic acid response elements (RAREs), RARE1 at -1041 (TGACCTCGTGATCC), RARE2 at -859 (TGACCTCCTATGA) and RARE3 at -765 (TGACCTCCTGTGA), each with a half-site of a canonical sequence (TGACCT; reverse complement AGGTCA). Tretinoin 127-140 keratin 10 Homo sapiens 50-54
32006898-0 2020 Decitabine and all-trans retinoic acid synergistically exhibit cytotoxicity against elderly AML patients via miR-34a/MYCN axis. Tretinoin 15-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 117-121
31659279-0 2020 Caspase-8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3 regulate retinoic acid-induced cell differentiation and necroptosis. Tretinoin 77-90 caspase 8 Mus musculus 0-9
16760641-0 2006 9-cis retinoic acid induces insulin-like growth factor binding protein-3 through DR-8 retinoic acid responsive elements. Tretinoin 6-19 insulin like growth factor binding protein 3 Homo sapiens 28-72
16760641-1 2006 Retinoic acids, which have shown potential chemopreventive and therapeutic activities for several neoplastic diseases in vitro, modulate the growth-promoting and anti-apoptotic activities of insulin-like growth factors (IGFs), in part by influencing the expression of insulin-like growth factor binding protein-3 (IGFBP-3). Tretinoin 0-14 insulin like growth factor binding protein 3 Homo sapiens 268-312
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 112-125 caspase 8 Mus musculus 32-41
16760641-1 2006 Retinoic acids, which have shown potential chemopreventive and therapeutic activities for several neoplastic diseases in vitro, modulate the growth-promoting and anti-apoptotic activities of insulin-like growth factors (IGFs), in part by influencing the expression of insulin-like growth factor binding protein-3 (IGFBP-3). Tretinoin 0-14 insulin like growth factor binding protein 3 Homo sapiens 314-321
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 127-129 caspase 8 Mus musculus 32-41
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 253-255 caspase 8 Mus musculus 32-41
16497785-10 2006 The improved alveolarization in animals given RA + hyperoxia, in conjunction with the attenuation of CYP1A1 and 1A2 expression in these animals, suggests that this phenomenon may play a role in the beneficial effects of RA. Tretinoin 46-48 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 101-115
31659279-7 2020 In Caspase-8-deficient as well as Caspase-8- and Mlkl-deficient mouse embryos, the expression of RA-specific target genes was obviously enhanced. Tretinoin 97-99 caspase 8 Mus musculus 3-12
16497785-10 2006 The improved alveolarization in animals given RA + hyperoxia, in conjunction with the attenuation of CYP1A1 and 1A2 expression in these animals, suggests that this phenomenon may play a role in the beneficial effects of RA. Tretinoin 220-222 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 101-115
31659279-7 2020 In Caspase-8-deficient as well as Caspase-8- and Mlkl-deficient mouse embryos, the expression of RA-specific target genes was obviously enhanced. Tretinoin 97-99 caspase 8 Mus musculus 34-43
31659279-8 2020 Thus, Caspase-8, RIPK1, and RIPK3 regulate RA-induced cell differentiation and necroptosis both in vitro and in vivo. Tretinoin 43-45 caspase 8 Mus musculus 6-15
31597015-1 2020 AIMS/INTRODUCTION: Electronegative low-density lipoprotein (L5) is the most atherogenic fraction of low-density lipoprotein and is elevated in people with metabolic syndrome (MetS), whereas the retinol-binding protein 4 receptor (stimulated by retinoic acid 6 [STRA6]) cascade is disrupted in various organs of patients with obesity-related diseases. Tretinoin 244-257 signaling receptor and transporter of retinol STRA6 Homo sapiens 194-228
16501610-3 2006 In the NB4 cell line, which was derived from an APL patient and expresses PML:RARalpha, we observed a retinoic acid-dependent change in the modification of specific proteins by SUMO-1. Tretinoin 102-115 PML nuclear body scaffold Homo sapiens 74-77
16501610-3 2006 In the NB4 cell line, which was derived from an APL patient and expresses PML:RARalpha, we observed a retinoic acid-dependent change in the modification of specific proteins by SUMO-1. Tretinoin 102-115 retinoic acid receptor alpha Homo sapiens 78-86
32293355-8 2020 Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Tretinoin 15-19 aldehyde dehydrogenase 1 family member A1 Homo sapiens 82-89
16638120-9 2006 In NB4 cells undergoing retinoic acid mediated differentiation, the level of endogenous hARD1 and NATH protein decreases while the level of hARD2 protein is stable. Tretinoin 24-37 N-alpha-acetyltransferase 11, NatA catalytic subunit Homo sapiens 140-145
32293355-8 2020 Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Tretinoin 15-19 aldehyde dehydrogenase 1 family member A1 Homo sapiens 203-210
32293355-8 2020 Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Tretinoin 168-172 aldehyde dehydrogenase 1 family member A1 Homo sapiens 82-89
16618747-0 2006 Retinoic acid induces p27Kip1 nuclear accumulation by modulating its phosphorylation. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 22-29
32293355-8 2020 Treatment with ATRA was found to significantly reduce the increased expression of ALDH1A1 and CD44 and the IC50 values for gefitinib in A549GSC and H1650GSC cells, and ATRA could directly inhibit active ALDH1A1 as compared to DEAB. Tretinoin 168-172 aldehyde dehydrogenase 1 family member A1 Homo sapiens 203-210
16618747-4 2006 Here, we investigate the mechanisms by which ATRA regulates p27Kip1 level in LAN-5, a neuroblastoma cell line. Tretinoin 45-49 cyclin dependent kinase inhibitor 1B Homo sapiens 60-67
32293355-9 2020 CONCLUSION: Our findings suggest that combination treatment with ATRA prevents gefitinib-induced enrichment of ALDH1A1bright/CD44high CSCs and enhances gefitinib-induced growth inhibition of NSCLC/ADC cells. Tretinoin 65-69 aldehyde dehydrogenase 1 family member A1 Homo sapiens 111-118
16618747-5 2006 When added to the cells, ATRA causes a rapid nuclear increase of p27Kip1, which clearly precedes growth arrest. Tretinoin 25-29 cyclin dependent kinase inhibitor 1B Homo sapiens 65-72
32006103-9 2020 Furthermore, atRA upregulated CLDN7 in the cytoplasm but not in cell-cell contacts. Tretinoin 13-17 claudin 7 Mus musculus 30-35
16618747-9 2006 The characterization of CDKI isoforms by two-dimensional PAGE/immunoblotting showed that ATRA induces an early nuclear up-regulation of monophosphorylated p27Kip1. Tretinoin 89-93 cyclin dependent kinase inhibitor 1B Homo sapiens 155-162
16618747-12 2006 Finally, ATRA-treated nuclear LAN-5 extracts showed an enhanced capability of phosphorylating p27Kip1 on S10, thus explaining the nuclear up-regulation of the isoform. Tretinoin 9-13 cyclin dependent kinase inhibitor 1B Homo sapiens 94-101
32255397-2 2020 Materials & methods: All-trans retinoic acid (ATRA)-poly(lactide-co-glycolide acid) (PLGA)-poly(ethylene glycol) (PEG)-programmed death-ligand 1 (PD-L1) nanomedicines were fabricated by loading ATRA into PLGA-PEG nanocarriers and modification using an anti-PD-L1 antibody. Tretinoin 21-44 CD274 molecule Homo sapiens 146-151
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 47-60 heparin binding EGF like growth factor Homo sapiens 88-112
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 62-65 heparin binding EGF like growth factor Homo sapiens 88-112
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 18-20 integrin subunit alpha E Homo sapiens 82-87
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 18-20 integrin subunit alpha E Homo sapiens 193-198
32274275-4 2020 With the initiation of all-trans retinoic acid, arsenic trioxide and gemtuzumab, the patient achieved remission, with absent PML/RARalpha by fluorescence in situ hybridization analysis. Tretinoin 23-46 PML nuclear body scaffold Homo sapiens 125-128
16437139-1 2006 Relapse of acute promyelocytic leukemia (APL) following all-trans retinoic acid (ATRA) therapy has been associated with the acquisition of mutations in the high-affinity ATRA binding site in PML-RARalpha, but little information is available about the selection dynamics of the mutation-harboring subclones. Tretinoin 66-79 PML nuclear body scaffold Homo sapiens 191-194
16437139-1 2006 Relapse of acute promyelocytic leukemia (APL) following all-trans retinoic acid (ATRA) therapy has been associated with the acquisition of mutations in the high-affinity ATRA binding site in PML-RARalpha, but little information is available about the selection dynamics of the mutation-harboring subclones. Tretinoin 66-79 retinoic acid receptor alpha Homo sapiens 195-203
16437139-1 2006 Relapse of acute promyelocytic leukemia (APL) following all-trans retinoic acid (ATRA) therapy has been associated with the acquisition of mutations in the high-affinity ATRA binding site in PML-RARalpha, but little information is available about the selection dynamics of the mutation-harboring subclones. Tretinoin 81-85 PML nuclear body scaffold Homo sapiens 191-194
16437139-1 2006 Relapse of acute promyelocytic leukemia (APL) following all-trans retinoic acid (ATRA) therapy has been associated with the acquisition of mutations in the high-affinity ATRA binding site in PML-RARalpha, but little information is available about the selection dynamics of the mutation-harboring subclones. Tretinoin 81-85 retinoic acid receptor alpha Homo sapiens 195-203
16437139-1 2006 Relapse of acute promyelocytic leukemia (APL) following all-trans retinoic acid (ATRA) therapy has been associated with the acquisition of mutations in the high-affinity ATRA binding site in PML-RARalpha, but little information is available about the selection dynamics of the mutation-harboring subclones. Tretinoin 170-174 PML nuclear body scaffold Homo sapiens 191-194
16437139-1 2006 Relapse of acute promyelocytic leukemia (APL) following all-trans retinoic acid (ATRA) therapy has been associated with the acquisition of mutations in the high-affinity ATRA binding site in PML-RARalpha, but little information is available about the selection dynamics of the mutation-harboring subclones. Tretinoin 170-174 retinoic acid receptor alpha Homo sapiens 195-203
16437139-2 2006 In this study, 6/18 patients treated with sequential ATRA and chemotherapy on protocol INT0129 relapsed with complete replacement of the nonmutant pretreatment APL cell population by a PML-RARalpha mutant subclone. Tretinoin 53-57 PML nuclear body scaffold Homo sapiens 185-188
16437139-2 2006 In this study, 6/18 patients treated with sequential ATRA and chemotherapy on protocol INT0129 relapsed with complete replacement of the nonmutant pretreatment APL cell population by a PML-RARalpha mutant subclone. Tretinoin 53-57 retinoic acid receptor alpha Homo sapiens 189-197
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 162-175 retinoic acid receptor alpha Homo sapiens 72-81
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 162-175 PML nuclear body scaffold Homo sapiens 86-99
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 162-175 retinoic acid receptor alpha Homo sapiens 90-99
32274275-4 2020 With the initiation of all-trans retinoic acid, arsenic trioxide and gemtuzumab, the patient achieved remission, with absent PML/RARalpha by fluorescence in situ hybridization analysis. Tretinoin 23-46 retinoic acid receptor alpha Homo sapiens 129-137
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 177-181 retinoic acid receptor alpha Homo sapiens 72-81
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 177-181 PML nuclear body scaffold Homo sapiens 86-99
32054698-5 2020 ZGLP1 overexpression induces differentiation of in vitro primordial germ cell-like cells (PGCLCs) into fetal oocytes by activating the oogenic programs repressed by Polycomb activities, whereas RA signaling contributes to the oogenic program maturation and PGC program repression. Tretinoin 194-196 zinc finger, GATA-like protein 1 Mus musculus 0-5
16331271-11 2006 Similarly to what was observed in human APL patients, we found that NPM/RAR alpha and PML/RAR alpha, but not PLZF/RAR alpha leukemia, was responsive to all-trans retinoic acid (ATRA) or As2O3 treatments. Tretinoin 177-181 retinoic acid receptor alpha Homo sapiens 90-99
16410462-9 2006 Cultured TG2-/- macrophages demonstrated diminished phagocytosis of apoptotic leukocytes, unaltered endocytosis, and degradation of oxidized LDL but decreased retinoic acid induction of the reverse cholesterol transport and apoptotic cell uptake mediator ABCA1. Tretinoin 159-172 transglutaminase 2, C polypeptide Mus musculus 9-12
31646671-5 2020 The Stra8 gene expression increased in the RA groups on all days. Tretinoin 43-45 stimulated by retinoic acid gene 8 Mus musculus 4-9
16452093-4 2006 We show that RA synthesized in the anterior paraxial mesoderm adjacent to the foregut is necessary for the development of insulin-expressing beta-cells. Tretinoin 13-15 preproinsulin Danio rerio 122-129
16452093-6 2006 We further show that activation of RA signal transduction in endoderm alone is sufficient to induce insulin expression. Tretinoin 35-37 preproinsulin Danio rerio 100-107
31187490-0 2020 ALDH1A1 in patient-derived bladder cancer spheroids activates retinoic acid signaling leading to TUBB3 overexpression and tumor progression. Tretinoin 62-75 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7
16461896-7 2006 Our work shows that signaling by retinoic acid (RA), an active derivative of vitamin A, is required for Stra8 expression and thereby meiotic initiation in embryonic ovaries. Tretinoin 33-46 stimulated by retinoic acid gene 8 Mus musculus 104-109
16461896-7 2006 Our work shows that signaling by retinoic acid (RA), an active derivative of vitamin A, is required for Stra8 expression and thereby meiotic initiation in embryonic ovaries. Tretinoin 48-50 stimulated by retinoic acid gene 8 Mus musculus 104-109
16461896-8 2006 We also discovered that RA is sufficient to induce Stra8 expression in embryonic testes and in vitamin A-deficient adult testes in vivo. Tretinoin 24-26 stimulated by retinoic acid gene 8 Mus musculus 51-56
31187490-6 2020 Notably, CSC marker aldehyde dehydrogenase 1A1 (ALDH1A1), a critical enzyme that synthesizes retinoic acid (RA), was abundantly expressed in PDCs. Tretinoin 93-106 aldehyde dehydrogenase 1 family member A1 Homo sapiens 20-46
16461896-9 2006 Finally, our results show that cytochrome p450 (CYP)-mediated RA metabolism prevents premature Stra8 expression in embryonic testes. Tretinoin 62-64 stimulated by retinoic acid gene 8 Mus musculus 95-100
31187490-6 2020 Notably, CSC marker aldehyde dehydrogenase 1A1 (ALDH1A1), a critical enzyme that synthesizes retinoic acid (RA), was abundantly expressed in PDCs. Tretinoin 93-106 aldehyde dehydrogenase 1 family member A1 Homo sapiens 48-55
16461896-10 2006 Treatment with an inhibitor specific to RA-metabolizing enzymes indicates that a cytochrome p450 from the 26 family (CYP26) is responsible for delaying Stra8 expression in embryonic testes. Tretinoin 40-42 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 117-122
16461896-10 2006 Treatment with an inhibitor specific to RA-metabolizing enzymes indicates that a cytochrome p450 from the 26 family (CYP26) is responsible for delaying Stra8 expression in embryonic testes. Tretinoin 40-42 stimulated by retinoic acid gene 8 Mus musculus 152-157
31187490-6 2020 Notably, CSC marker aldehyde dehydrogenase 1A1 (ALDH1A1), a critical enzyme that synthesizes retinoic acid (RA), was abundantly expressed in PDCs. Tretinoin 108-110 aldehyde dehydrogenase 1 family member A1 Homo sapiens 20-46
16410076-0 2006 All-trans retinoic acid inhibited chondrogenesis of mouse embryonic palate mesenchymal cells by down-regulation of TGF-beta/Smad signaling. Tretinoin 10-23 transforming growth factor, beta 3 Mus musculus 115-123
16410076-7 2006 atRA led to an increase in mRNA expression of TGF-beta3 and an instantaneous decrease in TGF-beta type II receptor (TbetaRII) as determined by real-time RT-PCR. Tretinoin 0-4 transforming growth factor, beta 3 Mus musculus 46-55
31187490-6 2020 Notably, CSC marker aldehyde dehydrogenase 1A1 (ALDH1A1), a critical enzyme that synthesizes retinoic acid (RA), was abundantly expressed in PDCs. Tretinoin 108-110 aldehyde dehydrogenase 1 family member A1 Homo sapiens 48-55
31187490-7 2020 ALDH1A1 inhibitors and shRNAs repressed both PDC proliferation and spheroid formation, whereas all-trans RA could rescue ALDH1A1 shRNA-suppressed spheroid formation. Tretinoin 105-107 aldehyde dehydrogenase 1 family member A1 Homo sapiens 121-128
16428452-7 2006 Interaction between TGIF and RXRalpha is reduced by the addition of retinoic acid, consistent with a role for TGIF as an RXRalpha transcriptional corepressor. Tretinoin 68-81 TGFB-induced factor homeobox 1 Mus musculus 20-24
31666191-6 2020 Using RNA sequencing, bioinformatic analyses, and literature searching, we predicted transglutaminase 2 (TG2) to be an all-trans retinoic acid (ATRA)-induced secretory protein in cultured C2C12 myotubes. Tretinoin 119-142 transglutaminase 2, C polypeptide Mus musculus 85-103
16428452-8 2006 We created a Tgif null mutation in mice and tested the sensitivity of mutant mice to increased levels of retinoic acid. Tretinoin 105-118 TGFB-induced factor homeobox 1 Mus musculus 13-17
16428452-9 2006 Tgif mutant embryos are more sensitive to retinoic acid-induced teratogenesis, and retinoid target genes are expressed at a higher level in tissues from Tgif null mice. Tretinoin 42-55 TGFB-induced factor homeobox 1 Mus musculus 0-4
31666191-6 2020 Using RNA sequencing, bioinformatic analyses, and literature searching, we predicted transglutaminase 2 (TG2) to be an all-trans retinoic acid (ATRA)-induced secretory protein in cultured C2C12 myotubes. Tretinoin 119-142 transglutaminase 2, C polypeptide Mus musculus 105-108
16428452-10 2006 These results demonstrate an important role for TGIF as a transcriptional corepressor, which regulates developmental signaling by retinoic acid, and raises the possibility that TGIF may repress other RXR-dependent transcriptional responses. Tretinoin 130-143 TGFB-induced factor homeobox 1 Mus musculus 48-52
31666191-6 2020 Using RNA sequencing, bioinformatic analyses, and literature searching, we predicted transglutaminase 2 (TG2) to be an all-trans retinoic acid (ATRA)-induced secretory protein in cultured C2C12 myotubes. Tretinoin 144-148 transglutaminase 2, C polypeptide Mus musculus 85-103
31666191-6 2020 Using RNA sequencing, bioinformatic analyses, and literature searching, we predicted transglutaminase 2 (TG2) to be an all-trans retinoic acid (ATRA)-induced secretory protein in cultured C2C12 myotubes. Tretinoin 144-148 transglutaminase 2, C polypeptide Mus musculus 105-108
31666191-7 2020 Tg2 mRNA expression increased in ATRA- or beta-carotene-stimulated myotubes and in the soleus muscle of beta-carotene-treated mice. Tretinoin 33-37 transglutaminase 2, C polypeptide Mus musculus 0-3
31666191-9 2020 ATRA increased endogenous TG2 levels in conditioned medium from myotubes. Tretinoin 0-4 transglutaminase 2, C polypeptide Mus musculus 26-29
31866203-8 2020 NF-kappaB signaling acts upstream of retinoic acid (RA) signaling, which also needs to be downregulated for dedifferentiation to occur, via suppression of the RA-degrading enzyme cyp26b1. Tretinoin 37-50 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 179-186
16111716-3 2006 However, MGF showed the result as RA, which was verified to suppress the production of proteoglycan. Tretinoin 34-36 kit ligand Mus musculus 9-12
16003389-4 2006 Granulocyte colony-stimulating factor (G-CSF) increases mitochondrial respiration and calcium accumulation capacity and subsequently blocks ATRA-induced apoptosis. Tretinoin 140-144 colony stimulating factor 3 Homo sapiens 0-37
31866203-8 2020 NF-kappaB signaling acts upstream of retinoic acid (RA) signaling, which also needs to be downregulated for dedifferentiation to occur, via suppression of the RA-degrading enzyme cyp26b1. Tretinoin 52-54 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 179-186
16003389-4 2006 Granulocyte colony-stimulating factor (G-CSF) increases mitochondrial respiration and calcium accumulation capacity and subsequently blocks ATRA-induced apoptosis. Tretinoin 140-144 colony stimulating factor 3 Homo sapiens 39-44
31866203-8 2020 NF-kappaB signaling acts upstream of retinoic acid (RA) signaling, which also needs to be downregulated for dedifferentiation to occur, via suppression of the RA-degrading enzyme cyp26b1. Tretinoin 159-161 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 179-186
31953251-0 2020 Correction: An alternative retinoic acid-responsive Stra6 promoter regulated in response to retinol deficiency. Tretinoin 27-40 signaling receptor and transporter of retinol STRA6 Homo sapiens 52-57
16436339-1 2006 Retinoic acid regulates keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors, including retinoic acid receptor (RAR-alpha,beta,gamma) and the common heterodimer partners (RXR-alpha,beta,gamma). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 188-197
31936807-5 2020 Retinoic acid induced differentiation of ES cells, decreased the short form of NFYA (NFYAs), increased phosphorylation of STAT3, and decreased B3GALT5-LTR expression. Tretinoin 0-13 beta-1,3-galactosyltransferase 5 Homo sapiens 143-150
16043492-8 2006 RESULTS: Retinol, ATRA, and 9-RA significantly inhibited: (i) cell proliferation, (ii) expression of alpha-SMA, collagen I, fibronectin, and laminin, and (iii) activation of all three classes of MAPKs. Tretinoin 18-22 actin gamma 2, smooth muscle Rattus norvegicus 101-110
16043492-8 2006 RESULTS: Retinol, ATRA, and 9-RA significantly inhibited: (i) cell proliferation, (ii) expression of alpha-SMA, collagen I, fibronectin, and laminin, and (iii) activation of all three classes of MAPKs. Tretinoin 18-22 fibronectin 1 Rattus norvegicus 124-135
17170094-7 2007 The ATRA-induced tube formation was inhibited by coincubation with RAR antagonist LE540/LE135. Tretinoin 4-8 retinoic acid receptor alpha Homo sapiens 67-70
17067568-2 2007 Although both CYP26A1 and CYP26C1, retinoic acid-degrading enzymes that are expressed at the anterior end of the gastrulating mouse embryo, have been thought to play an important role in central nervous system patterning, the detailed mechanism of their contribution has remained largely unknown. Tretinoin 35-48 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 14-21
31936807-8 2020 Retinoic acid decreased the binding of NFYA to B3GALT5-LTR promoter and increased phospho-STAT3 binding. Tretinoin 0-13 beta-1,3-galactosyltransferase 5 Homo sapiens 47-54
16752155-3 2007 RA treatment resulted in an increase of p21, p27 and p53 protein levels and G1 arrest in UM cells, which correlated with significant down-modulation of surface Her2/neu proto-oncogene expression. Tretinoin 0-2 H3 histone pseudogene 16 Homo sapiens 40-43
32064173-0 2020 Erratum: Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells. Tretinoin 40-63 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 134-138
16752155-3 2007 RA treatment resulted in an increase of p21, p27 and p53 protein levels and G1 arrest in UM cells, which correlated with significant down-modulation of surface Her2/neu proto-oncogene expression. Tretinoin 0-2 interferon alpha inducible protein 27 Homo sapiens 45-48
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 synaptonemal complex protein 3 Mus musculus 228-258
17283134-8 2007 These results strongly suggest that XAB2 is a component of the RAR corepressor complex with an inhibitory effect on ATRA-induced cellular differentiation and that XAB2 plays a role in ATRA-mediated cellular differentiation as an important aspect of cancer therapy. Tretinoin 116-120 retinoic acid receptor alpha Homo sapiens 63-66
17283134-8 2007 These results strongly suggest that XAB2 is a component of the RAR corepressor complex with an inhibitory effect on ATRA-induced cellular differentiation and that XAB2 plays a role in ATRA-mediated cellular differentiation as an important aspect of cancer therapy. Tretinoin 184-188 retinoic acid receptor alpha Homo sapiens 63-66
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 63-76 synaptonemal complex protein 3 Mus musculus 260-265
17393088-1 2007 Restin, belonging to the melanoma-associated antigen superfamily, was firstly cloned from the differentiated HL-60 cells when induced by all-trans retinoic acid (ATRA) in our lab. Tretinoin 147-160 ankyrin repeat domain 36B Homo sapiens 25-52
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 synaptonemal complex protein 3 Mus musculus 228-258
17393088-1 2007 Restin, belonging to the melanoma-associated antigen superfamily, was firstly cloned from the differentiated HL-60 cells when induced by all-trans retinoic acid (ATRA) in our lab. Tretinoin 162-166 ankyrin repeat domain 36B Homo sapiens 25-52
31210146-7 2020 In GC-1 cells cultured in vitro, Shp2 knockdown suppressed the retinoic acid (RA)-induced phosphorylation of extracellular-regulated protein kinase (Erk) and protein kinase B (Akt/PKB) and the expression of target genes such as synaptonemal complex protein 3 (Sycp3) and Dmc1. Tretinoin 78-80 synaptonemal complex protein 3 Mus musculus 260-265
17184907-3 2007 Several peptides including D22, PGC1alpha, SRC3-2, PRIP/RAP250 and SRC1-4 also formed a complex with RXRbeta LBD in the presence of all-trans retinoic acid (at-RA) and the fatty acids, phytanic acid (PA) and docosahexaenoic acid (DHA). Tretinoin 142-155 nuclear receptor coactivator 6 Homo sapiens 51-55
31536749-8 2020 The increase in RA content was in line with the identified upregulation of retinoic acid anabolizing enzymes ALDH1A3 and DHRS3. Tretinoin 16-18 aldehyde dehydrogenase 1 family member A3 Homo sapiens 109-116
17184907-3 2007 Several peptides including D22, PGC1alpha, SRC3-2, PRIP/RAP250 and SRC1-4 also formed a complex with RXRbeta LBD in the presence of all-trans retinoic acid (at-RA) and the fatty acids, phytanic acid (PA) and docosahexaenoic acid (DHA). Tretinoin 142-155 nuclear receptor coactivator 6 Homo sapiens 56-62
31536749-8 2020 The increase in RA content was in line with the identified upregulation of retinoic acid anabolizing enzymes ALDH1A3 and DHRS3. Tretinoin 75-88 aldehyde dehydrogenase 1 family member A3 Homo sapiens 109-116
17239227-11 2007 We further show that application of a low dose of retinoic acid that does not perturb patterning of the anterior neural plate leads to expansion of foxi1 and to a massive Fgf-dependent otic induction. Tretinoin 50-63 forkhead box i1 Danio rerio 148-153
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 vascular endothelial growth factor A Rattus norvegicus 233-237
17239240-9 2007 These findings are supported by ChIP-on-chip data from retinoic acid-treated HL60 cells revealing RAR binding to several Alu-DR2 motifs. Tretinoin 55-68 retinoic acid receptor alpha Homo sapiens 98-101
31847204-7 2019 Interestingly, it has been reported that several drugs like lenalidomide, panobinostat, the all-trans retinoic acid and the DNA methyltransferase inhibitors may increase the expression of CD38. Tretinoin 102-115 CD38 molecule Homo sapiens 188-192
17234770-0 2007 Suppression of mammary carcinoma cell growth by retinoic acid: the cell cycle control gene Btg2 is a direct target for retinoic acid receptor signaling. Tretinoin 48-61 BTG anti-proliferation factor 2 Homo sapiens 91-95
17234770-1 2007 The anticarcinogenic activities of retinoic acid (RA) are believed to be mediated by the nuclear RA receptor (RAR) and by the RA-binding protein cellular RA-binding protein-II (CRABP-II). Tretinoin 35-48 retinoic acid receptor alpha Homo sapiens 97-108
17234770-1 2007 The anticarcinogenic activities of retinoic acid (RA) are believed to be mediated by the nuclear RA receptor (RAR) and by the RA-binding protein cellular RA-binding protein-II (CRABP-II). Tretinoin 35-48 retinoic acid receptor alpha Homo sapiens 110-113
17234770-1 2007 The anticarcinogenic activities of retinoic acid (RA) are believed to be mediated by the nuclear RA receptor (RAR) and by the RA-binding protein cellular RA-binding protein-II (CRABP-II). Tretinoin 50-52 retinoic acid receptor alpha Homo sapiens 97-108
17234770-1 2007 The anticarcinogenic activities of retinoic acid (RA) are believed to be mediated by the nuclear RA receptor (RAR) and by the RA-binding protein cellular RA-binding protein-II (CRABP-II). Tretinoin 50-52 retinoic acid receptor alpha Homo sapiens 110-113
32042778-9 2019 The qPCR results showed that NONMMUT004850.2 (P=5E-05), NONMMUT024276.2 (P=0.0012), and Prkar1alpha (P=3E-05) were up-regulated, whereas miR-741-3p (P=0.006) and miR-465b-5p (P=1E-04) were down-regulated in ATRA-treated mice compared to the control samples. Tretinoin 207-211 protein kinase, cAMP dependent regulatory, type I, alpha Mus musculus 88-99
17234770-4 2007 We show that a 3- to 5-h RA pulse is sufficient for inducing a robust growth arrest 2 to 4 days later, demonstrating inhibition of the G1-S transition by RA is triggered by immediate-early RAR targets and does not require the continuous presence of the hormone throughout the arrest program. Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 189-192
17234770-4 2007 We show that a 3- to 5-h RA pulse is sufficient for inducing a robust growth arrest 2 to 4 days later, demonstrating inhibition of the G1-S transition by RA is triggered by immediate-early RAR targets and does not require the continuous presence of the hormone throughout the arrest program. Tretinoin 154-156 retinoic acid receptor alpha Homo sapiens 189-192
17234770-5 2007 Expression array analyses revealed that RA induces the expression of several genes involved in cell cycle regulation, including the p53-controlled antiproliferative gene B-cell translocation gene, member 2 (Btg2) and the BTG family member Tob1. Tretinoin 40-42 BTG anti-proliferation factor 2 Homo sapiens 207-211
17234770-5 2007 Expression array analyses revealed that RA induces the expression of several genes involved in cell cycle regulation, including the p53-controlled antiproliferative gene B-cell translocation gene, member 2 (Btg2) and the BTG family member Tob1. Tretinoin 40-42 transducer of ERBB2, 1 Homo sapiens 239-243
17234770-6 2007 We show that induction of Btg2 by RA does not require de novo protein synthesis and is augmented by overexpression of CRABP-II. Tretinoin 34-36 BTG anti-proliferation factor 2 Homo sapiens 26-30
17234770-7 2007 Additionally, we identify a RA response element in the Btg2 promoter and show that the element binds retinoid X receptor/RAR heterodimers in vitro, is occupied by the heterodimers in cells, and can drive RA-induced activation of a reporter gene. Tretinoin 28-30 BTG anti-proliferation factor 2 Homo sapiens 55-59
17234770-7 2007 Additionally, we identify a RA response element in the Btg2 promoter and show that the element binds retinoid X receptor/RAR heterodimers in vitro, is occupied by the heterodimers in cells, and can drive RA-induced activation of a reporter gene. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 121-124
17234770-7 2007 Additionally, we identify a RA response element in the Btg2 promoter and show that the element binds retinoid X receptor/RAR heterodimers in vitro, is occupied by the heterodimers in cells, and can drive RA-induced activation of a reporter gene. Tretinoin 121-123 BTG anti-proliferation factor 2 Homo sapiens 55-59
17234770-8 2007 Hence, Btg2 is a novel direct target for RA signaling. Tretinoin 41-43 BTG anti-proliferation factor 2 Homo sapiens 7-11
17234770-9 2007 In concert with the reports that Btg2 inhibits cell cycle progression by down-regulating cyclin D1, induction of Btg2 by RA was accompanied by a marked decrease in cyclin D1 expression. Tretinoin 121-123 BTG anti-proliferation factor 2 Homo sapiens 113-117
31264378-8 2019 Furthermore, we demonstrated that expressions of c-Myc and miR-17-92 are markedly suppressed during ATRA-induced NB4 cell differentiation. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 49-54
17010966-4 2007 Different combinations of signals are responsible for different aspects of this early transient induction: FGF initiates expression of Sox3 and ERNI, retinoic acid can induce Cyp26A1 and only a combination of low levels of FGF8 together with Wnt- and BMP-antagonists can induce Otx2. Tretinoin 150-163 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 175-182
17078027-1 2007 It was investigated whether retinoic acid (RA) and the proinflammatory cytokines IL-1beta, IL-6, and TNFalpha influence the intracellular distribution of retinoic acid receptors (RAR) and retinoid X receptors (RXR) in Schwann cells. Tretinoin 28-41 retinoic acid receptor, alpha Rattus norvegicus 179-182
31264378-8 2019 Furthermore, we demonstrated that expressions of c-Myc and miR-17-92 are markedly suppressed during ATRA-induced NB4 cell differentiation. Tretinoin 100-104 miR-17-92a-1 cluster host gene Homo sapiens 59-68
17078027-1 2007 It was investigated whether retinoic acid (RA) and the proinflammatory cytokines IL-1beta, IL-6, and TNFalpha influence the intracellular distribution of retinoic acid receptors (RAR) and retinoid X receptors (RXR) in Schwann cells. Tretinoin 43-45 retinoic acid receptor, alpha Rattus norvegicus 179-182
31596288-7 2019 Luciferase report showed RA binding to RARalpha regulated stimulated by RA 8 (Stra8) promoter activity during SSC formation, while mutations in RAR binding sites inhibited the Stra8 expression and SSC formation. Tretinoin 25-27 retinoic acid receptor alpha Gallus gallus 39-47
31635381-5 2019 We describe the role of hyaluronan mixed esters of butyric and retinoic acids as synthetic intracrines, controlling prodynorphin gene expression, cardiogenesis, and cardiac repair. Tretinoin 63-77 prodynorphin Homo sapiens 116-128
17202112-2 2007 Patients with APL respond to differentiation therapy with all-trans-retinoic acid, which induces PML/RAR alpha degradation. Tretinoin 58-81 PML nuclear body scaffold Homo sapiens 97-110
17113559-6 2007 Tau/P19 cells underwent drastic apoptosis during neural differentiation induced by retinoic acid (RA). Tretinoin 83-96 microtubule associated protein tau Homo sapiens 0-3
31570593-1 2019 Retinoic acid-related orphan receptor alpha (RORalpha) functions as a transcription factor for various biological processes, including circadian rhythm, cancer, and metabolism. Tretinoin 0-13 RAR-related orphan receptor alpha Mus musculus 45-53
16614850-6 2007 The addition of ATRA also exhibited additional inhibitory effects on ALDH activity and increased 4-HC toxicity when added to single siRNA aimed at one of the enzymes. Tretinoin 16-20 aldehyde dehydrogenase 1 family member A1 Homo sapiens 69-73
16614850-7 2007 On the other hand, ATRA had minimal and insignificant additional inhibitory effects on ALDH enzyme activity when added to a combination of siRNAs against both enzymes, but still increased 4-HC toxicity beyond that seen with RNAi-mediated inhibition of both enzymes together. Tretinoin 19-23 aldehyde dehydrogenase 1 family member A1 Homo sapiens 87-91
31591086-0 2019 Perturbed development of cranial neural crest cells in association with reduced sonic hedgehog signaling underlies the pathogenesis of retinoic-acid-induced cleft palate. Tretinoin 135-148 sonic hedgehog signaling molecule Homo sapiens 80-94
17573612-12 2007 Differentiation of USSC with growth factors, retinoic acid, matrigel matrix and different co-cultures led to an increased expression of albumin and also to the detection of GSC, SOX 17, Cyp2B6, Cyp3A4, Gys2, HNF4a, ISL-1 and Nkx6.1. Tretinoin 45-58 SRY-box transcription factor 17 Homo sapiens 178-184
17337438-4 2007 During retinoic-acid-induced P19 stem cell differentiation, the expression of CoAA undergoes a rapid switch to its dominant negative splice variant CoAM in the cavity of the embryoid body. Tretinoin 7-20 interleukin 23 subunit alpha Homo sapiens 29-32
17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 10-23 nuclear receptor subfamily 2 group C member 1 Homo sapiens 101-104
31591086-5 2019 In the RA-treated group, we observed altered expression of Sox10, which marks cranial neural crest cells (CNCCs). Tretinoin 7-9 SRY-box transcription factor 10 Homo sapiens 59-64
17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 10-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175
31591086-8 2019 RNA-sequencing comparisons of RA-treated embryos compared to controls revealed alterations in Sonic hedgehog (Shh) signaling. Tretinoin 30-32 sonic hedgehog signaling molecule Homo sapiens 94-108
17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 25-27 nuclear receptor subfamily 2 group C member 1 Homo sapiens 101-104
17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 25-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175
17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 125-127 nuclear receptor subfamily 2 group C member 1 Homo sapiens 101-104
31591086-8 2019 RNA-sequencing comparisons of RA-treated embryos compared to controls revealed alterations in Sonic hedgehog (Shh) signaling. Tretinoin 30-32 sonic hedgehog signaling molecule Homo sapiens 110-113
17389641-3 2007 All-trans retinoic acid (RA) stimulates cellular proliferation in 3T3-L1 preadipocytes by activating TR2 through an IR0-type RA response element, which further activates c-Myc expression. Tretinoin 125-127 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-175
31591086-9 2019 More specifically, the expression of Shh and its downstream genes Ptch1 and Gli1 was spatiotemporally downregulated in the developing face of RA-treated embryos. Tretinoin 142-144 sonic hedgehog signaling molecule Homo sapiens 37-40
17389641-4 2007 In post-differentiated adipocytes, RA becomes a repressive signal for TR2 and rapidly down-regulates its expression. Tretinoin 35-37 nuclear receptor subfamily 2 group C member 1 Homo sapiens 70-73
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 23-25 nuclear receptor subfamily 2 group C member 1 Homo sapiens 29-32
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 23-25 glutamate receptor interacting protein 1 Homo sapiens 126-180
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 23-25 glutamate receptor interacting protein 1 Homo sapiens 182-187
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 23-25 nuclear receptor subfamily 2 group C member 1 Homo sapiens 219-222
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 82-84 nuclear receptor subfamily 2 group C member 1 Homo sapiens 29-32
31591086-10 2019 Consistent with these findings, the incidence of CP in association with excessive RA signaling was reduced by administration of the Shh signaling agonist SAG (Smoothened agonist). Tretinoin 82-84 sonic hedgehog signaling molecule Homo sapiens 132-135
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 82-84 glutamate receptor interacting protein 1 Homo sapiens 126-180
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 82-84 glutamate receptor interacting protein 1 Homo sapiens 182-187
31591086-11 2019 Altogether, our results uncovered a novel mechanistic association between RA-induced CP with decreased Shh signaling and elevated CNCC apoptosis. Tretinoin 74-76 sonic hedgehog signaling molecule Homo sapiens 103-106
17389641-5 2007 The biphasic effect of RA on TR2 expression in 3T3-L1 is mediated by differential RA-dependent coregulator recruitment to the receptor/Glucocorticoid Receptor-Interacting Protein 1 (GRIP1) complex that binds IR0 on the TR2 promoter. Tretinoin 82-84 nuclear receptor subfamily 2 group C member 1 Homo sapiens 219-222
17389641-6 2007 RA induces the recruitment of histone acetyl transferase-containing/GRIP1/p300/CBP-associated factor (PCAF) complex to the TR2 promoter in undifferentiated cells, whereas it triggers recruitment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in differentiated cells. Tretinoin 0-2 glutamate receptor interacting protein 1 Homo sapiens 68-73
31592194-0 2019 KDM3B suppresses APL progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARalpha. Tretinoin 93-97 lysine demethylase 3B Homo sapiens 0-5
17389641-6 2007 RA induces the recruitment of histone acetyl transferase-containing/GRIP1/p300/CBP-associated factor (PCAF) complex to the TR2 promoter in undifferentiated cells, whereas it triggers recruitment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in differentiated cells. Tretinoin 0-2 nuclear receptor subfamily 2 group C member 1 Homo sapiens 123-126
17389641-6 2007 RA induces the recruitment of histone acetyl transferase-containing/GRIP1/p300/CBP-associated factor (PCAF) complex to the TR2 promoter in undifferentiated cells, whereas it triggers recruitment of histone deacetylase-containing/GRIP1/receptor-interacting protein 140 (RIP140) complex in differentiated cells. Tretinoin 0-2 glutamate receptor interacting protein 1 Homo sapiens 229-234
31592194-0 2019 KDM3B suppresses APL progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARalpha. Tretinoin 93-97 PML nuclear body scaffold Homo sapiens 122-125
17389641-9 2007 This results in a biphasic effect of RA on the expression of TR2 in undifferentiated and differentiated cells, which is required for RA-stimulated preadipocyte proliferation. Tretinoin 37-39 nuclear receptor subfamily 2 group C member 1 Homo sapiens 61-64
31592194-0 2019 KDM3B suppresses APL progression by restricting chromatin accessibility and facilitating the ATRA-mediated degradation of PML/RARalpha. Tretinoin 93-97 retinoic acid receptor alpha Homo sapiens 126-134
17389641-9 2007 This results in a biphasic effect of RA on the expression of TR2 in undifferentiated and differentiated cells, which is required for RA-stimulated preadipocyte proliferation. Tretinoin 133-135 nuclear receptor subfamily 2 group C member 1 Homo sapiens 61-64
31592194-7 2019 Finally, molecular biological techniques and a multi-omics analysis were used to explore the role of KDM3B in differentiation of the leukemia cells after ATRA treatment. Tretinoin 154-158 lysine demethylase 3B Homo sapiens 101-106
17159378-1 2007 All-trans retinoic acid (ATRA) increases the expression of COX-1 and COX-2 and the production of PGE2, a prostaglandin with anti-inflammatory effects in human mesangial cells (MC). Tretinoin 0-23 mitochondrially encoded cytochrome c oxidase I Homo sapiens 59-64
17159378-1 2007 All-trans retinoic acid (ATRA) increases the expression of COX-1 and COX-2 and the production of PGE2, a prostaglandin with anti-inflammatory effects in human mesangial cells (MC). Tretinoin 25-29 mitochondrially encoded cytochrome c oxidase I Homo sapiens 59-64
31592194-10 2019 Moreover, knocking down KDM3B inhibited the ATRA-induced degradation of the PML/RARalpha oncoprotein. Tretinoin 44-48 lysine demethylase 3B Homo sapiens 24-29
31592194-10 2019 Moreover, knocking down KDM3B inhibited the ATRA-induced degradation of the PML/RARalpha oncoprotein. Tretinoin 44-48 PML nuclear body scaffold Homo sapiens 76-79
16340750-13 2006 CONCLUSIONS: These results suggest that the inhibitory effects of EB1089 on 9-cis RA-induced apoptosis lie upstream of caspase activation and could be associated with reduction of p27Kip1 protein levels. Tretinoin 82-84 cyclin dependent kinase inhibitor 1B Homo sapiens 180-187
31592194-10 2019 Moreover, knocking down KDM3B inhibited the ATRA-induced degradation of the PML/RARalpha oncoprotein. Tretinoin 44-48 retinoic acid receptor alpha Homo sapiens 80-88
17047027-1 2006 Cyp26a1, a gene required for retinoic acid (RA) inactivation during embryogenesis, was previously identified as a potential Tbx1 target from a microarray screen comparing wild-type and null Tbx1 mouse embryo pharyngeal arches (pa) at E9.5. Tretinoin 29-42 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
31592194-11 2019 Conclusion: Our study suggested that KDM3B was able to inhibit APL progression by maintaining chromatin in a compact state and facilitating the ATRA-mediated degradation of PML/RARalpha. Tretinoin 144-148 lysine demethylase 3B Homo sapiens 37-42
17047027-1 2006 Cyp26a1, a gene required for retinoic acid (RA) inactivation during embryogenesis, was previously identified as a potential Tbx1 target from a microarray screen comparing wild-type and null Tbx1 mouse embryo pharyngeal arches (pa) at E9.5. Tretinoin 29-42 T-box 1 Mus musculus 124-128
17047027-1 2006 Cyp26a1, a gene required for retinoic acid (RA) inactivation during embryogenesis, was previously identified as a potential Tbx1 target from a microarray screen comparing wild-type and null Tbx1 mouse embryo pharyngeal arches (pa) at E9.5. Tretinoin 44-46 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
17047027-1 2006 Cyp26a1, a gene required for retinoic acid (RA) inactivation during embryogenesis, was previously identified as a potential Tbx1 target from a microarray screen comparing wild-type and null Tbx1 mouse embryo pharyngeal arches (pa) at E9.5. Tretinoin 44-46 T-box 1 Mus musculus 124-128
17047027-6 2006 Down-regulation of Tbx1 itself was observed, in accordance with previous observations that RA represses Tbx1 expression. Tretinoin 91-93 T-box 1 Mus musculus 19-23
17047027-6 2006 Down-regulation of Tbx1 itself was observed, in accordance with previous observations that RA represses Tbx1 expression. Tretinoin 91-93 T-box 1 Mus musculus 104-108
16373280-10 2006 Since the disturbance of retinoic acid supply has been implicated in carcinogenicity, this finding may, at least in part, explain the high incidence of esophageal cancer in alcoholics, especially in those with inactive ALDH 2 whose blood acetaldehyde levels become higher than those with active ALDH 2. Tretinoin 25-38 aldehyde dehydrogenase 2 family member Rattus norvegicus 295-301
31592194-11 2019 Conclusion: Our study suggested that KDM3B was able to inhibit APL progression by maintaining chromatin in a compact state and facilitating the ATRA-mediated degradation of PML/RARalpha. Tretinoin 144-148 PML nuclear body scaffold Homo sapiens 173-176
17047027-7 2006 Thus, by specifically blocking the action of the Cyp26 enzymes we can recapitulate many elements of the Tbx1 mutant mouse, supporting the hypothesis that the dysregulation of RA-controlled morphogenesis contributes to the Tbx1 loss of function phenotype. Tretinoin 175-177 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 49-54
17047027-7 2006 Thus, by specifically blocking the action of the Cyp26 enzymes we can recapitulate many elements of the Tbx1 mutant mouse, supporting the hypothesis that the dysregulation of RA-controlled morphogenesis contributes to the Tbx1 loss of function phenotype. Tretinoin 175-177 T-box 1 Mus musculus 104-108
31592194-11 2019 Conclusion: Our study suggested that KDM3B was able to inhibit APL progression by maintaining chromatin in a compact state and facilitating the ATRA-mediated degradation of PML/RARalpha. Tretinoin 144-148 retinoic acid receptor alpha Homo sapiens 177-185
17047027-7 2006 Thus, by specifically blocking the action of the Cyp26 enzymes we can recapitulate many elements of the Tbx1 mutant mouse, supporting the hypothesis that the dysregulation of RA-controlled morphogenesis contributes to the Tbx1 loss of function phenotype. Tretinoin 175-177 T-box 1 Mus musculus 222-226
16289102-0 2005 Retinoic acid via RARalpha inhibits the expression of 24-hydroxylase in human prostate stromal cells. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 18-26
31395337-1 2019 Upon viral infection, retinoic acid-inducible gene-I (RIG-I)-like receptors detect viral foreign RNAs and transmit anti-viral signals via direct interaction with the downstream mitochondrial adaptor molecule, interferon (IFN)-beta promoter stimulator-1 (IPS-1), to inhibit viral replication. Tretinoin 22-35 mitochondrial antiviral signaling protein Homo sapiens 254-259
16289102-5 2005 By using transfection and RAR-selective ligands, we found that the inhibitory effect of ATRA on 24-hydroxylase expression in stromal cells was mediated by RARalpha but not by RARbeta. Tretinoin 88-92 retinoic acid receptor alpha Homo sapiens 26-29
16289102-5 2005 By using transfection and RAR-selective ligands, we found that the inhibitory effect of ATRA on 24-hydroxylase expression in stromal cells was mediated by RARalpha but not by RARbeta. Tretinoin 88-92 retinoic acid receptor alpha Homo sapiens 155-163
16289102-6 2005 Moreover, the ATRA-induced expression of RARbeta was also mediated by RARalpha. Tretinoin 14-18 retinoic acid receptor alpha Homo sapiens 70-78
16289102-8 2005 Our data suggest that ATRA suppresses 24-hydroxylase expression through RARalpha-dependent signaling pathway and can enhance vitamin D action in suppression of cell growth. Tretinoin 22-26 retinoic acid receptor alpha Homo sapiens 72-80
16985168-0 2006 Differentiation-specific factors modulate epidermal CYP1-4 gene expression in human skin in response to retinoic acid and classic aryl hydrocarbon receptor ligands. Tretinoin 104-117 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 52-58
17140143-4 2006 For instance, cells treated with retinoic acid show an increased expression of alpha-smooth muscle actin. Tretinoin 33-46 actin gamma 2, smooth muscle Rattus norvegicus 79-104
31337269-6 2019 Loss-of-function studies revealed that 7-like 2 (Tcf7l2) was the key transcription factor that Wnt operate through during RA-induced differentiation. Tretinoin 122-124 transcription factor 7 like 2 Homo sapiens 49-55
16757074-5 2006 Commencement of ATRA induces APL blast cell differentiation and is associated with a rapid resolution of the bleeding tendency through a combination of effects which include up regulation of thrombomodulin and down regulation of TF and CP production and cell surface expression of annexin II. Tretinoin 16-20 coagulation factor III, tissue factor Homo sapiens 229-231
16757074-5 2006 Commencement of ATRA induces APL blast cell differentiation and is associated with a rapid resolution of the bleeding tendency through a combination of effects which include up regulation of thrombomodulin and down regulation of TF and CP production and cell surface expression of annexin II. Tretinoin 16-20 annexin A2 Homo sapiens 281-291
17079450-2 2006 Here, we show for the first time that RA, via the RA receptor alpha (RARalpha), epigenetically regulates in a concerted fashion the transcription of two RA-responsive genes, the RA receptor beta2 (RARbeta2) and the cellular retinol-binding protein 1 (CRBP1). Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 69-77
16217742-4 2005 It was found that inhibition of RA signaling in vivo leads to excessive mammary ductal morphogenesis through upregulation of cyclin D1 and MMP-3 expression. Tretinoin 32-34 matrix metallopeptidase 3 Mus musculus 139-144
16149052-6 2005 MEK1/2 inhibitors, such as PD98059 and U0126, reduced RA-induced ERK1/2 activity, but could not block the genistein effects. Tretinoin 54-56 mitogen-activated protein kinase kinase 1 Homo sapiens 0-6
31370073-7 2019 ATRA inhibited platelet aggregation and adenosine triphosphate release induced by collagen (5 mug/mL) or thrombin (0.05 U/mL) in a dose-dependent manner without affecting P-selectin expression or surface levels of glycoprotein (GP) Ibalpha, GPVI, or alphaIIbbeta3. Tretinoin 0-4 glycoprotein VI platelet Homo sapiens 241-245
17079450-3 2006 Specifically, an impaired RA signal through RARalpha in human breast epithelial cells triggers a repressive epigenetic domino effect, involving first RARbeta2 and second CRBP1. Tretinoin 26-28 retinoic acid receptor alpha Homo sapiens 44-52
31561560-2 2019 Retinoic acid (RA) is considered the main inducer of meiotic entry, as it stimulates Stra8 which is required for the mitotic/meiotic switch. Tretinoin 0-13 stimulated by retinoic acid gene 8 Mus musculus 85-90
17050680-1 2006 The RIG-G gene, originally isolated from an acute promyelocytic leukemia cell line NB4, codes for a 60-kDa cytoplasmic protein that is induced by all-trans retinoic acid (ATRA) treatment along with the induction of morphological differentiation of NB4 cells. Tretinoin 156-169 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 4-9
17050680-1 2006 The RIG-G gene, originally isolated from an acute promyelocytic leukemia cell line NB4, codes for a 60-kDa cytoplasmic protein that is induced by all-trans retinoic acid (ATRA) treatment along with the induction of morphological differentiation of NB4 cells. Tretinoin 171-175 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 4-9
17050680-7 2006 Considering that IFN-alpha and ATRA synergistically inhibit growth along the intracellular pathways triggered by the two compounds in many cell types, we suggest that Rig-G may also represent one of the key molecular nodes of signaling cross-talk between ATRA and IFN-alpha. Tretinoin 31-35 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 167-172
17050680-7 2006 Considering that IFN-alpha and ATRA synergistically inhibit growth along the intracellular pathways triggered by the two compounds in many cell types, we suggest that Rig-G may also represent one of the key molecular nodes of signaling cross-talk between ATRA and IFN-alpha. Tretinoin 255-259 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 167-172
16832676-7 2006 However, the histone acetylase inhibitor SAHA combined with ATRA significantly reactivated RARbeta2 mRNA both in NB4 and MR2 cells with degradation of PML-RARalpha, which was associated with maturation. Tretinoin 60-64 PML nuclear body scaffold Homo sapiens 151-154
16044313-11 2005 We found that RA leads to enhanced cell death and up-regulation of CD38 and CD117. Tretinoin 14-16 CD38 molecule Homo sapiens 67-71
16267017-1 2005 Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). Tretinoin 91-114 retinoic acid receptor alpha Homo sapiens 157-180
16267017-1 2005 Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). Tretinoin 91-114 retinoic acid receptor alpha Homo sapiens 182-185
16267017-1 2005 Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). Tretinoin 116-120 retinoic acid receptor alpha Homo sapiens 157-180
16267017-1 2005 Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). Tretinoin 116-120 retinoic acid receptor alpha Homo sapiens 182-185
16267017-1 2005 Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). Tretinoin 101-114 retinoic acid receptor alpha Homo sapiens 157-180
16267017-1 2005 Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). Tretinoin 101-114 retinoic acid receptor alpha Homo sapiens 182-185
16832676-7 2006 However, the histone acetylase inhibitor SAHA combined with ATRA significantly reactivated RARbeta2 mRNA both in NB4 and MR2 cells with degradation of PML-RARalpha, which was associated with maturation. Tretinoin 60-64 retinoic acid receptor alpha Homo sapiens 155-163
31561560-2 2019 Retinoic acid (RA) is considered the main inducer of meiotic entry, as it stimulates Stra8 which is required for the mitotic/meiotic switch. Tretinoin 15-17 stimulated by retinoic acid gene 8 Mus musculus 85-90
16197938-3 2005 Exposure to exogenous RA increased the number of photoreceptors expressing rod opsin and red cone opsin, and decreased the number of photoreceptors expressing the blue and UV cone opsins, suggesting targeted effects of RA on photoreceptor development. Tretinoin 22-24 parapinopsin b Danio rerio 79-84
31561560-10 2019 CYP26A1, a very potent RA degrading enzyme, does not impair the formation of STRA8-positive cells, but decreases Stra8 transcription. Tretinoin 23-25 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
16197938-3 2005 Exposure to exogenous RA increased the number of photoreceptors expressing rod opsin and red cone opsin, and decreased the number of photoreceptors expressing the blue and UV cone opsins, suggesting targeted effects of RA on photoreceptor development. Tretinoin 22-24 parapinopsin b Danio rerio 98-103
16197938-6 2005 These observations collectively indicate that RA treatment does not affect photoreceptor fate, but rather differentially influences opsin transcription in determined photoreceptors. Tretinoin 46-48 parapinopsin b Danio rerio 132-137
31561560-11 2019 Collectively, our data reveal that CYP26B1 has other activities apart from metabolizing RA in fetal gonads and suggest a role of endogenous RA in amplifying Stra8, rather than being the initial inducer of Stra8. Tretinoin 140-142 stimulated by retinoic acid gene 8 Mus musculus 157-162
16085646-7 2005 Expression of IFNgamma receptor-1 on the cell surface was also increased upon atRA pretreatment. Tretinoin 78-82 interferon gamma receptor 1 Homo sapiens 14-33
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 124-128 retinoic acid receptor alpha Homo sapiens 73-101
16859680-9 2006 Our data suggest that Src tyrosine kinases are involved in the terminal differentiation of excitatory neuronal phenotype during ES cell neural differentiation after RA induction. Tretinoin 165-167 Rous sarcoma oncogene Mus musculus 22-25
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 124-128 retinoic acid receptor alpha Homo sapiens 103-111
31527569-0 2019 Retinoic Acid Promotes Retinoic Acid Signaling by Suppression of Pitx1 In Tendon Cells: A Possible Mechanism of a Clubfoot-Like Phenotype Induced by Retinoic Acid. Tretinoin 0-13 paired like homeodomain 1 Homo sapiens 65-70
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 124-128 interferon gamma receptor 1 Homo sapiens 199-218
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 124-128 retinoic acid receptor alpha Homo sapiens 304-312
16935935-0 2006 Retinoic acid induces leukemia cell G1 arrest and transition into differentiation by inhibiting cyclin-dependent kinase-activating kinase binding and phosphorylation of PML/RARalpha. Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 169-172
16935935-0 2006 Retinoic acid induces leukemia cell G1 arrest and transition into differentiation by inhibiting cyclin-dependent kinase-activating kinase binding and phosphorylation of PML/RARalpha. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 173-181
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 PML nuclear body scaffold Homo sapiens 21-24
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 25-33
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 PML nuclear body scaffold Homo sapiens 136-139
16935935-6 2006 In response to ATRA, PML/RARalpha is dissociated from CAK, leading to MAT1 degradation, G1 arrest, and decreased CAK phosphorylation of PML/RARalpha. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 140-148
16112651-6 2005 We found that retinoic acid that dissociates PML-RARalpha from the DNA, and which is used to treat acute promyelocytic leukemia patients, restores heparanase expression to normal levels in an acute promyelocytic leukemia cell line. Tretinoin 14-27 PML nuclear body scaffold Homo sapiens 45-48
16935935-8 2006 Both MAT1 degradation and PML/RARalpha hypophosphorylation occur in ATRA-induced G1-arresting cells undergoing differentiation but not in the synchronized G1 cells that do not differentiate. Tretinoin 68-72 PML nuclear body scaffold Homo sapiens 26-29
31238067-0 2019 All-trans retinoic acid attenuates isoproterenol-induced cardiac dysfunction through Crabp1 to dampen CaMKII activation. Tretinoin 0-23 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 102-108
16935935-8 2006 Both MAT1 degradation and PML/RARalpha hypophosphorylation occur in ATRA-induced G1-arresting cells undergoing differentiation but not in the synchronized G1 cells that do not differentiate. Tretinoin 68-72 retinoic acid receptor alpha Homo sapiens 30-38
16112651-6 2005 We found that retinoic acid that dissociates PML-RARalpha from the DNA, and which is used to treat acute promyelocytic leukemia patients, restores heparanase expression to normal levels in an acute promyelocytic leukemia cell line. Tretinoin 14-27 retinoic acid receptor alpha Homo sapiens 49-57
31447065-0 2019 Characterization of a rarely reported STAT5B/RARA gene fusion in a young adult with newly diagnosed acute promyelocytic leukemia with resistance to ATRA therapy. Tretinoin 148-152 retinoic acid receptor alpha Homo sapiens 45-49
16197459-0 2005 All-trans retinoic acid-induced downregulation of annexin II expression in myeloid leukaemia cell lines is not confined to acute promyelocytic leukaemia. Tretinoin 10-23 annexin A2 Homo sapiens 50-60
16197459-6 2005 The results confirmed that AnII expression in the APL cell line (NB4) was significantly downregulated in response to ATRA (P < 0.01), with associated morphological and immunophenotypical evidence of myeloid differentiation. Tretinoin 117-121 annexin A2 Homo sapiens 27-31
16197459-8 2005 The results provide evidence that ATRA may resolve the hyperfibrinolysis in APL by downregulation of AnII expression. Tretinoin 34-38 annexin A2 Homo sapiens 101-105
16885501-0 2006 Granulocyte macrophage colony-stimulating factor enhances retinoic acid-induced gene expression. Tretinoin 58-71 colony stimulating factor 2 Homo sapiens 0-48
16885501-1 2006 We reported previously that treatment of human myeloblastic leukemia ML-1 cells with all-trans retinoic acid (ATRA) in combination with GM-CSF enhances the granulocytic differentiation, which is induced only slightly by ATRA alone. Tretinoin 220-224 colony stimulating factor 2 Homo sapiens 136-142
16885501-2 2006 To investigate the mechanism underlying this differentiation and the synergistic effect of ATRA and GM-CSF, we used cDNA microarray to examine gene expression profiles of ML-1 cells treated with ATRA and/or GM-CSF. Tretinoin 195-199 colony stimulating factor 2 Homo sapiens 100-106
16885501-4 2006 Comparison of cells treated with both reagents and cells treated with ATRA or GM-CSF alone revealed that expression of nine of the 19 genes was induced synergistically by combined treatment with ATRA and GM-CSF. Tretinoin 70-74 colony stimulating factor 2 Homo sapiens 204-210
16054129-5 2005 It was found that the kinetics of c-Myc correlates most closely with the telomerase activity suggesting in agreement with previous studies that this protein is a major intermediate of the RA-induced downregulation of telomerase activity. Tretinoin 188-190 MYC proto-oncogene, bHLH transcription factor Homo sapiens 34-39
16885501-4 2006 Comparison of cells treated with both reagents and cells treated with ATRA or GM-CSF alone revealed that expression of nine of the 19 genes was induced synergistically by combined treatment with ATRA and GM-CSF. Tretinoin 195-199 colony stimulating factor 2 Homo sapiens 78-84
31447065-2 2019 While most cases of APL harboring the PML/RARA fusion respond to all-trans retinoic acid (ATRA), some variant RARA rearrangements are ATRA insensitive. Tretinoin 68-88 PML nuclear body scaffold Homo sapiens 38-41
16885501-6 2006 These results indicate that GM-CSF enhances ATRA-induced gene expression. Tretinoin 44-48 colony stimulating factor 2 Homo sapiens 28-34
16885501-9 2006 It is likely that the enhancer effect of GM-CSF on ATRA-induced gene expression leads to the differentiation induced synergistically by ATRA combined with GM-CSF. Tretinoin 51-55 colony stimulating factor 2 Homo sapiens 41-47
31447065-2 2019 While most cases of APL harboring the PML/RARA fusion respond to all-trans retinoic acid (ATRA), some variant RARA rearrangements are ATRA insensitive. Tretinoin 68-88 retinoic acid receptor alpha Homo sapiens 42-46
16885501-9 2006 It is likely that the enhancer effect of GM-CSF on ATRA-induced gene expression leads to the differentiation induced synergistically by ATRA combined with GM-CSF. Tretinoin 51-55 colony stimulating factor 2 Homo sapiens 155-161
16885501-9 2006 It is likely that the enhancer effect of GM-CSF on ATRA-induced gene expression leads to the differentiation induced synergistically by ATRA combined with GM-CSF. Tretinoin 136-140 colony stimulating factor 2 Homo sapiens 41-47
31447065-2 2019 While most cases of APL harboring the PML/RARA fusion respond to all-trans retinoic acid (ATRA), some variant RARA rearrangements are ATRA insensitive. Tretinoin 90-94 PML nuclear body scaffold Homo sapiens 38-41
16179254-4 2005 PRAME binds to RAR in the presence of RA, preventing ligand-induced receptor activation and target gene transcription through recruitment of Polycomb proteins. Tretinoin 1-3 retinoic acid receptor alpha Homo sapiens 15-18
31447065-2 2019 While most cases of APL harboring the PML/RARA fusion respond to all-trans retinoic acid (ATRA), some variant RARA rearrangements are ATRA insensitive. Tretinoin 90-94 retinoic acid receptor alpha Homo sapiens 42-46
16179254-6 2005 Conversely, knockdown of PRAME expression by RNA interference in RA-resistant human melanoma restores RAR signaling and reinstates sensitivity to the antiproliferative effects of RA in vitro and in vivo. Tretinoin 26-28 retinoic acid receptor alpha Homo sapiens 102-105
16157890-6 2005 Although RA alone increased the neonatal anti-TT antibody response, it selectively increased anti-TT IgG1 and IL-5, resulting in a skewed type 2 response. Tretinoin 9-11 interleukin 5 Mus musculus 110-114
16740652-1 2006 Murine epididymal retinoic acid-binding protein [or lipocalin 5 (Lcn5)] is synthesized and secreted by the principal cells of the mouse middle/distal caput epididymidis. Tretinoin 18-31 lipocalin 5 Mus musculus 52-63
16740652-1 2006 Murine epididymal retinoic acid-binding protein [or lipocalin 5 (Lcn5)] is synthesized and secreted by the principal cells of the mouse middle/distal caput epididymidis. Tretinoin 18-31 lipocalin 5 Mus musculus 65-69
31447065-2 2019 While most cases of APL harboring the PML/RARA fusion respond to all-trans retinoic acid (ATRA), some variant RARA rearrangements are ATRA insensitive. Tretinoin 134-138 retinoic acid receptor alpha Homo sapiens 110-114
31447065-3 2019 Herein, we report a 27-year-old male with newly diagnosed, rapidly progressive APL and a rarely described STAT5B/RARA fusion with known resistance to ATRA therapy. Tretinoin 150-154 retinoic acid receptor alpha Homo sapiens 113-117
17172655-5 2006 EGF could not induce AP-1 activity or S-phase entry in density-arrested cells, but could do so after pretreatment with retinoic acid, which enhances EGF receptor expression. Tretinoin 119-132 epidermal growth factor Rattus norvegicus 0-3
31006867-5 2019 OBJECTIVES: To investigate whether all-trans-RA (ATRA) activates mast cells via MRGPRX2/MrgprB2 (the mouse orthologue), contributing to the pathogenesis of retinoid-induced dermatitis. Tretinoin 35-47 MAS-related GPR, member B2 Mus musculus 88-95
17172655-5 2006 EGF could not induce AP-1 activity or S-phase entry in density-arrested cells, but could do so after pretreatment with retinoic acid, which enhances EGF receptor expression. Tretinoin 119-132 epidermal growth factor Rattus norvegicus 149-152
18404486-3 2006 DNA array analysis showed that treatment of normal human epidermal keratinocytes (NHEKs) with all-trans-retinoic acid (ATRA), an agonist to RAR (retinoic acid receptor), enhanced the expression of mRNA for the P2Y2 receptor, a metabotropic P2 receptor that is known to be involved in the proliferation of the epidermis. Tretinoin 94-117 retinoic acid receptor alpha Homo sapiens 140-143
16023837-6 2005 In NTERA2, but not in 2102Ep cells, retinoic acid induces up-regulation of p27 expression, suggesting that 2102Ep cells lack this capacity. Tretinoin 36-49 cyclin dependent kinase inhibitor 1B Homo sapiens 75-78
16188211-9 2005 The treatment of LA-N-1 cells with 12-O-tetradecanoyl-phorbol-13 acetate (TPA) and RA increases diacylglycerol (DAG) levels indicating the stimulation of PLC activity. Tretinoin 83-85 heparan sulfate proteoglycan 2 Homo sapiens 154-157
18404486-3 2006 DNA array analysis showed that treatment of normal human epidermal keratinocytes (NHEKs) with all-trans-retinoic acid (ATRA), an agonist to RAR (retinoic acid receptor), enhanced the expression of mRNA for the P2Y2 receptor, a metabotropic P2 receptor that is known to be involved in the proliferation of the epidermis. Tretinoin 119-123 retinoic acid receptor alpha Homo sapiens 140-143
31006867-8 2019 RESULTS: As compared with WT mice, MrgprB2-/- mice showed resistance to ATRA-triggered contact dermatitis and local inflammatory reactions in the paws. Tretinoin 72-76 MAS-related GPR, member B2 Mus musculus 35-42
15950969-3 2005 Previously, we described a system of retinoic acid (RA) synthesis in the cycling rat uterus consisting of cellular retinol binding protein (Crbp), epithelial retinol dehydrogenase (eRoldh), retinal dehydrogenase 2 (Aldh1a2), and cellular retinoic acid binding protein type II (Crabp2). Tretinoin 52-54 cellular retinoic acid binding protein 2 Rattus norvegicus 277-283
31006867-10 2019 CONCLUSIONS: ATRA-induced dermatitis could be achieved by activating mast cells via MRGPRX2/MrgprB2, which may provide a potential therapy target to reduce the side-effect. Tretinoin 13-17 MAS-related GPR, member B2 Mus musculus 92-99
16882163-13 2006 In contrast, CYP1A1 and CYP1A2 expression was suppressed by atRA, and gamma-GCS and MRP1 by clobetasol 17-propionate. Tretinoin 60-64 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 13-19
31180720-6 2019 In the mechanism, ZIKV nonstructural (NS) 3 and NS2B3 negatively regulate IFN-related retinoic acid-inducible gene I-like receptor signaling pathway by targeting MAVS and MITA, respectively. Tretinoin 86-99 mitochondrial antiviral signaling protein Homo sapiens 162-166
16882163-13 2006 In contrast, CYP1A1 and CYP1A2 expression was suppressed by atRA, and gamma-GCS and MRP1 by clobetasol 17-propionate. Tretinoin 60-64 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 24-30
16818722-3 2006 We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Tretinoin 36-49 bone morphogenetic protein 1 Homo sapiens 105-108
15870697-1 2005 Human breast cancer cell lines expressing the estrogen receptor alpha (ERalpha), all-trans-retinoic acid (ATRA) receptor alpha (RARalpha) and cellular retinoic acid binding protein II (CRABPII) genes are sensitive to ATRA-mediated growth inhibition. Tretinoin 106-110 retinoic acid receptor alpha Homo sapiens 128-136
15872003-3 2005 We demonstrate in mouse embryos that an RA signal initially travels from the paraxial mesoderm to r3, forming a boundary next to the r2 expression domain of Cyp26a1 (which encodes an RA-degrading enzyme). Tretinoin 40-42 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 157-164
15872003-3 2005 We demonstrate in mouse embryos that an RA signal initially travels from the paraxial mesoderm to r3, forming a boundary next to the r2 expression domain of Cyp26a1 (which encodes an RA-degrading enzyme). Tretinoin 183-185 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 157-164
16818722-3 2006 We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Tretinoin 51-53 bone morphogenetic protein 1 Homo sapiens 105-108
31235250-0 2019 The isoflavone puerarin induces Foxp3+ regulatory T cells by augmenting retinoic acid production, thereby inducing mucosal immune tolerance in a murine food allergy model. Tretinoin 72-85 forkhead box P3 Mus musculus 32-37
15949682-5 2005 Thereby, a novel retinoic acid-responsive element could be located within 191 bp of the proximal CYP27A1 promoter. Tretinoin 17-30 cytochrome P450 family 27 subfamily A member 1 Homo sapiens 97-104
16888198-0 2006 Retinoic acid-induced human secretin gene expression in neuronal cells is mediated by cyclin-dependent kinase 1. Tretinoin 0-13 cyclin dependent kinase 1 Homo sapiens 86-111
31434807-7 2019 We found that retinoic acid-related orphan receptor alpha (RORalpha) was increased by inflammatory mediators, such as IL-1beta, and bound to ANGPTL4 promoter in MSCs. Tretinoin 14-27 interleukin 1 alpha Homo sapiens 118-126
16619266-0 2006 Endodermal differentiation of murine embryonic carcinoma cells by retinoic acid requires JLP, a JNK-scaffolding protein. Tretinoin 66-79 sperm associated antigen 9 Mus musculus 89-92
16619266-5 2006 Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Tretinoin 21-23 sperm associated antigen 9 Mus musculus 53-91
16619266-5 2006 Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Tretinoin 21-23 sperm associated antigen 9 Mus musculus 93-96
16619266-5 2006 Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Tretinoin 167-169 sperm associated antigen 9 Mus musculus 53-91
16619266-5 2006 Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Tretinoin 167-169 sperm associated antigen 9 Mus musculus 93-96
16619266-7 2006 More interestingly, silencing JLP abrogates RA-mediated endodermal differentiation of P19 cells analogous to the effects seen with the silencing of G alpha13 or JNK. Tretinoin 44-46 sperm associated antigen 9 Mus musculus 30-33
16029656-0 2005 [Effects of all-trans retinoic acid on expression of connexin genes and gap junction communication in hepatocellular carcinoma cell lines]. Tretinoin 12-35 LOC100128922 Homo sapiens 53-61
15907482-6 2005 These results, as a whole, indicate that SH3BGRL3 may function as a regulator in all-trans retinoic acid-induced pathway. Tretinoin 91-104 SH3 domain binding glutamate rich protein like 3 Homo sapiens 41-49
15628969-10 2005 These data provide the first analytically robust quantification of atRA in animal brain and in CRBP-null mice. Tretinoin 67-71 retinol binding protein 1, cellular Mus musculus 95-99
31434807-7 2019 We found that retinoic acid-related orphan receptor alpha (RORalpha) was increased by inflammatory mediators, such as IL-1beta, and bound to ANGPTL4 promoter in MSCs. Tretinoin 14-27 angiopoietin like 4 Homo sapiens 141-148
16455818-0 2006 A novel cytochrome P450, zebrafish Cyp26D1, is involved in metabolism of all-trans retinoic acid. Tretinoin 83-96 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 35-42
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 119-142 glutamic-oxaloacetic transaminase 2 Homo sapiens 61-87
16455818-3 2006 Using reverse-phase HPLC analyses, we show here that zebrafish Cyp26D1 expressed in 293T cells could metabolize all-trans RA, 9-cis RA, and 13-cis RA, but could not metabolize retinol or retinal. Tretinoin 122-124 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 63-70
16455818-3 2006 Using reverse-phase HPLC analyses, we show here that zebrafish Cyp26D1 expressed in 293T cells could metabolize all-trans RA, 9-cis RA, and 13-cis RA, but could not metabolize retinol or retinal. Tretinoin 132-134 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 63-70
16455818-3 2006 Using reverse-phase HPLC analyses, we show here that zebrafish Cyp26D1 expressed in 293T cells could metabolize all-trans RA, 9-cis RA, and 13-cis RA, but could not metabolize retinol or retinal. Tretinoin 132-134 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 63-70
16455818-4 2006 The metabolites of all-trans RA produced by Cyp26D1 were the same as that produced by Cyp26A1, which are mainly 4-hydroxy-all-trans-RA and 4-oxo-all-trans-RA. Tretinoin 29-31 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 44-51
16455818-4 2006 The metabolites of all-trans RA produced by Cyp26D1 were the same as that produced by Cyp26A1, which are mainly 4-hydroxy-all-trans-RA and 4-oxo-all-trans-RA. Tretinoin 132-134 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 44-51
16455818-7 2006 Together, our in vitro and in vivo results provided direct evidence that zebrafish Cyp26D1 is involved in RA metabolism. Tretinoin 106-108 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 83-90
15866332-6 2005 Since Nano-atRA which is prepared following to this new DDS system developmentally improved the permeability to the stratum corneum, the remarkable pharmacological effects were resulted in comparison with atRA as such as follows: (1) thicker epidermis than classical atRA treatment and (2) the overexpression of mRNA for heparin-binding epidermal growth factor (HB-EGF) as the provocation epidermal hyperplasia. Tretinoin 11-15 heparin binding EGF like growth factor Homo sapiens 321-360
15867264-6 2005 RESULTS: We identified aberrant expression of several components of the retinoic acid (RA) signaling pathway (RARalpha, MUC4, Id-1, MMP9, uPAR, HB-EGF, HOXB6, and HOXB2), many of which are known to be aberrantly expressed in pancreatic cancer and PanIN. Tretinoin 87-89 retinoic acid receptor alpha Homo sapiens 110-118
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 119-142 glutamic-oxaloacetic transaminase 2 Homo sapiens 89-93
16187701-1 2005 The results of the treatment of 14 patients with promyelocytic leukemia (PML) treated with all trans-retinoic acid (ATRA), combined chemotherapy (CT) and prophylactic prednisone are reported; the median age was 30 years (range 7 - 49). Tretinoin 95-114 PML nuclear body scaffold Homo sapiens 49-71
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 43-45 glutamic-oxaloacetic transaminase 2 Homo sapiens 61-87
16584924-5 2006 In retinoic acid-induced differentiating HL-60 cells, the d2EGFP expression is diminished in the same manner as the hTERT expression. Tretinoin 3-16 telomerase reverse transcriptase Homo sapiens 116-121
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 43-45 glutamic-oxaloacetic transaminase 2 Homo sapiens 89-93
30916783-8 2019 Molecular analysis identified increased RA signalling as one factor contributing to the delay in SMC differentiation, possibly caused by reduced direct transcriptional activation of Cyp26a1, which encodes an RA-degrading enzyme. Tretinoin 40-42 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 182-189
16889531-4 2006 Interestingly, vitamin D and RA demonstrated a consistent, dose-dependent enhancement of osteogenesis and upregulated osteoblast specific markers including osteopontin and osteocalcin. Tretinoin 29-31 bone gamma-carboxyglutamate protein 2 Mus musculus 172-183
15924754-11 2005 The level of RARalpha gene expression of B cells (lg copies/50 ng RNA) in the RA group was significantly higher than that in the control (24 h: 7.03 +/- 1.36 vs. 5.79 +/- 2.05; 48 h: 7.91 +/- 1.60 vs. 6.21 +/- 1.88) (P < 0.05), and that in the LPS + RA group was significantly higher than that in the LPS group (24 h: 7.29 +/- 1.53 vs. 5.98 +/- 1.48; 48 h: 7.83 +/- 1.66 vs. 5.79 +/- 2.36)(P < 0.05). Tretinoin 78-80 retinoic acid receptor alpha Homo sapiens 13-21
30916783-8 2019 Molecular analysis identified increased RA signalling as one factor contributing to the delay in SMC differentiation, possibly caused by reduced direct transcriptional activation of Cyp26a1, which encodes an RA-degrading enzyme. Tretinoin 208-210 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 182-189
15857687-2 2005 We have previously shown that bone morphogenetic protein-2 (BMP2) and retinoic acid synergistically induce the responsiveness of developing sympathetic neurons to neurotrophic factors, neurotrophin 3 (NT-3), and GDNF by upregulating corresponding receptors concomitantly with the induction of other neuron-specific genes including BRINP1, a neuron-specific cell-cycle regulatory protein. Tretinoin 70-83 BMP/retinoic acid inducible neural specific 1 Homo sapiens 331-337
15677473-8 2005 In the present study, we present evidence suggesting that chicken ovalbumin upstream promoter-transcription factor (COUP-TF) members antagonize RA-induced Cdx1 expression by competing with retinoid X receptor-retinoic acid receptor heterodimers for binding to the Cdx1 RA response element. Tretinoin 144-146 caudal type homeobox 1 Gallus gallus 155-159
15677473-8 2005 In the present study, we present evidence suggesting that chicken ovalbumin upstream promoter-transcription factor (COUP-TF) members antagonize RA-induced Cdx1 expression by competing with retinoid X receptor-retinoic acid receptor heterodimers for binding to the Cdx1 RA response element. Tretinoin 144-146 caudal type homeobox 1 Gallus gallus 264-268
16606617-1 2006 Additional sex comb-like 1 (ASXL1, 170 kDa), a mammalian homolog of Drosophila ASX, was identified as a protein that interacts with retinoic acid receptor (RAR) in the presence of retinoic acid (RA). Tretinoin 132-145 retinoic acid receptor alpha Homo sapiens 156-159
16606617-1 2006 Additional sex comb-like 1 (ASXL1, 170 kDa), a mammalian homolog of Drosophila ASX, was identified as a protein that interacts with retinoic acid receptor (RAR) in the presence of retinoic acid (RA). Tretinoin 156-158 retinoic acid receptor alpha Homo sapiens 132-154
16636064-6 2006 Following RA treatment, we also observed increased nuclear EBBP levels in aggregates with the promyelocytic leukemia protein at promyelocytic leukemia nuclear bodies. Tretinoin 10-12 PML nuclear body scaffold Homo sapiens 94-124
15677473-10 2005 Together with other data, these findings suggest a model by which COUP-TF expression is induced by RA in the trunk region as a negative feedback mechanism to restrict Cdx1 expression to the caudal embryo. Tretinoin 99-101 caudal type homeobox 1 Gallus gallus 167-171
31147716-4 2019 Enhancer deletion significantly inhibited expression of RA-induced Hoxa1 and endoderm master control genes such as Gata4 and Gata6. Tretinoin 56-58 GATA binding protein 6 Homo sapiens 125-130
15735731-0 2005 Retinoic acid stabilizes p27Kip1 in EBV-immortalized lymphoblastoid B cell lines through enhanced proteasome-dependent degradation of the p45Skp2 and Cks1 proteins. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 25-32
15735731-1 2005 Retinoic acid (RA) arrests the growth of EBV-immortalized lymphoblastoid B cell lines (LCLs) by upregulating the cyclin-dependent kinase inhibitor p27Kip1. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 147-154
16690024-5 2006 cADPRP was detectable in retinoic acid-differentiated, CD38+ HL-60 cells, but not in undifferentiated, CD38- cells. Tretinoin 25-38 CD38 molecule Homo sapiens 55-59
31320612-6 2019 Moreover, RA treatment leads to suppression of BMP signaling by reducing the level of FBXO30 in mammalian cells and in mouse embryos with NTDs. Tretinoin 10-12 bone morphogenetic protein 1 Homo sapiens 47-50
16556444-6 2006 Our results revealed that ANT1 and ANT3 over-expressing HeLa cells increased their atRA sensitivity. Tretinoin 83-87 solute carrier family 25 member 4 Homo sapiens 26-30
16556444-6 2006 Our results revealed that ANT1 and ANT3 over-expressing HeLa cells increased their atRA sensitivity. Tretinoin 83-87 solute carrier family 25 member 6 Homo sapiens 35-39
15735731-1 2005 Retinoic acid (RA) arrests the growth of EBV-immortalized lymphoblastoid B cell lines (LCLs) by upregulating the cyclin-dependent kinase inhibitor p27Kip1. Tretinoin 15-17 cyclin dependent kinase inhibitor 1B Homo sapiens 147-154
15735731-2 2005 Here, we show that in LCLs, RA inhibits ubiquitination and proteasome-dependent degradation of p27Kip1, a phenomenon that is associated with downregulation of Thr187 phosphorylation of the protein, whereas the phosphorylation on Ser10 is unaffected. Tretinoin 28-30 cyclin dependent kinase inhibitor 1B Homo sapiens 95-102
15735731-3 2005 Furthermore, we demonstrate that RA downregulates the expression of the p45Skp2 and Cks1 proteins, two essential components of the SCF(Skp2) ubiquitin ligase complex that target p27Kip1 for degradation. Tretinoin 33-35 cyclin dependent kinase inhibitor 1B Homo sapiens 178-185
15735731-9 2005 These results indicate that downregulation of p45Skp2 is a key element underlying RA-induced p27Kip1 stabilization in B cells, resulting in an impaired targeting of the protein to the ubiquitin-proteasome pathway and probably contributing to the nuclear accumulation of p27Kip1. Tretinoin 82-84 cyclin dependent kinase inhibitor 1B Homo sapiens 93-100
15735731-9 2005 These results indicate that downregulation of p45Skp2 is a key element underlying RA-induced p27Kip1 stabilization in B cells, resulting in an impaired targeting of the protein to the ubiquitin-proteasome pathway and probably contributing to the nuclear accumulation of p27Kip1. Tretinoin 82-84 cyclin dependent kinase inhibitor 1B Homo sapiens 270-277
15736167-0 2005 Retinoic acid down-regulates Tbx1 expression in vivo and in vitro. Tretinoin 0-13 T-box 1 Mus musculus 29-33
16556444-7 2006 Thus, our results not only demonstrate the different functional activities of ANT isoforms, but also contribute to a better understanding of the properties of atRA as an anti-tumoral agent used in cancer therapy. Tretinoin 159-163 solute carrier family 25 member 6 Homo sapiens 78-81
15736167-1 2005 Both Tbx1 and retinoic acid (RA) are key players in embryonic pharyngeal development; loss of Tbx1 produces DiGeorge syndrome-like phenotypes in mouse models as does disruption of retinoic acid homeostasis. Tretinoin 14-27 T-box 1 Mus musculus 94-98
31231034-3 2019 Gata6 expression is maintained in a non-cell autonomous manner and is elicited by the vitamin A metabolite, retinoic acid. Tretinoin 108-121 GATA binding protein 6 Homo sapiens 0-5
15736167-1 2005 Both Tbx1 and retinoic acid (RA) are key players in embryonic pharyngeal development; loss of Tbx1 produces DiGeorge syndrome-like phenotypes in mouse models as does disruption of retinoic acid homeostasis. Tretinoin 29-31 T-box 1 Mus musculus 94-98
15736167-1 2005 Both Tbx1 and retinoic acid (RA) are key players in embryonic pharyngeal development; loss of Tbx1 produces DiGeorge syndrome-like phenotypes in mouse models as does disruption of retinoic acid homeostasis. Tretinoin 180-193 T-box 1 Mus musculus 5-9
15736167-2 2005 We have demonstrated that perturbation of retinoic acid levels in the avian embryo produces altered Tbx1 expression. Tretinoin 42-55 T-box 1 Mus musculus 100-104
15736167-3 2005 In vitamin A-deficient quails, which lack endogenous retinoic acid, Tbx1 expression patterns were disrupted early in development and expression was subsequently lost in all tissues. Tretinoin 53-66 T-box 1 Mus musculus 68-72
15736167-4 2005 "Gain-of-function" experiments where RA-soaked beads were grafted into the pharyngeal region produced localized down-regulation of Tbx1 expression. Tretinoin 37-39 T-box 1 Mus musculus 131-135
15736167-6 2005 Real-time polymerase chain reaction analysis of retinoic acid-treated P19 cells showed a dose-dependent repression of Tbx1 by retinoic acid. Tretinoin 48-61 T-box 1 Mus musculus 118-122
15736167-6 2005 Real-time polymerase chain reaction analysis of retinoic acid-treated P19 cells showed a dose-dependent repression of Tbx1 by retinoic acid. Tretinoin 126-139 T-box 1 Mus musculus 118-122
16615129-9 2006 The downregulation of Cyp26s and the upregulation of Raldhs after birth during inner ear maturation suggest tissue changes in the sensitivity to retinoic acid concentrations. Tretinoin 145-158 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 22-27
16434964-4 2006 PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA). Tretinoin 216-229 PML nuclear body scaffold Homo sapiens 0-3
16434964-4 2006 PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA). Tretinoin 216-229 retinoic acid receptor alpha Homo sapiens 4-12
16434964-4 2006 PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA). Tretinoin 216-229 PML nuclear body scaffold Homo sapiens 155-158
16434964-4 2006 PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA). Tretinoin 231-235 PML nuclear body scaffold Homo sapiens 0-3
16434964-4 2006 PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA). Tretinoin 231-235 retinoic acid receptor alpha Homo sapiens 4-12
16434964-4 2006 PML-RARalpha has been shown to promote transcriptional repression of genes involved in myeloid terminal differentiation and to disrupt the architecture of PML bodies, a phenotype reversed by treatment with all trans retinoic acid (ATRA). Tretinoin 231-235 PML nuclear body scaffold Homo sapiens 155-158
15736167-7 2005 Repression of Tbx1 transcript levels was first evident after 8-12 hr in culture in the presence of retinoic acid, and to achieve the highest levels of repression, de novo protein synthesis was required. Tretinoin 99-112 T-box 1 Mus musculus 14-18
16434964-8 2006 The activity of the PML-RARalphaL is completely sensitive to ATRA. Tretinoin 61-65 PML nuclear body scaffold Homo sapiens 20-23
31231034-5 2019 Retinoic acid-dependent and -independent hallmark genes of GATA6+ macrophages were induced by mesothelial and fibroblastic stromal cells that express the transcription factor Wilms" Tumor 1 (WT1), which drives the expression of two rate-limiting enzymes in retinol metabolism. Tretinoin 0-13 GATA binding protein 6 Homo sapiens 59-64
16688765-3 2006 The eye contains a highly intricate architecture of RA-synthesizing (RALDH) and degrading (CYP26) enzymes. Tretinoin 52-54 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 91-96
30982491-3 2019 We found that RREB1 is overexpressed in AML patients and myeloid leukemia cell lines (NB4 and HL-60), and RREB1 expression was significantly decreased during granulocytic differentiation of myeloid leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 234-247 ras responsive element binding protein 1 Homo sapiens 14-19
16688765-6 2006 Throughout development CYP26A1 degrades RA in a horizontal region that extends across the retina, but during later embryonic and postnatal retina maturation this function is reinforced by another enzyme, CYP26C1. Tretinoin 40-42 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 23-30
16819260-2 2006 The most important endogeneous retinoid is all-trans-retinoic acid (ATRA) which is an RARalpha, beta and gamma ligand. Tretinoin 43-66 retinoic acid receptor alpha Homo sapiens 86-94
16819260-2 2006 The most important endogeneous retinoid is all-trans-retinoic acid (ATRA) which is an RARalpha, beta and gamma ligand. Tretinoin 68-72 retinoic acid receptor alpha Homo sapiens 86-94
30982491-3 2019 We found that RREB1 is overexpressed in AML patients and myeloid leukemia cell lines (NB4 and HL-60), and RREB1 expression was significantly decreased during granulocytic differentiation of myeloid leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 234-247 ras responsive element binding protein 1 Homo sapiens 106-111
30982491-3 2019 We found that RREB1 is overexpressed in AML patients and myeloid leukemia cell lines (NB4 and HL-60), and RREB1 expression was significantly decreased during granulocytic differentiation of myeloid leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 249-253 ras responsive element binding protein 1 Homo sapiens 14-19
16636311-6 2006 Although a second dose of ATRA or Am580 (a related retinoid selective for retinoic acid receptor-alpha [RARalpha]), given 16 hrs after the first dose, restimulated IRF-1 mRNA and protein levels to a similar level to that obtained by the first dose, IRF-1 was predominantly concentrated in the nucleus after restimulation. Tretinoin 26-30 retinoic acid receptor alpha Homo sapiens 74-102
30982491-3 2019 We found that RREB1 is overexpressed in AML patients and myeloid leukemia cell lines (NB4 and HL-60), and RREB1 expression was significantly decreased during granulocytic differentiation of myeloid leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 249-253 ras responsive element binding protein 1 Homo sapiens 106-111
16636311-6 2006 Although a second dose of ATRA or Am580 (a related retinoid selective for retinoic acid receptor-alpha [RARalpha]), given 16 hrs after the first dose, restimulated IRF-1 mRNA and protein levels to a similar level to that obtained by the first dose, IRF-1 was predominantly concentrated in the nucleus after restimulation. Tretinoin 26-30 retinoic acid receptor alpha Homo sapiens 104-112
16636311-7 2006 ATRA and Am580 also increased nuclear RARalpha, whereas retinoid X receptor-alpha (RXRalpha)--a dimerization partner for RARalpha, was localized to the nucleus upon second exposure to ATRA. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 38-46
31291979-0 2019 Involvement of epigenetic modification of TERT promoter in response to all-trans retinoic acid in ovarian cancer cell lines. Tretinoin 81-94 telomerase reverse transcriptase Homo sapiens 42-46
16680587-3 2006 Retinoic acid (RA), a derivative of vitamin A, is a ligand for the IGF II receptor (IGF2R). Tretinoin 0-13 insulin like growth factor 2 receptor Homo sapiens 67-82
16680587-3 2006 Retinoic acid (RA), a derivative of vitamin A, is a ligand for the IGF II receptor (IGF2R). Tretinoin 0-13 insulin like growth factor 2 receptor Homo sapiens 84-89
16680587-3 2006 Retinoic acid (RA), a derivative of vitamin A, is a ligand for the IGF II receptor (IGF2R). Tretinoin 15-17 insulin like growth factor 2 receptor Homo sapiens 67-82
16680587-3 2006 Retinoic acid (RA), a derivative of vitamin A, is a ligand for the IGF II receptor (IGF2R). Tretinoin 15-17 insulin like growth factor 2 receptor Homo sapiens 84-89
16680587-10 2006 Retinoic acid x10(-5) M completely abrogated the proliferative actions of IGF II (70.2% +/- 9.7%, P < 0.05) but had no significant effect on the IGF I response (P > 0.05). Tretinoin 0-13 insulin like growth factor 2 Homo sapiens 74-80
16680587-12 2006 The IGF II inhibitory effect of RA was enhanced in the presence of analogs [Leu27]IGF II (P = 0.052) but not with des(1-6)IGF II (P > 0.05), compared with wild-type IGF II. Tretinoin 32-34 insulin like growth factor 2 Homo sapiens 4-10
16680587-12 2006 The IGF II inhibitory effect of RA was enhanced in the presence of analogs [Leu27]IGF II (P = 0.052) but not with des(1-6)IGF II (P > 0.05), compared with wild-type IGF II. Tretinoin 32-34 insulin like growth factor 2 Homo sapiens 82-88
16680587-12 2006 The IGF II inhibitory effect of RA was enhanced in the presence of analogs [Leu27]IGF II (P = 0.052) but not with des(1-6)IGF II (P > 0.05), compared with wild-type IGF II. Tretinoin 32-34 insulin like growth factor 2 Homo sapiens 82-88
16680587-12 2006 The IGF II inhibitory effect of RA was enhanced in the presence of analogs [Leu27]IGF II (P = 0.052) but not with des(1-6)IGF II (P > 0.05), compared with wild-type IGF II. Tretinoin 32-34 insulin like growth factor 2 Homo sapiens 82-88
16680587-13 2006 CONCLUSIONS: These data implicate a novel antiproliferative role for RA in enhancing the pericellular clearance of IGF II via the IGF2R preventing ligand activation of the IGF I receptor. Tretinoin 69-71 insulin like growth factor 2 Homo sapiens 115-121
16680587-13 2006 CONCLUSIONS: These data implicate a novel antiproliferative role for RA in enhancing the pericellular clearance of IGF II via the IGF2R preventing ligand activation of the IGF I receptor. Tretinoin 69-71 insulin like growth factor 2 receptor Homo sapiens 130-135
16329108-0 2006 Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels. Tretinoin 0-13 CD38 molecule Homo sapiens 22-26
16329108-1 2006 Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RARalpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell. Tretinoin 0-13 CD38 molecule Homo sapiens 40-44
16329108-1 2006 Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RARalpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 124-132
16329108-4 2006 Expression of CD38 enhanced retinoic acid-induced myeloid differentiation and G0 cell cycle arrest, but at higher expression levels, induced differentiation was blocked and retinoic acid induced a loss of cell viability instead. Tretinoin 28-41 CD38 molecule Homo sapiens 14-18
16329108-4 2006 Expression of CD38 enhanced retinoic acid-induced myeloid differentiation and G0 cell cycle arrest, but at higher expression levels, induced differentiation was blocked and retinoic acid induced a loss of cell viability instead. Tretinoin 173-186 CD38 molecule Homo sapiens 14-18
16329108-6 2006 Expression levels of CD38 thus regulated the cellular response to retinoic acid, either propelling cell differentiation or loss of viability. Tretinoin 66-79 CD38 molecule Homo sapiens 21-25
16482212-2 2006 Recently, we have shown that long-term treatment with all-trans retinoic acid (ATRA), a compound clinically approved for differentiation therapy of acute promyelocytic leukemia (APL), represses hTERT in differentiation-resistant APL cell lines leading to telomere shortening and death. Tretinoin 54-77 telomerase reverse transcriptase Homo sapiens 194-199
16482212-2 2006 Recently, we have shown that long-term treatment with all-trans retinoic acid (ATRA), a compound clinically approved for differentiation therapy of acute promyelocytic leukemia (APL), represses hTERT in differentiation-resistant APL cell lines leading to telomere shortening and death. Tretinoin 79-83 telomerase reverse transcriptase Homo sapiens 194-199
16482212-5 2006 Here, we demonstrate that repression of hTERT occurs in fresh blasts cells from patients with myeloid leukemias of various subtypes exposed ex vivo to ATRA or synthetic retinoids. Tretinoin 151-155 telomerase reverse transcriptase Homo sapiens 40-45
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 CCAAT enhancer binding protein epsilon Homo sapiens 216-254
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 telomerase reverse transcriptase Homo sapiens 329-334
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 MYC proto-oncogene, bHLH transcription factor Homo sapiens 336-341
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 359-407
16569247-0 2006 In vitro and in vivo effects of the PPAR-alpha agonists fenofibrate and retinoic acid in endometrial cancer. Tretinoin 72-85 peroxisome proliferator activated receptor alpha Homo sapiens 36-46
16257998-6 2006 Irradiation also increased the levels of mRNA for IL-6R and gp130, which were blocked by coexisting ATRA. Tretinoin 100-104 interleukin 6 cytokine family signal transducer Homo sapiens 60-65
16757381-3 2006 Two retinoic acid response elements (RAREs) to which retinoid X receptor alpha (RXRalpha) and retinoic acid receptor alpha (RARalpha) bind and activate transcription are present in the human PDK4 (hPDK4) proximal promoter. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 94-122
16757381-3 2006 Two retinoic acid response elements (RAREs) to which retinoid X receptor alpha (RXRalpha) and retinoic acid receptor alpha (RARalpha) bind and activate transcription are present in the human PDK4 (hPDK4) proximal promoter. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 124-132
16530516-0 2006 All-trans retinoic acid induces XAF1 expression through an interferon regulatory factor-1 element in colon cancer. Tretinoin 10-23 interferon regulatory factor 1 Mus musculus 59-89
16530516-2 2006 All-trans retinoic acid (ATRA) exerts an antiproliferative effect on tumor cells through up-regulation of IFN regulatory factor 1 (IRF-1) and the downstream IFN-stimulated genes. Tretinoin 0-23 interferon regulatory factor 1 Mus musculus 106-129
16530516-2 2006 All-trans retinoic acid (ATRA) exerts an antiproliferative effect on tumor cells through up-regulation of IFN regulatory factor 1 (IRF-1) and the downstream IFN-stimulated genes. Tretinoin 0-23 interferon regulatory factor 1 Mus musculus 131-136
16530516-2 2006 All-trans retinoic acid (ATRA) exerts an antiproliferative effect on tumor cells through up-regulation of IFN regulatory factor 1 (IRF-1) and the downstream IFN-stimulated genes. Tretinoin 25-29 interferon regulatory factor 1 Mus musculus 106-129
16530516-2 2006 All-trans retinoic acid (ATRA) exerts an antiproliferative effect on tumor cells through up-regulation of IFN regulatory factor 1 (IRF-1) and the downstream IFN-stimulated genes. Tretinoin 25-29 interferon regulatory factor 1 Mus musculus 131-136
16408307-4 2006 First, we analyzed whether the retinoic acid (RA)-treated hNT neurons and the NT2 precursor cells expressed two transcription factors required for development of the midbrain DA neurons. Tretinoin 31-44 ras responsive element binding protein 1 Homo sapiens 58-61
16408307-4 2006 First, we analyzed whether the retinoic acid (RA)-treated hNT neurons and the NT2 precursor cells expressed two transcription factors required for development of the midbrain DA neurons. Tretinoin 46-48 ras responsive element binding protein 1 Homo sapiens 58-61
16408307-5 2006 We report that NT2 cells endogenously expressed Engrailed-1 and Ptx3, whereas RA-treated hNT neurons did not express Engrailed-1 or Ptx3. Tretinoin 78-80 ras responsive element binding protein 1 Homo sapiens 89-92
16594593-3 2006 To evaluate the correlation between the degree of expression of retinoic acid receptor alpha (RARalpha) mRNA and the antiproliferative effects of all-trans retinoic acid (ATRA) treatments, expression analysis of RARalpha mRNA and cell growth inhibition assay were performed on 17 established canine tumor cell lines, including 6 mammary gland tumor (MGT) cell lines, 3 osteosarcoma cell lines, 5 melanoma cell lines, and 3 mast cell tumor (MCT) cell lines. Tretinoin 64-77 retinoic acid receptor alpha Canis lupus familiaris 94-102
16594593-3 2006 To evaluate the correlation between the degree of expression of retinoic acid receptor alpha (RARalpha) mRNA and the antiproliferative effects of all-trans retinoic acid (ATRA) treatments, expression analysis of RARalpha mRNA and cell growth inhibition assay were performed on 17 established canine tumor cell lines, including 6 mammary gland tumor (MGT) cell lines, 3 osteosarcoma cell lines, 5 melanoma cell lines, and 3 mast cell tumor (MCT) cell lines. Tretinoin 171-175 retinoic acid receptor alpha Canis lupus familiaris 64-92
16594593-3 2006 To evaluate the correlation between the degree of expression of retinoic acid receptor alpha (RARalpha) mRNA and the antiproliferative effects of all-trans retinoic acid (ATRA) treatments, expression analysis of RARalpha mRNA and cell growth inhibition assay were performed on 17 established canine tumor cell lines, including 6 mammary gland tumor (MGT) cell lines, 3 osteosarcoma cell lines, 5 melanoma cell lines, and 3 mast cell tumor (MCT) cell lines. Tretinoin 171-175 retinoic acid receptor alpha Canis lupus familiaris 94-102
16594593-4 2006 Among the cell lines investigated, all 3 MCT cell lines showed high expression of RARalpha, and the most effective cell growth inhibition was observed in ATRA-treated MCT cell lines. Tretinoin 154-158 retinoic acid receptor alpha Canis lupus familiaris 82-90
16594593-5 2006 However, remarkable antiproliferative effects of ATRA treatments were not observed on other tumor cell lines with moderate or low RARalpha mRNA expression. Tretinoin 49-53 retinoic acid receptor alpha Canis lupus familiaris 130-138
16594593-8 2006 These results suggest that ATRA may be an effective antitumor agent for MCT in dogs, and that prior measurement of expression of RARalpha mRNA may be a good indicator of the effectiveness of ATRA treatment. Tretinoin 191-195 retinoic acid receptor alpha Canis lupus familiaris 129-137
16424870-8 2006 We also found that overexpression of wild-type Ski inhibited the prodifferentiating effects of retinoic acid in U937 leukemia cells. Tretinoin 95-108 SKI proto-oncogene Homo sapiens 47-50
16274701-4 2006 Similarly, the increase of Akt activation, as well as PTEN inactivation, was accompanied both by a decrease of CKIepsilon expression induced by all-trans retinoic acid and by the addition of a specific inhibitor for CKIepsilon in HL-60 cells. Tretinoin 154-167 phosphatase and tensin homolog Homo sapiens 54-58
16456540-2 2006 Here we show that during RA-dependent activation of the RARalpha isotype, the p160 coactivator pCIP/ACTR/AIB-1/RAC-3/TRAM-1/SRC-3 is phosphorylated by p38MAPK. Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 56-64
16456540-2 2006 Here we show that during RA-dependent activation of the RARalpha isotype, the p160 coactivator pCIP/ACTR/AIB-1/RAC-3/TRAM-1/SRC-3 is phosphorylated by p38MAPK. Tretinoin 25-27 nuclear receptor coactivator 3 Homo sapiens 105-110
16456540-2 2006 Here we show that during RA-dependent activation of the RARalpha isotype, the p160 coactivator pCIP/ACTR/AIB-1/RAC-3/TRAM-1/SRC-3 is phosphorylated by p38MAPK. Tretinoin 25-27 nuclear receptor coactivator 3 Homo sapiens 124-129
16456540-7 2006 We propose a model in which RARalpha transcriptional activity is regulated by SRC-3 through coordinated events that are fine-tuned by RA and p38MAPK. Tretinoin 28-30 nuclear receptor coactivator 3 Homo sapiens 78-83
16397143-3 2006 All trans-retinoic acid treatment of A404 cells induced a strong increase in LPP, as well as SM alpha-actin, SM myosin heavy chain, and smoothelin mRNA levels, in a Rho kinase (ROK)-dependent manner. Tretinoin 4-23 LOC100738983 Sus scrofa 77-80
16232120-0 2006 Post-translational and transcriptional regulation of DMT1 during P19 embryonic carcinoma cell differentiation by retinoic acid. Tretinoin 113-126 solute carrier family 11 member 2 Homo sapiens 53-57
16232120-1 2006 Studies were performed to determine the regulation of DMT1 (divalent metal transporter 1) during RA (retinoic acid)-induced differentiation of P19 embryonic carcinoma cells. Tretinoin 97-99 solute carrier family 11 member 2 Homo sapiens 54-58
16232120-1 2006 Studies were performed to determine the regulation of DMT1 (divalent metal transporter 1) during RA (retinoic acid)-induced differentiation of P19 embryonic carcinoma cells. Tretinoin 97-99 solute carrier family 11 member 2 Homo sapiens 60-88
16232120-1 2006 Studies were performed to determine the regulation of DMT1 (divalent metal transporter 1) during RA (retinoic acid)-induced differentiation of P19 embryonic carcinoma cells. Tretinoin 101-114 solute carrier family 11 member 2 Homo sapiens 54-58
16232120-1 2006 Studies were performed to determine the regulation of DMT1 (divalent metal transporter 1) during RA (retinoic acid)-induced differentiation of P19 embryonic carcinoma cells. Tretinoin 101-114 solute carrier family 11 member 2 Homo sapiens 60-88
16232120-2 2006 Protein and mRNA expression for the +/-IRE (iron response element) forms of DMT1, but not the 1A isoform, were down-regulated within the first few hours upon removal of RA, at which time the cells began to differentiate. Tretinoin 169-171 solute carrier family 11 member 2 Homo sapiens 76-80
16406622-0 2006 Inhibition of benzo(a)pyrene-induced cell cycle progression by all-trans retinoic acid partly through cyclin D1/E2F-1 pathway in human embryo lung fibroblasts. Tretinoin 73-86 E2F transcription factor 1 Homo sapiens 112-117
16406622-5 2006 There were almost no changes of CDK4 and E2F-4 expression by treatment with B(a)P. As expected, pretreatment with ATRA could efficiently decrease B(a)P-induced overexpression of cyclin D1 and E2F-1. Tretinoin 114-118 E2F transcription factor 1 Homo sapiens 192-197
16406622-8 2006 Pretreatment with ATRA, cells expressing antisense cyclinD1 or antisense CDK4 showed a lesser decrease of B(a)P-induced overexpression of E2F-1 compared with similarly treated HELF. Tretinoin 18-22 E2F transcription factor 1 Homo sapiens 138-143
16406622-10 2006 It was suggested that ATRA could block B(a)P-induced cell cycle promotion partly through the cyclin D1/E2F-1 pathway in HELF. Tretinoin 22-26 E2F transcription factor 1 Homo sapiens 103-108
16322758-4 2006 Notably, an element was characterized in the cyclin-dependent kinase (CDK) inhibitor p19ink4d gene, and 1,25D3- or RA-induced p19INK4D) expression. Tretinoin 115-117 cyclin dependent kinase inhibitor 2D Homo sapiens 126-134
16206244-0 2006 Interaction of PP2A catalytic subunit with Rb2/p130 is required for all-trans retinoic acid suppression of ovarian carcinoma cell growth. Tretinoin 78-91 protein phosphatase 2 catalytic subunit alpha Homo sapiens 15-37
16206244-8 2006 These studies suggest that ATRA treatment suppresses the growth of CAOV3 cells via a novel posttranscriptional mechanism involving PP2A. Tretinoin 27-31 protein phosphatase 2 phosphatase activator Homo sapiens 131-135
16141360-6 2006 In contrast, simultaneous transfection of Ngn2 and HB9 cDNA increased the expression of Isl1/2, a motoneuron marker, when the cells were maintained in medium supplemented with retinoic acid, forskolin, and sonic hedgehog. Tretinoin 176-189 neurogenin 2 Homo sapiens 42-46
16141360-6 2006 In contrast, simultaneous transfection of Ngn2 and HB9 cDNA increased the expression of Isl1/2, a motoneuron marker, when the cells were maintained in medium supplemented with retinoic acid, forskolin, and sonic hedgehog. Tretinoin 176-189 motor neuron and pancreas homeobox 1 Homo sapiens 51-54
16141360-6 2006 In contrast, simultaneous transfection of Ngn2 and HB9 cDNA increased the expression of Isl1/2, a motoneuron marker, when the cells were maintained in medium supplemented with retinoic acid, forskolin, and sonic hedgehog. Tretinoin 176-189 ISL LIM homeobox 1 Homo sapiens 88-94
16158052-4 2006 RA receptor (RAR) agonist (4-(E-2-[5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl]-1-propenyl) benzoic acid) and RAR/retinoid X receptor (RXR) agonist (9-cis-RA) promote expression of TGase, migration and invasion of SH-SY5Y cells, while RXR agonist has no significant effect. Tretinoin 159-167 retinoic acid receptor alpha Homo sapiens 0-11
16158052-4 2006 RA receptor (RAR) agonist (4-(E-2-[5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl]-1-propenyl) benzoic acid) and RAR/retinoid X receptor (RXR) agonist (9-cis-RA) promote expression of TGase, migration and invasion of SH-SY5Y cells, while RXR agonist has no significant effect. Tretinoin 159-167 retinoic acid receptor alpha Homo sapiens 13-16
16111716-0 2006 Milk growth factor (MGF) induces transformation into ATDC5 cells, prechondrocytes, and cooperates with retinoic acid to transform the cells into new forms. Tretinoin 103-116 kit ligand Mus musculus 0-18
16111716-0 2006 Milk growth factor (MGF) induces transformation into ATDC5 cells, prechondrocytes, and cooperates with retinoic acid to transform the cells into new forms. Tretinoin 103-116 kit ligand Mus musculus 20-23
16399080-4 2006 We can partially rescue one salient feature of DGS in Crkl+/-;Tbx1+/- embryos by genetically reducing the amount of RA produced in the embryo. Tretinoin 116-118 v-crk avian sarcoma virus CT10 oncogene homolog-like Mus musculus 54-58
16399080-4 2006 We can partially rescue one salient feature of DGS in Crkl+/-;Tbx1+/- embryos by genetically reducing the amount of RA produced in the embryo. Tretinoin 116-118 T-box 1 Mus musculus 62-66
16195406-7 2006 Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do not respond to BMP-4. Tretinoin 8-21 SMAD family member 4 Mus musculus 117-123
15778294-3 2005 Here, we show that Sonic hedgehog (Shh) and retinoic acid (RA), signaling molecules secreted from tissues in the vicinity of peripheral sensory ganglia during embryogenesis, exert synergistic effects on neural-competent MSCs to express a comprehensive set of glutamatergic sensory neuron markers. Tretinoin 59-61 sonic hedgehog signaling molecule Homo sapiens 19-33
15800190-7 2005 Chromatin immunoprecipitation assay demonstrated RA induced replacement of the c-Myc/Max complex with the Max/Mad1 complex on the E box located within nucleosome N1, coinciding with reduced Sp1 binding to GC boxes located within nucleosome N2 and recruitment of chromatin remodeling factor Brahma-related gene 1 (BRG-1) to this promoter. Tretinoin 49-51 MAX dimerization protein 1 Mus musculus 110-114
15688037-1 2005 The acute promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) fusion product recruits histone deacetylase (HDAC) and DNA methyltransferase (DNMT) activities on retinoic acid (RA)-target promoters causing their silencing and differentiation block. Tretinoin 39-52 retinoic acid receptor alpha Homo sapiens 69-77
15592517-5 2005 Following treatment with 10 muM RA for 6 days, the MYCN-amplified IGR-N-91 cell lines underwent neuronal differentiation as assessed by reduced MYCN gene expression and neuritic extension. Tretinoin 32-34 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 51-55
15592517-5 2005 Following treatment with 10 muM RA for 6 days, the MYCN-amplified IGR-N-91 cell lines underwent neuronal differentiation as assessed by reduced MYCN gene expression and neuritic extension. Tretinoin 32-34 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 144-148
15572023-0 2005 Nuclear CD38 in retinoic acid-induced HL-60 cells. Tretinoin 16-29 CD38 molecule Homo sapiens 8-12
15572023-3 2005 All-trans-retinoic acid (RA) is a potent and specific inducer of CD38 in myeloid cells. Tretinoin 0-23 CD38 molecule Homo sapiens 65-69
15572023-3 2005 All-trans-retinoic acid (RA) is a potent and specific inducer of CD38 in myeloid cells. Tretinoin 25-27 CD38 molecule Homo sapiens 65-69
15572023-4 2005 In this report, we demonstrate that the nuclei of RA-treated human HL-60 myeloblastic cells reveal enzymatic activities inherent to CD38. Tretinoin 50-52 CD38 molecule Homo sapiens 132-136
15572023-6 2005 With Western blotting, we detected in the nuclear protein fraction from RA-treated cells a approximately 43-kDa protein band which was reactive with the CD38-specific monoclonal antibody OKT10. Tretinoin 72-74 CD38 molecule Homo sapiens 153-157
15661642-3 2005 cDNA transfection assays showed that like human cyp26b1, zebrafish cyp26b1 is involved in limiting the activity of retinoic acid. Tretinoin 115-128 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 67-74
16448778-0 2006 Insulin-like growth factor I and II expression and modulation in amoeboid microglial cells by lipopolysaccharide and retinoic acid. Tretinoin 117-130 insulin-like growth factor 1 Rattus norvegicus 0-28
31291979-3 2019 When hypomethylated, ATRA-inducible TERT repressors can bind the promoter, repressing transcription of TERT, the rate-limiting component of telomerase. Tretinoin 21-25 telomerase reverse transcriptase Homo sapiens 36-40
31291979-3 2019 When hypomethylated, ATRA-inducible TERT repressors can bind the promoter, repressing transcription of TERT, the rate-limiting component of telomerase. Tretinoin 21-25 telomerase reverse transcriptase Homo sapiens 103-107
16309824-5 2005 The retinoic acid receptor (RAR)alpha agonist Ro 4060-55 but not the pan-retinoid X receptors (RXRs) agonist Ro 2573-86 mimicked the effects of atRA on LBP expression suggesting that atRA enhances LBP expression through a RARalpha-mediated pathway. Tretinoin 144-148 retinoic acid receptor, alpha Rattus norvegicus 28-31
31291979-6 2019 Our aim was to investigate the potential role of ATRA as an anticancer drug in a sub-group of ovarian carcinoma where the TERT promoter was hypomethylated. Tretinoin 49-53 telomerase reverse transcriptase Homo sapiens 122-126
31291979-7 2019 METHODS: The potential antiproliferative and cytotoxic effect of ATRA was investigated in seven serous ovarian carcinoma and one teratocarcinoma cell lines and the results were compared to the methylation status of their TERT promoter. Tretinoin 65-69 telomerase reverse transcriptase Homo sapiens 221-225
16309824-7 2005 In sharp contrast to our previous observations that atRA supplementation enhances IFN-gamma expression and NOS2 pathway activation in LPS-challenged rats [Devaux, Y., Grosjean, S., Seguin, C., David, C., Dousset, B., Zannad, F., Meistelman, C., de Talance, N., Mertes, P.M., Ungureanu-Longrois, D., 2000. Tretinoin 52-56 interferon gamma Rattus norvegicus 82-91
31291979-11 2019 CONCLUSIONS: Our results demonstrate an inverse correlation between the methylation level of TERT promoter and ATRA efficacy in ovarian carcinoma cell lines. Tretinoin 111-115 telomerase reverse transcriptase Homo sapiens 93-97
31291979-12 2019 Although these results are preliminary, ATRA treatment could become a new powerful, personalized therapy in serous ovarian carcinoma patients, but only in those with tumors harboring a hypomethylated TERT promoter. Tretinoin 40-44 telomerase reverse transcriptase Homo sapiens 200-204
31299141-5 2019 Recent work from our laboratory indicates that the E3 ubiquitin ligase Hectd1 is required for full activation of retinoic acid signaling during cardiac development. Tretinoin 113-126 HECT domain E3 ubiquitin protein ligase 1 Homo sapiens 71-77
16375665-5 2005 This PML-RAR alpha fusion protein is responsible for the proliferative and de-differentiated phenotype of the leukemic cells and is the target of all-trans retinoic acid (ATRA). Tretinoin 156-169 PML nuclear body scaffold Homo sapiens 5-8
16375665-5 2005 This PML-RAR alpha fusion protein is responsible for the proliferative and de-differentiated phenotype of the leukemic cells and is the target of all-trans retinoic acid (ATRA). Tretinoin 171-175 PML nuclear body scaffold Homo sapiens 5-8
16126938-8 2005 The NR ligands, vitamin D(3), trans/cis RA, glucocorticoids, and thiazolidines, induce dramatic changes in the physiology of cells harboring high Wnt/beta-catenin/Tcf activity. Tretinoin 40-42 catenin beta 1 Homo sapiens 150-162
31053627-3 2019 We showed that dendritic cells (DCs), engineered to de novo produce high concentrations of both 1,25-dihydroxyvitamin D, the active vitamin D metabolite, and retinoic acid, an active vitamin A metabolite, augmented the induction of T cells that express both the regulatory molecule Foxp3 and the gut-homing receptor CCR9 in vitro and in vivo. Tretinoin 158-171 forkhead box P3 Mus musculus 282-287
16126301-4 2005 In this work, we describe for the first time that Brn-3a is phosphorylated in IMR-32 neuroblastoma cells in response to differentiation induced by retinoic acid treatment and that its post-translational modification is potentially mediated by the activation of the MAPK/ERK pathway. Tretinoin 147-160 POU class 4 homeobox 1 Homo sapiens 50-56
30760649-5 2019 Retinoic acid significantly reduced the mRNA transcript levels of apoptosis-related genes, including BAX and P53, and reduced the BAX/BCL2 ratio. Tretinoin 0-13 apoptosis regulator BAX Camelus dromedarius 101-104
16053444-0 2005 Transcriptional co-operativity between distant retinoic acid response elements in regulation of Cyp26A1 inducibility. Tretinoin 47-60 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 96-103
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 19-21 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 19-21 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 51-54
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 19-21 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 56-71
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 23-36 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
30760649-5 2019 Retinoic acid significantly reduced the mRNA transcript levels of apoptosis-related genes, including BAX and P53, and reduced the BAX/BCL2 ratio. Tretinoin 0-13 apoptosis regulator BAX Camelus dromedarius 130-133
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 23-36 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 51-54
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 23-36 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 56-71
31024166-8 2019 Strikingly, we demonstrate that the combination of ATRA and ATO proves to be a powerfully synergistic and effective therapy in a number of mouse and human mIDH1/2 leukemic models. Tretinoin 51-55 isocitrate dehydrogenase 1 (NADP+), soluble Mus musculus 155-162
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 122-124 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 122-124 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 51-54
16053444-1 2005 Cyp26A1 encodes an RA (retinoic acid)-catabolizing CYP (cytochrome P450) protein that plays a critical role in regulating RA distribution in vivo. Tretinoin 122-124 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 56-71
16053444-2 2005 Cyp26A1 expression is inducible by RA, and the locus has previously been shown to contain a RARE (RA response element), R1, within the minimal promoter [Loudig, Babichuk, White, Abu-Abed, Mueller and Petkovich (2000) Mol. Tretinoin 35-37 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
31186810-5 2019 Following induced differentiation of U87 glioblastoma cells with all-trans retinoic acid, the expression levels of NSPc1 decreased initially, reaching its lowest point on day 6, but then subsequently increased until day 10. Tretinoin 75-88 polycomb group ring finger 1 Homo sapiens 115-120
31135261-7 2019 These results suggest that PML-RARalpha initiates ATRA-induced transcription through its interaction with MED1. Tretinoin 50-54 PML nuclear body scaffold Homo sapiens 27-30
31072004-4 2019 Using genetic and experimental approaches in the mouse, we show that during development of ontogenetically different organs, including the tail, genital tubercle, and secondary palate, Sonic hedgehog (SHH) loss-of-function causes anomalies phenocopying those induced by enhanced retinoic acid signaling and that SHH is required to prevent supraphysiological activation of retinoic signaling through maintenance and reinforcement of expression of the Cyp26 genes. Tretinoin 279-292 sonic hedgehog Mus musculus 185-199
16094422-7 2005 Overexpression of LYL1 in U937 cells blocked all-trans retinoic acid-induced monocytic differentiation. Tretinoin 55-68 LYL1 basic helix-loop-helix family member Homo sapiens 18-22
16392701-9 2005 Bone Gla protein mRNA expression was inhibited by 10 and 100 nM 9-cis RA and by 100 nM ATRA on day 14. Tretinoin 87-91 bone gamma carboxyglutamate protein Mus musculus 0-16
31072004-4 2019 Using genetic and experimental approaches in the mouse, we show that during development of ontogenetically different organs, including the tail, genital tubercle, and secondary palate, Sonic hedgehog (SHH) loss-of-function causes anomalies phenocopying those induced by enhanced retinoic acid signaling and that SHH is required to prevent supraphysiological activation of retinoic signaling through maintenance and reinforcement of expression of the Cyp26 genes. Tretinoin 279-292 sonic hedgehog Mus musculus 201-204
31059511-2 2019 Stimulated by retinoic acid gene 8 (Stra8) is an essential gatekeeper of meiotic initiation in vertebrates; yet, the molecular role of STRA8 remains principally unknown. Tretinoin 14-27 stimulated by retinoic acid gene 8 Mus musculus 36-41
16166294-0 2005 Suppression of mammary carcinoma growth by retinoic acid: proapoptotic genes are targets for retinoic acid receptor and cellular retinoic acid-binding protein II signaling. Tretinoin 43-56 retinoic acid receptor alpha Homo sapiens 93-115
16166294-5 2005 Accordingly, expression array analyses revealed that RA induces the expression of several proapoptotic genes, including caspase 7 and caspase 9. Tretinoin 53-55 caspase 7 Homo sapiens 120-129
16166294-5 2005 Accordingly, expression array analyses revealed that RA induces the expression of several proapoptotic genes, including caspase 7 and caspase 9. Tretinoin 53-55 caspase 9 Homo sapiens 134-143
16166294-6 2005 Whereas caspase 7 is an indirect responder to RA signaling, caspase 9 is a novel direct target for RAR, and it harbors a functional retinoic acid response element in its second intron. Tretinoin 46-48 caspase 7 Homo sapiens 8-17
16166294-6 2005 Whereas caspase 7 is an indirect responder to RA signaling, caspase 9 is a novel direct target for RAR, and it harbors a functional retinoic acid response element in its second intron. Tretinoin 132-145 caspase 9 Homo sapiens 60-69
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 37-39 retinoic acid receptor alpha Homo sapiens 90-93
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 37-39 caspase 9 Homo sapiens 153-162
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 37-39 caspase 7 Homo sapiens 202-211
31059511-2 2019 Stimulated by retinoic acid gene 8 (Stra8) is an essential gatekeeper of meiotic initiation in vertebrates; yet, the molecular role of STRA8 remains principally unknown. Tretinoin 14-27 stimulated by retinoic acid gene 8 Mus musculus 135-140
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 90-92 caspase 9 Homo sapiens 153-162
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 90-92 caspase 7 Homo sapiens 202-211
30862546-4 2019 HL-60 cell differentiation with dimethyl sulfoxide caused a large decrease in expression of both Prxs, and all-trans retinoic acid also decreased Prx1 expression. Tretinoin 117-130 peroxiredoxin 1 Homo sapiens 146-150
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 90-92 caspase 9 Homo sapiens 153-162
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 90-92 caspase 7 Homo sapiens 202-211
16166294-9 2005 Specifically, overexpression of CRABP-II, in the absence of RA, up-regulated the expression of Apaf1 and triggered caspase 7 and caspase 9 cleavage. Tretinoin 33-35 caspase 7 Homo sapiens 115-124
16166294-9 2005 Specifically, overexpression of CRABP-II, in the absence of RA, up-regulated the expression of Apaf1 and triggered caspase 7 and caspase 9 cleavage. Tretinoin 33-35 caspase 9 Homo sapiens 129-138
15839205-0 2005 [Different impacts of DMSO and RA on GPI-80 expression]. Tretinoin 31-33 vanin 2 Homo sapiens 37-43
15839205-4 2005 RT-PCR, flow cytometry and western-blot assays were used to detect the GPI-80 expression on HL-60 cells induced by DMSO or RA and to analyze the relationship between GPI-80 expression and CD11b or transferrin receptor (CD71) expression. Tretinoin 123-125 vanin 2 Homo sapiens 71-77
30710527-9 2019 Treg cells from patients with CD incubated with rapamycin and an agonist of RARA (RAR568) expressed high levels of integrin alpha4beta7, as well as CD62L and FOXP3, compared with cells incubated with rapamycin or rapamycin and all-trans retinoic acid. Tretinoin 237-250 retinoic acid receptor alpha Homo sapiens 76-80
15748426-4 2005 The ability of ATRA to modify the recruitment of nuclear receptor co-repressor with PML-RAR alpha but not PLZF-RAR alpha caused by the variant chromosome translocation elucidated the therapeutic mechanism of ATRA from the molecular level and provides new insight into transcription-modulating therapy. Tretinoin 15-19 PML nuclear body scaffold Homo sapiens 84-87
16109390-5 2005 Mice absent in the three proteins CRBP I, CRABP I, and CRABP II (CI/CAI/CAII-/-) displayed significantly lower hepatic retinyl ester, retinol, and all-trans-retinoic acid levels compared to wildtype mice, whereas the liver concentrations of 9-cis-4-oxo-13,14-dihydro-retinoic acid was considerably higher. Tretinoin 151-170 retinol binding protein 1, cellular Mus musculus 34-40
16350840-7 2005 In this system, RA upregulates the mRNA level of Runx2/Cbfa1 (type II), a positive regulator for mineralization, and downregulates the mRNA of Indian hedgehog (Ihh), parathyroid hormone related protein (PTHrP), negative regulators for terminal differentiation. Tretinoin 16-18 runt related transcription factor 2 Mus musculus 49-54
16350840-7 2005 In this system, RA upregulates the mRNA level of Runx2/Cbfa1 (type II), a positive regulator for mineralization, and downregulates the mRNA of Indian hedgehog (Ihh), parathyroid hormone related protein (PTHrP), negative regulators for terminal differentiation. Tretinoin 16-18 runt related transcription factor 2 Mus musculus 55-60
15695403-3 2005 RA induces cell accumulation in G(0)-G(1) together with a marked up-regulation of p27(Kip1) by inhibiting ubiquitination and proteasome-dependent degradation of the protein. Tretinoin 0-2 interferon alpha inducible protein 27 Homo sapiens 82-85
31083206-14 2019 LESSONS: Both STAT5b-RARalpha-positive APL and PLZF-RARalpha-positive APL appear to be resistant to both ATRA and ATO, so combined chemotherapy and allo-HSCT should be considered. Tretinoin 105-109 retinoic acid receptor alpha Homo sapiens 52-60
15695403-3 2005 RA induces cell accumulation in G(0)-G(1) together with a marked up-regulation of p27(Kip1) by inhibiting ubiquitination and proteasome-dependent degradation of the protein. Tretinoin 0-2 cyclin dependent kinase inhibitor 1B Homo sapiens 86-90
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 8-10 interferon alpha inducible protein 27 Homo sapiens 19-22
16479313-0 2005 Effects of high dose retinoic acid on TGF-beta2 expression during pancreatic organogenesis. Tretinoin 21-34 transforming growth factor, beta 2 Rattus norvegicus 38-47
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 8-10 cyclin dependent kinase inhibitor 1B Homo sapiens 23-27
30824184-1 2019 Genetic mutations on PML-RARalpha in acute promyelocytic leukemia (APL) are reported to associate with arsenic trioxide (ATO) or all-trans retinoic acid (ATRA) resistance. Tretinoin 139-152 PML nuclear body scaffold Homo sapiens 21-24
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 210-212 interferon alpha inducible protein 27 Homo sapiens 19-22
15695403-5 2005 Most of RA-induced p27(Kip1) was bound to cyclin D1/cyclin-dependent kinase 4 complexes, probably contributing to the decreased cyclin-dependent kinase 4 kinase activity and pRb hypophosphorylation observed in RA-treated cells. Tretinoin 210-212 cyclin dependent kinase inhibitor 1B Homo sapiens 23-27
16038477-10 2005 Stavudine caused a specific induction of UCP1 gene expression through direct interaction with a retinoic acid-dependent pathway. Tretinoin 96-109 uncoupling protein 1 Homo sapiens 41-45
16479313-1 2005 The aim of this study was to investigate the effects of excess all-trans retinoic acid, a vitamin A metabolite, on pancreatic organogenesis and TGF-beta2 expression during prenatal development in rats. Tretinoin 73-86 transforming growth factor, beta 2 Rattus norvegicus 144-153
16479313-8 2005 In view of the present findings we suggest that TGF-beta2 plays important role in pancreatic morphogenesis and administration of excess all-trans retinoic acid before neurulation inhibit TGF-beta2 expression disrupted pancreatic morphogenesis particularly Langerhans islets. Tretinoin 146-159 transforming growth factor, beta 2 Rattus norvegicus 187-196
16054184-11 2005 The observed ubiquitous tissue distribution, as well as the expression of CYP2S1 throughout embryogenesis suggest that CYP2S1 is likely to metabolize important endogenous substrates; thus far, retinoic acid has been identified. Tretinoin 193-206 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 119-125
15897880-4 2005 Several genes like RARRES1, RARRES3, CTGF, CKS2, CCNA2, IGFBP3, UBE2C, CCL2 or ITM2B that were previously found to be deregulated in advanced tumors exhibited opposite expression changes after ATRA treatment. Tretinoin 193-197 insulin like growth factor binding protein 3 Homo sapiens 56-62
15897880-4 2005 Several genes like RARRES1, RARRES3, CTGF, CKS2, CCNA2, IGFBP3, UBE2C, CCL2 or ITM2B that were previously found to be deregulated in advanced tumors exhibited opposite expression changes after ATRA treatment. Tretinoin 193-197 integral membrane protein 2B Homo sapiens 79-84
30824184-1 2019 Genetic mutations on PML-RARalpha in acute promyelocytic leukemia (APL) are reported to associate with arsenic trioxide (ATO) or all-trans retinoic acid (ATRA) resistance. Tretinoin 139-152 retinoic acid receptor alpha Homo sapiens 25-33
16010410-12 2005 All-trans-retinoic acid was demonstrated in PC-3 to up-regulate LGR8 gene activity in a dose- and time-dependent manner while having no effect on INSL3 gene activity. Tretinoin 0-23 chromobox 8 Homo sapiens 44-48
16010410-12 2005 All-trans-retinoic acid was demonstrated in PC-3 to up-regulate LGR8 gene activity in a dose- and time-dependent manner while having no effect on INSL3 gene activity. Tretinoin 0-23 relaxin family peptide receptor 2 Homo sapiens 64-68
15733733-9 2005 The present review focuses on the regulation of glyceroneogenesis and of PEPCK-C gene expression and activity by FAs, retinoic acids, glucocorticoids and the hypolipidemic class of drugs, thiazolidinediones. Tretinoin 118-132 phosphoenolpyruvate carboxykinase 1 Homo sapiens 73-80
30824184-1 2019 Genetic mutations on PML-RARalpha in acute promyelocytic leukemia (APL) are reported to associate with arsenic trioxide (ATO) or all-trans retinoic acid (ATRA) resistance. Tretinoin 154-158 PML nuclear body scaffold Homo sapiens 21-24
30824184-1 2019 Genetic mutations on PML-RARalpha in acute promyelocytic leukemia (APL) are reported to associate with arsenic trioxide (ATO) or all-trans retinoic acid (ATRA) resistance. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 25-33
30824184-2 2019 Here we performed a retrospective analysis of APL patients and identified that the patient with S214L mutation on the PML moiety of PML-RARalpha showed resistance to both ATO and ATRA. Tretinoin 179-183 PML nuclear body scaffold Homo sapiens 118-121
30824184-2 2019 Here we performed a retrospective analysis of APL patients and identified that the patient with S214L mutation on the PML moiety of PML-RARalpha showed resistance to both ATO and ATRA. Tretinoin 179-183 PML nuclear body scaffold Homo sapiens 132-135
15946654-6 2005 We showed that both MMP-1 and MMP-13 mRNA expression, protein production and enzyme activity induced by either IL-1 or TNF-alpha were suppressed by t-RA or different retinoid derivatives. Tretinoin 148-152 matrix metallopeptidase 1 Homo sapiens 20-25
15668483-7 2005 The effects of retinoic acid and sodium butyrate on the CD97/CD55 expression in OSCC cell lines were determined by quantitative PCR, immunocytochemistry, and flow cytometry. Tretinoin 15-28 adhesion G protein-coupled receptor E5 Homo sapiens 56-60
30824184-2 2019 Here we performed a retrospective analysis of APL patients and identified that the patient with S214L mutation on the PML moiety of PML-RARalpha showed resistance to both ATO and ATRA. Tretinoin 179-183 retinoic acid receptor alpha Homo sapiens 136-144
15668483-14 2005 Sodium butyrate and retinoic acid inhibited CD97 mRNA and protein in OSCC cell lines. Tretinoin 20-33 adhesion G protein-coupled receptor E5 Homo sapiens 44-48
31019453-2 2019 Our data demonstrate that Drp1 regulates the transcriptional program induced by retinoic acid (RA), leading to neuronal differentiation. Tretinoin 80-93 dynamin 1 like Homo sapiens 26-30
15717686-6 2005 In contrast, the expression of PU.1, a transcription factor reportedly involved in the basal expression of p67phox in monocytic cells, was only slightly up-regulated by DHEA and ATRA. Tretinoin 178-182 Spi-1 proto-oncogene Homo sapiens 31-35
15850806-11 2005 Deletion and mutation of the DR5, but not the IR6 element, abolished the atRA-mediated activity. Tretinoin 73-77 TNF receptor superfamily member 10b Homo sapiens 29-32
15850806-13 2005 In addition to the functional DR5, the region contains many other potential sequence elements that are required to maximize the atRA-mediated induction. Tretinoin 128-132 TNF receptor superfamily member 10b Homo sapiens 30-33
15583048-11 2005 These results indicate that retinoic acid inhibits porcine preadipocyte differentiation by a mechanism that involves activation of the RAR and downregulation of PPARgamma, RXRalpha, and SREBP-1C mRNA. Tretinoin 28-41 peroxisome proliferator activated receptor gamma Sus scrofa 161-170
31019453-2 2019 Our data demonstrate that Drp1 regulates the transcriptional program induced by retinoic acid (RA), leading to neuronal differentiation. Tretinoin 95-97 dynamin 1 like Homo sapiens 26-30
15583048-11 2005 These results indicate that retinoic acid inhibits porcine preadipocyte differentiation by a mechanism that involves activation of the RAR and downregulation of PPARgamma, RXRalpha, and SREBP-1C mRNA. Tretinoin 28-41 retinoid X receptor alpha Sus scrofa 172-180
15769996-1 2005 IGF binding protein (IGFBP)-3, the principal carrier of IGFs in the circulation, contributes to both endocrine and autocrine/paracrine growth control; it can be induced by GH, cytokines, retinoic acid, and tumor suppressors. Tretinoin 187-200 insulin like growth factor binding protein 3 Homo sapiens 0-29
30322324-0 2019 An analysis of the impact of CD56 expression in de novo acute promyelocytic leukemia patients treated with upfront all-trans retinoic acid and anthracycline-based regimens. Tretinoin 115-138 neural cell adhesion molecule 1 Homo sapiens 29-33
16092758-1 2005 Restin, a member of melanoma-associated antigen superfamily gene, was first cloned from differentiated leukemia cell induced by all trans-retinoic acid, and was able to inhibit cell proliferation, but the molecular mechanism was not clear. Tretinoin 132-151 ankyrin repeat domain 36B Homo sapiens 20-47
17142856-6 2005 Retinoic acids bind to the retinoic acid receptor (RAR alpha) component of the fusion product, resulting in degradation of the fusion protein by ubiquitinization. Tretinoin 0-14 retinoic acid receptor alpha Homo sapiens 51-60
15597047-3 2004 Injections of all-trans RA suppressed the expression of dorsal signals Tbx5, BMP4 and to a lesser extent of ephrinB1, whereas the injection of citral, an inhibitor of RA synthesis, enhanced the expression of BMP4 and Tbx5. Tretinoin 24-26 T-box 5 Gallus gallus 71-75
15589822-0 2004 c-Myc-mediated expression of nucleophosmin/B23 decreases during retinoic acid-induced differentiation of human leukemia HL-60 cells. Tretinoin 64-77 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
15949693-1 2005 Retinoic acid (RA) administration and chronic vitamin A supplementation were reported to inhibit adipose tissue leptin expression in rodents, but the impact of this effect on food intake and its relationship with changes of body adiposity was not analyzed. Tretinoin 0-13 WD and tetratricopeptide repeats 1 Mus musculus 97-104
15949693-1 2005 Retinoic acid (RA) administration and chronic vitamin A supplementation were reported to inhibit adipose tissue leptin expression in rodents, but the impact of this effect on food intake and its relationship with changes of body adiposity was not analyzed. Tretinoin 0-13 leptin Mus musculus 112-118
15949693-1 2005 Retinoic acid (RA) administration and chronic vitamin A supplementation were reported to inhibit adipose tissue leptin expression in rodents, but the impact of this effect on food intake and its relationship with changes of body adiposity was not analyzed. Tretinoin 15-17 WD and tetratricopeptide repeats 1 Mus musculus 97-104
15949693-1 2005 Retinoic acid (RA) administration and chronic vitamin A supplementation were reported to inhibit adipose tissue leptin expression in rodents, but the impact of this effect on food intake and its relationship with changes of body adiposity was not analyzed. Tretinoin 15-17 leptin Mus musculus 112-118
15949693-4 2005 They also demonstrate a direct inhibitory effect of RA on leptin expression in both white and brown adipocyte cell cultures, and constitute first proof of the involvement of both RA receptors (RARs) and rexinoid receptors (RXRs) in this effect. Tretinoin 52-54 leptin Mus musculus 58-64
15589822-1 2004 The retinoic acid-induced differentiation of human leukemia HL-60 cells towards mature granulocytic cells was accompanied by the decline in the protein levels of c-myc, nucleophosmin/B23 and its promoter activity. Tretinoin 4-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167
30674471-8 2019 Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication. Tretinoin 31-35 transformation related protein 53, pseudogene Mus musculus 163-166
15319284-2 2004 Acute promyelocytic leukemia (APL) is characterized by a translocation, t(15;17), that produces a PML/RARalpha fusion oncoprotein, whose abnormal transcriptional function is successfully targeted by pharmacologic levels of all-trans-retinoic acid (ATRA). Tretinoin 226-246 PML nuclear body scaffold Homo sapiens 98-101
30894514-6 2019 We demonstrate that resveratrol interferes with the reprogramming of the retinoic acid signaling pathway in decidualizing HESCs by accelerating down-regulation of cellular retinoic acid-binding protein 2 (CRABP2) and retinoic acid receptor (RAR). Tretinoin 73-86 retinoic acid receptor alpha Homo sapiens 217-239
15319284-2 2004 Acute promyelocytic leukemia (APL) is characterized by a translocation, t(15;17), that produces a PML/RARalpha fusion oncoprotein, whose abnormal transcriptional function is successfully targeted by pharmacologic levels of all-trans-retinoic acid (ATRA). Tretinoin 226-246 retinoic acid receptor alpha Homo sapiens 102-110
15319284-2 2004 Acute promyelocytic leukemia (APL) is characterized by a translocation, t(15;17), that produces a PML/RARalpha fusion oncoprotein, whose abnormal transcriptional function is successfully targeted by pharmacologic levels of all-trans-retinoic acid (ATRA). Tretinoin 248-252 PML nuclear body scaffold Homo sapiens 98-101
15319284-2 2004 Acute promyelocytic leukemia (APL) is characterized by a translocation, t(15;17), that produces a PML/RARalpha fusion oncoprotein, whose abnormal transcriptional function is successfully targeted by pharmacologic levels of all-trans-retinoic acid (ATRA). Tretinoin 248-252 retinoic acid receptor alpha Homo sapiens 102-110
15319284-7 2004 This effect may not be limited to abnormal nuclear receptors, because overexpression of SMRTbeta increased ATRA-induced binding and transcriptional activation of wild-type receptors PML/RARalpha and RARalpha. Tretinoin 107-111 PML nuclear body scaffold Homo sapiens 182-185
15319284-7 2004 This effect may not be limited to abnormal nuclear receptors, because overexpression of SMRTbeta increased ATRA-induced binding and transcriptional activation of wild-type receptors PML/RARalpha and RARalpha. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 186-194
15319284-7 2004 This effect may not be limited to abnormal nuclear receptors, because overexpression of SMRTbeta increased ATRA-induced binding and transcriptional activation of wild-type receptors PML/RARalpha and RARalpha. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 199-207
16185481-1 2005 OBJECTIVE: To investigate the role of Mcl-1 gene in resistance of all-trans retinoic acid (ATRA) of leukemia cells. Tretinoin 76-89 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 38-43
16185481-1 2005 OBJECTIVE: To investigate the role of Mcl-1 gene in resistance of all-trans retinoic acid (ATRA) of leukemia cells. Tretinoin 91-95 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 38-43
16185481-6 2005 RESULTS: The HL-60/ATRA could keep its undifferentiated and proliferative status to a high concentration of ATRA (100 nmol/L) with highly expressed Mcl-1 protein (relative grey scale 0.624 +/- 0.127). Tretinoin 19-23 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 148-153
15910691-10 2005 CONCLUSION: The data show that RARalpha regulates MDR1/ Pgp activity in human leukemic cells, in the first place, Pgp activity induced by ATRA. Tretinoin 138-142 retinoic acid receptor alpha Homo sapiens 31-39
30894514-6 2019 We demonstrate that resveratrol interferes with the reprogramming of the retinoic acid signaling pathway in decidualizing HESCs by accelerating down-regulation of cellular retinoic acid-binding protein 2 (CRABP2) and retinoic acid receptor (RAR). Tretinoin 73-86 retinoic acid receptor alpha Homo sapiens 241-244
30806631-8 2019 Moreover, the treatment of MDA-MB-231 cells with triorganotin compounds together with ATRA resulted in an additional reduction of annexin 5, vimentin and nucleoside diphosphate kinase B. Tretinoin 86-90 annexin A5 Homo sapiens 130-139
15866332-6 2005 Since Nano-atRA which is prepared following to this new DDS system developmentally improved the permeability to the stratum corneum, the remarkable pharmacological effects were resulted in comparison with atRA as such as follows: (1) thicker epidermis than classical atRA treatment and (2) the overexpression of mRNA for heparin-binding epidermal growth factor (HB-EGF) as the provocation epidermal hyperplasia. Tretinoin 11-15 heparin binding EGF like growth factor Homo sapiens 362-368
15604289-0 2004 Vdelta1 T lymphocytes from B-CLL patients recognize ULBP3 expressed on leukemic B cells and up-regulated by trans-retinoic acid. Tretinoin 108-127 UL16 binding protein 3 Homo sapiens 52-57
15604289-7 2004 More importantly, they also lysed autologous B-CLL cells when transcription and expression of MIC-A or up-regulation of ULBP3 were achieved either by activation or by exposure to trans-retinoic acid. Tretinoin 179-198 UL16 binding protein 3 Homo sapiens 120-125
15623634-6 2004 We also investigated the regulation of AP-2gamma by steroids and retinoic acid. Tretinoin 65-78 transcription factor AP-2 gamma Homo sapiens 39-48
15855632-0 2005 Implication of Wt1 in the pathogenesis of nephrogenic failure in a mouse model of retinoic acid-induced caudal regression syndrome. Tretinoin 82-95 WT1 transcription factor Mus musculus 15-18
15855632-7 2005 Wt1 expression and organogenesis were both restored, however, when metanephroi from retinoic acid-treated pregnancies were grown in serum-containing media. Tretinoin 84-97 WT1 transcription factor Mus musculus 0-3
16187701-1 2005 The results of the treatment of 14 patients with promyelocytic leukemia (PML) treated with all trans-retinoic acid (ATRA), combined chemotherapy (CT) and prophylactic prednisone are reported; the median age was 30 years (range 7 - 49). Tretinoin 95-114 PML nuclear body scaffold Homo sapiens 73-76
15623634-8 2004 We found that AP-2gamma expression was regulated by retinoic acid in an embryonal carcinoma cell line (NT2). Tretinoin 52-65 transcription factor AP-2 gamma Homo sapiens 14-23
30806631-8 2019 Moreover, the treatment of MDA-MB-231 cells with triorganotin compounds together with ATRA resulted in an additional reduction of annexin 5, vimentin and nucleoside diphosphate kinase B. Tretinoin 86-90 vimentin Homo sapiens 141-149
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 insulin receptor substrate 1 Homo sapiens 95-100
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 insulin receptor substrate 1 Homo sapiens 95-100
16187701-1 2005 The results of the treatment of 14 patients with promyelocytic leukemia (PML) treated with all trans-retinoic acid (ATRA), combined chemotherapy (CT) and prophylactic prednisone are reported; the median age was 30 years (range 7 - 49). Tretinoin 116-120 PML nuclear body scaffold Homo sapiens 49-71
16187701-1 2005 The results of the treatment of 14 patients with promyelocytic leukemia (PML) treated with all trans-retinoic acid (ATRA), combined chemotherapy (CT) and prophylactic prednisone are reported; the median age was 30 years (range 7 - 49). Tretinoin 116-120 PML nuclear body scaffold Homo sapiens 73-76
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 insulin receptor substrate 1 Homo sapiens 95-100
30806631-8 2019 Moreover, the treatment of MDA-MB-231 cells with triorganotin compounds together with ATRA resulted in an additional reduction of annexin 5, vimentin and nucleoside diphosphate kinase B. Tretinoin 86-90 NME/NM23 nucleoside diphosphate kinase 2 Homo sapiens 154-185
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 insulin receptor substrate 1 Homo sapiens 61-66
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 insulin receptor substrate 1 Homo sapiens 95-100
30764845-0 2019 Analysis of the role of thrombomodulin in all-trans retinoic acid treatment of coagulation disorders in cancer patients. Tretinoin 52-65 thrombomodulin Homo sapiens 24-38
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 insulin receptor substrate 1 Homo sapiens 95-100
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 113-115 insulin receptor substrate 1 Homo sapiens 95-100
15489899-4 2004 In leukemic cell lines treated with all-trans retinoic acid (ATRA), cyclin A1 localized to the nucleus. Tretinoin 36-59 cyclin A1 Homo sapiens 68-77
15489899-4 2004 In leukemic cell lines treated with all-trans retinoic acid (ATRA), cyclin A1 localized to the nucleus. Tretinoin 61-65 cyclin A1 Homo sapiens 68-77
15489899-5 2004 Further, there was a direct interaction between cyclin A1 and cyclin-dependent kinase 1, as well as a major ATRA receptor, RARalpha, in ATRA-treated cells but not in untreated leukemic cells. Tretinoin 108-112 retinoic acid receptor alpha Homo sapiens 123-131
15467735-4 2004 Estrogen treatment of T47D cells caused increased expression of E2F-1, and this expression was inhibited by cotreatment with all-trans retinoic acid. Tretinoin 135-148 E2F transcription factor 1 Homo sapiens 64-69
15467735-8 2004 In addition, we found that two important downstream target genes of estrogen and heregulin-beta1 that are regulated through E2F-1, cyclin E and NPAT, were both regulated in a similar fashion by all-trans retinoic acid, and these effects were antagonized by dominant-negative HES-1. Tretinoin 204-217 E2F transcription factor 1 Homo sapiens 124-129
15467735-8 2004 In addition, we found that two important downstream target genes of estrogen and heregulin-beta1 that are regulated through E2F-1, cyclin E and NPAT, were both regulated in a similar fashion by all-trans retinoic acid, and these effects were antagonized by dominant-negative HES-1. Tretinoin 204-217 nuclear protein, coactivator of histone transcription Homo sapiens 144-148
15520197-0 2004 Retinoic acid induces neuroblastoma cell death by inhibiting proteasomal degradation of retinoic acid receptor alpha. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 88-116
15520197-2 2004 SK-N-DZ cells expressed relatively high levels of retinoic acid receptor alpha (RAR-alpha) and underwent ATRA-induced cell death that was blocked by an RAR-alpha antagonist. Tretinoin 105-109 retinoic acid receptor alpha Homo sapiens 152-161
15520197-4 2004 We report here the ubiquitin-dependent down-regulation of RAR-alpha expression during ATRA treatment. Tretinoin 86-90 retinoic acid receptor alpha Homo sapiens 58-67
15520197-5 2004 Our data suggest that SK-N-DZ cells have a defect in RAR-alpha down-regulation, resulting in sustained high expression of RAR-alpha that confers high sensitivity to ATRA. Tretinoin 165-169 retinoic acid receptor alpha Homo sapiens 53-62
15520197-5 2004 Our data suggest that SK-N-DZ cells have a defect in RAR-alpha down-regulation, resulting in sustained high expression of RAR-alpha that confers high sensitivity to ATRA. Tretinoin 165-169 retinoic acid receptor alpha Homo sapiens 122-131
15520197-7 2004 Our results reveal the crucial involvement of the RAR-alpha signaling pathway in NBL cell death and show that three NBL cell lines are differentially sensitive to ATRA. Tretinoin 163-167 retinoic acid receptor alpha Homo sapiens 50-59
15464577-4 2004 The induction of the more ventral phenotype was due to the higher expression level of the N-terminus of sonic hedgehog protein (Shh-N) when treated with low concentration RA, as it was abrogated by an inhibitor of Shh signaling, cyclopamine. Tretinoin 171-173 sonic hedgehog Mus musculus 104-126
15345685-3 2004 Recent studies demonstrate that retinoic acid (RA)-induced human HL60 cell proliferation/differentiation (P/D) transition is accompanied by MAT1 degradation and decreased CAK phosphorylation of retinoic acid receptor alpha (RARa). Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 194-222
15345685-3 2004 Recent studies demonstrate that retinoic acid (RA)-induced human HL60 cell proliferation/differentiation (P/D) transition is accompanied by MAT1 degradation and decreased CAK phosphorylation of retinoic acid receptor alpha (RARa). Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 224-228
15345685-3 2004 Recent studies demonstrate that retinoic acid (RA)-induced human HL60 cell proliferation/differentiation (P/D) transition is accompanied by MAT1 degradation and decreased CAK phosphorylation of retinoic acid receptor alpha (RARa). Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 194-222
15345685-3 2004 Recent studies demonstrate that retinoic acid (RA)-induced human HL60 cell proliferation/differentiation (P/D) transition is accompanied by MAT1 degradation and decreased CAK phosphorylation of retinoic acid receptor alpha (RARa). Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 224-228
15345685-7 2004 These findings reveal that RA induces MAT1 ubiquitination to decrease CAK phosphorylation of RARalpha, suggesting a novel mechanism of RA-mediated P/D transition in which MAT1 ubiquitination may act as an integral part of RA-effect to decrease CAK activity in the switch from proliferation to differentiation. Tretinoin 27-29 retinoic acid receptor alpha Homo sapiens 93-101
15762481-0 2004 [SERS spectra of vitamin A acid in silver solution]. Tretinoin 17-31 seryl-tRNA synthetase 2, mitochondrial Homo sapiens 1-5
15762481-2 2004 After sufficient shaking, collect SERS spectra of VAA with silver sol layer solution. Tretinoin 50-53 seryl-tRNA synthetase 2, mitochondrial Homo sapiens 34-38
15485494-0 2004 Induction of cyclin-dependent kinase 5 and its activator p35 through the extracellular-signal-regulated kinase and protein kinase A pathways during retinoic-acid mediated neuronal differentiation in human neuroblastoma SK-N-BE(2)C cells. Tretinoin 148-161 cyclin dependent kinase 5 Homo sapiens 13-38
15485494-3 2004 In this study we newly found that RA treatment of SK-N-BE(2)C, human neuroblastoma cells, increased the expression of Cdk5 and its neuron specific activator p35 through the extracellular-signal-regulated kinase1/2 (ERK1/2) and cAMP-dependent protein kinase A (PKA) pathway. Tretinoin 34-36 cyclin dependent kinase 5 Homo sapiens 118-122
15485494-4 2004 Inhibition of Cdk5 activity either by an inhibitor, roscovitine, or by transfection with a dominant negative form of Cdk5 caused a dramatic decrease in RA-induced differentiation, suggesting the requirement of Cdk5 kinase activity for the RA-induced neurite outgrowth. Tretinoin 152-154 cyclin dependent kinase 5 Homo sapiens 14-18
15485494-4 2004 Inhibition of Cdk5 activity either by an inhibitor, roscovitine, or by transfection with a dominant negative form of Cdk5 caused a dramatic decrease in RA-induced differentiation, suggesting the requirement of Cdk5 kinase activity for the RA-induced neurite outgrowth. Tretinoin 152-154 cyclin dependent kinase 5 Homo sapiens 117-121
15485494-4 2004 Inhibition of Cdk5 activity either by an inhibitor, roscovitine, or by transfection with a dominant negative form of Cdk5 caused a dramatic decrease in RA-induced differentiation, suggesting the requirement of Cdk5 kinase activity for the RA-induced neurite outgrowth. Tretinoin 152-154 cyclin dependent kinase 5 Homo sapiens 117-121
15485494-4 2004 Inhibition of Cdk5 activity either by an inhibitor, roscovitine, or by transfection with a dominant negative form of Cdk5 caused a dramatic decrease in RA-induced differentiation, suggesting the requirement of Cdk5 kinase activity for the RA-induced neurite outgrowth. Tretinoin 239-241 cyclin dependent kinase 5 Homo sapiens 14-18
15485494-4 2004 Inhibition of Cdk5 activity either by an inhibitor, roscovitine, or by transfection with a dominant negative form of Cdk5 caused a dramatic decrease in RA-induced differentiation, suggesting the requirement of Cdk5 kinase activity for the RA-induced neurite outgrowth. Tretinoin 239-241 cyclin dependent kinase 5 Homo sapiens 117-121
15485494-4 2004 Inhibition of Cdk5 activity either by an inhibitor, roscovitine, or by transfection with a dominant negative form of Cdk5 caused a dramatic decrease in RA-induced differentiation, suggesting the requirement of Cdk5 kinase activity for the RA-induced neurite outgrowth. Tretinoin 239-241 cyclin dependent kinase 5 Homo sapiens 117-121
15485494-6 2004 In addition, a transcription factor early growth response 1 (Egr-1) was induced by RA through the ERK1/2 pathway, suggesting its possible involvement in the p35 induction. Tretinoin 83-85 early growth response 1 Homo sapiens 36-59
15485494-6 2004 In addition, a transcription factor early growth response 1 (Egr-1) was induced by RA through the ERK1/2 pathway, suggesting its possible involvement in the p35 induction. Tretinoin 83-85 early growth response 1 Homo sapiens 61-66
15485494-7 2004 RA treatment also induced c-fos mediated AP-1 binding, and cAMP-responsive element binding protein (CREB) mediated CRE binding via ERK1/2 and PKA pathway, respectively, in the Cdk5 promoter region, resulting in the induction of Cdk5. Tretinoin 0-2 cyclin dependent kinase 5 Homo sapiens 176-180
15485494-7 2004 RA treatment also induced c-fos mediated AP-1 binding, and cAMP-responsive element binding protein (CREB) mediated CRE binding via ERK1/2 and PKA pathway, respectively, in the Cdk5 promoter region, resulting in the induction of Cdk5. Tretinoin 0-2 cyclin dependent kinase 5 Homo sapiens 228-232
15485494-8 2004 Our results suggest that ERK1/2 and PKA-induced regulation of Cdk5 activity possibly through Egr-1, c-fos, and CREB plays a critical role in the RA-induced neuronal differentiation. Tretinoin 145-147 cyclin dependent kinase 5 Homo sapiens 62-66
15485494-8 2004 Our results suggest that ERK1/2 and PKA-induced regulation of Cdk5 activity possibly through Egr-1, c-fos, and CREB plays a critical role in the RA-induced neuronal differentiation. Tretinoin 145-147 early growth response 1 Homo sapiens 93-98
15512805-4 2004 It is now well established that all-trans-retinoic acid when administered at pharmacological doses can reverse the dominant-negative effects that the PML-RARalpha oncoprotein exhibits on the functions of the wild type PML and RARalpha proteins. Tretinoin 32-55 PML nuclear body scaffold Homo sapiens 150-153
15512805-4 2004 It is now well established that all-trans-retinoic acid when administered at pharmacological doses can reverse the dominant-negative effects that the PML-RARalpha oncoprotein exhibits on the functions of the wild type PML and RARalpha proteins. Tretinoin 32-55 retinoic acid receptor alpha Homo sapiens 154-162
15512805-4 2004 It is now well established that all-trans-retinoic acid when administered at pharmacological doses can reverse the dominant-negative effects that the PML-RARalpha oncoprotein exhibits on the functions of the wild type PML and RARalpha proteins. Tretinoin 32-55 PML nuclear body scaffold Homo sapiens 218-221
15512805-4 2004 It is now well established that all-trans-retinoic acid when administered at pharmacological doses can reverse the dominant-negative effects that the PML-RARalpha oncoprotein exhibits on the functions of the wild type PML and RARalpha proteins. Tretinoin 32-55 retinoic acid receptor alpha Homo sapiens 226-234
15347642-3 2004 Recently, gluconeogenic conditions have been shown to modulate homocysteine metabolism and treatment with glucocorticoids and/or all-trans-retinoic acid (RA)-induced active GNMT protein, thereby leading to methyl group loss. Tretinoin 129-152 glycine N-methyltransferase Rattus norvegicus 173-177
15347642-3 2004 Recently, gluconeogenic conditions have been shown to modulate homocysteine metabolism and treatment with glucocorticoids and/or all-trans-retinoic acid (RA)-induced active GNMT protein, thereby leading to methyl group loss. Tretinoin 154-156 glycine N-methyltransferase Rattus norvegicus 173-177
15347642-4 2004 This study was conducted to determine the effect of diabetes, alone and in combination with RA, on GNMT regulation. Tretinoin 92-94 glycine N-methyltransferase Rattus norvegicus 99-103
15347642-7 2004 Cell culture studies demonstrated that pretreatment with insulin prevented GNMT induction by both RA and dexamethasone. Tretinoin 98-100 glycine N-methyltransferase Rattus norvegicus 75-79
15464216-4 2004 Incubation with retinoic acid (RA) (0.5 microM) lead to an increase in the number of cultured cells showing positive immunoreactivity for the neuronal marker, microtubule-associated protein (MAP)-2ab. Tretinoin 16-29 regulator of microtubule dynamics 1 Homo sapiens 159-189
15464216-4 2004 Incubation with retinoic acid (RA) (0.5 microM) lead to an increase in the number of cultured cells showing positive immunoreactivity for the neuronal marker, microtubule-associated protein (MAP)-2ab. Tretinoin 16-29 regulator of microtubule dynamics 1 Homo sapiens 191-194
15464216-4 2004 Incubation with retinoic acid (RA) (0.5 microM) lead to an increase in the number of cultured cells showing positive immunoreactivity for the neuronal marker, microtubule-associated protein (MAP)-2ab. Tretinoin 31-33 regulator of microtubule dynamics 1 Homo sapiens 159-189
15464216-4 2004 Incubation with retinoic acid (RA) (0.5 microM) lead to an increase in the number of cultured cells showing positive immunoreactivity for the neuronal marker, microtubule-associated protein (MAP)-2ab. Tretinoin 31-33 regulator of microtubule dynamics 1 Homo sapiens 191-194
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 0-13 epidermal growth factor Mus musculus 193-216
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 0-13 epidermal growth factor Mus musculus 218-221
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 15-17 epidermal growth factor Mus musculus 193-216
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 15-17 epidermal growth factor Mus musculus 218-221
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 104-106 epidermal growth factor Mus musculus 193-216
15272014-3 2004 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblasts co-stimulated with epidermal growth factor (EGF). Tretinoin 104-106 epidermal growth factor Mus musculus 218-221
15272014-4 2004 Here we investigate whether EGF also antagonized RA-induced TGase expression in breast cancer cells. Tretinoin 49-51 epidermal growth factor Homo sapiens 28-31
15467265-4 2004 In this study, we observed the role of alternative splicing of hTERT in the regulation of telomerase activity in all-trans-retinoic acid (ATRA)-induced, differentiated HL-60 cells. Tretinoin 113-136 telomerase reverse transcriptase Homo sapiens 63-68
15467265-4 2004 In this study, we observed the role of alternative splicing of hTERT in the regulation of telomerase activity in all-trans-retinoic acid (ATRA)-induced, differentiated HL-60 cells. Tretinoin 138-142 telomerase reverse transcriptase Homo sapiens 63-68
15467265-5 2004 ATRA-induced down-regulation of telomerase activity in differentiated HL-60 cells was associated with a decrease in hTERT and an increase in human telomerase-associated protein-1 (hTP1) transcription. Tretinoin 0-4 telomerase reverse transcriptase Homo sapiens 116-121
15467265-8 2004 hTERT alpha- and hTERT alpha- beta- mRNA were reduced dramatically after ATRA treatment. Tretinoin 73-77 telomerase reverse transcriptase Homo sapiens 0-5
15467265-8 2004 hTERT alpha- and hTERT alpha- beta- mRNA were reduced dramatically after ATRA treatment. Tretinoin 73-77 telomerase reverse transcriptase Homo sapiens 17-22
15467265-9 2004 In the dose-effect study, hTERT alpha+ beta+ and hTERT beta- maintained a relatively stable ratio when telomerase activity decreased largely from treatment with 1 to 5 microM ATRA. Tretinoin 175-179 telomerase reverse transcriptase Homo sapiens 26-31
15467265-9 2004 In the dose-effect study, hTERT alpha+ beta+ and hTERT beta- maintained a relatively stable ratio when telomerase activity decreased largely from treatment with 1 to 5 microM ATRA. Tretinoin 175-179 telomerase reverse transcriptase Homo sapiens 49-54
15305337-3 2004 RESULTS: Initial studies demonstrated that exposure of TRAMP-derived C2N prostate tumor cells to ATRA in vitro decreased total viable cell numbers with a concomitant decrease in the fraction of cells in S phase. Tretinoin 97-101 dermatopontin Mus musculus 55-60
15305337-4 2004 When TRAMP mice were treated in vivo with ATRA for either 6 or 8 weeks at low, medium, or high dose, mice on average presented with lower grade and more differentiated tumors. Tretinoin 42-46 dermatopontin Mus musculus 5-10
15305337-6 2004 Nevertheless, we were able to observe a significant decrease in the expression of synaptophysin, a marker of neuroendocrine differentiation, in tumors of mice receiving the highest dose of ATRA. Tretinoin 189-193 synaptophysin Mus musculus 82-95
15374966-8 2004 Inhibition of p53 and caspases with alpha-pifithrin and z-Val-Ala-Asp-fluoromethyl ketone, respectively, blocked UVB- and doxorubicin-induced apoptosis in ATRA-treated KCs. Tretinoin 155-159 caspase 6 Homo sapiens 22-30
15231515-6 2004 Stable overexpression of dominant-negative myocardin in A404 cells resulted in impaired induction of SM alpha-actin and SM-MHC by all trans-retinoic acid but had no effect on induction of smoothelin-B and aortic carboxypeptidase-like protein expression. Tretinoin 134-153 myocardin Mus musculus 43-52
15554945-6 2004 However, in the present study, we show that the RA-induced expression of endodermal markers such as EndoA, collagen IV, and t-PA are inhibited by exogenous MyoR expression and that the level of inhibition of these markers correlates with the level of MyoR expressed. Tretinoin 48-50 musculin Homo sapiens 156-160
15554945-6 2004 However, in the present study, we show that the RA-induced expression of endodermal markers such as EndoA, collagen IV, and t-PA are inhibited by exogenous MyoR expression and that the level of inhibition of these markers correlates with the level of MyoR expressed. Tretinoin 48-50 musculin Homo sapiens 251-255
15236314-2 2004 To elucidate how TERT is inactivated during differentiation, we applied all-trans retinoic acid (ATRA) to induce the differentiation of human teratocarcinoma (HT) cells and human acute myeloid leukemia (HL60) cells. Tretinoin 82-95 telomerase reverse transcriptase Homo sapiens 17-21
15236314-2 2004 To elucidate how TERT is inactivated during differentiation, we applied all-trans retinoic acid (ATRA) to induce the differentiation of human teratocarcinoma (HT) cells and human acute myeloid leukemia (HL60) cells. Tretinoin 97-101 telomerase reverse transcriptase Homo sapiens 17-21
15234573-3 2004 Moreover, in the presence of 1 microM ATRA, approximately 50% of UF-1 cells expressing annexin V, an early-apoptotic marker, was negative for CD11b and showed immature morphology. Tretinoin 38-42 annexin A5 Homo sapiens 87-96
15234273-4 2004 In the presence of RA, the coactivators SRC-1 and GRIP-1 formed complexes with RAR beta and RXR alpha which are bound to an oligonucleotide specifying a RARE site in the promoter. Tretinoin 19-21 glutamate receptor interacting protein 1 Homo sapiens 50-56
15234273-5 2004 In conclusion, this study shows that in the presence of retinoic acid, the coactivators SRC-1 and GRIP-1 augment, while the corepressor N-CoR abolishes, the suppressive effects of RAR beta and RXR alpha on alpha 2(I) collagen promoter activity. Tretinoin 56-69 glutamate receptor interacting protein 1 Homo sapiens 98-104
15234273-5 2004 In conclusion, this study shows that in the presence of retinoic acid, the coactivators SRC-1 and GRIP-1 augment, while the corepressor N-CoR abolishes, the suppressive effects of RAR beta and RXR alpha on alpha 2(I) collagen promoter activity. Tretinoin 56-69 nuclear receptor corepressor 1 Homo sapiens 136-141
15262180-0 2004 Possible involvement of p44/p42 MAP kinase in retinoic acid-stimulated vascular endothelial growth factor release in aortic smooth muscle cells. Tretinoin 46-59 cyclin dependent kinase 20 Homo sapiens 28-31
15262180-6 2004 Retinoic acid induced the phosphorylation of p44/p42 mitogen-activated protein (MAP) kinase but not p38 MAP kinase or stress-activated protein kinase/c-Jun N-terminal kinase among the MAP kinase superfamily. Tretinoin 0-13 cyclin dependent kinase 20 Homo sapiens 49-52
15262180-8 2004 The retinoic acid-stimulated release of VEGF was significantly reduced by PD98059 and U0126, specific MEK inhibitors, which attenuated the retinoic acid-induced phosphorylation of p44/p42 MAP kinase. Tretinoin 4-17 cyclin dependent kinase 20 Homo sapiens 184-187
15262180-8 2004 The retinoic acid-stimulated release of VEGF was significantly reduced by PD98059 and U0126, specific MEK inhibitors, which attenuated the retinoic acid-induced phosphorylation of p44/p42 MAP kinase. Tretinoin 139-152 cyclin dependent kinase 20 Homo sapiens 184-187
15304040-5 2004 ATRA treatment was associated with a significant decrease in TF gene expression in bone marrow cells during the first 30 days of treatment, whereas IL-1 beta gene expression, which decreased in the cells of six patients treated with either chemotherapy or ATRA, actually increased in the remaining six patients treated with either chemotherapy or ATRA. Tretinoin 0-4 coagulation factor III, tissue factor Homo sapiens 61-63
15190260-11 2004 In conclusion, COX-1 is induced during ATRA-dependent maturation and appears to contribute to myeloid differentiation both in vitro and ex vivo, and COX-1 activity may potentiate the differentiation of human APL.Leukemia (2004) 18, 1373-1379. doi:10.1038/sj.leu.2403407 Published online 10 June 2004 Tretinoin 39-43 mitochondrially encoded cytochrome c oxidase I Homo sapiens 15-20
15219855-2 2004 Retinoic acid (RA)-induced differentiation of P19 embryonic carcinoma cells, in which A-type lamins are absent, increases the expression of lamin A/C. Tretinoin 0-13 lamin A/C Homo sapiens 140-149
15219855-2 2004 Retinoic acid (RA)-induced differentiation of P19 embryonic carcinoma cells, in which A-type lamins are absent, increases the expression of lamin A/C. Tretinoin 15-17 lamin A/C Homo sapiens 140-149
15219855-3 2004 We previously showed, using P19 cells as a model system, that the lamin A/C promoter has a retinoic acid-responsive element (L-RARE), and that Sp1 and Sp3 bind the CACCC box of the L-RARE. Tretinoin 91-104 lamin A/C Homo sapiens 66-75
15312521-0 2004 [Effects of retinoic acid on the signal transduction of beta-catenin /Tcf of cultured bronchial epithelial cells]. Tretinoin 12-25 catenin beta 1 Homo sapiens 56-68
15026310-4 2004 In both atRA-treated VPC cultures and CAM tissues underneath the chorionic epithelial layer, the expression of angiopoietin-2 (Ang-2; competitor for Ang-1) was enhanced, whereas that of Tie2 (a receptor for Angs) was reduced. Tretinoin 8-12 angiopoietin 2 Mus musculus 111-125
15026310-4 2004 In both atRA-treated VPC cultures and CAM tissues underneath the chorionic epithelial layer, the expression of angiopoietin-2 (Ang-2; competitor for Ang-1) was enhanced, whereas that of Tie2 (a receptor for Angs) was reduced. Tretinoin 8-12 angiopoietin 2 Mus musculus 127-132
15196957-4 2004 As a result of RA treatment, the expression of Sonic Hedgehog (Shh), a known inhibitor of pancreas development in other vertebrate systems, is negatively regulated in the dorsal prepancreatic endoderm. Tretinoin 15-17 sonic hedgehog L homeolog Xenopus laevis 47-61
15196957-4 2004 As a result of RA treatment, the expression of Sonic Hedgehog (Shh), a known inhibitor of pancreas development in other vertebrate systems, is negatively regulated in the dorsal prepancreatic endoderm. Tretinoin 15-17 sonic hedgehog L homeolog Xenopus laevis 63-66
15246741-6 2004 Furthermore, addition of all-trans retinoic acid (RA) to cultures of RAR alpha-transfected COS-1 cells diminishes RAR alpha and returns levels of MMP-1 to those approaching baseline. Tretinoin 35-48 retinoic acid receptor alpha Homo sapiens 69-78
15246741-6 2004 Furthermore, addition of all-trans retinoic acid (RA) to cultures of RAR alpha-transfected COS-1 cells diminishes RAR alpha and returns levels of MMP-1 to those approaching baseline. Tretinoin 35-48 retinoic acid receptor alpha Homo sapiens 114-123
15792532-0 2005 The mouse chemerin receptor gene, mcmklr1, utilizes alternative promoters for transcription and is regulated by all-trans retinoic acid. Tretinoin 122-135 chemokine-like receptor 1 Mus musculus 10-27
15792532-0 2005 The mouse chemerin receptor gene, mcmklr1, utilizes alternative promoters for transcription and is regulated by all-trans retinoic acid. Tretinoin 122-135 chemokine-like receptor 1 Mus musculus 34-41
15888413-6 2005 Avian UCP protein was specifically immunodetected and retinoic acid, which belongs to the carotenoid family, was found to trigger its activity. Tretinoin 54-67 uncoupling protein 1 Homo sapiens 6-9
15888413-8 2005 However, when activated by retinoic acid, avian UCP can also operate as the mammalian thermogenic UCP1. Tretinoin 27-40 uncoupling protein 1 Homo sapiens 48-51
15888413-8 2005 However, when activated by retinoic acid, avian UCP can also operate as the mammalian thermogenic UCP1. Tretinoin 27-40 uncoupling protein 1 Homo sapiens 98-102
15677473-0 2005 Chicken ovalbumin upstream promoter-transcription factor members repress retinoic acid-induced Cdx1 expression. Tretinoin 73-86 caudal type homeobox 1 Gallus gallus 95-99
15766748-0 2005 Retinoic acid, hypoxia, and GATA factors cooperatively control the onset of fetal liver erythropoietin expression and erythropoietic differentiation. Tretinoin 0-13 erythropoietin Mus musculus 88-102
15766748-3 2005 Our previous work demonstrated that the Epo gene is a direct target of retinoic acid action, via a retinoic acid receptor binding site in the Epo gene enhancer. Tretinoin 71-84 erythropoietin Mus musculus 40-43
15766748-3 2005 Our previous work demonstrated that the Epo gene is a direct target of retinoic acid action, via a retinoic acid receptor binding site in the Epo gene enhancer. Tretinoin 71-84 erythropoietin Mus musculus 142-145
15623509-7 2005 Moreover, activating the endogenous gene coding for GI-GPx by all-trans-retinoic acid (RA) was sufficient to cause down-regulation of the HCV replicon. Tretinoin 62-85 glutathione peroxidase 2 Homo sapiens 52-58
15707588-2 2005 In this study, using luciferase assay of a reporter gene containing PPAR response element (PPRE), we found PPRE transactivity was additively induced by PPAR gamma activator (15dPGJ2) and RXR activator (9-cis retinoic acid, 9-cis RA). Tretinoin 208-221 peroxisome proliferator activated receptor alpha Homo sapiens 68-72
15734096-1 2005 PURPOSE: The aim of the study was to evaluate a soluble form of APO-1/Fas antigen in supernatants from HeLa cell line culture after 24 and 72 h of incubation with selected retinoic acid concentrations. Tretinoin 172-185 Fas cell surface death receptor Homo sapiens 64-69
15734096-1 2005 PURPOSE: The aim of the study was to evaluate a soluble form of APO-1/Fas antigen in supernatants from HeLa cell line culture after 24 and 72 h of incubation with selected retinoic acid concentrations. Tretinoin 172-185 Fas cell surface death receptor Homo sapiens 70-81
15644206-11 2005 Consequently, RA has a co-dominant effect with EGF: when present simultaneously, their effects balance each other. Tretinoin 14-16 epidermal growth factor Homo sapiens 47-50
15645120-2 2005 Treatment of SCC25 oral squamous carcinoma cells with sodium butyrate (SB) at 0.5-5 mM or all-trans retinoic acid (ATRA) at 3-300 microM inhibited cell growth and induced apoptosis in a dose-dependent manner with concomittant increases in expression of keratin 13, p21WAF1/Cip1 and p27Kip1 and decreases in expression of COX-2. Tretinoin 115-119 keratin 13 Homo sapiens 253-263
15645120-2 2005 Treatment of SCC25 oral squamous carcinoma cells with sodium butyrate (SB) at 0.5-5 mM or all-trans retinoic acid (ATRA) at 3-300 microM inhibited cell growth and induced apoptosis in a dose-dependent manner with concomittant increases in expression of keratin 13, p21WAF1/Cip1 and p27Kip1 and decreases in expression of COX-2. Tretinoin 115-119 cyclin dependent kinase inhibitor 1B Homo sapiens 282-289
15839205-8 2005 RA inhibits the GPI-80 expression on DMSO induced HL-60 cells suggests that different signal conduction has been activated by DMSO and RA when they induce the HL-60 cells to the neutrophilic differentiation. Tretinoin 0-2 vanin 2 Homo sapiens 16-22
15839205-8 2005 RA inhibits the GPI-80 expression on DMSO induced HL-60 cells suggests that different signal conduction has been activated by DMSO and RA when they induce the HL-60 cells to the neutrophilic differentiation. Tretinoin 135-137 vanin 2 Homo sapiens 16-22
15725742-4 2005 The NTera2/D1 teratocarcinoma cell-line (or NT2-N cells) gives rise to neuron-like cells called hNT neurons after exposure to retinoic acid. Tretinoin 126-139 neurotrimin Homo sapiens 96-99
15725742-6 2005 However, when the NT2 cells are treated with retinoic acid to produce hNT cells, they terminally differentiate into post-mitotic neurons with no sign of tumorigenicity. Tretinoin 45-58 neurotrimin Homo sapiens 70-73
15339853-3 2005 We demonstrate here that myelomonocytic growth factors (granulocyte colony-stimulating factor [G-CSF] and/or granulocyte macrophage colony-stimulating factor [GM-CSF]) potentiate differentiation effects of ATRA in different AML cell lines and primary cells from patients with myeloid leukemia. Tretinoin 206-210 colony stimulating factor 2 Homo sapiens 109-157
15339853-3 2005 We demonstrate here that myelomonocytic growth factors (granulocyte colony-stimulating factor [G-CSF] and/or granulocyte macrophage colony-stimulating factor [GM-CSF]) potentiate differentiation effects of ATRA in different AML cell lines and primary cells from patients with myeloid leukemia. Tretinoin 206-210 colony stimulating factor 2 Homo sapiens 159-166
15339853-5 2005 Specific inhibitors of mitogen mitogen-activated protein kinase (MAPK) (MEK)-1/-2 or p38 extracellular signal-related kinase (ERK) kinase diminish the ATRA as well as ATRA and G/GM-CSF-induced activation of the RARalpha proteins and decreased the differentiation-induced decline in cell numbers. Tretinoin 151-155 mitogen-activated protein kinase kinase 1 Homo sapiens 72-81
15339853-5 2005 Specific inhibitors of mitogen mitogen-activated protein kinase (MAPK) (MEK)-1/-2 or p38 extracellular signal-related kinase (ERK) kinase diminish the ATRA as well as ATRA and G/GM-CSF-induced activation of the RARalpha proteins and decreased the differentiation-induced decline in cell numbers. Tretinoin 151-155 retinoic acid receptor alpha Homo sapiens 211-219
15339853-5 2005 Specific inhibitors of mitogen mitogen-activated protein kinase (MAPK) (MEK)-1/-2 or p38 extracellular signal-related kinase (ERK) kinase diminish the ATRA as well as ATRA and G/GM-CSF-induced activation of the RARalpha proteins and decreased the differentiation-induced decline in cell numbers. Tretinoin 167-171 mitogen-activated protein kinase kinase 1 Homo sapiens 72-81
15339853-5 2005 Specific inhibitors of mitogen mitogen-activated protein kinase (MAPK) (MEK)-1/-2 or p38 extracellular signal-related kinase (ERK) kinase diminish the ATRA as well as ATRA and G/GM-CSF-induced activation of the RARalpha proteins and decreased the differentiation-induced decline in cell numbers. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 211-219
15617756-5 2005 Activation of the caudal marker genes such as Hoxb9 is observed in a dose-dependent manner over the range of 2x10(-9)-2x10(-6) M. Suppression of the forebrain genes has a narrow critical period of RA response during the early culture phase. Tretinoin 197-199 homeobox B9 Homo sapiens 46-51
15529177-10 2005 RA enhanced the expression of adenovirus-cytomegalovirus-promoted PML at both transcription and protein levels within 12 hours after treatment; however, the PML protein was significantly degraded in the presence of RA at days 3-5 postinfection. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 66-69
15529177-10 2005 RA enhanced the expression of adenovirus-cytomegalovirus-promoted PML at both transcription and protein levels within 12 hours after treatment; however, the PML protein was significantly degraded in the presence of RA at days 3-5 postinfection. Tretinoin 215-217 PML nuclear body scaffold Homo sapiens 157-160
15529177-11 2005 PML degradation was also observed in SK-BR3 breast cancer cells treated with RA. Tretinoin 77-79 PML nuclear body scaffold Homo sapiens 0-3
15529177-12 2005 Taken together, our findings strongly support the hypothesis that PML acts as a strong independent cell death inducer and that RA conversely abolishes the therapeutic effects of the PML proteins through proteasomal degradation of the protein. Tretinoin 127-129 PML nuclear body scaffold Homo sapiens 182-185
16357442-0 2005 Soluble form of heparin-binding EGF-like growth factor contributes to retinoic acid-induced epidermal hyperplasia. Tretinoin 70-83 heparin-binding EGF-like growth factor Mus musculus 16-54
16357442-3 2005 Here we investigate the role of HB-EGF in epidermal hyperplasia induced by all-trans retinoic acid (tRA) treatment. Tretinoin 85-98 heparin-binding EGF-like growth factor Mus musculus 32-38
16357442-3 2005 Here we investigate the role of HB-EGF in epidermal hyperplasia induced by all-trans retinoic acid (tRA) treatment. Tretinoin 100-103 heparin-binding EGF-like growth factor Mus musculus 32-38
15912649-4 2005 Our studies show that 25 microM AR-t triggers mesangial cell apoptosis assessed by light and fluorescence microscopy (Giemsa stain and acridine orange stain, respectively), DNA electrophoresis, flow cytometry (annexin-V) and immunocytochemistry (TUNEL). Tretinoin 32-36 annexin A5 Homo sapiens 210-219
15641927-0 2005 Retinoic acid-induced neural differentiation of P19 embryonal carcinoma cells is potentiated by leukemia inhibitory factor. Tretinoin 0-13 LIF interleukin 6 family cytokine Homo sapiens 96-122
15641927-2 2005 Here we show that LIF potentiates retinoic acid-mediated neural induction in pluripotent P19 embryonal carcinoma cells. Tretinoin 34-47 LIF interleukin 6 family cytokine Homo sapiens 18-21
15589975-1 2005 Five organochlorine pesticides, namely, chlordane, dieldrin, aldrin, endrin, and endosulfan, activate human retinoic acid receptor (RAR)-mediated gene transcription via a retinoic acid response element (RARE). Tretinoin 108-121 retinoic acid receptor alpha Homo sapiens 132-135
15492006-7 2004 Expression of the dominant negative p115RhoGEF was able to inhibit activation of both RhoA and JNK1 in response to either retinoic acid or the expression of a constitutively activated mutant of G alpha(13). Tretinoin 122-135 rho/rac guanine nucleotide exchange factor (GEF) 2 Mus musculus 36-46
15308577-11 2004 RA signaling in granulocytic differentiation involves regulated expression of CHOP and C/EBPepsilon in a coordinated fashion. Tretinoin 0-2 CCAAT enhancer binding protein epsilon Homo sapiens 87-99
15358764-10 2004 Downstream of retinoic acid production, we identified hoxc8 as a retinoic acid-induced gene that, when ectopically expressed, rescued phenotypes of APC- and zRDHB-deficient zebrafish. Tretinoin 14-27 homeobox C8a Danio rerio 54-59
15606784-2 2004 Retinoic acid (RARalpha, beta, gamma) and retinoid X (RXRalpha, beta, gamma) receptors mediate the retinoid/rexinoid signal to the transcriptional machineries by interacting at the first level with coactivators or corepressors, which leads to the recruitment of enzymatically active noncovalent complexes at target gene promoters. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 15-86
15246741-6 2004 Furthermore, addition of all-trans retinoic acid (RA) to cultures of RAR alpha-transfected COS-1 cells diminishes RAR alpha and returns levels of MMP-1 to those approaching baseline. Tretinoin 35-48 matrix metallopeptidase 1 Homo sapiens 146-151
15047706-0 2004 Cyclophilin A is required for retinoic acid-induced neuronal differentiation in p19 cells. Tretinoin 30-43 peptidylprolyl isomerase A Homo sapiens 0-13
15047706-1 2004 Stable transfectants with expression of small interfering RNA for targeting cyclophilin A (CypA) in p19 cells lose their potential for retinoic acid (RA)-induced neuronal differentiation but not Me(2)SO-induced mesodermal differentiation. Tretinoin 135-148 peptidylprolyl isomerase A Homo sapiens 76-89
15047706-1 2004 Stable transfectants with expression of small interfering RNA for targeting cyclophilin A (CypA) in p19 cells lose their potential for retinoic acid (RA)-induced neuronal differentiation but not Me(2)SO-induced mesodermal differentiation. Tretinoin 135-148 peptidylprolyl isomerase A Homo sapiens 91-95
15047706-1 2004 Stable transfectants with expression of small interfering RNA for targeting cyclophilin A (CypA) in p19 cells lose their potential for retinoic acid (RA)-induced neuronal differentiation but not Me(2)SO-induced mesodermal differentiation. Tretinoin 150-152 peptidylprolyl isomerase A Homo sapiens 76-89
15047706-1 2004 Stable transfectants with expression of small interfering RNA for targeting cyclophilin A (CypA) in p19 cells lose their potential for retinoic acid (RA)-induced neuronal differentiation but not Me(2)SO-induced mesodermal differentiation. Tretinoin 150-152 peptidylprolyl isomerase A Homo sapiens 91-95
15047706-2 2004 This difference suggests that CypA is specifically required for the RA-induced neuronal pathway. Tretinoin 68-70 peptidylprolyl isomerase A Homo sapiens 30-34
15047706-5 2004 Collectively, our data reveal that a novel function of CypA is required in the processing of RA-induced neuronal differentiation in p19 embryonal carcinoma cells. Tretinoin 93-95 peptidylprolyl isomerase A Homo sapiens 55-59
15028729-2 2004 However, when HL-60 cells are induced to differentiate to granulocytes by treatment with retinoic acid (RA), they express CD38 and accumulate cADPR. Tretinoin 89-102 CD38 molecule Homo sapiens 122-126
15028729-2 2004 However, when HL-60 cells are induced to differentiate to granulocytes by treatment with retinoic acid (RA), they express CD38 and accumulate cADPR. Tretinoin 104-106 CD38 molecule Homo sapiens 122-126
30764845-3 2019 In vitro studies have reported that RA upregulates thrombomodulin (TM) expression on the endothelial cell surface. Tretinoin 36-38 thrombomodulin Homo sapiens 51-65
15108357-0 2004 Tissue-specific regulation of leptin expression and secretion by all-trans retinoic acid. Tretinoin 75-88 leptin Homo sapiens 30-36
30764845-3 2019 In vitro studies have reported that RA upregulates thrombomodulin (TM) expression on the endothelial cell surface. Tretinoin 36-38 thrombomodulin Homo sapiens 67-69
15108357-3 2004 Retinoic acid (RA) is a ligand of some nuclear receptors and previous reports have demonstrated contradictory effects on plasma leptin levels. Tretinoin 0-13 leptin Homo sapiens 128-134
15108357-3 2004 Retinoic acid (RA) is a ligand of some nuclear receptors and previous reports have demonstrated contradictory effects on plasma leptin levels. Tretinoin 15-17 leptin Homo sapiens 128-134
30764845-4 2019 The objective of this study was to investigate how and to what extent the TM concentration changes after RA treatment in cancer patients, and how this variation influences the blood coagulation cascade. Tretinoin 105-107 thrombomodulin Homo sapiens 74-76
15108357-4 2004 Thus, we examined the effect of RA on expression of leptin in adipocytes of murine and human origin. Tretinoin 32-34 leptin Mus musculus 52-58
30764845-5 2019 RESULTS: In this study, we introduced an ordinary differential equation (ODE) model of gene expression for the RA-induced upregulation of TM concentration. Tretinoin 111-113 thrombomodulin Homo sapiens 138-140
15133197-5 2004 Transcription assays in COS-1 cells indicated that the N-acylated derivatives (2A-5A) and 4-HPR (1A) were much weaker ligands for all three subtypes of retinoic acid receptor (RAR) than all-trans retinoic acid (ATRA), although they showed some selectivity for RARbeta and RARgamma. Tretinoin 152-165 retinoic acid receptor alpha Homo sapiens 176-179
30764845-6 2019 Coupling the gene expression model with a two-compartment pharmacokinetic model of RA, we obtained the time-dependent changes in TM and thrombomodulin-mRNA (TMR) concentrations following oral administration of RA. Tretinoin 83-85 thrombomodulin Homo sapiens 129-131
15133197-6 2004 In contrast, the O-acylated retinoate derivatives (1B-5B) activated all three RAR isotypes without specificity to an extent similar to ATRA. Tretinoin 28-37 retinoic acid receptor alpha Homo sapiens 78-81
30764845-6 2019 Coupling the gene expression model with a two-compartment pharmacokinetic model of RA, we obtained the time-dependent changes in TM and thrombomodulin-mRNA (TMR) concentrations following oral administration of RA. Tretinoin 83-85 thrombomodulin Homo sapiens 136-150
15133197-8 2004 When retinoate derivative 5B was coupled to organic acid salts, the resulting salt derivatives 5C and 5D had RAR activation and cytotoxicity similar to those of 5B. Tretinoin 5-14 retinoic acid receptor alpha Homo sapiens 109-112
30764845-8 2019 Continuous treatment with RA resulted in oscillatory expression of TM on the endothelial cell surface. Tretinoin 26-28 thrombomodulin Homo sapiens 67-69
15095411-0 2004 Retinoic acid regulates the expression of PBX1, PBX2, and PBX3 in P19 cells both transcriptionally and post-translationally. Tretinoin 0-13 pre B cell leukemia homeobox 1 Mus musculus 42-46
30764845-12 2019 CONCLUSIONS: Our results indicate that the oscillatory upregulation of TM expression on the endothelial cells over the course of RA therapy could potentially contribute to the treatment of coagulation abnormalities in cancer patients. Tretinoin 129-131 thrombomodulin Homo sapiens 71-73
15095411-3 2004 In this report, we demonstrate that PBX1a, PBX1b, PBX2, and PBX3 mRNAs and PBX1/2/3 proteins are induced during endodermal and neuronal differentiation of P19 cells in a RAR-dependent subtype-unspecific manner following RA treatment. Tretinoin 170-172 pre B cell leukemia homeobox 1 Mus musculus 75-83
15095411-4 2004 The increases in both PBX1 mRNA and PBX3 mRNA levels are secondary responses to RA treatment requiring new proteins synthesis while the increase in PBX2 mRNA is a primary response. Tretinoin 80-82 pre B cell leukemia homeobox 1 Mus musculus 22-26
15095411-6 2004 In addition, the half-lives of PBX1/2/3 proteins are significantly extended by RA treatment. Tretinoin 79-81 pre B cell leukemia homeobox 1 Mus musculus 31-39
15291362-6 2004 Based on these findings, combined treatment with ATRA and TSA may be clinically useful in therapy for acute leukemia displaying MLL-AF9 fusion gene. Tretinoin 49-53 lysine methyltransferase 2A Homo sapiens 128-131
30906641-0 2019 Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells. Tretinoin 41-54 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 67-72
15291363-2 2004 Retinoids, such as all-trans retinoic acid (ATRA), have been shown to induce CD38 expression. Tretinoin 19-42 CD38 molecule Homo sapiens 77-81
15291363-2 2004 Retinoids, such as all-trans retinoic acid (ATRA), have been shown to induce CD38 expression. Tretinoin 44-48 CD38 molecule Homo sapiens 77-81
14976209-1 2004 Acute promyelocytic leukemia (APL) cases expressing the t(15,17) product, promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARalpha), have clinical remissions through leukemic cell differentiation after all-trans-retinoic acid (RA) treatment. Tretinoin 217-236 PML nuclear body scaffold Homo sapiens 98-101
14976209-1 2004 Acute promyelocytic leukemia (APL) cases expressing the t(15,17) product, promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARalpha), have clinical remissions through leukemic cell differentiation after all-trans-retinoic acid (RA) treatment. Tretinoin 217-236 retinoic acid receptor alpha Homo sapiens 103-131
14976209-1 2004 Acute promyelocytic leukemia (APL) cases expressing the t(15,17) product, promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARalpha), have clinical remissions through leukemic cell differentiation after all-trans-retinoic acid (RA) treatment. Tretinoin 217-236 retinoic acid receptor alpha Homo sapiens 133-141
14976209-1 2004 Acute promyelocytic leukemia (APL) cases expressing the t(15,17) product, promyelocytic leukemia (PML)/retinoic acid receptor alpha (RARalpha), have clinical remissions through leukemic cell differentiation after all-trans-retinoic acid (RA) treatment. Tretinoin 133-135 retinoic acid receptor alpha Homo sapiens 103-131
15563759-7 2004 The amount of surfactant also had a marked effect on the oral absorption of ATRA with SLN formulations. Tretinoin 76-80 sarcolipin Rattus norvegicus 86-89
15609095-0 2004 Teratogenicity of retinoic acid and its effects on TGF-beta2 expression in the developing cerebral cortex of the rat. Tretinoin 18-31 transforming growth factor, beta 2 Rattus norvegicus 51-60
30906641-0 2019 Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells. Tretinoin 41-54 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 125-129
15609095-7 2004 In the 15-day-old fetus from mothers who had been fed by gavage a single dose of 60 mg/kg body weight of all-trans retinoic acid on the 8th day of gestation, TGF-beta2 immunoreactivity in the brain was decreased. Tretinoin 115-128 transforming growth factor, beta 2 Rattus norvegicus 158-167
30906641-7 2019 However, the clinical outcome has not been sufficient with the use of retinoids, including all-trans retinoic acid (ATRA), mainly because of the inhibition of differentiation caused by N-Myc. Tretinoin 91-114 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 185-190
15609095-9 2004 The expression of TGF-beta2 in fetuses whose mothers had been given all-trans retinoic acid after the neurulation period (on day 12 of gestation) was generally similar to that in a control group. Tretinoin 78-91 transforming growth factor, beta 2 Rattus norvegicus 18-27
15609095-11 2004 Further, retinoic acid has a variable effect on the expression of TGF-beta2. Tretinoin 9-22 transforming growth factor, beta 2 Rattus norvegicus 66-75
14742427-6 2004 Furthermore we demonstrated that PBX proteins regulate the RA-dependent induction in the mRNA levels of bone morphogenetic protein 4 (BMP4) and Decorin (DCN) in P19 cells using both PBX1b-AS cells and PBX1 small interfering RNA. Tretinoin 59-61 pre B cell leukemia homeobox 1 Mus musculus 182-186
30906641-7 2019 However, the clinical outcome has not been sufficient with the use of retinoids, including all-trans retinoic acid (ATRA), mainly because of the inhibition of differentiation caused by N-Myc. Tretinoin 116-120 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 185-190
30906641-8 2019 In the present study, we succeeded in synergistically accelerating the ATRA-induced neuronal differentiation of MYCN-amplified neuroblastoma cells by combining a peptide derived from tenascin-C, termed TNIIIA2, which has a potent ability to activate beta1-integrins. Tretinoin 71-75 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 112-116
30906641-9 2019 Accelerated differentiation was caused by a decrease in N-Myc protein level in neuroblastoma cells after the combined treatment of TNIIIA2 with ATRA. Tretinoin 144-148 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 56-61
15073138-6 2004 RESULTS: RA treatment triggered degradation of cyclin E protein, and ALLN, a proteasomal inhibitor, inhibited this degradation. Tretinoin 9-11 proliferating cell nuclear antigen Homo sapiens 47-53
15482329-5 2004 RESULTS: Retinoic acid caused immunohistochemical diminution of keratin 4, keratin 13, and desmoglein. Tretinoin 9-22 keratin 13 Homo sapiens 75-85
30906641-10 2019 That is, combination treatment using ATRA with TNIIIA2 induced proteasomal degradation in the N-Myc oncoprotein of neuroblastoma cells with MYCN gene amplification, and this caused acceleration of neuronal differentiation and attenuation of malignant properties. Tretinoin 37-41 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 94-99
15482329-7 2004 RA significantly decreased the transcript levels of keratin 13, keratin 14, desmoglein 1, and desmocollin 1 in a dose-dependent manner. Tretinoin 0-2 keratin 13 Homo sapiens 52-62
15073138-8 2004 Transfection experiments in BEAS-2B cells indicated that RA treatment repressed expression of wild-type cyclin D1 and cyclin E, but ALLN inhibited this degradation. Tretinoin 57-59 proliferating cell nuclear antigen Homo sapiens 104-110
15482329-7 2004 RA significantly decreased the transcript levels of keratin 13, keratin 14, desmoglein 1, and desmocollin 1 in a dose-dependent manner. Tretinoin 0-2 keratin 14 Homo sapiens 64-74
30906641-10 2019 That is, combination treatment using ATRA with TNIIIA2 induced proteasomal degradation in the N-Myc oncoprotein of neuroblastoma cells with MYCN gene amplification, and this caused acceleration of neuronal differentiation and attenuation of malignant properties. Tretinoin 37-41 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 140-144
15482329-9 2004 CONCLUSION: These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. Tretinoin 41-43 keratin 13 Homo sapiens 133-143
15482329-9 2004 CONCLUSION: These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. Tretinoin 41-43 keratin 14 Homo sapiens 224-234
15160934-4 2004 The mechanism of action of both ATRA and As2O3 appears to be by inducing granulocytic differentiation and this cellular differentiation seems to depend on PML-RARalpha proteolysis. Tretinoin 32-36 PML nuclear body scaffold Homo sapiens 155-158
15160934-4 2004 The mechanism of action of both ATRA and As2O3 appears to be by inducing granulocytic differentiation and this cellular differentiation seems to depend on PML-RARalpha proteolysis. Tretinoin 32-36 retinoic acid receptor alpha Homo sapiens 159-167
15160934-5 2004 ATRA treatment results in partial cleavage and complete degradation of PML-RARalpha protein in differentiation sensitive, but not in differentiation resistant APL cells. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 71-74
15160934-5 2004 ATRA treatment results in partial cleavage and complete degradation of PML-RARalpha protein in differentiation sensitive, but not in differentiation resistant APL cells. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 75-83
15160934-8 2004 Therefore, PML-RARalpha proteolysis induced by ATRA and As2O3 may play an important role in overcoming the repressive activity of PML-RARalpha and allowing cellular differentiation to proceed. Tretinoin 47-51 PML nuclear body scaffold Homo sapiens 11-14
15369820-3 2004 Thus, ADH1 and ADH4 provide a metabolic pathway for the synthesis of the corresponding retinoic acids. Tretinoin 87-101 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 6-10
30709378-0 2019 Correction to: Stemness marker ALDH1A1 promotes tumor angiogenesis via retinoic acid/HIF-1alpha/VEGF signalling in MCF-7 breast cancer cells. Tretinoin 71-84 aldehyde dehydrogenase 1 family member A1 Homo sapiens 31-38
15369700-3 2004 We demonstrated that nanomolar EGF further enhances transglutaminase activity previously induced by all-trans retinoic acid. Tretinoin 110-123 epidermal growth factor Homo sapiens 31-34
15160934-8 2004 Therefore, PML-RARalpha proteolysis induced by ATRA and As2O3 may play an important role in overcoming the repressive activity of PML-RARalpha and allowing cellular differentiation to proceed. Tretinoin 47-51 retinoic acid receptor alpha Homo sapiens 15-23
15160934-8 2004 Therefore, PML-RARalpha proteolysis induced by ATRA and As2O3 may play an important role in overcoming the repressive activity of PML-RARalpha and allowing cellular differentiation to proceed. Tretinoin 47-51 PML nuclear body scaffold Homo sapiens 130-133
15160934-8 2004 Therefore, PML-RARalpha proteolysis induced by ATRA and As2O3 may play an important role in overcoming the repressive activity of PML-RARalpha and allowing cellular differentiation to proceed. Tretinoin 47-51 retinoic acid receptor alpha Homo sapiens 134-142
30250298-5 2019 Moreover, we demonstrated that pharmacological inhibition of 15-PGDH enhanced CYP26A1 expression, leading to depletion of all-trans retinoic acid (ATRA) and expansion of the ALDH1-positive subset in both human PDAC cells and tumor cells of KrasLSL-G12D/+; Ptf1aCre/+ (KC) mice. Tretinoin 132-145 15-hydroxyprostaglandin dehydrogenase Homo sapiens 61-68
30578278-0 2019 The ubiquitin ligase HECTD1 promotes retinoic acid signaling required for development of the aortic arch. Tretinoin 37-50 HECT domain E3 ubiquitin protein ligase 1 Mus musculus 21-27
15003502-6 2004 After transfer to the stem cell maintenance culture, they changed morphologically and became immunoreactive for MAP5 and neurofilament200 after inducement with retinoic acid. Tretinoin 160-173 microtubule associated protein 1B Homo sapiens 112-116
15498118-0 2004 [Effect of sodium butyrate in combination with ATRA on the proliferation/differentiation of MDS cell line SKM-1]. Tretinoin 47-51 sodium voltage-gated channel alpha subunit 4 Homo sapiens 106-111
15273718-5 2004 We found that RA+GF induce apoptosis, as shown by an increase in fragmented DNA, Annexin-V-positive cells and caspase-3 activation. Tretinoin 14-16 annexin A5 Homo sapiens 81-90
30578278-3 2019 Here, we identify the HECTD1 ubiquitin ligase as a novel modulator of retinoic acid signaling during this process. Tretinoin 70-83 HECT domain E3 ubiquitin protein ligase 1 Mus musculus 22-28
15383262-5 2004 The expression of Bcl-2 was higher in the Bugu Mixture group than that in the all-trans retinoic acid (ATRA) induced group, and the expression of Bax was lower in the Bugu Mixture group than that in the ATRA induced group. Tretinoin 203-207 BCL2 associated X, apoptosis regulator Rattus norvegicus 146-149
30578278-7 2019 Furthermore, reduced activation of a retinoic acid response element (RARE) reporter is detected in Hectd1 mutant cells and embryos. Tretinoin 37-50 HECT domain E3 ubiquitin protein ligase 1 Mus musculus 99-105
14630830-1 2004 The promyelocytic leukemia (PML) tumor suppressor of acute promyelocytic leukemia (APL) is essential for a number of proapoptotic and growth-suppressive pathways as well as for the activity of differentiating agents such as retinoic acid (RA). Tretinoin 224-237 PML nuclear body scaffold Homo sapiens 4-27
30578278-8 2019 Interestingly, Hectd1opm/+ heterozygous embryos exhibit reduced retinoic acid signaling, along with intermediate increased expression of SHF markers; however, heterozygotes show normal development of the aortic arch. Tretinoin 64-77 HECT domain E3 ubiquitin protein ligase 1 Mus musculus 15-21
14630830-1 2004 The promyelocytic leukemia (PML) tumor suppressor of acute promyelocytic leukemia (APL) is essential for a number of proapoptotic and growth-suppressive pathways as well as for the activity of differentiating agents such as retinoic acid (RA). Tretinoin 239-241 PML nuclear body scaffold Homo sapiens 4-27
14630830-6 2004 Complete functional loss of PML is therefore selected by the APL phenotype and associates with poor prognosis and RA unresponsiveness. Tretinoin 114-116 PML nuclear body scaffold Homo sapiens 28-31
15317450-3 2004 The transcriptional antagonism of the 3"-n-butyl analogue was demonstrated by its blockade of retinoic acid receptor (RAR) beta expression induced by the RXRalpha/peroxisome proliferator-activated receptor (PPAR) gamma heterodimer complexed with an RXRalpha agonist plus the PPARgamma agonist ciglitazone and the inhibition of 9-cis-RA-induced coactivator SRC-1a recruitment to RXRalpha. Tretinoin 327-335 peroxisome proliferator activated receptor alpha Homo sapiens 154-205
30578278-9 2019 Decreasing retinoic acid synthesis by reducing Raldh2 (also known as Aldh1a2) gene dosage in Hectd1opm/+ heterozygous embryos reveals a genetic interaction. Tretinoin 11-24 HECT domain E3 ubiquitin protein ligase 1 Mus musculus 93-99
15317450-3 2004 The transcriptional antagonism of the 3"-n-butyl analogue was demonstrated by its blockade of retinoic acid receptor (RAR) beta expression induced by the RXRalpha/peroxisome proliferator-activated receptor (PPAR) gamma heterodimer complexed with an RXRalpha agonist plus the PPARgamma agonist ciglitazone and the inhibition of 9-cis-RA-induced coactivator SRC-1a recruitment to RXRalpha. Tretinoin 327-335 peroxisome proliferator activated receptor alpha Homo sapiens 207-211
30578278-11 2019 Together, our data establish that HECTD1 is a novel regulator of retinoic acid signaling required for proper aortic arch development. Tretinoin 65-78 HECT domain E3 ubiquitin protein ligase 1 Mus musculus 34-40
30123996-10 2019 Stra8 expression was significantly higher in RA group in comparison to other groups. Tretinoin 45-47 stimulated by retinoic acid gene 8 Mus musculus 0-5
14988223-0 2004 Ionizing radiation-induced E-selectin gene expression and tumor cell adhesion is inhibited by lovastatin and all-trans retinoic acid. Tretinoin 119-132 selectin E Homo sapiens 27-37
14988223-6 2004 Radiation-induced expression of E-selectin was also blocked by all-trans retinoic acid (at-RA), whereas 9-cis retinoic acid was ineffective. Tretinoin 63-86 selectin E Homo sapiens 32-42
14758549-6 2004 As retinoic acid also upregulated retinoic acid receptor beta ( Rar-beta), we assume that cROR-1 upregulation is mediated by Rar-beta. Tretinoin 3-16 retinoic acid receptor beta Gallus gallus 34-61
14758549-6 2004 As retinoic acid also upregulated retinoic acid receptor beta ( Rar-beta), we assume that cROR-1 upregulation is mediated by Rar-beta. Tretinoin 3-16 retinoic acid receptor beta Gallus gallus 64-72
14758549-6 2004 As retinoic acid also upregulated retinoic acid receptor beta ( Rar-beta), we assume that cROR-1 upregulation is mediated by Rar-beta. Tretinoin 3-16 retinoic acid receptor beta Gallus gallus 125-133
14613895-10 2004 These results suggest that retinoic acid acting through RARalpha negatively affects fetal Sertoli cell differentiation and gonocyte survival and blocks the migration of mesonephric cells, thereby leading to inhibition of the XY gonad development. Tretinoin 27-40 retinoic acid receptor, alpha Rattus norvegicus 56-64
14988223-6 2004 Radiation-induced expression of E-selectin was also blocked by all-trans retinoic acid (at-RA), whereas 9-cis retinoic acid was ineffective. Tretinoin 88-93 selectin E Homo sapiens 32-42
15262888-9 2004 Neurons induced by beta-catenin overexpression either alone or in association with RA express the caudal neuronal marker Hoxc4. Tretinoin 83-85 catenin beta 1 Homo sapiens 19-31
15262888-10 2004 However, RA treatment inhibits the beta-catenin-mediated generation of tyrosine hydroxylase-positive neurons, suggesting that not all of the effects of RA are dependent upon beta-catenin signaling. Tretinoin 9-11 catenin beta 1 Homo sapiens 35-47
31682209-4 2019 RESULTS: Decreased vitamin A, and its retinoic acid metabolites, lead to a decrease in CD38 and associated changes that underpin a wide array of data on the biological underpinnings of ASD, including decreased oxytocin, with relevance both prenatally and in the gut. Tretinoin 38-51 CD38 molecule Homo sapiens 87-91
15262888-11 2004 These observations suggest that beta-catenin signaling promotes neural lineage commitment by ES cells, and that beta-catenin signaling may be a necessary co-factor for RA-mediated neuronal differentiation. Tretinoin 168-170 catenin beta 1 Homo sapiens 112-124
15262888-12 2004 Further, enhancement of beta-catenin signaling with RA treatment significantly increases the numbers of neurons generated from ES cells, thus suggesting a method for obtaining large numbers of neural species for possible use in for ES cell transplantation. Tretinoin 52-54 catenin beta 1 Homo sapiens 24-36
15190260-2 2004 We investigated the expression and activity of COX-1 and -2 during granulocyte-oriented maturation induced by all-trans-retinoic acid (ATRA) of NB4 cells, originated from a human acute promyelocytic leukemia (APL), and in blasts from APL patients. Tretinoin 110-133 mitochondrially encoded cytochrome c oxidase I Homo sapiens 47-59
15190260-2 2004 We investigated the expression and activity of COX-1 and -2 during granulocyte-oriented maturation induced by all-trans-retinoic acid (ATRA) of NB4 cells, originated from a human acute promyelocytic leukemia (APL), and in blasts from APL patients. Tretinoin 135-139 mitochondrially encoded cytochrome c oxidase I Homo sapiens 47-59
14998970-9 2004 When in vitro differentiation of hES cells was induced by retinoic acid, three embryonic germ layer cells were identified by RT-PCR or indirect immunocytochemistry. Tretinoin 58-71 ribosome binding protein 1 Homo sapiens 33-36
15160908-0 2004 Clinico-biological features and prognostic significance of PML/RARalpha isoforms in adult patients with acute promyelocytic leukemia treated with all trans retinoic acid (ATRA) and chemotherapy. Tretinoin 156-169 PML nuclear body scaffold Homo sapiens 59-62
15481529-7 2004 ATRA(1 x 10(-6) mol/L), however, inhibited the effect of E2 on regulation of IGF- II gene and IGFBP-6 gene as well as MC-3T3-E1 cell proliferation. Tretinoin 0-4 insulin-like growth factor 2 Mus musculus 77-84
31359390-3 2019 Consequently, loss of normal RAR function in the presence of physiological levels of retinoic acid (RA) is often observed in cancers, and pharmacological reactivation of RAR signaling has been considered a promising strategy for cancer therapy and prevention. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 29-32
14976384-7 2004 We observed that RA and retinol markedly induced the expression of HA synthase-3 (HAS3) mRNA. Tretinoin 17-19 hyaluronan synthase 3 Homo sapiens 67-80
14976384-7 2004 We observed that RA and retinol markedly induced the expression of HA synthase-3 (HAS3) mRNA. Tretinoin 17-19 hyaluronan synthase 3 Homo sapiens 82-86
31695003-3 2019 All-trans retinoic acid (ATRA) treatment was initiated, but promyelocytic leukemia/retinoic acid receptor alpha gene fusion without remission was identified by fluorescence in situ hybridization. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 83-111
14871822-0 2004 Restoration of promyelocytic leukemia protein-nuclear bodies in neuroblastoma cells enhances retinoic acid responsiveness. Tretinoin 93-106 PML nuclear body scaffold Homo sapiens 15-45
14871822-6 2004 Expression of PML in neuroblastoma cells restored PML-nuclear bodies, enhanced responsiveness to all-trans-retinoic acid, and induced cellular differentiation. Tretinoin 97-120 PML nuclear body scaffold Homo sapiens 14-17
15082719-4 2004 At least five SOX genes, Sox2, Sox6, Sox7, Sox13, and Sox17, were expressed in F9 cells, and of these, Sox7 and Sox17 were dramatically induced in parallel with Fgf-3 following differentiation into parietal endoderm-like cells with retinoic acid and dibutyryl cAMP. Tretinoin 232-245 SRY (sex determining region Y)-box 7 Mus musculus 103-107
15082719-4 2004 At least five SOX genes, Sox2, Sox6, Sox7, Sox13, and Sox17, were expressed in F9 cells, and of these, Sox7 and Sox17 were dramatically induced in parallel with Fgf-3 following differentiation into parietal endoderm-like cells with retinoic acid and dibutyryl cAMP. Tretinoin 232-245 SRY (sex determining region Y)-box 17 Mus musculus 112-117
30662778-4 2018 We describe the efficacy and feasibility of the consecutive use of all-trans retinoic acid and arsenic trioxide-containing regimen for the treatment of promyelocytic leukemia and high-dose methotrexate plus cytarabine to treat lymphoproliferative involvement of the central nervous system. Tretinoin 77-90 PML nuclear body scaffold Homo sapiens 152-174
15256728-3 2004 The expression of p21 and p27 among the CDK inhibitors we examined increased during the differentiation induced with ATRA. Tretinoin 117-121 interferon alpha inducible protein 27 Homo sapiens 26-29
15256728-6 2004 These results suggest that increased expression of CDK inhibitors, p21 and p27, is necessary for the differentiation of HL-60 cells induced with ATRA. Tretinoin 145-149 interferon alpha inducible protein 27 Homo sapiens 75-78
14706456-0 2004 Characterization of the murine orphan G-protein-coupled receptor gene Rai3 and its regulation by retinoic acid. Tretinoin 97-110 G protein-coupled receptor, family C, group 5, member A Mus musculus 70-74
14603524-6 2004 We conclude that RA induces CCE ES cell differentiation in the presence of LIF, in part, by disrupting signaling between the LIFR/gp130 receptor and nuclear targets that are required to prevent ES cell differentiation. Tretinoin 17-19 leukemia inhibitory factor Mus musculus 75-78
30389142-0 2018 Retinoic acid co-treatment aggravates severity of dioxin-induced skin lesions in hairless mice via induction of inflammatory response. Tretinoin 0-13 lysine demethylase and nuclear receptor corepressor Mus musculus 81-89
14603524-6 2004 We conclude that RA induces CCE ES cell differentiation in the presence of LIF, in part, by disrupting signaling between the LIFR/gp130 receptor and nuclear targets that are required to prevent ES cell differentiation. Tretinoin 17-19 LIF receptor alpha Mus musculus 125-129
14603524-7 2004 Our data indicate that RA-induced inhibition of LIF signaling does not involve Erk1/2-dependent actions. Tretinoin 23-25 leukemia inhibitory factor Mus musculus 48-51
14977075-9 2004 In addition, the expression of cornifin-alpha mRNA was suppressed, and the expressions of mucin gene 5AC (MUC5AC) and MUC5B mRNA increased progressively with RA treatment. Tretinoin 158-160 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 90-104
14977075-9 2004 In addition, the expression of cornifin-alpha mRNA was suppressed, and the expressions of mucin gene 5AC (MUC5AC) and MUC5B mRNA increased progressively with RA treatment. Tretinoin 158-160 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 106-112
12829450-6 2004 CCT alpha promoter-reporter activity, CCT alpha transcript levels, and immunoreactive protein levels increased significantly in the presence of all-trans retinoic acid. Tretinoin 154-167 phosphate cytidylyltransferase 1, choline, alpha isoform Mus musculus 0-9
12829450-6 2004 CCT alpha promoter-reporter activity, CCT alpha transcript levels, and immunoreactive protein levels increased significantly in the presence of all-trans retinoic acid. Tretinoin 154-167 phosphate cytidylyltransferase 1, choline, alpha isoform Mus musculus 38-47
15194426-5 2004 Concomitantly, RA increased the level of the cyclin-dependent kinase inhibitor p27 (Kip-1). Tretinoin 15-17 cyclin dependent kinase inhibitor 1B Homo sapiens 84-89
15069081-8 2004 Our findings indicate the existence of an early phase of RA signaling acting upstream of Tbx5, Meis2, and dHand, followed by a late phase of RA signaling needed to expand AER structure fully along the distal ectoderm. Tretinoin 57-59 Meis homeobox 2 Homo sapiens 95-100
30389142-8 2018 However, in hairless mice (in vivo), RA/TCDD co-treatment produced more severe effects, than treatment with either of the two compounds individually. Tretinoin 37-39 lysine demethylase and nuclear receptor corepressor Mus musculus 12-20
14960491-5 2004 The negative effect of RA did not result from a diminution in the number of Leydig cells but from a decrease in P450c17 mRNA levels and in LH-stimulated cAMP production. Tretinoin 23-25 cytochrome P450, family 17, subfamily a, polypeptide 1 Rattus norvegicus 112-119
14960491-6 2004 However, the RA-induced decrease in P450C17 mRNA levels was also observed with neonatal testes, suggesting that this enzymatic step is no longer rate limiting at this developmental stage. Tretinoin 13-15 cytochrome P450, family 17, subfamily a, polypeptide 1 Rattus norvegicus 36-43
30409702-1 2018 The retinaldehyde dehydrogenase (RALDH) enzymes, RALDH1, RALDH2, and RALDH3, catalyze the irreversible oxidation of retinaldehyde to all-trans-retinoic acid (ATRA). Tretinoin 137-156 aldehyde dehydrogenase 1 family member A1 Homo sapiens 49-55
29616859-6 2018 In addition, all-trans retinoic acid was shown to increase the levels of FR-alpha and FR-beta in two myeloma cell lines. Tretinoin 23-36 rabaptin, RAB GTPase binding effector protein 2 Homo sapiens 73-81
15159275-10 2004 Expression of the CD11b cell surface marker and C/EBPepsilon was increased when the cells were treated for 4 days with 0.3 microm AF and a physiological concentration of all-trans retinoic acid (ATRA, 5 nm). Tretinoin 180-193 CCAAT enhancer binding protein epsilon Homo sapiens 48-60
15159275-10 2004 Expression of the CD11b cell surface marker and C/EBPepsilon was increased when the cells were treated for 4 days with 0.3 microm AF and a physiological concentration of all-trans retinoic acid (ATRA, 5 nm). Tretinoin 195-199 CCAAT enhancer binding protein epsilon Homo sapiens 48-60
14514656-0 2004 Dietary retinoic acid supplementation stimulates intestinal tumour formation and growth in multiple intestinal neoplasia (Min)/+ mice. Tretinoin 8-21 APC, WNT signaling pathway regulator Mus musculus 91-120
14514656-0 2004 Dietary retinoic acid supplementation stimulates intestinal tumour formation and growth in multiple intestinal neoplasia (Min)/+ mice. Tretinoin 8-21 APC, WNT signaling pathway regulator Mus musculus 122-125
14514656-4 2004 Our hypothesis was therefore that dietary supplementation with all-trans RA may inhibit the Apc-driven tumourigenesis in Min/+ mice. Tretinoin 73-75 APC, WNT signaling pathway regulator Mus musculus 92-95
14514656-4 2004 Our hypothesis was therefore that dietary supplementation with all-trans RA may inhibit the Apc-driven tumourigenesis in Min/+ mice. Tretinoin 73-75 APC, WNT signaling pathway regulator Mus musculus 121-124
15354417-10 2004 We also observed a reduction in expression of the telomerase components, hTERT and hTR in ATRA treated ovarian carcinoma cells. Tretinoin 90-94 telomerase reverse transcriptase Homo sapiens 73-78
29616859-6 2018 In addition, all-trans retinoic acid was shown to increase the levels of FR-alpha and FR-beta in two myeloma cell lines. Tretinoin 23-36 folate receptor beta Homo sapiens 86-93
14657669-0 2004 Inhibition of phosphatidylinositol 3-kinase causes apoptosis in retinoic acid differentiated hl-60 leukemia cells. Tretinoin 64-77 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 14-43
30397335-0 2018 Retinoic acid and BMP4 cooperate with p63 to alter chromatin dynamics during surface epithelial commitment. Tretinoin 0-13 tumor protein p63 Homo sapiens 38-41
15587392-0 2004 The effect of sodium butyrate in combination with ATRA on the proliferation/differentiation of SKM-1. Tretinoin 50-54 sodium voltage-gated channel alpha subunit 4 Homo sapiens 95-100
15046780-6 2004 We demonstrate that retinoic acid already affects in the early stage of germ layer formation, which was demonstrated by a change of Oct-4 and Brachyury gene expression. Tretinoin 20-33 POU class 5 homeobox 1 Homo sapiens 132-137
30555939-6 2019 Expression of a RA metabolizing enzyme, CYP26A1, was high in the epithelium of caudal MD and urogenital sinus, indicating that the enzyme causes the absence of RA signaling in the region. Tretinoin 16-18 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 40-47
17150542-0 2004 Histone modification activities of JDP2 associated with retinoic acid-induced differentiation of F9 cells. Tretinoin 56-69 Jun dimerization protein 2 Homo sapiens 35-39
30555939-6 2019 Expression of a RA metabolizing enzyme, CYP26A1, was high in the epithelium of caudal MD and urogenital sinus, indicating that the enzyme causes the absence of RA signaling in the region. Tretinoin 160-162 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 40-47
30459947-13 2018 Furthermore, we found that RA, a key bioactive metabolite of vitamin A, activated PPARGC1A promoter, which explains the upregulated expression of PPARGC1A in skeletal muscle. Tretinoin 27-29 PPARG coactivator 1 alpha Bos taurus 82-90
14964780-8 2003 In this study, we used a model of neuronal differentiation to demonstrate that the nuclear translocation of CypA, the appearance of hypophosphorylated RB and the enhancement of RB: CypA complex formation correlates with retinoic acid induced neuronal differentiation. Tretinoin 220-233 peptidylprolyl isomerase A Homo sapiens 108-112
14964780-8 2003 In this study, we used a model of neuronal differentiation to demonstrate that the nuclear translocation of CypA, the appearance of hypophosphorylated RB and the enhancement of RB: CypA complex formation correlates with retinoic acid induced neuronal differentiation. Tretinoin 220-233 peptidylprolyl isomerase A Homo sapiens 181-185
14623956-5 2003 This malformation, which is similar to isolated congenital CA in humans and may result from impaired RA-controlled down-regulation of Fgf8 expression in nasal fins, can be prevented by a simple maternal treatment with RA. Tretinoin 101-103 fibroblast growth factor 8 Homo sapiens 134-138
30459947-13 2018 Furthermore, we found that RA, a key bioactive metabolite of vitamin A, activated PPARGC1A promoter, which explains the upregulated expression of PPARGC1A in skeletal muscle. Tretinoin 27-29 PPARG coactivator 1 alpha Bos taurus 146-154
12915404-8 2003 Obligate CDK4 phosphorylation sites seemed most important to the stability of the protein and are among the candidate sites that are dephosphorylated by PP2A following ATRA treatment. Tretinoin 168-172 protein phosphatase 2 phosphatase activator Homo sapiens 153-157
30142332-5 2018 HB-EGF levels increase in response to different forms of injuries as well as stimuli, such as lysophosphatidic acid, retinoic acid, and 17beta-estradiol. Tretinoin 117-130 heparin binding EGF like growth factor Homo sapiens 0-6
12841847-8 2003 When breast cancer cell lines were treated with all- trans -retinoic acid, OCT3 expression was repressed, associated with decreased cell proliferation. Tretinoin 48-73 POU class 5 homeobox 1 Homo sapiens 75-79
30106128-1 2018 Stimulated by retinoic acid 8 (Stra8), one of genes induced by retinoic acid (RA), is required for the meiotic initiation of male spermatogenesis. Tretinoin 14-27 stimulated by retinoic acid gene 8 Mus musculus 31-36
30106128-1 2018 Stimulated by retinoic acid 8 (Stra8), one of genes induced by retinoic acid (RA), is required for the meiotic initiation of male spermatogenesis. Tretinoin 78-80 stimulated by retinoic acid gene 8 Mus musculus 31-36
30379862-8 2018 Retinaldehyde dehydrogenase 1 family, member A2 (ALDH1A2) and retinaldehyde dehydrogenase 1 family, member A3 (ALDH1A3), key enzymes for retinoic acid synthesis, were underexpressed in SS (-1.48 and -2.3-fold, respectively) and NASH (-1.47 and -2.6-fold, respectively) versus LD. Tretinoin 137-150 aldehyde dehydrogenase 1 family member A3 Homo sapiens 111-118
30379862-9 2018 In NASH, hepatic ALDH1A2 and ALDH1A3 were underexpressed and inversely correlated with plasma retinol levels, which may reduce retinoic acid in the liver. Tretinoin 127-140 aldehyde dehydrogenase 1 family member A3 Homo sapiens 29-36
30153436-8 2018 We next characterize the epigenetic mechanisms that contribute to RA-induced transcriptional activation of CRABP2 and NR2F1 in mESCs and show for the first time that CARM1 is required for this activation. Tretinoin 66-68 nuclear receptor subfamily 2, group F, member 1 Mus musculus 118-123
30349665-13 2018 It is known that retinoic acid (RA) signaling regulates pronephros segmentation in vertebrates and we show that Efhc2 function is crucial for nephron segmentation in zebrafish. Tretinoin 17-30 EF-hand domain (C-terminal) containing 2 Danio rerio 112-117
30349665-13 2018 It is known that retinoic acid (RA) signaling regulates pronephros segmentation in vertebrates and we show that Efhc2 function is crucial for nephron segmentation in zebrafish. Tretinoin 32-34 EF-hand domain (C-terminal) containing 2 Danio rerio 112-117
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 145-167
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 169-172
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 88-90 retinoic acid receptor alpha Homo sapiens 145-167
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 88-90 retinoic acid receptor alpha Homo sapiens 169-172
30322383-6 2018 RESULTS: Our results show that CRABP2 and RAR are the most and the least important proteins, respectively, in controlling the model performance at physiological concentrations of RA (1-10 nM). Tretinoin 32-34 retinoic acid receptor alpha Homo sapiens 42-45
30322383-7 2018 However, at higher concentrations of RA, CYP and RAR are the most sensitive parameters of the system. Tretinoin 37-39 retinoic acid receptor alpha Homo sapiens 49-52
30104253-0 2018 E2F1 Mediates the Retinoic Acid-Induced Transcription of Tshz1 during Neuronal Differentiation in a Cell Division-Dependent Manner. Tretinoin 18-31 E2F transcription factor 1 Homo sapiens 0-4
30104253-8 2018 A series of experiments was used to identify E2F1 as the induction factor for the RA-dependent transcription of Tshz1 We propose that E2F1 mediates neuronal differentiation in a cell division-dependent manner. Tretinoin 82-84 E2F transcription factor 1 Homo sapiens 45-49
30104253-8 2018 A series of experiments was used to identify E2F1 as the induction factor for the RA-dependent transcription of Tshz1 We propose that E2F1 mediates neuronal differentiation in a cell division-dependent manner. Tretinoin 82-84 E2F transcription factor 1 Homo sapiens 134-138
30233705-8 2018 RAR-alpha mRNA expression was observed to be decreased in PC12 cells following OGD-induced injury, and this decrease can be reversed by 4 micromol/l ATRA treatment. Tretinoin 149-153 retinoic acid receptor, alpha Rattus norvegicus 0-9
30254197-2 2018 Because retinoic acid receptor alpha (RARalpha) is highly expressed by LCs, we investigate the functions of RARalpha and retinoic acid (RA) in regulating the langerin-expressing DCs. Tretinoin 8-21 retinoic acid receptor alpha Homo sapiens 38-46
30254197-2 2018 Because retinoic acid receptor alpha (RARalpha) is highly expressed by LCs, we investigate the functions of RARalpha and retinoic acid (RA) in regulating the langerin-expressing DCs. Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 8-36
30206209-4 2018 Furthermore, treatment of the APL cell line, NB4 with all-trans retinoic acid (ATRA) causes the rapid loss of p36 and p11 protein. Tretinoin 54-77 annexin A2 Homo sapiens 110-113
30206209-4 2018 Furthermore, treatment of the APL cell line, NB4 with all-trans retinoic acid (ATRA) causes the rapid loss of p36 and p11 protein. Tretinoin 79-83 annexin A2 Homo sapiens 110-113
30194441-1 2018 Retinoic acid-inducible gene I-like receptor (RLR) is one of the most important pattern recognition receptors of the innate immune system that detects positive and/or negative stranded RNA viruses. Tretinoin 0-13 DExH-box helicase 58 Homo sapiens 46-49
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 retinol dehydrogenase 10 Rattus norvegicus 101-106
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 14-27 retinoic acid receptor alpha Homo sapiens 66-70
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 29-31 retinoic acid receptor alpha Homo sapiens 66-70
15064739-10 2004 Moreover, levels of endogenous Staf50 mRNA correlated to all-trans retinoic acid-induced differentiation of promyelocytic NB-4 and HL60 cells, suggesting that Staf50 could be involved in proliferation and/or differentiation of leukemic cells. Tretinoin 67-80 tripartite motif containing 22 Homo sapiens 31-37
30225259-10 2018 Our results suggest that ATRA enhances MMP-2 expression and secretion in human myeloid leukemia THP-1 cells in a calcium ion dependent manner through RAR/RXR signaling pathways, and this enhanced expression and secretion may be associated with the possible mechanisms of RAS. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 150-153
15064739-10 2004 Moreover, levels of endogenous Staf50 mRNA correlated to all-trans retinoic acid-induced differentiation of promyelocytic NB-4 and HL60 cells, suggesting that Staf50 could be involved in proliferation and/or differentiation of leukemic cells. Tretinoin 67-80 tripartite motif containing 22 Homo sapiens 159-165
15108365-11 2004 We conclude that HSC are the site of the liver beta-carotene storage and release, which can be used for RA production as well as for maintenance of the homeostasis of circulating carotenoids in periods of low dietary uptake. Tretinoin 104-106 fucosyltransferase 1 (H blood group) Homo sapiens 17-20
30158832-2 2018 RA promotes dendritic cells to express CD103 and to produce RA, enhances the differentiation of Foxp3+ inducible regulatory T cells, and induces gut-homing specificity in T cells. Tretinoin 0-2 integrin subunit alpha E Homo sapiens 39-44
15218975-0 2004 Tetraploid acute promyelocytic leukemia with double PML/RARA gene rearrangements successfully treated with all-trans retinoic acid. Tretinoin 117-130 PML nuclear body scaffold Homo sapiens 52-55
15218975-0 2004 Tetraploid acute promyelocytic leukemia with double PML/RARA gene rearrangements successfully treated with all-trans retinoic acid. Tretinoin 117-130 retinoic acid receptor alpha Homo sapiens 56-60
30123134-12 2018 In validating experiments, combination of Lapatinib and all-trans retinoic acid (ATRA) synergistically suppresses cell growth, and accompanied by decreased expression of MYC. Tretinoin 60-79 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-173
15040006-0 2004 p27/Kip1 mediates retinoic acid-induced suppression of ovarian carcinoma cell growth. Tretinoin 18-31 cyclin dependent kinase inhibitor 1B Homo sapiens 4-8
15040006-3 2004 We have found that treatment of CAOV3 cells with ATRA causes a 5-10 fold increase in the protein level of the cyclin dependent kinase inhibitor p27/Kip1. Tretinoin 49-53 cyclin dependent kinase inhibitor 1B Homo sapiens 148-152
15040006-5 2004 The increase in p27/Kip1 is detected by day 3 of ATRA treatment of CAOV3 cells, and is maximal by day 5. Tretinoin 49-53 cyclin dependent kinase inhibitor 1B Homo sapiens 20-24
14745140-2 2003 Granulocyte colony-stimulating factor (G-CSF), although not having detectable effect by itself, exerted the additive effects on lipid droplet formation in NB4 cells when combined with ATRA. Tretinoin 184-188 colony stimulating factor 3 Homo sapiens 0-37
30123134-12 2018 In validating experiments, combination of Lapatinib and all-trans retinoic acid (ATRA) synergistically suppresses cell growth, and accompanied by decreased expression of MYC. Tretinoin 81-85 MYC proto-oncogene, bHLH transcription factor Homo sapiens 170-173
14745140-2 2003 Granulocyte colony-stimulating factor (G-CSF), although not having detectable effect by itself, exerted the additive effects on lipid droplet formation in NB4 cells when combined with ATRA. Tretinoin 184-188 colony stimulating factor 3 Homo sapiens 39-44
15068906-0 2004 Induction of differentiation of retinoic acid-resistant acute promyelocytic leukemia cells by the combination of all-trans retinoic acid and granulocyte colony-stimulating factor. Tretinoin 32-45 colony stimulating factor 3 Homo sapiens 141-178
15068906-1 2004 An acute promyelocytic leukemia (APL) cell line with natural resistance to all-trans retinoic acid (ATRA), UF-1, was induced to differentiate into mature granulocyte when treated with the combination of ATRA and granulocyte colony-stimulating factor (G-CSF), while neither of them alone was capable of inducing the differentiation effectively. Tretinoin 85-98 colony stimulating factor 3 Homo sapiens 212-249
14508522-6 2003 Cotreatment of U937/NPM-RARalpha cells with all-trans retinoic acid (atRA) abrogated the induction of apoptosis by TG. Tretinoin 54-67 retinoic acid receptor alpha Homo sapiens 24-32
14508522-6 2003 Cotreatment of U937/NPM-RARalpha cells with all-trans retinoic acid (atRA) abrogated the induction of apoptosis by TG. Tretinoin 69-73 retinoic acid receptor alpha Homo sapiens 24-32
29945211-6 2018 Moreover, exposure to beta-CYP and 3-PBA at 100 muM inhibited all-trans retinoic acid (ATRA)-induced mRNA expressions of the granulocytic differentiation-related genes, CD11b and CSF-3R. Tretinoin 72-85 colony stimulating factor 3 receptor Homo sapiens 179-185
15068906-1 2004 An acute promyelocytic leukemia (APL) cell line with natural resistance to all-trans retinoic acid (ATRA), UF-1, was induced to differentiate into mature granulocyte when treated with the combination of ATRA and granulocyte colony-stimulating factor (G-CSF), while neither of them alone was capable of inducing the differentiation effectively. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 212-249
15068906-1 2004 An acute promyelocytic leukemia (APL) cell line with natural resistance to all-trans retinoic acid (ATRA), UF-1, was induced to differentiate into mature granulocyte when treated with the combination of ATRA and granulocyte colony-stimulating factor (G-CSF), while neither of them alone was capable of inducing the differentiation effectively. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 251-256
15291358-4 2004 We treated HL-60 and ATRA-resistant HL-60 (HL-60R) cells that express mutated RARalpha and very low levels of RARbeta, RARgamma and RXRalpha with 4-HPR (2 microM) for 3 days. Tretinoin 21-25 retinoic acid receptor alpha Homo sapiens 78-86
29945211-6 2018 Moreover, exposure to beta-CYP and 3-PBA at 100 muM inhibited all-trans retinoic acid (ATRA)-induced mRNA expressions of the granulocytic differentiation-related genes, CD11b and CSF-3R. Tretinoin 87-91 peptidylprolyl isomerase G Homo sapiens 27-30
29945211-6 2018 Moreover, exposure to beta-CYP and 3-PBA at 100 muM inhibited all-trans retinoic acid (ATRA)-induced mRNA expressions of the granulocytic differentiation-related genes, CD11b and CSF-3R. Tretinoin 87-91 colony stimulating factor 3 receptor Homo sapiens 179-185
12842898-1 2003 It has been suggested that cellular retinoic acid-binding protein (II) (CRABP(II)) may have a role in the movement of retinoic acid (RA) to its nuclear receptors, thereby enhancing the action of RA in the cells in which it is expressed. Tretinoin 36-49 cellular retinoic acid binding protein 2 Rattus norvegicus 72-81
12842898-1 2003 It has been suggested that cellular retinoic acid-binding protein (II) (CRABP(II)) may have a role in the movement of retinoic acid (RA) to its nuclear receptors, thereby enhancing the action of RA in the cells in which it is expressed. Tretinoin 73-75 cellular retinoic acid binding protein 2 Rattus norvegicus 27-70
29940355-3 2018 Here we report that transcriptional activation of TM in both immortalized vascular endothelial cells (EAhy926) and primary human aortic endothelial cells (HAEC) by all-trans retinoic acid (RA) paralleled accumulation of trimethylated histone H3K4, a prominent marker for active chromatin, surrounding the THBD promoter. Tretinoin 174-187 thrombomodulin Homo sapiens 50-52
12842898-1 2003 It has been suggested that cellular retinoic acid-binding protein (II) (CRABP(II)) may have a role in the movement of retinoic acid (RA) to its nuclear receptors, thereby enhancing the action of RA in the cells in which it is expressed. Tretinoin 133-135 cellular retinoic acid binding protein 2 Rattus norvegicus 27-70
12842898-1 2003 It has been suggested that cellular retinoic acid-binding protein (II) (CRABP(II)) may have a role in the movement of retinoic acid (RA) to its nuclear receptors, thereby enhancing the action of RA in the cells in which it is expressed. Tretinoin 133-135 cellular retinoic acid binding protein 2 Rattus norvegicus 72-81
14734562-0 2004 Activation and interaction of ATF2 with the coactivator ASC-2 are responsive for granulocytic differentiation by retinoic acid. Tretinoin 113-126 nuclear receptor coactivator 6 Homo sapiens 56-61
14734562-8 2004 Furthermore, the molecular interaction of ATF2 and ASC-2 was stimulated by RA treatment and inhibited by p38beta kinase inhibitor. Tretinoin 75-77 nuclear receptor coactivator 6 Homo sapiens 51-56
15047602-4 2004 RA administration to normal mice resulted in reduced resistin mRNA levels in brown and white adipose tissues, reduced circulating resistin levels, reduced body weight, and improved glucose tolerance. Tretinoin 0-2 resistin Mus musculus 130-138
27265573-4 2003 ATRA-induced differentiation of APL cells is strictly dependent on the presence of PML-RAR alpha. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 83-86
27265573-4 2003 ATRA-induced differentiation of APL cells is strictly dependent on the presence of PML-RAR alpha. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 87-96
29940355-3 2018 Here we report that transcriptional activation of TM in both immortalized vascular endothelial cells (EAhy926) and primary human aortic endothelial cells (HAEC) by all-trans retinoic acid (RA) paralleled accumulation of trimethylated histone H3K4, a prominent marker for active chromatin, surrounding the THBD promoter. Tretinoin 189-191 thrombomodulin Homo sapiens 50-52
14754907-7 2004 Two classes of nuclear receptors, the retinoic acid receptor (RAR) and the retinoid X receptor (RXR), mediate retinoic acid signaling. Tretinoin 38-51 retinoic acid receptor alpha Homo sapiens 62-65
29940355-4 2018 RA treatment up-regulated the expression of SETD1A (SET1), a dedicated H3K4 methyltransferase, and augmented SETD1A occupancies on the THBD promoter. Tretinoin 0-2 thrombomodulin Homo sapiens 135-139
14754907-8 2004 Specific RAR and RXR agonists were used to identify the nuclear receptor responsible for LPLA(2) induction by retinoic acid. Tretinoin 110-123 retinoic acid receptor alpha Homo sapiens 9-12
14506398-1 2003 BACKGROUND: Cytosolic aldehyde dehydrogenase, or ALDH1A1, functions in ethanol detoxification, metabolism of neurotransmitters, and synthesis of retinoic acid. Tretinoin 145-158 aldehyde dehydrogenase 1 family member A1 Homo sapiens 49-56
30055648-4 2018 Therefore, we established a nude mouse model to investigate if treatment of xenografts derived from NF1 associated S462 and T265 MPNST cells respond to ATRA and the MEKi PD0325901. Tretinoin 152-156 neurofibromin 1 Mus musculus 100-103
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 nuclear receptor coactivator 3 Homo sapiens 288-317
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 33-35 nuclear receptor coactivator 3 Homo sapiens 319-324
12915310-2 2003 RA distribution and concentration is precisely regulated during embryogenesis by balanced complementary activities of RA synthesizing (RALDH) and metabolizing (CYP26) enzymes. Tretinoin 0-2 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 160-165
12882839-8 2003 The optimal enhancement of Th2 development in the second system, however, was achieved with a delayed addition of RA. Tretinoin 114-116 heart and neural crest derivatives expressed 2 Mus musculus 27-30
12882839-9 2003 The presence of RA during the initial stimulation period often suppressed Th2 development. Tretinoin 16-18 heart and neural crest derivatives expressed 2 Mus musculus 74-77
15124139-5 2004 The majority of patients with promyelocytic leukemia with the PML/RARalpha fusion gene can be cured with an all-trans-retinoic acid and anthracycline-based treatment program. Tretinoin 108-131 PML nuclear body scaffold Homo sapiens 62-65
12882839-10 2003 The RA receptor (RAR) antagonists, LE540 and LE135, but not the retinoic X receptor (RXR) antagonist, PA452, inhibited the effect of RA on Th1/Th2 development. Tretinoin 4-6 heart and neural crest derivatives expressed 2 Mus musculus 143-146
30046590-4 2018 By inducing cell differentiation with all-trans retinoic acid and a modified neuronal medium, MSCs and MSCs-FTH1 were successfully differentiated into neuron-like cells (Neurons and Neurons-FTH1), and the neural differentiation rates were (91.56+-7.89)% and (92.23+-7.64)%, respectively. Tretinoin 48-61 ferritin heavy chain 1 Homo sapiens 108-112
12882839-13 2003 These results indicate that, via RAR, RA directly suppresses Th1 development and directly enhances Th2 development with its timely addition. Tretinoin 33-35 heart and neural crest derivatives expressed 2 Mus musculus 99-102
12754318-2 2003 Differentiation of SHSY-5Y cells with either retinoic acid (RA) or 12-o-tetradecanoyl-phorbol-13-acetate (TPA) significantly increased MOR mRNA levels. Tretinoin 45-58 opioid receptor mu 1 Homo sapiens 135-138
15124139-5 2004 The majority of patients with promyelocytic leukemia with the PML/RARalpha fusion gene can be cured with an all-trans-retinoic acid and anthracycline-based treatment program. Tretinoin 108-131 retinoic acid receptor alpha Homo sapiens 66-74
14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 99-122 colony stimulating factor 3 Homo sapiens 44-81
14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 99-122 colony stimulating factor 3 Homo sapiens 83-88
14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 124-128 colony stimulating factor 3 Homo sapiens 44-81
14604978-1 2004 Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL). Tretinoin 124-128 colony stimulating factor 3 Homo sapiens 83-88
14604978-9 2004 ATRA induction of NB4 cells resulted in morphologic differentiation and up-regulation of C/EBPepsilon and G-CSFR, but not in STAT3 phosphorylation. Tretinoin 0-4 CCAAT enhancer binding protein epsilon Homo sapiens 89-101
14604978-9 2004 ATRA induction of NB4 cells resulted in morphologic differentiation and up-regulation of C/EBPepsilon and G-CSFR, but not in STAT3 phosphorylation. Tretinoin 0-4 colony stimulating factor 3 receptor Homo sapiens 106-112
12754318-2 2003 Differentiation of SHSY-5Y cells with either retinoic acid (RA) or 12-o-tetradecanoyl-phorbol-13-acetate (TPA) significantly increased MOR mRNA levels. Tretinoin 60-62 opioid receptor mu 1 Homo sapiens 135-138
12879006-12 2003 The pan-RAR antagonists AGN193109 and the RARalpha antagonist Ro 41-5253 blocked TIG3 induction by ATRA. Tretinoin 99-103 retinoic acid receptor alpha Homo sapiens 42-50
14604978-10 2004 The addition of G-CSF with ATRA during NB4 induction resulted in STAT3 phosphorylation but did not enhance differentiation. Tretinoin 27-31 colony stimulating factor 3 Homo sapiens 16-21
29748133-1 2018 Retinoic acid is the active metabolite of vitamin A and regulates several important cellular processes by activating retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 117-140
15026555-0 2004 Retinoic acid-induced CD38 antigen as a target for immunotoxin-mediated killing of leukemia cells. Tretinoin 0-13 CD38 molecule Homo sapiens 22-26
15026555-2 2004 We reported previously that retinoic acid (RA) is a potent and selective inducer of the cell-surface antigen CD38 in myeloid leukemia cells. Tretinoin 28-41 CD38 molecule Homo sapiens 109-113
14983057-9 2004 In a model system for neural differentiation, Nolz-1 mRNA was dramatically induced on neural induction of P19 embryonal carcinoma cells by retinoic acid, suggesting that Nolz-1 activation may be involved in neural differentiation. Tretinoin 139-152 zinc finger protein 503 Homo sapiens 46-52
12836159-4 2003 Retinoic acid caused an increase in nuclear beta-catenin levels in SH-SY5Y cells, which was followed by an increase in cyclin D1 protein levels. Tretinoin 0-13 catenin beta 1 Homo sapiens 44-56
12810068-3 2003 Retinoic acid (RA)-induced differentiation led to hTERT gene silencing and increased methylation of the hTERT promoter. Tretinoin 0-13 telomerase reverse transcriptase Homo sapiens 50-55
12810068-3 2003 Retinoic acid (RA)-induced differentiation led to hTERT gene silencing and increased methylation of the hTERT promoter. Tretinoin 0-13 telomerase reverse transcriptase Homo sapiens 104-109
12810068-3 2003 Retinoic acid (RA)-induced differentiation led to hTERT gene silencing and increased methylation of the hTERT promoter. Tretinoin 15-17 telomerase reverse transcriptase Homo sapiens 50-55
12810068-3 2003 Retinoic acid (RA)-induced differentiation led to hTERT gene silencing and increased methylation of the hTERT promoter. Tretinoin 15-17 telomerase reverse transcriptase Homo sapiens 104-109
14983057-9 2004 In a model system for neural differentiation, Nolz-1 mRNA was dramatically induced on neural induction of P19 embryonal carcinoma cells by retinoic acid, suggesting that Nolz-1 activation may be involved in neural differentiation. Tretinoin 139-152 interleukin 23 subunit alpha Homo sapiens 106-109
14983057-9 2004 In a model system for neural differentiation, Nolz-1 mRNA was dramatically induced on neural induction of P19 embryonal carcinoma cells by retinoic acid, suggesting that Nolz-1 activation may be involved in neural differentiation. Tretinoin 139-152 zinc finger protein 503 Homo sapiens 170-176
29748133-1 2018 Retinoic acid is the active metabolite of vitamin A and regulates several important cellular processes by activating retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 142-145
29748133-11 2018 These effects of retinoic acid are thought to be at least partially mediated by the retinoid receptors, as treatment of the neurons with synthetic RAR and RXR agonists produced a similar inhibition of ICa. Tretinoin 17-30 retinoic acid receptor alpha Homo sapiens 147-150
12637327-0 2003 Ser727/Tyr701-phosphorylated Stat1 is required for the regulation of c-Myc, cyclins, and p27Kip1 associated with ATRA-induced G0/G1 arrest of U-937 cells. Tretinoin 113-117 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74
29699387-5 2018 In this study, we investigated the combined effect of ATRA and bromodomain inhibitor JQ1, proven to have potent anti-cancer activity mainly through inhibition of c-Myc. Tretinoin 54-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167
12637327-0 2003 Ser727/Tyr701-phosphorylated Stat1 is required for the regulation of c-Myc, cyclins, and p27Kip1 associated with ATRA-induced G0/G1 arrest of U-937 cells. Tretinoin 113-117 cyclin dependent kinase inhibitor 1B Homo sapiens 89-96
12637327-1 2003 All-trans retinoic acid (ATRA)-induced growth arrest of myeloid cells is associated with a sequential regulation of cyclins and cyclin-dependent kinase inhibitors (CKIs), which modulates the cell cycle machinery and inhibits the G1-S phase progression. Tretinoin 4-23 proliferating cell nuclear antigen Homo sapiens 116-122
12637327-1 2003 All-trans retinoic acid (ATRA)-induced growth arrest of myeloid cells is associated with a sequential regulation of cyclins and cyclin-dependent kinase inhibitors (CKIs), which modulates the cell cycle machinery and inhibits the G1-S phase progression. Tretinoin 25-29 proliferating cell nuclear antigen Homo sapiens 116-122
12637327-7 2003 Our results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and the simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase of the cell cycle. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 132-137
12637327-7 2003 Our results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and the simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase of the cell cycle. Tretinoin 100-104 cyclin dependent kinase inhibitor 1B Homo sapiens 206-213
15179005-8 2004 In PML-RARA-positive APL about 70% of patients are expected to be cured with a combination of ATRA and anthracycline-based chemotherapy. Tretinoin 94-98 PML nuclear body scaffold Homo sapiens 3-6
15179005-8 2004 In PML-RARA-positive APL about 70% of patients are expected to be cured with a combination of ATRA and anthracycline-based chemotherapy. Tretinoin 94-98 retinoic acid receptor alpha Homo sapiens 7-11
15500294-3 2004 Results showed that retinoic acid treatment increases the amount of beta-catenin bound to E-cadherin by decreasing its tyrosine-phosphorylation level. Tretinoin 20-33 catenin beta 1 Homo sapiens 68-80
29757260-8 2018 The knockdown of RARα or MAFB counteracted the ATRA-mediated suppression of HuH7 cell invasion while the knockdown of MAFF inhibited the invasion. Tretinoin 57-61 retinoic acid receptor alpha Homo sapiens 17-20
15061197-0 2004 Alterations in Fas (CD 95/Apo-1) and Fas ligand (CD178) expression in acute promyelocytic leukemia during treatment with ATRA. Tretinoin 121-125 Fas ligand Homo sapiens 37-47
15061197-0 2004 Alterations in Fas (CD 95/Apo-1) and Fas ligand (CD178) expression in acute promyelocytic leukemia during treatment with ATRA. Tretinoin 121-125 Fas cell surface death receptor Homo sapiens 20-25
12756180-3 2003 Grafting of somites or retinoic acid-loaded beads beneath the rostral hindbrain induced the formation of somatic motoneurones in rhombomere 4 only, and Hox genes normally expressed more caudally (Hoxa3, Hoxd4) were induced in this region. Tretinoin 23-36 homeobox D4 Homo sapiens 203-208
12858348-7 2003 However, RA treatment caused sustained expression of N-cadherin and its associated proteins including alpha- and beta-catenin suggesting that modulation of expression of these molecules is associated with RA-induced inhibition of chondrogenesis. Tretinoin 9-11 catenin beta 1 Homo sapiens 113-125
15061197-0 2004 Alterations in Fas (CD 95/Apo-1) and Fas ligand (CD178) expression in acute promyelocytic leukemia during treatment with ATRA. Tretinoin 121-125 Fas cell surface death receptor Homo sapiens 26-31
29716520-5 2018 We analyzed the NUP26L-PIH1D3 bidirectional gene pair during Retinoic acid mediated differentiation of embryonic carcinoma cells. Tretinoin 61-74 dynein axonemal assembly factor 6 Homo sapiens 16-29
15061197-0 2004 Alterations in Fas (CD 95/Apo-1) and Fas ligand (CD178) expression in acute promyelocytic leukemia during treatment with ATRA. Tretinoin 121-125 Fas ligand Homo sapiens 49-54
15061197-3 2004 Data from in vivo and in vitro studies have demonstrated that during ATRA treatment of APL there are significant changes not only in the expression of the apoptotic molecules Fas and Fas ligand, but also in the expression of other molecules involved both in the regulation of apoptosis and in interactions between host immune and leukemia cells. Tretinoin 69-73 Fas ligand Homo sapiens 183-193
15061197-6 2004 We focus on ATRA-induced changes in apoptotic pathways, particularly as it relates to the Fas/Fas ligand system. Tretinoin 12-16 Fas ligand Homo sapiens 94-104
14668795-4 2003 Recently, we have shown that, independently of maturation, a long-term all-trans retinoic acid (ATRA) treatment of the maturation-resistant APL cell line (NB4-LR1) represses telomerase (hTERT), leading to telomere shortening and death. Tretinoin 75-94 telomerase reverse transcriptase Homo sapiens 186-191
14668795-4 2003 Recently, we have shown that, independently of maturation, a long-term all-trans retinoic acid (ATRA) treatment of the maturation-resistant APL cell line (NB4-LR1) represses telomerase (hTERT), leading to telomere shortening and death. Tretinoin 96-100 telomerase reverse transcriptase Homo sapiens 186-191
12858348-7 2003 However, RA treatment caused sustained expression of N-cadherin and its associated proteins including alpha- and beta-catenin suggesting that modulation of expression of these molecules is associated with RA-induced inhibition of chondrogenesis. Tretinoin 205-207 catenin beta 1 Homo sapiens 113-125
12821942-0 2003 The cleavage product deltaPML-RARalpha contributes to all-trans retinoic acid-mediated differentiation in acute promyelocytic leukemia cells. Tretinoin 64-77 retinoic acid receptor alpha Homo sapiens 30-38
12821942-1 2003 PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncated form termed deltaPML-RARalpha during all-trans retinoic acid (ATRA)-induced differentiation of NB4 cells. Tretinoin 167-180 PML nuclear body scaffold Homo sapiens 0-3
12821942-1 2003 PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncated form termed deltaPML-RARalpha during all-trans retinoic acid (ATRA)-induced differentiation of NB4 cells. Tretinoin 167-180 retinoic acid receptor alpha Homo sapiens 4-12
12821942-1 2003 PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncated form termed deltaPML-RARalpha during all-trans retinoic acid (ATRA)-induced differentiation of NB4 cells. Tretinoin 167-180 retinoic acid receptor alpha Homo sapiens 141-149
12821942-1 2003 PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncated form termed deltaPML-RARalpha during all-trans retinoic acid (ATRA)-induced differentiation of NB4 cells. Tretinoin 182-186 PML nuclear body scaffold Homo sapiens 0-3
14623241-8 2003 Our studies suggest that RA signaling provides proximodistal information for limb buds that counterbalances Bmp signaling, which in turn helps mediate proximodistal and anteroposterior patterning of Hgf expression to correctly direct migration of Met-expressing myogenic precursor cells. Tretinoin 25-27 bone morphogenetic protein 1 Homo sapiens 108-111
12821942-1 2003 PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncated form termed deltaPML-RARalpha during all-trans retinoic acid (ATRA)-induced differentiation of NB4 cells. Tretinoin 182-186 retinoic acid receptor alpha Homo sapiens 4-12
29439915-1 2018 Retinoids, such as all-trans-retinoic acid (ATRA), regulate cellular differentiation and signalling pathways in chordates by binding to nuclear retinoic acid receptors (RARalpha/beta/gamma). Tretinoin 19-42 retinoic acid receptor alpha Homo sapiens 169-177
12821942-1 2003 PML-RARalpha protein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncated form termed deltaPML-RARalpha during all-trans retinoic acid (ATRA)-induced differentiation of NB4 cells. Tretinoin 182-186 retinoic acid receptor alpha Homo sapiens 141-149
12821942-4 2003 Treatment with hexamethylene bisacetamide (HMBA) combined with ATRA enhances ATRA-induced differentiation in ATRA-insensitive NB4-CI and arsenic-resistant NB4/As cells, and is associated with stabilization of PML-RARalpha protein and increased deltaPML-RARalpha formation. Tretinoin 63-67 PML nuclear body scaffold Homo sapiens 209-212
12821942-4 2003 Treatment with hexamethylene bisacetamide (HMBA) combined with ATRA enhances ATRA-induced differentiation in ATRA-insensitive NB4-CI and arsenic-resistant NB4/As cells, and is associated with stabilization of PML-RARalpha protein and increased deltaPML-RARalpha formation. Tretinoin 63-67 retinoic acid receptor alpha Homo sapiens 213-221
12821942-4 2003 Treatment with hexamethylene bisacetamide (HMBA) combined with ATRA enhances ATRA-induced differentiation in ATRA-insensitive NB4-CI and arsenic-resistant NB4/As cells, and is associated with stabilization of PML-RARalpha protein and increased deltaPML-RARalpha formation. Tretinoin 63-67 retinoic acid receptor alpha Homo sapiens 253-261
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 PML nuclear body scaffold Homo sapiens 51-54
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 55-63
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 176-184
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 PML nuclear body scaffold Homo sapiens 172-175
14534139-9 2003 For the posterior hindbrain, we identify retinoic acid as an important signal to induce NA differentiation in the medulla oblongata and area postrema, where it expands the tfap2a expression domain and thus acts upstream of tfap2a. Tretinoin 41-54 transcription factor AP-2 alpha Danio rerio 172-178
14534139-9 2003 For the posterior hindbrain, we identify retinoic acid as an important signal to induce NA differentiation in the medulla oblongata and area postrema, where it expands the tfap2a expression domain and thus acts upstream of tfap2a. Tretinoin 41-54 transcription factor AP-2 alpha Danio rerio 223-229
14959844-1 2003 Acute promyelocytic leukemia (APL) is a form of acute myelogenous leukemia characterized by chromosomal alterations involving the retinoic acid receptor-alpha (RARalpha) gene that generate unique chimeric proteins (N-RARalpha) and by clinical responsiveness to all-trans-retinoic acid (ATRA) treatment. Tretinoin 265-284 retinoic acid receptor alpha Homo sapiens 130-158
14959844-1 2003 Acute promyelocytic leukemia (APL) is a form of acute myelogenous leukemia characterized by chromosomal alterations involving the retinoic acid receptor-alpha (RARalpha) gene that generate unique chimeric proteins (N-RARalpha) and by clinical responsiveness to all-trans-retinoic acid (ATRA) treatment. Tretinoin 265-284 retinoic acid receptor alpha Homo sapiens 160-168
14959844-1 2003 Acute promyelocytic leukemia (APL) is a form of acute myelogenous leukemia characterized by chromosomal alterations involving the retinoic acid receptor-alpha (RARalpha) gene that generate unique chimeric proteins (N-RARalpha) and by clinical responsiveness to all-trans-retinoic acid (ATRA) treatment. Tretinoin 286-290 retinoic acid receptor alpha Homo sapiens 130-158
14959844-1 2003 Acute promyelocytic leukemia (APL) is a form of acute myelogenous leukemia characterized by chromosomal alterations involving the retinoic acid receptor-alpha (RARalpha) gene that generate unique chimeric proteins (N-RARalpha) and by clinical responsiveness to all-trans-retinoic acid (ATRA) treatment. Tretinoin 286-290 retinoic acid receptor alpha Homo sapiens 160-168
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 176-184
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 176-184
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 PML nuclear body scaffold Homo sapiens 172-175
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 176-184
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 176-184
12821942-8 2003 These data suggest that (a) ATRA treatment induces PML-RARalpha cleavage by induction of unknown enzymes independent of proteasome- and caspase-mediated pathways; (b) deltaPML-RARalpha might function differently from both PML-RARalpha and RARalpha; (c) failure to cleave PML-RARalpha and form deltaPML-RARalpha after ATRA treatment may contribute to ATRA resistance in APL cells. Tretinoin 317-321 PML nuclear body scaffold Homo sapiens 51-54
14706140-1 2003 Detection of the PML/RARalpha fusion gene by RT-PCR in acute promyelocytic leukemia (APL) blasts is not only critical to commence promptly the specific therapy with all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)), but also essential for the definition of PML breakpoint type and subsequent monitoring of minimal residual disease (MRD). Tretinoin 175-188 PML nuclear body scaffold Homo sapiens 17-20
14706140-1 2003 Detection of the PML/RARalpha fusion gene by RT-PCR in acute promyelocytic leukemia (APL) blasts is not only critical to commence promptly the specific therapy with all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)), but also essential for the definition of PML breakpoint type and subsequent monitoring of minimal residual disease (MRD). Tretinoin 175-188 retinoic acid receptor alpha Homo sapiens 21-29
14706140-1 2003 Detection of the PML/RARalpha fusion gene by RT-PCR in acute promyelocytic leukemia (APL) blasts is not only critical to commence promptly the specific therapy with all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)), but also essential for the definition of PML breakpoint type and subsequent monitoring of minimal residual disease (MRD). Tretinoin 190-194 PML nuclear body scaffold Homo sapiens 17-20
14706140-1 2003 Detection of the PML/RARalpha fusion gene by RT-PCR in acute promyelocytic leukemia (APL) blasts is not only critical to commence promptly the specific therapy with all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)), but also essential for the definition of PML breakpoint type and subsequent monitoring of minimal residual disease (MRD). Tretinoin 190-194 retinoic acid receptor alpha Homo sapiens 21-29
29439915-1 2018 Retinoids, such as all-trans-retinoic acid (ATRA), regulate cellular differentiation and signalling pathways in chordates by binding to nuclear retinoic acid receptors (RARalpha/beta/gamma). Tretinoin 44-48 retinoic acid receptor alpha Homo sapiens 169-177
14706140-1 2003 Detection of the PML/RARalpha fusion gene by RT-PCR in acute promyelocytic leukemia (APL) blasts is not only critical to commence promptly the specific therapy with all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)), but also essential for the definition of PML breakpoint type and subsequent monitoring of minimal residual disease (MRD). Tretinoin 190-194 PML nuclear body scaffold Homo sapiens 270-273
12904257-4 2003 RESULTS: Direct protein-protein interaction studies demonstrate that the RXR agonist 9-cis-RA increases interaction of CAR/RXR heterodimers with the coactivator SRC-3, but also inhibits the ability of TCPOBOP to increase and androstanol to decrease coactivator binding. Tretinoin 85-93 CXADR pseudogene 1 Homo sapiens 119-122
29110208-9 2018 In addition, using SH-SY5Y cells differentiated with retinoic acid as a neuronal model, we found that extracellular Gas1 promotes neurite outgrowth, increases the levels of tyrosine hydroxylase, and stimulates the inhibition of GSK3beta. Tretinoin 53-66 growth arrest specific 1 Homo sapiens 116-120
12904257-4 2003 RESULTS: Direct protein-protein interaction studies demonstrate that the RXR agonist 9-cis-RA increases interaction of CAR/RXR heterodimers with the coactivator SRC-3, but also inhibits the ability of TCPOBOP to increase and androstanol to decrease coactivator binding. Tretinoin 85-93 nuclear receptor coactivator 3 Homo sapiens 161-166
12813000-7 2003 In another set of experiments, cells treated for 10-12 days with vehicle (ethanol) or retinoic acid were challenged with ET-1 or sarafotoxin S6c, and various determinations were made at 24 h. 3 Retinoic acid inhibited transformation and proliferation of HSC as assessed by morphological characteristics, expression of alpha-sma, bromodeoxyuridine incorporation and cell count. Tretinoin 194-207 actin gamma 2, smooth muscle Rattus norvegicus 318-327
12813000-11 2003 The presence of retinoic acid in the medium during treatment with ET-1 caused further reduction in the expression of alpha-smooth muscle actin. Tretinoin 16-29 actin gamma 2, smooth muscle Rattus norvegicus 117-142
12746314-3 2003 Both RA and BMP-2 induced expression of the chondrocyte maturational marker, colX, in chondrocyte cultures by 8 d. Though the RA effect was small, it synergistically enhanced the effect of BMP-2 on colX and phosphatase activity. Tretinoin 5-7 bone morphogenetic protein 2 Gallus gallus 189-194
12746314-3 2003 Both RA and BMP-2 induced expression of the chondrocyte maturational marker, colX, in chondrocyte cultures by 8 d. Though the RA effect was small, it synergistically enhanced the effect of BMP-2 on colX and phosphatase activity. Tretinoin 126-128 bone morphogenetic protein 2 Gallus gallus 12-17
12746314-3 2003 Both RA and BMP-2 induced expression of the chondrocyte maturational marker, colX, in chondrocyte cultures by 8 d. Though the RA effect was small, it synergistically enhanced the effect of BMP-2 on colX and phosphatase activity. Tretinoin 126-128 bone morphogenetic protein 2 Gallus gallus 189-194
12746314-4 2003 Inhibition of either RA or BMP signaling, with selective inhibitors, interfered with the inductive effects of these agents but also inhibited the complementary pathway, demonstrating a codependence of RA and BMP signaling during chondrocyte maturation. Tretinoin 201-203 bone morphogenetic protein 1 Homo sapiens 27-30
12746314-7 2003 RA did not increase the expression of the type IA BMP receptor but did markedly up-regulate the expression of Smad1 and Smad5 proteins, important participants in the BMP pathway. Tretinoin 0-2 bone morphogenetic protein 1 Homo sapiens 166-169
12746314-9 2003 These findings demonstrate that RA induces the expression of BMP-signaling molecules and enhances BMP effects in chondrocytes. Tretinoin 32-34 bone morphogenetic protein 1 Homo sapiens 61-64
29689192-7 2018 Lats1/2 mutant cells displayed an arrested developmental trajectory with persistence of epicardial markers and expanded expression of Yap targets Dhrs3, an inhibitor of retinoic acid synthesis, and Dpp4, a protease that modulates extracellular matrix (ECM) composition. Tretinoin 169-182 large tumor suppressor kinase 1 Homo sapiens 0-5
12746314-9 2003 These findings demonstrate that RA induces the expression of BMP-signaling molecules and enhances BMP effects in chondrocytes. Tretinoin 32-34 bone morphogenetic protein 1 Homo sapiens 98-101
12782018-0 2003 Modulation of p53 after maternal exposure to all-trans-retinoic acid in Swiss Webster mouse fetuses. Tretinoin 45-68 transformation related protein 53, pseudogene Mus musculus 14-17
12782018-3 2003 We have recently reported the modulation of p53 in murine stem cells by RA. Tretinoin 72-74 transformation related protein 53, pseudogene Mus musculus 44-47
29486153-3 2018 In the neural tube PAX6 expression is initiated in neural progenitors through the positive action of retinoic acid signaling and downregulated in neuronal precursors by the bHLH transcription factor NEUROG2. Tretinoin 101-114 paired box 6a Danio rerio 19-23
12782018-5 2003 RA treatment resulted in a decreased p53 mRNA level in fetuses 24, 48, and 72 h after maternal treatment as detected by semiquantitative reverse transcriptase polymerase chain reaction. Tretinoin 0-2 transformation related protein 53, pseudogene Mus musculus 37-40
12782018-6 2003 Western blot analysis showed a decrease in p53 protein at 24 and 48 h. Immunohistochemistry revealed decreased localization of p53 in the neuroepithelium of fetuses exposed to RA in utero. Tretinoin 176-178 transformation related protein 53, pseudogene Mus musculus 43-46
12782018-6 2003 Western blot analysis showed a decrease in p53 protein at 24 and 48 h. Immunohistochemistry revealed decreased localization of p53 in the neuroepithelium of fetuses exposed to RA in utero. Tretinoin 176-178 transformation related protein 53, pseudogene Mus musculus 127-130
12782018-7 2003 RA treatment also resulted in decreased nuclear p21 and decreased expression of cytosolic as well as nuclear p27 at 72 h in the fetuses. Tretinoin 0-2 dynactin 6 Mus musculus 109-112
29543331-5 2018 We show that in response to RA, TRIM24 serves as an adapter linking RARalpha to the proteasome for its degradation. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 68-76
12955881-4 2003 We demonstrate that RA induces growth arrest and differentiation in HepG2 cells by influencing the activities of cyclin-cdk complexes involved in the regulation of G1/S transition and S-phase progression, in particular by modifying the binding of these complexes to p21 and p27 inhibitors. Tretinoin 20-22 interferon alpha inducible protein 27 Homo sapiens 274-277
12955881-6 2003 Retinoic acid also modulates c-myc and Bcl-2 expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 29-34
12704731-9 2003 As both RARalpha and RXRalpha are present in fetal and neonatal gonocytes, we suggest that retinoic acid exerts its effects on gonocytes via a RARalpha-RXRalpha heterodimer, with RARalpha functioning as an active partner and RXRalpha as a passive partner. Tretinoin 91-104 retinoic acid receptor, alpha Rattus norvegicus 8-16
12704731-9 2003 As both RARalpha and RXRalpha are present in fetal and neonatal gonocytes, we suggest that retinoic acid exerts its effects on gonocytes via a RARalpha-RXRalpha heterodimer, with RARalpha functioning as an active partner and RXRalpha as a passive partner. Tretinoin 91-104 retinoic acid receptor, alpha Rattus norvegicus 143-151
12704731-9 2003 As both RARalpha and RXRalpha are present in fetal and neonatal gonocytes, we suggest that retinoic acid exerts its effects on gonocytes via a RARalpha-RXRalpha heterodimer, with RARalpha functioning as an active partner and RXRalpha as a passive partner. Tretinoin 91-104 retinoic acid receptor, alpha Rattus norvegicus 143-151
12844477-7 2003 Since LMNA is regulated by a retinoic acid responsive element (L-RARE) in the promoter region, we propose that indinavir impairs retinoic acid homeostasis and/or interact via the L-RARE within the LMNA promoter. Tretinoin 29-42 lamin A/C Homo sapiens 6-10
12844477-7 2003 Since LMNA is regulated by a retinoic acid responsive element (L-RARE) in the promoter region, we propose that indinavir impairs retinoic acid homeostasis and/or interact via the L-RARE within the LMNA promoter. Tretinoin 129-142 lamin A/C Homo sapiens 6-10
12606540-8 2003 In addition, ATRA induced multiple features of hypertrophic differentiation (including type X collagen, alkaline phosphatase, and MMP-13), and these effects required TG2. Tretinoin 13-17 transglutaminase 2, C polypeptide Mus musculus 166-169
12606540-9 2003 Significantly, TG2 (-/-) chondrocytes lost the capacity for ATRA-induced expression of Cbfa1, a transcription factor necessary for ATRA-induced chondrocyte hypertrophy. Tretinoin 60-64 transglutaminase 2, C polypeptide Mus musculus 15-18
12606540-9 2003 Significantly, TG2 (-/-) chondrocytes lost the capacity for ATRA-induced expression of Cbfa1, a transcription factor necessary for ATRA-induced chondrocyte hypertrophy. Tretinoin 60-64 runt related transcription factor 2 Mus musculus 87-92
12604597-0 2003 Activation of the Ras-ERK pathway inhibits retinoic acid-induced stimulation of tissue transglutaminase expression in NIH3T3 cells. Tretinoin 43-56 transglutaminase 2, C polypeptide Mus musculus 80-103
12604597-1 2003 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosphoinositide 3-kinase (PI3K) activity was required for RA to increase TGase protein levels. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 44-67
12604597-1 2003 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosphoinositide 3-kinase (PI3K) activity was required for RA to increase TGase protein levels. Tretinoin 0-13 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 119-144
12604597-1 2003 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosphoinositide 3-kinase (PI3K) activity was required for RA to increase TGase protein levels. Tretinoin 15-17 transglutaminase 2, C polypeptide Mus musculus 44-67
12604597-1 2003 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosphoinositide 3-kinase (PI3K) activity was required for RA to increase TGase protein levels. Tretinoin 15-17 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 119-144
12604597-1 2003 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosphoinositide 3-kinase (PI3K) activity was required for RA to increase TGase protein levels. Tretinoin 178-180 transglutaminase 2, C polypeptide Mus musculus 44-67
12604597-1 2003 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosphoinositide 3-kinase (PI3K) activity was required for RA to increase TGase protein levels. Tretinoin 178-180 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 119-144
12711858-0 2003 Retinoic acid increases expression of the calcium-binding protein S100P in human gastric cancer cells. Tretinoin 0-13 S100 calcium binding protein P Homo sapiens 66-71
12754300-9 2003 In contrast, higher doses of RA (40 nM to 1 micro M) inhibited ERK1 expression, caused accumulation of G(1) phase cyclins and cdks, decreased Rb phosphorylation, and increased Rb/E2F-1 association. Tretinoin 29-31 E2F transcription factor 1 Homo sapiens 179-184
12711469-6 2003 Cutaneous expression of CYP2S1 was induced by ultraviolet radiation, PUVA, coal tar, and all-trans retinoic acid; expression was significantly higher in lesional psoriatic skin than in adjacent non-lesional skin (geometric mean 3.38 [95% CI 2.64-4.34] times higher; p<0.0001), which implies that topical drugs are differentially metabolised in psoriatic plaque and non-lesional skin. Tretinoin 99-112 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 24-30
12711469-7 2003 We showed that all-trans retinoic acid is metabolised by CYP2S1, which has higher cutaneous expression than CYP26, previously described as the specific cutaneous P450 retinoic-acid-metabolising enzyme. Tretinoin 25-38 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 57-63
12711469-7 2003 We showed that all-trans retinoic acid is metabolised by CYP2S1, which has higher cutaneous expression than CYP26, previously described as the specific cutaneous P450 retinoic-acid-metabolising enzyme. Tretinoin 167-180 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 57-63
12515718-0 2003 Enhancement of ATRA-induced cell differentiation by inhibition of calcium accumulation into the endoplasmic reticulum: cross-talk between RAR alpha and calcium-dependent signaling. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 138-147
12515718-7 2003 In addition, we found that retinoic acid receptor alpha (RAR alpha) and PML-RAR alpha proteins are protected from ATRA-induced proteolytic degradation by SERCA inhibition, indicating that cellular calcium homeostasis may interact with signaling systems involved in the control of ATRA-dependent transcriptional activity. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 27-55
12515718-7 2003 In addition, we found that retinoic acid receptor alpha (RAR alpha) and PML-RAR alpha proteins are protected from ATRA-induced proteolytic degradation by SERCA inhibition, indicating that cellular calcium homeostasis may interact with signaling systems involved in the control of ATRA-dependent transcriptional activity. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 57-66
12515718-7 2003 In addition, we found that retinoic acid receptor alpha (RAR alpha) and PML-RAR alpha proteins are protected from ATRA-induced proteolytic degradation by SERCA inhibition, indicating that cellular calcium homeostasis may interact with signaling systems involved in the control of ATRA-dependent transcriptional activity. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 76-85
12531892-0 2003 Elements of the glucocorticoid and retinoic acid response units are involved in cAMP-mediated expression of the PEPCK gene. Tretinoin 35-48 phosphoenolpyruvate carboxykinase 1 Gallus gallus 112-117
12487626-4 2003 We show that, in P19 embryonal carcinoma cells, GCs potentiate RA-induced expression of the murine Hoxb -1 gene through an autoregulatory element, b1-ARE, recognized by the Pbx1 and HOXB1 homoeodomain proteins. Tretinoin 63-65 pre B cell leukemia homeobox 1 Mus musculus 173-177
12820386-3 2003 RESULTS & CONCLUSION: ATRA, BMP-6 and ATRA + BMP-6 treatments each induced dopaminergic neuronal differentiation of the IMR-32 cells as judged by expression of GAP-43, tyrosine hydroxylase and microtubule-associated protein 2ab. Tretinoin 26-30 growth associated protein 43 Homo sapiens 164-170
12820386-3 2003 RESULTS & CONCLUSION: ATRA, BMP-6 and ATRA + BMP-6 treatments each induced dopaminergic neuronal differentiation of the IMR-32 cells as judged by expression of GAP-43, tyrosine hydroxylase and microtubule-associated protein 2ab. Tretinoin 42-46 growth associated protein 43 Homo sapiens 164-170
12586765-14 2003 Altogether, our data demonstrate that mEP17 spatial expression, regulation, and fate are different from that of the highly related mouse epididymal retinoic acid binding protein. Tretinoin 148-161 lipocalin 8 Mus musculus 38-43
12554770-5 2003 These differing transcriptional properties appear to reflect the differing abilities of the three RAR isotypes to interact with the SMRT (silencing mediator of retinoic acid and thyroid hormone receptor) corepressor protein: RARalpha binds to SMRT strongly both in vitro and in vivo, whereas RARbeta and RARgamma interact only weakly with SMRT. Tretinoin 160-173 retinoic acid receptor alpha Homo sapiens 98-101
12554770-5 2003 These differing transcriptional properties appear to reflect the differing abilities of the three RAR isotypes to interact with the SMRT (silencing mediator of retinoic acid and thyroid hormone receptor) corepressor protein: RARalpha binds to SMRT strongly both in vitro and in vivo, whereas RARbeta and RARgamma interact only weakly with SMRT. Tretinoin 160-173 retinoic acid receptor alpha Homo sapiens 225-233
12642900-6 2003 Endogenous expression of ACCbeta in differentiated H9C2 myotube was significantly increased by retinoic acid treatment. Tretinoin 95-108 acetyl-CoA carboxylase beta Homo sapiens 25-32
12584566-3 2003 In gel-shift assays, NuMA-RARalpha bound to retinoic acid response elements (RAREs) both as a homodimer and as a heterodimer with RXRalpha. Tretinoin 44-57 retinoic acid receptor alpha Homo sapiens 26-34
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 retinoic acid receptor alpha Homo sapiens 35-43
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 152-165 retinoic acid receptor alpha Homo sapiens 115-123
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 35-43
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 115-123
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 254-258 retinoic acid receptor alpha Homo sapiens 35-43
12584566-6 2003 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid (ATRA) at 10(-7)-10(-6) M and became associated with the coactivator TRAM-1 at 10(-8) M ATRA. Tretinoin 254-258 retinoic acid receptor alpha Homo sapiens 115-123
26680915-0 2003 Correlation between Retinoic Acid Sensitivity and IGFBP-3, AFP Protein Expression in Hepatoma Cell Lines. Tretinoin 20-33 insulin like growth factor binding protein 3 Homo sapiens 50-57
26680915-9 2003 We supposed that RA-induced cell growth inhibition may be related to the expressions of IGFBP-3 and AFP, but no exact correlation exists between the growth inhibition and receptor expression status in hepatoma cell lines. Tretinoin 17-19 insulin like growth factor binding protein 3 Homo sapiens 88-95
12570742-5 2003 RA exerts its molecular actions mainly through RAR and RXR nuclear receptors. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 47-50
12615366-4 2003 RESULTS: From CAT assays, TR2 can suppress retinoic acid (RA)-induced transactivation by 44.7% in HaCaT keratinocytes. Tretinoin 43-56 nuclear receptor subfamily 2 group C member 1 Homo sapiens 26-29
12615366-4 2003 RESULTS: From CAT assays, TR2 can suppress retinoic acid (RA)-induced transactivation by 44.7% in HaCaT keratinocytes. Tretinoin 58-60 nuclear receptor subfamily 2 group C member 1 Homo sapiens 26-29
12538081-2 2003 Recently, studies in vivo and in cell lines have shown that vitamin A and its active metabolite, retinoic acid, regulate the expression of fatty acid desaturases including stearoyl-CoA desaturase and delta-5 desaturase. Tretinoin 97-110 fatty acid desaturase 1 Homo sapiens 200-218
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 26-39 retinoic acid receptor alpha Homo sapiens 86-94
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 41-43 retinoic acid receptor alpha Homo sapiens 86-94
12514132-3 2003 A retinoic acid response element (RARE) was identified downstream of Hoxb5 and shown to be essential for expression of Hoxb5 and Hoxb8 reporter transgenes in the anterior neural tube. Tretinoin 2-15 homeobox B5 Mus musculus 69-74
12514132-3 2003 A retinoic acid response element (RARE) was identified downstream of Hoxb5 and shown to be essential for expression of Hoxb5 and Hoxb8 reporter transgenes in the anterior neural tube. Tretinoin 2-15 homeobox B5 Mus musculus 119-124
12524175-4 2003 The expression of Trip15/CSN2 mRNA was induced at an early stage of neuronal differentiation in the retinoic acid (RA)-treated P19 cells, but not in the triiodothyronine (T3)-primed cardiac muscular cell differentiation. Tretinoin 100-113 COP9 signalosome subunit 2 Rattus norvegicus 18-24
12524175-4 2003 The expression of Trip15/CSN2 mRNA was induced at an early stage of neuronal differentiation in the retinoic acid (RA)-treated P19 cells, but not in the triiodothyronine (T3)-primed cardiac muscular cell differentiation. Tretinoin 115-117 COP9 signalosome subunit 2 Rattus norvegicus 18-24
12524175-6 2003 Enforced expression of sense rat Trip15/CSN2 mRNA caused the downregulation of Oct-3/4 mRNA expression and was sufficient to convert P19 cells into neurons, but not glial cells, only after the aggregation without RA. Tretinoin 213-215 COP9 signalosome subunit 2 Rattus norvegicus 33-39
12524175-7 2003 In the presence of RA, exogenous expression of the sense mRNA caused the intense and rapid induction of neurogenic Brn-2 and Mash-1 mRNA expressions accompanying the strong downregulation of Oct-3/4 mRNA expression, and stimulated both neuronal and glial cell differentiations of P19 cells. Tretinoin 19-21 achaete-scute family bHLH transcription factor 1 Rattus norvegicus 125-131
12524175-7 2003 In the presence of RA, exogenous expression of the sense mRNA caused the intense and rapid induction of neurogenic Brn-2 and Mash-1 mRNA expressions accompanying the strong downregulation of Oct-3/4 mRNA expression, and stimulated both neuronal and glial cell differentiations of P19 cells. Tretinoin 19-21 solute carrier family 22 member 8 Rattus norvegicus 191-198
12532224-12 2003 Sec61alpha, Hsp47 and type IV collagen levels were increased after retinoic acid treatment. Tretinoin 67-80 serine (or cysteine) peptidase inhibitor, clade H, member 1 Mus musculus 12-17
14708090-11 2003 Analysis of gene expression demonstrated changes in the anterior boundaries of Hoxa7 expression domains in embryos treated on GD 6 and 8 with RA. Tretinoin 142-144 homeobox A7 Mus musculus 79-84
14708090-13 2003 The studies indicate that RA GD 6 treatment-induced Hoxa7 shifts were rostral (posteriorization) while the RA-induced GD 8 anterior expression boundary shift was caudal (anteriorization), correlating with the axial skeletal changes noted. Tretinoin 26-28 homeobox A7 Mus musculus 52-57
12645859-8 2003 The addition of atRA to cell culture produced a marked increase in the amounts of RAR-beta2 mRNA (2.2- to 41-fold). Tretinoin 16-20 retinoic acid receptor alpha Homo sapiens 82-85
12645859-12 2003 Our results suggest that the expressions of the RAR-alpha2 and -beta2 isoforms in lymphoid cells are highly controlled by atRA. Tretinoin 122-126 retinoic acid receptor alpha Homo sapiens 48-51
12893766-0 2003 Comparative analysis of genes regulated by PML/RAR alpha and PLZF/RAR alpha in response to retinoic acid using oligonucleotide arrays. Tretinoin 91-104 PML nuclear body scaffold Homo sapiens 43-56
12893766-0 2003 Comparative analysis of genes regulated by PML/RAR alpha and PLZF/RAR alpha in response to retinoic acid using oligonucleotide arrays. Tretinoin 91-104 retinoic acid receptor alpha Homo sapiens 47-56
14592454-7 2003 Mechanistically, inhibition of telomerase by endogenous ceramide in response to ATRA treatment involves, at least in part, down-regulation of the expression of telomerase reverse transcriptase (hTERT) mRNA, as determined by semi-quantitative RT-PCR, in these cells. Tretinoin 80-84 telomerase reverse transcriptase Homo sapiens 194-199
14649406-1 2003 Effects of two natural (retinol and retinoic acid, RA) and one synthetic N-(4-hydroxyphenyl) retinamide (4-HPR) retinoids on proliferation and expression of urokinase-plasminogen activator (u-PA) by bovine mammary epithelial cells were examined. Tretinoin 36-49 plasminogen activator, urokinase Bos taurus 157-188
12888564-9 2003 Finally, mNAT1 and mARD1 are expressed in proliferating mouse P19 embryonic carcinoma cells; treatment of these cells with retinoic acid initiates exit from the cell cycle, neuronal differentiation, and down-regulation of mNAT1 and mARD1 as the NMOA receptor 1 gene is induced. Tretinoin 123-136 N-acetyl transferase 1 Mus musculus 9-14
12888564-9 2003 Finally, mNAT1 and mARD1 are expressed in proliferating mouse P19 embryonic carcinoma cells; treatment of these cells with retinoic acid initiates exit from the cell cycle, neuronal differentiation, and down-regulation of mNAT1 and mARD1 as the NMOA receptor 1 gene is induced. Tretinoin 123-136 N(alpha)-acetyltransferase 10, NatA catalytic subunit Mus musculus 19-24
12888564-9 2003 Finally, mNAT1 and mARD1 are expressed in proliferating mouse P19 embryonic carcinoma cells; treatment of these cells with retinoic acid initiates exit from the cell cycle, neuronal differentiation, and down-regulation of mNAT1 and mARD1 as the NMOA receptor 1 gene is induced. Tretinoin 123-136 N-acetyl transferase 1 Mus musculus 222-227
12888564-9 2003 Finally, mNAT1 and mARD1 are expressed in proliferating mouse P19 embryonic carcinoma cells; treatment of these cells with retinoic acid initiates exit from the cell cycle, neuronal differentiation, and down-regulation of mNAT1 and mARD1 as the NMOA receptor 1 gene is induced. Tretinoin 123-136 N(alpha)-acetyltransferase 10, NatA catalytic subunit Mus musculus 232-237
14519498-1 2003 Human, neuronally committed hNT or NT2-N cells, originally derived from the Ntera2/D1 (NT2) clone after exposure to retinoic acid (RA), represent a potentially important source of cells to treat neurodegenerative diseases. Tretinoin 116-129 ras responsive element binding protein 1 Homo sapiens 28-31
14519498-1 2003 Human, neuronally committed hNT or NT2-N cells, originally derived from the Ntera2/D1 (NT2) clone after exposure to retinoic acid (RA), represent a potentially important source of cells to treat neurodegenerative diseases. Tretinoin 131-133 ras responsive element binding protein 1 Homo sapiens 28-31
14613030-3 2003 Support for the concept of targeting products of fusion genes found in specific cancers was first provided by the efficacy of all-trans retinoic acid in acute promyelocytic leukemia where the RARalpha all-trans retinoic acid target is the target of multiple different chromosomal rearrangements. Tretinoin 136-149 retinoic acid receptor alpha Homo sapiens 192-200
14613030-3 2003 Support for the concept of targeting products of fusion genes found in specific cancers was first provided by the efficacy of all-trans retinoic acid in acute promyelocytic leukemia where the RARalpha all-trans retinoic acid target is the target of multiple different chromosomal rearrangements. Tretinoin 211-224 retinoic acid receptor alpha Homo sapiens 192-200
12949900-4 2003 Further support for these allegations was obtained by culturing b2T cells in defined medium and by assessing the expression of Krox20, an odd-numbered rhombomere marker, which appeared to be modulated by a complex interplay between FGF, retinoic acid (RA), and noggin. Tretinoin 237-250 early growth response 2 Mus musculus 127-133
12949900-4 2003 Further support for these allegations was obtained by culturing b2T cells in defined medium and by assessing the expression of Krox20, an odd-numbered rhombomere marker, which appeared to be modulated by a complex interplay between FGF, retinoic acid (RA), and noggin. Tretinoin 252-254 early growth response 2 Mus musculus 127-133
12914961-4 2003 Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway. Tretinoin 43-56 ret proto-oncogene Homo sapiens 75-78
12914961-4 2003 Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway. Tretinoin 43-56 ret proto-oncogene Homo sapiens 111-114
12895391-2 2003 Reverse-transcription polymerase chain reaction (RT-PCR) amplification of PML-RARalpha messenger RNA can establish the diagnosis of APL, predict response to all-trans retinoic acid and arsenic trioxide, detect minimal residual disease, and predict relapse. Tretinoin 167-180 PML nuclear body scaffold Homo sapiens 74-77
12895391-2 2003 Reverse-transcription polymerase chain reaction (RT-PCR) amplification of PML-RARalpha messenger RNA can establish the diagnosis of APL, predict response to all-trans retinoic acid and arsenic trioxide, detect minimal residual disease, and predict relapse. Tretinoin 167-180 retinoic acid receptor alpha Homo sapiens 78-86
12970771-5 2003 Treatment with pharmacological RA dosages overcomes the dominant-negative effects of PML/RARalpha to activate transcription of retinoid target genes. Tretinoin 31-33 PML nuclear body scaffold Homo sapiens 85-88
12865321-3 2003 In the current study, we examined the regulation of PSA promoter-directed NIS expression and therapeutic effectiveness of (131)I in LNCaP cells by all-trans-retinoic acid (atRA). Tretinoin 147-170 kallikrein related peptidase 3 Homo sapiens 52-55
12865321-3 2003 In the current study, we examined the regulation of PSA promoter-directed NIS expression and therapeutic effectiveness of (131)I in LNCaP cells by all-trans-retinoic acid (atRA). Tretinoin 172-176 kallikrein related peptidase 3 Homo sapiens 52-55
12865321-10 2003 In conclusion, treatment with atRA increases NIS expression levels and selective killing effect of (131)I in prostate cancer cells stably expressing NIS under the control of the PSA promoter. Tretinoin 30-34 kallikrein related peptidase 3 Homo sapiens 178-181
12865321-11 2003 Therefore atRA may be used to enhance the therapeutic response to radioiodine in prostate cancer cells following PSA promoter-directed NIS gene delivery. Tretinoin 10-14 kallikrein related peptidase 3 Homo sapiens 113-116
12645859-13 2003 Differences in the regulation of RAR isoforms by atRA in human lymphoid cells may be an important factor in the modulation of cytokine production and the augmentation in Ig synthesis by atRA. Tretinoin 49-53 retinoic acid receptor alpha Homo sapiens 33-36
12648520-4 2003 In the absence of the RAR-specific ligand all trans retinoic acid, RAR/RXR heterodimers are associated with the nuclear receptor corepressor N-CoR or the related SMRT. Tretinoin 52-65 nuclear receptor corepressor 1 Homo sapiens 112-140
12648520-4 2003 In the absence of the RAR-specific ligand all trans retinoic acid, RAR/RXR heterodimers are associated with the nuclear receptor corepressor N-CoR or the related SMRT. Tretinoin 52-65 nuclear receptor corepressor 1 Homo sapiens 141-146
12529666-4 2003 Furthermore, gel-shift analysis of APL cells showed elevated levels of PU.1 binding activity to the M-CSF receptor promoter, particularly after ATRA stimulation. Tretinoin 144-148 colony stimulating factor 1 Homo sapiens 100-105
12529666-6 2003 A variable proportion of ATRA-induced APL cells exhibited monocyte-like morphology and immunophenotype: the proportion of monocytic cells was consistently increased by combined treatment with ATRA and diverse hematopoietic growth factors cocktails, which always comprised M-CSF. Tretinoin 25-29 colony stimulating factor 1 Homo sapiens 272-277
12529666-6 2003 A variable proportion of ATRA-induced APL cells exhibited monocyte-like morphology and immunophenotype: the proportion of monocytic cells was consistently increased by combined treatment with ATRA and diverse hematopoietic growth factors cocktails, which always comprised M-CSF. Tretinoin 192-196 colony stimulating factor 1 Homo sapiens 272-277
14510502-3 2003 Previously we showed that JDP2 inhibits the retinoic acid (RA) dependent transcription by recruiting a histone deacetylase 3 (HDAC3) complex to the promoter region of the target genes. Tretinoin 44-57 Jun dimerization protein 2 Homo sapiens 26-30
14510502-3 2003 Previously we showed that JDP2 inhibits the retinoic acid (RA) dependent transcription by recruiting a histone deacetylase 3 (HDAC3) complex to the promoter region of the target genes. Tretinoin 59-61 Jun dimerization protein 2 Homo sapiens 26-30
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 nuclear receptor coactivator 3 Homo sapiens 288-317
14535629-1 2003 In the process of retinoic acid (RA) signaling, retinoic acid receptor interacts with a coactivator complex composed of various transcription cofactors such as CREB-binding protein (CBP)/p300 and p160 family member proteins represented by steroid receptor coactivator-1 (SRC-1)/NCoA1 and p300/CBP cointegrator protein (p/CIP)/ACTR. Tretinoin 18-31 nuclear receptor coactivator 3 Homo sapiens 319-324
12882839-0 2003 Retinoic acids exert direct effects on T cells to suppress Th1 development and enhance Th2 development via retinoic acid receptors. Tretinoin 0-14 heart and neural crest derivatives expressed 2 Mus musculus 87-90
12882839-1 2003 The vitamin A metabolite, retinoic acid (RA), affects Th1 and Th2 development. Tretinoin 26-39 heart and neural crest derivatives expressed 2 Mus musculus 62-65
12882839-1 2003 The vitamin A metabolite, retinoic acid (RA), affects Th1 and Th2 development. Tretinoin 41-43 heart and neural crest derivatives expressed 2 Mus musculus 62-65
12403723-5 2002 Conversely, the low level of beta-catenin in differentiated articular chondrocytes was increased by post-translational stabilization during phenotypic loss caused by a serial monolayer culture or exposure to retinoic acid or interleukin-1beta. Tretinoin 208-221 catenin beta 1 Homo sapiens 29-41
29516351-5 2018 ATRA significantly decreased the nuclear to cytoplasmic ratio of SIRT1 and SIRT2.1, while sirtinol inhibited that of SIRT1, and TSA increased that of SIRT1 and SIRT2.1 during early differentiation. Tretinoin 0-4 sirtuin 2 Homo sapiens 160-165
12213824-4 2002 The switch to CAK hypophosphorylation of RARalpha is accompanied by decreased MAT1 expression and MAT1 fragmentation that occurs in the differentiating cells through the all-trans-retinoic acid (ATRA)-mediated proteasome degradation pathway. Tretinoin 170-193 retinoic acid receptor alpha Homo sapiens 41-49
12213824-4 2002 The switch to CAK hypophosphorylation of RARalpha is accompanied by decreased MAT1 expression and MAT1 fragmentation that occurs in the differentiating cells through the all-trans-retinoic acid (ATRA)-mediated proteasome degradation pathway. Tretinoin 195-199 retinoic acid receptor alpha Homo sapiens 41-49
29496480-0 2018 Coordinate regulation of retinoic acid synthesis by pbx genes and fibroblast growth factor signaling by hoxb1b is required for hindbrain patterning and development. Tretinoin 25-38 pbx/knotted 1 homeobox 1.2 Danio rerio 52-55
12423348-11 2002 Cells stimulated with all-trans retinoic acid to differentiate them towards a granulocytic pathway, showed a strong ( approximately 18-fold) down-regulation of intracellular cystatin F and almost abolished secreted levels of the inhibitor. Tretinoin 32-45 cystatin F Homo sapiens 174-184
12397630-7 2002 In addition to the two PBX1 isoforms, the mRNA level of the other two subtypes (PBX2 and PBX3) and the level of PBX1/2/3 protein were also found to be elevated in limb buds after RA treatment. Tretinoin 179-181 pre B cell leukemia homeobox 1 Mus musculus 112-120
12831362-3 2003 Increased FR-beta expression in these cells can be induced by all-trans retinoic acid (ATRA) and other retinoid compounds in the absence of terminal differentiation or cell growth inhibition. Tretinoin 72-85 folate receptor beta Homo sapiens 10-17
12831362-3 2003 Increased FR-beta expression in these cells can be induced by all-trans retinoic acid (ATRA) and other retinoid compounds in the absence of terminal differentiation or cell growth inhibition. Tretinoin 87-91 folate receptor beta Homo sapiens 10-17
12642121-3 2003 Paradoxically, the X-RARalpha fusion protein has the potential to mediate myeloid differentiation at pharmacological doses of its ligand (all trans-retinoic acid (ATRA)), which is dependent on the dissociation of the HDAC/co-repressor complex. Tretinoin 142-161 retinoic acid receptor alpha Homo sapiens 21-29
29523306-6 2018 Such suppression is in response to a retinoic acid-RARalpha binding initiated pathway and results in the upregulation of gut-homing chemokine receptor CCR9 and downregulation of lymphoid tissue-homing receptor CCR7, which can then guide ILC3 cells to intestine. Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 51-59
12642121-3 2003 Paradoxically, the X-RARalpha fusion protein has the potential to mediate myeloid differentiation at pharmacological doses of its ligand (all trans-retinoic acid (ATRA)), which is dependent on the dissociation of the HDAC/co-repressor complex. Tretinoin 163-167 retinoic acid receptor alpha Homo sapiens 21-29
12642121-5 2003 It is now apparent that the nature of the RARalpha-fusion partner is a critical determinant of response to ATRA and arsenic, underlining the importance of cytogenetic and molecular characterisation of patients with suspected APL to determine the most appropriate treatment approach. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 42-50
12642121-6 2003 Standard protocols involving ATRA combined with anthracycline-based chemotherapy, lead to cure of approximately 70% patients with PML-RARalpha-associated APL. Tretinoin 29-33 PML nuclear body scaffold Homo sapiens 130-133
12171913-6 2002 Collectively, enhanced binding of Sp1 to promoter I of the KOR gene as a result of inhibiting the ERK pathway contributes to RA induction of this gene in P19. Tretinoin 125-127 cyclin dependent kinase inhibitor 2D Mus musculus 154-157
12642121-6 2003 Standard protocols involving ATRA combined with anthracycline-based chemotherapy, lead to cure of approximately 70% patients with PML-RARalpha-associated APL. Tretinoin 29-33 retinoic acid receptor alpha Homo sapiens 134-142
29253589-5 2018 We report that differentiation of H9c2 cells with retinoic acid towards cardiomyocytes is accompanied by increased expression of mitochondrial proteins, oxygen consumption, and expression of the PA/PI binding protein, PITPNC1, and CDS1 immunoreactivity. Tretinoin 50-63 CDP-diacylglycerol synthase 1 Rattus norvegicus 231-235
12846418-3 2003 9-cis retinoic acid (9-cis RA), a ligand for both retinoic acid receptor (RAR)/retinoic X receptor (RXR) heterodimers as well as RXR/RXR homodimers, markedly induced NIS mRNA expression in MCF-7 breast cancer cells in a dose- and time-dependent fashion, with maximal levels occurring at 12 h. All-trans retinoic acid, ATRA, a RAR specific ligand had a similar potency. Tretinoin 6-19 retinoic acid receptor alpha Homo sapiens 50-72
12846418-3 2003 9-cis retinoic acid (9-cis RA), a ligand for both retinoic acid receptor (RAR)/retinoic X receptor (RXR) heterodimers as well as RXR/RXR homodimers, markedly induced NIS mRNA expression in MCF-7 breast cancer cells in a dose- and time-dependent fashion, with maximal levels occurring at 12 h. All-trans retinoic acid, ATRA, a RAR specific ligand had a similar potency. Tretinoin 6-19 retinoic acid receptor alpha Homo sapiens 74-77
12846418-3 2003 9-cis retinoic acid (9-cis RA), a ligand for both retinoic acid receptor (RAR)/retinoic X receptor (RXR) heterodimers as well as RXR/RXR homodimers, markedly induced NIS mRNA expression in MCF-7 breast cancer cells in a dose- and time-dependent fashion, with maximal levels occurring at 12 h. All-trans retinoic acid, ATRA, a RAR specific ligand had a similar potency. Tretinoin 6-19 retinoic acid receptor alpha Homo sapiens 326-329
12782018-8 2003 These results demonstrated that RA-mediated teratogenesis is accompanied by a reduction in the temporal and spatial pattern of p53 gene and protein expression in addition to the disruption of the cell cycle by modulation of p21 and p27. Tretinoin 32-34 transformation related protein 53, pseudogene Mus musculus 127-130
12239632-10 2002 WNT7B, but not WNT7A, was slightly up-regulated by all-trans retinoic acid in NT2 cells. Tretinoin 61-74 Wnt family member 7B Homo sapiens 0-5
12357342-3 2002 The treatment of APL patients with all-trans retinoic acid (ATRA) results in clinical remission associated with blast cell differentiation and reformation of the PML nuclear bodies. Tretinoin 39-58 PML nuclear body scaffold Homo sapiens 162-165
12357342-3 2002 The treatment of APL patients with all-trans retinoic acid (ATRA) results in clinical remission associated with blast cell differentiation and reformation of the PML nuclear bodies. Tretinoin 60-64 PML nuclear body scaffold Homo sapiens 162-165
12357343-5 2002 According to this idea the PML-RARalpha fusion protein promotes leukemogenesis not only through repression of retinoic acid responsive genes, but also by way of interfering with several tumor suppressor proteins that cooperate to establish senescence. Tretinoin 110-123 PML nuclear body scaffold Homo sapiens 27-30
12357343-5 2002 According to this idea the PML-RARalpha fusion protein promotes leukemogenesis not only through repression of retinoic acid responsive genes, but also by way of interfering with several tumor suppressor proteins that cooperate to establish senescence. Tretinoin 110-123 retinoic acid receptor alpha Homo sapiens 31-39
12357345-5 2002 It is also likely that treatment of APL cells by retinoic acid induces de novo up-regulation of the same genes which are dominantly repressed by PML-RARalpha and whose expression is required for reactivation of the differentiation program. Tretinoin 49-62 PML nuclear body scaffold Homo sapiens 145-148
12357345-5 2002 It is also likely that treatment of APL cells by retinoic acid induces de novo up-regulation of the same genes which are dominantly repressed by PML-RARalpha and whose expression is required for reactivation of the differentiation program. Tretinoin 49-62 retinoic acid receptor alpha Homo sapiens 149-157
12782018-8 2003 These results demonstrated that RA-mediated teratogenesis is accompanied by a reduction in the temporal and spatial pattern of p53 gene and protein expression in addition to the disruption of the cell cycle by modulation of p21 and p27. Tretinoin 32-34 dynactin 6 Mus musculus 232-235
12841631-0 2003 Retinoic acid inhibits the growth of bone marrow mesenchymal stem cells and induces p27Kip1 and p16INK4A up-regulation. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 84-91
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 forkhead box P3 Mus musculus 158-163
12606456-7 2003 We show that peroxisome proliferators were able to disrupt the retinoic acid-induced nuclear localization of RARalpha and the retinoic acid-stimulated increase in transcriptional activity of a retinoic acid-responsive reporter gene in Sertoli cells. Tretinoin 63-76 retinoic acid receptor alpha Homo sapiens 109-117
12513735-0 2002 [Study on telomerase activity and expression of hTERT, c-myc and bcl-2 during terminal differentiation of HL-60 cells induced by retinoic acid]. Tretinoin 129-142 telomerase reverse transcriptase Homo sapiens 48-53
12513735-1 2002 The study was to explore the telomerase activity and the expression of hTERT, c-myc and bcl-2 mRNA during terminal differentiation of HL-60 cells induced by all trans-retinoic acid (ATRA) and to study the possible molecular mechanism. Tretinoin 182-186 telomerase reverse transcriptase Homo sapiens 71-76
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 embryonic ectoderm development Mus musculus 168-171
12513735-4 2002 It is concluded that the telomerase activity is related to decrease expression of hTERT, c-myc and bcl-2 mRNA during HL-60 cell differentiation induced by ATRA. Tretinoin 155-159 telomerase reverse transcriptase Homo sapiens 82-87
12513735-4 2002 It is concluded that the telomerase activity is related to decrease expression of hTERT, c-myc and bcl-2 mRNA during HL-60 cell differentiation induced by ATRA. Tretinoin 155-159 MYC proto-oncogene, bHLH transcription factor Homo sapiens 89-94
12666206-8 2003 Respecification of the anterior mesoderm as occurs secondarily to Sonic hedgehog (SHH) or retinoic acid application to the anterior border leads to down-regulation of eHAND expression. Tretinoin 90-103 heart and neural crest derivatives expressed 1 Gallus gallus 167-172
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 embryonic ectoderm development Mus musculus 264-267
29305158-0 2018 TBR2 antagonizes retinoic acid dependent neuronal differentiation by repressing Zfp423 during corticogenesis. Tretinoin 17-30 zinc finger protein 423 Homo sapiens 80-86
12660332-6 2003 Daily administration of ATRA ameliorated proteinuria, which was accompanied by the improvement in the effacement of the foot processes and by the induction of nephrin and midkine. Tretinoin 24-28 NPHS1 adhesion molecule, nephrin Rattus norvegicus 159-166
12354671-7 2002 Taken together, these results indicate that the PEPCK retinoic acid response element (RARE)1 is required for 9-cis RA induction-but not all-trans RA induction-of the PEPCK gene. Tretinoin 115-117 retinoic acid response element 1 Mus musculus 86-92
29301505-5 2018 METHODS: As a proof of principle, differentiation upon ATRA treatment of two MYCN-amplified neuroblastoma cell lines, IMR32 and BE2C, was measured both in cell cultures and in tumours formed on the chick chorioallantoic membrane (CAM). Tretinoin 55-59 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 77-81
12165812-9 2002 WNT5A and WNT5B were expressed together in 5 embryonal tumor cell lines, and were slightly down-regulated by all-trans retinoic acid in NT2 cells. Tretinoin 119-132 Wnt family member 5B Homo sapiens 10-15
12070176-3 2002 To better understand the mechanism of action of ATRA metabolites and isomers, we assessed their binding to retinoic acid receptors (RARs) and activation of RAR-mediated transcription via a retinoic acid response element (RARE). Tretinoin 48-52 retinoic acid receptor alpha Homo sapiens 132-135
12070176-7 2002 The lowest EC(50) value for RAR alpha was with 9-cis-RA (13 nM), followed by 4-oxo-RA (33 nM), 5,6-epoxy-RA (77 nM), 13-cis-RA (124 nM), 18-OH-RA (162 nM), ATRA (169 nM), and 4-OH-RA (791 nM). Tretinoin 47-55 retinoic acid receptor alpha Homo sapiens 28-37
12070176-7 2002 The lowest EC(50) value for RAR alpha was with 9-cis-RA (13 nM), followed by 4-oxo-RA (33 nM), 5,6-epoxy-RA (77 nM), 13-cis-RA (124 nM), 18-OH-RA (162 nM), ATRA (169 nM), and 4-OH-RA (791 nM). Tretinoin 156-160 retinoic acid receptor alpha Homo sapiens 28-37
12769347-6 2003 In the present study, we investigated the relationship between induction of CD38 expression and induction of myeloid differentiation by retinoic acid (RA) in normal and leukemic human hematopoietic cells. Tretinoin 136-149 CD38 molecule Homo sapiens 76-80
12769347-6 2003 In the present study, we investigated the relationship between induction of CD38 expression and induction of myeloid differentiation by retinoic acid (RA) in normal and leukemic human hematopoietic cells. Tretinoin 151-153 CD38 molecule Homo sapiens 76-80
12769347-10 2003 The results suggest that while in normal hematopoietic cells and in PML CD34 - cells induction of CD38 antigen expression by RA results in terminal differentiation along the myeloid lineage, in early myeloblastic leukemic CD34 + cells, induction of CD38 and differentiation are not functionally related. Tretinoin 125-127 PML nuclear body scaffold Homo sapiens 68-71
12769347-10 2003 The results suggest that while in normal hematopoietic cells and in PML CD34 - cells induction of CD38 antigen expression by RA results in terminal differentiation along the myeloid lineage, in early myeloblastic leukemic CD34 + cells, induction of CD38 and differentiation are not functionally related. Tretinoin 125-127 CD38 molecule Homo sapiens 98-102
12769347-10 2003 The results suggest that while in normal hematopoietic cells and in PML CD34 - cells induction of CD38 antigen expression by RA results in terminal differentiation along the myeloid lineage, in early myeloblastic leukemic CD34 + cells, induction of CD38 and differentiation are not functionally related. Tretinoin 125-127 CD38 molecule Homo sapiens 249-253
12769347-11 2003 Since, several lines of evidence suggest that the CD38 - cells are the targets of leukemic transformation, transition of these cellsinto CD38 + phenotype by RA or other drugs may have therapeutic effect, either alone or in conjunction with cytotoxic drugs, regardless the ability of the cells to undergo differentiation. Tretinoin 157-159 CD38 molecule Homo sapiens 50-54
12769347-11 2003 Since, several lines of evidence suggest that the CD38 - cells are the targets of leukemic transformation, transition of these cellsinto CD38 + phenotype by RA or other drugs may have therapeutic effect, either alone or in conjunction with cytotoxic drugs, regardless the ability of the cells to undergo differentiation. Tretinoin 157-159 CD38 molecule Homo sapiens 137-141
12615055-2 2003 In this study, we found that three different neuroblastoma cell lines exhibited wide variation in their responsiveness to the growth inhibitory effects of the retinoic acid receptor (RAR) agonist, all-trans-retinoic acid (aRA). Tretinoin 197-220 retinoic acid receptor alpha Homo sapiens 183-186
12208505-0 2002 Photoaffinity labeling of the uncoupling protein UCP1 with retinoic acid: ubiquinone favors binding. Tretinoin 59-72 uncoupling protein 1 Homo sapiens 49-53
12208505-1 2002 Retinoic acid is a potent activator of the uncoupling protein-1 (UCP1) both at the gene and mitochondrial level. Tretinoin 0-13 uncoupling protein 1 Homo sapiens 43-69
12208505-4 2002 All-trans-retinoic acid binds to UCP1 with high affinity and the labeling is only partially protected by guanosine diphosphate. Tretinoin 0-23 uncoupling protein 1 Homo sapiens 33-37
12208505-5 2002 Ubiquinone (UQ) has been described to be an obligatory cofactor for uncoupling protein function and we demonstrate that it greatly increases the affinity of UCP1 for retinoic acid. Tretinoin 166-179 uncoupling protein 1 Homo sapiens 157-161
12615055-5 2003 Combination of receptor-specific retinoid agonists for RXR and RAR alpha significantly enhanced the sensitivity of N-myc-amplified neuroblastoma cells to the growth inhibitory effects of aRA. Tretinoin 187-190 retinoic acid receptor alpha Homo sapiens 63-72
12615055-5 2003 Combination of receptor-specific retinoid agonists for RXR and RAR alpha significantly enhanced the sensitivity of N-myc-amplified neuroblastoma cells to the growth inhibitory effects of aRA. Tretinoin 187-190 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 115-120
29301505-9 2018 RESULTS: Treatment of IMR32 and BE2C cells in vitro with 10 muM ATRA resulted in a change in cell morphology, a 65% decrease in cell proliferation, upregulation of STMN4 and ROBO2 and downregulation of KLF4. Tretinoin 64-68 roundabout guidance receptor 2 Homo sapiens 174-179
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 138-157 thioredoxin Homo sapiens 14-25
12619135-14 2003 Addition of retinoic acid or sodium butyrate to F9 EC cells showed a rapid decrease in expression of DENTT protein occurring by 1 hr that continued to decrease to almost undetectable levels after 24 hr. Tretinoin 12-25 TSPY-like 2 Mus musculus 101-106
12165554-1 2002 Previous analyses of gene expression in a mouse model of Huntington"s disease (R6/2) indicated that an N-terminal fragment of mutant huntingtin causes downregulation of striatal signaling genes and particularly those normally induced by cAMP and retinoic acid. Tretinoin 246-259 huntingtin Mus musculus 133-143
12139742-0 2002 Phosphatidylinositol 3-kinases are involved in the all-trans retinoic acid-induced upregulation of CD38 antigen on human haematopoietic cells. Tretinoin 61-74 CD38 molecule Homo sapiens 99-103
12139742-1 2002 All-trans retinoic acid (ATRA) is a specific inducer of CD38 antigen on marrow CD34+ cells as well as on blast cells in acute promyelocytic and myeloblastic leukaemia. Tretinoin 0-23 CD38 molecule Homo sapiens 56-60
12139742-1 2002 All-trans retinoic acid (ATRA) is a specific inducer of CD38 antigen on marrow CD34+ cells as well as on blast cells in acute promyelocytic and myeloblastic leukaemia. Tretinoin 25-29 CD38 molecule Homo sapiens 56-60
12139742-3 2002 The aim of this study was to determine whether phosphoinositide 3-kinase (PI3-K) is involved in the modification of CD38 antigen expression on myeloid cells, as PI3-K plays a major role in the ATRA-induced granulocytic differentiation of HL-60 cells. Tretinoin 193-197 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 47-72
12139742-6 2002 Interestingly, PI3-K activity was also necessary for CD38 expression on normal marrow CD34+ cells and for the ATRA-induced upregulation of CD157, a CD38-related antigen. Tretinoin 110-114 CD38 molecule Homo sapiens 148-152
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 138-157 thioredoxin Homo sapiens 107-110
12601020-9 2003 The cell-cycle-arrest stage correlated with the observed microarray results in which the RA treatment downregulated critical genes such as cyclins (cyclin E, cyclin D3) and cyclin-dependent kinases (CDK5, CDK10). Tretinoin 89-91 cyclin dependent kinase 5 Homo sapiens 199-203
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 159-163 thioredoxin Homo sapiens 14-25
28322443-4 2018 We found that thioredoxin interacting protein (TXNIP), which inhibits antioxidant activity of thioredoxin (TRX), was downregulated by all-trans retinoic acid (ATRA). Tretinoin 159-163 thioredoxin Homo sapiens 107-110
12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 36-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 210-215
29387217-1 2018 Acute promyelocytic leukemia (APL), characterized by the presence of the promyelocytic leukemia (PML)-retinoic acid alpha receptor (RARalpha) fusion protein, responds to treatment with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 102-115 PML nuclear body scaffold Homo sapiens 97-100
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 68-70 neuronal differentiation 1 Homo sapiens 273-280
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 57-59 catenin beta 1 Homo sapiens 236-248
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 171-173 catenin beta 1 Homo sapiens 236-248
11983505-0 2002 RAR-RXR selectivity and biological activity of new retinoic acid analogues with heterocyclic or polycyclic aromatic systems. Tretinoin 51-64 retinoic acid receptor alpha Homo sapiens 0-3
12581870-6 2003 Serglycin expression was increased by treatment of ES cells with retinoic acid (RA) and dibutyryl cAMP (dbcAMP). Tretinoin 65-78 serglycin Mus musculus 0-9
12581870-6 2003 Serglycin expression was increased by treatment of ES cells with retinoic acid (RA) and dibutyryl cAMP (dbcAMP). Tretinoin 80-82 serglycin Mus musculus 0-9
12581870-8 2003 Only the lower Mr band is present in serglycin secreted from RA-treated and the higher Mr band in RA+dbcAMP-treated cells, suggesting that core protein structure is affected by differentiation. Tretinoin 61-63 serglycin Mus musculus 37-46
29387217-1 2018 Acute promyelocytic leukemia (APL), characterized by the presence of the promyelocytic leukemia (PML)-retinoic acid alpha receptor (RARalpha) fusion protein, responds to treatment with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 102-115 retinoic acid receptor alpha Homo sapiens 132-140
12565908-5 2003 Constitutively active forms of BMP type I receptors (BMPR-IA and BMPR-IB) and those of activin receptor-like kinase (ALK)-1 and ALK-2 maintained differentiation of chondrocytes in the presence of retinoic acid. Tretinoin 196-209 activin A receptor like type 1 Homo sapiens 87-123
29387217-1 2018 Acute promyelocytic leukemia (APL), characterized by the presence of the promyelocytic leukemia (PML)-retinoic acid alpha receptor (RARalpha) fusion protein, responds to treatment with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 210-214 PML nuclear body scaffold Homo sapiens 97-100
12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 64-69
12700651-0 2003 Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 119-124
12079996-7 2002 However, the mechanism by which retinoic acid positively influences the nuclear localization of RARalpha is not due to retinoic acid directly increasing protein kinase C or mitogen-activated protein kinase activities. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 96-104
29387217-1 2018 Acute promyelocytic leukemia (APL), characterized by the presence of the promyelocytic leukemia (PML)-retinoic acid alpha receptor (RARalpha) fusion protein, responds to treatment with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 210-214 retinoic acid receptor alpha Homo sapiens 132-140
12700651-2 2003 Retinoic acid (RA) decreases N-myc levels and induces cell cycle arrest in vitro and increases event-free survival in advanced stage NB patients. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 29-34
12700651-2 2003 Retinoic acid (RA) decreases N-myc levels and induces cell cycle arrest in vitro and increases event-free survival in advanced stage NB patients. Tretinoin 15-17 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 29-34
29070519-7 2017 ATRA could induce a RARalpha increase; however, the expression of RARbeta and RARgamma were unchanged. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 20-28
12700651-11 2003 Thus, RA induces both N-myc-dependent and -independent mechanisms to minimize the degradation of p27 and arrest NB cell growth. Tretinoin 6-8 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 22-27
12494454-7 2003 However, clones expressing the dominant-negative fos had a markedly decreased sensitivity to RA-induced inhibition of anchorage-dependent and -independent growth. Tretinoin 93-95 FBJ osteosarcoma oncogene Mus musculus 49-52
12494454-8 2003 Treatment of wt B16 cells for 48 h with RA increased melanin production by two to fourfold, but this effect was completely lost in the A-fos clones. Tretinoin 40-42 FBJ osteosarcoma oncogene Mus musculus 137-140
12393416-7 2003 In HL-60R mutant cells, which harbor a defective retinoic acid receptor-alpha (RAR-alpha), ATRA is unable to reduce levels of TGF-beta-induced phospho-Smad2/3, coincident with its inability to differentiate these cells along granulocytic pathways. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 49-77
12186376-4 2002 The cell lines (MCF-7, T-47D, ZR-75-1), which expressed both BRCA1 and p27, were extremely sensitive to the inhibitory effect of the combination of TGZ and either ATRA or 9-cis-RA (ED90, 2-5 x 10(-11) M). Tretinoin 163-167 interferon alpha inducible protein 27 Homo sapiens 71-74
12186376-4 2002 The cell lines (MCF-7, T-47D, ZR-75-1), which expressed both BRCA1 and p27, were extremely sensitive to the inhibitory effect of the combination of TGZ and either ATRA or 9-cis-RA (ED90, 2-5 x 10(-11) M). Tretinoin 171-179 interferon alpha inducible protein 27 Homo sapiens 71-74
12069693-2 2002 METHOD: In this study, we examined the interactions between T and retinoic acid (RA) in cell growth of human prostate carcinoma cells, LNCaP, and their relationship with the expression of RAR and epidermal growth factor receptor (EGF-R). Tretinoin 66-79 retinoic acid receptor alpha Homo sapiens 188-191
12069693-2 2002 METHOD: In this study, we examined the interactions between T and retinoic acid (RA) in cell growth of human prostate carcinoma cells, LNCaP, and their relationship with the expression of RAR and epidermal growth factor receptor (EGF-R). Tretinoin 81-83 retinoic acid receptor alpha Homo sapiens 188-191
12393416-7 2003 In HL-60R mutant cells, which harbor a defective retinoic acid receptor-alpha (RAR-alpha), ATRA is unable to reduce levels of TGF-beta-induced phospho-Smad2/3, coincident with its inability to differentiate these cells along granulocytic pathways. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 79-88
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 sonic hedgehog signaling molecule Homo sapiens 231-234
12069693-10 2002 The opposite effects of T and RA on the expression of RAR and EGF-R suggest that signal events of these receptors might be involved in the interaction between T and RA in the control of LNCaP cell growth. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 54-57
28762645-15 2017 AHA-Ret induced less Erythema vs retinol and was more tolerable vs retinol and tretinoin. Tretinoin 79-88 ret proto-oncogene Homo sapiens 4-7
11979502-6 2002 RA stimulated MAO B but not MAO A activity, in a dose- and time-dependent way, and only in the presence of serum. Tretinoin 0-2 monoamine oxidase B Gallus gallus 14-19
11979502-8 2002 In conclusion, the present work shows that RA selectively elicits MAO B activity in cultured chick embryonic hepatocytes, this stimulation requires the presence of some factors present in the serum and is probably due to an increase in the number of enzyme molecules. Tretinoin 43-45 monoamine oxidase B Gallus gallus 66-71
12042033-6 2002 We previously reported that induction of MUC2, MUC5AC, and MUC5B gene expressions by retinoic acid is mediated by the retinoic acid receptor (RARalpha), and inhibited by the specific RARalpha antagonist Ro 41-5253. Tretinoin 85-98 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 47-53
12042033-6 2002 We previously reported that induction of MUC2, MUC5AC, and MUC5B gene expressions by retinoic acid is mediated by the retinoic acid receptor (RARalpha), and inhibited by the specific RARalpha antagonist Ro 41-5253. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 142-150
12042033-6 2002 We previously reported that induction of MUC2, MUC5AC, and MUC5B gene expressions by retinoic acid is mediated by the retinoic acid receptor (RARalpha), and inhibited by the specific RARalpha antagonist Ro 41-5253. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 183-191
14515147-1 2003 In the retinoic acid-differentiated neuroblastoma SH-SY5Y cells, IL-1 induced binding activity of NFkappaB and up-regulated the expression and activity of MnSOD. Tretinoin 7-20 interleukin 1 alpha Homo sapiens 65-69
12485937-3 2003 We identified a retinoic acid response element (RARE) that lies nearly 900 nucleotides upstream of the CD18 transcriptional start site that was bound by the RA receptors, retinoic acid receptor (RAR) and retinoic X receptor (RXR). Tretinoin 16-29 retinoic acid receptor alpha Homo sapiens 171-193
12485937-3 2003 We identified a retinoic acid response element (RARE) that lies nearly 900 nucleotides upstream of the CD18 transcriptional start site that was bound by the RA receptors, retinoic acid receptor (RAR) and retinoic X receptor (RXR). Tretinoin 16-29 retinoic acid receptor alpha Homo sapiens 48-51
14529416-2 2003 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RAR alpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 57-70 retinoic acid receptor alpha Homo sapiens 168-177
12757021-2 2003 This role is primarily mediated by binding of retinoic acid to retinoic acid receptor alpha (RARalpha), a nuclear receptor that modulates the expression of multiple downstream targets via retinoic acid response elements. Tretinoin 46-59 retinoic acid receptor alpha Homo sapiens 63-91
12757021-2 2003 This role is primarily mediated by binding of retinoic acid to retinoic acid receptor alpha (RARalpha), a nuclear receptor that modulates the expression of multiple downstream targets via retinoic acid response elements. Tretinoin 46-59 retinoic acid receptor alpha Homo sapiens 93-101
28951425-4 2017 Colon APCs also expressed lower levels of retinoic acid-producing enzymes that are known to control the mucosal homing of T cells. Tretinoin 42-55 amyloid P component, serum Homo sapiens 6-10
12393611-5 2002 We observe that the retinoic acid response element (RARE) used in our RA responsive reporter harbors overlapping Stat/RAR-binding sites. Tretinoin 20-33 retinoic acid receptor alpha Homo sapiens 52-55
12163000-7 2002 HT-29 cells treated with retinoic acid had dose-dependent increases in IGFBP-4 and reduced IGF-II expression. Tretinoin 25-38 insulin like growth factor 2 Homo sapiens 91-97
28978663-2 2017 In this study, we aimed at further understanding DAPK2 function and regulation during arsenic trioxide (ATO) cytotoxic or all-trans retinoic acid (ATRA) differentiation therapy in APL cells. Tretinoin 132-145 death associated protein kinase 2 Homo sapiens 49-54
12054474-0 2002 Cloning of rat cytochrome P450RAI (CYP26) cDNA and regulation of its gene expression by all-trans-retinoic acid in vivo. Tretinoin 88-111 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 35-40
12453892-1 2002 All-trans-retinoic acid (RA) is known to increase the rate of transcription of the PEPCK gene upon engagement of the RA receptor (RAR). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 117-128
12453892-1 2002 All-trans-retinoic acid (RA) is known to increase the rate of transcription of the PEPCK gene upon engagement of the RA receptor (RAR). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 130-133
12453892-1 2002 All-trans-retinoic acid (RA) is known to increase the rate of transcription of the PEPCK gene upon engagement of the RA receptor (RAR). Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 117-128
28978663-2 2017 In this study, we aimed at further understanding DAPK2 function and regulation during arsenic trioxide (ATO) cytotoxic or all-trans retinoic acid (ATRA) differentiation therapy in APL cells. Tretinoin 147-151 death associated protein kinase 2 Homo sapiens 49-54
12453892-1 2002 All-trans-retinoic acid (RA) is known to increase the rate of transcription of the PEPCK gene upon engagement of the RA receptor (RAR). Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 130-133
29344139-10 2017 An electrophoresis mobility shift assay (EMSA) indicated that NLS-RARalpha could bind retinoic acid response elements (RAREs) in the presence of ATRA. Tretinoin 86-99 retinoic acid receptor alpha Homo sapiens 66-74
12429992-7 2002 FZD4 and FZD10 are up-regulated in NT2 cells after ATRA treatment. Tretinoin 51-55 frizzled class receptor 10 Homo sapiens 9-14
12775111-7 2002 When VA-deficient rats received a single injection of retinoic acid (2 mg/rat), tissue IGF-I and IGF-IR gene expression did not change after 4 or 8 h, while the expression of IGF-II, IGFBP-4, and IGFBP-6 mRNAs in some tissues increased rapidly. Tretinoin 54-67 insulin-like growth factor 1 Rattus norvegicus 87-92
12404122-5 2002 Luciferase assays of promoter activity indicate that B-myb-dependent transactivation is enhanced in LAN-5 cells treated with retinoic acid (RA) for 24 h. The enhancement is independent from cyclin A but is suppressed by a degradation-resistant mutant form of cyclin D1. Tretinoin 125-138 MYB proto-oncogene like 2 Homo sapiens 53-58
12404122-5 2002 Luciferase assays of promoter activity indicate that B-myb-dependent transactivation is enhanced in LAN-5 cells treated with retinoic acid (RA) for 24 h. The enhancement is independent from cyclin A but is suppressed by a degradation-resistant mutant form of cyclin D1. Tretinoin 140-142 MYB proto-oncogene like 2 Homo sapiens 53-58
12404122-6 2002 The importance of cyclin D1 in controlling B-myb activity is further suggested by co-immunoprecipitation experiments, showing that the amount of cyclin D1 co-immunoprecipitated with B-myb decreased after RA treatment. Tretinoin 204-206 MYB proto-oncogene like 2 Homo sapiens 43-48
12404122-6 2002 The importance of cyclin D1 in controlling B-myb activity is further suggested by co-immunoprecipitation experiments, showing that the amount of cyclin D1 co-immunoprecipitated with B-myb decreased after RA treatment. Tretinoin 204-206 MYB proto-oncogene like 2 Homo sapiens 182-187
11970916-2 2002 We previously demonstrated, based on nuclear run-on assay, that retinoic acid (RA) stimulated Trx gene expression in airway epithelial cells at the transcriptional level. Tretinoin 64-77 thioredoxin Homo sapiens 94-97
11970916-2 2002 We previously demonstrated, based on nuclear run-on assay, that retinoic acid (RA) stimulated Trx gene expression in airway epithelial cells at the transcriptional level. Tretinoin 79-81 thioredoxin Homo sapiens 94-97
11970916-3 2002 Nucleotide sequencing of the 5"-flanking region of the human Trx gene revealed the presence of a TATA box at -28 and four RA response element (RARE)-like half sites at -426, -453, -507, and -626 nt. Tretinoin 122-124 thioredoxin Homo sapiens 61-64
12027902-0 2002 Interaction between p21-activated protein kinase and Rac during differentiation of HL-60 human promyelocytic leukemia cell induced by all-trans-retinoic acid. Tretinoin 134-157 H3 histone pseudogene 16 Homo sapiens 20-23
12068955-0 2002 Retinoic acid response element in HOXA-7 regulatory region affects the rate, not the formation of anterior boundary expression. Tretinoin 0-13 homeobox A7 Mus musculus 34-40
11832495-8 2002 Administration of retinoic acid to mice bearing tumors driven by activation of the Wnt-1/beta-catenin pathway resulted in increased expression of stra6 in the tumors but not in normal tissue. Tretinoin 18-31 stimulated by retinoic acid gene 6 Mus musculus 146-151
12399974-6 2002 SS (400 microg/ml, 6 days) induced 60% and 55% of NBT-positive cells in HL-60 and U937 cell lines, which were augmented in the presence of GM-CSF (25 ng/ml) to levels (85% and 81%, respectively) comparable to those induced by ATRA. Tretinoin 226-230 colony stimulating factor 2 Homo sapiens 139-145
11929748-2 2002 Initially described in a patient with all-trans retinoic acid (ATRA)-unresponsive disease, STAT5b-RARalpha resulted from an interstitial deletion on chromosome 17. Tretinoin 48-61 retinoic acid receptor alpha Homo sapiens 98-106
29344139-10 2017 An electrophoresis mobility shift assay (EMSA) indicated that NLS-RARalpha could bind retinoic acid response elements (RAREs) in the presence of ATRA. Tretinoin 145-149 retinoic acid receptor alpha Homo sapiens 66-74
11929748-4 2002 STAT5b-RARalpha bound to retinoic acid response elements (RAREs) both as a homodimer and as a heterodimer with RXRalpha and inhibited wild-type RARalpha/RXRalpha transactivation. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 7-15
29344218-0 2017 ATRA increases iodine uptake and inhibits the proliferation and invasiveness of human anaplastic thyroid carcinoma SW1736 cells: Involvement of beta-catenin phosphorylation inhibition. Tretinoin 0-4 catenin beta 1 Homo sapiens 144-156
11929749-5 2002 Oligomerization of this domain in the Stat5-RARalpha fusion protein leads to stable binding of the corepressor SMRT independent of all-trans retinoic acid (ATRA) stimulation and is accompanied by an impaired response to differentiation signals in hematopoietic cells. Tretinoin 141-154 signal transducer and activator of transcription 5A Homo sapiens 38-43
11929749-5 2002 Oligomerization of this domain in the Stat5-RARalpha fusion protein leads to stable binding of the corepressor SMRT independent of all-trans retinoic acid (ATRA) stimulation and is accompanied by an impaired response to differentiation signals in hematopoietic cells. Tretinoin 141-154 retinoic acid receptor alpha Homo sapiens 44-52
11929749-5 2002 Oligomerization of this domain in the Stat5-RARalpha fusion protein leads to stable binding of the corepressor SMRT independent of all-trans retinoic acid (ATRA) stimulation and is accompanied by an impaired response to differentiation signals in hematopoietic cells. Tretinoin 156-160 signal transducer and activator of transcription 5A Homo sapiens 38-43
12239173-0 2002 Response to histone deacetylase inhibition of novel PML/RARalpha mutants detected in retinoic acid-resistant APL cells. Tretinoin 85-98 PML nuclear body scaffold Homo sapiens 52-55
12239173-0 2002 Response to histone deacetylase inhibition of novel PML/RARalpha mutants detected in retinoic acid-resistant APL cells. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 56-64
12239173-7 2002 Cotreatment with ATRA and TSA restored RARbeta gene expression in NB4-MRA1 cells, whose PML/RARalpha mutation is in helix 12 of the LBD, but not in an APL cell line harboring the patient-derived PML/RARalpha mutation, which was between helix 5 and 6. Tretinoin 17-21 PML nuclear body scaffold Homo sapiens 88-91
11929749-5 2002 Oligomerization of this domain in the Stat5-RARalpha fusion protein leads to stable binding of the corepressor SMRT independent of all-trans retinoic acid (ATRA) stimulation and is accompanied by an impaired response to differentiation signals in hematopoietic cells. Tretinoin 156-160 retinoic acid receptor alpha Homo sapiens 44-52
29344218-14 2017 ATRA treatment decreased the expression of phosphorylated (p-)beta-catenin, p-GSK-3beta, vimentin, and fibronectin, and increased the expression of NIS and E-cadherin, compared with the control. Tretinoin 0-4 catenin beta 1 Homo sapiens 62-74
12239173-7 2002 Cotreatment with ATRA and TSA restored RARbeta gene expression in NB4-MRA1 cells, whose PML/RARalpha mutation is in helix 12 of the LBD, but not in an APL cell line harboring the patient-derived PML/RARalpha mutation, which was between helix 5 and 6. Tretinoin 17-21 retinoic acid receptor alpha Homo sapiens 92-100
12239173-7 2002 Cotreatment with ATRA and TSA restored RARbeta gene expression in NB4-MRA1 cells, whose PML/RARalpha mutation is in helix 12 of the LBD, but not in an APL cell line harboring the patient-derived PML/RARalpha mutation, which was between helix 5 and 6. Tretinoin 17-21 PML nuclear body scaffold Homo sapiens 195-198
29344218-14 2017 ATRA treatment decreased the expression of phosphorylated (p-)beta-catenin, p-GSK-3beta, vimentin, and fibronectin, and increased the expression of NIS and E-cadherin, compared with the control. Tretinoin 0-4 vimentin Homo sapiens 89-97
12239173-7 2002 Cotreatment with ATRA and TSA restored RARbeta gene expression in NB4-MRA1 cells, whose PML/RARalpha mutation is in helix 12 of the LBD, but not in an APL cell line harboring the patient-derived PML/RARalpha mutation, which was between helix 5 and 6. Tretinoin 17-21 retinoic acid receptor alpha Homo sapiens 199-207
11904524-4 2002 Northern blot analysis showed that all-trans retinoic acid (atRA) and 9-cis retinoic acid (9cRA) increased PAI-1 mRNA levels in a dose-dependent manner. Tretinoin 39-58 serpin family E member 1 Homo sapiens 107-112
11904524-4 2002 Northern blot analysis showed that all-trans retinoic acid (atRA) and 9-cis retinoic acid (9cRA) increased PAI-1 mRNA levels in a dose-dependent manner. Tretinoin 60-64 serpin family E member 1 Homo sapiens 107-112
29344218-15 2017 ATRA increased the iodine uptake and inhibited the proliferation and invasion of SW1736 cells, involving beta-catenin phosphorylation. Tretinoin 0-4 catenin beta 1 Homo sapiens 105-117
11904524-7 2002 Stable and transient transfection assays of the human PAI-1 promoter-luciferase constructs indicate that DNA sequence responsive to either ligand-stimulated or overexpressed retinoic acid receptor-alpha expression vector lies downstream of -363 relative to the transcription start site, where no putative retinoic acid response element is found. Tretinoin 174-187 serpin family E member 1 Homo sapiens 54-59
29109271-6 2017 We measured RA concentrations and found that they changed periodically, as also reflected in the expression patterns of an RA-responsive gene, STRA8; RA levels were low before the four transitions, increased when the transitions occurred, and remained elevated thereafter. Tretinoin 12-14 stimulated by retinoic acid gene 8 Mus musculus 143-148
11904524-9 2002 Because PAI-1 inhibits the production of fibrinolytic protein plasmin that facilitates SMC migration, induction of the PAI-1 gene expression by atRA may at least partly account for the role of atRA as an important inhibitor of neointima formation. Tretinoin 144-148 serpin family E member 1 Homo sapiens 119-124
11904524-9 2002 Because PAI-1 inhibits the production of fibrinolytic protein plasmin that facilitates SMC migration, induction of the PAI-1 gene expression by atRA may at least partly account for the role of atRA as an important inhibitor of neointima formation. Tretinoin 193-197 serpin family E member 1 Homo sapiens 8-13
11904524-9 2002 Because PAI-1 inhibits the production of fibrinolytic protein plasmin that facilitates SMC migration, induction of the PAI-1 gene expression by atRA may at least partly account for the role of atRA as an important inhibitor of neointima formation. Tretinoin 193-197 serpin family E member 1 Homo sapiens 119-124
12165291-0 2002 Arsenic trioxide, retinoic acid and Ara-c regulated the expression of annexin II on the surface of APL cells, a novel co-receptor for plasminogen/tissue plasminogen activator. Tretinoin 18-31 annexin A2 Homo sapiens 70-80
12165291-3 2002 We investigated patients with APL receiving all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)) treatment, contributing to the downregulation of the expression of annexin II on APL cells, and decreasing the generation of plasmin by tissue plasminogen activator (t-PA). Tretinoin 44-67 annexin A2 Homo sapiens 174-184
12165291-3 2002 We investigated patients with APL receiving all-trans retinoic acid (ATRA) or arsenic trioxide (As(2)O(3)) treatment, contributing to the downregulation of the expression of annexin II on APL cells, and decreasing the generation of plasmin by tissue plasminogen activator (t-PA). Tretinoin 69-73 annexin A2 Homo sapiens 174-184
12431242-2 2002 ATRA induced apoptosis in all the B-CLL samples tested, and this was accompanied by a specific reduction in Bcl-2 and Mcl-1 protein expression in the apoptotic cells. Tretinoin 0-4 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 118-123
12431242-4 2002 Caspase-3 activation was shown to be a prerequisite for ATRA-induced apoptosis, which was inhibited by the pan-caspase inhibitor Z-VAD-FMK and the caspase-9 inhibitor Z-LEHD-FMK. Tretinoin 56-60 caspase 9 Homo sapiens 147-156
12169446-0 2002 Enhancement of the inducible NO synthase activation by retinoic acid is mimicked by RARalpha agonist in vivo. Tretinoin 55-68 retinoic acid receptor, alpha Rattus norvegicus 84-92
12169446-4 2002 Both atRA and the RARalpha agonist (but not the RXR agonist) increased the number of peripheral T helper lymphocytes and plasma interferon-gamma concentration. Tretinoin 5-9 interferon gamma Rattus norvegicus 128-144
12165291-5 2002 Consistent with in vivo findings, annexin II on NB(4) cell surface and its mRNA content were downregulated with 1 microM As(2)O(3) or 1 microM ATRA, while 2 microg Ara-c enhanced the expression of annexin II and the generation of cell-surface plasmin before its induction of apoptosis. Tretinoin 143-147 annexin A2 Homo sapiens 34-44
12165291-6 2002 Our data indicate that the inhibition of annexin II expression with ATRA is transcriptionally mediated while As(2)O(3) induces an accelerated degradation of annexin II mRNA. Tretinoin 68-72 annexin A2 Homo sapiens 41-51
12169446-6 2002 These results suggest that, in vivo, atRA activates NOS II through RARalpha and contributes to characterizing the complex effect of retinoids on the host inflammatory/immune response. Tretinoin 37-41 retinoic acid receptor, alpha Rattus norvegicus 67-75
29109271-6 2017 We measured RA concentrations and found that they changed periodically, as also reflected in the expression patterns of an RA-responsive gene, STRA8; RA levels were low before the four transitions, increased when the transitions occurred, and remained elevated thereafter. Tretinoin 123-125 stimulated by retinoic acid gene 8 Mus musculus 143-148
28911263-9 2017 In the presence of RA, we observed a decrease of OCT4 expression, associated with a loss of clonogenic and proliferation capacities, cell cycle arrest, and upregulation of p21, in HL60, NB4, KASUMI, and Me-1 cell lines. Tretinoin 19-21 POU class 5 homeobox 1 Homo sapiens 49-53
12196475-5 2002 By studying the vestigial tail (Wnt-3a(vt)) mutant, we provide evidence that Wnt-3a, a gene that controls the development of the caudal region, is directly involved in the pathogenic pathway of RA-induced caudal regression. Tretinoin 194-196 wingless-type MMTV integration site family, member 3A Mus musculus 32-38
12196475-5 2002 By studying the vestigial tail (Wnt-3a(vt)) mutant, we provide evidence that Wnt-3a, a gene that controls the development of the caudal region, is directly involved in the pathogenic pathway of RA-induced caudal regression. Tretinoin 194-196 wingless-type MMTV integration site family, member 3A Mus musculus 77-83
11788590-5 2002 Interleukin 6 and interleukin 11, known to activate STAT3 synergistically, stimulated the SP-B promoter activity with retinoic acid, which is at least partially mediated through interactions between STAT3 and retinoid nuclear receptor enhanceosome proteins in pulmonary epithelial cells. Tretinoin 118-131 interleukin 11 Homo sapiens 18-32
12009305-0 2002 Anticancer effect of retinoic acid via AP-1 activity repression is mediated by retinoic acid receptor alpha and beta in gastric cancer cells. Tretinoin 21-34 retinoic acid receptor alpha Homo sapiens 79-107
28911263-9 2017 In the presence of RA, we observed a decrease of OCT4 expression, associated with a loss of clonogenic and proliferation capacities, cell cycle arrest, and upregulation of p21, in HL60, NB4, KASUMI, and Me-1 cell lines. Tretinoin 19-21 H3 histone pseudogene 16 Homo sapiens 172-175
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 73-81
11948401-9 2002 The transcriptional activities of full-length JunB and full-length Fra-1, but not the transactivation domain fusions, were increased by TPA treatment and suppressed by RA. Tretinoin 168-170 FOS like 1, AP-1 transcription factor subunit Homo sapiens 67-72
11948401-10 2002 Since these full-length fusions have bzip domains, the results suggest that JunB and/or Fra-1-containing dimers may constitute one target of RA for transrepression of AP-1. Tretinoin 141-143 FOS like 1, AP-1 transcription factor subunit Homo sapiens 88-93
12009305-2 2002 All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells (RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo), RARbeta(-)). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 73-81
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 10-23 interferon regulatory factor 8 Homo sapiens 79-83
12009305-5 2002 Transient transfection of RARalpha into MKN-45 cells however, displayed receptor concentration-dependent AP-1 activity inhibition only in the presence of ATRA. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 26-34
28851699-9 2017 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IRF8 ratio, abrogated BCR-NOTCH hyperactivation, and reduced NOTCH2 expression in cGVHD B cells without compromising viability. Tretinoin 25-29 interferon regulatory factor 8 Homo sapiens 79-83
12009305-7 2002 For AP-1 binding activity induced by TPA, the repressive effect of ATRA was only observed in BGC-823 and RARalpha and RARbeta stably transfected MKN-45 cells, but not in intact MKN-45 cells. Tretinoin 67-71 retinoic acid receptor alpha Homo sapiens 105-113
11914039-11 2002 IGF-1 protein decreased in the presence of retinoic acid after oxygen exposure but not in room air. Tretinoin 43-56 insulin-like growth factor 1 Rattus norvegicus 0-5
28886987-7 2017 We determined that derivatives of retinoic acid led to significantly reduced level of proteins belonging to metabolic pathway (e.g. glyceraldehyde-3-phosphate dehydrogenase or pyruvate kinase 2) or to other cellular processes as apoptosis, regulation of transcription process or epithelial-mesenchymal transition (e.g. annexins, nucleoside diphosphate kinase B, vimentin). Tretinoin 34-47 vimentin Homo sapiens 362-370
12130515-8 2002 As2O3 in combination with tRA induces gene (Bfl-1/A1 and C/EBPepsilon) expression and partial differentiation. Tretinoin 26-29 CCAAT enhancer binding protein epsilon Homo sapiens 57-69
12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 21-34 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 210-215
12091353-7 2002 In the FR-beta-expressing KG-1 human AML cells, treatment with ATRA further increased this specificity. Tretinoin 63-67 folate receptor beta Homo sapiens 7-14
11896582-0 2002 Retinoic acid inhibits hepatic Jun N-terminal kinase-dependent signaling pathway in ethanol-fed rats. Tretinoin 0-13 mitogen-activated protein kinase 8 Rattus norvegicus 31-52
11896582-11 2002 The results from these studies indicate that restoration of RA homeostasis is critical for the regulation of JNK-dependent signaling pathway and apoptosis in the liver of ethanol-fed rats. Tretinoin 60-62 mitogen-activated protein kinase 8 Rattus norvegicus 109-112
12091353-10 2002 The above combined data from our 2 laboratories further support the feasibility and potential usefulness of selective ATRA-facilitated liposomal drug delivery in FR-beta + AMLs. Tretinoin 118-122 folate receptor beta Homo sapiens 162-169
28692043-7 2017 Retinoic acid (RA) treatment blocked the P4 increase in CK5+ cells and prevented the P4 increase in mammosphere size. Tretinoin 0-13 keratin 5 Homo sapiens 56-59
12511087-6 2002 Application of exogenous retinoic acid (RA) increased the number of GFP-expressing cells throughout the retina, and possibly the level of expressed rhodopsin. Tretinoin 25-38 rhodopsin Danio rerio 148-157
12511087-6 2002 Application of exogenous retinoic acid (RA) increased the number of GFP-expressing cells throughout the retina, and possibly the level of expressed rhodopsin. Tretinoin 40-42 rhodopsin Danio rerio 148-157
12069693-0 2002 Androgen and retinoic acid interaction in LNCaP cells, effects on cell proliferation and expression of retinoic acid receptors and epidermal growth factor receptor. Tretinoin 13-26 retinoic acid receptor alpha Homo sapiens 103-126
11856352-0 2002 Repression of FasL expression by retinoic acid involves a novel mechanism of inhibition of transactivation function of the nuclear factors of activated T-cells. Tretinoin 33-46 Fas ligand Homo sapiens 14-18
11803116-0 2002 Retinoic acid influences the expression of the neuronal regulatory genes Mash-1 and c-ret in the developing rat heart. Tretinoin 0-13 achaete-scute family bHLH transcription factor 1 Rattus norvegicus 73-79
28692043-7 2017 Retinoic acid (RA) treatment blocked the P4 increase in CK5+ cells and prevented the P4 increase in mammosphere size. Tretinoin 15-17 keratin 5 Homo sapiens 56-59
11803116-1 2002 We analyzed the expression of neuronal regulatory genes Mash-1 and c-ret by immunohistochemistry and reverse transcriptase-polymerase chain reaction in the developing heart of rat embryos following exogenous retinoic acid (RA) treatment of the pregnant dams. Tretinoin 208-221 achaete-scute family bHLH transcription factor 1 Rattus norvegicus 56-62
28692043-12 2017 Interestingly, RARalpha was recruited to the -1.1 kb PRE and the -130 bp PRE/RARE regions with P4, but not RA alone or RA plus P4. Tretinoin 77-79 retinoic acid receptor alpha Homo sapiens 15-23
11803116-1 2002 We analyzed the expression of neuronal regulatory genes Mash-1 and c-ret by immunohistochemistry and reverse transcriptase-polymerase chain reaction in the developing heart of rat embryos following exogenous retinoic acid (RA) treatment of the pregnant dams. Tretinoin 223-225 achaete-scute family bHLH transcription factor 1 Rattus norvegicus 56-62
11803116-5 2002 RA-treated hearts showed a down-regulation of both Mash-1 and c-Ret at the mRNA as well as at the protein level on E16.5. Tretinoin 0-2 achaete-scute family bHLH transcription factor 1 Rattus norvegicus 51-57
12225397-0 2002 GM-CSF induces expression of gp91phox and stimulates retinoic acid-induced p47phox expression in human myeloblastic leukemia cells. Tretinoin 53-66 colony stimulating factor 2 Homo sapiens 0-6
28241900-2 2017 PCDH11Y is upregulated by retinoic acid signalling and is essential for spermatogonial differentiation and initiation of meiosis. Tretinoin 26-39 protocadherin 11 X-linked Homo sapiens 0-6
12225397-8 2002 These results indicate that GM-CSF induces expression of gp91phox and enhances ATRA-induced p47phox expression. Tretinoin 79-83 colony stimulating factor 2 Homo sapiens 28-34
12225397-8 2002 These results indicate that GM-CSF induces expression of gp91phox and enhances ATRA-induced p47phox expression. Tretinoin 79-83 pleckstrin Homo sapiens 92-95
11803116-6 2002 The present results show that differentiation of cardiac ganglionic cells is affected after RA treatment, by the down-regulation of Mash-1 and c-Ret. Tretinoin 92-94 achaete-scute family bHLH transcription factor 1 Rattus norvegicus 132-138
11818666-1 2002 The presence of the characteristic fusion transcript gene, promyelocytic leukemia-retinoic acid receptor-alpha (PML-RARalpha), provided hematologists with a rationale for the use of all-trans retinoic acid (ATRA) for differentiation therapy for acute promyelocytic leukemia (APL). Tretinoin 182-205 PML nuclear body scaffold Homo sapiens 112-115
11818666-1 2002 The presence of the characteristic fusion transcript gene, promyelocytic leukemia-retinoic acid receptor-alpha (PML-RARalpha), provided hematologists with a rationale for the use of all-trans retinoic acid (ATRA) for differentiation therapy for acute promyelocytic leukemia (APL). Tretinoin 182-205 retinoic acid receptor alpha Homo sapiens 116-124
12112877-6 2002 We also found the difference between the effects of Shh and retinoic acid, another possible ventralizing factor, suggesting that Shh could promote ventralization independently of retinoic acid. Tretinoin 60-73 sonic hedgehog L homeolog Xenopus laevis 129-132
28746836-4 2017 The retinoic acid receptor alpha (RARalpha)-selective antagonist Ro 41-5253 inhibited the cystine perturbation caused by all-trans-retinoic acid, TTNPB, 13-cis-retinoic acid, 9-cis-retinoic acid, and acitretin. Tretinoin 121-144 retinoic acid receptor alpha Homo sapiens 4-32
12095687-6 2002 Sequence analysis of the 960 bp upstream of the transcription start site of the mouse Mix gene revealed the presence of a putative initiator region and TATA box as well as potential Smad, FoxH1/FAST, T-box, COUP-TF, C/EBP, GATA, HNF3 binding sites and retinoic acid response elements. Tretinoin 252-265 Mix paired-like homeobox Homo sapiens 86-89
12054474-7 2002 The CYP26 dose response to RA was nearly linear (R(2)=0.9638). Tretinoin 27-29 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 4-9
12054474-8 2002 Additionally, significant regulation of CYP26 gene expression was observed in the vitamin-A-deficient, control, and RA-treated condition in lung, testis, and small intestine. Tretinoin 116-118 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 40-45
11818666-1 2002 The presence of the characteristic fusion transcript gene, promyelocytic leukemia-retinoic acid receptor-alpha (PML-RARalpha), provided hematologists with a rationale for the use of all-trans retinoic acid (ATRA) for differentiation therapy for acute promyelocytic leukemia (APL). Tretinoin 207-211 PML nuclear body scaffold Homo sapiens 112-115
11876525-4 2002 Both URA liposomes and retinoic acid decreased markers of keratinocyte differentiation (keratin 1, keratin 10 and involucrin) in cultured NHEK. Tretinoin 23-36 keratin 10 Homo sapiens 99-109
11872149-0 2002 4-(N,N-dipropylamino)benzaldehyde inhibits the oxidation of all-trans retinal to all-trans retinoic acid by ALDH1A1, but not the differentiation of HL-60 promyelocytic leukemia cells exposed to all-trans retinal. Tretinoin 91-104 aldehyde dehydrogenase 1 family member A1 Homo sapiens 108-115
11872149-2 2002 Following the reports that two members of the superfamily of aldehyde dehydrogenase (ALDH) enzymes, ALDH1A1 and ALDH1A2, were capable of catalyzing the oxidation of all-trans retinal to all-trans retinoic acid with submicromolar Km values, we initiated an investigation of the ability of 4-(N,N-dipropylamino)benzaldehyde (DPAB) to inhibit the oxidation of retinal by purified mouse and human ALDH1A1. Tretinoin 186-209 aldehyde dehydrogenase 1 family member A1 Homo sapiens 393-400
12054474-9 2002 We conclude that CYP26 mRNA expression is dynamically regulated in vivo by diet and RA in hepatic and extrahepatic tissues. Tretinoin 84-86 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 17-22
28746836-4 2017 The retinoic acid receptor alpha (RARalpha)-selective antagonist Ro 41-5253 inhibited the cystine perturbation caused by all-trans-retinoic acid, TTNPB, 13-cis-retinoic acid, 9-cis-retinoic acid, and acitretin. Tretinoin 121-144 retinoic acid receptor alpha Homo sapiens 34-42
11875072-5 2002 As in rodents, PGC-1 is involved in the transcriptional regulation of the UCP1 gene in humans and mediates the effects of PPARalpha and PPARgamma agonists and retinoic acid. Tretinoin 159-172 uncoupling protein 1 Homo sapiens 74-78
29317828-4 2017 The analysis was performed by determining copy numbers of a genome of O volvulus present in skin snip samples of persons with onchocerciacis, and correlating these numbers with expression levels of retinoic acid receptor-alpha (RAR-alpha), which is inducible by retinoic acid. Tretinoin 198-211 retinoic acid receptor alpha Homo sapiens 228-237
11979432-4 2002 Therefore, we analyzed the expression of OVCA1 and OVCA2 in cells in response to treatment with all-trans retinoic acid (RA) and N-(4-hydroxyphenyl)retinamide (4HPR), or under conditions of low serum and confluence, to determine further the roles of OVCA1 and OVCA2 in cell growth, apoptosis and differentiation. Tretinoin 106-119 OVCA2 serine hydrolase domain containing Homo sapiens 51-56
11994980-6 2002 Retinoic acid receptor-alpha (RARalpha) specific antagonist (CD2503) totally abolished the ATRA-induced expression of CYP26 mRNA in HL-60 and NB4 cells. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 0-28
11994980-6 2002 Retinoic acid receptor-alpha (RARalpha) specific antagonist (CD2503) totally abolished the ATRA-induced expression of CYP26 mRNA in HL-60 and NB4 cells. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 30-38
11994980-8 2002 ATRA-induced expression of CYP26 was restored in HL-60R cells retrovirally transduced with RARalpha, but not in those cells transduced with the other retinoid receptors. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 91-99
11801540-6 2002 RA effects on epidermal growth factor (EGF) induction of EGFR-phosphotyrosine levels, cyclin D1 expression and mitogenesis were examined in BEAS-2B cells. Tretinoin 0-2 epidermal growth factor Homo sapiens 14-37
11801540-6 2002 RA effects on epidermal growth factor (EGF) induction of EGFR-phosphotyrosine levels, cyclin D1 expression and mitogenesis were examined in BEAS-2B cells. Tretinoin 0-2 epidermal growth factor Homo sapiens 39-42
11994980-9 2002 In conclusion, ATRA induces expression of CYP26 in myeloid and promyelocytic leukemia cells and this expression is modulated by RARalpha. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 128-136
28928446-4 2017 Upon treating APL with all-trans retinoic acid and achieving complete remission, the levels of PGD2, NKp30, ILC2s, IL-13 and M-MDSCs are restored. Tretinoin 33-46 natural cytotoxicity triggering receptor 3 Homo sapiens 101-106
12054489-7 2002 Hepatic GNMT activity was also elevated in female rats treated with all-trans-retinoic acid, but to a lesser extent compared to males. Tretinoin 68-91 glycine N-methyltransferase Rattus norvegicus 8-12
12189565-2 2002 MATERIALS AND METHODS: ATRA was administered orally at 45 mg/m(2)/day on days 1-14 and 25 mg/m(2)/day on days 15-28 of two standard cycles (idarubicin, etoposide, cytarabine, G-CSF) and of up to three high-dose courses (cytarabine, G-CSF). Tretinoin 23-27 colony stimulating factor 3 Homo sapiens 175-180
12189565-2 2002 MATERIALS AND METHODS: ATRA was administered orally at 45 mg/m(2)/day on days 1-14 and 25 mg/m(2)/day on days 15-28 of two standard cycles (idarubicin, etoposide, cytarabine, G-CSF) and of up to three high-dose courses (cytarabine, G-CSF). Tretinoin 23-27 colony stimulating factor 3 Homo sapiens 232-237
28779023-4 2017 Rbpj-deficient DCs expressed little Aldh1a2 protein that is required for generating retinoic acid. Tretinoin 84-97 recombination signal binding protein for immunoglobulin kappa J region Mus musculus 0-4
11743650-3 2002 Here, effects of beta-estradiol, retinoic acid, and inflammatory cytokines on expression of FZD10 mRNA in human cancer cell lines were investigated. Tretinoin 33-46 frizzled class receptor 10 Homo sapiens 92-97
11743650-5 2002 FZD10 mRNA was expressed in NT2 cells, which are reported to differentiate into neuronal cells after exposure to retinoic acid. Tretinoin 113-126 frizzled class receptor 10 Homo sapiens 0-5
11743650-6 2002 Although expression level of FZD10 mRNA was unchanged until 36 h after retinoic-acid treatment, FZD10 mRNA was up-regulated at 48 and 72 h after retinoic-acid treatment in NT2 cells. Tretinoin 145-158 frizzled class receptor 10 Homo sapiens 96-101
11962657-3 2002 Significant increase of thrombomodulin was observed when endothelial cells were treated with all-trans retinoic acid (ATRA). Tretinoin 93-116 thrombomodulin Homo sapiens 24-38
11962657-3 2002 Significant increase of thrombomodulin was observed when endothelial cells were treated with all-trans retinoic acid (ATRA). Tretinoin 118-122 thrombomodulin Homo sapiens 24-38
11962657-4 2002 ATRA induced the increase of thrombomodulin also in cells incubated with cement extracts. Tretinoin 0-4 thrombomodulin Homo sapiens 29-43
28877686-11 2017 Our analyses of primary AML cells during in vivo treatment suggest that ATRA modulates HOX activity (i.e. decreased expression of HOXA3, HOXA4 and HOXA5 and their regulator PBX3), but altered function of DNA methyl transferase 3A (DNMT3A) and G-protein coupled receptor signaling may also contribute to the effect of the overall treatment. Tretinoin 72-76 homeobox A5 Homo sapiens 147-152
28877686-11 2017 Our analyses of primary AML cells during in vivo treatment suggest that ATRA modulates HOX activity (i.e. decreased expression of HOXA3, HOXA4 and HOXA5 and their regulator PBX3), but altered function of DNA methyl transferase 3A (DNMT3A) and G-protein coupled receptor signaling may also contribute to the effect of the overall treatment. Tretinoin 72-76 DNA methyltransferase 3 alpha Homo sapiens 204-229
28877686-11 2017 Our analyses of primary AML cells during in vivo treatment suggest that ATRA modulates HOX activity (i.e. decreased expression of HOXA3, HOXA4 and HOXA5 and their regulator PBX3), but altered function of DNA methyl transferase 3A (DNMT3A) and G-protein coupled receptor signaling may also contribute to the effect of the overall treatment. Tretinoin 72-76 DNA methyltransferase 3 alpha Homo sapiens 231-237
11986943-3 2002 Recently, we have shown that telomerase can be repressed by all-trans retinoic acid (ATRA) independently of terminal maturation during long-term ATRA treatment of the maturation-resistant promyelocytic leukemia cell line (NB4-R1), leading to shortening of telomeres and cell death, events overcome by ectopic hTERT expression. Tretinoin 85-89 telomerase reverse transcriptase Homo sapiens 309-314
28687976-8 2017 Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Tretinoin 66-89 Picrotoxin-resistant Drosophila melanogaster 31-34
11953746-2 2002 The Cyp26a1 (cytochrome p450, 26) protein metabolizes retinoic acid into more polar hydroxylated and oxidized derivatives. Tretinoin 54-67 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 4-11
11953746-2 2002 The Cyp26a1 (cytochrome p450, 26) protein metabolizes retinoic acid into more polar hydroxylated and oxidized derivatives. Tretinoin 54-67 cytochrome P450, family 21, subfamily a, polypeptide 1 Mus musculus 13-32
11953746-4 2002 Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration, indicating that human CYP26A1 may be essential in controlling retinoic acid levels during development. Tretinoin 100-113 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
11953746-4 2002 Cyp26a1(-/-) mouse fetuses have lethal morphogenetic phenotypes mimicking those generated by excess retinoic acid administration, indicating that human CYP26A1 may be essential in controlling retinoic acid levels during development. Tretinoin 192-205 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
11953746-5 2002 This hypothesis suggests that the Cyp26a1(-/-) phenotype could be rescued under conditions in which embryonic retinoic acid levels are decreased. Tretinoin 110-123 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 34-41
11953746-6 2002 We show that Cyp26a1(-/-) mice are phenotypically rescued by heterozygous disruption of Aldh1a2 (also known as Raldh2), which encodes a retinaldehyde dehydrogenase responsible for the synthesis of retinoic acid during early embryonic development. Tretinoin 197-210 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 13-20
11953746-10 2002 We provide genetic evidence that ALDH1A2 and CYP26A1 activities concurrently establish local embryonic retinoic acid levels that must be finely tuned to allow posterior organ development and to prevent spina bifida. Tretinoin 103-116 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 45-52
12455619-3 2002 There is a particular focus on the discovery that retinoic acid could mimic signalling of the polarizing activity and this finding is then set in the context of more recent work which implicates Shh and BMPs in mediating polarizing activity. Tretinoin 50-63 sonic hedgehog signaling molecule Homo sapiens 195-198
11851873-5 2002 After treatment with all-trans retinoic acid, many of the cells became tyrosinase- and dihydroxyphenylalanine-reaction-positive, changed from polygonal to dendritic in shape, and had stage III to IV melanosomes. Tretinoin 31-44 tyrosinase Mus musculus 71-81
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 Jun dimerization protein 2 Homo sapiens 39-43
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 Jun dimerization protein 2 Homo sapiens 45-71
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 Jun dimerization protein 2 Homo sapiens 39-43
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 Jun dimerization protein 2 Homo sapiens 45-71
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 Jun dimerization protein 2 Homo sapiens 39-43
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 Jun dimerization protein 2 Homo sapiens 45-71
11854287-0 2002 Phosphoinositide 3-kinase activity is required for retinoic acid-induced expression and activation of the tissue transglutaminase. Tretinoin 51-64 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 0-25
11854287-0 2002 Phosphoinositide 3-kinase activity is required for retinoic acid-induced expression and activation of the tissue transglutaminase. Tretinoin 51-64 transglutaminase 2, C polypeptide Mus musculus 106-129
11854287-4 2002 It was found that RA stimulation of NIH3T3 cells activated ERK and phosphoinositide 3-kinase (PI3K); however, only PI3K activation was necessary for RA-induced TGase expression. Tretinoin 18-20 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 67-92
11595732-2 2001 We show here that the decrease in D-type cyclin levels observed following ATRA treatment correlates with an increase in the rate of cyclin D1 ubiquitylation in both T-47D and MCF-7 breast cancer cell lines. Tretinoin 74-78 proliferating cell nuclear antigen Homo sapiens 41-47
28687976-8 2017 Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Tretinoin 66-89 annexin A2 Homo sapiens 132-137
11595732-4 2001 We found a striking difference between these cells in that while ATRA induces an elevation in the cdk inhibitor p27 in T-47D cells, this is not observed in the ATRA-resistant MCF-7 cells. Tretinoin 65-69 interferon alpha inducible protein 27 Homo sapiens 112-115
11595732-5 2001 Furthermore, we demonstrate that ATRA promotes the ubiquitylation of Skp2, an F-box protein that targets p27 for degradation. Tretinoin 33-37 interferon alpha inducible protein 27 Homo sapiens 105-108
12054580-2 2002 In this report, we have shown that overexpression of Wnt-1 can direct embryonic carcinoma P19 cells to differentiate into neuron-like cells in the absence of retinoic acid. Tretinoin 158-171 wingless Drosophila melanogaster 53-58
28687976-8 2017 Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Tretinoin 91-95 Picrotoxin-resistant Drosophila melanogaster 31-34
28687976-8 2017 Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Tretinoin 91-95 annexin A2 Homo sapiens 132-137
28766684-0 2017 Epigallocatechin-3-gallate promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells via PTEN. Tretinoin 46-59 phosphatase and tensin homolog Homo sapiens 121-125
12223078-6 2002 Inhibiting the inducible expression of TF by monocytes can be achieved by "deactivating" cytokines, such as interleukin (IL)-4, -10 and -13, or by certain prostanoids; by drugs that modify signal transduction, such as pentoxifylline, retinoic acid or vitamin D(3), or by antisense oligonucleotides. Tretinoin 234-247 coagulation factor III, tissue factor Homo sapiens 39-41
11960350-6 2002 Pretreatment of cells with 5 microM of the MEK-1/-2-specific inhibitor U0126 abrogated PMA- or RA-induced activation of ERK-1/MAPK and ERK-2/MAPK. Tretinoin 95-97 mitogen-activated protein kinase kinase 1 Homo sapiens 43-51
11751425-8 2001 Following RA treatment, both receptors cause an early, transient increase in the cyclin-dependent kinase inhibitor (CDKI) p21 proteins, while only RARalpha causes a simultaneous sharp, brief increase in the CDKI p16 protein. Tretinoin 10-12 cyclin-dependent kinase inhibitor 1C (P57) Mus musculus 81-114
11751425-8 2001 Following RA treatment, both receptors cause an early, transient increase in the cyclin-dependent kinase inhibitor (CDKI) p21 proteins, while only RARalpha causes a simultaneous sharp, brief increase in the CDKI p16 protein. Tretinoin 10-12 cyclin-dependent kinase inhibitor 1C (P57) Mus musculus 116-120
11753676-4 2001 However, RA sensitive CA-OV3 cells expressed higher levels of p53, p27, p21, and p16 compared to RA resistant SK-OV3 cells. Tretinoin 9-11 H3 histone pseudogene 16 Homo sapiens 72-75
11720446-5 2001 Conversely, we found that the same NB tumour cell line overexpressing the full-length MRP1 cDNA in sense orientation (MRP-S) demonstrated resistance to the neuritogenic effect of the differentiating agent, all-trans-retinoic acid. Tretinoin 210-229 mitochondrial ribosomal protein S7 Homo sapiens 118-123
28766684-4 2017 A significant increase of PTEN levels was found in NB4, HL-60 and THP-1 cells upon ATRA combined with EGCG treatment, paralleled by increased myeloid differentiation marker CD11b. Tretinoin 83-87 phosphatase and tensin homolog Homo sapiens 26-30
11909957-0 2002 Direct channeling of retinoic acid between cellular retinoic acid-binding protein II and retinoic acid receptor sensitizes mammary carcinoma cells to retinoic acid-induced growth arrest. Tretinoin 21-34 retinoic acid receptor alpha Homo sapiens 89-111
11909957-2 2002 We previously showed that CRABP-II enhances the transcriptional activity of the nuclear receptor with which it shares a common ligand, namely, the retinoic acid receptor (RAR), and we suggested that it may act by delivering retinoic acid to this receptor. Tretinoin 147-160 retinoic acid receptor alpha Homo sapiens 171-174
28766684-5 2017 EGCG in synergy with ATRA promote degradation of PML/RARalpha and restores PML expression, and increase the level of nuclear PTEN. Tretinoin 21-25 PML nuclear body scaffold Homo sapiens 49-52
11909957-5 2002 The data establish that potentiation of the transcriptional activity of RAR stems directly from the ability of CRABP-II to channel retinoic acid to the receptor. Tretinoin 131-144 retinoic acid receptor alpha Homo sapiens 72-75
11909957-8 2002 Taken together, the data unequivocally establish the function of CRABP-II in modulating the RAR-mediated biological activities of retinoic acid. Tretinoin 130-143 retinoic acid receptor alpha Homo sapiens 92-95
11689255-6 2001 The RA-loaded nanoparticles were more potent stimulators of hepatocyte DNA synthesis than the free RA system in the presence of epidermal growth factor (EGF) owing to the controlled release of RA from the RA-loaded nanoparticles. Tretinoin 4-6 epidermal growth factor Homo sapiens 128-151
28766684-5 2017 EGCG in synergy with ATRA promote degradation of PML/RARalpha and restores PML expression, and increase the level of nuclear PTEN. Tretinoin 21-25 retinoic acid receptor alpha Homo sapiens 53-61
28766684-5 2017 EGCG in synergy with ATRA promote degradation of PML/RARalpha and restores PML expression, and increase the level of nuclear PTEN. Tretinoin 21-25 PML nuclear body scaffold Homo sapiens 75-78
11713105-3 2001 Since cytokines can induce matrix metalloproteinase (MMP) production in fibroblasts and neutrophil elastase (NE) can activate MMPs, we hypothesized that retinoic acid could attenuate collagen degradation by modifying MMP production and activation. Tretinoin 153-166 matrix metallopeptidase 1 Homo sapiens 53-56
11713105-3 2001 Since cytokines can induce matrix metalloproteinase (MMP) production in fibroblasts and neutrophil elastase (NE) can activate MMPs, we hypothesized that retinoic acid could attenuate collagen degradation by modifying MMP production and activation. Tretinoin 153-166 matrix metallopeptidase 1 Homo sapiens 126-130
28766684-5 2017 EGCG in synergy with ATRA promote degradation of PML/RARalpha and restores PML expression, and increase the level of nuclear PTEN. Tretinoin 21-25 phosphatase and tensin homolog Homo sapiens 125-129
11713105-3 2001 Since cytokines can induce matrix metalloproteinase (MMP) production in fibroblasts and neutrophil elastase (NE) can activate MMPs, we hypothesized that retinoic acid could attenuate collagen degradation by modifying MMP production and activation. Tretinoin 153-166 matrix metallopeptidase 1 Homo sapiens 126-129
11713105-8 2001 Retinoic acid attenuated the induction and activation of MMP-1 and MMP-3. Tretinoin 0-13 matrix metallopeptidase 1 Homo sapiens 57-62
11972796-4 2002 By Northern blot analysis, the levels of Nogo-A mRNA were elevated markedly in NTera2 cells following RA-induced neuronal differentiation, accompanied by an increased expression of the neurite growth-associated protein GAP-43 mRNA. Tretinoin 102-104 reticulon 4 Homo sapiens 41-47
11891284-1 2002 All-trans-retinoic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, promyelocytic leukemia (PML)/RA receptor alpha (RARalpha). Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 159-162
28766684-8 2017 These results therefore indicate that EGCG targets PML/RARalpha oncoprotein for degradation and potentiates differentiation of promyelocytic leukemia cells in combination with ATRA via PTEN. Tretinoin 176-180 phosphatase and tensin homolog Homo sapiens 185-189
11891284-1 2002 All-trans-retinoic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, promyelocytic leukemia (PML)/RA receptor alpha (RARalpha). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 183-191
28568315-11 2017 The retinoate biosynthesis pathway was also enriched due to the differential expression of the genes AKR1C3, ALDH8A1, RDH8, RDH13 and SDR9C7. Tretinoin 4-13 aldo-keto reductase family 1, member C3 (3-alpha hydroxysteroid dehydrogenase, type II) Bos taurus 101-107
11891284-1 2002 All-trans-retinoic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, promyelocytic leukemia (PML)/RA receptor alpha (RARalpha). Tretinoin 25-27 PML nuclear body scaffold Homo sapiens 159-162
11891284-1 2002 All-trans-retinoic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, promyelocytic leukemia (PML)/RA receptor alpha (RARalpha). Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 183-191
11640888-0 2001 Retinoic acid and vitamin E modulate expression and release of CD178 in carcinoma cells: consequences for induction of apoptosis in CD95-sensitive cells. Tretinoin 0-13 Fas ligand Homo sapiens 63-68
11640888-0 2001 Retinoic acid and vitamin E modulate expression and release of CD178 in carcinoma cells: consequences for induction of apoptosis in CD95-sensitive cells. Tretinoin 0-13 Fas cell surface death receptor Homo sapiens 132-136
29044428-2 2017 In the mouse, retinoic acid induces ovarian Stra8 expression and entry of germ cells into meiosis. Tretinoin 14-27 stimulated by retinoic acid gene 8 Mus musculus 44-49
11640888-4 2001 Vitamin E succinate (VES) and retinoic acid (RA) were found to reduce CD178 surface expression, whereas interferon-gamma stimulated a slight upregulation. Tretinoin 30-43 Fas ligand Homo sapiens 70-75
11640888-4 2001 Vitamin E succinate (VES) and retinoic acid (RA) were found to reduce CD178 surface expression, whereas interferon-gamma stimulated a slight upregulation. Tretinoin 45-47 Fas ligand Homo sapiens 70-75
11872252-4 2002 These results suggest that RA disrupts the differentiation of cardiac neural crest cells into ganglionic cells destined to contribute to the parasympathetic innervation of the heart, by regulating the expression of Phox2a and Phox2b. Tretinoin 27-29 paired-like homeobox 2a Rattus norvegicus 215-221
11870076-12 2002 Expression of mRNA for RXR alpha, RXR beta, RALDH2, and PPAR gamma suggests that the early embryo may be competent to synthesize retinoic acid and regulate gene expression during preattachment development in vitro. Tretinoin 129-142 retinoid X receptor alpha Bos taurus 23-32
12536483-1 2001 OBJECTIVE: The expressions of HOXB5, HOXB6, HOXB7, and HOXB8 genes of U251 cell infected by human cytomegalovirus and/or treated with all trans-retinoic acid(ATRA) were detected by semi-quantitative RT-PCR. Tretinoin 138-157 homeobox B8 Homo sapiens 55-60
29044428-3 2017 In developing mouse testes, cytochrome P450 family 26, subfamily b, polypeptide 1 (CYP26B1) produced by the Sertoli cells degrades retinoic acid, preventing Stimulated by Retinoic Acid Gene 8 (Stra8), expression and inhibiting meiosis. Tretinoin 131-144 stimulated by retinoic acid gene 8 Mus musculus 157-191
12536483-1 2001 OBJECTIVE: The expressions of HOXB5, HOXB6, HOXB7, and HOXB8 genes of U251 cell infected by human cytomegalovirus and/or treated with all trans-retinoic acid(ATRA) were detected by semi-quantitative RT-PCR. Tretinoin 158-162 homeobox B8 Homo sapiens 55-60
12536483-3 2001 After infected with HCMV and/or treated with ATRA, the expressions of HOXB7 and HOXB8 were up-regulated and the expression of HOXB7 lasted the fourth generation, while HOXB8 was up-regulated only in the second generation. Tretinoin 45-49 homeobox B8 Homo sapiens 80-85
29044428-3 2017 In developing mouse testes, cytochrome P450 family 26, subfamily b, polypeptide 1 (CYP26B1) produced by the Sertoli cells degrades retinoic acid, preventing Stimulated by Retinoic Acid Gene 8 (Stra8), expression and inhibiting meiosis. Tretinoin 131-144 stimulated by retinoic acid gene 8 Mus musculus 193-198
12536483-3 2001 After infected with HCMV and/or treated with ATRA, the expressions of HOXB7 and HOXB8 were up-regulated and the expression of HOXB7 lasted the fourth generation, while HOXB8 was up-regulated only in the second generation. Tretinoin 45-49 homeobox B8 Homo sapiens 168-173
11880556-3 2002 Previously, we demonstrated that the retinoid derivatives 13-cis- (CRA) and all-trans-retinoic acid (ATRA) mediated both the activity of GNMT and its abundance. Tretinoin 76-99 glycine N-methyltransferase Rattus norvegicus 137-141
11880556-3 2002 Previously, we demonstrated that the retinoid derivatives 13-cis- (CRA) and all-trans-retinoic acid (ATRA) mediated both the activity of GNMT and its abundance. Tretinoin 101-105 glycine N-methyltransferase Rattus norvegicus 137-141
29044428-5 2017 We therefore examined aspects of the retinoic acid/STRA8/CYP26B1 pathway during gonadal development in the tammar wallaby, a marsupial, to understand whether retinoic acid stimulation of STRA8 and CYP26B1 degradation of retinoic acid was conserved between widely divergent mammals. Tretinoin 158-171 stimulated by retinoic acid gene 8 Mus musculus 187-192
11694457-0 2001 Retinoic acid protects against hyperoxia-mediated cell-cycle arrest of lung alveolar epithelial cells by preserving late G1 cyclin activities. Tretinoin 0-13 proliferating cell nuclear antigen Homo sapiens 124-130
11694457-5 2001 To gain insights into the mechanisms involved, we studied the effects of RA on the cyclin-dependent kinase (CDK) system. Tretinoin 73-75 proliferating cell nuclear antigen Homo sapiens 83-89
11880556-6 2002 Moreover, the retinoid-mediated changes in GNMT activity were reflected in GNMT abundance (38, 89 and 107% increases for RP-, CRA-, and ATRA-treated rats, respectively). Tretinoin 136-140 glycine N-methyltransferase Rattus norvegicus 43-47
28992291-7 2017 Inhibition of Zfp423 expression due to RA contributes to the enhanced brown adipogenesis. Tretinoin 39-41 zinc finger protein 423 Homo sapiens 14-20
11880556-6 2002 Moreover, the retinoid-mediated changes in GNMT activity were reflected in GNMT abundance (38, 89 and 107% increases for RP-, CRA-, and ATRA-treated rats, respectively). Tretinoin 136-140 glycine N-methyltransferase Rattus norvegicus 75-79
11694457-9 2001 These effects were associated with a reduced association of p21(CIP1) with cyclin E-CDK2 complexes in the presence of RA. Tretinoin 118-120 proliferating cell nuclear antigen Homo sapiens 75-81
11694457-10 2001 In addition, studies of Smad activity strongly suggest that the mechanisms through which RA preserves late G(1) cyclin-CDK complex activity may involve interference with the transforming growth factor-beta signaling pathway. Tretinoin 89-91 proliferating cell nuclear antigen Homo sapiens 112-118
28992291-8 2017 In summary, RA inhibits white adipogenesis by inducing RAR and ING1 interaction and inhibiting Gadd45a expression, which prevents GADD45A-mediated DNA demethylation. Tretinoin 12-14 retinoic acid receptor alpha Homo sapiens 55-58
28992291-8 2017 In summary, RA inhibits white adipogenesis by inducing RAR and ING1 interaction and inhibiting Gadd45a expression, which prevents GADD45A-mediated DNA demethylation. Tretinoin 12-14 inhibitor of growth family member 1 Homo sapiens 63-67
11830487-1 2002 This study identified missense mutations in the ligand binding domain of the oncoprotein PML-RARalpha in 5 of 8 patients with acute promyelocytic leukemia (APL) with 2 or more relapses and 2 or more previous courses of all-trans retinoic acid (RA)-containing therapy. Tretinoin 229-242 PML nuclear body scaffold Homo sapiens 89-92
28684780-0 2017 Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition. Tretinoin 0-13 GATA binding protein 6 Homo sapiens 81-86
11830487-1 2002 This study identified missense mutations in the ligand binding domain of the oncoprotein PML-RARalpha in 5 of 8 patients with acute promyelocytic leukemia (APL) with 2 or more relapses and 2 or more previous courses of all-trans retinoic acid (RA)-containing therapy. Tretinoin 229-242 retinoic acid receptor alpha Homo sapiens 93-101
11830487-1 2002 This study identified missense mutations in the ligand binding domain of the oncoprotein PML-RARalpha in 5 of 8 patients with acute promyelocytic leukemia (APL) with 2 or more relapses and 2 or more previous courses of all-trans retinoic acid (RA)-containing therapy. Tretinoin 93-95 PML nuclear body scaffold Homo sapiens 89-92
11830487-4 2002 Of the 5 RA + PB-treated patients, 4 had PML-RARalpha mutations. Tretinoin 9-11 PML nuclear body scaffold Homo sapiens 41-44
11830487-4 2002 Of the 5 RA + PB-treated patients, 4 had PML-RARalpha mutations. Tretinoin 9-11 retinoic acid receptor alpha Homo sapiens 45-53
11830487-5 2002 The Gly289Arg mutation in the clinical responder produced the most defective PML-RARalpha function in the presence of RA with or without sodium butyrate (NaB) or trichostatin A. Tretinoin 81-83 PML nuclear body scaffold Homo sapiens 77-80
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 32-34 PML nuclear body scaffold Homo sapiens 28-31
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 95-97 PML nuclear body scaffold Homo sapiens 28-31
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 95-97 retinoic acid receptor alpha Homo sapiens 32-40
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 95-97 PML nuclear body scaffold Homo sapiens 28-31
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 95-97 retinoic acid receptor alpha Homo sapiens 32-40
11676881-1 2001 OBJECTIVE: To study the effects of retinoic acid on regulation of expressions of cyclin-dependent kinase inhibitors, i.e. p16, p21 and p27 in cultured rat hepatic stellate cells. Tretinoin 35-48 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 135-138
11520679-0 2001 Cloning of a novel retinoic-acid metabolizing cytochrome P450, Cyp26B1, and comparative expression analysis with Cyp26A1 during early murine development. Tretinoin 19-32 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 113-120
11520679-2 2001 The RA-metabolizing enzymes Cyp26A1 and Cyp26B1 are believed to play important roles in protecting certain embryonic tissues from inappropriate RA signaling. Tretinoin 4-6 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 28-35
11520048-5 2001 These results suggest that activation of SphK disengages cells from their liver-specific phenotype, and that 9-cis RA further induces differentiation of hepatoma cells when SphK activity is inhibited. Tretinoin 115-117 sphingosine kinase 1 Homo sapiens 173-177
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 95-97 PML nuclear body scaffold Homo sapiens 28-31
11830487-8 2002 These results indicate that PML-RARalpha mutations occurred with high frequency after multiple RA treatment relapses, indicate that the functional potential of PML-RARalpha was not correlated with clinical response to RA + PB treatment, and suggest that the response to RA + PB therapy in one patient was related to the ability of PB to circumvent the blocked RA-regulated gene response pathway. Tretinoin 95-97 retinoic acid receptor alpha Homo sapiens 32-40
28684780-4 2017 In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved in the physiological differentiation of the distal lung. Tretinoin 29-31 GATA binding protein 6 Homo sapiens 173-178
28684780-6 2017 Furthermore, we uncovered a novel mechanism in NSCLC that shows how RA exerts its function; we found that RA-mediated GATA6 activation is necessary for EGFR and Wnt inhibition, thus leading to 1) increased differentiation and 2) loss of proliferation. Tretinoin 68-70 GATA binding protein 6 Homo sapiens 118-123
11856352-2 2002 In this study, we demonstrate that all-trans-retinoic acid (all-trans-RA) directly represses the transcriptional activity of the nuclear factors of activated T-cells (NFAT), which is an important transactivator of the FasL promoter. Tretinoin 35-58 nuclear factor of activated T cells 2 Homo sapiens 167-171
11856352-2 2002 In this study, we demonstrate that all-trans-retinoic acid (all-trans-RA) directly represses the transcriptional activity of the nuclear factors of activated T-cells (NFAT), which is an important transactivator of the FasL promoter. Tretinoin 35-58 Fas ligand Homo sapiens 218-222
11397803-7 2001 These results indicate the involvement of RAR alpha in the induction of SCD expression by retinoic acid. Tretinoin 90-103 retinoic acid receptor alpha Homo sapiens 42-51
11683493-0 2001 Retinoic acid causes MEK-dependent RAF phosphorylation through RARalpha plus RXR activation in HL-60 cells. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 63-71
28684780-6 2017 Furthermore, we uncovered a novel mechanism in NSCLC that shows how RA exerts its function; we found that RA-mediated GATA6 activation is necessary for EGFR and Wnt inhibition, thus leading to 1) increased differentiation and 2) loss of proliferation. Tretinoin 106-108 GATA binding protein 6 Homo sapiens 118-123
11856352-2 2002 In this study, we demonstrate that all-trans-retinoic acid (all-trans-RA) directly represses the transcriptional activity of the nuclear factors of activated T-cells (NFAT), which is an important transactivator of the FasL promoter. Tretinoin 60-72 nuclear factor of activated T cells 2 Homo sapiens 167-171
11856352-2 2002 In this study, we demonstrate that all-trans-retinoic acid (all-trans-RA) directly represses the transcriptional activity of the nuclear factors of activated T-cells (NFAT), which is an important transactivator of the FasL promoter. Tretinoin 60-72 Fas ligand Homo sapiens 218-222
28483168-5 2017 Based on retinoic acid (RA) induction of ESCs to SSCs in vitro, Gli1 overexpression has the ability to induce ESCs differentiation and SSCs-like cells formation and high expression of related reproductive genes, like Cvh, C-kit, Blamp1, Prmd14, Stra8, Dazl, integrin alpha6 and integrin beta1 and so on in vitro. Tretinoin 9-22 GLI family zinc finger 1 Gallus gallus 64-68
12503607-1 2002 The ligand-activated retinoid receptors RXR and RAR control development, homeostasis and disease by regulating transcription of retinoic acid (RA) responsive target genes or crosstalk with other signalling pathways. Tretinoin 128-141 retinoic acid receptor alpha Homo sapiens 48-51
11536433-6 2001 Several factors known to be expressed in hypoblast, and retinoic acid, synergistically induce Gnot-1 and Gnot-2 expression in blastoderm cell culture. Tretinoin 56-69 notochord homeobox Gallus gallus 94-100
11536433-6 2001 Several factors known to be expressed in hypoblast, and retinoic acid, synergistically induce Gnot-1 and Gnot-2 expression in blastoderm cell culture. Tretinoin 56-69 Gnot2 homeodomain protein Gallus gallus 105-111
28483168-5 2017 Based on retinoic acid (RA) induction of ESCs to SSCs in vitro, Gli1 overexpression has the ability to induce ESCs differentiation and SSCs-like cells formation and high expression of related reproductive genes, like Cvh, C-kit, Blamp1, Prmd14, Stra8, Dazl, integrin alpha6 and integrin beta1 and so on in vitro. Tretinoin 24-26 GLI family zinc finger 1 Gallus gallus 64-68
11438209-0 2001 Novel mutation in the PML/RARalpha chimeric gene exhibits dramatically decreased ligand-binding activity and confers acquired resistance to retinoic acid in acute promyelocytic leukemia. Tretinoin 140-153 PML nuclear body scaffold Homo sapiens 22-25
11438209-0 2001 Novel mutation in the PML/RARalpha chimeric gene exhibits dramatically decreased ligand-binding activity and confers acquired resistance to retinoic acid in acute promyelocytic leukemia. Tretinoin 140-153 retinoic acid receptor alpha Homo sapiens 26-34
11438209-9 2001 Interestingly, RA-binding activity was dramatically decreased in the mutant PML/RARalpha compared with that of the wild-type chimeric protein, suggesting that this single amino acid substitution is critical for RA binding. Tretinoin 15-17 PML nuclear body scaffold Homo sapiens 76-79
11438209-9 2001 Interestingly, RA-binding activity was dramatically decreased in the mutant PML/RARalpha compared with that of the wild-type chimeric protein, suggesting that this single amino acid substitution is critical for RA binding. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 80-88
11438209-9 2001 Interestingly, RA-binding activity was dramatically decreased in the mutant PML/RARalpha compared with that of the wild-type chimeric protein, suggesting that this single amino acid substitution is critical for RA binding. Tretinoin 80-82 PML nuclear body scaffold Homo sapiens 76-79
11840342-7 2002 Other important regulators of Cyr61 expression in breast cancer cells that we found are the phorbol ester TPA, vitamin D, and retinoic acid. Tretinoin 126-139 cellular communication network factor 1 Homo sapiens 30-35
11840342-10 2002 Lastly, retinoic acid has a negative effect on Cyr61 expression and downregulates its expression in MCF-7 cells. Tretinoin 8-21 cellular communication network factor 1 Homo sapiens 47-52
11682484-1 2002 In acute promyelocytic leukemia (APL) cells harboring the promyelocytic leukemia retinoic acid receptor alpha (PML-RARalpha) chimeric protein, retinoic acid (RA)-induced differentiation is triggered through a PML-RARalpha signaling resulting in activation of critical target genes. Tretinoin 81-94 PML nuclear body scaffold Homo sapiens 111-114
11682484-1 2002 In acute promyelocytic leukemia (APL) cells harboring the promyelocytic leukemia retinoic acid receptor alpha (PML-RARalpha) chimeric protein, retinoic acid (RA)-induced differentiation is triggered through a PML-RARalpha signaling resulting in activation of critical target genes. Tretinoin 81-94 retinoic acid receptor alpha Homo sapiens 115-123
11682484-1 2002 In acute promyelocytic leukemia (APL) cells harboring the promyelocytic leukemia retinoic acid receptor alpha (PML-RARalpha) chimeric protein, retinoic acid (RA)-induced differentiation is triggered through a PML-RARalpha signaling resulting in activation of critical target genes. Tretinoin 115-117 retinoic acid receptor alpha Homo sapiens 81-109
11438209-11 2001 We conclude that acquisition of the PML/RARalpha mutation is one possible mechanism for development of RA resistance in patients with APL in vivo. Tretinoin 40-42 PML nuclear body scaffold Homo sapiens 36-39
11682484-1 2002 In acute promyelocytic leukemia (APL) cells harboring the promyelocytic leukemia retinoic acid receptor alpha (PML-RARalpha) chimeric protein, retinoic acid (RA)-induced differentiation is triggered through a PML-RARalpha signaling resulting in activation of critical target genes. Tretinoin 115-117 PML nuclear body scaffold Homo sapiens 111-114
28446509-0 2017 Inhibition of the all-trans Retinoic Acid (atRA) Hydroxylases CYP26A1 and CYP26B1 Results in Dynamic, Tissue-Specific Changes in Endogenous atRA Signaling. Tretinoin 43-47 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 62-69
11682484-4 2002 PML-RARalpha strongly enhanced RA-induced ASB-2 mRNA expression. Tretinoin 4-6 PML nuclear body scaffold Homo sapiens 0-3
12206137-0 2002 All-trans-retinoic acid-mediated modulation of p53 during neural differentiation in murine embryonic stem cells. Tretinoin 0-23 transformation related protein 53, pseudogene Mus musculus 47-50
12206137-3 2002 Temporal modulation of p53 by retinoic acid was investigated in murine embryonic stem cells during differentiation and apoptosis. Tretinoin 30-43 transformation related protein 53, pseudogene Mus musculus 23-26
12206137-5 2002 The addition of retinoic acid during 8-10 days of differentiation increased the levels of p53 mRNA and protein, accompanied by accelerated neural differentiation and apoptosis. Tretinoin 16-29 transformation related protein 53, pseudogene Mus musculus 90-93
12536675-10 2001 Treated with all-trans retinoic acid (ATRA), the expression of HOXB9 gene in HEL cells infected by HCMV was significantly increased. Tretinoin 13-36 homeobox B9 Homo sapiens 63-68
12536675-10 2001 Treated with all-trans retinoic acid (ATRA), the expression of HOXB9 gene in HEL cells infected by HCMV was significantly increased. Tretinoin 38-42 homeobox B9 Homo sapiens 63-68
12206137-8 2002 Maximum increase in p53 mRNA in retinoic acid-treated cells occurred on day 17, whereas maximum protein synthesis occurred on days 14-17, which coincided with increased neural differentiation and proliferation. Tretinoin 32-45 transformation related protein 53, pseudogene Mus musculus 20-23
28446509-2 2017 The cytochrome P450 family 26 (CYP26) enzymes are responsible for atRA clearance, and are potential drug targets to increase concentrations of endogenous atRA in a tissue-specific manner. Tretinoin 66-70 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 4-29
12206137-9 2002 Increased p53 levels did not induce p21 transactivation, interestingly a decrease in p21 was observed on day 17 on exposure to retinoic acid. Tretinoin 127-140 tumor protein, translationally-controlled 1 Mus musculus 85-88
12206137-12 2002 However, retinoic acid accelerated neural differentiation and increased the expression of p53 in proliferating neural cells, corroborated by decreased p21 levels, indicating the importance of cell type and stage specificity of p53 function. Tretinoin 9-22 transformation related protein 53, pseudogene Mus musculus 90-93
11371621-8 2001 A second pathway of hTERT regulation, identified in the RAR-responsive, maturation-resistant NB4-R1 cell line, results in a down-regulation of telomerase that develops slowly during two weeks of all-trans retinoic acid (ATRA) treatment. Tretinoin 205-218 telomerase reverse transcriptase Homo sapiens 20-25
11371621-8 2001 A second pathway of hTERT regulation, identified in the RAR-responsive, maturation-resistant NB4-R1 cell line, results in a down-regulation of telomerase that develops slowly during two weeks of all-trans retinoic acid (ATRA) treatment. Tretinoin 205-218 retinoic acid receptor alpha Homo sapiens 56-59
11371621-8 2001 A second pathway of hTERT regulation, identified in the RAR-responsive, maturation-resistant NB4-R1 cell line, results in a down-regulation of telomerase that develops slowly during two weeks of all-trans retinoic acid (ATRA) treatment. Tretinoin 220-224 telomerase reverse transcriptase Homo sapiens 20-25
12206137-12 2002 However, retinoic acid accelerated neural differentiation and increased the expression of p53 in proliferating neural cells, corroborated by decreased p21 levels, indicating the importance of cell type and stage specificity of p53 function. Tretinoin 9-22 tumor protein, translationally-controlled 1 Mus musculus 151-154
28446509-2 2017 The cytochrome P450 family 26 (CYP26) enzymes are responsible for atRA clearance, and are potential drug targets to increase concentrations of endogenous atRA in a tissue-specific manner. Tretinoin 66-70 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 31-36
12206137-12 2002 However, retinoic acid accelerated neural differentiation and increased the expression of p53 in proliferating neural cells, corroborated by decreased p21 levels, indicating the importance of cell type and stage specificity of p53 function. Tretinoin 9-22 transformation related protein 53, pseudogene Mus musculus 227-230
11744378-0 2002 Differential expression of the retinoic acid-metabolizing enzymes CYP26A1 and CYP26B1 during murine organogenesis. Tretinoin 31-44 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 66-73
11731283-4 2002 We followed by competitive PCR the expression of DAP complex components during retinoic acid (RA)-induced neuronal differentiation of P19 cells. Tretinoin 79-92 interleukin 23 subunit alpha Homo sapiens 134-137
11371621-8 2001 A second pathway of hTERT regulation, identified in the RAR-responsive, maturation-resistant NB4-R1 cell line, results in a down-regulation of telomerase that develops slowly during two weeks of all-trans retinoic acid (ATRA) treatment. Tretinoin 220-224 retinoic acid receptor alpha Homo sapiens 56-59
11731283-4 2002 We followed by competitive PCR the expression of DAP complex components during retinoic acid (RA)-induced neuronal differentiation of P19 cells. Tretinoin 94-96 interleukin 23 subunit alpha Homo sapiens 134-137
28446509-6 2017 Following a single 2.5-mg/kg dose of talarozole to mice, atRA concentrations increased up to 5.7-, 2.7-, and 2.5-fold in serum, liver, and testis, respectively, resulting in induction of Cyp26a1 in the liver and testis and Rar beta and Pgc 1beta in liver. Tretinoin 57-61 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 187-194
11319755-3 2001 The aim of the present study has been to investigate the relationships between retinoic acid and TGF-beta in regulating the expression of CRBP-1 and alpha-smooth muscle actin in cultured rat subcutaneous tissue fibroblasts. Tretinoin 79-92 actin gamma 2, smooth muscle Rattus norvegicus 149-174
28446509-7 2017 The increase in atRA concentrations was well predicted from talarozole pharmacokinetics and in vitro data of CYP26 inhibition. Tretinoin 16-20 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 109-114
28343272-0 2017 Effect of ATRA and ATO on the expression of tissue factor in NB4 acute promyelocytic leukemia cells and regulatory function of the inflammatory cytokines TNF and IL-1beta. Tretinoin 10-14 coagulation factor III, tissue factor Homo sapiens 44-57
11699203-0 2001 Acute promyelocytic leukemia with apparently normal karyotype: molecular findings and response to all-trans retinoic acid. Tretinoin 108-121 PML nuclear body scaffold Homo sapiens 6-28
11699203-7 2001 The present study shows the key role of the fusion of PML-RARA in the responsiveness to ATRA as well as in the leukemogenesis of APL. Tretinoin 88-92 PML nuclear body scaffold Homo sapiens 54-57
11699203-7 2001 The present study shows the key role of the fusion of PML-RARA in the responsiveness to ATRA as well as in the leukemogenesis of APL. Tretinoin 88-92 retinoic acid receptor alpha Homo sapiens 58-62
16206674-7 2001 Abnormal high expression of TF in APL cell was downregulated in patients treated with ATRA or As2O3. Tretinoin 86-90 coagulation factor III, tissue factor Homo sapiens 28-30
11716987-9 2001 Neuronal differentiation of the P19 cells by retinoic acid did not affect the basal or PMA stimulated-PLD activity. Tretinoin 45-58 cyclin dependent kinase inhibitor 2D Mus musculus 32-35
28238841-10 2017 Insulin + RA treatment further induced the Cyp26a1 and Gck expressions in STZ-VAD rats. Tretinoin 10-12 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 43-50
11753687-10 2001 RC-58T/hTERT cells showed growth inhibition when exposed to retinoic acid and transforming growth factor (TGF)-beta1 known potent inhibitors of prostate epithelial cell growth. Tretinoin 60-73 telomerase reverse transcriptase Homo sapiens 7-12
11342454-0 2001 Tyrosine kinase inhibitor STI571 potentiates the pharmacologic activity of retinoic acid in acute promyelocytic leukemia cells: effects on the degradation of RARalpha and PML-RARalpha. Tretinoin 75-88 PML nuclear body scaffold Homo sapiens 171-174
11342454-5 2001 In NB4 promyelocytes, a RARalpha agonist, but not an RXR agonist, can substitute for ATRA and interact with STI571. Tretinoin 85-89 retinoic acid receptor alpha Homo sapiens 24-32
27797397-3 2017 Expression of KLK5 and KLK7 is controlled and upregulated by stimulants such as calcium, 1,25-dihydroxyvitamin D3 [1,25(OH)2 VD3 ] and retinoic acid (RA). Tretinoin 135-148 kallikrein related peptidase 7 Homo sapiens 23-27
11681409-0 2001 Pulsed ATRA as single therapy restores long-term remission in PML-RARalpha-positive acute promyelocytic leukemia patients: real time quantification of minimal residual disease. Tretinoin 7-11 PML nuclear body scaffold Homo sapiens 62-65
11681409-0 2001 Pulsed ATRA as single therapy restores long-term remission in PML-RARalpha-positive acute promyelocytic leukemia patients: real time quantification of minimal residual disease. Tretinoin 7-11 retinoic acid receptor alpha Homo sapiens 66-74
27797397-3 2017 Expression of KLK5 and KLK7 is controlled and upregulated by stimulants such as calcium, 1,25-dihydroxyvitamin D3 [1,25(OH)2 VD3 ] and retinoic acid (RA). Tretinoin 150-152 kallikrein related peptidase 7 Homo sapiens 23-27
11278809-0 2001 Selective roles of retinoic acid receptor and retinoid x receptor in the suppression of apoptosis by all-trans-retinoic acid. Tretinoin 101-124 retinoic acid receptor alpha Homo sapiens 19-41
28488421-0 2017 Retinoic acid modulates lipid accumulation glucose concentration dependently through inverse regulation of SREBP-1 expression in 3T3L1 adipocytes. Tretinoin 0-13 sterol regulatory element binding transcription factor 1 Mus musculus 107-114
11278809-4 2001 In this report, we investigated the involvement of retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H(2)O(2)-exposed cells. Tretinoin 141-145 retinoic acid receptor alpha Homo sapiens 51-73
11278809-4 2001 In this report, we investigated the involvement of retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H(2)O(2)-exposed cells. Tretinoin 141-145 retinoic acid receptor alpha Homo sapiens 75-78
11278809-6 2001 Similarly, transient transfection with a dominant-negative mutant of RAR or a dominant-negative RXR diminished the antiapoptotic effect of t-RA. Tretinoin 139-143 retinoic acid receptor alpha Homo sapiens 69-72
11278809-10 2001 Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Tretinoin 46-50 retinoic acid receptor alpha Homo sapiens 88-91
11704843-5 2001 The effect of As(2)O(3) has been shown to be related to the expression of APL-specific PML-RARalpha oncoprotein, and there is a synergistic effect between As(2)O(3) and ATRA in an APL mouse model. Tretinoin 169-173 PML nuclear body scaffold Homo sapiens 87-90
11704848-2 2001 This finding, coupled with the remarkable success of retinoic acid (RA), the natural ligand of RARalpha, in the treatment of APL, has made APL a unique model system in the study of oncogenic conversion of transcription factors in hematological malignancies. Tretinoin 53-66 retinoic acid receptor alpha Homo sapiens 95-103
28488421-6 2017 Transfection of SREBP-1 siRNA suppressed RA-induced enhancement of lipid accumulation and FAS expression in the cells cultured with HG. Tretinoin 41-43 sterol regulatory element binding transcription factor 1 Mus musculus 16-23
11704848-2 2001 This finding, coupled with the remarkable success of retinoic acid (RA), the natural ligand of RARalpha, in the treatment of APL, has made APL a unique model system in the study of oncogenic conversion of transcription factors in hematological malignancies. Tretinoin 68-70 retinoic acid receptor alpha Homo sapiens 95-103
11704854-0 2001 Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission. Tretinoin 12-25 PML nuclear body scaffold Homo sapiens 55-58
11704854-0 2001 Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission. Tretinoin 12-25 retinoic acid receptor alpha Homo sapiens 59-67
11704854-4 2001 Each drug targets a specific moiety of the fusion protein (RARalpha for retinoic acid, PML for arsenic) to the proteasome. Tretinoin 72-85 retinoic acid receptor alpha Homo sapiens 59-67
11297512-2 2001 We have found that the Epo gene is a direct transcriptional target gene of retinoic acid signaling during early erythropoiesis (prior to embryonic day E12.5) in the fetal liver. Tretinoin 75-88 erythropoietin Mus musculus 23-26
11297512-8 2001 We propose that Epo expression is regulated during the E9.5--E11.5 phase of fetal liver erythropoiesis by RXR alpha and retinoic acid, and that expression then becomes dominated by HNF4 activity from E11.5 onward. Tretinoin 120-133 erythropoietin Mus musculus 16-19
28488421-7 2017 Transfection of the nuclear form of SREBP-1a cDNA into the cells cultured with NG inhibited RA-induced suppression of lipid accumulation and FAS expression. Tretinoin 92-94 sterol regulatory element binding transcription factor 1 Mus musculus 36-44
28488421-8 2017 Moreover, RA- and HG-induced SREBP-1a expression occurred at the early phase of adipogenesis and was dependent on glucocorticoid to induce liver X receptor (LXR) beta, peroxisomal proliferator-activated receptor (PPAR) gamma and retinoid X receptor (RXR), the key nuclear factors influencing the SREBP-1a gene expression. Tretinoin 10-12 sterol regulatory element binding transcription factor 1 Mus musculus 29-37
11668484-5 2001 Our results show that combined treatment with IFN-gamma and RA or the phorbol ester 12-O-tetradecanoyl-phorbol acetate (TPA) had synergistic or enhancing effects on morphologic differentiation and neurite outgrowth in 5 of 5 neuroblastoma cell lines, 3 of which expressed very high levels of N-myc mRNA due to N-myc amplification. Tretinoin 60-62 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 292-297
11668484-5 2001 Our results show that combined treatment with IFN-gamma and RA or the phorbol ester 12-O-tetradecanoyl-phorbol acetate (TPA) had synergistic or enhancing effects on morphologic differentiation and neurite outgrowth in 5 of 5 neuroblastoma cell lines, 3 of which expressed very high levels of N-myc mRNA due to N-myc amplification. Tretinoin 60-62 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 310-315
28488421-8 2017 Moreover, RA- and HG-induced SREBP-1a expression occurred at the early phase of adipogenesis and was dependent on glucocorticoid to induce liver X receptor (LXR) beta, peroxisomal proliferator-activated receptor (PPAR) gamma and retinoid X receptor (RXR), the key nuclear factors influencing the SREBP-1a gene expression. Tretinoin 10-12 nuclear receptor subfamily 1, group H, member 2 Mus musculus 139-166
11318877-6 2001 Two lines of evidence suggested functions of p48 in neurogenesis: (i) expression of p48 was induced in P19 cells when they committed to neural fate upon retinoic acid treatment, and (ii) p48 over-expressed in Xenopus embryos repressed the development of neuronal precursors. Tretinoin 153-166 interferon regulatory factor 9 Mus musculus 45-48
28488421-8 2017 Moreover, RA- and HG-induced SREBP-1a expression occurred at the early phase of adipogenesis and was dependent on glucocorticoid to induce liver X receptor (LXR) beta, peroxisomal proliferator-activated receptor (PPAR) gamma and retinoid X receptor (RXR), the key nuclear factors influencing the SREBP-1a gene expression. Tretinoin 10-12 sterol regulatory element binding transcription factor 1 Mus musculus 296-304
11318877-6 2001 Two lines of evidence suggested functions of p48 in neurogenesis: (i) expression of p48 was induced in P19 cells when they committed to neural fate upon retinoic acid treatment, and (ii) p48 over-expressed in Xenopus embryos repressed the development of neuronal precursors. Tretinoin 153-166 interferon regulatory factor 9 Mus musculus 84-87
11318877-6 2001 Two lines of evidence suggested functions of p48 in neurogenesis: (i) expression of p48 was induced in P19 cells when they committed to neural fate upon retinoic acid treatment, and (ii) p48 over-expressed in Xenopus embryos repressed the development of neuronal precursors. Tretinoin 153-166 interferon regulatory factor 9 Mus musculus 84-87
11819850-0 2001 The effect pathway of retinoic acid through regulation of retinoic acid receptor alpha in gastric cancer cells. Tretinoin 22-35 retinoic acid receptor alpha Homo sapiens 58-86
28488421-9 2017 These results suggest that RA suppresses and enhances lipid accumulation through extracellular glucose concentration-dependent modulation of SREBP-1 expression. Tretinoin 27-29 sterol regulatory element binding transcription factor 1 Mus musculus 141-148
11819850-1 2001 AIM: To evaluate the role of RARalpha gene in mediating the growth inhibitory effect of all-trans retinoic acid (ATRA) on gastric cancer cells. Tretinoin 88-111 retinoic acid receptor alpha Homo sapiens 29-37
11819850-1 2001 AIM: To evaluate the role of RARalpha gene in mediating the growth inhibitory effect of all-trans retinoic acid (ATRA) on gastric cancer cells. Tretinoin 113-117 retinoic acid receptor alpha Homo sapiens 29-37
11230985-9 2001 Immunostainings and Northern blotting demonstrated an enhanced alpha-smooth muscle actin and heavy chain myosin expression in haSMC after atRA-treatment. Tretinoin 138-142 myosin heavy chain 14 Homo sapiens 105-111
11819850-6 2001 RESULTS: ATRA could induce expression level of RARalpha in MGC80-3, BGC-823 and SGC-7901 cells obviously, resulting in growth inhibition of these cell lines. Tretinoin 9-13 retinoic acid receptor alpha Homo sapiens 47-55
27862257-4 2017 In Retinoic acid (RA) induced in vitro differentiation assay, the expression of two germ cell marker genes, integrin alpha6, and integrin beta1, was observed to significantly increase, while it decreased dramatically when IHH was knocked down. Tretinoin 3-16 integrin subunit beta 1 Gallus gallus 129-143
11819850-8 2001 In contrast, when antisense RARalpha gene was transfected into BGC-823 cells, a little inhibitory effect by ATRA was seen, compared with the parallel BGC-823 cells. Tretinoin 108-112 retinoic acid receptor alpha Homo sapiens 28-36
11819850-9 2001 In transient transfection assay, ATRA effectively induced transcriptional activity of betaRARE in MGC80-3, BGC-823, SGC-7902 and MKN/RARalpha cell lines, but not in MKN-45 and BGC/aRARalpha cell lines. Tretinoin 33-37 retinoic acid receptor alpha Homo sapiens 133-141
11234892-8 2001 A 24-h exposure to ATRA increased the expression of RAR alpha, RAR beta, RAR gamma, and RXR alpha in 46%, 77%, 30%, and 38% of the samples, respectively. Tretinoin 19-23 retinoic acid receptor alpha Homo sapiens 52-61
11234892-13 2001 We conclude that RAR alpha, RAR beta, RAR gamma, and RXR alpha are expressed in non-M3 AML blast cells and that ATRA-induced expression of RAR beta may be a marker for retinoid sensitivity. Tretinoin 112-116 retinoic acid receptor alpha Homo sapiens 17-26
11161715-4 2001 We show that RA induces the TJ structure and expression of several TJ-associated molecules, such as ZO-1, occludin, claudin-6, and claudin-7, as well as a barrier function in the genetically engineered cell line F9:rtTA:Cre-ER(T) L32T2, which allows sophisticated genetic manipulations simply by addition of ligands (H. Chiba et al., 2000, Exp. Tretinoin 13-15 claudin 7 Mus musculus 131-140
11704352-3 2001 The human Neuro-Teratocarcinoma (hNT) neurons constitute a terminally differentiated human neuronal cell line that is derived from the Ntera-2/clone D1 (NT2) precursors upon retinoic acid (RA) treatment. Tretinoin 174-187 ras responsive element binding protein 1 Homo sapiens 33-36
11525643-1 2001 Retinoic acid activation of retinoic acid receptor alpha (RARalpha) induces protein kinase Calpha (PKCalpha) expression and inhibits proliferation of the hormone-dependent T-47D breast cancer cell line. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 28-56
11525643-1 2001 Retinoic acid activation of retinoic acid receptor alpha (RARalpha) induces protein kinase Calpha (PKCalpha) expression and inhibits proliferation of the hormone-dependent T-47D breast cancer cell line. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 58-66
11525643-7 2001 Expression of RARalpha in PKCalpha expressing MDA-MB-231 cells resulted in even greater retinoic acid responses, as measured by effects on cell proliferation, inhibition of serum signaling, and transactivation of an RARE-CAT reporter plasmid. Tretinoin 88-101 retinoic acid receptor alpha Homo sapiens 14-22
11172606-8 2001 RA also induced ets-1 expression, a transcription factor known to be phosphorylated by ERK1, in RA sensitive but not RA resistant lines. Tretinoin 0-2 ETS proto-oncogene 1, transcription factor Homo sapiens 16-21
11172606-8 2001 RA also induced ets-1 expression, a transcription factor known to be phosphorylated by ERK1, in RA sensitive but not RA resistant lines. Tretinoin 96-98 ETS proto-oncogene 1, transcription factor Homo sapiens 16-21
11172606-11 2001 The results of these experiments indicate that induction of hypophosphorylated ets-1 as the result of RA and ECM mediated decreases in ERK1 activity represents a novel mechanism by which RA regulates MMP-9 gene expression. Tretinoin 102-104 ETS proto-oncogene 1, transcription factor Homo sapiens 79-84
11172606-11 2001 The results of these experiments indicate that induction of hypophosphorylated ets-1 as the result of RA and ECM mediated decreases in ERK1 activity represents a novel mechanism by which RA regulates MMP-9 gene expression. Tretinoin 187-189 ETS proto-oncogene 1, transcription factor Homo sapiens 79-84
27862257-4 2017 In Retinoic acid (RA) induced in vitro differentiation assay, the expression of two germ cell marker genes, integrin alpha6, and integrin beta1, was observed to significantly increase, while it decreased dramatically when IHH was knocked down. Tretinoin 18-20 integrin subunit beta 1 Gallus gallus 129-143
11306066-4 2001 Simulations of the oxidation of retinol to retinoic acid with mouse ADH4 and human aldehyde dehydrogenase (ALDH1), using rate constants estimated for all steps in the mechanism, suggest that ethanol (50 mM) would modestly decrease production of retinoic acid. Tretinoin 245-258 aldehyde dehydrogenase 1 family member A1 Homo sapiens 107-112
27862257-5 2017 Fluorescence activated cell sorting analysis showed that the proportion of integrin alpha6+ and integrin beta1+ cells in the RA group was significantly higher than that in the RA + siRNA- Indian Hedgehog (IHH) group. Tretinoin 125-127 integrin subunit beta 1 Gallus gallus 96-110
11212271-9 2001 The ATRA metabolites were found to exert their differentiation effects via the RAR alpha nuclear receptors, because the RAR alpha-specific antagonist BMS614 blocked metabolite-induced CD11c expression in NB4 cells. Tretinoin 4-8 retinoic acid receptor alpha Homo sapiens 79-88
11472875-4 2001 The levels of alpha-synuclein expression were elevated markedly in NTera2 teratocarcinoma cells following retinoic acid-induced neuronal differentiation, accompanied with an increased expression of synphilin-1, while they were unaltered in NTera2-derived differentiated neurons by exposure to TNF-alpha, IL-1beta, BDNF or GDNF. Tretinoin 106-119 synuclein alpha Homo sapiens 14-29
28503683-9 2017 Additionally, ATRA treatment also inhibited the DSNA-mediated up-regulation of a repair gene RAD51, suggesting possible involvement of basal Nrf2 in the anti-genotoxic effect of DSNA. Tretinoin 14-18 DNA repair protein RAD51 homolog 1 Cricetulus griseus 93-98
11507036-9 2001 957E/hTERT cells showed growth inhibition when exposed to retinoic acid and transforming growth factor beta1, potent inhibitors of prostate epithelial cell growth. Tretinoin 58-71 telomerase reverse transcriptase Homo sapiens 5-10
11313705-0 2001 A functionally active RARalpha nuclear receptor is expressed in retinoic acid non responsive early myeloblastic cell lines. Tretinoin 64-77 retinoic acid receptor alpha Homo sapiens 22-30
11313705-3 2001 Our results indicate that a functionally active RARalpha nuclear receptor is expressed in all the analyzed cell lines, regardless of their differentiation capacity following exposure to ATRA. Tretinoin 186-190 retinoic acid receptor alpha Homo sapiens 48-56
11313705-6 2001 Further investigation is needed to clarify whether myeloid transcription factors, distinct to RARalpha, play a role in the resistance of these cells to ATRA treatment. Tretinoin 152-156 retinoic acid receptor alpha Homo sapiens 94-102
11478838-3 2001 Immunoblotting analyses and capillary zone electrophoresis demonstrated that following RA treatment: lamins A/C and B1, and vimentin decreased to negligible amounts; LAP2 beta, lamin B2 and emerin remained essentially unchanged; lamin B receptor (LBR) increased markedly; histone subtypes H1.4 and 1.5 exhibited dephosphorylation. Tretinoin 87-89 membrane spanning 4-domains A1 Homo sapiens 110-118
11478838-3 2001 Immunoblotting analyses and capillary zone electrophoresis demonstrated that following RA treatment: lamins A/C and B1, and vimentin decreased to negligible amounts; LAP2 beta, lamin B2 and emerin remained essentially unchanged; lamin B receptor (LBR) increased markedly; histone subtypes H1.4 and 1.5 exhibited dephosphorylation. Tretinoin 87-89 vimentin Homo sapiens 124-132
28422378-2 2017 We found that RA depletion caused by expression of the RA-metabolizing enzyme CYP26A1 promotes carcinogenesis, implicating CYP26A1 as a candidate oncogene. Tretinoin 14-16 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 78-85
11478838-3 2001 Immunoblotting analyses and capillary zone electrophoresis demonstrated that following RA treatment: lamins A/C and B1, and vimentin decreased to negligible amounts; LAP2 beta, lamin B2 and emerin remained essentially unchanged; lamin B receptor (LBR) increased markedly; histone subtypes H1.4 and 1.5 exhibited dephosphorylation. Tretinoin 87-89 emerin Homo sapiens 190-196
11478839-0 2001 Retinoic acid- and bone morphogenetic protein 4-induced apoptosis in P19 embryonal carcinoma cells requires p27. Tretinoin 0-13 interferon alpha inducible protein 27 Homo sapiens 108-111
11478839-3 2001 Retinoic acid (RA) and bone morphogenetic protein (BMP) 4 induce rapidly dividing P19 embryonal carcinoma cells to undergo apoptosis. Tretinoin 0-13 cyclin dependent kinase inhibitor 2D Homo sapiens 82-85
11478839-3 2001 Retinoic acid (RA) and bone morphogenetic protein (BMP) 4 induce rapidly dividing P19 embryonal carcinoma cells to undergo apoptosis. Tretinoin 15-17 cyclin dependent kinase inhibitor 2D Homo sapiens 82-85
11478839-8 2001 In contrast, RA and BMP4 induce the Cdk inhibitor p27. Tretinoin 13-15 interferon alpha inducible protein 27 Homo sapiens 50-53
11779431-0 2001 Effect of all-trans retinoic acid and arsenic trioxide on tissue factor expression in acute promyelocytic leukemia cells. Tretinoin 10-33 coagulation factor III, tissue factor Homo sapiens 58-71
11779431-1 2001 OBJECTIVE: To study the effect of all-trans retinoic acid (ATRA) and arsenic troxide (As2O3) on tissue factor (TF) expression and procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells in vivo and in vitro. Tretinoin 34-57 coagulation factor III, tissue factor Homo sapiens 96-109
11779431-1 2001 OBJECTIVE: To study the effect of all-trans retinoic acid (ATRA) and arsenic troxide (As2O3) on tissue factor (TF) expression and procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells in vivo and in vitro. Tretinoin 34-57 coagulation factor III, tissue factor Homo sapiens 111-113
11779431-1 2001 OBJECTIVE: To study the effect of all-trans retinoic acid (ATRA) and arsenic troxide (As2O3) on tissue factor (TF) expression and procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells in vivo and in vitro. Tretinoin 59-63 coagulation factor III, tissue factor Homo sapiens 96-109
11779431-1 2001 OBJECTIVE: To study the effect of all-trans retinoic acid (ATRA) and arsenic troxide (As2O3) on tissue factor (TF) expression and procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells in vivo and in vitro. Tretinoin 59-63 coagulation factor III, tissue factor Homo sapiens 111-113
11779431-5 2001 RESULTS: Both ATRA and As2O3 can down-regulate the TF antigen, its mRNA transcription and membrane PCA of APL cells in vivo and in vitro, in a time-dependent manner. Tretinoin 14-18 coagulation factor III, tissue factor Homo sapiens 51-53
11779431-7 2001 Both ATRA and As2O3 can also down-regulate the TF antigen in U937 cells transfected with or without PML-RARa. Tretinoin 5-9 coagulation factor III, tissue factor Homo sapiens 47-49
11779431-7 2001 Both ATRA and As2O3 can also down-regulate the TF antigen in U937 cells transfected with or without PML-RARa. Tretinoin 5-9 PML nuclear body scaffold Homo sapiens 100-103
11779431-7 2001 Both ATRA and As2O3 can also down-regulate the TF antigen in U937 cells transfected with or without PML-RARa. Tretinoin 5-9 retinoic acid receptor alpha Homo sapiens 104-108
11779431-8 2001 CONCLUSION: Tissue factor expression and PCA in APL cells may be down-regulated by ATRA and As2O3. Tretinoin 83-87 coagulation factor III, tissue factor Homo sapiens 12-25
11478839-13 2001 These data support the hypothesis that RA and BMP4 together induce the p27 protein leading to Rb activation and ultimately apoptosis. Tretinoin 39-41 interferon alpha inducible protein 27 Homo sapiens 71-74
11688558-5 2001 We use mosaic analysis to show that the reduction in hoxb4 expression in the nervous system is a non-cell autonomous effect, reflecting a requirement for retinoic acid signalling from adjacent paraxial mesoderm. Tretinoin 154-167 homeobox B4a Danio rerio 53-58
28422378-2 2017 We found that RA depletion caused by expression of the RA-metabolizing enzyme CYP26A1 promotes carcinogenesis, implicating CYP26A1 as a candidate oncogene. Tretinoin 14-16 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 123-130
28422378-2 2017 We found that RA depletion caused by expression of the RA-metabolizing enzyme CYP26A1 promotes carcinogenesis, implicating CYP26A1 as a candidate oncogene. Tretinoin 55-57 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 78-85
11479138-0 2001 Retinoic acid and vitamin D(3) powerfully inhibit in vitro leptin secretion by human adipose tissue. Tretinoin 0-13 leptin Homo sapiens 59-65
11424001-10 2001 ATRA also inhibited CD34+ JCML monocytic growth and GM-CSF hypersensitivity. Tretinoin 0-4 colony stimulating factor 2 Homo sapiens 52-58
28422378-2 2017 We found that RA depletion caused by expression of the RA-metabolizing enzyme CYP26A1 promotes carcinogenesis, implicating CYP26A1 as a candidate oncogene. Tretinoin 55-57 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 123-130
11479138-8 2001 In conclusion, in vitro leptin secretion by human adipose tissue is negatively controlled by either RA or vitamin D(3). Tretinoin 100-102 leptin Homo sapiens 24-30
28087752-6 2017 Localisation of RA synthetic (RALDH-1) and degrading (cytochrome P450 subfamily 26 A1 (CYP26A1)) enzymes in human lung was determined by immunofluorescence. Tretinoin 16-18 aldehyde dehydrogenase 1 family member A1 Homo sapiens 30-37
11480559-9 2001 In conclusion, a combination of As2O3 and GM-CSF appears to be a novel differentiation-inducing therapy in patients with APL, including relapsed or RA-resistant cases. Tretinoin 148-150 colony stimulating factor 2 Homo sapiens 42-48
12488603-2 2001 The pretreatment of the cells by compactin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl (HMG) CoA reductase, during 24 hours, enhances the ATRA-induced cell differentiation. Tretinoin 149-153 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 71-117
28087752-8 2017 RESULTS: RA stimulated HLMVEC angiogenesis in vitro; this was partially reproduced with a RAR-alpha agonist. Tretinoin 9-11 retinoic acid receptor alpha Homo sapiens 90-99
28558014-0 2017 Correction: Retinoic acid exacerbates chlorpyrifos action in ensuing adipogenic differentiation of C3H10T1/2 cells in a GSK3beta dependent pathway. Tretinoin 12-25 glycogen synthase kinase 3 beta Mus musculus 120-128
11137376-3 2001 We have previously demonstrated that all-trans-retinoic acid administered to pregnant CD-1 mice on gestational day 11 or 13 produced limb defects and cleft palate near term in a dose-responsive manner. Tretinoin 37-60 CD1 antigen complex Mus musculus 86-90
11331281-0 2001 Regulation of interferon and retinoic acid-induced cell death activation through thioredoxin reductase. Tretinoin 29-42 peroxiredoxin 5 Homo sapiens 81-102
11331281-8 2001 IFN/all-trans-retinoic acid-induced cytochrome c release from the mitochondrion was promoted in the presence of wild type and was inhibited in the presence of mutant TR. Tretinoin 4-27 peroxiredoxin 5 Homo sapiens 166-168
28526071-3 2017 Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKIIdelta pathway through miR-31-5p in embryonic tongue. Tretinoin 38-40 microRNA 31 Homo sapiens 85-91
11399257-4 2001 We examined the effects of all-trans-retinoic acid (atRA), either alone or in combination with mitogenic growth factor, basic fibroblast growth factor (bFGF), on the PAI-1 expression in cultured vascular smooth muscle cells (SMCs). Tretinoin 52-56 serpin family E member 1 Homo sapiens 166-171
11399257-6 2001 RESULTS: Treatment of vascular SMCs with atRA in combination with bFGF resulted in an additional increase in PAI-1 expression both at the mRNA and protein levels. Tretinoin 41-45 serpin family E member 1 Homo sapiens 109-114
11399257-12 2001 In agreement with the role of PAI-1 in the inhibition of fibrinolytic activity which stimulates ECM degradation, cell migration was inhibited by treatment with atRA and bFGF. Tretinoin 160-164 serpin family E member 1 Homo sapiens 30-35
11104669-6 2000 Unlike p96, p67 largely resides in RA-treated F9 cell nuclei. Tretinoin 35-37 methionine aminopeptidase 2 Mus musculus 12-15
28526071-5 2017 RESULTS: RA stimulated the expression of miR-31-5p in both embryonic tongue and C2C12 myoblasts. Tretinoin 9-11 microRNA 31 Homo sapiens 41-47
28526071-7 2017 MiR-31-5p mimics disrupted CamkIIdelta expression, C2C12 proliferation and differentiation as excess RA did, while miR-31-5p inhibitor partially rescued these defects in the presence of RA. Tretinoin 101-103 microRNA 31 Homo sapiens 0-6
11090075-5 2000 This elevation of cyclin A1 was reversed by treatment with all-trans retinoic acid (ATRA) in cells expressing PML-RAR alpha but not PLZF-RAR alpha. Tretinoin 59-82 cyclin A1 Homo sapiens 18-27
11435507-4 2001 Here, we examined the ability of CRA, as well as all-trans-retinoic acid (ATRA), to regulate hepatic GNMT as a potential basis for our earlier observations. Tretinoin 49-72 glycine N-methyltransferase Rattus norvegicus 101-105
28526071-7 2017 MiR-31-5p mimics disrupted CamkIIdelta expression, C2C12 proliferation and differentiation as excess RA did, while miR-31-5p inhibitor partially rescued these defects in the presence of RA. Tretinoin 186-188 microRNA 31 Homo sapiens 115-121
11435507-4 2001 Here, we examined the ability of CRA, as well as all-trans-retinoic acid (ATRA), to regulate hepatic GNMT as a potential basis for our earlier observations. Tretinoin 74-78 glycine N-methyltransferase Rattus norvegicus 101-105
11435507-6 2001 Rats from each group were orally given ATRA, CRA (both at 30 micromol/kg body), or vehicle daily for 7 d. For control rats, administration of both CRA and ATRA elevated the hepatic GNMT activity 49% and 34%, respectively, compared with the control group. Tretinoin 155-159 glycine N-methyltransferase Rattus norvegicus 181-185
11090075-5 2000 This elevation of cyclin A1 was reversed by treatment with all-trans retinoic acid (ATRA) in cells expressing PML-RAR alpha but not PLZF-RAR alpha. Tretinoin 59-82 retinoic acid receptor alpha Homo sapiens 114-123
11090075-5 2000 This elevation of cyclin A1 was reversed by treatment with all-trans retinoic acid (ATRA) in cells expressing PML-RAR alpha but not PLZF-RAR alpha. Tretinoin 84-88 cyclin A1 Homo sapiens 18-27
11090075-5 2000 This elevation of cyclin A1 was reversed by treatment with all-trans retinoic acid (ATRA) in cells expressing PML-RAR alpha but not PLZF-RAR alpha. Tretinoin 84-88 retinoic acid receptor alpha Homo sapiens 114-123
11090075-10 2000 Addition of ATRA inhibited PML-RAR alpha-induced cyclin A1 promoter activity. Tretinoin 12-16 retinoic acid receptor alpha Homo sapiens 31-40
11090075-10 2000 Addition of ATRA inhibited PML-RAR alpha-induced cyclin A1 promoter activity. Tretinoin 12-16 cyclin A1 Homo sapiens 49-58
28526071-8 2017 CONCLUSIONS: Excess RA can stimulate miR-31-5p expression to suppress CamkIIdelta, which represses the proliferation and differentiation of tongue myoblasts. Tretinoin 20-22 microRNA 31 Homo sapiens 37-43
11283017-9 2001 3) The beta3Gn-T5 expression was up-regulated by stimulation with retinoic acid and down-regulated with 12-O-tetradecanoylphorbol-13-acetate in HL-60 cells. Tretinoin 66-79 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 5 Homo sapiens 7-17
28486108-6 2017 Genetically inhibiting TRIB3 expression or combination of a peptide disturbing TRIB3/PML-RARalpha interaction with ATRA/As2O3 eradicates APL by accelerating PML-RARalpha degradation. Tretinoin 115-119 PML nuclear body scaffold Homo sapiens 85-88
11301322-0 2001 PRAM-1 is a novel adaptor protein regulated by retinoic acid (RA) and promyelocytic leukemia (PML)-RA receptor alpha in acute promyelocytic leukemia cells. Tretinoin 1-3 PML nuclear body scaffold Homo sapiens 70-92
11301322-0 2001 PRAM-1 is a novel adaptor protein regulated by retinoic acid (RA) and promyelocytic leukemia (PML)-RA receptor alpha in acute promyelocytic leukemia cells. Tretinoin 1-3 PML nuclear body scaffold Homo sapiens 94-97
11301322-2 2001 Complete remission of acute promyelocytic leukemia can be obtained by treating patients with all-trans retinoic acid, and PML-RARalpha plays a major role in mediating retinoic acid effects in leukemia cells. Tretinoin 167-180 PML nuclear body scaffold Homo sapiens 122-125
11301322-2 2001 Complete remission of acute promyelocytic leukemia can be obtained by treating patients with all-trans retinoic acid, and PML-RARalpha plays a major role in mediating retinoic acid effects in leukemia cells. Tretinoin 167-180 retinoic acid receptor alpha Homo sapiens 126-134
11301322-4 2001 By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARalpha target gene encoding an Adaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. Tretinoin 87-100 PML nuclear body scaffold Homo sapiens 41-63
11301322-4 2001 By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARalpha target gene encoding an Adaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. Tretinoin 87-100 PML nuclear body scaffold Homo sapiens 123-126
11301322-4 2001 By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARalpha target gene encoding an Adaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. Tretinoin 87-100 retinoic acid receptor alpha Homo sapiens 127-135
11301322-4 2001 By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARalpha target gene encoding an Adaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. Tretinoin 87-100 FYN binding protein 1 Homo sapiens 258-266
11301322-4 2001 By applying subtraction cloning to acute promyelocytic leukemia cells, we identified a retinoic acid-induced gene, PRAM-1 (PML-RARalpha target gene encoding an Adaptor Molecule-1), which encodes a novel adaptor protein sharing structural homologies with the SLAP-130/fyb adaptor. Tretinoin 87-100 FYN binding protein 1 Homo sapiens 267-270
11301322-8 2001 By providing the first evidence that PML-RARalpha dysregulates expression of an adaptor protein, our data open new insights into signaling events that are disrupted during transformation by PML-RARalpha and induced by retinoic acid during de novo differentiation of acute promyelocytic leukemia cells. Tretinoin 218-231 PML nuclear body scaffold Homo sapiens 37-40
11301322-8 2001 By providing the first evidence that PML-RARalpha dysregulates expression of an adaptor protein, our data open new insights into signaling events that are disrupted during transformation by PML-RARalpha and induced by retinoic acid during de novo differentiation of acute promyelocytic leukemia cells. Tretinoin 218-231 retinoic acid receptor alpha Homo sapiens 41-49
11429697-10 2001 We conclude that constitutive expression of cyclin D1 sensitizes ER-positive breast cancer cells to a retinoic acid-induced mitochondrial death pathway involving Bax activation, cytochrome c release and caspase-9 cleavage. Tretinoin 102-115 caspase 9 Homo sapiens 203-212
11384110-5 2001 ATRA inhibited docetaxel-induced phosphorylation of cdc2 resulting in activation of cdc2 kinase and partial reversal of the G2/M arrest. Tretinoin 0-4 cyclin dependent kinase 1 Homo sapiens 52-56
11384110-5 2001 ATRA inhibited docetaxel-induced phosphorylation of cdc2 resulting in activation of cdc2 kinase and partial reversal of the G2/M arrest. Tretinoin 0-4 cyclin dependent kinase 1 Homo sapiens 84-88
11384110-6 2001 ATRA also inhibited docetaxel-induced activation of MAPK indicating that the effects of docetaxel and ATRA on cdc2 phosphorylation are dependent on MAPK. Tretinoin 0-4 cyclin dependent kinase 1 Homo sapiens 110-114
11413229-5 2001 The presence of the GluRzeta1 protein was detected throughout neural induction, whereas retinoic acid-induced neuron formation elevated the amount of exon 21 (C1)- and exon 22 (C2)-containing GluRzeta1 mRNAs and resulted in the appearance of exon 5 (N1)-containing transcripts. Tretinoin 88-101 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 192-201
11519864-6 2001 Both 1,25(OH)2D3 and ATRA individually induced an accumulation of MCF-7 cells in the G1 phase of the cell cycle and an associated increase in p21WAFI/CiP1, p27KiP1 and a dephosphorylation of Rb but the effects were not additive. Tretinoin 21-25 cyclin dependent kinase inhibitor 1B Homo sapiens 156-163
11504380-7 2001 Retinol and retinoic acid also inhibited proliferation of cells growth-stimulated by insulin and other growth factors from the IGF growth factor family (des(1-3)IGF-I and IGF-II), as well as growth factors from the epidermal growth factor family (EGF and TGF-alpha), with retinoic acid being more effective than retinol. Tretinoin 12-25 insulin Bos taurus 85-92
11504380-7 2001 Retinol and retinoic acid also inhibited proliferation of cells growth-stimulated by insulin and other growth factors from the IGF growth factor family (des(1-3)IGF-I and IGF-II), as well as growth factors from the epidermal growth factor family (EGF and TGF-alpha), with retinoic acid being more effective than retinol. Tretinoin 12-25 insulin like growth factor 1 Bos taurus 161-166
11504380-7 2001 Retinol and retinoic acid also inhibited proliferation of cells growth-stimulated by insulin and other growth factors from the IGF growth factor family (des(1-3)IGF-I and IGF-II), as well as growth factors from the epidermal growth factor family (EGF and TGF-alpha), with retinoic acid being more effective than retinol. Tretinoin 12-25 epidermal growth factor Bos taurus 247-250
11504380-9 2001 The growth-stimulating effect of insulin, EGF and TGF-alpha was inhibited 42-64% by retinol and retinoic acid at 100 ng/ml, and 64-84% at 10,000 ng/ml. Tretinoin 96-109 insulin Bos taurus 33-40
11504380-9 2001 The growth-stimulating effect of insulin, EGF and TGF-alpha was inhibited 42-64% by retinol and retinoic acid at 100 ng/ml, and 64-84% at 10,000 ng/ml. Tretinoin 96-109 epidermal growth factor Bos taurus 42-45
11331403-7 2001 Using neuroblastoma cells as an in vitro model for neuronal differentiation, we found that retinoic acid stimulated the expression of the three Kif3 and the kinesin-associated protein genes, although with different time courses. Tretinoin 91-104 kinesin family member 3A Mus musculus 144-148
11311979-4 2001 After exposure to retinoic acid for 4 days AQP4 mRNA expression started at the initiation of astrocytic differentiation of P19 cells at 6 days, and increased markedly by 21 days. Tretinoin 18-31 interleukin 23 subunit alpha Homo sapiens 123-126
11290607-12 2001 Furthermore, other inducers of differentiation, all-trans-retinoic acid and 12-O-tetradecanoylphorbol 13-acetate, increased PTEN expression in HL-60. Tretinoin 48-71 phosphatase and tensin homolog Homo sapiens 124-128
11299304-0 2001 Up-regulation of cyclooxygenase-1 in neuroblastoma cell lines by retinoic acid and corticosteroids. Tretinoin 65-78 prostaglandin-endoperoxide synthase 1 Mus musculus 17-33
11299304-3 2001 Differentiation of the cells with retinoic acid increased cyclooxygenase-1 mRNA and protein expression within 24 and 48 h, respectively. Tretinoin 34-47 prostaglandin-endoperoxide synthase 1 Mus musculus 58-74
11299304-7 2001 Retinoic acid increased the transcription of cyclooxygenase-1 mRNA, determined with a luciferase-coupled promoter construct. Tretinoin 0-13 prostaglandin-endoperoxide synthase 1 Mus musculus 45-61
11264371-6 2001 After treatment with retinoic acid, NT2 cells differentiate into neuron-like hNT cells which express very high levels of both PML and Sp100. Tretinoin 21-34 PML nuclear body scaffold Homo sapiens 126-129
11264371-6 2001 After treatment with retinoic acid, NT2 cells differentiate into neuron-like hNT cells which express very high levels of both PML and Sp100. Tretinoin 21-34 SP100 nuclear antigen Homo sapiens 134-139
11346880-0 2001 Retinoic acid-induced expression of autotaxin in N-myc-amplified neuroblastoma cells. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 49-54
11246122-3 2001 Mucous differentiation and expression of MUC2, MUC5AC, MUC5B and MUC7, but not MUCi, MUC4, and MUC8 mucin genes, were shown to be retinoic acid- (RA) or retinol-dependent. Tretinoin 130-143 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 47-53
11245923-0 2001 A functional retinoic acid response element (RARE) is present within the distal promoter of the rat gonadotropin-releasing hormone (GnRH) gene. Tretinoin 13-26 gonadotropin releasing hormone 1 Rattus norvegicus 100-130
11245923-0 2001 A functional retinoic acid response element (RARE) is present within the distal promoter of the rat gonadotropin-releasing hormone (GnRH) gene. Tretinoin 13-26 gonadotropin releasing hormone 1 Rattus norvegicus 132-136
11245923-1 2001 We previously demonstrated that all-trans-retinoic acid (all-trans-RA) regulates gonadotropin-releasing hormone (GnRH) release and gene expression in rat hypothalamic fragments and GT1-1 neuronal cells. Tretinoin 32-55 gonadotropin releasing hormone 1 Rattus norvegicus 81-111
11245923-1 2001 We previously demonstrated that all-trans-retinoic acid (all-trans-RA) regulates gonadotropin-releasing hormone (GnRH) release and gene expression in rat hypothalamic fragments and GT1-1 neuronal cells. Tretinoin 32-55 gonadotropin releasing hormone 1 Rattus norvegicus 113-117
11245923-3 2001 In the present study, we attempted to localize functional retinoic acid response elements (RAREs) within the all-trans-RA-responsive region of the rat GnRH gene. Tretinoin 58-71 gonadotropin releasing hormone 1 Rattus norvegicus 151-155
11245924-0 2001 9-cis-Retinoic acid represses transcription of the gonadotropin-releasing hormone (GnRH) gene via proximal promoter region that is distinct from all-trans-retinoic acid response element. Tretinoin 149-168 gonadotropin releasing hormone 1 Mus musculus 51-81
11245924-0 2001 9-cis-Retinoic acid represses transcription of the gonadotropin-releasing hormone (GnRH) gene via proximal promoter region that is distinct from all-trans-retinoic acid response element. Tretinoin 149-168 gonadotropin releasing hormone 1 Mus musculus 83-87
11245924-1 2001 We previously reported an enhancing effect of all-trans-retinoic acid (all-trans-RA) on gonadotropin-releasing hormone (GnRH) gene transcription via distal promoter elements of the rat GnRH gene. Tretinoin 46-69 gonadotropin releasing hormone 1 Rattus norvegicus 88-118
11245924-1 2001 We previously reported an enhancing effect of all-trans-retinoic acid (all-trans-RA) on gonadotropin-releasing hormone (GnRH) gene transcription via distal promoter elements of the rat GnRH gene. Tretinoin 46-69 gonadotropin releasing hormone 1 Rattus norvegicus 120-124
11245924-1 2001 We previously reported an enhancing effect of all-trans-retinoic acid (all-trans-RA) on gonadotropin-releasing hormone (GnRH) gene transcription via distal promoter elements of the rat GnRH gene. Tretinoin 46-69 gonadotropin releasing hormone 1 Rattus norvegicus 185-189
11245924-1 2001 We previously reported an enhancing effect of all-trans-retinoic acid (all-trans-RA) on gonadotropin-releasing hormone (GnRH) gene transcription via distal promoter elements of the rat GnRH gene. Tretinoin 71-83 gonadotropin releasing hormone 1 Rattus norvegicus 88-118
11245924-1 2001 We previously reported an enhancing effect of all-trans-retinoic acid (all-trans-RA) on gonadotropin-releasing hormone (GnRH) gene transcription via distal promoter elements of the rat GnRH gene. Tretinoin 71-83 gonadotropin releasing hormone 1 Rattus norvegicus 120-124
11245924-1 2001 We previously reported an enhancing effect of all-trans-retinoic acid (all-trans-RA) on gonadotropin-releasing hormone (GnRH) gene transcription via distal promoter elements of the rat GnRH gene. Tretinoin 71-83 gonadotropin releasing hormone 1 Rattus norvegicus 185-189
11092879-0 2001 An intronic Ikaros-binding element mediates retinoic acid suppression of the kappa opioid receptor gene, accompanied by histone deacetylation on the promoters. Tretinoin 44-57 IKAROS family zinc finger 1 Mus musculus 12-18
11171071-1 2001 We reported previously that the expression of the gene encoding MUC5AC mucin in human airway epithelial cells is controlled by retinoic acid via the retinoic acid receptor (RAR)-alpha and that 3,3",5-tri-iodothyronine (T(3)) inhibits the expression of MUC5AC. Tretinoin 127-140 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 64-70
11171071-1 2001 We reported previously that the expression of the gene encoding MUC5AC mucin in human airway epithelial cells is controlled by retinoic acid via the retinoic acid receptor (RAR)-alpha and that 3,3",5-tri-iodothyronine (T(3)) inhibits the expression of MUC5AC. Tretinoin 127-140 retinoic acid receptor alpha Homo sapiens 149-171
11171071-1 2001 We reported previously that the expression of the gene encoding MUC5AC mucin in human airway epithelial cells is controlled by retinoic acid via the retinoic acid receptor (RAR)-alpha and that 3,3",5-tri-iodothyronine (T(3)) inhibits the expression of MUC5AC. Tretinoin 127-140 retinoic acid receptor alpha Homo sapiens 173-176
11168401-8 2001 Expression of COUP-TFII induced by either retinoic acid or dimethyl sulfoxide in differentiating P19 cells increases NHE expression. Tretinoin 42-55 nuclear receptor subfamily 2, group F, member 2 Mus musculus 14-23
11306054-6 2001 The recombinant xALDH1 protein exhibited both T(3)-binding activity and ALDH activity converting retinal to retinoic acid (RA), which were similar to those of xCTBP purified from liver cytosol. Tretinoin 108-121 aldehyde dehydrogenase 1 family member A1 Homo sapiens 17-21
11306054-6 2001 The recombinant xALDH1 protein exhibited both T(3)-binding activity and ALDH activity converting retinal to retinoic acid (RA), which were similar to those of xCTBP purified from liver cytosol. Tretinoin 123-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 17-21
11306066-4 2001 Simulations of the oxidation of retinol to retinoic acid with mouse ADH4 and human aldehyde dehydrogenase (ALDH1), using rate constants estimated for all steps in the mechanism, suggest that ethanol (50 mM) would modestly decrease production of retinoic acid. Tretinoin 43-56 aldehyde dehydrogenase 1 family member A1 Homo sapiens 107-112
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 110-133
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 135-138
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 retinoic acid receptor alpha Homo sapiens 110-133
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 retinoic acid receptor alpha Homo sapiens 135-138
11313967-5 2001 When SN-1 cells were treated with MLL-CBP antisense oligonucleotide, the cells were induced to differentiate by ATRA or VD3, suggesting that the MLL-CBP fusion gene dominant-negatively suppresses ATRA- or VD3-induced differentiation. Tretinoin 112-116 lysine methyltransferase 2A Homo sapiens 34-37
11313967-5 2001 When SN-1 cells were treated with MLL-CBP antisense oligonucleotide, the cells were induced to differentiate by ATRA or VD3, suggesting that the MLL-CBP fusion gene dominant-negatively suppresses ATRA- or VD3-induced differentiation. Tretinoin 112-116 lysine methyltransferase 2A Homo sapiens 145-148
11313967-8 2001 These findings suggest that RXR agonists or a clinically applicable combination of ATRA and butyrate derivatives might be useful for differentiation therapy in leukemia patients with the MLL-CBP fusion gene. Tretinoin 83-87 lysine methyltransferase 2A Homo sapiens 187-190
11212249-0 2001 Increased retinoic acid responsiveness in lung carcinoma cells that are nonresponsive despite the presence of endogenous retinoic acid receptor (RAR) beta by expression of exogenous retinoid receptors retinoid X receptor alpha, RAR alpha, and RAR gamma. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 145-148
11212249-0 2001 Increased retinoic acid responsiveness in lung carcinoma cells that are nonresponsive despite the presence of endogenous retinoic acid receptor (RAR) beta by expression of exogenous retinoid receptors retinoid X receptor alpha, RAR alpha, and RAR gamma. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 228-237
11212249-6 2001 RXR alpha and RAR alpha enhanced growth inhibition by all-trans-retinoic acid or 9-cis-retinoic acid, whereas RAR gamma was less effective, and RAR beta was ineffective. Tretinoin 54-77 retinoic acid receptor alpha Homo sapiens 14-23
11151452-1 2000 Retinal dehydrogenase type 1 (RALDH1) is involved in the biosynthesis of retinoic acid (RA), a modulator of gene expression and cell differentiation. Tretinoin 73-86 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-28
11151452-1 2000 Retinal dehydrogenase type 1 (RALDH1) is involved in the biosynthesis of retinoic acid (RA), a modulator of gene expression and cell differentiation. Tretinoin 73-86 aldehyde dehydrogenase 1 family member A1 Homo sapiens 30-36
11151452-1 2000 Retinal dehydrogenase type 1 (RALDH1) is involved in the biosynthesis of retinoic acid (RA), a modulator of gene expression and cell differentiation. Tretinoin 30-32 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-28
11327309-2 2000 The effects of RA on target gene expression are mediated by a family of ligand dependent nuclear transcription factors known as retinoic acid receptors (RAR). Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 128-151
11327309-2 2000 The effects of RA on target gene expression are mediated by a family of ligand dependent nuclear transcription factors known as retinoic acid receptors (RAR). Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 153-156
11327309-8 2000 Finally, RA mediates induction of the human ets-1 gene at the mRNA and protein levels. Tretinoin 9-11 ETS proto-oncogene 1, transcription factor Homo sapiens 44-49
11327309-9 2000 These data suggest that induction of ets-1 expression by RA is mediated by a novel retinoic acid response element in the promoter region of this gene. Tretinoin 57-59 ETS proto-oncogene 1, transcription factor Homo sapiens 37-42
11327309-9 2000 These data suggest that induction of ets-1 expression by RA is mediated by a novel retinoic acid response element in the promoter region of this gene. Tretinoin 83-96 ETS proto-oncogene 1, transcription factor Homo sapiens 37-42
11073974-2 2000 An early target gene of the retinoid metabolite, retinoic acid (RA), is that encoding one of its own receptors, the retinoic acid receptor beta (RARbeta). Tretinoin 49-62 retinoic acid receptor beta Gallus gallus 116-143
11073974-2 2000 An early target gene of the retinoid metabolite, retinoic acid (RA), is that encoding one of its own receptors, the retinoic acid receptor beta (RARbeta). Tretinoin 49-62 retinoic acid receptor beta Gallus gallus 145-152
11073974-2 2000 An early target gene of the retinoid metabolite, retinoic acid (RA), is that encoding one of its own receptors, the retinoic acid receptor beta (RARbeta). Tretinoin 64-66 retinoic acid receptor beta Gallus gallus 116-143
11073974-2 2000 An early target gene of the retinoid metabolite, retinoic acid (RA), is that encoding one of its own receptors, the retinoic acid receptor beta (RARbeta). Tretinoin 64-66 retinoic acid receptor beta Gallus gallus 145-152
11819702-1 2000 AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA. Tretinoin 41-54 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 155-158
11071651-2 2000 FR-beta expression was elevated up to 20-fold by all-trans retinoic acid (ATRA) in KG-1 myeloid leukemia cells in a dose-dependent and reversible manner in the absence of terminal differentiation or cell growth inhibition. Tretinoin 59-72 folate receptor beta Homo sapiens 0-7
11071651-2 2000 FR-beta expression was elevated up to 20-fold by all-trans retinoic acid (ATRA) in KG-1 myeloid leukemia cells in a dose-dependent and reversible manner in the absence of terminal differentiation or cell growth inhibition. Tretinoin 74-78 folate receptor beta Homo sapiens 0-7
11071651-6 2000 The ATRA-induced increase in FR-beta expression in KG-1 cells occurred at the level of messenger RNA synthesis, and in 293 cells containing a stably integrated FR-beta promoter-luciferase reporter construct, ATRA induced expression of the reporter. Tretinoin 4-8 folate receptor beta Homo sapiens 29-36
11071651-6 2000 The ATRA-induced increase in FR-beta expression in KG-1 cells occurred at the level of messenger RNA synthesis, and in 293 cells containing a stably integrated FR-beta promoter-luciferase reporter construct, ATRA induced expression of the reporter. Tretinoin 4-8 folate receptor beta Homo sapiens 160-167
11071651-6 2000 The ATRA-induced increase in FR-beta expression in KG-1 cells occurred at the level of messenger RNA synthesis, and in 293 cells containing a stably integrated FR-beta promoter-luciferase reporter construct, ATRA induced expression of the reporter. Tretinoin 208-212 folate receptor beta Homo sapiens 29-36
11071651-6 2000 The ATRA-induced increase in FR-beta expression in KG-1 cells occurred at the level of messenger RNA synthesis, and in 293 cells containing a stably integrated FR-beta promoter-luciferase reporter construct, ATRA induced expression of the reporter. Tretinoin 208-212 folate receptor beta Homo sapiens 160-167
11050004-0 2000 Altered ligand binding and transcriptional regulation by mutations in the PML/RARalpha ligand-binding domain arising in retinoic acid-resistant patients with acute promyelocytic leukemia. Tretinoin 120-133 PML nuclear body scaffold Homo sapiens 74-77
11050004-0 2000 Altered ligand binding and transcriptional regulation by mutations in the PML/RARalpha ligand-binding domain arising in retinoic acid-resistant patients with acute promyelocytic leukemia. Tretinoin 120-133 retinoic acid receptor alpha Homo sapiens 78-86
11050004-4 2000 Recently, mutations in PML/RARalpha have been described in APL cells from patients clinically resistant to RA therapy. Tretinoin 27-29 PML nuclear body scaffold Homo sapiens 23-26
11029500-6 2000 However, MCF-10A cells showed a reduction of telomerase activity and down-regulation of hTERT after 4 days of RA treatment. Tretinoin 110-112 telomerase reverse transcriptase Homo sapiens 88-93
11092983-1 2000 Retinoic acid (RAR) and retinoid X receptors (RXR) are essential in the transcriptional actions of retinoids. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 15-18
11044606-10 2000 These results suggested that Raldh-3 is the key enzyme in the formation of an RA gradient along the dorso-ventral axis during the early eye development, and also in the development of the olfactory system. Tretinoin 78-80 aldehyde dehydrogenase 1 family member A3 Homo sapiens 29-36
11120388-0 2000 Interaction of ethanol with retinol and retinoic acid in RAR beta and GAP-43 expression. Tretinoin 40-53 growth associated protein 43 Homo sapiens 70-76
10938282-11 2000 In conclusion, induction of MUC4 expression in pancreatic carcinoma by RA is mediated through the RAR-alpha signaling pathway, and TGF-beta2 may serve as an interim mediator of this regulated expression. Tretinoin 71-73 retinoic acid receptor alpha Homo sapiens 98-107
11032820-6 2000 However, NAT1(-/-) cells exhibited an impaired ability to differentiate: they were resistant to differentiation induced by retinoic acid, and teratomas derived from them consisted of undifferentiated and poorly differentiated tissues. Tretinoin 123-136 N-acetyl transferase 1 Mus musculus 9-13
11032820-7 2000 The expression of retinoic acid-responsive genes, such as the cell-cycle inhibitor p21(WAF1), was selectively impaired in NAT1(-/-) cells. Tretinoin 18-31 N-acetyl transferase 1 Mus musculus 122-126
11089918-2 2000 Also CD38, a homologous gene to CD157, is upregulated in promyelocytic HL-60 cells by the monocyte and granulocyte differentiation-inducing 1alpha,25dihydroxyvitamin D3 (VD3) and all-trans retinoic acid (ATRA), respectively. Tretinoin 189-202 CD38 molecule Homo sapiens 5-9
11089918-2 2000 Also CD38, a homologous gene to CD157, is upregulated in promyelocytic HL-60 cells by the monocyte and granulocyte differentiation-inducing 1alpha,25dihydroxyvitamin D3 (VD3) and all-trans retinoic acid (ATRA), respectively. Tretinoin 204-208 CD38 molecule Homo sapiens 5-9
11034409-11 2000 Both capsaicin and SK&F96365 also inhibited PAF-induced cytosolic superoxide generation in HL-60 cells differentiated by all-trans-retinoic acid. Tretinoin 129-148 PCNA clamp associated factor Homo sapiens 48-51
10952894-3 2000 We show here that retinoic acid (RA) is an upstream activator of the proximal determinant genes Meis1 and Meis2. Tretinoin 18-31 Meis homeobox 2 Homo sapiens 106-111
10952894-3 2000 We show here that retinoic acid (RA) is an upstream activator of the proximal determinant genes Meis1 and Meis2. Tretinoin 33-35 Meis homeobox 2 Homo sapiens 106-111
11022230-1 2000 Retinoic acids (RA) play a key role in myeloid differentiation through their agonistic nuclear receptors (RAR alpha/RXR) to modulate the expression of target genes. Tretinoin 0-14 retinoic acid receptor alpha Homo sapiens 106-115
11022230-3 2000 Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Tretinoin 24-47 retinoic acid receptor alpha Homo sapiens 78-87
11022230-3 2000 Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Tretinoin 24-47 retinoic acid receptor alpha Homo sapiens 185-194
11022230-3 2000 Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Tretinoin 49-53 retinoic acid receptor alpha Homo sapiens 78-87
11022230-3 2000 Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Tretinoin 49-53 retinoic acid receptor alpha Homo sapiens 185-194
10933889-4 2000 Here we have examined the role of the hydroxyl group of RARgamma Ser(289) and its homologous amino acid residues in RARalpha (Ser(287)) and RARbeta (Ser(280)) alone and in conjunction with their respective RARgamma Arg(278) homologs for RA binding and RA-dependent transactivation activity. Tretinoin 56-58 retinoic acid receptor alpha Homo sapiens 116-124
10969805-1 2000 We reported previously that treatment with all-trans retinoic acid (ATRA) and granulocyte macrophage colony-stimulating factor (GM-CSF) induces differentiation of human myeloblastic leukemia ML-1 cells to granulocytes, whereas treatment with ATRA alone induces practically no differentiation of these cells. Tretinoin 242-246 colony stimulating factor 2 Homo sapiens 78-126
10969805-1 2000 We reported previously that treatment with all-trans retinoic acid (ATRA) and granulocyte macrophage colony-stimulating factor (GM-CSF) induces differentiation of human myeloblastic leukemia ML-1 cells to granulocytes, whereas treatment with ATRA alone induces practically no differentiation of these cells. Tretinoin 242-246 colony stimulating factor 2 Homo sapiens 128-134
10969805-4 2000 Furthermore, expression of CD38 mRNA mediated through RAR alpha is induced synergistically by treatment with ATRA + GM-CSF. Tretinoin 109-113 CD38 molecule Homo sapiens 27-31
10969805-4 2000 Furthermore, expression of CD38 mRNA mediated through RAR alpha is induced synergistically by treatment with ATRA + GM-CSF. Tretinoin 109-113 retinoic acid receptor alpha Homo sapiens 54-63
10896783-0 2000 Retinoic acid-mediated G1 arrest is associated with induction of p27(Kip1) and inhibition of cyclin-dependent kinase 3 in human lung squamous carcinoma CH27 cells. Tretinoin 0-13 interferon alpha inducible protein 27 Homo sapiens 65-68
10896783-0 2000 Retinoic acid-mediated G1 arrest is associated with induction of p27(Kip1) and inhibition of cyclin-dependent kinase 3 in human lung squamous carcinoma CH27 cells. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 69-73
10896783-0 2000 Retinoic acid-mediated G1 arrest is associated with induction of p27(Kip1) and inhibition of cyclin-dependent kinase 3 in human lung squamous carcinoma CH27 cells. Tretinoin 0-13 cyclin dependent kinase 3 Homo sapiens 93-118
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 interferon alpha inducible protein 27 Homo sapiens 124-127
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 cyclin dependent kinase inhibitor 1B Homo sapiens 128-132
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 cyclin dependent kinase 3 Homo sapiens 165-190
10896783-3 2000 Here we report that RA mediated the dose- and time-dependent growth arrest in G1 phase, accompanied by the up-regulation of p27(Kip1) and the down-regulation of the cyclin-dependent kinase 3 (Cdk3) and p21(CIP1/Waf1) proteins. Tretinoin 20-22 cyclin dependent kinase 3 Homo sapiens 192-196
10896783-4 2000 Furthermore, RA-induced growth arrest of CH27 cells was also associated with increased retinoic acid receptor beta (RARbeta) and reduced c-Myc expression. Tretinoin 13-15 MYC proto-oncogene, bHLH transcription factor Homo sapiens 137-142
10946899-10 2000 Moreover, all-trans-retinoic acid increased the mRNA expression of thyroglobulin and decreased both the mRNA expression and secretion of interleukin-6 and leukemia inhibitory factor while significantly stimulating growth. Tretinoin 10-33 LIF interleukin 6 family cytokine Homo sapiens 155-181
10915218-5 2000 When cells were exposed to RA in the immature stage (before the addition of FSH) or the early stage of development (0-24 h after the addition of FSH), expression of LH receptor mRNA was greatly diminished. Tretinoin 27-29 luteinizing hormone/choriogonadotropin receptor Homo sapiens 165-176
10915218-6 2000 When the immature cells were cultured for 15 h with RA, then washed and cultured for 48 h with FSH and for 24 h with LH, the expression of LH receptor mRNA was not reversed. Tretinoin 52-54 luteinizing hormone/choriogonadotropin receptor Homo sapiens 139-150
10951230-4 2000 We also studied the regulation of Fas and Fas ligand in skin cells by retinoic acid, vitamin D3, and dexamethasone as well as various cytokines. Tretinoin 70-83 Fas ligand Homo sapiens 42-52
10951230-5 2000 Among the molecules and cells tested, retinoic acid selectively upregulated the expression of Fas ligand molecule by fibroblasts. Tretinoin 38-51 Fas ligand Homo sapiens 94-104
10951230-6 2000 Retinoic acid-induced Fas ligand+ fibroblasts killed Fas+ target cells, and this killing was blocked by anti-Fas ligand antibody. Tretinoin 0-13 Fas ligand Homo sapiens 22-32
10951230-6 2000 Retinoic acid-induced Fas ligand+ fibroblasts killed Fas+ target cells, and this killing was blocked by anti-Fas ligand antibody. Tretinoin 0-13 Fas ligand Homo sapiens 109-119
10951230-9 2000 Daily local injection of retinoic acid blocked inflammation and extended graft survival for more than 10 d. Injection of retinoic acid into Fas ligand mutated gld/gld donor skin did not prevent leukocyte infiltration into the allograft or prolong graft survival. Tretinoin 121-134 Fas ligand Homo sapiens 140-150
10951230-10 2000 These experiments indicate that, in skin, retinoic acid selectively increases Fas ligand expression by fibroblasts and that retinoic acid has potent Fas/Fas ligand-dependent immunosuppressive activity. Tretinoin 42-55 Fas ligand Homo sapiens 78-88
10951230-10 2000 These experiments indicate that, in skin, retinoic acid selectively increases Fas ligand expression by fibroblasts and that retinoic acid has potent Fas/Fas ligand-dependent immunosuppressive activity. Tretinoin 124-137 Fas ligand Homo sapiens 153-163
10951254-7 2000 De novo mRNA expression of cytochrome P450 1A1, a major xenobiotic metabolizing enzyme, in SZ95 sebocytes was induced by all-trans retinoic acid, but not by 13-cis retinoic acid. Tretinoin 131-144 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 27-46
10951254-9 2000 Both 13-cis retinoic acid and all-trans retinoic acid suppressed mRNA expression of cytochrome P450 1A2. Tretinoin 12-25 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 84-103
10899079-0 2000 Retinoic acid upregulates beta(1)-integrin in vascular smooth muscle cells and alters adhesion to fibronectin. Tretinoin 0-13 fibronectin 1 Rattus norvegicus 98-109
10907644-5 2000 MATERIALS AND METHODS: The effects of RA treatment on CBL and CrkL phosphorylation, as well as on protein-protein interactions, were determined in studies involving immunoprecipitations of cell extracts with specific antibodies and Western blots. Tretinoin 38-40 Cbl proto-oncogene Homo sapiens 54-57
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 200-202 Cbl proto-oncogene Homo sapiens 123-126
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 200-202 Cbl proto-oncogene Homo sapiens 123-126
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 200-202 CRK like proto-oncogene, adaptor protein Homo sapiens 91-95
10907644-11 2000 CONCLUSIONS: These findings demonstrate that the CBL-CrkL pathway is one of the mediators of the effects of RA on APL cells and suggest that one of the mechanisms of synergy between RA and interferons may involve regulation of components of this signaling cascade. Tretinoin 108-110 Cbl proto-oncogene Homo sapiens 49-52
10907644-11 2000 CONCLUSIONS: These findings demonstrate that the CBL-CrkL pathway is one of the mediators of the effects of RA on APL cells and suggest that one of the mechanisms of synergy between RA and interferons may involve regulation of components of this signaling cascade. Tretinoin 108-110 CRK like proto-oncogene, adaptor protein Homo sapiens 53-57
10907644-11 2000 CONCLUSIONS: These findings demonstrate that the CBL-CrkL pathway is one of the mediators of the effects of RA on APL cells and suggest that one of the mechanisms of synergy between RA and interferons may involve regulation of components of this signaling cascade. Tretinoin 182-184 Cbl proto-oncogene Homo sapiens 49-52
10907644-11 2000 CONCLUSIONS: These findings demonstrate that the CBL-CrkL pathway is one of the mediators of the effects of RA on APL cells and suggest that one of the mechanisms of synergy between RA and interferons may involve regulation of components of this signaling cascade. Tretinoin 182-184 CRK like proto-oncogene, adaptor protein Homo sapiens 53-57
10945465-8 2000 In addition, expression of RAIG-2 and RAIG-3 mRNA was increased following treatment with all-trans-retinoic acid in a manner similar to that previously described for RAIG-1. Tretinoin 92-112 G protein-coupled receptor class C group 5 member B Homo sapiens 27-33
10945465-8 2000 In addition, expression of RAIG-2 and RAIG-3 mRNA was increased following treatment with all-trans-retinoic acid in a manner similar to that previously described for RAIG-1. Tretinoin 92-112 G protein-coupled receptor class C group 5 member C Homo sapiens 38-44
10945465-10 2000 These results suggest that RAIG-1, RAIG-2, and RAIG-3 represent a novel family of retinoic acid-inducible receptors, most closely related to the type 3 GPCR subfamily, and provide further evidence for a linkage between retinoic acid and G-protein-coupled receptor signal transduction pathways. Tretinoin 82-95 G protein-coupled receptor class C group 5 member B Homo sapiens 35-41
10945465-10 2000 These results suggest that RAIG-1, RAIG-2, and RAIG-3 represent a novel family of retinoic acid-inducible receptors, most closely related to the type 3 GPCR subfamily, and provide further evidence for a linkage between retinoic acid and G-protein-coupled receptor signal transduction pathways. Tretinoin 82-95 G protein-coupled receptor class C group 5 member C Homo sapiens 47-53
11205873-14 2001 The treatment of retinoic acid induced expression of mucin and CFTR, whereas it inhibited expression of cornifin. Tretinoin 17-30 small proline rich protein 1B Homo sapiens 104-112
11133770-1 2001 All-trans retinoic acid (tRA) and arsenic trioxide (As(2)O(3)) induce non-cross-resistant complete clinical remission in patients with acute promyelocytic leukemia with t(15;17) translocation and target PML-RARalpha, the leukemogenic protein, by different pathways suggesting a possible therapeutic synergism. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 203-206
11133770-1 2001 All-trans retinoic acid (tRA) and arsenic trioxide (As(2)O(3)) induce non-cross-resistant complete clinical remission in patients with acute promyelocytic leukemia with t(15;17) translocation and target PML-RARalpha, the leukemogenic protein, by different pathways suggesting a possible therapeutic synergism. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 207-215
11133770-1 2001 All-trans retinoic acid (tRA) and arsenic trioxide (As(2)O(3)) induce non-cross-resistant complete clinical remission in patients with acute promyelocytic leukemia with t(15;17) translocation and target PML-RARalpha, the leukemogenic protein, by different pathways suggesting a possible therapeutic synergism. Tretinoin 25-28 PML nuclear body scaffold Homo sapiens 203-206
11133770-1 2001 All-trans retinoic acid (tRA) and arsenic trioxide (As(2)O(3)) induce non-cross-resistant complete clinical remission in patients with acute promyelocytic leukemia with t(15;17) translocation and target PML-RARalpha, the leukemogenic protein, by different pathways suggesting a possible therapeutic synergism. Tretinoin 25-28 retinoic acid receptor alpha Homo sapiens 207-215
27419349-1 2001 The interaction of an exogenous PML/RARalpha fusion gene, associated with acute promyelocytic leukemia, with all-trans retinoic acid (ATRA) was examined in B-lymphoid cell lines. Tretinoin 134-138 retinoic acid receptor alpha Homo sapiens 36-44
27419349-5 2001 When these results are taken together, it can be observed that the exogenous PML/RARalpha fusion gene responds to ATRA, which results in cell differentiation of the human B cell line. Tretinoin 114-118 PML nuclear body scaffold Homo sapiens 77-80
27419349-5 2001 When these results are taken together, it can be observed that the exogenous PML/RARalpha fusion gene responds to ATRA, which results in cell differentiation of the human B cell line. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 81-89
11306979-2 2001 We could previously show that retinoic acid (RA) strongly inhibits CD40 + IL-4-mediated IgE production in vitro. Tretinoin 30-43 interleukin 4 Mus musculus 74-78
11306979-2 2001 We could previously show that retinoic acid (RA) strongly inhibits CD40 + IL-4-mediated IgE production in vitro. Tretinoin 45-47 interleukin 4 Mus musculus 74-78
11112687-6 2001 Moreover, retinoic acid treatment, which causes remission of APL in patients and reformation of PML-containing bodies in NB4 cells, relocalized PA28 to this site. Tretinoin 10-23 PML nuclear body scaffold Homo sapiens 96-99
11108612-6 2001 In the present study, the mRNA expression of ST8SiaII and ST8SiaIV was comparatively analyzed in neuronal differentiation of PSA-positive human neuroblastoma cell lines induced by retinoic acid (RA), phorbolester, or growth factors. Tretinoin 180-193 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2 Homo sapiens 45-53
11108612-6 2001 In the present study, the mRNA expression of ST8SiaII and ST8SiaIV was comparatively analyzed in neuronal differentiation of PSA-positive human neuroblastoma cell lines induced by retinoic acid (RA), phorbolester, or growth factors. Tretinoin 195-197 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2 Homo sapiens 45-53
11464913-3 2001 DR-nm23 expression increased after retinoic acid induction of differentiation in human cell lines SK-N-SH and LAN-5. Tretinoin 35-48 NME/NM23 nucleoside diphosphate kinase 3 Homo sapiens 0-7
11464914-2 2001 RESULTS AND CONCLUSIONS: Within 2 days of RA treatment, and prior to the arrest of NB cells in the G1 phase of the cell cycle, there was a complete downregulation of GI cyclin/cdk activities. Tretinoin 42-44 proliferating cell nuclear antigen Homo sapiens 169-175
11464914-5 2001 Within 24 hr of RA treatment, there was a 4-fold increase in the expression of p27Kip1, although p27 mRNA levels were unchanged. Tretinoin 16-18 cyclin dependent kinase inhibitor 1B Homo sapiens 79-86
11464914-5 2001 Within 24 hr of RA treatment, there was a 4-fold increase in the expression of p27Kip1, although p27 mRNA levels were unchanged. Tretinoin 16-18 interferon alpha inducible protein 27 Homo sapiens 79-82
10876035-3 2000 Retinoic acid reduced the expression of CK14 and CKs recognized by polyclonal anti-keratin antibody, whereas it induced nestin. Tretinoin 0-13 keratin 14 Mus musculus 40-44
10861789-0 2000 Retinoic acid potentiated the protective effect of NGF against staurosporine-induced apoptosis in cultured chick neurons by increasing the trkA protein expression. Tretinoin 0-13 neurotrophic receptor tyrosine kinase 1 Gallus gallus 139-143
28486108-6 2017 Genetically inhibiting TRIB3 expression or combination of a peptide disturbing TRIB3/PML-RARalpha interaction with ATRA/As2O3 eradicates APL by accelerating PML-RARalpha degradation. Tretinoin 115-119 retinoic acid receptor alpha Homo sapiens 89-97
10861789-4 2000 TrkA protein expression in chick neurons was markedly reduced by staurosporine, but was found to be increased in the presence of RA and NGF compared with the treatment with staurosporine alone. Tretinoin 129-131 neurotrophic receptor tyrosine kinase 1 Gallus gallus 0-4
10861789-5 2000 The antiapoptotic effect caused by RA and NGF was abolished by the tyrosine kinase inhibitor K-252a, as well as by anti-trkA antibodies and anti-NGF antibodies suggesting that the increase in trkA protein expression contributed to its mechanism of action. Tretinoin 35-37 neurotrophic receptor tyrosine kinase 1 Gallus gallus 192-196
28486108-6 2017 Genetically inhibiting TRIB3 expression or combination of a peptide disturbing TRIB3/PML-RARalpha interaction with ATRA/As2O3 eradicates APL by accelerating PML-RARalpha degradation. Tretinoin 115-119 PML nuclear body scaffold Homo sapiens 157-160
12075932-4 2001 To determine whether the novel human gene was involved in hematopoietic differentiation process as mouse Myadm did, we examined the mRNA expressive abundance of this gene between normal bone marrow cells and peripheral blood leukocytes, and detected the expression change in NB4 cells induced by all-trans retinoic acid at different induce time by the semi-quantitative RT-PCR. Tretinoin 306-319 myeloid-associated differentiation marker Mus musculus 105-110
10821786-6 2000 The in vivo administration of 9-cis-RA resulted in the inhibition of IL-12 production by macrophages stimulated in vitro with either LPS or HKL, leading to the inhibition of Th1 cytokine profile (decreased IFN-gamma and increased IL-4 production) in CD4(+) T cells. Tretinoin 30-38 interleukin 4 Mus musculus 230-234
28486108-6 2017 Genetically inhibiting TRIB3 expression or combination of a peptide disturbing TRIB3/PML-RARalpha interaction with ATRA/As2O3 eradicates APL by accelerating PML-RARalpha degradation. Tretinoin 115-119 retinoic acid receptor alpha Homo sapiens 161-169
11172538-6 2001 Targeting of the PLZF-RARalpha-bound corepressor complexes using a combination of all-trans retinoic acid (ATRA) and deacetylase inhibitors has shown that the repression of target genes can be relieved, allowing differentiation of the cells. Tretinoin 92-105 retinoic acid receptor alpha Homo sapiens 22-30
11172538-6 2001 Targeting of the PLZF-RARalpha-bound corepressor complexes using a combination of all-trans retinoic acid (ATRA) and deacetylase inhibitors has shown that the repression of target genes can be relieved, allowing differentiation of the cells. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 22-30
28286014-1 2017 BACKGROUND: We have demonstrated that intramyocardial delivery of human mesenchymal stem cells preconditioned with a hyaluronan mixed ester of butyric and retinoic acid (MSCp+) is more effective in preventing the decay of regional myocardial contractility in a swine model of myocardial infarction (MI). Tretinoin 155-168 musculin Homo sapiens 170-174
11172538-7 2001 In addition, when a combination of retinoic acid and the hematopoietic growth factor granulocyte colony-stimulating factor (G-CSF) is applied, the cells may be forced to undergo terminal differentiation, both in vitro and in vivo. Tretinoin 35-48 colony stimulating factor 3 Homo sapiens 124-129
11162441-5 2000 In contrast, cotransfection with RARalpha decreased reporter activity by retinoic acid 30%. Tretinoin 73-86 retinoic acid receptor alpha Homo sapiens 33-41
11162441-6 2000 Three regions in the CYP4F2 gene are responsive to retinoic acid with the DR1 RARE element (CCTCCT G TGACCT) at -708 able to bind RXRalpha/RARalpha heterodimers and mediate the repressive response of ATRA. Tretinoin 51-64 retinoic acid receptor alpha Homo sapiens 139-147
10929040-0 2000 Respiratory failure during induction chemotherapy for acute myelomonocytic leukaemia (FAB M4Eo) with ara-C and all-trans retinoic acid. Tretinoin 121-134 FA complementation group B Homo sapiens 86-89
10965999-5 2000 MCF-7 cells treated sequentially with Mlt and atRA also demonstrated an enhanced sensitivity to the apoptotic effects of atRA, which did not appear to be due to increased expression of the retinoic acid receptors, RAR alpha or RXR alpha, but rather to enhanced transcriptional activity of the RAR alpha. Tretinoin 46-50 retinoic acid receptor alpha Homo sapiens 293-302
28363907-0 2017 Retinoic Acid Regulates Immune Responses by Promoting IL-22 and Modulating S100 Proteins in Viral Hepatitis. Tretinoin 0-13 interleukin 22 Mus musculus 54-59
10874164-5 2000 Activin also participates in kidney organogenesis in combination with retinoic acid. Tretinoin 70-83 inhibin subunit beta E Homo sapiens 0-7
11077050-0 2000 Differential regulation of a fibroblast growth factor-binding protein by receptor-selective analogs of retinoic acid. Tretinoin 103-116 fibroblast growth factor binding protein 1 Homo sapiens 29-69
28363907-3 2017 RA can promote gammadelta T cells to produce mTORC1-dependent IL-22 in the liver, but inhibits IFN-gamma and IL-17. Tretinoin 0-2 interleukin 22 Mus musculus 62-67
28363907-8 2017 Our study has demonstrated a crucial role for RA in promoting IL-22 production and tempering DC function through downregulating S100 family proteins during viral hepatitis. Tretinoin 46-48 interleukin 22 Mus musculus 62-67
28423611-5 2017 ALDH1A3, as well as other members of the ALDH1 subfamily, can function in cells as a retinaldehyde dehydrogenase to generate retinoic acid (RA) from retinal. Tretinoin 125-138 aldehyde dehydrogenase 1 family member A3 Homo sapiens 0-7
11076660-5 2000 In fact, HMGI(Y) gene expression is differentially regulated by retinoic acid in retinoid-sensitive and -resistant neuroblastoma cells, while HMGI-C participates in conferring retinoic acid resistance in some neuroblastoma cells. Tretinoin 176-189 high mobility group AT-hook 2 Homo sapiens 142-148
11090461-5 2000 The mE-RABP protein belongs to the lipocalin superfamily and may be involved in the trafficking of retinoic acid within the epididymis. Tretinoin 99-112 lipocalin 5 Mus musculus 4-11
10910131-7 2000 The expression of COL1A1 was increased in posteriorized embryos resulting from treatment with retinoic acid but decreased in hyper-dorsalized embryos resulting from lithium chloride treatment. Tretinoin 94-107 collagen, type I, alpha 1 S homeolog Xenopus laevis 18-24
10929428-15 2000 Although RA at the concentration of 10(-6) mmol/l caused lower p21 expression, Ni(RA)2.3H2O did not affect p21 expression in EJ cells. Tretinoin 9-11 H3 histone pseudogene 16 Homo sapiens 63-66
10837916-5 2000 In a mutant P19 cell line, RAC65, treatment with ATRA induced neither p27 accumulation nor neuronal differentiation, but p21 mRNA expression increased markedly. Tretinoin 49-53 interleukin 23 subunit alpha Homo sapiens 12-15
11108247-0 2000 Retinoic acids and thyroid hormone act synergistically with dexamethasone to increase growth hormone-releasing hormone receptor messenger ribonucleic acid expression. Tretinoin 0-14 growth hormone releasing hormone receptor Rattus norvegicus 86-127
28423611-5 2017 ALDH1A3, as well as other members of the ALDH1 subfamily, can function in cells as a retinaldehyde dehydrogenase to generate retinoic acid (RA) from retinal. Tretinoin 125-138 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-5
28232094-0 2017 Chromatin reader ZMYND8 is a key target of all trans retinoic acid-mediated inhibition of cancer cell proliferation. Tretinoin 53-66 zinc finger, MYND-type containing 8 Mus musculus 17-23
11107126-3 2000 RESULTS: After 12 exposures to 10 microM ATRA, the two MYCN-amplified cell lines (KCNR 12X RR and LA-N-5 12X RR) showed partial resistance to the cytostatic/differentiation effects of ATRA; complete resistance was seen in LHN 12X RR. Tretinoin 41-45 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 55-59
11107126-3 2000 RESULTS: After 12 exposures to 10 microM ATRA, the two MYCN-amplified cell lines (KCNR 12X RR and LA-N-5 12X RR) showed partial resistance to the cytostatic/differentiation effects of ATRA; complete resistance was seen in LHN 12X RR. Tretinoin 184-188 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 55-59
10928085-0 2000 Synergistic down-regulation of telomerase activity and hTERT mRNA expression by combination of retinoic acid and GM-CSF in human myeloblastic leukemia ML-1 cells. Tretinoin 95-108 telomerase reverse transcriptase Homo sapiens 55-60
10928085-2 2000 In this study, we investigated telomerase activity and expression of genes involved in telomerase activity in human myeloblastic leukemia ML-1 cells, differentiated synergistically by treatment with all-trans retinoic acid (ATRA) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Tretinoin 224-228 colony stimulating factor 2 Homo sapiens 234-282
10928085-2 2000 In this study, we investigated telomerase activity and expression of genes involved in telomerase activity in human myeloblastic leukemia ML-1 cells, differentiated synergistically by treatment with all-trans retinoic acid (ATRA) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Tretinoin 224-228 colony stimulating factor 2 Homo sapiens 284-290
10928085-5 2000 We also detected remarkable suppression of hTERT mRNA expression in ML-1 cells treated with ATRA and GM-CSF. Tretinoin 92-96 telomerase reverse transcriptase Homo sapiens 43-48
10928085-6 2000 These results indicate that a synergistic down-regulation of telomerase activity and hTERT mRNA expression is induced by treatment with ATRA and GM-CSF in ML-1 cells. Tretinoin 136-140 telomerase reverse transcriptase Homo sapiens 85-90
11078926-4 2000 Moreover, retinoic acid increases polysialated-neural cell adhesion molecules (PSA-NCAM)-immunoreactivity. Tretinoin 10-23 neural cell adhesion molecule 1 Rattus norvegicus 83-87
28232094-2 2017 Previously, we identified a dual histone reader ZMYND8 (zinc finger MYND (Myeloid, Nervy and DEAF-1)-type containing 8), to be a novel target of ATRA. Tretinoin 145-149 zinc finger, MYND-type containing 8 Mus musculus 48-54
28232094-6 2017 We show here that ATRA causes dynamic changes in recruitment of transcription factor YY1 in concert with HDAC1 at ZMYND8 promoter. Tretinoin 18-22 histone deacetylase 1 Mus musculus 105-110
28232094-6 2017 We show here that ATRA causes dynamic changes in recruitment of transcription factor YY1 in concert with HDAC1 at ZMYND8 promoter. Tretinoin 18-22 zinc finger, MYND-type containing 8 Mus musculus 114-120
11443279-4 2000 An increase in the levels of the polysialic acid (PSA) epitope was associated with a parallel increase in the levels of the neural cell adhesion molecule (NCAM) protein backbone although there was no overall change in the PSA:NCAM ratio following RA treatment. Tretinoin 247-249 neural cell adhesion molecule 1 Homo sapiens 155-159
28232094-7 2017 Further, we show that ATRA treatment triggers an anti-proliferative activity in cancer cells through regulation of ZMYND8 expression. Tretinoin 22-26 zinc finger, MYND-type containing 8 Mus musculus 115-121
28232094-8 2017 Subsequently, in 4T1-induced syngenic tumor mouse model, ATRA injection caused significant upregulation of ZMYND8. Tretinoin 57-61 zinc finger, MYND-type containing 8 Mus musculus 107-113
28232094-9 2017 Overall our findings highlight a novel mechanism underlying ATRA-mediated changes in ZMYND8 expression which, in turn, activates the anti-proliferative program in a cancer cell. Tretinoin 60-64 zinc finger, MYND-type containing 8 Mus musculus 85-91
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 23-25 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 45-74
11069026-4 2000 In contrast, following treatment of HL-60 cells with retinoic acid (RA) which results in a granulocytic differentiation of these cells, 4E-BP1 protein expression is decreased whereas 4E-BP2 protein expression is strongly increased. Tretinoin 53-66 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 136-142
11069026-4 2000 In contrast, following treatment of HL-60 cells with retinoic acid (RA) which results in a granulocytic differentiation of these cells, 4E-BP1 protein expression is decreased whereas 4E-BP2 protein expression is strongly increased. Tretinoin 68-70 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 136-142
11069026-6 2000 RA treatment resulted in a decrease in 4E-BP1 protein and mRNA expression and concomitant increase in 4E-BP2 protein expression, in NB4 cells, but not in NB4-R1 and NB4-R2 cells. Tretinoin 0-2 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 39-45
11069028-10 2000 Retinoic acid (RA) inhibited 3H-thymidine incorporation in response to GM-CSF. Tretinoin 0-13 colony stimulating factor 2 Homo sapiens 71-77
10938282-0 2000 Retinoic acid-dependent transforming growth factor-beta 2-mediated induction of MUC4 mucin expression in human pancreatic tumor cells follows retinoic acid receptor-alpha signaling pathway. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 142-170
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 63-67 interleukin 3 Homo sapiens 14-19
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 63-67 colony stimulating factor 2 Homo sapiens 23-29
28379293-4 2017 We recently found that RA stimulation of the Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian target of rapamycin (mTOR) kinase signaling pathway is required for differentiation, and that short-term inhibition of mTOR complex 1 (mTORC1) by rapamycin blocked spermatogonial differentiation in vivo and prevented RA-induced translational activation. Tretinoin 23-25 mechanistic target of rapamycin kinase Mus musculus 215-219
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 63-67 colony stimulating factor 3 Homo sapiens 168-173
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 156-160 interleukin 3 Homo sapiens 14-19
11042692-1 2000 Type I Interferon (IFN) and all-trans retinoic acid (RA) inhibit cell proliferation of squamous carcinoma cell lines (SCC). Tretinoin 38-51 serpin family B member 3 Homo sapiens 118-121
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 156-160 colony stimulating factor 2 Homo sapiens 23-29
11042692-1 2000 Type I Interferon (IFN) and all-trans retinoic acid (RA) inhibit cell proliferation of squamous carcinoma cell lines (SCC). Tretinoin 53-55 serpin family B member 3 Homo sapiens 118-121
28291828-0 2017 Retinoic acid exacerbates chlorpyrifos action in ensuing adipogenic differentiation of C3H10T1/2 cells in a GSK3beta dependent pathway. Tretinoin 0-13 glycogen synthase kinase 3 beta Mus musculus 108-116
11042692-3 2000 In combination treatment RA potentiates IFN-beta effect in SCC ME-180 but not in SiHa cell line, partially resistant to RA antiproliferative action. Tretinoin 25-27 serpin family B member 3 Homo sapiens 59-62
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 156-160 interleukin 3 Homo sapiens 14-19
10803520-3 2000 The number of IL-3- or GM-CSF-induced CFU-GM with 3 x 10(-7) M ATRA was 3.25+/-1.13, and 2.17+/-0.8-fold greater respectively, compared to controls without ATRA, while G-CSF had no effect and the ratio of colony-induced with or without ATRA was 1.06+/-0.17 (P = 0.00012). Tretinoin 156-160 colony stimulating factor 2 Homo sapiens 23-29
10803520-5 2000 Maximum enhancing effect on IL-3-induced CFU-GM occurred when ATRA was added on day 2, gradually diminished when delaying ATRA, and in cultures of day 9 or older adding ATRA had no effect. Tretinoin 62-66 interleukin 3 Homo sapiens 28-32
10803520-5 2000 Maximum enhancing effect on IL-3-induced CFU-GM occurred when ATRA was added on day 2, gradually diminished when delaying ATRA, and in cultures of day 9 or older adding ATRA had no effect. Tretinoin 122-126 interleukin 3 Homo sapiens 28-32
10803520-5 2000 Maximum enhancing effect on IL-3-induced CFU-GM occurred when ATRA was added on day 2, gradually diminished when delaying ATRA, and in cultures of day 9 or older adding ATRA had no effect. Tretinoin 122-126 interleukin 3 Homo sapiens 28-32
10803520-6 2000 In 14 days liquid cultures of purified CD34+ cells with IL-3, ATRA increased the number of myeloid differentiated cells to 91-95%, compared to 37-70% with IL-3 alone. Tretinoin 62-66 interleukin 3 Homo sapiens 56-60
10803520-9 2000 This effect is dependent on the stimulating cytokine, suggesting the myeloid cells responding to ATRA are the less mature CFU-GMs that are targets of IL-3 and GM-CSF and not the G-CSF-responding mature progenitors. Tretinoin 97-101 interleukin 3 Homo sapiens 150-154
10803520-9 2000 This effect is dependent on the stimulating cytokine, suggesting the myeloid cells responding to ATRA are the less mature CFU-GMs that are targets of IL-3 and GM-CSF and not the G-CSF-responding mature progenitors. Tretinoin 97-101 colony stimulating factor 2 Homo sapiens 159-165
10921912-3 2000 The activatory effects of norepinephrine and retinoic acid (RA) on rodent ucp1 gene transcription have been well characterized. Tretinoin 45-58 uncoupling protein 1 Homo sapiens 74-78
10921912-3 2000 The activatory effects of norepinephrine and retinoic acid (RA) on rodent ucp1 gene transcription have been well characterized. Tretinoin 60-62 uncoupling protein 1 Homo sapiens 74-78
27862498-8 2017 RESULTS: In ATRA-treated MSCs, expressions of COX-2, HIF-1, CXCR4, CCR2, VEGF, Ang-2 and Ang-4 increased compared to control groups. Tretinoin 12-16 vascular endothelial growth factor A Rattus norvegicus 73-77
11010814-4 2000 The exogenous expression of dominant-negative MEK1 efficiently abrogated RA-mediated induction of the cytokeratins EndoA and EndoC in the F9 cells. Tretinoin 73-75 keratin 8 Mus musculus 115-120
11010814-4 2000 The exogenous expression of dominant-negative MEK1 efficiently abrogated RA-mediated induction of the cytokeratins EndoA and EndoC in the F9 cells. Tretinoin 73-75 keratin 19 Mus musculus 125-130
11778229-5 2000 RESULTS: ATRA could induce expression of RAR alpha in BGC-823 cells, but not in MKN-45 cells. Tretinoin 9-13 retinoic acid receptor alpha Homo sapiens 41-50
11778229-6 2000 In stable clones, ATRA could inhibit growth of MKN-45 cells transfected with RAR alpha gene, but could not inhibit that of BGC-823 cells transfected with antisense RAR alpha. Tretinoin 18-22 retinoic acid receptor alpha Homo sapiens 77-86
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 12-25 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 128-135
28153738-7 2017 This regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha/RXRalpha heterodimer. Tretinoin 19-32 retinoic acid receptor alpha Homo sapiens 215-223
11200589-7 2000 Omission of retinoic acid (RA) caused decrease in the secretion of mucin and lysozyme, and in the cellular expression of MUC 2, MUC 5AC and MUC 5B mRNA. Tretinoin 27-29 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 128-135
10996843-0 2000 Retinoic acid combines with interleukin-1 to promote the degradation of collagen from bovine nasal cartilage: matrix metalloproteinases-1 and -13 are involved in cartilage collagen breakdown. Tretinoin 0-13 interstitial collagenase Bos taurus 110-145
11798779-0 2000 [Effects of all-trans retinoic acid and arsenic trioxide on tissue factor expression of acute promyelocytic leukemia cells]. Tretinoin 12-35 coagulation factor III, tissue factor Homo sapiens 60-73
11798779-1 2000 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)) on both tissue factor (TF) expression and procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells in vivo and in vitro. Tretinoin 41-64 coagulation factor III, tissue factor Homo sapiens 113-126
11798779-1 2000 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)) on both tissue factor (TF) expression and procoagulant activity (PCA) of acute promyelocytic leukemia (APL) cells in vivo and in vitro. Tretinoin 66-70 coagulation factor III, tissue factor Homo sapiens 113-126
28153738-7 2017 This regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha/RXRalpha heterodimer. Tretinoin 106-119 retinoic acid receptor alpha Homo sapiens 215-223
11200828-2 2000 As 1,25-dihydroxyvitamin D3, retinoic acid and triiodothyronine are known to exert effects on skin and hair follicle growth through similar receptors, we decided to investigate both the expression pattern of the PPAR alpha, -delta and -gamma subtypes and their role in human hair follicles. Tretinoin 29-42 peroxisome proliferator activated receptor alpha Homo sapiens 212-241
30108774-1 2017 All-trans-retinoic acid (ATRA) and its synthetic analogues EC23 and EC19 direct cellular differentiation by interacting as ligands for the retinoic acid receptor (RARalpha, beta and gamma) family of nuclear receptor proteins. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 163-171
11776079-0 2000 c-myc gene inactivation during induction of nasopharyngeal carcinoma cells with retinoic acid. Tretinoin 80-93 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
11776079-9 2000 c-myc was down-regulated at 48 h of RA treatment. Tretinoin 36-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
10772914-0 2000 Retinoic acid inhibits nitric oxide synthase-2 expression through the retinoic acid receptor-alpha. Tretinoin 0-13 retinoic acid receptor, alpha Rattus norvegicus 70-98
10766166-2 2000 The purpose of this study was to identify genes that are regulated in a PML-RARalpha-dependent fashion by retinoic acid (RA), because such genes may be integrally involved in APL pathogenesis and/or myeloid differentiation. Tretinoin 106-119 PML nuclear body scaffold Homo sapiens 72-75
11776079-13 2000 However, only 1 hypersensitive site was found in c-Ha-ras of RA treated cells and controls. Tretinoin 61-63 transcription factor like 5 Homo sapiens 49-53
30108774-1 2017 All-trans-retinoic acid (ATRA) and its synthetic analogues EC23 and EC19 direct cellular differentiation by interacting as ligands for the retinoic acid receptor (RARalpha, beta and gamma) family of nuclear receptor proteins. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 163-171
11776079-15 2000 CONCLUSION: RA can induce differentiation in a nasopharyngeal carcinoma cell line at high concentration of RA; HNE1 shows some similar patterns of DNase I hypersensitive sites with the common one in other types of cells expressing c-myc. Tretinoin 12-14 MYC proto-oncogene, bHLH transcription factor Homo sapiens 231-236
10974645-0 2000 Opposite effects of feeding a vitamin A-deficient diet and retinoic acid treatment on brown adipose tissue uncoupling protein 1 (UCP1), UCP2 and leptin expression. Tretinoin 59-72 leptin Mus musculus 145-151
10933889-0 2000 Role of Ser(289) in RARgamma and its homologous amino acid residue of RARalpha and RARbeta in the binding of retinoic acid. Tretinoin 109-122 retinoic acid receptor alpha Homo sapiens 70-78
10766166-2 2000 The purpose of this study was to identify genes that are regulated in a PML-RARalpha-dependent fashion by retinoic acid (RA), because such genes may be integrally involved in APL pathogenesis and/or myeloid differentiation. Tretinoin 106-119 retinoic acid receptor alpha Homo sapiens 76-84
10766166-2 2000 The purpose of this study was to identify genes that are regulated in a PML-RARalpha-dependent fashion by retinoic acid (RA), because such genes may be integrally involved in APL pathogenesis and/or myeloid differentiation. Tretinoin 76-78 PML nuclear body scaffold Homo sapiens 72-75
10766166-7 2000 B94 was also induced by RA in NB4, UF1, and HL-60 cells, but not in other hematopoietic cell lines tested, suggesting that its up-regulation by RA may be specific to cells that express PML-RARalpha or are at the late myeloblast or promyelocyte stage of myeloid development. Tretinoin 144-146 PML nuclear body scaffold Homo sapiens 185-188
10766166-7 2000 B94 was also induced by RA in NB4, UF1, and HL-60 cells, but not in other hematopoietic cell lines tested, suggesting that its up-regulation by RA may be specific to cells that express PML-RARalpha or are at the late myeloblast or promyelocyte stage of myeloid development. Tretinoin 144-146 retinoic acid receptor alpha Homo sapiens 189-197
10725232-7 2000 Alterations in the endodermal expression pattern of Hoxa1, Hoxb1, Pax1, Pax9, Fgf3 and Fgf8 in response to the antagonist-induced block in RA signal transduction demonstrate for the first time that RA signaling is indispensable for the specification of the pharyngeal endoderm and suggest that this signaling is necessary to provide a permissive environment locally for the migration of NCC and mesodermal cells. Tretinoin 139-141 homeobox B1 Homo sapiens 59-64
10725232-7 2000 Alterations in the endodermal expression pattern of Hoxa1, Hoxb1, Pax1, Pax9, Fgf3 and Fgf8 in response to the antagonist-induced block in RA signal transduction demonstrate for the first time that RA signaling is indispensable for the specification of the pharyngeal endoderm and suggest that this signaling is necessary to provide a permissive environment locally for the migration of NCC and mesodermal cells. Tretinoin 139-141 fibroblast growth factor 8 Homo sapiens 87-91
10933889-1 2000 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, -beta, and -gamma) and retinoid X receptors (RXRalpha, -beta, and -gamma). Tretinoin 26-39 retinoic acid receptor alpha Homo sapiens 86-168
10933889-1 2000 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, -beta, and -gamma) and retinoid X receptors (RXRalpha, -beta, and -gamma). Tretinoin 41-43 retinoic acid receptor alpha Homo sapiens 86-168
10933889-3 2000 We have previously demonstrated the importance for RA binding and RA-dependent transactivation of Arg(276) in RARalpha and Arg(278) in RARgamma; however, in RARbeta Arg(269) functions in conjunction with Lys(220). Tretinoin 66-68 retinoic acid receptor alpha Homo sapiens 110-118
10983416-8 2000 Level of keratin-10 (K10) mRNA was strongly inhibited by all-trans-retinoic acid, 9-cis-retinoic acid and 11-cis-retinoic acid as compared to 13-cis-retinoic acid and 9,13-di-cis-retinoic acids. Tretinoin 57-80 keratin 10 Homo sapiens 9-19
30108774-4 2017 Therefore, we have used molecular modelling techniques to define RAR interactions with ATRA and two synthetic analogues, EC19 and EC23, and compared their predicted biochemical activities to experimental measurements of relative ligand affinity and recruitment of coactivator proteins. Tretinoin 87-91 retinoic acid receptor alpha Homo sapiens 65-68
10983416-8 2000 Level of keratin-10 (K10) mRNA was strongly inhibited by all-trans-retinoic acid, 9-cis-retinoic acid and 11-cis-retinoic acid as compared to 13-cis-retinoic acid and 9,13-di-cis-retinoic acids. Tretinoin 57-80 keratin 10 Homo sapiens 21-24
10983416-9 2000 The mRNA level of keratin-14 (K14) was suppressed by all-trans-retinoic acid, 9-cis-retinoic acid and 11-cis-retinoic acid but not influenced by 13-cis-retinoic acid and 9,13-di-cis-retinoic acid. Tretinoin 56-76 keratin 14 Homo sapiens 18-28
30108774-5 2017 A comprehensive molecular docking approach that explored the conformational space of the ligands indicated that ATRA is able to bind the three RAR proteins in a number of conformations with one extended structure being favoured. Tretinoin 112-116 retinoic acid receptor alpha Homo sapiens 143-146
10983416-9 2000 The mRNA level of keratin-14 (K14) was suppressed by all-trans-retinoic acid, 9-cis-retinoic acid and 11-cis-retinoic acid but not influenced by 13-cis-retinoic acid and 9,13-di-cis-retinoic acid. Tretinoin 56-76 keratin 14 Homo sapiens 30-33
10913834-5 2000 RA-treated lungs had elongated primary branches but decreased further branching with increased Hoxb-5 immunostaining in subepithelial regions underlying these elongated airways. Tretinoin 0-2 homeobox B5 Mus musculus 95-101
28017614-5 2017 FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulating expression of targets such as ASB2 and RARA by reducing m6A levels in these mRNA transcripts. Tretinoin 93-116 FTO alpha-ketoglutarate dependent dioxygenase Homo sapiens 0-3
10913834-7 2000 In contrast, lungs treated with Hoxb-5 antisense oligos plus RA had foreshortened primary branches with rudimentary distal clefts resulting in decreased numbers of primary and subsequent branches. Tretinoin 61-63 homeobox B5 Mus musculus 32-38
10913834-8 2000 Immunohistochemistry confirmed that Hoxb-5 antisense oligos inhibited Hoxb-5 protein expression even in the presence of RA. Tretinoin 120-122 homeobox B5 Mus musculus 36-42
10913834-10 2000 RA-induced alterations in branching are mediated in part through regulated Hoxb-5 expression. Tretinoin 0-2 homeobox B5 Mus musculus 75-81
10734183-4 2000 In vitro, nanomolar concentrations of R115866 inhibited the conversion of RA by CYP26, a RA-inducible RA metabolizing enzyme. Tretinoin 74-76 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 80-85
10734183-4 2000 In vitro, nanomolar concentrations of R115866 inhibited the conversion of RA by CYP26, a RA-inducible RA metabolizing enzyme. Tretinoin 89-91 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 80-85
10734183-4 2000 In vitro, nanomolar concentrations of R115866 inhibited the conversion of RA by CYP26, a RA-inducible RA metabolizing enzyme. Tretinoin 89-91 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 80-85
10694383-2 2000 Binding of RA to RARalpha, beta, and gamma is sensitive to nitration with tetranitromethane, a tyrosine-specific modifying reagent. Tretinoin 11-13 retinoic acid receptor alpha Homo sapiens 17-25
10893206-2 2000 We report that RA and 1,25-dihydroxyvitamin D(3) (Vit D), alone and in combination, significantly increase [(3)H]thymidine incorporation in cultured fetal and postnatal rat lung fibroblasts (P < 0.05). Tretinoin 15-17 vitrin Rattus norvegicus 50-53
28017614-5 2017 FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulating expression of targets such as ASB2 and RARA by reducing m6A levels in these mRNA transcripts. Tretinoin 118-122 FTO alpha-ketoglutarate dependent dioxygenase Homo sapiens 0-3
10893206-8 2000 Thus exogenous RA may influence alveolarization by stimulating fibroblast proliferation through a PDGF-mediated autocrine mechanism, which is enhanced when RA and Vit D are administered in combination. Tretinoin 15-17 vitrin Rattus norvegicus 163-166
10694383-3 2000 To identify tyrosine residue(s) that are important for RA binding, we carried out chemical modification experiments with purified RARalpha ligand-binding domain (RARalpha-LBD) subjected to partial acid hydrolysis and selective proteolysis. Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 130-138
10694383-3 2000 To identify tyrosine residue(s) that are important for RA binding, we carried out chemical modification experiments with purified RARalpha ligand-binding domain (RARalpha-LBD) subjected to partial acid hydrolysis and selective proteolysis. Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 162-170
10694383-5 2000 We found that RA binding to RARalpha-LBD protected Tyr(277)-containing peptides from nitration. Tretinoin 14-16 retinoic acid receptor alpha Homo sapiens 28-36
10953340-0 2000 All trans-retinoic acid suppresses in vitro growth and down-regulates LIF gene expression as well as telomerase activity of human medulloblastoma cells. Tretinoin 4-23 LIF interleukin 6 family cytokine Homo sapiens 70-73
28111553-6 2016 We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. Tretinoin 167-169 odontogenic, ameloblast asssociated Mus musculus 83-124
11603759-3 2000 However, exogenous application of retinoic acid has been shown to stimulate the formation of supernumerary hair cells in organ of Corti explants from E13 to E16 mouse embryos. Tretinoin 34-47 skull morphology 19 Mus musculus 150-153
28111553-6 2016 We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. Tretinoin 167-169 odontogenic, ameloblast asssociated Mus musculus 126-130
28529810-1 2017 Several variant RARA translocations have been reported in acute promyelocytic leukemia (APL) of which the t(11;17)(q23;q21), which results in a ZBTB16-RARA fusion, is the most widely identified and is largely resistant to therapy with all-trans retinoic acid (ATRA). Tretinoin 245-258 retinoic acid receptor alpha Homo sapiens 16-20
10715300-0 2000 CD56 expression is an indicator of poor clinical outcome in patients with acute promyelocytic leukemia treated with simultaneous all-trans-retinoic acid and chemotherapy. Tretinoin 129-152 neural cell adhesion molecule 1 Homo sapiens 0-4
10699459-8 2000 Our data suggests for the first time that the effect of RA on FSH-R expression is possibly mediated by the reduction of the FSH-R mRNA level due to a negative regulation of the FSH-R gene in the presence of FSH. Tretinoin 56-58 follicle stimulating hormone receptor Rattus norvegicus 62-67
10699459-8 2000 Our data suggests for the first time that the effect of RA on FSH-R expression is possibly mediated by the reduction of the FSH-R mRNA level due to a negative regulation of the FSH-R gene in the presence of FSH. Tretinoin 56-58 follicle stimulating hormone receptor Rattus norvegicus 124-129
10699459-8 2000 Our data suggests for the first time that the effect of RA on FSH-R expression is possibly mediated by the reduction of the FSH-R mRNA level due to a negative regulation of the FSH-R gene in the presence of FSH. Tretinoin 56-58 follicle stimulating hormone receptor Rattus norvegicus 124-129
10880953-5 2000 Dehydrogenases catalyzing the reversible oxidation/reduction of retinol and retinal are members of either the alcohol dehydrogenase (ADH) or short-chain dehydrogenase/reductase (SDR) enzyme families, whereas dehydrogenases catalyzing the oxidation of retinal to retinoic acid are members of the aldehyde dehydrogenase (ALDH) family. Tretinoin 262-275 aldehyde dehydrogenase 1 family member A1 Homo sapiens 319-323
10907644-0 2000 All-trans-retinoic acid induces tyrosine phosphorylation of the CrkL adapter in acute promyelocytic leukemia cells. Tretinoin 0-23 CRK like proto-oncogene, adaptor protein Homo sapiens 64-68
10907644-5 2000 MATERIALS AND METHODS: The effects of RA treatment on CBL and CrkL phosphorylation, as well as on protein-protein interactions, were determined in studies involving immunoprecipitations of cell extracts with specific antibodies and Western blots. Tretinoin 38-40 CRK like proto-oncogene, adaptor protein Homo sapiens 62-66
10907644-6 2000 In addition, glutathione-S-transferase fusion proteins were used in binding studies to determine whether the SH2 domain of CrkL interacts with CBL in a RA-dependent manner and whether Rapl is activated by RA. Tretinoin 152-154 CRK like proto-oncogene, adaptor protein Homo sapiens 123-127
10907644-7 2000 RESULTS: Treatment of NB-4 or HL-60 cells with RA resulted in strong tyrosine phosphorylation of CBL, which was time and dose dependent. Tretinoin 47-49 Cbl proto-oncogene Homo sapiens 97-100
10907644-8 2000 Similarly, RA induced tyrosine phosphorylation of the CrkL adapter and the association of CrkL with CBL. Tretinoin 11-13 CRK like proto-oncogene, adaptor protein Homo sapiens 54-58
10907644-8 2000 Similarly, RA induced tyrosine phosphorylation of the CrkL adapter and the association of CrkL with CBL. Tretinoin 11-13 CRK like proto-oncogene, adaptor protein Homo sapiens 90-94
10907644-8 2000 Similarly, RA induced tyrosine phosphorylation of the CrkL adapter and the association of CrkL with CBL. Tretinoin 11-13 Cbl proto-oncogene Homo sapiens 100-103
28529810-1 2017 Several variant RARA translocations have been reported in acute promyelocytic leukemia (APL) of which the t(11;17)(q23;q21), which results in a ZBTB16-RARA fusion, is the most widely identified and is largely resistant to therapy with all-trans retinoic acid (ATRA). Tretinoin 260-264 retinoic acid receptor alpha Homo sapiens 16-20
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 4-6 CRK like proto-oncogene, adaptor protein Homo sapiens 32-36
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 4-6 Cbl proto-oncogene Homo sapiens 42-45
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 4-6 CRK like proto-oncogene, adaptor protein Homo sapiens 91-95
10684855-7 2000 Upon retinoic acid treatment, which induces disease remission in APL, Daxx relocalizes to the PML NBs. Tretinoin 5-18 PML nuclear body scaffold Homo sapiens 94-97
29241165-5 2017 RESULTS: SC1 regulates the expressions of pluripotency and differentiation factors, and antagonizes the retinoic acid (RA)-induced differentiation in the presence or absence of LIF. Tretinoin 104-117 spinal cord QTL 1 Mus musculus 9-12
10689181-7 2000 Increased centre of nucleus-to-gene and gene-to-gene distances of c-myc genes, centromeric region of chromosome 8 and chromosome 8 domains were found early after the induction of granulocytic differentiation by dimethyl sulfoxide (DMSO) or retinoic acid (RA); the size of the chromosome 8 domains was rapidly reduced. Tretinoin 240-253 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-71
10689181-7 2000 Increased centre of nucleus-to-gene and gene-to-gene distances of c-myc genes, centromeric region of chromosome 8 and chromosome 8 domains were found early after the induction of granulocytic differentiation by dimethyl sulfoxide (DMSO) or retinoic acid (RA); the size of the chromosome 8 domains was rapidly reduced. Tretinoin 255-257 MYC proto-oncogene, bHLH transcription factor Homo sapiens 66-71
10716617-9 2000 BMP-3 mRNA expression were almost negative in either control or retinoic acid-treated groups during all stages. Tretinoin 64-77 bone morphogenetic protein 3 Mus musculus 0-5
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 4-6 Cbl proto-oncogene Homo sapiens 123-126
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 4-6 Cbl proto-oncogene Homo sapiens 123-126
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 4-6 CRK like proto-oncogene, adaptor protein Homo sapiens 91-95
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 200-202 CRK like proto-oncogene, adaptor protein Homo sapiens 32-36
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 200-202 Cbl proto-oncogene Homo sapiens 42-45
10907644-9 2000 The RA-dependent interaction of CrkL with CBL was mediated by binding of the SH2 domain of CrkL to tyrosine phosphorylated CBL, suggesting that CBL provides a docking site for engagement of CrkL in a RA-activated cellular pathway. Tretinoin 200-202 CRK like proto-oncogene, adaptor protein Homo sapiens 91-95
11100817-7 2000 Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53. Tretinoin 20-33 GSM1 Homo sapiens 82-85
11100817-7 2000 Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53. Tretinoin 35-37 GSM1 Homo sapiens 82-85
10695998-2 2000 In the present study, we examined the ability of RA to induce the expression of gp130, the signal-transducing receptor component for IL-6, in HL-60 and a RA-supersensitive cell line HL-60/S4. Tretinoin 49-51 interleukin 6 cytokine family signal transducer Homo sapiens 80-85
10695998-2 2000 In the present study, we examined the ability of RA to induce the expression of gp130, the signal-transducing receptor component for IL-6, in HL-60 and a RA-supersensitive cell line HL-60/S4. Tretinoin 154-156 interleukin 6 cytokine family signal transducer Homo sapiens 80-85
10695998-3 2000 We found that RA induced the expression of gp130, at both the mRNA and protein levels, in HL-60 and HL-60/S4 cells. Tretinoin 14-16 interleukin 6 cytokine family signal transducer Homo sapiens 43-48
29241165-5 2017 RESULTS: SC1 regulates the expressions of pluripotency and differentiation factors, and antagonizes the retinoic acid (RA)-induced differentiation in the presence or absence of LIF. Tretinoin 119-121 spinal cord QTL 1 Mus musculus 9-12
10695998-4 2000 Interestingly, the induction of gp 130 expression observed in the RA-supersensitive HL-60/S4 cells was much more pronounced than that observed in HL-60 cells. Tretinoin 66-68 interleukin 6 cytokine family signal transducer Homo sapiens 32-38
10695998-5 2000 Furthermore, activation of the RA-induced gp130 by exogenous IL-6 potentiated the differentiating effects of RA. Tretinoin 31-33 interleukin 6 cytokine family signal transducer Homo sapiens 42-47
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 290-303 retinoic acid receptor alpha Homo sapiens 45-48
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 290-303 retinoic acid receptor alpha Homo sapiens 59-67
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 retinoic acid receptor alpha Homo sapiens 59-67
10695998-7 2000 Our findings suggest that the differentiating effects of RA may partially be mediated by the up-regulation of IL-6/gp130 signaling in HL-60 and HL-60/S4 cells. Tretinoin 57-59 interleukin 6 cytokine family signal transducer Homo sapiens 115-120
28904317-0 2017 Notch signaling partly regulates the osteogenic differentiation of retinoic acid-treated murine induced pluripotent stem cells. Tretinoin 67-80 notch 1 Mus musculus 0-5
10654448-1 2000 We evaluated the in vitro effect on clonogenic potential (CFU-GM) and apoptosis in myelodysplastic syndromes (MDS) progenitors of an anti-oxidant (N-acetylcysteine, NAC) and/or a differentiating (all-trans retinoic acid, ATRA) agent. Tretinoin 196-219 synuclein alpha Homo sapiens 165-168
10654448-1 2000 We evaluated the in vitro effect on clonogenic potential (CFU-GM) and apoptosis in myelodysplastic syndromes (MDS) progenitors of an anti-oxidant (N-acetylcysteine, NAC) and/or a differentiating (all-trans retinoic acid, ATRA) agent. Tretinoin 221-225 synuclein alpha Homo sapiens 165-168
10654448-3 2000 NAC + ATRA conferred a significant advantage in terms of CFU-GM with respect to NAC and ATRA alone. Tretinoin 6-10 synuclein alpha Homo sapiens 80-83
10654448-3 2000 NAC + ATRA conferred a significant advantage in terms of CFU-GM with respect to NAC and ATRA alone. Tretinoin 88-92 synuclein alpha Homo sapiens 0-3
10854854-2 2000 Our Northern blotting experiments have shown that P2Y(2) and P2Y(11) messengers were up-regulated in these cells, rapidly and independently of protein synthesis, following treatment with granulocytic differentiating agents such as retinoic acid, dimethylsulfoxide, granulocyte-colony stimulating factor, dibutyryl cyclic AMP and ATP. Tretinoin 231-244 purinergic receptor P2Y11 Homo sapiens 61-68
28904317-2 2017 Here, we investigated the involvement of Notch signaling in the osteogenic differentiation of retinoic acid-treated embryoid bodies derived from mouse gingival fibroblast-derived induced pluripotent stem cells (mGF-iPSCs). Tretinoin 94-107 notch 1 Mus musculus 41-46
28904317-2 2017 Here, we investigated the involvement of Notch signaling in the osteogenic differentiation of retinoic acid-treated embryoid bodies derived from mouse gingival fibroblast-derived induced pluripotent stem cells (mGF-iPSCs). Tretinoin 94-107 kit ligand Mus musculus 211-214
10828067-1 2000 A novel, retinoic acid-induced gene, GRP1-associated scaffold protein (GRASP), was isolated from P19 embryonal carcinoma cells using a subtractive screening strategy. Tretinoin 9-22 trafficking regulator and scaffold protein tamalin Homo sapiens 37-69
10828067-1 2000 A novel, retinoic acid-induced gene, GRP1-associated scaffold protein (GRASP), was isolated from P19 embryonal carcinoma cells using a subtractive screening strategy. Tretinoin 9-22 trafficking regulator and scaffold protein tamalin Homo sapiens 71-76
10680847-9 2000 Moreover, this RevM10 vector transduced the neuronal precursor cell line NT2, retinoic acid-differentiated human neurons (hNT) from the precursor cells, and primary isolated human brain MVECs with high efficiency. Tretinoin 78-91 neurotrimin Homo sapiens 122-125
27894085-0 2016 Tracing anti-cancer and cancer-promoting actions of all-trans retinoic acid in breast cancer to a RARalpha epigenetic mechanism of mammary epithelial cell fate. Tretinoin 62-75 retinoic acid receptor alpha Homo sapiens 98-106
10645005-0 2000 Regulation of CD26/DPPIV gene expression by interferons and retinoic acid in tumor B cells. Tretinoin 60-73 dipeptidyl peptidase 4 Homo sapiens 14-18
10645005-0 2000 Regulation of CD26/DPPIV gene expression by interferons and retinoic acid in tumor B cells. Tretinoin 60-73 dipeptidyl peptidase 4 Homo sapiens 19-24
11775865-8 2000 RA can potentiate As2O3-induced apoptosis even in RA-resistant HL-60 cells in which the classical ATRA response pathway is repressed owing to a homozygous inactivating mutation in the retinoic acid receptor alpha. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 184-212
10816385-12 2000 In addition, retinoic acid induced a relocalization of gelsolin from the plasma membrane to the cytoplasm. Tretinoin 13-26 gelsolin Homo sapiens 55-63
27894085-5 2016 Indeed, factors that hamper the RARA epigenetic function make physiological RA drive aberrant morphogenesis via non-transcriptional RARA, thus leading to cell transformation. Tretinoin 32-34 retinoic acid receptor alpha Homo sapiens 132-136
27793834-5 2016 The 25 nM RA dataset yielded a cohort of previously known caudal RA target genes including Fgf8 (repressed) and Sox2 (activated), plus novel early RA signaling targets with nearby conserved RA response elements. Tretinoin 10-12 fibroblast growth factor 8 Homo sapiens 91-95
10872810-0 2000 Retinoic acid switches differential expression of FGF8 isoforms in LNCaP cells. Tretinoin 0-13 fibroblast growth factor 8 Homo sapiens 50-54
10809758-3 2000 Here we show that endogenous p73 levels increase in neuroblastoma cells induced to differentiate by retinoic acid and that exogenously expressed p73, but not p53, is sufficient to induce both morphological (neurite outgrowth) and biochemical (expression of neurofilaments and neural cell adhesion molecule (N-CAM); down-regulation of N-MYC and up-regulation of pRB) markers of neuronal differentiation. Tretinoin 100-113 transformation related protein 73 Mus musculus 29-32
10940651-3 2000 Exposure of the cell lines to 1.0 microM ATRA for 72 h caused induction of apoptosis detectable by morphology and the annexin V assay. Tretinoin 41-45 annexin A5 Homo sapiens 118-127
10940651-4 2000 The number of apoptotic cells according to the annexin V assay varied from 16 +/- 8% (OU-AML-7) to 61 +/- 4% (OU-AML-3) in ATRA-treated cells, while it was 7 +/- 6% in control cells. Tretinoin 123-127 annexin A5 Homo sapiens 47-56
10679930-0 2000 Regulation of the Hoxa4 and Hoxa5 genes in the embryonic mouse lung by retinoic acid and TGFbeta1: implications for lung development and patterning. Tretinoin 71-84 homeobox A4 Mus musculus 18-23
10679930-0 2000 Regulation of the Hoxa4 and Hoxa5 genes in the embryonic mouse lung by retinoic acid and TGFbeta1: implications for lung development and patterning. Tretinoin 71-84 homeobox A5 Mus musculus 28-33
10679930-5 2000 We show that both Hoxa4 and Hoxa5 are upregulated when cultured in the presence of all-trans retinoic acid. Tretinoin 93-106 homeobox A4 Mus musculus 18-23
10679930-5 2000 We show that both Hoxa4 and Hoxa5 are upregulated when cultured in the presence of all-trans retinoic acid. Tretinoin 93-106 homeobox A5 Mus musculus 28-33
10679930-6 2000 In addition, retinoic acid extends the domain of Hoxa4 and Hoxa5 expression to the periphery of the explants where the distal epithelia are developing. Tretinoin 13-26 homeobox A4 Mus musculus 49-54
10679930-6 2000 In addition, retinoic acid extends the domain of Hoxa4 and Hoxa5 expression to the periphery of the explants where the distal epithelia are developing. Tretinoin 13-26 homeobox A5 Mus musculus 59-64
27888400-5 2016 Furthermore, all-trans retinoic acid treatment induced CDKN2C expression by releasing the PML/RARalpha binding on chromatin in NB4 cells. Tretinoin 23-36 PML nuclear body scaffold Homo sapiens 90-93
10679930-7 2000 Interestingly, the effect of retinoic acid on Hoxa5 expression was not observed in a Hoxa4 mutant background. Tretinoin 29-42 homeobox A5 Mus musculus 46-51
10679930-10 2000 Lungs from Hoxa4 mutant embryos exhibited a similar response to retinoic acid, suggesting that Hoxa4 alone is not required for the proximalizing effect. Tretinoin 64-77 homeobox A4 Mus musculus 11-16
10840075-5 2000 On the other hand, treatment with RA profoundly increased the soluble receptor gp130 released from the four-week bone marrow stroma by 7.5-fold from only 145 +/- 2.1 pg per ml in control cultures to 1,069.9 +/- 3.8 pg per ml in RA-treated cultures. Tretinoin 34-36 interleukin 6 cytokine family signal transducer Homo sapiens 79-84
10870476-4 2000 In the presence of high levels of all-trans retinoic acid (ATRA), both PML-dependent apoptotic mechanisms and myeloid-specific gene expression programs are reactivated. Tretinoin 44-57 PML nuclear body scaffold Homo sapiens 71-74
10870476-4 2000 In the presence of high levels of all-trans retinoic acid (ATRA), both PML-dependent apoptotic mechanisms and myeloid-specific gene expression programs are reactivated. Tretinoin 59-63 PML nuclear body scaffold Homo sapiens 71-74
10760826-0 2000 Retinoic acid induces persistent, RARalpha-mediated anti-proliferative responses in Epstein-Barr virus-immortalized b lymphoblasts carrying an activated C-MYC oncogene but not in Burkitt"s lymphoma cell lines. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 34-42
10760826-0 2000 Retinoic acid induces persistent, RARalpha-mediated anti-proliferative responses in Epstein-Barr virus-immortalized b lymphoblasts carrying an activated C-MYC oncogene but not in Burkitt"s lymphoma cell lines. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158
10840075-5 2000 On the other hand, treatment with RA profoundly increased the soluble receptor gp130 released from the four-week bone marrow stroma by 7.5-fold from only 145 +/- 2.1 pg per ml in control cultures to 1,069.9 +/- 3.8 pg per ml in RA-treated cultures. Tretinoin 228-230 interleukin 6 cytokine family signal transducer Homo sapiens 79-84
27888400-5 2016 Furthermore, all-trans retinoic acid treatment induced CDKN2C expression by releasing the PML/RARalpha binding on chromatin in NB4 cells. Tretinoin 23-36 retinoic acid receptor alpha Homo sapiens 94-102
10840075-10 2000 The profound and rapid 7.5-fold increase in the natural antagonist of human IL-6 cytokine family after RA treatment could abrogate the gp130 signaling required for proliferation and/or expansion of human primitive hemopoietic stem cells and lead to the observed inhibitory effect of RA on CAFC. Tretinoin 103-105 interleukin 6 cytokine family signal transducer Homo sapiens 135-140
10840075-10 2000 The profound and rapid 7.5-fold increase in the natural antagonist of human IL-6 cytokine family after RA treatment could abrogate the gp130 signaling required for proliferation and/or expansion of human primitive hemopoietic stem cells and lead to the observed inhibitory effect of RA on CAFC. Tretinoin 283-285 interleukin 6 cytokine family signal transducer Homo sapiens 135-140
10840075-13 2000 In conclusion, the RA inhibitory effect on the proliferation of primitive human hemopoietic stem cells could be mediated through: A) an impaired hemopoietic stem cell adhesion due to the significant increase in soluble adhesion molecules released from the marrow stroma after RA treatment, and B) a significantly reduced gp130 signaling that is necessary for stem cell proliferation due to the natural antagonistic effect of the profoundly increased level of soluble gp130 released from the marrow stroma after treatment with RA. Tretinoin 19-21 interleukin 6 cytokine family signal transducer Homo sapiens 321-326
10840075-13 2000 In conclusion, the RA inhibitory effect on the proliferation of primitive human hemopoietic stem cells could be mediated through: A) an impaired hemopoietic stem cell adhesion due to the significant increase in soluble adhesion molecules released from the marrow stroma after RA treatment, and B) a significantly reduced gp130 signaling that is necessary for stem cell proliferation due to the natural antagonistic effect of the profoundly increased level of soluble gp130 released from the marrow stroma after treatment with RA. Tretinoin 19-21 interleukin 6 cytokine family signal transducer Homo sapiens 467-472
10714240-2 2000 The biological action of retinoic acid and synthetic analogs, referred to as retinoids, is mediated by RAR alpha, RAR beta, or RAR gamma and/or by RXR alpha, RXR beta, or RXR gamma, all being nuclear receptors. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 103-112
10797533-7 2000 In addition, we found that the expression of the vesicular monoamine transporter 2 (VMAT2) and the vesicular acetylcholine transporter (VAChT) was increased in those cells treated with retinoic acid. Tretinoin 185-198 solute carrier family 18 member A3 Homo sapiens 99-134
10797533-7 2000 In addition, we found that the expression of the vesicular monoamine transporter 2 (VMAT2) and the vesicular acetylcholine transporter (VAChT) was increased in those cells treated with retinoic acid. Tretinoin 185-198 solute carrier family 18 member A3 Homo sapiens 136-141
10797533-8 2000 Immunostaining revealed that retinoic acid treatment changed the cellular distribution of both vesicular monoamine transporter 2 and vesicular acetylcholine transporter. Tretinoin 29-42 solute carrier family 18 member A3 Homo sapiens 95-168
10797535-9 2000 All-trans-retinoic acid had the opposite inhibitory effect on PPARalpha and PPARdelta expression. Tretinoin 0-23 peroxisome proliferator activated receptor alpha Rattus norvegicus 62-71
10793354-8 2000 This was accomplished by use of 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] and all-trans -retinoic acid to indirectly stimulate PP-2A activity through their capacity to elevated intracellular levels of the second messenger ceramide. Tretinoin 86-110 protein phosphatase 2 phosphatase activator Homo sapiens 135-140
27840989-6 2016 Cell Counting Kit-8 and flow cytometry analysis revealed that the efficient overexpression of NLS-RARalpha significantly promoted NB4 cell proliferation and inhibited all-trans retinoic acid-induced cell differentiation. Tretinoin 177-190 retinoic acid receptor alpha Homo sapiens 98-106
11778229-0 2000 [Mechanism of retinoic acid receptor alpha-mediated growth inhibition of gastric cancer cells by all-trans retinoic acid]. Tretinoin 97-120 retinoic acid receptor alpha Homo sapiens 14-42
11778229-1 2000 OBJECTIVE: To study the mechanism of retinoic acid receptor alpha(RAR alpha) in mediating growth inhibition of gastric cancer cells by all-trans retinoic acid(ATRA). Tretinoin 135-158 retinoic acid receptor alpha Homo sapiens 60-75
11778229-1 2000 OBJECTIVE: To study the mechanism of retinoic acid receptor alpha(RAR alpha) in mediating growth inhibition of gastric cancer cells by all-trans retinoic acid(ATRA). Tretinoin 159-163 retinoic acid receptor alpha Homo sapiens 60-75
11876987-0 2000 [Mechanism of tissue factor expression on NB4 cells down-regulated by all-trans retinoic acid and arsenic trioxide]. Tretinoin 80-93 coagulation factor III, tissue factor Homo sapiens 14-27
11876987-1 2000 OBJECTIVE: To investigate molecular mechanism of tissue factor (TF) expression on acute promyelocytic leukemia cell line NB4 cells down-regulated by all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)). Tretinoin 159-172 coagulation factor III, tissue factor Homo sapiens 49-62
11876987-1 2000 OBJECTIVE: To investigate molecular mechanism of tissue factor (TF) expression on acute promyelocytic leukemia cell line NB4 cells down-regulated by all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)). Tretinoin 159-172 coagulation factor III, tissue factor Homo sapiens 64-66
11876987-1 2000 OBJECTIVE: To investigate molecular mechanism of tissue factor (TF) expression on acute promyelocytic leukemia cell line NB4 cells down-regulated by all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)). Tretinoin 174-178 coagulation factor III, tissue factor Homo sapiens 49-62
11876987-1 2000 OBJECTIVE: To investigate molecular mechanism of tissue factor (TF) expression on acute promyelocytic leukemia cell line NB4 cells down-regulated by all-trans retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)). Tretinoin 174-178 coagulation factor III, tissue factor Homo sapiens 64-66
11876987-2 2000 METHODS: Cyclohexamide (CHX) inhibition test for de novo protein synthesis and actinomycin D (Act D) inhibition test for RNA synthesis were used to check the effect of ATRA on the TF expression. Tretinoin 168-172 coagulation factor III, tissue factor Homo sapiens 180-182
11876987-3 2000 TF antigen of U937 cells transfected with pMSCV-PML-RARalpha treated with or without ATRA and As(2)O(3) was detected. Tretinoin 85-89 coagulation factor III, tissue factor Homo sapiens 0-2
11876987-4 2000 RESULTS: CHX treatment completely suppressed the down-regulation effect of ATRA on the TF mRNA expression, Act D inhibition test showed that half-life of TF mRNA in treated NB4 cells was shortened to about 30 min from that of around 60 min in untreated NB4 cells. Tretinoin 75-79 coagulation factor III, tissue factor Homo sapiens 87-89
11876987-4 2000 RESULTS: CHX treatment completely suppressed the down-regulation effect of ATRA on the TF mRNA expression, Act D inhibition test showed that half-life of TF mRNA in treated NB4 cells was shortened to about 30 min from that of around 60 min in untreated NB4 cells. Tretinoin 75-79 coagulation factor III, tissue factor Homo sapiens 154-156
10777552-4 2000 The aim of this investigation was to determine the effects of retinoic acid derivatives on the expression of FATP-1 and ACS. Tretinoin 62-75 solute carrier family 27 member 1 Rattus norvegicus 109-123
10753864-13 2000 Furthermore, RA treatment enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence in TC6 cells. Tretinoin 13-15 sex determining region of Chr Y Mus musculus 103-106
10745031-13 2000 Taking these data together, a novel mechanism is proposed in which ATRA activates promoter activity of IL-8 gene through TRX-dependent NF-kappaB activation. Tretinoin 67-71 thioredoxin Homo sapiens 121-124
11798775-8 2000 1.0 micromol/L ATRA also exerted, to a less extent than As(2)O(3), growth-inhibitory effects in K(V) sublines, which became more obvious in K(PML) but not in K(PLZF) sublines. Tretinoin 15-19 PML nuclear body scaffold Homo sapiens 142-145
10694435-10 2000 The differential expression of PS1 and PS2 within the P19 cells following retinoic acid treatment indicates different utilization or temporal requirements for these proteins during neuronal differentiation. Tretinoin 74-87 presenilin 1 Mus musculus 31-34
10694499-3 2000 Here we report that a novel RA-responsive element, termed lamin A/C-RA-responsive element (L-RARE), is located within the lamin A/C promoter. Tretinoin 28-30 lamin A/C Homo sapiens 58-67
10694499-3 2000 Here we report that a novel RA-responsive element, termed lamin A/C-RA-responsive element (L-RARE), is located within the lamin A/C promoter. Tretinoin 28-30 lamin A/C Homo sapiens 122-131
10694499-3 2000 Here we report that a novel RA-responsive element, termed lamin A/C-RA-responsive element (L-RARE), is located within the lamin A/C promoter. Tretinoin 68-70 lamin A/C Homo sapiens 58-67
10694499-3 2000 Here we report that a novel RA-responsive element, termed lamin A/C-RA-responsive element (L-RARE), is located within the lamin A/C promoter. Tretinoin 68-70 lamin A/C Homo sapiens 122-131
10681373-2 2000 We examined the retinoic acid synthetic activity of human cDNA-expressed CYP1A1, 1A2, 1B1, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, 3A4, 3A4+ cytochrome b(5) (b(5)), 3A5, and 4A11, expressed individually in insect cells together with NADPH-P-450 reductase. Tretinoin 16-29 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 73-79
10681373-3 2000 Only CYP1A1, 1A2, 1B1, and 3A4+b(5) converted all-trans-retinal (20 microM) to all-trans-retinoic acid with turnover numbers of 0.53, 0.18, 0.20, and 0.41 nmol/min/nmol P-450, respectively. Tretinoin 79-102 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 5-11
10614788-3 1999 However, the BM2 v-myb-transformed chicken monoblastic cell line is resistant to retinoic acid treatment. Tretinoin 81-94 MYB proto-oncogene, transcription factor Gallus gallus 19-22
10598586-1 1999 Nuclear receptor corepressor (NCoR) mediates repression (silencing) of basal gene transcription by nuclear receptors for thyroid hormone and retinoic acid. Tretinoin 141-154 nuclear receptor corepressor 1 Homo sapiens 30-34
10597230-0 1999 Formation of PML/RAR alpha high molecular weight nuclear complexes through the PML coiled-coil region is essential for the PML/RAR alpha-mediated retinoic acid response. Tretinoin 146-159 PML nuclear body scaffold Homo sapiens 13-26
10597230-0 1999 Formation of PML/RAR alpha high molecular weight nuclear complexes through the PML coiled-coil region is essential for the PML/RAR alpha-mediated retinoic acid response. Tretinoin 146-159 PML nuclear body scaffold Homo sapiens 13-16
10597230-0 1999 Formation of PML/RAR alpha high molecular weight nuclear complexes through the PML coiled-coil region is essential for the PML/RAR alpha-mediated retinoic acid response. Tretinoin 146-159 PML nuclear body scaffold Homo sapiens 123-136
10597230-2 1999 RA-sensitivity in APL is mediated by its oncogenic protein, which results from the recombination of the PML and the RA receptor alpha (RAR alpha) genes (PML/RAR alpha fusion protein). Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 104-107
10597230-2 1999 RA-sensitivity in APL is mediated by its oncogenic protein, which results from the recombination of the PML and the RA receptor alpha (RAR alpha) genes (PML/RAR alpha fusion protein). Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 135-144
10597230-2 1999 RA-sensitivity in APL is mediated by its oncogenic protein, which results from the recombination of the PML and the RA receptor alpha (RAR alpha) genes (PML/RAR alpha fusion protein). Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 153-166
10583214-3 1999 ATRA caused a dose-dependent (range 0.01-10 microM) accumulation of PAI-2 antigen and activity into the cell culture medium, with a maximal increase (about 5-fold over control) at a concentration of 1-10 microM. Tretinoin 0-4 serpin family B member 2 Homo sapiens 68-73
10583214-4 1999 Similarly, a dose-dependent increase in PAI-2 antigen was observed in cell extracts upon ATRA stimulation. Tretinoin 89-93 serpin family B member 2 Homo sapiens 40-45
10583214-5 1999 Northern blot analysis showed a parallel increase in the amount of PAI-2 mRNA in ATRA-treated cells. Tretinoin 81-85 serpin family B member 2 Homo sapiens 67-72
10583214-6 1999 Time-course experiments with 1 microM ATRA showed enhanced PAI-2 mRNA expression as early as 2 h, reaching a maximum at 4-6 h and then declining at 18-24 h, and a time-dependent increase in PAI-2 antigen in the cell culture medium. Tretinoin 38-42 serpin family B member 2 Homo sapiens 59-64
10583214-6 1999 Time-course experiments with 1 microM ATRA showed enhanced PAI-2 mRNA expression as early as 2 h, reaching a maximum at 4-6 h and then declining at 18-24 h, and a time-dependent increase in PAI-2 antigen in the cell culture medium. Tretinoin 38-42 serpin family B member 2 Homo sapiens 190-195
10583214-10 1999 The effect was due to enhanced extracellular PAI-2 accumulation since it was observed with conditioned medium from ATRA-treated cells; it was abolished by the addition of neutralizing anti-PAI-2 antibodies and was negligible when single-chain t-PA was used instead of u-PA. Tretinoin 115-119 serpin family B member 2 Homo sapiens 45-50
10583214-10 1999 The effect was due to enhanced extracellular PAI-2 accumulation since it was observed with conditioned medium from ATRA-treated cells; it was abolished by the addition of neutralizing anti-PAI-2 antibodies and was negligible when single-chain t-PA was used instead of u-PA. Tretinoin 115-119 serpin family B member 2 Homo sapiens 189-194
10612431-4 1999 In Hs578T cells, retinoic acid (10-100 nM) increased IGFBP-3 phosphorylation to a maximum of 150% of control. Tretinoin 17-30 insulin like growth factor binding protein 3 Homo sapiens 53-60
10520028-6 1999 After ATRA treatment, > 80% of initial NB-4 cell attachment to endothelial cells was E-selectin dependent. Tretinoin 6-10 selectin E Homo sapiens 88-98
10520028-10 1999 Thus, ATRA dramatically altered the adhesion phenotype on NB-4 cells: ATRA induced rolling largely attributable to E-selectin, abrogated alpha4 integrin dependent rolling, and promoted acquisition of beta2 integrin dependent firm adherence and transmigration. Tretinoin 6-10 selectin E Homo sapiens 115-125
10477294-3 1999 We show that retinoic acid expands the N-tubulin, X-ngnr-1, X-MyT1, X-&Dgr;-1 and Gli3 domains and inhibits the expression of Zic2 and sonic hedgehog in the neural ectoderm, whereas a retinoid antagonist produces opposite changes. Tretinoin 13-26 neurogenin 2 L homeolog Xenopus laevis 50-58
10477294-3 1999 We show that retinoic acid expands the N-tubulin, X-ngnr-1, X-MyT1, X-&Dgr;-1 and Gli3 domains and inhibits the expression of Zic2 and sonic hedgehog in the neural ectoderm, whereas a retinoid antagonist produces opposite changes. Tretinoin 13-26 sonic hedgehog L homeolog Xenopus laevis 145-153
10498757-0 1999 Retinoic acid induces Gpx2 gene expression in MCF-7 human breast cancer cells. Tretinoin 0-13 glutathione peroxidase 2 Homo sapiens 22-26
10498757-4 1999 Because we identified three putative retinoic acid response elements (RARE) in the Gpx2 gene, we examined the regulation of the Gpx2 gene expression by all-trans retinoic acid (RA) in RA-sensitive MCF-7 cells and RA-resistant HT29 cells. Tretinoin 37-50 glutathione peroxidase 2 Homo sapiens 83-87
10498757-4 1999 Because we identified three putative retinoic acid response elements (RARE) in the Gpx2 gene, we examined the regulation of the Gpx2 gene expression by all-trans retinoic acid (RA) in RA-sensitive MCF-7 cells and RA-resistant HT29 cells. Tretinoin 162-175 glutathione peroxidase 2 Homo sapiens 128-132
10498757-4 1999 Because we identified three putative retinoic acid response elements (RARE) in the Gpx2 gene, we examined the regulation of the Gpx2 gene expression by all-trans retinoic acid (RA) in RA-sensitive MCF-7 cells and RA-resistant HT29 cells. Tretinoin 70-72 glutathione peroxidase 2 Homo sapiens 83-87
10498757-4 1999 Because we identified three putative retinoic acid response elements (RARE) in the Gpx2 gene, we examined the regulation of the Gpx2 gene expression by all-trans retinoic acid (RA) in RA-sensitive MCF-7 cells and RA-resistant HT29 cells. Tretinoin 177-179 glutathione peroxidase 2 Homo sapiens 128-132
10498757-6 1999 RA treatment increased Gpx2 mRNA level 3- to 11-fold and resulted in a fourfold increase of GPX activity (80 mU/mg protein) in MCF-7 cells. Tretinoin 0-2 glutathione peroxidase 2 Homo sapiens 23-27
10498757-8 1999 These results show that the Gpx2 gene is expressed in both breast and intestinal epithelium cells, and suggest that its expression can be highly regulated by retinoic acid, a known differentiation agent. Tretinoin 158-171 glutathione peroxidase 2 Homo sapiens 28-32
10706449-8 1999 The levels of CDK2 activity were inhibited approximately 60% in ATRA-treated cells, suggesting that the increased p21 levels were sufficient to inhibit CDK activity and cause RB hypophosphorylation. Tretinoin 64-68 H3 histone pseudogene 16 Homo sapiens 114-117
10540944-9 1999 In situ staining for IL-1alpha mRNA was slightly more abundant in mice treated for 3 weeks with UV and UV + tretinoin than in controls whereas 5 weeks of UV + tretinoin treatment gave strongly positive staining. Tretinoin 108-117 interleukin 1 alpha Mus musculus 21-30
10580834-8 1999 R1881 decreased and atRA increased the mRNA levels of IGFBP-3 and these effects were confirmed by Western ligand blotting and by radioimmunoassay. Tretinoin 20-24 insulin like growth factor binding protein 3 Homo sapiens 54-61
10485269-3 1999 On the other hand, 10(-12) M ATRA significantly promoted the growth of CFU-meg, in the presence either of thrombopoietin or of IL-3+ GM-CSF, and induced a reproducible stimulation of the immature CD34+DR- subset. Tretinoin 29-33 interleukin 3 Homo sapiens 127-131
10485269-3 1999 On the other hand, 10(-12) M ATRA significantly promoted the growth of CFU-meg, in the presence either of thrombopoietin or of IL-3+ GM-CSF, and induced a reproducible stimulation of the immature CD34+DR- subset. Tretinoin 29-33 colony stimulating factor 2 Homo sapiens 133-139
10662597-1 1999 We studied the regulation of the human Galbeta1, 3GalNAc/Galbeta1,4GlcNAc alpha2,3-sialyltransferase (hST3Gal IV) gene during HL-60 cell differentiation induced by dimethyl sulfoxide (DMSO), all trans-retinoic acid (ATRA), and phorbol myristate acetate (PMA). Tretinoin 195-214 ST3 beta-galactoside alpha-2,3-sialyltransferase 4 Homo sapiens 102-113
10662597-1 1999 We studied the regulation of the human Galbeta1, 3GalNAc/Galbeta1,4GlcNAc alpha2,3-sialyltransferase (hST3Gal IV) gene during HL-60 cell differentiation induced by dimethyl sulfoxide (DMSO), all trans-retinoic acid (ATRA), and phorbol myristate acetate (PMA). Tretinoin 216-220 ST3 beta-galactoside alpha-2,3-sialyltransferase 4 Homo sapiens 102-113
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 83-96 retinoic acid receptor alpha Homo sapiens 4-26
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 83-96 retinoic acid receptor alpha Homo sapiens 28-31
10441468-4 1999 Treatment with the selective RARalpha agonist Ro 40-6055 completely mimicked the effects of ATRA on growth and transactivation of a betaRAREx2-luciferase reporter construct, while RARbeta- and gamma-specific analogues were ineffective. Tretinoin 92-96 retinoic acid receptor alpha Homo sapiens 29-37
10441468-6 1999 Thus, ATRA potently inhibits anchorage-independent growth in HT29 cells and this effect is mainly if not exclusively mediated by the retinoic acid receptor alpha. Tretinoin 6-10 retinoic acid receptor alpha Homo sapiens 133-161
10480290-5 1999 Exposure of U-937 cells to 1alpha,25-dihydroxycholecalciferol (VitD3) and all-trans retinoic acid (ATRA) resulted in down-regulation of TF expression and PCA. Tretinoin 74-97 coagulation factor III, tissue factor Homo sapiens 136-138
10480290-5 1999 Exposure of U-937 cells to 1alpha,25-dihydroxycholecalciferol (VitD3) and all-trans retinoic acid (ATRA) resulted in down-regulation of TF expression and PCA. Tretinoin 99-103 coagulation factor III, tissue factor Homo sapiens 136-138
10480290-6 1999 In NB4 cells induction by ATRA, but not VitD3, resulted in the down-regulation of TF expression and PCA. Tretinoin 26-30 coagulation factor III, tissue factor Homo sapiens 82-84
10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Tretinoin 78-101 RUNX family transcription factor 3 Homo sapiens 15-19
10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Tretinoin 103-105 RUNX family transcription factor 3 Homo sapiens 15-19
10419474-4 1999 In HL-60 cells AML2 expression can be induced by all three natural retinoids, all-trans-retinoic acid (RA), 13-cis-RA, and 9-cis-RA in a dose-dependent manner. Tretinoin 115-117 RUNX family transcription factor 3 Homo sapiens 15-19
10419474-7 1999 Our study further showed that AGN193109, a potent RARalpha antagonist, suppressed AML2 expression induced by RA and that a retinoic X receptor pan agonist AGN194204 had no effect on its expression. Tretinoin 50-52 RUNX family transcription factor 3 Homo sapiens 82-86
10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 colony stimulating factor 3 Homo sapiens 161-166
10414449-7 1999 Furthermore, G-CSF, through its potent differentiating activity, may increase the risk of such complications during ATRA treatment. Tretinoin 116-120 colony stimulating factor 3 Homo sapiens 13-18
10417615-11 1999 Additionally, protein C inhibitor could contribute to the regulation of retinoid supply in the epidermis, as we have shown recently that retinoic acid binds specifically to protein C inhibitor. Tretinoin 137-150 protein C, inactivator of coagulation factors Va and VIIIa Homo sapiens 14-23
10386957-4 1999 Upon differentiation of SHSY5Y cells with retinoic acid, we found that the phosphorylation of high molecular mass (NF-H) and medium molecular mass (NF-M) NFs increased, whereas the CDK-5 protein level and kinase activity were unaffected. Tretinoin 42-55 neurofilament heavy chain Homo sapiens 115-119
10386957-4 1999 Upon differentiation of SHSY5Y cells with retinoic acid, we found that the phosphorylation of high molecular mass (NF-H) and medium molecular mass (NF-M) NFs increased, whereas the CDK-5 protein level and kinase activity were unaffected. Tretinoin 42-55 cyclin dependent kinase 5 Homo sapiens 181-186
10400422-3 1999 Notably, clinical improvement was also correlated to ATRA/As2O3-induced rapid decrease of membrane procoagulant activity (PCA) and TF contents of APL blasts. Tretinoin 53-57 coagulation factor III, tissue factor Homo sapiens 131-133
10400422-4 1999 Consistent with the in vivo findings, the membrane PCA, TF antigen and its mRNA level within NB4 cells were rapidly down-regulated by 1 microM ATRA or As2O3, while 0.2 microg/ml DNR increased these TF parameters prior to its effect upon apoptosis induction. Tretinoin 143-147 coagulation factor III, tissue factor Homo sapiens 56-58
10400422-4 1999 Consistent with the in vivo findings, the membrane PCA, TF antigen and its mRNA level within NB4 cells were rapidly down-regulated by 1 microM ATRA or As2O3, while 0.2 microg/ml DNR increased these TF parameters prior to its effect upon apoptosis induction. Tretinoin 143-147 coagulation factor III, tissue factor Homo sapiens 198-200
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 31-33 PML nuclear body scaffold Homo sapiens 132-135
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 31-33 PML nuclear body scaffold Homo sapiens 132-135
10373566-3 1999 Recently it has been shown that complete remission can be achieved upon treatment with arsenic trioxide (As2O3) in PML-RARalpha-positive APL, even when the patient has relapsed and the disease is RA resistant. Tretinoin 119-121 PML nuclear body scaffold Homo sapiens 115-118
10393242-7 1999 The intensity of PPAR binding was also increased by the treatment of retinoic acid (RA) and 9-cis retinoic acid (9-cis RA). Tretinoin 69-82 peroxisome proliferator activated receptor alpha Rattus norvegicus 17-21
10361124-3 1999 Upon stimulation with RA, mRNA levels of RARalpha and beta transiently increased in parallel with the induction of uPA, and this increase was inhibited by cycloheximide. Tretinoin 22-24 retinoic acid receptor alpha Homo sapiens 41-49
27461974-0 2016 All-Trans Retinoic Acid Increases Aquaporin 3 Expression in Human Vaginal Epithelial Cells. Tretinoin 10-23 aquaporin 3 (Gill blood group) Homo sapiens 34-45
10361124-10 1999 These results suggest that (1) RA induces RARs mainly via RARalpha and that (2) RAR/RXR physically and functionally interact with Sp1, resulting in a potentiation of uPA transcription. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 58-66
10361124-10 1999 These results suggest that (1) RA induces RARs mainly via RARalpha and that (2) RAR/RXR physically and functionally interact with Sp1, resulting in a potentiation of uPA transcription. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 42-45
10364073-0 1999 Retinoic acid regulates arterial smooth muscle cell proliferation and phenotypic features in vivo and in vitro through an RARalpha-dependent signaling pathway. Tretinoin 0-13 retinoic acid receptor, alpha Rattus norvegicus 122-130
27461974-3 2016 AIM: To investigate the effect of ATRA on the expression of AQP3 in human vaginal epithelial cells. Tretinoin 34-38 aquaporin 3 (Gill blood group) Homo sapiens 60-64
28331816-10 2017 Furthermore, we were able to show that microRNA 27a and/or microRNA 96 are important regulators of gap junction signalling, the rearrangement of the actin cytoskeleton as well as the citric acid cycle, which represent the most affected pathways with regard to inhibitory effects of ATRA in 3T3-L1 preadipocytes. Tretinoin 282-286 microRNA 96 Mus musculus 59-70
10362099-3 1999 In addition, 13-cis RA treatment results in an increase of MMP-1 mRNA stability. Tretinoin 20-22 matrix metallopeptidase 1 Homo sapiens 59-64
10362099-4 1999 These data demonstrate that RA stimulates MMP-1 gene expression in human pancreatic carcinoma cells by transcriptional and post-transcriptional mechanisms. Tretinoin 28-30 matrix metallopeptidase 1 Homo sapiens 42-47
10357800-0 1999 Retinoic acid and 4-hydroxyphenylretinamide induce growth inhibition and tissue transglutaminase through different signal transduction pathways in mouse fibroblasts (NIH 3T3 cells). Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 73-96
10357800-3 1999 We have previously reported that stable expression of a truncated retinoic acid receptor alpha, RARalpha403, transduced in NIH 3T3 cells by a retroviral vector, rendered the cells resistant to retinoic acid for growth inhibition and induction of tissue transglutaminase (TGase II). Tretinoin 66-79 transglutaminase 2, C polypeptide Mus musculus 246-269
10699977-4 2000 Profuse dendritic growth was observed upon exposure to BMP-7, and this was reduced by approximately 70% by RA. Tretinoin 107-109 bone morphogenetic protein 7 Rattus norvegicus 55-60
10720132-7 2000 Comparing HLA frequencies, clinical features at diagnosis and clinical outcome of the 64 patients homogeneously treated with all-trans retinoic acid and idarubicin (AIDA protocol) we observed a statistically significant association between HLA-B*13 and risk of relapse by univariate and multivariate regression analysis. Tretinoin 135-148 major histocompatibility complex, class I, B Homo sapiens 240-245
27638841-7 2016 Conversely, restoration of RA by pharmacologic blockade of the RA-catabolizing enzyme CYP26A1 attenuated inflammation and diminished tumor burden. Tretinoin 27-29 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 86-93
10736240-1 2000 The EAT/mcl-1 gene was isolated during the early differentiation of a retinoic acid-induced human embryonal carcinoma cell line to the trophectoderm lineage. Tretinoin 70-83 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 8-13
10381141-2 1999 We recently reported that rat CYP 1A1 induced by 3-methylcholanthrene (3-MC) catalyzed the conversion of retinal to retinoic acid. Tretinoin 116-129 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 30-37
10473117-0 1999 Retinoic acid induces down-regulation of Wnt-3a, apoptosis and diversion of tail bud cells to a neural fate in the mouse embryo. Tretinoin 0-13 wingless-type MMTV integration site family, member 3A Mus musculus 41-47
10746412-1 2000 BACKGROUND: Rapid and accurate diagnosis of acute promyelocytic leukemia (APL) is essential for management of the disease, as all-trans retinoic acid (ATRA) therapy only induces complete remission in patients whose leukemic cells harbor a t(15;17) translocation, resulting in promyelocytic-retinoic acid receptor alpha (PML-RAR alpha) fusion transcripts. Tretinoin 136-149 retinoic acid receptor alpha Homo sapiens 290-318
10473117-8 1999 Wnt-3a, a gene that has been shown to be essential for tail bud formation, is specifically down-regulated in the tail bud of retinoic acid-treated embryos, as early as 2 h after retinoic acid treatment and Wnt-3a transcripts become undetectable by 10 h. In contrast, Wnt-5a and RAR-gamma are still detectable in the tail bud at that time. Tretinoin 125-138 wingless-type MMTV integration site family, member 3A Mus musculus 0-6
27638841-7 2016 Conversely, restoration of RA by pharmacologic blockade of the RA-catabolizing enzyme CYP26A1 attenuated inflammation and diminished tumor burden. Tretinoin 63-65 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 86-93
10473117-8 1999 Wnt-3a, a gene that has been shown to be essential for tail bud formation, is specifically down-regulated in the tail bud of retinoic acid-treated embryos, as early as 2 h after retinoic acid treatment and Wnt-3a transcripts become undetectable by 10 h. In contrast, Wnt-5a and RAR-gamma are still detectable in the tail bud at that time. Tretinoin 125-138 wingless-type MMTV integration site family, member 3A Mus musculus 206-212
10746412-1 2000 BACKGROUND: Rapid and accurate diagnosis of acute promyelocytic leukemia (APL) is essential for management of the disease, as all-trans retinoic acid (ATRA) therapy only induces complete remission in patients whose leukemic cells harbor a t(15;17) translocation, resulting in promyelocytic-retinoic acid receptor alpha (PML-RAR alpha) fusion transcripts. Tretinoin 151-155 retinoic acid receptor alpha Homo sapiens 290-318
10699459-0 2000 The mechanisms of retinoic acid-induced regulation on the follicle-stimulating hormone receptor in rat granulosa cells. Tretinoin 18-31 follicle stimulating hormone receptor Rattus norvegicus 58-95
10473117-8 1999 Wnt-3a, a gene that has been shown to be essential for tail bud formation, is specifically down-regulated in the tail bud of retinoic acid-treated embryos, as early as 2 h after retinoic acid treatment and Wnt-3a transcripts become undetectable by 10 h. In contrast, Wnt-5a and RAR-gamma are still detectable in the tail bud at that time. Tretinoin 178-191 wingless-type MMTV integration site family, member 3A Mus musculus 0-6
10473117-11 1999 These results suggest that retinoic acid induces down-regulation of Wnt-3a which may play an important role in the pathogenesis of axial truncation, involving induction of widespread apoptosis, followed by an alteration of tail bud cell fate to form multiple ectopic neural tubes. Tretinoin 27-40 wingless-type MMTV integration site family, member 3A Mus musculus 68-74
10699459-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on follicle-stimulating hormone receptor (FSH-R) in rat granulosa cells. Tretinoin 85-98 follicle stimulating hormone receptor Rattus norvegicus 107-144
10699459-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on follicle-stimulating hormone receptor (FSH-R) in rat granulosa cells. Tretinoin 85-98 follicle stimulating hormone receptor Rattus norvegicus 146-151
10699459-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on follicle-stimulating hormone receptor (FSH-R) in rat granulosa cells. Tretinoin 100-102 follicle stimulating hormone receptor Rattus norvegicus 107-144
10699459-1 2000 The present study was undertaken to identify the mechanisms underlying the effect of retinoic acid (RA) on follicle-stimulating hormone receptor (FSH-R) in rat granulosa cells. Tretinoin 100-102 follicle stimulating hormone receptor Rattus norvegicus 146-151
10699459-2 2000 Treatment with FSH produced a substantial increase in FSH-R mRNA level, as was expected, while concurrent treatment with increasing concentrations of RA brought about dose-dependent decreases in FSH-induced FSH-R mRNA, with a maximal inhibition one-third lower than that induced by FSH alone. Tretinoin 150-152 follicle stimulating hormone receptor Rattus norvegicus 207-212
10339585-4 1999 In contrast to bone marrow cells from PLZF-RARalpha transgenic mice, those from NPM-RARalpha transgenic mice could be induced to differentiate by all-trans-retinoic acid (ATRA). Tretinoin 146-169 nucleophosmin 1 Mus musculus 80-83
10339585-4 1999 In contrast to bone marrow cells from PLZF-RARalpha transgenic mice, those from NPM-RARalpha transgenic mice could be induced to differentiate by all-trans-retinoic acid (ATRA). Tretinoin 171-175 nucleophosmin 1 Mus musculus 80-83
10699459-4 2000 These results suggested that RA diminished the action of FSH on FSH-R expression at sites distal to cAMP generation in the granulosa cells. Tretinoin 29-31 follicle stimulating hormone receptor Rattus norvegicus 64-69
27242163-3 2016 Immunocytochemistry was used to localize different components of RA signaling within sections of the retina and optic tectum, namely, the synthetic enzyme retinaldehyde dehydrogenase (RALDH), the RA binding proteins CRABPI and II, the retinoic acid receptors RARalpha, beta and gamma, and finally the catabolic enzyme CYP26A1. Tretinoin 65-67 retinoic acid receptor alpha Homo sapiens 259-267
10645966-8 2000 ELISA assays revealed that retinoic acid treated myocyte cultures contained significantly more hLAMP-1 and fibronectin than either normal or DMSO controls. Tretinoin 27-40 fibronectin 1 Mus musculus 107-118
10642512-0 2000 Induction of Myc-intron-binding polypeptides MIBP1 and RFX1 during retinoic acid-mediated differentiation of haemopoietic cells. Tretinoin 67-80 HIVEP zinc finger 2 Homo sapiens 45-50
10642512-1 2000 Retinoic acid-mediated differentiation of HL60 cells is associated with an alteration of chromatin structure that maps to protein-binding sequences within intron I of the c-myc gene and with down-regulation of c-myc expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 171-176
10339585-6 1999 Dissociation of SMRT from different receptors was observed at ATRA concentrations of 0.01 microM, 0.1 microM, and 1.0 microM for RARalpha-RXRalpha, NPM-RARalpha, and PML-RARalpha, respectively, but not observed for PLZF-RARalpha even in the presence of 10 microM ATRA. Tretinoin 62-66 nuclear receptor co-repressor 2 Mus musculus 16-20
10330422-4 1999 Reporter gene studies showed that C/EBPepsilon promoter/enhancer activity increased in a retinoid-dependent fashion via the retinoic acid response element (RARE) present in the promoter region of C/EBPepsilon. Tretinoin 124-137 CCAAT enhancer binding protein epsilon Homo sapiens 196-208
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 CCAAT enhancer binding protein epsilon Homo sapiens 29-41
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 137-145
10642512-1 2000 Retinoic acid-mediated differentiation of HL60 cells is associated with an alteration of chromatin structure that maps to protein-binding sequences within intron I of the c-myc gene and with down-regulation of c-myc expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 210-215
10642512-4 2000 In addition, we show that treatment with retinoic acid induces both MIBP1 and RFX1 protein, as well as their DNA-binding activity, upon granulocytic differentiation of HL60 cells, with a gel mobility pattern identical to that of HeLa cells. Tretinoin 41-54 HIVEP zinc finger 2 Homo sapiens 68-73
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 PML nuclear body scaffold Homo sapiens 147-150
10642512-6 2000 We also show that the time course of MIBP1 and RFX1 induction is inversely correlated with the down-regulation of c-myc levels during the treatment of HL60 cells with retinoic acid. Tretinoin 167-180 HIVEP zinc finger 2 Homo sapiens 37-42
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 151-159
10642512-6 2000 We also show that the time course of MIBP1 and RFX1 induction is inversely correlated with the down-regulation of c-myc levels during the treatment of HL60 cells with retinoic acid. Tretinoin 167-180 MYC proto-oncogene, bHLH transcription factor Homo sapiens 114-119
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 151-159
27348405-4 2016 Acute RA treatment increases spontaneous inhibitory synaptic transmission in L2/3 pyramidal neurons of the somatosensory cortex, and this effect requires expression of RA"s receptor RARalpha both pre- and post-synaptically. Tretinoin 6-8 retinoic acid receptor alpha Homo sapiens 182-190
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 151-159
10330422-6 1999 In retinoid-resistant APL cell lines, C/EBPepsilon either is not induced or is induced only at very high concentrations of RA (>/=10(-6) M). Tretinoin 123-125 CCAAT enhancer binding protein epsilon Homo sapiens 38-50
10344762-0 1999 HMGI(Y) and HMGI-C genes are expressed in neuroblastoma cell lines and tumors and affect retinoic acid responsiveness. Tretinoin 89-102 high mobility group AT-hook 1 Homo sapiens 0-7
10344762-0 1999 HMGI(Y) and HMGI-C genes are expressed in neuroblastoma cell lines and tumors and affect retinoic acid responsiveness. Tretinoin 89-102 high mobility group AT-hook 2 Homo sapiens 12-18
10344762-5 1999 Although HMGI(Y) is constitutively expressed in the embryonal and adult adrenal gland and in all of the NB cell lines and ex vivo tumors examined, its regulation appears to be associated to growth inhibition and differentiation because we observed that HMGI(Y) expression is reduced by retinoic acid (RA) in several NB cell lines that are induced to differentiate into postmitotic neurons, whereas it is up-regulated by RA in cells that fail to differentiate. Tretinoin 286-299 high mobility group AT-hook 1 Homo sapiens 9-16
10650963-1 2000 Decidualization of stromal cells at the site of embryo implantation in the rat uterus is accompanied by expression of cellular retinol-binding protein and cellular retinoic acid-binding protein [CRABP(II)], whose presence has been shown to correlate with gain of ability to synthesize retinoic acid in other cells. Tretinoin 164-177 cellular retinoic acid binding protein 2 Rattus norvegicus 195-205
10650963-11 2000 Thus, expression of CRABP(II) was correlated with gain of ability to synthesize retinoic acid. Tretinoin 80-93 cellular retinoic acid binding protein 2 Rattus norvegicus 20-29
10640639-3 2000 Here we show that neuroectodermal differentiation stimulated by retinoic acid (RA) in the embryonal carcinoma (EC) line P19 is accompanied by upregulation of GAP-43 expression in neuroepithelial precursor cells. Tretinoin 64-77 interleukin 23 subunit alpha Homo sapiens 120-123
10640639-3 2000 Here we show that neuroectodermal differentiation stimulated by retinoic acid (RA) in the embryonal carcinoma (EC) line P19 is accompanied by upregulation of GAP-43 expression in neuroepithelial precursor cells. Tretinoin 64-77 growth associated protein 43 Homo sapiens 158-164
10640639-3 2000 Here we show that neuroectodermal differentiation stimulated by retinoic acid (RA) in the embryonal carcinoma (EC) line P19 is accompanied by upregulation of GAP-43 expression in neuroepithelial precursor cells. Tretinoin 79-81 interleukin 23 subunit alpha Homo sapiens 120-123
10344762-5 1999 Although HMGI(Y) is constitutively expressed in the embryonal and adult adrenal gland and in all of the NB cell lines and ex vivo tumors examined, its regulation appears to be associated to growth inhibition and differentiation because we observed that HMGI(Y) expression is reduced by retinoic acid (RA) in several NB cell lines that are induced to differentiate into postmitotic neurons, whereas it is up-regulated by RA in cells that fail to differentiate. Tretinoin 301-303 high mobility group AT-hook 1 Homo sapiens 9-16
10344762-5 1999 Although HMGI(Y) is constitutively expressed in the embryonal and adult adrenal gland and in all of the NB cell lines and ex vivo tumors examined, its regulation appears to be associated to growth inhibition and differentiation because we observed that HMGI(Y) expression is reduced by retinoic acid (RA) in several NB cell lines that are induced to differentiate into postmitotic neurons, whereas it is up-regulated by RA in cells that fail to differentiate. Tretinoin 420-422 high mobility group AT-hook 1 Homo sapiens 9-16
10640639-3 2000 Here we show that neuroectodermal differentiation stimulated by retinoic acid (RA) in the embryonal carcinoma (EC) line P19 is accompanied by upregulation of GAP-43 expression in neuroepithelial precursor cells. Tretinoin 79-81 growth associated protein 43 Homo sapiens 158-164
27348405-9 2016 Here, the authors show that in layer 2/3 (L2/3) of the somatosensory cortex (S1), acute RA induces increases in spontaneous but not action-potential evoked transmission, and that this requires retinoic acid receptor (RARalpha) both in presynaptic PV-positive interneurons and postsynaptic pyramidal (PN) neurons. Tretinoin 88-90 retinoic acid receptor alpha Homo sapiens 217-225
27157616-8 2016 Finally, 2 weeks of daily ATRA treatment were sufficient to inhibit gastric tumor progression in vivo, which was associated with a decrease in CD44, ALDH1, Ki67 and PCNA expression in the remaining tumor cells. Tretinoin 26-30 aldehyde dehydrogenase 1 family member A1 Homo sapiens 149-154
10634605-1 2000 PURPOSE: To study effects of depletion of retinoic acid on expression of the mucins ASGP (rMuc4), rMuc5AC, and rMuc1, by the corneal and conjunctival epithelia of the rat. Tretinoin 42-55 mucin 4, cell surface associated Rattus norvegicus 84-88
10209963-1 1999 The natural ligands of the nuclear receptors vitamin D receptor (VDR) and retinoic acid receptor (RAR), i.e., 1alpha,25-dihydroxyvitamin D3 (VD) and all-trans retinoic acid, have important effects on the proliferation, differentiation and apoptosis of a variety of malignant cells, including melanoma. Tretinoin 74-87 retinoic acid receptor alpha Homo sapiens 98-101
10634605-1 2000 PURPOSE: To study effects of depletion of retinoic acid on expression of the mucins ASGP (rMuc4), rMuc5AC, and rMuc1, by the corneal and conjunctival epithelia of the rat. Tretinoin 42-55 mucin 4, cell surface associated Rattus norvegicus 90-95
27157616-8 2016 Finally, 2 weeks of daily ATRA treatment were sufficient to inhibit gastric tumor progression in vivo, which was associated with a decrease in CD44, ALDH1, Ki67 and PCNA expression in the remaining tumor cells. Tretinoin 26-30 proliferating cell nuclear antigen Homo sapiens 165-169
10791768-8 2000 Appearance of both IGFBP-3 and lactoferrin in conditioned media of primary cultures of bovine mammary cells was stimulated by all trans retinoic acid (atRA). Tretinoin 136-149 lactotransferrin Bos taurus 31-42
10215635-5 1999 The IL-2-mediated c-myc overexpression and CYP down-regulation were prevented by 1) genistein (a tyrosine kinase inhibitor that blocks the initial transduction of the IL-2R signal), 2) retinoic acid, butyric acid, or dimethyl sulfoxide (three agents that block c-myc transcription), or 3) an antisense c-myc oligonucleotide (which may cause rapid degradation of the c-myc transcript). Tretinoin 185-198 interleukin 2 Rattus norvegicus 4-8
10791768-8 2000 Appearance of both IGFBP-3 and lactoferrin in conditioned media of primary cultures of bovine mammary cells was stimulated by all trans retinoic acid (atRA). Tretinoin 151-155 lactotransferrin Bos taurus 31-42
27759097-4 2016 Here we report the first crystal structure of human ALDH1A3 complexed with NAD+ and the product all-trans retinoic acid (REA). Tretinoin 106-119 aldehyde dehydrogenase 1 family member A3 Homo sapiens 52-59
10791768-9 2000 Furthermore, atRA was necessary for the entry of exogenously added lactoferrin into the mammary cell nucleus, while IGFBP-3 entry into the nuclei of atRA treated cells required the presence of lactoferrin. Tretinoin 13-17 lactotransferrin Bos taurus 67-78
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 188-201 retinoic acid receptor alpha Homo sapiens 41-44
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 188-201 nuclear receptor corepressor 1 Homo sapiens 131-136
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 retinoic acid receptor alpha Homo sapiens 41-44
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 nuclear receptor corepressor 1 Homo sapiens 131-136
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 nuclear receptor corepressor 1 Homo sapiens 225-230
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 retinoic acid receptor alpha Homo sapiens 251-259
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 PML nuclear body scaffold Homo sapiens 100-104
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 retinoic acid receptor alpha Homo sapiens 104-112
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 retinoic acid receptor alpha Homo sapiens 129-137
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 nuclear receptor corepressor 1 Homo sapiens 257-262
10637480-3 2000 We demonstrate that SMRT association, as with PML-RARalpha, can be released from NPM-RARalpha at pharmacological concentration of ATRA (10-6 M). Tretinoin 130-134 PML nuclear body scaffold Homo sapiens 46-50
10637480-3 2000 We demonstrate that SMRT association, as with PML-RARalpha, can be released from NPM-RARalpha at pharmacological concentration of ATRA (10-6 M). Tretinoin 130-134 retinoic acid receptor alpha Homo sapiens 50-58
10637480-3 2000 We demonstrate that SMRT association, as with PML-RARalpha, can be released from NPM-RARalpha at pharmacological concentration of ATRA (10-6 M). Tretinoin 130-134 retinoic acid receptor alpha Homo sapiens 85-93
10356361-4 1999 We showed in this study that PML/RARalpha increased the transcription of p21WAF1/CIP1 gene and the activation was further induced by RA treatment. Tretinoin 33-35 PML nuclear body scaffold Homo sapiens 29-32
10356361-7 1999 These results suggest that the induction of APL cells differentiation by RA may be a result of the activation of p21WAF1/CIP1 by PML/RARalpha. Tretinoin 73-75 PML nuclear body scaffold Homo sapiens 129-132
10356361-7 1999 These results suggest that the induction of APL cells differentiation by RA may be a result of the activation of p21WAF1/CIP1 by PML/RARalpha. Tretinoin 73-75 retinoic acid receptor alpha Homo sapiens 133-141
10191271-1 1999 Mammalian class I aldehyde dehydrogenase (ALDH1) has been implicated as a retinal dehydrogenase in the biosynthesis of retinoic acid, a modulator of gene expression and cell differentiation. Tretinoin 119-132 aldehyde dehydrogenase 1 family member A1 Homo sapiens 42-47
10094816-0 1999 Induction of p21(CIP1/Waf1) and activation of p34(cdc2) involved in retinoic acid-induced apoptosis in human hepatoma Hep3B cells. Tretinoin 68-81 cyclin dependent kinase 1 Homo sapiens 50-54
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 cyclin dependent kinase 1 Homo sapiens 151-155
10090931-0 1999 1,25-Dihydroxyvitamin D3 induces differentiation of a retinoic acid-resistant acute promyelocytic leukemia cell line (UF-1) associated with expression of p21(WAF1/CIP1) and p27(KIP1). Tretinoin 54-67 interferon alpha inducible protein 27 Homo sapiens 173-176
10090931-0 1999 1,25-Dihydroxyvitamin D3 induces differentiation of a retinoic acid-resistant acute promyelocytic leukemia cell line (UF-1) associated with expression of p21(WAF1/CIP1) and p27(KIP1). Tretinoin 54-67 cyclin dependent kinase inhibitor 1B Homo sapiens 177-181
10090931-14 1999 Interestingly, the combination of 1, 25(OH)2D3 and RA markedly enhanced the levels of p27(KIP1) transcript and protein as compared with levels induced by 1, 25(OH)2D3 alone. Tretinoin 51-53 interferon alpha inducible protein 27 Homo sapiens 86-89
10090931-14 1999 Interestingly, the combination of 1, 25(OH)2D3 and RA markedly enhanced the levels of p27(KIP1) transcript and protein as compared with levels induced by 1, 25(OH)2D3 alone. Tretinoin 51-53 cyclin dependent kinase inhibitor 1B Homo sapiens 90-94
27759097-4 2016 Here we report the first crystal structure of human ALDH1A3 complexed with NAD+ and the product all-trans retinoic acid (REA). Tretinoin 121-124 aldehyde dehydrogenase 1 family member A3 Homo sapiens 52-59
10965525-8 2000 Long-term BC or RA treatment elicited a substantial decrement in reduced glutathione content and gamma-glutamyltranspeptidase activity and an increment in cytochrome P-450 content and glutathione peroxidase and glutathione S-transferase activities in the HNs and NNSP, which were otherwise reversed in rats that received DEN-PB treatment alone. Tretinoin 16-18 hematopoietic prostaglandin D synthase Rattus norvegicus 211-236
27755557-4 2016 The activation of FGF and Retinoic Acid along with the inhibition of BMP, SHH and TGF-beta led to the generation of 75% NKX6.1+/NGN3+ Endocrine Progenitors. Tretinoin 26-39 neurogenin 3 Homo sapiens 128-132
10601023-1 1999 Although retinoic acid receptor alpha (RARalpha) agonists induce the maturation of t(15;17) acute promyelocytic leukemia (APL) cells, drug treatment also selects leukemic blasts expressing PML-RARalpha fusion proteins with mutated ligand-binding domains that no longer respond to all-trans retinoic acid (ATRA). Tretinoin 9-22 retinoic acid receptor alpha Homo sapiens 39-47
10601023-1 1999 Although retinoic acid receptor alpha (RARalpha) agonists induce the maturation of t(15;17) acute promyelocytic leukemia (APL) cells, drug treatment also selects leukemic blasts expressing PML-RARalpha fusion proteins with mutated ligand-binding domains that no longer respond to all-trans retinoic acid (ATRA). Tretinoin 305-309 retinoic acid receptor alpha Homo sapiens 9-37
10601023-1 1999 Although retinoic acid receptor alpha (RARalpha) agonists induce the maturation of t(15;17) acute promyelocytic leukemia (APL) cells, drug treatment also selects leukemic blasts expressing PML-RARalpha fusion proteins with mutated ligand-binding domains that no longer respond to all-trans retinoic acid (ATRA). Tretinoin 305-309 retinoic acid receptor alpha Homo sapiens 39-47
10601023-2 1999 Here we report a novel RARalpha-independent signaling pathway that induces maturation of both ATRA-sensitive and ATRA-resistant APL NB4 cells, and does not invoke the ligand-induced alteration of PML-RARalpha signaling, stability or compartmentalization. Tretinoin 94-98 retinoic acid receptor alpha Homo sapiens 23-31
10233362-5 1999 Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation. Tretinoin 237-250 ret proto-oncogene Homo sapiens 106-109
10233362-5 1999 Consistent with this observation, when THP-1 monocytic and HL-60 promyelocytic leukaemia cells expressing Ret were differentiated toward macrophages or granulocytes by treatment of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans retinoic acid (RA), Ret expression strikingly decreased during differentiation. Tretinoin 252-254 ret proto-oncogene Homo sapiens 106-109
10233384-6 1999 Similarly, blasts from this case were found to be sensitive to ATRA in vitro as determined by NBT reduction test and by normalization of the PML nuclear body staining pattern. Tretinoin 63-67 PML nuclear body scaffold Homo sapiens 141-144
10075839-11 1999 As retinoic acid response elements are present in the promoter regions of both tTG and stromelysin-3 genes, we propose that RA might increase the amount of cell death in the INZs through a direct modulation of tTG expression and that it also contributes to the process of tissue remodeling, which accompanies cell death, through an up-regulation of stromelysin-3 expression in the INZs. Tretinoin 3-16 transglutaminase 2, C polypeptide Mus musculus 79-82
10102285-0 1999 Differential inhibition of collagenase and interleukin-1alpha gene expression in cultured corneal fibroblasts by TGF-beta, dexamethasone, and retinoic acid. Tretinoin 142-155 interleukin 1 alpha Homo sapiens 43-61
27626703-3 2016 We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. Tretinoin 23-36 phosphatase and tensin homolog Homo sapiens 130-134
10099141-4 1999 We also determined the effect of all-trans-retinoic acid on the expression of annexin II and the generation of cell-surface plasmin. Tretinoin 33-56 annexin A2 Homo sapiens 78-88
10099141-8 1999 The t(15;17)-positive APL cells contained abundant messenger RNA for annexin II, which disappeared through a transcriptional mechanism after treatment with all-trans-retinoic acid. Tretinoin 156-179 annexin A2 Homo sapiens 69-79
10620391-4 1999 We provide evidence that IBMX, as well as the rod promoting molecules taurine and RA, all act on postmitotic rhodopsin(-)cells to accelerate their differentiation into rhodopsin(+)cells. Tretinoin 82-84 rhodopsin Rattus norvegicus 109-118
10620391-4 1999 We provide evidence that IBMX, as well as the rod promoting molecules taurine and RA, all act on postmitotic rhodopsin(-)cells to accelerate their differentiation into rhodopsin(+)cells. Tretinoin 82-84 rhodopsin Rattus norvegicus 168-177
10582595-7 1999 Furthermore, differentiation of P19 mouse embryonal carcinoma cells to neuronal cells with retinoic acid induced the expression of gamma2 and a decrease of gamma5, the major isoform in the undifferentiated state. Tretinoin 91-104 gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2 Mus musculus 131-137
27626703-3 2016 We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. Tretinoin 23-36 Spi-1 proto-oncogene Homo sapiens 216-220
10068679-14 1999 We conclude that retinoids or combination of retinoids with specificities for both RAR and RXR may markedly enhance the ability of ATRA to inhibit clonal growth and induce differentiation of HL-60 and NB4 leukemic cells. Tretinoin 131-135 retinoic acid receptor alpha Homo sapiens 83-86
27626703-3 2016 We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. Tretinoin 23-36 phosphatase and tensin homolog Homo sapiens 269-273
27626703-3 2016 We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. Tretinoin 38-42 phosphatase and tensin homolog Homo sapiens 130-134
27626703-3 2016 We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. Tretinoin 38-42 Spi-1 proto-oncogene Homo sapiens 216-220
10619646-2 1999 Since the expression of its receptor TrkB can be induced by the transcriptional activator retinoic acid (RA), we have investigated the possibility that RA promotes axonal regeneration of differentiated chick RGC synergistically with BDNF. Tretinoin 90-103 neurotrophic receptor tyrosine kinase 2 Gallus gallus 37-41
10619646-2 1999 Since the expression of its receptor TrkB can be induced by the transcriptional activator retinoic acid (RA), we have investigated the possibility that RA promotes axonal regeneration of differentiated chick RGC synergistically with BDNF. Tretinoin 105-107 neurotrophic receptor tyrosine kinase 2 Gallus gallus 37-41
10092805-6 1999 Dephosphorylation of 4E-BP1 was also observed when U-937 cells were induced to differentiate into monocytes/macrophages following treatment with retinoic acid or DMSO. Tretinoin 145-158 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 21-27
10619646-2 1999 Since the expression of its receptor TrkB can be induced by the transcriptional activator retinoic acid (RA), we have investigated the possibility that RA promotes axonal regeneration of differentiated chick RGC synergistically with BDNF. Tretinoin 152-154 neurotrophic receptor tyrosine kinase 2 Gallus gallus 37-41
10092805-7 1999 In contrast, treatment of HL-60 cells with retinoic acid or DMSO, which results in a granulocytic differentiation of these cells, decreases 4E-BP1 amount without affecting its phosphorylation and strongly increases 4E-BP2 amount. Tretinoin 43-56 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 140-146
10024536-2 1999 In the present study we describe the effects of all-trans-retinoic acid (RA) on the levels of GPT protein and enzymic activity, and on the transcription rate of the GPT gene, in mouse P19 teratocarcinoma cells. Tretinoin 48-71 glutamic pyruvic transaminase, soluble Mus musculus 94-97
10024536-2 1999 In the present study we describe the effects of all-trans-retinoic acid (RA) on the levels of GPT protein and enzymic activity, and on the transcription rate of the GPT gene, in mouse P19 teratocarcinoma cells. Tretinoin 73-75 glutamic pyruvic transaminase, soluble Mus musculus 94-97
10539879-1 1999 The results of the treatment of 43 patients with acute promyelocytic leukemia (PML) are reported: 27 were treated initially with all-trans-retinoic acid (ATRA), whereas 16 were treated with conventional chemotherapy. Tretinoin 129-152 PML nuclear body scaffold Homo sapiens 79-82
27626703-3 2016 We show that All-Trans Retinoic Acid (ATRA) triggers in APL cells an active chromatin status at the core regulatory region of the PTEN promoter, that allows the binding of the myeloid-regulating transcription factor PU.1, and, in turn, the transcriptional induction of PTEN. Tretinoin 38-42 phosphatase and tensin homolog Homo sapiens 269-273
10583214-0 1999 Retinoic acid stimulates plasminogen activator inhibitor 2 production by blood mononuclear cells and inhibits urokinase-induced extracellular proteolysis. Tretinoin 0-13 serpin family B member 2 Homo sapiens 25-58
10024536-4 1999 The maximum induction of GPT activity (about 3-fold) required 2 days of exposure to 1 microM RA. Tretinoin 93-95 glutamic pyruvic transaminase, soluble Mus musculus 25-28
10024536-7 1999 The GPT gene was induced (2-fold) after 7 h of RA treatment. Tretinoin 47-49 glutamic pyruvic transaminase, soluble Mus musculus 4-7
27166374-4 2016 This involves feed forward regulation of Raldh2, a rate-limiting enzyme for RA biosynthesis, and requires Med25 to coordinate RAR, STAT6 and chromatin remodeler, Brg1 to remodel the +1 nucleosome of Arg1 for transcription initiation. Tretinoin 76-78 signal transducer and activator of transcription 6 Homo sapiens 131-136
10024536-10 1999 4-fold increases in the levels of three GPT transcripts (1.8, 2.0 and 2.2 kb) were observed after 2 days of RA treatment. Tretinoin 108-110 glutamic pyruvic transaminase, soluble Mus musculus 40-43
10578180-0 1999 BMP-4 and retinoic acid synergistically induce activation of caspase-9 and cause apoptosis of P19 embryonal carcinoma cells cultured as a monolayer. Tretinoin 10-23 caspase 9 Homo sapiens 61-70
27531891-6 2016 Wnt and retinoic acid co-treatments synergise, representing a promising combination treatment for MYCN-amplified neuroblastoma. Tretinoin 8-21 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 98-102
10493748-6 1999 Exogenous application of retinoic acid induced NRTN responsiveness and Ret protein expression from E9 vestibular ganglion neurons, suggesting that retinoic acid can regulate Ret protein expression in peripheral sensory neurons in vitro. Tretinoin 25-38 ret proto-oncogene Gallus gallus 71-74
10026096-0 1999 Retinoic acid stimulates the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human choriocarcinoma JEG-3 cells. Tretinoin 0-13 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 43-85
10026096-7 1999 Results from semi-quantitative reverse transcription-polymerase chain reaction demonstrated that there was a corresponding increase in 11beta-HSD2 mRNA after RA treatment. Tretinoin 158-160 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 135-146
10026096-9 1999 In conclusion, the present study has demonstrated for the first time that RA, at physiological concentrations, induces 11beta-HSD2 gene expression and enzyme activity in JEG-3 cells. Tretinoin 74-76 hydroxysteroid 11-beta dehydrogenase 2 Homo sapiens 119-130
10493748-6 1999 Exogenous application of retinoic acid induced NRTN responsiveness and Ret protein expression from E9 vestibular ganglion neurons, suggesting that retinoic acid can regulate Ret protein expression in peripheral sensory neurons in vitro. Tretinoin 25-38 ret proto-oncogene Gallus gallus 174-177
10493748-6 1999 Exogenous application of retinoic acid induced NRTN responsiveness and Ret protein expression from E9 vestibular ganglion neurons, suggesting that retinoic acid can regulate Ret protein expression in peripheral sensory neurons in vitro. Tretinoin 147-160 ret proto-oncogene Gallus gallus 71-74
27600527-3 2016 Here we report that ATRA, an active metabolite of vitamin A, restores mechanical quiescence in PSCs via a mechanism involving a retinoic acid receptor beta (RAR-beta)-dependent downregulation of actomyosin (MLC-2) contractility. Tretinoin 20-24 myosin light chain 2 Homo sapiens 207-212
10493748-6 1999 Exogenous application of retinoic acid induced NRTN responsiveness and Ret protein expression from E9 vestibular ganglion neurons, suggesting that retinoic acid can regulate Ret protein expression in peripheral sensory neurons in vitro. Tretinoin 147-160 ret proto-oncogene Gallus gallus 174-177
10706449-6 1999 ATRA decreased the level of phosphorylation of the RB protein at doses > 5 x 10(-9) M and also induced a five fold increase in p21WAF1, while levels of p27KIP1 and CDK2 were unchanged. Tretinoin 0-4 cyclin dependent kinase inhibitor 1B Homo sapiens 155-162
10706449-7 1999 The ATRA-mediated increase in p21 preceded the change in RB phosphorylation and G1 arrest and was not reversed by the addition of exogenous IL-6. Tretinoin 4-8 H3 histone pseudogene 16 Homo sapiens 30-33
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 89-102 retinoic acid receptor alpha Homo sapiens 113-116
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 104-106 retinoic acid receptor alpha Homo sapiens 113-116
10029601-9 1999 Factors relevant to the biology of leukemic growth, such as tumor necrosis factor-alpha (TNF-alpha), 1alpha,25-(OH)2D3, and especially all-trans retinoic acid (ATRA), upregulated HB-EGF mRNA in HL-60 or ML-3 cells. Tretinoin 145-158 heparin binding EGF like growth factor Homo sapiens 179-185
10029601-9 1999 Factors relevant to the biology of leukemic growth, such as tumor necrosis factor-alpha (TNF-alpha), 1alpha,25-(OH)2D3, and especially all-trans retinoic acid (ATRA), upregulated HB-EGF mRNA in HL-60 or ML-3 cells. Tretinoin 160-164 heparin binding EGF like growth factor Homo sapiens 179-185
27626069-3 2016 Thirteen months after the start of ATRA maintenance, the patient suffered clinically overt meningeal relapse along with minute molecular traces of PML/RARA (promyelocytic leukemia/retinoic acid receptor alpha) in the bone marrow. Tretinoin 35-39 PML nuclear body scaffold Homo sapiens 147-155
10084602-2 1999 The aim of this study was to analyze the expression of the CD97 protein in thyroid carcinomas and the role of all-trans-retinoic acid (RA) in the regulation of CD97 protein in monolayer culture of the human follicular thyroid carcinoma cell line FTC-133. Tretinoin 110-133 adhesion G protein-coupled receptor E5 Homo sapiens 160-164
10084602-2 1999 The aim of this study was to analyze the expression of the CD97 protein in thyroid carcinomas and the role of all-trans-retinoic acid (RA) in the regulation of CD97 protein in monolayer culture of the human follicular thyroid carcinoma cell line FTC-133. Tretinoin 135-137 adhesion G protein-coupled receptor E5 Homo sapiens 160-164
10084602-9 1999 Under basal conditions, RA treatment for 72 h led to a decrease in total cell number by 33% and in CD97-positive cells from 50% to 30%. Tretinoin 24-26 adhesion G protein-coupled receptor E5 Homo sapiens 99-103
10488123-3 1999 We found that PAD activity in human myeloid leukemia HL-60 cells was induced with the granulocyte-inducing agents retinoic acid and dimethyl sulfoxide and with the monocyte-inducing agent 1alpha,25-dihydroxyvitamin D(3). Tretinoin 114-127 peptidyl arginine deiminase 4 Homo sapiens 14-17
10479651-11 1999 These studies identify RA as a nuclear signal for MCP-1 induction in undifferentiated human monocytic cells. Tretinoin 23-25 C-C motif chemokine ligand 2 Homo sapiens 50-55
10460485-5 1999 Retinoic acid (RA) treatment will drive these cells to differentiation toward the neuronal lineage and cause an increase in expression of the cyclin-dependent kinase inhibitor p21 protein, which leads to an inhibition in cellular proliferation. Tretinoin 0-13 H3 histone pseudogene 16 Homo sapiens 176-179
10460485-5 1999 Retinoic acid (RA) treatment will drive these cells to differentiation toward the neuronal lineage and cause an increase in expression of the cyclin-dependent kinase inhibitor p21 protein, which leads to an inhibition in cellular proliferation. Tretinoin 15-17 H3 histone pseudogene 16 Homo sapiens 176-179
10495774-12 1999 The expression of the reporter was driven by a retinoic acid response element (RARE) from the RAR beta gene, which was incorporated into the reporter plasmid. Tretinoin 47-60 retinoic acid receptor alpha Homo sapiens 79-82
10469600-6 1999 Misexpression of the normally left-sided signals Nodal, Lefty2 and Shh on the right side, or ectopic application of retinoic acid (RA), resulted in upregulation of NKX3.2 contralateral to its normal expression in left LPM. Tretinoin 116-129 NK3 homeobox 2 Mus musculus 164-170
10469600-6 1999 Misexpression of the normally left-sided signals Nodal, Lefty2 and Shh on the right side, or ectopic application of retinoic acid (RA), resulted in upregulation of NKX3.2 contralateral to its normal expression in left LPM. Tretinoin 131-133 NK3 homeobox 2 Mus musculus 164-170
10509805-0 1999 Opposite regulation of PPAR-alpha and -gamma gene expression by both their ligands and retinoic acid in brown adipocytes. Tretinoin 87-100 peroxisome proliferator activated receptor alpha Homo sapiens 23-44
10509805-6 1999 Both retinoic acid isomers and PPAR agonists, specific for either PPARalpha or PPARgamma, regulate expression of each PPAR subtype gene in the opposite way: they up-regulate PPARalpha and down-regulate PPARgamma. Tretinoin 5-18 peroxisome proliferator activated receptor alpha Homo sapiens 66-75
10509805-6 1999 Both retinoic acid isomers and PPAR agonists, specific for either PPARalpha or PPARgamma, regulate expression of each PPAR subtype gene in the opposite way: they up-regulate PPARalpha and down-regulate PPARgamma. Tretinoin 5-18 peroxisome proliferator activated receptor alpha Homo sapiens 66-70
10509805-6 1999 Both retinoic acid isomers and PPAR agonists, specific for either PPARalpha or PPARgamma, regulate expression of each PPAR subtype gene in the opposite way: they up-regulate PPARalpha and down-regulate PPARgamma. Tretinoin 5-18 peroxisome proliferator activated receptor alpha Homo sapiens 174-183
10447003-0 1999 Posttranslational mechanisms contribute to the suppression of specific cyclin:CDK complexes by all-trans retinoic acid in human bronchial epithelial cells. Tretinoin 105-118 proliferating cell nuclear antigen Homo sapiens 71-77
10428509-8 1999 Simultaneous treatment with G-CSF and zVAD-fmk additively blocked ATRA-induced apoptosis. Tretinoin 66-70 colony stimulating factor 3 Homo sapiens 28-33
10810558-9 1999 The concurrent treatment of dams with 3-MC and RA led to an increased inducibility of cytochrome P-450 and subsequently, CYP1A1 dependent enzyme activity higher than those observed after the injection of 3-MC alone. Tretinoin 47-49 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 121-127
10542138-0 1999 High-cell-density phorbol ester and retinoic acid upregulate involucrin and downregulate suprabasal keratin 10 in autocrine cultures of human epidermal keratinocytes. Tretinoin 36-49 keratin 10 Homo sapiens 100-110
10542138-6 1999 Treatment of confluent keratinocytes with RA downregulates K10, but upregulates involucrin. Tretinoin 42-44 keratin 10 Homo sapiens 59-62
10388516-0 1999 The HNF-3alpha transcription factor is a primary target for retinoic acid action. Tretinoin 60-73 forkhead box A1 Homo sapiens 4-14
10388516-1 1999 We have previously demonstrated that gene expression of the hepatocyte nuclear factor 3alpha (HNF-3alpha) transcription factor is activated during retinoic-acid-induced differentiation of F9 embryonal carcinoma cells (A. Jacob et al. Tretinoin 147-160 forkhead box A1 Homo sapiens 60-92
10388516-1 1999 We have previously demonstrated that gene expression of the hepatocyte nuclear factor 3alpha (HNF-3alpha) transcription factor is activated during retinoic-acid-induced differentiation of F9 embryonal carcinoma cells (A. Jacob et al. Tretinoin 147-160 forkhead box A1 Homo sapiens 94-104
10388516-5 1999 We have extended these studies and now show that HNF-3alpha mRNA is induced approximately 6 h after addition of retinoic acid to the cells, peaks at 1 day postdifferentiation, and then declines to undetectable levels. Tretinoin 112-125 forkhead box A1 Homo sapiens 49-59
10388516-6 1999 Furthermore, HNF-3alpha induction occurs in the absence of de novo protein synthesis, suggesting that it is a primary target for retinoic acid action. Tretinoin 129-142 forkhead box A1 Homo sapiens 13-23
10388516-7 1999 In order to corroborate this hypothesis, we have mapped the cis-acting HNF-3alpha promoter site that mediates the retinoic acid response. Tretinoin 114-127 forkhead box A1 Homo sapiens 71-81
10388516-8 1999 DNA sequence analysis indicates that the HNF-3alpha promoter contains an authentic retinoic acid response element (RARE) of the DR5 class. Tretinoin 83-96 forkhead box A1 Homo sapiens 41-51
10388516-11 1999 Since HNF-3alpha is induced early during mammalian neurogenesis, our data shed new light on the connection between retinoic-acid-mediated HNF-3alpha activation and establishment of the neuronal phenotype. Tretinoin 115-128 forkhead box A1 Homo sapiens 6-16
10388516-11 1999 Since HNF-3alpha is induced early during mammalian neurogenesis, our data shed new light on the connection between retinoic-acid-mediated HNF-3alpha activation and establishment of the neuronal phenotype. Tretinoin 115-128 forkhead box A1 Homo sapiens 138-148
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 88-101 PML nuclear body scaffold Homo sapiens 10-13
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 88-101 retinoic acid receptor alpha Homo sapiens 31-39
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 88-101 PML nuclear body scaffold Homo sapiens 132-135
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 88-101 retinoic acid receptor alpha Homo sapiens 31-39
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 88-101 retinoic acid receptor alpha Homo sapiens 31-39
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 14-16 PML nuclear body scaffold Homo sapiens 10-13
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 14-16 PML nuclear body scaffold Homo sapiens 132-135
10502453-3 1999 Previous studies have demonstrated that these inhibitory effects of RA, and the combination of TNFalpha and IFN-gamma are associated with increased accumulation of IGFBP-3 in the culture medium of HSG cells. Tretinoin 68-70 insulin like growth factor binding protein 3 Homo sapiens 164-171
10502453-7 1999 Retinoic acid with TNFalpha and IFN-gamma had a marked inhibitory effect (P<0.05) which was similarly reversed by increasing concentrations of IGFBP-3 antibody. Tretinoin 0-13 insulin like growth factor binding protein 3 Homo sapiens 146-153
10502453-8 1999 The present data support the hypothesis that the combination of TNFalpha and IFN-gamma with retinoic acid exert their anti-proliferative effect on HSG cells by reducing the mitogenic effect of IGF-I due to a shift in IGF-I from the free to the IGFBP-3-bound form. Tretinoin 92-105 insulin like growth factor binding protein 3 Homo sapiens 244-251
10429659-11 1999 Taken together, these data indicate that the resistance to RA is caused by the mutation in RAR alpha of HL-60-R9, but by other factor(s), which also affect the VD-response pathways, in HL-60-R2. Tretinoin 59-61 retinoic acid receptor alpha Homo sapiens 91-100
10217254-5 1999 It is interesting that in retinoic acid-induced neural differentiated mouse embryonic carcinoma P19 cells, GDAP mRNA expression levels were also up-regulated (except that of GDAP3), ranging from three to >10 times compared with nondifferentiated P19 cells. Tretinoin 26-39 mitochondrial ribosomal protein S33 Mus musculus 174-179
10216260-0 1999 Retinoic acid-dependent upregulation of mouse folate receptor-alpha expression in embryonic stem cells, and conservation of alternative splicing patterns. Tretinoin 0-13 folate receptor 1 (adult) Mus musculus 46-67
10216260-2 1999 We used differential display reverse transcriptase polymerase chain reaction (RT-PCR) to identify RA-responsive genes expressed in embryonic stem (ES) cells and found that murine folate receptor-alpha (FR-alpha) expression is rapidly induced by RA treatment. Tretinoin 98-100 folate receptor 1 (adult) Mus musculus 179-200
10216260-2 1999 We used differential display reverse transcriptase polymerase chain reaction (RT-PCR) to identify RA-responsive genes expressed in embryonic stem (ES) cells and found that murine folate receptor-alpha (FR-alpha) expression is rapidly induced by RA treatment. Tretinoin 245-247 folate receptor 1 (adult) Mus musculus 179-200
10094816-6 1999 Olomoucine, a potent p34(cdc2) and Cdk2 inhibitor, effectively blocked RA-mediated p34(cdc2) kinase activation and prevented RA-induced apoptosis. Tretinoin 71-73 cyclin dependent kinase 1 Homo sapiens 25-29
10094816-6 1999 Olomoucine, a potent p34(cdc2) and Cdk2 inhibitor, effectively blocked RA-mediated p34(cdc2) kinase activation and prevented RA-induced apoptosis. Tretinoin 71-73 cyclin dependent kinase 1 Homo sapiens 87-91
10094816-7 1999 Furthermore, antisense oligonucleotide complementary to p21(CIP2/Waf1) and p34(cdc2) mRNA significantly rescued RA-induced apoptosis. Tretinoin 112-114 cyclin dependent kinase 1 Homo sapiens 79-83
10094816-11 1999 These findings suggest that inappropriate regulation of the cell cycle regulators p21(CIP2/Waf1) and p34(cdc2) is coupled with induction of Bax and involved in cell death with apoptosis when Hep3B cells are exposed to RA. Tretinoin 218-220 cyclin dependent kinase 1 Homo sapiens 105-109
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 3 Homo sapiens 60-65
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 2 Homo sapiens 70-76
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 3 Homo sapiens 93-98
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 3 Homo sapiens 93-98
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 2 Homo sapiens 141-147
10210322-8 1999 However, we found that RA opposed anti-apoptotic effects of G-CSF and GM-CSF on CD34+ cells (G-CSF: 8% dead cells at day 6; G-CSF + RA: 20%; GM-CSF: 12%; GM-CSF + RA: 27%). Tretinoin 23-25 colony stimulating factor 2 Homo sapiens 141-147
10221506-6 1999 Among them, granulocyte colony-stimulating factor (G-CSF) is unique in that it preferentially stimulates clonal growth, but not self-renewal, in many APL cases, and synergistically enhances the differentiation-inducing effect of ATRA when used in combination. Tretinoin 229-233 colony stimulating factor 3 Homo sapiens 12-49
10221506-6 1999 Among them, granulocyte colony-stimulating factor (G-CSF) is unique in that it preferentially stimulates clonal growth, but not self-renewal, in many APL cases, and synergistically enhances the differentiation-inducing effect of ATRA when used in combination. Tretinoin 229-233 colony stimulating factor 3 Homo sapiens 51-56
10354476-2 1999 Here we show that in the early eye vesicle of the mouse embryo, expression of the dorsal dehydrogenase is preceded by, and transiently overlaps with, the RA-degrading oxidase CYP26. Tretinoin 154-156 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 175-180
10354476-3 1999 Subsequently in the embryonic retina, CYP26 forms a narrow horizontal boundary between the dorsal and ventral dehydrogenases, creating a trough between very high ventral and moderately high dorsal RA levels. Tretinoin 197-199 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 38-43
10354476-5 1999 The orphan receptor COUP-TFII, which modulates RA responses, colocalizes with the dorsal dehydrogenase. Tretinoin 47-49 nuclear receptor subfamily 2, group F, member 2 Mus musculus 20-29
10354487-2 1999 The retinoic acid (RA) 4-hydroxylase, belonging to the cytochrome P450 family CYP26, is an enzyme catalyzing the 4-hydroxylation of RA, thereby regulating RA homeostasis. Tretinoin 19-21 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 78-83
10074929-0 1999 Retinoic acid-mediated growth inhibition of small cell lung cancer cells is associated with reduced myc and increased p27Kip1 expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 100-103
10074929-0 1999 Retinoic acid-mediated growth inhibition of small cell lung cancer cells is associated with reduced myc and increased p27Kip1 expression. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 118-125
10074929-5 1999 RA treatment of H209-RAR-beta cells was also accompanied by increased expression of the cdk inhibitor p27Kip1, whereas no differences in the expression of L-myc or p27Kip1 were detected upon RA treatment of parental H209 cells. Tretinoin 0-2 cyclin dependent kinase inhibitor 1B Homo sapiens 102-109
10024536-14 1999 The results indicate that the RA-induced enzyme activity was mainly determined by increased transcription of the GPT gene. Tretinoin 30-32 glutamic pyruvic transaminase, soluble Mus musculus 113-116
10024536-15 1999 RA-treated P19 cells were about 4-fold more resistant to tunicamycin, a fungal antibiotic which inhibits GPT, than were control cells. Tretinoin 0-2 glutamic pyruvic transaminase, soluble Mus musculus 105-108
10024536-16 1999 In addition, GPT activity in membranes from RA-treated P19 cells exhibited approx. Tretinoin 44-46 glutamic pyruvic transaminase, soluble Mus musculus 13-16
10024536-19 1999 Together, the data provide additional insights into the hormonal regulation of GPT and present evidence that the RA-mediated induction of GPT has a regulatory impact on the dolichol pathway. Tretinoin 113-115 glutamic pyruvic transaminase, soluble Mus musculus 79-82
10024536-19 1999 Together, the data provide additional insights into the hormonal regulation of GPT and present evidence that the RA-mediated induction of GPT has a regulatory impact on the dolichol pathway. Tretinoin 113-115 glutamic pyruvic transaminase, soluble Mus musculus 138-141
10029573-0 1999 Constitutive degradation of PML/RARalpha through the proteasome pathway mediates retinoic acid resistance. Tretinoin 81-94 PML nuclear body scaffold Homo sapiens 28-31
10029573-0 1999 Constitutive degradation of PML/RARalpha through the proteasome pathway mediates retinoic acid resistance. Tretinoin 81-94 retinoic acid receptor alpha Homo sapiens 32-40
10029573-2 1999 Treatment with retinoic acid (RA) induces degradation of PML/RARalpha, differentiation of leukaemic blasts, and disease remission. Tretinoin 15-28 PML nuclear body scaffold Homo sapiens 57-60
10029573-2 1999 Treatment with retinoic acid (RA) induces degradation of PML/RARalpha, differentiation of leukaemic blasts, and disease remission. Tretinoin 15-28 retinoic acid receptor alpha Homo sapiens 61-69
10029573-2 1999 Treatment with retinoic acid (RA) induces degradation of PML/RARalpha, differentiation of leukaemic blasts, and disease remission. Tretinoin 30-32 PML nuclear body scaffold Homo sapiens 57-60
10029573-2 1999 Treatment with retinoic acid (RA) induces degradation of PML/RARalpha, differentiation of leukaemic blasts, and disease remission. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 61-69
10029573-8 1999 Similarly, forced expression of PML/RARalpha, but not RARalpha, into the NB4/007.6 cells restored sensitivity to RA treatment to levels comparable to those of the NB4 cells. Tretinoin 36-38 PML nuclear body scaffold Homo sapiens 32-35
10067828-7 1999 Both RBP and PTH/PTHrP inhibited the dedifferentiative activity of RA on growth plate chondrocytes when added to the culture medium. Tretinoin 67-69 parathyroid hormone-related protein Oryctolagus cuniculus 17-22
10067828-8 1999 These results demonstrate that chondrocytes synthesize and secrete RBP in vivo and in vitro and suggest that PTH/PTHrP modulates the effect of RA by means of RBP production in chondrocytes. Tretinoin 143-145 parathyroid hormone-related protein Oryctolagus cuniculus 113-118
10066345-0 1999 The regulatory effects of all-trans-retinoic acid on isotype switching: retinoic acid induces IgA switch rearrangement in cooperation with IL-5 and inhibits IgG1 switching. Tretinoin 26-49 interleukin 5 Mus musculus 139-143
10066345-3 1999 RA alone could not induce switch rearrangement but required the cooperation of IL-5. Tretinoin 0-2 interleukin 5 Mus musculus 79-83
10066345-4 1999 RA has another effect on isotype switching; RA strongly inhibits IL-4-dependent IgG1 and IgE production. Tretinoin 0-2 interleukin 4 Mus musculus 65-69
10066345-4 1999 RA has another effect on isotype switching; RA strongly inhibits IL-4-dependent IgG1 and IgE production. Tretinoin 44-46 interleukin 4 Mus musculus 65-69
10066345-5 1999 To analyze the mechanism of IgG1 inhibition, we tested whether RA can inhibit IL-4-dependent Smu-Sgamma1 switch rearrangement. Tretinoin 63-65 interleukin 4 Mus musculus 78-82
10066345-11 1999 These results indicated that RA can regulate isotype switching at the level of germline transcription and directs switching to IgA with the help of IL-5 and inhibits IgG1 switching. Tretinoin 29-31 interleukin 5 Mus musculus 148-152
10225671-0 1999 Acute myelogenous leukemia with a t(2;17;4)(p13;q21;p16) aberration: effective treatment with all-trans retinoic acid and granulocyte colony-stimulating factor. Tretinoin 104-117 H3 histone pseudogene 6 Homo sapiens 44-47
9973257-1 1999 In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Tretinoin 19-32 retinoic acid receptor alpha Homo sapiens 87-90
9973257-1 1999 In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Tretinoin 34-36 retinoic acid receptor alpha Homo sapiens 87-90
9989778-8 1999 All-trans retinoic acid was effective in reducing the levels of focal adhesion kinase and paxillin protein. Tretinoin 10-23 paxillin Homo sapiens 90-98
9973257-5 1999 Using a mammalian two-hybrid system, we report here that human RARalpha (hRARalpha) can disrupt in a RA-dependent manner the homo- and heterodimerization properties of c-Jun and c-Fos. Tretinoin 63-65 retinoic acid receptor alpha Homo sapiens 73-82
27089940-1 2016 Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. Tretinoin 0-13 forkhead box P3 Mus musculus 61-66
27089940-1 2016 Retinoic acid (RA) in the steady state enhances induction of Foxp3(+) regulatory T (Treg) cells and inhibits differentiation of Th1 and Th17 cells, thereby maintaining tolerance, but can in inflammatory conditions promote effector Th1 and Th17 cells that mediate inflammation. Tretinoin 15-17 forkhead box P3 Mus musculus 61-66
10023688-6 1999 RA treatment led to PLZF/RARalpha degradation. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 25-33
9988753-5 1999 In contrast, only hsp27 can protect dorsal root ganglion neurons from apoptosis induced by nerve growth factor withdrawal, and hsp27 also protects the ND7 neuronal cell line from retinoic acid-induced apoptosis. Tretinoin 179-192 heat shock protein family B (small) member 1 Homo sapiens 127-132
27089940-4 2016 We found that RA had a dramatic suppressive effect on IL-17A and IL-17F production by gammadelta T cells stimulated with IL-1beta and IL-23. Tretinoin 14-16 interleukin 17F Mus musculus 65-71
9949174-1 1999 We recently demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme of de novo cholesterol synthesis, was a potential mediator of the biological effects of retinoic acid on human neuroblastoma cells. Tretinoin 202-215 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 30-87
9935210-6 1999 Here, we show that a synthetic retinoid, CD-271, that activates selectively the RAR gamma subtype in a given context, shows increased anti-proliferative activity against certain carcinoma cells over all-trans-retinoic acid (tRA). Tretinoin 203-222 nerve growth factor receptor Homo sapiens 41-47
9935210-6 1999 Here, we show that a synthetic retinoid, CD-271, that activates selectively the RAR gamma subtype in a given context, shows increased anti-proliferative activity against certain carcinoma cells over all-trans-retinoic acid (tRA). Tretinoin 224-227 nerve growth factor receptor Homo sapiens 41-47
9989277-6 1999 In parallel with this, unesterified retinol and retinoic acid concentrations in SCC were significantly elevated over those in normal cells. Tretinoin 48-61 serpin family B member 3 Homo sapiens 80-83
9989277-10 1999 Challenging cells with increasing medium retinol concentrations resulted in dose-dependent increases in retinol and retinoic acid within SCC. Tretinoin 116-129 serpin family B member 3 Homo sapiens 137-140
27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 85-98 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-192
10599447-10 1999 Relative gene expression before (constitutive) and after treatment with 10 microM all-trans-retinoic acid (aTRA) was measured for androgen and estrogen receptor; a set of genes involved with retinoid metabolism and action, hRAR alpha nd beta, hRXR alpha and beta CRBP, CRABP I and II; and for signaling genes that are known to be sensitive to retinoic acid, EGFR, cytokine MK, ICAM I and transglutaminase. Tretinoin 92-105 retinoic acid receptor alpha Homo sapiens 223-233
10224351-5 1999 Both retinoic acid and corticosteroids were able to downregulate IL-3- and IL-5-induced expression of IL-5R on cord-blood-derived as well as HL-60 cloned Eo-B progenitors. Tretinoin 5-18 interleukin 3 Homo sapiens 65-79
9920669-1 1999 We have studied the effect of retinoic acid on the expression of the neurotrophin receptors trkA, trkC, and p75 by neuroblasts and neurons at different axial levels along the embryonic mouse paravertebral sympathetic chain. Tretinoin 30-43 neurotrophic tyrosine kinase, receptor, type 1 Mus musculus 92-96
27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 85-98 PML nuclear body scaffold Homo sapiens 197-200
9920669-2 1999 In dissociated cultures of sympathetic neuroblasts, retinoic acid inhibited the developmental increase in trkA mRNA expression and the developmental decrease in trkC mRNA expression that normally occurs in these cells but did not affect p75 mRNA expression. Tretinoin 52-65 neurotrophic tyrosine kinase, receptor, type 1 Mus musculus 106-110
9920669-6 1999 The observation that alpha-antagonists increased trkA mRNA expression in intact sympathetic ganglion explants suggests that endogenous retinoic acid is a physiological regulator of trkA receptor expression. Tretinoin 135-148 neurotrophic tyrosine kinase, receptor, type 1 Mus musculus 49-53
9920669-6 1999 The observation that alpha-antagonists increased trkA mRNA expression in intact sympathetic ganglion explants suggests that endogenous retinoic acid is a physiological regulator of trkA receptor expression. Tretinoin 135-148 neurotrophic tyrosine kinase, receptor, type 1 Mus musculus 181-185
9858493-0 1999 Synthesis of retinoic acid by rat ovarian cells that express cellular retinoic acid-binding protein-II. Tretinoin 13-26 cellular retinoic acid binding protein 2 Rattus norvegicus 61-102
9858493-2 1999 We have previously demonstrated that the uterine epithelial cells from the pseudopregnant rat have gained the ability to synthesize retinoic acid from retinol, in correlation with the induced expression of CRABP(II). Tretinoin 132-145 cellular retinoic acid binding protein 2 Rattus norvegicus 206-215
9858493-3 1999 If this is true for other sites of CRABP(II) expression, then local production of retinoic acid is intimately connected with various stages of reproduction in the female. Tretinoin 82-95 cellular retinoic acid binding protein 2 Rattus norvegicus 35-44
10023688-0 1999 Retinoic acid, but not arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in a RA-therapy resistant t(11;17)(q23;q21) APL patient. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 59-67
27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 201-209
9858493-4 1999 Here we report that granulosa cells from the ovary of the eCG-treated immature rat and luteal cells from the ovary of the eCG/hCG-treated immature rat (both of which express CRABP[II]) synthesized markedly higher amounts of retinoic acid when cultured, compared to granulosa cells cultured from the ovary of the prepubertal rat treated with control vehicle. Tretinoin 224-237 cellular retinoic acid binding protein 2 Rattus norvegicus 174-183
9858493-6 1999 These data are consistent with our hypothesis that CRABP(II) expression is associated with retinoic acid synthesis and strengthen the case that local generation of retinoic acid plays an important role in reproduction. Tretinoin 91-104 cellular retinoic acid binding protein 2 Rattus norvegicus 51-60
27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 100-104 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-192
27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 100-104 PML nuclear body scaffold Homo sapiens 197-200
27486764-6 2016 We also show that let-7 microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARalpha through altering miRNA targets. Tretinoin 100-104 retinoic acid receptor alpha Homo sapiens 201-209
9890568-3 1999 To understand the role of human liver cytosolic aldehyde dehydrogenase (ALDH1) in retinoic acid synthesis, we examined the ability of ALDH 1 to catalyze the oxidation of the naturally occurring retinal isomers. Tretinoin 82-95 aldehyde dehydrogenase 1 family member A1 Homo sapiens 72-77
27343556-0 2016 Activation of Notch1 inhibits medial edge epithelium apoptosis in all-trans retinoic acid-induced cleft palate in mice. Tretinoin 76-89 notch 1 Mus musculus 14-20
9880512-3 1999 Retinoic acid, combined with cAMP analogs, sharply induces the Bmp2 mRNA during the differentiation of F9 embryonal carcinoma cells into parietal endoderm. Tretinoin 0-13 bone morphogenetic protein 2 Gallus gallus 63-67
9880512-4 1999 Retinoic acid (RA) also induces the Bmp2 gene in chick limb buds. Tretinoin 0-13 bone morphogenetic protein 2 Gallus gallus 36-40
9880512-4 1999 Retinoic acid (RA) also induces the Bmp2 gene in chick limb buds. Tretinoin 15-17 bone morphogenetic protein 2 Gallus gallus 36-40
9876133-3 1999 In this paper we present a study of the hormone binding/unbinding process in order to clarify the role of some of the amino acid contacts and identify possible pathways of the all-trans retinoic acid binding/unbinding to/from human retinoic acid receptor (hRAR)-gamma. Tretinoin 186-199 retinoic acid receptor alpha Homo sapiens 232-254
9892191-0 1999 Retinoic acid increases tyrosine phosphorylation of focal adhesion kinase and paxillin in MCF-7 human breast cancer cells. Tretinoin 0-13 paxillin Homo sapiens 78-86
9892191-5 1999 Focal adhesion kinase and paxillin, which localize in focal adhesion plaques and may play important roles in the integrin signaling pathway, were identified as the major proteins showing RA-induced tyrosine phosphorylation. Tretinoin 187-189 paxillin Homo sapiens 26-34
9886825-0 1999 Expression of hepatocyte growth factor-like protein is repressed by retinoic acid and enhanced by cyclic adenosine 3",5"-monophosphate response element-binding protein (CREB)-binding protein (CBP). Tretinoin 68-81 LOC105369252 Homo sapiens 14-51
9886825-1 1999 In an effort to understand the molecular mechanisms involved in the regulation of expression of the gene encoding hepatocyte growth factor-like protein (HGFL), it was found that all-trans-retinoic acid dramatically represses expression of the endogenous HGFL gene in HepG2 cells, a human hepatocyte-derived cell line. Tretinoin 182-201 LOC105369252 Homo sapiens 114-151
9886825-1 1999 In an effort to understand the molecular mechanisms involved in the regulation of expression of the gene encoding hepatocyte growth factor-like protein (HGFL), it was found that all-trans-retinoic acid dramatically represses expression of the endogenous HGFL gene in HepG2 cells, a human hepatocyte-derived cell line. Tretinoin 182-201 LOC105369252 Homo sapiens 153-157
9886825-1 1999 In an effort to understand the molecular mechanisms involved in the regulation of expression of the gene encoding hepatocyte growth factor-like protein (HGFL), it was found that all-trans-retinoic acid dramatically represses expression of the endogenous HGFL gene in HepG2 cells, a human hepatocyte-derived cell line. Tretinoin 182-201 LOC105369252 Homo sapiens 254-258
9886825-4 1999 However, the transcriptional coactivator, CREB-binding protein (CBP) coactivates expression of this gene through an indirect interaction with the HNF-4-binding site, and overexpression of CBP in HepG2 cells eliminates retinoic acid repression of reporter gene expression driven by the HGFL promoter. Tretinoin 218-231 LOC105369252 Homo sapiens 285-289
9886825-5 1999 Overexpression of CBP also protects the endogenous HGFL gene from down-regulation by retinoic acid. Tretinoin 85-98 LOC105369252 Homo sapiens 51-55
10094571-6 1999 Retinoic acid (RA) has a specific effect on brown adipose tissue, because it activates transcription of the gene for uncoupling protein-1, responsible for brown fat thermogenesis. Tretinoin 0-13 uncoupling protein 1 Homo sapiens 117-137
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 115-128 retinoic acid receptor alpha Homo sapiens 253-275
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 115-128 retinoic acid receptor alpha Homo sapiens 277-280
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 130-132 retinoic acid receptor alpha Homo sapiens 253-275
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 130-132 retinoic acid receptor alpha Homo sapiens 277-280
10609868-3 1999 Both RAR and VDR form heterodimers preferentially with the nuclear receptor for 9-cis RA, referred to as the retinoid X receptor (RXR), but functional RAR-VDR heterodimers have also been observed. Tretinoin 5-7 retinoic acid receptor alpha Homo sapiens 151-154
27343556-4 2016 Notch1 was up-regulated in MEE cells in the atRA-treated group compared with the controls at E15.0, together with reduced apoptosis and elevated proliferation. Tretinoin 44-48 notch 1 Mus musculus 0-6
9888458-0 1999 Retinoic acid modulates prolactin receptor expression and prolactin-induced STAT-5 activation in breast cancer cells in vitro. Tretinoin 0-13 signal transducer and activator of transcription 5A Homo sapiens 76-82
10027563-5 1999 An accompanying effect of RA was to sustain or up-regulate trkA, trkB, trkC, and p75NGFR expression. Tretinoin 26-28 neurotrophic receptor tyrosine kinase 3 Rattus norvegicus 71-75
27343556-6 2016 Our results revealed that down-regulation of Notch1 partially rescued the inhibition of atRA-induced palate fusion. Tretinoin 88-92 notch 1 Mus musculus 45-51
9888458-6 1999 Pretreatment with retinoic acid also reduced the prolactin-/prolactin receptor-dependent signal transduction and activation of transcription 5 (STAT-5) activation in T47D cells. Tretinoin 18-31 signal transducer and activator of transcription 5A Homo sapiens 89-142
9888458-6 1999 Pretreatment with retinoic acid also reduced the prolactin-/prolactin receptor-dependent signal transduction and activation of transcription 5 (STAT-5) activation in T47D cells. Tretinoin 18-31 signal transducer and activator of transcription 5A Homo sapiens 144-150
27343556-9 2016 Moreover, inhibition of Rbpj expression partially reversed atRA-induced MEE persistence and increased P21 expression. Tretinoin 59-63 recombination signal binding protein for immunoglobulin kappa J region Mus musculus 24-28
27343556-10 2016 These findings demonstrate that atRA inhibits MEE degradation, which in turn induces a cleft palate, possibly through the Notch1/RBPjk/P21 signaling pathway. Tretinoin 32-36 notch 1 Mus musculus 122-128
10625211-5 1999 In the mean time, concerning expression of TF antigens, if at all, only a very slight decrease was observed by costimulation with estradiol-17beta and MK4 in U937 and NB4 cells, whereas all-trans-retinoic acid (ATRA) showed a remarkable decrease in surface TF antigen levels in NB4 cells and also a modest decrease in U937 cells. Tretinoin 189-209 coagulation factor III, tissue factor Homo sapiens 43-45
27343556-10 2016 These findings demonstrate that atRA inhibits MEE degradation, which in turn induces a cleft palate, possibly through the Notch1/RBPjk/P21 signaling pathway. Tretinoin 32-36 recombination signal binding protein for immunoglobulin kappa J region Mus musculus 129-134
10625211-5 1999 In the mean time, concerning expression of TF antigens, if at all, only a very slight decrease was observed by costimulation with estradiol-17beta and MK4 in U937 and NB4 cells, whereas all-trans-retinoic acid (ATRA) showed a remarkable decrease in surface TF antigen levels in NB4 cells and also a modest decrease in U937 cells. Tretinoin 211-215 coagulation factor III, tissue factor Homo sapiens 43-45
9858142-2 1998 Here we report that mRNA expression of heparin-binding EGF-like growth factor (HB-EGF), a member of the EGF family of growth factors, is induced by RA in human keratinocytes and skin, and is overexpressed in the context of epidermal hyperplasia in vivo. Tretinoin 148-150 heparin binding EGF like growth factor Homo sapiens 39-77
9858142-2 1998 Here we report that mRNA expression of heparin-binding EGF-like growth factor (HB-EGF), a member of the EGF family of growth factors, is induced by RA in human keratinocytes and skin, and is overexpressed in the context of epidermal hyperplasia in vivo. Tretinoin 148-150 heparin binding EGF like growth factor Homo sapiens 79-85
9858142-3 1998 Treatment of normal adult human keratinocytes with micromolar concentrations of RA significantly induced the expression of HB-EGF. Tretinoin 80-82 heparin binding EGF like growth factor Homo sapiens 123-129
9858142-5 1998 RA also enhanced the induction of HB-EGF mRNA in human skin organ culture, an ex vivo model system displaying many similarities to wound healing in vivo. Tretinoin 0-2 heparin binding EGF like growth factor Homo sapiens 34-40
10505667-5 1999 Three short but complex modules, within 400 bp from the transcription initiation site of the mouse LF gene, contain the response elements that are responsible for estrogen, retinoic acid, mitogen, and growth factor stimulation. Tretinoin 173-186 lactotransferrin Mus musculus 99-101
10208011-5 1999 In the nucleus, the RA signal is transduced by binding to a heterodimeric pair of retinoid receptors (RAR/RXR). Tretinoin 20-22 retinoic acid receptor alpha Homo sapiens 102-105
9858142-6 1998 HB-EGF transcripts were markedly increased in human skin by topical treatment with RA under conditions known to provoke epidermal hyperplasia. Tretinoin 83-85 heparin binding EGF like growth factor Homo sapiens 0-6
27307294-9 2016 All-trans retinoic acid increased CD38 levels and decreased CD55 and CD59 expression on MM cells from patients who developed daratumumab resistance, to approximately pretreatment values. Tretinoin 10-23 CD38 molecule Homo sapiens 34-38
9858142-8 1998 These results support the hypothesis that the effects of RA on epidermal hyperplasia are mediated at least in part by HB-EGF, and suggest that signal transduction mechanisms other than or in addition to nuclear RA receptors contribute to this effect. Tretinoin 57-59 heparin binding EGF like growth factor Homo sapiens 118-124
9811861-2 1998 Here, we show that RA, after 2-3 h of incubation with cultured neonatal-rat cardiac fibroblasts, dramatically alters the intracellular distribution of M6P/IGF2R as well as that of cathepsin B (a lysosomal protease bearing M6P). Tretinoin 19-21 cathepsin B Rattus norvegicus 180-191
12142928-1 1999 P19 EC cells can be induced to differentiate into neurons in vitro when they were treated with 1x10(-6) mol/L retinoic acid. Tretinoin 110-123 interleukin 23 subunit alpha Homo sapiens 0-3
9852056-1 1998 The diverse biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, beta and gamma) and retinoid X receptors (RXR alpha, beta, and gamma). Tretinoin 34-47 retinoic acid receptor alpha Homo sapiens 94-172
9852056-1 1998 The diverse biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, beta and gamma) and retinoid X receptors (RXR alpha, beta, and gamma). Tretinoin 49-51 retinoic acid receptor alpha Homo sapiens 94-172
9827903-0 1998 All-trans-retinoic acid up-regulates CD38 but not c-Kit antigens on human marrow CD34+ cells without recruitment into cell cycle. Tretinoin 0-23 CD38 molecule Homo sapiens 37-41
9852056-3 1998 Previously we have demonstrated the importance for RA binding and RA-dependent transactivation of Arg276 of RARalpha alone and in RARbeta Arg269 in conjunction with Lys220. Tretinoin 51-53 retinoic acid receptor alpha Homo sapiens 108-116
9827903-2 1998 Moreover ATRA induces CD38 antigen overexpression on these cells. Tretinoin 9-13 CD38 molecule Homo sapiens 22-26
27256846-0 2016 The BRPF2/BRD1-MOZ complex is involved in retinoic acid-induced differentiation of embryonic stem cells. Tretinoin 42-55 K(lysine) acetyltransferase 6A Mus musculus 15-18
9827903-10 1998 Contrary to steady-state cells, CD34+ cells treated with pharmacological doses of ATRA alone displayed CD38 over-expression without change in c-Kit levels and cycle status, suggesting an absence of maturation pressure. Tretinoin 82-86 CD38 molecule Homo sapiens 103-107
9826179-3 1998 We found CRBP to be expressed in the choroid plexus and, in an in-vitro assay, addition of recombinant CRBP to RALDH-2 increased RA synthesis from retinaldehyde, with the amount of increase depending on the CRBP/retinaldehyde ratio. Tretinoin 111-113 retinol binding protein 1, cellular Mus musculus 9-13
9826179-3 1998 We found CRBP to be expressed in the choroid plexus and, in an in-vitro assay, addition of recombinant CRBP to RALDH-2 increased RA synthesis from retinaldehyde, with the amount of increase depending on the CRBP/retinaldehyde ratio. Tretinoin 111-113 retinol binding protein 1, cellular Mus musculus 103-107
9826179-3 1998 We found CRBP to be expressed in the choroid plexus and, in an in-vitro assay, addition of recombinant CRBP to RALDH-2 increased RA synthesis from retinaldehyde, with the amount of increase depending on the CRBP/retinaldehyde ratio. Tretinoin 111-113 retinol binding protein 1, cellular Mus musculus 103-107
9852056-3 1998 Previously we have demonstrated the importance for RA binding and RA-dependent transactivation of Arg276 of RARalpha alone and in RARbeta Arg269 in conjunction with Lys220. Tretinoin 66-68 retinoic acid receptor alpha Homo sapiens 108-116
9852056-8 1998 It is likely that Lys236 in RARgamma and its homologs in RARalpha and RARbeta are solvent exposed rather than pointing into the RA-binding pocket. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 57-65
18505519-1 1998 The influence of all-trans retinoic acid (RA), either in its free or encapsulated form into wheat ceramides (CER), on the production of collagenase (MMP-1), and tissue inhibitor of metalloproteinase (TIMP-1) by human skin fibroblasts (HSF) at early and late stages of their proliferative life span (PLS) was examined. Tretinoin 17-40 matrix metallopeptidase 1 Homo sapiens 149-154
18505519-1 1998 The influence of all-trans retinoic acid (RA), either in its free or encapsulated form into wheat ceramides (CER), on the production of collagenase (MMP-1), and tissue inhibitor of metalloproteinase (TIMP-1) by human skin fibroblasts (HSF) at early and late stages of their proliferative life span (PLS) was examined. Tretinoin 42-44 matrix metallopeptidase 1 Homo sapiens 149-154
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 10-23 matrix metallopeptidase 1 Homo sapiens 80-85
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 10-23 matrix metallopeptidase 1 Homo sapiens 223-228
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 176-178 matrix metallopeptidase 1 Homo sapiens 80-85
18505519-3 1998 All-trans retinoic acid significantly decreased and increased the secretions of MMP-1 and TIMP-1 respectively, in a dose-dependent manner, from 10-7 m to 10-5 m. Entrapment of RA into CER vesicles potentiated its effect on MMP-1 and TIMP-1 secretions by HSF, independently of cell passages. Tretinoin 176-178 matrix metallopeptidase 1 Homo sapiens 223-228
18505519-4 1998 The extent of variations obtained on MMP-1 and TIMP-1 levels, when HSF culture medium was supplemented with 10-5 m RA, could be obtained using a 100-fold lower concentration of RA encapsulated into CER vesicles. Tretinoin 115-117 matrix metallopeptidase 1 Homo sapiens 37-42
18505519-4 1998 The extent of variations obtained on MMP-1 and TIMP-1 levels, when HSF culture medium was supplemented with 10-5 m RA, could be obtained using a 100-fold lower concentration of RA encapsulated into CER vesicles. Tretinoin 177-179 matrix metallopeptidase 1 Homo sapiens 37-42
9770359-3 1998 In order to begin to understand the tissue-specific roles of these interacting factors, we determined the expression pattern and activity of the pRB, E2F, cyclin, cdk, and CKI families of cell cycle regulatory proteins during retinoic acid-induced (neuronal pathway) and DMSO-induced (cardiac muscle pathway) differentiation of the pluripotent murine embryonal carcinoma cell line, P19. Tretinoin 226-239 choline kinase alpha Homo sapiens 172-175
9778041-2 1998 PML/RAR alpha expression is linked to leukemogenesis and to clinical sensitivity to all-trans retinoic acid (RA). Tretinoin 94-107 PML nuclear body scaffold Homo sapiens 0-13
27531765-1 2016 OBJECTIVE: To explore effect of all-trans retinoic acid(ATRA) on annexin II expression in NB4 cells and to analyze the luciferase activity of annexinII promoter in condition of ATRA-induced treatment. Tretinoin 32-55 annexin A2 Homo sapiens 65-75
9746761-0 1998 Caspases mediate retinoic acid-induced degradation of the acute promyelocytic leukemia PML/RARalpha fusion protein. Tretinoin 17-30 retinoic acid receptor alpha Homo sapiens 91-99
9746761-1 1998 All-trans-retinoic acid (RA) treatment induces morphological remission in acute promyelocytic leukemia (APL) patients carrying the t(15;17) and expressing the PML/RARalpha product by inducing terminal differentiation of the leukemic clone. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 159-162
27445154-8 2016 Using both gain and loss of RA signaling approaches, we show that RA signaling in brain endothelial cells can inhibit WNT-beta-catenin transcriptional activity and that this is required to moderate the expression of WNT target Sox17. Tretinoin 28-30 SRY (sex determining region Y)-box 17 Mus musculus 227-232
9746761-1 1998 All-trans-retinoic acid (RA) treatment induces morphological remission in acute promyelocytic leukemia (APL) patients carrying the t(15;17) and expressing the PML/RARalpha product by inducing terminal differentiation of the leukemic clone. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 163-171
9746761-1 1998 All-trans-retinoic acid (RA) treatment induces morphological remission in acute promyelocytic leukemia (APL) patients carrying the t(15;17) and expressing the PML/RARalpha product by inducing terminal differentiation of the leukemic clone. Tretinoin 25-27 PML nuclear body scaffold Homo sapiens 159-162
9746761-1 1998 All-trans-retinoic acid (RA) treatment induces morphological remission in acute promyelocytic leukemia (APL) patients carrying the t(15;17) and expressing the PML/RARalpha product by inducing terminal differentiation of the leukemic clone. Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 163-171
9746761-2 1998 RA treatment induces downregulation of PML/RARalpha and reorganization of the PML-nuclear bodies. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 39-42
9746761-2 1998 RA treatment induces downregulation of PML/RARalpha and reorganization of the PML-nuclear bodies. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 43-51
9746761-2 1998 RA treatment induces downregulation of PML/RARalpha and reorganization of the PML-nuclear bodies. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 78-81
9746761-4 1998 Here, we show that in the APL-derived NB4 cell line as well as in myeloid precursor U937 cells expressing the PML/RARalpha (U937/PR9) and in blasts from APL patients, the PML/RARalpha fusion protein is cleaved by a caspase 3-like activity induced by RA treatment. Tretinoin 114-116 PML nuclear body scaffold Homo sapiens 110-113
9869047-10 1998 A transcriptional reduction of the N-myc gene by retinoic acid (RA) decreased the motility, which thus resulted in a marked decline of invasiveness in IMR-32 and GOTO. Tretinoin 49-62 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-40
9869047-10 1998 A transcriptional reduction of the N-myc gene by retinoic acid (RA) decreased the motility, which thus resulted in a marked decline of invasiveness in IMR-32 and GOTO. Tretinoin 64-66 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-40
9819390-8 1998 This result suggests that expression of Aldh1 protein is negatively regulated by Hox11 and that abnormal expression of Aldh1 in Hox11 null mice may cause loss of splenic precursor cells by aberrant retinoic acid metabolism. Tretinoin 198-211 homeobox A7 Mus musculus 128-133
27445154-8 2016 Using both gain and loss of RA signaling approaches, we show that RA signaling in brain endothelial cells can inhibit WNT-beta-catenin transcriptional activity and that this is required to moderate the expression of WNT target Sox17. Tretinoin 66-68 SRY (sex determining region Y)-box 17 Mus musculus 227-232
9746761-5 1998 In fact, a caspase 3-like activity is detectable in PML/RARalpha expressing cells after RA treatment, and selective caspase inhibitor peptides are able to prevent the RA-induced degradation of the fusion protein in vivo and in vitro. Tretinoin 56-58 PML nuclear body scaffold Homo sapiens 52-55
9746761-5 1998 In fact, a caspase 3-like activity is detectable in PML/RARalpha expressing cells after RA treatment, and selective caspase inhibitor peptides are able to prevent the RA-induced degradation of the fusion protein in vivo and in vitro. Tretinoin 88-90 PML nuclear body scaffold Homo sapiens 52-55
27445154-14 2016 Therefore, RA may act as a "brake" on endothelial WNT signaling and Sox17 to ensure normal brain vascular development. Tretinoin 11-13 SRY (sex determining region Y)-box 17 Mus musculus 68-73
9746761-5 1998 In fact, a caspase 3-like activity is detectable in PML/RARalpha expressing cells after RA treatment, and selective caspase inhibitor peptides are able to prevent the RA-induced degradation of the fusion protein in vivo and in vitro. Tretinoin 88-90 retinoic acid receptor alpha Homo sapiens 56-64
9746761-7 1998 The extent of PML/RARalpha cleavage directly correlates with the ability of RA to restore the normal PML nuclear bodies (NBs) pattern. Tretinoin 18-20 PML nuclear body scaffold Homo sapiens 101-104
9822698-5 1998 We show that the expression levels of proteins that bind to the beta-retinoic acid response element (RAR/retinoid X receptors and orphan receptors) and also the differential expression of a number of coactivators modulate the RA response on both natural and synthetic reporters. Tretinoin 64-82 retinoic acid receptor alpha Homo sapiens 101-104
9746761-9 1998 These results indicate that PML/RARalpha is directly involved in conferring RA sensitivity of APL cells and that the RA-induced reassembly of PML NBs is the consequence of the disappearance of PML/RARalpha. Tretinoin 76-78 PML nuclear body scaffold Homo sapiens 28-31
27130522-0 2016 Retinoic acid induces nuclear FAK translocation and reduces breast cancer cell adhesion through Moesin, FAK, and Paxillin. Tretinoin 0-13 paxillin Homo sapiens 113-121
9746761-9 1998 These results indicate that PML/RARalpha is directly involved in conferring RA sensitivity of APL cells and that the RA-induced reassembly of PML NBs is the consequence of the disappearance of PML/RARalpha. Tretinoin 76-78 retinoic acid receptor alpha Homo sapiens 32-40
9731743-6 1998 RA also increased TGF-beta2 mRNA expression; we have previously shown that RA upregulates TGF-beta3 mRNA in these cells. Tretinoin 0-2 transforming growth factor, beta 3 Mus musculus 90-99
9731565-7 1998 To investigate the molecular mechanism of the effects of RA, we evaluated the expression of two proteins, c-myc and p53, which are known to be involved in both cell differentiation and apoptosis. Tretinoin 57-59 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 116-119
9699512-8 1998 The RAR alpha-specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXR alpha in mediating the biological effects of retinoids on JEG-3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. Tretinoin 257-259 retinoic acid receptor alpha Homo sapiens 4-13
9828104-7 1998 Total amounts of lamins A/C and cytoplasmic vimentin were reduced by RA treatment. Tretinoin 69-71 vimentin Homo sapiens 44-52
9813049-6 1998 The order of potency of different ligands to compete against 55Fe-hemin binding to p22 HBP was hemin = protoporphyrin IX > coproporphyrin III > bilirubin > palmitic acid > all-trans-retinoic acid. Tretinoin 184-207 heme binding protein 1 Mus musculus 83-90
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 44-57 retinoic acid receptor alpha Homo sapiens 97-100
27130522-2 2016 In previous works we have demonstrated that retinoic acid (RA), the main retinoic acid receptor (RAR) ligand, is involved in the metastatic process by inhibiting migration through a reduced expression of the specific migration-related proteins Moesin, c-Src, and FAK. Tretinoin 59-61 retinoic acid receptor alpha Homo sapiens 97-100
27130522-4 2016 Here we identify that the administration of 10(-6) M RA (10-20 min) induces the activation of the migration-related proteins Moesin, FAK, and Paxillin in T-47D breast cancer cells. Tretinoin 53-55 paxillin Homo sapiens 142-150
9694705-0 1998 Leukemic cellular retinoic acid resistance and missense mutations in the PML-RARalpha fusion gene after relapse of acute promyelocytic leukemia from treatment with all-trans retinoic acid and intensive chemotherapy. Tretinoin 174-187 PML nuclear body scaffold Homo sapiens 73-76
27130522-5 2016 The phosphorylation exerted by the selective agonists for RARalpha and RARbeta, on Moesin, FAK, and Paxillin was comparable to the activation exerted by RA. Tretinoin 58-60 paxillin Homo sapiens 100-108
9694705-0 1998 Leukemic cellular retinoic acid resistance and missense mutations in the PML-RARalpha fusion gene after relapse of acute promyelocytic leukemia from treatment with all-trans retinoic acid and intensive chemotherapy. Tretinoin 174-187 retinoic acid receptor alpha Homo sapiens 77-85
9694705-1 1998 This study evaluated whether relapse of acute promyelocytic leukemia (APL) patients from clinical remissions achieved and/or maintained with all-trans retinoic acid (RA) in combination with intensive chemotherapy is associated with leukemic cellular resistance to RA and with alterations in the PML-RARalpha fusion gene. Tretinoin 166-168 PML nuclear body scaffold Homo sapiens 295-298
9806904-10 1998 Additions of polyclonal rabbit antiserum for human GSTP1-1 to the reaction resulted in a significant decrease in generation of t-RA (70-80%). Tretinoin 127-131 glutathione S-transferase pi 1 Homo sapiens 51-58
9806904-11 1998 In addition, ethacrynic acid, a selective substrate for Pi isoforms of GST, also inhibited the isomerization of 13-cRA to t-RA catalysed by GSTP1-1. Tretinoin 122-126 glutathione S-transferase pi 1 Homo sapiens 140-147
9806904-12 1998 Under the same reaction conditions, GSTP1-1 was much less effective in catalysing the steric conversion of 9-cis-retinoic acid to t-RA, indicating that the enzyme was stereospecific for the conversion of 13-cRA to t-RA. Tretinoin 130-134 glutathione S-transferase pi 1 Homo sapiens 36-43
9694705-1 1998 This study evaluated whether relapse of acute promyelocytic leukemia (APL) patients from clinical remissions achieved and/or maintained with all-trans retinoic acid (RA) in combination with intensive chemotherapy is associated with leukemic cellular resistance to RA and with alterations in the PML-RARalpha fusion gene. Tretinoin 166-168 retinoic acid receptor alpha Homo sapiens 299-307
26868909-5 2016 Studies showed that miR-17-92 cluster regulation was, surprisingly, independent of transcription factors c-MYC and E2F in these cells; instead all-trans-retinoic acid (ATRA), a drug used for terminally differentiating AML subtypes, markedly suppressed miR-17-92 expression and increased PHLPP2 protein levels and phosphatase activity. Tretinoin 147-166 miR-17-92a-1 cluster host gene Homo sapiens 20-29
9694705-10 1998 We conclude that APL cellular resistance occurs with high incidence after relapse from RA + DA therapy administered in a nonconcurrent manner and that mutations in the RARalpha region of the PML-RARalpha gene are present in and likely mechanistically involved in RA resistance in a subset of these cases. Tretinoin 87-89 PML nuclear body scaffold Homo sapiens 191-194
9792441-1 1998 Expression of CD95 (Apo-1/Fas) ligand and its two receptor isoforms, in response to all-trans retinoic acid and interferon gamma (IFNgamma), was analyzed atthe mRNA and protein levels in human Tera-2 embryonal carcinoma cells. Tretinoin 94-107 Fas cell surface death receptor Homo sapiens 14-18
9804832-0 1998 c-Myc is a major mediator of the synergistic growth inhibitory effects of retinoic acid and interferon in breast cancer cells. Tretinoin 74-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
9804832-3 1998 In MCF-7 cells, all-trans-retinoic acid potentiated the effects of interferon-alpha by up-regulating the expression of the RNA-dependent protein kinase (PKR). Tretinoin 16-39 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 153-156
9804832-7 1998 When c-Myc was overexpressed ectopically via a c-Myc expression vector, MCF-7 cells became resistant to growth inhibition by all-trans-retinoic acid plus interferon-alpha. Tretinoin 125-148 MYC proto-oncogene, bHLH transcription factor Homo sapiens 5-10
9792441-1 1998 Expression of CD95 (Apo-1/Fas) ligand and its two receptor isoforms, in response to all-trans retinoic acid and interferon gamma (IFNgamma), was analyzed atthe mRNA and protein levels in human Tera-2 embryonal carcinoma cells. Tretinoin 94-107 Fas cell surface death receptor Homo sapiens 20-25
9792441-2 1998 Exposure of Tera-2 cells to all-trans retinoic acid for up to 16 days led to a decrease of CD95 ligand expression when compared to the control conditions, whereas expression of both CD95 isoforms increased. Tretinoin 38-51 Fas cell surface death receptor Homo sapiens 91-95
9804832-7 1998 When c-Myc was overexpressed ectopically via a c-Myc expression vector, MCF-7 cells became resistant to growth inhibition by all-trans-retinoic acid plus interferon-alpha. Tretinoin 125-148 MYC proto-oncogene, bHLH transcription factor Homo sapiens 47-52
26868909-5 2016 Studies showed that miR-17-92 cluster regulation was, surprisingly, independent of transcription factors c-MYC and E2F in these cells; instead all-trans-retinoic acid (ATRA), a drug used for terminally differentiating AML subtypes, markedly suppressed miR-17-92 expression and increased PHLPP2 protein levels and phosphatase activity. Tretinoin 168-172 miR-17-92a-1 cluster host gene Homo sapiens 20-29
9804832-8 1998 These experiments define the following pathway as a major pathway in the synergistic growth inhibition of MCF-7 cells by all-trans-retinoic acid plus interferon-alpha: all-trans-retinoic acid + interferon-alpha --> upward arrow double-stranded RNA-dependent protein kinase --> downward arrow c-Myc --> cell growth inhibition. Tretinoin 131-144 MYC proto-oncogene, bHLH transcription factor Homo sapiens 298-303
9792441-2 1998 Exposure of Tera-2 cells to all-trans retinoic acid for up to 16 days led to a decrease of CD95 ligand expression when compared to the control conditions, whereas expression of both CD95 isoforms increased. Tretinoin 38-51 Fas cell surface death receptor Homo sapiens 182-186
9792441-3 1998 These changes were functionally significant since Tera-2 cells treated with all-trans retinoic acid for six to 16 days were more susceptible to CD95-mediated apoptosis. Tretinoin 86-99 Fas cell surface death receptor Homo sapiens 144-148
9716179-10 1998 RXR-gamma expression produced significant reduction in levels of RA-responsive genes including the cyclin-dependent kinase inhibitors p21Cip1/WAF1 and p27Kip1, resulting in increased cdc2 and cdk2 kinase activity and RB phosphorylation. Tretinoin 65-67 cyclin dependent kinase inhibitor 1B Homo sapiens 151-158
9716180-3 1998 Stable introduction of different RA receptor (RAR) subtypes in HCT 116 cells showed that CYP26 expression is dependent on RARalpha and RARgamma and, to a lesser extent, on RARbeta and closely paralleled RA metabolism, suggesting that it represents the major RA 4-hydroxylase in these human cells. Tretinoin 33-35 retinoic acid receptor alpha Homo sapiens 46-49
9823968-7 1998 Furthermore, all-trans-retinoic acid-mediated growth inhibition and transactivation was completely blocked by the RAR-alpha-specific antagonist Ro 41-5253. Tretinoin 13-36 retinoic acid receptor, alpha Rattus norvegicus 114-123
26868909-5 2016 Studies showed that miR-17-92 cluster regulation was, surprisingly, independent of transcription factors c-MYC and E2F in these cells; instead all-trans-retinoic acid (ATRA), a drug used for terminally differentiating AML subtypes, markedly suppressed miR-17-92 expression and increased PHLPP2 protein levels and phosphatase activity. Tretinoin 168-172 miR-17-92a-1 cluster host gene Homo sapiens 252-261
26868909-5 2016 Studies showed that miR-17-92 cluster regulation was, surprisingly, independent of transcription factors c-MYC and E2F in these cells; instead all-trans-retinoic acid (ATRA), a drug used for terminally differentiating AML subtypes, markedly suppressed miR-17-92 expression and increased PHLPP2 protein levels and phosphatase activity. Tretinoin 168-172 PH domain and leucine rich repeat protein phosphatase 2 Homo sapiens 287-293
26868909-6 2016 Finally, we demonstrate that the effect of ATRA on miR-17-92 expression is mediated through its target, transcription factor C/EBPbeta, which interacts with the intronic promoter of the miR-17-92 gene to inhibit transactivation of the cluster. Tretinoin 43-47 miR-17-92a-1 cluster host gene Homo sapiens 51-60
9783809-4 1998 In the present study, we examined the effect of RA on IL-1beta and IL-1ra production by human alveolar macrophages in order to clarify the mechanism in pulmonary infiltration of neutrophils, since IL-1 has been shown to initiate neutrophil recruitment into the lung through up-regulated expression of adhesion molecules on vascular endothelium. Tretinoin 48-50 interleukin 1 receptor antagonist Homo sapiens 67-73
9669522-6 1998 Comparison of the DNA sequence of the promoter and coding regions with that of the rat epididymal secretory protein I (ESP I) gene showed that the mE-RABP gene is the orthologue of the ESP I gene that encodes a rat epididymal retinoic acid-binding protein. Tretinoin 226-239 lipocalin 5 Rattus norvegicus 119-124
9669522-6 1998 Comparison of the DNA sequence of the promoter and coding regions with that of the rat epididymal secretory protein I (ESP I) gene showed that the mE-RABP gene is the orthologue of the ESP I gene that encodes a rat epididymal retinoic acid-binding protein. Tretinoin 226-239 lipocalin 5 Mus musculus 147-154
9669522-6 1998 Comparison of the DNA sequence of the promoter and coding regions with that of the rat epididymal secretory protein I (ESP I) gene showed that the mE-RABP gene is the orthologue of the ESP I gene that encodes a rat epididymal retinoic acid-binding protein. Tretinoin 226-239 lipocalin 5 Rattus norvegicus 185-190
9783809-5 1998 RA enhanced IL-1beta and inhibited IL-1ra production by 4beta phorbol 12beta-myristate-13alpha acetate (PMA)- and lipopolysaccharide (LPS)-stimulated human alveolar macrophages. Tretinoin 0-2 interleukin 1 receptor antagonist Homo sapiens 35-41
26868909-6 2016 Finally, we demonstrate that the effect of ATRA on miR-17-92 expression is mediated through its target, transcription factor C/EBPbeta, which interacts with the intronic promoter of the miR-17-92 gene to inhibit transactivation of the cluster. Tretinoin 43-47 miR-17-92a-1 cluster host gene Homo sapiens 186-195
28591946-9 2016 The serum levels of TNF-alpha, IFN-gamma and IL-17A were decreased in both ATRA groups; ATRA also can increase the serum level of IL-4. Tretinoin 75-79 interferon gamma Rattus norvegicus 31-40
28591946-9 2016 The serum levels of TNF-alpha, IFN-gamma and IL-17A were decreased in both ATRA groups; ATRA also can increase the serum level of IL-4. Tretinoin 75-79 interleukin 17A Rattus norvegicus 45-51
9922051-9 1998 HOX B6 mRNA expression in HL-60, NB4, and NKM-1 cultured with ATRA increased on day 3 and decreased on day 5. Tretinoin 62-66 homeobox B6 Homo sapiens 0-6
9651402-3 1998 Here we demonstrate that retinoic acid can induce the accumulation of alphaB-crystallin in N/N1003A lens cells and that retinoic acid receptor heterodimers (retinoic acid receptor/retinoid X receptor; RAR/RXR) can transactivate LSR1 and LSR2 in cotransfection experiments. Tretinoin 25-38 alpha-crystallin B chain Oryctolagus cuniculus 70-87
27107124-1 2016 UNLABELLED: A novel bacterial aldehyde dehydrogenase (ALDH) that converts retinal to retinoic acid was first identified in Bacillus cereus The amino acid sequence of ALDH from B. cereus (BcALDH) was more closely related to mammalian ALDHs than to bacterial ALDHs. Tretinoin 85-98 aldehyde dehydrogenase 1 family member A1 Homo sapiens 54-58
9651402-4 1998 DNase I footprinting experiments demonstrated that purified RAR/RXR heterodimers will occupy sequences resembling retinoic acid response elements within LSR1 and LSR2. Tretinoin 114-127 listeria resistance Mus musculus 153-157
9639510-0 1998 Cancer procoagulant and tissue factor are differently modulated by all-trans-retinoic acid in acute promyelocytic leukemia cells. Tretinoin 67-90 coagulation factor III, tissue factor Homo sapiens 24-37
9639510-1 1998 All-trans-retinoic acid (ATRA) downregulates the expression of two cellular procoagulants, tissue factor (TF) and cancer procoagulant (CP), in human promyelocytic leukemia cells. Tretinoin 0-23 coagulation factor III, tissue factor Homo sapiens 91-104
9639510-1 1998 All-trans-retinoic acid (ATRA) downregulates the expression of two cellular procoagulants, tissue factor (TF) and cancer procoagulant (CP), in human promyelocytic leukemia cells. Tretinoin 0-23 coagulation factor III, tissue factor Homo sapiens 106-108
9639510-1 1998 All-trans-retinoic acid (ATRA) downregulates the expression of two cellular procoagulants, tissue factor (TF) and cancer procoagulant (CP), in human promyelocytic leukemia cells. Tretinoin 25-29 coagulation factor III, tissue factor Homo sapiens 91-104
9774665-0 1998 Thioredoxin reductase mediates cell death effects of the combination of beta interferon and retinoic acid. Tretinoin 92-105 peroxiredoxin 5 Homo sapiens 0-21
9831119-0 1998 All-trans-retinoic acid upregulates the expression of COUP-TFI in early-somite mouse embryos cultured in vitro. Tretinoin 0-23 nuclear receptor subfamily 2, group F, member 1 Mus musculus 54-62
9831119-5 1998 The aim of this work is to assess whether RA-induced modifications in the expression of Krox-20 and Hox genes correlate with alterations of the expression of COUP-TF genes. Tretinoin 42-44 early growth response 2 Mus musculus 88-95
9839358-12 1998 The increases in mRNA steady-state levels for TGF-beta 2 and TGF-beta 3, as for TGF-beta 1, were rapid and transient in nature, again arguing for direct mediation by RA. Tretinoin 166-168 transforming growth factor, beta 3 Mus musculus 61-71
9778049-0 1998 Retinoic acid-mediated growth arrest of EBV-immortalized B lymphocytes is associated with multiple changes in G1 regulatory proteins: p27Kip1 up-regulation is a relevant early event. Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 134-141
9778049-5 1998 In addition, RA-treated LCLs showed a marked up-regulation of the CDK inhibitor (CKI) p27Kip-1 at the protein but not mRNA level, which correlated with a progressive increase of p27Kip-1 in CDK2 complexes (more than 2.5-fold) and with a reduction in the active phosphorylated form of CDK2. Tretinoin 13-15 cyclin dependent kinase inhibitor 1B Homo sapiens 86-94
9778049-5 1998 In addition, RA-treated LCLs showed a marked up-regulation of the CDK inhibitor (CKI) p27Kip-1 at the protein but not mRNA level, which correlated with a progressive increase of p27Kip-1 in CDK2 complexes (more than 2.5-fold) and with a reduction in the active phosphorylated form of CDK2. Tretinoin 13-15 cyclin dependent kinase inhibitor 1B Homo sapiens 178-186
9639510-1 1998 All-trans-retinoic acid (ATRA) downregulates the expression of two cellular procoagulants, tissue factor (TF) and cancer procoagulant (CP), in human promyelocytic leukemia cells. Tretinoin 25-29 coagulation factor III, tissue factor Homo sapiens 106-108
9639510-2 1998 To evaluate whether or not changes of the procoagulant activities (PCAs) may share mechanisms with the ATRA-induced cyto-differentiation process, we have characterized the effect of ATRA on the TF and CP expression by NB4 cells, an ATRA maturation-inducible cell line, and two NB4-derived cell lines resistant to ATRA-induced maturation, the NB4. Tretinoin 182-186 coagulation factor III, tissue factor Homo sapiens 194-196
9639510-2 1998 To evaluate whether or not changes of the procoagulant activities (PCAs) may share mechanisms with the ATRA-induced cyto-differentiation process, we have characterized the effect of ATRA on the TF and CP expression by NB4 cells, an ATRA maturation-inducible cell line, and two NB4-derived cell lines resistant to ATRA-induced maturation, the NB4. Tretinoin 182-186 coagulation factor III, tissue factor Homo sapiens 194-196
9778049-6 1998 p27Kip-1 may also contribute to the inhibition of CDK4 kinase activity, as the amount of CDK4-associated p27Kip-1 was increased by 50% after RA exposure. Tretinoin 141-143 cyclin dependent kinase inhibitor 1B Homo sapiens 0-8
27107124-1 2016 UNLABELLED: A novel bacterial aldehyde dehydrogenase (ALDH) that converts retinal to retinoic acid was first identified in Bacillus cereus The amino acid sequence of ALDH from B. cereus (BcALDH) was more closely related to mammalian ALDHs than to bacterial ALDHs. Tretinoin 85-98 aldehyde dehydrogenase 1 family member A1 Homo sapiens 166-170
9778049-6 1998 p27Kip-1 may also contribute to the inhibition of CDK4 kinase activity, as the amount of CDK4-associated p27Kip-1 was increased by 50% after RA exposure. Tretinoin 141-143 cyclin dependent kinase inhibitor 1B Homo sapiens 105-113
9778049-9 1998 Overall, these results demonstrate that RA treatment of EBV-immortalized B lymphocytes is associated with multiple effects on G1 regulatory proteins, including p27Kip1 up-regulation, decreased levels of cyclins D2, D3 and A, and inhibition of CDK2, CDK4 and CDK6 activity, which ultimately result in reduced pRb phosphorylation and G0/G1 growth arrest. Tretinoin 40-42 cyclin dependent kinase inhibitor 1B Homo sapiens 160-167
9697305-8 1998 Long-term treatment with RA at 1 microM completely abolished the level of osteocalcin mRNA on both days 12 and 16, as revealed by Northern blot analysis. Tretinoin 25-27 bone gamma-carboxyglutamate protein 2 Mus musculus 74-85
27107124-2 2016 This enzyme converted not only small aldehydes to carboxylic acids but also the large aldehyde all-trans-retinal to all-trans-retinoic acid with NAD(P)(+) We newly found that BcALDH and human ALDH (ALDH1A1) could reduce all-trans-retinal to all-trans-retinol with NADPH. Tretinoin 120-139 aldehyde dehydrogenase 1 family member A1 Homo sapiens 177-181
27107124-2 2016 This enzyme converted not only small aldehydes to carboxylic acids but also the large aldehyde all-trans-retinal to all-trans-retinoic acid with NAD(P)(+) We newly found that BcALDH and human ALDH (ALDH1A1) could reduce all-trans-retinal to all-trans-retinol with NADPH. Tretinoin 120-139 aldehyde dehydrogenase 1 family member A1 Homo sapiens 198-205
27107124-9 2016 IMPORTANCE: Although mammalian ALDHs have catalyzed the conversion of retinal to retinoic acid with NAD(P)(+) as a cofactor, a bacterial ALDH involved in the conversion is first characterized. Tretinoin 81-94 aldehyde dehydrogenase 1 family member A1 Homo sapiens 31-35
9624536-6 1998 The two cases expressing PML/RARA presented with an immunostaining pattern typical of APL and a positive response to ATRA, whereas the APL case expressing only a RARA/PML fusion transcript exhibited an immunostaining pattern typical of non-APL cells, and was resistant to ATRA. Tretinoin 117-121 PML nuclear body scaffold Homo sapiens 25-28
9792294-6 1998 A serum-independent HL60 cell line was induced towards the neutrophil lineage by treatment with all-trans retinoic acid (ATRA) for 24 h. CD38+ cells committed towards this lineage were enriched and a population of these cells treated with dihydroxyvitamin D3 to induce neutrophil maturation. Tretinoin 96-119 CD38 molecule Homo sapiens 137-141
9792294-6 1998 A serum-independent HL60 cell line was induced towards the neutrophil lineage by treatment with all-trans retinoic acid (ATRA) for 24 h. CD38+ cells committed towards this lineage were enriched and a population of these cells treated with dihydroxyvitamin D3 to induce neutrophil maturation. Tretinoin 121-125 CD38 molecule Homo sapiens 137-141
9624536-6 1998 The two cases expressing PML/RARA presented with an immunostaining pattern typical of APL and a positive response to ATRA, whereas the APL case expressing only a RARA/PML fusion transcript exhibited an immunostaining pattern typical of non-APL cells, and was resistant to ATRA. Tretinoin 117-121 retinoic acid receptor alpha Homo sapiens 29-33
9792294-7 1998 RNA extracted from uninduced, ATRA-induced CD38+ cells, and vitamin D3 treated maturing cell cultures were amplified using the degenerate primers. Tretinoin 30-34 CD38 molecule Homo sapiens 43-47
27107124-10 2016 The biotransformation of all-trans-retinal to all-trans-retinoic acid by BcALDH and human ALDH was altered to the biotransformation to all-trans-retinol by a cofactor switch using NADPH. Tretinoin 46-69 aldehyde dehydrogenase 1 family member A1 Homo sapiens 75-79
9716606-8 1998 Reducing PML/RARalpha protein in NB4-R1 cells rendered these cells more sensitive to ATRA. Tretinoin 85-89 PML nuclear body scaffold Homo sapiens 9-12
9624536-7 1998 Our results confirm that sensitivity to ATRA requires expression of PML/RARA and strongly correlates with immunostaining, and demonstrate that expression of RARA/PML alone is sufficient for a cytological APL phenotype, but does not confer sensitivity to ATRA. Tretinoin 40-44 PML nuclear body scaffold Homo sapiens 68-71
9624536-7 1998 Our results confirm that sensitivity to ATRA requires expression of PML/RARA and strongly correlates with immunostaining, and demonstrate that expression of RARA/PML alone is sufficient for a cytological APL phenotype, but does not confer sensitivity to ATRA. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 72-76
9716606-8 1998 Reducing PML/RARalpha protein in NB4-R1 cells rendered these cells more sensitive to ATRA. Tretinoin 85-89 retinoic acid receptor alpha Homo sapiens 13-21
9699509-1 1998 Retinoic acid (RA) induces the activation of latent transforming growth factor-beta (TGF-beta) in bovine aortic endothelial cells (BAECs) via enhancement of cellular plasminogen activator (PA)/plasmin levels. Tretinoin 0-13 plasminogen Bos taurus 166-173
9699509-1 1998 Retinoic acid (RA) induces the activation of latent transforming growth factor-beta (TGF-beta) in bovine aortic endothelial cells (BAECs) via enhancement of cellular plasminogen activator (PA)/plasmin levels. Tretinoin 15-17 plasminogen Bos taurus 166-173
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 70-83 polymeric immunoglobulin receptor Homo sapiens 123-127
9649586-2 1998 We have tested the hypothesis that the vitamin A metabolite all-trans retinoic acid (RA) is required for the regulation of pIgR expression by the cytokines interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in HT-29 cells, a well-differentiated human epithelial cell line derived from a colonic carcinoma. Tretinoin 85-87 polymeric immunoglobulin receptor Homo sapiens 123-127
9649586-4 1998 Treatment with RA at concentrations from 10(-9) to 10(-5) mol/L restored normal levels of pIgR expression. Tretinoin 15-17 polymeric immunoglobulin receptor Homo sapiens 90-94
9649586-5 1998 The percentages of cells expressing cell-surface pIgR after 24, 48 and 72 h of treatment with RA, IL-4 and IFN-gamma were 66 +/- 10, 90 +/- 5 and 92 +/- 1, respectively, significantly higher than the percentages seen without RA treatment, which were 32 +/- 2.3, 72 +/- 1.2 and 30 +/- 7, respectively. Tretinoin 94-96 polymeric immunoglobulin receptor Homo sapiens 49-53
27299863-4 2016 Using a murine embryonic stem cell system, we revealed that shRNAi of the mammalian homologue of hyd, Ubr5, effectively prevented retinoic-acid-induced Sonic hedgehog (Shh) expression. Tretinoin 130-143 ubiquitin protein ligase E3 component n-recognin 5 Homo sapiens 102-106
9624127-0 1998 Molecular mechanism of human CD38 gene expression by retinoic acid. Tretinoin 53-66 CD38 molecule Homo sapiens 29-33
9624127-4 1998 We previously reported that CD38 was specifically induced by all-trans-retinoic acid (RA) in human promyelocytic leukemia HL-60 cells. Tretinoin 61-84 CD38 molecule Homo sapiens 28-32
9624127-4 1998 We previously reported that CD38 was specifically induced by all-trans-retinoic acid (RA) in human promyelocytic leukemia HL-60 cells. Tretinoin 86-88 CD38 molecule Homo sapiens 28-32
9624127-5 1998 Here we studied the molecular mechanism of the RA-dependent induction of human CD38. Tretinoin 47-49 CD38 molecule Homo sapiens 79-83
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 thrombomodulin Homo sapiens 92-106
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 thrombomodulin Homo sapiens 108-110
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 coagulation factor III, tissue factor Homo sapiens 131-144
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 coagulation factor III, tissue factor Homo sapiens 146-148
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 thrombomodulin Homo sapiens 92-106
9624127-10 1998 Thus, the RA-induced expression of the human CD38 gene was demonstrated to be mediated through the RARE located in the first intron. Tretinoin 10-12 CD38 molecule Homo sapiens 45-49
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 thrombomodulin Homo sapiens 108-110
27299863-4 2016 Using a murine embryonic stem cell system, we revealed that shRNAi of the mammalian homologue of hyd, Ubr5, effectively prevented retinoic-acid-induced Sonic hedgehog (Shh) expression. Tretinoin 130-143 sonic hedgehog signaling molecule Homo sapiens 152-166
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 coagulation factor III, tissue factor Homo sapiens 131-144
9720716-1 1998 We have recently found that retinoic acids (RAs) evoke anticoagulant effect by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 coagulation factor III, tissue factor Homo sapiens 146-148
9720716-6 1998 A specific RARalpha antagonist Ro41-5253 efficiently suppressed the upregulation of TM by ATRA and Am80 in NB4 cells, U937 cells and HUVECs. Tretinoin 90-94 retinoic acid receptor alpha Homo sapiens 11-19
27299863-4 2016 Using a murine embryonic stem cell system, we revealed that shRNAi of the mammalian homologue of hyd, Ubr5, effectively prevented retinoic-acid-induced Sonic hedgehog (Shh) expression. Tretinoin 130-143 sonic hedgehog signaling molecule Homo sapiens 168-171
9671405-8 1998 The addition of retinoic acid abrogated the PMLRARalpha, but not PML-induced stimulation of GAL4/Fos activity in a dose-dependent manner. Tretinoin 16-29 PML nuclear body scaffold Homo sapiens 44-47
26916447-0 2016 Correlation of proliferation, TGF-beta3 promoter methylation, and Smad signaling in MEPM cells during the development of ATRA-induced cleft palate. Tretinoin 121-125 transforming growth factor, beta 3 Mus musculus 30-39
9607808-4 1998 A computer analysis of the predicted three-dimensional structure confirmed that mE-RABP can accommodate retinoic acid as ligand. Tretinoin 104-117 lipocalin 5 Mus musculus 80-87
9620283-0 1998 All-trans retinoic acid modulates Fas antigen expression and affects cell proliferation and apoptosis in combination with anti-Fas monoclonal antibody in the human myeloma cell line, U266B1. Tretinoin 10-23 Fas cell surface death receptor Homo sapiens 34-45
9688304-7 1998 Upon treatment with retinoic acid (RA), HGCT-1 cells lost the expression of desmin, but exhibited abundant CK filaments. Tretinoin 20-33 desmin Homo sapiens 76-82
9688304-7 1998 Upon treatment with retinoic acid (RA), HGCT-1 cells lost the expression of desmin, but exhibited abundant CK filaments. Tretinoin 35-37 desmin Homo sapiens 76-82
26916447-4 2016 In the present study, we demonstrate that atRA promotes TGF-beta3 promoter demethylation and protein expression, but can cause depression of mesenchymal cell proliferation, especially at embryonic day 14 (E14). Tretinoin 42-46 transforming growth factor, beta 3 Mus musculus 56-65
26916447-5 2016 Moreover, the inhibition of MEPM cell proliferation by atRA results in the downregulation of Smad signaling mediated by transforming growth interacting factor (TGIF). Tretinoin 55-59 TGFB-induced factor homeobox 1 Mus musculus 120-158
11189487-0 1998 [Tissue factor expression during all-trans retinoic acid or arsenic trioxide treatment in acute promyelocytic leukemia]. Tretinoin 43-56 coagulation factor III, tissue factor Homo sapiens 1-14
11189487-1 1998 OBJECTIVE: In order to study the effect of all-trans retinoic acid (ATRA) or arsenic trioxide (As2O3) treatment on the expression of tissue factor (TF) in acute promyelocytic leukemia(APL). Tretinoin 43-66 coagulation factor III, tissue factor Homo sapiens 133-146
11189487-1 1998 OBJECTIVE: In order to study the effect of all-trans retinoic acid (ATRA) or arsenic trioxide (As2O3) treatment on the expression of tissue factor (TF) in acute promyelocytic leukemia(APL). Tretinoin 43-66 coagulation factor III, tissue factor Homo sapiens 148-150
11189487-1 1998 OBJECTIVE: In order to study the effect of all-trans retinoic acid (ATRA) or arsenic trioxide (As2O3) treatment on the expression of tissue factor (TF) in acute promyelocytic leukemia(APL). Tretinoin 68-72 coagulation factor III, tissue factor Homo sapiens 133-146
11189487-1 1998 OBJECTIVE: In order to study the effect of all-trans retinoic acid (ATRA) or arsenic trioxide (As2O3) treatment on the expression of tissue factor (TF) in acute promyelocytic leukemia(APL). Tretinoin 68-72 coagulation factor III, tissue factor Homo sapiens 148-150
26916447-5 2016 Moreover, the inhibition of MEPM cell proliferation by atRA results in the downregulation of Smad signaling mediated by transforming growth interacting factor (TGIF). Tretinoin 55-59 TGFB-induced factor homeobox 1 Mus musculus 160-164
11189487-4 1998 CONCLUSION: Both ATRA and As2O3 downregulated the expression of TF mRNA, decreased the PCA and TF levels in APL cells, inhibited coagulation activation and secondary hyperfibrinolysis, thus greatly relieved the bleeding symptom in the early stage of treatment. Tretinoin 17-21 coagulation factor III, tissue factor Homo sapiens 64-66
11189487-4 1998 CONCLUSION: Both ATRA and As2O3 downregulated the expression of TF mRNA, decreased the PCA and TF levels in APL cells, inhibited coagulation activation and secondary hyperfibrinolysis, thus greatly relieved the bleeding symptom in the early stage of treatment. Tretinoin 17-21 coagulation factor III, tissue factor Homo sapiens 95-97
26916447-6 2016 We speculate that the effects of atRA on MEPM cell proliferation may be mediated by Smad pathways, which are regulated by TGIF but are not related to TGF-beta3 expression. Tretinoin 33-37 TGFB-induced factor homeobox 1 Mus musculus 122-126
27187787-8 2016 Similarly, exposure of Tgif1 mutant embryos to retinoic acid at E8.5 increased the severity and penetrance of the Tgif1 phenotype. Tretinoin 47-60 TGFB-induced factor homeobox 1 Mus musculus 23-28
9665814-0 1998 BMP4- and RA-induced apoptosis is mediated through the activation of retinoic acid receptor alpha and gamma in P19 embryonal carcinoma cells. Tretinoin 10-12 retinoic acid receptor alpha Homo sapiens 69-97
27187787-8 2016 Similarly, exposure of Tgif1 mutant embryos to retinoic acid at E8.5 increased the severity and penetrance of the Tgif1 phenotype. Tretinoin 47-60 TGFB-induced factor homeobox 1 Mus musculus 114-119
9648858-3 1998 When mouse embryonal carcinoma P19 cells were differentiated by retinoic acid into neural cells, the amount of AK1 protein and enzyme activity increased about fivefold concomitantly with neurofilament (NF). Tretinoin 64-77 adenylate kinase 1 Mus musculus 111-114
27187787-9 2016 This suggests that Tgif1 and Tgif2 regulate axial patterning and that reduced TGIF function sensitizes embryos to the effects of retinoic acid. Tretinoin 129-142 TGFB-induced factor homeobox 1 Mus musculus 78-82
27176797-0 2016 All-trans retinoic acid and interferon-alpha increase CD38 expression on adult T-cell leukemia cells and sensitize them to T cells bearing anti-CD38 chimeric antigen receptors. Tretinoin 10-23 CD38 molecule Homo sapiens 54-58
9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 109-114
9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 109-114
9616179-6 1998 Northern analysis showed that the M-CSF mRNA expression was only slightly reduced by RA treatment, suggesting regulation on the posttranscriptional level. Tretinoin 85-87 colony stimulating factor 1 Homo sapiens 34-39
9616179-8 1998 Because M-CSF is not only a survival-promoting but also a differentiation-promoting factor for myeloid cells, we analyzed the effect of RA on MO to MAC maturation. Tretinoin 136-138 colony stimulating factor 1 Homo sapiens 8-13
9616179-9 1998 RA suppressed the expression of the maturation-associated antigen carboxypeptidase M (CPM)/MAX.1 at both the protein and mRNA levels and modulated the lipopolysaccharide-stimulated cytokine secretion of MO/MAC. Tretinoin 0-2 carboxypeptidase M Homo sapiens 66-84
27176797-0 2016 All-trans retinoic acid and interferon-alpha increase CD38 expression on adult T-cell leukemia cells and sensitize them to T cells bearing anti-CD38 chimeric antigen receptors. Tretinoin 10-23 CD38 molecule Homo sapiens 144-148
9616179-10 1998 The addition of exogenous M-CSF to RA-containing MO cultures fails to overcome the RA-induced inhibition of MO differentiation. Tretinoin 35-37 colony stimulating factor 1 Homo sapiens 26-31
9616179-12 1998 We conclude that RA acts via two different mechanisms on monocyte survival and differentiation: posttranscriptionally by controlling M-CSF secretion, which decreases MO survival, and transcriptionally regulating the expression of differentiation-associated genes. Tretinoin 17-19 colony stimulating factor 1 Homo sapiens 133-138
26762983-5 2016 Here, we show that the H3K27 demethylase UTX (also called KDM6A) is required for the resolution and activation of numerous retinoic acid (RA)-inducible bivalent genes during the RA-driven differentiation of mouse embryonic stem cells (ESCs). Tretinoin 123-136 lysine (K)-specific demethylase 6A Mus musculus 41-44
9616179-13 1998 The regulation of M-CSF production may contribute to the antileukemic effect of RA in vivo by reducing autocrine M-CSF production by leukemic cells. Tretinoin 80-82 colony stimulating factor 1 Homo sapiens 18-23
9616179-13 1998 The regulation of M-CSF production may contribute to the antileukemic effect of RA in vivo by reducing autocrine M-CSF production by leukemic cells. Tretinoin 80-82 colony stimulating factor 1 Homo sapiens 113-118
9616182-0 1998 Secondary leukemia responsive to retinoic acid with abnormal localization of RARalpha protein: a report of two cases. Tretinoin 33-46 retinoic acid receptor alpha Homo sapiens 77-85
26762983-5 2016 Here, we show that the H3K27 demethylase UTX (also called KDM6A) is required for the resolution and activation of numerous retinoic acid (RA)-inducible bivalent genes during the RA-driven differentiation of mouse embryonic stem cells (ESCs). Tretinoin 123-136 lysine (K)-specific demethylase 6A Mus musculus 58-63
26762983-5 2016 Here, we show that the H3K27 demethylase UTX (also called KDM6A) is required for the resolution and activation of numerous retinoic acid (RA)-inducible bivalent genes during the RA-driven differentiation of mouse embryonic stem cells (ESCs). Tretinoin 138-140 lysine (K)-specific demethylase 6A Mus musculus 41-44
9596679-5 1998 Thus, As2O3- or retinoic acid (RA)-induced PML/RARalpha degradation may be a prerequisite, but is not sufficient for the full differentiative/apoptotic response to these drugs. Tretinoin 16-29 PML nuclear body scaffold Homo sapiens 43-46
9596679-5 1998 Thus, As2O3- or retinoic acid (RA)-induced PML/RARalpha degradation may be a prerequisite, but is not sufficient for the full differentiative/apoptotic response to these drugs. Tretinoin 16-29 retinoic acid receptor alpha Homo sapiens 47-55
26762983-5 2016 Here, we show that the H3K27 demethylase UTX (also called KDM6A) is required for the resolution and activation of numerous retinoic acid (RA)-inducible bivalent genes during the RA-driven differentiation of mouse embryonic stem cells (ESCs). Tretinoin 138-140 lysine (K)-specific demethylase 6A Mus musculus 58-63
26762983-6 2016 Notably, UTX loss in mouse ESCs inhibited the RA-driven bivalency resolution and activation of most developmentally critical homeobox (Hox) a-d genes. Tretinoin 46-48 lysine (K)-specific demethylase 6A Mus musculus 9-12
9714701-5 1998 Conversely, v-Myb protein interferes with RAR alpha transactivation function as well as with retinoic acid-induced apoptosis of HL-60 cells. Tretinoin 93-106 MYB proto-oncogene, transcription factor Homo sapiens 12-17
26762983-7 2016 The UTX-mediated resolution and activation of many bivalent Hox genes during mouse ESC differentiation were recapitulated during RA-driven differentiation of human NT2/D1 embryonal carcinoma cells. Tretinoin 129-131 lysine (K)-specific demethylase 6A Mus musculus 4-7
26848712-9 2016 The RARalpha ligand all-trans retinoic acid (atRA) disrupted RARalpha-Arp2/3 interactions. Tretinoin 30-43 retinoic acid receptor alpha Homo sapiens 4-12
9570764-0 1998 Expression of the murine Hoxa4 gene requires both autoregulation and a conserved retinoic acid response element. Tretinoin 81-94 homeobox A4 Mus musculus 25-30
9570764-6 1998 We also identify three potential retinoic acid response elements in the Hoxa4 5" flanking region, one of which is identical to a well-characterized element flanking the Hoxd4 gene. Tretinoin 33-46 homeobox A4 Mus musculus 72-77
9570764-7 1998 Administration of retinoic acid to Hoxa4/lacZ transgenic embryos resulted in stage-dependent ectopic expression of the reporter gene in the neural tube and hindbrain. Tretinoin 18-31 homeobox A4 Mus musculus 35-40
9570764-8 1998 When administered to Hoxa4 null embryos, however, persistent ectopic expression was not observed, suggesting that autoregulation is required for maintenance of the retinoic acid-induced expression. Tretinoin 164-177 homeobox A4 Mus musculus 21-26
26848712-9 2016 The RARalpha ligand all-trans retinoic acid (atRA) disrupted RARalpha-Arp2/3 interactions. Tretinoin 30-43 retinoic acid receptor alpha Homo sapiens 61-69
26848712-9 2016 The RARalpha ligand all-trans retinoic acid (atRA) disrupted RARalpha-Arp2/3 interactions. Tretinoin 30-43 actin related protein 2 Homo sapiens 70-74
26848712-9 2016 The RARalpha ligand all-trans retinoic acid (atRA) disrupted RARalpha-Arp2/3 interactions. Tretinoin 45-49 retinoic acid receptor alpha Homo sapiens 4-12
26848712-9 2016 The RARalpha ligand all-trans retinoic acid (atRA) disrupted RARalpha-Arp2/3 interactions. Tretinoin 45-49 retinoic acid receptor alpha Homo sapiens 61-69
9633525-1 1998 The heparin-binding growth-associated molecule HB-GAM (also named pleiotrophin) and the retinoic acid-induced heparin-binding protein RIHB (chicken midkine) are developmentally regulated proteins forming a new family of heparin-binding molecules with putative functions during cell growth and differentiation. Tretinoin 88-101 pleiotrophin Gallus gallus 47-53
9633525-1 1998 The heparin-binding growth-associated molecule HB-GAM (also named pleiotrophin) and the retinoic acid-induced heparin-binding protein RIHB (chicken midkine) are developmentally regulated proteins forming a new family of heparin-binding molecules with putative functions during cell growth and differentiation. Tretinoin 88-101 pleiotrophin Gallus gallus 66-78
26848712-9 2016 The RARalpha ligand all-trans retinoic acid (atRA) disrupted RARalpha-Arp2/3 interactions. Tretinoin 45-49 actin related protein 2 Homo sapiens 70-74
27052693-0 2016 Effect of ATRA on the expression of HOXA5 gene in K562 cells and its relationship with cell cycle and apoptosis. Tretinoin 10-14 homeobox A5 Homo sapiens 36-41
9619634-0 1998 Contrasting levels of p21ras activation and expression of neurofibromin in peripheral primitive neuroectodermal tumour and neuroblastoma cells, and their response to retinoic acid. Tretinoin 166-179 HRas proto-oncogene, GTPase Homo sapiens 22-28
9619634-8 1998 Retinoic acid (RA)-induced differentiation and growth inhibition of neuroblastoma cells was associated with an increase in type 1 GAP120 and neurofibromin mRNA, and a decrease in p21ras-GTP. Tretinoin 0-13 HRas proto-oncogene, GTPase Homo sapiens 179-185
27052693-2 2016 The aim of the present study was to examine the changes in the expression of homeobox (Hox) A5 gene and its relationship with cell cycle and apoptosis through the intervention of human K562 myeloid leukemia cell line by all-trans retinoic acid (ATRA), to analyze the role of HOXA5 in the pathogenesis and development process of myeloid leukemia. Tretinoin 230-243 homeobox A5 Homo sapiens 77-94
9579574-4 1998 Electrophoretic mobility shift and super-shift assays using a DR2 ("direct repeat" 2) RA response element demonstrated DNA-binding of RARalpha, RARgamma, RXRalpha and RXRbeta in nuclear extracts of FTC-133 and anaplastic HTh74 cells. Tretinoin 86-88 retinoic acid receptor alpha Homo sapiens 134-142
27052693-2 2016 The aim of the present study was to examine the changes in the expression of homeobox (Hox) A5 gene and its relationship with cell cycle and apoptosis through the intervention of human K562 myeloid leukemia cell line by all-trans retinoic acid (ATRA), to analyze the role of HOXA5 in the pathogenesis and development process of myeloid leukemia. Tretinoin 245-249 homeobox A5 Homo sapiens 77-94
27052693-6 2016 The HOXA5 mRNA and protein expression levels were increased following treatment with ATRA in K562 cells. Tretinoin 85-89 homeobox A5 Homo sapiens 4-9
27052693-12 2016 In conclusion, the expression of HOXA5 in cells was increased following treatment with ATRA in K562 cells, in a time-dependent manner. Tretinoin 87-91 homeobox A5 Homo sapiens 33-38
27052693-13 2016 Additionally, ATRA may inhibit the proliferation of K562 cells and promote apoptosis by upregulating the HOXA5 mRNA and protein expression. Tretinoin 14-18 homeobox A5 Homo sapiens 105-110
9578604-2 1998 G-CSF enhanced O-2 generating ability of HL-60 cells whose differentiation had been initiated by dimethylsulfoxide (DMSO) or retinoic acid (RA). Tretinoin 140-142 colony stimulating factor 3 Homo sapiens 0-5
26950191-0 2016 Loss-of-Function of HtrA1 Abrogates All-Trans Retinoic Acid-Induced Osteogenic Differentiation of Mouse Adipose-Derived Stromal Cells Through Deficiencies in p70S6K Activation. Tretinoin 46-59 WD and tetratricopeptide repeats 1 Mus musculus 104-111
9560322-0 1998 Synergistic transcriptional activation of the mouse urokinase plasminogen activator (uPA) gene and of its enhancer activator protein 1 (AP1) site by cAMP and retinoic acid. Tretinoin 158-171 plasminogen activator, urokinase Mus musculus 52-83
9560322-0 1998 Synergistic transcriptional activation of the mouse urokinase plasminogen activator (uPA) gene and of its enhancer activator protein 1 (AP1) site by cAMP and retinoic acid. Tretinoin 158-171 plasminogen activator, urokinase Mus musculus 85-88
9560322-1 1998 We have investigated the mechanism whereby all-trans retinoic acid (tRA) potentiates the 8-bromo-cAMP (8-BrcAMP)-dependent transcription of the urokinase plasminogen activator (uPA) gene in SC115 mouse mammary carcinoma cells. Tretinoin 53-66 plasminogen activator, urokinase Mus musculus 144-175
9560322-1 1998 We have investigated the mechanism whereby all-trans retinoic acid (tRA) potentiates the 8-bromo-cAMP (8-BrcAMP)-dependent transcription of the urokinase plasminogen activator (uPA) gene in SC115 mouse mammary carcinoma cells. Tretinoin 53-66 plasminogen activator, urokinase Mus musculus 177-180
9560322-1 1998 We have investigated the mechanism whereby all-trans retinoic acid (tRA) potentiates the 8-bromo-cAMP (8-BrcAMP)-dependent transcription of the urokinase plasminogen activator (uPA) gene in SC115 mouse mammary carcinoma cells. Tretinoin 68-71 plasminogen activator, urokinase Mus musculus 144-175
9560322-1 1998 We have investigated the mechanism whereby all-trans retinoic acid (tRA) potentiates the 8-bromo-cAMP (8-BrcAMP)-dependent transcription of the urokinase plasminogen activator (uPA) gene in SC115 mouse mammary carcinoma cells. Tretinoin 68-71 plasminogen activator, urokinase Mus musculus 177-180
26950191-1 2016 All-trans retinoic acid (ATRA) is a potent inducer of osteogenic differentiation in mouse adipose-derived stromal cells (mASCs), although the underlying mechanisms responsible for its mode of action have yet to be completely elucidated. Tretinoin 0-23 WD and tetratricopeptide repeats 1 Mus musculus 90-97
9593266-0 1998 The myeloid zinc finger gene (MZF-1) delays retinoic acid-induced apoptosis and differentiation in myeloid leukemia cells. Tretinoin 44-57 myeloid zinc finger 1 Homo sapiens 30-35
9593266-4 1998 However, HL-60-MZF-1 cells exposed to RA continue to proliferate in response to RA as evidenced by a higher percentage of cells in S phase, higher peak cell counts, and later peak cell counts. Tretinoin 38-40 myeloid zinc finger 1 Homo sapiens 15-20
26950191-1 2016 All-trans retinoic acid (ATRA) is a potent inducer of osteogenic differentiation in mouse adipose-derived stromal cells (mASCs), although the underlying mechanisms responsible for its mode of action have yet to be completely elucidated. Tretinoin 25-29 WD and tetratricopeptide repeats 1 Mus musculus 90-97
9593266-4 1998 However, HL-60-MZF-1 cells exposed to RA continue to proliferate in response to RA as evidenced by a higher percentage of cells in S phase, higher peak cell counts, and later peak cell counts. Tretinoin 80-82 myeloid zinc finger 1 Homo sapiens 15-20
9593266-5 1998 Morphologic differentiation of the RA-induced HL-60-MZF-1 cells is delayed with half as many of the HL-60-MZF-1 cells compared to the wild-type HL-60 cells that are differentiated after 3 days of RA, although both cells types responded with 80-95% mature granulocytes after 6 days of RA. Tretinoin 35-37 myeloid zinc finger 1 Homo sapiens 52-57
27104669-4 2016 alpha-Mangostin also can reverse the drug resistance of retinoic acid in RARa siRNA-transduced sk-mel-2 cells. Tretinoin 56-69 retinoic acid receptor alpha Homo sapiens 73-77
9593266-5 1998 Morphologic differentiation of the RA-induced HL-60-MZF-1 cells is delayed with half as many of the HL-60-MZF-1 cells compared to the wild-type HL-60 cells that are differentiated after 3 days of RA, although both cells types responded with 80-95% mature granulocytes after 6 days of RA. Tretinoin 35-37 myeloid zinc finger 1 Homo sapiens 106-111
9593266-5 1998 Morphologic differentiation of the RA-induced HL-60-MZF-1 cells is delayed with half as many of the HL-60-MZF-1 cells compared to the wild-type HL-60 cells that are differentiated after 3 days of RA, although both cells types responded with 80-95% mature granulocytes after 6 days of RA. Tretinoin 196-198 myeloid zinc finger 1 Homo sapiens 52-57
9593266-5 1998 Morphologic differentiation of the RA-induced HL-60-MZF-1 cells is delayed with half as many of the HL-60-MZF-1 cells compared to the wild-type HL-60 cells that are differentiated after 3 days of RA, although both cells types responded with 80-95% mature granulocytes after 6 days of RA. Tretinoin 196-198 myeloid zinc finger 1 Homo sapiens 52-57
9593266-8 1998 However, following 6 days of RA, only half as many HL-60-MZF-1 cells expressed CD18 compared to the wild-type HL-60 cells. Tretinoin 29-31 myeloid zinc finger 1 Homo sapiens 57-62
27074819-0 2016 The HER2 inhibitor TAK165 Sensitizes Human Acute Myeloid Leukemia Cells to Retinoic Acid-Induced Myeloid Differentiation by activating MEK/ERK mediated RARalpha/STAT1 axis. Tretinoin 75-88 retinoic acid receptor alpha Homo sapiens 152-160
9609098-1 1998 Mutations in receptors for the vitamin A metabolite retinoic acid (RAR) that repress retinoic acid (RA)-responsive gene expression have been identified and characterized. Tretinoin 52-65 retinoic acid receptor alpha Homo sapiens 67-70
9609098-1 1998 Mutations in receptors for the vitamin A metabolite retinoic acid (RAR) that repress retinoic acid (RA)-responsive gene expression have been identified and characterized. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 67-70
26951332-4 2016 We show that treatment with all-trans retinoic acid (ATRA) at clinically achievable doses markedly enhanced terminal granulocytic differentiation in AML cell lines, primary patient samples, and a xenograft mouse model carrying mutant IDH1. Tretinoin 38-51 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 234-238
9555083-0 1998 Negative regulation of Apo A-I gene expression by retinoic acid in rat hepatocytes maintained in a coculture system. Tretinoin 50-63 apolipoprotein A1 Rattus norvegicus 23-30
9555083-1 1998 Rat hepatocytes cocultured with rat liver epithelial cells (RLEC) were used to investigate the influence of all-trans retinoic acid (RA) on the regulation of apolipoproteins (Apo) A-I and A-II gene expression, the major protein constituent of high-density lipoproteins. Tretinoin 133-135 apolipoprotein A1 Rattus norvegicus 175-192
9555083-3 1998 Treatment of cocultured rat hepatocytes with RA resulted in a specific decrease in Apo A-I mRNA levels whereas no marked difference in Apo A-II mRNA levels was observed. Tretinoin 45-47 apolipoprotein A1 Rattus norvegicus 83-90
9555083-9 1998 Furthermore, they demonstrate that RA can directly act on hepatocytes and differently affect Apo A-I and Apo A-II gene expression. Tretinoin 35-37 apolipoprotein A1 Rattus norvegicus 93-100
9590146-4 1998 Based on these observations, we administered recombinant human G-CSF to a patient with APL in the third relapse that was resistant to both cytotoxic agents and all trans retinoic acid, in an attempt to sensitize the leukemic cells to cell-cycle-dependent agents. Tretinoin 170-183 colony stimulating factor 3 Homo sapiens 63-68
26951332-4 2016 We show that treatment with all-trans retinoic acid (ATRA) at clinically achievable doses markedly enhanced terminal granulocytic differentiation in AML cell lines, primary patient samples, and a xenograft mouse model carrying mutant IDH1. Tretinoin 53-57 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 234-238
26951332-5 2016 Moreover, treatment with a cell-permeable form of 2-HG sensitized wild-type IDH1 AML cells to ATRA-induced myeloid differentiation, whereas inhibition of 2-HG production significantly reduced ATRA effects in mutant IDH1 cells. Tretinoin 192-196 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 215-219
9558392-0 1998 Constitutive expression of the promyelocytic leukemia-associated oncogene PML-RARalpha in TF1 cells: isoform-specific and retinoic acid-dependent effects on growth, bcl-2 expression, and apoptosis. Tretinoin 122-135 PML nuclear body scaffold Homo sapiens 74-77
9558392-0 1998 Constitutive expression of the promyelocytic leukemia-associated oncogene PML-RARalpha in TF1 cells: isoform-specific and retinoic acid-dependent effects on growth, bcl-2 expression, and apoptosis. Tretinoin 122-135 retinoic acid receptor alpha Homo sapiens 78-86
9490815-13 1998 Down-regulation of h-eag by long-term exposure to retinoic acid was paralleled by a right shift in the activation potential of HERG-like channels. Tretinoin 50-63 potassium voltage-gated channel subfamily H member 2 Homo sapiens 127-131
9506453-2 1998 RAR directly bind and are activated by two naturally occurring isomers of retinoic acid (RA), all-trans retinoic acid (t-RA) and 9-cis retinoic acid (9c-RA). Tretinoin 74-87 retinoic acid receptor alpha Homo sapiens 0-3
9506453-2 1998 RAR directly bind and are activated by two naturally occurring isomers of retinoic acid (RA), all-trans retinoic acid (t-RA) and 9-cis retinoic acid (9c-RA). Tretinoin 94-117 retinoic acid receptor alpha Homo sapiens 0-3
9558392-5 1998 Treatment with all-trans retinoic acid (ATRA) inhibited cell growth and caused apoptosis only in PML-RARalpha-expressing cells, and these effects of ATRA were more marked in cells expressing the L isoform. Tretinoin 15-38 PML nuclear body scaffold Homo sapiens 97-100
9558392-5 1998 Treatment with all-trans retinoic acid (ATRA) inhibited cell growth and caused apoptosis only in PML-RARalpha-expressing cells, and these effects of ATRA were more marked in cells expressing the L isoform. Tretinoin 15-38 retinoic acid receptor alpha Homo sapiens 101-109
9558392-5 1998 Treatment with all-trans retinoic acid (ATRA) inhibited cell growth and caused apoptosis only in PML-RARalpha-expressing cells, and these effects of ATRA were more marked in cells expressing the L isoform. Tretinoin 40-44 PML nuclear body scaffold Homo sapiens 97-100
9558392-5 1998 Treatment with all-trans retinoic acid (ATRA) inhibited cell growth and caused apoptosis only in PML-RARalpha-expressing cells, and these effects of ATRA were more marked in cells expressing the L isoform. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 101-109
9558392-6 1998 ATRA treatment also led to downregulation of bcl-2 and endogenous RARalpha in PML-RARalpha-expressing cells, but had little effect on the level of exogenously expressed PML-RARalpha. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 66-74
9558392-6 1998 ATRA treatment also led to downregulation of bcl-2 and endogenous RARalpha in PML-RARalpha-expressing cells, but had little effect on the level of exogenously expressed PML-RARalpha. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 78-81
26951332-6 2016 ATRA treatment specifically decreased cell viability and induced apoptosis of mutant IDH1 blasts in vitro. Tretinoin 0-4 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 85-89
9558392-6 1998 ATRA treatment also led to downregulation of bcl-2 and endogenous RARalpha in PML-RARalpha-expressing cells, but had little effect on the level of exogenously expressed PML-RARalpha. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 82-90
9558392-6 1998 ATRA treatment also led to downregulation of bcl-2 and endogenous RARalpha in PML-RARalpha-expressing cells, but had little effect on the level of exogenously expressed PML-RARalpha. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 82-90
9514149-2 1998 Evidence by in vivo deoxyribonuclease I (DNase I) hypersensitivity assay indicates that RA treatment of these cells results in an alteration of chromatin structure in and near the promoter. Tretinoin 88-90 uncharacterized protein MGC64462 Xenopus laevis 20-39
9514149-2 1998 Evidence by in vivo deoxyribonuclease I (DNase I) hypersensitivity assay indicates that RA treatment of these cells results in an alteration of chromatin structure in and near the promoter. Tretinoin 88-90 uncharacterized protein MGC64462 Xenopus laevis 41-48
9558392-7 1998 We conclude that (1) subtle differences exist in the biologic activities of the L and S isoforms of PML-RARalpha, and (2) both isoforms are capable of transducing an ATRA-mediated signal that leads to downregulation of bcl-2 and induction of programmed cell death. Tretinoin 166-170 PML nuclear body scaffold Homo sapiens 100-103
26951332-7 2016 ATRA also reduced tumor burden of mutant IDH1 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased overall survival, revealing a potent antileukemic effect of ATRA in the presence of IDH1 mutation. Tretinoin 0-4 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 41-45
9558392-7 1998 We conclude that (1) subtle differences exist in the biologic activities of the L and S isoforms of PML-RARalpha, and (2) both isoforms are capable of transducing an ATRA-mediated signal that leads to downregulation of bcl-2 and induction of programmed cell death. Tretinoin 166-170 retinoic acid receptor alpha Homo sapiens 104-112
9537651-7 1998 Retinoic acid, which inhibits the progression of certain cancers, repressed v-src-induced MMP-1 transcription. Tretinoin 0-13 matrix metallopeptidase 1 Homo sapiens 90-95
26951332-7 2016 ATRA also reduced tumor burden of mutant IDH1 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased overall survival, revealing a potent antileukemic effect of ATRA in the presence of IDH1 mutation. Tretinoin 0-4 isocitrate dehydrogenase 1 (NADP+), soluble Mus musculus 207-211
9659296-9 1998 However, retinoic acid (10(-6) M) stimulated both IGFBP-2 and IGFBP-6 protein and mRNA levels, but it decreased IGFBP-3 mRNA levels relative to controls. Tretinoin 9-22 insulin like growth factor binding protein 6 Bos taurus 62-69
26951332-7 2016 ATRA also reduced tumor burden of mutant IDH1 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased overall survival, revealing a potent antileukemic effect of ATRA in the presence of IDH1 mutation. Tretinoin 183-187 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 41-45
9516082-6 1998 The IGF-independent action of IGFBP-3 requires interaction with cell-surface association proteins, presumably putative IGFBP-3 specific receptors, and is responsible for growth inhibitory action of the known growth suppressing factors such as TGF-beta, retinoic acid, and antiestrogens in breast cancer cells. Tretinoin 253-266 insulin like growth factor binding protein 3 Homo sapiens 30-37
26915804-6 2016 We found that centlein overexpression inhibited neurite formation in retinoic acid (RA)-induced SH-SY5Y and N2a cells. Tretinoin 69-82 centlein Homo sapiens 14-22
9442029-5 1998 The interaction between eIF-5A and TGase is specific for the GDP-bound form of the TGase and is not detected when the TGase is pre-loaded with GTP gamma S. The TGase-eIF-5A interaction also is promoted by Ca2+, Mg2+, and RA treatment of HeLa cells. Tretinoin 221-223 eukaryotic translation initiation factor 5A Homo sapiens 24-30
9442029-5 1998 The interaction between eIF-5A and TGase is specific for the GDP-bound form of the TGase and is not detected when the TGase is pre-loaded with GTP gamma S. The TGase-eIF-5A interaction also is promoted by Ca2+, Mg2+, and RA treatment of HeLa cells. Tretinoin 221-223 eukaryotic translation initiation factor 5A Homo sapiens 166-172
9442029-6 1998 In the presence of retinoic acid, millimolar levels of Ca2+ are no longer required for the TGase-eIF-5A interaction. Tretinoin 19-32 eukaryotic translation initiation factor 5A Homo sapiens 97-103
9442029-8 1998 The interaction between TGase and eIF-5A and its sensitivity to the nucleotide-occupied state of the TGase provides a potentially interesting connection between RA signaling and protein synthesis and/or RNA trafficking activities. Tretinoin 161-163 eukaryotic translation initiation factor 5A Homo sapiens 34-40
9531570-0 1998 Reduced retinoic acid-sensitivities of nuclear receptor corepressor binding to PML- and PLZF-RARalpha underlie molecular pathogenesis and treatment of acute promyelocytic leukemia. Tretinoin 8-21 PML nuclear body scaffold Homo sapiens 79-83
9531570-0 1998 Reduced retinoic acid-sensitivities of nuclear receptor corepressor binding to PML- and PLZF-RARalpha underlie molecular pathogenesis and treatment of acute promyelocytic leukemia. Tretinoin 8-21 retinoic acid receptor alpha Homo sapiens 93-101
9531570-1 1998 Typical acute promyelocytic leukemia (APL) is associated with expression of the PML-RARalpha fusion protein and responsiveness to treatment with all-trans retinoic acid (ATRA). Tretinoin 145-168 PML nuclear body scaffold Homo sapiens 80-84
9531570-1 1998 Typical acute promyelocytic leukemia (APL) is associated with expression of the PML-RARalpha fusion protein and responsiveness to treatment with all-trans retinoic acid (ATRA). Tretinoin 145-168 retinoic acid receptor alpha Homo sapiens 84-92
9531570-1 1998 Typical acute promyelocytic leukemia (APL) is associated with expression of the PML-RARalpha fusion protein and responsiveness to treatment with all-trans retinoic acid (ATRA). Tretinoin 170-174 PML nuclear body scaffold Homo sapiens 80-84
9531570-1 1998 Typical acute promyelocytic leukemia (APL) is associated with expression of the PML-RARalpha fusion protein and responsiveness to treatment with all-trans retinoic acid (ATRA). Tretinoin 170-174 retinoic acid receptor alpha Homo sapiens 84-92
9531570-4 1998 We now show that the above-mentioned oncogenic fusion proteins interact with the nuclear receptor corepressor N-CoR and, in comparison with the wild-type RARalpha protein, their interactions display reduced sensitivities to ATRA. Tretinoin 224-228 nuclear receptor corepressor 1 Homo sapiens 110-115
9457077-6 1998 In this paper, we have examined the RA-mediated regulation of the RAR, RXR, peroxisome proliferator-activated receptor (PPAR), and AFP genes in Hep3B cells. Tretinoin 36-38 retinoic acid receptor alpha Homo sapiens 66-69
9457077-6 1998 In this paper, we have examined the RA-mediated regulation of the RAR, RXR, peroxisome proliferator-activated receptor (PPAR), and AFP genes in Hep3B cells. Tretinoin 36-38 peroxisome proliferator activated receptor alpha Homo sapiens 76-118
9457077-6 1998 In this paper, we have examined the RA-mediated regulation of the RAR, RXR, peroxisome proliferator-activated receptor (PPAR), and AFP genes in Hep3B cells. Tretinoin 36-38 peroxisome proliferator activated receptor alpha Homo sapiens 120-124
9457077-7 1998 RA induced the expression of RAR alpha, beta, and gamma mRNA in Hep3B cells. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 29-38
9457077-10 1998 Gel retardation assays demonstrated that RA decreased the overall binding of nuclear receptors to the RA and PPAR response elements. Tretinoin 41-43 peroxisome proliferator activated receptor alpha Homo sapiens 109-113
9531570-4 1998 We now show that the above-mentioned oncogenic fusion proteins interact with the nuclear receptor corepressor N-CoR and, in comparison with the wild-type RARalpha protein, their interactions display reduced sensitivities to ATRA. Tretinoin 224-228 retinoic acid receptor alpha Homo sapiens 154-162
9531570-5 1998 Although pharmacologic concentration of ATRA could still induce dissociation of N-CoR from PML-RARalpha, it had a very little effect on its association with the PLZF-RARalpha fusion protein. Tretinoin 40-44 nuclear receptor corepressor 1 Homo sapiens 80-85
26915804-6 2016 We found that centlein overexpression inhibited neurite formation in retinoic acid (RA)-induced SH-SY5Y and N2a cells. Tretinoin 84-86 centlein Homo sapiens 14-22
9531570-5 1998 Although pharmacologic concentration of ATRA could still induce dissociation of N-CoR from PML-RARalpha, it had a very little effect on its association with the PLZF-RARalpha fusion protein. Tretinoin 40-44 PML nuclear body scaffold Homo sapiens 91-95
9600389-3 1998 In this study we investigated whether the well-known retinoic acid-induced differentiation of ES cells into neurons (identified by immunostaining for neuron-specific enolase and synaptophysin) was accompanied by cells expressing astroglial (GFAP), oligodendroglial (O4), and microglial (5C6, galectin-3) markers. Tretinoin 53-66 synaptophysin Mus musculus 178-191
9531570-5 1998 Although pharmacologic concentration of ATRA could still induce dissociation of N-CoR from PML-RARalpha, it had a very little effect on its association with the PLZF-RARalpha fusion protein. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 95-103
26818829-3 2016 atRA-mediated increase of both ligands and receptor expression correlated with the elevated level of retinoic acid receptor alpha (RARalpha) expression, while the level of another atRA receptor, peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta), was decreased. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 101-129
9531570-6 1998 This ATRA-insensitive interaction between N-CoR and PLZF-RARalpha was mediated by the N-terminal PLZF moiety of the chimera. Tretinoin 5-9 nuclear receptor corepressor 1 Homo sapiens 42-47
9531570-6 1998 This ATRA-insensitive interaction between N-CoR and PLZF-RARalpha was mediated by the N-terminal PLZF moiety of the chimera. Tretinoin 5-9 retinoic acid receptor alpha Homo sapiens 57-65
9600389-3 1998 In this study we investigated whether the well-known retinoic acid-induced differentiation of ES cells into neurons (identified by immunostaining for neuron-specific enolase and synaptophysin) was accompanied by cells expressing astroglial (GFAP), oligodendroglial (O4), and microglial (5C6, galectin-3) markers. Tretinoin 53-66 glial fibrillary acidic protein Mus musculus 241-245
26818829-3 2016 atRA-mediated increase of both ligands and receptor expression correlated with the elevated level of retinoic acid receptor alpha (RARalpha) expression, while the level of another atRA receptor, peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta), was decreased. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 131-139
9576187-2 1998 To investigate whether the biochemical events following the binding of GM-CSF to its receptor are differentiation dependent we analysed GM-CSF mediated activation of the JAK 2-STAT 5 and MAP kinase pathways in undifferentiated HL-60 cells and HL-60 cells induced to differentiate with dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 315-328 colony stimulating factor 2 Homo sapiens 71-77
9576187-2 1998 To investigate whether the biochemical events following the binding of GM-CSF to its receptor are differentiation dependent we analysed GM-CSF mediated activation of the JAK 2-STAT 5 and MAP kinase pathways in undifferentiated HL-60 cells and HL-60 cells induced to differentiate with dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 330-332 colony stimulating factor 2 Homo sapiens 71-77
9808423-0 1998 Transcriptional regulation of human transcription factor IIB in SMMC-7721 human hepatocellular carcinoma cells by all-trans-retinoic acid and phorbol 12-myristate 13-acetate. Tretinoin 114-137 cilia and flagella associated protein 20 Homo sapiens 36-60
9808423-2 1998 Human transcription factor IIB (TFIIB) was discovered to be decreased on the 3rd day after the cells had been treated with retinoic acid and increased by phorbol 12-myristate 13-acetate, which stimulated the proliferation of human hepatocellular carcinoma cells. Tretinoin 123-136 cilia and flagella associated protein 20 Homo sapiens 6-30
26818829-5 2016 On the contrary, the nuclear quantity of another possible RARalpha counterpart, transcription factor Sp1, was increased after atRA treatment. Tretinoin 126-130 retinoic acid receptor alpha Homo sapiens 58-66
9808423-2 1998 Human transcription factor IIB (TFIIB) was discovered to be decreased on the 3rd day after the cells had been treated with retinoic acid and increased by phorbol 12-myristate 13-acetate, which stimulated the proliferation of human hepatocellular carcinoma cells. Tretinoin 123-136 cilia and flagella associated protein 20 Homo sapiens 32-37
9535729-0 1998 Long-term exposure to retinoic acid induces the expression of IRK1 channels in HERG channel-endowed neuroblastoma cells. Tretinoin 22-35 potassium voltage-gated channel subfamily H member 2 Homo sapiens 79-83
9535729-3 1998 After 10-20 days exposure to Retinoic Acid (RA), SH-SY5Y cells showed, in addition to HERG currents, a novel current characterized by inward rectification, dependence on the extracellular K+ concentration, and blockade by Cs+ and Ba2+, the main features of the IRK1 current. Tretinoin 29-42 potassium voltage-gated channel subfamily H member 2 Homo sapiens 86-90
9535729-3 1998 After 10-20 days exposure to Retinoic Acid (RA), SH-SY5Y cells showed, in addition to HERG currents, a novel current characterized by inward rectification, dependence on the extracellular K+ concentration, and blockade by Cs+ and Ba2+, the main features of the IRK1 current. Tretinoin 44-46 potassium voltage-gated channel subfamily H member 2 Homo sapiens 86-90
9535729-6 1998 On the whole, data here presented demonstrate that RA-induced neuronal differentiation of neuroblastoma cells is accompanied by the switch from a HERG-driven to a IRK1-driven control of Vrest, similarly to what happens in normal differentiating neurons; however, in tumor cells, this switch does not imply the abolition of HERG channel expression. Tretinoin 51-53 potassium voltage-gated channel subfamily H member 2 Homo sapiens 146-150
9535729-6 1998 On the whole, data here presented demonstrate that RA-induced neuronal differentiation of neuroblastoma cells is accompanied by the switch from a HERG-driven to a IRK1-driven control of Vrest, similarly to what happens in normal differentiating neurons; however, in tumor cells, this switch does not imply the abolition of HERG channel expression. Tretinoin 51-53 potassium voltage-gated channel subfamily H member 2 Homo sapiens 323-327
9507016-8 1998 Furthermore, c-fos expression was inhibited by agonists of retinoic acid receptors (RARs) or retinoid X receptors (RXRs), and suppression of c-fos promoter activity by t-RA was abrogated by treatment with antagonists of RAR-alpha or of all the RXRs. Tretinoin 168-172 retinoic acid receptor alpha Homo sapiens 220-229
9412494-8 1998 These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Tretinoin 56-69 erb-b2 receptor tyrosine kinase 2 Mus musculus 28-33
26671998-2 2016 In this study, we showed that activation of CB2with the specific agonist JWH133 [3-(1",1"-dimethylbutyl)-1-deoxy-8-THC] (IC5010(-6)M) mimics epigenetic events induced by RA (IC5010(-7)M) in spermatogonia. Tretinoin 170-172 cannabinoid receptor 2 Homo sapiens 44-47
27050967-0 2016 All-trans retinoic acid prevents the development of type 1 diabetes by affecting the levels of interferon gamma and interleukin 4 in streptozotocin-induced murine diabetes model. Tretinoin 10-23 interleukin 4 Mus musculus 116-129
9701451-1 1998 We have recently found that retinoic acids (RAs) evoke an anticoagulant effect by upregulating thrombomodulin (TM) and downregulating expression of tissue factor (TF) in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 thrombomodulin Homo sapiens 95-109
9521849-0 1998 A putative G-protein-coupled receptor, H218, is down-regulated during the retinoic acid-induced differentiation of F9 embryonal carcinoma cells. Tretinoin 74-87 sphingosine-1-phosphate receptor 2 Homo sapiens 39-43
26811260-3 2016 In the present study, we used TaqMan RT-qPCR to characterize Piwil1 mRNA expression in different types of spermatogenic cells, including primordial germ cells (PGCs), spermatogonial stem cells (SSCs), spermatogonia cells (Sa), tetraploid cells (Tp), round sperm cells (Rs), mature sperm, and in PGCs treated with retinoic acid. Tretinoin 313-326 piwi like RNA-mediated gene silencing 1 Gallus gallus 61-67
9472103-5 1998 The FKBP12 expression increased during ATRA-induced differentiation and expression of cyclophilin A remained unchanged. Tretinoin 39-43 FKBP prolyl isomerase 1A pseudogene 4 Homo sapiens 4-10
9701451-1 1998 We have recently found that retinoic acids (RAs) evoke an anticoagulant effect by upregulating thrombomodulin (TM) and downregulating expression of tissue factor (TF) in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 coagulation factor III, tissue factor Homo sapiens 148-161
9701451-1 1998 We have recently found that retinoic acids (RAs) evoke an anticoagulant effect by upregulating thrombomodulin (TM) and downregulating expression of tissue factor (TF) in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 28-42 coagulation factor III, tissue factor Homo sapiens 163-165
9701451-1 1998 We have recently found that retinoic acids (RAs) evoke an anticoagulant effect by upregulating thrombomodulin (TM) and downregulating expression of tissue factor (TF) in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 thrombomodulin Homo sapiens 95-109
9701451-1 1998 We have recently found that retinoic acids (RAs) evoke an anticoagulant effect by upregulating thrombomodulin (TM) and downregulating expression of tissue factor (TF) in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 coagulation factor III, tissue factor Homo sapiens 148-161
9701451-1 1998 We have recently found that retinoic acids (RAs) evoke an anticoagulant effect by upregulating thrombomodulin (TM) and downregulating expression of tissue factor (TF) in acute promyelocytic leukemia (APL) and monoblastic leukemia cells. Tretinoin 44-47 coagulation factor III, tissue factor Homo sapiens 163-165
9701451-6 1998 A specific RARalpha antagonist, Ro41-5253, efficiently suppressed the upregulation of TM by ATRA and Am80 in NB4 cells, U937 cells and HUVECs. Tretinoin 92-96 retinoic acid receptor alpha Homo sapiens 11-19
9621899-0 1998 Bone morphogenetic protein-7 in growth-plate chondrocytes: regulation by retinoic acid is dependent on the stage of chondrocyte maturation. Tretinoin 73-86 bone morphogenetic protein 7 Gallus gallus 0-28
9621899-3 1998 Low basal levels of bone morphogenetic protein-7 mRNA and protein expression were stimulated by increasing doses of all-trans retinoic acid, a metabolite of vitamin A. Tretinoin 126-139 bone morphogenetic protein 7 Gallus gallus 20-48
9621899-4 1998 The addition of 10 microM retinoic acid resulted in approximately a 6-fold increase in bone morphogenetic protein-7 mRNA levels. Tretinoin 26-39 bone morphogenetic protein 7 Gallus gallus 87-115
26811260-6 2016 Retinoic acid significantly upregulated Piwil1 and Stra8 mRNA expression as well as Piwil1 levels in chicken PGCs. Tretinoin 0-13 piwi like RNA-mediated gene silencing 1 Gallus gallus 40-46
9621899-6 1998 The increase in bone morphogenetic protein-7 transcripts, although present at 6 hours, was maximal following a 12-hour exposure to retinoic acid. Tretinoin 131-144 bone morphogenetic protein 7 Gallus gallus 16-44
9405388-6 1997 The level of P2Y11 transcripts was strongly increased in these cells after granulocyte differentiation induced by retinoic acid or dimethyl sulfoxide. Tretinoin 114-127 purinergic receptor P2Y11 Homo sapiens 13-18
9621899-7 1998 Retinoic acid induction of bone morphogenetic protein-7 transcript levels was dependent on protein synthesis because the induction could be blocked by cyclohexamide. Tretinoin 0-13 bone morphogenetic protein 7 Gallus gallus 27-55
26811260-6 2016 Retinoic acid significantly upregulated Piwil1 and Stra8 mRNA expression as well as Piwil1 levels in chicken PGCs. Tretinoin 0-13 piwi like RNA-mediated gene silencing 1 Gallus gallus 84-90
9621899-8 1998 In maturationally distinct subpopulations of chondrocytes separated by countercurrent centrifugal elutriation, retinoic acid markedly induced bone morphogenetic protein-7 mRNA levels in the least differentiated chondrocytes but had no effect in the most terminally differentiated hypertrophic chondrocytes. Tretinoin 111-124 bone morphogenetic protein 7 Gallus gallus 142-170
26811260-11 2016 Treatment of PGCs with retinoic acid further demonstrated that Piwil1 plays a key role in meiosis during chicken spermatogenesis. Tretinoin 23-36 piwi like RNA-mediated gene silencing 1 Gallus gallus 63-69
9570357-4 1997 Our previous work has shown that RA works synergistically with other agents, such as interferon-gamma (IFN-gamma), to down-regulate N-myc expression and induce differentiation. Tretinoin 33-35 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 132-137
9621899-12 1998 Regulation of bone morphogenetic protein-7 by retinoic acid may be important in normal growth and development as well as in pathologic conditions of an excess or deficiency of vitamin A. Tretinoin 46-59 bone morphogenetic protein 7 Gallus gallus 14-42
9486654-3 1998 PML-RARalpha APL patients achieve complete remission following treatments with pharmacological doses of retinoic acids (RA); in contrast, PLZF-RARalpha patients respond very poorly, if at all. Tretinoin 104-118 PML nuclear body scaffold Homo sapiens 0-3
26271478-0 2016 Retinoic Acid Inhibits Adipogenesis Modulating C/EBPbeta Phosphorylation and Down Regulating Srebf1a Expression. Tretinoin 0-13 sterol regulatory element binding transcription factor 1 Homo sapiens 93-99
9486654-3 1998 PML-RARalpha APL patients achieve complete remission following treatments with pharmacological doses of retinoic acids (RA); in contrast, PLZF-RARalpha patients respond very poorly, if at all. Tretinoin 104-118 retinoic acid receptor alpha Homo sapiens 4-12
9486654-3 1998 PML-RARalpha APL patients achieve complete remission following treatments with pharmacological doses of retinoic acids (RA); in contrast, PLZF-RARalpha patients respond very poorly, if at all. Tretinoin 4-6 PML nuclear body scaffold Homo sapiens 0-3
9486655-4 1998 However, treatment with RA induces differentiation of leukaemic blast cells and disease remission in PML-RARalpha APLs, whereas PLZF-RARa APLs are resistant to RA. Tretinoin 24-26 PML nuclear body scaffold Homo sapiens 101-104
9486655-4 1998 However, treatment with RA induces differentiation of leukaemic blast cells and disease remission in PML-RARalpha APLs, whereas PLZF-RARa APLs are resistant to RA. Tretinoin 24-26 retinoic acid receptor alpha Homo sapiens 105-113
9486655-4 1998 However, treatment with RA induces differentiation of leukaemic blast cells and disease remission in PML-RARalpha APLs, whereas PLZF-RARa APLs are resistant to RA. Tretinoin 24-26 retinoic acid receptor alpha Homo sapiens 105-109
9486655-4 1998 However, treatment with RA induces differentiation of leukaemic blast cells and disease remission in PML-RARalpha APLs, whereas PLZF-RARa APLs are resistant to RA. Tretinoin 105-107 PML nuclear body scaffold Homo sapiens 101-104
9486655-8 1998 High doses of RA release histone deacetylase activity from PML-RARalpha, but not from PLZF-RARalpha. Tretinoin 14-16 PML nuclear body scaffold Homo sapiens 59-62
9486655-8 1998 High doses of RA release histone deacetylase activity from PML-RARalpha, but not from PLZF-RARalpha. Tretinoin 14-16 retinoic acid receptor alpha Homo sapiens 63-71
9486655-10 1998 Therefore, recruitment of histone deacetylase is crucial to the transforming potential of APL fusion proteins, and the different effects of RA on the stability of the PML-RARalpha and PLZF-RARalpha co-repressor complexes determines the differential response of APLs to RA. Tretinoin 140-142 PML nuclear body scaffold Homo sapiens 167-170
9486655-10 1998 Therefore, recruitment of histone deacetylase is crucial to the transforming potential of APL fusion proteins, and the different effects of RA on the stability of the PML-RARalpha and PLZF-RARalpha co-repressor complexes determines the differential response of APLs to RA. Tretinoin 140-142 retinoic acid receptor alpha Homo sapiens 171-179
9415455-7 1997 In the RA-treated heart, an intermittent patchy staining for fibronectin and a sparse distribution of type I collagen were observed in the thin cardiac jelly. Tretinoin 7-9 fibronectin 1 Mus musculus 61-72
9373269-5 1997 We show that prior incubation of human myeloid leukemic cells with ATRA or 1,25(OH)2 D3 induced resistance to idarubicin-induced apoptosis, which was modulated by coincubation with GM-CSF. Tretinoin 67-71 colony stimulating factor 2 Homo sapiens 181-187
9486655-10 1998 Therefore, recruitment of histone deacetylase is crucial to the transforming potential of APL fusion proteins, and the different effects of RA on the stability of the PML-RARalpha and PLZF-RARalpha co-repressor complexes determines the differential response of APLs to RA. Tretinoin 140-142 retinoic acid receptor alpha Homo sapiens 189-197
26659823-12 2016 In addition, CDDP/ATRA co-treatment significantly increased RAR-alpha, RXR-alpha, fibrin, and iNOS protein expression compared to CDDP alone. Tretinoin 18-22 retinoic acid receptor, alpha Rattus norvegicus 60-69
9486655-10 1998 Therefore, recruitment of histone deacetylase is crucial to the transforming potential of APL fusion proteins, and the different effects of RA on the stability of the PML-RARalpha and PLZF-RARalpha co-repressor complexes determines the differential response of APLs to RA. Tretinoin 171-173 PML nuclear body scaffold Homo sapiens 167-170
9452473-5 1998 Interestingly, the serine at position 232 in RARalpha gives an explanation for the observed differences in the affinity of the naturally occurring ligand, all-trans-retinoic acid (t-RA), in this receptor compared with that for the other receptors, since hydrogen bonding would not be permitted between the hydroxyl of serine and the hydrophobic linker of t-RA. Tretinoin 155-178 retinoic acid receptor alpha Homo sapiens 45-53
9361184-1 1997 The receptors for retinoic acid (RA) and for 1 alpha,25-dihydroxyvitamin D3 (VD), RAR, RXR, and VDR are ligand-inducible members of the nuclear receptor superfamily. Tretinoin 18-31 retinoic acid receptor alpha Homo sapiens 82-85
9417874-0 1997 Reduction of both RAR and RXR levels is required to maximally alter sensitivity of CA-OV3 ovarian tumor cells to growth suppression by all-trans-retinoic acid. Tretinoin 135-158 retinoic acid receptor alpha Homo sapiens 18-21
9452473-5 1998 Interestingly, the serine at position 232 in RARalpha gives an explanation for the observed differences in the affinity of the naturally occurring ligand, all-trans-retinoic acid (t-RA), in this receptor compared with that for the other receptors, since hydrogen bonding would not be permitted between the hydroxyl of serine and the hydrophobic linker of t-RA. Tretinoin 180-184 retinoic acid receptor alpha Homo sapiens 45-53
26566904-6 2016 Inhibition of RA synthesis in newborn mice decreased FGF-18 and elastin expression and impaired alveolarization. Tretinoin 14-16 elastin Mus musculus 64-71
9488621-1 1998 Acute myeloid leukaemia (AML) of FAB subtype M3 is associated with t(15;17)(q22;q21) and a relatively good prognosis when treated with all-trans retinoic acid (ATRA) and combination chemotherapy. Tretinoin 145-158 FA complementation group B Homo sapiens 33-36
9488621-1 1998 Acute myeloid leukaemia (AML) of FAB subtype M3 is associated with t(15;17)(q22;q21) and a relatively good prognosis when treated with all-trans retinoic acid (ATRA) and combination chemotherapy. Tretinoin 160-164 FA complementation group B Homo sapiens 33-36
9488621-3 1998 The translocation t(11;17)(q23;q21) leading to a PLZF/RARalpha rearrangement has been described in a very small number of cases and has been associated with a poor response to ATRA and an adverse prognosis. Tretinoin 176-180 retinoic acid receptor alpha Homo sapiens 54-62
9488621-4 1998 We describe a case of AML FAB type M3 with this translocation who entered morphological and cytogenetic complete remission after concurrent prolonged ATRA and one course of induction chemotherapy and remains in morphological and molecular remission at 10 months after presentation. Tretinoin 150-154 FA complementation group B Homo sapiens 26-29
9488639-0 1998 Establishment of a GM-CSF-dependent megakaryoblastic cell line with the potential to differentiate into an eosinophilic lineage in response to retinoic acids. Tretinoin 143-157 colony stimulating factor 2 Homo sapiens 19-25
9351827-0 1997 Phosphorylation of activation functions AF-1 and AF-2 of RAR alpha and RAR gamma is indispensable for differentiation of F9 cells upon retinoic acid and cAMP treatment. Tretinoin 135-148 retinoic acid receptor alpha Homo sapiens 57-66
9345016-0 1997 Induction of apoptosis without differentiation by retinoic acid in PLB-985 cells requires the activation of both RAR and RXR. Tretinoin 50-63 retinoic acid receptor alpha Homo sapiens 113-116
9367652-10 1997 Although the synthesis of Retinoid and Fatty Acid Binding Glycoprotein does not require chromophore precursors as does that of opsin, the control of Retinoid and Fatty Acid Binding Glycoprotein and opsin transcription by retinoids including retinoic acid might very well be the same. Tretinoin 241-254 neither inactivation nor afterpotential E Drosophila melanogaster 198-203
9488639-4 1998 All-trans-RA, 13-cis-RA and 9-cis-RA at 10(-8) mol/l to 10(-5) mol/l inhibited the GM-CSF-dependent cell growth. Tretinoin 10-12 colony stimulating factor 2 Homo sapiens 83-89
9526050-0 1998 Retinoic acid regulates gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 0-13 gonadotropin releasing hormone 1 Rattus norvegicus 24-54
9526050-0 1998 Retinoic acid regulates gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 0-13 gonadotropin releasing hormone 1 Rattus norvegicus 56-60
9526050-1 1998 The present study attempts to examine the possible involvement of retinoic acid (RA) in the regulation of gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 66-79 gonadotropin releasing hormone 1 Rattus norvegicus 106-136
26673819-4 2016 The expression of peptidylarginine deiminase 4 (PADI4), encoding PAD4, a protein that post-translationally converts arginine into citrulline, was restored during ATRA-induced differentiation. Tretinoin 162-166 peptidyl arginine deiminase 4 Homo sapiens 18-46
9526050-1 1998 The present study attempts to examine the possible involvement of retinoic acid (RA) in the regulation of gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 66-79 gonadotropin releasing hormone 1 Rattus norvegicus 138-142
9526050-1 1998 The present study attempts to examine the possible involvement of retinoic acid (RA) in the regulation of gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 81-83 gonadotropin releasing hormone 1 Rattus norvegicus 106-136
9526050-1 1998 The present study attempts to examine the possible involvement of retinoic acid (RA) in the regulation of gonadotropin-releasing hormone (GnRH) release and gene expression in the rat hypothalamic fragments and GT1-1 neuronal cells in vitro. Tretinoin 81-83 gonadotropin releasing hormone 1 Rattus norvegicus 138-142
9526050-2 1998 During a short-term period (2h), RA (0.01-1 microM) increased GnRH release in a dose-related manner. Tretinoin 33-35 gonadotropin releasing hormone 1 Mus musculus 62-66
9526050-3 1998 Time-course experiments showed that RA rapidly increased GnRH release by 30 min in both cells. Tretinoin 36-38 gonadotropin releasing hormone 1 Mus musculus 57-61
9526050-4 1998 RA-induced GnRH release was slowly attenuated in the next incubation period in hypothalamic fragments, but rapidly returned to control levels in GT-1 cells. Tretinoin 0-2 gonadotropin releasing hormone 1 Mus musculus 11-15
9365540-0 1997 Retinoic acid downregulates growth, fibronectin and RAR alpha in 3T3 cells: Ha-ras blocks this response and RA metabolism. Tretinoin 0-13 fibronectin 1 Mus musculus 36-47
9365540-1 1997 Retinoic acid (RA) reduced growth, fibronectin, and retinoic acid receptor (RAR alpha) in NIH 3T3 cells but not in cells transformed by the Ha-ras oncogene. Tretinoin 0-13 fibronectin 1 Mus musculus 35-46
9526050-12 1998 Taken together, the present study strongly suggests that RA is an important regulator of the GnRH neurons. Tretinoin 57-59 gonadotropin releasing hormone 1 Mus musculus 93-97
26673819-4 2016 The expression of peptidylarginine deiminase 4 (PADI4), encoding PAD4, a protein that post-translationally converts arginine into citrulline, was restored during ATRA-induced differentiation. Tretinoin 162-166 peptidyl arginine deiminase 4 Homo sapiens 48-53
26673819-4 2016 The expression of peptidylarginine deiminase 4 (PADI4), encoding PAD4, a protein that post-translationally converts arginine into citrulline, was restored during ATRA-induced differentiation. Tretinoin 162-166 peptidyl arginine deiminase 4 Homo sapiens 65-69
9376579-9 1997 ATRA also induced expression of C/EBP epsilon protein in NB4 cells, as shown by Western blotting. Tretinoin 0-4 CCAAT enhancer binding protein epsilon Homo sapiens 32-45
26673819-6 2016 Functionally, PAD4 translocated into the nucleus upon ATRA exposure and promoted ATRA-mediated differentiation. Tretinoin 54-58 peptidyl arginine deiminase 4 Homo sapiens 14-18
9438553-10 1998 To test the hypothesis that GST-catalyzed GSH conjugation can effectively prevent inhibition of t-RA synthesis by aldehydic products of lipid peroxidation, triethyltin bromide (TEB, a potent inhibitor of GST, 20 microM) was added to ARHC-catalyzed reactions when hexanal or tNE were present in the incubations. Tretinoin 96-100 hematopoietic prostaglandin D synthase Rattus norvegicus 28-31
9376579-13 1997 We suspect that the C/EBP epsilon promoter/enhancer contains a retinoic acid-response element that is directly stimulated by retinoids. Tretinoin 63-76 CCAAT enhancer binding protein epsilon Homo sapiens 20-33
25645024-2 2016 RESULTS: The serum osteocalcin levels in the Mix and SPA-IS groups decreased compared with the model group (mice showing retinoic acid-induced osteoporosis) (P < 0.05). Tretinoin 121-134 bone gamma-carboxyglutamate protein 2 Mus musculus 19-30
9377582-3 1997 Parental and vector-transfected MCF7 cells, which were sensitive to the growth-inhibitory effects of atRA, exhibited atRA-dependent retinoic acid receptor (RAR) transactivation and transrepression of 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity. Tretinoin 101-105 retinoic acid receptor alpha Homo sapiens 156-159
9462740-1 1998 Acute promyelocytic leukaemia (APL), associated with chromosomal translocations involving the retinoic acid receptor alpha gene (RARA) and the PML gene, is sensitive to retinoic acid (RA) treatment, while APL patients harbouring translocations between RARA and the PLZF gene do not respond to RA. Tretinoin 94-107 retinoic acid receptor alpha Homo sapiens 129-133
9462740-1 1998 Acute promyelocytic leukaemia (APL), associated with chromosomal translocations involving the retinoic acid receptor alpha gene (RARA) and the PML gene, is sensitive to retinoic acid (RA) treatment, while APL patients harbouring translocations between RARA and the PLZF gene do not respond to RA. Tretinoin 129-131 retinoic acid receptor alpha Homo sapiens 94-122
9462740-1 1998 Acute promyelocytic leukaemia (APL), associated with chromosomal translocations involving the retinoic acid receptor alpha gene (RARA) and the PML gene, is sensitive to retinoic acid (RA) treatment, while APL patients harbouring translocations between RARA and the PLZF gene do not respond to RA. Tretinoin 131-133 retinoic acid receptor alpha Homo sapiens 94-122
9442029-0 1998 Identification of the eukaryotic initiation factor 5A as a retinoic acid-stimulated cellular binding partner for tissue transglutaminase II. Tretinoin 59-72 eukaryotic translation initiation factor 5A Homo sapiens 22-53
9442090-3 1998 Like its human and zibrafish counterparts, the mouse P450RAI cDNA catalyzes metabolism of retinoic acid into 4-OH-retinoic acid, 4-oxo-retinoic acid, 18-OH-retinoic acid, and unidentified water-soluble metabolites when transfected into COS-1 cells. Tretinoin 90-103 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 53-60
9442090-5 1998 We were interested in determining whether P450RAI could be responsible for retinoic acid metabolism in F9 cells and in studying the effect of retinoid receptor ablation on P450RAI expression. Tretinoin 75-88 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 42-49
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 141-154 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 200-207
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 178-191 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 200-207
9442090-7 1998 These experiments, as well as others using synthetic receptor subtype-specific retinoids, suggest that the RAR gamma and RXR alpha receptors mediate the effects of retinoic acid on the expression of the P450RAI gene. Tretinoin 164-177 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 203-210
9473674-0 1998 Bone morphogenetic protein-2 and retinoic acid induce neurotrophin-3 responsiveness in developing rat sympathetic neurons. Tretinoin 33-46 neurotrophin 3 Rattus norvegicus 54-68
9473674-6 1998 Treatment of SCG neurons with retinoic acid (RA) promoted the effect of BMP2 on the induction of trkC mRNA levels. Tretinoin 30-43 neurotrophic receptor tyrosine kinase 3 Rattus norvegicus 97-101
9473674-6 1998 Treatment of SCG neurons with retinoic acid (RA) promoted the effect of BMP2 on the induction of trkC mRNA levels. Tretinoin 45-47 neurotrophic receptor tyrosine kinase 3 Rattus norvegicus 97-101
9387884-5 1997 When RA-treated aggregates of P19 cells were cultured under conditions permissive for neurite outgrowth, we observed a significant increase in the amount of detectable NF-L protein localized within morphologically distinct neurons. Tretinoin 5-7 interleukin 23 subunit alpha Homo sapiens 30-33
14555966-6 1997 In these stably transfected HeLa cells both the endogenous tissue transglutaminase gene and transfected mouse tissue transglutaminase promoter are activated by all-trans retinoic acid and by retinoic acid receptor (RAR)-specific and retinoid X receptor (RXR)-specific retinoids. Tretinoin 170-183 transglutaminase 2, C polypeptide Mus musculus 110-133
9473674-8 1998 Furthermore, BMP2/RA treatment induced the endogenous expression of NT3. Tretinoin 18-20 neurotrophin 3 Rattus norvegicus 68-71
26374632-2 2016 We explored these questions in the context of acute promyelocytic leukemia cells (NB4) expressing oncogenic fusion protein, PML-RARa and exquisitely sensitive to its clinically used antagonist, the all-trans retinoic acid (ATRA). Tretinoin 208-221 PML nuclear body scaffold Homo sapiens 124-127
9426070-2 1998 The effects of RA are mediated by a family of ligand-dependent transcription factors, the retinoic acid receptors (RAR) and the retinoid X receptors. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 90-113
9426070-2 1998 The effects of RA are mediated by a family of ligand-dependent transcription factors, the retinoic acid receptors (RAR) and the retinoid X receptors. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 115-118
9402230-1 1997 In vitro neural differentiation was induced in a p53-deficient immortalized neuroectodermal progenitor cell line, NE-4C, by treatment with retinoic acid [K. Schlett and E. Madarasz (1997) J. Neurosci. Tretinoin 139-152 transformation related protein 53, pseudogene Mus musculus 49-52
9305907-6 1997 Expression of the constitutively active form of Galpha13 (Q226L) stimulates differentiation of the cells from embryonal to endodermal, in the absence of retinoic acid. Tretinoin 153-166 guanine nucleotide binding protein, alpha 13 Mus musculus 48-56
9305907-7 1997 Thus, both Galpha12 and Galpha13 are essential to stimulation of cell differentiation by retinoic acid. Tretinoin 89-102 guanine nucleotide binding protein, alpha 13 Mus musculus 24-32
9305908-1 1997 Retinoic acid induces P19 mouse embryonal carcinoma cells to differentiate to endoderm and increases expression of the heterotrimeric G-protein subunits Galpha12 and Galpha13. Tretinoin 0-13 guanine nucleotide binding protein, alpha 13 Mus musculus 166-174
9305908-3 1997 Much like retinoic acid, expression of constitutively active forms of Galpha12 and Galpha13 induced differentiation and constitutive activation of c-Jun amino-terminal kinase. Tretinoin 10-23 guanine nucleotide binding protein, alpha 13 Mus musculus 83-91
26374632-2 2016 We explored these questions in the context of acute promyelocytic leukemia cells (NB4) expressing oncogenic fusion protein, PML-RARa and exquisitely sensitive to its clinically used antagonist, the all-trans retinoic acid (ATRA). Tretinoin 223-227 PML nuclear body scaffold Homo sapiens 124-127
9305908-5 1997 These data implicate c-Jun amino-terminal kinase as a downstream element of activation of Galpha12 or Galpha13 obligate for retinoic acid-induced differentiation. Tretinoin 124-137 guanine nucleotide binding protein, alpha 13 Mus musculus 102-110
26374632-7 2016 Endothelial cell uptake of NB4-derived EVs renders these cells more TF-positive and procoagulant, and this effect is diminished by pre-treatment of EV donor cells with ATRA. Tretinoin 168-172 coagulation factor III, tissue factor Homo sapiens 68-70
9496783-1 1998 We report the structure, chromosomal localization and expression features of Stra3, a novel mouse gene whose expression is upregulated by retinoic acid in P19 embryonal carcinoma cells. Tretinoin 138-151 left right determination factor 1 Mus musculus 77-82
26783748-0 2016 All-Trans Retinoic Acid Attenuates Hypoxia-Induced Injury in NRK52E Cells via Inhibiting NF-x03BA;B/VEGF and TGF-beta2/VEGF Pathway. Tretinoin 10-23 vascular endothelial growth factor A Rattus norvegicus 100-104
9496783-5 1998 We also show that Stra3/lefty is ectopically induced in the endodermal and ectodermal layers following in vivo administration of retinoic acid to gastrulating mouse embryos. Tretinoin 129-142 left right determination factor 1 Mus musculus 18-23
9496783-5 1998 We also show that Stra3/lefty is ectopically induced in the endodermal and ectodermal layers following in vivo administration of retinoic acid to gastrulating mouse embryos. Tretinoin 129-142 left right determination factor 1 Mus musculus 24-29
9269772-1 1997 We recently found that retinoic acids (RAs) exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) cells and monoblastic leukemia cells. Tretinoin 23-37 thrombomodulin Homo sapiens 88-102
9269772-1 1997 We recently found that retinoic acids (RAs) exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) cells and monoblastic leukemia cells. Tretinoin 23-37 coagulation factor III, tissue factor Homo sapiens 127-140
9269772-1 1997 We recently found that retinoic acids (RAs) exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) cells and monoblastic leukemia cells. Tretinoin 23-37 coagulation factor III, tissue factor Homo sapiens 142-144
9269772-1 1997 We recently found that retinoic acids (RAs) exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) cells and monoblastic leukemia cells. Tretinoin 39-42 thrombomodulin Homo sapiens 88-102
9269772-1 1997 We recently found that retinoic acids (RAs) exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) cells and monoblastic leukemia cells. Tretinoin 39-42 coagulation factor III, tissue factor Homo sapiens 127-140
9269772-1 1997 We recently found that retinoic acids (RAs) exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia (APL) cells and monoblastic leukemia cells. Tretinoin 39-42 coagulation factor III, tissue factor Homo sapiens 142-144
9269772-6 1997 A specific RAR alpha antagonist, Ro41-5253, significantly suppressed the upregulation of TM by ATRA and Am80 in NB4 cells, U937 cells, and HUVECs. Tretinoin 95-99 retinoic acid receptor alpha Homo sapiens 11-20
9852221-0 1998 CD95 predicts responsiveness to tretinoin in acute promyelocytic leukemia. Tretinoin 32-41 Fas cell surface death receptor Homo sapiens 0-4
9852221-1 1998 We describe a predictive marker (CD95) for the responsiveness to tretinoin (RA) in acute promyelocytic leukemia (APL). Tretinoin 65-74 Fas cell surface death receptor Homo sapiens 33-37
9439457-2 1997 Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. Tretinoin 205-218 lipoprotein lipase Homo sapiens 78-96
9439457-2 1997 Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. Tretinoin 205-218 lipoprotein lipase Homo sapiens 98-101
9242550-3 1997 T-RA is an effective inducer of clinical remission only in patients carrying the t(15;17) and expressing the PML/RAR alpha products. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 109-122
9242550-9 1997 Moreover, two different high-affinity 9-cis-RA binding sites (Kd = 0.45 and 0.075 nmol/L) were detectable in the bcr3-PML/RAR alpha product but not in the bcr1-PML/RAR alpha product (Kd = 0.77 nmol/L). Tretinoin 38-46 PML nuclear body scaffold Homo sapiens 118-121
9439457-2 1997 Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. Tretinoin 205-218 peroxisome proliferator activated receptor alpha Homo sapiens 155-197
9242550-9 1997 Moreover, two different high-affinity 9-cis-RA binding sites (Kd = 0.45 and 0.075 nmol/L) were detectable in the bcr3-PML/RAR alpha product but not in the bcr1-PML/RAR alpha product (Kd = 0.77 nmol/L). Tretinoin 38-46 retinoic acid receptor alpha Homo sapiens 122-131
9439457-2 1997 Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. Tretinoin 205-218 peroxisome proliferator activated receptor alpha Homo sapiens 199-203
9242550-9 1997 Moreover, two different high-affinity 9-cis-RA binding sites (Kd = 0.45 and 0.075 nmol/L) were detectable in the bcr3-PML/RAR alpha product but not in the bcr1-PML/RAR alpha product (Kd = 0.77 nmol/L). Tretinoin 38-46 PML nuclear body scaffold Homo sapiens 160-163
26783748-0 2016 All-Trans Retinoic Acid Attenuates Hypoxia-Induced Injury in NRK52E Cells via Inhibiting NF-x03BA;B/VEGF and TGF-beta2/VEGF Pathway. Tretinoin 10-23 transforming growth factor, beta 2 Rattus norvegicus 109-118
9242550-9 1997 Moreover, two different high-affinity 9-cis-RA binding sites (Kd = 0.45 and 0.075 nmol/L) were detectable in the bcr3-PML/RAR alpha product but not in the bcr1-PML/RAR alpha product (Kd = 0.77 nmol/L). Tretinoin 38-46 retinoic acid receptor alpha Homo sapiens 164-173
9242550-10 1997 By competition binding experiments we showed that 9-cis-RA binds with higher specificity to the bcr3-PML/RAR alpha isoform than to the bcr1-PML/RAR alpha or RAR alpha. Tretinoin 50-58 retinoic acid receptor alpha Homo sapiens 96-114
9447831-7 1997 Addition of ATRA induced the progressive expression and accumulation of p22phox, p91phox, p47phox and p67phox. Tretinoin 12-16 cytochrome b-245 alpha chain Homo sapiens 72-79
26783748-0 2016 All-Trans Retinoic Acid Attenuates Hypoxia-Induced Injury in NRK52E Cells via Inhibiting NF-x03BA;B/VEGF and TGF-beta2/VEGF Pathway. Tretinoin 10-23 vascular endothelial growth factor A Rattus norvegicus 119-123
9242550-10 1997 By competition binding experiments we showed that 9-cis-RA binds with higher specificity to the bcr3-PML/RAR alpha isoform than to the bcr1-PML/RAR alpha or RAR alpha. Tretinoin 50-58 BCR pseudogene 1 Homo sapiens 135-139
9242550-10 1997 By competition binding experiments we showed that 9-cis-RA binds with higher specificity to the bcr3-PML/RAR alpha isoform than to the bcr1-PML/RAR alpha or RAR alpha. Tretinoin 50-58 PML nuclear body scaffold Homo sapiens 101-104
26783748-14 2016 CONCLUSIONS: This study indicated that ATRA may attenuate hypoxia-induced injury in NRK52E cells via inhibiting NF-x03BA;B/VEGF and TGF-beta2/VEGF pathway. Tretinoin 39-43 vascular endothelial growth factor A Rattus norvegicus 123-127
9242550-10 1997 By competition binding experiments we showed that 9-cis-RA binds with higher specificity to the bcr3-PML/RAR alpha isoform than to the bcr1-PML/RAR alpha or RAR alpha. Tretinoin 50-58 retinoic acid receptor alpha Homo sapiens 105-114
9242550-10 1997 By competition binding experiments we showed that 9-cis-RA binds with higher specificity to the bcr3-PML/RAR alpha isoform than to the bcr1-PML/RAR alpha or RAR alpha. Tretinoin 50-58 retinoic acid receptor alpha Homo sapiens 144-153
9395213-0 1997 Inhibition by N-(4-hydroxyphenyl)retinamide and all-trans-retinoic acid of exogenous and endogenous development of putative preneoplastic, glutathione S-transferase placental form-positive lesions in the livers of rats. Tretinoin 48-71 hematopoietic prostaglandin D synthase Rattus norvegicus 139-164
9242550-11 1997 Consistent with these data, the binding of 9-cis-RA to the bcr3-PML/RAR alpha product resulted in increased transcriptional activation of the RA-responsive element (RARE) TRE, but not of the betaRARE, in transiently transfected COS-1 cells. Tretinoin 43-51 retinoic acid receptor alpha Homo sapiens 59-77
26783748-14 2016 CONCLUSIONS: This study indicated that ATRA may attenuate hypoxia-induced injury in NRK52E cells via inhibiting NF-x03BA;B/VEGF and TGF-beta2/VEGF pathway. Tretinoin 39-43 transforming growth factor, beta 2 Rattus norvegicus 132-141
9268495-5 1997 Enhancement of IL-2Ralpha/beta by RA was accompanied by upregulation of the expression of CD38, CD69, CD45RO, and HLA-DR, surface molecules known to be associated with T-cell activation. Tretinoin 34-36 CD38 molecule Homo sapiens 90-94
26783748-14 2016 CONCLUSIONS: This study indicated that ATRA may attenuate hypoxia-induced injury in NRK52E cells via inhibiting NF-x03BA;B/VEGF and TGF-beta2/VEGF pathway. Tretinoin 39-43 vascular endothelial growth factor A Rattus norvegicus 142-146
9550098-6 1997 Since these enzymes (EROD, CYP 1A1/2 and PROD, CYP2B1) activate polycyclic hydrocarbons, aromatic amines and aliphatic halogenated hydrocarbons to their ultimate mutagenic or carcinogenic forms, and are effective in producing reactive oxygen species such as superoxide, hydroxyl radical and hydrogen peroxide, the new compound, BITN, appears to have a greater anticarcinogenic and antioxidant potential than RA and BHT. Tretinoin 408-410 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 27-34
9365540-1 1997 Retinoic acid (RA) reduced growth, fibronectin, and retinoic acid receptor (RAR alpha) in NIH 3T3 cells but not in cells transformed by the Ha-ras oncogene. Tretinoin 15-17 fibronectin 1 Mus musculus 35-46
9272954-3 1997 In addition to directing expression in the central nervous system (CNS) up to the correct rhombomere 6/7 boundary in the hindbrain, the neural enhancer also mediates a three rhombomere anterior shift from this boundary in response to retinoic acid (RA), mimicking the endogenous Hoxd4 response. Tretinoin 249-251 homeobox D4 Homo sapiens 279-284
25980532-5 2016 Mass spectrometry analysis of the CSF identified retinol binding protein 4 (Rbp4), which transports retinol, the precursor to retinoic acid (RA). Tretinoin 126-139 retinol binding protein 4, plasma Danio rerio 49-74
9272954-5 1997 Comparative analysis of the retinoid responses of Hoxd4, Hoxa4 and Hoxb4 reveals that, while they can be rapidly induced by RA, there is a window of competence for this response, which is different to that of more 3" Hox genes. Tretinoin 124-126 homeobox D4 Homo sapiens 50-55
9277051-0 1997 Prediction of growth sensitivity of acute promyelocytic leukemia cells to granulocyte colony-stimulating factor using 7AAD/PY during administration of all-trans retinoic acid. Tretinoin 161-174 colony stimulating factor 3 Homo sapiens 74-111
9277051-5 1997 In one patient, APL cells harvested from marrow during the first 3 weeks of ATRA administration showed distinct growth sensitivity to G-CSF ex vivo, and the cells harvested after a 4-week exposure to ATRA appeared to have lost this sensitivity. Tretinoin 76-80 colony stimulating factor 3 Homo sapiens 134-139
9277051-6 1997 In this patient, G-CSF could be safely administered after 4 weeks of ATRA therapy. Tretinoin 69-73 colony stimulating factor 3 Homo sapiens 17-22
9277051-7 1997 7AAD/PY analysis is useful for predicting growth sensitivity of APL cells to G-CSF during ATRA administration. Tretinoin 90-94 colony stimulating factor 3 Homo sapiens 77-82
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 38-51 PML nuclear body scaffold Homo sapiens 22-25
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 38-51 retinoic acid receptor alpha Homo sapiens 26-34
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 38-51 PML nuclear body scaffold Homo sapiens 133-136
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 38-51 retinoic acid receptor alpha Homo sapiens 137-145
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 26-28 PML nuclear body scaffold Homo sapiens 22-25
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 26-28 PML nuclear body scaffold Homo sapiens 133-136
9369431-0 1997 Mutant AF-2 domain of PML-RARalpha in retinoic acid-resistant NB4 cells: differentiation induced by RA is triggered directly through PML-RARalpha and its down-regulation in acute promyelocytic leukemia. Tretinoin 26-28 retinoic acid receptor alpha Homo sapiens 137-145
9369431-4 1997 Immunostaining of NB4/RA cells using anti-PML antibody showed a microgranular pattern which was not restored even by the combination of RA and 8-CPT-cAMP, whereas the microgranular pattern in NB4 cells was rapidly restored to the normal speckled pattern by RA. Tretinoin 22-24 PML nuclear body scaffold Homo sapiens 42-45
9369431-4 1997 Immunostaining of NB4/RA cells using anti-PML antibody showed a microgranular pattern which was not restored even by the combination of RA and 8-CPT-cAMP, whereas the microgranular pattern in NB4 cells was rapidly restored to the normal speckled pattern by RA. Tretinoin 136-138 PML nuclear body scaffold Homo sapiens 42-45
9369431-8 1997 These data suggest that differentiation of APL by RA is triggered directly through PML-RARalpha, and is associated with its degradation. Tretinoin 50-52 PML nuclear body scaffold Homo sapiens 83-86
9234742-0 1997 Opposite effects of the acute promyelocytic leukemia PML-retinoic acid receptor alpha (RAR alpha) and PLZF-RAR alpha fusion proteins on retinoic acid signalling. Tretinoin 57-70 retinoic acid receptor alpha Homo sapiens 87-96
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 150-163 PML nuclear body scaffold Homo sapiens 14-17
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 150-163 retinoic acid receptor alpha Homo sapiens 40-49
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 150-163 PML nuclear body scaffold Homo sapiens 194-197
9369431-8 1997 These data suggest that differentiation of APL by RA is triggered directly through PML-RARalpha, and is associated with its degradation. Tretinoin 50-52 retinoic acid receptor alpha Homo sapiens 87-95
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 150-163 retinoic acid receptor alpha Homo sapiens 40-49
9366521-3 1997 RA-induced cell cycle arrest is also associated with induction of p27Kip1 expression, inhibition of cdk2-associated kinase activity and alteration of the phosphorylation state of the pRB-family proteins. Tretinoin 0-2 cyclin dependent kinase inhibitor 1B Homo sapiens 66-73
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 150-163 retinoic acid receptor alpha Homo sapiens 40-49
9366521-8 1997 Interestingly, when U343 cells are growth arrested by p16, p21 or p27 induction and treated simultaneously with RA, a dramatic morphological change occurs, cells acquiring multiple long, tapering processes reminiscent of primary astrocytes. Tretinoin 112-114 interferon alpha inducible protein 27 Homo sapiens 66-69
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 18-20 PML nuclear body scaffold Homo sapiens 14-17
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 18-20 PML nuclear body scaffold Homo sapiens 194-197
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 40-42 PML nuclear body scaffold Homo sapiens 194-197
25980532-5 2016 Mass spectrometry analysis of the CSF identified retinol binding protein 4 (Rbp4), which transports retinol, the precursor to retinoic acid (RA). Tretinoin 126-139 retinol binding protein 4, plasma Danio rerio 76-80
9344581-4 1997 Suppression of RAR function in HMECs resulted in reduced growth inhibition mediated by all-trans-retinoic acid (ATRA). Tretinoin 87-110 retinoic acid receptor alpha Homo sapiens 15-18
25980532-5 2016 Mass spectrometry analysis of the CSF identified retinol binding protein 4 (Rbp4), which transports retinol, the precursor to retinoic acid (RA). Tretinoin 141-143 retinol binding protein 4, plasma Danio rerio 49-74
9344581-4 1997 Suppression of RAR function in HMECs resulted in reduced growth inhibition mediated by all-trans-retinoic acid (ATRA). Tretinoin 112-116 retinoic acid receptor alpha Homo sapiens 15-18
9224725-8 1997 Treatment with TPA subsequent to a 120-h pretreatment with retinoic acid (RA), 9-cis-RA, or calcitriol resulted in a potentiation of the induction of OPN mRNA. Tretinoin 59-72 secreted phosphoprotein 1 Homo sapiens 150-153
9224725-8 1997 Treatment with TPA subsequent to a 120-h pretreatment with retinoic acid (RA), 9-cis-RA, or calcitriol resulted in a potentiation of the induction of OPN mRNA. Tretinoin 74-76 secreted phosphoprotein 1 Homo sapiens 150-153
25980532-5 2016 Mass spectrometry analysis of the CSF identified retinol binding protein 4 (Rbp4), which transports retinol, the precursor to retinoic acid (RA). Tretinoin 141-143 retinol binding protein 4, plasma Danio rerio 76-80
25980532-8 2016 Zebrafish rbp4 is highly expressed in the yolk syncytial layer, suggesting Rbp4 protein and retinol/RA precursors can be transported into the CSF from the yolk. Tretinoin 100-102 retinol binding protein 4, plasma Danio rerio 10-14
9230184-2 1997 Levels of expression of the retinoic acid 4-hydroxylase, P450RAI, did not change, whereas cytochrome P4501A2 levels were lower in the null mouse, as shown earlier; however, this enzyme was found not to be active toward retinoic acid. Tretinoin 28-41 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 57-64
9421176-0 1997 TrkA expression levels of sympathetic neurons correlate with NGF-dependent survival during development and after treatment with retinoic acid. Tretinoin 128-141 neurotrophic receptor tyrosine kinase 1 Gallus gallus 0-4
25980532-10 2016 Together, these data support the model that Rbp4 and RA precursors are present within the CSF and used for synthesis of RA, which promotes embryonic neuroepithelial survival. Tretinoin 120-122 retinol binding protein 4, plasma Danio rerio 44-48
9421176-7 1997 To define the correlation between trkA expression and NGF-mediated survival in more detail, trkA expression was adjusted to different levels by treatment with increasing concentrations of retinoic acid. Tretinoin 188-201 neurotrophic receptor tyrosine kinase 1 Gallus gallus 92-96
9218607-2 1997 In the human U937 promonocytic cell line, STAT5 activation occurred in response to several inducers of monocytic differentiation (phorbol ester, 1alpha,25-dihydroxyvitamin D3, and retinoic acid). Tretinoin 180-193 signal transducer and activator of transcription 5A Homo sapiens 42-47
9305907-0 1997 Galpha12 and Galpha13 mediate differentiation of P19 mouse embryonal carcinoma cells in response to retinoic acid. Tretinoin 100-113 guanine nucleotide binding protein, alpha 13 Mus musculus 13-21
26722220-4 2016 RA attenuated BSCB permeability and decreased the loss of tight junction (TJ) molecules such as P120, beta-catenin, Occludin and Claudin5 after injury in vivo as well as in Brain Microvascular Endothelial Cells (BMECs). Tretinoin 0-2 catenin beta 1 Rattus norvegicus 102-114
9305907-3 1997 The Galpha12 and Galpha13 subunits of heterotrimeric G-proteins are expressed in the embryonal P19 cells and stimulated in response to retinoic acid as the cells differentiate to endodermal or neuroectodermal phenotypes. Tretinoin 135-148 guanine nucleotide binding protein, alpha 13 Mus musculus 17-25
9331973-9 1997 In conclusion, DMSO- or RA-treated HL-60 cells are useful for the measurement of bioactivity of hG-CSF. Tretinoin 24-26 colony stimulating factor 3 Homo sapiens 96-102
9207104-0 1997 Cloning of a gene (RIG-G) associated with retinoic acid-induced differentiation of acute promyelocytic leukemia cells and representing a new member of a family of interferon-stimulated genes. Tretinoin 42-55 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 19-24
9207104-1 1997 In a cell line (NB4) derived from a patient with acute promyelocytic leukemia, all-trans-retinoic acid (ATRA) and interferon (IFN) induce the expression of a novel gene we call RIG-G (for retinoic acid-induced gene G). Tretinoin 79-102 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 177-182
9207104-1 1997 In a cell line (NB4) derived from a patient with acute promyelocytic leukemia, all-trans-retinoic acid (ATRA) and interferon (IFN) induce the expression of a novel gene we call RIG-G (for retinoic acid-induced gene G). Tretinoin 79-102 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 188-216
9207104-1 1997 In a cell line (NB4) derived from a patient with acute promyelocytic leukemia, all-trans-retinoic acid (ATRA) and interferon (IFN) induce the expression of a novel gene we call RIG-G (for retinoic acid-induced gene G). Tretinoin 104-108 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 177-182
9207104-1 1997 In a cell line (NB4) derived from a patient with acute promyelocytic leukemia, all-trans-retinoic acid (ATRA) and interferon (IFN) induce the expression of a novel gene we call RIG-G (for retinoic acid-induced gene G). Tretinoin 104-108 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 188-216
9207104-4 1997 ATRA treatment induces the transcriptional expression of RIG-G relatively late (12-24 hr) in a protein synthesis-dependent manner, whereas IFN-alpha induces its expression early (30 min to 3 hr). Tretinoin 0-4 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 57-62
9207104-7 1997 A synergistic induction of RIG-G expression in NB4 cells by combined treatment with ATRA and IFNs suggests that a collaboration exists between their respective signaling pathways. Tretinoin 84-88 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 27-32
9332729-1 1997 Post-mitotic, human neurons (hNT cells) which have a phenotype similar to that of terminally differentiated neurons of the central nervous system were generated by treating the NT2/D1 human teratocarcinoma cell line with retinoic acid. Tretinoin 221-234 ras responsive element binding protein 1 Homo sapiens 29-32
26722220-6 2016 RA inhibited the expression of CHOP and caspase-12 by induction of autophagic flux. Tretinoin 0-2 DNA-damage inducible transcript 3 Rattus norvegicus 31-35
9436034-8 1997 In summary, retinoic acids could mediate cell growth and differentiation of testicular tumor through RAR-alpha. Tretinoin 12-26 retinoic acid receptor alpha Homo sapiens 101-110
9211495-8 1997 Retinoic acid increased insulin secretion from INS-1 cells as observed previously in RINm5F cells. Tretinoin 0-13 insulin 1 Rattus norvegicus 47-52
26686474-0 2016 RIG-G inhibits the proliferation of NB4 cells and propels ATRA-induced differentiation of APL cells. Tretinoin 58-62 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 0-5
9211495-9 1997 In conclusion, retinoic acid increases transglutaminase activity in both rat islets and two insulin-secreting from INS-1 cells. Tretinoin 15-28 insulin 1 Rattus norvegicus 115-120
9191474-5 1997 Removal of RA from the media caused a drastic decrease in mucin secretion and a decrease in expression of the mucin genes MUC2 and MUC5AC.LZ and SLPI secretions were increased in these cultures. Tretinoin 11-13 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 131-137
9451807-0 1997 Molecular cloning of the bovine alpha 1(IV) procollagen gene (COL4A1) and its use in investigating the regulation of expression of type IV procollagen by retinoic acid in bovine lens epithelial cells. Tretinoin 154-167 collagen type IV alpha 1 chain Bos taurus 62-68
9260895-3 1997 HNF-3alpha transcription was detected 2 h after addition of retinoic acid and took place in the absence of de novo protein synthesis. Tretinoin 60-73 forkhead box A1 Homo sapiens 0-10
9260895-4 1997 This suggests that HNF-3alpha is a primary target for retinoic acid action. Tretinoin 54-67 forkhead box A1 Homo sapiens 19-29
9169853-10 1997 However, blocking experiments with a dominant-inhibitory FGF receptor and a dominant-inhibitory retinoic acid receptor suggest that Pax-3 inductive activities arising from Hensen"s node and posterior non-axial mesoderm do not strictly depend on FGF or retinoic acid. Tretinoin 96-109 paired box 3 Gallus gallus 132-137
26686474-1 2016 RIG-G (retinoic acid-induced gene G) was originally identified in ATRA (all-trans retinoic acid)-treated NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 66-70 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 0-5
9260895-8 1997 According to our studies, the retinoic acid-mediated induction of HNF-3alpha occurs at the level of transcriptional initiation and is conferred by distal promoter sequences. Tretinoin 30-43 forkhead box A1 Homo sapiens 66-76
9260897-2 1997 RA did not affect cyclins D1, A, and E and cyclin-dependent kinase 2 (CDK2) expression, but significantly reduced cyclin D3 and CDK4 expression after 24 h. RA also inhibited cyclin B1 and CDC2 expression, possibly responsible for the reduction of the proportion of cells in G2 + M and S phases. Tretinoin 0-2 cyclin B1 Homo sapiens 174-183
9260897-2 1997 RA did not affect cyclins D1, A, and E and cyclin-dependent kinase 2 (CDK2) expression, but significantly reduced cyclin D3 and CDK4 expression after 24 h. RA also inhibited cyclin B1 and CDC2 expression, possibly responsible for the reduction of the proportion of cells in G2 + M and S phases. Tretinoin 0-2 cyclin dependent kinase 1 Homo sapiens 188-192
9260897-3 1997 RA did not induce p16 and p27 expression, but obviously reduced p21 level in MCF-7 cells. Tretinoin 0-2 H3 histone pseudogene 16 Homo sapiens 64-67
9191046-7 1997 MIC cells co-cultured with 14-day intestinal endoderms promoted endodermal cell adhesion and growth, and the addition of exogeneous RA enhanced epithelial cell polarization and differentiation assessed by cytokeratin and lactase immunostaining. Tretinoin 132-134 lactase Rattus norvegicus 221-228
26686474-1 2016 RIG-G (retinoic acid-induced gene G) was originally identified in ATRA (all-trans retinoic acid)-treated NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 66-70 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 7-35
26686474-1 2016 RIG-G (retinoic acid-induced gene G) was originally identified in ATRA (all-trans retinoic acid)-treated NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 72-95 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 0-5
9228041-2 1997 CYP26 mRNA is up-regulated during the retinoic acid (RA)-induced neural differentiation of mouse embryonic stem cells in vitro and is transiently expressed by embryonic stem cells undergoing predominantly non-neural differentiation. Tretinoin 38-51 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-5
26686474-1 2016 RIG-G (retinoic acid-induced gene G) was originally identified in ATRA (all-trans retinoic acid)-treated NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 72-95 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 7-35
9228041-2 1997 CYP26 mRNA is up-regulated during the retinoic acid (RA)-induced neural differentiation of mouse embryonic stem cells in vitro and is transiently expressed by embryonic stem cells undergoing predominantly non-neural differentiation. Tretinoin 53-55 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-5
26686474-5 2016 By using the transformant, we showed that expression of RIG-G in NB4 cells not only arrested the cells at G1/G0 transition phase and inhibited their proliferation, but also markedly drive the maturation of NB4 cells in the presence of very low concentration of ATRA (10(-9)mol/L). Tretinoin 261-265 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 56-61
9165460-3 1997 METHODS: Competitive NPY binding studies were performed on normal and RA-treated cells, followed by Scatchard analysis. Tretinoin 70-72 neuropeptide Y Homo sapiens 21-24
9165460-5 1997 The mitogenic effect of NPY was evaluated by growing normal or RA-treated cell in the presence of various concentrations of NPY. Tretinoin 63-65 neuropeptide Y Homo sapiens 24-27
9218465-0 1997 Mutational analysis reveals that all-trans-retinoic acid, 9-cis-retinoic acid, and antagonist interact with distinct binding determinants of RARalpha. Tretinoin 33-56 retinoic acid receptor alpha Homo sapiens 141-149
26129652-3 2016 Here we show that RA acts cell intrinsically in developing gut-tropic pre-mucosal dendritic cell (pre-muDC) to effect the differentiation and drive the specialization of intestinal CD103(+)CD11b(-) (cDC1) and of CD103(+)CD11b(+) (cDC2). Tretinoin 18-20 integrin subunit alpha E Homo sapiens 181-186
9165460-9 1997 NPY stimulated growth was significantly attenuated after RA treatment, possibly as a result of decreased NPY receptor expression. Tretinoin 57-59 neuropeptide Y Homo sapiens 0-3
9165460-9 1997 NPY stimulated growth was significantly attenuated after RA treatment, possibly as a result of decreased NPY receptor expression. Tretinoin 57-59 neuropeptide Y Homo sapiens 105-108
9165460-10 1997 CONCLUSIONS: Treatment of SK-N-MC cells with RA, a known differentiating agent, leads to decreased expression of functional NPY receptors and a concomitant decrease in the mitogenic effect of NPY. Tretinoin 45-47 neuropeptide Y Homo sapiens 124-127
9165460-10 1997 CONCLUSIONS: Treatment of SK-N-MC cells with RA, a known differentiating agent, leads to decreased expression of functional NPY receptors and a concomitant decrease in the mitogenic effect of NPY. Tretinoin 45-47 neuropeptide Y Homo sapiens 192-195
26129652-3 2016 Here we show that RA acts cell intrinsically in developing gut-tropic pre-mucosal dendritic cell (pre-muDC) to effect the differentiation and drive the specialization of intestinal CD103(+)CD11b(-) (cDC1) and of CD103(+)CD11b(+) (cDC2). Tretinoin 18-20 integrin subunit alpha E Homo sapiens 212-217
9111003-0 1997 Stromelysin-3 induction and interstitial collagenase repression by retinoic acid. Tretinoin 67-80 matrix metallopeptidase 1 Homo sapiens 28-52
9111003-4 1997 Physiological concentrations of retinoic acid were found to simultaneously induce stromelysin-3 and repress interstitial collagenase. Tretinoin 32-45 matrix metallopeptidase 1 Homo sapiens 108-132
26129652-3 2016 Here we show that RA acts cell intrinsically in developing gut-tropic pre-mucosal dendritic cell (pre-muDC) to effect the differentiation and drive the specialization of intestinal CD103(+)CD11b(-) (cDC1) and of CD103(+)CD11b(+) (cDC2). Tretinoin 18-20 cyclin dependent kinase 1 Homo sapiens 230-234
26129652-4 2016 Systemic deficiency or DC-restricted antagonism of RA signaling resulted in altered phenotypes of intestinal cDC1 and cDC2, and reduced numbers of cDC2. Tretinoin 51-53 cyclin dependent kinase 1 Homo sapiens 118-122
9109417-0 1997 Retinoic acid modulates retinoid X receptor alpha and retinoic acid receptor alpha levels of cultured brown adipocytes. Tretinoin 0-13 retinoic acid receptor alpha Cricetulus griseus 54-82
26129652-4 2016 Systemic deficiency or DC-restricted antagonism of RA signaling resulted in altered phenotypes of intestinal cDC1 and cDC2, and reduced numbers of cDC2. Tretinoin 51-53 cyclin dependent kinase 1 Homo sapiens 147-151
9109417-2 1997 Here we provide evidence that the UCP responsiveness to RA in primary cultures of brown adipocytes involves RA receptor alpha (RAR alpha), and show, in the same system and also in CHO cells, that RA down-regulates the steady-state levels of RAR alpha and especially of retinoid X receptor alpha, suggesting autoregulation of the retinoid pathway and therefore supporting the idea of a physiological role for it in controlling the thermogenic capacity of BAT. Tretinoin 56-58 retinoic acid receptor alpha Cricetulus griseus 127-136
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 24-26 glutamic-oxaloacetic transaminase 2 Homo sapiens 184-210
9122176-3 1997 In this report, we present evidence that RA down-regulates MGP gene expression in different rat and human cell lines via endogenous retinoid receptors [RA receptor (RAR) and retinoid X receptor (RXR)]. Tretinoin 41-43 retinoic acid receptor alpha Homo sapiens 152-163
9122176-3 1997 In this report, we present evidence that RA down-regulates MGP gene expression in different rat and human cell lines via endogenous retinoid receptors [RA receptor (RAR) and retinoid X receptor (RXR)]. Tretinoin 41-43 retinoic acid receptor alpha Homo sapiens 165-168
9122176-7 1997 Furthermore, electrophoretic mobility-shift assays performed with proteins from RA-treated cells show that endogenous RAR/RXR binds to the NRE. Tretinoin 80-82 retinoic acid receptor alpha Homo sapiens 118-121
26058416-4 2015 It has been found that all-trans-retinoic acid (ATRA) or arsenic trioxide (ATO) alone exerts therapeutic effect on APL patients with the PML-RARalpha fusion gene, and the combination of both drugs can act synergistically to further enhance the cure rate of the patients. Tretinoin 23-46 PML nuclear body scaffold Homo sapiens 137-140
9122176-9 1997 Our results indicate that RA-mediated repression of the hMGP gene is due to binding of liganded RAR/RXR to a novel negative RA response element. Tretinoin 26-28 retinoic acid receptor alpha Homo sapiens 96-99
9056251-0 1997 The interconversion of protein phosphatase 2A between PP2A1 and PP2A0 during retinoic acid-induced granulocytic differentiation and a modification on the catalytic subunit in S phase of HL-60 cells. Tretinoin 77-90 protein phosphatase 2 phosphatase activator Homo sapiens 31-45
26058416-4 2015 It has been found that all-trans-retinoic acid (ATRA) or arsenic trioxide (ATO) alone exerts therapeutic effect on APL patients with the PML-RARalpha fusion gene, and the combination of both drugs can act synergistically to further enhance the cure rate of the patients. Tretinoin 23-46 retinoic acid receptor alpha Homo sapiens 141-149
9056251-1 1997 Alterations in protein phosphatase 2A (PP2A) during retinoic acid-induced differentiation of HL-60 cells have been investigated. Tretinoin 52-65 protein phosphatase 2 phosphatase activator Homo sapiens 23-37
26058416-4 2015 It has been found that all-trans-retinoic acid (ATRA) or arsenic trioxide (ATO) alone exerts therapeutic effect on APL patients with the PML-RARalpha fusion gene, and the combination of both drugs can act synergistically to further enhance the cure rate of the patients. Tretinoin 48-52 PML nuclear body scaffold Homo sapiens 137-140
9056251-1 1997 Alterations in protein phosphatase 2A (PP2A) during retinoic acid-induced differentiation of HL-60 cells have been investigated. Tretinoin 52-65 protein phosphatase 2 phosphatase activator Homo sapiens 39-43
9056251-2 1997 PP2A activity of HL-60 cells for phosphorylated myelin basic protein showed a sharp and transient increase after 18-h treatment with 1 microM retinoic acid, which corresponded to G1/S boundary of the cell cycle. Tretinoin 142-155 protein phosphatase 2 phosphatase activator Homo sapiens 0-4
26058416-4 2015 It has been found that all-trans-retinoic acid (ATRA) or arsenic trioxide (ATO) alone exerts therapeutic effect on APL patients with the PML-RARalpha fusion gene, and the combination of both drugs can act synergistically to further enhance the cure rate of the patients. Tretinoin 48-52 retinoic acid receptor alpha Homo sapiens 141-149
9056251-5 1997 Immunoblot analyses with antisera against B" and B alpha subunits showed that the PP2A in the 0.13 M NaCl eluate from 18-h retinoic acid-treated cells was PP2A0 (AC-B"), whereas the PP2A eluted with 0.23 M NaCl from 24-h retinoic acid-treated cells and 0-, 18-, and 24-h control cells was PP2A1 (AC-B alpha). Tretinoin 123-136 protein phosphatase 2 phosphatase activator Homo sapiens 82-86
9056251-5 1997 Immunoblot analyses with antisera against B" and B alpha subunits showed that the PP2A in the 0.13 M NaCl eluate from 18-h retinoic acid-treated cells was PP2A0 (AC-B"), whereas the PP2A eluted with 0.23 M NaCl from 24-h retinoic acid-treated cells and 0-, 18-, and 24-h control cells was PP2A1 (AC-B alpha). Tretinoin 123-136 protein phosphatase 2 phosphatase activator Homo sapiens 155-159
26516929-6 2015 Furthermore, AKR1B10 silencing increased retinoic acid (RA) levels in the serum of tumor-bearing mice and RA treatment attenuated 14-3-3epsilon-induced HCC cell proliferation. Tretinoin 41-54 aldo-keto reductase family 1, member B10 (aldose reductase) Mus musculus 13-20
9056251-5 1997 Immunoblot analyses with antisera against B" and B alpha subunits showed that the PP2A in the 0.13 M NaCl eluate from 18-h retinoic acid-treated cells was PP2A0 (AC-B"), whereas the PP2A eluted with 0.23 M NaCl from 24-h retinoic acid-treated cells and 0-, 18-, and 24-h control cells was PP2A1 (AC-B alpha). Tretinoin 221-234 protein phosphatase 2 phosphatase activator Homo sapiens 82-86
9056251-6 1997 These results strongly suggest that PP2A undergoes a transient and reversible interconversion of holoenzyme forms during the initial stage of retinoic acid-induced granulocytic differentiation. Tretinoin 142-155 protein phosphatase 2 phosphatase activator Homo sapiens 36-40
9056251-7 1997 PP2A activity assayed after dissociation of the catalytic subunit, for phosphorylase as substrate, showed a sharp and transient decrease in S phase of HL-60 cells irrespective of the presence or absence of retinoic acid. Tretinoin 206-219 protein phosphatase 2 phosphatase activator Homo sapiens 0-4
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 151-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 64-69
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 151-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 213-218
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 166-168 MYC proto-oncogene, bHLH transcription factor Homo sapiens 64-69
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 166-168 MYC proto-oncogene, bHLH transcription factor Homo sapiens 213-218
26571119-0 2015 All-Trans Retinoic Acid-Induced Deficiency of the Wnt/beta-Catenin Pathway Enhances Hepatic Carcinoma Stem Cell Differentiation. Tretinoin 10-23 catenin beta 1 Homo sapiens 54-66
9070313-5 1997 On the other hand, RA completely inhibited IL-4-induced I gamma 1C gamma 1 expression. Tretinoin 19-21 interleukin 4 Mus musculus 43-47
26571119-4 2015 All-trans retinoic acid (ATRA) differentiated hCSCs through inhibiting the function of beta-catenin in vitro. Tretinoin 0-23 catenin beta 1 Homo sapiens 87-99
26571119-4 2015 All-trans retinoic acid (ATRA) differentiated hCSCs through inhibiting the function of beta-catenin in vitro. Tretinoin 25-29 catenin beta 1 Homo sapiens 87-99
26571119-5 2015 ATRA also inhibited the function of PI3K-AKT and enhanced GSK-3beta-dependent degradation of phosphorylated beta-catenin. Tretinoin 0-4 catenin beta 1 Homo sapiens 108-120
9128763-0 1997 Thrombomodulin, a functional surface protein on human keratinocytes, is regulated by retinoic acid. Tretinoin 85-98 thrombomodulin Homo sapiens 0-14
26571119-7 2015 Our results suggest that targeting beta-catenin will provide extra benefits for ATRA-mediated treatment of hepatic cancer patients. Tretinoin 80-84 catenin beta 1 Homo sapiens 35-47
9128763-3 1997 The role of retinoic acid in keratinocyte differentiation prompted us to study retinoic acid regulation of thrombomodulin expression in primary cultures of keratinocytes isolated from adult human skin, grown at low (undifferentiated keratinocytes) and normal calcium levels (differentiated keratinocytes). Tretinoin 79-92 thrombomodulin Homo sapiens 107-121
26556479-7 2015 Wnt 2 and beta-catenin protein levels were markedly down-regulated, while Axin 2 expression level was up-regulated in the presence of RA, both in vivo and in vitro. Tretinoin 134-136 axin 2 Mus musculus 74-80
9128763-7 1997 In contrast, retinoic acid induced significant increases in the total antigen level and in surface and intracellular thrombomodulin activities only in keratinocytes grown in a low-calcium medium. Tretinoin 13-26 thrombomodulin Homo sapiens 117-131
9128763-9 1997 Thus, functional thrombomodulin is a human keratinocyte surface protein whose expression is controlled through the keratinocyte differentiation program and is modulated in vitro by retinoic acid. Tretinoin 181-194 thrombomodulin Homo sapiens 17-31
26556479-9 2015 Furthermore, RA induced significant PSC apoptosis, inhibited proliferation, suppressed TCF/LEF-dependent transcriptional activity and ECM production of PSC via down-regulation of TGFbetaRII, PDGFRbeta and collagen 1alpha1 in vitro. Tretinoin 13-15 platelet derived growth factor receptor, beta polypeptide Mus musculus 191-200
9028736-2 1997 Retinoic acid (RA) inhibition of estrogen receptor (ER)-positive breast carcinoma seems to be mediated through RAR alpha. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 111-120
26397153-0 2015 Restoration of CCAAT enhancer binding protein alpha P42 induces myeloid differentiation and overcomes all-trans retinoic acid resistance in human acute promyelocytic leukemia NB4-R1 cells. Tretinoin 112-125 cyclin dependent kinase 20 Homo sapiens 52-55
9147069-1 1997 Increasing evidence suggests that the retinoid-X receptors (RXR-alpha,-beta,-gamma) play a crucial role in regulating the transcriptional activity of several steroid hormone receptors, including the receptors for retinoic acid (RAR-alpha,-beta,-gamma), 1,25-dihydroxyvitamin D3 and thyroid hormone. Tretinoin 213-226 retinoic acid receptor alpha Homo sapiens 228-237
26397153-10 2015 Further upregulating of CD11b expression and differential morphological changes were found in NB4-R1 cells with restored C/EBPalpha P42 after ATRA treatment. Tretinoin 142-146 cyclin dependent kinase 20 Homo sapiens 132-135
26256243-0 2015 All-trans retinoic acid modulates the balance of ADAMTS13 and VWF in human microvascular endothelial cells. Tretinoin 10-23 ADAM metallopeptidase with thrombospondin type 1 motif 13 Homo sapiens 49-57
9193684-2 1997 We previously demonstrated that an ecto-form NAD+ glycohydrolase (NADase) activity induced by all-trans retinoic acid in HL-60 cells is due to the extracellular domain of CD38. Tretinoin 104-117 CD38 molecule Homo sapiens 171-175
9193684-3 1997 In the present study, we investigated a possible signal transduction mediated through CD38 in the retinoic acid-differentiated HL-60 cells with anti-CD38 monoclonal antibodies (mAbs). Tretinoin 98-111 CD38 molecule Homo sapiens 86-90
9193684-3 1997 In the present study, we investigated a possible signal transduction mediated through CD38 in the retinoic acid-differentiated HL-60 cells with anti-CD38 monoclonal antibodies (mAbs). Tretinoin 98-111 CD38 molecule Homo sapiens 149-153
26256243-1 2015 PURPOSE: To better understand the antithrombotic property of All-trans retinoic acid (ATRA), we investigated whether ATRA may affect the balance between ADAMTS13 and von Willebrand factor (VWF) in human microvascular endothelial cell. Tretinoin 117-121 ADAM metallopeptidase with thrombospondin type 1 motif 13 Homo sapiens 153-161
26256243-2 2015 METHODS: Compared to tumor necrosis factor-alpha (TNF-alpha), we observed the effects of ATRA on the expression of ADAMTS13 and VWF. Tretinoin 89-93 ADAM metallopeptidase with thrombospondin type 1 motif 13 Homo sapiens 115-123
9397535-7 1997 Retinoic acid produced a decrease in connexin43 mRNA, protein, and functional gap junctions. Tretinoin 0-13 gap junction protein, beta 1 Mus musculus 37-47
9397535-10 1997 Connexin26 was detected at sites of cell-cell and cell-neurite contact within 3 days following differentiation with retinoic acid. Tretinoin 116-129 gap junction protein, beta 2 Mus musculus 0-10
26256243-6 2015 ATRA could reverse the inhibition expression of ADAMTS13 by TNF-alpha. Tretinoin 0-4 ADAM metallopeptidase with thrombospondin type 1 motif 13 Homo sapiens 48-56
26256243-8 2015 CONCLUSIONS: This study provides the evidence that ATRA modulates the balance of ADAMTS13 and VWF in human microvascular endothelial cell, which might be a very relevant compartment for the antithrombotic property of ATRA. Tretinoin 51-55 ADAM metallopeptidase with thrombospondin type 1 motif 13 Homo sapiens 81-89
8989665-7 1997 In addition, levels of mRNA for both the CNTF receptor alpha and gp130 subunits increased twofold as measured by RNase protection after treatment with retinoic acid for 30 h. The increase in CNTF receptor alpha subunit mRNA was not due to a decrease in its turnover rate, and therefore, was likely due to an increase in gene expression. Tretinoin 151-164 interleukin 6 cytokine family signal transducer Homo sapiens 65-70
26775483-6 2015 RESULTS: MAT combined ATRA could significantly elevate positive rates of NBT and CD11 b in NB4-R1 cells, and significantly down-regulate the expression of PML/RARapha-fusion protein/gene (P < 0.05, P < 0.01). Tretinoin 22-26 PML nuclear body scaffold Homo sapiens 155-158
9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 33-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70
9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 224-228 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70
9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 39-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 65-70
9290118-4 1997 An increase in c-myc expression after supplementation was observed in 6 of 12 subjects, but 5 of these 6 subjects had decreased total serum retinoic acid concentration and 4 had decreased ATRA concentration. Tretinoin 140-153 MYC proto-oncogene, bHLH transcription factor Homo sapiens 15-20
26775483-13 2015 CONCLUSION: MAT combined ATRA could significantly induce the differentiation of NB4-R1 cells, and inhibit the expression of PML/RARalpha fusion gene/protein, which might be associated with up-regulating PLSCR1 expression. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 124-127
9290118-4 1997 An increase in c-myc expression after supplementation was observed in 6 of 12 subjects, but 5 of these 6 subjects had decreased total serum retinoic acid concentration and 4 had decreased ATRA concentration. Tretinoin 188-192 MYC proto-oncogene, bHLH transcription factor Homo sapiens 15-20
9290118-6 1997 Conversely, c-myc expression was increased in only two of five paired samples from subjects whose total serum retinoic acid concentration increased during the 90-day supplementation period. Tretinoin 110-123 MYC proto-oncogene, bHLH transcription factor Homo sapiens 12-17
26775483-13 2015 CONCLUSION: MAT combined ATRA could significantly induce the differentiation of NB4-R1 cells, and inhibit the expression of PML/RARalpha fusion gene/protein, which might be associated with up-regulating PLSCR1 expression. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 128-136
26439802-2 2015 We have previously demonstrated that knockdown of the nuclear envelope component Lamin A/C in human neuroblastoma cells inhibits retinoic acid-mediated differentiation and results in a more aggressive phenotype. Tretinoin 129-142 lamin A/C Homo sapiens 81-90
8943235-3 1996 AF1 and AF2 also partially account for the response of the PEPCK gene to retinoic acid and insulin, respectively. Tretinoin 73-86 phosphoenolpyruvate carboxykinase 1 Gallus gallus 59-64
8943263-0 1996 Retinoic acid-induced expression of apolipoprotein D and concomitant growth arrest in human breast cancer cells are mediated through a retinoic acid receptor RARalpha-dependent signaling pathway. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 158-166
8940196-6 1996 In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene"s promoter which is required to confer RA induction through RAR.RXR heterodimers. Tretinoin 67-69 retinoic acid receptor alpha Homo sapiens 216-219
8940196-6 1996 In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene"s promoter which is required to confer RA induction through RAR.RXR heterodimers. Tretinoin 123-125 retinoic acid receptor alpha Homo sapiens 216-219
8940196-7 1996 These results correlate the RA induction of monocytic differentiation of U937 cells with the transcriptional activation of the p21 gene and suggest a role for this cyclin/cyclin-dependent kinase complex inhibitor in facilitating this differentiation pathway. Tretinoin 28-30 proliferating cell nuclear antigen Homo sapiens 164-170
8940196-7 1996 These results correlate the RA induction of monocytic differentiation of U937 cells with the transcriptional activation of the p21 gene and suggest a role for this cyclin/cyclin-dependent kinase complex inhibitor in facilitating this differentiation pathway. Tretinoin 28-30 proliferating cell nuclear antigen Homo sapiens 171-177
26251460-15 2015 In cultured fetal ovaries treated with RA, an increased number of meiotic germ cells (P < 0.05) and DMRT1-positive oogonia initiating meiosis (P < 0.05) was observed, which is in agreement with a previous study. Tretinoin 39-41 doublesex and mab-3 related transcription factor 1 Homo sapiens 103-108
8959336-2 1996 The addition of retinoic acid (RA) to P19-EC cell aggregates results in a transient activation of receptor protein tyrosine phosphatase-alpha (RPTP alpha). Tretinoin 16-29 protein tyrosine phosphatase, receptor type, A Mus musculus 143-153
8959336-2 1996 The addition of retinoic acid (RA) to P19-EC cell aggregates results in a transient activation of receptor protein tyrosine phosphatase-alpha (RPTP alpha). Tretinoin 31-33 protein tyrosine phosphatase, receptor type, A Mus musculus 143-153
8959336-4 1996 P19-EC cells expressing constitutively active RPTP alpha (P19-RPTP alpha) show extensive neuronal differentiation upon RA treatment in monolayer. Tretinoin 119-121 protein tyrosine phosphatase, receptor type, A Mus musculus 46-56
8959336-4 1996 P19-EC cells expressing constitutively active RPTP alpha (P19-RPTP alpha) show extensive neuronal differentiation upon RA treatment in monolayer. Tretinoin 119-121 protein tyrosine phosphatase, receptor type, A Mus musculus 62-72
8959336-13 1996 Activin and bFGF appeared to exert differential actions on RA-induced neuronal differentiation. Tretinoin 59-61 inhibin subunit beta E Homo sapiens 0-7
26427057-6 2015 They add to the mechanisms through which ATRA promote expression of the KIT tyrosine kinase receptor to trigger a critical step in spermatogonia differentiation. Tretinoin 41-45 KIT proto-oncogene receptor tyrosine kinase Mus musculus 72-75
8939936-2 1996 The cellular effects of RA are dependent upon the complement of nuclear receptors expressed (RARs and RXRs), which transduce retinoid signals into transcriptional regulation, the presence of cellular retinoid-binding proteins (CRABP and CRBP), which may be involved in RA metabolism, and the activity of RA metabolizing enzymes. Tretinoin 24-26 retinol binding protein 2a, cellular Danio rerio 237-241
26318046-8 2015 G0S2 is strongly induced in acute promyelocytic leukemia (APL) cells in response to all trans retinoic acid (ATRA) and we show that inhibition of ATGL in these cells by G0S2 is required for efficacy of ATRA treatment. Tretinoin 94-107 patatin like phospholipase domain containing 2 Homo sapiens 146-150
26617752-13 2015 ATRA decreased anti-oxygen protein Nrf2 and HO-1, and increases inflammatory factors NF-kappaB and TNF-alpha. Tretinoin 0-4 heme oxygenase 1 Homo sapiens 44-48
8941725-1 1996 We reported that ecto-NAD+ glycohydrolase activity induced upon differentiation of HL-60 cells with retinoic acid is localized on the extracellular domain of CD38 and that CD38 ligation by a specific monoclonal antibody, HB-7, is followed by rapid tyrosine phosphorylation of cellular proteins including a proto-oncogene product, Cbl. Tretinoin 100-113 CD38 molecule Homo sapiens 158-162
8941725-1 1996 We reported that ecto-NAD+ glycohydrolase activity induced upon differentiation of HL-60 cells with retinoic acid is localized on the extracellular domain of CD38 and that CD38 ligation by a specific monoclonal antibody, HB-7, is followed by rapid tyrosine phosphorylation of cellular proteins including a proto-oncogene product, Cbl. Tretinoin 100-113 Cbl proto-oncogene Homo sapiens 330-333
8934535-2 1996 We have previously reported that all-trans-retinoic acid (RA) inhibits the growth of NCI-H82 SCLC cells in association with increased neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression. Tretinoin 33-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 212-217
8934535-2 1996 We have previously reported that all-trans-retinoic acid (RA) inhibits the growth of NCI-H82 SCLC cells in association with increased neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression. Tretinoin 58-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 212-217
8895377-10 1996 We observed that CRABP-II was expressed in certain cells that synthesized retinoic acid in the uterus and ovary (unpublished). Tretinoin 74-87 cellular retinoic acid binding protein 2 Rattus norvegicus 17-25
26066585-5 2015 In this study, we determined that the injection of RA for 4 consecutive days resulted in increases in zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin) expression, which are crucial components of the BBB structure. Tretinoin 51-53 tight junction protein 1 Rattus norvegicus 102-120
8895377-13 1996 The reported expression of CRABP-II in embryonal tissues, which are RA responsive and undergoing morphogenesis, coupled with CRABP-II expression in the testis at a critical morphogenic stage suggest that RA may play a prominent role in the morphogenesis of the testis. Tretinoin 68-70 cellular retinoic acid binding protein 2 Rattus norvegicus 27-35
26066585-5 2015 In this study, we determined that the injection of RA for 4 consecutive days resulted in increases in zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin) expression, which are crucial components of the BBB structure. Tretinoin 51-53 tight junction protein 1 Rattus norvegicus 122-126
26066585-6 2015 We demonstrated that RA pretreatment could alleviate the ischemic stroke-induced enlargement of vascular permeability, which is related to the up-regulated expression of ZO-1 and VE-cadherin proteins in rat models of middle cerebral artery occlusion (MCAO). Tretinoin 21-23 tight junction protein 1 Rattus norvegicus 170-174
26228249-9 2015 In addition, ATRA treatment decreased the mRNA expression of 17-beta-dehydrogenase 2 (HSD17B2) which converts estradiol into estrone in a dose-dependent manner, and the ELISA measurements indicated that estradiol production in the OEC tissue was inhibited by ATRA treatment. Tretinoin 13-17 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 86-93
8994352-0 1996 Control of Drosophila opsin gene expression by carotenoids and retinoic acid: northern and western analyses. Tretinoin 63-76 neither inactivation nor afterpotential E Drosophila melanogaster 22-27
9387294-1 1996 The relationship between the effect of retinoic acid (RA) on the growth of breast cancer cell and their estrogen receptor (ER) status as well as the relationship between RA effect and the expression of retinoic acid receptorsd (RAR alpha) were studied by cell growth assay, Northern Blot and gene transfection. Tretinoin 170-172 retinoic acid receptor alpha Homo sapiens 228-237
9250660-11 1997 These results suggest that P450RA regulates the intracellular level of RA and may be involved in setting up the uneven distribution of active RA in mammalian embryos. Tretinoin 71-73 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 27-33
26228249-9 2015 In addition, ATRA treatment decreased the mRNA expression of 17-beta-dehydrogenase 2 (HSD17B2) which converts estradiol into estrone in a dose-dependent manner, and the ELISA measurements indicated that estradiol production in the OEC tissue was inhibited by ATRA treatment. Tretinoin 259-263 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 86-93
8824230-2 1996 In this study, we demonstrated that the neurofilament-L (NF-L) mRNA and protein levels of these cells were enhanced in accordance with their retinoic acid-induced neural differentiation. Tretinoin 141-154 neurofilament, light polypeptide Mus musculus 40-55
26225425-6 2015 RESULTS: AtRA-treatment of IEC6 cells selectively increased TGF-beta2 mRNA and protein expression in a time- and dose-dependent fashion, and increased the activity of the TGF-beta2 promoter. Tretinoin 9-13 transforming growth factor, beta 2 Rattus norvegicus 60-69
8824230-2 1996 In this study, we demonstrated that the neurofilament-L (NF-L) mRNA and protein levels of these cells were enhanced in accordance with their retinoic acid-induced neural differentiation. Tretinoin 141-154 neurofilament, light polypeptide Mus musculus 57-61
8982293-3 1996 After 5 d exposure to ATRA 10(-6) M APL-treated samples showed a significant reduction of IL-6 (p = 0.008) and GM-CSF (p = 0.03) and a significant increase of IL-1 alpha (p = 0.01) production, if compared to untreated APL samples. Tretinoin 22-26 colony stimulating factor 2 Homo sapiens 111-117
9224671-0 1997 Sonic hedgehog participates in craniofacial morphogenesis and is down-regulated by teratogenic doses of retinoic acid. Tretinoin 104-117 sonic hedgehog signaling molecule Homo sapiens 0-14
9224671-6 1997 High doses of retinoic acid, which are known to truncate the growth of the frontonasal and maxillary processes and thus produce bilateral clefting of the lip and palate, inhibited the expression of shh and patched but not fgf8, in the craniofacial primordia, and abolished polarizing activity of these tissues. Tretinoin 14-27 sonic hedgehog signaling molecule Homo sapiens 198-201
9224671-6 1997 High doses of retinoic acid, which are known to truncate the growth of the frontonasal and maxillary processes and thus produce bilateral clefting of the lip and palate, inhibited the expression of shh and patched but not fgf8, in the craniofacial primordia, and abolished polarizing activity of these tissues. Tretinoin 14-27 fibroblast growth factor 8 Homo sapiens 222-226
9260053-9 1997 Provocative data were also presented suggesting that retinoic acid may induce synthesis of a protein that selectively degrades PML/RAR alpha, and that interferons may regulate PML/RAR alpha expression. Tretinoin 53-66 retinoic acid receptor alpha Homo sapiens 127-140
8982293-3 1996 After 5 d exposure to ATRA 10(-6) M APL-treated samples showed a significant reduction of IL-6 (p = 0.008) and GM-CSF (p = 0.03) and a significant increase of IL-1 alpha (p = 0.01) production, if compared to untreated APL samples. Tretinoin 22-26 interleukin 1 alpha Homo sapiens 159-169
26225425-6 2015 RESULTS: AtRA-treatment of IEC6 cells selectively increased TGF-beta2 mRNA and protein expression in a time- and dose-dependent fashion, and increased the activity of the TGF-beta2 promoter. Tretinoin 9-13 transforming growth factor, beta 2 Rattus norvegicus 171-180
8896602-1 1996 The full-length cDNA corresponding to Stra8, a novel gene inducible by retinoic acid (RA) in P19 embryonal carcinoma cells, has been isolated and shown to encode a 45-kD protein. Tretinoin 71-84 stimulated by retinoic acid gene 8 Mus musculus 38-43
8896602-1 1996 The full-length cDNA corresponding to Stra8, a novel gene inducible by retinoic acid (RA) in P19 embryonal carcinoma cells, has been isolated and shown to encode a 45-kD protein. Tretinoin 86-88 stimulated by retinoic acid gene 8 Mus musculus 38-43
8896602-2 1996 Both Stra8 mRNA and protein were induced in cells treated by all-trans and 9-cis retinoic acids. Tretinoin 81-95 stimulated by retinoic acid gene 8 Mus musculus 5-10
8896602-3 1996 Two-dimensional gel analysis and dephosphorylation experiments revealed that the two stereoisomers of RA differentially regulate the phosphorylation status of the Stra8 protein, which was shown to exist in differently phosphorylated forms. Tretinoin 102-104 stimulated by retinoic acid gene 8 Mus musculus 163-168
9202205-3 1997 Here, we report that the LIF-JAK-STAT signal transduction pathway is blocked in cellular E1A-expressing undifferentiated F9 cells, and that the block is overcome by retinoic acid-induced differentiation. Tretinoin 165-178 leukemia inhibitory factor Mus musculus 25-28
26186635-8 2015 Western blot analysis also revealed that ATRA pre-treatment increased a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (0.65 +- 0.20 vs. 0.41+-0.02 in vivo) and reduced the level of receptor for advanced glycation end-products (RAGE) (0.38 +- 0.17 vs. 0.52 +- 0.11 in vivo). Tretinoin 41-45 a disintegrin and metallopeptidase domain 10 Mus musculus 72-134
9204954-6 1997 Moreover, Northern and Western blot analysis demonstrated that retinoic acid opposed VD-induced accumulation of transforming growth factor-beta1, p21WAF1, and p27KIP1. Tretinoin 63-76 cyclin dependent kinase inhibitor 1B Homo sapiens 159-166
26186635-8 2015 Western blot analysis also revealed that ATRA pre-treatment increased a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (0.65 +- 0.20 vs. 0.41+-0.02 in vivo) and reduced the level of receptor for advanced glycation end-products (RAGE) (0.38 +- 0.17 vs. 0.52 +- 0.11 in vivo). Tretinoin 41-45 a disintegrin and metallopeptidase domain 10 Mus musculus 136-142
9181055-0 1996 Ha-ras oncogene transformation abolishes retinoic acid-induced reduction of intracellular fibronectin. Tretinoin 41-54 fibronectin 1 Mus musculus 90-101
9181055-2 1996 Therefore, we were interested in the effect of RA on the biosynthesis of fibronectin (FN). Tretinoin 47-49 fibronectin 1 Mus musculus 73-84
26186635-11 2015 One possible mechanism underlying these effects is that ATRA could increase ADAM10 expression and thus cleave RAGE, which is the main receptor up-stream of MAPKs in myocardial I/R injury, resulting in the down-regulation of MAPK signaling and protective role on myocardial I/R injury. Tretinoin 56-60 a disintegrin and metallopeptidase domain 10 Mus musculus 76-82
9181055-2 1996 Therefore, we were interested in the effect of RA on the biosynthesis of fibronectin (FN). Tretinoin 47-49 fibronectin 1 Mus musculus 86-88
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 159-172 PML nuclear body scaffold Homo sapiens 24-27
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 159-172 retinoic acid receptor alpha Homo sapiens 28-36
9181055-3 1996 RA reduced the level of intracellular FN in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 0-2 fibronectin 1 Mus musculus 38-40
9181055-7 1996 A variety of approaches permitted the following conclusions: 1) RA-dependent FN downmodulation is mediated by RARs, 2) retinoid X receptors (RXRs) mediate the observed reduction of RAR alpha by RA, and 3) the blockade of RA responsiveness by Ha-ras-transfected cells cannot be overcome by overexpression of RAR alpha. Tretinoin 64-66 fibronectin 1 Mus musculus 77-79
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 159-172 retinoic acid receptor alpha Homo sapiens 46-54
9181055-8 1996 These studies have identified fibronectin and RAR alpha as RA targets in fibroblast cells and have shown that oncogenic transformation renders the cells resistant to RA action. Tretinoin 59-61 fibronectin 1 Mus musculus 30-41
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 174-178 PML nuclear body scaffold Homo sapiens 24-27
25880909-9 2015 All-trans retinoic acid treatment reduced MYCN, NCYM, and OCT4 expression, accompanied by the decreased amount of OCT4 recruited onto the intron 1 region of MYCN. Tretinoin 10-23 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 157-161
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 174-178 retinoic acid receptor alpha Homo sapiens 46-54
25738595-0 2015 All-trans-retinoic acid inhibits chondrogenesis of rat embryo hindlimb bud mesenchymal cells by downregulating p53 expression. Tretinoin 0-23 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 111-114
9188753-5 1997 The restricted pattern of beta-galactosidase expression in the heart can be disrupted with retinoic acid exposure and extended posteriorly along the anterior-posterior axis in hemizygous mice. Tretinoin 91-104 galactosidase, beta 1 Mus musculus 26-44
9202388-8 1997 Analysis of expression of potential adipogenic genes, such as peroxisome proliferator-activated receptors gamma and delta and CCAAT/enhancer binding protein beta, during differentiation of retinoic acid-treated embryoid bodies has been performed. Tretinoin 189-202 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 73-161
9025876-7 1996 [125I]IGF-II ligand blotting of conditioned medium from RA-treated cultures revealed a dramatic alteration in the pattern of expression of insulin-like growth factor binding proteins (IGFBPs). Tretinoin 56-58 insulin like growth factor 2 Homo sapiens 6-12
8865855-7 1996 In conclusion, it is evident that the original differentiation status of cells and their responsiveness to the agents are not clearly associated, and that RA responsiveness correlates with upregulation of RAR-alpha and -gamma mRNA. Tretinoin 155-157 retinoic acid receptor alpha Homo sapiens 205-225
9220339-6 1997 To test whether this acceleration of cardiac differentiation and RA-induced increase of the MLC-2v promotor/beta-galactosidase activity reflects an increase of cardiac- and ventricle-specific gene expression, a semi-quantitative RT-PCR analysis was performed for alpha-cardiac myosin heavy chain (alpha-MHC) and MLC-2v genes. Tretinoin 65-67 myosin light chain 2 Homo sapiens 92-98
25738595-9 2015 The present study demonstrated that ATRA decreases the chondrogenesis of rEHBMCs by inhibiting cartilage-specific molecules, including aggrecan, Sox9 and Col2al, via regulating the expression of p53 and p21. Tretinoin 36-40 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 195-198
9220339-6 1997 To test whether this acceleration of cardiac differentiation and RA-induced increase of the MLC-2v promotor/beta-galactosidase activity reflects an increase of cardiac- and ventricle-specific gene expression, a semi-quantitative RT-PCR analysis was performed for alpha-cardiac myosin heavy chain (alpha-MHC) and MLC-2v genes. Tretinoin 65-67 myosin light chain 2 Homo sapiens 312-318
9220339-7 1997 It was shown that both 10(-8) M and 10(-9) M RA resulted in an increased level of alpha-cardiac MHC and MLC-2v mRNA in embryoid bodies in early, but not in terminal developmental stages. Tretinoin 45-47 myosin light chain 2 Homo sapiens 104-110
8752277-3 1996 6) human acute promyelocytic leukaemia cells treated with either an RAR-alpha-selective agonist alone, or certain RAR-alpha antagonists in combination with an RXR agonist, receptor-DNA binding is induced in vivo, resulting in expression of the target genes of retinoic acid as well as acute promyelocytic leukaemia protein (PML) relocation to nuclear bodies and differentiation before apoptosis. Tretinoin 260-273 retinoic acid receptor alpha Homo sapiens 114-123
25753732-0 2015 The orphan GPCR, Gpr161, regulates the retinoic acid and canonical Wnt pathways during neurulation. Tretinoin 39-52 G protein-coupled receptor 161 Mus musculus 17-23
8806447-0 1996 Regulation of connexin31 gene expression upon retinoic acid treatment in rat choriocarcinoma cells. Tretinoin 46-59 gap junction protein, beta 3 Rattus norvegicus 14-24
8806447-5 1996 Upon retinoic acid treatment, Rcho-1 cells irreversibly lost cx31 expression, accompanied by a loss of functional coupling. Tretinoin 5-18 gap junction protein, beta 3 Rattus norvegicus 61-65
9160665-2 1997 In this study, we demonstrate the nature of retinoid receptors involved in retinoic acid-induced expression of CD38 protein in the human myeloblastic leukemia cell line HL-60. Tretinoin 75-88 CD38 molecule Homo sapiens 111-115
9115293-0 1997 Identification and characterization of a retinoic acid-regulated human homologue of the unc-33-like phosphoprotein gene (hUlip) from neuroblastoma cells. Tretinoin 41-54 Amidohydro-rel domain-containing protein;Protein unc-33 Caenorhabditis elegans 88-94
26041547-9 2015 In the cells pre-treated with BMP4 and then exposed to RA in the monolayer differentiation protocol, the gene expression levels of germ cell, Mvh, and maturation markers, Cx37, Zp2, and Gdf9, were also upregulated significantly. Tretinoin 55-57 growth differentiation factor 9 Mus musculus 186-190
9174604-0 1997 CD43 (leukosialin, sialophorin) expression is differentially regulated by retinoic acids. Tretinoin 74-88 LOC105369247 Homo sapiens 6-17
9125573-4 1997 Whereas tumor necrosis factor alpha, gamma interferon, bufalin, or granulocyte-macrophage colony-stimulating factor only marginally increased the ability of monocytic MonoMac-6 and myelomonocytic JOSK-M cells to interact with the bacteria, retinoic acid and vitamin D3 treatment for 2 to 4 days led to highly phagocytic cells that internalized gonococci in an Opa protein-specific manner. Tretinoin 240-253 colony stimulating factor 2 Homo sapiens 37-115
9111026-6 1997 In addition, Arg276 of RARalpha, like its homologous residue Arg269 of RARbeta, was found to play an important role in the binding of RA most likely by interacting with the carboxylate group of RA. Tretinoin 71-73 retinoic acid receptor alpha Homo sapiens 23-31
8761481-4 1996 Stimulation of the hepatoma cell line HepG2 with the receptor ligands L-3,5,3"-tri-iodothyronine, all-trans retinoic acid, or their combination, increased production of antithrombin into the culture medium by 1.3-, 1.6-, and 2.0-fold, respectively. Tretinoin 108-121 serpin family C member 1 Homo sapiens 169-181
8706939-4 1996 All-trans retinoic acid and dibutyryl cyclic AMP have cell type specific effects on COUP-TF II promoter activity. Tretinoin 10-23 nuclear receptor subfamily 2, group F, member 2 Mus musculus 84-94
25687389-7 2015 RA exposure resulted in up-regulation of the RA metabolizing enzyme genes cyp26a1, cyp26b1 and cyp26c1 in vitro and in vivo. Tretinoin 0-2 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 83-90
8810554-1 1996 We studied the quantitative changes in PML/retinoic acid receptor alpha (PML/RAR alpha) fusion mRNA using the reverse transcriptase-polymerase chain reaction (RT-PCR) and the in vitro differentiation of leukemic cells from eight acute promyelocytic leukemia (APL) patients during treatment with all-trans retinoic acid (ATRA). Tretinoin 43-56 PML nuclear body scaffold Homo sapiens 73-86
8810554-2 1996 In three patients, the intensity of the chimeric PML/RAR alpha bands decreased rapidly after the start of ATRA therapy. Tretinoin 106-110 PML nuclear body scaffold Homo sapiens 49-62
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 115-139
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 0-3
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 115-139
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 115-139
9108090-1 1997 Acute promyelocytic leukemia (APL) is associated with the t(15;17) translocation, which generates a PML/RAR alpha fusion protein between PML, a growth suppressor localized on nuclear matrix-associated bodies, and RAR alpha, a nuclear receptor for retinoic acid (RA). Tretinoin 247-260 PML nuclear body scaffold Homo sapiens 100-113
9108090-1 1997 Acute promyelocytic leukemia (APL) is associated with the t(15;17) translocation, which generates a PML/RAR alpha fusion protein between PML, a growth suppressor localized on nuclear matrix-associated bodies, and RAR alpha, a nuclear receptor for retinoic acid (RA). Tretinoin 247-260 PML nuclear body scaffold Homo sapiens 100-103
9108090-1 1997 Acute promyelocytic leukemia (APL) is associated with the t(15;17) translocation, which generates a PML/RAR alpha fusion protein between PML, a growth suppressor localized on nuclear matrix-associated bodies, and RAR alpha, a nuclear receptor for retinoic acid (RA). Tretinoin 247-260 retinoic acid receptor alpha Homo sapiens 183-222
9108090-1 1997 Acute promyelocytic leukemia (APL) is associated with the t(15;17) translocation, which generates a PML/RAR alpha fusion protein between PML, a growth suppressor localized on nuclear matrix-associated bodies, and RAR alpha, a nuclear receptor for retinoic acid (RA). Tretinoin 104-106 PML nuclear body scaffold Homo sapiens 100-103
9108090-8 1997 Thus, RA and arsenic target RAR alpha and PML, respectively, but both induce the degradation of the PML/RAR alpha fusion protein, which should contribute to their therapeutic effects. Tretinoin 6-8 retinoic acid receptor alpha Homo sapiens 28-37
9108090-8 1997 Thus, RA and arsenic target RAR alpha and PML, respectively, but both induce the degradation of the PML/RAR alpha fusion protein, which should contribute to their therapeutic effects. Tretinoin 6-8 PML nuclear body scaffold Homo sapiens 42-45
9108090-8 1997 Thus, RA and arsenic target RAR alpha and PML, respectively, but both induce the degradation of the PML/RAR alpha fusion protein, which should contribute to their therapeutic effects. Tretinoin 6-8 retinoic acid receptor alpha Homo sapiens 100-113
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 0-3
8702428-0 1996 Retinoic acid regulates differentially the expression of IL-1 beta and IL-1 receptor antagonist (IL-1ra) in PMA-activated human monocytes. Tretinoin 0-13 interleukin 1 receptor antagonist Homo sapiens 71-95
8702428-0 1996 Retinoic acid regulates differentially the expression of IL-1 beta and IL-1 receptor antagonist (IL-1ra) in PMA-activated human monocytes. Tretinoin 0-13 interleukin 1 receptor antagonist Homo sapiens 97-103
8702428-2 1996 Although it has been shown that RA stimulates IL-1 expression in monocytes, it is of interest for understanding of the regulatory role of RA in inflammation to examine whether RA also modulates the expression of the IL-1 receptor antagonist (IL-1ra), which is reported to reduce IL-1 beta-mediated inflammation. Tretinoin 32-34 interleukin 1 receptor antagonist Homo sapiens 242-248
9174119-3 1997 The IC50 plots of DDRA for inhibition of [3H]RA binding to CRABP I and II and to RAR alpha, beta and gamma illustrate that this retinoid binds with the same affinity as RA to these proteins. Tretinoin 20-22 retinoic acid receptor alpha Homo sapiens 81-90
9174119-3 1997 The IC50 plots of DDRA for inhibition of [3H]RA binding to CRABP I and II and to RAR alpha, beta and gamma illustrate that this retinoid binds with the same affinity as RA to these proteins. Tretinoin 45-47 retinoic acid receptor alpha Homo sapiens 81-90
9174119-5 1997 Evaluation of the transcriptional activation potential of DDRA in CV-1 cells showed that this retinoid induced RAR alpha-mediated transcription to the same magnitude as RA in the 10(-9) to 10(-6) M concentration range. Tretinoin 60-62 retinoic acid receptor alpha Homo sapiens 111-120
25687389-7 2015 RA exposure resulted in up-regulation of the RA metabolizing enzyme genes cyp26a1, cyp26b1 and cyp26c1 in vitro and in vivo. Tretinoin 0-2 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 95-102
25687389-7 2015 RA exposure resulted in up-regulation of the RA metabolizing enzyme genes cyp26a1, cyp26b1 and cyp26c1 in vitro and in vivo. Tretinoin 45-47 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 83-90
8706705-4 1996 Such dual effects of Zn2+ were also observed in the native membrane-bound CD38 of HL-60 cells which had been caused to differentiate by retinoic acid. Tretinoin 136-149 CD38 molecule Homo sapiens 74-78
25687389-7 2015 RA exposure resulted in up-regulation of the RA metabolizing enzyme genes cyp26a1, cyp26b1 and cyp26c1 in vitro and in vivo. Tretinoin 45-47 cytochrome P450, family 26, subfamily C, polypeptide 1 Danio rerio 95-102
9150345-1 1997 All-trans-retinoic acid (ATRA) has been used as a potent therapeutic agent to induce differentiation of acute promyelocytic leukemia (APL) cells, and granulocyte colony-stimulating factor (G-CSF) has been reported to enhance this effect of ATRA in vitro. Tretinoin 0-23 colony stimulating factor 3 Homo sapiens 189-194
9150345-1 1997 All-trans-retinoic acid (ATRA) has been used as a potent therapeutic agent to induce differentiation of acute promyelocytic leukemia (APL) cells, and granulocyte colony-stimulating factor (G-CSF) has been reported to enhance this effect of ATRA in vitro. Tretinoin 240-244 colony stimulating factor 3 Homo sapiens 150-187
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein, alpha-crystallin-related, B6 Mus musculus 60-65
9150345-1 1997 All-trans-retinoic acid (ATRA) has been used as a potent therapeutic agent to induce differentiation of acute promyelocytic leukemia (APL) cells, and granulocyte colony-stimulating factor (G-CSF) has been reported to enhance this effect of ATRA in vitro. Tretinoin 240-244 colony stimulating factor 3 Homo sapiens 189-194
9125129-1 1997 P19 EC cells undergoes apoptosis during neuronal differentiation induced by retinoic acid. Tretinoin 76-89 interleukin 23 subunit alpha Homo sapiens 0-3
9125129-2 1997 Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. Tretinoin 74-87 caspase 7 Homo sapiens 36-41
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 185-198 PML nuclear body scaffold Homo sapiens 68-71
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 185-198 retinoic acid receptor alpha Homo sapiens 72-76
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 185-198 retinoic acid receptor alpha Homo sapiens 98-102
9125129-2 1997 Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. Tretinoin 74-87 interleukin 23 subunit alpha Homo sapiens 96-99
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 185-198 PML nuclear body scaffold Homo sapiens 103-106
9125129-5 1997 Wortmannin, PI-3K inhibitor, enhances the CPP32-like activity of the retinoic acid-treated P19 EC cells. Tretinoin 69-82 interleukin 23 subunit alpha Homo sapiens 91-94
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 DnaJ heat shock protein family (Hsp40) member B1 Mus musculus 86-91
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 200-204 PML nuclear body scaffold Homo sapiens 68-71
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 200-204 retinoic acid receptor alpha Homo sapiens 72-76
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein, alpha-crystallin-related, B6 Mus musculus 60-65
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 200-204 retinoic acid receptor alpha Homo sapiens 98-102
8819070-2 1996 The t(15;17) leads to the formation of two reciprocal fusion genes, PML/RARA on chromosome 15 and RARA/PML on chromosome 17; it is responsible for the unique response of the disease to retinoic acid (ATRA) treatment. Tretinoin 200-204 PML nuclear body scaffold Homo sapiens 103-106
8832580-0 1996 Retinoic acid induction of the tissue transglutaminase promoter is mediated by a novel response element. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 31-54
8832580-7 1996 Our results suggest that this novel retinoid response element is responsible for the retinoic acid induction of mouse tissue transglutaminase gene expression observed in numerous cells. Tretinoin 85-98 transglutaminase 2, C polypeptide Mus musculus 118-141
9137463-7 1997 After a two-week treatment with all-trans retinoic acid, all the cells became spindle shaped, vimentin filaments reappeared in the cytoplasm of J82-NVB cells and desmosomes disappeared from the membranes of these cells. Tretinoin 32-55 vimentin Homo sapiens 94-102
8843397-6 1996 Differential effects of RA on the expression of GATA-1 and GATA-2 suggest that RA has a direct action on haematopoietic differentiation, rather than on the formation of haematopoietic mesoderm. Tretinoin 24-26 GATA binding protein 2 L homeolog Xenopus laevis 59-65
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 DnaJ heat shock protein family (Hsp40) member B1 Mus musculus 86-91
8843397-6 1996 Differential effects of RA on the expression of GATA-1 and GATA-2 suggest that RA has a direct action on haematopoietic differentiation, rather than on the formation of haematopoietic mesoderm. Tretinoin 79-81 GATA binding protein 2 L homeolog Xenopus laevis 59-65
9048588-0 1997 Retinoic acids increase 17 beta-hydroxysteroid dehydrogenase type 1 expression in JEG-3 and T47D cells, but the stimulation is potentiated by epidermal growth factor, 12-O-tetradecanoylphorbol-13-acetate, and cyclic adenosine 3",5"-monophosphate only in JEG-3 cells. Tretinoin 0-14 epidermal growth factor Homo sapiens 142-165
25911751-4 2015 Regulatory functions can be corrected, even in T cells isolated from aged, diabetic mice, by a synergistic activity of retinoic acid, TGF-beta, and IL-2, which enhance connexin 43 and Foxp3 expression in T(regs) and restore the ability of conventional CD4(+) T cells to upregulate Foxp3 and generate peripherally derived T(regs). Tretinoin 119-132 forkhead box P3 Mus musculus 184-189
9068616-3 1997 Here we show that retinoic acid, injected intraperitoneally into dark-adapted mice, increases the arrestin mRNA levels and mimics the effect of light. Tretinoin 18-31 S-antigen, retina and pineal gland (arrestin) Mus musculus 98-106
8645577-6 1996 Addition of all-trans-retinoic acid increased the amount of RAR-alpha mRNA in the three cell lines and induced RAR-beta mRNA in Capan 1 and Capan 2 cells. Tretinoin 12-35 retinoic acid receptor alpha Homo sapiens 60-69
8674421-2 1996 Retinoic acid and Sonic Hedgehog (SHH) can act as polarizing signals; when applied anteriorly in the limb bud, they induce mirror-image digit duplications and ectopic Bmp-2 expression in anterior mesenchyme. Tretinoin 0-13 bone morphogenetic protein 2 Gallus gallus 167-172
8655603-9 1996 Retinoic acid was less effective in inhibiting thymidine incorporation when cells were stimulated with insulin, des(1-3) IGF-I, or Long(R3) IGF-I when compared to cells stimulated with native IGF-I or serum. Tretinoin 0-13 insulin Bos taurus 103-110
9068616-4 1997 Injection of 1 mumol of retinoic acid produces a maximal increase in arrestin mRNA levels. Tretinoin 24-37 S-antigen, retina and pineal gland (arrestin) Mus musculus 69-77
9068616-6 1997 The observations suggest that retinoic acid may mediate the increase in arrestin mRNA produced by light. Tretinoin 30-43 S-antigen, retina and pineal gland (arrestin) Mus musculus 72-80
25911751-4 2015 Regulatory functions can be corrected, even in T cells isolated from aged, diabetic mice, by a synergistic activity of retinoic acid, TGF-beta, and IL-2, which enhance connexin 43 and Foxp3 expression in T(regs) and restore the ability of conventional CD4(+) T cells to upregulate Foxp3 and generate peripherally derived T(regs). Tretinoin 119-132 forkhead box P3 Mus musculus 281-286
24285572-6 2015 Proteomics tentatively identified this protein as aldehyde dehydrogenase 1A1 (ALDH1A1), a key enzyme regulating retinoic acid synthesis, and ALDH1A1 protein deficiency in GDFs was confirmed by Western blot. Tretinoin 112-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 50-76
9089745-1 1997 We describe here the first case of childhood acute promyelocytic leukemia (APL) with cutaneous infiltration of leukemic cells following treatment with all-trans retinoic acid (ATRA) confirmed by immunostaining and polymerase chain reaction for PML/RAR alpha. Tretinoin 151-174 PML nuclear body scaffold Homo sapiens 244-257
8782080-4 1996 Mobility shift assays demonstrated that ARP-1 binds specifically to a composite steroid response element on the hPL promoter that confers retinoic acid and T3 responsiveness. Tretinoin 138-151 galectin 1 Homo sapiens 112-115
8639801-0 1996 Infrequent alterations of the RAR alpha gene in acute myelogenous leukemias, retinoic acid-resistant acute promyelocytic leukemias, myelodysplastic syndromes, and cell lines. Tretinoin 77-90 retinoic acid receptor alpha Homo sapiens 30-39
9089745-1 1997 We describe here the first case of childhood acute promyelocytic leukemia (APL) with cutaneous infiltration of leukemic cells following treatment with all-trans retinoic acid (ATRA) confirmed by immunostaining and polymerase chain reaction for PML/RAR alpha. Tretinoin 176-180 PML nuclear body scaffold Homo sapiens 244-257
8639801-2 1996 All-trans retinoic acid (RA) induces complete remission in patients with acute promyelocytic leukemia (APL) presumably by binding directly to RAR alpha of APL cells. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 142-151
24285572-6 2015 Proteomics tentatively identified this protein as aldehyde dehydrogenase 1A1 (ALDH1A1), a key enzyme regulating retinoic acid synthesis, and ALDH1A1 protein deficiency in GDFs was confirmed by Western blot. Tretinoin 112-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 78-85
8639801-2 1996 All-trans retinoic acid (RA) induces complete remission in patients with acute promyelocytic leukemia (APL) presumably by binding directly to RAR alpha of APL cells. Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 142-151
8639801-4 1996 HL-60 myeloblasts cultured with RA have developed mutations of the ligand-binding region of RAR alpha and have become resistant to RA. Tretinoin 32-34 retinoic acid receptor alpha Homo sapiens 92-101
9113387-8 1997 These results suggested that the inhibitory effect of RA on the mineralization of human osteoblasts is mediated by the activation of RAR alpha and/or RAR beta and that RAR gamma preferentially regulates the expression of osteocalcin without influence on mineralization. Tretinoin 54-56 retinoic acid receptor alpha Homo sapiens 133-142
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 polo like kinase 2 Homo sapiens 246-264
25727910-10 2015 We propose the relevance of estrogen-related receptor gamma (ERRgamma) in regulating dopaminergic neuronal phenotype: ERRgamma is up-regulated by retinoic acid in SH-SY5Y cells, and enhances dopaminergic phenotypes and induces neurite outgrowth; Polo-like kinase 2 (PLK2) and glycogen synthase kinase 3 beta/nuclear factor of activated T cells (GSK3beta/NFAT) signaling are responsible for the ERRgamma effect. Tretinoin 146-159 polo like kinase 2 Homo sapiens 266-270
9081214-0 1997 Paxillin increases as retinoic acid or vitamin D3 induce HL-60 cell differentiation. Tretinoin 22-35 paxillin Homo sapiens 0-8
8626453-0 1996 Retinoic acid down-regulation of fibronectin and retinoic acid receptor alpha proteins in NIH-3T3 cells. Tretinoin 0-13 fibronectin 1 Mus musculus 33-44
8626453-2 1996 All-trans-retinoic acid (RA) markedly reduced the level of intracellular fibronectin (FN) in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 0-23 fibronectin 1 Mus musculus 73-84
8626453-2 1996 All-trans-retinoic acid (RA) markedly reduced the level of intracellular fibronectin (FN) in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 0-23 fibronectin 1 Mus musculus 86-88
25849135-0 2015 Active Pin1 is a key target of all-trans retinoic acid in acute promyelocytic leukemia and breast cancer. Tretinoin 41-54 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 7-11
8626453-2 1996 All-trans-retinoic acid (RA) markedly reduced the level of intracellular fibronectin (FN) in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 25-27 fibronectin 1 Mus musculus 73-84
8626453-2 1996 All-trans-retinoic acid (RA) markedly reduced the level of intracellular fibronectin (FN) in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 25-27 fibronectin 1 Mus musculus 86-88
8626453-3 1996 Pulse/chase experiments indicated that RA affects FN biosynthesis rather than its turnover rate. Tretinoin 39-41 fibronectin 1 Mus musculus 50-52
9155047-9 1997 Additionally, RA was shown to enhance the expression of retinoic acid receptor alpha (RAR alpha) in SC-M1 cells, and to have no effect on the expression of RARbeta or RARgamma. Tretinoin 14-16 retinoic acid receptor alpha Homo sapiens 56-84
9155047-9 1997 Additionally, RA was shown to enhance the expression of retinoic acid receptor alpha (RAR alpha) in SC-M1 cells, and to have no effect on the expression of RARbeta or RARgamma. Tretinoin 14-16 retinoic acid receptor alpha Homo sapiens 86-95
25933005-2 2015 The biological action of retinoic acid is mediated by three nuclear receptors denoted RARalpha, beta and gamma. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 86-94
9181129-2 1997 Members of the RAR family (types alpha, beta and gamma and their isoforms alpha 1, alpha 2, beta 1 to beta 4, and gamma 1 and gamma 2) are activated by most physiologically occurring retinoids (all-trans RA, 9-cis RA, 4oxo RA and 3,4 dihyroRA). Tretinoin 15-17 hemoglobin, beta adult major chain Mus musculus 92-133
9181129-2 1997 Members of the RAR family (types alpha, beta and gamma and their isoforms alpha 1, alpha 2, beta 1 to beta 4, and gamma 1 and gamma 2) are activated by most physiologically occurring retinoids (all-trans RA, 9-cis RA, 4oxo RA and 3,4 dihyroRA). Tretinoin 204-206 hemoglobin, beta adult major chain Mus musculus 92-133
8634442-2 1996 In the present study, we show that t-RA treatment dramatically induced type II transglutaminase (type II TGase) expression in cells carrying the t(15;17) translocation and expressing the PML-RARalpha product such as the APL-derived NB4 cell line and fresh leukemic cells from APL patients. Tretinoin 35-39 PML nuclear body scaffold Homo sapiens 187-190
8634442-2 1996 In the present study, we show that t-RA treatment dramatically induced type II transglutaminase (type II TGase) expression in cells carrying the t(15;17) translocation and expressing the PML-RARalpha product such as the APL-derived NB4 cell line and fresh leukemic cells from APL patients. Tretinoin 35-39 retinoic acid receptor alpha Homo sapiens 191-199
8634447-10 1996 We conclude that the RAR/RXR pathway is more important than RXR/RXR pathway for differentiation and proliferation of acute myeloid leukemic cells, and certain retinoids or combination of retinoids with both RAR and RXR specificities may synergistically enhance the differentiation activity of ATRA, which may be relevant in several clinical situations. Tretinoin 293-297 retinoic acid receptor alpha Homo sapiens 21-24
25546009-6 2015 In addition, when coexpressed with LRH1, RA receptors (RARs) can promote reprogramming in the absence of both exogenous and endogenously synthesized RA. Tretinoin 41-43 nuclear receptor subfamily 5, group A, member 2 Mus musculus 35-39
8631256-6 1996 In addition, r4 gene expression is also partially altered by RA; within 6 hours of r4 exposure to RA, ectopic expression of Krox-20 is seen in r4 and Hoxb-1 expression is lost while Hoxa-2 expression continues normally. Tretinoin 61-63 early growth response 2 Homo sapiens 124-131
8631256-6 1996 In addition, r4 gene expression is also partially altered by RA; within 6 hours of r4 exposure to RA, ectopic expression of Krox-20 is seen in r4 and Hoxb-1 expression is lost while Hoxa-2 expression continues normally. Tretinoin 98-100 early growth response 2 Homo sapiens 124-131
8631256-6 1996 In addition, r4 gene expression is also partially altered by RA; within 6 hours of r4 exposure to RA, ectopic expression of Krox-20 is seen in r4 and Hoxb-1 expression is lost while Hoxa-2 expression continues normally. Tretinoin 98-100 homeobox B1 Homo sapiens 150-156
8603611-4 1996 The most dramatic effect of RA on IGFBPs++ in all cell types tested was to increase IGFBP-6 messenger RNA (mRNA) abundance more than 1000% of the control value. Tretinoin 28-30 insulin like growth factor binding protein 3 Homo sapiens 34-40
8603611-7 1996 The levels of the 24-, 29- to 32-, and 38- to 42 kDa IGFBPs in the conditioned medium of RA-treated cultures increased, as determined by ligand blot analysis, whereas the amount of IGFBP-5 was reduced, as determined by RIA. Tretinoin 89-91 insulin like growth factor binding protein 3 Homo sapiens 53-59
8603611-8 1996 Cycloheximide abolished the RA-stimulated increase in IGFBP-6 mRNA and reduced baseline IGFBP-5 mRNA levels, but did not affect RA-modulated mRNA levels of the other IGFBPs. Tretinoin 28-30 insulin like growth factor binding protein 3 Homo sapiens 166-172
8603611-9 1996 RA modestly increased the stabilities of all four IGFBP mRNAs, which could contribute to the observed increases in IGFBP-3 and IGFBP-4 mRNA levels; however, the 217% increase in the IGFBP-5 mRNA half- life in the presence of RA could not contribute to the reduction in mRNA levels. Tretinoin 0-2 insulin like growth factor binding protein 3 Homo sapiens 115-122
9216065-0 1997 Lens-preferred activity of chicken delta 1- and delta 2-crystallin enhancers in transgenic mice and evidence for retinoic acid-responsive regulation of the delta 1-crystallin gene. Tretinoin 113-126 delta-1 crystallin Gallus gallus 156-174
9216065-6 1997 Finally, retinoic acid receptors (RAR beta) activated the delta 1-crystallin, but not the delta 2-crystallin enhancer in teh recombinant plasmids in cotransfected embryonic chicken lens epithelial cells treated with retinoic acid. Tretinoin 9-22 retinoic acid receptor beta Gallus gallus 34-42
9216065-6 1997 Finally, retinoic acid receptors (RAR beta) activated the delta 1-crystallin, but not the delta 2-crystallin enhancer in teh recombinant plasmids in cotransfected embryonic chicken lens epithelial cells treated with retinoic acid. Tretinoin 9-22 delta-1 crystallin Gallus gallus 58-76
9027555-8 1997 Following a 24-h exposure of porcine preadipocytes to retinoic acid at d 1, Northern blot analysis showed that there was a decrease in lipoprotein lipase and adipsin mRNA levels. Tretinoin 54-67 complement factor D Sus scrofa 158-165
8717447-5 1996 Growth was decreased to a greater extent by deletion of growth factors from medium with KGF versus EGF, and retinoic acid was 10-fold more potent at inducing growth inhibition and differentiation-associated keratin with KGF compared with EGF. Tretinoin 108-121 epidermal growth factor Homo sapiens 238-241
8981241-5 1997 In contrast, NMDAR1-like immunoreactivity (NMDAR1-LI) in the RA-treated cells was detected in the cell soma and processes only with the higher concentration of the antiserum. Tretinoin 61-63 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 13-19
25929268-7 2015 FGF8 and Isl1 expression were downregulated in retinoic acid-exposed AHF, and differentiation and expansion of cardiomyocytes were suppressed in cultured AHF in medium supplemented with retinoic acid. Tretinoin 47-60 fibroblast growth factor 8 Homo sapiens 0-4
8981241-5 1997 In contrast, NMDAR1-like immunoreactivity (NMDAR1-LI) in the RA-treated cells was detected in the cell soma and processes only with the higher concentration of the antiserum. Tretinoin 61-63 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 43-49
8986606-0 1996 The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic. Tretinoin 83-96 PML nuclear body scaffold Homo sapiens 4-7
9183635-4 1996 Retinoic acid receptor (RAR) of HSG cells revealed a transcriptional activity in vivo, and the heterodimerization between RAR and 9-cis retinoic acid receptor (RXR) is requisite for the binding with a specific DNA element termed RA response element in vitro. Tretinoin 24-26 retinoic acid receptor alpha Homo sapiens 0-22
9183635-4 1996 Retinoic acid receptor (RAR) of HSG cells revealed a transcriptional activity in vivo, and the heterodimerization between RAR and 9-cis retinoic acid receptor (RXR) is requisite for the binding with a specific DNA element termed RA response element in vitro. Tretinoin 24-26 retinoic acid receptor alpha Homo sapiens 122-125
9183635-4 1996 Retinoic acid receptor (RAR) of HSG cells revealed a transcriptional activity in vivo, and the heterodimerization between RAR and 9-cis retinoic acid receptor (RXR) is requisite for the binding with a specific DNA element termed RA response element in vitro. Tretinoin 24-26 retinoic acid receptor alpha Homo sapiens 136-158
8986606-0 1996 The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic. Tretinoin 83-96 PML nuclear body scaffold Homo sapiens 12-15
8986606-0 1996 The PML and PML/RARalpha domains: from autoimmunity to molecular oncology and from retinoic acid to arsenic. Tretinoin 83-96 retinoic acid receptor alpha Homo sapiens 16-24
25929268-7 2015 FGF8 and Isl1 expression were downregulated in retinoic acid-exposed AHF, and differentiation and expansion of cardiomyocytes were suppressed in cultured AHF in medium supplemented with retinoic acid. Tretinoin 47-60 ISL LIM homeobox 1 Homo sapiens 9-13
8986606-5 1996 In APL, the PML/RARalpha fusion interferes with both the retinoic acid (RA) response and PML localization on nuclear bodies, but the respective contribution of each defect to leukemogenesis is unclear. Tretinoin 57-70 PML nuclear body scaffold Homo sapiens 12-15
8986606-5 1996 In APL, the PML/RARalpha fusion interferes with both the retinoic acid (RA) response and PML localization on nuclear bodies, but the respective contribution of each defect to leukemogenesis is unclear. Tretinoin 57-70 retinoic acid receptor alpha Homo sapiens 16-24
25929268-7 2015 FGF8 and Isl1 expression were downregulated in retinoic acid-exposed AHF, and differentiation and expansion of cardiomyocytes were suppressed in cultured AHF in medium supplemented with retinoic acid. Tretinoin 186-199 fibroblast growth factor 8 Homo sapiens 0-4
8986606-5 1996 In APL, the PML/RARalpha fusion interferes with both the retinoic acid (RA) response and PML localization on nuclear bodies, but the respective contribution of each defect to leukemogenesis is unclear. Tretinoin 16-18 PML nuclear body scaffold Homo sapiens 12-15
8986606-5 1996 In APL, the PML/RARalpha fusion interferes with both the retinoic acid (RA) response and PML localization on nuclear bodies, but the respective contribution of each defect to leukemogenesis is unclear. Tretinoin 16-18 PML nuclear body scaffold Homo sapiens 89-92
8612233-0 1996 HMG-CoA reductase mediates the biological effects of retinoic acid on human neuroblastoma cells: lovastatin specifically targets P-glycoprotein-expressing cells. Tretinoin 53-66 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-17
8852383-2 1996 RNAase protection and western blot analysis revealed that E14-ES cells up regulate RPTP alpha expression upon neuronal differentiation with retinoic acid. Tretinoin 140-153 nuclear protein, coactivator of histone transcription Homo sapiens 58-61
25929268-7 2015 FGF8 and Isl1 expression were downregulated in retinoic acid-exposed AHF, and differentiation and expansion of cardiomyocytes were suppressed in cultured AHF in medium supplemented with retinoic acid. Tretinoin 186-199 ISL LIM homeobox 1 Homo sapiens 9-13
8852383-3 1996 Overexpression of RPTP alpha, by stable DNA transfection, and subsequent differentiation with retinoic acid, resulted in a temporally enhanced expression of the neuronal markers GAP-43 and NF-164. Tretinoin 94-107 growth associated protein 43 Homo sapiens 178-184
8980637-5 1996 Retinoic acid and 13-cis-retinoic acid produced transient, but significant, depressions of both serum retinol and RBP concentrations, when the individual retinoids were administered orally to rats. Tretinoin 0-13 retinol binding protein 4 Rattus norvegicus 114-117
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 117-130 apoptotic chromatin condensation inducer 1 Homo sapiens 5-11
8574972-7 1996 These results suggest that the clinical effects of RA in SCCHN patients may be due to a downmodulation of TGF-alpha and EGFR mRNA production. Tretinoin 51-53 epidermal growth factor Homo sapiens 120-124
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 117-130 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
8997128-9 1996 These findings suggest that combined therapy of ATRA and G-CSF is effective to the low responder to ATRA and that combined use of ATRA and prednisolone reduces the side effect of ATRA without diminishing the favorable effect on differentiation. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 57-62
8997128-9 1996 These findings suggest that combined therapy of ATRA and G-CSF is effective to the low responder to ATRA and that combined use of ATRA and prednisolone reduces the side effect of ATRA without diminishing the favorable effect on differentiation. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 57-62
8576149-2 1996 We demonstrated previously that the extracellular domain of CD38 has NAD+ glycohydrolase (NADase) activity and that the ecto-form NADase activity induced in HL-60 cells during cell differentiation by retinoic acid is due to CD38. Tretinoin 200-213 CD38 molecule Homo sapiens 60-64
8997128-9 1996 These findings suggest that combined therapy of ATRA and G-CSF is effective to the low responder to ATRA and that combined use of ATRA and prednisolone reduces the side effect of ATRA without diminishing the favorable effect on differentiation. Tretinoin 100-104 colony stimulating factor 3 Homo sapiens 57-62
8576149-2 1996 We demonstrated previously that the extracellular domain of CD38 has NAD+ glycohydrolase (NADase) activity and that the ecto-form NADase activity induced in HL-60 cells during cell differentiation by retinoic acid is due to CD38. Tretinoin 200-213 CD38 molecule Homo sapiens 224-228
8576149-3 1996 In the present study, we investigated the intracellular signaling mediated by CD38 in retinoic acid-differentiated HL-60 cells with an anti-CD38 monoclonal antibody. Tretinoin 86-99 CD38 molecule Homo sapiens 78-82
8576149-3 1996 In the present study, we investigated the intracellular signaling mediated by CD38 in retinoic acid-differentiated HL-60 cells with an anti-CD38 monoclonal antibody. Tretinoin 86-99 CD38 molecule Homo sapiens 140-144
8555497-11 1996 Possible mechanisms for accelerated clearance of RA include the induction of non-CYP1A1 cytochrome P450 enzymes and P-glycoprotein. Tretinoin 49-51 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 81-87
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 117-130 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
8881287-5 1996 The fusion protein PML-RAR, which is not localized in nuclear bodies, also enhanced the transactivating activity of PR but this effect was totally suppressed by the administration of retinoic acid. Tretinoin 183-196 PML nuclear body scaffold Homo sapiens 19-22
8956873-4 1996 The unusual PML-RARA fusion may be related to this patient"s poor response to induction therapy with all-trans-retinoic acid. Tretinoin 101-124 PML nuclear body scaffold Homo sapiens 12-15
25205379-3 2015 Both Acinus-L and Acinus-S", with the activity of Acinus-L higher than that of Acinus-S", increase the splicing of a retinoic acid (RA)-responsive minigene containing a weak 5" splice site but not a RA-responsive minigene containing a strong 5" splice site. Tretinoin 117-130 apoptotic chromatin condensation inducer 1 Homo sapiens 18-24
8956873-4 1996 The unusual PML-RARA fusion may be related to this patient"s poor response to induction therapy with all-trans-retinoic acid. Tretinoin 101-124 retinoic acid receptor alpha Homo sapiens 16-20
8881287-5 1996 The fusion protein PML-RAR, which is not localized in nuclear bodies, also enhanced the transactivating activity of PR but this effect was totally suppressed by the administration of retinoic acid. Tretinoin 183-196 retinoic acid receptor alpha Homo sapiens 23-26
25578258-10 2015 These findings support that in addition to the "classic" retinoic acid receptor alpha-mediated transcriptional control of CRF expression, disruption in CRF-modulating systems constitutes a novel pathway that underlies ATRA-induced HPA axis hyperactivity in vivo. Tretinoin 218-222 retinoic acid receptor, alpha Rattus norvegicus 57-85
8547646-4 1996 An RAR alpha-selective ligand used with an RXR-selective ligand generated the same responses as did all-trans RA or 9-cis RA, which affect both families of receptors, suggesting an important role for RAR alpha among RAR subtypes in eliciting cellular response. Tretinoin 3-5 retinoic acid receptor alpha Homo sapiens 200-203
8706045-3 1996 We have now identified the p65 gene as a novel member of the superfamily of genes that encode nuclear receptors for various hydrophobic ligands such as steroids, vitamin D, retinoic acid, and thyroid hormones. Tretinoin 173-186 golgi reassembly stacking protein 1 Homo sapiens 27-30
8887661-7 1996 The cooperative enhancement by TFIIB and IRF-1 was independent of the TATA sequence in the ISRE promoter but dependent on the initiator sequence (Inr) and was abolished when P19 cells were induced to differentiate by retinoic acid treatment. Tretinoin 217-230 interferon regulatory factor 1 Mus musculus 41-46
9387294-0 1996 [Growth inhibitory effect of retinoic acid in human breast cancer cells correlates with retinoic acid receptor alpha (RAR alpha) expression]. Tretinoin 29-42 retinoic acid receptor alpha Homo sapiens 88-116
9387294-0 1996 [Growth inhibitory effect of retinoic acid in human breast cancer cells correlates with retinoic acid receptor alpha (RAR alpha) expression]. Tretinoin 29-42 retinoic acid receptor alpha Homo sapiens 118-127
8792612-4 1996 We show that as well as retinyl palmitate, other retinoids such as all-trans-retinoic acid and TTNPB, which is a RAR specific retinoid, can induce the homeotic transformation. Tretinoin 67-90 retinoic acid receptor alpha Homo sapiens 113-116
25805962-0 2015 Granulocyte colony-stimulating factor potentiates all-trans retinoic acid-induced granulocytic differentiation in acute promyelocytic leukemia cell line HT93A. Tretinoin 60-73 colony stimulating factor 3 Homo sapiens 0-37
25805962-7 2015 RESULTS: ATRA (100 nM) induced granulocytic differentiation (upregulation of CD11b and downregulation of CD34) and the effect was potentiated by addition of G-CSF, while G-CSF alone had no effect on HT93A cells. Tretinoin 9-13 colony stimulating factor 3 Homo sapiens 157-162
8558945-0 1996 All-trans retinoic acid rapidly decreases cathepsin G synthesis and mRNA expression in acute promyelocytic leukemia. Tretinoin 0-23 cathepsin G Homo sapiens 42-53
8874178-0 1996 The PML/RAR alpha oncoprotein is a direct molecular target of retinoic acid in acute promyelocytic leukemia cells. Tretinoin 62-75 retinoic acid receptor alpha Homo sapiens 4-17
25805962-7 2015 RESULTS: ATRA (100 nM) induced granulocytic differentiation (upregulation of CD11b and downregulation of CD34) and the effect was potentiated by addition of G-CSF, while G-CSF alone had no effect on HT93A cells. Tretinoin 9-13 colony stimulating factor 3 Homo sapiens 170-175
8874178-3 1996 We now show that the PML/RAR alpha fusion product is directly downregulated in response to retinoic acid (tRA) treatment in the human APL cell line, NB4. Tretinoin 91-104 PML nuclear body scaffold Homo sapiens 21-34
8558945-2 1996 We have analyzed the expression of the mRNA for cathepsin G, a promyelocyte stage-specific transcript, in the leukemia and in retinoic acid responsive cell lines. Tretinoin 126-139 cathepsin G Homo sapiens 48-59
25805962-9 2015 G-CSF receptor expression was reduced by ATRA treatment in a time-dependent manner. Tretinoin 41-45 colony stimulating factor 3 receptor Homo sapiens 0-14
25805962-10 2015 After 5 days" incubation with ATRA, the expression levels of signal transducer and activator of transcription (STAT) 3, and phosphorylated STAT3 and STAT5, were significantly reduced. Tretinoin 30-34 signal transducer and activator of transcription 5A Homo sapiens 149-154
25343668-4 2015 We also found that RA reduced extracellular signal-regulated kinase (ERK) phosphorylation, but increased phosphatase 2A (PP2A) activity in TCR/CD28-stimulated NKT cells. Tretinoin 19-21 protein phosphatase 2 phosphatase activator Homo sapiens 121-125
8786690-3 1996 DR1 elements are also activated by RXR homodimers formed in the presence of 9-cis retinoic acid (9 cis RA) suggesting that PP and 9 cis RA might regulate an overlapping set of target genes. Tretinoin 103-105 down-regulator of transcription 1 Rattus norvegicus 0-3
25568183-7 2015 Hence, beta-catenin/TCF4 signaling induces local regulatory DC and regulatory T-cell phenotypes via the RA pathway, identifying this pathway as an important target for anticancer immunotherapy. Tretinoin 104-106 transcription factor 4 Mus musculus 20-24
8786690-3 1996 DR1 elements are also activated by RXR homodimers formed in the presence of 9-cis retinoic acid (9 cis RA) suggesting that PP and 9 cis RA might regulate an overlapping set of target genes. Tretinoin 136-138 down-regulator of transcription 1 Rattus norvegicus 0-3
8839844-1 1996 Retinoic acid (RA)-induced maturation mediated by the retinoic acid receptor alpha (RAR alpha) has been implicated in myeloid development. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 54-82
8839844-1 1996 Retinoic acid (RA)-induced maturation mediated by the retinoic acid receptor alpha (RAR alpha) has been implicated in myeloid development. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 84-93
8839844-1 1996 Retinoic acid (RA)-induced maturation mediated by the retinoic acid receptor alpha (RAR alpha) has been implicated in myeloid development. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 54-82
8839844-1 1996 Retinoic acid (RA)-induced maturation mediated by the retinoic acid receptor alpha (RAR alpha) has been implicated in myeloid development. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 84-93
8923783-0 1996 Administration of granulocyte colony-stimulating factor during remission induction therapy with all-trans retinoic acid for acute promyelocytic leukemia. Tretinoin 106-119 colony stimulating factor 3 Homo sapiens 18-55
8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 140-153 colony stimulating factor 3 Homo sapiens 0-37
8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 140-153 colony stimulating factor 3 Homo sapiens 39-44
25247321-2 2015 Acute promyelocytic leukaemia (APL) driven by chimeric transcription factors encoding retinoic acid receptor alpha fusions is the paradigm of targeted cancer therapy, in which the application of all-trans retinoic acid (ATRA) treatments have markedly transformed this highly fatal cancer to a highly manageable disease. Tretinoin 220-224 retinoic acid receptor alpha Homo sapiens 86-114
8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 155-159 colony stimulating factor 3 Homo sapiens 0-37
8923783-1 1996 Granulocyte colony-stimulating factor (G-CSF) enhances the differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA) in vitro. Tretinoin 155-159 colony stimulating factor 3 Homo sapiens 39-44
8923783-2 1996 Accordingly, we initiated a pilot study on G-CSF in APL patients who developed neutropenia and severe infection during remission induction therapy with ATRA. Tretinoin 152-156 colony stimulating factor 3 Homo sapiens 43-48
8923783-5 1996 Our findings suggest that administration of G-CSF combined with ATRA can improve the hematological state in APL patients not previously receiving ATRA therapy. Tretinoin 146-150 colony stimulating factor 3 Homo sapiens 44-49
8841418-1 1996 Retinoic acid has important actions on cell differentiation and osteoblastic function, and some of these actions may be mediated by changes in the insulin-like growth factor (IGF) axis. Tretinoin 0-13 insulin-like growth factor 1 Rattus norvegicus 147-173
8841418-1 1996 Retinoic acid has important actions on cell differentiation and osteoblastic function, and some of these actions may be mediated by changes in the insulin-like growth factor (IGF) axis. Tretinoin 0-13 insulin-like growth factor 1 Rattus norvegicus 175-178
25502770-3 2015 While ALDH1A1, ALDH1A2, and ALDH1A3 all form RA, the expression pattern and relative contribution of these enzymes to RA formation in the testis is unknown. Tretinoin 45-47 aldehyde dehydrogenase 1 family member A1 Homo sapiens 6-13
9121491-0 1996 An adipogenic basic helix-loop-helix-leucine zipper type transcription factor (ADD1) mRNA is expressed and regulated by retinoic acid in osteoblastic cells. Tretinoin 120-133 adducin 1 Rattus norvegicus 79-83
9121491-5 1996 Treatment with retinoic acid (RA) enhanced the ADD1 mRNA expression several fold in these cells within 4 h in a dose-dependent manner. Tretinoin 15-28 adducin 1 Rattus norvegicus 47-51
9121491-5 1996 Treatment with retinoic acid (RA) enhanced the ADD1 mRNA expression several fold in these cells within 4 h in a dose-dependent manner. Tretinoin 30-32 adducin 1 Rattus norvegicus 47-51
25502770-3 2015 While ALDH1A1, ALDH1A2, and ALDH1A3 all form RA, the expression pattern and relative contribution of these enzymes to RA formation in the testis is unknown. Tretinoin 45-47 aldehyde dehydrogenase 1 family member A3 Homo sapiens 28-35
9121491-11 1996 RA treatment also enhanced the ADD1 mRNA expression in another rat calvaria-derived cell line, RCT1, and in the primary cultures of newborn rat calvaria cells. Tretinoin 0-2 adducin 1 Rattus norvegicus 31-35
25502770-7 2015 In the absence of cellular retinol binding protein (CRBP)1, ALDH1A1 was predicted to be the main contributor to intratesticular RA formation, but when CRBP1 was present, ALDH1A2 was predicted to be equally important in RA formation as ALDH1A1. Tretinoin 128-130 aldehyde dehydrogenase 1 family member A1 Homo sapiens 60-67
25560970-4 2015 Genetic studies later revealed that endogenous RA promotes forelimb initiation by repressing fibroblast growth factor 8 (Fgf8). Tretinoin 47-49 fibroblast growth factor 8 Homo sapiens 93-119
8822923-3 1996 We examined thrombomodulin function and regulation of thrombomodulin expression by all-trans retinoic acid (ATRA) and TNF in human keratinocytes and endothelial cells. Tretinoin 83-106 thrombomodulin Homo sapiens 54-68
8822923-3 1996 We examined thrombomodulin function and regulation of thrombomodulin expression by all-trans retinoic acid (ATRA) and TNF in human keratinocytes and endothelial cells. Tretinoin 108-112 thrombomodulin Homo sapiens 54-68
8822923-5 1996 Incubation of keratinocytes with 10 mumol/L ATRA for 24 hours increased thrombomodulin activity 5.4 +/- 0.9-fold (mean +/- SE), with equivalent increases observed in thrombomodulin protein (5.5 +/- 2.1-fold) and mRNA (4.2 +/- 1.2-fold). Tretinoin 44-48 thrombomodulin Homo sapiens 72-86
8822923-5 1996 Incubation of keratinocytes with 10 mumol/L ATRA for 24 hours increased thrombomodulin activity 5.4 +/- 0.9-fold (mean +/- SE), with equivalent increases observed in thrombomodulin protein (5.5 +/- 2.1-fold) and mRNA (4.2 +/- 1.2-fold). Tretinoin 44-48 thrombomodulin Homo sapiens 166-180
8822923-7 1996 In endothelial cells, ATRA produced a small increase in thrombomodulin activity (1.9 +/- 0.1-fold), and incubation with TNF for 24 hours decreased thrombomodulin activity 83% +/- 7%. Tretinoin 22-26 thrombomodulin Homo sapiens 56-70
25560970-4 2015 Genetic studies later revealed that endogenous RA promotes forelimb initiation by repressing fibroblast growth factor 8 (Fgf8). Tretinoin 47-49 fibroblast growth factor 8 Homo sapiens 121-125
25973309-7 2015 HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy. Tretinoin 157-161 PML nuclear body scaffold Homo sapiens 89-92
8806687-9 1996 However, following all trans retinoic acid treatment of NB4 cells a significant relocalisation of PIC1 and PML is observed. Tretinoin 29-42 PML nuclear body scaffold Homo sapiens 107-110
25973309-7 2015 HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy. Tretinoin 157-161 retinoic acid receptor alpha Homo sapiens 93-101
25973309-7 2015 HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy. Tretinoin 157-161 PML nuclear body scaffold Homo sapiens 137-140
25973309-7 2015 HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy. Tretinoin 157-161 retinoic acid receptor alpha Homo sapiens 141-149
8790159-13 1996 However, although PML immunofluorescence staining is suitable for rapid determination of patients likely to benefit from ATRA, this approach does not obviate the need for cytogenetic and RT-PCR analysis of all patients entered into APL clinical trials, because both techniques provide additional information which may prove to be of independent prognostic significance. Tretinoin 121-125 PML nuclear body scaffold Homo sapiens 18-21
25427913-6 2015 RA is synthesized from retinaldehyde by the retinaldehyde dehydrogenases, specifically ALDH1A1, ALDH1A2, ALDH1A3, and ALDH8A1. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A1 Homo sapiens 87-94
8826895-2 1996 Treatment with all-trans-retinoic-acid (ATRA) resulted in rapid normalization of the coagulopathy and complete remission of PML within 2 weeks. Tretinoin 15-38 PML nuclear body scaffold Homo sapiens 124-127
8826895-2 1996 Treatment with all-trans-retinoic-acid (ATRA) resulted in rapid normalization of the coagulopathy and complete remission of PML within 2 weeks. Tretinoin 40-44 PML nuclear body scaffold Homo sapiens 124-127
8826895-4 1996 ATRA therapy for PML during late pregnancy was effective in reversing the maternal bleeding tendency and inducing a complete remission of the PML without evidence of teratogenicity. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 17-20
8826895-4 1996 ATRA therapy for PML during late pregnancy was effective in reversing the maternal bleeding tendency and inducing a complete remission of the PML without evidence of teratogenicity. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 142-145
25427913-6 2015 RA is synthesized from retinaldehyde by the retinaldehyde dehydrogenases, specifically ALDH1A1, ALDH1A2, ALDH1A3, and ALDH8A1. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A3 Homo sapiens 105-112
8947586-8 1996 This mutation in the retinoic acid receptor alpha of the HL-60/RA cells may be responsible for drug resistance to ATRA and 9-cis-retinoic acid and increased sensitivity to vitamin D3 analogs. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 21-49
26557664-3 2015 In this study, we demonstrate that treatment with ATRA can activate the ERK signaling pathway by a transcription-independent mechanism through a signaling cascade that involves RARalpha and PI3K, promoting growth, survival, and migration in lung cancer cells. Tretinoin 50-54 retinoic acid receptor alpha Homo sapiens 177-185
8702769-5 1996 Expression of RARs with deletions of amino acids 413 and 414 in the transactivation-2 (AF-2) domain also reduced RA inhibition, while deletions and point mutations beyond amino acid 414 behaved like the wild-type RARalpha. Tretinoin 14-16 retinoic acid receptor alpha Homo sapiens 213-221
8753812-0 1996 Production of granulocyte colony-stimulating factor by THP-1 cells in response to retinoic acid and phorbol ester is mediated through the autocrine production of interleukin-1. Tretinoin 82-95 colony stimulating factor 3 Homo sapiens 14-51
25052690-4 2015 Both RA and BMP4 induced OCT4, MVH, DAZL, STELLA, NANOG and C-KIT expression, but RNF17, PIWIL2, STRA8, and SCP3 were only expressed after RA treatment. Tretinoin 5-7 LOC102184271 Capra hircus 36-40
8753812-0 1996 Production of granulocyte colony-stimulating factor by THP-1 cells in response to retinoic acid and phorbol ester is mediated through the autocrine production of interleukin-1. Tretinoin 82-95 interleukin 1 alpha Homo sapiens 162-175
25052690-4 2015 Both RA and BMP4 induced OCT4, MVH, DAZL, STELLA, NANOG and C-KIT expression, but RNF17, PIWIL2, STRA8, and SCP3 were only expressed after RA treatment. Tretinoin 5-7 Nanog homeobox Capra hircus 50-55
25052690-4 2015 Both RA and BMP4 induced OCT4, MVH, DAZL, STELLA, NANOG and C-KIT expression, but RNF17, PIWIL2, STRA8, and SCP3 were only expressed after RA treatment. Tretinoin 5-7 RING finger protein 17 Capra hircus 82-87
8663150-2 1996 All-trans-retinoic acid (RA) is a potent and specific inducer of CD38 in myeloid cells. Tretinoin 0-23 CD38 molecule Homo sapiens 65-69
8663150-2 1996 All-trans-retinoic acid (RA) is a potent and specific inducer of CD38 in myeloid cells. Tretinoin 25-27 CD38 molecule Homo sapiens 65-69
25052690-6 2015 Compared with the RA treated group, DAZL ectopic expression upregulated the transcription and translation of MVH, and SCP3 was also increased at the mRNA level. Tretinoin 18-20 LOC102184271 Capra hircus 36-40
8663150-3 1996 In this report, we demonstrate that RA-induced CD38 protein from human myeloid (HL-60) leukemia cells coimmunoprecipitates with another protein of molecular mass approximately190 kDa (p190). Tretinoin 36-38 CD38 molecule Homo sapiens 47-51
25052690-8 2015 Ectopic expression of the DAZL gene enhanced trans-differentiation compared to the RA-treated group. Tretinoin 83-85 LOC102184271 Capra hircus 26-30
25603532-1 2015 As the name implies, Stimulated by Retinoic Acid 8 is an early retinoic acid (RA) responsive gene pivotal for the beginning of meiosis in female and male germ cells. Tretinoin 63-76 stimulated by retinoic acid gene 8 Mus musculus 21-50
8674046-0 1996 Accelerated degradation of PML-retinoic acid receptor alpha (PML-RARA) oncoprotein by all-trans-retinoic acid in acute promyelocytic leukemia: possible role of the proteasome pathway. Tretinoin 86-109 retinoic acid receptor alpha Homo sapiens 65-69
8674046-3 1996 However, the molecular effect of ATRA on PML-RARA is unknown. Tretinoin 33-37 retinoic acid receptor alpha Homo sapiens 45-49
8674046-4 1996 In this study, we showed by means of immunoblotting that the expression of PML-RARA decreased within 12 h in APL cells treated with ATRA at concentrations greater than 0.1 microM. Tretinoin 132-136 retinoic acid receptor alpha Homo sapiens 79-83
8674046-8 1996 These data indicate that the PML-RARA degradation is accelerated by pharmacological concentrations of ATRA, suggesting that ATRA allows APL cells to differentiate by relieving the differentiation block. Tretinoin 102-106 retinoic acid receptor alpha Homo sapiens 33-37
25603532-1 2015 As the name implies, Stimulated by Retinoic Acid 8 is an early retinoic acid (RA) responsive gene pivotal for the beginning of meiosis in female and male germ cells. Tretinoin 78-80 stimulated by retinoic acid gene 8 Mus musculus 21-50
25106087-3 2015 Analysis of breast patient tumors revealed that high levels of ALDH1A3 correlated with expression of RA-inducible genes with retinoic acid response elements (RAREs), poorer patient survival and triple-negative breast cancers. Tretinoin 101-103 aldehyde dehydrogenase 1 family member A3 Homo sapiens 63-70
8765055-8 1996 A representative RA-resistant clone, NT2/D1-R1, overcame the antitumorigenic actions of RA as assessed in athymic mice. Tretinoin 17-19 zinc finger protein 263 Mus musculus 37-46
25106087-3 2015 Analysis of breast patient tumors revealed that high levels of ALDH1A3 correlated with expression of RA-inducible genes with retinoic acid response elements (RAREs), poorer patient survival and triple-negative breast cancers. Tretinoin 125-138 aldehyde dehydrogenase 1 family member A3 Homo sapiens 63-70
25106087-7 2015 Exogenous RA replaced ALDH1A3 in inducing the same opposing tumor growth and metastasis effects, suggesting that ALDH1A3 mediates these effects by promoting RA signaling. Tretinoin 10-12 aldehyde dehydrogenase 1 family member A3 Homo sapiens 113-120
8813719-8 1996 Using synthetic RA analogs, which selectively activate RARs and RXRs, the RAR partner within the heterodimeric complex appeared to be sufficient while the RXR partner was insufficient to independently activate transcription. Tretinoin 16-18 retinoic acid receptor alpha Homo sapiens 55-58
25106087-7 2015 Exogenous RA replaced ALDH1A3 in inducing the same opposing tumor growth and metastasis effects, suggesting that ALDH1A3 mediates these effects by promoting RA signaling. Tretinoin 157-159 aldehyde dehydrogenase 1 family member A3 Homo sapiens 113-120
8660822-1 1996 All trans retinoic acid (RA) enhanced the production of IgA at high concentrations (10-100 nM) in the presence of IL-5. Tretinoin 10-23 interleukin 5 Mus musculus 114-118
8660822-1 1996 All trans retinoic acid (RA) enhanced the production of IgA at high concentrations (10-100 nM) in the presence of IL-5. Tretinoin 25-27 interleukin 5 Mus musculus 114-118
8660822-5 1996 Addition of IL-5 to the system showed a synergistic effect which could be attenuated by addition of low concentrations of RA (about 1 nM). Tretinoin 122-124 interleukin 5 Mus musculus 12-16
25106087-10 2015 In summary, ALDH1A3 induces differential RA signaling in breast cancer cells which affects the rate of breast cancer progression. Tretinoin 41-43 aldehyde dehydrogenase 1 family member A3 Homo sapiens 12-19
26496651-8 2015 Retinoic acid also significantly reduced the expression of matrix metalloproteases 1, 3 and 9 while not increasing alpha-smooth muscle actin and fibronectin expression. Tretinoin 0-13 matrix metallopeptidase 1 Homo sapiens 59-93
8649786-0 1996 Differential changes of retinoid-X-receptor (RXR alpha) and its RAR alpha and PML-RAR alpha partners induced by retinoic acid and cAMP distinguish maturation sensitive and resistant t(15;17) promyelocytic leukemia NB4 cells. Tretinoin 112-125 retinoic acid receptor alpha Homo sapiens 64-73
8649786-0 1996 Differential changes of retinoid-X-receptor (RXR alpha) and its RAR alpha and PML-RAR alpha partners induced by retinoic acid and cAMP distinguish maturation sensitive and resistant t(15;17) promyelocytic leukemia NB4 cells. Tretinoin 112-125 PML nuclear body scaffold Homo sapiens 78-81
8649786-0 1996 Differential changes of retinoid-X-receptor (RXR alpha) and its RAR alpha and PML-RAR alpha partners induced by retinoic acid and cAMP distinguish maturation sensitive and resistant t(15;17) promyelocytic leukemia NB4 cells. Tretinoin 112-125 retinoic acid receptor alpha Homo sapiens 82-91
8674428-5 1996 Administration of retinoic acid to developing embryos causes alterations in the spatial restriction of the transgene expression domain, indicating that the HOXD4 enhancer is also a retinoid-responsive element in vivo. Tretinoin 18-31 homeobox D4 Homo sapiens 156-161
25258343-4 2014 Whereas RA elicits transcriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Tretinoin 8-10 PML nuclear body scaffold Homo sapiens 49-52
8674436-3 1996 In animal cap explants treated with activin A together with retinoic acid, we induced HNF1alpha in pronephric tubules and epithelial gut cells, i.e. in mesodermal as well as in endodermal tissues. Tretinoin 60-73 HNF1 homeobox A S homeolog Xenopus laevis 86-95
8674436-4 1996 HNF1alpha can also be induced by activin A, but not by retinoic acid alone. Tretinoin 55-68 HNF1 homeobox A S homeolog Xenopus laevis 0-9
8762813-0 1996 Regulation of egr-1 gene expression by retinoic acid in a human growth factor-dependent cell line. Tretinoin 39-52 early growth response 1 Homo sapiens 14-19
25258343-4 2014 Whereas RA elicits transcriptional activation of PML/RARA targets, how arsenic triggers differentiation remains unclear. Tretinoin 8-10 retinoic acid receptor alpha Homo sapiens 53-57
8762813-3 1996 Suppression of egr-1 gene expression by RA was dosage-dependent and reached maximum at 4 h after RA addition. Tretinoin 40-42 early growth response 1 Homo sapiens 15-20
8762813-3 1996 Suppression of egr-1 gene expression by RA was dosage-dependent and reached maximum at 4 h after RA addition. Tretinoin 97-99 early growth response 1 Homo sapiens 15-20
25320093-3 2014 The classical function of this protein is to directly deliver retinoic acid (RA) to RA receptor (RAR), a nuclear receptor activated by this hormone, in turn inducing the expression of multiple antiproliferative genes. Tretinoin 62-75 retinoic acid receptor alpha Homo sapiens 84-95
8762813-4 1996 The decay of egr-1 mRNA was similar in M07e cells treated with or without RA. Tretinoin 74-76 early growth response 1 Homo sapiens 13-18
8762813-5 1996 The transcriptional activity of the promoter region up to -600 or -480 bp upstream of the egr-1 gene was greatly reduced by RA treatment. Tretinoin 124-126 early growth response 1 Homo sapiens 90-95
8762813-6 1996 These data suggest that biological effects of RA on hematopoietic cells may, in part, be mediated by transcriptional suppression of egr-1 gene through its promoter region within -480 bp. Tretinoin 46-48 early growth response 1 Homo sapiens 132-137
8623511-8 1996 Many factors may influence PSA synthesis and production, and among them the most important are androgen, retinoic acid and growth factor stimulation. Tretinoin 105-118 kallikrein related peptidase 3 Homo sapiens 27-30
8530418-2 1995 When binding to natural HREs, TR2 orphan receptor remains flexible with higher binding affinities to (a) cellular retinol-binding protein II promoter region (CRBPIIp) (DR1), SV40 +55 region (DR2), and retinoic acid response element beta (RARE beta) (DR5) than to (b) NGFI-B response element (NBRE) and also to (c) the palindromic thyroid hormone response element (TREpal). Tretinoin 201-214 nuclear receptor subfamily 2 group C member 1 Homo sapiens 30-33
25320093-3 2014 The classical function of this protein is to directly deliver retinoic acid (RA) to RA receptor (RAR), a nuclear receptor activated by this hormone, in turn inducing the expression of multiple antiproliferative genes. Tretinoin 62-75 retinoic acid receptor alpha Homo sapiens 97-100
8655609-0 1996 Regulation of human dermal papilla cell production of insulin-like growth factor binding protein-3 by retinoic acid, glucocorticoids, and insulin-like growth factor-1. Tretinoin 102-115 insulin like growth factor binding protein 3 Homo sapiens 54-98
25252214-7 2014 Nevertheless, real-time RT-PCR results showed that LPL gene expression was up-regulated in both protocols 1 and 2, whereas LEPR was up-regulated only in protocol 2 (fortified with retinoic acid). Tretinoin 180-193 leptin receptor Homo sapiens 123-127
8655609-7 1996 IGFBP-3 levels are increased fivefold by retinoic acid, eightfold by dexamethasone, and tenfold by IGF1. Tretinoin 41-54 insulin like growth factor binding protein 3 Homo sapiens 0-7
7585542-2 1995 Estradiol enhances RAR alpha mRNA expression in different ER-positive HBCs by 2-3-fold, which in turn results in increased sensitivity of ER-positive HBCs to the growth inhibitory effects of retinoic acid. Tretinoin 191-204 retinoic acid receptor alpha Homo sapiens 19-28
24846581-1 2014 All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 4-23 retinoic acid receptor alpha Homo sapiens 148-157
8648436-1 1996 Retinoic acid bound to the nuclear retinoic acid receptor-alpha is required for the differentiation of promyelocytes to mature neutrophils. Tretinoin 0-13 retinoic acid receptor, alpha Rattus norvegicus 35-63
24846581-1 2014 All-trans retinoic acid (ATRA) plays an essential role in cell survival and differentiation by binding to retinoic acid receptors (RARs), including RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 148-157
24846581-3 2014 This study was performed to investigate which of the RAR subtypes is involved in the signal pathway of ATRA-induced differentiation of injured podocytes. Tretinoin 103-107 retinoic acid receptor alpha Homo sapiens 53-56
8584029-0 1995 Retinoic acid regulates the expression of the calcium binding protein, calbindin-D28K. Tretinoin 0-13 calbindin 1 Homo sapiens 71-80
8584029-4 1995 These findings are the first evidence of RA-mediated regulation of calbindin. Tretinoin 41-43 calbindin 1 Homo sapiens 67-76
8584029-6 1995 The induction of calbindin mRNA by RA was preceded by an induction of retinoic acid receptor-alpha mRNA and was accompanied by an induction of retinoid X receptor-alpha mRNA. Tretinoin 35-37 calbindin 1 Homo sapiens 17-26
8584029-6 1995 The induction of calbindin mRNA by RA was preceded by an induction of retinoic acid receptor-alpha mRNA and was accompanied by an induction of retinoid X receptor-alpha mRNA. Tretinoin 35-37 retinoic acid receptor alpha Homo sapiens 70-98
8584029-7 1995 Calbindin-D28k mRNA levels in D283 medulloblastoma cells as well as the induction of calbindin mRNA by RA were not significantly affected by 1,25-dihydroxyvitamin D3 treatment. Tretinoin 103-105 calbindin 1 Homo sapiens 85-94
8584029-9 1995 Studies of calbindin-D28k mRNA in control and RA-pretreated D283 medulloblastoma cells at various times (3-24 h) after treatment with 4 micrograms/ml actinomycin D indicated that the half-life of calbindin-D28k mRNA was significantly increased in the presence of RA, suggesting regulation of calbindin-D28k mRNA stability by RA. Tretinoin 46-48 calbindin 1 Homo sapiens 196-205
8662799-7 1996 Gangliosides GM1a and GQ1balpha inhibited the NADase activity in the immunoprecipitate of anti-CD38 antibody from the membrane extract of retinoic acid-treated human leukemic HL-60 cells. Tretinoin 138-151 CD38 molecule Homo sapiens 95-99
8804707-0 1996 All-trans retinoic acid affects the expression of orphan receptors COUP-TF I and COUP-TF II in the developing neural tube. Tretinoin 10-23 nuclear receptor subfamily 2, group F, member 1 Mus musculus 67-76
8804707-0 1996 All-trans retinoic acid affects the expression of orphan receptors COUP-TF I and COUP-TF II in the developing neural tube. Tretinoin 10-23 nuclear receptor subfamily 2, group F, member 2 Mus musculus 81-91
8804707-2 1996 All-trans RA treatment results in changes in expression of COUP-TF I and COUP-TF II genes in the spinal cord and telencephalon. Tretinoin 10-12 nuclear receptor subfamily 2, group F, member 1 Mus musculus 59-68
8584029-9 1995 Studies of calbindin-D28k mRNA in control and RA-pretreated D283 medulloblastoma cells at various times (3-24 h) after treatment with 4 micrograms/ml actinomycin D indicated that the half-life of calbindin-D28k mRNA was significantly increased in the presence of RA, suggesting regulation of calbindin-D28k mRNA stability by RA. Tretinoin 46-48 calbindin 1 Homo sapiens 196-205
8584029-10 1995 Thus, calbindin-D28k is one of the few known targets of RA action in cells that express a neuronal phenotype. Tretinoin 56-58 calbindin 1 Homo sapiens 6-15
8804707-2 1996 All-trans RA treatment results in changes in expression of COUP-TF I and COUP-TF II genes in the spinal cord and telencephalon. Tretinoin 10-12 nuclear receptor subfamily 2, group F, member 2 Mus musculus 73-83
24846581-9 2014 Compared with the injured podocytes, the protein/mRNA expression of RAR-alpha and RAR-gamma was significantly increased after ATRA exposure; however, the expression level of RAR-beta was not significantly different. Tretinoin 126-130 retinoic acid receptor alpha Homo sapiens 68-77
24846581-12 2014 In conclusion, RAR-alpha/gamma (and RAR-beta to a lesser degree) may be involved in the signal pathway of ATRA-induced differentiation in injured podocytes. Tretinoin 106-110 retinoic acid receptor alpha Homo sapiens 15-24
25330951-7 2014 We hypothesized that prenatal treatment with ATRA increases pulmonary Lep and Lep-R expression in the nitrofen model of CDH-associated PH. Tretinoin 45-49 leptin receptor Rattus norvegicus 78-83
8670216-0 1996 Retinoic acid differentially up-regulates the gene expression of retinoic acid receptor alpha and gamma isoforms in embryo and adult rats. Tretinoin 0-13 retinoic acid receptor, alpha Rattus norvegicus 65-93
25330951-17 2014 Relative mRNA expression of Lep and Lep-R was significantly increased in Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 82-86 leptin receptor Rattus norvegicus 36-41
8670216-7 1996 The gene expression of RAR-alpha 2, which was not affected by RA in the maternal tissues, was up-regulated in embryos, though there were no significant effects of RA on the levels of RAR-alpha 1 and the alpha total in the maternal tissues and the embryos. Tretinoin 62-64 retinoic acid receptor, alpha Rattus norvegicus 23-32
8770562-0 1995 Identification of the control regions for mouse c-kit gene transcription induced by retinoic acid. Tretinoin 84-97 KIT proto-oncogene receptor tyrosine kinase Mus musculus 48-53
25330951-18 2014 Lep and Lep-R immunoreactivity was markedly increased in interstitial and alveolar epithelial cells of Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 112-116 leptin receptor Rattus norvegicus 8-13
8770562-3 1995 F9 teratocarcinoma cells differentiated and expressed the c-kit gene upon exposure to retinoic acid (RA). Tretinoin 86-99 KIT proto-oncogene receptor tyrosine kinase Mus musculus 58-63
25403085-9 2014 CONCLUSIONS: According to our modeling of metabolic and signalization pathways using differentially expressed genes we have identified a network with major nodes (including Sirt3, Il1b, Cpt1b and Pparg) likely to underlie the observed strain specific response to ATRA. Tretinoin 263-267 sirtuin 3 Rattus norvegicus 173-178
8770562-3 1995 F9 teratocarcinoma cells differentiated and expressed the c-kit gene upon exposure to retinoic acid (RA). Tretinoin 101-103 KIT proto-oncogene receptor tyrosine kinase Mus musculus 58-63
8770562-8 1995 Cyclic AMP augmented the expression of the c-kit gene induced by RA; when combined with RA, it was less effective on the reporter gene activity. Tretinoin 65-67 KIT proto-oncogene receptor tyrosine kinase Mus musculus 43-48
8770562-8 1995 Cyclic AMP augmented the expression of the c-kit gene induced by RA; when combined with RA, it was less effective on the reporter gene activity. Tretinoin 88-90 KIT proto-oncogene receptor tyrosine kinase Mus musculus 43-48
8770562-10 1995 These findings suggested that transcription of the c-kit gene is regulated by complex controls and that there are different control regions responsive to RA and cyclic AMP. Tretinoin 154-156 KIT proto-oncogene receptor tyrosine kinase Mus musculus 51-56
8805274-10 1996 CONCLUSIONS: These results demonstrate that the ability of RA to respecify proximodistal identity is mediated by a specific RAR isoform, delta 2. Tretinoin 59-61 retinoic acid receptor alpha Homo sapiens 124-127
25261715-5 2014 Functional studies in mouse organ cultures that faithfully reproduce the initiation of prostate development indicate that one of the roles of retinoic acid signaling in the male is to inhibit the expression of Inhba, which encodes the betaA subunit of Activin, in the UGS mesenchyme. Tretinoin 142-155 inhibin subunit beta E Homo sapiens 252-259
8767533-7 1996 A patient with Vaquez"s disease, in remission for 15 years and presenting a progressive increase in bone marrow and peripheral myeloblasts, did not have a positive response to the administration of ATRA; however, the association of G-CSF to ATRA was followed by a complete remission. Tretinoin 241-245 colony stimulating factor 3 Homo sapiens 232-237
7566126-2 1995 On response elements consisting of direct repeats spaced by five base pairs (DR + 5 elements), RAR/RXR heterodimers activate transcription in response to RAR-specific ligands, such as all-trans-retinoic acid (RA). Tretinoin 188-207 retinoic acid receptor alpha Homo sapiens 95-98
7566126-2 1995 On response elements consisting of direct repeats spaced by five base pairs (DR + 5 elements), RAR/RXR heterodimers activate transcription in response to RAR-specific ligands, such as all-trans-retinoic acid (RA). Tretinoin 188-207 retinoic acid receptor alpha Homo sapiens 154-157
7566126-2 1995 On response elements consisting of direct repeats spaced by five base pairs (DR + 5 elements), RAR/RXR heterodimers activate transcription in response to RAR-specific ligands, such as all-trans-retinoic acid (RA). Tretinoin 95-97 retinoic acid receptor alpha Homo sapiens 154-157
8634095-0 1996 Coordinate control of growth and cytokeratin 13 expression by retinoic acid. Tretinoin 62-75 keratin 13 Homo sapiens 33-47
8634095-6 1996 Our data suggest that low K13 expression may be mechanistically related to resistance to RA-induced growth inhibition. Tretinoin 89-91 keratin 13 Homo sapiens 26-29
7556928-0 1995 The organizer-associated chick homeobox gene, Gnot1, is expressed before gastrulation and regulated synergistically by activin and retinoic acid. Tretinoin 131-144 notochord homeobox Gallus gallus 46-51
25261715-6 2014 Through in vivo genetic analysis and culture studies we show that inhibition of Activin signaling in the female UGS leads to a similar phenotype to that of retinoic acid treatment, namely bud formation in the absence of androgens. Tretinoin 156-169 inhibin subunit beta E Homo sapiens 80-87
7556928-3 1995 Both activin and retinoic acid are able to activate Gnot1 expression in cultured blastodermal cells and show a strong synergistic effect when applied in combination. Tretinoin 17-30 notochord homeobox Gallus gallus 52-57
25305491-2 2014 CYP26 enzymes degrade RA and have specific expression patterns that produce a RA gradient, which regulates the patterning of various structures in the embryo. Tretinoin 22-24 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-5
7672129-2 1995 The formation of this cyclic nucleotide is catalyzed by not only Aplysia ADP-ribosyl cyclase but also an ecto-form enzyme of NAD+ glycohydrolase (NADase), which was previously identified as all-trans-retinoic acid (RA)-inducible CD38 in human leukemic HL-60 cells. Tretinoin 190-213 CD38 molecule Homo sapiens 229-233
7672129-2 1995 The formation of this cyclic nucleotide is catalyzed by not only Aplysia ADP-ribosyl cyclase but also an ecto-form enzyme of NAD+ glycohydrolase (NADase), which was previously identified as all-trans-retinoic acid (RA)-inducible CD38 in human leukemic HL-60 cells. Tretinoin 215-217 CD38 molecule Homo sapiens 229-233
8622986-4 1996 PLZF-RARalpha and PML-RARalpha have essentially the same ligand-binding affinities and can bind in vitro to retinoic acid response elements (RAREs) as homodimers or heterodimers with RXRalpha. Tretinoin 108-121 retinoic acid receptor alpha Homo sapiens 5-13
8622986-4 1996 PLZF-RARalpha and PML-RARalpha have essentially the same ligand-binding affinities and can bind in vitro to retinoic acid response elements (RAREs) as homodimers or heterodimers with RXRalpha. Tretinoin 108-121 PML nuclear body scaffold Homo sapiens 18-21
8622986-4 1996 PLZF-RARalpha and PML-RARalpha have essentially the same ligand-binding affinities and can bind in vitro to retinoic acid response elements (RAREs) as homodimers or heterodimers with RXRalpha. Tretinoin 108-121 retinoic acid receptor alpha Homo sapiens 22-30
8622986-8 1996 These different protein-protein interactions and the target gene specificities of PLZF-RARalpha and PML-RARalpha may underlie, at least in part, the apparent resistance of APL with t(11;17) to differentiation effects of all-trans-retinoic acid. Tretinoin 224-243 PML nuclear body scaffold Homo sapiens 100-103
8622986-8 1996 These different protein-protein interactions and the target gene specificities of PLZF-RARalpha and PML-RARalpha may underlie, at least in part, the apparent resistance of APL with t(11;17) to differentiation effects of all-trans-retinoic acid. Tretinoin 224-243 retinoic acid receptor alpha Homo sapiens 104-112
8609382-9 1996 Retinoic acid inhibited IFN-gamma synthesis when the CD28 costimulatory pathway was activated in addition to the TCR/CD3 pathway, suggesting it blocks some step in the CD28 pathway. Tretinoin 0-13 CD28 antigen Mus musculus 53-57
8609382-9 1996 Retinoic acid inhibited IFN-gamma synthesis when the CD28 costimulatory pathway was activated in addition to the TCR/CD3 pathway, suggesting it blocks some step in the CD28 pathway. Tretinoin 0-13 CD28 antigen Mus musculus 168-172
25305491-2 2014 CYP26 enzymes degrade RA and have specific expression patterns that produce a RA gradient, which regulates the patterning of various structures in the embryo. Tretinoin 78-80 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-5
7670594-6 1995 Embryo cells cultured on poly-D-lysine substrate in the presence of retinoic acid or Buffalo rat liver cell-conditioned medium (BRL-CM) and a reduced serum concentration differentiated into neuronal cell types exhibiting elevated levels of acetylcholinesterase enzyme activity and expression of neurofilament and glial fibrillary acidic protein. Tretinoin 68-81 acetylcholinesterase Rattus norvegicus 240-260
25231683-0 2014 All-trans retinoic acid suppresses apoptosis in PC12 cells injured by oxygen and glucose deprivation via the retinoic acid receptor alpha signaling pathway. Tretinoin 10-23 retinoic acid receptor, alpha Rattus norvegicus 109-137
7646519-0 1995 Reduced level of octamer binding transcription factor (Oct-1) is correlated with H2B histone gene repression during differentiation of HL-60 cells by all-trans retinoic acid. Tretinoin 160-173 POU class 2 homeobox 1 Homo sapiens 55-60
7646519-4 1995 In DNase I footprinting analysis, a nuclear factor (octamer binding transcription factor, Oct-1) bound at -42 bp (ATTTGCAT) both before and after retinoic-acid-induced differentiation of HL-60 cells. Tretinoin 146-159 POU class 2 homeobox 1 Homo sapiens 90-95
7646519-5 1995 One DNA-protein complex was formed by DNA mobility shift assay, and the level of Oct-1 decreased during retinoic-acid-induced differentiation. Tretinoin 104-117 POU class 2 homeobox 1 Homo sapiens 81-86
8624378-12 1996 This pilot study demonstrates that treatment with ATRA/G-CSF/EPO/tocopherol is well tolerated, leading to normalization of neutrophil counts in most, and to improvement of platelets and red blood cells in a significant subgroup of patients. Tretinoin 50-54 colony stimulating factor 3 Homo sapiens 55-60
8603400-11 1996 This effect was not observed when RA- or TGF-beta2-exposed cells were treated with sense IGFBP-3 ODN. Tretinoin 34-36 insulin like growth factor binding protein 3 Homo sapiens 89-96
8640300-7 1996 The mitogenic effect of RA therefore reflects its stimulation of IGF-II production. Tretinoin 24-26 insulin like growth factor 2 Homo sapiens 65-71
7646519-7 1995 These results suggest that the transcriptional repression of H2B histone gene during retinoic-acid-induced differentiation in HL-60 cells may be mediated by reduced level of Oct-1. Tretinoin 85-98 POU class 2 homeobox 1 Homo sapiens 174-179
25231683-7 2014 ATRA at 4 micromol/l also reduced the expression levels of Bax and enhanced the expression of B-cell lymphoma 2. Tretinoin 0-4 BCL2 associated X, apoptosis regulator Rattus norvegicus 59-62
25231683-8 2014 Furthermore, RNA interference with retinoic acid receptor alpha (RARalpha) reversed the observed effect in PC12 cells following ATRA treatment at 4 micromol/l alone. Tretinoin 128-132 retinoic acid receptor, alpha Rattus norvegicus 35-63
25231683-8 2014 Furthermore, RNA interference with retinoic acid receptor alpha (RARalpha) reversed the observed effect in PC12 cells following ATRA treatment at 4 micromol/l alone. Tretinoin 128-132 retinoic acid receptor, alpha Rattus norvegicus 65-73
25231683-9 2014 In conclusion, the present study suggested that treatment with ATRA at 4 micromol/l suppressed apoptosis of PC12 cells following OGD injury, potentially through regulation of the RARalpha signaling pathway. Tretinoin 63-67 retinoic acid receptor, alpha Rattus norvegicus 179-187
7639724-0 1995 Characterization of nuclear retinoic acid binding activity in sensitive leukemic cell lines: cell specific uptake of ATRA and RAR alpha protein modulation. Tretinoin 28-41 retinoic acid receptor alpha Homo sapiens 126-135
7639724-2 1995 Although it is not known to what extent each RAR contributes to the different effects of ATRA, several studies have demonstrated that ATRA induced granulocytic differentiation in human myeloid leukemic cell lines is mediated by RAR alpha. Tretinoin 134-138 retinoic acid receptor alpha Homo sapiens 45-48
7639724-2 1995 Although it is not known to what extent each RAR contributes to the different effects of ATRA, several studies have demonstrated that ATRA induced granulocytic differentiation in human myeloid leukemic cell lines is mediated by RAR alpha. Tretinoin 134-138 retinoic acid receptor alpha Homo sapiens 228-237
7639724-5 1995 Modulation of RAR alpha protein (5 fold excess) was found in NB4 cells after 24 hours ATRA exposure, whereas HL-60 cells required a 72-hour culture period to weakly increase the RAR alpha protein level. Tretinoin 86-90 retinoic acid receptor alpha Homo sapiens 14-23
7639684-0 1995 Retinoic acid directly stimulates osteoclastic bone resorption and gene expression of cathepsin K/OC-2. Tretinoin 0-13 cathepsin K Oryctolagus cuniculus 86-97
8726400-3 1996 In vitro treatment with ATRA dramatically modifies the adhesion phenotype of APL blast cells, promoting a consistently striking up-regulation of CD11b, CD11c, CD15, CD65, CD54, and CD38. Tretinoin 24-28 CD38 molecule Homo sapiens 181-185
8600988-5 1996 A clear example of a naturally existing RAR-selective retinoid is all-trans retinoic acid. Tretinoin 76-89 retinoic acid receptor alpha Homo sapiens 40-43
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 33-46 colony stimulating factor 2 Homo sapiens 208-256
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 33-46 colony stimulating factor 2 Homo sapiens 258-264
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 33-46 interleukin 3 Homo sapiens 270-283
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 33-46 interleukin 3 Homo sapiens 285-289
7639684-0 1995 Retinoic acid directly stimulates osteoclastic bone resorption and gene expression of cathepsin K/OC-2. Tretinoin 0-13 cathepsin K Oryctolagus cuniculus 98-102
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 Mus musculus 133-137
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 33-46 colony stimulating factor 3 Homo sapiens 341-346
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 48-50 colony stimulating factor 2 Homo sapiens 208-256
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 48-50 colony stimulating factor 2 Homo sapiens 258-264
7620182-7 1995 Reorganization of the PML labeling into PODs with normal appearance was observed in cells from patients who received RA. Tretinoin 117-119 PML nuclear body scaffold Homo sapiens 22-25
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 48-50 interleukin 3 Homo sapiens 270-283
25275592-8 2014 Furthermore, all-trans retinoic acid (ATRA) significantly induced CDKN2D expression in APL cells and knockdown of CDKN2D expression during ATRA treatment partially blocked the ATRA-induced differentiation and cell cycle arrest. Tretinoin 13-36 cyclin dependent kinase inhibitor 2D Homo sapiens 66-72
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 48-50 interleukin 3 Homo sapiens 285-289
8634418-1 1996 Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. Tretinoin 48-50 colony stimulating factor 3 Homo sapiens 341-346
8721678-7 1996 Current data suggest that PML-RAR alpha and PLZF-RAR alpha fusion receptors may play an important role in the development of APL and that PML-RAR alpha could be the target of ATRA differentiation therapy. Tretinoin 175-179 PML nuclear body scaffold Homo sapiens 138-141
7543855-5 1995 G-CSFR-expressing clones (a) acquired the capacity to respond to the differentiation-inducing properties of G-CSF and retinoic acid, (b) formed colonies which exhibited a dispersed phenotype, and (c) exhibited near diploid DNA ploidy. Tretinoin 118-131 colony stimulating factor 3 receptor Homo sapiens 0-6
7543855-5 1995 G-CSFR-expressing clones (a) acquired the capacity to respond to the differentiation-inducing properties of G-CSF and retinoic acid, (b) formed colonies which exhibited a dispersed phenotype, and (c) exhibited near diploid DNA ploidy. Tretinoin 118-131 colony stimulating factor 3 Homo sapiens 0-5
8590777-0 1995 Epidermal growth factor in acute promyelocytic leukemia treated with retinoic acid. Tretinoin 69-82 epidermal growth factor Homo sapiens 0-23
8622645-6 1996 Although VDR can bind as a homodimer to the osteopontin gene vitamin D response element, we find that a RXR-VDR heterodimer must be the transactivating species from the element in vivo, since RXR enhances and 9-cis RA and other RXR-specific ligands attenuate this induction. Tretinoin 215-217 secreted phosphoprotein 1 Homo sapiens 44-55
7795226-0 1995 Retinoic acid reduces induction of monocyte tissue factor and tissue factor/factor VIIa-dependent arterial thrombus formation. Tretinoin 0-13 coagulation factor III, tissue factor Homo sapiens 44-57
25275592-8 2014 Furthermore, all-trans retinoic acid (ATRA) significantly induced CDKN2D expression in APL cells and knockdown of CDKN2D expression during ATRA treatment partially blocked the ATRA-induced differentiation and cell cycle arrest. Tretinoin 38-42 cyclin dependent kinase inhibitor 2D Homo sapiens 66-72
7795226-0 1995 Retinoic acid reduces induction of monocyte tissue factor and tissue factor/factor VIIa-dependent arterial thrombus formation. Tretinoin 0-13 coagulation factor III, tissue factor Homo sapiens 62-75
7795226-3 1995 Ishii et al (Blood 80:2556, 1992) reported that induction of endothelial TF is downregulated by all-trans retinoic acid (ATRA), and Conese et al (Thromb Haemost 66:662, 1991) reported that retinoids downregulate monocyte procoagulant activity (PCA). Tretinoin 106-119 coagulation factor III, tissue factor Homo sapiens 73-75
9238678-6 1996 RA treatment significantly (P < 0.05) suppressed prolactin and IGFBP-1 production associated with stromal cells decidualization. Tretinoin 0-2 insulin like growth factor binding protein 1 Homo sapiens 66-73
9238678-9 1996 With RA treatment, RAR-alpha and RAR-gamma mRNA concentrations were approximately 70 and 25% respectively of those in cells decidualized in the absence of RA. Tretinoin 5-7 retinoic acid receptor alpha Homo sapiens 19-28
7795226-3 1995 Ishii et al (Blood 80:2556, 1992) reported that induction of endothelial TF is downregulated by all-trans retinoic acid (ATRA), and Conese et al (Thromb Haemost 66:662, 1991) reported that retinoids downregulate monocyte procoagulant activity (PCA). Tretinoin 121-125 coagulation factor III, tissue factor Homo sapiens 73-75
25275592-8 2014 Furthermore, all-trans retinoic acid (ATRA) significantly induced CDKN2D expression in APL cells and knockdown of CDKN2D expression during ATRA treatment partially blocked the ATRA-induced differentiation and cell cycle arrest. Tretinoin 139-143 cyclin dependent kinase inhibitor 2D Homo sapiens 114-120
7795226-4 1995 These findings led us to investigate the effect of ATRA on monocyte TF expression, and to study the effect of ATRA on monocyte-induced thrombus formation in a model system of human arterial thrombogenesis. Tretinoin 51-55 coagulation factor III, tissue factor Homo sapiens 68-70
25275592-8 2014 Furthermore, all-trans retinoic acid (ATRA) significantly induced CDKN2D expression in APL cells and knockdown of CDKN2D expression during ATRA treatment partially blocked the ATRA-induced differentiation and cell cycle arrest. Tretinoin 139-143 cyclin dependent kinase inhibitor 2D Homo sapiens 114-120
8528505-11 1995 Inhibition of endogenous CRABP expression renders MEPM cells less responsive to RA with respect to induction of TGF-beta 3, RAR-beta, and tenascin gene expression. Tretinoin 26-28 transforming growth factor, beta 3 Mus musculus 112-122
8631309-0 1996 Retinoic acid-mediated down-regulation of Oct3/4 coincides with the loss of promoter occupancy in vivo. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 42-48
25126724-4 2014 MIR125B1 overexpression enhanced PML-RARA expression and inhibited the ATRA-induced degradation of the PML-RARA oncoprotein. Tretinoin 71-75 microRNA 125b-1 Homo sapiens 0-8
8604312-0 1996 A novel type of retinoic acid response element in the second intron of the mouse H2Kb gene is activated by the RAR/RXR heterodimer. Tretinoin 16-29 histocompatibility 2, K1, K region Mus musculus 81-85
21552804-0 1995 Retinoic Acid potently stimulates the production of granulocyte-colony-stimulating factor in the human monocytic thp-1 cell-line. Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 52-89
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 colony stimulating factor 3 Homo sapiens 94-131
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 colony stimulating factor 3 Homo sapiens 133-138
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 colony stimulating factor 2 Homo sapiens 135-138
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 colony stimulating factor 3 Homo sapiens 94-131
8604312-1 1996 We have identified and characterized a novel retinoic acid (RA) response element (Hi-RARE) in the second intron of the mouse major histocompatibility H2Kb gene. Tretinoin 45-58 histocompatibility 2, K1, K region Mus musculus 150-154
8604312-1 1996 We have identified and characterized a novel retinoic acid (RA) response element (Hi-RARE) in the second intron of the mouse major histocompatibility H2Kb gene. Tretinoin 60-62 histocompatibility 2, K1, K region Mus musculus 150-154
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 colony stimulating factor 3 Homo sapiens 133-138
25126724-4 2014 MIR125B1 overexpression enhanced PML-RARA expression and inhibited the ATRA-induced degradation of the PML-RARA oncoprotein. Tretinoin 71-75 PML nuclear body scaffold Homo sapiens 103-106
21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 colony stimulating factor 2 Homo sapiens 135-138
8605251-2 1996 Differentiation of Tera-2 cells in media containing retinoic acid restored the ability of the upstream region to downregulate H2AZ gene promoter activity. Tretinoin 52-65 H2A.Z variant histone 1 Homo sapiens 126-130
25126724-4 2014 MIR125B1 overexpression enhanced PML-RARA expression and inhibited the ATRA-induced degradation of the PML-RARA oncoprotein. Tretinoin 71-75 retinoic acid receptor alpha Homo sapiens 107-111
8562957-8 1996 In transcriptional assays using a retinoic acid response element reporter construct, both NPM-RAR fusion proteins act as retinoic acid-dependent transcriptional activators. Tretinoin 34-47 retinoic acid receptor alpha Homo sapiens 94-97
25126724-10 2014 Thus, MIR125B1 dysregulation may interfere with the effectiveness of ATRA-mediated differentiation through an autophagy-dependent pathway, representing a novel potential APL therapeutic target. Tretinoin 69-73 microRNA 125b-1 Homo sapiens 6-14
8562957-8 1996 In transcriptional assays using a retinoic acid response element reporter construct, both NPM-RAR fusion proteins act as retinoic acid-dependent transcriptional activators. Tretinoin 121-134 retinoic acid receptor alpha Homo sapiens 94-97
7598688-0 1995 Increased expression of AML1 during retinoic-acid-induced differentiation of U937 cells. Tretinoin 36-49 RUNX family transcription factor 1 Homo sapiens 24-28
7598688-5 1995 It was revealed that AML1b and AML1c are the major AML1 proteins in these cell lines and that prior to morphological and functional differentiation, their expressions increase in U937 cells when treated with all-trans retinoic acid. Tretinoin 218-231 RUNX family transcription factor 1 Homo sapiens 21-25
8603437-10 1996 All-trans retinoic acid (RA) inhibited FasL induction, but had little effect on Fas up-regulation. Tretinoin 0-23 Fas ligand Homo sapiens 39-43
25209250-5 2014 Moreover, Nepn expression is modulated by Activin signaling, with high levels inhibiting and low levels enhancing RA-dependent expression. Tretinoin 114-116 nephrocan Mus musculus 10-14
8574972-0 1996 Retinoic acid normalizes the increased gene transcription rate of TGF-alpha and EGFR in head and neck cancer cell lines. Tretinoin 0-13 epidermal growth factor Homo sapiens 80-84
8574972-4 1996 In this report, we examined the hypothesis that the action of RA on the mucosa of the upper aerodigestive tract is mediated via downregulation of steady-state TGF-alpha and/or EGFR mRNA levels. Tretinoin 62-64 epidermal growth factor Homo sapiens 176-180
8574972-6 1996 Nuclear run-on analysis indicated that the RA-mediated reduction of TGF-alpha and EGFR steady-state mRNA levels was a result of decreased gene transcription. Tretinoin 43-45 epidermal growth factor Homo sapiens 82-86
7784078-3 1995 Clinical remissions induced by all-trans-retinoic acid (RA) treatment of APL patients are linked to expression of PML/RAR apha, a transcription factor with reported dominant negative functions. Tretinoin 31-54 PML nuclear body scaffold Homo sapiens 114-117
7784078-3 1995 Clinical remissions induced by all-trans-retinoic acid (RA) treatment of APL patients are linked to expression of PML/RAR apha, a transcription factor with reported dominant negative functions. Tretinoin 56-58 PML nuclear body scaffold Homo sapiens 114-117
25368812-10 2014 RA enhanced the conversion of CD103(+) DCs, which paralleled the antigen-specific Treg-stimulating effect, though the differences failed to reach statistical significance. Tretinoin 0-2 integrin subunit alpha E Homo sapiens 30-35
7786028-1 1995 Two families of nuclear retinoid receptors, retinoic acid receptor and retinoid X receptor (RAR and RXR respectively), and a family of cellular retinoic acid-binding proteins (CRABPI and II) participate in the retinoic acid (RA) signaling pathway. Tretinoin 44-57 retinoic acid receptor alpha Homo sapiens 92-95
7786028-6 1995 Furthermore, 9-cis RA, a ligand that binds to both the RAR and the RXR families, selectively activates the CRABPII gene. Tretinoin 19-21 retinoic acid receptor alpha Homo sapiens 55-58
8637715-0 1996 Overexpression of both RAR and RXR restores AP-1 repression in ovarian adenocarcinoma cells resistant to retinoic acid-dependent growth inhibition. Tretinoin 105-118 retinoic acid receptor alpha Homo sapiens 23-26
9053826-0 1996 Retinoic acid response elements as positive and negative regulators of the expression of the homeobox b-1 gene. Tretinoin 0-13 homeobox B1 Homo sapiens 93-105
9053826-2 1996 A paradigm for the transduction of positive and negative signaling is the discovery that retinoic acid response elements (RAREs), positioned in the 3" enhancer and 5" promoter of the Hoxb-1 gene, may function respectively as positive and negative regulators, thereby permitting a diffused (early positive) as well as segmentally specified and limited (late negative) expression of the gene. Tretinoin 89-102 homeobox B1 Homo sapiens 183-189
25368812-12 2014 RA was an effective reagent that induces mature DCs with the typical phenotypic expression of CD103 that demonstrated the functional capability to promote antigen-specific Tregs. Tretinoin 0-2 integrin subunit alpha E Homo sapiens 94-99
8570209-8 1996 Leukemogenesis in t(11;17) APL may be related to interference with ATRA-mediated differentiation due to sequestration of RXR by the PLZF-RAR alpha chimera. Tretinoin 67-71 retinoic acid receptor alpha Homo sapiens 137-146
25070893-0 2014 The E3 deubiquitinase USP17 is a positive regulator of retinoic acid-related orphan nuclear receptor gammat (RORgammat) in Th17 cells. Tretinoin 55-68 ubiquitin specific peptidase 17 like family member 9, pseudogene Homo sapiens 22-27
8570225-0 1996 Retinoic acid-induced growth arrest and differentiation of neuroblastoma cells are counteracted by N-myc and enhanced by max overexpressions. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 99-104
8570225-1 1996 N-myc expression is negatively regulated by retinoic acid (RA) which induces the growth arrest and differentiation of neuroblastoma (NB) cells. Tretinoin 44-57 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-5
8570225-1 1996 N-myc expression is negatively regulated by retinoic acid (RA) which induces the growth arrest and differentiation of neuroblastoma (NB) cells. Tretinoin 59-61 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 0-5
8570225-5 1996 In contrast to N-Myc, Max strongly induced the differentiation by enhancing the effects of RA. Tretinoin 91-93 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 15-20
8546677-0 1996 The organization of the human GSTP1-1 gene promoter and its response to retinoic acid and cellular redox status. Tretinoin 72-85 glutathione S-transferase pi 1 Homo sapiens 30-37
8546677-3 1996 We have previously shown that the expression of GSTP1 is suppressed by retinoic acid (RA) in the presence of the retinoic acid receptor (RAR) as a result of decreased transcription from its promoter. Tretinoin 71-84 glutathione S-transferase pi 1 Homo sapiens 48-53
24952353-7 2014 Additionally we observed a correlation between ZNF143 downregulation and miR-590-3p up-regulation in retinoic acid treated teratocarcinoma cells. Tretinoin 101-114 zinc finger protein 143 Homo sapiens 47-53
8546677-3 1996 We have previously shown that the expression of GSTP1 is suppressed by retinoic acid (RA) in the presence of the retinoic acid receptor (RAR) as a result of decreased transcription from its promoter. Tretinoin 86-88 glutathione S-transferase pi 1 Homo sapiens 48-53
8547662-6 1996 Retinoic acid (RA) was the strongest inducer of defensin mRNA accumulation, even at doses too low to effect morphologic changes; the initial (first 48 hours), gradual increase resulted from transcriptional activation and was enhanced by granulocyte colony-stimulating factor. Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 237-274
8557772-7 1996 The ability of RA to upregulate fibronectin and thrombospondin expression in NRP-152 cells was also blocked by the monoclonal antibody. Tretinoin 15-17 fibronectin 1 Rattus norvegicus 32-43
8762455-5 1996 The results suggest that RA can induce the expression of MDR1 gene but perhaps inhibit the function of pump glycoprotein 170 (Pgp-170) through phosphorylation/dephosphorylation pathway. Tretinoin 25-27 phosphoglycolate phosphatase Homo sapiens 126-129
25047539-0 2014 Granulosa cells and retinoic acid co-treatment enrich potential germ cells from manually selected Oct4-EGFP expressing human embryonic stem cells. Tretinoin 20-33 POU class 5 homeobox 1 Homo sapiens 98-102
8845378-7 1995 In HL-60 cells, MZF-1 mRNA levels are increased by granulopoietic inducers including retinoic acid and GM-CSF. Tretinoin 85-98 myeloid zinc finger 1 Homo sapiens 16-21
8605120-11 1995 Whereas RARA rearrangement appears sufficient for an APL-like phenotype, it seems that the presence of a classical PML/RARA is required for typical APL with response to ATRA. Tretinoin 169-173 PML nuclear body scaffold Homo sapiens 115-118
8605120-11 1995 Whereas RARA rearrangement appears sufficient for an APL-like phenotype, it seems that the presence of a classical PML/RARA is required for typical APL with response to ATRA. Tretinoin 169-173 retinoic acid receptor alpha Homo sapiens 119-123
7592926-5 1995 The expression of ATBF1-A transcripts increased to high levels when P19 and NT2/D1 cells were treated with retinoic acid to induce neuronal differentiation. Tretinoin 107-120 zinc finger homeobox 3 Homo sapiens 18-23
7556459-1 1995 We have previously shown that both transforming growth factor-beta (TGF-beta) and retinoic acid (RA) regulate the expression of cellular retinoic acid binding proteins (CRABP) I and II and TGF-beta 3 mRNAs in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Tretinoin 82-95 transforming growth factor, beta 3 Mus musculus 189-199
7556459-1 1995 We have previously shown that both transforming growth factor-beta (TGF-beta) and retinoic acid (RA) regulate the expression of cellular retinoic acid binding proteins (CRABP) I and II and TGF-beta 3 mRNAs in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Tretinoin 97-99 transforming growth factor, beta 3 Mus musculus 189-199
25136833-8 2014 Here we present data to show that, upon treatment with retinoic acid, the HLXB9 gene becomes over-expressed during the early stages of neuronal differentiation and that this corresponds to a reposition of the gene in the nucleus. Tretinoin 55-68 motor neuron and pancreas homeobox 1 Homo sapiens 74-79
7559803-9 1995 Treatment with the IGF-I receptor blocking antibody, alpha IR-3, restores RA-induced growth inhibition of IGF-I-treated or IGF-II-overexpressing MCF-7 cells, indicating that the IGF-I receptor is mediating these effects. Tretinoin 74-76 insulin like growth factor 2 Homo sapiens 123-129
7559803-10 1995 IGFs cannot reverse all RA effects since the altered cell culture morphology of RA-treated cells is similar in growth-inhibited cultures and in IGF-II expressing clones that are resistant to RA-induced growth inhibition. Tretinoin 80-82 insulin like growth factor 2 Homo sapiens 144-150
7559803-10 1995 IGFs cannot reverse all RA effects since the altered cell culture morphology of RA-treated cells is similar in growth-inhibited cultures and in IGF-II expressing clones that are resistant to RA-induced growth inhibition. Tretinoin 80-82 insulin like growth factor 2 Homo sapiens 144-150
25127121-3 2014 c-Myc over-expression in leukemic cells induced resistance to chemotherapeutic drugs, enhanced colony formation capacity and inhibited cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 177-190 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
7545670-8 1995 However, following RA treatment, the AP-1 element is repressed and the RARE is activated, resulting in an overall stimulation of the enhancer by RA in the BMGE+H cells used in our study. Tretinoin 19-21 Jun proto-oncogene, AP-1 transcription factor subunit Bos taurus 37-41
7654186-1 1995 Functional retinoic acid response elements (RAREs) have been described wherein the direct repeats are separated by 1, 2 or 5 bp (termed DR1, DR2 and DR5 respectively). Tretinoin 11-24 TNF receptor superfamily member 10b Homo sapiens 149-152
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 30-43 retinoic acid receptor alpha Homo sapiens 74-77
8574944-1 1995 The effects of retinoic acid (RA), and calcitriol are mediated by specific nuclear receptors (RARs and VDR, respectively). Tretinoin 15-28 arginyl-tRNA synthetase Mus musculus 94-98
8574944-1 1995 The effects of retinoic acid (RA), and calcitriol are mediated by specific nuclear receptors (RARs and VDR, respectively). Tretinoin 30-32 arginyl-tRNA synthetase Mus musculus 94-98
25127121-3 2014 c-Myc over-expression in leukemic cells induced resistance to chemotherapeutic drugs, enhanced colony formation capacity and inhibited cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 192-196 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
25124193-0 2014 Implications of the Wnt5a/CaMKII pathway in retinoic acid-induced myogenic tongue abnormalities of developing mice. Tretinoin 44-57 calcium/calmodulin-dependent protein kinase II, delta Mus musculus 26-32
8619133-3 1995 We have studied the retinoic acid response of five cell lines, compared to P19 cells, by observing three markers of retinoic acid induced P19 differentiation--cell morphology, RAR alpha and Wnt1 transcription. Tretinoin 116-129 interleukin 23 subunit alpha Homo sapiens 138-141
7642623-2 1995 Treatment with retinoic acid and dibutyryl cyclic AMP, which induces F9 cells to differentiate into endoderm-like cells, produced a 50-fold increase in the expression of LRP-2. Tretinoin 15-28 low density lipoprotein receptor-related protein 2 Mus musculus 170-175
7642623-8 1995 In cell assays, LRP-2 antibodies blocked the elevated 125I-LDL internalization and degradation observed in the retinoic acid/dibutyryl cyclic AMP-treated F9 cells. Tretinoin 111-124 low density lipoprotein receptor-related protein 2 Mus musculus 16-21
24954410-4 2014 In a microarray analysis, integrin-alpha1 and integrin-beta3 showed the largest variation in the ATRA-treated group compared with the controls. Tretinoin 97-101 integrin subunit alpha 1 Homo sapiens 26-41
7500381-9 1995 P19 cells induced with retinoic acid and plated in N2 were exposed to bFGF and EGF, which are known to be mitogens for neuronal precursor cells. Tretinoin 23-36 interleukin 23 subunit alpha Homo sapiens 0-3
24782508-2 2014 Although the PML-RARalpha fusion gene can be detected in >98% of APL cases, RARalpha is also found to be fused with other partner genes, which are also related to all-trans retinoic acid (ATRA)-dependent transcriptional activity and cell differentiation. Tretinoin 176-189 retinoic acid receptor alpha Homo sapiens 79-87
7644503-1 1995 Disruption of retinoic acid receptor (RAR) gamma in F9 embryonal carcinoma cells leads to aberrent differentiation and reduced activation of expression of several all-trans-retinoic acid (RA)-induced genes. Tretinoin 14-27 retinoic acid receptor alpha Homo sapiens 38-41
7644503-1 1995 Disruption of retinoic acid receptor (RAR) gamma in F9 embryonal carcinoma cells leads to aberrent differentiation and reduced activation of expression of several all-trans-retinoic acid (RA)-induced genes. Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 14-36
24782508-2 2014 Although the PML-RARalpha fusion gene can be detected in >98% of APL cases, RARalpha is also found to be fused with other partner genes, which are also related to all-trans retinoic acid (ATRA)-dependent transcriptional activity and cell differentiation. Tretinoin 191-195 retinoic acid receptor alpha Homo sapiens 17-25
8578578-4 1995 Induction of monocytoid and granulocytoid differentiation with phorbor ester and ATRA was accompanied by increased expression of HSP73 and HSP90 with distinct kinetics. Tretinoin 81-85 heat shock protein 90 alpha family class A member 1 Homo sapiens 139-144
24782508-2 2014 Although the PML-RARalpha fusion gene can be detected in >98% of APL cases, RARalpha is also found to be fused with other partner genes, which are also related to all-trans retinoic acid (ATRA)-dependent transcriptional activity and cell differentiation. Tretinoin 191-195 retinoic acid receptor alpha Homo sapiens 79-87
24782508-8 2014 In the presence of pharmacologic doses of ATRA, TBLR1-RARalpha could be degraded, and its homodimerization was abrogated. Tretinoin 42-46 retinoic acid receptor alpha Homo sapiens 54-62
7615557-2 1995 Human cytosolic aldehyde dehydrogenase 1 (ALDH1) plays a role in the biosynthesis of retinoic acid that is a modulator for gene expression and cell differentiation. Tretinoin 85-98 aldehyde dehydrogenase 1 family member A1 Homo sapiens 42-47
24782508-9 2014 Moreover, when treated with ATRA, TBLR1-RARalpha could mediate the dissociation and degradation of transcriptional corepressors, consequent transactivation of RARalpha target genes, and cell differentiation induction in a dose- and time-dependent manner. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 40-48
7673487-1 1995 Retinoic acid (RA) induces a human teratocarcinoma cell line (NTera-2 or NT2) to give rise exclusively to post-mitotic neuron-like (NT2N) cells, but NT2N cells never acquire a fully mature neuronal phenotype in vitro. Tretinoin 0-13 zinc finger protein 263 Mus musculus 73-76
24782508-9 2014 Moreover, when treated with ATRA, TBLR1-RARalpha could mediate the dissociation and degradation of transcriptional corepressors, consequent transactivation of RARalpha target genes, and cell differentiation induction in a dose- and time-dependent manner. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 159-167
24789671-5 2014 After 7 days of induction with neurotrophin-3 (NT-3) and retinoic acid (RA) in vitro, we observed a significant increase in TrkC mRNA transcription by Real-time PCR and this was confirmed by in situ hybridization. Tretinoin 57-70 neurotrophic receptor tyrosine kinase 3 Rattus norvegicus 124-128
7549784-4 1995 To determine if this growth arrest is mediated by the same pathway underlying contact inhibition of proliferation, the expression of a gene associated with the induction of contact inhibition, protein disulfide isomerase (PDI), was quantified by Northern blot analysis and enzymatic activity after retinoic acid treatment. Tretinoin 298-311 prolyl 4-hydroxylase, beta polypeptide Mus musculus 193-220
7549784-4 1995 To determine if this growth arrest is mediated by the same pathway underlying contact inhibition of proliferation, the expression of a gene associated with the induction of contact inhibition, protein disulfide isomerase (PDI), was quantified by Northern blot analysis and enzymatic activity after retinoic acid treatment. Tretinoin 298-311 prolyl 4-hydroxylase, beta polypeptide Mus musculus 222-225
7549784-5 1995 Retinoic acid caused a significant elevation of PDI-mRNA within 24 hrs. Tretinoin 0-13 prolyl 4-hydroxylase, beta polypeptide Mus musculus 48-51
7549784-7 1995 Bacitracin, a specific inhibitor of PDI, abrogated the ability of retinoic acid to induce differentiation. Tretinoin 66-79 prolyl 4-hydroxylase, beta polypeptide Mus musculus 36-39
7750498-7 1995 This suggests that CRABP(II) may be expressed to restrict retinoic acid from occupying nuclear retinoic acid receptors, implying that the differentiation and maintenance of the rat corpus luteum may involve in part a release of certain pathways from retinoid suppression. Tretinoin 58-71 cellular retinoic acid binding protein 2 Rattus norvegicus 19-28
24789671-5 2014 After 7 days of induction with neurotrophin-3 (NT-3) and retinoic acid (RA) in vitro, we observed a significant increase in TrkC mRNA transcription by Real-time PCR and this was confirmed by in situ hybridization. Tretinoin 72-74 neurotrophic receptor tyrosine kinase 3 Rattus norvegicus 124-128
24971534-4 2014 Real-time PCR analysis revealed that OCT4 levels were high in undifferentiated NCCIT cells but significantly decreased upon retinoic acid-mediated differentiation, concomitant with up-regulation of ESE-1 expression. Tretinoin 124-137 POU class 5 homeobox 1 Homo sapiens 37-41
7775578-5 1995 RA inhibited MLC-CAT transgene but not alpha sk actin-CAT transgene expression in primary cultures from these mice. Tretinoin 0-2 megalencephalic leukoencephalopathy with subcortical cysts 1 homolog (human) Mus musculus 13-16
7775578-6 1995 Analysis of MLC-CAT expression in transgenic mouse primary cultures and in stably transfected C2C12 cells demonstrated that repression of MLC-CAT activity by RA was dependent upon diffusible factors in chick embryo extract. Tretinoin 158-160 megalencephalic leukoencephalopathy with subcortical cysts 1 homolog (human) Mus musculus 12-15
7775578-6 1995 Analysis of MLC-CAT expression in transgenic mouse primary cultures and in stably transfected C2C12 cells demonstrated that repression of MLC-CAT activity by RA was dependent upon diffusible factors in chick embryo extract. Tretinoin 158-160 megalencephalic leukoencephalopathy with subcortical cysts 1 homolog (human) Mus musculus 138-141
7651608-15 1995 Induction of differentiation with retinoic acid produced cells with a neuronal morphology and a redistribution of the expression of PHF-1 tau in the long neurites. Tretinoin 34-47 microtubule associated protein tau Homo sapiens 138-141
7769256-8 1995 Addition of 10(-7) M retinoic acid to cultured differentiating keratinocytes significantly down-regulated the expression of SPRR2 and SPRR3 transcripts and slightly decreased that of SPRR1. Tretinoin 21-34 small proline rich protein 1B Homo sapiens 183-188
7496626-0 1995 Retinoic acid-mediated increase in TrkA expression is sufficient to elicit NGF-dependent survival of sympathetic neurons. Tretinoin 0-13 neurotrophic receptor tyrosine kinase 1 Gallus gallus 35-39
7496626-3 1995 Treatment with retinoic acid (RA) leads to increased levels of both trkA mRNA and protein, a response mediated through retinoic acid receptor alpha (RAR alpha). Tretinoin 15-28 neurotrophic receptor tyrosine kinase 1 Gallus gallus 68-72
7496626-3 1995 Treatment with retinoic acid (RA) leads to increased levels of both trkA mRNA and protein, a response mediated through retinoic acid receptor alpha (RAR alpha). Tretinoin 15-28 retinoic acid receptor alpha Gallus gallus 119-147
7496626-3 1995 Treatment with retinoic acid (RA) leads to increased levels of both trkA mRNA and protein, a response mediated through retinoic acid receptor alpha (RAR alpha). Tretinoin 15-28 retinoic acid receptor alpha Gallus gallus 149-158
24971534-4 2014 Real-time PCR analysis revealed that OCT4 levels were high in undifferentiated NCCIT cells but significantly decreased upon retinoic acid-mediated differentiation, concomitant with up-regulation of ESE-1 expression. Tretinoin 124-137 E74 like ETS transcription factor 3 Homo sapiens 198-203
7496626-3 1995 Treatment with retinoic acid (RA) leads to increased levels of both trkA mRNA and protein, a response mediated through retinoic acid receptor alpha (RAR alpha). Tretinoin 30-32 neurotrophic receptor tyrosine kinase 1 Gallus gallus 68-72
7496626-3 1995 Treatment with retinoic acid (RA) leads to increased levels of both trkA mRNA and protein, a response mediated through retinoic acid receptor alpha (RAR alpha). Tretinoin 30-32 retinoic acid receptor alpha Gallus gallus 119-147
7656409-7 1995 Conversely, the adverse effects of 0.25% alcohol on neurite extension, GAP43/B50, N-myc, and c-myc were prevented by 15 and 45 nM retinoic acid. Tretinoin 130-143 growth associated protein 43 Homo sapiens 71-76
7496626-3 1995 Treatment with retinoic acid (RA) leads to increased levels of both trkA mRNA and protein, a response mediated through retinoic acid receptor alpha (RAR alpha). Tretinoin 30-32 retinoic acid receptor alpha Gallus gallus 149-158
7656409-7 1995 Conversely, the adverse effects of 0.25% alcohol on neurite extension, GAP43/B50, N-myc, and c-myc were prevented by 15 and 45 nM retinoic acid. Tretinoin 130-143 growth associated protein 43 Homo sapiens 77-80
7496626-4 1995 Ectopic expression of trkA in these cells results in the ability to survive with NGF, suggesting that RA-induced trkA expression is sufficient to elicit NGF-dependent survival. Tretinoin 102-104 neurotrophic receptor tyrosine kinase 1 Gallus gallus 22-26
24821728-3 2014 We found that PLZF-RARalpha can repress transcription of the p21WAF/CDKN1A gene, which encodes the negative cell cycle regulator p21 by binding to its proximal promoter Sp1-binding GC-boxes 3, 4, 5/6, a retinoic acid response element (RARE), and distal p53-responsive elements (p53REs). Tretinoin 203-216 retinoic acid receptor alpha Homo sapiens 19-27
7496626-4 1995 Ectopic expression of trkA in these cells results in the ability to survive with NGF, suggesting that RA-induced trkA expression is sufficient to elicit NGF-dependent survival. Tretinoin 102-104 neurotrophic receptor tyrosine kinase 1 Gallus gallus 113-117
7643455-9 1995 These successful cases treated with M-CSF combining chemotherapy may suggest a new therapeutic strategy for APL in addition to all-trans retinoic acid. Tretinoin 137-150 colony stimulating factor 1 Homo sapiens 36-41
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 140-153 interleukin 1 alpha Homo sapiens 66-85
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 140-153 interleukin 1 alpha Homo sapiens 87-97
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 155-159 interleukin 1 alpha Homo sapiens 66-85
7763262-1 1995 We have studied the relationship between interleukin-8 (IL-8) and interleukin-1 alpha (IL-1 alpha) release after stimulation with all-trans retinoic acid (ATRA) and tumor necrosis factor-alpha (TNF-alpha) in the human epithelial ovarian cancer cell line HOC-7. Tretinoin 155-159 interleukin 1 alpha Homo sapiens 87-97
7763262-2 1995 Both IL-1 alpha and IL-8 protein release were enhanced by treatment with ATRA and TNF-alpha after 48 h exposure. Tretinoin 73-77 interleukin 1 alpha Homo sapiens 5-15
7656409-7 1995 Conversely, the adverse effects of 0.25% alcohol on neurite extension, GAP43/B50, N-myc, and c-myc were prevented by 15 and 45 nM retinoic acid. Tretinoin 130-143 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 82-87
7656409-7 1995 Conversely, the adverse effects of 0.25% alcohol on neurite extension, GAP43/B50, N-myc, and c-myc were prevented by 15 and 45 nM retinoic acid. Tretinoin 130-143 MYC proto-oncogene, bHLH transcription factor Homo sapiens 93-98
7656409-8 1995 These results suggest that inhibition of neuronal differentiation by alcohol and prevention of such effects by retinoic acid are related to changes in GAP43/B50, N-myc and c-myc. Tretinoin 111-124 growth associated protein 43 Homo sapiens 151-156
7656409-8 1995 These results suggest that inhibition of neuronal differentiation by alcohol and prevention of such effects by retinoic acid are related to changes in GAP43/B50, N-myc and c-myc. Tretinoin 111-124 growth associated protein 43 Homo sapiens 157-160
7656409-8 1995 These results suggest that inhibition of neuronal differentiation by alcohol and prevention of such effects by retinoic acid are related to changes in GAP43/B50, N-myc and c-myc. Tretinoin 111-124 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 162-167
7656409-8 1995 These results suggest that inhibition of neuronal differentiation by alcohol and prevention of such effects by retinoic acid are related to changes in GAP43/B50, N-myc and c-myc. Tretinoin 111-124 MYC proto-oncogene, bHLH transcription factor Homo sapiens 172-177
7768638-0 1995 Retinoic acid induced death of ovarian carcinoma cells correlates with c-myc stimulation. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 71-76
7768638-3 1995 Exposure of N.I cells to increasing concentrations of ATRA was accompanied by a considerable up-regulation of c-myc transcript levels that correlated with the rate of cell killing, which itself was an active process as judged by sustained transcriptional expression. Tretinoin 54-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 110-115
7768638-6 1995 The accompanying c-myc up-regulation seems to be mediated by retinoic-acid-receptor-independent pathways involving membrane-associated phospholipases instead, because manoalide partly suppressed c-myc induction by ATRA but left constitutive c-myc expression unaffected. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 17-22
7768638-6 1995 The accompanying c-myc up-regulation seems to be mediated by retinoic-acid-receptor-independent pathways involving membrane-associated phospholipases instead, because manoalide partly suppressed c-myc induction by ATRA but left constitutive c-myc expression unaffected. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 195-200
7768638-6 1995 The accompanying c-myc up-regulation seems to be mediated by retinoic-acid-receptor-independent pathways involving membrane-associated phospholipases instead, because manoalide partly suppressed c-myc induction by ATRA but left constitutive c-myc expression unaffected. Tretinoin 214-218 MYC proto-oncogene, bHLH transcription factor Homo sapiens 195-200
7763262-3 1995 Blocking of IL-1 alpha activity in HOC-7 cells with either IL-1 receptor antagonist (IL-1ra) or a neutralizing antibody directed against IL-1 alpha resulted in a dose-dependent decrease of IL-8 release by ATRA, TNF-alpha and IL-1 alpha treated HOC-7 cells. Tretinoin 205-209 interleukin 1 alpha Homo sapiens 12-22
7763262-3 1995 Blocking of IL-1 alpha activity in HOC-7 cells with either IL-1 receptor antagonist (IL-1ra) or a neutralizing antibody directed against IL-1 alpha resulted in a dose-dependent decrease of IL-8 release by ATRA, TNF-alpha and IL-1 alpha treated HOC-7 cells. Tretinoin 205-209 interleukin 1 receptor antagonist Homo sapiens 59-83
7763262-3 1995 Blocking of IL-1 alpha activity in HOC-7 cells with either IL-1 receptor antagonist (IL-1ra) or a neutralizing antibody directed against IL-1 alpha resulted in a dose-dependent decrease of IL-8 release by ATRA, TNF-alpha and IL-1 alpha treated HOC-7 cells. Tretinoin 205-209 interleukin 1 receptor antagonist Homo sapiens 85-91
7763262-3 1995 Blocking of IL-1 alpha activity in HOC-7 cells with either IL-1 receptor antagonist (IL-1ra) or a neutralizing antibody directed against IL-1 alpha resulted in a dose-dependent decrease of IL-8 release by ATRA, TNF-alpha and IL-1 alpha treated HOC-7 cells. Tretinoin 205-209 interleukin 1 alpha Homo sapiens 137-147
7763262-3 1995 Blocking of IL-1 alpha activity in HOC-7 cells with either IL-1 receptor antagonist (IL-1ra) or a neutralizing antibody directed against IL-1 alpha resulted in a dose-dependent decrease of IL-8 release by ATRA, TNF-alpha and IL-1 alpha treated HOC-7 cells. Tretinoin 205-209 interleukin 1 alpha Homo sapiens 137-147
24991767-6 2014 As AML cells are blocked in their differentiation, we tested if the expression levels of WIPI-1 and WIPI-2 increase during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of APL. Tretinoin 133-146 WD repeat domain, phosphoinositide interacting 1 Homo sapiens 89-95
7771807-0 1995 All-trans-retinoic acid interacts synergistically with basic fibroblast growth factor and epidermal growth factor to stimulate the production of tissue inhibitor of metalloproteinases from fibroblasts. Tretinoin 0-23 epidermal growth factor Homo sapiens 90-113
7771807-2 1995 When 10(-5) M retinoic acid is applied in combination with 1, 10, and 100 ng/ml of either FGF or EGF to foreskin or synovial fibroblasts, this results in a dose-dependent synergistic increase in TIMP protein production which is greater than the additive effect of the agents by up to fourfold. Tretinoin 14-27 epidermal growth factor Homo sapiens 97-100
7771807-4 1995 We have also found that retinoic acid potently inhibits bFGF- and EGF-stimulated collagenase protein production in both skin and synovial fibroblasts. Tretinoin 24-37 epidermal growth factor Homo sapiens 66-69
7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 44-57 RUNX family transcription factor 3 Homo sapiens 16-21
7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 59-82 RUNX family transcription factor 3 Homo sapiens 16-21
7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 84-88 RUNX family transcription factor 3 Homo sapiens 16-21
7536793-0 1995 Fas and activation-induced Fas ligand mediate apoptosis of T cell hybridomas: inhibition of Fas ligand expression by retinoic acid and glucocorticoids. Tretinoin 117-130 Fas ligand Homo sapiens 27-37
7536793-0 1995 Fas and activation-induced Fas ligand mediate apoptosis of T cell hybridomas: inhibition of Fas ligand expression by retinoic acid and glucocorticoids. Tretinoin 117-130 Fas ligand Homo sapiens 92-102
7536793-10 1995 We conclude that up-regulated expression of FasL and its subsequent interaction with Fas accounts for the apoptotic response of T cell hybridomas to activation, and that retinoic acid and corticosteroids inhibit activation-induced apoptosis by preventing up-regulation of FasL. Tretinoin 170-183 Fas ligand Homo sapiens 44-48
7536793-10 1995 We conclude that up-regulated expression of FasL and its subsequent interaction with Fas accounts for the apoptotic response of T cell hybridomas to activation, and that retinoic acid and corticosteroids inhibit activation-induced apoptosis by preventing up-regulation of FasL. Tretinoin 170-183 Fas ligand Homo sapiens 272-276
7731708-2 1995 The effects of RA are mediated through multiple members of the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families of nuclear transcription factors. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 87-90
7731708-4 1995 Using NTera2/clone D1 (NT2/D1) human embryonal carcinoma cells as a model, we report that the RA induced terminal differentiation of these cells into a neuronal phenotype is characterized by an increase in expression of RAR alpha, RAR beta, RAR gamma, and a slight induction of RXR alpha. Tretinoin 94-96 retinoic acid receptor alpha Homo sapiens 220-229
7704904-1 1995 The effects of retinoids (all-trans-retinoic acid (RA) and vitamin A) and hydrocortisone (HC) on the IL-4-dependent IgE and IgG1 response by mouse whole spleen cells and splenic B cells were studied. Tretinoin 26-49 interleukin 4 Mus musculus 101-105
7704904-1 1995 The effects of retinoids (all-trans-retinoic acid (RA) and vitamin A) and hydrocortisone (HC) on the IL-4-dependent IgE and IgG1 response by mouse whole spleen cells and splenic B cells were studied. Tretinoin 51-53 interleukin 4 Mus musculus 101-105
7739532-4 1995 We have found that transcriptional activation of a Myb-responsive reporter gene can be inhibited by RA in a human monocytic cell line. Tretinoin 100-102 MYB proto-oncogene, transcription factor Homo sapiens 51-54
7739532-9 1995 The introduction of an inducible, exogenous RAR alpha into v-myb-transformed monoblasts permitted an RA-dependent differentiation into macrophage-like cells similar to those induced by TPA. Tretinoin 44-46 MYB proto-oncogene, transcription factor Homo sapiens 59-64
7739532-10 1995 These results demonstrate that transformation by v-myb is recessive to RAR alpha and imply that many types of non-RA-responsive leukemia cells may become responsive following the introduction of the RAR. Tretinoin 71-73 MYB proto-oncogene, transcription factor Homo sapiens 49-54
24991767-6 2014 As AML cells are blocked in their differentiation, we tested if the expression levels of WIPI-1 and WIPI-2 increase during all-trans retinoic acid (ATRA)-induced neutrophil differentiation of APL. Tretinoin 148-152 WD repeat domain, phosphoinositide interacting 1 Homo sapiens 89-95
24819975-0 2014 Small ubiquitin-related modifier-1 modification regulates all-trans-retinoic acid-induced differentiation via stabilization of retinoic acid receptor alpha. Tretinoin 68-81 retinoic acid receptor alpha Homo sapiens 127-155
7706767-0 1995 Differential regulation of decorin and biglycan gene expression by dexamethasone and retinoic acid in cultured human skin fibroblasts. Tretinoin 85-98 decorin Homo sapiens 27-34
7721753-3 1995 Here we demonstrate that B-myb expression is down-regulated during retinoic acid-induced neural and glial differentiation of neuroblastoma cells. Tretinoin 67-80 MYB proto-oncogene like 2 Homo sapiens 25-30
24819975-6 2014 We also found that RARalpha enhanced the transcription of its target genes, which might also contribute to the enhanced differentiating effects of ATRA; however, mutation of Lys399 of RARalpha inhibits the extents of both SUMO-1 modification and ATRA-induced differentiation. Tretinoin 147-151 retinoic acid receptor alpha Homo sapiens 19-27
7706767-2 1995 We have studied the regulation of gene expression of two small extracellular matrix chondroitin/dermatan sulfate proteoglycans, decorin and biglycan, by dexamethasone and retinoic acid in cultured human skin fibroblasts. Tretinoin 171-184 decorin Homo sapiens 128-135
7706767-6 1995 Retinoic acid dose dependently reduced decorin mRNA levels (by 51%) and production (by 72%), but had no effect on biglycan gene expression. Tretinoin 0-13 decorin Homo sapiens 39-46
24819975-6 2014 We also found that RARalpha enhanced the transcription of its target genes, which might also contribute to the enhanced differentiating effects of ATRA; however, mutation of Lys399 of RARalpha inhibits the extents of both SUMO-1 modification and ATRA-induced differentiation. Tretinoin 246-250 retinoic acid receptor alpha Homo sapiens 19-27
7705951-4 1995 In contrast, expression of matrilysin was down-regulated by all trans-retinoic acid or by introduction of anti-sense matrilysin in BM314 colon cancer cells. Tretinoin 64-83 matrix metallopeptidase 7 Homo sapiens 27-37
24819975-6 2014 We also found that RARalpha enhanced the transcription of its target genes, which might also contribute to the enhanced differentiating effects of ATRA; however, mutation of Lys399 of RARalpha inhibits the extents of both SUMO-1 modification and ATRA-induced differentiation. Tretinoin 246-250 retinoic acid receptor alpha Homo sapiens 184-192
25161869-10 2014 Stimulation with RA at 1 muM for 24 h augmented AQP3 expression and down-regulated AQP9 expression. Tretinoin 17-19 aquaporin 3 (Gill blood group) Homo sapiens 48-52
7532580-7 1995 In the presence of 100 nM RA, the stimulation elicited by these agents was enhanced, with IGFBP-3 levels increasing to 6-fold above that seen with RA alone. Tretinoin 26-28 insulin like growth factor binding protein 3 Homo sapiens 90-97
7532580-7 1995 In the presence of 100 nM RA, the stimulation elicited by these agents was enhanced, with IGFBP-3 levels increasing to 6-fold above that seen with RA alone. Tretinoin 147-149 insulin like growth factor binding protein 3 Homo sapiens 90-97
24699546-6 2014 Dlg1 null mice showed reduced Ret expression and apoptosis during ureter maturation and evidence of reduced retinoic acid signaling in the kidney. Tretinoin 108-121 discs large MAGUK scaffold protein 1 Mus musculus 0-4
7532580-10 1995 The stimulatory effect of RA + forskolin on IGFBP-3 was partially reversed by estrogen, whereas RA + forskolin-stimulated IGFBP-6 levels were further increased by estrogen. Tretinoin 26-28 insulin like growth factor binding protein 3 Homo sapiens 44-51
7532580-11 1995 Increased IGFBP-3 and -6 production in response to RA + forskolin was accompanied by a decrease in IGF-stimulated thymidine incorporation into DNA; by contrast, the bioactivity of an IGF analog that does not bind with IGFBPs, [Gln3, Ala4, Tyr15, Leu16]IGF-I, was unchanged under these conditions. Tretinoin 51-53 insulin like growth factor binding protein 3 Homo sapiens 10-24
7532580-11 1995 Increased IGFBP-3 and -6 production in response to RA + forskolin was accompanied by a decrease in IGF-stimulated thymidine incorporation into DNA; by contrast, the bioactivity of an IGF analog that does not bind with IGFBPs, [Gln3, Ala4, Tyr15, Leu16]IGF-I, was unchanged under these conditions. Tretinoin 51-53 insulin like growth factor binding protein 3 Homo sapiens 218-224
7532580-11 1995 Increased IGFBP-3 and -6 production in response to RA + forskolin was accompanied by a decrease in IGF-stimulated thymidine incorporation into DNA; by contrast, the bioactivity of an IGF analog that does not bind with IGFBPs, [Gln3, Ala4, Tyr15, Leu16]IGF-I, was unchanged under these conditions. Tretinoin 51-53 membrane spanning 4-domains A1 Homo sapiens 246-251
7823919-3 1995 Similarly, Oct-3/4 is expressed in embryonal carcinoma (EC) cells and is repressed in retinoic acid (RA)-differentiated EC cells. Tretinoin 86-99 POU class 5 homeobox 1 Homo sapiens 11-18
7823919-3 1995 Similarly, Oct-3/4 is expressed in embryonal carcinoma (EC) cells and is repressed in retinoic acid (RA)-differentiated EC cells. Tretinoin 101-103 POU class 5 homeobox 1 Homo sapiens 11-18
7823919-5 1995 Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. Tretinoin 48-50 interleukin 23 subunit alpha Homo sapiens 59-62
7823919-5 1995 Our present results demonstrate that in P19 and RA-treated P19 cells, the orphan receptors ARP-1/COUP-TFII and EAR-3/COUP-TFI repress Oct-3/4 promoter activity through the RAREoct site in a dose-dependent manner. Tretinoin 48-50 POU class 5 homeobox 1 Homo sapiens 134-141
7823919-14 1995 Most interestingly, in RA-treated EC cells, the kinetics of Oct-3/4 repression inversely correlates with the kinetics of ARP-1/COUP-TFII and EAR-3/COUP-TFI activation. Tretinoin 23-25 POU class 5 homeobox 1 Homo sapiens 60-67
7823950-0 1995 Targeted disruption of retinoic acid receptor alpha (RAR alpha) and RAR gamma results in receptor-specific alterations in retinoic acid-mediated differentiation and retinoic acid metabolism. Tretinoin 23-36 retinoic acid receptor alpha Homo sapiens 53-62
7823950-0 1995 Targeted disruption of retinoic acid receptor alpha (RAR alpha) and RAR gamma results in receptor-specific alterations in retinoic acid-mediated differentiation and retinoic acid metabolism. Tretinoin 122-135 retinoic acid receptor alpha Homo sapiens 23-51
7823950-0 1995 Targeted disruption of retinoic acid receptor alpha (RAR alpha) and RAR gamma results in receptor-specific alterations in retinoic acid-mediated differentiation and retinoic acid metabolism. Tretinoin 122-135 retinoic acid receptor alpha Homo sapiens 53-62
7736436-4 1995 Positive response to retinoic acid treatment suggests molecular rearrangement of retinoic acid receptor alpha. Tretinoin 21-34 retinoic acid receptor alpha Homo sapiens 81-109
7615664-2 1995 In F9 embryonal carcinoma cells, expression of RAP mRNA increases when differentiation is induced with retinoic acid and dibutyryl-cyclic AMP. Tretinoin 103-116 LDL receptor related protein associated protein 1 Homo sapiens 47-50
7706770-0 1995 Topical tretinoin increases the tropoelastin and fibronectin content of photoaged hairless mouse skin. Tretinoin 8-17 elastin Mus musculus 32-44
7706770-0 1995 Topical tretinoin increases the tropoelastin and fibronectin content of photoaged hairless mouse skin. Tretinoin 8-17 fibronectin 1 Mus musculus 49-60
7706770-6 1995 The distribution of elastin and fibronectin was examined by immunofluorescence microscopy, which revealed fine fibrils in the subepidermal zone in tretinoin-treated skin. Tretinoin 147-156 elastin Mus musculus 20-27
7706770-6 1995 The distribution of elastin and fibronectin was examined by immunofluorescence microscopy, which revealed fine fibrils in the subepidermal zone in tretinoin-treated skin. Tretinoin 147-156 fibronectin 1 Mus musculus 32-43
7706770-7 1995 A quantitative slot-blot immunobinding assay showed that tretinoin induced a threefold higher amount of tropoelastin compared with controls. Tretinoin 57-66 elastin Mus musculus 104-116
7706775-5 1995 Increasing RA concentrations altered the in vivo-like terminal differentiation of oral keratinocytes by disruption of organized stratification, inhibition of filaggrin/profilaggrin and K1 expression, and stimulation of K13 and K19 expression. Tretinoin 11-13 keratin 13 Homo sapiens 219-222
7823950-4 1995 The absence of RAR alpha is associated with a reduction in the RA-induced expression of both the CRABP-II and Hoxb-1 (formerly 2.9) genes. Tretinoin 15-17 homeobox B1 Homo sapiens 110-116
7775378-1 1995 An ecto-enzyme of NAD glycohydrolase (NADase) induced by retinoic acid in HL-60 cells is attributed to the molecule of CD38 antigen [Kontani, K., Nishina, H., Ohoka, Y., Takahashi, K., and Katada, T. (1993) J. Biol. Tretinoin 57-70 CD38 molecule Homo sapiens 119-123
7620342-6 1995 Retinoic acid at various concentrations (0.1-1 microM) evoked a standard increase in IL-2 production. Tretinoin 0-13 interleukin 2 Mus musculus 85-89
24799257-5 2014 These three natural RAR agonists with diterpene structures, while structurally different from ATRA, were able to increase the mRNA levels of the constitutive androstane receptor in HepG2 cells, induce F9 cell differentiation followed by Cyp26a1 mRNA expression, and differentiate HL-60 cells via RAR activation in a different manner from ATRA. Tretinoin 94-98 retinoic acid receptor alpha Homo sapiens 20-23
7535055-4 1995 Challenge of NB4 cells with G-CSF, dbcAMP and ATRA causes a much higher induction of LAP relative to that observed in the presence of ATRA+G-CSF or ATRA+dbcAMP. Tretinoin 46-50 colony stimulating factor 3 Homo sapiens 139-144
7719237-0 1995 Acute promyelocytic leukaemia cells resistant to retinoic acid show further perturbation of the RAR alpha signal transduction system. Tretinoin 49-62 retinoic acid receptor alpha Homo sapiens 96-105
24799257-6 2014 These results demonstrate that some diterpenes exist as naturally occurring RAR agonists and that the differences in chemical structure between ATRA and these diterpenes may induce distinct gene activation and a specific cellular response. Tretinoin 144-148 retinoic acid receptor alpha Homo sapiens 76-79
24856513-5 2014 We find that DMRT1 blocks testicular retinoic acid (RA) signaling from activating genes normally involved in female sex determination and ovarian development and show that inappropriate activation of these genes can drive sexual transdifferentiation. Tretinoin 37-50 doublesex and mab-3 related transcription factor 1 Homo sapiens 13-18
7697779-0 1994 Synthesis of 9E- and 9Z-locked retinoic acid analogs as ligands for RAR and RXR. Tretinoin 31-44 retinoic acid receptor alpha Homo sapiens 68-71
7697808-0 1995 Retinoic acid antagonizes basal as well as coal tar and glucocorticoid-induced cytochrome P4501A1 expression in human skin. Tretinoin 0-13 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 79-97
7867726-3 1995 A marked increase in RET mRNA levels was observed in all the cell lines examined shortly after retinoic acid (RA) treatment and before the onset of detectable morphological changes. Tretinoin 95-108 ret proto-oncogene Homo sapiens 21-24
7867726-3 1995 A marked increase in RET mRNA levels was observed in all the cell lines examined shortly after retinoic acid (RA) treatment and before the onset of detectable morphological changes. Tretinoin 110-112 ret proto-oncogene Homo sapiens 21-24
7867726-5 1995 Induction of RET expression by RA occurred in the absence of de novo protein synthesis. Tretinoin 31-33 ret proto-oncogene Homo sapiens 13-16
21559717-3 1994 In order to develop new alternatives for therapy of metastatic melanoma, we tested the biological activity of eight synthetic retinoids with high affinity and/or selectivity for the retinoic acid receptors (RAR) alpha, beta and gamma in comparison to all-trans retinoic acid, arotinoid acid and CD 367 in four human melanoma cell lines. Tretinoin 182-195 retinoic acid receptor alpha Homo sapiens 207-210
7526151-0 1994 AP-1, ETS, and transcriptional silencers regulate retinoic acid-dependent induction of keratin 18 in embryonic cells. Tretinoin 50-63 keratin 18 Homo sapiens 87-97
24856513-5 2014 We find that DMRT1 blocks testicular retinoic acid (RA) signaling from activating genes normally involved in female sex determination and ovarian development and show that inappropriate activation of these genes can drive sexual transdifferentiation. Tretinoin 52-54 doublesex and mab-3 related transcription factor 1 Homo sapiens 13-18
7526151-1 1994 The differentiation of both embryonal carcinoma (EC) and embryonic stem (ES) cells can be triggered in culture by exposure to retinoic acid and results in the transcriptional induction of both the endogenous mouse keratin 18 (mK18) intermediate filament gene and an experimentally introduced human keratin 18 (K18) gene as well as a variety of other markers characteristic of extraembryonic endoderm. Tretinoin 126-139 keratin 18 Homo sapiens 298-308
7526151-1 1994 The differentiation of both embryonal carcinoma (EC) and embryonic stem (ES) cells can be triggered in culture by exposure to retinoic acid and results in the transcriptional induction of both the endogenous mouse keratin 18 (mK18) intermediate filament gene and an experimentally introduced human keratin 18 (K18) gene as well as a variety of other markers characteristic of extraembryonic endoderm. Tretinoin 126-139 keratin 18 Homo sapiens 227-230
7533101-7 1995 The exposure to 1 microM ATRA resulted in downregulation of PP2A catalytic subunit protein in HL-60 cells, but ATRA did not affect PP2A expression in HL60RAr cells. Tretinoin 25-29 protein phosphatase 2 phosphatase activator Homo sapiens 60-64
26237391-3 2014 Retinoic acid, the active metabolite of vitamin A, is involved in a wide range of biological processes, through binding and activation of nuclear receptors: retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 157-180
7533101-10 1995 Our results show a correlation between the extent of PP2A expression and the response of HL-60 and HL-60RAr cells to the differentiative effects of ATRA. Tretinoin 148-152 protein phosphatase 2 phosphatase activator Homo sapiens 53-57
7949172-0 1994 All-trans retinoic acid upregulates thrombomodulin and downregulates tissue-factor expression in acute promyelocytic leukemia cells: distinct expression of thrombomodulin and tissue factor in human leukemic cells. Tretinoin 10-23 thrombomodulin Homo sapiens 36-50
7949172-0 1994 All-trans retinoic acid upregulates thrombomodulin and downregulates tissue-factor expression in acute promyelocytic leukemia cells: distinct expression of thrombomodulin and tissue factor in human leukemic cells. Tretinoin 10-23 coagulation factor III, tissue factor Homo sapiens 69-82
7949172-0 1994 All-trans retinoic acid upregulates thrombomodulin and downregulates tissue-factor expression in acute promyelocytic leukemia cells: distinct expression of thrombomodulin and tissue factor in human leukemic cells. Tretinoin 10-23 thrombomodulin Homo sapiens 156-170
7949172-0 1994 All-trans retinoic acid upregulates thrombomodulin and downregulates tissue-factor expression in acute promyelocytic leukemia cells: distinct expression of thrombomodulin and tissue factor in human leukemic cells. Tretinoin 10-23 coagulation factor III, tissue factor Homo sapiens 175-188
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 75-88 thrombomodulin Homo sapiens 19-33
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 75-88 thrombomodulin Homo sapiens 35-37
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 75-88 coagulation factor III, tissue factor Homo sapiens 43-56
7850796-3 1995 In the present study, the effects of two potent retinoids, all-trans-retinoic acid (RA) and 13-cis-RA, on the expression of retinoic acid receptor alpha and the growth of AIDS-related KS (AIDS-KS) cells were examined. Tretinoin 59-82 retinoic acid receptor alpha Homo sapiens 124-152
7850796-3 1995 In the present study, the effects of two potent retinoids, all-trans-retinoic acid (RA) and 13-cis-RA, on the expression of retinoic acid receptor alpha and the growth of AIDS-related KS (AIDS-KS) cells were examined. Tretinoin 84-86 retinoic acid receptor alpha Homo sapiens 124-152
7850796-8 1995 The effects of RA were accompanied by a dramatic increase in nuclear staining for retinoic acid receptor alpha and in the relative number of strongly positive retinoic acid receptor alpha nuclei. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 82-110
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 75-88 coagulation factor III, tissue factor Homo sapiens 58-60
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 90-94 thrombomodulin Homo sapiens 19-33
7850796-8 1995 The effects of RA were accompanied by a dramatic increase in nuclear staining for retinoic acid receptor alpha and in the relative number of strongly positive retinoic acid receptor alpha nuclei. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 159-187
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 90-94 coagulation factor III, tissue factor Homo sapiens 43-56
26237391-3 2014 Retinoic acid, the active metabolite of vitamin A, is involved in a wide range of biological processes, through binding and activation of nuclear receptors: retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 182-185
7949172-1 1994 The expressions of thrombomodulin (TM) and tissue factor (TF) by all-trans retinoic acid (ATRA) were studied in human leukemic cell lines including NB4 (acute promyelocytic leukemia) and U937 (monoblastic leukemia). Tretinoin 90-94 coagulation factor III, tissue factor Homo sapiens 58-60
7949172-4 1994 Inherently procoagulant NB4 cells contained markedly higher content of TF, which was efficiently reduced by ATRA. Tretinoin 108-112 coagulation factor III, tissue factor Homo sapiens 71-73
7949172-6 1994 On the other hand, both ATRA and dbcAMP showed dramatic increase of TM antigen level and modest decrease of TF antigen in U937 cells. Tretinoin 24-28 thrombomodulin Homo sapiens 68-70
7949172-6 1994 On the other hand, both ATRA and dbcAMP showed dramatic increase of TM antigen level and modest decrease of TF antigen in U937 cells. Tretinoin 24-28 coagulation factor III, tissue factor Homo sapiens 108-110
7949172-7 1994 These results suggest that ATRA regulates expressions of TM and TF antigens and activity in NB4 and U937 cell lines, and provide evidence for a potential efficiency of ATRA as a preventive and therapeutic agent for disseminated intravascular coagulation in promyelocytic and monocytic leukemia. Tretinoin 27-31 thrombomodulin Homo sapiens 57-59
7949172-7 1994 These results suggest that ATRA regulates expressions of TM and TF antigens and activity in NB4 and U937 cell lines, and provide evidence for a potential efficiency of ATRA as a preventive and therapeutic agent for disseminated intravascular coagulation in promyelocytic and monocytic leukemia. Tretinoin 27-31 coagulation factor III, tissue factor Homo sapiens 64-66
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 31-44 retinoic acid receptor alpha Homo sapiens 230-239
7530211-1 1995 All trans-retinoic acid (ATRA) can induce granulocytic differentiation both in vitro and in vivo, and its activity is mediated by the retinoic acid receptor-alpha (RAR-alpha). Tretinoin 4-23 retinoic acid receptor alpha Homo sapiens 134-162
7530211-1 1995 All trans-retinoic acid (ATRA) can induce granulocytic differentiation both in vitro and in vivo, and its activity is mediated by the retinoic acid receptor-alpha (RAR-alpha). Tretinoin 4-23 retinoic acid receptor alpha Homo sapiens 164-173
7949175-5 1994 These data suggest that ATRA may inhibit the proliferation of myeloma cells both by the downregulation of IL-6R and gp130 expression on myeloma cells and by the inhibition of IL-6 production from myeloma and stromal cells. Tretinoin 24-28 interleukin 6 cytokine family signal transducer Homo sapiens 116-121
24576683-10 2014 This positive effect of retinoic acid resulted from the inhibition of Smad3/TGF-beta1 signaling via reduced Smad4 mRNA and increased Smad7 protein expression. Tretinoin 24-37 SMAD family member 4 Mus musculus 108-113
7530211-1 1995 All trans-retinoic acid (ATRA) can induce granulocytic differentiation both in vitro and in vivo, and its activity is mediated by the retinoic acid receptor-alpha (RAR-alpha). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 134-162
7530211-1 1995 All trans-retinoic acid (ATRA) can induce granulocytic differentiation both in vitro and in vivo, and its activity is mediated by the retinoic acid receptor-alpha (RAR-alpha). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 164-173
7530213-0 1995 The combination of Steel factor and GM-CSF blocks apoptosis induced by retinoic acid and upregulates AP-1 in a human growth factor-dependent cell line. Tretinoin 71-84 colony stimulating factor 2 Homo sapiens 36-42
7530213-4 1995 Treatment of cells with RA resulted in apoptotic cell death associated with internucleosomal DNA fragmentation in the presence of either SLF or GM-CSF. Tretinoin 24-26 colony stimulating factor 2 Homo sapiens 144-150
7957668-3 1994 HNF-3 alpha expression increased upon retinoic acid-induced GCT 27 X-1 differentiation. Tretinoin 38-51 forkhead box A1 Homo sapiens 0-11
24576683-11 2014 Retinoic acid also induced alveolarization and restricted Smad3/TGF-beta1 signaling by decreasing Smad4 mRNA in healthy mice. Tretinoin 0-13 SMAD family member 4 Mus musculus 98-103
24798219-6 2014 Further studies demonstrated that RA treatment increased Wnt/beta-catenin signaling, as demonstrated by Wnt/beta-catenin target gene expression analysis and a luciferase-based beta-catenin-activated reporter assay. Tretinoin 34-36 catenin beta 1 Homo sapiens 61-73
7965197-0 1994 Retinoic acid receptor-alpha gene expression is modulated by dietary vitamin A and by retinoic acid in chicken T lymphocytes. Tretinoin 86-99 retinoic acid receptor alpha Gallus gallus 0-28
7965197-4 1994 In vitro effects of retinoic acid on the modulation of RAR-alpha mRNA were studied in stimulated T lymphocytes. Tretinoin 20-33 retinoic acid receptor alpha Gallus gallus 55-64
7965197-5 1994 Retinoic acid (0.01 mumol/L) increased RAR-alpha mRNA levels within 2 or 16 h of incubation with concanavalin A- or beta-casein-stimulated T cells, respectively. Tretinoin 0-13 retinoic acid receptor alpha Gallus gallus 39-48
7965197-7 1994 Expression of RAR-alpha mRNA in concanavalin A-stimulated T lymphocytes was up-regulated by retinoic acid in a dose-dependent manner, and maximal expression occurred in response to 1 mumol/L retinoic acid. Tretinoin 92-105 retinoic acid receptor alpha Gallus gallus 14-23
7829878-5 1995 Increasing RA concentrations altered the in vivo-like terminal differentiation of oral keratinocytes by disruption of organized stratification, inhibition of filaggrin/profilaggrin and K1 expression, and stimulation of K13 and K19 expression. Tretinoin 11-13 keratin 13 Homo sapiens 219-222
7738588-10 1995 Instead, p36 gene expression was modulated in both proliferating and non-proliferating PNET cell cultures by treatment with 50 mIU/ml of insulin, 100 mM ethanol, or 5 microM retinoic acid. Tretinoin 174-187 annexin A2 Homo sapiens 9-12
7823957-8 1995 Investigations of retinoic acid-induced differentiation in P19 cells provided further support for a strong correlation of ets-1 with the pathway for astrocyte differentiation. Tretinoin 18-31 interleukin 23 subunit alpha Homo sapiens 59-62
7823957-8 1995 Investigations of retinoic acid-induced differentiation in P19 cells provided further support for a strong correlation of ets-1 with the pathway for astrocyte differentiation. Tretinoin 18-31 ETS proto-oncogene 1, transcription factor Homo sapiens 122-127
7965197-7 1994 Expression of RAR-alpha mRNA in concanavalin A-stimulated T lymphocytes was up-regulated by retinoic acid in a dose-dependent manner, and maximal expression occurred in response to 1 mumol/L retinoic acid. Tretinoin 191-204 retinoic acid receptor alpha Gallus gallus 14-23
7965197-9 1994 Our results indicate that RAR-alpha mRNA expression and antigen-specific proliferative responses of T lymphocytes are influenced by vitamin A status in vivo, and directly modulated by retinoic acid. Tretinoin 184-197 retinoic acid receptor alpha Gallus gallus 26-35
7576949-0 1995 Effect of retinoic acid on p21ras and regulators of its activity in neuroblastoma. Tretinoin 10-23 H3 histone pseudogene 16 Homo sapiens 27-30
24798219-6 2014 Further studies demonstrated that RA treatment increased Wnt/beta-catenin signaling, as demonstrated by Wnt/beta-catenin target gene expression analysis and a luciferase-based beta-catenin-activated reporter assay. Tretinoin 34-36 catenin beta 1 Homo sapiens 108-120
7576949-3 1995 Therefore, the aim of the present study was to examine the role of p21ras and regulators of its activity in the differentiation of neuroblastoma cells induced by retinoic acid (RA). Tretinoin 162-175 H3 histone pseudogene 16 Homo sapiens 67-70
24798219-6 2014 Further studies demonstrated that RA treatment increased Wnt/beta-catenin signaling, as demonstrated by Wnt/beta-catenin target gene expression analysis and a luciferase-based beta-catenin-activated reporter assay. Tretinoin 34-36 catenin beta 1 Homo sapiens 108-120
7576949-3 1995 Therefore, the aim of the present study was to examine the role of p21ras and regulators of its activity in the differentiation of neuroblastoma cells induced by retinoic acid (RA). Tretinoin 177-179 H3 histone pseudogene 16 Homo sapiens 67-70
7522960-7 1994 RA treatment increased the levels of the three RAR mRNAs in most of the cell lines but had no effect on the RXR mRNAs. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 47-50
7537744-4 1995 Despite tRAR gamma"s capacity to interfere with RAR-mediated transactivation of retinoic acid response elements (RAREs) in keratinocytes, the effects of the truncated receptor are independent of its ability to bind DNA and directly interact with endogenous RARs. Tretinoin 80-93 retinoic acid receptor alpha Homo sapiens 9-12
24798219-8 2014 In summary, excessive all-trans retinoic acid inhibited proliferation and promoted ossification of hFPCs by upregulation of Wnt/beta-catenin signaling. Tretinoin 26-45 catenin beta 1 Homo sapiens 128-140
25099890-6 2014 Furthermore, we show that defects in Hox gene expression known to occur in embryos lacking the histone acetyltransferase MOZ (also called MYST3 or KAT6A) were masked in Moz-deficient ESCs when excessive RA (0.5-5 microM) was used. Tretinoin 203-205 lysine acetyltransferase 6A Homo sapiens 121-124
7537079-0 1995 Retinoic acid upregulates c-kit ligand production by murine keratinocyte in vitro and increases cutaneous mast cell in vivo. Tretinoin 0-13 kit ligand Mus musculus 26-38
7537079-3 1995 Anti-c-kit ligand antibody abrogated MC9-GF activity and RT-PCR analysis demonstrated that retinoic acid upregulates c-kit ligand mRNA expression by Pam cells. Tretinoin 91-104 kit ligand Mus musculus 5-17
7537079-3 1995 Anti-c-kit ligand antibody abrogated MC9-GF activity and RT-PCR analysis demonstrated that retinoic acid upregulates c-kit ligand mRNA expression by Pam cells. Tretinoin 91-104 kit ligand Mus musculus 117-129
7919389-0 1994 Monocyte chemoattractant protein-1 gene is expressed in activated neutrophils and retinoic acid-induced human myeloid cell lines. Tretinoin 82-95 C-C motif chemokine ligand 2 Homo sapiens 0-34
7919389-2 1994 Three of the cDNAs cloned hybridized to RA-inducible transcripts on Northern blots, one of which was shown to encode sequences for monocyte chemoattractant protein-1 (MCP-1), a recently described cytokine that is chemotactic for monocytes but not for neutrophils. Tretinoin 40-42 C-C motif chemokine ligand 2 Homo sapiens 131-165
7919389-2 1994 Three of the cDNAs cloned hybridized to RA-inducible transcripts on Northern blots, one of which was shown to encode sequences for monocyte chemoattractant protein-1 (MCP-1), a recently described cytokine that is chemotactic for monocytes but not for neutrophils. Tretinoin 40-42 C-C motif chemokine ligand 2 Homo sapiens 167-172
7919389-4 1994 MCP-1 transcript levels also increased after RA treatment of the NB4 acute promyelocytic cell line. Tretinoin 45-47 C-C motif chemokine ligand 2 Homo sapiens 0-5
7845010-10 1995 Disappearance of the PML/RAR alpha rearrangement after ATRA suggests that ATRA is effective against minimal residual disease. Tretinoin 55-59 PML nuclear body scaffold Homo sapiens 21-34
25099890-6 2014 Furthermore, we show that defects in Hox gene expression known to occur in embryos lacking the histone acetyltransferase MOZ (also called MYST3 or KAT6A) were masked in Moz-deficient ESCs when excessive RA (0.5-5 microM) was used. Tretinoin 203-205 lysine acetyltransferase 6A Homo sapiens 138-143
7845010-10 1995 Disappearance of the PML/RAR alpha rearrangement after ATRA suggests that ATRA is effective against minimal residual disease. Tretinoin 74-78 PML nuclear body scaffold Homo sapiens 21-34
7924741-11 1994 All-trans-retinoic acid had similar stimulatory effect on EGF-induced DNA synthesis. Tretinoin 0-23 epidermal growth factor Homo sapiens 58-61
25099890-6 2014 Furthermore, we show that defects in Hox gene expression known to occur in embryos lacking the histone acetyltransferase MOZ (also called MYST3 or KAT6A) were masked in Moz-deficient ESCs when excessive RA (0.5-5 microM) was used. Tretinoin 203-205 lysine acetyltransferase 6A Homo sapiens 147-152
25099890-6 2014 Furthermore, we show that defects in Hox gene expression known to occur in embryos lacking the histone acetyltransferase MOZ (also called MYST3 or KAT6A) were masked in Moz-deficient ESCs when excessive RA (0.5-5 microM) was used. Tretinoin 203-205 lysine acetyltransferase 6A Homo sapiens 169-172
25099890-7 2014 The role of MOZ in Hox gene activation was only evident when ESCs were differentiated at low concentrations of RA, namely 20 nM, which is similar to RA levels in vivo. Tretinoin 111-113 lysine acetyltransferase 6A Homo sapiens 12-15
25099890-7 2014 The role of MOZ in Hox gene activation was only evident when ESCs were differentiated at low concentrations of RA, namely 20 nM, which is similar to RA levels in vivo. Tretinoin 149-151 lysine acetyltransferase 6A Homo sapiens 12-15
7523800-0 1994 Modulation of IL-8, IL-1 beta, and G-CSF secretion by all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 64-77 colony stimulating factor 3 Homo sapiens 35-40
18475624-5 1995 Co-incubation of RA inhibited PAF-induced PMN aggregation, the release of acid phosphatase from PMNs, and PMN chemotaxis to zymosan-activated serum and histamine while the expression of ICAM-1 and ELAM-1 did not change. Tretinoin 17-19 selectin E Homo sapiens 197-203
7523800-9 1994 Interestingly, the increase of IL-1 beta and G-CSF production in the presence of ATRA was highly correlated to an increase in APL cell count in vitro and in vivo hyperleukocytosis, resulting in fatal outcome. Tretinoin 81-85 colony stimulating factor 3 Homo sapiens 45-50
24887554-9 2014 We show that the ALDH1A1 isoform, through its function in the retinoic acid metabolism, affects the proliferation and/or early differentiation of stem/progenitor cells and is important for branching morphogenesis. Tretinoin 62-75 aldehyde dehydrogenase 1 family member A1 Homo sapiens 17-24
7878635-0 1994 Thrombomodulin induction by all-trans retinoic acid is independent of HL-60 cells differentiation to neutrophilic cells. Tretinoin 28-51 thrombomodulin Homo sapiens 0-14
7878635-1 1994 The expression of thrombomodulin (TM), an antithrombotic factor, was investigated during neutrophilic differentiation of the HL-60 human myeloblastic cell line treated with all-trans retinoic acid (ATRA) or dimethyl sulfoxide (DMSO). Tretinoin 183-196 thrombomodulin Homo sapiens 18-32
7878635-1 1994 The expression of thrombomodulin (TM), an antithrombotic factor, was investigated during neutrophilic differentiation of the HL-60 human myeloblastic cell line treated with all-trans retinoic acid (ATRA) or dimethyl sulfoxide (DMSO). Tretinoin 183-196 thrombomodulin Homo sapiens 34-36
7811230-2 1994 In vitamin A-deficient rats, the hepatic level of apoAI mRNA was increased and enhanced by an oral administration of excess retinoic acid(RA). Tretinoin 124-137 apolipoprotein A1 Rattus norvegicus 50-55
7878635-1 1994 The expression of thrombomodulin (TM), an antithrombotic factor, was investigated during neutrophilic differentiation of the HL-60 human myeloblastic cell line treated with all-trans retinoic acid (ATRA) or dimethyl sulfoxide (DMSO). Tretinoin 198-202 thrombomodulin Homo sapiens 18-32
24792964-4 2014 Here, we identified retinoic acid as a signal that induces tissue-specific localization and functional polarization of peritoneal macrophages through the reversible induction of transcription factor GATA6. Tretinoin 20-33 GATA binding protein 6 Homo sapiens 199-204
7878635-1 1994 The expression of thrombomodulin (TM), an antithrombotic factor, was investigated during neutrophilic differentiation of the HL-60 human myeloblastic cell line treated with all-trans retinoic acid (ATRA) or dimethyl sulfoxide (DMSO). Tretinoin 198-202 thrombomodulin Homo sapiens 34-36
7878635-3 1994 TM antigen and cofactor activity for thrombin-dependent protein C activation were not detected in untreated HL-60 cells and the cells cultured with DMSO, but were expressed in a time-dependent manner in the cells cultured with ATRA. Tretinoin 227-231 thrombomodulin Homo sapiens 0-2
7878635-4 1994 The level of TM expression in the HL-60 cells was not dose-dependent on ATRA concentrations, but maximum TM expression was obtained at 10(-7) M ATRA. Tretinoin 144-148 thrombomodulin Homo sapiens 105-107
7878635-5 1994 TM expression levels decreased in cells cultured with greater than 10(-6) M ATRA, although the extent of cell differentiation into neutrophilic cells progressed at the higher ATRA concentrations. Tretinoin 76-80 thrombomodulin Homo sapiens 0-2
7878635-6 1994 Since the TM antigen levels in the ATRA-treated cells also paralleled the TM mRNA levels, the data suggests that TM induction in the HL-60 cells cultured with ATRA reflected the levels of TM biosynthesis and was independent of HL-60 differentiation into neutrophilic cells. Tretinoin 35-39 thrombomodulin Homo sapiens 10-12
8063765-0 1994 Retinoic acid suppression of c-fos gene inhibits expression of tumor necrosis factor-alpha-induced monocyte chemoattractant JE/MCP-1 in clonal osteoblastic MC3T3-E1 cells. Tretinoin 0-13 FBJ osteosarcoma oncogene Mus musculus 29-34
8063765-8 1994 RA pretreatment transcriptionally suppressed the expression of the c-fos gene but not that of the c-jun gene in TNF-alpha-treated cells. Tretinoin 0-2 FBJ osteosarcoma oncogene Mus musculus 67-72
7697468-9 1994 Recently it has been shown that PML/RAR alpha can be modulated directly by ATRA. Tretinoin 75-79 PML nuclear body scaffold Homo sapiens 32-45
7735895-9 1994 Substances as fibrates, retinoic acid, polyunsaturated fatty acids activate specific types of receptors-PPAR (peroxisome proliferators activated receptors) belonging to the superfamily of receptors activated by steroid hormones, thyroid hormones, and D-vitamins. Tretinoin 24-37 peroxisome proliferator activated receptor alpha Homo sapiens 104-108
7979398-0 1994 Transforming growth factor-beta and insulin-like growth factor-1 restore proteoglycan metabolism of bovine articular cartilage after depletion by retinoic acid. Tretinoin 146-159 insulin like growth factor 1 Bos taurus 36-64
24522204-0 2014 Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells. Tretinoin 71-84 prohibitin 2 Homo sapiens 0-12
7979398-10 1994 TGF-beta (10 ng/ml) or IGF-1 (10 ng/ml) added for 7 days to serum-free medium following retinoic acid treatment led to recoveries of proteoglycan synthesis of 74 +/- 24% (n = 12) and 69 +/- 18% (n = 12), respectively, as compared to controls switched from serum-free conditions to corresponding cytokine treatments. Tretinoin 88-101 insulin like growth factor 1 Bos taurus 23-28
7963135-5 1994 The biosynthesis of retinoic acid (RA) from beta-C via central and eccentric cleavage pathways is reviewed. Tretinoin 20-33 colony stimulating factor 2 receptor subunit beta Homo sapiens 44-50
24769646-0 2014 Sensitivity of MLL-rearranged AML cells to all-trans retinoic acid is associated with the level of H3K4me2 in the RARalpha promoter region. Tretinoin 53-66 lysine methyltransferase 2A Homo sapiens 15-18
8034721-4 1994 No structural information is available concerning the nature of the amino acids which are responsible for binding of RA within the ligand binding domain of any RAR. Tretinoin 117-119 retinoic acid receptor alpha Homo sapiens 160-163
7524761-0 1994 All-trans retinoic acid directly inhibits granulocyte colony-stimulating factor-induced proliferation of CD34+ human hematopoietic progenitor cells. Tretinoin 10-23 colony stimulating factor 3 Homo sapiens 42-79
7524761-6 1994 Retinoids also significantly inhibited G-CSF-induced colony formation in semisolid medium, with 88% inhibition observed at a concentration of retinoic acid of 1 mumol/L. Tretinoin 142-155 colony stimulating factor 3 Homo sapiens 39-44
8034721-9 1994 Furthermore, this double mutant RAR-beta acted as a dominant negative mutant when transfected with wild type RAR-alpha, -beta, or -gamma in a RA concentration-dependent fashion. Tretinoin 32-34 retinoic acid receptor alpha Homo sapiens 109-118
24769646-0 2014 Sensitivity of MLL-rearranged AML cells to all-trans retinoic acid is associated with the level of H3K4me2 in the RARalpha promoter region. Tretinoin 53-66 retinoic acid receptor alpha Homo sapiens 114-122
24769646-1 2014 All-trans retinoic acid (ATRA) is well established as differentiation therapy for acute promyelocytic leukemia (APL) in which the PML-RARalpha (promyelocytic leukemia-retinoic acid receptor alpha) fusion protein causes blockade of the retinoic acid (RA) pathway; however, in types of acute myeloid leukemia (AML) other than APL, the mechanism of RA pathway inactivation is not fully understood. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 134-142
7935794-7 1994 Moreover, Shh expression in mesenchyme can be activated by FGF4 in combination with retinoic acid. Tretinoin 84-97 sonic hedgehog Mus musculus 10-13
24769646-1 2014 All-trans retinoic acid (ATRA) is well established as differentiation therapy for acute promyelocytic leukemia (APL) in which the PML-RARalpha (promyelocytic leukemia-retinoic acid receptor alpha) fusion protein causes blockade of the retinoic acid (RA) pathway; however, in types of acute myeloid leukemia (AML) other than APL, the mechanism of RA pathway inactivation is not fully understood. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 134-142
24769646-1 2014 All-trans retinoic acid (ATRA) is well established as differentiation therapy for acute promyelocytic leukemia (APL) in which the PML-RARalpha (promyelocytic leukemia-retinoic acid receptor alpha) fusion protein causes blockade of the retinoic acid (RA) pathway; however, in types of acute myeloid leukemia (AML) other than APL, the mechanism of RA pathway inactivation is not fully understood. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 134-142
24769646-1 2014 All-trans retinoic acid (ATRA) is well established as differentiation therapy for acute promyelocytic leukemia (APL) in which the PML-RARalpha (promyelocytic leukemia-retinoic acid receptor alpha) fusion protein causes blockade of the retinoic acid (RA) pathway; however, in types of acute myeloid leukemia (AML) other than APL, the mechanism of RA pathway inactivation is not fully understood. Tretinoin 27-29 retinoic acid receptor alpha Homo sapiens 134-142
8207015-0 1994 Characterization of thrombomodulin expression in response to retinoic acid and identification of a retinoic acid response element in the human thrombomodulin gene. Tretinoin 61-74 thrombomodulin Homo sapiens 20-34
8207015-0 1994 Characterization of thrombomodulin expression in response to retinoic acid and identification of a retinoic acid response element in the human thrombomodulin gene. Tretinoin 99-112 thrombomodulin Homo sapiens 143-157
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 95-103
8207015-2 1994 We have observed that the expression of TM mRNA in response to retinoic acid was markedly increased in human U937 monoblast-like cells, and human MEG01 megakaryocyte-like cells, but not in human umbilical vein cells, murine hemangioma cells, human K562 erythroblast-like cells, and murine HSD fibroblast-like cells. Tretinoin 63-76 thrombomodulin Homo sapiens 40-42
7923112-6 1994 Decreased expression of the N-myc oncogene in neuroblastoma cell lines SH-SY5Y and BE(2)-C, following treatment with retinoic acid, was paralleled by down-regulation of MRP gene expression, contrasting with increased expression of the MDR1 gene. Tretinoin 117-130 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 28-33
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 CCAAT enhancer binding protein epsilon Homo sapiens 117-123
7889981-4 1994 In normal HL-60 cells retinoic acid is known to induce a colony-stimulating factor-1 (CSF-1)-dependent metabolic cascade culminating in G0 arrest and phenotypic conversion. Tretinoin 22-35 colony stimulating factor 1 Homo sapiens 57-84
7889981-4 1994 In normal HL-60 cells retinoic acid is known to induce a colony-stimulating factor-1 (CSF-1)-dependent metabolic cascade culminating in G0 arrest and phenotypic conversion. Tretinoin 22-35 colony stimulating factor 1 Homo sapiens 86-91
8202477-5 1994 However, in the presence of RA (100 nM), a PAF-dependent (1-50 nM) synergistic activation of luciferase reporter constructs driven by regulatory regions of the TIS10/PGS-2 gene was found. Tretinoin 28-30 PCNA clamp associated factor Homo sapiens 43-46
8202477-5 1994 However, in the presence of RA (100 nM), a PAF-dependent (1-50 nM) synergistic activation of luciferase reporter constructs driven by regulatory regions of the TIS10/PGS-2 gene was found. Tretinoin 28-30 decorin Homo sapiens 166-171
24722286-0 2014 MicroRNA-181a-mediated downregulation of AC9 protein decreases intracellular cAMP level and inhibits ATRA-induced APL cell differentiation. Tretinoin 101-105 adenylate cyclase 9 Homo sapiens 41-44
8050357-6 1994 Igf2, H19 and Igf2r were all appropriately expressed in the PGES derived cells following induction of differentiation in vitro with all-trans retinoic acid or DMSO, when compared with control (D3) and androgenetic ES cells (AGES). Tretinoin 142-155 insulin like growth factor 2 Homo sapiens 0-4
8050357-6 1994 Igf2, H19 and Igf2r were all appropriately expressed in the PGES derived cells following induction of differentiation in vitro with all-trans retinoic acid or DMSO, when compared with control (D3) and androgenetic ES cells (AGES). Tretinoin 142-155 insulin like growth factor 2 receptor Homo sapiens 14-19
7934172-0 1994 Induction of high-affinity GM-CSF receptors during all-trans retinoic acid treatment of acute promyelocytic leukemia. Tretinoin 61-74 colony stimulating factor 2 Homo sapiens 27-33
7934172-5 1994 The data presented show that modulation of GM-CSF receptors cells is correlated to the degree of ATRA-induced granulocytic differentiation but not to increased cell growth. Tretinoin 97-101 colony stimulating factor 2 Homo sapiens 43-49
24722286-4 2014 Knockdown of AC9 in APL cell line NB4 could obviously inhibit ATRA-induced differentiation. Tretinoin 62-66 adenylate cyclase 9 Homo sapiens 13-16
24524833-5 2014 INTERVENTION(S): Measurement of the three enzymes necessary for retinoic acid biosynthesis, aldehyde dehydrogenase (ALDH) 1A1, 1A2, and 1A3, in testicular tissue by a novel liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) peptide assay. Tretinoin 64-77 aldehyde dehydrogenase 1 family member A1 Homo sapiens 92-125
7754440-1 1994 PURPOSE: To assess the results attained with all-trans-retinoic acid (ATRA) in a group of Cuban patients with acute promyelocytic leukaemia (PML). Tretinoin 45-68 PML nuclear body scaffold Homo sapiens 141-144
7754440-1 1994 PURPOSE: To assess the results attained with all-trans-retinoic acid (ATRA) in a group of Cuban patients with acute promyelocytic leukaemia (PML). Tretinoin 70-74 PML nuclear body scaffold Homo sapiens 141-144
7754440-20 1994 The efficacy of ATRA, in general terms, in the induction of CR in PML seems confirmed by these results. Tretinoin 16-20 PML nuclear body scaffold Homo sapiens 66-69
8200985-9 1994 The upregulation of VEGF expression by PGE2 in the preosteoblastic RCT-1 cells was potentiated by treatment with retinoic acid, which induces the differentiation of these cells. Tretinoin 113-126 vascular endothelial growth factor A Rattus norvegicus 20-24
8176254-0 1994 Retinoic acid induces expression of early growth response gene-1 (Egr-1) in human skin in vivo and in cultured skin fibroblasts. Tretinoin 0-13 early growth response 1 Homo sapiens 36-64
24659788-3 2014 RA production by CD103(+) dendritic cells and alveolar macrophages functions with TGF-beta to promote conversion of naive T cells into Foxp3(+) regulatory T cells and, thereby, maintain mucosal tolerance. Tretinoin 0-2 forkhead box P3 Mus musculus 135-140
8176254-0 1994 Retinoic acid induces expression of early growth response gene-1 (Egr-1) in human skin in vivo and in cultured skin fibroblasts. Tretinoin 0-13 early growth response 1 Homo sapiens 66-71
8176254-2 1994 Retinoic acid has been shown to markedly induce Egr-1 gene expression in mouse embryonal carcinoma cells and rat preosteoblastic cells. Tretinoin 0-13 early growth response 1 Mus musculus 48-53
8176254-3 1994 In this study we demonstrate that treatment of cultured human skin fibroblasts with retinoic acid results in a rapid transient four-fold induction of Egr-1 transcripts, being maximum at 60 min and returning to a basal level by 120 min. Tretinoin 84-97 early growth response 1 Homo sapiens 150-155
8176254-6 1994 Topical application of 0.1% retinoic acid cream in vivo resulted in a two- to threefold induction of Egr-1 transcripts following treatment for 24 and 48 h, returning to nearly basal levels by 96 h. Taken together, these data are consistent with the possibility that Egr-1 is a proximal component of an intracellular molecular cascade that may give rise to alterations in cell phenotype in response to retinoic acid. Tretinoin 28-41 early growth response 1 Homo sapiens 101-106
8176254-6 1994 Topical application of 0.1% retinoic acid cream in vivo resulted in a two- to threefold induction of Egr-1 transcripts following treatment for 24 and 48 h, returning to nearly basal levels by 96 h. Taken together, these data are consistent with the possibility that Egr-1 is a proximal component of an intracellular molecular cascade that may give rise to alterations in cell phenotype in response to retinoic acid. Tretinoin 28-41 early growth response 1 Homo sapiens 266-271
8176254-6 1994 Topical application of 0.1% retinoic acid cream in vivo resulted in a two- to threefold induction of Egr-1 transcripts following treatment for 24 and 48 h, returning to nearly basal levels by 96 h. Taken together, these data are consistent with the possibility that Egr-1 is a proximal component of an intracellular molecular cascade that may give rise to alterations in cell phenotype in response to retinoic acid. Tretinoin 401-414 early growth response 1 Homo sapiens 101-106
8083217-0 1994 Induction of human interleukin-1 gene expression by retinoic acid and its regulation at processing of precursor transcripts. Tretinoin 52-65 interleukin 1 alpha Homo sapiens 19-32
8083217-1 1994 Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tretinoin 0-13 interleukin 1 alpha Homo sapiens 123-142
8083217-1 1994 Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tretinoin 0-13 interleukin 1 alpha Homo sapiens 144-154
8083217-1 1994 Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tretinoin 15-17 interleukin 1 alpha Homo sapiens 123-142
8083217-1 1994 Retinoic acid (RA), we show, induces in peripheral blood mononuclear cells a transient wave of newly transcribed, unstable interleukin-1 alpha (IL-1 alpha) and IL-1 beta mRNA. Tretinoin 15-17 interleukin 1 alpha Homo sapiens 144-154
8069853-1 1994 To elucidate the regulation of protein phosphatases types 1 (PP1) and 2A (PP2A) during all-trans retinoic acid (ATRA)-induced granulocytic differentiation of HL-60 cells, the phosphatase activity, proteins, and gene expressions of PP1 and PP2A were examined. Tretinoin 97-110 protein phosphatase 2 phosphatase activator Homo sapiens 74-78
8069853-1 1994 To elucidate the regulation of protein phosphatases types 1 (PP1) and 2A (PP2A) during all-trans retinoic acid (ATRA)-induced granulocytic differentiation of HL-60 cells, the phosphatase activity, proteins, and gene expressions of PP1 and PP2A were examined. Tretinoin 112-116 protein phosphatase 2 phosphatase activator Homo sapiens 74-78
8069853-2 1994 Treatment with 1 microM ATRA caused an 85% decrease in the PP2A activity in extracts from HL-60 cells, while the PP1 activity was constant. Tretinoin 24-28 protein phosphatase 2 phosphatase activator Homo sapiens 59-63
8069853-3 1994 This reduction in PP2A activity appeared to parallel phenotypic and functional changes of HL-60 cells induced by ATRA. Tretinoin 113-117 protein phosphatase 2 phosphatase activator Homo sapiens 18-22
7918086-3 1994 The RAR alpha rearranged band in the Southern blot analysis and a chimaeric product of PML-RAR alpha by polymerase chain reaction were strongly visible before ATRA treatment, but at the time of maximal basophilia both of them were markedly diminished. Tretinoin 159-163 retinoic acid receptor alpha Homo sapiens 4-13
7912076-4 1994 In B16-ML8 cells, retinoic acid reduced mts1 expression together with a reduction of p53 positivity. Tretinoin 18-31 transformation related protein 53, pseudogene Mus musculus 85-88
8069853-4 1994 Western blot analysis showed that the level of PP2A catalytic subunit (PP2A-C) decreased during the course of ATRA-induced differentiation, whereas expressions of A and B (M(r) 55,000) regulatory subunits of PP2A were relatively unaltered. Tretinoin 110-114 protein phosphatase 2 catalytic subunit alpha Homo sapiens 47-69
24406248-5 2014 ATRA treatment caused decreased Mcl-1, caspase-3 activation, and PARP cleavage following the inactivation of phosphatidylinositol 3-kinase/AKT and the activation of GSK-3beta. Tretinoin 0-4 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 32-37
8069853-4 1994 Western blot analysis showed that the level of PP2A catalytic subunit (PP2A-C) decreased during the course of ATRA-induced differentiation, whereas expressions of A and B (M(r) 55,000) regulatory subunits of PP2A were relatively unaltered. Tretinoin 110-114 protein phosphatase 2 catalytic subunit alpha Homo sapiens 71-77
8069853-4 1994 Western blot analysis showed that the level of PP2A catalytic subunit (PP2A-C) decreased during the course of ATRA-induced differentiation, whereas expressions of A and B (M(r) 55,000) regulatory subunits of PP2A were relatively unaltered. Tretinoin 110-114 protein phosphatase 2 phosphatase activator Homo sapiens 47-51
8069853-6 1994 Northern blot analysis revealed that mRNA levels of PP2A-C beta and A alpha regulatory subunits were decreased following treatment with ATRA, while levels of PP2A-C alpha and B (M(r) 55,000) alpha regulatory subunit transcripts were relatively constant. Tretinoin 136-140 protein phosphatase 2 catalytic subunit alpha Homo sapiens 52-58
24406248-6 2014 Pharmacologically and genetically inhibiting GSK-3beta effectively retarded ATRA-induced Mcl-1 degradation and apoptosis. Tretinoin 76-80 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 89-94
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 17-21 pleckstrin Homo sapiens 133-142
21566987-5 1994 Further experiments indicated that interleukin 1 (IL-1), one of the mediators of LPS activity, also synergized with t-RA to stimulate G-CSF secretion. Tretinoin 116-120 interleukin 1 alpha Homo sapiens 35-54
21566987-5 1994 Further experiments indicated that interleukin 1 (IL-1), one of the mediators of LPS activity, also synergized with t-RA to stimulate G-CSF secretion. Tretinoin 116-120 colony stimulating factor 3 Homo sapiens 134-139
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 17-21 pleckstrin Homo sapiens 137-141
8071352-4 1994 We also determined whether retinoic acid (RA) altered this IL-11 production. Tretinoin 27-40 interleukin 11 Homo sapiens 59-64
8071352-4 1994 We also determined whether retinoic acid (RA) altered this IL-11 production. Tretinoin 42-44 interleukin 11 Homo sapiens 59-64
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 172-176 pleckstrin Homo sapiens 133-142
24406248-8 2014 Mechanistically, ATRA caused the generation of reactive oxygen species (ROS) through increased expression of NADPH oxidase subunits (p47(phox) and p67(phox)) to facilitate ATRA-induced GSK-3beta activation and cell apoptosis. Tretinoin 172-176 pleckstrin Homo sapiens 137-141
24596215-1 2014 PML-RARA degradation and PML nuclear body reformation underlie APL clearance by retinoic acid (RA). Tretinoin 80-93 PML nuclear body scaffold Homo sapiens 0-3
7982090-1 1994 The BE (2)-M17 human neuroblastoma has previously been shown to express corticotropin-releasing factor (CRF) mRNA following retinoic acid treatment. Tretinoin 124-137 corticotropin releasing hormone Homo sapiens 72-102
8053676-3 1994 Retinoic acid was not detected when a boiled incubation mixture was incubated in the presence of 9-cis-beta-C. Tretinoin 0-13 colony stimulating factor 2 receptor subunit beta Homo sapiens 103-109
8056833-10 1994 RA inhibition of UVB-induced melanogenesis acts at the post-transcriptional level leading to a decreased tyrosinase and TRP-1 synthesis. Tretinoin 0-2 tyrosinase Mus musculus 105-115
8200851-4 1994 For the samples in group C, RA inhibited the colonies formed by granulocyte colony-stimulating factor (G-CSF) but stimulated those by granulocyte macrophage CSF (GM-CSF). Tretinoin 28-30 colony stimulating factor 3 Homo sapiens 64-101
8200851-4 1994 For the samples in group C, RA inhibited the colonies formed by granulocyte colony-stimulating factor (G-CSF) but stimulated those by granulocyte macrophage CSF (GM-CSF). Tretinoin 28-30 colony stimulating factor 3 Homo sapiens 103-108
8200851-4 1994 For the samples in group C, RA inhibited the colonies formed by granulocyte colony-stimulating factor (G-CSF) but stimulated those by granulocyte macrophage CSF (GM-CSF). Tretinoin 28-30 colony stimulating factor 2 Homo sapiens 105-108
8200851-4 1994 For the samples in group C, RA inhibited the colonies formed by granulocyte colony-stimulating factor (G-CSF) but stimulated those by granulocyte macrophage CSF (GM-CSF). Tretinoin 28-30 colony stimulating factor 2 Homo sapiens 162-168
8200851-8 1994 This finding supports the hypothesis that the increase of GMR is one of the causes of the stimulative effects of RA on cells cultured with GM-CSF in group C. Tretinoin 113-115 colony stimulating factor 2 Homo sapiens 139-145
8050571-0 1994 Retinoic acid up-regulates erythropoietin production in hepatoma cells and in vitamin A-depleted rats. Tretinoin 0-13 erythropoietin Rattus norvegicus 27-41
8050571-4 1994 Oral administration of RA to the vitamin A-depleted rats elevated the concentration of Epo in serum. Tretinoin 23-25 erythropoietin Rattus norvegicus 87-90
24596215-1 2014 PML-RARA degradation and PML nuclear body reformation underlie APL clearance by retinoic acid (RA). Tretinoin 80-93 PML nuclear body scaffold Homo sapiens 25-28
8050575-1 1994 Uteroglobin, a progesterone-binding secretory protein, was shown to bind retinoic acid and retinol in a non-saturable manner, at least up to concentrations of retinoids of 20 microM. Tretinoin 73-86 secretoglobin family 1A member 1 Homo sapiens 0-11
7518821-3 1994 In the present report we study the effects of epidermal growth factor (EGF) and all-trans-retinoic acid (RA) on IGFBP-3 RNA and protein levels in human papillomavirus-immortalized cervical epithelial cells. Tretinoin 80-103 insulin like growth factor binding protein 3 Homo sapiens 112-119
8152308-6 1994 We expressed the PML/RAR alpha protein in U937 myeloid precursor cell line and show that they: 1) lose the capacity to differentiate under the action of different stimuli (vitamin D3, transforming growth factor beta 1); ii) acquire enhanced sensitivity to retinoic acid; iii) exhibit a higher growth rate that is due to a reduction in apoptotic cell death. Tretinoin 256-269 PML nuclear body scaffold Homo sapiens 17-30
7518821-3 1994 In the present report we study the effects of epidermal growth factor (EGF) and all-trans-retinoic acid (RA) on IGFBP-3 RNA and protein levels in human papillomavirus-immortalized cervical epithelial cells. Tretinoin 105-107 insulin like growth factor binding protein 3 Homo sapiens 112-119
24596215-1 2014 PML-RARA degradation and PML nuclear body reformation underlie APL clearance by retinoic acid (RA). Tretinoin 4-6 PML nuclear body scaffold Homo sapiens 0-3
7518821-5 1994 In contrast, 1 microM RA increases IGFBP-3 mRNA and protein levels in the presence or absence of 20 ng/ml EGF. Tretinoin 22-24 insulin like growth factor binding protein 3 Homo sapiens 35-42
7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 16-29 colony stimulating factor 3 Homo sapiens 323-328
7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 31-35 colony stimulating factor 3 Homo sapiens 323-328
7518821-8 1994 Conversely, when cells are treated with RA, IGFBP-3 levels increase within 24 h and subsequent addition of EGF is without effect. Tretinoin 40-42 insulin like growth factor binding protein 3 Homo sapiens 44-51
7518821-8 1994 Conversely, when cells are treated with RA, IGFBP-3 levels increase within 24 h and subsequent addition of EGF is without effect. Tretinoin 40-42 epidermal growth factor Homo sapiens 107-110
7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 314-318 colony stimulating factor 3 Homo sapiens 41-78
24325348-9 2014 These results provided more evidence for the signal messenger role of RA in cyp26a1 regulation from the other side. Tretinoin 70-72 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 76-83
7510354-1 1994 Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. Tretinoin 314-318 colony stimulating factor 3 Homo sapiens 80-85
8149912-4 1994 Both chi alpha 1 and chi delta 1 were comparable in their ability to stimulate transcription of a synthetic reporter construct through a RA response element after activation with T3 in situ. Tretinoin 137-139 adrenoceptor alpha 1D Homo sapiens 9-32
7518821-9 1994 Thus, the RA-dependent increase in IGFBP-3 levels is dominant over the EGF suppression. Tretinoin 10-12 insulin like growth factor binding protein 3 Homo sapiens 35-42
7518821-11 1994 Similar RA effects on IGFBP-3 mRNA levels were observed in other cervical epithelial cell lines (i.e., ECE16-D1, ECE16-D2, and CaSki). Tretinoin 8-10 insulin like growth factor binding protein 3 Homo sapiens 22-29
7518821-12 1994 These results suggest that RA may act to inhibit cervical cell growth by increasing IGFBP-3 levels and reducing the extracellular concentration of free insulin-like growth factor I (IGFI) and/or alternatively, IGFBP-3 may inhibit cell growth by direct effects on the cell, independent of IGFI. Tretinoin 27-29 insulin like growth factor binding protein 3 Homo sapiens 84-91
7518821-12 1994 These results suggest that RA may act to inhibit cervical cell growth by increasing IGFBP-3 levels and reducing the extracellular concentration of free insulin-like growth factor I (IGFI) and/or alternatively, IGFBP-3 may inhibit cell growth by direct effects on the cell, independent of IGFI. Tretinoin 27-29 insulin like growth factor binding protein 3 Homo sapiens 210-217
7913468-8 1994 The mutated RAR can suppress the wild-type RAR function, especially at the physiological concentration of retinoic acid. Tretinoin 106-119 retinoic acid receptor alpha Homo sapiens 12-15
7913468-8 1994 The mutated RAR can suppress the wild-type RAR function, especially at the physiological concentration of retinoic acid. Tretinoin 106-119 retinoic acid receptor alpha Homo sapiens 43-46
24470498-5 2014 Retinoic acid-stimulated endothelial cells promoted dendritic cell adhesion under shear stress conditions and transmigration in a ChemR23-dependent manner. Tretinoin 0-13 chemokine-like receptor 1 Mus musculus 130-137
7979182-3 1994 The expression of the hyperphosphorylated retinoblastoma protein species (RB p110) was observed to be increased fivefold to tenfold in NSCLC cells within 16 h of exposure to retinoic acid. Tretinoin 174-187 spliceosome associated factor 3, U4/U6 recycling protein Homo sapiens 77-81
7979182-4 1994 In the H460a and H226b cell lines, p110 showed some conversion to the underphosphorylated p105 form after 24 h of retinoic acid treatment. Tretinoin 114-127 spliceosome associated factor 3, U4/U6 recycling protein Homo sapiens 35-39
7979182-8 1994 In these cells, both p110 and p105 were induced within 8 h of retinoic acid treatment. Tretinoin 62-75 spliceosome associated factor 3, U4/U6 recycling protein Homo sapiens 21-25
8106754-0 1994 In vivo prevention of corticosteroid-induced skin atrophy by tretinoin in the hairless mouse is accompanied by modulation of collagen, glycosaminoglycans, and fibronectin. Tretinoin 61-70 fibronectin 1 Mus musculus 159-170
8106754-11 1994 Fibronectin, which was increased by the steroid:vehicle treatment, was reduced to more normal levels by steroid:tretinoin. Tretinoin 112-121 fibronectin 1 Mus musculus 0-11
8290265-0 1994 The PML-RAR alpha gene product of the t(15;17) translocation inhibits retinoic acid-induced granulocytic differentiation and mediated transactivation in human myeloid cells. Tretinoin 70-83 PML nuclear body scaffold Homo sapiens 4-7
8290265-0 1994 The PML-RAR alpha gene product of the t(15;17) translocation inhibits retinoic acid-induced granulocytic differentiation and mediated transactivation in human myeloid cells. Tretinoin 70-83 retinoic acid receptor alpha Homo sapiens 8-17
8290265-3 1994 In non hematopoietic cells, the transfected PML-RAR alpha product binds all trans retinoic acid and exhibits altered transactivating properties when compared with RAR alpha. Tretinoin 82-95 PML nuclear body scaffold Homo sapiens 44-47
8290265-3 1994 In non hematopoietic cells, the transfected PML-RAR alpha product binds all trans retinoic acid and exhibits altered transactivating properties when compared with RAR alpha. Tretinoin 82-95 retinoic acid receptor alpha Homo sapiens 48-57
8290265-5 1994 We find that in myeloid cell lines responsive to retinoic acid, PML-RAR alpha blocks retinoic acid mediated transactivation and totally abrogates the retinoic acid mediated granulocytic differentiation. Tretinoin 49-62 PML nuclear body scaffold Homo sapiens 64-67
8290265-5 1994 We find that in myeloid cell lines responsive to retinoic acid, PML-RAR alpha blocks retinoic acid mediated transactivation and totally abrogates the retinoic acid mediated granulocytic differentiation. Tretinoin 49-62 retinoic acid receptor alpha Homo sapiens 68-77
8290265-5 1994 We find that in myeloid cell lines responsive to retinoic acid, PML-RAR alpha blocks retinoic acid mediated transactivation and totally abrogates the retinoic acid mediated granulocytic differentiation. Tretinoin 85-98 PML nuclear body scaffold Homo sapiens 64-67
8290265-5 1994 We find that in myeloid cell lines responsive to retinoic acid, PML-RAR alpha blocks retinoic acid mediated transactivation and totally abrogates the retinoic acid mediated granulocytic differentiation. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 68-77
8018933-3 1994 Similarly, HL-60 cells pretreated with retinoic acid or 1,25 dihydroxyvitamin D3 were also capable of responding to GM-CSF. Tretinoin 39-52 colony stimulating factor 2 Homo sapiens 116-122
24470498-9 2014 In conclusion, this study reports that retinoic acid-activated endothelial cells can promote myeloid and plasmacytoid dendritic cell transmigration across endothelial cell monolayers through the endogenous production of chemerin, the upregulation of CCRL2, and the activation of dendritic cell beta1 integrin affinity. Tretinoin 39-52 chemokine (C-C motif) receptor-like 2 Mus musculus 250-255
8020193-0 1994 Retinoic acid effects on endothelial cell function: interaction with interleukin 1. Tretinoin 0-13 interleukin 1 alpha Homo sapiens 69-82
8020193-3 1994 To explore alternate hypotheses, we examined the interaction of retinoic acid and IL-1 on endothelial cell (EC) function and found that RA directly affects and modifies the effects of IL-1 on EC proliferation, prostacyclin production, and plasminogen activator inhibitor capacity (PAI-1). Tretinoin 136-138 interleukin 1 alpha Homo sapiens 82-86
8290265-5 1994 We find that in myeloid cell lines responsive to retinoic acid, PML-RAR alpha blocks retinoic acid mediated transactivation and totally abrogates the retinoic acid mediated granulocytic differentiation. Tretinoin 85-98 PML nuclear body scaffold Homo sapiens 64-67
8290265-5 1994 We find that in myeloid cell lines responsive to retinoic acid, PML-RAR alpha blocks retinoic acid mediated transactivation and totally abrogates the retinoic acid mediated granulocytic differentiation. Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 68-77
8290265-7 1994 The fact that high doses of all-trans retinoic acid relieve the inhibitory effect of PML-RAR alpha corroborates the therapeutic effect of all-trans retinoic acid in APL patients. Tretinoin 32-51 PML nuclear body scaffold Homo sapiens 85-88
8020193-3 1994 To explore alternate hypotheses, we examined the interaction of retinoic acid and IL-1 on endothelial cell (EC) function and found that RA directly affects and modifies the effects of IL-1 on EC proliferation, prostacyclin production, and plasminogen activator inhibitor capacity (PAI-1). Tretinoin 136-138 interleukin 1 alpha Homo sapiens 184-188
8020193-3 1994 To explore alternate hypotheses, we examined the interaction of retinoic acid and IL-1 on endothelial cell (EC) function and found that RA directly affects and modifies the effects of IL-1 on EC proliferation, prostacyclin production, and plasminogen activator inhibitor capacity (PAI-1). Tretinoin 136-138 serpin family E member 1 Homo sapiens 281-286
8290265-7 1994 The fact that high doses of all-trans retinoic acid relieve the inhibitory effect of PML-RAR alpha corroborates the therapeutic effect of all-trans retinoic acid in APL patients. Tretinoin 32-51 retinoic acid receptor alpha Homo sapiens 89-98
24357327-9 2014 Thus, diminished 22q11 gene dosage, including but not limited to Tbx1, disrupts oro-facial and CN development by modifying RA-modulated anterior-posterior hindbrain differentiation. Tretinoin 123-125 T-box 1 Mus musculus 65-69
8302850-3 1994 In transient-expression assays, both the PLZF(A)-RAR alpha and PLZF(B)-RAR alpha fusion proteins like the PML-RAR alpha protein resulting from the well-known t(15;17) translocation in APL, antagonized endogenous and transfected wild-type RAR alpha in the presence of retinoic acid. Tretinoin 267-280 retinoic acid receptor alpha Homo sapiens 71-80
8302850-3 1994 In transient-expression assays, both the PLZF(A)-RAR alpha and PLZF(B)-RAR alpha fusion proteins like the PML-RAR alpha protein resulting from the well-known t(15;17) translocation in APL, antagonized endogenous and transfected wild-type RAR alpha in the presence of retinoic acid. Tretinoin 267-280 retinoic acid receptor alpha Homo sapiens 71-80
8302850-3 1994 In transient-expression assays, both the PLZF(A)-RAR alpha and PLZF(B)-RAR alpha fusion proteins like the PML-RAR alpha protein resulting from the well-known t(15;17) translocation in APL, antagonized endogenous and transfected wild-type RAR alpha in the presence of retinoic acid. Tretinoin 267-280 retinoic acid receptor alpha Homo sapiens 71-80
8020193-6 1994 With respect to EC prostacyclin production, although retinoic acid alone had no effect, cis and trans-retinoic acid and retinol all induced a dose-dependent increase in IL-1-mediated prostacyclin production, which was most marked at higher concentrations (20 U/ml) of IL-1. Tretinoin 53-66 interleukin 1 alpha Homo sapiens 169-173
8020193-8 1994 With respect to plasminogen activator inhibitor capacity, both IL-1 and retinoic acid stimulated EC PAI-1 synthesis, but the individual effects were additive, with RA augmenting the known IL-1 effects on EC PAI-1 production. Tretinoin 72-85 serpin family E member 1 Homo sapiens 100-105
8020193-8 1994 With respect to plasminogen activator inhibitor capacity, both IL-1 and retinoic acid stimulated EC PAI-1 synthesis, but the individual effects were additive, with RA augmenting the known IL-1 effects on EC PAI-1 production. Tretinoin 164-166 interleukin 1 alpha Homo sapiens 188-192
8020193-8 1994 With respect to plasminogen activator inhibitor capacity, both IL-1 and retinoic acid stimulated EC PAI-1 synthesis, but the individual effects were additive, with RA augmenting the known IL-1 effects on EC PAI-1 production. Tretinoin 164-166 serpin family E member 1 Homo sapiens 207-212
8020193-9 1994 The interaction between RA and IL-1 on the endothelium, described in this study, may play a role in the fashion through which retinoic acid alters the expression of synovitis in certain types of experimental inflammatory arthritis. Tretinoin 126-139 interleukin 1 alpha Homo sapiens 31-35
8058062-11 1994 When the AHD-M1 and AHD-2 cDNAs were inserted into the expression vector pSG5 and transfected into cultured COS cells, 3-5-fold and 100-fold increases, respectively, in the conversion of [3H]retinaldehyde to [3H]retinoic acid could be detected by high performance liquid chromatographic assay. Tretinoin 212-225 aldehyde dehydrogenase 2, mitochondrial Mus musculus 9-15
8302850-6 1994 These abnormal transactivation properties observed in retinoic acid-sensitive myeloid cells strongly implicate the PLZF-RAR alpha fusion proteins in the molecular pathogenesis of APL. Tretinoin 54-67 retinoic acid receptor alpha Homo sapiens 120-129
8022710-6 1994 Androgen-induced levels of both prostate-specific antigen (PSA) and human glandular kallikrein-1 (hKLK2) mRNAs were significantly repressed by RA in a dose- and time-dependent manner. Tretinoin 143-145 kallikrein related peptidase 3 Homo sapiens 32-63
24265455-3 2014 In this study we demonstrate that all-trans retinoic acid (atRA) enhances StAR expression, but not its phosphorylation (P-StAR), and progesterone production in MA-10 mouse Leydig cells. Tretinoin 44-57 steroidogenic acute regulatory protein Mus musculus 74-78
8022710-7 1994 Consistent with this finding, androgen induction of PSA glycoprotein was also repressed by RA, with maximal inhibition occurring at 10(-5) M. These data suggest that the suppression of proliferation and function of prostatic cells by RA may be via modulatory effects on the AR. Tretinoin 91-93 kallikrein related peptidase 3 Homo sapiens 52-55
8022710-7 1994 Consistent with this finding, androgen induction of PSA glycoprotein was also repressed by RA, with maximal inhibition occurring at 10(-5) M. These data suggest that the suppression of proliferation and function of prostatic cells by RA may be via modulatory effects on the AR. Tretinoin 234-236 kallikrein related peptidase 3 Homo sapiens 52-55
8024563-3 1994 We investigated, in cultured normal human keratinocytes (NHK), the effects of retinoic acid (RA) and synthetic analogs on the regulation of the CYP1A1 gene. Tretinoin 78-91 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 144-150
8293468-0 1994 Retinoic acid regulates aberrant nuclear localization of PML-RAR alpha in acute promyelocytic leukemia cells. Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 57-60
8293468-0 1994 Retinoic acid regulates aberrant nuclear localization of PML-RAR alpha in acute promyelocytic leukemia cells. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 61-70
8293468-2 1994 The involvement of RAR alpha is particularly intriguing in view of the efficient therapeutic effect of retinoic acid (RA) in this disease. Tretinoin 103-116 retinoic acid receptor alpha Homo sapiens 19-28
8288643-3 1994 The element RE3 which is the major retinoic acid (RA) response element also binds the transcription factors HNF-4 and ARP-1. Tretinoin 35-48 ARP1 actin-related protein 1A, centractin alpha Mus musculus 118-123
8288643-3 1994 The element RE3 which is the major retinoic acid (RA) response element also binds the transcription factors HNF-4 and ARP-1. Tretinoin 50-52 ARP1 actin-related protein 1A, centractin alpha Mus musculus 118-123
8024563-3 1994 We investigated, in cultured normal human keratinocytes (NHK), the effects of retinoic acid (RA) and synthetic analogs on the regulation of the CYP1A1 gene. Tretinoin 93-95 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 144-150
24265455-3 2014 In this study we demonstrate that all-trans retinoic acid (atRA) enhances StAR expression, but not its phosphorylation (P-StAR), and progesterone production in MA-10 mouse Leydig cells. Tretinoin 59-63 steroidogenic acute regulatory protein Mus musculus 74-78
8207015-3 1994 TM activity in U937 cells and MEG01 cells was not detectable in untreated cells, but developed rapidly after treatment with retinoic acid. Tretinoin 124-137 thrombomodulin Homo sapiens 0-2
8123593-0 1994 All-trans-retinoic acid alters myc gene expression and inhibits in vitro progression in small cell lung cancer. Tretinoin 0-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 31-34
24394593-0 2014 A TDG/CBP/RARalpha ternary complex mediates the retinoic acid-dependent expression of DNA methylation-sensitive genes. Tretinoin 48-61 retinoic acid receptor alpha Homo sapiens 10-18
8123593-4 1994 We now report that treatment of NCI-H82 cells with 1 microM all-trans-retinoic acid resulted in decreased cellular growth, decreased c-myc mRNA levels, and increased L-myc mRNA levels. Tretinoin 60-83 MYC proto-oncogene, bHLH transcription factor Homo sapiens 133-138
8123593-7 1994 These data show that all-trans-retinoic acid, a clinically relevant compound, inhibits small cell lung cancer progression in our in vitro model and alters the expression of the c-myc and L-myc oncogenes. Tretinoin 21-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 177-182
8152429-2 1994 The retinoic acid receptor (RAR), as a heterodimer with the retinoid-x receptor (RXR), binds to DNA recognition sites, referred to as retinoic acid response elements (RAREs), that are generally composed of a direct repeat of the half-site core motif PuGGTCA spaced by 2 (DR-2) or 5 (DR-5) basepairs. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 28-31
8193365-0 1994 Retinoic acid-resistant HL-60 cells exclusively contain mutant retinoic acid receptor-alpha. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 63-91
24300824-7 2014 Mechanistically, ATRA was shown to elevate BMP9 expression and activate BMP/Smad signaling. Tretinoin 17-21 bone morphogenetic protein 1 Homo sapiens 43-46
8193365-1 1994 Sequence analysis of the retinoic acid receptor-alpha (RAR alpha) gene from a subline of HL-60 cells (RA-res) stably resistant to all-trans retinoic acid (RA) disclosed a single-base change in codon number 411, the same C to T transition previously reported in an independently selected HL-60 RA resistant clone by Robertson et al (Blood 80:1885, 1992). Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 55-64
8193365-1 1994 Sequence analysis of the retinoic acid receptor-alpha (RAR alpha) gene from a subline of HL-60 cells (RA-res) stably resistant to all-trans retinoic acid (RA) disclosed a single-base change in codon number 411, the same C to T transition previously reported in an independently selected HL-60 RA resistant clone by Robertson et al (Blood 80:1885, 1992). Tretinoin 55-57 retinoic acid receptor alpha Homo sapiens 25-53
8264595-4 1994 In a limited trypsin digestion assay, complexation of RAR alpha with retinoic acid or several other agonistic retinoids altered the degradation of the receptor such that a 30-kDa proteolytic fragment became resistant to proteolysis. Tretinoin 69-82 retinoic acid receptor alpha Homo sapiens 54-63
24300824-8 2014 Additionally, BMP9 and ATRA exerted a synergistic effect on activation of Wnt/beta-catenin signaling. Tretinoin 23-27 catenin beta 1 Homo sapiens 78-90
8269518-3 1993 Retinoic acid, which can convert anterior limb bud tissue into tissue with polarizing activity, concomitantly induces Sonic hedgehog expression in the anterior limb bud. Tretinoin 0-13 hedgehog Drosophila melanogaster 124-132
24300824-9 2014 Knockdown of beta-catenin abolished the stimulatory effect of ATRA on BMP9-induced alkaline phosphatase activity and reversed the inhibitory effect of ATRA on BMP9-induced adipogenesis in preadipocytes. Tretinoin 62-66 catenin beta 1 Homo sapiens 13-25
7522652-0 1994 Effect of in ovo retinoic acid exposure on forebrain neural crest: in vitro analysis reveals up-regulation of N-CAM and loss of mesenchymal phenotype. Tretinoin 17-30 neural cell adhesion molecule 1 Homo sapiens 110-115
24300824-9 2014 Knockdown of beta-catenin abolished the stimulatory effect of ATRA on BMP9-induced alkaline phosphatase activity and reversed the inhibitory effect of ATRA on BMP9-induced adipogenesis in preadipocytes. Tretinoin 151-155 catenin beta 1 Homo sapiens 13-25
7522652-1 1994 In a prior study of in ovo exogenous retinoic acid (RA) exposure, we observed a prolonged expression of cell surface N-CAM in cranial neural crest (NC) cells exhibiting migratory failure. Tretinoin 37-50 neural cell adhesion molecule 1 Homo sapiens 117-122
7522652-1 1994 In a prior study of in ovo exogenous retinoic acid (RA) exposure, we observed a prolonged expression of cell surface N-CAM in cranial neural crest (NC) cells exhibiting migratory failure. Tretinoin 52-54 neural cell adhesion molecule 1 Homo sapiens 117-122
7522652-7 1994 These observations indicate that RA modulates NC cell N-CAM expression and microanatomical phenotype, a finding consistent with prior in ovo studies of RA-exposure. Tretinoin 33-35 neural cell adhesion molecule 1 Homo sapiens 54-59
8280165-1 1993 P19 embryonal carcinoma cells can be induced to differentiate into neuron-like cells by retinoic acid. Tretinoin 88-101 interleukin 23 subunit alpha Homo sapiens 0-3
8280165-5 1993 Nuclease protection assays revealed a large quantitative induction of GluR6 transcripts following retinoic acid treatment. Tretinoin 98-111 glutamate ionotropic receptor kainate type subunit 2 Homo sapiens 70-75
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 phosphatase and tensin homolog Homo sapiens 225-229
8155579-4 1993 Higher doses of RA led to progressively more severe truncations in the brain and a loss of XLPOU 1 expression. Tretinoin 16-18 POU class 3 homeobox 1 S homeolog Xenopus laevis 91-98
8194470-0 1994 Regulation of interstitial collagenase expression and collagen degradation by retinoic acid in bone cells. Tretinoin 78-91 matrix metallopeptidase 1 Rattus norvegicus 14-38
8194470-2 1994 However, little is known about the effects of RA on the regulation of interstitial collagenase synthesis and collagen degradation. Tretinoin 46-48 matrix metallopeptidase 1 Rattus norvegicus 70-94
24300824-10 2014 Furthermore, ATRA and BMP9 synergistically repressed glycogen synthase kinase 3beta (GSK3beta) activity and promoted Akt phosphorylation, and inhibited expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) that antagonizes phosphatidylinositol-3-kinase (PI3K) function, suggesting that Wnt/beta-catenin signaling was activated at least partly through PI3K/Akt/GSK3beta pathway. Tretinoin 13-17 catenin beta 1 Homo sapiens 315-327
24300824-11 2014 Collectively, ATRA mediated BMP9-induced osteogenic or adipogenic differentiation of 3T3-L1 preadipocytes by BMP/Smad and Wnt/beta-catenin signaling. Tretinoin 14-18 bone morphogenetic protein 1 Homo sapiens 28-31
24300824-11 2014 Collectively, ATRA mediated BMP9-induced osteogenic or adipogenic differentiation of 3T3-L1 preadipocytes by BMP/Smad and Wnt/beta-catenin signaling. Tretinoin 14-18 catenin beta 1 Homo sapiens 126-138
24317203-0 2014 Connexin-dependent gap junction enhancement is involved in the synergistic effect of sorafenib and all-trans retinoic acid on HCC growth inhibition. Tretinoin 99-122 LOC100128922 Homo sapiens 0-8
7982904-0 1994 Retinoic acid-induced gene expression of tissue transglutaminase via protein kinase C-dependent pathway in mouse peritoneal macrophages. Tretinoin 0-13 transglutaminase 2, C polypeptide Mus musculus 41-64
7982904-1 1994 Culture of mouse resident peritoneal macrophages with retinoic acid resulted in increased expression of the tissue transglutaminase gene as revealed by increases in the maximal velocity of the enzyme reaction in the cytosol and in the enzyme mRNA level. Tretinoin 54-67 transglutaminase 2, C polypeptide Mus musculus 108-131
8145770-7 1993 However, direct in vitro phosphorylation of hRAR alpha by PKC diminished its ability to form heterodimeric or homodimeric complexes on a retinoic acid response element, suggesting that the DNA-binding capacity of hRAR alpha in intact cells is indirectly controlled by a PKC-dependent mechanism. Tretinoin 137-150 retinoic acid receptor alpha Homo sapiens 44-54
8145770-7 1993 However, direct in vitro phosphorylation of hRAR alpha by PKC diminished its ability to form heterodimeric or homodimeric complexes on a retinoic acid response element, suggesting that the DNA-binding capacity of hRAR alpha in intact cells is indirectly controlled by a PKC-dependent mechanism. Tretinoin 137-150 retinoic acid receptor alpha Homo sapiens 213-223
24516348-12 2014 By contrast, cell differentiation was stimulated by all trans retinoic acid (ATRA) (2.5micromol/L) at 24h after virus infection of pAd-NLS-RARalpha, and then detected by CD11b labeling two days later. Tretinoin 77-81 retinoic acid receptor alpha Homo sapiens 139-147
8218362-6 1993 In these studies a constitutively active PKC-gamma augmented the RA-mediated transactivation of a luciferase reporter containing the native RAR-beta promoter which has a retinoic-acid-response element (RARE). Tretinoin 65-67 protein kinase C gamma Homo sapiens 41-50
8218362-7 1993 These findings reveal that PKC pathway activation is an early step in RA-mediated human TC differentiation and that PKC-gamma can potentiate the effects of RA on RAR transcriptional activation. Tretinoin 70-72 protein kinase C gamma Homo sapiens 27-30
8218362-7 1993 These findings reveal that PKC pathway activation is an early step in RA-mediated human TC differentiation and that PKC-gamma can potentiate the effects of RA on RAR transcriptional activation. Tretinoin 156-158 protein kinase C gamma Homo sapiens 116-125
8218362-7 1993 These findings reveal that PKC pathway activation is an early step in RA-mediated human TC differentiation and that PKC-gamma can potentiate the effects of RA on RAR transcriptional activation. Tretinoin 156-158 retinoic acid receptor alpha Homo sapiens 162-165
8402688-10 1993 Conversely, stimulation of this I-type clone with retinoic acid resulted in an accumulation of N-type cells (which are thought to represent embryonic precursors of sympathetic neurons), decreased vimentin and beta-2-microglobulin, increased neurofilament-M, and a marked elevation in p26-Bcl-2. Tretinoin 50-63 vimentin Homo sapiens 196-204
8402688-10 1993 Conversely, stimulation of this I-type clone with retinoic acid resulted in an accumulation of N-type cells (which are thought to represent embryonic precursors of sympathetic neurons), decreased vimentin and beta-2-microglobulin, increased neurofilament-M, and a marked elevation in p26-Bcl-2. Tretinoin 50-63 beta-2-microglobulin Homo sapiens 209-229
7518108-0 1994 Retinoic acid inhibits expression of E-selectin in endothelial cells and prolongs discordant xenograft survival. Tretinoin 0-13 selectin E Homo sapiens 37-47
8195167-7 1994 An analysis of the temporal expression pattern of zif268/egr-1 and synapsin I during neuronal differentiation of P19 embryonal carcinoma cells revealed that zif268/egr-1 mRNA was induced on day 5 and synapsin I mRNA on day 8 after retinoic acid treatment. Tretinoin 231-244 early growth response 1 Homo sapiens 157-163
8195167-7 1994 An analysis of the temporal expression pattern of zif268/egr-1 and synapsin I during neuronal differentiation of P19 embryonal carcinoma cells revealed that zif268/egr-1 mRNA was induced on day 5 and synapsin I mRNA on day 8 after retinoic acid treatment. Tretinoin 231-244 early growth response 1 Homo sapiens 164-169
24516348-13 2014 The transcription and translation of C-MYC was detected in HL-60/pAd-NLS-RARalpha cells which treated by ATRA. Tretinoin 105-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 37-42
24516348-13 2014 The transcription and translation of C-MYC was detected in HL-60/pAd-NLS-RARalpha cells which treated by ATRA. Tretinoin 105-109 retinoic acid receptor alpha Homo sapiens 73-81
8399088-1 1993 Addition of retinol (vitamin A) and retinoic acid to the culture medium resulted in a time- and dose-dependent increase in the secretion of apoA-I. Tretinoin 36-49 apolipoprotein A-I Macaca fascicularis 140-146
24516348-16 2014 FCM outcome revealed the differentiation increased in HL-60/pNLS-RARalpha-shRNA cells, and decreased in the HL-60/pAd-NLS-RARalpha cells treated with 2.5micromol/L ATRA. Tretinoin 164-168 retinoic acid receptor alpha Homo sapiens 122-130
8399088-2 1993 No effect was observed during the first 24-hour incubation period; however, apoA-I secretion was enhanced 1.5-fold in the following 24-hour period in the presence of 10 mumol/L retinoic acid. Tretinoin 177-190 apolipoprotein A-I Macaca fascicularis 76-82
8399088-7 1993 Among different natural and synthetic retinoids, retinoic acid and its 9-cis and 13-cis isomers were equally active and were the most potent inducers of apoA-I synthesis, whereas the maximal stimulation induced by retinol was lower (1.6-fold). Tretinoin 49-62 apolipoprotein A-I Macaca fascicularis 153-159
8399088-8 1993 ApoA-I mRNA abundance was increased threefold in hepatocytes exposed for 72 hours to 10 mumol/L retinoic acid, which was associated with a twofold increase in the transcriptional rate of the apoA-I gene. Tretinoin 96-109 apolipoprotein A-I Macaca fascicularis 0-6
8399088-8 1993 ApoA-I mRNA abundance was increased threefold in hepatocytes exposed for 72 hours to 10 mumol/L retinoic acid, which was associated with a twofold increase in the transcriptional rate of the apoA-I gene. Tretinoin 96-109 apolipoprotein A-I Macaca fascicularis 191-197
8169976-10 1994 Induction of neuronal differentiation in SMS-KCNR neuroblastoma cells using retinoic acid resulted in an increase in Hsp27. Tretinoin 76-89 heat shock protein family B (small) member 1 Homo sapiens 117-122
8274449-4 1993 Of interest, 5 SCLC lines with high levels of myc gene family expression related to c-, N-, or L-myc gene amplification exhibited growth inhibition (28-87%), whereas 2 non-SCLC lines actually showed growth stimulation after treatment with 1 microM RA. Tretinoin 248-250 MYC proto-oncogene, bHLH transcription factor Homo sapiens 46-49
8184881-0 1994 Interferon alpha and all-trans retinoic acid-induced in vivo differentiation in a patient with nonlymphoblastic leukemia (FAB:M4) Tretinoin 31-44 FA complementation group B Homo sapiens 122-125
24516348-17 2014 The expression of C-MYC increased strikingly in HL-60/pAd-NLS-RARalpha cells treated with 2.5micromol/L ATRA. Tretinoin 104-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 18-23
7521152-6 1994 Although GM-CSF, IL-3 and IL-1 significantly modulated the ATRA-induced morphological changes, they did not induce CD14 expression, a typical marker of monocytic differentiation. Tretinoin 59-63 colony stimulating factor 2 Homo sapiens 9-15
24516348-17 2014 The expression of C-MYC increased strikingly in HL-60/pAd-NLS-RARalpha cells treated with 2.5micromol/L ATRA. Tretinoin 104-108 retinoic acid receptor alpha Homo sapiens 62-70
7521152-6 1994 Although GM-CSF, IL-3 and IL-1 significantly modulated the ATRA-induced morphological changes, they did not induce CD14 expression, a typical marker of monocytic differentiation. Tretinoin 59-63 interleukin 3 Homo sapiens 17-21
24516348-19 2014 On the contrary, over-expression of NLS-RARalpha promoted proliferation and reduced the ATRA-induced differentiation of HL-60 cells. Tretinoin 88-92 retinoic acid receptor alpha Homo sapiens 40-48
7521152-7 1994 In the presence of ATRA, GM-CSF potentiated production and secretion of tumor necrosis factor-alpha (TNF) in response to lipopolysaccharide, as well as interferon-gamma which is a potent inducer of monocytic differentiation in APL cells. Tretinoin 19-23 colony stimulating factor 2 Homo sapiens 25-31
7505755-3 1993 Comparable to normal keratinocytes, HaCaT cells and ras clones showed increased expression of the epidermal suprabasal keratins K1 and K10 upon RA depletion of the media (delipidized serum), while simple epithelial type keratins K7, K8 and K18 as well as K19 and K13 (typical of internal stratified epithelia) were almost completely suppressed. Tretinoin 144-146 keratin 10 Homo sapiens 135-138
7505755-4 1993 The cell density-dependent increase of K1 and K10 at intermediate RA levels (as in regular media with untreated serum) was also observed at Ca2+ levels below 0.1 mM, thus being clearly unrelated to stratification, whereas K13 synthesis was Ca(2+)-dependent and initiated with stratification. Tretinoin 66-68 keratin 10 Homo sapiens 46-49
8269032-4 1993 The stimulatory effect of RA was inhibited by a blocking monoclonal antibody directed against the binding domain of the EGF receptor. Tretinoin 26-28 epidermal growth factor Homo sapiens 120-123
24551289-7 2014 Moreover, compared with the control group, lower expression of Bcl-2 and higher expression of BAX were found in the ATRA-exposed group in both mRNA and protein level. Tretinoin 116-120 BCL2 associated X, apoptosis regulator Rattus norvegicus 94-97
8269032-7 1993 Decreased TGF alpha binding capacity is thought to be due to the ability of RA to stimulate TGF alpha, thereby resulting in EGF receptor binding and internalization. Tretinoin 76-78 epidermal growth factor Homo sapiens 124-127
8413217-1 1993 Retinoic acid (RA) treatment of human embryonal carcinoma (EC) NTera-2 (NT2) cells induces expression of major histocompatibility complex (MHC) class I and beta-2 microglobulin surface molecules. Tretinoin 0-13 beta-2-microglobulin Homo sapiens 156-176
8413217-1 1993 Retinoic acid (RA) treatment of human embryonal carcinoma (EC) NTera-2 (NT2) cells induces expression of major histocompatibility complex (MHC) class I and beta-2 microglobulin surface molecules. Tretinoin 15-17 beta-2-microglobulin Homo sapiens 156-176
8156927-0 1994 Synergistic induction of gene 33 expression by retinoic acid and insulin. Tretinoin 47-60 ERBB receptor feedback inhibitor 1 Rattus norvegicus 25-32
7918098-1 1994 The cDNAs encoding the zebrafish homologs of retinoic acid receptor alpha(zRAR alpha) and gamma (zRAR gamma) were isolated and their expression studied in normal and retinoic acid (RA) treated embryos. Tretinoin 45-58 retinoic acid receptor gamma a Danio rerio 97-107
24551289-8 2014 Immunohistochemical labeling of Bcl-2 in the control group was more intense while BAX labeling in the ATRA-exposed group was more intense. Tretinoin 102-106 BCL2 associated X, apoptosis regulator Rattus norvegicus 82-85
24851929-0 2014 All-trans retinoic acid induces DU145 cell cycle arrest through Cdk5 activation. Tretinoin 10-23 cyclin dependent kinase 5 Homo sapiens 64-68
8061301-5 1994 RA-induced neuronal differentiation led to a decrease in the content of GM2, GD3, and GD2 and to a 3-7 fold increased concentration of the ganglio-tetraosyl gangliosides GM1, GD1a, GT1a, GD1b, and GT1b. Tretinoin 0-2 GRDX Homo sapiens 77-80
7512172-6 1994 Indomethacin shifted the G-CSF dose-response curve of cells treated with 10 nM RA to lower G-CSF concentrations. Tretinoin 79-81 colony stimulating factor 3 Homo sapiens 25-30
7512172-6 1994 Indomethacin shifted the G-CSF dose-response curve of cells treated with 10 nM RA to lower G-CSF concentrations. Tretinoin 79-81 colony stimulating factor 3 Homo sapiens 91-96
7690555-0 1993 Rapid induction of CD38 antigen on myeloid leukemia cells by all trans-retinoic acid. Tretinoin 65-84 CD38 molecule Homo sapiens 19-23
7690555-3 1993 Using human promyelocytic leukemia cells, we demonstrate that all trans-retinoic acid is a potent and specific inducer of CD38 expression in myeloid lineage. Tretinoin 66-85 CD38 molecule Homo sapiens 122-126
7690555-4 1993 At physiological doses, all trans-retinoic acid induces significant levels (8 to 10-fold) of CD38. Tretinoin 28-47 CD38 molecule Homo sapiens 93-97
7690555-5 1993 Similarly, in patients with promyelocytic leukemia, a significant increase (3 to 6-fold) in CD38 expression was observed in vivo following single oral dose administration of all trans-retinoic acid. Tretinoin 178-197 CD38 molecule Homo sapiens 92-96
7690555-6 1993 The induction of CD38 is a specific response of myeloid cells to retinoic acid and is not seen with other agents that induce differentiation. Tretinoin 65-78 CD38 molecule Homo sapiens 17-21
8400236-6 1993 RA treatment of NB4 cells or clones expressing PML/RAR alpha gradually leads to a PML pattern before apparent morphologic maturation. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 47-60
8400236-6 1993 RA treatment of NB4 cells or clones expressing PML/RAR alpha gradually leads to a PML pattern before apparent morphologic maturation. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 47-50
8119774-0 1994 Retinoic acid up-regulates nuclear retinoic acid receptor-alpha expression in human neuroblastoma cells. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 35-63
8119774-3 1994 In this study, we show that in human neuroblastoma, a cell type exceptionally sensitive to RA-induced differentiation, RAR alpha as well as RAR beta is markedly up-regulated by RA treatment. Tretinoin 91-93 retinoic acid receptor alpha Homo sapiens 119-128
24851929-2 2014 It has been indicated that cyclin-dependent kinase 5 (Cdk5) activity can be affected by ATRA treatment. Tretinoin 88-92 cyclin dependent kinase 5 Homo sapiens 27-52
8119774-8 1994 These findings, showing direct activation by RA of RAR alpha gene transcription in human neuroblastoma cells, suggest differences in the overall regulation of this receptor from that found in most other RA-inducible tissue. Tretinoin 45-47 retinoic acid receptor alpha Homo sapiens 51-60
8400236-8 1993 Strikingly, in 4 patients, after 1 to 2 weeks of RA therapy, the speckled nuclear PML pattern reappeared concomitant with the onset of differentiation. Tretinoin 49-51 PML nuclear body scaffold Homo sapiens 82-85
8400236-9 1993 These results establish that fusion of PML to RAR alpha results in an altered localization of PML that is reverted upon RA treatment. Tretinoin 46-48 PML nuclear body scaffold Homo sapiens 39-42
8400236-9 1993 These results establish that fusion of PML to RAR alpha results in an altered localization of PML that is reverted upon RA treatment. Tretinoin 46-48 PML nuclear body scaffold Homo sapiens 94-97
8018987-10 1994 Although the promoter of the human counterpart of Adh-1 contains a retinoic acid response element (Duester et al. Tretinoin 67-80 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 50-55
24851929-2 2014 It has been indicated that cyclin-dependent kinase 5 (Cdk5) activity can be affected by ATRA treatment. Tretinoin 88-92 cyclin dependent kinase 5 Homo sapiens 54-58
24851929-4 2014 The purpose of this study is to examine whether Cdk5 is involved in ATRA-induced growth arrest of the castration-resistant cancer cell line DU145 through up-regulating Cdk inhibitor protein, p27. Tretinoin 68-72 cyclin dependent kinase 5 Homo sapiens 48-52
24851929-4 2014 The purpose of this study is to examine whether Cdk5 is involved in ATRA-induced growth arrest of the castration-resistant cancer cell line DU145 through up-regulating Cdk inhibitor protein, p27. Tretinoin 68-72 interferon alpha inducible protein 27 Homo sapiens 191-194
8395394-6 1993 Retinoic acid greatly inhibited vimentin expression in HL-60 cells, but it had little effect on A/C lamin expression. Tretinoin 0-13 vimentin Homo sapiens 32-40
24851929-7 2014 RESULTS: ATRA treatment inhibited DU145 cell proliferation and significantly increased p27 expression through Cdk5 up-regulation. Tretinoin 9-13 interferon alpha inducible protein 27 Homo sapiens 87-90
8395395-7 1993 The expression of the retinoic acid receptors RAR alpha and gamma was not affected by treatment in any of the cultures examined, while RAR beta was expressed only by the organ cultures and was transcriptionally induced by retinoic acid treatment. Tretinoin 22-35 retinoic acid receptor, alpha Rattus norvegicus 46-55
8180134-0 1994 Retinoic acid differentially affects platelet-derived growth factor and epidermal growth factor-regulated cell growth of mouse osteoblast-like cells. Tretinoin 0-13 epidermal growth factor Mus musculus 72-95
24851929-7 2014 RESULTS: ATRA treatment inhibited DU145 cell proliferation and significantly increased p27 expression through Cdk5 up-regulation. Tretinoin 9-13 cyclin dependent kinase 5 Homo sapiens 110-114
24851929-8 2014 Immunocytochemical data showed that a Cdk5 inhibitor reduced ATRA-triggered nuclear distribution of p27 in DU145 cells. Tretinoin 61-65 cyclin dependent kinase 5 Homo sapiens 38-42
24851929-8 2014 Immunocytochemical data showed that a Cdk5 inhibitor reduced ATRA-triggered nuclear distribution of p27 in DU145 cells. Tretinoin 61-65 interferon alpha inducible protein 27 Homo sapiens 100-103
8144129-2 1994 We examined bone marrow cells by reverse transcriptase-polymerase chain reaction (RT-PCR) to detect residual PML/RAR alpha mRNA-containing cells following treatment with all-trans retinoic acid (ATRA) and cytotoxic chemotherapy in a patient with APL. Tretinoin 180-193 PML nuclear body scaffold Homo sapiens 109-122
8377475-7 1993 RESULTS: Epidermal growth factor, cholera toxin, calcium, 1,25-dihydroxyvitamin D, ionomycin, trans-retinoic acid, transforming growth factor-beta 1 and hydrocortisone stimulated production of PTHrP by SCC 2/88 cells to various degrees. Tretinoin 94-113 parathyroid hormone like hormone Canis lupus familiaris 193-198
8144129-2 1994 We examined bone marrow cells by reverse transcriptase-polymerase chain reaction (RT-PCR) to detect residual PML/RAR alpha mRNA-containing cells following treatment with all-trans retinoic acid (ATRA) and cytotoxic chemotherapy in a patient with APL. Tretinoin 195-199 PML nuclear body scaffold Homo sapiens 109-122
24851929-10 2014 CONCLUSIONS: Our results demonstrate that ATRA induced growth inhibition in castration-resistant prostate cancer cells through activating Cdk5 and p27. Tretinoin 42-46 cyclin dependent kinase 5 Homo sapiens 138-142
8396695-4 1993 In addition, we observed that RA and 16-23-D3 interact additively with respect to the reduction of c-myc mRNA expression. Tretinoin 30-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 99-104
8144129-4 1994 We show that PML/RAR alpha mRNA was still detectable despite clinical remission following ATRA treatment, but undetectable following consolidation with chemotherapy. Tretinoin 90-94 PML nuclear body scaffold Homo sapiens 13-26
24851929-10 2014 CONCLUSIONS: Our results demonstrate that ATRA induced growth inhibition in castration-resistant prostate cancer cells through activating Cdk5 and p27. Tretinoin 42-46 interferon alpha inducible protein 27 Homo sapiens 147-150
24962883-1 2014 The nuclear retinoic acid receptors (RAR alpha, beta and gamma) and their isoforms are ligand-dependent regulators of transcription Transcription , which mediate the effects of all-trans retinoic acid (RA), the active endogenous metabolite of Vitamin A. Tretinoin 12-25 retinoic acid receptor alpha Homo sapiens 37-62
8289783-0 1994 Retinoic acid represses Oct-3/4 gene expression through several retinoic acid-responsive elements located in the promoter-enhancer region. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 24-31
8289783-3 1994 Retinoic acid (RA)-induced differentiation of embryonal carcinoma (EC) cells is accompanied by decreased expression of the Oct-3/4 gene. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 123-130
8289783-3 1994 Retinoic acid (RA)-induced differentiation of embryonal carcinoma (EC) cells is accompanied by decreased expression of the Oct-3/4 gene. Tretinoin 15-17 POU class 5 homeobox 1 Homo sapiens 123-130
8289783-4 1994 Previous findings show that sequences in the Oct-3/4 enhancer region (designated RARE1) are targets for RA-mediated repression (H. Okazawa, K. Okamoto, F. Ishino, T. Ishino-Kaneko, S. Takeda, Y. Toyoda, M. Muramatsu, and H. Hamada, EMBO J. Tretinoin 81-83 POU class 5 homeobox 1 Homo sapiens 45-52
8289783-7 1994 We identified a novel cis element in the Oct-3/4 promoter harbors a putative Sp1 binding site and a RA-responsive element (designated RAREoct), which are juxtaposed to one another. Tretinoin 100-102 POU class 5 homeobox 1 Homo sapiens 41-48
8289783-12 1994 Using site-directed mutagenesis, we show that the RAREoct contributes to the transcriptional activation of Oct-3/4 promoter in P19 cells and, most interestingly, mediates the RA-induced repression in RA-differentiated EC cells. Tretinoin 50-52 POU class 5 homeobox 1 Homo sapiens 107-114
8289783-14 1994 In accordance with the suggestion that suppression of Oct-3/4 expression is a crucial step during embryogenesis, the Oct-3/4 upstream region contains multiple targets for RA-induced repression, probably to ensure accurate and prompt repression of Oct-3/4 expression. Tretinoin 171-173 POU class 5 homeobox 1 Homo sapiens 117-124
24344243-3 2013 The empirical discoveries that PML-RARa-associated APL is sensitive to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding of the mechanisms of action of these drugs, have led to efforts to understand the contribution of molecular events to APL cell differentiation, leukemia-initiating cell (LIC) clearance, and disease eradication in vitro and in vivo. Tretinoin 76-99 PML nuclear body scaffold Homo sapiens 31-34
8119128-5 1994 Retinoic acid application, which mimics the effects of polarizing region grafts, activates Bmp-2 gene expression in anterior cells. Tretinoin 0-13 bone morphogenetic protein 2 Gallus gallus 91-96
8119128-11 1994 There is a close relationship, both temporal and spatial, between the activation of the Bmp-2 and Hoxd-13 genes in response to retinoic acid and polarizing region grafts, suggesting that expression of the two genes might be linked. Tretinoin 127-140 bone morphogenetic protein 2 Gallus gallus 88-93
8119128-11 1994 There is a close relationship, both temporal and spatial, between the activation of the Bmp-2 and Hoxd-13 genes in response to retinoic acid and polarizing region grafts, suggesting that expression of the two genes might be linked. Tretinoin 127-140 homeobox D13 Gallus gallus 98-105
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 66-100
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 102-105
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 66-100
24344243-3 2013 The empirical discoveries that PML-RARa-associated APL is sensitive to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding of the mechanisms of action of these drugs, have led to efforts to understand the contribution of molecular events to APL cell differentiation, leukemia-initiating cell (LIC) clearance, and disease eradication in vitro and in vivo. Tretinoin 76-99 retinoic acid receptor alpha Homo sapiens 35-39
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 102-105
24344243-3 2013 The empirical discoveries that PML-RARa-associated APL is sensitive to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding of the mechanisms of action of these drugs, have led to efforts to understand the contribution of molecular events to APL cell differentiation, leukemia-initiating cell (LIC) clearance, and disease eradication in vitro and in vivo. Tretinoin 101-105 PML nuclear body scaffold Homo sapiens 31-34
24344243-3 2013 The empirical discoveries that PML-RARa-associated APL is sensitive to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding of the mechanisms of action of these drugs, have led to efforts to understand the contribution of molecular events to APL cell differentiation, leukemia-initiating cell (LIC) clearance, and disease eradication in vitro and in vivo. Tretinoin 101-105 retinoic acid receptor alpha Homo sapiens 35-39
24100014-1 2013 TG-interacting factor 1 (TGIF1) is a transcriptional repressor that can modulate retinoic acid and transforming growth factor beta signaling pathways. Tretinoin 81-94 TGFB-induced factor homeobox 1 Mus musculus 0-23
7505280-5 1994 We have previously demonstrated that retinoic acid (RA) inhibition of IGF-I-stimulated MCF-7 cell proliferation is associated with increased IGFBP-3 levels in the conditioned media. Tretinoin 37-50 insulin like growth factor binding protein 3 Homo sapiens 141-148
24100014-1 2013 TG-interacting factor 1 (TGIF1) is a transcriptional repressor that can modulate retinoic acid and transforming growth factor beta signaling pathways. Tretinoin 81-94 TGFB-induced factor homeobox 1 Mus musculus 25-30
8136307-5 1994 The RAR expression in F9 cells was slightly down-regulated in charcoal-stripped culture medium and returned to normal level after retinoic acid treatment. Tretinoin 130-143 retinoic acid receptor alpha Homo sapiens 4-7
23821302-0 2013 Regulation of URG4/URGCP and PPARalpha gene expressions after retinoic acid treatment in neuroblastoma cells. Tretinoin 62-75 peroxisome proliferator activated receptor alpha Homo sapiens 29-38
7808017-9 1994 These mutated RAR receptors exhibit a reduced affinity for retinoic acid while retaining the ability to bind to a retinoic acid response element on DNA. Tretinoin 59-72 retinoic acid receptor alpha Homo sapiens 14-17
7808017-9 1994 These mutated RAR receptors exhibit a reduced affinity for retinoic acid while retaining the ability to bind to a retinoic acid response element on DNA. Tretinoin 114-127 retinoic acid receptor alpha Homo sapiens 14-17
23821302-6 2013 This study aims to detect gene expression patterns of PPARalpha and URG4/URGCP genes in SH-SY5Y NB cell line after RA treatment. Tretinoin 115-117 peroxisome proliferator activated receptor alpha Homo sapiens 54-63
7808033-1 1994 Retinoic acids exert a wide range of biological activities following binding to the cognate nuclear receptors, which has several members (RAR-alpha, beta, gamma and RXR-alpha, beta, gamma). Tretinoin 0-14 retinoic acid receptor alpha Homo sapiens 138-147
24121663-4 2013 Specifically, we demonstrate that TAp73 regulates GLS2 during retinoic acid-induced terminal neuronal differentiation of neuroblastoma cells, and overexpression or inhibition of GLS2 modulates neuronal differentiation and intracellular levels of ATP. Tretinoin 62-75 transformation related protein 73 Mus musculus 34-39
8264603-2 1994 To address the role of RXRs in retinoic acid- (RA) mediated gene regulation, we designed a dominant negative RXR beta. Tretinoin 31-44 retinoid X receptor beta Mus musculus 109-117
8264603-2 1994 To address the role of RXRs in retinoic acid- (RA) mediated gene regulation, we designed a dominant negative RXR beta. Tretinoin 47-49 retinoid X receptor beta Mus musculus 109-117
8264603-8 1994 Gel mobility shift assays demonstrated that RA treatment of control P19 cells induces RARE-binding activity, of which RXR beta is a major component. Tretinoin 44-46 retinoid X receptor beta Mus musculus 118-126
23760752-0 2013 Over-expression of Mcl-1 impairs the ability of ATRA to induce growth arrest and differentiation in acute promyelocytic leukemia cells. Tretinoin 48-52 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 19-24
8260698-0 1993 Effects of novel retinoic acid compound, 9-cis-retinoic acid, on proliferation, differentiation, and expression of retinoic acid receptor-alpha and retinoid X receptor-alpha RNA by HL-60 cells. Tretinoin 17-30 retinoic acid receptor alpha Homo sapiens 115-173
8260698-2 1993 A stereoisomer of retinoic acid, 9-cis-retinoic acid, is a high-affinity ligand for RXR and binds efficiently to RAR. Tretinoin 18-31 retinoic acid receptor alpha Homo sapiens 113-116
8250033-4 1993 On the other hand, retinoic acid induced a concentration-dependent increase in EGF binding that was maximal at 1 mumol/L. Tretinoin 19-32 epidermal growth factor Sus scrofa 79-82
8250033-5 1993 One micromolar of retinoic acid increased EGF binding from 0.38 +/- 0.01 fmol/10(6) cells in controls to 1.10 +/- 0.03 fmol/10(6) in treated cells at 18 hours (n = 8, P < 0.001). Tretinoin 18-31 epidermal growth factor Sus scrofa 42-45
8250033-7 1993 The upregulation of the EGF receptor induced by retinoic acid was associated with enhanced EGF-induced growth promotion. Tretinoin 48-61 epidermal growth factor Sus scrofa 24-27
8250033-7 1993 The upregulation of the EGF receptor induced by retinoic acid was associated with enhanced EGF-induced growth promotion. Tretinoin 48-61 epidermal growth factor Sus scrofa 91-94
8250033-8 1993 A 45-minute incubation of cells with phorbol 12-myristate 13-acetate caused a concentration-dependent decrease in EGF binding that was prevented by a 40-hour, 2 mumol/L pre-exposure to phorbol 12-myristate 13-acetate; 10(-8) mol/L EGF also caused a downregulation of the EGF receptor that was not prevented by phorbol 12-myristate 13-acetate or retinoic acid. Tretinoin 345-358 epidermal growth factor Sus scrofa 114-117
23760752-1 2013 Exposure of acute promyelocytic leukemia (APL) cells to all-trans retinoic acid (ATRA) increases levels of Mcl-1, however, the implication of ATRA-mediated expressions of Mcl-1 in these cells remains to be fully elucidated. Tretinoin 66-79 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 107-112
23760752-1 2013 Exposure of acute promyelocytic leukemia (APL) cells to all-trans retinoic acid (ATRA) increases levels of Mcl-1, however, the implication of ATRA-mediated expressions of Mcl-1 in these cells remains to be fully elucidated. Tretinoin 66-79 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 171-176
8243317-0 1993 Embryonic stem cells express growth hormone receptors: regulation by retinoic acid. Tretinoin 69-82 growth hormone Mus musculus 29-43
23760752-1 2013 Exposure of acute promyelocytic leukemia (APL) cells to all-trans retinoic acid (ATRA) increases levels of Mcl-1, however, the implication of ATRA-mediated expressions of Mcl-1 in these cells remains to be fully elucidated. Tretinoin 81-85 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 107-112
23760752-1 2013 Exposure of acute promyelocytic leukemia (APL) cells to all-trans retinoic acid (ATRA) increases levels of Mcl-1, however, the implication of ATRA-mediated expressions of Mcl-1 in these cells remains to be fully elucidated. Tretinoin 81-85 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 171-176
23760752-1 2013 Exposure of acute promyelocytic leukemia (APL) cells to all-trans retinoic acid (ATRA) increases levels of Mcl-1, however, the implication of ATRA-mediated expressions of Mcl-1 in these cells remains to be fully elucidated. Tretinoin 142-146 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 107-112
7504151-4 1993 G-CSF markedly enhanced RA-induced granulocytic differentiation in APL cells obtained from all four cases. Tretinoin 24-26 colony stimulating factor 3 Homo sapiens 0-5
23760752-1 2013 Exposure of acute promyelocytic leukemia (APL) cells to all-trans retinoic acid (ATRA) increases levels of Mcl-1, however, the implication of ATRA-mediated expressions of Mcl-1 in these cells remains to be fully elucidated. Tretinoin 142-146 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 171-176
8108182-4 1993 Using SK-N-SH neuroblastoma cells, we found that RA induced differentiation of SK-N-SH cells as demonstrated by down-regulation of N-myc gene expression, cell-cycle arrest in G1 phase, and phenotypic change. Tretinoin 49-51 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 131-136
23760752-2 2013 This study found that exposure of NB4 and PL-21 cells to ATRA increased levels of Mcl-1 in association with phosphorylation of c-jun N-terminus kinases. Tretinoin 57-61 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 82-87
23760752-3 2013 Down-regulation of Mcl-1 by a small interfering (siRNA) or an inhibitor of JNK significantly potentiated the ability of ATRA to induce differentiation and apoptosis in these cells. Tretinoin 120-124 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 19-24
23760752-4 2013 On the other hand, the anti-leukemia effects of ATRA were blunted when Mcl-1 was forced expressed in NB4 and PL-21 cells as well as leukemia cells isolated from individuals with APL. Tretinoin 48-52 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 71-76
8241133-4 1993 Following purification and thrombin cleavage, a predominant monomeric (stokes radius = 2.3 nm, molecular mass of 32 kDa) [3H]retinoic acid hRAR alpha LBD complex was characterized by high-performance size-exclusion chromatography. Tretinoin 125-138 retinoic acid receptor alpha Homo sapiens 139-143
23760752-6 2013 Taken together, inhibition of Mcl-1 might be useful to potentiate the action of ATRA in APL as well as non-APL AML cells. Tretinoin 80-84 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 30-35
8241133-5 1993 The purified hRAR alpha LBD bound retinoic acid with an apparent Kd of 9 nM, a value close to the Kd of the full-length hRAR alpha expressed in COS cells. Tretinoin 34-47 retinoic acid receptor alpha Homo sapiens 13-23
23607934-5 2013 Retinoic acid (RA) induced gut-homing markers (beta7 and CCR9) and a regulatory phenotype and function [decreased human leucocyte antigen D-related (HLA-DR) and increased ILT3 and fluorescein isothiocyanate (FITC-dextran uptake) in MoDC]. Tretinoin 0-13 leukocyte immunoglobulin like receptor B4 Homo sapiens 171-175
7504461-0 1993 Transformation of NIH3T3 cells with ras oncogenes abrogates the retinoic acid induction of tissue transglutaminase. Tretinoin 64-77 transglutaminase 2, C polypeptide Mus musculus 91-114
23830798-3 2013 We therefore investigated whether RARA gene amplification could be associated with sensitivity to retinoic acid derivatives in breast cancers. Tretinoin 98-111 retinoic acid receptor alpha Homo sapiens 34-38
8218362-1 1993 We previously reported that protein kinase C (PKC) stimulation through phorbol ester (TPA) treatment enhances the effects of all-trans retinoic acid (RA) on immunophenotypic differentiation and RA nuclear receptor (RAR) activation in the multipotential human teratocarcinoma (TC) cell line NTera-2/clone D1 (abbreviated NT2/D1). Tretinoin 135-148 protein kinase C gamma Homo sapiens 46-49
8218362-1 1993 We previously reported that protein kinase C (PKC) stimulation through phorbol ester (TPA) treatment enhances the effects of all-trans retinoic acid (RA) on immunophenotypic differentiation and RA nuclear receptor (RAR) activation in the multipotential human teratocarcinoma (TC) cell line NTera-2/clone D1 (abbreviated NT2/D1). Tretinoin 150-152 protein kinase C gamma Homo sapiens 46-49
8218362-2 1993 This study extends prior work in NT2/D1 cells by demonstrating that PKC pathway activation is an early effect of RA treatment which regulates RAR transcriptional activity. Tretinoin 113-115 protein kinase C gamma Homo sapiens 68-71
8218362-2 1993 This study extends prior work in NT2/D1 cells by demonstrating that PKC pathway activation is an early effect of RA treatment which regulates RAR transcriptional activity. Tretinoin 113-115 retinoic acid receptor alpha Homo sapiens 142-145
8218362-3 1993 RA activated the PKC pathway prior to induction of RAR-beta expression at 6 h, which is an established early marker of RAR activation in NT2/D1 cells. Tretinoin 0-2 protein kinase C gamma Homo sapiens 17-20
8218362-4 1993 RA caused a transient 1.3-fold increase in intracellular diacylglycerol (DG) at 2 min and a translocation of the gamma isozyme of PKC (PKC-gamma) within 5 min. Tretinoin 0-2 protein kinase C gamma Homo sapiens 130-133
8218362-4 1993 RA caused a transient 1.3-fold increase in intracellular diacylglycerol (DG) at 2 min and a translocation of the gamma isozyme of PKC (PKC-gamma) within 5 min. Tretinoin 0-2 protein kinase C gamma Homo sapiens 135-144
23830798-9 2013 All-trans-retinoic acid reduced cell viability of RARA-amplified, but not RARA-normal, cell lines through apoptosis. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 50-54
21573453-5 1993 Induction of proliferin by the tumour promoters butylated hydroxytoluene or TPA was efficiently inhibited at certain concentrations of catalase and superoxide dismutase, but retinoic acid had no effect. Tretinoin 174-187 prolactin family 2, subfamily c, member 2 Mus musculus 13-23
23830798-10 2013 Gene expression arrays showed that ATRA-induced apoptosis in RARA-amplified cell lines was related to an increase in CASP1 and IRF1. Tretinoin 35-39 retinoic acid receptor alpha Homo sapiens 61-65
21573453-6 1993 Proliferin induction by a recently identified promoter of transformation, tri-n-butyltin chloride, was stimulated by catalase, superoxide dismutase and retinoic acid, but inhibited at higher concentrations of N-acetyl cysteine. Tretinoin 152-165 prolactin family 2, subfamily c, member 2 Mus musculus 0-10
23830798-11 2013 CONCLUSION: The results of this study suggest that breast cancers exhibiting RARA amplifications could be sensitive to retinoic acid. Tretinoin 119-132 retinoic acid receptor alpha Homo sapiens 77-81
8231235-6 1993 Treatment of NB-4 cells with all-trans retinoic acid (ATRA) or the phorbol ester TPA induced terminal differentiation and down-regulated annexin VIII mRNA expression rapidly within a few hours; vitamin D3 was ineffective in this regard; the protein kinase C activator Bryostatin 1 up-regulated the expression. Tretinoin 39-52 annexin A8 like 1 Homo sapiens 137-149
8231235-6 1993 Treatment of NB-4 cells with all-trans retinoic acid (ATRA) or the phorbol ester TPA induced terminal differentiation and down-regulated annexin VIII mRNA expression rapidly within a few hours; vitamin D3 was ineffective in this regard; the protein kinase C activator Bryostatin 1 up-regulated the expression. Tretinoin 54-58 annexin A8 like 1 Homo sapiens 137-149
23975865-4 2013 Genes involved in RA biosynthesis and metabolism, such as Adh1 and Raldh2, as well as RA receptors and IL-10, were induced in dendritic cells (DCs) via TLR2-dependent ERK signaling. Tretinoin 18-20 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 58-62
23980207-1 2013 Retinoic acid (RA) enhances TGF-beta-dependent differentiation of Foxp3(+) inducible regulatory T cells (iTregs) and inhibits Th17 differentiation by binding to the RA receptor (RAR)/retinoid X receptor (RXR) heterodimer. Tretinoin 0-13 forkhead box P3 Mus musculus 66-71
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 145-158 PML nuclear body scaffold Homo sapiens 34-37
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 145-158 retinoic acid receptor alpha Homo sapiens 175-184
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 145-158 retinoic acid receptor alpha Homo sapiens 198-207
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 175-177 PML nuclear body scaffold Homo sapiens 34-37
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 175-177 retinoic acid receptor alpha Homo sapiens 145-173
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 175-177 retinoic acid receptor alpha Homo sapiens 198-207
23980207-1 2013 Retinoic acid (RA) enhances TGF-beta-dependent differentiation of Foxp3(+) inducible regulatory T cells (iTregs) and inhibits Th17 differentiation by binding to the RA receptor (RAR)/retinoid X receptor (RXR) heterodimer. Tretinoin 15-17 forkhead box P3 Mus musculus 66-71
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 198-200 PML nuclear body scaffold Homo sapiens 34-37
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 198-200 retinoic acid receptor alpha Homo sapiens 145-173
24074870-4 2013 Wnt signaling completely blocked the HSC inductive effects of RA modulators, whereas inhibition of the pathway promoted the development of HSCs in the absence of RA signaling. Tretinoin 62-64 fucosyltransferase 1 (H blood group) Homo sapiens 37-40
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 198-200 retinoic acid receptor alpha Homo sapiens 175-184
8415704-3 1993 Stimulation is dependent on the concentration of RA and its dose-response curve is comparable to that for activation by RAR alpha of transcription on RA-responsive genes. Tretinoin 49-51 retinoic acid receptor alpha Homo sapiens 120-129
8415704-6 1993 In view of the association between AP-1 activity and hemopoietic differentiation, we suggest that these properties of PML-RAR alpha could contribute to the leukemic phenotype and its response to RA. Tretinoin 122-124 PML nuclear body scaffold Homo sapiens 118-121
23765726-6 2013 This resulting DeltaCAK acted as a dominant negative to inhibit the growth and metastasis of different leukemic myeloblasts, with or without RA resistance, by concurrently suppressing CAK and TFIIH kinase activities to inhibit cell cycle and gene transcription. Tretinoin 141-143 cyclin-dependent kinase 7 Mus musculus 20-23
8402622-5 1993 ECE16-1 but not normal ectocervical epithelial cells are growth inhibited by trans-retinoic acid which attenuates the stimulatory effect of EGF on ECE16-1 cell growth. Tretinoin 77-96 epidermal growth factor Homo sapiens 140-143
8402622-6 1993 Retinoic acid reduces both EGF binding and EGF receptor protein levels in ECE16-1 cells but not in normal ectocervical cells. Tretinoin 0-13 epidermal growth factor Homo sapiens 27-30
8402622-6 1993 Retinoic acid reduces both EGF binding and EGF receptor protein levels in ECE16-1 cells but not in normal ectocervical cells. Tretinoin 0-13 epidermal growth factor Homo sapiens 43-46
23765726-6 2013 This resulting DeltaCAK acted as a dominant negative to inhibit the growth and metastasis of different leukemic myeloblasts, with or without RA resistance, by concurrently suppressing CAK and TFIIH kinase activities to inhibit cell cycle and gene transcription. Tretinoin 141-143 general transcription factor IIH, polypeptide 3 Mus musculus 192-197
8404615-4 1993 However, RA potentiated PMA-mediated induction of PAI-2 mRNA in HL-60 and U937 cells and PAI-2 antigen in all four cell lines. Tretinoin 9-11 serpin family B member 2 Homo sapiens 50-55
23937294-6 2013 The vagal motor neuron phenotype caused by loss of Zic2a/2b mimics a depletion of Aldh1a2 and is rescued by exogenously supplied retinoic acid. Tretinoin 129-142 zic family member 2 (odd-paired homolog, Drosophila), a Danio rerio 51-56
8404615-9 1993 In fact, in U937 cells, RA inhibited PMA-induced PAI-1 antigen secretion by approximately 60%. Tretinoin 24-26 serpin family E member 1 Homo sapiens 49-54
8405671-0 1993 Retinoic acid stimulates mouse lung development by a mechanism involving epithelial-mesenchymal interaction and regulation of epidermal growth factor receptors. Tretinoin 0-13 epidermal growth factor Mus musculus 126-149
8405671-6 1993 The cellular response to RA was correlated with an increase in the expression of epidermal growth factor receptor (EGFR). Tretinoin 25-27 epidermal growth factor receptor Mus musculus 81-113
8405671-6 1993 The cellular response to RA was correlated with an increase in the expression of epidermal growth factor receptor (EGFR). Tretinoin 25-27 epidermal growth factor receptor Mus musculus 115-119
23950971-8 2013 Moreover, we report for the first time the protective effect of GDF3 against retinoic acid-induced apoptosis in cells with stem cell-like properties. Tretinoin 77-90 growth differentiation factor 3 Homo sapiens 64-68
8405671-13 1993 Further studies identified the mesenchyme as a major source of EGF in the embryonic lung, suggesting that mesenchymal EGF may represent a paracrine factor involved in the epithelial response to RA. Tretinoin 194-196 epidermal growth factor Mus musculus 118-121
23803888-3 2013 Retinoic acid reduces the invasiveness in cancer, through inhibition of matrix metalloproteinases (MMPs). Tretinoin 0-13 matrix metallopeptidase 7 Homo sapiens 99-103
7693329-5 1993 RA increased CK19 expression in both cell lines and CK19 was also present in tumors developed in nude mice from both RA untreated (CK19 negative) and RA-treated (CK19 positive) K248C and K266 cells. Tretinoin 0-2 keratin 19 Mus musculus 13-17
7693329-9 1993 These findings suggest that the modulation of CK19 and CKs 5/14 expression observed in mammary carcinoma cells upon RA treatment might be regulated through different pathways. Tretinoin 116-118 keratin 19 Mus musculus 46-50
23562973-7 2013 ATRA consistently and significantly inhibited LPS-induced release of the pro-inflammatory cytokines tumor necrosis factor, interleukin (IL)-6, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta. Tretinoin 0-4 C-C motif chemokine ligand 3 Homo sapiens 143-187
8239509-1 1993 Retinoic acid (RA) modulation of c-myc and max gene expression was investigated in human breast carcinoma (HBC) cell lines. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38
23562973-7 2013 ATRA consistently and significantly inhibited LPS-induced release of the pro-inflammatory cytokines tumor necrosis factor, interleukin (IL)-6, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta. Tretinoin 0-4 C-C motif chemokine ligand 4 Homo sapiens 192-201
8239509-1 1993 Retinoic acid (RA) modulation of c-myc and max gene expression was investigated in human breast carcinoma (HBC) cell lines. Tretinoin 15-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38
8239509-3 1993 RA-mediated increase in c-myc mRNA levels were noticed as early as 30 min. Tretinoin 0-2 MYC proto-oncogene, bHLH transcription factor Homo sapiens 24-29
23998577-0 2013 Expression of PML-RARalpha is up-regulated during ATRA and arsenics combined induction without influence on long-term prognosis of acute promyelocytic leukemia. Tretinoin 50-54 PML nuclear body scaffold Homo sapiens 14-17
8239509-5 1993 We thus report for the first time that RA, during its growth inhibitory effects on MCF-7 HBC cells, positively regulates the gene expression of c-myc and max. Tretinoin 39-41 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149
8220153-13 1993 Although the mechanism by which this occurs has not been established, preliminary data suggest that ATRA blocks the downregulation of the thrombomodulin gene and the up-regulation of the tissue factor gene induced by tumor necrosis factor. Tretinoin 100-104 thrombomodulin Homo sapiens 138-152
8220153-13 1993 Although the mechanism by which this occurs has not been established, preliminary data suggest that ATRA blocks the downregulation of the thrombomodulin gene and the up-regulation of the tissue factor gene induced by tumor necrosis factor. Tretinoin 100-104 coagulation factor III, tissue factor Homo sapiens 187-200
23998577-0 2013 Expression of PML-RARalpha is up-regulated during ATRA and arsenics combined induction without influence on long-term prognosis of acute promyelocytic leukemia. Tretinoin 50-54 retinoic acid receptor alpha Homo sapiens 18-26
23998577-9 2013 It is concluded that up-regulation of PML-RARa expression is a common event during induction therapy with ATRA plus arsenics. Tretinoin 106-110 PML nuclear body scaffold Homo sapiens 38-41
23998577-9 2013 It is concluded that up-regulation of PML-RARa expression is a common event during induction therapy with ATRA plus arsenics. Tretinoin 106-110 retinoic acid receptor alpha Homo sapiens 42-46
8394351-7 1993 The responsiveness of the osteocalcin element to all-trans-retinoic acid is mediated neither by RAR homodimers nor by RAR-RXR heterodimers. Tretinoin 49-72 retinoic acid receptor alpha Homo sapiens 96-99
8394351-8 1993 However, a VDR-RAR heterodimer binds to the osteocalcin response element and mediates activation by all-trans-retinoic acid. Tretinoin 100-123 retinoic acid receptor alpha Homo sapiens 15-18
23874626-4 2013 Recently, we have shown that, after encounter of retinoic acid during differentiation, circulating gut-imprinted T cells express CD62L(neg)CD38(+). Tretinoin 49-62 selectin L Homo sapiens 129-134
8394351-10 1993 In combination with all-trans-retinoic acid, however, vitamin D enhances VDR-RAR heterodimer-mediated gene expression. Tretinoin 20-43 retinoic acid receptor alpha Homo sapiens 77-80
8394323-3 1993 The NADase specifically induced by retinoic acid appeared to be encoded by human leukocyte cell surface antigen CD38 as follows. Tretinoin 35-48 CD38 molecule Homo sapiens 112-116
23874626-4 2013 Recently, we have shown that, after encounter of retinoic acid during differentiation, circulating gut-imprinted T cells express CD62L(neg)CD38(+). Tretinoin 49-62 CD38 molecule Homo sapiens 139-143
8394323-4 1993 1) There was an early expression of CD38 mRNA, together with the induction of the NADase activity, in the retinoic acid-treated HL-60 cells. Tretinoin 106-119 CD38 molecule Homo sapiens 36-40
8394323-9 1993 These results clearly indicated that the dithiothreitol-sensitive NADase activity induced by retinoic acid in HL-60 cells is attributed to the molecule of human leukocyte cell surface antigen CD38, which contains cysteine-rich cytoplasmic domain within its molecule. Tretinoin 93-106 CD38 molecule Homo sapiens 192-196
23449393-1 2013 Stra6 is the retinoic acid (RA)-inducible gene encoding the cellular receptor for holo-retinol binding protein. Tretinoin 13-26 signaling receptor and transporter of retinol STRA6 Homo sapiens 0-5
8393772-7 1993 1,25-dihydroxyvitamin D3 and retinoic acid increase thrombomodulin expression and activity in a dose-dependent manner whereas tumor necrosis factor alpha and interleukin 1 decrease these parameters. Tretinoin 29-42 thrombomodulin Homo sapiens 52-66
23449393-1 2013 Stra6 is the retinoic acid (RA)-inducible gene encoding the cellular receptor for holo-retinol binding protein. Tretinoin 28-30 signaling receptor and transporter of retinol STRA6 Homo sapiens 0-5
23472658-0 2013 IL-23/IL-17A axis correlates with the nitric oxide pathway in inflammatory bowel disease: immunomodulatory effect of retinoic acid. Tretinoin 117-130 interleukin 23 subunit alpha Homo sapiens 0-5
7508772-5 1993 This case supports the concept that G-CSF accelerates ATRA-induced neutrophilic differentiation of blast cells in APL. Tretinoin 54-58 colony stimulating factor 3 Homo sapiens 36-41
22797059-8 2013 Intriguingly, it was determined that miR-340 is upregulated by demethylation of an upstream genomic region that occurs during the process of neuroblastoma cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 197-210 microRNA 340 Homo sapiens 37-44
8393014-16 1993 In cultured hypertrophic chondrocytes treated with 500 nM retinoic acid, ovotransferrin is maximally expressed 3 d after retinoic acid addition, when the cartilage-bone-specific collagen shift occurs, and decays between the 5th and the 10th day, when cells have fully acquired the osteoblast-like phenotype. Tretinoin 58-71 transferrin (ovotransferrin) Gallus gallus 73-87
8393014-16 1993 In cultured hypertrophic chondrocytes treated with 500 nM retinoic acid, ovotransferrin is maximally expressed 3 d after retinoic acid addition, when the cartilage-bone-specific collagen shift occurs, and decays between the 5th and the 10th day, when cells have fully acquired the osteoblast-like phenotype. Tretinoin 121-134 transferrin (ovotransferrin) Gallus gallus 73-87
7689128-1 1993 Recombinant human granulocyte colony-stimulating factor (rhG-CSF) not only enhanced the growth of HL-60 cells, but also significantly increased NBT-reducing ability and alkaline phosphatase (ALP) activity of the cells, which were enhanced by the treatment with retinoic acid (RA). Tretinoin 261-274 colony stimulating factor 3 Homo sapiens 18-55
8174476-6 1993 The analysis of lactic acid dehydrogenase (LDH) isoenzyme showed that the activity of LDH3 increased after RA treatment but without LDH1 and LDH2 expression. Tretinoin 107-109 lactate dehydrogenase C Homo sapiens 43-46
8174476-6 1993 The analysis of lactic acid dehydrogenase (LDH) isoenzyme showed that the activity of LDH3 increased after RA treatment but without LDH1 and LDH2 expression. Tretinoin 107-109 lactate dehydrogenase C Homo sapiens 86-90
8394219-5 1993 We expressed the PML-RAR alpha protein in U937 myeloid precursor cells and showed that they lost the capacity to differentiate under the action of different stimuli (vitamin D3 and transforming growth factor beta 1), acquired enhanced sensitivity to retinoic acid, and exhibited a higher growth rate consequent to diminished apoptotic cell death. Tretinoin 250-263 PML nuclear body scaffold Homo sapiens 17-20
8394219-5 1993 We expressed the PML-RAR alpha protein in U937 myeloid precursor cells and showed that they lost the capacity to differentiate under the action of different stimuli (vitamin D3 and transforming growth factor beta 1), acquired enhanced sensitivity to retinoic acid, and exhibited a higher growth rate consequent to diminished apoptotic cell death. Tretinoin 250-263 retinoic acid receptor alpha Homo sapiens 21-30
8344389-6 1993 Within 4 days of treatment, RA dramatically induced expression of the alkaline phosphatase (APase), osteonectin, and osteopontin genes, caused a several-fold increase in APase activity, and provoked massive mineral formation while it left type X collagen gene expression largely unchanged. Tretinoin 28-30 secreted phosphoprotein 1 Homo sapiens 117-128
22797059-8 2013 Intriguingly, it was determined that miR-340 is upregulated by demethylation of an upstream genomic region that occurs during the process of neuroblastoma cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 212-216 microRNA 340 Homo sapiens 37-44
23665324-6 2013 Interestingly, mAchR inhibitors also reduced the expression of Cyp26a1, an enzyme involved in the catabolism of retinoic acid (RA). Tretinoin 112-125 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 63-70
8391258-2 1993 It is shown that the expression of human glutathione S-transferase P1-1 (GSTP1-1) is suppressed by retinoic acid (RA) as the result of decreased transcription from its gene, GSTP1. Tretinoin 99-112 glutathione S-transferase pi 1 Homo sapiens 73-80
8391258-2 1993 It is shown that the expression of human glutathione S-transferase P1-1 (GSTP1-1) is suppressed by retinoic acid (RA) as the result of decreased transcription from its gene, GSTP1. Tretinoin 99-112 glutathione S-transferase pi 1 Homo sapiens 73-78
7686602-2 1993 Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF). Tretinoin 56-69 colony stimulating factor 3 Homo sapiens 274-311
7686602-2 1993 Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF). Tretinoin 56-69 colony stimulating factor 3 Homo sapiens 313-318
7686602-2 1993 Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF). Tretinoin 56-69 colony stimulating factor 2 Homo sapiens 379-405
7686602-2 1993 Previous studies have shown: (i) blast cells exposed to retinoic acid before cytosine arabinoside (Ara-C) usually show increased sensitivity, but after some retinoic acid exposure times, sensitivity may be decreased; (ii) factor-sensitive or responsive blasts cultured with granulocyte colony-stimulating factor (G-CSF) are regularly more Ara-C-sensitive than when cultured with granulocyte-macrophage CSF (GM-CSF). Tretinoin 56-69 colony stimulating factor 2 Homo sapiens 407-413
8391258-2 1993 It is shown that the expression of human glutathione S-transferase P1-1 (GSTP1-1) is suppressed by retinoic acid (RA) as the result of decreased transcription from its gene, GSTP1. Tretinoin 114-116 glutathione S-transferase pi 1 Homo sapiens 73-80
8401251-11 1993 During retinoic acid treatment, N-myc oncogene expression decreases and other genes are deregulated. Tretinoin 7-20 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 32-37
23665324-6 2013 Interestingly, mAchR inhibitors also reduced the expression of Cyp26a1, an enzyme involved in the catabolism of retinoic acid (RA). Tretinoin 127-129 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 63-70
8396481-7 1993 Preliminary results suggest that the PML/RAR alpha fusion protein is responsible for two important properties of the APL phenotype: the differentiation block characteristic of the leukemic blasts and the high sensitivity of the blasts to the differentiative action of retinoic acid (RA) both in vivo and in vitro. Tretinoin 268-281 PML nuclear body scaffold Homo sapiens 37-50
8162329-9 1993 Pretreatment of cultures with retinoic acid (10(-5)-10(-7) M) significantly inhibited the induction of ODC by EGF. Tretinoin 30-43 epidermal growth factor Homo sapiens 110-113
23600975-4 2013 PCDH11X and PCDH11Y, differentially regulated by retinoic acid, are highly expressed in the ventricular zone, subplate, and cortical plate of the developing cerebral cortex. Tretinoin 49-62 protocadherin 11 X-linked Homo sapiens 0-7
7684042-6 1993 Treatment of MDA-MB-231 and MDA-MB-468 cells with RA increased the levels in conditioned media of a M(r) 42-46-kDa IGFBP, which was immunoprecipitated by an IGFBP-3 antibody. Tretinoin 50-52 insulin like growth factor binding protein 3 Homo sapiens 157-164
7684042-9 1993 The difference in the magnitude of the RA enhancement of IGFBP-3 mRNA levels (1.5-fold) and RA stimulation of IGFBP-3 levels in conditioned media (3.5-4-fold) suggests that some of the effect of RA is at a posttranscriptional level. Tretinoin 39-41 insulin like growth factor binding protein 3 Homo sapiens 57-64
7684042-9 1993 The difference in the magnitude of the RA enhancement of IGFBP-3 mRNA levels (1.5-fold) and RA stimulation of IGFBP-3 levels in conditioned media (3.5-4-fold) suggests that some of the effect of RA is at a posttranscriptional level. Tretinoin 92-94 insulin like growth factor binding protein 3 Homo sapiens 110-117
8389144-4 1993 Trace amounts of TM antigen were induced in neutrophilic cells differentiated from HL-60 by treatment with retinoic acid. Tretinoin 107-120 thrombomodulin Homo sapiens 17-19
23528537-0 2013 Retinoic acid-induced HOXA5 expression is co-regulated by HuR and miR-130a. Tretinoin 0-13 homeobox A5 Homo sapiens 22-27
8389207-4 1993 This site was used in BALB/c 3T3 cells constitutively expressing TM, and when TM expression was induced in F9 teratocarcinoma cells in response to retinoic acid (RA) and dibutyryl cAMP (dbcAMP). Tretinoin 147-160 thrombomodulin Mus musculus 78-80
8389207-4 1993 This site was used in BALB/c 3T3 cells constitutively expressing TM, and when TM expression was induced in F9 teratocarcinoma cells in response to retinoic acid (RA) and dibutyryl cAMP (dbcAMP). Tretinoin 162-164 thrombomodulin Mus musculus 78-80
8389207-6 1993 CAT activity was induced on exposure to RA and dbcAMP and mimicked the pattern of expression of the endogenous TM gene. Tretinoin 40-42 thrombomodulin Mus musculus 111-113
23528537-0 2013 Retinoic acid-induced HOXA5 expression is co-regulated by HuR and miR-130a. Tretinoin 0-13 ELAV like RNA binding protein 1 Homo sapiens 58-61
23528537-6 2013 Upon RA treatment, c-Myc is quickly degraded via the proteasome-dependent pathway. Tretinoin 5-7 MYC proto-oncogene, bHLH transcription factor Homo sapiens 19-24
23528537-9 2013 Collectively, these results demonstrate that HuR and miR-130a dynamically regulate HOXA5 gene expression via modulating HOXA5 mRNA turnover and translation, respectively, thereby contributing to RA-induced growth inhibition. Tretinoin 195-197 ELAV like RNA binding protein 1 Homo sapiens 45-48
8097725-3 1993 We have investigated the role of retinoic acid receptor alpha (RAR alpha) in retinoic acid-dependent induction of HOX-2 gene expression in embryocarcinoma (EC) cells by using the P19 RAC65 EC cell line, which is retinoic acid-resistant due to the expression of a dominant negative RAR alpha. Tretinoin 33-46 homeobox B cluster Mus musculus 114-119
8097725-3 1993 We have investigated the role of retinoic acid receptor alpha (RAR alpha) in retinoic acid-dependent induction of HOX-2 gene expression in embryocarcinoma (EC) cells by using the P19 RAC65 EC cell line, which is retinoic acid-resistant due to the expression of a dominant negative RAR alpha. Tretinoin 77-90 homeobox B cluster Mus musculus 114-119
23528537-9 2013 Collectively, these results demonstrate that HuR and miR-130a dynamically regulate HOXA5 gene expression via modulating HOXA5 mRNA turnover and translation, respectively, thereby contributing to RA-induced growth inhibition. Tretinoin 195-197 homeobox A5 Homo sapiens 83-88
23528537-9 2013 Collectively, these results demonstrate that HuR and miR-130a dynamically regulate HOXA5 gene expression via modulating HOXA5 mRNA turnover and translation, respectively, thereby contributing to RA-induced growth inhibition. Tretinoin 195-197 homeobox A5 Homo sapiens 120-125
23441061-5 2013 Blocking retinoic acid signaling using a retinoic acid antagonist results in a corresponding decrease in the levels of ski mRNA. Tretinoin 9-22 SKI proto-oncogene Homo sapiens 119-122
8505143-3 1993 Peak potentiation of IL-2 responses occurred over a pharmacologic range of retinoic acid (RA) concentration (10(-10)-10(-8) M) in the presence of 20 U/ml rIL-2. Tretinoin 75-88 interleukin 2 Mus musculus 21-25
23441061-5 2013 Blocking retinoic acid signaling using a retinoic acid antagonist results in a corresponding decrease in the levels of ski mRNA. Tretinoin 41-54 SKI proto-oncogene Homo sapiens 119-122
8505143-3 1993 Peak potentiation of IL-2 responses occurred over a pharmacologic range of retinoic acid (RA) concentration (10(-10)-10(-8) M) in the presence of 20 U/ml rIL-2. Tretinoin 90-92 interleukin 2 Mus musculus 21-25
8505143-3 1993 Peak potentiation of IL-2 responses occurred over a pharmacologic range of retinoic acid (RA) concentration (10(-10)-10(-8) M) in the presence of 20 U/ml rIL-2. Tretinoin 90-92 interleukin 2 Rattus norvegicus 154-159
23441061-6 2013 Finally, overexpression of SKI in human cells results in reduced levels of CYP26A1 mRNA, a known target of retinoic acid signaling. Tretinoin 107-120 SKI proto-oncogene Homo sapiens 27-30
8505143-5 1993 Preincubation of the spleen cells with Con A plus RA without the subsequent addition of IL-2 resulted in a proliferative response that was potentiated nearly to the level of the response produced by subsequent addition of IL-2 to Con A-activated cells. Tretinoin 50-52 interleukin 2 Mus musculus 222-226
8505143-6 1993 Preincubation of the cells with Con A in the presence of RA produced a true synergy with IL-2; the resulting increase in response was greater than the sum of the increases produced by RA or IL-2 alone. Tretinoin 57-59 interleukin 2 Mus musculus 89-93
8505143-6 1993 Preincubation of the cells with Con A in the presence of RA produced a true synergy with IL-2; the resulting increase in response was greater than the sum of the increases produced by RA or IL-2 alone. Tretinoin 57-59 interleukin 2 Mus musculus 190-194
23441061-7 2013 CONCLUSIONS: Our results, coupled with the known ability of Ski to repress retinoic acid signaling, demonstrate that Ski expression is a novel negative feedback mechanism acting on retinoic acid signaling. Tretinoin 75-88 SKI proto-oncogene Homo sapiens 60-63
8505143-6 1993 Preincubation of the cells with Con A in the presence of RA produced a true synergy with IL-2; the resulting increase in response was greater than the sum of the increases produced by RA or IL-2 alone. Tretinoin 184-186 interleukin 2 Mus musculus 89-93
23441061-7 2013 CONCLUSIONS: Our results, coupled with the known ability of Ski to repress retinoic acid signaling, demonstrate that Ski expression is a novel negative feedback mechanism acting on retinoic acid signaling. Tretinoin 75-88 SKI proto-oncogene Homo sapiens 117-120
8497851-0 1993 Retinoic acid enhances fibrinolytic activity in-vivo by enhancing tissue type plasminogen activator (t-PA) activity and inhibits venous thrombosis. Tretinoin 0-13 plasminogen activator, tissue type Rattus norvegicus 66-99
8497851-0 1993 Retinoic acid enhances fibrinolytic activity in-vivo by enhancing tissue type plasminogen activator (t-PA) activity and inhibits venous thrombosis. Tretinoin 0-13 plasminogen activator, tissue type Rattus norvegicus 101-105
8497851-8 1993 Lysis of blood clots from vehicle and retinoic acid treated rats could be completely blocked by addition of tranexamic acid or antibodies against rat t-PA before clot formation. Tretinoin 38-51 plasminogen activator, tissue type Rattus norvegicus 150-154
8497851-10 1993 t-PA activity in lung and kidney was marginally enhanced by retinoic acid but in heart and aortic tissue extracts t-PA activity was increased by about 50%. Tretinoin 60-73 plasminogen activator, tissue type Rattus norvegicus 0-4
23441061-7 2013 CONCLUSIONS: Our results, coupled with the known ability of Ski to repress retinoic acid signaling, demonstrate that Ski expression is a novel negative feedback mechanism acting on retinoic acid signaling. Tretinoin 181-194 SKI proto-oncogene Homo sapiens 60-63
23441061-7 2013 CONCLUSIONS: Our results, coupled with the known ability of Ski to repress retinoic acid signaling, demonstrate that Ski expression is a novel negative feedback mechanism acting on retinoic acid signaling. Tretinoin 181-194 SKI proto-oncogene Homo sapiens 117-120
8385052-0 1993 Bovine urokinase-type plasminogen activator and its receptor: cloning and induction by retinoic acid. Tretinoin 87-100 plasminogen activator, urokinase Bos taurus 7-43
23587393-7 2013 Retinoic acid-induced differentiation of MAC-T cells was associated with an increase in the mRNA expression of alphaS1-casein (3.9-fold), alphaS2-casein (4.5-fold), and beta-casein (4.4-fold) compared with the control group. Tretinoin 0-13 casein alpha s1 Bos taurus 111-125
8385052-5 1993 Northern blot hybridization demonstrated a moderate induction of u-PA and u-PAR mRNA in bovine aortic endothelial cells after treatment with 10 nM and 1 microM retinoic acid for 8 hours. Tretinoin 160-173 plasminogen activator, urokinase Bos taurus 65-69
8385314-2 1993 We found that in Drosophila SL-3 cells that are devoid of endogenous RARs and RXRs the presence of RAR is sufficient to confer a response to all-trans retinoic acid (RA). Tretinoin 151-164 retinoic acid receptor alpha Homo sapiens 69-72
23528261-2 2013 In NB4 and HL60 cell lines, BMPs reduced the percentage of differentiated cells, and suppressed PU.1 and C/EBPepsilon gene expression induced by ATRA. Tretinoin 145-149 Spi-1 proto-oncogene Homo sapiens 96-100
8382210-8 1993 RA treatment of both mouse C2 and chicken satellite cells caused rapid induction of the RAR-alpha mRNA levels. Tretinoin 0-2 retinoic acid receptor alpha Gallus gallus 88-97
8445950-7 1993 The induction of c-fms transcripts by ATRA is associated with induction of M-CSF-binding ability, suggesting cell surface expression of the monocyte growth factor receptor. Tretinoin 38-42 colony stimulating factor 1 Homo sapiens 75-80
23528261-2 2013 In NB4 and HL60 cell lines, BMPs reduced the percentage of differentiated cells, and suppressed PU.1 and C/EBPepsilon gene expression induced by ATRA. Tretinoin 145-149 CCAAT enhancer binding protein epsilon Homo sapiens 105-117
23588859-0 2013 c-myc but not Hif-1alpha-dependent downregulation of VEGF influences the proliferation and differentiation of HL-60 cells induced by ATRA. Tretinoin 133-137 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
8442757-0 1993 Effects of retinoic acid on lipoprotein lipase activity and mRNA level in vitro and in vivo. Tretinoin 11-24 lipoprotein lipase Homo sapiens 28-46
23588859-10 2013 In conclusion, our data demonstrate that VEGF plays an important role in the differentiation and proliferation of HL-60 cells; c-myc-dependent downregulation of VEGF induced by ATRA contributes to the differentiation of HL-60 cells. Tretinoin 177-181 MYC proto-oncogene, bHLH transcription factor Homo sapiens 127-132
8442757-4 1993 Feeding all-trans retinoic acid for 4 days led to a significant decrease in adipose tissue LPL activity but no change in heart enzyme activity. Tretinoin 11-31 lipoprotein lipase Homo sapiens 91-94
8442757-8 1993 The observed decrease in adipose tissue LPL activity in vivo is not due to alterations in mRNA levels and may be a secondary effect of retinoic acid. Tretinoin 135-148 lipoprotein lipase Homo sapiens 40-43
23693014-10 2013 Interestingly, ATRA treatment induces the translocation of RARalpha to the plasma membrane, where it colocalizes with Akt. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 59-67
8381482-4 1993 Teratogenic doses of RA increase the level of RAR-beta 2 mRNA, RAR-alpha 2 mRNA, CRBP-I mRNA and CRABP-II mRNA in mouse conceptuses and embryos. Tretinoin 21-23 retinol binding protein 1, cellular Mus musculus 81-87
7678695-1 1993 In this study we evaluate, for the first time, the molecular mechanism that underlies the extinction of a tissue-specific transcription factor, Oct-3/4, in somatic cell hybrids and compared it with its down-regulation in retinoic acid (RA)-treated embryonal carcinoma (EC) cells. Tretinoin 221-234 POU class 5 homeobox 1 Homo sapiens 144-151
23321499-5 2013 Consistently, RA-induced cancer cell cytotoxicity was significantly impaired by Zyxin or PTOV1. Tretinoin 14-16 zyxin Homo sapiens 80-85
8018944-8 1993 (5) It seems likely that the fusion gene PML-RARA plays an important role in APL leukemogenesis and in its response to the ATRA treatment. Tretinoin 123-127 PML nuclear body scaffold Homo sapiens 41-44
8018944-8 1993 (5) It seems likely that the fusion gene PML-RARA plays an important role in APL leukemogenesis and in its response to the ATRA treatment. Tretinoin 123-127 retinoic acid receptor alpha Homo sapiens 45-49
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 26-45 synaptosome associated protein 25 Homo sapiens 240-274
8518028-4 1993 Recombinant human granulocyte-macrophage colony-stimulating factor (RhGM-CSF) can increase and retinoic acid/alpha-interferon can decrease c-myc expression in myeloid cells in vivo. Tretinoin 95-108 MYC proto-oncogene, bHLH transcription factor Homo sapiens 139-144
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 26-45 synaptosome associated protein 25 Homo sapiens 276-283
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 47-49 synaptosome associated protein 25 Homo sapiens 240-274
8416796-1 1993 P19 teratoma cells differentiate to neural-like cells in the presence of retinoic acid. Tretinoin 73-86 interleukin 23 subunit alpha Homo sapiens 0-3
23597229-6 2013 Cells treated with 10 muM trans-retinoic acid (RA) for 72 hrs exhibited marked changes in morphology to include neurite extensions; presence of P/Q, N and T-type voltage-gated Ca2+ channels; and expression of neuron specific enolase (NSE), synaptosomal-associated protein 25 (SNAP-25), nicotinic acetylcholine receptor alpha7 (nAChR-alpha7) and other neuronal markers. Tretinoin 47-49 synaptosome associated protein 25 Homo sapiens 276-283
8416796-2 1993 If they are plated in N2 synthetic, serum-free medium without being exposed to retinoic acid, they die within 48-72 h. This model has allowed the discovery of the neuron survival-promoting capacity of activin. Tretinoin 79-92 inhibin subunit beta E Homo sapiens 201-208
23613978-2 2013 We found that the expression of Csn3 was induced by all-trans retinoic acid (ATRA) during neural differentiation in P19 embryonal carcinoma cells from our study using DNA microarray. Tretinoin 52-75 casein kappa Mus musculus 32-36
8093325-4 1993 The expression of murine Hox-4.2 and its human homolog, HOX4B, is increased in embryonal carcinoma (EC) cell lines upon RA treatment (M. S. Featherstone, A. Baron, S. J. Gaunt, M.-G. Mattei, and D. Duboule, Proc. Tretinoin 120-122 homeobox D4 Homo sapiens 56-61
23613978-2 2013 We found that the expression of Csn3 was induced by all-trans retinoic acid (ATRA) during neural differentiation in P19 embryonal carcinoma cells from our study using DNA microarray. Tretinoin 77-81 casein kappa Mus musculus 32-36
1472015-8 1992 The present report describes the induction of LTC4 synthase activity during differentiation of human erythroleukemia (HEL) cells by the protein kinase C stimulator 12-O-tetradecanoyl phorbol 13-acetate (TPA), ligands of the steroid-thyroid hormone receptor superfamily: all-trans-retinoic acid (RA) and 1 alpha, 25-dihydroxy-vitamin D3 and in addition dimethylsulfoxide (DMSO). Tretinoin 270-293 leukotriene C4 synthase Homo sapiens 46-59
23613978-4 2013 The Csn3 expression was induced rapidly and transiently within 24 h of ATRA treatment. Tretinoin 71-75 casein kappa Mus musculus 4-8
1472015-8 1992 The present report describes the induction of LTC4 synthase activity during differentiation of human erythroleukemia (HEL) cells by the protein kinase C stimulator 12-O-tetradecanoyl phorbol 13-acetate (TPA), ligands of the steroid-thyroid hormone receptor superfamily: all-trans-retinoic acid (RA) and 1 alpha, 25-dihydroxy-vitamin D3 and in addition dimethylsulfoxide (DMSO). Tretinoin 295-297 leukotriene C4 synthase Homo sapiens 46-59
23613978-5 2013 Retinoic acid receptor (RAR)-specific agonists were used in expression analysis to identify the RAR subtype involved upregulation of Csn3; a RARalpha-specific agonist mimicked the effects of ATRA on induction of Csn3 expression. Tretinoin 191-195 casein kappa Mus musculus 133-137
23613978-5 2013 Retinoic acid receptor (RAR)-specific agonists were used in expression analysis to identify the RAR subtype involved upregulation of Csn3; a RARalpha-specific agonist mimicked the effects of ATRA on induction of Csn3 expression. Tretinoin 191-195 casein kappa Mus musculus 212-216
23613978-6 2013 Therefore, RARalpha may be the RAR subtype mediating the effects of ATRA on the induction of Csn3 gene transcription in this differentiation-promoting process of P19 cells. Tretinoin 68-72 casein kappa Mus musculus 93-97
1460033-0 1992 Differential regulation of biglycan and decorin by retinoic acid in bovine chondrocytes. Tretinoin 51-64 biglycan Bos taurus 27-35
23613978-7 2013 We found that the promoter region of Csn3 contained a typical consensus retinoic acid response element (RARE), and this RARE was necessary for ATRA-dependent transcriptional regulation. Tretinoin 72-85 casein kappa Mus musculus 37-41
1460033-2 1992 We have examined the effects of retinoic acid (RA) on the expression of biglycan and decorin at the protein and mRNA levels in cultured bovine articular chondrocytes. Tretinoin 32-45 biglycan Bos taurus 72-80
1460033-2 1992 We have examined the effects of retinoic acid (RA) on the expression of biglycan and decorin at the protein and mRNA levels in cultured bovine articular chondrocytes. Tretinoin 47-49 biglycan Bos taurus 72-80
23428742-7 2013 Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. Tretinoin 37-39 matrix metallopeptidase 1 Homo sapiens 108-143
1460033-3 1992 Biglycan protein expression is rapidly turned off after 1-2 days of treatment with RA. Tretinoin 83-85 biglycan Bos taurus 0-8
1460033-11 1992 In contrast, the repression of biglycan by RA was not significantly altered by cycloheximide, showing that the repression was a direct effect. Tretinoin 43-45 biglycan Bos taurus 31-39
23042455-5 2013 This process is dependent on protein phosphatase 2A (PP2A) activity since selective PP2A inhibitors prevented the ability of RA to dephosphorylate Cx43. Tretinoin 125-127 protein phosphatase 2 phosphatase activator Homo sapiens 53-57
1285021-4 1992 L2 cells produced tPA, which production was stimulated by retinoic acid, phorbol myristate acetate, butyrate and cAMP; serum factors blunted their response, whereas in the synthetic serum substituting medium Ultraculture and with cocktail Ultroser the action of tPA stimulators was enhanced. Tretinoin 58-71 plasminogen activator, tissue type Rattus norvegicus 18-21
23042455-5 2013 This process is dependent on protein phosphatase 2A (PP2A) activity since selective PP2A inhibitors prevented the ability of RA to dephosphorylate Cx43. Tretinoin 125-127 protein phosphatase 2 phosphatase activator Homo sapiens 84-88
23042455-6 2013 Although RA had no effect on total PP2A expression or activity, it significantly increased the intracellular association of Cx43 and PP2A. Tretinoin 9-11 protein phosphatase 2 phosphatase activator Homo sapiens 133-137
23042455-9 2013 Our data indicate that RA stimulates physical association of PP2A with Cx43, resulting in the dephosphorylation of Cx43 and, as a consequence, up-regulation of GJIC in ESCs. Tretinoin 23-25 protein phosphatase 2 phosphatase activator Homo sapiens 61-65
1333043-2 1992 We demonstrate here that retinoic acid receptor alpha (RAR alpha) binds to a sequence within the AF1 element, TGACCT (site B), that is a consensus retinoic acid response element (RARE) half-site. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 55-64
22560855-16 2013 Compared with the I/R group, ATRA treatment increased IkappaBalpha expression and suppressed NF-kappaB p65 expression. Tretinoin 29-33 NFKB inhibitor alpha Rattus norvegicus 54-66
1333043-5 1992 Mutational analysis of the AF1 element shows that the RAR alpha/CR complex is the trans-acting unit that mediates the retinoic acid response of the PEPCK gene. Tretinoin 118-131 retinoic acid receptor alpha Homo sapiens 54-63
1330076-0 1992 Retinoic acid counteracts both the downregulation of thrombomodulin and the induction of tissue factor in cultured human endothelial cells exposed to tumor necrosis factor. Tretinoin 0-13 thrombomodulin Homo sapiens 53-67
1330076-0 1992 Retinoic acid counteracts both the downregulation of thrombomodulin and the induction of tissue factor in cultured human endothelial cells exposed to tumor necrosis factor. Tretinoin 0-13 coagulation factor III, tissue factor Homo sapiens 89-102
1330076-3 1992 The approximate 50% downregulation of TM antigen and cofactor activity induced by TNF-alpha (10 U/mL for 24 hours) was completely prevented when the cells were coincubated with both TNF-alpha and 10 mumol/L RA. Tretinoin 207-209 thrombomodulin Homo sapiens 38-40
8498603-2 1993 Hypervitaminosis A and retinoic acid treatment increased plasma TPA activity by approximately 50%, but PAI-1 activity was not affected. Tretinoin 23-36 plasminogen activator, tissue type Rattus norvegicus 64-67
8498603-6 1993 Modulation of plasma TPA activity by vitamin A status and retinoic acid treatment was associated with similar changes in tissue TPA activity. Tretinoin 58-71 plasminogen activator, tissue type Rattus norvegicus 21-24
8498603-6 1993 Modulation of plasma TPA activity by vitamin A status and retinoic acid treatment was associated with similar changes in tissue TPA activity. Tretinoin 58-71 plasminogen activator, tissue type Rattus norvegicus 128-131
8386680-0 1993 Down-regulation by retinoic acid of the catalytic subunit of protein phosphatase type 2A during granulocytic differentiation of HL-60 cells. Tretinoin 19-32 protein phosphatase 2 phosphatase activator Homo sapiens 69-88
8386680-2 1993 Treatment of HL-60 cells with ATRA led to a dramatic decrease in the amount of protein phosphatase type 2A (PP2A) protein, whereas that of protein phosphatase type 1 (PP1) protein was relatively constant, as detected by immunoblotting with antibodies specific to PP1 and PP2A. Tretinoin 30-34 protein phosphatase 2 phosphatase activator Homo sapiens 87-106
8386680-2 1993 Treatment of HL-60 cells with ATRA led to a dramatic decrease in the amount of protein phosphatase type 2A (PP2A) protein, whereas that of protein phosphatase type 1 (PP1) protein was relatively constant, as detected by immunoblotting with antibodies specific to PP1 and PP2A. Tretinoin 30-34 protein phosphatase 2 phosphatase activator Homo sapiens 108-112
8386680-2 1993 Treatment of HL-60 cells with ATRA led to a dramatic decrease in the amount of protein phosphatase type 2A (PP2A) protein, whereas that of protein phosphatase type 1 (PP1) protein was relatively constant, as detected by immunoblotting with antibodies specific to PP1 and PP2A. Tretinoin 30-34 protein phosphatase 2 phosphatase activator Homo sapiens 271-275
8386680-6 1993 Thus, PP2A is down-regulated during ATRA-induced differentiation of HL-60 cells into granulocytes. Tretinoin 36-40 protein phosphatase 2 phosphatase activator Homo sapiens 6-10
1328864-3 1992 When F9 cells are stably transfected with a truncated RAR alpha lacking the E/F domain necessary for ligand binding and RAR/RXR dimerization, action at retinoid response elements is suppressed and cells produce a retinoic acid-resistant phenotype; i.e., they are blocked in differentiation (A. S. Espeseth, S. P. Murphy, and E. Linney, Genes Dev. Tretinoin 213-226 retinoic acid receptor alpha Homo sapiens 54-63
23590952-3 2013 The aims of this study were to examine the effects of maternal retinoic acid treatment on lung VEGF expression and angiogenesis in oligohydramnios-exposed fetal rats. Tretinoin 63-76 vascular endothelial growth factor A Rattus norvegicus 95-99
1437149-10 1992 We also analysed IP-1 regulation upon differentiation of P19 embryonal carcinoma cells by retinoic acid. Tretinoin 90-103 inhibitor of nuclear factor kappa B kinase regulatory subunit gamma Homo sapiens 17-21
8387013-8 1993 RA treatment markedly induced expression of the gene encoding the beta isoform of retinoic acid receptor (RAR beta) and also provoked a moderate 2.5-fold increase in RAR alpha gene expression. Tretinoin 0-2 retinoic acid receptor beta Gallus gallus 106-114
8387013-8 1993 RA treatment markedly induced expression of the gene encoding the beta isoform of retinoic acid receptor (RAR beta) and also provoked a moderate 2.5-fold increase in RAR alpha gene expression. Tretinoin 0-2 retinoic acid receptor alpha Gallus gallus 166-175
23637584-3 2013 Regulation of these receptors occurs through the binding of hormones, and in the case of the retinoic acid receptor (RAR), through the binding of retinoic acid (RA). Tretinoin 93-106 retinoic acid receptor alpha Homo sapiens 117-120
8483267-2 1993 Retinoic acid is an oxidative metabolite which is produced intracellularly and plays role in gene expression via nuclear retinoic acid receptor (RAR), a family of steroid receptor. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 121-143
8483267-2 1993 Retinoic acid is an oxidative metabolite which is produced intracellularly and plays role in gene expression via nuclear retinoic acid receptor (RAR), a family of steroid receptor. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 145-148
8483267-3 1993 Recently, clinical use of retinoic acid in acute pro-myelocytic leukemia (APL) was proposed to induce complete remission in the leukemic cells, which have the t(15:17) of chromosomal anomaly producing a different protein from the normal RAR. Tretinoin 26-39 retinoic acid receptor alpha Homo sapiens 237-240
7748347-4 1993 We have shown that expression of the human ADH3 gene is induced by retinoic acid, thus further supporting the role of ADH in retinoic acid synthesis and suggesting the existence of a positive feedback loop. Tretinoin 67-80 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 43-47
1382709-2 1992 GM-CSF or IL-3 stimulation of HL-60 cells pretreated with either dimethyl sulfoxide (DMSO) or retinoic acid results in increases in proliferative response as well as both tyrosine and serine phosphorylation. Tretinoin 94-107 colony stimulating factor 2 Homo sapiens 0-6
1382709-2 1992 GM-CSF or IL-3 stimulation of HL-60 cells pretreated with either dimethyl sulfoxide (DMSO) or retinoic acid results in increases in proliferative response as well as both tyrosine and serine phosphorylation. Tretinoin 94-107 interleukin 3 Homo sapiens 10-14
1328196-4 1992 The retinoic acid-induced activation was 3-4-fold higher with RXR alpha than with either RAR alpha or RAR beta. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 89-98
7748347-4 1993 We have shown that expression of the human ADH3 gene is induced by retinoic acid, thus further supporting the role of ADH in retinoic acid synthesis and suggesting the existence of a positive feedback loop. Tretinoin 67-80 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 43-46
7748347-4 1993 We have shown that expression of the human ADH3 gene is induced by retinoic acid, thus further supporting the role of ADH in retinoic acid synthesis and suggesting the existence of a positive feedback loop. Tretinoin 125-138 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 43-47
23486062-2 2013 In mouse female PGCs, expression of stimulated by retinoic acid gene 8 (Stra8) and meiosis are induced in response to retinoic acid provided from the mesonephroi. Tretinoin 50-63 stimulated by retinoic acid gene 8 Mus musculus 72-77
7748347-4 1993 We have shown that expression of the human ADH3 gene is induced by retinoic acid, thus further supporting the role of ADH in retinoic acid synthesis and suggesting the existence of a positive feedback loop. Tretinoin 125-138 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 43-46
8093685-8 1993 Treatment of neuroblastoma cells in culture with retinoic acid, which induces differentiation, resulted in a substantial decrease in PCNA. Tretinoin 49-62 proliferating cell nuclear antigen Homo sapiens 133-137
1339190-6 1992 The DNA-binding motifs of both the RARA and PML proteins, together with the ligand-binding domain of RARA, are combined in a single fusion protein which may dysregulate either retinoic acid or PML-sensitive pathways. Tretinoin 176-189 retinoic acid receptor alpha Homo sapiens 35-39
1339190-6 1992 The DNA-binding motifs of both the RARA and PML proteins, together with the ligand-binding domain of RARA, are combined in a single fusion protein which may dysregulate either retinoic acid or PML-sensitive pathways. Tretinoin 176-189 PML nuclear body scaffold Homo sapiens 44-47
1339190-6 1992 The DNA-binding motifs of both the RARA and PML proteins, together with the ligand-binding domain of RARA, are combined in a single fusion protein which may dysregulate either retinoic acid or PML-sensitive pathways. Tretinoin 176-189 retinoic acid receptor alpha Homo sapiens 101-105
1339190-9 1992 The PML-RARA chimaeric protein is presumably the target during the striking differentiation therapy achieved with all-trans retinoic acid. Tretinoin 124-137 PML nuclear body scaffold Homo sapiens 4-7
1339190-9 1992 The PML-RARA chimaeric protein is presumably the target during the striking differentiation therapy achieved with all-trans retinoic acid. Tretinoin 124-137 retinoic acid receptor alpha Homo sapiens 8-12
1363087-6 1992 Expression of Hox-2.6 and Hox-2.1 was ectopically induced anteriorly in neurectoderm in response to RA on day 8. Tretinoin 100-102 homeobox B5 Mus musculus 26-33
1363087-11 1992 Krox-20 expression was reduced in a stage- and region-specific manner by RA. Tretinoin 73-75 early growth response 2 Mus musculus 0-7
1363087-14 1992 The ectopic expression of the 3" Hox-2 genes in response to RA is consistent with a role for these genes in mediating the teratogenic effects of RA; the rapid response of the Hox-C genes to RA is consistent with a role for endogenous RA in refining 3" Hox-C gene expression boundaries early in development. Tretinoin 60-62 homeobox B cluster Mus musculus 33-38
1363087-14 1992 The ectopic expression of the 3" Hox-2 genes in response to RA is consistent with a role for these genes in mediating the teratogenic effects of RA; the rapid response of the Hox-C genes to RA is consistent with a role for endogenous RA in refining 3" Hox-C gene expression boundaries early in development. Tretinoin 145-147 homeobox B cluster Mus musculus 33-38
23486062-7 2013 Chemical inhibition of retinoic acid signalling partially suppresses precocious Oct4 downregulation and Stra8 activation in Rnf2-deficient female PGCs. Tretinoin 23-36 stimulated by retinoic acid gene 8 Mus musculus 104-109
1363087-14 1992 The ectopic expression of the 3" Hox-2 genes in response to RA is consistent with a role for these genes in mediating the teratogenic effects of RA; the rapid response of the Hox-C genes to RA is consistent with a role for endogenous RA in refining 3" Hox-C gene expression boundaries early in development. Tretinoin 145-147 homeobox B cluster Mus musculus 33-38
1363087-14 1992 The ectopic expression of the 3" Hox-2 genes in response to RA is consistent with a role for these genes in mediating the teratogenic effects of RA; the rapid response of the Hox-C genes to RA is consistent with a role for endogenous RA in refining 3" Hox-C gene expression boundaries early in development. Tretinoin 145-147 homeobox B cluster Mus musculus 33-38
22358703-2 1993 We have covalently linked a polylysine chain (10,000-20,000 mW) to compounds as folic acid, retinoic acid, transferrin, insulin and estradiol, to deliver c-myb antisense oligonucleotide into tumor cells. Tretinoin 92-105 MYB proto-oncogene, transcription factor Homo sapiens 154-159
7764059-2 1993 We have covalently linked a polylysine chain (10,000-20,000 mw) to compounds as folic acid, retinoic acid, transferrin, insulin and estradiol, to deliver c-myb antisense oligonucleotide into tumor cells. Tretinoin 92-105 MYB proto-oncogene, transcription factor Homo sapiens 154-159
23486062-7 2013 Chemical inhibition of retinoic acid signalling partially suppresses precocious Oct4 downregulation and Stra8 activation in Rnf2-deficient female PGCs. Tretinoin 23-36 ring finger protein 2 Mus musculus 124-128
23298258-0 2013 All-trans retinoic acid protects hepatocellular carcinoma cells against serum-starvation-induced cell death by upregulating collagen 8A2. Tretinoin 10-23 collagen type VIII alpha 2 chain Homo sapiens 124-136
7915184-3 1993 These include the proposal that retinoic acid and/or related retinoids are the morphogens responsible for the morphogenetic gradient giving rise to anterior-posterior pattern formation of the limb bud, the suggestion that the HOX4 complex and other homeotic genes may also be involved in patterning, and a greater understanding of other mechanisms such as programmed cell death in the shaping of the final hand and foot. Tretinoin 32-45 homeobox D11 Homo sapiens 226-230
1478951-6 1992 Densitometer evaluation of electrophoresed proteins revealed a 50% DMSO- and a 25% RA-induced myc reduction. Tretinoin 83-85 MYC proto-oncogene, bHLH transcription factor Homo sapiens 94-97
1478951-7 1992 Apart from growth reduction, which was seen for both inducers, inhibition of myc gene expression was the only response of HOC-7 cells to RA-treatment. Tretinoin 137-139 MYC proto-oncogene, bHLH transcription factor Homo sapiens 77-80
8217219-7 1993 The glucocorticoid, dexamethasone, and the retinoid, all-trans retinoic acid, stimulated M-CSF formation. Tretinoin 57-76 colony stimulating factor 1 Homo sapiens 89-94
23298258-8 2013 Knockdown of COL8A2 blocked enhancement in the early stage of cell adhesion by atRA treatment. Tretinoin 79-83 collagen type VIII alpha 2 chain Homo sapiens 13-19
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 48-61 retinoic acid receptor alpha Homo sapiens 161-183
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 48-61 retinoic acid receptor alpha Homo sapiens 185-188
23292364-8 2013 This effect, which was significantly associated and linearly correlated with PCNA expression, was abolished by the presence of retinoic acid in the culture medium. Tretinoin 151-164 proliferating cell nuclear antigen Homo sapiens 89-93
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 63-65 retinoic acid receptor alpha Homo sapiens 161-183
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 63-65 retinoic acid receptor alpha Homo sapiens 185-188
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 185-187 retinoic acid receptor alpha Homo sapiens 161-183
8381386-1 1993 The murine retinoid X receptor beta (mRXR beta) is a nuclear hormone receptor that activates transcription of murine major histocompatibility complex (MHC) class I genes in response to retinoic acid. Tretinoin 185-198 retinoid X receptor beta Mus musculus 37-46
8396187-0 1993 Retinoic acid-induced decrease of DNA synthesis and peroxidase mRNA levels in human thyroid cells expressing retinoic acid receptor alpha mRNA. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 109-137
1335685-5 1992 The molecular basis for the efficacy of ATRA in APL appears to be the involvement of the retinoic acid receptor alpha locus in the t(15;17) translocation breakpoint characteristic of APL. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 89-117
23429425-0 2013 Expression of claudins -2 and -4 and cingulin is coordinated with the start of stratification and differentiation in corneal epithelial cells: retinoic acid reversibly disrupts epithelial barrier. Tretinoin 143-156 claudin-2 Oryctolagus cuniculus 14-32
1324405-4 1992 To test this hypothesis in hematopoietic cells, we used retrovirus-mediated gene transduction to introduce the RA receptors RAR-alpha, RAR-beta, and RAR-gamma as well as RXR-alpha into a mutant subclone of the HL-60 promyelocytic leukemia cell line (designated HL-60R) that is relatively resistant to RA-induced granulocytic differentiation. Tretinoin 111-113 retinoic acid receptor alpha Homo sapiens 124-133
1323613-0 1992 Retinoic acid and phorbol ester synergistically up-regulate IL-8 expression and specifically modulate protein kinase C-epsilon in human skin fibroblasts. Tretinoin 0-13 protein kinase C epsilon Homo sapiens 102-126
7678054-4 1993 Cotransfection of ICSBP into cells treated with retinoic acid or any of the IFNs (alpha, beta, or gamma) repressed expression of a chloramphenicol acetyltransferase reporter driven by the major histocompatibility complex class I gene promoter. Tretinoin 48-61 interferon regulatory factor 8 Homo sapiens 18-23
7678054-10 1993 Taken together, these results suggest that ICSBP is a negative regulatory factor capable of repressing transcription of target genes induced by IFN, retinoic acid, or IRF-1. Tretinoin 149-162 interferon regulatory factor 8 Homo sapiens 43-48
1361214-4 1992 Here we follow the changes induced by retinoic acid to hindbrain segmentation and the branchial arches using transgenic mice which contain lacZ reporter genes that reveal the endogenous segment-restricted expression of the Hox-B1 (Hox-2.9), Hox-B2(Hox-2.8) and Krox-20 genes. Tretinoin 38-51 early growth response 2 Mus musculus 261-268
1365641-12 1992 In contrast, retinoic acid strongly increased phorbol myristate acetate-induced MCP-1 expression and potentiated the effects of IL-1 and LPS. Tretinoin 13-26 C-C motif chemokine ligand 2 Homo sapiens 80-85
1363523-2 1992 The expression of Thy-1 at the mRNA and protein levels is down-regulated during differentiation induced by retinoic acid (RA). Tretinoin 107-120 Thy-1 cell surface antigen Homo sapiens 18-23
23331247-9 2013 RA treatment resulted in Nrf2 inactivation by increasing RA receptor-alpha (RARalpha) activity, suggesting that RA acts as an inhibitor of Nrf2. Tretinoin 0-2 retinoic acid receptor, alpha Rattus norvegicus 76-84
1363523-2 1992 The expression of Thy-1 at the mRNA and protein levels is down-regulated during differentiation induced by retinoic acid (RA). Tretinoin 122-124 Thy-1 cell surface antigen Homo sapiens 18-23
1321136-3 1992 A region in the human ADH3 promoter from -328 to -272 base pairs was shown previously to function as a retinoic acid response element (RARE), prompting an hypothesis for a positive feedback mechanism controlling retinoic acid synthesis (Duester, G., Shean, M. L., McBride, M. S., and Stewart, M. J. Tretinoin 212-225 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 22-26
1423259-3 1992 Growth of UNC and E-3 was inhibited by either OHTAM (10(-7) M) or RA (10(-6) M), and this inhibition could not be overcome by the simultaneous addition of estradiol. Tretinoin 66-68 small nucleolar RNA, H/ACA box 63 Homo sapiens 18-21
23331247-9 2013 RA treatment resulted in Nrf2 inactivation by increasing RA receptor-alpha (RARalpha) activity, suggesting that RA acts as an inhibitor of Nrf2. Tretinoin 57-59 retinoic acid receptor, alpha Rattus norvegicus 76-84
1423259-5 1992 RR was resistant to RA at all concentrations tested between 10(-9) M and 10(-6) M. The inhibition of uncloned MCF-7 cells by RA was dose dependent between 10(-9) M and 10(-6) M. Subline E-3, however, exhibited a mixed response to RA. Tretinoin 125-127 small nucleolar RNA, H/ACA box 63 Homo sapiens 186-189
1637683-8 1992 All four agents inhibited myc oncoprotein expression reversibly (1% DMSO greater than 0.5% DMF greater than 10 microM RA greater than 10 ng ml-1 TGF-beta 1) and in time-dependent manner. Tretinoin 118-120 MYC proto-oncogene, bHLH transcription factor Homo sapiens 26-29
1324421-6 1992 RXR alpha complexes with RAR alpha, RAR beta, and RAR gamma bound selectively to retinoic acid responsive elements from the human RAR beta 2 gene (hRAR beta 2), the gene of the rat cellular retinol binding protein I and the human apolipoprotein A1 gene. Tretinoin 81-94 retinoic acid receptor alpha Homo sapiens 25-34
1423259-5 1992 RR was resistant to RA at all concentrations tested between 10(-9) M and 10(-6) M. The inhibition of uncloned MCF-7 cells by RA was dose dependent between 10(-9) M and 10(-6) M. Subline E-3, however, exhibited a mixed response to RA. Tretinoin 125-127 small nucleolar RNA, H/ACA box 63 Homo sapiens 186-189
22718360-6 2013 The inhibitory effect of RA on NF-kappaB activation was mediated through inhibition of IKK/IkappaBalpha phosphorylation. Tretinoin 25-27 NFKB inhibitor alpha Rattus norvegicus 91-103
22961837-4 2013 In this study, MafB gene expression was regulated by both the VA status of the mother (VA-marginal, adequate, and supplemented diets) and by direct oral supplementation of the neonates with VARA (VA mixed with 10% RA). Tretinoin 192-194 MAF bZIP transcription factor B Rattus norvegicus 15-19
1446821-8 1992 Treatment of TM4 cells with retinoic acid (RA) increases the level of LNGFR mRNA twofold, while testosterone treatment results in a tenfold decrease. Tretinoin 28-41 tropomyosin 4 Rattus norvegicus 13-16
1446821-8 1992 Treatment of TM4 cells with retinoic acid (RA) increases the level of LNGFR mRNA twofold, while testosterone treatment results in a tenfold decrease. Tretinoin 43-45 tropomyosin 4 Rattus norvegicus 13-16
1446821-9 1992 Regions of the promoter responsive to testosterone and RA in TM4 cells were found at -610 to -860 bp and -1840 to -4800 bp upstream from the translation start codon, respectively. Tretinoin 55-57 tropomyosin 4 Rattus norvegicus 61-64
1318236-2 1992 In transient transfection, an RAR alpha-beta-galactosidase fusion protein (RAR-LacZ) was able to transactivate expression in the absence of RA. Tretinoin 30-32 galactosidase, beta 1 Mus musculus 40-58
1590797-0 1992 Activin synergistically increased c-jun mRNA in P19 embryonal carcinoma cells in the presence of retinoic acid. Tretinoin 97-110 inhibin subunit beta E Homo sapiens 0-7
22961837-10 2013 These results support a role for MafB as a regulator of chondrocyte gene expression and matrix formation via control of aggrecan, MMP3 and MMP13 expression, and indicate an important role for RA in the regulation of MafB. Tretinoin 192-194 MAF bZIP transcription factor B Rattus norvegicus 216-220
1590797-3 1992 Activin (lng/ml) was sufficient to induce the synergistic increase of c-jun mRNA in P19 EC cells with all-trans-retinoic acid. Tretinoin 102-125 inhibin subunit beta E Homo sapiens 0-7
23243061-1 2013 All-trans-retinoic acid (ATRA) has held great promise for differentiation-based therapy but reportedly downregulates retinoic acid receptor-alpha (RARalpha) in a proteasome-dependent manner, which leads to decreased acute myeloid leukemia (AML) cell differentiation efficiency. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 147-155
1397312-2 1992 Furthermore, plasma membrane redox activity is partially inhibited by retinoic acid in neuroblastoma cells with multiple copies of the N-myc oncogene but not in neuroblastoma cells with only one copy of this gene. Tretinoin 70-83 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 135-140
23484687-1 2013 To verify the differential expression of non-metastasis cell 3 (NME3) protein in HL-60 cells when they were induced to differentiate into monocyte and granulocyte like cells, and study its value in diagnosis of acute myeloid leukemia, all-trans retinoic acid (ATRA) and a new steroidal drug NSC67657 were employed to induce acute myeloid leukemia HL-60 cells into monocyte and granulocyte like cells. Tretinoin 245-258 NME/NM23 nucleoside diphosphate kinase 3 Homo sapiens 64-68
1327285-2 1992 In the HL-60 promyelocytic leukemia cell line, this RA-induced granulocytic differentiation appears to be directly mediated through the RA receptor (RAR-alpha). Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 149-158
1400313-0 1992 Inhibition of mitogen-induced c-fos expression in melanoma cells by retinoic acid involves the serum response element. Tretinoin 68-81 FBJ osteosarcoma oncogene Mus musculus 30-35
1400313-1 1992 To investigate the mechanism(s) by which all-transretinoic acid (RA) inhibits cell growth, we studied its effect on the expression of c-fos and c-jun in B16 melanoma cells. Tretinoin 45-63 FBJ osteosarcoma oncogene Mus musculus 134-139
1316240-1 1992 In embryonal carcinoma (EC) cells retinoic acid (RA) strongly induces transcription from the RA receptor beta 2 (RAR beta 2) promoter through an RA response element (RARE) located in close proximity to the TATA box. Tretinoin 34-47 retinoic acid receptor alpha Homo sapiens 113-116
1316240-1 1992 In embryonal carcinoma (EC) cells retinoic acid (RA) strongly induces transcription from the RA receptor beta 2 (RAR beta 2) promoter through an RA response element (RARE) located in close proximity to the TATA box. Tretinoin 49-51 retinoic acid receptor alpha Homo sapiens 113-116
1316240-1 1992 In embryonal carcinoma (EC) cells retinoic acid (RA) strongly induces transcription from the RA receptor beta 2 (RAR beta 2) promoter through an RA response element (RARE) located in close proximity to the TATA box. Tretinoin 93-95 retinoic acid receptor alpha Homo sapiens 113-116
1316240-2 1992 Here we demonstrate that recombinant human TATA box-binding protein, hTFIID, and RAR functionally cooperate in transactivation of the RAR beta 2 promoter in EC cells in a strictly RA-dependent manner. Tretinoin 81-83 retinoic acid receptor alpha Homo sapiens 134-137
1572288-4 1992 Treatment of C6 cells with dexamethasone or retinoic acid decreased IGF-I mRNA levels in a time-dependent fashion. Tretinoin 44-57 insulin-like growth factor 1 Rattus norvegicus 68-73
1572288-5 1992 The time course of the effect of the two agents differed, with the peak effect of dexamethasone between 6 and 12 h and the peak effect of retinoic acid at 27 h. In dose-response studies, IGF-I mRNA levels decreased to 27% of control levels (cells maintained in serum-free media) after treatment with 5 ng/ml dexamethasone, while half-maximal inhibition was achieved with approximately 0.5 ng/ml (1.4 nM) dexamethasone. Tretinoin 138-151 insulin-like growth factor 1 Rattus norvegicus 187-192
1572288-6 1992 Treatment with 10 microM retinoic acid decreased IGF-I mRNA levels to 24% of control levels with half-maximal inhibition occurring with approximately 0.5 microM retinoic acid. Tretinoin 25-38 insulin-like growth factor 1 Rattus norvegicus 49-54
1572288-6 1992 Treatment with 10 microM retinoic acid decreased IGF-I mRNA levels to 24% of control levels with half-maximal inhibition occurring with approximately 0.5 microM retinoic acid. Tretinoin 161-174 insulin-like growth factor 1 Rattus norvegicus 49-54
1327537-0 1992 All-trans and 9-cis retinoic acid induction of CRABPII transcription is mediated by RAR-RXR heterodimers bound to DR1 and DR2 repeated motifs. Tretinoin 20-33 retinoic acid receptor alpha Homo sapiens 84-87
23484687-1 2013 To verify the differential expression of non-metastasis cell 3 (NME3) protein in HL-60 cells when they were induced to differentiate into monocyte and granulocyte like cells, and study its value in diagnosis of acute myeloid leukemia, all-trans retinoic acid (ATRA) and a new steroidal drug NSC67657 were employed to induce acute myeloid leukemia HL-60 cells into monocyte and granulocyte like cells. Tretinoin 260-264 NME/NM23 nucleoside diphosphate kinase 3 Homo sapiens 64-68
1572288-8 1992 Immunoreactive IGF-I levels in media conditioned for 48 h by cells treated with dexamethasone or retinoic acid decreased to 32% and 42% of control levels, respectively. Tretinoin 97-110 insulin-like growth factor 1 Rattus norvegicus 15-20
1429370-6 1992 Amongst the agents considered, retinoic acid was the only one that caused a significant parallel reduction in RB and c-myc expression in the HL-60 human promyelocytic leukemia cells tested. Tretinoin 31-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 117-122
23221369-7 2013 Growth factors that promote maintenance of undifferentiated spermatogonia upregulate miR-221/222 expression; whereas exposure to retinoic acid, an inducer of spermatogonial differentiation, downregulates miR-221/222 abundance. Tretinoin 129-142 microRNA 221 Homo sapiens 204-211
1453015-5 1992 ATRA increased the number of these colonies in a concentration-dependent manner, with maximal stimulation (3.5-fold) occurring at 30 nM in the presence of 5.5 ng/ml IL-3, 0.1 mM hemin, 3.0 U/ml Epo and 30 nM IGF-I. Tretinoin 0-4 interleukin 3 Homo sapiens 165-169
1318502-10 1992 These results demonstrate that the control of NHEK differentiation by RA is consistent with the interaction of the retinoid with RAR and the regulation of transcription by that ligand-receptor complex. Tretinoin 70-72 retinoic acid receptor alpha Homo sapiens 129-132
1313739-12 1992 However, the mRNA loss was transient, and recovery of RAR alpha and RAR gamma mRNA levels was noted 12-24 h after retinoic acid treatment. Tretinoin 114-127 retinoic acid receptor alpha Homo sapiens 54-63
23221369-8 2013 Furthermore, undifferentiated spermatogonia overexpressing miR-221/222 are resistant to retinoic acid-induced transition to a KIT(+) state and are incapable of differentiation in vivo. Tretinoin 88-101 microRNA 221 Homo sapiens 59-66
22504942-8 2013 Furthermore, ATRA decreased the KRT10 transcripts 200-fold as well as diminished the ratio of mutant to wild-type transcripts from 0.41 to 0.35, thus providing a plausible rational for retinoid therapy of EI due to K10 mutations. Tretinoin 13-17 keratin 10 Homo sapiens 32-37
1313714-11 1992 Thus, increased expression of RARA preceded the downregulation of annexin VIII after ATRA induction, suggesting an inverse relationship between RARA and annexin VIII expression. Tretinoin 85-89 retinoic acid receptor alpha Homo sapiens 30-34
1313714-11 1992 Thus, increased expression of RARA preceded the downregulation of annexin VIII after ATRA induction, suggesting an inverse relationship between RARA and annexin VIII expression. Tretinoin 85-89 annexin A8 like 1 Homo sapiens 66-78
1313714-11 1992 Thus, increased expression of RARA preceded the downregulation of annexin VIII after ATRA induction, suggesting an inverse relationship between RARA and annexin VIII expression. Tretinoin 85-89 annexin A8 like 1 Homo sapiens 153-165
1515368-6 1992 RA enhances the proliferative response of cultured keratinocytes to EGF, increases the number of EGFRs on the surface of some cells, and induces EGFR promoter activity in most cells. Tretinoin 0-2 epidermal growth factor Homo sapiens 68-71
1380150-4 1992 To address the role of the retinoic acid receptor (RAR-alpha) in mediating the transformation-inhibitory effect of retinoic acid, we have overexpressed either RAR-alpha or cellular retinoic acid-binding protein I (CRABP) cDNAs in F111 cells. Tretinoin 27-40 retinoic acid receptor, alpha Rattus norvegicus 51-60
1380150-6 1992 In contrast, overexpression of RAR-alpha increased the sensitivity of F111 cells to the transformation-inhibitory action of retinoic acid by 10- to 100-fold. Tretinoin 124-137 retinoic acid receptor, alpha Rattus norvegicus 31-40
1323988-4 1992 Paradoxically, this rearrangement of RAR-alpha results in clinical sensitivity to retinoic acid. Tretinoin 82-95 retinoic acid receptor alpha Homo sapiens 37-46
22504942-8 2013 Furthermore, ATRA decreased the KRT10 transcripts 200-fold as well as diminished the ratio of mutant to wild-type transcripts from 0.41 to 0.35, thus providing a plausible rational for retinoid therapy of EI due to K10 mutations. Tretinoin 13-17 keratin 10 Homo sapiens 215-218
23392891-0 2013 Differential regulation of TauT by calcitriol and retinoic acid via VDR/RXR in LLC-PK1 and MCF-7 cells. Tretinoin 50-63 solute carrier family 6 member 6 Sus scrofa 27-31
1312715-0 1992 Thrombomodulin gene regulation by cAMP and retinoic acid in F9 embryonal carcinoma cells. Tretinoin 43-56 thrombomodulin Homo sapiens 0-14
1312715-2 1992 Exposure of F9 cells to retinoic acid (RA) triggers differentiation into primitive endoderm and induces the appearance of barely detectable amounts of TM mRNA, whereas treatment with dibutyryl cAMP plus theophylline (CT) augments the levels of TM mRNA to a 4-fold greater extent than RA. Tretinoin 24-37 thrombomodulin Homo sapiens 151-153
1312715-2 1992 Exposure of F9 cells to retinoic acid (RA) triggers differentiation into primitive endoderm and induces the appearance of barely detectable amounts of TM mRNA, whereas treatment with dibutyryl cAMP plus theophylline (CT) augments the levels of TM mRNA to a 4-fold greater extent than RA. Tretinoin 24-37 thrombomodulin Homo sapiens 244-246
1312715-2 1992 Exposure of F9 cells to retinoic acid (RA) triggers differentiation into primitive endoderm and induces the appearance of barely detectable amounts of TM mRNA, whereas treatment with dibutyryl cAMP plus theophylline (CT) augments the levels of TM mRNA to a 4-fold greater extent than RA. Tretinoin 39-41 thrombomodulin Homo sapiens 151-153
1312715-2 1992 Exposure of F9 cells to retinoic acid (RA) triggers differentiation into primitive endoderm and induces the appearance of barely detectable amounts of TM mRNA, whereas treatment with dibutyryl cAMP plus theophylline (CT) augments the levels of TM mRNA to a 4-fold greater extent than RA. Tretinoin 39-41 thrombomodulin Homo sapiens 244-246
1624809-4 1992 Expression of the MCP-1 gene is inducible by activators of the protein kinase A (cAMP) and C (PMA) signal transduction pathways and is differentially regulated by the steroids dexamethasone and retinoic acid. Tretinoin 194-207 C-C motif chemokine ligand 2 Homo sapiens 18-23
23392891-6 2013 Expression of TauT was significantly increased by RA, which was synergized by the addition of VD(3) after RXR activation in LLC-PK1 cells. Tretinoin 50-52 solute carrier family 6 member 6 Sus scrofa 14-18
1623557-7 1992 Retinoic acid-differentiated F9 cells and P19 cells expressing H-2 antigen after exposure to MAF (IFN-gamma) were sensitive to the killing by nonactivated macrophages. Tretinoin 0-13 avian musculoaponeurotic fibrosarcoma oncogene homolog Mus musculus 93-96
23442244-4 2013 In addition, we found that supplementation of 10 muM ATRA enhanced CK-18 expression and induced cluster-formation in cells grown on the thick collagen gel. Tretinoin 53-57 keratin 18 Homo sapiens 67-72
1317794-2 1992 Two-dimensional gel electrophoresis and immunoprecipitation studies showed that the expression of HSP47 was significantly induced during the differentiation of mouse teratocarcinoma F9 cells by treatment with retinoic acid alone or with retinoic acid and dibutyryladenosine 3",5"-phosphate. Tretinoin 209-222 serine (or cysteine) peptidase inhibitor, clade H, member 1 Mus musculus 98-103
1317794-2 1992 Two-dimensional gel electrophoresis and immunoprecipitation studies showed that the expression of HSP47 was significantly induced during the differentiation of mouse teratocarcinoma F9 cells by treatment with retinoic acid alone or with retinoic acid and dibutyryladenosine 3",5"-phosphate. Tretinoin 237-250 serine (or cysteine) peptidase inhibitor, clade H, member 1 Mus musculus 98-103
1540946-4 1992 When c-myc levels and responses to serum induction were analyzed in the presence of inducers of differentiation, i.e., dimethylformamide, retinoic acid, sodium butyrate and TGF-beta, distinct patterns of sensitivity and resistance emerged. Tretinoin 138-151 MYC proto-oncogene, bHLH transcription factor Homo sapiens 5-10
1315216-8 1992 Northern blot and slot-blot analyses revealed that neuronal cells overexpressing RAR alpha-mRNA exhibited an enhanced sensitivity to exogenous and endogenous retinoic acid in terms of thymosin beta 10 mRNA. Tretinoin 158-171 retinoic acid receptor, alpha Rattus norvegicus 81-90
23527294-3 2013 Here we report membrane localization of beta-catenin during retinoic acid (RA)--induced epithelial differentiation. Tretinoin 60-73 catenin beta 1 Homo sapiens 40-52
1352781-7 1992 Moreover, RA is capable of delaying the early induction of vimentin expression caused by TPA and SB, without affecting the normal expression of differentiation markers. Tretinoin 10-12 vimentin Homo sapiens 59-67
1370835-4 1992 Normally, P19 cells are induced to differentiate along a neural lineage when allowed to form extensive cell-cell contacts in large multicellular aggregates during exposure to RA. Tretinoin 175-177 interleukin 23 subunit alpha Homo sapiens 10-13
1353130-2 1992 Treatment of HL-60 cells with retinoic acid (1 microM) induced granulocytic differentiation which was accompanied with a 2.4-fold increase in GMPR and 55% decrease in IMPDH activities. Tretinoin 30-43 guanosine monophosphate reductase Homo sapiens 142-146
1313791-1 1992 Activin acts mitogenically on P19 cells as well as being inhibitory of the differentiation of retinoic acid-treated P19 cells and some neuroblastoma cell lines. Tretinoin 94-107 inhibin subunit beta E Homo sapiens 0-7
1370835-5 1992 Through analysis of markers of epithelial (keratin and desmosomal proteins) and neuronal (neurofilament) cells we have found that RA-induced P19 cells transiently express epithelial markers before neuronal differentiation. Tretinoin 130-132 interleukin 23 subunit alpha Homo sapiens 141-144
23527294-3 2013 Here we report membrane localization of beta-catenin during retinoic acid (RA)--induced epithelial differentiation. Tretinoin 75-77 catenin beta 1 Homo sapiens 40-52
1370835-8 1992 The effects of pp60v-src on cell fate and cell-cell adhesion could be mimicked by direct modulation of Ca+(+)-dependent cell-cell contact during RA induction of normal P19 cells. Tretinoin 145-147 interleukin 23 subunit alpha Homo sapiens 168-171
1550338-3 1992 We found that RA treatment of B16 cells resulted in an increase in PKC alpha mRNA beginning at 4-8 h and reached a maximum of 10- to 12-fold over control levels by 48 h. There was also a small amount of PKC gamma mRNA, present only in 48-h RA-treated cells, but no PKC beta mRNA was detected. Tretinoin 14-16 protein kinase C, gamma Mus musculus 203-212
23472160-0 2013 CoupTFI interacts with retinoic acid signaling during cortical development. Tretinoin 23-36 nuclear receptor subfamily 2, group F, member 1 Mus musculus 0-7
1350056-0 1992 Inhibition of tyrosine aminotransferase gene expression by retinoic acid. Tretinoin 59-72 tyrosine aminotransferase Rattus norvegicus 14-39
1370673-3 1992 In this study, we compared, in dose-response experiments, the biologic activities of retinoic acid and CD271, a substance unable to bind to CRABP, but able to bind to nuclear retinoic acid receptors (RAR). Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 175-198
1370673-3 1992 In this study, we compared, in dose-response experiments, the biologic activities of retinoic acid and CD271, a substance unable to bind to CRABP, but able to bind to nuclear retinoic acid receptors (RAR). Tretinoin 85-98 retinoic acid receptor alpha Homo sapiens 200-203
1730652-1 1992 We previously reported that retinoic acid (RA) augmented mouse (BALB/c) lymphokine (interleukin-2)-activated killer (LAK) cell activity in a dose and time dependent manner. Tretinoin 28-41 interleukin 2 Mus musculus 84-97
1730652-1 1992 We previously reported that retinoic acid (RA) augmented mouse (BALB/c) lymphokine (interleukin-2)-activated killer (LAK) cell activity in a dose and time dependent manner. Tretinoin 28-41 alpha-kinase 1 Mus musculus 117-120
1730652-1 1992 We previously reported that retinoic acid (RA) augmented mouse (BALB/c) lymphokine (interleukin-2)-activated killer (LAK) cell activity in a dose and time dependent manner. Tretinoin 43-45 interleukin 2 Mus musculus 84-97
23472160-2 2013 CoupTFI is a regulator of cortical development known to collaborate with retinoic acid (RA) signaling in other systems. Tretinoin 73-86 nuclear receptor subfamily 2, group F, member 1 Mus musculus 0-7
1730652-1 1992 We previously reported that retinoic acid (RA) augmented mouse (BALB/c) lymphokine (interleukin-2)-activated killer (LAK) cell activity in a dose and time dependent manner. Tretinoin 43-45 alpha-kinase 1 Mus musculus 117-120
1730652-7 1992 Kinetics study revealed that the increase in PKC was a time-dependent process and the enhancement was detectable as early as 8 h after the addition of RA to LAK cell culture. Tretinoin 151-153 alpha-kinase 1 Mus musculus 157-160
1730652-11 1992 Taken together, these results indicate that the mechanism of the augmentation of LAK cell activity by RA may in part result from the increase in PKC, especially PKC alpha isozyme. Tretinoin 102-104 alpha-kinase 1 Mus musculus 81-84
1565467-6 1992 All tested constructs retaining promoter activity showed decreased activity in parallel with the down-regulation of endogenous N-myc in response to treatment of transfected cells with retinoic acid. Tretinoin 184-197 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 127-132
1327453-4 1992 The RARA gene configuration was investigated in two APL patients during the course of treatment with all-trans retinoic acid (ATRA). Tretinoin 101-124 retinoic acid receptor alpha Homo sapiens 4-8
1327453-4 1992 The RARA gene configuration was investigated in two APL patients during the course of treatment with all-trans retinoic acid (ATRA). Tretinoin 126-130 retinoic acid receptor alpha Homo sapiens 4-8
1327453-5 1992 It was shown that phenotypically differentiated bone marrow myelocytes under ATRA therapy could still carry RARA gene rearrangement. Tretinoin 77-81 retinoic acid receptor alpha Homo sapiens 108-112
23472160-2 2013 CoupTFI is a regulator of cortical development known to collaborate with retinoic acid (RA) signaling in other systems. Tretinoin 88-90 nuclear receptor subfamily 2, group F, member 1 Mus musculus 0-7
1425010-6 1992 Osteoblasts have been shown to produce LIF, and the amount is increased by treatment with retinoic acid or TNF-alpha. Tretinoin 90-103 leukemia inhibitory factor Mus musculus 39-42
23472160-4 2013 By analyzing CoupTFI(-/-);Foxc1(H/L) double mutant mice we provide evidence that CoupTFI is required for RA rescue of the ventricular zone and the neurogenic phenotypes in Foxc1-mutants. Tretinoin 105-107 nuclear receptor subfamily 2, group F, member 1 Mus musculus 13-20
23472160-4 2013 By analyzing CoupTFI(-/-);Foxc1(H/L) double mutant mice we provide evidence that CoupTFI is required for RA rescue of the ventricular zone and the neurogenic phenotypes in Foxc1-mutants. Tretinoin 105-107 forkhead box C1 Mus musculus 26-31
1310471-3 1992 When treated with retinoic acid and dibutyryl cAMP, F9 cells differentiate into PE and SPARC mRNA is increased approximately 20-fold. Tretinoin 18-31 secreted protein acidic and cysteine rich Homo sapiens 87-92
23472160-4 2013 By analyzing CoupTFI(-/-);Foxc1(H/L) double mutant mice we provide evidence that CoupTFI is required for RA rescue of the ventricular zone and the neurogenic phenotypes in Foxc1-mutants. Tretinoin 105-107 nuclear receptor subfamily 2, group F, member 1 Mus musculus 81-88
1315216-9 1992 Although the RAR-alpha gene was expressed (at low levels) a priori in these neuroblastoma cells, retinoic acid (2 x 10(-7) M for 3 days) slightly stimulated RAR-alpha-mRNA accumulation. Tretinoin 97-110 retinoic acid receptor, alpha Rattus norvegicus 157-166
1292933-1 1992 The major cytosolic aldehyde dehydrogenase isozyme (ALDH1) exhibits strong activity for oxidation of retinal to retinoic acid, while the major mitochondrial ALDH2 and the stomach cytosolic ALDH3 have no such activity. Tretinoin 112-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 52-57
1292933-3 1992 Thus, ALDH1 can efficiently produce retinoic acid from retinal in tissues with low retinal concentrations (< 0.01 mumol/l). Tretinoin 36-49 aldehyde dehydrogenase 1 family member A1 Homo sapiens 6-11
23472160-4 2013 By analyzing CoupTFI(-/-);Foxc1(H/L) double mutant mice we provide evidence that CoupTFI is required for RA rescue of the ventricular zone and the neurogenic phenotypes in Foxc1-mutants. Tretinoin 105-107 forkhead box C1 Mus musculus 172-177
1292933-5 1992 These findings suggest that the major physiological substrate of human ALDH1 is retinal, and that its primary biological role is generation of retinoic acid resulting in modulation of cell differentiation including hormone-mediated development. Tretinoin 143-156 aldehyde dehydrogenase 1 family member A1 Homo sapiens 71-76
23472160-6 2013 These results suggest that CoupTFI collaborates with RA signaling to regulate both cortical ventricular zone progenitor cell behavior and cortical neurogenesis. Tretinoin 53-55 nuclear receptor subfamily 2, group F, member 1 Mus musculus 27-34
23102850-0 2013 Retinoic acid signaling biomarkers after treatment with retinoic acid and retinoic acid receptor alpha antagonist (Ro 41-5253) in canine testis: an in vitro organ culture study. Tretinoin 0-13 retinoic acid receptor alpha Canis lupus familiaris 74-102
1315557-1 1992 From a series of naphthalene and benzoic acid derivatives we have identified synthetic retinoic acid analogues exhibiting high selectivity for the nuclear retinoic acid receptors RAR alpha (Am 580), RAR beta (CD 2019) and RAR gamma (CD 437) as well as ligands sharing high affinities for all RAR subtypes (CD 367). Tretinoin 87-100 retinoic acid receptor alpha Homo sapiens 179-188
1315557-1 1992 From a series of naphthalene and benzoic acid derivatives we have identified synthetic retinoic acid analogues exhibiting high selectivity for the nuclear retinoic acid receptors RAR alpha (Am 580), RAR beta (CD 2019) and RAR gamma (CD 437) as well as ligands sharing high affinities for all RAR subtypes (CD 367). Tretinoin 87-100 retinoic acid receptor alpha Homo sapiens 179-182
1734039-7 1992 Retinoic acid also has contrasting effects on chondrocytes and myocytes either increasing or decreasing, respectively, expression of TGF-beta s 2 and 3 mRNAs and TGF-beta 2 protein. Tretinoin 0-13 transforming growth factor beta 2 Gallus gallus 162-172
1372669-6 1992 The combination of retinoic acid with interferon gamma was most effective in reducing CFU-L recovering (8 responsive/15 AML cases), G-CSF and M-CSF displayed either inhibitory or stimulatory activity in different AML cases. Tretinoin 19-32 colony stimulating factor 3 Homo sapiens 132-137
1372669-6 1992 The combination of retinoic acid with interferon gamma was most effective in reducing CFU-L recovering (8 responsive/15 AML cases), G-CSF and M-CSF displayed either inhibitory or stimulatory activity in different AML cases. Tretinoin 19-32 colony stimulating factor 1 Homo sapiens 142-147
1839359-0 1991 Up-regulation of the integrin alpha 1/beta 1 in human neuroblastoma cells differentiated by retinoic acid: correlation with increased neurite outgrowth response to laminin. Tretinoin 92-105 integrin subunit alpha 1 Homo sapiens 21-44
23102850-3 2013 The objective was to elucidate the effects of exogenous RA and a RARalpha antagonist on gene expression of ALDH1, CYP26b1, RARalpha, cellular RA-binding protein II, and STRA8 in an in vitro organ culture model of canine testis. Tretinoin 56-58 retinoic acid receptor alpha Canis lupus familiaris 123-131
1839359-2 1991 Here we show that treatment of two human neuroblastoma cell lines, SY5Y and IMR32, with RA resulted in a fivefold increase of the integrin alpha 1/beta 1 expression. Tretinoin 88-90 integrin subunit alpha 1 Homo sapiens 130-146
1839359-8 1991 Affinity chromatography experiments showed that alpha 1/beta 1 is the major laminin receptor in both untreated and RA-treated SY5Y cells. Tretinoin 115-117 adrenoceptor alpha 1D Homo sapiens 48-62
1310350-5 1992 Transfection experiments show that RXR alpha can greatly enhance the transcriptional activity of TR and RAR at low retinoic acid concentrations that do not significantly activate RXR alpha itself. Tretinoin 115-128 retinoic acid receptor alpha Homo sapiens 104-107
1310351-1 1992 Cellular responsiveness to retinoic acid and its metabolites is conferred through two structurally and pharmacologically distinct families of receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 157-180
1310351-1 1992 Cellular responsiveness to retinoic acid and its metabolites is conferred through two structurally and pharmacologically distinct families of receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 182-185
1839359-9 1991 These data show that RA, a naturally occurring morphogen implicated in embryonic development, can selectively regulate the expression of integrin complexes in neuronal cells and suggest an important role of the alpha 1/beta 1 laminin receptor in the morphological differentiation of nerve cells. Tretinoin 21-23 adrenoceptor alpha 1D Homo sapiens 211-218
23102850-8 2013 In conclusion, exogenous RA decreased mRNA abundance of ALDH1 and increased mRNA abundance of RA signaling molecules and its downstream effectors (CYP26b1, CRABII, and STRA8), whereas treatment with a RARalpha antagonist effectively decreased RARalpha and RA metabolism molecules and its downstream effectors in canine testis. Tretinoin 25-27 retinoic acid receptor alpha Canis lupus familiaris 201-209
1668609-6 1991 Simultaneous molecular and cytologic studies showed that the RARA gene rearrangements persisted during the first 2 to 3 weeks of all-trans retinoic acid (ATRA) therapy when differentiated granulocytes predominated in bone marrow, while these rearrangements disappeared after achieving complete remission. Tretinoin 139-152 retinoic acid receptor alpha Homo sapiens 61-65
1310606-4 1992 When the effect of EGF (2.5 ng/ml) was tested against the growth inhibition produced by a range of doses of RA, EGF stimulated growth and reduced the degree of inhibition produced by RA at all dose levels. Tretinoin 108-110 epidermal growth factor Homo sapiens 112-115
1310606-5 1992 Conversely, a single dose of 10(-8) M RA tested against a range of EGF concentrations reduced the dose-related EGF-induced increase in anchorage-independent growth. Tretinoin 38-40 epidermal growth factor Homo sapiens 67-70
1668609-6 1991 Simultaneous molecular and cytologic studies showed that the RARA gene rearrangements persisted during the first 2 to 3 weeks of all-trans retinoic acid (ATRA) therapy when differentiated granulocytes predominated in bone marrow, while these rearrangements disappeared after achieving complete remission. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 61-65
1310606-5 1992 Conversely, a single dose of 10(-8) M RA tested against a range of EGF concentrations reduced the dose-related EGF-induced increase in anchorage-independent growth. Tretinoin 38-40 epidermal growth factor Homo sapiens 111-114
23102850-8 2013 In conclusion, exogenous RA decreased mRNA abundance of ALDH1 and increased mRNA abundance of RA signaling molecules and its downstream effectors (CYP26b1, CRABII, and STRA8), whereas treatment with a RARalpha antagonist effectively decreased RARalpha and RA metabolism molecules and its downstream effectors in canine testis. Tretinoin 25-27 retinoic acid receptor alpha Canis lupus familiaris 243-251
1935958-0 1991 Effect of retinoic acid on the synthesis of tissue-type plasminogen activator and plasminogen activator inhibitor-1 in human endothelial cells. Tretinoin 10-23 serpin family E member 1 Homo sapiens 82-115
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 0-13 fatty acid binding protein 5, epidermal Mus musculus 243-248
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 15-17 fatty acid binding protein 5, epidermal Mus musculus 243-248
1503781-2 1992 We have examined the effects of LIF in nullipotent embryonal carcinoma cell lines, and have found that LIF blocks differentiation induced by retinoic acid and at low temperature in OTF9 cells. Tretinoin 141-154 leukemia inhibitory factor Mus musculus 103-106
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 fatty acid binding protein 5, epidermal Mus musculus 137-142
1662118-3 1991 This protein, termed RXR beta, forms heterodimers with RAR, preferentially increasing its DNA binding and transcriptional activity on promoters containing retinoic acid, but not thyroid hormone or vitamin D, response elements. Tretinoin 155-168 retinoic acid receptor alpha Homo sapiens 55-58
1751405-0 1991 Retinoic acid negatively regulates p34cdc2 expression during human neuroblastoma differentiation. Tretinoin 0-13 cyclin dependent kinase 1 Homo sapiens 35-42
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 sirtuin 1 Mus musculus 227-232
1751405-2 1991 In this work, we show that the arrest of cell growth and induction of differentiation in a tumorigenic neuroblastoma cell line by retinoic acid (RA) is associated with a 75-fold decrease in the level of p34cdc2 protein. Tretinoin 130-143 cyclin dependent kinase 1 Homo sapiens 203-210
23105114-6 2012 The switch in RA signaling is accomplished by a transient up-regulation of RARbeta concomitantly with a transient increase in the CRABP-II/FABP5 ratio at early stages of differentiation. Tretinoin 14-16 fatty acid binding protein 5, epidermal Mus musculus 139-144
23011350-5 2012 RESULTS: This study reveals, for the first time, that activin/TGF-beta signalling blocks pancreatic specification induced by retinoic acid while promoting hepatic specification in combination with bone morphogenetic protein and fibroblast growth factor. Tretinoin 125-138 inhibin subunit beta E Homo sapiens 54-61
1717348-6 1991 This CpG cluster region was found to be hypomethylated in endodermal PYS-2 cells, retinoic acid-treated F9 cells, and F9 embryonal carcinoma cells, but hypermethylated in BALB/C 3T3 fibroblast cells that do not express EndoA. Tretinoin 82-95 keratin 8 Mus musculus 219-224
1936556-0 1991 The transcription factor, Egr-1, is rapidly modulated in response to retinoic acid in P19 embryonal carcinoma cells. Tretinoin 69-82 early growth response 1 Mus musculus 26-31
1936556-9 1991 The response was more rapid at high RA concentrations and this suggests that the Egr-1 transcription factor could play a role in initiation of differentiation pathways of P19 EC cells. Tretinoin 36-38 early growth response 1 Mus musculus 81-86
22942074-3 2012 We found that exposure of embryos to exogenous RA induces a dramatic anterior expansion of the number of pharyngeal teeth that later form and shifts anteriorly the expression patterns of genes normally expressed in the posterior tooth-forming region, such as pitx2 and dlx2b. Tretinoin 47-49 paired-like homeodomain 2 Danio rerio 259-264
1748717-3 1991 Northern blot analysis demonstrates a tenfold increase in EGF mRNA following retinoic acid treatment and a 60% decrease in receptor message levels after dexamethasone treatment. Tretinoin 77-90 epidermal growth factor Rattus norvegicus 58-61
1748717-7 1991 In contrast, the mechanism by which retinoic acid increases the expression of EGF receptor mRNA requires protein synthesis. Tretinoin 36-49 epidermal growth factor Rattus norvegicus 78-81
1961035-3 1991 Some blast cells were stimulated by RA in the presence of rGM-CSF and rIL-3 and inhibited when cultured with RA and rG-CSF. Tretinoin 36-38 colony stimulating factor 2 Homo sapiens 62-65
1961035-7 1991 Colony formation was stimulated by RA in the presence of rGM-CSF or rIL-3 but inhibited by RA with rG-CSF. Tretinoin 35-37 colony stimulating factor 2 Homo sapiens 61-64
1713586-8 1991 We demonstrate that serum deprivation; placement of cells into primary culture; and growth factors such as transforming growth factor beta 1, retinoic acid, and 1,25-dihydroxyvitamin D3 can all change the alternative splicing of fibronectin pre-mRNA in the ED-A, ED-B, and type III connecting sequence exons. Tretinoin 142-155 fibronectin 1 Rattus norvegicus 229-240
1713586-8 1991 We demonstrate that serum deprivation; placement of cells into primary culture; and growth factors such as transforming growth factor beta 1, retinoic acid, and 1,25-dihydroxyvitamin D3 can all change the alternative splicing of fibronectin pre-mRNA in the ED-A, ED-B, and type III connecting sequence exons. Tretinoin 142-155 ectodysplasin-A Rattus norvegicus 257-261
1880152-0 1991 Differential regulation of the expression of transforming growth factor-beta s 1 and 2 by retinoic acid, epidermal growth factor, and dexamethasone in NRK-49F and A549 cells. Tretinoin 90-103 transforming growth factor, beta 2 Rattus norvegicus 45-86
1880152-3 1991 We show that epidermal growth factor (EGF) induces secretion of TGF-beta 1 and not TGF-beta 2, whereas retinoic acid (RA) induces secretion of TGF-beta 2 and not TGF-beta 1 in NRK-49F normal rat kidney fibroblasts and A549 human lung carcinoma cells. Tretinoin 103-116 transforming growth factor, beta 2 Rattus norvegicus 143-153
1880152-3 1991 We show that epidermal growth factor (EGF) induces secretion of TGF-beta 1 and not TGF-beta 2, whereas retinoic acid (RA) induces secretion of TGF-beta 2 and not TGF-beta 1 in NRK-49F normal rat kidney fibroblasts and A549 human lung carcinoma cells. Tretinoin 118-120 transforming growth factor, beta 2 Rattus norvegicus 143-153
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 32-34 transforming growth factor, beta 2 Rattus norvegicus 174-184
1880152-6 1991 The interactive effects of EGF, RA, and Dex on the production of TGF-beta 1 and TGF-beta 2, which were studied on NRK-49F cells, demonstrate that EGF blocks the induction of TGF-beta 2 mRNA and peptide by RA, while Dex inhibits the induction of TGF-beta 1 mRNA and peptide by EGF. Tretinoin 205-207 transforming growth factor, beta 2 Rattus norvegicus 174-184
1719965-1 1991 The effects of three retinoids, all-trans-retinoic acid (all-trans-RA), 13-cis-RA, and etretin were examined on mRNA abundance of nuclear retinoic acid receptors (RAR-alpha, beta, and gamma) in lung and liver of retinol deficient and chow fed rats. Tretinoin 32-55 retinoic acid receptor, alpha Rattus norvegicus 163-172
22989886-8 2012 Accordingly, all-trans-retinoic acid, alone or together with gemfibrozil, up-regulated TPP1. Tretinoin 13-36 tripeptidyl peptidase I Mus musculus 87-91
1915273-0 1991 Effects of retinoic acid excess on expression of Hox-2.9 and Krox-20 and on morphological segmentation in the hindbrain of mouse embryos. Tretinoin 11-24 early growth response 2 Mus musculus 61-68
1915274-1 1991 Oct3 is an embryonic octamer-binding transcription factor, whose expression is rapidly repressed by retinoic acid (RA). Tretinoin 100-113 POU class 5 homeobox 1 Homo sapiens 0-4
1915274-1 1991 Oct3 is an embryonic octamer-binding transcription factor, whose expression is rapidly repressed by retinoic acid (RA). Tretinoin 115-117 POU class 5 homeobox 1 Homo sapiens 0-4
2069569-2 1991 The cDNA insert (4B) hybridized with a single 1.7 kb mRNA, whose abundance was markedly increased in P19 cells after retinoic acid treatment. Tretinoin 117-130 interleukin 23 subunit alpha Homo sapiens 101-104
22906706-4 2012 The large cell population responds to retinoic acid differentiation with greater than a 50% reduction in cell number and loss of Oct-4 expression, whereas the number of the small cell population does not change and Oct-4 protein expression is maintained. Tretinoin 38-51 POU class 5 homeobox 1 Homo sapiens 129-134
2055691-4 1991 After being fed a retinoid-deficient diet containing retinoic acid for 26 weeks, the rhodopsin content of rat retinas was reduced by over 85%. Tretinoin 53-66 rhodopsin Rattus norvegicus 85-94
1915274-2 1991 In this report, we have determined the transcriptional control region of the oct3 gene and studied the mechanism of the RA-mediated repression. Tretinoin 120-122 POU class 5 homeobox 1 Homo sapiens 77-81
1915274-10 1991 We suggest that RARE1 is a critical cis element for oct3 gene expression in embryonic stem cells and for the RA-mediated repression. Tretinoin 16-18 POU class 5 homeobox 1 Homo sapiens 52-56
1645738-3 1991 In A126-1B2 cells, RA also induced the expression of other markers of differentiation including acetylcholinesterase and the mRNAs for neurofilament (NF-M) and GAP-43 as effectively as nerve growth factor (NGF). Tretinoin 19-21 neurofilament medium chain Rattus norvegicus 135-148
22640830-0 2012 All-trans-retinoic acid inhibits growth of head and neck cancer stem cells by suppression of Wnt/beta-catenin pathway. Tretinoin 0-23 catenin beta 1 Homo sapiens 97-109
1645738-3 1991 In A126-1B2 cells, RA also induced the expression of other markers of differentiation including acetylcholinesterase and the mRNAs for neurofilament (NF-M) and GAP-43 as effectively as nerve growth factor (NGF). Tretinoin 19-21 neurofilament medium chain Rattus norvegicus 150-154
1890978-1 1991 A biological hypothesis which is based upon the response of AML blast cells to retinoic acid alone and in combinations with other differentiating agents in primary culture, is proposed for the FAB classification of Acute Myeloid Leukaemias. Tretinoin 79-92 FA complementation group B Homo sapiens 193-196
1666409-1 1991 Two types of retinoic acid-binding proteins, designated as epididymal retinoic acid-binding protein (ERABP) types A and B, have been purified to homogeneity from rat genital organs. Tretinoin 13-26 lipocalin 5 Rattus norvegicus 101-106
1666409-3 1991 The absorption spectrum of ERABP complex with retinoic acid had two peaks at 277 and 354 nm, and showed similar uncorrected fluorescence spectra to that of cellular retinoic acid-binding protein (CRABP). Tretinoin 46-59 lipocalin 5 Rattus norvegicus 27-32
1666409-6 1991 The existence of ERABP strongly suggests that retinoic acid might be involved in the maturation of spermatozoa. Tretinoin 46-59 lipocalin 5 Rattus norvegicus 17-22
1656191-1 1991 Biological effects of retinoic acid (RA) are mediated through its binding to three closely related nuclear receptors (RAR alpha, RAR beta, and RAR gamma) belonging to the steroid-thyroid nuclear receptor family. Tretinoin 22-35 retinoic acid receptor alpha Homo sapiens 118-127
1656191-1 1991 Biological effects of retinoic acid (RA) are mediated through its binding to three closely related nuclear receptors (RAR alpha, RAR beta, and RAR gamma) belonging to the steroid-thyroid nuclear receptor family. Tretinoin 37-39 retinoic acid receptor alpha Homo sapiens 118-127
1656958-1 1991 The biological response to retinoic acid (RA) and synthetic derivatives (retinoids) is mediated by three nuclear retinoic acid receptors, RAR alpha, beta and gamma. Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 138-147
1656958-1 1991 The biological response to retinoic acid (RA) and synthetic derivatives (retinoids) is mediated by three nuclear retinoic acid receptors, RAR alpha, beta and gamma. Tretinoin 42-44 retinoic acid receptor alpha Homo sapiens 138-147
1656958-4 1991 In response to retinoic acid, the three hybrid receptors ER-RAR alpha, ER-RAR beta and ER-RAR gamma exhibited the same induction profile as the corresponding wild type receptors RAR alpha, RAR beta, and RAR gamma. Tretinoin 15-28 retinoic acid receptor alpha Homo sapiens 60-69
1656958-4 1991 In response to retinoic acid, the three hybrid receptors ER-RAR alpha, ER-RAR beta and ER-RAR gamma exhibited the same induction profile as the corresponding wild type receptors RAR alpha, RAR beta, and RAR gamma. Tretinoin 15-28 retinoic acid receptor alpha Homo sapiens 178-187
1652063-4 1991 RA-induced down-regulation of the IL-2 enhancer is mediated by RAR, since overexpression of transfected RARs increased RA sensitivity of the IL-2 promoter. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 63-66
1903722-2 1991 We here report that both D factor/LIF and IL-6 inhibit the differentiation of mouse teratocarcinoma F9 cells induced by retinoic acid alone or combined with dibutyryl cAMP. Tretinoin 120-133 leukemia inhibitory factor Mus musculus 25-33
1903722-2 1991 We here report that both D factor/LIF and IL-6 inhibit the differentiation of mouse teratocarcinoma F9 cells induced by retinoic acid alone or combined with dibutyryl cAMP. Tretinoin 120-133 leukemia inhibitory factor Mus musculus 34-37
1850696-0 1991 The late retinoic acid induction of laminin B1 gene transcription involves RAR binding to the responsive element. Tretinoin 9-22 retinoic acid receptor alpha Homo sapiens 75-78
22640830-7 2012 ATRA suppressed the expression of the stem cell markers Oct4, Sox2, Nestin and CD44 in HNSC CSCs and inhibited the proliferation of HNSC CSCs in vitro and in vivo. Tretinoin 0-4 POU class 5 homeobox 1 Homo sapiens 56-60
22640830-9 2012 The anti-tumour effects of ATRA may be associated with down-regulation of Wnt/beta-catenin signalling. Tretinoin 27-31 catenin beta 1 Homo sapiens 78-90
1850832-0 1991 Characterization of DNA binding and retinoic acid binding properties of retinoic acid receptor. Tretinoin 36-49 retinoic acid receptor alpha Homo sapiens 72-94
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 194-205
1850832-3 1991 Both intact RAR molecules and the DNA binding domain bind to the cognate DNA response element with high specificity in the absence of retinoic acid. Tretinoin 134-147 retinoic acid receptor alpha Homo sapiens 12-15
1850832-7 1991 The hormone binding ability of the RAR alpha protein was assayed by a charcoal absorption assay and the RAR protein was found to bind to retinoic acid with a Kd of 2.1 x 10(-10) M. Tretinoin 137-150 retinoic acid receptor alpha Homo sapiens 35-44
1850832-7 1991 The hormone binding ability of the RAR alpha protein was assayed by a charcoal absorption assay and the RAR protein was found to bind to retinoic acid with a Kd of 2.1 x 10(-10) M. Tretinoin 137-150 retinoic acid receptor alpha Homo sapiens 35-38
1849758-2 1991 We studied the response to RA by molecularly analyzing the RA receptor alpha (RAR alpha) locus, which has recently been shown to be rearranged in all APLs. Tretinoin 27-29 retinoic acid receptor alpha Homo sapiens 78-87
1860835-0 1991 A retinoic acid-responsive human zinc finger gene, MZF-1, preferentially expressed in myeloid cells. Tretinoin 2-15 myeloid zinc finger 1 Homo sapiens 51-56
1648481-0 1991 A retinoic acid response element is present in the mouse cellular retinol binding protein I (mCRBPI) promoter. Tretinoin 2-15 retinol binding protein 1, cellular Mus musculus 57-91
1648481-0 1991 A retinoic acid response element is present in the mouse cellular retinol binding protein I (mCRBPI) promoter. Tretinoin 2-15 retinol binding protein 1, cellular Mus musculus 93-99
1648481-2 1991 A specific cis-acting element responsible for retinoic acid (RA) inducibility of the mCRBPI promoter was identified and characterized. Tretinoin 46-59 retinol binding protein 1, cellular Mus musculus 85-91
1648481-2 1991 A specific cis-acting element responsible for retinoic acid (RA) inducibility of the mCRBPI promoter was identified and characterized. Tretinoin 61-63 retinol binding protein 1, cellular Mus musculus 85-91
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 25-38 retinoic acid receptor alpha Homo sapiens 207-210
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 40-42 retinoic acid receptor alpha Homo sapiens 194-205
1652423-10 1991 Treatment of stage 20 embryos with retinoic acid altered the distribution of RAR-beta transcripts in the maxillary primordia, such that high levels of transcripts were present throughout, rather than being confined to the anterior part. Tretinoin 35-48 retinoic acid receptor beta Gallus gallus 77-85
1909429-3 1991 Transcriptional regulation accounts at least partly for the increased steady-state levels of Egr-1 mRNA in differentiating teratocarcinoma cells; this rate increases threefold over the 7-10 days of differentiation of P19 embryonal carcinoma cells with both 0.5% DMSO (to give predominantly cardiac muscle) and 1 microM retinoic acid (to give nerve and glial cells). Tretinoin 319-332 early growth response 1 Homo sapiens 93-98
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 40-42 retinoic acid receptor alpha Homo sapiens 207-210
1652423-13 1991 These results show that RAR-beta transcripts are particularly concentrated in regions of the primordia that give rise to the upper beak, the development of which is specifically affected by retinoic acid. Tretinoin 190-203 retinoic acid receptor beta Gallus gallus 24-32
22871568-6 2012 We conclude that ATRA treatment enhances fatty acid catabolism in hepatocytes through RXR-mediated mechanisms that likely involve the transactivation of the PPARalpha:RXR heterodimer. Tretinoin 17-21 peroxisome proliferator activated receptor alpha Homo sapiens 157-166
1652423-14 1991 In addition, they demonstrate that retinoic acid can induce changes in the pattern of expression of RAR-beta transcripts in vivo. Tretinoin 35-48 retinoic acid receptor beta Gallus gallus 100-108
22344541-0 2012 All-trans retinoic acid inhibits mesangial cell proliferation by up-regulating p21Waf1/Cip1 and p27Kip1 and down-regulating Skp2. Tretinoin 10-23 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 96-103
1771617-2 1991 Differentiation-linked expression of PAI-2 was investigated by adding cell-differentiation promoting agents [such as phorbol myristate acetate (PMA), retinoic acid (RA), dexamethasone (Dex), and recombinant cytokines, including tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), granulocyte-colony stimulating factor (G-CSF), and interleukin-6 (IL-6)] into the culture medium of PL-21 cells. Tretinoin 150-163 serpin family B member 2 Homo sapiens 37-42
1771617-2 1991 Differentiation-linked expression of PAI-2 was investigated by adding cell-differentiation promoting agents [such as phorbol myristate acetate (PMA), retinoic acid (RA), dexamethasone (Dex), and recombinant cytokines, including tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), granulocyte-colony stimulating factor (G-CSF), and interleukin-6 (IL-6)] into the culture medium of PL-21 cells. Tretinoin 165-167 serpin family B member 2 Homo sapiens 37-42
1645361-0 1991 Retinoic acid priming potentiates the induction of urokinase-type plasminogen activator by cyclic adenosine monophosphate in mouse mammary carcinoma cells. Tretinoin 0-13 plasminogen activator, urokinase Mus musculus 51-87
1645361-1 1991 Interactive regulation of gene expression by retinoic acid (RA) and adenosine monophosphate (cAMP) in mammary tumor cells was explored using Shionogi mouse mammary carcinoma cells (SC115) as a model and urokinase-type plasminogen activator (uPA) as a target gene product. Tretinoin 45-58 plasminogen activator, urokinase Mus musculus 203-239
1645361-13 1991 In conclusion, RA treatment of SC115 cells potentiates the effect of cAMP on uPA expression at the single cell level via a partially irreversible mechanism independent of protein kinase C. The molecular target of RA and whether SC115 cell differentiation underlies the effect of RA remain to be established. Tretinoin 15-17 plasminogen activator, urokinase Mus musculus 77-80
1675998-13 1991 Treatment of HBF cells with retinoic acid increased the level of RAR beta mRNA in a time-dependent manner; the maximal induction was about 15-fold. Tretinoin 28-41 retinoic acid receptor alpha Homo sapiens 65-68
22836912-6 2012 Conversely, we find that RA positively regulates nr2f1a expression in trunk endoderm and mesoderm. Tretinoin 25-27 nuclear receptor subfamily 2, group F, member 1a Danio rerio 49-55
1657899-2 1991 A combination of Bt2cAMP (1 mM) and RA (1 microM) yielded the most significant networks of neurites after 3 to 4 days, this being associated with the reduction of N-myc mRNA levels. Tretinoin 36-38 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 163-168
2013316-0 1991 Expression of protein kinase C-alpha (PKC-alpha) and MYCN mRNAs in human neuroblastoma cells and modulation during morphological differentiation induced by retinoic acid. Tretinoin 156-169 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 53-57
22836912-10 2012 Our finding that RA positively regulates nr2f1a expression in the trunk supports the possibility that Nr2fs function in a negative feedback loop to modulate RA signaling in this region. Tretinoin 17-19 nuclear receptor subfamily 2, group F, member 1a Danio rerio 41-47
1650576-1 1991 As in other embryocarcinoma (EC) cell lines retinoic acid (RA) rapidly induces expression of the nuclear retinoic acid receptor (RAR) beta in murine P19 EC cells, while RAR alpha is expressed constitutively. Tretinoin 44-57 retinoic acid receptor alpha Homo sapiens 129-132
1650576-1 1991 As in other embryocarcinoma (EC) cell lines retinoic acid (RA) rapidly induces expression of the nuclear retinoic acid receptor (RAR) beta in murine P19 EC cells, while RAR alpha is expressed constitutively. Tretinoin 59-61 retinoic acid receptor alpha Homo sapiens 129-132
1675427-3 1991 We now report that six different genes of the cluster HOX 1 are sequentially induced by RA in a similar temporal pattern, beginning with genes at the 3" end of the cluster. Tretinoin 88-90 homeobox A5 Homo sapiens 54-59
1675427-5 1991 Hox 1.4 and Hox 1.3, genes abundantly induced in nontransformed clones after 3 days of RA treatment, are expressed in N-ras-transformed cells only after 10 days of RA treatment. Tretinoin 87-89 homeobox A5 Homo sapiens 0-5
1650576-6 1991 On the contrary no activity can be observed in the RA-resistant RAC65 cells; however, co-transfection of hRAR alpha, hRAR beta or hRAR gamma 1 restores the RA-dependent induction of CAT activity. Tretinoin 51-53 retinoic acid receptor alpha Homo sapiens 105-115
1675427-5 1991 Hox 1.4 and Hox 1.3, genes abundantly induced in nontransformed clones after 3 days of RA treatment, are expressed in N-ras-transformed cells only after 10 days of RA treatment. Tretinoin 87-89 homeobox A5 Homo sapiens 12-19
22836912-10 2012 Our finding that RA positively regulates nr2f1a expression in the trunk supports the possibility that Nr2fs function in a negative feedback loop to modulate RA signaling in this region. Tretinoin 157-159 nuclear receptor subfamily 2, group F, member 1a Danio rerio 41-47
1675427-5 1991 Hox 1.4 and Hox 1.3, genes abundantly induced in nontransformed clones after 3 days of RA treatment, are expressed in N-ras-transformed cells only after 10 days of RA treatment. Tretinoin 164-166 homeobox A5 Homo sapiens 0-5
1996113-2 1991 Promoter activity of human ADH3, but not ADH1 or ADH2, was shown to be activated by retinoic acid in transient transfection assays of Hep3B human hepatoma cells. Tretinoin 84-97 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 27-31
1996113-3 1991 Deletion mapping experiments identified a region in the ADH3 promoter located between -328 and -272 bp which confers retinoic acid activation. Tretinoin 117-130 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 56-60
1675427-5 1991 Hox 1.4 and Hox 1.3, genes abundantly induced in nontransformed clones after 3 days of RA treatment, are expressed in N-ras-transformed cells only after 10 days of RA treatment. Tretinoin 164-166 homeobox A5 Homo sapiens 12-19
22406829-4 2012 The expression of TM is negatively regulated by NF-kappaB- and GSK3-beta-dependent signalling pathways and positively regulated by retinoic acid and transcription factor Sp1 in PrEC, LNCaP and PC-3 cells, but not in DU-145 cells. Tretinoin 131-144 thrombomodulin Homo sapiens 18-20
1675427-7 1991 Constitutive expression of a transfected Hox 1.4 gene under the control of a simian virus 40 promotor leads to differentiated cell morphology similar to that of the RA-induced phenotype and restores the growth-inhibitory effects of RA in N-ras-transformed cells. Tretinoin 165-167 homeobox A5 Homo sapiens 41-46
2033252-1 1991 In this report we demonstrate that retinoic acid (RA) down-regulated the number of IL-6R on human leukocyte cell lines, including the myeloma cell line AF10, and two B cell hybridomas that correspond to cells at earlier stages of B cell development. Tretinoin 35-48 MLLT10 histone lysine methyltransferase DOT1L cofactor Homo sapiens 152-156
2033252-1 1991 In this report we demonstrate that retinoic acid (RA) down-regulated the number of IL-6R on human leukocyte cell lines, including the myeloma cell line AF10, and two B cell hybridomas that correspond to cells at earlier stages of B cell development. Tretinoin 50-52 MLLT10 histone lysine methyltransferase DOT1L cofactor Homo sapiens 152-156
2033252-2 1991 Using AF10 cells, whose growth was determined to be mediated by the autocrine action of IL-6, we found that RA reduction of IL-6R was concentration-dependent over a range of 10(-11) to 10(-5) M and corresponded to the ability of the retinoid to inhibit cell proliferation. Tretinoin 108-110 MLLT10 histone lysine methyltransferase DOT1L cofactor Homo sapiens 6-10
1711202-3 1991 Our studies revealed that the epidermal keratins, K5, K6, K14, and K16, their mRNAs, and their transcripts were diminished relative to actin as a consequence of retinoic acid (RA) treatment. Tretinoin 161-174 keratin 14 Homo sapiens 58-61
1996113-5 1991 Within a 34-bp stretch, the ADH3 retinoic acid response element (RARE) contains two TGACC motifs and one TGAAC motif, both of which exist in RAREs controlling other genes. Tretinoin 33-46 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 28-32
1996113-8 1991 Since ADH catalyzes the conversion of retinol to retinal, which can be further converted to retinoic acid by aldehyde dehydrogenase, these results suggest that retinoic acid activation of ADH3 constitutes a positive feedback loop regulating retinoic acid synthesis. Tretinoin 92-105 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 188-192
1996113-8 1991 Since ADH catalyzes the conversion of retinol to retinal, which can be further converted to retinoic acid by aldehyde dehydrogenase, these results suggest that retinoic acid activation of ADH3 constitutes a positive feedback loop regulating retinoic acid synthesis. Tretinoin 160-173 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 188-192
1703480-4 1991 Since the effects of both IGF-I and IGF-II may be modulated by specific binding proteins (IGF-BPs) we examined the possibility that one mechanism by which retinoic acid may inhibit cancer growth is by an alteration in these BPs, thereby blocking IGF"s growth effect. Tretinoin 155-168 insulin like growth factor 2 Homo sapiens 36-42
1704851-3 1991 Treatment of neutrophils with both G-CSF and retinoic acid augmented the amount of mRNA for NAP over the amount obtained by G-CSF alone, which was most marked at 24 h. These results show that both G-CSF-mediated NAP induction and its potentiation by retinoic acid are due to the increased levels of mRNA for NAP. Tretinoin 45-58 colony stimulating factor 3 Homo sapiens 124-129
1704851-3 1991 Treatment of neutrophils with both G-CSF and retinoic acid augmented the amount of mRNA for NAP over the amount obtained by G-CSF alone, which was most marked at 24 h. These results show that both G-CSF-mediated NAP induction and its potentiation by retinoic acid are due to the increased levels of mRNA for NAP. Tretinoin 45-58 colony stimulating factor 3 Homo sapiens 124-129
1711202-3 1991 Our studies revealed that the epidermal keratins, K5, K6, K14, and K16, their mRNAs, and their transcripts were diminished relative to actin as a consequence of retinoic acid (RA) treatment. Tretinoin 176-178 keratin 14 Homo sapiens 58-61
1710118-6 1991 The distribution of three RARs in adipose tissue suggests the physiological role of retinoic acid in the regulation of specific genes via RARs in adipocytes. Tretinoin 84-97 arginyl-tRNA synthetase 1 Rattus norvegicus 26-30
1704851-3 1991 Treatment of neutrophils with both G-CSF and retinoic acid augmented the amount of mRNA for NAP over the amount obtained by G-CSF alone, which was most marked at 24 h. These results show that both G-CSF-mediated NAP induction and its potentiation by retinoic acid are due to the increased levels of mRNA for NAP. Tretinoin 250-263 colony stimulating factor 3 Homo sapiens 35-40
22896640-1 2012 Dendritic cells (DC) in the gut promote immune tolerance by expressing retinal dehydrogenase (RALDH), an enzyme that promotes retinoic acid, which aids differentiation of Foxp3+ inducible regulatory T cells (iTreg) in the intestinal mucosa. Tretinoin 126-139 forkhead box P3 Mus musculus 171-176
2068135-0 1991 Patterns of regulation of nuclear proto-oncogenes MYCN and MYB in retinoic acid treated neuroblastoma cells. Tretinoin 66-79 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 50-54
2068135-0 1991 Patterns of regulation of nuclear proto-oncogenes MYCN and MYB in retinoic acid treated neuroblastoma cells. Tretinoin 66-79 MYB proto-oncogene, transcription factor Homo sapiens 59-62
1710118-6 1991 The distribution of three RARs in adipose tissue suggests the physiological role of retinoic acid in the regulation of specific genes via RARs in adipocytes. Tretinoin 84-97 arginyl-tRNA synthetase 1 Rattus norvegicus 138-142
1652423-0 1991 Retinoic acid treatment alters the distribution of retinoic acid receptor-beta transcripts in the embryonic chick face. Tretinoin 0-13 retinoic acid receptor beta Gallus gallus 51-78
1879351-1 1991 We report the results of a histochemical study, using polyclonal antipeptide antibodies to the different TGF beta isoforms, which demonstrates that retinoic acid regulates the expression of TGF beta 2 in the vitamin A-deficient rat. Tretinoin 148-161 transforming growth factor, beta 2 Rattus norvegicus 190-200
1879351-3 1991 Treatment with retinoic acid caused a rapid and transient induction of TGF beta 2 and TGF beta 3 in the epidermis, tracheobronchial and alveolar epithelium, and intestinal mucosa. Tretinoin 15-28 transforming growth factor, beta 2 Rattus norvegicus 71-81
2176462-3 1990 RA binding to the wild-type and truncated forms of the receptor was identical for both RAR alpha and RAR beta, indicating that the ligand-binding domains have retained the binding characteristics of the intact receptors. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 87-96
22969159-3 2012 We developed specific antibodies against the amino-terminal segment of CD38 and showed that two opposing orientations of CD38, type II and type III (which has its catalytic domain inside the cell), were both present on the surface of HL-60 cells during retinoic acid-induced differentiation. Tretinoin 253-266 CD38 molecule Homo sapiens 71-75
2176462-4 1990 Furthermore, RA bound with the same affinity to both RAR alpha and RAR beta. Tretinoin 13-15 retinoic acid receptor alpha Homo sapiens 53-62
1707036-4 1991 Addition of fetuin or epidermal growth factor (EGF) to incubates with serum-deprived cells increased the ability of TPA to affect growth, but addition of platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-beta) or retinoic acid (RA) was without effect. Tretinoin 239-252 epidermal growth factor Homo sapiens 22-45
1707036-4 1991 Addition of fetuin or epidermal growth factor (EGF) to incubates with serum-deprived cells increased the ability of TPA to affect growth, but addition of platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-beta) or retinoic acid (RA) was without effect. Tretinoin 239-252 epidermal growth factor Homo sapiens 47-50
1707036-4 1991 Addition of fetuin or epidermal growth factor (EGF) to incubates with serum-deprived cells increased the ability of TPA to affect growth, but addition of platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-beta) or retinoic acid (RA) was without effect. Tretinoin 254-256 epidermal growth factor Homo sapiens 22-45
1707036-4 1991 Addition of fetuin or epidermal growth factor (EGF) to incubates with serum-deprived cells increased the ability of TPA to affect growth, but addition of platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-beta) or retinoic acid (RA) was without effect. Tretinoin 254-256 epidermal growth factor Homo sapiens 47-50
2090523-0 1990 Filaggrin production by cultured human epidermal keratinocytes and its regulation by retinoic acid. Tretinoin 85-98 filaggrin Homo sapiens 0-9
2090523-7 1990 Finally, we show that the accumulation of filaggrin in the outermost layers of submerged cultured human keratinocytes can be triggered by extensive removal (double delipidization) of retinoids from the serum supplement and inhibited when small concentrations (10(-11)-10(-10) M) of retinoic acid are readded to the culture medium. Tretinoin 282-295 filaggrin Homo sapiens 42-51
22969159-3 2012 We developed specific antibodies against the amino-terminal segment of CD38 and showed that two opposing orientations of CD38, type II and type III (which has its catalytic domain inside the cell), were both present on the surface of HL-60 cells during retinoic acid-induced differentiation. Tretinoin 253-266 CD38 molecule Homo sapiens 121-125
2090523-8 1990 Altogether, the data reported suggest that not only the synthesis of profilaggrin, but also the conversion of profilaggrin into filaggrin are negatively controlled by retinoic acid. Tretinoin 167-180 filaggrin Homo sapiens 72-81
2090523-9 1990 Further, it seems that retinoic acid acts directly on the conversion of profilaggrin into filaggrin rather than on the production of terminally differentiating cells capable of accumulating this protein. Tretinoin 23-36 filaggrin Homo sapiens 75-84
1708372-3 1991 At 10(-8) M retinoic acid, the cells form a stratified squamous epithelium which expresses the differentiation-specific keratin K13. Tretinoin 12-25 keratin 13 Homo sapiens 128-131
23098119-3 2012 The molecular hallmark of the disease is the presence of a balanced reciprocal translocation resulting in the PML/RAR-alpha gene fusion, which represents the target of the all-trans retinoic acid (ATRA) therapy. Tretinoin 182-195 PML nuclear body scaffold Homo sapiens 110-123
1932206-6 1991 Two nuclear matrix proteins, p52 and p55, incorporated [3H] retinoic acid rapidly, were cell-cycle-related, and disappeared within 12 h of dosing. Tretinoin 60-73 H3 histone pseudogene 44 Homo sapiens 37-40
1705636-8 1991 The results suggest that G-CSF stimulates RA-induced morphological and functional differentiation of HL-60 cells, but the differentiation-enhancing effects of GM-CSF are limited, whereas the growth-stimulating effect of GM-CSF on HL-60 cells is greater than that of G-CSF. Tretinoin 42-44 colony stimulating factor 3 Homo sapiens 25-30
1964179-7 1990 Also, the expression of different species of NGFR could be modified by treatment with retinoic acid (RA). Tretinoin 86-99 nerve growth factor receptor Homo sapiens 45-49
1964179-7 1990 Also, the expression of different species of NGFR could be modified by treatment with retinoic acid (RA). Tretinoin 101-103 nerve growth factor receptor Homo sapiens 45-49
23098119-3 2012 The molecular hallmark of the disease is the presence of a balanced reciprocal translocation resulting in the PML/RAR-alpha gene fusion, which represents the target of the all-trans retinoic acid (ATRA) therapy. Tretinoin 197-201 PML nuclear body scaffold Homo sapiens 110-123
23159076-15 2012 CD34 was expressed in all xenografts, most highly in the control group and lowest in the RGZ + ATRA group. Tretinoin 95-99 CD34 antigen Mus musculus 0-4
1703522-4 1990 We studied the effects of acyclic retinoid, the 7-hydroxy derivative of acyclic retinoid (7OH-acyclic retinoid) and retinoic acid on a human hepatoma-derived cell line PLC/PRF/5 (Alexander cells). Tretinoin 116-129 heparan sulfate proteoglycan 2 Homo sapiens 168-171
1846233-0 1991 Effects of retinoic acid and bromodeoxyuridine on human melanoma-associated antigen expression in small cell lung carcinoma cells. Tretinoin 11-24 ankyrin repeat domain 36B Homo sapiens 56-83
22592496-4 2012 We found that addition of the proteasome inhibitor lactacystin to isolated gonocytes inhibited their retinoic acid-induced differentiation in a dose-dependent manner, blocking the induction of the spermatogonial gene markers Stra8 and Dazl. Tretinoin 101-114 deleted in azoospermia-like Rattus norvegicus 235-239
1700022-3 1990 Chronic application of tretinoin causes epidermal thickening (25 of 25 samples), stratum granulosum thickening (15 of 25), parakeratosis (13 of 25), a marked increase in the number of cell layers expressing epidermal transglutaminase (13 of 25), and focal expression of two keratins, K6 (12 of 25) and K13 (8 of 25), not normally expressed in the epidermis. Tretinoin 23-32 keratin 13 Homo sapiens 302-305
2206968-0 1990 Effect of topical retinoic acid on the interleukin 1 alpha and beta immunoreactive pool in normal human epidermis. Tretinoin 18-31 interleukin 1 alpha Homo sapiens 39-58
2172246-1 1990 Differentiation of the murine embryonal carcinoma (EC) cell lines F-9 and PC-13, induced by beta-all transretinoic acid (RA) resulted in an increased level of two lysosomal-associated membrane glycoproteins (LAMP-1 and LAMP-2). Tretinoin 92-119 lysosomal-associated membrane protein 2 Mus musculus 219-225
1982997-4 1990 However, RA treatment concomitant with MDI addition inhibited triacylglycerol accumulation (I0.5 = 6 nM) and the accumulation of the differentiation-dependent mRNAs encoding the adipocyte lipid-binding protein (ALBP) and stearoyl-CoA desaturase 1 (SCD1). Tretinoin 9-11 fatty acid binding protein 4, adipocyte Mus musculus 178-209
1982997-4 1990 However, RA treatment concomitant with MDI addition inhibited triacylglycerol accumulation (I0.5 = 6 nM) and the accumulation of the differentiation-dependent mRNAs encoding the adipocyte lipid-binding protein (ALBP) and stearoyl-CoA desaturase 1 (SCD1). Tretinoin 9-11 fatty acid binding protein 4, adipocyte Mus musculus 211-215
1982997-9 1990 Examination of immediate-early transcription factor expression during the MDI regimen revealed that RA mediated an elevated, prolonged expression of c-Jun mRNA accompanied by diminished expression of c-Fos and Jun-B mRNAs. Tretinoin 100-102 FBJ osteosarcoma oncogene Mus musculus 200-205
1982997-9 1990 Examination of immediate-early transcription factor expression during the MDI regimen revealed that RA mediated an elevated, prolonged expression of c-Jun mRNA accompanied by diminished expression of c-Fos and Jun-B mRNAs. Tretinoin 100-102 jun B proto-oncogene Mus musculus 210-215
22521346-6 2012 An assay of hepatocyte cell lines of differing AFP expression showed that cytoplasmic AFP is able to block ATRA-induced nuclear translocation of RAR and expression of the Fn14 gene. Tretinoin 107-111 retinoic acid receptor alpha Homo sapiens 145-148
2267130-5 1990 Treatment of the neuroblastoma cell line SMS-KCNR, which contains 75 copies of the N-myc gene, with retinoic acid for ten days resulted in an increase in Op18 phosphorylation. Tretinoin 100-113 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 83-88
1697169-1 1990 Expression of myc-box genes can be reduced by Interferon (c-myc in Daudi cells) or Retinoic acid (N-myc in neuroblastoma cells). Tretinoin 83-96 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 98-103
2267130-5 1990 Treatment of the neuroblastoma cell line SMS-KCNR, which contains 75 copies of the N-myc gene, with retinoic acid for ten days resulted in an increase in Op18 phosphorylation. Tretinoin 100-113 stathmin 1 Homo sapiens 154-158
22056878-5 2012 In estrogen-receptor-negative cellular models showing coamplification of ERBB2 and RARA, simultaneous targeting of the corresponding gene products with combinations of lapatinib and ATRA causes synergistic growth inhibition, cyto-differentiation and apoptosis. Tretinoin 182-186 retinoic acid receptor alpha Homo sapiens 83-87
2169566-0 1990 Thymosin beta 10 levels in developing human brain and its regulation by retinoic acid in the HTB-10 neuroblastoma. Tretinoin 72-85 thymosin beta 10 Homo sapiens 0-16
2169566-5 1990 However, in the HTB-10 neuroblastoma, retinoic acid caused a reduction in the level of thymosin beta 10. Tretinoin 38-51 thymosin beta 10 Homo sapiens 87-103
2165854-9 1990 These results would suggest that enhancement of the B-1 F cell growth is mediated through interaction of retinoic acid with retinoic acid receptor alpha. Tretinoin 105-118 retinoic acid receptor alpha Homo sapiens 124-152
22806070-8 2012 42: 1685-1694] show that RA ameliorates Con A-induced murine hepatitis by selectively downmodulating IFN-gamma and IL-4 production in disease-causing NKT cells in the liver. Tretinoin 25-27 interleukin 4 Mus musculus 115-119
1975093-2 1990 The multiple transcripts of the human HOX-5.1 gene are expressed differentially in tissue- and stage-specific patterns during embryogenesis, and differentially induced by retinoic acid (RA) in human embryonal carcinoma (EC) NT2/D1 cells. Tretinoin 171-184 homeobox D4 Homo sapiens 38-45
1975093-2 1990 The multiple transcripts of the human HOX-5.1 gene are expressed differentially in tissue- and stage-specific patterns during embryogenesis, and differentially induced by retinoic acid (RA) in human embryonal carcinoma (EC) NT2/D1 cells. Tretinoin 186-188 homeobox D4 Homo sapiens 38-45
2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tretinoin 128-141 interleukin 1 alpha Homo sapiens 26-30
2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tretinoin 128-141 interleukin 1 alpha Homo sapiens 151-155
2162058-5 1990 In contrast, RAR-alpha mRNA in F9 stem cells was affected less (1.2- to 1.4-fold increase) by retinoic acid and decreased 3-fold transiently when fresh serum was added to the medium. Tretinoin 94-107 retinoic acid receptor alpha Homo sapiens 13-22
22327096-0 2012 Thrombomodulin enhances the antifibrinolytic and antileukemic effects of all-trans retinoic acid in acute promyelocytic leukemia cells. Tretinoin 83-96 thrombomodulin Homo sapiens 0-14
2162058-8 1990 These results distinguish the effects of serum, cAMP, and retinoic acid on the expression of RAR from the effects mediated by differentiation. Tretinoin 58-71 retinoic acid receptor alpha Homo sapiens 93-96
1970118-0 1990 Retinoic acid-induced granulocytic differentiation of HL-60 myeloid leukemia cells is mediated directly through the retinoic acid receptor (RAR-alpha). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 140-149
2226349-14 1990 In the postnatal period, thyroid and steroid hormones including retinoic acid have been shown to modulate EGF and/or EGF receptors in several tissues. Tretinoin 64-77 epidermal growth factor Homo sapiens 106-109
2226349-14 1990 In the postnatal period, thyroid and steroid hormones including retinoic acid have been shown to modulate EGF and/or EGF receptors in several tissues. Tretinoin 64-77 epidermal growth factor Homo sapiens 117-120
2163993-1 1990 Retinoic acid (RA) treatment of F-9 embryonal carcinoma cells resulted in cell flattening and increased production of laminin B1 chain, both indicating differentiation to endoderm-like cells. Tretinoin 0-13 laminin subunit beta 1 Homo sapiens 118-134
2163993-1 1990 Retinoic acid (RA) treatment of F-9 embryonal carcinoma cells resulted in cell flattening and increased production of laminin B1 chain, both indicating differentiation to endoderm-like cells. Tretinoin 15-17 laminin subunit beta 1 Homo sapiens 118-134
22496486-7 2012 Interestingly, PKCdelta was involved in ATRA-induced increased NSMase2 transcription. Tretinoin 40-44 sphingomyelin phosphodiesterase 3 Homo sapiens 63-70
22588303-4 2012 We show that Activin directly inhibits the mitogenic sonic hedgehog pathway in a Gli3-dependent manner while enhancing retinoic acid signalling, the pro-neurogenic pathway. Tretinoin 119-132 inhibin subunit beta E Homo sapiens 13-20
2161334-4 1990 The mixed populations of endoderm- and mesoderm-like cells that were obtained after the introduction of c-jun morphologically and biochemically resembled P19 cells differentiated in monolayer by retinoic acid (RA). Tretinoin 195-208 interleukin 23 subunit alpha Homo sapiens 154-157
2161334-4 1990 The mixed populations of endoderm- and mesoderm-like cells that were obtained after the introduction of c-jun morphologically and biochemically resembled P19 cells differentiated in monolayer by retinoic acid (RA). Tretinoin 210-212 interleukin 23 subunit alpha Homo sapiens 154-157
1691021-2 1990 cDNAs corresponding to K8 and K18 mRNAs were cloned and used to study the change in the abundance of these mRNAs during differentiation of F9 cells into parietal endoderm-like cells by treatment with retinoic acid (RA) or with RA and dibutyryl cAMP (Bt2cAMP). Tretinoin 200-213 keratin 18 Homo sapiens 30-33
2107263-7 1990 The effects of RA were not limited to MSH or to Cloudman melanoma cells since RA blocked cholera toxin-inducible melanogenesis in Cloudman cells, as well as the induction of tyrosinase activity by L-tyrosine in Bomirski hamster melanoma cells. Tretinoin 15-17 tyrosinase Mus musculus 174-184
2110809-3 1990 Since we have previously shown that all-trans retinoic acid (RA) prevented the induction of uPA in mouse peritoneal macrophages, we have now assessed whether teratogenic doses of this agent could also interfere with uPA activity in mouse embryo in vitro and in vivo. Tretinoin 46-59 plasminogen activator, urokinase Mus musculus 92-95
22997710-4 2012 Down- regulation of MMP-1 by dihydroquercetin and its synthetic derivatives surpassed the activity of a standard (retinoic acid). Tretinoin 114-127 matrix metallopeptidase 1 Homo sapiens 20-25
2110809-3 1990 Since we have previously shown that all-trans retinoic acid (RA) prevented the induction of uPA in mouse peritoneal macrophages, we have now assessed whether teratogenic doses of this agent could also interfere with uPA activity in mouse embryo in vitro and in vivo. Tretinoin 61-63 plasminogen activator, urokinase Mus musculus 92-95
2164349-1 1990 The effect of retinoic acid (RA)-induced suppression of in vitro invasive ability of A549 human lung carcinoma cells on cellular binding of RA and epidermal growth factor (EGF) was investigated. Tretinoin 14-27 epidermal growth factor Homo sapiens 147-170
2164349-1 1990 The effect of retinoic acid (RA)-induced suppression of in vitro invasive ability of A549 human lung carcinoma cells on cellular binding of RA and epidermal growth factor (EGF) was investigated. Tretinoin 14-27 epidermal growth factor Homo sapiens 172-175
2164349-1 1990 The effect of retinoic acid (RA)-induced suppression of in vitro invasive ability of A549 human lung carcinoma cells on cellular binding of RA and epidermal growth factor (EGF) was investigated. Tretinoin 29-31 epidermal growth factor Homo sapiens 147-170
2164349-1 1990 The effect of retinoic acid (RA)-induced suppression of in vitro invasive ability of A549 human lung carcinoma cells on cellular binding of RA and epidermal growth factor (EGF) was investigated. Tretinoin 29-31 epidermal growth factor Homo sapiens 172-175
1689682-1 1990 P19 embryonal carcinoma cells can be induced to differentiate with a pulse of only 4 hr in retinoic acid (RA). Tretinoin 91-104 interleukin 23 subunit alpha Homo sapiens 0-3
1689682-1 1990 P19 embryonal carcinoma cells can be induced to differentiate with a pulse of only 4 hr in retinoic acid (RA). Tretinoin 106-108 interleukin 23 subunit alpha Homo sapiens 0-3
1689682-2 1990 The efficiency of RA-induced differentiation is independent of the position of P19 cells in the cell cycle but is critically dependent on the ratio between the number of cells and the number of moles of RA in the culture medium. Tretinoin 18-20 interleukin 23 subunit alpha Homo sapiens 79-82
22916501-9 2012 Combination of ATRA and MNM induced MSCs into neural-like cells which expressed neuronal specific markers, Nestin, NSE, MAP-2, and Tau. Tretinoin 15-19 enolase 2 Rattus norvegicus 115-118
2405249-0 1990 Rapid and transient decrease of N-myc expression in retinoic acid-induced differentiation of OTF9 teratocarcinoma stem cells. Tretinoin 52-65 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 32-37
2405249-2 1990 Previous studies have shown that N-myc expression significantly decreases when the stem cells are subjected to long-term induction for differentiation by retinoic acid (RA). Tretinoin 154-167 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 33-38
2405249-2 1990 Previous studies have shown that N-myc expression significantly decreases when the stem cells are subjected to long-term induction for differentiation by retinoic acid (RA). Tretinoin 169-171 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 33-38
2405249-3 1990 We found that in a stem cell line, OTF9, a steep yet transient decrease of N-myc expression takes place much earlier, immediately after induction by RA. Tretinoin 149-151 POU domain, class 3, transcription factor 4 Mus musculus 35-39
2405249-3 1990 We found that in a stem cell line, OTF9, a steep yet transient decrease of N-myc expression takes place much earlier, immediately after induction by RA. Tretinoin 149-151 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 75-80
2405249-6 1990 Therefore, transient decrease of N-myc expression may be the consequence of RA-induced differentiation, even though it occurs very early in the process. Tretinoin 76-78 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 33-38
2156569-1 1990 Two different species of cellular retinoic acid binding proteins, CRABP-I and CRABP-II, have been found in neonatal rat pups (Bailey, J. S. and Siu, C.-H. (1988) J. Biol. Tretinoin 34-47 cellular retinoic acid binding protein 2 Rattus norvegicus 78-86
2188740-3 1990 In the presence of retinoic acid the fibrillar vimentin immunoreactivity diminished rapidly, while it was increased when the cells were exposed to hemin or butyric acid. Tretinoin 19-32 vimentin Homo sapiens 47-55
22916501-9 2012 Combination of ATRA and MNM induced MSCs into neural-like cells which expressed neuronal specific markers, Nestin, NSE, MAP-2, and Tau. Tretinoin 15-19 microtubule-associated protein 2 Rattus norvegicus 120-125
2295827-0 1990 Trans retinoic acid enhances the growth response of epidermal keratinocytes to epidermal growth factor and transforming growth factor beta. Tretinoin 6-19 epidermal growth factor Mus musculus 79-102
2295827-3 1990 Incubation with all-trans retinoic acid (RA) greatly enhanced the stimulatory effect of EGF. Tretinoin 26-39 epidermal growth factor Mus musculus 88-91
22844234-4 2012 Single-point energy calculations performed with the M06-2x density functional were found to yield similar results to MP2/CBS for the low-energy retinoic acid conformations. Tretinoin 144-157 tryptase pseudogene 1 Homo sapiens 117-120
2295827-3 1990 Incubation with all-trans retinoic acid (RA) greatly enhanced the stimulatory effect of EGF. Tretinoin 41-43 epidermal growth factor Mus musculus 88-91
2295827-4 1990 Transforming growth factor beta (TGF beta) inhibited the EGF-induced DNA synthesis in a dose-dependent manner, and the inhibition was greatly enhanced by a low dose of RA. Tretinoin 168-170 epidermal growth factor Mus musculus 57-60
33819809-7 2021 Mechanistically, the retinoic acid-inducible gene I (RIG-I) pathway in MDMs was stimulated by EBV-encoded small RNA-1 (EBER-1) whereas the inhibition of these pathways by BX-795 almost abolished the production of these two cytokines and IDO induction. Tretinoin 21-34 indoleamine 2,3-dioxygenase 1 Homo sapiens 237-240
22374841-4 2012 Patients with untreated AML showed increased HSP90 levels and a distinct serum cytokine profile when compared with healthy controls, and low pre-therapy HSP90 levels were associated with a prolonged survival during treatment with ATRA + valproic acid + theophyllin. Tretinoin 230-234 heat shock protein 90 alpha family class A member 1 Homo sapiens 153-158
33972682-6 2021 DPP4 expression can be inducible by retinoic acid and repressed by ALDH1A inhibition. Tretinoin 36-49 dipeptidyl peptidase 4 Homo sapiens 0-4
2152965-0 1990 Cyclic AMP analogs and retinoic acid influence the expression of retinoic acid receptor alpha, beta, and gamma mRNAs in F9 teratocarcinoma cells. Tretinoin 23-36 retinoic acid receptor alpha Homo sapiens 65-93
2152965-1 1990 Retinoic acid (RA) receptor alpha (RAR alpha) and RAR gamma steady-state mRNA levels remained relatively constant over time after the addition of RA to F9 teratocarcinoma stem cells. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 35-44
2152965-3 1990 In the presence of RA, cyclic AMP analogs also greatly reduced the RAR alpha and RAR gamma mRNA levels, even though cyclic AMP analogs alone did not alter these mRNA levels. Tretinoin 19-21 retinoic acid receptor alpha Homo sapiens 67-76
22374841-6 2012 Furthermore, disease-stabilizing therapy altered the serum-cytokine profile, but the correlations between HSP70/HSP90/IL-1ra/HGF were maintained only when ATRA + valproic acid were combined with theophyllin but not when combined with cytarabine. Tretinoin 155-159 heat shock protein 90 alpha family class A member 1 Homo sapiens 112-117
22374841-6 2012 Furthermore, disease-stabilizing therapy altered the serum-cytokine profile, but the correlations between HSP70/HSP90/IL-1ra/HGF were maintained only when ATRA + valproic acid were combined with theophyllin but not when combined with cytarabine. Tretinoin 155-159 interleukin 1 receptor antagonist Homo sapiens 118-124
33654219-9 2021 We further demonstrated that BMSC-Exs protected against apoptosis and promoted the restoration of barrier function against SM through upregulating G protein-coupled receptor family C group 5 type A (GPRC5A), a retinoic acid target gene predominately expressed in the epithelial cells of the lung. Tretinoin 210-223 G protein-coupled receptor, family C, group 5, member A Mus musculus 147-197
33654219-9 2021 We further demonstrated that BMSC-Exs protected against apoptosis and promoted the restoration of barrier function against SM through upregulating G protein-coupled receptor family C group 5 type A (GPRC5A), a retinoic acid target gene predominately expressed in the epithelial cells of the lung. Tretinoin 210-223 G protein-coupled receptor, family C, group 5, member A Mus musculus 199-205
33807534-1 2021 The mitochondrial antiviral-signaling protein (MAVS, also known as VISA, IPS-1, or CARDIF) plays an essential role in the type I interferon (IFN) response and in retinoic acid-inducible gene I (RIG-I) mediated antiviral innate immunity in mammals. Tretinoin 162-175 mitochondrial antiviral signaling protein Homo sapiens 4-45
33807534-1 2021 The mitochondrial antiviral-signaling protein (MAVS, also known as VISA, IPS-1, or CARDIF) plays an essential role in the type I interferon (IFN) response and in retinoic acid-inducible gene I (RIG-I) mediated antiviral innate immunity in mammals. Tretinoin 162-175 mitochondrial antiviral signaling protein Homo sapiens 47-51
33807534-1 2021 The mitochondrial antiviral-signaling protein (MAVS, also known as VISA, IPS-1, or CARDIF) plays an essential role in the type I interferon (IFN) response and in retinoic acid-inducible gene I (RIG-I) mediated antiviral innate immunity in mammals. Tretinoin 162-175 mitochondrial antiviral signaling protein Homo sapiens 67-71
22343121-8 2012 Pretreatment of wild-type mice with retinoic acid before renal ischemia-reperfusion blunted the induction of Nur77, conferred protection of renal function, attenuated renal histologic injury, and reduced the expression of epithelial-derived proinflammatory cytokines. Tretinoin 36-49 nuclear receptor subfamily 4, group A, member 1 Mus musculus 109-114
33807534-1 2021 The mitochondrial antiviral-signaling protein (MAVS, also known as VISA, IPS-1, or CARDIF) plays an essential role in the type I interferon (IFN) response and in retinoic acid-inducible gene I (RIG-I) mediated antiviral innate immunity in mammals. Tretinoin 162-175 mitochondrial antiviral signaling protein Homo sapiens 73-78
33807534-1 2021 The mitochondrial antiviral-signaling protein (MAVS, also known as VISA, IPS-1, or CARDIF) plays an essential role in the type I interferon (IFN) response and in retinoic acid-inducible gene I (RIG-I) mediated antiviral innate immunity in mammals. Tretinoin 162-175 mitochondrial antiviral signaling protein Homo sapiens 83-89
23624502-0 2013 Small GTPase Rab39A interacts with UACA and regulates the retinoic acid-induced neurite morphology of Neuro2A cells. Tretinoin 58-71 RAB39, member RAS oncogene family Mus musculus 13-19
22343121-10 2012 Results obtained from proximal tubule cultures derived from Nur77-deficient mice suggested that the inhibition of Nur77 expression mediated the renoprotective effects of retinoic acid. Tretinoin 170-183 nuclear receptor subfamily 4, group A, member 1 Mus musculus 60-65
23624502-3 2013 shRNA-mediated knockdown of endogenous Rab39A or UACA in mouse neuroblastoma Neuro2A cells resulted in a change in retinoic acid-induced neurite morphology from a multipolar morphology to a bipolar morphology. Tretinoin 115-128 RAB39, member RAS oncogene family Mus musculus 39-45
23624502-4 2013 Taken together, these findings indicate that UACA functions as a Rab39A effector in the retinoic acid-induced differentiation of Neuro2A cells. Tretinoin 88-101 RAB39, member RAS oncogene family Mus musculus 65-71
30309678-6 2018 But, retinoic acid with estrogen group-treated cells exhibited increased mRNA expression of Stra8, Fragilis, Sycp3, GDF9, and Stella compared to untreated controls. Tretinoin 5-18 stimulated by retinoic acid gene 8 Mus musculus 92-97
30309678-6 2018 But, retinoic acid with estrogen group-treated cells exhibited increased mRNA expression of Stra8, Fragilis, Sycp3, GDF9, and Stella compared to untreated controls. Tretinoin 5-18 synaptonemal complex protein 3 Mus musculus 109-114
30309678-6 2018 But, retinoic acid with estrogen group-treated cells exhibited increased mRNA expression of Stra8, Fragilis, Sycp3, GDF9, and Stella compared to untreated controls. Tretinoin 5-18 growth differentiation factor 9 Mus musculus 116-120
22343121-11 2012 In summary, Nur77 promotes epithelial apoptosis after ischemia-reperfusion injury, and retinoic acid-mediated inhibition of Nur77 expression is a promising therapeutic strategy for the prevention of AKI. Tretinoin 87-100 nuclear receptor subfamily 4, group A, member 1 Mus musculus 124-129
22366455-5 2012 Absence of cytochrome P450, family 26, subfamily b, polypeptide 1 (Cyp26b1), a retinoic-acid-degrading enzyme, results in aberrant epidermal differentiation and filaggrin expression, defective cornified envelopes and skin barrier formation, in conjunction with peridermal retention. Tretinoin 79-92 filaggrin Homo sapiens 161-170
15894607-0 2005 Systems analysis of transcriptome and proteome in retinoic acid/arsenic trioxide-induced cell differentiation/apoptosis of promyelocytic leukemia. Tretinoin 50-63 PML nuclear body scaffold Homo sapiens 123-145
34910930-5 2022 These phenotypes resulted from the action of food-derived retinoic acid (ATRA), which enhanced actomyosin contractility and promoted LP cDC2 transmigration into the epithelium. Tretinoin 58-71 cyclin dependent kinase 1 Homo sapiens 136-140
34910930-5 2022 These phenotypes resulted from the action of food-derived retinoic acid (ATRA), which enhanced actomyosin contractility and promoted LP cDC2 transmigration into the epithelium. Tretinoin 73-77 cyclin dependent kinase 1 Homo sapiens 136-140
34625791-13 2021 Flow cytometric analysis revealed that ATRA temporarily increased CD38 expression on immune cell subsets. Tretinoin 39-43 CD38 molecule Homo sapiens 66-70
22228505-3 2012 The standard treatment for APL includes anthracycline-based chemotherapeutic agents plus the RARalpha agonist all-trans retinoic acid (ATRA). Tretinoin 120-133 retinoic acid receptor alpha Homo sapiens 93-101
34625791-14 2021 In conclusion, the addition of ATRA and re-intensification of daratumumab had limited activity in daratumumab-refractory patients, which may be explained by the transient upregulation of CD38 expression. Tretinoin 31-35 CD38 molecule Homo sapiens 187-191
34516292-3 2022 Synthetic retinoid agonists have major advantages over endogenous RAR agonists such as RA. Tretinoin 87-89 retinoic acid receptor alpha Homo sapiens 66-69
34516292-4 2022 Because they act through a specific RAR, side effects may be minimized, and synthetic retinoids often have better pharmaceutical properties than does RA. Tretinoin 150-152 retinoic acid receptor alpha Homo sapiens 36-39
22228505-3 2012 The standard treatment for APL includes anthracycline-based chemotherapeutic agents plus the RARalpha agonist all-trans retinoic acid (ATRA). Tretinoin 135-139 retinoic acid receptor alpha Homo sapiens 93-101
34288810-6 2021 Sox9 and Col2a1 in rEHBMCs were downregulated by ATRA in a dose-dependent manner at both mRNA and protein levels. Tretinoin 49-53 collagen type II alpha 1 chain Rattus norvegicus 9-15
22228505-7 2012 Here, we studied the molecular consequence of ATRA resistance by use of circular dichroism, protease resistance, and fluorescence anisotropy assays employing peptides derived from the NCOR nuclear corepressor and the ACTR nuclear coactivator. Tretinoin 46-50 nuclear receptor corepressor 1 Homo sapiens 184-188
34288810-7 2021 Similarly, HoxD9 was downregulated by ATRA in a dose-dependent manner, in parallel with the cartilage-specific molecules Sox9 and Col2a1. Tretinoin 38-42 collagen type II alpha 1 chain Rattus norvegicus 130-136
34934174-7 2021 The inhibitory effect of MCI-INI-3 on retinoic acid biosynthesis is comparable with that of ALDH1A3 knockout, suggesting that effective inhibition of ALDH1A3 is achieved with MCI-INI-3. Tretinoin 38-51 aldehyde dehydrogenase 1 family member A3 Homo sapiens 150-157
22367590-7 2012 In adherent culture conditions, EGAM1C partly inhibited the progression of differentiation at least within a 4-day culture period in the presence of retinoic acid by preventing the downregulation of LIF signaling with a robust increase in TBX3 expression. Tretinoin 149-162 leukemia inhibitory factor Mus musculus 199-202
34737147-8 2021 All compounds showed stimulating effects on the cholesterol biosynthesis related marker Msmo1 after 24 h exposure and tridemorph showed inhibition of Cyp26a1 which codes for one of the enzymes that metabolises retinoic acid. Tretinoin 210-223 methylsterol monooxygenase 1 Rattus norvegicus 88-93
34737147-8 2021 All compounds showed stimulating effects on the cholesterol biosynthesis related marker Msmo1 after 24 h exposure and tridemorph showed inhibition of Cyp26a1 which codes for one of the enzymes that metabolises retinoic acid. Tretinoin 210-223 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 150-157
34405393-7 2021 In conclusion, the present long-term follow-up study further confirmed the high cure probability of ATRA plus oral arsenic as front-line therapy for non-high-risk APL and showed that the PML-RARA transcript level at the end of induction therapy was associated with relapse. Tretinoin 100-104 PML nuclear body scaffold Homo sapiens 187-190
34405393-7 2021 In conclusion, the present long-term follow-up study further confirmed the high cure probability of ATRA plus oral arsenic as front-line therapy for non-high-risk APL and showed that the PML-RARA transcript level at the end of induction therapy was associated with relapse. Tretinoin 100-104 retinoic acid receptor alpha Homo sapiens 191-195
22337869-8 2012 These results suggest that RARalpha serves as an essential co-activator for ATRA signaling and that the recruitment of RARalpha to the KLF4-Sp1-YB1 complex, which leads to Klf4 expression in VSMCs, is independent of a retinoic acid response element. Tretinoin 218-231 retinoic acid receptor alpha Homo sapiens 119-127
34850159-2 2022 In these IDH-mutant gliomas, retinoic acid-related gene expression is commonly silenced by DNA hypermethylation. Tretinoin 29-42 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 9-12
34850159-5 2022 This was the rationale for a preclinical evaluation combining the DNA demethylating agent, 5-Azacytidine (5-Aza), and retinoic acid pathway activation with all-trans retinoic acid (atRA) in IDH-mutant glioma. Tretinoin 181-185 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 190-193
34288810-10 2021 These results demonstrate that ATRA suppresses chondrogenesis in rEHBMCs by inhibiting the expression of HoxD9 and its downstream protein targets, including Sox9 and Col2a1. Tretinoin 31-35 collagen type II alpha 1 chain Rattus norvegicus 166-172
34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin 38-51 H19 imprinted maternally expressed transcript Homo sapiens 320-323
34784434-2 2021 Previous studies have postulated that retinoic acid (RA), an active metabolite of vitamin A and high-affinity ligand for RA receptor (RAR), is reduced in airway inflammatory condition and contributes to multiple features of asthma including airway hyperresponsiveness and excessive accumulation of airway smooth muscle (ASM) cells. Tretinoin 53-55 H19 imprinted maternally expressed transcript Homo sapiens 320-323
34848785-10 2021 Our studies suggest RDH14 as a candidate for autosomal recessive ID and cerebellar atrophy, implicating either disrupted retinoic acid signaling, or, through PACC1, disrupted chloride ion homeostasis in the brain as a putative disease mechanism. Tretinoin 121-134 retinol dehydrogenase 14 Homo sapiens 20-25
34840990-9 2021 Moreover, retinoic acid (RA) released from TLR5+ LPDCs could play a key role in modulating TH1 polarization. Tretinoin 10-23 toll-like receptor 5 Mus musculus 43-47
34840990-9 2021 Moreover, retinoic acid (RA) released from TLR5+ LPDCs could play a key role in modulating TH1 polarization. Tretinoin 25-27 toll-like receptor 5 Mus musculus 43-47
22291023-6 2012 Analyses of retinoic acid levels using either endogenous retinoic acid-sensitive gene hoxd4 or retinoic acid reporter cell line both show that the levels of retinoic acid are significantly decreased in rdhe2 morphants. Tretinoin 57-70 homeobox D4 Homo sapiens 86-91
34731624-5 2021 The RA signaling pathway is not required for ketamine-mediated antidepressant action; however, direct activation of the retinoic acid receptor alpha (RARalpha) evokes rapid antidepressant action resembling ketamine. Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 120-148
34731624-5 2021 The RA signaling pathway is not required for ketamine-mediated antidepressant action; however, direct activation of the retinoic acid receptor alpha (RARalpha) evokes rapid antidepressant action resembling ketamine. Tretinoin 4-6 retinoic acid receptor alpha Homo sapiens 150-158
34837603-8 2022 Our data confirmed that STMN1 was highly expressed in early hematopoietic progenitors and reduced during cell differentiation, including the ATRA-induced granulocytic differentiation model. Tretinoin 141-145 stathmin 1 Homo sapiens 24-29
34775955-11 2021 Furthermore, our results revealed that CRBP-1 could increase the intracellular levels of retinoic acid, which induced the activation of RARs/RXRs leading to the transcriptional expression of WIF1, a secreted antagonist of the Wnt/beta-catenin signaling pathway, by physically interacting with the region on WIF1 promoter. Tretinoin 89-102 catenin beta 1 Homo sapiens 230-242
22291023-6 2012 Analyses of retinoic acid levels using either endogenous retinoic acid-sensitive gene hoxd4 or retinoic acid reporter cell line both show that the levels of retinoic acid are significantly decreased in rdhe2 morphants. Tretinoin 57-70 homeobox D4 Homo sapiens 86-91
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 4-8 retinoic acid receptor alpha Homo sapiens 61-70
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 137-141 retinoic acid receptor alpha Homo sapiens 61-70
22291023-8 2012 Importantly, the retinol oxidizing activity of frog rdhe2 is conserved in its mouse homologs, suggesting that rdhe2-related enzymes may represent the previously unrecognized physiologically relevant retinol dehydrogenases that contribute to retinoic acid biosynthesis in higher vertebrates. Tretinoin 241-254 short chain dehydrogenase/reductase family 16C, member 5 Mus musculus 52-57
34830183-10 2021 Our findings indicated that ATRA suppresses cell proliferation through the downregulation of OR7A17 via RAR alpha- and gamma-mediated retinoid signaling. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 104-113
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 266-279 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 54-104
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 266-279 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 106-111
22291023-8 2012 Importantly, the retinol oxidizing activity of frog rdhe2 is conserved in its mouse homologs, suggesting that rdhe2-related enzymes may represent the previously unrecognized physiologically relevant retinol dehydrogenases that contribute to retinoic acid biosynthesis in higher vertebrates. Tretinoin 241-254 short chain dehydrogenase/reductase family 16C, member 5 Mus musculus 110-115
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 266-279 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 183-188
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 281-285 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 54-104
22328502-8 2012 Expression of SOHLH1, but not SOHLH2, was increased in postnatal mitotic germ cells by treatment with all-trans retinoic acid. Tretinoin 112-125 spermatogenesis and oogenesis specific basic helix-loop-helix 1 Mus musculus 14-20
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 281-285 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 183-188
34498703-4 2021 Here, we demonstrate that BM ILC2s highly express the receptor activator of nuclear factor kappaB ligand (RANKL), a robust cytokine for osteoclast differentiation and activation, and RANKL expression on ILC2s is upregulated by interleukin (IL)-2, IL-7 and all-trans retinoic acid (ATRA). Tretinoin 281-285 interleukin 2 Mus musculus 227-245
34625492-5 2021 Correspondingly, mice deficient in VIP or VPAC1 suffer a paucity of intestinal ILC3s along with impaired production of the cytokine IL-22, rendering them highly susceptible to the enteric pathogen Citrobacter rodentium This heightened susceptibility to C. rodentium infection was ameliorated by RA supplementation, adoptive transfer of ILC3s, or by recombinant IL-22. Tretinoin 295-297 interleukin 22 Mus musculus 132-137
34764342-4 2021 CD38 expression in AML cells proved to depend on microenvironmental cues and could be significantly enforced through addition of tretinoin. Tretinoin 129-138 CD38 molecule Homo sapiens 0-4
22154861-9 2012 In particular, scaffold-based controlled delivery of RA enhanced MAP2 and RIP expression compared with bolus delivery despite lower amounts of drug (>8 times lower). Tretinoin 53-55 receptor interacting serine/threonine kinase 1 Homo sapiens 74-77
34695489-3 2022 METHODS: We differentiated hES-TEPs by mimicking developmental queues with FGF8, Retinoic Acid, Sonic Hedgehog, Noggin and BMP4. Tretinoin 81-94 ribosome binding protein 1 Homo sapiens 27-30
34464682-0 2021 Interaction between retinoic acid and FGF/ERK signals are involved in Dexamethasone-induced abnormal myogenesis during embryonic development. Tretinoin 20-33 fibroblast growth factor 8 Gallus gallus 38-41
34680392-4 2021 Here, using a panel of human AML cell lines and primary AML patient specimens harboring IDH mutations, we showed that the production of an oncometabolite (R)-2-HG by IDH mutant enzymes induces vitamin D receptor-related transcriptional changes, priming these AML cells to differentiate with pharmacological doses of ATRA and/or VD. Tretinoin 316-320 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 166-169
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 glutamic pyruvic transaminase, soluble Mus musculus 129-132
34643182-6 2021 We find that Tbx5/Aldh1a2-dependent RA signaling directly activates shh transcription in the adjacent foregut endoderm through a conserved MACS1 enhancer. Tretinoin 36-38 sonic hedgehog Mus musculus 68-71
34439217-9 2021 Overall, the response of iPMOL cells to ATRA and 5-AZA-CdR treatment was variable and is dependent on several factors, including RARbeta-promoter methylation. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 129-136
34447371-0 2021 Retinoic Acid Induces Functionally Suppressive Foxp3+RORgammat+ T Cells In Vitro. Tretinoin 0-13 forkhead box P3 Mus musculus 47-52
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 152-174
34447371-2 2021 This study aimed to discern the role played by IL-6 and retinoic acid (RA) in the in vitro generation of Foxp3+RORgammat+ T cells and to investigate whether such cells have suppressive properties. Tretinoin 56-69 forkhead box P3 Mus musculus 105-110
34733553-13 2021 ACE2 expression slightly increased in CRL-127 post RA-treatment. Tretinoin 51-53 interleukin 31 receptor A Homo sapiens 38-41
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 176-179
22039172-9 2012 P450-dependent atRA metabolism was demonstrated in HaCaT cells, with a very similar metabolite profile to that produced by our CYP2S1-expressing CHO cells. Tretinoin 15-19 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 127-133
34282811-7 2021 LP22A3 induced TGF-beta secretion from the IECs of the small intestine with retinoic acid production probably through TLR2, resulting in an increase in CD103+ DCs and the Foxp3+ Treg population. Tretinoin 76-89 forkhead box P3 Mus musculus 171-176
34091189-17 2021 Low MYB protein expression was associated with longer duration of stability on ATRA (P < 0.01). Tretinoin 79-83 MYB proto-oncogene, transcription factor Homo sapiens 4-7
20686816-1 2012 Unlike its cytotoxicity in p53-functional cell lines, Nutlin-1, the small-molecule inhibitor of murine double minute (MDM2), significantly enhanced the differentiation-inducing activity of all-trans retinoic acid (ATRA) in HL60 and NB4 cells (p53-nonfunctional) but not in U937 cells (p53 wild-type). Tretinoin 214-218 transformed mouse 3T3 cell double minute 2 Mus musculus 118-122
34346557-8 2021 We identified and validated new compounds, tretinoin, chondroitin sulfate, and hyaluronic acid, for their ability to restore age-related decline of collagen homeostasis and increase lifespan. Tretinoin 43-52 Col_cuticle_N domain-containing protein Caenorhabditis elegans 148-156
34362483-1 2021 OBJECTIVE: To investigate the expression of peptidylarginine deiminase 4 (PADI4) during the process of differentiation into granulocyte of NB4 cells induced by all-trans-retinoic acid (ATRA) and whether PADI4 is involved in the inflammatory cytokines expression. Tretinoin 160-183 peptidyl arginine deiminase 4 Homo sapiens 44-72
20686816-6 2012 Additionally, the expression of retinoic acid receptor alpha (RARalpha) was further reduced in cells treated with ATRA in combination with Nutlin-1. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 32-60
34362483-1 2021 OBJECTIVE: To investigate the expression of peptidylarginine deiminase 4 (PADI4) during the process of differentiation into granulocyte of NB4 cells induced by all-trans-retinoic acid (ATRA) and whether PADI4 is involved in the inflammatory cytokines expression. Tretinoin 160-183 peptidyl arginine deiminase 4 Homo sapiens 74-79
34362483-1 2021 OBJECTIVE: To investigate the expression of peptidylarginine deiminase 4 (PADI4) during the process of differentiation into granulocyte of NB4 cells induced by all-trans-retinoic acid (ATRA) and whether PADI4 is involved in the inflammatory cytokines expression. Tretinoin 185-189 peptidyl arginine deiminase 4 Homo sapiens 44-72
34362483-1 2021 OBJECTIVE: To investigate the expression of peptidylarginine deiminase 4 (PADI4) during the process of differentiation into granulocyte of NB4 cells induced by all-trans-retinoic acid (ATRA) and whether PADI4 is involved in the inflammatory cytokines expression. Tretinoin 185-189 peptidyl arginine deiminase 4 Homo sapiens 74-79
20686816-6 2012 Additionally, the expression of retinoic acid receptor alpha (RARalpha) was further reduced in cells treated with ATRA in combination with Nutlin-1. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 62-70
34362483-12 2021 CONCLUSION: During the differentiation into granulocyte of NB4 cells induced by ATRA, PADI4 expression increased. Tretinoin 80-84 peptidyl arginine deiminase 4 Homo sapiens 86-91
34419635-8 2021 Using the optimized concentration of -TTNPB, we found that RARalpha is the functionally dominant subtype and controls the RA-mediated neurogenesis of hESCs. Tretinoin 122-124 retinoic acid receptor alpha Homo sapiens 59-67
22239913-4 2012 RESULTS: Herein, we investigated the effects of bacterial-induced COPD-like inflammation and tobacco carcinogen-enhanced tumorigenesis/inflammation in the retinoic acid inducible G protein coupled receptor knock out mouse model (Gprc5a-/- mouse) characterized by late-onset, low multiplicity tumor formation. Tretinoin 155-168 G protein-coupled receptor, family C, group 5, member A Mus musculus 229-235
34166781-3 2021 We have found that MEPM-cell proliferation was regulated by atRA and exogenous TGF-beta3 could significantly antagonize the atRA-mediated suppression of MEPM cell proliferation, which is closely associated with the regulation of TGF-beta/Smad signaling pathway. Tretinoin 60-64 transforming growth factor alpha Mus musculus 229-237
34166781-3 2021 We have found that MEPM-cell proliferation was regulated by atRA and exogenous TGF-beta3 could significantly antagonize the atRA-mediated suppression of MEPM cell proliferation, which is closely associated with the regulation of TGF-beta/Smad signaling pathway. Tretinoin 124-128 transforming growth factor, beta 3 Mus musculus 79-88
34938986-3 2021 The identification of a balanced reciprocal translocation between chromosomes 15 and 17, resulting in fusion between the promyelocytic leukemia gene and the retinoic acid receptor alpha, has been crucial in understanding the mechanisms of leukemogenesis, and responsible for the peculiar response to targeted therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 322-345 retinoic acid receptor alpha Homo sapiens 157-185
34938986-3 2021 The identification of a balanced reciprocal translocation between chromosomes 15 and 17, resulting in fusion between the promyelocytic leukemia gene and the retinoic acid receptor alpha, has been crucial in understanding the mechanisms of leukemogenesis, and responsible for the peculiar response to targeted therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 347-351 retinoic acid receptor alpha Homo sapiens 157-185
34166781-3 2021 We have found that MEPM-cell proliferation was regulated by atRA and exogenous TGF-beta3 could significantly antagonize the atRA-mediated suppression of MEPM cell proliferation, which is closely associated with the regulation of TGF-beta/Smad signaling pathway. Tretinoin 124-128 transforming growth factor alpha Mus musculus 229-237
34166781-5 2021 Here, we found that Meg3 expression increased significantly in atRA-treated MEPM cells while TGF-beta3 treatment markedly inhibited Meg3 expression and antagonized the effect of atRA on Meg3. Tretinoin 178-182 transforming growth factor, beta 3 Mus musculus 93-102
34166781-7 2021 After Meg3 deletion, the effects of atRA on the proliferation of MEPM cells and TGF-beta3-dependent protein expression were lost. Tretinoin 36-40 transforming growth factor, beta 3 Mus musculus 80-89
34356051-0 2021 Retinoic Acid-Induced Gene G(RIG-G) as a Novel Monitoring Biomarker in Leukemia and Its Clinical Applications. Tretinoin 0-13 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 29-34
22490698-12 2012 CONCLUSIONS: RIG-G gene expression is closely correlated with the cross-talk between ATRA and IFN-alpha-induced signaling pathways. Tretinoin 85-89 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 13-18
34356051-1 2021 Retinoic acid inducible gene G (RIG-G) is an inducible gene produced during the treatment of acute promyelocytic leukemia with all-trans retinoic acid (ATRA). Tretinoin 127-150 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 0-30
34356051-1 2021 Retinoic acid inducible gene G (RIG-G) is an inducible gene produced during the treatment of acute promyelocytic leukemia with all-trans retinoic acid (ATRA). Tretinoin 127-150 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 32-37
34356051-1 2021 Retinoic acid inducible gene G (RIG-G) is an inducible gene produced during the treatment of acute promyelocytic leukemia with all-trans retinoic acid (ATRA). Tretinoin 152-156 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 0-30
34324169-0 2021 Selective Inhibition of JAK1 Primes STAT5-Driven Human Leukemia Cells for ATRA-Induced Differentiation. Tretinoin 74-78 signal transducer and activator of transcription 5A Homo sapiens 36-41
23254580-7 2012 Replicon-harboring cells showed higher expression of retinal dehydrogenase 1 (RALDH-1), which converts retinol to retinoic acid, and the cured cells showed higher expression of retinol-binding protein (RBP), which transports retinol from the liver to target tissues. Tretinoin 114-127 aldehyde dehydrogenase 1 family member A1 Homo sapiens 78-85
34278502-4 2021 The present study aimed to investigate the function of retinoic acid-related orphan receptor beta (RORbeta) in GC. Tretinoin 55-68 RAR-related orphan receptor alpha Mus musculus 99-106
34356051-1 2021 Retinoic acid inducible gene G (RIG-G) is an inducible gene produced during the treatment of acute promyelocytic leukemia with all-trans retinoic acid (ATRA). Tretinoin 152-156 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 32-37
34356051-5 2021 U test was used to analyze the expression level of RIG-G in the peripheral blood of 40 normal specimens and 20 APL patients to observe the prognostic monitoring effect of RIG-G gene in the ATRA treatment process. Tretinoin 189-193 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 51-56
34356051-5 2021 U test was used to analyze the expression level of RIG-G in the peripheral blood of 40 normal specimens and 20 APL patients to observe the prognostic monitoring effect of RIG-G gene in the ATRA treatment process. Tretinoin 189-193 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 171-176
34356051-9 2021 The changes in the expression level of RIG-G in peripheral blood changed indicates the remission and recurrence of APL patients after ATRA treatment, and the ROC curve shows that it has a better diagnostic power for APL. Tretinoin 134-138 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 39-44
34236140-0 2021 All-trans retinoic acid induces leukemia resistance to NK cell cytotoxicity by down-regulating B7-H6 expression via c-Myc signaling. Tretinoin 3-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 116-121
34236140-6 2021 We used CRISPR/Cas9 to knockdown B7-H6 expression and siRNA to knockdown c-Myc in U-937 cells to evaluate the role of B7-H6 and c-Myc in atRA-induced tumor resistance against NK cells. Tretinoin 137-141 MYC proto-oncogene, bHLH transcription factor Homo sapiens 128-133
34305901-6 2021 We observed that naive B cells lack the enzymatic machinery to produce RA, but use exogenous retinoic acid to enhance CD38 expression. Tretinoin 93-106 CD38 molecule Homo sapiens 118-122
21704731-7 2012 Retinoic acid is generated from retinaldehyde in adipose tissue by the aldehyde dehydrogenase-1 family of enzymes (Aldh1). Tretinoin 0-13 aldehyde dehydrogenase 1 family member A1 Homo sapiens 115-120
34305901-7 2021 Furthermore, we showed that human DCs metabolize retinal into retinoic acid, which in co-culture with naive B cells led to of the induction of CD38 expression. Tretinoin 62-75 CD38 molecule Homo sapiens 143-147
34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 FOS like 1, AP-1 transcription factor subunit Homo sapiens 118-122
34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 ETS proto-oncogene 1, transcription factor Homo sapiens 134-138
21704731-8 2012 In this review, we discuss the role of Aldh1 enzymes in the generation of retinoic acid during adipogenesis, in the regulation of the transcriptional network of PPARgamma in a fat-depot-specific manner, and the important contribution of this autocrine pathway in the development of visceral obesity. Tretinoin 74-87 aldehyde dehydrogenase 1 family member A1 Homo sapiens 39-44
22973984-7 2012 The findings indicate that ADAM23 suppresses neuronal differentiation through its disintegrin domain, and Adam23 KD up-regulates P27KIP1 in P19/ADAM23KD cells, one reason that P19/ADAM23KD cells can differentiate into neurons without RA induction. Tretinoin 234-236 a disintegrin and metallopeptidase domain 23 Mus musculus 106-112
34215687-12 2021 Increasing the CD38:CIP ratio through sequential CIP knockdown, followed by CD38 upregulation via All-Trans Retinoic Acid treatment, potently augments complement-mediated lysis in cells previously resistant to daratumumab. Tretinoin 98-121 CD38 molecule Homo sapiens 76-80
21954838-3 2012 METHODS: Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Tretinoin 52-65 keratin 18 Homo sapiens 99-113
34723044-7 2021 Combination treatment with RA enhanced the abscopal response when radiation and PD-L1 blockade were used together. Tretinoin 27-29 CD274 molecule Homo sapiens 80-85
34178631-13 2021 RA can normalize RARbeta levels and limit cell migration but does not have a significant effect on proliferation. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 17-24
21954838-3 2012 METHODS: Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Tretinoin 52-65 keratin 18 Homo sapiens 115-119
34085926-5 2021 Mechanistically, Rela deletion suppresses expression of Aldh1a1, an enzyme required for retinoic acid synthesis from vitamin A. Tretinoin 88-101 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 17-21
21954838-3 2012 METHODS: Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Tretinoin 67-71 keratin 18 Homo sapiens 99-113
34085926-6 2021 Retinoic acid administration blocks development of ocular anomalies in Krt14-Cre; Relaf/f mice and naturally aged mice. Tretinoin 0-13 keratin 14 Mus musculus 71-76
21954838-3 2012 METHODS: Previous studies have shown that all trans retinoic acid (ATRA) induces the expression of cytokeratin 18 (CK18), indicating the beginning of differentiation into the epithelial lineage. Tretinoin 67-71 keratin 18 Homo sapiens 115-119
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 integrin subunit alpha E Homo sapiens 124-129
21954838-10 2012 The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Tretinoin 83-87 keratin 18 Homo sapiens 147-151
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 integrin subunit alpha E Homo sapiens 241-246
34236140-11 2021 On the other hand, atRA treatment reduced c-Myc expression, which in turn inhibited the transcription of B7-H6 on leukemia cells. Tretinoin 19-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-47
22129829-7 2012 Therefore, Osr genes act as a relay within the genetic cascade of fin bud formation: by controlling the expression of the signaling molecule Wnt2ba in the IM they play an essential function transmitting the RA signaling originated in the somites to the LPM. Tretinoin 207-209 wingless-type MMTV integration site family, member 2Ba Danio rerio 141-147
34236140-12 2021 CONCLUSION: atRA treatment promotes tumor cell resistance against NK cell-mediated lysis by down-regulating B7-H6 expression via the c-Myc signaling pathway, suggesting that more attention needs to be paid to the immunological adverse effects in the clinical use of atRA treatment. Tretinoin 12-16 MYC proto-oncogene, bHLH transcription factor Homo sapiens 133-138
23300507-0 2012 Anti-PML-RARalpha shRNA sensitises promyelocytic leukaemia cells to all-trans retinoic acid. Tretinoin 78-91 PML nuclear body scaffold Homo sapiens 5-8
35490242-0 2022 The MYCN inhibitor BGA002 restores the retinoic acid response leading to differentiation or apoptosis by the mTOR block in MYCN-amplified neuroblastoma. Tretinoin 39-52 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 123-127
35490242-6 2022 RESULTS: We found that MYCN-specific inhibition by BGA002 in combination with RA (BGA002-RA) act synergistically and overcame resistance in NB cell lines. Tretinoin 78-80 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 23-27
35490242-10 2022 CONCLUSION: Taken together, MYCN modulation mediates the therapeutic efficacy of RA and the development of RA resistance in MNA-NB. Tretinoin 81-83 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 28-32
35490242-10 2022 CONCLUSION: Taken together, MYCN modulation mediates the therapeutic efficacy of RA and the development of RA resistance in MNA-NB. Tretinoin 107-109 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 28-32
23300507-0 2012 Anti-PML-RARalpha shRNA sensitises promyelocytic leukaemia cells to all-trans retinoic acid. Tretinoin 78-91 retinoic acid receptor alpha Homo sapiens 9-17
23300507-4 2012 When combined with ATRA administration, this down regulation of the fusion gene strongly inhibited proliferation in the NB4 PML cell line. Tretinoin 19-23 PML nuclear body scaffold Homo sapiens 124-127
23259068-0 2012 PKCdelta Regulates Translation Initiation through PKR and eIF2alpha in Response to Retinoic Acid in Acute Myeloid Leukemia Cells. Tretinoin 83-96 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 50-53
35468223-5 2022 In combination with BEZ235, ATRA treatment led to almost complete eradication of cellular MYC, G1 arrest, loss of clonal capacity and terminal granulocytic differentiation. Tretinoin 28-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 90-93
35468223-6 2022 We demonstrate that PAM inhibitor/ATRA treatment targets MYC via independent mechanisms. Tretinoin 34-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-60
35468223-7 2022 While inhibition of the PAM pathway causes MYC phosphorylation at threonine 58 via glycogen synthase kinase 3 beta and subsequent degradation, ATRA reduces its expression. Tretinoin 143-147 MYC proto-oncogene, bHLH transcription factor Homo sapiens 43-46
23259068-3 2012 ATRA and ATO induce Ser-51 phosphorylation (inactivation) of eIF2alpha, through the induction of protein kinase C delta (PKCdelta) and PKR, but not other eIF2alpha kinases, such as GCN2 and PERK in APL (NB4) and AML cells (HL60, U937, and THP-1). Tretinoin 0-4 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 135-138
23259068-3 2012 ATRA and ATO induce Ser-51 phosphorylation (inactivation) of eIF2alpha, through the induction of protein kinase C delta (PKCdelta) and PKR, but not other eIF2alpha kinases, such as GCN2 and PERK in APL (NB4) and AML cells (HL60, U937, and THP-1). Tretinoin 0-4 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 190-194
22690121-7 2012 RESULTS: We demonstrated that FRMD7 can promote neurite outgrowth following retinoic acid-induced differentiation in Neuro-2a cells. Tretinoin 76-89 FERM domain containing 7 Mus musculus 30-35
35412614-5 2022 We show that one such target gene, ALDH1A1, which regulates a key step in retinoic acid biosynthesis, is consistently upregulated with PBRM1 loss in ccRCC cell lines and primary tumors, as well as non-malignant cells. Tretinoin 74-87 aldehyde dehydrogenase 1 family member A1 Homo sapiens 35-42
22876133-0 2012 ATRA enhances the bystander effect of suicide gene therapy driven by the specific promoter LEP 503 in human lens epithelial cells. Tretinoin 0-4 lens epithelial protein Homo sapiens 91-98
35454359-10 2022 This observation suggests that ATRA may be partially effective in some ZBTB16-RARA APLs. Tretinoin 31-35 retinoic acid receptor alpha Homo sapiens 78-82
22876133-7 2012 RESULTS: The promoter LEP503-mediated HSV-tk was specifically expressed in HLECs, and ATRA dose-dependently strengthened the bystander effect following LEP503-mediated HSV-tk/GCV gene therapy against lens cells by upregulating the expression of the gap junction protein Cx43. Tretinoin 86-90 lens epithelial protein Homo sapiens 22-28
35406069-2 2022 Acting through the retinoic acid receptors RARalpha, RARbeta, and RARgamma, all-trans-retinoic acid, an active metabolite of VA, is a potent regulator of numerous biological pathways, including embryonic and somatic cellular differentiation, immune functions, and energy metabolism. Tretinoin 76-99 retinoic acid receptor alpha Homo sapiens 43-51
35406069-2 2022 Acting through the retinoic acid receptors RARalpha, RARbeta, and RARgamma, all-trans-retinoic acid, an active metabolite of VA, is a potent regulator of numerous biological pathways, including embryonic and somatic cellular differentiation, immune functions, and energy metabolism. Tretinoin 76-99 retinoic acid receptor alpha Homo sapiens 53-60
22876133-7 2012 RESULTS: The promoter LEP503-mediated HSV-tk was specifically expressed in HLECs, and ATRA dose-dependently strengthened the bystander effect following LEP503-mediated HSV-tk/GCV gene therapy against lens cells by upregulating the expression of the gap junction protein Cx43. Tretinoin 86-90 lens epithelial protein Homo sapiens 152-158
35328499-6 2022 All-trans retinoic acid (RA, 5 or 10 microM) inhibited the Wnt signaling pathway via suppressing the translocation of beta-catenin from the cytoplasm into the nucleus. Tretinoin 0-23 catenin beta 1 Homo sapiens 118-130
21911359-3 2012 Through microarray expression analysis, we identified transcripts differentially expressed between F9 wild-type (Wt) and RARalpha knockout cells cultured in the absence or presence of the RAR-specific ligand all trans retinoic acid (RA). Tretinoin 218-231 retinoic acid receptor alpha Homo sapiens 121-129
21911359-3 2012 Through microarray expression analysis, we identified transcripts differentially expressed between F9 wild-type (Wt) and RARalpha knockout cells cultured in the absence or presence of the RAR-specific ligand all trans retinoic acid (RA). Tretinoin 218-231 retinoic acid receptor alpha Homo sapiens 121-124
35092119-0 2022 LncSIK1 enhanced the sensitivity of AML cells to retinoic acid by the E2F1/autophagy pathway. Tretinoin 49-62 E2F transcription factor 1 Homo sapiens 70-74
23285066-8 2012 Overexpression of transcription factor Nanog was possibly achieved through a RA-induced non-genomic c-Src/Stat3/Nanog signaling pathway mediated by the subcellular c-Src mRNA localization for the maintenance of pluripotency in tNSCs. Tretinoin 77-79 signal transducer and activator of transcription 3 Rattus norvegicus 106-111
35167919-11 2022 Our data suggested that CD35+ FDCs can support differentiation of B cells into IgA+GL7+ GC B-like cells in environments that are not limited to MLNs, which can be stimulated by retinoic acid. Tretinoin 177-190 natriuretic peptide receptor 2 Mus musculus 88-92
22147914-0 2011 Cullin 3 mediates SRC-3 ubiquitination and degradation to control the retinoic acid response. Tretinoin 70-83 nuclear receptor coactivator 3 Homo sapiens 18-23
22147914-4 2011 Here, by using an RNAi E3-ubiquitin ligase entry screen, we identified CUL-3 and RBX1 as components of the E3 ubiquitin ligase involved in the RA-induced ubiquitination and subsequent degradation of SRC-3. Tretinoin 143-145 nuclear receptor coactivator 3 Homo sapiens 199-204
22147914-5 2011 We also show that the RA-induced ubiquitination of SRC-3 depends on its prior phosphorylation at serine 860 that promotes binding of the CUL-3-based E3 ligase in the nucleus. Tretinoin 22-24 nuclear receptor coactivator 3 Homo sapiens 51-56
21859732-1 2011 BACKGROUND: Combined treatment with all-trans-retinoic acid and chemotherapy is extremely efficient in patients with acute promyelocytic leukemia with t(15;17)/PML-RARA, but up to 15% of patients relapse. Tretinoin 36-59 PML nuclear body scaffold Homo sapiens 160-163
35225106-8 2022 Consistently, in the GPL rat model, we observed a similar disorder; however, ATRA supplementation significantly not only corrected the disorder by increasing Rdh10, Aldh1a1 and decreasing Cyp26b1, but also reduced claudin-18 (P < 0.05). Tretinoin 77-81 retinol dehydrogenase 10 Rattus norvegicus 158-163
35007564-3 2022 MATERIALS AND METHODS: ChIP-seq was utilized to identify binding sites of DDX5 and DDX17 in both human pluripotent stem cell (hPSC) line NTERA2 and their retinoic acid-induced neural derivatives. Tretinoin 154-167 DEAD-box helicase 5 Homo sapiens 74-78
21859732-1 2011 BACKGROUND: Combined treatment with all-trans-retinoic acid and chemotherapy is extremely efficient in patients with acute promyelocytic leukemia with t(15;17)/PML-RARA, but up to 15% of patients relapse. Tretinoin 36-59 retinoic acid receptor alpha Homo sapiens 164-168
35063128-2 2022 Combining an in vitro reconstitution of this process based on mouse embryonic stem cells (mESCs) with a collection of knockouts in reporter mESC lines, we identified retinoic acid (RA) as a critical mediator of early neural induction triggered by TGFbeta or Wnt signaling inhibition. Tretinoin 166-179 transforming growth factor alpha Mus musculus 247-254
35063128-2 2022 Combining an in vitro reconstitution of this process based on mouse embryonic stem cells (mESCs) with a collection of knockouts in reporter mESC lines, we identified retinoic acid (RA) as a critical mediator of early neural induction triggered by TGFbeta or Wnt signaling inhibition. Tretinoin 181-183 transforming growth factor alpha Mus musculus 247-254
21725974-7 2011 SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Tretinoin 35-39 angiopoietin like 4 Homo sapiens 84-91
35063128-5 2022 Genetic evidence showed that the RA-degrading enzyme Cyp26a1 protected PS-like cells from neural induction, even in the absence of TGFbeta and Wnt antagonists. Tretinoin 33-35 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 53-60
21725974-7 2011 SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Tretinoin 35-39 NPR2 like, GATOR1 complex subunit Homo sapiens 110-115
35149382-12 2022 CONCLUSIONS: High-dose ATRA intake over a short period of time can reduce GH-IGF1-IGFBP3 levels, affect cartilage and bone homeostasis, and inhibit bone growth in developing animals. Tretinoin 23-27 insulin-like growth factor 1 Rattus norvegicus 77-81
21988834-9 2011 Our analysis provides a dynamic view of RA signalling during cell differentiation, reveals RAR heterodimer dynamics and promiscuity, and predicts decisions that diversify the RA signal into distinct gene-regulatory programs. Tretinoin 40-42 retinoic acid receptor alpha Homo sapiens 91-94
35149382-12 2022 CONCLUSIONS: High-dose ATRA intake over a short period of time can reduce GH-IGF1-IGFBP3 levels, affect cartilage and bone homeostasis, and inhibit bone growth in developing animals. Tretinoin 23-27 insulin-like growth factor binding protein 3 Rattus norvegicus 82-88
35197751-6 2022 ATRA also supported ADMSCs by a significant down-regulation of caspase-3, il-6 and TGFbeta1, and a significant up-regulation of HIF1, VEGF and CD31 compared to group of cisplatin which reversed the cisplatin effect. Tretinoin 0-4 vascular endothelial growth factor A Rattus norvegicus 134-138
35204719-10 2022 Moreover, the ATRA treatment significantly induced the upregulation of the GABAergic-specific SLC32A1, while the UDP-4 treatment led to the significant upregulation of the adrenergic-specific TH. Tretinoin 14-18 solute carrier family 32 member 1 Homo sapiens 94-101
34673934-6 2022 Mechanistically, we showed that NUP98-JADE2 could impair all-trans retinoic acid (ATRA)-mediated transcriptional control and myeloid differentiation. Tretinoin 67-80 jade family PHD finger 2 Homo sapiens 38-43
34673934-7 2022 Intriguingly, NUP98-JADE2 was found to alter the subcellular distribution of wild-type JADE2, whose down-regulation similarly led to attenuated ATRA-induced responses and myeloid activation, suggesting that NUP98-JADE2 may mediate JADE2 inhibition. Tretinoin 144-148 jade family PHD finger 2 Homo sapiens 20-25
34673934-7 2022 Intriguingly, NUP98-JADE2 was found to alter the subcellular distribution of wild-type JADE2, whose down-regulation similarly led to attenuated ATRA-induced responses and myeloid activation, suggesting that NUP98-JADE2 may mediate JADE2 inhibition. Tretinoin 144-148 jade family PHD finger 2 Homo sapiens 87-92
34673934-9 2022 Our findings suggest JADE2 as a novel myeloid player involved in retinoic acid-induced differentiation. Tretinoin 65-78 jade family PHD finger 2 Homo sapiens 21-26
34673934-10 2022 Despite lacking a rearranged RARA, our findings implicate that altered retinoic acid signaling by JADE2 disruption may underlie the APL-like features in our case, corroborating the importance of this signaling in APL pathogenesis. Tretinoin 71-84 jade family PHD finger 2 Homo sapiens 98-103
21843507-0 2011 All-trans retinoic acid induces cellular senescence by up-regulating levels of p16 and p21 via promoter hypomethylation. Tretinoin 10-23 H3 histone pseudogene 16 Homo sapiens 87-90
21843507-1 2011 All-trans retinoic acid (ATRA) induces cellular senescence via up-regulation of p16 and p21; however, the action mechanism of ATRA is unknown. Tretinoin 0-23 H3 histone pseudogene 16 Homo sapiens 88-91
21843507-1 2011 All-trans retinoic acid (ATRA) induces cellular senescence via up-regulation of p16 and p21; however, the action mechanism of ATRA is unknown. Tretinoin 25-29 H3 histone pseudogene 16 Homo sapiens 88-91
21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 H3 histone pseudogene 16 Homo sapiens 68-71
35056791-1 2022 Aldehyde dehydrogenase-1a1 (ALDH1a1), the enzyme responsible for the oxidation of retinal into retinoic acid, represents a key therapeutic target for the treatment of debilitating disorders such as cancer, obesity, and inflammation. Tretinoin 95-108 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-26
35056791-1 2022 Aldehyde dehydrogenase-1a1 (ALDH1a1), the enzyme responsible for the oxidation of retinal into retinoic acid, represents a key therapeutic target for the treatment of debilitating disorders such as cancer, obesity, and inflammation. Tretinoin 95-108 aldehyde dehydrogenase 1 family member A1 Homo sapiens 28-35
21843507-2 2011 Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells. Tretinoin 19-23 H3 histone pseudogene 16 Homo sapiens 199-202
21383690-4 2011 RA treatment rapidly induced morphology changes, induced growth arrest at G1/G0 to S transition, decreased cyclin D1 expression and increased p27 expression. Tretinoin 0-2 interferon alpha inducible protein 27 Homo sapiens 142-145
21554977-3 2011 ATRA activates another set of transcription factors, the retinoic acid receptors (RAR) alpha, beta and gamma, which mediate its effects on target genes. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 82-85
21393419-0 2011 All-trans retinoic acid and a novel synthetic retinoid tamibarotene (Am80) differentially regulate CD38 expression in human leukemia HL-60 cells: possible involvement of protein kinase C-delta. Tretinoin 0-23 CD38 molecule Homo sapiens 99-103
21393419-2 2011 ATRA induces CD38 antigen during HL-60 cell differentiation, which interacts with CD31 antigen on the vascular EC surface and may induce disadvantages in the therapy. Tretinoin 0-4 CD38 molecule Homo sapiens 13-17
21393419-3 2011 We here examined the mechanisms of the ATRA-mediated CD38 induction and compared the difference between ATRA- and tamibarotene-mediated induction. Tretinoin 39-43 CD38 molecule Homo sapiens 53-57
21393419-7 2011 Cycloheximide and rottlerin suppressed the delayed-phase induction of CD38 expression by ATRA but did not affect the early-phase induction. Tretinoin 89-93 CD38 molecule Homo sapiens 70-74
21430230-3 2011 Retinoic acid significantly leads to the induction of Mirlet7 miRNAs through suppression of Lin28. Tretinoin 0-13 lin-28 homolog A Mus musculus 92-97
35213790-8 2022 Formation velocity of atRA was approximately threefold higher (p = 0.0001) in omental AT (9.8 (7.6, 11.2)) pmol/min/mg) than subcutaneous AT (3.2 (2.1, 4.0) pmol/min/mg) and correlated with ALDH1A2 expression in omental AT (beta-coefficient = 3.07, p = 0.0007) and with ALDH1A1 expression in subcutaneous AT (beta-coefficient = 0.13, p = 0.003). Tretinoin 22-26 aldehyde dehydrogenase 1 family member A1 Homo sapiens 270-277
35213790-10 2022 Our findings suggest that ALDH1A2 is the primary mediator of atRA formation in omental AT, whereas ALDH1A1 is the principal atRA-synthesizing enzyme in subcutaneous AT. Tretinoin 124-128 aldehyde dehydrogenase 1 family member A1 Homo sapiens 99-106
22586354-4 2011 In acute promyelocytic leukemia, the cooperative degradation of PML/RARA by arsenic and retinoic acid cures most patients. Tretinoin 88-101 PML nuclear body scaffold Homo sapiens 64-67
35545255-6 2022 In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner. Tretinoin 37-41 solute carrier organic anion transporter family member 1B1 Homo sapiens 70-77
35545255-6 2022 In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner. Tretinoin 37-41 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 79-85
35545255-6 2022 In human hepatocytes (n=3), 13cisRA, atRA and 4-oxo-13cisRA decreased OATP1B1, CYP1A2, CYP2C9, and CYP2D6 mRNA and increased CYP2B6 and CYP3A4 mRNA in a concentration-dependent manner. Tretinoin 37-41 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 87-93
22586354-4 2011 In acute promyelocytic leukemia, the cooperative degradation of PML/RARA by arsenic and retinoic acid cures most patients. Tretinoin 88-101 retinoic acid receptor alpha Homo sapiens 68-72
20815727-6 2011 ET-1 and dHAND protein levels were significantly increased in vitamin B12-supplemented embryos compared to the RA-exposed group in embryonic branchial region. Tretinoin 111-113 endothelin 1 Mus musculus 0-4
35467087-14 2022 CONCLUSIONS: Arsenic trioxide may reactivate the expression of HoxC9 by downregulating EZH2, which leads to restoring RA sensitivity and promoting the differentiation and apoptosis of RA-resistant NB cells. Tretinoin 118-120 homeobox C9 Homo sapiens 63-68
35467087-14 2022 CONCLUSIONS: Arsenic trioxide may reactivate the expression of HoxC9 by downregulating EZH2, which leads to restoring RA sensitivity and promoting the differentiation and apoptosis of RA-resistant NB cells. Tretinoin 184-186 homeobox C9 Homo sapiens 63-68
20815727-7 2011 CONCLUSIONS: These results suggest that vitamin B12 may prevent RA-induced craniofacial abnormalities via prevention of an RA-induced decrease of ET-1 and dHAND protein levels in the branchial region during the organogenic period. Tretinoin 123-125 endothelin 1 Mus musculus 146-150
21355853-7 2011 Our results indicate that HSC (heat shock constant)70 and HSP60 expressions decreased following RA treatment, EB formation and in mature neural cells derived from heat-stressed single cells and not heat-treated EBs. Tretinoin 96-98 heat shock protein 1 (chaperonin) Mus musculus 58-63
35452677-0 2022 Activity-dependent modulation of neuronal KV channels by retinoic acid enhances CaV channel activity. Tretinoin 57-70 caveolin 2 Homo sapiens 80-83
35452677-6 2022 The prolonged depolarizations observed during RA-modulated spiking lead to an increase in Ca2+ influx through CaV channels, though we also show an opposing effect of RA on the same neurons to inhibit Ca2+ influx. Tretinoin 46-48 caveolin 2 Homo sapiens 110-113
35452677-8 2022 Examining the interaction between the spike-modulating effects of RA and its inhibition of CaV channels, we found that inhibition of CaV2 channels limits the Ca2+ influx resulting from spike modulation. Tretinoin 66-68 caveolin 2 Homo sapiens 91-94
35452677-8 2022 Examining the interaction between the spike-modulating effects of RA and its inhibition of CaV channels, we found that inhibition of CaV2 channels limits the Ca2+ influx resulting from spike modulation. Tretinoin 66-68 caveolin 2 Homo sapiens 133-137
35436742-0 2022 All-trans retinoic acid inhibits the osteogenesis of periodontal ligament stem cells by promoting IL-1beta production via NF-kappaB signaling. Tretinoin 0-23 interleukin 1 alpha Homo sapiens 98-106
35436742-12 2022 Levels of interleukin-1beta (IL-1beta) were increased at varied time points after ATRA treatment. Tretinoin 82-86 interleukin 1 alpha Homo sapiens 29-37
35436742-13 2022 The inhibitive influence of ATRA on the osteogenesis of PDLSCs was partially reversed after neutralizing IL-1beta. Tretinoin 28-32 interleukin 1 alpha Homo sapiens 105-113
35436742-15 2022 Taken together, our results demonstrate that ATRA disrupts the osteogenesis and mineralizationof PDLSCs by promoting IL-1beta expression via activating NF-kappaB signaling and NLRP3 inflammasome, which may offer a new method for improving the ATRA-induced disruption of osteoblast differentiation. Tretinoin 45-49 interleukin 1 alpha Homo sapiens 117-125
21539831-0 2011 Hmx4 regulates Sonic hedgehog signaling through control of retinoic acid synthesis during forebrain patterning. Tretinoin 59-72 sonic hedgehog signaling molecule Homo sapiens 15-29
35436742-15 2022 Taken together, our results demonstrate that ATRA disrupts the osteogenesis and mineralizationof PDLSCs by promoting IL-1beta expression via activating NF-kappaB signaling and NLRP3 inflammasome, which may offer a new method for improving the ATRA-induced disruption of osteoblast differentiation. Tretinoin 243-247 interleukin 1 alpha Homo sapiens 117-125
21596042-1 2011 BACKGROUND & AIMS: Gut-associated dendritic cells (DC) metabolize vitamin A into all-trans retinoic acid (RA), which is required to induce lymphocytes to localize to the gastrointestinal tract and promotes the differentiation of Foxp3+ regulatory T cells and IgA antibody-secreting cells. Tretinoin 85-108 forkhead box P3 Mus musculus 233-238
35455744-5 2022 Most importantly, we show that induction of the specific retinoic acid receptor alpha (RARalpha) increased the efficiency of atrial differentiation to 72% compared with 45% after modulating the retinoic acid (RA) pathway with all-trans RA (atRA). Tretinoin 236-238 retinoic acid receptor alpha Homo sapiens 57-85
35455744-5 2022 Most importantly, we show that induction of the specific retinoic acid receptor alpha (RARalpha) increased the efficiency of atrial differentiation to 72% compared with 45% after modulating the retinoic acid (RA) pathway with all-trans RA (atRA). Tretinoin 240-244 retinoic acid receptor alpha Homo sapiens 57-85
35248720-0 2022 Aberrant epigenetic regulation of RARbeta by TET2 is involved in cutaneous squamous cell carcinoma resistance to retinoic acid. Tretinoin 113-126 retinoic acid receptor alpha Homo sapiens 34-41
21596042-1 2011 BACKGROUND & AIMS: Gut-associated dendritic cells (DC) metabolize vitamin A into all-trans retinoic acid (RA), which is required to induce lymphocytes to localize to the gastrointestinal tract and promotes the differentiation of Foxp3+ regulatory T cells and IgA antibody-secreting cells. Tretinoin 110-112 forkhead box P3 Mus musculus 233-238
35248720-2 2022 Retinoic acid receptor beta (RARbeta) functions as a tumor suppressor gene and is associated with the proliferation inhibition to retinoic acid. Tretinoin 130-143 retinoic acid receptor alpha Homo sapiens 29-36
35248720-11 2022 We upregulated TET2 could reverse promoter hypermethylation and showed a significantly increased expression of RARbeta, which enhanced the sensitivity of tumor cells to retinoic acid treatment. Tretinoin 169-182 retinoic acid receptor alpha Homo sapiens 111-118
21608077-4 2011 When compared with wild-type ESCs and gastrulating embryos, Oct4 repression is lost and its proximal promoter is significantly hypomethylated in retinoic acid (RA)-differentiated GCNF(-/-) ESCs and GCNF(-/-) embryos. Tretinoin 145-158 POU class 5 homeobox 1 Homo sapiens 60-64
35248720-13 2022 While reversing the hypermethylation of the RARbeta promoter by recovering the TET2 could enhance tumor cells to be sensitive to retinoic acid. Tretinoin 129-142 retinoic acid receptor alpha Homo sapiens 44-51
21608077-4 2011 When compared with wild-type ESCs and gastrulating embryos, Oct4 repression is lost and its proximal promoter is significantly hypomethylated in retinoic acid (RA)-differentiated GCNF(-/-) ESCs and GCNF(-/-) embryos. Tretinoin 160-162 POU class 5 homeobox 1 Homo sapiens 60-64
35198449-4 2022 In this report, we identified THRAP3 as novel RARA fusion in resembling APL, which was resistant to all-trans retinoic acid (ATRA) combined arsenic trioxide (ATO) chemotherapy. Tretinoin 100-123 retinoic acid receptor alpha Homo sapiens 46-50
35198449-4 2022 In this report, we identified THRAP3 as novel RARA fusion in resembling APL, which was resistant to all-trans retinoic acid (ATRA) combined arsenic trioxide (ATO) chemotherapy. Tretinoin 125-129 retinoic acid receptor alpha Homo sapiens 46-50
21498506-2 2011 We show here that Amer1 directly interacts with the armadillo repeats of beta-catenin via a domain consisting of repeated arginine-glutamic acid-alanine (REA) motifs, and that Amer1 assembles the beta-catenin destruction complex at the plasma membrane by recruiting beta-catenin, adenomatous polyposis coli, and Axin/Conductin. Tretinoin 154-157 catenin beta 1 Homo sapiens 196-208
35173714-6 2022 However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1beta, IL-6, IL-8 and TNF-alpha. Tretinoin 9-13 interleukin 1 alpha Homo sapiens 127-135
21498506-2 2011 We show here that Amer1 directly interacts with the armadillo repeats of beta-catenin via a domain consisting of repeated arginine-glutamic acid-alanine (REA) motifs, and that Amer1 assembles the beta-catenin destruction complex at the plasma membrane by recruiting beta-catenin, adenomatous polyposis coli, and Axin/Conductin. Tretinoin 154-157 catenin beta 1 Homo sapiens 196-208
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 interferon induced with helicase C domain 1 Homo sapiens 119-123
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 TNF receptor associated factor 6 Homo sapiens 186-191
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 mitochondrial antiviral signaling protein Homo sapiens 196-200
21594970-3 2011 The expression of some genes (Shh, Ptch-1, Gsc, and Msx2) controlled by retinoic acid is downregulated in rat embryos exposed at the phylotypic stage to the triazole triadimefon (FON). Tretinoin 72-85 msh homeobox 2 Rattus norvegicus 52-56
35145497-3 2021 Retinoic acid-induced gene I-like receptor (RLRs) recognize virus RNA in virus infection, and LGP2 is a member of RLRs. Tretinoin 0-13 DExH-box helicase 58 Homo sapiens 94-98
21671919-6 2011 In addition, as a model experiment of gene expression analysis using this staging series, we performed in situ hybridization of aldh1a2, aldh1a3 and cyp26a1 that play regulatory roles in retinoic acid (RA) metabolism essential for embryogenesis. Tretinoin 187-200 retinal dehydrogenase 2 Takifugu rubripes 128-135
35145896-8 2022 In addition, vitamin D3+ATRA supplementation increased miR-126 expression (p=0.014). Tretinoin 24-28 microRNA 126b Rattus norvegicus 55-62
35145896-11 2022 Also, vitamin D3+ATRA can be considered a new therapeutic agent that can elevate miR-126 expression and prevent diabetes-related cardiovascular complications. Tretinoin 17-21 microRNA 126b Rattus norvegicus 81-88
21671919-6 2011 In addition, as a model experiment of gene expression analysis using this staging series, we performed in situ hybridization of aldh1a2, aldh1a3 and cyp26a1 that play regulatory roles in retinoic acid (RA) metabolism essential for embryogenesis. Tretinoin 202-204 retinal dehydrogenase 2 Takifugu rubripes 128-135
21514413-6 2011 Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. Tretinoin 21-23 aldehyde dehydrogenase 1 family member A1 Homo sapiens 139-146
21514413-6 2011 Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. Tretinoin 170-172 aldehyde dehydrogenase 1 family member A1 Homo sapiens 139-146
21514413-6 2011 Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. Tretinoin 170-172 aldehyde dehydrogenase 1 family member A1 Homo sapiens 139-146
21228214-10 2011 Additionally, RA exposure resulted in increased Cyp26a1 expression of the RA-degrading enzyme. Tretinoin 14-16 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 48-55
21228214-10 2011 Additionally, RA exposure resulted in increased Cyp26a1 expression of the RA-degrading enzyme. Tretinoin 74-76 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 48-55
21471156-0 2011 SHH propagates distal limb bud development by enhancing CYP26B1-mediated retinoic acid clearance via AER-FGF signalling. Tretinoin 73-86 sonic hedgehog Mus musculus 0-3
21504909-3 2011 Sirenomelia occurs in mice lacking Cyp26a1, an enzyme that degrades retinoic acid (RA), and in mice that develop with reduced bone morphogenetic protein (Bmp) signaling in the caudal embryonic region. Tretinoin 68-81 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 35-42
21225541-1 2011 In thyroid cells, the effects of all- TRANS retinoic acid (ATRA) on sodium/iodide symporter (NIS) and CCAAT/enhancer-binding protein-homologous protein (CHOP) under condition of endoplasmic reticulum (ER) stress have not been evaluated. Tretinoin 59-63 DNA-damage inducible transcript 3 Rattus norvegicus 102-151
21225541-2 2011 In the present study, the relationships between NIS, CHOP, and p38 MAPK, and the effects of ATRA on NIS and CHOP expression as well as on p38 MAPK activation under condition of ER stress in thyroid cells were investigated. Tretinoin 92-96 DNA-damage inducible transcript 3 Rattus norvegicus 108-112
21436255-7 2011 These effects were recovered to some extent either by RA stimulation or overexpression of any of the Aldh1 enzymes in Aldh1a1(-/-) cells arguing that Aldh1a1 plays a dominant role in autocrine RA production. Tretinoin 193-195 aldehyde dehydrogenase 1 family member A1 Homo sapiens 101-106
21436255-7 2011 These effects were recovered to some extent either by RA stimulation or overexpression of any of the Aldh1 enzymes in Aldh1a1(-/-) cells arguing that Aldh1a1 plays a dominant role in autocrine RA production. Tretinoin 193-195 aldehyde dehydrogenase 1 family member A1 Homo sapiens 150-157
21436255-10 2011 This loss of RA-producing enzymes was accompanied by 70% decreased expression of ZFP423, PPARgamma, and Fabp4 in visceral fat of Aldh1a1(-/-) vs. wild-type mice and by the predominant loss of visceral fat. Tretinoin 13-15 fatty acid binding protein 4, adipocyte Mus musculus 104-109
21156171-0 2011 ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary. Tretinoin 0-4 CD38 molecule Homo sapiens 72-76
21156171-0 2011 ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary. Tretinoin 0-4 CD38 molecule Homo sapiens 130-134
21156171-1 2011 Leukocyte antigen CD38 expression is an early marker of all-trans retinoic acid (ATRA) stimulated differentiation in the leukemic cell line HL-60. Tretinoin 66-79 CD38 molecule Homo sapiens 18-22
21156171-1 2011 Leukocyte antigen CD38 expression is an early marker of all-trans retinoic acid (ATRA) stimulated differentiation in the leukemic cell line HL-60. Tretinoin 81-85 CD38 molecule Homo sapiens 18-22
21156171-4 2011 Here we determined whether CD38 enzymatic activity or the cytoplasmic tail is required for ATRA-induced differentiation. Tretinoin 91-95 CD38 molecule Homo sapiens 27-31
21156171-9 2011 Another is Vav1, which also showed only basal expression after ATRA treatment in CD38 Delta11-20 expressing cells. Tretinoin 63-67 CD38 molecule Homo sapiens 81-85
21307853-5 2011 Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. Tretinoin 124-137 interleukin 23 subunit alpha Homo sapiens 279-284
20717697-3 2011 In this study, proliferation-promoting effect of RA on chicken PGCs was investigated by revealing changes in adhesive proteins E-cadherin and alpha/beta catenins. Tretinoin 49-51 cadherin 1 Gallus gallus 127-137
20717697-6 2011 Furthermore, E-cadherin and beta-catenin protein expression levels were increased by RA treatment. Tretinoin 85-87 cadherin 1 Gallus gallus 13-23
20717697-8 2011 In addition, the number and area of PGC colonies were increased by RA treatment at 10(-7)-10(-5) M. Again, this increase was reduced by combined treatment of H(7). Tretinoin 67-69 progastricsin Gallus gallus 36-39
20717697-9 2011 The proliferating effect of RA on PGCs was further confirmed by increased mRNA expression of cyclins, CCND1 and CCNE1, and cyclin-dependent kinases 6 and 2, which are critical for G1-S progression in cell cycle. Tretinoin 28-30 cyclin dependent kinase 6 Gallus gallus 123-155
20717697-10 2011 Moreover, flow cytometry analysis confirmed that RA-treated PGC populations displayed a significant increase in the proportion of S and G2 phase cells. Tretinoin 49-51 progastricsin Gallus gallus 60-63
20717697-12 2011 These results indicate that RA, as a bioactive metabolite of vitamin A, may promote PGC proliferation and increase intercellular aggregation of PGCs via E-cadherin and alpha/beta-catenins expression through the PKC signaling pathway. Tretinoin 28-30 progastricsin Gallus gallus 84-87
20717697-12 2011 These results indicate that RA, as a bioactive metabolite of vitamin A, may promote PGC proliferation and increase intercellular aggregation of PGCs via E-cadherin and alpha/beta-catenins expression through the PKC signaling pathway. Tretinoin 28-30 cadherin 1 Gallus gallus 153-163
20354914-11 2011 Co-addition of atRA and calcitriol had no additive effects on cell viability but did increase ngn3 responses. Tretinoin 15-19 neurogenin 3 Homo sapiens 94-98
21138835-7 2011 siRNA knockdown indicates that Rdh10, Rdh2 (mRdh1), and Raldh1, -2, and -3 contribute to atRA production. Tretinoin 89-93 retinol dehydrogenase 10 Rattus norvegicus 31-36
21118818-0 2011 MicroRNAs-10a and -10b contribute to retinoic acid-induced differentiation of neuroblastoma cells and target the alternative splicing regulatory factor SFRS1 (SF2/ASF). Tretinoin 37-50 microRNA 10a Homo sapiens 0-22
21118818-7 2011 Induction of miR-10a and -10b by RA also could be detected in LA-N-1 neuroblastoma cells. Tretinoin 33-35 microRNA 10a Homo sapiens 13-20
21111795-9 2011 Non significant Oct-4 modulation in co-exposure with ATRA was observed at compounds, which potentiated ATRA-mediated effects in the reporter gene assay. Tretinoin 53-57 POU class 5 homeobox 1 Homo sapiens 16-21
21111795-9 2011 Non significant Oct-4 modulation in co-exposure with ATRA was observed at compounds, which potentiated ATRA-mediated effects in the reporter gene assay. Tretinoin 103-107 POU class 5 homeobox 1 Homo sapiens 16-21
21145646-0 2011 The expression of peroxisomal protein transcripts increased by retinoic acid during neural differentiation. Tretinoin 63-76 fibronectin type III domain containing 5 Mus musculus 18-37
20473866-4 2011 Knockdown of AFP mRNA or inhibition of AFP expression by all trans-retinoic acid resulted in enhancement of the PTEN level with a synchronous decrease in phosphorylated AKT. Tretinoin 61-80 phosphatase and tensin homolog Homo sapiens 112-116
20473866-6 2011 The inhibition of PI3K signaling by LY 294002 was simultaneously reversed by transfection, accompanied by diminution of all trans-retinoic acid-induced upregulation of PTEN and enhancement of cell growth. Tretinoin 124-143 phosphatase and tensin homolog Homo sapiens 168-172
20857416-4 2011 Addition of RA causes removal of H2A.Z and Suz12 from RARgamma target genes when the genes are transcriptionally activated. Tretinoin 12-14 H2A.Z variant histone 1 Homo sapiens 33-38
21176776-0 2011 PU.1 directly regulates retinoic acid-induced expression of RIG-G in leukemia cells. Tretinoin 24-37 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 60-65
21176776-2 2011 However, the mechanism underlying ATRA-induced RIG-G induction is not completely understood. Tretinoin 34-38 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 47-52
21176776-3 2011 Here, we demonstrate that ATRA up-regulates the expression of PU.1, which in turn directly binds to the promoter and increases the expression of RIG-G gene. Tretinoin 26-30 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 145-150
21176776-6 2011 These data provide new insight into the mechanism of ATRA-induced RIG-G expression. Tretinoin 53-57 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 66-71
21249211-2 2011 Dendritic cells in gut-related lymphoid organs can produce RA, thereby imprinting gut-homing specificity on T cells and enhancing transforming growth factor (TGF)-beta-dependent induction of Foxp3+ regulatory T cells upon antigen presentation. Tretinoin 59-61 forkhead box P3 Mus musculus 191-196
21138976-7 2011 Chromatin immunoprecipitation studies support Epo as a direct target of RA signaling in embryonic liver. Tretinoin 72-74 erythropoietin Mus musculus 46-49
21138976-11 2011 We propose a new model for the mechanism of RA-mediated myocardial expansion in which RA directly induces hepatic Epo resulting in activation of epicardial Igf2 that stimulates compact zone growth. Tretinoin 44-46 erythropoietin Mus musculus 114-117
21138976-11 2011 We propose a new model for the mechanism of RA-mediated myocardial expansion in which RA directly induces hepatic Epo resulting in activation of epicardial Igf2 that stimulates compact zone growth. Tretinoin 44-46 insulin-like growth factor 2 Mus musculus 156-160
21138976-11 2011 We propose a new model for the mechanism of RA-mediated myocardial expansion in which RA directly induces hepatic Epo resulting in activation of epicardial Igf2 that stimulates compact zone growth. Tretinoin 86-88 erythropoietin Mus musculus 114-117
21138976-11 2011 We propose a new model for the mechanism of RA-mediated myocardial expansion in which RA directly induces hepatic Epo resulting in activation of epicardial Igf2 that stimulates compact zone growth. Tretinoin 86-88 insulin-like growth factor 2 Mus musculus 156-160
21148184-0 2011 Vax2 regulates retinoic acid distribution and cone opsin expression in the vertebrate eye. Tretinoin 15-28 ventral anterior homeobox 2 Mus musculus 0-4
21148184-4 2011 In particular, we detected an expansion of the expression domains of the RA-catabolizing enzymes Cyp26a1 and Cyp26c1, and a downregulation of the RA-synthesizing enzyme Raldh3. Tretinoin 73-75 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 97-104
21148184-6 2011 At postnatal stages of eye development, Vax2 inactivation led to alterations of the regional expression of the cone photoreceptor genes Opn1sw (S-Opsin) and Opn1mw (M-Opsin), which were significantly rescued after RA administration. Tretinoin 214-216 ventral anterior homeobox 2 Mus musculus 40-44
21084447-9 2011 The Cyp26 inhibitor R115866 stimulated the proliferation of primary cultured mouse granulosa cells, and a similar effect was observed with RA and activin. Tretinoin 139-141 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 4-9
21425084-3 2011 By use of beta-galactosidase chemiluminescence, we show that a mouse Cdx1/lacZ reporter expressed in P19 EC cells responds to RA by the combined activities of an intron retinoic acid response element (RARE) and an upstream RARE. Tretinoin 126-128 galactosidase, beta 1 Mus musculus 10-28
21425084-3 2011 By use of beta-galactosidase chemiluminescence, we show that a mouse Cdx1/lacZ reporter expressed in P19 EC cells responds to RA by the combined activities of an intron retinoic acid response element (RARE) and an upstream RARE. Tretinoin 169-182 galactosidase, beta 1 Mus musculus 10-28
21528155-0 2011 All-trans retinoic acid upregulates reduced CD38 transcription in lymphoblastoid cell lines from Autism spectrum disorder. Tretinoin 10-23 CD38 molecule Homo sapiens 44-48
21528155-5 2011 One of these, all-trans retinoic acid (ATRA), a known inducer of CD38, was added during cell culture and tested on a large sample of N = 120 lymphoblastoid cell (LBC) lines from ASD patients and their parents. Tretinoin 14-37 CD38 molecule Homo sapiens 65-69
21528155-5 2011 One of these, all-trans retinoic acid (ATRA), a known inducer of CD38, was added during cell culture and tested on a large sample of N = 120 lymphoblastoid cell (LBC) lines from ASD patients and their parents. Tretinoin 39-43 CD38 molecule Homo sapiens 65-69
21528155-6 2011 Analysis of CD38 mRNA levels shows that ATRA has an upmodulatory potential on LBC derived from ASD patients as well as from their parents. Tretinoin 40-44 CD38 molecule Homo sapiens 12-16
21528155-9 2011 In addition, analysis of the role of genetic polymorphisms in the dynamics of the molecule revealed that the genotype of a single-nucleotide polymorphism (rs6449182; C>G variation) in the CpG island of intron 1, harboring the retinoic-acid response element, exerts differential roles in CD38 expression in ASD and in parental LBC. Tretinoin 229-242 CD38 molecule Homo sapiens 290-294
21695257-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: In the present study, differential gene expression profiling revealed a faster silencing of pluripotency-associated genes, like Nanog, Oct4, and Lin28, during retinoic acid-induced neuronal differentiation of LRRK2-deficient mouse embryonic stem cells compared to wildtype cultures. Tretinoin 191-204 lin-28 homolog A Mus musculus 177-182
20883757-1 2010 Our previous data demonstrated that folate receptor beta (FR-beta) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-beta upregulation by all-trans retinoic acid (ATRA) in AML blast cells. Tretinoin 273-286 folate receptor beta Homo sapiens 36-56
20883757-1 2010 Our previous data demonstrated that folate receptor beta (FR-beta) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-beta upregulation by all-trans retinoic acid (ATRA) in AML blast cells. Tretinoin 273-286 folate receptor beta Homo sapiens 58-65
20883757-1 2010 Our previous data demonstrated that folate receptor beta (FR-beta) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-beta upregulation by all-trans retinoic acid (ATRA) in AML blast cells. Tretinoin 288-292 folate receptor beta Homo sapiens 36-56
20883757-1 2010 Our previous data demonstrated that folate receptor beta (FR-beta) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-beta upregulation by all-trans retinoic acid (ATRA) in AML blast cells. Tretinoin 288-292 folate receptor beta Homo sapiens 58-65
20883757-10 2010 The results demonstrate that the efficiency of FR-mediated targeting of FT-L-DOX was preferentially enhanced by ATRA induced FR-beta upregulation in AML clonogenic cells. Tretinoin 112-116 folate receptor beta Homo sapiens 125-132
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 45-58 interleukin 12a Mus musculus 198-206
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 60-62 interleukin 12a Mus musculus 198-206
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 184-203 retinoic acid receptor alpha Homo sapiens 25-53
20724538-4 2010 We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)-induced transactivation of the OLFM4 gene. Tretinoin 205-209 retinoic acid receptor alpha Homo sapiens 25-53
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 130-150
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 152-158
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 248-254
20724538-7 2010 Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Tretinoin 66-70 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 248-254
20528759-4 2010 All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), which are the major molecularly targeted therapies in APL, affect the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 129-132
20528759-4 2010 All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), which are the major molecularly targeted therapies in APL, affect the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 133-137
20528759-4 2010 All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), which are the major molecularly targeted therapies in APL, affect the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 129-132
20528759-4 2010 All-trans retinoic acid (ATRA) and arsenic trioxide (ATO), which are the major molecularly targeted therapies in APL, affect the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 133-137
20632143-0 2010 All-trans retinoic acid is capable of inducing folate receptor beta expression in KG-1 cells. Tretinoin 10-23 folate receptor beta Homo sapiens 47-67
20632143-4 2010 The results revealed that ATRA was capable of upregulating the expression of FR-beta protein in KG-1 cells in a dosage-dependent manner, not in KG-1a, NB4, HL60, 293, L1210, JAR, and Hela cells. Tretinoin 26-30 folate receptor beta Homo sapiens 77-84
20632143-5 2010 FR-beta mRNA expression in KG-1 cells was higher when ATRA was present in culture medium at 10-6 mol/L for 5 days, and it went down to baseline when ATRA was removed from the medium, vice versa. Tretinoin 54-58 folate receptor beta Homo sapiens 0-7
20632143-5 2010 FR-beta mRNA expression in KG-1 cells was higher when ATRA was present in culture medium at 10-6 mol/L for 5 days, and it went down to baseline when ATRA was removed from the medium, vice versa. Tretinoin 149-153 folate receptor beta Homo sapiens 0-7
20632143-6 2010 The upregulation of FR-beta expression in KG-1 cells by ATRA was not associated with cell proliferation and differentiation. Tretinoin 56-60 folate receptor beta Homo sapiens 20-27
21176354-0 2010 [Expression change of IL-3 receptor system in all-trans retinoic acid induced differentiation of NB4 cells]. Tretinoin 56-69 interleukin 3 Homo sapiens 22-26
21176354-4 2010 In order to investigate the role of IL-3 receptor system (IL-3Ralpha, GM-CSFRalpha and hbetac) in myeloid differentiation, the expression level of IL-3 receptor system gene in all-trans retinoic acid (ATRA)-induced NB4 cell differentiation was detected by quantitative real time RT-PCR. Tretinoin 186-199 interleukin 3 Homo sapiens 36-40
21068375-6 2010 ITE acts not only on T cells, but also directly on dendritic cells to induce tolerogenic dendritic cells that support FoxP3(+) T(reg) differentiation in a retinoic acid-dependent manner. Tretinoin 155-168 forkhead box P3 Mus musculus 118-123
20864529-5 2010 As confirmed by gel shift and chromatin immunoprecipitation assays, ATRA enhanced the binding of both Ets-1 and Sp1 to the Npr1 promoter. Tretinoin 68-72 ETS proto-oncogene 1, transcription factor Homo sapiens 102-107
20864529-7 2010 Interestingly, ATRA also increased the acetylation of histones H3 and H4 and enhanced their recruitment to Ets-1 and Sp1 binding sites within the Npr1 promoter. Tretinoin 15-19 ETS proto-oncogene 1, transcription factor Homo sapiens 107-112
20650878-2 2010 Retinoic acid (RA) and a downstream target, Stra8, are required for complete spermatogenesis. Tretinoin 0-13 stimulated by retinoic acid gene 8 Mus musculus 44-49
20650878-2 2010 Retinoic acid (RA) and a downstream target, Stra8, are required for complete spermatogenesis. Tretinoin 15-17 stimulated by retinoic acid gene 8 Mus musculus 44-49
20123703-7 2010 Furthermore, stimulation with retinoic acid resulted in down-regulation of OCT4 expression, however, without multilineage differentiation. Tretinoin 30-43 POU class 5 homeobox 1 Homo sapiens 75-79
21327094-7 2010 During in vitro granulopoiesis induced with retinoic acid, the LBR knockdown cells retain an ovoid shaped nucleus with reduced levels of lamin A/C; while, the parent cells develop highly lobulated nuclei. Tretinoin 44-57 lamin A/C Homo sapiens 137-146
20951351-7 2010 DMRT1 acts in spermatogonia to restrict RA responsiveness, directly repress Stra8 transcription, and activate transcription of the spermatogonial differentiation factor Sohlh1, thereby preventing meiosis and promoting spermatogonial development. Tretinoin 40-42 doublesex and mab-3 related transcription factor 1 Homo sapiens 0-5
20842651-0 2010 The role of CYP26 enzymes in defining appropriate retinoic acid exposure during embryogenesis. Tretinoin 50-63 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 12-17
20842651-4 2010 This review will discuss our current understanding of the role of RA in teratogenesis, with specific emphasis on the essential function of the RA catabolic CYP26 enzymes in preventing teratogenic consequences caused by uncontrolled distribution of RA. Tretinoin 66-68 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 156-161
20842651-4 2010 This review will discuss our current understanding of the role of RA in teratogenesis, with specific emphasis on the essential function of the RA catabolic CYP26 enzymes in preventing teratogenic consequences caused by uncontrolled distribution of RA. Tretinoin 143-145 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 156-161
20842651-4 2010 This review will discuss our current understanding of the role of RA in teratogenesis, with specific emphasis on the essential function of the RA catabolic CYP26 enzymes in preventing teratogenic consequences caused by uncontrolled distribution of RA. Tretinoin 143-145 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 156-161
20525643-10 2010 Conversely, blockage of dopamine biosynthesis and loss of TH activity decreased AMHC1 and Tbx5 expression, whereas exposure to retinoic acid (RA) induced TH expression in parallel to that of AMHC1 and Tbx5. Tretinoin 127-140 T-box 5 Gallus gallus 201-205
20525643-10 2010 Conversely, blockage of dopamine biosynthesis and loss of TH activity decreased AMHC1 and Tbx5 expression, whereas exposure to retinoic acid (RA) induced TH expression in parallel to that of AMHC1 and Tbx5. Tretinoin 142-144 T-box 5 Gallus gallus 201-205
20525643-11 2010 Concordantly, inhibition of endogenous RA synthesis decreased TH expression as well as that of AMHC1 and Tbx5. Tretinoin 39-41 T-box 5 Gallus gallus 105-109
20435626-3 2010 This study focuses on the role of Ets-1 during granulocytic differentiation of NB4 promyelocytic and HL60 myeloblastic leukemia cell lines induced by all-trans retinoic acid. Tretinoin 160-173 ETS proto-oncogene 1, transcription factor Homo sapiens 34-39
20435626-7 2010 The addition of all-trans retinoic acid reduced p51 Ets-1 levels and induced inhibitory phosphorylation of the remaining protein. Tretinoin 16-39 tumor protein p63 Homo sapiens 48-51
20435626-7 2010 The addition of all-trans retinoic acid reduced p51 Ets-1 levels and induced inhibitory phosphorylation of the remaining protein. Tretinoin 16-39 ETS proto-oncogene 1, transcription factor Homo sapiens 52-57
20435626-8 2010 Expression of Ets-1 was also reduced during dimethylsulfoxide-induced differentiation and during granulocytic differentiation of human CD34(+) hematopoietic progenitor cells but not in NB4.R2 and HL60R cells resistant to all-trans retinoic acid. Tretinoin 231-244 ETS proto-oncogene 1, transcription factor Homo sapiens 14-19
20435626-10 2010 Consistently, Ets-1 knockdown by small interfering RNA increased the number of mature neutrophils upon addition of all-trans retinoic acid. Tretinoin 125-138 ETS proto-oncogene 1, transcription factor Homo sapiens 14-19
20839318-4 2010 In cell cultures, induction of chondrocyte maturation, by retinoic acid (RA) or transforming growth factor (TGF)-beta treatment led to a significant upregulation of F-spondin (p < 0.05). Tretinoin 58-71 spondin 1 Gallus gallus 165-174
20950777-4 2010 The mutation of the region responsible for inhibition of histone acetyltransferase activity within JDP2 eliminates repression of transcription from the c-jun promoter by JDP2, as well as JDP2-mediated inhibition of retinoic-acid-induced differentiation. Tretinoin 215-228 Jun dimerization protein 2 Homo sapiens 99-103
20350780-5 2010 Inhibition of CRABP-II enhanced RA-induced apoptosis and sensitized RA-resistant HCC cells to RA cytotoxicity by attenuating p42/44 MAPK and Akt activation. Tretinoin 15-17 cyclin dependent kinase 20 Homo sapiens 125-128
20664956-2 2010 All-trans retinoic acid (ATRA), a family of retinoids, is an internal ligand of RAR and well known as a useful differentiation inducer to treat acute promyelocytic leukemia (APL). Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 80-83
20664956-2 2010 All-trans retinoic acid (ATRA), a family of retinoids, is an internal ligand of RAR and well known as a useful differentiation inducer to treat acute promyelocytic leukemia (APL). Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 80-83
20664956-4 2010 Recently, to improve therapeutic potency and reduce adverse effects of ATRA, a novel synthetic selective agonist for RARalpha and beta, Am80, was developed and applied to APL treatment. Tretinoin 71-75 retinoic acid receptor alpha Homo sapiens 117-134
20615082-4 2010 ATO augmented ATRA-induced RAF/MEK/ERK axis signaling, expression of CD11b and p47(PHOX), and inducible oxidative metabolism. Tretinoin 14-18 pleckstrin Homo sapiens 79-82
20615082-8 2010 In summary, our results indicate that ATO in conjunction with ATRA is of potential chemotherapeutic use in PML-RARalpha negative leukemias. Tretinoin 62-66 PML nuclear body scaffold Homo sapiens 107-110
20084480-1 2010 Retinoic acid (RA), similar to specific growth factors, can induce differentiation of proliferating promyelocytic precursors into terminally differentiated granulocytes, although little is known about effects of its 13-cis isomer on promyelocytic leukemia (PML). Tretinoin 0-13 PML nuclear body scaffold Homo sapiens 257-260
20084480-1 2010 Retinoic acid (RA), similar to specific growth factors, can induce differentiation of proliferating promyelocytic precursors into terminally differentiated granulocytes, although little is known about effects of its 13-cis isomer on promyelocytic leukemia (PML). Tretinoin 15-17 PML nuclear body scaffold Homo sapiens 257-260
20562004-7 2010 Thus, atRA was shown to induce BCRP gene expression probably via the RAR/RXR signalling pathway, resulting in effective removal of B[a]P metabolites from intestinal cells. Tretinoin 6-10 retinoic acid receptor alpha Homo sapiens 69-72
20189646-0 2010 ATRA is effective to an acute promyelocytic leukemia patient without RARA gene rearrangement. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 69-73
20423710-7 2010 Experiments of loss of function with prep1.2 morpholinos change the shape of the hyoid and third pharyngeal cartilages while arches 4-7 and pectoral fins are absent, a phenotype strikingly similar to that caused by loss of retinoic acid (RA). Tretinoin 223-236 pbx/knotted 1 homeobox 1.2 Danio rerio 37-44
20577838-5 2010 These data suggested that miR-146a might influence proliferation of APL cells through TGF-beta1/Smad signal transduction pathway during ATRA induction. Tretinoin 136-140 microRNA 146a Homo sapiens 26-34
20598227-0 2010 Role of acetylated p53 in regulating the expression of map2 in retinoic acid-induced P19 cells. Tretinoin 63-76 interleukin 23 subunit alpha Homo sapiens 85-88
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 193-206 interleukin 23 subunit alpha Homo sapiens 162-165
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 208-210 interleukin 23 subunit alpha Homo sapiens 162-165
20598227-2 2010 METHODS: Neuronal differentiation of P19 cells was initiated with 4-day RA treatment. Tretinoin 72-74 interleukin 23 subunit alpha Homo sapiens 37-40
20061533-0 2010 ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production. Tretinoin 9-22 intestine specific homeobox Mus musculus 0-3
20618457-6 2010 Expression of ADH1/2/3, RDH5/10/11, DHRS3 and RALDH1/3 was increased in NAFLD, suggesting that oxidation process from retinol to all-trans retinoic acid (ATRA) was enhanced. Tretinoin 154-158 alcohol dehydrogenase 1A (class I), alpha polypeptide Homo sapiens 14-22
19651460-0 2010 Uncoupling between CD1d upregulation induced by retinoic acid and conduritol-B-epoxide and iNKT cell responsiveness. Tretinoin 48-61 CD1d molecule Homo sapiens 19-23
19651460-4 2010 We also show that retinoic acid (RA) and the beta-glucocerebrosidase inhibitor conduritol-B-epoxide (CBE) lead to upregulation of CD1d expression by THP-1 cells, which correlated with an increase in mRNA expression. Tretinoin 18-31 CD1d molecule Homo sapiens 130-134
19651460-4 2010 We also show that retinoic acid (RA) and the beta-glucocerebrosidase inhibitor conduritol-B-epoxide (CBE) lead to upregulation of CD1d expression by THP-1 cells, which correlated with an increase in mRNA expression. Tretinoin 33-35 CD1d molecule Homo sapiens 130-134
20187766-0 2010 All-trans retinoic acid ameliorates trinitrobenzene sulfonic acid-induced colitis by shifting Th1 to Th2 profile. Tretinoin 0-23 heart and neural crest derivatives expressed 2 Mus musculus 101-104
20228061-1 2010 In preadipocytes, retinoic acid (RA) regulates gene expression by activating the nuclear RA receptor (RAR) and its cognate intracellular lipid-binding protein CRABP-II. Tretinoin 18-31 retinoic acid receptor alpha Homo sapiens 89-100
20228061-1 2010 In preadipocytes, retinoic acid (RA) regulates gene expression by activating the nuclear RA receptor (RAR) and its cognate intracellular lipid-binding protein CRABP-II. Tretinoin 18-31 retinoic acid receptor alpha Homo sapiens 102-105
20228061-1 2010 In preadipocytes, retinoic acid (RA) regulates gene expression by activating the nuclear RA receptor (RAR) and its cognate intracellular lipid-binding protein CRABP-II. Tretinoin 33-35 retinoic acid receptor alpha Homo sapiens 89-100
20228061-1 2010 In preadipocytes, retinoic acid (RA) regulates gene expression by activating the nuclear RA receptor (RAR) and its cognate intracellular lipid-binding protein CRABP-II. Tretinoin 33-35 retinoic acid receptor alpha Homo sapiens 102-105
20228061-3 2010 The data presented here indicate that the diminished ability of RA to activate RAR following induction of differentiation stems from down-regulation of CRABP-II. Tretinoin 64-66 retinoic acid receptor alpha Homo sapiens 79-82
19778331-10 2010 Along with the change of claudin species, the expressions of keratin 7, keratin 8 and keratin 18, as markers for the simple epithelium, were clearly stimulated by retinoic acid. Tretinoin 163-176 keratin 18 Homo sapiens 86-96
20197308-10 2010 We confirmed a role for RA in reversal of TGF-beta1-induced changes associated with epithelial-mesenchymal transition, including expression changes in Snail, E-cadherin, vimetin, and redistribution of beta-catenin. Tretinoin 24-26 catenin beta 1 Homo sapiens 201-213
20206130-8 2010 Here we show that exposure to ATRA and TGF-beta induces CD8(+)Foxp3(+) T cells ex vivo, which suppress diabetogenic T cells in vitro and in vivo. Tretinoin 30-34 forkhead box P3 Mus musculus 62-67
20118242-4 2010 Loss-of-function approaches using miR-10a inhibitors uncovered that miR-10a is a critical mediator for SMC lineage determination in our retinoic acid-induced ESC/SMC differentiation system. Tretinoin 136-149 microRNA 10a Mus musculus 34-41
20118242-4 2010 Loss-of-function approaches using miR-10a inhibitors uncovered that miR-10a is a critical mediator for SMC lineage determination in our retinoic acid-induced ESC/SMC differentiation system. Tretinoin 136-149 microRNA 10a Mus musculus 68-75
20118242-6 2010 To determine the molecular mechanism through which retinoic acid induced miR-10a expression, a consensus NF-kappaB element was identified in the miR-10a gene promoter by bioinformatics analysis, and chromatin immunoprecipitation assay confirmed that NF-kappaB could bind to this element. Tretinoin 51-64 microRNA 10a Mus musculus 73-80
20118242-6 2010 To determine the molecular mechanism through which retinoic acid induced miR-10a expression, a consensus NF-kappaB element was identified in the miR-10a gene promoter by bioinformatics analysis, and chromatin immunoprecipitation assay confirmed that NF-kappaB could bind to this element. Tretinoin 51-64 microRNA 10a Mus musculus 145-152
20147374-4 2010 Sox10-GFP-positive cells are produced transiently from mouse embryonic stem (ES) cells by treatment with retinoic acid in combination with Fgf8b and the cytokine leukaemia inhibitory factor (Lif). Tretinoin 105-118 SRY (sex determining region Y)-box 10 Mus musculus 0-5
19263240-7 2010 Moreover, exposure of the reprogrammed cells to all trans-retinoic acid (RA) medium elicited the generation of neuronal class IIIbeta-tubulin-positive, neuron-specific enolase (NSE)-positive, nestin-positive, and neurofilament light chain (NF-L)-positive neural-like cells. Tretinoin 52-71 neurofilament, light polypeptide Mus musculus 240-244
19263240-7 2010 Moreover, exposure of the reprogrammed cells to all trans-retinoic acid (RA) medium elicited the generation of neuronal class IIIbeta-tubulin-positive, neuron-specific enolase (NSE)-positive, nestin-positive, and neurofilament light chain (NF-L)-positive neural-like cells. Tretinoin 73-75 neurofilament, light polypeptide Mus musculus 240-244
20236590-3 2010 The differentiation of SCC cells were induced with all-trans-retinoic acid (ATRA). Tretinoin 51-74 serpin family B member 3 Homo sapiens 23-26
20236590-3 2010 The differentiation of SCC cells were induced with all-trans-retinoic acid (ATRA). Tretinoin 76-80 serpin family B member 3 Homo sapiens 23-26
20152184-3 2010 The nonneurogenic zone at segment centers comprises a distinct progenitor population that expresses fibroblast growth factor (fgfr) 2, erm, sox9b, and the retinoic acid degrading enzyme, cyp26b1. Tretinoin 155-168 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 187-194
20009537-2 2010 Germ cell meiotic commitment requires expression of Stimulated by retinoic acid gene 8 (Stra8), which is transcriptionally activated by retinoic acid (RA). Tretinoin 66-79 stimulated by retinoic acid gene 8 Mus musculus 88-93
20009537-2 2010 Germ cell meiotic commitment requires expression of Stimulated by retinoic acid gene 8 (Stra8), which is transcriptionally activated by retinoic acid (RA). Tretinoin 151-153 stimulated by retinoic acid gene 8 Mus musculus 52-86
20009537-2 2010 Germ cell meiotic commitment requires expression of Stimulated by retinoic acid gene 8 (Stra8), which is transcriptionally activated by retinoic acid (RA). Tretinoin 151-153 stimulated by retinoic acid gene 8 Mus musculus 88-93
20009537-4 2010 Here we show in mice that RA-induced Stra8 transcription is epigenetically controlled and requires a co-activator that binds proximal to the RA response elements (RAREs) in the Stra8 promoter. Tretinoin 26-28 stimulated by retinoic acid gene 8 Mus musculus 37-42
20009537-4 2010 Here we show in mice that RA-induced Stra8 transcription is epigenetically controlled and requires a co-activator that binds proximal to the RA response elements (RAREs) in the Stra8 promoter. Tretinoin 26-28 stimulated by retinoic acid gene 8 Mus musculus 177-182
20009537-4 2010 Here we show in mice that RA-induced Stra8 transcription is epigenetically controlled and requires a co-activator that binds proximal to the RA response elements (RAREs) in the Stra8 promoter. Tretinoin 141-143 stimulated by retinoic acid gene 8 Mus musculus 37-42
20009537-4 2010 Here we show in mice that RA-induced Stra8 transcription is epigenetically controlled and requires a co-activator that binds proximal to the RA response elements (RAREs) in the Stra8 promoter. Tretinoin 141-143 stimulated by retinoic acid gene 8 Mus musculus 177-182
20009537-9 2010 Thus, the ability of RA to transcriptionally induce expression of the meiosis-commitment gene, Stra8, is epigenetically controlled and this process involves a novel co-activator that functions upstream of the RAREs. Tretinoin 21-23 stimulated by retinoic acid gene 8 Mus musculus 95-100
20224268-3 2010 The data presented in this study demonstrated that ider(17q), which resulted in an extra RARA-PML fusion gene, was more frequent in males than females (male/female ratio of 2.12/1), was associated with a rather low initial white blood cell count and did not confer an adverse prognosis in APL patients treated with all-trans-retinoic acid and chemotherapy. Tretinoin 319-338 retinoic acid receptor alpha Homo sapiens 89-93
20224268-3 2010 The data presented in this study demonstrated that ider(17q), which resulted in an extra RARA-PML fusion gene, was more frequent in males than females (male/female ratio of 2.12/1), was associated with a rather low initial white blood cell count and did not confer an adverse prognosis in APL patients treated with all-trans-retinoic acid and chemotherapy. Tretinoin 319-338 PML nuclear body scaffold Homo sapiens 94-97
19550295-15 2010 Retinoic acid combined with vincristine is the most effective combination to reduce Myc-N expression. Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 84-87
2573410-0 1989 Cholinergic differentiation of clonal rat pheochromocytoma cells (PC12) induced by retinoic acid: increase of choline acetyltransferase activity and decrease of tyrosine hydroxylase activity. Tretinoin 83-96 choline O-acetyltransferase Rattus norvegicus 110-135
2573410-3 1989 In PC12 cells cultured in the presence of 10 microM RA for 8 days, the specific activity of choline acetyltransferase (ChAT) was increased 2-fold, while the specific activity of tyrosine hydroxylase (TH) was decreased 0.5-fold compared with cells cultured in the absence of RA. Tretinoin 52-54 choline O-acetyltransferase Rattus norvegicus 92-117
20040491-1 2010 Tgif1 and Tgif2 are transcriptional co-repressors that limit the response to TGFbeta signaling and play a role in regulating retinoic-acid-mediated gene expression. Tretinoin 125-138 TGFB induced factor homeobox 2 Homo sapiens 10-15
2573410-3 1989 In PC12 cells cultured in the presence of 10 microM RA for 8 days, the specific activity of choline acetyltransferase (ChAT) was increased 2-fold, while the specific activity of tyrosine hydroxylase (TH) was decreased 0.5-fold compared with cells cultured in the absence of RA. Tretinoin 274-276 choline O-acetyltransferase Rattus norvegicus 92-117
2553481-2 1989 The effects of RA on the retinoic acid receptor (RAR) mRNA level were investigated in P19 cells and an RA non-responsive mutant RAC65. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 49-52
19747912-0 2010 Vav1 and PU.1 are recruited to the CD11b promoter in APL-derived promyelocytes: role of Vav1 in modulating PU.1-containing complexes during ATRA-induced differentiation. Tretinoin 140-144 Spi-1 proto-oncogene Homo sapiens 107-111
2553481-3 1989 RA induced a rapid accumulation of RAR alpha within 2 h and this was followed by an increase in the RAR beta mRNA. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 35-44
19747912-6 2010 The reported data suggest that the ATRA-induced increase of Vav1 expression and tyrosine phosphorylation may be involved in recruiting PU.1 to its consensus sequence on the CD11b promoter and, ultimately, in regulating CD11b expression during the late stages of neutrophil differentiation of APL-derived promyelocytes. Tretinoin 35-39 Spi-1 proto-oncogene Homo sapiens 135-139
19757389-5 2010 We show by loss of function using the inhibitor citral, that RA signalling within the limb bud is required to maintain Pax3 and Meox2 in the progenitor and Myf5 and MyoD in the differentiating myoblasts. Tretinoin 61-63 paired box 3 Gallus gallus 119-123
2848718-1 1988 Treatment with 10(-5) M retinoic acid causes loss of anchorage-independent growth in src-transformed RR1022 cells but not in ras-transformed KNRK cells. Tretinoin 24-37 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 85-88
19757389-5 2010 We show by loss of function using the inhibitor citral, that RA signalling within the limb bud is required to maintain Pax3 and Meox2 in the progenitor and Myf5 and MyoD in the differentiating myoblasts. Tretinoin 61-63 mesenchyme homeobox 2 Gallus gallus 128-133
19757389-6 2010 Treatment with excess RA showed a differential effect: Meox2 and Pax3 showed localised down-regulation of expression in the limb. Tretinoin 22-24 mesenchyme homeobox 2 Gallus gallus 55-60
19757389-6 2010 Treatment with excess RA showed a differential effect: Meox2 and Pax3 showed localised down-regulation of expression in the limb. Tretinoin 22-24 paired box 3 Gallus gallus 65-69
2461362-3 1988 However, TTR mRNA and RBP mRNA were both detected in F9 cell aggregates differentiated to embryoid bodies (which contain visceral endoderm-like cells) by treatment of the aggregates in suspension with retinoic acid. Tretinoin 201-214 transthyretin Homo sapiens 9-12
2461362-3 1988 However, TTR mRNA and RBP mRNA were both detected in F9 cell aggregates differentiated to embryoid bodies (which contain visceral endoderm-like cells) by treatment of the aggregates in suspension with retinoic acid. Tretinoin 201-214 retinol binding protein 4 Homo sapiens 22-25
19934264-0 2010 Reciprocal roles of SIRT1 and SKIP in the regulation of RAR activity: implication in the retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 89-102 retinoic acid receptor alpha Homo sapiens 56-59
2461362-4 1988 TTR mRNA was observed at 3 days, and RBP mRNA at 5 days, after treatment of the F9 cell aggregates with retinoic acid. Tretinoin 104-117 transthyretin Homo sapiens 0-3
3167862-5 1988 Retinoic acid modulated expression of lipid and CA125, while dimethyl sulfoxide reduced expression of CA125. Tretinoin 0-13 mucin 16, cell surface associated Homo sapiens 48-53
20042001-2 2010 Carrier proteins that move the RA from the cytosol into the nucleus are the fatty acid-binding protein 5 (FABP5), activating PPARdelta, and the cellular retinoic acid-binding protein II (CRABPII), activating RAR. Tretinoin 31-33 fatty acid binding protein 5, epidermal Mus musculus 76-104
2459072-11 1988 C-fos responded differently to the retinoic acid treatment. Tretinoin 35-48 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5
20042001-2 2010 Carrier proteins that move the RA from the cytosol into the nucleus are the fatty acid-binding protein 5 (FABP5), activating PPARdelta, and the cellular retinoic acid-binding protein II (CRABPII), activating RAR. Tretinoin 31-33 fatty acid binding protein 5, epidermal Mus musculus 106-111
19580869-5 2010 Fluorescence spectroscopy experiments show that mLcn6 prepared according to our procedure has high affinities to both retinoic acid (K(d)=810nM) and retinol (K(d)=210nM). Tretinoin 118-131 lipocalin 6 Mus musculus 48-53
3276363-6 1988 An increase in c-fos expression was also found in HL-60 cells differentiated along the granulocytic pathway after exposure to hypoxanthine, hexamethylene bisacetamide, and the combination of retinoic acid and dibutyryl adenosine 3"5" cyclic monophosphate. Tretinoin 191-204 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-20
20008524-2 2009 Other studies identified CD103(+) DCs in the mucosa, which, through their ability to synthesize retinoic acid (RA), appear to be capable of generating typical signatures of intestinal adaptive immune responses. Tretinoin 96-109 integrin subunit alpha E Homo sapiens 25-30
3426588-0 1987 Retinoic acid increases the expression of NGF gene in mouse L cells. Tretinoin 0-13 nerve growth factor Mus musculus 42-45
19799567-4 2009 PBX1 is present in the protein complex formed at this site with nuclear proteins from uninduced cells, whereas both PBX1 and MEIS1 proteins were detected in the complex created with extract from RA (retinoic acid)-induced NT2/D1 cells. Tretinoin 195-197 PBX homeobox 1 Homo sapiens 116-120
3426588-1 1987 Retinoic acid (RA), the acid form of vitamin A, is shown to enhance the synthesis of nerve growth factor (NGF) in cultures of mouse L cells. Tretinoin 0-13 nerve growth factor Mus musculus 85-104
3426588-1 1987 Retinoic acid (RA), the acid form of vitamin A, is shown to enhance the synthesis of nerve growth factor (NGF) in cultures of mouse L cells. Tretinoin 0-13 nerve growth factor Mus musculus 106-109
3426588-1 1987 Retinoic acid (RA), the acid form of vitamin A, is shown to enhance the synthesis of nerve growth factor (NGF) in cultures of mouse L cells. Tretinoin 15-17 nerve growth factor Mus musculus 85-104
3426588-1 1987 Retinoic acid (RA), the acid form of vitamin A, is shown to enhance the synthesis of nerve growth factor (NGF) in cultures of mouse L cells. Tretinoin 15-17 nerve growth factor Mus musculus 106-109
3426588-2 1987 Maximal stimulation was observed in cells growing in a serum-free medium supplemented with 10(-6)M RA during 48 h. The drug increased both the level of NGF mRNA and the amount of mature NGF protein secreted by the cells. Tretinoin 99-101 nerve growth factor Mus musculus 152-155
3426588-2 1987 Maximal stimulation was observed in cells growing in a serum-free medium supplemented with 10(-6)M RA during 48 h. The drug increased both the level of NGF mRNA and the amount of mature NGF protein secreted by the cells. Tretinoin 99-101 nerve growth factor Mus musculus 186-189
3426588-3 1987 RA was previously reported to increase the number of NGF receptors on some neuroblastoma cells (Haskell et al., 1987 Cell and Tiss. Tretinoin 0-2 nerve growth factor Mus musculus 53-56
19799567-4 2009 PBX1 is present in the protein complex formed at this site with nuclear proteins from uninduced cells, whereas both PBX1 and MEIS1 proteins were detected in the complex created with extract from RA (retinoic acid)-induced NT2/D1 cells. Tretinoin 199-212 PBX homeobox 1 Homo sapiens 116-120
19799567-5 2009 By functional analysis we also showed that mutations of the PBX1/MEIS1-binding sites resulted in profound reduction of SOX3 promoter responsiveness to RA. Tretinoin 151-153 PBX homeobox 1 Homo sapiens 60-64
19770350-7 2009 Although (R)-all-trans-13,14-dihydroretinoic acid exhibited comparable potency to retinoic acid in promoting the interaction of RARs with a coactivator peptide in vitro, its potency in activating RAR-controlled genes in cell-based assays was much lower than that of retinoic acid. Tretinoin 36-49 retinoic acid receptor alpha Homo sapiens 128-131
2822401-2 1987 Sonication or DNase I digestion followed by extraction with 0.6 M NaCl released 20-40% of the nuclear-associated retinoic acid. Tretinoin 113-126 deoxyribonuclease I Mus musculus 14-21
19770350-7 2009 Although (R)-all-trans-13,14-dihydroretinoic acid exhibited comparable potency to retinoic acid in promoting the interaction of RARs with a coactivator peptide in vitro, its potency in activating RAR-controlled genes in cell-based assays was much lower than that of retinoic acid. Tretinoin 82-95 retinoic acid receptor alpha Homo sapiens 128-131
3600758-4 1987 This resemblance raises an intriguing possibility: that RA is related to the as yet unidentified inducer substance thought to be released by the ZPA. Tretinoin 56-58 zona pellucida glycoprotein 2 Gallus gallus 145-148
19770350-8 2009 As an explanation for the weak RAR agonist activity of dihydroretinoids in cell-based assays, we propose that both delivery of ligand to the nucleus and RAR activation favor retinoic acid over dihydroretinoids. Tretinoin 174-187 retinoic acid receptor alpha Homo sapiens 153-156
3600758-5 1987 Here we report that chick limb buds contain endogenous RA and we show that RA, but not its biosynthetic precursor retinol, forms a concentration gradient across the limb anlage with a high-point in the posterior domain of the limb bud, the part that also contains the ZPA. Tretinoin 75-77 zona pellucida glycoprotein 2 Gallus gallus 268-271
19211146-7 2009 However, administration of ATRA to NOD mice in which the proportion and function of CD4(+)Foxp3(+) Treg cells was abrogated by cyclophosphamide (CY), failed to permit progression to T1D. Tretinoin 27-31 forkhead box P3 Mus musculus 90-95
3034940-1 1987 Radical species were detected in the incubation mixtures of some retinoids (retinoic acid, retinal, retinol and retinyl acetate) by using the spin-trapping technique. Tretinoin 76-89 spindlin 1 Homo sapiens 142-146
3034940-3 1987 The spin-adducts were eluted in the order retinoic acid, retinol, retinyl acetate, in a similar manner to the retinoids themselves. Tretinoin 42-55 spindlin 1 Homo sapiens 4-8
19812389-1 2009 Retinoic acid (RA) signaling is mediated by the retinoic acid receptor (RAR), belonging to the nuclear hormone receptor superfamily. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 48-70
19812389-1 2009 Retinoic acid (RA) signaling is mediated by the retinoic acid receptor (RAR), belonging to the nuclear hormone receptor superfamily. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 72-75
3102507-3 1987 IFNs induce Class I antigen expression in F9 cells in a highly selective manner: unlike retinoic acid treatment which also stimulates the antigen expression, IFNs induce neither morphological differentiation, increased binding of epidermal growth factor, nor reduction of expression of stage specific embryonic antigen. Tretinoin 88-101 ATPase, aminophospholipid transporter (APLT), class I, type 8A, member 1 Mus musculus 12-19
19812389-1 2009 Retinoic acid (RA) signaling is mediated by the retinoic acid receptor (RAR), belonging to the nuclear hormone receptor superfamily. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 48-70
3428508-5 1987 NG2-2.16 cells were induced to differentiate by exposure to retinoic acid, suggesting that the mutation affects the regulation of differentiation rather than the potential for differentiation. Tretinoin 60-73 chondroitin sulfate proteoglycan 4 Mus musculus 0-3
2511439-0 1989 Expression of REX-1, a gene containing zinc finger motifs, is rapidly reduced by retinoic acid in F9 teratocarcinoma cells. Tretinoin 81-94 zinc finger protein 42 Mus musculus 14-19
2511439-3 1989 By 48 to 96 h after RA treatment of F9 cells in monolayer culture, the REX-1 steady-state mRNA level was more than sevenfold lower than the level in undifferentiated F9 stem cells. Tretinoin 20-22 zinc finger protein 42 Mus musculus 71-76
19812389-1 2009 Retinoic acid (RA) signaling is mediated by the retinoic acid receptor (RAR), belonging to the nuclear hormone receptor superfamily. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 72-75
19812389-8 2009 We conclude that RA activation of signaling pathways can indeed regulate mRNA processing as part of a cellular response orchestrated by the nuclear receptor RAR. Tretinoin 17-19 retinoic acid receptor alpha Homo sapiens 157-160
2482225-1 1989 The expression of the transcription factor AP-2 recently has been shown to be enhanced during retinoic acid (RA)-induced differentiation of NT2 cells, a human teratocarcinoma cell line. Tretinoin 94-107 transcription factor AP-2 alpha Homo sapiens 43-47
2482225-1 1989 The expression of the transcription factor AP-2 recently has been shown to be enhanced during retinoic acid (RA)-induced differentiation of NT2 cells, a human teratocarcinoma cell line. Tretinoin 109-111 transcription factor AP-2 alpha Homo sapiens 43-47
19609931-3 2009 We show here that retinoic acid (RA) facilitates LIF-induced astrocyte differentiation of NPCs. Tretinoin 18-31 LIF interleukin 6 family cytokine Homo sapiens 49-52
2482225-2 1989 Here we show that this induction of AP-2 mRNA is at the level of transcription and is transient, reaching a peak 48-72 hr after the addition of RA and declining thereafter, even in the continuous presence of RA. Tretinoin 144-146 transcription factor AP-2 alpha Homo sapiens 36-40
3770209-0 1986 all-trans-Retinoic acid inhibits the appearance of two phorbol ester-induced ornithine decarboxylase mRNAs in mouse epidermis. Tretinoin 0-23 ornithine decarboxylase, structural 1 Mus musculus 77-100
3769135-5 1986 trans-Retinoic acid, a potent inhibitor of tumor promotion, markedly inhibited the epidermal induction of ornithine decarboxylase activity that resulted from the topical administration of sn-1,2-didecanoylglycerol or TPA. Tretinoin 0-19 ornithine decarboxylase, structural 1 Mus musculus 106-129
19609931-3 2009 We show here that retinoic acid (RA) facilitates LIF-induced astrocyte differentiation of NPCs. Tretinoin 33-35 LIF interleukin 6 family cytokine Homo sapiens 49-52
2522491-4 1989 Retinoic acid and 13-cis retinoic acid (13-cRA) produced significant increases in the percentage of cells with markers for total T-helper cells, with a minimal effect on percentage of lymphocytes with markers for NK cells. Tretinoin 0-13 myotubularin related protein 11 Homo sapiens 43-46
19647057-9 2009 This novel SLN formulation represents a promising alternative for topical treatment of acne with RA. Tretinoin 97-99 sarcolipin Homo sapiens 11-14
2783693-0 1989 Regulation of epidermal growth factor receptor gene expression by retinoic acid and epidermal growth factor. Tretinoin 66-79 epidermal growth factor receptor Rattus norvegicus 14-46
2472150-10 1989 Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells. Tretinoin 131-144 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 52-57
2428876-11 1986 Retinoic acid stimulated myeloid differentiation of HL-60 cells and induced expression of both Mac-1 and p150,95. Tretinoin 0-13 integrin subunit alpha M Homo sapiens 95-100
19427305-5 2009 RA coordinates these processes by regulating biological activities of a family of non-steroid hormone receptors, RARalpha/beta/gamma, and RXRalpha/beta/gamma. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 113-157
2423265-5 1986 This specific ODC staining in cells surrounding hair follicles was inhibited by pretreatment of mice with either retinoic acid or cycloheximide 1 h before TPA treatment. Tretinoin 113-126 ornithine decarboxylase, structural 1 Mus musculus 14-17
2472150-10 1989 Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells. Tretinoin 131-144 platelet derived growth factor subunit B Rattus norvegicus 66-71
2472150-10 1989 Nuclear runoff transcription of the proto-oncogenes c-src, c-fms, c-sis, N-ras, c-myc, and c-fos was observed in proliferating and retinoic acid-treated cells. Tretinoin 131-144 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 91-96
2477289-0 1989 Decreased content of the 35 kDa cytoskeletal protein p35 in Friend erythroleukemia cells exposed to dimethyl sulfoxide and retinoic acid is associated with entrance into a quiescent substrate. Tretinoin 123-136 interleukin 12A Homo sapiens 53-56
2477289-2 1989 The effect of all-trans-retinoic acid (RA) on cell cycle kinetics, RNA content, and expression of the 35 kDa cytoskeletal protein p35 in exponentially-growing Friend erythroleukemia (FL) cells was compared with the prototypic differentiation-inducer dimethylsulfoxide (DMSO). Tretinoin 39-41 interleukin 12A Homo sapiens 130-133
2477289-6 1989 Decreases in the cellular content of p35 occurred in both DMSO- and RA-treated FL cells, correlating with the onset of accumulation of cells into G1, and stabilized by 48 hr after initial exposure to either inducer. Tretinoin 68-70 interleukin 12A Homo sapiens 37-40
3081453-7 1986 Inhibition by topical retinoic acid of ODC induction by TPA was partially overcome in a dose-response fashion by PGE. Tretinoin 22-35 ornithine decarboxylase, structural 1 Mus musculus 39-42
19427305-7 2009 RA-binding to RAR receptors induces a conformational change in the receptor, followed by the replacement of co-repressor with co-activator complexes. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 14-17
2645590-2 1989 Polyacrylamide gel electrophoresis (PAGE), followed by protein blotting with an antiserum specific to retinol-binding protein (RBP), the plasma carrier of retinol, showed that: (1) retinoic acid induced striking conformational changes when bound to RBP, and (2) none of the several synthetic retinoids used in human therapy were found to bind to RBP. Tretinoin 181-194 retinol binding protein 4 Homo sapiens 102-125
19539783-5 2009 Following loss of RA signaling, the caudal expression domains of Fgf8, Wnt8a, and Wnt3a expand anteriorly into the trunk, but no change is observed in caudal expression of Fgf4 or Fgf17 plus caudal expression of Fgf18 and Cdx1 is reduced. Tretinoin 18-20 wingless-type MMTV integration site family, member 3A Mus musculus 82-87
2645590-2 1989 Polyacrylamide gel electrophoresis (PAGE), followed by protein blotting with an antiserum specific to retinol-binding protein (RBP), the plasma carrier of retinol, showed that: (1) retinoic acid induced striking conformational changes when bound to RBP, and (2) none of the several synthetic retinoids used in human therapy were found to bind to RBP. Tretinoin 181-194 retinol binding protein 4 Homo sapiens 127-130
2645590-2 1989 Polyacrylamide gel electrophoresis (PAGE), followed by protein blotting with an antiserum specific to retinol-binding protein (RBP), the plasma carrier of retinol, showed that: (1) retinoic acid induced striking conformational changes when bound to RBP, and (2) none of the several synthetic retinoids used in human therapy were found to bind to RBP. Tretinoin 181-194 retinol binding protein 4 Homo sapiens 249-252
2645590-2 1989 Polyacrylamide gel electrophoresis (PAGE), followed by protein blotting with an antiserum specific to retinol-binding protein (RBP), the plasma carrier of retinol, showed that: (1) retinoic acid induced striking conformational changes when bound to RBP, and (2) none of the several synthetic retinoids used in human therapy were found to bind to RBP. Tretinoin 181-194 retinol binding protein 4 Homo sapiens 249-252
3180083-0 1988 Changes in c-myc, c-fms, and N-ras proto-oncogene expression associated with retinoic acid-induced monocytic differentiation of human leukemia HL60/MRI cells. Tretinoin 77-90 NRAS proto-oncogene, GTPase Homo sapiens 29-34
3930245-9 1985 Although retinoic acid can inhibit ODC activity and putrescine accumulation, it is unlikely that this mechanism of action is responsible for retinoic acid-induced F9 cell differentiation, inasmuch as putrescine addition did not prevent the expression of the differentiated phenotype. Tretinoin 9-22 ornithine decarboxylase, structural 1 Mus musculus 35-38
2998635-7 1985 The tissue distribution of CRBP and CRABP, together with their relation to lipid transporting proteins suggests that CRBP and CRABP are cellular transporting proteins for retinol and retinoic acid, respectively. Tretinoin 183-196 retinol binding protein 1 Rattus norvegicus 27-31
18926686-6 2009 Retinoic acid also repressed LPS-induced transcription of NF-kappaB target genes such as IL-6, MCP-1 and COX-2. Tretinoin 0-13 C-C motif chemokine ligand 2 Homo sapiens 95-100
2998635-7 1985 The tissue distribution of CRBP and CRABP, together with their relation to lipid transporting proteins suggests that CRBP and CRABP are cellular transporting proteins for retinol and retinoic acid, respectively. Tretinoin 183-196 retinol binding protein 1 Rattus norvegicus 117-121
19723072-1 2009 Acute promyelocytic leukemia KG1 cells with t(11;17) PLZF-RARalpha respond poorly to the differentiation inducer all-trans retinoic acid (RA), and the reason for the RA resistance is the recruitment of histone deacetylase by PLZF-RARalpha. Tretinoin 123-136 retinoic acid receptor alpha Homo sapiens 58-66
2861859-0 1985 Inhibition of phorbol ester-caused synthesis of mouse epidermal ornithine decarboxylase by retinoic acid. Tretinoin 91-104 ornithine decarboxylase, structural 1 Mus musculus 64-87
2861859-1 1985 The mechanisms by which topically applied retinoic acid to mouse skin inhibits tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced epidermal ornithine decarboxylase activity were analyzed. Tretinoin 42-55 ornithine decarboxylase, structural 1 Mus musculus 155-178
2861859-4 1985 We found that retinoic acid inhibits the synthesis of ornithine decarboxylase caused by TPA. Tretinoin 14-27 ornithine decarboxylase, structural 1 Mus musculus 54-77
3404291-10 1988 In contrast, the activity of RO, the enzyme that regulates the irreversible oxidation of retinal to retinoic acid, was significantly increased in ZD rats. Tretinoin 100-113 aldehyde oxidase 4 Rattus norvegicus 29-31
2861859-6 1985 Application of 17 nmol retinoic acid 1 h prior to application of 10 nmol TPA to skin resulted in inhibition of the induction of activity which accompanied inhibition of [3H]difluoromethylornithine binding and [35S]methionine incorporation into ornithine decarboxylase protein as determined by the tube-gel electrophoresis of the enzyme immunoprecipitated with monoclonal antibodies to it. Tretinoin 23-36 ornithine decarboxylase, structural 1 Mus musculus 244-267
2454869-4 1988 Clones expressing c-fos antisense RNA grew as rapidly as control F9 cells, and underwent differentiation after retinoic acid treatment. Tretinoin 111-124 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 18-23
19723072-1 2009 Acute promyelocytic leukemia KG1 cells with t(11;17) PLZF-RARalpha respond poorly to the differentiation inducer all-trans retinoic acid (RA), and the reason for the RA resistance is the recruitment of histone deacetylase by PLZF-RARalpha. Tretinoin 138-140 retinoic acid receptor alpha Homo sapiens 58-66
2470302-0 1988 Interleukin-1 alpha mRNA induced by cycloheximide PMA, and retinoic acid is reduced by dexamethasone in PAM-212 keratinocytes. Tretinoin 59-72 peptidylglycine alpha-amidating monooxygenase Homo sapiens 104-107
2861859-8 1985 The results indicate that retinoic acid possibly inhibits TPA-caused synthesis of ornithine decarboxylase protein selectively. Tretinoin 26-39 ornithine decarboxylase, structural 1 Mus musculus 82-105
19723072-5 2009 Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites. Tretinoin 94-96 H3 histone pseudogene 16 Homo sapiens 148-151
19767821-8 2009 Together, results indicate that the coordinate signaling by two independent pathways, one involving canonical Wnt-beta-catenin activation of target genes and the other with Galpha13 signaling to ERM proteins to modulate cytoarchitectural changes, is required during the retinoic acid induced differentiation of F9 cells to primitive endoderm. Tretinoin 270-283 guanine nucleotide binding protein, alpha 13 Mus musculus 173-181
2992315-1 1985 A one-step procedure to detect cellular [3H]retinol and [3H]retinoic acid binding proteins (CRBP and CRABP) from rat testis cytosolic extract was devised. Tretinoin 60-73 retinol binding protein 1 Rattus norvegicus 92-96
3600758-3 1987 Hence, RA closely mimics posterior limb bud tissue (the zone of polarizing activity, ZPA) that causes very similar duplications when grafted to an anterior site of a host limb bud. Tretinoin 7-9 zona pellucida glycoprotein 2 Gallus gallus 85-88
2826263-2 1987 One is the retinol-binding protein (RBP, the plasma carrier of natural vitamin A, retinol, which was found to also bind retinoic acid (RA) in vitro. Tretinoin 120-133 retinol binding protein 4 Homo sapiens 36-39
19375825-3 2009 Interestingly, while the effect of ATRA was RARalpha-dependent, the effect of its active analogues was not inhibited by a selective RARalpha antagonist. Tretinoin 35-39 retinoic acid receptor alpha Homo sapiens 44-52
2826263-2 1987 One is the retinol-binding protein (RBP, the plasma carrier of natural vitamin A, retinol, which was found to also bind retinoic acid (RA) in vitro. Tretinoin 135-137 retinol binding protein 4 Homo sapiens 36-39
2826263-4 1987 This technique allowed us to study the binding of several natural and synthetic retinoids to the plasma RBP; it was found that only natural retinoids bind to RBP in vitro; RA binding was found to induce major conformational changes in the protein. Tretinoin 172-174 retinol binding protein 4 Homo sapiens 104-107
3475513-4 1987 Strong inhibition of colony cell growth (greater than or equal to 50%) was observed in 4/10 cases treated with rINF-alpha A alone, but only at high concentration (greater than or equal to 2500 U/ml) and in 4/10 cases treated with RA alone (5 X 10(-8) M or 5 X 10(-7) M). Tretinoin 230-232 cobalamin binding intrinsic factor Rattus norvegicus 111-115
6616453-1 1983 The ability of all-trans-retinoic acid (RA) and other retinoid derivatives to enhance DNA synthesis and to induce ornithine decarboxylase [L-ornithine carboxylyase; EC 4.1.1.17 (ODC)] activity has been investigated in normal and tape-stripped hairless mouse epidermis. Tretinoin 15-38 ornithine decarboxylase, structural 1 Mus musculus 114-137
6616453-1 1983 The ability of all-trans-retinoic acid (RA) and other retinoid derivatives to enhance DNA synthesis and to induce ornithine decarboxylase [L-ornithine carboxylyase; EC 4.1.1.17 (ODC)] activity has been investigated in normal and tape-stripped hairless mouse epidermis. Tretinoin 15-38 ornithine decarboxylase, structural 1 Mus musculus 178-181
6616453-1 1983 The ability of all-trans-retinoic acid (RA) and other retinoid derivatives to enhance DNA synthesis and to induce ornithine decarboxylase [L-ornithine carboxylyase; EC 4.1.1.17 (ODC)] activity has been investigated in normal and tape-stripped hairless mouse epidermis. Tretinoin 40-42 ornithine decarboxylase, structural 1 Mus musculus 114-137
6616453-4 1983 Induction of epidermal ODC activity was inhibited by arotinoid ethyl ester but not by RA, 13-cis-RA, or aromatic retinoid when they were applied to the skin at 24 hr prior to tape stripping. Tretinoin 86-88 ornithine decarboxylase, structural 1 Mus musculus 23-26
6616453-5 1983 RA applied topically to normal hairless mouse skin induced a dose-dependent increase in epidermal ODC activity, detectable 24 hr or more after treatment. Tretinoin 0-2 ornithine decarboxylase, structural 1 Mus musculus 98-101
6616453-6 1983 RA induced epidermal ODC activity to levels only 15- to 30-fold less than found after treatment with the potent tumor promoter tetradecanoylphorbol-13-acetate. Tretinoin 0-2 ornithine decarboxylase, structural 1 Mus musculus 21-24
6616453-7 1983 Epidermal ODC activity was also induced by topical 13-cis-RA, aromatic retinoid, and arotinoid ethyl ester at this time, although in lower amounts than after RA treatment. Tretinoin 58-60 ornithine decarboxylase, structural 1 Mus musculus 10-13
6616453-8 1983 The induction of ODC activity by RA was itself inhibited by topical arotinoid ethyl ester treatment. Tretinoin 33-35 ornithine decarboxylase, structural 1 Mus musculus 17-20
6616453-9 1983 RA, 13-cis-RA, and aromatic retinoid induced ODC activity at doses below those required to enhance epidermal DNA synthesis. Tretinoin 0-2 ornithine decarboxylase, structural 1 Mus musculus 45-48
3025324-1 1986 A study was conducted to explore the effects of retinoic acid, fed to retinol-deficient rats, on the tissue distribution and levels of cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP). Tretinoin 48-61 retinol binding protein 1 Rattus norvegicus 135-167
3025324-1 1986 A study was conducted to explore the effects of retinoic acid, fed to retinol-deficient rats, on the tissue distribution and levels of cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP). Tretinoin 48-61 retinol binding protein 1 Rattus norvegicus 169-173
6194034-0 1983 Changes in the rate of laminin and entactin synthesis in F9 embryonal carcinoma cells treated with retinoic acid and cyclic amp. Tretinoin 99-112 nidogen 1 Mus musculus 35-43
19605690-0 2009 Removal of maternal retinoic acid by embryonic CYP26 is required for correct Nodal expression during early embryonic patterning. Tretinoin 20-33 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 47-52
6194034-1 1983 The synthesis of laminin A and B chains, and of entactin, has been measured in murine F9 embryonal carcinoma cells differentiating in response to retinoic acid and cyclic AMP. Tretinoin 146-159 nidogen 1 Mus musculus 48-56
6406052-8 1983 Application of 17 nmol of retinoic acid or 76 nmol of dexamethasone inhibited the induction of ornithine decarboxylase activity by BrMBA. Tretinoin 26-39 ornithine decarboxylase, structural 1 Mus musculus 95-118
6846105-3 1983 SDS-PAGE of (2-(3)H)-mannose labelled glycoproteins indicates that both retinoic acid and retinol treatments stimulate the incorporation of the radiolabelled sugar into a glycoprotein with subunit MW 180,000 (Gp 180) and, to a lesser extent, into other glycoproteins. Tretinoin 72-85 carboxypeptidase D Mus musculus 209-215
6846105-5 1983 A retinoic acid induced increase in the amount of Gp 180 can also be shown by lactoperoxidase catalyzed radioiodination of cultured 3T12 cells, and controlled trypsin digestion experiments indicate that Gp 180 is a component of the cell surface. Tretinoin 2-15 carboxypeptidase D Mus musculus 50-56
6846105-5 1983 A retinoic acid induced increase in the amount of Gp 180 can also be shown by lactoperoxidase catalyzed radioiodination of cultured 3T12 cells, and controlled trypsin digestion experiments indicate that Gp 180 is a component of the cell surface. Tretinoin 2-15 carboxypeptidase D Mus musculus 203-209
6847765-0 1983 Inhibition of ultraviolet-B skin carcinogenesis by all-trans-retinoic acid regimens that inhibit ornithine decarboxylase induction. Tretinoin 61-74 ornithine decarboxylase, structural 1 Mus musculus 97-120
6847765-3 1983 In this study, all-trans-retinoic acid (RA) regimens that inhibited the induction of epidermal ODC by ultraviolet-B (UVB) were tested for their ability to inhibit UVB skin carcinogenesis. Tretinoin 15-38 ornithine decarboxylase, structural 1 Mus musculus 95-98
6847765-3 1983 In this study, all-trans-retinoic acid (RA) regimens that inhibited the induction of epidermal ODC by ultraviolet-B (UVB) were tested for their ability to inhibit UVB skin carcinogenesis. Tretinoin 40-42 ornithine decarboxylase, structural 1 Mus musculus 95-98
6847765-9 1983 These results show that RA treatments that inhibit epidermal ODC induction may be effective in reducing the carcinogenicity of UVB. Tretinoin 24-26 ornithine decarboxylase, structural 1 Mus musculus 61-64
7082807-1 1982 A study was made of antitumor and toxic properties of retinoid C15 which has some characteristic structural features of retinoic acid natural metabolites; such as ethyl-2E, 4E-3-methyl-5-/2,6-dimethyl-6-ethoxycarbonyl-/3-oxo-1-cyclohexene-1-yl/-2,4-pentadienoate. Tretinoin 120-133 placenta associated 8 Homo sapiens 63-66
7068980-5 1982 The ability of retinoic acid and its congeners to inhibit tumor promotion by the phorbol ester correlated with the effect of dose, structure, and time of treatment on the induction of ornithine decarboxylase. Tretinoin 15-28 ornithine decarboxylase, structural 1 Mus musculus 184-207
6892133-11 1982 We have established that, like serum retinol-binding protein, IRBP can be also bind retinoic acid, although it has not been established that retinoic acid is an endogenous ligand. Tretinoin 84-97 retinol binding protein 3 Bos taurus 62-66
6770995-4 1980 For example, in clone A6, beta-all-transretinoic acid stimulated tyrosinase activity by 48% but caused only a 7% inhibition of cellular proliferation. Tretinoin 26-53 tyrosinase Homo sapiens 65-75
11219836-2 1980 Retinoic acid (0.17-68 nmol), a potent inhibitor of both the induction of ODC activity and tumor formation by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), failed to inhibit both the induction of ODC activity and tumor formation by DMBA. Tretinoin 0-13 ornithine decarboxylase, structural 1 Mus musculus 74-77
11219836-4 1980 These results indicate that (a) the mechanism of the induction of ODC activity and tumor formation by a complete carcinogen appears to be different from that of the tumor promoter TPA, (b) DMBA-induced ODC activity may be an important component of the mechanism of DMBA carcinogenesis, and (c) the protective effect of retinoic acid on skin carcinogenesis is not universal; it inhibits skin tumor formation by some agents and not by others. Tretinoin 319-332 ornithine decarboxylase, structural 1 Mus musculus 66-69
11219836-4 1980 These results indicate that (a) the mechanism of the induction of ODC activity and tumor formation by a complete carcinogen appears to be different from that of the tumor promoter TPA, (b) DMBA-induced ODC activity may be an important component of the mechanism of DMBA carcinogenesis, and (c) the protective effect of retinoic acid on skin carcinogenesis is not universal; it inhibits skin tumor formation by some agents and not by others. Tretinoin 319-332 ornithine decarboxylase, structural 1 Mus musculus 202-205
1035129-1 1976 Cellular retinol and retinoic acid binding proteins were detected in mouse skin papillomas, human adenocarcinoma HAD-1, Dunning Leukemia, Walker 256 carcinosarcoma and mammary adenocarcinoma MAC-1. Tretinoin 21-34 integrin subunit alpha M Homo sapiens 191-196
4337154-13 1972 In contrast, retinoic acid bound to apo-RBP almost as effectively as did retinol. Tretinoin 13-26 retinol binding protein 4 Homo sapiens 40-43
14258729-1 1965 The major metabolite in rat bile of injected C(14)-retinoic acid was purified by ion-exchange and silicic acid chromatography; it has the spectrum of methyl retinoate, releases retinoic acid upon basic hydrolysis or by treatment with beta-glucuronidase, and contains glucuronic acid. Tretinoin 51-64 glucuronidase, beta Rattus norvegicus 234-252
34051632-0 2021 All-trans-retinoic acid restores CD4+ T cell response after sepsis by inhibiting the expansion and activation of myeloid-derived suppressor cells. Tretinoin 0-23 CD4 antigen Mus musculus 33-36
34001245-0 2021 The role of Serpina3n in the reversal effect of ATRA on dexamethasone-inhibited osteogenic differentiation in mesenchymal stem cells. Tretinoin 48-52 serine (or cysteine) peptidase inhibitor, clade A, member 3N Mus musculus 12-21
34001245-12 2021 RESULTS: ATRA enhanced BMP9-induced ALP, RUNX2 expressions, ALP activities, and matrix mineralization in mouse embryonic fibroblasts as well as C3H10T1/2 and C2C12 cells, while a high concentration of DEX attenuated these markers. Tretinoin 9-13 growth differentiation factor 2 Mus musculus 23-27
34001245-15 2021 During the reversal process of ATRA, the expression of retinoic acid receptor beta (RARbeta) was elevated. Tretinoin 31-35 retinoic acid receptor, alpha Mus musculus 84-91
34001245-16 2021 RARbeta inhibitor Le135 partly blocked the reversal effect of ATRA. Tretinoin 62-66 retinoic acid receptor, alpha Mus musculus 0-7
34001245-17 2021 Meanwhile, RNA-seq demonstrated that serine protease inhibitor, clade A, member 3N (Serpina3n) was remarkably upregulated by DEX but downregulated when combined with ATRA. Tretinoin 166-170 serine (or cysteine) peptidase inhibitor, clade A, member 3N Mus musculus 37-82
34001245-17 2021 Meanwhile, RNA-seq demonstrated that serine protease inhibitor, clade A, member 3N (Serpina3n) was remarkably upregulated by DEX but downregulated when combined with ATRA. Tretinoin 166-170 serine (or cysteine) peptidase inhibitor, clade A, member 3N Mus musculus 84-93
34001245-18 2021 Overexpression of Serpina3n attenuated ATRA-promoted osteogenic differentiation, whereas knockdown of Serpina3n blocked DEX-inhibited osteogenic differentiation. Tretinoin 39-43 serine (or cysteine) peptidase inhibitor, clade A, member 3N Mus musculus 18-27
34001245-20 2021 CONCLUSION: ATRA can reverse DEX-inhibited osteogenic differentiation both in vitro and in vivo, which may be closely related to the downregulation of DEX-promoted Serpina3n. Tretinoin 12-16 serine (or cysteine) peptidase inhibitor, clade A, member 3N Mus musculus 164-173
33989617-7 2021 Additionally, upregulated transcriptions of spermatogenic differentiation marker C-KIT and meiotic marker SYCP3 were detected in these cells after retinoic acid-induced differentiation. Tretinoin 147-160 KIT proto-oncogene, receptor tyrosine kinase Bos taurus 81-86
33976430-4 2021 Here we show that retinoic acid-inducible gene-I (RIG-I) sufficiently restrains SARS-CoV-2 replication in human lung cells in a type I/III interferon (IFN)-independent manner. Tretinoin 18-31 DExD/H-box helicase 58 Homo sapiens 50-55
33976430-9 2021 By contrast, the anti-SARS-CoV-2 activity was restored by all-trans retinoic acid treatment through upregulation of RIG-I protein expression in primary lung cells derived from patients with chronic obstructive pulmonary disease. Tretinoin 68-81 DExD/H-box helicase 58 Homo sapiens 116-121
33565183-3 2021 ALDH1A2 is involved in conversion of retinol (vitamin A) into retinoic acid, which is an essential regulator of diaphragm and cardiovascular formation during embryogenesis. Tretinoin 62-75 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-7
33928787-2 2021 With the aim of developing an in vivo model to monitor retinoic acid receptor (RAR) transactivation real-time in intact animals, we generated transgenic mice carrying a luciferase (luc) reporter gene under the control of retinoic acid response elements (RAREs) consisting of three copies of a direct repeat with five spacing nucleotides (DR5). Tretinoin 55-68 retinoic acid receptor, alpha Mus musculus 79-82
33995343-4 2021 VSV activates innate immunity via retinoic acid-inducible gene I (RIG-I), a sensor for viral RNA. Tretinoin 34-47 DExD/H-box helicase 58 Homo sapiens 66-71
33742137-3 2021 Accordingly, FASN levels decreased during all-trans retinoic acid (ATRA)-mediated granulocytic differentiation of acute promyelocytic leukemia (APL) cells, partially via autophagic degradation. Tretinoin 52-65 fatty acid synthase Homo sapiens 13-17
33742137-3 2021 Accordingly, FASN levels decreased during all-trans retinoic acid (ATRA)-mediated granulocytic differentiation of acute promyelocytic leukemia (APL) cells, partially via autophagic degradation. Tretinoin 67-71 fatty acid synthase Homo sapiens 13-17
33742137-4 2021 Furthermore, our data suggest that inhibition of FASN expression levels using RNAi or (-)-epigallocatechin-3-gallate (EGCG) accelerated the differentiation of APL cell lines and significantly re-sensitized ATRA refractory non-APL AML cells. Tretinoin 206-210 fatty acid synthase Homo sapiens 49-53
3025324-5 1986 Analysis of the data indicated that only the CRBP level of the proximal epididymis in the retinol-deficient/retinoic acid group differed significantly from (was lower than) the corresponding control level, at the 1% confidence level. Tretinoin 108-121 retinol binding protein 1 Rattus norvegicus 45-49
3008983-1 1986 The intracisternal injection of either all-trans-retinoic acid or [alpha]-difluoromethylornithine (DFMO) into the brain of 9-day-old mice blocked (greater than 90%) phorbol ester-induced ornithine decarboxylase (ODC, EC 4.1.1.17) activity in a concentration-dependent fashion; this inhibition was not evident with the use of the biologically impotent furyl analog of retinoic acid. Tretinoin 39-62 ornithine decarboxylase, structural 1 Mus musculus 187-210
3008983-1 1986 The intracisternal injection of either all-trans-retinoic acid or [alpha]-difluoromethylornithine (DFMO) into the brain of 9-day-old mice blocked (greater than 90%) phorbol ester-induced ornithine decarboxylase (ODC, EC 4.1.1.17) activity in a concentration-dependent fashion; this inhibition was not evident with the use of the biologically impotent furyl analog of retinoic acid. Tretinoin 39-62 ornithine decarboxylase, structural 1 Mus musculus 212-215
3008983-1 1986 The intracisternal injection of either all-trans-retinoic acid or [alpha]-difluoromethylornithine (DFMO) into the brain of 9-day-old mice blocked (greater than 90%) phorbol ester-induced ornithine decarboxylase (ODC, EC 4.1.1.17) activity in a concentration-dependent fashion; this inhibition was not evident with the use of the biologically impotent furyl analog of retinoic acid. Tretinoin 49-62 ornithine decarboxylase, structural 1 Mus musculus 187-210
3008983-1 1986 The intracisternal injection of either all-trans-retinoic acid or [alpha]-difluoromethylornithine (DFMO) into the brain of 9-day-old mice blocked (greater than 90%) phorbol ester-induced ornithine decarboxylase (ODC, EC 4.1.1.17) activity in a concentration-dependent fashion; this inhibition was not evident with the use of the biologically impotent furyl analog of retinoic acid. Tretinoin 49-62 ornithine decarboxylase, structural 1 Mus musculus 212-215
3027712-0 1986 The regulation of collagen type IV(alpha 1) and other genes during the retinoic acid induced differentiation of wild type and mutant mouse teratocarcinoma stem cells. Tretinoin 71-84 collagen, type IV, alpha 1 Mus musculus 18-42
2988756-2 1985 The reduction was inhibited by phospholipase A2 inhibitors, such as dibromoacetophenone, the lipoxygenase inhibitor nordihydroguaiaretic acid, an NADH-dehydrogenase inhibitor, the microfilament inhibitor cytochalasin B, oxygen radical scavengers such as superoxide dismutase, antioxidants such as butyl hydroxyanisole and non-specific inhibitors such as retinoic acid. Tretinoin 354-367 phospholipase A2, group IB, pancreas Mus musculus 31-47
6498840-1 1984 Retinoic acid inhibits the proliferation of the murine melanoma clone S91-C-2 cells, enhances the glycosylation of specific cell surface sialoglycoproteins, and stimulates sialytransferase activity. Tretinoin 0-13 complement component 2 (within H-2S) Mus musculus 74-77
6498840-6 1984 The results demonstrated that retinoic acid enhanced [3H]glucosamine incorporation into a Mr 160,000 glycoprotein in the S91-C-2 cells but not in any of the resistant mutant clones, while the pattern of [35S]methionine-labeled proteins was not modified in either the sensitive or the resistant clones. Tretinoin 30-43 complement component 2 (within H-2S) Mus musculus 125-128
6498840-7 1984 Radiolabeling of a Mr 160,000 sialoglycoprotein on the surface of S91-C-2 and of several retinoic acid-sensitive subclones of S91-C-2 was augmented by retinoic acid. Tretinoin 89-102 complement component 2 (within H-2S) Mus musculus 130-133
6498840-7 1984 Radiolabeling of a Mr 160,000 sialoglycoprotein on the surface of S91-C-2 and of several retinoic acid-sensitive subclones of S91-C-2 was augmented by retinoic acid. Tretinoin 151-164 complement component 2 (within H-2S) Mus musculus 70-73
6498840-7 1984 Radiolabeling of a Mr 160,000 sialoglycoprotein on the surface of S91-C-2 and of several retinoic acid-sensitive subclones of S91-C-2 was augmented by retinoic acid. Tretinoin 151-164 complement component 2 (within H-2S) Mus musculus 130-133
6498840-9 1984 Sialytransferase activity was increased 2- to 3-fold by retinoic acid in the S91-C-2 cells and in several sensitive subclones, but not in any of the resistant mutant clones. Tretinoin 56-69 complement component 2 (within H-2S) Mus musculus 81-84
6486823-6 1984 In a system reconstituted with NADPH-cytochrome P-450 reductase, NADPH, and phospholipid, purified cytochromes P-450f and b were discovered to promote conversion of retinoic acid to polar metabolites, including 4-hydroxy-retinoic acid. Tretinoin 165-178 cytochrome p450 oxidoreductase Rattus norvegicus 31-63
6486823-6 1984 In a system reconstituted with NADPH-cytochrome P-450 reductase, NADPH, and phospholipid, purified cytochromes P-450f and b were discovered to promote conversion of retinoic acid to polar metabolites, including 4-hydroxy-retinoic acid. Tretinoin 165-178 cytochrome P450, family 2, subfamily c, polypeptide 7 Rattus norvegicus 111-117
6611208-5 1984 Our results indicate that RA is required early in the PHA activation process and that thymocytes affected by RA treatment already express the "mature" T3 antigen but lack T6 and Fc mu receptors. Tretinoin 109-111 PRSS3 pseudogene 2 Homo sapiens 171-193
6331639-4 1984 Both TPA-dependent and developmental increases in mouse brain ODC activity were significantly reduced by intracisternal injection of retinoic acid (RA). Tretinoin 133-146 ornithine decarboxylase, structural 1 Mus musculus 62-65
6331639-4 1984 Both TPA-dependent and developmental increases in mouse brain ODC activity were significantly reduced by intracisternal injection of retinoic acid (RA). Tretinoin 148-150 ornithine decarboxylase, structural 1 Mus musculus 62-65
6427217-4 1984 IRBP also binds exogenous cholesterol, alpha-tocopherol, and all-trans retinoic acid, all of which are completely displaced by all trans retinol. Tretinoin 71-84 retinol binding protein 3 Bos taurus 0-4
6423272-5 1984 The dose required for 50% inhibition was 0.063 micrograms, or 0.15 nmol, which is about one-half that of retinoic acid, a known inhibitor of induction of ODC activity by TPA. Tretinoin 105-118 ornithine decarboxylase, structural 1 Mus musculus 154-157
6580493-1 1983 A phase I trial was conducted of the vitamin A derivative beta-all-trans-retinoic acid (vitamin A acid; TRA), delivered via a collagen sponge and cervical cap for mild or moderate intraepithelial cervical neoplasia. Tretinoin 88-102 T cell receptor alpha locus Homo sapiens 104-107
7057047-0 1982 Retinoic acid modulation of ultraviolet light-induced epidermal ornithine decarboxylase activity. Tretinoin 0-13 ornithine decarboxylase, structural 1 Mus musculus 64-87
7057047-2 1982 Induction of epidermal ornithine decarboxylase also occurs following application of the tumor promoting agent 12-0-tetradecanoylphorbol-13 acetate and topical retinoic acid is able to block both this ornithine decarboxylase induction and skin tumor promotion. Tretinoin 159-172 ornithine decarboxylase, structural 1 Mus musculus 23-46
7057047-2 1982 Induction of epidermal ornithine decarboxylase also occurs following application of the tumor promoting agent 12-0-tetradecanoylphorbol-13 acetate and topical retinoic acid is able to block both this ornithine decarboxylase induction and skin tumor promotion. Tretinoin 159-172 ornithine decarboxylase, structural 1 Mus musculus 200-223
7057047-3 1982 In the studies described below, topical application of retinoic acid to hairless mouse skin leads to a significant inhibition of UVB-induced epidermal ornithine decarboxylase activity. Tretinoin 55-68 ornithine decarboxylase, structural 1 Mus musculus 151-174
7057047-5 1982 To show significant inhibition of UVB-induced ornithine decarboxylase the retinoic acid had to be applied within 5 hr of UVB irradiation. Tretinoin 74-87 ornithine decarboxylase, structural 1 Mus musculus 46-69
7057047-7 1982 The quantities of retinoic acid used (1.7 nmol and 3.4 nmol) have been shown effective at inhibiting 12-0-tetradecanoyl phorbol-13 acetate induced ornithine decarboxylase. Tretinoin 18-31 ornithine decarboxylase, structural 1 Mus musculus 147-170
7057047-8 1982 The results show that these concentrations of topical retinoic acid applied either before or immediately following UVB irradiation reduces the UVB induction of epidermal ornithine decarboxylase. Tretinoin 54-67 ornithine decarboxylase, structural 1 Mus musculus 170-193
6802491-3 1982 Retinoic acid, a potent inhibitor of both the induction of ODC activity and tumor promotion by TPA, failed to inhibit both the induction of ODC activity and tumor formation by DMBA. Tretinoin 0-13 ornithine decarboxylase, structural 1 Mus musculus 59-62
7083472-4 1982 Retinoic acid inhibited the TPA-induced ODC activity and the ensuing accumulation of putrescine, but did not alter the TPA-induced SAM-D activity or the molar ratio of spermidine/spermine. Tretinoin 0-13 ornithine decarboxylase, structural 1 Mus musculus 40-43
6253061-3 1980 These effects of retinoic acid progressed lin-early in a time-dependent and a dose-dependent fashion such that at the end of a seven-day treatment cell growth was inhibited by approximately 65%, and both melanin content and tyrosinase activity increased more than three-fold over the control. Tretinoin 17-30 tyrosinase Homo sapiens 224-234
6253061-6 1980 In the presence of the tyrosinase inhibitor phenylthiocarbamate, retinoic acid was capable of inhibiting cell proliferation without enhancing melanin synthesis. Tretinoin 65-78 tyrosinase Homo sapiens 23-33
7388798-1 1980 The ability of 5,6-epoxyretinoic acid, a biologically active metabolites of retinoic acid, to inhibit both the induction of ornithine decarboxylase (ODC) activity and skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA) was evaluated. Tretinoin 24-37 ornithine decarboxylase, structural 1 Mus musculus 124-147
7388798-1 1980 The ability of 5,6-epoxyretinoic acid, a biologically active metabolites of retinoic acid, to inhibit both the induction of ornithine decarboxylase (ODC) activity and skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA) was evaluated. Tretinoin 24-37 ornithine decarboxylase, structural 1 Mus musculus 149-152
7388798-4 1980 5,6-Epoxyretinoic acid, 5,6-dihydroretinoic acid, and retinoic acid were equally effective in inhibiting the induction of ODC activity by TPA. Tretinoin 9-22 ornithine decarboxylase, structural 1 Mus musculus 122-125
1062896-0 1975 Inhibition of glucose-6-phosphate dehydrogenase activity by tretinoin. Tretinoin 60-69 glucose-6-phosphate dehydrogenase Homo sapiens 14-47
33713958-1 2021 Retinoic acid-inducible gene I (RIG-I) plays a critical role in the recognition of intracytoplasmic viral RNA. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 32-37
34051632-6 2021 ATRA administration eventually reduced mortality of secondary infection by Legionella pneumophila in CLP-surviving mice, which might be associated with the restoration of CD4+ T cells proliferating and secreting activity. Tretinoin 0-4 CD4 antigen Mus musculus 171-174
34051632-7 2021 CONCLUSION: ATRA can restore CD4+ T cells dysfunction in sepsis by modulating the expansion and function of MDSCs and therefore provides a potential therapy that targets the immunosuppressive state of sepsis. Tretinoin 12-16 CD4 antigen Mus musculus 29-32
34015278-11 2021 Treatment with free ATRA and the selected formulations led to a significant amelioration of DN by reducing of creatinine, urea, TNF-alpha, ICAM-1, GM-CSF, VEGF levels as well as elevating AMPK and LKB1 levels. Tretinoin 20-24 intercellular adhesion molecule 1 Rattus norvegicus 139-145
34015278-11 2021 Treatment with free ATRA and the selected formulations led to a significant amelioration of DN by reducing of creatinine, urea, TNF-alpha, ICAM-1, GM-CSF, VEGF levels as well as elevating AMPK and LKB1 levels. Tretinoin 20-24 colony stimulating factor 2 Rattus norvegicus 147-153
33835049-3 2021 Dogmatically, progenitor spermatogonia that express retinoic acid receptor gamma (RARG) at these stages will differentiate in response to RA, but this has yet to be tested functionally. Tretinoin 82-84 retinoic acid receptor, gamma Mus musculus 52-80
33835049-7 2021 Following acute RA treatment (2-4hr), significantly more Dppa3+ late progenitors induced KIT, including at the midpoint of the cycle (stages VI-IX), than Dppa3- late progenitors. Tretinoin 16-18 developmental pluripotency-associated 3 Mus musculus 57-62
33878891-7 2021 High levels of FABP5 can reduce the delivery of all-trans-retinoic acid to RXRA. Tretinoin 48-71 fatty acid binding protein 5 Homo sapiens 15-20
33878891-7 2021 High levels of FABP5 can reduce the delivery of all-trans-retinoic acid to RXRA. Tretinoin 48-71 retinoid X receptor alpha Homo sapiens 75-79
33878891-9 2021 Conclusion: The authors propose that HDAC7 controls the uptake of all-trans-retinoic acid, thus influencing RXRA activity and IGF1 signaling. Tretinoin 66-89 retinoid X receptor alpha Homo sapiens 108-112
33995501-3 2021 Here, we performed transcriptome profiling in the hippocampus of Ube3a m+/p+ and Ube3a m-/p+ mice, and determined that the expression of the retinoic acid (RA) signalling pathway was downregulated in Ube3a-deficient mice compared to WT mice. Tretinoin 141-154 ubiquitin protein ligase E3A Mus musculus 65-70
33995501-3 2021 Here, we performed transcriptome profiling in the hippocampus of Ube3a m+/p+ and Ube3a m-/p+ mice, and determined that the expression of the retinoic acid (RA) signalling pathway was downregulated in Ube3a-deficient mice compared to WT mice. Tretinoin 141-154 ubiquitin protein ligase E3A Mus musculus 81-86
33995501-3 2021 Here, we performed transcriptome profiling in the hippocampus of Ube3a m+/p+ and Ube3a m-/p+ mice, and determined that the expression of the retinoic acid (RA) signalling pathway was downregulated in Ube3a-deficient mice compared to WT mice. Tretinoin 141-154 ubiquitin protein ligase E3A Mus musculus 81-86
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 ubiquitin protein ligase E3A Mus musculus 8-13
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 calbindin 1 Mus musculus 115-120
33995501-5 2021 Loss of UBE3A expression caused the downregulation of the expression of RA-related genes, including Erbb4, Dpysl3, Calb1, Pten, and Arhgap5 in Ube3a m-/p+ mice brain tissues. Tretinoin 72-74 ubiquitin protein ligase E3A Mus musculus 143-148
33995501-6 2021 This work revealed a new role for UBE3A in regulating retinoic acid (RA) signalling downstream genes and hopefully to shed light on the potential drug target of AS. Tretinoin 54-67 ubiquitin protein ligase E3A Mus musculus 34-39
33995501-6 2021 This work revealed a new role for UBE3A in regulating retinoic acid (RA) signalling downstream genes and hopefully to shed light on the potential drug target of AS. Tretinoin 69-71 ubiquitin protein ligase E3A Mus musculus 34-39
33901013-7 2021 Moreover, silencing of C/EBPalpha attenuated ATRA-induced NEAT1 upregulation and APL cell differentiation. Tretinoin 45-49 nuclear paraspeckle assembly transcript 1 Homo sapiens 58-63
33075145-1 2021 AIM: To assess the expression of Retinoic acid-related orphan receptor beta (Ror beta) in human inflamed dental pulp stem cells (hI-DPSCs) and during macrophage phenotypic conversion. Tretinoin 33-46 RAR related orphan receptor A Homo sapiens 77-85
33531433-0 2021 Retinoic acid production, regulation, and containment through Zic1, Pitx2c and Cyp26c1 control cranial placode specification. Tretinoin 0-13 paired like homeodomain 2 L homeolog Xenopus laevis 68-74
33531433-3 2021 Here we identified two Zic1 targets, the RA catabolizing enzyme Cyp26c1 and the transcription factor Pitx2c, expressed in the vicinity of the PPR as crucially required for maintaining low RA levels in a spatially restricted, PPR-adjacent domain. Tretinoin 188-190 paired like homeodomain 2 L homeolog Xenopus laevis 101-107
33576062-10 2021 Additionally, FSK and ATRA ameliorated oxidative stress and inflammation, reduced TGF-beta1 levels and reversed the effect of BLM on the mRNA expression of Ptch-1, Smo and Gli-2. Tretinoin 22-26 GLI family zinc finger 2 Rattus norvegicus 172-177
33581110-8 2021 Collectively, these results provide new insight into RA-induced HoxA expression during early ESC differentiation, also highlight precise regulatory roles of the CTCF-binding element in orchestrating high-order chromatin structure. Tretinoin 53-55 CCCTC-binding factor Homo sapiens 161-165
33450188-3 2021 We demonstrate that KLRG1+ but not KLRG1- ILC2 produced IL-10 upon activation with IL-33 and retinoic acid. Tretinoin 93-106 killer cell lectin like receptor G1 Homo sapiens 20-25
33450188-3 2021 We demonstrate that KLRG1+ but not KLRG1- ILC2 produced IL-10 upon activation with IL-33 and retinoic acid. Tretinoin 93-106 interleukin 10 Homo sapiens 56-61
32905596-0 2021 Retinoic acid-responsive CD8 effector T-cells are selectively increased in IL-23-rich tissue in gastrointestinal GvHD. Tretinoin 0-13 CD8a molecule Homo sapiens 25-28
32905596-2 2021 The metabolite retinoic acid (RA) potentiates GI-GvHD in mice via alloreactive T-cells expressing the RA-receptor-alpha (RARalpha), but the role of RA-responsive cells in human GI-GvHD remains undefined. Tretinoin 15-28 retinoic acid receptor, alpha Mus musculus 121-129
32905596-2 2021 The metabolite retinoic acid (RA) potentiates GI-GvHD in mice via alloreactive T-cells expressing the RA-receptor-alpha (RARalpha), but the role of RA-responsive cells in human GI-GvHD remains undefined. Tretinoin 30-32 retinoic acid receptor, alpha Mus musculus 121-129
32905596-2 2021 The metabolite retinoic acid (RA) potentiates GI-GvHD in mice via alloreactive T-cells expressing the RA-receptor-alpha (RARalpha), but the role of RA-responsive cells in human GI-GvHD remains undefined. Tretinoin 102-104 retinoic acid receptor, alpha Mus musculus 121-129
32905596-9 2021 Finally, functional approaches demonstrated RA predominantly increased alloreactive GI-tropic RARahi CD8 effector T-cells, including cells with the phenotype identified in vivo. Tretinoin 44-46 CD8a molecule Homo sapiens 101-104
33531604-7 2021 Furthermore, we treated PCa cells with all trans retinoic acid (ATRA) and found that the reduced HOXB13 expression can be reverted. Tretinoin 43-62 homeobox B13 Homo sapiens 97-103
33531604-7 2021 Furthermore, we treated PCa cells with all trans retinoic acid (ATRA) and found that the reduced HOXB13 expression can be reverted. Tretinoin 64-68 homeobox B13 Homo sapiens 97-103
33901013-8 2021 Finally, simultaneous knockdown of C/EBPalpha and C/EBPbeta reduces ATRA-induced upregulation of C/EBPepsilon and dramatically impaired NEAT1 activation and APL cell differentiation. Tretinoin 68-72 nuclear paraspeckle assembly transcript 1 Homo sapiens 136-141
33942021-4 2021 As in mammals, stra8 expression was restricted to germ cells in the testis, transcript levels increased during the start of puberty, and decreased when blocking the production of retinoic acid. Tretinoin 179-192 stimulated by retinoic acid 8 Homo sapiens 15-20
33551168-5 2021 All concentrations of ATRA inhibited preconfluent preadipocyte proliferation with decreased proportion of S-phase cells and reduced protein abundance of cyclins (CCND1, CCND2, CCND3, CCNE1) and cyclin-dependent kinases (CDK2, CDK4, CDK6). Tretinoin 22-26 cyclin E1 Bos taurus 183-188
19605690-1 2009 The abundance of retinoic acid (RA) is determined by the balance between its synthesis by retinaldehyde dehydrogenase (RALDH) and its degradation by CYP26. Tretinoin 17-30 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 149-154
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 0-13 stearoyl-CoA desaturase (delta-9-desaturase) Danio rerio 68-71
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 151-164 stearoyl-CoA desaturase (delta-9-desaturase) Danio rerio 68-71
33429301-5 2021 Retinoic acid (cyp26b1, cyp3a65, lrata) and lipid metabolism (fasn, scd, elovl6) related genes were up-regulated by tributyltin chloride and all-trans retinoic acid, while only all-trans retinoic acid down-regulated the expression of dgat1a. Tretinoin 187-200 stearoyl-CoA desaturase (delta-9-desaturase) Danio rerio 68-71
19605690-1 2009 The abundance of retinoic acid (RA) is determined by the balance between its synthesis by retinaldehyde dehydrogenase (RALDH) and its degradation by CYP26. Tretinoin 32-34 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 149-154
19605690-2 2009 In particular, the dynamic expression of three CYP26 genes controls the regional level of RA within the body. Tretinoin 90-92 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 47-52
33360628-5 2021 The cell-binding efficiencies of substrates modified with anti-CD13 and anti-CD11b decreased and increased, respectively, with increasing duration of cell culture in medium containing differentiation-inducing agents, including all-trans retinoic acid. Tretinoin 237-250 integrin subunit alpha M Homo sapiens 77-82
19605690-7 2009 These observations suggest that maternal RA must be removed by embryonic CYP26 for correct Nodal expression during embryonic patterning. Tretinoin 41-43 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 73-78
19557639-0 2009 Function of retinoid acid receptor alpha and p21 in all-trans-retinoic acid-induced acute T-lymphoblastic leukemia apoptosis. Tretinoin 62-75 H3 histone pseudogene 16 Homo sapiens 45-48
33648532-9 2021 A final modular analysis identified an upregulation of ALDH1A2, a key rate-limiting enzyme of retinoic acid signaling pathway. Tretinoin 94-107 aldehyde dehydrogenase 1 family member A2 Homo sapiens 55-62
33653777-10 2021 Furthermore, ATRA treatment also effectively induced differentiation of cancer stem-like cells as represented by reduced expression of CD44 and inhibited Wnt signaling pathway activity. Tretinoin 13-17 CD44 molecule (Indian blood group) Homo sapiens 135-139
33177108-7 2021 Mechanistically, RA could restrain the glycolytic capacity of myeloid cells, which in turn activated the AMP-activated protein kinase (AMPK) pathway, further impairing the suppressive capacity of myeloid cells. Tretinoin 17-19 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 105-133
33177108-7 2021 Mechanistically, RA could restrain the glycolytic capacity of myeloid cells, which in turn activated the AMP-activated protein kinase (AMPK) pathway, further impairing the suppressive capacity of myeloid cells. Tretinoin 17-19 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 135-139
19557639-4 2009 Among these components, RARalpha is preferentially bound to ATRA, which is used to treat acute T-lymphoblastic leukemia, yet the conditions and mechanisms remain unknown. Tretinoin 60-64 retinoic acid receptor alpha Homo sapiens 24-32
32866959-5 2021 In summary, we conclude that epidermal hyperproliferation of mouse skin in response to a topically administered vitamin D receptor antagonist/partial agonist (ZK159222) is induced via increased retinoic acid synthesis, retinoic acid levels and increased RARgamma-mediated pathways. Tretinoin 194-207 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 112-130
19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 41-43 H3 histone pseudogene 16 Homo sapiens 81-84
32866959-5 2021 In summary, we conclude that epidermal hyperproliferation of mouse skin in response to a topically administered vitamin D receptor antagonist/partial agonist (ZK159222) is induced via increased retinoic acid synthesis, retinoic acid levels and increased RARgamma-mediated pathways. Tretinoin 219-232 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 112-130
33668324-0 2021 FOXC1 Downregulates Nanog Expression by Recruiting HDAC2 to Its Promoter in F9 Cells Treated by Retinoic Acid. Tretinoin 96-109 Nanog homeobox Homo sapiens 20-25
33668324-2 2021 FOXC1 is up-regulated in retinoic acid-induced differentiation of F9 Embryonal Carcinoma (EC) cells; furthermore, FOXC1 specifically inhibits the core pluripotency factor Nanog by binding to the proximal promoter. Tretinoin 25-38 Nanog homeobox Homo sapiens 171-176
19557639-7 2009 Consequently, it has been shown that, in RA-treated Molt3 cells, upregulation of p21 due to RA accompanies caspase 3/PARP activation which precedes the occurrence of apoptosis. Tretinoin 92-94 H3 histone pseudogene 16 Homo sapiens 81-84
33605051-8 2021 Remarkably, the cleavage site on the RNA helicases MDA5 and LGP2, two relevant immune sensors of the retinoic acid-inducible gene-I (RIG-I)-like receptors family, resembles the L target site of Gemin5 and Daxx, and similar cleavage sites have been reported in ISG15 and TBK1, two proteins involved in type I interferon response and signaling pathway, respectively. Tretinoin 101-114 gem nuclear organelle associated protein 5 Homo sapiens 194-200
19954601-11 2009 Methylation levels of HOX A4, A6 and A10 in HL-60 cells and of HOX A6 in K562 cells were reduced by ATRA treatment. Tretinoin 100-104 homeobox A4 Mus musculus 22-28
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 240-263 transforming growth factor beta induced Homo sapiens 40-79
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 240-263 transforming growth factor beta induced Homo sapiens 81-86
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 240-263 transforming growth factor beta induced Homo sapiens 172-177
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 265-269 transforming growth factor beta induced Homo sapiens 40-79
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 265-269 transforming growth factor beta induced Homo sapiens 81-86
33668680-7 2021 We further show that treatment with retinoic acid, prednisolone, and dorsomorphin all alter Smad9 expression, consistent with the effects of these drugs on the skeletal system. Tretinoin 36-49 SMAD family member 9 Danio rerio 92-97
19516907-11 2009 Our results show that the induction of CdxA, a midgut marker, and pancreas induction require direct RA signaling in endoderm. Tretinoin 100-102 caudal type homeobox 1 Gallus gallus 39-43
33709028-12 2021 Pathway enrichment analysis showed that the DEGs were significantly enriched in the retinoate biosynthesis II, signaling pathways regulating pluripotency of stem cells, ALK2 signaling events, vitamin D3 biosynthesis, cell cycle and aurora B signaling. Tretinoin 84-93 delta 4-desaturase, sphingolipid 1 Homo sapiens 44-48
33709028-12 2021 Pathway enrichment analysis showed that the DEGs were significantly enriched in the retinoate biosynthesis II, signaling pathways regulating pluripotency of stem cells, ALK2 signaling events, vitamin D3 biosynthesis, cell cycle and aurora B signaling. Tretinoin 84-93 activin A receptor type 1 Homo sapiens 169-173
33709028-12 2021 Pathway enrichment analysis showed that the DEGs were significantly enriched in the retinoate biosynthesis II, signaling pathways regulating pluripotency of stem cells, ALK2 signaling events, vitamin D3 biosynthesis, cell cycle and aurora B signaling. Tretinoin 84-93 aurora kinase B Homo sapiens 232-240
33128580-3 2021 Mechanistic investigation revealed that transforming growth factor beta-induced (TGFBI) acts as a potential downstream target of HMGB1 and lentivirus-mediated knockdown of TGFBI expression impaired phorbol-12-myristate-13-acetate (PMA) and all-trans retinoic acid (ATRA)-induced myeloid differentiation of AML cell lines. Tretinoin 265-269 transforming growth factor beta induced Homo sapiens 172-177
33969133-0 2021 Retinoic Acid Correlates with Reduced Serum IL-10 And TGF-beta in Allergic Rhinitis. Tretinoin 0-13 interleukin 10 Homo sapiens 44-49
33969133-7 2021 Conclusion: Our data suggest that RA may influence AR risk via affecting the TGF-beta and IL-10 production. Tretinoin 34-36 interleukin 10 Homo sapiens 90-95
33832420-1 2021 Retinoic acid (RA) binding proteins, CRABP1 and CRABP2, are molecular chaperones that mediate intracellular activity of RA, the key promoter of cell differentiation with tumor suppressor activity. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 48-54
19341714-1 2009 Recent data has implicated the Ski protein as being a physiologically relevant negative regulator of signaling by retinoic acid (RA). Tretinoin 114-127 SKI proto-oncogene Homo sapiens 31-34
33832420-1 2021 Retinoic acid (RA) binding proteins, CRABP1 and CRABP2, are molecular chaperones that mediate intracellular activity of RA, the key promoter of cell differentiation with tumor suppressor activity. Tretinoin 15-17 cellular retinoic acid binding protein 2 Homo sapiens 48-54
33832420-2 2021 One of the main functions of CRABP2 is delivery and transfer of RA to the nuclear receptors RAR/RXR, which leads to activation of the transcription of a wide range of retinoid-responsive genes. Tretinoin 30-32 retinoid X receptor alpha Homo sapiens 96-99
33832420-7 2021 At the same time, we found strong correlation between the expression of CRABP1 and CRABP2 proteins in all studied cell types, regardless of their origin and RA-sensitivity/resistance. Tretinoin 73-75 cellular retinoic acid binding protein 2 Homo sapiens 83-89
33832420-8 2021 Moreover, suppression of the CRABP1 level in both RA-sensitive and RA-resistant cells was shown in the cells with cells with knockdown of CRABP2 gene. Tretinoin 30-32 cellular retinoic acid binding protein 2 Homo sapiens 138-144
33832420-8 2021 Moreover, suppression of the CRABP1 level in both RA-sensitive and RA-resistant cells was shown in the cells with cells with knockdown of CRABP2 gene. Tretinoin 50-52 cellular retinoic acid binding protein 2 Homo sapiens 138-144
33490645-7 2021 Immunoblotting also revealed that ATRA plus urolithin A-treatment up-regulated protein levels of p22-phox (to ~160%) and gp91-phox (to ~170%) although ATRA plus ellagic acid-treatment down-regulated protein levels of p22-phox (to ~70%) and gp91-phox (to ~60%). Tretinoin 34-38 cytochrome b-245 beta chain Homo sapiens 121-130
33490645-7 2021 Immunoblotting also revealed that ATRA plus urolithin A-treatment up-regulated protein levels of p22-phox (to ~160%) and gp91-phox (to ~170%) although ATRA plus ellagic acid-treatment down-regulated protein levels of p22-phox (to ~70%) and gp91-phox (to ~60%). Tretinoin 34-38 cytochrome b-245 beta chain Homo sapiens 240-249
33378690-7 2021 RESULTS: PN induced a unique gene expression profile in mDC, including the gene that encodes retinaldehyde dehydrogenase 2 (RALDH2), a rate-limiting enzyme in the retinoic acid (RA)-producing pathway. Tretinoin 163-176 aldehyde dehydrogenase 1 family member A2 Homo sapiens 124-130
33160998-6 2020 Furthermore, using retinoic acid (RA), we induced hPGCLCs in embryoid bodies and identified positive staining for the meiotic initiation marker STRA8. Tretinoin 19-32 stimulated by retinoic acid 8 Homo sapiens 144-149
33160998-6 2020 Furthermore, using retinoic acid (RA), we induced hPGCLCs in embryoid bodies and identified positive staining for the meiotic initiation marker STRA8. Tretinoin 34-36 stimulated by retinoic acid 8 Homo sapiens 144-149
19341714-1 2009 Recent data has implicated the Ski protein as being a physiologically relevant negative regulator of signaling by retinoic acid (RA). Tretinoin 129-131 SKI proto-oncogene Homo sapiens 31-34
19341714-2 2009 The mechanism by which Ski represses RA signaling is unknown. Tretinoin 37-39 SKI proto-oncogene Homo sapiens 23-26
19341714-3 2009 Co-immunoprecipitation and immunofluorescence assay showed that Ski and RARalpha are in the same complex in both the absence and presence of RA, which makes Ski different from other corepressors. Tretinoin 72-74 SKI proto-oncogene Homo sapiens 157-160
19341714-5 2009 These results suggest that Ski represses RA signaling by stabilizing corepressor complex. Tretinoin 41-43 SKI proto-oncogene Homo sapiens 27-30
32964418-7 2020 ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO). Tretinoin 0-4 caspase 3 Mus musculus 108-117
32964418-7 2020 ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO). Tretinoin 0-4 BCL2-associated X protein Mus musculus 122-125
32964418-7 2020 ATRA mitigated gene expression of markers for damage-associated molecular pattern (DAMP, HMGB1), apoptosis (caspase-3 and Bax), activated microglia (TSPO), and reactive astrogliosis (GFAP, SerpinA3N) at 7 dpi and a subset of markers at 30 dpi (GFAP, TSPO). Tretinoin 0-4 serine (or cysteine) peptidase inhibitor, clade A, member 3N Mus musculus 189-198
33682692-4 2021 OBJECTIVE: The goal of this research is to assess the effect of the vitamin A derivative all-trans retinoic acid (RA) and polyphenol pentagalloyl glucose (PGG) on the expression of elastin in human aortic smooth muscle cells (hASMC). Tretinoin 89-112 elastin Homo sapiens 181-188
32469071-0 2021 Retinoic Acid Is Elevated in the Mucosa of Patients With Active Ulcerative Colitis and Displays a Proinflammatory Role by Augmenting IL-17 and IFNgamma Production. Tretinoin 0-13 interleukin 17A Homo sapiens 133-138
32469071-2 2021 Our previous research highlighted that in the face of inflammatory conditions, RA plays a contrary role where it aggravates intestinal inflammation by promoting interferon (IFN) gamma and interleukin (IL)-17 differentiation in vitro. Tretinoin 79-81 interleukin 17A Homo sapiens 188-207
19324018-0 2009 All-trans retinoic acid induces Thrombospondin-1 expression in acute promyelocytic leukemia cells though down-regulation of its transcription repressor, c-MYC oncoprotein. Tretinoin 10-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 153-158
32469071-6 2021 Moreover, the raised RA levels in patients with active disease showed a positive correlation with proinflammatory cytokines (IL-17, IFNgamma) and a negative correlation with IL-10. Tretinoin 21-23 interleukin 17A Homo sapiens 125-130
32469071-6 2021 Moreover, the raised RA levels in patients with active disease showed a positive correlation with proinflammatory cytokines (IL-17, IFNgamma) and a negative correlation with IL-10. Tretinoin 21-23 interleukin 10 Homo sapiens 174-179
33241870-3 2021 The protein ankyrin repeat domain 17 (Ankrd17), a positive regulator of inflammatory responses via the retinoic acid-inducible gene-I (RIG-I)-like receptor (RLR) signaling pathway, was identified as a specific PA-X binding partner that preferred PA-X to the PA protein. Tretinoin 103-116 ankyrin repeat domain 17 Homo sapiens 12-36
33241870-3 2021 The protein ankyrin repeat domain 17 (Ankrd17), a positive regulator of inflammatory responses via the retinoic acid-inducible gene-I (RIG-I)-like receptor (RLR) signaling pathway, was identified as a specific PA-X binding partner that preferred PA-X to the PA protein. Tretinoin 103-116 ankyrin repeat domain 17 Homo sapiens 38-45
32536235-6 2020 Further studies revealed that ATO/ATRA may suppress the Expression of FLT3-ITD by promoting the UBE2L6-mediated ubiquitination pathway and decreasing the expression of C-MYC. Tretinoin 34-38 ubiquitin conjugating enzyme E2 L6 Homo sapiens 96-102
19324018-2 2009 The aim of the present study was to evaluate the role of c-MYC, a key transcription factor that contributes to the genesis of many human tumors, in TSP-1 induction by ATRA in acute promyelocytic leukemia (APL). Tretinoin 167-171 MYC proto-oncogene, bHLH transcription factor Homo sapiens 57-62
33254555-10 2020 Despite compensatory mechanisms, causes such as high fever, serious catabolic process and excessively large viral genome (SARS-CoV-2), excessive use of RIG-I and Type I interferon synthesis pathway using retinoic acid causes emptying of retinoic acid stores. Tretinoin 204-217 DExD/H-box helicase 58 Homo sapiens 152-157
33254555-10 2020 Despite compensatory mechanisms, causes such as high fever, serious catabolic process and excessively large viral genome (SARS-CoV-2), excessive use of RIG-I and Type I interferon synthesis pathway using retinoic acid causes emptying of retinoic acid stores. Tretinoin 237-250 DExD/H-box helicase 58 Homo sapiens 152-157
33375774-7 2022 Furthermore, the cytotoxic potential of CD38 CAR-NK cells was augmented by pre-treatment of the AML cells with all-trans retinoic acid which drove enhanced CD38 expression offering a rational combination therapy. Tretinoin 121-134 nuclear receptor subfamily 1 group I member 3 Homo sapiens 45-48
19324018-3 2009 ATRA treatment markedly increased TSP-1 level and inhibited c-MYC expression in NB4 APL leukemic cells compared with controls. Tretinoin 0-4 MYC proto-oncogene, bHLH transcription factor Homo sapiens 60-65
32865844-9 2020 The expression of T-bet and IFN-gamma genes in the splenocytes of ATRA, calcitriol and combination- treated mice were significantly reduced compared to vehicle group (p < 0.05). Tretinoin 66-70 T-box 21 Mus musculus 18-23
32865844-10 2020 A significant decrease in T-bet expression was observed in the combination-treated group compared to the ATRA-treated group (p < 0.05). Tretinoin 105-109 T-box 21 Mus musculus 26-31
33112876-0 2020 APC mutations in human colon lead to decreased neuroendocrine maturation of ALDH+ stem cells that alters GLP-2 and SST feedback signaling: Clue to a link between WNT and retinoic acid signalling in colon cancer development. Tretinoin 170-183 somatostatin Homo sapiens 115-118
19324018-5 2009 c-MYC recruitment to TSP-1 promoter was dramatically decreased in NB4 cells following ATRA treatment. Tretinoin 86-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 0-5
33113163-7 2021 The expression of both EGR3 and RELN were decreased during neuronal differentiation induced by retinoic acid (RA) in SH-SY5Y cells, and EGR3 overexpression reduced neurite outgrowth which could be partially reversed by the knockdown of RELN. Tretinoin 95-108 reelin Homo sapiens 32-36
32927254-13 2020 CONCLUSION: Therapeutic supplementation of ATRA rectifies the deregulated Notch, Hedgehog, Wnt, BMP and TGFbeta pathways in emphysema condition, resulting in alveolar epithelium regeneration. Tretinoin 43-47 transforming growth factor alpha Rattus norvegicus 104-111
19324018-7 2009 Moreover, transient over-expression of c-MYC totally abolished TSP-1 induction by ATRA in NB4 cells. Tretinoin 82-86 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-44
33113163-7 2021 The expression of both EGR3 and RELN were decreased during neuronal differentiation induced by retinoic acid (RA) in SH-SY5Y cells, and EGR3 overexpression reduced neurite outgrowth which could be partially reversed by the knockdown of RELN. Tretinoin 110-112 reelin Homo sapiens 32-36
19324018-8 2009 Collectively, our results indicate that ATRA induces TSP-1 expression in APL cells though down-regulation of its transcription repressor, c-MYC oncoprotein. Tretinoin 40-44 MYC proto-oncogene, bHLH transcription factor Homo sapiens 138-143
19451220-4 2009 Here we show that, like PML/RARA, PLZF/RARA expression leads to recruitment of the Polycomb-repressive complex 2 (PRC2) Polycomb group (PcG) complex to RA response elements. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 39-43
33105751-8 2020 CYP26C1 plays a vital role in tissue-specific regulation of retinoic acid (RA) during embryonic development. Tretinoin 60-73 cytochrome P450 26C1 Bos taurus 0-7
33105751-8 2020 CYP26C1 plays a vital role in tissue-specific regulation of retinoic acid (RA) during embryonic development. Tretinoin 75-77 cytochrome P450 26C1 Bos taurus 0-7
33028897-4 2020 Firstly, by using RNASeq we identified two relevant pathways that are activated during 9 days of retinoic acid (RA) induced differentiation i.e. RA receptor (RAR) activation and the cAMP response element-binding protein (CREB) signalling pathways. Tretinoin 97-110 cAMP responsive element binding protein 1 Homo sapiens 182-219
33028897-4 2020 Firstly, by using RNASeq we identified two relevant pathways that are activated during 9 days of retinoic acid (RA) induced differentiation i.e. RA receptor (RAR) activation and the cAMP response element-binding protein (CREB) signalling pathways. Tretinoin 97-110 cAMP responsive element binding protein 1 Homo sapiens 221-225
32048472-4 2020 Differentiation of nephrin (NPHS1)-green fluorescent protein (GFP) iPSCs into kidney podocytes (iPSC-PODs) was performed by the addition of Activin A, bone morphogenetic protein 7 (BMP7), and retinoic acid over 10 days of culture. Tretinoin 192-205 nephrosis 1, nephrin Mus musculus 19-26
33105751-9 2020 Dysregulation of RA can result in teratogenesis by altering the endothelin-1 signaling pathway affecting the expression of Dlx genes, critical to mandibulofacial development. Tretinoin 17-19 endothelin 1 Bos taurus 64-76
33105751-10 2020 We postulate that this recessive missense mutation in CYP26C1 impacts the catalytic activity of the encoded enzyme, leading to excess RA resulting in the observed MD phenotype. Tretinoin 134-136 cytochrome P450 26C1 Bos taurus 54-61
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 PML nuclear body scaffold Homo sapiens 64-67
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 retinoic acid receptor alpha Homo sapiens 68-72
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 retinoic acid receptor alpha Homo sapiens 81-85
33194073-11 2020 These findings suggest that ATRA induces autophagy and autophagic cell death through the Bcl-2/Beclin1 pathway. Tretinoin 28-32 beclin 1 Homo sapiens 95-102
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 retinoic acid receptor alpha Homo sapiens 81-85
33190441-6 2020 ATRA acted on the ERS-related PERK/eif2alpha signaling pathway and continued to increase the ERS of FLT3-ITD cells, resulting in an upregulation of apoptotic gene CHOP expression. Tretinoin 0-4 eukaryotic translation initiation factor 2A Homo sapiens 35-44
19094985-4 2009 The results indicated that atRA treatment up-regulated de novo synthesis of collagen type I, but decreased that of laminin beta1 in a dose-dependent manner. Tretinoin 27-31 laminin subunit beta 1 Homo sapiens 115-128
33190441-9 2020 Conclusions: ATRA further raises the ERS level of FLT3-ITD cells continuously by activating the ERS-related PERK/eif2alpha signal pathway and induces FLT3-ITD protein autophagy degradation through ERAA pathway, which induces apoptosis of FLT3-ITD-mutated leukemia cells. Tretinoin 13-17 eukaryotic translation initiation factor 2A Homo sapiens 113-122
19351818-7 2009 Moreover, the induction of RIG-G by retinoic acid in NB4 cells resulted, to some extent, from an IFNalpha autocrine pathway, a finding that suggests a novel mechanism for the signal cross-talk between IFNalpha and retinoic acid. Tretinoin 36-49 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 27-32
33102941-5 2021 These effects are mainly ascribed to the stereoselective interaction between chiral helical nanofibers and retinol-binding protein 4 (RBP4, a key protein in the retinoic acid (RA) metabolic pathway). Tretinoin 176-178 retinol binding protein 4 Homo sapiens 134-138
32916897-0 2020 Enhanced Antiproliferative Effect of Combined Treatment with Calcitriol and All-Trans Retinoic Acid in Relation to Vitamin D Receptor and Retinoic Acid Receptor alpha Expression in Osteosarcoma Cell Lines. Tretinoin 86-99 vitamin D receptor Homo sapiens 115-133
19351818-7 2009 Moreover, the induction of RIG-G by retinoic acid in NB4 cells resulted, to some extent, from an IFNalpha autocrine pathway, a finding that suggests a novel mechanism for the signal cross-talk between IFNalpha and retinoic acid. Tretinoin 214-227 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 27-32
32916897-4 2020 Although the levels of respective nuclear receptors did not correlate with the sensitivity of cells to these drugs, vitamin D receptor (VDR) upregulation induced by ATRA was found in cell lines that were the most sensitive to the combined treatment. Tretinoin 165-169 vitamin D receptor Homo sapiens 116-134
19345323-3 2009 demonstrate that the Kruppel zinc-finger protein ZNF423 is critical for retinoic acid signaling and is likely a favorable prognostic marker for neuroblastoma. Tretinoin 72-85 zinc finger protein 423 Homo sapiens 49-55
32916897-4 2020 Although the levels of respective nuclear receptors did not correlate with the sensitivity of cells to these drugs, vitamin D receptor (VDR) upregulation induced by ATRA was found in cell lines that were the most sensitive to the combined treatment. Tretinoin 165-169 vitamin D receptor Homo sapiens 136-139
32916897-7 2020 Moreover, we provide the first evidence that ATRA is able to upregulate VDR expression in human osteosarcoma cells. Tretinoin 45-49 vitamin D receptor Homo sapiens 72-75
32916897-8 2020 According to our results, the endogenous levels of RARalpha and VDR could be used as a predictor of possible synergy between ATRA and calcitriol in osteosarcoma cells. Tretinoin 125-129 vitamin D receptor Homo sapiens 64-67
19345331-0 2009 ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome. Tretinoin 34-47 zinc finger protein 423 Homo sapiens 0-6
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 189-214
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 161-174 zinc finger protein 423 Homo sapiens 77-83
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 216-220
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoid X receptor gamma Homo sapiens 260-285
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 161-174 zinc finger protein 423 Homo sapiens 99-104
32770619-2 2020 RA activates downstream pathways through its receptors (retinoic acid receptor alpha [RARA], retinoic acid receptor beta, and retinoic acid receptor gamma [RARG]) and retinoid X receptors (retinoid X receptor alpha [RXRA], retinoid X receptor beta [RXRB], and retinoid X receptor gamma [RXRG]). Tretinoin 0-2 retinoid X receptor gamma Homo sapiens 287-291
32823855-5 2020 The first cancer showing ANXA8 upregulation was reported in acute promyelocytic leukemia (APL), which induces the differentiation arrest of promyelocytes due to defective RA signaling caused by RARA fusion genes as the PML-RARA gene. Tretinoin 171-173 retinoic acid receptor, alpha Mus musculus 194-198
19345331-2 2009 Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OAZ, or Zfp423) as a component critically required for retinoic acid (RA)-induced differentiation. Tretinoin 161-174 zinc finger protein 423 Homo sapiens 106-109
19190084-0 2009 GM-CSF and IL-4 synergistically trigger dendritic cells to acquire retinoic acid-producing capacity. Tretinoin 67-80 interleukin 4 Mus musculus 11-15
32929351-10 2020 The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy. Tretinoin 53-57 tribbles pseudokinase 3 Homo sapiens 13-18
32929351-10 2020 The elevated TRIB3 expression in response to arsenic/ATRA therapy suppressed PPARgamma activity by disrupting the PPARgamma/RXR dimer, which resulted in dyslipidemia in APL patients undergoing therapy. Tretinoin 53-57 retinoid X receptor alpha Homo sapiens 124-127
32929351-11 2020 Indeed, the PPAR activator not only enhanced the anti-APL effects of arsenic/ATRA by suppressing TRIB3 expression but also reduced therapy-induced dyslipidemia in APL patients. Tretinoin 77-81 tribbles pseudokinase 3 Homo sapiens 97-102
32929351-12 2020 Conclusion: Our work reveals the critical role of the PML-RARalpha/PPARgamma/TRIB3 axis in the development of dyslipidemia in APL patients, potentially conferring a rationale for combining ATRA/arsenic with the PPAR activator for APL treatment. Tretinoin 189-193 tribbles pseudokinase 3 Homo sapiens 77-82
19190084-1 2009 Retinoic acid (RA) produced by intestinal dendritic cells (DCs) imprints gut-homing specificity on lymphocytes and enhances Foxp3(+) regulatory T-cell differentiation. Tretinoin 0-13 forkhead box P3 Mus musculus 124-129
19190084-1 2009 Retinoic acid (RA) produced by intestinal dendritic cells (DCs) imprints gut-homing specificity on lymphocytes and enhances Foxp3(+) regulatory T-cell differentiation. Tretinoin 15-17 forkhead box P3 Mus musculus 124-129
19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 nuclear receptor corepressor 1 Homo sapiens 442-446
32437860-7 2020 Furthermore, LjUSP5 inhibited the activation of zebrafish IFN 1 promoter induced by key genes of retinoic acid-inducible gene I-like receptors signaling pathway. Tretinoin 97-110 interferon phi 1 Danio rerio 58-63
32171039-8 2020 Interestingly, the data suggest that all-trans retinoic acid (ATRA)-induced ADAM17-mediated MerTK cleavage plays a critical role in regulating the levels of MerTK receptor on macrophages and that this pathway is impaired in NASH fibrosis. Tretinoin 37-60 ADAM metallopeptidase domain 17 Homo sapiens 76-82
19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 nuclear receptor corepressor 1 Homo sapiens 442-446
19120344-2 2009 Epidermal expression of the heparin-binding epidermal growth factor-like growth factor (HB-EGF) is induced by RA treatment and HB-EGF is responsible for RA-mediated epidermal hyperplasia in vivo. Tretinoin 110-112 heparin binding EGF like growth factor Homo sapiens 88-94
32774702-6 2020 Bioinformatics results indicated that retinoic acid (RA) was likely to be the signaling pathway that Baicalin targeted on, and this was confirmed by whole-mount RALDH2 in situ hybridization and quantitative PCR of HH10 chick embryos in the absence/presence of Baicalin. Tretinoin 53-55 aldehyde dehydrogenase 1 family member A2 Gallus gallus 161-167
19120344-2 2009 Epidermal expression of the heparin-binding epidermal growth factor-like growth factor (HB-EGF) is induced by RA treatment and HB-EGF is responsible for RA-mediated epidermal hyperplasia in vivo. Tretinoin 153-155 heparin binding EGF like growth factor Homo sapiens 88-94
19120344-2 2009 Epidermal expression of the heparin-binding epidermal growth factor-like growth factor (HB-EGF) is induced by RA treatment and HB-EGF is responsible for RA-mediated epidermal hyperplasia in vivo. Tretinoin 153-155 heparin binding EGF like growth factor Homo sapiens 127-133
32513696-1 2020 Retinoic acid-inducible gene I (RIG-I) is up-regulated during granulocytic differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA). Tretinoin 146-169 DExD/H-box helicase 58 Homo sapiens 0-30
32513696-1 2020 Retinoic acid-inducible gene I (RIG-I) is up-regulated during granulocytic differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA). Tretinoin 146-169 DExD/H-box helicase 58 Homo sapiens 32-37
19120344-3 2009 RA also induces HB-EGF expression in cultured keratinocytes and alters their differentiating phenotype. Tretinoin 0-2 heparin binding EGF like growth factor Homo sapiens 16-22
32513696-1 2020 Retinoic acid-inducible gene I (RIG-I) is up-regulated during granulocytic differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA). Tretinoin 171-175 DExD/H-box helicase 58 Homo sapiens 0-30
32513696-1 2020 Retinoic acid-inducible gene I (RIG-I) is up-regulated during granulocytic differentiation of acute promyelocytic leukemia (APL) cells induced by all-trans retinoic acid (ATRA). Tretinoin 171-175 DExD/H-box helicase 58 Homo sapiens 32-37
32513696-4 2020 Herein, we identified a number of RIG-I-binding endogenous RNAs in APL cells following ATRA treatment, including the tripartite motif-containing protein 25 (TRIM25) messenger RNA (mRNA). Tretinoin 87-91 DExD/H-box helicase 58 Homo sapiens 34-39
19120344-8 2009 RESULTS: RA induced HB-EGF and involucrin expression in a concentration-dependent manner, whereas it inhibited keratin 10 expression. Tretinoin 9-11 heparin binding EGF like growth factor Homo sapiens 20-26
32295917-2 2020 Both cellular and viral RNA cleavage products of RNase L bind pattern recognition receptors (PRR) like Retinoic acid-inducible I (Rig-I) and or melanoma differentiation-associated protein 5 (MDA5) to further amplify interferon (IFN) production and antiviral response. Tretinoin 103-116 DExD/H-box helicase 58 Homo sapiens 130-135
19120344-8 2009 RESULTS: RA induced HB-EGF and involucrin expression in a concentration-dependent manner, whereas it inhibited keratin 10 expression. Tretinoin 9-11 keratin 10 Homo sapiens 111-121
32124141-7 2020 CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 77-90 MDM2 proto-oncogene Homo sapiens 227-231
32125053-0 2020 RXRalpha and MRTF-A have a synergistic effect in the retinoic acid-induced neural-like differentiation of adult bone marrow-derived mesenchymal stem cells. Tretinoin 53-66 retinoid X receptor alpha Homo sapiens 0-8
32125053-4 2020 Here, we show that RXRalpha collaborated with myocardin-related transcription factor-A (MRTF-A) to strongly promote the RA-induced process as evidenced by the increase in NF-H expression and NF-H promoter transcription activity. Tretinoin 120-122 retinoid X receptor alpha Homo sapiens 19-27
32125053-7 2020 These findings reveal the important roles of RXRalpha and MRTF-A signaling in RA-induced neural-like differentiation of MSCs and describe a new mechanism underlying the synergistic interaction of RXRalpha and MRTF-A. Tretinoin 78-80 retinoid X receptor alpha Homo sapiens 45-53
32125053-7 2020 These findings reveal the important roles of RXRalpha and MRTF-A signaling in RA-induced neural-like differentiation of MSCs and describe a new mechanism underlying the synergistic interaction of RXRalpha and MRTF-A. Tretinoin 78-80 retinoid X receptor alpha Homo sapiens 196-204
19120344-10 2009 However, when R115866 was combined with low concentrations of RA, HB-EGF and involucrin expression was induced. Tretinoin 62-64 heparin binding EGF like growth factor Homo sapiens 66-72
19385038-9 2009 After induction by retinoic acid for 7 days, some isolated cells differentiated to spermatogonial stem-like cells, expressing Mvh, Stra-8, Hsp90-a, integrinb1 and a6. Tretinoin 19-32 stimulated by retinoic acid gene 8 Mus musculus 131-137
32251704-10 2020 Unexpectedly, VPA showed also a weak, but not marginal, capability to enter the CYP 26A1 and CYP 26C1 catalytic sites, suggesting a possible role of VPA in decreasing RA catabolism, acting as an additional MIE. Tretinoin 167-169 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 93-101
19468269-3 2009 The use of all-trans-retinoic acid (ATRA) and arsenic trioxide, both of which induce degradation of the progressive multifocal leukoencephalopathy/retinoic acid receptor alpha oncoprotein, in combination with chemotherapy is currently the accepted treatment of APL, presenting a potential paradigm for differentiation therapy in clinical oncology. Tretinoin 11-34 retinoic acid receptor alpha Homo sapiens 147-175
31820845-0 2020 Inhibition of UBE2L6 attenuates ISGylation and impedes ATRA-induced differentiation of leukemic cells. Tretinoin 55-59 ubiquitin conjugating enzyme E2 L6 Homo sapiens 14-20
31820845-2 2020 Previous gene expression studies in acute promyelocytic leukemia (APL) cells showed that all-trans-retinoic acid (ATRA) altered the expression of many genes, including UBE2L6 (200-fold) and other members of the ISGylation pathway. Tretinoin 89-112 ubiquitin conjugating enzyme E2 L6 Homo sapiens 168-174
31820845-2 2020 Previous gene expression studies in acute promyelocytic leukemia (APL) cells showed that all-trans-retinoic acid (ATRA) altered the expression of many genes, including UBE2L6 (200-fold) and other members of the ISGylation pathway. Tretinoin 114-118 ubiquitin conjugating enzyme E2 L6 Homo sapiens 168-174
31820845-6 2020 ATRA strongly induced UBE2L6 in NB4 APL cells and in ATRA-sensitive HL60 AML cells, but not in the ATRA-resistant NB4R and HL60R cells. Tretinoin 0-4 ubiquitin conjugating enzyme E2 L6 Homo sapiens 22-28
31820845-7 2020 Furthermore, short hairpin (sh)RNA-mediated UBE2L6 depletion in NB4 cells impeded ATRA-mediated differentiation, suggesting a functional role for UBE2L6 in leukemic cell differentiation. Tretinoin 82-86 ubiquitin conjugating enzyme E2 L6 Homo sapiens 44-50
31820845-9 2020 UBE2L6 depletion attenuated ATRA-induced ISG15 conjugation. Tretinoin 28-32 ubiquitin conjugating enzyme E2 L6 Homo sapiens 0-6
31820845-11 2020 In summary, we demonstrate the functional importance of UBE2L6 in ATRA induced neutrophil differentiation of APL cells and propose that this may be mediated by its catalytic role in ISGylation. Tretinoin 66-70 ubiquitin conjugating enzyme E2 L6 Homo sapiens 56-62
19468269-3 2009 The use of all-trans-retinoic acid (ATRA) and arsenic trioxide, both of which induce degradation of the progressive multifocal leukoencephalopathy/retinoic acid receptor alpha oncoprotein, in combination with chemotherapy is currently the accepted treatment of APL, presenting a potential paradigm for differentiation therapy in clinical oncology. Tretinoin 36-40 retinoic acid receptor alpha Homo sapiens 147-175
18652909-9 2009 In addition, we found that both retinoic acid and retinol induced transcripts for the STRA6 gene, which encodes a membrane receptor involved in retinol (vitamin A) uptake, in PrEC cells but not in PC-3 cells. Tretinoin 32-45 signaling receptor and transporter of retinol STRA6 Homo sapiens 86-91
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 141-160 interleukin 4 Sus scrofa 32-35
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 141-160 C-C motif chemokine ligand 26 Homo sapiens 54-59
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 162-166 interleukin 4 Sus scrofa 32-35
32431691-1 2020 We previously demonstrated that IL4, IL13, CLCA1, and CCL26 mRNA were significantly upregulated in the lungs of pigs given a low dose of all trans-retinoic acid (ATRA) and infected with Ascaris suum. Tretinoin 162-166 C-C motif chemokine ligand 26 Homo sapiens 54-59
32431691-4 2020 ATRA also increased IL-4 induced phosphorylation of signal transducer and activator of transcription 6 (STAT6) and mRNA expression of the chloride channel, calcium activated, family member 1 (CLCA1), important for mucus formation, and chemokine (C-C motif) ligand 26 (CCL26), a potent eosinophil chemoattractant. Tretinoin 0-4 C-C motif chemokine ligand 26 Homo sapiens 268-273
19135033-1 2009 The POU family transcription factor Brn-3a is required for the differentiation and survival of sensory neurones, and is phosphorylated in neuroblastoma cells following treatment with all-trans retinoic acid (RA). Tretinoin 193-206 POU class 4 homeobox 1 Homo sapiens 36-42
32431691-5 2020 We extended these findings to human Mphi THP-1 cells and showed that ATRA synergistically increased IL-4-induced CCL2, CCL13, and CCL26 mRNA and protein levels. Tretinoin 69-73 C-C motif chemokine ligand 26 Homo sapiens 130-135
19135033-1 2009 The POU family transcription factor Brn-3a is required for the differentiation and survival of sensory neurones, and is phosphorylated in neuroblastoma cells following treatment with all-trans retinoic acid (RA). Tretinoin 208-210 POU class 4 homeobox 1 Homo sapiens 36-42
19135033-2 2009 Mutation of serines-121 and -122 of Brn-3a to alanine blocks its phosphorylation and impairs RA-mediated neurite outgrowth. Tretinoin 93-95 POU class 4 homeobox 1 Homo sapiens 36-42
31868199-2 2020 Vitamin A circulates mainly as retinol bound to retinol-binding protein 4 (RBP4), and is delivered to tissues and converted to retinoic acid, which is a ligand for several nuclear receptors. Tretinoin 127-140 retinol binding protein 4 Homo sapiens 75-79
19135033-5 2009 We show that Brn-3a over-expression acts synergistically with RA treatment to up-regulate Galanin promoter activity; that the activity of the N-terminal transcriptional activation domain of Brn-3a is increased following RA treatment; and that both these effects require threonine-39 and serine-122. Tretinoin 220-222 POU class 4 homeobox 1 Homo sapiens 13-19
32323852-5 2020 In addition, through transient expression assays in breast cancer cells, it was revealed that a transcriptional mechanism dependent on protein kinase A and susceptible to retinoic acid in ER-positive cells induces GPR30 expression through a cis-regulatory element for E26 transformation-specific transcription factors, located between -631 and -625 bp from the GPR30 translation start codon. Tretinoin 171-184 G protein-coupled estrogen receptor 1 Homo sapiens 214-219
33029001-7 2020 By combining quantitative imaging with RNA sequencing, we show the role of endogenous retinoic acid metabolism in initiating transcriptional programs that guide the cell-fate transitions of intestinal epithelium, and we identify an inhibitor of the retinoid X receptor that improves intestinal regeneration in vivo. Tretinoin 86-99 retinoid X receptor alpha Homo sapiens 249-268
32323852-5 2020 In addition, through transient expression assays in breast cancer cells, it was revealed that a transcriptional mechanism dependent on protein kinase A and susceptible to retinoic acid in ER-positive cells induces GPR30 expression through a cis-regulatory element for E26 transformation-specific transcription factors, located between -631 and -625 bp from the GPR30 translation start codon. Tretinoin 171-184 G protein-coupled estrogen receptor 1 Homo sapiens 361-366
32970669-8 2020 Importantly, inhibition of retinoic acid signaling by the aldehyde dehydrogenase (Aldh) and retinoic acid receptor inhibitors promoted Pou4f3 expression in the cochlear tissue and suppressed the progression of hearing loss in the mutant mice. Tretinoin 27-40 POU domain, class 4, transcription factor 3 Mus musculus 135-141
19135033-5 2009 We show that Brn-3a over-expression acts synergistically with RA treatment to up-regulate Galanin promoter activity; that the activity of the N-terminal transcriptional activation domain of Brn-3a is increased following RA treatment; and that both these effects require threonine-39 and serine-122. Tretinoin 220-222 POU class 4 homeobox 1 Homo sapiens 190-196
19028692-7 2009 Deletion of the enzyme specifically in the epidermis causes alopecia, indicating that the regulation of RA homeostasis by DGAT1 is autonomous in the epidermis. Tretinoin 104-106 diacylglycerol O-acyltransferase 1 Mus musculus 122-127
32680882-5 2020 Thereby, Nsp1 effectively blocks retinoic acid-inducible gene I-dependent innate immune responses that would otherwise facilitate clearance of the infection. Tretinoin 33-46 SH2 domain containing 3A Homo sapiens 9-13
31858119-6 2020 Butyrate upregulated the production of transforming growth factor beta1 and all-trans retinoic acid by CD103+CD11b+ dendritic cells, both of which are critical for T-cell-independent IgA CSR. Tretinoin 86-99 integrin subunit alpha M Homo sapiens 109-114
32020743-4 2020 Here, we show that RA directly downregulates Gdnf mRNA levels in primary murine Sertoli cells through binding of RARalpha to a novel DR5-RARE on Gdnf promoter. Tretinoin 19-21 retinoic acid receptor, alpha Mus musculus 113-121
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 125-127 integrin subunit alpha M Homo sapiens 187-192
32256976-8 2020 Roscovitine also enhanced the ATRA-induced nuclear enrichment of other signaling molecules traditionally perceived as cytoplasmic promoters of proliferation, but now known to promote differentiation; in particular: SFKs, Lyn, Fgr; adaptor proteins, c-Cbl, SLP-76; a guanine exchange factor, Vav1; and a transcription factor, IRF-1. Tretinoin 30-34 lymphocyte cytosolic protein 2 Homo sapiens 256-262
31676951-8 2020 Furthermore, CYP26A1 a retinoic acid receptor-specific target was revealed as a new player mediating the suppressive effect of fish oil-supplemented diet on SCD1 and ELOVL6 hepatic gene expression. Tretinoin 23-36 stearoyl-Coenzyme A desaturase 1 Mus musculus 157-161
19216755-0 2009 Chmp 1A is a mediator of the anti-proliferative effects of all-trans retinoic acid in human pancreatic cancer cells. Tretinoin 69-82 charged multivesicular body protein 1A Homo sapiens 0-7
32705508-2 2020 HEPC-CB.1 cells" potential to differentiate into endothelial cells was revealed after treating the cells with a mixture of ATRA, cAMP and VEGF, as shown by the reduced expression levels of CD133, CD271 and CD90 antigens, augmentation of CD146 and CD31, and a decrease in cell clonogenicity. Tretinoin 123-127 melanoma cell adhesion molecule Homo sapiens 237-242
32169218-3 2020 Using multiple murine sarcoma models, we find that the TME induces tumor cells to produce retinoic acid (RA), which polarizes intratumoral monocyte differentiation toward TAMs and away from DCs via suppression of DC-promoting transcription factor Irf4. Tretinoin 90-103 interferon regulatory factor 4 Mus musculus 247-251
32169218-3 2020 Using multiple murine sarcoma models, we find that the TME induces tumor cells to produce retinoic acid (RA), which polarizes intratumoral monocyte differentiation toward TAMs and away from DCs via suppression of DC-promoting transcription factor Irf4. Tretinoin 105-107 interferon regulatory factor 4 Mus musculus 247-251
19216755-5 2009 The objective of our study was to investigate whether Chmp1A is involved in ATRA-mediated growth inhibition of human pancreatic tumor cells. Tretinoin 76-80 charged multivesicular body protein 1A Homo sapiens 54-60
32258025-0 2020 Inhibition of GSK3 Represses the Expression of Retinoic Acid Synthetic Enzyme ALDH1A2 via Wnt/beta-Catenin Signaling in WiT49 Cells. Tretinoin 47-60 aldehyde dehydrogenase 1 family member A2 Homo sapiens 78-85
32548665-7 2020 ATRA could completely reverse the impaired retinoic acid receptor alpha (RARalpha) signal in the spinal cord of ALS mice. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 43-71
32548665-7 2020 ATRA could completely reverse the impaired retinoic acid receptor alpha (RARalpha) signal in the spinal cord of ALS mice. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 73-81
19216755-8 2009 Since our microarray data indicates a potential involvement of Chmp1A in ATRA signaling, we tested this hypothesis by treating pancreatic tumor cells with ATRA in vitro. Tretinoin 73-77 charged multivesicular body protein 1A Homo sapiens 63-69
32193285-8 2020 Together our study reveals that Pin1 inhibition with widely used ATRA acts as an effective HR disrupter that sensitizes BRCA1-proficient tumors to PARP inhibition. Tretinoin 65-69 BRCA1 DNA repair associated Homo sapiens 120-125
19216755-10 2009 We found that knockdown of Chmp1A via shRNA abolished the ATRA-mediated growth inhibition of PanC-1 cells. Tretinoin 58-62 charged multivesicular body protein 1A Homo sapiens 27-33
32630207-8 2020 We show that ATRA alleviates the negative feedback loop effect of IL-10 anti-inflammatory cytokine on NLRP3 inflammasome function by inhibiting the Akt-mTOR-STAT3 signaling axis. Tretinoin 13-17 interleukin 10 Homo sapiens 66-71
31634391-9 2020 All-trans retinoic acid altered IFN-gamma signaling via blocking IFN-gamma-induced tyrosine phosphorylation of STAT-1. Tretinoin 0-23 signal transducer and activator of transcription 1 Homo sapiens 111-117
19216755-11 2009 Also, Chmp1A silencing diminished the increase of Chmp1A, P53 and phospho-P53 protein expression induced by ATRA. Tretinoin 108-112 charged multivesicular body protein 1A Homo sapiens 6-12
31634391-12 2020 CONCLUSION: Our data showing upregulation of DRA under normal and inflammatory conditions by ATRA demonstrate a novel role of this micronutrient in alleviating IBD-associated diarrhea. Tretinoin 93-97 solute carrier family 26, member 3 Mus musculus 45-48
19216755-11 2009 Also, Chmp1A silencing diminished the increase of Chmp1A, P53 and phospho-P53 protein expression induced by ATRA. Tretinoin 108-112 charged multivesicular body protein 1A Homo sapiens 50-56
19216755-14 2009 Interestingly, in ATRA responsive cells Chmp1A is localized to the nucleus, which became robust upon ATRA treatment. Tretinoin 18-22 charged multivesicular body protein 1A Homo sapiens 40-46
31862304-11 2020 Together, our data demonstrate that SNAI2 maintains progenitor-like features in neuroblastoma cells while interfering with RA-induced growth inhibition. Tretinoin 123-125 snail family transcriptional repressor 2 Homo sapiens 36-41
32685464-1 2020 Cellular retinoic acid-binding protein 2 (CRABP2) binds retinoic acid (RA) in the cytoplasm and transports it into the nucleus, allowing for the regulation of specific downstream signal pathway. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 42-48
32685464-1 2020 Cellular retinoic acid-binding protein 2 (CRABP2) binds retinoic acid (RA) in the cytoplasm and transports it into the nucleus, allowing for the regulation of specific downstream signal pathway. Tretinoin 43-45 cellular retinoic acid binding protein 2 Homo sapiens 0-40
31862304-12 2020 We propose that targeting gene regulatory circuits, such as those controlling SNAI2 function, may allow reversion of RA-therapy resistant neuroblastoma cells to a more differentiated and therapy responsive phenotype. Tretinoin 117-119 snail family transcriptional repressor 2 Homo sapiens 78-83
19216755-15 2009 In the ATRA-non-responsive cells, Chmp1A was mainly translocated to the plasma membrane upon ATRA treatment. Tretinoin 7-11 charged multivesicular body protein 1A Homo sapiens 34-40
19216755-16 2009 CONCLUSION: Collectively our data provides evidence that Chmp1A mediates the growth inhibitory activity of ATRA in human pancreatic cancer cells via regulation of CRBP-1. Tretinoin 107-111 charged multivesicular body protein 1A Homo sapiens 57-63
32027669-2 2020 Cyp1b1 is not expressed in perinatal liver but appears in the E9.5 embryo, close to sites of retinoic acid (RA) signaling. Tretinoin 108-110 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 0-6
19027885-1 2009 A tetracycline inducible transfectant cell line (3D5) capable of producing soluble and sarkosyl-insoluble assemblies of wild-type human alpha-synuclein (alpha-Syn) upon differentiation with retinoic acid was used to study the impact of alpha-Syn accumulation on protein phosphorylation and glycosylation. Tretinoin 190-203 synuclein alpha Homo sapiens 136-151
31666191-14 2020 These results indicated that TG2 expression was upregulated through ATRA-mediated RARgamma and that extracellular TG2 induced myotube hypertrophy by activating mTOR signaling-mediated protein synthesis through GPR56, independent of transglutaminase activity. Tretinoin 68-72 retinoic acid receptor, gamma Mus musculus 82-90
31706164-1 2020 Hepatitis B virus (HBV) X protein (HBx) has been reported to counteract the innate immune responses through interfering with the pattern recognition receptors signaling activated by retinoic acid-inducible gene-I (RIG-I)-mitochondrial antiviral signaling protein (MAVS). Tretinoin 182-195 DExD/H-box helicase 58 Homo sapiens 214-219
32013828-2 2020 The RA transporter, Cellular Retinoic-Acid Binding Protein 2 (CRABP2), abnormally expressed in various tumor types. Tretinoin 4-6 cellular retinoic acid binding protein 2 Homo sapiens 20-60
32013828-2 2020 The RA transporter, Cellular Retinoic-Acid Binding Protein 2 (CRABP2), abnormally expressed in various tumor types. Tretinoin 4-6 cellular retinoic acid binding protein 2 Homo sapiens 62-68
32173553-5 2020 The ERRgamma agonist GSK4716 increased DAT and TH expression, and the ERRgamma inverse agonist GSK5182 attenuated the retinoic acid-induced upregulation of DAT and TH in differentiated SH-SY5Y cells. Tretinoin 118-131 solute carrier family 6 member 3 Homo sapiens 156-159
32455804-2 2020 Resistance to all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) has been suggested in PLZF/RARalpha and other variant APLs. Tretinoin 14-37 zinc finger and BTB domain containing 16 Homo sapiens 94-98
32455804-2 2020 Resistance to all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) has been suggested in PLZF/RARalpha and other variant APLs. Tretinoin 39-43 zinc finger and BTB domain containing 16 Homo sapiens 94-98
32217463-8 2020 After RA treatment, chromatin immunoprecipitation assays using an antibody against NCOR1, revealed that NCOR1 binding to RARbeta promoters was significantly lower in Sirt1-/- mESCs than in Sirt1+/+ mESCs, and luciferase reporter assays showed SIRT1 knockdown decreased RA-induced RARalpha activity. Tretinoin 6-8 retinoic acid receptor, alpha Mus musculus 121-128
32258025-1 2020 Organogenesis, including renal development, requires an appropriate retinoic acid concentration, which is established by differential expression of aldehyde dehydrogenase 1 family member A2 (ALDH1A2) and cytochrome P450 family 26 subfamily A/B/C member 1 (CYP26A1/B1/C1). Tretinoin 68-81 aldehyde dehydrogenase 1 family member A2 Homo sapiens 148-189
32258025-1 2020 Organogenesis, including renal development, requires an appropriate retinoic acid concentration, which is established by differential expression of aldehyde dehydrogenase 1 family member A2 (ALDH1A2) and cytochrome P450 family 26 subfamily A/B/C member 1 (CYP26A1/B1/C1). Tretinoin 68-81 aldehyde dehydrogenase 1 family member A2 Homo sapiens 191-198
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 matrix metallopeptidase 9 Rattus norvegicus 242-247
19027885-1 2009 A tetracycline inducible transfectant cell line (3D5) capable of producing soluble and sarkosyl-insoluble assemblies of wild-type human alpha-synuclein (alpha-Syn) upon differentiation with retinoic acid was used to study the impact of alpha-Syn accumulation on protein phosphorylation and glycosylation. Tretinoin 190-203 synuclein alpha Homo sapiens 153-162
31732869-2 2020 RA signaling is mediated by nuclear retinoic acid receptors, alpha, beta, and gamma (RARalpha, RARbeta, and RARgamma). Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 85-93
19141675-3 2009 We have recently identified the Xenopus homologue of retinol dehydrogenase 10 (XRDH10) that mediates the first step in RA synthesis from retinol to retinal. Tretinoin 119-121 retinol dehydrogenase 10 L homeolog Xenopus laevis 79-85
31732869-2 2020 RA signaling is mediated by nuclear retinoic acid receptors, alpha, beta, and gamma (RARalpha, RARbeta, and RARgamma). Tretinoin 0-2 retinoic acid receptor, gamma Mus musculus 108-116
31732869-2 2020 RA signaling is mediated by nuclear retinoic acid receptors, alpha, beta, and gamma (RARalpha, RARbeta, and RARgamma). Tretinoin 36-49 retinoic acid receptor, alpha Mus musculus 85-93
31732869-2 2020 RA signaling is mediated by nuclear retinoic acid receptors, alpha, beta, and gamma (RARalpha, RARbeta, and RARgamma). Tretinoin 36-49 retinoic acid receptor, gamma Mus musculus 108-116
31862304-0 2020 The transcriptional repressor SNAI2 impairs neuroblastoma differentiation and inhibits response to retinoic acid therapy. Tretinoin 99-112 snail family transcriptional repressor 2 Homo sapiens 30-35
31862304-10 2020 Loss of SNAI2 function reduces self-renewal, 3D invasion as well as metastatic spread in vivo, while strongly sensitizing neuroblastoma cells to RA-induced growth inhibition. Tretinoin 145-147 snail family transcriptional repressor 2 Homo sapiens 8-13
31449909-4 2019 Knockdown of the retinoic acid degradation enzyme cytochrome p450 family 26 subfamily b member 1 (Cyp26b1) in the nucleus accumbens shell increased depression-related behavior while decreasing anxiety-like behavior. Tretinoin 17-30 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 50-96
31449909-4 2019 Knockdown of the retinoic acid degradation enzyme cytochrome p450 family 26 subfamily b member 1 (Cyp26b1) in the nucleus accumbens shell increased depression-related behavior while decreasing anxiety-like behavior. Tretinoin 17-30 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 98-105
31921854-6 2019 The lncRNA maternally expressed 3 is up-regulated by the ATRA/cAMP/CREB pathway, and it, in turn, is directly down-regulated by miR-128-3p to increase the amount of neuron differentiation. Tretinoin 57-61 cAMP responsive element binding protein 1 Homo sapiens 67-71
19141675-5 2009 We show that endogenous RA suppresses XRDH10 gene expression, suggesting negative-feedback regulation. Tretinoin 24-26 retinol dehydrogenase 10 L homeolog Xenopus laevis 38-44
19246282-1 2009 OBJECTIVE: To investigate the molecular mechanism of dermal damage in heat shock-induced skin aging by observing the expressions of metalloproteinase-1 (MMP-1) and tissue inhibitor of MMP-1 (TIMP-1) in retinoic acid-treated cultured human fibroblasts with heat shock. Tretinoin 202-215 matrix metallopeptidase 1 Homo sapiens 153-158
31822659-0 2019 All-trans retinoic acid enhances, and a pan-RAR antagonist counteracts, the stem cell promoting activity of EVI1 in acute myeloid leukemia. Tretinoin 10-23 MDS1 and EVI1 complex locus Homo sapiens 108-112
31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 185-205 MDS1 and EVI1 complex locus Homo sapiens 0-34
31400045-3 2020 Interestingly, CYP1B1, a cytochrome P450 enzyme, is able to mediate the oxidative metabolisms also leading to RA generation, its expression patterns being associated with many known sites of RA activity. Tretinoin 110-112 cytochrome P450 family 1 subfamily B member 1 Gallus gallus 15-21
31400045-3 2020 Interestingly, CYP1B1, a cytochrome P450 enzyme, is able to mediate the oxidative metabolisms also leading to RA generation, its expression patterns being associated with many known sites of RA activity. Tretinoin 191-193 cytochrome P450 family 1 subfamily B member 1 Gallus gallus 15-21
31400045-4 2020 RESULTS: This study describes for the first time the presence of CYP1B1 in the developing chick inner ear as a RALDH-independent RA-signaling mechanism. Tretinoin 111-113 cytochrome P450 family 1 subfamily B member 1 Gallus gallus 65-71
31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 185-205 MDS1 and EVI1 complex locus Homo sapiens 36-40
31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 207-211 MDS1 and EVI1 complex locus Homo sapiens 0-34
19255510-0 2009 Negative functional interaction of retinoic acid and TGF-beta signaling mediated by TG-interacting factor during chondrogenesis. Tretinoin 35-48 TGFB-induced factor homeobox 1 Mus musculus 84-105
31822659-1 2019 Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. Tretinoin 207-211 MDS1 and EVI1 complex locus Homo sapiens 36-40
31822659-5 2019 atRA further augmented these effects in an Evi1 dependent manner. Tretinoin 0-4 MDS1 and EVI1 complex locus Mus musculus 43-47
19255510-5 2009 Functional assays indicated that TGF-beta3 treatment or co-transfection of expressing Smad2/3 vectors suppressed atRA-induced RARE-tk-Luc activity. Tretinoin 113-117 transforming growth factor, beta 3 Mus musculus 33-42
31957262-9 2020 Short-term (2 h) co-administration of 10 muM ATRA and Hst1 to pre-osteoblasts resulted in significantly higher spreading of pre-osteoblasts compared to ATRA or Hst1 alone. Tretinoin 45-49 histatin 1 Homo sapiens 160-164
31957262-9 2020 Short-term (2 h) co-administration of 10 muM ATRA and Hst1 to pre-osteoblasts resulted in significantly higher spreading of pre-osteoblasts compared to ATRA or Hst1 alone. Tretinoin 152-156 histatin 1 Homo sapiens 54-58
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 TGFB-induced factor homeobox 1 Mus musculus 35-39
31957262-11 2020 Co-administration of ATRA and Hst1 was associated with significantly higher metabolic activity, DNA content and ALP activity than either ATRA or Hst1 alone. Tretinoin 21-25 histatin 1 Homo sapiens 145-149
31957262-11 2020 Co-administration of ATRA and Hst1 was associated with significantly higher metabolic activity, DNA content and ALP activity than either ATRA or Hst1 alone. Tretinoin 137-141 histatin 1 Homo sapiens 30-34
31805626-8 2019 Finally, we identified the signaling pathways regulated by LSD1 in HCC, including the retinoic acid (RA) pathway. Tretinoin 86-99 lysine demethylase 1A Homo sapiens 59-63
31805626-8 2019 Finally, we identified the signaling pathways regulated by LSD1 in HCC, including the retinoic acid (RA) pathway. Tretinoin 101-103 lysine demethylase 1A Homo sapiens 59-63
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 TGFB-induced factor homeobox 1 Mus musculus 142-146
31646671-10 2020 The expression of Mvh protein significantly increased in the RA group on day 7. Tretinoin 61-63 DEAD box helicase 4 Mus musculus 18-21
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 transforming growth factor, beta 3 Mus musculus 199-208
31646671-11 2020 The Mvh expression was also enhanced in the P group on day 4, but it decreased on day 7, while this protein upregulated on day 0 and 7 in the RA + P group. Tretinoin 142-144 DEAD box helicase 4 Mus musculus 4-7
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 TGFB-induced factor homeobox 1 Mus musculus 142-146
31586630-9 2019 Moreover, ATRA/TGF-beta MPs treatment resulted in increased Treg proliferation and frequency of CTLA-4+PD1+ and CD39+IL-10+ Tregs, suggestive of their higher suppressive capacity. Tretinoin 10-14 cytotoxic T-lymphocyte-associated protein 4 Mus musculus 96-102
31372995-5 2019 In mesenteric lymph nodes, retinoic acid (RA) released by CD103+ dendritic cells downregulated lamin A/C in CD4+ T-cells, enhancing Treg differentiation. Tretinoin 27-40 CD4 antigen Mus musculus 108-111
31372995-5 2019 In mesenteric lymph nodes, retinoic acid (RA) released by CD103+ dendritic cells downregulated lamin A/C in CD4+ T-cells, enhancing Treg differentiation. Tretinoin 42-44 CD4 antigen Mus musculus 108-111
31165892-6 2020 The second-most significant site (P = 1.38 x 10-9, q = 0.013) was located in ALDH1A2, which encodes an enzyme for astrocyte-derived retinoic acid-a key neuronal morphogen with relevance for schizophrenia. Tretinoin 132-145 aldehyde dehydrogenase 1 family member A2 Homo sapiens 77-84
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 transforming growth factor, beta 3 Mus musculus 290-299
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 311-315 TGFB-induced factor homeobox 1 Mus musculus 35-39
31806367-1 2020 The retinoic-acid inducible gene (RIG)-I is a cytoplasmic pattern recognition receptor that senses single-stranded (ss) or double-stranded (ds) RNA. Tretinoin 4-17 DExD/H-box helicase 58 Homo sapiens 34-40
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 99-118 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 53-60
31419517-2 2019 The three CYP26 family enzymes, CYP26A1, CYP26B1 and CYP26C1 have all been shown to metabolize all-trans-retinoic acid (atRA) it"s 9-cisRA and 13-cisRA isomers and primary metabolites 4-OH-RA and 4-oxo-RA with high efficiency. Tretinoin 120-124 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 53-60
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 311-315 TGFB-induced factor homeobox 1 Mus musculus 142-146
31768440-1 2019 Objective: To identify an agonist of RXRalpha and RARalpha with reduced undesired profiles of all-trans retinoic acid for differentiation-inducing therapy of acute promyelocytic leukemia (APL), such as its susceptibility to P450 enzyme, induction of P450 enzyme, increased sequestration by cellular retinoic acid binding protein and increased expression of P-glycoprotein, a virtual screening was performed. Tretinoin 94-117 retinoid X receptor alpha Homo sapiens 37-45
19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 311-315 TGFB-induced factor homeobox 1 Mus musculus 142-146
31768440-1 2019 Objective: To identify an agonist of RXRalpha and RARalpha with reduced undesired profiles of all-trans retinoic acid for differentiation-inducing therapy of acute promyelocytic leukemia (APL), such as its susceptibility to P450 enzyme, induction of P450 enzyme, increased sequestration by cellular retinoic acid binding protein and increased expression of P-glycoprotein, a virtual screening was performed. Tretinoin 104-117 retinoid X receptor alpha Homo sapiens 37-45
19255510-9 2009 Furthermore, we demonstrated that the effects of atRA on TGF-beta-dependent gene activation and of TGF-beta on RA-dependent gene activation are mediated by TGIF with siRNA to downregulate TGIF. Tretinoin 49-53 TGFB-induced factor homeobox 1 Mus musculus 156-160
32030959-17 2020 qRT-PCR test showed that the combined use of ATRA and Ad-VEGF also increased the relative mRNA expressions of early-stage osteogenesis-related markers ALP, OPN, and collagen type I ( P<0.05); the relative mRNA expressions of angiogenesis-related markers VEGF, EMCN, and ANGPT1 increased at 7 days ( P<0.05). Tretinoin 45-49 vascular endothelial growth factor A Mus musculus 257-261
32030959-18 2020 Immunohistochemical staining showed that ATRA combined with Ad-VEGF not only enhanced OPN protein expression, but also increased VEGF protein expression on 7th day. Tretinoin 41-45 vascular endothelial growth factor A Mus musculus 129-133
19255510-9 2009 Furthermore, we demonstrated that the effects of atRA on TGF-beta-dependent gene activation and of TGF-beta on RA-dependent gene activation are mediated by TGIF with siRNA to downregulate TGIF. Tretinoin 49-53 TGFB-induced factor homeobox 1 Mus musculus 188-192
31597660-1 2019 Retinoic acid (RA) is critical for mammalian spermatogonia differentiation, and stimulates Stra8 expression, a gene required for meiosis. Tretinoin 0-13 stimulated by retinoic acid 8 Homo sapiens 91-96
19088275-2 2009 Here we show that retinoic acid-inducible gene (RIG)-I-like receptors (RLRs) in cooperation with Toll-like receptor (TLR) 9 is required for expression of type I interferons (IFNs) after infection with herpes simplex virus (HSV). Tretinoin 18-31 toll like receptor 4 Homo sapiens 97-101
31597660-1 2019 Retinoic acid (RA) is critical for mammalian spermatogonia differentiation, and stimulates Stra8 expression, a gene required for meiosis. Tretinoin 15-17 stimulated by retinoic acid 8 Homo sapiens 91-96
31682623-5 2019 MEK1/2 inhibitor (U0126) treatment suppressed the mRNA expressions of RA-induced Stra8 and meiotic marker genes (Rec8, Spo11, Dmc1, and Sycp3) in both XX and XY fetal germ cells. Tretinoin 70-72 SPO11 initiator of meiotic double stranded breaks Mus musculus 119-124
32075033-2 2020 Here, the HSER (Homo sapiens retinoic acid receptor) peptide was designed from retinoic acid receptor responder protein 2 of Homo sapiens, and was conjugated with synthesized CQDs (carbon quantum dots) for enhanced antibacterial activity in combination, as individually they are not highly effective. Tretinoin 29-42 retinoic acid receptor responder 2 Homo sapiens 79-121
19088275-2 2009 Here we show that retinoic acid-inducible gene (RIG)-I-like receptors (RLRs) in cooperation with Toll-like receptor (TLR) 9 is required for expression of type I interferons (IFNs) after infection with herpes simplex virus (HSV). Tretinoin 18-31 toll like receptor 4 Homo sapiens 117-120
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 61-63 CD38 molecule Homo sapiens 108-112
31298420-0 2020 Upregulation of amphiregulin by retinoic acid and Wnt signalling promotes liver cancer cell proliferation. Tretinoin 32-45 amphiregulin Homo sapiens 16-28
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 184-186 CD38 molecule Homo sapiens 108-112
31898934-3 2020 Transcriptome screen and in vivo functional studies revealed that the elevated level of retinoic acid (RA) caused by de-repression of RA metabolic process genes as a result of RBP-J deletion in HFSCs triggers ectopic McSCs differentiation in the niche. Tretinoin 88-101 retinol binding protein 4, plasma Mus musculus 176-179
31898934-3 2020 Transcriptome screen and in vivo functional studies revealed that the elevated level of retinoic acid (RA) caused by de-repression of RA metabolic process genes as a result of RBP-J deletion in HFSCs triggers ectopic McSCs differentiation in the niche. Tretinoin 103-105 retinol binding protein 4, plasma Mus musculus 176-179
31648727-6 2019 Mechanically, we found that JEV infection increases the expression of retinoic acid-inducible gene I (RIG-I) and activates transcription factor NF-kappaB. Tretinoin 70-83 DExD/H-box helicase 58 Homo sapiens 102-107
31898934-3 2020 Transcriptome screen and in vivo functional studies revealed that the elevated level of retinoic acid (RA) caused by de-repression of RA metabolic process genes as a result of RBP-J deletion in HFSCs triggers ectopic McSCs differentiation in the niche. Tretinoin 134-136 retinol binding protein 4, plasma Mus musculus 176-179
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 24-47 nuclear receptor subfamily 2 group C member 1 Homo sapiens 151-154
31615043-1 2019 Aldehyde dehydrogenase 1 family member A2 (ALDH1A2) is a rate-limiting enzyme involved in cellular retinoic acid synthesis. Tretinoin 99-112 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-41
31615043-1 2019 Aldehyde dehydrogenase 1 family member A2 (ALDH1A2) is a rate-limiting enzyme involved in cellular retinoic acid synthesis. Tretinoin 99-112 aldehyde dehydrogenase 1 family member A2 Homo sapiens 43-50
19204783-7 2009 Recently, we found that all-trans retinoic acid (atRA) triggers the activation of extracellular-signal-regulated kinase 2 (ERK2), which phosphorylates TR2 and stimulates its partitioning to promyelocytic leukemia (PML) nuclear bodies, thereby converting the activator function of TR2 into repression (Gupta et al. Tretinoin 24-47 PML nuclear body scaffold Homo sapiens 214-217
33583383-8 2020 However, the electrophysiological properties of the Retinoic Acid + Brain-Derived Neurotrophic Factor differentiated cells were significantly altered after Amyloid Beta treatment. Tretinoin 52-65 brain derived neurotrophic factor Homo sapiens 68-101
18976680-2 2009 The postulated mechanism for the dysmorphogenetic effects is the inhibition of retinoic acid (RA)-degrading enzyme CYP26. Tretinoin 79-92 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 115-120
32359644-7 2020 Retinoic acid incorporation into the ligand-binding domain leads to a conformational change enabling the formation of RAR homodimers or RAR/RXR heterodimers that in turn bind specifically to target DNA sequences. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 140-143
31606046-8 2019 H1d knockdown primed ATRA-mediated differentiation of OCI-AML3 and U937 AML cell lines, as assessed on CD11b/CD11c markers, morphological and gene expression analyses. Tretinoin 21-25 integrin subunit alpha M Homo sapiens 103-108
31394504-8 2019 The enhanced inhibitory interaction between RA and BMP-4 pathways occurs also in another relevant corticotroph gene promoter, the Corticotropin-releasing hormone receptor 1 (CRH-R1). Tretinoin 44-46 corticotropin releasing hormone receptor 1 Mus musculus 130-172
31394504-8 2019 The enhanced inhibitory interaction between RA and BMP-4 pathways occurs also in another relevant corticotroph gene promoter, the Corticotropin-releasing hormone receptor 1 (CRH-R1). Tretinoin 44-46 corticotropin releasing hormone receptor 1 Mus musculus 174-180
31370073-8 2019 ATRA-treated platelets demonstrated reduced spreading on immobilized fibrinogen or collagen and reduced thrombin-induced clot retraction together with reduced phosphorylation of Syk and PLCgamma2. Tretinoin 0-4 spleen associated tyrosine kinase Homo sapiens 178-181
32359645-3 2020 The (patho)physiological functions of RAR-RXR heterodimers rely on a dynamic sequence of protein-protein interactions, many of which being modulated by natural (retinoic acid) or synthetic ligands. Tretinoin 161-174 retinoid X receptor alpha Homo sapiens 42-45
18976680-2 2009 The postulated mechanism for the dysmorphogenetic effects is the inhibition of retinoic acid (RA)-degrading enzyme CYP26. Tretinoin 94-96 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 115-120
19489262-4 2009 RESULTS: The expression rates of CK-13 in KB cells in the ATRA group and As2 O3 group were significantly higher than that in the control (P < 0.05), but there was no significant difference in the expression between ATRA and As2 O3 group(P > 0.05). Tretinoin 58-62 keratin 13 Homo sapiens 33-38
31527426-9 2019 In conclusion, selective agonists of RAR demonstrate comparable protective effects against NIHL to retinoic acid. Tretinoin 99-112 retinoic acid receptor, alpha Mus musculus 37-40
32066035-5 2020 RESULTS: The uptake of [18F]FPGLU in C6 cells increased significantly after induced by ATRA for 24, 48, and 72 h, which was closely related to expression of EAAC1 in C6 cells (R2 = 0.939). Tretinoin 87-91 solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1 Mus musculus 157-162
19073915-8 2008 Moreover, RARalpha association with the GluR1 mRNA directly underlies the translational control of GluR1 by RA: RARalpha represses GluR1 translation, while RA binding to RARalpha reduces its association with the GluR1 mRNA and relieves translational repression. Tretinoin 10-12 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 40-45
31950055-3 2019 ATRA treatment significantly enhanced the flagellin-induced NF-kappaB/AP-1 activity in THP-1 via the RAR/RXR pathway. Tretinoin 0-4 retinoid X receptor alpha Homo sapiens 105-108
31238067-8 2019 Cell culture experiments confirm that RA inhibits CaMKII phosphorylation, which requires Crabp1. Tretinoin 38-40 cellular retinoic acid binding protein I Mus musculus 89-95
31238067-9 2019 Molecular data reveal interaction of Crabp1 with the kinase and regulatory domains of CaMKII, and that RA selectively enhances Crabp1 interaction with the regulatory domain, suggesting a potential regulatory role for holo-Crabp1 in CaMKII activation. Tretinoin 103-105 cellular retinoic acid binding protein I Mus musculus 127-133
31238067-9 2019 Molecular data reveal interaction of Crabp1 with the kinase and regulatory domains of CaMKII, and that RA selectively enhances Crabp1 interaction with the regulatory domain, suggesting a potential regulatory role for holo-Crabp1 in CaMKII activation. Tretinoin 103-105 cellular retinoic acid binding protein I Mus musculus 127-133
19073915-8 2008 Moreover, RARalpha association with the GluR1 mRNA directly underlies the translational control of GluR1 by RA: RARalpha represses GluR1 translation, while RA binding to RARalpha reduces its association with the GluR1 mRNA and relieves translational repression. Tretinoin 10-12 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 99-104
31238067-10 2019 Together, these data demonstrate that RA bound Crabp1 plays a protective role in beta-adrenergic stimulated cardiac remodeling, which is partially attributed to its dampening CaMKII activation. Tretinoin 38-40 cellular retinoic acid binding protein I Mus musculus 47-53
19073915-8 2008 Moreover, RARalpha association with the GluR1 mRNA directly underlies the translational control of GluR1 by RA: RARalpha represses GluR1 translation, while RA binding to RARalpha reduces its association with the GluR1 mRNA and relieves translational repression. Tretinoin 10-12 retinoic acid receptor alpha Homo sapiens 112-120
31283017-9 2019 mRNAs of genes involved in retinoic acid (RA) synthesis (Stra6 and Rdh10) were also increased by EtOH, AcH, and 4-HNE treatment. Tretinoin 27-40 retinol dehydrogenase 10 Homo sapiens 67-72
31283017-9 2019 mRNAs of genes involved in retinoic acid (RA) synthesis (Stra6 and Rdh10) were also increased by EtOH, AcH, and 4-HNE treatment. Tretinoin 42-44 retinol dehydrogenase 10 Homo sapiens 67-72
32699982-0 2019 Efficacy of All-Trans-Retinoic Acid in High-Risk Acute Myeloid Leukemia with Overexpression of EVI1. Tretinoin 12-35 MDS1 and EVI1 complex locus Homo sapiens 95-99
32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 106-129 MDS1 and EVI1 complex locus Homo sapiens 14-18
32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 106-129 MDS1 and EVI1 complex locus Homo sapiens 20-25
32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 131-135 MDS1 and EVI1 complex locus Homo sapiens 14-18
19073915-8 2008 Moreover, RARalpha association with the GluR1 mRNA directly underlies the translational control of GluR1 by RA: RARalpha represses GluR1 translation, while RA binding to RARalpha reduces its association with the GluR1 mRNA and relieves translational repression. Tretinoin 10-12 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 99-104
32699982-1 2019 INTRODUCTION: EVI1 (MECOM)-positive acute myeloid leukemia (AML) cells have shown in vitro sensitivity to all-trans-retinoic acid (ATRA) by inducing differentiation, cell death, and decreased leukemic engraftment. Tretinoin 131-135 MDS1 and EVI1 complex locus Homo sapiens 20-25
32699982-2 2019 METHODS: In this pilot study, we investigated the response to ATRA in 13 high-risk AML patients with overexpression of EVI1. Tretinoin 62-66 MDS1 and EVI1 complex locus Homo sapiens 119-123
31200068-6 2019 In addition, the capabilities of a retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) system to activate IFN promoter were decreased during the overexpression of FGFR3. Tretinoin 35-48 fibroblast growth factor receptor 3 Homo sapiens 170-175
32699982-4 2019 CONCLUSION: These primary results tend to confirm in vitro results and suggest that addition of ATRA might be of benefit in the treatment of patients with EVI1-positive AML. Tretinoin 96-100 MDS1 and EVI1 complex locus Homo sapiens 155-159
19073915-8 2008 Moreover, RARalpha association with the GluR1 mRNA directly underlies the translational control of GluR1 by RA: RARalpha represses GluR1 translation, while RA binding to RARalpha reduces its association with the GluR1 mRNA and relieves translational repression. Tretinoin 10-12 retinoic acid receptor alpha Homo sapiens 112-120
19073915-8 2008 Moreover, RARalpha association with the GluR1 mRNA directly underlies the translational control of GluR1 by RA: RARalpha represses GluR1 translation, while RA binding to RARalpha reduces its association with the GluR1 mRNA and relieves translational repression. Tretinoin 10-12 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 99-104
18845239-4 2008 Using in vitro cell and in vivo mouse models, we report that RA, specifically all-trans-RA (atRA) at concentrations implicated in toxicity, can activate NRF2 and induce NRF2 target genes, particularly the subunits of the rate-limiting enzyme of glutathione biosynthesis, glutamate cysteine ligase (GCLM/GCLC). Tretinoin 92-96 glutamate-cysteine ligase, modifier subunit Mus musculus 298-302
31694317-1 2019 The three subtypes (alpha, beta, and gamma) of the retinoic acid receptor (RAR) are ligand-dependent transcription factors that mediate retinoic acid signaling by forming heterodimers with the retinoid X receptor (RXR). Tretinoin 51-64 retinoid X receptor alpha Homo sapiens 193-212
31694317-1 2019 The three subtypes (alpha, beta, and gamma) of the retinoic acid receptor (RAR) are ligand-dependent transcription factors that mediate retinoic acid signaling by forming heterodimers with the retinoid X receptor (RXR). Tretinoin 51-64 retinoid X receptor alpha Homo sapiens 214-217
31109648-3 2019 Our objective was to characterize the action of ATRA in mature adipocytes of mice by ablating RAR signaling through overexpression of a well-characterized dominant negative RARalpha mutant (RARdn) form specifically in adipocytes. Tretinoin 48-52 retinoic acid receptor, alpha Mus musculus 94-97
31109648-3 2019 Our objective was to characterize the action of ATRA in mature adipocytes of mice by ablating RAR signaling through overexpression of a well-characterized dominant negative RARalpha mutant (RARdn) form specifically in adipocytes. Tretinoin 48-52 retinoic acid receptor, alpha Mus musculus 173-181
31109648-4 2019 Altered RAR signaling in adipocytes resulted in a significant decrease in ATRA levels in visceral and brown adipose tissues as well as liver tissue. Tretinoin 74-78 retinoic acid receptor, alpha Mus musculus 8-11
31479736-10 2019 Also, RA significantly reduced Sp7 expression at days 14 and 21 (p < 0.05). Tretinoin 6-8 Sp7 transcription factor 7 Mus musculus 31-34
18845239-5 2008 RNA interference-mediated silencing of NRF2, but not of retinoid X receptor-alpha and -beta, reduced basal and atRA-induced GCLM/GCLC gene expression. Tretinoin 111-115 glutamate-cysteine ligase, modifier subunit Mus musculus 124-128
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 0-13 CCAAT enhancer binding protein epsilon Homo sapiens 221-233
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 15-17 lysine methyltransferase 2A Homo sapiens 91-94
18776924-4 2008 Retinoic acid (RA) induced monocytic differentiation in the myelomonocytic cell lines with MLL-fusion genes, THP-1, MOLM-14 and HF-6 cells, accompanied by monocytic differentiation with the upregulation of C/EBPalpha and C/EBPepsilon. Tretinoin 15-17 CCAAT enhancer binding protein epsilon Homo sapiens 221-233
31037648-9 2019 RA + BDNF-induced differentiation resulted in remarkable neuronal morphology alterations characterized by increased neurite density. Tretinoin 0-2 brain derived neurotrophic factor Homo sapiens 5-9
30682454-5 2019 METHODS: IL-10+ ILCregs induced from ILC2s by using retinoic acid (RA) were analyzed with RNA-sequencing and flow cytometry. Tretinoin 52-65 interleukin 10 Homo sapiens 9-14
18922886-0 2008 Retinoic acid-dependent activation of the polycystic kidney disease-1 (PKD1) promoter. Tretinoin 0-13 polycystin 1, transient receptor potential channel interacting Homo sapiens 71-75
30556162-2 2019 Differentiation of dsASCs with ATRA and a combination of growth factors induced expression of simple epithelial markers (KRT7, KRT8, KRT18, and KRT19), along with low levels of stratified epithelial markers (KRT5, KRT10, KRT13, and KRT14). Tretinoin 31-35 keratin 8 Homo sapiens 127-131
31135261-7 2019 These results suggest that PML-RARalpha initiates ATRA-induced transcription through its interaction with MED1. Tretinoin 50-54 mediator complex subunit 1 Homo sapiens 106-110
31143119-9 2019 In addition, ATRA dose-dependently reduced the phosphorylation levels of mTOR and mTOR target proteins p70 S6 kinase (p70S6K) and 4E-binding protein 1 (4EBP1) in A7r5 and HASMC. Tretinoin 13-17 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 103-116
31143119-9 2019 In addition, ATRA dose-dependently reduced the phosphorylation levels of mTOR and mTOR target proteins p70 S6 kinase (p70S6K) and 4E-binding protein 1 (4EBP1) in A7r5 and HASMC. Tretinoin 13-17 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 118-124
31736873-1 2019 Background: Cellular retinoic acid binding protein 2 (CRABP2) mediates retinoic acid/RA anti-cancer pathways. Tretinoin 21-34 cellular retinoic acid binding protein 2 Homo sapiens 54-60
18922886-1 2008 The retinoic acids all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9C-RA) and the retinoic acid receptors RAR and RXR significantly induce transcriptional activity from a 200-bp PKD1 proximal promoter in transfected mammalian cells. Tretinoin 4-18 retinoic acid receptor alpha Homo sapiens 115-118
31235507-0 2019 TRIB3 Stabilizes High TWIST1 Expression to Promote Rapid APL Progression and ATRA Resistance. Tretinoin 77-81 tribbles pseudokinase 3 Homo sapiens 0-5
31235507-8 2019 TRIB3 depletion promoting TWIST1 degradation reverses resistance to induction therapy and improves sensitivity to ATRA. Tretinoin 114-118 tribbles pseudokinase 3 Homo sapiens 0-5
18922886-1 2008 The retinoic acids all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9C-RA) and the retinoic acid receptors RAR and RXR significantly induce transcriptional activity from a 200-bp PKD1 proximal promoter in transfected mammalian cells. Tretinoin 4-18 polycystin 1, transient receptor potential channel interacting Homo sapiens 187-191
30876849-4 2019 Here we show that retinoic acid (RA), signaling through its receptor (RAR), is the trigger for hyperactivity. Tretinoin 18-31 Rab40B, member RAS oncogene family Mus musculus 70-73
18922886-1 2008 The retinoic acids all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9C-RA) and the retinoic acid receptors RAR and RXR significantly induce transcriptional activity from a 200-bp PKD1 proximal promoter in transfected mammalian cells. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 115-118
30876849-4 2019 Here we show that retinoic acid (RA), signaling through its receptor (RAR), is the trigger for hyperactivity. Tretinoin 33-35 Rab40B, member RAS oncogene family Mus musculus 70-73
18922886-1 2008 The retinoic acids all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9C-RA) and the retinoic acid receptors RAR and RXR significantly induce transcriptional activity from a 200-bp PKD1 proximal promoter in transfected mammalian cells. Tretinoin 4-17 polycystin 1, transient receptor potential channel interacting Homo sapiens 187-191
18922886-8 2008 These data indicate that induction of the PKD1 promoter by retinoic acid is mediated through Sp1 elements. Tretinoin 59-72 polycystin 1, transient receptor potential channel interacting Homo sapiens 42-46
30939964-0 2019 Retinoic acid worsens ATG10-dependent autophagy impairment in TBK1-mutant hiPSC-derived motoneurons through SQSTM1/p62 accumulation. Tretinoin 0-13 autophagy related 10 Homo sapiens 22-27
19041605-2 2008 Most patients are treated with all-trans retinoic acid (ATRA), which targets the RAR-alpha moiety of the PML/RAR-alpha fusion transcript, and anthracycline-based chemotherapy. Tretinoin 41-54 retinoic acid receptor alpha Homo sapiens 81-90
30939964-0 2019 Retinoic acid worsens ATG10-dependent autophagy impairment in TBK1-mutant hiPSC-derived motoneurons through SQSTM1/p62 accumulation. Tretinoin 0-13 sequestosome 1 Homo sapiens 108-114
30939964-0 2019 Retinoic acid worsens ATG10-dependent autophagy impairment in TBK1-mutant hiPSC-derived motoneurons through SQSTM1/p62 accumulation. Tretinoin 0-13 sequestosome 1 Homo sapiens 115-118
30879180-2 2019 In the present study, we examined the role of SST in all-trans retinoic acid (RA)-induced progression of neurite outgrowth in SH-SY5Y cells. Tretinoin 63-76 somatostatin Homo sapiens 46-49
30879180-2 2019 In the present study, we examined the role of SST in all-trans retinoic acid (RA)-induced progression of neurite outgrowth in SH-SY5Y cells. Tretinoin 78-80 somatostatin Homo sapiens 46-49
30879180-4 2019 Here, we present evidence that SST is a molecular determinant in regulating the transition of SH-SY5Y cells from non-neuronal entity to neuronal phenotype in response to RA. Tretinoin 170-172 somatostatin Homo sapiens 31-34
31035455-0 2019 Retinoic Acid Induces Differentiation of Mouse F9 Embryonic Carcinoma Cell by Modulating the miR-485 Targeting of Abhd2. Tretinoin 0-13 abhydrolase domain containing 2 Mus musculus 114-119
31035455-4 2019 RA up-regulates miR-485 and concurrently down-regulates Abhd2. Tretinoin 0-2 abhydrolase domain containing 2 Mus musculus 56-61
31485618-4 2019 The present study investigates, to the best of our knowledge, for the first time, the influence of CIF in combination with RSV or ATRA on the expression of relevant modifiers of DNA methylation machinery, including DNA Methyltransferase 1 (DNMT1) and Cyclin dependent kinase inhibitor 1A (CDKN1A) in CML cells. Tretinoin 130-134 DNA methyltransferase 1 Homo sapiens 240-245
31035455-6 2019 In summary, RA can mediate cell differentiation by phosphorylating Erk1/2 via miR-485 and Abhd2. Tretinoin 12-14 abhydrolase domain containing 2 Mus musculus 90-95
19041605-2 2008 Most patients are treated with all-trans retinoic acid (ATRA), which targets the RAR-alpha moiety of the PML/RAR-alpha fusion transcript, and anthracycline-based chemotherapy. Tretinoin 41-54 PML nuclear body scaffold Homo sapiens 105-118
19041605-2 2008 Most patients are treated with all-trans retinoic acid (ATRA), which targets the RAR-alpha moiety of the PML/RAR-alpha fusion transcript, and anthracycline-based chemotherapy. Tretinoin 56-60 retinoic acid receptor alpha Homo sapiens 81-90
19041605-2 2008 Most patients are treated with all-trans retinoic acid (ATRA), which targets the RAR-alpha moiety of the PML/RAR-alpha fusion transcript, and anthracycline-based chemotherapy. Tretinoin 56-60 PML nuclear body scaffold Homo sapiens 105-118
31344789-0 2019 All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1. Tretinoin 0-23 cellular retinoic acid binding protein I Mus musculus 78-84
31344789-3 2019 Most of these rapid atRA responses are the outcome of its binding to cellular retinoic acid binding protein 1 (CRABP1) that is predominantly localized in cytoplasm and binds to atRA with a high affinity. Tretinoin 20-24 cellular retinoic acid binding protein I Mus musculus 69-109
19029830-2 2008 RA exerts its biological functions primarily through binding to and activating nuclear RA receptors (RARs, which include the RAR alpha, beta and gamma isotypes RARA, RARB and RARC). Tretinoin 0-2 arginyl-tRNA synthetase Mus musculus 101-105
31344789-3 2019 Most of these rapid atRA responses are the outcome of its binding to cellular retinoic acid binding protein 1 (CRABP1) that is predominantly localized in cytoplasm and binds to atRA with a high affinity. Tretinoin 20-24 cellular retinoic acid binding protein I Mus musculus 111-117
31344789-3 2019 Most of these rapid atRA responses are the outcome of its binding to cellular retinoic acid binding protein 1 (CRABP1) that is predominantly localized in cytoplasm and binds to atRA with a high affinity. Tretinoin 177-181 cellular retinoic acid binding protein I Mus musculus 69-109
30706710-5 2019 The inhibition of XIAP with the restoration of PPARgamma signaling using a SMAC-mimetic (Compound A (CmpdA)) and rosiglitazone (RGZ)/retinoic acid (RA), respectively, reduced cell proliferation and induced apoptosis in the KGN cells. Tretinoin 133-146 X-linked inhibitor of apoptosis Homo sapiens 18-22
30706710-5 2019 The inhibition of XIAP with the restoration of PPARgamma signaling using a SMAC-mimetic (Compound A (CmpdA)) and rosiglitazone (RGZ)/retinoic acid (RA), respectively, reduced cell proliferation and induced apoptosis in the KGN cells. Tretinoin 148-150 X-linked inhibitor of apoptosis Homo sapiens 18-22
31344789-3 2019 Most of these rapid atRA responses are the outcome of its binding to cellular retinoic acid binding protein 1 (CRABP1) that is predominantly localized in cytoplasm and binds to atRA with a high affinity. Tretinoin 177-181 cellular retinoic acid binding protein I Mus musculus 111-117
19046160-0 2008 Retinoic acid affects craniofacial patterning by changing Fgf8 expression in the pharyngeal ectoderm. Tretinoin 0-13 fibroblast growth factor 8 Homo sapiens 58-62
30937689-0 2019 Vitronectin is Involved in the Morphological Transition of Neurites in Retinoic Acid-Induced Neurogenesis of Neuroblastoma Cell Line Neuro2a. Tretinoin 71-84 vitronectin Mus musculus 0-11
30937689-5 2019 Treatment with an antibody for Vtn suppressed the RA-induced cell cycle exit and multipolar-to-bipolar transition. Tretinoin 50-52 vitronectin Mus musculus 31-34
31234811-11 2019 Analysis of conserved SDH-loss master regulators in human tumors and MEFs implicated ZNF423, a known modulator of retinoic acid response in neuroblastoma. Tretinoin 114-127 succinate dehydrogenase complex iron sulfur subunit B Homo sapiens 22-25
31234811-12 2019 Subsequent functional analysis revealed a blunted cell death response to retinoic acid in SDH-loss MEFs and blunted differentiation response in SDH-inhibited SH-SY5Y neuroblastoma cells. Tretinoin 73-86 succinate dehydrogenase complex iron sulfur subunit B Homo sapiens 90-93
30728260-6 2019 In contrast, ATRA binding to CRABP2 potently inhibited HCV via suppression of LD accumulation. Tretinoin 13-17 cellular retinoic acid binding protein 2 Homo sapiens 29-35
30632787-4 2019 The expression of Raldh2, which encodes the key enzyme in RA synthesis, was reduced in Gen1 mutant metanephros through RNA sequencing. Tretinoin 58-60 aldehyde dehydrogenase 1 family member A2 Homo sapiens 18-24
30709353-0 2019 All-trans retinoic acid inhibits lipopolysaccharide-induced inflammatory responses in bovine adipocytes via TGFbeta1/Smad3 signaling pathway. Tretinoin 0-23 SMAD family member 3 Bos taurus 117-122
18669599-5 2008 Light-triggered alterations in circulatory ATRA levels regulated ecto-5"-nucleotidase gene expression by retinoic acid receptor retinoic acid receptor-alpha and modulated 5"-AMP levels in blood and were associated with mPlrp2 and mClps expression in the livers. Tretinoin 43-47 5' nucleotidase, ecto Mus musculus 65-85
30658598-0 2019 All-trans retinoic acid stimulates the secretion of TGF-beta2 via the phospholipase C but not the adenylyl cyclase signaling pathway in retinal pigment epithelium cells. Tretinoin 10-23 transforming growth factor beta 2 Homo sapiens 52-61
31202261-7 2019 The autism-associated gene ubiquitin-protein ligase E3A (UBE3A) has been reported to influence WNT, BMP, and RA signaling pathways, suggesting crosstalk between various signaling pathways during autistic brain development. Tretinoin 109-111 ubiquitin protein ligase E3A Homo sapiens 27-55
31202261-7 2019 The autism-associated gene ubiquitin-protein ligase E3A (UBE3A) has been reported to influence WNT, BMP, and RA signaling pathways, suggesting crosstalk between various signaling pathways during autistic brain development. Tretinoin 109-111 ubiquitin protein ligase E3A Homo sapiens 57-62
30658598-1 2019 BACKGROUND: By investigating that (i) all-trans retinoic acid (ATRA) affects human retinal pigment epithelium (RPE) in expressing and secreting transforming growth factor (TGF)-beta2 and (ii) U73122 (phospholipase C inhibitor) and SQ22536 (adenylyl cyclase inhibitor) regulate the ATRA-induced secretion of TGF-beta2 in human RPE, we sought to interpret the signaling pathway of ATRA in promoting the development of myopia. Tretinoin 48-61 transforming growth factor beta 2 Homo sapiens 144-182
30658598-1 2019 BACKGROUND: By investigating that (i) all-trans retinoic acid (ATRA) affects human retinal pigment epithelium (RPE) in expressing and secreting transforming growth factor (TGF)-beta2 and (ii) U73122 (phospholipase C inhibitor) and SQ22536 (adenylyl cyclase inhibitor) regulate the ATRA-induced secretion of TGF-beta2 in human RPE, we sought to interpret the signaling pathway of ATRA in promoting the development of myopia. Tretinoin 48-61 transforming growth factor beta 2 Homo sapiens 307-316
18767146-7 2008 Differential expression of the retinoic acid target genes, RARB, CRABP1, and CRABP2, indicated that deletion of TBL1XR1 compromised the function of SMRT/N-CoR in the appropriate control of gene expression. Tretinoin 31-44 nuclear receptor corepressor 1 Homo sapiens 153-158
30658598-1 2019 BACKGROUND: By investigating that (i) all-trans retinoic acid (ATRA) affects human retinal pigment epithelium (RPE) in expressing and secreting transforming growth factor (TGF)-beta2 and (ii) U73122 (phospholipase C inhibitor) and SQ22536 (adenylyl cyclase inhibitor) regulate the ATRA-induced secretion of TGF-beta2 in human RPE, we sought to interpret the signaling pathway of ATRA in promoting the development of myopia. Tretinoin 63-67 transforming growth factor beta 2 Homo sapiens 144-182
30658598-1 2019 BACKGROUND: By investigating that (i) all-trans retinoic acid (ATRA) affects human retinal pigment epithelium (RPE) in expressing and secreting transforming growth factor (TGF)-beta2 and (ii) U73122 (phospholipase C inhibitor) and SQ22536 (adenylyl cyclase inhibitor) regulate the ATRA-induced secretion of TGF-beta2 in human RPE, we sought to interpret the signaling pathway of ATRA in promoting the development of myopia. Tretinoin 63-67 transforming growth factor beta 2 Homo sapiens 307-316
30658598-5 2019 RESULTS: TGF-beta2 in the cytoplasm was time-dependent increased by ATRA (p < 0.001). Tretinoin 68-72 transforming growth factor beta 2 Homo sapiens 9-18
30658598-6 2019 A time-dependent increase in the TGF-beta2 protein of the supernatant was induced by ATRA (p < 0.001). Tretinoin 85-89 transforming growth factor beta 2 Homo sapiens 33-42
30658598-7 2019 U73122 (in the range of 5 to 40 muM) could suppress the secretion of TGF-beta2 induced by ATRA (p < 0.001), and 40 muM U73122 could completely inhibit the up-regulated effect of 10 muM ATRA. Tretinoin 90-94 transforming growth factor beta 2 Homo sapiens 69-78
30461012-0 2019 Upregulation of transient receptor potential melastatin 6 channel expression by rosiglitazone and all-trans-retinoic acid in erlotinib-treated renal tubular epithelial cells. Tretinoin 98-121 transient receptor potential cation channel, subfamily M, member 6 Rattus norvegicus 16-57
30461012-5 2019 Here, we found that rosiglitazone, an antidiabetic drug, and all- trans-retinoic acid (ATRA), a vitamin A derivative, increase the messenger RNA (mRNA) level of TRPM6 in the presence of erlotinib. Tretinoin 61-85 transient receptor potential cation channel, subfamily M, member 6 Rattus norvegicus 161-166
30461012-5 2019 Here, we found that rosiglitazone, an antidiabetic drug, and all- trans-retinoic acid (ATRA), a vitamin A derivative, increase the messenger RNA (mRNA) level of TRPM6 in the presence of erlotinib. Tretinoin 87-91 transient receptor potential cation channel, subfamily M, member 6 Rattus norvegicus 161-166
30461012-6 2019 The rosiglitazone- and ATRA-induced elevation of mRNA level, Mg 2+ influx, and promoter activity of TRPM6 were inhibited by GW-9662, a potent antagonist of peroxisome proliferator-activated receptor (PPAR)gamma, and LE135, a retinoic acid receptor (RAR) antagonist, respectively. Tretinoin 23-27 transient receptor potential cation channel, subfamily M, member 6 Rattus norvegicus 100-105
30461012-6 2019 The rosiglitazone- and ATRA-induced elevation of mRNA level, Mg 2+ influx, and promoter activity of TRPM6 were inhibited by GW-9662, a potent antagonist of peroxisome proliferator-activated receptor (PPAR)gamma, and LE135, a retinoic acid receptor (RAR) antagonist, respectively. Tretinoin 23-27 peroxisome proliferator-activated receptor gamma Rattus norvegicus 200-210
30461012-11 2019 These results suggest that rosiglitazone and ATRA reverse the reduction in Mg 2+ reabsorption caused by anti-EGFR drugs. Tretinoin 45-49 epidermal growth factor receptor Rattus norvegicus 109-113
31141879-10 2019 Retinoic acid-induced activation of retinoic acid receptor response element (RARE)-tk-luciferase is dependent on exogenous expression of retinoic acid receptor alpha (RARa)/RXRa heterodimer in MDA-MB 231 but not in MCF7 and KAIMRC1 cell lines. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 173-177
30229860-5 2019 Dose-response analysis of selected combinations from the initial combinatorial screen revealed that the combined treatment of all-trans retinoic acid (RA) with the glycogen synthase kinase 3 inhibitor CHIR-99021 (CHIR) enhances neurogenesis while simultaneously decreases astrocyte differentiation, whereas the combined treatment of brain-derived neurotrophic factor and the small azide neuropathiazol enhances the differentiation into neurons and astrocytes. Tretinoin 136-149 brain derived neurotrophic factor Homo sapiens 333-366
18641177-8 2008 The expressions of connective tissue growth factor, AXL receptor tyrosine kinase, stromal membrane-associated protein 1-like, and retinoic acid-induced 14 were significantly downregulated during adipocyte differentiation in vitro (P < 0.05), and the expressions of Rho/Rac guanine nucleotide exchange factor 2 and secreted frizzled-related protein 4 also tended to be decreased, although not significantly. Tretinoin 130-143 Rho/Rac guanine nucleotide exchange factor 2 Sus scrofa 268-352
30229860-5 2019 Dose-response analysis of selected combinations from the initial combinatorial screen revealed that the combined treatment of all-trans retinoic acid (RA) with the glycogen synthase kinase 3 inhibitor CHIR-99021 (CHIR) enhances neurogenesis while simultaneously decreases astrocyte differentiation, whereas the combined treatment of brain-derived neurotrophic factor and the small azide neuropathiazol enhances the differentiation into neurons and astrocytes. Tretinoin 151-153 brain derived neurotrophic factor Homo sapiens 333-366
30825428-5 2019 This regulation of CDX4 over Pax6 is restricted to the rostral pre-neural tube by Retinoic Acid signaling. Tretinoin 82-95 caudal type homeobox 4 Gallus gallus 19-23
30825428-5 2019 This regulation of CDX4 over Pax6 is restricted to the rostral pre-neural tube by Retinoic Acid signaling. Tretinoin 82-95 paired box 6 Gallus gallus 29-33
18534676-1 2008 The nuclear arrangement of promyelocytic leukaemia nuclear bodies (PML NBs) was studied in vitro after the cell treatment by clinically used agents such as all-trans retinoic acid (RA) in human leukaemia and cytostatics or gamma radiation in multiple myeloma cells. Tretinoin 181-183 PML nuclear body scaffold Homo sapiens 67-70
30879360-8 2019 TFAP2A (transcription factor AP-2-alpha [activating enhancer-binding protein 2 alpha]), a different transcription factor was upregulated in normotensive DSCs but not in preeclampsia DSCs after RA treatment. Tretinoin 193-195 transcription factor AP-2 alpha Homo sapiens 0-6
30076181-8 2019 Mutation of both cysteines largely abrogates the synergistic effect of 2-Bromopalmitate on all-trans retinoic acid-induced differentiation, demonstrating that 2-Bromopalmitate promotes all-trans retinoic acid-induced differentiation through binding RARalpha. Tretinoin 91-114 retinoic acid receptor, alpha Mus musculus 249-257
30076181-8 2019 Mutation of both cysteines largely abrogates the synergistic effect of 2-Bromopalmitate on all-trans retinoic acid-induced differentiation, demonstrating that 2-Bromopalmitate promotes all-trans retinoic acid-induced differentiation through binding RARalpha. Tretinoin 101-114 retinoic acid receptor, alpha Mus musculus 249-257
18534676-3 2008 A reduced number of PML bodies, which led to relocation of PML NBs closer to the nuclear interior, mostly accompanied RA- and PMA-induced differentiation. Tretinoin 118-120 PML nuclear body scaffold Homo sapiens 20-23
30806286-3 2019 ATRA treatment causes ~12-fold increase in the number of acidic vesicular organelles and induces marked up-regulation of LC3-II, autophagy-related 5 (ATG5), and Beclin-1. Tretinoin 0-4 beclin 1 Homo sapiens 161-169
30816486-7 2019 Furthermore, all-trans-retinoic acid treatment significantly downregulated CDC20 expression in cSCC. Tretinoin 13-36 cell division cycle 20 Homo sapiens 75-80
30806286-8 2019 ATRA inhibits Bcl-2, up-regulates Beclin-1 expression, and reduces induction of mTOR activation/phosphorylation in NB4 cells. Tretinoin 0-4 beclin 1 Homo sapiens 34-42
18534676-3 2008 A reduced number of PML bodies, which led to relocation of PML NBs closer to the nuclear interior, mostly accompanied RA- and PMA-induced differentiation. Tretinoin 118-120 PML nuclear body scaffold Homo sapiens 59-62
18987198-3 2008 Here we report a robust decrease in brain Abeta deposition and tau phosphorylation in the blinded study of APP/PS1 transgenic mice treated intraperitoneally for 8 weeks with ATRA (20 mg/kg, three times weekly, initiated when the mice were 5 months old). Tretinoin 174-178 amyloid beta (A4) precursor protein Mus musculus 42-47
18987198-3 2008 Here we report a robust decrease in brain Abeta deposition and tau phosphorylation in the blinded study of APP/PS1 transgenic mice treated intraperitoneally for 8 weeks with ATRA (20 mg/kg, three times weekly, initiated when the mice were 5 months old). Tretinoin 174-178 presenilin 1 Mus musculus 111-114
30885956-1 2019 Recent studies have underscored the critical role of retinoic acid (RA) in the development of lineage-committed CD4 and CD8 T cells in vivo. Tretinoin 53-66 CD8a molecule Homo sapiens 120-123
18987198-6 2008 The ATRA-treated APP/PS1 mice showed decreased activation of microglia and astrocytes, attenuated neuronal degeneration, and improved spatial learning and memory compared with the vehicle-treated APP/PS1 mice. Tretinoin 4-8 presenilin 1 Mus musculus 21-24
30885956-1 2019 Recent studies have underscored the critical role of retinoic acid (RA) in the development of lineage-committed CD4 and CD8 T cells in vivo. Tretinoin 68-70 CD8a molecule Homo sapiens 120-123
30885956-5 2019 RA production is facilitated by retinaldehyde isoform-2 (RALDH2) preferentially expressed in dendritic cells (DCs). Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 32-55
30203271-4 2019 The cells differentiated with retinoic acid and 12-o-tetradecanoylphorbol-13-acetate show a significant increase in the expression of tyrosine hydroxylase, vesicular monoamine transporter-2, and dopamine transporter. Tretinoin 30-43 solute carrier family 6 member 3 Homo sapiens 195-215
30885956-5 2019 RA production is facilitated by retinaldehyde isoform-2 (RALDH2) preferentially expressed in dendritic cells (DCs). Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 57-63
18987198-6 2008 The ATRA-treated APP/PS1 mice showed decreased activation of microglia and astrocytes, attenuated neuronal degeneration, and improved spatial learning and memory compared with the vehicle-treated APP/PS1 mice. Tretinoin 4-8 presenilin 1 Mus musculus 200-203
30885956-6 2019 Conditionally deleted RA-synthesizing enzyme RALDH2 in host or to a lesser extent donor DCs reduced GVHD lethality. Tretinoin 22-24 aldehyde dehydrogenase 1 family member A2 Homo sapiens 45-51
18974118-8 2008 RA causes the gradual down-regulation and eventual loss of c-Cbl expression, resulting in loss of the Cbl-CD38 interaction, suggesting that c-Cbl plays a relatively early role in promoting RA-induced differentiation. Tretinoin 189-191 CD38 molecule Homo sapiens 106-110
18974118-8 2008 RA causes the gradual down-regulation and eventual loss of c-Cbl expression, resulting in loss of the Cbl-CD38 interaction, suggesting that c-Cbl plays a relatively early role in promoting RA-induced differentiation. Tretinoin 189-191 Cbl proto-oncogene Homo sapiens 140-145
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 forkhead box M1 Homo sapiens 125-130
18974118-9 2008 RA-induced differentiation can thus be propelled by c-Cbl and by CD38, both of which bind together, enhance the expression of each other, and cause MAPK signaling. Tretinoin 0-2 Cbl proto-oncogene Homo sapiens 52-57
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 aurora kinase B Homo sapiens 132-147
18974118-9 2008 RA-induced differentiation can thus be propelled by c-Cbl and by CD38, both of which bind together, enhance the expression of each other, and cause MAPK signaling. Tretinoin 0-2 CD38 molecule Homo sapiens 65-69
30978209-4 2019 RA and/or bexarotene increased the transcript levels of FOXO1, FOXO3A, and TRAIL receptors; reduced the transcript levels of FOXM1, Aurora kinase B (AURKB), and vascular endothelial growth factor A (VEGFA); and decreased the proliferation of OSCC-derived cell lines. Tretinoin 0-2 aurora kinase B Homo sapiens 149-154
30978209-5 2019 Also, RA and/or bexarotene influenced the recruitment of FOXO3A and FOXM1 to target genes. Tretinoin 6-8 forkhead box M1 Homo sapiens 68-73
18974118-10 2008 There thus seems to be a cooperative role for c-Cbl and CD38, reflected in their direct binding, in propulsion of RA-induced differentiation. Tretinoin 114-116 Cbl proto-oncogene Homo sapiens 46-51
30978209-8 2019 This research suggests novel influences of the drugs RA and bexarotene on the expression of FOXM1 and FOXO3A in transcriptional regulatory pathways of human OSCC. Tretinoin 53-55 forkhead box M1 Homo sapiens 92-97
18974118-10 2008 There thus seems to be a cooperative role for c-Cbl and CD38, reflected in their direct binding, in propulsion of RA-induced differentiation. Tretinoin 114-116 CD38 molecule Homo sapiens 56-60
18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 275-278
30816426-0 2019 All-trans retinoic acid alters the expression of the tight junction proteins Claudin-1 and -4 and epidermal barrier function-associated genes in the epidermis. Tretinoin 10-23 claudin 1 Mus musculus 77-93
30816426-12 2019 In conclusion, ATRA exerts a dual effect on epidermal barrier genes: It downregulates the expression of Claudin-1 and upregulates the expression of Claudin-4. Tretinoin 15-19 claudin 1 Mus musculus 104-113
18719224-0 2008 Spermatogonial stem cell self-renewal requires OCT4, a factor downregulated during retinoic acid-induced differentiation. Tretinoin 83-96 POU class 5 homeobox 1 Homo sapiens 47-51
30709899-0 2019 Repression of hepatocyte nuclear factor 4 alpha by AP-1 underlies dyslipidemia associated with retinoic acid. Tretinoin 95-108 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-55
30709899-11 2019 Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4alpha transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia. Tretinoin 42-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108
18719224-6 2008 In addition to developing a method to test specific gene function in GS cells, we demonstrate that retinoic acid (RA) triggers GS cells to shift to a differentiated, premeiotic state lacking OCT4 and PLZF expression and colonization activity. Tretinoin 99-112 POU class 5 homeobox 1 Homo sapiens 191-195
18719224-6 2008 In addition to developing a method to test specific gene function in GS cells, we demonstrate that retinoic acid (RA) triggers GS cells to shift to a differentiated, premeiotic state lacking OCT4 and PLZF expression and colonization activity. Tretinoin 114-116 POU class 5 homeobox 1 Homo sapiens 191-195
30539216-3 2019 As ATRA exhibits its therapeutic effect through its receptors, this study was focused to investigate the effect and action of liposomal-ATRA treatment on the expression of RAR-beta protein which is also a tumor suppressor. Tretinoin 3-7 retinoic acid receptor, alpha Mus musculus 172-180
18719224-7 2008 Our data support a model in which OCT4 and PLZF maintain SSCs in an undifferentiated state and RA triggers spermatogonial differentiation through the direct or indirect downregulation of OCT4 and PLZF. Tretinoin 95-97 POU class 5 homeobox 1 Homo sapiens 187-191
30539216-3 2019 As ATRA exhibits its therapeutic effect through its receptors, this study was focused to investigate the effect and action of liposomal-ATRA treatment on the expression of RAR-beta protein which is also a tumor suppressor. Tretinoin 136-140 retinoic acid receptor, alpha Mus musculus 172-180
18959816-4 2008 Protein levels of NF-kappaB p65 and relB were clearly enhanced during retinoic acid-induced differentiation. Tretinoin 70-83 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 28-31
30539216-9 2019 Interestingly, the liposomal-ATRA treatment demonstrated a significantly (p <= 0.01) higher RAR-beta expression in lung (35.20 +- 3.398% band intensity and score 4+ in the 120th day) than that of in ATRA alone treatment. Tretinoin 29-33 retinoic acid receptor, alpha Mus musculus 92-100
30539216-11 2019 The treatment could reactivate the suppression and the lipo-ATRA treatment could show significantly higher RAR-beta expression on the 120th day, which implies that it accumulated more ATRA in target site and sustained it for enhanced action. Tretinoin 60-64 retinoic acid receptor, alpha Mus musculus 107-115
30532072-2 2019 The pharmacological activity of ATRA is mediated by the ligand-activated RAR and RXR transcription factors. Tretinoin 32-36 retinoid X receptor alpha Homo sapiens 81-84
18806776-5 2008 miR-134, miR-296 and miR-470, upregulated on retinoic-acid-induced differentiation of mouse embryonic stem cells, target the CDS of each transcription factor in various combinations, leading to transcriptional and morphological changes characteristic of differentiating mouse embryonic stem cells, and resulting in a new phenotype. Tretinoin 45-58 microRNA 296 Homo sapiens 9-16
30674471-0 2019 FLT3-ITD impedes retinoic acid, but not arsenic, responses in murine acute promyelocytic leukemias. Tretinoin 17-30 FMS-like tyrosine kinase 3 Mus musculus 0-4
30674471-3 2019 APL is a model for oncogene-targeted therapies: all-trans retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor alpha (PML/RARA) driver. Tretinoin 58-71 retinoic acid receptor, alpha Mus musculus 176-180
30674471-3 2019 APL is a model for oncogene-targeted therapies: all-trans retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor alpha (PML/RARA) driver. Tretinoin 73-77 retinoic acid receptor, alpha Mus musculus 176-180
30674471-6 2019 Using mouse APL models, we unexpectedly demonstrate that FLT3-ITD severely blunts ATRA response. Tretinoin 82-86 FMS-like tyrosine kinase 3 Mus musculus 57-61
30674471-7 2019 Remarkably, although the transcriptional output of initial ATRA response is unaffected, ATRA-induced PML/RARA degradation is blunted, as is PML nuclear body reformation and activation of P53 signaling. Tretinoin 88-92 retinoic acid receptor, alpha Mus musculus 105-109
30674471-8 2019 Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication. Tretinoin 31-35 FMS-like tyrosine kinase 3 Mus musculus 86-90
30674471-8 2019 Critically, the combination of ATRA and arsenic fully rescues therapeutic response in FLT3-ITD APLs, restoring PML/RARA degradation, PML nuclear body reformation, P53 activation, and APL eradication. Tretinoin 31-35 retinoic acid receptor, alpha Mus musculus 115-119
18847503-15 2008 Pathway analysis suggests that CDC2, CHEK1, CDC45L and MCM6 are key players in mediating the biological activity of RA in B16 melanoma cells. Tretinoin 116-118 cell division cycle 45 Mus musculus 44-50
30661714-6 2019 Healthy proximal tubules expressed retinaldehyde dehydrogenase 2 (RALDH2), a rate-limiting enzyme in retinoic acid biosynthesis. Tretinoin 101-114 aldehyde dehydrogenase 1 family member A2 Homo sapiens 35-64
30709353-8 2019 Treatment with ATRA could over-activate TGFbeta1/Smad3 signaling pathway in bovine adipocytes and reversed the over-production of pro-inflammatory cytokines and inhibition of anti-inflammatory cytokines induced by LPS. Tretinoin 15-19 SMAD family member 3 Bos taurus 49-54
30709353-9 2019 Importantly, inhibition of TGFbeta1/Smad3 signaling diminished the effects of ATRA on suppressing the proinflammatory responses induced by LPS. Tretinoin 78-82 SMAD family member 3 Bos taurus 36-41
18847503-15 2008 Pathway analysis suggests that CDC2, CHEK1, CDC45L and MCM6 are key players in mediating the biological activity of RA in B16 melanoma cells. Tretinoin 116-118 minichromosome maintenance complex component 6 Mus musculus 55-59
30709353-10 2019 Furthermore, activation of TGFbeta1/Smad3 signaling further extended the effects of ATRA on suppressing the proinflammatory responses on LPS stimulation. Tretinoin 84-88 SMAD family member 3 Bos taurus 36-41
30709353-11 2019 CONCLUSION: In conclusion, ATRA stimulates TGFbeta1/Smad3 signaling pathway and further suppresses bovine adipocytes inflammatory responses induced by LPS. Tretinoin 27-31 SMAD family member 3 Bos taurus 52-57
18716620-6 2008 Remarkably, treatment with drugs that trigger PML-RARalpha degradation, such as all-trans retinoic acid or arsenic trioxide, restore nuclear PTEN. Tretinoin 80-103 PML nuclear body scaffold Homo sapiens 46-49
18716620-6 2008 Remarkably, treatment with drugs that trigger PML-RARalpha degradation, such as all-trans retinoic acid or arsenic trioxide, restore nuclear PTEN. Tretinoin 80-103 phosphatase and tensin homolog Homo sapiens 141-145
18838813-4 2008 ATRA inhibited the expression of tyrosinase and TRP-1, and retinol inhibited the expression of tyrosinase, in a dose-dependent manner. Tretinoin 0-4 tyrosinase Mus musculus 33-43
30472261-0 2019 Znfl1s are essential for patterning the anterior-posterior axis of zebrafish posterior hindbrain by acting as direct target genes of retinoic acid. Tretinoin 133-146 zinc finger-like gene 1 Danio rerio 0-5
30472261-4 2019 Here, we revealed that znfl1s play a critical role in patterning the posterior axis of hindbrain by maintaining the homeostasis of RA signaling in zebrafish embryos. Tretinoin 131-133 zinc finger-like gene 1 Danio rerio 23-28
18838813-7 2008 Therefore, the depigmenting effect of ATRA and retinol might be due to inhibition of the signaling pathway between cAMP and tyrosinase transcription bound to tyrosinase expression. Tretinoin 38-42 tyrosinase Mus musculus 124-134
18838813-7 2008 Therefore, the depigmenting effect of ATRA and retinol might be due to inhibition of the signaling pathway between cAMP and tyrosinase transcription bound to tyrosinase expression. Tretinoin 38-42 tyrosinase Mus musculus 158-168
18810488-2 2008 The hOct4 promoter is unmethylated in mESCs and it undergoes methylation during retinoic acid-induced differentiation. Tretinoin 80-93 POU class 5 homeobox 1 Homo sapiens 4-9
30329139-7 2019 Real-time RT-PCR analysis confirmed that ATRA enhanced the expression of the key ovarian development gene Wnt4 and the antitestis gene Nr0b1 in a concentration-dependent manner. Tretinoin 41-45 nuclear receptor subfamily 0, group B, member 1 Rattus norvegicus 135-140
30329139-8 2019 After 3 days of culture, ATRA-treated testes contained both immunohistochemically DMRT1-positive and FOXL2-positive somatic cells, providing evidence of disrupted testicular cell fate maintenance following ATRA exposure. Tretinoin 25-29 forkhead box L2 Rattus norvegicus 101-106
30329139-8 2019 After 3 days of culture, ATRA-treated testes contained both immunohistochemically DMRT1-positive and FOXL2-positive somatic cells, providing evidence of disrupted testicular cell fate maintenance following ATRA exposure. Tretinoin 206-210 forkhead box L2 Rattus norvegicus 101-106
18816858-0 2008 Retinoic acid down-regulates Tbx1 expression and induces abnormal differentiation of tongue muscles in fetal mice. Tretinoin 0-13 T-box 1 Mus musculus 29-33
30761250-4 2019 Here, we demonstrate that hypoxic conditions result in upregulated expression of Slc7a5 in differentiated neuronal cells (Neuro2A cells induced to differentiate using all-trans retinoic acid). Tretinoin 177-190 solute carrier family 7 (cationic amino acid transporter, y+ system), member 5 Mus musculus 81-87
18816858-3 2008 RA-degrading enzymes (Cyp26a1 and Cyp26b1) were expressed at early stages of normal tongue development, but exogenous RA perturbed their expression in the fetal tongue. Tretinoin 0-2 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 22-29
18816858-6 2008 Tbx1, a candidate gene of DiGeorge syndrome, was down-regulated in the fetal tongue in response to excess RA. Tretinoin 106-108 T-box 1 Mus musculus 0-4
18816858-8 2008 Our study suggests that RA signaling may play an essential role in tongue muscle differentiation via the regulation of Tbx1. Tretinoin 24-26 T-box 1 Mus musculus 119-123
30631055-8 2019 In addition, we show that KDM6B functions downstream of the retinoic acid-HOXC9 axis in inducing neuroblastoma cell differentiation: KDM6B expression is upregulated by retinoic acid via HOXC9, and KDM6B is required for HOXC9-induced neuroblastoma cell differentiation. Tretinoin 60-73 lysine demethylase 6B Homo sapiens 26-31
19007082-1 2008 OBJECTIVE: To study the effect of retinoic acid (RA) on cell proliferation and apoptosis of palatal shelves by 5-bromo-2-deoxyuridine (BrdU) and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL). Tretinoin 34-47 deoxynucleotidyltransferase, terminal Mus musculus 145-182
30631055-8 2019 In addition, we show that KDM6B functions downstream of the retinoic acid-HOXC9 axis in inducing neuroblastoma cell differentiation: KDM6B expression is upregulated by retinoic acid via HOXC9, and KDM6B is required for HOXC9-induced neuroblastoma cell differentiation. Tretinoin 60-73 lysine demethylase 6B Homo sapiens 133-138
30631055-8 2019 In addition, we show that KDM6B functions downstream of the retinoic acid-HOXC9 axis in inducing neuroblastoma cell differentiation: KDM6B expression is upregulated by retinoic acid via HOXC9, and KDM6B is required for HOXC9-induced neuroblastoma cell differentiation. Tretinoin 60-73 lysine demethylase 6B Homo sapiens 133-138
30310934-3 2019 We established a chemically defined protocol by application of Activin A, BMP4, and Retinoic acid followed by GDNF, which steered hPSCs to the renal lineage and resulted in populations of SIX2+/CITED1+ metanephric mesenchyme- (MM) and of HOXB7+/GRHL2+ ureteric bud (UB)-like cells already by 6 days. Tretinoin 84-97 grainyhead like transcription factor 2 Homo sapiens 245-250
19007082-1 2008 OBJECTIVE: To study the effect of retinoic acid (RA) on cell proliferation and apoptosis of palatal shelves by 5-bromo-2-deoxyuridine (BrdU) and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL). Tretinoin 49-51 deoxynucleotidyltransferase, terminal Mus musculus 145-182
30016600-4 2019 Microarray analysis of mouse articular cartilage cells indicated that retinoic acid, a destructive stimulus in articular cartilage, up-regulated expression of sex-determining region Y-box (Sox)4, a SoxC family transcription factor, together with increases in Adamts4 and Adamts5, both of which are aggrecanases of articular cartilages. Tretinoin 70-83 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2) Mus musculus 271-278
18799751-0 2008 Stra8 and its inducer, retinoic acid, regulate meiotic initiation in both spermatogenesis and oogenesis in mice. Tretinoin 23-36 stimulated by retinoic acid gene 8 Mus musculus 0-5
18799751-5 2008 Stra8 is a vertebrate-specific, cytoplasmic factor expressed by germ cells in response to retinoic acid. Tretinoin 90-103 stimulated by retinoic acid gene 8 Mus musculus 0-5
30587607-7 2019 In chondrogenic ATDC5 cells, an RARgamma agonist induced the gene expression of type-X collagen (Col10A1), transglutaminase-2 (Tg2), matrix metalloproteinase-13 (Mmp13), and Ccn2 mRNA, whereas a retinoic acid pan-agonist suppressed RARgamma agonist-stimulated gene expression. Tretinoin 195-208 retinoic acid receptor, gamma Mus musculus 32-40
18799751-11 2008 Taken together with previous observations, our present findings indicate that, in both the male and female germ lines, meiosis is initiated through retinoic acid induction of Stra8. Tretinoin 148-161 stimulated by retinoic acid gene 8 Mus musculus 175-180
18718172-8 2008 CONCLUSION: These results indicate that atRA inhibits the increases in fibronectin that are induced by TGF-beta1 and Ang II in cultured glomerular mesangial cells. Tretinoin 40-44 fibronectin 1 Rattus norvegicus 71-82
18437159-6 2008 In addition, we have demonstrated that some genes, similarly regulated by both inhibitors (upregulated as Bcl2, Id2, Cd24a or downregulated as Nodal), are bona fide p38alpha targets involved in neurogenesis and found a correlation with their expression profiles and the onset of neuronal differentiation triggered upon retinoic acid treatment. Tretinoin 319-332 CD24a antigen Mus musculus 117-122
30562901-2 2019 Retinol binding protein 4 (RBP4) is an adipocyte-secreted hormone (adipokine) that regulates insulin signaling and is also a key transporter of retinoic acid and its derivatives. Tretinoin 144-157 retinol binding protein 4 Homo sapiens 0-25
30562901-2 2019 Retinol binding protein 4 (RBP4) is an adipocyte-secreted hormone (adipokine) that regulates insulin signaling and is also a key transporter of retinoic acid and its derivatives. Tretinoin 144-157 retinol binding protein 4 Homo sapiens 27-31
18548108-2 2008 AQP3 expression in human skin is increased in response to skin stress in diseases such as atopic eczema, to various agents such as retinoic acid, and in skin carcinomas. Tretinoin 131-144 aquaporin 3 (Gill blood group) Homo sapiens 0-4
30472251-6 2019 On the molecular level, ATRA signalling causes induction of TXNIP, a potent inhibitor of the physiological antioxidant thioredoxin (TRX1) and sensitizes cells to necrotic cell death upon hypoxia. Tretinoin 24-28 thioredoxin interacting protein Rattus norvegicus 60-65
30814416-11 2019 In the ATRA-experiment, ATRA suppressed the expression of IL-6, TNF-alpha, NO, a disintegrin and metalloprotease with thrombospondin motifs-4 (ADAMTS-4), MMP-3, and MMP-9. Tretinoin 7-11 matrix metallopeptidase 3 Rattus norvegicus 154-159
30814416-11 2019 In the ATRA-experiment, ATRA suppressed the expression of IL-6, TNF-alpha, NO, a disintegrin and metalloprotease with thrombospondin motifs-4 (ADAMTS-4), MMP-3, and MMP-9. Tretinoin 7-11 matrix metallopeptidase 9 Rattus norvegicus 165-170
30266657-4 2018 When undifferentiated spermatogonia were treated with Retinoic acid (RA), miR-26b was increased, further promoting RA-induced differentiation of spermatogonia. Tretinoin 54-67 microRNA 26b Mus musculus 74-81
30266657-4 2018 When undifferentiated spermatogonia were treated with Retinoic acid (RA), miR-26b was increased, further promoting RA-induced differentiation of spermatogonia. Tretinoin 69-71 microRNA 26b Mus musculus 74-81
30266657-4 2018 When undifferentiated spermatogonia were treated with Retinoic acid (RA), miR-26b was increased, further promoting RA-induced differentiation of spermatogonia. Tretinoin 115-117 microRNA 26b Mus musculus 74-81
18552205-9 2008 CD1d expression was also induced by ATRA in HL-60 cells and ligation with anti-CD1d antibody-induced apoptosis. Tretinoin 36-40 CD1d molecule Homo sapiens 0-4
30019299-0 2019 RACK1 deficiency synergizes with all-trans retinoic acid to induce apoptosis in human acute promyelocytic leukemia cells. Tretinoin 33-56 receptor for activated C kinase 1 Homo sapiens 0-5
30019299-5 2019 In the present study, we demonstrate that silencing of endogenous RACK1 expression synergized with ATRA to promote the death of NB4 and HL-60 APL cells without effect on cell differentiation induced by ATRA. Tretinoin 99-103 receptor for activated C kinase 1 Homo sapiens 66-71
30355624-2 2018 Retinoic acid (RA) and its receptor RARalpha have been established as critical mediators of homeostatic synaptic plasticity. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 36-44
18684916-0 2008 Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression. Tretinoin 0-13 interleukin 23 receptor Homo sapiens 158-172
30355624-2 2018 Retinoic acid (RA) and its receptor RARalpha have been established as critical mediators of homeostatic synaptic plasticity. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 36-44
30355624-9 2018 RARalpha deletion in PV+ interneurons blocked visual deprivation-induced changes in mIPSCs, demonstrating the critical involvement of RA signaling in PV+ interneurons in vivo Moreover, visual deprivation- or RA-induced downregulation of synaptic inhibition was absent in the visual cortical circuit of constitutive and PV-specific Fmr1 KO mice, strongly suggesting a functional interaction between fragile X mental retardation protein and RA signaling pathways. Tretinoin 0-2 fragile X messenger ribonucleoprotein 1 Mus musculus 331-335
30355624-9 2018 RARalpha deletion in PV+ interneurons blocked visual deprivation-induced changes in mIPSCs, demonstrating the critical involvement of RA signaling in PV+ interneurons in vivo Moreover, visual deprivation- or RA-induced downregulation of synaptic inhibition was absent in the visual cortical circuit of constitutive and PV-specific Fmr1 KO mice, strongly suggesting a functional interaction between fragile X mental retardation protein and RA signaling pathways. Tretinoin 134-136 retinoic acid receptor, alpha Mus musculus 0-8
30355624-9 2018 RARalpha deletion in PV+ interneurons blocked visual deprivation-induced changes in mIPSCs, demonstrating the critical involvement of RA signaling in PV+ interneurons in vivo Moreover, visual deprivation- or RA-induced downregulation of synaptic inhibition was absent in the visual cortical circuit of constitutive and PV-specific Fmr1 KO mice, strongly suggesting a functional interaction between fragile X mental retardation protein and RA signaling pathways. Tretinoin 134-136 retinoic acid receptor, alpha Mus musculus 0-8
30355624-10 2018 Together, our results demonstrate that RA/RARalpha signaling acts as a key component for homeostatic regulation of synaptic transmission at the inhibitory synapses of the visual cortex.SIGNIFICANCE STATEMENT In vitro studies established that retinoic acid (RA) and its receptor RARalpha play key roles in homeostatic synaptic plasticity, a mechanism by which synaptic excitation/inhibition balance and network stability are maintained. Tretinoin 242-255 retinoic acid receptor, alpha Mus musculus 42-50
30355624-10 2018 Together, our results demonstrate that RA/RARalpha signaling acts as a key component for homeostatic regulation of synaptic transmission at the inhibitory synapses of the visual cortex.SIGNIFICANCE STATEMENT In vitro studies established that retinoic acid (RA) and its receptor RARalpha play key roles in homeostatic synaptic plasticity, a mechanism by which synaptic excitation/inhibition balance and network stability are maintained. Tretinoin 242-255 retinoic acid receptor, alpha Mus musculus 278-286
30355624-10 2018 Together, our results demonstrate that RA/RARalpha signaling acts as a key component for homeostatic regulation of synaptic transmission at the inhibitory synapses of the visual cortex.SIGNIFICANCE STATEMENT In vitro studies established that retinoic acid (RA) and its receptor RARalpha play key roles in homeostatic synaptic plasticity, a mechanism by which synaptic excitation/inhibition balance and network stability are maintained. Tretinoin 39-41 retinoic acid receptor, alpha Mus musculus 42-50
30355624-10 2018 Together, our results demonstrate that RA/RARalpha signaling acts as a key component for homeostatic regulation of synaptic transmission at the inhibitory synapses of the visual cortex.SIGNIFICANCE STATEMENT In vitro studies established that retinoic acid (RA) and its receptor RARalpha play key roles in homeostatic synaptic plasticity, a mechanism by which synaptic excitation/inhibition balance and network stability are maintained. Tretinoin 39-41 retinoic acid receptor, alpha Mus musculus 278-286
30019299-5 2019 In the present study, we demonstrate that silencing of endogenous RACK1 expression synergized with ATRA to promote the death of NB4 and HL-60 APL cells without effect on cell differentiation induced by ATRA. Tretinoin 202-206 receptor for activated C kinase 1 Homo sapiens 66-71
30568578-0 2018 Retinoic Acid Regulates Endothelial beta-catenin Expression and Pericyte Numbers in the Developing Brain Vasculature. Tretinoin 0-13 catenin (cadherin associated protein), beta 1 Mus musculus 36-48
30409702-1 2018 The retinaldehyde dehydrogenase (RALDH) enzymes, RALDH1, RALDH2, and RALDH3, catalyze the irreversible oxidation of retinaldehyde to all-trans-retinoic acid (ATRA). Tretinoin 137-156 aldehyde dehydrogenase 1 family member A2 Homo sapiens 57-63
30409702-1 2018 The retinaldehyde dehydrogenase (RALDH) enzymes, RALDH1, RALDH2, and RALDH3, catalyze the irreversible oxidation of retinaldehyde to all-trans-retinoic acid (ATRA). Tretinoin 158-162 aldehyde dehydrogenase 1 family member A2 Homo sapiens 57-63
18539269-1 2008 Retinoic acid (RA) is known to be required at various levels of eye patterning via Retinoic Acid Receptors (RAR); however the molecular and cellular mechanisms triggered by these nuclear receptors are still obscure. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 108-111
18555216-8 2008 We also showed that retinoic acid (RA) stimulates the mannosylation of OA protein. Tretinoin 20-33 glycoprotein (transmembrane) nmb Mus musculus 71-73
30059166-8 2018 ATRA inhibited physiologically induced (RANKL) osteoclast formation of human peripheral blood monocytes and mouse BMM as well as human monocytes stimulated with the pro-inflammatory compounds, TNF-alpha and LPS. Tretinoin 0-4 TNF superfamily member 11 Homo sapiens 40-45
29619741-5 2018 In our recently published study, we have identified a set of miRNAs including miR-145 and miR-29b families differentially expressed in SH-SY5Y cells exposed sequentially with retinoic acid + brain-derived neurotrophic factor (RA+BDNF) for differentiation into mature neurons (Mol Neurobiol (2016) doi: https://doi.org/10.1007/s12035-016-0042-9 ). Tretinoin 175-188 brain derived neurotrophic factor Homo sapiens 229-233
30372846-8 2018 RESULTS AND DISCUSSION: In silico docking, analysis confirms that ATRA interferes with the normal binding of ligands (TNF-alpha, IL6ST) and receptors (TNFR1, IL6) of ERK/JAK-STAT pathways respectively. Tretinoin 66-70 TNF receptor superfamily member 1A Rattus norvegicus 151-156
29350420-1 2018 Differentiated embryo chondrocyte 1 (DEC1), a member of basic-helix-loop-helix transcription factor Bhlhe40, also called stimulated by retinoic acid 13, STRA13, plays an important role in the regulation of adipogenesis, tumorigenesis, peripheral circadian output, response to hypoxia, and development of metabolic syndrome. Tretinoin 135-148 basic helix-loop-helix family member e40 Bos taurus 100-107
18636162-1 2008 All-trans-retinoic acid (RA) treatment of acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, PML/RARalpha, is a successful example of differentiation therapy. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 116-119
18636162-1 2008 All-trans-retinoic acid (RA) treatment of acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, PML/RARalpha, is a successful example of differentiation therapy. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 120-128
30366671-0 2018 Adenylate cyclase 7 regulated by miR-192 promotes ATRA-induced differentiation of acute promyelocytic leukemia cells. Tretinoin 50-54 adenylate cyclase 7 Homo sapiens 0-19
18636162-1 2008 All-trans-retinoic acid (RA) treatment of acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, PML/RARalpha, is a successful example of differentiation therapy. Tretinoin 25-27 PML nuclear body scaffold Homo sapiens 116-119
30366671-2 2018 However, the roles of AC7 in all-trans retinoic acid (ATRA)-induced differentiation of acute promyelocytic leukemia (APL) cells are still unknown. Tretinoin 33-52 adenylate cyclase 7 Homo sapiens 22-25
30522558-7 2018 At the same time, RA could arrest the cell cycle of CSCs and reduce the expression of Sox-2, Oct-4 in CSCs of melanoma, thereby induced the differentiation of CSCs and increased its sensitivity to paclitaxel. Tretinoin 18-20 SRY-box transcription factor 2 Homo sapiens 86-91
30366671-2 2018 However, the roles of AC7 in all-trans retinoic acid (ATRA)-induced differentiation of acute promyelocytic leukemia (APL) cells are still unknown. Tretinoin 54-58 adenylate cyclase 7 Homo sapiens 22-25
18636162-1 2008 All-trans-retinoic acid (RA) treatment of acute promyelocytic leukemia (APL) cases expressing the t(15;17) product, PML/RARalpha, is a successful example of differentiation therapy. Tretinoin 25-27 retinoic acid receptor alpha Homo sapiens 120-128
30366671-3 2018 In this study, firstly, our results showed that AC7 affected intracellular cAMP level and influenced ATRA-induced differentiation of APL cells. Tretinoin 101-105 adenylate cyclase 7 Homo sapiens 48-51
18305572-5 2008 The effects of norepinephrine (NE) and 9-cis retinoic acid (RA) on UCP expression were also investigated. Tretinoin 60-62 uncoupling protein 1 Homo sapiens 67-70
30224377-3 2018 In agreement with reports in other cancers, we observe loss, downregulation, or mutation of the innate viral nucleotide sensor retinoic acid-inducible gene I (RIG-I/DDX58) in only 1% of clinical breast cancers, suggesting potentially widespread applicability for therapeutic RIG-I agonists that activate innate immunity. Tretinoin 127-140 DExD/H-box helicase 58 Homo sapiens 159-164
30224377-3 2018 In agreement with reports in other cancers, we observe loss, downregulation, or mutation of the innate viral nucleotide sensor retinoic acid-inducible gene I (RIG-I/DDX58) in only 1% of clinical breast cancers, suggesting potentially widespread applicability for therapeutic RIG-I agonists that activate innate immunity. Tretinoin 127-140 DExD/H-box helicase 58 Homo sapiens 165-170
30224377-3 2018 In agreement with reports in other cancers, we observe loss, downregulation, or mutation of the innate viral nucleotide sensor retinoic acid-inducible gene I (RIG-I/DDX58) in only 1% of clinical breast cancers, suggesting potentially widespread applicability for therapeutic RIG-I agonists that activate innate immunity. Tretinoin 127-140 DExD/H-box helicase 58 Homo sapiens 275-280
30145807-3 2018 The expression of TNFAIP2 is regulated by multiple transcription factors and signalling pathways, including NF-kappaB, KLF5 and retinoic acid. Tretinoin 128-141 TNF alpha induced protein 2 Homo sapiens 18-25
29377254-7 2018 Retinoic acid, an agonist of GnT-V, further increased glycosylated CD147, and activated matrix metalloproteinase-2/-9 (MMP-2 and MMP-9) in the hypertrophied left ventricle of 2K1C rat. Tretinoin 0-13 matrix metallopeptidase 9 Rattus norvegicus 129-134
30420837-11 2018 ADH1 could increase retinoic acid (RA) synthesis, then RA facilitates Leydig cell differentiation by activating the steroidogenic factor 1 gene (Nr5a1) promoter activity, which consequently promotes Leydig cell specific gene expression, resulting in progenitor Leydig cells differentiation into functional Leydig cells. Tretinoin 20-33 nuclear receptor subfamily 5, group A, member 1 Mus musculus 145-150
30420837-11 2018 ADH1 could increase retinoic acid (RA) synthesis, then RA facilitates Leydig cell differentiation by activating the steroidogenic factor 1 gene (Nr5a1) promoter activity, which consequently promotes Leydig cell specific gene expression, resulting in progenitor Leydig cells differentiation into functional Leydig cells. Tretinoin 55-57 nuclear receptor subfamily 5, group A, member 1 Mus musculus 116-138
30420837-11 2018 ADH1 could increase retinoic acid (RA) synthesis, then RA facilitates Leydig cell differentiation by activating the steroidogenic factor 1 gene (Nr5a1) promoter activity, which consequently promotes Leydig cell specific gene expression, resulting in progenitor Leydig cells differentiation into functional Leydig cells. Tretinoin 55-57 nuclear receptor subfamily 5, group A, member 1 Mus musculus 145-150
32254654-4 2018 The release profile, DNA, and elastin analysis of direct and transwell seeded RA-loaded PCL electrospun scaffolds showed desirable controlled release at 15 kV fabrication, with 0.01% RA as the optimum concentration. Tretinoin 78-80 elastin Homo sapiens 30-37
32254654-8 2018 For both hMSC and HDF cultures, exposure to RA-loaded PCL scaffolds provided a significant increase in elastin production per cell. Tretinoin 44-46 elastin Homo sapiens 103-110
18305572-7 2008 UCP1 expression in keratinocytes was synergistically upregulated by NE and RA treatment. Tretinoin 75-77 uncoupling protein 1 Homo sapiens 0-4
18458045-9 2008 Results from experiments with several species of RA and with retinoic acid receptor (RAR) and retinoid X receptor (RXR) antagonists showed that the effect of RA on PGIS expression was mediated by RAR. Tretinoin 85-87 retinoic acid receptor alpha Homo sapiens 61-83
30360758-12 2018 Accordingly, TFEB was observed to be mainly expressed in differentiating spermatogonia and was activated for nuclear translocation by RA treatment. Tretinoin 134-136 transcription factor EB Mus musculus 13-17
30360758-14 2018 CONCLUSION: These findings imply that regionally distinct expression and activation of TFEB was strongly associated with RA signaling, and therefore may promote cell migration across the BTB and transport along the seminiferous epithelium. Tretinoin 121-123 transcription factor EB Mus musculus 87-91
30289902-8 2018 In deletion PML-RARA-transduced cells, the CD11b expression levels and NBT reducing ability were significantly decreased compared with control cells and the formation of PML nuclear bodies was rarely observed after RA treatment. Tretinoin 16-18 integrin subunit alpha M Homo sapiens 43-48
30425691-6 2018 Combining ATRA with a non-ablative fractional laser (NAFL), which represents a new category of vaccine adjuvant utilizing physical stimuli to induce self-immune stimulators, further enhanced the efficacy of influenza vaccines with a more balanced Th1/Th2 immune response. Tretinoin 10-14 negative elongation factor complex member C/D Homo sapiens 247-250
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 40-53 retinoid X receptor alpha Homo sapiens 178-197
30190278-0 2018 Variant PRC1 competes with retinoic acid-related signals to repress Meis2 in the mouse distal forelimb bud. Tretinoin 27-40 Meis homeobox 2 Mus musculus 68-73
18458045-9 2008 Results from experiments with several species of RA and with retinoic acid receptor (RAR) and retinoid X receptor (RXR) antagonists showed that the effect of RA on PGIS expression was mediated by RAR. Tretinoin 85-87 retinoic acid receptor alpha Homo sapiens 196-199
30190278-4 2018 Here, we reveal that PcG factors and RA-related signals antagonize each other to polarize Meis2 expression along the PD axis in mouse. Tretinoin 37-39 Meis homeobox 2 Mus musculus 90-95
18495661-1 2008 All-trans-retinoic acid stimulates dendritic growth in hippocampal neurons within minutes by activating mitogen-activated protein kinase and mTOR and increasing dendritic translation of calcium calmodulin-dependent protein kinase II alpha and the alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate receptor subunit GluR1. Tretinoin 0-23 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 319-324
30190278-5 2018 Supported by mathematical modeling and simulation, we propose that PcG factors are required to adjust the threshold for RA-related signaling to regulate Meis2 expression. Tretinoin 120-122 Meis homeobox 2 Mus musculus 153-158
30209067-0 2018 Zebrafish blastomere screen identifies retinoic acid suppression of MYB in adenoid cystic carcinoma. Tretinoin 39-52 v-myb avian myeloblastosis viral oncogene homolog Danio rerio 68-71
30209067-3 2018 We performed a chemical genetic screen and identified retinoic acid agonists as suppressors of c-myb expression. Tretinoin 54-67 v-myb avian myeloblastosis viral oncogene homolog Danio rerio 95-100
30121453-10 2018 Additionally, ATRA reduces the expression of immunosuppressive genes including PD-L1, IL-10, and indoleamine 2,3-dioxygenase by MDSCs. Tretinoin 14-18 interleukin 10 Homo sapiens 86-91
18495661-2 2008 Hippocampal neurons express RARalpha in dendrites, and knocking down RARalpha prevents all-trans-retinoic acid effects on dendritic growth. Tretinoin 87-110 retinoic acid receptor alpha Homo sapiens 69-77
18491231-0 2008 Death-associated protein 5 (DAP5/p97/NAT1) contributes to retinoic acid-induced granulocytic differentiation and arsenic trioxide-induced apoptosis in acute promyelocytic leukemia. Tretinoin 58-71 N-acetyltransferase 1 Homo sapiens 37-41
30275368-3 2018 The bioactive derivatives of these retinoids are the retinoic acids, which can potently activate nuclear hormone receptors such as the retinoic acid receptor and the retinoid X receptor. Tretinoin 53-67 retinoid X receptor alpha Homo sapiens 166-185
30217263-11 2018 Interestingly, rhein potentiated all-trans retinoic acid (ATRA)-induced macrophage differentiation in NB4 cells by inducing changes in morphology, expression of the differentiation markers CD11b and CD14, ROS production, phagocytic activity, and expression of CCR1 and CCR2. Tretinoin 58-62 integrin subunit alpha M Homo sapiens 189-194
18445086-2 2008 PML/RARalpha is directly targeted by all-trans-retinoic acid (ATRA), which degrades the oncoprotein and induces complete remission of malignancies. Tretinoin 37-60 PML nuclear body scaffold Homo sapiens 0-3
30195874-11 2018 The combination treatment with allicin and ATRA significantly reduced the IC50 value obtained for ATRA alone in CD44+ melanoma cells. Tretinoin 43-47 CD44 molecule (Indian blood group) Homo sapiens 112-116
30195874-11 2018 The combination treatment with allicin and ATRA significantly reduced the IC50 value obtained for ATRA alone in CD44+ melanoma cells. Tretinoin 98-102 CD44 molecule (Indian blood group) Homo sapiens 112-116
30195874-12 2018 In CD44+ cells, the IC50 value of ATRA was 37.43 +- 0.54, while the IC50 value of allicin/ATRA treatment was 17.53 +- 0.2 microM. Tretinoin 34-38 CD44 molecule (Indian blood group) Homo sapiens 3-7
30195874-14 2018 The combination treatment caused the inhibition of CD44+ and CD117+ melanoma cells at the S phases compared to ATRA alone. Tretinoin 111-115 CD44 molecule (Indian blood group) Homo sapiens 51-55
30195874-15 2018 Allicin, ATRA, and allicin/ATRA increased the expression of cyclin D1 mRNA in both CD44+ and CD117+ cells. Tretinoin 9-13 CD44 molecule (Indian blood group) Homo sapiens 83-87
30195874-15 2018 Allicin, ATRA, and allicin/ATRA increased the expression of cyclin D1 mRNA in both CD44+ and CD117+ cells. Tretinoin 27-31 CD44 molecule (Indian blood group) Homo sapiens 83-87
30028046-5 2018 Furthermore, SC1 inhibits downregulation of pluripotency-related genes caused by retinoic acid and promotes the proliferation of cBCs. Tretinoin 81-94 activated leukocyte cell adhesion molecule Gallus gallus 13-16
30195874-0 2018 Molecular mechanism and cytotoxicity of allicin and all-trans retinoic acid against CD44+ versus CD117+ melanoma cells. Tretinoin 62-75 CD44 molecule (Indian blood group) Homo sapiens 84-88
30195874-4 2018 To clarify this mechanism, we determined the sensitivity to ATRA, allicin and allicin/ATRA in CD44+ and CD117+ melanoma cell subpopulations. Tretinoin 86-90 CD44 molecule (Indian blood group) Homo sapiens 94-98
30195874-9 2018 RESULTS: Here, we demonstrated that CD44+ melanoma cells were more resistant to allicin and ATRA than CD117+ cells. Tretinoin 92-96 CD44 molecule (Indian blood group) Homo sapiens 36-40
29940355-7 2018 In summary, our data illustrate a previously unrecognized pathway in which SETD1A contributes to RA-induced TM expression in vascular endothelial cells by modulating the activity and expression of KLF4. Tretinoin 97-99 Kruppel like factor 4 Homo sapiens 197-201
29936250-10 2018 Fluorescence-activated cell sorting (FACS) analysis demonstrated a marked increase in systemic CD34+/Flk-1+ EPCs in ATRA-treated rat. Tretinoin 116-120 CD34 molecule Rattus norvegicus 95-99
29936250-11 2018 The expression of ANG2 and VEGF was increased in diabetic flap tissues under ATRA administration. Tretinoin 77-81 angiogenin, ribonuclease A family, member 2 Rattus norvegicus 18-22
30195874-18 2018 In contrast, ATRA and the combination treatment significantly increased MMP-9 gene expression in CD44+ cells. Tretinoin 13-17 matrix metallopeptidase 9 Homo sapiens 72-77
30195874-18 2018 In contrast, ATRA and the combination treatment significantly increased MMP-9 gene expression in CD44+ cells. Tretinoin 13-17 CD44 molecule (Indian blood group) Homo sapiens 97-101
18445086-2 2008 PML/RARalpha is directly targeted by all-trans-retinoic acid (ATRA), which degrades the oncoprotein and induces complete remission of malignancies. Tretinoin 37-60 retinoic acid receptor alpha Homo sapiens 4-12
30195874-19 2018 CONCLUSION: Overall, our results indicate that allicin reinforces the ATRA-mediated inhibitory effects on CD44+ and CD117+ melanoma cells and may provide a new approach for the treatment of malignant melanoma. Tretinoin 70-74 CD44 molecule (Indian blood group) Homo sapiens 106-110
18445086-2 2008 PML/RARalpha is directly targeted by all-trans-retinoic acid (ATRA), which degrades the oncoprotein and induces complete remission of malignancies. Tretinoin 62-66 PML nuclear body scaffold Homo sapiens 0-3
28536942-0 2018 LRRC25 plays a key role in all-trans retinoic acid-induced granulocytic differentiation as a novel potential leukocyte differentiation antigen. Tretinoin 37-50 CD1e molecule Homo sapiens 109-142
28536942-8 2018 Therefore, LRRC25, a potential leukocyte differentiation antigen, is a key regulator of ATRA-induced granulocytic differentiation. Tretinoin 88-92 CD1e molecule Homo sapiens 31-64
18445086-2 2008 PML/RARalpha is directly targeted by all-trans-retinoic acid (ATRA), which degrades the oncoprotein and induces complete remission of malignancies. Tretinoin 62-66 retinoic acid receptor alpha Homo sapiens 4-12
30225259-7 2018 Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. Tretinoin 154-158 retinoid X receptor alpha Homo sapiens 65-68
29848550-0 2018 Combinatorial knockout of RARalpha, RARbeta, and RARgamma completely abrogates transcriptional responses to retinoic acid in murine embryonic stem cells. Tretinoin 108-121 retinoic acid receptor, alpha Mus musculus 26-34
18394023-10 2008 In the absence of LPS, RA enhanced the expression of COX-1 mRNA. Tretinoin 23-25 mitochondrially encoded cytochrome c oxidase I Homo sapiens 53-58
29848550-0 2018 Combinatorial knockout of RARalpha, RARbeta, and RARgamma completely abrogates transcriptional responses to retinoic acid in murine embryonic stem cells. Tretinoin 108-121 retinoic acid receptor, gamma Mus musculus 49-57
29848550-1 2018 All-trans-retinoic acid (RA), a potent inducer of cellular differentiation, functions as a ligand for retinoic acid receptors (RARalpha, beta, and gamma). Tretinoin 0-23 retinoic acid receptor, alpha Mus musculus 127-135
29848550-1 2018 All-trans-retinoic acid (RA), a potent inducer of cellular differentiation, functions as a ligand for retinoic acid receptors (RARalpha, beta, and gamma). Tretinoin 25-27 retinoic acid receptor, alpha Mus musculus 127-135
30225259-7 2018 Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. Tretinoin 154-158 retinoid X receptor alpha Homo sapiens 118-121
29986869-4 2018 In this study, we show that retinoic acid (RA) signaling activity at the site of gland initiation is colocalized with expression of retinol metabolic genes Rdh10 and Aldh1a2 in the underlying SMG mesenchyme. Tretinoin 28-41 retinol dehydrogenase 10 Homo sapiens 156-161
29986869-4 2018 In this study, we show that retinoic acid (RA) signaling activity at the site of gland initiation is colocalized with expression of retinol metabolic genes Rdh10 and Aldh1a2 in the underlying SMG mesenchyme. Tretinoin 28-41 aldehyde dehydrogenase 1 family member A2 Homo sapiens 166-173
19035179-6 2008 Western blot displayed that ATRA could decrease the expression of cyclin A, up-regulate the expression of p21 and p27, and down-regulate the expression of p27 related proteins Skp2. Tretinoin 28-32 interferon alpha inducible protein 27 Homo sapiens 114-117
29945211-6 2018 Moreover, exposure to beta-CYP and 3-PBA at 100 muM inhibited all-trans retinoic acid (ATRA)-induced mRNA expressions of the granulocytic differentiation-related genes, CD11b and CSF-3R. Tretinoin 72-85 integrin subunit alpha M Homo sapiens 169-174
30089026-7 2018 Flow cytometry analysis showed that mean number of Mvh-positive cells in the +RA group was greater as compared with ESCs, -RA and EB7 groups (p = 0.00). Tretinoin 78-80 DEAD box helicase 4 Mus musculus 51-54
29941555-2 2018 Here, we show that the expression of ZNF281, a zinc finger factor involved in several cellular processes, decreases during terminal differentiation of murine cortical neurons and in retinoic acid-induced differentiation of neuroblastoma (NB) cells. Tretinoin 182-195 zinc finger protein 281 Mus musculus 37-43
29730892-8 2018 However, transfer of p70S6k1 over-expressing-MSCs together with ATRA resulted in further improvements over those seen following WT MSCs together with ATRA. Tretinoin 150-154 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 21-28
29730892-9 2018 ATRA activated p70S6k1 in MSCs in vitro, which was completely inhibited by rapamycin. Tretinoin 0-4 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 15-22
29688535-9 2018 The treatment of ATRA (1,000 nM) also increased (P < 0.05) mRNA gene expression of SMAD3. Tretinoin 17-21 SMAD family member 3 Bos taurus 86-91
19035179-6 2008 Western blot displayed that ATRA could decrease the expression of cyclin A, up-regulate the expression of p21 and p27, and down-regulate the expression of p27 related proteins Skp2. Tretinoin 28-32 interferon alpha inducible protein 27 Homo sapiens 155-158
18082256-2 2008 The ALDH1A1 gene, whose product participates in retinoic acid synthesis, was previously identified as a TLX1-responsive gene. Tretinoin 48-61 T cell leukemia, homeobox 1 Mus musculus 104-108
29945667-1 2018 BACKGROUND: Previous work aimed at understanding the gene regulatory networks (GRNs) governing caudal hindbrain formation identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Tretinoin 152-165 homeobox B1b Danio rerio 247-253
29945667-1 2018 BACKGROUND: Previous work aimed at understanding the gene regulatory networks (GRNs) governing caudal hindbrain formation identified morphogens such as Retinoic Acid (RA) and Fibroblast growth factors (FGFs), as well as transcription factors like hoxb1b, hoxb1a, hnf1ba, and valentino as being required for rhombomere (r) r4-r6 formation in zebrafish. Tretinoin 167-169 homeobox B1b Danio rerio 247-253
29880835-7 2018 In effect, ATRA increased the resistance to apoptosis despite the high CRABP2/FABP5 ratio of RA FLS; and CRABP2 suppression sensitized RA FLS to Fas-induced apoptosis. Tretinoin 11-15 fatty acid binding protein 5 Homo sapiens 78-83
29891447-5 2018 RESULTS: Compared with the control cells, the hepatocytes treated with ATRA showed a concentration-dependent decrease in AFP expression and increase in the expressions of ALB, CK18, TAT and ApoB. Tretinoin 71-75 alpha fetoprotein Mus musculus 121-124
29891447-8 2018 ATRA treatment resulted in significantly increased the expressions of autophagy-related markers LC3-II, Beclin-1, RAB7 and P62 and also an increased ratio of LC3-II/LC3-I(P<0.05). Tretinoin 0-4 nucleoporin 62 Mus musculus 123-126
29892071-3 2018 Embryos can generate retinoic acid from maternal circulating beta-carotene upon oxidation of retinaldehyde produced via the symmetric cleavage enzyme beta-carotene 15,15"-oxygenase (BCO1). Tretinoin 21-34 beta-carotene oxygenase 1 Homo sapiens 182-186
18400747-7 2008 Retinoic acid has also been shown to suppress loss of Foxp3 induced by TGF-beta1. Tretinoin 0-13 forkhead box P3 Mus musculus 54-59
18400747-8 2008 Retinoic acid in the presence of TGF-beta1 reduced STAT6 binding to the Foxp3 promoter and enhanced histone acetylation, thereby reverting the effect of IL-4. Tretinoin 0-13 forkhead box P3 Mus musculus 72-77
29760176-9 2018 However, whether RA signaling mediated by RARalpha contributes to neural circuit functions in vivo remains largely unknown. Tretinoin 17-19 retinoic acid receptor, alpha Mus musculus 42-50
18400747-8 2008 Retinoic acid in the presence of TGF-beta1 reduced STAT6 binding to the Foxp3 promoter and enhanced histone acetylation, thereby reverting the effect of IL-4. Tretinoin 0-13 interleukin 4 Mus musculus 153-157
29868013-8 2018 We also found that Con A administration led to an increase in the retinoic acid early inducible (RAE-1) surface expression on wild-type hepatocytes. Tretinoin 66-79 ribonucleic acid export 1 Mus musculus 97-102
29802528-5 2018 We demonstrated that ATRA pretreatment could alleviate CIR-induced neurological deficits, increase of BBB permeability, infarct volume, degradation of tight junction proteins, inhibit MMP-9 protein expression and activity. Tretinoin 21-25 matrix metallopeptidase 9 Rattus norvegicus 184-189
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 154-157
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 351-354
28993924-5 2018 In order to better understand the biological role of ACh in AD, we studied the effect of Abeta on the phosphorylation of the cytosolic phospholipase A2 (cPLA2) in the TB neuroectodermal cell line, which differentiates toward a neuronal phenotype when cultured in the presence of retinoic acid (RA). Tretinoin 279-292 phospholipase A2 group IVA Homo sapiens 153-158
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 retinoic acid receptor alpha Homo sapiens 154-157
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 retinoic acid receptor alpha Homo sapiens 351-354
29972129-13 2018 Compared with the ATRA group, the OM-85BV+ATRA group had significantly increased levels of IL-10 and IL-17 in BALF (P<0.05). Tretinoin 42-46 interleukin 17A Mus musculus 101-106
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 retinoic acid receptor alpha Homo sapiens 154-157
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 retinoic acid receptor alpha Homo sapiens 351-354
18453568-6 2008 Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Tretinoin 58-71 interleukin 4 Mus musculus 146-150
29844435-9 2018 Detailed functional experiments demonstrated that circ-HIPK2, one of the differentially expressed circRNAs, significantly influenced ATRA-induced differentiation of APL cells. Tretinoin 133-137 homeodomain interacting protein kinase 2 Homo sapiens 55-60
29111326-2 2018 LncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) is indispensable during acute promyelocytic leukemia (APL) cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 155-168 nuclear paraspeckle assembly transcript 1 Homo sapiens 7-45
29111326-2 2018 LncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) is indispensable during acute promyelocytic leukemia (APL) cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 155-168 nuclear paraspeckle assembly transcript 1 Homo sapiens 47-52
29111326-2 2018 LncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) is indispensable during acute promyelocytic leukemia (APL) cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 170-174 nuclear paraspeckle assembly transcript 1 Homo sapiens 7-45
29139475-5 2018 Mechanistically, lack of RARalpha resulted in increased KLF4+ goblet cell precursors in the distal bowel, whereas RA treatment inhibited klf4 expression and goblet cell differentiation in zebrafish. Tretinoin 25-27 Kruppel-like factor 4 Danio rerio 56-60
29326073-2 2018 Here, we show that RA transcriptionally upregulates cystic fibrosis transmembrane conductance regulator (Cftr) by promoting the direct binding of its receptor RARalpha to Cftr promoter in mouse spermatogonia and embryonic stem (ES) cells. Tretinoin 19-21 cystic fibrosis transmembrane conductance regulator Mus musculus 52-103
29111326-2 2018 LncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) is indispensable during acute promyelocytic leukemia (APL) cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 170-174 nuclear paraspeckle assembly transcript 1 Homo sapiens 47-52
18453568-6 2008 Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Tretinoin 73-75 interleukin 4 Mus musculus 146-150
29111326-5 2018 Moreover, the expression of C/EBPbeta was increased after ATRA treatment, and the binding of C/EBPbeta in the NEAT1 promoter was also dramatically increased. Tretinoin 58-62 nuclear paraspeckle assembly transcript 1 Homo sapiens 110-115
29111326-6 2018 Finally, knockdown of C/EBPbeta significantly reduced the ATRA-induced upregulation of NEAT1. Tretinoin 58-62 nuclear paraspeckle assembly transcript 1 Homo sapiens 87-92
29326073-2 2018 Here, we show that RA transcriptionally upregulates cystic fibrosis transmembrane conductance regulator (Cftr) by promoting the direct binding of its receptor RARalpha to Cftr promoter in mouse spermatogonia and embryonic stem (ES) cells. Tretinoin 19-21 cystic fibrosis transmembrane conductance regulator Mus musculus 105-109
18453568-6 2008 Consistent with the finding that the vitamin A metabolite retinoic acid (RA) induces gut-homing molecules on T cells, we further demonstrate that IL-4 up-regulated retinaldehyde dehydrogenase 2 mRNA on MLN-DC, a critical enzyme involved in the synthesis of RA. Tretinoin 257-259 interleukin 4 Mus musculus 146-150
29326073-2 2018 Here, we show that RA transcriptionally upregulates cystic fibrosis transmembrane conductance regulator (Cftr) by promoting the direct binding of its receptor RARalpha to Cftr promoter in mouse spermatogonia and embryonic stem (ES) cells. Tretinoin 19-21 retinoic acid receptor, alpha Mus musculus 159-167
29326073-2 2018 Here, we show that RA transcriptionally upregulates cystic fibrosis transmembrane conductance regulator (Cftr) by promoting the direct binding of its receptor RARalpha to Cftr promoter in mouse spermatogonia and embryonic stem (ES) cells. Tretinoin 19-21 cystic fibrosis transmembrane conductance regulator Mus musculus 171-175
29111326-8 2018 Knockdown of C/EBPbeta impairs ATRA-induced transcriptional activation of NEAT1. Tretinoin 31-35 nuclear paraspeckle assembly transcript 1 Homo sapiens 74-79
29111326-9 2018 Our data indicate that C/EBPbeta contributes to ATRA-induced activation of NEAT1 during APL cell differentiation. Tretinoin 48-52 nuclear paraspeckle assembly transcript 1 Homo sapiens 75-80
18216048-2 2008 The current study investigated the role of monocyte chemotactic protein (MCP)-1 in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4) APL cells toward A549 alveolar epithelial cells. Tretinoin 117-121 C-C motif chemokine ligand 2 Homo sapiens 43-79
29476041-0 2018 CYP26C1 Is a Hydroxylase of Multiple Active Retinoids and Interacts with Cellular Retinoic Acid Binding Proteins. Tretinoin 82-95 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
29428877-4 2018 The association RA plus MPA provided the most complete and mature neuron phenotype, as demonstrated by high levels of beta-Tubulin III, MAP-2, and tyrosine hydroxylase. Tretinoin 16-18 microtubule associated protein 2 Homo sapiens 136-141
18216048-6 2008 The secretion of MCP-1 was enhanced by ATRA treatment in both A549 and NB4 cells. Tretinoin 39-43 C-C motif chemokine ligand 2 Homo sapiens 17-22
29476041-2 2018 The goal of this study was to establish the substrate specificity of CYP26C1, and determine whether CYP26C1 interacts with cellular retinoic acid binding proteins (CRABPs). Tretinoin 132-145 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 100-107
29476041-3 2018 CYP26C1 was found to effectively metabolize all-trans retinoic acid (atRA), 9-cis-retinoic acid (9-cis-RA), 13-cis-retinoic acid, and 4-oxo-atRA with the highest intrinsic clearance toward 9-cis-RA. Tretinoin 44-67 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
18216048-10 2008 Monocyte chemotactic protein-1 secreted from alveolar epithelial cells plays an important role in the cell-cell interaction involved in the chemotactic transmigration of all-trans retinoic acid-treated acute promyelocytic leukaemia cells toward alveolar epithelial cells. Tretinoin 180-193 C-C motif chemokine ligand 2 Homo sapiens 0-30
29476041-3 2018 CYP26C1 was found to effectively metabolize all-trans retinoic acid (atRA), 9-cis-retinoic acid (9-cis-RA), 13-cis-retinoic acid, and 4-oxo-atRA with the highest intrinsic clearance toward 9-cis-RA. Tretinoin 69-73 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
29337257-5 2018 Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51. Tretinoin 57-70 dehydrogenase/reductase 3 Homo sapiens 260-265
29337257-5 2018 Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51. Tretinoin 57-70 methylsterol monooxygenase 1 Homo sapiens 270-275
18064629-6 2008 All-trans retinoic acid or atRA, while alone inducing AQP3 expression, attenuates UV-induced down-regulation of AQP3 and water permeability. Tretinoin 10-23 aquaporin 3 (Gill blood group) Homo sapiens 54-58
29596381-9 2018 Our results demonstrate for the first time: (1) the therapeutic value of resveratrol by itself or in combination with RA in the management of ATCs, (2) the capacity of resveratrol to overcome RA resistance in ATC cells by reprogramming CRABP2/RAR- and fatty acid-binding protein 5 (FABP5)/PPAR-beta/delta-mediated RA signaling, and (3) the redifferentiating potential of resveratrol in ATC cells. Tretinoin 192-194 cellular retinoic acid binding protein 2 Homo sapiens 236-242
18064629-6 2008 All-trans retinoic acid or atRA, while alone inducing AQP3 expression, attenuates UV-induced down-regulation of AQP3 and water permeability. Tretinoin 10-23 aquaporin 3 (Gill blood group) Homo sapiens 112-116
29596381-9 2018 Our results demonstrate for the first time: (1) the therapeutic value of resveratrol by itself or in combination with RA in the management of ATCs, (2) the capacity of resveratrol to overcome RA resistance in ATC cells by reprogramming CRABP2/RAR- and fatty acid-binding protein 5 (FABP5)/PPAR-beta/delta-mediated RA signaling, and (3) the redifferentiating potential of resveratrol in ATC cells. Tretinoin 192-194 fatty acid binding protein 5 Homo sapiens 252-280
29596381-9 2018 Our results demonstrate for the first time: (1) the therapeutic value of resveratrol by itself or in combination with RA in the management of ATCs, (2) the capacity of resveratrol to overcome RA resistance in ATC cells by reprogramming CRABP2/RAR- and fatty acid-binding protein 5 (FABP5)/PPAR-beta/delta-mediated RA signaling, and (3) the redifferentiating potential of resveratrol in ATC cells. Tretinoin 192-194 fatty acid binding protein 5 Homo sapiens 282-287
29596381-9 2018 Our results demonstrate for the first time: (1) the therapeutic value of resveratrol by itself or in combination with RA in the management of ATCs, (2) the capacity of resveratrol to overcome RA resistance in ATC cells by reprogramming CRABP2/RAR- and fatty acid-binding protein 5 (FABP5)/PPAR-beta/delta-mediated RA signaling, and (3) the redifferentiating potential of resveratrol in ATC cells. Tretinoin 192-194 peroxisome proliferator activated receptor delta Homo sapiens 289-298
29534930-1 2018 Crystallography has identified stearic acid, ALRT 1550 and ATRA as ligands that bind RORbeta, however, none of these molecules represent good starting points to develop optimized small molecule modulators. Tretinoin 59-63 RAR related orphan receptor B Homo sapiens 85-92
29620445-6 2018 RA induction led to slender spindles and tadpole-like changes of cell morphology, and the expression of germ cell-specific markers (Oct4, Piwil2, Itgb1, SSEA-1, and Stra8) presented significant upregulation in the RA treatment group according to the polymerase chain reaction and immunofluorescence results. Tretinoin 0-2 piwi like RNA-mediated gene silencing 2 Homo sapiens 138-144
29620445-6 2018 RA induction led to slender spindles and tadpole-like changes of cell morphology, and the expression of germ cell-specific markers (Oct4, Piwil2, Itgb1, SSEA-1, and Stra8) presented significant upregulation in the RA treatment group according to the polymerase chain reaction and immunofluorescence results. Tretinoin 0-2 integrin subunit beta 1 Homo sapiens 146-151
18064629-6 2008 All-trans retinoic acid or atRA, while alone inducing AQP3 expression, attenuates UV-induced down-regulation of AQP3 and water permeability. Tretinoin 27-31 aquaporin 3 (Gill blood group) Homo sapiens 54-58
29620445-6 2018 RA induction led to slender spindles and tadpole-like changes of cell morphology, and the expression of germ cell-specific markers (Oct4, Piwil2, Itgb1, SSEA-1, and Stra8) presented significant upregulation in the RA treatment group according to the polymerase chain reaction and immunofluorescence results. Tretinoin 0-2 stimulated by retinoic acid 8 Homo sapiens 165-170
29743969-4 2018 Supporting the notion of noncanonical autophagy, we found that ATRA-induced autophagy was Beclin1-independent compared to starvation- or arsenic trioxide- (ATO-) induced autophagy. Tretinoin 63-67 beclin 1 Homo sapiens 90-97
29516351-5 2018 ATRA significantly decreased the nuclear to cytoplasmic ratio of SIRT1 and SIRT2.1, while sirtinol inhibited that of SIRT1, and TSA increased that of SIRT1 and SIRT2.1 during early differentiation. Tretinoin 0-4 sirtuin 1 Homo sapiens 65-70
18064629-6 2008 All-trans retinoic acid or atRA, while alone inducing AQP3 expression, attenuates UV-induced down-regulation of AQP3 and water permeability. Tretinoin 27-31 aquaporin 3 (Gill blood group) Homo sapiens 112-116
18064629-10 2008 We conclude that atRA protects against UV-induced down-regulation AQP3 and decrease in water permeability, reduction in cell migration and delayed in vitro wound healing via trans-activation of EGFR and inhibition on ROS-mediated MEK/ERK pathway. Tretinoin 17-21 aquaporin 3 (Gill blood group) Homo sapiens 66-70
18183617-7 2008 Moreover, ATRA selectively up-regulated the expression of a PGE(2) synthase, mPGES-1, but had little effect on the PGD(2) synthase, H-PGDS. Tretinoin 10-14 prostaglandin E synthase Mus musculus 77-84
29356182-0 2018 Retinoic acid signalling is a candidate regulator of the expression of pituitary-specific transcription factor Prop1 in the developing rodent pituitary. Tretinoin 0-13 PROP paired-like homeobox 1 Rattus norvegicus 111-116
18416830-2 2008 Here, we have demonstrated that the observed effects using ATRA and 9-cis RA are shared with the clinically useful RAR ligand, 13-cis retinoic acid (13-cis RA), and the retinoic acid receptor-alpha (RAR-alpha)-selective agonist, AM580 but not with the RAR-beta/gamma ligand, 4-hydroxyphenylretinamide (4-HPR). Tretinoin 59-63 retinoic acid receptor alpha Homo sapiens 169-197
29356182-4 2018 The present study aimed to clarify the relationship between endogenous RA signalling and mRNA expression of the pituitary-specific transcription factor Prop1 in the pituitary primordium of Rathke"s pouch. Tretinoin 71-73 PROP paired-like homeobox 1 Rattus norvegicus 152-157
29356182-8 2018 This is the first report of a relationship between RA signalling and Prop1-expression during early pituitary development. Tretinoin 51-53 PROP paired-like homeobox 1 Rattus norvegicus 69-74
29240402-2 2018 ALDH1A2 is the primary RA-synthesizing enzyme in mammalian spermatogenesis and is therefore considered a viable drug target for male contraceptive development. Tretinoin 23-25 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-7
18416830-2 2008 Here, we have demonstrated that the observed effects using ATRA and 9-cis RA are shared with the clinically useful RAR ligand, 13-cis retinoic acid (13-cis RA), and the retinoic acid receptor-alpha (RAR-alpha)-selective agonist, AM580 but not with the RAR-beta/gamma ligand, 4-hydroxyphenylretinamide (4-HPR). Tretinoin 59-63 retinoic acid receptor alpha Homo sapiens 199-208
18318772-4 2008 HIC1 mRNA was induced in a patient with t(15;17)-positive acute promyelocytic leukaemia receiving all-trans retinoic acid (ATRA) therapy. Tretinoin 108-121 HIC ZBTB transcriptional repressor 1 Homo sapiens 0-4
29242118-2 2018 In this study, we investigated the regulation of TG2 transamidase activity by NGF in retinoic acid-induced differentiating mouse N2a and human SH-SY5Y neuroblastoma cells. Tretinoin 85-98 nerve growth factor Mus musculus 78-81
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 18-20 integrin subunit alpha 6 Gallus gallus 208-223
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 281-283 Wnt family member 5A Gallus gallus 68-71
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 281-283 Wnt family member 5A Gallus gallus 110-115
28815778-4 2018 In Retinoic acid (RA) induced in vitro differentiation assays, the expression of germ cell marker genes, cvh, c-kit, integrin alpha6 and integrin beta1, was observed to upregulate while activating JNK signaling significantly. Tretinoin 3-16 integrin subunit alpha 6 Gallus gallus 117-132
28815778-4 2018 In Retinoic acid (RA) induced in vitro differentiation assays, the expression of germ cell marker genes, cvh, c-kit, integrin alpha6 and integrin beta1, was observed to upregulate while activating JNK signaling significantly. Tretinoin 18-20 integrin subunit alpha 6 Gallus gallus 117-132
29407582-5 2018 NM23 expression decreased and EDG2 expression increased during all-trans retinoic acid (ATRA)-induced myeloid differentiation of HL-60, NB4, and THP-1 leukemia cells. Tretinoin 73-86 lysophosphatidic acid receptor 1 Homo sapiens 30-34
29407582-5 2018 NM23 expression decreased and EDG2 expression increased during all-trans retinoic acid (ATRA)-induced myeloid differentiation of HL-60, NB4, and THP-1 leukemia cells. Tretinoin 88-92 lysophosphatidic acid receptor 1 Homo sapiens 30-34
29407582-8 2018 ATRA plus LPA enhanced the motility of leukemia cells as well as breast cancer cells in an EDG2-dependent manner. Tretinoin 0-4 lysophosphatidic acid receptor 1 Homo sapiens 91-95
29193451-7 2018 Levels of Pax6, Klf4, and cFos were upregulated in MGPCs by RA agonists and downregulated in MGPCs by RA antagonists. Tretinoin 60-62 paired box 6 Gallus gallus 10-14
29193451-7 2018 Levels of Pax6, Klf4, and cFos were upregulated in MGPCs by RA agonists and downregulated in MGPCs by RA antagonists. Tretinoin 60-62 Kruppel like factor 4 Gallus gallus 16-20
18318772-4 2008 HIC1 mRNA was induced in a patient with t(15;17)-positive acute promyelocytic leukaemia receiving all-trans retinoic acid (ATRA) therapy. Tretinoin 123-127 HIC ZBTB transcriptional repressor 1 Homo sapiens 0-4
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 CD4 antigen Mus musculus 172-175
18318772-6 2008 We evaluated HIC1 mRNA levels in HL-60 and U-937 cells upon ATRA-induced differentiation and in CD34+ progenitor cells after granulocyte colony-stimulating factor-induced differentiation. Tretinoin 60-64 HIC ZBTB transcriptional repressor 1 Homo sapiens 13-17
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 CD4 antigen Mus musculus 239-242
29207193-0 2018 All-trans retinoic acid reduces endothelin-1 expression and increases endothelial nitric oxide synthase phosphorylation in rabbits with atherosclerosis. Tretinoin 0-23 endothelin-1 Oryctolagus cuniculus 32-44
18008394-0 2008 Effect of retinoic acid on transglutaminase and ornithine decarboxylase activities during liver regeneration. Tretinoin 10-23 ornithine decarboxylase 1 Rattus norvegicus 48-71
29207193-0 2018 All-trans retinoic acid reduces endothelin-1 expression and increases endothelial nitric oxide synthase phosphorylation in rabbits with atherosclerosis. Tretinoin 0-23 nitric oxide synthase, endothelial Oryctolagus cuniculus 70-103
29207193-8 2018 Western blotting demonstrated significantly decreased ET-1 expression levels in the arterial tissue of rabbits in the ATRA group compared with the high fat group, together with increased p-eNOS level (P<0.05), however, no difference was observed in the expression of eNOS (P>0.05). Tretinoin 118-122 endothelin-1 Oryctolagus cuniculus 54-58
29207193-8 2018 Western blotting demonstrated significantly decreased ET-1 expression levels in the arterial tissue of rabbits in the ATRA group compared with the high fat group, together with increased p-eNOS level (P<0.05), however, no difference was observed in the expression of eNOS (P>0.05). Tretinoin 118-122 nitric oxide synthase, endothelial Oryctolagus cuniculus 189-193
29207193-8 2018 Western blotting demonstrated significantly decreased ET-1 expression levels in the arterial tissue of rabbits in the ATRA group compared with the high fat group, together with increased p-eNOS level (P<0.05), however, no difference was observed in the expression of eNOS (P>0.05). Tretinoin 118-122 nitric oxide synthase, endothelial Oryctolagus cuniculus 270-274
29207193-10 2018 Therefore, the present study demonstrated that ATRA may regulate the grade of AS by the reduction of ET-1 secretion and increased NO formation via increased phosphorylation of eNOS. Tretinoin 47-51 endothelin-1 Oryctolagus cuniculus 101-105
29207193-10 2018 Therefore, the present study demonstrated that ATRA may regulate the grade of AS by the reduction of ET-1 secretion and increased NO formation via increased phosphorylation of eNOS. Tretinoin 47-51 nitric oxide synthase, endothelial Oryctolagus cuniculus 176-180
28436029-14 2018 Collectively, WNT4 may act downstream of BMP2 to mediate the effects of ATRA on the terminal differentiation of antler chondrocytes through targeting RUNX1. Tretinoin 72-76 Wnt family member 4 Homo sapiens 14-18
29177441-7 2018 These variants altered the expression of CYP26A1, a direct CDX2 target encoding the major retinoic acid (RA)-degrading enzyme. Tretinoin 90-103 caudal type homeobox 2 Homo sapiens 59-63
18008394-3 2008 To investigate the role of TG2 and ODC activities in regenerating liver, we used retinoic acid (RA), an inducer of TG2 and a suppressor of ODC. Tretinoin 81-94 ornithine decarboxylase 1 Rattus norvegicus 139-142
29177441-7 2018 These variants altered the expression of CYP26A1, a direct CDX2 target encoding the major retinoic acid (RA)-degrading enzyme. Tretinoin 105-107 caudal type homeobox 2 Homo sapiens 59-63
18008394-3 2008 To investigate the role of TG2 and ODC activities in regenerating liver, we used retinoic acid (RA), an inducer of TG2 and a suppressor of ODC. Tretinoin 96-98 ornithine decarboxylase 1 Rattus norvegicus 139-142
18354155-2 2008 TCI induced Ag-specific IgA Ab-secreting cells expressing CCR9 and CCR10 in the small intestine in a retinoic acid-dependent manner. Tretinoin 101-114 chemokine (C-C motif) receptor 10 Mus musculus 67-72
29183727-0 2018 Resveratrol strongly enhances the retinoic acid-induced superoxide generating activity via up-regulation of gp91-phox gene expression in U937 cells. Tretinoin 34-47 cytochrome b-245 beta chain Homo sapiens 108-117
29183727-4 2018 Semiquantitative RT-PCR showed that co-treatment with RA and resveratrol strongly enhanced transcription of the gp91-phox compared with those of the RA-treatment only. Tretinoin 54-56 cytochrome b-245 beta chain Homo sapiens 112-121
29183727-5 2018 On the other hand, immunoblot analysis revealed that co-treatment with RA and resveratrol caused remarkable accumulation of protein levels of gp91-phox (to 4-fold), p22-phox (to 5-fold) and p47-phox (to 4-fold) compared with those of the RA-treatment alone. Tretinoin 71-73 cytochrome b-245 beta chain Homo sapiens 142-151
30423583-0 2018 Novel Zinc Finger Transcription Factor ZFP580 Facilitates All-Trans Retinoic Acid -Induced Vascular Smooth Muscle Cells Differentiation by Raralpha-Mediated PI3K/Akt and ERK Signaling. Tretinoin 68-81 zinc finger protein 354C Rattus norvegicus 6-38
29321611-3 2018 In the embryo, RA production by RALDH2 (ALDH1A2), the main retinaldehyde dehydrogenase expressed at that stage, is inhibited by ethanol exposure. Tretinoin 15-17 aldehyde dehydrogenase 1 family member A2 Homo sapiens 32-38
29321611-3 2018 In the embryo, RA production by RALDH2 (ALDH1A2), the main retinaldehyde dehydrogenase expressed at that stage, is inhibited by ethanol exposure. Tretinoin 15-17 aldehyde dehydrogenase 1 family member A2 Homo sapiens 40-47
29321611-5 2018 Acetaldehyde-mediated reduction of RA can be rescued by RALDH2 or retinaldehyde supplementation. Tretinoin 35-37 aldehyde dehydrogenase 1 family member A2 Homo sapiens 56-62
29321611-7 2018 RA production by hRALDH2 is efficiently inhibited by acetaldehyde but not by ethanol itself. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 17-24
29225170-0 2018 Dihydromyricetin sensitizes human acute myeloid leukemia cells to retinoic acid-induced myeloid differentiation by activating STAT1. Tretinoin 66-79 signal transducer and activator of transcription 1 Homo sapiens 126-131
30423583-4 2018 Here, we have investigated the probable roles and underlying mechanisms of the novel C2H2 zinc finger transcription factor ZFP580 on ATRA-induced VSMC differentiation. Tretinoin 133-137 zinc finger protein 354C Rattus norvegicus 90-122
30423583-17 2018 CONCLUSION: The novel zinc finger transcription factor ZFP580 facilitates ATRA-induced VSMC differentiation by the RARalpha-mediated PI3K/Akt and ERK signaling pathways. Tretinoin 74-78 zinc finger protein 354C Rattus norvegicus 22-54
29301505-9 2018 RESULTS: Treatment of IMR32 and BE2C cells in vitro with 10 muM ATRA resulted in a change in cell morphology, a 65% decrease in cell proliferation, upregulation of STMN4 and ROBO2 and downregulation of KLF4. Tretinoin 64-68 Kruppel like factor 4 Homo sapiens 202-206
17554788-0 2008 Retinoic acid induced downregulation of MYCN is not mediated through changes in Sp1/Sp3. Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 40-44
29183727-5 2018 On the other hand, immunoblot analysis revealed that co-treatment with RA and resveratrol caused remarkable accumulation of protein levels of gp91-phox (to 4-fold), p22-phox (to 5-fold) and p47-phox (to 4-fold) compared with those of the RA-treatment alone. Tretinoin 71-73 neutrophil cytosolic factor 1 Homo sapiens 190-198
29183727-7 2018 These results suggested that resveratrol strongly enhances the RA-induced O2--generating activity via up-regulation of gp91-phox gene expression in U937 cells. Tretinoin 63-65 cytochrome b-245 beta chain Homo sapiens 119-128
29634397-7 2018 Results: RA-induced differentiation in the NT2/D1 cells significantly increased the expression of MAP2, NRG1, NRP1, NRP2, NEUROG1 and EN1 genes (genes linked to neural differentiation) compared with undifferentiated NT2/D1 cells. Tretinoin 9-11 microtubule associated protein 2 Homo sapiens 98-102
29634397-7 2018 Results: RA-induced differentiation in the NT2/D1 cells significantly increased the expression of MAP2, NRG1, NRP1, NRP2, NEUROG1 and EN1 genes (genes linked to neural differentiation) compared with undifferentiated NT2/D1 cells. Tretinoin 9-11 neuropilin 2 Homo sapiens 116-120
29634397-7 2018 Results: RA-induced differentiation in the NT2/D1 cells significantly increased the expression of MAP2, NRG1, NRP1, NRP2, NEUROG1 and EN1 genes (genes linked to neural differentiation) compared with undifferentiated NT2/D1 cells. Tretinoin 9-11 neurogenin 1 Homo sapiens 122-129
29076503-3 2018 Here we report that the functionality of ALDH1A2, the rate-limiting enzyme of retinoic acid (RA) synthesis, is negatively regulated by UBE3A in a ubiquitylation-dependent manner. Tretinoin 78-91 ubiquitin protein ligase E3A Homo sapiens 135-140
29321952-8 2018 The analysis of gene expression showed that only in the presence of retinoic acid did FEZ1 induce hoxb4 gene expression. Tretinoin 68-81 homeobox B4 Homo sapiens 98-103
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 peripheral myelin protein 22 Homo sapiens 182-187
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 growth associated protein 43 Homo sapiens 195-200
18026954-4 2008 NB4 and R4 cells express BP1, bcl-2, and c-myc; the expression of all three genes was repressed after ATRA treatment of NB4 cells but not R4 cells. Tretinoin 102-106 MYC proto-oncogene, bHLH transcription factor Homo sapiens 41-46
28857306-10 2017 RESULTS: A Dose Enhancement Factor (DEF) was determined in order to undertake a quantitative assessment of the effect of ATRA on tumour control. Tretinoin 121-125 UTP25 small subunit processome component Homo sapiens 36-39
32984754-0 2018 Increased Musashi-2 and Decreased NUMB Protein Levels Observed in Human Colorectal Cancer are reverted to Normal Levels by ATRA-Induced Cell Differentiation. Tretinoin 123-127 musashi RNA binding protein 2 Homo sapiens 10-19
32984754-6 2018 We also determined whether induction of cellular differentiation by all-trans retinoic acid (ATRA) influences MSI-2 and NUMB expression. Tretinoin 68-91 musashi RNA binding protein 2 Homo sapiens 110-115
32984754-6 2018 We also determined whether induction of cellular differentiation by all-trans retinoic acid (ATRA) influences MSI-2 and NUMB expression. Tretinoin 68-91 NUMB endocytic adaptor protein Homo sapiens 120-124
32984754-6 2018 We also determined whether induction of cellular differentiation by all-trans retinoic acid (ATRA) influences MSI-2 and NUMB expression. Tretinoin 93-97 musashi RNA binding protein 2 Homo sapiens 110-115
32984754-6 2018 We also determined whether induction of cellular differentiation by all-trans retinoic acid (ATRA) influences MSI-2 and NUMB expression. Tretinoin 93-97 NUMB endocytic adaptor protein Homo sapiens 120-124
29042055-3 2017 We found that RA down-regulated IgE class switching recombination (CSR) mainly through RA receptor alpha (RARalpha). Tretinoin 14-16 retinoic acid receptor, alpha Mus musculus 106-114
18323656-2 2008 CD38 expression was increased by isonicotinic acid and all-trans-retinoic acid (ATRA). Tretinoin 55-78 CD38 molecule Homo sapiens 0-4
28756872-0 2017 Retinoic acid improves nephrotoxic serum-induced glomerulonephritis through activation of podocyte retinoic acid receptor alpha. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 99-127
32984754-9 2018 Moreover, promoting cellular differentiation by ATRA reduces MSI-2 protein levels, while increasing NUMB protein levels in human CRC cell lines. Tretinoin 48-52 musashi RNA binding protein 2 Homo sapiens 61-66
18323656-2 2008 CD38 expression was increased by isonicotinic acid and all-trans-retinoic acid (ATRA). Tretinoin 80-84 CD38 molecule Homo sapiens 0-4
29267673-2 2017 Recent studies have demonstrated that CRABP2 plays important roles in the retinoic acid, beta-catenin and Notch signaling pathways, as well as in the interaction between epithelial and mesenchymal cells, which are important for human dental pulp stem cells (hDPSCs) and tooth development. Tretinoin 74-87 cellular retinoic acid binding protein 2 Homo sapiens 38-44
28756872-2 2017 We previously found that retinoic acid (RA) inhibits proliferation and induces differentiation of podocytes by activating RA receptor-alpha (RARalpha) in a murine model of HIV-associated nephropathy. Tretinoin 25-38 retinoic acid receptor, alpha Mus musculus 141-149
28756872-2 2017 We previously found that retinoic acid (RA) inhibits proliferation and induces differentiation of podocytes by activating RA receptor-alpha (RARalpha) in a murine model of HIV-associated nephropathy. Tretinoin 40-42 retinoic acid receptor, alpha Mus musculus 141-149
28756872-4 2017 RA treatment markedly improved renal function and reduced the number of crescentic lesions in nephritic wild-type mice, while this protection was largely lost in mice with podocyte-specific ablation of Rara (Pod-Rara knockout). Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 202-206
28756872-4 2017 RA treatment markedly improved renal function and reduced the number of crescentic lesions in nephritic wild-type mice, while this protection was largely lost in mice with podocyte-specific ablation of Rara (Pod-Rara knockout). Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 212-216
28756872-6 2017 Furthermore, RA suppressed the expression of cell injury, proliferation, and parietal epithelial cell markers in nephritic wild-type mice, all of which were significantly dampened in nephritic Pod-Rara knockout mice. Tretinoin 13-15 retinoic acid receptor, alpha Mus musculus 197-201
28756872-10 2017 Thus, RA attenuates crescentic glomerulonephritis primarily through RARalpha-mediated protection of podocytes and in part through the inhibition of parietal epithelial cell proliferation and induction of their transdifferentiation into podocytes. Tretinoin 6-8 retinoic acid receptor, alpha Mus musculus 68-76
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 transforming growth factor beta 2 Homo sapiens 78-86
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 inhibitor of DNA binding 2 Homo sapiens 92-95
28735443-8 2017 In situ hybridization analysis showed that RA is able to alter cyp26a1, sox9, tgfbeta2, and id2 spatial distribution; to increase rarbeta, meis2, and hoxb5 expression levels; and has a very modest effect on sox2, fgf10, fgfr2, and shh expression levels. Tretinoin 43-45 SRY-box transcription factor 2 Homo sapiens 207-211
18063688-6 2008 Treatment of cardiomyocytes with ciglitazone, a PPARgamma agonist, or 9-cis retinoic acid (RA), a RXR agonist, increased insulin- and metabolic stress-stimulated glucose transport, whereas agonists of PPARalpha or PPARbeta/delta had no effect. Tretinoin 91-93 peroxisome proliferator activated receptor alpha Rattus norvegicus 201-210
29312596-4 2017 Moreover, RA-induced hypercholesterolemia was completely corrected by omega-3 PUFA supplementation. Tretinoin 10-12 pumilio RNA binding family member 3 Homo sapiens 78-82
29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 intercellular adhesion molecule 1 Homo sapiens 283-316
29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 intercellular adhesion molecule 1 Homo sapiens 318-323
29055789-7 2017 Importantly, addition of rTM to this co-culture system inhibited the RA-induced phosphorylation of p38 and VE-cadherin and decreased ICAM1 and vascular permeability in EA.hy926 cells, without a decrease inthe levels of TNF-alpha. Tretinoin 69-71 intercellular adhesion molecule 1 Homo sapiens 133-138
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 114-127 retinoic acid receptor gamma a Danio rerio 193-198
29131833-10 2017 We furthermore demonstrated that ATRA signaling was functional for common targets, and that mRNA expression of CRABP2 and its targets was raised by ATRA therapy, whereas alternative pathways via FABP5 were not induced. Tretinoin 33-37 cellular retinoic acid binding protein 2 Homo sapiens 111-117
29131833-10 2017 We furthermore demonstrated that ATRA signaling was functional for common targets, and that mRNA expression of CRABP2 and its targets was raised by ATRA therapy, whereas alternative pathways via FABP5 were not induced. Tretinoin 148-152 cellular retinoic acid binding protein 2 Homo sapiens 111-117
29068287-0 2017 Hepatitis B virus X protein suppresses all-trans retinoic acid-induced apoptosis in human hepatocytes by repressing p14 expression via DNA methylation. Tretinoin 49-62 ribonuclease P/MRP subunit p14 Homo sapiens 116-119
29068287-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes. Tretinoin 0-23 ribonuclease P/MRP subunit p14 Homo sapiens 107-110
29166590-0 2017 Interleukin-33-Activated Islet-Resident Innate Lymphoid Cells Promote Insulin Secretion through Myeloid Cell Retinoic Acid Production. Tretinoin 109-122 interleukin 33 Mus musculus 0-14
29166590-4 2017 IL-33 promoted beta cell function through islet-resident group 2 innate lymphoid cells (ILC2s) that elicited retinoic acid (RA)-producing capacities in macrophages and dendritic cells via the secretion of IL-13 and colony-stimulating factor 2. Tretinoin 109-122 interleukin 33 Mus musculus 0-5
29166590-4 2017 IL-33 promoted beta cell function through islet-resident group 2 innate lymphoid cells (ILC2s) that elicited retinoic acid (RA)-producing capacities in macrophages and dendritic cells via the secretion of IL-13 and colony-stimulating factor 2. Tretinoin 124-126 interleukin 33 Mus musculus 0-5
29068287-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes. Tretinoin 25-29 ribonuclease P/MRP subunit p14 Homo sapiens 107-110
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 129-131 retinoic acid receptor gamma a Danio rerio 193-198
28849147-0 2017 Retinoic acid ameliorates photoaged skin through RAR-mediated pathway in mice. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 49-52
18292940-4 2008 This study demonstrates the epigenetic changes associated with ATRA-induced inhibition of telomerase activity, including the hypoacetylation and hypermethylation of the hTERT promoter. Tretinoin 63-67 telomerase reverse transcriptase Homo sapiens 169-174
28849147-2 2017 The aim of the present study was to examine whether the therapeutic effects of RA on photoaged skin are mediated by retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) in mice, and to investigate the underlying mechanism. Tretinoin 79-81 retinoic acid receptor, alpha Mus musculus 116-138
28849147-2 2017 The aim of the present study was to examine whether the therapeutic effects of RA on photoaged skin are mediated by retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) in mice, and to investigate the underlying mechanism. Tretinoin 79-81 retinoic acid receptor, alpha Mus musculus 140-143
29073082-8 2017 In the intestine, it increased the expression of retinoic acid-inducible target genes such as Aldh1a2, Dhrs3, and Ccr9 The beta-carotene-inducible disruption of retinoid homeostasis affected gut-homing and differentiation of lymphocytes and displayed morphologically in large lymphoid follicles along the intestine. Tretinoin 49-62 chemokine (C-C motif) receptor 9 Mus musculus 114-118
28849085-1 2017 The current study was designed to elucidate the mechanism of retinol binding protein 4 (RBP4) in cleft palate induced by all-trans retinoic acid (atRA). Tretinoin 121-144 retinol binding protein 4, plasma Mus musculus 61-86
28849085-1 2017 The current study was designed to elucidate the mechanism of retinol binding protein 4 (RBP4) in cleft palate induced by all-trans retinoic acid (atRA). Tretinoin 121-144 retinol binding protein 4, plasma Mus musculus 88-92
28849085-1 2017 The current study was designed to elucidate the mechanism of retinol binding protein 4 (RBP4) in cleft palate induced by all-trans retinoic acid (atRA). Tretinoin 146-150 retinol binding protein 4, plasma Mus musculus 61-86
28849085-1 2017 The current study was designed to elucidate the mechanism of retinol binding protein 4 (RBP4) in cleft palate induced by all-trans retinoic acid (atRA). Tretinoin 146-150 retinol binding protein 4, plasma Mus musculus 88-92
28849085-6 2017 Human embryonic palatal mesenchymal cells were exposed to atRA to detect the variation in RBP4 induced by atRA in vitro. Tretinoin 106-110 retinol binding protein 4 Homo sapiens 90-94
28849085-11 2017 In vitro experiments indicated that atRA suppressed the expression of RBP4 and altered the expression of p27 and cyclin D1 to cause growth inhibition. Tretinoin 36-40 retinol binding protein 4, plasma Mus musculus 70-74
28849085-11 2017 In vitro experiments indicated that atRA suppressed the expression of RBP4 and altered the expression of p27 and cyclin D1 to cause growth inhibition. Tretinoin 36-40 cyclin-dependent kinase inhibitor 1B Mus musculus 105-108
28802580-0 2017 Suppressive role of OGT-mediated O-GlcNAcylation of BAP1 in retinoic acid signaling. Tretinoin 60-73 Brca1 associated protein 1 Mus musculus 52-56
28802580-6 2017 OGT promoted the BAP1-induced repression of retinoic acid (RA)-induced RA receptor (RAR) activation. Tretinoin 44-57 Brca1 associated protein 1 Mus musculus 17-21
28802580-6 2017 OGT promoted the BAP1-induced repression of retinoic acid (RA)-induced RA receptor (RAR) activation. Tretinoin 59-61 Brca1 associated protein 1 Mus musculus 17-21
28849085-11 2017 In vitro experiments indicated that atRA suppressed the expression of RBP4 and altered the expression of p27 and cyclin D1 to cause growth inhibition. Tretinoin 36-40 cyclin D1 Mus musculus 113-122
18269766-10 2008 The "freed-up" Jun can then form a heterodimer with Fos, resulting in the increased AP-1 activity observed in RA-treated B16 cells. Tretinoin 110-112 FBJ osteosarcoma oncogene Mus musculus 52-55
28849085-13 2017 Overexpression of RBP4 reversed the inhibitory effect of atRA and promoted proliferation via the ERK1/2 and AKT signaling pathways. Tretinoin 57-61 retinol binding protein 4, plasma Mus musculus 18-22
28849085-14 2017 These results suggested that RBP4 was involved in cleft palate induced by atRA and it can be suppressed by atRA to cause growth inhibition in the embryonic palate. Tretinoin 74-78 retinol binding protein 4, plasma Mus musculus 29-33
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 21-23 gastricsin Bubalus bubalis 136-139
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 gastricsin Bubalus bubalis 136-139
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 growth/differentiation factor 9 Bubalus bubalis 291-295
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 gastricsin Bubalus bubalis 136-139
28849085-14 2017 These results suggested that RBP4 was involved in cleft palate induced by atRA and it can be suppressed by atRA to cause growth inhibition in the embryonic palate. Tretinoin 107-111 retinol binding protein 4, plasma Mus musculus 29-33
18269766-11 2008 Shifting the balance from predominantly ATF-2:Jun dimers to a higher amount of Jun:Fos dimers could lead a change in target gene expression that reduces resistance to chemotherapeutic drugs and contributes to the pathway by which RA arrests proliferation and induces differentiation. Tretinoin 230-232 FBJ osteosarcoma oncogene Mus musculus 83-86
18156191-7 2008 RA restored the ratio of Bcl-2 to Bax, inhibited cleavage of caspase-3 and -9, and prevented the decreases in the levels of SOD-1 and SOD-2. Tretinoin 0-2 BCL2 associated X, apoptosis regulator Rattus norvegicus 34-37
18156191-8 2008 Pressure overload-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by RA, via upregulation of mitogen-activated protein kinase phosphatase (MKP)-1 and MKP-2. Tretinoin 83-85 mitogen-activated protein kinase 8 Rattus norvegicus 53-56
29285249-1 2017 Retinol dehydrogenase-10 (RDH10) is a member of the short-chain dehydrogenase/reductase family, which plays an important role in retinoic acid (RA) synthesis. Tretinoin 129-142 retinol dehydrogenase 10 Homo sapiens 0-24
28923935-6 2017 Our results suggest that the repressive activity of RXR on prometastatic genes is mediated primarily through direct DNA binding of the receptor along with nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors and is largely unresponsive to ligand activation. Tretinoin 217-230 retinoid X receptor alpha Homo sapiens 52-55
18156191-8 2008 Pressure overload-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by RA, via upregulation of mitogen-activated protein kinase phosphatase (MKP)-1 and MKP-2. Tretinoin 83-85 dual specificity phosphatase 1 Rattus norvegicus 107-159
29285249-1 2017 Retinol dehydrogenase-10 (RDH10) is a member of the short-chain dehydrogenase/reductase family, which plays an important role in retinoic acid (RA) synthesis. Tretinoin 129-142 retinol dehydrogenase 10 Homo sapiens 26-31
29285249-1 2017 Retinol dehydrogenase-10 (RDH10) is a member of the short-chain dehydrogenase/reductase family, which plays an important role in retinoic acid (RA) synthesis. Tretinoin 144-146 retinol dehydrogenase 10 Homo sapiens 0-24
18025157-2 2008 At physiological concentrations of retinoic acid, PML-RARalpha silences RARalpha target genes, blocking differentiation of the cells. Tretinoin 35-48 PML nuclear body scaffold Homo sapiens 50-53
29285249-1 2017 Retinol dehydrogenase-10 (RDH10) is a member of the short-chain dehydrogenase/reductase family, which plays an important role in retinoic acid (RA) synthesis. Tretinoin 144-146 retinol dehydrogenase 10 Homo sapiens 26-31
27793605-3 2017 It is well established that retinol dehydrogenase 10 (RDH10, SDR16C4), which belongs to the 16C family of the short chain dehydrogenase/reductase (SDR) superfamily of proteins, is the major enzyme responsible for the oxidation of retinol to retinaldehyde for RA biosynthesis during embryogenesis. Tretinoin 259-261 retinol dehydrogenase 10 Homo sapiens 28-52
27793605-3 2017 It is well established that retinol dehydrogenase 10 (RDH10, SDR16C4), which belongs to the 16C family of the short chain dehydrogenase/reductase (SDR) superfamily of proteins, is the major enzyme responsible for the oxidation of retinol to retinaldehyde for RA biosynthesis during embryogenesis. Tretinoin 259-261 retinol dehydrogenase 10 Homo sapiens 54-59
27793605-3 2017 It is well established that retinol dehydrogenase 10 (RDH10, SDR16C4), which belongs to the 16C family of the short chain dehydrogenase/reductase (SDR) superfamily of proteins, is the major enzyme responsible for the oxidation of retinol to retinaldehyde for RA biosynthesis during embryogenesis. Tretinoin 259-261 retinol dehydrogenase 10 Homo sapiens 61-68
27793605-10 2017 Expression of the native RDHE2 is downregulated in the presence of elevated levels of RA. Tretinoin 86-88 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 25-30
29119099-7 2017 The expected increase in Wnt/beta-catenin-dependent TCF-LEF reporter activity and PrE markers induced by RA was, however, blocked by cyclopamine. Tretinoin 105-107 catenin (cadherin associated protein), beta 1 Mus musculus 29-41
17634073-10 2008 In conclusion, multipotent hMSC failed to differentiate into E-cadherin- or cytokeratin-expressing cells under optimized organotypic culture conditions for keratinocytes but differentiated into myofibroblast-like cells contracting the extracellular matrix, a phenomenon that was enhanced by RA and 5-azacytidine. Tretinoin 291-293 musculin Homo sapiens 27-31
29021535-6 2017 In this study, we aimed at identifying if the autophagy-linked FYVE-domain containing protein (ALFY/WDFY3) is involved in autophagic degradation of protein aggregates contributes to ATRA therapy-induced autophagy. Tretinoin 182-186 WD repeat and FYVE domain containing 3 Homo sapiens 95-99
29021535-6 2017 In this study, we aimed at identifying if the autophagy-linked FYVE-domain containing protein (ALFY/WDFY3) is involved in autophagic degradation of protein aggregates contributes to ATRA therapy-induced autophagy. Tretinoin 182-186 WD repeat and FYVE domain containing 3 Homo sapiens 100-105
28681415-6 2017 Retinoic acid represses many anteriorly expressed genes, including Bmp4, Lhx9, Msx2, and Alx4. Tretinoin 0-13 bone morphogenetic protein 4 Gallus gallus 67-71
28681415-7 2017 We provide evidence that retinoic acid influences transcription via induction of dHAND and inhibition of Gli3 to establish a new anteroposterior pre-pattern. Tretinoin 25-38 hand Drosophila melanogaster 81-86
27525675-5 2017 Differentiation of SH-SY5Y cells by retinoic acid (RA) or RA + brain-derived neurotrophic factor (BDNF) induced dramatic changes in global miRNA expression. Tretinoin 58-60 brain derived neurotrophic factor Homo sapiens 98-102
29021535-7 2017 We found that ALFY mRNA levels increase significantly during the course of ATRA-induced differentiation of APL and AML cell lines. Tretinoin 75-79 WD repeat and FYVE domain containing 3 Homo sapiens 14-18
29021535-9 2017 In agreement with its function in aggrephagy, knockdown of ALFY results in reduced ATRA-induced proteolysis. Tretinoin 83-87 WD repeat and FYVE domain containing 3 Homo sapiens 59-63
22504453-7 2008 It strongly inhibited in vitro proliferation of alloantigenstimulated donor T lymphocytes, and RAR-alpha seemed to play an exclusive role in this effect since inhibition by all-trans retinoic acid, which can activate all subtypes of RAR, was completely reversed by an RAR-alpha selective antagonist. Tretinoin 184-197 retinoic acid receptor alpha Homo sapiens 95-104
29021914-3 2017 Here we report that RA induces white adipose tissue browning via activating vascular endothelial growth factor (VEGF) signaling. Tretinoin 20-22 vascular endothelial growth factor A Mus musculus 76-110
29021914-3 2017 Here we report that RA induces white adipose tissue browning via activating vascular endothelial growth factor (VEGF) signaling. Tretinoin 20-22 vascular endothelial growth factor A Mus musculus 112-116
29021914-4 2017 RA triggered angiogenesis and elicited de novo generation of platelet-derived growth factor receptor alpha positive (PDGFRalpha+) adipose precursor cells via VEGFA/VEGFR2 signaling. Tretinoin 0-2 vascular endothelial growth factor A Mus musculus 158-163
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 growth/differentiation factor 9 Bubalus bubalis 291-295
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 gastricsin Bubalus bubalis 136-139
28713967-8 2017 In addition, the atRA-induced cyclin D1 downregulation and p21 upregulation were partially reversed following Notch2 silencing, whereas the atRA-induced inhibition of cellular proliferation was also attenuated. Tretinoin 17-21 cyclin D1 Mus musculus 30-39
28713967-8 2017 In addition, the atRA-induced cyclin D1 downregulation and p21 upregulation were partially reversed following Notch2 silencing, whereas the atRA-induced inhibition of cellular proliferation was also attenuated. Tretinoin 17-21 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 59-62
28713967-9 2017 Furthermore, it was revealed that Notch2 expression was upregulated, whereas Ki-67 expression was downregulated following atRA exposure, as assessed using resin bead-released atRA in MEPM cells. Tretinoin 122-126 antigen identified by monoclonal antibody Ki 67 Mus musculus 77-82
28713967-9 2017 Furthermore, it was revealed that Notch2 expression was upregulated, whereas Ki-67 expression was downregulated following atRA exposure, as assessed using resin bead-released atRA in MEPM cells. Tretinoin 175-179 antigen identified by monoclonal antibody Ki 67 Mus musculus 77-82
28736154-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 growth/differentiation factor 9 Bubalus bubalis 291-295
22504453-7 2008 It strongly inhibited in vitro proliferation of alloantigenstimulated donor T lymphocytes, and RAR-alpha seemed to play an exclusive role in this effect since inhibition by all-trans retinoic acid, which can activate all subtypes of RAR, was completely reversed by an RAR-alpha selective antagonist. Tretinoin 184-197 retinoic acid receptor alpha Homo sapiens 95-98
28780376-0 2017 Retinoic acid induction of CD1d expression primes chronic lymphocytic leukemia B cells for killing by CD8+ invariant natural killer T cells. Tretinoin 0-13 CD8a molecule Homo sapiens 102-105
29156743-0 2017 Hepatitis C virus Core overcomes all-trans retinoic acid-induced apoptosis in human hepatoma cells by inhibiting p14 expression via DNA methylation. Tretinoin 43-56 ribonuclease P/MRP subunit p14 Homo sapiens 113-116
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 0-23 ribonuclease P/MRP subunit p14 Homo sapiens 105-108
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 0-23 ribonuclease P/MRP subunit p14 Homo sapiens 165-168
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 0-23 MDM2 proto-oncogene Homo sapiens 169-173
17561254-3 2008 For HL60 cells, ATRA induced major increases in descending order of CD38, CD11b, CD45RO, CD11c, CD54 and CD36 with repression of CD117 and CD44. Tretinoin 16-20 CD38 molecule Homo sapiens 68-72
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 25-29 ribonuclease P/MRP subunit p14 Homo sapiens 105-108
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 25-29 ribonuclease P/MRP subunit p14 Homo sapiens 165-168
29156743-1 2017 All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. Tretinoin 25-29 MDM2 proto-oncogene Homo sapiens 169-173
29156743-3 2017 For this effect, HCV Core upregulated both protein levels and enzyme activities of DNA methyltransferase 1 (DNMT1), DNMT3a, and DNMT3b and thereby repressed p14 expression via promoter hypermethylation, resulting in inactivation of the pathway leading to p53 accumulation in the presence of ATRA. Tretinoin 291-295 ribonuclease P/MRP subunit p14 Homo sapiens 157-160
28836501-5 2017 Both RXRalpha and RXRbeta protein levels decrease was found also by combination ATRA+TBT-Cl/TPT-Cl. Tretinoin 80-84 retinoid X receptor alpha Homo sapiens 5-13
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 CEA cell adhesion molecule 6 Homo sapiens 113-118
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 CD38 molecule Homo sapiens 186-190
17561254-6 2008 Approximately half of the antigens up-regulated by ATRA on NB4 cells were adhesion molecules, including CD11a, CD11b, CD11c, CD54, CD66c and CD138, consistent with the increased adhesiveness of leukaemia cells observed for APL patients treated with ATRA. Tretinoin 51-55 CEA cell adhesion molecule 6 Homo sapiens 131-136
28840512-6 2017 In addition, nanomolar levels of retinoic acid elicited increased nuclear trafficking of the CRABP2, which is traditionally associated with gene expression of cellular pathways related to neuronal differentiation. Tretinoin 33-46 cellular retinoic acid binding protein 2 Homo sapiens 93-99
28840512-7 2017 Collectively, these results show that nanomolar concentrations of retinoic acid are capable of inducing both structural and functional neuron-like features in HTB-11 cells using CRABP2, suggesting differentiation in neuroblastoma cells into neuronal phenotypes. Tretinoin 66-79 cellular retinoic acid binding protein 2 Homo sapiens 178-184
29050312-6 2017 Mutant mice exhibited increased levels of retinoic acid-responsive genes, including p21, and decreased oxidative stress as evaluated by serum and liver markers. Tretinoin 42-55 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 84-87
17561254-7 2008 On HL60 cells, ATRA induced expression of CD38, CD43 and CD45RO and repressed CD117, while the converse was true on NB4 cells that contain chimeric PML-RARalpha. Tretinoin 15-19 CD38 molecule Homo sapiens 42-46
17561254-8 2008 For NB4 cells, ATRA induced some remarkable increases in CD antigens not seen for HL60: CD14 (16.6-fold), CD32 (27.8), CD53 (20.5), CD65 (139), CD66c (79.7), CD126 (15.1), and CD138 (57.6). Tretinoin 15-19 CEA cell adhesion molecule 6 Homo sapiens 144-149
18039708-4 2008 We show a functional RA response element in the DIF2 promoter, which is constitutively bound by PML/RARalpha in APL cells. Tretinoin 21-23 PML nuclear body scaffold Homo sapiens 96-99
28768913-3 2017 In an effort to identify mechanisms governing HIV-1 permissiveness/persistence in gut-homing Th17 cells, we analyzed the transcriptome of CCR6+ versus CCR6- T cells exposed to the gut-homing inducer retinoic acid (RA) and performed functional validations in colon biopsies of HIV-infected individuals receiving ART (HIV+ART). Tretinoin 199-212 C-C motif chemokine receptor 6 Homo sapiens 138-142
28768913-6 2017 Of note, mTOR expression/phosphorylation was distinctively induced by RA in CCR6+ T cells. Tretinoin 70-72 C-C motif chemokine receptor 6 Homo sapiens 76-80
29296827-3 2017 We also demonstrated that BAALC overexpression was associated with shorter disease-free survival (DFS) (hazard ratio [HR], 4.43; 95% confidence interval [CI], 1.29-15.2; P = .018) in 221 consecutive patients (median age, 35 years; range, 18-82 years) with newly diagnosed APL homogeneously treated with all-trans retinoic acid and anthracycline-based chemotherapy. Tretinoin 313-326 BAALC binder of MAP3K1 and KLF4 Homo sapiens 26-31
18039708-4 2008 We show a functional RA response element in the DIF2 promoter, which is constitutively bound by PML/RARalpha in APL cells. Tretinoin 21-23 retinoic acid receptor alpha Homo sapiens 100-108
27966552-4 2017 We found that P2X7 upregulation on CD4+ effector T cells is induced by retinoic acid through retinoic acid receptor alpha binding to an intragenic enhancer region of the P2rx7 gene. Tretinoin 71-84 retinoic acid receptor, alpha Mus musculus 93-121
28423181-6 2017 This subset expressed Aldh1a2 and Itgb8 genes, which are involved in retinoic acid metabolism and transforming growth factor-beta (TGF-beta) activation, respectively. Tretinoin 69-82 aldehyde dehydrogenase 1 family member A2 Homo sapiens 22-29
17962700-3 2008 RA strongly upregulated expression of keratin 18 and the transcription factor p63, which is involved in epidermal morphogenesis and ectodermal specification, while repressing early neural marker transcription. Tretinoin 0-2 keratin 18 Homo sapiens 38-48
28677722-2 2017 Enzymes that catalyze the oxidation of retinol to generate atRA, including aldehyde dehydrogenase 1 family (ALDH1)A1, ALDH1A2 and ALDH1A3, exhibit complex expression patterns at different stages of renal development. Tretinoin 59-63 aldehyde dehydrogenase 1 family member A2 Homo sapiens 118-125
28677722-4 2017 In this study, we provide in vitro evidence to demonstrate that Wilms" tumor 1 (WT1) negatively regulates the expression of the atRA synthetic enzymes, ALDH1A1, ALDH1A2 and ALDH1A3, in the 293 cell line, leading to significant blockage of atRA production. Tretinoin 128-132 aldehyde dehydrogenase 1 family member A2 Homo sapiens 161-168
28739877-3 2017 We report that PALLD is highly induced along with all-trans-retinoic acid-induced maturation of myeloid leukemia cells, to promote Ig- or complement-opsonized phagocytosis. Tretinoin 60-73 palladin, cytoskeletal associated protein Homo sapiens 15-20
28392548-0 2017 Effect of retinoic acid on midkine gene expression in rat anterior pituitary cells. Tretinoin 10-23 midkine Rattus norvegicus 27-34
28392548-3 2017 Midkine (MK) is an RA-inducible growth factor, and MK production in the rat anterior pituitary gland was recently reported. Tretinoin 19-21 midkine Rattus norvegicus 0-7
28392548-3 2017 Midkine (MK) is an RA-inducible growth factor, and MK production in the rat anterior pituitary gland was recently reported. Tretinoin 19-21 midkine Rattus norvegicus 9-11
28392548-8 2017 Using isolated anterior pituitary cells of rats, we examined the effect of RA on gene expression of MK. Tretinoin 75-77 midkine Rattus norvegicus 100-102
28392548-9 2017 Quantitative real-time PCR revealed that 72 h exposure to a concentration of 10-6 M of retinal and all-trans retinoic acid increased MK mRNA levels by about 2-fold. Tretinoin 109-122 midkine Rattus norvegicus 133-135
28392548-11 2017 This is the first report to show that RA is important in regulating MK expression in rat anterior pituitary gland. Tretinoin 38-40 midkine Rattus norvegicus 68-70
28656276-1 2017 Retinoic acid inducible gene I (RIG-I) is upregulated during all-trans retinoic acid (ATRA)-induced terminal granulocytic differentiation of NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 71-84 DExD/H-box helicase 58 Homo sapiens 0-30
28656276-1 2017 Retinoic acid inducible gene I (RIG-I) is upregulated during all-trans retinoic acid (ATRA)-induced terminal granulocytic differentiation of NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 71-84 DExD/H-box helicase 58 Homo sapiens 32-37
17962700-3 2008 RA strongly upregulated expression of keratin 18 and the transcription factor p63, which is involved in epidermal morphogenesis and ectodermal specification, while repressing early neural marker transcription. Tretinoin 0-2 tumor protein p63 Homo sapiens 78-81
28656276-1 2017 Retinoic acid inducible gene I (RIG-I) is upregulated during all-trans retinoic acid (ATRA)-induced terminal granulocytic differentiation of NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 86-90 DExD/H-box helicase 58 Homo sapiens 0-30
28656276-1 2017 Retinoic acid inducible gene I (RIG-I) is upregulated during all-trans retinoic acid (ATRA)-induced terminal granulocytic differentiation of NB4 acute promyelocytic leukemia (APL) cells. Tretinoin 86-90 DExD/H-box helicase 58 Homo sapiens 32-37
17962700-4 2008 RA-induced hESCs efficiently differentiated to keratin 14-expressing epithelial cells, although this effect was dependent upon on the context of bone morphogenetic protein signaling. Tretinoin 0-2 keratin 14 Homo sapiens 47-57
28656276-5 2017 The results showed that the ATRA-induced expression of RIG-I was specifically and effectively knocked down at the mRNA and protein levels by lentivirus mediated RIG-I short hairpin RNA. Tretinoin 28-32 DExD/H-box helicase 58 Homo sapiens 55-60
28656276-5 2017 The results showed that the ATRA-induced expression of RIG-I was specifically and effectively knocked down at the mRNA and protein levels by lentivirus mediated RIG-I short hairpin RNA. Tretinoin 28-32 DExD/H-box helicase 58 Homo sapiens 161-166
28635660-0 2017 Diverse Regulation of Vitamin D Receptor Gene Expression by 1,25-Dihydroxyvitamin D and ATRA in Murine and Human Blood Cells at Early Stages of Their Differentiation. Tretinoin 88-92 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 22-40
28635660-4 2017 This is why we decided to examine the effects of the combination of 1,25D and all-trans-retinoic acid (ATRA) on VDR gene expression in normal human and murine blood cells at various steps of their development. Tretinoin 78-101 vitamin D receptor Homo sapiens 112-115
28635660-4 2017 This is why we decided to examine the effects of the combination of 1,25D and all-trans-retinoic acid (ATRA) on VDR gene expression in normal human and murine blood cells at various steps of their development. Tretinoin 103-107 vitamin D receptor Homo sapiens 112-115
28656276-6 2017 In addition, silencing of RIG-I reduced the ATRA-induced inhibition of NB4 cell proliferation, cell cycle arrest and apoptosis. Tretinoin 44-48 DExD/H-box helicase 58 Homo sapiens 26-31
28656276-7 2017 Further investigations indicated that with ATRA-induced expression of RIG-I, levels of phosphorylated (p)AKT-Thr308 and pForkhead Box (FOX) O3A-Thr32 were decreased, the expression levels of cell cycle arrest protein p27 and the apoptotic protein, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), directly transcribed by FOXO3A were increased. Tretinoin 43-47 DExD/H-box helicase 58 Homo sapiens 70-75
17991421-6 2008 In addition, we revealed that co-repressor SMRT co-localized with PML-RARalpha, resulting in the immobilization of SMRT while ATRA treatment eliminated their association and reversed the immobile effect of SMRT. Tretinoin 126-130 PML nuclear body scaffold Homo sapiens 66-69
28656276-8 2017 By contrast, following the knockdown of ATRA-induced expression of RIG-I, the levels of pAKT-Thr308 and pFOXO3A-Thr32 were increased, and the protein expression levels of p27 and TRAIL were decreased. Tretinoin 40-44 DExD/H-box helicase 58 Homo sapiens 67-72
28656276-9 2017 Taken together, these results showed that the knockdown of RIG-I reduced the inhibition of cell proliferation, cell cycle arrest and apoptosis in the ATRA-induced NB4 cells via the AKT-FOXO3A signaling pathway. Tretinoin 150-154 DExD/H-box helicase 58 Homo sapiens 59-64
28465486-4 2017 Here we show that SphK2 overexpression contributes to the resistance of all-trans retinoic acid (ATRA) therapy in colon cancer through rapid degradation of cytoplasmic retinoid X receptor alpha (RXRalpha) by lysine 48 (K48)- and lysine 63 (K63)-based polyubiquitination. Tretinoin 82-95 retinoid X receptor alpha Homo sapiens 168-193
28465486-4 2017 Here we show that SphK2 overexpression contributes to the resistance of all-trans retinoic acid (ATRA) therapy in colon cancer through rapid degradation of cytoplasmic retinoid X receptor alpha (RXRalpha) by lysine 48 (K48)- and lysine 63 (K63)-based polyubiquitination. Tretinoin 82-95 retinoid X receptor alpha Homo sapiens 195-203
28465486-4 2017 Here we show that SphK2 overexpression contributes to the resistance of all-trans retinoic acid (ATRA) therapy in colon cancer through rapid degradation of cytoplasmic retinoid X receptor alpha (RXRalpha) by lysine 48 (K48)- and lysine 63 (K63)-based polyubiquitination. Tretinoin 97-101 retinoid X receptor alpha Homo sapiens 168-193
28465486-4 2017 Here we show that SphK2 overexpression contributes to the resistance of all-trans retinoic acid (ATRA) therapy in colon cancer through rapid degradation of cytoplasmic retinoid X receptor alpha (RXRalpha) by lysine 48 (K48)- and lysine 63 (K63)-based polyubiquitination. Tretinoin 97-101 retinoid X receptor alpha Homo sapiens 195-203
28927033-6 2017 After the RA+TMZ treatment of U251 cells, autophagy associated proteins Beclin 1 and LC3B were significantly increased, and the TEM analysis were consistent with autophagy protein levels. Tretinoin 10-12 beclin 1 Homo sapiens 72-80
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 21-23 gastricsin Bubalus bubalis 136-139
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 gastricsin Bubalus bubalis 136-139
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 growth/differentiation factor 9 Bubalus bubalis 291-295
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 gastricsin Bubalus bubalis 136-139
28195391-5 2017 We identified retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated protein 5, and IFN regulatory factor 1 (IRF1) as the key anti-HEV ISGs. Tretinoin 14-27 DExD/H-box helicase 58 Homo sapiens 46-51
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 growth/differentiation factor 9 Bubalus bubalis 291-295
17991421-6 2008 In addition, we revealed that co-repressor SMRT co-localized with PML-RARalpha, resulting in the immobilization of SMRT while ATRA treatment eliminated their association and reversed the immobile effect of SMRT. Tretinoin 126-130 retinoic acid receptor alpha Homo sapiens 70-78
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 gastricsin Bubalus bubalis 136-139
28526652-4 2017 Out of the series of RA doses (2, 4, 8, 16, 20 and 30muM), 16muM RA for 8day culture interval was found to induce highest expression of PGC- and meiosis-associated genes like DAZL, VASA, SYCP3, MLH1, TNP1/2 and PRM2, while mature germ cell genes like BOULE and TEKT1 (Spermatocyte markers), GDF9 and ZP2 (Oocyte markers) showed higher expression at 2muM RA dose, suggesting functional concentration-gradient of RA activity. Tretinoin 65-67 growth/differentiation factor 9 Bubalus bubalis 291-295
17712061-5 2008 In synaptoneurosomes, atRA rapidly increased phosphorylation of ERK1/2, its target 4E-BP, and p70S6K, and its substrate, ribosome protein S6, indicating activation of MAPK and mammalian target of rapamycin (mTOR). Tretinoin 22-26 ribosomal protein S6 kinase B1 Homo sapiens 94-100
28568315-11 2017 The retinoate biosynthesis pathway was also enriched due to the differential expression of the genes AKR1C3, ALDH8A1, RDH8, RDH13 and SDR9C7. Tretinoin 4-13 short chain dehydrogenase/reductase family 9C member 7 Bos taurus 134-140
28106276-6 2017 Immunofluorescent staining revealed that the mutagenized ESCs (RA (Retinoic Acid) with C1EIS Knock out) expressed lower levels of integrin alpha6 and integrin beta1 compared to wild type cells. Tretinoin 63-65 integrin subunit alpha 6 Gallus gallus 130-145
28106276-6 2017 Immunofluorescent staining revealed that the mutagenized ESCs (RA (Retinoic Acid) with C1EIS Knock out) expressed lower levels of integrin alpha6 and integrin beta1 compared to wild type cells. Tretinoin 67-80 integrin subunit alpha 6 Gallus gallus 130-145
33429696-3 2017 The overall objective of this study was to manufacture an all-trans retinoic acid (atRA)-loaded bilayered collagen-hyaluronate (atRA-B) scaffold as a platform technology for tracheal tissue regeneration. Tretinoin 58-81 C2H2 and C2HC zinc fingers superfamily protein Arabidopsis thaliana 128-134
33429696-3 2017 The overall objective of this study was to manufacture an all-trans retinoic acid (atRA)-loaded bilayered collagen-hyaluronate (atRA-B) scaffold as a platform technology for tracheal tissue regeneration. Tretinoin 83-87 C2H2 and C2HC zinc fingers superfamily protein Arabidopsis thaliana 128-134
28727051-12 2017 Liver fat and MUFA content nonlinearly declined with liver all- retinoic acid, indicating a saturation point at relatively low all- retinoic acid content. Tretinoin 64-77 Monounsaturated fatty acid percentage Sus scrofa 14-18
28087752-9 2017 RA induced mRNA expression of vascular endothelial growth factor A (VEGFA) and VEGFR2. Tretinoin 0-2 kinase insert domain receptor Homo sapiens 79-85
28215943-8 2017 These results indicate that ATRA enhances gemcitabine cytotoxicity by increasing dCK expression in gemcitabine-resistant human pancreatic cancer cells. Tretinoin 28-32 Calcium/calmodulin-dependent protein kinase II Drosophila melanogaster 81-84
17910894-3 2008 Vitamin A (retinoic acid [RA]) and the active form of vitamin D3 (1,25 dihydroxyvitamin D3 [1,25D(3)]) have been used to treat certain T cell-mediated inflammatory skin diseases, as well as cutaneous T-cell lymphomas; however, their effect on CLA expression has not been studied. Tretinoin 11-24 selectin P ligand Homo sapiens 243-246
28025671-6 2017 Retinoic acid inhibits the expression of early and late muscle differentiation markers and enhances the expression of myogenic specification genes, such as PAX7 and PAX3. Tretinoin 0-13 paired box 7 Homo sapiens 156-160
28477983-5 2017 Roscovitine, a pharmacological CDK5 inhibitor, or a siRNA against CDK5 prevented RA potentiation of GR phosphorylation. Tretinoin 81-83 cyclin-dependent kinase 5 Mus musculus 66-70
28465486-6 2017 Sphk2 overexpression increases the ATRA-induced nuclear RXRalpha export to cytoplasm and then rapidly degrades RXRalpha through the polyubiquitination pathway. Tretinoin 35-39 retinoid X receptor alpha Homo sapiens 56-64
28465486-6 2017 Sphk2 overexpression increases the ATRA-induced nuclear RXRalpha export to cytoplasm and then rapidly degrades RXRalpha through the polyubiquitination pathway. Tretinoin 35-39 retinoid X receptor alpha Homo sapiens 111-119
28601081-3 2017 We demonstrated decrease in OCT4 and NANOG mRNA and protein levels following exposure to retinoic acid. Tretinoin 89-102 Nanog homeobox Homo sapiens 37-42
27996177-3 2017 In the present study, PPARbeta/delta was over-expressed in three human neuroblastoma cell lines, NGP, SK-N-BE(2), and IMR-32, that exhibit high, medium, and low sensitivity, respectively, to retinoic acid-induced differentiation to determine if PPARbeta/delta and retinoic acid receptors (RARs) could be jointly targeted to increase the efficacy of treatment. Tretinoin 191-204 peroxisome proliferator activated receptor delta Homo sapiens 22-30
17910894-3 2008 Vitamin A (retinoic acid [RA]) and the active form of vitamin D3 (1,25 dihydroxyvitamin D3 [1,25D(3)]) have been used to treat certain T cell-mediated inflammatory skin diseases, as well as cutaneous T-cell lymphomas; however, their effect on CLA expression has not been studied. Tretinoin 26-28 selectin P ligand Homo sapiens 243-246
28155214-0 2017 RA Differentiation Enhances Dopaminergic Features, Changes Redox Parameters, and Increases Dopamine Transporter Dependency in 6-Hydroxydopamine-Induced Neurotoxicity in SH-SY5Y Cells. Tretinoin 0-2 solute carrier family 6 member 3 Homo sapiens 91-111
28424257-1 2017 Background: Few studies have examined the impact of local animal-source foods (ASFs) on the nutritional status of reproductive-age women in developing countries.Objective: We hypothesized that a midmorning snack of local ASF for 6 mo would reduce dietary micronutrient deficiencies [usual intake less than the estimated average requirement (EAR)] and improve blood biomarkers of iron, zinc, and vitamins A and B-12 status among nonpregnant, reproductive-age women in rural Vietnam.Methods: One hundred seventeen women, 18-30 y old, were randomly assigned to receive either an ASF (mean: 144 kcal, 8.9 mg Fe, 2.7 mg Zn, 1050 mug retinoic acid equivalent vitamin A, and 5.5 mug vitamin B-12) or a control snack (mean: 150 kcal, 2.0 mg Fe, 0.9 mg Zn, 0 mug retinoic acid equivalent vitamin A, and 0 mug vitamin B-12) 5 d/wk for 6 mo. Tretinoin 628-641 arylsulfatase F Homo sapiens 221-224
28424257-1 2017 Background: Few studies have examined the impact of local animal-source foods (ASFs) on the nutritional status of reproductive-age women in developing countries.Objective: We hypothesized that a midmorning snack of local ASF for 6 mo would reduce dietary micronutrient deficiencies [usual intake less than the estimated average requirement (EAR)] and improve blood biomarkers of iron, zinc, and vitamins A and B-12 status among nonpregnant, reproductive-age women in rural Vietnam.Methods: One hundred seventeen women, 18-30 y old, were randomly assigned to receive either an ASF (mean: 144 kcal, 8.9 mg Fe, 2.7 mg Zn, 1050 mug retinoic acid equivalent vitamin A, and 5.5 mug vitamin B-12) or a control snack (mean: 150 kcal, 2.0 mg Fe, 0.9 mg Zn, 0 mug retinoic acid equivalent vitamin A, and 0 mug vitamin B-12) 5 d/wk for 6 mo. Tretinoin 754-767 arylsulfatase F Homo sapiens 221-224
28155214-6 2017 DAT inhibition by 3alpha-bis-4-fluorophenyl-methoxytropane and dithiothreitol (a cell-permeable thiol-reducing agent) protected RA-differentiated, but not undifferentiated, SH-SY5Y cells from oxidative damage and cell death caused by 6-OHDA. Tretinoin 128-130 solute carrier family 6 member 3 Homo sapiens 0-3
17986232-4 2008 Using two different human neuroblastoma cell lines, SH-SY5Y and LA-N-5, we show here that PML protein leads to the formation of nuclear bodies (PML-NB) after only 1 h of retinoic acid treatment and that this formation is mediated by the extracellular signal-regulated kinase (ERK) pathway. Tretinoin 170-183 PML nuclear body scaffold Homo sapiens 90-93
28408241-4 2017 Furthermore, RA-induced beige adipogenesis was blocked following vascular endothelial growth factor receptor (VEGFR) 2 knock out in PDGFRalpha+ cells, suggesting its mediatory role. Tretinoin 13-15 kinase insert domain receptor Homo sapiens 65-108
28408241-4 2017 Furthermore, RA-induced beige adipogenesis was blocked following vascular endothelial growth factor receptor (VEGFR) 2 knock out in PDGFRalpha+ cells, suggesting its mediatory role. Tretinoin 13-15 kinase insert domain receptor Homo sapiens 110-115
28559980-0 2017 All-trans-retinoic acid activates SDF-1/CXCR4/ROCK2 signaling pathway to inhibit chondrogenesis. Tretinoin 0-23 C-X-C motif chemokine receptor 4 Rattus norvegicus 40-45
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 ras homolog family member A Rattus norvegicus 3-7
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 C-X-C motif chemokine receptor 4 Rattus norvegicus 23-28
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 ras homolog family member A Rattus norvegicus 128-132
28559980-3 2017 As RhoA/ROCK and SDF-1/CXCR4 signaling play important molecular roles for a variety of cellular processes, we hypothesized that RhoA/ROCK2 and SDF-1/CXCR4 signaling are involved in ATRA-induced chondrogenesis in rat embryo hind limb bud mesenchymal cells (rEHBMCs). Tretinoin 181-185 C-X-C motif chemokine receptor 4 Rattus norvegicus 149-154
28559980-4 2017 We found that ATRA dose-dependently inhibits proliferation and expression of chondrogenic transcription factors (SOX9 and COL2A1) in rEHBMCs. Tretinoin 14-18 SRY-box transcription factor 9 Rattus norvegicus 113-117
28559980-5 2017 In contrast, ATRA increases the expression of ROCK2, SDF-1 and CXCR4. Tretinoin 13-17 C-X-C motif chemokine receptor 4 Rattus norvegicus 63-68
28559980-7 2017 In addition, we found that disturbing SDF-1/CXCR4 signaling by AMD3100 decreases ATRA-induced ROCK2 expression. Tretinoin 81-85 C-X-C motif chemokine receptor 4 Rattus norvegicus 44-49
28559980-8 2017 In vivo studies we also confirm that SOX9 expression of early-stage cartilage progenitors in the proliferative zone and COL2A1 expression in prehypertrophic chondrocytes are decreased in ATRA-treated rat embryo hind limb. Tretinoin 187-191 SRY-box transcription factor 9 Rattus norvegicus 37-41
28253328-7 2017 Decidualization was also associated with increased expression of retinol-binding protein 4 (RBP4) and various enzymes involved in the metabolism of RA and its precursor, retinaldehyde (Rald), including CYP26A1, DHRS3, and RDH12. Tretinoin 148-150 retinol binding protein 4 Homo sapiens 65-90
28559980-9 2017 Together, these results show that ATRA activates SDF-1/CXCR4/ROCK2 signaling to inhibit chondrogenesis to lead to CCF by suppressing differentiation through down-regulation of SOX9 and COL2A1 expression in rat embryo hind limb bud mesenchymal cells. Tretinoin 34-38 C-X-C motif chemokine receptor 4 Rattus norvegicus 55-60
28253328-7 2017 Decidualization was also associated with increased expression of retinol-binding protein 4 (RBP4) and various enzymes involved in the metabolism of RA and its precursor, retinaldehyde (Rald), including CYP26A1, DHRS3, and RDH12. Tretinoin 148-150 retinol binding protein 4 Homo sapiens 92-96
28559980-9 2017 Together, these results show that ATRA activates SDF-1/CXCR4/ROCK2 signaling to inhibit chondrogenesis to lead to CCF by suppressing differentiation through down-regulation of SOX9 and COL2A1 expression in rat embryo hind limb bud mesenchymal cells. Tretinoin 34-38 SRY-box transcription factor 9 Rattus norvegicus 176-180
17986232-4 2008 Using two different human neuroblastoma cell lines, SH-SY5Y and LA-N-5, we show here that PML protein leads to the formation of nuclear bodies (PML-NB) after only 1 h of retinoic acid treatment and that this formation is mediated by the extracellular signal-regulated kinase (ERK) pathway. Tretinoin 170-183 PML nuclear body scaffold Homo sapiens 144-147
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 DEAD box helicase 4 Mus musculus 207-210
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 27-40 developmental pluripotency-associated 3 Mus musculus 226-232
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 DEAD box helicase 4 Mus musculus 207-210
28314787-4 2017 Interestingly, addition of retinoic acid (RA) into SSC conditions enabled efficient differentiation of mouse ESCs into germ-like cells, as shown by the activation of spermatogenesis-associated genes such as Mvh, Dazl, Prdm14, Stella, Scp1, Scp3, Stra8 and Rec8 In contrast, for cells cultured in control medium, the activation of the above genes barely occurred. Tretinoin 42-44 developmental pluripotency-associated 3 Mus musculus 226-232
28611979-2 2017 The function of retinoids is exerted by the complex of retinoic acid (RA) with the heterodimer of retinoid X receptor and the RA receptor. Tretinoin 55-68 retinoid X receptor alpha Homo sapiens 98-117
28611979-2 2017 The function of retinoids is exerted by the complex of retinoic acid (RA) with the heterodimer of retinoid X receptor and the RA receptor. Tretinoin 70-72 retinoid X receptor alpha Homo sapiens 98-117
18505338-0 2008 v-Myb suppresses phorbol ester- and modifies retinoic acid-induced differentiation of human promonocytic U937 cells. Tretinoin 45-58 MYB proto-oncogene, transcription factor Homo sapiens 2-5
28122350-5 2017 miR-27 asignificantly rescued differentiation and inhibited beta-catenin, LEF1, OCT4 and SOX2 in Wnt/beta-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Tretinoin 150-154 SRY-box transcription factor 2 Homo sapiens 89-93
28129653-4 2017 Here we showed that compound Z-10, a nitro-ligand of retinoid X receptor alpha (RXRalpha), strongly promoted the cAMP-independent apoptosis of both ATRA- sensitive and resistant NB4 cells via the induction of caspase-mediated PML-RARalpha degradation. Tretinoin 148-152 retinoid X receptor alpha Homo sapiens 53-78
28129653-4 2017 Here we showed that compound Z-10, a nitro-ligand of retinoid X receptor alpha (RXRalpha), strongly promoted the cAMP-independent apoptosis of both ATRA- sensitive and resistant NB4 cells via the induction of caspase-mediated PML-RARalpha degradation. Tretinoin 148-152 retinoid X receptor alpha Homo sapiens 80-88
27995495-0 2017 Downregulation of Oxytocin Receptor Decreases the Length of Projections Stimulated by Retinoic Acid in the U-87MG Cells. Tretinoin 86-99 oxytocin/neurophysin I prepropeptide Homo sapiens 18-26
27995495-7 2017 Retinoic acid"s and oxytocin"s stimulation of projections length was significantly blunted in U-87MG cells with oxytocin receptor knockdown. Tretinoin 0-13 oxytocin/neurophysin I prepropeptide Homo sapiens 112-120
28350049-0 2017 Activation of the CRABPII/RAR pathway by curcumin induces retinoic acid mediated apoptosis in retinoic acid resistant breast cancer cells. Tretinoin 58-71 cellular retinoic acid binding protein 2 Homo sapiens 18-25
18505338-8 2008 Some features of granulocytic differentiation of retinoic acid-treated U937 cells were affected by the v-Myb protein as well. Tretinoin 49-62 MYB proto-oncogene, transcription factor Homo sapiens 103-108
28350049-0 2017 Activation of the CRABPII/RAR pathway by curcumin induces retinoic acid mediated apoptosis in retinoic acid resistant breast cancer cells. Tretinoin 94-107 cellular retinoic acid binding protein 2 Homo sapiens 18-25
28350049-9 2017 These findings provide mechanistic insights into sensitizing TNBC cells to RA-mediated cell death by curcumin-induced upregulation of the CRABPII/RAR pathway. Tretinoin 75-77 cellular retinoic acid binding protein 2 Homo sapiens 138-145
28980226-6 2017 Retinoic acid controls meiotic entry in developing chicken gonads through the expressions of retinaldehyde dehydrogenase 2, a major retinoic acid synthesizing enzyme, and cytochrome P450 family 26, subfamily B member 1, a major retinoic acid-degrading enzyme. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A2 Gallus gallus 93-122
28980226-6 2017 Retinoic acid controls meiotic entry in developing chicken gonads through the expressions of retinaldehyde dehydrogenase 2, a major retinoic acid synthesizing enzyme, and cytochrome P450 family 26, subfamily B member 1, a major retinoic acid-degrading enzyme. Tretinoin 132-145 aldehyde dehydrogenase 1 family member A2 Gallus gallus 93-122
18773862-8 2008 Cyclin B1 and cyclin E expression was slightly decreased in the SB- and ATRA + SB-treated groups, but did not change in the ATRA-treated group. Tretinoin 72-76 cyclin B1 Homo sapiens 0-9
18048326-0 2007 Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha. Tretinoin 18-31 retinoic acid receptor alpha Homo sapiens 99-127
27840199-8 2017 Retinoic acid (RA) addition and inhibition studies revealed that tbx2a and tbx2b are negatively regulated by RA signaling. Tretinoin 0-13 T-box transcription factor 2a Danio rerio 65-70
27840199-8 2017 Retinoic acid (RA) addition and inhibition studies revealed that tbx2a and tbx2b are negatively regulated by RA signaling. Tretinoin 15-17 T-box transcription factor 2a Danio rerio 65-70
27840199-8 2017 Retinoic acid (RA) addition and inhibition studies revealed that tbx2a and tbx2b are negatively regulated by RA signaling. Tretinoin 109-111 T-box transcription factor 2a Danio rerio 65-70
27840199-13 2017 Taken together, these data reveal for the first time that tbx2a/b mitigate pronephros segmentation downstream of RA, and that interplay between Notch signaling and tbx2a/b regulate CS formation, thus providing several novel insights into the genetic regulatory networks that influence these lineages. Tretinoin 113-115 T-box transcription factor 2a Danio rerio 58-63
28361034-10 2017 Two genes comprising OGS (CYP26A1 and RDH10) are strongly associated with ALDH1A2 in the retinoic acid (RA) pathways, suggesting a major role of RA signaling in early PCa progression. Tretinoin 89-102 retinol dehydrogenase 10 Homo sapiens 38-43
28361034-10 2017 Two genes comprising OGS (CYP26A1 and RDH10) are strongly associated with ALDH1A2 in the retinoic acid (RA) pathways, suggesting a major role of RA signaling in early PCa progression. Tretinoin 89-102 aldehyde dehydrogenase 1 family member A2 Homo sapiens 74-81
28427488-0 2017 Nr2e1 Downregulation Is Involved in Excess Retinoic Acid-induced Developmental Abnormality in the Mouse Brain. Tretinoin 43-56 nuclear receptor subfamily 2, group E, member 1 Mus musculus 0-5
18048326-2 2007 Using a human mammary MCF7-derived AREc32 reporter cell line, we now report that all-trans retinoic acid (ATRA), and other retinoic acid receptor alpha (RARalpha) agonists, markedly reduces the ability of Nrf2 to mediate induction of ARE-driven genes by cancer chemopreventive agents including the metabolite of butylated hydroxyanisole, tert-butylhydroquinone (tBHQ). Tretinoin 91-104 retinoic acid receptor alpha Homo sapiens 123-151
28427488-1 2017 OBJECTIVE: This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 (Nr2e1) in retinoic acid (RA)-induced brain abnormality. Tretinoin 139-152 nuclear receptor subfamily 2, group E, member 1 Mus musculus 82-127
28427488-1 2017 OBJECTIVE: This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 (Nr2e1) in retinoic acid (RA)-induced brain abnormality. Tretinoin 139-152 nuclear receptor subfamily 2, group E, member 1 Mus musculus 129-134
28063140-3 2017 We used real-time quantitative PCR to determine whether PML/RARalpha affects the expression of S100A9 in NB4 and PR9 cells upon ATRA treatment. Tretinoin 128-132 S100 calcium binding protein A9 Homo sapiens 95-101
28063140-6 2017 Results showed that S100A9 was an ATRA-responsive gene, and PML/RARalpha was necessary for the ATRA-induced expression of S100A9 in APL cells. Tretinoin 34-38 S100 calcium binding protein A9 Homo sapiens 20-26
28063140-7 2017 In addition, PU.1 could bind to the promoter of S100A9, especially when treated with ATRA in NB4 cells, and promote its activity. Tretinoin 85-89 S100 calcium binding protein A9 Homo sapiens 48-54
28361317-13 2017 These SOX2-expressing foregut spheroids can be further patterned into posterior foregut by addition of retinoic acid. Tretinoin 103-116 SRY-box transcription factor 2 Homo sapiens 6-10
27166558-4 2017 A major subset of oral cDCs with the CD103-CD11b+ phenotype showed retinoic acid (RA)-producing activity and converted naive CD4+ T cells to Foxp3+ Treg cells in a transforming growth factor-beta- and RA-dependent manner in vitro. Tretinoin 67-80 integrin subunit alpha M Homo sapiens 43-48
27166558-4 2017 A major subset of oral cDCs with the CD103-CD11b+ phenotype showed retinoic acid (RA)-producing activity and converted naive CD4+ T cells to Foxp3+ Treg cells in a transforming growth factor-beta- and RA-dependent manner in vitro. Tretinoin 82-84 integrin subunit alpha M Homo sapiens 43-48
27166558-5 2017 In the ManLNs, migratory CD103-CD11b+ cDCs also showed RA-producing activity. Tretinoin 55-57 integrin subunit alpha M Homo sapiens 31-36
28063140-9 2017 Collectively, our data indicated that PML/RARalpha and PU.1 were necessary for the ATRA-induced expression of S100A9 in APL cells. Tretinoin 83-87 S100 calcium binding protein A9 Homo sapiens 110-116
18048326-2 2007 Using a human mammary MCF7-derived AREc32 reporter cell line, we now report that all-trans retinoic acid (ATRA), and other retinoic acid receptor alpha (RARalpha) agonists, markedly reduces the ability of Nrf2 to mediate induction of ARE-driven genes by cancer chemopreventive agents including the metabolite of butylated hydroxyanisole, tert-butylhydroquinone (tBHQ). Tretinoin 91-104 retinoic acid receptor alpha Homo sapiens 153-161
28049897-4 2017 The atRA-RARalpha complex is known to bind to a characteristic retinoic acid response element (RARE) located in the promoter of target genes. Tretinoin 63-76 retinoic acid receptor, alpha Mus musculus 9-17
18048326-7 2007 In MCF7 cells, ATRA did not block the nuclear accumulation of Nrf2 but reduced the binding of Nrf2 to the ARE enhancer as a consequence of forming a complex with RARalpha. Tretinoin 15-19 retinoic acid receptor alpha Homo sapiens 162-170
27798106-4 2016 Here, we show that DNA methylation-independent removable CTCF insulator is responsible for retinoic acid (RA)-mediated higher-order chromatin remodeling in the human HOXA gene locus. Tretinoin 91-104 CCCTC-binding factor Homo sapiens 57-61
18029486-5 2007 Expression of IFNgamma and inducible nitric oxide synthetase messenger RNA (mRNA) was higher in the infected lung tissues of RA-treated rats than in control rats. Tretinoin 125-127 interleukin 18 Rattus norvegicus 14-22
27798106-4 2016 Here, we show that DNA methylation-independent removable CTCF insulator is responsible for retinoic acid (RA)-mediated higher-order chromatin remodeling in the human HOXA gene locus. Tretinoin 106-108 CCCTC-binding factor Homo sapiens 57-61
27798106-7 2016 Notably, upon RA signaling, the RAR/RXR transcription factor induced loss of adjacent CTCF binding and changed the higher-order chromatin conformation of the overall locus. Tretinoin 14-16 retinoid X receptor alpha Homo sapiens 36-39
27798106-7 2016 Notably, upon RA signaling, the RAR/RXR transcription factor induced loss of adjacent CTCF binding and changed the higher-order chromatin conformation of the overall locus. Tretinoin 14-16 CCCTC-binding factor Homo sapiens 86-90
27989561-4 2017 SERPINA5 binds glycosaminoglycans, phospholipids, and retinoic acid. Tretinoin 54-67 serine (or cysteine) peptidase inhibitor, clade A, member 5 Mus musculus 0-8
27999196-5 2017 Moreover, meiosis was initiated in CHIR99021 and retinoic acid co-treated cultures as evidenced by a significant expression of the punctate synaptonemal complex protein 3 (SCP3). Tretinoin 49-62 synaptonemal complex protein 3 Homo sapiens 140-170
27999196-5 2017 Moreover, meiosis was initiated in CHIR99021 and retinoic acid co-treated cultures as evidenced by a significant expression of the punctate synaptonemal complex protein 3 (SCP3). Tretinoin 49-62 synaptonemal complex protein 3 Homo sapiens 172-176
28111553-3 2016 Robust expression of RA-degrading enzymes Cyp26b1 and Cyp26c1 in developing murine teeth suggested RA excess would reduce tooth hard tissue mineralization, adversely affecting enamel. Tretinoin 21-23 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 54-61
28111553-3 2016 Robust expression of RA-degrading enzymes Cyp26b1 and Cyp26c1 in developing murine teeth suggested RA excess would reduce tooth hard tissue mineralization, adversely affecting enamel. Tretinoin 99-101 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 54-61
27670072-4 2016 We hypothesized that increasing in vivo production of retinoic acid (RA) during vaccination with a DNA vector expressing retinaldehyde dehydrogenase 2 (RALDH2), the rate-limiting enzyme in RA biosynthesis, could similarly provide enhanced programming of mucosal homing to T cell responses while avoiding teratogenic effects. Tretinoin 54-67 aldehyde dehydrogenase 1 family member A2 Homo sapiens 121-150
27670072-4 2016 We hypothesized that increasing in vivo production of retinoic acid (RA) during vaccination with a DNA vector expressing retinaldehyde dehydrogenase 2 (RALDH2), the rate-limiting enzyme in RA biosynthesis, could similarly provide enhanced programming of mucosal homing to T cell responses while avoiding teratogenic effects. Tretinoin 54-67 aldehyde dehydrogenase 1 family member A2 Homo sapiens 152-158
18029491-6 2007 In vitro incubation of mouse splenocytes or purified spleen cluster of differentiation (CD) 4-positive T lymphocytes, with ATRA, increased, respectively, OVA- and anti-CD 3 antibody-induced IL-4 and IL-5 production and inhibited IFNgamma release. Tretinoin 123-127 interleukin 4 Mus musculus 190-194
27670072-4 2016 We hypothesized that increasing in vivo production of retinoic acid (RA) during vaccination with a DNA vector expressing retinaldehyde dehydrogenase 2 (RALDH2), the rate-limiting enzyme in RA biosynthesis, could similarly provide enhanced programming of mucosal homing to T cell responses while avoiding teratogenic effects. Tretinoin 69-71 aldehyde dehydrogenase 1 family member A2 Homo sapiens 121-150
27670072-4 2016 We hypothesized that increasing in vivo production of retinoic acid (RA) during vaccination with a DNA vector expressing retinaldehyde dehydrogenase 2 (RALDH2), the rate-limiting enzyme in RA biosynthesis, could similarly provide enhanced programming of mucosal homing to T cell responses while avoiding teratogenic effects. Tretinoin 69-71 aldehyde dehydrogenase 1 family member A2 Homo sapiens 152-158
27835617-10 2017 HIV reactivation was induced by TCR triggering and/or retinoic acid exposure at higher levels in CCR6 versus CCR6 TM, TCM, and TEM. Tretinoin 54-67 C-C motif chemokine receptor 6 Homo sapiens 97-101
27835617-10 2017 HIV reactivation was induced by TCR triggering and/or retinoic acid exposure at higher levels in CCR6 versus CCR6 TM, TCM, and TEM. Tretinoin 54-67 C-C motif chemokine receptor 6 Homo sapiens 109-113
18029491-6 2007 In vitro incubation of mouse splenocytes or purified spleen cluster of differentiation (CD) 4-positive T lymphocytes, with ATRA, increased, respectively, OVA- and anti-CD 3 antibody-induced IL-4 and IL-5 production and inhibited IFNgamma release. Tretinoin 123-127 interleukin 5 Mus musculus 199-203
27889102-10 2017 Using berberine or retinoic acid (which can regulate the activities of Hnf4a and Foxd3, respectively), we demonstrated suppression of C2H9orf152 by the chemicals in chicken primary hepatocytes. Tretinoin 19-32 forkhead box D3 Gallus gallus 81-86
27889102-10 2017 Using berberine or retinoic acid (which can regulate the activities of Hnf4a and Foxd3, respectively), we demonstrated suppression of C2H9orf152 by the chemicals in chicken primary hepatocytes. Tretinoin 19-32 chromosome 2 open reading frame, human C9orf152 Gallus gallus 134-144
27737899-2 2016 Am80, a retinoic acid (RA) agonist that enhances granulocytic differentiation by selectively activating transcription factor RA receptor alpha (RARalpha), alternatively promotes RA-target gene expression. Tretinoin 23-25 retinoic acid receptor, alpha Mus musculus 144-152
17616812-5 2007 Treatment with ATRA plus IFN-gamma stimulated PTEN expression and suppressed Akt activation in T98G cells, whereas no PTEN expression but Akt activation in U87MG cells under the same conditions. Tretinoin 15-19 phosphatase and tensin homolog Homo sapiens 46-50
27444966-1 2016 Retinoic acid early induced transcript-1 (RAE-1) glycoproteins are ligands of the activating immune receptor NKG2D. Tretinoin 0-13 ribonucleic acid export 1 Mus musculus 42-47
28680330-0 2017 Differentiated all-trans retinoic acid response of naive CD4+CD25- cells isolated from rats with collagen-induced arthritis and healthy ones under in vitro conditions. Tretinoin 25-38 Cd4 molecule Rattus norvegicus 57-60
17945029-6 2007 We demonstrated that rbp4 expression was negatively regulated by Nodal and Hedgehog (Hh) signalling and positively controlled by retinoic acid (RA). Tretinoin 129-142 retinol binding protein 4, plasma Danio rerio 21-25
27320333-5 2017 Conversely, RXR is able to form "nonpermissive" heterodimers with vitamin D receptor (VDR), thyroid receptor (TR) and retinoic acid receptor (RAR), which function only in the presence of vitamin D, T3 and retinoic acid, respectively. Tretinoin 118-131 retinoid X receptor alpha Homo sapiens 12-15
29154149-2 2017 In culture, ES cells can be differentiated into mature neurons by treatment with Retinoic Acid (RA) and this effect is mediated mainly through the activation of the RA nuclear receptors (RAR alpha, beta, and gamma), and their isoforms. Tretinoin 81-94 retinoic acid receptor, alpha Mus musculus 187-213
27007678-6 2016 Addition of exogenous GM-CSF to CD45RAG-/- mice rescued RA production, increased colonic T-cell numbers, and increased weight loss. Tretinoin 36-38 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 22-28
27299363-7 2016 Retinoic acid can posteriorize and at the same time dorsalize the foregut toward a PDX1-positive pancreatic duodenal cell type whereas active Wnt/beta-catenin signaling synergistically with FGF-2, BMP-4, and RA induces the formation of CDX2-positive posterior endoderm. Tretinoin 0-13 caudal type homeobox 2 Homo sapiens 236-240
27724856-2 2016 The subfamily of aldehyde dehydrogenases 1 (ALDH1) isoenzymes, which comprises ALDH1A1, ALDH1A2, and ALDH1A3, is involved in the synthesis of retinoic acid, and has been identified as functional stem cell markers in diverse cancers. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A2 Homo sapiens 88-95
17945029-6 2007 We demonstrated that rbp4 expression was negatively regulated by Nodal and Hedgehog (Hh) signalling and positively controlled by retinoic acid (RA). Tretinoin 144-146 retinol binding protein 4, plasma Danio rerio 21-25
17917245-8 2007 Finally, ATRA-induced differentiation and eotaxin-2/CCL24 production were greatly enhanced in the GATA-1-overexpressed clones. Tretinoin 9-13 C-C motif chemokine ligand 24 Homo sapiens 42-51
27546489-2 2016 We found that the PRRs, retinoic acid-inducible gene 1 (RIG-I) and melanoma differentiation-associated protein 5 (MDA5), which have been implicated as interferon (IFN)-stimulated genes, were dominantly responsible for the recognition of IAV in lungs of mice at 3 and 7 days post infection (dpi). Tretinoin 24-37 DEAD/H box helicase 58 Mus musculus 56-61
27964926-4 2017 The pan-RAR agonist, all-trans retinoic acid (ATRA), directly inhibited differentiation and mineralisation of early osteoprogenitors and impaired the differentiation of more mature osteoblast populations. Tretinoin 21-44 retinoic acid receptor, alpha Mus musculus 8-11
27964926-4 2017 The pan-RAR agonist, all-trans retinoic acid (ATRA), directly inhibited differentiation and mineralisation of early osteoprogenitors and impaired the differentiation of more mature osteoblast populations. Tretinoin 46-50 retinoic acid receptor, alpha Mus musculus 8-11
27546489-2 2016 We found that the PRRs, retinoic acid-inducible gene 1 (RIG-I) and melanoma differentiation-associated protein 5 (MDA5), which have been implicated as interferon (IFN)-stimulated genes, were dominantly responsible for the recognition of IAV in lungs of mice at 3 and 7 days post infection (dpi). Tretinoin 24-37 interferon induced with helicase C domain 1 Mus musculus 114-118
17917245-8 2007 Finally, ATRA-induced differentiation and eotaxin-2/CCL24 production were greatly enhanced in the GATA-1-overexpressed clones. Tretinoin 9-13 C-C motif chemokine ligand 24 Homo sapiens 52-57
17929112-0 2007 PML-RARalpha inhibitors (ATRA, tamibaroten, arsenic troxide) for acute promyelocytic leukemia. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 0-3
26776160-0 2016 The E3 ubiquitin protein ligase MDM2 dictates all-trans retinoic acid-induced osteoblastic differentiation of osteosarcoma cells by modulating the degradation of RARalpha. Tretinoin 56-69 MDM2 proto-oncogene Homo sapiens 32-36
26776160-7 2016 Moreover, MDM2 impairs the ATRA-induced osteoblastic differentiation of osteosarcoma cells, whereas an inhibitor of the MDM2 ubiquitin ligase synergizes with ATRA to enhance the differentiation of osteosarcoma cells and primary osteosarcoma blasts. Tretinoin 27-31 MDM2 proto-oncogene Homo sapiens 10-14
26776160-7 2016 Moreover, MDM2 impairs the ATRA-induced osteoblastic differentiation of osteosarcoma cells, whereas an inhibitor of the MDM2 ubiquitin ligase synergizes with ATRA to enhance the differentiation of osteosarcoma cells and primary osteosarcoma blasts. Tretinoin 158-162 MDM2 proto-oncogene Homo sapiens 120-124
26776160-8 2016 Therefore, our study indicates that MDM2 serves as an E3 ubiquitin ligase to regulate the degradation of RARalpha and suggests that MDM2 is a novel therapeutic target for ATRA-based differentiation therapeutic approaches in osteosarcoma. Tretinoin 171-175 MDM2 proto-oncogene Homo sapiens 36-40
17988991-0 2007 Successful all-trans retinoic acid treatment of acute promyelocytic leukemia in a patient with NPM/RAR fusion. Tretinoin 21-34 retinoic acid receptor alpha Homo sapiens 99-102
26776160-8 2016 Therefore, our study indicates that MDM2 serves as an E3 ubiquitin ligase to regulate the degradation of RARalpha and suggests that MDM2 is a novel therapeutic target for ATRA-based differentiation therapeutic approaches in osteosarcoma. Tretinoin 171-175 MDM2 proto-oncogene Homo sapiens 132-136
17988991-6 2007 These findings suggest that ATRA can be used to treat APL patients with NPM/RAR as well as APL with PML/RAR. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 76-79
27402696-1 2016 The vitamin A metabolite all-trans retinoic acid (ATRA) induces a gut-homing phenotype in activated CD4(+) conventional T cells (Tconv) by upregulating the integrin alpha4beta7 and the chemokine receptor CCR9. Tretinoin 35-48 CD4 antigen Mus musculus 100-103
27402696-1 2016 The vitamin A metabolite all-trans retinoic acid (ATRA) induces a gut-homing phenotype in activated CD4(+) conventional T cells (Tconv) by upregulating the integrin alpha4beta7 and the chemokine receptor CCR9. Tretinoin 35-48 chemokine (C-C motif) receptor 9 Mus musculus 204-208
17988991-6 2007 These findings suggest that ATRA can be used to treat APL patients with NPM/RAR as well as APL with PML/RAR. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 104-107
27402696-1 2016 The vitamin A metabolite all-trans retinoic acid (ATRA) induces a gut-homing phenotype in activated CD4(+) conventional T cells (Tconv) by upregulating the integrin alpha4beta7 and the chemokine receptor CCR9. Tretinoin 50-54 CD4 antigen Mus musculus 100-103
17655486-4 2007 RA-treated EBs were subsequently exposed to sodium butyrate (SB), betacellulin (BTC) or activin A (AA). Tretinoin 0-2 betacellulin, epidermal growth factor family member Mus musculus 66-78
27402696-1 2016 The vitamin A metabolite all-trans retinoic acid (ATRA) induces a gut-homing phenotype in activated CD4(+) conventional T cells (Tconv) by upregulating the integrin alpha4beta7 and the chemokine receptor CCR9. Tretinoin 50-54 chemokine (C-C motif) receptor 9 Mus musculus 204-208
27402696-2 2016 We report that, in contrast to mouse Tconv, only ~50% of regulatory T cells (Treg) upregulate CCR9 when stimulated by physiological levels of ATRA, even though Tconv and Treg express similar levels of the retinoic acid receptor (RAR). Tretinoin 142-146 chemokine (C-C motif) receptor 9 Mus musculus 94-98
27402696-5 2016 This suggests that in Treg, ATRA-induced upregulation of CCR9 and alpha4beta7 is dependent on activation of a mTOR signaling pathway. Tretinoin 28-32 chemokine (C-C motif) receptor 9 Mus musculus 57-61
17538076-4 2007 RA significantly induced HSD17B2 mRNA levels and enzyme activity in a dose- and time-dependent manner. Tretinoin 0-2 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 25-32
27281783-8 2016 Retinoic acid induced AIRE expression in GC1-spg cells. Tretinoin 0-13 autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy) Mus musculus 22-26
17538076-6 2007 RNA interference directed against RARA or RXRA led to reduced basal levels of HSD17B2 mRNA levels and significantly abolished RA-stimulated HSD17B2 expression. Tretinoin 34-36 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 78-85
17538076-6 2007 RNA interference directed against RARA or RXRA led to reduced basal levels of HSD17B2 mRNA levels and significantly abolished RA-stimulated HSD17B2 expression. Tretinoin 34-36 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 140-147
17538076-7 2007 Together, these data indicate that regulation of HSD17B2 mRNA levels and enzymatic activity by RA in the placenta is mediated by RARA and RXRA. Tretinoin 95-97 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 49-56
27462186-7 2016 On the other hand, Top2beta expression markedly decreased upon the induction of differentiation by all trans-retinoic acid. Tretinoin 103-122 DNA topoisomerase II beta Homo sapiens 19-27
17538076-7 2007 Together, these data indicate that regulation of HSD17B2 mRNA levels and enzymatic activity by RA in the placenta is mediated by RARA and RXRA. Tretinoin 95-97 retinoic acid receptor alpha Homo sapiens 129-133
17804711-0 2007 HOXA5 acts directly downstream of retinoic acid receptor beta and contributes to retinoic acid-induced apoptosis and growth inhibition. Tretinoin 34-47 homeobox A5 Homo sapiens 0-5
17804711-5 2007 We have, for the first time, identified the RA response element in HOXA5, which was found to be located in the 3" end of the gene. Tretinoin 44-46 homeobox A5 Homo sapiens 67-72
27329592-7 2016 The differentiated APL cells derived from the excised tumor mass exhibited decreased CD44 expression in fucoidan+ATRA treated mice. Tretinoin 113-117 CD44 antigen Mus musculus 85-89
17804711-7 2007 Overexpression of RARbeta strongly enhances RA responsiveness, and knocking down RARbeta expression abolishes RA-mediated induction of HOXA5 expression in breast cancer cells. Tretinoin 18-20 homeobox A5 Homo sapiens 135-140
17694576-4 2007 Using a specific agonist and antagonist, as well as retroviral over-expression, we also provide evidence that the effects of ATRA are likely to be at least partially mediated by the nuclear retinoic acid receptor-alpha (RARalpha). Tretinoin 125-129 retinoic acid receptor alpha Homo sapiens 190-218
26980802-1 2016 All-trans-retinoic acid plays a central role in mucosal immunity, where it promotes its synthesis by up-regulating CD103 expression on dendritic cells, induces gut tropic (alpha4beta7(+) and CCR9(+)) T cells, and inhibits Th1/Th17 differentiation. Tretinoin 0-23 negative elongation factor complex member C/D Homo sapiens 222-225
26980802-3 2016 However, as a result of limited human data, we investigated the effect of retinoic acid on human dendritic cells and CD4(+) T cell responses in the presence of polarizing (Th1/Th9/Th17) and inflammatory (LPS-induced dendritic cells) conditions. Tretinoin 74-87 negative elongation factor complex member C/D Homo sapiens 172-175
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 26-39 negative elongation factor complex member C/D Homo sapiens 262-265
17694576-4 2007 Using a specific agonist and antagonist, as well as retroviral over-expression, we also provide evidence that the effects of ATRA are likely to be at least partially mediated by the nuclear retinoic acid receptor-alpha (RARalpha). Tretinoin 125-129 retinoic acid receptor alpha Homo sapiens 220-228
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 72-85 negative elongation factor complex member C/D Homo sapiens 262-265
26980802-4 2016 We report a novel role of retinoic acid in an inflammatory setup, where retinoic acid-primed dendritic cells (retinoic acid-monocyte-derived dendritic cells) up-regulated CCR9(+)T cells, which were observed to express high levels of IFN-gamma in the presence of Th1/Th17 conditions. Tretinoin 72-85 negative elongation factor complex member C/D Homo sapiens 262-265
18063853-1 2007 In the present work, the effects of colchicine (COL) and/or all-trans retinoic acid (ATRA) on expression of rexinoid receptors (RXRs) (alpha, beta, gamma), thyroid hormone receptor alpha and coregulators N-CoR, SMRT and SRC-1 mRNA in primary rat hepatocytes as a model of no-proliferating cells were investigated. Tretinoin 85-89 nuclear receptor coactivator 1 Rattus norvegicus 220-225
26980802-7 2016 Experiments with naive CD4(+) T cells, activated in the presence of Th1/Th17 conditions and absence of DCs, indicated that retinoic acid inhibited IFN-gamma and IL-17 expression on T cells. Tretinoin 123-136 negative elongation factor complex member C/D Homo sapiens 68-71
26980802-7 2016 Experiments with naive CD4(+) T cells, activated in the presence of Th1/Th17 conditions and absence of DCs, indicated that retinoic acid inhibited IFN-gamma and IL-17 expression on T cells. Tretinoin 123-136 interleukin 17A Homo sapiens 161-166
27363269-7 2016 The expressions of p-JAK2 and p-STAT3 were down-regulated while the expressions of GRIM-19 and Bax were up-regulated after treated with IFN-beta or ATRA on HepG2 cells, especially the combination of IFN-beta and ATRA. Tretinoin 148-152 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 83-90
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 40-53 lysine acetyltransferase 6A Homo sapiens 21-24
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 55-57 lysine acetyltransferase 6A Homo sapiens 21-24
17611697-2 2007 Am-80, Tamibarotene, binds to retinoic acid receptor alpha (RARalpha) more specifically than all-trans retinoic acid. Tretinoin 30-43 retinoic acid receptor alpha Homo sapiens 60-68
27349479-2 2016 Here, we showed that Retinoic acid (RA)-inducible gene I (RIG-I) responds to nutrient signals and induces loss of beta cell mass through G1 cell cycle arrest. Tretinoin 21-34 DExD/H-box helicase 58 Homo sapiens 58-63
27349479-2 2016 Here, we showed that Retinoic acid (RA)-inducible gene I (RIG-I) responds to nutrient signals and induces loss of beta cell mass through G1 cell cycle arrest. Tretinoin 36-38 DExD/H-box helicase 58 Homo sapiens 58-63
18489360-7 2007 Through this mechanism, RA was shown to reduce the levels of matrix metalloproteases (MMPs) and the increase levels of extracellular matrix proteins. Tretinoin 24-26 matrix metallopeptidase 1 Homo sapiens 86-90
27129260-4 2016 We document that overexpression of EVI1 abrogates retinoic acid-induced maturation of EML cells into committed myeloid cells, a process that can be documented by the down-regulation of stem cell antigen-1 and acquisition of responsiveness to granulocyte-macrophage colony-stimulating factor. Tretinoin 50-63 MDS1 and EVI1 complex locus Homo sapiens 35-39
17226773-4 2007 We found that Oct4 and SF-1 were co-expressed in undifferentiated human embryonal carcinoma NCCIT cells and downregulated during retinoic acid-mediated differentiation. Tretinoin 129-142 POU class 5 homeobox 1 Homo sapiens 14-18
27334688-8 2016 Induction of neural differentiation with retinoic acid resulted in downregulation of Sox2 and VRK1 that inversely correlated with the expression of differentiation markers such as N-cadherin, Pax6, mH2A1.2 and mH2A2. Tretinoin 41-54 SRY-box transcription factor 2 Homo sapiens 85-89
27244900-0 2016 Retinoic acid treated human dendritic cells induce T regulatory cells via the expression of CD141 and GARP which is impaired with age. Tretinoin 0-13 leucine rich repeat containing 32 Homo sapiens 102-106
27244900-5 2016 Our investigations revealed that compared to young DCs, RA stimulated DCs from aged subjects are defective in inducing IL-10 and T regulatory cells. Tretinoin 56-58 interleukin 10 Homo sapiens 119-124
17867372-3 2007 Recently, it was identified as an integral transmembrane protein named STRA6 that is inducible by retinoic acid in certain cancer cells. Tretinoin 98-111 signaling receptor and transporter of retinol STRA6 Homo sapiens 71-76
27244900-6 2016 Examinations of the underlying mechanisms indicated that RA exposure led to the upregulation of CD141 and GARP on DCs which rendered the DCs tolerogenic. Tretinoin 57-59 leucine rich repeat containing 32 Homo sapiens 106-110
26945879-2 2016 Retinoic acid binding protein II (CRABP-II) is a cytoplasmic receptor that critically regulates all-trans-retinoic acid (ATRA) trafficking. Tretinoin 96-119 cellular retinoic acid binding protein 2 Homo sapiens 34-42
26945879-2 2016 Retinoic acid binding protein II (CRABP-II) is a cytoplasmic receptor that critically regulates all-trans-retinoic acid (ATRA) trafficking. Tretinoin 121-125 cellular retinoic acid binding protein 2 Homo sapiens 34-42
26945879-6 2016 CRABP-II-transfected HaCaT, FaDu, and A431 cells showed expression of differentiation markers, retinoic acid receptor-beta/-gamma signaling, ATRA sensitivity, and suppression of EGFR/v-akt murine thymoma viral oncogene homolog 1 (AKT) pathways in a fatty acid binding protein 5/peroxisome proliferator-activated receptor-beta/-delta-independent manner. Tretinoin 141-145 cellular retinoic acid binding protein 2 Homo sapiens 0-8
17297443-3 2007 GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. Tretinoin 84-97 HtrA serine peptidase 2 Homo sapiens 34-39
26945879-9 2016 Our results showed reduced CRABP-II expression in human poorly differentiated squamous cell carcinomas, and its gene deletion favored experimental skin carcinogenesis and impaired ATRA antitumor efficacy, likely modulating EGFR/AKT pathways and retinoic acid receptor-beta/-gamma signaling. Tretinoin 180-184 cellular retinoic acid binding protein 2 Homo sapiens 27-35
26662056-5 2016 Overexpression of Btg1 up-regulates the expression of retinoic acid and thyroid hormone receptors, but, different from other systems, the influence of BTG1 in connective tissue differentiation appears to be independent of retinoic acid and thyroid hormone signaling. Tretinoin 54-67 BTG anti-proliferation factor 1 Homo sapiens 18-22
17297443-3 2007 GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. Tretinoin 99-101 HtrA serine peptidase 2 Homo sapiens 34-39
17522161-4 2007 Excess RA leads to ectopic foxi1 expression throughout the entire preplacodal domain. Tretinoin 7-9 forkhead box i1 Danio rerio 27-32
27080036-0 2016 Retinoic acid facilitates inactivated transmissible gastroenteritis virus induction of CD8(+) T-cell migration to the porcine gut. Tretinoin 0-13 CD8a molecule Homo sapiens 87-90
27080036-6 2016 We demonstrated that elevated numbers of gut-homing CD8(+) T cells (which express alpha4beta7 and CCR9 molecules) were presented in porcine inguinal lymph nodes and were recruited to the small intestine by RA. Tretinoin 206-208 CD8a molecule Homo sapiens 52-55
27078158-0 2016 Retinoid X Receptor Agonists Upregulate Genes Responsible for the Biosynthesis of All-Trans-Retinoic Acid in Human Epidermis. Tretinoin 82-105 retinoid X receptor alpha Homo sapiens 0-19
17522161-11 2007 We show that rhombomere 5 wnt8b expression is absent in both RA-signaling-depleted embryos and in fgf3;tcf2 double mutants, and inactivation of wnt8b in fgf3 mutants by morpholino injection results in small otic vesicles, similar to RA depletion in wild type. Tretinoin 61-63 wingless-type MMTV integration site family, member 8b Danio rerio 26-31
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 142-161 vascular endothelial growth factor D Homo sapiens 72-78
17522161-12 2007 Thus, excess RA expands otic competence, whereas the loss of RA impairs the expression of fgf3 and wnt8b in the hindbrain, compromising the induction and maintenance of otic fate. Tretinoin 61-63 wingless-type MMTV integration site family, member 8b Danio rerio 99-104
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 142-161 fms related receptor tyrosine kinase 4 Homo sapiens 100-106
17185354-11 2007 LCA and ATRA caused a synergistic increase in RA signalling as shown by increased p21 (p<0.01). Tretinoin 8-12 H3 histone pseudogene 16 Homo sapiens 82-85
17185354-11 2007 LCA and ATRA caused a synergistic increase in RA signalling as shown by increased p21 (p<0.01). Tretinoin 10-12 H3 histone pseudogene 16 Homo sapiens 82-85
17317642-16 2007 Strikingly, a clearance of PML-RARalpha transcript in an earlier and more thorough manner, and a higher quality remission and survival in newly diagnosed APL are achieved when ATRA is combined with ATO, as compared to either monotherapy, making APL a curable disease. Tretinoin 176-180 PML nuclear body scaffold Homo sapiens 27-30
17317642-16 2007 Strikingly, a clearance of PML-RARalpha transcript in an earlier and more thorough manner, and a higher quality remission and survival in newly diagnosed APL are achieved when ATRA is combined with ATO, as compared to either monotherapy, making APL a curable disease. Tretinoin 176-180 retinoic acid receptor alpha Homo sapiens 31-39
17503335-2 2007 STRA6 encodes an integral cell-membrane protein that favors RA uptake from soluble retinol-binding protein; its transcription is directly regulated by RA levels. Tretinoin 60-62 signaling receptor and transporter of retinol STRA6 Homo sapiens 0-5
17451432-8 2007 Treatment of cells with the RARalpha/RXRalpha ligands, all-trans retinoic acid and 9-cis-retinoic acid, reduced and increased GnRH II gene expression in TE671 and JEG-3 cells, respectively. Tretinoin 65-78 retinoic acid receptor alpha Homo sapiens 28-36
17426037-0 2007 Activation of the kinase activity of ATM by retinoic acid is required for CREB-dependent differentiation of neuroblastoma cells. Tretinoin 44-57 ATM serine/threonine kinase Homo sapiens 37-40
17426037-3 2007 In addition to this well characterized role in DNA repair, we now demonstrate a novel role for ATM in the retinoic acid (RA)-induced differentiation of SH-SY5Y neuroblastoma cells into post-mitotic, neuronal-like cells. Tretinoin 106-119 ATM serine/threonine kinase Homo sapiens 95-98
17426037-3 2007 In addition to this well characterized role in DNA repair, we now demonstrate a novel role for ATM in the retinoic acid (RA)-induced differentiation of SH-SY5Y neuroblastoma cells into post-mitotic, neuronal-like cells. Tretinoin 121-123 ATM serine/threonine kinase Homo sapiens 95-98
17426037-4 2007 RA rapidly activates the activity of ATM kinase, leading to the ATM-dependent phosphorylation of the CREB protein, extrusion of neuritic processes, and differentiation of SH-SY5Y cells into neuronal-like cells. Tretinoin 0-2 ATM serine/threonine kinase Homo sapiens 37-40
17347302-5 2007 In addition, all-trans retinoic acid (ATRA)-induced neutrophil differentiation of two leukemic cell lines, NB4 and U937, revealed significantly higher DAPK2 mRNA expression paralleled by protein induction. Tretinoin 13-36 death associated protein kinase 2 Homo sapiens 151-156
17347302-5 2007 In addition, all-trans retinoic acid (ATRA)-induced neutrophil differentiation of two leukemic cell lines, NB4 and U937, revealed significantly higher DAPK2 mRNA expression paralleled by protein induction. Tretinoin 38-42 death associated protein kinase 2 Homo sapiens 151-156
17347302-8 2007 Lentiviral vector-mediated expression of DAPK2 in NB4 cells enhanced, whereas small interfering RNA-mediated DAPK2 knockdown reduced ATRA-induced granulocytic differentiation, as evidenced by morphology and neutrophil stage-specific maturation genes, such as CD11b, G-CSF receptor, C/EBPepsilon, and lactoferrin. Tretinoin 133-137 death associated protein kinase 2 Homo sapiens 109-114
17522305-11 2007 Furthermore, activation of GFR alpha2b inhibited neurite outgrowth induced by retinoic acid and activated RhoA. Tretinoin 78-91 GDNF family receptor alpha 2 Homo sapiens 27-37
17244680-2 2007 Here, we show that AML1/ETO, the most common translocation fusion product in acute myeloid leukemia (AML), counteracts the activity of retinoic acid (RA), a transcriptional regulator of myelopoiesis. Tretinoin 135-148 RUNX family transcription factor 1 Homo sapiens 19-23
17244680-2 2007 Here, we show that AML1/ETO, the most common translocation fusion product in acute myeloid leukemia (AML), counteracts the activity of retinoic acid (RA), a transcriptional regulator of myelopoiesis. Tretinoin 150-152 RUNX family transcription factor 1 Homo sapiens 19-23
17244680-5 2007 The link among AML1/ETO, heterochromatic RARbeta2 repression, RA resistance, and myeloid differentiation block is indicated by the ability of either siRNA-AML1/ETO or the DNA methylation inhibitor 5-azacytidine to revert these epigenetic alterations and to restore RA differentiation response in AML1/ETO blasts. Tretinoin 62-64 RUNX family transcription factor 1 Homo sapiens 15-19
17244680-5 2007 The link among AML1/ETO, heterochromatic RARbeta2 repression, RA resistance, and myeloid differentiation block is indicated by the ability of either siRNA-AML1/ETO or the DNA methylation inhibitor 5-azacytidine to revert these epigenetic alterations and to restore RA differentiation response in AML1/ETO blasts. Tretinoin 62-64 RUNX family transcription factor 1 Homo sapiens 155-159
17244680-5 2007 The link among AML1/ETO, heterochromatic RARbeta2 repression, RA resistance, and myeloid differentiation block is indicated by the ability of either siRNA-AML1/ETO or the DNA methylation inhibitor 5-azacytidine to revert these epigenetic alterations and to restore RA differentiation response in AML1/ETO blasts. Tretinoin 62-64 RUNX family transcription factor 1 Homo sapiens 155-159
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 16-29 neurofilament, light polypeptide Mus musculus 41-44
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 16-29 glial fibrillary acidic protein Mus musculus 151-155
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 31-33 neurofilament, light polypeptide Mus musculus 41-44
17395374-5 2007 When exposed to retinoic acid (RA), both NFL-/- and normal MSCs could express several markers of neuronal lineage, such as Nestin, MAP-2, NeuN, O4 and GFAP. Tretinoin 31-33 glial fibrillary acidic protein Mus musculus 151-155
17483073-5 2007 Both U937 and NB4 cells treated with 10-7 M all-trans retinoic acid (ATRA) for 6 days displayed increased levels of BPI protein and accompanying up-regulated C/EBP epsilon expression. Tretinoin 44-67 bactericidal permeability increasing protein Homo sapiens 116-119
17483073-5 2007 Both U937 and NB4 cells treated with 10-7 M all-trans retinoic acid (ATRA) for 6 days displayed increased levels of BPI protein and accompanying up-regulated C/EBP epsilon expression. Tretinoin 44-67 CCAAT enhancer binding protein epsilon Homo sapiens 158-171
17483073-5 2007 Both U937 and NB4 cells treated with 10-7 M all-trans retinoic acid (ATRA) for 6 days displayed increased levels of BPI protein and accompanying up-regulated C/EBP epsilon expression. Tretinoin 69-73 bactericidal permeability increasing protein Homo sapiens 116-119
17483073-5 2007 Both U937 and NB4 cells treated with 10-7 M all-trans retinoic acid (ATRA) for 6 days displayed increased levels of BPI protein and accompanying up-regulated C/EBP epsilon expression. Tretinoin 69-73 CCAAT enhancer binding protein epsilon Homo sapiens 158-171
17203325-5 2007 Cyp26 (a1,b1, and c1), which is a member of the cytochrome P450 family, acts by reducing the activity of RA. Tretinoin 105-107 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 0-5
17463084-3 2007 The present work reports that TLR3 signaling by polyinosinic-polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8alphaalpha intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. Tretinoin 146-159 toll-like receptor 3 Mus musculus 30-34
17317001-4 2007 Retinoic acid induced marked increase in p47phox expression and in catalytic activity of PKC delta: the upregulation of a pathway involving NADPH oxidase and PKC delta is likely to be responsible for neuronal susceptibility to AGE. Tretinoin 0-13 pleckstrin Homo sapiens 41-44
28300657-8 2017 Interestingly, in silico analysis of prune2 promoter found retinoic acid (RA) response elements (AGGTCAcaTGACCA) located at -3 to -16 relative to the first exon. Tretinoin 59-72 prune homolog 2 with BCH domain Danio rerio 37-43
28300657-8 2017 Interestingly, in silico analysis of prune2 promoter found retinoic acid (RA) response elements (AGGTCAcaTGACCA) located at -3 to -16 relative to the first exon. Tretinoin 74-76 prune homolog 2 with BCH domain Danio rerio 37-43
28300657-9 2017 It turned out that RA signaling altered the expression pattern of prune2 in the hindbrain. Tretinoin 19-21 prune homolog 2 with BCH domain Danio rerio 66-72
17185629-0 2007 Lipopolysaccharide opposes the induction of CYP26A1 and CYP26B1 gene expression by retinoic acid in the rat liver in vivo. Tretinoin 83-96 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 44-51
27840957-0 2017 Upregulation of CD54 and downregulation of HLA-ABC contribute to the novel enhancement of the susceptibility of HL-60 cells to NK cell-mediated cytolysis induced by ATRA plus VPA. Tretinoin 165-169 intercellular adhesion molecule 1 Homo sapiens 16-20
27840957-9 2017 In conclusion, the combination of VPA and ATRA not only induced the differentiation of HL-60 cells, but also induced enhancement of the sensitivity of HL-60 cells to NK cells by downregulating the expression of HLA-ABC and upregulating the expression of CD54, but not MICA/MICB. Tretinoin 42-46 intercellular adhesion molecule 1 Homo sapiens 254-258
17185629-3 2007 The cytochrome P450 (CYP) gene family CYP26, which encodes RA-4-hydroxylase activity, is strongly implicated in the oxidation of RA. Tretinoin 59-61 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 38-43
17185629-5 2007 We investigated the regulation of CYP26A1 and CYP26B1 mRNA levels by RA and LPS in the rat liver, as the liver is centrally involved in retinoid metabolism and the acute-phase response to LPS. Tretinoin 69-71 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 34-41
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 0-2 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 29-36
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 0-2 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 196-203
27919949-0 2016 1alpha-Dihydroxyvitamin D3 and Retinoic Acid Increase Nuclear Vitamin D Receptor Expression in Monocytic THP-1 Cells. Tretinoin 31-44 vitamin D receptor Homo sapiens 62-80
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 157-159 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 29-36
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 157-159 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 29-36
17185629-8 2007 When RA and LPS were administered simultaneously (6-h study), LPS alone had little effect on either CYP26A1 or CP26B1 mRNA, but LPS reduced by 80% the RA-induced increase in CYP26A1 mRNA (P<0.02), with a similar trend for CYP26B1 mRNA. Tretinoin 5-7 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 174-181
17392484-3 2007 Here we show that all-trans-retinoic acid (RA), the active metabolite of vitamin A, rapidly (1 hr after treatment) increases CD1d mRNA in human and rodent monocytic cells at a physiologic dose (10 nM). Tretinoin 18-41 CD1d molecule Homo sapiens 125-129
27861128-0 2016 Retinoic acid catabolizing enzyme CYP26C1 is a genetic modifier in SHOX deficiency. Tretinoin 0-13 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 34-41
27861128-4 2016 The variant p.Phe508Cys of the retinoic acid catabolizing enzyme CYP26C1 co-segregated with the SHOX variant p.Val161Ala in the affected individuals, while the SHOX mutant alone was present in asymptomatic individuals. Tretinoin 31-44 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 65-72
27861128-4 2016 The variant p.Phe508Cys of the retinoic acid catabolizing enzyme CYP26C1 co-segregated with the SHOX variant p.Val161Ala in the affected individuals, while the SHOX mutant alone was present in asymptomatic individuals. Tretinoin 31-44 short stature homeobox Homo sapiens 96-100
27861128-4 2016 The variant p.Phe508Cys of the retinoic acid catabolizing enzyme CYP26C1 co-segregated with the SHOX variant p.Val161Ala in the affected individuals, while the SHOX mutant alone was present in asymptomatic individuals. Tretinoin 31-44 short stature homeobox Homo sapiens 160-164
27861128-5 2016 Two further cases with SHOX deficiency and damaging CYP26C1 variants were identified in a cohort of 68 individuals with LWD The identified CYP26C1 variants affected its catabolic activity, leading to an increased level of retinoic acid. Tretinoin 222-235 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 52-59
27861128-5 2016 Two further cases with SHOX deficiency and damaging CYP26C1 variants were identified in a cohort of 68 individuals with LWD The identified CYP26C1 variants affected its catabolic activity, leading to an increased level of retinoic acid. Tretinoin 222-235 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 139-146
27337917-7 2016 Compared with DMSO control group, a low concentration (1 x 10(-7) mol x L(-1)) of RA could up-regulate the expression of mRNA (barx1, dlx2a) in neural crest. Tretinoin 82-84 BARX homeobox 1 Danio rerio 127-132
27861128-6 2016 High levels of retinoic acid significantly decrease SHOX expression in human primary chondrocytes and zebrafish embryos. Tretinoin 15-28 short stature homeobox Homo sapiens 52-56
17392484-3 2007 Here we show that all-trans-retinoic acid (RA), the active metabolite of vitamin A, rapidly (1 hr after treatment) increases CD1d mRNA in human and rodent monocytic cells at a physiologic dose (10 nM). Tretinoin 43-45 CD1d molecule Homo sapiens 125-129
27337917-7 2016 Compared with DMSO control group, a low concentration (1 x 10(-7) mol x L(-1)) of RA could up-regulate the expression of mRNA (barx1, dlx2a) in neural crest. Tretinoin 82-84 distal-less homeobox 2a Danio rerio 134-139
17392484-6 2007 A putative RA-response element was identified in the distal 5" flanking region of the CD1d gene, which binds nuclear retinoid receptors and was responsive to RA in both gel mobility shift assay and transient transfection assay in THP-1 cells. Tretinoin 11-13 CD1d molecule Homo sapiens 86-90
26678800-7 2016 Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression. Tretinoin 24-28 neurofilament medium chain Homo sapiens 120-124
26678800-7 2016 Finally, treatment with ATRA for 96h in the presence of MnSOD siRNA or PEG-catalase inhibited ATRA induced increases in NF-M expression. Tretinoin 94-98 neurofilament medium chain Homo sapiens 120-124
27647308-0 2016 A Novel Combination of Docosahexaenoic Acid, All-Trans Retinoic Acid, and 1, 25-Dihydroxyvitamin D3 Reduces T-Bet Gene Expression, Serum Interferon Gamma, and Clinical Scores but Promotes PPARgamma Gene Expression in Experimental Autoimmune Encephalomyelitis. Tretinoin 45-68 T-box 21 Mus musculus 108-113
27647308-9 2016 These findings highlighted that ATRA, D3, and DHA combination modulated PPARgamma and T-bet gene expression and resulted in decrease in Th1 response and lymphocyte invasion into the central nervous system (CNS) and resultant inflammation. Tretinoin 32-36 T-box 21 Mus musculus 86-91
27569851-4 2016 The objective was to elucidate gene expression of these RA-metabolizing enzymes (ALDH1A1, ALDH1A2, ALDH1A3, CYP26A1, CYP26B1 and CYP26C1) and their protein presence in testes of young, peripubertal and adult dogs. Tretinoin 56-58 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 117-124
27569851-5 2016 Genes encoding RA-synthesizing isozymes ALDH1A1, ALDH1A2 and ALDH1A3 and RA-catabolizing isomers CYP26A1, CYP26B1 and CYP26C1 were expressed in testis at varying levels during testicular development from birth to adulthood in dogs. Tretinoin 73-75 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 106-113
26901853-10 2016 ATRA therapy could significantly increase the percentage of Treg cell, IL-10 level and Foxp3 expression. Tretinoin 0-4 interleukin 10 Homo sapiens 71-76
17392484-6 2007 A putative RA-response element was identified in the distal 5" flanking region of the CD1d gene, which binds nuclear retinoid receptors and was responsive to RA in both gel mobility shift assay and transient transfection assay in THP-1 cells. Tretinoin 158-160 CD1d molecule Homo sapiens 86-90
27569851-6 2016 Based on detailed analyses of mRNA expression patterns, ALDH1A2 was regarded as a primary RA-synthesizing enzyme and CYP26B1 as a critical RA-hydrolysing enzyme; presumably, these genes have vital roles in maintaining RA homeostasis, which is imperative to spermatogenesis and other testicular functions in post-natal canine testis. Tretinoin 139-141 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 117-124
27569851-6 2016 Based on detailed analyses of mRNA expression patterns, ALDH1A2 was regarded as a primary RA-synthesizing enzyme and CYP26B1 as a critical RA-hydrolysing enzyme; presumably, these genes have vital roles in maintaining RA homeostasis, which is imperative to spermatogenesis and other testicular functions in post-natal canine testis. Tretinoin 139-141 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 117-124
17392484-9 2007 These studies together provide evidence for a previously unknown mechanism of CD1d gene expression regulation by RA and suggest that RA is a significant modulator of NKT cell activation. Tretinoin 113-115 CD1d molecule Homo sapiens 78-82
26797574-6 2016 ATRA in the presence of tamoxifen increased NBT reduction and the expression of CD11b in HL-60 cells more effectively than ATRA alone. Tretinoin 0-4 integrin subunit alpha M Homo sapiens 80-85
17392484-9 2007 These studies together provide evidence for a previously unknown mechanism of CD1d gene expression regulation by RA and suggest that RA is a significant modulator of NKT cell activation. Tretinoin 133-135 CD1d molecule Homo sapiens 78-82
17483060-5 2007 HL-60 cells treated with either a PPARgamma ligand (ciglitazone) or a RAR ligand (all-trans retinoic acid [ATRA]) up-regulated PTEN in HL-60 cells. Tretinoin 107-111 phosphatase and tensin homolog Homo sapiens 127-131
17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 H3 histone pseudogene 16 Homo sapiens 150-153
26578346-8 2016 RESULTS: Four weeks of retinoic acid and retinol treatments both increased epidermal thickness, and upregulated genes for collagen type 1 (COL1A1), and collagen type 3 (COL3A1) with corresponding increases in procollagen I and procollagen III protein expression. Tretinoin 23-36 collagen type I alpha 1 chain Homo sapiens 139-145
27688150-5 2016 Significantly, it is found that the differentiation-inducing factor all-trans retinoic acid, but not the proinflammatory cytokine tumor necrosis factor-alpha, enhances this ACAT2-dependent lipoprotein excretion. Tretinoin 78-91 sterol O-acyltransferase 2 Homo sapiens 173-178
26277894-0 2016 Retinoic acid enhances lactoferrin-induced IgA responses by increasing betaglycan expression. Tretinoin 0-13 transforming growth factor beta receptor 3 Homo sapiens 71-81
16914201-0 2007 Retinoic acid therapy served by ligands cross linking and masking CD38. Tretinoin 0-13 CD38 molecule Homo sapiens 66-70
27725760-6 2016 Regarding the mechanism of differentiation and proliferation, EdU+CCR9+Mphis with a proliferative potential were detected specifically in the inflamed liver, and in vitro study revealed that BM-derived CD11b+ cells co-cultured with hepatic stellate cells (HSCs) or stimulated with retinoic acids could acquire CCR9 with antigen-presenting ability. Tretinoin 281-295 integrin subunit alpha M Homo sapiens 202-207
27506116-0 2016 Nuclear receptor corepressors Ncor1 and Ncor2 (Smrt) are required for retinoic acid-dependent repression of Fgf8 during somitogenesis. Tretinoin 70-83 fibroblast growth factor 8 Mus musculus 108-112
26843326-10 2016 Short-term treatment of mice with all-trans retinoic acid resulted in increased PreB lymphopoiesis in BM and an increase in thymic double-negative 4 T cells, inverse to that observed upon Nes cell-specific deletion of Rargamma. Tretinoin 44-57 prolactin regulatory element binding Mus musculus 80-84
26843326-10 2016 Short-term treatment of mice with all-trans retinoic acid resulted in increased PreB lymphopoiesis in BM and an increase in thymic double-negative 4 T cells, inverse to that observed upon Nes cell-specific deletion of Rargamma. Tretinoin 44-57 retinoic acid receptor, gamma Mus musculus 218-226
26506232-7 2016 We further showed that ATRA inhibited E6AP and stabilized MNT expression by protecting it from E6AP mediated ubiquitin-proteasome degradation. Tretinoin 23-27 ubiquitin protein ligase E3A Homo sapiens 38-42
26506232-7 2016 We further showed that ATRA inhibited E6AP and stabilized MNT expression by protecting it from E6AP mediated ubiquitin-proteasome degradation. Tretinoin 23-27 ubiquitin protein ligase E3A Homo sapiens 95-99
27506116-1 2016 Retinoic acid (RA) repression of Fgf8 is required for many different aspects of organogenesis, however relatively little is known about how endogenous RA controls gene repression as opposed to gene activation. Tretinoin 0-13 fibroblast growth factor 8 Mus musculus 33-37
27506116-1 2016 Retinoic acid (RA) repression of Fgf8 is required for many different aspects of organogenesis, however relatively little is known about how endogenous RA controls gene repression as opposed to gene activation. Tretinoin 15-17 fibroblast growth factor 8 Mus musculus 33-37
26566904-8 2016 Thus we identified RA as a lung angiocrine that regulates alveolarization through autocrine regulation of endothelial development and paracrine regulation of elastin synthesis via induction of FGF-18 in mesenchymal cells. Tretinoin 19-21 elastin Homo sapiens 158-165
16920192-0 2007 Retinoic acid-induced CD38 antigen promotes leukemia cells attachment and interferon-gamma/interleukin-1beta-dependent apoptosis of endothelial cells: implications in the etiology of retinoic acid syndrome. Tretinoin 0-13 CD38 molecule Homo sapiens 22-26
26566904-8 2016 Thus we identified RA as a lung angiocrine that regulates alveolarization through autocrine regulation of endothelial development and paracrine regulation of elastin synthesis via induction of FGF-18 in mesenchymal cells. Tretinoin 19-21 fibroblast growth factor 18 Homo sapiens 193-199
27506116-2 2016 Here, we show that nuclear receptor corepressors NCOR1 and NCOR2 (SMRT) redundantly mediate the ability of RA to repress Fgf8. Tretinoin 107-109 fibroblast growth factor 8 Mus musculus 121-125
27506116-4 2016 Embryo chromatin immunoprecipitation studies revealed that NCOR1/2 but not coactivators are recruited to the Fgf8 RA response element (RARE) in an RA-dependent manner, whereas coactivators but not NCOR1/2 are recruited RA-dependently to a RARE near Rarb that is activated by RA. Tretinoin 114-116 fibroblast growth factor 8 Mus musculus 109-113
27506116-4 2016 Embryo chromatin immunoprecipitation studies revealed that NCOR1/2 but not coactivators are recruited to the Fgf8 RA response element (RARE) in an RA-dependent manner, whereas coactivators but not NCOR1/2 are recruited RA-dependently to a RARE near Rarb that is activated by RA. Tretinoin 135-137 fibroblast growth factor 8 Mus musculus 109-113
27506116-4 2016 Embryo chromatin immunoprecipitation studies revealed that NCOR1/2 but not coactivators are recruited to the Fgf8 RA response element (RARE) in an RA-dependent manner, whereas coactivators but not NCOR1/2 are recruited RA-dependently to a RARE near Rarb that is activated by RA. Tretinoin 135-137 fibroblast growth factor 8 Mus musculus 109-113
27506116-7 2016 Our studies support a model in which NCOR1/2 mediates direct RA-dependent repression of Fgf8 in caudal progenitors in order to control somitogenesis. Tretinoin 61-63 fibroblast growth factor 8 Mus musculus 88-92
26742640-7 2016 We observed that differentiation of SH-SY5Y human neuroblastoma cells induced by retinoic acid (RA), the phorbol ester PMA, or the gamma-secretase inhibitor DAPT resulted in an electrophoretic mobility shift of Fe65. Tretinoin 81-94 amyloid beta precursor protein binding family B member 1 Homo sapiens 211-215
26742640-7 2016 We observed that differentiation of SH-SY5Y human neuroblastoma cells induced by retinoic acid (RA), the phorbol ester PMA, or the gamma-secretase inhibitor DAPT resulted in an electrophoretic mobility shift of Fe65. Tretinoin 96-98 amyloid beta precursor protein binding family B member 1 Homo sapiens 211-215
17207476-1 2007 Retinoic acid (RA) synthesized by Raldh3 in the frontonasal surface ectoderm of chick embryos has been suggested to function in early forebrain patterning by regulating Fgf8, Shh, and Meis2 expression. Tretinoin 0-13 fibroblast growth factor 8 Gallus gallus 169-173
27086067-4 2016 Retinoic acid, an active metabolite of vitamin A, activates both retinoic acid receptors (RAR) and retinoid X receptors (RXR), inducing epigenetic changes in key regulatory genes governing adipogenesis. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 99-119
27086067-4 2016 Retinoic acid, an active metabolite of vitamin A, activates both retinoic acid receptors (RAR) and retinoid X receptors (RXR), inducing epigenetic changes in key regulatory genes governing adipogenesis. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 121-124
17031849-3 2007 We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1. Tretinoin 78-82 X-box binding protein 1 Homo sapiens 222-226
27590114-5 2016 The benefit of atRA treatment was mediated by cytotoxic CD8(+) T cells, which were activated due to MHCI upregulation on tumor cells. Tretinoin 15-19 CD8a molecule Homo sapiens 56-59
27590114-6 2016 Consistent with these findings, increased colonic expression of the atRA-catabolizing enzyme, CYP26A1, correlated with reduced frequencies of tumoral cytotoxic CD8(+) T cells and with worse disease prognosis in human CRC. Tretinoin 68-72 CD8a molecule Homo sapiens 160-163
26598443-9 2016 By contrast, knockdown of TFAP2B by lentiviral transduction of shRNAs abrogated RA-induced neuronal differentiation of SH-SY5Y and SK-N-BE(2)c neuroblastoma cells almost completely. Tretinoin 80-82 transcription factor AP-2 beta Homo sapiens 26-32
26598443-10 2016 Taken together, our results suggest that TFAP2B is playing a vital role in retaining RA responsiveness and mediating noradrenergic neuronal differentiation in neuroblastoma. Tretinoin 85-87 transcription factor AP-2 beta Homo sapiens 41-47
17283129-4 2007 Interestingly, we found that miRNA expression levels substantially change in a MYCN-amplified cell line following exposure to retinoic acid, a compound which is well known for causing reductions in MYCN expression and for inducing neuroblastoma cell lines to undergo neuronal differentiation. Tretinoin 126-139 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 79-83
26712806-5 2016 After intranasal immunization with inactive cholera toxin (CT), LDCs stimulated retinoic acid-dependent up-regulation of alpha4beta7 and CCR9 gut-homing receptors on local IgA-expressing B cells. Tretinoin 80-93 chemokine (C-C motif) receptor 9 Mus musculus 137-141
27608010-8 2016 Silencing TSPO expression in gonocytes increased the stimulatory effect of RA on the expression of the differentiation marker Stra8, suggesting that TSPO exerts a repressive role on differentiation. Tretinoin 75-77 translocator protein Homo sapiens 10-14
17283129-4 2007 Interestingly, we found that miRNA expression levels substantially change in a MYCN-amplified cell line following exposure to retinoic acid, a compound which is well known for causing reductions in MYCN expression and for inducing neuroblastoma cell lines to undergo neuronal differentiation. Tretinoin 126-139 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 198-202
27608010-8 2016 Silencing TSPO expression in gonocytes increased the stimulatory effect of RA on the expression of the differentiation marker Stra8, suggesting that TSPO exerts a repressive role on differentiation. Tretinoin 75-77 stimulated by retinoic acid 8 Homo sapiens 126-131
27608010-8 2016 Silencing TSPO expression in gonocytes increased the stimulatory effect of RA on the expression of the differentiation marker Stra8, suggesting that TSPO exerts a repressive role on differentiation. Tretinoin 75-77 translocator protein Homo sapiens 149-153
16955405-0 2007 Regulation of expression of the retinoic acid metabolizing enzyme CYP26A1 in uteri of ovariectomized mice after treatment with ovarian steroid hormones. Tretinoin 32-45 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 66-73
27357360-7 2016 After RA treatment, NLRR2 expression was increased and correlated with the upregulation of c-Jun, a member of the activator protein-1 (AP-1) family in NB cells. Tretinoin 6-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96
26728137-0 2016 All-trans retinoic acid synergizes with topotecan to suppress AML cells via promoting RARalpha-mediated DNA damage. Tretinoin 10-23 retinoic acid receptor, alpha Mus musculus 86-94
16955405-3 2007 In this study, we determined the influence of progesterone and 17-ss-estradiol on the uterine expression of the RA-metabolizing enzyme CYP26A1 after specific time intervals (1, 4, 24, and 48 hr after treatment of ovariectomized mice). Tretinoin 112-114 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 135-142
26548461-12 2016 The mRNA expression of mesenchymal markers N-cadherin, vimentin, snail and twist decreased, while expression of epithelial marker E-cadherin increased in hepa1-6 cells after treated with ATRA. Tretinoin 187-191 cadherin 2 Mus musculus 43-53
27357360-7 2016 After RA treatment, NLRR2 expression was increased and correlated with the upregulation of c-Jun, a member of the activator protein-1 (AP-1) family in NB cells. Tretinoin 6-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-133
27357360-7 2016 After RA treatment, NLRR2 expression was increased and correlated with the upregulation of c-Jun, a member of the activator protein-1 (AP-1) family in NB cells. Tretinoin 6-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 135-139
27236299-8 2016 When mice CD4(+)CD45 RA(+) T cells were co-cultured with PF-treated DCs stimulated with/without DNCB, the gene expression of the Th17 cell markers such as retinoic acid-related orphan nuclear hormone receptor gammat (RORgammat), IL-17A, and IL-23R decreased, in accordance with the less secretions of IL-17 and IL-23 in vitro and in vivo. Tretinoin 155-168 CD4 antigen Mus musculus 10-13
26548461-12 2016 The mRNA expression of mesenchymal markers N-cadherin, vimentin, snail and twist decreased, while expression of epithelial marker E-cadherin increased in hepa1-6 cells after treated with ATRA. Tretinoin 187-191 vimentin Mus musculus 55-63
26548461-12 2016 The mRNA expression of mesenchymal markers N-cadherin, vimentin, snail and twist decreased, while expression of epithelial marker E-cadherin increased in hepa1-6 cells after treated with ATRA. Tretinoin 187-191 snail family zinc finger 1 Mus musculus 65-70
16955405-9 2007 These data indicate an additional level of hormonal control of endogenous RA levels in the mouse uterus, where its synthesis would rely on estrogen-dependent expression of RALDH enzymes, whereas its active metabolism would be triggered by progesterone-induced CYP26A1 expression. Tretinoin 74-76 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 260-267
17234757-6 2007 In the embryonal carcinoma cell line NT2/D1, ectopic DeltaN-p63-alpha disrupts retinoic acid-induced differentiation, thereby preserving expression of nestin; however, small interfering RNA-mediated ablation of nestin is insufficient to promote differentiation, indicating that whereas nestin may identify cells within the regenerative compartment of the mammary gland, it is insufficient to block differentiation and preserve replicative capacity. Tretinoin 79-92 tumor protein p63 Homo sapiens 60-63
26400044-8 2016 To test the significance of phosphorylation of these proteins further, we administered all-trans-retinoic acid (ATRA) to the 3xTg mice, which downregulates Cdk5 and GSK3beta activity. Tretinoin 87-110 cyclin-dependent kinase 5 Mus musculus 156-160
26400044-8 2016 To test the significance of phosphorylation of these proteins further, we administered all-trans-retinoic acid (ATRA) to the 3xTg mice, which downregulates Cdk5 and GSK3beta activity. Tretinoin 112-116 cyclin-dependent kinase 5 Mus musculus 156-160
27402843-2 2016 In mammalian tissues, beta-carotene 15,15"-oxygenase (BCO1) converts beta-carotene to retinaldehyde, which is then oxidized to retinoic acid, the biologically active form of vitamin A that acts as a transcription factor ligand to regulate gene expression. Tretinoin 127-140 beta-carotene oxygenase 1 Homo sapiens 54-58
17202324-8 2007 Conversely, retinoic acid produced by the intestinal dendritic cells may suppress NKG2A expression. Tretinoin 12-25 killer cell lectin like receptor C1 Homo sapiens 82-87
27830500-5 2016 Intracellular retinoic acid binding-proteins (CRABP1 and 2, and FABP5) seem to have more diverse functions distinctive to each, such as directing retinoic acid to catabolism, delivering retinoic acid to specific nuclear receptors, and generating non-canonical actions. Tretinoin 14-27 fatty acid binding protein 5 Homo sapiens 64-69
27830500-5 2016 Intracellular retinoic acid binding-proteins (CRABP1 and 2, and FABP5) seem to have more diverse functions distinctive to each, such as directing retinoic acid to catabolism, delivering retinoic acid to specific nuclear receptors, and generating non-canonical actions. Tretinoin 146-159 fatty acid binding protein 5 Homo sapiens 64-69
27830500-5 2016 Intracellular retinoic acid binding-proteins (CRABP1 and 2, and FABP5) seem to have more diverse functions distinctive to each, such as directing retinoic acid to catabolism, delivering retinoic acid to specific nuclear receptors, and generating non-canonical actions. Tretinoin 146-159 fatty acid binding protein 5 Homo sapiens 64-69
27830505-2 2016 More recent observations have established that RA also activates an additional nuclear receptor, PPARbeta/delta. Tretinoin 47-49 peroxisome proliferator activated receptor delta Homo sapiens 97-105
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 peroxisome proliferator activated receptor delta Homo sapiens 33-41
27559173-9 2016 Functionally, Cyp1b1 generated retinoic acid as well as 20-hydroxyeicosatetraenoic acid that regulated P-glycoprotein and junction proteins, respectively, thereby modulating BBB properties. Tretinoin 31-44 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 14-20
17107666-6 2007 Our results demonstrated that ATRA suppressed NF-kappaB activity and prevented IkappaBalpha degradation in a dose-dependent way, inhibited IFN-gamma production and gene expression of granzyme B and NKp46. Tretinoin 30-34 granzyme B Homo sapiens 183-193
29541688-5 2016 Our results demonstrated that atRA enhanced progesterone production by upregulating the levels of steroidogenic acute regulatory protein (StAR) and cytochrome P450scc (Cyp11a1) mRNAs, but not 3beta-hydroxysteroid dehydrogenase mRNA in immature rat GCs. Tretinoin 30-34 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 148-166
29541688-5 2016 Our results demonstrated that atRA enhanced progesterone production by upregulating the levels of steroidogenic acute regulatory protein (StAR) and cytochrome P450scc (Cyp11a1) mRNAs, but not 3beta-hydroxysteroid dehydrogenase mRNA in immature rat GCs. Tretinoin 30-34 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 168-175
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 cellular retinoic acid binding protein 2 Homo sapiens 111-140
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 cellular retinoic acid binding protein 2 Homo sapiens 142-148
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 fatty acid binding protein 5 Homo sapiens 212-217
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 13-15 peroxisome proliferator activated receptor delta Homo sapiens 268-276
27505250-7 2016 Next, we examined effects of 10 different agents on the expression of CD44 transcripts in cultured human keratinocytes, and found that several agents, particularly epidermal growth factor, hydrogen peroxide, phorbol 12-myristate 13-acetate, retinoic acid, calcium and fetal calf serum differently regulated their expressions in various patterns. Tretinoin 241-254 CD44 molecule (Indian blood group) Homo sapiens 70-74
17204142-15 2007 Pre-incubation of SH-SY5Y human neuroblastoma cells with either RAR-pan-antagonist LE540 or MAP kinase kinase 1 (MEK-1) inhibitor PD98059 resulted in the abolition of ATRA-induced COX-2 promoter activity, COX-2 protein expression and PGE2 production whereas the retinoid X receptor pan-antagonist HX531, the p38 MAPK inhibitor SB203580 or the c-Jun kinase inhibitor SP600125 did not have any effect. Tretinoin 167-171 retinoic acid receptor alpha Homo sapiens 64-67
27185863-0 2016 Retinoic-acid-mediated HRas stabilization induces neuronal differentiation of neural stem cells during brain development. Tretinoin 0-13 Harvey rat sarcoma virus oncogene Mus musculus 23-27
27185863-5 2016 Retinoic acid, an active metabolite of vitamin A, promoted neuronal differentiation of NSCs by stabilizing HRas, and HRas knockdown blocked the retinoic acid effect. Tretinoin 0-13 Harvey rat sarcoma virus oncogene Mus musculus 107-111
27185863-5 2016 Retinoic acid, an active metabolite of vitamin A, promoted neuronal differentiation of NSCs by stabilizing HRas, and HRas knockdown blocked the retinoic acid effect. Tretinoin 144-157 Harvey rat sarcoma virus oncogene Mus musculus 117-121
27185863-7 2016 All of these abnormal phenotypes were rescued with the restoration of HRas protein levels achieved upon feeding with a retinoic-acid-supplemented diet. Tretinoin 119-132 Harvey rat sarcoma virus oncogene Mus musculus 70-74
27185863-8 2016 In summary, this study shows that retinoic acid stabilizes HRas protein during neurogenesis, and that this is required for NSC differentiation into neurons and murine brain development. Tretinoin 34-47 Harvey rat sarcoma virus oncogene Mus musculus 59-63
26504088-1 2015 The biological actions of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are mediated by the vitamin D receptor (VDR), whose expression in bone cells is regulated positively by 1,25(OH)2D3, retinoic acid, and parathyroid hormone through both intergenic and intronic enhancers. Tretinoin 182-195 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 85-103
26504088-1 2015 The biological actions of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) are mediated by the vitamin D receptor (VDR), whose expression in bone cells is regulated positively by 1,25(OH)2D3, retinoic acid, and parathyroid hormone through both intergenic and intronic enhancers. Tretinoin 182-195 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 105-108
17204142-15 2007 Pre-incubation of SH-SY5Y human neuroblastoma cells with either RAR-pan-antagonist LE540 or MAP kinase kinase 1 (MEK-1) inhibitor PD98059 resulted in the abolition of ATRA-induced COX-2 promoter activity, COX-2 protein expression and PGE2 production whereas the retinoid X receptor pan-antagonist HX531, the p38 MAPK inhibitor SB203580 or the c-Jun kinase inhibitor SP600125 did not have any effect. Tretinoin 167-171 mitogen-activated protein kinase kinase 1 Homo sapiens 92-111
26634247-7 2015 Moreover, an ALDH1A2(high)CRABP2(high) staining pattern served as an independent predictor for progression-free (HR: 0.395, p = 0.007) and overall survival (HR: 0.303, p = 0.002), suggesting a critical impact of RA metabolism and signaling on clinical outcome. Tretinoin 27-29 aldehyde dehydrogenase 1 family member A2 Homo sapiens 13-20
26634247-8 2015 Functionally, ALDH1A2 expression and activity in tumor cell lines were related to RA levels. Tretinoin 82-84 aldehyde dehydrogenase 1 family member A2 Homo sapiens 14-21
27282572-4 2016 Adding carbachol which is a cholinergic agonist to the ATRA treatment resulted in an increase of a granulocytic differentiation marker (CD11b) as compared with ATRA treatment alone (p<0.05), indicating that cholinergic activation enhanced ATRA in inducing NB-4 maturation. Tretinoin 55-59 integrin subunit alpha M Homo sapiens 136-141
17204142-15 2007 Pre-incubation of SH-SY5Y human neuroblastoma cells with either RAR-pan-antagonist LE540 or MAP kinase kinase 1 (MEK-1) inhibitor PD98059 resulted in the abolition of ATRA-induced COX-2 promoter activity, COX-2 protein expression and PGE2 production whereas the retinoid X receptor pan-antagonist HX531, the p38 MAPK inhibitor SB203580 or the c-Jun kinase inhibitor SP600125 did not have any effect. Tretinoin 167-171 mitogen-activated protein kinase kinase 1 Homo sapiens 113-118
17204142-17 2007 CONCLUSION: These results highlight the importance of RAR-dependent and kinase-dependent mechanisms for ATRA-induced COX-2 expression and activity. Tretinoin 104-108 retinoic acid receptor alpha Homo sapiens 54-57
17976305-3 2007 Recently, we have shown that LIF potentiated retinoic acid-induced neural differentiation of pluripotent mouse embryonal carcinoma P19 cells. Tretinoin 45-58 leukemia inhibitory factor Mus musculus 29-32
26374207-8 2016 The expression of CYP26A1 and CYP26B1 was also investigated in the adult human brain and colocalization of CYP26A1 and the RA synthetic enzyme RALDH2 indicated a different, autocrine role for RA in human hippocampal neurons. Tretinoin 123-125 aldehyde dehydrogenase 1 family member A2 Homo sapiens 143-149
27540526-0 2016 Differential Incorporation of beta-actin as A Component of RNA Polymerase II into Regulatory Regions of Stemness/Differentiation Genes in Retinoic Acid-Induced Differentiated Human Embryonic Carcinoma Cells. Tretinoin 138-151 POTE ankyrin domain family member F Homo sapiens 30-40
25923039-4 2015 We studied RA signaling and its relation to IL-15 in the lung during cigarette smoke (CS) exposure and influenza virus infection. Tretinoin 11-13 interleukin 15 Mus musculus 44-49
17976305-4 2007 Here we demonstrate that pro-neural effects of LIF and partially also of retinoic acid are abolished by inhibition of the JAK2->STAT3 signalling pathway. Tretinoin 73-86 Janus kinase 2 Mus musculus 122-126
26416905-6 2015 Effectively, after Encephalitozoon cuniculi infection, CD11b(-) CD8(+) DC were activated in the lamina propria (LP) and acquired the ability to process retinoic acid (RA). Tretinoin 152-165 integrin subunit alpha M Homo sapiens 55-60
17976305-6 2007 These results suggest that in neurogenic regions, cooperative action of LIF and other neuro-differentiation-inducing factors, such as retinoic acid, may be mediated by the STAT3 signalling pathway. Tretinoin 134-147 leukemia inhibitory factor Mus musculus 72-75
26416905-6 2015 Effectively, after Encephalitozoon cuniculi infection, CD11b(-) CD8(+) DC were activated in the lamina propria (LP) and acquired the ability to process retinoic acid (RA). Tretinoin 152-165 CD8a molecule Homo sapiens 64-67
27294875-5 2016 Retinoic acid (RA)-inducible gene I (RIG-I, encoded by DDX58) forms one class of PRRs that mediates apoptosis and the elimination of infected cells after recognition of viral RNA. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 37-42
17468032-2 2007 The ability of retinoic acid (RA) and arsenic trioxide to directly target the oncogenic promyelocytic leukemia-retinoic receptor A (PML-RARA) fusion protein also made this disease the first model for oncogene-targeted therapies. Tretinoin 15-28 PML nuclear body scaffold Homo sapiens 132-135
27294875-5 2016 Retinoic acid (RA)-inducible gene I (RIG-I, encoded by DDX58) forms one class of PRRs that mediates apoptosis and the elimination of infected cells after recognition of viral RNA. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 55-60
27294875-5 2016 Retinoic acid (RA)-inducible gene I (RIG-I, encoded by DDX58) forms one class of PRRs that mediates apoptosis and the elimination of infected cells after recognition of viral RNA. Tretinoin 15-17 DExD/H-box helicase 58 Homo sapiens 37-42
27294875-5 2016 Retinoic acid (RA)-inducible gene I (RIG-I, encoded by DDX58) forms one class of PRRs that mediates apoptosis and the elimination of infected cells after recognition of viral RNA. Tretinoin 15-17 DExD/H-box helicase 58 Homo sapiens 55-60
26476360-5 2015 Additionally, expression of BAX and SHC1 were lower in both non-encapsulated tretinoin (TTN) and TTN-LNC-treated groups. Tretinoin 77-86 SHC adaptor protein 1 Bos taurus 36-40
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 14-16 CD4 antigen Mus musculus 43-46
25899567-6 2015 Functionally, RA increased DC induction of CD4(+) T-cell IL-10, while reducing CD4(+) T-cell IL-4 and IL-13, revealing a previously unidentified role for RA in regulating the ability of alternatively activated DCs to influence Th2 polarization. Tretinoin 14-16 CD4 antigen Mus musculus 79-82
27199456-0 2016 Retinoic acid and sodium butyrate suppress the cardiac expression of hypertrophic markers and proinflammatory mediators in Npr1 gene-disrupted haplotype mice. Tretinoin 0-13 natriuretic peptide receptor 1 Mus musculus 123-127
27334688-8 2016 Induction of neural differentiation with retinoic acid resulted in downregulation of Sox2 and VRK1 that inversely correlated with the expression of differentiation markers such as N-cadherin, Pax6, mH2A1.2 and mH2A2. Tretinoin 41-54 cadherin 2 Homo sapiens 180-190
27334688-8 2016 Induction of neural differentiation with retinoic acid resulted in downregulation of Sox2 and VRK1 that inversely correlated with the expression of differentiation markers such as N-cadherin, Pax6, mH2A1.2 and mH2A2. Tretinoin 41-54 H2A clustered histone 4 Mus musculus 198-203
17468032-2 2007 The ability of retinoic acid (RA) and arsenic trioxide to directly target the oncogenic promyelocytic leukemia-retinoic receptor A (PML-RARA) fusion protein also made this disease the first model for oncogene-targeted therapies. Tretinoin 15-28 retinoic acid receptor alpha Homo sapiens 136-140
26517695-7 2015 Consistent with the ability of retinoic acid to foster inducible Tregs, miR-33-depleted macrophages had an enhanced capacity to induce forkhead box P3 (FOXP3) expression in naive CD4(+) T cells. Tretinoin 31-44 microRNA 33 Mus musculus 72-78
17468032-2 2007 The ability of retinoic acid (RA) and arsenic trioxide to directly target the oncogenic promyelocytic leukemia-retinoic receptor A (PML-RARA) fusion protein also made this disease the first model for oncogene-targeted therapies. Tretinoin 30-32 PML nuclear body scaffold Homo sapiens 132-135
26893190-6 2016 Treatment of malignant glioma cell lines with RA results in a dose-dependent increase in accumulation of CRABP2 in the cytoplasm. Tretinoin 46-48 cellular retinoic acid binding protein 2 Homo sapiens 105-111
17468032-2 2007 The ability of retinoic acid (RA) and arsenic trioxide to directly target the oncogenic promyelocytic leukemia-retinoic receptor A (PML-RARA) fusion protein also made this disease the first model for oncogene-targeted therapies. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 136-140
26893190-10 2016 Our combined in vivo and in vitro data indicate that: (i) CRABP2 is an important determinant of clinical outcome in GBM patients, and (ii) the mechanism of action of CRABP2 in GBM involves sequestration of RA in the cytoplasm and activation of an anti-apoptotic pathway, thereby enhancing proliferation and preventing RA-mediated cell death and differentiation. Tretinoin 59-61 cellular retinoic acid binding protein 2 Homo sapiens 166-172
17616924-1 2007 We have investigated the function of the retinoic acid metabolising enzyme, CYP26B1, by administering an antisense morpholino oligonucleotide to zebrafish embryos. Tretinoin 41-54 cytochrome P450, family 26, subfamily b, polypeptide 1 Danio rerio 76-83
26464515-9 2015 Furthermore, differentiation of the neuroblastoma cell line SH-SY5Y induced by all-trans retinoic acid (ATRA) increased both TXNRD1_v1 and TXNRD1_v2 expressions along with several of the identified genes associated with differentiation and adhesion. Tretinoin 89-102 thioredoxin reductase 1 Homo sapiens 125-131
26464515-9 2015 Furthermore, differentiation of the neuroblastoma cell line SH-SY5Y induced by all-trans retinoic acid (ATRA) increased both TXNRD1_v1 and TXNRD1_v2 expressions along with several of the identified genes associated with differentiation and adhesion. Tretinoin 89-102 thioredoxin reductase 1 Homo sapiens 139-145
26464515-9 2015 Furthermore, differentiation of the neuroblastoma cell line SH-SY5Y induced by all-trans retinoic acid (ATRA) increased both TXNRD1_v1 and TXNRD1_v2 expressions along with several of the identified genes associated with differentiation and adhesion. Tretinoin 104-108 thioredoxin reductase 1 Homo sapiens 125-131
26464515-9 2015 Furthermore, differentiation of the neuroblastoma cell line SH-SY5Y induced by all-trans retinoic acid (ATRA) increased both TXNRD1_v1 and TXNRD1_v2 expressions along with several of the identified genes associated with differentiation and adhesion. Tretinoin 104-108 thioredoxin reductase 1 Homo sapiens 139-145
26873005-0 2016 Erratum to: Phospholipase C-eta2 interacts with nuclear and cytoplasmic LIMK-1 during retinoic acid-stimulated neurite growth. Tretinoin 86-99 phospholipase C eta 2 Homo sapiens 12-32
17182884-6 2007 RARalpha antagonists blocked atRA-induced cAMP production and its antiproliferative and prodifferentiation effects on podocytes, suggesting that RARalpha is required. Tretinoin 29-33 retinoic acid receptor alpha Homo sapiens 0-8
26768478-4 2016 Bone marrow-derived macrophages do not express the diethylaminobenzaldehyde-sensitive enzymes Aldh1a1, Aldh1a2, or Aldh1a3 but instead, express Aldh3b1, which we found is capable of diethylaminobenzaldehyde-insensitive synthesis of all trans-retinoic acid. Tretinoin 236-255 aldehyde dehydrogenase 3 family, member B1 Mus musculus 144-151
26414475-4 2015 It is important to identify these cryptic and variant translocations because certain variants, including ZBTB16/RARA and STAT5B/RARA, are resistant to treatment with all-trans retinoic acid, arsenic trioxide, and anthracyclines. Tretinoin 176-189 zinc finger and BTB domain containing 16 Homo sapiens 105-111
17182884-6 2007 RARalpha antagonists blocked atRA-induced cAMP production and its antiproliferative and prodifferentiation effects on podocytes, suggesting that RARalpha is required. Tretinoin 29-33 retinoic acid receptor alpha Homo sapiens 145-153
26208884-5 2015 Most interestingly, TLR ligation in the presence of recombinant IL-10 (rIL-10) or retinoic acid (RA) led to ERK1/2 activation independent of MEK1 in BMDMs derived from Mek1(d/d)Sox2(Cre) mice and led to inhibition of STAT4 and decreased IL-12 levels. Tretinoin 82-95 SRY (sex determining region Y)-box 2 Mus musculus 177-181
26208884-5 2015 Most interestingly, TLR ligation in the presence of recombinant IL-10 (rIL-10) or retinoic acid (RA) led to ERK1/2 activation independent of MEK1 in BMDMs derived from Mek1(d/d)Sox2(Cre) mice and led to inhibition of STAT4 and decreased IL-12 levels. Tretinoin 82-95 signal transducer and activator of transcription 4 Mus musculus 217-222
17182884-12 2007 These findings suggest that atRA reverses the abnormal phenotype in HIV-1-infected podocytes by stimulating RARalpha-mediated intracellular cAMP production. Tretinoin 28-32 retinoic acid receptor alpha Homo sapiens 108-116
17516864-1 2007 Retinol inhibits the growth of all-trans-retinoic acid (ATRA)-resistant human colon cancer cell lines through a retinoic acid receptor (RAR)-independent mechanism. Tretinoin 31-54 retinoic acid receptor alpha Homo sapiens 112-134
25864619-5 2015 Interestingly, CD4(+)Foxp3(+) regulatory T cells were markedly increased in the spleens of atRA-treated mice. Tretinoin 91-95 CD4 antigen Mus musculus 15-18
27001866-0 2016 Kinetic characterization and regulation of the human retinaldehyde dehydrogenase 2 enzyme during production of retinoic acid. Tretinoin 111-124 aldehyde dehydrogenase 1 family member A2 Homo sapiens 53-82
27001866-4 2016 The main enzyme producing RA in the early embryo is retinaldehyde dehydrogenase 2 (RALDH2, ALDH1A2). Tretinoin 26-28 aldehyde dehydrogenase 1 family member A2 Homo sapiens 52-81
27001866-4 2016 The main enzyme producing RA in the early embryo is retinaldehyde dehydrogenase 2 (RALDH2, ALDH1A2). Tretinoin 26-28 aldehyde dehydrogenase 1 family member A2 Homo sapiens 83-89
27001866-4 2016 The main enzyme producing RA in the early embryo is retinaldehyde dehydrogenase 2 (RALDH2, ALDH1A2). Tretinoin 26-28 aldehyde dehydrogenase 1 family member A2 Homo sapiens 91-98
27001866-10 2016 In addition, RA was studied as a possible inhibitor of hRALDH2 and a regulator of its activity. Tretinoin 13-15 aldehyde dehydrogenase 1 family member A2 Homo sapiens 55-62
26935255-4 2016 Detailed in-vitro and in-vivo investigations on the antitumor effects of ATRA via Cx32 mediation were performed, and the possible underlying mechanisms of action of the compound were then examined. Tretinoin 73-77 gap junction protein beta 1 Homo sapiens 82-86
26935255-7 2016 The protein expression levels of Cx32 in ATRA-untreated or ATRA-treated tissues were quantified by immunohistochemical analysis and Western blot assays. Tretinoin 41-45 gap junction protein beta 1 Homo sapiens 33-37
26367011-8 2015 Further, in silico knockouts of genes and reactions in the vitamin A pathway predict that deletion of Lipe, hormone-sensitive lipase, disrupts the RA pulse thereby causing spermatogenic defects. Tretinoin 147-149 lipase, hormone sensitive Mus musculus 102-106
26367011-8 2015 Further, in silico knockouts of genes and reactions in the vitamin A pathway predict that deletion of Lipe, hormone-sensitive lipase, disrupts the RA pulse thereby causing spermatogenic defects. Tretinoin 147-149 lipase, hormone sensitive Mus musculus 108-132
26935255-7 2016 The protein expression levels of Cx32 in ATRA-untreated or ATRA-treated tissues were quantified by immunohistochemical analysis and Western blot assays. Tretinoin 59-63 gap junction protein beta 1 Homo sapiens 33-37
17516864-1 2007 Retinol inhibits the growth of all-trans-retinoic acid (ATRA)-resistant human colon cancer cell lines through a retinoic acid receptor (RAR)-independent mechanism. Tretinoin 31-54 retinoic acid receptor alpha Homo sapiens 136-139
26935255-10 2016 ATRA significantly increased the expression of Cx32 in the hepatoma tissues (P<0.01). Tretinoin 0-4 gap junction protein beta 1 Homo sapiens 47-51
26368825-8 2015 Thus, RA activity in the neural plate is sufficient to prevent anterior expansion of caudal Fgf8 expression associated with a small somite defect. Tretinoin 6-8 fibroblast growth factor 8 Mus musculus 92-96
17516864-1 2007 Retinol inhibits the growth of all-trans-retinoic acid (ATRA)-resistant human colon cancer cell lines through a retinoic acid receptor (RAR)-independent mechanism. Tretinoin 56-60 retinoic acid receptor alpha Homo sapiens 112-134
27081671-8 2016 Overexpression of StAR in mouse RAW 264.7 macrophages increased the effects of both all-trans retinoic acid (atRA) and 9-cis RA on cholesterol efflux, suggesting StAR enhances the efficacy of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) ligands. Tretinoin 94-107 retinoic acid receptor, alpha Mus musculus 192-214
27081671-8 2016 Overexpression of StAR in mouse RAW 264.7 macrophages increased the effects of both all-trans retinoic acid (atRA) and 9-cis RA on cholesterol efflux, suggesting StAR enhances the efficacy of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) ligands. Tretinoin 94-107 retinoic acid receptor, alpha Mus musculus 216-219
17516864-1 2007 Retinol inhibits the growth of all-trans-retinoic acid (ATRA)-resistant human colon cancer cell lines through a retinoic acid receptor (RAR)-independent mechanism. Tretinoin 56-60 retinoic acid receptor alpha Homo sapiens 136-139
27081671-8 2016 Overexpression of StAR in mouse RAW 264.7 macrophages increased the effects of both all-trans retinoic acid (atRA) and 9-cis RA on cholesterol efflux, suggesting StAR enhances the efficacy of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) ligands. Tretinoin 109-113 retinoic acid receptor, alpha Mus musculus 192-214
27081671-8 2016 Overexpression of StAR in mouse RAW 264.7 macrophages increased the effects of both all-trans retinoic acid (atRA) and 9-cis RA on cholesterol efflux, suggesting StAR enhances the efficacy of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR) ligands. Tretinoin 109-113 retinoic acid receptor, alpha Mus musculus 216-219
26352270-6 2015 Conserved Retinoic Acid Response Elements (RAREs) upstream of human ALDH1A3 and FOXN1 and in mouse Aldh1a3 and Foxn1 genes were revealed using bioinformatic approximation. Tretinoin 10-23 forkhead box N1 Mus musculus 111-116
18274629-3 2007 Using these criteria, it was recently demonstrated that all-trans-retinoic acid (RA), the activator of the classical retinoic acid receptor RAR, also serves as a ligand for PPARbeta/delta. Tretinoin 56-79 retinoic acid receptor alpha Homo sapiens 140-143
25986473-6 2015 We found that autophagy is increased during all-trans-retinoic acid (ATRA)-induced granulocytic differentiation of the APL cell line NB4 and that this is associated with increased expression of LC3II and GATE-16 proteins involved in autophagosome formation. Tretinoin 44-67 GABA type A receptor associated protein like 2 Homo sapiens 204-211
25986473-6 2015 We found that autophagy is increased during all-trans-retinoic acid (ATRA)-induced granulocytic differentiation of the APL cell line NB4 and that this is associated with increased expression of LC3II and GATE-16 proteins involved in autophagosome formation. Tretinoin 69-73 GABA type A receptor associated protein like 2 Homo sapiens 204-211
26902400-0 2016 PHOX2A and PHOX2B are differentially regulated during retinoic acid-driven differentiation of SK-N-BE(2)C neuroblastoma cell line. Tretinoin 54-67 paired like homeobox 2B Homo sapiens 11-17
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 57-70 paired like homeobox 2B Homo sapiens 185-191
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 57-70 paired like homeobox 2B Homo sapiens 287-293
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 72-76 paired like homeobox 2B Homo sapiens 185-191
26902400-2 2016 We used the SK-N-BE(2)C cell line to show that all-trans retinoic acid (ATRA), a drug that is widely used to inhibit growth and induce differentiation in NBs, regulates both PHOX2A and PHOX2B expression, albeit by means of different mechanisms: it up-regulates PHOX2A and down-regulates PHOX2B. Tretinoin 72-76 paired like homeobox 2B Homo sapiens 287-293
18274629-3 2007 Using these criteria, it was recently demonstrated that all-trans-retinoic acid (RA), the activator of the classical retinoic acid receptor RAR, also serves as a ligand for PPARbeta/delta. Tretinoin 81-83 retinoic acid receptor alpha Homo sapiens 140-143
26201974-9 2015 Moreover, treatment with 9-cis-RA significantly increased the protein expression levels of ABCA1 and ABCG1 in J774A.1 macrophages in a dose-dependent manner. Tretinoin 30-33 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 91-96
26009309-0 2016 Elevated expression of the retinoic acid-metabolizing enzyme CYP26C1 in primary breast carcinomas. Tretinoin 27-40 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 61-68
26009309-9 2016 Based on the RA-catabolizing activity of CYP26C1, our data suggest that CYP26C1 expression may contribute to neoplasia in the breast. Tretinoin 13-15 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 41-48
26009309-9 2016 Based on the RA-catabolizing activity of CYP26C1, our data suggest that CYP26C1 expression may contribute to neoplasia in the breast. Tretinoin 13-15 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 72-79
26287494-3 2015 FICZ enhances RA-induced differentiation, assessed by expression of the membrane differentiation markers CD38 and CD11b, cell cycle arrest and the functional differentiation marker, inducible oxidative metabolism. Tretinoin 14-16 integrin subunit alpha M Homo sapiens 114-119
18274629-4 2007 Partitioning of RA between its two receptors was found to be regulated by FABP5, which delivers it to PPARbeta/delta, and cellular RA binding protein II (CRABP-II), which targets it to RAR. Tretinoin 16-18 retinoic acid receptor alpha Homo sapiens 185-188
26349992-0 2015 Low-dose all-trans retinoic acid enhances cytotoxicity of cisplatin and 5-fluorouracil on CD44(+) cancer stem cells. Tretinoin 19-32 CD44 molecule (Indian blood group) Homo sapiens 90-94
17166369-10 2006 CONCLUSIONS: ATRA and 1,25(OH)2D3 could inhibit growth and induce apoptosis of HepG2 cells, and the molecular basis of the cell cycle blockade by 1,25(OH)2D3 may be associated with the up-regulation of CDK inhibitors p21(WAF/CIP1) and p27(KIP1), which mediate G1 arrest. Tretinoin 13-17 cyclin dependent kinase inhibitor 1B Homo sapiens 239-243
26349992-6 2015 We allowed the CD44(+-) cells to grow 6 days at a subtoxic concentration of ATRA and then treated with different concentration of CDDP and 5-FU for 24h. Tretinoin 76-80 CD44 molecule (Indian blood group) Homo sapiens 15-19
27113312-6 2016 As the ATRA concentration enhanced and action time prolonged, the survival rate of RPE cells was reduced, but the expressions of HGF and MMP-2 increased, so did the secretion of HGF. Tretinoin 7-11 hepatocyte growth factor Oryctolagus cuniculus 129-132
27113312-6 2016 As the ATRA concentration enhanced and action time prolonged, the survival rate of RPE cells was reduced, but the expressions of HGF and MMP-2 increased, so did the secretion of HGF. Tretinoin 7-11 hepatocyte growth factor Oryctolagus cuniculus 178-181
26839961-2 2016 Cellular retinoic acid binding protein 2 (CRABP2) is a member of the retinoic acid (RA) and lipocalin/cytosolic fatty-acid binding protein family and plays a completely contrary role in tumorigenesis through the retinoid signaling pathway, depending on the nuclear RA receptors (RAR) and PPARbeta/delta receptors. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 42-48
25991604-0 2015 Loss of MT1-MMP causes cell senescence and nuclear defects which can be reversed by retinoic acid. Tretinoin 84-97 matrix metallopeptidase 14 (membrane-inserted) Mus musculus 8-15
26839961-2 2016 Cellular retinoic acid binding protein 2 (CRABP2) is a member of the retinoic acid (RA) and lipocalin/cytosolic fatty-acid binding protein family and plays a completely contrary role in tumorigenesis through the retinoid signaling pathway, depending on the nuclear RA receptors (RAR) and PPARbeta/delta receptors. Tretinoin 9-22 peroxisome proliferator activated receptor delta Homo sapiens 288-296
16963447-1 2006 We cloned a novel mouse cDNA, Mcpr1 (mouse cleft palate-related gene 1), between retinoic acid (RA)-treated murine embryonic palatal and control shelves by improved subtractive hybridization. Tretinoin 81-94 cDNA sequence AY074887 Mus musculus 30-35
26839961-2 2016 Cellular retinoic acid binding protein 2 (CRABP2) is a member of the retinoic acid (RA) and lipocalin/cytosolic fatty-acid binding protein family and plays a completely contrary role in tumorigenesis through the retinoid signaling pathway, depending on the nuclear RA receptors (RAR) and PPARbeta/delta receptors. Tretinoin 43-45 cellular retinoic acid binding protein 2 Homo sapiens 0-40
26839961-2 2016 Cellular retinoic acid binding protein 2 (CRABP2) is a member of the retinoic acid (RA) and lipocalin/cytosolic fatty-acid binding protein family and plays a completely contrary role in tumorigenesis through the retinoid signaling pathway, depending on the nuclear RA receptors (RAR) and PPARbeta/delta receptors. Tretinoin 43-45 peroxisome proliferator activated receptor delta Homo sapiens 288-296
26671787-0 2016 Phospholipase C-eta2 interacts with nuclear and cytoplasmic LIMK-1 during retinoic acid-stimulated neurite growth. Tretinoin 74-87 phospholipase C, eta 2 Mus musculus 0-20
26671787-0 2016 Phospholipase C-eta2 interacts with nuclear and cytoplasmic LIMK-1 during retinoic acid-stimulated neurite growth. Tretinoin 74-87 LIM-domain containing, protein kinase Mus musculus 60-66
25991604-5 2015 Consistent with the role of retinoic acid signaling in nuclear lamina stabilization, treatment of Mmp14(-/-) mice with all-trans retinoic acid reversed the nuclear lamina alterations, partially rescued the cell senescence phenotypes, ameliorated the pathological defects in bone, skin, and heart, and extended their life span. Tretinoin 28-41 matrix metallopeptidase 14 (membrane-inserted) Mus musculus 98-103
25991604-5 2015 Consistent with the role of retinoic acid signaling in nuclear lamina stabilization, treatment of Mmp14(-/-) mice with all-trans retinoic acid reversed the nuclear lamina alterations, partially rescued the cell senescence phenotypes, ameliorated the pathological defects in bone, skin, and heart, and extended their life span. Tretinoin 129-142 matrix metallopeptidase 14 (membrane-inserted) Mus musculus 98-103
26020124-5 2015 Pretreatment with differentiating agent all-trans retinoic acid counteracts cisplatin resistance specifically of the slowly dividing compartment indicating effect on CD133+/CXCR4+ cells. Tretinoin 44-63 C-X-C motif chemokine receptor 4 Homo sapiens 173-178
26671787-2 2016 Here we investigate the function of PLCeta2 in neuritogenesis using Neuro2A cells, which upon stimulation with retinoic acid differentiate and form neurites. Tretinoin 111-124 phospholipase C, eta 2 Mus musculus 36-43
26671787-5 2016 Retinoic acid-induced neuritogenesis was highly dependent on PLCeta2 activity, with the H460Q mutant exhibiting a strong dominant-negative effect. Tretinoin 0-13 phospholipase C, eta 2 Mus musculus 61-68
16963447-1 2006 We cloned a novel mouse cDNA, Mcpr1 (mouse cleft palate-related gene 1), between retinoic acid (RA)-treated murine embryonic palatal and control shelves by improved subtractive hybridization. Tretinoin 96-98 cDNA sequence AY074887 Mus musculus 30-35
16963447-9 2006 Furthermore, knockdown of MCPR1 protein levels by antisense oligodeoxynucleotides promoted progression of cells from the G1 to S phase and completely abolished the RA-induced block of the cell cycle from the G1 to S phase. Tretinoin 164-166 cDNA sequence AY074887 Mus musculus 26-31
25760394-6 2015 The results showed that the expression levels of GFAP, beta-tubulin III and Galc were upregulated following treatment with ATRA in a dose-dependent manner. Tretinoin 123-127 glial fibrillary acidic protein Homo sapiens 49-53
26582376-0 2016 Primary acute myeloid leukemia cells with overexpression of EVI-1 are sensitive to all-trans retinoic acid. Tretinoin 93-106 MDS1 and EVI1 complex locus Homo sapiens 60-65
25760394-6 2015 The results showed that the expression levels of GFAP, beta-tubulin III and Galc were upregulated following treatment with ATRA in a dose-dependent manner. Tretinoin 123-127 galactosylceramidase Homo sapiens 76-80
17075312-0 2006 Influence of the level of gamma-glutamyltranspeptidase activity on the response of poorly and moderately differentiated rhabdomyosarcoma cell lines to all-trans-retinoic acid. Tretinoin 155-174 gamma-glutamyltransferase 1 Rattus norvegicus 26-54
25827071-0 2015 All-trans retinoic acid induces p53-depenent apoptosis in human hepatocytes by activating p14 expression via promoter hypomethylation. Tretinoin 10-23 ribonuclease P/MRP subunit p14 Homo sapiens 90-93
25827071-3 2015 For this effect, ATRA activated p14 expression via promoter hypomethylation, resulting in ubiquitin-dependent degradation of mouse double minute 2 (MDM2) and subsequent stabilization of p53. Tretinoin 17-21 S100 calcium binding protein A9 (calgranulin B) Mus musculus 32-35
26121141-10 2015 Additional sequence analysis also uncovered deleterious variants in genes associated with retinoic acid signaling, including NODAL and retinol dehydrogenase 10. Tretinoin 90-103 retinol dehydrogenase 10 Homo sapiens 135-159
25592248-6 2015 Lastly, we observed that IFN-gamma and IL-17 production by ex vivo re-stimulated dLNs cells is greatly increased during rejection, which it turns depends on RA synthesis, as shown in experiments using a specific RALDH inhibitor. Tretinoin 157-159 interleukin 17A Homo sapiens 39-44
26582376-3 2016 Because treatment of acute promyelocytic patients with all-trans retinoic acid (ATRA) has improved the survival of these patients substantially, we investigated whether ATRA might also be effective for the subgroup of AML patients with EVI-1 overexpression. Tretinoin 169-173 MDS1 and EVI1 complex locus Homo sapiens 236-241
26582376-4 2016 Here, we show that a substantial part of the EVI-1-positive AML cases respond to ATRA by induction of differentiation and decreased clonogenic capacity of myeloid blasts. Tretinoin 81-85 MDS1 and EVI1 complex locus Homo sapiens 45-50
26582376-5 2016 Most importantly, we demonstrate that in vivo treatment of primary EVI-1-positive AML with ATRA leads to a significant reduction in leukemic engraftment. Tretinoin 91-95 MDS1 and EVI1 complex locus Homo sapiens 67-72
26582376-6 2016 Altogether, our results show that a considerable part of the EVI-1-positive primary AML cases are sensitive to ATRA, suggesting that combining ATRA with the currently used conventional chemotherapy might be a promising treatment strategy decreasing relapse rates and enhancing complete remissions in this poor prognostic subgroup of AML patients. Tretinoin 111-115 MDS1 and EVI1 complex locus Homo sapiens 61-66
26582376-6 2016 Altogether, our results show that a considerable part of the EVI-1-positive primary AML cases are sensitive to ATRA, suggesting that combining ATRA with the currently used conventional chemotherapy might be a promising treatment strategy decreasing relapse rates and enhancing complete remissions in this poor prognostic subgroup of AML patients. Tretinoin 143-147 MDS1 and EVI1 complex locus Homo sapiens 61-66
26863034-6 2016 Beads soaked in a retinoic acid antagonist can potentiate premature MyoD induction by FGF18. Tretinoin 18-31 fibroblast growth factor 18 Gallus gallus 86-91
17075312-5 2006 These effects were in consonance with the activity level of gamma-glutamyltranspeptidase, which was significantly increased in F21 cells, but not in S4MH cells, in response to the all-trans-retinoic acid-induced increase in reactive oxygen species. Tretinoin 184-203 gamma-glutamyltransferase 1 Rattus norvegicus 60-88
17075312-8 2006 Our findings suggest that the response to all-trans-retinoic-acid of the tumour cell lines studied is influenced by the strong relationship between intracellular glutathione content, gamma-glutamyltranspeptidase activity and degree of differentiation of the rhabdomyosarcoma cell line, and that this relationship should be taken into account when identifying "retinoid-sensitive" tumours. Tretinoin 42-65 gamma-glutamyltransferase 1 Rattus norvegicus 183-211
27073891-2 2016 Increasing evidence suggested that retinoic acid (RA) signaling selectively induces IgA isotype switching and basic leucine zipper transcription factor, ATF-like (BATF) controls the global regulators of class switch recombination (CSR) in lymphocytes. Tretinoin 35-48 basic leucine zipper ATF-like transcription factor Homo sapiens 163-167
16891362-0 2006 Unbinding of retinoic acid from the retinoic acid receptor by random expulsion molecular dynamics. Tretinoin 13-26 retinoic acid receptor alpha Homo sapiens 36-58
27073891-2 2016 Increasing evidence suggested that retinoic acid (RA) signaling selectively induces IgA isotype switching and basic leucine zipper transcription factor, ATF-like (BATF) controls the global regulators of class switch recombination (CSR) in lymphocytes. Tretinoin 50-52 basic leucine zipper ATF-like transcription factor Homo sapiens 163-167
26372689-0 2016 Retinoic Acid Induces Ubiquitination-Resistant RIP140/LSD1 Complex to Fine-Tune Pax6 Gene in Neuronal Differentiation. Tretinoin 0-13 lysine demethylase 1A Homo sapiens 54-58
26372689-2 2016 Here, we identify RIP140 as an immediate retinoic acid (RA)-induced dual-function chaperone for LSD1 (lysine-specific demethylase 1). Tretinoin 41-54 lysine demethylase 1A Homo sapiens 96-100
26372689-2 2016 Here, we identify RIP140 as an immediate retinoic acid (RA)-induced dual-function chaperone for LSD1 (lysine-specific demethylase 1). Tretinoin 41-54 lysine demethylase 1A Homo sapiens 102-131
16891362-1 2006 Unbinding pathways of retinoic acid (RA) bound to retinoic acid receptor (RAR) have been explored by the random expulsion molecular dynamics (REMD) method. Tretinoin 22-35 retinoic acid receptor alpha Homo sapiens 50-72
26372689-2 2016 Here, we identify RIP140 as an immediate retinoic acid (RA)-induced dual-function chaperone for LSD1 (lysine-specific demethylase 1). Tretinoin 56-58 lysine demethylase 1A Homo sapiens 96-100
26372689-2 2016 Here, we identify RIP140 as an immediate retinoic acid (RA)-induced dual-function chaperone for LSD1 (lysine-specific demethylase 1). Tretinoin 56-58 lysine demethylase 1A Homo sapiens 102-131
16891362-1 2006 Unbinding pathways of retinoic acid (RA) bound to retinoic acid receptor (RAR) have been explored by the random expulsion molecular dynamics (REMD) method. Tretinoin 22-35 retinoic acid receptor alpha Homo sapiens 74-77
26372689-4 2016 In RA-induced neuronal differentiation, the increased RIP140/LSD1 complex is recruited by RA-elevated Pit-1 to specifically reduce H3K4me2 modification on the Pax6 promoter, thereby repressing RA-induction of Pax6. Tretinoin 3-5 lysine demethylase 1A Homo sapiens 61-65
26372689-5 2016 This study reveals a new RA-induced gene repressive mechanism that modulates the abundance, enzyme quality, and recruitment of histone modifier LSD1 to neuronal regulator Pax6, which provides a homeostatic control for RA induction of neuronal differentiation. Tretinoin 25-27 lysine demethylase 1A Homo sapiens 144-148
17167544-1 2006 Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase (ALDH) family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active. Tretinoin 111-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-28
26372689-5 2016 This study reveals a new RA-induced gene repressive mechanism that modulates the abundance, enzyme quality, and recruitment of histone modifier LSD1 to neuronal regulator Pax6, which provides a homeostatic control for RA induction of neuronal differentiation. Tretinoin 218-220 lysine demethylase 1A Homo sapiens 144-148
26464195-0 2015 The retinoic acid derivative, ABPN, inhibits pancreatic cancer through induction of Nrdp1. Tretinoin 4-17 ring finger protein 41 Homo sapiens 84-89
26592976-0 2015 Saturated fatty acids regulate retinoic acid signalling and suppress tumorigenesis by targeting fatty acid-binding protein 5. Tretinoin 31-44 fatty acid binding protein 5 Homo sapiens 96-124
17167544-1 2006 Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase (ALDH) family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active. Tretinoin 111-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 30-36
26592976-2 2015 Here we show that these biological compounds also regulate gene expression and that they do so by controlling the transcriptional activities of the retinoic acid (RA)-activated nuclear receptors RAR and PPARbeta/delta. Tretinoin 148-161 peroxisome proliferator activated receptor delta Homo sapiens 203-211
26592976-2 2015 Here we show that these biological compounds also regulate gene expression and that they do so by controlling the transcriptional activities of the retinoic acid (RA)-activated nuclear receptors RAR and PPARbeta/delta. Tretinoin 163-165 peroxisome proliferator activated receptor delta Homo sapiens 203-211
17167544-1 2006 Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase (ALDH) family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active. Tretinoin 111-125 aldehyde dehydrogenase 1 family member A1 Homo sapiens 31-35
26581770-4 2015 Subsequent addition of retinoic acid and BMP4 at specific time points and concentrations yielded a high population of neural crest progenitor cells (AP2alpha(+), P75(+)), which further differentiated into nociceptive neurons (TRKA(+), Nav1.7(+), P2X3(+)). Tretinoin 23-36 transcription factor AP-2 alpha Homo sapiens 149-157
16554086-5 2006 This study also focused to find out the association of serum ATRA level with the proliferation status in terms of proliferating cell nuclear antigen (PCNA) expression as it is an anti-proliferation agent and with the grades of cervical lesions, using SPSS statistical package. Tretinoin 61-65 proliferating cell nuclear antigen Homo sapiens 114-148
26581770-4 2015 Subsequent addition of retinoic acid and BMP4 at specific time points and concentrations yielded a high population of neural crest progenitor cells (AP2alpha(+), P75(+)), which further differentiated into nociceptive neurons (TRKA(+), Nav1.7(+), P2X3(+)). Tretinoin 23-36 sodium voltage-gated channel alpha subunit 9 Homo sapiens 235-241
26416422-5 2015 The partitioning of RA between these receptors is regulated by two carrier proteins: cellular retinoic acid-binding protein 2 (CRABP2), which delivers RA to RARs, and fatty acid-binding protein 5 (FABP5), which shuttles ligands to PPARbeta/delta. Tretinoin 20-22 cellular retinoic acid binding protein 2 Homo sapiens 85-125
26416422-5 2015 The partitioning of RA between these receptors is regulated by two carrier proteins: cellular retinoic acid-binding protein 2 (CRABP2), which delivers RA to RARs, and fatty acid-binding protein 5 (FABP5), which shuttles ligands to PPARbeta/delta. Tretinoin 20-22 cellular retinoic acid binding protein 2 Homo sapiens 127-133
16554086-5 2006 This study also focused to find out the association of serum ATRA level with the proliferation status in terms of proliferating cell nuclear antigen (PCNA) expression as it is an anti-proliferation agent and with the grades of cervical lesions, using SPSS statistical package. Tretinoin 61-65 proliferating cell nuclear antigen Homo sapiens 150-154
26416422-5 2015 The partitioning of RA between these receptors is regulated by two carrier proteins: cellular retinoic acid-binding protein 2 (CRABP2), which delivers RA to RARs, and fatty acid-binding protein 5 (FABP5), which shuttles ligands to PPARbeta/delta. Tretinoin 20-22 fatty acid binding protein 5 Homo sapiens 167-195
26416422-5 2015 The partitioning of RA between these receptors is regulated by two carrier proteins: cellular retinoic acid-binding protein 2 (CRABP2), which delivers RA to RARs, and fatty acid-binding protein 5 (FABP5), which shuttles ligands to PPARbeta/delta. Tretinoin 20-22 fatty acid binding protein 5 Homo sapiens 197-202
16554086-6 2006 RESULTS: The results showed a highly significant negative association for serum ATRA level with different stages of cervical lesions (F = 3.305; P = 0.000) by one-way ANOVA and with intensity of PCNA expression (r = -0.825; P < 0.01) by Pearson"s correlation test. Tretinoin 80-84 proliferating cell nuclear antigen Homo sapiens 195-199
26416422-5 2015 The partitioning of RA between these receptors is regulated by two carrier proteins: cellular retinoic acid-binding protein 2 (CRABP2), which delivers RA to RARs, and fatty acid-binding protein 5 (FABP5), which shuttles ligands to PPARbeta/delta. Tretinoin 20-22 peroxisome proliferator activated receptor delta Homo sapiens 231-245
16728697-1 2006 In an acute promyelocytic leukemia (APL)-transplantable mouse model, we previously reported the presence of antibodies recognizing PML-RARalpha and RARalpha in the sera of ATRA-treated mice. Tretinoin 172-176 retinoic acid receptor alpha Homo sapiens 135-143
26181105-7 2015 In addition, RA treatment increased expression of CCAAT/enhancer-binding protein alpha. Tretinoin 13-15 CCAAT enhancer binding protein alpha Danio rerio 50-86
25975191-6 2015 Importantly, all-trans retinoic acid (ATRA) increased CD38 expression levels but also reduced expression of the complement-inhibitory proteins CD55 and CD59 in both cell lines and primary MM samples. Tretinoin 13-36 CD55 molecule (Cromer blood group) Homo sapiens 143-147
16728697-5 2006 In the patients with APL, anti-RARalpha antibodies were detected at diagnosis and after maintenance therapy, reminiscent of the ATRA-treated APL mice. Tretinoin 128-132 retinoic acid receptor alpha Homo sapiens 31-39
25975191-6 2015 Importantly, all-trans retinoic acid (ATRA) increased CD38 expression levels but also reduced expression of the complement-inhibitory proteins CD55 and CD59 in both cell lines and primary MM samples. Tretinoin 38-42 CD55 molecule (Cromer blood group) Homo sapiens 143-147
16782282-9 2006 Experiments with Schwann cell primary cultures revealed an effect of retinoic acid on the expression of the neuregulin receptor ErbB3, suggesting that one function of retinoic acid consists in the regulation of neuroglial interactions after peripheral nerve injury. Tretinoin 69-82 erb-b2 receptor tyrosine kinase 3 Rattus norvegicus 128-133
26093056-6 2015 Therefore, we propose that this PCAN could be a potentially powerful carrier for effective RA delivery to direct hiPSC fate to neuronal lineage. Tretinoin 91-93 podocan Homo sapiens 32-36
16782282-9 2006 Experiments with Schwann cell primary cultures revealed an effect of retinoic acid on the expression of the neuregulin receptor ErbB3, suggesting that one function of retinoic acid consists in the regulation of neuroglial interactions after peripheral nerve injury. Tretinoin 167-180 erb-b2 receptor tyrosine kinase 3 Rattus norvegicus 128-133
16847438-12 2006 The COX inhibitor dexketoprofen and the interleukin-1 receptor antagonist IL-1ra inhibited ATRA effect. Tretinoin 91-95 coproporphyrinogen oxidase Rattus norvegicus 4-7
26305673-9 2015 In conclusion, ALDH1 expression in tumor-associated stromal cells indicates reduced BrCa progression, possibly via RA secretion. Tretinoin 115-117 BRCA1 DNA repair associated Homo sapiens 84-88
16847438-13 2006 The results indicate that COX and interleukin-1 are involved in the effects of ATRA in the spinal cord, similar to that seen in inflammation. Tretinoin 79-83 coproporphyrinogen oxidase Rattus norvegicus 26-29
16838369-1 2006 GFP labeled/NE-4C neural progenitor cells cloned from primary neuroectodermal cultures of p53- mouse embryos give rise to neurons when exposed to retinoic acid in vitro. Tretinoin 146-159 transformation related protein 53, pseudogene Mus musculus 90-93
16989981-6 2006 Additionally, teratogenic (4-yn-VPA) and nonteratogenic analogs of VPA (IE-VPA), retinoic acid (RA), and saline were compared for effects on Hoxa1 expression on d12. Tretinoin 96-98 homeobox A1 Rattus norvegicus 141-146
16989981-10 2006 RA significantly elevated Hoxa1 expression at all time points except 24-h post-treatment. Tretinoin 0-2 homeobox A1 Rattus norvegicus 26-31
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 protein phosphatase 2 phosphatase activator Homo sapiens 41-45
16823827-0 2006 All-trans retinoic acid induces p62DOK1 and p56DOK2 expression which enhances induced differentiation and G0 arrest of HL-60 leukemia cells. Tretinoin 10-23 docking protein 2 Homo sapiens 44-51
16823827-5 2006 The data in this report show that both the DOK1 and the DOK2 adaptor proteins are constitutively expressed in the myelomonoblastic leukemia cell line, HL-60, and that expression of both proteins is induced by the chemotherapeutic differentiation causing agents, all-trans retinoic acid (atRA) and 1,25-dihydroxyvitamin D3 (VD3). Tretinoin 272-285 docking protein 2 Homo sapiens 56-60
16823827-5 2006 The data in this report show that both the DOK1 and the DOK2 adaptor proteins are constitutively expressed in the myelomonoblastic leukemia cell line, HL-60, and that expression of both proteins is induced by the chemotherapeutic differentiation causing agents, all-trans retinoic acid (atRA) and 1,25-dihydroxyvitamin D3 (VD3). Tretinoin 287-291 docking protein 2 Homo sapiens 56-60
16845368-4 2006 By contrast, in retinoic-acid-induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of Hoxb1, at the 3" boundary of the HoxB domain. Tretinoin 16-29 homeobox B cluster Mus musculus 65-69
16845368-4 2006 By contrast, in retinoic-acid-induced differentiated cells, when HoxB transcription is activated, a general silencing of DNA replication origins occurs in the locus except one located downstream of Hoxb1, at the 3" boundary of the HoxB domain. Tretinoin 16-29 homeobox B cluster Mus musculus 231-235
16978060-1 2006 We describe a method of generating an enriched population of NCAM-positive cells from a human teratocarcinoma cell line (NTera2/D1) and their differentiation into midbrain dopaminergic neurons in the absence of the caudalizing factor retinoic acid (RA). Tretinoin 234-247 neural cell adhesion molecule 1 Homo sapiens 61-65
25839652-1 2015 Apoptosis Related Protein 3 (APR3) is an important protein which is involved in retinoic acid-induced apoptosis, osteoblast differentiation and cervical squamous cell carcinoma progression. Tretinoin 80-93 all-trans retinoic acid induced differentiation factor Homo sapiens 0-27
25839652-1 2015 Apoptosis Related Protein 3 (APR3) is an important protein which is involved in retinoic acid-induced apoptosis, osteoblast differentiation and cervical squamous cell carcinoma progression. Tretinoin 80-93 all-trans retinoic acid induced differentiation factor Homo sapiens 29-33
16978060-1 2006 We describe a method of generating an enriched population of NCAM-positive cells from a human teratocarcinoma cell line (NTera2/D1) and their differentiation into midbrain dopaminergic neurons in the absence of the caudalizing factor retinoic acid (RA). Tretinoin 249-251 neural cell adhesion molecule 1 Homo sapiens 61-65
16510162-7 2006 In HL-60 cells induced to differentiate with retinoic acid (RA), a similar increase in FasL expression, but no associated changes in CD16 gene expression, was observed following clozapine treatments. Tretinoin 45-58 Fas ligand Homo sapiens 87-91
25866159-2 2015 We present a piggyBac transposon gain of function screen in human ES cells that identifies DENND2C, which genetically cooperates with NANOG to maintain self-renewal in the presence of retinoic acid. Tretinoin 184-197 DENN domain containing 2C Homo sapiens 91-98
25866159-2 2015 We present a piggyBac transposon gain of function screen in human ES cells that identifies DENND2C, which genetically cooperates with NANOG to maintain self-renewal in the presence of retinoic acid. Tretinoin 184-197 Nanog homeobox Homo sapiens 134-139
16510162-7 2006 In HL-60 cells induced to differentiate with retinoic acid (RA), a similar increase in FasL expression, but no associated changes in CD16 gene expression, was observed following clozapine treatments. Tretinoin 60-62 Fas ligand Homo sapiens 87-91
16684888-0 2006 All-trans retinoic acid-induced expression of bactericidal/permeability-increasing protein (BPI) in human myeloid cells correlates to binding of C/EBPbeta and C/EBPepsilon to the BPI promoter. Tretinoin 10-23 bactericidal permeability increasing protein Homo sapiens 46-90
25510432-4 2015 In contrast to other NUP98 fusions, cells transformed by the NUP98-RARG fusion were extremely sensitive to all-trans retinoic acid (ATRA) treatment. Tretinoin 117-130 retinoic acid receptor, gamma Mus musculus 67-71
16684888-0 2006 All-trans retinoic acid-induced expression of bactericidal/permeability-increasing protein (BPI) in human myeloid cells correlates to binding of C/EBPbeta and C/EBPepsilon to the BPI promoter. Tretinoin 10-23 bactericidal permeability increasing protein Homo sapiens 92-95
16684888-0 2006 All-trans retinoic acid-induced expression of bactericidal/permeability-increasing protein (BPI) in human myeloid cells correlates to binding of C/EBPbeta and C/EBPepsilon to the BPI promoter. Tretinoin 10-23 CCAAT enhancer binding protein epsilon Homo sapiens 159-171
25843047-4 2015 Switching to retinoic acid treatment at any point during this process halts colinear HOX activation and transitions the neuromesoderm into SOX2(+)/PAX6(+) neuroectoderm with predictable, discrete HOX gene/protein profiles that can be further differentiated into region-specific cells, e.g., motor neurons. Tretinoin 13-26 SRY-box transcription factor 2 Homo sapiens 139-143
16684888-0 2006 All-trans retinoic acid-induced expression of bactericidal/permeability-increasing protein (BPI) in human myeloid cells correlates to binding of C/EBPbeta and C/EBPepsilon to the BPI promoter. Tretinoin 10-23 bactericidal permeability increasing protein Homo sapiens 179-182
16684888-6 2006 We show that treatment of NB4 cells with all-trans retinoic acid (ATRA) induces BPI expression at mRNA and at protein level. Tretinoin 51-64 bactericidal permeability increasing protein Homo sapiens 80-83
16684888-6 2006 We show that treatment of NB4 cells with all-trans retinoic acid (ATRA) induces BPI expression at mRNA and at protein level. Tretinoin 66-70 bactericidal permeability increasing protein Homo sapiens 80-83
16684888-9 2006 Here, we show that induction of NB4 cells with ATRA correlates to direct binding of C/EBPbeta and C/EBPepsilon to the proximal BPI promoter, as determined by electrophoretic mobility shift analysis and chromatin immunoprecipitation. Tretinoin 47-51 CCAAT enhancer binding protein epsilon Homo sapiens 98-110
25797252-0 2015 CRABP-II- and FABP5-independent responsiveness of human glioblastoma cells to all-trans retinoic acid. Tretinoin 88-101 cellular retinoic acid binding protein 2 Homo sapiens 0-8
25797252-0 2015 CRABP-II- and FABP5-independent responsiveness of human glioblastoma cells to all-trans retinoic acid. Tretinoin 88-101 fatty acid binding protein 5 Homo sapiens 14-19
16684888-9 2006 Here, we show that induction of NB4 cells with ATRA correlates to direct binding of C/EBPbeta and C/EBPepsilon to the proximal BPI promoter, as determined by electrophoretic mobility shift analysis and chromatin immunoprecipitation. Tretinoin 47-51 bactericidal permeability increasing protein Homo sapiens 127-130
16849523-0 2006 An autocrine loop involving ret and glial cell-derived neurotrophic factor mediates retinoic acid-induced neuroblastoma cell differentiation. Tretinoin 84-97 ret proto-oncogene Homo sapiens 28-31
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 37-50 ret proto-oncogene Homo sapiens 248-251
25861444-0 2015 Retinoic acid-independent expression of Meis2 during autopod patterning in the developing bat and mouse limb. Tretinoin 0-13 Meis homeobox 2 Mus musculus 40-45
25861444-7 2015 This interdigital Meis2 expression is not activated by retinoic acid (RA) signalling as it is present in the retained interdigital tissue of Rdh10 (trex/trex) mice, which lack RA. Tretinoin 176-178 Meis homeobox 2 Mus musculus 18-23
25027601-0 2015 Retinoic acid primes human dendritic cells to induce gut-homing, IL-10-producing regulatory T cells. Tretinoin 0-13 interleukin 10 Homo sapiens 65-70
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 52-54 ret proto-oncogene Homo sapiens 248-251
25027601-4 2015 We report a novel role of RA in immune regulation by showing that RA-conditioned human DCs did not substantially enhance Foxp3 but induced alpha4beta7(+) CCR9(+) T cells expressing high levels of interleukin (IL)-10, which were functional suppressive Treg cells. Tretinoin 26-28 interleukin 10 Homo sapiens 196-215
16849523-5 2006 Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release. Tretinoin 102-104 ret proto-oncogene Homo sapiens 46-49
25027601-7 2015 Experiments with naive CD4(+) T cells stimulated by anti-CD3 and anti-CD28 antibodies in the absence of DCs emphasized that RA induces IL-10 in face of inflammatory mediators. Tretinoin 124-126 interleukin 10 Homo sapiens 135-140
25027601-8 2015 The data thus show for the first time that RA induces IL-10-producing Treg cells and postulates a novel mechanism for IL-10 in maintaining tolerance to the intestinal microbiome. Tretinoin 43-45 interleukin 10 Homo sapiens 54-59
16849523-5 2006 Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release. Tretinoin 102-104 ret proto-oncogene Homo sapiens 84-87
25027601-8 2015 The data thus show for the first time that RA induces IL-10-producing Treg cells and postulates a novel mechanism for IL-10 in maintaining tolerance to the intestinal microbiome. Tretinoin 43-45 interleukin 10 Homo sapiens 118-123
16849523-5 2006 Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release. Tretinoin 102-104 ret proto-oncogene Homo sapiens 84-87
16849523-6 2006 This report shows that in SK-N-BE(2) cells, stimulation of Ret is a major upstream mechanism needed to mediate RA-induced differentiation. Tretinoin 111-113 ret proto-oncogene Homo sapiens 59-62
16740727-8 2006 Finally, FR-beta selectively mediated growth inhibition by (6S) dideazatetrahydrofolate in a manner that was greatly potentiated in AML cells by ATRA and HDAC inhibition. Tretinoin 145-149 folate receptor beta Homo sapiens 9-16
16800923-9 2006 There was a substantial decrease in c-myc mRNA levels when 100 microg/ml bestatin was added to 10 nmol/L ATRA (P < 0.05). Tretinoin 105-109 MYC proto-oncogene, bHLH transcription factor Homo sapiens 36-41
26312847-5 2015 METHODS: We used a mouse model in which retinoic acid signalling is specifically ablated within the T-cell compartment through overexpression of a dominant negative retinoic acid receptor alpha (RARalpha) (dnRARalpha mice) to investigate its role in the regulation of Th1 lineage stability. Tretinoin 40-53 retinoic acid receptor, alpha Mus musculus 165-193
26312847-5 2015 METHODS: We used a mouse model in which retinoic acid signalling is specifically ablated within the T-cell compartment through overexpression of a dominant negative retinoic acid receptor alpha (RARalpha) (dnRARalpha mice) to investigate its role in the regulation of Th1 lineage stability. Tretinoin 40-53 retinoic acid receptor, alpha Mus musculus 195-203
26312847-10 2015 Abrogation of retinoic acid signalling in Th1 cells resulted in loss of T-bet expression and STAT4 activity. Tretinoin 14-27 T-box 21 Mus musculus 72-77
26312847-10 2015 Abrogation of retinoic acid signalling in Th1 cells resulted in loss of T-bet expression and STAT4 activity. Tretinoin 14-27 signal transducer and activator of transcription 4 Mus musculus 93-98
16800923-10 2006 Various concentrations (50, 75, 100 microg/ml) of bestatin combined with 10 nmol/L ATRA down-regulated the expression of c-Myc protein, which was negatively correlated with the NBT reduction activity of NB4 cells induced by 10 nmol/L ATRA alone or plus bestatin at various concentrations (r = -0.940, P = 0.017). Tretinoin 83-87 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126
25351211-6 2015 Retinoic acid treatment led to GATA3 downregulation together with neuronal differentiation, suppression of cell proliferation and inhibition of tumorigenecity in neuroblastoma cells. Tretinoin 0-13 GATA binding protein 3 Homo sapiens 31-36
16800923-10 2006 Various concentrations (50, 75, 100 microg/ml) of bestatin combined with 10 nmol/L ATRA down-regulated the expression of c-Myc protein, which was negatively correlated with the NBT reduction activity of NB4 cells induced by 10 nmol/L ATRA alone or plus bestatin at various concentrations (r = -0.940, P = 0.017). Tretinoin 234-238 MYC proto-oncogene, bHLH transcription factor Homo sapiens 121-126
16800923-12 2006 It is concluded that an aminopeptidase inhibitor bestatin can potentiate ATRA-inducing differentiation of NB4 cells, possibly by down-regulating c-myc expression in synergy with ATRA. Tretinoin 73-77 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150
16540467-7 2006 Remarkably, Mut PML stabilizes PML-RARalpha and inhibits differentiation induced by pharmacological doses of RA. Tretinoin 35-37 PML nuclear body scaffold Homo sapiens 16-19
25595247-4 2015 RA revealed the same ability to induce IL-10 as did interferon-beta-1b (IFN-beta-1b), and B-cells from patients treated with glatiramer acetate or IFN-beta-1b still displayed the beneficial effects of RA on the IL-10/TNF-alpha ratio. Tretinoin 0-2 interleukin 10 Homo sapiens 39-44
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 0-13 fibroblast growth factor 8 Mus musculus 59-85
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 0-13 fibroblast growth factor 8 Mus musculus 87-91
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 0-13 fibroblast growth factor 8 Mus musculus 266-270
16540467-7 2006 Remarkably, Mut PML stabilizes PML-RARalpha and inhibits differentiation induced by pharmacological doses of RA. Tretinoin 35-37 PML nuclear body scaffold Homo sapiens 31-34
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 15-17 fibroblast growth factor 8 Mus musculus 59-85
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 15-17 fibroblast growth factor 8 Mus musculus 87-91
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 15-17 fibroblast growth factor 8 Mus musculus 266-270
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 214-216 fibroblast growth factor 8 Mus musculus 59-85
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 214-216 fibroblast growth factor 8 Mus musculus 87-91
26500786-0 2015 NRG1 and KITL Signal Downstream of Retinoic Acid in the Germline to Support Soma-Free Syncytial Growth of Differentiating Spermatogonia. Tretinoin 35-48 KIT ligand Homo sapiens 9-13
26500786-3 2015 Here, we analyzed EGF superfamily receptor and ligand diversity in rat testis cells, and delineated germline-intrinsic signaling via an ERBB3 co-transducer, ERBB2, as essential for retinoic acid-induced syncytial growth by differentiating spermatogonia. Tretinoin 181-194 erb-b2 receptor tyrosine kinase 2 Rattus norvegicus 157-162
26500786-6 2015 Thus, we report NRG1 and KITL activate alternative pathways downstream of retinoic acid signaling in the germline that are essential for stem cells to undergo pre-meiotic steps of spermatogenesis in culture. Tretinoin 74-87 KIT ligand Homo sapiens 25-29
25537091-6 2015 Bmp3, egr3, and stra8 are stimulated after 1 d of RA treatment and then recover to normal after 3 d of RA treatment. Tretinoin 50-52 early growth response 3 Bos taurus 6-10
26368825-2 2015 Retinoic acid (RA) restricts the anterior extent of caudal fibroblast growth factor 8 (Fgf8) expression in both mesoderm and neural plate to control somitogenesis and neurogenesis, however it remains unclear where RA acts to control the spatial expression of caudal Fgf8. Tretinoin 214-216 fibroblast growth factor 8 Mus musculus 266-270
16414179-7 2006 Lipocalin 5 [Lcn5 or epididymal retinoic acid-binding protein (E-RABP)] is a member of this epididymis-specific lipocalin gene cluster, which binds hydrophobic molecules such as retinoic acid. Tretinoin 32-45 lipocalin 5 Mus musculus 0-11
26045160-5 2015 All-trans-retinoic acid has high affinity (kd<=0.4nM) for its nuclear receptors (RARalpha, -beta, and -gamma), whereas retinal has low (if any) affinity for these receptors, making it unlikely that these retinal concentrations would activate RAR. Tretinoin 0-23 retinoic acid receptor, alpha Mus musculus 84-111
26045160-5 2015 All-trans-retinoic acid has high affinity (kd<=0.4nM) for its nuclear receptors (RARalpha, -beta, and -gamma), whereas retinal has low (if any) affinity for these receptors, making it unlikely that these retinal concentrations would activate RAR. Tretinoin 0-23 retinoic acid receptor, alpha Mus musculus 84-87
24938743-2 2015 Here, we identified a stromal cell (SC) population in the intestinal lamina propria (LP), which is capable of inducing RA production in DCs in a RA- and granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent fashion. Tretinoin 119-121 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 153-201
24938743-2 2015 Here, we identified a stromal cell (SC) population in the intestinal lamina propria (LP), which is capable of inducing RA production in DCs in a RA- and granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent fashion. Tretinoin 119-121 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 203-209
25611428-5 2015 Although addition of IL-21 counteracted the proliferative effect of ATRA in normal B cells, it significantly enhanced the growth of tumor B cells in presence of CpG and ATRA. Tretinoin 68-72 interleukin 21 Homo sapiens 21-26
25611428-5 2015 Although addition of IL-21 counteracted the proliferative effect of ATRA in normal B cells, it significantly enhanced the growth of tumor B cells in presence of CpG and ATRA. Tretinoin 169-173 interleukin 21 Homo sapiens 21-26
26713527-10 2015 The combination of RAD001 with ATRA significantly inhibited mTOR signaling downstream proteins P-P70S6K, P-4E-BP1 and enhanced autophagy-related protein LC3-II and Beclin 1. Tretinoin 31-35 beclin 1 Homo sapiens 164-172
16414179-7 2006 Lipocalin 5 [Lcn5 or epididymal retinoic acid-binding protein (E-RABP)] is a member of this epididymis-specific lipocalin gene cluster, which binds hydrophobic molecules such as retinoic acid. Tretinoin 32-45 lipocalin 5 Mus musculus 13-17
16414179-7 2006 Lipocalin 5 [Lcn5 or epididymal retinoic acid-binding protein (E-RABP)] is a member of this epididymis-specific lipocalin gene cluster, which binds hydrophobic molecules such as retinoic acid. Tretinoin 32-45 lipocalin 5 Mus musculus 63-69
16636307-9 2006 With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. Tretinoin 53-57 NPHS1 adhesion molecule, nephrin Rattus norvegicus 88-95
27308362-1 2014 Retinoic acid inducible gene-I (RIG-I), named for the observation that its mRNA expression is highly upregulated in the progression of all-trans retinoic acid (ATRA)-induced maturation of acute promyelocytic leukemia (APL) cells, has been well documented as a pivotal virus-associated molecular pattern recognition receptor (PRR) responsible for triggering innate immunity. Tretinoin 139-158 DExD/H-box helicase 58 Homo sapiens 0-30
27308362-1 2014 Retinoic acid inducible gene-I (RIG-I), named for the observation that its mRNA expression is highly upregulated in the progression of all-trans retinoic acid (ATRA)-induced maturation of acute promyelocytic leukemia (APL) cells, has been well documented as a pivotal virus-associated molecular pattern recognition receptor (PRR) responsible for triggering innate immunity. Tretinoin 139-158 DExD/H-box helicase 58 Homo sapiens 32-37
16636307-12 2006 In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. Tretinoin 88-92 NPHS1 adhesion molecule, nephrin Rattus norvegicus 189-196
27308362-1 2014 Retinoic acid inducible gene-I (RIG-I), named for the observation that its mRNA expression is highly upregulated in the progression of all-trans retinoic acid (ATRA)-induced maturation of acute promyelocytic leukemia (APL) cells, has been well documented as a pivotal virus-associated molecular pattern recognition receptor (PRR) responsible for triggering innate immunity. Tretinoin 160-164 DExD/H-box helicase 58 Homo sapiens 0-30
27308362-1 2014 Retinoic acid inducible gene-I (RIG-I), named for the observation that its mRNA expression is highly upregulated in the progression of all-trans retinoic acid (ATRA)-induced maturation of acute promyelocytic leukemia (APL) cells, has been well documented as a pivotal virus-associated molecular pattern recognition receptor (PRR) responsible for triggering innate immunity. Tretinoin 160-164 DExD/H-box helicase 58 Homo sapiens 32-37
27308379-2 2014 Recently, we reported that p62 is upregulated during all-trans retinoic acid (ATRA)-induced terminal differentiation of acute myeloid leukemia (AML) cells. Tretinoin 63-76 nucleoporin 62 Homo sapiens 27-30
27308379-2 2014 Recently, we reported that p62 is upregulated during all-trans retinoic acid (ATRA)-induced terminal differentiation of acute myeloid leukemia (AML) cells. Tretinoin 78-82 nucleoporin 62 Homo sapiens 27-30
26079152-2 2015 Astrocyte elevated gene-1 (AEG-1) plays a pivotal role in hepatocarcinogenesis and inhibits retinoic acid-induced gene expression and cell death. Tretinoin 92-105 metadherin Mus musculus 0-25
26079152-2 2015 Astrocyte elevated gene-1 (AEG-1) plays a pivotal role in hepatocarcinogenesis and inhibits retinoic acid-induced gene expression and cell death. Tretinoin 92-105 metadherin Mus musculus 27-32
16242776-4 2006 Inhibition of ATRA-induced apoptosis by TGF-beta1 was associated with an increased level of Mcl-1 protein, an anti-apoptotic member of Bcl-2 family, but not with inhibition of mitochondrial membrane depolarization. Tretinoin 14-18 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 92-97
25351459-10 2014 Both flow cytometric and antibody-mediated neutralization studies showed that liver NKT cells up-regulate the natural killer group 2, member D (NKG2D) ligand and bind with the NKG2D ligand, retinoic acid early inducible 1 (Rae1), and positively activated HSCs to ameliorate liver fibrosis. Tretinoin 190-203 ribonucleic acid export 1 Mus musculus 223-227
25450689-2 2014 Although it is appreciated that isomers of retinoic acid activate the retinoic acid receptor (RAR) and retinoid X receptor (RXR) family of nuclear receptors to elicit cellular changes, the molecular details of retinoic acid action remain poorly defined in immune processes. Tretinoin 43-56 retinoid X receptor alpha Homo sapiens 103-122
25450689-2 2014 Although it is appreciated that isomers of retinoic acid activate the retinoic acid receptor (RAR) and retinoid X receptor (RXR) family of nuclear receptors to elicit cellular changes, the molecular details of retinoic acid action remain poorly defined in immune processes. Tretinoin 43-56 retinoid X receptor alpha Homo sapiens 124-127
16352814-3 2006 Here we found that conditional expression of promyelocytic leukemia-retinoic acid receptor alpha (PML-RARA), the protein encoded by the t(15;17) translocation found in acute promyelocytic leukemia (APL), suppressed PU.1 expression, while treatment of APL cell lines and primary cells with all-trans retinoic acid (ATRA) restored PU.1 expression and induced neutrophil differentiation. Tretinoin 68-81 Spi-1 proto-oncogene Homo sapiens 215-219
25149081-5 2014 Immunohistochemical analysis revealed that retinaldehyde dehydrogenase 2 (RALDH2), a key enzyme for RA synthesis, is highly expressed by reactive astrocytes throughout white matter lesions compared to control and normal appearing white matter. Tretinoin 74-76 aldehyde dehydrogenase 1 family member A2 Homo sapiens 43-72
16352814-3 2006 Here we found that conditional expression of promyelocytic leukemia-retinoic acid receptor alpha (PML-RARA), the protein encoded by the t(15;17) translocation found in acute promyelocytic leukemia (APL), suppressed PU.1 expression, while treatment of APL cell lines and primary cells with all-trans retinoic acid (ATRA) restored PU.1 expression and induced neutrophil differentiation. Tretinoin 68-81 Spi-1 proto-oncogene Homo sapiens 329-333
16352814-3 2006 Here we found that conditional expression of promyelocytic leukemia-retinoic acid receptor alpha (PML-RARA), the protein encoded by the t(15;17) translocation found in acute promyelocytic leukemia (APL), suppressed PU.1 expression, while treatment of APL cell lines and primary cells with all-trans retinoic acid (ATRA) restored PU.1 expression and induced neutrophil differentiation. Tretinoin 314-318 Spi-1 proto-oncogene Homo sapiens 215-219
16352814-4 2006 ATRA-induced activation was mediated by a region in the PU.1 promoter to which CEBPB and OCT-1 binding were induced. Tretinoin 0-4 Spi-1 proto-oncogene Homo sapiens 56-60
16352814-5 2006 Finally, conditional expression of PU.1 in human APL cells was sufficient to trigger neutrophil differentiation, whereas reduction of PU.1 by small interfering RNA (siRNA) blocked ATRA-induced neutrophil differentiation. Tretinoin 180-184 Spi-1 proto-oncogene Homo sapiens 134-138
25164272-5 2014 Both BC and RE supplementation increased retinoic acid mediated transcriptional responses in intestine (on Isx and Bco1) and the liver (on Cyp26a1 and Cpt1a). Tretinoin 41-54 beta-carotene oxygenase 1 Rattus norvegicus 115-119
16527258-4 2006 While the levels of Neurensin-1 mRNA and protein in retinoic acid-exposed mouse neuroblastoma Neuro2a cells increased, those of Neurensin-2 mRNA and protein remained unchanged. Tretinoin 52-65 neurensin 1 Mus musculus 20-31
25239423-6 2014 CD11b and CD11c were negative in all untreated APLs but positive in 76% and 88% of ATRA-treated APLs, respectively. Tretinoin 83-87 integrin subunit alpha M Homo sapiens 0-5
16569592-6 2006 HP1 and MNEI levels inversely correlate in a number of normal and leukemia myeloid cells and show strikingly opposite coordinated changes during differentiation of U937 cell line induced by retinoic acid. Tretinoin 190-203 chromobox 5 Homo sapiens 0-3
24801450-7 2014 After incubation with 10 muM RA for 3-5 days, a majority of the cells exited the cell cycle to become postmitotic neurons, characterized by the presence of longer neurite outgrowths and expression of the neuronal marker microtubule-associated protein-2 (MAP2). Tretinoin 29-31 microtubule associated protein 2 Homo sapiens 220-252
24801450-7 2014 After incubation with 10 muM RA for 3-5 days, a majority of the cells exited the cell cycle to become postmitotic neurons, characterized by the presence of longer neurite outgrowths and expression of the neuronal marker microtubule-associated protein-2 (MAP2). Tretinoin 29-31 microtubule associated protein 2 Homo sapiens 254-258
24801450-9 2014 Chromatin immunoprecipitation assay demonstrated an increased recruitment of Sp1 to the top IIbeta promoter after RA treatment. Tretinoin 114-116 DNA topoisomerase II beta Homo sapiens 88-98
24694005-0 2014 Potential signal pathway of all-trans retinoic acid for MMP-2 and MMP-9 expression in injury podocyte induced by adriamycin. Tretinoin 38-51 matrix metallopeptidase 9 Homo sapiens 66-71
16646664-3 2006 Steady-state protein levels of the TFIIA tau, alphabeta, and gamma subunits were significantly reduced when human embryonal (ec) and hepatic carcinoma cell lines were stimulated to differentiate with either all-trans-retinoic acid (ATRA) or sodium butyrate. Tretinoin 207-230 general transcription factor IIA subunit 2 Homo sapiens 35-40
25268355-5 2014 All-trans retinoic acid in vitro induced IL-10 in CD4(+)CD25(high)Foxp3(+) T cells; IL-10 and TGF-beta production in CD4(+)CD25-Foxp3- T cells, and IL-10 in monocytes isolated from healthy children. Tretinoin 10-23 interleukin 10 Homo sapiens 41-46
25268355-6 2014 However, the use of all-trans retinoic acid together with leishmanial antigens in vitro prevented increases in IL-10 production in Treg cells and monocytes isolated from VL children. Tretinoin 30-43 interleukin 10 Homo sapiens 111-116
16646664-3 2006 Steady-state protein levels of the TFIIA tau, alphabeta, and gamma subunits were significantly reduced when human embryonal (ec) and hepatic carcinoma cell lines were stimulated to differentiate with either all-trans-retinoic acid (ATRA) or sodium butyrate. Tretinoin 232-236 general transcription factor IIA subunit 2 Homo sapiens 35-40
16646664-4 2006 ATRA-treated NT2-ec cells required replating to induce a neuronal phenotype and loss of detectable TFIIA tau and gamma proteins. Tretinoin 0-4 general transcription factor IIA subunit 2 Homo sapiens 99-104
24793539-1 2014 Retinoic acid (RA) is an active derivative of vitamin A, and it has different isomers, including ATRA (all-trans-retinoic acid), 13-cRA (13-cis-retinoic acid) and 9-cRA (9-cis-retinoic acid), etc. Tretinoin 0-13 myotubularin related protein 11 Homo sapiens 132-135
16288212-3 2006 We report that, in mouse embryocarcinoma cells (F9 cells), RA induces an early activation of PI3K and Akt via an increase in the expression of the p85alpha regulatory subunit. Tretinoin 59-61 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 147-155
24793539-1 2014 Retinoic acid (RA) is an active derivative of vitamin A, and it has different isomers, including ATRA (all-trans-retinoic acid), 13-cRA (13-cis-retinoic acid) and 9-cRA (9-cis-retinoic acid), etc. Tretinoin 0-13 myotubularin related protein 11 Homo sapiens 165-168
24833708-3 2014 The current study examines the hepatic binding profile of two RA receptor isoforms, RARA (RARalpha) and RARB (RARbeta), in response to RA treatment in mouse livers. Tretinoin 62-64 retinoic acid receptor, alpha Mus musculus 84-88
16261163-3 2006 Here we demonstrate that the genes for the RA-receptor RARbeta2 and the cytochrome P450 RA-specific hydrolase Cyp26a1 involved in RA catabolism are coordinately regulated by RA. Tretinoin 43-45 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 110-117
24833708-3 2014 The current study examines the hepatic binding profile of two RA receptor isoforms, RARA (RARalpha) and RARB (RARbeta), in response to RA treatment in mouse livers. Tretinoin 62-64 retinoic acid receptor, alpha Mus musculus 90-98
16405439-4 2006 We report a unique case of a PML/RARA positive APL patient exhibiting extensive monocytic differentiation after ATRA therapy as documented by morphology, flow cytometry, and FISH studies. Tretinoin 112-116 PML nuclear body scaffold Homo sapiens 29-32
24967705-0 2014 ATRA-induced cellular differentiation and CD38 expression inhibits acquisition of BCR-ABL mutations for CML acquired resistance. Tretinoin 0-4 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 82-89
24967705-4 2014 Forced myeloid differentiation by all-trans-retinoic acid (ATRA) effectively blocked acquisition of BCR-ABL mutations and resistance to the TKIs imatinib, nilotinib or dasatinib in our previously described in vitro models of acquired TKI resistance. Tretinoin 34-57 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 100-107
24967705-4 2014 Forced myeloid differentiation by all-trans-retinoic acid (ATRA) effectively blocked acquisition of BCR-ABL mutations and resistance to the TKIs imatinib, nilotinib or dasatinib in our previously described in vitro models of acquired TKI resistance. Tretinoin 59-63 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 100-107
24967705-7 2014 Consequently, ATRA treatment decreased DNA damage repair and suppressed acquisition of BCR-ABL mutations. Tretinoin 14-18 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 87-94
16405439-4 2006 We report a unique case of a PML/RARA positive APL patient exhibiting extensive monocytic differentiation after ATRA therapy as documented by morphology, flow cytometry, and FISH studies. Tretinoin 112-116 retinoic acid receptor alpha Homo sapiens 33-37
16291826-4 2006 A broad caspase inhibitor (z-VAD-fmk), caspase-9 inhibitor z-LEHD-fmk and caspase-3 inhibitor (z-DEVD-fmk) blocked atRA-induced DNA fragmentation and sub-G1 fraction, but not caspase-8 inhibitor z-IETD-fmk. Tretinoin 115-119 caspase 8 Mus musculus 175-184
16273324-0 2006 Retinoic acids increase expression of GLUT4 in dedifferentiated and hypertrophied cardiac myocytes. Tretinoin 0-14 solute carrier family 2 member 4 Rattus norvegicus 38-43
24888826-10 2014 Immunofluorescence-double-staining confirmed markedly increased LIF expression in alveolar walls of Nitrofen+ATRA compared to Nitrofen+Placebo. Tretinoin 109-113 LIF, interleukin 6 family cytokine Rattus norvegicus 64-67
24888826-11 2014 CONCLUSIONS: Increased LIF expression after prenatal treatment with ATRA in nitrofen-induced PH suggests that ATRA may have a therapeutic potential in attenuating CDH-associated PH by stimulating alveolar development. Tretinoin 110-114 LIF, interleukin 6 family cytokine Rattus norvegicus 23-26
16273324-9 2006 In conclusion, treatment with RA can restore the down-regulated expression of GLUT4 in cardiomyocytes in association with a partial improvement of the differentiated phenotype. Tretinoin 30-32 solute carrier family 2 member 4 Rattus norvegicus 78-83
24867581-0 2014 Up-regulation of VEGF by retinoic acid during hyperoxia prevents retinal neovascularization and retinopathy. Tretinoin 25-38 vascular endothelial growth factor A Mus musculus 17-21
16420438-2 2006 RA exerts its effects by binding to retinoic acid receptors (RAR) which heterodimerize with retinoid X receptors (RXR) and then act as ligand-activated transcription factors. Tretinoin 0-2 retinoic acid receptor, alpha Rattus norvegicus 61-64
24867581-2 2014 This study was to investigate whether the systemic administration of retinoic acid (RA) regulates retinal VEGF expression and prevents retinal neovascularization and retinopathy in the oxygen-induced retinopathy (OIR) mouse model. Tretinoin 69-82 vascular endothelial growth factor A Mus musculus 106-110
24867581-2 2014 This study was to investigate whether the systemic administration of retinoic acid (RA) regulates retinal VEGF expression and prevents retinal neovascularization and retinopathy in the oxygen-induced retinopathy (OIR) mouse model. Tretinoin 84-86 vascular endothelial growth factor A Mus musculus 106-110
24867581-6 2014 RESULTS: Systemic administration of RA in OIR mice promoted retinal VEGF mRNA and protein expression in phase I; the stabilized level of VEGF in phase I supported retinal vascular development and counteracted vaso-obliteration in OIR mice. Tretinoin 36-38 vascular endothelial growth factor A Mus musculus 68-72
24867581-9 2014 CONCLUSIONS: Systemic administration of RA regulates retinal VEGF expression and supports retinal vascular development in OIR mouse model. Tretinoin 40-42 vascular endothelial growth factor A Mus musculus 61-65
24845860-4 2014 In vitro experiments showed that RA is necessary and sufficient to induce the development of distal-like hair cell phenotypes and promotes expression of the actin-crosslinking proteins, Espin and Fscn2. Tretinoin 33-35 fascin actin-bundling protein 2, retinal Gallus gallus 196-201
17124055-4 2006 The unique PML/RARalpha aberration serves as a molecular marker for rapid diagnosis and prediction of response to ATRA-and ATO-containing therapies. Tretinoin 114-118 PML nuclear body scaffold Homo sapiens 11-14
24038081-6 2014 The Hes6 promoter is specifically activated by the retinoic acid receptor (RAR) in response to its natural agonist ligand, all-trans retinoic acid (atRA), and is repressed by SHP. Tretinoin 123-146 retinoic acid receptor, alpha Mus musculus 75-78
24038081-6 2014 The Hes6 promoter is specifically activated by the retinoic acid receptor (RAR) in response to its natural agonist ligand, all-trans retinoic acid (atRA), and is repressed by SHP. Tretinoin 148-152 retinoic acid receptor, alpha Mus musculus 75-78
25112011-5 2014 In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. Tretinoin 13-15 Nanog homeobox Homo sapiens 138-143
25112011-5 2014 In addition, RA induced differentiation of H9 ESC coupled with morphology changes, decreased expression of undifferentiated markers Oct4, Nanog, Sox2 and OCT4 mRNA binding protein Lin28 at mRNA level, and reduced expression of Oct4 at protein level. Tretinoin 13-15 SRY-box transcription factor 2 Homo sapiens 145-149
24769646-3 2014 Treatment with ATRA induced significant myeloid differentiation accompanied by upregulation of RARalpha, C/EBPalpha, C/EBPe and PU.1 in MLL-AF9-positive but not in MLL-AF4/5q31-positive cells. Tretinoin 15-19 AF4/FMR2 family member 1 Homo sapiens 168-171
26119689-3 2015 In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1). Tretinoin 92-105 apolipoprotein A-I Mus musculus 174-191
26119689-3 2015 In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1). Tretinoin 92-105 apolipoprotein A-I Mus musculus 193-199
17124055-4 2006 The unique PML/RARalpha aberration serves as a molecular marker for rapid diagnosis and prediction of response to ATRA-and ATO-containing therapies. Tretinoin 114-118 retinoic acid receptor alpha Homo sapiens 15-23
26119689-3 2015 In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1). Tretinoin 107-111 apolipoprotein A-I Mus musculus 174-191
26119689-3 2015 In the present study, treatment of mouse macrophages with retinoids, particularly all-trans retinoic acid (atRA) and 9-cis RA, resulted in increases in cholesterol efflux to apolipoprotein AI (Apo-A1). Tretinoin 107-111 apolipoprotein A-I Mus musculus 193-199
16517207-0 2006 Increased expression of cyclin A1 protein is associated with all-trans retinoic acid-induced apoptosis. Tretinoin 71-84 cyclin A1 Homo sapiens 24-33
26263556-3 2015 To address the role of H3K27me3 in the retinoic acid (RA)-induced differentiation of the human carcinoma NCCIT cell line, we inhibited JMJD3 and UTX using the H3K27me3 demethylase inhibitor GSK-J4. Tretinoin 39-52 lysine demethylase 6B Homo sapiens 135-140
24739462-5 2014 The differentiation agent, retinoic acid, increases IKKalpha expression by suppressing EZH2-mediated H3K27 histone methylation, resulting in enhanced differentiation of NPC cells. Tretinoin 27-40 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 52-60
24566867-3 2014 In acute promyelocytic leukemia (APL), repression by the PML-RARalpha oncofusion protein is mediated by an HDAC-containing complex that can be dissociated by pharmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the expense of side effects and recurrence. Tretinoin 191-204 histone deacetylase 9 Homo sapiens 107-111
24566867-3 2014 In acute promyelocytic leukemia (APL), repression by the PML-RARalpha oncofusion protein is mediated by an HDAC-containing complex that can be dissociated by pharmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the expense of side effects and recurrence. Tretinoin 206-210 histone deacetylase 9 Homo sapiens 107-111
24566867-4 2014 We hypothesized that the context-specific close physical proximity of a retinoid and HDACi-binding protein in the repressive PML-RARalpha-HDAC complex may permit selective targeting by a hybrid molecule of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS-275, yielding MC2392. Tretinoin 206-210 histone deacetylase 9 Homo sapiens 85-89
24566867-4 2014 We hypothesized that the context-specific close physical proximity of a retinoid and HDACi-binding protein in the repressive PML-RARalpha-HDAC complex may permit selective targeting by a hybrid molecule of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS-275, yielding MC2392. Tretinoin 206-210 histone deacetylase 9 Homo sapiens 138-142
26263556-3 2015 To address the role of H3K27me3 in the retinoic acid (RA)-induced differentiation of the human carcinoma NCCIT cell line, we inhibited JMJD3 and UTX using the H3K27me3 demethylase inhibitor GSK-J4. Tretinoin 54-56 lysine demethylase 6B Homo sapiens 135-140
26225425-9 2015 CONCLUSIONS: AtRA induces TGF-beta2 expression in IECs via RhoA- and p38alpha MAPK-mediated activation of the transcription factor ATF2. Tretinoin 13-17 activating transcription factor 2 Homo sapiens 131-135
16517207-5 2006 In the present study, we investigated whether cyclin A1 might be involved in all-trans retinoic acid-induced apoptosis in U-937 leukemic cells. Tretinoin 87-100 cyclin A1 Homo sapiens 46-55
16517207-6 2006 We found that all-trans retinoic acid-induced apoptosis was associated with concomitant increase in cyclin A1 expression. Tretinoin 24-37 cyclin A1 Homo sapiens 100-109
16517207-10 2006 Further, U-937 cells overexpressing cyclin A1 appeared to be more sensitive to all-trans retinoic acid-induced apoptosis indicating the ability of cyclin A1 to mediate all-trans retinoic acid-induced apoptosis. Tretinoin 83-102 cyclin A1 Homo sapiens 36-45
26162091-4 2015 Moreover, RA modulated the DNA methylation of mESCs by altering the expression of epigenetic-associated genes such as Dnmt3b and Dnmt3l. Tretinoin 10-12 DNA (cytosine-5-)-methyltransferase 3-like Mus musculus 129-135
26142905-3 2015 The expression and subcellular distribution of two RA-binding proteins, FABP5 and CRABP2, has already been shown to play critical roles in breast cancer cell response to RA. Tretinoin 51-53 fatty acid binding protein 5 Homo sapiens 72-77
24496080-11 2014 Notably, this enhanced Ptch1 expression was preceded by induction of the homeobox transcription factor Meis1, a direct RA target. Tretinoin 119-121 Meis homeobox 1 Homo sapiens 103-108
24440757-0 2014 All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity. Tretinoin 0-23 microRNA 23a Homo sapiens 39-46
24440757-0 2014 All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity. Tretinoin 25-29 microRNA 23a Homo sapiens 39-46
26142905-3 2015 The expression and subcellular distribution of two RA-binding proteins, FABP5 and CRABP2, has already been shown to play critical roles in breast cancer cell response to RA. Tretinoin 51-53 cellular retinoic acid binding protein 2 Homo sapiens 82-88
16517207-10 2006 Further, U-937 cells overexpressing cyclin A1 appeared to be more sensitive to all-trans retinoic acid-induced apoptosis indicating the ability of cyclin A1 to mediate all-trans retinoic acid-induced apoptosis. Tretinoin 83-102 cyclin A1 Homo sapiens 147-156
26142905-17 2015 We propose that these three RA-binding proteins can serve as biomarkers for predicting triple-negative breast cancer response to RA, with elevated levels of either cytoplasmic CRABP1 or FABP5 associated with RA resistance, and elevated levels of nuclear CRABP2 associated with sensitivity to RA. Tretinoin 28-30 cellular retinoic acid binding protein 2 Homo sapiens 254-260
26142905-17 2015 We propose that these three RA-binding proteins can serve as biomarkers for predicting triple-negative breast cancer response to RA, with elevated levels of either cytoplasmic CRABP1 or FABP5 associated with RA resistance, and elevated levels of nuclear CRABP2 associated with sensitivity to RA. Tretinoin 129-131 cellular retinoic acid binding protein 2 Homo sapiens 254-260
16517207-10 2006 Further, U-937 cells overexpressing cyclin A1 appeared to be more sensitive to all-trans retinoic acid-induced apoptosis indicating the ability of cyclin A1 to mediate all-trans retinoic acid-induced apoptosis. Tretinoin 89-102 cyclin A1 Homo sapiens 36-45
26142905-17 2015 We propose that these three RA-binding proteins can serve as biomarkers for predicting triple-negative breast cancer response to RA, with elevated levels of either cytoplasmic CRABP1 or FABP5 associated with RA resistance, and elevated levels of nuclear CRABP2 associated with sensitivity to RA. Tretinoin 129-131 cellular retinoic acid binding protein 2 Homo sapiens 254-260
25991548-0 2015 A Brn2-Zic1 axis specifies the neuronal fate of retinoic-acid-treated embryonic stem cells. Tretinoin 48-61 zinc finger protein of the cerebellum 1 Mus musculus 7-11
24388784-2 2014 We have investigated if neuron specific anti-betaIII-tubulin antibodies are useful in a microplate assay of neurite outgrowth of retinoic acid-induced neurons from mouse P19 embryonal carcinoma cells. Tretinoin 129-142 tubulin, beta 3 class III Mus musculus 45-60
16517207-10 2006 Further, U-937 cells overexpressing cyclin A1 appeared to be more sensitive to all-trans retinoic acid-induced apoptosis indicating the ability of cyclin A1 to mediate all-trans retinoic acid-induced apoptosis. Tretinoin 89-102 cyclin A1 Homo sapiens 147-156
25991548-7 2015 Small hairpin RNA (shRNA)-mediated silencing of Zic1 prevented ESCs from differentiating into neuronal precursors, thus defining a hierarchical Brn2-Zic1 axis that is essential to specify neural fate in retinoic-acid-treated ESCs. Tretinoin 203-216 zinc finger protein of the cerebellum 1 Mus musculus 48-52
16517207-12 2006 Our results indicate that cyclin A1 might have a role in apoptosis by mediating all-trans retinoic acid-induced apoptosis. Tretinoin 90-103 cyclin A1 Homo sapiens 26-35
24584857-4 2014 In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 96-109 hexokinase 3 Homo sapiens 52-55
16837774-7 2006 The results show an increased uptake of atROH in intimal SMCs compared to medial SMCs as well as increased expression of the retinoid-metabolizing enzymes retinol dehydrogenase-5 and retinal dehydrogenase-1 and, in conjunction with this gene expression, increased production of all-trans retinoic acid (atRA). Tretinoin 288-301 aldehyde dehydrogenase 1 family member A1 Homo sapiens 183-206
24584857-4 2014 In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Tretinoin 111-115 hexokinase 3 Homo sapiens 52-55
24548459-8 2014 We found that day 7 MCs differentiated in the presence of RA had an increase in the percent positive and relative expression levels of both maturation (CD80, CD86, and MHCII) and inhibitory (PD-L1 and PD-L2) markers compared to control cells. Tretinoin 58-60 programmed cell death 1 ligand 2 Homo sapiens 201-206
26146052-5 2015 RESULTS: Compared with NB4 cells treated with ATRA alone, NB4 cells treated with ATRA plus TNF-alpha showed slower proliferation and a higher rate of apoptosis during the whole process of differentiation, and had a higher ratio of CD11b positive cells on the second day of differentiation. Tretinoin 81-85 integrin subunit alpha M Homo sapiens 231-236
24548459-10 2014 CONCLUSION: RA induced mature regulatory myeloid cells that were suppressive and had a CD11b+ CD11c-Ly6C low/intermediate monocyte phenotype. Tretinoin 12-14 integrin subunit alpha M Homo sapiens 87-92
16837774-7 2006 The results show an increased uptake of atROH in intimal SMCs compared to medial SMCs as well as increased expression of the retinoid-metabolizing enzymes retinol dehydrogenase-5 and retinal dehydrogenase-1 and, in conjunction with this gene expression, increased production of all-trans retinoic acid (atRA). Tretinoin 303-307 aldehyde dehydrogenase 1 family member A1 Homo sapiens 183-206
16083310-0 2006 Inhibition of vascular endothelial growth factor-induced retinal neovascularization by retinoic acid in experimental retinopathy of prematurity. Tretinoin 87-100 vascular endothelial growth factor A Rattus norvegicus 14-48
24360906-9 2014 In addition, they may modulate the transcriptional output of multiple signaling pathways involved in neural crest development (Wnt, Retinoic Acid) through the induction of key pathway regulators (Axin2 and Cyp26c1). Tretinoin 132-145 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 206-213
24570662-8 2014 Moreover, we show that the beneficial effect of RA on memory is associated to an increase in hippocampal PSD-95 expression. Tretinoin 48-50 discs large MAGUK scaffold protein 4 Mus musculus 105-111
26101153-5 2015 Among them we show that retinaldehyde dehydrogenase 2 (RALDH2) and lipocalin-type prostaglandin D2 synthase (LPGDS), which, respectively, regulate the synthesis and transport of RA, directly participate in the establishment of the PPR. Tretinoin 55-57 aldehyde dehydrogenase 1 family member A2 Homo sapiens 24-53
16083310-3 2006 The aim of this study was to demonstrate the preventive effect of retinoic acid (RA) on the VEGF-induced retinal neovascularization in a rat model of ROP. Tretinoin 66-79 vascular endothelial growth factor A Rattus norvegicus 92-96
24570662-11 2014 Interestingly, RA treatment induces a modulation of RA receptors RARalpha and RARbeta expression in middle-aged mice, a finding which has been correlated with the amplitude of intrahippocampal CORT levels after novelty-induced stress. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 65-73
25451588-3 2015 The reductive reaction catalysed by DHRS3 seems to be physiological, and recent studies proved the importance of DHRS3 for maintaining suitable retinoic acid levels during embryonic development in vivo. Tretinoin 144-157 dehydrogenase/reductase 3 Homo sapiens 36-41
16083310-3 2006 The aim of this study was to demonstrate the preventive effect of retinoic acid (RA) on the VEGF-induced retinal neovascularization in a rat model of ROP. Tretinoin 81-83 vascular endothelial growth factor A Rattus norvegicus 92-96
25451588-3 2015 The reductive reaction catalysed by DHRS3 seems to be physiological, and recent studies proved the importance of DHRS3 for maintaining suitable retinoic acid levels during embryonic development in vivo. Tretinoin 144-157 dehydrogenase/reductase 3 Homo sapiens 113-118
16083310-13 2006 The VEGF immunostaining score significantly decreased in the RA-treated ROP group compared to that in the saline-administered ROP group. Tretinoin 61-63 vascular endothelial growth factor A Rattus norvegicus 4-8
24503540-5 2014 We found that ASCs cultured with ATRA or transfected with miRNA let-7e expressed epithelial markers such as cytokeratin-18 and early renal organogenesis markers such as Pax2, Wt1, Wnt4 and megalin. Tretinoin 33-37 paired box 2 Homo sapiens 169-173
16083310-14 2006 RA treatment might be beneficial in preventing neovascularization resulting from oxygen-induced retinopathy by downregulation of VEGF expression. Tretinoin 0-2 vascular endothelial growth factor A Rattus norvegicus 129-133
24503540-5 2014 We found that ASCs cultured with ATRA or transfected with miRNA let-7e expressed epithelial markers such as cytokeratin-18 and early renal organogenesis markers such as Pax2, Wt1, Wnt4 and megalin. Tretinoin 33-37 Wnt family member 4 Homo sapiens 180-184
16251210-5 2005 A dominant-negative form of the retinoic acid receptor alpha (DNhRARalpha) was expressed in the chick retina to block RA activity. Tretinoin 65-67 retinoic acid receptor alpha Gallus gallus 32-60
24412064-1 2014 Retinoic acid (RA)-inducible gene I (RIG-I) is highly upregulated and functionally implicated in the RA-induced maturation of acute myeloid leukemia (AML) blasts. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 37-42
24412064-1 2014 Retinoic acid (RA)-inducible gene I (RIG-I) is highly upregulated and functionally implicated in the RA-induced maturation of acute myeloid leukemia (AML) blasts. Tretinoin 15-17 DExD/H-box helicase 58 Homo sapiens 37-42
24412064-1 2014 Retinoic acid (RA)-inducible gene I (RIG-I) is highly upregulated and functionally implicated in the RA-induced maturation of acute myeloid leukemia (AML) blasts. Tretinoin 101-103 DExD/H-box helicase 58 Homo sapiens 37-42
25809880-7 2015 Similar to Fgf8, Wnt8a requires retinoic acid (RA) signaling to restrict its caudal expression boundary and possesses an upstream RA response element that binds RA receptors. Tretinoin 32-45 Wnt family member 8A Homo sapiens 17-22
25809880-7 2015 Similar to Fgf8, Wnt8a requires retinoic acid (RA) signaling to restrict its caudal expression boundary and possesses an upstream RA response element that binds RA receptors. Tretinoin 47-49 Wnt family member 8A Homo sapiens 17-22
25809880-7 2015 Similar to Fgf8, Wnt8a requires retinoic acid (RA) signaling to restrict its caudal expression boundary and possesses an upstream RA response element that binds RA receptors. Tretinoin 130-132 Wnt family member 8A Homo sapiens 17-22
25941336-0 2015 RAI2: Linking Retinoic Acid Signaling with Metastasis Suppression. Tretinoin 14-27 retinoic acid induced 2 Homo sapiens 0-4
16251210-7 2005 Blocking RA signaling by misexpression of a RA degrading enzyme, Cyp26A1 recapitulated some but not all the effects of DNhRARalpha. Tretinoin 9-11 cytochrome P450 family 26 subfamily A member 1 Gallus gallus 65-72
25843403-5 2015 Moreover, RA-induced AMPAR trafficking utilized the Q-SNARE syntaxin-4, whereas LTP utilized syntaxin-3; both additionally required the Q-SNARE SNAP-47 and the R-SNARE synatobrevin-2. Tretinoin 10-12 syntaxin 4 Homo sapiens 60-70
24395056-10 2014 The 2-nM retinoic acid exposure also led to alterations of neurobehavior- and optic nerve-related genes, with the transforming growth factor-beta signal transduction inhibitor noggin (nog) and the spinal cord marker homeobox c3a (hox) being underexpressed and the retinal G protein-coupled receptor a (rgr), the photoreceptor cell marker rhodopsin (rho), and the short wave-sensitive cone pigment opsin 1 (opn1sw1) being overexpressed. Tretinoin 9-22 retinal G protein coupled receptor a Danio rerio 264-300
24395056-10 2014 The 2-nM retinoic acid exposure also led to alterations of neurobehavior- and optic nerve-related genes, with the transforming growth factor-beta signal transduction inhibitor noggin (nog) and the spinal cord marker homeobox c3a (hox) being underexpressed and the retinal G protein-coupled receptor a (rgr), the photoreceptor cell marker rhodopsin (rho), and the short wave-sensitive cone pigment opsin 1 (opn1sw1) being overexpressed. Tretinoin 9-22 retinal G protein coupled receptor a Danio rerio 302-305
25941627-5 2015 Our results show that VAF347 enhanced RA-induced cell cycle arrest, CD11b integrin expression and neutrophil respiratory burst. Tretinoin 38-40 integrin subunit alpha M Homo sapiens 68-73
16251210-7 2005 Blocking RA signaling by misexpression of a RA degrading enzyme, Cyp26A1 recapitulated some but not all the effects of DNhRARalpha. Tretinoin 44-46 cytochrome P450 family 26 subfamily A member 1 Gallus gallus 65-72
25742746-8 2015 We conclude that ATRA downregulates ALDH1/FoxM1/Notch1 signalling and suppresses tumour formation in ovarian cancer cells. Tretinoin 17-21 forkhead box M1 Homo sapiens 42-47
24475288-8 2014 Forced expression of NANOG prevented the induction of resistance to cisplatin by retinoic acid. Tretinoin 81-94 Nanog homeobox Homo sapiens 21-26
16275619-5 2005 When the kinetics of B cells with different phenotypic characteristics were monitored during 9 days culture period by flow cytometric analysis, it displayed the increase of the B cells with plasma cell phenotype (CD38+/CD20-/IgD-) in the presence of RA. Tretinoin 250-252 CD38 molecule Homo sapiens 213-217
24269351-5 2014 Changes observed in the expression of factors involved in the retinoid pathway under ATRA, namely an upregulation of CRBP and CRABP2, were also reflected in GCT tissues of different histologies, providing further insight into factors involved in the differentiation of these pluripotent tumors. Tretinoin 85-89 cellular retinoic acid binding protein 2 Homo sapiens 126-132
16102944-8 2005 RESULTS: EGCG, like RA, decreased the level of MMPs production and increased TIMP-1 expression level. Tretinoin 20-22 matrix metallopeptidase 1 Homo sapiens 47-51
25477000-7 2015 Furthermore, we have identified a novel pathway involving all-trans retinoic acid (ATRA) and its receptor (RARgamma) signaling that inhibits type I NKT cells and, consequently, ALD. Tretinoin 83-87 retinoic acid receptor, gamma Mus musculus 107-115
16102944-10 2005 RA decreased the MMP-1 and MMP-3 expression levels to a greater extent than EGCG. Tretinoin 0-2 matrix metallopeptidase 1 Homo sapiens 17-22
25793304-1 2015 BACKGROUND/OBJECTIVES: Retinaldehyde dehydrogenase 2 (RALDH2) has been implicated in regulating all-trans-retinoic acid (atRA) synthesis in response to visual signals in animal models of myopia. Tretinoin 96-119 aldehyde dehydrogenase 1 family member A2 Homo sapiens 23-52
25793304-1 2015 BACKGROUND/OBJECTIVES: Retinaldehyde dehydrogenase 2 (RALDH2) has been implicated in regulating all-trans-retinoic acid (atRA) synthesis in response to visual signals in animal models of myopia. Tretinoin 96-119 aldehyde dehydrogenase 1 family member A2 Homo sapiens 54-60
23810783-11 2014 Furthermore, our immunofluorescent microscopy and Western blotting assays indicated that Pitx1 was mainly expressed in the cartilage nodules and the levels of Pitx1, Sox9 and Col2al were also downregulated by ATRA dose-dependently. Tretinoin 209-213 paired-like homeodomain 1 Rattus norvegicus 89-94
23810783-11 2014 Furthermore, our immunofluorescent microscopy and Western blotting assays indicated that Pitx1 was mainly expressed in the cartilage nodules and the levels of Pitx1, Sox9 and Col2al were also downregulated by ATRA dose-dependently. Tretinoin 209-213 paired-like homeodomain 1 Rattus norvegicus 159-164
23810783-11 2014 Furthermore, our immunofluorescent microscopy and Western blotting assays indicated that Pitx1 was mainly expressed in the cartilage nodules and the levels of Pitx1, Sox9 and Col2al were also downregulated by ATRA dose-dependently. Tretinoin 209-213 SRY-box transcription factor 9 Rattus norvegicus 166-170
25793304-1 2015 BACKGROUND/OBJECTIVES: Retinaldehyde dehydrogenase 2 (RALDH2) has been implicated in regulating all-trans-retinoic acid (atRA) synthesis in response to visual signals in animal models of myopia. Tretinoin 121-125 aldehyde dehydrogenase 1 family member A2 Homo sapiens 23-52
25793304-1 2015 BACKGROUND/OBJECTIVES: Retinaldehyde dehydrogenase 2 (RALDH2) has been implicated in regulating all-trans-retinoic acid (atRA) synthesis in response to visual signals in animal models of myopia. Tretinoin 121-125 aldehyde dehydrogenase 1 family member A2 Homo sapiens 54-60
24416428-4 2014 ATRA rapidly activated p38-MSK (mitogen- and stress activated protein kinase) cascade to phosphorylate cAMP response element-binding protein (CREB). Tretinoin 0-4 cAMP responsive element binding protein 1 Homo sapiens 103-140
16195347-9 2005 Retinoic acid triggers Oct4 down-regulation, de novo activation of A-type lamins, and nestin. Tretinoin 0-13 POU class 5 homeobox 1 Homo sapiens 23-27
24416428-4 2014 ATRA rapidly activated p38-MSK (mitogen- and stress activated protein kinase) cascade to phosphorylate cAMP response element-binding protein (CREB). Tretinoin 0-4 cAMP responsive element binding protein 1 Homo sapiens 142-146
25742608-0 2015 Correction: ATRA-induced cellular differentiation and CD38 expression inhibits acquisition of BCR-ABL mutations for CML acquired resistance. Tretinoin 12-16 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 94-101
25435432-6 2015 Activated NF-kappaB enhanced the degree of ATRA-induced differentiation of HL-60 cells to macrophages, rather than granulocytes, as assessed by morphologic examination and expressions of differentiation markers such as CD11b, CD38, CD68, MMP9 and Btg2. Tretinoin 43-47 integrin subunit alpha M Homo sapiens 219-224
25435432-6 2015 Activated NF-kappaB enhanced the degree of ATRA-induced differentiation of HL-60 cells to macrophages, rather than granulocytes, as assessed by morphologic examination and expressions of differentiation markers such as CD11b, CD38, CD68, MMP9 and Btg2. Tretinoin 43-47 CD68 molecule Homo sapiens 232-236
25435432-6 2015 Activated NF-kappaB enhanced the degree of ATRA-induced differentiation of HL-60 cells to macrophages, rather than granulocytes, as assessed by morphologic examination and expressions of differentiation markers such as CD11b, CD38, CD68, MMP9 and Btg2. Tretinoin 43-47 matrix metallopeptidase 9 Homo sapiens 238-242
24264050-2 2014 To better understand the mechanism underlying OST gene regulation, the effects of retinoic acid (RA) on OSTalpha/beta gene expression were investigated. Tretinoin 82-95 solute carrier family 51 subunit alpha Homo sapiens 104-117
16287870-5 2005 Here we show that interfering with RA signal through RARalpha (which was achieved by use of a dominant-negative RARalpha, by downregulation of RARalpha by RNA interference, and by use of RARalpha antagonists) induces an exacerbation of the repressed chromatin status of RARbeta2 and leads to RARbeta2 transcriptional silencing. Tretinoin 35-37 retinoic acid receptor alpha Homo sapiens 53-61
25036122-0 2014 Attenuation of migration properties of CD4+ T cells from aged mice correlates with decrease in chemokine receptor expression, response to retinoic acid, and RALDH expression compared to young mice. Tretinoin 138-151 CD4 antigen Mus musculus 39-42
25773996-4 2015 We selected these cells with Geneticin-418 to obtain BDNF-BMSCs, which were induced with retinoic acid to obtain induced BDNF-BMSCs. Tretinoin 89-102 brain derived neurotrophic factor Homo sapiens 53-57
25773996-4 2015 We selected these cells with Geneticin-418 to obtain BDNF-BMSCs, which were induced with retinoic acid to obtain induced BDNF-BMSCs. Tretinoin 89-102 brain derived neurotrophic factor Homo sapiens 121-125
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 17-30 CD4 antigen Mus musculus 37-40
16287870-5 2005 Here we show that interfering with RA signal through RARalpha (which was achieved by use of a dominant-negative RARalpha, by downregulation of RARalpha by RNA interference, and by use of RARalpha antagonists) induces an exacerbation of the repressed chromatin status of RARbeta2 and leads to RARbeta2 transcriptional silencing. Tretinoin 35-37 retinoic acid receptor alpha Homo sapiens 112-120
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 17-30 chemokine (C-C motif) receptor 9 Mus musculus 84-88
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 17-30 CD4 antigen Mus musculus 158-161
16287870-5 2005 Here we show that interfering with RA signal through RARalpha (which was achieved by use of a dominant-negative RARalpha, by downregulation of RARalpha by RNA interference, and by use of RARalpha antagonists) induces an exacerbation of the repressed chromatin status of RARbeta2 and leads to RARbeta2 transcriptional silencing. Tretinoin 35-37 retinoic acid receptor alpha Homo sapiens 112-120
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 32-34 CD4 antigen Mus musculus 37-40
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 32-34 chemokine (C-C motif) receptor 9 Mus musculus 84-88
25239070-4 2015 Since retinoid is a potential patterning influence on the developing face, we have examined whether retinoic acid (RA) signaling regulated Lhx8, Msx1 and Msx2 transcription through fibroblast growth factor (FGF) signals in the maxillary prominence. Tretinoin 115-117 msh homeobox 1 Gallus gallus 145-149
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 147-166
25036122-4 2014 Upon addition of retinoic acid (RA), CD4(+) T cells from aged mice showed decreased CCR9 expression level compared to young mice and the migration ability of CD4(+) T cells from aged mice toward CCL25 was attenuated compared to young mice. Tretinoin 32-34 CD4 antigen Mus musculus 158-161
16287870-5 2005 Here we show that interfering with RA signal through RARalpha (which was achieved by use of a dominant-negative RARalpha, by downregulation of RARalpha by RNA interference, and by use of RARalpha antagonists) induces an exacerbation of the repressed chromatin status of RARbeta2 and leads to RARbeta2 transcriptional silencing. Tretinoin 35-37 retinoic acid receptor alpha Homo sapiens 112-120
24310731-3 2014 Our results indicated that atRA and retinol could induce GM-CSF and IL-16 expression, whereas all these tested substances enhanced MMP-9 production. Tretinoin 27-31 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 57-63
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 168-171
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 147-166
24310731-3 2014 Our results indicated that atRA and retinol could induce GM-CSF and IL-16 expression, whereas all these tested substances enhanced MMP-9 production. Tretinoin 27-31 interleukin 16 Mus musculus 68-73
24310731-5 2014 AtRA and retinol affected GM-CSF and IL-16 expression mainly through RA receptor beta (RARbeta). Tretinoin 0-4 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 26-32
16287870-8 2005 Conversely, we demonstrate that restoration of RA signal at a silent RARbeta2 through RARalpha leads to RARbeta2 reactivation. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 86-94
24310731-5 2014 AtRA and retinol affected GM-CSF and IL-16 expression mainly through RA receptor beta (RARbeta). Tretinoin 0-4 interleukin 16 Mus musculus 37-42
25134739-1 2015 Retinoic acid (RA) is a terpenoid that is synthesized from vitamin A/retinol (ROL) and binds to the nuclear receptors retinoic acid receptor (RAR)/retinoid X receptor (RXR) to control multiple developmental processes in vertebrates. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 168-171
16279945-8 2005 Retinoic acid treatment of two neuroblastoma cell lines upregulated the expression of both APLP2 and ADAM10, thus leading to an increased release of soluble APLP2. Tretinoin 0-13 a disintegrin and metallopeptidase domain 10 Mus musculus 101-107
25468951-0 2015 Impact of retinoic acid exposure on midfacial shape variation and manifestation of holoprosencephaly in Twsg1 mutant mice. Tretinoin 10-23 twisted gastrulation BMP signaling modulator 1 Mus musculus 104-109
25468951-3 2015 The goal of this study was to examine whether mice carrying a mutation in a gene encoding the bone morphogenetic protein (BMP) antagonist twisted gastrulation (Twsg1), which is associated with a low penetrance of HPE, are sensitized to retinoic acid (RA) teratogenesis. Tretinoin 236-249 twisted gastrulation BMP signaling modulator 1 Mus musculus 160-165
25468951-3 2015 The goal of this study was to examine whether mice carrying a mutation in a gene encoding the bone morphogenetic protein (BMP) antagonist twisted gastrulation (Twsg1), which is associated with a low penetrance of HPE, are sensitized to retinoic acid (RA) teratogenesis. Tretinoin 251-253 twisted gastrulation BMP signaling modulator 1 Mus musculus 160-165
25468951-7 2015 Although only 7% of wild-type embryos exposed to RA showed overt HPE or neural tube defects (NTDs), 100% of Twsg1(-/-) mutants exposed to RA manifested severe HPE compared to 17% without RA. Tretinoin 138-140 twisted gastrulation BMP signaling modulator 1 Mus musculus 108-113
25468951-7 2015 Although only 7% of wild-type embryos exposed to RA showed overt HPE or neural tube defects (NTDs), 100% of Twsg1(-/-) mutants exposed to RA manifested severe HPE compared to 17% without RA. Tretinoin 138-140 twisted gastrulation BMP signaling modulator 1 Mus musculus 108-113
23653115-6 2014 In humans, IL-22BP was expressed in immature monocyte-derived DC and strongly induced by retinoic acid but dramatically reduced upon maturation. Tretinoin 89-102 interleukin 22 receptor subunit alpha 2 Homo sapiens 11-18
25030439-0 2014 Effect of 9-cis retinoic acid and all-trans retinoic acid in combination with verapamil on P-glycoprotein expression in L1210 cells. Tretinoin 16-29 retinol dehydrogenase 5 Mus musculus 10-15
25030439-0 2014 Effect of 9-cis retinoic acid and all-trans retinoic acid in combination with verapamil on P-glycoprotein expression in L1210 cells. Tretinoin 16-29 phosphoglycolate phosphatase Mus musculus 91-105
25030439-3 2014 Several authors have described the induction of P-gp expression/activity in malignant cell lines after treatment with all-trans retinoic acid (AtRA; ligand of retinoic acid nuclear receptors, RARs). Tretinoin 122-141 phosphoglycolate phosphatase Mus musculus 48-52
25030439-3 2014 Several authors have described the induction of P-gp expression/activity in malignant cell lines after treatment with all-trans retinoic acid (AtRA; ligand of retinoic acid nuclear receptors, RARs). Tretinoin 143-147 phosphoglycolate phosphatase Mus musculus 48-52
25030439-4 2014 An isomer of AtRA also exists, 9-cis retinoic acid, which is a ligand of both RARs and nuclear retinoid X receptors (RXRs). Tretinoin 13-17 retinol dehydrogenase 5 Mus musculus 31-36
25030439-5 2014 In a previous work, we described that the combined treatment of R cells with verapamil and AtRA induces the downregulation of P-gp expression/activity. Tretinoin 91-95 phosphoglycolate phosphatase Mus musculus 126-130
25030439-6 2014 In the current study, we studied the expression of RARs and RXRs in S, R and T cells and the effects of treatment with AtRA, 9cRA and verapamil on P-gp expression, cellular localization and efflux activity in R and T cells. Tretinoin 119-123 phosphoglycolate phosphatase Mus musculus 147-151
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 359-363 retinoic acid receptor alpha Homo sapiens 73-101
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 359-363 retinoic acid receptor alpha Homo sapiens 103-111
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 359-363 interferon gamma receptor 1 Homo sapiens 199-218
25389133-3 2015 atRA signaling was ablated in beta-cells by overexpressing a dominant-negative retinoic acid receptor (RAR)-alpha mutant (RARdn) using an inducible Cre-Lox system under the control of the pancreas duodenal homeobox gene promoter. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 103-113
16040168-5 2005 The IgG2a/IgG1 ratio was lower in mice treated with ATRA. Tretinoin 52-56 immunoglobulin heavy variable V1-9 Mus musculus 4-9
25335858-6 2015 Conversely, over-expression of Hes5 in pMN-like progenitor cells during the differentiation interfered with retinoic acid- and purmorphamine-induced motor neuron differentiation and inhibited the emergence of motor neurons. Tretinoin 108-121 hes family bHLH transcription factor 5 Homo sapiens 31-35
15964596-7 2005 These results suggest that the possible perinatal RA production by RALDHs might regulate various RA-target genes including CRBPII and RARalpha through RXRalpha or HNF-4 in the small intestine. Tretinoin 50-52 retinol binding protein 2 Rattus norvegicus 123-129
25120220-3 2015 A highly conserved complex retinoic acid response element (RARE) is located 485 base pairs (bp) upstream of exon 2B in the promoter of the Nedd9 gene. Tretinoin 27-40 neural precursor cell expressed, developmentally down-regulated gene 9 Mus musculus 139-144
25120220-7 2015 When the 5.2 kb construct is modified (eight point mutations) to eliminate responsiveness of the RARE to all-trans retinoic acid (atRA) [Nedd9(mutRARE)-lacZ], virtually all beta-galactosidase (beta-gal, lacZ) expression is lost. Tretinoin 115-128 neural precursor cell expressed, developmentally down-regulated gene 9 Mus musculus 137-142
25120220-7 2015 When the 5.2 kb construct is modified (eight point mutations) to eliminate responsiveness of the RARE to all-trans retinoic acid (atRA) [Nedd9(mutRARE)-lacZ], virtually all beta-galactosidase (beta-gal, lacZ) expression is lost. Tretinoin 130-134 neural precursor cell expressed, developmentally down-regulated gene 9 Mus musculus 137-142
25120220-9 2015 Thus the RARE upstream of the Nedd9 2B promoter is necessary for much of the endogenous gene expression during early development as well as ectopic expression in response to atRA. Tretinoin 174-178 neural precursor cell expressed, developmentally down-regulated gene 9 Mus musculus 30-35
25749095-2 2015 Thus, RA enhanced autophagy in TLR9- and CD180-stimulated peripheral blood B cells, as revealed by increased levels of the autophagosomal marker LC3B-II, enhanced colocalization between LC3B and the lysosomal marker Lyso-ID, by a larger percentage of cells with more than 5 characteristic LC3B puncta, and by the concomitant reduction in the level of SQSTM1/p62. Tretinoin 6-8 sequestosome 1 Homo sapiens 351-357
25749095-2 2015 Thus, RA enhanced autophagy in TLR9- and CD180-stimulated peripheral blood B cells, as revealed by increased levels of the autophagosomal marker LC3B-II, enhanced colocalization between LC3B and the lysosomal marker Lyso-ID, by a larger percentage of cells with more than 5 characteristic LC3B puncta, and by the concomitant reduction in the level of SQSTM1/p62. Tretinoin 6-8 sequestosome 1 Homo sapiens 358-361
25208926-7 2015 Evidence that such genes may be targets of regulation via RA signalling initiated by ALDH1A activity was provided by the TNFRSF10B gene, encoding the apoptotic death receptor TNFRSF10B (also termed TRAIL-R2), which negatively correlated with ALDH1A2 and showed elevated transcription following treatment of T-ALL cell lines with the ALDH1A inhibitor citral (3,7-dimethyl-2,6-octadienal). Tretinoin 58-60 aldehyde dehydrogenase 1 family member A2 Homo sapiens 242-249
15964596-7 2005 These results suggest that the possible perinatal RA production by RALDHs might regulate various RA-target genes including CRBPII and RARalpha through RXRalpha or HNF-4 in the small intestine. Tretinoin 50-52 retinoic acid receptor, alpha Rattus norvegicus 134-142
15964596-7 2005 These results suggest that the possible perinatal RA production by RALDHs might regulate various RA-target genes including CRBPII and RARalpha through RXRalpha or HNF-4 in the small intestine. Tretinoin 50-52 hepatocyte nuclear factor 4, alpha Rattus norvegicus 163-168
26036413-1 2015 Article title: The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid. Tretinoin 119-132 MDS1 and EVI1 complex locus Homo sapiens 28-32
16316409-8 2005 As CRABPI was elevated far more than any other genes, we observed that the retinoids, all-trans retinoic acid and 9-cis retinoic acid, that bind CRABPI, promoted nitroblue tetrazolium-associated functional cell differentiation in p75NTR PC-3 cells, but not in neo control PC-3 cells. Tretinoin 96-109 nerve growth factor receptor Homo sapiens 230-236
16142401-6 2005 RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. Tretinoin 97-101 retinoic acid receptor alpha Homo sapiens 0-9
25403801-7 2015 In addition, the high levels of tumor necrosis factor-alpha, interleukin-1beta, and receptor activator of nuclear factor-kappa B ligand (RANKL) expression induced by LPS were inhibited after treatment with atRA. Tretinoin 206-210 TNF superfamily member 11 Homo sapiens 84-135
25403801-7 2015 In addition, the high levels of tumor necrosis factor-alpha, interleukin-1beta, and receptor activator of nuclear factor-kappa B ligand (RANKL) expression induced by LPS were inhibited after treatment with atRA. Tretinoin 206-210 TNF superfamily member 11 Homo sapiens 137-142
16142401-6 2005 RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. Tretinoin 97-101 retinoic acid receptor alpha Homo sapiens 0-3
26278415-0 2015 All-trans-retinoic acid modulates nitric oxide and interleukin-17A production by peripheral blood mononuclear cells from patients with Alzheimer"s disease. Tretinoin 0-23 interleukin 17A Homo sapiens 51-66
16142401-6 2005 RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. Tretinoin 97-101 retinoic acid receptor alpha Homo sapiens 14-17
16051514-2 2005 The exposed RNA template of hTR is an ideal target for antisense oligonucleotides (As-ODN); while recent findings indicate all-trans retinoid acid (ATRA) could effectively inhibit the expression of catalytic subunit-hTERT. Tretinoin 148-152 telomerase reverse transcriptase Homo sapiens 216-221
25721651-14 2015 Thus, our data suggest that LRAT overexpression represents a novel mechanism by which tumor cells can escape high supplementary ATRA levels that mediate tumor-suppressive RAR signaling. Tretinoin 128-132 retinoic acid receptor, alpha Mus musculus 171-174
16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 3-16 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-39
26401661-4 2015 These 2 ovarian factors, together with retinoic acid (RA) action, promote feminization partially through the repression of the masculinizing activities of SOX9, FGF9 and DMRT1. Tretinoin 39-52 fibroblast growth factor 9 Homo sapiens 161-165
26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 interleukin 17A Homo sapiens 177-183
25446536-6 2014 We also show that retinoic acid (RA) can inhibit the myogenic activity of FGF18 and that blocking RA signalling allows premature induction of MyoD by FGF18 at HH19. Tretinoin 18-31 fibroblast growth factor 18 Gallus gallus 74-79
25446536-6 2014 We also show that retinoic acid (RA) can inhibit the myogenic activity of FGF18 and that blocking RA signalling allows premature induction of MyoD by FGF18 at HH19. Tretinoin 33-35 fibroblast growth factor 18 Gallus gallus 74-79
25446536-6 2014 We also show that retinoic acid (RA) can inhibit the myogenic activity of FGF18 and that blocking RA signalling allows premature induction of MyoD by FGF18 at HH19. Tretinoin 98-100 fibroblast growth factor 18 Gallus gallus 150-155
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 141-154 retinoid X receptor alpha Homo sapiens 90-115
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 245-249 retinoid X receptor alpha Homo sapiens 90-115
25230277-6 2014 The activation of NEK2 in myeloma cells relied on the ALDH1A1-dependent generation of the retinoid X receptor alpha (RXRalpha) ligand, 9-cis retinoic acid (9CRA) - not the retinoic acid receptor alpha (RARalpha) ligand, all-trans retinoic acid (ATRA). Tretinoin 245-249 retinoid X receptor alpha Homo sapiens 117-125
25173565-0 2014 RARgamma-C-Fos-PPARgamma2 signaling rather than ROS generation is critical for all-trans retinoic acid-inhibited adipocyte differentiation. Tretinoin 89-102 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-14
25173565-12 2014 ATRA induced a profound interaction between RARgamma and C-Fos protein, reflected by Co-IP results. Tretinoin 0-4 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 44-48 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 44-48 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 297-301 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88
25173565-14 2014 RARgamma inhibitor significantly suppressed ATRA-inhibited DNA binding activity of C-Fos to PPARgamma2 promoter, indicating that downregulation of C-Fos activity mediated activation of RARgamma-exerted reduction of PPARgamma2 expression and thus inhibition of adipocyte differentiation induced by ATRA. Tretinoin 297-301 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152
25540002-3 2014 Considering growing evidence indicating that SOX2 expression level must be tightly controlled for proper neural development, the aim of this research was to analyze the effects of constitutive SOX2 overexpression on outcome of retinoic acid-induced neural differentiation of pluripotent NT2/D1 cells. Tretinoin 227-240 SRY-box transcription factor 2 Homo sapiens 193-197
25201493-3 2014 The present study investigated the effects of ATRA on the expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1alpha (HIF-1alpha) in various glioma cell lines under normoxia and hypoxia. Tretinoin 46-50 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 118-149
25201493-9 2014 Following ATRA treatment, the expression of VEGF and HIF-1alpha was found to vary among the different concentration groups. Tretinoin 10-14 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 53-63
25201493-10 2014 In the glioma cells in the lower concentration groups (5 and 10 micromol/l ATRA), a significant increase in VEGF and HIF-1alpha expression was observed. Tretinoin 75-79 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 117-127
25201493-11 2014 Conversely, a significant decrease in VEGF and HIF-1alpha expression was found in the glioma cells in the high ATRA concentration group (40 micromol/l), compared with that in the cells in the control group. Tretinoin 111-115 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 47-57
25175738-8 2014 All-trans RA also decreased the hepatic mRNA levels of Lrh-1 (Nr5a2) and Hnf4alpha (Nr2a1), which positively regulate the gene expression of Cyp7a1 and Cyp8b1. Tretinoin 10-12 hepatic nuclear factor 4, alpha Mus musculus 73-82
25175738-8 2014 All-trans RA also decreased the hepatic mRNA levels of Lrh-1 (Nr5a2) and Hnf4alpha (Nr2a1), which positively regulate the gene expression of Cyp7a1 and Cyp8b1. Tretinoin 10-12 hepatic nuclear factor 4, alpha Mus musculus 84-89
25175738-9 2014 Moreover, all-trans RA induced the gene expression levels of negative regulators of bile acid synthesis including hepatic Fgfr4, Fxr, and Shp (Nr0b2) as well as ileal Fgf15. Tretinoin 20-22 nuclear receptor subfamily 0, group B, member 2 Mus musculus 138-141
25175738-9 2014 Moreover, all-trans RA induced the gene expression levels of negative regulators of bile acid synthesis including hepatic Fgfr4, Fxr, and Shp (Nr0b2) as well as ileal Fgf15. Tretinoin 20-22 nuclear receptor subfamily 0, group B, member 2 Mus musculus 143-148
25175738-12 2014 The data suggest that all-trans RA-induced SHP may contribute to the inhibition of CYP7A1 and CYP8B1, which in turn reduces bile acid synthesis and affects lipid absorption in the gastrointestinal tract. Tretinoin 32-34 nuclear receptor subfamily 0, group B, member 2 Mus musculus 43-46
25256744-3 2014 According to our present observations, NLRR3-ICD was induced to accumulate in cell nucleus of neuroblastoma SH-SY5Y cells following ATRA treatment. Tretinoin 132-136 leucine rich repeat neuronal 3 Homo sapiens 39-44
25256744-8 2014 Together, our present results strongly suggest that NLRR3-ICD produced by the secretase-mediated proteolytic processing of NLRR3 plays a crucial role in ATRA-mediated neuronal differentiation, and provide a clue to develop a novel therapeutic strategy against aggressive neuroblastomas. Tretinoin 153-157 leucine rich repeat neuronal 3 Homo sapiens 52-57
25256744-8 2014 Together, our present results strongly suggest that NLRR3-ICD produced by the secretase-mediated proteolytic processing of NLRR3 plays a crucial role in ATRA-mediated neuronal differentiation, and provide a clue to develop a novel therapeutic strategy against aggressive neuroblastomas. Tretinoin 153-157 leucine rich repeat neuronal 3 Homo sapiens 123-128
25275461-11 2014 Retinoic acid (RA) partially rescued the inhibitory action of RAGE. Tretinoin 0-13 long intergenic non-protein coding RNA 914 Homo sapiens 62-66
25275461-11 2014 Retinoic acid (RA) partially rescued the inhibitory action of RAGE. Tretinoin 15-17 long intergenic non-protein coding RNA 914 Homo sapiens 62-66
24694005-3 2014 This study was performed to study the potential signal pathway of ATRA in the expression of matrix metalloproteinases-2 (MMP-2) and matrix metalloproteinases-9 (MMP-9) in injury podocyte. Tretinoin 66-70 matrix metallopeptidase 9 Homo sapiens 132-159
24694005-3 2014 This study was performed to study the potential signal pathway of ATRA in the expression of matrix metalloproteinases-2 (MMP-2) and matrix metalloproteinases-9 (MMP-9) in injury podocyte. Tretinoin 66-70 matrix metallopeptidase 9 Homo sapiens 161-166
24694005-8 2014 Enzymatic activity of MMP-2 and MMP-9 in group AA was significantly enhanced compared to AI group after ATRA-treated 24 h (p < 0.05). Tretinoin 104-108 matrix metallopeptidase 9 Homo sapiens 32-37
24694005-13 2014 In conclusion, ATRA may increase expression of MMP-2 and MMP-9 by the potential signal pathway of RAR-alpha and RAR-gamma in injury podocyte induced by adriamycin, but not RAR-beta. Tretinoin 15-19 matrix metallopeptidase 9 Homo sapiens 57-62
25155613-3 2014 Here we demonstrate that SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, contributes to homeostatic retinoic acid (RA) signaling and modulates mouse embryonic stem cell (mESC) differentiation in part through deacetylation of cellular retinoic acid binding protein II (CRABPII). Tretinoin 124-137 sirtuin 1 Homo sapiens 25-30
25155613-3 2014 Here we demonstrate that SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, contributes to homeostatic retinoic acid (RA) signaling and modulates mouse embryonic stem cell (mESC) differentiation in part through deacetylation of cellular retinoic acid binding protein II (CRABPII). Tretinoin 139-141 sirtuin 1 Homo sapiens 25-30
24800886-9 2014 Combined treatment with belinostat and RA dose dependently accelerated and reinforced granulocytic differentiation, accompanied by changes in the expression of CD11b, C/EBPalpha (CCAAT/enhancer binding protein-alpha), and C/EBPepsilon. Tretinoin 39-41 integrin subunit alpha M Homo sapiens 160-165
25136779-12 2014 Western blotting assays additionally showed that ATRA dose-dependently reduced the expression of Sox9, Col2al and p63 (P<0.05 in all vs. controls). Tretinoin 49-53 SRY-box transcription factor 9 Rattus norvegicus 97-101
25136779-13 2014 Together, our results suggest that ATRA suppresses chondrogenesis by modulating the expression of Sox9, Col2al and p63 in primary hind limb bud mesenchymal cells. Tretinoin 35-39 SRY-box transcription factor 9 Rattus norvegicus 98-102
25099355-4 2014 atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Tretinoin 0-4 negative elongation factor complex member C/D Homo sapiens 46-49
24803390-1 2014 Transcription factor Foxa1 plays a critical role during neural differentiation and is induced immediately after retinoic acid (RA)-initiated differentiation of pluripotent P19 embryonal carcinoma cells, correlated with the downregulated expression of pluripotency-related genes such as Nanog. Tretinoin 112-125 Nanog homeobox Homo sapiens 286-291
24803390-1 2014 Transcription factor Foxa1 plays a critical role during neural differentiation and is induced immediately after retinoic acid (RA)-initiated differentiation of pluripotent P19 embryonal carcinoma cells, correlated with the downregulated expression of pluripotency-related genes such as Nanog. Tretinoin 127-129 Nanog homeobox Homo sapiens 286-291
25119106-6 2014 Some retinoic acid target genes regulated by PML/RARA are involved in not only differentiation block but also hematopoietic cell self-renewal. Tretinoin 5-18 retinoic acid receptor, alpha Mus musculus 49-53
25116125-2 2014 However, ATRA treatment also increases cytokine, chemokine, and adhesive molecule (mainly ICAM-1) expression, which can cause clinical complications, including a severe situation known as differentiation syndrome (DS) which can cause death. Tretinoin 9-13 intercellular adhesion molecule 1 Homo sapiens 90-96
25116125-6 2014 Celastrol"s effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. Tretinoin 32-36 intercellular adhesion molecule 1 Homo sapiens 22-28
24994461-4 2014 We found that RA increased IgA production and the expression of germ-line IgA1 and IgA2 transcripts (GLTalpha1 and GLTalpha2). Tretinoin 14-16 immunoglobulin heavy constant alpha 1 Homo sapiens 74-78
25422748-6 2014 The expression of protamine 1 (Prm1) gene was checked as post meiotic marker in differentiated mESCs after 5, 10, 15, 21 and 30 days after RA induction. Tretinoin 139-141 protamine 1 Mus musculus 18-29
25422748-9 2014 The protamine 1 gene was expressed after 21 days of RA induction. Tretinoin 52-54 protamine 1 Mus musculus 4-15
24647975-2 2014 We have previously shown that all-trans retinoic acid (ATRA) increases local content of neural growth factor (NGF), improving peripheral neuropathy of diverse origins. Tretinoin 30-53 nerve growth factor Mus musculus 88-108
24647975-2 2014 We have previously shown that all-trans retinoic acid (ATRA) increases local content of neural growth factor (NGF), improving peripheral neuropathy of diverse origins. Tretinoin 55-59 nerve growth factor Mus musculus 88-108
24953245-5 2014 Treatment of NB4 cells with 1 muM of ATRA, 0.5 muM of ATO, or 10 muM of PP2 for 72 h induced expression of CD11b-positive cells by 13.01%, 11.53% or 13.28%, respectively. Tretinoin 37-41 integrin subunit alpha M Homo sapiens 107-112
24953245-6 2014 However, the combination of ATRA and ATO and the combination of three agents (ATRA, ATO, and PP2) led to a significantly higher expression of CD11b-positive cells (30.96% and 63.17%, respectively). Tretinoin 28-32 integrin subunit alpha M Homo sapiens 142-147
24953245-6 2014 However, the combination of ATRA and ATO and the combination of three agents (ATRA, ATO, and PP2) led to a significantly higher expression of CD11b-positive cells (30.96% and 63.17%, respectively). Tretinoin 78-82 integrin subunit alpha M Homo sapiens 142-147
24932660-7 2014 The hydrophobic retinoic acid (RA) molecule was directly incorporated into PCL films. Tretinoin 16-29 PHD finger protein 1 Homo sapiens 75-78
24377748-6 2013 CONCLUSION: Vital for retinoic acid synthesis during early development, ALDH1A2 has previously been demonstrated in animal models to have a strong association with congenital heart disease and diaphragmatic hernia, two key elements comprising pentalogy of Cantrell. Tretinoin 22-35 aldehyde dehydrogenase 1 family member A2 Homo sapiens 72-79
24324757-0 2013 An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-beta and retinoic acid. Tretinoin 100-113 immunoglobulin heavy constant alpha Mus musculus 68-71
24324757-4 2013 When TGF-beta was combined with retinoic acid (RA), switching to IgA was even more pronounced. Tretinoin 32-45 immunoglobulin heavy constant alpha Mus musculus 65-68
24324757-4 2013 When TGF-beta was combined with retinoic acid (RA), switching to IgA was even more pronounced. Tretinoin 47-49 immunoglobulin heavy constant alpha Mus musculus 65-68
24324757-7 2013 Besides IgA induction, RA treatment of sorted PEC and splenic B cells led to expression of gut homing molecules - alpha4beta7 and CCR9. Tretinoin 23-25 chemokine (C-C motif) receptor 9 Mus musculus 130-134
24324757-8 2013 Intraperitoneal transfer of RA-treated B1 cells into Rag1(-/-) recipients resulted in IgA in serum and gut lavage, most efficiently amongst B1b cell recipients. Tretinoin 28-30 immunoglobulin heavy constant alpha Mus musculus 86-89
24011394-8 2013 We found that DPYSL3 levels increased during RA-induced cell differentiation. Tretinoin 45-47 dihydropyrimidinase like 3 Homo sapiens 14-20
24204796-4 2013 Here we show that ATRA increases ORMDL3 production in vitro via inducing PKA-dependent CREB phosphorylation which in turn binds to the CRE element in promoter region of ORMDL3 and initiates ORMDL3 transcription. Tretinoin 18-22 cAMP responsive element binding protein 1 Homo sapiens 87-91
24006462-0 2013 Retinoic acid improves defective TLR9/RP105-induced immune responses in common variable immunodeficiency-derived B cells. Tretinoin 0-13 CD180 molecule Homo sapiens 38-43
24006462-4 2013 We demonstrate that RA almost normalizes proliferation and IL-10 secretion in patient-derived B cells. Tretinoin 20-22 interleukin 10 Homo sapiens 59-64
24006462-6 2013 This can be explained by impaired RA-mediated isotype switching in TLR9/RP105-stimulated CVID-derived B cells owing to reduced induction of activation-induced deaminase. Tretinoin 34-36 CD180 molecule Homo sapiens 72-77
24006462-8 2013 The ability of RA to improve critical immune parameters in CVID-derived B cells stimulated through TLR9 and RP105 support the possibility of combining RA with TLR stimulation for the treatment of CVID. Tretinoin 15-17 CD180 molecule Homo sapiens 108-113
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 48-50 aldehyde dehydrogenase 1 family member A2 Homo sapiens 212-235
24074870-3 2013 Here, we show that activation of retinoic acid (RA) signaling in aorta-gonad-mesonephros-derived HE ex vivo dramatically enhanced its HSC potential, whereas conditional inactivation of the RA metabolizing enzyme retinal dehydrogenase 2 in VE-cadherin expressing endothelial cells in vivo abrogated HSC development. Tretinoin 189-191 aldehyde dehydrogenase 1 family member A2 Homo sapiens 212-235
23999499-3 2013 Here, we report that retinoic acid (RA), a vitamin A derivative, controls the homeostasis of pre-DC (precursor of DC)-derived splenic CD11b(+)CD8alpha(-)Esam(high) DCs and the developmentally related CD11b(+)CD103(+) subset within the gut. Tretinoin 21-34 integrin subunit alpha M Homo sapiens 134-139
23999499-3 2013 Here, we report that retinoic acid (RA), a vitamin A derivative, controls the homeostasis of pre-DC (precursor of DC)-derived splenic CD11b(+)CD8alpha(-)Esam(high) DCs and the developmentally related CD11b(+)CD103(+) subset within the gut. Tretinoin 21-34 CD8a molecule Homo sapiens 142-150
23999499-3 2013 Here, we report that retinoic acid (RA), a vitamin A derivative, controls the homeostasis of pre-DC (precursor of DC)-derived splenic CD11b(+)CD8alpha(-)Esam(high) DCs and the developmentally related CD11b(+)CD103(+) subset within the gut. Tretinoin 21-34 integrin subunit alpha M Homo sapiens 200-205
23999499-3 2013 Here, we report that retinoic acid (RA), a vitamin A derivative, controls the homeostasis of pre-DC (precursor of DC)-derived splenic CD11b(+)CD8alpha(-)Esam(high) DCs and the developmentally related CD11b(+)CD103(+) subset within the gut. Tretinoin 36-38 integrin subunit alpha M Homo sapiens 134-139
23849428-0 2013 Calcium prevents retinoic acid-induced disruption of the spectrin-based cytoskeleton in keratinocytes through the Src/PI3K-p85alpha/AKT/PKCdelta/beta-adducin pathways. Tretinoin 17-30 adducin 2 Homo sapiens 145-157
23849428-5 2013 RA also enhanced AKT expression and dramatically induced phosphorylation of AKT((Thr308)), accompanied by phosphorylation of both PKCdelta((Thr505)) and beta-adducin((Ser662)) and upregulated cyclin D2 and down-regulated cyclin B1. Tretinoin 0-2 adducin 2 Homo sapiens 153-165
23849428-6 2013 On the other hand, Ca2+ overcame the inhibitory effects of RA on expression of Src, PI3K-p85alpha and cyclin B1 by maintaining high levels of phosphorylation of both Src((Tyr527)) and PI3K-p85alpha and preventing phosphorylation of AKT((Thr308)), PKCdelta((Thr505)) and beta-adducin((Ser662)). Tretinoin 59-61 adducin 2 Homo sapiens 270-282
23624141-1 2013 The retinoic acid (RA, a vitamin A metabolite) receptor (RAR) is a transcription factor. Tretinoin 4-17 retinoic acid receptor, alpha Mus musculus 57-60
23624141-1 2013 The retinoic acid (RA, a vitamin A metabolite) receptor (RAR) is a transcription factor. Tretinoin 19-21 retinoic acid receptor, alpha Mus musculus 57-60
24406343-3 2013 Here, NT2-D1 teratocarcinoma cells -a model of Hox gene expression- were used to show that upon retinoic acid induction, Pknox1 co-localizes with polymeric nuclear actin. Tretinoin 96-109 PBX/knotted 1 homeobox 1 Homo sapiens 121-127
23952237-5 2013 Our results show that RsTSPO behaves as a dimer in the purified state and binds with low micromolar affinity to many of these ligands, including retinoic acid, curcumin, and a known Bcl-2 inhibitor, gossypol, suggesting a possible direct role for TSPO in their regulation of apoptosis. Tretinoin 145-158 translocator protein Homo sapiens 24-28
23891751-0 2013 Inhibition of GATE-16 attenuates ATRA-induced neutrophil differentiation of APL cells and interferes with autophagosome formation. Tretinoin 33-37 GABA type A receptor associated protein like 2 Homo sapiens 14-21
23991089-0 2013 The retinoic acid-metabolizing enzyme Cyp26b1 regulates CD4 T cell differentiation and function. Tretinoin 4-17 CD4 antigen Mus musculus 56-59
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 11-34 Rab40B, member RAS oncogene family Mus musculus 172-175
23977003-3 2013 Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARdelta signaling whereas Crabp2 promotes RAR signaling. Tretinoin 36-40 Rab40B, member RAS oncogene family Mus musculus 172-175
23242600-7 2013 In contrast, all-trans retinoic acid treatment generates regulatory T cells that retain the capacity to secrete IL-17. Tretinoin 23-36 interleukin 17A Homo sapiens 112-117
23242600-8 2013 However, combined use of rapamycin and all-trans retinoic acid abolishes IL-17 production and confers a specific chemokine receptor homing profile upon regulatory T cells. Tretinoin 49-62 interleukin 17A Homo sapiens 73-78
23242600-9 2013 The use of purified regulatory T-cell subpopulations provided direct evidence that rapamycin can confer an early selective advantage to CD45RA(+) regulatory T cells, while all-trans retinoic acid favors CD45RA(-) regulatory T-cell subset. Tretinoin 182-195 protein tyrosine phosphatase receptor type C Homo sapiens 203-207
25152123-1 2014 OBJECTIVE: To explore the effect of RNA interference of human I2PP2A gene on the proliferation and apoptosis of retinoic acid-resistant human acute promyelocytic leukemia (APL) cell line NB4-R1. Tretinoin 112-125 SET nuclear proto-oncogene Homo sapiens 62-68
24686085-5 2014 We observed that Lyn inhibition blocked c-Cbl and p85/p55 PI3K phosphorylation driven by the anti-CD38 agonistic mAb IB4 in ATRA-treated HL-60 cells and untreated CD38+ transfectants. Tretinoin 124-128 LYN proto-oncogene, Src family tyrosine kinase Mus musculus 17-20
24686085-5 2014 We observed that Lyn inhibition blocked c-Cbl and p85/p55 PI3K phosphorylation driven by the anti-CD38 agonistic mAb IB4 in ATRA-treated HL-60 cells and untreated CD38+ transfectants. Tretinoin 124-128 CD38 antigen Mus musculus 98-102
24686085-8 2014 In contrast another SFK inhibitor (dasatinib) which blocks Lyn activity with ATRA co-treatment prevented ATRA-induced c-Cbl phosphorylation and crippled p85 PI3K phosphorylation, indicating Lyn kinase activity is important for ATRA-propelled events potentially regulated by CD38. Tretinoin 77-81 phosphoinositide-3-kinase regulatory subunit 2 Homo sapiens 153-156
24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 179-184
24894398-11 2014 CONCLUSIONS: All-trans-retinoic acid inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, most likely by attenuating the formation of actin stress fibers and focal adhesions as well as signaling by MAPKs, c-Jun, and Smads. Tretinoin 13-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 222-227
16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 3-16 high mobility group AT-hook 1 Homo sapiens 76-81
24357672-5 2014 However, the sequential treatment of hPSCs with CHIR99021 followed by fibroblast growth factor-2 and retinoic acid generated PAX2(+)LHX1(+) cells with 70%-80% efficiency after 3 days of differentiation. Tretinoin 101-114 paired box 2 Homo sapiens 125-129
16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 3-16 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 130-134
24888826-3 2014 Previous studies have demonstrated that ATRA positively affects LIF expression in developing lungs. Tretinoin 40-44 LIF, interleukin 6 family cytokine Rattus norvegicus 64-67
23775127-0 2013 The corepressor CTBP2 is a coactivator of retinoic acid receptor/retinoid X receptor in retinoic acid signaling. Tretinoin 42-55 C-terminal binding protein 2 Mus musculus 16-21
24888826-4 2014 We hypothesized that pulmonary LIF expression is increased after prenatal ATRA treatment in the nitrofen model of CDH-associated PH. Tretinoin 74-78 LIF, interleukin 6 family cytokine Rattus norvegicus 31-34
16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 18-20 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 35-39
16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 18-20 high mobility group AT-hook 1 Homo sapiens 76-81
23775127-3 2013 Using an RNA interference-based genetic screen in mouse F9 cells, we identified the transcriptional corepressor CTBP2 (C-terminal binding protein 2) as a coactivator critically required for retinoic acid (RA)-induced transcription. Tretinoin 190-203 C-terminal binding protein 2 Mus musculus 112-117
23775127-3 2013 Using an RNA interference-based genetic screen in mouse F9 cells, we identified the transcriptional corepressor CTBP2 (C-terminal binding protein 2) as a coactivator critically required for retinoic acid (RA)-induced transcription. Tretinoin 190-203 C-terminal binding protein 2 Mus musculus 119-147
24904835-10 2014 We found that one of the possible reasons might be due to a very low expression level of vitamin D receptor (VDR) mRNA in resistant cells, which can be increased by exposing the cells to ATRA. Tretinoin 187-191 vitamin D receptor Homo sapiens 89-107
23775127-3 2013 Using an RNA interference-based genetic screen in mouse F9 cells, we identified the transcriptional corepressor CTBP2 (C-terminal binding protein 2) as a coactivator critically required for retinoic acid (RA)-induced transcription. Tretinoin 205-207 C-terminal binding protein 2 Mus musculus 112-117
23775127-3 2013 Using an RNA interference-based genetic screen in mouse F9 cells, we identified the transcriptional corepressor CTBP2 (C-terminal binding protein 2) as a coactivator critically required for retinoic acid (RA)-induced transcription. Tretinoin 205-207 C-terminal binding protein 2 Mus musculus 119-147
23775127-4 2013 CTBP2 suppression by RNA interference confers resistance to RA-induced differentiation in diverse murine and human cells. Tretinoin 60-62 C-terminal binding protein 2 Mus musculus 0-5
23775127-5 2013 Mechanistically, we find that CTBP2 associates with RAR/RXR at RA target gene promoters and is essential for their transactivation in response to RA. Tretinoin 52-54 C-terminal binding protein 2 Mus musculus 30-35
24904835-10 2014 We found that one of the possible reasons might be due to a very low expression level of vitamin D receptor (VDR) mRNA in resistant cells, which can be increased by exposing the cells to ATRA. Tretinoin 187-191 vitamin D receptor Homo sapiens 109-112
24576537-3 2014 In CYP26B1-null XY gonads, germ cells are exposed to a higher level of RA than in normal XY gonads and this activates Stra8 to induce meiosis while male-specific gene expression is suppressed. Tretinoin 71-73 stimulated by retinoic acid 8 Homo sapiens 118-123
23850490-0 2013 Retracted: Histone H2B ubquitination regulates retinoic acid signaling through the cooperation of ASXL1 and BAP1. Tretinoin 47-60 ASXL transcriptional regulator 1 Homo sapiens 98-103
16166307-4 2005 On retinoic acid (RA) treatment of MYCN-amplified neuroblastoma cell lines, HMGA1 decreases with a kinetics that strictly follows MYCN repression. Tretinoin 18-20 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 130-134
23850490-7 2013 Both ASXL1 and BAP1 were downregulated during RA-induced P19 cell differentiation with concomitant increase of ubiquitinated H2B, leading to activation of Hox genes. Tretinoin 46-48 ASXL transcriptional regulator 1 Homo sapiens 5-10
24576537-10 2014 Taken together, we conclude that inhibition of RA is one of the essential factors to promote male germ cell differentiation, and that CYP26B1 suppresses two distinct genetic programs induced by RA: a Stra8-dependent meiotic pathway, and a Stra8-independent mitotic pathway. Tretinoin 194-196 stimulated by retinoic acid 8 Homo sapiens 200-205
16853176-1 2005 To examine the mechanisms of electron injection to TiO2 in retinoic acid (RA) and carotenoic acids (CAs), including RA5, CA6, CA7, CA8, CA9, and CA11 having the number of conjugated double bonds n = 5, 6, 7, 8, 9, and 11, respectively, their subpicosecond time-resolved absorption spectra were recorded free in solution and bound to TiO2 nanoparticles in suspension. Tretinoin 74-76 carbonic anhydrase 11 Homo sapiens 145-149
24788806-0 2014 Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A2 Homo sapiens 45-68
24788806-0 2014 Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A2 Homo sapiens 70-76
24788806-0 2014 Retinoic acid and GM-CSF coordinately induce retinal dehydrogenase 2 (RALDH2) expression through cooperation between the RAR/RXR complex and Sp1 in dendritic cells. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 125-128
24788806-2 2014 Retinal dehydrogenase 2 (RALDH2) encoded by Aldh1a2 is a key enzyme for generating RA in DCs. Tretinoin 25-27 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-23
24788806-2 2014 Retinal dehydrogenase 2 (RALDH2) encoded by Aldh1a2 is a key enzyme for generating RA in DCs. Tretinoin 25-27 aldehyde dehydrogenase 1 family member A2 Homo sapiens 44-51
24788806-3 2014 Granulocyte-macrophage colony-stimulating factor (GM-CSF) potently induces RALDH2 expression in DCs in an RA-dependent manner, and RA alone weakly induces the expression. Tretinoin 106-108 aldehyde dehydrogenase 1 family member A2 Homo sapiens 75-81
23850490-8 2013 Our data demonstrate the critical role of ASXL1 cooperation with BAP1 in cell differentiation through the regulation of RA signaling associated with H2B ubiquitination. Tretinoin 120-122 ASXL transcriptional regulator 1 Homo sapiens 42-47
23843516-3 2013 Similar to its action at excitatory synapses, action of RA at inhibitory synapses requires protein translation and is mediated by a nontranscriptional function of the RA-receptor RARalpha. Tretinoin 56-58 retinoic acid receptor, alpha Mus musculus 179-187
23843516-6 2013 Thus, the action of RA at inhibitory and excitatory synapses diverges significantly after the step of RARalpha-mediated protein synthesis, and the regulations of GABAAR and AMPAR trafficking are independent processes. Tretinoin 20-22 retinoic acid receptor, alpha Mus musculus 102-110
23843516-8 2013 Importantly, RA-mediated downscaling of synaptic inhibition is completely absent in Fmr1 knock-out neurons. Tretinoin 13-15 fragile X messenger ribonucleoprotein 1 Mus musculus 84-88
24788806-10 2014 In the presence of RA, ectopic expression of RARalpha/RXRalpha and Sp1 synergistically enhanced Aldh1a2 promoter-reporter activity. Tretinoin 19-21 retinoid X receptor alpha Homo sapiens 54-62
24788806-10 2014 In the presence of RA, ectopic expression of RARalpha/RXRalpha and Sp1 synergistically enhanced Aldh1a2 promoter-reporter activity. Tretinoin 19-21 aldehyde dehydrogenase 1 family member A2 Homo sapiens 96-103
16140954-7 2005 The differentiation effect of NSC656243 was associated with enhanced ATRA-mediated up-regulation of cell cycle regulatory proteins p21waf1 and p27kip1, retinoblastoma dephosphorylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation of the myeloperoxidase (MPO) gene. Tretinoin 69-73 cyclin dependent kinase inhibitor 1B Homo sapiens 143-150
24606396-8 2014 These findings suggest that stimulation of 5-HT4 receptors may enhance ATRA-induced neural differentiation of mouse iPS cells through activation of PKA and CREB. Tretinoin 71-75 mitogen-activated protein kinase kinase kinase 14 Mus musculus 148-151
23837398-5 2013 The overlapping region included two genes, EXOC6B and CYP26B1, which are involved in exocytosis/Notch signaling and retinoic acid (RA) metabolism, respectively, and are of critical importance for early morphogenesis, symmetry as well as craniofacial, skeleton and brain development. Tretinoin 116-129 exocyst complex component 6B Homo sapiens 43-49
23991366-2 2013 In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARgamma to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. Tretinoin 18-20 retinoic acid receptor, gamma Mus musculus 80-88
16140954-7 2005 The differentiation effect of NSC656243 was associated with enhanced ATRA-mediated up-regulation of cell cycle regulatory proteins p21waf1 and p27kip1, retinoblastoma dephosphorylation, expression of RIG-E and RIG-G, and myelomonocytic differentiation-specific down-regulation of the myeloperoxidase (MPO) gene. Tretinoin 69-73 interferon induced protein with tetratricopeptide repeats 3 Homo sapiens 210-215
16140955-5 2005 Investigating the mechanism underlying the effects of these drugs on ATRA-induced APL cell differentiation, we have shown that benzodithiophenes enhance ATRA-mediated dissociation and association of corepressor N-CoR and coactivator p300 acetyltransferase, respectively, with retinoic acid receptor (RAR) alpha proteins. Tretinoin 69-73 nuclear receptor corepressor 1 Homo sapiens 211-216
23742077-0 2013 Retinoic acids up-regulate functional eosinophil-driving receptor CCR3. Tretinoin 0-14 C-C motif chemokine receptor 3 Homo sapiens 66-70
24582848-9 2014 Reports depict that retinoic acid isomers enhance, the expression of genes linked with cholesterol efflux e.g. apoe, abca-1 and abcg-1 proteins in astrocytes. Tretinoin 20-33 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 117-123
24591564-6 2014 Importantly, we also uncovered a vital role for BRCA1 and PALB2 in response to retinoic acid (RA), a growth inhibitory signal in breast cancer cells, which may constitute the basis for their tumor suppressor activity. Tretinoin 79-92 BRCA1 DNA repair associated Homo sapiens 48-53
24591564-6 2014 Importantly, we also uncovered a vital role for BRCA1 and PALB2 in response to retinoic acid (RA), a growth inhibitory signal in breast cancer cells, which may constitute the basis for their tumor suppressor activity. Tretinoin 79-92 partner and localizer of BRCA2 Homo sapiens 58-63
16140955-5 2005 Investigating the mechanism underlying the effects of these drugs on ATRA-induced APL cell differentiation, we have shown that benzodithiophenes enhance ATRA-mediated dissociation and association of corepressor N-CoR and coactivator p300 acetyltransferase, respectively, with retinoic acid receptor (RAR) alpha proteins. Tretinoin 69-73 retinoic acid receptor alpha Homo sapiens 300-303
24591564-6 2014 Importantly, we also uncovered a vital role for BRCA1 and PALB2 in response to retinoic acid (RA), a growth inhibitory signal in breast cancer cells, which may constitute the basis for their tumor suppressor activity. Tretinoin 94-96 BRCA1 DNA repair associated Homo sapiens 48-53
24591564-6 2014 Importantly, we also uncovered a vital role for BRCA1 and PALB2 in response to retinoic acid (RA), a growth inhibitory signal in breast cancer cells, which may constitute the basis for their tumor suppressor activity. Tretinoin 94-96 partner and localizer of BRCA2 Homo sapiens 58-63
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 74-87 membrane associated ring-CH-type finger 8 Homo sapiens 185-188
16140955-5 2005 Investigating the mechanism underlying the effects of these drugs on ATRA-induced APL cell differentiation, we have shown that benzodithiophenes enhance ATRA-mediated dissociation and association of corepressor N-CoR and coactivator p300 acetyltransferase, respectively, with retinoic acid receptor (RAR) alpha proteins. Tretinoin 153-157 nuclear receptor corepressor 1 Homo sapiens 211-216
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 74-87 membrane associated ring-CH-type finger 8 Homo sapiens 286-289
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 89-91 membrane associated ring-CH-type finger 8 Homo sapiens 185-188
24440820-6 2014 We demonstrate that during neuronal differentiation of Neuro-2a cells, RA induces Chka expression by a mechanism that involves ERK1/2 activation which triggers C/EBPbeta expression. Tretinoin 71-73 choline kinase alpha Mus musculus 82-86
24489122-5 2014 The current study examines RA repression of the Nanog gene and compares the results with RA repression of the Oct4 gene on the chromatin level. Tretinoin 27-29 Nanog homeobox Homo sapiens 48-53
23541638-3 2013 During neuronal differentiation of P 19 cells induced by the treatment of retinoic acid (RA), in vitro and in vivo imaging demonstrated that the expression and activity of NIS from the miR-9 NIS reporter gene was clearly repressed by the increased expression and functional activity of miR-9 that bound with the target sequences in the NIS reporter gene and resulted in destabilized the transcriptional activity of NIS gene, compared with the undifferentiated P19 cells. Tretinoin 89-91 membrane associated ring-CH-type finger 8 Homo sapiens 286-289
24489122-7 2014 On RA treatment, the Nanog gene locus remodels specifically in the CR1 region of its proximal promoter, with the insertion of a nucleosome and compaction of this region. Tretinoin 3-5 Nanog homeobox Homo sapiens 21-26
16140955-5 2005 Investigating the mechanism underlying the effects of these drugs on ATRA-induced APL cell differentiation, we have shown that benzodithiophenes enhance ATRA-mediated dissociation and association of corepressor N-CoR and coactivator p300 acetyltransferase, respectively, with retinoic acid receptor (RAR) alpha proteins. Tretinoin 153-157 retinoic acid receptor alpha Homo sapiens 300-303
24489122-8 2014 Further, RA induces coordinated chromatin-remodeling of both Nanog and Oct4 gene loci, which requires RA receptor-alpha, RIP140 and Brm. Tretinoin 9-11 Nanog homeobox Homo sapiens 61-66
16052510-6 2005 However, the activity of the protein phosphatase PP2A was found to increase 24 h following atRA treatment in CA-OV3 cells. Tretinoin 91-95 protein phosphatase 2 phosphatase activator Homo sapiens 49-53
24767374-6 2014 Additionally, an in vitro study demonstrated that the down-regulation of brain-derived neurotrophic factor (BDNF) gene expression by CRP treatment in retinoic acid (RA) differentiated SH-SY5Y neuroblastoma cells. Tretinoin 150-163 brain derived neurotrophic factor Homo sapiens 73-106
23571271-7 2013 Furthermore, overexpressed NFAT1 either alone or in combination with the ATRA-driven signalling pathway deregulated cyclin A and retinoic acid receptor proteins in BM2 cells. Tretinoin 73-77 cyclin A2 Gallus gallus 116-124
16052510-8 2005 Since the inhibition of AP-1 activity following atRA treatment of CA-OV3 cells was abolished in the presence of specific PP2A inhibitors, it is likely that PP2A plays an important role in the atRA-induced repression of AP-1. Tretinoin 48-52 protein phosphatase 2 phosphatase activator Homo sapiens 121-125
24767374-6 2014 Additionally, an in vitro study demonstrated that the down-regulation of brain-derived neurotrophic factor (BDNF) gene expression by CRP treatment in retinoic acid (RA) differentiated SH-SY5Y neuroblastoma cells. Tretinoin 150-163 brain derived neurotrophic factor Homo sapiens 108-112
24767374-6 2014 Additionally, an in vitro study demonstrated that the down-regulation of brain-derived neurotrophic factor (BDNF) gene expression by CRP treatment in retinoic acid (RA) differentiated SH-SY5Y neuroblastoma cells. Tretinoin 165-167 brain derived neurotrophic factor Homo sapiens 73-106
16052510-8 2005 Since the inhibition of AP-1 activity following atRA treatment of CA-OV3 cells was abolished in the presence of specific PP2A inhibitors, it is likely that PP2A plays an important role in the atRA-induced repression of AP-1. Tretinoin 48-52 protein phosphatase 2 phosphatase activator Homo sapiens 156-160
24767374-6 2014 Additionally, an in vitro study demonstrated that the down-regulation of brain-derived neurotrophic factor (BDNF) gene expression by CRP treatment in retinoic acid (RA) differentiated SH-SY5Y neuroblastoma cells. Tretinoin 165-167 brain derived neurotrophic factor Homo sapiens 108-112
23524428-9 2013 CONCLUSION: Our results indicated that restoration of GJIC via enhanced Cx32 and Cx43 expression might serve as a novel mechanism for the anti-tumor effect of ATRA in OSCC. Tretinoin 159-163 gap junction protein beta 1 Homo sapiens 72-76
16052510-8 2005 Since the inhibition of AP-1 activity following atRA treatment of CA-OV3 cells was abolished in the presence of specific PP2A inhibitors, it is likely that PP2A plays an important role in the atRA-induced repression of AP-1. Tretinoin 192-196 protein phosphatase 2 phosphatase activator Homo sapiens 121-125
16052510-8 2005 Since the inhibition of AP-1 activity following atRA treatment of CA-OV3 cells was abolished in the presence of specific PP2A inhibitors, it is likely that PP2A plays an important role in the atRA-induced repression of AP-1. Tretinoin 192-196 protein phosphatase 2 phosphatase activator Homo sapiens 156-160
23519987-0 2013 A crucial role for retinoic acid in the development of Notch-dependent murine splenic CD8- CD4- and CD4+ dendritic cells. Tretinoin 19-32 CD4 antigen Mus musculus 91-94
24559867-2 2014 The RAR agonist: all-trans retinoic acid was reported to be an RORbeta inverse agonist, but no information is available regarding ROR activity of its synthetic analogue Am580. Tretinoin 17-40 RAR related orphan receptor B Homo sapiens 63-70
23519987-0 2013 A crucial role for retinoic acid in the development of Notch-dependent murine splenic CD8- CD4- and CD4+ dendritic cells. Tretinoin 19-32 CD4 antigen Mus musculus 100-103
24594504-2 2014 We focus on the characterization of the aldehyde dehydrogenase-1 family of enzymes (ALDH1A1, ALDH1A2, ALDH1A3) that catalyze conversion of retinaldehyde to retinoic acid. Tretinoin 156-169 aldehyde dehydrogenase 1 family member A2 Homo sapiens 93-100
15987645-4 2005 CYP2S1 has been shown to metabolize all-trans retinoic acid and CYP2R1 is a major vitamin D 25-hydroxylase. Tretinoin 46-59 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 0-6
24594504-4 2014 Although estrogen does not directly influence expression of Aldh1a1, it has the ability to suppress Aldh1a2 and Aldh1a3, thereby establishing a female-specific mechanism for retinoic acid generation in target tissues. Tretinoin 174-187 aldehyde dehydrogenase 1 family member A2 Homo sapiens 100-107
24374174-3 2014 RA dose-dependently inhibited cell proliferation and mRNA and protein levels of ECM components fibronectin, tenascin C and fibrillin-2. Tretinoin 0-2 tenascin C Homo sapiens 108-118
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 87-93
23587393-7 2013 Retinoic acid-induced differentiation of MAC-T cells was associated with an increase in the mRNA expression of alphaS1-casein (3.9-fold), alphaS2-casein (4.5-fold), and beta-casein (4.4-fold) compared with the control group. Tretinoin 0-13 alpha-S2-casein Bos taurus 138-152
23587393-8 2013 Expression of alphaS1-casein, alphaS2-casein, and beta-casein was increased 12.9-fold, 11.9-fold, and 19.3-fold, respectively, following treatment with RA and PRL combined compared with the control group. Tretinoin 152-154 alpha-S2-casein Bos taurus 30-44
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 ATP binding cassette subfamily A member 1 Homo sapiens 133-138
16043647-9 2005 ATRA-induced NO increase was abolished by coincubation with RAR antagonist LE540. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 60-63
23807211-10 2014 Ten genes have been successfully validated involved in: (1) steroid hormone secretion (HSD3B1, HSD3B2), (2) retinoic acid signaling (ABCA1, ABCG1, HMGCR), (3) cell-cycle damage (GADD45A, CCNE2, UHRF1), and the (4) immune response (MAP2K6, IL1R2). Tretinoin 108-121 ubiquitin like with PHD and ring finger domains 1 Homo sapiens 194-199
23584676-4 2013 In this work, we report that signaling through retinoic acid receptor alpha (RARalpha) inhibits CMA and apply structure-based chemical design to develop synthetic derivatives of all-trans-retinoic acid to specifically neutralize this inhibitory effect. Tretinoin 181-201 retinoic acid receptor, alpha Mus musculus 47-75
23584676-4 2013 In this work, we report that signaling through retinoic acid receptor alpha (RARalpha) inhibits CMA and apply structure-based chemical design to develop synthetic derivatives of all-trans-retinoic acid to specifically neutralize this inhibitory effect. Tretinoin 181-201 retinoic acid receptor, alpha Mus musculus 77-85
23741453-9 2013 Together, we conclude that RA activated Ndrg1a represses Wnt/beta-catenin signaling to allow the specification of pancreas, oesophagus, stomach, and duodenum progenitor cells in Xenopus embryos. Tretinoin 27-29 N-myc downstream regulated 1 Xenopus tropicalis 40-46
23741453-9 2013 Together, we conclude that RA activated Ndrg1a represses Wnt/beta-catenin signaling to allow the specification of pancreas, oesophagus, stomach, and duodenum progenitor cells in Xenopus embryos. Tretinoin 27-29 catenin beta 1 Xenopus tropicalis 61-73
16043647-16 2005 CONCLUSIONS: ATRA increases NO production by eNOS phosphorylation through RAR-mediated PI3K/Akt pathway activation in vascular ECs and possibly plays beneficial roles in vascular endothelium. Tretinoin 13-17 retinoic acid receptor alpha Homo sapiens 74-77
15977162-5 2005 Homologs of vertebrate genes involved in neurogenesis and/or neuronal functions (e.g., COUP-TF, Ci-Hox1, and SCO-spondin) were expressed in the central nervous system of Ciona embryos, and activated by retinoic acid. Tretinoin 202-215 SCO-spondin Ciona intestinalis 109-120
23507259-0 2013 Retinoic acid impairs estrogen signaling in breast cancer cells by interfering with activation of LSD1 via PKA. Tretinoin 0-13 lysine demethylase 1A Homo sapiens 98-102
23934681-8 2014 Moreover, our results showed that OA displayed synergistic effects with all-trans retinoic acid and VD3 in part related to reduction of intranuclear phosphorylated RXRalpha that has been reported to block nuclear receptor/RXRalpha heterodimer transcriptional activity. Tretinoin 82-95 retinoid X receptor alpha Homo sapiens 164-172
24619838-4 2014 We observed that the combination of all-trans retinoic acid and matrine can increase the level of cyclic adenosine monophosphate and protein kinase A activity, reduce telomerase activity, and downregulate the protein expression of topoisomerase II beta in NB4-LR1 cells. Tretinoin 46-59 DNA topoisomerase II beta Homo sapiens 231-252
16055921-6 2005 This interaction affects the transcriptional response to retinoic acid in a promoter-specific manner, conferring an unanticipated role to PCNA in transcriptional regulation. Tretinoin 57-70 proliferating cell nuclear antigen Homo sapiens 138-142
24333507-5 2014 Upon retinoic acid-induced differentiation, we found that depletion of DNMT3B leads to a decrease in expression of the surface antigen A2B5 and of neural tube-associated genes PAX7 and BRN3A. Tretinoin 5-18 paired box 7 Homo sapiens 176-180
24082012-0 2014 Differential role of all-trans retinoic acid in promoting the development of CD4+ and CD8+ regulatory T cells. Tretinoin 21-44 CD8a molecule Homo sapiens 86-89
24082012-1 2014 It is known that ATRA promotes the development of TGF-beta-induced CD4(+)Foxp3(+) iTregs, which play a vital role in the prevention of autoimmune diseases; however, the role of ATRA in facilitating the differentiation and function of CD8(+)Foxp3(+) iTregs remains elusive. Tretinoin 17-21 CD8a molecule Homo sapiens 234-237
24082012-5 2014 ATRA did not boost but, conversely, impaired the differentiation and function of human CD8(+) iTregs. Tretinoin 0-4 CD8a molecule Homo sapiens 87-90
24082012-6 2014 CD8(+) cells expressed the ATRA receptor RAR and responded to ATRA, similar to CD4(+) cells. Tretinoin 27-31 CD8a molecule Homo sapiens 0-3
24082012-7 2014 We have identified the differential role of ATRA in promoting Foxp3(+) Tregs in CD4(+) and CD8(+) cell populations. Tretinoin 44-48 CD8a molecule Homo sapiens 91-94
23710639-5 2013 Under the all-trans-retinoic acid (RA)-induced differentiation condition, spheroids extended neurites and further up-regulated the expression of synaptophysin, NSE, CAMs, and ECM proteins. Tretinoin 10-33 synaptophysin Homo sapiens 145-158
23710639-5 2013 Under the all-trans-retinoic acid (RA)-induced differentiation condition, spheroids extended neurites and further up-regulated the expression of synaptophysin, NSE, CAMs, and ECM proteins. Tretinoin 35-37 synaptophysin Homo sapiens 145-158
23611991-0 2013 Retinoic acid inhibits CD25+ dendritic cell expansion and gammadelta T-cell activation in experimental autoimmune uveitis. Tretinoin 0-13 interleukin 2 receptor, alpha chain Mus musculus 23-27
23611991-5 2013 RESULTS: Administration of ATRA to B6 mice in which EAU was induced suppressed the response of Th17 autoreactive T cells, which was associated with decreased generation of the CD25(+) DC subset and suppressed activation of gammadelta T cells. Tretinoin 27-31 interleukin 2 receptor, alpha chain Mus musculus 176-180
23611991-7 2013 CONCLUSIONS: ATRA inhibits the expansion of CD25(+) DCs and gammadelta T-cell activation, thereby restraining the Th17 autoreactive T-cell response. Tretinoin 13-17 interleukin 2 receptor, alpha chain Mus musculus 44-48
15927671-3 2005 The RNase protection assay using a multi-probe template set for human chemokines revealed that ATRA induced gene expressions of a number of CC chemokines, such as monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1alpha and MIP-1beta in NB4 cells. Tretinoin 95-99 C-C motif chemokine ligand 2 Homo sapiens 163-197
23509325-1 2013 In PML/RARA-driven acute promyelocytic leukemia (APL), retinoic acid (RA) induces leukemia cell differentiation and transiently clears the disease. Tretinoin 55-68 retinoic acid receptor, alpha Mus musculus 7-11
24234421-6 2014 To determine whether dynamic RA production acutely regulates Apoc3 expression, its mRNA levels in response to retinoid treatments or adenovirus-mediated overexpression of hepatocyte nuclear factor 4 alpha (HNF4alpha) and chicken ovalbumin upstream-transcription factor II (COUP-TFII) were analyzed. Tretinoin 29-31 apolipoprotein C3 Gallus gallus 61-66
15927671-3 2005 The RNase protection assay using a multi-probe template set for human chemokines revealed that ATRA induced gene expressions of a number of CC chemokines, such as monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1alpha and MIP-1beta in NB4 cells. Tretinoin 95-99 C-C motif chemokine ligand 2 Homo sapiens 199-204
24412926-2 2014 APL is the only malignancy definitively cured by targeted therapies: retinoic acid (RA) and/or arsenic trioxide, which both trigger PML-RARA degradation through nonoverlapping pathways. Tretinoin 69-82 retinoic acid receptor, alpha Mus musculus 136-140
23396089-10 2013 Most genes regulated by fenretinide and ATRA were bound by RXRalpha, suggesting a direct effect. Tretinoin 40-44 retinoid X receptor alpha Homo sapiens 59-67
15927671-3 2005 The RNase protection assay using a multi-probe template set for human chemokines revealed that ATRA induced gene expressions of a number of CC chemokines, such as monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1alpha and MIP-1beta in NB4 cells. Tretinoin 95-99 C-C motif chemokine ligand 3 Homo sapiens 207-251
24412926-2 2014 APL is the only malignancy definitively cured by targeted therapies: retinoic acid (RA) and/or arsenic trioxide, which both trigger PML-RARA degradation through nonoverlapping pathways. Tretinoin 84-86 retinoic acid receptor, alpha Mus musculus 136-140
24412926-5 2014 Upon RA-induced PML-RARA degradation, normal Pml elicits NB reformation and induces a Trp53 response exhibiting features of senescence but not apoptosis, ultimately abrogating APL-initiating activity. Tretinoin 5-7 retinoic acid receptor, alpha Mus musculus 20-24
15927671-3 2005 The RNase protection assay using a multi-probe template set for human chemokines revealed that ATRA induced gene expressions of a number of CC chemokines, such as monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1alpha and MIP-1beta in NB4 cells. Tretinoin 95-99 C-C motif chemokine ligand 4 Homo sapiens 256-265
24352370-0 2014 Prenatal administration of retinoic acid increases the trophoblastic insulin-like growth factor 2 protein expression in the nitrofen model of congenital diaphragmatic hernia. Tretinoin 27-40 insulin-like growth factor 2 Rattus norvegicus 69-97
15927671-5 2005 APL cells prepared from two APL patients showed gene expression of chemokines, such as IL-8, MCP-1, MIP-1alpha, and MIP-1beta when stimulated with ATRA in vitro. Tretinoin 147-151 C-C motif chemokine ligand 2 Homo sapiens 93-98
24352370-15 2014 Significantly decreased IGF2 protein levels were detected in serum, intra-amniotic fluid and left lungs in the CDH group compared to control and nitrofen+RA group. Tretinoin 154-156 insulin-like growth factor 2 Rattus norvegicus 24-28
24352370-17 2014 Prenatal administration of RA may promote lung and placental growth by increasing trophoblastic IGF2 expression. Tretinoin 27-29 insulin-like growth factor 2 Rattus norvegicus 96-100
22788718-5 2013 When EBs were cultured in the presence of 1 or 2% DMSO or 10(-8) M or 10(-7) M retinoic acid for 25 days, ES cells could be directed to form muscle cell-like cells, the identity of which was confirmed by expression of alpha-actinin by immunofluorescence and of MYF-5, MYOD and MYOGENIN genes by RT-PCR. Tretinoin 79-92 myogenic factor 5 Bubalus bubalis 261-266
22788718-5 2013 When EBs were cultured in the presence of 1 or 2% DMSO or 10(-8) M or 10(-7) M retinoic acid for 25 days, ES cells could be directed to form muscle cell-like cells, the identity of which was confirmed by expression of alpha-actinin by immunofluorescence and of MYF-5, MYOD and MYOGENIN genes by RT-PCR. Tretinoin 79-92 myogenin Bubalus bubalis 277-285
15927671-5 2005 APL cells prepared from two APL patients showed gene expression of chemokines, such as IL-8, MCP-1, MIP-1alpha, and MIP-1beta when stimulated with ATRA in vitro. Tretinoin 147-151 C-C motif chemokine ligand 3 Homo sapiens 100-110
22788718-6 2013 MYOD was first detected on Day 10 in both treatment groups and on Day 15 in controls, whereas MYOGENIN was first detected on Day 10, Day 15 and Day 25 in the presence of retinoic acid, in the presence of DMSO and in controls, respectively. Tretinoin 170-183 myogenin Bubalus bubalis 94-102
15927671-5 2005 APL cells prepared from two APL patients showed gene expression of chemokines, such as IL-8, MCP-1, MIP-1alpha, and MIP-1beta when stimulated with ATRA in vitro. Tretinoin 147-151 C-C motif chemokine ligand 4 Homo sapiens 116-125
23352986-1 2013 All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. Tretinoin 0-23 retinoid X receptor alpha Homo sapiens 129-148
23352986-1 2013 All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. Tretinoin 0-23 retinoid X receptor alpha Homo sapiens 150-153
23352986-1 2013 All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. Tretinoin 25-29 retinoid X receptor alpha Homo sapiens 129-148
23352986-1 2013 All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. Tretinoin 25-29 retinoid X receptor alpha Homo sapiens 150-153
23352986-3 2013 Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5 muM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). Tretinoin 79-83 solute carrier family 22 member 7 Homo sapiens 284-317
15927671-6 2005 Furthermore, serum levels of IL-8, MIP-1beta and RANTES were increased during the course of ATRA treatment in both APL patients who developed APL differentiation syndrome. Tretinoin 92-96 C-C motif chemokine ligand 4 Homo sapiens 35-44
23352986-5 2013 Some transporters such as OATP1B3 and the bile salt export pump (BSEP) were however down-regulated by atRA in primary human hepatocytes, but induced in HepaRG cells, thus pointing out discrepancies between these two liver cell models in terms of detoxifying protein regulation. Tretinoin 102-106 ATP binding cassette subfamily B member 11 Homo sapiens 42-63
23352986-5 2013 Some transporters such as OATP1B3 and the bile salt export pump (BSEP) were however down-regulated by atRA in primary human hepatocytes, but induced in HepaRG cells, thus pointing out discrepancies between these two liver cell models in terms of detoxifying protein regulation. Tretinoin 102-106 ATP binding cassette subfamily B member 11 Homo sapiens 65-69
15872003-7 2005 Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. Tretinoin 75-77 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 37-42
23352986-6 2013 atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARalpha and RXRalpha through siRNA transfection in HepaRG cells. Tretinoin 0-4 solute carrier family 22 member 7 Homo sapiens 47-51
23352986-6 2013 atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARalpha and RXRalpha through siRNA transfection in HepaRG cells. Tretinoin 0-4 retinoid X receptor alpha Homo sapiens 159-167
15872003-7 2005 Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. Tretinoin 130-132 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 37-42
15872003-7 2005 Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. Tretinoin 130-132 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 37-42
15949696-1 2005 The effects of fatty acids and retinoic acid (carotene) on brown adipose tissue differentiation are mediated by activation of the transcription factors PPARgamma and PPARalpha in combination with RXR. Tretinoin 31-44 peroxisome proliferator activated receptor alpha Homo sapiens 166-175
23239029-7 2013 Inhibition of CXCR4 signaling in primary cultures of mouse undifferentiated spermatogonia resulted in SSC loss, in part by reducing proliferation and increasing the transition to a progenitor state primed for differentiation upon stimulation by retinoic acid. Tretinoin 245-258 chemokine (C-X-C motif) receptor 4 Mus musculus 14-19
15746941-3 2005 The results show that CDDO-Im selectively downregulates expression of the PML/retinoic receptor alpha fusion protein by a caspase-dependent mechanism and sensitizes APL cells to the differentiating effects of all-trans retinoic acid (ATRA). Tretinoin 219-232 PML nuclear body scaffold Homo sapiens 74-77
23264745-5 2013 Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm"s tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARgamma(-/-) cells. Tretinoin 177-179 Meis homeobox 1 Homo sapiens 112-117
23264745-5 2013 Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm"s tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARgamma(-/-) cells. Tretinoin 177-179 Meis homeobox 1 Homo sapiens 119-161
15746941-3 2005 The results show that CDDO-Im selectively downregulates expression of the PML/retinoic receptor alpha fusion protein by a caspase-dependent mechanism and sensitizes APL cells to the differentiating effects of all-trans retinoic acid (ATRA). Tretinoin 234-238 PML nuclear body scaffold Homo sapiens 74-77
22733143-0 2013 RALDH2, the enzyme for retinoic acid synthesis, mediates meiosis initiation in germ cells of the female embryonic chickens. Tretinoin 23-36 aldehyde dehydrogenase 1 family member A2 Gallus gallus 0-6
22733143-3 2013 In the present study, we investigated the role of the enzyme retinaldehyde dehydrogenase 2 (RALDH2) which catalyzes RA synthesizes by initiating meiosis in chicken ovarian germ cells. Tretinoin 92-94 aldehyde dehydrogenase 1 family member A2 Gallus gallus 61-90
15970678-8 2005 Cotreatment with the RAR-alpha antagonist, Ro41-5253 or pan-TGF-beta neutralizing antibody abolished the phenotypic and antiproliferative effects of all-trans retinoic acid. Tretinoin 159-172 retinoic acid receptor alpha Homo sapiens 21-30
22733143-6 2013 This was also revealed by RA stimulation of the cultured ovaries with the initiation of meiosis response, and the knocking down of the Raldh2 expression during meiosis, leading to abolishment of RA-dependent action. Tretinoin 195-197 aldehyde dehydrogenase 1 family member A2 Gallus gallus 135-141
22733143-7 2013 Altogether, these studies indicate that RA synthesis by the enzyme RALDH2 and signaling through its receptor is crucial for meiosis initiation in chicken embryonic ovary. Tretinoin 40-42 aldehyde dehydrogenase 1 family member A2 Gallus gallus 67-73
23243061-0 2013 Bortezomib sensitizes human acute myeloid leukemia cells to all-trans-retinoic acid-induced differentiation by modifying the RARalpha/STAT1 axis. Tretinoin 70-83 signal transducer and activator of transcription 1 Homo sapiens 134-139
15813899-5 2005 In contrast, melatonin potentiates the action of all-trans-retinoic acid on RARalpha transcriptional activation and enhances RARalpha/DNA binding activity, an action which is not PTX-sensitive. Tretinoin 49-72 retinoic acid receptor alpha Homo sapiens 76-84
23319320-6 2013 Expression of fatty acid synthase (FAS) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) proteins was increased in ATRA-treated cells. Tretinoin 132-136 fatty acid synthase Homo sapiens 14-33
23319320-6 2013 Expression of fatty acid synthase (FAS) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) proteins was increased in ATRA-treated cells. Tretinoin 132-136 fatty acid synthase Homo sapiens 35-38
15691824-2 2005 TG2-/- mouse chondrocytes demonstrate markedly inhibited progression to hypertrophic differentiation in response to both retinoic acid and the chemokine CXCL1. Tretinoin 121-134 transglutaminase 2, C polypeptide Mus musculus 0-3
23327868-1 2013 BACKGROUND: The cellular retinoic acid-binding protein II (CRABPII) and epidermal fatty acid-binding protein (E-FABP) both serving as the transport protein of retinoic acid (RA), through RA signal transduction pathway, commit the cell to opposite fate, apoptosis or survival. Tretinoin 25-38 cellular retinoic acid binding protein 2 Homo sapiens 59-66
23327868-1 2013 BACKGROUND: The cellular retinoic acid-binding protein II (CRABPII) and epidermal fatty acid-binding protein (E-FABP) both serving as the transport protein of retinoic acid (RA), through RA signal transduction pathway, commit the cell to opposite fate, apoptosis or survival. Tretinoin 60-62 cellular retinoic acid binding protein 2 Homo sapiens 16-57
15721283-0 2005 Anti-inflammatory roles of retinoic acid in rat brain astrocytes: Suppression of interferon-gamma-induced JAK/STAT phosphorylation. Tretinoin 27-40 interferon gamma Rattus norvegicus 81-97
22998816-3 2012 When treated with neural induction medium containing Noggin/retinoic acid, the encapsulated cells expressed much higher levels of neural progenitor markers SOX1 and PAX6 than those in other treatment conditions. Tretinoin 60-73 SRY-box transcription factor 1 Homo sapiens 156-160
15721283-5 2005 Both RA isoforms also reduced IFN-gamma-induced activation of signal transducers and activators of transcription (STAT)1, STAT3, Janus kinase (JAK)1, and JAK2. Tretinoin 5-7 interferon gamma Rattus norvegicus 30-39
15721283-5 2005 Both RA isoforms also reduced IFN-gamma-induced activation of signal transducers and activators of transcription (STAT)1, STAT3, Janus kinase (JAK)1, and JAK2. Tretinoin 5-7 signal transducer and activator of transcription 3 Rattus norvegicus 122-127
15721283-6 2005 This inhibitory effect was significant when cells were pre-treated with RA prior to IFN-gamma. Tretinoin 72-74 interferon gamma Rattus norvegicus 84-93
15721283-10 2005 These results suggest that RA induces an anti-inflammatory effect by suppressing the activation of the JAK/STAT pathway in IFN-gamma-treated astrocytes. Tretinoin 27-29 interferon gamma Rattus norvegicus 123-132
15781332-5 2005 RESULTS: All-trans retinoic acid (1 mumol/L) reduced expansion of CD34+CD38-Lin- TNC and CFUs after 2 to 5 weeks of culture. Tretinoin 9-32 CD38 molecule Homo sapiens 71-75
22884502-4 2012 F9 cells treated with retinoic acid differentiate to primitive endoderm and this is accompanied by the activation of canonical Wnt-beta-catenin signalling. Tretinoin 22-35 catenin (cadherin associated protein), beta 1 Mus musculus 131-143
22378018-0 2012 Annexin A1 mediates the anti-inflammatory effects during the granulocytic differentiation process in all-trans retinoic acid-treated acute promyelocytic leukemic cells. Tretinoin 111-124 annexin A1 Homo sapiens 0-10
22378018-5 2012 We found that ATRA was able to enhance the surface expression of AnxA1 and its receptor (FPR2/ALX) and the release of AnxA1-containing MPs from ATRA-NB4 cells, while the expression of annexin V was not elevated on the latter cells. Tretinoin 14-18 annexin A1 Homo sapiens 65-70
22378018-5 2012 We found that ATRA was able to enhance the surface expression of AnxA1 and its receptor (FPR2/ALX) and the release of AnxA1-containing MPs from ATRA-NB4 cells, while the expression of annexin V was not elevated on the latter cells. Tretinoin 14-18 annexin A1 Homo sapiens 118-123
15845083-0 2005 Retinoic acid synthesis by a population of NG2-positive cells in the injured spinal cord. Tretinoin 0-13 chondroitin sulfate proteoglycan 4 Rattus norvegicus 43-46
22902413-0 2012 A retinoic acid--rich tumor microenvironment provides clonal survival cues for tumor-specific CD8(+) T cells. Tretinoin 2-15 CD8a molecule Homo sapiens 94-97
22902413-3 2012 Conditional disruption of RA signaling in CD8(+) T cells using a dominant negative retinoic acid receptor alpha (dnRARalpha) established that RA signaling is required for tumor-specific CD8(+) T-cell expansion/accumulation and protective antitumor immunity. Tretinoin 26-28 CD8a molecule Homo sapiens 42-45
22902413-3 2012 Conditional disruption of RA signaling in CD8(+) T cells using a dominant negative retinoic acid receptor alpha (dnRARalpha) established that RA signaling is required for tumor-specific CD8(+) T-cell expansion/accumulation and protective antitumor immunity. Tretinoin 26-28 CD8a molecule Homo sapiens 186-189
22902413-5 2012 Our findings indicate that RA function is essential for the survival of tumor-reactive CD8(+) T cells within the TME. Tretinoin 27-29 CD8a molecule Homo sapiens 87-90
22982681-2 2012 RA responses are mediated by transcriptional activation by the retinoic acid receptor (RAR) and retinoid X receptor (RXR) in cooperation with various types of coregulators at RA-responsive gene promoters. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 96-115
22982681-2 2012 RA responses are mediated by transcriptional activation by the retinoic acid receptor (RAR) and retinoid X receptor (RXR) in cooperation with various types of coregulators at RA-responsive gene promoters. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 117-120
15845083-10 2005 Instead, RALDH2 was present in a cell type not previously identified as capable of synthesizing RA, that expressed NG2 and that was negative for markers of astrocytes, oligodendroglia, microglia, neurons, Schwann cells and immature lymphocytes. Tretinoin 9-11 chondroitin sulfate proteoglycan 4 Rattus norvegicus 115-118
15667595-5 2005 The present investigation evaluates the role of retinoic acid on the expression of aryl sulfotransferase IV and hydroxysteroid sulfotransferase a in male and female Sprague-Dawley rat liver and intestine. Tretinoin 48-61 sulfotransferase family 2A, dehydroepiandrosterone (DHEA)-preferring, member 6 Rattus norvegicus 112-145
22828480-7 2012 Pretreatment of EBs with either atenolol (a selective beta(1)-adrenoceptor antagonist) or H89 (a protein kinase A inhibitor) significantly inhibited the l-isoproterenol-enhancement of ATRA-induced Nestin expression. Tretinoin 184-188 adrenergic receptor, beta 1 Mus musculus 54-74
22828480-9 2012 These findings suggest that beta(1)-adrenoceptor stimulation enhances ATRA-induced neural differentiation of mouse iPS cells. Tretinoin 70-74 adrenergic receptor, beta 1 Mus musculus 28-48
15606616-10 2005 A single administration of ATRA reduced the Th1 [interleukin (IL)-2, interferon (IFN)-gamma and IL-12], and a Th2 (IL-4) cytokine level, as effectively as administration of PSL. Tretinoin 27-31 heart and neural crest derivatives expressed 2 Mus musculus 110-113
22539306-6 2012 RXR and FGFR1 co-associate with 5"-Fluorouridine-labeled transcription sites and with RA Responsive Elements (RARE). Tretinoin 86-88 retinoid X receptor alpha Homo sapiens 0-3
23071480-7 2012 The variant APL with t(11;17)(q23;q21) cases that are associated with the ZBTB16/RARA fusion gene have been reported as being resistant to all-trans-retinoic acid (ATRA). Tretinoin 142-162 zinc finger and BTB domain containing 16 Homo sapiens 74-80
15606616-10 2005 A single administration of ATRA reduced the Th1 [interleukin (IL)-2, interferon (IFN)-gamma and IL-12], and a Th2 (IL-4) cytokine level, as effectively as administration of PSL. Tretinoin 27-31 interleukin 4 Mus musculus 115-119
23071480-7 2012 The variant APL with t(11;17)(q23;q21) cases that are associated with the ZBTB16/RARA fusion gene have been reported as being resistant to all-trans-retinoic acid (ATRA). Tretinoin 164-168 zinc finger and BTB domain containing 16 Homo sapiens 74-80
15615521-2 2004 The synthetic features include introduction of nucleophilic ligands at C-4 of all-trans-retinoic acid (ATRA) and 13-cis-retinoic acid, and modification of terminal carboxylic acid group. Tretinoin 82-101 complement C4A (Rodgers blood group) Homo sapiens 71-74
22513004-12 2012 The factors regulating NGAL expression are numerous and range from pro-inflammatory cytokines like interleukins, tumor necrosis factor-alpha and interferons to vitamins like retinoic acid. Tretinoin 174-187 lipocalin 2 Homo sapiens 23-27
22696440-6 2012 In vitro treatment with ATRA induced the expression of Foxp3 and repressed the IL-17 expression in the CD4(+) T cells in mice. Tretinoin 24-28 interleukin 17A Mus musculus 79-84
22696440-6 2012 In vitro treatment with ATRA induced the expression of Foxp3 and repressed the IL-17 expression in the CD4(+) T cells in mice. Tretinoin 24-28 CD4 antigen Mus musculus 103-106
15615521-2 2004 The synthetic features include introduction of nucleophilic ligands at C-4 of all-trans-retinoic acid (ATRA) and 13-cis-retinoic acid, and modification of terminal carboxylic acid group. Tretinoin 103-107 complement C4A (Rodgers blood group) Homo sapiens 71-74
15454112-6 2004 Upregulation of CD83 was also detected on the surface of ATRA-treated NB4 cells versus untreated cells. Tretinoin 57-61 CD83 molecule Homo sapiens 16-20
22676378-0 2012 Retinoic acid and liver X receptor agonist synergistically inhibit HIV infection in CD4+ T cells by up-regulating ABCA1-mediated cholesterol efflux. Tretinoin 0-13 ATP binding cassette subfamily A member 1 Homo sapiens 114-119
22676378-1 2012 BACKGROUND: Retinoic acids regulate the reverse cholesterol transport by inducing the ATP binding cassette transporter A1 (ABCA1) dependent cholesterol efflux in macrophages, neuronal as well as intestine cells. Tretinoin 12-26 ATP binding cassette subfamily A member 1 Homo sapiens 86-121
22676378-1 2012 BACKGROUND: Retinoic acids regulate the reverse cholesterol transport by inducing the ATP binding cassette transporter A1 (ABCA1) dependent cholesterol efflux in macrophages, neuronal as well as intestine cells. Tretinoin 12-26 ATP binding cassette subfamily A member 1 Homo sapiens 123-128
22676378-2 2012 In the present study, we aim to test the effect of all trans retinoic acid (ATRA) on ABCA1 expression in human CD4+ T cells and the involvement of cholesterol in ATRA mediated anti-HIV effect. Tretinoin 61-74 ATP binding cassette subfamily A member 1 Homo sapiens 85-90
23955575-9 2014 Secondly, all-trans retinoic acid (ATRA) resulted in an inhibition of ALDH activity, and induction of the differentiation and radiosensitization of SQ20B/SP/CD44(+)/ALDH(high) cells. Tretinoin 10-33 CD44 molecule (Indian blood group) Homo sapiens 157-161
23955575-9 2014 Secondly, all-trans retinoic acid (ATRA) resulted in an inhibition of ALDH activity, and induction of the differentiation and radiosensitization of SQ20B/SP/CD44(+)/ALDH(high) cells. Tretinoin 35-39 CD44 molecule (Indian blood group) Homo sapiens 157-161
22676378-2 2012 In the present study, we aim to test the effect of all trans retinoic acid (ATRA) on ABCA1 expression in human CD4+ T cells and the involvement of cholesterol in ATRA mediated anti-HIV effect. Tretinoin 76-80 ATP binding cassette subfamily A member 1 Homo sapiens 85-90
15454112-7 2004 The addition of cytokines alone, such as GM-CSF or CD40 ligand, did not affect the expression of CD83 in untreated NB4 cells but they up-regulated CD83 in ATRA-treated cells. Tretinoin 155-159 colony stimulating factor 2 Homo sapiens 41-47
22676378-10 2012 METHODS: ABCA1 RNA and protein were determined by real-time PCR and immuno blot methods in cells treated with ATRA. Tretinoin 110-114 ATP binding cassette subfamily A member 1 Homo sapiens 9-14
22676378-13 2012 Increased cholesterol efflux contributed to reduced HIV-1 entry, suggesting that anti-HIV effect of ATRA is mediated through ABCA1. Tretinoin 100-104 ATP binding cassette subfamily A member 1 Homo sapiens 125-130
15454112-7 2004 The addition of cytokines alone, such as GM-CSF or CD40 ligand, did not affect the expression of CD83 in untreated NB4 cells but they up-regulated CD83 in ATRA-treated cells. Tretinoin 155-159 CD83 molecule Homo sapiens 147-151
24076097-3 2014 Evidence suggests that retinoic acid (RA) induces expression of the critical pre-meiosis gene Stra8 in germ cells of the fetal ovary, pubertal testis and adult testis. Tretinoin 23-36 stimulated by retinoic acid 8 Homo sapiens 94-99
24076097-3 2014 Evidence suggests that retinoic acid (RA) induces expression of the critical pre-meiosis gene Stra8 in germ cells of the fetal ovary, pubertal testis and adult testis. Tretinoin 38-40 stimulated by retinoic acid 8 Homo sapiens 94-99
15516986-0 2004 Retinoic acid mediates degradation of IRS-1 by the ubiquitin-proteasome pathway, via a PKC-dependant mechanism. Tretinoin 0-13 insulin receptor substrate 1 Homo sapiens 38-43
24076097-4 2014 In the fetal testis, CYP26B1 degrades RA, while FGF9 further antagonises RA signalling to suppress meiosis. Tretinoin 73-75 fibroblast growth factor 9 Homo sapiens 48-52
22568433-6 2012 Retinoic acid-induced differentiation of human precursor NT2 cells into dopaminergic cells increased expression of TH, NURR1, D2 R and SRY. Tretinoin 0-13 nuclear receptor subfamily 4 group A member 2 Homo sapiens 119-124
24475288-3 2014 Using the human embryonal carcinoma cell line NTera2/D1, we confirmed that exposure to the differentiating agent retinoic acid produced a reduction in pluripotency markers NANOG and POU5F1 (Oct3/4) and an acute concentration-dependent increase in resistance to both cisplatin and paclitaxel that reached as high as 18-fold for cisplatin and 61-fold for paclitaxel within four days. Tretinoin 113-126 Nanog homeobox Homo sapiens 172-177
15516986-2 2004 We found that all-trans retinoic acid (RA) decreases IRS-1 protein levels in MCF-7, T47-D, and ZR75.1 breast cancer cells, which are growth arrested by RA, but not in the RA-resistant MDA-MB-231 and MDA-MB-468 cells. Tretinoin 24-37 insulin receptor substrate 1 Homo sapiens 53-58
15516986-2 2004 We found that all-trans retinoic acid (RA) decreases IRS-1 protein levels in MCF-7, T47-D, and ZR75.1 breast cancer cells, which are growth arrested by RA, but not in the RA-resistant MDA-MB-231 and MDA-MB-468 cells. Tretinoin 39-41 insulin receptor substrate 1 Homo sapiens 53-58
15516986-4 2004 Two proteasome inhibitors, MG-132 and lactacystin, blocked the RA-mediated degradation of IRS-1, and RA increased ubiquitination of IRS-1 in the RA-sensitive breast cancer cells. Tretinoin 63-65 insulin receptor substrate 1 Homo sapiens 90-95
15516986-4 2004 Two proteasome inhibitors, MG-132 and lactacystin, blocked the RA-mediated degradation of IRS-1, and RA increased ubiquitination of IRS-1 in the RA-sensitive breast cancer cells. Tretinoin 101-103 insulin receptor substrate 1 Homo sapiens 132-137
22402911-1 2012 We investigated the role of homeobox B4 (HOXB4) mRNA/protein expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) in proliferation and committed differentiation of human cord blood hematopoietic stem cells (HSCs) into colony-forming-units of T-lymphocyte (CFU-TL) and erythroid (CFU-E) progenitors in vitro. Tretinoin 129-142 homeobox B4 Homo sapiens 41-46
24026680-7 2014 Our findings demonstrate critical, cooperative roles for RA and CHD7 in SVZ neural stem cell function and inner ear development, suggesting that altered RA signaling may be an effective method for treating Chd7 deficiency. Tretinoin 153-155 chromodomain helicase DNA binding protein 7 Mus musculus 64-68
22402911-1 2012 We investigated the role of homeobox B4 (HOXB4) mRNA/protein expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) in proliferation and committed differentiation of human cord blood hematopoietic stem cells (HSCs) into colony-forming-units of T-lymphocyte (CFU-TL) and erythroid (CFU-E) progenitors in vitro. Tretinoin 144-148 homeobox B4 Homo sapiens 41-46
15516986-5 2004 In addition, we found that RA increases serine phosphorylation of IRS-1. Tretinoin 27-29 insulin receptor substrate 1 Homo sapiens 66-71
22402911-4 2012 HOXB4 mRNA/protein expression in CFU-TL and CFU-E was detected in control, ATRA, HCMV and ATRA + HCMV groups on days 3, 7, and 12 of culture by fluorescent qRT-PCR/western blot. Tretinoin 75-79 homeobox B4 Homo sapiens 0-5
22402911-4 2012 HOXB4 mRNA/protein expression in CFU-TL and CFU-E was detected in control, ATRA, HCMV and ATRA + HCMV groups on days 3, 7, and 12 of culture by fluorescent qRT-PCR/western blot. Tretinoin 90-94 homeobox B4 Homo sapiens 0-5
22402911-9 2012 ATRA, at the concentration used, significantly up-regulated HOXB4 mRNA/protein expression in normal lymphocyte and erythrocyte progenitor cells as well as in HCMV-infected cells. Tretinoin 0-4 homeobox B4 Homo sapiens 60-65
23810783-0 2014 All-trans-retinoid acid (ATRA) may have inhibited chondrogenesis of primary hind limb bud mesenchymal cells by downregulating Pitx1 expression. Tretinoin 25-29 paired-like homeodomain 1 Rattus norvegicus 126-131
24416428-7 2014 Moreover, ATRA-mediated Ape/Ref-1 upregulation was correlated with histone modification and activation of CBP/p300, an important cofactors for CREB transcriptional activity. Tretinoin 10-14 cAMP responsive element binding protein 1 Homo sapiens 143-147
24416428-10 2014 Hence, our study suggests the existence of a noncanonical mechanism involving p38-MSK-CREB cascade and CBP induction to mediate ATRA-induced Ape/Ref-1 expression and acquired chemoresistance in myeloma cells. Tretinoin 128-132 cAMP responsive element binding protein 1 Homo sapiens 86-90
15516986-7 2004 Two PKC inhibitors, but not a MAPK inhibitor, blocked the RA-induced degradation and serine phosphorylation of IRS-1. Tretinoin 58-60 insulin receptor substrate 1 Homo sapiens 111-116
15516986-8 2004 We demonstrate that RA activates PKC-delta in the sensitive, but not in the resistant cells, with a time course that is consistent with the RA-induced decrease of IRS-1. Tretinoin 20-22 insulin receptor substrate 1 Homo sapiens 163-168
22464761-9 2012 Concomitant with these effects on day 14, CD38, CD11b, and F4/80 were higher on macrophages from RA-treated mice versus controls. Tretinoin 97-99 CD38 antigen Mus musculus 42-46
15516986-8 2004 We demonstrate that RA activates PKC-delta in the sensitive, but not in the resistant cells, with a time course that is consistent with the RA-induced decrease of IRS-1. Tretinoin 140-142 insulin receptor substrate 1 Homo sapiens 163-168
22464761-9 2012 Concomitant with these effects on day 14, CD38, CD11b, and F4/80 were higher on macrophages from RA-treated mice versus controls. Tretinoin 97-99 adhesion G protein-coupled receptor E1 Mus musculus 59-64
25486480-0 2014 The oncogene EVI1 enhances transcriptional and biological responses of human myeloid cells to all-trans retinoic acid. Tretinoin 104-117 MDS1 and EVI1 complex locus Homo sapiens 13-17
15516986-9 2004 We also show that: (1) RA-activated PKC-delta phosphorylates IRS-1 in vitro, (2) PKC-delta and IRS-1 interact in RA-treated cells, and (3) mutation of three PKC-delta serine sites in IRS-1 to alanines results in no RA-induced in vitro phosphorylation of IRS-1. Tretinoin 23-25 insulin receptor substrate 1 Homo sapiens 61-66
15650238-7 2004 The exogenous expression of HMGA2 is sufficient to convert RA-sensitive SY5Y NB cells into RA-resistant cells, thus suggesting that HMGA2 might be a relevant player in determining NB cell responses to endogenous or therapeutically important growth inhibitory substances. Tretinoin 59-61 high mobility group AT-hook 2 Homo sapiens 28-33
25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 153-176 MDS1 and EVI1 complex locus Homo sapiens 53-57
25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 153-176 MDS1 and EVI1 complex locus Homo sapiens 303-307
25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 178-182 MDS1 and EVI1 complex locus Homo sapiens 53-57
21938722-6 2012 In addition, the targeting of p300 in combination with a differential enrichment of Brm to Brg1 change at the distal promoter region of the gene is induced under RA treatment. Tretinoin 162-164 E1A binding protein p300 Mus musculus 30-34
25486480-2 2014 Previous results from our laboratory have shown that EVI1 influenced transcription regulation in response to the myeloid differentiation inducing agent, all-trans retinoic acid (ATRA), in a dual manner: it enhanced ATRA induced transcription of the RARbeta gene, but repressed the ATRA induction of the EVI1 gene itself. Tretinoin 178-182 MDS1 and EVI1 complex locus Homo sapiens 303-307
21938722-6 2012 In addition, the targeting of p300 in combination with a differential enrichment of Brm to Brg1 change at the distal promoter region of the gene is induced under RA treatment. Tretinoin 162-164 SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2 Mus musculus 84-87
15650238-7 2004 The exogenous expression of HMGA2 is sufficient to convert RA-sensitive SY5Y NB cells into RA-resistant cells, thus suggesting that HMGA2 might be a relevant player in determining NB cell responses to endogenous or therapeutically important growth inhibitory substances. Tretinoin 59-61 high mobility group AT-hook 2 Homo sapiens 132-137
25486480-6 2014 A particularly strong synergy between EVI1 and ATRA was observed for GDF15, which codes for a member of the TGF-beta superfamily of cytokines. Tretinoin 47-51 growth differentiation factor 15 Homo sapiens 69-74
25486480-7 2014 In line with the gene expression results, EVI1 enhanced cell cycle arrest, differentiation, and apoptosis in response to ATRA, and knockdown of GDF15 counteracted some of these effects. Tretinoin 121-125 MDS1 and EVI1 complex locus Homo sapiens 42-46
15650238-9 2004 Interestingly, RA increases HMGA1 expression in RA-resistant NB cells but inhibits it in cells undergoing RA-induced growth inhibition and neuronal differentiation. Tretinoin 15-17 high mobility group AT-hook 1 Homo sapiens 28-33
24310731-10 2014 Taken together, we provide evidence here for the first time that atRA, retinol, and beta-carotene differentially regulate GM-CSF, IL-16, and MMP-9 production in macrophages, explaining at least in part why these vitamin A-related substances are beneficial for immunity. Tretinoin 65-69 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 122-128
24310731-10 2014 Taken together, we provide evidence here for the first time that atRA, retinol, and beta-carotene differentially regulate GM-CSF, IL-16, and MMP-9 production in macrophages, explaining at least in part why these vitamin A-related substances are beneficial for immunity. Tretinoin 65-69 interleukin 16 Mus musculus 130-135
22475041-8 2012 In this context, we review the published reports and draw a hypothesis that: (i) The distributions of RARs isoforms are different in different cells; (ii) ATRA activates the different RARs isoforms in different cells; (iii) The roles of different RARs isoforms for regulating the expression of MMP-2 or MMP-9 are different in different cells. Tretinoin 155-159 matrix metallopeptidase 9 Homo sapiens 303-308
25030439-8 2014 We also demonstrated that treatment with AtRA, 9cRA and verapamil induces alterations in P-gp expression in R and T cells. Tretinoin 41-45 phosphoglycolate phosphatase Mus musculus 89-93
25030439-9 2014 Particularly, combined treatment of R cells with verapamil and AtRA induced downregulation of P-gp content/activity. Tretinoin 63-67 phosphoglycolate phosphatase Mus musculus 94-98
15506985-7 2004 The results demonstrated that annexin A2 expression was affected when the cells were induced to differentiate by stimulation with all-trans-retinoic acid. Tretinoin 130-153 annexin A2 Homo sapiens 30-40
25509416-5 2014 As induction of neuronal differentiation in the studied MSCs using differentiation medium containing B27 and N2 supplements, 5-azacytidine, retinoic acid, IBMX and dbcAMF caused changes in the cells morphology, the increased expression of beta-III-tubulin, and the appearance of neuronal markers GFAP, NF-H, NeuN and MAP2. Tretinoin 140-153 glial fibrillary acidic protein Homo sapiens 296-300
25509416-5 2014 As induction of neuronal differentiation in the studied MSCs using differentiation medium containing B27 and N2 supplements, 5-azacytidine, retinoic acid, IBMX and dbcAMF caused changes in the cells morphology, the increased expression of beta-III-tubulin, and the appearance of neuronal markers GFAP, NF-H, NeuN and MAP2. Tretinoin 140-153 microtubule associated protein 2 Homo sapiens 317-321
22441042-6 2012 In the all-trans retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cells, the BDNF transcription rate measured by a nuclear run-on assay was significantly suppressed by Abeta(25-35) and elevated by SMI, but the BDNF degradation rate measured by half-life determination was unchanged by Abeta(25-35) and SMI. Tretinoin 17-30 brain derived neurotrophic factor Homo sapiens 84-88
22441042-6 2012 In the all-trans retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cells, the BDNF transcription rate measured by a nuclear run-on assay was significantly suppressed by Abeta(25-35) and elevated by SMI, but the BDNF degradation rate measured by half-life determination was unchanged by Abeta(25-35) and SMI. Tretinoin 17-30 brain derived neurotrophic factor Homo sapiens 217-221
22441042-6 2012 In the all-trans retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cells, the BDNF transcription rate measured by a nuclear run-on assay was significantly suppressed by Abeta(25-35) and elevated by SMI, but the BDNF degradation rate measured by half-life determination was unchanged by Abeta(25-35) and SMI. Tretinoin 32-34 brain derived neurotrophic factor Homo sapiens 84-88
22441042-6 2012 In the all-trans retinoic acid (RA)-differentiated SH-SY5Y neuroblastoma cells, the BDNF transcription rate measured by a nuclear run-on assay was significantly suppressed by Abeta(25-35) and elevated by SMI, but the BDNF degradation rate measured by half-life determination was unchanged by Abeta(25-35) and SMI. Tretinoin 32-34 brain derived neurotrophic factor Homo sapiens 217-221
22339500-0 2012 Induction of NANOG expression by targeting promoter sequence with small activating RNA antagonizes retinoic acid-induced differentiation. Tretinoin 99-112 Nanog homeobox Homo sapiens 13-18
22339500-7 2012 Treatment with RA (retinoic acid) triggers NCCIT cell differentiation, reducing NANOG and OCT4 expression and up-regulating several neural markers [i.e. ASCL1 (achaete-scute complex homologue 1), NEUROD1 (neuronal differentiation 1) and PAX6 (paired box 6)]. Tretinoin 19-32 Nanog homeobox Homo sapiens 80-85
24130925-7 2012 Matrix metalloproteinase-9 (MMP-9) and MMP-2, well known genes involved in invasion of cancer cells were induced in the ATRA-induced invasion of the SH-SH5Y cells. Tretinoin 120-124 matrix metallopeptidase 9 Homo sapiens 0-26
24130925-7 2012 Matrix metalloproteinase-9 (MMP-9) and MMP-2, well known genes involved in invasion of cancer cells were induced in the ATRA-induced invasion of the SH-SH5Y cells. Tretinoin 120-124 matrix metallopeptidase 9 Homo sapiens 28-33
24130925-8 2012 Treatment of CTM suppressed the MMP-9 and MMP-2 enzyme activities in the ATRA-induced invasion of the SH-SY5Y cells. Tretinoin 73-77 matrix metallopeptidase 9 Homo sapiens 32-37
24346134-0 2013 All-trans retinoic acid-induced hypothalamus-pituitary-adrenal hyperactivity involves glucocorticoid receptor dysregulation. Tretinoin 10-23 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 86-109
24346134-3 2013 Here we show that all-trans retinoic acid (RA)-induced HPA activation involves impairments in glucocorticoid receptor (GR) negative feedback. Tretinoin 28-41 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 94-117
24346134-3 2013 Here we show that all-trans retinoic acid (RA)-induced HPA activation involves impairments in glucocorticoid receptor (GR) negative feedback. Tretinoin 28-41 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 119-121
15531370-0 2004 CYP26A1 and CYP26C1 cooperate in degrading retinoic acid within the equatorial retina during later eye development. Tretinoin 43-56 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-7
24346134-3 2013 Here we show that all-trans retinoic acid (RA)-induced HPA activation involves impairments in glucocorticoid receptor (GR) negative feedback. Tretinoin 43-45 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 94-117
24346134-3 2013 Here we show that all-trans retinoic acid (RA)-induced HPA activation involves impairments in glucocorticoid receptor (GR) negative feedback. Tretinoin 43-45 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 119-121
24346134-9 2013 Additional in vitro studies confirmed that RA abolished GR-mediated glucocorticoid-induced suppression of CRH expression, indicating a negative cross-talk between RAR-alpha and GR signaling pathways. Tretinoin 43-45 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 56-58
24324637-9 2013 RB1 significantly reduced renal injury and apoptosis as compared with IIR group, which was reversed by ATRA treatment. Tretinoin 103-107 RB transcriptional corepressor 1 Mus musculus 0-3
22387209-11 2012 Reduced retinoic acid synthesis altered the expression of genes involved in retinoic acid homeostasis and also demonstrated that retinoic acid signaling is required for Tbx3 expression, whereas high levels of retinoic acid signaling inhibited Bmp4 expression and repressed Wnt signaling. Tretinoin 8-21 T-box 3 Mus musculus 169-173
22396202-5 2012 In this study, we show that RA inhibits adipocyte differentiation by activating the CRABP-II/RARgamma path in preadipose cells, thereby upregulating the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2). Tretinoin 28-30 retinoic acid receptor, gamma Mus musculus 93-101
24324637-10 2013 Immunohistochemistry and Western blot analysis demonstrated that RB1 significantly upregulated the protein expression of heme oxygenase-1 (HO-1) and Nrf2, which were attenuated by ATRA treatment. Tretinoin 180-184 RB transcriptional corepressor 1 Mus musculus 65-68
15531370-1 2004 In the embryonic mouse retina, retinoic acid (RA) is unevenly distributed along the dorsoventral axis: RA-rich zones in dorsal and ventral retina are separated by a horizontal RA-poor stripe that contains the RA-inactivating enzyme CYP26A1. Tretinoin 31-44 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 232-239
24161943-5 2013 Knockdown of 14-3-3epsilon leads to a decrease in atRA-mediated neurite outgrowth, similar to the elongation defects observed when NAV2 is depleted or mutated. Tretinoin 50-54 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein epsilon Homo sapiens 13-26
22648617-5 2012 The aim of this study was to investigate the potential of orally administered lycopene and all-trans retinoic acid (ATRA) for the induction of the retinoic acid receptor (RAR) in a transgenic retinoic acid response-element (RARE)-reporter mouse system. Tretinoin 101-114 retinoic acid receptor, alpha Mus musculus 171-174
22648617-5 2012 The aim of this study was to investigate the potential of orally administered lycopene and all-trans retinoic acid (ATRA) for the induction of the retinoic acid receptor (RAR) in a transgenic retinoic acid response-element (RARE)-reporter mouse system. Tretinoin 116-120 retinoic acid receptor, alpha Mus musculus 171-174
22544395-0 2012 TGF-beta and retinoic acid induce the microRNA miR-10a, which targets Bcl-6 and constrains the plasticity of helper T cells. Tretinoin 13-26 BCL6 transcription repressor Homo sapiens 70-75
23891972-10 2013 In KPC mice, administration of ATRA, which renders PSCs quiescent, increased numbers of CD8(+) T cells in juxtatumoral compartments. Tretinoin 31-35 CD8a molecule Homo sapiens 88-91
22537161-0 2012 Nicotine, IFN-gamma and retinoic acid mediated induction of MUC4 in pancreatic cancer requires E2F1 and STAT-1 transcription factors and utilize different signaling cascades. Tretinoin 24-37 signal transducer and activator of transcription 1 Homo sapiens 104-110
15531370-7 2004 While RA applications increased retinal Cyp26a1 expression, they slightly reduced Cyp26c1. Tretinoin 6-8 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 40-47
22406747-3 2012 Here we show that, through epigenetic reprogramming, inhibitors of lysine-specific demethylase 1 (LSD1, also called KDM1A), including tranylcypromine (TCP), unlocked the ATRA-driven therapeutic response in non-APL AML. Tretinoin 170-174 lysine demethylase 1A Homo sapiens 116-121
24490497-6 2013 Cell surface differentiation antigen CD11b of infected HL-60 cell induced by ATRA was examined by FCM. Tretinoin 77-81 integrin subunit alpha M Homo sapiens 37-42
24204796-5 2013 This finding is in consistent with the previous reports that ATRA could regulate target genes without the presence of retinoic acid response element (RARE) in promoter region but through other signals such as PKA/CREB. Tretinoin 61-65 cAMP responsive element binding protein 1 Homo sapiens 213-217
15550114-9 2004 Treatment with retinoic acid tended to suppress the MCP-1 gene transcript, and significantly inhibited MCP-1 protein synthesis induced by high glucose stimulation. Tretinoin 15-28 C-C motif chemokine ligand 2 Rattus norvegicus 52-57
24926434-7 2013 Retinoic acid was identified as sufficient to induce the specification of neuroectoderm direct from the pluripotent state of hESCs and trigger a cascade of neuronal lineage-specific progression to human neuronal progenitors and neurons of the developing CNS in high efficiency, purity, and neuronal lineage specificity by promoting nuclear translocation of the neuronal specific transcription factor Nurr-1. Tretinoin 0-13 nuclear receptor subfamily 4 group A member 2 Homo sapiens 400-406
23960232-0 2013 IL-4 and retinoic acid synergistically induce regulatory dendritic cells expressing Aldh1a2. Tretinoin 9-22 aldehyde dehydrogenase 1 family member A2 Homo sapiens 84-91
23960232-5 2013 IL-4 plus RA-treated IDCs strongly induced CD4+Foxp3+ regulatory T cell differentiation and suppressed Th1 and Th17 differentiation. Tretinoin 10-12 negative elongation factor complex member C/D Homo sapiens 103-106
22355136-4 2012 We previously demonstrated that retinoic acid (RAR-RXR) and vitamin D3 receptors (VDR-RXR) heterodimers recruit only one coactivator molecule asymmetrically without steric hindrance for the binding of a second cofactor. Tretinoin 32-45 retinoid X receptor alpha Homo sapiens 51-54
22355136-4 2012 We previously demonstrated that retinoic acid (RAR-RXR) and vitamin D3 receptors (VDR-RXR) heterodimers recruit only one coactivator molecule asymmetrically without steric hindrance for the binding of a second cofactor. Tretinoin 32-45 vitamin D receptor Homo sapiens 82-85
22355136-4 2012 We previously demonstrated that retinoic acid (RAR-RXR) and vitamin D3 receptors (VDR-RXR) heterodimers recruit only one coactivator molecule asymmetrically without steric hindrance for the binding of a second cofactor. Tretinoin 32-45 retinoid X receptor alpha Homo sapiens 86-89
22154861-11 2012 In addition, positive staining for synaptophysin was detected only in cells cultured on aligned scaffolds in the presence of RA. Tretinoin 125-127 synaptophysin Homo sapiens 35-48
15550114-9 2004 Treatment with retinoic acid tended to suppress the MCP-1 gene transcript, and significantly inhibited MCP-1 protein synthesis induced by high glucose stimulation. Tretinoin 15-28 C-C motif chemokine ligand 2 Rattus norvegicus 103-108
22354841-0 2012 RIPPLY3 is a retinoic acid-inducible repressor required for setting the borders of the pre-placodal ectoderm. Tretinoin 13-26 ripply transcriptional repressor 3 Homo sapiens 0-7
15550114-12 2004 Retinoic acid treatment resulted in 30% reduction of the urinary level of MCP-1 compared with vehicle-treated diabetic rats (119.3+/-74.2 vs 78.1+/-62.7 pg/mgCr, P=0.078). Tretinoin 0-13 C-C motif chemokine ligand 2 Rattus norvegicus 74-79
23806210-3 2013 Because RA is produced locally in the tissues where it acts by stimulating RAR and RXR receptors, RA signaling during development is absolutely dependent on the rate of RA synthesis and degradation. Tretinoin 8-10 Rab40B, member RAS oncogene family Mus musculus 75-78
15550114-13 2004 Immunohistochemistry revealed a significant increase in staining for MCP-1 and anti-monocyte/macrophage (ED-1) protein in the diabetic kidney, and retinoic acid treatment significantly suppressed intrarenal MCP-1 and ED-1 protein synthesis. Tretinoin 147-160 C-C motif chemokine ligand 2 Rattus norvegicus 207-212
15563759-5 2004 Drug release from two sorts of ATRA-SLN was studied and compared with the diffusion from ATRA solution in 0.1 M HCl, distilled water and phosphate buffer (pH 7.40), using a dialysis bag method. Tretinoin 31-35 sarcolipin Rattus norvegicus 36-39
23833249-3 2013 Here we present that only a subset of murine and human DCs express the necessary enzymes, including RDH10, RALDH2, and transporter cellular retinoic acid binding protein (CRABP)2, to produce ATRA and efficient signaling. Tretinoin 191-195 retinol dehydrogenase 10 Homo sapiens 100-105
22250783-15 2012 ATRA may ease the bleomycin-induced pulmonary fibrosis by inhibiting the expression of IL-6 and TGF-beta, shifting the Treg/Th17 ratio and reducing the secretion of IL-17A. Tretinoin 0-4 interleukin 17A Mus musculus 165-171
22293198-5 2012 In a monolayer culture, RA significantly induced both the expression of the early germ-specific genes, Stra8, Dazl and Mvh, and prolonged activation of Smad1/5 (for at least 24h). Tretinoin 24-26 DEAD box helicase 4 Mus musculus 119-122
23833249-3 2013 Here we present that only a subset of murine and human DCs express the necessary enzymes, including RDH10, RALDH2, and transporter cellular retinoic acid binding protein (CRABP)2, to produce ATRA and efficient signaling. Tretinoin 191-195 aldehyde dehydrogenase 1 family member A2 Homo sapiens 107-113
15371543-0 2004 Rapid effects of retinoic acid on CREB and ERK phosphorylation in neuronal cells. Tretinoin 17-30 cAMP responsive element binding protein 1 Rattus norvegicus 34-38
23833249-3 2013 Here we present that only a subset of murine and human DCs express the necessary enzymes, including RDH10, RALDH2, and transporter cellular retinoic acid binding protein (CRABP)2, to produce ATRA and efficient signaling. Tretinoin 191-195 cellular retinoic acid binding protein 2 Homo sapiens 171-178
23833249-6 2013 In our model of human mo-DCs, all three proteins (RDH10, RALDH2, and CRABP2) appeared to be required for ATRA production induced by activation of PPARgamma and therefore form a linear pathway. Tretinoin 105-109 retinol dehydrogenase 10 Homo sapiens 50-55
23833249-6 2013 In our model of human mo-DCs, all three proteins (RDH10, RALDH2, and CRABP2) appeared to be required for ATRA production induced by activation of PPARgamma and therefore form a linear pathway. Tretinoin 105-109 aldehyde dehydrogenase 1 family member A2 Homo sapiens 57-63
23833249-6 2013 In our model of human mo-DCs, all three proteins (RDH10, RALDH2, and CRABP2) appeared to be required for ATRA production induced by activation of PPARgamma and therefore form a linear pathway. Tretinoin 105-109 cellular retinoic acid binding protein 2 Homo sapiens 69-75
22419906-5 2012 This action of RA was suggested to be mediated by its canonical receptor RARalpha but no genetic evidence was available. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 73-81
15371543-3 2004 We show here that in PC12 cell subclones in which the retinoid causes neurite extension, RA induces a rapid and sustained phosphorylation of CREB (cyclic AMP response element binding protein), compatible with a nongenomic effect. Tretinoin 89-91 cAMP responsive element binding protein 1 Rattus norvegicus 141-145
24137725-0 2013 Retraction notice to: Histone H2B ubquitination regulates retinoic acid signaling through the cooperation of ASXL1 and BAP1. Tretinoin 58-71 ASXL transcriptional regulator 1 Homo sapiens 109-114
15371543-3 2004 We show here that in PC12 cell subclones in which the retinoid causes neurite extension, RA induces a rapid and sustained phosphorylation of CREB (cyclic AMP response element binding protein), compatible with a nongenomic effect. Tretinoin 89-91 cAMP responsive element binding protein 1 Rattus norvegicus 147-190
15371543-4 2004 RA also causes a rapid increase of CREB phosphorylation in primary cultures of cerebrocortical cells and of dorsal root ganglia neurons from rat embryos. Tretinoin 0-2 cAMP responsive element binding protein 1 Rattus norvegicus 35-39
23903816-3 2013 The neuronal differentiation triggered by exposure to retinoic acid (RA) was characterized in the control culture by mRNA expression analysis of neuronal specific markers such as MAP2, NF-200, Tubulin betaIII, MAPT-tau, synaptophysin as well as excitatory (NMDA, AMPA) and inhibitory (GABA) receptors. Tretinoin 54-67 microtubule associated protein 2 Homo sapiens 179-183
15371543-5 2004 RA-mediated phosphorylation of CREB leads to a direct stimulation of CREB-dependent transcriptional activity and to activation of the expression of genes such as c-fos, which do not contain RAREs but contain cAMP response elements (CREs) in their promoters. Tretinoin 0-2 cAMP responsive element binding protein 1 Rattus norvegicus 31-35
15371543-5 2004 RA-mediated phosphorylation of CREB leads to a direct stimulation of CREB-dependent transcriptional activity and to activation of the expression of genes such as c-fos, which do not contain RAREs but contain cAMP response elements (CREs) in their promoters. Tretinoin 0-2 cAMP responsive element binding protein 1 Rattus norvegicus 69-73
15371543-6 2004 CREB is a major target of extracellular signal regulated kinase ERK1/2 signaling in neuronal cells, and we demonstrate here that RA induces an early stimulation of ERK1/2, which is required both for CREB phosphorylation and transcriptional activity. Tretinoin 129-131 cAMP responsive element binding protein 1 Rattus norvegicus 0-4
23773919-4 2013 Data presented in this study demonstrated that intraperitoneal injection of ATRA ameliorated EAMG pathology in rats associated with reduced total anti-acetylcholine receptor (AChR) serum IgG levels. Tretinoin 76-80 cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus 146-173
15371543-6 2004 CREB is a major target of extracellular signal regulated kinase ERK1/2 signaling in neuronal cells, and we demonstrate here that RA induces an early stimulation of ERK1/2, which is required both for CREB phosphorylation and transcriptional activity. Tretinoin 129-131 cAMP responsive element binding protein 1 Rattus norvegicus 199-203
23773919-4 2013 Data presented in this study demonstrated that intraperitoneal injection of ATRA ameliorated EAMG pathology in rats associated with reduced total anti-acetylcholine receptor (AChR) serum IgG levels. Tretinoin 76-80 cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus 175-179
23773919-7 2013 In vitro, ATRA inhibited AChR-specific cell proliferation and eliciting apoptosis in these cells without affecting the cell cycle. Tretinoin 10-14 cholinergic receptor nicotinic alpha 2 subunit Rattus norvegicus 25-29
15376324-0 2004 Crk-associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all-trans retinoic acid. Tretinoin 139-152 BCAR1 scaffold protein, Cas family member Homo sapiens 0-24
23530929-0 2013 Retinoic acid-elicited RARalpha/RXRalpha signaling attenuates Abeta production by directly inhibiting gamma-secretase-mediated cleavage of amyloid precursor protein. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 23-31
23530929-9 2013 Finally, we have established that RA inhibits gamma-secretase through nuclear retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-alpha (RXRalpha). Tretinoin 34-36 retinoic acid receptor, alpha Mus musculus 108-116
15376324-0 2004 Crk-associated substrate (Cas) family member, NEDD9, is regulated in human neuroblastoma cells and in the embryonic hindbrain by all-trans retinoic acid. Tretinoin 139-152 BCAR1 scaffold protein, Cas family member Homo sapiens 26-29
15376324-2 2004 In the human neuroblastoma cell line, SH-SY5Y, atRA rapidly induces (within 4 hr) the expression of the Crk-associated substrate (Cas) family member, neural precursor cell-expressed, developmentally down-regulated gene 9 (NEDD9) also called the human enhancer of filamentation (HEF1). Tretinoin 47-51 BCAR1 scaffold protein, Cas family member Homo sapiens 104-128
15376324-2 2004 In the human neuroblastoma cell line, SH-SY5Y, atRA rapidly induces (within 4 hr) the expression of the Crk-associated substrate (Cas) family member, neural precursor cell-expressed, developmentally down-regulated gene 9 (NEDD9) also called the human enhancer of filamentation (HEF1). Tretinoin 47-51 BCAR1 scaffold protein, Cas family member Homo sapiens 130-133
23541806-5 2013 Of note, myocardin-related transcription factor-A (MRTF-A), a major co-activator of serum response factor (SRF), was significantly activated and its nuclear localization was observed during RA-induced neural-like differentiation. Tretinoin 190-192 serum response factor Homo sapiens 107-110
15451545-0 2004 Delivery of all trans-retinoic acid (RA) to hepatocyte cell line from RA/galactosyl alpha-cyclodextrin inclusion complex. Tretinoin 16-35 glutaryl-CoA dehydrogenase Homo sapiens 70-102
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 25-38 Rab40B, member RAS oncogene family Mus musculus 109-112
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 25-38 Rab40B, member RAS oncogene family Mus musculus 204-207
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 40-42 Rab40B, member RAS oncogene family Mus musculus 109-112
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 40-42 Rab40B, member RAS oncogene family Mus musculus 204-207
23991366-1 2013 The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPARbeta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPARbeta/delta. Tretinoin 109-111 Rab40B, member RAS oncogene family Mus musculus 204-207
23991366-2 2013 In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RARgamma to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. Tretinoin 18-20 Rab40B, member RAS oncogene family Mus musculus 68-71
15492811-0 2004 Expression of p27 and MAPK proteins involved in all-trans retinoic acid-induced apoptosis and cell cycle arrest in matched primary and metastatic melanoma cells. Tretinoin 58-71 interferon alpha inducible protein 27 Homo sapiens 14-17
23657628-6 2013 We found that RA significantly enhanced TGF-beta-induced expression of Foxp3 on naive and committed T cells in vitro and that this was blocked by an antagonist of RARalpha (RARi). Tretinoin 14-16 retinoic acid receptor, alpha Mus musculus 163-171
15492811-1 2004 We investigated whether p27 and mitogen-activated protein kinase (MAPK) proteins were involved in all-trans retinoic acid (atRA)-induced apoptosis and cell cycle arrest. Tretinoin 108-121 interferon alpha inducible protein 27 Homo sapiens 24-27
23600914-4 2013 The expression of ABCA1 and ABCG1 was induced by 24-OHC, as well as TO901317 and retinoic acid, which are ligands of the nuclear receptors liver X receptor/retinoid X receptor (LXR/RXR). Tretinoin 81-94 ATP binding cassette subfamily A member 1 Homo sapiens 18-23
15492811-1 2004 We investigated whether p27 and mitogen-activated protein kinase (MAPK) proteins were involved in all-trans retinoic acid (atRA)-induced apoptosis and cell cycle arrest. Tretinoin 123-127 interferon alpha inducible protein 27 Homo sapiens 24-27
23600914-4 2013 The expression of ABCA1 and ABCG1 was induced by 24-OHC, as well as TO901317 and retinoic acid, which are ligands of the nuclear receptors liver X receptor/retinoid X receptor (LXR/RXR). Tretinoin 81-94 retinoid X receptor alpha Homo sapiens 181-184
15492811-9 2004 These data indicate that up-regulation of p27 and down-regulation of MAPK proteins were involved in atRA-induced apoptosis and cell cycle arrest in melanoma. Tretinoin 100-104 interferon alpha inducible protein 27 Homo sapiens 42-45
23785470-1 2013 In mammalian germ cells, meiotic commitment requires the expression of Stimulated by retinoic acid gene 8 (Stra8), which is transcriptionally activated by retinoic acid (RA). Tretinoin 85-98 stimulated by retinoic acid 8 Homo sapiens 107-112
15514252-0 2004 Triiodothyronine treatment attenuates the induction of hepatic glycine N-methyltransferase by retinoic acid and elevates plasma homocysteine concentrations in rats. Tretinoin 94-107 glycine N-methyltransferase Rattus norvegicus 63-90
23785470-1 2013 In mammalian germ cells, meiotic commitment requires the expression of Stimulated by retinoic acid gene 8 (Stra8), which is transcriptionally activated by retinoic acid (RA). Tretinoin 170-172 stimulated by retinoic acid 8 Homo sapiens 71-105
23785470-1 2013 In mammalian germ cells, meiotic commitment requires the expression of Stimulated by retinoic acid gene 8 (Stra8), which is transcriptionally activated by retinoic acid (RA). Tretinoin 170-172 stimulated by retinoic acid 8 Homo sapiens 107-112
15514252-2 2004 Retinoic acid (RA) was shown to induce hepatic glycine N-methyltransferase (GNMT), a key regulatory protein in methyl group metabolism, and to reduce circulating homocysteine levels. Tretinoin 0-13 glycine N-methyltransferase Rattus norvegicus 47-74
15514252-2 2004 Retinoic acid (RA) was shown to induce hepatic glycine N-methyltransferase (GNMT), a key regulatory protein in methyl group metabolism, and to reduce circulating homocysteine levels. Tretinoin 0-13 glycine N-methyltransferase Rattus norvegicus 76-80
23763947-6 2013 Gdf11 also coordinates reallocation of bipotent neuromesodermal progenitors from the anterior primitive streak to the tail bud, in part by reducing the retinoic acid available to the progenitors. Tretinoin 152-165 growth differentiation factor 11 Homo sapiens 0-5
15514252-2 2004 Retinoic acid (RA) was shown to induce hepatic glycine N-methyltransferase (GNMT), a key regulatory protein in methyl group metabolism, and to reduce circulating homocysteine levels. Tretinoin 15-17 glycine N-methyltransferase Rattus norvegicus 47-74
15514252-2 2004 Retinoic acid (RA) was shown to induce hepatic glycine N-methyltransferase (GNMT), a key regulatory protein in methyl group metabolism, and to reduce circulating homocysteine levels. Tretinoin 15-17 glycine N-methyltransferase Rattus norvegicus 76-80
15514252-7 2004 d)] the last 4 d. T(3) treatment prevented the RA-mediated increase in GNMT activity. Tretinoin 47-49 glycine N-methyltransferase Rattus norvegicus 71-75
23711709-4 2013 RESULTS: Of them, 82 were mapped in proximity to known or previously predicted genes; 7 were randomly picked up for further confirmation by ChIP-PCR and 3 genes (GALM, ITPR2 and ORM2) were found to be specifically up-regulated in the ATRA-treated NB4 cells, indicating that they might be the down-stream target genes of ATRA. Tretinoin 234-238 orosomucoid 2 Homo sapiens 178-182
23711709-4 2013 RESULTS: Of them, 82 were mapped in proximity to known or previously predicted genes; 7 were randomly picked up for further confirmation by ChIP-PCR and 3 genes (GALM, ITPR2 and ORM2) were found to be specifically up-regulated in the ATRA-treated NB4 cells, indicating that they might be the down-stream target genes of ATRA. Tretinoin 320-324 orosomucoid 2 Homo sapiens 178-182
15514258-0 2004 Alcohol-reduced plasma IGF-I levels and hepatic IGF-I expression can be partially restored by retinoic acid supplementation in rats. Tretinoin 94-107 insulin-like growth factor 1 Rattus norvegicus 23-28
15514258-0 2004 Alcohol-reduced plasma IGF-I levels and hepatic IGF-I expression can be partially restored by retinoic acid supplementation in rats. Tretinoin 94-107 insulin-like growth factor 1 Rattus norvegicus 48-53
23330981-3 2013 Here, we examined the molecular mechanisms underlying the deregulation of HIPK2 activity in two cellular models, HEK-293 cells and SH-SY5Y neuroblastoma cells differentiated with retinoic acid over-expressing the amyloid precursor protein, focusing on the evidence that zyxin expression is important to maintain HIPK2 protein stability. Tretinoin 179-192 homeodomain interacting protein kinase 2 Homo sapiens 74-79
15514258-6 2004 In contrast, RA supplementation in ethanol-fed rats partially restored both hepatic IGF-I mRNA levels and plasma IGF-I concentration compared with rats fed ethanol alone. Tretinoin 13-15 insulin-like growth factor 1 Rattus norvegicus 84-89
15514258-6 2004 In contrast, RA supplementation in ethanol-fed rats partially restored both hepatic IGF-I mRNA levels and plasma IGF-I concentration compared with rats fed ethanol alone. Tretinoin 13-15 insulin-like growth factor 1 Rattus norvegicus 113-118
15597079-1 2004 BACKGROUND: Cytosolic aldehyde dehydrogenase (ALDH1A1) is an important enzyme in the metabolism of acetaldehyde and the synthesis of retinoic acid. Tretinoin 133-146 aldehyde dehydrogenase 1 family member A1 Homo sapiens 46-53
23228968-0 2013 ATRA and the specific RARalpha agonist, NRX195183, have opposing effects on the clonogenicity of pre-leukemic murine AML1-ETO bone marrow cells. Tretinoin 0-4 runt related transcription factor 1 Mus musculus 117-121
23228968-2 2013 ATRA enhances hematopoietic stem cell self-renewal through retinoic acid receptor (RAR)gamma activation while promoting differentiation of committed myeloid progenitors through RARalpha activation. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 83-86
23228968-2 2013 ATRA enhances hematopoietic stem cell self-renewal through retinoic acid receptor (RAR)gamma activation while promoting differentiation of committed myeloid progenitors through RARalpha activation. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 177-185
23583383-4 2013 We found that RA treatment resulted in a dramatic inhibition of adipogenesis, especially at an early phase of differentiation, and led to increased beta-catenin protein expression. Tretinoin 14-16 catenin (cadherin associated protein), beta 1 Mus musculus 148-160
15554945-7 2004 Conversely, knock-down of MyoR expression via RNA interference enhances RA-induced differentiation of EC cells, promoting earlier and much higher expression of the above-mentioned endodermal markers following RA treatment. Tretinoin 72-74 musculin Homo sapiens 26-30
23583383-5 2013 Moreover, RA enhances the transcriptional activity of beta-catenin as well as Wnt gene expression during adipogenesis. Tretinoin 10-12 catenin (cadherin associated protein), beta 1 Mus musculus 54-66
23583383-6 2013 Taken together, the present study demonstrated that Wnt/beta-catenin signaling may be associated with the RA-induced suppression of adipogenesis and may cooperatively inhibit adipocyte differentiation. Tretinoin 106-108 catenin (cadherin associated protein), beta 1 Mus musculus 56-68
23656719-11 2013 RESULTS: We demonstrate that FICZ enhances RA-induced differentiation, assessed by the expression of the membrane differentiation marker CD11b; cell cycle arrest; and the functional differentiation marker, inducible-oxidative metabolism. Tretinoin 43-45 integrin subunit alpha M Homo sapiens 137-142
23656719-14 2013 Moreover, FICZ in combination with RA also increases expression of AhR and even more so of both Cyp1A2 and p47phox, which are known to be transcriptionally regulated by AhR. Tretinoin 35-37 neutrophil cytosolic factor 1 Homo sapiens 107-114
15554945-7 2004 Conversely, knock-down of MyoR expression via RNA interference enhances RA-induced differentiation of EC cells, promoting earlier and much higher expression of the above-mentioned endodermal markers following RA treatment. Tretinoin 209-211 musculin Homo sapiens 26-30
15358589-4 2004 The t(15;17)(q22;q21) gene rearrangement and PML/RARalpha fusion product in acute promyelocytic leukemia played the key role to leukemogenesis and to sensitivity to differentiation-inducing therapy of all-trans retinoic acid. Tretinoin 211-224 PML nuclear body scaffold Homo sapiens 45-48
23542713-11 2013 On the other hand, retinoic acid enhanced the expression of VEGF despite inhibiting the TGZ-induced differentiation. Tretinoin 19-32 vascular endothelial growth factor A Mus musculus 60-64
15358589-4 2004 The t(15;17)(q22;q21) gene rearrangement and PML/RARalpha fusion product in acute promyelocytic leukemia played the key role to leukemogenesis and to sensitivity to differentiation-inducing therapy of all-trans retinoic acid. Tretinoin 211-224 retinoic acid receptor alpha Homo sapiens 49-57
15223636-10 2004 These results suggested that CD56 expression was associated with the leukemogenetic mutation at the primitive hematopoietic progenitor cell level and extramedullary relapse in APL patients treated with ATRA and chemotherapy. Tretinoin 202-206 neural cell adhesion molecule 1 Homo sapiens 29-33
15234573-0 2004 Alteration in the cellular response to retinoic acid of a human acute promyelocytic leukemia cell line, UF-1, carrying a patient-derived mutant PML-RARalpha chimeric gene. Tretinoin 39-52 PML nuclear body scaffold Homo sapiens 144-147
15234573-0 2004 Alteration in the cellular response to retinoic acid of a human acute promyelocytic leukemia cell line, UF-1, carrying a patient-derived mutant PML-RARalpha chimeric gene. Tretinoin 39-52 retinoic acid receptor alpha Homo sapiens 148-156
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 31-44 PML nuclear body scaffold Homo sapiens 118-121
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 31-44 PML nuclear body scaffold Homo sapiens 152-155
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 31-44 retinoic acid receptor alpha Homo sapiens 156-164
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 31-44 PML nuclear body scaffold Homo sapiens 152-155
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 46-50 PML nuclear body scaffold Homo sapiens 118-121
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 46-50 PML nuclear body scaffold Homo sapiens 152-155
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 46-50 retinoic acid receptor alpha Homo sapiens 156-164
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 46-50 PML nuclear body scaffold Homo sapiens 152-155
15234573-1 2004 Cellular response to all-trans retinoic acid (ATRA) of acute promyelocytic leukemia (APL) with patient-derived mutant PML-retinoic acid receptor-alpha (PML-RARalpha) was investigated using an APL cell line, UF-1, carrying Arg611Trp mutation in PML-RARalpha. Tretinoin 46-50 retinoic acid receptor alpha Homo sapiens 248-256
22153617-0 2012 CRABP-II methylation: a critical determinant of retinoic acid resistance of medulloblastoma cells. Tretinoin 48-61 cellular retinoic acid binding protein 2 Homo sapiens 0-8
15262180-9 2004 These results strongly suggest that retinoic acid stimulates the release of VEGF in a p44/p42 MAP kinase-dependent manner in aortic smooth muscle cells. Tretinoin 36-49 cyclin dependent kinase 20 Homo sapiens 90-93
22153617-12 2012 In conclusion, aberrant methylation in CRABP-II reduces the expression of CRABP-II that in turn confers RA resistance in medulloblastoma cells. Tretinoin 40-42 cellular retinoic acid binding protein 2 Homo sapiens 74-82
15268896-8 2004 BMP"s stimulatory effects on SOST were further enhanced by retinoic acid or 1,25-dihydroxyvitamin D3. Tretinoin 59-72 bone morphogenetic protein 1 Homo sapiens 0-3
22197812-10 2012 Additionally, two ER-resident E3 ubiquitin ligases, gp78 and Hrd1, were both upregulated in H9 cells following 5 days of exposure to RA. Tretinoin 133-135 autocrine motility factor receptor Homo sapiens 52-56
23124249-3 2012 ATRA treatment causes neuronal differentiation by inducing tropomyosin-related kinase B (TrkB) expression and increasing the sensitivity to brain-derived neurotrophic factor (BDNF), a TrkB ligand. Tretinoin 0-4 brain derived neurotrophic factor Homo sapiens 140-173
23124249-3 2012 ATRA treatment causes neuronal differentiation by inducing tropomyosin-related kinase B (TrkB) expression and increasing the sensitivity to brain-derived neurotrophic factor (BDNF), a TrkB ligand. Tretinoin 0-4 brain derived neurotrophic factor Homo sapiens 175-179
15254726-5 2004 Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. Tretinoin 106-110 H3 histone pseudogene 16 Homo sapiens 19-22
22010213-5 2012 RESULTS: Response to ATRA was observed to be dependent upon differential expression of FABP5 versus CRABP2. Tretinoin 21-25 fatty acid binding protein 5 Homo sapiens 87-92
22010213-5 2012 RESULTS: Response to ATRA was observed to be dependent upon differential expression of FABP5 versus CRABP2. Tretinoin 21-25 cellular retinoic acid binding protein 2 Homo sapiens 100-106
22010213-7 2012 Conversely, CRABP2 expression in the absence of FABP5 was associated with significant tumor growth inhibition with ATRA, even in gemcitabine-resistant tumors. Tretinoin 115-119 cellular retinoic acid binding protein 2 Homo sapiens 12-18
15254726-8 2004 These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Tretinoin 75-79 H3 histone pseudogene 16 Homo sapiens 30-33
22010213-8 2012 The ATRA-resistant phenotype of FABP5(high)CRABP2(null) cells could be circumvented by ectopic expression of CRABP2. Tretinoin 4-8 fatty acid binding protein 5 Homo sapiens 32-37
22010213-8 2012 The ATRA-resistant phenotype of FABP5(high)CRABP2(null) cells could be circumvented by ectopic expression of CRABP2. Tretinoin 4-8 cellular retinoic acid binding protein 2 Homo sapiens 43-49
15184080-0 2004 The retinoic acid and brain-derived neurotrophic factor differentiated SH-SY5Y cell line as a model for Alzheimer"s disease-like tau phosphorylation. Tretinoin 4-17 microtubule associated protein tau Homo sapiens 129-132
22010213-8 2012 The ATRA-resistant phenotype of FABP5(high)CRABP2(null) cells could be circumvented by ectopic expression of CRABP2. Tretinoin 4-8 cellular retinoic acid binding protein 2 Homo sapiens 109-115
15215172-11 2004 In the presence of RA, active forms of both MMP-1 and MMP-9 were reduced. Tretinoin 19-21 matrix metallopeptidase 1 Homo sapiens 44-49
23296452-1 2012 Retinoid-X receptor (RXR)- and retinoic acid receptor (RAR)-mediated signaling is induced by retinoic acids (RA), which are involved in the regulation of skin permeability, differentiation and immune response. Tretinoin 93-107 retinoic acid receptor, alpha Mus musculus 31-53
23296452-1 2012 Retinoid-X receptor (RXR)- and retinoic acid receptor (RAR)-mediated signaling is induced by retinoic acids (RA), which are involved in the regulation of skin permeability, differentiation and immune response. Tretinoin 93-107 retinoic acid receptor, alpha Mus musculus 55-58
23296452-1 2012 Retinoid-X receptor (RXR)- and retinoic acid receptor (RAR)-mediated signaling is induced by retinoic acids (RA), which are involved in the regulation of skin permeability, differentiation and immune response. Tretinoin 55-57 retinoic acid receptor, alpha Mus musculus 31-53
22045663-3 2012 Here, we show that 1) RARG is expressed by A aligned (A(al)) spermatogonia, as well as during the transition from A(al) to A(1) spermatogonia, which is known to require RA; and 2) ablation of Rarg, either in the whole mouse or specifically in spermatogonia, does not affect meiosis and spermiogenesis but impairs the A(al) to A(1) transition in the course of some of the seminiferous epithelium cycles. Tretinoin 22-24 retinoic acid receptor, gamma Mus musculus 192-196
15188435-1 2004 We have cloned a novel retinoic acid (RA) catabolizing enzyme, Cyp26C1, in the chick and describe here its distribution during early stages of chick embryogenesis. Tretinoin 23-36 cytochrome P450 family 26 subfamily C member 1 Gallus gallus 63-70
23304206-7 2012 In conclusion, we report a new mechanism in which RA could cause apoptosis of androgen-independent prostate cancer cells through p35 cleavage and Cdk5 over-activation. Tretinoin 50-52 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 129-132
15188435-1 2004 We have cloned a novel retinoic acid (RA) catabolizing enzyme, Cyp26C1, in the chick and describe here its distribution during early stages of chick embryogenesis. Tretinoin 38-40 cytochrome P450 family 26 subfamily C member 1 Gallus gallus 63-70
15188435-5 2004 We suggest that a gradient of RA within the mesoderm generated by Raldh2 and catabolized by Cyp26C1 could be responsible for patterning the hindbrain. Tretinoin 30-32 cytochrome P450 family 26 subfamily C member 1 Gallus gallus 92-99
22072421-6 2012 However, CD44-deficient tail skin challenged with retinoic acid or tape stripping revealed diffuse accumulation of hyaluronan in the superficial epidermal layers, normally negative for hyaluronan. Tretinoin 50-63 CD44 molecule (Indian blood group) Homo sapiens 9-13
15580810-4 2004 Phorbol-myristate-acetate (PMA)/ionomycin-stimulated SMC (splenic mononuclear cells) from mice fed with ATRA and the vitamin A-deficient diet group showed increased interleukin-4 (IL-4) responses in non-sensitized mice. Tretinoin 104-108 interleukin 4 Mus musculus 165-178
21859520-6 2012 However, alpha-SMA and MHC expression were affected by differentiation factors in strain culture, in particular, showing that treatment with retinoic acid significantly increased the expression of alpha-SMA (3.6-fold) and MHC (2-fold) as compared to strain alone. Tretinoin 141-154 major histocompatibility complex, class I, C Homo sapiens 23-26
21859520-6 2012 However, alpha-SMA and MHC expression were affected by differentiation factors in strain culture, in particular, showing that treatment with retinoic acid significantly increased the expression of alpha-SMA (3.6-fold) and MHC (2-fold) as compared to strain alone. Tretinoin 141-154 major histocompatibility complex, class I, C Homo sapiens 222-225
15580810-4 2004 Phorbol-myristate-acetate (PMA)/ionomycin-stimulated SMC (splenic mononuclear cells) from mice fed with ATRA and the vitamin A-deficient diet group showed increased interleukin-4 (IL-4) responses in non-sensitized mice. Tretinoin 104-108 interleukin 4 Mus musculus 180-184
15103387-3 2004 PML/RARalpha is the central leukemia-inducing lesion in APL and is directly targeted by all trans retinoic acid (t-RA) as well as by arsenic, both compounds able to induce complete remissions. Tretinoin 92-111 PML nuclear body scaffold Homo sapiens 0-3
21842375-7 2012 Zebularine alone or in sequential combination with RA decreased expression of DNMT1, caused fast and time-dependent expression of pan-cadherin and partial demethylation of E-cadherin but not tumor suppressor p15. Tretinoin 51-53 DNA methyltransferase 1 Homo sapiens 78-83
15103387-3 2004 PML/RARalpha is the central leukemia-inducing lesion in APL and is directly targeted by all trans retinoic acid (t-RA) as well as by arsenic, both compounds able to induce complete remissions. Tretinoin 92-111 retinoic acid receptor alpha Homo sapiens 4-12
15103387-3 2004 PML/RARalpha is the central leukemia-inducing lesion in APL and is directly targeted by all trans retinoic acid (t-RA) as well as by arsenic, both compounds able to induce complete remissions. Tretinoin 113-117 PML nuclear body scaffold Homo sapiens 0-3
15103387-3 2004 PML/RARalpha is the central leukemia-inducing lesion in APL and is directly targeted by all trans retinoic acid (t-RA) as well as by arsenic, both compounds able to induce complete remissions. Tretinoin 113-117 retinoic acid receptor alpha Homo sapiens 4-12
21818148-8 2012 By contrast, Zfp36 expression in murine macrophages (RAW 264.7) was not enhanced by exposure to Dex but was stimulated by retinoic acid (RA). Tretinoin 122-135 zinc finger protein 36 Mus musculus 13-18
21818148-8 2012 By contrast, Zfp36 expression in murine macrophages (RAW 264.7) was not enhanced by exposure to Dex but was stimulated by retinoic acid (RA). Tretinoin 53-55 zinc finger protein 36 Mus musculus 13-18
15116119-7 2004 This was associated with a right-shift and sharpening of the ATRA-induced maturation response compared to ATRA-sensitive NB4 cells, which corresponded to the transcriptional activation by PML-RARalphaPro900Ser of a cotransfected ATRA-targeted reporter vector in COS-1 cells. Tretinoin 61-65 PML nuclear body scaffold Homo sapiens 188-191
22389628-4 2012 In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24. Tretinoin 15-28 MDM2 proto-oncogene Homo sapiens 123-127
15116119-7 2004 This was associated with a right-shift and sharpening of the ATRA-induced maturation response compared to ATRA-sensitive NB4 cells, which corresponded to the transcriptional activation by PML-RARalphaPro900Ser of a cotransfected ATRA-targeted reporter vector in COS-1 cells. Tretinoin 106-110 PML nuclear body scaffold Homo sapiens 188-191
22389628-4 2012 In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24. Tretinoin 15-28 tripartite motif containing 24 Homo sapiens 132-138
15158163-3 2004 In this study, the presence and the intracellular distribution of torsinA protein in SH-SY5Y neuroblastoma cells were evaluated by immunofluorescence and Western blot analysis following differentiation with retinoic acid and BDNF. Tretinoin 207-220 torsin family 1 member A Homo sapiens 66-73
22629307-1 2012 Human Ntera2/cl.D1 (NT2) cells treated with retinoic acid (RA) differentiate towards a well characterized neuronal phenotype sharing many features with human fetal neurons. Tretinoin 44-57 claudin 1 Homo sapiens 6-18
22629307-1 2012 Human Ntera2/cl.D1 (NT2) cells treated with retinoic acid (RA) differentiate towards a well characterized neuronal phenotype sharing many features with human fetal neurons. Tretinoin 59-61 claudin 1 Homo sapiens 6-18
22629307-5 2012 The RA-induced expression of neuronal markers, i.e. neural cell adhesion molecule (NCAM), microtubule associated protein-2 (MAP2) and tyrosine hydroxylase (TH) mRNAs and proteins, was decreased in si-Casp9, but markedly increased in si-Casp2 cells. Tretinoin 4-6 microtubule associated protein 2 Homo sapiens 90-122
23539512-0 2013 Preincubation of pituitary tumor cells with the epidrugs zebularine and trichostatin A are permissive for retinoic acid-augmented expression of the BMP-4 and D2R genes. Tretinoin 106-119 bone morphogenetic protein 4 Rattus norvegicus 148-153
23539512-1 2013 Retinoic acid (RA)-induced expression of bone morphogenetic protein-4 (BMP-4) inhibits in vitro and in vivo cell proliferation and ACTH synthesis in corticotroph-derived tumor cells. Tretinoin 0-13 bone morphogenetic protein 4 Rattus norvegicus 41-69
23539512-1 2013 Retinoic acid (RA)-induced expression of bone morphogenetic protein-4 (BMP-4) inhibits in vitro and in vivo cell proliferation and ACTH synthesis in corticotroph-derived tumor cells. Tretinoin 0-13 bone morphogenetic protein 4 Rattus norvegicus 71-76
23539512-1 2013 Retinoic acid (RA)-induced expression of bone morphogenetic protein-4 (BMP-4) inhibits in vitro and in vivo cell proliferation and ACTH synthesis in corticotroph-derived tumor cells. Tretinoin 15-17 bone morphogenetic protein 4 Rattus norvegicus 41-69
23539512-1 2013 Retinoic acid (RA)-induced expression of bone morphogenetic protein-4 (BMP-4) inhibits in vitro and in vivo cell proliferation and ACTH synthesis in corticotroph-derived tumor cells. Tretinoin 15-17 bone morphogenetic protein 4 Rattus norvegicus 71-76
22629307-5 2012 The RA-induced expression of neuronal markers, i.e. neural cell adhesion molecule (NCAM), microtubule associated protein-2 (MAP2) and tyrosine hydroxylase (TH) mRNAs and proteins, was decreased in si-Casp9, but markedly increased in si-Casp2 cells. Tretinoin 4-6 microtubule associated protein 2 Homo sapiens 124-128
22629307-6 2012 During RA-induced NT2 differentiation, the class III histone deacetylase Sirt1, a putative caspase substrate implicated in the regulation of the proneural bHLH MASH1 gene expression, was cleaved to a ~100 kDa fragment. Tretinoin 7-9 sirtuin 1 Homo sapiens 73-78
23539512-2 2013 Reduced expression of BMP-4 in this adenoma subtype is associated with epigenomic silencing, and similar silencing mechanisms are also associated with the RA-responsive dopamine D2 receptor (D2R) in somatolactotroph cells. Tretinoin 155-157 bone morphogenetic protein 4 Rattus norvegicus 22-27
15075337-4 2004 Therefore, we examined the effect of TCDD and all-trans retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagenase), one of the proteolytic enzymes that degrade type I collagen, in normal human keratinocytes. Tretinoin 46-69 matrix metallopeptidase 1 Homo sapiens 98-124
23539512-3 2013 We now show that preincubation with the epidrugs zebularine and trichostatin A is obligate and permissive for RA-induced expression of the BMP-4 and the D2R genes in pituitary tumor cells. Tretinoin 110-112 bone morphogenetic protein 4 Rattus norvegicus 139-144
23614737-5 2013 The authors demonstrated that ALDH1A1 substrate 9-cis retinal and its corresponding product 9-cis retinoic acid potently induced the accumulation of MITF mRNA, tyrosinase mRNA and melanin. Tretinoin 98-111 tyrosinase Homo sapiens 160-170
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 13-26 glial fibrillary acidic protein Homo sapiens 159-190
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 13-26 glial fibrillary acidic protein Homo sapiens 192-196
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 28-30 glial fibrillary acidic protein Homo sapiens 159-190
23489885-8 2013 Furthermore, Retinoic acid (RA) treatment confirmed the expression of the multipotent differentiation markers in the SP cells, including TUJ1, pancytokeratin, glial fibrillary acidic protein (GFAP), and p27(Kip1). Tretinoin 28-30 glial fibrillary acidic protein Homo sapiens 192-196
22470433-0 2012 The colocalization potential of HIV-specific CD8+ and CD4+ T-cells is mediated by integrin beta7 but not CCR6 and regulated by retinoic acid. Tretinoin 127-140 CD8a molecule Homo sapiens 45-48
22363502-7 2012 However, the RA treatment blocks the increased primitive myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Tretinoin 13-15 GATA binding protein 4 Danio rerio 95-102
22363502-7 2012 However, the RA treatment blocks the increased primitive myelopoiesis caused by overexpressing gata4/6 whereas the abolished primitive myelopoiesis in gata4/5/6 depleted embryos is well rescued by 4-diethylamino-benzaldehyde, a retinal dehydrogenase inhibitor, or partially rescued by knocking down aldh1a2, the major retinal dehydrogenase gene that is responsible for RA synthesis during early development. Tretinoin 13-15 GATA binding protein 4 Danio rerio 95-100
22363502-9 2012 The results reveal that RA signaling acts downstream of gata4/5/6 to control primitive myelopoiesis. Tretinoin 24-26 GATA binding protein 4 Danio rerio 56-65
22363502-11 2012 Taken together, our results demonstrate that RA signaling restricts zebrafish primitive myelopoiesis through acting downstream of gata4/5/6, upstream of, or parallel to, cloche, and upstream of scl. Tretinoin 45-47 GATA binding protein 4 Danio rerio 130-139
23423514-1 2013 The ratio between FABP5 and CRABPII determines cellular response to physiological level of retinoic acid; tumor cells undergo proliferation with high level of FABP5 and apoptosis with high level of CRABPII. Tretinoin 91-104 fatty acid binding protein 5 Homo sapiens 18-23
23423514-1 2013 The ratio between FABP5 and CRABPII determines cellular response to physiological level of retinoic acid; tumor cells undergo proliferation with high level of FABP5 and apoptosis with high level of CRABPII. Tretinoin 91-104 cellular retinoic acid binding protein 2 Homo sapiens 28-35
23423514-1 2013 The ratio between FABP5 and CRABPII determines cellular response to physiological level of retinoic acid; tumor cells undergo proliferation with high level of FABP5 and apoptosis with high level of CRABPII. Tretinoin 91-104 fatty acid binding protein 5 Homo sapiens 159-164
23423514-1 2013 The ratio between FABP5 and CRABPII determines cellular response to physiological level of retinoic acid; tumor cells undergo proliferation with high level of FABP5 and apoptosis with high level of CRABPII. Tretinoin 91-104 cellular retinoic acid binding protein 2 Homo sapiens 198-205
21987446-6 2011 Here, we treated the seminoma-like cell line TCam-2 with the HDAC-inhibitor Depsipeptide, the global demethylating agent 5-aza-2"-deocycytidine, all-trans retinoic acid and the monaminooxidase inhibitor Tranylcipromine and also used knock down approaches to reduce expression of the pluripotency marker NANOG and/or the inhibitor of primordial germ cell differentiation TFAP2C. Tretinoin 155-168 histone deacetylase 9 Homo sapiens 61-65
23423514-2 2013 We intended to study FABP5 and CRABPII expression in craniopharyngiomas, to establish craniopharyngioma cell model using explants method, and to study the effect of pharmacological dose of retinoic acid on craniopharyngioma cells. Tretinoin 189-202 fatty acid binding protein 5 Homo sapiens 21-26
15075337-4 2004 Therefore, we examined the effect of TCDD and all-trans retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagenase), one of the proteolytic enzymes that degrade type I collagen, in normal human keratinocytes. Tretinoin 46-69 matrix metallopeptidase 1 Homo sapiens 126-131
23423514-2 2013 We intended to study FABP5 and CRABPII expression in craniopharyngiomas, to establish craniopharyngioma cell model using explants method, and to study the effect of pharmacological dose of retinoic acid on craniopharyngioma cells. Tretinoin 189-202 cellular retinoic acid binding protein 2 Homo sapiens 31-38
23423514-9 2013 Also, retinoic acid increased CRABPII, and decreased FABP5 and NF-kappaB expression in craniopharyngioma cells. Tretinoin 6-19 cellular retinoic acid binding protein 2 Homo sapiens 30-37
21720768-4 2011 In HL-60 cells treated with ATRA, the increase of beta3GnT-8 was more than beta3GnT-2, while in NB4 cells treated with DMSO, the increase of beta3GnT-2 was more than beta3GnT-8. Tretinoin 28-32 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 50-60
15075337-4 2004 Therefore, we examined the effect of TCDD and all-trans retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagenase), one of the proteolytic enzymes that degrade type I collagen, in normal human keratinocytes. Tretinoin 46-69 matrix metallopeptidase 1 Homo sapiens 133-157
21720768-4 2011 In HL-60 cells treated with ATRA, the increase of beta3GnT-8 was more than beta3GnT-2, while in NB4 cells treated with DMSO, the increase of beta3GnT-2 was more than beta3GnT-8. Tretinoin 28-32 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 75-85
23423514-9 2013 Also, retinoic acid increased CRABPII, and decreased FABP5 and NF-kappaB expression in craniopharyngioma cells. Tretinoin 6-19 fatty acid binding protein 5 Homo sapiens 53-58
23423514-11 2013 Retinoic acid at pharmacological level induced craniopharyngioma cell apoptosis via increasing FABP5/CRABPII ratio and inhibiting NF-kappaB signaling pathway. Tretinoin 0-13 fatty acid binding protein 5 Homo sapiens 95-100
23423514-11 2013 Retinoic acid at pharmacological level induced craniopharyngioma cell apoptosis via increasing FABP5/CRABPII ratio and inhibiting NF-kappaB signaling pathway. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 101-108
21720768-4 2011 In HL-60 cells treated with ATRA, the increase of beta3GnT-8 was more than beta3GnT-2, while in NB4 cells treated with DMSO, the increase of beta3GnT-2 was more than beta3GnT-8. Tretinoin 28-32 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 141-151
21720768-4 2011 In HL-60 cells treated with ATRA, the increase of beta3GnT-8 was more than beta3GnT-2, while in NB4 cells treated with DMSO, the increase of beta3GnT-2 was more than beta3GnT-8. Tretinoin 28-32 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 8 Homo sapiens 166-176
15075337-4 2004 Therefore, we examined the effect of TCDD and all-trans retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagenase), one of the proteolytic enzymes that degrade type I collagen, in normal human keratinocytes. Tretinoin 71-75 matrix metallopeptidase 1 Homo sapiens 98-124
21555390-7 2011 RESULTS: In this study, we demonstrate a substantial increase in the expression of the NKG2D ligands retinoic acid early inducible-1 (RAE-1), murine ULBP-like transcript 1 (MULT-1) and histocompatibility-60 (H-60) in mouse kidneys during renal IRI. Tretinoin 101-114 ribonucleic acid export 1 Mus musculus 134-139
23638129-4 2013 We observed pronounced epidermal hyperproliferation upon application of ATRA and synthetic agonists for RARgamma and RXR. Tretinoin 72-76 retinoic acid receptor, gamma Mus musculus 104-112
23638129-6 2013 In contrast, a RARalpha agonist strongly decreased the expression of ATRA-synthesis enzymes, of retinoid target genes, markers of skin homeostasis, and various cytokines in the skin, thereby markedly resembling the expression profile induced by RXR and RAR antagonists. Tretinoin 69-73 retinoic acid receptor, alpha Mus musculus 15-23
23638129-6 2013 In contrast, a RARalpha agonist strongly decreased the expression of ATRA-synthesis enzymes, of retinoid target genes, markers of skin homeostasis, and various cytokines in the skin, thereby markedly resembling the expression profile induced by RXR and RAR antagonists. Tretinoin 69-73 retinoic acid receptor, alpha Mus musculus 15-18
15075337-4 2004 Therefore, we examined the effect of TCDD and all-trans retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagenase), one of the proteolytic enzymes that degrade type I collagen, in normal human keratinocytes. Tretinoin 71-75 matrix metallopeptidase 1 Homo sapiens 126-131
23518499-10 2013 In addition, expression of wee1 kinase and Cdc25A/C phosphatases also coincide with CDK1 expression and its subcellular localization in response to ATRA treatment. Tretinoin 148-152 WEE1 G2 checkpoint kinase Homo sapiens 27-31
15075337-4 2004 Therefore, we examined the effect of TCDD and all-trans retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagenase), one of the proteolytic enzymes that degrade type I collagen, in normal human keratinocytes. Tretinoin 71-75 matrix metallopeptidase 1 Homo sapiens 133-157
23518499-10 2013 In addition, expression of wee1 kinase and Cdc25A/C phosphatases also coincide with CDK1 expression and its subcellular localization in response to ATRA treatment. Tretinoin 148-152 cell division cycle 25A Homo sapiens 43-49
21908575-7 2011 RESULTS: The expression of NLRR3 mRNA was upregulated during differentiation of NBL cells induced by retinoic acid, accompanied with reduced expression of MYCN, suggesting that NLRR3 expression was inversely correlated with MYCN in differentiation. Tretinoin 101-114 leucine rich repeat neuronal 3 Homo sapiens 27-32
15075337-5 2004 The data show that TCDD exposure results in increased MMP-1 expression in keratinocytes that is further enhanced by co-treatment with all-trans retinoic acid. Tretinoin 144-157 matrix metallopeptidase 1 Homo sapiens 54-59
21626648-0 2013 Retinoic acid influences the embryoid body formation in mouse embryonic stem cells by induction of caspase and p38 MAPK/JNK-mediated apoptosis. Tretinoin 0-13 mitogen-activated protein kinase 8 Mus musculus 120-123
15075337-7 2004 However, retinoic acid-mediated induction of keratinocyte MMP-1 is a result of both promoter activation and increased mRNA stability. Tretinoin 9-22 matrix metallopeptidase 1 Homo sapiens 58-63
21626648-6 2013 JNK, P-38 and caspase activation were shown in the nature of RA-triggered apoptotic signaling in ES cells. Tretinoin 61-63 mitogen-activated protein kinase 8 Mus musculus 0-3
15175265-5 2004 Exogenous provision of RA or Fn to Raldh2(-/-) explants in whole mouse embryo culture restored vascular remodeling, visceral endoderm survival, as well as integrin alpha5 expression and its downstream signaling that controls endothelial growth. Tretinoin 23-25 integrin alpha 5 (fibronectin receptor alpha) Mus musculus 155-170
23379615-0 2013 Amyloid beta inhibits retinoic acid synthesis exacerbating Alzheimer disease pathology which can be attenuated by an retinoic acid receptor alpha agonist. Tretinoin 22-35 retinoic acid receptor, alpha Mus musculus 117-145
23379615-2 2013 Here we show that RARalpha signalling is down-regulated by amyloid beta (Abeta), which inhibits the synthesis of the endogenous ligand, retinoic acid (RA). Tretinoin 136-149 retinoic acid receptor, alpha Mus musculus 18-26
15171703-1 2004 Retinoic acid receptor alpha (RARalpha) plays an important role in mediating all-trans retinoic acid (ATRA) signals. Tretinoin 87-100 retinoic acid receptor alpha Homo sapiens 0-28
15171703-1 2004 Retinoic acid receptor alpha (RARalpha) plays an important role in mediating all-trans retinoic acid (ATRA) signals. Tretinoin 87-100 retinoic acid receptor alpha Homo sapiens 30-38
15171703-1 2004 Retinoic acid receptor alpha (RARalpha) plays an important role in mediating all-trans retinoic acid (ATRA) signals. Tretinoin 102-106 retinoic acid receptor alpha Homo sapiens 0-28
15171703-1 2004 Retinoic acid receptor alpha (RARalpha) plays an important role in mediating all-trans retinoic acid (ATRA) signals. Tretinoin 102-106 retinoic acid receptor alpha Homo sapiens 30-38
15171703-2 2004 In this study, we found that ATRA up-regulated RARalpha mRNA and protein expression in gastric cancer BGC-823 cells. Tretinoin 29-33 retinoic acid receptor alpha Homo sapiens 47-55
15171703-5 2004 In MCF-7 cells, ATRA treatment enhanced the ubiquitination of RARalpha and the subsequent degradation of RARalpha through the ubiquitin/proteasome pathway. Tretinoin 16-20 retinoic acid receptor alpha Homo sapiens 62-70
15171703-5 2004 In MCF-7 cells, ATRA treatment enhanced the ubiquitination of RARalpha and the subsequent degradation of RARalpha through the ubiquitin/proteasome pathway. Tretinoin 16-20 retinoic acid receptor alpha Homo sapiens 105-113
15223604-7 2004 Moreover, in vitro and in vivo studies demonstrated that G-CSF may act as a co-stimulus augmenting the response of PML-RARalpha acute promyelocytic leukemia cells to all-trans-retinoic acid treatment. Tretinoin 176-189 colony stimulating factor 3 Homo sapiens 57-62
15274337-2 2004 MATERIALS AND METHODS: We studied the expression and the possible role of histamine receptors H1 and H2 in retinoic-acid mediated differentiation by semiquantitative RT-PCR. Tretinoin 107-120 histamine receptor H1 Homo sapiens 74-103
15040006-6 2004 Messenger RNA levels of p27/Kip1 do not change in CAOV3 cells following ATRA treatment, however, we have shown that p27/Kip1 mRNA is more stable in ATRA treated CAOV3 cells. Tretinoin 148-152 cyclin dependent kinase inhibitor 1B Homo sapiens 28-32
15040006-6 2004 Messenger RNA levels of p27/Kip1 do not change in CAOV3 cells following ATRA treatment, however, we have shown that p27/Kip1 mRNA is more stable in ATRA treated CAOV3 cells. Tretinoin 148-152 cyclin dependent kinase inhibitor 1B Homo sapiens 120-124
15040006-9 2004 We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Tretinoin 28-32 cyclin dependent kinase inhibitor 1B Homo sapiens 59-63
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 139-143 cyclin dependent kinase inhibitor 1B Homo sapiens 65-69
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 139-143 cyclin dependent kinase inhibitor 1B Homo sapiens 124-128
15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 216-220 cyclin dependent kinase inhibitor 1B Homo sapiens 65-69
15040006-11 2004 Taken together our data suggest ATRA-induced growth inhibition in CAOV3 ovarian carcinoma cells involves modulation of the CDK inhibitor p27/kip1. Tretinoin 32-36 cyclin dependent kinase inhibitor 1B Homo sapiens 141-145
15189689-12 2004 When RA was added to the medium and the culture was continued for nine days, the percent of immature DC (CD1a + HLA-DR+) was much higher than that of the control (absence of RA) (58.93 +/- 4.70 vs. 45.80 +/- 7.88, t = 6.575, P < 0.001); whereas, mature DC (CD83 + HLA-DR+) percentage was markedly lower than that of the control (17.25 +/- 8.49 vs. 27.92 +/- 13.94, t = 4.435, P = 0.002). Tretinoin 5-7 CD83 molecule Homo sapiens 260-264
14976428-4 2004 We proposed that C/EBPbeta is an ATRA-dependent PML/RARA target gene and that its activation is critical during ATRA-induced differentiation of APL cells. Tretinoin 33-37 PML nuclear body scaffold Homo sapiens 48-51
14976428-4 2004 We proposed that C/EBPbeta is an ATRA-dependent PML/RARA target gene and that its activation is critical during ATRA-induced differentiation of APL cells. Tretinoin 33-37 retinoic acid receptor alpha Homo sapiens 52-56
15047602-0 2004 Modulation of resistin expression by retinoic acid and vitamin A status. Tretinoin 37-50 resistin Mus musculus 14-22
15047602-1 2004 This work identifies retinoic acid (RA), the acid form of vitamin A, as a signal that inhibits the expression of resistin, an adipocyte-secreted protein previously proposed to act as an inhibitor of adipocyte differentiation and as a systemic insulin resistance factor. Tretinoin 21-34 resistin Mus musculus 113-121
15047602-1 2004 This work identifies retinoic acid (RA), the acid form of vitamin A, as a signal that inhibits the expression of resistin, an adipocyte-secreted protein previously proposed to act as an inhibitor of adipocyte differentiation and as a systemic insulin resistance factor. Tretinoin 36-38 resistin Mus musculus 113-121
15047602-4 2004 RA administration to normal mice resulted in reduced resistin mRNA levels in brown and white adipose tissues, reduced circulating resistin levels, reduced body weight, and improved glucose tolerance. Tretinoin 0-2 resistin Mus musculus 53-61
14980522-0 2004 Retinoic acid causes cell growth arrest and an increase in p27 in F9 wild type but not in F9 retinoic acid receptor beta2 knockout cells. Tretinoin 0-13 interferon alpha inducible protein 27 Homo sapiens 59-62
14980522-5 2004 In F9 Wt cells, cyclin D1, D3, and cyclin E protein levels decreased, while cyclin D2 and p27 levels increased after RA treatment. Tretinoin 117-119 interferon alpha inducible protein 27 Homo sapiens 90-93
14980522-9 2004 Moreover, RA increased the half-life of p27 protein in F9 Wt cells. Tretinoin 10-12 interferon alpha inducible protein 27 Homo sapiens 40-43
14980522-11 2004 Using both genetic and molecular approaches, we have identified some of the molecular mechanisms, such as the large elevation of p27, through which RARbeta(2) mediates these growth inhibitory effects of RA in F9 cells. Tretinoin 148-150 interferon alpha inducible protein 27 Homo sapiens 129-132
15008977-0 2004 Retinoic acid enhances the gene expression of human polymeric immunoglobulin receptor (pIgR) by TNF-alpha. Tretinoin 0-13 polymeric immunoglobulin receptor Homo sapiens 52-85
15008977-0 2004 Retinoic acid enhances the gene expression of human polymeric immunoglobulin receptor (pIgR) by TNF-alpha. Tretinoin 0-13 polymeric immunoglobulin receptor Homo sapiens 87-91
15008977-2 2004 Expression of the pIgR by tumour necrosis factor (TNF-alpha) was enhanced by the addition of all-trans retinoic acid (ATRA) or 9-cis retinoic acid (9CRA). Tretinoin 93-116 polymeric immunoglobulin receptor Homo sapiens 18-22
15008977-2 2004 Expression of the pIgR by tumour necrosis factor (TNF-alpha) was enhanced by the addition of all-trans retinoic acid (ATRA) or 9-cis retinoic acid (9CRA). Tretinoin 118-122 polymeric immunoglobulin receptor Homo sapiens 18-22
15160908-0 2004 Clinico-biological features and prognostic significance of PML/RARalpha isoforms in adult patients with acute promyelocytic leukemia treated with all trans retinoic acid (ATRA) and chemotherapy. Tretinoin 156-169 retinoic acid receptor alpha Homo sapiens 63-71
15160908-0 2004 Clinico-biological features and prognostic significance of PML/RARalpha isoforms in adult patients with acute promyelocytic leukemia treated with all trans retinoic acid (ATRA) and chemotherapy. Tretinoin 171-175 PML nuclear body scaffold Homo sapiens 59-62
15160908-0 2004 Clinico-biological features and prognostic significance of PML/RARalpha isoforms in adult patients with acute promyelocytic leukemia treated with all trans retinoic acid (ATRA) and chemotherapy. Tretinoin 171-175 retinoic acid receptor alpha Homo sapiens 63-71
15160922-4 2004 Confirming previous results, our data showed that both the leukemic and normal cells increased their CD38 expression when grown in serum-containing medium or when treated with retinoic acid. Tretinoin 176-189 CD38 molecule Homo sapiens 101-105
14988021-3 2004 Aggregation of embryonic carcinoma P19 cells with retinoic acid (RA) results in the development of neurons, glia and fibroblast-like cells. Tretinoin 50-63 interleukin 23 subunit alpha Homo sapiens 35-38
14988021-3 2004 Aggregation of embryonic carcinoma P19 cells with retinoic acid (RA) results in the development of neurons, glia and fibroblast-like cells. Tretinoin 65-67 interleukin 23 subunit alpha Homo sapiens 35-38
14988021-6 2004 These P19[Sox6] had acquired both characteristics of the wild-type P19 induced by RA. Tretinoin 82-84 interleukin 23 subunit alpha Homo sapiens 6-9
14988021-6 2004 These P19[Sox6] had acquired both characteristics of the wild-type P19 induced by RA. Tretinoin 82-84 interleukin 23 subunit alpha Homo sapiens 67-70
14988021-8 2004 Second, P19[Sox6] could differentiate into microtubule-associated protein 2 (MAP2)-expressing neuronal cells in the absence of RA. Tretinoin 127-129 interleukin 23 subunit alpha Homo sapiens 8-11
14758042-6 2004 Decreased TGase activities by CCl(4) in the liver from guinea pigs and rats were significantly recovered by retinoic acid treatment that was reported to increase TGase. Tretinoin 108-121 protein-glutamine gamma-glutamyltransferase 2 Cavia porcellus 10-15
14758042-6 2004 Decreased TGase activities by CCl(4) in the liver from guinea pigs and rats were significantly recovered by retinoic acid treatment that was reported to increase TGase. Tretinoin 108-121 protein-glutamine gamma-glutamyltransferase 2 Cavia porcellus 162-167
14758042-8 2004 These results suggested that the distinction of the effect of retinoic acid on serum ALT level in CCl(4)-treated animals was due to the different TGase activity that increased membrane stability. Tretinoin 62-75 protein-glutamine gamma-glutamyltransferase 2 Cavia porcellus 146-151
14603524-0 2004 Retinoic acid inhibits leukemia inhibitory factor signaling pathways in mouse embryonic stem cells. Tretinoin 0-13 leukemia inhibitory factor Mus musculus 23-49
23036366-1 2013 The apoptosis-related protein 3 (APR3) gene was first cloned from HL-60 cells treated with all-trans-retinoic acid and was thought to be related to tumor cell apoptosis or differentiation. Tretinoin 91-114 all-trans retinoic acid induced differentiation factor Homo sapiens 4-31
23036366-1 2013 The apoptosis-related protein 3 (APR3) gene was first cloned from HL-60 cells treated with all-trans-retinoic acid and was thought to be related to tumor cell apoptosis or differentiation. Tretinoin 91-114 all-trans retinoic acid induced differentiation factor Homo sapiens 33-37
14603524-3 2004 Addition of RA to the culture media overrides the self-renewing effects of LIF to induce ES cell differentiation. Tretinoin 12-14 leukemia inhibitory factor Mus musculus 75-78
21989909-6 2011 We have used the zebrafish to uncover genes that function downstream of RA signaling, and here we identify mnx1 (hb9) as an RA-regulated endoderm transcription factor-encoding gene. Tretinoin 72-74 motor neuron and pancreas homeobox 1 Danio rerio 107-111
14603524-4 2004 Therefore, we hypothesized that RA-induced differentiation of ES cells may be accomplished by antagonism of LIF-induced signaling pathways. Tretinoin 32-34 leukemia inhibitory factor Mus musculus 108-111
21989909-6 2011 We have used the zebrafish to uncover genes that function downstream of RA signaling, and here we identify mnx1 (hb9) as an RA-regulated endoderm transcription factor-encoding gene. Tretinoin 72-74 motor neuron and pancreas homeobox 1 Danio rerio 113-116
14603524-5 2004 We demonstrate that RA-induced differentiation of CCE ES cells is associated with (1) downregulation of the LIF receptor (LIFR); (2) decreased tyrosine phosphorylation of signal transducer and activator of transcription 3 protein (Stat3); and (3) increased activation of extracellular regulated kinase (Erk1/2). Tretinoin 20-22 LIF receptor alpha Mus musculus 108-120
14603524-5 2004 We demonstrate that RA-induced differentiation of CCE ES cells is associated with (1) downregulation of the LIF receptor (LIFR); (2) decreased tyrosine phosphorylation of signal transducer and activator of transcription 3 protein (Stat3); and (3) increased activation of extracellular regulated kinase (Erk1/2). Tretinoin 20-22 LIF receptor alpha Mus musculus 122-126
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 43-56 sonic hedgehog Mus musculus 98-112
21879259-1 2011 The aim of the present study was to investigate the role of Hoxb2 and Hoxb4 gene expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) on the proliferation and committed differentiation process of human cord blood hematopoietic stem cells (HSCs) to colony-forming erythroid progenitor cells (CFU-Es) in vitro. Tretinoin 149-162 homeobox B2 Homo sapiens 60-65
21879259-1 2011 The aim of the present study was to investigate the role of Hoxb2 and Hoxb4 gene expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) on the proliferation and committed differentiation process of human cord blood hematopoietic stem cells (HSCs) to colony-forming erythroid progenitor cells (CFU-Es) in vitro. Tretinoin 149-162 homeobox B4 Homo sapiens 70-75
21879259-1 2011 The aim of the present study was to investigate the role of Hoxb2 and Hoxb4 gene expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) on the proliferation and committed differentiation process of human cord blood hematopoietic stem cells (HSCs) to colony-forming erythroid progenitor cells (CFU-Es) in vitro. Tretinoin 164-168 homeobox B2 Homo sapiens 60-65
21879259-1 2011 The aim of the present study was to investigate the role of Hoxb2 and Hoxb4 gene expression induced by human cytomegalovirus (HCMV) and/or all-trans retinoic acid (ATRA) on the proliferation and committed differentiation process of human cord blood hematopoietic stem cells (HSCs) to colony-forming erythroid progenitor cells (CFU-Es) in vitro. Tretinoin 164-168 homeobox B4 Homo sapiens 70-75
21879259-7 2011 However, expression levels of the Hoxb2 and Hoxb4 genes were significantly up-regulated in the HCMV + ATRA group compared with the HCMV group (P<0.05). Tretinoin 102-106 homeobox B2 Homo sapiens 34-39
21879259-7 2011 However, expression levels of the Hoxb2 and Hoxb4 genes were significantly up-regulated in the HCMV + ATRA group compared with the HCMV group (P<0.05). Tretinoin 102-106 homeobox B4 Homo sapiens 44-49
22991072-1 2013 Annexin A1 (AnxA1) is an important anti-inflammatory mediator during granulocytic differentiation in all trans-retinoic acid (ATRA) treated acute promyelocytic leukemic (APL) cells. Tretinoin 105-124 annexin A1 Homo sapiens 0-10
22991072-1 2013 Annexin A1 (AnxA1) is an important anti-inflammatory mediator during granulocytic differentiation in all trans-retinoic acid (ATRA) treated acute promyelocytic leukemic (APL) cells. Tretinoin 105-124 annexin A1 Homo sapiens 12-17
22991072-1 2013 Annexin A1 (AnxA1) is an important anti-inflammatory mediator during granulocytic differentiation in all trans-retinoic acid (ATRA) treated acute promyelocytic leukemic (APL) cells. Tretinoin 126-130 annexin A1 Homo sapiens 0-10
22991072-1 2013 Annexin A1 (AnxA1) is an important anti-inflammatory mediator during granulocytic differentiation in all trans-retinoic acid (ATRA) treated acute promyelocytic leukemic (APL) cells. Tretinoin 126-130 annexin A1 Homo sapiens 12-17
23337719-11 2013 CONCLUSIONS: Simvastatin interacts with the RA system, inducing the expression of the key protein regulating the uptake of retinol (STRA6) and the expression of apoptosis-promoting CRABP2. Tretinoin 44-46 cellular retinoic acid binding protein 2 Homo sapiens 181-187
21987218-1 2011 Pluripotent mouse embryonal carcinoma (mEC) and mouse embryonic stem (mES) cells differentiate into several cell lineages upon retinoic acid (RA) addition. Tretinoin 127-140 chemokine (C-C motif) ligand 28 Mus musculus 39-42
21987218-1 2011 Pluripotent mouse embryonal carcinoma (mEC) and mouse embryonic stem (mES) cells differentiate into several cell lineages upon retinoic acid (RA) addition. Tretinoin 142-144 chemokine (C-C motif) ligand 28 Mus musculus 39-42
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 43-56 sonic hedgehog Mus musculus 114-117
23338237-0 2013 Critical role for all-trans retinoic acid for optimal effector and effector memory CD8 T cell differentiation. Tretinoin 28-41 CD8a molecule Homo sapiens 83-86
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 58-62 sonic hedgehog Mus musculus 98-112
23338237-7 2013 Collectively, these results introduce a new role for RA in CD8 T cell activation and differentiation. Tretinoin 53-55 CD8a molecule Homo sapiens 59-62
14966734-2 2004 The authors investigated whether all-trans retinoic acid (ATRA) affects the expression pattern of Sonic hedgehog (Shh) and Bone morphogenetic protein 4 (BMP4), which play important roles in anorectal morphogenesis in vertebrates. Tretinoin 58-62 sonic hedgehog Mus musculus 114-117
21704588-6 2011 In the organotypic model, and in mice, ATRA induced quiescence of PSCs and thereby reduced cancer cell proliferation and translocation of beta-catenin to the nucleus, increased cancer cell apoptosis, and altered tumor morphology. Tretinoin 39-43 catenin (cadherin associated protein), beta 1 Mus musculus 138-150
14715249-0 2004 Insulin-like growth factor binding protein-3 prevents retinoid receptor heterodimerization: implications for retinoic acid-sensitivity in human breast cancer cells. Tretinoin 109-122 insulin like growth factor binding protein 3 Homo sapiens 0-44
21538808-2 2011 Excessive RA down-regulates Fgf8 and triggers premature termination of body axis extension, suggesting that endogenous RA may function in normal termination of body axis extension. Tretinoin 10-12 fibroblast growth factor 8 Mus musculus 28-32
21538808-2 2011 Excessive RA down-regulates Fgf8 and triggers premature termination of body axis extension, suggesting that endogenous RA may function in normal termination of body axis extension. Tretinoin 119-121 fibroblast growth factor 8 Mus musculus 28-32
23237262-0 2013 Phospholipase C-eta2 is required for retinoic acid-stimulated neurite growth. Tretinoin 37-50 phospholipase C, eta 2 Mus musculus 0-20
23237262-3 2013 The role of PLCeta2 in neuritogenesis was assessed during retinoic acid (RA)-induced Neuro2A cell differentiation. Tretinoin 58-71 phospholipase C, eta 2 Mus musculus 12-19
23237262-3 2013 The role of PLCeta2 in neuritogenesis was assessed during retinoic acid (RA)-induced Neuro2A cell differentiation. Tretinoin 73-75 phospholipase C, eta 2 Mus musculus 12-19
23237262-5 2013 Stable expression of PLCeta2-targetted shRNA led to a decrease in the number of differentiated cells and total length of neurites following RA-treatment. Tretinoin 140-142 phospholipase C, eta 2 Mus musculus 21-28
23237262-6 2013 Furthermore, RA response element activation was perturbed by PLCeta2 knockdown. Tretinoin 13-15 phospholipase C, eta 2 Mus musculus 61-68
23237262-9 2013 RA-induced phosphorylation of LIMK1 and cAMP-responsive element-binding protein was reduced in PLCeta2 knock-down cells. Tretinoin 0-2 LIM-domain containing, protein kinase Mus musculus 30-35
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 94-98 insulin like growth factor binding protein 3 Homo sapiens 39-46
23237262-9 2013 RA-induced phosphorylation of LIMK1 and cAMP-responsive element-binding protein was reduced in PLCeta2 knock-down cells. Tretinoin 0-2 phospholipase C, eta 2 Mus musculus 95-102
22000442-7 2011 RESULTS: The expression of MMP-9 in lung tissues in the ATRA treatment group was significantly higher than that in the control group, but the airway responsiveness in the ATRA treatment group was not significantly different from that in the control group. Tretinoin 56-60 matrix metallopeptidase 9 Rattus norvegicus 27-32
22000442-8 2011 The airway responsiveness and the expression of MMP-9 in lung tissues were significantly reduced in the ATRA treatment group compared with the asthma model group. Tretinoin 104-108 matrix metallopeptidase 9 Rattus norvegicus 48-53
21715325-8 2011 Stimulation of Rankl mRNA by ATRA was competitively inhibited by the RARalpha antagonist GR110. Tretinoin 29-33 retinoic acid receptor, alpha Mus musculus 69-77
21715325-12 2011 The data suggest that ATRA enhances periosteal bone resorption by increasing the RANKL/OPG ratio via RARalpha receptors, a response that can be inhibited by monomeric GR. Tretinoin 22-26 tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin) Mus musculus 87-90
23087051-6 2013 Our results showed that alveolar hypoplasia caused by caloric restriction can be reversed with refeeding, and that retinoic acid prevents the alveolar hypoplasia coincident with the increased expression of elastin and retinoic acid receptor-alpha and decreased transforming growth factor-beta activity in developing rat lungs. Tretinoin 115-128 elastin Rattus norvegicus 206-213
21715325-12 2011 The data suggest that ATRA enhances periosteal bone resorption by increasing the RANKL/OPG ratio via RARalpha receptors, a response that can be inhibited by monomeric GR. Tretinoin 22-26 retinoic acid receptor, alpha Mus musculus 101-109
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 151-155 insulin like growth factor binding protein 3 Homo sapiens 39-46
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 151-155 insulin like growth factor binding protein 3 Homo sapiens 126-133
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 151-155 insulin like growth factor binding protein 3 Homo sapiens 126-133
22931413-10 2013 However, several substances that have been proven to not be transportable by P-gp (such as cisplatin or alltrans retinoic acid) could induce minor improvements in P-gp overexpression. Tretinoin 113-126 phosphoglycolate phosphatase Mus musculus 163-167
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 151-155 insulin like growth factor binding protein 3 Homo sapiens 39-46
22040429-7 2011 The protein and mRNA levels of VEGF were down-regulated after being treated with ATRA and 5-FU compared to the control group (P < 0.05). Tretinoin 81-85 vascular endothelial growth factor A Mus musculus 31-35
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 151-155 insulin like growth factor binding protein 3 Homo sapiens 126-133
14715249-5 2004 To investigate whether the presence of IGFBP-3 regulates breast cancer cell responsiveness to atRA, we immuno-neutralized the IGFBP-3 expressed by the atRA-resistant Hs578T and MDA-MB-231 BCCs (which express IGFBP-3 constitutively) and showed that they become more sensitive to the growth-inhibitory effects of atRA. Tretinoin 151-155 insulin like growth factor binding protein 3 Homo sapiens 126-133
23509752-6 2013 mRNA expression of Stra8, Odf2, Act, and Prm1 was upregulated in iPS cells by retinoic acid or testosterone induction, whereas Oct-4 transcription was reduced in these cells compared to the controls. Tretinoin 78-91 outer dense fiber of sperm tails 2 Mus musculus 26-30
14715249-6 2004 Similarly, in Hs578T cells expressing a reporter gene under the control of an RAR response element (RARE), depletion of IGFBP-3 resulted in the induction of reporter gene expression in response to atRA. Tretinoin 197-201 retinoic acid receptor alpha Homo sapiens 78-81
23509752-6 2013 mRNA expression of Stra8, Odf2, Act, and Prm1 was upregulated in iPS cells by retinoic acid or testosterone induction, whereas Oct-4 transcription was reduced in these cells compared to the controls. Tretinoin 78-91 protamine 1 Mus musculus 41-45
24516726-4 2011 We demonstrate that murine fully competent CD8(+) regulatory T cells can be induced by stimulating naive CD8(+) T cells in the presence of TGF-beta and retinoic acid (RA). Tretinoin 152-165 CD8a molecule Homo sapiens 43-46
14715249-6 2004 Similarly, in Hs578T cells expressing a reporter gene under the control of an RAR response element (RARE), depletion of IGFBP-3 resulted in the induction of reporter gene expression in response to atRA. Tretinoin 197-201 insulin like growth factor binding protein 3 Homo sapiens 120-127
24516726-4 2011 We demonstrate that murine fully competent CD8(+) regulatory T cells can be induced by stimulating naive CD8(+) T cells in the presence of TGF-beta and retinoic acid (RA). Tretinoin 152-165 CD8a molecule Homo sapiens 105-108
24516726-4 2011 We demonstrate that murine fully competent CD8(+) regulatory T cells can be induced by stimulating naive CD8(+) T cells in the presence of TGF-beta and retinoic acid (RA). Tretinoin 167-169 CD8a molecule Homo sapiens 43-46
23856557-0 2013 Prdm12 is induced by retinoic acid and exhibits anti-proliferative properties through the cell cycle modulation of P19 embryonic carcinoma cells. Tretinoin 21-34 PR/SET domain 12 Homo sapiens 0-6
23856557-4 2013 In P19 cells, Prdm12 is induced by Retinoic acid (RA). Tretinoin 35-48 PR/SET domain 12 Homo sapiens 14-20
23856557-4 2013 In P19 cells, Prdm12 is induced by Retinoic acid (RA). Tretinoin 50-52 PR/SET domain 12 Homo sapiens 14-20
14715249-7 2004 In investigating possible mechanisms for IGFBP-3 regulation of atRA-sensitivity, we found that IGFBP-3 blocked the formation of RAR:RXR heterodimers and disrupted the ligand-inducible receptor complex. Tretinoin 63-67 insulin like growth factor binding protein 3 Homo sapiens 41-48
24516726-4 2011 We demonstrate that murine fully competent CD8(+) regulatory T cells can be induced by stimulating naive CD8(+) T cells in the presence of TGF-beta and retinoic acid (RA). Tretinoin 167-169 CD8a molecule Homo sapiens 105-108
23856557-6 2013 In contrast, the knockdown of Prdm12 increases the number of cells in a suspension culture of RA-induced neural differentiation. Tretinoin 94-96 PR/SET domain 12 Homo sapiens 30-36
14715249-7 2004 In investigating possible mechanisms for IGFBP-3 regulation of atRA-sensitivity, we found that IGFBP-3 blocked the formation of RAR:RXR heterodimers and disrupted the ligand-inducible receptor complex. Tretinoin 63-67 insulin like growth factor binding protein 3 Homo sapiens 95-102
23856557-8 2013 While the data in this study is based on in vitro models, the results suggest that Prdm12 is induced by the RA signaling in vivo, and may regulate neural differentiation during animal development. Tretinoin 108-110 PR/SET domain 12 Homo sapiens 83-89
21711349-0 2011 Generation and function of immunosuppressive human and murine CD8+ T cells by transforming growth factor-beta and retinoic acid. Tretinoin 114-127 CD8a molecule Homo sapiens 62-65
14715249-7 2004 In investigating possible mechanisms for IGFBP-3 regulation of atRA-sensitivity, we found that IGFBP-3 blocked the formation of RAR:RXR heterodimers and disrupted the ligand-inducible receptor complex. Tretinoin 63-67 retinoic acid receptor alpha Homo sapiens 128-131
23178692-11 2013 The caspase assay demonstrated that the overexpression of GRIM-19 enhanced the cellular sensitivity to interferon(IFN)-beta- and retinoic acid (RA)-induced death in HeLa cells. Tretinoin 129-142 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 58-65
14715249-8 2004 Thus, IGFBP-3 has the potential to reduce the RARE-mediated transactivation of target genes and modulate the atRA-response in BCCs. Tretinoin 109-113 insulin like growth factor binding protein 3 Homo sapiens 6-13
23178692-11 2013 The caspase assay demonstrated that the overexpression of GRIM-19 enhanced the cellular sensitivity to interferon(IFN)-beta- and retinoic acid (RA)-induced death in HeLa cells. Tretinoin 144-146 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 58-65
21663736-12 2011 Wnt5a, a prototypic non-canonical Wnt with enriched epicardial expression, and Raldh2, a key regulator of retinoic acid signaling confined to the epicardium, were also markedly downregulated in Wt1(KO) epicardium. Tretinoin 106-119 aldehyde dehydrogenase 1 family member A2 Homo sapiens 79-85
14702386-7 2004 Adenoviral introduction of Runx2 or treatment with transforming growth factor-beta, retinoic acid, interleukin-1 beta, basic fibroblast growth factor, platelet-derived growth factor or parathyroid hormone inhibited the adipogenic changes in Runx2-/- chondrocytes. Tretinoin 84-97 runt related transcription factor 2 Mus musculus 241-246
21273387-12 2011 MMP-7 was highly induced by ATRA in healthy but not in emphysematous lungs. Tretinoin 28-32 matrix metallopeptidase 7 Rattus norvegicus 0-5
23554907-2 2013 Using HL60 model human myeloid leukemia cells, where all-trans retinoic acid (RA) induces granulocytic differentiation, we developed two emergent RA-resistant HL60 cell lines which are characterized by loss of RA-inducible G1/G0 arrest, CD11b expression, inducible oxidative metabolism and p47(phox) expression. Tretinoin 146-148 integrin subunit alpha M Homo sapiens 237-242
23554907-2 2013 Using HL60 model human myeloid leukemia cells, where all-trans retinoic acid (RA) induces granulocytic differentiation, we developed two emergent RA-resistant HL60 cell lines which are characterized by loss of RA-inducible G1/G0 arrest, CD11b expression, inducible oxidative metabolism and p47(phox) expression. Tretinoin 146-148 integrin subunit alpha M Homo sapiens 237-242
23451234-3 2013 The arginine-glutamic acid dipeptide (RE) repeats gene (RERE) is located in this region and encodes a nuclear receptor coregulator that plays a critical role in embryonic development as a positive regulator of retinoic acid signaling. Tretinoin 210-223 arginine glutamic acid dipeptide (RE) repeats Mus musculus 56-60
21273387-13 2011 ATRA reduced both MMP-2 and TIMP-1 activity in BAL fluid of emphysematous lungs. Tretinoin 0-4 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 28-34
14670623-0 2004 Differential regulation of vimentin mRNA by 12-O-tetradecanoylphorbol 13-acetate and all-trans-retinoic acid correlates with motility of Hep 3B human hepatocellular carcinoma cells. Tretinoin 85-108 vimentin Homo sapiens 27-35
21653670-0 2011 Retinoic acid as a vaccine adjuvant enhances CD8+ T cell response and mucosal protection from viral challenge. Tretinoin 0-13 CD8a molecule Homo sapiens 45-48
21653670-3 2011 We tested whether the administration of exogenous ATRA during a systemic vaccination of mice could enhance the generation of mucosal CD8(+) T cell immunity, which might represent a strategy for establishing better protection from viral infection via mucosal routes. Tretinoin 50-54 CD8a molecule Homo sapiens 133-136
21653670-4 2011 ATRA induced the expression of CCR9 and alpha4beta7 on both mouse and human CD8(+) T cells activated in vitro. Tretinoin 0-4 chemokine (C-C motif) receptor 9 Mus musculus 31-35
23169621-3 2012 The mouse CMV MHC class I (MHC-I)-like m152/gp40 glycoprotein down-regulates retinoic acid early inducible-1 (RAE1) NKG2D ligands as well as host MHC-I. Tretinoin 77-90 ribonucleic acid export 1 Mus musculus 110-114
23053054-9 2012 Taken together, these results suggest that the accumulation of RA in the stroma during mouse embryo implantation has an inhibitory effect on the expression of the three implantation-essential genes, LIF, HB-EGF and CSF-1. Tretinoin 63-65 colony stimulating factor 1 (macrophage) Mus musculus 215-220
21653670-4 2011 ATRA induced the expression of CCR9 and alpha4beta7 on both mouse and human CD8(+) T cells activated in vitro. Tretinoin 0-4 CD8a molecule Homo sapiens 76-79
14670623-3 2004 We studied the regulation of vimentin mRNA and multistep invasion processes following treatment of 12-O-tetradecanoylphorbol 13-acetate (TPA) and all-trans-retinoic acid (RA) in Hep 3B hepatocellular carcinoma cells. Tretinoin 146-169 vimentin Homo sapiens 29-37
20812861-5 2011 RA did not affect the levels of upstream regulators of autophagy, such as Beclin-1, phospho-mTOR, and phospho-Akt1, but induced redistribution of both endogenous cation-independent mannose-6-phosphate receptor CIMPR and transiently transfected GFP and RFP full-length CIMPR fusion proteins from the trans-Golgi region to acidified AUT structures. Tretinoin 0-2 tripartite motif containing 27 Homo sapiens 252-255
14670623-3 2004 We studied the regulation of vimentin mRNA and multistep invasion processes following treatment of 12-O-tetradecanoylphorbol 13-acetate (TPA) and all-trans-retinoic acid (RA) in Hep 3B hepatocellular carcinoma cells. Tretinoin 171-173 vimentin Homo sapiens 29-37
14670623-7 2004 These findings suggest that TPA and RA could modulate the invasive potential of Hep 3B cells by altering cellular motility related to differential regulation of vimentin mRNA. Tretinoin 36-38 vimentin Homo sapiens 161-169
23268390-5 2012 RESULTS: RA treatment significantly increased gamma-globin and hemoglobin expressions in K562 cells (P<0.01), causing also significantly enhanced AQP1 mRNA and protein expressions over time (P<0.01). Tretinoin 9-11 hemoglobin subunit gamma 1 Homo sapiens 46-58
15448735-13 2004 TGF-beta1, isotretinoin and tretinoin added to the culture resulted in the lowest percentage of PCNA positive cells. Tretinoin 14-23 proliferating cell nuclear antigen Homo sapiens 96-100
22689466-2 2012 This study describes the source of RA for the rodent hippocampus in the meninges via the key RA synthetic enzyme retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 35-37 aldehyde dehydrogenase 1 family member A2 Homo sapiens 113-142
22689466-2 2012 This study describes the source of RA for the rodent hippocampus in the meninges via the key RA synthetic enzyme retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 35-37 aldehyde dehydrogenase 1 family member A2 Homo sapiens 144-150
22689466-2 2012 This study describes the source of RA for the rodent hippocampus in the meninges via the key RA synthetic enzyme retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 93-95 aldehyde dehydrogenase 1 family member A2 Homo sapiens 113-142
22689466-2 2012 This study describes the source of RA for the rodent hippocampus in the meninges via the key RA synthetic enzyme retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 93-95 aldehyde dehydrogenase 1 family member A2 Homo sapiens 144-150
21252119-1 2011 AIMS: Kruppel-like factor 4 (KLF4) is implicated in all-trans retinoic acid (ATRA)-induced and platelet-derived growth factor-BB (PDGF-BB)-repressed SM22alpha expression in vascular smooth muscle cells (VSMCs). Tretinoin 62-75 Kruppel like factor 4 Homo sapiens 6-27
21252119-1 2011 AIMS: Kruppel-like factor 4 (KLF4) is implicated in all-trans retinoic acid (ATRA)-induced and platelet-derived growth factor-BB (PDGF-BB)-repressed SM22alpha expression in vascular smooth muscle cells (VSMCs). Tretinoin 62-75 Kruppel like factor 4 Homo sapiens 29-33
21252119-1 2011 AIMS: Kruppel-like factor 4 (KLF4) is implicated in all-trans retinoic acid (ATRA)-induced and platelet-derived growth factor-BB (PDGF-BB)-repressed SM22alpha expression in vascular smooth muscle cells (VSMCs). Tretinoin 77-81 Kruppel like factor 4 Homo sapiens 6-27
21252119-1 2011 AIMS: Kruppel-like factor 4 (KLF4) is implicated in all-trans retinoic acid (ATRA)-induced and platelet-derived growth factor-BB (PDGF-BB)-repressed SM22alpha expression in vascular smooth muscle cells (VSMCs). Tretinoin 77-81 Kruppel like factor 4 Homo sapiens 29-33
21252119-6 2011 ATRA increased the binding of KLF4 to site 2, whereas PDGF-BB decreased the binding of KLF4 to site 1. Tretinoin 0-4 Kruppel like factor 4 Homo sapiens 30-34
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 Kruppel like factor 4 Homo sapiens 16-20
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 Kruppel like factor 4 Homo sapiens 45-49
21252119-7 2011 ATRA stimulated KLF4 acetylation by inducing KLF4 phosphorylation and increasing its interaction with p300 via activating c-Jun NH(2)-terminal kinase (JNK) and p38 pathways, and acetylated KLF4 increased its binding activity to site 2. Tretinoin 0-4 Kruppel like factor 4 Homo sapiens 45-49
21252119-9 2011 CONCLUSIONS: In VSMCs, ATRA activates and PDGF-BB represses SM22alpha expression through KLF4 binding to, or dissociating from, its different cis-elements in an acetylation-dependent manner. Tretinoin 23-27 Kruppel like factor 4 Homo sapiens 89-93
22344541-8 2012 ATRA dose-dependently reversed both TGF-beta(1)-induced decreases in p21(Waf1/Cip1) mRNA and protein levels and p27(Kip1) protein level and increases in Skp2 mRNA and protein levels, and inhibited TGF-beta(1)-induced proliferation through G(1) arrest. Tretinoin 0-4 KRAS proto-oncogene, GTPase Rattus norvegicus 69-72
22344541-10 2012 CONCLUSION: ATRA inhibited TGF-beta(1)-induced mesangial cell proliferation by up-regulating p21(Waf1/Cip1) mRNA and protein levels, and p27(Kip1) protein level, and down-regulating Skp2 mRNA and protein levels, but it had no significant effect on apoptosis in rat mesangial cells. Tretinoin 12-16 KRAS proto-oncogene, GTPase Rattus norvegicus 93-96
22531980-8 2012 In agreement with these observations, in vitro experiments showed that in the presence of leptin, ATRA directly induced LEPR gene expression through RARalpha, resulting in enhancement of STAT3 and insulin-induced insulin receptor substrate 1 phosphorylation. Tretinoin 98-102 retinoic acid receptor, alpha Mus musculus 149-157
21573029-8 2011 Furthermore, SEB-1 sebocytes treated with retinol and SCD inhibitor also display an elevation in retinoic acid-induced genes. Tretinoin 97-110 stearoyl-Coenzyme A desaturase 1 Mus musculus 54-57
14725900-10 2004 In addition, [gamma-32P]-labeled TPO-RARE probe bound to KM101 nuclear protein extract was supershifted by anti-RARalpha antibody and modified by treatment with ATRA. Tretinoin 161-165 retinoic acid receptor alpha Homo sapiens 112-120
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 45-58 integrin subunit alpha M Homo sapiens 231-236
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 45-58 integrin subunit alpha M Homo sapiens 263-268
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 60-64 integrin subunit alpha M Homo sapiens 231-236
21237205-3 2011 In this study, we demonstrate that all-trans retinoic acid (ATRA) significantly up-regulated TLR-5 expression in human macrophage THP-1 cells by co-activating NF-kappaB and the RARalpha receptor and inducing the differentiation of CD11b(-)CD11c(-) THP-1 cells to CD11b(+)CD11c(low) cells. Tretinoin 60-64 integrin subunit alpha M Homo sapiens 263-268
23335538-5 2012 Contrary to this, RA treatment increased the expression of inhibitory KIR CD158b. Tretinoin 18-20 killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 2 Homo sapiens 74-80
22815530-7 2012 Consistent with an established antagonistic relationship between AP1 expression and retinoic acid receptor activity, increased differentiation was seen in the DNMT3B7-expressing neuroblastoma cells following treatment with all-trans retinoic acid (ATRA) compared to controls. Tretinoin 248-252 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-68
14592536-0 2004 Distinct role and functional mode of TR3 and RARalpha in mediating ATRA-induced signalling pathway in breast and gastric cancer cells. Tretinoin 67-71 retinoic acid receptor alpha Homo sapiens 45-53
22790594-0 2012 DHRS3, a retinal reductase, is differentially regulated by retinoic acid and lipopolysaccharide-induced inflammation in THP-1 cells and rat liver. Tretinoin 59-72 dehydrogenase/reductase 3 Homo sapiens 0-5
21345790-5 2011 The results of this study demonstrate that ectopic expression of retinol dehydrogenase 10 (RDH10, SDR16C4) in skin rafts dramatically increases proliferation and inhibits differentiation of keratinocytes, consistent with the increased steady-state levels of retinoic acid and activation of retinoic acid-inducible genes in RDH10 rafts. Tretinoin 258-271 retinol dehydrogenase 10 Homo sapiens 65-89
21345790-5 2011 The results of this study demonstrate that ectopic expression of retinol dehydrogenase 10 (RDH10, SDR16C4) in skin rafts dramatically increases proliferation and inhibits differentiation of keratinocytes, consistent with the increased steady-state levels of retinoic acid and activation of retinoic acid-inducible genes in RDH10 rafts. Tretinoin 258-271 retinol dehydrogenase 10 Homo sapiens 91-96
21345790-5 2011 The results of this study demonstrate that ectopic expression of retinol dehydrogenase 10 (RDH10, SDR16C4) in skin rafts dramatically increases proliferation and inhibits differentiation of keratinocytes, consistent with the increased steady-state levels of retinoic acid and activation of retinoic acid-inducible genes in RDH10 rafts. Tretinoin 258-271 retinol dehydrogenase 10 Homo sapiens 98-105
14592536-6 2004 However, in ATRA-induced gastric cancer cells MGC80-3, RXRalpha heterodimerised with RARalpha but not with TR3, and remained in the nucleus exerting its effect on cell cycle regulation. Tretinoin 12-16 retinoic acid receptor alpha Homo sapiens 85-93
21187718-7 2011 Furthermore, knockdown of p62/SQSTM1 inhibited ATRA-induced PML-RARalpha degradation and myeloid cell differentiation. Tretinoin 47-51 sequestosome 1 Homo sapiens 26-29
23103284-0 2012 TLR9-signaling is required for turning retinoic acid into a potent stimulator of RP105 (CD180)-mediated proliferation and IgG synthesis in human memory B cells. Tretinoin 39-52 CD180 molecule Homo sapiens 81-86
23103284-0 2012 TLR9-signaling is required for turning retinoic acid into a potent stimulator of RP105 (CD180)-mediated proliferation and IgG synthesis in human memory B cells. Tretinoin 39-52 CD180 molecule Homo sapiens 88-93
23103284-3 2012 Here we explore the impact of all-trans retinoic acid (RA) on B cell responses mediated via the TLR homolog RP105 (CD180). Tretinoin 40-53 CD180 molecule Homo sapiens 108-113
23103284-3 2012 Here we explore the impact of all-trans retinoic acid (RA) on B cell responses mediated via the TLR homolog RP105 (CD180). Tretinoin 40-53 CD180 molecule Homo sapiens 115-120
21187718-7 2011 Furthermore, knockdown of p62/SQSTM1 inhibited ATRA-induced PML-RARalpha degradation and myeloid cell differentiation. Tretinoin 47-51 sequestosome 1 Homo sapiens 30-36
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 RB transcriptional corepressor like 2 Homo sapiens 176-180
23103284-3 2012 Here we explore the impact of all-trans retinoic acid (RA) on B cell responses mediated via the TLR homolog RP105 (CD180). Tretinoin 55-57 CD180 molecule Homo sapiens 108-113
14592536-7 2004 When transfected with antisense-RARalpha, MGC80-3 cells changed from ATRA-sensitive to ATRA-resistant and most cells were arrested in the S phase, implying the importance of RARalpha in cell cycle regulation. Tretinoin 69-73 retinoic acid receptor alpha Homo sapiens 32-40
23103284-3 2012 Here we explore the impact of all-trans retinoic acid (RA) on B cell responses mediated via the TLR homolog RP105 (CD180). Tretinoin 55-57 CD180 molecule Homo sapiens 115-120
23103284-4 2012 We show that RA slightly reduces the proliferation and IgG production in CD27+ memory B cells stimulated by anti-RP105 alone. Tretinoin 13-15 CD180 molecule Homo sapiens 113-118
14592536-7 2004 When transfected with antisense-RARalpha, MGC80-3 cells changed from ATRA-sensitive to ATRA-resistant and most cells were arrested in the S phase, implying the importance of RARalpha in cell cycle regulation. Tretinoin 87-91 retinoic acid receptor alpha Homo sapiens 32-40
23103284-5 2012 However, co-stimulation with the TLR9-ligand CpG results in turning RA into a potent stimulator of RP105-induced proliferation and IgG synthesis in memory B cells. Tretinoin 68-70 CD180 molecule Homo sapiens 99-104
21343363-0 2011 Wt1 controls retinoic acid signalling in embryonic epicardium through transcriptional activation of Raldh2. Tretinoin 13-26 aldehyde dehydrogenase 1 family member A2 Homo sapiens 100-106
14592536-8 2004 Furthermore, we demonstrated that the effects of ATRA depend on the relative levels of TR3, RARalpha and RXRalpha expression in cancer cells. Tretinoin 49-53 retinoic acid receptor alpha Homo sapiens 92-100
21343363-3 2011 RA is a potent morphogen synthesised by Raldh enzymes, Raldh2 being the predominant one in mesodermal tissues. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 55-61
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoic acid receptor alpha Homo sapiens 212-220
21343363-11 2011 Taken together, our results indicate that Wt1 critically regulates epicardial RA signalling via direct activation of the Raldh2 gene, and identify a role for Wt1 in the regulation of morphogen receptors involved in the proliferation, migration, and differentiation of epicardial and epicardially-derived cells (EPDC). Tretinoin 78-80 aldehyde dehydrogenase 1 family member A2 Homo sapiens 121-127
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoic acid receptor alpha Homo sapiens 246-254
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoic acid receptor alpha Homo sapiens 246-254
22614235-10 2012 Differentiation induction with all-trans retinoic acid induced the upregulation of Reelin and DAB1. Tretinoin 41-54 reelin Homo sapiens 83-89
15587392-10 2004 Both ATRA and/or sodium butyrate stimulated p21 expression at the mRNA levels. Tretinoin 5-9 H3 histone pseudogene 16 Homo sapiens 44-47
22696440-5 2012 Interestingly, Foxp3(+) regulatory T cells were markedly increased and IL-17-producing CD4(+) T cells (Th17 cells) were decreased in the spleens of ATRA-treated mice. Tretinoin 148-152 interleukin 17A Mus musculus 71-76
22696440-5 2012 Interestingly, Foxp3(+) regulatory T cells were markedly increased and IL-17-producing CD4(+) T cells (Th17 cells) were decreased in the spleens of ATRA-treated mice. Tretinoin 148-152 CD4 antigen Mus musculus 87-90
20666879-2 2011 Salicylic acid (SA), tretinoin (all-TRA) and clindamycin phosphate (CDP) are known to to be effective agents depending on their comedolytic and anti-inflammatory properties. Tretinoin 21-30 T cell receptor alpha locus Homo sapiens 36-39
15641681-0 2004 Effects of retinoic acid on the beta-catenin/TCF pathway in cultured porcine tracheobronchial epithelial cells. Tretinoin 11-24 catenin beta 1 Homo sapiens 32-44
22504877-7 2012 iPS cell-derived EBs were induced by retinoic acid to differentiate into spermatogonial stem cells (SSCs), as evidenced by their expression of VASA, as well as CDH1 and GFRalpha1, which are markers of SSCs. Tretinoin 37-50 glial cell line derived neurotrophic factor family receptor alpha 1 Mus musculus 169-178
15641681-2 2004 After TBEC were treated with retinoic acid at various concentrations, mRNA and protein changes of beta-catenin in cytoplasm, nucleus and whole cell of the TBEC were observed by immunocytochemical stain, RT-PCR and Western blotting. Tretinoin 29-42 catenin beta 1 Homo sapiens 98-110
15641681-5 2004 However, the expression of beta-catenin in the whole cell and cytoplasm was elevated with the increase of retinoic acid concentration (P<0. Tretinoin 106-119 catenin beta 1 Homo sapiens 27-39
21150871-2 2011 In vitro, all-trans retinoic acid inhibits HIV-induced podocyte proliferation and restores podocyte differentiation markers by activating its receptor-alpha (RARalpha). Tretinoin 10-33 retinoic acid receptor, alpha Mus musculus 158-166
15641681-8 2004 It was indicated that retinoic acid could increase beta-catenin level of the whole cell protein and decrease nuclear beta-catenin, downregulating beta-cat/TCF signaling activity and reducing target gene cyclinD1 protein level. Tretinoin 22-35 catenin beta 1 Homo sapiens 51-63
20354914-12 2011 In conclusion, RAR, RXR and VDR are expressed in human fetal PPCs and PPC proliferation can be promoted by calcitriol, atRA or both together, data valuable for elucidating mechanisms underlying islet development and for developing clinical islet transplantation. Tretinoin 119-123 vitamin D receptor Homo sapiens 28-31
22658364-3 2012 As a CRABP-II-recognizing moiety, all-trans retinoic acid (ATRA, 3), a physiological ligand of CRABP, was chosen. Tretinoin 44-57 cellular retinoic acid binding protein 2 Homo sapiens 5-13
22658364-3 2012 As a CRABP-II-recognizing moiety, all-trans retinoic acid (ATRA, 3), a physiological ligand of CRABP, was chosen. Tretinoin 59-63 cellular retinoic acid binding protein 2 Homo sapiens 5-13
15641681-8 2004 It was indicated that retinoic acid could increase beta-catenin level of the whole cell protein and decrease nuclear beta-catenin, downregulating beta-cat/TCF signaling activity and reducing target gene cyclinD1 protein level. Tretinoin 22-35 catenin beta 1 Homo sapiens 117-129
22333881-9 2012 However, in combination with ATRA, VPA synergized for PML-RARA degradation and LIC eradication in vivo. Tretinoin 29-33 retinoic acid receptor, alpha Mus musculus 58-62
21047566-6 2011 Of these proteins, FABP7 is a marker of NS cells, CRMP2 is involved in axon guidance, and CRABP1 is thought to regulate retinoic acid access to its nuclear receptors. Tretinoin 120-133 cellular retinoic acid-binding protein 1 Macaca fascicularis 90-96
15641681-9 2004 As a result, retinoic acid can downregulate beta-catenin/TCF pathway in porcine tracheobronchial epithelial cell, suggesting that retinoic acid can inhibit the proliferation and accelerate differentiation of tracheobronchial epithelial cells. Tretinoin 13-26 catenin beta 1 Homo sapiens 44-56
15641681-9 2004 As a result, retinoic acid can downregulate beta-catenin/TCF pathway in porcine tracheobronchial epithelial cell, suggesting that retinoic acid can inhibit the proliferation and accelerate differentiation of tracheobronchial epithelial cells. Tretinoin 130-143 catenin beta 1 Homo sapiens 44-56
14643679-9 2003 We also observed that Lin-28 expression is repressed during the retinoic acid-induced differentiation of mouse P19 cells into neuronal cells, suggesting that down-regulation of Lin-28 in some tissues may occur in response to hormonal signals that govern development. Tretinoin 64-77 lin-28 homolog A Mus musculus 22-28
20969843-5 2011 Furthermore, reporter expression expanded anteriorly when transgenic embryos were exposed to retinoic acid (RA) or LiCl, or injected with fgf3/8 mRNA, implicating the flanking DNA examined here in the responsiveness of hoxb1b to posteriorizing signals. Tretinoin 93-106 homeobox B1b Danio rerio 219-225
22659417-2 2012 Here, we report that the EBV oncoprotein, latent membrane protein 1 (LMP1), suppresses apoptotic cell death provoked by all-trans retinoic acid (ATRA) in NPC cells. Tretinoin 130-143 PDZ and LIM domain 7 Homo sapiens 69-73
22659417-2 2012 Here, we report that the EBV oncoprotein, latent membrane protein 1 (LMP1), suppresses apoptotic cell death provoked by all-trans retinoic acid (ATRA) in NPC cells. Tretinoin 145-149 PDZ and LIM domain 7 Homo sapiens 69-73
22659417-4 2012 In addition, LMP1 suppressed ATRA-mediated activation of Caspase 9, Caspase 3, and PARP but not Caspase 8 in Ad-AH cells, suggesting that LMP1 acts by blocking the activation of intrinsic apoptosis pathway by ATRA. Tretinoin 29-33 PDZ and LIM domain 7 Homo sapiens 13-17
22659417-4 2012 In addition, LMP1 suppressed ATRA-mediated activation of Caspase 9, Caspase 3, and PARP but not Caspase 8 in Ad-AH cells, suggesting that LMP1 acts by blocking the activation of intrinsic apoptosis pathway by ATRA. Tretinoin 29-33 PDZ and LIM domain 7 Homo sapiens 138-142
21274875-10 2011 atRA alone or in combination with UDCA greatly repressed CYP7A1 expression in human hepatocytes and significantly inhibited COL1A1, MMP2, and alpha-SMA expression and/or activity in primary human hepatic stellate cells and LX-2 cells. Tretinoin 0-4 collagen type I alpha 1 chain Homo sapiens 124-130
14643679-9 2003 We also observed that Lin-28 expression is repressed during the retinoic acid-induced differentiation of mouse P19 cells into neuronal cells, suggesting that down-regulation of Lin-28 in some tissues may occur in response to hormonal signals that govern development. Tretinoin 64-77 lin-28 homolog A Mus musculus 177-183
21069354-0 2011 Downregulation of Midkine gene expression and its response to retinoic acid treatment in the nitrofen-induced hypoplastic lung. Tretinoin 62-75 midkine Rattus norvegicus 18-25
14652353-0 2003 All-trans-retinoic acid rapidly induces glycine N-methyltransferase in a dose-dependent manner and reduces circulating methionine and homocysteine levels in rats. Tretinoin 0-23 glycine N-methyltransferase Rattus norvegicus 40-67
21069354-6 2011 We designed this study to investigate the hypothesis that the pulmonary MK gene expression is downregulated in the early lung morphogenesis in the nitrofen-induced PH, and to evaluate the effect of prenatal RA treatment on pulmonary MK gene expression in the nitrofen-induced CDH model. Tretinoin 207-209 midkine Rattus norvegicus 233-235
21069354-13 2011 MK gene expression levels were significantly upregulated in nitrofen + RA (0.71 +- 0.17) compared to the control (0.35 +- 0.16), CDH(-) (0.24 +- 0.15), CDH(+) (0.39 +- 0.19) and control + RA (0.47 +- 0.13) (*p < 0.05). Tretinoin 71-73 midkine Rattus norvegicus 0-2
21069354-13 2011 MK gene expression levels were significantly upregulated in nitrofen + RA (0.71 +- 0.17) compared to the control (0.35 +- 0.16), CDH(-) (0.24 +- 0.15), CDH(+) (0.39 +- 0.19) and control + RA (0.47 +- 0.13) (*p < 0.05). Tretinoin 188-190 midkine Rattus norvegicus 0-2
21069354-14 2011 Immunoreactivity of MK was also markedly decreased in nitrofen lungs compared to controls on D15, and increased in nitrofen + RA lungs compared to the other lungs on D21. Tretinoin 126-128 midkine Rattus norvegicus 20-22
21069354-16 2011 Upregulation of MK gene after RA treatment in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential to rescue PH in CDH through RA-responsive growth factor signaling. Tretinoin 30-32 midkine Rattus norvegicus 16-18
21069354-16 2011 Upregulation of MK gene after RA treatment in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential to rescue PH in CDH through RA-responsive growth factor signaling. Tretinoin 98-100 midkine Rattus norvegicus 16-18
21069354-16 2011 Upregulation of MK gene after RA treatment in the nitrofen-induced hypoplastic lung suggests that RA may have a therapeutic potential to rescue PH in CDH through RA-responsive growth factor signaling. Tretinoin 98-100 midkine Rattus norvegicus 16-18
22109893-0 2012 Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid. Tretinoin 102-115 CD4 antigen Mus musculus 85-88
22344976-6 2012 Moreover, blocking the activation of RAGE with neutralizing antibody in the presence of retinoic acid disrupted the progression of normal neuronal differentiation. Tretinoin 88-101 advanced glycosylation end-product specific receptor Homo sapiens 37-41
22535523-0 2012 The ulnar-mammary syndrome gene, Tbx3, is a direct target of the retinoic acid signaling pathway, which regulates its expression during mouse limb development. Tretinoin 65-78 T-box 3 Mus musculus 33-37
14652353-5 2003 Induction of hepatic GNMT by ATRA was rapid, exhibiting a 31% increase after a single dose (1 d) and achieving maximal induction (95%) after 4 d. Plasma methionine and homocysteine concentrations were decreased 42 and 53%, respectively, in ATRA-treated rats compared with controls. Tretinoin 29-33 glycine N-methyltransferase Rattus norvegicus 21-25
22535523-5 2012 Here we show, using in vitro and in vivo assays, that retinoic acid (RA) activates endogenous TBX3 expression, which is mediated by an RA-receptor complex directly binding and activating the TBX3 promoter, and we provide evidence that this regulation may be functionally relevant in mouse embryonic limb development. Tretinoin 54-67 T-box 3 Mus musculus 94-98
22535523-5 2012 Here we show, using in vitro and in vivo assays, that retinoic acid (RA) activates endogenous TBX3 expression, which is mediated by an RA-receptor complex directly binding and activating the TBX3 promoter, and we provide evidence that this regulation may be functionally relevant in mouse embryonic limb development. Tretinoin 54-67 T-box 3 Mus musculus 191-195
22535523-5 2012 Here we show, using in vitro and in vivo assays, that retinoic acid (RA) activates endogenous TBX3 expression, which is mediated by an RA-receptor complex directly binding and activating the TBX3 promoter, and we provide evidence that this regulation may be functionally relevant in mouse embryonic limb development. Tretinoin 69-71 T-box 3 Mus musculus 94-98
22535523-5 2012 Here we show, using in vitro and in vivo assays, that retinoic acid (RA) activates endogenous TBX3 expression, which is mediated by an RA-receptor complex directly binding and activating the TBX3 promoter, and we provide evidence that this regulation may be functionally relevant in mouse embryonic limb development. Tretinoin 69-71 T-box 3 Mus musculus 191-195
22535523-6 2012 Our data identify TBX3 as a direct target of the RA signaling pathway and extend our understanding of the role and regulation of TBX3 in limb development. Tretinoin 49-51 T-box 3 Mus musculus 18-22
21148038-0 2011 Retinoic acid-induced CCR9 expression requires transient TCR stimulation and cooperativity between NFATc2 and the retinoic acid receptor/retinoid X receptor complex. Tretinoin 0-13 chemokine (C-C motif) receptor 9 Mus musculus 22-26
21148038-1 2011 Retinoic acid (RA) imprints gut-homing specificity on T cells upon activation by inducing the expression of chemokine receptor CCR9 and integrin alpha4beta7. Tretinoin 0-13 chemokine (C-C motif) receptor 9 Mus musculus 127-131
21148038-1 2011 Retinoic acid (RA) imprints gut-homing specificity on T cells upon activation by inducing the expression of chemokine receptor CCR9 and integrin alpha4beta7. Tretinoin 15-17 chemokine (C-C motif) receptor 9 Mus musculus 127-131
21148038-2 2011 CCR9 expression seemed to be more highly dependent on RA than was the alpha4beta7 expression, but its molecular mechanism remained unclear. Tretinoin 54-56 chemokine (C-C motif) receptor 9 Mus musculus 0-4
14652353-5 2003 Induction of hepatic GNMT by ATRA was rapid, exhibiting a 31% increase after a single dose (1 d) and achieving maximal induction (95%) after 4 d. Plasma methionine and homocysteine concentrations were decreased 42 and 53%, respectively, in ATRA-treated rats compared with controls. Tretinoin 240-244 glycine N-methyltransferase Rattus norvegicus 21-25
22498432-8 2012 Cell death was not evident in short forelimb, and ATRA inhibited the expression of Ccnb1 and Ccna1, thus retarding chondrocyte maturation. Tretinoin 50-54 cyclin A1 Mus musculus 93-98
21409183-0 2011 Expression of cellular retinoic acid-binding protein I and II (CRABP I and II) in embryonic mouse hearts treated with retinoic acid. Tretinoin 23-36 cellular retinoic acid binding protein I Mus musculus 63-77
14585314-2 2003 In its active form, retinoic acid, it controls the regular differentiation as a ligand for retinoic acid receptors (RAR, RXR) and is involved in the integration (gap junction formation) of cell formations [Nature 37 (1994) 528; International Review of Cytology. Tretinoin 20-33 retinoic acid receptor alpha Homo sapiens 91-114
21409183-4 2011 RA treatment at 8.5dpc affects production of CRABP I and II in the heart in the 48-h period. Tretinoin 0-2 cellular retinoic acid binding protein I Mus musculus 45-59
21409183-5 2011 Changes in expression of mRNA for retinaldehyde dehydrogenase II (Raldh2), Crabp1 and Crabp2 genes also occur within the same time window (i.e. 10-11dpc) after RA treatment. Tretinoin 160-162 cellular retinoic acid binding protein I Mus musculus 75-81
21736279-2 2011 The effects of ATRA on the proliferation of cells and gene regulation are mediated by retinoid receptors (RAR and RXR), which belong to the nuclear receptor superfamily of ligand- inducible transcription factors. Tretinoin 15-19 retinoid X receptor alpha Homo sapiens 114-117
21099229-7 2011 Timed exposure of mouse and Xenopus embryos to excess of RA upregulated LYVE-1 and VEGFR-3 on embryonic veins and increased formation of Prox1-positive lymphatic progenitors. Tretinoin 57-59 prospero homeobox 1 L homeolog Xenopus laevis 137-142
22653585-7 2012 After 21 days of induction by retinoic acid, expression of neural markers (neuroD1 and synaptophysin) was higher in induced cell clones than in induced parental cells. Tretinoin 30-43 synaptophysin Homo sapiens 88-101
22653585-10 2012 Taken together, we developed two SOX2-overexpressing cell clones, with constitutive SOX2 expression after three weeks of retinoic acid treatment. Tretinoin 122-136 SRY-box transcription factor 2 Homo sapiens 33-37
22653585-11 2012 SOX2 overexpression resulted in altered expression of pluripotency-related genes, increased proliferation, and altered expression of neural markers after three weeks of retinoic acid treatment. Tretinoin 171-184 SRY-box transcription factor 2 Homo sapiens 0-4
14585314-2 2003 In its active form, retinoic acid, it controls the regular differentiation as a ligand for retinoic acid receptors (RAR, RXR) and is involved in the integration (gap junction formation) of cell formations [Nature 37 (1994) 528; International Review of Cytology. Tretinoin 20-33 retinoic acid receptor alpha Homo sapiens 116-119
22525672-3 2012 During the RA-induced differentiation process, Dab2 expression is induced by the GATA factors in a coherent feed-forward loop; on the other hand, we showed that p96 regulates GATA-4 in a positive feed-back manner in this study. Tretinoin 11-13 GATA binding protein 4 Homo sapiens 81-85
22525672-3 2012 During the RA-induced differentiation process, Dab2 expression is induced by the GATA factors in a coherent feed-forward loop; on the other hand, we showed that p96 regulates GATA-4 in a positive feed-back manner in this study. Tretinoin 11-13 GATA binding protein 4 Homo sapiens 175-181
20941602-5 2011 We present a detailed protocol demonstrating that polyclonal activation of conventional CD4(+) T cells in the presence of IL-2, TGFbeta, and all trans retinoic acid induces >90% conversion of these T cells to Foxp3-expressing iTregs as well as promotes a three- to fourfold increase in proliferation following a 4-day incubation period in vitro. Tretinoin 151-164 CD4 antigen Mus musculus 88-91
14647461-5 2003 In THP-1 cells differentiated to mature macrophage-like cells by PMA/TPA or ATRA, MLL-AF9 expression was downregulated. Tretinoin 76-80 lysine methyltransferase 2A Homo sapiens 82-85
22110697-0 2011 A retinoic acid responsive Hoxa3 transgene expressed in embryonic pharyngeal endoderm, cardiac neural crest and a subdomain of the second heart field. Tretinoin 2-15 homeobox A3 Mus musculus 27-32
21818590-9 2012 Pre-treatment of cell populations with DEAB or ATRA had no effect on ALDH(low)CD44(-) cells, but resulted in significant initial sensitization of ALDH(hi)CD44(+) cells to chemotherapy/radiotherapy. Tretinoin 47-51 CD44 molecule (Indian blood group) Homo sapiens 154-158
14608049-0 2003 Retinoic acid and glucocorticoid treatment induce hepatic glycine N-methyltransferase and lower plasma homocysteine concentrations in rats and rat hepatoma cells. Tretinoin 0-13 glycine N-methyltransferase Rattus norvegicus 58-85
22438569-5 2012 Additionally, we discovered that genes expressed in pre-meiotic embryonic female and adult male germ cells, including cyclin D1 (Ccnd1) and stimulated by retinoic acid 8 (Stra8), were prematurely expressed in teratoma-susceptible germ cells and, in rare instances, induced entry into meiosis. Tretinoin 154-167 cyclin D1 Mus musculus 118-127
22258322-2 2012 Our recent in vitro studies suggest that all-trans retinoic acid induces podocyte differentiation by activating the retinoic acid receptor-alpha (RARalpha)/cAMP/PKA/CREB pathway. Tretinoin 51-64 cAMP responsive element binding protein 1 Homo sapiens 165-169
21991333-4 2011 Hoxd4 transcription is regulated by a 3" neural enhancer that harbours a retinoic acid response element (RARE). Tretinoin 73-86 homeobox D4 Mus musculus 0-5
21674038-6 2011 Using immunohistochemistry to detect RA receptors RARalpha, beta and RXRalpha, we find germ cells to be the predominant target of RA signalling in the fetal human ovary, but also reveal widespread receptor nuclear localization indicative of signalling in the testis, suggesting that human fetal testicular germ cells are not efficiently shielded from RA by the action of the RA-metabolising enzyme CYP26B1. Tretinoin 37-39 retinoid X receptor alpha Homo sapiens 69-77
22292422-4 2012 VA activities are mediated by the metabolite of retinol catabolism, retinoic acid, which activates the retinoic acid receptor and retinoid X receptor (RXR). Tretinoin 68-81 retinoid X receptor alpha Homo sapiens 130-149
14608049-6 2003 Intact adrenal function was not required for RA to induce and activate hepatic GNMT; however, treatment of rats with dexamethasone (DEX) was as effective as RA in inducing GNMT in rat liver. Tretinoin 157-159 glycine N-methyltransferase Rattus norvegicus 172-176
22292422-4 2012 VA activities are mediated by the metabolite of retinol catabolism, retinoic acid, which activates the retinoic acid receptor and retinoid X receptor (RXR). Tretinoin 68-81 retinoid X receptor alpha Homo sapiens 151-154
21674038-8 2011 Finally, we demonstrate that RA induces a two-fold increase in STRA8 expression in cultures of human fetal testis, but is not sufficient to cause widespread meiosis-associated gene expression. Tretinoin 29-31 stimulated by retinoic acid 8 Homo sapiens 63-68
21280163-0 2011 Distinct roles for Wnt-4 and Wnt-11 during retinoic acid-induced neuronal differentiation. Tretinoin 43-56 Wnt family member 4 Homo sapiens 19-24
22353356-5 2012 The stimulatory effects of ATRA on ABCG1 expression were completely abolished in the presence of RAR/RXR antagonists but were only partially canceled in the presence of an LXR antagonist. Tretinoin 27-31 retinoid X receptor alpha Homo sapiens 101-104
14608049-8 2003 Moreover, coadministration of RA and DEX had an additive effect on GNMT induction. Tretinoin 30-32 glycine N-methyltransferase Rattus norvegicus 67-71
21280163-6 2011 Retinoic acid treatment of NTERA-2 cells induced the expression of Wnt-4 and Wnt-11, both of which were able to inhibit beta-catenin/Tcf activity. Tretinoin 0-13 Wnt family member 4 Homo sapiens 67-72
14608049-10 2003 Taken together, these results demonstrate that both RA and DEX independently induce GNMT, thereby having substantial implications for the potential interaction of retinoid administration with diabetes. Tretinoin 52-54 glycine N-methyltransferase Rattus norvegicus 84-88
14624395-9 2003 Moreover, we show that RA and 4HPR are able to induce morphologic changes, inhibition of cell growth, and apoptosis in FGO exerting their effects through RAR-modulated pathways. Tretinoin 23-25 retinoic acid receptor alpha Homo sapiens 154-157
20935222-6 2010 RA treatment induced UBE1L, ISG15, and UBP43 expression in RA-sensitive but not RA-resistant APL cells. Tretinoin 0-2 ubiquitin specific peptidase 18 Homo sapiens 39-44
20935222-8 2010 UBP43 knockdown repressed PML/RARalpha protein levels and inhibited RA-sensitive or RA-resistant cell growth by destabilizing the PML domain of PML/RARalpha. Tretinoin 30-32 ubiquitin specific peptidase 18 Homo sapiens 0-5
20935222-8 2010 UBP43 knockdown repressed PML/RARalpha protein levels and inhibited RA-sensitive or RA-resistant cell growth by destabilizing the PML domain of PML/RARalpha. Tretinoin 68-70 ubiquitin specific peptidase 18 Homo sapiens 0-5
21678401-0 2012 Role of SF-1 and DAX-1 during differentiation of P19 cells by retinoic acid. Tretinoin 62-75 splicing factor 1 Homo sapiens 8-12
14597990-2 2003 In this study we examined the transcriptional mechanisms of all-trans retinoic acid (ATRA)-induced down-regulation of TF in the APL cell line NB4, by analysis of stable clones expressing the luciferase gene under the control of 5" flanking regions of the TF gene. Tretinoin 70-83 coagulation factor III, tissue factor Homo sapiens 118-120
22245250-0 2012 The retinoic acid-induced up-regulation of insulin-like growth factor 1 and 2 is associated with prolidase-dependent collagen synthesis in UVA-irradiated human dermal equivalents. Tretinoin 4-17 peptidase D Homo sapiens 97-106
22245250-6 2012 RESULTS: In addition to the expected changes in MMPs and collagen synthesis in HDEs in response to ATRA, prolidase, an important enzyme in the recycling of proline and hydroxyproline from degraded collagen molecules, was significantly decreased by UVA irradiation, and its down-regulation was antagonized by ATRA. Tretinoin 99-103 peptidase D Homo sapiens 105-114
22245250-8 2012 ATRA inhibited the UVA irradiation-induced decrease in prolidase activity through an insulin-like growth factor (IGF) receptor signaling pathway in HDEs. Tretinoin 0-4 peptidase D Homo sapiens 55-64
22245250-10 2012 CONCLUSIONS: These data demonstrate that ATRA regulates prolidase activity in HDEs via IGF receptor signaling, suggesting one of the pharmacological mechanisms by which improves photo-aged human skin. Tretinoin 41-45 peptidase D Homo sapiens 56-65
22116806-3 2012 The repression of microRNA clusters Mir-17-92 (Mirc1) and Mir-106b-25 (Mirc3) by retinoic acid in turn potentially upregulates the expression of Bim, Kit, Socs3, and Stat3. Tretinoin 81-94 BCL2-like 11 (apoptosis facilitator) Mus musculus 145-148
22406747-0 2012 Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia. Tretinoin 59-82 lysine demethylase 1A Homo sapiens 18-22
22406747-0 2012 Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia. Tretinoin 59-82 lysine demethylase 1A Homo sapiens 24-29
21223795-9 2010 The average gray value of caspase-3 protein expressed in the control group was 46.12 +- 0.33 and the relative expression of caspase-3 mRNA was 0.14 +- 0.03, both were significantly lower than that in the ATRA group, 5-Fu group and the two-drugs combination group (P < 0.05). Tretinoin 204-208 caspase 3 Mus musculus 26-35
21223795-9 2010 The average gray value of caspase-3 protein expressed in the control group was 46.12 +- 0.33 and the relative expression of caspase-3 mRNA was 0.14 +- 0.03, both were significantly lower than that in the ATRA group, 5-Fu group and the two-drugs combination group (P < 0.05). Tretinoin 204-208 caspase 3 Mus musculus 124-133
20944006-3 2010 RA induced bone marrow-derived DCs to express CCR9 and ALDH1a2 and conferred upon them mucosal DC functions, including induction of Foxp3(+) regulatory T cells, IgA-secreting B cells, and gut-homing molecules. Tretinoin 0-2 chemokine (C-C motif) receptor 9 Mus musculus 46-50
20944006-7 2010 Furthermore, MyD88 signaling enhanced RA-educated DC ALDH1a2 expression and was required for optimal TGF-beta production. Tretinoin 38-40 myeloid differentiation primary response gene 88 Mus musculus 13-18
22406747-3 2012 Here we show that, through epigenetic reprogramming, inhibitors of lysine-specific demethylase 1 (LSD1, also called KDM1A), including tranylcypromine (TCP), unlocked the ATRA-driven therapeutic response in non-APL AML. Tretinoin 170-174 lysine demethylase 1A Homo sapiens 67-96
14597990-2 2003 In this study we examined the transcriptional mechanisms of all-trans retinoic acid (ATRA)-induced down-regulation of TF in the APL cell line NB4, by analysis of stable clones expressing the luciferase gene under the control of 5" flanking regions of the TF gene. Tretinoin 70-83 coagulation factor III, tissue factor Homo sapiens 255-257
22406747-3 2012 Here we show that, through epigenetic reprogramming, inhibitors of lysine-specific demethylase 1 (LSD1, also called KDM1A), including tranylcypromine (TCP), unlocked the ATRA-driven therapeutic response in non-APL AML. Tretinoin 170-174 lysine demethylase 1A Homo sapiens 98-102
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 C-reactive protein, pentraxin-related Mus musculus 247-250
20881191-1 2010 The active vitamin A metabolite retinoic acid (RA) imprints gut-homing specificity on lymphocytes upon activation by inducing the expression of alpha4beta7 integrin and CCR9. Tretinoin 32-45 chemokine (C-C motif) receptor 9 Mus musculus 169-173
20881191-1 2010 The active vitamin A metabolite retinoic acid (RA) imprints gut-homing specificity on lymphocytes upon activation by inducing the expression of alpha4beta7 integrin and CCR9. Tretinoin 47-49 chemokine (C-C motif) receptor 9 Mus musculus 169-173
20881191-4 2010 The major physiological RA, all-trans-RA, binds to RAR but not to RXR at physiological concentrations. Tretinoin 24-26 retinoic acid receptor, alpha Mus musculus 51-54
14597990-2 2003 In this study we examined the transcriptional mechanisms of all-trans retinoic acid (ATRA)-induced down-regulation of TF in the APL cell line NB4, by analysis of stable clones expressing the luciferase gene under the control of 5" flanking regions of the TF gene. Tretinoin 85-89 coagulation factor III, tissue factor Homo sapiens 118-120
14597990-2 2003 In this study we examined the transcriptional mechanisms of all-trans retinoic acid (ATRA)-induced down-regulation of TF in the APL cell line NB4, by analysis of stable clones expressing the luciferase gene under the control of 5" flanking regions of the TF gene. Tretinoin 85-89 coagulation factor III, tissue factor Homo sapiens 255-257
22154532-8 2012 In the in vitro experiments, all-trans-retinoic acid induced a decrease of the IRP2 mRNA level in hepatocytes, whereas the Fn, TfR, and IRP2 mRNA levels regulated by all-trans-retinoic acid were reversed by the vitamin A receptor blocker Ro41-5253. Tretinoin 29-52 iron responsive element binding protein 2 Rattus norvegicus 79-83
22154532-8 2012 In the in vitro experiments, all-trans-retinoic acid induced a decrease of the IRP2 mRNA level in hepatocytes, whereas the Fn, TfR, and IRP2 mRNA levels regulated by all-trans-retinoic acid were reversed by the vitamin A receptor blocker Ro41-5253. Tretinoin 32-52 iron responsive element binding protein 2 Rattus norvegicus 79-83
20869773-3 2010 Here we show that, although purified naive cells are highly susceptible to Treg generation, total CD4(+) T-cell populations from different mouse strains display significantly different sensitivities to TGF-beta/ATRA-induced Treg conversion. Tretinoin 211-215 CD4 antigen Mus musculus 98-101
14597990-4 2003 Basal activity and ATRA-induced suppression of TF promoter is determined by the proximal -383 to +121 bp of the promoter. Tretinoin 19-23 coagulation factor III, tissue factor Homo sapiens 47-49
14597990-8 2003 Interestingly, this PML/RARalpha-mediated increase in TF promoter activity is sensitive to ATRA treatment. Tretinoin 91-95 PML nuclear body scaffold Homo sapiens 20-23
14597990-8 2003 Interestingly, this PML/RARalpha-mediated increase in TF promoter activity is sensitive to ATRA treatment. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 24-32
20513800-12 2010 To confirm our observation that RACGAP-1 declines during retinoic acid-mediated differentiation, we used multiple reaction monitoring, a targeted mass spectrometry-based quantitation method, and determined that RACGAP-1 levels decline by half during retinoic acid-mediated differentiation. Tretinoin 57-70 Rac GTPase-activating protein 1 Mus musculus 32-40
22357317-3 2012 In a set of retinoic-acid (RA) and carotenoic-acid (CA) sensitizers, having n conjugated double bonds, CA7 gave rise to the highest performance, which was reduced toward RA5 and CA13. Tretinoin 12-25 RA5 Homo sapiens 170-173
14597990-8 2003 Interestingly, this PML/RARalpha-mediated increase in TF promoter activity is sensitive to ATRA treatment. Tretinoin 91-95 coagulation factor III, tissue factor Homo sapiens 54-56
22357317-3 2012 In a set of retinoic-acid (RA) and carotenoic-acid (CA) sensitizers, having n conjugated double bonds, CA7 gave rise to the highest performance, which was reduced toward RA5 and CA13. Tretinoin 27-29 RA5 Homo sapiens 170-173
20513800-12 2010 To confirm our observation that RACGAP-1 declines during retinoic acid-mediated differentiation, we used multiple reaction monitoring, a targeted mass spectrometry-based quantitation method, and determined that RACGAP-1 levels decline by half during retinoic acid-mediated differentiation. Tretinoin 250-263 Rac GTPase-activating protein 1 Mus musculus 32-40
14597990-9 2003 These data indicate that TF expression in APL cells is exacerbated by the presence of the PML/RARalpha fusion protein, and implicates the loss of Fos/Jun binding to the TF promoter in ATRA-induced suppression of TF. Tretinoin 184-188 coagulation factor III, tissue factor Homo sapiens 25-27
14597990-9 2003 These data indicate that TF expression in APL cells is exacerbated by the presence of the PML/RARalpha fusion protein, and implicates the loss of Fos/Jun binding to the TF promoter in ATRA-induced suppression of TF. Tretinoin 184-188 PML nuclear body scaffold Homo sapiens 90-93
14597990-9 2003 These data indicate that TF expression in APL cells is exacerbated by the presence of the PML/RARalpha fusion protein, and implicates the loss of Fos/Jun binding to the TF promoter in ATRA-induced suppression of TF. Tretinoin 184-188 retinoic acid receptor alpha Homo sapiens 94-102
21487509-7 2010 We demonstrate that RA containing PLGA nanoparticles suppress IL-17 production and ROR-gamma(t) expression in T cells polarized towards the Th17 phenotype in vitro with similar potency to that of free drug. Tretinoin 20-22 interleukin 17A Homo sapiens 62-67
22262177-1 2012 Through microarray analyses, we identified the Mpped2 gene as differentially expressed in two neuroblastoma cell lines induced to differentiation with all-trans retinoic acid. Tretinoin 161-174 metallophosphoesterase domain containing 2 Homo sapiens 47-53
14561891-5 2003 We found that hES cell differentiation and organization can be influenced by the scaffold and directed by growth factors such as retinoic acid, transforming growth factor beta, activin-A, or insulin-like growth factor. Tretinoin 129-142 ribosome binding protein 1 Homo sapiens 14-17
22108894-1 2012 Retinoic acid (RA) is a vitamin A derivative, which modifies the appearance of fine wrinkles and roughness of facial skin and treats acne and activates gene transcription by binding to heterodimers of the retinoic acid receptor (RAR) and the retinoic X receptor (RXR). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 242-261
22108894-1 2012 Retinoic acid (RA) is a vitamin A derivative, which modifies the appearance of fine wrinkles and roughness of facial skin and treats acne and activates gene transcription by binding to heterodimers of the retinoic acid receptor (RAR) and the retinoic X receptor (RXR). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 263-266
22108894-1 2012 Retinoic acid (RA) is a vitamin A derivative, which modifies the appearance of fine wrinkles and roughness of facial skin and treats acne and activates gene transcription by binding to heterodimers of the retinoic acid receptor (RAR) and the retinoic X receptor (RXR). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 242-261
22108894-1 2012 Retinoic acid (RA) is a vitamin A derivative, which modifies the appearance of fine wrinkles and roughness of facial skin and treats acne and activates gene transcription by binding to heterodimers of the retinoic acid receptor (RAR) and the retinoic X receptor (RXR). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 263-266
22490698-3 2012 The protein levels of tyrosine-phosphorylated STAT2 in ATRA-treated NB4 cells were detected by Western blot. Tretinoin 55-59 signal transducer and activator of transcription 2 Homo sapiens 46-51
19916800-1 2010 Transcription factor FoxA1 plays a critical role during embryonic development and is activated during retinoic acid (RA)-induced neural differentiation of pluripotent P19 embryonal carcinoma cells at the early stage, which is marked by decreased expression of Nanog and increased expression of neural stem cell marker Nestin. Tretinoin 102-115 Nanog homeobox Homo sapiens 260-265
19916800-1 2010 Transcription factor FoxA1 plays a critical role during embryonic development and is activated during retinoic acid (RA)-induced neural differentiation of pluripotent P19 embryonal carcinoma cells at the early stage, which is marked by decreased expression of Nanog and increased expression of neural stem cell marker Nestin. Tretinoin 117-119 Nanog homeobox Homo sapiens 260-265
20493242-8 2010 The amount of adducin co-immunoprecipitated with EAAC1 increases after the treatment of C6 cells with retinoic acid, a differentiating agent that induces EAAC1 overexpression in this cell model. Tretinoin 102-115 solute carrier family 1 member 1 Rattus norvegicus 49-54
20493242-8 2010 The amount of adducin co-immunoprecipitated with EAAC1 increases after the treatment of C6 cells with retinoic acid, a differentiating agent that induces EAAC1 overexpression in this cell model. Tretinoin 102-115 solute carrier family 1 member 1 Rattus norvegicus 154-159
20525991-3 2010 We demonstrate that during retinoic acid (RA)-induced differentiation of Neuro-2a cells, PtdCho synthesis was promoted by an ordered and sequential activation of choline kinase alpha (CK(alpha)) and choline cytidylyltransferase alpha (CCT(alpha)). Tretinoin 27-40 choline kinase alpha Mus musculus 162-193
20525991-3 2010 We demonstrate that during retinoic acid (RA)-induced differentiation of Neuro-2a cells, PtdCho synthesis was promoted by an ordered and sequential activation of choline kinase alpha (CK(alpha)) and choline cytidylyltransferase alpha (CCT(alpha)). Tretinoin 42-44 choline kinase alpha Mus musculus 162-193
23317920-9 2012 In response to daily intraperitoneal injections of retinoic acid, a portion of transplanted NPPFV cells exhibited retinal ganglion cell-like morphology and expressed mature neuronal markers (beta-III-tubulin and synaptophysin). Tretinoin 51-64 synaptophysin Homo sapiens 213-226
12915404-10 2003 Our data suggest that ATRA mediates growth inhibition by stabilizing Rb2/p130 via a mechanism that involves induction of PP2A, an enzyme that can potentially dephosphorylate Rb2/p130, thereby protecting it from degradation by the proteasome. Tretinoin 22-26 protein phosphatase 2 phosphatase activator Homo sapiens 121-125
20505682-1 2010 Gene associated with Retinoid-Interferon-induced Mortality (GRIM)-19 was originally identified as a regulatory gene necessary for interferon-beta and retinoic acid-induced cell death. Tretinoin 150-163 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 21-68
14706069-9 2003 Exogenous RA specifically inhibits the mesenchymal condensation prior to the proximal radial formation together with the down-regulation of sonic hedgehog (shh) and patched (pta) expression, resulting in the loss of proximal radials. Tretinoin 10-12 sonic hedgehog protein Takifugu rubripes 156-159
20534877-6 2010 Mouse myeloid DC cultured with atRA demonstrated increased gelatinase activity compared with cells cultured with retinoic acid receptor (RAR)-alpha antagonist. Tretinoin 31-35 retinoic acid receptor, alpha Mus musculus 137-147
20534877-11 2010 Chromatin immunoprecipitation assays indicated RARalpha and histone acetyltransferase p300 recruitment to, and acetylation of, histone H3 at the Mmp-9 promoter was greater after atRA treatment. Tretinoin 178-182 retinoic acid receptor, alpha Mus musculus 47-55
20534877-11 2010 Chromatin immunoprecipitation assays indicated RARalpha and histone acetyltransferase p300 recruitment to, and acetylation of, histone H3 at the Mmp-9 promoter was greater after atRA treatment. Tretinoin 178-182 E1A binding protein p300 Mus musculus 60-90
22186728-0 2012 Ectopic retinoic acid signaling affects outflow tract cushion development through suppression of the myocardial Tbx2-Tgfbeta2 pathway. Tretinoin 8-21 T-box transcription factor 2 Homo sapiens 112-116
22186728-0 2012 Ectopic retinoic acid signaling affects outflow tract cushion development through suppression of the myocardial Tbx2-Tgfbeta2 pathway. Tretinoin 8-21 transforming growth factor beta 2 Homo sapiens 117-125
22186728-5 2012 We herein demonstrate that the expression of Tbx2 in the OFT myocardium is responsive to RA, and its downregulation is associated with abnormal OFT development. Tretinoin 89-91 T-box transcription factor 2 Homo sapiens 45-49
22186728-6 2012 We found that RA could directly downregulate the Tbx2 expression through a functional retinoic acid response element (RARE) in the Tbx2 promoter region, which is also required for the initiation of Tbx2 transcription during OFT development. Tretinoin 14-16 T-box transcription factor 2 Homo sapiens 49-53
22186728-6 2012 We found that RA could directly downregulate the Tbx2 expression through a functional retinoic acid response element (RARE) in the Tbx2 promoter region, which is also required for the initiation of Tbx2 transcription during OFT development. Tretinoin 14-16 T-box transcription factor 2 Homo sapiens 131-135
14584898-18 2003 Mineralization of RA-treated cultures was inhibited by antibodies specific for annexin V but not mineralization of staurosporine-treated cultures. Tretinoin 18-20 annexin A5 Homo sapiens 79-88
22186728-6 2012 We found that RA could directly downregulate the Tbx2 expression through a functional retinoic acid response element (RARE) in the Tbx2 promoter region, which is also required for the initiation of Tbx2 transcription during OFT development. Tretinoin 14-16 T-box transcription factor 2 Homo sapiens 131-135
22186728-6 2012 We found that RA could directly downregulate the Tbx2 expression through a functional retinoic acid response element (RARE) in the Tbx2 promoter region, which is also required for the initiation of Tbx2 transcription during OFT development. Tretinoin 86-99 T-box transcription factor 2 Homo sapiens 49-53
22186728-6 2012 We found that RA could directly downregulate the Tbx2 expression through a functional retinoic acid response element (RARE) in the Tbx2 promoter region, which is also required for the initiation of Tbx2 transcription during OFT development. Tretinoin 86-99 T-box transcription factor 2 Homo sapiens 131-135
22186728-6 2012 We found that RA could directly downregulate the Tbx2 expression through a functional retinoic acid response element (RARE) in the Tbx2 promoter region, which is also required for the initiation of Tbx2 transcription during OFT development. Tretinoin 86-99 T-box transcription factor 2 Homo sapiens 131-135
22186728-7 2012 Tgfb2 expression was also downregulated in the RA-treated OFT region and was upregulated by Tbx2 in a culture system. Tretinoin 47-49 transforming growth factor beta 2 Homo sapiens 0-5
22186728-8 2012 Moreover, defective epithelial-mesenchymal transition caused by the excess RA was rescued by the addition of Tgfbeta2 in an organ culture system. Tretinoin 75-77 transforming growth factor beta 2 Homo sapiens 109-117
22186728-9 2012 These data suggest that RA signaling participates in the Tbx2 transcriptional mechanism during OFT development and that the Tbx2-Tgfbeta2 cascade is one of the key pathways involved in inducing the TGA phenotype. Tretinoin 24-26 T-box transcription factor 2 Homo sapiens 57-61
20689858-2 2010 Expression of proteoglycans and tenascin-C increased after retinoic acid induction of SSEA1-positive ES (embryonic stem) cells to nestin-positive neural stem cells, and after neural differentiation, proteoglycans and tenascin-C are expressed by both neurons and astrocytes, where they surround cell bodies and processes and in certain cases show distinctive expression patterns. Tretinoin 59-72 tenascin C Homo sapiens 32-42
20507312-9 2010 At ATRA concentrations that induced apoptosis, expression levels of retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-gamma (RXRgamma) were increased. Tretinoin 3-7 retinoid X receptor gamma Homo sapiens 112-137
20507312-9 2010 At ATRA concentrations that induced apoptosis, expression levels of retinoic acid receptor-alpha (RARalpha) and retinoid X receptor-gamma (RXRgamma) were increased. Tretinoin 3-7 retinoid X receptor gamma Homo sapiens 139-147
20421725-0 2010 All-trans retinoic acid (ATRA) downregulates MMP-9 by modulating its regulatory molecules. Tretinoin 0-23 matrix metallopeptidase 9 Homo sapiens 45-50
20421725-0 2010 All-trans retinoic acid (ATRA) downregulates MMP-9 by modulating its regulatory molecules. Tretinoin 25-29 matrix metallopeptidase 9 Homo sapiens 45-50
12914961-4 2003 Interestingly, treating SH-SY5Y cells with retinoic acid greatly increases Ret protein levels and GDNF-induced Ret tyrosine phosphorylation, but does not affect the mitogenic action of GDNF and the activation of the Akt/p70S6K pathway. Tretinoin 43-56 ribosomal protein S6 kinase B1 Homo sapiens 220-226
20421725-2 2010 We aimed to study the effect of ATRA on MMP-9 in MDA-MB-231, human breast cancer cells and the probable molecular mechanisms through which ATRA exerts its effect. Tretinoin 32-36 matrix metallopeptidase 9 Homo sapiens 40-45
22082219-0 2012 CRABP-II- and FABP5-independent all-trans retinoic acid resistance in COLO 16 human cutaneous squamous cancer cells. Tretinoin 42-55 cellular retinoic acid binding protein 2 Homo sapiens 0-8
12941622-4 2003 At all sites, expression of additional RA signaling molecules (RARalpha, RARbeta, RXR, CRABP1) depends on M/E interactions. Tretinoin 39-41 retinoic acid receptor alpha Homo sapiens 63-71
22116001-2 2012 Retinoic acid (RA) enhances induction of CD4(+) Tregs in the presence of TGFbeta. Tretinoin 0-13 CD4 antigen Mus musculus 41-44
22116001-2 2012 Retinoic acid (RA) enhances induction of CD4(+) Tregs in the presence of TGFbeta. Tretinoin 15-17 CD4 antigen Mus musculus 41-44
20511190-0 2010 Evaluation of retinoic acid therapy for OTX2-positive medulloblastomas. Tretinoin 14-27 orthodenticle homeobox 2 Mus musculus 40-44
20511190-3 2010 Retinoic acids (RAs) can suppress OTX2 expression and inhibit MB growth. Tretinoin 0-14 orthodenticle homeobox 2 Mus musculus 34-38
20511190-3 2010 Retinoic acids (RAs) can suppress OTX2 expression and inhibit MB growth. Tretinoin 16-19 orthodenticle homeobox 2 Mus musculus 34-38
20511190-5 2010 9-cis RA functions through the downregulation of OTX2 expression, which subsequently induces neuronal differentiation of OTX2-expressing cells. Tretinoin 6-8 orthodenticle homeobox 2 Mus musculus 49-53
22489124-0 2012 All-trans retinoic acid treatment is associated with prohibitin expression in renal interstitial fibrosis rats. Tretinoin 10-23 prohibitin 1 Rattus norvegicus 53-63
20511190-5 2010 9-cis RA functions through the downregulation of OTX2 expression, which subsequently induces neuronal differentiation of OTX2-expressing cells. Tretinoin 6-8 orthodenticle homeobox 2 Mus musculus 121-125
22489124-1 2012 This study was performed to investigate the association of prohibitin with renal interstitial fibrosis (RIF) lesion and to explore the association of all-trans retinoic acid (ATRA) treatment with prohibitin expression in RIF rats. Tretinoin 150-173 prohibitin 1 Rattus norvegicus 196-206
12941622-6 2003 Expression of Fgf8, shh, and Bmp4, all of which are thought to influence RA signaling, is also regulated by M/E interactions independent of RA at all sites. Tretinoin 73-75 fibroblast growth factor 8 Homo sapiens 14-18
22489124-1 2012 This study was performed to investigate the association of prohibitin with renal interstitial fibrosis (RIF) lesion and to explore the association of all-trans retinoic acid (ATRA) treatment with prohibitin expression in RIF rats. Tretinoin 175-179 prohibitin 1 Rattus norvegicus 196-206
20511190-8 2010 These findings suggest a mechanism for RA-mediated anti-tumor effect on OTX2-positive MB cells and indicate that therapeutic targeting of OTX2 might be effective if FGF pathway-mediated resistance can be overcome. Tretinoin 39-41 orthodenticle homeobox 2 Mus musculus 72-76
20511190-8 2010 These findings suggest a mechanism for RA-mediated anti-tumor effect on OTX2-positive MB cells and indicate that therapeutic targeting of OTX2 might be effective if FGF pathway-mediated resistance can be overcome. Tretinoin 39-41 orthodenticle homeobox 2 Mus musculus 138-142
22489124-9 2012 In conclusion, lower expression of prohibitin is associated with the RIF, and ATRA treatment is associated with increased prohibitin, which can prevent the progression of RIF. Tretinoin 78-82 prohibitin 1 Rattus norvegicus 122-132
12941622-6 2003 Expression of Fgf8, shh, and Bmp4, all of which are thought to influence RA signaling, is also regulated by M/E interactions independent of RA at all sites. Tretinoin 73-75 sonic hedgehog signaling molecule Homo sapiens 20-23
12970771-5 2003 Treatment with pharmacological RA dosages overcomes the dominant-negative effects of PML/RARalpha to activate transcription of retinoid target genes. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 89-97
22848172-3 2012 Here we describe targeting of TrkB-binding peptide-conjugated liposomes (PCL) to the TrkB-expressing mouse macrophage-like cell line RAW264, and to all-trans-retinoic acid-treated neuron-like TrkB+ SH-SY5Y human neuroblastoma cells. Tretinoin 158-171 neurotrophic tyrosine kinase, receptor, type 2 Mus musculus 30-34
20548792-5 2010 METHODOLOGY/PRINCIPAL FINDINGS: All-trans-retinoic acid (ATRA) enhanced the expression of the 67-kDa laminin receptor (67LR) and increased EGCG-induced cell growth inhibition in B16 melanoma cells. Tretinoin 32-55 ribosomal protein SA Mus musculus 94-117
20548792-5 2010 METHODOLOGY/PRINCIPAL FINDINGS: All-trans-retinoic acid (ATRA) enhanced the expression of the 67-kDa laminin receptor (67LR) and increased EGCG-induced cell growth inhibition in B16 melanoma cells. Tretinoin 32-55 ribosomal protein SA Mus musculus 119-123
20548792-5 2010 METHODOLOGY/PRINCIPAL FINDINGS: All-trans-retinoic acid (ATRA) enhanced the expression of the 67-kDa laminin receptor (67LR) and increased EGCG-induced cell growth inhibition in B16 melanoma cells. Tretinoin 57-61 ribosomal protein SA Mus musculus 94-117
20548792-5 2010 METHODOLOGY/PRINCIPAL FINDINGS: All-trans-retinoic acid (ATRA) enhanced the expression of the 67-kDa laminin receptor (67LR) and increased EGCG-induced cell growth inhibition in B16 melanoma cells. Tretinoin 57-61 ribosomal protein SA Mus musculus 119-123
23300837-0 2012 All-trans-retinoic acid modulates ICAM-1 N-glycan composition by influencing GnT-III levels and inhibits cell adhesion and trans-endothelial migration. Tretinoin 0-23 intercellular adhesion molecule 1 Homo sapiens 34-40
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 35-58 intercellular adhesion molecule 1 Homo sapiens 104-137
20548792-6 2010 The cell growth inhibition seen with the combined EGCG and ATRA treatment was abolished by treatment with an anti-67LR antibody. Tretinoin 59-63 ribosomal protein SA Mus musculus 114-118
12970771-6 2003 This regulation is linked directly to RA effects in APL, including PML/RARalpha degradation and induction of differentiation. Tretinoin 38-40 PML nuclear body scaffold Homo sapiens 67-70
20548792-8 2010 Expression of 67LR in the tumor increased upon oral administration of ATRA or a combined treatment of EGCG and ATRA treatment. Tretinoin 70-74 ribosomal protein SA Mus musculus 14-18
20548792-8 2010 Expression of 67LR in the tumor increased upon oral administration of ATRA or a combined treatment of EGCG and ATRA treatment. Tretinoin 111-115 ribosomal protein SA Mus musculus 14-18
20548792-9 2010 Furthermore, RNAi-mediated silencing of the retinoic acid receptor (RAR) alpha attenuated the ATRA-induced enhancement of 67LR expression in the melanoma cells. Tretinoin 94-98 retinoic acid receptor, alpha Mus musculus 44-66
20548792-9 2010 Furthermore, RNAi-mediated silencing of the retinoic acid receptor (RAR) alpha attenuated the ATRA-induced enhancement of 67LR expression in the melanoma cells. Tretinoin 94-98 retinoic acid receptor, alpha Mus musculus 68-71
20548792-9 2010 Furthermore, RNAi-mediated silencing of the retinoic acid receptor (RAR) alpha attenuated the ATRA-induced enhancement of 67LR expression in the melanoma cells. Tretinoin 94-98 ribosomal protein SA Mus musculus 122-126
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 35-58 intercellular adhesion molecule 1 Homo sapiens 139-145
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 60-64 intercellular adhesion molecule 1 Homo sapiens 104-137
23300837-2 2012 In the present study, we show that all-trans-retinoic acid (ATRA) modulates the N-glycan composition of intercellular adhesion molecule-1 (ICAM-1) by manipulating the expression of two N-acetylglucosaminyltransferases, GnT-III and GnT-V, via the ERK signaling pathway. Tretinoin 60-64 intercellular adhesion molecule 1 Homo sapiens 139-145
23300837-3 2012 Exposure of various cells to ATRA caused a remarkable gel mobility down-shift of ICAM-1. Tretinoin 29-33 intercellular adhesion molecule 1 Homo sapiens 81-87
23300837-10 2012 These data indicate that the alteration of ICAM-1 N-glycan composition by ATRA-induced GnT-III activities hindered cell adhesion and cell migration functions simultaneously, pinpointing a unique regulatory role of specific glycosyltransferases in the biological behaviors of tumor cells and a novel function of ATRA in the modulation of ICAM-1 N-glycan composition. Tretinoin 74-78 intercellular adhesion molecule 1 Homo sapiens 43-49
23300837-10 2012 These data indicate that the alteration of ICAM-1 N-glycan composition by ATRA-induced GnT-III activities hindered cell adhesion and cell migration functions simultaneously, pinpointing a unique regulatory role of specific glycosyltransferases in the biological behaviors of tumor cells and a novel function of ATRA in the modulation of ICAM-1 N-glycan composition. Tretinoin 74-78 intercellular adhesion molecule 1 Homo sapiens 337-343
23300837-10 2012 These data indicate that the alteration of ICAM-1 N-glycan composition by ATRA-induced GnT-III activities hindered cell adhesion and cell migration functions simultaneously, pinpointing a unique regulatory role of specific glycosyltransferases in the biological behaviors of tumor cells and a novel function of ATRA in the modulation of ICAM-1 N-glycan composition. Tretinoin 311-315 intercellular adhesion molecule 1 Homo sapiens 43-49
20455087-7 2010 The RA/arsenic trioxide association, which dramatically synergizes for PML/RARA degradation but not for differentiation, rapidly clears LIC in a proteasome-dependent manner, resulting in APL eradication in murine models and patients. Tretinoin 4-6 retinoic acid receptor, alpha Mus musculus 75-79
21120193-2 2010 The variant APL with t(11;17)(q23;q12); ZBTB16-RARA subgroup has been reported to have leukemic cells with regular nuclei, many granules, absence of Auer rods, an increased number of Pelgeroid neutrophils, strong myeloperoxidase (MPO) activity, and all-trans-retinoic-acid (ATRA) resistance. Tretinoin 253-272 zinc finger and BTB domain containing 16 Homo sapiens 40-46
12970771-6 2003 This regulation is linked directly to RA effects in APL, including PML/RARalpha degradation and induction of differentiation. Tretinoin 38-40 retinoic acid receptor alpha Homo sapiens 71-79
21120193-2 2010 The variant APL with t(11;17)(q23;q12); ZBTB16-RARA subgroup has been reported to have leukemic cells with regular nuclei, many granules, absence of Auer rods, an increased number of Pelgeroid neutrophils, strong myeloperoxidase (MPO) activity, and all-trans-retinoic-acid (ATRA) resistance. Tretinoin 274-278 zinc finger and BTB domain containing 16 Homo sapiens 40-46
12794076-2 2003 These oncoproteins retain the ability to bind DNA and retinoic acid through the RARalpha moiety. Tretinoin 54-67 retinoic acid receptor alpha Homo sapiens 80-88
20428830-0 2010 The cleavage fragment of retinoid X receptor-alpha ligand binding domain inhibits radiosensitization by retinoic acid. Tretinoin 104-117 retinoid X receptor alpha Homo sapiens 25-50
20428830-2 2010 Previous finding that ligand binding domain (LBD) fragment of RXR alpha specifically inhibits retinoic acid receptor-gamma (RAR gamma) activity led us to investigate the functional role of RXR alpha LBD fragment in radiosensitization by retinoic acid (RA). Tretinoin 94-107 retinoid X receptor alpha Homo sapiens 62-71
20428830-2 2010 Previous finding that ligand binding domain (LBD) fragment of RXR alpha specifically inhibits retinoic acid receptor-gamma (RAR gamma) activity led us to investigate the functional role of RXR alpha LBD fragment in radiosensitization by retinoic acid (RA). Tretinoin 124-126 retinoid X receptor alpha Homo sapiens 62-71
20428830-3 2010 Ectopic expression of RXR alpha LBD fragment in cells that do not have a detectable endogenous RXR alpha LBD fragment, blocked synergistic radiosensitizing action of RA, as determined by growth inhibition, cell death and colony formation assays. Tretinoin 166-168 retinoid X receptor alpha Homo sapiens 22-31
20428830-6 2010 Taken together, we hypothesize that the RXR alpha LBD fragment may act as a negative regulator of radiosensitizing effect of RA by restricting the RAR gamma-mediated biological response to RA. Tretinoin 125-127 retinoid X receptor alpha Homo sapiens 40-49
23185633-7 2012 In vitro treatment with PPARgamma agonists and ATRA also induced modest increase in the expression of neuronal beta-III tubulin and astrocyte-specific GFAP in NSCs in 3-7 days. Tretinoin 47-51 tubulin, beta 3 class III Mus musculus 111-127
23152790-6 2012 PML/RARalpha without the "coiled-coil" fails to block differentiation and mediates an all-trans retinoic acid-response. Tretinoin 96-109 retinoic acid receptor, alpha Mus musculus 4-12
20428830-6 2010 Taken together, we hypothesize that the RXR alpha LBD fragment may act as a negative regulator of radiosensitizing effect of RA by restricting the RAR gamma-mediated biological response to RA. Tretinoin 147-149 retinoid X receptor alpha Homo sapiens 40-49
12930299-5 2003 Interestingly, insulin-like growth factor-II (IGF-II, 50 ng/ml) was able to significantly (67.3%; P < 0.05) reduce RA effects, whereas IGF-I (50 ng/ml) and insulin (75 ng/ml) were without effect. Tretinoin 118-120 insulin like growth factor 2 Homo sapiens 15-52
23110224-3 2012 METHODOLOGY/PRINCIPAL FINDINGS: The full-length coding region of rat GlnT was inserted into a vector for gene transfection along with selection by G418, followed by culture with all-trans retinoic acid under floating conditions and subsequent dispersion for spontaneous differentiation under adherent conditions. Tretinoin 188-201 solute carrier family 38, member 1 Rattus norvegicus 69-73
22848373-0 2012 A new module in neural differentiation control: two microRNAs upregulated by retinoic acid, miR-9 and -103, target the differentiation inhibitor ID2. Tretinoin 77-90 inhibitor of DNA binding 2 Homo sapiens 145-148
20090765-0 2010 Kallikrein expression and cathelicidin processing are independently controlled in keratinocytes by calcium, vitamin D(3), and retinoic acid. Tretinoin 126-139 kallikrein related peptidase 4 Homo sapiens 0-10
12930299-10 2003 The inhibition of RA action by IGF-II was independent of its ability to signal through the IGF-I receptor or to interact with IGFBPs. Tretinoin 18-20 insulin like growth factor 2 Homo sapiens 31-37
22848373-4 2012 Notably, the two miRNAs show an inverse correlation with ID2 during neuroblastoma cell differentiation induced by retinoic acid. Tretinoin 114-127 inhibitor of DNA binding 2 Homo sapiens 57-60
22848373-6 2012 Conversely, an ID2 mutant that cannot be targeted by either miRNA prevents retinoic acid-induced differentiation more efficient than wild-type ID2. Tretinoin 75-88 inhibitor of DNA binding 2 Homo sapiens 15-18
12801531-1 2003 We investigated the dynamics of bone morphogenetic protein (BMP) and their receptor mRNA expression in relation to combined treatment with all trans-retinoic acid (ATRA) and chemotherapy in four patients with acute promyelocytic leukemia (APL). Tretinoin 143-162 bone morphogenetic protein 1 Homo sapiens 32-58
22848373-6 2012 Conversely, an ID2 mutant that cannot be targeted by either miRNA prevents retinoic acid-induced differentiation more efficient than wild-type ID2. Tretinoin 75-88 inhibitor of DNA binding 2 Homo sapiens 143-146
20346917-0 2010 Curcumin dramatically enhances retinoic acid-induced superoxide generating activity via accumulation of p47-phox and p67-phox proteins in U937 cells. Tretinoin 31-44 neutrophil cytosolic factor 1 Homo sapiens 104-112
20060826-9 2010 In retinoic acid-induced granulocytic differentiation, the activation of ERK and upregulation of tescalcin occurs slowly (16-48 h). Tretinoin 3-16 tescalcin Homo sapiens 97-106
22808286-0 2012 ATRA inhibits the proliferation of DU145 prostate cancer cells through reducing the methylation level of HOXB13 gene. Tretinoin 0-4 homeobox B13 Homo sapiens 105-111
22808286-4 2012 We discovered that ATRA was able to induce the growth arrest and to increase HOXB13 expression in AR(-) prostate cancer cells. Tretinoin 19-23 homeobox B13 Homo sapiens 77-83
12801531-1 2003 We investigated the dynamics of bone morphogenetic protein (BMP) and their receptor mRNA expression in relation to combined treatment with all trans-retinoic acid (ATRA) and chemotherapy in four patients with acute promyelocytic leukemia (APL). Tretinoin 143-162 bone morphogenetic protein 1 Homo sapiens 60-63
22808286-8 2012 Concurrently, the methylation level of the HOXB13 promoter was reduced upon the treatment of ATRA. Tretinoin 93-97 homeobox B13 Homo sapiens 43-49
22808286-9 2012 Results from this study implicated a novel effect of ATRA in inhibition of the growth of AR(-) resistant human prostate cancer cells through alteration of HOXB13 expression as a result of epigenetic modifications. Tretinoin 53-57 homeobox B13 Homo sapiens 155-161
12801531-1 2003 We investigated the dynamics of bone morphogenetic protein (BMP) and their receptor mRNA expression in relation to combined treatment with all trans-retinoic acid (ATRA) and chemotherapy in four patients with acute promyelocytic leukemia (APL). Tretinoin 164-168 bone morphogenetic protein 1 Homo sapiens 32-58
12801531-1 2003 We investigated the dynamics of bone morphogenetic protein (BMP) and their receptor mRNA expression in relation to combined treatment with all trans-retinoic acid (ATRA) and chemotherapy in four patients with acute promyelocytic leukemia (APL). Tretinoin 164-168 bone morphogenetic protein 1 Homo sapiens 60-63
20200558-0 2010 Targeting PKC delta-mediated topoisomerase II beta overexpression subverts the differentiation block in a retinoic acid-resistant APL cell line. Tretinoin 106-119 DNA topoisomerase II beta Homo sapiens 29-50
20200558-6 2010 Co-treatment with a pharmacologic inhibitor of PRKCD and RA resulted in the induction of an RA responsive reporter construct, as well as the endogenous RA target genes, CEBPE, CYP26A1 and RIG-I. Tretinoin 57-59 DExD/H-box helicase 58 Homo sapiens 188-193
22514600-6 2012 Our results showed that 9-cis-retinoic acid and all-trans retinoic acid enhanced the assembly of connexin32 into gap junctions. Tretinoin 30-43 gap junction protein beta 1 Homo sapiens 97-107
12842195-6 2003 Both RA isomers caused the enhancement of PGE2 production and the up-regulation of COX-1 expression at the protein and mRNA levels. Tretinoin 5-7 mitochondrially encoded cytochrome c oxidase I Homo sapiens 83-88
22514600-8 2012 Finally, our findings showed that formation of gap junctions sensitized connexin32-expressing LNCaP cells to the growth modifying effects of 9-cis-retinoic acid, all-trans-retinoic acid and androgens. Tretinoin 162-185 gap junction protein beta 1 Homo sapiens 72-82
21998312-1 2011 Cellular retinoic acid-binding protein II (CRABP-II) undergoes nuclear translocation upon binding of retinoic acid (RA). Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 43-51
21998312-1 2011 Cellular retinoic acid-binding protein II (CRABP-II) undergoes nuclear translocation upon binding of retinoic acid (RA). Tretinoin 44-46 cellular retinoic acid binding protein 2 Homo sapiens 0-41
21998312-5 2011 We show here that RA induces interactions of CRABP-II with the E2 SUMO ligase Ubc9 and triggers SUMOylation of the protein both in vitro and in cultured cells. Tretinoin 18-20 cellular retinoic acid binding protein 2 Homo sapiens 45-53
21998312-9 2011 Furthermore, we show that RA-induced dissociation of CRABP-II from the ER requires SUMOylation of K102. Tretinoin 26-28 cellular retinoic acid binding protein 2 Homo sapiens 53-61
20200558-8 2010 Cumulatively, our data suggest a model whereby inhibition of PRKCD decreases TOP2B protein levels, leading to a loss of TOP2B-mediated repressive effects on RA-induced transcription and granulocytic differentiation. Tretinoin 157-159 DNA topoisomerase II beta Homo sapiens 120-125
20043900-0 2010 Analysis of Cyp26b1/Rarg compound-null mice reveals two genetically separable effects of retinoic acid on limb outgrowth. Tretinoin 89-102 retinoic acid receptor, gamma Mus musculus 20-24
21998312-10 2011 Hence, SUMOylation of K102 in response to RA binding is critical for dissociation of CRABP-II from ER and, consequently, for mobilization of the protein to nucleus and for its cooperation with RAR. Tretinoin 42-44 cellular retinoic acid binding protein 2 Homo sapiens 85-93
12835288-2 2003 One putative genetic risk factor for these conditions is the retinoic acid receptor alpha (RARA) locus, which is involved in cell-specific responses to retinoic acid. Tretinoin 61-74 retinoic acid receptor alpha Homo sapiens 91-95
19775754-5 2010 Moreover, NDRG1 mRNA levels increased in two acute promyelocytic leukemia (APL) patients as well as in NB4 and HT93 APL cells upon all-trans retinoic acid (ATRA) therapy. Tretinoin 141-154 N-myc downstream regulated 1 Homo sapiens 10-15
19775754-5 2010 Moreover, NDRG1 mRNA levels increased in two acute promyelocytic leukemia (APL) patients as well as in NB4 and HT93 APL cells upon all-trans retinoic acid (ATRA) therapy. Tretinoin 156-160 N-myc downstream regulated 1 Homo sapiens 10-15
12543860-2 2003 Here we identify functional elements in the FR-beta gene and examine the molecular mechanism of transcriptional induction of FR-beta by ATRA. Tretinoin 136-140 folate receptor beta Homo sapiens 125-132
20142486-3 2010 We show that eve1 is involved in establishing trunk and tail neural ectoderm by two independent mechanisms: First, eve1 posteriorizes neural ectoderm via induction of aldh1a2, which encodes an enzyme that synthesizes retinoic acid; second, eve1 is involved in neural induction in the posterior ectoderm by attenuating BMP expression. Tretinoin 217-230 even-skipped-like1 Danio rerio 13-17
20142486-3 2010 We show that eve1 is involved in establishing trunk and tail neural ectoderm by two independent mechanisms: First, eve1 posteriorizes neural ectoderm via induction of aldh1a2, which encodes an enzyme that synthesizes retinoic acid; second, eve1 is involved in neural induction in the posterior ectoderm by attenuating BMP expression. Tretinoin 217-230 even-skipped-like1 Danio rerio 115-119
20142486-3 2010 We show that eve1 is involved in establishing trunk and tail neural ectoderm by two independent mechanisms: First, eve1 posteriorizes neural ectoderm via induction of aldh1a2, which encodes an enzyme that synthesizes retinoic acid; second, eve1 is involved in neural induction in the posterior ectoderm by attenuating BMP expression. Tretinoin 217-230 even-skipped-like1 Danio rerio 115-119
21963687-3 2011 In microarray experiments, the set of genes regulated by apo-10-lycac treatments was compared to the set of genes regulated by all-trans retinoic acid (ATRA), the natural ligand of RAR, in adipocytes. Tretinoin 137-150 retinoic acid receptor, alpha Mus musculus 181-184
21963687-3 2011 In microarray experiments, the set of genes regulated by apo-10-lycac treatments was compared to the set of genes regulated by all-trans retinoic acid (ATRA), the natural ligand of RAR, in adipocytes. Tretinoin 152-156 retinoic acid receptor, alpha Mus musculus 181-184
21917910-3 2011 Here, we examined ligand-dependent dynamic interactions of VDR with retinoid X receptor (RXR), steroid receptor coactivator 1 (SRC-1), and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) in cells using fluorescence resonance energy transfer (FRET) and chromatin immunoprecipitation (ChIP) assays. Tretinoin 161-174 vitamin D receptor Homo sapiens 59-62
21523764-0 2011 Retinoic acid induces REST degradation and neuronal differentiation by modulating the expression of SCF(beta-TRCP) in neuroblastoma cells. Tretinoin 0-13 KIT ligand Homo sapiens 100-103
12543860-5 2003 The repressor elements bound Fos family proteins; association of the proteins with the repressor elements correlated negatively with FR-beta expression in peripheral blood neutrophils and monocytes and also in KG-1 (AML) cells grown in the absence or in the presence of ATRA. Tretinoin 270-274 folate receptor beta Homo sapiens 133-140
21523764-12 2011 CONCLUSIONS: The current results indicated that elevated transcription of REST compounded by its impaired degradation by SCF(beta-TRCP) may contribute to the failure of these tumors to differentiate in response to retinoic acid. Tretinoin 214-227 KIT ligand Homo sapiens 121-124
12543860-10 2003 The multiple mechanisms favor the prediction that ATRA will induce FR-beta expression in a broad spectrum of AML cells. Tretinoin 50-54 folate receptor beta Homo sapiens 67-74
14626352-6 2003 Retinoic acid (RA) as well as 9-cis-RA increased LTBP-1 expression in both cell lines, probably through post-transcriptional mechanisms. Tretinoin 0-13 latent transforming growth factor beta binding protein 1 Homo sapiens 49-55
21903586-6 2011 Interestingly, we found that this novel pathway including CDX2, miR-125b, and CBFbeta was mediated by undergoing all-trans-retinoic acid induction. Tretinoin 113-136 caudal type homeobox 2 Homo sapiens 58-62
14626352-6 2003 Retinoic acid (RA) as well as 9-cis-RA increased LTBP-1 expression in both cell lines, probably through post-transcriptional mechanisms. Tretinoin 15-17 latent transforming growth factor beta binding protein 1 Homo sapiens 49-55
12773567-8 2003 All-trans-retinoic acid induced reorganization of the PML nuclear body (NB) and reappearance of the IR-induced TopBP1 foci. Tretinoin 0-23 PML nuclear body scaffold Homo sapiens 54-57
22148010-6 2011 RA significantly decreased DSG1 and DSC1 expression at the mRNA and protein levels in keratinocytes that were cultured in both low- and high-calcium media. Tretinoin 0-2 desmoglein 1 Homo sapiens 27-31
22148010-9 2011 CONCLUSION: Our results indicate that DSG1 and DSC1 downregulation by RA could be related to the increased degradation of corneodesmosomes and consequent desquamation induced by retinoids. Tretinoin 70-72 desmoglein 1 Homo sapiens 38-42
12776186-0 2003 Retinoic acid-induced growth arrest of MCF-7 cells involves the selective regulation of the IRS-1/PI 3-kinase/AKT pathway. Tretinoin 0-13 insulin receptor substrate 1 Homo sapiens 92-97
21906690-8 2011 CYP26C1 metabolism of all trans-RA could also be effectively competed with 9-cis RA, with IC(50) of 62nM, and was sensitive to ketoconazole inhibition. Tretinoin 32-34 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
21801775-0 2011 Retinoic acid-induced upregulation of the metalloendopeptidase nardilysin is accelerated by co-expression of the brain-specific protein p42(IP4) (centaurin alpha 1; ADAP1) in neuroblastoma cells. Tretinoin 0-13 erythrocyte membrane protein band 4.2 Homo sapiens 136-139
21801775-11 2011 Interestingly, SH-SY5Y cells, which we stably transfected with GFP-tagged-p42(IP4) showed an enhanced NRD protein expression already at an earlier time point after RA stimulation. Tretinoin 164-166 erythrocyte membrane protein band 4.2 Homo sapiens 74-77
12776186-4 2003 Treatment of MCF-7 cells with RA caused a significant reduction in IRS-1 protein and tyrosine phosphorylation levels at a concentration and time consistent with RA-mediated growth inhibition. Tretinoin 30-32 insulin receptor substrate 1 Homo sapiens 67-72
12776186-4 2003 Treatment of MCF-7 cells with RA caused a significant reduction in IRS-1 protein and tyrosine phosphorylation levels at a concentration and time consistent with RA-mediated growth inhibition. Tretinoin 161-163 insulin receptor substrate 1 Homo sapiens 67-72
12776186-5 2003 IRS-1 regulation is selective, as RA did not influence IRS-2 or SHC levels. Tretinoin 34-36 insulin receptor substrate 1 Homo sapiens 0-5
21691148-0 2011 ATRA-induced upregulation of Beclin 1 prolongs the life span of differentiated acute promyelocytic leukemia cells. Tretinoin 0-4 beclin 1 Homo sapiens 29-37
12776186-7 2003 To confirm the importance of IRS-1 regulation by RA, we examined the response to RA in MCF-7 cells overexpressing IGF-IR and IRS-1. Tretinoin 49-51 insulin receptor substrate 1 Homo sapiens 29-34
12776186-8 2003 RA resistance was observed in MCF-7 cells overexpressing IRS-1 but not IGF-IR. Tretinoin 0-2 insulin receptor substrate 1 Homo sapiens 57-62
12776186-9 2003 This suggests that RA-mediated growth inhibition requires the selective downregulation of IRS-1 and AKT. Tretinoin 19-21 insulin receptor substrate 1 Homo sapiens 90-95
12776186-10 2003 Therapeutic agents targeting the IRS-1/PI 3-kinase/AKT pathway may enhance the cytostatic effects of RA in breast cancer, since overexpression of IRS-1 and AKT have been reported in primary breast tumors. Tretinoin 101-103 insulin receptor substrate 1 Homo sapiens 33-38
21401418-7 2011 These results suggest that a RARgamma-dependent functional crosstalk is present between the retinoic acid and BMP2 signaling to induce osteogenic transdifferentiation in myoblastic C2C12 cells. Tretinoin 92-105 retinoic acid receptor, gamma Mus musculus 29-37
12776186-10 2003 Therapeutic agents targeting the IRS-1/PI 3-kinase/AKT pathway may enhance the cytostatic effects of RA in breast cancer, since overexpression of IRS-1 and AKT have been reported in primary breast tumors. Tretinoin 101-103 insulin receptor substrate 1 Homo sapiens 146-151
12529176-0 2003 Neurogenin3 triggers beta-cell differentiation of retinoic acid-derived endoderm cells. Tretinoin 50-63 neurogenin 3 Homo sapiens 0-11
21782811-0 2011 RDH10 is the primary enzyme responsible for the first step of embryonic Vitamin A metabolism and retinoic acid synthesis. Tretinoin 97-110 retinol dehydrogenase 10 Homo sapiens 0-5
21278145-9 2011 LRAT deficiency decreased diethylnitrosamine-induced injury and tumour load and increased the expression of the retinoic acid responsive genes Cyp26a1, RARb and p21, suggesting that the lower tumour load of LRAT-deficient mice was a result of increased retinoid signalling and subsequent p21-mediated inhibition of proliferation. Tretinoin 112-125 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 161-164
12529176-5 2003 By using retinoic acid-derived-endoderm F9 cells as a model, the present study indicates that the ectopic expression of Neurogenin3 is able to start the differentiation pathway of endocrine pancreas. Tretinoin 9-22 neurogenin 3 Homo sapiens 120-131
12873158-9 2003 Our results indicated that ATRA supplemented with vitamin D(3) and granulocyte colony-stimulating factor affords robust, rapid, and reproducible differentiation of both cell types. Tretinoin 27-31 colony stimulating factor 3 Homo sapiens 67-104
21373967-7 2011 Time-dependent induction of cell cycle-related genes, such as cyclin D1 and retinoblastoma protein, and amplification of the neural progenitor cell marker, brain lipid binding protein, were suppressed by GGA treatment and were completely abolished by ATRA. Tretinoin 251-255 fatty acid binding protein 7 Homo sapiens 156-183
12671705-5 2003 In cells treated with 9-cis-retinoic acid or all-trans-retinoic acid, we found that two PTKs (Eph and Hek5) appeared to be upregulated. Tretinoin 45-68 EPH receptor B2 Homo sapiens 102-106
21519922-6 2011 Retinol, retinal, and retinoic acid (RA) induced Pck1 expression dose-dependently in primary hepatocytes. Tretinoin 37-39 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 49-53
21519922-9 2011 Disruption of the proximal, but not the distal, RA responsive element in the Pck1 promoter eliminated the RA response of Pck1 promoter reporter constructs in primary hepatocytes. Tretinoin 106-108 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 77-81
21519922-9 2011 Disruption of the proximal, but not the distal, RA responsive element in the Pck1 promoter eliminated the RA response of Pck1 promoter reporter constructs in primary hepatocytes. Tretinoin 106-108 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 121-125
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 37-50 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 76-83
21336564-4 2011 Rapamycin potentiated differentiation of ATRA-treated NB4 cells, but the combination of rapamycin and LY 294002 inhibited the expression of CD11b in both ATRA- and phorbol myristate acetate (PMA)-stimulated cells more than PI3K inhibitor alone. Tretinoin 154-158 integrin subunit alpha M Homo sapiens 140-145
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 37-50 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 233-240
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 52-54 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 76-83
21653693-3 2011 Retinoic acid, acting through the retinoic acid receptor (RAR) and retinoid X receptor (RXR), affects stem cell fate determination in a concentration-dependent manner, but it only has a modest efficacy on the commitment of ES cells into skeletal muscle lineage. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 34-56
21653693-3 2011 Retinoic acid, acting through the retinoic acid receptor (RAR) and retinoid X receptor (RXR), affects stem cell fate determination in a concentration-dependent manner, but it only has a modest efficacy on the commitment of ES cells into skeletal muscle lineage. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 58-61
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 52-54 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 233-240
12588859-1 2003 We have previously reported that the retinoic acid (RA) catabolizing enzyme CYP26A1 plays an important role in protecting tail bud tissues from inappropriate exposure to RA generated in the adjacent trunk tissues by RALDH2, and that Cyp26a1-null animals exhibit spina bifida and caudal agenesis. Tretinoin 170-172 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 76-83
21596042-8 2011 RA-mediated regulation of DC required signaling through the mitogen-activated protein kinase signaling pathway and unexpectedly required MyD88, which is conventionally associated with Toll-like receptor, interleukin-1, and interleukin-18 signaling. Tretinoin 0-2 myeloid differentiation primary response gene 88 Mus musculus 137-142
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 25-27 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 49-56
21672091-9 2011 These results suggest that Sp1 plays a critical role in RA-induced CADM1 expression through possible interaction with RARalpha in the neural differentiation of P19. Tretinoin 56-58 retinoic acid receptor, alpha Mus musculus 118-126
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 25-27 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 149-156
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 25-27 wingless-type MMTV integration site family, member 3A Mus musculus 202-207
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 172-174 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 49-56
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 172-174 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 149-156
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 172-174 wingless-type MMTV integration site family, member 3A Mus musculus 202-207
21646294-2 2011 Gut-associated DC from MyD88(-/-) mice, which lack most TLR signals, expressed low levels of retinal dehydrogenases (critical enzymes for all-trans retinoic acid biosynthesis) and were significantly impaired in their ability to induce gut-homing T cells. Tretinoin 148-161 myeloid differentiation primary response gene 88 Mus musculus 23-28
12632092-4 2003 Since ABCA1 is highly regulated by liver X receptor (LXR) we also analysed the mRNA and protein expressions of LXR-alpha and LXR-beta in the THP-1 cells after treatment with atRA. Tretinoin 174-178 nuclear receptor subfamily 1 group H member 2 Homo sapiens 125-133
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 14-27 reticulon 4 receptor Homo sapiens 109-112
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 14-27 reticulon 4 receptor Homo sapiens 169-172
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 29-31 reticulon 4 receptor Homo sapiens 109-112
21690307-4 2011 Specifically, retinoic acid (RA), acting through the RA receptor beta (RAR-beta), inhibited myelin-activated NgR signaling through the transcriptional repression of the NgR complex member Lingo-1. Tretinoin 29-31 reticulon 4 receptor Homo sapiens 169-172
21605549-5 2011 This could be inhibited by RA exposure during the BMP4 treatment stage (commitment stage before adipogenic hormonal inducers were given), as was observed by reductions in key adipogenic genes/transcription factors (C/EBPalpha, PPARgamma, aP2), lipogenic genes (LPL, FAS, GLUT4), and lipid accumulation. Tretinoin 27-29 lipoprotein lipase Mus musculus 261-264
12769347-0 2003 Retinoic acid induction of CD38 antigen expression on normal and leukemic human myeloid cells: relationship with cell differentiation. Tretinoin 0-13 CD38 molecule Homo sapiens 27-31
12676320-3 2003 Here, we show that RA treatment of Xenopus embryos enhances xEmGCNF expression. Tretinoin 19-21 nuclear receptor subfamily 6 group A member 1 S homeolog Xenopus laevis 60-67
21651349-0 2011 IL-15 modulates the effect of retinoic acid, promoting inflammation rather than oral tolerance to dietary antigens. Tretinoin 30-43 interleukin 15 Homo sapiens 0-5
20195526-5 2010 Furthermore, functional dissection of components in the differentiation medium revealed that dibutyryl-cAMP (db-cAMP), 3-isobutyl-1-methylxanthine (IBMX) and retinoic acid (RA) are involved in the regulation of Nurr1 and Neurofilament-L expression as well as in the differential phosphorylation of TH. Tretinoin 158-171 nuclear receptor subfamily 4 group A member 2 Homo sapiens 211-216
20034106-1 2010 Previous studies on retinoic acid receptor (RAR) mutants suggested that retinoic acid (RA) is required for loss of interdigital mesenchyme during digit formation. Tretinoin 20-33 retinoic acid receptor, alpha Mus musculus 44-47
20034106-1 2010 Previous studies on retinoic acid receptor (RAR) mutants suggested that retinoic acid (RA) is required for loss of interdigital mesenchyme during digit formation. Tretinoin 44-46 retinoic acid receptor, alpha Mus musculus 20-42
20028206-0 2010 Differentiation of human SH-SY5Y neuroblastoma cells by all-trans retinoic acid activates the interleukin-18 system. Tretinoin 66-79 interleukin 18 Homo sapiens 94-108
21609483-6 2011 Epigenetic drugs (retinoic acid and MS-275) induced F9 cell differentiation with enhanced Rhox5 expression and dynamic changes of epigenetic marks. Tretinoin 18-31 reproductive homeobox 5 Mus musculus 90-95
12676320-6 2003 Our loss-of-function analyses using a xEmGCNF-specific morpholino antisense oligonucleotide indicate that xEmGCNF is required for the effect of RA on primary neurogenesis. Tretinoin 144-146 nuclear receptor subfamily 6 group A member 1 S homeolog Xenopus laevis 38-45
20028206-4 2010 Herein, we examined the effect of ATRA on the activity of the interleukin-18 (IL-18) system in human SH-SY5Y neuroblastoma cells. Tretinoin 34-38 interleukin 18 Homo sapiens 62-76
20028206-4 2010 Herein, we examined the effect of ATRA on the activity of the interleukin-18 (IL-18) system in human SH-SY5Y neuroblastoma cells. Tretinoin 34-38 interleukin 18 Homo sapiens 78-83
12676320-6 2003 Our loss-of-function analyses using a xEmGCNF-specific morpholino antisense oligonucleotide indicate that xEmGCNF is required for the effect of RA on primary neurogenesis. Tretinoin 144-146 nuclear receptor subfamily 6 group A member 1 S homeolog Xenopus laevis 106-113
12699690-0 2003 Human CYP1A1 allelic variants: baculovirus expression and purification, hydrodynamic, spectral, and catalytical properties and their potency in the formation of all-trans-retinoic acid. Tretinoin 161-184 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 6-12
19965660-3 2010 In gel-shift assays, R1A-RARalpha was able to bind to a panel of retinoic acid response elements both as a homodimer and as a heterodimer with RXRalpha, and demonstrated distinct DNA-binding characteristics compared with wild-type RARalpha/RXRalpha or other X-RARalpha chimeric proteins. Tretinoin 65-78 retinoic acid receptor, alpha Mus musculus 25-33
19965660-4 2010 The ratio of R1A-RARalpha to RXRalpha proteins affected the retinoic acid response element interaction pattern of R1A-RARalpha/RXRalpha complexes. Tretinoin 60-73 retinoic acid receptor, alpha Mus musculus 17-25
19965660-4 2010 The ratio of R1A-RARalpha to RXRalpha proteins affected the retinoic acid response element interaction pattern of R1A-RARalpha/RXRalpha complexes. Tretinoin 60-73 retinoic acid receptor, alpha Mus musculus 118-126
21072052-5 2011 The effect is mediated by retinoic acid receptor (RAR) alpha/retinoid X receptor (RXR) heterodimers, and occurs when both RARalpha and RXR are ligated by retinoic acids. Tretinoin 154-168 retinoic acid receptor, alpha Mus musculus 50-53
21072052-5 2011 The effect is mediated by retinoic acid receptor (RAR) alpha/retinoid X receptor (RXR) heterodimers, and occurs when both RARalpha and RXR are ligated by retinoic acids. Tretinoin 154-168 retinoic acid receptor, alpha Mus musculus 122-130
21360789-1 2011 Retinoic acid (RA) is purported to be required for expression of genes controlling proximodistal (Meis2) or anteroposterior (Shh) limb patterning. Tretinoin 0-13 Meis homeobox 2 Mus musculus 98-103
21360789-1 2011 Retinoic acid (RA) is purported to be required for expression of genes controlling proximodistal (Meis2) or anteroposterior (Shh) limb patterning. Tretinoin 15-17 Meis homeobox 2 Mus musculus 98-103
19965687-0 2010 DNA vaccination with all-trans retinoic acid treatment induces long-term survival and elicits specific immune responses requiring CD4+ and CD8+ T-cell activation in an acute promyelocytic leukemia mouse model. Tretinoin 31-44 CD4 antigen Mus musculus 130-133
12699690-10 2003 All three variants are able to produce significant amounts of all-trans-retinoic acid from all-trans-retinal with V(max) of 4.0, 3.3, and 5.6 nmol/min/nmol CYP1A1 and K(m) values of 111, 83, and 250 microM for CYP1A1.1, CYP1A1.2, and CYP1A1.4, respectively. Tretinoin 66-85 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 156-162
12699690-10 2003 All three variants are able to produce significant amounts of all-trans-retinoic acid from all-trans-retinal with V(max) of 4.0, 3.3, and 5.6 nmol/min/nmol CYP1A1 and K(m) values of 111, 83, and 250 microM for CYP1A1.1, CYP1A1.2, and CYP1A1.4, respectively. Tretinoin 66-85 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 210-216
19918205-5 2010 Cdh1 was upregulated, whereas Id2 (one downstream substrate of Cdh1-APC) was downregulated when primary neural stem cells were induced to differentiate into neurons by all-trans retinoic acid. Tretinoin 178-191 inhibitor of DNA binding 2 Homo sapiens 30-33
20563989-7 2010 In the case of co-localisation with Cyp1B1 in the hindbrain mesenchyme, this reveals that retinol is taken up into the cells for conversion to RA by Cyp1B1 and used in establishing ventral progenitor domains in the hindbrain. Tretinoin 143-145 cytochrome P450 family 1 subfamily B member 1 Gallus gallus 149-155
21437295-4 2011 Initially, we focused on the role of the BLR1 receptor in RA-induced differentiation and G1/0-arrest in HL-60. Tretinoin 58-60 C-X-C motif chemokine receptor 5 Homo sapiens 41-45
21437295-5 2011 BLR1, a putative G protein-coupled receptor expressed following RA exposure, is required for RA-induced cell-cycle arrest and differentiation and causes persistent MAPK signaling. Tretinoin 64-66 C-X-C motif chemokine receptor 5 Homo sapiens 0-4
21437295-5 2011 BLR1, a putative G protein-coupled receptor expressed following RA exposure, is required for RA-induced cell-cycle arrest and differentiation and causes persistent MAPK signaling. Tretinoin 93-95 C-X-C motif chemokine receptor 5 Homo sapiens 0-4
12699690-10 2003 All three variants are able to produce significant amounts of all-trans-retinoic acid from all-trans-retinal with V(max) of 4.0, 3.3, and 5.6 nmol/min/nmol CYP1A1 and K(m) values of 111, 83, and 250 microM for CYP1A1.1, CYP1A1.2, and CYP1A1.4, respectively. Tretinoin 66-85 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 210-216
21481001-9 2011 Compared with the control or the ATRA+FA group, ATRA had little effect on TGF-beta3 in MEPM cells but significantly inhibited TGF-beta receptor II. Tretinoin 48-52 transforming growth factor, beta receptor II Mus musculus 126-146
12699690-10 2003 All three variants are able to produce significant amounts of all-trans-retinoic acid from all-trans-retinal with V(max) of 4.0, 3.3, and 5.6 nmol/min/nmol CYP1A1 and K(m) values of 111, 83, and 250 microM for CYP1A1.1, CYP1A1.2, and CYP1A1.4, respectively. Tretinoin 66-85 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 210-216
21362455-6 2011 Overexpressed p53 induces marked DUOXA1 expression in P19 cells and intensifies neuronal differentiation in the presence of retinoic acid, which suggests that p53 and DUOXA1 possess a neural differentiation potential. Tretinoin 124-137 dual oxidase maturation factor 1 Mus musculus 33-39
19858186-3 2010 We found that all-trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta-catenin signaling in the absence or presence of exogenous Wnt3a, as revealed by lymphoid enhancer factor/T-cell factor/beta-catenin reporter activity and beta-catenin nuclear accumulation. Tretinoin 14-37 catenin (cadherin associated protein), beta 1 Mus musculus 114-126
21362455-6 2011 Overexpressed p53 induces marked DUOXA1 expression in P19 cells and intensifies neuronal differentiation in the presence of retinoic acid, which suggests that p53 and DUOXA1 possess a neural differentiation potential. Tretinoin 124-137 dual oxidase maturation factor 1 Mus musculus 167-173
12522100-6 2003 Although Nif3l1 was mainly detected in the cytoplasm, the translocation of Nif3l1 into the nuclei was observed in retinoic acid-primed neural differentiation of P19 cells and enhanced by the enforced expression of Trip15/CSN2. Tretinoin 114-127 casein beta Homo sapiens 221-225
21362455-7 2011 At day 3 of retinoic acid induced differentiation when cells showed a typical morphology of neuronal progenies, CD133 expression was down-regulated. Tretinoin 12-25 prominin 1 Mus musculus 112-117
19858186-3 2010 We found that all-trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta-catenin signaling in the absence or presence of exogenous Wnt3a, as revealed by lymphoid enhancer factor/T-cell factor/beta-catenin reporter activity and beta-catenin nuclear accumulation. Tretinoin 14-37 catenin (cadherin associated protein), beta 1 Mus musculus 238-250
19858186-3 2010 We found that all-trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta-catenin signaling in the absence or presence of exogenous Wnt3a, as revealed by lymphoid enhancer factor/T-cell factor/beta-catenin reporter activity and beta-catenin nuclear accumulation. Tretinoin 14-37 catenin (cadherin associated protein), beta 1 Mus musculus 238-250
19858186-3 2010 We found that all-trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta-catenin signaling in the absence or presence of exogenous Wnt3a, as revealed by lymphoid enhancer factor/T-cell factor/beta-catenin reporter activity and beta-catenin nuclear accumulation. Tretinoin 39-41 catenin (cadherin associated protein), beta 1 Mus musculus 114-126
19858186-3 2010 We found that all-trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta-catenin signaling in the absence or presence of exogenous Wnt3a, as revealed by lymphoid enhancer factor/T-cell factor/beta-catenin reporter activity and beta-catenin nuclear accumulation. Tretinoin 39-41 catenin (cadherin associated protein), beta 1 Mus musculus 238-250
19858186-3 2010 We found that all-trans-retinoic acid (RA) treatment of mouse epiphyseal chondrocytes in culture did increase Wnt/beta-catenin signaling in the absence or presence of exogenous Wnt3a, as revealed by lymphoid enhancer factor/T-cell factor/beta-catenin reporter activity and beta-catenin nuclear accumulation. Tretinoin 39-41 catenin (cadherin associated protein), beta 1 Mus musculus 238-250
19858186-4 2010 This stimulation was accompanied by increased gene expression of Wnt proteins and receptors and was inhibited by co-treatment with Dickkopf-related protein-1, an extracellular inhibitor of Wnt/beta-catenin signaling, suggesting that RA modulates Wnt signaling at Wnt cell surface receptor level. Tretinoin 233-235 catenin (cadherin associated protein), beta 1 Mus musculus 193-205
19858186-5 2010 RA also enhanced matrix loss triggered by Wnt/beta-catenin signaling, whereas treatment with a retinoid antagonist reduced it. Tretinoin 0-2 catenin (cadherin associated protein), beta 1 Mus musculus 46-58
21414315-2 2011 Here we show that cellular retinoic acid binding protein-II (CRABP-II) can be specifically degraded by a novel compound, SNIPER-4, consisting of (--)-N-[(2S,3R)-3-amino-2-hydroxy-4-phenyl-butyryl]-L-leucine methyl ester and all-trans retinoic acid that are ligands for cellular inhibitor of apoptosis protein 1 (cIAP1) and CRABP-II, respectively. Tretinoin 227-247 cellular retinoic acid binding protein 2 Homo sapiens 18-59
21414315-2 2011 Here we show that cellular retinoic acid binding protein-II (CRABP-II) can be specifically degraded by a novel compound, SNIPER-4, consisting of (--)-N-[(2S,3R)-3-amino-2-hydroxy-4-phenyl-butyryl]-L-leucine methyl ester and all-trans retinoic acid that are ligands for cellular inhibitor of apoptosis protein 1 (cIAP1) and CRABP-II, respectively. Tretinoin 227-247 cellular retinoic acid binding protein 2 Homo sapiens 61-69
21414315-2 2011 Here we show that cellular retinoic acid binding protein-II (CRABP-II) can be specifically degraded by a novel compound, SNIPER-4, consisting of (--)-N-[(2S,3R)-3-amino-2-hydroxy-4-phenyl-butyryl]-L-leucine methyl ester and all-trans retinoic acid that are ligands for cellular inhibitor of apoptosis protein 1 (cIAP1) and CRABP-II, respectively. Tretinoin 227-247 cellular retinoic acid binding protein 2 Homo sapiens 323-331
21345790-7 2011 These results reveal essential differences in the metabolic contribution of RDH10 versus retinol/sterol dehydrogenases to retinoic acid biosynthesis and provide the first evidence that non-retinoid metabolic products of retinol/sterol dehydrogenases affect gene expression in human epidermis. Tretinoin 122-135 retinol dehydrogenase 10 Homo sapiens 76-81
20942599-5 2010 Our results show that treatment with ATRA (10-11 M) and VPA (2 x 10-3 M) induces megakaryopoiesis of MEG-01 cells as estimated by polyploidy, formation of characteristic proplatelets and elevated expression of the megakaryocytic markers CD41 and CD61. Tretinoin 37-41 integrin subunit alpha 2b Homo sapiens 237-241
12646247-3 2003 Expression of RAR-beta 2 in MCF-7 cells resulted in increased sensitivity to ATRA-induced growth arrest and correlated with induction of CBP/p300 mRNA and protein. Tretinoin 77-81 retinoic acid receptor alpha Homo sapiens 14-17
19861119-7 2009 Moreover, via up-regulation of FABP5 Nurr1 can enhance retinoic acid-induced signaling of PPARbeta/delta and DHA-induced activation of RXR. Tretinoin 55-68 fatty acid binding protein 5 Homo sapiens 31-36
19861119-7 2009 Moreover, via up-regulation of FABP5 Nurr1 can enhance retinoic acid-induced signaling of PPARbeta/delta and DHA-induced activation of RXR. Tretinoin 55-68 nuclear receptor subfamily 4 group A member 2 Homo sapiens 37-42
19861119-7 2009 Moreover, via up-regulation of FABP5 Nurr1 can enhance retinoic acid-induced signaling of PPARbeta/delta and DHA-induced activation of RXR. Tretinoin 55-68 peroxisome proliferator activated receptor delta Homo sapiens 90-98
19861119-7 2009 Moreover, via up-regulation of FABP5 Nurr1 can enhance retinoic acid-induced signaling of PPARbeta/delta and DHA-induced activation of RXR. Tretinoin 55-68 retinoid X receptor alpha Homo sapiens 135-138
21398606-4 2011 In this study, we investigated whether memory T cells coexpressing CCR6 and integrin beta(7) are selective HIV targets and whether retinoic acid (RA)-induced imprinting for gut-homing selectively increases CCR6(+) T cell permissiveness to infection. Tretinoin 131-144 C-C motif chemokine receptor 6 Homo sapiens 206-210
21398606-4 2011 In this study, we investigated whether memory T cells coexpressing CCR6 and integrin beta(7) are selective HIV targets and whether retinoic acid (RA)-induced imprinting for gut-homing selectively increases CCR6(+) T cell permissiveness to infection. Tretinoin 146-148 C-C motif chemokine receptor 6 Homo sapiens 206-210
12646247-4 2003 Inhibition of RAR function in HMECs resulted in resistance to ATRA-induced growth arrest and loss of CBP/p300 induction. Tretinoin 62-66 retinoic acid receptor alpha Homo sapiens 14-17
12584240-1 2003 Megalin is a receptor expressed by embryonic epithelia that mediates endocytosis of numerous ligands, including sonic hedgehog (Shh) and retinol, the precursor to retinoic acid (RA). Tretinoin 163-176 low density lipoprotein receptor-related protein 2 Mus musculus 0-7
21486496-9 2011 Fluorescence and Luciferase activity, reflecting the Msi1 transcriptional activity, were observed in a stable BAC-carrying embryonic stem cell line when it was induced toward neural lineage differentiation by retinoic acid treatment. Tretinoin 209-222 musashi RNA-binding protein 1 Mus musculus 53-57
20857408-0 2011 PP2A interaction with Rb2/p130 mediates translocation of Rb2/p130 into the nucleus in all-trans retinoic acid-treated ovarian carcinoma cells. Tretinoin 96-109 RB transcriptional corepressor like 2 Homo sapiens 22-25
20857408-0 2011 PP2A interaction with Rb2/p130 mediates translocation of Rb2/p130 into the nucleus in all-trans retinoic acid-treated ovarian carcinoma cells. Tretinoin 96-109 RB transcriptional corepressor like 2 Homo sapiens 26-30
20857408-0 2011 PP2A interaction with Rb2/p130 mediates translocation of Rb2/p130 into the nucleus in all-trans retinoic acid-treated ovarian carcinoma cells. Tretinoin 96-109 RB transcriptional corepressor like 2 Homo sapiens 57-60
19855079-5 2009 RA induced the differentiation of PLZF-RARalpha-transformed murine hematopoietic cells and reduced the frequency of clonogenic progenitors, concomitant with c-Myc down-regulation. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 39-47
19855079-6 2009 Surviving RA-treated cells retained the ability to be replated and this was associated with sustained c-Myc expression and repression of Dusp6, suggesting a role for these genes in maintaining a self-renewal pathway triggered by PLZF-RARalpha. Tretinoin 10-12 dual specificity phosphatase 6 Mus musculus 137-142
19855079-6 2009 Surviving RA-treated cells retained the ability to be replated and this was associated with sustained c-Myc expression and repression of Dusp6, suggesting a role for these genes in maintaining a self-renewal pathway triggered by PLZF-RARalpha. Tretinoin 10-12 retinoic acid receptor, alpha Mus musculus 234-242
20857408-0 2011 PP2A interaction with Rb2/p130 mediates translocation of Rb2/p130 into the nucleus in all-trans retinoic acid-treated ovarian carcinoma cells. Tretinoin 96-109 RB transcriptional corepressor like 2 Homo sapiens 61-65
20857408-1 2011 One of the mechanisms by which all-trans retinoic acid (ATRA) has been shown to suppress the growth of CAOV3 ovarian carcinoma cells involves an increase in the accumulation of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 41-54 RB transcriptional corepressor like 2 Homo sapiens 177-180
12584240-1 2003 Megalin is a receptor expressed by embryonic epithelia that mediates endocytosis of numerous ligands, including sonic hedgehog (Shh) and retinol, the precursor to retinoic acid (RA). Tretinoin 163-176 sonic hedgehog Mus musculus 112-126
20857408-1 2011 One of the mechanisms by which all-trans retinoic acid (ATRA) has been shown to suppress the growth of CAOV3 ovarian carcinoma cells involves an increase in the accumulation of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 41-54 RB transcriptional corepressor like 2 Homo sapiens 181-185
20857408-1 2011 One of the mechanisms by which all-trans retinoic acid (ATRA) has been shown to suppress the growth of CAOV3 ovarian carcinoma cells involves an increase in the accumulation of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 56-60 RB transcriptional corepressor like 2 Homo sapiens 177-180
19631020-7 2009 RA treatment resulted in a slight decrease in adiposity, decreased cell lipid accumulation and increased UCP1 content, suggesting that the effects of BC on thermogenic capacity are not through RA. Tretinoin 0-2 mitochondrial brown fat uncoupling protein 1 Mustela putorius furo 105-109
12584240-1 2003 Megalin is a receptor expressed by embryonic epithelia that mediates endocytosis of numerous ligands, including sonic hedgehog (Shh) and retinol, the precursor to retinoic acid (RA). Tretinoin 178-180 low density lipoprotein receptor-related protein 2 Mus musculus 0-7
20857408-1 2011 One of the mechanisms by which all-trans retinoic acid (ATRA) has been shown to suppress the growth of CAOV3 ovarian carcinoma cells involves an increase in the accumulation of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 56-60 RB transcriptional corepressor like 2 Homo sapiens 181-185
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 RB transcriptional corepressor like 2 Homo sapiens 58-61
12584240-3 2003 Several mechanisms could explain how megalin influences Shh and RA signaling in the context of neurodevelopment. Tretinoin 64-66 low density lipoprotein receptor-related protein 2 Mus musculus 37-44
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 RB transcriptional corepressor like 2 Homo sapiens 62-66
20857408-3 2011 We show that upon ATRA treatment, PP2A interacts with the Rb2/p130 C-terminus and specifically dephosphorylates two residues (S1080 and T1097) adjacent to NLS1 and NLS2 of Rb2/p130. Tretinoin 18-22 RB transcriptional corepressor like 2 Homo sapiens 172-175
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 RB transcriptional corepressor like 2 Homo sapiens 153-156
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 RB transcriptional corepressor like 2 Homo sapiens 157-161
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 RB transcriptional corepressor like 2 Homo sapiens 275-278
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 RB transcriptional corepressor like 2 Homo sapiens 279-283
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 RB transcriptional corepressor like 2 Homo sapiens 275-278
27635169-7 2009 Considering the mitogenic effects of RA, the RA-activated RXRalpha would likely then influence hepatocyte proliferation and liver tissue repair. Tretinoin 37-39 retinoid X receptor alpha Homo sapiens 58-66
27635169-9 2009 This review summarizes the activation of nuclear receptors (peroxisome proliferator activated receptor-alpha, pregnane x receptor, constitutive androstane receptor, and farnesoid x receptor) in an RXRalpha dependent manner to induce hepatocyte proliferation, providing a link between RA and its proliferative role. Tretinoin 284-286 nuclear receptor subfamily 1 group I member 3 Homo sapiens 131-189
27635169-9 2009 This review summarizes the activation of nuclear receptors (peroxisome proliferator activated receptor-alpha, pregnane x receptor, constitutive androstane receptor, and farnesoid x receptor) in an RXRalpha dependent manner to induce hepatocyte proliferation, providing a link between RA and its proliferative role. Tretinoin 284-286 retinoid X receptor alpha Homo sapiens 197-205
19749800-5 2009 Patients successfully treated with all-trans-retinoic acid (ATRA) and chemotherapy showed downregulation of miR-181b and upregulation of miR-15b, -16, -107, -223, -342 and let-7c. Tretinoin 35-58 microRNA 15b Homo sapiens 137-144
19749800-5 2009 Patients successfully treated with all-trans-retinoic acid (ATRA) and chemotherapy showed downregulation of miR-181b and upregulation of miR-15b, -16, -107, -223, -342 and let-7c. Tretinoin 60-64 microRNA 15b Homo sapiens 137-144
20857408-6 2011 Our studies suggest that one mechanism by which ATRA treatment of CAOV3 cells induces G0/G1 arrest involves the recruitment of PP2A to the C-terminus of Rb2/p130, resulting in the dephosphorylation of the S1080 and T1097 adjacent to the NLS and the subsequent interaction of Rb2/p130 with importins leading to transport of the Rb2/p130 to the nucleus where it inhibits cell-cycle progression. Tretinoin 48-52 RB transcriptional corepressor like 2 Homo sapiens 279-283
12645566-6 2003 Furthermore, constitutive expression of ZPR9 in human neuroblastoma cells induces apoptosis in the presence of retinoic acid. Tretinoin 111-124 zinc finger protein 622 Homo sapiens 40-44
21344951-6 2011 Surprisingly, eukaryotic initiation factor 5A (Eif5a), a protein which is essential for cell proliferation and differentiation, was significantly down-regulated under RA treatment. Tretinoin 167-169 eukaryotic translation initiation factor 5A2 Mus musculus 14-45
21360626-3 2011 Retinoic acid (RA) rapidly downregulates Pml, resulting in the replacement of BRGC with Brm-containing remodeling complex, disassociation of SF1 and Sp1, retaining of TR2, recruitment of receptor-interaction protein 140, G9a and HP1gamma, and sequential insertion of two nucleosomes on CR1 that progressively displays repressive heterochromatin marks. Tretinoin 0-13 splicing factor 1 Homo sapiens 141-144
21360626-3 2011 Retinoic acid (RA) rapidly downregulates Pml, resulting in the replacement of BRGC with Brm-containing remodeling complex, disassociation of SF1 and Sp1, retaining of TR2, recruitment of receptor-interaction protein 140, G9a and HP1gamma, and sequential insertion of two nucleosomes on CR1 that progressively displays repressive heterochromatin marks. Tretinoin 0-13 euchromatic histone lysine methyltransferase 2 Homo sapiens 187-224
19683536-0 2009 Cell cycle regulatory effects of retinoic Acid and forskolin are mediated by the cyclin C gene. Tretinoin 33-46 cyclin C Homo sapiens 81-89
19683536-2 2009 In this study, we showed that the highly expressed Cyclin C gene is a direct target of the nuclear hormone all-trans retinoic acid (RA) in HEK293 human embryonal kidney cells. Tretinoin 117-130 cyclin C Homo sapiens 51-59
21262915-4 2011 RA effects are mediated by RAR/RXR receptors that we show are modified by interactions with the aryl hydrocarbon receptor (AhR), a protein functioning both as a transcription factor and a ligand-dependent adaptor in an ubiquitin ligase complex. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 31-34
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 73-86 sphingosine-1-phosphate receptor 2 Homo sapiens 164-170
21193583-10 2011 RA also promoted an oxygen contraction in the Cyp3a(-/-) DA. Tretinoin 0-2 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 46-51
21193583-11 2011 However, responses of RA-treated WT and Cyp3a(-/-) mice differed in that only the former abated with ET-1 suppression. Tretinoin 22-24 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 40-45
19834598-12 2009 Moreover, the transcriptional response of SY5Y cells to Gli1 transduction closely resembled the transcriptional response to the differentiation agent retinoic acid (p<0.00001). Tretinoin 150-163 GLI family zinc finger 1 Homo sapiens 56-60
19474283-2 2009 We previously reported that all-trans retinoic acid (ATRA) and 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] induced expression of nephrin in murine podocytes. Tretinoin 28-51 nephrosis 1, nephrin Mus musculus 130-137
19474283-2 2009 We previously reported that all-trans retinoic acid (ATRA) and 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] induced expression of nephrin in murine podocytes. Tretinoin 53-57 nephrosis 1, nephrin Mus musculus 130-137
19474283-7 2009 ATRA-triggered, RAR-mediated activation of the nephrin gene promoter was not suppressed by the VDR antagonist. Tretinoin 0-4 nephrosis 1, nephrin Mus musculus 47-54
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 retinoic acid receptor, alpha Mus musculus 62-65
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 70-73
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 nephrosis 1, nephrin Mus musculus 99-106
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 nephrosis 1, nephrin Mus musculus 135-142
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 retinoic acid receptor, alpha Mus musculus 163-166
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 nephrosis 1, nephrin Mus musculus 135-142
21356353-0 2011 Association of FABP5 expression with poor survival in triple-negative breast cancer: implication for retinoic acid therapy. Tretinoin 101-114 fatty acid binding protein 5 Homo sapiens 15-20
21356353-1 2011 Recent studies using animal models suggest that expression of FABP5 drives the stimulation of cell growth observed in estrogen receptor (ER)-negative breast cancer cells on exposure to retinoic acid (RA). Tretinoin 185-198 fatty acid binding protein 5 Homo sapiens 62-67
21356353-1 2011 Recent studies using animal models suggest that expression of FABP5 drives the stimulation of cell growth observed in estrogen receptor (ER)-negative breast cancer cells on exposure to retinoic acid (RA). Tretinoin 200-202 fatty acid binding protein 5 Homo sapiens 62-67
21356353-8 2011 We propose a model whereby growth-promoting FABP5 competes with growth-inhibiting CRABP2 for RA, with retention of RA in the cytoplasm by FABP5 preventing the inhibition of tumor growth. Tretinoin 93-95 fatty acid binding protein 5 Homo sapiens 44-49
21356353-8 2011 We propose a model whereby growth-promoting FABP5 competes with growth-inhibiting CRABP2 for RA, with retention of RA in the cytoplasm by FABP5 preventing the inhibition of tumor growth. Tretinoin 93-95 cellular retinoic acid binding protein 2 Homo sapiens 82-88
19474283-11 2009 CONCLUSIONS: These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)(2)D(3) induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR. Tretinoin 122-126 retinoic acid receptor, alpha Mus musculus 163-166
19633294-7 2009 RA down-regulates expression of CaMKIV and one of its upstream activators, CaMKK1 (calmodulin-dependent protein kinase kinase 1). Tretinoin 0-2 calcium/calmodulin dependent protein kinase kinase 1 Homo sapiens 75-81
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 73-86 sphingosine-1-phosphate receptor 2 Homo sapiens 172-177
19633294-7 2009 RA down-regulates expression of CaMKIV and one of its upstream activators, CaMKK1 (calmodulin-dependent protein kinase kinase 1). Tretinoin 0-2 calcium/calmodulin dependent protein kinase kinase 1 Homo sapiens 83-127
19633294-8 2009 This is accompanied by RA-induced suppression of activating phosphorylation of CREB with a time course paralleling that of CaMKIV down-regulation. Tretinoin 23-25 cAMP responsive element binding protein 1 Homo sapiens 79-83
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 0-2 cAMP responsive element binding protein 1 Homo sapiens 86-90
21547672-7 2011 Furthermore, the activity of MMP-2, a key enzyme in tumor cell invasion, was significantly decreased in cells treated with the combination of paclitaxel and ATRA while other combinations and single agents did not significantly affect its activity. Tretinoin 157-161 matrix metallopeptidase 2 Mus musculus 29-34
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 252-254 cAMP responsive element binding protein 1 Homo sapiens 86-90
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 88-90 sphingosine-1-phosphate receptor 2 Homo sapiens 164-170
19633294-9 2009 RA-induced repression of the Ca(2+)/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating the timing of neuronal differentiation, as shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation of p21/Cip1 and doublecortin expression and RA-promoted neurite outgrowth. Tretinoin 252-254 cAMP responsive element binding protein 1 Homo sapiens 86-90
21061155-4 2011 Laser confocal microscopy results reveal that PHB colocalized with the expression products of c-myc, c-fos, p53, and Rb, but the colocalization region was altered after RA treatment. Tretinoin 169-171 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 101-106
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 88-90 sphingosine-1-phosphate receptor 2 Homo sapiens 172-177
21284970-1 2011 OBJECTIVE: The objective of this study was to determine whether amniotic fluid levels of glial acidic fibrillary protein (GFAP) would reflect myelomeningocele-related neurodegeneration in the rat model of retinoic acid-induced myelomeningocele, which is a model that is very similar to human myelomeningocele and develops the entire spectrum of disease severity including features of the Chiari II malformation. Tretinoin 205-218 glial fibrillary acidic protein Rattus norvegicus 89-120
19482004-4 2009 To enable the search for nonretinoid molecules with fenretinide-like activities we developed a HTS-compatible homogeneous TR-FRET assay monitoring the displacement of retinoic acid derivatives from RBP4 in high-density 384-well and 1536-well microtiter plate formats. Tretinoin 167-180 retinol binding protein 4, plasma Mus musculus 198-202
21284970-1 2011 OBJECTIVE: The objective of this study was to determine whether amniotic fluid levels of glial acidic fibrillary protein (GFAP) would reflect myelomeningocele-related neurodegeneration in the rat model of retinoic acid-induced myelomeningocele, which is a model that is very similar to human myelomeningocele and develops the entire spectrum of disease severity including features of the Chiari II malformation. Tretinoin 205-218 glial fibrillary acidic protein Rattus norvegicus 122-126
12577307-4 2003 S1P-evoked increases in [Ca(2+)](i) in S1P(3) R-predominant BCCs were suppressed by concentrations of VD3 and RA which decreased expression of S1P(3) Rs, despite RA-induced increases in S1P(2) Rs. Tretinoin 110-112 sphingosine-1-phosphate receptor 2 Homo sapiens 186-192
12577307-6 2003 The RA-induced increase in expression of S1P(2) Rs did not prevent suppression by RA of S1P-elicited chemokinesis, which appears to be mediated by S1P(3) Rs, but instead exposed S1P(2) R-mediated inhibition of epidermal growth factor-stimulated chemotaxis of BCCs. Tretinoin 4-6 sphingosine-1-phosphate receptor 2 Homo sapiens 41-47
12577307-6 2003 The RA-induced increase in expression of S1P(2) Rs did not prevent suppression by RA of S1P-elicited chemokinesis, which appears to be mediated by S1P(3) Rs, but instead exposed S1P(2) R-mediated inhibition of epidermal growth factor-stimulated chemotaxis of BCCs. Tretinoin 4-6 sphingosine-1-phosphate receptor 2 Homo sapiens 178-184
19464348-8 2009 Retinoic acid (RA) was found to regulate Nedd9 expression in NCCs. Tretinoin 0-13 neural precursor cell expressed, developmentally down-regulated 9 Gallus gallus 41-46
12647219-3 2003 The expression of PML, revealed as speckled or microgranular staining in the nuclei, was positively correlated with the differentiation status of NB cells in vivo, and was upregulated during the differentiation of KCNR and SY5Y cells following retinoic acid treatment. Tretinoin 244-257 PML nuclear body scaffold Homo sapiens 18-21
19556237-4 2009 An evolutionarily conserved gene, beta,beta-carotene 15,15"-monooxygenase (BCMO), which is involved in retinoic acid biosynthesis, was studied in both Caenorhabditis elegans and murine Hepa 1-6 cells. Tretinoin 103-116 Beta-Carotene 15,15'-MonoOxygenase Caenorhabditis elegans 34-73
20376700-2 2011 We found that in AN(3)CA and F9 cells, this hCOX-2 DR1 mediates responsiveness to all-trans-retinoic acid (tRA) or 9-cis-retinoic acid (9cRA), but this effect was suppressed by PPARdelta. Tretinoin 82-105 peroxisome proliferator activated receptor delta Homo sapiens 177-186
20376700-2 2011 We found that in AN(3)CA and F9 cells, this hCOX-2 DR1 mediates responsiveness to all-trans-retinoic acid (tRA) or 9-cis-retinoic acid (9cRA), but this effect was suppressed by PPARdelta. Tretinoin 107-110 peroxisome proliferator activated receptor delta Homo sapiens 177-186
12606034-1 2003 In an earlier study, we showed that expressions of GD3, GT1b, and GQ1b gangliosides in P19 embryonic carcinoma (EC) cells were enhanced during their neural differentiation induced by retinoic acid. Tretinoin 183-196 GRDX Homo sapiens 51-54
21220944-4 2011 We found that while retinoic acid-inducible gene expression tends to be uniformly dependent on CBP/p300, dsRNA- and serum-inducible genes displayed non-uniform requirements for CBP/p300, with the dsRNA-inducible expression of Ifnb1 (interferon-beta) being particularly dependent on CBP/p300. Tretinoin 20-33 CREB binding protein Mus musculus 95-98
21220944-4 2011 We found that while retinoic acid-inducible gene expression tends to be uniformly dependent on CBP/p300, dsRNA- and serum-inducible genes displayed non-uniform requirements for CBP/p300, with the dsRNA-inducible expression of Ifnb1 (interferon-beta) being particularly dependent on CBP/p300. Tretinoin 20-33 E1A binding protein p300 Mus musculus 99-103
21220944-4 2011 We found that while retinoic acid-inducible gene expression tends to be uniformly dependent on CBP/p300, dsRNA- and serum-inducible genes displayed non-uniform requirements for CBP/p300, with the dsRNA-inducible expression of Ifnb1 (interferon-beta) being particularly dependent on CBP/p300. Tretinoin 20-33 CREB binding protein Mus musculus 95-103
19388084-8 2009 The protein expression levels of p21, Smad2/3, phospho-Smad2, and phospho-Smad3 were increased, while phospho-Rb was decreased in MEPM after atRA treatment on GD 10. Tretinoin 141-145 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 33-36
19388084-13 2009 Our study demonstrated that Smad2/3 regulation of p21 was partly required for atRA-induced cell cycle perturbations in MEPM cells. Tretinoin 78-82 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 50-53
12482873-1 2003 Ligand-induced transcription activation of retinoic acid (RA) target genes by nuclear receptors (retinoic acid (RAR) and retinoid X (RXR) receptors) depends on the recruitment of coactivators. Tretinoin 43-56 retinoic acid receptor alpha Homo sapiens 112-115
19585150-4 2009 The present data demonstrate that retinoic acid (RA) treatment and the activation of Wnt signaling induce Hoxa2 and Hoxd9 expression, respectively, in mouse mesencephalic neural crest cells, which never express Hox genes in vivo. Tretinoin 34-47 homeobox D9 Mus musculus 116-121
19156541-6 2009 In retinoic acid-differentiated SH-SY5Y neuronal cells where ObRb was induced, leptin increased the expression of Cdk5, p35, and p25 kinases. Tretinoin 3-16 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 120-123
19156541-6 2009 In retinoic acid-differentiated SH-SY5Y neuronal cells where ObRb was induced, leptin increased the expression of Cdk5, p35, and p25 kinases. Tretinoin 3-16 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 129-132
21232103-1 2011 BACKGROUND: Among its many roles in development, retinoic acid determines the anterior-posterior identity of differentiating motor neurons by activating retinoic acid receptor (RAR)-mediated transcription. Tretinoin 49-62 retinoic acid receptor, alpha Mus musculus 153-175
21232103-1 2011 BACKGROUND: Among its many roles in development, retinoic acid determines the anterior-posterior identity of differentiating motor neurons by activating retinoic acid receptor (RAR)-mediated transcription. Tretinoin 49-62 retinoic acid receptor, alpha Mus musculus 177-180
21232103-4 2011 RESULTS: We tested the constitutive RAR binding model using the retinoic acid-driven differentiation of mouse embryonic stem cells into differentiated motor neurons. Tretinoin 64-77 retinoic acid receptor, alpha Mus musculus 36-39
21232103-5 2011 We find that retinoic acid treatment results in widespread changes in RAR genomic binding, including novel binding to genes directly responsible for anterior-posterior specification, as well as the subsequent recruitment of the basal polymerase machinery. Tretinoin 13-26 retinoic acid receptor, alpha Mus musculus 70-73
19294396-6 2009 The mRNA expression of RA-regulated genes (KRT2, KRT4, CRABPII and HBEGF) was altered within 24 h after RA exposure. Tretinoin 23-25 keratin 4 Homo sapiens 49-53
12482873-1 2003 Ligand-induced transcription activation of retinoic acid (RA) target genes by nuclear receptors (retinoic acid (RAR) and retinoid X (RXR) receptors) depends on the recruitment of coactivators. Tretinoin 58-60 retinoic acid receptor alpha Homo sapiens 112-115
19618472-2 2009 Upon all-trans retinoic acid induced differentiation of murine embryonic stem (ES) cells, Rex1 mRNA levels decrease several fold. Tretinoin 15-28 zinc finger protein 42 Mus musculus 90-94
22553627-1 2011 AIM: All-trans retinoic acid (RA) is the only extrinsic biochemical candidate known to date that could act as a growth controller, the aim of this study was to investigate the expression cellular retinoic acid binding proteins I (CRABP-I) and retinoic acid receptor-beta (RAR-beta) in retina of the guinea pig eyes with experimental myopia. Tretinoin 15-28 retinoic acid receptor beta Cavia porcellus 243-270
12569362-7 2003 A DR5 retinoic acid responsive element was observed in the LTR. Tretinoin 6-19 TNF receptor superfamily member 10b Homo sapiens 2-5
22553627-1 2011 AIM: All-trans retinoic acid (RA) is the only extrinsic biochemical candidate known to date that could act as a growth controller, the aim of this study was to investigate the expression cellular retinoic acid binding proteins I (CRABP-I) and retinoic acid receptor-beta (RAR-beta) in retina of the guinea pig eyes with experimental myopia. Tretinoin 15-28 retinoic acid receptor beta Cavia porcellus 272-280
22553627-1 2011 AIM: All-trans retinoic acid (RA) is the only extrinsic biochemical candidate known to date that could act as a growth controller, the aim of this study was to investigate the expression cellular retinoic acid binding proteins I (CRABP-I) and retinoic acid receptor-beta (RAR-beta) in retina of the guinea pig eyes with experimental myopia. Tretinoin 30-32 retinoic acid receptor beta Cavia porcellus 243-270
22553627-1 2011 AIM: All-trans retinoic acid (RA) is the only extrinsic biochemical candidate known to date that could act as a growth controller, the aim of this study was to investigate the expression cellular retinoic acid binding proteins I (CRABP-I) and retinoic acid receptor-beta (RAR-beta) in retina of the guinea pig eyes with experimental myopia. Tretinoin 30-32 retinoic acid receptor beta Cavia porcellus 272-280
22553627-12 2011 During the progression of experimental myopia, the retinal RA level increased rapidly, and there might be a positive feedback between the increase of RA and up-regulation of RAR-beta. Tretinoin 59-61 retinoic acid receptor beta Cavia porcellus 174-182
19357873-0 2009 Effect of all-trans retinoic acid on renal expressions of matrix metalloproteinase-2, matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in rats with glomerulosclerosis. Tretinoin 10-33 matrix metallopeptidase 9 Rattus norvegicus 86-112
19357873-0 2009 Effect of all-trans retinoic acid on renal expressions of matrix metalloproteinase-2, matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in rats with glomerulosclerosis. Tretinoin 10-33 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 117-156
19886770-2 2009 Removal of dietary vitamin A or a targeted deletion of retinoic acid receptor alpha gene (Rara), the receptor for retinoic acid, in mice, led to testicular degeneration by a dramatic loss of germ cells and a loss of control of the spermatogenic cycle. Tretinoin 55-68 retinoic acid receptor, alpha Mus musculus 90-94
12570784-8 2003 Interestingly, some agents, like retinoic acid, have been shown to modulate the expression of both NPY and NPY-Rs in the same direction, thus providing a fine mechanism for the tuning of the system. Tretinoin 33-46 neuropeptide Y Homo sapiens 99-102
20857298-0 2011 Prenatal treatment with retinoic acid activates parathyroid hormone-related protein signaling in the nitrofen-induced hypoplastic lung. Tretinoin 24-37 parathyroid hormone-like hormone Rattus norvegicus 48-83
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 42-44 parathyroid hormone-like hormone Rattus norvegicus 13-18
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 42-44 parathyroid hormone-like hormone Rattus norvegicus 23-28
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 42-44 parathyroid hormone-like hormone Rattus norvegicus 23-28
19578722-2 2009 Here, we try to reveal how PRC2, PRC2-mediated repressive histone marker H3K27me3, and active histone marker histone H4 acetylation (acH4) regulate the CD11b transcription during alltrans retinoic acid (ATRA)-induced HL-60 leukemia cell differentiation. Tretinoin 188-201 integrin subunit alpha M Homo sapiens 152-157
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 42-44 parathyroid hormone-like hormone Rattus norvegicus 23-28
19578722-2 2009 Here, we try to reveal how PRC2, PRC2-mediated repressive histone marker H3K27me3, and active histone marker histone H4 acetylation (acH4) regulate the CD11b transcription during alltrans retinoic acid (ATRA)-induced HL-60 leukemia cell differentiation. Tretinoin 203-207 integrin subunit alpha M Homo sapiens 152-157
12570784-8 2003 Interestingly, some agents, like retinoic acid, have been shown to modulate the expression of both NPY and NPY-Rs in the same direction, thus providing a fine mechanism for the tuning of the system. Tretinoin 33-46 neuropeptide Y Homo sapiens 107-110
19578722-6 2009 By using chromatin immunoprecipitation assay, we compared the local changes in SUZ12 binding and PRC2-mediated H3K27me3 at the promoter of CD11b during ATRA-induced HL-60 differentiation. Tretinoin 152-156 integrin subunit alpha M Homo sapiens 139-144
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 112-114 parathyroid hormone-like hormone Rattus norvegicus 13-18
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 112-114 parathyroid hormone-like hormone Rattus norvegicus 23-28
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 112-114 parathyroid hormone-like hormone Rattus norvegicus 23-28
12627849-2 2003 Granulocyte colony-stimulating factor (G-CSF) by itself had no effect on NB4 cells but exerted additional enhancing effects on the respiratory burst activity in the presence of ATRA. Tretinoin 177-181 colony stimulating factor 3 Homo sapiens 0-37
20857298-5 2011 Because both PTHrP and PTHrP-R genes have RA-inducible element, we hypothesized that prenatal administration of RA upregulates pulmonary gene expression of PTHrP and PTHrP-R in the nitrofen-induced HL. Tretinoin 112-114 parathyroid hormone-like hormone Rattus norvegicus 23-28
20857298-10 2011 RESULTS: The pulmonary gene expression levels of PTHrP and PTHrP-R were significantly increased in nitrofen + RA group compared to nitrofen group (p < 0.05). Tretinoin 110-112 parathyroid hormone-like hormone Rattus norvegicus 49-54
20857298-10 2011 RESULTS: The pulmonary gene expression levels of PTHrP and PTHrP-R were significantly increased in nitrofen + RA group compared to nitrofen group (p < 0.05). Tretinoin 110-112 parathyroid hormone-like hormone Rattus norvegicus 59-64
20857298-11 2011 Immunoreactivity of PTHrP and PTHrP-R was also remarkably increased in nitrofen + RA group compared to nitrofen group. Tretinoin 82-84 parathyroid hormone-like hormone Rattus norvegicus 20-25
20857298-11 2011 Immunoreactivity of PTHrP and PTHrP-R was also remarkably increased in nitrofen + RA group compared to nitrofen group. Tretinoin 82-84 parathyroid hormone-like hormone Rattus norvegicus 30-35
19244314-5 2009 These molecules regulate Cdc42 and p38MAPK activities, which increase in a Cdo-dependent manner during neuronal differentiation of C17.2 cells and retinoic acid-treated P19 cells. Tretinoin 147-160 cysteine dioxygenase 1, cytosolic Mus musculus 75-78
19246492-3 2009 The expression of retinoic acid (RA)-regulated genes and retinoid metabolites were measured in high-fat diet fed HSL-null mice using real-time quantitative PCR and triple-stage liquid chromatography/tandem mass spectrometry, respectively. Tretinoin 33-35 lipase, hormone sensitive Mus musculus 113-116
19246492-8 2009 Dietary RA supplementation partly restored WAT mass and the expression of RA-regulated genes in WAT of HSL-null mice. Tretinoin 8-10 lipase, hormone sensitive Mus musculus 103-106
19246492-8 2009 Dietary RA supplementation partly restored WAT mass and the expression of RA-regulated genes in WAT of HSL-null mice. Tretinoin 74-76 lipase, hormone sensitive Mus musculus 103-106
19246492-9 2009 These findings demonstrate the importance of HSL as an REH of adipose tissue and suggest that HSL via this action provides RA and other retinoids for signaling events that are crucial for adipocyte differentiation and lineage commitment. Tretinoin 123-125 lipase, hormone sensitive Mus musculus 94-97
22022577-5 2011 More intriguingly, the level of GRP75/RARalpha/RXRalpha tripartite complexes was tightly associated with the RA-induced suppression of tumor growth in animals and the histological grade of differentiation in human NB tumors. Tretinoin 38-40 retinoid X receptor alpha Homo sapiens 47-55
21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 45-58 CD4 antigen Mus musculus 111-114
19398580-0 2009 ZNF536, a novel zinc finger protein specifically expressed in the brain, negatively regulates neuron differentiation by repressing retinoic acid-induced gene transcription. Tretinoin 131-144 zinc finger protein 536 Homo sapiens 0-6
12627849-2 2003 Granulocyte colony-stimulating factor (G-CSF) by itself had no effect on NB4 cells but exerted additional enhancing effects on the respiratory burst activity in the presence of ATRA. Tretinoin 177-181 colony stimulating factor 3 Homo sapiens 39-44
19398580-4 2009 During neuronal differentiation of P19 cells induced by retinoic acid (RA), ZNF536 expression is increased at an early stage, and it is maintained at a constant level in later stages. Tretinoin 56-69 zinc finger protein 536 Homo sapiens 76-82
19398580-4 2009 During neuronal differentiation of P19 cells induced by retinoic acid (RA), ZNF536 expression is increased at an early stage, and it is maintained at a constant level in later stages. Tretinoin 71-73 zinc finger protein 536 Homo sapiens 76-82
21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 60-64 CD4 antigen Mus musculus 111-114
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 CD4 antigen Mus musculus 58-61
21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 interleukin 2 receptor, alpha chain Mus musculus 64-68
21931768-6 2011 atRA did not significantly affect the phosphorylation levels of Smad2/3 and still promoted iTreg differentiation in CD4(+) cells isolated from Smad3 KO and Smad2 conditional KO mice. Tretinoin 0-4 CD4 antigen Mus musculus 116-119
19398580-5 2009 Overexpression of ZNF536 results in an inhibition of RA-induced neuronal differentiation, while depletion or mutation of the ZNF536 gene results in an enhancement of differentiation. Tretinoin 53-55 zinc finger protein 536 Homo sapiens 18-24
19398580-6 2009 We further demonstrated that ZNF536 inhibits expression of neuron-specific marker genes, possibly through the inhibition of RA response element-mediated transcriptional activity, as overexpression of RA receptor alpha can rescue the inhibitory role of ZNF536 in neuronal differentiation and neuron-specific gene expression. Tretinoin 124-126 zinc finger protein 536 Homo sapiens 29-35
12627849-7 2003 Fundamentally identical but slightly different phenomena for the cell surface expression of CD33 and CD10 were observed in the normal human bone marrow mononuclear cells; G-CSF induced CD10 even in the absence of ATRA and down-regulated CD33 in normal cells. Tretinoin 213-217 colony stimulating factor 3 Homo sapiens 171-176
12438307-6 2003 In addition, we provide evidence that E2F proteins are involved in the negative regulation of MYCN by TGF-beta and retinoic acid. Tretinoin 115-128 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 94-98
19715998-7 2009 Also, supplementation of the cultures with RA induced the expression of the intestinal homing receptors CCR9 and alpha4beta7. Tretinoin 43-45 chemokine (C-C motif) receptor 9 Mus musculus 104-108
21731740-9 2011 And then induced differentiation of ESCC cells by all-trans retinoic acid treatment led to decreased expression of CD44. Tretinoin 60-73 CD44 antigen Mus musculus 115-119
14756521-1 2003 It was recently revealed that epidermal growth following topical treatment with all-trans retinoic acid (atRA) was at least partly induced by heparin-binding epidermal growth factor-like growth factor (HB-EGF) released from suprabasal keratinocytes. Tretinoin 80-103 heparin binding EGF like growth factor Homo sapiens 202-208
21419270-6 2011 RA itself is essential for the GM-CSF-induced RALDH2 expression. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 46-52
19401466-0 2009 Retinoic acid activates monoamine oxidase B promoter in human neuronal cells. Tretinoin 0-13 monoamine oxidase B Homo sapiens 24-43
19401466-2 2009 Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line. Tretinoin 65-78 monoamine oxidase B Homo sapiens 30-35
19401466-2 2009 Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line. Tretinoin 65-78 monoamine oxidase B Homo sapiens 113-118
19401466-2 2009 Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line. Tretinoin 80-82 monoamine oxidase B Homo sapiens 30-35
19401466-2 2009 Among hormonal regulations of MAO B, we have recently found that retinoic acid (RA) significantly activates both MAO B promoter activity and mRNA expression in a human neuroblastoma BE(2)C cell line. Tretinoin 80-82 monoamine oxidase B Homo sapiens 113-118
19401466-4 2009 There are four retinoic acid response elements (RAREs) as identified in the MAO B 2-kb promoter, and mutation of the third RARE reduced RA-induced MAO B promoter activation by 50%, suggesting this element is important. Tretinoin 15-28 monoamine oxidase B Homo sapiens 76-81
19401466-9 2009 Taken together, this study provides evidence for the first time showing the stimulating effect of RA on MAO B and new insight into the molecular mechanisms of MAO B regulation by hormones. Tretinoin 98-100 monoamine oxidase B Homo sapiens 104-109
19401466-9 2009 Taken together, this study provides evidence for the first time showing the stimulating effect of RA on MAO B and new insight into the molecular mechanisms of MAO B regulation by hormones. Tretinoin 98-100 monoamine oxidase B Homo sapiens 159-164
22041695-7 2011 Kinetic studies and molecular docking studies based on the result of NMR titration experiments provide the direct evidence for two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS. Tretinoin 160-173 prostaglandin D2 synthase (brain) Mus musculus 197-203
21159962-0 2010 Fragile X protein FMRP is required for homeostatic plasticity and regulation of synaptic strength by retinoic acid. Tretinoin 101-114 fragile X messenger ribonucleoprotein 1 Mus musculus 18-22
21159962-3 2010 Here, we show that fragile X mental retardation protein (FMRP), an RNA-binding protein that regulates dendritic protein synthesis, is essential for increases in synaptic strength induced by RA or by blockade of neural activity in the mouse hippocampus. Tretinoin 190-192 fragile X messenger ribonucleoprotein 1 Mus musculus 19-55
21159962-3 2010 Here, we show that fragile X mental retardation protein (FMRP), an RNA-binding protein that regulates dendritic protein synthesis, is essential for increases in synaptic strength induced by RA or by blockade of neural activity in the mouse hippocampus. Tretinoin 190-192 fragile X messenger ribonucleoprotein 1 Mus musculus 57-61
14756521-1 2003 It was recently revealed that epidermal growth following topical treatment with all-trans retinoic acid (atRA) was at least partly induced by heparin-binding epidermal growth factor-like growth factor (HB-EGF) released from suprabasal keratinocytes. Tretinoin 105-109 heparin binding EGF like growth factor Homo sapiens 202-208
19306865-5 2009 We also provide evidence that Hoxd11 suppresses the expression of Hoxd10 and the retinoic acid synthetic enzyme, retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 81-94 aldehyde dehydrogenase 1 family member A2 Gallus gallus 113-142
14756521-3 2003 In this study, HB-EGF mRNA expression in normal human keratinocytes after atRA treatment was examined, and the effects of a variety of natural and synthetic retinoids were compared. Tretinoin 74-78 heparin binding EGF like growth factor Homo sapiens 15-21
20876578-0 2010 Synergistic effect of retinoic acid and cytokines on the regulation of glial fibrillary acidic protein expression. Tretinoin 22-35 glial fibrillary acidic protein Homo sapiens 71-102
14756521-6 2003 HB-EGF mRNA was upregulated in differentiation-induced keratinocytes by all retinoids used in this study at 1 micromol/l, and marked upregulation was seen when treated with three isotypes of retinoic acid (atRA, and 9-cis and 13-cis retinoic acid). Tretinoin 191-204 heparin binding EGF like growth factor Homo sapiens 0-6
20876578-2 2010 Activation of the JAK/STAT pathway by the IL-6 family of cytokines is the canonical pathway regulating GFAP expression, whereas retinoic acid is thought to be the only inducer of GFAP to operate independently of this pathway. Tretinoin 128-141 glial fibrillary acidic protein Homo sapiens 179-183
14756521-6 2003 HB-EGF mRNA was upregulated in differentiation-induced keratinocytes by all retinoids used in this study at 1 micromol/l, and marked upregulation was seen when treated with three isotypes of retinoic acid (atRA, and 9-cis and 13-cis retinoic acid). Tretinoin 206-210 heparin binding EGF like growth factor Homo sapiens 0-6
14756521-6 2003 HB-EGF mRNA was upregulated in differentiation-induced keratinocytes by all retinoids used in this study at 1 micromol/l, and marked upregulation was seen when treated with three isotypes of retinoic acid (atRA, and 9-cis and 13-cis retinoic acid). Tretinoin 233-246 heparin binding EGF like growth factor Homo sapiens 0-6
20427702-6 2010 The RA-treated cells highly expressed definitive hematopoietic genes, formed large numbers of multilineage and myeloid colonies, and gave rise to greater than 45% CD45(+) hematopoietic cells. Tretinoin 4-6 protein tyrosine phosphatase receptor type C Homo sapiens 163-167
19179438-0 2009 Retinoic acid reduces glucocorticoid sensitivity in C2C12 myotubes by decreasing 11beta-hydroxysteroid dehydrogenase type 1 and glucocorticoid receptor activities. Tretinoin 0-13 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 81-151
19179438-4 2009 Here, we investigated whether RA might counteract glucocorticoid effects in skeletal muscle cells by lowering 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1)-dependent local glucocorticoid activation and/or activation of glucocorticoid receptor (GR). Tretinoin 30-32 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 154-165
19179438-5 2009 We found a dose-dependent down-regulation of 11beta-HSD1 mRNA expression and activity upon incubation of fully differentiated mouse C2C12 myotubes with RA. Tretinoin 152-154 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 45-56
14756522-7 2003 MMP-1 mRNA expression in the control group was significantly upregulated after the addition of tretinoin, whereas no significant change was observed in the keloid group. Tretinoin 95-104 matrix metallopeptidase 1 Homo sapiens 0-5
19179438-6 2009 In addition, RA inhibited GR transactivation by an 11beta-HSD1-independent mechanism. Tretinoin 13-15 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 51-62
12757021-2 2003 This role is primarily mediated by binding of retinoic acid to retinoic acid receptor alpha (RARalpha), a nuclear receptor that modulates the expression of multiple downstream targets via retinoic acid response elements. Tretinoin 63-76 retinoic acid receptor alpha Homo sapiens 93-101
19179438-7 2009 The presence of RA during myogenesis did not prevent myotube formation but resulted in relatively glucocorticoid-resistant myotubes, exhibiting very low 11beta-HSD1 expression and GR activity. Tretinoin 16-18 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 153-164
19179438-9 2009 Importantly, short hairpin RNA against RARgamma abolished the effect of RA on 11beta-HSD1 and GR. Tretinoin 39-41 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 78-89
19472184-2 2009 Previous studies have shown that RA activates p38 mitogen-activated protein kinase (MAPK) and steroid receptor coactivator (SRC)-3 in tumor cells in vitro. Tretinoin 33-35 nuclear receptor coactivator 3 Mus musculus 94-130
20573444-0 2010 Hypoxia and retinoic acid-inducible NDRG1 expression is responsible for doxorubicin and retinoic acid resistance in hepatocellular carcinoma cells. Tretinoin 12-25 N-myc downstream regulated 1 Homo sapiens 36-41
20573444-0 2010 Hypoxia and retinoic acid-inducible NDRG1 expression is responsible for doxorubicin and retinoic acid resistance in hepatocellular carcinoma cells. Tretinoin 88-101 N-myc downstream regulated 1 Homo sapiens 36-41
20573444-5 2010 HCC cells expressed NDRG1 protein, and the expression of this protein was hypoxia- and RA-inducible. Tretinoin 87-89 N-myc downstream regulated 1 Homo sapiens 20-25
20573444-9 2010 The suppression of NDRG1 expression also sensitized RA-resistant HCC cells to RA-induced apoptosis, and this sensitization was more apparent in hypoxic HCC cells than in normoxic cells. Tretinoin 52-54 N-myc downstream regulated 1 Homo sapiens 19-24
20573444-11 2010 These results show that hypoxia- and RA-inducible NDRG1 expression is responsible for doxorubicin and RA resistance in HCC cells. Tretinoin 37-39 N-myc downstream regulated 1 Homo sapiens 50-55
20573444-11 2010 These results show that hypoxia- and RA-inducible NDRG1 expression is responsible for doxorubicin and RA resistance in HCC cells. Tretinoin 102-104 N-myc downstream regulated 1 Homo sapiens 50-55
19472184-5 2009 Results showed that ATRA treatment rapidly activated p38 MAPK, which in turn resulted in phosphorylation with subsequent degradation of SRC-3. Tretinoin 20-24 nuclear receptor coactivator 3 Mus musculus 136-141
19472184-7 2009 The binding of RARalpha to retinoic acid responsive element (RARE) was rapidly increased in neurons following ATRA treatment. Tretinoin 27-40 retinoic acid receptor, alpha Mus musculus 15-23
19472184-7 2009 The binding of RARalpha to retinoic acid responsive element (RARE) was rapidly increased in neurons following ATRA treatment. Tretinoin 110-114 retinoic acid receptor, alpha Mus musculus 15-23
19428697-0 2009 Neurotrophin-3 improves retinoic acid-induced neural differentiation of skin-derived precursors through a p75NTR-dependent signaling pathway. Tretinoin 24-37 neurotrophin 3 Homo sapiens 0-14
19428697-3 2009 When treated sequentially with neurotrophin-3 (NT-3) after RA induction, the survival and neural differentiation of SKPs were enhanced significantly, and cell apoptosis induced by RA was decreased. Tretinoin 59-61 neurotrophin 3 Homo sapiens 31-45
12925606-6 2003 In addition, real-time polymerase chain reaction was used to examine the effects of retinoic acid on expression of genes encoding BMP-2, 4, and 6. Tretinoin 84-97 bone morphogenetic protein 2 Gallus gallus 130-138
19428697-3 2009 When treated sequentially with neurotrophin-3 (NT-3) after RA induction, the survival and neural differentiation of SKPs were enhanced significantly, and cell apoptosis induced by RA was decreased. Tretinoin 59-61 neurotrophin 3 Homo sapiens 47-51
19428697-3 2009 When treated sequentially with neurotrophin-3 (NT-3) after RA induction, the survival and neural differentiation of SKPs were enhanced significantly, and cell apoptosis induced by RA was decreased. Tretinoin 180-182 neurotrophin 3 Homo sapiens 31-45
19428697-3 2009 When treated sequentially with neurotrophin-3 (NT-3) after RA induction, the survival and neural differentiation of SKPs were enhanced significantly, and cell apoptosis induced by RA was decreased. Tretinoin 180-182 neurotrophin 3 Homo sapiens 47-51
19428697-5 2009 The results indicate that NT-3 improves the neural differentiation of SKPs induced by RA through a p75NTR-dependent signaling pathway. Tretinoin 86-88 neurotrophin 3 Homo sapiens 26-30
19118439-6 2009 To induce granulocytic differentiation, HL-60 cells were treated for 5 d with ATRA and differentiation was confirmed by examining superoxide anion production, nuclear morphology, and changes in the expression of CD11b, CD13, and CD15. Tretinoin 78-82 integrin subunit alpha M Homo sapiens 212-217
21086135-7 2010 In addition, in cells induced to differentiate by ATRA or VD3, Nitroblue-tetrazolium (NBT) reduction and esterase activity, were blocked either by LY294002, a PI3K inhibitor, or by BIM, a PKC inhibitor, without affecting cell surface markers such as CD11b or CD14. Tretinoin 50-54 integrin subunit alpha M Homo sapiens 250-255
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 213-219
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 matrix metallopeptidase 3 Rattus norvegicus 289-294
21181362-7 2010 The results showed that ATRA inhibited HSCs proliferation and diminished the mRNA expression of collagen genes [procollagen alpha1 (I), procollagen alpha1 (III)] and profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly stimulated the mRNA expression of MMP-3 and MMP-13 in HSCs by suppressing the mRNA expression of JNK and AP-1. Tretinoin 24-28 matrix metallopeptidase 13 Rattus norvegicus 299-305
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 256-262
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 matrix metallopeptidase 3 Rattus norvegicus 328-333
21181362-8 2010 These findings suggested that ATRA could inhibit proliferation and collagen production of HSCs via the suppression of active protein-1 and c-Jun N-terminal kinase signal, then decrease the mRNAs expression of profibrogenic genes (TGF-beta(1), CTGF, MMP-2, TIMP-1, TIMP-2, PAI-1), and significantly induce the mRNA expression of MMP-3 and MMP-13. Tretinoin 30-34 matrix metallopeptidase 13 Rattus norvegicus 338-344
12925606-9 2003 Retinoic acid rapidly and dramatically stimulated accumulation of BMP-2 and BMP-6 messenger RNAs. Tretinoin 0-13 bone morphogenetic protein 2 Gallus gallus 66-71
12478612-3 2003 By using the annexin V labeling as a marker of apoptosis, a significant apoptotic cell death was quantified during the third and the fourth days of the RA treatment. Tretinoin 152-154 annexin A5 Homo sapiens 13-22
20576349-0 2010 All-trans retinoic acid downregulates ALK in neuroblastoma cell lines and induces apoptosis in neuroblastoma cell lines with activated ALK. Tretinoin 10-23 ALK receptor tyrosine kinase Homo sapiens 38-41
20576349-0 2010 All-trans retinoic acid downregulates ALK in neuroblastoma cell lines and induces apoptosis in neuroblastoma cell lines with activated ALK. Tretinoin 10-23 ALK receptor tyrosine kinase Homo sapiens 135-138
20576349-3 2010 We report that all-trans retinoic acid (ATRA) downregulates ALK in neuroblastoma cell lines. Tretinoin 15-38 ALK receptor tyrosine kinase Homo sapiens 60-63
20576349-3 2010 We report that all-trans retinoic acid (ATRA) downregulates ALK in neuroblastoma cell lines. Tretinoin 40-44 ALK receptor tyrosine kinase Homo sapiens 60-63
20850164-2 2010 We report that the PRRSV nonstructural protein 1alpha (Nsp1alpha) subunit of Nsp1 is a nuclear-cytoplasmic protein distributed to the nucleus and contains a strong suppressive activity for IFN-beta production that is mediated through the retinoic acid-inducible gene I (RIG-I) signaling pathway. Tretinoin 238-251 DExD/H-box helicase 58 Homo sapiens 270-275
19102727-3 2009 A recent study showed that RDH10 is essential for generating retinoic acid at early embryonic stages. Tretinoin 61-74 retinol dehydrogenase 10 Homo sapiens 27-32
18926804-6 2009 This finding led the authors to propose that RDH-E2 may be involved in the pathogenesis of psoriasis through its potential role in retinoic acid biosynthesis and stimulation of keratinocyte proliferation. Tretinoin 131-144 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 45-51
18926804-9 2009 In this study, we began the characterization of RDH-E2 protein in order to determine whether it might play a role in retinoic acid biosynthesis. Tretinoin 117-130 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 48-54
18926804-13 2009 The preference for NAD(+) suggests that RDH-E2 is likely to function in the oxidative direction in vivo, further supporting its potential role in the oxidation of retinol to retinaldehyde for retinoic acid biosynthesis in human keratinocytes. Tretinoin 192-205 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 40-46
19177594-3 2009 Injection of poly I:C/D-GalN into mice could promote tumor necrosis factor-alpha production and surface retinoic acid early inducible-1 (Rae1) protein expression by Kupffer cells, which then activated NK cells to produce interferon-gamma via NKG2D-Rae1 recognition. Tretinoin 104-117 ribonucleic acid export 1 Mus musculus 137-141
12488555-5 2003 We demonstrated for the first time that retinoic acids inhibit adenine nucleotide translocase (ANT) activity in heart and liver mitochondria. Tretinoin 40-54 solute carrier family 25 member 6 Homo sapiens 95-98
19550115-11 2009 The positive rates of both CD11b and CD14 in HL-60 cells were over 90% after 5-day treatment (2 micromol/L ATRA or 10 micromol/L NSC67657); cell morphology also represented characteristics of differentiation. Tretinoin 107-111 integrin subunit alpha M Homo sapiens 27-32
19068090-3 2009 Our study demonstrated that combining ATRA with vaccination not only decreased the number of Gr-1+ CD11b+ ImC, but for the first time also suppressed the function of Gr-1+ CD11b+ ImC with decreased expression of CD80. Tretinoin 38-42 integrin subunit alpha M Homo sapiens 99-104
19068090-3 2009 Our study demonstrated that combining ATRA with vaccination not only decreased the number of Gr-1+ CD11b+ ImC, but for the first time also suppressed the function of Gr-1+ CD11b+ ImC with decreased expression of CD80. Tretinoin 38-42 integrin subunit alpha M Homo sapiens 172-177
21076177-5 2010 We showed that the Npm1/Sox2 complex was sustained when cells were induced to differentiate by retinoic acid, while decreased in the other differentiation pathways. Tretinoin 95-108 SRY-box transcription factor 2 Homo sapiens 24-28
21061289-6 2010 BMPR-IB and Smad5 mRNA levels increased significantly in cells cultured in OM and declined following treatment with ATRA, whereas the expression of the BMPR-IA mRNA was up-regulated by ATRA. Tretinoin 185-189 bone morphogenetic protein receptor, type 1A Mus musculus 152-159
20949013-0 2010 Retinoic acid increases proliferation of human osteoclast progenitors and inhibits RANKL-stimulated osteoclast differentiation by suppressing RANK. Tretinoin 0-13 TNF superfamily member 11 Homo sapiens 83-88
12488555-6 2003 Kinetic studies revealed atRA as an uncompetitive inhibitor of ANT. Tretinoin 25-29 solute carrier family 25 member 6 Homo sapiens 63-66
20949013-7 2010 In contrast, RA inhibited differentiation of the receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclastogenesis of human and murine osteoclast progenitors via retinoic acid receptors (RARs). Tretinoin 13-15 TNF superfamily member 11 Homo sapiens 49-99
12488555-9 2003 The specific photolabeling of ANT was also prevented in a concentration-dependent manner by nonlabeled atRA, whereas palmitic acid was ineffective. Tretinoin 103-107 solute carrier family 25 member 6 Homo sapiens 30-33
20949013-7 2010 In contrast, RA inhibited differentiation of the receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclastogenesis of human and murine osteoclast progenitors via retinoic acid receptors (RARs). Tretinoin 13-15 TNF superfamily member 11 Homo sapiens 101-106
20949013-11 2010 Furthermore, RA treatment suppressed the expression of the transcription factor nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and increased the expression of interferon regulatory factor-8 (IRF-8) in osteoclast progenitors via RARs. Tretinoin 13-15 nuclear factor of activated T cells 1 Homo sapiens 80-129
19091570-7 2009 There was stable down-regulation of MDM2 and UGB as well as overexpression of SOD2, CSTB, and G3BP when RA-treated SHG-44 was compared with normal SHG-44. Tretinoin 104-106 MDM2 proto-oncogene Homo sapiens 36-40
19091570-7 2009 There was stable down-regulation of MDM2 and UGB as well as overexpression of SOD2, CSTB, and G3BP when RA-treated SHG-44 was compared with normal SHG-44. Tretinoin 104-106 G3BP stress granule assembly factor 1 Homo sapiens 94-98
20949013-11 2010 Furthermore, RA treatment suppressed the expression of the transcription factor nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and increased the expression of interferon regulatory factor-8 (IRF-8) in osteoclast progenitors via RARs. Tretinoin 13-15 nuclear factor of activated T cells 1 Homo sapiens 131-137
12414989-11 2002 Moreover, co-addition of Ro 41-5253, an antagonist of RARalpha, abrogated the lumen-inducing activity of both RA and DCS, indicating that this biological response is mediated through an RARalpha-dependent signaling pathway. Tretinoin 54-56 retinoic acid receptor alpha Homo sapiens 186-194
20711222-0 2010 Kruppel-like factor 4 interacts with p300 to activate mitofusin 2 gene expression induced by all-trans retinoic acid in VSMCs. Tretinoin 103-116 Kruppel like factor 4 Homo sapiens 0-21
18803283-2 2009 In cultured human osteosarcoma cells, RA enhances the expression of bone morphogenetic protein-7 (BMP7), a trophic factor that reduces ischemia- or neurotoxin-mediated neurodegeneration in vivo. Tretinoin 38-40 bone morphogenetic protein 7 Homo sapiens 68-96
18803283-2 2009 In cultured human osteosarcoma cells, RA enhances the expression of bone morphogenetic protein-7 (BMP7), a trophic factor that reduces ischemia- or neurotoxin-mediated neurodegeneration in vivo. Tretinoin 38-40 bone morphogenetic protein 7 Homo sapiens 98-102
20711222-0 2010 Kruppel-like factor 4 interacts with p300 to activate mitofusin 2 gene expression induced by all-trans retinoic acid in VSMCs. Tretinoin 103-116 mitofusin 2 Homo sapiens 54-65
12421932-5 2002 The presence of atRA led to elevated levels of cyclin D3, -E, and -A, decreased levels of p27(Kip1), increased activity of cyclin-dependent kinase 2, and enhanced phosphorylation of the retinoblastoma protein (pRB). Tretinoin 16-20 interferon alpha inducible protein 27 Homo sapiens 90-93
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 105-118 Kruppel like factor 4 Homo sapiens 22-43
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 105-118 Kruppel like factor 4 Homo sapiens 45-49
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 105-118 mitofusin 2 Homo sapiens 61-72
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 105-118 mitofusin 2 Homo sapiens 74-79
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 120-124 Kruppel like factor 4 Homo sapiens 22-43
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 120-124 Kruppel like factor 4 Homo sapiens 45-49
19317219-9 2009 We demonstrated that histone acetylation by the PPARgamma agonist CDDO, RAR/RXR agonist ATRA, and/or histone deacetylase inhibitors (HDACIs) reversed the silenced RARbeta and MDR1 genes in acute promyelocytic leukemia, and that HDACI induced apoptosis with phagocytosis through the induction of Annexin A1 in AML1/ETO-positive acute myelocytic leukemia (AML) cells. Tretinoin 88-92 retinoid X receptor alpha Homo sapiens 76-79
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 120-124 mitofusin 2 Homo sapiens 61-72
12421932-5 2002 The presence of atRA led to elevated levels of cyclin D3, -E, and -A, decreased levels of p27(Kip1), increased activity of cyclin-dependent kinase 2, and enhanced phosphorylation of the retinoblastoma protein (pRB). Tretinoin 16-20 cyclin dependent kinase inhibitor 1B Homo sapiens 94-98
20711222-1 2010 AIM: To elucidate how kruppel-like factor 4 (KLF4) activates mitofusin 2 (mfn-2) expression in all-trans retinoic acid (ATRA)-induced vascular smooth muscle cell (VSMC) differentiation. Tretinoin 120-124 mitofusin 2 Homo sapiens 74-79
20711222-6 2010 RESULTS: KLF4 mediated ATRA-induced mfn-2 expression in VSMCs. Tretinoin 23-27 Kruppel like factor 4 Homo sapiens 9-13
18936944-0 2009 Apoptosis induced by synthetic retinoic acid CD437 on human melanoma A375 cells involves RIG-I pathway. Tretinoin 31-44 DExD/H-box helicase 58 Homo sapiens 89-94
20711222-6 2010 RESULTS: KLF4 mediated ATRA-induced mfn-2 expression in VSMCs. Tretinoin 23-27 mitofusin 2 Homo sapiens 36-41
12421932-9 2002 rIL-2 was able to substitute for the effects of atRA on the cell cycle machinery and on DNA synthesis, and blocking the IL-2R markedly inhibited atRA-induced cell proliferation and pRB phosphorylation. Tretinoin 48-52 interleukin 2 Rattus norvegicus 0-5
20711222-8 2010 ATRA increased the interaction of KLF4 with p300 by inducing KLF4 phosphorylation via activation of JNK and p38 MAPK signaling. Tretinoin 0-4 Kruppel like factor 4 Homo sapiens 34-38
19636436-13 2009 This inhibitory effect of ATRA on MMP-2 activity in human breast cancer cells (MCF-7) may result due to its inhibitory effect on MT1-MMP, EMMPRIN, and upregulation of TIMP-2. Tretinoin 26-30 TIMP metallopeptidase inhibitor 2 Homo sapiens 167-173
12171913-0 2002 Induction of the mouse kappa-opioid receptor gene by retinoic acid in P19 cells. Tretinoin 53-66 cyclin dependent kinase inhibitor 2D Mus musculus 70-73
20711222-8 2010 ATRA increased the interaction of KLF4 with p300 by inducing KLF4 phosphorylation via activation of JNK and p38 MAPK signaling. Tretinoin 0-4 Kruppel like factor 4 Homo sapiens 61-65
20711222-10 2010 CONCLUSION: ATRA induces KLF4 acetylation by p300 and increases the ability of KLF4 to transactivate the mfn-2 promoter in VSMCs. Tretinoin 12-16 Kruppel like factor 4 Homo sapiens 25-29
20711222-10 2010 CONCLUSION: ATRA induces KLF4 acetylation by p300 and increases the ability of KLF4 to transactivate the mfn-2 promoter in VSMCs. Tretinoin 12-16 Kruppel like factor 4 Homo sapiens 79-83
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 110-123 cyclin dependent kinase inhibitor 2D Mus musculus 85-88
20711222-10 2010 CONCLUSION: ATRA induces KLF4 acetylation by p300 and increases the ability of KLF4 to transactivate the mfn-2 promoter in VSMCs. Tretinoin 12-16 mitofusin 2 Homo sapiens 105-110
19492242-2 2009 Our previous studies demonstrated that JWA is a pro-apoptotic molecule and required for arsenic trioxide and all-trans-retinoic acid-induced cancer cell apoptosis. Tretinoin 109-132 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 39-42
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 145-147 cyclin dependent kinase inhibitor 2D Mus musculus 85-88
12370804-4 2002 Estrogen levels present in fetal calf serum are sufficient to maintain AIB1 mRNA and protein at low basal levels, and this repression is reversed by the addition of antiestrogens or all-trans retinoic acid. Tretinoin 192-205 HEAT repeat containing 6 Homo sapiens 71-75
18368485-4 2009 Indeed, treatment of cells with 1 muM all-trans retinoic acid (ATRA) or 1 muM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation with upregulation of glial fibrillary acidic protein (GFAP) and down regulation of telomerase activity. Tretinoin 42-61 glial fibrillary acidic protein Homo sapiens 175-206
18368485-4 2009 Indeed, treatment of cells with 1 muM all-trans retinoic acid (ATRA) or 1 muM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation with upregulation of glial fibrillary acidic protein (GFAP) and down regulation of telomerase activity. Tretinoin 42-61 glial fibrillary acidic protein Homo sapiens 208-212
18368485-4 2009 Indeed, treatment of cells with 1 muM all-trans retinoic acid (ATRA) or 1 muM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation with upregulation of glial fibrillary acidic protein (GFAP) and down regulation of telomerase activity. Tretinoin 63-67 glial fibrillary acidic protein Homo sapiens 175-206
18368485-4 2009 Indeed, treatment of cells with 1 muM all-trans retinoic acid (ATRA) or 1 muM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation with upregulation of glial fibrillary acidic protein (GFAP) and down regulation of telomerase activity. Tretinoin 63-67 glial fibrillary acidic protein Homo sapiens 208-212
20706998-6 2010 For forelimb ectrodactyly, a locus on chromosome 11, Rafar, has linkage to the strain difference, and mRNA localization has shown that specific genes (Fgf8, Dlx3, Bmp4, and Sp8) in the postaxial preAER (prior to formation of the apical ectodermal ridge) of the developing limb bud (the site of the defect) were downregulated hours after atRA administration more in the susceptible C57 than in the SWV strain. Tretinoin 337-341 fibroblast growth factor 8 Mus musculus 151-155
20706998-6 2010 For forelimb ectrodactyly, a locus on chromosome 11, Rafar, has linkage to the strain difference, and mRNA localization has shown that specific genes (Fgf8, Dlx3, Bmp4, and Sp8) in the postaxial preAER (prior to formation of the apical ectodermal ridge) of the developing limb bud (the site of the defect) were downregulated hours after atRA administration more in the susceptible C57 than in the SWV strain. Tretinoin 337-341 trans-acting transcription factor 8 Mus musculus 173-176
20850014-4 2010 Mechanistically, the demethylase genes are directly activated by Pou5f1 and Cebpbeta and are indirectly repressed by retinoic acid, which antagonizes Pou5f1 and Cebpbeta. Tretinoin 117-130 POU domain, class 5, transcription factor 3 Danio rerio 65-71
20850014-4 2010 Mechanistically, the demethylase genes are directly activated by Pou5f1 and Cebpbeta and are indirectly repressed by retinoic acid, which antagonizes Pou5f1 and Cebpbeta. Tretinoin 117-130 POU domain, class 5, transcription factor 3 Danio rerio 150-156
20850014-5 2010 Apc mutants lack retinoic acid as a result of the transcriptional repression of retinol dehydrogenase l1 via a complex that includes Lef1, Groucho2, Ctbp1, Lsd1, and Corest. Tretinoin 17-30 APC regulator of WNT signaling pathway Danio rerio 0-3
18840407-3 2008 Cells with low membrane potential treated with 9-cis RA showed significantly lower amounts of RXRalpha in mitochondria. Tretinoin 53-55 retinoid X receptor alpha Homo sapiens 94-102
12392597-1 2002 BACKGROUND: The effects of the vitamin A metabolite retinoic acid (RA) are mediated at the transcriptional level by retinoic acid receptors (RAR). Tretinoin 52-65 retinoic acid receptor alpha Homo sapiens 141-144
18840764-2 2008 In the cytosol, CRBP-III binds retinol, the precursor of retinyl ester and the active metabolite retinoic acid. Tretinoin 97-110 retinol binding protein 7, cellular Mus musculus 16-24
20398728-5 2010 The modulation of BMP-4 also plays an important role in the therapeutic mechanism of action of bromocriptine, somatostatin analogs and retinoic acid. Tretinoin 135-148 bone morphogenetic protein 4 Rattus norvegicus 18-23
12392597-1 2002 BACKGROUND: The effects of the vitamin A metabolite retinoic acid (RA) are mediated at the transcriptional level by retinoic acid receptors (RAR). Tretinoin 67-69 retinoic acid receptor alpha Homo sapiens 141-144
12392597-5 2002 RESULTS: We have determined that RA inhibits cyclin H and cdk7 expression thereby decreasing levels of phosphorylated RARalpha in human cancer cell lines. Tretinoin 33-35 retinoic acid receptor alpha Homo sapiens 118-126
19029980-1 2008 Retinoic acid and arsenic trioxide target the protein stability and transcriptional repression activity of the fusion oncoprotein PML-RARA, resulting in regression of acute promyelocytic leukemia (APL). Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 134-138
19029980-3 2008 Here we show that retinoic acid also triggers growth arrest of leukemia-initiating cells (LICs) ex vivo and their clearance in PML-RARA mouse APL in vivo. Tretinoin 18-31 retinoic acid receptor, alpha Mus musculus 131-135
20395453-4 2010 In retinoic acid (RA)-stimulated human promyelocytic leukemia (HL-60) cells, the transcription of the BLT1 gene was found to be significantly activated. Tretinoin 3-16 leukotriene B4 receptor Homo sapiens 102-106
19029980-4 2008 Retinoic acid treatment of mouse APLs expressing the fusion protein PLZF-RARA triggers full differentiation, but not LIC loss or disease remission, establishing that differentiation and LIC loss can be uncoupled. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 73-77
12242693-2 2002 One member of this family, IGFBP-3, mediates the growth-inhibitory and apoptosis-inducing effects of a number of growth factors and hormones such as transforming growth factor-beta, retinoic acid, and 1,25-dihydroxyvitamin D3. Tretinoin 182-195 insulin like growth factor binding protein 3 Homo sapiens 27-34
19029980-5 2008 Although retinoic acid and arsenic synergize to clear LICs through cooperative PML-RARA degradation, this combination does not enhance differentiation. Tretinoin 9-22 retinoic acid receptor, alpha Mus musculus 83-87
18809380-3 2008 The MMP-9 activity of certain cell lines was significantly inhibited with retinoic acid treatment, and this effect was reversed in the presence of a TGase 2 inhibitor. Tretinoin 74-87 matrix metallopeptidase 9 Homo sapiens 4-9
20395453-4 2010 In retinoic acid (RA)-stimulated human promyelocytic leukemia (HL-60) cells, the transcription of the BLT1 gene was found to be significantly activated. Tretinoin 18-20 leukotriene B4 receptor Homo sapiens 102-106
20705860-4 2010 beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Tretinoin 114-127 catenin (cadherin associated protein), beta 1 Mus musculus 0-12
12242694-7 2002 Inhibition of RAR function in HMECs by DNRAR suppressed expression of CBP/p300 and expression of RARbeta2 in MCF-7 cells promoted induction of CBP/p300 when cells were treated with 1.0 microM all-trans-retinoic acid (ATRA). Tretinoin 192-215 retinoic acid receptor alpha Homo sapiens 14-17
20506167-9 2010 The localization of CRBP1 within Muller cells and the RPE and its demonstrated role in modulating the proper folding of nascent outer segment membranes through retinoic acid further elucidates the role of these cells in directly influencing photoreceptor physiology. Tretinoin 160-173 ribulose-5-phosphate-3-epimerase Homo sapiens 54-57
12242694-7 2002 Inhibition of RAR function in HMECs by DNRAR suppressed expression of CBP/p300 and expression of RARbeta2 in MCF-7 cells promoted induction of CBP/p300 when cells were treated with 1.0 microM all-trans-retinoic acid (ATRA). Tretinoin 217-221 retinoic acid receptor alpha Homo sapiens 14-17
20723292-8 2010 Furthermore, HL-60 cells in ATRA + hucMSC group had stronger CD11b expression than ATRA group (48 hours p < 0.05, 72 hours p < 0.01). Tretinoin 28-32 integrin subunit alpha M Homo sapiens 61-66
19006694-0 2008 Retinoic acid enhances Foxp3 induction indirectly by relieving inhibition from CD4+CD44hi Cells. Tretinoin 0-13 CD44 molecule (Indian blood group) Homo sapiens 83-87
18637026-6 2008 The differentiation-inhibitory effect of RA was mimicked by conditioned medium from RA-treated ESCs and was accompanied with up-regulated expression of leukemia inhibitory factor (LIF), Wnt3a, Wnt5a, and Wnt6. Tretinoin 41-43 wingless-type MMTV integration site family, member 5A Mus musculus 193-198
20689834-0 2010 Retinoic acids potentiate BMP9-induced osteogenic differentiation of mesenchymal progenitor cells. Tretinoin 0-14 growth differentiation factor 2 Mus musculus 26-30
12213675-8 2002 RESULTS: We found that RA increased the expression of both trkA and p75 NGF receptors in NCI-N-592 and GLC8 cell lines and prevented the loss of both NGF production and NGF receptor expression occurring when NGF treatment was discontinued. Tretinoin 23-25 nerve growth factor receptor Homo sapiens 72-84
20689834-3 2010 In this study, we investigate the effect of RA signaling on BMP9-induced osteogenic differentiation of mesenchymal progenitor cells (MPCs). Tretinoin 44-46 growth differentiation factor 2 Mus musculus 60-64
18637026-6 2008 The differentiation-inhibitory effect of RA was mimicked by conditioned medium from RA-treated ESCs and was accompanied with up-regulated expression of leukemia inhibitory factor (LIF), Wnt3a, Wnt5a, and Wnt6. Tretinoin 84-86 wingless-type MMTV integration site family, member 5A Mus musculus 193-198
18637026-8 2008 Furthermore, knock-down of beta-catenin, a component of the Wnt signaling pathway, by small interfering RNA counteracted the effect of RA. Tretinoin 135-137 catenin (cadherin associated protein), beta 1 Mus musculus 27-39
18637026-9 2008 In addition, RA treatment enhanced expression of endodermal markers GATA4 and AFP but inhibited expression of primitive ectodermal marker Fgf-5 and mesodermal marker Brachyury. Tretinoin 13-15 alpha fetoprotein Mus musculus 78-81
20643338-3 2010 We showed here that direct stimulation of FDCs by bacterial products and retinoic acid synergistically enhanced the expression of the chemokine CXCL13, the survival factor BAFF, and molecules that facilitate the secretion and activation of the cytokine TGF-beta1. Tretinoin 73-86 C-X-C motif chemokine ligand 13 Homo sapiens 144-150
12176302-12 2002 Taken together, SLN formulation of ATRA with similar characteristics to those of parenteral emulsions could be obtained even after freeze-drying. Tretinoin 35-39 sarcolipin Homo sapiens 16-19
20410509-4 2010 Treatment with an inhibitor of RA biosynthesis or a retinoic acid receptor antagonist increases gata1(+) erythroid progenitors in the posterior mesoderm of wild-type embryos and anemic cdx4(-/-) mutants, indicating a link between the cdx-hox signaling pathway and RA. Tretinoin 31-33 GATA binding protein 1a Danio rerio 96-101
20644631-4 2010 Upon stimulation with micromolar concentrations of RA, ESCs significantly downregulated the pluripotency factor OCT-4 but markedly upregulated UP1A, UP1B, UP2, UP3A, and UP3B mRNA levels in comparison to naive ESCs and spontaneously differentiating controls. Tretinoin 51-53 POU domain, class 5, transcription factor 1 Mus musculus 112-117
20644631-4 2010 Upon stimulation with micromolar concentrations of RA, ESCs significantly downregulated the pluripotency factor OCT-4 but markedly upregulated UP1A, UP1B, UP2, UP3A, and UP3B mRNA levels in comparison to naive ESCs and spontaneously differentiating controls. Tretinoin 51-53 uroplakin 3B Mus musculus 170-174
18622580-5 2008 We show forced expression of EWS-FLI1 causes absence of retinoic acid-induced neural morphology, and decreases expression of neural-specific proteins MAPT and NCAM. Tretinoin 56-69 Fli-1 proto-oncogene, ETS transcription factor Homo sapiens 33-37
18713813-5 2008 Altogether, these findings support the conclusion that RXRB heterodimerized with a RA-liganded RARA transduces signals required in SC for spermatid release. Tretinoin 83-85 retinoic acid receptor, alpha Mus musculus 95-99
20456496-5 2010 Addition of ATRA to the medium for 48 h caused a dose-dependent increase in KRT4/KRT13 and a down-regulation of KRT2 mRNA. Tretinoin 12-16 keratin 4 Homo sapiens 76-80
12063257-6 2002 Clones stably transfected to express the dominant-negative Tcf4 displayed a block in retinoic acid-induced activation of Lef-Tcf-sensitive transcription and primitive endoderm formation. Tretinoin 85-98 transcription factor 4 Mus musculus 59-63
20559758-4 2010 EA activated the caspase-3 pathway and enhanced the expressions of myeloid differentiation markers (CD11b, MRP-14 protein, granulocytic morphology) induced by ATRA treatment. Tretinoin 159-163 integrin subunit alpha M Homo sapiens 100-105
20559758-4 2010 EA activated the caspase-3 pathway and enhanced the expressions of myeloid differentiation markers (CD11b, MRP-14 protein, granulocytic morphology) induced by ATRA treatment. Tretinoin 159-163 S100 calcium binding protein A9 Homo sapiens 107-113
18621984-1 2008 BACKGROUND: All-trans retinoic acid (ATRA) stimulates elastin synthesis by lung fibroblasts and induces alveolar regeneration in animal models of pulmonary emphysema. Tretinoin 12-35 elastin Homo sapiens 54-61
18621984-1 2008 BACKGROUND: All-trans retinoic acid (ATRA) stimulates elastin synthesis by lung fibroblasts and induces alveolar regeneration in animal models of pulmonary emphysema. Tretinoin 37-41 elastin Homo sapiens 54-61
18621984-7 2008 The effect of CRABP2 silencing on elastin and RAR-beta expression in response to ATRA was measured in MRC5 lung fibroblasts. Tretinoin 81-85 cellular retinoic acid binding protein 2 Homo sapiens 14-20
18621984-7 2008 The effect of CRABP2 silencing on elastin and RAR-beta expression in response to ATRA was measured in MRC5 lung fibroblasts. Tretinoin 81-85 elastin Homo sapiens 34-41
20483764-2 2010 In the current study, we demonstrate that naive CD4+CD25-Foxp3- T cells specific for the myelin proteolipid protein (PLP)139-151 peptide can be converted into CD25+Foxp3+ induced Treg cells (iTregs) when stimulated in the presence of TGF-beta, retinoic acid, and IL-2. Tretinoin 244-257 interleukin 2 receptor, alpha chain Mus musculus 159-163
12139723-0 2002 Superior effect of 9-cis retinoic acid (RA) compared with all-trans RA and 13-cis RA on the inhibition of clonogenic cell growth and the induction of apoptosis in OCI/AML-2 subclones: is the p53 pathway involved? Tretinoin 40-42 RUNX family transcription factor 3 Homo sapiens 167-172
18957096-3 2008 FINDINGS: SH-SY5Y-A cells differentiated in the presence of RA, whereas RA-treated SH-SY5Y-E cells required additional treatment with brain-derived neurotrophic factor (BDNF) for full differentiation. Tretinoin 72-74 brain derived neurotrophic factor Homo sapiens 134-167
18957096-3 2008 FINDINGS: SH-SY5Y-A cells differentiated in the presence of RA, whereas RA-treated SH-SY5Y-E cells required additional treatment with brain-derived neurotrophic factor (BDNF) for full differentiation. Tretinoin 72-74 brain derived neurotrophic factor Homo sapiens 169-173
12139723-7 2002 In conclusion, this study shows that 9-cis RA was a more potent agent than ATRA or 13-cis RA in inducing growth arrest and apoptosis in the OCI/AML-2 subclones. Tretinoin 43-45 RUNX family transcription factor 3 Homo sapiens 144-149
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 PDZ and LIM domain 7 Homo sapiens 13-17
20233719-2 2010 The expression of Nip1 was detected in the developing mouse brain, embryonic stem cells, primary neuronal stem cells, and retinoic acid-treated P19 embryonal carcinoma cells. Tretinoin 122-135 dual oxidase maturation factor 1 Mus musculus 18-22
12115542-7 2002 Owing to a decrease in the secretion of MCP-1 and transforming growth factor-beta 1 (TGF-beta 1), tumor cells treated with RA were unable to induce peripheral blood monocyte (PBM) chemotaxis. Tretinoin 123-125 C-C motif chemokine ligand 2 Homo sapiens 40-45
20237236-2 2010 We previously reported that 1) expression of nephrin in cultured podocytes is reinforced by retinoic acid (RA) and 1,25-dihydroxyvitamin D(3), 2) these effects are mediated by retinoic acid receptor (RAR) and vitamin D receptor (VDR), and 3) basal and inducible expression of nephrin is downregulated by TNF-alpha. Tretinoin 92-105 NPHS1 adhesion molecule, nephrin Homo sapiens 45-52
20237236-2 2010 We previously reported that 1) expression of nephrin in cultured podocytes is reinforced by retinoic acid (RA) and 1,25-dihydroxyvitamin D(3), 2) these effects are mediated by retinoic acid receptor (RAR) and vitamin D receptor (VDR), and 3) basal and inducible expression of nephrin is downregulated by TNF-alpha. Tretinoin 107-109 NPHS1 adhesion molecule, nephrin Homo sapiens 45-52
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 PDZ and LIM domain 7 Homo sapiens 13-17
18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 185-187 PDZ and LIM domain 7 Homo sapiens 13-17
18539384-4 2008 As a consequence, LMP1 could abrogate the growth-inhibitory effect of RA by releasing cell cycle arrest at G1 phase. Tretinoin 70-72 PDZ and LIM domain 7 Homo sapiens 18-22
18692045-8 2008 To a lesser degree they also diminished retinoic acid-induced earlier markers of cell differentiation, namely CD38 and CD11b. Tretinoin 40-53 integrin subunit alpha M Homo sapiens 119-124
19965837-7 2010 RESULTS: ATRA synergised with TGF-beta to induce Foxp3(+) T regulatory cells (Treg) and reciprocally inhibited development of IL-17-producing T helper cells (Th17) induced by TGF-beta and IL-6. Tretinoin 9-13 interleukin 17A Mus musculus 126-131
12032135-0 2002 Down-regulation of the phosphatidylinositol 3-kinase/Akt pathway is involved in retinoic acid-induced phosphorylation, degradation, and transcriptional activity of retinoic acid receptor gamma 2. Tretinoin 80-93 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 23-52
19965837-8 2010 ATRA treatment reduced the severity of EAU clinically, and IFN-gamma and IL-17 production were significantly reduced in ATRA-treated mice. Tretinoin 120-124 interleukin 17A Mus musculus 73-78
20507360-7 2010 Overexpression and knockdown experiments for PTB in HEK293 cells and Xenopus embryos indicated that PTB is required for repression by retinoic acid. Tretinoin 134-147 polypyrimidine tract binding protein 1 Homo sapiens 45-48
20507360-7 2010 Overexpression and knockdown experiments for PTB in HEK293 cells and Xenopus embryos indicated that PTB is required for repression by retinoic acid. Tretinoin 134-147 polypyrimidine tract binding protein 1 S homeolog Xenopus laevis 100-103
20507360-10 2010 Our results indicate that PTB plays a role in the repression of gene expression by retinoic acid through binding to the TG/CA repeats. Tretinoin 83-96 polypyrimidine tract binding protein 1 S homeolog Xenopus laevis 26-29
18846337-10 2008 The expression of COL I and TIMP-1 proteins in group A was increased, while decreased in ATRA-treated CBDL groups (P<0.05). Tretinoin 89-93 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 28-34
18846337-12 2008 ATRA treatment increased the protein levels of MMP2 and MMP13. Tretinoin 0-4 matrix metallopeptidase 13 Rattus norvegicus 56-61
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 165-171
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 matrix metallopeptidase 13 Rattus norvegicus 184-189
18846337-15 2008 It was concluded that ATRA could inhibit CBDL-induced liver fibrosis in rats by suppressing the expression of TGF-beta1 and CTGF so as to diminish the inhibition of TIMP-1 on MMP2 and MMP13 and increase the activity of MMP2 and MMP13. Tretinoin 22-26 matrix metallopeptidase 13 Rattus norvegicus 228-233
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 retinoid X receptor alpha Homo sapiens 129-138
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 69-71 retinoid X receptor alpha Homo sapiens 208-217
12032135-3 2002 We show here that this RA-induced phosphorylation of RARgamma2 resulted from the down-regulation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Tretinoin 23-25 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 104-133
19538480-8 2010 Chromatin immunoprecipitation demonstrated that interactions between RARs, RXRs and t-PA promoter were time dependent: RAR-alpha/RXR-alpha bound DR5 motif before and up to 12 hrs of RA exposure, and RAR-beta/RXR-alpha bound DR5 response element after 12 hrs of RA treatment. Tretinoin 119-121 retinoid X receptor alpha Homo sapiens 208-217
18799012-10 2008 In particular, the retinoic acid-synthesising enzyme, RALDH2, is expressed in the left ovarian cortex at the time of STRA8 up-regulation, prior to meiosis. Tretinoin 19-32 aldehyde dehydrogenase 1 family member A2 Gallus gallus 54-60
12100164-8 2002 ATRA-treated CD34+ cells displayed changes in apoptotic status compared with control cultures, particularly in lower annexin V-binding. Tretinoin 0-4 annexin A5 Homo sapiens 117-126
18505683-11 2008 In addition significant differences of ADH isoenzymes activities between cancer tissues and healthy organs may be a factor intensifying carcinogenesis by the increased ability to acetaldehyde formation from ethanol and disorders in metabolism of some biologically important substances (e.g. retinoic acid). Tretinoin 291-304 aldo-keto reductase family 1 member A1 Homo sapiens 39-42
19761519-7 2010 Cortical thickness and area of glomerular tuft were significantly decreased after vascular endothelial growth factor (VEGF) inhibitor, and were significantly restored by RA. Tretinoin 170-172 vascular endothelial growth factor A Mus musculus 118-122
12120653-1 2002 OBJECT: Human neuroteratocarcinoma (hNT)-derived neurons are differentiated postmitotic neurons derived from a human teratocarcinoma cell line following treatment with retinoic acid. Tretinoin 168-181 neurotrimin Homo sapiens 36-39
20308937-6 2010 However, we found that the (A) allele of the rs12591551 single nucleotide polymorphism (SNP) in the ALDH1A2 gene (ALDH1A2rs12591551(A)), occurring in 19% of newborns, was associated with 2.5-fold higher serum RA levels. Tretinoin 209-211 aldehyde dehydrogenase 1 family member A2 Homo sapiens 100-107
20308937-6 2010 However, we found that the (A) allele of the rs12591551 single nucleotide polymorphism (SNP) in the ALDH1A2 gene (ALDH1A2rs12591551(A)), occurring in 19% of newborns, was associated with 2.5-fold higher serum RA levels. Tretinoin 209-211 aldehyde dehydrogenase 1 family member A2 Homo sapiens 114-121
18550535-4 2008 Recently we found that the retinoic acid-inducible gene I (RIG-I) is a major intracellular RSV sensor upstream of the canonical pathway. Tretinoin 27-40 DExD/H-box helicase 58 Homo sapiens 59-64
18641199-4 2008 Male BALB/cJ mouse bone marrow cells cultured with granulocyte-macrophage colony-stimulating factor in the presence of retinoic acid receptor (RAR) alpha-specific antagonist showed an increase in the percentage of developing DC that remained adherent compared with cells rescued with atRA treatment from d 8 to 10 of culture (P < 0.05). Tretinoin 284-288 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 51-99
18641199-4 2008 Male BALB/cJ mouse bone marrow cells cultured with granulocyte-macrophage colony-stimulating factor in the presence of retinoic acid receptor (RAR) alpha-specific antagonist showed an increase in the percentage of developing DC that remained adherent compared with cells rescued with atRA treatment from d 8 to 10 of culture (P < 0.05). Tretinoin 284-288 retinoic acid receptor, alpha Mus musculus 143-146
20561408-4 2010 The level of CD11b expression in HL-60 cells was up-regulated gradually during ATRA-induced cell differentiation. Tretinoin 79-83 integrin subunit alpha M Homo sapiens 13-18
12052888-0 2002 JDP2, a repressor of AP-1, recruits a histone deacetylase 3 complex to inhibit the retinoic acid-induced differentiation of F9 cells. Tretinoin 83-96 Jun dimerization protein 2 Homo sapiens 0-4
20074641-4 2010 Retinoic acid induces neuronal differentiation as revealed by the increased expression of MAP2, the decreased cell doubling rate, and the gain in neuronal morphological features and these events are accompanied by the increased expression level of PKC delta and p67(phox), one of the components of NADPH oxidase. Tretinoin 0-13 microtubule associated protein 2 Homo sapiens 90-94
20074641-6 2010 Moreover, using rottlerin to inhibit PKC delta or transfection experiments to overexpress it, we show that retinoic acid acts through this enzyme to induce MAP2 expression and to increase p67(phox) membrane translocation leading to NADPH oxidase activation. Tretinoin 107-120 microtubule associated protein 2 Homo sapiens 156-160
18502750-7 2008 The dual cis/trans substrate specificity suggests a dual physiological role for RDH10: in the biosynthesis of 11-cis-retinaldehyde for vision as well as the biosynthesis of all-trans-retinoic acid for differentiation and development. Tretinoin 173-196 retinol dehydrogenase 10 Homo sapiens 80-85
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 58-77 aldehyde dehydrogenase 1 family member A2 Homo sapiens 123-129
18502188-6 2008 And during P19 cell neural differentiation induced by all trans-retinoic acid (ATRA) and cell aggregate formation, RALDH1, RALDH2, CYP26A1, and CYP26B1 could be notably upregulated by ATRA, and keeping the high-level expression of RALDH1 and RALDH2 was dependent on the further neural differentiation, but not continuous ATRA induction. Tretinoin 184-188 aldehyde dehydrogenase 1 family member A2 Homo sapiens 123-129
18502188-8 2008 CYP26C1 transcription was significantly repressed by ATRA, and this downregulation also showed a neural differentiation-dependent pattern, in respect that CYP26C1 expression was kept in low-level even after the withdrawal of ATRA. Tretinoin 53-57 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
18502188-8 2008 CYP26C1 transcription was significantly repressed by ATRA, and this downregulation also showed a neural differentiation-dependent pattern, in respect that CYP26C1 expression was kept in low-level even after the withdrawal of ATRA. Tretinoin 225-229 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
20215566-4 2010 Given that retinoic acid, the ligand for RARA, is known to regulate cell proliferation and differentiation, we investigated whether FSH regulates RARA by a direct posttranslational phosphorylation mechanism. Tretinoin 11-24 retinoic acid receptor, alpha Mus musculus 41-45
12052888-4 2002 Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. Tretinoin 239-241 Jun dimerization protein 2 Homo sapiens 63-67
20090765-5 2010 However, 1,25(OH)(2) vitamin D(3), 9-cis retinoic acid (RA), and 13-cis RA also induced the KLKs, but the timing and pattern of KLK induction for each were different and distinct from changes in differentiation markers. Tretinoin 56-58 kallikrein related peptidase 4 Homo sapiens 92-96
20090765-5 2010 However, 1,25(OH)(2) vitamin D(3), 9-cis retinoic acid (RA), and 13-cis RA also induced the KLKs, but the timing and pattern of KLK induction for each were different and distinct from changes in differentiation markers. Tretinoin 72-74 kallikrein related peptidase 4 Homo sapiens 92-96
12225397-9 2002 We speculate that the remarkable induction of gp91phox and p47phox protein is associated with an increase in superoxide-generating activity due to the synergistic effect of ATRA plus GM-CSF. Tretinoin 173-177 pleckstrin Homo sapiens 59-62
18485106-5 2008 Using pharmacologic inhibitors of various isoforms of protein kinase C (PKC), we also demonstrate that DARPP-32 induction by RA in vitro is dependent on PKC zeta (PKCzeta). Tretinoin 125-127 protein kinase C zeta Homo sapiens 72-75
18485106-5 2008 Using pharmacologic inhibitors of various isoforms of protein kinase C (PKC), we also demonstrate that DARPP-32 induction by RA in vitro is dependent on PKC zeta (PKCzeta). Tretinoin 125-127 protein kinase C zeta Homo sapiens 153-161
18485106-5 2008 Using pharmacologic inhibitors of various isoforms of protein kinase C (PKC), we also demonstrate that DARPP-32 induction by RA in vitro is dependent on PKC zeta (PKCzeta). Tretinoin 125-127 protein kinase C zeta Homo sapiens 163-170
12012012-7 2002 Our results indicate that ATRA-pretreatment modified the CDDP-induced regulation of CDK2 activity by the CDK inhibitors p21 and p27. Tretinoin 26-30 interferon alpha inducible protein 27 Homo sapiens 128-131
18474614-7 2008 While normal DNER was actively endocytosed and inhibited the retinoic-acid-induced neurite outgrowth of Neuro-2A cells, pleiotrophin stimulation increased the tyrosine phosphorylation level of DNER and suppressed the endocytosis of this protein, which led to the reversal of this inhibition, thus allowing neurite extension. Tretinoin 61-74 delta/notch-like EGF repeat containing Mus musculus 13-17
20134361-8 2010 RESULTS: Mouse sutures were found to express genes necessary for retinoic acid synthesis, binding, and signal transduction, demonstrated by quantitative real-time polymerase chain reaction (Raldh1, Raldh2, Raldh3, and Rbp4). Tretinoin 65-78 retinol binding protein 4, plasma Mus musculus 218-222
20346917-7 2010 These results suggested that curcumin dramatically enhances RA-induced O(2)(-)-generating activity via accumulation of cytosolic p47-phox and p67-phox proteins in U937 cells. Tretinoin 60-62 neutrophil cytosolic factor 1 Homo sapiens 129-137
20130111-4 2010 GRp58 interacted with RARA in the presence of all-trans retinoic acid (ATRA) ligand and, as a complex, it was translocated from the cytoplasm to the nucleus and, then with time, GRp58 dissociated from RARA and was found in the cytoplasm. Tretinoin 56-69 retinoic acid receptor, alpha Mus musculus 22-26
20130111-4 2010 GRp58 interacted with RARA in the presence of all-trans retinoic acid (ATRA) ligand and, as a complex, it was translocated from the cytoplasm to the nucleus and, then with time, GRp58 dissociated from RARA and was found in the cytoplasm. Tretinoin 71-75 retinoic acid receptor, alpha Mus musculus 22-26
20130111-6 2010 Moreover, treatment with sulfhydryl-modifying agents that oxidize SH-groups of cysteine residues to disulfide bonds abolished ATRA-mediated RARA nuclear localization, suggesting that the thiol oxidoreductase activity of GRp58 may be required for RARA nuclear import. Tretinoin 126-130 retinoic acid receptor, alpha Mus musculus 140-144
12032336-0 2002 Variant-type PML-RAR(alpha) fusion transcript in acute promyelocytic leukemia: use of a cryptic coding sequence from intron 2 of the RAR(alpha) gene and identification of a new clinical subtype resistant to retinoic acid therapy. Tretinoin 207-220 PML nuclear body scaffold Homo sapiens 13-16
20130111-6 2010 Moreover, treatment with sulfhydryl-modifying agents that oxidize SH-groups of cysteine residues to disulfide bonds abolished ATRA-mediated RARA nuclear localization, suggesting that the thiol oxidoreductase activity of GRp58 may be required for RARA nuclear import. Tretinoin 126-130 retinoic acid receptor, alpha Mus musculus 246-250
19955695-4 2010 RKIP(+) cells showed accelerated neurite outgrowth, formation of elaborated neuronal networks and increased neuronal marker expression both in RA-induced differentiation and to some extent even in non-RA-treated cells. Tretinoin 143-145 phosphatidylethanolamine binding protein 1 Homo sapiens 0-4
18387645-2 2008 JWA, a novel retinoic acid-inducible gene, is known to be involved in apoptosis induced by various agents, for example, 12-O-tetradecanoylphorbol 13-acetate, N-4-hydroxy-phenyl-retinamide and arsenic trioxide. Tretinoin 13-26 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 0-3
12032336-0 2002 Variant-type PML-RAR(alpha) fusion transcript in acute promyelocytic leukemia: use of a cryptic coding sequence from intron 2 of the RAR(alpha) gene and identification of a new clinical subtype resistant to retinoic acid therapy. Tretinoin 207-220 retinoic acid receptor alpha Homo sapiens 17-27
18399539-2 2008 One of these signaling molecules is retinoic acid (RA), an active vitamin A derivative, which in mammalian embryos is synthesized from maternal retinol by two oxidative reactions involving alcohol/retinol dehydrogenases (ADH/RDHs) and retinaldehyde dehydrogenases (RALDHs), respectively. Tretinoin 36-49 short chain dehydrogenase/reductase family 9C member 7 Homo sapiens 225-229
18399539-2 2008 One of these signaling molecules is retinoic acid (RA), an active vitamin A derivative, which in mammalian embryos is synthesized from maternal retinol by two oxidative reactions involving alcohol/retinol dehydrogenases (ADH/RDHs) and retinaldehyde dehydrogenases (RALDHs), respectively. Tretinoin 51-53 short chain dehydrogenase/reductase family 9C member 7 Homo sapiens 225-229
19955695-4 2010 RKIP(+) cells showed accelerated neurite outgrowth, formation of elaborated neuronal networks and increased neuronal marker expression both in RA-induced differentiation and to some extent even in non-RA-treated cells. Tretinoin 201-203 phosphatidylethanolamine binding protein 1 Homo sapiens 0-4
19917671-3 2010 We report here that in both human myeloid leukemia and mouse embryonic teratocarcinoma stem cells, either RA-suppressed CAK phosphorylation of RARalpha or mutation of RARalphaS77 to alanine (RARalphaS77A) coordinates CAK-dependent G(1) arrest with cancer cell differentiation by transactivating RA-target genes. Tretinoin 106-108 retinoic acid receptor, alpha Mus musculus 143-151
12032336-10 2002 In these cases, the aberrant V-type PML-RAR(alpha) protein displayed increased affinity to the nuclear corepressor protein SMRT, providing further evidence that RA exerts the therapeutic effect on APL through modulation of the RAR-corepressor interaction. Tretinoin 40-42 PML nuclear body scaffold Homo sapiens 36-39
12051745-7 2002 Electrophoretic mobility shift assay (EMSA) experiment demonstrated that two slowly migrated complexes (C1 and C2) capable of binding the RARE sequence were present in nuclear extracts prepared from cells and the complex C1 was strongly increased in nuclear extracts by RA stimulation. Tretinoin 138-140 heterogeneous nuclear ribonucleoprotein C Homo sapiens 104-113
20159609-4 2010 Genome-wide epigenetic studies revealed that treatment with pharmacological doses of all-trans retinoic acid induces changes in H3 acetylation, but not H3K27me3, H3K9me3, or DNA methylation at the PML-RARalpha/RXR binding sites or at nearby target genes. Tretinoin 95-108 retinoid X receptor alpha Homo sapiens 210-213
20164929-0 2010 Rere controls retinoic acid signalling and somite bilateral symmetry. Tretinoin 14-27 arginine-glutamic acid dipeptide repeats Homo sapiens 0-4
18520998-3 2008 RBP is an all-trans retinol carrier, a molecule that can be metabolized into retinoic acid, a morphogen involved in central nervous system (CNS) morphogenesis and patterning. Tretinoin 77-90 retinol binding protein 4 Homo sapiens 0-3
18492817-4 2008 Besides E(2), retinoic acid (RA) and P4 play an important role in the regulation of STC2 expression, not only in MCF-7 but also in other breast cancer and non-breast cell lines. Tretinoin 14-27 stanniocalcin 2 Homo sapiens 84-88
12392175-6 2002 Application of exogenous retinoic acid (RA) increased the number of GFP-expressing cells throughout the retina, and possibly the level of expressed rhodopsin. Tretinoin 25-38 rhodopsin Danio rerio 148-157
18492817-4 2008 Besides E(2), retinoic acid (RA) and P4 play an important role in the regulation of STC2 expression, not only in MCF-7 but also in other breast cancer and non-breast cell lines. Tretinoin 29-31 stanniocalcin 2 Homo sapiens 84-88
18492826-4 2008 Three RXR-binding elements [retinoic acid response element (RARE)1/PCK1, RARE2, and RARE3/PCK2] were previously located in the promoter of Pck1. Tretinoin 28-41 retinoid X receptor alpha Homo sapiens 6-9
18497940-4 2008 During the all-trans-retinoic acid (ATRA)-mediated neuronal differentiation in neuroblastoma-derived RTBM1 cells, the expression levels of ERAP140/Nbla10993 increased at the mRNA level. Tretinoin 36-40 nuclear receptor coactivator 7 Homo sapiens 139-146
18497940-4 2008 During the all-trans-retinoic acid (ATRA)-mediated neuronal differentiation in neuroblastoma-derived RTBM1 cells, the expression levels of ERAP140/Nbla10993 increased at the mRNA level. Tretinoin 36-40 nuclear receptor coactivator 7 Homo sapiens 147-156
18497940-5 2008 Consistent with these observations, the luciferase reporter analysis demonstrated that the ERAP140/Nbla10993 promoter responds to ATRA. Tretinoin 130-134 nuclear receptor coactivator 7 Homo sapiens 91-98
18497940-5 2008 Consistent with these observations, the luciferase reporter analysis demonstrated that the ERAP140/Nbla10993 promoter responds to ATRA. Tretinoin 130-134 nuclear receptor coactivator 7 Homo sapiens 99-108
20164929-2 2010 Here we show that a mutation in Rere (also known as atrophin2) leads to the formation of asymmetrical somites in mouse embryos, similar to embryos deprived of retinoic acid. Tretinoin 159-172 arginine glutamic acid dipeptide (RE) repeats Mus musculus 32-36
20164929-2 2010 Here we show that a mutation in Rere (also known as atrophin2) leads to the formation of asymmetrical somites in mouse embryos, similar to embryos deprived of retinoic acid. Tretinoin 159-172 arginine glutamic acid dipeptide (RE) repeats Mus musculus 52-61
20164929-5 2010 Furthermore, the knockdown of Nr2f2 and/or Rere decreases retinoic acid signalling, suggesting that this complex is required to promote transcriptional activation of retinoic acid targets. Tretinoin 58-71 arginine-glutamic acid dipeptide repeats Homo sapiens 43-47
20164929-5 2010 Furthermore, the knockdown of Nr2f2 and/or Rere decreases retinoic acid signalling, suggesting that this complex is required to promote transcriptional activation of retinoic acid targets. Tretinoin 166-179 arginine-glutamic acid dipeptide repeats Homo sapiens 43-47
20028078-6 2010 In fact, the overexpression of a mutated form of Vav1, in which Y745 was replaced with a phenylalanine, significantly reduced the ATRA-induced CD11b expression and essentially abrogated the differentiation-related acquisition of the migratory capability. Tretinoin 130-134 integrin subunit alpha M Homo sapiens 143-148
20137113-2 2010 The results showed that the expression of STAT2, IRF-9 and IRF-1 could be upregulated by ATRA with different kinetics in NB4 cells. Tretinoin 89-93 signal transducer and activator of transcription 2 Homo sapiens 42-47
20137113-5 2010 It is concluded that during ATRA-induced APL cell differentiation, IRF-1 is first upregulated by ATRA, and then IRF-1 increases the protein levels of IRF-9 and STAT2 with the downregulation of C/EBPalpha. Tretinoin 28-32 signal transducer and activator of transcription 2 Homo sapiens 160-165
18497940-8 2008 Taken together, our present findings indicate that ERAP140/Nbla10993 plays an important role in the regulation of ATRA-mediated neuronal differentiation, and is a novel member of prognostic indicators for neuroblastoma. Tretinoin 114-118 nuclear receptor coactivator 7 Homo sapiens 51-58
18497940-8 2008 Taken together, our present findings indicate that ERAP140/Nbla10993 plays an important role in the regulation of ATRA-mediated neuronal differentiation, and is a novel member of prognostic indicators for neuroblastoma. Tretinoin 114-118 nuclear receptor coactivator 7 Homo sapiens 59-68
12392175-6 2002 Application of exogenous retinoic acid (RA) increased the number of GFP-expressing cells throughout the retina, and possibly the level of expressed rhodopsin. Tretinoin 40-42 rhodopsin Danio rerio 148-157
19035249-15 2008 After the ATRA treatment, cells were stained strongly positive, strongly positive and moderately positive by NSE, vimentin and GFAP antibodies, respectively. Tretinoin 10-14 glial fibrillary acidic protein Homo sapiens 127-131
18495924-0 2008 Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR. Tretinoin 11-24 peroxisome proliferator activated receptor delta Homo sapiens 90-98
18495924-0 2008 Overcoming retinoic acid-resistance of mammary carcinomas by diverting retinoic acid from PPARbeta/delta to RAR. Tretinoin 71-84 peroxisome proliferator activated receptor delta Homo sapiens 90-98
18495924-4 2008 A clue to this paradoxical behavior was recently suggested by the findings that RA also activates PPARbeta/delta, a receptor involved in mitogenic and anti-apoptotic activities. Tretinoin 80-82 peroxisome proliferator activated receptor delta Homo sapiens 98-106
20082710-9 2010 Furthermore, our results suggest the interesting possibility that Pax6 regulates anterior-posterior patterning of the hindbrain via activation of Cyp26b1, an enzyme that metabolizes retinoic acid. Tretinoin 182-195 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 146-153
19653098-9 2010 Retinoic acid signaling via the retinoid X-receptor (RXR) has shown promise to be a major regulator of reproductive tract recrudescence. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 32-51
11929749-7 2002 We conclude that Stat5 is capable of interacting with a corepressor complex that alters the pattern of corepressor binding to RARalpha and its dissociation in response to ATRA stimulation, leading to enhanced repressor activity and a block of hematopoietic differentiation. Tretinoin 171-175 signal transducer and activator of transcription 5A Homo sapiens 17-22
19653098-9 2010 Retinoic acid signaling via the retinoid X-receptor (RXR) has shown promise to be a major regulator of reproductive tract recrudescence. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 53-56
11929749-7 2002 We conclude that Stat5 is capable of interacting with a corepressor complex that alters the pattern of corepressor binding to RARalpha and its dissociation in response to ATRA stimulation, leading to enhanced repressor activity and a block of hematopoietic differentiation. Tretinoin 171-175 retinoic acid receptor alpha Homo sapiens 126-134
19787411-2 2010 We cultured type II pneumocytes at confluent, high cell density (10(4) cells/mm(2)) and found that RA (10(-6) M) inhibited thymidine incorporation to 60% of control, despite a dose-dependent increase in epidermal growth factor receptor (EGFR) levels. Tretinoin 99-101 epidermal growth factor receptor Rattus norvegicus 203-235
19787411-2 2010 We cultured type II pneumocytes at confluent, high cell density (10(4) cells/mm(2)) and found that RA (10(-6) M) inhibited thymidine incorporation to 60% of control, despite a dose-dependent increase in epidermal growth factor receptor (EGFR) levels. Tretinoin 99-101 epidermal growth factor receptor Rattus norvegicus 237-241
18383274-5 2008 Moreover, RA increased the expression of active CREB by enhancing the activity of JNK. Tretinoin 10-12 mitogen-activated protein kinase 8 Mus musculus 82-85
18383274-6 2008 Our research suggests that CREB plays a role in RA-induced NPC differentiation by increasing the expression of active JNK. Tretinoin 48-50 mitogen-activated protein kinase 8 Mus musculus 118-121
11788605-1 2002 All-trans-retinoic acid (ATRA) induces myeloid differentiation of a human promyelocytic leukemia cell line, NB4, but does not affect its subclone NB4/RA harboring a point-mutated ligand-binding domain (AF2) in retinoic acid receptor alpha (RARalpha) gene. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 210-238
18407549-0 2008 Autoregulatory loop and retinoic acid repression regulate pou2/pou5f1 gene expression in the zebrafish embryonic brain. Tretinoin 24-37 POU domain, class 5, transcription factor 3 Danio rerio 58-62
18407549-0 2008 Autoregulatory loop and retinoic acid repression regulate pou2/pou5f1 gene expression in the zebrafish embryonic brain. Tretinoin 24-37 POU domain, class 5, transcription factor 3 Danio rerio 63-69
18217212-0 2008 ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of beta-catenin via up-regulation of Axin. Tretinoin 0-4 axin 1 Homo sapiens 128-132
18217212-3 2008 In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of beta-catenin. Tretinoin 28-51 axin 1 Homo sapiens 160-164
19903244-9 2010 The electrophoresis mobility shift assay revealed that ATRA produced two retarded bands, which were erased by antibody against chicken ovalbumin upstream promoter transcription factor I (COUP-TFI), RARalpha, and RXRalpha, respectively. Tretinoin 55-59 retinoid X receptor alpha Gallus gallus 212-220
21189168-9 2010 The expression levels of GATA-4 and AFP were the highest after induction of differentiation with retinoic acid. Tretinoin 97-110 alpha fetoprotein Mus musculus 36-39
18217212-3 2008 In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of beta-catenin. Tretinoin 53-57 axin 1 Homo sapiens 160-164
11788605-1 2002 All-trans-retinoic acid (ATRA) induces myeloid differentiation of a human promyelocytic leukemia cell line, NB4, but does not affect its subclone NB4/RA harboring a point-mutated ligand-binding domain (AF2) in retinoic acid receptor alpha (RARalpha) gene. Tretinoin 25-29 retinoic acid receptor alpha Homo sapiens 240-248
18217212-5 2008 Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines. Tretinoin 64-66 axin 1 Homo sapiens 27-31
11788605-7 2002 Luciferase activity in transformed cells markedly increased in response to ATRA stimulation when the wild type RARalpha or the PML/RARalpha hybrid protein was co-expressed. Tretinoin 75-79 retinoic acid receptor alpha Homo sapiens 111-119
20369475-7 2010 With increase of ATRA-induced cell differentiation, MtF mRNA expressions were downregulated progressively. Tretinoin 17-21 metallothionein 1L, pseudogene Homo sapiens 52-55
20369475-8 2010 After 5 days of induced cell differentiation, expression levels of MtF and TfR1 mRNA were just 86.5% and 79.2% of that before ATRA treatment. Tretinoin 126-130 metallothionein 1L, pseudogene Homo sapiens 67-70
11788605-7 2002 Luciferase activity in transformed cells markedly increased in response to ATRA stimulation when the wild type RARalpha or the PML/RARalpha hybrid protein was co-expressed. Tretinoin 75-79 PML nuclear body scaffold Homo sapiens 127-130
20369475-10 2010 CONCLUSION: MtF expression is downregulated during ATRA-induced K562 cell differentiation, with concomitant downregulation of TfR1 and upregulation of Fn. Tretinoin 51-55 metallothionein 1L, pseudogene Homo sapiens 12-15
11788605-7 2002 Luciferase activity in transformed cells markedly increased in response to ATRA stimulation when the wild type RARalpha or the PML/RARalpha hybrid protein was co-expressed. Tretinoin 75-79 retinoic acid receptor alpha Homo sapiens 131-139
18390749-6 2008 In addition, inducible expression of KLF4 in the HL60 human acute myeloid leukemia cell line stimulated monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage differentiation, but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells. Tretinoin 232-251 Kruppel like factor 4 Homo sapiens 37-41
11877298-0 2002 Retinoic acid-induced cell cycle arrest of human myeloid cell lines is associated with sequential down-regulation of c-Myc and cyclin E and posttranscriptional up-regulation of p27(Kip1). Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 117-122
19744992-5 2009 ATRA also strongly induced the expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) (an increase of 5- and 50-fold, respectively). Tretinoin 0-4 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 95-129
19744992-5 2009 ATRA also strongly induced the expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) (an increase of 5- and 50-fold, respectively). Tretinoin 0-4 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 131-140
18004512-5 2008 Further BCMO function in mammalian cells was analyzed by a retinoic acid receptor reporter assay, which responds to the metabolic conversion of beta-carotene to retinoic acid in vivo. Tretinoin 59-72 beta-carotene oxygenase 1 Homo sapiens 8-12
18412219-0 2008 Retinoic acid-induced inner ear teratogenesis caused by defective Fgf3/Fgf10-dependent Dlx5 signaling. Tretinoin 0-13 fibroblast growth factor 10 Mus musculus 71-76
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 93-95 fibroblast growth factor 10 Mus musculus 37-42
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 190-192 fibroblast growth factor 10 Mus musculus 136-141
18412219-9 2008 Before Dlx5 downregulation, Fgf3 and Fgf10 expression is modified in the inner ear by excess RA, with the ability of exogenous Fgf3 and Fgf10 to rescue chondrogenesis and Dlx5 expression in RA-treated cultures of periotic mesenchyme containing otic epithelium supporting these fibroblast growth factors (FGFs) as intermediary genes by which RA mediates its effects. Tretinoin 190-192 fibroblast growth factor 10 Mus musculus 136-141
19885578-9 2009 Actinomycin-D, cyclohexamide, retinoic acid and dexamethasone inhibited MMP-2 in both cancer cell lines and inhibited MMP-9 in MM. Tretinoin 30-43 matrix metallopeptidase 9 Homo sapiens 118-123
11877298-0 2002 Retinoic acid-induced cell cycle arrest of human myeloid cell lines is associated with sequential down-regulation of c-Myc and cyclin E and posttranscriptional up-regulation of p27(Kip1). Tretinoin 0-13 interferon alpha inducible protein 27 Homo sapiens 177-180
11877298-0 2002 Retinoic acid-induced cell cycle arrest of human myeloid cell lines is associated with sequential down-regulation of c-Myc and cyclin E and posttranscriptional up-regulation of p27(Kip1). Tretinoin 0-13 cyclin dependent kinase inhibitor 1B Homo sapiens 181-185
11877298-3 2002 In this study, we show that the onset of ATRA-induced G(0)/G(1) arrest of human monoblastic U-937 cells is linked to a sharp down-regulation of c-Myc and cyclin E levels and an increase in p21(WAF1/CIP1) expression. Tretinoin 41-45 MYC proto-oncogene, bHLH transcription factor Homo sapiens 144-149
20005394-1 2009 BACKGROUND: Ligands for the natural killer cell-activating receptor NKG2D, such as retinoic acid early inducible (Rae-1), minor histocompatibility antigen H60 (mouse), and major histocompatibility complex class I chain-related (human) may be expressed by tissues in response to stress. Tretinoin 83-96 ribonucleic acid export 1 Mus musculus 114-119
11877298-5 2002 The importance of an early decrease in Myc expression for these events was demonstrated by the failure of a U-937 subline with constitutive exogenous expression of v-Myc to cell cycle arrest and regulate cyclin E and p27(Kip1) in response to ATRA. Tretinoin 242-246 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-42
11877298-5 2002 The importance of an early decrease in Myc expression for these events was demonstrated by the failure of a U-937 subline with constitutive exogenous expression of v-Myc to cell cycle arrest and regulate cyclin E and p27(Kip1) in response to ATRA. Tretinoin 242-246 cyclin dependent kinase inhibitor 1B Homo sapiens 221-225
18278797-5 2008 Based on marker expression, retinoic acid increased the yield of neurons and the percentage of sensory neurons obtained and caused a sharp increase in Pax2, a key transcription factor of cranial placodes. Tretinoin 28-41 paired box 2 Homo sapiens 151-155
11877298-8 2002 These results thus identify a decrease in c-Myc and cyclin E levels and a posttranscriptional up-regulation of p27(Kip1) as important early changes, and position them in the complex chain of events regulating ATRA-induced cell cycle arrest of myeloid cells. Tretinoin 209-213 MYC proto-oncogene, bHLH transcription factor Homo sapiens 42-47
11877298-8 2002 These results thus identify a decrease in c-Myc and cyclin E levels and a posttranscriptional up-regulation of p27(Kip1) as important early changes, and position them in the complex chain of events regulating ATRA-induced cell cycle arrest of myeloid cells. Tretinoin 209-213 interferon alpha inducible protein 27 Homo sapiens 111-114
17943186-0 2008 All-trans retinoic acid-induced hyaluronan production and hyperplasia are partly mediated by EGFR signaling in epidermal keratinocytes. Tretinoin 10-23 epidermal growth factor receptor Rattus norvegicus 93-97
20030938-0 2009 [Effect of ATRA on the expression of genes Hoxb2 and Hoxb4 in cord blood erythroid progenitors]. Tretinoin 11-15 homeobox B2 Homo sapiens 43-48
20030938-0 2009 [Effect of ATRA on the expression of genes Hoxb2 and Hoxb4 in cord blood erythroid progenitors]. Tretinoin 11-15 homeobox B4 Homo sapiens 53-58
11877298-8 2002 These results thus identify a decrease in c-Myc and cyclin E levels and a posttranscriptional up-regulation of p27(Kip1) as important early changes, and position them in the complex chain of events regulating ATRA-induced cell cycle arrest of myeloid cells. Tretinoin 209-213 cyclin dependent kinase inhibitor 1B Homo sapiens 115-119
20030938-1 2009 This study was aimed to investigate the expressions of genes hoxb2 and hoxb4 after interference of the proliferation and differentiation of hematopoietic stem cells (HSC) to the erythroid progenitors (CFU-E) in vitro by using all-trans retinoic acid (ATRA). Tretinoin 236-249 homeobox B2 Homo sapiens 61-66
20030938-1 2009 This study was aimed to investigate the expressions of genes hoxb2 and hoxb4 after interference of the proliferation and differentiation of hematopoietic stem cells (HSC) to the erythroid progenitors (CFU-E) in vitro by using all-trans retinoic acid (ATRA). Tretinoin 236-249 homeobox B4 Homo sapiens 71-76
11867758-4 2002 The predicted amino acid sequence is similar to that of GRP-1-associated protein (GRASP), a recently identified retinoic acid-induced cytohesin-binding protein. Tretinoin 112-125 trafficking regulator and scaffold protein tamalin Homo sapiens 56-80
20030938-1 2009 This study was aimed to investigate the expressions of genes hoxb2 and hoxb4 after interference of the proliferation and differentiation of hematopoietic stem cells (HSC) to the erythroid progenitors (CFU-E) in vitro by using all-trans retinoic acid (ATRA). Tretinoin 251-255 homeobox B2 Homo sapiens 61-66
20030938-1 2009 This study was aimed to investigate the expressions of genes hoxb2 and hoxb4 after interference of the proliferation and differentiation of hematopoietic stem cells (HSC) to the erythroid progenitors (CFU-E) in vitro by using all-trans retinoic acid (ATRA). Tretinoin 251-255 homeobox B4 Homo sapiens 71-76
20030938-7 2009 As compared with blank control group, the expressions of genes hoxb2 and hoxb4 in the ATRA group were significantly up-regulated. Tretinoin 86-90 homeobox B2 Homo sapiens 63-68
20030938-7 2009 As compared with blank control group, the expressions of genes hoxb2 and hoxb4 in the ATRA group were significantly up-regulated. Tretinoin 86-90 homeobox B4 Homo sapiens 73-78
19843176-0 2009 Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response. Tretinoin 92-105 MDS1 and EVI1 complex locus Homo sapiens 33-67
19843176-0 2009 Zinc finger transcription factor ecotropic viral integration site 1 is induced by all-trans retinoic acid (ATRA) and acts as a dual modulator of the ATRA response. Tretinoin 107-111 MDS1 and EVI1 complex locus Homo sapiens 33-67
17922036-4 2008 Dab2 levels induced during retinoic acid-induced differentiation of F9, or during transforming growth factor-beta-induced epithelial-mesenchymal transdifferentiation of mouse mammary epithelial cells result in the stabilization of Axin and concomitant inhibition of beta-catenin signaling. Tretinoin 27-40 disabled 2, mitogen-responsive phosphoprotein Mus musculus 0-4
17922036-4 2008 Dab2 levels induced during retinoic acid-induced differentiation of F9, or during transforming growth factor-beta-induced epithelial-mesenchymal transdifferentiation of mouse mammary epithelial cells result in the stabilization of Axin and concomitant inhibition of beta-catenin signaling. Tretinoin 27-40 axin 1 Mus musculus 231-235
18020317-1 2008 The ab initio fragment molecular orbital (FMO) calculations were performed for retinoid X receptor (RXR) complexes with its ligand 9-cis retinoic acid (9cRA) and steroid receptor coactivator-1 (SRC1) to examine the influence of mutations in transcriptional activation function 2 activating domain core (AF2C) of RXR on molecular interactions between 9cRA liganded RXR and SRC1 coactivator. Tretinoin 137-150 retinoid X receptor alpha Homo sapiens 79-98
18020317-1 2008 The ab initio fragment molecular orbital (FMO) calculations were performed for retinoid X receptor (RXR) complexes with its ligand 9-cis retinoic acid (9cRA) and steroid receptor coactivator-1 (SRC1) to examine the influence of mutations in transcriptional activation function 2 activating domain core (AF2C) of RXR on molecular interactions between 9cRA liganded RXR and SRC1 coactivator. Tretinoin 137-150 retinoid X receptor alpha Homo sapiens 100-103
18437907-9 2008 BMP-7 mRNA and protein levels in MC-3T3-E1 cells treated with 1 x 10(-6) mol/L ATRA decreased by 60% and 80%, respectively, compared with ATRA-untreated cells (P < 0.05). Tretinoin 79-83 bone morphogenetic protein 7 Mus musculus 0-5
18437907-9 2008 BMP-7 mRNA and protein levels in MC-3T3-E1 cells treated with 1 x 10(-6) mol/L ATRA decreased by 60% and 80%, respectively, compared with ATRA-untreated cells (P < 0.05). Tretinoin 138-142 bone morphogenetic protein 7 Mus musculus 0-5
19843176-3 2009 Here we describe the identification of a retinoic acid response element that was located in the most distal of several alternative first exons of the human EVI1 gene and was constitutively bound by canonical retinoid receptors in NTERA-2 teratocarcinoma cells. Tretinoin 41-54 MDS1 and EVI1 complex locus Homo sapiens 156-160
19843176-4 2009 Furthermore, it was the target of negative feedback by EVI1 on the induction of its own promoter by retinoic acid. Tretinoin 100-113 MDS1 and EVI1 complex locus Homo sapiens 55-59
19843176-6 2009 Extending its role as a modulator of the retinoic acid response, EVI1 had the opposite effect on the RARbeta retinoic acid response element, whose induction by all-trans retinoic acid it enhanced through a mechanism that involved almost all of its known functional domains. Tretinoin 41-54 MDS1 and EVI1 complex locus Homo sapiens 65-69
19843176-7 2009 Augmentation of the retinoic acid response by EVI1 was also observed for the endogenous RARbeta gene. Tretinoin 20-33 MDS1 and EVI1 complex locus Homo sapiens 46-50
11867758-4 2002 The predicted amino acid sequence is similar to that of GRP-1-associated protein (GRASP), a recently identified retinoic acid-induced cytohesin-binding protein. Tretinoin 112-125 trafficking regulator and scaffold protein tamalin Homo sapiens 82-87
19843176-8 2009 Thus, we have established EVI1 as a novel type of modulator of the retinoic acid response, which can both enhance and repress induction by this agent in a promoter-specific manner. Tretinoin 67-80 MDS1 and EVI1 complex locus Homo sapiens 26-30
11945128-0 2002 Discovery and design of retinoic acid receptor and retinoid X receptor class- and subtype-selective synthetic analogs of all-trans-retinoic acid and 9-cis-retinoic acid. Tretinoin 121-144 retinoic acid receptor alpha Homo sapiens 24-46
19783990-0 2009 Chemokine CXCL13 is essential for lymph node initiation and is induced by retinoic acid and neuronal stimulation. Tretinoin 74-87 C-X-C motif chemokine ligand 13 Homo sapiens 10-16
19783990-3 2009 Retinoic acid (RA) induced early CXCL13 expression in stromal organizer cells independently of lymphotoxin signaling. Tretinoin 0-13 C-X-C motif chemokine ligand 13 Homo sapiens 33-39
19783990-3 2009 Retinoic acid (RA) induced early CXCL13 expression in stromal organizer cells independently of lymphotoxin signaling. Tretinoin 15-17 C-X-C motif chemokine ligand 13 Homo sapiens 33-39
18360785-0 2008 Eicosapentaenoic acid (EPA) increases cell viability and expression of neurotrophin receptors in retinoic acid and brain-derived neurotrophic factor differentiated SH-SY5Y cells. Tretinoin 97-110 brain derived neurotrophic factor Homo sapiens 71-83
18360785-5 2008 METHODS: Both undifferentiated and retinoic acid (RA)-BDNF differentiated SH-SY5Y cells were treated with EPA and/or BDNF. Tretinoin 35-48 brain derived neurotrophic factor Homo sapiens 54-58
18360785-5 2008 METHODS: Both undifferentiated and retinoic acid (RA)-BDNF differentiated SH-SY5Y cells were treated with EPA and/or BDNF. Tretinoin 50-52 brain derived neurotrophic factor Homo sapiens 54-58
19783990-6 2009 Therefore, our data show that the initiation of lymph node development is controlled by RA-mediated expression of CXCL13 and suggest that RA may be provided by adjacent neurons. Tretinoin 88-90 C-X-C motif chemokine ligand 13 Homo sapiens 114-120
12058867-0 2002 1Alpha25(OH)2D3 interferes with retinoic acid-induced inhibition of c-fos gene expression for AP-1 formation in osteoblastic cells. Tretinoin 32-45 FBJ osteosarcoma oncogene Mus musculus 68-73
19814781-5 2009 RESULTS: Treatment of P19 or mouse ES cells with low levels of RA led to an enhancement of skeletal myogenesis by upregulating the expression of the mesodermal marker, Wnt3a, the skeletal muscle progenitor factors Pax3 and Meox1, and the myogenic regulatory factors (MRFs) MyoD and myogenin. Tretinoin 63-65 mesenchyme homeobox 1 Mus musculus 223-228
17987264-2 2008 Treatment of cells with 1 microM all-trans retinoic acid (ATRA) or 1 microM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation, overexpression of glial fibrillary acidic protein (GFAP), and also down regulated telomerase expression and activity, thereby increased sensitivity to TXL for apoptosis. Tretinoin 37-56 glial fibrillary acidic protein Homo sapiens 171-202
17987264-2 2008 Treatment of cells with 1 microM all-trans retinoic acid (ATRA) or 1 microM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation, overexpression of glial fibrillary acidic protein (GFAP), and also down regulated telomerase expression and activity, thereby increased sensitivity to TXL for apoptosis. Tretinoin 37-56 glial fibrillary acidic protein Homo sapiens 204-208
17987264-2 2008 Treatment of cells with 1 microM all-trans retinoic acid (ATRA) or 1 microM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation, overexpression of glial fibrillary acidic protein (GFAP), and also down regulated telomerase expression and activity, thereby increased sensitivity to TXL for apoptosis. Tretinoin 58-62 glial fibrillary acidic protein Homo sapiens 171-202
17987264-2 2008 Treatment of cells with 1 microM all-trans retinoic acid (ATRA) or 1 microM 13-cis retinoic acid (13-CRA) for 7 days induced astrocytic differentiation, overexpression of glial fibrillary acidic protein (GFAP), and also down regulated telomerase expression and activity, thereby increased sensitivity to TXL for apoptosis. Tretinoin 58-62 glial fibrillary acidic protein Homo sapiens 204-208
19814781-12 2009 CONCLUSION: RA can enhance skeletal myogenesis in stem cells at the muscle specification/progenitor stage by activating RARs bound directly to mesoderm and skeletal muscle progenitor genes, activating beta-catenin function and inhibiting bone morphogenetic protein (BMP) signalling. Tretinoin 12-14 catenin (cadherin associated protein), beta 1 Mus musculus 201-213
19546303-4 2009 In BMMs, spleen cells, and RAW264.7 cells, osteoclast differentiation and formation stimulated by M-CSF/RANKL were inhibited (IC(50) = 0.3 nM) by ATRA. Tretinoin 146-150 colony stimulating factor 1 (macrophage) Mus musculus 98-103
12058867-1 2002 Our previous studies demonstrated retinoic acid (RA) inhibition of activation protein-1 (AP-1) formation in TNF-alpha-treated osteoblastic MC3T3-E1 cells via c-fos suppression. Tretinoin 34-47 FBJ osteosarcoma oncogene Mus musculus 158-163
19340880-11 2009 RA may be a useful clinical treatment for Th1-mediated inflammatory diseases, especially those such as Crohn"s disease occurring in the gut. Tretinoin 0-2 negative elongation factor complex member C/D Homo sapiens 42-45
18212063-3 2008 Here, we report that topoisomerase II beta (TopoIIbeta) associates with and negatively modulates RARalpha transcriptional activity and that increased levels of and association with TopoIIbeta cause resistance to RA in APL cell lines. Tretinoin 97-99 DNA topoisomerase II beta Homo sapiens 21-42
12058867-1 2002 Our previous studies demonstrated retinoic acid (RA) inhibition of activation protein-1 (AP-1) formation in TNF-alpha-treated osteoblastic MC3T3-E1 cells via c-fos suppression. Tretinoin 49-51 FBJ osteosarcoma oncogene Mus musculus 158-163
18212063-3 2008 Here, we report that topoisomerase II beta (TopoIIbeta) associates with and negatively modulates RARalpha transcriptional activity and that increased levels of and association with TopoIIbeta cause resistance to RA in APL cell lines. Tretinoin 97-99 DNA topoisomerase II beta Homo sapiens 44-54
18212063-6 2008 Chromatin immunoprecipitation assays indicated that TopoIIbeta is bound to an RA response element and that inhibition of TopoIIbeta causes hyperacetylation of histone 3 at lysine 9 and activation of transcription. Tretinoin 78-80 DNA topoisomerase II beta Homo sapiens 52-62
12058867-2 2002 In the present study, we observed that 1alpha25(OH)2D3 was able to interfere at the transcriptional level with RA inhibition of TNF-alpha-induced c-fos gene expression in cells when the cells were incubated with the vitamin for 24 hr before the RA treatment. Tretinoin 111-113 FBJ osteosarcoma oncogene Mus musculus 146-151
18212063-6 2008 Chromatin immunoprecipitation assays indicated that TopoIIbeta is bound to an RA response element and that inhibition of TopoIIbeta causes hyperacetylation of histone 3 at lysine 9 and activation of transcription. Tretinoin 78-80 DNA topoisomerase II beta Homo sapiens 121-131
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 84-88 Kruppel like factor 4 Homo sapiens 190-194
19486889-4 2009 Inhibiting JNK by JNK inhibitor SP600125 or knockdown of JNK by JNK siRNA abrogated ATRA-induced HDAC2 phosphorylation and reversed ATRA-induced suppression of the interaction of HDAC2 with KLF4. Tretinoin 132-136 Kruppel like factor 4 Homo sapiens 190-194
18207650-0 2008 C6 glioma cells differentiated by retinoic acid overexpress the glutamate transporter excitatory amino acid carrier 1 (EAAC1). Tretinoin 34-47 solute carrier family 1 member 1 Rattus norvegicus 86-117
12058867-2 2002 In the present study, we observed that 1alpha25(OH)2D3 was able to interfere at the transcriptional level with RA inhibition of TNF-alpha-induced c-fos gene expression in cells when the cells were incubated with the vitamin for 24 hr before the RA treatment. Tretinoin 245-247 FBJ osteosarcoma oncogene Mus musculus 146-151
18207650-0 2008 C6 glioma cells differentiated by retinoic acid overexpress the glutamate transporter excitatory amino acid carrier 1 (EAAC1). Tretinoin 34-47 solute carrier family 1 member 1 Rattus norvegicus 119-124
19486889-5 2009 We further demonstrated that HDAC2 directly deacetylated KLF4, and that KLF4 acetylation and binding activity of KLF4 to the SM22alpha promoter were significantly increased in ATRA-treated VSMCs. Tretinoin 176-180 Kruppel like factor 4 Homo sapiens 57-61
19486889-5 2009 We further demonstrated that HDAC2 directly deacetylated KLF4, and that KLF4 acetylation and binding activity of KLF4 to the SM22alpha promoter were significantly increased in ATRA-treated VSMCs. Tretinoin 176-180 Kruppel like factor 4 Homo sapiens 72-76
19486889-5 2009 We further demonstrated that HDAC2 directly deacetylated KLF4, and that KLF4 acetylation and binding activity of KLF4 to the SM22alpha promoter were significantly increased in ATRA-treated VSMCs. Tretinoin 176-180 Kruppel like factor 4 Homo sapiens 72-76
18207650-4 2008 Here we report that, in C6 rat glioma cells, a line recently described to contain neural stem-like cells, EAAC1 is markedly induced by all trans-retinoic acid (ATRA), a well known differentiating agent. Tretinoin 139-158 solute carrier family 1 member 1 Rattus norvegicus 106-111
18207650-4 2008 Here we report that, in C6 rat glioma cells, a line recently described to contain neural stem-like cells, EAAC1 is markedly induced by all trans-retinoic acid (ATRA), a well known differentiating agent. Tretinoin 160-164 solute carrier family 1 member 1 Rattus norvegicus 106-111
19486889-6 2009 Collectively, our results indicate that ATRA induces HDAC2 phosphorylation mediated by JNK signaling, and thus causes HDAC2 dissociation from KLF4, subsequently leading to the increase in KLF4 acetylation. Tretinoin 40-44 Kruppel like factor 4 Homo sapiens 142-146
18207650-6 2008 After 4 days of treatment with 10 microM ATRA, the transport Vmax is fivefold enhanced, Slc1a1 mRNA is increased by 400% compared with control, EAAC1 carrier is sixfold overexpressed and the C6 culture is greatly enriched of cells with bipolar morphology strongly positive for EAAC1 immunoreactivity. Tretinoin 41-45 solute carrier family 1 member 1 Rattus norvegicus 88-94
11700306-1 2002 Galpha13 mediates the ability of the morphogen retinoic acid to promote primitive endoderm formation from mouse P19 embryonal carcinoma stem cells, a process that includes the obligate activation of Jun N-terminal kinase. Tretinoin 47-60 guanine nucleotide binding protein, alpha 13 Mus musculus 0-8
18207650-6 2008 After 4 days of treatment with 10 microM ATRA, the transport Vmax is fivefold enhanced, Slc1a1 mRNA is increased by 400% compared with control, EAAC1 carrier is sixfold overexpressed and the C6 culture is greatly enriched of cells with bipolar morphology strongly positive for EAAC1 immunoreactivity. Tretinoin 41-45 solute carrier family 1 member 1 Rattus norvegicus 144-149
18207650-6 2008 After 4 days of treatment with 10 microM ATRA, the transport Vmax is fivefold enhanced, Slc1a1 mRNA is increased by 400% compared with control, EAAC1 carrier is sixfold overexpressed and the C6 culture is greatly enriched of cells with bipolar morphology strongly positive for EAAC1 immunoreactivity. Tretinoin 41-45 solute carrier family 1 member 1 Rattus norvegicus 277-282
18207650-10 2008 These results indicate that, in C6 cells, ATRA stimulates the expression of EAAC1, possibly as a step toward oligodendrocytic differentiation, and constitute the first demonstration of the induction of this transporter by a differentiating agent. Tretinoin 42-46 solute carrier family 1 member 1 Rattus norvegicus 76-81
18006504-4 2008 Unlike wild-type parental cells, RA-treated BLR1 knock-out cells failed to show RAF and consequential MEK and ERK phosphorylation, failed to accumulate CDK inhibitors that control G(1)/S transition, and failed to differentiate and arrest in response to RA, whereas ectopically overexpressing BLR1 enhanced MAPK signaling and caused accelerated RA-induced differentiation and arrest. Tretinoin 33-35 C-X-C motif chemokine receptor 5 Homo sapiens 292-296
18006504-6 2008 Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. Tretinoin 26-28 C-X-C motif chemokine receptor 5 Homo sapiens 75-79
18006504-6 2008 Ectopic expression of the RAF CR3, the catalytically active domain, in the BLR1 knock-out restored RA-induced MAPK activation and the ability to differentiate and arrest, indicating that RAF effects MAPK signaling by BLR1 to propel differentiation/arrest. Tretinoin 26-28 C-X-C motif chemokine receptor 5 Homo sapiens 217-221
18006504-7 2008 Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. Tretinoin 16-18 C-X-C motif chemokine receptor 5 Homo sapiens 114-118
18006504-7 2008 Taken together, RA induces cell differentiation and growth arrest through activation of a novel MAPK pathway with BLR1 as a critical component in a positive feedback mechanism that may contribute to the prolonged MAPK signaling propelling RA-induced cell cycle arrest and differentiation. Tretinoin 239-241 C-X-C motif chemokine receptor 5 Homo sapiens 114-118
17962516-0 2008 Role of pregnane X receptor in control of all-trans retinoic acid (ATRA) metabolism and its potential contribution to ATRA resistance. Tretinoin 42-65 nuclear receptor subfamily 1, group I, member 2 Mus musculus 8-27
17962516-0 2008 Role of pregnane X receptor in control of all-trans retinoic acid (ATRA) metabolism and its potential contribution to ATRA resistance. Tretinoin 67-71 nuclear receptor subfamily 1, group I, member 2 Mus musculus 8-27
17962516-0 2008 Role of pregnane X receptor in control of all-trans retinoic acid (ATRA) metabolism and its potential contribution to ATRA resistance. Tretinoin 118-122 nuclear receptor subfamily 1, group I, member 2 Mus musculus 8-27
17962516-6 2008 The present study was designed to examine the role of PXR in ATRA metabolism. Tretinoin 61-65 nuclear receptor subfamily 1, group I, member 2 Mus musculus 54-57
17962516-8 2008 In addition to pregnenolone 16alpha-carbonitrile, several clinically relevant PXR ligands (rifampicin and dexamethasone) all increased ATRA metabolism both in vitro and in vivo, which was PXR-dependent, and up-regulation of Cyp3a was the major contributor. Tretinoin 135-139 nuclear receptor subfamily 1, group I, member 2 Mus musculus 78-81
17962516-8 2008 In addition to pregnenolone 16alpha-carbonitrile, several clinically relevant PXR ligands (rifampicin and dexamethasone) all increased ATRA metabolism both in vitro and in vivo, which was PXR-dependent, and up-regulation of Cyp3a was the major contributor. Tretinoin 135-139 nuclear receptor subfamily 1, group I, member 2 Mus musculus 188-191
17962516-8 2008 In addition to pregnenolone 16alpha-carbonitrile, several clinically relevant PXR ligands (rifampicin and dexamethasone) all increased ATRA metabolism both in vitro and in vivo, which was PXR-dependent, and up-regulation of Cyp3a was the major contributor. Tretinoin 135-139 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 224-229
17962516-10 2008 This study suggested that coadministration of PXR ligands can increase ATRA metabolism through activation of the PXR-CYP3A pathway, which might be a mechanism for some form of ATRA resistance. Tretinoin 71-75 nuclear receptor subfamily 1, group I, member 2 Mus musculus 46-49
17962516-10 2008 This study suggested that coadministration of PXR ligands can increase ATRA metabolism through activation of the PXR-CYP3A pathway, which might be a mechanism for some form of ATRA resistance. Tretinoin 71-75 nuclear receptor subfamily 1, group I, member 2 Mus musculus 113-116
17962516-10 2008 This study suggested that coadministration of PXR ligands can increase ATRA metabolism through activation of the PXR-CYP3A pathway, which might be a mechanism for some form of ATRA resistance. Tretinoin 71-75 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 117-122
17962516-10 2008 This study suggested that coadministration of PXR ligands can increase ATRA metabolism through activation of the PXR-CYP3A pathway, which might be a mechanism for some form of ATRA resistance. Tretinoin 176-180 nuclear receptor subfamily 1, group I, member 2 Mus musculus 46-49
17962516-10 2008 This study suggested that coadministration of PXR ligands can increase ATRA metabolism through activation of the PXR-CYP3A pathway, which might be a mechanism for some form of ATRA resistance. Tretinoin 176-180 nuclear receptor subfamily 1, group I, member 2 Mus musculus 113-116
17962516-10 2008 This study suggested that coadministration of PXR ligands can increase ATRA metabolism through activation of the PXR-CYP3A pathway, which might be a mechanism for some form of ATRA resistance. Tretinoin 176-180 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 117-122
18230156-0 2008 Retinoic acid reduces human neuroblastoma cell migration and invasiveness: effects on DCX, LIS1, neurofilaments-68 and vimentin expression. Tretinoin 0-13 platelet activating factor acetylhydrolase 1b regulatory subunit 1 Homo sapiens 91-95
17637745-7 2008 Consistent with its role as an important neurodevelopmental gene, forced overexpression of wild-type PHOX2B in neuroblastoma cell lines suppressed cell proliferation and synergized with all-trans retinoic acid to promote differentiation. Tretinoin 196-209 paired like homeobox 2B Homo sapiens 101-107
17986385-3 2008 Western blot analysis showed that exposure to retinoic acid resulted in significantly increased levels of ADAM10 and TACE, suggesting that regulation of alpha-secretases causes the effects on APP processing. Tretinoin 46-59 ADAM metallopeptidase domain 17 Homo sapiens 117-121
18156812-1 2008 GRIM-19, a gene associated with retinoid interferon-induced mortality, was originally identified as a critical regulatory protein for interferon-beta and retinoic acid-induced cell death. Tretinoin 154-167 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 0-7
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 26-30 CCAAT/enhancer binding protein beta Rattus norvegicus 83-102
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 26-30 CCAAT/enhancer binding protein beta Rattus norvegicus 104-111
18769064-0 2008 All-trans retinoic acid decreases murine adipose retinol binding protein 4 production. Tretinoin 10-23 retinol binding protein 4, plasma Mus musculus 49-74
18769064-4 2008 METHODS: Changes in RBP4 expression were analyzed in adipose tissues and liver of mice treated in vivo with all-trans retinoic acid (ATRA), and in 3T3-L1 adipocytes and adipocytes derived from mouse embryonic fibroblasts exposed to ATRA. Tretinoin 118-131 retinol binding protein 4, plasma Mus musculus 20-24
18769064-4 2008 METHODS: Changes in RBP4 expression were analyzed in adipose tissues and liver of mice treated in vivo with all-trans retinoic acid (ATRA), and in 3T3-L1 adipocytes and adipocytes derived from mouse embryonic fibroblasts exposed to ATRA. Tretinoin 133-137 retinol binding protein 4, plasma Mus musculus 20-24
18769064-4 2008 METHODS: Changes in RBP4 expression were analyzed in adipose tissues and liver of mice treated in vivo with all-trans retinoic acid (ATRA), and in 3T3-L1 adipocytes and adipocytes derived from mouse embryonic fibroblasts exposed to ATRA. Tretinoin 232-236 retinol binding protein 4, plasma Mus musculus 20-24
18769064-5 2008 RESULTS: ATRA treatment in mice increased insulin sensitivity as assessed by the homeostatic model assessment for insulin resistance, and led to a reduction of RBP4 mRNA and protein levels in adipose tissues, a reduction of RBP4 protein but not RBP4 mRNA levels in the liver, and a marked increase in circulating RBP4 protein levels. Tretinoin 9-13 retinol binding protein 4, plasma Mus musculus 160-164
18769064-5 2008 RESULTS: ATRA treatment in mice increased insulin sensitivity as assessed by the homeostatic model assessment for insulin resistance, and led to a reduction of RBP4 mRNA and protein levels in adipose tissues, a reduction of RBP4 protein but not RBP4 mRNA levels in the liver, and a marked increase in circulating RBP4 protein levels. Tretinoin 9-13 retinol binding protein 4, plasma Mus musculus 224-228
18769064-5 2008 RESULTS: ATRA treatment in mice increased insulin sensitivity as assessed by the homeostatic model assessment for insulin resistance, and led to a reduction of RBP4 mRNA and protein levels in adipose tissues, a reduction of RBP4 protein but not RBP4 mRNA levels in the liver, and a marked increase in circulating RBP4 protein levels. Tretinoin 9-13 retinol binding protein 4, plasma Mus musculus 224-228
18769064-5 2008 RESULTS: ATRA treatment in mice increased insulin sensitivity as assessed by the homeostatic model assessment for insulin resistance, and led to a reduction of RBP4 mRNA and protein levels in adipose tissues, a reduction of RBP4 protein but not RBP4 mRNA levels in the liver, and a marked increase in circulating RBP4 protein levels. Tretinoin 9-13 retinol binding protein 4, plasma Mus musculus 224-228
18769064-6 2008 In adipocyte cell models, ATRA down-regulated RBP4 mRNA levels in a dose-dependent manner: this effect was reproduced by retinaldehyde and retinoid receptors agonists, and correlated with a reduced accumulation of RBP4 protein in the culture medium. Tretinoin 26-30 retinol binding protein 4, plasma Mus musculus 46-50
18769064-6 2008 In adipocyte cell models, ATRA down-regulated RBP4 mRNA levels in a dose-dependent manner: this effect was reproduced by retinaldehyde and retinoid receptors agonists, and correlated with a reduced accumulation of RBP4 protein in the culture medium. Tretinoin 26-30 retinol binding protein 4, plasma Mus musculus 214-218
18769064-7 2008 CONCLUSION: These results reveal a selective effect of ATRA inhibiting RBP4 expression specifically in adipocytes, and reinforce the concept that vitamin A vitamers may affect insulin sensitivity through effects on adipokine production. Tretinoin 55-59 retinol binding protein 4, plasma Mus musculus 71-75
17727842-6 2008 ATRA treatment (10 microM) resulted in a 59.9+/-9.8% increase (p<0.05) in the BrdU labeling index in K10/FLAG-CRABPI TG(+) mice vs. TG(-) mice. Tretinoin 0-4 cellular retinoic acid binding protein I Mus musculus 113-119
17828619-4 2008 In in vitro culture, all-transretinoic acid promoted the maturation from CD4+CD8+ cells to CD4+ cells but inhibited the differentiation from CD4+CD8+ cells to CD8+ cells. Tretinoin 25-43 CD8a molecule Homo sapiens 77-80
17828619-4 2008 In in vitro culture, all-transretinoic acid promoted the maturation from CD4+CD8+ cells to CD4+ cells but inhibited the differentiation from CD4+CD8+ cells to CD8+ cells. Tretinoin 25-43 CD8a molecule Homo sapiens 145-148
17828619-4 2008 In in vitro culture, all-transretinoic acid promoted the maturation from CD4+CD8+ cells to CD4+ cells but inhibited the differentiation from CD4+CD8+ cells to CD8+ cells. Tretinoin 25-43 CD8a molecule Homo sapiens 145-148
18444141-1 2008 Retinol utilizes a retinoid X receptor (RXR)-mediated degradation pathway to decrease beta-catenin protein in all-trans retinoic acid (ATRA)-resistant human colon cancer cells. Tretinoin 120-133 retinoid X receptor alpha Homo sapiens 19-38
18444141-1 2008 Retinol utilizes a retinoid X receptor (RXR)-mediated degradation pathway to decrease beta-catenin protein in all-trans retinoic acid (ATRA)-resistant human colon cancer cells. Tretinoin 120-133 retinoid X receptor alpha Homo sapiens 40-43
18444141-1 2008 Retinol utilizes a retinoid X receptor (RXR)-mediated degradation pathway to decrease beta-catenin protein in all-trans retinoic acid (ATRA)-resistant human colon cancer cells. Tretinoin 135-139 retinoid X receptor alpha Homo sapiens 19-38
18444141-1 2008 Retinol utilizes a retinoid X receptor (RXR)-mediated degradation pathway to decrease beta-catenin protein in all-trans retinoic acid (ATRA)-resistant human colon cancer cells. Tretinoin 135-139 retinoid X receptor alpha Homo sapiens 40-43
18345250-2 2007 Both retinoids and rexinoids are either natural or synthetic compounds related to retinoic acids that act through interaction with two basic types of nuclear receptors belonging to the nuclear receptor superfamily: All-trans retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 82-96 retinoid X receptor alpha Homo sapiens 309-317
18000064-2 2007 We show that CRABPI (encoding cellular retinoic acid binding protein I) is a target of PLZF, which is fused to RARalpha by the t(11;17)(q23;q21) translocation associated with retinoic acid (RA)-resistant acute promyelocytic leukemia (APL). Tretinoin 14-16 cellular retinoic acid binding protein I Mus musculus 30-70
18000064-2 2007 We show that CRABPI (encoding cellular retinoic acid binding protein I) is a target of PLZF, which is fused to RARalpha by the t(11;17)(q23;q21) translocation associated with retinoic acid (RA)-resistant acute promyelocytic leukemia (APL). Tretinoin 14-16 retinoic acid receptor, alpha Mus musculus 111-119
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 retinoic acid receptor, alpha Mus musculus 58-66
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 retinoic acid receptor, alpha Mus musculus 67-75
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 cellular retinoic acid binding protein I Mus musculus 122-128
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 33-35 retinoic acid receptor, alpha Mus musculus 67-75
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 58-60 retinoic acid receptor, alpha Mus musculus 67-75
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 58-60 cellular retinoic acid binding protein I Mus musculus 122-128
18000064-5 2007 In line with these observations, RA-resistant murine PLZF/RARalpha+RARalpha/PLZF APL blasts express much higher levels of CRABPI than standard RA-sensitive PML/RARalpha APL. Tretinoin 58-60 retinoic acid receptor, alpha Mus musculus 67-75
18000064-6 2007 RARalpha-PLZF confers RA resistance to a retinoid-sensitive acute myeloid leukemia (AML) cell line in a CRABPI-dependent fashion. Tretinoin 0-2 cellular retinoic acid binding protein I Mus musculus 104-110
17646067-6 2007 These cultures can be expanded in vitro for several months and differentiating markers such as ATOH1/HATH1 and POU4F3/BRN3C can be induced by manipulating the culture conditions using specific growth factors such as bFGF, EGF and retinoic acid. Tretinoin 230-243 atonal bHLH transcription factor 1 Homo sapiens 95-100
17715133-0 2007 NMR solution structure of lipocalin-type prostaglandin D synthase: evidence for partial overlapping of catalytic pocket and retinoic acid-binding pocket within the central cavity. Tretinoin 124-137 prostaglandin D2 synthase (brain) Mus musculus 26-65
17715133-8 2007 These results indicated that the two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS were responsible for the broad ligand specificity of L-PGDS and the non-competitive inhibition of L-PGDS activity by retinoic acid. Tretinoin 66-79 prostaglandin D2 synthase (brain) Mus musculus 103-109
17715133-8 2007 These results indicated that the two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS were responsible for the broad ligand specificity of L-PGDS and the non-competitive inhibition of L-PGDS activity by retinoic acid. Tretinoin 66-79 prostaglandin D2 synthase (brain) Mus musculus 163-169
17715133-8 2007 These results indicated that the two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS were responsible for the broad ligand specificity of L-PGDS and the non-competitive inhibition of L-PGDS activity by retinoic acid. Tretinoin 66-79 prostaglandin D2 synthase (brain) Mus musculus 163-169
17715133-8 2007 These results indicated that the two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS were responsible for the broad ligand specificity of L-PGDS and the non-competitive inhibition of L-PGDS activity by retinoic acid. Tretinoin 227-240 prostaglandin D2 synthase (brain) Mus musculus 103-109
17715133-8 2007 These results indicated that the two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS were responsible for the broad ligand specificity of L-PGDS and the non-competitive inhibition of L-PGDS activity by retinoic acid. Tretinoin 227-240 prostaglandin D2 synthase (brain) Mus musculus 163-169
17656367-4 2007 Structural overlap of a retinoic acid response element with these retinoid X response elements led to a high affinity binding of retinoic acid receptor/RXR heterodimer to the retinoic acid response element, resulting in the prevention of RXR ligand-mediated p21 transactivation. Tretinoin 24-37 retinoid X receptor alpha Homo sapiens 152-155
17656367-4 2007 Structural overlap of a retinoic acid response element with these retinoid X response elements led to a high affinity binding of retinoic acid receptor/RXR heterodimer to the retinoic acid response element, resulting in the prevention of RXR ligand-mediated p21 transactivation. Tretinoin 24-37 retinoid X receptor alpha Homo sapiens 238-241
17656367-4 2007 Structural overlap of a retinoic acid response element with these retinoid X response elements led to a high affinity binding of retinoic acid receptor/RXR heterodimer to the retinoic acid response element, resulting in the prevention of RXR ligand-mediated p21 transactivation. Tretinoin 129-142 retinoid X receptor alpha Homo sapiens 152-155
17656367-4 2007 Structural overlap of a retinoic acid response element with these retinoid X response elements led to a high affinity binding of retinoic acid receptor/RXR heterodimer to the retinoic acid response element, resulting in the prevention of RXR ligand-mediated p21 transactivation. Tretinoin 129-142 retinoid X receptor alpha Homo sapiens 238-241
17673467-3 2007 Here we showed that treatment of zebrafish expressing a truncated form of Apc with either retinoic acid or a selective COX-2 inhibitor decreased beta-catenin protein levels and downstream signaling events. Tretinoin 90-103 APC regulator of WNT signaling pathway Danio rerio 74-77
17673467-5 2007 These findings support roles for retinoic acid and Cox-2 in regulating the stability of beta-catenin following Apc loss. Tretinoin 33-46 APC regulator of WNT signaling pathway Danio rerio 111-114
17670908-0 2007 LGL1, a novel branching morphogen in developing kidney, is induced by retinoic acid. Tretinoin 70-83 cysteine-rich secretory protein LCCL domain containing 2 Mus musculus 0-4
17670908-4 2007 However, early branching morphogenesis in the lung and kidney is stimulated by retinoic acid, and we identified putative retinoic acid response elements in the Lgl1 promoter. Tretinoin 121-134 cysteine-rich secretory protein LCCL domain containing 2 Mus musculus 160-164
17670908-5 2007 All-trans-retinoic acid (10(-6) M) stimulated Lgl1 promoter activity and endogenous Lgl1 mRNA expression in vitro. Tretinoin 0-23 cysteine-rich secretory protein LCCL domain containing 2 Mus musculus 46-50
17670908-5 2007 All-trans-retinoic acid (10(-6) M) stimulated Lgl1 promoter activity and endogenous Lgl1 mRNA expression in vitro. Tretinoin 0-23 cysteine-rich secretory protein LCCL domain containing 2 Mus musculus 84-88
17670908-9 2007 We propose a model in which retinoic acid stimulates branching morphogenesis by activating Lgl1 early in development. Tretinoin 28-41 cysteine-rich secretory protein LCCL domain containing 2 Mus musculus 91-95
17893708-8 2007 By contrast, upregulation of Rig-I in NB4 cells that are treated with ATRA is accompanied by elevated G alpha i2 expression. Tretinoin 70-74 DExD/H-box helicase 58 Homo sapiens 29-34
19486889-6 2009 Collectively, our results indicate that ATRA induces HDAC2 phosphorylation mediated by JNK signaling, and thus causes HDAC2 dissociation from KLF4, subsequently leading to the increase in KLF4 acetylation. Tretinoin 40-44 Kruppel like factor 4 Homo sapiens 188-192
19877527-8 2009 AtRA supplementation inhibited the increase in IRP2 mRNA expression. Tretinoin 0-4 iron responsive element binding protein 2 Rattus norvegicus 47-51
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 20-33 aldehyde dehydrogenase 1 family member A2 Homo sapiens 107-113
19294396-1 2009 The biosynthesis of retinoic acid (RA) from retinol is controlled by several enzymes, e.g. dehydrogenases (RalDH2, RoDH-4) and retinol-esterifying enzyme (LRAT), whereas its degradation mainly involves CYP26 enzymes. Tretinoin 35-37 aldehyde dehydrogenase 1 family member A2 Homo sapiens 107-113
19357873-3 2009 Therefore, a rat model of GS was established to investigate the effect of all-trans retinoic acid (ATRA) on the renal expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Tretinoin 99-103 matrix metallopeptidase 9 Rattus norvegicus 169-195
19357873-12 2009 ATRA and benazepril also significantly down-regulated Col-IV, FN expression and TIMP-1 expression (protein and mRNA) (P < 0.05). Tretinoin 0-4 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 80-86
19357873-15 2009 In conclusion, ATRA may protect renal function and step down the progression of GS by reducing the expression of TIMP-1, enhancing the expression and activity of MMP-2 and MMP-9, and regulating the ratio of MMPs/TIMPs to dynamic balance, so as to reduce the accumulation of ECM. Tretinoin 15-19 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 113-119
19357873-15 2009 In conclusion, ATRA may protect renal function and step down the progression of GS by reducing the expression of TIMP-1, enhancing the expression and activity of MMP-2 and MMP-9, and regulating the ratio of MMPs/TIMPs to dynamic balance, so as to reduce the accumulation of ECM. Tretinoin 15-19 matrix metallopeptidase 9 Rattus norvegicus 172-177
19156818-1 2009 The binding of retinoic acid to mutants of Cellular Retinoic Acid Binding Protein II (CRABPII) was evaluated to better understand the importance of the direct protein/ligand interactions. Tretinoin 15-28 cellular retinoic acid binding protein 2 Homo sapiens 43-84
19156818-1 2009 The binding of retinoic acid to mutants of Cellular Retinoic Acid Binding Protein II (CRABPII) was evaluated to better understand the importance of the direct protein/ligand interactions. Tretinoin 15-28 cellular retinoic acid binding protein 2 Homo sapiens 86-93
19156818-3 2009 Furthermore, retinoic acid binding to CRABPII mutants that lack all previously identified interacting amino acids was rescued by providing a carboxylic acid dimer partner in the form of a Glu residue. Tretinoin 13-26 cellular retinoic acid binding protein 2 Homo sapiens 38-45
19417068-7 2009 FHL2 expression was remarkably up-regulated during retinoic acid-induced differentiation of neuroblastoma cells, during which the expression of Id2 was opposite to that. Tretinoin 51-64 inhibitor of DNA binding 2 Homo sapiens 144-147
19464179-1 2009 Retinoic acid (RA) is thought to be a key signaling molecule involved in limb bud patterning along the proximodistal or anteroposterior axes functioning through induction of Meis2 and Shh, respectively. Tretinoin 0-13 Meis homeobox 2 Mus musculus 174-179
19464179-1 2009 Retinoic acid (RA) is thought to be a key signaling molecule involved in limb bud patterning along the proximodistal or anteroposterior axes functioning through induction of Meis2 and Shh, respectively. Tretinoin 15-17 Meis homeobox 2 Mus musculus 174-179
19464179-4 2009 We provide evidence for a model of trunk mesodermal RA action in which forelimb induction requires RA repression of Fgf8 in the developing trunk similar to how RA controls somitogenesis and heart development. Tretinoin 52-54 fibroblast growth factor 8 Mus musculus 116-120
19464179-4 2009 We provide evidence for a model of trunk mesodermal RA action in which forelimb induction requires RA repression of Fgf8 in the developing trunk similar to how RA controls somitogenesis and heart development. Tretinoin 99-101 fibroblast growth factor 8 Mus musculus 116-120
19464179-4 2009 We provide evidence for a model of trunk mesodermal RA action in which forelimb induction requires RA repression of Fgf8 in the developing trunk similar to how RA controls somitogenesis and heart development. Tretinoin 99-101 fibroblast growth factor 8 Mus musculus 116-120
19464179-7 2009 Our findings suggest that RA signaling is not required for limb proximodistal or anteroposterior patterning but that RA inhibition of FGF8 signaling during the early stages of body axis extension provides an environment permissive for induction of forelimb buds. Tretinoin 117-119 fibroblast growth factor 8 Mus musculus 134-138
18752469-1 2009 Signalling by small molecules, such as retinoic acid, is mediated by heterodimers comprising a class II nuclear receptor and an RXR (retinoid X receptor) subunit. Tretinoin 39-52 retinoid X receptor alpha Homo sapiens 128-131
18752469-1 2009 Signalling by small molecules, such as retinoic acid, is mediated by heterodimers comprising a class II nuclear receptor and an RXR (retinoid X receptor) subunit. Tretinoin 39-52 retinoid X receptor alpha Homo sapiens 133-152
19306865-5 2009 We also provide evidence that Hoxd11 suppresses the expression of Hoxd10 and the retinoic acid synthetic enzyme, retinaldehyde dehydrogenase 2 (RALDH2). Tretinoin 81-94 aldehyde dehydrogenase 1 family member A2 Gallus gallus 144-150
19508691-7 2009 Treatment of aphakia embryonic stem cell cultures with retinoic acid resulted in a significant increase in mesodiencephalic tyrosine hydroxylase-positive neurons, providing further support for the role of Pitx3 in dopaminergic neuron specification through the retinoic acid pathway. Tretinoin 55-68 paired-like homeodomain transcription factor 3 Mus musculus 205-210
19508691-7 2009 Treatment of aphakia embryonic stem cell cultures with retinoic acid resulted in a significant increase in mesodiencephalic tyrosine hydroxylase-positive neurons, providing further support for the role of Pitx3 in dopaminergic neuron specification through the retinoic acid pathway. Tretinoin 260-273 paired-like homeodomain transcription factor 3 Mus musculus 205-210
19332534-6 2009 Expression of IL4, IL13, IL1B, IL6, CCL11, and CCL26 was increased in the lungs of infected pigs treated with ATRA. Tretinoin 110-114 interleukin 4 Sus scrofa 14-17
22666666-7 2009 Treatment with stem cell factor (SCF), nerve growth factor (NGF), retinoic acid (RA) or dimethyl sulphoxide (DMSO) enhanced CD23 expression in HT29 cells. Tretinoin 81-83 KIT ligand Homo sapiens 15-31
17595318-3 2007 Activation of PI3K by RA appears to involve the classical nuclear receptor, retinoic acid receptor (RAR), on the basis of the pharmacological profile of the activation, loss, and gain of function experiments with mouse embryo fibroblast-RAR(alpha beta gamma)(L-/L-) null cells, and the physical association between liganded RAR and PI3K activity. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 76-98
17595318-3 2007 Activation of PI3K by RA appears to involve the classical nuclear receptor, retinoic acid receptor (RAR), on the basis of the pharmacological profile of the activation, loss, and gain of function experiments with mouse embryo fibroblast-RAR(alpha beta gamma)(L-/L-) null cells, and the physical association between liganded RAR and PI3K activity. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 100-103
17595318-3 2007 Activation of PI3K by RA appears to involve the classical nuclear receptor, retinoic acid receptor (RAR), on the basis of the pharmacological profile of the activation, loss, and gain of function experiments with mouse embryo fibroblast-RAR(alpha beta gamma)(L-/L-) null cells, and the physical association between liganded RAR and PI3K activity. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 237-240
17595318-3 2007 Activation of PI3K by RA appears to involve the classical nuclear receptor, retinoic acid receptor (RAR), on the basis of the pharmacological profile of the activation, loss, and gain of function experiments with mouse embryo fibroblast-RAR(alpha beta gamma)(L-/L-) null cells, and the physical association between liganded RAR and PI3K activity. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 237-240
17595318-5 2007 Immunoprecipitation experiments performed in SH-SY5Y cells showed stable association between RARalpha and p85, the regulatory subunit of PI3K, independently of the presence of RA. Tretinoin 93-95 phosphoinositide-3-kinase regulatory subunit 2 Homo sapiens 106-109
17805463-0 2007 Modulation of Dishevelled and Vangl2 by all-trans-retinoic acid in the developing mouse central nervous system and its relationship to teratogenesis. Tretinoin 40-63 VANGL planar cell polarity 2 Mus musculus 30-36
17805463-3 2007 The effects of RA-mediated teratogenesis might be due to its misregulation of Vangl2 and Dishevelled genes. Tretinoin 15-17 VANGL planar cell polarity 2 Mus musculus 78-84
17805463-7 2007 RA treatment also led to a pronounced decrease of Vangl2 mRNA at 4 and 18 h and a pronounced increase at 66 h after maternal treatment, as detected by reverse transcription-polymerase chain reaction. Tretinoin 0-2 VANGL planar cell polarity 2 Mus musculus 50-56
17805463-9 2007 Dishevelled1/2/3 mRNA was significantly down-regulated at 4 and 18 h and up-regulated at 42 h in the fetus after RA treatment, except for an up-regulation of Dishevelled3 at 66 h. The Dishevelled2 mRNA and its protein matched each other. Tretinoin 113-115 dishevelled segment polarity protein 1 Mus musculus 0-16
17884779-4 2007 RESULTS: Tretinoin induced obvious changes in bone structure and contents of bone calcium and other elements, causing also significantly increased tartrate-resistant acid phosphatase (TRAP) and alkaline phosphatase (AKP), which suggested the development of osteoporosis. Tretinoin 9-18 acid phosphatase 5, tartrate resistant Rattus norvegicus 147-182
17884779-4 2007 RESULTS: Tretinoin induced obvious changes in bone structure and contents of bone calcium and other elements, causing also significantly increased tartrate-resistant acid phosphatase (TRAP) and alkaline phosphatase (AKP), which suggested the development of osteoporosis. Tretinoin 9-18 acid phosphatase 5, tartrate resistant Rattus norvegicus 184-188
11700306-2 2002 Expression of the constitutively activated (Q226L) GTPase-deficient form of Galpha13 mimics retinoic acid and was used to investigate the signaling upstream of primitive endoderm formation. Tretinoin 92-105 guanine nucleotide binding protein, alpha 13 Mus musculus 76-84
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 41-54 mediator complex subunit 25 Homo sapiens 12-17
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 41-54 retinoid X receptor alpha Homo sapiens 183-186
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 56-58 mediator complex subunit 25 Homo sapiens 12-17
11836298-0 2002 Divergent effects of retinoic acids on the expression of ERalpha and 17beta-hydroxysteroid dehydrogenase type 2 in endometrial carcinoma cells (RL 95-2). Tretinoin 21-35 hydroxysteroid 17-beta dehydrogenase 2 Homo sapiens 69-111
17641689-1 2007 We isolated MED25, which associates with retinoic acid (RA)-bound retinoic acid receptor (RAR) through the C-terminal nuclear hormone receptor (NR) box/LxxLL motif, and increases RAR/RXR-mediated transcription. Tretinoin 56-58 retinoid X receptor alpha Homo sapiens 183-186
17641689-5 2007 Stimulation of RAR by MED25 was correlated with enhanced RA cytotoxicity in vivo. Tretinoin 15-17 mediator complex subunit 25 Homo sapiens 22-27
17431131-1 2007 Palladin was originally found up-regulated with NB4 cell differentiation induced by all-trans retinoic acid. Tretinoin 94-107 palladin, cytoskeletal associated protein Homo sapiens 0-8
19380308-4 2009 Retinaldehyde dehydrogenase 2 (RALDH2) is required to activate RA signaling at the onset of gastrulation. Tretinoin 31-33 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-29
19476501-5 2009 Furthermore, ATRA demonstrates substrate specificity for beta-site amyloid precursor protein-cleaving enzyme (BACE) 1 over nonamyloidogenic BACE2 in beta-secretase regulation, which probably promotes competition for amyloid precursor protein between ADAM17 and BACE1. Tretinoin 13-17 beta-secretase 2 Homo sapiens 140-145
19476501-5 2009 Furthermore, ATRA demonstrates substrate specificity for beta-site amyloid precursor protein-cleaving enzyme (BACE) 1 over nonamyloidogenic BACE2 in beta-secretase regulation, which probably promotes competition for amyloid precursor protein between ADAM17 and BACE1. Tretinoin 13-17 ADAM metallopeptidase domain 17 Homo sapiens 250-256
12015078-5 2002 (2) After treatment with ATRA, the fusion protein disappeared and PML protein resumed in NB4 cells, while in HL-60 and K562 cells there was no difference from control cells. Tretinoin 25-29 PML nuclear body scaffold Homo sapiens 66-69
19285077-1 2009 To examine the function of SIRT1 in neuronal differentiation, we employed all-trans retinoic acid (ATRA)-induced differentiation of neuroblastoma cells. Tretinoin 99-103 sirtuin 1 Homo sapiens 27-32
19285077-6 2009 SIRT1 and FOXO3a siRNA inhibited ATRA-induced up-regulation of TH and differentiation. Tretinoin 33-37 sirtuin 1 Homo sapiens 0-5
17847715-3 2007 Here, we show that buttermilk xanthine oxidase was capable to oxidizing all-trans-retinol (t-ROL) to all-trans-retinaldehyde (t-RAL) that was successively oxidized to all-trans-retinoic acid (t-RA). Tretinoin 167-190 RAS like proto-oncogene A Homo sapiens 128-131
17297443-3 2007 GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. Tretinoin 84-97 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 0-7
11777343-5 2002 All-trans-retinoic acid (ATRA) treatment of HPV-immortalized HEN-16-2 cells and transformed/MDR HEN-16-2/CDDP cells inhibited telomerase activity and downregulated expression of hTERT mRNAs containing full-length functional and a defective RT motif, but there were no changes in hTR and TP1 expression. Tretinoin 0-23 telomerase reverse transcriptase Homo sapiens 178-183
17478430-11 2007 Retinoic acid, which induces teratogenic effects similarly to ethanol, also caused up-regulation of ABCA1 and ABCG1. Tretinoin 0-13 ATP binding cassette subfamily A member 1 Rattus norvegicus 100-105
19285077-7 2009 Taken together, these results indicate that SIRT1 is involved in ATRA-induced differentiation of neuroblastoma cells via FOXO3a. Tretinoin 65-69 sirtuin 1 Homo sapiens 44-49
11777343-5 2002 All-trans-retinoic acid (ATRA) treatment of HPV-immortalized HEN-16-2 cells and transformed/MDR HEN-16-2/CDDP cells inhibited telomerase activity and downregulated expression of hTERT mRNAs containing full-length functional and a defective RT motif, but there were no changes in hTR and TP1 expression. Tretinoin 25-29 telomerase reverse transcriptase Homo sapiens 178-183
19144990-6 2009 Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes. Tretinoin 45-47 integrin subunit alpha M Homo sapiens 225-230
17335046-5 2007 RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Tretinoin 53-55 fibroblast growth factor 8 Mus musculus 199-203
11930660-11 2002 This implies that there may be a pathway other than PML/RAR alpha fusion gene product which mediates ATRA-induced myeloid maturation in leukemia cells. Tretinoin 101-105 PML nuclear body scaffold Homo sapiens 52-65
17335046-5 2007 RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Tretinoin 53-55 trans-acting transcription factor 8 Mus musculus 217-220
17335046-5 2007 RESULTS: In the C57BL/6N limb bud following maternal RA administration, gene-specific perturbations were observed within hours of the RA injection in the posterior pre-AER (apical ectodermal ridge) (Fgf8, Dlx3, Bmp4, Sp8, but not Dlx2 or p63), whereas these genes were normally expressed in the SWV/Fnn limb bud. Tretinoin 53-55 distal-less homeobox 2 Mus musculus 230-234
17512397-3 2007 (2007) demonstrate that retinoic acid also activates the peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta). Tretinoin 24-37 peroxisome proliferator activated receptor delta Homo sapiens 57-110
17512397-3 2007 (2007) demonstrate that retinoic acid also activates the peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta). Tretinoin 24-37 peroxisome proliferator activated receptor delta Homo sapiens 112-120
17512397-4 2007 Remarkably, retinoic acid signaling through RAR or PPARbeta/delta-which depends on cytoplasmic retinoic acid transporters-commits the cell to opposite fates, apoptosis or survival, respectively. Tretinoin 12-25 peroxisome proliferator activated receptor delta Homo sapiens 51-59
17512406-3 2007 Here, we show that, in addition to functioning through RAR, RA activates the "orphan" nuclear receptor PPARbeta/delta, which, in turn, induces the expression of prosurvival genes. Tretinoin 55-57 peroxisome proliferator activated receptor delta Homo sapiens 103-111
19122199-0 2009 Retinoic acid-induced gene-1 (RIG-I) associates with the actin cytoskeleton via caspase activation and recruitment domain-dependent interactions. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 30-35
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 10-23 aldehyde dehydrogenase 1 family member A2 Homo sapiens 98-104
19171200-1 2009 All-trans retinoic acid (RA) levels are controlled by enzymes of the vitamin A metabolism (RDH16, RalDH2, and LRAT) and RA catabolism (CYP26 and CYP2S1). Tretinoin 25-27 aldehyde dehydrogenase 1 family member A2 Homo sapiens 98-104
19171200-4 2009 RA (1 microM) induced CYP26A1, CYP26B1, CYP2S1, CRABPII and LRAT mRNA. Tretinoin 0-2 cellular retinoic acid binding protein 2 Homo sapiens 48-55
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 246-249
19764350-10 2009 In addition, our results also indicated that Cdk5 activity was involved in RA-induced HeLa apoptosis by detecting cleavages of caspase-3 and its substrate, PARP (poly (ADP-ribose) polymerases) Interestingly, the nuclear localizations of Cdk5 and p35 proteins were increased by RA treatment, which, again, suggests the involvement of Cdk5 and p35 in RA-induced apoptotic effects. Tretinoin 75-77 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 342-345
17512406-4 2007 Partitioning of RA between the two receptors is regulated by the intracellular lipid binding proteins CRABP-II and FABP5. Tretinoin 16-18 cellular retinoic acid binding protein 2 Homo sapiens 102-110
17512406-4 2007 Partitioning of RA between the two receptors is regulated by the intracellular lipid binding proteins CRABP-II and FABP5. Tretinoin 16-18 fatty acid binding protein 5 Homo sapiens 115-120
17512406-5 2007 These proteins specifically deliver RA from the cytosol to nuclear RAR and PPARbeta/delta, respectively, thereby selectively enhancing the transcriptional activity of their cognate receptors. Tretinoin 36-38 peroxisome proliferator activated receptor delta Homo sapiens 75-83
19176369-2 2009 ATRA-induced phosphorylation of the Akt kinase and ribosomal S6 protein in APL cells was sensitive to class I PI3K, and p110beta or p110delta inhibitors, and to the mammalian target of rapamycin (mTOR) inhibitor rapamycin. Tretinoin 0-4 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta Homo sapiens 120-128
17512406-6 2007 Consequently, RA functions through RAR and is a proapoptotic agent in cells with high CRABP-II/FABP5 ratio, but it signals through PPARbeta/delta and promotes survival in cells that highly express FABP5. Tretinoin 14-16 cellular retinoic acid binding protein 2 Homo sapiens 86-94
19176369-6 2009 In summary, class I PI3K signaling, mediated by p110beta and p110delta, plays an important role in basal and ATRA-induced cell survival mechanisms in APL. Tretinoin 109-113 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta Homo sapiens 48-56
11968022-11 2002 Leptin also protected against RA-induced apoptosis, as estimated by soluble DNA fractions and DNA laddering patterns subsequent to 10 days of culture. Tretinoin 30-32 leptin Homo sapiens 0-6
17512406-6 2007 Consequently, RA functions through RAR and is a proapoptotic agent in cells with high CRABP-II/FABP5 ratio, but it signals through PPARbeta/delta and promotes survival in cells that highly express FABP5. Tretinoin 14-16 fatty acid binding protein 5 Homo sapiens 95-100
17512406-6 2007 Consequently, RA functions through RAR and is a proapoptotic agent in cells with high CRABP-II/FABP5 ratio, but it signals through PPARbeta/delta and promotes survival in cells that highly express FABP5. Tretinoin 14-16 peroxisome proliferator activated receptor delta Homo sapiens 131-139
17512406-6 2007 Consequently, RA functions through RAR and is a proapoptotic agent in cells with high CRABP-II/FABP5 ratio, but it signals through PPARbeta/delta and promotes survival in cells that highly express FABP5. Tretinoin 14-16 fatty acid binding protein 5 Homo sapiens 197-202
19010342-10 2009 Chemical and immuno-inhibition metabolism studies suggested that Cyp26a1, Cyp2b, and Cyp3a, but not Cyp1a1 proteins were involved in atRA metabolism. Tretinoin 133-137 cytochrome P450, family 3, subfamily a, polypeptide 11 Mus musculus 85-90
11851886-8 2002 These data suggest that p63 expression in human keratinocytes is affected by all-trans retinoic acid and this influence might contribute to the fine tuned keratinocyte proliferation and differentiation equilibrium in the mammalian epidermis. Tretinoin 87-100 tumor protein p63 Homo sapiens 24-27
19540457-1 2009 All-trans-retinoic acid (atRA) appears to affect Th1-Th2 differentiation and its effects on immune responses might also be mediated by dendritic cell (DC). Tretinoin 0-23 negative elongation factor complex member C/D Homo sapiens 49-52
17442359-6 2007 In addition, RA was found to prevent the G(1)/S progression of palatal mesenchymal cells through upregulation of p21(Cip1), leading to Rb hypophospholylation. Tretinoin 13-15 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 113-116
17442359-6 2007 In addition, RA was found to prevent the G(1)/S progression of palatal mesenchymal cells through upregulation of p21(Cip1), leading to Rb hypophospholylation. Tretinoin 13-15 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 117-121
19540457-1 2009 All-trans-retinoic acid (atRA) appears to affect Th1-Th2 differentiation and its effects on immune responses might also be mediated by dendritic cell (DC). Tretinoin 25-29 negative elongation factor complex member C/D Homo sapiens 49-52
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 89-92
17303670-5 2007 The embryonic teratocarcinoma F9 cells, in which differentiation is driven by retinoic acid (RA), express V1-PDGFRbeta, but not wild-type PDGFRbeta. Tretinoin 93-95 platelet derived growth factor receptor beta Rattus norvegicus 109-118
17303670-8 2007 Treatment of F9 cells with RA induced V1-PDGFRbeta gene expression, concomitant with changes in morphology and increased mRNA expression of collagen IV and laminin B1, suggesting that V1-PFGRbeta is involved in cell differentiation. Tretinoin 27-29 platelet derived growth factor receptor beta Rattus norvegicus 41-50
17303670-9 2007 Similarly, treatment of postnatal d 3 rat gonocytes with RA induced a dose-dependent increase in V1-PDGFRbeta expression together with an increase in c-kit and Stra8, markers of more differentiated germ cells and a concomitant decrease in GFRalpha1, a marker of spermatogonial stem cells. Tretinoin 57-59 platelet derived growth factor receptor beta Rattus norvegicus 100-109
17303670-9 2007 Similarly, treatment of postnatal d 3 rat gonocytes with RA induced a dose-dependent increase in V1-PDGFRbeta expression together with an increase in c-kit and Stra8, markers of more differentiated germ cells and a concomitant decrease in GFRalpha1, a marker of spermatogonial stem cells. Tretinoin 57-59 stimulated by retinoic acid 8 Rattus norvegicus 160-165
17303670-10 2007 However, an excess of V1-PDGFRbeta inhibited RA-mediated collagen IV and laminin B1 expression and altered both RA-dependent and RA-independent morphological changes in F9 cells, while increasing cell survival. Tretinoin 45-47 platelet derived growth factor receptor beta Rattus norvegicus 25-34
17303670-10 2007 However, an excess of V1-PDGFRbeta inhibited RA-mediated collagen IV and laminin B1 expression and altered both RA-dependent and RA-independent morphological changes in F9 cells, while increasing cell survival. Tretinoin 112-114 platelet derived growth factor receptor beta Rattus norvegicus 25-34
17303670-10 2007 However, an excess of V1-PDGFRbeta inhibited RA-mediated collagen IV and laminin B1 expression and altered both RA-dependent and RA-independent morphological changes in F9 cells, while increasing cell survival. Tretinoin 112-114 platelet derived growth factor receptor beta Rattus norvegicus 25-34
18952085-4 2009 METHODS: The effect of retinoids on the iron metabolism was examined in HuH7 cells treated with all-trans retinoic acid and acyclic retinoid NIK-333. Tretinoin 106-119 MIR7-3 host gene Homo sapiens 72-76
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 89-92
18981221-0 2009 Role of the molybdoflavoenzyme aldehyde oxidase homolog 2 in the biosynthesis of retinoic acid: generation and characterization of a knockout mouse. Tretinoin 81-94 aldehyde oxidase 4 Mus musculus 31-57
18981221-5 2009 Purified AOH2 oxidizes retinaldehyde into retinoic acid, while it is devoid of pyridoxal-oxidizing activity. Tretinoin 42-55 aldehyde oxidase 4 Mus musculus 9-13
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 65-78 retinoic acid receptor alpha Homo sapiens 89-92
17523870-0 2007 The IFN-beta and retinoic acid-induced cell death regulator GRIM-19 is upregulated during focal cerebral ischemia. Tretinoin 17-30 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 60-67
11795432-9 2001 Incubation of RA-treated but not the control cellular extracts with in vitro translated cyclin D1 led to cyclin degradation. Tretinoin 14-16 proliferating cell nuclear antigen Homo sapiens 88-94
17523870-1 2007 The induction of GRIM-19 has been shown to be essential for interferon-beta (IFN-beta)-induced and retinoic acid (RA)-induced tumor cell death. Tretinoin 99-112 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 17-24
17523870-1 2007 The induction of GRIM-19 has been shown to be essential for interferon-beta (IFN-beta)-induced and retinoic acid (RA)-induced tumor cell death. Tretinoin 114-116 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 17-24
17463084-3 2007 The present work reports that TLR3 signaling by polyinosinic-polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8alphaalpha intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. Tretinoin 146-159 interleukin 15 Mus musculus 289-294
19056420-6 2009 The differentiation property of RA was confirmed by showing an extensive outgrowth of neurites, increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin and synaptic associated protein-97, and decreased expression of inhibitor of differentiation-1. Tretinoin 32-34 synaptophysin Homo sapiens 163-176
11767100-0 2001 Characterization of nuclear factors that bind to the human thymidylate synthase gene in HL-60 cells differentiated by all-trans retinoic acid treatment. Tretinoin 128-141 thymidylate synthetase Homo sapiens 59-79
18805411-3 2008 We show that cellular RA-binding proteins CRABP1 and CRABP2 and the fatty acid-binding protein FABP5 are dynamically expressed during skin development and in adult tissue. Tretinoin 22-24 cellular retinoic acid binding protein 2 Homo sapiens 53-59
19081079-0 2008 Hoxb5b acts downstream of retinoic acid signaling in the forelimb field to restrict heart field potential in zebrafish. Tretinoin 26-39 homeobox B5b Danio rerio 0-6
18989765-0 2008 Effects of all-trans retinoic acid on Th1- and Th2-related chemokines production in monocytes. Tretinoin 11-34 negative elongation factor complex member C/D Homo sapiens 38-41
17387344-6 2007 Retinoic acid metabolism blocking agents induced cell differentiation as determined by increased expression of cytokeratin 8/18 and oestrogen receptor-alpha (ER-alpha). Tretinoin 0-13 keratin 8 Homo sapiens 111-156
17306764-0 2007 Retinoic acid activates human inducible nitric oxide synthase gene through binding of RARalpha/RXRalpha heterodimer to a novel retinoic acid response element in the promoter. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 95-103
17306764-0 2007 Retinoic acid activates human inducible nitric oxide synthase gene through binding of RARalpha/RXRalpha heterodimer to a novel retinoic acid response element in the promoter. Tretinoin 127-140 retinoid X receptor alpha Homo sapiens 95-103
17407572-13 2007 Lastly, estrogen affects retinoic acid (RA) synthesis and mobilization by regulating expression of CRABP2 and ALDH1A1. Tretinoin 25-38 cellular retinoic acid binding protein 2 Homo sapiens 99-105
17407572-13 2007 Lastly, estrogen affects retinoic acid (RA) synthesis and mobilization by regulating expression of CRABP2 and ALDH1A1. Tretinoin 40-42 cellular retinoic acid binding protein 2 Homo sapiens 99-105
18989765-7 2008 To survey whether ATRA and ascorbic acid effect Th1- and Th2-related chemokine expression in monocytes. Tretinoin 18-22 negative elongation factor complex member C/D Homo sapiens 48-51
18989765-14 2008 In conclusion, ATRA suppressed Th2- and Th1-related chemokines expression in THP-1 cells, at least in part via the c-Raf-MKK1/2-ERK/MAPK pathway. Tretinoin 15-19 negative elongation factor complex member C/D Homo sapiens 40-43
17329364-3 2007 Although the majority of the early effects of RA can be attributed to the activity of RALDH2, many other effects are suggestive of the presence of an as yet unidentified RA source. Tretinoin 46-48 aldehyde dehydrogenase 1 family member A2 Homo sapiens 86-92
11728801-7 2001 Due to the reactivity of TrxR, the enzyme is inhibited by many clinically used electrophilic compounds including nitrosoureas, aurothioglucose, platinum compounds, and retinoic acid derivatives. Tretinoin 168-181 peroxiredoxin 5 Homo sapiens 25-29
17272500-5 2007 We used Q(2)ChIP to monitor changes in histone H3 modifications on the 5" regulatory regions of the developmentally regulated genes OCT4, NANOG, LMNA, and PAX6 in the context of retinoic-acid-mediated human embryonal carcinoma cell differentiation. Tretinoin 178-191 Nanog homeobox Homo sapiens 138-143
17491551-1 2007 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RARalpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as ligand-activated, DNA-binding, transacting, transcription-modulating proteins involved in a general molecular mechanism responsible for transcriptional responses in target genes. Tretinoin 57-70 retinoid X receptor alpha Homo sapiens 226-234
19176038-3 2008 RESULTS: The combination of 5 nmol/L bufalin and 30 nmol/L ATRA induced HL-60 cells differentiation in a time-dependent manner, the percentages of CD11b positive cells treated for 2 d and 4 d being (20.0 +/- 2.8)% and (75.0 +/- 5.3)%, respectively, with the increasing of cellular adherence ability. Tretinoin 59-63 integrin subunit alpha M Homo sapiens 147-152
18495959-6 2008 RA generated by RALDH2 in basophils modulates IL-3-induced gene expression in an autocrine manner, providing positive (CD25) as well as negative (granzyme B) regulation. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 16-22
18701617-0 2008 Ligand-mediated regulation of peroxisome proliferator-activated receptor (PPAR) beta/delta: a comparative analysis of PPAR-selective agonists and all-trans retinoic acid. Tretinoin 156-169 peroxisome proliferator activated receptor delta Homo sapiens 30-84
11746830-0 2001 Decreased mitogenic response to epidermal growth factor in human squamous cell carcinoma lines overexpressing epidermal growth factor receptor owing to limiting amounts of the adaptor protein Grb2: rescue by retinoic acid treatment. Tretinoin 208-221 epidermal growth factor Homo sapiens 32-55
18701617-2 2008 It is noteworthy that all trans-retinoic acid (atRA) has recently been reported to act as a ligand for PPARbeta/delta, to activate its transcriptional activity, and, in contrast to the "classic" function of atRA, to stimulate cell proliferation (Schug et al., 2007). Tretinoin 26-45 peroxisome proliferator activated receptor delta Homo sapiens 103-117
18701617-2 2008 It is noteworthy that all trans-retinoic acid (atRA) has recently been reported to act as a ligand for PPARbeta/delta, to activate its transcriptional activity, and, in contrast to the "classic" function of atRA, to stimulate cell proliferation (Schug et al., 2007). Tretinoin 47-51 peroxisome proliferator activated receptor delta Homo sapiens 103-117
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 40-53 retinoid X receptor alpha Homo sapiens 84-87
18632758-4 2008 Combining MN1 expression with all-trans retinoic acid (ATRA), the ligand of the RAR/RXR dimer, showed that MN1 could both enhance and repress ATRA effects. Tretinoin 55-59 retinoid X receptor alpha Homo sapiens 84-87
17235257-15 2007 CONCLUSIONS: IL-8 and GRO-alpha secreted from alveolar epithelial cells play an important role in the cell-cell interaction involved in the chemotactic transmigration of ATRA-treated APL cells toward alveolar epithelial cells. Tretinoin 170-174 C-X-C motif chemokine ligand 1 Homo sapiens 22-31
17170094-9 2007 The ATRA-induced tube formation was completely abolished by coincubation with vascular endothelial growth factor (VEGF) neutralizing antibody or with VEGF receptor (VEGFR)-2 (KDR) neutralizing antibody, but not VEGFR-1 (Flt-1) neutralizing antibody. Tretinoin 4-8 kinase insert domain receptor Homo sapiens 150-163
17170094-9 2007 The ATRA-induced tube formation was completely abolished by coincubation with vascular endothelial growth factor (VEGF) neutralizing antibody or with VEGF receptor (VEGFR)-2 (KDR) neutralizing antibody, but not VEGFR-1 (Flt-1) neutralizing antibody. Tretinoin 4-8 kinase insert domain receptor Homo sapiens 165-170
17170094-9 2007 The ATRA-induced tube formation was completely abolished by coincubation with vascular endothelial growth factor (VEGF) neutralizing antibody or with VEGF receptor (VEGFR)-2 (KDR) neutralizing antibody, but not VEGFR-1 (Flt-1) neutralizing antibody. Tretinoin 4-8 kinase insert domain receptor Homo sapiens 175-178
11746830-5 2001 The vitamin A metabolite retinoic acid (RA) has been used as a chemotherapeutic drug in the treatment of SCC. Tretinoin 25-38 serpin family B member 3 Homo sapiens 105-108
11746830-5 2001 The vitamin A metabolite retinoic acid (RA) has been used as a chemotherapeutic drug in the treatment of SCC. Tretinoin 40-42 serpin family B member 3 Homo sapiens 105-108
17267746-9 2007 Finally, 4-wk treatment with all-trans retinoic acid restored the impaired endothelium-dependent vasodilation and reversed the expression of eNOS but not DDAH-II. Tretinoin 39-52 nitric oxide synthase 3 Canis lupus familiaris 141-145
18781795-3 2008 Here we report two monomethylated residues, Lys (109) and Lys (171) identified by LC-ESI-MS/MS in the DNA binding domain (DBD) and the hinge region, which affect retinoic acid (RA) sensitivity, coregulator interaction and heterodimerization with retinoid X receptor (RXR) in the context of the full-length protein. Tretinoin 162-175 retinoid X receptor alpha Homo sapiens 246-265
11746830-7 2001 However, we previously found that treatment of SCC lines with inhibitory doses of RA sensitized cells to the proliferative effects of EGF. Tretinoin 82-84 serpin family B member 3 Homo sapiens 47-50
18781795-3 2008 Here we report two monomethylated residues, Lys (109) and Lys (171) identified by LC-ESI-MS/MS in the DNA binding domain (DBD) and the hinge region, which affect retinoic acid (RA) sensitivity, coregulator interaction and heterodimerization with retinoid X receptor (RXR) in the context of the full-length protein. Tretinoin 162-175 retinoid X receptor alpha Homo sapiens 267-270
18781795-3 2008 Here we report two monomethylated residues, Lys (109) and Lys (171) identified by LC-ESI-MS/MS in the DNA binding domain (DBD) and the hinge region, which affect retinoic acid (RA) sensitivity, coregulator interaction and heterodimerization with retinoid X receptor (RXR) in the context of the full-length protein. Tretinoin 177-179 retinoid X receptor alpha Homo sapiens 246-265
11746830-7 2001 However, we previously found that treatment of SCC lines with inhibitory doses of RA sensitized cells to the proliferative effects of EGF. Tretinoin 82-84 epidermal growth factor Homo sapiens 134-137
18781795-3 2008 Here we report two monomethylated residues, Lys (109) and Lys (171) identified by LC-ESI-MS/MS in the DNA binding domain (DBD) and the hinge region, which affect retinoic acid (RA) sensitivity, coregulator interaction and heterodimerization with retinoid X receptor (RXR) in the context of the full-length protein. Tretinoin 177-179 retinoid X receptor alpha Homo sapiens 267-270
17253143-7 2007 The addition of atRA to cell cultures potentiated the LPS-induced IL-10 mRNA expression and the number of IL-10 secreting cells from THP-1 cells and cord blood mononuclear cells. Tretinoin 16-20 interleukin 10 Homo sapiens 66-71
11746830-11 2001 RA also inhibited autocrine secretion of EGF, which returned to basal levels with slower kinetics. Tretinoin 0-2 epidermal growth factor Homo sapiens 41-44
11698455-3 2001 In retinoic acid-differentiated HL-60 cells, cross-linking of FcgammaRs resulted in a marked increase in the tyrosine phosphorylation of FcgammaRIIa, p58(lyn), and p120(c-cbl), which was inhibited by a specific inhibitor of Src family protein tyrosine kinases. Tretinoin 3-16 Cbl proto-oncogene Homo sapiens 169-174
17332617-6 2007 After incubation with 10(-6) mol/L ATRA, the mRNA level in Rad-NIS-infected MCF-7 cells increased to 118.5 times that of wild-type MCF-7 cells, whereas the mRNA level in wild-type MCF-7 cells showed only a 2.1-fold increase. Tretinoin 35-39 RRAD, Ras related glycolysis inhibitor and calcium channel regulator Homo sapiens 59-62
17332617-7 2007 Western blot, immunocytochemical staining, and flow cytometry analyses showed that NIS protein expression in MCF-7 cells infected with Rad-NIS increased after ATRA treatment. Tretinoin 159-163 RRAD, Ras related glycolysis inhibitor and calcium channel regulator Homo sapiens 135-138
17332617-11 2007 Treatment of Rad-NIS-infected cells with 10(-8), 10(-7), and 10(-6) mol/L ATRA increased (125)I uptake by 4.9-, 8.2-, and 27.6-fold, respectively, compared with wild-type MCF-7 cells. Tretinoin 74-78 RRAD, Ras related glycolysis inhibitor and calcium channel regulator Homo sapiens 13-16
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 86-90 RRAD, Ras related glycolysis inhibitor and calcium channel regulator Homo sapiens 31-34
17332617-12 2007 The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. Tretinoin 188-192 RRAD, Ras related glycolysis inhibitor and calcium channel regulator Homo sapiens 31-34
18282598-0 2008 Effect of the combination of ATRA, ATO and DNR on CD11b expression in NB4 cells. Tretinoin 29-33 integrin subunit alpha M Homo sapiens 50-55
18789152-0 2008 Enhancement of docetaxel-induced cytotoxicity and apoptosis by all-trans retinoic acid (ATRA) through downregulation of survivin (BIRC5), MCL-1 and LTbeta-R in hormone- and drug resistant prostate cancer cell line, DU-145. Tretinoin 67-86 baculoviral IAP repeat containing 5 Homo sapiens 130-135
18789152-0 2008 Enhancement of docetaxel-induced cytotoxicity and apoptosis by all-trans retinoic acid (ATRA) through downregulation of survivin (BIRC5), MCL-1 and LTbeta-R in hormone- and drug resistant prostate cancer cell line, DU-145. Tretinoin 88-92 baculoviral IAP repeat containing 5 Homo sapiens 130-135
18789152-11 2008 We have found out that docetaxel-ATRA combination significantly downregulates survivin (BIRC5), myeloid cell leukemia-1 (MCL-1) and lymphotoxin beta-receptor (LTbetaR) genes, which all three have pivotal roles in regulation of apoptosis and cell cycle progression. Tretinoin 33-37 baculoviral IAP repeat containing 5 Homo sapiens 88-93
17067568-2 2007 Although both CYP26A1 and CYP26C1, retinoic acid-degrading enzymes that are expressed at the anterior end of the gastrulating mouse embryo, have been thought to play an important role in central nervous system patterning, the detailed mechanism of their contribution has remained largely unknown. Tretinoin 35-48 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 26-33
11911279-0 2001 Remodeling of vimentin cytoskeleton correlates with enhanced motility of promyelocytic leukemia cells during differentiation induced by retinoic acid. Tretinoin 136-149 vimentin Homo sapiens 14-22
17283134-5 2007 In the present study, we showed that overexpression of XAB2 inhibited ATRA-induced cellular differentiation in human rhabdomyosarcoma cell line, and that knockdown of XAB2 by small interfering RNA (siRNA) increased ATRA-sensitive cellular differentiation in the human promyelocytic leukemia cell line HL60 at both physiologic (10(-9)-10(-8) mol/L) and therapeutic (10(-7) mol/L) concentrations of ATRA. Tretinoin 215-219 XPA binding protein 2 Homo sapiens 167-171
17283134-5 2007 In the present study, we showed that overexpression of XAB2 inhibited ATRA-induced cellular differentiation in human rhabdomyosarcoma cell line, and that knockdown of XAB2 by small interfering RNA (siRNA) increased ATRA-sensitive cellular differentiation in the human promyelocytic leukemia cell line HL60 at both physiologic (10(-9)-10(-8) mol/L) and therapeutic (10(-7) mol/L) concentrations of ATRA. Tretinoin 215-219 XPA binding protein 2 Homo sapiens 167-171
17283134-7 2007 Finally, using siRNA against XAB2, we showed that the ATRA-resistant neuroblastoma cell line IMR-32 underwent cellular differentiation induced by ATRA at a therapeutic concentration (10(-6) mol/L). Tretinoin 54-58 XPA binding protein 2 Homo sapiens 29-33
17283134-8 2007 These results strongly suggest that XAB2 is a component of the RAR corepressor complex with an inhibitory effect on ATRA-induced cellular differentiation and that XAB2 plays a role in ATRA-mediated cellular differentiation as an important aspect of cancer therapy. Tretinoin 116-120 XPA binding protein 2 Homo sapiens 36-40
17283134-8 2007 These results strongly suggest that XAB2 is a component of the RAR corepressor complex with an inhibitory effect on ATRA-induced cellular differentiation and that XAB2 plays a role in ATRA-mediated cellular differentiation as an important aspect of cancer therapy. Tretinoin 184-188 XPA binding protein 2 Homo sapiens 163-167
18511453-0 2008 Kruppel-like factor 4 is required for the expression of vascular smooth muscle cell differentiation marker genes induced by all-trans retinoic acid. Tretinoin 134-147 Kruppel like factor 4 Homo sapiens 0-21
18511453-4 2008 Here, we show that treatment of VSMCs with ATRA resulted in significant inhibition of proliferation and migration of VSMCs, as well as up-regulation of KLF4 and the VSMC differentiation marker genes SM22alpha and SM alpha-actin (alpha-SMA). Tretinoin 43-47 Kruppel like factor 4 Homo sapiens 152-156
18511453-7 2008 Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22alpha and alpha-SMA expression and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration. Tretinoin 110-114 Kruppel like factor 4 Homo sapiens 13-17
18511453-7 2008 Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22alpha and alpha-SMA expression and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration. Tretinoin 110-114 Kruppel like factor 4 Homo sapiens 32-36
18511453-7 2008 Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22alpha and alpha-SMA expression and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration. Tretinoin 200-204 Kruppel like factor 4 Homo sapiens 13-17
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 196-200 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 55-58
17349212-4 2007 In the present study, we investigated whether ATRA or HMBA induced the growth arrest of HL-60 cells by down-regulating the expression of CD44. Tretinoin 46-50 CD44 molecule (Indian blood group) Homo sapiens 137-141
11911279-5 2001 We demonstrated a down-regulation of vimentin after ATRA treatment of NB4 cells by immunoblotting and immunofluorescence. Tretinoin 52-56 vimentin Homo sapiens 37-45
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 196-200 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 153-156
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 196-200 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 153-156
18425745-9 2008 Moreover, the induction of p21 by atRA was partially attenuated when RAR was silenced with specific siRNA. Tretinoin 34-38 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 27-30
18425745-9 2008 Moreover, the induction of p21 by atRA was partially attenuated when RAR was silenced with specific siRNA. Tretinoin 34-38 Rab40B, member RAS oncogene family Mus musculus 69-72
18425745-12 2008 Taken together, our results indicate p21 is responsible for atRA-induced growth inhibition of MEPM cells and RAR plays a role during this process. Tretinoin 60-64 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 37-40
17331193-3 2007 Retinoic acid did not increase cell proliferation but led to up-regulation of myosin VIIa and formation of prominent actin rings that gave rise to numerous large, linear actin bundles. Tretinoin 0-13 myosin VIIA Homo sapiens 78-89
11911279-8 2001 The structural features of the vimentin cytoskeleton obtained by image analysis showed significant differences in network density and directionality between ATRA-treated NB4 cells and controls. Tretinoin 157-161 vimentin Homo sapiens 31-39
11601984-6 2001 Competition studies between cis-parinaric acid and the natural ligands indicated a decreasing affinity of chicken Lb-FABP for PA, OA, and retinoic acid (RA). Tretinoin 138-151 liver basic fatty acid binding protein Gallus gallus 114-121
17223708-7 2007 The RXR ligand, 9-cis-RA, generates a second SRC-1 site and increases the affinity by improving the entropic component of binding. Tretinoin 16-24 retinoid X receptor alpha Homo sapiens 4-7
17234770-1 2007 The anticarcinogenic activities of retinoic acid (RA) are believed to be mediated by the nuclear RA receptor (RAR) and by the RA-binding protein cellular RA-binding protein-II (CRABP-II). Tretinoin 35-48 cellular retinoic acid binding protein 2 Homo sapiens 177-185
17234770-1 2007 The anticarcinogenic activities of retinoic acid (RA) are believed to be mediated by the nuclear RA receptor (RAR) and by the RA-binding protein cellular RA-binding protein-II (CRABP-II). Tretinoin 50-52 cellular retinoic acid binding protein 2 Homo sapiens 177-185
17234770-6 2007 We show that induction of Btg2 by RA does not require de novo protein synthesis and is augmented by overexpression of CRABP-II. Tretinoin 34-36 cellular retinoic acid binding protein 2 Homo sapiens 118-126
18466335-3 2008 The present experiments were performed to see whether 13-cis-RA and all-trans-RA could alter the dendritic morphology of cultured hippocampal neurons via RA receptors: retinoic acid receptor (RAR) and retinoid X receptor (RXR). Tretinoin 61-63 retinoic acid receptor, alpha Mus musculus 168-190
18466335-3 2008 The present experiments were performed to see whether 13-cis-RA and all-trans-RA could alter the dendritic morphology of cultured hippocampal neurons via RA receptors: retinoic acid receptor (RAR) and retinoid X receptor (RXR). Tretinoin 61-63 retinoic acid receptor, alpha Mus musculus 192-195
18466335-5 2008 The negative changes induced by 13-cis-RA and all-trans-RA were antagonized by RXR antagonists and RAR antagonists, respectively. Tretinoin 39-41 retinoic acid receptor, alpha Mus musculus 99-102
18502750-1 2008 Human retinol dehydrogenase 10 (RDH10) was implicated in the oxidation of all-trans-retinol for biosynthesis of all-trans-retinoic acid, however, initial assays suggested that RDH10 prefers NADP(+) as a cofactor, undermining its role as an oxidative enzyme. Tretinoin 112-135 retinol dehydrogenase 10 Homo sapiens 6-30
17234770-7 2007 Additionally, we identify a RA response element in the Btg2 promoter and show that the element binds retinoid X receptor/RAR heterodimers in vitro, is occupied by the heterodimers in cells, and can drive RA-induced activation of a reporter gene. Tretinoin 28-30 retinoid X receptor alpha Homo sapiens 101-120
17234770-7 2007 Additionally, we identify a RA response element in the Btg2 promoter and show that the element binds retinoid X receptor/RAR heterodimers in vitro, is occupied by the heterodimers in cells, and can drive RA-induced activation of a reporter gene. Tretinoin 121-123 retinoid X receptor alpha Homo sapiens 101-120
18502750-1 2008 Human retinol dehydrogenase 10 (RDH10) was implicated in the oxidation of all-trans-retinol for biosynthesis of all-trans-retinoic acid, however, initial assays suggested that RDH10 prefers NADP(+) as a cofactor, undermining its role as an oxidative enzyme. Tretinoin 112-135 retinol dehydrogenase 10 Homo sapiens 32-37
18502750-1 2008 Human retinol dehydrogenase 10 (RDH10) was implicated in the oxidation of all-trans-retinol for biosynthesis of all-trans-retinoic acid, however, initial assays suggested that RDH10 prefers NADP(+) as a cofactor, undermining its role as an oxidative enzyme. Tretinoin 112-135 retinol dehydrogenase 10 Homo sapiens 176-181
11585737-0 2001 Retinoic acid biosynthesis by normal human breast epithelium is via aldehyde dehydrogenase 6, absent in MCF-7 cells. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A3 Homo sapiens 68-92
18502750-5 2008 Consistent with its preference for NAD(+), RDH10 functions exclusively in the oxidative direction in the cells, increasing the levels of retinaldehyde and retinoic acid. Tretinoin 155-168 retinol dehydrogenase 10 Homo sapiens 43-48
18502750-6 2008 Targeted small interfering RNA-mediated silencing of endogenous RDH10 or RoDH4 expression in human cells results in a significant decrease in retinoic acid production from retinol, identifying both human enzymes as physiologically relevant retinol dehydrogenases. Tretinoin 142-155 retinol dehydrogenase 10 Homo sapiens 64-69
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 132-151 cubilin Homo sapiens 63-70
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 153-155 cubilin Homo sapiens 63-70
18567755-5 2008 Using immunoblotting and real-time PCR, we found that megalin, cubilin, and Dab2 were expressed and dose dependently induced by all-trans-retinoic acid (RA) in T-47D human breast cancer cells and that RA-treated T-47D cells exhibited enhanced DBP internalization. Tretinoin 201-203 cubilin Homo sapiens 63-70
17010966-4 2007 Different combinations of signals are responsible for different aspects of this early transient induction: FGF initiates expression of Sox3 and ERNI, retinoic acid can induce Cyp26A1 and only a combination of low levels of FGF8 together with Wnt- and BMP-antagonists can induce Otx2. Tretinoin 150-163 orthodenticle homeobox 2 Mus musculus 278-282
17079289-0 2007 Inhibition of retinoic acid-inducible gene I-mediated induction of beta interferon by the NS1 protein of influenza A virus. Tretinoin 14-27 influenza virus NS1A binding protein Homo sapiens 90-93
18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 0-13 matrix metallopeptidase 9 Homo sapiens 28-54
11585737-6 2001 Immunohistochemical analysis of normal human breast with antibodies to ALDH6 showed expression of this enzyme in the glandular epithelia colocalized with cellular RA-binding protein type II, a possible marker for certain cells able to synthesize RA. Tretinoin 163-165 aldehyde dehydrogenase 1 family member A3 Homo sapiens 71-76
18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 0-13 matrix metallopeptidase 9 Homo sapiens 56-61
18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85
18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 15-17 matrix metallopeptidase 9 Homo sapiens 28-54
18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 15-17 matrix metallopeptidase 9 Homo sapiens 56-61
18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 15-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85
17035595-2 2007 We have demonstrated previously that all-trans retinoic acid (atRA) plays an important role in forming functional TJs through a specific retinoic acid receptor (RAR)/retinoid X receptor heterodimer in epithelial cells. Tretinoin 47-60 retinoic acid receptor, alpha Mus musculus 161-164
17035595-2 2007 We have demonstrated previously that all-trans retinoic acid (atRA) plays an important role in forming functional TJs through a specific retinoic acid receptor (RAR)/retinoid X receptor heterodimer in epithelial cells. Tretinoin 62-66 retinoic acid receptor, alpha Mus musculus 161-164
17035595-6 2007 This RA-mediated enhancement of barrier function is potentially associated with the increased expression of TJ-associated genes such as occludin, claudin-1, claudin-4, and zonula occludens-1. Tretinoin 5-7 claudin 1 Mus musculus 146-155
18443043-5 2008 CREB binding protein (CBP) and p300/CBP-associated factor (PCAF) were displaced from transcription factor binding sites on the MMP-9 promoter within minutes of RA treatment. Tretinoin 160-162 matrix metallopeptidase 9 Homo sapiens 127-132
11585737-8 2001 When MCF-7 cells were then transfected with ALDH6, they (re)gained the ability to oxidize retinal to RA as well as some ability to synthesize RA when provided with retinol. Tretinoin 101-103 aldehyde dehydrogenase 1 family member A3 Homo sapiens 44-49
11585737-8 2001 When MCF-7 cells were then transfected with ALDH6, they (re)gained the ability to oxidize retinal to RA as well as some ability to synthesize RA when provided with retinol. Tretinoin 142-144 aldehyde dehydrogenase 1 family member A3 Homo sapiens 44-49
18342014-0 2008 Retinoic acid induces caspase-8 transcription via phospho-CREB and increases apoptotic responses to death stimuli in neuroblastoma cells. Tretinoin 0-13 cAMP responsive element binding protein 1 Homo sapiens 58-62
18391515-7 2007 Expression profiling at P1 and P2 in Dmrt1 mutant testes indicates defects in several important testicular signaling pathways (Gdnf, retinoic acid, TGFbeta, FSH), and detects elevated expression of the pluripotency marker Stella/Dppa3/Pgc7, providing insight into the molecular basis of Dmrt1 testis defects. Tretinoin 133-146 doublesex and mab-3 related transcription factor 1 Mus musculus 37-42
11585737-9 2001 This suggests that loss of ALDH6 expression is the defect in RA biosynthesis in these cells. Tretinoin 61-63 aldehyde dehydrogenase 1 family member A3 Homo sapiens 27-32
11585737-10 2001 Identification of ALDH6 as the retinaldehyde dehydrogenase present in normal human breast epithelia provides the first tool necessary for studying the loss of RA synthetic ability in cancer cells and the relationship of this process to malignant transformation. Tretinoin 159-161 aldehyde dehydrogenase 1 family member A3 Homo sapiens 18-23
18498088-0 2008 Retinoic acid controls heart anteroposterior patterning by down-regulating Isl1 through the Fgf8 pathway. Tretinoin 0-13 ISL1 transcription factor, LIM/homeodomain Mus musculus 75-79
11584082-2 2001 The effects of RA on phospholipase A(2) (PLA(2)) and cyclooxygenase (COX) isoforms in vitro are controversial, and few in vivo studies exist. Tretinoin 15-17 phospholipase A2 group IB Rattus norvegicus 21-39
18498088-0 2008 Retinoic acid controls heart anteroposterior patterning by down-regulating Isl1 through the Fgf8 pathway. Tretinoin 0-13 fibroblast growth factor 8 Mus musculus 92-96
18498088-6 2008 We provide evidence that retinoic acid acts specifically in the posterior-medial region of the cardiac field to establish the heart posterior boundary potentially by reducing Fgf8 expression which restricts the Isl1 domain. Tretinoin 25-38 fibroblast growth factor 8 Mus musculus 175-179
18498088-6 2008 We provide evidence that retinoic acid acts specifically in the posterior-medial region of the cardiac field to establish the heart posterior boundary potentially by reducing Fgf8 expression which restricts the Isl1 domain. Tretinoin 25-38 ISL1 transcription factor, LIM/homeodomain Mus musculus 211-215
17097063-6 2006 Taken together, our data indicate that atRA increases AQP5 expression through transactivation of Sp1, leading to an increase in plasma membrane water permeability. Tretinoin 39-43 aquaporin 5 Mus musculus 54-58
11584082-2 2001 The effects of RA on phospholipase A(2) (PLA(2)) and cyclooxygenase (COX) isoforms in vitro are controversial, and few in vivo studies exist. Tretinoin 15-17 phospholipase A2 group IB Rattus norvegicus 41-47
17173184-2 2006 Although the original work showed that PLSCR1 contributes to the transbilayer movement of phospholipids, the following studies revealed that PLSCR1 expression can be induced by some cytokines such as interferon, epidermal growth factor, and also by leukemic cell differentiation-inducing agents such as all-trans retinoic acid (ATRA) and phorbol 12-myristate 13-acetate (PMA). Tretinoin 313-326 phospholipid scramblase 1 Homo sapiens 141-147
17173184-2 2006 Although the original work showed that PLSCR1 contributes to the transbilayer movement of phospholipids, the following studies revealed that PLSCR1 expression can be induced by some cytokines such as interferon, epidermal growth factor, and also by leukemic cell differentiation-inducing agents such as all-trans retinoic acid (ATRA) and phorbol 12-myristate 13-acetate (PMA). Tretinoin 328-332 phospholipid scramblase 1 Homo sapiens 141-147
11584082-8 2001 In addition, RA and LPS induced the expression of the microsomal isoform of PGE synthase (mPGES). Tretinoin 13-15 prostaglandin E synthase Mus musculus 90-95
18471880-4 2008 In addition, the helicases retinoic acid induced protein I (RIG-I)/melanoma differentiation associated gene 5 (MDA5) binds cytoplasmic dsRNA generated during viral replication. Tretinoin 27-40 DExD/H-box helicase 58 Homo sapiens 60-65
11676881-5 2001 RESULTS: Retinoic acid markedly inhibited hepatic stellate cells proliferation (41.50%, P<0.05), decreased the protein level of alpha-smooth muscle actin (55.09%, P<0.05), and induced hepatic stellate cells to express retinoic acid receptor beta 2 mRNA. Tretinoin 9-22 actin gamma 2, smooth muscle Rattus norvegicus 131-156
18212744-0 2008 Retinoic acid downregulates Rae1 leading to APC(Cdh1) activation and neuroblastoma SH-SY5Y differentiation. Tretinoin 0-13 ribonucleic acid export 1 Homo sapiens 28-32
18212744-5 2008 The mRNA and protein abundance of Rae1-a nuclear export factor that limits APC(Cdh1) activity in mitosis-decreased upon retinoic acid-induced inhibition of neuroblastoma cell proliferation. Tretinoin 120-133 ribonucleic acid export 1 Homo sapiens 34-38
18212744-6 2008 Furthermore, either Rae1 overexpression or Cdh1 inhibition promoted Skp2 accumulation, p27 destabilization and prevented retinoic acid-induced cell cycle arrest and differentiation. Tretinoin 121-134 ribonucleic acid export 1 Homo sapiens 20-24
18212744-7 2008 Conversely, inhibition of Rae1 accelerated retinoic acid-induced differentiation. Tretinoin 43-56 ribonucleic acid export 1 Homo sapiens 26-30
18212744-8 2008 Thus, retinoic acid downregulates Rae1, hence facilitating APC(Cdh1)-mediated Skp2 degradation leading to the arrest of cell cycle progression and neuroblastoma differentiation. Tretinoin 6-19 ribonucleic acid export 1 Homo sapiens 34-38
17116711-5 2006 Rats received a single injection of streptozotocin (60 mg/kg body wt) or vehicle followed by administration of ATRA (30 mumol/kg body wt) or vehicle for 5 d. The hepatic activity of PEMT increased 50% in both diabetic rat groups, whereas administration of ATRA was without effect. Tretinoin 256-260 phosphatidylethanolamine N-methyltransferase Rattus norvegicus 182-186
18241033-4 2008 The study revealed that expression of GLI1 and its direct transcriptional target Patched (PTCH) is downregulated in the early stages of retinoic acid-induced neuronal differentiation of NT2 cells. Tretinoin 136-149 GLI family zinc finger 1 Homo sapiens 38-42
11676881-6 2001 In addition, retinoic acid increased the protein level of p16 (218.75%, P <0.05) and induced p21 protein expression; meanwhile, p27 was undetectable by immunocytochemistry in both control and retinoic acid-treated hepatic stellate cells. Tretinoin 195-208 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 131-134
17109623-3 2006 Here we describe a modified in vitro procedure to direct differentiation of three clonal hESC lines, hES 3.1, hES 3.2 and hES 3.3 efficiently to spinal motor neurons by using various differentiation factors namely retinoic acid (RA), sonic hedgehog (Shh), bone morphogenetic protein-2 (BMP-2) and Wnt3A. Tretinoin 214-227 carboxylesterase 3 Homo sapiens 101-108
11566889-5 2001 These results suggest that TH and RA activate the same intracellular pathway leading to oligodendrocyte differentiation, and that this pathway depends on a p53 family protein. Tretinoin 34-36 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 156-159
17032197-2 2006 Recently, we have demonstrated that MUC4 expression in pancreatic tumor cells is regulated by interferon-gamma (IFNgamma) and by retinoic acid via transforming growth factor beta 2 (TGFbeta-2). Tretinoin 129-142 transforming growth factor beta 2 Homo sapiens 147-180
17032197-2 2006 Recently, we have demonstrated that MUC4 expression in pancreatic tumor cells is regulated by interferon-gamma (IFNgamma) and by retinoic acid via transforming growth factor beta 2 (TGFbeta-2). Tretinoin 129-142 transforming growth factor beta 2 Homo sapiens 182-191
18439490-6 2008 Treatment with a RARgamma selective agonist plus a retinoid X receptor agonist (LGD1069) increased Tie1 mRNA levels by 11- +/- 2.5-fold 48 hours after RA addition in F9 WT, but not in F9 RARgamma-/- cells, by quantitative reverse transcription polymerase chain reaction. Tretinoin 17-19 tyrosine kinase with immunoglobulin like and EGF like domains 1 Homo sapiens 99-103
18270252-11 2008 Finally, immunoprecipitationimmunoblotting demonstrated RA-induced interactions between RARalpha/RXRalpha and SP1/SP3 in intact endometrial cells. Tretinoin 56-58 retinoid X receptor alpha Homo sapiens 97-105
18270252-12 2008 CONCLUSIONS: In endometrial epithelial cells, RA stimulates formation of a multimeric complex comprised of RARalpha/RXRalpha tethered to transcription factors SP1 and SP3 on the HSD17B2 promoter. Tretinoin 46-48 retinoid X receptor alpha Homo sapiens 116-124
11520943-6 2001 Using a quantitative PCR assay, trkA and p75(NTR) mRNAs, but not trkC mRNA, were increased ( approximately 1.5- to 2-fold) after 72 and 48 hr of exposure of the cultures to atRA, respectively. Tretinoin 173-177 neurotrophic receptor tyrosine kinase 1 Gallus gallus 32-36
17066417-0 2006 PDGF-C controls proliferation and is down-regulated by retinoic acid in mouse embryonic palatal mesenchymal cells. Tretinoin 55-68 platelet-derived growth factor, C polypeptide Mus musculus 0-6
17066417-8 2006 CONCLUSIONS: These demonstrate that PDGF-C is a potent mitogen for MEPM cells, implying that inactivated PDGF-C by gene-targeting or reduced PDGF-C by RA may both cause inhibition of proliferation in palatal shelves, which might account for the pathogenesis of cleft palate in Pdgfc(-/-) mouse or RA-treated mouse. Tretinoin 297-299 platelet-derived growth factor, C polypeptide Mus musculus 36-42
11520943-7 2001 The atRA-induced increase in trkA mRNA may play a role in the enhanced survival of neurons cultured in the presence of either NGF or NT-3, as both neurotrophins have been shown to signal through this receptor. Tretinoin 4-8 neurotrophic receptor tyrosine kinase 1 Gallus gallus 29-33
17066417-8 2006 CONCLUSIONS: These demonstrate that PDGF-C is a potent mitogen for MEPM cells, implying that inactivated PDGF-C by gene-targeting or reduced PDGF-C by RA may both cause inhibition of proliferation in palatal shelves, which might account for the pathogenesis of cleft palate in Pdgfc(-/-) mouse or RA-treated mouse. Tretinoin 297-299 platelet-derived growth factor, C polypeptide Mus musculus 105-111
17066417-8 2006 CONCLUSIONS: These demonstrate that PDGF-C is a potent mitogen for MEPM cells, implying that inactivated PDGF-C by gene-targeting or reduced PDGF-C by RA may both cause inhibition of proliferation in palatal shelves, which might account for the pathogenesis of cleft palate in Pdgfc(-/-) mouse or RA-treated mouse. Tretinoin 297-299 platelet-derived growth factor, C polypeptide Mus musculus 105-111
17066417-9 2006 In conclusion, our results suggest that PDGF-C signaling is a new mechanism of cleft palate induced by RA. Tretinoin 103-105 platelet-derived growth factor, C polypeptide Mus musculus 40-46
18058943-4 2008 RAGE knockdown inhibited retinoic acid-induced activation and blocked nuclear translocation of NF-kappaB, suggesting RAGE regulates activation of NF-kappaB. Tretinoin 25-38 advanced glycosylation end-product specific receptor Homo sapiens 0-4
11520679-2 2001 The RA-metabolizing enzymes Cyp26A1 and Cyp26B1 are believed to play important roles in protecting certain embryonic tissues from inappropriate RA signaling. Tretinoin 144-146 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 28-35
18058943-4 2008 RAGE knockdown inhibited retinoic acid-induced activation and blocked nuclear translocation of NF-kappaB, suggesting RAGE regulates activation of NF-kappaB. Tretinoin 25-38 advanced glycosylation end-product specific receptor Homo sapiens 117-121
18058943-5 2008 RAGE was also shown to be involved in survival of P19 cells during retinoic acid differentiation. Tretinoin 67-80 advanced glycosylation end-product specific receptor Homo sapiens 0-4
18058943-7 2008 Retinoic acid-treated P19 cells activated GTPases, Rac1, and Cdc42. Tretinoin 0-13 Rac family small GTPase 1 Homo sapiens 51-55
11511297-10 2001 In contrast, all-trans retinoic acid and clobetasol were equally effective in blocking ultraviolet induction of MMP-1 and degradation of collagen in human skin in vivo. Tretinoin 23-36 matrix metallopeptidase 1 Homo sapiens 112-117
19099751-12 2008 The pups treated with RA in the hyperoxic environment expressed significantly lower mRNA levels of MMP-2 and MMP-9 than the hyperoxic control pups on each experimental day (P < 0.05 for all). Tretinoin 22-24 matrix metallopeptidase 9 Rattus norvegicus 109-114
19099751-13 2008 The levels of active MMP-2 and pro/active MMP-9 decreased to a different degree after RA treatment in hyperoxia exposure rat pups. Tretinoin 86-88 matrix metallopeptidase 9 Rattus norvegicus 42-47
19099751-16 2008 RA could have a protective effect on hyperoxia induced lung injury by decreasing active levels of JNK and p38, which subsequently reduce the expression and activation of MMP-2 and MMP-9. Tretinoin 0-2 matrix metallopeptidase 9 Rattus norvegicus 180-185
18280804-3 2008 We now demonstrate that treatment of acute promyelocytic leukemia (APL)-derived NB4 cells with ATRA results in dissociation of the translational repressor 4E-BP1 from the eukaryotic initiation factor eIF4E, and subsequent formation of eIF4G-eIF4E complexes. Tretinoin 95-99 eukaryotic translation initiation factor 4 gamma 1 Homo sapiens 235-240
18342301-3 2008 Distal embryonic lung epithelium showed high levels of Mia1 expression, which was suppressed by treatment with either retinoic acid or the FGF signaling antagonist SU5402. Tretinoin 118-131 MIA SH3 domain containing Mus musculus 55-59
16984259-6 2006 In culture MMP-21 was upregulated by phorbol myristate acetate in THP-1 cells and by retinoic acid (RA) in U937 cells, and downregulated by transforming growth factor beta 1 (TGF-beta1) in HEL 299 as assessed by Taqman quantitative polymerase chain reaction (PCR). Tretinoin 85-98 matrix metallopeptidase 21 Homo sapiens 11-17
16984259-6 2006 In culture MMP-21 was upregulated by phorbol myristate acetate in THP-1 cells and by retinoic acid (RA) in U937 cells, and downregulated by transforming growth factor beta 1 (TGF-beta1) in HEL 299 as assessed by Taqman quantitative polymerase chain reaction (PCR). Tretinoin 100-102 matrix metallopeptidase 21 Homo sapiens 11-17
16619265-6 2006 We observed atRA can regulate the dHAND expression in a dose- and time-dependent manner. Tretinoin 12-16 hand Drosophila melanogaster 34-39
16922813-0 2006 JWA is required for the antiproliferative and pro-apoptotic effects of all-trans retinoic acid in Hela cells. Tretinoin 81-94 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 0-3
16922813-8 2006 Western blot analysis revealed that ATRA caused increased expression of JWA in HeLa cells in a dose- and time-dependent manner, accompanied by activation of extracellular signal-regulated kinase (ERK) 1/2 phosphorylation. Tretinoin 36-40 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 72-75
16922813-9 2006 However, ERK1/2 phosphorylation induced by ATRA was inhibited in JWA-deficient HeLa cells. Tretinoin 43-47 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 65-68
18234667-3 2008 Incubation of cells with retinoic acid in the absence of mitogens enhanced basal neuronal differentiation that was accompanied by an up-regulation of neuronal gene expression and a down-regulation of GFAP and nestin expression. Tretinoin 25-38 glial fibrillary acidic protein Homo sapiens 200-204
18234667-4 2008 Retinoic acid treatment changed the histone code of neuronal genes encoding synapsin I, synaptophysin, and synaptotagmins II, IV, and VII from a transcriptionally inactive (methylation of lysine residue 9 of histone 3) to a transcriptionally active state (methylation of lysine residue 4 of histone 3). Tretinoin 0-13 synapsin I Homo sapiens 76-86
16922813-10 2006 In JWA-overexpressing HeLa cells, ATRA showed more significant antiproliferative effects and induced more apoptosis. Tretinoin 34-38 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 3-6
11437362-3 2001 The inhibition of human mammary cancer (MCF-7) cell growth and the transactivation of the retinoic acid receptor (RAR) reporter gene by synthetic acyclo-retinoic acid, the open chain analog of retinoic acid, was compared to the effects of lycopene and retinoic acid in the same systems. Tretinoin 90-103 retinoic acid receptor alpha Homo sapiens 114-117
16922813-12 2006 The reporter gene assay showed that ATRA (5 mmol/L) enhanced the transcriptional activity of JWA by interacting with its promoter in the region from -194 to +107 bp (P < 0.01). Tretinoin 36-40 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 93-96
16922813-14 2006 Therefore, ATRA-inhibited cellular proliferation and -induced apoptosis in HeLa cells may be dependent on JWA transactivation via its C/EBP-binding motifs. Tretinoin 11-15 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 106-109
16922813-17 2006 The findings may represent a novel mechanism by which the effects of ATRA in regulating cellular proliferation and apoptosis are mediated, at least in part, by JWA expression. Tretinoin 69-73 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 160-163
18234667-4 2008 Retinoic acid treatment changed the histone code of neuronal genes encoding synapsin I, synaptophysin, and synaptotagmins II, IV, and VII from a transcriptionally inactive (methylation of lysine residue 9 of histone 3) to a transcriptionally active state (methylation of lysine residue 4 of histone 3). Tretinoin 0-13 synaptophysin Homo sapiens 88-101
17943186-5 2008 These effects were consistent with the findings that all-trans RA upregulated heparin-binding epidermal growth factor-like growth factor mRNA expression and increased the phosphorylation of EGFR and extracellular signal-regulated kinase 1/2 (ERK1/2). Tretinoin 63-65 epidermal growth factor receptor Rattus norvegicus 190-194
17943186-6 2008 Interestingly, the activation of EGFR and ERK1/2 was seen already 30 minutes after all-trans RA treatment, suggesting that the activation of this signaling pathway is a primary response to all-trans RA. Tretinoin 93-95 epidermal growth factor receptor Rattus norvegicus 33-37
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 homeobox A3 Mus musculus 139-144
18164278-8 2008 Genes specifically induced by RA at 6h with the protein synthesis inhibitor cycloheximide in F9 Wt, but not in RARgamma-/- cells, included Hoxa3, Hoxa5, Gas1, Cyp26a1, Sfrp2, Fbp2, and Emp1. Tretinoin 30-32 secreted frizzled-related protein 2 Mus musculus 168-173
16820792-6 2006 Among the bioactive substances tested, three physiological ligands of nuclear receptors including all-trans-retinoic acid, 1,25-dihydroxyvitamin D3, and dexamethasone significantly activated the nephrin gene promoter in a dose-dependent manner. Tretinoin 98-121 NPHS1 adhesion molecule, nephrin Homo sapiens 195-202
11437362-3 2001 The inhibition of human mammary cancer (MCF-7) cell growth and the transactivation of the retinoic acid receptor (RAR) reporter gene by synthetic acyclo-retinoic acid, the open chain analog of retinoic acid, was compared to the effects of lycopene and retinoic acid in the same systems. Tretinoin 153-166 retinoic acid receptor alpha Homo sapiens 90-112
18404486-3 2006 DNA array analysis showed that treatment of normal human epidermal keratinocytes (NHEKs) with all-trans-retinoic acid (ATRA), an agonist to RAR (retinoic acid receptor), enhanced the expression of mRNA for the P2Y2 receptor, a metabotropic P2 receptor that is known to be involved in the proliferation of the epidermis. Tretinoin 94-117 purinergic receptor P2Y2 Homo sapiens 210-214
11437362-3 2001 The inhibition of human mammary cancer (MCF-7) cell growth and the transactivation of the retinoic acid receptor (RAR) reporter gene by synthetic acyclo-retinoic acid, the open chain analog of retinoic acid, was compared to the effects of lycopene and retinoic acid in the same systems. Tretinoin 153-166 retinoic acid receptor alpha Homo sapiens 114-117
18404486-3 2006 DNA array analysis showed that treatment of normal human epidermal keratinocytes (NHEKs) with all-trans-retinoic acid (ATRA), an agonist to RAR (retinoic acid receptor), enhanced the expression of mRNA for the P2Y2 receptor, a metabotropic P2 receptor that is known to be involved in the proliferation of the epidermis. Tretinoin 119-123 purinergic receptor P2Y2 Homo sapiens 210-214
18249135-6 2008 Moreover, the activity of the promoter-luciferase construct ostensibly paralleled endogenous Nav1.7 mRNA levels in vitro, with both increased in a quantitatively and qualitatively similar manner by numerous factors (including NGF, phorbol esters, retinoic acid, and Brn-3a transcription factor over-expression). Tretinoin 247-260 sodium voltage-gated channel alpha subunit 9 Homo sapiens 93-99
16712891-8 2006 Importantly, atRA-induced DNA fragmentation and capase-3 activation were prevented by pretreatment with the JNK inhibitor (SP600125) and the p38 MAPK inhibitor (SB202190), but not by pretreatment with MEK inhibitor (U0126). Tretinoin 13-17 mitogen-activated protein kinase 8 Mus musculus 108-111
11404231-5 2001 A single injection of retinoic acid or retinol to VA-deficient quail did not affect the levels of IGFBP-2 mRNA, but it rapidly induced the expression of IGFBP-5 mRNAs in some tissues. Tretinoin 22-35 insulin-like growth factor-binding protein 5 Coturnix japonica 153-160
16885356-9 2006 These findings support a novel role for APC in balancing retinoic acid biosynthesis and catabolism through WNT-independent and WNT-dependent mechanisms. Tretinoin 57-70 APC regulator of WNT signaling pathway Danio rerio 40-43
16872448-0 2006 Epigenetic regulation of the imprinted U2af1-rs1 gene during retinoic acid-induced differentiation of embryonic stem cells. Tretinoin 61-74 ZRSR2 pseudogene 1 Homo sapiens 39-48
17937658-2 2008 We recently reported that RA (retinoic acid) rapidly activates CREB without using RARs (RA receptors) or RXRs (retinoid X receptors) in NHTBE cells (normal human tracheobronchial epithelial cells). Tretinoin 26-28 cAMP responsive element binding protein 1 Homo sapiens 63-67
17937658-2 2008 We recently reported that RA (retinoic acid) rapidly activates CREB without using RARs (RA receptors) or RXRs (retinoid X receptors) in NHTBE cells (normal human tracheobronchial epithelial cells). Tretinoin 30-43 cAMP responsive element binding protein 1 Homo sapiens 63-67
18207673-1 2008 The aim of this study is to investigate the chemical retinoic acid (RA) disruption at the level of retinoid X receptor (RXR) functioning. Tretinoin 53-66 retinoid X receptor alpha Homo sapiens 120-123
18207673-1 2008 The aim of this study is to investigate the chemical retinoic acid (RA) disruption at the level of retinoid X receptor (RXR) functioning. Tretinoin 68-70 retinoid X receptor alpha Homo sapiens 120-123
18207673-2 2008 This assay makes use of recombined human RXR gene and reporter gene yeast, which specifically expresses beta-galactosidase when incubated with exogenous 9-cis retinoic acid (9-cis RA). Tretinoin 180-182 retinoid X receptor alpha Homo sapiens 41-44
16872448-3 2006 The present work analyzes the involvement of these mechanisms in the expression of the U2af1-rs1 imprinted gene during the differentiation process of embryonic stem (ES) cells induced by retinoic acid. Tretinoin 187-200 ZRSR2 pseudogene 1 Homo sapiens 87-96
11414679-0 2001 Fatty acid delta(5)-desaturase mRNA is regulated by dietary vitamin A and exogenous retinoic acid in liver of adult rats. Tretinoin 84-97 fatty acid desaturase 1 Rattus norvegicus 11-30
16928291-10 2006 CD117- CD11b+ phenotype was detected in all patients recovering from APL with CD117+ CD11b- phenotype at diagnosis and after treatment with all-trans-retinoic acid (ARTA) for 2 months. Tretinoin 140-163 integrin subunit alpha M Homo sapiens 7-12
16928291-10 2006 CD117- CD11b+ phenotype was detected in all patients recovering from APL with CD117+ CD11b- phenotype at diagnosis and after treatment with all-trans-retinoic acid (ARTA) for 2 months. Tretinoin 165-169 integrin subunit alpha M Homo sapiens 7-12
16818722-3 2006 We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Tretinoin 36-49 aldehyde dehydrogenase 1 family member A2 Homo sapiens 72-79
18156191-9 2008 The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Tretinoin 76-78 angiotensin I converting enzyme 2 Rattus norvegicus 144-149
18199582-4 2008 Asymmetric PITX2 expression in the left presumptive gonad leads to the asymmetric expression of the retinoic-acid (RA)-synthesizing enzyme, RALDH2, in the right presumptive gonad. Tretinoin 100-113 aldehyde dehydrogenase 1 family member A2 Gallus gallus 140-146
18199582-4 2008 Asymmetric PITX2 expression in the left presumptive gonad leads to the asymmetric expression of the retinoic-acid (RA)-synthesizing enzyme, RALDH2, in the right presumptive gonad. Tretinoin 115-117 aldehyde dehydrogenase 1 family member A2 Gallus gallus 140-146
16818722-3 2006 We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Tretinoin 36-49 aldehyde dehydrogenase 1 family member A2 Homo sapiens 172-179
16818722-3 2006 We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Tretinoin 51-53 aldehyde dehydrogenase 1 family member A2 Homo sapiens 72-79
18199619-9 2008 The miR-23a expression in P19 cells before and after neuronal differentiation with retinoic acid treatment showed an increase in Fluc activity and a concomitant decrease in Gluc activity in vitro. Tretinoin 83-96 microRNA 23a Homo sapiens 4-11
16818722-3 2006 We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Tretinoin 51-53 aldehyde dehydrogenase 1 family member A2 Homo sapiens 172-179
11414679-4 2001 Treatment of VA-deficient rats with all-trans-retinoic acid lowered the level of expression of D5D mRNA toward that of VA-sufficient rats. Tretinoin 40-59 fatty acid desaturase 1 Rattus norvegicus 95-98
11451739-7 2001 tRA-induced apoptosis associated with an increased ratio of bax to bcl-2 by bax overexpression and cleavage of caspase-3. Tretinoin 0-3 BCL2 associated X, apoptosis regulator Rattus norvegicus 60-63
16888198-0 2006 Retinoic acid-induced human secretin gene expression in neuronal cells is mediated by cyclin-dependent kinase 1. Tretinoin 0-13 secretin Homo sapiens 28-36
16888198-1 2006 Previously, we found that secretin transcript levels were induced by all-trans retinoic acid (RA) in a neuroblastoma cell model, SH-SY5Y. Tretinoin 79-92 secretin Homo sapiens 26-34
16619266-0 2006 Endodermal differentiation of murine embryonic carcinoma cells by retinoic acid requires JLP, a JNK-scaffolding protein. Tretinoin 66-79 mitogen-activated protein kinase 8 Mus musculus 96-99
18280292-4 2008 We hypothesized that retinoids promote alveologenesis by stimulating differentiation of AECs-II to AECs-I at the end of gestation; and therefore, we investigated the effect of RA on the pulmonary expression of intercellular adhesion molecule 1 (ICAM-1), a marker for AECs-I, and thyroid transcription factor 1 (Ttf-1), a marker for AECs-II, in nitrofen-induced hypoplastic lungs. Tretinoin 176-178 intercellular adhesion molecule 1 Rattus norvegicus 210-243
18280292-11 2008 Expression levels of Ttf-1 were significantly decreased in lungs from RA-treated CDH animals compared with CDH without RA (P < .05). Tretinoin 70-72 transcription termination factor 1 Rattus norvegicus 21-26
18280292-11 2008 Expression levels of Ttf-1 were significantly decreased in lungs from RA-treated CDH animals compared with CDH without RA (P < .05). Tretinoin 119-121 transcription termination factor 1 Rattus norvegicus 21-26
17920233-6 2008 Several authors have described that all-trans retinoic acid (ATRA, ligand of retinoic acid receptors, RARs) may induce alterations in P-gp expression and/or activity in drug resistant malignant cell lines. Tretinoin 46-59 phosphoglycolate phosphatase Mus musculus 134-138
17920233-6 2008 Several authors have described that all-trans retinoic acid (ATRA, ligand of retinoic acid receptors, RARs) may induce alterations in P-gp expression and/or activity in drug resistant malignant cell lines. Tretinoin 61-65 phosphoglycolate phosphatase Mus musculus 134-138
17920233-14 2008 In contrast, when ATRA was applied together with verapamil (an often used P-gp inhibitor), a significant decrease in P-gp expression and transport activity were observed. Tretinoin 18-22 phosphoglycolate phosphatase Mus musculus 74-78
16619266-5 2006 Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Tretinoin 21-23 mitogen-activated protein kinase 8 Mus musculus 53-56
16619266-5 2006 Here, we report that RA stimulates the expression of JNK-interacting leucine zipper protein (JLP), a newly identified JNK-scaffolding protein and its critical role in RA-mediated endodermal differentiation. Tretinoin 167-169 mitogen-activated protein kinase 8 Mus musculus 53-56
16819395-8 2006 FXR activity requires heterodimerization with the 9-cis retinoid receptor (RXR alpha), and when bound by bile acids and retinoic acid, the complex effectively activates the transcription of BSEP. Tretinoin 120-133 retinoid X receptor alpha Homo sapiens 75-84
17920233-14 2008 In contrast, when ATRA was applied together with verapamil (an often used P-gp inhibitor), a significant decrease in P-gp expression and transport activity were observed. Tretinoin 18-22 phosphoglycolate phosphatase Mus musculus 117-121
17920233-17 2008 Thus, we can conclude that the combined treatment of L1210/VCR cells with ATRA and verapamil is able to depress P-gp expression, and consequently its activity. Tretinoin 74-78 phosphoglycolate phosphatase Mus musculus 112-116
16819395-8 2006 FXR activity requires heterodimerization with the 9-cis retinoid receptor (RXR alpha), and when bound by bile acids and retinoic acid, the complex effectively activates the transcription of BSEP. Tretinoin 120-133 ATP binding cassette subfamily B member 11 Homo sapiens 190-194
11451739-7 2001 tRA-induced apoptosis associated with an increased ratio of bax to bcl-2 by bax overexpression and cleavage of caspase-3. Tretinoin 0-3 BCL2 associated X, apoptosis regulator Rattus norvegicus 76-79
11399257-0 2001 Combined effect of retinoic acid and basic FGF on PAI-1 gene expression in vascular smooth muscle cells. Tretinoin 19-32 serpin family E member 1 Homo sapiens 50-55
11399257-4 2001 We examined the effects of all-trans-retinoic acid (atRA), either alone or in combination with mitogenic growth factor, basic fibroblast growth factor (bFGF), on the PAI-1 expression in cultured vascular smooth muscle cells (SMCs). Tretinoin 27-50 serpin family E member 1 Homo sapiens 166-171
16638968-4 2006 In rat pheochromocytoma PC-12 cells, treatment with 9-cis-retinoic acid as well as all-trans-retinoic acid significantly increased the mRNA and protein level of P2X2 receptor. Tretinoin 83-106 purinergic receptor P2X 2 Rattus norvegicus 161-165
18836242-0 2008 Evidence for species differences in the regulation of MMPs by all-trans retinoic acid in cytokine-stimulated chondrocytes. Tretinoin 72-85 matrix metallopeptidase 9 Homo sapiens 54-58
18836242-5 2008 ATRA displayed controversial effects on MMPs between rat and human chondrocytes, especially for MMP-9 expression. Tretinoin 0-4 matrix metallopeptidase 9 Homo sapiens 40-44
11399950-0 2001 Retinoic acids reduce matrilysin (matrix metalloproteinase 7) and inhibit tumor cell invasion in human colon cancer. Tretinoin 0-14 matrix metallopeptidase 7 Homo sapiens 22-32
18836242-5 2008 ATRA displayed controversial effects on MMPs between rat and human chondrocytes, especially for MMP-9 expression. Tretinoin 0-4 matrix metallopeptidase 9 Homo sapiens 96-101
18974614-3 2008 In this study, the effects of all-trans retinoic acid (atRA), 9-cis RA, and the RAR agonist TTNPB, on UGT2B7 and UGT2B15 mRNA expression in Caco-2 cells have been examined. Tretinoin 40-53 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 102-108
18974614-3 2008 In this study, the effects of all-trans retinoic acid (atRA), 9-cis RA, and the RAR agonist TTNPB, on UGT2B7 and UGT2B15 mRNA expression in Caco-2 cells have been examined. Tretinoin 55-59 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 102-108
16606617-1 2006 Additional sex comb-like 1 (ASXL1, 170 kDa), a mammalian homolog of Drosophila ASX, was identified as a protein that interacts with retinoic acid receptor (RAR) in the presence of retinoic acid (RA). Tretinoin 132-145 ASXL transcriptional regulator 1 Homo sapiens 0-26
16606617-1 2006 Additional sex comb-like 1 (ASXL1, 170 kDa), a mammalian homolog of Drosophila ASX, was identified as a protein that interacts with retinoic acid receptor (RAR) in the presence of retinoic acid (RA). Tretinoin 132-145 ASXL transcriptional regulator 1 Homo sapiens 28-33
16606617-1 2006 Additional sex comb-like 1 (ASXL1, 170 kDa), a mammalian homolog of Drosophila ASX, was identified as a protein that interacts with retinoic acid receptor (RAR) in the presence of retinoic acid (RA). Tretinoin 156-158 ASXL transcriptional regulator 1 Homo sapiens 0-26
16606617-1 2006 Additional sex comb-like 1 (ASXL1, 170 kDa), a mammalian homolog of Drosophila ASX, was identified as a protein that interacts with retinoic acid receptor (RAR) in the presence of retinoic acid (RA). Tretinoin 156-158 ASXL transcriptional regulator 1 Homo sapiens 28-33
16606617-9 2006 Overall, these results suggest that ASXL1 is a novel coactivator of RAR that cooperates with SRC-1 and implicates it as a potential antitumor target of RA in RA-resistant cancer cells. Tretinoin 68-70 ASXL transcriptional regulator 1 Homo sapiens 36-41
16688771-3 2006 In both cases the RA-synthesizing enzyme is RALDH-2. Tretinoin 18-20 aldehyde dehydrogenase 1 family member A2 Homo sapiens 44-51
11399950-0 2001 Retinoic acids reduce matrilysin (matrix metalloproteinase 7) and inhibit tumor cell invasion in human colon cancer. Tretinoin 0-14 matrix metallopeptidase 7 Homo sapiens 34-60
11399950-5 2001 All three retinoic acids tested reduced matrilysin expression and suppressed the invasiveness of colon cancer cell lines in vitro. Tretinoin 10-24 matrix metallopeptidase 7 Homo sapiens 40-50
11413191-2 2001 In acute promyelocytic leukemia, PML/retinoic acid receptor (RAR) alpha expression disrupts NBs, but therapies such as retinoic acid or arsenic trioxide (As2O3) restore them. Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 61-64
16674946-1 2006 Vitamin A (all-trans retinol) and all-trans retinoid acid (ATRA) interacted with human annexin A6 (AnxA6) as evidenced by AnxA6-induced blue shift of retinoid absorption maxima, by AnxA6-Trp fluorescence quenching and by a fluorescence resonance energy transfer from a Trp residue of AnxA6 to retinol. Tretinoin 59-63 annexin A6 Homo sapiens 87-97
16674946-1 2006 Vitamin A (all-trans retinol) and all-trans retinoid acid (ATRA) interacted with human annexin A6 (AnxA6) as evidenced by AnxA6-induced blue shift of retinoid absorption maxima, by AnxA6-Trp fluorescence quenching and by a fluorescence resonance energy transfer from a Trp residue of AnxA6 to retinol. Tretinoin 59-63 annexin A6 Homo sapiens 99-104
16674946-1 2006 Vitamin A (all-trans retinol) and all-trans retinoid acid (ATRA) interacted with human annexin A6 (AnxA6) as evidenced by AnxA6-induced blue shift of retinoid absorption maxima, by AnxA6-Trp fluorescence quenching and by a fluorescence resonance energy transfer from a Trp residue of AnxA6 to retinol. Tretinoin 59-63 annexin A6 Homo sapiens 122-127
16674946-1 2006 Vitamin A (all-trans retinol) and all-trans retinoid acid (ATRA) interacted with human annexin A6 (AnxA6) as evidenced by AnxA6-induced blue shift of retinoid absorption maxima, by AnxA6-Trp fluorescence quenching and by a fluorescence resonance energy transfer from a Trp residue of AnxA6 to retinol. Tretinoin 59-63 annexin A6 Homo sapiens 122-127
16674946-1 2006 Vitamin A (all-trans retinol) and all-trans retinoid acid (ATRA) interacted with human annexin A6 (AnxA6) as evidenced by AnxA6-induced blue shift of retinoid absorption maxima, by AnxA6-Trp fluorescence quenching and by a fluorescence resonance energy transfer from a Trp residue of AnxA6 to retinol. Tretinoin 59-63 annexin A6 Homo sapiens 122-127
18085670-2 2008 Experimental evidence suggests that the active metabolites of vitamin A that mediate its effects on the immune system are the retinoic acids (RA), which are ligands for the nuclear RA receptor (RAR) family. Tretinoin 126-140 retinoic acid receptor, alpha Mus musculus 181-192
18085670-2 2008 Experimental evidence suggests that the active metabolites of vitamin A that mediate its effects on the immune system are the retinoic acids (RA), which are ligands for the nuclear RA receptor (RAR) family. Tretinoin 126-140 retinoic acid receptor, alpha Mus musculus 194-197
18085670-2 2008 Experimental evidence suggests that the active metabolites of vitamin A that mediate its effects on the immune system are the retinoic acids (RA), which are ligands for the nuclear RA receptor (RAR) family. Tretinoin 142-144 retinoic acid receptor, alpha Mus musculus 181-192
18085670-2 2008 Experimental evidence suggests that the active metabolites of vitamin A that mediate its effects on the immune system are the retinoic acids (RA), which are ligands for the nuclear RA receptor (RAR) family. Tretinoin 142-144 retinoic acid receptor, alpha Mus musculus 194-197
18157915-6 2007 Retinoic acid increased TGF-beta2 mRNA content and secretion of the active and latent forms of TGF-beta2 (measured by ELISA and bioassay). Tretinoin 0-13 transforming growth factor beta 2 Homo sapiens 24-33
18157915-6 2007 Retinoic acid increased TGF-beta2 mRNA content and secretion of the active and latent forms of TGF-beta2 (measured by ELISA and bioassay). Tretinoin 0-13 transforming growth factor beta 2 Homo sapiens 95-104
18157915-7 2007 The concentrations of active and TGF-beta2 secreted in response to 0.1 - 10 muM retinoic acid were between 1-5 pM. Tretinoin 80-93 transforming growth factor beta 2 Homo sapiens 33-42
16914095-3 2006 Since all-trans retinoic acid (ATRA) can regulate some interferon -responsive genes, we studied here the effects of all-trans retinoic acid onto matrix metalloproteinase-9 levels in these cells. Tretinoin 6-29 matrix metallopeptidase 9 Homo sapiens 145-171
16914095-3 2006 Since all-trans retinoic acid (ATRA) can regulate some interferon -responsive genes, we studied here the effects of all-trans retinoic acid onto matrix metalloproteinase-9 levels in these cells. Tretinoin 31-35 matrix metallopeptidase 9 Homo sapiens 145-171
11274148-9 2001 RAR DBD greatly enhanced TTF-1 homeodomain DNA binding activity to a hSP-B enhancer oligonucleotide, in which retinoic acid-responsive element and TTF-1 DNA binding sites overlap. Tretinoin 110-123 retinoic acid receptor alpha Homo sapiens 0-3
16914095-3 2006 Since all-trans retinoic acid (ATRA) can regulate some interferon -responsive genes, we studied here the effects of all-trans retinoic acid onto matrix metalloproteinase-9 levels in these cells. Tretinoin 16-29 matrix metallopeptidase 9 Homo sapiens 145-171
16914095-5 2006 The inhibitory action of all-trans retinoic acid toward matrix metalloproteinase-9 was however not associated with the STAT1/IRF-1 pathway involved in interferon-mediated matrix metalloproteinase-9 inhibition indicating that all-trans retinoic acid did not bypass IFN receptor signaling. Tretinoin 35-48 matrix metallopeptidase 9 Homo sapiens 56-82
18026104-5 2007 We further show that deletion of a single retinoic acid receptor alpha (Rara) allele in a Trim24-null background suppresses HCC development and restores wild-type expression of retinoic acid-responsive genes in the liver, thus demonstrating that in this genetic background Rara expresses an oncogenic activity correlating with a dysregulation of the retinoic acid signaling pathway. Tretinoin 42-55 retinoic acid receptor, alpha Mus musculus 72-76
18026104-5 2007 We further show that deletion of a single retinoic acid receptor alpha (Rara) allele in a Trim24-null background suppresses HCC development and restores wild-type expression of retinoic acid-responsive genes in the liver, thus demonstrating that in this genetic background Rara expresses an oncogenic activity correlating with a dysregulation of the retinoic acid signaling pathway. Tretinoin 42-55 retinoic acid receptor, alpha Mus musculus 273-277
18026104-5 2007 We further show that deletion of a single retinoic acid receptor alpha (Rara) allele in a Trim24-null background suppresses HCC development and restores wild-type expression of retinoic acid-responsive genes in the liver, thus demonstrating that in this genetic background Rara expresses an oncogenic activity correlating with a dysregulation of the retinoic acid signaling pathway. Tretinoin 177-190 retinoic acid receptor, alpha Mus musculus 42-70
16914095-8 2006 Furthermore, we showed that all-trans retinoic acid down-regulated matrix metalloproteinase-9 expression in lymphocytes of untreated patients with early stage B chronic lymphocytic leukemia. Tretinoin 38-51 matrix metallopeptidase 9 Homo sapiens 67-93
16914095-9 2006 Together, our data suggest the potential relevance of all-trans retinoic acid as a pharmacological tool to attenuate matrix metalloproteinase-9 secretion in pathological situations. Tretinoin 64-77 matrix metallopeptidase 9 Homo sapiens 117-143
18026104-5 2007 We further show that deletion of a single retinoic acid receptor alpha (Rara) allele in a Trim24-null background suppresses HCC development and restores wild-type expression of retinoic acid-responsive genes in the liver, thus demonstrating that in this genetic background Rara expresses an oncogenic activity correlating with a dysregulation of the retinoic acid signaling pathway. Tretinoin 177-190 retinoic acid receptor, alpha Mus musculus 72-76
11274148-10 2001 Chromatin immunoprecipitation assay demonstrated that retinoic acid treatment of H441 cells greatly stimulated both RAR and TTF-1 DNA binding to the hSP-B enhancer region in H441 cells. Tretinoin 54-67 retinoic acid receptor alpha Homo sapiens 116-119
16680587-13 2006 CONCLUSIONS: These data implicate a novel antiproliferative role for RA in enhancing the pericellular clearance of IGF II via the IGF2R preventing ligand activation of the IGF I receptor. Tretinoin 69-71 insulin like growth factor 1 receptor Homo sapiens 172-186
11399774-8 2001 In the monocytic cell line THP-1 cell, the combination of IFN-gamma and all-trans-retinoic acid (a known differentiation agent) enhances the ACAT-1 P1 promoter but not the P7 promoter. Tretinoin 72-95 acetyl-CoA acetyltransferase 1 Homo sapiens 141-145
16329108-1 2006 Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RARalpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 137-140
15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 integrin subunit alpha M Homo sapiens 202-207
16780682-7 2006 RESULTS: Bufalin combined with ATRA can induce differentiation of APL cells towards mature stages, NBT reduction was increased 15% - 52% and CD(11)b expression was also increased 16% - 69% in combination of bufalin and ATRA as compared with that of ATRA alone, while the concentration of ATRA needed in the combination group was reduced to 30% and the time of differentiation was reduced from 7 days to 4 days. Tretinoin 31-35 integrin subunit alpha M Homo sapiens 141-148
16780682-7 2006 RESULTS: Bufalin combined with ATRA can induce differentiation of APL cells towards mature stages, NBT reduction was increased 15% - 52% and CD(11)b expression was also increased 16% - 69% in combination of bufalin and ATRA as compared with that of ATRA alone, while the concentration of ATRA needed in the combination group was reduced to 30% and the time of differentiation was reduced from 7 days to 4 days. Tretinoin 219-223 integrin subunit alpha M Homo sapiens 141-148
18476589-2 2007 METHODS: SDF-1 alpha mRNA from healthy adult lung tissue was measured by RT-PCR, CXCR4 protein expression on the cell membrane of APL cells induced by ATRA (APL-ATRA) was tested by FCM, and the rotary cell culture system (RCCS) was used to build a modal for in vitro stimulation of APL-ATRA infiltrating human lung tissue. Tretinoin 151-155 C-X-C motif chemokine receptor 4 Homo sapiens 81-86
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 64-77 retinoic acid receptor, alpha Mus musculus 197-225
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 64-77 retinoic acid receptor, alpha Mus musculus 227-235
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 79-81 retinoic acid receptor, alpha Mus musculus 197-225
17968018-4 2007 We report here that ectopic expression of two genes that act on retinoic acid (RA) signaling can cause resistance to growth arrest and apoptosis induced by HDACI of different chemical classes: the retinoic acid receptor alpha (RARalpha) and preferentially expressed antigen of melanoma (PRAME), a repressor of RA signaling. Tretinoin 79-81 retinoic acid receptor, alpha Mus musculus 227-235
16780682-7 2006 RESULTS: Bufalin combined with ATRA can induce differentiation of APL cells towards mature stages, NBT reduction was increased 15% - 52% and CD(11)b expression was also increased 16% - 69% in combination of bufalin and ATRA as compared with that of ATRA alone, while the concentration of ATRA needed in the combination group was reduced to 30% and the time of differentiation was reduced from 7 days to 4 days. Tretinoin 219-223 integrin subunit alpha M Homo sapiens 141-148
16780682-7 2006 RESULTS: Bufalin combined with ATRA can induce differentiation of APL cells towards mature stages, NBT reduction was increased 15% - 52% and CD(11)b expression was also increased 16% - 69% in combination of bufalin and ATRA as compared with that of ATRA alone, while the concentration of ATRA needed in the combination group was reduced to 30% and the time of differentiation was reduced from 7 days to 4 days. Tretinoin 219-223 integrin subunit alpha M Homo sapiens 141-148
11394905-3 2001 Culturing retinoic acid treated ES cells in the presence of the osteogenic supplements ascorbic acid and beta-glycerophosphate resulted in the expression of several osteoblast marker genes, osteocalcin, alkaline phosphatase, and osteopontin. Tretinoin 10-23 bone gamma-carboxyglutamate protein 2 Mus musculus 190-201
16549780-7 2006 Conversely, silencing of ENH by RNA interference prevents cytoplasmic relocation of Id2 in neuroblastoma cells differentiated with retinoic acid. Tretinoin 131-144 inhibitor of DNA binding 2 Homo sapiens 84-87
17875935-3 2007 p160 and Pbx1 compete for Prep1 in vitro, and p160 inhibits Prep1-dependent HoxB2 expression in retinoic acid-treated NT2-D1 cells. Tretinoin 96-109 PBX/knotted 1 homeobox 1 Homo sapiens 60-65
17875935-3 2007 p160 and Pbx1 compete for Prep1 in vitro, and p160 inhibits Prep1-dependent HoxB2 expression in retinoic acid-treated NT2-D1 cells. Tretinoin 96-109 homeobox B2 Homo sapiens 76-81
11558869-8 2001 Five out of 6 patients with KRT10 mutations benefited from treatment with oral acitretin (5-25mg/day) or topical tretinoin/tazarotene, but none of the patients with KRT1 mutations derived any benefit. Tretinoin 113-122 keratin 10 Homo sapiens 28-33
17715133-8 2007 These results indicated that the two binding sites for PGH(2) and retinoic acid in the large cavity of L-PGDS were responsible for the broad ligand specificity of L-PGDS and the non-competitive inhibition of L-PGDS activity by retinoic acid. Tretinoin 227-240 prostaglandin D2 synthase (brain) Mus musculus 163-169
17673545-0 2007 Retinoic acid signaling sensitizes hepatic stellate cells to NK cell killing via upregulation of NK cell activating ligand RAE1. Tretinoin 0-13 ribonucleic acid export 1 Mus musculus 123-127
17673545-7 2007 Blocking RA synthesis by the Raldh inhibitor or blocking RA signaling by the retinoic acid receptor antagonist abolished upregulation of RAE-1 whereas treatment with RA induced RAE-1 expression in HSCs. Tretinoin 9-11 ribonucleic acid export 1 Mus musculus 137-142
17673545-7 2007 Blocking RA synthesis by the Raldh inhibitor or blocking RA signaling by the retinoic acid receptor antagonist abolished upregulation of RAE-1 whereas treatment with RA induced RAE-1 expression in HSCs. Tretinoin 57-59 ribonucleic acid export 1 Mus musculus 137-142
17917245-4 2007 Since only 20 to 30% cells incubated with ATRA became positive for CCR3, CCR3(+) population was enriched by a magnetic activated cell sorter (MACS). Tretinoin 42-46 C-C motif chemokine receptor 3 Homo sapiens 67-71
16569247-2 2006 We show that these effects are potentiated by retinoic acid, an agonist of the retinoid-X-receptor. Tretinoin 46-59 retinoid X receptor alpha Homo sapiens 79-98
16288218-7 2006 Furthermore, the proapoptotic function of BMCC1 was also suggested by increased expression in CHP134 NBL cells undergoing apoptosis after treatment with retinoic acid, and by an enhanced apoptosis after depletion of NGF in the SCG neurons obtained from newborn mice transgenic with BMCC1 in primary culture. Tretinoin 153-166 prune homolog 2 with BCH domain Homo sapiens 42-47
16352598-7 2006 Luciferase reporter assay mediated by the oct-3/4 promoter revealed that cyclophilin A could act as a transcriptional activator and that its activity was suppressed by the beta-variant, suggesting that cyclophilin A takes part in the induction of oct-3/4 gene expression, which might lead to neuroectodermal otx2 expression within 12 h of the immediate-early stages of retinoic acid-primed neural differentiation. Tretinoin 369-382 POU domain, class 5, transcription factor 1 Mus musculus 42-49
16352598-7 2006 Luciferase reporter assay mediated by the oct-3/4 promoter revealed that cyclophilin A could act as a transcriptional activator and that its activity was suppressed by the beta-variant, suggesting that cyclophilin A takes part in the induction of oct-3/4 gene expression, which might lead to neuroectodermal otx2 expression within 12 h of the immediate-early stages of retinoic acid-primed neural differentiation. Tretinoin 369-382 peptidylprolyl isomerase A Mus musculus 73-86
16352598-7 2006 Luciferase reporter assay mediated by the oct-3/4 promoter revealed that cyclophilin A could act as a transcriptional activator and that its activity was suppressed by the beta-variant, suggesting that cyclophilin A takes part in the induction of oct-3/4 gene expression, which might lead to neuroectodermal otx2 expression within 12 h of the immediate-early stages of retinoic acid-primed neural differentiation. Tretinoin 369-382 peptidylprolyl isomerase A Mus musculus 202-215
16757381-3 2006 Two retinoic acid response elements (RAREs) to which retinoid X receptor alpha (RXRalpha) and retinoic acid receptor alpha (RARalpha) bind and activate transcription are present in the human PDK4 (hPDK4) proximal promoter. Tretinoin 4-17 retinoid X receptor alpha Homo sapiens 53-78
16757381-3 2006 Two retinoic acid response elements (RAREs) to which retinoid X receptor alpha (RXRalpha) and retinoic acid receptor alpha (RARalpha) bind and activate transcription are present in the human PDK4 (hPDK4) proximal promoter. Tretinoin 4-17 retinoid X receptor alpha Homo sapiens 80-88
17666047-0 2007 Induction of the reelin promoter by retinoic acid is mediated by Sp1. Tretinoin 36-49 reelin Homo sapiens 17-23
17666047-4 2007 We examined reelin mRNA and promoter induction following a 6-day treatment of these cells with retinoic acid (RA). Tretinoin 95-108 reelin Homo sapiens 12-18
17666047-4 2007 We examined reelin mRNA and promoter induction following a 6-day treatment of these cells with retinoic acid (RA). Tretinoin 110-112 reelin Homo sapiens 12-18
17666047-7 2007 Based on our results, it appears likely that RA-induces reelin expression through a critical Sp1 site that resides adjacent to the Pax6 site within this multisite enhancer region. Tretinoin 45-47 reelin Homo sapiens 56-62
11331070-2 2001 We aimed to study the effect of RA on RAR protein levels in MCF-7 human breast cancer cells. Tretinoin 32-34 retinoic acid receptor alpha Homo sapiens 38-41
17646388-2 2007 We previously showed that RA rapidly activated cyclic AMP response element-binding protein (CREB) in a nonclassical manner in normal human tracheobronchial epithelial (NHTBE) cells. Tretinoin 26-28 cAMP responsive element binding protein 1 Homo sapiens 47-90
17646388-2 2007 We previously showed that RA rapidly activated cyclic AMP response element-binding protein (CREB) in a nonclassical manner in normal human tracheobronchial epithelial (NHTBE) cells. Tretinoin 26-28 cAMP responsive element binding protein 1 Homo sapiens 92-96
17646388-3 2007 In the present study, we further demonstrated that this nonclassical signaling of RA on the activation of CREB plays a critical role in regulating the expression of airway epithelial cell differentiation markers, the MUC2, MUC5AC, and MUC5B genes. Tretinoin 82-84 cAMP responsive element binding protein 1 Homo sapiens 106-110
17646388-4 2007 We found that RA rapidly activates the protein kinase Calpha isozyme and transmits the activation signal to CREB via the Raf/MEK/extracellular signal-regulated kinase/p90 ribosomal S6 kinase (RSK) pathway. Tretinoin 14-16 cAMP responsive element binding protein 1 Homo sapiens 108-112
17646388-8 2007 Taken together, our findings demonstrate that CREB activation via this nonclassical RA signaling pathway may play an important role in regulating the expression of mucin genes and mediating the early biological effects of RA during normal mucous differentiation in NHTBE cells. Tretinoin 84-86 cAMP responsive element binding protein 1 Homo sapiens 46-50
16423341-3 2006 Early in cardiogenesis, retinoic acid alters the expression of key genes in the lateral plate mesoderm including Nkx2.5 and HAND1, indicating that early patterning of the lateral plate mesoderm is, in part, controlled by retinoic acid. Tretinoin 24-37 NK2 homeobox 5 S homeolog Xenopus laevis 113-119
16423341-3 2006 Early in cardiogenesis, retinoic acid alters the expression of key genes in the lateral plate mesoderm including Nkx2.5 and HAND1, indicating that early patterning of the lateral plate mesoderm is, in part, controlled by retinoic acid. Tretinoin 221-234 NK2 homeobox 5 S homeolog Xenopus laevis 113-119
16489341-8 2006 Our findings suggest that antagonism of Fgf8 expression by retinoic acid occurs in the ectoderm and that failure of this mechanism generates excessive FGF8 signalling to adjacent mesoderm, resulting initially in smaller somites and then left-right asymmetry. Tretinoin 59-72 fibroblast growth factor 8 Mus musculus 40-44
17646388-8 2007 Taken together, our findings demonstrate that CREB activation via this nonclassical RA signaling pathway may play an important role in regulating the expression of mucin genes and mediating the early biological effects of RA during normal mucous differentiation in NHTBE cells. Tretinoin 222-224 cAMP responsive element binding protein 1 Homo sapiens 46-50
11331070-3 2001 Incubation of these cells with 10(-6) M RA induced a rapid breakdown of both RARalpha and RARgamma in spite of the accumulation of their mRNAs. Tretinoin 40-42 retinoic acid receptor alpha Homo sapiens 77-85
17785809-2 2007 We found that the major vitamin A metabolite all-trans-retinoic acid induces histone acetylation at the FoxP3 gene promoter and expression of the FoxP3 protein in CD4+ T cells. Tretinoin 45-68 CD4 antigen Mus musculus 163-166
11331070-5 2001 Furthermore, RA enhanced the formation of the complex between RARalpha and ubiquitin in a concentration- and time-dependent manner, suggesting the involvement of ubiquitin and proteasome in this reaction. Tretinoin 13-15 retinoic acid receptor alpha Homo sapiens 62-70
16603817-3 2006 To investigate the effects of divalent cations on the dehydrogenase activity of Xenopus laevis ALDH1A1, the formation of acetate and retinoic acid from acetaldehyde and retinal, respectively, was investigated in the presence of Ca2+, Mg2+, Mn2+ or Zn2+. Tretinoin 133-146 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 95-102
11331070-8 2001 An electrophoretic mobility shift assay, using nuclear extracts from RA-treated cells, showed that a reduction in complex formation with hormone response elements correlated with the reduction of RAR and RXR protein. Tretinoin 69-71 retinoic acid receptor alpha Homo sapiens 196-199
17611083-4 2007 RA treatment for 24 h transiently increased invasion and expression of MMP9 in SH-SY5Y, LA-N-5 and MMP2 in SMS-KCNR cells. Tretinoin 0-2 matrix metallopeptidase 9 Homo sapiens 71-75
11384110-6 2001 ATRA also inhibited docetaxel-induced activation of MAPK indicating that the effects of docetaxel and ATRA on cdc2 phosphorylation are dependent on MAPK. Tretinoin 102-106 cyclin dependent kinase 1 Homo sapiens 110-114
16397143-3 2006 All trans-retinoic acid treatment of A404 cells induced a strong increase in LPP, as well as SM alpha-actin, SM myosin heavy chain, and smoothelin mRNA levels, in a Rho kinase (ROK)-dependent manner. Tretinoin 4-23 smoothelin Sus scrofa 136-146
11384110-7 2001 We conclude that ATRA synergistically enhances docetaxel toxicity by down-regulating Bcl-2 expression and partially reverses the docetaxel-induced G2/M arrest by inhibiting docetaxel-induced cdc2 phosphorylation in a pathway that is dependent on MAPK. Tretinoin 17-21 cyclin dependent kinase 1 Homo sapiens 191-195
17538007-10 2007 As has been described for rodent P19 embryonal carcinoma stem cells, retinoic acid treatment markedly suppressed KOR mRNA expression in human NPCs. Tretinoin 69-82 opioid receptor kappa 1 Homo sapiens 113-116
11378441-0 2001 Low synthesis of retinoic acid due to impaired cytochrome P450 1a1 expression in mouse xeroderma pigmentosum fibroblasts. Tretinoin 17-30 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 47-66
17579210-8 2007 ATRA, the effects of which are mediated by retinoic acid receptor alpha and gamma in C3H10T1/2 cells, stimulates the dissociation of C/EBPbeta from this element and promotes Runx2 expression. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 43-71
17825229-0 2007 [Effects of arsenic trioxide and ATRA on PLZF-RARalpha-positive U937 leukemic cells]. Tretinoin 33-37 zinc finger and BTB domain containing 16 Homo sapiens 41-45
17825229-1 2007 AIM: To investigate effects of arsenic trioxide (As(2)O(3)) and alltrans retinoic acid (ATRA) on PLZF-RARalpha-positive cells. Tretinoin 73-86 zinc finger and BTB domain containing 16 Homo sapiens 97-101
17825229-1 2007 AIM: To investigate effects of arsenic trioxide (As(2)O(3)) and alltrans retinoic acid (ATRA) on PLZF-RARalpha-positive cells. Tretinoin 88-92 zinc finger and BTB domain containing 16 Homo sapiens 97-101
16461020-6 2006 As result, merely two lipocalins, RBP and beta-trace, revealed high affinities both for retinol and for RA, which probably reflects a specialized physiological function in retinoid complexation. Tretinoin 104-106 retinol binding protein 4 Homo sapiens 34-37
17825229-9 2007 After treated with As(2)O(3) (0.5 micromol/L) and ATRA (1 mumol/L), U937/PLZF cells presented some changes such as decreased nuclear/cytoplasm ratio, and partial disappearance of nucleoli, suggesting a certain degree of morphological differentiation. Tretinoin 50-54 zinc finger and BTB domain containing 16 Homo sapiens 73-77
11378441-7 2001 These results suggest that decreased structure activity of RA synthesis, resulting from impaired mRNA expression of cytochrome P450 1a1 may, at least together with UV irradiation, involve in skin carcinogenesis in XP patients. Tretinoin 59-61 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 116-135
16472205-3 2006 Here we demonstrate that the alpha-secretase-cleaved fragment of the amyloid precursor protein (sAPPalpha), a potent neurotrophic factor, potentiates the nerve growth factor (NGF)/retinoic acid (RA) induced transdifferentiation of bone marrow-derived adult progenitor cells (MAPCs) into neural progenitor cells and, more specifically, enhances their terminal differentiation into a cholinergic-like neuronal phenotype. Tretinoin 180-193 nerve growth factor Mus musculus 154-173
16472205-3 2006 Here we demonstrate that the alpha-secretase-cleaved fragment of the amyloid precursor protein (sAPPalpha), a potent neurotrophic factor, potentiates the nerve growth factor (NGF)/retinoic acid (RA) induced transdifferentiation of bone marrow-derived adult progenitor cells (MAPCs) into neural progenitor cells and, more specifically, enhances their terminal differentiation into a cholinergic-like neuronal phenotype. Tretinoin 180-193 nerve growth factor Mus musculus 175-178
11413229-1 2001 NE-7C2 neuroectodermal cells derived from forebrain vesicles of p53-deficient mouse embryos (E9) produce neurons and astrocytes in vitro if induced by all-trans retinoic acid. Tretinoin 161-174 transformation related protein 53, pseudogene Mus musculus 64-67
16472205-3 2006 Here we demonstrate that the alpha-secretase-cleaved fragment of the amyloid precursor protein (sAPPalpha), a potent neurotrophic factor, potentiates the nerve growth factor (NGF)/retinoic acid (RA) induced transdifferentiation of bone marrow-derived adult progenitor cells (MAPCs) into neural progenitor cells and, more specifically, enhances their terminal differentiation into a cholinergic-like neuronal phenotype. Tretinoin 195-197 nerve growth factor Mus musculus 154-173
11404087-6 2001 Expression analysis in swirl and chordino mutants as well as in retinoic acid treated embryos indicate that noz1 is activated by BMP antagonists and neural posteriorizing signals. Tretinoin 64-77 decapentaplegic Drosophila melanogaster 129-132
16472205-3 2006 Here we demonstrate that the alpha-secretase-cleaved fragment of the amyloid precursor protein (sAPPalpha), a potent neurotrophic factor, potentiates the nerve growth factor (NGF)/retinoic acid (RA) induced transdifferentiation of bone marrow-derived adult progenitor cells (MAPCs) into neural progenitor cells and, more specifically, enhances their terminal differentiation into a cholinergic-like neuronal phenotype. Tretinoin 195-197 nerve growth factor Mus musculus 175-178
16439309-0 2006 Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Tretinoin 94-107 lymphocyte cytosolic protein 2 Homo sapiens 36-42
17310985-2 2007 In HaCaT keratinocytes, we found that atRA significantly suppressed the expression of Id2, a member of the inhibitor of differentiation family of transcription factors that regulate cell growth and differentiation. Tretinoin 38-42 inhibitor of DNA binding 2 Homo sapiens 86-89
16439309-2 2006 The present studies show that RA up-regulated expression of SLP-76 (Src-homology 2 domain-containing leukocyte-specific phospho-protein of 76 kDa), which became a prominent tyrosine-phosphorylated protein in RA-treated cells. Tretinoin 30-32 lymphocyte cytosolic protein 2 Homo sapiens 60-66
17475324-0 2007 RXRalpha regulates the pregnancy-specific glycoprotein 5 gene transcription through a functional retinoic acid responsive element. Tretinoin 97-110 retinoid X receptor alpha Homo sapiens 0-8
11434680-8 2001 In cells induced to differentiate by ATRA, CD11b expression seems more closely related to inositol uptake than to PKC activity while the expression of TF and TM show the opposite pattern, which suggests cellular events regulated at a different level within a common signal transduction pathway. Tretinoin 37-41 coagulation factor III, tissue factor Homo sapiens 151-153
17524364-1 2007 Human Apr3 was first cloned from HL-60 cells treated by ATRA. Tretinoin 56-60 all-trans retinoic acid induced differentiation factor Homo sapiens 6-10
16439309-2 2006 The present studies show that RA up-regulated expression of SLP-76 (Src-homology 2 domain-containing leukocyte-specific phospho-protein of 76 kDa), which became a prominent tyrosine-phosphorylated protein in RA-treated cells. Tretinoin 208-210 lymphocyte cytosolic protein 2 Homo sapiens 60-66
16439309-7 2006 SLP-76 now enhanced RA-induced ERK activation, compared to parental c-FMS transfectants. Tretinoin 20-22 lymphocyte cytosolic protein 2 Homo sapiens 0-6
16439309-10 2006 A triple Y to F mutant SLP-76 known to be a dominant negative in T-cell receptor signaling failed to enhance RA-induced paxillin expression, but enhanced RA-induced ERK activation, differentiation and G0 arrest essentially as well as wild-type SLP-76. Tretinoin 154-156 lymphocyte cytosolic protein 2 Homo sapiens 23-29
16439309-12 2006 This is the first indication to our knowledge that RA induces the expression of an adapter molecule to facilitate induced differentiation via co-operation between c-FMS and SLP-76. Tretinoin 51-53 lymphocyte cytosolic protein 2 Homo sapiens 173-179
17524364-2 2007 In this study, we further demonstrated that Apr3 could be obviously upregulated by ATRA in many other ATRA sensitive cells, suggesting a common role of Apr3 in ATRA effects. Tretinoin 83-87 all-trans retinoic acid induced differentiation factor Homo sapiens 44-48
17524364-2 2007 In this study, we further demonstrated that Apr3 could be obviously upregulated by ATRA in many other ATRA sensitive cells, suggesting a common role of Apr3 in ATRA effects. Tretinoin 83-87 all-trans retinoic acid induced differentiation factor Homo sapiens 152-156
11358845-0 2001 Overexpression of the retinoic acid-responsive gene Stra6 in human cancers and its synergistic induction by Wnt-1 and retinoic acid. Tretinoin 22-35 signaling receptor and transporter of retinol STRA6 Homo sapiens 52-57
17592014-7 2007 The number of tyrosine hydroxylase-positive (TH+) neurons was significantly increased after RA treatment in the rostral mdDA region of Pitx3-/- embryos. Tretinoin 92-94 paired-like homeodomain transcription factor 3 Mus musculus 135-140
17592014-10 2007 This positions Pitx3 centrally in a mdDA developmental cascade linked to RA signaling. Tretinoin 73-75 paired-like homeodomain transcription factor 3 Mus musculus 15-20
16206244-0 2006 Interaction of PP2A catalytic subunit with Rb2/p130 is required for all-trans retinoic acid suppression of ovarian carcinoma cell growth. Tretinoin 78-91 RB transcriptional corepressor like 2 Homo sapiens 43-46
16206244-0 2006 Interaction of PP2A catalytic subunit with Rb2/p130 is required for all-trans retinoic acid suppression of ovarian carcinoma cell growth. Tretinoin 78-91 RB transcriptional corepressor like 2 Homo sapiens 47-51
16206244-1 2006 All-trans retinoic acid (ATRA) treatment causes CAOV3 ovarian carcinoma cells to growth arrest in the G0/G1 phase and to elevate the level of Rb2/p130 protein. Tretinoin 0-23 RB transcriptional corepressor like 2 Homo sapiens 142-145
16206244-1 2006 All-trans retinoic acid (ATRA) treatment causes CAOV3 ovarian carcinoma cells to growth arrest in the G0/G1 phase and to elevate the level of Rb2/p130 protein. Tretinoin 0-23 RB transcriptional corepressor like 2 Homo sapiens 146-150
16206244-1 2006 All-trans retinoic acid (ATRA) treatment causes CAOV3 ovarian carcinoma cells to growth arrest in the G0/G1 phase and to elevate the level of Rb2/p130 protein. Tretinoin 25-29 RB transcriptional corepressor like 2 Homo sapiens 142-145
16206244-1 2006 All-trans retinoic acid (ATRA) treatment causes CAOV3 ovarian carcinoma cells to growth arrest in the G0/G1 phase and to elevate the level of Rb2/p130 protein. Tretinoin 25-29 RB transcriptional corepressor like 2 Homo sapiens 146-150
16206244-6 2006 Furthermore, CAOV3 cells transfected with a truncated Rb2/p130 construct consisting of only the wt C-terminus grew more aggressively and were less sensitive to ATRA treatment when compared to parental CAOV3 cells. Tretinoin 160-164 RB transcriptional corepressor like 2 Homo sapiens 54-57
16206244-6 2006 Furthermore, CAOV3 cells transfected with a truncated Rb2/p130 construct consisting of only the wt C-terminus grew more aggressively and were less sensitive to ATRA treatment when compared to parental CAOV3 cells. Tretinoin 160-164 RB transcriptional corepressor like 2 Homo sapiens 58-62
16206244-7 2006 In contrast, CAOV3 cells transfected with a truncated Rb2/p130 construct consisting of only the C-terminus in which the NLS sites were mutated and which could not interact with PP2A, were as sensitive to ATRA treatment as parental CAOV3 cells. Tretinoin 204-208 RB transcriptional corepressor like 2 Homo sapiens 54-57
17568621-0 2007 Activation of p38/MEF2C pathway by all-trans retinoic acid in cardiac myoblasts. Tretinoin 45-58 myocyte enhancer factor 2C Rattus norvegicus 18-23
17568621-4 2007 Here, our results, obtained from Western blot and protein kinase assays, showed that the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and MEF2C was induced by atRA in H9c2 myocardial cells. Tretinoin 177-181 myocyte enhancer factor 2C Rattus norvegicus 156-161
11358845-2 2001 We screened mouse C57MG cells to isolate mRNAs induced by Wnt-1 and identified Stra6, an mRNA known to be up-regulated by retinoic acid. Tretinoin 122-135 stimulated by retinoic acid gene 6 Mus musculus 79-84
16280361-0 2006 Nonclassical action of retinoic acid on the activation of the cAMP response element-binding protein in normal human bronchial epithelial cells. Tretinoin 23-36 cAMP responsive element binding protein 1 Homo sapiens 62-99
16280361-7 2006 Inhibition of protein kinase C (PKC) or extracellular regulated kinase (ERK1/2) blocked the RA-mediated activation of CREB. Tretinoin 92-94 cAMP responsive element binding protein 1 Homo sapiens 118-122
11358845-4 2001 Stimulation of C57MG cells with retinoic acid plus Wnt-1 resulted in expression of Stra6 transcript to levels greatly exceeding that observed with either stimulus alone. Tretinoin 32-45 stimulated by retinoic acid gene 6 Mus musculus 83-88
16280361-9 2006 Altogether, this study provides the first evidence that RA rapidly activates CREB transcription factor via PKC, ERK, and RSK in a retinoid receptor-independent manner in normal bronchial epithelial cells. Tretinoin 56-58 cAMP responsive element binding protein 1 Homo sapiens 77-81
17531980-1 2007 Treatment of HepG2 with all-trans retinoic acid (RA) induces expression of fatty acid synthase (FAS) mRNA and protein. Tretinoin 34-47 fatty acid synthase Homo sapiens 75-94
17531980-1 2007 Treatment of HepG2 with all-trans retinoic acid (RA) induces expression of fatty acid synthase (FAS) mRNA and protein. Tretinoin 34-47 fatty acid synthase Homo sapiens 96-99
11358845-6 2001 Accordingly, treatment of human colorectal cancer cell lines with retinoic acid resulted in the up-regulation of Stra6 mRNA and accumulation of Stra6 protein at the cell membrane. Tretinoin 66-79 signaling receptor and transporter of retinol STRA6 Homo sapiens 113-118
17531980-1 2007 Treatment of HepG2 with all-trans retinoic acid (RA) induces expression of fatty acid synthase (FAS) mRNA and protein. Tretinoin 49-51 fatty acid synthase Homo sapiens 75-94
11358845-6 2001 Accordingly, treatment of human colorectal cancer cell lines with retinoic acid resulted in the up-regulation of Stra6 mRNA and accumulation of Stra6 protein at the cell membrane. Tretinoin 66-79 signaling receptor and transporter of retinol STRA6 Homo sapiens 144-149
17531980-1 2007 Treatment of HepG2 with all-trans retinoic acid (RA) induces expression of fatty acid synthase (FAS) mRNA and protein. Tretinoin 49-51 fatty acid synthase Homo sapiens 96-99
16195406-7 2006 Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do not respond to BMP-4. Tretinoin 8-21 noggin Mus musculus 131-137
11331971-6 2001 In addition retinoic acid increased the production of hLAMP-1 and fibronectin but not transferrin, confirming our earlier report. Tretinoin 12-25 fibronectin 1 Mus musculus 66-77
16309824-0 2005 Retinoic acid amplifies the host immune response to LPS through increased T lymphocytes number and LPS binding protein expression. Tretinoin 0-13 lipopolysaccharide binding protein Rattus norvegicus 99-118
16309824-5 2005 The retinoic acid receptor (RAR)alpha agonist Ro 4060-55 but not the pan-retinoid X receptors (RXRs) agonist Ro 2573-86 mimicked the effects of atRA on LBP expression suggesting that atRA enhances LBP expression through a RARalpha-mediated pathway. Tretinoin 144-148 lipopolysaccharide binding protein Rattus norvegicus 152-155
16309824-6 2005 In order to investigate the significance of increased LBP expression we challenged atRA-supplemented rats with the Gram-positive bacteria Listeria monocytogenes (LM) that activates the immune response independently from LBP. Tretinoin 83-87 lipopolysaccharide binding protein Rattus norvegicus 54-57
16309824-12 2005 Overall, these data demonstrate that although atRA induces a "priming" of the immune system characterized by increased T lymphocytes number and LBP expression, the profile of the immune response depends on the inflammatory/infectious stimulus. Tretinoin 46-50 lipopolysaccharide binding protein Rattus norvegicus 144-147
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 patched 2 Rattus norvegicus 344-349
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 regenerating family member 1 alpha Rattus norvegicus 414-418
17307727-7 2007 Data presented indicate that these proadaptive effects of retinoic acid may be mediated via changes in the extracellular matrix (e.g., by increasing collagen IV synthesis, decreasing E-cadherin expression, and reducing integrin beta(3) levels), via affects on Hedgehog signaling (e.g., by reducing expression of the Hedgehog receptors Ptch and Ptch2 and the Gli1 transcription factor), by increasing expression of Reg1 and Pap1, and by modulation of retinoid and peroxisome proliferator-activated receptor signaling pathways. Tretinoin 58-71 regenerating family member 3 beta Rattus norvegicus 423-427
19746216-7 2007 For the treatment of the human transfectant cells with chemical carcinogens, all-trans retinoic acid (5 mM) and 13-cis retinoic acid (5 mM) downregulated the cellular NF-kappaB activation up to 83% and 85% compared to the NF-kappaB activity that was upregulated by NMU (5microM) and NEU (5microM), respectively. Tretinoin 87-100 neuralized E3 ubiquitin protein ligase 1 Homo sapiens 283-286
11780404-9 2001 atRA inhibited the MMP-1 mRNA overexpression from Day 14 to Day 28 and reduced the hydroxyproline content (5.59 +/- 0.70 micrograms/mg vs 7.96 +/- 1.13 micrograms/mg and 7.77 +/- 0.96 micrograms/mg vs 9.93 +/- 1.27 micrograms/mg, P < 0.01) and the mean pulmonary artery pressure compared with the model group (19.6 +/- 3.2 mm Hg vs 25.7 +/- 4.3 mm Hg and 26.3 +/- 4.6 mm Hg vs 38.5 +/- 6.4 mm Hg, P < 0.01). Tretinoin 0-4 matrix metallopeptidase 1 Rattus norvegicus 19-24
17331771-6 2007 Functionally, we observed that axolotl NPDC-1 mRNA expression peaked late in embryogenesis, with highest levels of expression occurring during the time of limb development, a process regulated by retinoic acid signaling. Tretinoin 196-209 neural proliferation, differentiation and control 1 Homo sapiens 39-45
17331771-8 2007 These data justify axolotl as a model to further investigate NPDC-1 and its role in regulating retinoic acid signaling. Tretinoin 95-108 neural proliferation, differentiation and control 1 Homo sapiens 61-67
11780404-10 2001 CONCLUSION: atRA inhibits MMP-1 overexpression and the accumulation of collagen, which might elicit favorable geometric remodeling in rat pulmonary hypertension induced by monocrotaline. Tretinoin 12-16 matrix metallopeptidase 1 Rattus norvegicus 26-31
17426037-8 2007 Furthermore, when dominant negative CREB proteins with mutations in either the CREB phosphorylation site (CREBS133A) or the DNA binding domain (KCREB) were introduced into SH-SY5Y cells, retinoic acid-induced differentiation was blocked and the cells underwent cell death. Tretinoin 187-200 cAMP responsive element binding protein 1 Homo sapiens 36-40
17426037-9 2007 The results demonstrate that ATM is required for the retinoic acid-induced differentiation of SH-SY5Y cells through the ATM dependent-phosphorylation of serine 133 of CREB. Tretinoin 53-66 cAMP responsive element binding protein 1 Homo sapiens 167-171
11348454-5 2001 In this study, we have examined the abundance and distribution of fibrillin-1 prior to, and following, 192 wk of all-trans retinoic acid treatment. Tretinoin 123-136 fibrillin 1 Homo sapiens 66-77
17426037-10 2007 These results therefore define a novel mechanism for activation of the activity of ATM kinase by RA, and implicate ATM in the regulation of CREB function during RA-induced differentiation. Tretinoin 97-99 cAMP responsive element binding protein 1 Homo sapiens 140-144
17426037-10 2007 These results therefore define a novel mechanism for activation of the activity of ATM kinase by RA, and implicate ATM in the regulation of CREB function during RA-induced differentiation. Tretinoin 161-163 cAMP responsive element binding protein 1 Homo sapiens 140-144
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 71-84 microsomal triglyceride transfer protein Homo sapiens 149-189
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 71-84 microsomal triglyceride transfer protein Homo sapiens 191-194
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 86-88 microsomal triglyceride transfer protein Homo sapiens 149-189
11348454-14 2001 Significant increases (p < 0.05) were observed at the protein and mRNA levels for fibrillin-1 following all-trans retinoic acid and sodium lauryl sulfate treatments, with all-trans retinoic acid having a significantly greater effect than irritant control (p < 0.001); however, neither application had significant effect on the abundance of collagen VII or its mRNA. Tretinoin 117-130 fibrillin 1 Homo sapiens 85-96
17368571-2 2007 Here, we report that the GD3 synthase is involved in apoB secretion in retinoic acid (RA)-treated Chang liver cells via transcriptional induction of microsomal triglyceride transfer protein (MTP). Tretinoin 86-88 microsomal triglyceride transfer protein Homo sapiens 191-194
11348454-19 2001 This study indicates that all-trans retinoic acid can significantly affect fibrillin-1 content in photoaged skin. Tretinoin 36-49 fibrillin 1 Homo sapiens 75-86
11348470-8 2001 All-trans retinoic acid lead to a strong increase in urokinase-type plasminogen activator (enzyme-linked immunosorbent assay) and urokinase-type plasminogen activator receptor cell surface expression (flow cytometry) after 24 h. At this time-point, tissue-type plasminogen activator and plasminogen activator inhibitor-1 and -2 proteins were not or only slightly increased. Tretinoin 10-23 serpin family B member 2 Homo sapiens 287-327
11348470-9 2001 Northern blot analyses revealed that all-trans retinoic acid caused an early and short-lived increase of plasminogen activator inhibitor-1, but a prolonged induction of urokinase-type plasminogen activator and urokinase-type plasminogen activator receptor mRNA levels. Tretinoin 47-60 serpin family E member 1 Homo sapiens 105-138
17244893-4 2007 In any of these basal media, addition of 1,25-dihydroxyvitamin D(3), all-trans-retinoic acid or dexamethasone significantly increased activity of the nephrin promoter. Tretinoin 69-92 nephrosis 1, nephrin Mus musculus 150-157
11369412-1 2001 To study the in vivo effect of all-trans-retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)) on the expression of tissue factor (TF) and the other hemostatic disturbance, a series of parameters were measured either in bone marrow blasts or plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 31-54 coagulation factor III, tissue factor Homo sapiens 116-129
17209053-6 2007 By using specific inhibitors, all the RA-mediated events, including proliferation, cyclin D3 expression, IL-10 secretion, and Ig secretion, were shown to be dependent on p38MAPK. Tretinoin 38-40 interleukin 10 Homo sapiens 105-110
11369412-1 2001 To study the in vivo effect of all-trans-retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)) on the expression of tissue factor (TF) and the other hemostatic disturbance, a series of parameters were measured either in bone marrow blasts or plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 31-54 coagulation factor III, tissue factor Homo sapiens 131-133
17451530-0 2007 HSP110, caspase-3 and -9 expression in physiological apoptosis and apoptosis induced by in vivo embryonic exposition to all-trans retinoic acid or irradiation during early mouse eye development. Tretinoin 130-143 heat shock 105kDa/110kDa protein 1 Mus musculus 0-6
17451530-0 2007 HSP110, caspase-3 and -9 expression in physiological apoptosis and apoptosis induced by in vivo embryonic exposition to all-trans retinoic acid or irradiation during early mouse eye development. Tretinoin 130-143 caspase 3 Mus musculus 8-24
17451530-12 2007 HSP110 and caspase-3 expression presented similar topographic and chronological patterns, whereas expression of HSP110 was more precocious in retinoic acid-treated embryos. Tretinoin 142-155 heat shock 105kDa/110kDa protein 1 Mus musculus 112-118
11369412-1 2001 To study the in vivo effect of all-trans-retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)) on the expression of tissue factor (TF) and the other hemostatic disturbance, a series of parameters were measured either in bone marrow blasts or plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 56-60 coagulation factor III, tissue factor Homo sapiens 116-129
11369412-1 2001 To study the in vivo effect of all-trans-retinoic acid (ATRA) and arsenic trioxide (As(2)O(3)) on the expression of tissue factor (TF) and the other hemostatic disturbance, a series of parameters were measured either in bone marrow blasts or plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 56-60 coagulation factor III, tissue factor Homo sapiens 131-133
11290610-0 2001 Myeloblastin is an Myb target gene: mechanisms of regulation in myeloid leukemia cells growth-arrested by retinoic acid. Tretinoin 106-119 MYB proto-oncogene, transcription factor Homo sapiens 19-22
17498488-5 2007 RESULTS: ATRA caused remarkable elevation of intercellular adhesion molecule-1 (ICAM-1) in NB4 cells, which could be significantly reduced by tripterine (P<0.01). Tretinoin 9-13 intercellular adhesion molecule 1 Homo sapiens 45-78
17498488-5 2007 RESULTS: ATRA caused remarkable elevation of intercellular adhesion molecule-1 (ICAM-1) in NB4 cells, which could be significantly reduced by tripterine (P<0.01). Tretinoin 9-13 intercellular adhesion molecule 1 Homo sapiens 80-86
11290610-2 2001 Although Myb is a target of retinoic acid, little is known about the mechanisms by which it may contribute to induced growth arrest in leukemia cells. Tretinoin 28-41 MYB proto-oncogene, transcription factor Homo sapiens 9-12
17318229-3 2007 Among potential interactors, we found that activating protein transcription factor 2 (AP2)alpha forms a complex with NPM during retinoic-acid-induced cell differentiation. Tretinoin 128-141 transcription factor AP-2 alpha Homo sapiens 86-95
11290610-8 2001 Inhibition of myeloblastin expression in leukemia cells growth-arrested by retinoic acid is demonstrated to depend on Myb down-regulation. Tretinoin 75-88 MYB proto-oncogene, transcription factor Homo sapiens 118-121
11290610-9 2001 Myb is shown to induce myeloblastin expression and abolish its down-regulation by retinoic acid. Tretinoin 82-95 MYB proto-oncogene, transcription factor Homo sapiens 0-3
11290610-10 2001 Altogether, the data offer a clue as to how a myeloid-specific transcriptional machinery can be accessible to regulation by retinoic acid and point to myeloblastin as a novel target of Myb. Tretinoin 124-137 MYB proto-oncogene, transcription factor Homo sapiens 185-188
11290610-11 2001 This link between Myb and myeloblastin suggests a previously nonidentified Myb pathway through which growth arrest is induced by retinoic acid in myeloid leukemia cells. Tretinoin 129-142 MYB proto-oncogene, transcription factor Homo sapiens 18-21
17259635-8 2007 Accordingly we show that differentiation of Ntera2 cells with retinoic acid led to down-regulation of ZNF217. Tretinoin 62-75 zinc finger protein 217 Homo sapiens 102-108
11290610-11 2001 This link between Myb and myeloblastin suggests a previously nonidentified Myb pathway through which growth arrest is induced by retinoic acid in myeloid leukemia cells. Tretinoin 129-142 MYB proto-oncogene, transcription factor Homo sapiens 75-78
11237747-8 2001 NGFI-B nuclear receptors have been implicated in retinoic acid, vitamin D, and thyroid hormone signaling. Tretinoin 49-62 nuclear receptor subfamily 4, group A, member 1 Mus musculus 0-6
17244623-0 2007 Epstein-Barr virus lytic infection induces retinoic acid-responsive genes through induction of a retinol-metabolizing enzyme, DHRS9. Tretinoin 43-56 dehydrogenase/reductase 9 Homo sapiens 126-131
17244623-4 2007 Here we show that AGS gastric carcinoma cells containing the lytic form of EBV infection have enhanced expression of a gene (DHRS9) encoding an enzyme that mediates conversion of retinol into RA. Tretinoin 192-194 dehydrogenase/reductase 9 Homo sapiens 125-130
17183585-0 2007 Platelet-derived growth factor C plays a role in the branchial arch malformations induced by retinoic acid. Tretinoin 93-106 platelet-derived growth factor, C polypeptide Mus musculus 0-32
11237771-3 2001 A similar effect was observed with 13-cis retinoic acid (RA), which has been used in chemoprevention of SCC. Tretinoin 57-59 serpin family B member 3 Homo sapiens 104-107
17183585-4 2007 The roles of PDGF-C in branchial arch malformations induced by RA and possible mechanisms were investigated. Tretinoin 63-65 platelet-derived growth factor, C polypeptide Mus musculus 13-19
17183585-9 2007 RESULTS: PDGF-C was reduced by RA, and exogenous PDGF-C rescued the branchial arch malformations induced by RA. Tretinoin 31-33 platelet-derived growth factor, C polypeptide Mus musculus 9-15
17183585-9 2007 RESULTS: PDGF-C was reduced by RA, and exogenous PDGF-C rescued the branchial arch malformations induced by RA. Tretinoin 108-110 platelet-derived growth factor, C polypeptide Mus musculus 49-55
11170409-5 2001 In the present study, we examined the effect of exogenous gangliosides on the NADase activity of CD38 on the surface of retinoic acid-treated human leukemic HL60 cells and CD38-transfected THP-1 cells. Tretinoin 120-133 CD38 molecule Homo sapiens 97-101
17183585-10 2007 Moreover, PDGF-C prevented RA-induced inhibition of the migratory ability of mesenchymal cells in the first branchial arch, by regulating the expressions of MMP-2, MMP-14, and TIPM-2. Tretinoin 27-29 platelet-derived growth factor, C polypeptide Mus musculus 10-16
17183585-10 2007 Moreover, PDGF-C prevented RA-induced inhibition of the migratory ability of mesenchymal cells in the first branchial arch, by regulating the expressions of MMP-2, MMP-14, and TIPM-2. Tretinoin 27-29 matrix metallopeptidase 2 Mus musculus 157-162
17183585-10 2007 Moreover, PDGF-C prevented RA-induced inhibition of the migratory ability of mesenchymal cells in the first branchial arch, by regulating the expressions of MMP-2, MMP-14, and TIPM-2. Tretinoin 27-29 matrix metallopeptidase 14 (membrane-inserted) Mus musculus 164-170
17183585-11 2007 CONCLUSIONS: Our results suggest that RA exposure reduces the expression of PDGF-C. Tretinoin 38-40 platelet-derived growth factor, C polypeptide Mus musculus 76-82
17183585-12 2007 The branchial arch malformations resulting from fetal RA exposure are caused at least partially by loss of PDGF-C and subsequent misregulations of the expressions of MMP-2, MMP-14, and TIMP-2. Tretinoin 54-56 platelet-derived growth factor, C polypeptide Mus musculus 107-113
17183585-12 2007 The branchial arch malformations resulting from fetal RA exposure are caused at least partially by loss of PDGF-C and subsequent misregulations of the expressions of MMP-2, MMP-14, and TIMP-2. Tretinoin 54-56 matrix metallopeptidase 2 Mus musculus 166-171
17183585-12 2007 The branchial arch malformations resulting from fetal RA exposure are caused at least partially by loss of PDGF-C and subsequent misregulations of the expressions of MMP-2, MMP-14, and TIMP-2. Tretinoin 54-56 matrix metallopeptidase 14 (membrane-inserted) Mus musculus 173-179
17170094-12 2007 ATRA also induced VDGFR-2/KDR mRNA expression in HUVECs. Tretinoin 0-4 kinase insert domain receptor Homo sapiens 26-29
17339181-7 2007 Here we compared the effects of ATRA and arsenic on PML/RARalpha-positive stem cell compartments. Tretinoin 32-36 retinoic acid receptor, alpha Mus musculus 56-64
17253143-0 2007 Retinoic acid enhances the production of IL-10 while reducing the synthesis of IL-12 and TNF-alpha from LPS-stimulated monocytes/macrophages. Tretinoin 0-13 interleukin 10 Homo sapiens 41-46
17253143-7 2007 The addition of atRA to cell cultures potentiated the LPS-induced IL-10 mRNA expression and the number of IL-10 secreting cells from THP-1 cells and cord blood mononuclear cells. Tretinoin 16-20 interleukin 10 Homo sapiens 106-111
17253143-11 2007 While atRA downregulated the proinflammatory cytokines, e.g., IL-12 and TNF-alpha, the production of an immune modulating cytokine, IL-10 was enhanced by atRA. Tretinoin 154-158 interleukin 10 Homo sapiens 132-137
17275818-0 2007 Involvement of membrane protein GDE2 in retinoic acid-induced neurite formation in Neuro2A cells. Tretinoin 40-53 glycerophosphodiester phosphodiesterase domain containing 5 Mus musculus 32-36
17275818-1 2007 We show that a glycerophosphodiester phosphodiesterase homolog, GDE2, is widely expressed in brain tissues including primary neurons, and that the expression of GDE2 in neuroblastoma Neuro2A cells is significantly upregulated during neuronal differentiation by retinoic acid (RA) treatment. Tretinoin 261-274 glycerophosphodiester phosphodiesterase domain containing 5 Mus musculus 64-68
17275818-1 2007 We show that a glycerophosphodiester phosphodiesterase homolog, GDE2, is widely expressed in brain tissues including primary neurons, and that the expression of GDE2 in neuroblastoma Neuro2A cells is significantly upregulated during neuronal differentiation by retinoic acid (RA) treatment. Tretinoin 261-274 glycerophosphodiester phosphodiesterase domain containing 5 Mus musculus 161-165
17275818-1 2007 We show that a glycerophosphodiester phosphodiesterase homolog, GDE2, is widely expressed in brain tissues including primary neurons, and that the expression of GDE2 in neuroblastoma Neuro2A cells is significantly upregulated during neuronal differentiation by retinoic acid (RA) treatment. Tretinoin 276-278 glycerophosphodiester phosphodiesterase domain containing 5 Mus musculus 64-68
17275818-1 2007 We show that a glycerophosphodiester phosphodiesterase homolog, GDE2, is widely expressed in brain tissues including primary neurons, and that the expression of GDE2 in neuroblastoma Neuro2A cells is significantly upregulated during neuronal differentiation by retinoic acid (RA) treatment. Tretinoin 276-278 glycerophosphodiester phosphodiesterase domain containing 5 Mus musculus 161-165
17275818-3 2007 Furthermore, a loss-of-function of GDE2 in Neuro2A cells by RNAi blocked RA-induced neurite formation. Tretinoin 73-75 glycerophosphodiester phosphodiesterase domain containing 5 Mus musculus 35-39
17218779-1 2007 The constitutive over-expression of the retinol dehydrogenase 10 (RDH10) gene, involved in retinoic acid (RA) biosynthesis, produced in HepG2 cells a significant antiproliferative response, but not signs of apoptosis. Tretinoin 91-104 retinol dehydrogenase 10 Homo sapiens 40-64
17218779-1 2007 The constitutive over-expression of the retinol dehydrogenase 10 (RDH10) gene, involved in retinoic acid (RA) biosynthesis, produced in HepG2 cells a significant antiproliferative response, but not signs of apoptosis. Tretinoin 91-104 retinol dehydrogenase 10 Homo sapiens 66-71
17218779-1 2007 The constitutive over-expression of the retinol dehydrogenase 10 (RDH10) gene, involved in retinoic acid (RA) biosynthesis, produced in HepG2 cells a significant antiproliferative response, but not signs of apoptosis. Tretinoin 106-108 retinol dehydrogenase 10 Homo sapiens 40-64
17218779-1 2007 The constitutive over-expression of the retinol dehydrogenase 10 (RDH10) gene, involved in retinoic acid (RA) biosynthesis, produced in HepG2 cells a significant antiproliferative response, but not signs of apoptosis. Tretinoin 106-108 retinol dehydrogenase 10 Homo sapiens 66-71
17218779-4 2007 These results indicated that forced expression of RDH10 produces antiproliferative effects highly comparable to those achieved by retinoids treatment and thus the development of a gene therapy, finalized at the restoration of the enzymatic and receptorial machinery of the RA pathway, could be a possible curative strategy for hepatocellular carcinoma (HCC). Tretinoin 273-275 retinol dehydrogenase 10 Homo sapiens 50-55
17289919-6 2007 Independent of its action on androgen synthesis, SHP also determines the timing of germ cell differentiation by controlling testicular retinoic acid metabolism. Tretinoin 135-148 nuclear receptor subfamily 0, group B, member 2 Mus musculus 49-52
17289919-8 2007 Together, our data demonstrate new roles for SHP in testicular androgen and retinoic acid metabolism, making SHP a testicular gatekeeper of the timing of male sexual maturation. Tretinoin 76-89 nuclear receptor subfamily 0, group B, member 2 Mus musculus 45-48
17161435-4 2007 Expressions of all three genes (SLIM1, SM alpha-actin and CNN-1) were simultaneously elevated in the cells treated with 9-cis retinoic acid (RA). Tretinoin 141-143 four and a half LIM domains 1 Rattus norvegicus 32-37
17011172-2 2007 RA suppresses the expression of alpha2(I) collagen by means of the activities of specific nuclear receptors RARalpha, RXRbeta and their coregulators. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 108-116
17011172-3 2007 In this study, the effects of RA in fibrogenesis were examined in carbon tetrachloride (CCl4) induced liver fibrosis in mice. Tretinoin 30-32 chemokine (C-C motif) ligand 4 Mus musculus 88-92
17011172-5 2007 RA reduced the amount of histologically detectable fibrosis produced by CCl4. Tretinoin 0-2 chemokine (C-C motif) ligand 4 Mus musculus 72-76
17011172-7 2007 Furthermore, RA reduced the levels of 3-nitrotyrosine (3-NT) protein adducts and thiobarbituric acid (TBA) reactive substance (TBARS) in the liver, which are formed as results of oxidative stress induced by CCl4 treatment. Tretinoin 13-15 chemokine (C-C motif) ligand 4 Mus musculus 207-211
17011172-9 2007 The data also provide evidence that RA reduces CCl4 induced oxidative stress in liver, suggesting that the anti-fibrotic role of RA is not limited to the inhibition of type I collagen expression. Tretinoin 36-38 chemokine (C-C motif) ligand 4 Mus musculus 47-51
17164423-5 2007 In zebrafish embryos depleted of the orthologs of the three mammalian CYP26 genes CYP26A1, CYP26B1 and CYP26C1, the entire hindbrain expresses RA-responsive genes that are normally restricted to nested domains in the posterior hindbrain. Tretinoin 143-145 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 103-110
17035100-8 2007 Retinoic acid signaling influences tsh1 expression. Tretinoin 0-13 teashirt zinc finger homeobox 1 Danio rerio 35-39
17035100-9 2007 Zebrafish tsh1 expression was induced in the anterior neural tube in embryos treated briefly with exogenous retinoic acid. Tretinoin 108-121 teashirt zinc finger homeobox 1 Danio rerio 10-14
16873554-4 2006 All-trans retinoic acid (ATRA) increased pgrn mRNA levels in myelomonocytic cells (CD34(+) progenitors; monoblastic U-937; monocytic THP-1; progranulocytic HL-60; macrophage RAW 264.7) but not in nonmyeloid cells tested. Tretinoin 10-23 granulin Mus musculus 41-45
16873554-4 2006 All-trans retinoic acid (ATRA) increased pgrn mRNA levels in myelomonocytic cells (CD34(+) progenitors; monoblastic U-937; monocytic THP-1; progranulocytic HL-60; macrophage RAW 264.7) but not in nonmyeloid cells tested. Tretinoin 25-29 granulin Mus musculus 41-45
16873554-8 2006 In U-937, ATRA and chemical differentiation agents greatly increased pgrn mRNA stability, whereas, in HL-60, ATRA accelerated pgrn mRNA turnover. Tretinoin 10-14 granulin Mus musculus 69-73
16873554-9 2006 The initial upregulation of pgrn mRNA after stimulation with ATRA was independent of de novo protein synthesis in U-937 but not HL-60. Tretinoin 61-65 granulin Mus musculus 28-32
16873554-10 2006 Chemical blockade of nuclear factor-kappaB (NF-kappaB) activation impaired ATRA-stimulated pgrn expression in HL-60 but not U-937, whereas in U-937 it blocked PMA-induced pgrn mRNA expression, suggestive of cell-specific roles for NF-kappaB in determining pgrn mRNA levels. Tretinoin 75-79 granulin Mus musculus 91-95
16873554-10 2006 Chemical blockade of nuclear factor-kappaB (NF-kappaB) activation impaired ATRA-stimulated pgrn expression in HL-60 but not U-937, whereas in U-937 it blocked PMA-induced pgrn mRNA expression, suggestive of cell-specific roles for NF-kappaB in determining pgrn mRNA levels. Tretinoin 75-79 granulin Mus musculus 171-175
16873554-10 2006 Chemical blockade of nuclear factor-kappaB (NF-kappaB) activation impaired ATRA-stimulated pgrn expression in HL-60 but not U-937, whereas in U-937 it blocked PMA-induced pgrn mRNA expression, suggestive of cell-specific roles for NF-kappaB in determining pgrn mRNA levels. Tretinoin 75-79 granulin Mus musculus 171-175
17145891-8 2006 Administration of a retinoic acid to cancer-bearing mice reduced the population of CD11b(+) Gr-1(+) cells and effectively restored alpha-GalCer-induced protection. Tretinoin 20-33 integrin subunit alpha M Homo sapiens 83-88
17005281-0 2006 Mapping of the RXRalpha binding elements involved in retinoic acid induced transcriptional activation of the human SOX3 gene. Tretinoin 53-66 retinoid X receptor alpha Homo sapiens 15-23
17118196-6 2006 Real time RT-PCR analysis revealed a dampened expression of the Th1-associated gene, T-bet, and a time-dependent increase in the mRNA for the Th2-associated genes, GATA-3, c-MAF and STAT6, upon treatment with ATRA. Tretinoin 209-213 GATA binding protein 3 Homo sapiens 164-170
17118196-7 2006 Besides Th1 and Th2 cytokines, a number of additional proinflammatory and regulatory cytokines including several chemokines were also differentially regulated by ATRA treatment. Tretinoin 162-166 negative elongation factor complex member C/D Homo sapiens 8-11
17001652-13 2006 Furthermore, we were able to calculate in silico K(i)"s comparable to the published experimental values for the complexes of palmitic and retinoic acid with BLG. Tretinoin 138-151 beta-lactoglobulin Bos taurus 157-160
16996685-5 2006 RT-PCR analysis revealed that AdvNT-3 in combination with RA pretreatment could initiate the transcription of TrkC mRNA. Tretinoin 58-60 neurotrophic receptor tyrosine kinase 3 Homo sapiens 110-114
16919229-3 2006 We describe a fluorescence-based method for quantitating RA that takes advantage of the high affinity and selectivity of the intracellular lipid-binding protein termed CRABP-I and CRABP-II and that uses them as RA sensors. Tretinoin 57-59 cellular retinoic acid binding protein 2 Homo sapiens 180-188
16860319-2 2006 G protein signaling either blocks or mimics RA-induced differentiation, the latter signaling through the Wnt-beta-catenin pathway. Tretinoin 44-46 catenin (cadherin associated protein), beta 1 Mus musculus 109-121
16982809-4 2006 Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 (RALDH2). Tretinoin 45-58 retinol dehydrogenase 10 Homo sapiens 148-172
16982809-4 2006 Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 (RALDH2). Tretinoin 45-58 aldehyde dehydrogenase 1 family member A2 Homo sapiens 177-211
16982809-4 2006 Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 (RALDH2). Tretinoin 45-58 aldehyde dehydrogenase 1 family member A2 Homo sapiens 213-219
16854989-0 2006 Retinoic acid regulates the expression of photoreceptor transcription factor NRL. Tretinoin 0-13 neural retina leucine zipper Homo sapiens 77-80
16854989-4 2006 Here, we show that retinoic acid (RA), a diffusible factor implicated in rod development, activates the expression of NRL in serum-deprived Y79 human retinoblastoma cells and in primary cultures of rat and porcine photoreceptors. Tretinoin 19-32 neural retina leucine zipper Homo sapiens 118-121
16854989-4 2006 Here, we show that retinoic acid (RA), a diffusible factor implicated in rod development, activates the expression of NRL in serum-deprived Y79 human retinoblastoma cells and in primary cultures of rat and porcine photoreceptors. Tretinoin 34-36 neural retina leucine zipper Homo sapiens 118-121
16925845-0 2006 Prevention of retinoic acid-induced early craniofacial abnormalities by folinic acid and expression of endothelin-1/dHAND in the branchial arches in mouse. Tretinoin 14-27 hand Drosophila melanogaster 116-121
16115698-1 2006 The effects of ethanol consumption and ageing were investigated on the expression levels of retinoic acid (RA) and triiodothyronine (T3) nuclear receptors (RAR, RXR and TR) and of associated target genes involved in synaptic plasticity, neurogranin (RC3) and neuromodulin (GAP-43) in mice brain. Tretinoin 92-105 retinoic acid receptor, alpha Mus musculus 156-159
16918696-4 2006 We have previously shown that ATRA-induced differentiation and cell cycle arrest specifically requires Stat1 activation, through phosphorylation of tyrosine 701 and serine 727. Tretinoin 30-34 signal transducer and activator of transcription 1 Homo sapiens 103-108
16918696-6 2006 We demonstrate that ATRA-induced upregulation of Stat2, ICSBP/IRF8 and C/EBPepsilon, key transcription factors linked to myelomonocytic differentiation, is selectively impaired in cells expressing mutant Stat1. Tretinoin 20-24 signal transducer and activator of transcription 2 Homo sapiens 49-54
16280019-10 2005 In the in vitro luciferase assay, GRA resulted in significant dose-dependent RAR transactivation activity in a 100 times higher concentration range than RA. Tretinoin 35-37 retinoic acid receptor, alpha Mus musculus 77-80
16280019-12 2005 CONCLUSIONS: Topical GRA appears to be able to repair photoaged skin damage without any of the irritation caused by topical RA, probably via RAR transactivation activity. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 141-144
16249480-0 2005 Effect of retinoic acid on gene expression in human conjunctival epithelium: secretory phospholipase A2 mediates retinoic acid induction of MUC16. Tretinoin 113-126 mucin 16, cell surface associated Homo sapiens 140-145
16249480-8 2005 To investigate whether sPLA(2) is associated with RA-induced MUC16 upregulation, HCjE cells were incubated with RA and the broad-spectrum PLA(2) inhibitor aristolochic acid (ArA) or the specific sPLA(2)-IIA inhibitor LY315920, followed by analysis of MUC16 mRNA and protein by real-time PCR and Western blot analysis. Tretinoin 50-52 phospholipase A2 group IIA Homo sapiens 23-29
16249480-8 2005 To investigate whether sPLA(2) is associated with RA-induced MUC16 upregulation, HCjE cells were incubated with RA and the broad-spectrum PLA(2) inhibitor aristolochic acid (ArA) or the specific sPLA(2)-IIA inhibitor LY315920, followed by analysis of MUC16 mRNA and protein by real-time PCR and Western blot analysis. Tretinoin 50-52 mucin 16, cell surface associated Homo sapiens 61-66
16186334-10 2005 Application of exogenous retinoic acid downregulated BCO mRNA levels at higher concentrations (1 microM; -96%, P < 0.0005) and upregulated it at a lower concentration (0.01 microM; 399%, P < 0.005). Tretinoin 25-38 beta-carotene oxygenase 1 Homo sapiens 53-56
16277846-6 2005 In ATRA and TPA group, the change of HSP70 had positive correlation with JWA, and negative correlation with Bcl-2. Tretinoin 3-7 heat shock protein family A (Hsp70) member 4 Homo sapiens 37-42
16277846-6 2005 In ATRA and TPA group, the change of HSP70 had positive correlation with JWA, and negative correlation with Bcl-2. Tretinoin 3-7 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 73-76
16083855-5 2005 When a dominant negative form of NDRF protein was expressed during retinoic acid-induced neuronal differentiation of P19 cells, the BLBP gene, but not the Id1 gene, was potently repressed. Tretinoin 67-80 fatty acid binding protein 7, brain Mus musculus 132-136
16084493-9 2005 Phospho-JNK immunohistochemistry showed that ATRA inhibited the activation of JNK. Tretinoin 45-49 mitogen-activated protein kinase 8 Mus musculus 8-11
16084493-9 2005 Phospho-JNK immunohistochemistry showed that ATRA inhibited the activation of JNK. Tretinoin 45-49 mitogen-activated protein kinase 8 Mus musculus 78-81
16166285-0 2005 The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer. Tretinoin 4-17 aldehyde dehydrogenase 1 family member A2 Homo sapiens 33-40
16166285-4 2005 ALDH1a2 encodes an enzyme responsible for synthesis of retinoic acid (RA), a compound with prodifferentiation properties. Tretinoin 55-68 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-7
16166285-4 2005 ALDH1a2 encodes an enzyme responsible for synthesis of retinoic acid (RA), a compound with prodifferentiation properties. Tretinoin 70-72 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-7
16166285-7 2005 Finally, transfection-mediated reexpression of wild-type ALDH1a2 (but not a presumptive catalytically dead mutant) in the prostate cancer cell line DU145 resulted in decreased colony growth (P < 0.0001), comparable with treatment with either 5-aza-dC or RA. Tretinoin 257-259 aldehyde dehydrogenase 1 family member A2 Homo sapiens 57-64
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 90-92 cellular retinoic acid binding protein 2 Homo sapiens 36-44
16166294-7 2005 In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Tretinoin 90-92 cellular retinoic acid binding protein 2 Homo sapiens 36-44
16109390-5 2005 Mice absent in the three proteins CRBP I, CRABP I, and CRABP II (CI/CAI/CAII-/-) displayed significantly lower hepatic retinyl ester, retinol, and all-trans-retinoic acid levels compared to wildtype mice, whereas the liver concentrations of 9-cis-4-oxo-13,14-dihydro-retinoic acid was considerably higher. Tretinoin 151-170 cellular retinoic acid binding protein I Mus musculus 42-49
16096774-4 2005 Recent studies in vitro show that retinoic acid (RA) downregulates the release of MCP-1 and TGF-beta1 by tumor cells. Tretinoin 34-47 chemokine (C-C motif) ligand 2 Mus musculus 82-87
16096774-4 2005 Recent studies in vitro show that retinoic acid (RA) downregulates the release of MCP-1 and TGF-beta1 by tumor cells. Tretinoin 49-51 chemokine (C-C motif) ligand 2 Mus musculus 82-87
16096774-5 2005 Therefore, we investigated the ability of RA to modulate the ability of tumor cells to recruit and activate monocytes for participation in VEGF-mediated angiogenesis and immunosuppression in vivo. Tretinoin 42-44 vascular endothelial growth factor A Mus musculus 139-143
15950488-5 2005 Transcripts for the ligand-specifying receptors for GDNF and neurturin, GFRalpha-1 and GFRalpha-2, as well as the common signal transducing receptor Ret were all down-regulated by RA treatment in a dose-dependent manner. Tretinoin 180-182 GDNF family receptor alpha 1 Gallus gallus 72-97
16129031-8 2005 This rapid down-regulation of VEGF gene expression, during ATRA-induced NB4 cell differentiation, was accompanied by the up-regulation of CD11b expression and an increased NBT reduction rate. Tretinoin 59-63 integrin subunit alpha M Homo sapiens 138-143
16038410-10 2005 Despite a weak increase in cytosolic Hsp70, the percentage of Hsp70 membrane-positive cells dropped significantly after repeated treatments with 13-RA and ATRA in CX+ and ML-1 but not in CX- tumor cells. Tretinoin 155-159 heat shock protein family A (Hsp70) member 4 Homo sapiens 62-67
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 132-145 integrin subunit alpha M Homo sapiens 11-16
15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 147-149 integrin subunit alpha M Homo sapiens 11-16
15850806-12 2005 Electrophoretic mobility shift assays with nuclear extract from atRA-treated cells indicated the binding of retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers specifically to this response element. Tretinoin 64-68 retinoid X receptor alpha Homo sapiens 141-160
15850806-12 2005 Electrophoretic mobility shift assays with nuclear extract from atRA-treated cells indicated the binding of retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers specifically to this response element. Tretinoin 64-68 retinoid X receptor alpha Homo sapiens 162-165
15955085-0 2005 Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla. Tretinoin 77-90 transforming growth factor beta 2 Homo sapiens 163-195
15955085-9 2005 After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Tretinoin 13-17 transforming growth factor beta 2 Homo sapiens 29-38
15955085-10 2005 Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. Tretinoin 79-83 transforming growth factor beta 2 Homo sapiens 54-63
15955085-11 2005 This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Tretinoin 56-60 transforming growth factor beta 2 Homo sapiens 181-190
16110744-3 2005 The purpose of this work was to detect caspase 3 (which is associated with the apoptosis cascade) and p53 in cell death areas, both during physiological apoptosis and during apoptosis induced by three agents (retinoic acid, methyl-triazene, irradiation). Tretinoin 209-222 caspase 3 Mus musculus 39-48
15949692-5 2005 It is shown that RA reduces RB expression and enhances RB phosphorylation by a mechanism that involves down-regulation of the cyclin-dependent kinase inhibitor (CKI) p21(Cip1), having this fact as important consequences for both the cell cycle progression and the adipocyte differentiation process. Tretinoin 17-19 cyclin dependent kinase inhibitor 3 Homo sapiens 126-159
15809060-5 2005 In GAL4-DNA tethering assays, the DeltaC-C mutant completely lost the inhibitory effect on retinoic acid (RA)-mediated transactivation. Tretinoin 106-108 galectin 4 Homo sapiens 3-7
15790450-10 2005 CONCLUSIONS: The mechanism of RA radiosensitization does not require functional p53 and may involve c-fos in cervical cancer cell lines. Tretinoin 30-32 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 100-105
15816857-3 2005 High secretin transcript and peptide levels were found in this cell, and secretin gene expression and promoter activity were up-regulated upon all-trans retinoic acid (RA) treatment. Tretinoin 153-166 secretin Homo sapiens 73-81
15816857-3 2005 High secretin transcript and peptide levels were found in this cell, and secretin gene expression and promoter activity were up-regulated upon all-trans retinoic acid (RA) treatment. Tretinoin 168-170 secretin Homo sapiens 5-13
15816857-3 2005 High secretin transcript and peptide levels were found in this cell, and secretin gene expression and promoter activity were up-regulated upon all-trans retinoic acid (RA) treatment. Tretinoin 168-170 secretin Homo sapiens 73-81
15816857-5 2005 The human secretin gene in SH-SY5Y cells is controlled by the (Sp1 + Sp4)/Sp3 ratio and the RA-induced activation is a partial result of a decrease in Sp3 levels. Tretinoin 92-94 secretin Homo sapiens 10-18
15816857-10 2005 We conclude that RA induction of the secretin gene in neuronal cells is regulated by the combined actions of reducing Sp3 and increasing NFI-C expression. Tretinoin 17-19 secretin Homo sapiens 37-45
15777839-4 2005 Cholera toxin-induced activation of cAMP responsive element (CRE)-binding protein (CREB) was enhanced by pretreating cells with ATRA for 24 h. In contrast, HGF production induced by epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) was potently inhibited by ATRA. Tretinoin 128-132 cAMP responsive element binding protein 1 Homo sapiens 83-87
15777839-4 2005 Cholera toxin-induced activation of cAMP responsive element (CRE)-binding protein (CREB) was enhanced by pretreating cells with ATRA for 24 h. In contrast, HGF production induced by epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) was potently inhibited by ATRA. Tretinoin 279-283 cAMP responsive element binding protein 1 Homo sapiens 83-87
15707588-2 2005 In this study, using luciferase assay of a reporter gene containing PPAR response element (PPRE), we found PPRE transactivity was additively induced by PPAR gamma activator (15dPGJ2) and RXR activator (9-cis retinoic acid, 9-cis RA). Tretinoin 208-221 retinoid X receptor alpha Homo sapiens 187-190
15733075-12 2005 CONCLUSION: Our findings indicate that administration of RA increases serum and nerve contents of NGF in diabetic mice and suggest a potential therapeutic role for retinoic acid in diabetic patients. Tretinoin 57-59 nerve growth factor Mus musculus 98-101
15749933-3 2005 MSCs treated with retinoic acid resulted in synaptic transmission, based on immunostaining of synaptophysin and electrophysiological studies. Tretinoin 18-31 synaptophysin Homo sapiens 94-107
16918696-6 2006 We demonstrate that ATRA-induced upregulation of Stat2, ICSBP/IRF8 and C/EBPepsilon, key transcription factors linked to myelomonocytic differentiation, is selectively impaired in cells expressing mutant Stat1. Tretinoin 20-24 signal transducer and activator of transcription 1 Homo sapiens 204-209
16918696-8 2006 Taken together, our data suggest that ATRA-induced regulation of Stat2, ICSBP and C/EBPepsilon is dependent on active Stat1, and that a failure to correctly regulate these transcription factors is associated with the inhibition of monocytic differentiation. Tretinoin 38-42 signal transducer and activator of transcription 2 Homo sapiens 65-70
16918696-8 2006 Taken together, our data suggest that ATRA-induced regulation of Stat2, ICSBP and C/EBPepsilon is dependent on active Stat1, and that a failure to correctly regulate these transcription factors is associated with the inhibition of monocytic differentiation. Tretinoin 38-42 signal transducer and activator of transcription 1 Homo sapiens 118-123
16872382-5 2006 In addition, all-trans-retinoic acid-treated dendritic cells could drive T cells towards T-helper cell type 2 responses with decreased secretion of interleukin-12, interferon-gamma, and increased production of interleukin-10 and interleukin-4. Tretinoin 13-36 interleukin 10 Homo sapiens 210-224
16417921-1 2006 To study the function of S100A9 protein in HL-60 cells treated with all-trans retinoic acid (ATRA), we had designed and constructed retroviral vectors for expression of small hairpin RNAs (shRNAs), and silenced S100A9 expression in HL-60 cells treated with ATRA. Tretinoin 78-91 S100 calcium binding protein A9 Homo sapiens 25-31
16417921-1 2006 To study the function of S100A9 protein in HL-60 cells treated with all-trans retinoic acid (ATRA), we had designed and constructed retroviral vectors for expression of small hairpin RNAs (shRNAs), and silenced S100A9 expression in HL-60 cells treated with ATRA. Tretinoin 93-97 S100 calcium binding protein A9 Homo sapiens 25-31
16417921-4 2006 Western blot showed that shRNAs remarkably reduce of S100A9 expression in HL-60 cells when they were induced to differentiation by ATRA. Tretinoin 131-135 S100 calcium binding protein A9 Homo sapiens 53-59
16928318-3 2006 After treated with ATRA at 0.01, 0.1, or 1 micromol/L, expression of intercellular adhesion molecule-1 (ICAM-1) protein and vascular adhesion molecule-1 (VCAM-1) protein were detected by flow cytometry, and soluble ICAM-1 (sICAM-1) protein was determined by using radioimmunoassay. Tretinoin 19-23 intercellular adhesion molecule 1 Homo sapiens 69-102
16928318-3 2006 After treated with ATRA at 0.01, 0.1, or 1 micromol/L, expression of intercellular adhesion molecule-1 (ICAM-1) protein and vascular adhesion molecule-1 (VCAM-1) protein were detected by flow cytometry, and soluble ICAM-1 (sICAM-1) protein was determined by using radioimmunoassay. Tretinoin 19-23 intercellular adhesion molecule 1 Homo sapiens 104-110
16928318-3 2006 After treated with ATRA at 0.01, 0.1, or 1 micromol/L, expression of intercellular adhesion molecule-1 (ICAM-1) protein and vascular adhesion molecule-1 (VCAM-1) protein were detected by flow cytometry, and soluble ICAM-1 (sICAM-1) protein was determined by using radioimmunoassay. Tretinoin 19-23 intercellular adhesion molecule 1 Homo sapiens 215-221
15710892-3 2005 We demonstrate that disruption of retinoic acid-inducible gene I (RIG-I) signaling by the viral NS3/4A protease contributes to the ability of HCV to control innate antiviral defenses. Tretinoin 34-47 KRAS proto-oncogene, GTPase Homo sapiens 96-99
11036068-1 2001 The interactions between retinoic acid- (RA)-dependent transcriptional regulatory sequences of the 5"-untranslated region of the thrombomodulin gene and nuclear RA-responsive proteins were studied using human pancreas BxPC-3 cells. Tretinoin 25-38 thrombomodulin Homo sapiens 129-143
15591223-9 2005 CONCLUSIONS: Clusterin overexpression characterized neointimal SMCs; s-CLU expression decreased in IT cells during all-trans retinoic acid-induced proliferative arrest and redifferentiation, whereas n-CLU overexpression was characteristic of apoptosis. Tretinoin 125-138 clusterin Rattus norvegicus 71-74
15591223-12 2005 All-trans retinoic acid-induced proliferative arrest showed association with s-CLU reduction and n-CLU overexpression with apoptosis, supporting a different biological role of these isoforms. Tretinoin 10-23 clusterin Rattus norvegicus 79-82
16699180-4 2006 We report that COX-2 is up-regulated in APC mutant zebrafish because of a deficiency in retinoic acid biosynthesis. Tretinoin 88-101 APC regulator of WNT signaling pathway Danio rerio 40-43
16699180-5 2006 Treatment of both APC mutant zebrafish and human carcinoma cell lines with retinoic acid significantly reduces COX-2 expression. Tretinoin 75-88 APC regulator of WNT signaling pathway Danio rerio 18-21
16699180-6 2006 Retinoic acid regulates COX-2 levels by a mechanism that involves participation of the transcription factor C/EBP-beta. Tretinoin 0-13 CCAAT enhancer binding protein beta Danio rerio 108-118
16888198-1 2006 Previously, we found that secretin transcript levels were induced by all-trans retinoic acid (RA) in a neuroblastoma cell model, SH-SY5Y. Tretinoin 94-96 secretin Homo sapiens 26-34
16888198-4 2006 Together with our previous works, we propose here that the RA responsiveness of the secretin promotor is mediated by two different pathways. Tretinoin 59-61 secretin Homo sapiens 84-92
15774309-0 2005 Effects of ATRA on expression of mRNA binding protein p62 in human gastric cancer cells. Tretinoin 11-15 nucleoporin 62 Homo sapiens 54-57
15774309-2 2005 In control cells p62 was cytoplasmic in location and concentrated in the cytoplasmic matrix, but when cell growth was inhibited by treatment with 50 microM all-trans-retinoic acid (ATRA) for 5 days, p62 expression decreased and the protein was translocated from cytoplasm to nucleus. Tretinoin 156-179 nucleoporin 62 Homo sapiens 17-20
11036068-1 2001 The interactions between retinoic acid- (RA)-dependent transcriptional regulatory sequences of the 5"-untranslated region of the thrombomodulin gene and nuclear RA-responsive proteins were studied using human pancreas BxPC-3 cells. Tretinoin 41-43 thrombomodulin Homo sapiens 129-143
15774309-2 2005 In control cells p62 was cytoplasmic in location and concentrated in the cytoplasmic matrix, but when cell growth was inhibited by treatment with 50 microM all-trans-retinoic acid (ATRA) for 5 days, p62 expression decreased and the protein was translocated from cytoplasm to nucleus. Tretinoin 156-179 nucleoporin 62 Homo sapiens 199-202
15774309-2 2005 In control cells p62 was cytoplasmic in location and concentrated in the cytoplasmic matrix, but when cell growth was inhibited by treatment with 50 microM all-trans-retinoic acid (ATRA) for 5 days, p62 expression decreased and the protein was translocated from cytoplasm to nucleus. Tretinoin 181-185 nucleoporin 62 Homo sapiens 17-20
11036068-1 2001 The interactions between retinoic acid- (RA)-dependent transcriptional regulatory sequences of the 5"-untranslated region of the thrombomodulin gene and nuclear RA-responsive proteins were studied using human pancreas BxPC-3 cells. Tretinoin 161-163 thrombomodulin Homo sapiens 129-143
15774309-2 2005 In control cells p62 was cytoplasmic in location and concentrated in the cytoplasmic matrix, but when cell growth was inhibited by treatment with 50 microM all-trans-retinoic acid (ATRA) for 5 days, p62 expression decreased and the protein was translocated from cytoplasm to nucleus. Tretinoin 181-185 nucleoporin 62 Homo sapiens 199-202
16763719-1 2006 AIM: To study the regulatory effects of 9-cis retinoic acid (RA) on the expression of human homeobox gene NKX3.1 in prostate cancer cell line LNCaP. Tretinoin 61-63 NK3 homeobox 1 Homo sapiens 106-112
16763719-7 2006 CONCLUSION: Our results demonstrated that 9-cis RA as a differentiating agent can arrest prostate cancer cells in G(1) phase and reduce cell mitosis, and upregulate the expression of human homeobox gene NKX3.1, which is thought to play an important role in prostate differentiation and to act as a tumor suppressor gene in the prostate. Tretinoin 48-50 NK3 homeobox 1 Homo sapiens 203-209
16226872-3 2006 Treatment with ATRA at 1 muM for 5 days markedly inhibited the proliferation and increased the expression of differentiation markers (CD38, CD11b) in HL-60/Vect cells, but showed no such effect in HL-60/FAK cells. Tretinoin 15-19 integrin subunit alpha M Homo sapiens 140-145
15750294-6 2005 Furthermore, RA may promote cytoplasmic maturation of bovine oocytes via its modulatory effects on the gene expression of gonadotrophin receptors, midkine, cyclooxygenase-2, and nitric oxide synthase in cumulus-granulosa cells. Tretinoin 13-15 prostaglandin-endoperoxide synthase 2 Bos taurus 156-172
11157777-0 2001 The retinoic acid-inactivating enzyme CYP26 is essential for establishing an uneven distribution of retinoic acid along the anterio-posterior axis within the mouse embryo. Tretinoin 4-17 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 38-43
15629189-6 2005 CYP1A1 and 1A2 were both induced by treatment with beta-napthoflavone as indicated by RT-PCR and Western blotting, while CYP2C mRNA was upregulated by all-trans retinoic acid and farnesol. Tretinoin 161-174 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 121-126
16531051-3 2006 Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Tretinoin 73-86 beta-secretase 1 Rattus norvegicus 248-269
16531051-3 2006 Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Tretinoin 73-86 beta-secretase 1 Rattus norvegicus 271-275
16531051-3 2006 Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Tretinoin 88-90 beta-secretase 1 Rattus norvegicus 248-269
16531051-3 2006 Thus, the effect of vitamin A depletion and subsequent administration of retinoic acid (RA, the active metabolite of vitamin A) on the expression of RARbeta, and of proteins involved in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the whole brain, hippocampus, striatum, and cerebral cortex of rats. Tretinoin 88-90 beta-secretase 1 Rattus norvegicus 271-275
11157777-0 2001 The retinoic acid-inactivating enzyme CYP26 is essential for establishing an uneven distribution of retinoic acid along the anterio-posterior axis within the mouse embryo. Tretinoin 100-113 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 38-43
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 101-114 muscular LMNA interacting protein Homo sapiens 0-3
15567562-4 2005 In particular, we reported for the first time that RA treatment was followed by a modulation of endogenous Ngn1 and Math1 transcripts. Tretinoin 51-53 neurogenin 1 Homo sapiens 107-111
11157777-3 2001 We have examined the role of CYP26, a P450 enzyme that may degrade RA, by generating mutant mice that lack CYP26. Tretinoin 67-69 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 29-34
15567562-4 2005 In particular, we reported for the first time that RA treatment was followed by a modulation of endogenous Ngn1 and Math1 transcripts. Tretinoin 51-53 atonal bHLH transcription factor 1 Homo sapiens 116-121
15492006-7 2004 Expression of the dominant negative p115RhoGEF was able to inhibit activation of both RhoA and JNK1 in response to either retinoic acid or the expression of a constitutively activated mutant of G alpha(13). Tretinoin 122-135 mitogen-activated protein kinase 8 Mus musculus 95-99
15494319-8 2004 RA up-regulated the expression level of MAP kinase phosphatase-1 (MKP-1) and MKP-2, and the time course was correlated with the inhibitory effect of RA on activation of MAP kinases. Tretinoin 0-2 dual specificity phosphatase 4 Homo sapiens 77-82
16765349-1 2006 Cip/Kip family protein p21, a cyclin-dependent kinase (CDK) inhibitor, is directly transactivated by retinoic acid receptor alpha (RARalpha) upon retinoic acid (RA):RARalpha binding. Tretinoin 131-133 muscular LMNA interacting protein Homo sapiens 0-3
16586441-4 2006 They confirm that RA plays critical roles in controlling spermatogonia differentiation, spermatid adhesion to Sertoli cells, and spermiation, and suggest that the VAD-induced arrest of spermatogonia differentiation results from simultaneous blocks in RA-dependent events mediated by RA receptor gamma (RARgamma) in spermatogonia and by RARalpha in Sertoli cells. Tretinoin 18-20 retinoic acid receptor, gamma Mus musculus 283-300
15494319-8 2004 RA up-regulated the expression level of MAP kinase phosphatase-1 (MKP-1) and MKP-2, and the time course was correlated with the inhibitory effect of RA on activation of MAP kinases. Tretinoin 149-151 dual specificity phosphatase 4 Homo sapiens 77-82
16586441-4 2006 They confirm that RA plays critical roles in controlling spermatogonia differentiation, spermatid adhesion to Sertoli cells, and spermiation, and suggest that the VAD-induced arrest of spermatogonia differentiation results from simultaneous blocks in RA-dependent events mediated by RA receptor gamma (RARgamma) in spermatogonia and by RARalpha in Sertoli cells. Tretinoin 18-20 retinoic acid receptor, gamma Mus musculus 302-310
11157777-5 2001 The concentration of endogenous RA, as revealed by marker gene activity, was markedly increased in the tailbud of the mutant animals, in which CYP26 is normally expressed. Tretinoin 32-34 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 143-148
16586441-4 2006 They confirm that RA plays critical roles in controlling spermatogonia differentiation, spermatid adhesion to Sertoli cells, and spermiation, and suggest that the VAD-induced arrest of spermatogonia differentiation results from simultaneous blocks in RA-dependent events mediated by RA receptor gamma (RARgamma) in spermatogonia and by RARalpha in Sertoli cells. Tretinoin 18-20 retinoic acid receptor, alpha Mus musculus 336-344
11157777-7 2001 The lack of CYP26 also resulted in homeotic transformation of vertebrae as well as in misspecification of the rostral hindbrain associated with anterior expansion of RA-positive domains. Tretinoin 166-168 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 12-17
11157777-8 2001 These results suggest that local degradation of RA by CYP26 is required for establishing an uneven distribution of RA along the anterio-posterior axis, which is essential for patterning the hindbrain, vertebrae, and tailbud. Tretinoin 48-50 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 54-59
15530851-10 2004 RA treatment increased steady-state levels of the protein tyrosine phosphatase PTP-1C and all measured effects of RA on EGF receptor function were reversed by the tyrosine phosphate inhibitor orthovanadate. Tretinoin 0-2 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 79-85
11157777-8 2001 These results suggest that local degradation of RA by CYP26 is required for establishing an uneven distribution of RA along the anterio-posterior axis, which is essential for patterning the hindbrain, vertebrae, and tailbud. Tretinoin 115-117 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 54-59
15358764-9 2004 Treatment of either APC or zRDHB morphant embryos with retinoic acid rescued the defective phenotypes. Tretinoin 55-68 APC regulator of WNT signaling pathway Danio rerio 20-23
16813970-6 2006 Proteins involved in mediating the cellular responses to RA include the cellular retinoic acid binding proteins CRABP-I and CRABP-II and the nuclear retinoic acid receptors RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 57-59 cellular retinoic acid binding protein I Mus musculus 112-119
11157778-0 2001 The retinoic acid-metabolizing enzyme, CYP26A1, is essential for normal hindbrain patterning, vertebral identity, and development of posterior structures. Tretinoin 4-17 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 39-46
16813970-6 2006 Proteins involved in mediating the cellular responses to RA include the cellular retinoic acid binding proteins CRABP-I and CRABP-II and the nuclear retinoic acid receptors RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 57-59 retinoic acid receptor, alpha Mus musculus 173-182
15358764-11 2004 Our data establish a genetic link supporting a critical role for retinoic acid downstream of APC and confirm the importance of retinoic acid in enterocyte differentiation. Tretinoin 65-78 APC regulator of WNT signaling pathway Danio rerio 93-96
16813970-6 2006 Proteins involved in mediating the cellular responses to RA include the cellular retinoic acid binding proteins CRABP-I and CRABP-II and the nuclear retinoic acid receptors RAR-alpha, RAR-beta, and RAR-gamma. Tretinoin 57-59 retinoic acid receptor, gamma Mus musculus 198-207
11157778-4 2001 As a first step in understanding the developmental function of RA-metabolizing enzymes, we have disrupted the murine Cyp26A1 gene. Tretinoin 63-65 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 117-124
11157778-9 2001 Because all of the Cyp26A1(-/-) abnormalities closely resemble RA teratogenic effects, we postulate that the key function of CYP26A1 is to maintain specific embryonic areas in a RA-depleted state, to protect them against the deleterious effect of ectopic RA signaling. Tretinoin 178-180 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 125-132
15581624-0 2004 All-trans retinoic acid inhibits proliferation of intestinal epithelial cells by inhibiting expression of the gene encoding Kruppel-like factor 5. Tretinoin 10-23 Kruppel-like factor 5 Rattus norvegicus 124-145
11157778-9 2001 Because all of the Cyp26A1(-/-) abnormalities closely resemble RA teratogenic effects, we postulate that the key function of CYP26A1 is to maintain specific embryonic areas in a RA-depleted state, to protect them against the deleterious effect of ectopic RA signaling. Tretinoin 178-180 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 125-132
15581624-6 2004 In contrast, constitutive expression of KLF5 in stably transfected IEC6 cells with a KLF5-expressing plasmid driven by a viral promoter abrogated the growth inhibitory effect of ATRA. Tretinoin 178-182 Kruppel-like factor 5 Rattus norvegicus 40-44
16682494-6 2006 Furthermore, loss of RARgamma abrogated the potentiating effects of all-trans retinoic acid on the maintenance of HSCs in ex vivo culture. Tretinoin 78-91 retinoic acid receptor, gamma Mus musculus 21-29
11212271-9 2001 The ATRA metabolites were found to exert their differentiation effects via the RAR alpha nuclear receptors, because the RAR alpha-specific antagonist BMS614 blocked metabolite-induced CD11c expression in NB4 cells. Tretinoin 4-8 retinoic acid receptor alpha Homo sapiens 120-129
15581624-6 2004 In contrast, constitutive expression of KLF5 in stably transfected IEC6 cells with a KLF5-expressing plasmid driven by a viral promoter abrogated the growth inhibitory effect of ATRA. Tretinoin 178-182 Kruppel-like factor 5 Rattus norvegicus 85-89
15581624-8 2004 Our results indicate that KLF5 is a potential mediator for the inhibitory effect of ATRA on intestinal epithelial cell proliferation. Tretinoin 84-88 Kruppel-like factor 5 Rattus norvegicus 26-30
16517099-9 2006 Transient transfection experiments with RXRalpha promoter-luciferase reporter constructs in SRB12-p9 skin SCC cells, as well as with PC3 prostate carcinoma cells, revealed that RXRalpha transcription is relatively weak compared to the positive control thymidine kinase (TK) promoter and is stimulated by treatment with all-trans retinoic acid (ATRA), the biologically active form of vitamin A. Tretinoin 329-342 retinoid X receptor alpha Homo sapiens 177-185
16517099-9 2006 Transient transfection experiments with RXRalpha promoter-luciferase reporter constructs in SRB12-p9 skin SCC cells, as well as with PC3 prostate carcinoma cells, revealed that RXRalpha transcription is relatively weak compared to the positive control thymidine kinase (TK) promoter and is stimulated by treatment with all-trans retinoic acid (ATRA), the biologically active form of vitamin A. Tretinoin 344-348 retinoid X receptor alpha Homo sapiens 177-185
11245337-9 2001 In T-47D breast cancer cells, which express RARalpha, RXRalpha and ER, 17beta-HSD reductive activity increased 1.76-fold (p < 0.001), five days following treatment with 10 nM retinoic acid. Tretinoin 178-191 retinoic acid receptor alpha Homo sapiens 44-52
16408290-3 2006 We have demonstrated that phospholipase C-beta2 (PLC-beta2), highly expressed in neutrophils and nearly absent in tumoral promyelocytes, largely increases during ATRA treatment of APL-derived cells and strongly correlates with the responsiveness of APL patients to ATRA-based differentiating therapies. Tretinoin 162-166 phospholipase C beta 2 Homo sapiens 26-47
16408290-3 2006 We have demonstrated that phospholipase C-beta2 (PLC-beta2), highly expressed in neutrophils and nearly absent in tumoral promyelocytes, largely increases during ATRA treatment of APL-derived cells and strongly correlates with the responsiveness of APL patients to ATRA-based differentiating therapies. Tretinoin 162-166 phospholipase C beta 2 Homo sapiens 49-58
16408290-3 2006 We have demonstrated that phospholipase C-beta2 (PLC-beta2), highly expressed in neutrophils and nearly absent in tumoral promyelocytes, largely increases during ATRA treatment of APL-derived cells and strongly correlates with the responsiveness of APL patients to ATRA-based differentiating therapies. Tretinoin 265-269 phospholipase C beta 2 Homo sapiens 26-47
16408290-3 2006 We have demonstrated that phospholipase C-beta2 (PLC-beta2), highly expressed in neutrophils and nearly absent in tumoral promyelocytes, largely increases during ATRA treatment of APL-derived cells and strongly correlates with the responsiveness of APL patients to ATRA-based differentiating therapies. Tretinoin 265-269 phospholipase C beta 2 Homo sapiens 49-58
16408290-4 2006 Here we report that, in APL-derived cells, low doses of As3O3 induce a slight increase of PLC-beta2 together with a moderate maturation, and cooperate with ATRA to provoke a significant increase of PLC-beta2 expression. Tretinoin 156-160 phospholipase C beta 2 Homo sapiens 198-207
17166106-12 2004 On the other hand, the amount of elastin significantly (p = 0.02) decreased from a mean of 54.5% +/- 3.68 before treatment to 43.4% +/- 4.42 after 6 months of tretinoin application but with no significant change thereafter. Tretinoin 159-168 elastin Homo sapiens 33-40
15231690-2 2004 In rat liver, in particular, retinoic acid has been shown to inhibit regeneration after partial hepatectomy, most probably through repression of the expression of c-fos and c-jun. Tretinoin 29-42 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 163-168
15482329-5 2004 RESULTS: Retinoic acid caused immunohistochemical diminution of keratin 4, keratin 13, and desmoglein. Tretinoin 9-22 keratin 4 Homo sapiens 64-73
16408290-5 2006 Remarkably, the amounts of PLC-beta2 draw a parallel with the differentiation levels reached by both ATRA-responsive and -resistant cells treated with ATRA/As2O3 combinations. Tretinoin 101-105 phospholipase C beta 2 Homo sapiens 27-36
15482329-7 2004 RA significantly decreased the transcript levels of keratin 13, keratin 14, desmoglein 1, and desmocollin 1 in a dose-dependent manner. Tretinoin 0-2 desmoglein 1 Homo sapiens 76-88
11196162-5 2001 Accordingly, we show that AML1/ETO, the commonest AML-associated fusion protein, is an HDAC-dependent repressor of RA signaling. Tretinoin 115-117 RUNX family transcription factor 1 Homo sapiens 26-30
15482329-9 2004 CONCLUSION: These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. Tretinoin 41-43 desmoglein 1 Homo sapiens 104-116
15482329-9 2004 CONCLUSION: These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. Tretinoin 41-43 keratin 4 Homo sapiens 149-158
15482329-9 2004 CONCLUSION: These results indicated that RA disintegrated not only desmosomes by depriving the cells of desmoglein 1, desmocollin 1, keratin 13, and keratin 4, but also hemidesmosomes by reducing the expression of BPAG1 and keratin 14 in basal keratinocytes. Tretinoin 41-43 dystonin Homo sapiens 214-219
15646024-6 2004 RESULTS: ATRA-treatment resulted in a reduction of the specific RARalpha and especially RXRalpha content in BAT that paralleled the induction of UCP1 appearance in the tissue. Tretinoin 9-13 retinoic acid receptor, alpha Mus musculus 64-72
16468075-0 2006 JWA, a novel signaling molecule, involved in all-trans retinoic acid induced differentiation of HL-60 cells. Tretinoin 55-68 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 0-3
16468075-2 2006 For the notable performance achieved by ATRA in the differentiation induction therapy, we investigated the role of JWA in ATRA-mediated differentiation of the human myeloid leukemia HL-60 cells. Tretinoin 122-126 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 115-118
16468075-3 2006 We found that concomitant with the progressive cell differentiation, JWA expression was up-regulated by ATRA in a dose- and time-dependent manner. Tretinoin 104-108 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 69-72
16468075-4 2006 Inhibition of JWA expression by RNA interference partially blocked ATRA-induced differentiation and growth inhibition of HL-60 cells. Tretinoin 67-71 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 14-17
16468075-8 2006 All the data suggest that up-regulation of JWA expression is essential for ATRA-induced differentiation of HL-60 cells. Tretinoin 75-79 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 43-46
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 47-60 amphiregulin Homo sapiens 117-129
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 47-60 amphiregulin Homo sapiens 131-133
11779431-11 2001 The down-regulating effect of ATRA and As2O3 on TF expression in U937 cells might not involve this fusion protein. Tretinoin 30-34 coagulation factor III, tissue factor Homo sapiens 48-50
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 62-65 amphiregulin Homo sapiens 117-129
16470170-6 2006 Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Tretinoin 62-65 amphiregulin Homo sapiens 131-133
16410076-7 2006 atRA led to an increase in mRNA expression of TGF-beta3 and an instantaneous decrease in TGF-beta type II receptor (TbetaRII) as determined by real-time RT-PCR. Tretinoin 0-4 transforming growth factor, beta receptor II Mus musculus 89-114
16410076-7 2006 atRA led to an increase in mRNA expression of TGF-beta3 and an instantaneous decrease in TGF-beta type II receptor (TbetaRII) as determined by real-time RT-PCR. Tretinoin 0-4 transforming growth factor, beta receptor II Mus musculus 116-124
16410076-9 2006 Activation of the Smad pathways by transfection with Smad7deltaC mutant or constitutively active TbetaRII retroviral vector abolished atRA-induced inhibition of chondrogenesis as indicated by Alcian blue staining, indicating that Smad signaling is essential for this response. Tretinoin 134-138 transforming growth factor, beta receptor II Mus musculus 97-105
15364113-0 2004 Retinoic acid treated HL60 cells express CEACAM1 (CD66a) and phagocytose Neisseria gonorrhoeae. Tretinoin 0-13 CEA cell adhesion molecule 1 Homo sapiens 41-48
15364113-4 2004 The interaction of OpaI E. coli with RA-treated HL60 cells was inhibited by antibodies against CEACAM1. Tretinoin 37-39 CEA cell adhesion molecule 1 Homo sapiens 95-102
15364113-6 2004 Our results indicate that the level of expression of CEACAM1 in HL60 cells can be regulated by treatment with RA in a differentiation-dependent manner, and that this is important for phagocytosis of OpaI-expressing gonococci or E. coli. Tretinoin 110-112 CEA cell adhesion molecule 1 Homo sapiens 53-60
11211936-0 2001 Retinoic acid-induced blr1 expression requires RARalpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 47-55
15700765-0 2004 Retinoic acid reverses the PTU related decrease in neurogranin level in mice brain. Tretinoin 0-13 neurogranin Mus musculus 51-62
15317450-3 2004 The transcriptional antagonism of the 3"-n-butyl analogue was demonstrated by its blockade of retinoic acid receptor (RAR) beta expression induced by the RXRalpha/peroxisome proliferator-activated receptor (PPAR) gamma heterodimer complexed with an RXRalpha agonist plus the PPARgamma agonist ciglitazone and the inhibition of 9-cis-RA-induced coactivator SRC-1a recruitment to RXRalpha. Tretinoin 327-335 retinoid X receptor alpha Homo sapiens 154-162
16165408-3 2006 In cell homogenates, it has been found that GGOH can be metabolized to geranylgeranoic acid (GGA) which, like retinoic acid (RA), is a stimulator of retinoic acid receptor (RAR) expression. Tretinoin 110-123 retinoic acid receptor, alpha Mus musculus 149-171
16165408-3 2006 In cell homogenates, it has been found that GGOH can be metabolized to geranylgeranoic acid (GGA) which, like retinoic acid (RA), is a stimulator of retinoic acid receptor (RAR) expression. Tretinoin 110-123 retinoic acid receptor, alpha Mus musculus 173-176
16165408-3 2006 In cell homogenates, it has been found that GGOH can be metabolized to geranylgeranoic acid (GGA) which, like retinoic acid (RA), is a stimulator of retinoic acid receptor (RAR) expression. Tretinoin 125-127 retinoic acid receptor, alpha Mus musculus 149-171
11211936-2 2001 RA-induced myeloid differentiation and G1/G0 growth arrest of HL-60 cells is known to require the activation of the RARalpha and RXR retinoid receptors, as well as activation of the MAPK, ERK2. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 116-124
16165408-3 2006 In cell homogenates, it has been found that GGOH can be metabolized to geranylgeranoic acid (GGA) which, like retinoic acid (RA), is a stimulator of retinoic acid receptor (RAR) expression. Tretinoin 125-127 retinoic acid receptor, alpha Mus musculus 173-176
15238362-2 2004 Alcohol (ADH) and aldehyde (ALDH) dehydrogenases are implicated in cellular detoxification and conversion of vitamin A to RA. Tretinoin 122-124 aldehyde dehydrogenase 1 family member A2 Homo sapiens 28-32
27419349-0 2001 Exogenous PML/RARalpha Fusion Gene Responds to All-trans Retinoic Acid Results in Differentiation of the Human B Cell Line. Tretinoin 57-70 PML nuclear body scaffold Homo sapiens 10-13
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 153-178
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 180-189
16082379-8 2006 The results suggest that the combination of Ad-CD:UPRT/5-FC with TRA-8 produces an additive cytotoxic effect in cancer cells in vitro and in vivo. Tretinoin 65-68 uracil phosphoribosyltransferase homolog Homo sapiens 50-54
27419349-0 2001 Exogenous PML/RARalpha Fusion Gene Responds to All-trans Retinoic Acid Results in Differentiation of the Human B Cell Line. Tretinoin 57-70 retinoic acid receptor alpha Homo sapiens 14-22
16291826-3 2006 atRA-induced apoptosis is associated with activation of the initiator caspase-9 and the effector caspase-3, but not of the effector caspase-8. Tretinoin 0-4 caspase 3 Mus musculus 97-106
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 153-178
27419349-1 2001 The interaction of an exogenous PML/RARalpha fusion gene, associated with acute promyelocytic leukemia, with all-trans retinoic acid (ATRA) was examined in B-lymphoid cell lines. Tretinoin 119-132 PML nuclear body scaffold Homo sapiens 32-35
16111716-4 2006 The synthesis of vimentin in ATDC5 cells was slightly induced by RA, but its withdrawal induced the large-scale induction and the fibril formation of vimentin, which may indicate that the cells became fibroblastic cells, namely dedifferentiation. Tretinoin 65-67 vimentin Mus musculus 17-25
16111716-8 2006 The combination of MGF and RA enlarged the cells and enhanced the synthesis of vimentin due to RA under control, however, almost terminated alpha-SM-actin-synthesis in the cells. Tretinoin 27-29 vimentin Mus musculus 79-87
27419349-1 2001 The interaction of an exogenous PML/RARalpha fusion gene, associated with acute promyelocytic leukemia, with all-trans retinoic acid (ATRA) was examined in B-lymphoid cell lines. Tretinoin 119-132 retinoic acid receptor alpha Homo sapiens 36-44
27419349-1 2001 The interaction of an exogenous PML/RARalpha fusion gene, associated with acute promyelocytic leukemia, with all-trans retinoic acid (ATRA) was examined in B-lymphoid cell lines. Tretinoin 134-138 PML nuclear body scaffold Homo sapiens 32-35
15457346-1 2004 hRDH-E2 is a member of the short-chain alcohol dehydrogenase/reductase (SDR) family that converts retinol to retinaldehyde as the first and rate-limiting step in the retinoic acid synthetic pathway. Tretinoin 166-179 dehydrogenase/reductase 9 Homo sapiens 0-7
11108612-0 2001 Retinoic acid-induced changes in polysialyltransferase mRNA expression and NCAM polysialylation in human neuroblastoma cells. Tretinoin 0-13 neural cell adhesion molecule 1 Homo sapiens 75-79
16430309-17 2006 CYP3A7 has a specific role in hydroxylation of retinoic acid and 16alpha-hydroxylation of steroids, and is therefore of relevance both to normal development and carcinogenesis.CYP3A43 is the most recently discovered CYP3A isoform. Tretinoin 47-60 cytochrome P450 family 3 subfamily A member 43 Homo sapiens 176-183
16316642-4 2006 DEAB reduces expression of the myogenic markers myoD and myogenin in somites, whereas RA induces increased expression of these genes and strongly induces premature myoD expression in the presomitic mesoderm (psm). Tretinoin 86-88 myogenic differentiation 1 Danio rerio 164-168
15297736-3 2004 Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH-box family, which is involved in various reactions related to RNA metabolism, and is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. Tretinoin 177-190 DExD/H-box helicase 58 Homo sapiens 0-30
15297736-3 2004 Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH-box family, which is involved in various reactions related to RNA metabolism, and is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. Tretinoin 177-190 DExD/H-box helicase 58 Homo sapiens 32-37
11798557-1 2001 OBJECTIVES: To study the changes of tissue factor expression and hemostatic molecular markers in acute promyelocytic leukemia during all-trans retinoic acid (ATRA) or arsenic trioxide (AS(2)O(3)) treatment. Tretinoin 143-156 coagulation factor III, tissue factor Homo sapiens 36-49
15481529-7 2004 ATRA(1 x 10(-6) mol/L), however, inhibited the effect of E2 on regulation of IGF- II gene and IGFBP-6 gene as well as MC-3T3-E1 cell proliferation. Tretinoin 0-4 insulin-like growth factor binding protein 6 Mus musculus 94-101
16436339-1 2006 Retinoic acid regulates keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors, including retinoic acid receptor (RAR-alpha,beta,gamma) and the common heterodimer partners (RXR-alpha,beta,gamma). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 247-256
11798557-1 2001 OBJECTIVES: To study the changes of tissue factor expression and hemostatic molecular markers in acute promyelocytic leukemia during all-trans retinoic acid (ATRA) or arsenic trioxide (AS(2)O(3)) treatment. Tretinoin 158-162 coagulation factor III, tissue factor Homo sapiens 36-49
16260419-2 2005 The expression of PLSCR1 protein is also known to be markedly increased in response to IFN and to some differentiation inducing agents such as all-trans retinoic acid, but the precise mechanisms of this response remain to be investigated. Tretinoin 153-166 phospholipid scramblase 1 Homo sapiens 18-24
15219805-4 2004 RIG-I is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. Tretinoin 38-51 DExD/H-box helicase 58 Homo sapiens 0-5
11798557-7 2001 All-trans retinoic acid and arsenic trioxide down-regulate the expression of TF mRNA and decrease the TF contents in APL blasts. Tretinoin 0-23 coagulation factor III, tissue factor Homo sapiens 77-79
15271423-0 2004 Ornithine decarboxylase, polyamines and CD11b expression in HL-60 cells during differentiation induced by retinoic acid. Tretinoin 106-119 integrin subunit alpha M Homo sapiens 40-45
16289102-0 2005 Retinoic acid via RARalpha inhibits the expression of 24-hydroxylase in human prostate stromal cells. Tretinoin 0-13 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 54-68
16289102-4 2005 We demonstrate here that ATRA markedly reduced the expression of 24-hydroxylase mRNA induced by 25OHD3 and 1alpha,25-(OH)2D3 in human prostatic stromal cells P29SN and P32S but not in epithelial cells PrEC or cancer cells LNCaP. Tretinoin 25-29 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 65-79
11798557-7 2001 All-trans retinoic acid and arsenic trioxide down-regulate the expression of TF mRNA and decrease the TF contents in APL blasts. Tretinoin 0-23 coagulation factor III, tissue factor Homo sapiens 102-104
16289102-5 2005 By using transfection and RAR-selective ligands, we found that the inhibitory effect of ATRA on 24-hydroxylase expression in stromal cells was mediated by RARalpha but not by RARbeta. Tretinoin 88-92 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 96-110
16289102-8 2005 Our data suggest that ATRA suppresses 24-hydroxylase expression through RARalpha-dependent signaling pathway and can enhance vitamin D action in suppression of cell growth. Tretinoin 22-26 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 38-52
15271423-2 2004 Retinoic acid induces granulocytic differentiation of mieloid cell lines and, during this process, is responsible for the expression of CD11b, a surface antigen. Tretinoin 0-13 integrin subunit alpha M Homo sapiens 136-141
15271423-8 2004 CD11b expression, stimulated by retinoic acid treatment, is associated with the SPM trend. Tretinoin 32-45 integrin subunit alpha M Homo sapiens 0-5
11146121-2 2000 CaM kinase II activity was induced during the differentiation of P19 cells treated with retinoic acid. Tretinoin 88-101 cyclin dependent kinase inhibitor 2D Mus musculus 65-68
15194426-9 2004 Retinoic acid-induced changes in cell cycle-related proteins occurred in 4-6 h, including reduced cyclin E expression in bromodeoxyuridine (BrdU)-labeled cells, before the onset of cell differentiation as indicated by an increase in the percentage of G1 phase cells and a reduction in S phase cells at 24 h. The expression of CD11b, a cell surface marker of macrophage-like differentiation was increased by RA, as was phagocytic activity. Tretinoin 0-13 integrin subunit alpha M Homo sapiens 326-331
15239098-7 2004 Retinoic acid activated the human ASBT promoter fourfold. Tretinoin 0-13 solute carrier family 10 member 2 Homo sapiens 34-38
16217742-4 2005 It was found that inhibition of RA signaling in vivo leads to excessive mammary ductal morphogenesis through upregulation of cyclin D1 and MMP-3 expression. Tretinoin 32-34 cyclin D1 Mus musculus 125-134
10995752-0 2000 Feedback inhibition of the retinaldehyde dehydrogenase gene ALDH1 by retinoic acid through retinoic acid receptor alpha and CCAAT/enhancer-binding protein beta. Tretinoin 69-82 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 124-159
16317119-3 2005 We identified nuclear receptors that bind to retinoic acid response elements (RAREs) in the PEPCK promoter by electrophoretic mobility shift assay and verified these in vivo using chromatin immunoprecipitation in mouse liver. Tretinoin 45-58 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 92-97
15239098-10 2004 In conclusion, the human ASBT is positively regulated by retinoic acid. Tretinoin 57-70 solute carrier family 10 member 2 Homo sapiens 25-29
10995752-5 2000 Retinoic acid receptor alpha (RARalpha) transactivates the ALDH1 gene promoter through a complex with an RA response-like element (RARE) located at -91/-75 bp, which bound to the RARalpha/retinoid X receptor beta heterodimer. Tretinoin 30-32 retinoid X receptor beta Mus musculus 188-212
10995752-7 2000 Exposure of Hepa-1 cells to RA results in a decrease in C/EBPbeta mRNA levels; however, there was no difference in mRNA and protein levels between wild-type and AHR-null mouse liver. Tretinoin 28-30 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 56-65
15069081-0 2004 Retinoic acid synthesis controlled by Raldh2 is required early for limb bud initiation and then later as a proximodistal signal during apical ectodermal ridge formation. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A2 Homo sapiens 38-44
10995752-8 2000 These data support a model in which the RARalpha and C/EBPbeta activate the ALDH1 gene promoter through the RARE and C/EBP response elements, and in Hepa-1 cells, high levels of RA inhibit this activation by decreasing cellular levels of C/EBPbeta. Tretinoin 40-42 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 238-247
15069081-2 2004 Limb RA synthesis is under the control of retinaldehyde dehydrogenase-2 (Raldh2) expressed in the lateral plate mesoderm, which generates a proximodistal RA signal during limb outgrowth. Tretinoin 5-7 aldehyde dehydrogenase 1 family member A2 Homo sapiens 42-71
15069081-2 2004 Limb RA synthesis is under the control of retinaldehyde dehydrogenase-2 (Raldh2) expressed in the lateral plate mesoderm, which generates a proximodistal RA signal during limb outgrowth. Tretinoin 5-7 aldehyde dehydrogenase 1 family member A2 Homo sapiens 73-79
15069081-2 2004 Limb RA synthesis is under the control of retinaldehyde dehydrogenase-2 (Raldh2) expressed in the lateral plate mesoderm, which generates a proximodistal RA signal during limb outgrowth. Tretinoin 154-156 aldehyde dehydrogenase 1 family member A2 Homo sapiens 42-71
15069081-2 2004 Limb RA synthesis is under the control of retinaldehyde dehydrogenase-2 (Raldh2) expressed in the lateral plate mesoderm, which generates a proximodistal RA signal during limb outgrowth. Tretinoin 154-156 aldehyde dehydrogenase 1 family member A2 Homo sapiens 73-79
15069081-7 2004 AER formation in Raldh2(-/-) forelimbs is rescued by continuous RA treatment through E10, which restores RA to distal ectoderm fated to become the AER. Tretinoin 64-66 aldehyde dehydrogenase 1 family member A2 Homo sapiens 17-23
15069081-7 2004 AER formation in Raldh2(-/-) forelimbs is rescued by continuous RA treatment through E10, which restores RA to distal ectoderm fated to become the AER. Tretinoin 105-107 aldehyde dehydrogenase 1 family member A2 Homo sapiens 17-23
16403261-3 2005 By treatment of 1 micromol/L ATRA, cell differentiation antigen CD11b was gradually increased ([chi = 47.002, P = 0.000) and CD33 was gradually decreased (chi = 1.614, P = 0.806) with time. Tretinoin 29-33 integrin subunit alpha M Homo sapiens 64-69
16207763-2 2005 In POM, the effects of the paracrine RA signal are mediated by the nuclear RA receptors heterodimers RXRalpha/RARbeta and RXRalpha/RARgamma. Tretinoin 37-39 retinoic acid receptor, gamma Mus musculus 131-139
11076660-5 2000 In fact, HMGI(Y) gene expression is differentially regulated by retinoic acid in retinoid-sensitive and -resistant neuroblastoma cells, while HMGI-C participates in conferring retinoic acid resistance in some neuroblastoma cells. Tretinoin 64-77 high mobility group AT-hook 1 Homo sapiens 9-16
16211222-5 2005 CRABP2 is a main regulator of anti-carcinogenic activities of retinoic acid and may become a novel diagnostic marker and experimental therapeutic tool for prostate cancer. Tretinoin 62-75 cellular retinoic acid binding protein 2 Homo sapiens 0-6
16085646-8 2005 Experiments using receptor-selective retinoids revealed that ligands for retinoic acid receptor-alpha (RARalpha), including atRA, 9-cis-retinoic acid, and Am580, sequentially increased the levels of IFNgamma receptor-1, activated signal transducer and activator of transcription-1, and IRF-1 and that an RARalpha antagonist was able to inhibit the effects of atRA and Am580. Tretinoin 124-128 signal transducer and activator of transcription 1 Homo sapiens 230-280
15159275-10 2004 Expression of the CD11b cell surface marker and C/EBPepsilon was increased when the cells were treated for 4 days with 0.3 microm AF and a physiological concentration of all-trans retinoic acid (ATRA, 5 nm). Tretinoin 180-193 integrin subunit alpha M Homo sapiens 18-23
15159275-10 2004 Expression of the CD11b cell surface marker and C/EBPepsilon was increased when the cells were treated for 4 days with 0.3 microm AF and a physiological concentration of all-trans retinoic acid (ATRA, 5 nm). Tretinoin 195-199 integrin subunit alpha M Homo sapiens 18-23
11314085-0 2000 Alteration of Fas/FasL expression of oral squamous cell carcinoma cell line Tca83 induced by retinoic acid. Tretinoin 93-106 Fas ligand Homo sapiens 18-22
14729516-3 2004 This includes findings that nitrofen, which induces CDH in rodents, inhibits the key enzyme for retinoic acid (RA) production, retinaldehyde dehydrogenase-2 (RALDH2) in vitro. Tretinoin 96-109 aldehyde dehydrogenase 1 family member A2 Homo sapiens 127-156
14729516-3 2004 This includes findings that nitrofen, which induces CDH in rodents, inhibits the key enzyme for retinoic acid (RA) production, retinaldehyde dehydrogenase-2 (RALDH2) in vitro. Tretinoin 96-109 aldehyde dehydrogenase 1 family member A2 Homo sapiens 158-164
16266505-1 2005 OBJECTIVE: To investigate the reverse effect of all-trans retinoic acid (ATRA) on Benzo (a) pyrene (B (a) P)-induced cyclin D1, CDK4, E2F-1 and E2F-4 expression and cell cycle progression in human embryo lung fibroblast (HELF). Tretinoin 48-71 cyclin-dependent kinase 4 S homeolog Xenopus laevis 128-132
16157890-6 2005 Although RA alone increased the neonatal anti-TT antibody response, it selectively increased anti-TT IgG1 and IL-5, resulting in a skewed type 2 response. Tretinoin 9-11 LOC105243590 Mus musculus 101-105
11098153-0 2000 A novel cis-acting element regulates HES-1 gene expression in P19 embryonal carcinoma cells treated with retinoic acid. Tretinoin 105-118 interleukin 23 subunit alpha Homo sapiens 62-65
16101150-5 2005 The torsion angle C5"-C6"-C7"-C8", determining the conformation of the RBP-beta-ionone-ring relative to the isoprene tail, is rotated by 42 degrees for RPA compared to retinol and to retinoic acid, respectively. Tretinoin 183-196 retinol binding protein 4 Homo sapiens 71-74
16101150-9 2005 RPA was able to compete with retinoic acid for binding at RBP in human plasma. Tretinoin 29-42 retinol binding protein 4 Homo sapiens 58-61
15370293-3 2004 RIG-I is induced in leukemia cells by retinoic acid and in endothelial cells by lipopolysaccharide. Tretinoin 38-51 DExD/H-box helicase 58 Homo sapiens 0-5
15291358-4 2004 We treated HL-60 and ATRA-resistant HL-60 (HL-60R) cells that express mutated RARalpha and very low levels of RARbeta, RARgamma and RXRalpha with 4-HPR (2 microM) for 3 days. Tretinoin 21-25 retinoid X receptor alpha Homo sapiens 132-140
14734562-0 2004 Activation and interaction of ATF2 with the coactivator ASC-2 are responsive for granulocytic differentiation by retinoic acid. Tretinoin 113-126 activating transcription factor 2 Homo sapiens 30-34
11080189-5 2000 In P19 cells, retinoic acid induced neurite extensions after 3-4 days; these extensions were coincident with a fourfold increase in endogenous CaMK-II activity. Tretinoin 14-27 cyclin dependent kinase inhibitor 2D Mus musculus 3-6
14734562-3 2004 All-trans retinoic acid (RA) induced the phosphorylation and expression of ATF2 in the early and middle phase of granulocyte differentiation, respectively. Tretinoin 0-23 activating transcription factor 2 Homo sapiens 75-79
14734562-3 2004 All-trans retinoic acid (RA) induced the phosphorylation and expression of ATF2 in the early and middle phase of granulocyte differentiation, respectively. Tretinoin 25-27 activating transcription factor 2 Homo sapiens 75-79
14734562-8 2004 Furthermore, the molecular interaction of ATF2 and ASC-2 was stimulated by RA treatment and inhibited by p38beta kinase inhibitor. Tretinoin 75-77 activating transcription factor 2 Homo sapiens 42-46
14754907-8 2004 Specific RAR and RXR agonists were used to identify the nuclear receptor responsible for LPLA(2) induction by retinoic acid. Tretinoin 110-123 retinoid X receptor alpha Homo sapiens 17-20
16081783-5 2005 Specifically, IL-21 only demonstrated a therapeutic effect in mice challenged with a retinoic acid early inducible-1delta-bearing lymphoma but not in mice bearing parental RMA tumors lacking NKG2D ligands. Tretinoin 85-98 interleukin 21 Mus musculus 14-19
16081783-8 2005 We also observed that IL-21 treatment could enhance RMA-retinoic acid early inducible-1delta tumor rejection in RAG-1(-/-) deficient mice, thereby demonstrating that the IL-21-induced protective effect can be mediated by the innate immune system and that, in this case, IL-21 does not require the adaptive immune response. Tretinoin 56-69 interleukin 21 Mus musculus 22-27
16081783-8 2005 We also observed that IL-21 treatment could enhance RMA-retinoic acid early inducible-1delta tumor rejection in RAG-1(-/-) deficient mice, thereby demonstrating that the IL-21-induced protective effect can be mediated by the innate immune system and that, in this case, IL-21 does not require the adaptive immune response. Tretinoin 56-69 interleukin 21 Mus musculus 170-175
16081783-8 2005 We also observed that IL-21 treatment could enhance RMA-retinoic acid early inducible-1delta tumor rejection in RAG-1(-/-) deficient mice, thereby demonstrating that the IL-21-induced protective effect can be mediated by the innate immune system and that, in this case, IL-21 does not require the adaptive immune response. Tretinoin 56-69 interleukin 21 Mus musculus 170-175
14754907-13 2004 Thus, an RXR-dependent pathway controls LPLA(2) gene activation by retinoic acid in THP-1 cells. Tretinoin 67-80 retinoid X receptor alpha Homo sapiens 9-12
14961038-3 2004 Int-3-transduced human myeloid leukemia (HL-60) cells demonstrated significantly delayed expression of differentiation markers following retinoic acid and 12-0-tetradecanoylphorbol 13-acetate treatment. Tretinoin 137-150 notch receptor 4 Homo sapiens 0-5
15817812-9 2005 Finally, the activity of FXR was mapped to a retinoic acid response element (RARE) site containing an imbedded farnesoid X response element (FXRE) on the human ICAM-1 promoter and FXR and retinoid X receptor were demonstrated to bind to this site. Tretinoin 45-58 intercellular adhesion molecule 1 Homo sapiens 160-166
11080189-5 2000 In P19 cells, retinoic acid induced neurite extensions after 3-4 days; these extensions were coincident with a fourfold increase in endogenous CaMK-II activity. Tretinoin 14-27 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 143-150
15817812-9 2005 Finally, the activity of FXR was mapped to a retinoic acid response element (RARE) site containing an imbedded farnesoid X response element (FXRE) on the human ICAM-1 promoter and FXR and retinoid X receptor were demonstrated to bind to this site. Tretinoin 45-58 retinoid X receptor alpha Homo sapiens 188-207
11080189-7 2000 C-terminal CaMK-II constructs disrupted the ability of endogenous CaMK-II to autophosphorylate and blocked retinoic acid-induced differentiation. Tretinoin 107-120 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 11-18
15487511-8 2004 This is the first report suggesting the SDR participation of mammalian peroxisomers in retinoid metabolism and it provides a reliable foundation to further investigate the biological function of this protein and retinoic acid biosynthesis. Tretinoin 212-225 hydroxysteroid 17-beta dehydrogenase 14 Bos taurus 40-43
11080189-7 2000 C-terminal CaMK-II constructs disrupted the ability of endogenous CaMK-II to autophosphorylate and blocked retinoic acid-induced differentiation. Tretinoin 107-120 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 66-73
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 31-44 retinoic acid receptor alpha Homo sapiens 53-64
15035668-5 2004 Using Line 1 tumor cells as a model for signal regulation of metastatic gene expression, we investigated the reciprocal interactions between NFkappaB and RARs in response to the pan-RAR agonist, all-trans retinoic acid (at-RA) and the pan-RAR antagonist, AGN193109. Tretinoin 205-218 retinoic acid receptor, alpha Mus musculus 154-157
16033655-9 2005 VAD was also associated with a decrease in the concentration of parenchymal elastic fibers, which was restored and was accompanied by an increase in tropoelastin mRNA after 12 days of RA-treatment. Tretinoin 184-186 elastin Rattus norvegicus 149-161
16033655-10 2005 Lung elastin, which was resistant to 0.1 N NaOH at 98 degrees, decreased in VAD and was not restored after 21 days of RA-treatment. Tretinoin 118-120 elastin Rattus norvegicus 5-12
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 31-44 retinoic acid receptor alpha Homo sapiens 66-69
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 46-48 retinoic acid receptor alpha Homo sapiens 53-64
15954902-0 2005 ATRA induces podocyte differentiation and alters nephrin and podocin expression in vitro and in vivo. Tretinoin 0-4 nephrosis 1, nephrin Mus musculus 49-56
14991612-4 2004 Two groups of nuclear receptors for retinoic acids (RA) have been identified: retinoic acid receptors (RAR) and retinoid X receptors. Tretinoin 36-50 retinoic acid receptor, alpha Mus musculus 103-106
14991612-4 2004 Two groups of nuclear receptors for retinoic acids (RA) have been identified: retinoic acid receptors (RAR) and retinoid X receptors. Tretinoin 52-54 retinoic acid receptor, alpha Mus musculus 103-106
15954902-0 2005 ATRA induces podocyte differentiation and alters nephrin and podocin expression in vitro and in vivo. Tretinoin 0-4 nephrosis 2, podocin Mus musculus 61-68
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 46-48 retinoic acid receptor alpha Homo sapiens 66-69
15954902-10 2005 RESULTS: ATRA induced podocyte process formation in vitro, and significantly increased the expression of nephrin and podocin. Tretinoin 9-13 nephrosis 1, nephrin Mus musculus 105-112
15954902-10 2005 RESULTS: ATRA induced podocyte process formation in vitro, and significantly increased the expression of nephrin and podocin. Tretinoin 9-13 nephrosis 2, podocin Mus musculus 117-124
11071654-6 2000 Moreover, indinavir enhanced the ability of ATRA to induce expression of the myeloid differentiation-related transcription factor C/EBPepsilon messenger RNA in NB4 cells by 9.5-fold. Tretinoin 44-48 CCAAT enhancer binding protein epsilon Homo sapiens 130-142
15954902-12 2005 ATRA also significantly prevented the decrease in staining for synaptopodin, nephrin, and podocin in experimental animals (P < 0.05 vs. control). Tretinoin 0-4 nephrosis 1, nephrin Mus musculus 77-84
15954902-12 2005 ATRA also significantly prevented the decrease in staining for synaptopodin, nephrin, and podocin in experimental animals (P < 0.05 vs. control). Tretinoin 0-4 nephrosis 2, podocin Mus musculus 90-97
14981092-4 2004 An intact actin and microtubule cytoskeleton appears to be required for the restriction of MAPK nuclear entry induced by retinoic acid treatment because the cytoskeletal disrupting agents nocodazole, colchicine, and cytochalasin D are able to revert the suppression of c-Fos expression. Tretinoin 121-134 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 269-274
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 retinoic acid receptor alpha Homo sapiens 197-225
15318936-6 2004 Recently, RXR-selective ligands were discovered that inhibited proliferation of all-trans retinoic acid resistant breast cancer cells in vitro and caused regression of the disease in animal models. Tretinoin 90-103 retinoid X receptor alpha Homo sapiens 10-13
15318936-11 2004 Interestingly, RXR-alpha-overexpressing retinoic acid resistant breast cancer cell lines were more sensitive to the effects of the RXR-selective compound. Tretinoin 40-53 retinoid X receptor alpha Homo sapiens 15-24
21190613-0 2005 [Experimental study of effects of retinoic acid on IL-1beta and IFN-gamma induced C3 and factor B secretion in lung cancer cell line]. Tretinoin 34-47 complement C3 Homo sapiens 82-97
21190613-2 2005 The aim of this study is to investigate the regulated effects of retinoic acid (RA) on IL-1beta and IFN-gamma induced C3 and factor B secretion in human lung cancer cell line A549. Tretinoin 65-78 complement C3 Homo sapiens 118-133
21190613-2 2005 The aim of this study is to investigate the regulated effects of retinoic acid (RA) on IL-1beta and IFN-gamma induced C3 and factor B secretion in human lung cancer cell line A549. Tretinoin 80-82 complement C3 Homo sapiens 118-133
21190613-6 2005 CONCLUSIONS: RA can up-regulate C3 and factor B secretion induced by IL-1beta and IFN-gamma in human lung cancer cell A549. Tretinoin 13-15 complement C3 Homo sapiens 32-47
15318936-11 2004 Interestingly, RXR-alpha-overexpressing retinoic acid resistant breast cancer cell lines were more sensitive to the effects of the RXR-selective compound. Tretinoin 40-53 retinoid X receptor alpha Homo sapiens 15-18
15949692-5 2005 It is shown that RA reduces RB expression and enhances RB phosphorylation by a mechanism that involves down-regulation of the cyclin-dependent kinase inhibitor (CKI) p21(Cip1), having this fact as important consequences for both the cell cycle progression and the adipocyte differentiation process. Tretinoin 17-19 cyclin dependent kinase inhibitor 3 Homo sapiens 161-164
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 retinoic acid receptor alpha Homo sapiens 227-236
11776129-6 2000 One of the mechanisms for ATRA to inhibit the growth of gastric cancer cells may be through its inhibitory effect on the AP-1 activity and its influence on up-regulation of RAR alpha expression. Tretinoin 26-30 retinoic acid receptor alpha Homo sapiens 173-182
15200239-2 2004 Human septin 3 was originally cloned during a screening of genes expressed in human teratocarcinoma cells induced to differentiate with retinoic acid. Tretinoin 136-149 septin 3 Homo sapiens 6-14
15200239-4 2004 The purpose of the present study was to identify the expression patterns of human septin 3 isoforms in normal human brain and a human neuroblastoma cell line, SH-SY5Y, after retinoic acid-induced differentiation. Tretinoin 174-187 septin 3 Homo sapiens 82-90
11120388-6 2000 The mRNA expression of GAP-43, an important factor in neural development, increased with 10(-6) M retinol and 10(-5)-10(-9) M RA. Tretinoin 126-128 growth associated protein 43 Homo sapiens 23-29
14654966-0 2004 Retinoic acid delays keratinocyte senescence by suppression of betaig-h3 and p16 expression and induction of telomerase activity. Tretinoin 0-13 transforming growth factor beta induced Homo sapiens 63-72
14654966-4 2004 The levels of betaig-h3 and p16 in 1 nM of RA-treated cells remained significantly lower than that of the vehicle control at all population doublings. Tretinoin 43-45 transforming growth factor beta induced Homo sapiens 14-23
16029656-5 2005 RESULTS: CX26 mRNA and CX32 mRNA were not expressed in the cell lines SMMC-7721, however, expression of CX26 mRNA and expression of CX32 mRNA were found 48 and 72 hours after being induction by ATRA respectively. Tretinoin 194-198 gap junction protein beta 1 Homo sapiens 132-136
16029656-6 2005 CX26 mRNA and CX32 mRNA were not expressed in the cell lines BEL-7404, however, expression of CX26 mRNA and expression of CX32 mRNA were found 48 hours after induction by ATRA. Tretinoin 171-175 gap junction protein beta 1 Homo sapiens 122-126
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 15-28 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 84-89
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 15-28 activating transcription factor 2 Homo sapiens 155-160
11120388-9 2000 CX prevented the effects of both RA and ethanol on GAP-43 mRNA. Tretinoin 33-35 growth associated protein 43 Homo sapiens 51-57
15878332-6 2005 Consistent with an effect of Vav on the transcriptional machinery, array profiling shows that the inhibition of the Syk-dependent tyrosine phosphorylation of Vav reduces the number of ATRA-induced genes. Tretinoin 184-188 spleen associated tyrosine kinase Homo sapiens 116-119
11007958-3 2000 At the molecular level, PML protein has been shown to be a coactivator of nuclear hormone receptors, whereas its oncogenic counterpart PML-retinoic acid receptor alpha, which promotes POD disaggregation, has been found to activate activator protein-1 transcription in a retinoic acid-dependent manner. Tretinoin 139-152 PML nuclear body scaffold Homo sapiens 135-138
14691372-8 2003 Each of the three RXR isoforms alpha, beta, and gamma stimulated the expression of reporter constructs containing the FP330-3" sites in a 9-cis retinoic acid-dependent fashion in cells in culture. Tretinoin 144-157 retinoid X receptor alpha Homo sapiens 18-21
14623241-0 2003 Patterning of forelimb bud myogenic precursor cells requires retinoic acid signaling initiated by Raldh2. Tretinoin 61-74 aldehyde dehydrogenase 1 family member A2 Homo sapiens 98-104
14623241-3 2003 Here, we find that correct patterning of Hgf expression in forelimb buds is dependent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proximally. Tretinoin 89-102 aldehyde dehydrogenase 1 family member A2 Homo sapiens 123-152
15867264-7 2005 HOXB2, a downstream target of RA, was up-regulated 6.7-fold in pancreatic cancer compared with normal pancreas. Tretinoin 30-32 homeobox B2 Homo sapiens 0-5
11063125-0 2000 Retinoic acid induces neuronal differentiation of embryonal carcinoma cells by reducing proteasome-dependent proteolysis of the cyclin-dependent inhibitor p27. Tretinoin 0-13 interferon alpha inducible protein 27 Homo sapiens 155-158
15867264-10 2005 CONCLUSIONS: We identified aberrant expression of RA signaling components in pancreatic cancer, including HOXB2, which was expressed in a proportion of PanIN lesions. Tretinoin 50-52 homeobox B2 Homo sapiens 106-111
15824860-10 2005 Immunoblots showed that hypertrophic chondrocytes contained sizable levels of phosphorylated ERK1/2 and p38 MAP kinases that were dose- and time-dependently increased by RA treatment. Tretinoin 170-172 adapter molecule crk Gallus gallus 104-107
14623241-3 2003 Here, we find that correct patterning of Hgf expression in forelimb buds is dependent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proximally. Tretinoin 89-102 aldehyde dehydrogenase 1 family member A2 Homo sapiens 154-160
14623241-3 2003 Here, we find that correct patterning of Hgf expression in forelimb buds is dependent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proximally. Tretinoin 104-106 aldehyde dehydrogenase 1 family member A2 Homo sapiens 123-152
14623241-3 2003 Here, we find that correct patterning of Hgf expression in forelimb buds is dependent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proximally. Tretinoin 104-106 aldehyde dehydrogenase 1 family member A2 Homo sapiens 154-160
14623241-4 2003 Raldh2(-/-) forelimb buds lack RA and display an anteroproximal shift in expression of Hgf such that its normally separate dorsal and ventral expression domains are joined into a single anterior-proximal domain. Tretinoin 31-33 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-6
12893766-0 2003 Comparative analysis of genes regulated by PML/RAR alpha and PLZF/RAR alpha in response to retinoic acid using oligonucleotide arrays. Tretinoin 91-104 zinc finger and BTB domain containing 16 Homo sapiens 61-65
14605041-0 2003 All-trans retinoic acid modulates the balance of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in patients with emphysema. Tretinoin 0-23 matrix metallopeptidase 9 Homo sapiens 49-75
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 50-73 matrix metallopeptidase 9 Homo sapiens 99-125
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 50-73 matrix metallopeptidase 9 Homo sapiens 127-132
15836616-5 2005 RA-induced activation of Rac1 is mediated by phosphatidylinositol 3-kinase (PI3K), probably because of phosphorylation of the p85 regulatory subunit by Src kinases. Tretinoin 0-2 Rac family small GTPase 1 Homo sapiens 25-29
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 75-79 matrix metallopeptidase 9 Homo sapiens 99-125
11063125-2 2000 In the present study, we provide a functional link between RA and p27 function in the control of neuronal differentiation in NT2/D1 cells. Tretinoin 59-61 interferon alpha inducible protein 27 Homo sapiens 66-69
14605041-2 2003 This study was designed to evaluate the impact of all-trans retinoic acid (ATRA) on the balance of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with emphysema. Tretinoin 75-79 matrix metallopeptidase 9 Homo sapiens 127-132
14605041-3 2003 DESIGN AND SETTING: As part of a clinical study, ATRA was administered to 20 patients with emphysema for 12 weeks and evaluated for its effects on plasma levels of MMP-9 and TIMP-1. Tretinoin 49-53 matrix metallopeptidase 9 Homo sapiens 164-169
11063125-3 2000 We report that RA enhances p27 expression, which results in increased association with cyclin E/cyclin-dependent kinase 2 complexes and suppression of their activity; however, antisense clones, which have greatly reduced RA-dependent p27 inducibility (NT2-p27AS), continue to synthesize DNA and are unable to differentiate properly in response to RA as determined by lack of neurite outgrowth and by the failure to modify surface antigens. Tretinoin 15-17 interferon alpha inducible protein 27 Homo sapiens 27-30
15866176-3 2005 This work focuses on CRABP-II, a cytosolic protein that moves to the nucleus upon binding of retinoic acid. Tretinoin 93-106 cellular retinoic acid binding protein 2 Homo sapiens 21-29
15866176-5 2005 We map the retinoic acid-induced structural rearrangements that result in the presence of this NLS in holo- but not apo-CRABP-II. Tretinoin 11-24 cellular retinoic acid binding protein 2 Homo sapiens 120-128
14605041-6 2003 MEASUREMENTS AND RESULTS: Administration of ATRA to patients with emphysema produced a 45 +/- 14% reduction (mean +/- SEM) in plasma MMP-9 by enzyme-linked immunosorbent assay and a similar reduction in MMP-9 enzyme activity, while having little effect on TIMP-1 levels. Tretinoin 44-48 matrix metallopeptidase 9 Homo sapiens 133-138
11063125-4 2000 As to the mechanism involved in RA-dependent p27 upregulation, our data support the concept that RA reduces p27 protein degradation through the ubiquitin/proteasome-dependent pathway. Tretinoin 32-34 interferon alpha inducible protein 27 Homo sapiens 45-48
14605041-6 2003 MEASUREMENTS AND RESULTS: Administration of ATRA to patients with emphysema produced a 45 +/- 14% reduction (mean +/- SEM) in plasma MMP-9 by enzyme-linked immunosorbent assay and a similar reduction in MMP-9 enzyme activity, while having little effect on TIMP-1 levels. Tretinoin 44-48 matrix metallopeptidase 9 Homo sapiens 203-208
14605041-8 2003 In vitro, concentrations of ATRA similar to those achieved in the plasma of study subjects significantly reduced both the production and enzyme activity of MMP-9 by AM. Tretinoin 28-32 matrix metallopeptidase 9 Homo sapiens 156-161
11063125-4 2000 As to the mechanism involved in RA-dependent p27 upregulation, our data support the concept that RA reduces p27 protein degradation through the ubiquitin/proteasome-dependent pathway. Tretinoin 32-34 interferon alpha inducible protein 27 Homo sapiens 108-111
11063125-4 2000 As to the mechanism involved in RA-dependent p27 upregulation, our data support the concept that RA reduces p27 protein degradation through the ubiquitin/proteasome-dependent pathway. Tretinoin 97-99 interferon alpha inducible protein 27 Homo sapiens 45-48
11063125-4 2000 As to the mechanism involved in RA-dependent p27 upregulation, our data support the concept that RA reduces p27 protein degradation through the ubiquitin/proteasome-dependent pathway. Tretinoin 97-99 interferon alpha inducible protein 27 Homo sapiens 108-111
15857687-2 2005 We have previously shown that bone morphogenetic protein-2 (BMP2) and retinoic acid synergistically induce the responsiveness of developing sympathetic neurons to neurotrophic factors, neurotrophin 3 (NT-3), and GDNF by upregulating corresponding receptors concomitantly with the induction of other neuron-specific genes including BRINP1, a neuron-specific cell-cycle regulatory protein. Tretinoin 70-83 neurotrophin 3 Homo sapiens 185-199
12963727-0 2003 Retinoic acid is a high affinity selective ligand for the peroxisome proliferator-activated receptor beta/delta. Tretinoin 0-13 peroxisome proliferator activated receptor delta Homo sapiens 58-105
15735731-0 2005 Retinoic acid stabilizes p27Kip1 in EBV-immortalized lymphoblastoid B cell lines through enhanced proteasome-dependent degradation of the p45Skp2 and Cks1 proteins. Tretinoin 0-13 CDC28 protein kinase regulatory subunit 1B pseudogene 7 Homo sapiens 150-154
11014218-0 2000 Expression of enzymes synthesizing (aldehyde dehydrogenase 1 and reinaldehyde dehydrogenase 2) and metabolizaing (Cyp26) retinoic acid in the mouse female reproductive system. Tretinoin 121-134 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 114-119
15735731-3 2005 Furthermore, we demonstrate that RA downregulates the expression of the p45Skp2 and Cks1 proteins, two essential components of the SCF(Skp2) ubiquitin ligase complex that target p27Kip1 for degradation. Tretinoin 33-35 CDC28 protein kinase regulatory subunit 1B pseudogene 7 Homo sapiens 84-88
15735731-3 2005 Furthermore, we demonstrate that RA downregulates the expression of the p45Skp2 and Cks1 proteins, two essential components of the SCF(Skp2) ubiquitin ligase complex that target p27Kip1 for degradation. Tretinoin 33-35 KIT ligand Homo sapiens 131-134
12963727-7 2003 We demonstrate that while RA does not activate PPARalpha and PPARgamma, it binds to PPARbeta/delta with nanomolar affinity, modulates the conformation of the receptor, promotes interaction with the coactivator SRC-1, and efficiently activates PPARbeta/delta-mediated transcription. Tretinoin 26-28 peroxisome proliferator activated receptor delta Homo sapiens 84-92
12963727-7 2003 We demonstrate that while RA does not activate PPARalpha and PPARgamma, it binds to PPARbeta/delta with nanomolar affinity, modulates the conformation of the receptor, promotes interaction with the coactivator SRC-1, and efficiently activates PPARbeta/delta-mediated transcription. Tretinoin 26-28 peroxisome proliferator activated receptor delta Homo sapiens 243-251
12888559-0 2003 Concomitant increase of histone acetyltransferase activity and degradation of p300 during retinoic acid-induced differentiation of F9 cells. Tretinoin 90-103 E1A binding protein p300 Mus musculus 78-82
12888559-2 2003 Despite their similarities, p300 and CBP have distinct functions during retinoic acid-induced differentiation of mouse F9 embryonal carcinoma cells. Tretinoin 72-85 E1A binding protein p300 Mus musculus 28-32
12888559-2 2003 Despite their similarities, p300 and CBP have distinct functions during retinoic acid-induced differentiation of mouse F9 embryonal carcinoma cells. Tretinoin 72-85 CREB binding protein Mus musculus 37-40
12888559-6 2003 We report a dramatic decrease of p300, but not CBP protein levels, after 48 h of retinoic acid treatment. Tretinoin 81-94 E1A binding protein p300 Mus musculus 33-37
15602748-4 2005 RA acted in a dose-dependent manner (0.1-10 microM) by attenuating both TNF-alpha (29-97%) and iNOS (61-96%) mRNA expression in microglia exposed to Abeta or LPS. Tretinoin 0-2 amyloid beta precursor protein Rattus norvegicus 149-154
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 25-27 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 150-155
14519498-3 2003 In the current study, we sought to examine whether Nurr1, an orphan receptor of the nuclear receptor superfamily shown to be essential for the development, differentiation and survival of midbrain DA neurons, would be expressed in 3, 4, or 5 week RA-induced hNT neurons and their NT2 precursors. Tretinoin 247-249 nuclear receptor subfamily 4 group A member 2 Homo sapiens 51-56
11014218-3 2000 Here, we report that two RA-synthesizing enzymes [aldehyde dehydrogenase 1 (Aldh1) and retinaldehyde dehydrogenase 2 (Raldh2)] and a cytochrome P450 (Cyp26) that metabolizes vitamin A and RA into more polar metabolites exhibit dynamic expression patterns in the mouse uterus, both during the ovarian cycle and during early pregnancy. Tretinoin 188-190 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 150-155
11023996-3 2000 CYP26 (P450RAI), a novel cytochrome P450, is expressed during embryonic development, induced by all-trans RA, and capable of catalyzing the oxidation of [3H]RA to polar retinoids including 4-oxo-RA. Tretinoin 11-13 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 0-5
12933640-5 2003 We used real-time RT-PCR to examine the effects of these factors on the expression of mRNA encoding the Id proteins, demonstrating an increase in Id2 and Id3 expression in Sertoli cells treated with thyroid hormone, retinoic acid, or testosterone. Tretinoin 216-229 inhibitor of DNA binding 2 Rattus norvegicus 146-149
15688020-0 2005 Retinoic acid and arsenic trioxide cooperate for apoptosis through phosphorylated RXR alpha. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 82-91
15800190-0 2005 Retinoic acid-induced chromatin remodeling of mouse kappa opioid receptor gene. Tretinoin 0-13 opioid receptor, kappa 1 Mus musculus 52-73
11023996-3 2000 CYP26 (P450RAI), a novel cytochrome P450, is expressed during embryonic development, induced by all-trans RA, and capable of catalyzing the oxidation of [3H]RA to polar retinoids including 4-oxo-RA. Tretinoin 106-108 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 0-5
15800190-1 2005 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in P19 embryonic stem cells but is first suppressed and reactivated during retinoic acid (RA)-induced neuronal differentiation. Tretinoin 146-159 opioid receptor, kappa 1 Mus musculus 10-31
11023996-4 2000 Here we report that CYP26 expression in adult liver is regulated by all-trans RA and dietary vitamin A, and is correlated with the metabolism of all-trans RA to polar metabolites. Tretinoin 78-80 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 20-25
15800190-1 2005 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in P19 embryonic stem cells but is first suppressed and reactivated during retinoic acid (RA)-induced neuronal differentiation. Tretinoin 146-159 opioid receptor, kappa 1 Mus musculus 33-36
15800190-1 2005 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in P19 embryonic stem cells but is first suppressed and reactivated during retinoic acid (RA)-induced neuronal differentiation. Tretinoin 161-163 opioid receptor, kappa 1 Mus musculus 10-31
14582708-2 2003 We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. Tretinoin 37-50 inhibitor of DNA binding 2 Homo sapiens 96-99
14582708-2 2003 We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. Tretinoin 37-50 inhibitor of DNA binding 2 Homo sapiens 156-159
14582708-2 2003 We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. Tretinoin 52-56 inhibitor of DNA binding 2 Homo sapiens 96-99
15800190-1 2005 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in P19 embryonic stem cells but is first suppressed and reactivated during retinoic acid (RA)-induced neuronal differentiation. Tretinoin 161-163 opioid receptor, kappa 1 Mus musculus 33-36
15800190-3 2005 The suppression and reactivation of the KOR gene in this neuronal differentiation model suggested chromatin remodeling occurred on this gene promoter triggered by RA induction. Tretinoin 163-165 opioid receptor, kappa 1 Mus musculus 40-43
14582708-2 2003 We analyzed the effects of all-trans retinoic acid (atRA) on the gene and protein expression of Id2 in THP-1 cells and found a suppression of the levels of Id2. Tretinoin 52-56 inhibitor of DNA binding 2 Homo sapiens 156-159
11023996-4 2000 Here we report that CYP26 expression in adult liver is regulated by all-trans RA and dietary vitamin A, and is correlated with the metabolism of all-trans RA to polar metabolites. Tretinoin 155-157 cytochrome P450, family 26, subfamily a, polypeptide 1 Rattus norvegicus 20-25
15800190-9 2005 It is concluded that RA induces KOR gene suppression, as early neuronal differentiation marker, by inducing substitution of c-Myc/Max with Max/Mad on the E box and by BRG-1 involved nucleosome recruitment and chromatin condensation, thereby abolishing Sp1 binding. Tretinoin 21-23 opioid receptor, kappa 1 Mus musculus 32-35
10996843-9 2000 Both MMP-1 and MMP-13 were detected and appear to be involved in IL-1 + RetA induced bovine cartilage destruction. Tretinoin 72-76 interstitial collagenase Bos taurus 5-10
15688037-1 2005 The acute promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) fusion product recruits histone deacetylase (HDAC) and DNA methyltransferase (DNMT) activities on retinoic acid (RA)-target promoters causing their silencing and differentiation block. Tretinoin 39-52 DNA methyltransferase 1 Homo sapiens 134-155
15688037-1 2005 The acute promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) fusion product recruits histone deacetylase (HDAC) and DNA methyltransferase (DNMT) activities on retinoic acid (RA)-target promoters causing their silencing and differentiation block. Tretinoin 39-52 DNA methyltransferase 1 Homo sapiens 157-161
15688037-1 2005 The acute promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) fusion product recruits histone deacetylase (HDAC) and DNA methyltransferase (DNMT) activities on retinoic acid (RA)-target promoters causing their silencing and differentiation block. Tretinoin 69-71 DNA methyltransferase 1 Homo sapiens 134-155
15688037-1 2005 The acute promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) fusion product recruits histone deacetylase (HDAC) and DNA methyltransferase (DNMT) activities on retinoic acid (RA)-target promoters causing their silencing and differentiation block. Tretinoin 69-71 DNA methyltransferase 1 Homo sapiens 157-161
15688037-6 2005 The specific contribution of the HDAC and DNMT pathways to the response of APL cells to RA was also tested by inhibiting these enzymatic activities with TSA and/or 5-azacytidine. Tretinoin 88-90 DNA methyltransferase 1 Homo sapiens 42-46
12906928-7 2003 Furthermore, zymography experiments showed that supernatants of ATRA-exposed PSC cultures contained higher levels of matrix metalloproteinase-9 but not of matrix metalloproteinase-2 than untreated controls. Tretinoin 64-68 matrix metallopeptidase 9 Rattus norvegicus 117-143
12907615-2 2003 RA exerts its pleiotropic activities by activating the nuclear receptors, retinoic acid receptor (RAR), which, in turn, regulate transcription of multiple target genes. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 74-96
12907615-2 2003 RA exerts its pleiotropic activities by activating the nuclear receptors, retinoic acid receptor (RAR), which, in turn, regulate transcription of multiple target genes. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 98-101
12907615-6 2003 Stable expression of CRABP-II in mammary carcinoma SC115 cells enabled activation of RAR, considerably sensitized the cells to RA-induced growth inhibition, and dramatically suppressed their tumorigenicity in immunodeficient mice. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 85-88
15844314-6 2005 Furthermore, RA could suppress the expression of CA125 tumor marker in 3AO cells. Tretinoin 13-15 mucin 16, cell surface associated Homo sapiens 49-54
10999756-11 2000 Pharmacological dietary RA stimulated RARalpha, RARbeta, and RARgamma as early as day 1 by 2-, 4-, and 2.1-fold, respectively, without effect on lung RARs. Tretinoin 24-26 retinoic acid receptor, alpha Rattus norvegicus 38-46
15618018-0 2005 Effect of all-trans-retinoic acid on mRNA binding protein p62 in human gastric cancer cells. Tretinoin 10-33 nucleoporin 62 Homo sapiens 58-61
15618018-3 2005 Interestingly, we found that p62 was cytoplasmic in location, but it significantly decreased in cytoplasm and appeared in nucleus of cells when the cells were treated with 50 microM all-trans retinoic acid (ATRA) for 5 days. Tretinoin 192-205 nucleoporin 62 Homo sapiens 29-32
12767051-2 2003 LTC(4) S activity in rat basophilic leukemia-1 (RBL-1) cells increased after culture in the presence of retinoic acid (RA) analogues, which was inhibited by cycloheximide or actinomycin D (ACD). Tretinoin 104-117 leukotriene C4 synthase Rattus norvegicus 0-8
12767051-2 2003 LTC(4) S activity in rat basophilic leukemia-1 (RBL-1) cells increased after culture in the presence of retinoic acid (RA) analogues, which was inhibited by cycloheximide or actinomycin D (ACD). Tretinoin 119-121 leukotriene C4 synthase Rattus norvegicus 0-8
12767051-3 2003 Unexpectedly, the co-addition of a low dose of ACD with RA further potentiated the upregulation of the LTC(4) S activity. Tretinoin 56-58 leukotriene C4 synthase Rattus norvegicus 103-111
12767051-6 2003 While LTC(4) S mRNA and protein increased in the cells treated with RA, the co-addition of ACD further potentiated both in proportion to the LTC(4) S activity. Tretinoin 68-70 leukotriene C4 synthase Rattus norvegicus 6-14
15618018-3 2005 Interestingly, we found that p62 was cytoplasmic in location, but it significantly decreased in cytoplasm and appeared in nucleus of cells when the cells were treated with 50 microM all-trans retinoic acid (ATRA) for 5 days. Tretinoin 207-211 nucleoporin 62 Homo sapiens 29-32
15618018-5 2005 These results suggest that there is a significant association between expression and distribution of p62 and the growth arrest of tumor cells, in which p62 is associated with cell apoptosis induced by ATRA. Tretinoin 201-205 nucleoporin 62 Homo sapiens 101-104
12767051-11 2003 In consideration of RA-differentiation therapy, it may be of pathophysiological relevance that the antineoplastic agents potentiate RA-induced, steroid-sensitive, induction of LTC(4) S in RBL-1 cells. Tretinoin 20-22 leukotriene C4 synthase Rattus norvegicus 176-184
12767051-11 2003 In consideration of RA-differentiation therapy, it may be of pathophysiological relevance that the antineoplastic agents potentiate RA-induced, steroid-sensitive, induction of LTC(4) S in RBL-1 cells. Tretinoin 132-134 leukotriene C4 synthase Rattus norvegicus 176-184
15618018-5 2005 These results suggest that there is a significant association between expression and distribution of p62 and the growth arrest of tumor cells, in which p62 is associated with cell apoptosis induced by ATRA. Tretinoin 201-205 nucleoporin 62 Homo sapiens 152-155
10936200-4 2000 This biphasic response may be related to the different expression of TNF-alpha receptors (TNFRs); a significant increase in the density of TNFR1 was in fact observed following RA-induced differentiation. Tretinoin 176-178 TNF receptor superfamily member 1A Homo sapiens 139-144
15883744-7 2005 RESULTS: ATRA induced a dose-dependent increase of percent CD23 (3.4 fold) or CD54 (1.6 fold) positive B cells. Tretinoin 9-13 intercellular adhesion molecule 1 Homo sapiens 78-82
15883744-12 2005 CONCLUSIONS: ATRA interferes through several pathways with the anti-CD40 plus IL-4 mediated B cell activation, namely IL-6, CD23 and CD54. Tretinoin 13-17 intercellular adhesion molecule 1 Homo sapiens 133-137
12846418-3 2003 9-cis retinoic acid (9-cis RA), a ligand for both retinoic acid receptor (RAR)/retinoic X receptor (RXR) heterodimers as well as RXR/RXR homodimers, markedly induced NIS mRNA expression in MCF-7 breast cancer cells in a dose- and time-dependent fashion, with maximal levels occurring at 12 h. All-trans retinoic acid, ATRA, a RAR specific ligand had a similar potency. Tretinoin 6-19 retinoid X receptor alpha Homo sapiens 100-103
12782018-8 2003 These results demonstrated that RA-mediated teratogenesis is accompanied by a reduction in the temporal and spatial pattern of p53 gene and protein expression in addition to the disruption of the cell cycle by modulation of p21 and p27. Tretinoin 32-34 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 224-227
15664402-0 2005 Effects of all-trans retinoic acid on orphan receptor APJ signaling in spontaneously hypertensive rats. Tretinoin 11-34 apelin receptor Rattus norvegicus 54-57
10976925-0 2000 Cytochrome P450RAI(CYP26) promoter: a distinct composite retinoic acid response element underlies the complex regulation of retinoic acid metabolism. Tretinoin 57-70 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-25
15705891-0 2005 Identification of OTX2 as a medulloblastoma oncogene whose product can be targeted by all-trans retinoic acid. Tretinoin 96-109 orthodenticle homeobox 2 Homo sapiens 18-22
12755330-10 2003 The effects of the growth factors activin A, retinoic acid (RA) and basic fibroblast growth factor (bFGF) on the regulation of Xlmx1b were also studied. Tretinoin 60-62 LIM homeobox transcription factor 1, beta, gene 1 S homeolog Xenopus laevis 127-133
12569559-7 2003 Of interest is the finding that retinoic acid upregulated expression of MICA/B in Huh7 and HepG2 cells. Tretinoin 32-45 MIR7-3 host gene Homo sapiens 82-86
15705891-3 2005 Knockdown of OTX2 expression by siRNAs inhibited medulloblastoma cell growth in vitro, whereas pharmacologic doses of all-trans retinoic acid repressed OTX2 expression and induced apoptosis only in medulloblastoma cell lines that expressed OTX2. Tretinoin 128-141 orthodenticle homeobox 2 Homo sapiens 152-156
10976925-0 2000 Cytochrome P450RAI(CYP26) promoter: a distinct composite retinoic acid response element underlies the complex regulation of retinoic acid metabolism. Tretinoin 124-137 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-25
15705891-3 2005 Knockdown of OTX2 expression by siRNAs inhibited medulloblastoma cell growth in vitro, whereas pharmacologic doses of all-trans retinoic acid repressed OTX2 expression and induced apoptosis only in medulloblastoma cell lines that expressed OTX2. Tretinoin 128-141 orthodenticle homeobox 2 Homo sapiens 152-156
12660332-6 2003 Daily administration of ATRA ameliorated proteinuria, which was accompanied by the improvement in the effacement of the foot processes and by the induction of nephrin and midkine. Tretinoin 24-28 midkine Rattus norvegicus 171-178
12660332-8 2003 Consistently, the promoter region of human nephrin gene (NPHS1) contained three putative retinoic acid response elements (RARE) and showed the enhancer activity in response to ATRA in a dose-dependent manner. Tretinoin 89-102 NPHS1 adhesion molecule, nephrin Homo sapiens 43-50
12660332-8 2003 Consistently, the promoter region of human nephrin gene (NPHS1) contained three putative retinoic acid response elements (RARE) and showed the enhancer activity in response to ATRA in a dose-dependent manner. Tretinoin 89-102 NPHS1 adhesion molecule, nephrin Homo sapiens 57-62
12660332-8 2003 Consistently, the promoter region of human nephrin gene (NPHS1) contained three putative retinoic acid response elements (RARE) and showed the enhancer activity in response to ATRA in a dose-dependent manner. Tretinoin 176-180 NPHS1 adhesion molecule, nephrin Homo sapiens 43-50
15661643-1 2005 The cellular retinoic acid-binding protein 2 (CRABP2) is believed to be involved in regulating access of retinoic acid to nuclear retinoic acid receptors. Tretinoin 13-26 cellular retinoic acid binding protein 2, b Danio rerio 46-52
12660332-8 2003 Consistently, the promoter region of human nephrin gene (NPHS1) contained three putative retinoic acid response elements (RARE) and showed the enhancer activity in response to ATRA in a dose-dependent manner. Tretinoin 176-180 NPHS1 adhesion molecule, nephrin Homo sapiens 57-62
15661643-9 2005 Whole mount in situ hybridization detected crabp2b and crabp2a mRNA in a number of structures known to require retinoic acid signaling during embryonic development. Tretinoin 111-124 cellular retinoic acid binding protein 2, b Danio rerio 43-50
10976925-13 2000 Together, these results indicate that the P450RAI-RARE is atypical in that conserved flanking sequences may play a very important role in regulating RA inducibility and expression of P450RAI(CYP26). Tretinoin 46-48 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 183-196
15607726-6 2005 Concurrently, atRA also decreased the expressions of vascular endothelial growth factor (VEGF) and its receptor KDR/Flk-1, and Akt phosphorylation. Tretinoin 14-18 vascular endothelial growth factor A Bos taurus 53-87
15607726-6 2005 Concurrently, atRA also decreased the expressions of vascular endothelial growth factor (VEGF) and its receptor KDR/Flk-1, and Akt phosphorylation. Tretinoin 14-18 vascular endothelial growth factor A Bos taurus 89-93
15607726-7 2005 Co-treatment with troglitazone, an activator of VEGF expression, reversed the atRA-induced reductions in eNOS-Ser(1179) phosphorylation and NO production, with concomitant restoration in VEGF expression. Tretinoin 78-82 vascular endothelial growth factor A Bos taurus 48-52
12615055-5 2003 Combination of receptor-specific retinoid agonists for RXR and RAR alpha significantly enhanced the sensitivity of N-myc-amplified neuroblastoma cells to the growth inhibitory effects of aRA. Tretinoin 187-190 retinoid X receptor alpha Homo sapiens 55-58
12606150-6 2003 Levels of atRA and the expression of two potentially retinoic acid (RA)-controlled proteins critically involved in retinoid storage regulation, lecithin: retinol acyltransferase (LRAT) and cellular retinol binding protein I (CRBP I), were analyzed in liver and kidney. Tretinoin 53-66 lecithin retinol acyltransferase Rattus norvegicus 179-183
15607726-7 2005 Co-treatment with troglitazone, an activator of VEGF expression, reversed the atRA-induced reductions in eNOS-Ser(1179) phosphorylation and NO production, with concomitant restoration in VEGF expression. Tretinoin 78-82 vascular endothelial growth factor A Bos taurus 187-191
12606150-6 2003 Levels of atRA and the expression of two potentially retinoic acid (RA)-controlled proteins critically involved in retinoid storage regulation, lecithin: retinol acyltransferase (LRAT) and cellular retinol binding protein I (CRBP I), were analyzed in liver and kidney. Tretinoin 53-66 retinol binding protein 1 Rattus norvegicus 189-223
15607726-10 2005 Thus, atRA decreases eNOS-Ser(1179) phosphorylation through a mechanism that depends on VEGF-KDR/Flk-1-mediated Akt phosphorylation but is independent of RARE, leading to reduction in NO production. Tretinoin 6-10 vascular endothelial growth factor A Bos taurus 88-92
12606150-6 2003 Levels of atRA and the expression of two potentially retinoic acid (RA)-controlled proteins critically involved in retinoid storage regulation, lecithin: retinol acyltransferase (LRAT) and cellular retinol binding protein I (CRBP I), were analyzed in liver and kidney. Tretinoin 53-66 retinol binding protein 1 Rattus norvegicus 225-231
10984118-0 2000 A combination treatment of c-myc antisense DNA with all-trans-retinoic acid inhibits cell proliferation by downregulating c-myc expression in small cell lung cancer. Tretinoin 52-75 MYC proto-oncogene, bHLH transcription factor Homo sapiens 27-32
12393392-0 2003 All-trans-retinoic acid induces CD52 expression in acute promyelocytic leukemia. Tretinoin 0-23 CD52 molecule Homo sapiens 32-36
12393392-2 2003 In this study, we found that ATRA treatment of the APL cell line NB4 induced the expression of CD52, both at transcriptional and translational levels. Tretinoin 29-33 CD52 molecule Homo sapiens 95-99
12393392-4 2003 The ATRA-dependent induction of CD52 expression was not observed in non-promyelocytic leukemia cell lines such as K562, U937, and HL-60, suggesting that induction of CD52 by ATRA may be specific to leukemic cells that express promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) or are at the promyelocytic stage of myeloid development. Tretinoin 4-8 CD52 molecule Homo sapiens 32-36
12393392-4 2003 The ATRA-dependent induction of CD52 expression was not observed in non-promyelocytic leukemia cell lines such as K562, U937, and HL-60, suggesting that induction of CD52 by ATRA may be specific to leukemic cells that express promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) or are at the promyelocytic stage of myeloid development. Tretinoin 4-8 CD52 molecule Homo sapiens 166-170
12393392-6 2003 An ATRA-induced high level of CD52 expression might potentially serve as a novel therapeutic target in treatment of APL. Tretinoin 3-7 CD52 molecule Homo sapiens 30-34
15668483-7 2005 The effects of retinoic acid and sodium butyrate on the CD97/CD55 expression in OSCC cell lines were determined by quantitative PCR, immunocytochemistry, and flow cytometry. Tretinoin 15-28 CD55 molecule (Cromer blood group) Homo sapiens 61-65
16026305-4 2005 Retinoic acids (RA) are biologically active metabolites of vitamin A that regulate growth and differentiation of many cell types, by binding to specific nuclear receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 0-14 retinoid X receptor alpha Homo sapiens 214-234
16026305-4 2005 Retinoic acids (RA) are biologically active metabolites of vitamin A that regulate growth and differentiation of many cell types, by binding to specific nuclear receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 0-14 retinoid X receptor alpha Homo sapiens 236-239
16026305-4 2005 Retinoic acids (RA) are biologically active metabolites of vitamin A that regulate growth and differentiation of many cell types, by binding to specific nuclear receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 16-18 retinoid X receptor alpha Homo sapiens 214-234
16026305-4 2005 Retinoic acids (RA) are biologically active metabolites of vitamin A that regulate growth and differentiation of many cell types, by binding to specific nuclear receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 16-18 retinoid X receptor alpha Homo sapiens 236-239
10984118-0 2000 A combination treatment of c-myc antisense DNA with all-trans-retinoic acid inhibits cell proliferation by downregulating c-myc expression in small cell lung cancer. Tretinoin 52-75 MYC proto-oncogene, bHLH transcription factor Homo sapiens 122-127
15652522-4 2005 In this study, we investigated the effect of all-trans-retinoic acid on the production of an ECM protein, thrombospondin-1 (TSP-1), and two angiogenic factors, pigment epithelium-derived factor (PEDF) and vascular endothelial growth factor (VEGF) by RPE cells. Tretinoin 45-68 thrombospondin 1 Mus musculus 106-122
12653733-0 2003 Early vitronectin receptor downregulation in a melanoma cell line during all-trans retinoic acid-induced apoptosis. Tretinoin 83-96 vitronectin Homo sapiens 6-17
15717686-4 2005 The protein expression of p47phox, another component of phagocyte NADPH oxidase, was also up-regulated by DHEA and ATRA. Tretinoin 115-119 neutrophil cytosolic factor 1 Homo sapiens 26-33
10984118-2 2000 In this study, we investigated whether c-myc antisense oligodeoxynucleoside phosphorothioate (OPT) covering the translational initiation site of c-myc mRNA used in combination with all-trans-retinoic acid (RA) would be more effective than either agent alone in inhibiting the growth of an SCLC cell line, NCI-H82, overexpressing c-myc with amplification of this gene, and whether this combination could be an experimental therapeutic tool against SCLC. Tretinoin 206-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 39-44
12653733-8 2003 At this time point, decrease in the F-actin polymerization as well as inhibition of cell adhesive ability to vitronectin (Vn) was exerted by ATRA treatment. Tretinoin 141-145 vitronectin Homo sapiens 109-120
12653733-8 2003 At this time point, decrease in the F-actin polymerization as well as inhibition of cell adhesive ability to vitronectin (Vn) was exerted by ATRA treatment. Tretinoin 141-145 vitronectin Homo sapiens 122-124
15583048-11 2005 These results indicate that retinoic acid inhibits porcine preadipocyte differentiation by a mechanism that involves activation of the RAR and downregulation of PPARgamma, RXRalpha, and SREBP-1C mRNA. Tretinoin 28-41 sterol regulatory element binding transcription factor 1 Sus scrofa 186-194
12653733-10 2003 Functionally, the treatment of melanoma cells with 10 micromol L-1 ATRA for 48 h causes an inhibition of directional cell migration towards Vn-coated filters. Tretinoin 67-71 vitronectin Homo sapiens 140-142
10984118-2 2000 In this study, we investigated whether c-myc antisense oligodeoxynucleoside phosphorothioate (OPT) covering the translational initiation site of c-myc mRNA used in combination with all-trans-retinoic acid (RA) would be more effective than either agent alone in inhibiting the growth of an SCLC cell line, NCI-H82, overexpressing c-myc with amplification of this gene, and whether this combination could be an experimental therapeutic tool against SCLC. Tretinoin 206-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150
10984118-2 2000 In this study, we investigated whether c-myc antisense oligodeoxynucleoside phosphorothioate (OPT) covering the translational initiation site of c-myc mRNA used in combination with all-trans-retinoic acid (RA) would be more effective than either agent alone in inhibiting the growth of an SCLC cell line, NCI-H82, overexpressing c-myc with amplification of this gene, and whether this combination could be an experimental therapeutic tool against SCLC. Tretinoin 206-208 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 proliferating cell nuclear antigen Homo sapiens 37-43
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 interferon alpha inducible protein 27 Homo sapiens 83-86
12619131-5 2003 In F9 cells induced by retinoic acid to differentiate to VE, mMix is coordinately expressed with three other endodermal transcription factors, well before AFP, and its protein product is localized to the nucleus. Tretinoin 23-36 Mix1 homeobox-like 1 (Xenopus laevis) Mus musculus 61-65
15389522-8 2005 Analysis of PCNA protein confirmed inhibition of proliferation by retinoic acid. Tretinoin 66-79 proliferating cell nuclear antigen Rattus norvegicus 12-16
12616482-3 2003 As evidenced by flow cytometry, ATRA (at 1 microM) clearly and donor-independently suppressed the expression of all integrin chains investigated (CD11a, CD11b, CD11c, and CD18), most strikingly of CD11a. Tretinoin 32-36 integrin subunit alpha M Homo sapiens 153-158
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin dependent kinase inhibitor 1B Homo sapiens 87-91
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 proliferating cell nuclear antigen Homo sapiens 146-152
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 proliferating cell nuclear antigen Homo sapiens 146-152
10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 proliferating cell nuclear antigen Homo sapiens 146-152
12601020-8 2003 RA treatment also led to G(0)/G(1) cell cycle arrest and increased both the intensity of human cone arrestin (hCAR)-immunoreactivity and the number of apoptotic cells. Tretinoin 0-2 CXADR Ig-like cell adhesion molecule Homo sapiens 110-114
15730877-10 2005 The density of RARalpha-ir cells was higher in the operated left olfactory epithelium and highest after ATRA treatment. Tretinoin 104-108 retinoic acid receptor, alpha Mus musculus 15-23
10951230-0 2000 Selective upregulation of fibroblast Fas ligand expression, and prolongation of Fas/Fas ligand-mediated skin allograft survival, by retinoic acid: the skin as a retinoide-inducible immune privilege site. Tretinoin 132-145 Fas ligand Homo sapiens 84-94
10940477-6 2000 Most RARalpha fusion proteins can still be induced to transactivate genes, but only at very high doses of ligand, explaining why pharmacological doses of ATRA are necessary to obtain a therapeutic effect in these patients. Tretinoin 154-158 retinoic acid receptor alpha Homo sapiens 5-13
15717849-4 2005 Moreover, not only neural (Mash-1) and neuroectodermal (Pax-6), but also endodermal (GATA-4, alpha-fetoprotein) genes are expressed at early stages of differentiation driven by RA under serum-free conditions. Tretinoin 177-179 achaete-scute family bHLH transcription factor 1 Mus musculus 27-33
15717849-4 2005 Moreover, not only neural (Mash-1) and neuroectodermal (Pax-6), but also endodermal (GATA-4, alpha-fetoprotein) genes are expressed at early stages of differentiation driven by RA under serum-free conditions. Tretinoin 177-179 alpha fetoprotein Mus musculus 93-110
12655154-7 2003 Moreover, levels of SGP-2 and/or TF were significantly elevated in the cells treatment with sodium butyrate and retinoic acid, inducers of cellular differentiation. Tretinoin 112-125 clusterin Rattus norvegicus 20-25
12494454-9 2003 The ability of RA to induce RARbeta and PKCalpha expression was retained in A-fos clones, suggesting that A-fos was not interfering with RAR transcription activation functions. Tretinoin 15-17 Rab40B, member RAS oncogene family Mus musculus 28-31
12485937-3 2003 We identified a retinoic acid response element (RARE) that lies nearly 900 nucleotides upstream of the CD18 transcriptional start site that was bound by the RA receptors, retinoic acid receptor (RAR) and retinoic X receptor (RXR). Tretinoin 16-29 retinoid X receptor alpha Homo sapiens 225-228
10854907-0 2000 Retinoic acid negatively regulates neuropeptide Y expression in human neuroblastoma cells. Tretinoin 0-13 neuropeptide Y Homo sapiens 35-49
14529416-2 2003 Retinoids are natural and synthetic compounds related to retinoic acid that act through interaction with two basic types of nuclear receptors: retinoic acid receptors (RAR alpha, RARbeta and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta and RXRgamma) as retinoid-inducible transcription factors. Tretinoin 57-70 retinoid X receptor alpha Homo sapiens 227-235
16215318-8 2005 Using proliferation assays, CRABP-II overexpressing CAKI-2 cells did not exhibit a significant change in RA sensitivity, but appeared to be less sensitive toward RA-stimulation compared to CAKI-2 cells expressing naturally low levels of CRABP-II (maximum difference, 59% at 3 microM ATRA). Tretinoin 283-287 cellular retinoic acid binding protein 2 Homo sapiens 28-36
15597047-3 2004 Injections of all-trans RA suppressed the expression of dorsal signals Tbx5, BMP4 and to a lesser extent of ephrinB1, whereas the injection of citral, an inhibitor of RA synthesis, enhanced the expression of BMP4 and Tbx5. Tretinoin 24-26 bone morphogenetic protein 4 Gallus gallus 77-81
14535836-2 2003 The incubation of cells with 1 micromol/l all-trans retinoic acid (ATRA) for 72 h induced differentiation of HL-60 cells and increased the number of CD11b positive cells. Tretinoin 42-65 integrin subunit alpha M Homo sapiens 149-154
10854907-2 2000 In the present study, we evaluated the effects of all-trans retinoic acid (RA) on the biosynthesis and secretion of neuropeptide Y (NPY), a widely expressed neuroregulatory peptide. Tretinoin 60-73 neuropeptide Y Homo sapiens 116-130
14535836-2 2003 The incubation of cells with 1 micromol/l all-trans retinoic acid (ATRA) for 72 h induced differentiation of HL-60 cells and increased the number of CD11b positive cells. Tretinoin 67-71 integrin subunit alpha M Homo sapiens 149-154
15308560-3 2004 We show that all-trans retinoic acid (ATRA), an effective differentiation-inducing agent of acute promyelocytic leukemic (APL) cells, can elevate PLSCR1 expression in ATRA-sensitive APL cells NB4 and HL60, but not in maturation-resistant NB4-LR1 cells. Tretinoin 23-36 phospholipid scramblase 1 Homo sapiens 146-152
15308560-3 2004 We show that all-trans retinoic acid (ATRA), an effective differentiation-inducing agent of acute promyelocytic leukemic (APL) cells, can elevate PLSCR1 expression in ATRA-sensitive APL cells NB4 and HL60, but not in maturation-resistant NB4-LR1 cells. Tretinoin 38-42 phospholipid scramblase 1 Homo sapiens 146-152
10854907-2 2000 In the present study, we evaluated the effects of all-trans retinoic acid (RA) on the biosynthesis and secretion of neuropeptide Y (NPY), a widely expressed neuroregulatory peptide. Tretinoin 60-73 neuropeptide Y Homo sapiens 132-135
15308560-4 2004 ATRA- and phorbol 12-myristate 13-acetate (PMA)-induced monocytic differentiation is accompanied by increased PLSCR1 expression, whereas only a slight or no elevation of PLSCR1 expression is observed in U937 cells differentiated with dimethyl sulfoxide (DMSO), sodium butyrate, or vitamin D3. Tretinoin 0-4 phospholipid scramblase 1 Homo sapiens 110-116
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 26-30 phospholipid scramblase 1 Homo sapiens 241-247
10854907-2 2000 In the present study, we evaluated the effects of all-trans retinoic acid (RA) on the biosynthesis and secretion of neuropeptide Y (NPY), a widely expressed neuroregulatory peptide. Tretinoin 75-77 neuropeptide Y Homo sapiens 116-130
15308560-5 2004 Cell differentiation with ATRA and PMA, but not with vitamin D3 or DMSO, results in phosphorylation of protein kinase Cdelta (PKCdelta), and the PKCdelta-specific inhibitor rottlerin nearly eliminates the ATRA- and PMA-induced expression of PLSCR1, while ectopic expression of a constitutively active form of PKCdelta directly increases PLSCR1 expression. Tretinoin 26-30 phospholipid scramblase 1 Homo sapiens 337-343
10854907-2 2000 In the present study, we evaluated the effects of all-trans retinoic acid (RA) on the biosynthesis and secretion of neuropeptide Y (NPY), a widely expressed neuroregulatory peptide. Tretinoin 75-77 neuropeptide Y Homo sapiens 132-135
12429354-0 2002 Retinoic acid binding properties of the lipocalin member beta-lactoglobulin studied by circular dichroism, electronic absorption spectroscopy and molecular modeling methods. Tretinoin 0-13 beta-lactoglobulin Bos taurus 57-75
10854907-4 2000 Treatment with 10 microM RA induced a marked decrease in NPY gene expression after as little as 3-6 h of incubation and resulted in its almost complete suppression at 12-24 h and after a 6-day differentiating treatment. Tretinoin 25-27 neuropeptide Y Homo sapiens 57-60
12429354-4 2002 As the disappearing CD activity showed in the course of CD-pH titration experiment, retinoic acid molecules dissociate from BLG upon acidification but this release is completely reversible as proved by the reconstitution of the CD and absorption spectra after setting the pH back to neutral. Tretinoin 84-97 beta-lactoglobulin Bos taurus 124-127
12453892-0 2002 Activating transcription factor-2 mediates transcriptional regulation of gluconeogenic gene PEPCK by retinoic acid. Tretinoin 101-114 activating transcription factor 2 Homo sapiens 0-33
15610140-6 2004 Treatment with RA had only a slight effect on the mRNA expression of the tight junction-associated proteins occludin, ZO-1, claudin-1, -3, and -4, but enhanced the expression of claudin-2, which was recently suggested to form a paracellular ion channel. Tretinoin 15-17 claudin 1 Homo sapiens 124-145
10854907-5 2000 The NPY content in cell extracts and the NPY secreted and accumulated in the culture medium were also reduced by exposure to 10 microM RA at 12 and 24 h and at 6 days. Tretinoin 135-137 neuropeptide Y Homo sapiens 4-7
15485494-0 2004 Induction of cyclin-dependent kinase 5 and its activator p35 through the extracellular-signal-regulated kinase and protein kinase A pathways during retinoic-acid mediated neuronal differentiation in human neuroblastoma SK-N-BE(2)C cells. Tretinoin 148-161 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 57-60
15485494-3 2004 In this study we newly found that RA treatment of SK-N-BE(2)C, human neuroblastoma cells, increased the expression of Cdk5 and its neuron specific activator p35 through the extracellular-signal-regulated kinase1/2 (ERK1/2) and cAMP-dependent protein kinase A (PKA) pathway. Tretinoin 34-36 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 157-160
15485494-6 2004 In addition, a transcription factor early growth response 1 (Egr-1) was induced by RA through the ERK1/2 pathway, suggesting its possible involvement in the p35 induction. Tretinoin 83-85 cyclin dependent kinase 5 regulatory subunit 1 Homo sapiens 157-160
15485494-7 2004 RA treatment also induced c-fos mediated AP-1 binding, and cAMP-responsive element binding protein (CREB) mediated CRE binding via ERK1/2 and PKA pathway, respectively, in the Cdk5 promoter region, resulting in the induction of Cdk5. Tretinoin 0-2 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 26-31
15485494-7 2004 RA treatment also induced c-fos mediated AP-1 binding, and cAMP-responsive element binding protein (CREB) mediated CRE binding via ERK1/2 and PKA pathway, respectively, in the Cdk5 promoter region, resulting in the induction of Cdk5. Tretinoin 0-2 cAMP responsive element binding protein 1 Homo sapiens 100-104
15485494-8 2004 Our results suggest that ERK1/2 and PKA-induced regulation of Cdk5 activity possibly through Egr-1, c-fos, and CREB plays a critical role in the RA-induced neuronal differentiation. Tretinoin 145-147 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 100-105
12453892-0 2002 Activating transcription factor-2 mediates transcriptional regulation of gluconeogenic gene PEPCK by retinoic acid. Tretinoin 101-114 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 92-97
12453892-1 2002 All-trans-retinoic acid (RA) is known to increase the rate of transcription of the PEPCK gene upon engagement of the RA receptor (RAR). Tretinoin 0-23 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 83-88
12453892-1 2002 All-trans-retinoic acid (RA) is known to increase the rate of transcription of the PEPCK gene upon engagement of the RA receptor (RAR). Tretinoin 25-27 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 83-88
12453892-3 2002 Here we show that RA upregulation of PEPCK promoter activity requires the cAMP response element (CRE)-1 in addition to the RA-response element and that activating transcription factor-2 (ATF-2) binds the CRE element to mediate this effect. Tretinoin 18-20 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 37-42
12453892-3 2002 Here we show that RA upregulation of PEPCK promoter activity requires the cAMP response element (CRE)-1 in addition to the RA-response element and that activating transcription factor-2 (ATF-2) binds the CRE element to mediate this effect. Tretinoin 18-20 activating transcription factor 2 Homo sapiens 187-192
12453892-3 2002 Here we show that RA upregulation of PEPCK promoter activity requires the cAMP response element (CRE)-1 in addition to the RA-response element and that activating transcription factor-2 (ATF-2) binds the CRE element to mediate this effect. Tretinoin 123-125 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 37-42
12453892-4 2002 Furthermore, we show that RA treatment potentiates ATF-2-dependent transactivation by inducing specific phosphorylation of ATF-2 by p38beta kinase. Tretinoin 26-28 activating transcription factor 2 Homo sapiens 51-56
12453892-4 2002 Furthermore, we show that RA treatment potentiates ATF-2-dependent transactivation by inducing specific phosphorylation of ATF-2 by p38beta kinase. Tretinoin 26-28 activating transcription factor 2 Homo sapiens 123-128
12453892-5 2002 ATF-2 activation by RA blocked the inhibitory intramolecular interaction of ATF-2 amino and carboxyl terminal domains in a p38beta kinase-dependent manner. Tretinoin 20-22 activating transcription factor 2 Homo sapiens 0-5
15485494-8 2004 Our results suggest that ERK1/2 and PKA-induced regulation of Cdk5 activity possibly through Egr-1, c-fos, and CREB plays a critical role in the RA-induced neuronal differentiation. Tretinoin 145-147 cAMP responsive element binding protein 1 Homo sapiens 111-115
12453892-5 2002 ATF-2 activation by RA blocked the inhibitory intramolecular interaction of ATF-2 amino and carboxyl terminal domains in a p38beta kinase-dependent manner. Tretinoin 20-22 activating transcription factor 2 Homo sapiens 76-81
10854907-5 2000 The NPY content in cell extracts and the NPY secreted and accumulated in the culture medium were also reduced by exposure to 10 microM RA at 12 and 24 h and at 6 days. Tretinoin 135-137 neuropeptide Y Homo sapiens 41-44
12453892-6 2002 Consistent with these results, RA treatment increased the DNA binding activity of ATF-2 on the PEPCK CRE-1 sequence. Tretinoin 31-33 activating transcription factor 2 Homo sapiens 82-87
10854907-6 2000 Moreover, RA treatment for 6 days, but not for 24 h, resulted in a marked stimulation of proNPY processing to mature NPY. Tretinoin 10-12 neuropeptide Y Homo sapiens 92-95
12453892-6 2002 Consistent with these results, RA treatment increased the DNA binding activity of ATF-2 on the PEPCK CRE-1 sequence. Tretinoin 31-33 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 95-100
15284334-6 2004 The fact that binding of RXR-RAR on DR3 is not observed suggests that contrary to RA-induced granulocytic differentiation, 1 alpha,25-dihydroxyvitamin D(3)-mediated monocytic differentiation requires positive and negative transcriptional controls both likely mediated by the RXR-VDR heterodimer. Tretinoin 29-31 retinoid X receptor alpha Homo sapiens 25-28
12453892-7 2002 Taken together, the data suggest that RA activates the p38beta kinase pathway leading to phosphorylation and activation of ATF-2, thereby enhancing PEPCK gene transcription and glucose production. Tretinoin 38-40 activating transcription factor 2 Homo sapiens 123-128
10854907-7 2000 The presence of negative retinoic acid-response elements in the human NPY promoter (up to -1078 bp) was excluded by a computer search. Tretinoin 25-38 neuropeptide Y Homo sapiens 70-73
12453892-7 2002 Taken together, the data suggest that RA activates the p38beta kinase pathway leading to phosphorylation and activation of ATF-2, thereby enhancing PEPCK gene transcription and glucose production. Tretinoin 38-40 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 148-153
10864469-5 2000 The correlation between tbx5 expression and atrial lineage determination was examined in retinoic acid (RA)-treated chicken embryos. Tretinoin 89-102 T-box 5 Gallus gallus 24-28
12429992-6 2002 WNT3A, WNT8A, WNT8B, WNT10B and WNT11 are down-regulated in NT2 cells after ATRA treatment, while WNT2, WNT7B and WNT14B are up-regulated. Tretinoin 76-80 Wnt family member 8A Homo sapiens 7-12
12775111-7 2002 When VA-deficient rats received a single injection of retinoic acid (2 mg/rat), tissue IGF-I and IGF-IR gene expression did not change after 4 or 8 h, while the expression of IGF-II, IGFBP-4, and IGFBP-6 mRNAs in some tissues increased rapidly. Tretinoin 54-67 insulin-like growth factor 2 Rattus norvegicus 175-181
15299018-8 2004 Although RA pretreatment inhibits nuc-1 remodeling and HIV-1 transcription, it has no effect on histone acetylation. Tretinoin 9-11 peroxisome proliferator activated receptor delta Homo sapiens 34-39
15299009-1 2004 Retinaldehyde dehydrogenase II (RalDH2) converts retinal to the transcriptional regulator retinoic acid in the developing embryo. Tretinoin 90-103 aldehyde dehydrogenase 1 family member A2 Homo sapiens 32-38
10864469-5 2000 The correlation between tbx5 expression and atrial lineage determination was examined in retinoic acid (RA)-treated chicken embryos. Tretinoin 104-106 T-box 5 Gallus gallus 24-28
15467265-5 2004 ATRA-induced down-regulation of telomerase activity in differentiated HL-60 cells was associated with a decrease in hTERT and an increase in human telomerase-associated protein-1 (hTP1) transcription. Tretinoin 0-4 telomerase associated protein 1 Homo sapiens 147-178
15467265-5 2004 ATRA-induced down-regulation of telomerase activity in differentiated HL-60 cells was associated with a decrease in hTERT and an increase in human telomerase-associated protein-1 (hTP1) transcription. Tretinoin 0-4 telomerase associated protein 1 Homo sapiens 180-184
15305337-7 2004 As well, expression of the cell cycle inhibitor p21 was found to be elevated only in well-differentiated tumors of mice, treated with ATRA while expression of p27, was found to be elevated only in the poorly differentiated tumors. Tretinoin 134-138 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 48-51
15234573-3 2004 Moreover, in the presence of 1 microM ATRA, approximately 50% of UF-1 cells expressing annexin V, an early-apoptotic marker, was negative for CD11b and showed immature morphology. Tretinoin 38-42 integrin subunit alpha M Homo sapiens 142-147
12393164-7 2002 We found that retinoic acid (RA) and carbenoxolone, agents that block gap-junctional channels in coupled neurons and other cell types, also suppressed Cx38 hemichannel currents with an IC(50) of approximately 2 and 34 microM for RA and carbenoxolone, respectively. Tretinoin 14-27 connexin 38 S homeolog Xenopus laevis 151-155
12397370-0 2002 Retinoic acid enhances leukemia inhibitory factor expression in OLN-93 oligodendrocytes. Tretinoin 0-13 LIF, interleukin 6 family cytokine Rattus norvegicus 23-49
10864469-6 2000 tbx5 expression is maintained throughout the hearts of RA-treated embryos under conditions that also expand atrial-specific gene expression. Tretinoin 55-57 T-box 5 Gallus gallus 0-4
10820192-4 2000 Retinoic acid-mediated differentiation of NT2 precursor cells to the neuronal phenotype resulted in five- to 15-fold increases in the expression of PLC-beta1, PLC-beta4, and Galpha(q/11) (the prime G protein activator of these isozymes). Tretinoin 0-13 succinate-CoA ligase GDP/ADP-forming subunit alpha Homo sapiens 174-186
12186877-2 2002 All-trans-retinoic acid (t-RA) inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis by inhibiting the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Tretinoin 0-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-154
12186877-2 2002 All-trans-retinoic acid (t-RA) inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis by inhibiting the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Tretinoin 25-29 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-154
15229225-2 2004 Embryonic differentiation in brain and lung has classically been linked to retinoid signaling, and we have recently characterized NPDC-1 as a regulator of retinoic acid-mediated events. Tretinoin 155-168 neural proliferation, differentiation and control 1 Homo sapiens 130-136
10865976-2 2000 Retinoic acid has been shown to induce differentiation and reduce TF expression in acute promyelocytic leukaemia (APL) cells in vitro, and to induce remission in APL patients. Tretinoin 0-13 coagulation factor III, tissue factor Homo sapiens 66-68
15229225-8 2004 Deletion of the PEST motif increased NPDC-1 protein stability and NPDC-1 inhibitory effect on retinoic acid-mediated transcription. Tretinoin 94-107 neural proliferation, differentiation and control 1 Homo sapiens 66-72
15229225-12 2004 Together these results suggest that retinoic acid signaling can be modulated by the presence of NPDC-1 and that the protein level and activity of NPDC-1 can be regulated by phosphorylation-mediated proteasomal degradation. Tretinoin 36-49 neural proliferation, differentiation and control 1 Homo sapiens 96-102
15190067-13 2004 We propose a novel role for APC and CDX2 in controlling retinoic acid biosynthesis and in promoting a retinoid-induced program of colonocyte differentiation. Tretinoin 56-69 caudal type homeobox 2 Homo sapiens 36-40
12145292-5 2002 Upon endoderm differentiation of F9 cells induced by retinoic acid, c-Fos expression, the downstream target of the Ras pathway, is suppressed by uncoupling Elk-1 phosphorylation/activation to MAPK activity. Tretinoin 53-66 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-73
12145292-5 2002 Upon endoderm differentiation of F9 cells induced by retinoic acid, c-Fos expression, the downstream target of the Ras pathway, is suppressed by uncoupling Elk-1 phosphorylation/activation to MAPK activity. Tretinoin 53-66 ETS transcription factor ELK1 Homo sapiens 156-161
12239173-0 2002 Response to histone deacetylase inhibition of novel PML/RARalpha mutants detected in retinoic acid-resistant APL cells. Tretinoin 85-98 histone deacetylase 9 Homo sapiens 12-31
15234273-1 2004 Retinoic acid (RA) suppresses alpha 2(I) collagen expression in hepatic stellate cells through the binding of retinoic acid receptor beta (RAR beta) and retinoid X receptor alpha (RXR alpha) to RA response elements (RAREs) in the alpha 2(I) collagen promoter. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 180-189
15234273-4 2004 In the presence of RA, the coactivators SRC-1 and GRIP-1 formed complexes with RAR beta and RXR alpha which are bound to an oligonucleotide specifying a RARE site in the promoter. Tretinoin 19-21 retinoid X receptor alpha Homo sapiens 92-101
12239173-6 2002 We evaluated whether histone deacetylase (HDAC) inhibition could overcome the effects of these mutations on ATRA-induced gene expression. Tretinoin 108-112 histone deacetylase 9 Homo sapiens 42-46
10865965-16 2000 We conclude that (1) ATRA combined to EMA chemotherapy is effective in the treatment of relapsed APL; (2) allogeneic BMT may be too toxic after salvage treatment including EMA intensive chemotherapy; (3) clinical outcome of autografted patients and preliminary molecular results regarding detection of PML/RARalpha after autologous PBSCT are encouraging. Tretinoin 21-25 PML nuclear body scaffold Homo sapiens 302-305
12239173-10 2002 Thus, the ability of an HDAC inhibitor to restore ATRA sensitivity in resistant cells may depend on their specific molecular defects. Tretinoin 50-54 histone deacetylase 9 Homo sapiens 24-28
15234273-5 2004 In conclusion, this study shows that in the presence of retinoic acid, the coactivators SRC-1 and GRIP-1 augment, while the corepressor N-CoR abolishes, the suppressive effects of RAR beta and RXR alpha on alpha 2(I) collagen promoter activity. Tretinoin 56-69 retinoid X receptor alpha Homo sapiens 193-202
15219855-4 2004 In this study, we report that Sp1, Sp3, and c-Jun increase transactivation of the L-RARE during RA treatment. Tretinoin 84-86 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-49
15219855-5 2004 Sp1 and Sp3 regulate the lamin A/C promoter in Sp1-deficient SL2 cells and contribute to RA-dependent activation in GAL4-based transcriptional assays. Tretinoin 89-91 galectin 4 Homo sapiens 116-120
15219855-9 2004 Our data suggest that Sp1, Sp3, and c-Jun play an important role in gene expression through the L-RARE during RA treatment. Tretinoin 98-100 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41
10865965-16 2000 We conclude that (1) ATRA combined to EMA chemotherapy is effective in the treatment of relapsed APL; (2) allogeneic BMT may be too toxic after salvage treatment including EMA intensive chemotherapy; (3) clinical outcome of autografted patients and preliminary molecular results regarding detection of PML/RARalpha after autologous PBSCT are encouraging. Tretinoin 21-25 retinoic acid receptor alpha Homo sapiens 306-314
10845230-6 2000 These results suggest that the RAR index in untreated NB and PNET shows great individual variation since its determination is necessary for the evaluation of the efficacy of retinoic acid treatment. Tretinoin 174-187 retinoic acid receptor alpha Homo sapiens 31-34
15206818-5 2004 Treatment with retinoic acid (RA) induced expression of Ngn1 as well as NeuroD in P19 cells in early period of neuronal differentiation. Tretinoin 15-28 neurogenin 1 Homo sapiens 56-60
15162499-1 2004 Retinoic acid (RA) synthesizing and metabolizing enzymes are coordinately expressed with serotonin 2B (5-HT2B) receptors at sites of epithelial-mesenchymal (E-M) interaction in the mouse embryo (Bhasin et al., 1999). Tretinoin 0-13 5-hydroxytryptamine (serotonin) receptor 2B Mus musculus 89-109
12383199-0 2002 Opposing cytokine-specific effects of all trans-retinoic acid on the activation and expression of signal transducer and activator of transcription (STAT)-1 in THP-1 cells. Tretinoin 42-61 signal transducer and activator of transcription 1 Homo sapiens 98-155
12383199-1 2002 The regulation of signal transducer and activator of transcription-1 (STAT-1) by cytokines and all-trans-retinoic acid (RA) was investigated in THP-1 monocytic cells cultured with RA and stimulated with lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), and IFN-gamma, individually or in combinations. Tretinoin 95-118 signal transducer and activator of transcription 1 Homo sapiens 18-68
12383199-1 2002 The regulation of signal transducer and activator of transcription-1 (STAT-1) by cytokines and all-trans-retinoic acid (RA) was investigated in THP-1 monocytic cells cultured with RA and stimulated with lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), and IFN-gamma, individually or in combinations. Tretinoin 95-118 signal transducer and activator of transcription 1 Homo sapiens 70-76
12383199-1 2002 The regulation of signal transducer and activator of transcription-1 (STAT-1) by cytokines and all-trans-retinoic acid (RA) was investigated in THP-1 monocytic cells cultured with RA and stimulated with lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), and IFN-gamma, individually or in combinations. Tretinoin 120-122 signal transducer and activator of transcription 1 Homo sapiens 18-68
12383199-1 2002 The regulation of signal transducer and activator of transcription-1 (STAT-1) by cytokines and all-trans-retinoic acid (RA) was investigated in THP-1 monocytic cells cultured with RA and stimulated with lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), and IFN-gamma, individually or in combinations. Tretinoin 120-122 signal transducer and activator of transcription 1 Homo sapiens 70-76
12445277-5 2002 More recently, it has become clear that a stimulatory receptor expressed by NK cells, T cells and macrophages (NKG2D) recognizes ligands (MHC class I chain related [MIC], H6O, retinoic acid early inducible [Rae1] and UL16 binding proteins [ULBP]) that are up-regulated on tumor cells and virally infected cells but are not expressed well by normal cells. Tretinoin 176-189 ribonucleic acid export 1 Mus musculus 207-211
15162499-1 2004 Retinoic acid (RA) synthesizing and metabolizing enzymes are coordinately expressed with serotonin 2B (5-HT2B) receptors at sites of epithelial-mesenchymal (E-M) interaction in the mouse embryo (Bhasin et al., 1999). Tretinoin 15-17 5-hydroxytryptamine (serotonin) receptor 2B Mus musculus 89-109
10792961-12 2000 A decrease in proteolytic activity was noted on zymography at 68 kDa, 7 and 28 days following surgery in vein grafts from animals treated with atRA, corresponding with a decrease in the active form of MMP-2. Tretinoin 143-147 72 kDa type IV collagenase Oryctolagus cuniculus 201-206
15093729-9 2004 TBX2 expression and its induction by retinoic acid was also observed in normal human and nonmalignant mouse melanocytes. Tretinoin 37-50 T-box transcription factor 2 Homo sapiens 0-4
15170058-0 2004 Retionic acid and its receptors are required for expression of aryl hydrocarbon receptor mRNA and embryonic development of blood vessel and bone in the medaka fish, Oryzias latipes. Tretinoin 0-13 aryl hydrocarbon receptor 1b Oryzias latipes 63-88
12237335-0 2002 Regulation of mouse kappa opioid receptor gene expression by different 3"-untranslated regions and the effect of retinoic acid. Tretinoin 113-126 opioid receptor, kappa 1 Mus musculus 20-41
12237335-4 2002 Retinoic acid specifically suppresses the expression of KOR transcripts using the second poly(A) in P19 cells. Tretinoin 0-13 opioid receptor, kappa 1 Mus musculus 56-59
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 121-124
12204966-6 2002 High-dose (10(-4) M) ATRA increased binding of NF-kappaB and STAT1 proteins to sequences that originated from the IRF-1 promoter region, while low-dose (10(-6) M) ATRA induced only NF-kappaB binding. Tretinoin 21-25 signal transducer and activator of transcription 1 Homo sapiens 61-66
12204966-7 2002 A delayed tyrosine phosphorylation of the signal transducer and activator of transcription-1 (STAT1) was observed after high-dose (10(-4) M) but not low-dose (10(-6) M) ATRA treatment. Tretinoin 169-173 signal transducer and activator of transcription 1 Homo sapiens 42-92
12204966-7 2002 A delayed tyrosine phosphorylation of the signal transducer and activator of transcription-1 (STAT1) was observed after high-dose (10(-4) M) but not low-dose (10(-6) M) ATRA treatment. Tretinoin 169-173 signal transducer and activator of transcription 1 Homo sapiens 94-99
14709332-6 2004 The Vav/p85 interaction is essential for the ATRA-induced PI 3-K activity and for association of PI 3-K with actin, particularly in the nucleus. Tretinoin 45-49 phosphoinositide-3-kinase regulatory subunit 2 Homo sapiens 8-11
15157320-4 2004 The levels of VEGF-R on the surface of HL-60 cells also decreased after treatment with ATRA of 5 and 10 micro mol/L for 72 hours, but at 48 hours the expression rates of VEGF-R on HL-60 cells of the two ATRA treated groups were not significantly decreased. Tretinoin 87-91 kinase insert domain receptor Homo sapiens 14-20
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 1-3 retinoic acid receptor alpha Homo sapiens 121-124
15157320-4 2004 The levels of VEGF-R on the surface of HL-60 cells also decreased after treatment with ATRA of 5 and 10 micro mol/L for 72 hours, but at 48 hours the expression rates of VEGF-R on HL-60 cells of the two ATRA treated groups were not significantly decreased. Tretinoin 203-207 kinase insert domain receptor Homo sapiens 170-176
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 121-124
12163600-6 2002 The vIRF1 protein deregulates GRIM19-induced apoptosis in the presence of IFN/all-trans-retinoic acid (RA) and inhibits IFN/RA-induced cell death. Tretinoin 78-101 K9 Human gammaherpesvirus 8 4-9
10777532-1 2000 Silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is known to interact with Sin3 and recruit the histone deacetylases (HDACs) that lead to hypoacetylation of histones and transrepression of target transcription factors. Tretinoin 22-35 SIN3 transcription regulator family member A Homo sapiens 99-103
12163600-6 2002 The vIRF1 protein deregulates GRIM19-induced apoptosis in the presence of IFN/all-trans-retinoic acid (RA) and inhibits IFN/RA-induced cell death. Tretinoin 78-101 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 30-36
12193473-0 2002 All-trans-retinoic acid induces nuclear factor kappaB activation and matrix metalloproteinase-9 expression and enhances basement membrane invasivity of differentiation-resistant human SK-N-BE 9N neuroblastoma Cells. Tretinoin 0-23 matrix metallopeptidase 9 Homo sapiens 69-95
12087179-7 2002 Retinoic acid (RA)-induced differentiation of NT2 cells to hNT neurons was accompanied by increased reelin expression and by the appearance of three DNase I hypersensitive sites 5" to the RNA start site. Tretinoin 0-13 reelin Homo sapiens 100-106
14766225-9 2004 The mode of action of CRABP-II in skin is to mediate retinoic acid activity. Tretinoin 53-66 cellular retinoic acid binding protein 2 Homo sapiens 22-30
15147236-3 2004 The amino acid sequence of the VDR shows a significant homology with other members of the nuclear hormone receptor superfamily, including receptors for glucocorticoids (GR), oestrogen (ER), androgen (AR), progesteron (PR), thyroid hormone (T3R), retinoic acid (RAR), retinoid X (RXR) and over 150 orphan receptors. Tretinoin 246-259 vitamin D receptor Homo sapiens 31-34
12087179-7 2002 Retinoic acid (RA)-induced differentiation of NT2 cells to hNT neurons was accompanied by increased reelin expression and by the appearance of three DNase I hypersensitive sites 5" to the RNA start site. Tretinoin 15-17 reelin Homo sapiens 100-106
10751444-3 2000 Previously, we reported on the cooperative roles of bone morphogenetic protein-2 (BMP2) and retinoic acid (RA) in the enhancement of neurotrophin-3 (NT3) responsiveness in cultured sympathetic neurons dissociated from perinatal rat superior cervical ganglia (SCG). Tretinoin 92-105 neurotrophin 3 Rattus norvegicus 133-147
12087179-8 2002 RA-induced differentiation was also associated with demethylation of the reelin promoter. Tretinoin 0-2 reelin Homo sapiens 73-79
12225397-0 2002 GM-CSF induces expression of gp91phox and stimulates retinoic acid-induced p47phox expression in human myeloblastic leukemia cells. Tretinoin 53-66 neutrophil cytosolic factor 1 Homo sapiens 75-82
10751444-3 2000 Previously, we reported on the cooperative roles of bone morphogenetic protein-2 (BMP2) and retinoic acid (RA) in the enhancement of neurotrophin-3 (NT3) responsiveness in cultured sympathetic neurons dissociated from perinatal rat superior cervical ganglia (SCG). Tretinoin 107-109 neurotrophin 3 Rattus norvegicus 133-147
12225397-5 2002 p47phox expression was increased by ATRA alone, and the expression was increased synergistically by the combination of ATRA with GM-CSF. Tretinoin 36-40 neutrophil cytosolic factor 1 Homo sapiens 0-7
12225397-5 2002 p47phox expression was increased by ATRA alone, and the expression was increased synergistically by the combination of ATRA with GM-CSF. Tretinoin 119-123 neutrophil cytosolic factor 1 Homo sapiens 0-7
14668324-4 2004 However, we recently presented functional evidence suggesting that RXR in the TR/RXR heterodimer can bind its natural ligand 9-cis-RA in cells. Tretinoin 125-133 retinoid X receptor alpha Homo sapiens 67-70
10753851-5 2000 The NPM-RAR fusion proteins bind to retinoic acid response element sequences as either homodimers or as heterodimers with RXR. Tretinoin 36-49 retinoic acid receptor alpha Homo sapiens 8-11
14668324-4 2004 However, we recently presented functional evidence suggesting that RXR in the TR/RXR heterodimer can bind its natural ligand 9-cis-RA in cells. Tretinoin 125-133 retinoid X receptor alpha Homo sapiens 81-84
10753851-9 2000 Both NPM-RAR and PML-RAR interact with the co-repressor protein SMRTe in a manner that is less sensitive than RARalpha to dissociation by retinoic acid. Tretinoin 138-151 retinoic acid receptor alpha Homo sapiens 9-12
12163000-7 2002 HT-29 cells treated with retinoic acid had dose-dependent increases in IGFBP-4 and reduced IGF-II expression. Tretinoin 25-38 insulin like growth factor binding protein 4 Homo sapiens 71-78
10753851-9 2000 Both NPM-RAR and PML-RAR interact with the co-repressor protein SMRTe in a manner that is less sensitive than RARalpha to dissociation by retinoic acid. Tretinoin 138-151 retinoic acid receptor alpha Homo sapiens 110-118
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 synaptophysin Homo sapiens 121-134
10830441-6 2000 In addition to the morphological changes, expressions of the pancreas-specific molecular markers, XIHbox8 and insulin, were induced in retinoic acid-treated dorsal lip explants. Tretinoin 135-148 insulin S homeolog Xenopus laevis 110-117
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 microtubule associated protein 2 Homo sapiens 321-353
14743441-5 2004 RA-treated CD133+ cells expressed mRNA transcripts for neuron-specific markers neurofilament proteins (NF-L, -M, -H) and synaptophysin as determined by RT-PCR, structural proteins characteristic of neurons including tubulin beta III and neuron specific enolase (NSE) by Western blot, and neuron-specific markers NeuN and microtubule-associated protein-2 (MAP2) by immunocytochemistry. Tretinoin 0-2 microtubule associated protein 2 Homo sapiens 355-359
12188026-1 2002 The active form of vitamin D, 1,25-Dihydroxyvitamin D3 [l,25(OH)2D3], is a secosteroid hormone that binds to the vitamin D receptor (VDR), a member of the superfamily of nuclear receptors for steroid hormones, thyroid hormone, and retinoic acid. Tretinoin 231-244 vitamin D receptor Homo sapiens 113-131
12188026-1 2002 The active form of vitamin D, 1,25-Dihydroxyvitamin D3 [l,25(OH)2D3], is a secosteroid hormone that binds to the vitamin D receptor (VDR), a member of the superfamily of nuclear receptors for steroid hormones, thyroid hormone, and retinoic acid. Tretinoin 231-244 vitamin D receptor Homo sapiens 133-136
14627700-3 2004 Three cAMP response element-binding protein (CREB)-binding protein-dependent transcriptional pathways, regulated by cAMP response element (CRE), retinoic acid response element, and nuclear factor kappaB, show abnormalities in our exon 1 cell model. Tretinoin 145-158 CREB binding protein Rattus norvegicus 6-66
10692469-2 2000 For the first time, we have shown that SF1 and Oct-3/4 are co-expressed in embryonal carcinoma (EC) P19 cells, and their expression is down-regulated with very similar kinetics following retinoic acid (RA) induced differentiation of these cells, suggesting a functional relationship between the two. Tretinoin 187-200 POU class 5 homeobox 1 Homo sapiens 47-54
14736747-8 2004 In addition, a Tead2-Engrailed fusion protein is able to repress retinoic acid-induced Pax3 expression in P19 cells and in vivo. Tretinoin 65-78 TEA domain family member 2 Mus musculus 15-20
12050180-3 2002 We found that PLC-beta2, virtually absent in untreated NB4 cells, was strongly up-regulated after ATRA-induced granulocytic differentiation. Tretinoin 98-102 phospholipase C beta 2 Homo sapiens 14-23
12050180-4 2002 Remarkably, using primary blasts purified from bone marrow of patients affected by APL successfully induced to remission by treatment with ATRA, we showed a striking correlation between the amount of PLC-beta2 expression and the responsiveness of APL blasts to the differentiative activity of ATRA. Tretinoin 139-143 phospholipase C beta 2 Homo sapiens 200-209
12050180-4 2002 Remarkably, using primary blasts purified from bone marrow of patients affected by APL successfully induced to remission by treatment with ATRA, we showed a striking correlation between the amount of PLC-beta2 expression and the responsiveness of APL blasts to the differentiative activity of ATRA. Tretinoin 293-297 phospholipase C beta 2 Homo sapiens 200-209
14623888-9 2004 Catalytic assays of five recombinant mouse CYP2Cs expressed in Escherichia coli revealed that only CYP2C39 was competent for RA 4-hydroxylation (K(m) = 812.3 nm and V(max) 47.85 (fmol/min/pmol P450)). Tretinoin 125-127 cytochrome P450, family 2, subfamily c, polypeptide 39 Mus musculus 99-106
10692469-2 2000 For the first time, we have shown that SF1 and Oct-3/4 are co-expressed in embryonal carcinoma (EC) P19 cells, and their expression is down-regulated with very similar kinetics following retinoic acid (RA) induced differentiation of these cells, suggesting a functional relationship between the two. Tretinoin 202-204 POU class 5 homeobox 1 Homo sapiens 47-54
14623888-11 2004 These data show that CYP2C39 catalyzes RA catabolism and thus possibly controls RA levels in mouse liver. Tretinoin 39-41 cytochrome P450, family 2, subfamily c, polypeptide 39 Mus musculus 21-28
12042426-0 2002 Lecithin:retinol acyltransferase expression is regulated by dietary vitamin A and exogenous retinoic acid in the lung of adult rats. Tretinoin 92-105 lecithin retinol acyltransferase Rattus norvegicus 0-32
10692469-3 2000 Previously, we have shown that the Oct-3/4 promoter harbors an RA-responsive element, RAREoct, which functions in EC cells as a binding site for positive regulators of transcription, such as RAR and RXR. Tretinoin 63-65 POU class 5 homeobox 1 Homo sapiens 35-42
12042426-5 2002 Treatment of VA-deficient rats with 100 microg RA increased lung LRAT mRNA (P < 0.005) and specific activity (P < 0.0001), and treatment with 5 mg of RA increased LRAT mRNA level and specific activity more than approximately 15- and 6-fold above those in control lung, respectively (both P < or = 0.001). Tretinoin 47-49 lecithin retinol acyltransferase Rattus norvegicus 65-69
12042426-5 2002 Treatment of VA-deficient rats with 100 microg RA increased lung LRAT mRNA (P < 0.005) and specific activity (P < 0.0001), and treatment with 5 mg of RA increased LRAT mRNA level and specific activity more than approximately 15- and 6-fold above those in control lung, respectively (both P < or = 0.001). Tretinoin 47-49 lecithin retinol acyltransferase Rattus norvegicus 169-173
10702898-4 2000 The PML/RARa protein product is responsible for the leukemic phenotype in these patients, but is also able to respond to pharmacologic levels of retinoic acid and induce cell differentiation. Tretinoin 145-158 PML nuclear body scaffold Homo sapiens 4-7
12128071-5 2002 In addition, exposure of cells to retinoic acid alone or in combination with dibutyryl cAMP for 22 days markedly decreased the level of lysyl oxidase mRNA (52 or 35% of control) while increasing the level of mRNA of N-acetylglucosaminidase (NAG), a marker enzyme for lysosomes (162 or 142% of control). Tretinoin 34-47 protein-lysine 6-oxidase Oryctolagus cuniculus 136-149
14532297-0 2004 A novel human cytochrome P450, CYP26C1, involved in metabolism of 9-cis and all-trans isomers of retinoic acid. Tretinoin 97-110 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 31-38
14532297-6 2004 Transiently transfected cells expressing CYP26C1 convert atRA to polar water-soluble metabolites similar to those generated by CYP26A1 and -B1. Tretinoin 57-61 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 41-48
14532297-7 2004 Competition studies with all-trans, 13-cis, and 9-cis isomers of retinoic acid demonstrated that atRA was the preferred substrate for CYP26C1. Tretinoin 65-78 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 134-141
14532297-7 2004 Competition studies with all-trans, 13-cis, and 9-cis isomers of retinoic acid demonstrated that atRA was the preferred substrate for CYP26C1. Tretinoin 97-101 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 134-141
10702898-4 2000 The PML/RARa protein product is responsible for the leukemic phenotype in these patients, but is also able to respond to pharmacologic levels of retinoic acid and induce cell differentiation. Tretinoin 145-158 retinoic acid receptor alpha Homo sapiens 8-12
14532297-9 2004 Specifically, CYP26C1 can also recognize and metabolize 9-cis-RA and is much less sensitive than the other CYP26 family members to the inhibitory effects of ketoconazole. Tretinoin 56-64 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 14-21
11979432-4 2002 Therefore, we analyzed the expression of OVCA1 and OVCA2 in cells in response to treatment with all-trans retinoic acid (RA) and N-(4-hydroxyphenyl)retinamide (4HPR), or under conditions of low serum and confluence, to determine further the roles of OVCA1 and OVCA2 in cell growth, apoptosis and differentiation. Tretinoin 106-119 diphthamide biosynthesis 1 Homo sapiens 41-46
11775254-1 2000 OBJECTIVE: To study in vivo effect of all-trans-retinoic acid (ATRA) or arsenic trioxide (As2O3) on the expression of tissue factor (TF) and the hemostatic disorders, a series of parameters were measured in bone marrow blasts and plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 38-61 coagulation factor III, tissue factor Homo sapiens 118-131
12054801-4 2002 We have now determined the crystal structures of the complexes of the trigonal form of beta-Lg at pH 7.5 with bound retinol (R=21.4% for 7329 reflections between 20 and 2.4 A resolution, R(free)=30.6%) and with bound retinoic acid (R=22.7% for 7813 reflections between 20 and 2.34 A resolution, R(free)=29.8%). Tretinoin 217-230 beta-lactoglobulin Bos taurus 87-94
15225900-3 2004 Topical application of retinoic acid resulted in significant inhibition of benzoyl peroxide-induced epidermal ornithine decarboxylase activity and DNA synthesis. Tretinoin 23-36 ornithine decarboxylase, structural 1 Mus musculus 110-133
11775254-1 2000 OBJECTIVE: To study in vivo effect of all-trans-retinoic acid (ATRA) or arsenic trioxide (As2O3) on the expression of tissue factor (TF) and the hemostatic disorders, a series of parameters were measured in bone marrow blasts and plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 38-61 coagulation factor III, tissue factor Homo sapiens 133-135
11775254-1 2000 OBJECTIVE: To study in vivo effect of all-trans-retinoic acid (ATRA) or arsenic trioxide (As2O3) on the expression of tissue factor (TF) and the hemostatic disorders, a series of parameters were measured in bone marrow blasts and plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 63-67 coagulation factor III, tissue factor Homo sapiens 118-131
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 15-28 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-183
14694446-12 2004 Paired related homeobox gene 2 (Prx2)/S8 homeobox, and retinoic acid (RA)-regulated nur77 and cellular retinoic acid-binding protein II (CRABPII) transcription factors are expressed preferentially in P- cells. Tretinoin 55-68 cellular retinoic acid binding protein 2 Homo sapiens 94-135
11775254-1 2000 OBJECTIVE: To study in vivo effect of all-trans-retinoic acid (ATRA) or arsenic trioxide (As2O3) on the expression of tissue factor (TF) and the hemostatic disorders, a series of parameters were measured in bone marrow blasts and plasma from acute promyelocytic leukemia (APL) patients. Tretinoin 63-67 coagulation factor III, tissue factor Homo sapiens 133-135
14694446-12 2004 Paired related homeobox gene 2 (Prx2)/S8 homeobox, and retinoic acid (RA)-regulated nur77 and cellular retinoic acid-binding protein II (CRABPII) transcription factors are expressed preferentially in P- cells. Tretinoin 55-68 cellular retinoic acid binding protein 2 Homo sapiens 137-144
14694446-12 2004 Paired related homeobox gene 2 (Prx2)/S8 homeobox, and retinoic acid (RA)-regulated nur77 and cellular retinoic acid-binding protein II (CRABPII) transcription factors are expressed preferentially in P- cells. Tretinoin 70-72 cellular retinoic acid binding protein 2 Homo sapiens 94-135
14694446-12 2004 Paired related homeobox gene 2 (Prx2)/S8 homeobox, and retinoic acid (RA)-regulated nur77 and cellular retinoic acid-binding protein II (CRABPII) transcription factors are expressed preferentially in P- cells. Tretinoin 70-72 cellular retinoic acid binding protein 2 Homo sapiens 137-144
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 15-28 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 30-32 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-183
11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 30-32 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189
11775254-4 2000 RESULTS: The blast cell procoagulant activity (PCA), TF antigen of APL cell lysates, as well as the transcription of APL TF mRNA elevated at diagnosis, were reduced after ATRA or As2O3 therapy. Tretinoin 171-175 coagulation factor III, tissue factor Homo sapiens 53-55
14666262-3 2003 Receptor functional integrity was determined by testing whether RAR mRNA could be induced by retinoic acid. Tretinoin 95-108 Rab40B, member RAS oncogene family Mus musculus 64-67
11775254-7 2000 Both ATRA and As2O3 therapy down-regulated the expression of TF mRNA, decreased the PCA and TF level in APL cells, inhibited coagulation activation, secondary hyperfibrinolysis and recorrected other hemostatic abnormalities, thus greatly improved the bleeding symptom in early stage of the treatment. Tretinoin 5-9 coagulation factor III, tissue factor Homo sapiens 61-63
14666262-5 2003 The possibility that retinoic acid would induce the expression of the vitamin D receptor and synergize with vitamin D, a known inhibitor of HC11 cell growth, was also investigated. Tretinoin 21-34 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 70-88
11997213-5 2002 Retinoic acids also show a positive effect on AR expression, while exposure to glucocorticoid or estrogen blocks AR expression. Tretinoin 0-14 androgen receptor Mesocricetus auratus 46-48
11775254-7 2000 Both ATRA and As2O3 therapy down-regulated the expression of TF mRNA, decreased the PCA and TF level in APL cells, inhibited coagulation activation, secondary hyperfibrinolysis and recorrected other hemostatic abnormalities, thus greatly improved the bleeding symptom in early stage of the treatment. Tretinoin 5-9 coagulation factor III, tissue factor Homo sapiens 92-94
10681376-11 2000 CYP1A1 and CYP1B1 SUPERSOMES both exhibited exceptionally high activities, and in extrahepatic tissues, these isoforms could play important roles in biosynthesis of all-trans-retinoic acid from t-ROH. Tretinoin 165-188 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 0-6
14627725-5 2003 Raldh2(-/-) endothelial cells exhibited significantly increased expression of phosphohistone 3 and decreased expression of p21 and p27, suggesting that RA is required to control endothelial cell cycle progression during early vascular development. Tretinoin 152-154 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-6
10698945-0 2000 Structure of the RXR-RAR DNA-binding complex on the retinoic acid response element DR1. Tretinoin 52-65 retinoic acid receptor alpha Homo sapiens 21-24
12031648-5 2002 RESULTS: Expression of the MmTRA1b gene was markedly induced during granulocytic differentiation of promyelocytic leukemia NB4 and HT93 cells induced by all-trans retinoic acid (ATRA). Tretinoin 178-182 phospholipid scramblase 1 Homo sapiens 27-34
12031648-9 2002 ATRA-induced differentiation of antisense MmTRA1b-transfected NB4 cells was significantly suppressed. Tretinoin 0-4 phospholipid scramblase 1 Homo sapiens 42-49
10698945-2 2000 We describe the 1.70 A resolution structure of the ternary complex of RXR and RAR DNA-binding regions in complex with the retinoic acid response element DR1. Tretinoin 122-135 retinoic acid receptor alpha Homo sapiens 78-81
12031648-10 2002 On the other hand, ATRA induced the differentiation of MmTRA1b-transfected NB4 cells more efficiently than that of mock-transfected cells. Tretinoin 19-23 phospholipid scramblase 1 Homo sapiens 55-62
12968026-5 2003 Retinoic acid dramatically increased the expression of JSAP1 and JNK3, which were co-precipitated with anti-JNK3 in the neuroectoderm of wild type but not JSAP1-null embryoid bodies. Tretinoin 0-13 mitogen-activated protein kinase 10 Mus musculus 65-69
12031648-11 2002 MmTRA1b mRNA also was clearly induced in ATRA-treated primary acute promyelocytic leukemia cells during granulocytic differentiation. Tretinoin 41-45 phospholipid scramblase 1 Homo sapiens 0-7
10712606-5 2000 We searched for a suitable cell line expressing the MT-3 gene to be used for determination of MT-3 promoter tissue specificity, and showed that MT-3 expression is activated during neuroectodermal differentiation of P19 cells induced by retinoic acid to levels similar to those found in whole brain. Tretinoin 236-249 metallothionein 3 Mus musculus 94-98
11960970-4 2002 2) Treatment of atRA attenuated the ANG II-induced increase in total cell protein content. Tretinoin 16-20 angiogenin Rattus norvegicus 36-39
11960970-7 2002 4) atRA attenuated the ANG II-induced increase in intracellular Ca2+. Tretinoin 3-7 angiogenin Rattus norvegicus 23-26
12968026-5 2003 Retinoic acid dramatically increased the expression of JSAP1 and JNK3, which were co-precipitated with anti-JNK3 in the neuroectoderm of wild type but not JSAP1-null embryoid bodies. Tretinoin 0-13 mitogen-activated protein kinase 10 Mus musculus 108-112
14592467-4 2003 Studies in VAD rats showed that 4-HPR, like atRA, supports animal growth and induces CYP26B1 mRNA expression in lung whereas 4-HBR does not. Tretinoin 44-48 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 85-92
10712606-5 2000 We searched for a suitable cell line expressing the MT-3 gene to be used for determination of MT-3 promoter tissue specificity, and showed that MT-3 expression is activated during neuroectodermal differentiation of P19 cells induced by retinoic acid to levels similar to those found in whole brain. Tretinoin 236-249 metallothionein 3 Mus musculus 94-98
10694373-7 2000 RA (7.5 mg/kg) increased UCP1 mRNA but decreased UCP2 and UCP3 mRNA by 50%, whereas methylprednisolone (65 mg/kg, two doses 24 h apart) suppressed all three uncoupling proteins by greater than 60%. Tretinoin 0-2 uncoupling protein 3 Rattus norvegicus 58-62
14581068-1 2003 All-trans retinoic acid (tRA, or tretinoin) can be metabolized through stereoisomerization to 13-cis retinoic acid (13-cRA) in vivo. Tretinoin 0-23 myotubularin related protein 11 Homo sapiens 119-122
14581068-1 2003 All-trans retinoic acid (tRA, or tretinoin) can be metabolized through stereoisomerization to 13-cis retinoic acid (13-cRA) in vivo. Tretinoin 25-28 myotubularin related protein 11 Homo sapiens 119-122
14581068-1 2003 All-trans retinoic acid (tRA, or tretinoin) can be metabolized through stereoisomerization to 13-cis retinoic acid (13-cRA) in vivo. Tretinoin 33-42 myotubularin related protein 11 Homo sapiens 119-122
12148907-5 2002 In addition, IL-10 abolishes all trans retinoic acid (ATRA)-induced growth inhibition of myeloma cells. Tretinoin 39-52 interleukin 10 Homo sapiens 13-18
12148907-5 2002 In addition, IL-10 abolishes all trans retinoic acid (ATRA)-induced growth inhibition of myeloma cells. Tretinoin 54-58 interleukin 10 Homo sapiens 13-18
12128097-5 2002 In utero RA-treatment resulted in decreased expression of max, mad, caspases, bax, and bad genes at 48 h. Terminal uridinetriphosphate nick end-labeling (TUNEL) analysis revealed increased apoptosis at 24-48 h, followed by decreased apoptosis 72 h after in utero RA-exposure, which correlated with the decreased expression of pro-apoptotic genes noted at 48 h. Further investigations are needed to understand the role of Myc family genes during RA-mediated teratogenesis. Tretinoin 9-11 BCL2-associated X protein Mus musculus 78-81
10645966-4 2000 In this study we have tested the effect of retinoic acid on cardiac mesenchyme formation in vitro and then tested retinoic acid treated myocyte cultures for changes in the expression of hLAMP-1, fibronectin and transferrin members of the particulate matrix that is required for mesenchyme formation. Tretinoin 114-127 fibronectin 1 Mus musculus 195-206
11943730-0 2002 Expression of UGT2B7, a UDP-glucuronosyltransferase implicated in the metabolism of 4-hydroxyestrone and all-trans retinoic acid, in normal human breast parenchyma and in invasive and in situ breast cancers. Tretinoin 115-128 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 14-20
11943730-8 2002 Recent identification of all-trans retinoic acid as a substrate of UGT2B7 suggests that this function includes the generation of retinoyl-beta-glucuronide, a potent mediator of actions of retinoids important for maintaining epithelia in a differentiated state. Tretinoin 25-48 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 67-73
14596915-1 2003 A cDNA clone up-regulated in hydraulic lung edema in rabbit showed high similarity with human RDH10 mRNA, which encodes a protein involved in retinoic acid metabolism. Tretinoin 142-155 retinol dehydrogenase 10 Homo sapiens 94-99
11909957-0 2002 Direct channeling of retinoic acid between cellular retinoic acid-binding protein II and retinoic acid receptor sensitizes mammary carcinoma cells to retinoic acid-induced growth arrest. Tretinoin 21-34 cellular retinoic acid binding protein 2 Homo sapiens 43-84
10718371-3 2000 We found that HSP90 showed remarkably high expression in undifferentiated human embryonal carcinoma (EC) cells, which were subsequently dramatically down-regulated during in vitro cellular differentiation, following retinoic acid (RA) treatment, at the protein level. Tretinoin 216-229 heat shock protein 90 alpha family class A member 1 Homo sapiens 14-19
11909957-1 2002 Cellular retinoic acid-binding protein II (CRABP-II) is an intracellular lipid-binding protein that associates with retinoic acid with a subnanomolar affinity. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 43-51
11909957-2 2002 We previously showed that CRABP-II enhances the transcriptional activity of the nuclear receptor with which it shares a common ligand, namely, the retinoic acid receptor (RAR), and we suggested that it may act by delivering retinoic acid to this receptor. Tretinoin 147-160 cellular retinoic acid binding protein 2 Homo sapiens 26-34
11909957-4 2002 We show that CRABP-II, a predominantly cytosolic protein, massively undergoes nuclear localization upon binding of retinoic acid; that it interacts with RAR in a ligand-dependent fashion; and that, in the presence of retinoic acid, the CRABP-II-RAR complex is a short-lived intermediate. Tretinoin 115-128 cellular retinoic acid binding protein 2 Homo sapiens 13-21
11909957-4 2002 We show that CRABP-II, a predominantly cytosolic protein, massively undergoes nuclear localization upon binding of retinoic acid; that it interacts with RAR in a ligand-dependent fashion; and that, in the presence of retinoic acid, the CRABP-II-RAR complex is a short-lived intermediate. Tretinoin 217-230 cellular retinoic acid binding protein 2 Homo sapiens 13-21
11909957-5 2002 The data establish that potentiation of the transcriptional activity of RAR stems directly from the ability of CRABP-II to channel retinoic acid to the receptor. Tretinoin 131-144 cellular retinoic acid binding protein 2 Homo sapiens 111-119
11909957-6 2002 We demonstrate further that overexpression of CRABP-II in MCF-7 mammary carcinoma cells dramatically enhances their sensitivity to retinoic acid-induced growth inhibition. Tretinoin 131-144 cellular retinoic acid binding protein 2 Homo sapiens 46-54
11909957-7 2002 Conversely, diminished expression of CRABP-II renders these cells retinoic acid resistant. Tretinoin 66-79 cellular retinoic acid binding protein 2 Homo sapiens 37-45
14568882-6 2003 Whereas retinoic acid increased C/EBPbeta and PPARgamma mRNAs 1.5 times in ATII in vitro, vitamin-A deficiency strongly decreased fetal lung C/EBPalpha, beta, and PPARgamma transcripts in vivo. Tretinoin 8-21 CCAAT/enhancer binding protein beta Rattus norvegicus 32-41
14568882-6 2003 Whereas retinoic acid increased C/EBPbeta and PPARgamma mRNAs 1.5 times in ATII in vitro, vitamin-A deficiency strongly decreased fetal lung C/EBPalpha, beta, and PPARgamma transcripts in vivo. Tretinoin 8-21 peroxisome proliferator-activated receptor gamma Rattus norvegicus 46-55
14573779-5 2003 Of interest, the CD52 and protein kinase A regulatory subunit alpha (PKA-Rlalpha) genes, whose products are being used as therapeutic targets for certain human neoplasias in currently ongoing clinical trials, were among the genes observed to be markedly up-regulated after ATRA treatment. Tretinoin 273-277 CD52 molecule Homo sapiens 17-21
11909957-8 2002 Taken together, the data unequivocally establish the function of CRABP-II in modulating the RAR-mediated biological activities of retinoic acid. Tretinoin 130-143 cellular retinoic acid binding protein 2 Homo sapiens 65-73
10718371-3 2000 We found that HSP90 showed remarkably high expression in undifferentiated human embryonal carcinoma (EC) cells, which were subsequently dramatically down-regulated during in vitro cellular differentiation, following retinoic acid (RA) treatment, at the protein level. Tretinoin 231-233 heat shock protein 90 alpha family class A member 1 Homo sapiens 14-19
10718371-8 2000 We showed that the RA-induced differentiation of EC cells into a neural cell lineage was inhibited by overexpression of the HSP90alpha or -beta isoform via the gene transfer method. Tretinoin 19-21 heat shock protein 90 alpha family class A member 1 Homo sapiens 124-134
11948401-0 2002 AP-1 transrepressing retinoic acid does not deplete coactivators or AP-1 monomers but may target specific Jun or Fos containing dimers. Tretinoin 21-34 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-116
14560020-4 2003 Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RARgamma/RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RARalpha/RXR, and no binding of RARbeta/RXR. Tretinoin 145-149 retinoic acid receptor, gamma Mus musculus 79-87
10704061-0 2000 The influence of retinoic acid and retinoic acid derivatives on beta2 integrins and L-selectin expression in HL-60 cells in vitro. Tretinoin 17-30 selectin L Homo sapiens 84-94
14560020-4 2003 Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RARgamma/RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RARalpha/RXR, and no binding of RARbeta/RXR. Tretinoin 145-149 retinoid X receptor alpha Homo sapiens 88-91
14560020-4 2003 Chromatin immunoprecipitation analysis in macrophages confirmed the binding of RARgamma/RXR to the ABCA1 promoter DR4 element in the presence of ATRA, with weaker binding of RARalpha/RXR, and no binding of RARbeta/RXR. Tretinoin 145-149 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 99-104
12915404-1 2003 Levels of Rb2/p130 protein are increased 5-10-fold following all-trans-retinoic acid (ATRA) treatment of the retinoid-sensitive ovarian adenocarcinoma cell line CAOV3, but not the retinoid-resistant adenocarcinoma cell line SKOV3. Tretinoin 64-84 RB transcriptional corepressor like 2 Homo sapiens 10-13
12915404-1 2003 Levels of Rb2/p130 protein are increased 5-10-fold following all-trans-retinoic acid (ATRA) treatment of the retinoid-sensitive ovarian adenocarcinoma cell line CAOV3, but not the retinoid-resistant adenocarcinoma cell line SKOV3. Tretinoin 64-84 RB transcriptional corepressor like 2 Homo sapiens 14-18
12915404-1 2003 Levels of Rb2/p130 protein are increased 5-10-fold following all-trans-retinoic acid (ATRA) treatment of the retinoid-sensitive ovarian adenocarcinoma cell line CAOV3, but not the retinoid-resistant adenocarcinoma cell line SKOV3. Tretinoin 86-90 RB transcriptional corepressor like 2 Homo sapiens 10-13
11943482-5 2002 The Pax6-binding site is adjacent to a previously identified retinoic acid response element and is itself required for retinoic acid induction of the F- and E-crystallin genes, suggesting that Pax proteins and retinoic acid receptors cooperate in transcriptional regulation. Tretinoin 61-74 paired box 6 Gallus gallus 4-8
11943482-5 2002 The Pax6-binding site is adjacent to a previously identified retinoic acid response element and is itself required for retinoic acid induction of the F- and E-crystallin genes, suggesting that Pax proteins and retinoic acid receptors cooperate in transcriptional regulation. Tretinoin 119-132 paired box 6 Gallus gallus 4-8
12915404-1 2003 Levels of Rb2/p130 protein are increased 5-10-fold following all-trans-retinoic acid (ATRA) treatment of the retinoid-sensitive ovarian adenocarcinoma cell line CAOV3, but not the retinoid-resistant adenocarcinoma cell line SKOV3. Tretinoin 86-90 RB transcriptional corepressor like 2 Homo sapiens 14-18
10704061-0 2000 The influence of retinoic acid and retinoic acid derivatives on beta2 integrins and L-selectin expression in HL-60 cells in vitro. Tretinoin 35-48 selectin L Homo sapiens 84-94
12915404-2 2003 We found that this increase in Rb2/p130 protein levels in ATRA-treated CAOV3 cells was the result of an increased protein stability. Tretinoin 58-62 RB transcriptional corepressor like 2 Homo sapiens 31-34
12915404-2 2003 We found that this increase in Rb2/p130 protein levels in ATRA-treated CAOV3 cells was the result of an increased protein stability. Tretinoin 58-62 RB transcriptional corepressor like 2 Homo sapiens 35-39
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 cyclin dependent kinase inhibitor 3 Homo sapiens 239-244
12915404-3 2003 Moreover, Rb2/p130 exhibited a decreased ubiquitination following ATRA treatment. Tretinoin 66-70 RB transcriptional corepressor like 2 Homo sapiens 10-13
10673742-1 2000 The fusion protein PML/RARA, associated with acute promyelocytic leukemia behaves as an abnormal retinoic acid (RA) receptor with altered transactivation properties but is still inducible by RA. Tretinoin 23-25 PML nuclear body scaffold Homo sapiens 19-22
12915404-3 2003 Moreover, Rb2/p130 exhibited a decreased ubiquitination following ATRA treatment. Tretinoin 66-70 RB transcriptional corepressor like 2 Homo sapiens 14-18
12915404-7 2003 We have made use of a battery of Rb2/p130 mutants to determine the sites dephosphorylated in response to ATRA treatment of CAOV3 cells. Tretinoin 105-109 RB transcriptional corepressor like 2 Homo sapiens 33-36
12915404-7 2003 We have made use of a battery of Rb2/p130 mutants to determine the sites dephosphorylated in response to ATRA treatment of CAOV3 cells. Tretinoin 105-109 RB transcriptional corepressor like 2 Homo sapiens 37-41
11869806-0 2002 Retinoic acid regulation of mu opioid receptor and c-fos mRNAs and AP-1 DNA binding in SH-SY5Y neuroblastoma cells. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-56
11869806-0 2002 Retinoic acid regulation of mu opioid receptor and c-fos mRNAs and AP-1 DNA binding in SH-SY5Y neuroblastoma cells. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 67-71
11869806-2 2002 We examined the time course of the effects of all-trans retinoic acid (RA) on HMOR and c-fos mRNA levels as determined by solution hybridization (using HMOR and rat c-fos riboprobes) in RNA extracts from SH-SY5Y cells. Tretinoin 71-73 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 87-92
10673742-3 2000 This has been supported by works reporting that in vitro ATRA resistance is characterized by defects in the RARA/E-domain of PML/RARA. Tretinoin 57-61 retinoic acid receptor alpha Homo sapiens 108-112
11869806-5 2002 In contrast, c-fos mRNA levels were unchanged at 0.5 h, but increased by 50% after 18 and 168 h of RA exposure. Tretinoin 99-101 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18
12943671-3 2003 We report up-regulation of BLT1 expression by dexamethasone (Dex), a synthetic glucocorticoid, in a promyelocytic cell line HL-60 during differentiation by retinoic acid (RA) into neutrophilic phenotype. Tretinoin 156-169 leukotriene B4 receptor Homo sapiens 27-31
10673742-3 2000 This has been supported by works reporting that in vitro ATRA resistance is characterized by defects in the RARA/E-domain of PML/RARA. Tretinoin 57-61 PML nuclear body scaffold Homo sapiens 125-128
12943671-3 2003 We report up-regulation of BLT1 expression by dexamethasone (Dex), a synthetic glucocorticoid, in a promyelocytic cell line HL-60 during differentiation by retinoic acid (RA) into neutrophilic phenotype. Tretinoin 171-173 leukotriene B4 receptor Homo sapiens 27-31
10673742-3 2000 This has been supported by works reporting that in vitro ATRA resistance is characterized by defects in the RARA/E-domain of PML/RARA. Tretinoin 57-61 retinoic acid receptor alpha Homo sapiens 129-133
10673742-4 2000 In the present report, we identified a new mutation in the E domain of PML/RARA which is associated with a RA-resistant subline of NB4 cells; NB4-R2. Tretinoin 75-77 PML nuclear body scaffold Homo sapiens 71-74
11861404-7 2002 Both the retinoic acid-dependent and the exogenous expression of retSDR1 in SK-N-AS cells induce the accumulation of retinyl esters, which indicates that it is involved in generating storage forms of retinol in tissues exposed to physiological retinol concentrations. Tretinoin 9-22 dehydrogenase/reductase 3 Homo sapiens 65-72
10627451-2 2000 We previously reported that pharmacologic levels (1 micromol) of ATRA enhanced the generation of colony-forming cell (CFC) and colony-forming unit-spleen (CFU-S) in liquid suspension cultures of lin- c-kit+ Sca-1+ murine hematopoietic precursors. Tretinoin 65-69 KIT proto-oncogene receptor tyrosine kinase Mus musculus 200-205
11909638-7 2002 Retinoic acid, a vitamin A (retinol) metabolite, which alone had little effect on the HSP27 level, markedly enhanced the HSP27 accumulation stimulated by TGF-beta. Tretinoin 0-13 heat shock protein 1 Mus musculus 121-126
11909638-8 2002 Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27. Tretinoin 0-13 heat shock protein 1 Mus musculus 65-70
11909638-9 2002 The amplification of TGF-beta-stimulated HSP27 accumulation by retinoic acid was reduced by PD98059 or SB203580. Tretinoin 63-76 heat shock protein 1 Mus musculus 41-46
12824162-1 2003 In eukaryotic cells, liganded RAR gamma 2/RXR alpha heterodimers activate the transcription of retinoic acid (RA) target genes and then are degraded through the ubiquitin-proteasome pathway. Tretinoin 95-108 retinoid X receptor alpha Homo sapiens 42-51
12824162-1 2003 In eukaryotic cells, liganded RAR gamma 2/RXR alpha heterodimers activate the transcription of retinoic acid (RA) target genes and then are degraded through the ubiquitin-proteasome pathway. Tretinoin 30-32 retinoid X receptor alpha Homo sapiens 42-51
27265573-0 2003 Quantification of All-Trans-Retinoic Acid (ATRA) Dependent Expression of CXCR4 Gene in Acute Promyelocytic Leukaemia. Tretinoin 18-41 C-X-C motif chemokine receptor 4 Homo sapiens 73-78
27265573-0 2003 Quantification of All-Trans-Retinoic Acid (ATRA) Dependent Expression of CXCR4 Gene in Acute Promyelocytic Leukaemia. Tretinoin 43-47 C-X-C motif chemokine receptor 4 Homo sapiens 73-78
27265573-2 2003 We have investigated the CXCR4 gene expression during ATRA treatment in acute promyelocytic leukaemia (APL) patients. Tretinoin 54-58 C-X-C motif chemokine receptor 4 Homo sapiens 25-30
27265573-10 2003 These findings indicate that ATRA treatment might be effective in CXCR4 gene expression related to amount of the blast population in APL. Tretinoin 29-33 C-X-C motif chemokine receptor 4 Homo sapiens 66-71
12503607-1 2002 The ligand-activated retinoid receptors RXR and RAR control development, homeostasis and disease by regulating transcription of retinoic acid (RA) responsive target genes or crosstalk with other signalling pathways. Tretinoin 128-141 retinoid X receptor alpha Homo sapiens 40-43
12867595-2 2003 Antisense ablation of GRIM-19 caused resistance to cell death induced by IFN plus retinoic acid and conferred a growth advantage to cells. Tretinoin 82-95 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 22-29
10627451-4 2000 ATRA enhanced the ex vivo maintenance and production of competitive repopulating STRCs and LTRCs from lin- c-kit+ Sca-1+ cells cultured in liquid suspension for 14 days. Tretinoin 0-4 KIT proto-oncogene receptor tyrosine kinase Mus musculus 107-112
10644979-4 2000 Our findings demonstrate that the retinoic acid-dependent growth arrest of LAN-5 neuroblastoma cell line is associated to a very large accumulation (>tenfold) of p27Kip1 protein, a cyclin-dependent kinase inhibitor; the protein binds and inhibits cyclin-dependent kinase 2, 4 and 6 activities, thus hampering pRb and p107 phosphorylation. Tretinoin 34-47 cyclin dependent kinase inhibitor 1B Homo sapiens 165-172
12915310-0 2003 Cyp26C1 encodes a novel retinoic acid-metabolizing enzyme expressed in the hindbrain, inner ear, first branchial arch and tooth buds during murine development. Tretinoin 24-37 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 0-7
12397610-8 2002 The possibility that RXR-homodimers mediate, in part, the induction of CRABP-II by 9-cis RA and RXR-specific ligands is discussed. Tretinoin 72-74 retinoid X receptor alpha Homo sapiens 21-24
12397610-8 2002 The possibility that RXR-homodimers mediate, in part, the induction of CRABP-II by 9-cis RA and RXR-specific ligands is discussed. Tretinoin 72-74 retinoid X receptor alpha Homo sapiens 96-99
12915310-10 2003 This pattern of expression suggests that mCYP26C1 may play an important role in protecting the hindbrain, first branchial arch, otocyst and tooth buds against RA exposure during embryonic development. Tretinoin 159-161 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 41-49
10644979-12 2000 Our results indicate that retinoic acid strongly increases p27Kip1 levels by down-regulating the ubiquitin-proteasome p27Kip1 degrading pathway. Tretinoin 26-39 cyclin dependent kinase inhibitor 1B Homo sapiens 59-66
12882839-10 2003 The RA receptor (RAR) antagonists, LE540 and LE135, but not the retinoic X receptor (RXR) antagonist, PA452, inhibited the effect of RA on Th1/Th2 development. Tretinoin 4-6 retinoic acid receptor, alpha Mus musculus 17-20
10644979-12 2000 Our results indicate that retinoic acid strongly increases p27Kip1 levels by down-regulating the ubiquitin-proteasome p27Kip1 degrading pathway. Tretinoin 26-39 cyclin dependent kinase inhibitor 1B Homo sapiens 118-125
10721822-1 2000 Retinoic acid, vitamin D3 and triiodothyronine regulate keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors for retinoic acid (RAR-alpha,-gamma), vitamin D3 (VDR), thyroid hormone (TR-alpha,-beta) plus the common heterodimer partners, the 9-cis-retinoic acid receptors (RXR-alpha,-beta). Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 204-256
12887690-0 2003 Regulation of expression of sulfoglucuronyl carbohydrate (HNK-1), Amphoterin and RAGE in retinoic acid-differentiated P19 embryonal carcinoma cells. Tretinoin 89-102 advanced glycosylation end-product specific receptor Homo sapiens 81-85
12887690-10 2003 RA also upregulated the synthesis of Amphoterin and RAGE in P19 cells. Tretinoin 0-2 advanced glycosylation end-product specific receptor Homo sapiens 52-56
12386300-2 2002 In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1). Tretinoin 34-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 140-159
12386300-2 2002 In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1). Tretinoin 34-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-165
10721822-1 2000 Retinoic acid, vitamin D3 and triiodothyronine regulate keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors for retinoic acid (RAR-alpha,-gamma), vitamin D3 (VDR), thyroid hormone (TR-alpha,-beta) plus the common heterodimer partners, the 9-cis-retinoic acid receptors (RXR-alpha,-beta). Tretinoin 189-202 retinoic acid receptor alpha Homo sapiens 204-256
11577091-4 2001 We have recently shown that MAPK activation and c-Fos expression are uncoupled in F9 cells upon retinoic acid-induced endodermal differentiation. Tretinoin 96-109 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 48-53
12801520-9 2003 Retinoic acid, which alone failed to affect VEGF synthesis, markedly enhanced the VEGF synthesis stimulated by TGF-beta. Tretinoin 0-13 vascular endothelial growth factor A Mus musculus 82-86
12801520-10 2003 Retinoic acid enhanced the TGF-beta-increased levels of VEGF mRNA. Tretinoin 0-13 vascular endothelial growth factor A Mus musculus 56-60
10664010-11 2000 The finding that keratin 13 expression following treatment with all-trans-retinoic acid occurred exclusively in hyperproliferative skin suggests that retinoid-induced and hyperproliferation-associated differentiation are coupled. Tretinoin 64-87 keratin 13 Homo sapiens 17-27
12801520-11 2003 The amplifications by retinoic acid of TGF-beta-increased VEGF synthesis and levels of VEGF mRNA were reduced by PD98059 or SB203580. Tretinoin 22-35 vascular endothelial growth factor A Mus musculus 58-62
12637327-0 2003 Ser727/Tyr701-phosphorylated Stat1 is required for the regulation of c-Myc, cyclins, and p27Kip1 associated with ATRA-induced G0/G1 arrest of U-937 cells. Tretinoin 113-117 signal transducer and activator of transcription 1 Homo sapiens 29-34
12637327-2 2003 ATRA treatment of myeloid cells induces up-regulation and tyrosine phosphorylation of Stat1, a member of the STAT (signal transducer and activator of transcription) transcription factor family that has been implicated in growth arrest in response to interferons. Tretinoin 0-4 signal transducer and activator of transcription 1 Homo sapiens 86-91
12637327-3 2003 We have previously shown that ATRA-induced cell cycle arrest is dependent on tyrosinephosphorylated Stat1. Tretinoin 30-34 signal transducer and activator of transcription 1 Homo sapiens 100-105
12637327-4 2003 In this study, we show that there is a basal level of Stat1 Ser727 phosphorylation in U-937 cells, which is transiently increased in response to ATRA treatment. Tretinoin 145-149 signal transducer and activator of transcription 1 Homo sapiens 54-59
12637327-5 2003 Using Stat1Ser727Ala-expressing sublines, we provide evidence that Ser727 phosphorylation of Stat1 is required for ATRA-induced growth arrest. Tretinoin 115-119 signal transducer and activator of transcription 1 Homo sapiens 6-11
12637327-7 2003 Our results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and the simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase of the cell cycle. Tretinoin 100-104 signal transducer and activator of transcription 1 Homo sapiens 51-56
11577091-9 2001 Transfection and expression of Disabled-2 in PA-1 cells mimic the effects of retinoic acid on growth suppression; the Disabled-2-expressing cells reach a much lower saturation density, and serum-stimulated c-Fos expression is greatly suppressed and disassociated from MAPK activation. Tretinoin 77-90 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 206-211
11577091-10 2001 Thus, Dab2 is one of the principal genes induced by retinoic acid involved in cell growth suppression, and expression of Dab2 alone is sufficient for uncoupling of MAPK activation and c-Fos expression. Tretinoin 52-65 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 184-189
11724755-11 2001 Intake of the deficient diet containing all-trans-retinoic acid (ATRA) during the final week of the experiment restored CYP4A2 mRNA and CYP4A protein. Tretinoin 40-63 cytochrome P450, family 4, subfamily a, polypeptide 2 Rattus norvegicus 120-126
11724755-11 2001 Intake of the deficient diet containing all-trans-retinoic acid (ATRA) during the final week of the experiment restored CYP4A2 mRNA and CYP4A protein. Tretinoin 65-69 cytochrome P450, family 4, subfamily a, polypeptide 2 Rattus norvegicus 120-126
12858348-0 2003 Retinoic acid inhibits chondrogenesis of mesenchymal cells by sustaining expression of N-cadherin and its associated proteins. Tretinoin 0-13 cadherin 2 Homo sapiens 87-97
12858348-7 2003 However, RA treatment caused sustained expression of N-cadherin and its associated proteins including alpha- and beta-catenin suggesting that modulation of expression of these molecules is associated with RA-induced inhibition of chondrogenesis. Tretinoin 9-11 cadherin 2 Homo sapiens 53-63
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 41-54 retinoid X receptor beta Mus musculus 315-322
12858348-7 2003 However, RA treatment caused sustained expression of N-cadherin and its associated proteins including alpha- and beta-catenin suggesting that modulation of expression of these molecules is associated with RA-induced inhibition of chondrogenesis. Tretinoin 205-207 cadherin 2 Homo sapiens 53-63
12904257-4 2003 RESULTS: Direct protein-protein interaction studies demonstrate that the RXR agonist 9-cis-RA increases interaction of CAR/RXR heterodimers with the coactivator SRC-3, but also inhibits the ability of TCPOBOP to increase and androstanol to decrease coactivator binding. Tretinoin 85-93 retinoid X receptor alpha Homo sapiens 73-76
11748135-5 2001 As we demonstrate that the repression of Otx2 by retinoic acid is dependent on an induction of Gbx2 in the anterior brain, molecules other than retinoic acid must regulate the initial expression of Otx2 in vivo. Tretinoin 49-62 orthodenticle homeobox 2 Mus musculus 41-45
12904257-4 2003 RESULTS: Direct protein-protein interaction studies demonstrate that the RXR agonist 9-cis-RA increases interaction of CAR/RXR heterodimers with the coactivator SRC-3, but also inhibits the ability of TCPOBOP to increase and androstanol to decrease coactivator binding. Tretinoin 85-93 retinoid X receptor alpha Homo sapiens 123-126
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 56-58 retinoid X receptor beta Mus musculus 315-322
11914024-1 2001 All-trans -retinoic acid (atRA) inhibits osteoblast marker gene expression and markedly increases expression of insulin-like growth factor binding protein-6 (IGFBP-6) in human osteoblasts. Tretinoin 0-24 insulin like growth factor binding protein 6 Homo sapiens 112-156
11389537-5 2000 In t(15;17)-containing leukemic cells, the PML nuclear bodies are disrupted, but reform when the leukemic cells are induced to differentiate in the presence of all-trans retinoic acid. Tretinoin 170-183 PML nuclear body scaffold Homo sapiens 43-46
11914024-1 2001 All-trans -retinoic acid (atRA) inhibits osteoblast marker gene expression and markedly increases expression of insulin-like growth factor binding protein-6 (IGFBP-6) in human osteoblasts. Tretinoin 0-24 insulin like growth factor binding protein 6 Homo sapiens 158-165
11914024-1 2001 All-trans -retinoic acid (atRA) inhibits osteoblast marker gene expression and markedly increases expression of insulin-like growth factor binding protein-6 (IGFBP-6) in human osteoblasts. Tretinoin 26-30 insulin like growth factor binding protein 6 Homo sapiens 112-156
11914024-1 2001 All-trans -retinoic acid (atRA) inhibits osteoblast marker gene expression and markedly increases expression of insulin-like growth factor binding protein-6 (IGFBP-6) in human osteoblasts. Tretinoin 26-30 insulin like growth factor binding protein 6 Homo sapiens 158-165
11914024-2 2001 The possibility that IGFBP-6 inhibits the osteoblast phenotype and also mediates the inhibitory effect of atRA on osteoblast marker gene expression was explored using an antisense approach. Tretinoin 106-110 insulin like growth factor binding protein 6 Homo sapiens 21-28
11914024-7 2001 We reasoned that atRA would have little or no effect on ALP activity in IGFBP-6 antisense clones if atRA mediated its inhibitory effects by recruiting IGFBP-6. Tretinoin 100-104 insulin like growth factor binding protein 6 Homo sapiens 151-158
12702665-0 2003 The regional pattern of retinoic acid synthesis by RALDH2 is essential for the development of posterior pharyngeal arches and the enteric nervous system. Tretinoin 24-37 aldehyde dehydrogenase 1 family member A2 Homo sapiens 51-57
12808116-5 2003 trkB expression and BDNF responsiveness in neuroblastoma cells can be induced by all-trans-retinoic acid (RA). Tretinoin 81-104 brain derived neurotrophic factor Homo sapiens 20-24
12808116-5 2003 trkB expression and BDNF responsiveness in neuroblastoma cells can be induced by all-trans-retinoic acid (RA). Tretinoin 106-108 brain derived neurotrophic factor Homo sapiens 20-24
12844477-6 2003 Indinavir leads to altered retinoic acid signaling most likely by an activation of the RAR/RXR heterodimer, perhaps by displacing all-trans-retinoic acid from CRABP. Tretinoin 27-40 retinoid X receptor alpha Homo sapiens 91-94
12844477-6 2003 Indinavir leads to altered retinoic acid signaling most likely by an activation of the RAR/RXR heterodimer, perhaps by displacing all-trans-retinoic acid from CRABP. Tretinoin 130-153 retinoid X receptor alpha Homo sapiens 91-94
10678262-14 2000 High concentrations of retinoic acid decreased PPARgamma expression in early S-V cultures (p<0.05). Tretinoin 23-36 peroxisome proliferator activated receptor gamma Sus scrofa 47-56
12606540-6 2003 We treated chondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATRA), which promotes endochondral chondrocyte hypertrophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endochondral development. Tretinoin 95-108 natriuretic peptide type C Mus musculus 208-234
12606540-6 2003 We treated chondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATRA), which promotes endochondral chondrocyte hypertrophy and pathologic calcification, and with C-type natriuretic peptide, an essential factor in endochondral development. Tretinoin 110-114 natriuretic peptide type C Mus musculus 208-234
11716828-3 2001 RT-PCR, immunoblotting and immunocytochemistry showed the increased expression of N-syndecan, a transmembrane heparan sulfate proteoglycan, in the neural stem cells after the differentiation induced by retinoic acid. Tretinoin 202-215 syndecan 3 Rattus norvegicus 82-92
11731009-7 2001 We also examined the expression of Zfhep protein during retinoic acid-induced neurogenesis of P19 embryonal carcinoma cells. Tretinoin 56-69 zinc finger E-box binding homeobox 1 Homo sapiens 35-40
11687288-3 2001 In this study, we found that neural differentiation of multipotent mouse P19 embryonal carcinoma cells by retinoic acid led to the appearance of Scrt together with neuron-specific class III beta-tubulin (Tuj1), following the earlier elaboration of Mash1. Tretinoin 106-119 achaete-scute family bHLH transcription factor 1 Mus musculus 248-253
10608897-1 1999 Retinoic acid (RA) regulation of cellular proliferation and differentiation is mediated, at least in part, through two related nuclear receptors, RAR and RXR. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 146-149
11747199-4 2001 Molecular cloning and subsequent studies on RALDH2, the key embryonic retinaldehyde dehydrogenase in retinoic acid (RA) synthesis, provided the missing link between teratogenic studies on RA deficiency and excess and normal chamber morphogenesis. Tretinoin 101-114 aldehyde dehydrogenase 1 family member A2 Homo sapiens 44-50
12714583-3 2003 Indeed, ATRA treatment induced the expression of CCAAT/enhancer-binding protein beta (C/EBPbeta), a CRE-dependent transcription factor important in monocytic differentiation, and the inhibition of CRE-enhancer activity by the expression of a dominant-negative CRE-binding protein (dn-CREB) abolished the induction of C/EBPbeta. Tretinoin 8-12 cAMP responsive element binding protein 1 Homo sapiens 284-288
10608897-1 1999 Retinoic acid (RA) regulation of cellular proliferation and differentiation is mediated, at least in part, through two related nuclear receptors, RAR and RXR. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 146-149
12754300-5 2003 The effects of RA are mediated by a family of ligand-dependent transcription factors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXR). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 129-149
10611294-0 1999 Retinoic acid induces proteasome-dependent degradation of retinoic acid receptor alpha (RARalpha) and oncogenic RARalpha fusion proteins. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 58-86
12754300-5 2003 The effects of RA are mediated by a family of ligand-dependent transcription factors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXR). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 151-154
11588055-8 2001 Taken together, these results suggest that erythropoiesis and granulopoiesis require diminished and enhanced RARalpha activities, respectively, which at physiological all-trans-retinoic acid (RA) concentrations may be accomplished by reciprocal effects of EPO and myelomonocytic growth factors on its expression. Tretinoin 177-190 retinoic acid receptor, alpha Mus musculus 109-117
12778364-8 2003 ESM-1 expression in human adipocytes was stimulated by phorbol ester, an activator of protein kinase C, and by retinoic acid, an activator of nuclear receptors. Tretinoin 111-124 endothelial cell specific molecule 1 Homo sapiens 0-5
10611294-0 1999 Retinoic acid induces proteasome-dependent degradation of retinoic acid receptor alpha (RARalpha) and oncogenic RARalpha fusion proteins. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 88-96
11579380-8 2001 Up-regulation of GDF-15/MIC-1 in activated macrophages (Mstraight phi) is also supported by RT-PCR, ICC, and Western blot experiments showing pronounced induction of GDF-15/MIC-1 expression (mRNA and protein) in retinoic acid/phorbol ester-stimulated human M phi. Tretinoin 212-225 growth differentiation factor 15 Homo sapiens 17-23
10611294-0 1999 Retinoic acid induces proteasome-dependent degradation of retinoic acid receptor alpha (RARalpha) and oncogenic RARalpha fusion proteins. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 112-120
11579380-8 2001 Up-regulation of GDF-15/MIC-1 in activated macrophages (Mstraight phi) is also supported by RT-PCR, ICC, and Western blot experiments showing pronounced induction of GDF-15/MIC-1 expression (mRNA and protein) in retinoic acid/phorbol ester-stimulated human M phi. Tretinoin 212-225 growth differentiation factor 15 Homo sapiens 24-29
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 82-110
12640113-4 2003 The importance of this down-regulation is demonstrated in chicken embryos by showing that the retinoic acid effect on semicircular canal development can be overcome by exogenous BMP4. Tretinoin 94-107 bone morphogenetic protein 4 Gallus gallus 178-182
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 PML nuclear body scaffold Homo sapiens 112-115
11562472-0 2001 Ectopic expression of retinoic acid early inducible-1 gene (RAE-1) permits natural killer cell-mediated rejection of a MHC class I-bearing tumor in vivo. Tretinoin 22-35 ribonucleic acid export 1 Mus musculus 60-65
11562472-6 2001 In contrast, when RMA cells were transfected with the retinoic acid early inducible gene-1 gamma or delta (RAE-1), ligands for the activating receptor NKG2D, the tumors were rejected. Tretinoin 54-67 ribonucleic acid export 1 Mus musculus 107-112
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 116-124
11525643-5 2001 Retinoic acid treatment of PKCalpha-MDA-MB-231 cells decreased proliferation (by approximately 40%) and inhibited serum activation of MAP kinases and induction of c-fos. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 163-168
12623064-0 2003 Homozygous deletion of the CRABPI gene in AB1 embryonic stem cells results in increased CRABPII gene expression and decreased intracellular retinoic acid concentration. Tretinoin 140-153 cellular retinoic acid binding protein I Mus musculus 27-33
12623064-1 2003 The cellular retinoic acid (RA) binding proteins I and II (CRABPI and CRABPII), intracellular proteins which bind retinoic acid with high affinity, are involved in the actions of RA, though their exact roles are not fully understood. Tretinoin 13-26 cellular retinoic acid binding protein I Mus musculus 59-65
12623064-1 2003 The cellular retinoic acid (RA) binding proteins I and II (CRABPI and CRABPII), intracellular proteins which bind retinoic acid with high affinity, are involved in the actions of RA, though their exact roles are not fully understood. Tretinoin 28-30 cellular retinoic acid binding protein I Mus musculus 59-65
12623064-1 2003 The cellular retinoic acid (RA) binding proteins I and II (CRABPI and CRABPII), intracellular proteins which bind retinoic acid with high affinity, are involved in the actions of RA, though their exact roles are not fully understood. Tretinoin 114-127 cellular retinoic acid binding protein I Mus musculus 59-65
12623064-4 2003 Complete lack of CRABPI results in decreased intracellular [3H]RA concentrations under conditions in which external concentrations of [3H]RA are low (1-10nM) and in an altered distribution of [3H] polar metabolites of [3H]RA in the cell and in the medium. Tretinoin 63-65 cellular retinoic acid binding protein I Mus musculus 17-23
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 PML nuclear body scaffold Homo sapiens 223-226
12623064-4 2003 Complete lack of CRABPI results in decreased intracellular [3H]RA concentrations under conditions in which external concentrations of [3H]RA are low (1-10nM) and in an altered distribution of [3H] polar metabolites of [3H]RA in the cell and in the medium. Tretinoin 63-65 cellular retinoic acid binding protein I Mus musculus 17-23
12623064-6 2003 These data suggest that CRABPI functions to regulate the intracellular concentrations of retinoic acid and to maintain high levels of oxidized retinoic acid metabolites such as 4-oxoretinoic acid within cells. Tretinoin 89-102 cellular retinoic acid binding protein I Mus musculus 24-30
11675954-8 2001 In contrast, ATRA strongly suppressed the pRb kinase activities of the cyclin-dependent kinases (Cdks) Cdk4, Cdk6, and Cdk2. Tretinoin 13-17 cyclin dependent kinase 2 Rattus norvegicus 97-101
11675954-8 2001 In contrast, ATRA strongly suppressed the pRb kinase activities of the cyclin-dependent kinases (Cdks) Cdk4, Cdk6, and Cdk2. Tretinoin 13-17 cyclin dependent kinase 2 Rattus norvegicus 119-123
11675954-9 2001 ATRA did not influence the expressions of Cip/Kip family Cdk inhibitors or those of cyclins D1 and D2, whereas it strongly inhibited the expressions of cyclins D3 and E, Cdk4, Cdk6, and Cdk2. Tretinoin 0-4 cyclin dependent kinase 2 Rattus norvegicus 186-190
12623064-6 2003 These data suggest that CRABPI functions to regulate the intracellular concentrations of retinoic acid and to maintain high levels of oxidized retinoic acid metabolites such as 4-oxoretinoic acid within cells. Tretinoin 143-156 cellular retinoic acid binding protein I Mus musculus 24-30
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 227-235
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 PML nuclear body scaffold Homo sapiens 223-226
12622724-7 2003 Under conditions of serum stimulation, the formation of NBs coincides with the immediate-early expression of the endogenous c-fos gene in fibroblasts and in all-trans retinoic acid-treated acute promyelocytic leukaemia NB4 cells. Tretinoin 167-180 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 124-129
11479234-10 2001 These results suggest that an RXR-selective retinoic acid decreases SCCHN proliferation in part by interfering with TGF-alpha/EGFR autocrine signaling. Tretinoin 44-57 retinoid X receptor alpha Homo sapiens 30-33
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 227-235
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 227-235
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 82-110
11510982-6 2001 These studies lead to the conclusion that most RA-induced events (e.g. primitive and visceral differentiation, growth arrest, apoptosis and activation of expression of a number of genes) are transduced by RARgamma/RXRalpha heterodimers, whereas some other events (e.g. parietal differentiation) are mediated by RARalpha/RXRalpha. Tretinoin 47-49 retinoic acid receptor, gamma Mus musculus 205-213
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 PML nuclear body scaffold Homo sapiens 112-115
11510982-6 2001 These studies lead to the conclusion that most RA-induced events (e.g. primitive and visceral differentiation, growth arrest, apoptosis and activation of expression of a number of genes) are transduced by RARgamma/RXRalpha heterodimers, whereas some other events (e.g. parietal differentiation) are mediated by RARalpha/RXRalpha. Tretinoin 47-49 retinoic acid receptor, alpha Mus musculus 311-319
11369141-0 2001 Proteolysis of integrin alpha5 and beta1 subunits involved in retinoic acid-induced apoptosis in human hepatoma Hep3B cells. Tretinoin 62-75 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 35-40
12579317-1 2003 The human retinoic acid receptor beta (RARbeta) has three isoforms (beta1, beta2, and beta4), which play important, distinct roles in mediating the effects of retinoic acid on cell growth and apoptosis. Tretinoin 10-23 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 68-73
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 116-124
12642900-10 2003 These results explained that retinoic acids differentially affected the action of MRFs according to their types and RXRalpha specially elevates the expression of muscle specific genes by stimulating the action of MRF4. Tretinoin 29-43 retinoid X receptor alpha Homo sapiens 116-124
11369141-7 2001 Treatment with perturbing antibody against integrin alpha5 or beta1 subunits resulted in promotion of ATRA-induced apoptosis. Tretinoin 102-106 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 62-67
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 PML nuclear body scaffold Homo sapiens 223-226
11339830-2 2001 Retinoic acid-induced differentiation in the embryonal carcinoma (EC) cell line NCR-G3 triggers concurrent induction of apoptosis. Tretinoin 0-13 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 80-83
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 227-235
11339831-0 2001 Cell proliferation and CD11b expression are controlled independently during HL60 cell differentiation initiated by 1,25 alpha-dihydroxyvitamin D(3) or all-trans-retinoic acid. Tretinoin 151-174 integrin subunit alpha M Homo sapiens 23-28
11339831-5 2001 Cells treated with D(3) or ATRA start to express CD11b after 9--14 h, before completing the first maturation division. Tretinoin 27-31 integrin subunit alpha M Homo sapiens 49-54
12538081-2 2003 Recently, studies in vivo and in cell lines have shown that vitamin A and its active metabolite, retinoic acid, regulate the expression of fatty acid desaturases including stearoyl-CoA desaturase and delta-5 desaturase. Tretinoin 97-110 stearoyl-CoA desaturase Homo sapiens 172-195
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 PML nuclear body scaffold Homo sapiens 223-226
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 26-39 retinoid X receptor alpha Homo sapiens 145-153
11278635-1 2001 Receptor-interacting protein 140 (RIP140) interacts with retinoic acid receptor and retinoid X receptor in a ligand-dependent manner and suppresses retinoic acid (RA) induction of its target genes. Tretinoin 163-165 retinoid X receptor alpha Homo sapiens 84-103
11278635-4 2001 RA induces coimmunoprecipitation of histone deacetylase 3 with retinoic acid receptor/retinoid X receptor in the presence of wild type RIP140, but not in the presence of the C-terminal motif-deleted RIP140. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 86-105
12504905-1 2003 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Tretinoin 41-43 retinoid X receptor alpha Homo sapiens 145-153
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 227-235
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 47-49 retinoic acid receptor alpha Homo sapiens 227-235
10611294-1 1999 Analyzing the pathways by which retinoic acid (RA) induces promyelocytic leukemia/retinoic acid receptor alpha (PML/RARalpha) catabolism in acute promyelocytic leukemia (APL), we found that, in addition to caspase-mediated PML/RARalpha cleavage, RA triggers degradation of both PML/RARalpha and RARalpha. Tretinoin 116-118 retinoic acid receptor alpha Homo sapiens 82-110
11376874-8 2001 Retinoic acid elicited synergistic effects on the CNP secretion rate from HL-60 cells when administered with lipopolysaccharide, interferon-gamma, interleukin-1beta, tumor necrosis factor-alpha, or phorbol ester. Tretinoin 0-13 natriuretic peptide C Homo sapiens 50-53
10607566-6 1999 Here, we shown that retinoic acid (RA) decreases the activity of the beta-catenin-LEF/TCF signaling pathway. Tretinoin 20-33 catenin beta 1 Homo sapiens 69-81
11504380-7 2001 Retinol and retinoic acid also inhibited proliferation of cells growth-stimulated by insulin and other growth factors from the IGF growth factor family (des(1-3)IGF-I and IGF-II), as well as growth factors from the epidermal growth factor family (EGF and TGF-alpha), with retinoic acid being more effective than retinol. Tretinoin 12-25 insulin like growth factor 2 Bos taurus 171-177
12680251-7 2003 These results suggested the importance of both IRF-1 and STAT1 in high-dose ATRA-induced activation of caspase-1. Tretinoin 76-80 signal transducer and activator of transcription 1 Homo sapiens 57-62
12680256-6 2003 We concluded that activation of STAT1 and IRF-1 is crucial for the growth inhibitory action of ATRA, which is associated with the activation of p21WAF1. Tretinoin 95-99 signal transducer and activator of transcription 1 Homo sapiens 32-37
12532224-0 2003 Sec61alpha synthesis is enhanced during translocation of nascent chains of collagen type IV in F9 teratocarcinoma cells after retinoic acid treatment. Tretinoin 126-139 Sec61 alpha 1 subunit (S. cerevisiae) Mus musculus 0-10
11311979-4 2001 After exposure to retinoic acid for 4 days AQP4 mRNA expression started at the initiation of astrocytic differentiation of P19 cells at 6 days, and increased markedly by 21 days. Tretinoin 18-31 aquaporin 4 Homo sapiens 43-47
10607566-6 1999 Here, we shown that retinoic acid (RA) decreases the activity of the beta-catenin-LEF/TCF signaling pathway. Tretinoin 35-37 catenin beta 1 Homo sapiens 69-81
12532224-12 2003 Sec61alpha, Hsp47 and type IV collagen levels were increased after retinoic acid treatment. Tretinoin 67-80 Sec61 alpha 1 subunit (S. cerevisiae) Mus musculus 0-10
12532224-14 2003 These data indicate that the enhanced production of Sec61alpha in retinoic acid-induced F9 teratocarcinoma cells parallels the increased synthesis of Hsp47 and collagen type IV. Tretinoin 66-79 Sec61 alpha 1 subunit (S. cerevisiae) Mus musculus 52-62
10607566-7 1999 This activity of RA was independent of the adenomatous polyposis coli (APC) tumor suppressor and ubiquitination-dependent degradation of cytoplasmic beta-catenin. Tretinoin 17-19 catenin beta 1 Homo sapiens 149-161
10607566-10 1999 The data suggest that direct regulation of beta-catenin-LEF/TCF signaling is one mechanism whereby RA influences development, cell differentiation and cancer. Tretinoin 99-101 catenin beta 1 Homo sapiens 43-55
12502496-4 2003 Here we show the presence of endogenous retinaldehyde dehydrogenase 2 (RALDH2), the most effective RA-synthesizing enzyme, RA-binding proteins, and RA receptors (RARs) in embryonic pancreatic tissue. Tretinoin 71-73 aldehyde dehydrogenase 1 family member A2 Homo sapiens 40-69
11281644-4 2001 Retinoic acid (RA) and bone morphogenetic protein-2 enhanced Ihh mRNA expression, whereas PTH/PTH-related peptide (PTHrP) markedly suppressed Ihh expression. Tretinoin 0-13 indian hedgehog protein Oryctolagus cuniculus 61-64
11281644-4 2001 Retinoic acid (RA) and bone morphogenetic protein-2 enhanced Ihh mRNA expression, whereas PTH/PTH-related peptide (PTHrP) markedly suppressed Ihh expression. Tretinoin 15-17 indian hedgehog protein Oryctolagus cuniculus 61-64
11281644-6 2001 These findings suggest that RA is involved in the up-regulation of Ihh during endochondral bone formation. Tretinoin 28-30 indian hedgehog protein Oryctolagus cuniculus 67-70
11721444-0 1999 The relationship between the levels of granulocyte colony-stimulating factor and leukocytosis induced by all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 105-128 colony stimulating factor 3 Homo sapiens 39-76
11274229-2 2001 This study investigated the effect of all-trans-retinoic acid (t-RA) on the constitutive and cytokine-inducible expression of monocyte chemoattractant protein 1 (MCP-1) in rat mesangial cells. Tretinoin 38-61 chemokine (C-C motif) ligand 2 Mus musculus 126-160
11274229-2 2001 This study investigated the effect of all-trans-retinoic acid (t-RA) on the constitutive and cytokine-inducible expression of monocyte chemoattractant protein 1 (MCP-1) in rat mesangial cells. Tretinoin 38-61 chemokine (C-C motif) ligand 2 Mus musculus 162-167
12485405-4 2003 PCR analysis of total mRNA from RA-treated cells showed a biphasic early induction of CRBP-I, CRABP-II, and RARgamma2 genes. Tretinoin 32-34 cellular retinoic acid binding protein 2 Homo sapiens 94-102
12485405-8 2003 These data suggest that the RA-specific induction of CRBP-I and CRABP-II could be an early event in the process leading to neuronal differentiation of NT2 cells. Tretinoin 28-30 cellular retinoic acid binding protein 2 Homo sapiens 64-72
11274229-2 2001 This study investigated the effect of all-trans-retinoic acid (t-RA) on the constitutive and cytokine-inducible expression of monocyte chemoattractant protein 1 (MCP-1) in rat mesangial cells. Tretinoin 63-67 chemokine (C-C motif) ligand 2 Mus musculus 126-160
12558991-8 2003 The exposure of cells to BDNF after treatment with retinoic acid rapidly induced promoter activity during the initial five hours and phosphorylation of CRE-binding protein during the first two hours. Tretinoin 51-64 brain derived neurotrophic factor Homo sapiens 25-29
11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 229-242 colony stimulating factor 3 Homo sapiens 97-134
11274229-2 2001 This study investigated the effect of all-trans-retinoic acid (t-RA) on the constitutive and cytokine-inducible expression of monocyte chemoattractant protein 1 (MCP-1) in rat mesangial cells. Tretinoin 63-67 chemokine (C-C motif) ligand 2 Mus musculus 162-167
11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 229-242 colony stimulating factor 3 Homo sapiens 136-141
12514312-3 2003 Our research has examined the expression and function of two enzymes, lecithin:retinol acyltransferase (LRAT) and a cytochrome P450, CYP26, in the liver and lung of rats and mice, over a wide range of vitamin A status or after treatment of vitamin A-deficient animals with exogenous RA. Tretinoin 105-107 lecithin retinol acyltransferase Rattus norvegicus 70-102
11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 244-248 colony stimulating factor 3 Homo sapiens 97-134
12648520-4 2003 In the absence of the RAR-specific ligand all trans retinoic acid, RAR/RXR heterodimers are associated with the nuclear receptor corepressor N-CoR or the related SMRT. Tretinoin 52-65 retinoid X receptor alpha Homo sapiens 71-74
11721444-2 1999 METHODS: Enzyme linked immunosorbent assay (ELISA) method was used for detecting levels of serum granulocyte colony-stimulating factor (G-CSF) in 47 cases of acute promyelocytic leukemia (APL) during the treatment with all-trans retinoic acid (ATRA). Tretinoin 244-248 colony stimulating factor 3 Homo sapiens 136-141
11285324-9 2001 When vitamin A-deficient quail received a single injection of retinol or retinoic acid (0.1 mg/bird), tissue IGF-I, IGF-IR and IR gene expressions did not change after 4 h. These results suggest a possible physiologic role of the IGF system in mediating vitamin A-supported growth of Japanese quail. Tretinoin 73-86 insulin-like growth factor I Coturnix japonica 109-114
11721444-4 1999 After ATRA treatment, both serum G-CSF level and WBC number increased in 68.1% of the cases. Tretinoin 6-10 colony stimulating factor 3 Homo sapiens 33-38
10653359-11 1999 Scmh1 is strongly induced by retinoic acid in F9 and P19 embryonal carcinoma cells. Tretinoin 29-42 sex comb on midleg homolog 1 Mus musculus 0-5
11287065-5 2001 Using the terminal deoxynucleotidyl transferase (tdt)-labeling technique we found that the postmitotic hNT neuronal cells exposed to RA demonstrated significantly higher numbers of apoptotic cells (12.5-15.8%) in comparison to rapidly dividing NT2 precursor cell line (3.6-4.4%) at both studied (1 and 5 days in vitro, DIV) time points. Tretinoin 133-135 DNA nucleotidylexotransferase Homo sapiens 10-47
11287065-5 2001 Using the terminal deoxynucleotidyl transferase (tdt)-labeling technique we found that the postmitotic hNT neuronal cells exposed to RA demonstrated significantly higher numbers of apoptotic cells (12.5-15.8%) in comparison to rapidly dividing NT2 precursor cell line (3.6-4.4%) at both studied (1 and 5 days in vitro, DIV) time points. Tretinoin 133-135 DNA nucleotidylexotransferase Homo sapiens 49-52
12927207-0 2003 Induction of tyrosine kinase receptor b by retinoic acid allows brain-derived neurotrophic factor-induced amyloid precursor protein gene expression in human SH-SY5Y neuroblastoma cells. Tretinoin 43-56 brain derived neurotrophic factor Homo sapiens 64-97
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 21-23 brain derived neurotrophic factor Homo sapiens 89-122
12384498-6 2002 ABCA1 was induced by treatment with retinoic acid and several oxysterols, including 22(R)-hydroxycholesterol and 24-hydroxycholesterol. Tretinoin 36-49 ATP binding cassette subfamily A member 1 Rattus norvegicus 0-5
10536361-1 1999 The ability of retinoic acid to modulate glutathione S-transferase P1-1 (GSTP1-1) activity has important implications both for cancer prevention and for anticancer therapy. Tretinoin 15-28 glutathione S-transferase pi 1 Homo sapiens 73-80
12414989-13 2002 Using gelatin zymography, we observed a dose-dependent increase in latent and active forms of gelatinase B (MMP-9) upon RA treatment. Tretinoin 120-122 matrix metallopeptidase 9 Homo sapiens 108-113
12468615-8 2002 The striking Th2 enhancement was also observed when only antigen-presenting cells were treated with atRA before stimulation of untreated CD4(+) transgenic T cells, but not vice versa. Tretinoin 100-104 CD4 antigen Mus musculus 137-140
11230116-5 2001 Furthermore, RARalpha overexpression directly stimulated BAEC differentiation on Matrigel and potentiated the effects of ATRA in this assay. Tretinoin 121-125 retinoic acid receptor, alpha Mus musculus 13-21
11230116-7 2001 In conclusion, RA can stimulate endothelial cell proliferation and differentiation in vitro via enhanced RARalpha-dependent FGF-2 production, and it can also induce angiogenesis in vivo. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 105-113
11222375-6 2001 RARalpha stimulates differentiation in response to exogenous retinoic acid. Tretinoin 61-74 retinoic acid receptor, alpha Mus musculus 0-8
10536361-2 1999 We investigated GSTP1-1 expression and activity in the human neuroblastoma cell line SK-N-BE(2) (genotype A*/B*) under basal conditions and during 48-h incubation with 0.1 microM all-trans-retinoic acid. Tretinoin 179-202 glutathione S-transferase pi 1 Homo sapiens 16-23
12435367-10 2002 The RXR ligand, 9-cis-RA, is found in perichondrium, mineralised cartilage, and bone. Tretinoin 16-24 retinoid X receptor alpha Homo sapiens 4-7
10536361-4 1999 This reduction in enzymatic activity could not be ascribed to a differential action of retinoic acid on the gene variants A* and B*; indeed, the two GSTP1-1 isoforms have different affinities toward 1-chloro-2,4-dinitrobenzene (CDNB), while we found a substantial invariance of the K(m) (CDNB) in the cytosol during retinoid treatment. Tretinoin 87-100 glutathione S-transferase pi 1 Homo sapiens 149-156
12435367-11 2002 To further define sites of RA synthesis in antler, we immunolocalised retinaldehyde dehydrogenase type 2 (RALDH-2), a major retinoic acid-generating enzyme. Tretinoin 124-137 aldehyde dehydrogenase 1 family member A2 Homo sapiens 70-104
12435367-11 2002 To further define sites of RA synthesis in antler, we immunolocalised retinaldehyde dehydrogenase type 2 (RALDH-2), a major retinoic acid-generating enzyme. Tretinoin 124-137 aldehyde dehydrogenase 1 family member A2 Homo sapiens 106-113
11180971-9 2001 Moreover, the expression of TRP-2 mRNA was induced by retinoic acid in retinoblastoma cells but not noticeably affected by forskolin, a cAMP-elevating reagent, whereas in melanoma cells its expression was induced by forskolin but not by retinoic acid. Tretinoin 237-250 dopachrome tautomerase Homo sapiens 28-33
10536361-5 1999 A modulatory effect of retinoic acid on other enzymes involved in glutathione transferase P1-1 metabolism, such as the retinoic acid-induced tissue trans-glutaminase, might be hypothesized, as well as a direct inactivation of GSTP1-1 by the oxidative stress that characterizes the early phases of apoptosis. Tretinoin 23-36 glutathione S-transferase pi 1 Homo sapiens 226-233
10536361-5 1999 A modulatory effect of retinoic acid on other enzymes involved in glutathione transferase P1-1 metabolism, such as the retinoic acid-induced tissue trans-glutaminase, might be hypothesized, as well as a direct inactivation of GSTP1-1 by the oxidative stress that characterizes the early phases of apoptosis. Tretinoin 119-132 glutathione S-transferase pi 1 Homo sapiens 226-233
11222649-6 2001 The regulation of KOR gene by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic acid (RA), the most potent ingredient of vitamin A, was able to suppress the expression of all the three KOR isoforms and KOR protein. Tretinoin 117-130 opioid receptor, kappa 1 Mus musculus 18-21
11222649-6 2001 The regulation of KOR gene by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic acid (RA), the most potent ingredient of vitamin A, was able to suppress the expression of all the three KOR isoforms and KOR protein. Tretinoin 117-130 opioid receptor, kappa 1 Mus musculus 231-234
10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 41-54 colony stimulating factor 1 Homo sapiens 181-186
11222649-6 2001 The regulation of KOR gene by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic acid (RA), the most potent ingredient of vitamin A, was able to suppress the expression of all the three KOR isoforms and KOR protein. Tretinoin 117-130 opioid receptor, kappa 1 Mus musculus 231-234
11222649-6 2001 The regulation of KOR gene by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic acid (RA), the most potent ingredient of vitamin A, was able to suppress the expression of all the three KOR isoforms and KOR protein. Tretinoin 132-134 opioid receptor, kappa 1 Mus musculus 18-21
12324654-0 2002 Ectopic expression of CXCR5/BLR1 accelerates retinoic acid- and vitamin D(3)-induced monocytic differentiation of U937 cells. Tretinoin 45-58 C-X-C motif chemokine receptor 5 Homo sapiens 22-27
12324654-0 2002 Ectopic expression of CXCR5/BLR1 accelerates retinoic acid- and vitamin D(3)-induced monocytic differentiation of U937 cells. Tretinoin 45-58 C-X-C motif chemokine receptor 5 Homo sapiens 28-32
11222649-6 2001 The regulation of KOR gene by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic acid (RA), the most potent ingredient of vitamin A, was able to suppress the expression of all the three KOR isoforms and KOR protein. Tretinoin 132-134 opioid receptor, kappa 1 Mus musculus 231-234
10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 41-54 colony stimulating factor 1 Homo sapiens 187-192
11222649-6 2001 The regulation of KOR gene by vitamin A was substantiated in a mouse embryonal carcinoma P19 culture system in which retinoic acid (RA), the most potent ingredient of vitamin A, was able to suppress the expression of all the three KOR isoforms and KOR protein. Tretinoin 132-134 opioid receptor, kappa 1 Mus musculus 231-234
12324654-5 2002 Ectopic expression of blr1 caused no significant cell cycle or differentiation changes, but caused the U937/blr1 cells to differentiate faster when treated with either retinoic acid or 1alpha,25-dihydroxyvitamin D(3). Tretinoin 168-181 C-X-C motif chemokine receptor 5 Homo sapiens 22-26
12324654-5 2002 Ectopic expression of blr1 caused no significant cell cycle or differentiation changes, but caused the U937/blr1 cells to differentiate faster when treated with either retinoic acid or 1alpha,25-dihydroxyvitamin D(3). Tretinoin 168-181 C-X-C motif chemokine receptor 5 Homo sapiens 108-112
10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 56-58 colony stimulating factor 1 Homo sapiens 181-186
12324654-6 2002 Treated with retinoic acid, U937/blr1 cells showed a greater increase in the percentage of CD11b expressing cells than vector control cells. Tretinoin 13-26 C-X-C motif chemokine receptor 5 Homo sapiens 33-37
12324654-6 2002 Treated with retinoic acid, U937/blr1 cells showed a greater increase in the percentage of CD11b expressing cells than vector control cells. Tretinoin 13-26 integrin subunit alpha M Homo sapiens 91-96
10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 56-58 colony stimulating factor 1 Homo sapiens 187-192
12324654-7 2002 Retinoic acid also induced a higher percentage of functionally differentiated blr1 transfectants as assessed by nitroblue tetrazolium reduction. Tretinoin 0-13 C-X-C motif chemokine receptor 5 Homo sapiens 78-82
12324654-8 2002 U937/blr1 cells underwent moderate growth inhibition on treatment with retinoic acid. Tretinoin 71-84 C-X-C motif chemokine receptor 5 Homo sapiens 5-9
12383199-1 2002 The regulation of signal transducer and activator of transcription-1 (STAT-1) by cytokines and all-trans-retinoic acid (RA) was investigated in THP-1 monocytic cells cultured with RA and stimulated with lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), and IFN-gamma, individually or in combinations. Tretinoin 180-182 signal transducer and activator of transcription 1 Homo sapiens 18-68
12383199-1 2002 The regulation of signal transducer and activator of transcription-1 (STAT-1) by cytokines and all-trans-retinoic acid (RA) was investigated in THP-1 monocytic cells cultured with RA and stimulated with lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha), interferon-beta (IFN-beta), and IFN-gamma, individually or in combinations. Tretinoin 180-182 signal transducer and activator of transcription 1 Homo sapiens 70-76
11224525-2 2001 The natural ligands for murine NKG2D are distant major histocompatibility complex homologs, retinoic acid early transcript (Rae1) and H-60 minor histocompatibility antigen. Tretinoin 92-105 ribonucleic acid export 1 Mus musculus 124-128
11242046-10 2001 The expression of GTRAP3-18 can be upregulated by retinoic acid, which results in a specific reduction of EAAC1-mediated glutamate transport. Tretinoin 50-63 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 18-27
12383199-2 2002 While RA (10(-8) m) alone did not alter STAT-1 activation or expression in THP-1 cells, RA enhanced or prolonged STAT-1 activation (tyrosine 701 phosphorylation) and gene expression (mRNA and protein) induced by either IFN-beta or IFN-gamma. Tretinoin 88-90 signal transducer and activator of transcription 1 Homo sapiens 113-119
10554038-7 1999 Our results also showed that atRA, by itself and in the presence of CSF-1, can increase the ability of breast carcinoma cells to invade in vitro. Tretinoin 29-33 colony stimulating factor 1 Homo sapiens 68-73
12383199-4 2002 These results imply that RA can significantly rebalance STAT-1-dependent responses, and that one of the mechanisms may be through the inhibition of the NFkappaB pathway. Tretinoin 25-27 signal transducer and activator of transcription 1 Homo sapiens 56-62
10554038-8 1999 Furthermore, we demonstrated that atRA is able to abolish the CSF-1-induced increase in anchorage-independent growth of breast carcinoma cells without affecting the anchorage-dependent growth. Tretinoin 34-38 colony stimulating factor 1 Homo sapiens 62-67
10578180-1 1999 In monolayer cultures of P19 EC cells treated with both all-trans retinoic acid (RA) and bone morphogenetic protein (BMP)-4 (RA/BMP-4 treatment), many non-adherent apoptotic cells and activated caspase-3-positive cells were observed, but they were not observed in cells treated with RA or BMP-4 alone. Tretinoin 66-79 interleukin 23 subunit alpha Homo sapiens 25-28
12354671-4 2002 Inhibition of the PEPCK gene by vitamin A deficiency is reversed by all-trans or 9-cis retinoic acid (RA) treatment. Tretinoin 102-104 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 18-23
12354671-5 2002 In a transgenic mouse model, a -460 and -355 bp PEPCK promoter fragment confers susceptibility to inhibition by vitamin A deficiency and responsiveness to all-trans RA treatment. Tretinoin 165-167 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 48-53
12354671-6 2002 However, there is a differential effect of 9-cis RA on the PEPCK promoter; the -460 fragment confers responsiveness to 9-cis RA, but the -355 fragment does not. Tretinoin 49-51 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 59-64
12354671-6 2002 However, there is a differential effect of 9-cis RA on the PEPCK promoter; the -460 fragment confers responsiveness to 9-cis RA, but the -355 fragment does not. Tretinoin 125-127 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 59-64
11092879-0 2001 An intronic Ikaros-binding element mediates retinoic acid suppression of the kappa opioid receptor gene, accompanied by histone deacetylation on the promoters. Tretinoin 44-57 opioid receptor, kappa 1 Mus musculus 77-98
11092879-1 2001 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in mouse embryonal carcinoma P19 stem cells and suppressed by retinoic acid (RA) in cells undergoing neuronal differentiation. Tretinoin 133-146 opioid receptor, kappa 1 Mus musculus 10-31
11092879-1 2001 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in mouse embryonal carcinoma P19 stem cells and suppressed by retinoic acid (RA) in cells undergoing neuronal differentiation. Tretinoin 133-146 opioid receptor, kappa 1 Mus musculus 33-36
11092879-1 2001 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in mouse embryonal carcinoma P19 stem cells and suppressed by retinoic acid (RA) in cells undergoing neuronal differentiation. Tretinoin 148-150 opioid receptor, kappa 1 Mus musculus 10-31
11092879-1 2001 The mouse kappa opioid receptor (KOR) gene is constitutively expressed in mouse embryonal carcinoma P19 stem cells and suppressed by retinoic acid (RA) in cells undergoing neuronal differentiation. Tretinoin 148-150 opioid receptor, kappa 1 Mus musculus 33-36
11092879-7 2001 It is proposed that in an RA-induced P19 differentiation model, RA elevates Ik-1 expression, which recruits histone deacetylase to intron 1 of the KOR gene and silences KOR gene promoters. Tretinoin 26-28 opioid receptor, kappa 1 Mus musculus 147-150
11092879-7 2001 It is proposed that in an RA-induced P19 differentiation model, RA elevates Ik-1 expression, which recruits histone deacetylase to intron 1 of the KOR gene and silences KOR gene promoters. Tretinoin 26-28 opioid receptor, kappa 1 Mus musculus 169-172
10529422-12 1999 These data, which indicate that retinoic acid signaling through RARalpha and/or RARbeta is essential for the specification of rhombomere identities and for the control of caudal hindbrain segmentation by restricting the expression domains of kreisler and of Krox-20, also strongly suggest that this signaling plays a crucial role in the posteriorization of the hindbrain neurectoderm. Tretinoin 32-45 early growth response 2 Mus musculus 258-265
11058598-8 2001 Co-transfection of an expression vector encoding wild-type RARalpha increased enhancer activity, whereas a dominant negative mutant of RARalpha significantly attenuated retinoic acid-induced activity of the enhancer. Tretinoin 169-182 retinoic acid receptor, alpha Mus musculus 135-143
12354671-7 2002 Taken together, these results indicate that the PEPCK retinoic acid response element (RARE)1 is required for 9-cis RA induction-but not all-trans RA induction-of the PEPCK gene. Tretinoin 86-88 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 48-53
12354671-7 2002 Taken together, these results indicate that the PEPCK retinoic acid response element (RARE)1 is required for 9-cis RA induction-but not all-trans RA induction-of the PEPCK gene. Tretinoin 86-88 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 166-171
12354671-7 2002 Taken together, these results indicate that the PEPCK retinoic acid response element (RARE)1 is required for 9-cis RA induction-but not all-trans RA induction-of the PEPCK gene. Tretinoin 115-117 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 48-53
12354671-7 2002 Taken together, these results indicate that the PEPCK retinoic acid response element (RARE)1 is required for 9-cis RA induction-but not all-trans RA induction-of the PEPCK gene. Tretinoin 115-117 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 166-171
12354678-0 2002 Retinoic acid induces parietal endoderm but not primitive endoderm and visceral endoderm differentiation in F9 teratocarcinoma stem cells with a targeted deletion of the Rex-1 (Zfp-42) gene. Tretinoin 0-13 zinc finger protein 42 Mus musculus 170-175
12354678-0 2002 Retinoic acid induces parietal endoderm but not primitive endoderm and visceral endoderm differentiation in F9 teratocarcinoma stem cells with a targeted deletion of the Rex-1 (Zfp-42) gene. Tretinoin 0-13 zinc finger protein 42 Mus musculus 177-183
11159837-5 2001 Nurr1"s importance in retinoic acid, vitamin D, and thyroid hormone signaling has been hypothesized. Tretinoin 22-35 nuclear receptor subfamily 4, group A, member 2 Mus musculus 0-5
10553155-2 1999 All-trans retinoic acid probably induces differentiation of atypical promyelocytes and clinical remission in APL patients by binding to the ligand binding domain (LBD) of the RARa portion of the PML-RARa chimeric protein. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 175-179
11165476-5 2001 Hormonal regulation of Spz1 was investigated and downregulation of Spz1 expression by testosterone and retinoic acid was found. Tretinoin 103-116 spermatogenic leucine zipper 1 Mus musculus 67-71
12165811-11 2002 Expression level of SOX18 mRNA in NT2 cells was down-regulated by all-trans retinoic acid. Tretinoin 76-89 SRY-box transcription factor 18 Homo sapiens 20-25
12130525-1 2002 Acute leukemia with the t(11;17) expressing the PLZF-RARalpha gene fusion is a rare variant of acute promyelocytic leukemia (APL) that has been associated with poor clinical response to all-trans retinoic acid (ATRA) treatment. Tretinoin 196-209 zinc finger and BTB domain containing 16 Homo sapiens 48-52
12130525-1 2002 Acute leukemia with the t(11;17) expressing the PLZF-RARalpha gene fusion is a rare variant of acute promyelocytic leukemia (APL) that has been associated with poor clinical response to all-trans retinoic acid (ATRA) treatment. Tretinoin 211-215 zinc finger and BTB domain containing 16 Homo sapiens 48-52
12130525-3 2002 We describe here a patient with PLZF/RARalpha APL who was treated at relapse with ATRA and low-dose hydroxyurea. Tretinoin 82-86 zinc finger and BTB domain containing 16 Homo sapiens 32-36
11166829-7 2001 Induction of monocytic differentiation by various agents was associated with upregulation of IL-1 beta and IL-1ra expression, while a differentiation shift to the granulocytic lineage in the presence of retinoic acid (RA) led to a marked increase of macrophage chemoattractant protein-1 (MCP-1) producing cells. Tretinoin 203-216 chemokine (C-C motif) ligand 2 Mus musculus 250-286
10553155-2 1999 All-trans retinoic acid probably induces differentiation of atypical promyelocytes and clinical remission in APL patients by binding to the ligand binding domain (LBD) of the RARa portion of the PML-RARa chimeric protein. Tretinoin 10-23 PML nuclear body scaffold Homo sapiens 195-198
11306054-8 2001 Our results demonstrate that xCTBP is identical to ALDH1 and suggest that this protein might modulate RA synthesis and intracellular concentration of free T(3). Tretinoin 102-104 C-terminal binding protein 2 like S homeolog Xenopus laevis 29-34
12193473-1 2002 A comparison between retinoic acid (RA) differentiation-resistant and differentiation-sensitive SK-N-BE neuroblastoma (NB) cell lines revealed an association between resistance to differentiation, exhibited by N-myc stable transfected SK-N-BE 9N cells, with sensitivity to RA induction of p50/p65 nuclear factor kappaB (NF-kappaB) transcription factor activity and induction of matrix metalloproteinase (MMP)-9 expression leading to enhanced invasive behavior in vitro. Tretinoin 36-38 matrix metallopeptidase 9 Homo sapiens 378-410
11306054-8 2001 Our results demonstrate that xCTBP is identical to ALDH1 and suggest that this protein might modulate RA synthesis and intracellular concentration of free T(3). Tretinoin 102-104 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 51-56
10553155-2 1999 All-trans retinoic acid probably induces differentiation of atypical promyelocytes and clinical remission in APL patients by binding to the ligand binding domain (LBD) of the RARa portion of the PML-RARa chimeric protein. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 199-203
11306060-5 2001 Although the true physiological substrates of this zinc metalloenzyme are unknown, alcohol dehydrogenase effectively catalyzes not only the interconversion of all-trans-retinol and all-trans-retinal but also the oxidation of all-trans-retinal to the corresponding retinoic acid. Tretinoin 264-277 aldo-keto reductase family 1 member A1 Homo sapiens 83-104
10553155-3 1999 Structural alterations of the LBD of the PML/RARa have been revealed in ATRA-resistant APL cell lines and in a few APL patients with acquired clinical resistance to ATRA therapy. Tretinoin 72-76 PML nuclear body scaffold Homo sapiens 41-44
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 cellular retinoic acid binding protein 2 Homo sapiens 198-206
12000751-9 2002 The down-regulation of PKC also inhibited the binding of RAR to a retinoic acid response element and the retinoic acid induction of RAR beta expression. Tretinoin 66-79 retinoic acid receptor, alpha Mus musculus 57-60
12000751-10 2002 These findings suggest that PKC can influence retinoic acid signaling by altering the stability of RAR protein without directly phosphorylating this receptor. Tretinoin 46-59 retinoic acid receptor, alpha Mus musculus 99-102
11162104-1 2001 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR), and cellular retinoic acid binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 cellular retinoic acid binding protein 2 Homo sapiens 198-206
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 68-70 neuronal differentiation 6 Homo sapiens 245-252
10553155-3 1999 Structural alterations of the LBD of the PML/RARa have been revealed in ATRA-resistant APL cell lines and in a few APL patients with acquired clinical resistance to ATRA therapy. Tretinoin 72-76 retinoic acid receptor alpha Homo sapiens 45-49
12000752-4 2002 The expression of other basic helix-loop-helix genes changed during RA-induced differentiation: expression of neuroblast-specific ASCL1 (HASH-1) gene was promptly reduced after RA treatment, whereas expression of differentiation-promoting genes NEUROD6 (NEX-1, HATH-2) and NEUROD1 was increased. Tretinoin 68-70 neuronal differentiation 6 Homo sapiens 254-259
11212249-0 2001 Increased retinoic acid responsiveness in lung carcinoma cells that are nonresponsive despite the presence of endogenous retinoic acid receptor (RAR) beta by expression of exogenous retinoid receptors retinoid X receptor alpha, RAR alpha, and RAR gamma. Tretinoin 10-23 retinoid X receptor alpha Homo sapiens 201-226
11212249-6 2001 RXR alpha and RAR alpha enhanced growth inhibition by all-trans-retinoic acid or 9-cis-retinoic acid, whereas RAR gamma was less effective, and RAR beta was ineffective. Tretinoin 54-77 retinoid X receptor alpha Homo sapiens 0-9
11464866-2 2001 The cellular effects of 9-cis RA may, in part, result from activation of retinoid X receptor (RXR) homodimers. Tretinoin 30-32 retinoid X receptor alpha Homo sapiens 73-92
11464866-2 2001 The cellular effects of 9-cis RA may, in part, result from activation of retinoid X receptor (RXR) homodimers. Tretinoin 30-32 retinoid X receptor alpha Homo sapiens 94-97
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 57-59 retinoid X receptor alpha Homo sapiens 221-224
12000762-8 2002 These data indicate that the remarkably broad effects of RA on the growth and differentiation of many different epithelial cancers may well be explained by the ability of RA to differentially regulate the activity of RAR/RXR, AP-1, and beta-catenin/TCF pathways. Tretinoin 171-173 retinoid X receptor alpha Homo sapiens 221-224
10553155-4 1999 Two APL relapsed patients with clinical resistance to ATRA therapy were evaluated for the presence of nucleotide mutations in the LBD of PML/RARa gene and then treated with arsenic trioxide (As2O3). Tretinoin 54-58 PML nuclear body scaffold Homo sapiens 137-140
10553155-8 1999 RESULTS: In both patients, at the ATRA-resistant relapse, a missense point mutation in the LBD of the PML/RARa gene was found. Tretinoin 34-38 PML nuclear body scaffold Homo sapiens 102-105
11983505-0 2002 RAR-RXR selectivity and biological activity of new retinoic acid analogues with heterocyclic or polycyclic aromatic systems. Tretinoin 51-64 retinoid X receptor alpha Homo sapiens 4-7
10553155-8 1999 RESULTS: In both patients, at the ATRA-resistant relapse, a missense point mutation in the LBD of the PML/RARa gene was found. Tretinoin 34-38 retinoic acid receptor alpha Homo sapiens 106-110
10610177-2 1999 Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). Tretinoin 121-134 PML nuclear body scaffold Homo sapiens 18-21
12080019-0 2002 Retinoic acid mediates transcriptional repression of ovine follicle-stimulating hormone receptor gene via a pleiotropic nuclear receptor response element. Tretinoin 0-13 follicle stimulating hormone receptor Homo sapiens 59-96
12075932-0 2001 Cloning of human myeloid-associated differentiation marker (MYADM) gene whose expression was up-regulated in NB4 cells induced by all-trans retinoic acid. Tretinoin 140-153 myeloid associated differentiation marker Homo sapiens 17-58
12075932-0 2001 Cloning of human myeloid-associated differentiation marker (MYADM) gene whose expression was up-regulated in NB4 cells induced by all-trans retinoic acid. Tretinoin 140-153 myeloid associated differentiation marker Homo sapiens 60-65
10610177-2 1999 Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). Tretinoin 121-134 retinoic acid receptor alpha Homo sapiens 46-54
11697231-5 2001 RXR ligands include naturally occurring retinoic acid and synthetic rexinoids. Tretinoin 40-53 retinoid X receptor alpha Homo sapiens 0-3
12186376-4 2002 The cell lines (MCF-7, T-47D, ZR-75-1), which expressed both BRCA1 and p27, were extremely sensitive to the inhibitory effect of the combination of TGZ and either ATRA or 9-cis-RA (ED90, 2-5 x 10(-11) M). Tretinoin 163-167 BRCA1 DNA repair associated Homo sapiens 61-66
12186376-4 2002 The cell lines (MCF-7, T-47D, ZR-75-1), which expressed both BRCA1 and p27, were extremely sensitive to the inhibitory effect of the combination of TGZ and either ATRA or 9-cis-RA (ED90, 2-5 x 10(-11) M). Tretinoin 171-179 BRCA1 DNA repair associated Homo sapiens 61-66
10610177-2 1999 Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). Tretinoin 46-48 PML nuclear body scaffold Homo sapiens 18-21
12052888-4 2002 Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. Tretinoin 239-241 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-151
11172538-5 2001 At the molecular level, this has been explained by the retinoic acid-insensitive binding of corepressor proteins to the PLZF part of the fusion protein, leading to sustained repression of target genes that are important for cellular differentiation. Tretinoin 55-68 zinc finger and BTB domain containing 16 Homo sapiens 120-124
10610177-7 1999 T18, similar to PML-RARalpha, disrupts the RA-dependent activity of this complex in a dominant-negative manner resulting in a growth advantage. Tretinoin 20-22 PML nuclear body scaffold Homo sapiens 16-19
11172538-6 2001 Targeting of the PLZF-RARalpha-bound corepressor complexes using a combination of all-trans retinoic acid (ATRA) and deacetylase inhibitors has shown that the repression of target genes can be relieved, allowing differentiation of the cells. Tretinoin 92-105 zinc finger and BTB domain containing 16 Homo sapiens 17-21
11172538-6 2001 Targeting of the PLZF-RARalpha-bound corepressor complexes using a combination of all-trans retinoic acid (ATRA) and deacetylase inhibitors has shown that the repression of target genes can be relieved, allowing differentiation of the cells. Tretinoin 107-111 zinc finger and BTB domain containing 16 Homo sapiens 17-21
10477294-7 1999 Our results suggest that retinoic acid acts very early, upstream of sonic hedgehog, and we propose a model for regulation of differentiation and proliferation in the neural plate, showing that retinoic acid might be activating primary neurogenesis by repressing sonic hedgehog expression. Tretinoin 25-38 sonic hedgehog L homeolog Xenopus laevis 268-276
11162439-4 2000 In vivo transfection experiments in COS cells indicate that cyclic AMP represses retinoic acid-mediated transcriptional activation of RXRalpha and this repression is mediated by serine 27. Tretinoin 81-94 retinoid X receptor alpha Homo sapiens 134-142
11162441-6 2000 Three regions in the CYP4F2 gene are responsive to retinoic acid with the DR1 RARE element (CCTCCT G TGACCT) at -708 able to bind RXRalpha/RARalpha heterodimers and mediate the repressive response of ATRA. Tretinoin 51-64 retinoid X receptor alpha Homo sapiens 130-138
12054674-12 2002 CIP4 levels are modified by all-trans-retinoic acid. Tretinoin 28-51 thyroid hormone receptor interactor 10 Homo sapiens 0-4
10477294-7 1999 Our results suggest that retinoic acid acts very early, upstream of sonic hedgehog, and we propose a model for regulation of differentiation and proliferation in the neural plate, showing that retinoic acid might be activating primary neurogenesis by repressing sonic hedgehog expression. Tretinoin 193-206 sonic hedgehog L homeolog Xenopus laevis 268-276
11980644-6 2002 Treatment with RA stimulated an interaction between RA receptor-alpha and CBP/p300; a corresponding decrease in the interaction between CBP/p300 and c-Jun was observed. Tretinoin 15-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 149-154
11162441-7 2000 These results indicate that retinoic acid can regulate CYP4F2 gene activity with RXRalpha heterodimers stimulating while RARalpha functioning to repress CYP4F2 gene expression. Tretinoin 28-41 retinoid X receptor alpha Homo sapiens 81-89
10548048-1 1999 A retinoic acid binding protein isolated from the lumen of the rat epididymis (ERABP) is a member of the lipocalin superfamily. Tretinoin 2-15 lipocalin 5 Rattus norvegicus 79-84
11090462-6 2000 Cyclin D(2) was not expressed in the undifferentiated A spermatogonia in vitamin A-deficient testis but was strongly induced in these cells after the induction of differentiation of most of these cells into A(1) spermatogonia by administration of retinoic acid. Tretinoin 247-260 cyclin D2 Mus musculus 0-11
11150643-0 2000 Retinoic acid down-regulates VPAC(1) receptors and TGF-beta 3 but up-regulates TGF-beta 2 in lung cancer cells. Tretinoin 0-13 transforming growth factor beta 2 Homo sapiens 79-89
11150643-9 2000 These results suggest that RA may inhibit lung cancer growth by down-regulating VPAC(1) receptor and TGF-beta 3 mRNA but up-regulating TGF-beta 2 mRNA. Tretinoin 27-29 transforming growth factor beta 2 Homo sapiens 135-145
11956596-0 2002 Expression and regulation of WNT8A and WNT8B mRNAs in human tumor cell lines: up-regulation of WNT8B mRNA by beta-estradiol in MCF-7 cells, and down-regulation of WNT8A and WNT8B mRNAs by retinoic acid in NT2 cells. Tretinoin 188-201 Wnt family member 8A Homo sapiens 29-34
11956596-9 2002 Because NT2 cells differentiate into neuronal cells after all-trans retinoic-acid treatment, effects of all-trans retinoic acid on mRNA expression of WNT8A and WNT8B were next investigated. Tretinoin 114-127 Wnt family member 8A Homo sapiens 150-155
11956596-10 2002 WNT8A and WNT8B mRNAs were down-regulated together in NT2 cells after all-trans retinoic-acid treatment. Tretinoin 80-93 Wnt family member 8A Homo sapiens 0-5
11980849-1 2002 PURPOSE: This study was initiated to investigate the molecular mechanisms of activation of expression of the human cone arrestin (hCAR) gene by retinoic acid (RA), in an in vitro model of retinoblastoma cells. Tretinoin 144-157 CXADR Ig-like cell adhesion molecule Homo sapiens 130-134
11980849-1 2002 PURPOSE: This study was initiated to investigate the molecular mechanisms of activation of expression of the human cone arrestin (hCAR) gene by retinoic acid (RA), in an in vitro model of retinoblastoma cells. Tretinoin 159-161 CXADR Ig-like cell adhesion molecule Homo sapiens 130-134
11980849-5 2002 The hCAR promoter"s activity and its responsiveness to RA treatment was evaluated by transient transfection of the hCAR promotor-luciferase reporter constructs, followed by promoter deletion analysis to map the specific regions responsible for the RA response. Tretinoin 55-57 CXADR Ig-like cell adhesion molecule Homo sapiens 4-8
11980849-5 2002 The hCAR promoter"s activity and its responsiveness to RA treatment was evaluated by transient transfection of the hCAR promotor-luciferase reporter constructs, followed by promoter deletion analysis to map the specific regions responsible for the RA response. Tretinoin 55-57 CXADR Ig-like cell adhesion molecule Homo sapiens 115-119
11205272-0 2000 Retinoic acid modulates stem cell factor secretion by human neuroblastoma cell lines. Tretinoin 0-13 KIT ligand Homo sapiens 24-40
11205272-2 2000 We have investigated the effect of retinoic acid (RA), one of the most active differentiating agents on human NB cells, on the SCF production by human neuroblastoma cell lines. Tretinoin 35-48 KIT ligand Homo sapiens 127-130
10548048-2 1999 ERABP binds both the all-trans and 9-cis isomers of retinoic acid, as well as the synthetic retinoid (E)-4-[2-(5,6,7,8)-tetrahydro-5,5,8,8-tetramethyl-2 napthalenyl-1 propenyl]-benzoic acid (TTNPB), a structural analog of all-trans retinoic acid. Tretinoin 52-65 lipocalin 5 Rattus norvegicus 0-5
11205272-2 2000 We have investigated the effect of retinoic acid (RA), one of the most active differentiating agents on human NB cells, on the SCF production by human neuroblastoma cell lines. Tretinoin 50-52 KIT ligand Homo sapiens 127-130
11205272-5 2000 A progressive increase pattern of the SCF concentration over time, was common to all SCF secreting cell lines, both unstimulated and RA-stimulated. Tretinoin 133-135 KIT ligand Homo sapiens 38-41
11980849-11 2002 Subsequently, a region between -852 and -702 of the hCAR promoter, with RA-responsive elements (RAREs), was discovered to be responsible for the RA response. Tretinoin 72-74 CXADR Ig-like cell adhesion molecule Homo sapiens 52-56
11980849-12 2002 CONCLUSIONS: The hCAR gene is transcriptionally upregulated by RA acting through cis elements within -852 to -702 of the hCAR 5" flanking region. Tretinoin 63-65 CXADR Ig-like cell adhesion molecule Homo sapiens 17-21
10548048-2 1999 ERABP binds both the all-trans and 9-cis isomers of retinoic acid, as well as the synthetic retinoid (E)-4-[2-(5,6,7,8)-tetrahydro-5,5,8,8-tetramethyl-2 napthalenyl-1 propenyl]-benzoic acid (TTNPB), a structural analog of all-trans retinoic acid. Tretinoin 232-245 lipocalin 5 Rattus norvegicus 0-5
11980849-12 2002 CONCLUSIONS: The hCAR gene is transcriptionally upregulated by RA acting through cis elements within -852 to -702 of the hCAR 5" flanking region. Tretinoin 63-65 CXADR Ig-like cell adhesion molecule Homo sapiens 121-125
11205272-6 2000 Moreover, after 48 and 72 hours-exposure to RA, SCF concentrations were higher than in the untreated controls (p < 0.01). Tretinoin 44-46 KIT ligand Homo sapiens 48-51
10488123-0 1999 Molecular characterization of peptidylarginine deiminase in HL-60 cells induced by retinoic acid and 1alpha,25-dihydroxyvitamin D(3). Tretinoin 83-96 peptidyl arginine deiminase 4 Homo sapiens 30-56
11205272-8 2000 These effects demonstrated that RA, besides inducing neuronal differentiation, enhanced SCF production in neuroblastoma cell lines. Tretinoin 32-34 KIT ligand Homo sapiens 88-91
12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-18
12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-189
12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-189
12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-189
10924506-0 2000 Identification of GRIM-19, a novel cell death-regulatory gene induced by the interferon-beta and retinoic acid combination, using a genetic approach. Tretinoin 97-110 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 18-25
11342307-3 2000 Recent studies that identify novel interactions between RARalpha and the nuclear receptor co-activators and co-repressors, new functions of the oncogenic RARalpha fusion proteins and their catabolism in retinoic acid-induced differentiation, and the availability of new transgenic mice models have provided important insights into our understanding of the mechanisms by which mutant forms of RARalpha can be implicated in the development of leukemia. Tretinoin 203-216 retinoic acid receptor, alpha Mus musculus 154-162
11342307-3 2000 Recent studies that identify novel interactions between RARalpha and the nuclear receptor co-activators and co-repressors, new functions of the oncogenic RARalpha fusion proteins and their catabolism in retinoic acid-induced differentiation, and the availability of new transgenic mice models have provided important insights into our understanding of the mechanisms by which mutant forms of RARalpha can be implicated in the development of leukemia. Tretinoin 203-216 retinoic acid receptor, alpha Mus musculus 154-162
10488123-4 1999 We cloned and characterized a PAD cDNA from retinoic acid-induced cells. Tretinoin 44-57 peptidyl arginine deiminase 4 Homo sapiens 30-33
11832495-8 2002 Administration of retinoic acid to mice bearing tumors driven by activation of the Wnt-1/beta-catenin pathway resulted in increased expression of stra6 in the tumors but not in normal tissue. Tretinoin 18-31 catenin (cadherin associated protein), beta 1 Mus musculus 89-101
10500184-0 1999 Multiple left-right asymmetry defects in Shh(-/-) mutant mice unveil a convergence of the shh and retinoic acid pathways in the control of Lefty-1. Tretinoin 98-111 sonic hedgehog Mus musculus 41-44
11929748-4 2002 STAT5b-RARalpha bound to retinoic acid response elements (RAREs) both as a homodimer and as a heterodimer with RXRalpha and inhibited wild-type RARalpha/RXRalpha transactivation. Tretinoin 25-38 retinoid X receptor alpha Homo sapiens 153-161
12207051-5 2002 ES cells exposed to 1 microM all-trans-retinoic acid on day 8, 9 and 10 of differentiation revealed increased expression of Bax and Bad compared to the vehicle-treated cells. Tretinoin 29-52 BCL2-associated X protein Mus musculus 124-127
12207051-7 2002 Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Tretinoin 66-79 caspase 3 Mus musculus 29-38
12207051-7 2002 Increased mRNA expression of caspase 3 and caspase 6 in all-trans-retinoic acid-exposed ES cells suggested that caspases play an important role in retinoic acid-mediated apoptosis during ES differentiation. Tretinoin 147-160 caspase 3 Mus musculus 29-38
10974019-0 2000 c-Jun-dependent inhibition of cutaneous procollagen transcription following ultraviolet irradiation is reversed by all-trans retinoic acid. Tretinoin 125-138 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5
10500184-0 1999 Multiple left-right asymmetry defects in Shh(-/-) mutant mice unveil a convergence of the shh and retinoic acid pathways in the control of Lefty-1. Tretinoin 98-111 left right determination factor 1 Mus musculus 139-146
10974019-6 2000 Pretreatment of human skin in vivo with all-trans retinoic acid inhibits UV induction of c-Jun and protects skin against loss of procollagen synthesis. Tretinoin 50-63 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 89-94
12153175-2 2002 Intracellular retinoid signaling induced by endogenous or exogenous RA is regulated by retinoid binding proteins such as CRBPI, CRABPI and CRABPII and there are data suggesting that the expression of these proteins can influence the sensitivity to the growth inhibitory effects of ATRA. Tretinoin 68-70 cellular retinoic acid binding protein 2 Homo sapiens 139-146
12153175-2 2002 Intracellular retinoid signaling induced by endogenous or exogenous RA is regulated by retinoid binding proteins such as CRBPI, CRABPI and CRABPII and there are data suggesting that the expression of these proteins can influence the sensitivity to the growth inhibitory effects of ATRA. Tretinoin 281-285 cellular retinoic acid binding protein 2 Homo sapiens 139-146
10500184-4 1999 We also demonstrate that retinoic acid (RA) controls Lefty-1 expression in a pathway downstream or parallel to Shh. Tretinoin 25-38 left right determination factor 1 Mus musculus 53-60
12153175-8 2002 However, ATRA-induced upregulation of CRABPII did significantly correlate with the ATRA sensitivity (p < 0.005) as well as with ATRA-induced upregulation of the retinoid receptor RARbeta (p < 0.05). Tretinoin 9-13 cellular retinoic acid binding protein 2 Homo sapiens 38-45
12153175-8 2002 However, ATRA-induced upregulation of CRABPII did significantly correlate with the ATRA sensitivity (p < 0.005) as well as with ATRA-induced upregulation of the retinoid receptor RARbeta (p < 0.05). Tretinoin 83-87 cellular retinoic acid binding protein 2 Homo sapiens 38-45
10500184-4 1999 We also demonstrate that retinoic acid (RA) controls Lefty-1 expression in a pathway downstream or parallel to Shh. Tretinoin 25-38 sonic hedgehog Mus musculus 111-114
12153175-8 2002 However, ATRA-induced upregulation of CRABPII did significantly correlate with the ATRA sensitivity (p < 0.005) as well as with ATRA-induced upregulation of the retinoid receptor RARbeta (p < 0.05). Tretinoin 83-87 cellular retinoic acid binding protein 2 Homo sapiens 38-45
10500184-4 1999 We also demonstrate that retinoic acid (RA) controls Lefty-1 expression in a pathway downstream or parallel to Shh. Tretinoin 40-42 left right determination factor 1 Mus musculus 53-60
11886382-0 2002 Interleukin 10 abolishes the growth inhibitory effects of all-trans retinoic acid on human myeloma cells. Tretinoin 68-81 interleukin 10 Homo sapiens 0-14
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 173-181
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 191-199
10500184-4 1999 We also demonstrate that retinoic acid (RA) controls Lefty-1 expression in a pathway downstream or parallel to Shh. Tretinoin 40-42 sonic hedgehog Mus musculus 111-114
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 173-181
10954752-0 2000 Retinoic acid (RA) and As2O3 treatment in transgenic models of acute promyelocytic leukemia (APL) unravel the distinct nature of the leukemogenic process induced by the PML-RARalpha and PLZF-RARalpha oncoproteins. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 191-199
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 cyclin dependent kinase inhibitor 3 Homo sapiens 204-237
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 cyclin dependent kinase inhibitor 3 Homo sapiens 239-244
11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 cyclin dependent kinase inhibitor 3 Homo sapiens 204-237
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 35-37 retinoic acid receptor, alpha Mus musculus 126-134
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 35-37 retinoic acid receptor, alpha Mus musculus 143-151
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 42-44 retinoic acid receptor, alpha Mus musculus 126-134
10954752-6 2000 Unexpectedly, therapeutic doses of RA and RA + As(2)O(3) can induce, both in vivo and in vitro, the degradation of either PML-RARalpha or PLZF-RARalpha proteins, suggesting that the maintenance of the leukemic phenotype depends on the continuous presence of the former, but not the latter. Tretinoin 42-44 retinoic acid receptor, alpha Mus musculus 143-151
11856770-9 2002 In metanephroi explanted from 14-d-old fetuses and cultured in a defined medium, expression of MK mRNA was found to be stimulated when retinoic acid (100 nM) was added in the culture medium. Tretinoin 135-148 midkine Rattus norvegicus 95-97
10500184-6 1999 Thus, the roles of Shh and RA in left-right specification indeed are conserved among vertebrates, and the Shh and RA pathways converge in the control of Lefty-1. Tretinoin 114-116 left right determination factor 1 Mus musculus 153-160
10479651-3 1999 In the current study, we show 9-cis retinoic acid (RA), a ligand for the nuclear hormone receptor retinoid X receptor (RXR) and retinoic acid receptor (RAR), markedly induces the expression of MCP-1. Tretinoin 51-53 C-C motif chemokine ligand 2 Homo sapiens 193-198
11839811-0 2002 Chromosomal integration of retinoic acid response elements prevents cooperative transcriptional activation by retinoic acid receptor and retinoid X receptor. Tretinoin 27-40 retinoid X receptor alpha Homo sapiens 137-156
10944463-2 2000 It is markedly up regulated in retinoic acid (RA)-treated F9 cells, suggesting a role for mDab2 in the cell differentiation. Tretinoin 31-44 disabled 2, mitogen-responsive phosphoprotein Mus musculus 90-95
10944463-2 2000 It is markedly up regulated in retinoic acid (RA)-treated F9 cells, suggesting a role for mDab2 in the cell differentiation. Tretinoin 46-48 disabled 2, mitogen-responsive phosphoprotein Mus musculus 90-95
10479651-4 1999 In human THP-1 monocytic leukemia cells cultured with RA (0.05 to 500 nmol/L), MCP-1 expression was induced rapidly, significantly, and dose-dependently by as much as 165-fold. Tretinoin 54-56 C-C motif chemokine ligand 2 Homo sapiens 79-84
10469660-5 1999 Interestingly, retinoic acid (RA) treatment prevented TAF(II)30-null cell death and induced primitive endodermal differentiation. Tretinoin 15-28 TATA-box binding protein associated factor 10 Homo sapiens 54-63
10926763-0 2000 Altered retinoic acid sensitivity and temporal expression of Hox genes in polycomb-M33-deficient mice. Tretinoin 8-21 chromobox 2 Mus musculus 74-82
10926763-0 2000 Altered retinoic acid sensitivity and temporal expression of Hox genes in polycomb-M33-deficient mice. Tretinoin 8-21 chromobox 2 Mus musculus 83-86
10926763-4 2000 In this paper, we show that in the absence of M33, the window of Hoxd4 retinoic acid (RA) responsiveness is opened earlier and that Hoxd11 gene expression is activated earlier in development This indicates that M33 antagonizes the RA pathway and has a function in the establishment of the early temporal sequence of activation of Hox genes. Tretinoin 71-84 homeobox D4 Mus musculus 65-70
10926763-4 2000 In this paper, we show that in the absence of M33, the window of Hoxd4 retinoic acid (RA) responsiveness is opened earlier and that Hoxd11 gene expression is activated earlier in development This indicates that M33 antagonizes the RA pathway and has a function in the establishment of the early temporal sequence of activation of Hox genes. Tretinoin 86-88 homeobox D4 Mus musculus 65-70
11741009-1 2002 Hypoxia-hypoglycemia has played an important role in inducing both phospholipase A2 activation and the expression of the early gene c-fos, in the neuroblastoma cell line SK-N-BE, after it has been differentiated by retinoic acid. Tretinoin 215-228 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-137
10469660-5 1999 Interestingly, retinoic acid (RA) treatment prevented TAF(II)30-null cell death and induced primitive endodermal differentiation. Tretinoin 30-32 TATA-box binding protein associated factor 10 Homo sapiens 54-63
10926763-4 2000 In this paper, we show that in the absence of M33, the window of Hoxd4 retinoic acid (RA) responsiveness is opened earlier and that Hoxd11 gene expression is activated earlier in development This indicates that M33 antagonizes the RA pathway and has a function in the establishment of the early temporal sequence of activation of Hox genes. Tretinoin 86-88 chromobox 2 Mus musculus 211-214
10926763-4 2000 In this paper, we show that in the absence of M33, the window of Hoxd4 retinoic acid (RA) responsiveness is opened earlier and that Hoxd11 gene expression is activated earlier in development This indicates that M33 antagonizes the RA pathway and has a function in the establishment of the early temporal sequence of activation of Hox genes. Tretinoin 231-233 homeobox D4 Mus musculus 65-70
11807825-0 2002 Regulation of BMP-7 expression by retinoic acid and prostaglandin E(2). Tretinoin 34-47 bone morphogenetic protein 7 Homo sapiens 14-19
10926763-4 2000 In this paper, we show that in the absence of M33, the window of Hoxd4 retinoic acid (RA) responsiveness is opened earlier and that Hoxd11 gene expression is activated earlier in development This indicates that M33 antagonizes the RA pathway and has a function in the establishment of the early temporal sequence of activation of Hox genes. Tretinoin 231-233 chromobox 2 Mus musculus 211-214
11807825-8 2002 We show that retinoic acid (RA) treatment results in an upregulation of the hBMP-7p reporter activity. Tretinoin 13-26 bone morphogenetic protein 7 Homo sapiens 76-83
10469660-6 1999 In contrast, the RA- and cAMP-induced parietal endodermal differentiation was impaired in the TAF(II)30-null cells. Tretinoin 17-19 TATA-box binding protein associated factor 10 Homo sapiens 94-103
11807825-8 2002 We show that retinoic acid (RA) treatment results in an upregulation of the hBMP-7p reporter activity. Tretinoin 28-30 bone morphogenetic protein 7 Homo sapiens 76-83
10926763-7 2000 We propose that a function of the M33 protein is to control the accessibility of retinoic acid response elements in the vicinity of Hox genes regulatory regions by direct or indirect mechanisms or both. Tretinoin 81-94 chromobox 2 Mus musculus 34-37
10940626-0 2000 Murine hoxd4 expression in the CNS requires multiple elements including a retinoic acid response element. Tretinoin 74-87 homeobox D4 Mus musculus 7-12
11807825-9 2002 This regulation of the hBMP-7p was further confirmed by Northern blot, PCR, and Western blot analyses, which showed an increase in both BMP-7 mRNA and protein expression upon treatment with RA. Tretinoin 190-192 bone morphogenetic protein 7 Homo sapiens 23-30
11807825-9 2002 This regulation of the hBMP-7p was further confirmed by Northern blot, PCR, and Western blot analyses, which showed an increase in both BMP-7 mRNA and protein expression upon treatment with RA. Tretinoin 190-192 bone morphogenetic protein 7 Homo sapiens 24-29
11807825-10 2002 We further show that RA specifically upregulates expression of osteocalcin via activation of BMP-7 mRNA and protein in vitro. Tretinoin 21-23 bone morphogenetic protein 7 Homo sapiens 93-98
10579191-0 1999 [Analysis of expression of ets-1 and fli-1 proto-oncogenes in murine embryonic stem cells, induced to differentiation by retinoic acid]. Tretinoin 121-134 Friend leukemia integration 1 Mus musculus 37-42
12468379-5 2002 A noticeable effect was that of ATRA on the enzyme activity of PTP, for which four distinct patterns of oscillatory behaviour were identified. Tretinoin 32-36 protein tyrosine phosphatase non-receptor type 22 Homo sapiens 63-66
10940626-1 2000 We have identified a retinoic acid response element (RARE) within a neural enhancer located 3" to the Hoxd4 gene. Tretinoin 21-34 homeobox D4 Mus musculus 102-107
10940626-2 2000 This RARE is required for the initiation and maintenance of Hoxd4 transgene expression in neurectoderm, and for full anteriorized expression upon retinoic acid (RA) treatment. Tretinoin 146-159 homeobox D4 Mus musculus 60-65
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 110-133
10807954-5 2000 Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-alpha (RAR(alpha)) and retinoid receptor X-beta (RXR(beta)). Tretinoin 50-63 retinoic acid receptor, alpha Mus musculus 138-148
10807954-5 2000 Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-alpha (RAR(alpha)) and retinoid receptor X-beta (RXR(beta)). Tretinoin 65-67 retinoic acid receptor, alpha Mus musculus 138-148
11879576-6 2002 We hypothesize that the loss of CRBP1 and RBP expression disrupts retinol metabolism and retinoic acid production, which may facilitate the occurrence of genetic damage leading to the malignant transformation of the ovarian surface epithelium, the cells from which ovarian cancer arises. Tretinoin 89-102 retinol binding protein 4 Homo sapiens 33-36
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 135-138
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 retinoic acid receptor alpha Homo sapiens 110-133
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 retinoic acid receptor alpha Homo sapiens 135-138
10926209-4 2000 One such gene, gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), is essential for tumor cell death induced by interferon-beta (IFN-beta) and retinoic acid (RA). Tretinoin 164-177 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 78-85
10926209-4 2000 One such gene, gene associated with retinoid-interferon-induced mortality-19 (GRIM-19), is essential for tumor cell death induced by interferon-beta (IFN-beta) and retinoic acid (RA). Tretinoin 179-181 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 78-85
12455633-1 2002 We have performed a time course analysis of the expression of Sonichedgehog (shh) and patched1 (ptc1) in response to exogenous retinoic acid (RA) application to get some insight into the mechanism(s) underlying the formation of a mirror-image duplication of shh and ptc1 domains of expression in the pectoral fin buds of zebrafish. Tretinoin 127-140 patched 1 Danio rerio 86-94
10446126-5 1999 The mechanisms by which RA transfers from the CRABPs to RAR were thus investigated directly. Tretinoin 24-26 retinoic acid receptor alpha Homo sapiens 56-59
12455633-1 2002 We have performed a time course analysis of the expression of Sonichedgehog (shh) and patched1 (ptc1) in response to exogenous retinoic acid (RA) application to get some insight into the mechanism(s) underlying the formation of a mirror-image duplication of shh and ptc1 domains of expression in the pectoral fin buds of zebrafish. Tretinoin 127-140 patched 1 Danio rerio 96-100
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-181
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-226
12455633-1 2002 We have performed a time course analysis of the expression of Sonichedgehog (shh) and patched1 (ptc1) in response to exogenous retinoic acid (RA) application to get some insight into the mechanism(s) underlying the formation of a mirror-image duplication of shh and ptc1 domains of expression in the pectoral fin buds of zebrafish. Tretinoin 127-140 patched 1 Danio rerio 266-270
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 231-236
10446126-6 1999 The rate constant for movement of RA from CRABP-II, but not from CRABP-I, to RAR strongly depended on the concentration of the acceptor. Tretinoin 34-36 retinoic acid receptor alpha Homo sapiens 77-80
10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 240-244
10866321-6 2000 However, RARbeta showed a strong RA-independent inhibition of AP-1 activity, whereas inhibition of AP-1 activity by RARalpha and RARgamma was RA dependent. Tretinoin 9-11 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-66
11851873-11 2002 All-trans retinoic acid upregulated caspase-3 and downregulated bcl-2. Tretinoin 10-23 caspase 3 Mus musculus 36-45
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 activating transcription factor 2 Homo sapiens 124-129
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 260-265
10438723-9 1999 The retinoic acid receptor (RAR) agonist TTNPB mimicked the key events affected by retinoic acid, such as pRB phosphorylation, cyclin E expression, and expression of p21(Cip1), whereas the RAR-selective antagonist Ro 41-5253 counteracted the effects of retinoic acid. Tretinoin 4-17 retinoic acid receptor alpha Homo sapiens 28-31
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 activating transcription factor 2 Homo sapiens 124-129
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 260-265
10816444-3 2000 SC-M1 is an unique cell line which responds to retinoic acid (RA) treatment with reversible growth arrest [Shyu, Jiang, Huang, Chang, Wu, Roffler and Yeh (1995) Eur. Tretinoin 47-60 X-C motif chemokine ligand 1 Homo sapiens 0-5
10816444-3 2000 SC-M1 is an unique cell line which responds to retinoic acid (RA) treatment with reversible growth arrest [Shyu, Jiang, Huang, Chang, Wu, Roffler and Yeh (1995) Eur. Tretinoin 62-64 X-C motif chemokine ligand 1 Homo sapiens 0-5
10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 X-C motif chemokine ligand 1 Homo sapiens 37-42
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 activating transcription factor 2 Homo sapiens 124-129
10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 X-C motif chemokine ligand 1 Homo sapiens 92-97
10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 X-C motif chemokine ligand 1 Homo sapiens 92-97
12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 260-265
10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 X-C motif chemokine ligand 1 Homo sapiens 92-97
11751425-6 2001 Following all-trans retinoic acid (RA) treatment, RARalpha- and RARgamma-transduced cell lines exhibit a progressive, dose-dependent growth inhibition relative to the control LXSN cell lines. Tretinoin 20-33 retinoic acid receptor, alpha Mus musculus 50-72
10816444-8 2000 In addition to the accelerated growth arrest, RA-treated SC-M1/Bcl2 cells also recovered from growth arrest two days faster than SC-M1/neo cells after the removal of RA. Tretinoin 46-48 X-C motif chemokine ligand 1 Homo sapiens 57-62
10439807-2 1999 Since treatment response to all-trans retinoic acid correlates directly with PML/RAR alpha, expeditious documentation is critical to patient care. Tretinoin 38-51 PML nuclear body scaffold Homo sapiens 77-90
11775865-6 2000 Both all-trans retinoic acid (ATRA) and 9-cis retinoic acid (9cRA) potentiated As2O3-induced apoptosis, as measured by quantitative TdT fragment and labeling and flow cytometry assays in both HL-60S and HL-60R cells (P < 0.05, for all RA + As2O3 combinations vs As2O3 alone in both sublines). Tretinoin 15-28 DNA nucleotidylexotransferase Homo sapiens 132-135
11775865-6 2000 Both all-trans retinoic acid (ATRA) and 9-cis retinoic acid (9cRA) potentiated As2O3-induced apoptosis, as measured by quantitative TdT fragment and labeling and flow cytometry assays in both HL-60S and HL-60R cells (P < 0.05, for all RA + As2O3 combinations vs As2O3 alone in both sublines). Tretinoin 30-34 DNA nucleotidylexotransferase Homo sapiens 132-135
10842360-7 2000 Cx37 distribution was altered in both heart and aorta of mice that had been exposed to all-trans retinoic acid at the beginning of foetal development, whether or not these animals subsequently developed a transposition of great arteries. Tretinoin 97-110 gap junction protein, alpha 4 Mus musculus 0-4
10842360-8 2000 The data indicate that Cx37 is widely distributed in multiple compartments of cardiovascular system, in patterns which are modulated during development, by retinoic acid. Tretinoin 156-169 gap junction protein, alpha 4 Mus musculus 23-27
10816385-11 2000 Retinoic acid induced a relocalization and decrease in the amount of Shc protein, another actin-binding protein which is an adaptor protein for EGF-R signaling. Tretinoin 0-13 SHC adaptor protein 1 Homo sapiens 69-72
10797535-8 2000 All-trans-retinoic acid and prostaglandin E(2) (PGE(2)) selectively potentiated both basal and ROS-phagocytosis-induced PPARgamma expression. Tretinoin 0-23 peroxisome proliferator-activated receptor gamma Rattus norvegicus 120-129
10799277-6 2000 The putative porcine RNA helicase induced by virus (RHIV -1) showed 84% amino acid similarity to human retinoic acid-induced gene (RIG-I). Tretinoin 103-116 DEAD-box helicase 19A Homo sapiens 21-33
10799277-6 2000 The putative porcine RNA helicase induced by virus (RHIV -1) showed 84% amino acid similarity to human retinoic acid-induced gene (RIG-I). Tretinoin 103-116 DExD/H-box helicase 58 Homo sapiens 131-136
11798775-8 2000 1.0 micromol/L ATRA also exerted, to a less extent than As(2)O(3), growth-inhibitory effects in K(V) sublines, which became more obvious in K(PML) but not in K(PLZF) sublines. Tretinoin 15-19 zinc finger and BTB domain containing 16 Homo sapiens 160-164
10681376-1 2000 Oxidative conversion of all-trans-retinol (t-ROH) to all-trans-retinal (t-RAL) is recognized as the rate-limiting step for biosynthesis of all-trans-retinoic acid from t-ROH in mammalian hepatic tissues. Tretinoin 139-162 RAS like proto-oncogene A Homo sapiens 74-77
10840941-5 2000 Our experimental results clearly indicate that All Trans Retinoic Acid (ATRA) inhibit metastatic potential of highly metastatic B16F10 melanoma cells by 1) downregulating the cell surface integrin receptors against ECM proteins specially laminin and vitronectin and 2) by inhibiting the 72 kd collagenase activity. Tretinoin 57-70 vitronectin Mus musculus 250-267
10840941-5 2000 Our experimental results clearly indicate that All Trans Retinoic Acid (ATRA) inhibit metastatic potential of highly metastatic B16F10 melanoma cells by 1) downregulating the cell surface integrin receptors against ECM proteins specially laminin and vitronectin and 2) by inhibiting the 72 kd collagenase activity. Tretinoin 72-76 vitronectin Mus musculus 250-267
10699072-13 2000 The expression of PPARgamma and RXRalpha remained unchanged with the various treatments, whereas the expression of RARalpha was substantially reduced after treatment with the combination of retinoic acid and troglitazone. Tretinoin 190-203 retinoic acid receptor, alpha Mus musculus 115-123
10712807-4 2000 At the same concentration, 9-cis RA and cholecalciferol induced ALP of chondroblast and osteoblast cells, respectively; ATRA, 9-cis RA and cholecalciferol induced PIP of chondroblast and undifferentiated cells. Tretinoin 120-124 prolactin induced protein Canis lupus familiaris 163-166
10640427-0 2000 Retinoic acid-induced blr1 expression promotes ERK2 activation and cell differentiation in HL-60 cells. Tretinoin 0-13 C-X-C motif chemokine receptor 5 Homo sapiens 22-26
10646501-0 2000 Induction of matrix metalloproteinase MMP-9 (92-kDa gelatinase) by retinoic acid in human neuroblastoma SKNBE cells: relevance to neuronal differentiation. Tretinoin 67-80 matrix metallopeptidase 9 Homo sapiens 38-43
10634804-10 2000 Vessel sections exhibited significantly more alpha-actin and desmin immunostaining (P=0.01) in the atRA-treated group. Tretinoin 99-103 desmin Oryctolagus cuniculus 61-67
10630309-4 2000 Phorbol 12-myristate 13-acetate and all-trans-retinoic acid, which induce differentiation in U-937 cells, up-regulated CD11b (MAC1 alpha-integrin) and CD82 and down-regulated CD71 (transferrin receptor) in a time- and dose-dependent manner. Tretinoin 36-59 integrin subunit alpha M Homo sapiens 119-124
10630309-4 2000 Phorbol 12-myristate 13-acetate and all-trans-retinoic acid, which induce differentiation in U-937 cells, up-regulated CD11b (MAC1 alpha-integrin) and CD82 and down-regulated CD71 (transferrin receptor) in a time- and dose-dependent manner. Tretinoin 36-59 integrin subunit alpha M Homo sapiens 126-136
10630309-4 2000 Phorbol 12-myristate 13-acetate and all-trans-retinoic acid, which induce differentiation in U-937 cells, up-regulated CD11b (MAC1 alpha-integrin) and CD82 and down-regulated CD71 (transferrin receptor) in a time- and dose-dependent manner. Tretinoin 36-59 CD82 molecule Homo sapiens 151-155
10831072-7 2000 Oral treatment of animals with all-trans-retinoic acid for one and two days induced a significant decrease of FGF-BP protein in tissues from stomach, eye and lung suggesting that regulation of FGF-BP can be one effector mechanism through which retinoids affect normal and pathological processes. Tretinoin 31-54 fibroblast growth factor binding protein 1 Rattus norvegicus 110-116
10831072-7 2000 Oral treatment of animals with all-trans-retinoic acid for one and two days induced a significant decrease of FGF-BP protein in tissues from stomach, eye and lung suggesting that regulation of FGF-BP can be one effector mechanism through which retinoids affect normal and pathological processes. Tretinoin 31-54 fibroblast growth factor binding protein 1 Rattus norvegicus 193-199
11595822-3 2000 However, VDR/RXR heterodimers bind in a transcriptionally unproductive manner and without a defined polarity on certain RA response elements, and under these circumstances vitamin D inhibits the response to RA. Tretinoin 207-209 vitamin D receptor Homo sapiens 9-12
11595822-3 2000 However, VDR/RXR heterodimers bind in a transcriptionally unproductive manner and without a defined polarity on certain RA response elements, and under these circumstances vitamin D inhibits the response to RA. Tretinoin 207-209 retinoid X receptor alpha Homo sapiens 13-16
10634605-1 2000 PURPOSE: To study effects of depletion of retinoic acid on expression of the mucins ASGP (rMuc4), rMuc5AC, and rMuc1, by the corneal and conjunctival epithelia of the rat. Tretinoin 42-55 mucin 5AC, oligomeric mucus/gel-forming Rattus norvegicus 98-105
10634605-1 2000 PURPOSE: To study effects of depletion of retinoic acid on expression of the mucins ASGP (rMuc4), rMuc5AC, and rMuc1, by the corneal and conjunctival epithelia of the rat. Tretinoin 42-55 mucin 1, cell surface associated Rattus norvegicus 111-116
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 188-201 retinoid X receptor alpha Homo sapiens 45-48
10637480-1 2000 Retinoic acid receptor (RA) heterodimer (RAR/RXR) activities have been shown to be repressed by transcriptional co-repressor, SMRT/N-CoR, in the absence of the ligand while upon all-trans retionic acid (ATRA) treatment, SMRT/N-CoR is dissociated from RARalpha leading to gene expression by the recruitment of transcriptional co-activators to the transcriptional complex. Tretinoin 203-207 retinoid X receptor alpha Homo sapiens 45-48
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 zinc finger and BTB domain containing 16 Homo sapiens 124-129
10637480-2 2000 The difference in response to ATRA therapy between acute promyelocytic leukemia (APL) patients with PML-RARalpha fusion and PLZF-RARalpha fusion has recently been found to be partially due to the strong association of the transcriptional co-repressor, SMRT/N-CoR, with PLZF domain. Tretinoin 30-34 zinc finger and BTB domain containing 16 Homo sapiens 124-128
10572073-4 1999 Thus, BSAP/Pax5A was constitutively expressed in the multipotent EML cell line, which can be directed toward the myeloid lineage by culture with interleukin-3 (IL-3) and retinoic acid. Tretinoin 170-183 paired box 5 Homo sapiens 6-10
10572073-5 1999 EML cells expressing BSAP/Pax5A successfully acquired the myeloid lineage markers CD11b and F4/80 in response to IL-3 and retinoic acid, indicating differentiation to the myeloid lineage. Tretinoin 122-135 paired box 5 Homo sapiens 21-25
10572073-5 1999 EML cells expressing BSAP/Pax5A successfully acquired the myeloid lineage markers CD11b and F4/80 in response to IL-3 and retinoic acid, indicating differentiation to the myeloid lineage. Tretinoin 122-135 integrin subunit alpha M Homo sapiens 82-87
10633866-0 1999 Retinoic acid is essential for Shh/Hoxd signaling during rat limb outgrowth but not for limb initiation. Tretinoin 0-13 sonic hedgehog signaling molecule Rattus norvegicus 31-34
10559481-2 1999 In contrast to Rarg mutants, retinoic acid (RA) treatment on embryonic day 10.5 of Hoxd4 single or Hoxd4;Rarg double mutants does not rescue normal development of C2. Tretinoin 29-42 homeobox D4 Mus musculus 83-88
10551880-6 1999 In addition, differentiation of P19 cells with retinoic acid leads to the specific loss of expression of the 71- and 72-kDa Numb proteins, suggesting that the expression of certain forms of Numb protein is regulated in a cell type-specific manner. Tretinoin 47-60 NUMB endocytic adaptor protein Homo sapiens 124-128
10551880-6 1999 In addition, differentiation of P19 cells with retinoic acid leads to the specific loss of expression of the 71- and 72-kDa Numb proteins, suggesting that the expression of certain forms of Numb protein is regulated in a cell type-specific manner. Tretinoin 47-60 NUMB endocytic adaptor protein Homo sapiens 190-194
10509049-0 1999 All-trans retinoic acid (ATRA) potentiates the in vitro inhibitory effects of IFN-alpha in parental (32D) and p210-bcr/abl transfected (LG7) murine myeloid cell lines. Tretinoin 0-23 interferon alpha Mus musculus 78-87
10509049-0 1999 All-trans retinoic acid (ATRA) potentiates the in vitro inhibitory effects of IFN-alpha in parental (32D) and p210-bcr/abl transfected (LG7) murine myeloid cell lines. Tretinoin 0-23 envoplakin Mus musculus 110-114
10509049-0 1999 All-trans retinoic acid (ATRA) potentiates the in vitro inhibitory effects of IFN-alpha in parental (32D) and p210-bcr/abl transfected (LG7) murine myeloid cell lines. Tretinoin 25-29 interferon alpha Mus musculus 78-87
10509049-0 1999 All-trans retinoic acid (ATRA) potentiates the in vitro inhibitory effects of IFN-alpha in parental (32D) and p210-bcr/abl transfected (LG7) murine myeloid cell lines. Tretinoin 25-29 envoplakin Mus musculus 110-114
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 89-102 retinoid X receptor alpha Homo sapiens 121-124
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 89-102 cellular retinoic acid binding protein 2 Homo sapiens 251-258
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 104-106 retinoid X receptor alpha Homo sapiens 121-124
10490651-1 1999 Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). Tretinoin 104-106 cellular retinoic acid binding protein 2 Homo sapiens 251-258
10935488-4 1999 Retinoid X receptor alpha (RXRalpha), a 9-cis-retinoic acid stimulated (9-cis-RA) heterodimeric partner of PPARgamma, was also co-expressed in all TCCa tissues and cell lines. Tretinoin 72-80 retinoid X receptor alpha Homo sapiens 0-25
10935488-4 1999 Retinoid X receptor alpha (RXRalpha), a 9-cis-retinoic acid stimulated (9-cis-RA) heterodimeric partner of PPARgamma, was also co-expressed in all TCCa tissues and cell lines. Tretinoin 72-80 retinoid X receptor alpha Homo sapiens 27-35
10526130-0 1999 pRb phosphorylation is regulated differentially by cyclin-dependent kinase (Cdk) 2 and Cdk4 in retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 95-108 RB transcriptional corepressor 1 Mus musculus 0-3
10526130-0 1999 pRb phosphorylation is regulated differentially by cyclin-dependent kinase (Cdk) 2 and Cdk4 in retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 95-108 cyclin-dependent kinase 2 Mus musculus 51-82
10526130-4 1999 In this study, the phosphorylation of pRb during retinoic acid (RA)-induced neuronal differentiation of P19 cells was examined using site-specific antibodies against pRb phosphorylated at Ser601, Ser605 and Ser773. Tretinoin 49-62 RB transcriptional corepressor 1 Mus musculus 38-41
10526130-4 1999 In this study, the phosphorylation of pRb during retinoic acid (RA)-induced neuronal differentiation of P19 cells was examined using site-specific antibodies against pRb phosphorylated at Ser601, Ser605 and Ser773. Tretinoin 64-66 RB transcriptional corepressor 1 Mus musculus 38-41
10526130-8 1999 In contrast, Cdk2 kinase activity and the phosphorylation of Ser605 were observed in undifferentiated cells as well as in RA-treated cells. Tretinoin 122-124 cyclin-dependent kinase 2 Mus musculus 13-17
11751425-6 2001 Following all-trans retinoic acid (RA) treatment, RARalpha- and RARgamma-transduced cell lines exhibit a progressive, dose-dependent growth inhibition relative to the control LXSN cell lines. Tretinoin 35-37 retinoic acid receptor, alpha Mus musculus 50-72
11751425-7 2001 Further characterization of RAR-transduced cells following RA treatment reveals that both RARalpha and RARgamma cause a decrease in S-phase population, while only RARalpha causes a simultaneous G(0)/G(1) block as evidenced by reduced [(3)H]-thymidine incorporation and flow cytometric analysis of DNA content. Tretinoin 28-30 retinoic acid receptor, alpha Mus musculus 90-98
11751425-7 2001 Further characterization of RAR-transduced cells following RA treatment reveals that both RARalpha and RARgamma cause a decrease in S-phase population, while only RARalpha causes a simultaneous G(0)/G(1) block as evidenced by reduced [(3)H]-thymidine incorporation and flow cytometric analysis of DNA content. Tretinoin 28-30 retinoic acid receptor, gamma Mus musculus 103-111
11751425-8 2001 Following RA treatment, both receptors cause an early, transient increase in the cyclin-dependent kinase inhibitor (CDKI) p21 proteins, while only RARalpha causes a simultaneous sharp, brief increase in the CDKI p16 protein. Tretinoin 10-12 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 122-125
11753676-5 2001 In addition, RA treatment of CA-OV3 cells resulted in a significant decrease in hyperphosphorylated RB and RB-2/p130 and corresponding significant increases in the levels of hypophosphorylated and/or partially phosphorylated RB-2/p130 protein and hypophosphorylated RB. Tretinoin 13-15 RB transcriptional corepressor like 2 Homo sapiens 107-111
11753676-5 2001 In addition, RA treatment of CA-OV3 cells resulted in a significant decrease in hyperphosphorylated RB and RB-2/p130 and corresponding significant increases in the levels of hypophosphorylated and/or partially phosphorylated RB-2/p130 protein and hypophosphorylated RB. Tretinoin 13-15 RB transcriptional corepressor like 2 Homo sapiens 112-116
11753676-5 2001 In addition, RA treatment of CA-OV3 cells resulted in a significant decrease in hyperphosphorylated RB and RB-2/p130 and corresponding significant increases in the levels of hypophosphorylated and/or partially phosphorylated RB-2/p130 protein and hypophosphorylated RB. Tretinoin 13-15 RB transcriptional corepressor like 2 Homo sapiens 225-229
11753676-5 2001 In addition, RA treatment of CA-OV3 cells resulted in a significant decrease in hyperphosphorylated RB and RB-2/p130 and corresponding significant increases in the levels of hypophosphorylated and/or partially phosphorylated RB-2/p130 protein and hypophosphorylated RB. Tretinoin 13-15 RB transcriptional corepressor like 2 Homo sapiens 230-234
11602619-2 2001 We found that retinoic acid inhibits the transcriptional activity of AP-1 and the orphan receptors Nur77 and Nurr1 in ACTH-secreting tumor cells. Tretinoin 14-27 nuclear receptor subfamily 4 group A member 2 Homo sapiens 109-114
11676881-1 2001 OBJECTIVE: To study the effects of retinoic acid on regulation of expressions of cyclin-dependent kinase inhibitors, i.e. p16, p21 and p27 in cultured rat hepatic stellate cells. Tretinoin 35-48 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 122-125
11676881-1 2001 OBJECTIVE: To study the effects of retinoic acid on regulation of expressions of cyclin-dependent kinase inhibitors, i.e. p16, p21 and p27 in cultured rat hepatic stellate cells. Tretinoin 35-48 KRAS proto-oncogene, GTPase Rattus norvegicus 127-130
11507765-0 2001 Expression and regulation of the retinoic acid synthetic enzyme RALDH-2 in the embryonic chicken wing. Tretinoin 33-46 aldehyde dehydrogenase 1 family member A2 Gallus gallus 64-71
11507765-1 2001 Retinaldehyde dehydrogenase type 2 (RALDH-2) is a major retinoic acid (RA) generating enzyme in the embryo. Tretinoin 56-69 aldehyde dehydrogenase 1 family member A2 Gallus gallus 0-34
11507765-1 2001 Retinaldehyde dehydrogenase type 2 (RALDH-2) is a major retinoic acid (RA) generating enzyme in the embryo. Tretinoin 56-69 aldehyde dehydrogenase 1 family member A2 Gallus gallus 36-43
11507765-1 2001 Retinaldehyde dehydrogenase type 2 (RALDH-2) is a major retinoic acid (RA) generating enzyme in the embryo. Tretinoin 36-38 aldehyde dehydrogenase 1 family member A2 Gallus gallus 0-34
11555630-7 2001 During retinoic acid-induced neurogenesis of frataxin-deficient cells there was a striking rise in cell death, while cell division remained unaffected. Tretinoin 7-20 frataxin Mus musculus 45-53
11675954-8 2001 In contrast, ATRA strongly suppressed the pRb kinase activities of the cyclin-dependent kinases (Cdks) Cdk4, Cdk6, and Cdk2. Tretinoin 13-17 RB transcriptional corepressor 1 Rattus norvegicus 42-45
11402055-0 2001 Disassociation of MAPK activation and c-Fos expression in F9 embryonic carcinoma cells following retinoic acid-induced endoderm differentiation. Tretinoin 97-110 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43
11402055-5 2001 We found that retinoic acid treatment inhibited the phosphorylation of Elk-1, a target of activated MAPK required for c-Fos transcription. Tretinoin 14-27 ETS transcription factor ELK1 Homo sapiens 71-76
11402055-5 2001 We found that retinoic acid treatment inhibited the phosphorylation of Elk-1, a target of activated MAPK required for c-Fos transcription. Tretinoin 14-27 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-123
11402055-8 2001 Thus, we conclude that retinoic acid treatment to induce F9 cell differentiation uncouples Ras/MAPK activation from c-Fos expression by reduction of Elk-1 phosphorylation through a mechanism not involving the activation of phosphoprotein phosphatase 2B. Tretinoin 23-36 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-121
11402055-8 2001 Thus, we conclude that retinoic acid treatment to induce F9 cell differentiation uncouples Ras/MAPK activation from c-Fos expression by reduction of Elk-1 phosphorylation through a mechanism not involving the activation of phosphoprotein phosphatase 2B. Tretinoin 23-36 ETS transcription factor ELK1 Homo sapiens 149-154
11397803-3 2001 Differential display analysis of retinal pigment epithelial (ARPE-19) cells identified SCD as a gene regulated by retinoic acid. Tretinoin 114-127 stearoyl-CoA desaturase Homo sapiens 87-90
11397803-7 2001 These results indicate the involvement of RAR alpha in the induction of SCD expression by retinoic acid. Tretinoin 90-103 stearoyl-CoA desaturase Homo sapiens 72-75
11397803-10 2001 Thus, SCD expression in retinal pigment epithelial cells is regulated by retinoic acid, and the regulation appears to be mediated through RAR and RXR. Tretinoin 73-86 stearoyl-CoA desaturase Homo sapiens 6-9
11470752-10 2001 Moreover, RA supplementation at both doses markedly suppressed the ethanol-induced PCNA-positive hepatocytes by approximately 80%. Tretinoin 10-12 proliferating cell nuclear antigen Rattus norvegicus 83-87
11683493-0 2001 Retinoic acid causes MEK-dependent RAF phosphorylation through RARalpha plus RXR activation in HL-60 cells. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 77-80
11591891-6 2001 Immunocytochemistry was performed to assess variation of the intracellular distribution of RIZ protein on all- trans-retinoic acid treatment. Tretinoin 111-130 PR/SET domain 2 Homo sapiens 91-94
11591891-8 2001 RESULTS: Treatment with retinoic acid induced a selective expression of RIZ1 in HL60 cell line. Tretinoin 24-37 PR/SET domain 2 Homo sapiens 72-76
11591891-15 2001 CONCLUSIONS: The correlation between the selective expression of RIZ1 induced by retinoic acid, 12-O-tetradecanoyl-phorbol-13-acetate, or 1,25-dihydroxyvitamin D(3) and differentiation suggested that RIZ protein was involved in myeloid cell differentiation induced by these agents. Tretinoin 81-94 PR/SET domain 2 Homo sapiens 65-69
11591891-15 2001 CONCLUSIONS: The correlation between the selective expression of RIZ1 induced by retinoic acid, 12-O-tetradecanoyl-phorbol-13-acetate, or 1,25-dihydroxyvitamin D(3) and differentiation suggested that RIZ protein was involved in myeloid cell differentiation induced by these agents. Tretinoin 81-94 PR/SET domain 2 Homo sapiens 65-68
11414696-2 2001 In this report, we have shown that N-cadherin mRNA and protein were increased rapidly in retinoic acid (RA)-induced neuronal differentiation of embryonic carcinoma P19 cells. Tretinoin 89-102 cadherin 2 Homo sapiens 35-45
11414696-2 2001 In this report, we have shown that N-cadherin mRNA and protein were increased rapidly in retinoic acid (RA)-induced neuronal differentiation of embryonic carcinoma P19 cells. Tretinoin 104-106 cadherin 2 Homo sapiens 35-45
11460014-3 2001 We have attempted to determine whether ATRA is effective against DIC in rat models induced by tissue factor (TF) or lipopolysaccharide (LPS), because the anticoagulant effect of ATRA has been considered to induce thrombomodulin upregulation and TF downregulation on endothelial cells as well as on APL cells. Tretinoin 39-43 coagulation factor III, tissue factor Rattus norvegicus 94-107
11460014-3 2001 We have attempted to determine whether ATRA is effective against DIC in rat models induced by tissue factor (TF) or lipopolysaccharide (LPS), because the anticoagulant effect of ATRA has been considered to induce thrombomodulin upregulation and TF downregulation on endothelial cells as well as on APL cells. Tretinoin 39-43 coagulation factor III, tissue factor Rattus norvegicus 109-111
11342454-6 2001 By contrast, STI571 is unique among c-Abl-specific tyrosine kinase inhibitors in modulating the pharmacologic activity of ATRA. Tretinoin 122-126 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 36-41
11340642-3 2001 Here we show that brief treatment with retinoic acid (RA) rendered the human neuroblastoma lines SY5Y, NGP, SMS-KCNR, and SK-N-SH dependent on brain-derived neurotrophic factor (BDNF) for survival. Tretinoin 39-52 brain derived neurotrophic factor Homo sapiens 143-176
11340642-3 2001 Here we show that brief treatment with retinoic acid (RA) rendered the human neuroblastoma lines SY5Y, NGP, SMS-KCNR, and SK-N-SH dependent on brain-derived neurotrophic factor (BDNF) for survival. Tretinoin 39-52 brain derived neurotrophic factor Homo sapiens 178-182
11340642-3 2001 Here we show that brief treatment with retinoic acid (RA) rendered the human neuroblastoma lines SY5Y, NGP, SMS-KCNR, and SK-N-SH dependent on brain-derived neurotrophic factor (BDNF) for survival. Tretinoin 54-56 brain derived neurotrophic factor Homo sapiens 143-176
11340642-3 2001 Here we show that brief treatment with retinoic acid (RA) rendered the human neuroblastoma lines SY5Y, NGP, SMS-KCNR, and SK-N-SH dependent on brain-derived neurotrophic factor (BDNF) for survival. Tretinoin 54-56 brain derived neurotrophic factor Homo sapiens 178-182
11369496-2 2001 In this study, we determined the effect of RA on the mRNA and protein levels of the Cu-,Zn-superoxide dismutase (SOD-1) and Mn-superoxide dismutase (SOD-2) during staurosporine-induced apoptosis in primary cultures from neonatal rat hippocampus. Tretinoin 43-45 superoxide dismutase 2 Rattus norvegicus 149-154
11369496-7 2001 Compared with staurosporine-exposed controls, RA (10 nM)-treated cultures showed a significant increase in neuronal survival, a reduced neuronal ROS content, and enhanced protein levels of SOD-1 and SOD-2 24 and 48 h after the start of the exposure to staurosporine. Tretinoin 46-48 superoxide dismutase 2 Rattus norvegicus 199-204
11369496-8 2001 The results suggest that RA reduced staurosporine-induced oxidative stress and apoptosis by preventing the decrease in the protein levels of SOD-1 and SOD-2, and thus supported the antioxidant defense system. Tretinoin 25-27 superoxide dismutase 2 Rattus norvegicus 151-156
11296268-4 2001 A 15- to 20-fold overexpression of 5-MCDG results in the specific demethylation of a stably integrated ecdysone-retinoic acid responsive enhancer-promoter linked to a beta-galactosidase reporter gene. Tretinoin 112-125 thymine DNA glycosylase Gallus gallus 35-41
11278809-0 2001 Selective roles of retinoic acid receptor and retinoid x receptor in the suppression of apoptosis by all-trans-retinoic acid. Tretinoin 101-124 retinoid X receptor alpha Homo sapiens 46-65
11278809-2 2001 We previously reported that all-trans-retinoic acid (t-RA) protected mesangial cells from H(2)O(2)-triggered apoptosis by suppressing the activator protein 1 (AP-1) pathway. Tretinoin 28-51 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-157
11278809-2 2001 We previously reported that all-trans-retinoic acid (t-RA) protected mesangial cells from H(2)O(2)-triggered apoptosis by suppressing the activator protein 1 (AP-1) pathway. Tretinoin 28-51 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 159-163
11278809-4 2001 In this report, we investigated the involvement of retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H(2)O(2)-exposed cells. Tretinoin 141-145 retinoid X receptor alpha Homo sapiens 84-103
11278809-4 2001 In this report, we investigated the involvement of retinoic acid receptor (RAR) and retinoid X receptor (RXR) in the antiapoptotic effect of t-RA in H(2)O(2)-exposed cells. Tretinoin 141-145 retinoid X receptor alpha Homo sapiens 105-108
11278809-6 2001 Similarly, transient transfection with a dominant-negative mutant of RAR or a dominant-negative RXR diminished the antiapoptotic effect of t-RA. Tretinoin 139-143 retinoid X receptor alpha Homo sapiens 96-99
11278809-10 2001 Furthermore, suppression of JNK activation by t-RA was observed even in the presence of RAR and RXR antagonists. Tretinoin 46-50 retinoid X receptor alpha Homo sapiens 96-99
11318877-6 2001 Two lines of evidence suggested functions of p48 in neurogenesis: (i) expression of p48 was induced in P19 cells when they committed to neural fate upon retinoic acid treatment, and (ii) p48 over-expressed in Xenopus embryos repressed the development of neuronal precursors. Tretinoin 153-166 cyclin-dependent kinase inhibitor 2D S homeolog Xenopus laevis 103-106
11259452-3 2001 We have previously identified a new gene, BRE, that is responsive to DNA damage and retinoic acid. Tretinoin 84-97 BRISC and BRCA1 A complex member 2 Homo sapiens 42-45
11471571-0 2001 All trans-retinoic acid selectively down-regulates matrix metalloproteinase-9 (MMP-9) and up-regulates tissue inhibitor of metalloproteinase-1 (TIMP-1) in human bronchoalveolar lavage cells. Tretinoin 4-23 matrix metallopeptidase 9 Homo sapiens 51-77
11471571-0 2001 All trans-retinoic acid selectively down-regulates matrix metalloproteinase-9 (MMP-9) and up-regulates tissue inhibitor of metalloproteinase-1 (TIMP-1) in human bronchoalveolar lavage cells. Tretinoin 4-23 matrix metallopeptidase 9 Homo sapiens 79-84
11471571-4 2001 We therefore have analyzed the effects of free and liposomal all trans-retinoic acid (ATRA) on the expression of MMP-9 and TIMP-1 in bronchoalveolar lavage (BAL) cells from patients with COPD and patients with other lung diseases. Tretinoin 65-84 matrix metallopeptidase 9 Homo sapiens 113-118
11471571-4 2001 We therefore have analyzed the effects of free and liposomal all trans-retinoic acid (ATRA) on the expression of MMP-9 and TIMP-1 in bronchoalveolar lavage (BAL) cells from patients with COPD and patients with other lung diseases. Tretinoin 86-90 matrix metallopeptidase 9 Homo sapiens 113-118
11471571-7 2001 RESULTS: We demonstrate that either liposomal or free ATRA selectively down-regulates MMP-9 and up-regulates TIMP-1. Tretinoin 54-58 matrix metallopeptidase 9 Homo sapiens 86-91
11230985-12 2001 Finally, protein expression and activity of the matrix metalloproteinases MMP-2 and MMP-9 were inhibited significantly by atRA. Tretinoin 122-126 matrix metallopeptidase 9 Homo sapiens 84-89
11180971-9 2001 Moreover, the expression of TRP-2 mRNA was induced by retinoic acid in retinoblastoma cells but not noticeably affected by forskolin, a cAMP-elevating reagent, whereas in melanoma cells its expression was induced by forskolin but not by retinoic acid. Tretinoin 54-67 dopachrome tautomerase Homo sapiens 28-33
11261782-0 2001 Retinoic acid up-regulates myeloid ICAM-3 expression and function in a cell-specific fashion--evidence for retinoid signaling pathways in the mast cell lineage. Tretinoin 0-13 intercellular adhesion molecule 3 Homo sapiens 35-41
11261782-1 2001 Investigation of mast cell responsiveness toward retinoic acid (RA) revealed selective promotion of ICAM-3 expression in the human mast cell line HMC-1. Tretinoin 49-62 intercellular adhesion molecule 3 Homo sapiens 100-106
11261782-1 2001 Investigation of mast cell responsiveness toward retinoic acid (RA) revealed selective promotion of ICAM-3 expression in the human mast cell line HMC-1. Tretinoin 64-66 intercellular adhesion molecule 3 Homo sapiens 100-106
11261782-5 2001 RA-mediated effects on ICAM-1 expression, studied in parallel, were clearly distinct from those on ICAM-3. Tretinoin 0-2 intercellular adhesion molecule 1 Homo sapiens 23-29
11261782-7 2001 RAR beta, not expressed at baseline, was induced by RA in a fashion obviously correlating with ICAM-3 up-regulation. Tretinoin 0-2 intercellular adhesion molecule 3 Homo sapiens 95-101
11261782-8 2001 Increased ICAM-3 expression was of functional significance, such that processes stimulated or co-stimulated via ICAM-3 (homotypic aggregation, IL-8 secretion) were clearly enhanced upon RA pretreatment, suggesting that RA may contribute via hitherto unrecognized pathways to immune function and host defense. Tretinoin 186-188 intercellular adhesion molecule 3 Homo sapiens 10-16
11261782-8 2001 Increased ICAM-3 expression was of functional significance, such that processes stimulated or co-stimulated via ICAM-3 (homotypic aggregation, IL-8 secretion) were clearly enhanced upon RA pretreatment, suggesting that RA may contribute via hitherto unrecognized pathways to immune function and host defense. Tretinoin 186-188 intercellular adhesion molecule 3 Homo sapiens 112-118
11261782-8 2001 Increased ICAM-3 expression was of functional significance, such that processes stimulated or co-stimulated via ICAM-3 (homotypic aggregation, IL-8 secretion) were clearly enhanced upon RA pretreatment, suggesting that RA may contribute via hitherto unrecognized pathways to immune function and host defense. Tretinoin 219-221 intercellular adhesion molecule 3 Homo sapiens 10-16
11261782-8 2001 Increased ICAM-3 expression was of functional significance, such that processes stimulated or co-stimulated via ICAM-3 (homotypic aggregation, IL-8 secretion) were clearly enhanced upon RA pretreatment, suggesting that RA may contribute via hitherto unrecognized pathways to immune function and host defense. Tretinoin 219-221 intercellular adhesion molecule 3 Homo sapiens 112-118
11222649-10 2001 A role of RA in KOR gene regulation during developmental stages was discussed. Tretinoin 10-12 opioid receptor, kappa 1 Mus musculus 16-19
11060298-9 2001 Altogether, our findings demonstrate that the Rac1/p38 MAP kinase pathway is activated in a RA-dependent manner and exhibits negative regulatory effects on the induction of differentiation. Tretinoin 92-94 Rac family small GTPase 1 Homo sapiens 46-50
11234892-8 2001 A 24-h exposure to ATRA increased the expression of RAR alpha, RAR beta, RAR gamma, and RXR alpha in 46%, 77%, 30%, and 38% of the samples, respectively. Tretinoin 19-23 retinoid X receptor alpha Homo sapiens 88-97
11172606-5 2001 We determined that RA mediated inhibition of MMP-9 expression was dependent on ECM attachment in RA sensitive but not RA resistant human carcinoma lines. Tretinoin 19-21 matrix metallopeptidase 9 Homo sapiens 45-50
11172606-5 2001 We determined that RA mediated inhibition of MMP-9 expression was dependent on ECM attachment in RA sensitive but not RA resistant human carcinoma lines. Tretinoin 97-99 matrix metallopeptidase 9 Homo sapiens 45-50
11172606-11 2001 The results of these experiments indicate that induction of hypophosphorylated ets-1 as the result of RA and ECM mediated decreases in ERK1 activity represents a novel mechanism by which RA regulates MMP-9 gene expression. Tretinoin 102-104 matrix metallopeptidase 9 Homo sapiens 200-205
11172606-11 2001 The results of these experiments indicate that induction of hypophosphorylated ets-1 as the result of RA and ECM mediated decreases in ERK1 activity represents a novel mechanism by which RA regulates MMP-9 gene expression. Tretinoin 187-189 matrix metallopeptidase 9 Homo sapiens 200-205
10526130-9 1999 These observations suggest that Cdk2 and Cdk4 may phosphorylate different sites of pRb in vivo and that the two sites of pRb examined here are newly phosphorylated during RA-induced neuronal differentiation in P19 cells. Tretinoin 171-173 cyclin-dependent kinase 2 Mus musculus 32-36
10526130-9 1999 These observations suggest that Cdk2 and Cdk4 may phosphorylate different sites of pRb in vivo and that the two sites of pRb examined here are newly phosphorylated during RA-induced neuronal differentiation in P19 cells. Tretinoin 171-173 RB transcriptional corepressor 1 Mus musculus 83-86
10526130-9 1999 These observations suggest that Cdk2 and Cdk4 may phosphorylate different sites of pRb in vivo and that the two sites of pRb examined here are newly phosphorylated during RA-induced neuronal differentiation in P19 cells. Tretinoin 171-173 RB transcriptional corepressor 1 Mus musculus 121-124
10479451-6 1999 (2) Both TH and RA induce a transcriptionally dependent antigenic change in purified precursor cells within 2-4 h. (3) Unexpectedly, even before they differentiate, the precursor cells express ceramide galactosyltransferase (CGT), the enzyme that catalyzes the final step in the synthesis of galactocerebroside, an early marker of oligodendrocyte differentiation. Tretinoin 16-18 UDP glycosyltransferase 8 Homo sapiens 193-223
10479451-6 1999 (2) Both TH and RA induce a transcriptionally dependent antigenic change in purified precursor cells within 2-4 h. (3) Unexpectedly, even before they differentiate, the precursor cells express ceramide galactosyltransferase (CGT), the enzyme that catalyzes the final step in the synthesis of galactocerebroside, an early marker of oligodendrocyte differentiation. Tretinoin 16-18 UDP glycosyltransferase 8 Homo sapiens 225-228
10467405-7 1999 Additionally, we observed that while cyclin G expression is markedly reduced upon aggregate formation in embryonic carcinoma P19 cells, retrovirus-mediated over-expression of cyclin G enhances apoptotic cell death in aggregated P19 cells, and increases the extent of apoptosis caused by retinoic acid or serum starvation of these cells. Tretinoin 287-300 cyclin G1 Mus musculus 175-183
10446999-6 1999 VDR is functionally active in ATRA-treated Kasumi-1 cells because it efficiently heterodimerizes with retinoid X receptor, binds to a DR3-type vitamin D-responsive element, and activates the transcription of a vitamin D-responsive element-regulated reporter gene. Tretinoin 30-34 vitamin D receptor Homo sapiens 0-3
10446999-8 1999 The molecular mechanism by which ATRA increases the nuclear abundance of a functional VDR is still unknown, but our data clearly indicate that the M2 leukemic cell context is only permissive of monocytic differentiation. Tretinoin 33-37 vitamin D receptor Homo sapiens 86-89
10470856-3 1999 After retinoic acid (RA) treatment with aggregation, expression of Evi1 was detected during neural differentiation in P19 cells. Tretinoin 6-19 MDS1 and EVI1 complex locus Mus musculus 67-71
10470856-3 1999 After retinoic acid (RA) treatment with aggregation, expression of Evi1 was detected during neural differentiation in P19 cells. Tretinoin 21-23 MDS1 and EVI1 complex locus Mus musculus 67-71
10470856-5 1999 Enforced expression of Evi1 in P19 cells induced neuron-specific microtubule-associated protein-2 microtubule-associated protein-2 and TrkA expression in the absence of RA under monolayer culture. Tretinoin 169-171 MDS1 and EVI1 complex locus Mus musculus 23-27
10470856-6 1999 After incubation with RA with aggregation, the Evi1 clones expressed microtubule-associated protein-2 continuously but did not express glial fibrillary acidic protein as an astrocyte marker protein until 12 days of culture. Tretinoin 22-24 MDS1 and EVI1 complex locus Mus musculus 47-51
10470856-7 1999 Thus, the overexpression of Evi1 leads to neural differentiation of P19 cells and blocks further differentiation into astrocytes by RA treatment, suggesting that Evi1 might be an important transcription factor for regulation of early neuroectodermal differentiation. Tretinoin 132-134 MDS1 and EVI1 complex locus Mus musculus 28-32
10450744-7 1999 In various cell lines, including those derived from APL, RA induces directly the expression of two transcription factors, Stat1 and IRF-1 which play central roles in the IFN signal transduction. Tretinoin 57-59 signal transducer and activator of transcription 1 Homo sapiens 122-127
10450755-4 1999 ATRA augmented PB induction of the myelomonocytic marker CD11b at all doses of ATRA tested (0.0025-1 microM). Tretinoin 0-4 integrin subunit alpha M Homo sapiens 57-62
10450755-5 1999 Although ATRA did not significantly affect the ED50 of PB, the combination of ATRA (1 microM) and PB (0.5 mM) augmented PB-induced CD11b expression eight-fold. Tretinoin 78-82 integrin subunit alpha M Homo sapiens 131-136
10450755-8 1999 ATRA combined synergistically with PB to augment CD11b expression and inhibit colony formation. Tretinoin 0-4 integrin subunit alpha M Homo sapiens 49-54
10397747-0 1999 Overexpression of wild-type retinoic acid receptor alpha (RARalpha) recapitulates retinoic acid-sensitive transformation of primary myeloid progenitors by acute promyelocytic leukemia RARalpha-fusion genes. Tretinoin 28-41 retinoic acid receptor, alpha Mus musculus 58-66
11165018-12 2001 The ability of some these SDRs to access retinol bound with CRBP provides specificity in retinoid metabolism and allows retinoic acid biosynthesis and retinol esterification to continue, as CRBP protects retinol from the general cellular milieu. Tretinoin 120-133 retinol binding protein 1 Rattus norvegicus 60-64
11165018-12 2001 The ability of some these SDRs to access retinol bound with CRBP provides specificity in retinoid metabolism and allows retinoic acid biosynthesis and retinol esterification to continue, as CRBP protects retinol from the general cellular milieu. Tretinoin 120-133 retinol binding protein 1 Rattus norvegicus 190-194
11285139-2 2001 Differentiation requires the action of the receptors for all trans, and 9cis-retinoic acid (RAR and RXR, respectively) and is accompanied by growth inhibition, changes in cell morphology, increased apoptosis, proteolytic degradation of the RARgamma2 receptor, and induction of target genes. Tretinoin 77-90 Rab40B, member RAS oncogene family Mus musculus 92-95
10397747-0 1999 Overexpression of wild-type retinoic acid receptor alpha (RARalpha) recapitulates retinoic acid-sensitive transformation of primary myeloid progenitors by acute promyelocytic leukemia RARalpha-fusion genes. Tretinoin 28-41 retinoic acid receptor, alpha Mus musculus 184-192
10413451-1 1999 The modulation of herg gene and HERG currents (I(HERG)) was studied in SH-SY5Y neuroblastoma (NB) cells treated with all-trans-retinoic acid (RA) in the absence or presence of the neurotrophin brain-derived neurotrophic factor (BDNF). Tretinoin 142-144 potassium voltage-gated channel subfamily H member 2 Homo sapiens 18-22
10397747-7 1999 The cellular responses to retinoic acid were accompanied by a sharp decrease in the amount of the RARalpha-fusion proteins expressed in the cells. Tretinoin 26-39 retinoic acid receptor, alpha Mus musculus 98-106
10397747-8 1999 Our findings suggest that the oncogenicity of RARalpha-fusion proteins results from their nature to behave as unliganded RARalpha in the presence of physiological concentrations of retinoic acid. Tretinoin 181-194 retinoic acid receptor, alpha Mus musculus 46-54
10398536-0 1999 Retinoic acid biosynthetic enzyme ALDH1 localizes in a subset of retinoid-dependent tissues during xenopus development. Tretinoin 0-13 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 34-39
10398536-8 1999 These findings are consistent with ALDH1 contributing to retinoic acid synthesis needed for development of certain head structures (olfactory placodes, dorsal retina, lens placode) and certain trunk structures (pronephros and pronephric duct). Tretinoin 57-70 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 35-40
11133157-3 2001 mdk2 is expressed shortly after the onset of gastrulation in the presumptive neural plate cells of the epiblast, and this expression is enhanced by exogenous retinoic acid. Tretinoin 158-171 midkine b Danio rerio 0-4
11211936-8 2001 Previous studies showed that ectopic expression of blr1 also caused increased MAPK activation, in particular ERK2, and subsequently accelerated RA-induced differentiation and G1/G0 growth arrest. Tretinoin 144-146 C-X-C motif chemokine receptor 5 Homo sapiens 51-55
10413451-3 1999 Differentiation of NB cells was accompanied by an increase in herg gene transcription, which attained its maximum after 6 days of treatment with RA and was not further increased by BDNF. Tretinoin 145-147 potassium voltage-gated channel subfamily H member 2 Homo sapiens 62-66
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 88-101 zinc finger and BTB domain containing 16 Homo sapiens 26-30
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 31-33 zinc finger and BTB domain containing 16 Homo sapiens 26-30
10413451-4 1999 This effect evidently reflected on HERG currents: In fact, RA produced an increase in HERG current density which was strongly potentiated by BDNF. Tretinoin 59-61 potassium voltage-gated channel subfamily H member 2 Homo sapiens 35-39
11104669-3 2000 Recent studies have shown that the expression of mDab2 is markedly up-regulated during the retinoic acid (RA)-induced differentiation of F9 cells, suggesting another role for mDab2 in cell differentiation [Cho, Lee and Park (1999) Mol. Tretinoin 91-104 disabled 2, mitogen-responsive phosphoprotein Mus musculus 49-54
10413451-4 1999 This effect evidently reflected on HERG currents: In fact, RA produced an increase in HERG current density which was strongly potentiated by BDNF. Tretinoin 59-61 potassium voltage-gated channel subfamily H member 2 Homo sapiens 86-90
11104669-3 2000 Recent studies have shown that the expression of mDab2 is markedly up-regulated during the retinoic acid (RA)-induced differentiation of F9 cells, suggesting another role for mDab2 in cell differentiation [Cho, Lee and Park (1999) Mol. Tretinoin 106-108 disabled 2, mitogen-responsive phosphoprotein Mus musculus 49-54
10357892-3 1999 RALDH-2-IR indicates dynamic and discrete patterns of retinoic acid synthesis in the embryo, particularly within the somitic mesoderm, lateral mesoderm, kidney, heart, and spinal motor neurons. Tretinoin 54-67 aldehyde dehydrogenase 1 family member A2 Gallus gallus 0-7
10413451-5 1999 Moreover, RA treatment affected the biophysical properties of I(HERG), inducing an increase in the deactivation time constant and a left shift of the activation curve. Tretinoin 10-12 potassium voltage-gated channel subfamily H member 2 Homo sapiens 64-68
10357892-10 1999 Motor neuronal expression of RALDH-2-IR is present in the growing axons as they extend to the periphery, indicating a potential role of retinoic acid in nerve influences on peripheral differentiation. Tretinoin 136-149 aldehyde dehydrogenase 1 family member A2 Gallus gallus 29-36
11104676-1 2000 Activation of mitogen-activated protein kinases (MAPKs), their upstream activators MAPK kinases (MAPKKs or MEKs) and induction of MKP-1 (CL100/3CH134) and MKP-3 (Pyst1/rVH6) dual-specificity MAPK phosphatases (MKPs) were studied in the mouse embryonic stem cell line P19 during the 7 day induction of neuronal differentiation triggered by aggregation and retinoic acid. Tretinoin 355-368 dual specificity phosphatase 1 Mus musculus 130-135
11104676-1 2000 Activation of mitogen-activated protein kinases (MAPKs), their upstream activators MAPK kinases (MAPKKs or MEKs) and induction of MKP-1 (CL100/3CH134) and MKP-3 (Pyst1/rVH6) dual-specificity MAPK phosphatases (MKPs) were studied in the mouse embryonic stem cell line P19 during the 7 day induction of neuronal differentiation triggered by aggregation and retinoic acid. Tretinoin 355-368 dual specificity phosphatase 6 Mus musculus 155-160
10432387-12 1999 ATRA also reduced nuclear levels of both subunits (p50 and p65) of NF-kappaB. Tretinoin 0-4 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 59-62
10995752-0 2000 Feedback inhibition of the retinaldehyde dehydrogenase gene ALDH1 by retinoic acid through retinoic acid receptor alpha and CCAAT/enhancer-binding protein beta. Tretinoin 69-82 retinoic acid receptor, alpha Mus musculus 91-119
11426618-5 2000 Increased expression of the leukocyte integrins CD11b and CD18 as well as down-regulation of the anti-apoptotic gene bcl-2 are associated with late stage differentiation of the myeloid lineage and retinoic acid induced maturation of acute myeloid leukemic cells. Tretinoin 197-210 integrin subunit alpha M Homo sapiens 48-53
10366427-0 1999 Role of vitamin D3 receptor in the synergistic differentiation of WEHI-3B leukemia cells by vitamin D3 and retinoic acid. Tretinoin 107-120 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 8-27
10366427-4 1999 No VDR was detected in untreated WEHI-3B D- cells; however, RA and 1,25-(OH)2D3 when used as single agents caused a slight induction of the VDR and in combination produced a marked increase in the VDR. Tretinoin 60-62 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 140-143
10366427-4 1999 No VDR was detected in untreated WEHI-3B D- cells; however, RA and 1,25-(OH)2D3 when used as single agents caused a slight induction of the VDR and in combination produced a marked increase in the VDR. Tretinoin 60-62 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 140-143
10366427-9 1999 These findings suggest that (a) induction of VDR expression is a key component in the synergistic differentiation induced by 1,25-(OH)2D3 and RA and (b) RAR and not RXR must be activated for enhanced induction of the VDR and for the synergistic differentiation produced by RA and 1, 25-(OH)2D3. Tretinoin 142-144 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 45-48
10366427-9 1999 These findings suggest that (a) induction of VDR expression is a key component in the synergistic differentiation induced by 1,25-(OH)2D3 and RA and (b) RAR and not RXR must be activated for enhanced induction of the VDR and for the synergistic differentiation produced by RA and 1, 25-(OH)2D3. Tretinoin 153-155 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 45-48
10366427-9 1999 These findings suggest that (a) induction of VDR expression is a key component in the synergistic differentiation induced by 1,25-(OH)2D3 and RA and (b) RAR and not RXR must be activated for enhanced induction of the VDR and for the synergistic differentiation produced by RA and 1, 25-(OH)2D3. Tretinoin 153-155 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 217-220
11819702-1 2000 AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA. Tretinoin 41-54 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 142-145
10397716-0 1999 All-trans retinoic acid delays the differentiation of primitive hematopoietic precursors (lin-c-kit+Sca-1(+)) while enhancing the terminal maturation of committed granulocyte/monocyte progenitors. Tretinoin 10-23 KIT proto-oncogene receptor tyrosine kinase Mus musculus 94-99
11819702-1 2000 AIM:To study the molecular mechanisms of retinoic acid (RA)on prolix-feration and expression of cyclin-dependent kinase inhibitors (CKI), i.e.p16, p21 and p27 in cultured rat hepatic stellate cells (HSC) stimulated with transforming growth factor beta 1 (TGF-beta1).METHODS:HSC were isolated from healthy rat livers and cultured.After stimulated with 1mg/L TGF-beta1, subcultured HSC were treated with or without 1nmol/L RA. Tretinoin 41-54 KRAS proto-oncogene, GTPase Rattus norvegicus 147-150
10938282-8 2000 The antagonist of the retinoic acid receptor (RAR)-alpha (Ro41-5253) abrogated the expression of MUC4 and TGF-beta2 induced by RA. Tretinoin 46-48 transforming growth factor beta 2 Homo sapiens 106-115
10347207-6 1999 Because the time course of TRKB induction closely parallels phenotypic differentiation of these cells, it seems probable that ATRA induces differentiation of NB1643 cells by establishing an autocrine loop involving BDNF and TRKB. Tretinoin 126-130 brain derived neurotrophic factor Homo sapiens 215-219
10347207-7 1999 Exogenous BDNF treatment resulted in a further increase in neurite outgrowth, which again suggests that an autocrine loop is involved in differentiation of NB1643 cells in response to ATRA. Tretinoin 184-188 brain derived neurotrophic factor Homo sapiens 10-14
11023524-0 2000 Phosphorylation-deficient Stat1 inhibits retinoic acid-induced differentiation and cell cycle arrest in U-937 monoblasts. Tretinoin 41-54 signal transducer and activator of transcription 1 Homo sapiens 26-31
10652610-0 1999 Retinoic acid modulates RAR alpha and RAR beta receptors in human glioma cell lines. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 24-33
11023524-2 2000 Recent reports have shown that ATRA induces the expression of several interferon-regulated genes, including signal transducer and activator of transcription (Stat)1. Tretinoin 31-35 signal transducer and activator of transcription 1 Homo sapiens 108-164
11023524-4 2000 Results showed that ATRA induction leads to activation of Stat1 by the phosphorylation of tyrosine 701 and subsequent nuclear translocation. Tretinoin 20-24 signal transducer and activator of transcription 1 Homo sapiens 58-63
11023524-6 2000 Moreover, ATRA-induced growth arrest in the G(0)/G(1) phase of the cell cycle was inhibited by phosphorylation-deficient Stat1. Tretinoin 10-14 signal transducer and activator of transcription 1 Homo sapiens 121-126
11023524-7 2000 Taken together, these results indicate that Stat1 is a key mediator of ATRA-induced cell cycle arrest and differentiation of U-937 cells. Tretinoin 71-75 signal transducer and activator of transcription 1 Homo sapiens 44-49
11032820-7 2000 The expression of retinoic acid-responsive genes, such as the cell-cycle inhibitor p21(WAF1), was selectively impaired in NAT1(-/-) cells. Tretinoin 18-31 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 83-86
10224118-3 1999 In addition, VDR mediates a ligand-dependent repression of the response of the retinoic acid receptor beta2 promoter to retinoic acid, and the helix 3 and helix 12 mutants were unable to mediate transrepression. Tretinoin 79-92 vitamin D receptor Homo sapiens 13-16
10094816-7 1999 Furthermore, antisense oligonucleotide complementary to p21(CIP2/Waf1) and p34(cdc2) mRNA significantly rescued RA-induced apoptosis. Tretinoin 112-114 cyclin dependent kinase inhibitor 3 Homo sapiens 60-64
10094816-9 1999 RA treatment leads to Rb2 hyperphosphorylation, and p34(cdc2) kinase activation is coincident with an aberrant mitotic progression, followed by appearance of abnormal nucleus. Tretinoin 0-2 RB transcriptional corepressor like 2 Homo sapiens 22-25
10094816-11 1999 These findings suggest that inappropriate regulation of the cell cycle regulators p21(CIP2/Waf1) and p34(cdc2) is coupled with induction of Bax and involved in cell death with apoptosis when Hep3B cells are exposed to RA. Tretinoin 218-220 cyclin dependent kinase inhibitor 3 Homo sapiens 86-90
11032820-7 2000 The expression of retinoic acid-responsive genes, such as the cell-cycle inhibitor p21(WAF1), was selectively impaired in NAT1(-/-) cells. Tretinoin 18-31 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 87-91
10652610-0 1999 Retinoic acid modulates RAR alpha and RAR beta receptors in human glioma cell lines. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 24-27
10652610-6 1999 Interestingly, RA treatment up-regulated RAR beta proteins but not RAR alpha proteins, suggesting post-transcriptional regulations of RAR transcripts in glioma cells. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 41-44
10319996-0 1999 Retinoic acid is able to induce interferon regulatory factor 1 in squamous carcinoma cells via a STAT-1 independent signalling pathway. Tretinoin 0-13 signal transducer and activator of transcription 1 Homo sapiens 97-103
10992453-0 2000 Regulation of cathelicidin gene expression: induction by lipopolysaccharide, interleukin-6, retinoic acid, and Salmonella enterica serovar typhimurium infection. Tretinoin 92-105 antibacterial protein PR-39 Sus scrofa 14-26
10992453-7 2000 Similarly, interleukin-6 (IL-6) and all-trans retinoic acid (RA) markedly induced cathelicidin gene expression. Tretinoin 46-59 antibacterial protein PR-39 Sus scrofa 82-94
10381520-10 1999 Pretreatment with ATRA greatly reduced IL-6-induced gp130 phosphorylation in OPM-2 cells, reflecting a reduction in cellular IL-6Ralpha. Tretinoin 18-22 interleukin 6 cytokine family signal transducer Homo sapiens 52-57
10992453-7 2000 Similarly, interleukin-6 (IL-6) and all-trans retinoic acid (RA) markedly induced cathelicidin gene expression. Tretinoin 61-63 antibacterial protein PR-39 Sus scrofa 82-94
10369717-7 1999 RESULTS: ATRA exerted a significant inhibitory effect on the synthesis of procollagens type I, III, and IV, fibronectin, and laminin, but did not influence stellate cell proliferation, whereas 9RA showed a clear but late effect on proliferation. Tretinoin 9-13 fibronectin 1 Rattus norvegicus 108-119
11006104-0 2000 Myristoylation alters retinoic acid-induced down-regulation of MARCKS in immortalized hippocampal cells. Tretinoin 22-35 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 63-69
11006104-3 2000 In this study, we examined the role of the myristoylation signal in the regulation of MARCKS in transfected rat hippocampal cells (H19-7) following retinoic acid (RA) treatment. Tretinoin 148-161 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 86-92
10227457-1 1999 We investigated the modulation of the expression and phosphatase activity of SHP-1 during granulocytic differentiation of human myeloid leukemia cell line, HL60 and t(15;17) positive APL cell line, HT93, in response to all-trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO). Tretinoin 229-242 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 77-82
10227457-1 1999 We investigated the modulation of the expression and phosphatase activity of SHP-1 during granulocytic differentiation of human myeloid leukemia cell line, HL60 and t(15;17) positive APL cell line, HT93, in response to all-trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO). Tretinoin 244-248 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 77-82
11006104-3 2000 In this study, we examined the role of the myristoylation signal in the regulation of MARCKS in transfected rat hippocampal cells (H19-7) following retinoic acid (RA) treatment. Tretinoin 163-165 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 86-92
10091603-0 1999 Stimulation of premature retinoic acid synthesis in Xenopus embryos following premature expression of aldehyde dehydrogenase ALDH1. Tretinoin 25-38 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 125-130
11006104-5 2000 Exposure of the wild-type MARCKS-transfected cells to RA resulted in an apparent shift of MARCKS from the membrane to the cytosol, while the total protein of wild-type MARCKS was not significantly changed. Tretinoin 54-56 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 26-32
10091603-2 1999 Biochemical studies have shown that retinal can be metabolized in vitro to retinoic acid by members of the aldehyde dehydrogenase enzyme family, including ALDH1. Tretinoin 75-88 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 155-160
11006104-5 2000 Exposure of the wild-type MARCKS-transfected cells to RA resulted in an apparent shift of MARCKS from the membrane to the cytosol, while the total protein of wild-type MARCKS was not significantly changed. Tretinoin 54-56 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 90-96
10456660-3 1999 ATRA acts by down-regulating IL-6-receptor-alpha or gp130 on the surface of the myeloma cells. Tretinoin 0-4 interleukin 6 cytokine family signal transducer Homo sapiens 52-57
11006104-5 2000 Exposure of the wild-type MARCKS-transfected cells to RA resulted in an apparent shift of MARCKS from the membrane to the cytosol, while the total protein of wild-type MARCKS was not significantly changed. Tretinoin 54-56 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 90-96
11006104-6 2000 In contrast, RA-exposed cells transfected with the mutant MARCKS revealed a dramatic reduction of expression of MARCKS protein in both cytosol and total protein fractions. Tretinoin 13-15 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 58-64
11006104-6 2000 In contrast, RA-exposed cells transfected with the mutant MARCKS revealed a dramatic reduction of expression of MARCKS protein in both cytosol and total protein fractions. Tretinoin 13-15 myristoylated alanine rich protein kinase C substrate Rattus norvegicus 112-118
10091603-3 1999 Here we describe the first direct evidence that ALDH1 plays a physiological role in retinoic acid synthesis by analysis of retinoid signaling in Xenopus embryos, which have plentiful stores of maternally derived retinal. Tretinoin 84-97 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 48-53
10091603-7 1999 Overexpression of ALDH1 by injection of Xenopus embryos with mRNAs encoding the mouse, chick or Xenopus ALDH1 homologs induced high levels of retinoic acid detection during the blastula stage. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 18-23
10091603-7 1999 Overexpression of ALDH1 by injection of Xenopus embryos with mRNAs encoding the mouse, chick or Xenopus ALDH1 homologs induced high levels of retinoic acid detection during the blastula stage. Tretinoin 142-155 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 104-109
10091603-8 1999 Thus, premature expression of ALDH1 stimulates premature synthesis of retinoic acid. Tretinoin 70-83 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 30-35
10023688-0 1999 Retinoic acid, but not arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in a RA-therapy resistant t(11;17)(q23;q21) APL patient. Tretinoin 0-13 zinc finger and BTB domain containing 16 Homo sapiens 54-58
10023688-0 1999 Retinoic acid, but not arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in a RA-therapy resistant t(11;17)(q23;q21) APL patient. Tretinoin 59-61 zinc finger and BTB domain containing 16 Homo sapiens 54-58
10979975-2 2000 It was found that steady-state retinoic acid receptor alpha (RARalpha) protein levels were markedly reduced in these cells after exposure to ATRA. Tretinoin 141-145 retinoic acid receptor, alpha Mus musculus 31-59
10490294-4 1999 The orphan receptor COUP-TFII, which modulates RA responses, colocalizes with the dorsal dehydrogenase. Tretinoin 47-49 nuclear receptor subfamily 2, group F, member 2 Mus musculus 20-29
10979975-2 2000 It was found that steady-state retinoic acid receptor alpha (RARalpha) protein levels were markedly reduced in these cells after exposure to ATRA. Tretinoin 141-145 retinoic acid receptor, alpha Mus musculus 61-69
10979975-6 2000 These findings suggested that the prevention of RARalpha protein loss by G-CSF or LiCl in ATRA-treated cells functioned to extend the differentiation response to the retinoid and was responsible, at least in part, for the observed synergism. Tretinoin 90-94 retinoic acid receptor, alpha Mus musculus 48-56
10979975-8 2000 ATRA caused a reduction, but not a complete loss, of RARalpha protein in these transfectants, which were considerably more responsive than parental D(+) cells to ATRA as a single agent, supporting the concept that the protection of RARalpha pools results in a heightened differentiation response to ATRA. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 53-61
10979975-8 2000 ATRA caused a reduction, but not a complete loss, of RARalpha protein in these transfectants, which were considerably more responsive than parental D(+) cells to ATRA as a single agent, supporting the concept that the protection of RARalpha pools results in a heightened differentiation response to ATRA. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 232-240
10979975-8 2000 ATRA caused a reduction, but not a complete loss, of RARalpha protein in these transfectants, which were considerably more responsive than parental D(+) cells to ATRA as a single agent, supporting the concept that the protection of RARalpha pools results in a heightened differentiation response to ATRA. Tretinoin 162-166 retinoic acid receptor, alpha Mus musculus 53-61
10979975-8 2000 ATRA caused a reduction, but not a complete loss, of RARalpha protein in these transfectants, which were considerably more responsive than parental D(+) cells to ATRA as a single agent, supporting the concept that the protection of RARalpha pools results in a heightened differentiation response to ATRA. Tretinoin 162-166 retinoic acid receptor, alpha Mus musculus 53-61
10952894-3 2000 We show here that retinoic acid (RA) is an upstream activator of the proximal determinant genes Meis1 and Meis2. Tretinoin 18-31 Meis homeobox 1 Homo sapiens 96-101
9890568-1 1999 Retinoic acid exerts pleiotropic effects by acting through two families of nuclear receptors, RAR and RXR. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 102-105
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 115-128 vitamin D receptor Homo sapiens 286-304
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 115-128 vitamin D receptor Homo sapiens 306-309
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 130-132 vitamin D receptor Homo sapiens 286-304
10609868-1 1999 Vitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all-trans retinoic acid (RA) and 1alpha,25-dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Tretinoin 130-132 vitamin D receptor Homo sapiens 306-309
10952894-3 2000 We show here that retinoic acid (RA) is an upstream activator of the proximal determinant genes Meis1 and Meis2. Tretinoin 33-35 Meis homeobox 1 Homo sapiens 96-101
11022230-1 2000 Retinoic acids (RA) play a key role in myeloid differentiation through their agonistic nuclear receptors (RAR alpha/RXR) to modulate the expression of target genes. Tretinoin 0-14 retinoid X receptor alpha Homo sapiens 116-119
10609868-3 1999 Both RAR and VDR form heterodimers preferentially with the nuclear receptor for 9-cis RA, referred to as the retinoid X receptor (RXR), but functional RAR-VDR heterodimers have also been observed. Tretinoin 5-7 retinoid X receptor alpha Homo sapiens 109-128
10609868-3 1999 Both RAR and VDR form heterodimers preferentially with the nuclear receptor for 9-cis RA, referred to as the retinoid X receptor (RXR), but functional RAR-VDR heterodimers have also been observed. Tretinoin 5-7 retinoid X receptor alpha Homo sapiens 130-133
11022230-3 2000 Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Tretinoin 24-47 retinoid X receptor alpha Homo sapiens 195-198
10415749-10 1999 Only all-trans retinoic acid reduced MMP-1 synthesis in these cells. Tretinoin 15-28 matrix metallopeptidase 1 Homo sapiens 37-42
11022230-3 2000 Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Tretinoin 49-53 retinoid X receptor alpha Homo sapiens 195-198
10609868-3 1999 Both RAR and VDR form heterodimers preferentially with the nuclear receptor for 9-cis RA, referred to as the retinoid X receptor (RXR), but functional RAR-VDR heterodimers have also been observed. Tretinoin 5-7 vitamin D receptor Homo sapiens 155-158
9864179-6 1999 C-Jun amino-terminal kinase (JNK) was not tyrosine-phosphorylated by any cytokine despite the existence of JNK proteins in human neutrophils, whereas it was tyrosine-phosphorylated by TNF in undifferentiated and all-trans retinoic acid-differentiated HL-60 cells. Tretinoin 222-235 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5
11144530-0 2000 Inhibition of ATRA-induced myeloid differentiation in acute promyelocytic leukemia by a new protein tyrosine phosphatase inhibitor, 3,4-dephostatin. Tretinoin 14-18 protein tyrosine phosphatase non-receptor type 22 Homo sapiens 92-120
10364250-0 1999 Signal relay by retinoic acid receptors alpha and beta in the retinoic acid-induced expression of insulin-like growth factor-binding protein-3 in breast cancer cells. Tretinoin 16-29 insulin like growth factor binding protein 3 Homo sapiens 98-142
11144530-1 2000 We previously reported that the expression and the activity of SHP-1, a non-transmembrane protein tyrosine phosphatase (PTPase) increased during myeloid differentiation of an acute promyelocytic leukemia cell line (HT93) induced by all-trans retinoic acid (ATRA). Tretinoin 232-255 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 63-68
11144530-1 2000 We previously reported that the expression and the activity of SHP-1, a non-transmembrane protein tyrosine phosphatase (PTPase) increased during myeloid differentiation of an acute promyelocytic leukemia cell line (HT93) induced by all-trans retinoic acid (ATRA). Tretinoin 232-255 protein tyrosine phosphatase non-receptor type 22 Homo sapiens 90-118
11144530-1 2000 We previously reported that the expression and the activity of SHP-1, a non-transmembrane protein tyrosine phosphatase (PTPase) increased during myeloid differentiation of an acute promyelocytic leukemia cell line (HT93) induced by all-trans retinoic acid (ATRA). Tretinoin 232-255 protein tyrosine phosphatase non-receptor type 22 Homo sapiens 120-126
11144530-1 2000 We previously reported that the expression and the activity of SHP-1, a non-transmembrane protein tyrosine phosphatase (PTPase) increased during myeloid differentiation of an acute promyelocytic leukemia cell line (HT93) induced by all-trans retinoic acid (ATRA). Tretinoin 257-261 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 63-68
11144530-1 2000 We previously reported that the expression and the activity of SHP-1, a non-transmembrane protein tyrosine phosphatase (PTPase) increased during myeloid differentiation of an acute promyelocytic leukemia cell line (HT93) induced by all-trans retinoic acid (ATRA). Tretinoin 257-261 protein tyrosine phosphatase non-receptor type 22 Homo sapiens 90-118
11144530-1 2000 We previously reported that the expression and the activity of SHP-1, a non-transmembrane protein tyrosine phosphatase (PTPase) increased during myeloid differentiation of an acute promyelocytic leukemia cell line (HT93) induced by all-trans retinoic acid (ATRA). Tretinoin 257-261 protein tyrosine phosphatase non-receptor type 22 Homo sapiens 120-126
11076197-0 2000 [Regulation of neural differentiation & neurotrophic factor responsiveness by bone morphogenetic protein and retinoic acid]. Tretinoin 113-126 neurotrophin 3 Homo sapiens 44-63
10352886-0 1999 Modulation of alpha-actin and alpha-actinin proteins in cardiomyocytes by retinoic acid during development. Tretinoin 74-87 actin, alpha 2, smooth muscle, aorta Gallus gallus 14-25
10208011-4 1999 Embryonic tissues in which this receptor is present also contain the retinol-binding protein CRBP I and the enzymes involved in RA synthesis; the same tissues are particularly vulnerable to vitamin A deficiency. Tretinoin 128-130 retinol binding protein 4 Homo sapiens 69-92
10208011-5 1999 In the nucleus, the RA signal is transduced by binding to a heterodimeric pair of retinoid receptors (RAR/RXR). Tretinoin 20-22 retinoid X receptor alpha Homo sapiens 106-109
10208011-8 1999 Excess RA causes abnormalities of many systems; altered susceptibility to RA excess in mice lacking RAR gamma or RXR alpha suggests that the teratogenic signal is transduced through different receptors compared with physiological RA function in the same tissue. Tretinoin 74-76 retinoic acid receptor, gamma Mus musculus 100-109
10208011-8 1999 Excess RA causes abnormalities of many systems; altered susceptibility to RA excess in mice lacking RAR gamma or RXR alpha suggests that the teratogenic signal is transduced through different receptors compared with physiological RA function in the same tissue. Tretinoin 74-76 retinoic acid receptor, gamma Mus musculus 100-109
10364250-3 1999 By using an RARalpha-selective antagonist (Ro 41-5253), we demonstrated that RARbeta expression was induced by atRA through an RARalpha-dependent signaling pathway and that RARbeta induction was correlated with IGFBP-3 induction. Tretinoin 111-115 retinoic acid receptor alpha Homo sapiens 12-20
10821537-3 1999 Western analyses showed that continuous exposure for 48 h of HL-60 cells to the differentiation-inducing agents, all-trans retinoic acid, 1,25-dihydroxyvitamin D3, or N-methylformamide, resulted in decreases in mitochondrial HSP70 (mtHSP70), with little change in the levels of HSP70, HSC70, and GRP78. Tretinoin 123-136 heat shock protein family A (Hsp70) member 4 Homo sapiens 225-230
10821537-3 1999 Western analyses showed that continuous exposure for 48 h of HL-60 cells to the differentiation-inducing agents, all-trans retinoic acid, 1,25-dihydroxyvitamin D3, or N-methylformamide, resulted in decreases in mitochondrial HSP70 (mtHSP70), with little change in the levels of HSP70, HSC70, and GRP78. Tretinoin 123-136 heat shock protein family A (Hsp70) member 4 Homo sapiens 234-239
11032177-5 2000 We also provide evidence to suggest that at least some of the effects elicited by RA in human EC cells might be mediated through RA-induced expression of BMP-7. Tretinoin 82-84 bone morphogenetic protein 7 Homo sapiens 154-159
11032177-5 2000 We also provide evidence to suggest that at least some of the effects elicited by RA in human EC cells might be mediated through RA-induced expression of BMP-7. Tretinoin 129-131 bone morphogenetic protein 7 Homo sapiens 154-159
10821537-3 1999 Western analyses showed that continuous exposure for 48 h of HL-60 cells to the differentiation-inducing agents, all-trans retinoic acid, 1,25-dihydroxyvitamin D3, or N-methylformamide, resulted in decreases in mitochondrial HSP70 (mtHSP70), with little change in the levels of HSP70, HSC70, and GRP78. Tretinoin 123-136 heat shock protein family A (Hsp70) member 8 Homo sapiens 285-290
10915218-8 2000 When the immature cells were exposed to RA, FSH-induced expression of c-fos mRNA was markedly decreased. Tretinoin 40-42 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-75
10364250-3 1999 By using an RARalpha-selective antagonist (Ro 41-5253), we demonstrated that RARbeta expression was induced by atRA through an RARalpha-dependent signaling pathway and that RARbeta induction was correlated with IGFBP-3 induction. Tretinoin 111-115 retinoic acid receptor alpha Homo sapiens 127-135
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 78-82 insulin like growth factor binding protein 3 Homo sapiens 91-98
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 78-82 insulin like growth factor binding protein 3 Homo sapiens 176-183
9889406-0 1998 Apoptosis and growth inhibition of squamous carcinoma cells treated with interferon-alpha, IFN-beta and retinoic acid are associated with induction of the cyclin-dependent kinase inhibitor p21. Tretinoin 104-117 cyclin dependent kinase inhibitor 3 Homo sapiens 155-188
10913195-7 2000 The levels of Sp110 mRNA and protein in the human promyelocytic leukemia cell line NB4 increased following treatment with all-trans retinoic acid (ATRA), and Sp110 localized to PML-Sp100 nuclear bodies in ATRA-treated NB4 cells. Tretinoin 132-145 SP110 nuclear body protein Homo sapiens 14-19
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 197-201 insulin like growth factor binding protein 3 Homo sapiens 91-98
10913195-7 2000 The levels of Sp110 mRNA and protein in the human promyelocytic leukemia cell line NB4 increased following treatment with all-trans retinoic acid (ATRA), and Sp110 localized to PML-Sp100 nuclear bodies in ATRA-treated NB4 cells. Tretinoin 147-151 SP110 nuclear body protein Homo sapiens 14-19
10364250-5 1999 On the other hand, antisense RARbeta cDNA transfection of MCF-7 cells blocked atRA-induced IGFBP-3 expression, indicating that RARbeta is directly involved in the mediation of IGFBP-3 induction by atRA. Tretinoin 197-201 insulin like growth factor binding protein 3 Homo sapiens 176-183
10913195-7 2000 The levels of Sp110 mRNA and protein in the human promyelocytic leukemia cell line NB4 increased following treatment with all-trans retinoic acid (ATRA), and Sp110 localized to PML-Sp100 nuclear bodies in ATRA-treated NB4 cells. Tretinoin 205-209 SP110 nuclear body protein Homo sapiens 14-19
10913195-7 2000 The levels of Sp110 mRNA and protein in the human promyelocytic leukemia cell line NB4 increased following treatment with all-trans retinoic acid (ATRA), and Sp110 localized to PML-Sp100 nuclear bodies in ATRA-treated NB4 cells. Tretinoin 205-209 SP110 nuclear body protein Homo sapiens 158-163
9894676-0 1998 Retinoic acid-induced thymic abnormalities in the mouse are associated with altered pharyngeal morphology, thymocyte maturation defects, and altered expression of Hoxa3 and Pax1. Tretinoin 0-13 homeobox A3 Mus musculus 163-168
10913195-10 2000 In addition, Sp110 produced a marked increase in ATRA-mediated expression of a reporter gene containing a retinoic acid response element. Tretinoin 49-53 SP110 nuclear body protein Homo sapiens 13-18
10364250-7 1999 Finally, we showed that atRA-induced IGFBP-3 is functionally active in modulating the growth-promoting effect of IGF-I. Tretinoin 24-28 insulin like growth factor binding protein 3 Homo sapiens 37-44
10913195-12 2000 The predominant expression of Sp110 in leukocytes and the enhanced expression of Sp110 in NB4 cells treated with ATRA raise the possibility that Sp110 has a role in inducing differentiation of myeloid cells. Tretinoin 113-117 SP110 nuclear body protein Homo sapiens 81-86
10913195-12 2000 The predominant expression of Sp110 in leukocytes and the enhanced expression of Sp110 in NB4 cells treated with ATRA raise the possibility that Sp110 has a role in inducing differentiation of myeloid cells. Tretinoin 113-117 SP110 nuclear body protein Homo sapiens 81-86
9894676-0 1998 Retinoic acid-induced thymic abnormalities in the mouse are associated with altered pharyngeal morphology, thymocyte maturation defects, and altered expression of Hoxa3 and Pax1. Tretinoin 0-13 paired box 1 Mus musculus 173-177
9894676-9 1998 Further, the observed defects in thymus development may be mediated by RA-induced alterations in the expression of Hoxa3. Tretinoin 71-73 homeobox A3 Mus musculus 115-120
9806904-1 1998 The steric conversion of 13-cis-retinoic acid (13-cRA) to all-trans-retinoic acid (t-RA) has been proposed as an activation mechanism for the observed therapeutic and teratogenic activities of 13-cRA. Tretinoin 58-81 myotubularin related protein 11 Homo sapiens 50-53
9806904-1 1998 The steric conversion of 13-cis-retinoic acid (13-cRA) to all-trans-retinoic acid (t-RA) has been proposed as an activation mechanism for the observed therapeutic and teratogenic activities of 13-cRA. Tretinoin 58-81 myotubularin related protein 11 Homo sapiens 196-199
9806904-1 1998 The steric conversion of 13-cis-retinoic acid (13-cRA) to all-trans-retinoic acid (t-RA) has been proposed as an activation mechanism for the observed therapeutic and teratogenic activities of 13-cRA. Tretinoin 83-87 myotubularin related protein 11 Homo sapiens 50-53
9806904-1 1998 The steric conversion of 13-cis-retinoic acid (13-cRA) to all-trans-retinoic acid (t-RA) has been proposed as an activation mechanism for the observed therapeutic and teratogenic activities of 13-cRA. Tretinoin 83-87 myotubularin related protein 11 Homo sapiens 196-199
11055551-0 2000 Mouse retinol binding protein gene: cloning, expression and regulation by retinoic acid. Tretinoin 74-87 retinol binding protein 4, plasma Mus musculus 6-29
11055551-5 2000 Both all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9c-RA) induced RBP mRNA expression in a dose- and time-dependent manner. Tretinoin 5-28 retinol binding protein 4, plasma Mus musculus 77-80
9806904-11 1998 In addition, ethacrynic acid, a selective substrate for Pi isoforms of GST, also inhibited the isomerization of 13-cRA to t-RA catalysed by GSTP1-1. Tretinoin 122-126 myotubularin related protein 11 Homo sapiens 115-118
10361124-2 1999 We investigated the molecular mechanism by which RA stimulates the expression of uPA, which lacks a canonical RA receptor (RAR)-responsive element, in bovine and human aortic endothelial cells. Tretinoin 49-51 plasminogen activator, urokinase Bos taurus 81-84
10862743-3 2000 At the onset of lung development RA signaling is ubiquitously activated in primary buds, as shown by expression of the major RA-synthesizing enzyme, RALDH-2 and activation of a RARE-lacZ transgene. Tretinoin 33-35 aldehyde dehydrogenase 1 family member A2 Homo sapiens 149-156
10354508-0 1999 The relationship of p53 and stress proteins in response to bleomycin and retinoic acid in the p53 heterozygous mouse. Tretinoin 73-86 transformation related protein 53, pseudogene Mus musculus 20-23
10864463-8 2000 Only treatment with anti-TGFbeta2 antibody or retinoic acid inhibited Slug expression in AV canal explants. Tretinoin 46-59 snail family transcriptional repressor 2 Gallus gallus 70-74
10907644-10 2000 The guanine exchange factor C3G was found to be associated with CrkL at similar levels before and after RA treatment, but Rapl activation downstream of C3G was not inducible by RA. Tretinoin 104-106 Rap guanine nucleotide exchange factor 1 Homo sapiens 28-31
9753672-11 1998 Amputations of caudal fins immediately after the first branching point of the lepidotrichia, and global administration of all-trans-retinoic acid, two procedures known to cause fusion of adjacent rays, result in a transient decrease in the expression of shh, ptc1 and bmp2. Tretinoin 122-145 sonic hedgehog signaling molecule a Danio rerio 254-257
9753672-12 1998 The effects of retinoic acid on shh expression occur within minutes after the onset of treatment suggesting direct regulation of shh by retinoic acid. Tretinoin 15-28 sonic hedgehog signaling molecule a Danio rerio 32-35
9753672-12 1998 The effects of retinoic acid on shh expression occur within minutes after the onset of treatment suggesting direct regulation of shh by retinoic acid. Tretinoin 15-28 sonic hedgehog signaling molecule a Danio rerio 129-132
9753672-12 1998 The effects of retinoic acid on shh expression occur within minutes after the onset of treatment suggesting direct regulation of shh by retinoic acid. Tretinoin 136-149 sonic hedgehog signaling molecule a Danio rerio 32-35
10354508-0 1999 The relationship of p53 and stress proteins in response to bleomycin and retinoic acid in the p53 heterozygous mouse. Tretinoin 73-86 transformation related protein 53, pseudogene Mus musculus 94-97
9753672-12 1998 The effects of retinoic acid on shh expression occur within minutes after the onset of treatment suggesting direct regulation of shh by retinoic acid. Tretinoin 136-149 sonic hedgehog signaling molecule a Danio rerio 129-132
10854244-3 2000 Accumulating evidence now suggests that RXRalpha is a critical receptor component mediating the effects of RA during embryonic development. Tretinoin 107-109 retinoid X receptor alpha Homo sapiens 40-48
10362099-0 1999 Induction of matrix metalloprotease-1 gene expression by retinoic acid in the human pancreatic tumour cell line Dan-G. We have investigated the effects of retinoic acid (RA) on matrix metalloprotease-1 (MMP-1) gene expression in the human pancreatic tumour cell line Dan-G. 13-cis RA results in a time- and dose-dependent increase of MMP-1 protein concentration. Tretinoin 57-70 matrix metallopeptidase 1 Homo sapiens 13-37
10854244-6 2000 In particular, we found that RA treatment resulted in a biphasic up-regulation of RXRalpha expression in NT2 cells. Tretinoin 29-31 retinoid X receptor alpha Homo sapiens 82-90
10392906-2 1999 We report that treatment of U937 cells with all-trans retinoic acid (ATRA), but not the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, results in an increased gene expression of the phosphoinositide 3-kinase (PI3K) species PI3Kgamma. Tretinoin 44-67 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 228-237
10941258-0 2000 Retinoic acid induces the degradation of the leukemogenic protein encoded by the promyelocytic leukemia gene fused to the retinoic acid receptor alpha gene. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 122-150
10941258-4 2000 RAR alpha itself is also degraded by atRA treatment, a process representing a possible feedback mechanism to turn off RAR alpha"s stimulation of transcription. Tretinoin 37-41 retinoic acid receptor, alpha Mus musculus 0-9
10941258-4 2000 RAR alpha itself is also degraded by atRA treatment, a process representing a possible feedback mechanism to turn off RAR alpha"s stimulation of transcription. Tretinoin 37-41 retinoic acid receptor, alpha Mus musculus 118-127
9825862-1 1998 Mammalian alcohol dehydrogenases ADH1 (class I ADH) and ADH4 (class IV ADH) function as retinol dehydrogenases contributing to the synthesis of retinoic acid, the active form of vitamin A involved in growth and development. Tretinoin 144-157 alcohol dehydrogenase 4 (class II), pi polypeptide L homeolog Xenopus laevis 56-60
9808636-4 1998 Treatment of IEC-6 cells with all-trans retinoic acid (RA) increased the levels of activity, protein and mRNA of L/B/K ALP, whereas enterocyte-specific proteins, including intestinal ALP, sucrase-isomaltase and glucose transporter-2, were not induced. Tretinoin 40-53 PDZ and LIM domain 3 Rattus norvegicus 119-122
9808636-4 1998 Treatment of IEC-6 cells with all-trans retinoic acid (RA) increased the levels of activity, protein and mRNA of L/B/K ALP, whereas enterocyte-specific proteins, including intestinal ALP, sucrase-isomaltase and glucose transporter-2, were not induced. Tretinoin 55-57 PDZ and LIM domain 3 Rattus norvegicus 119-122
9791009-5 1998 All-trans (ATRA) and 9-cis retinoic acid (9cRA) reduce c-erbB-1 protein to 50-100%, c-erbB-2 to 20-30%, and c-erbB-3 to 10-50% of control, depending on the concentration, respectively, without influencing the tyrosine phosphorylation status. Tretinoin 11-15 myotubularin related protein 11 Homo sapiens 43-46
10748128-5 2000 Our results indicate that RARgamma is the principle receptor contributing to all-trans-retinoic acid (RA)-mediated growth arrest in this system. Tretinoin 87-100 retinoic acid receptor, gamma Mus musculus 26-34
9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 nucleolar and coiled-body phosphoprotein 1 Homo sapiens 245-249
10392906-2 1999 We report that treatment of U937 cells with all-trans retinoic acid (ATRA), but not the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, results in an increased gene expression of the phosphoinositide 3-kinase (PI3K) species PI3Kgamma. Tretinoin 69-73 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 228-237
10392906-8 1999 Our findings suggest that sustained MAPK activation via PI3Kgamma precedes ATRA -dependent differentiation or growth inhibition. Tretinoin 75-79 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 56-65
10821786-6 2000 The in vivo administration of 9-cis-RA resulted in the inhibition of IL-12 production by macrophages stimulated in vitro with either LPS or HKL, leading to the inhibition of Th1 cytokine profile (decreased IFN-gamma and increased IL-4 production) in CD4(+) T cells. Tretinoin 30-38 CD4 antigen Mus musculus 250-253
10342883-0 1999 Vitamin D represses retinoic acid-dependent transactivation of the retinoic acid receptor-beta2 promoter: the AF-2 domain of the vitamin D receptor is required for transrepression. Tretinoin 20-33 vitamin D receptor Rattus norvegicus 129-147
10894171-2 2000 These molecules are encoded by the retinoic acid early inducible (RAE-1) and H60 minor histocompatibility antigen genes on mouse chromosome 10 and show weak homology with MHC class I. Tretinoin 35-48 ribonucleic acid export 1 Mus musculus 66-71
9892899-10 1998 Immunohistochemically, both RA and SDS were shown to reduce epidermal staining for desmoplakin, desmoglein 1, plakophilin 1 and desmocollin 3 equally compared with vehicle-treated skin (P < 0.001). Tretinoin 28-30 desmoglein 1 Homo sapiens 96-108
9892899-10 1998 Immunohistochemically, both RA and SDS were shown to reduce epidermal staining for desmoplakin, desmoglein 1, plakophilin 1 and desmocollin 3 equally compared with vehicle-treated skin (P < 0.001). Tretinoin 28-30 plakophilin 1 Homo sapiens 110-123
9789841-0 1998 Influence of retinoic acid and of cyclic AMP on the expression of choline acetyltransferase and of vesicular acetylcholine transporter in NG108-15 cells. Tretinoin 13-26 solute carrier family 18 (vesicular monoamine), member 3 Mus musculus 99-134
10411631-1 1999 Low concentrations of citral (3,7-dimethyl-2,6-octadienal), an inhibitor of retinoic acid biosynthesis, inhibited E1, E2 and E3 isozymes of human aldehyde dehydrogenase (EC1.2.1.3). Tretinoin 76-89 small nucleolar RNA, H/ACA box 73A Homo sapiens 114-168
9789841-1 1998 Treatment of the cholinergic cell line NG108-15 with retinoic acid or cAMP results in an increase of choline acetyltransferase activity (ChAT) whereas none of these agents influences the amount of the vesicular acetylcholine transporter (VAChT) as judged from vesamicol binding and immunoblot studies. Tretinoin 53-66 solute carrier family 18 (vesicular monoamine), member 3 Mus musculus 201-236
10736427-9 2000 One possible explanation for this result is that an RXR-RAR heterodimer in which both receptors are liganded is required for maximum expression of this critical component of the ATRA-induced differentiation pathway. Tretinoin 178-182 retinoic acid receptor, alpha Mus musculus 56-59
10429942-11 1999 In contrast, ADAM-9 mRNA levels were decreased in human monolayer chondrocytes exposed to IL-1 or retinoic acid. Tretinoin 98-111 ADAM metallopeptidase domain 9 Homo sapiens 13-19
10837916-1 2000 We examined the expression and the regulation of p21(waf1) and p27(kip1) cdk inhibitors in P19 mouse embryonal carcinoma (EC) cells following treatment with all-trans retinoic acid (ATRA) to induce neuronal differentiation. Tretinoin 167-180 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 49-57
10837916-1 2000 We examined the expression and the regulation of p21(waf1) and p27(kip1) cdk inhibitors in P19 mouse embryonal carcinoma (EC) cells following treatment with all-trans retinoic acid (ATRA) to induce neuronal differentiation. Tretinoin 182-186 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 49-57
10837916-1 2000 We examined the expression and the regulation of p21(waf1) and p27(kip1) cdk inhibitors in P19 mouse embryonal carcinoma (EC) cells following treatment with all-trans retinoic acid (ATRA) to induce neuronal differentiation. Tretinoin 182-186 cyclin-dependent kinase inhibitor 1B Mus musculus 67-71
9737713-1 1998 A stress-responsive gene highly expressed in brain and reproductive organs (BRE) is down-regulated after UV irradiation, DNA damaging agents, or retinoic acid treatment. Tretinoin 145-158 BRISC and BRCA1 A complex member 2 Homo sapiens 76-79
9699509-3 1998 Here, we report that, in this regulatory system, RA simultaneously up-regulates the expression of TGF-beta receptor types I and II, resulting in enhancement of TGF-beta activity in the cells. Tretinoin 49-51 transforming growth factor beta receptor 1 Bos taurus 98-130
12548778-4 1999 In RA-sensitive cell lines, ATRA-induced G0/G1 arrest is associated with down regulaton of c-myc and hyperphosphorylated Rb expression, and up regulation of p21WAF1/CIP1 and p53 expression. Tretinoin 28-32 MYC proto-oncogene, bHLH transcription factor Homo sapiens 91-96
9744516-1 1998 The effects of three inducers of differentiation, phorbol myristate acetate (PMA), retinoic acid (RA) and interferon-gamma (IFN-gamma), on the temporal regulation of vitamin D receptor (VDR) expression in HL-60 cells were analyzed by Northern blotting and immunofluorescence assays. Tretinoin 98-100 vitamin D receptor Homo sapiens 166-184
10837916-6 2000 In contrast, treatment of RAC65 cells with 9-cis retinoic acid induced both p27 expression and neuronal differentiation. Tretinoin 49-62 cyclin-dependent kinase inhibitor 1B Mus musculus 76-79
10929206-2 2000 P19 cells constitutively express the retinoic acid receptor alpha (RAR alpha) and RAR gamma mRNAs while RAR beta expression is induced by RA through a consensus RA-response element in the RAR beta promoter. Tretinoin 67-69 retinoic acid receptor, alpha Mus musculus 37-65
10339585-6 1999 Dissociation of SMRT from different receptors was observed at ATRA concentrations of 0.01 microM, 0.1 microM, and 1.0 microM for RARalpha-RXRalpha, NPM-RARalpha, and PML-RARalpha, respectively, but not observed for PLZF-RARalpha even in the presence of 10 microM ATRA. Tretinoin 263-267 nuclear receptor co-repressor 2 Mus musculus 16-20
10771097-0 2000 Treatment of v-Ki-ras-transformed SVC1 cells with low retinoic acid induces malignancy reversion associated with ras p21 down-regulation. Tretinoin 54-67 KRAS proto-oncogene, GTPase Rattus norvegicus 117-120
9681997-5 1998 HL-60/hsp70 cells also rapidly differentiated into granulocytes by addition of all-trans-retinoic acid, as assessed by phenotypic changes after staining with Wright-Giemsa. Tretinoin 83-102 heat shock protein family A (Hsp70) member 4 Homo sapiens 6-11
10815803-7 2000 We show that constitutive expression of CREG in NTERA-2 cells enhances neuronal differentiation upon treatment with retinoic acid. Tretinoin 116-129 cellular repressor of E1A stimulated genes 1 Homo sapiens 40-44
10766166-4 2000 The B94 gene (TNFAIP2; Unigene Hs.101382), originally identified as a tumor necrosis factor alpha-inducible gene in endothelial cells, was one of several genes found to be induced by RA specifically in TF1-PR cells, but not in TF1-neo (control) cells. Tretinoin 183-185 TNF alpha induced protein 2 Homo sapiens 4-7
10766166-4 2000 The B94 gene (TNFAIP2; Unigene Hs.101382), originally identified as a tumor necrosis factor alpha-inducible gene in endothelial cells, was one of several genes found to be induced by RA specifically in TF1-PR cells, but not in TF1-neo (control) cells. Tretinoin 183-185 TNF alpha induced protein 2 Homo sapiens 14-21
9684745-0 1998 Differentiation of human epidermal keratinocytes is accompanied by increased expression of CRABP-II and increased cellular concentration of retinoic acids: retention of newly synthesized retinoic acids by CRABP-II. Tretinoin 187-201 cellular retinoic acid binding protein 2 Homo sapiens 205-213
10359529-5 1999 RA-treatment induced two peaks of p21 synthesis: early (from the 2nd to the 6th hour), dependent on PML/RAR alpha expression and associated with G1-S transition and high CDK activity; late (from 3rd to the 4th day), independent from PML/RAR alpha and associated with G1 block and low CDK activity. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 100-113
9684745-15 1998 Moreover, newly synthesized [3H]retinoic acids were retained within cells bound to CRABP-II. Tretinoin 32-46 cellular retinoic acid binding protein 2 Homo sapiens 83-91
9684745-16 1998 The results suggest that increasing cellular concentration of retinoic acids in in vitro differentiating keratinocytes is achieved by a combination of increased activity of the retinoic acid synthesis pathway and increased cellular content of CRABP-II. Tretinoin 62-76 cellular retinoic acid binding protein 2 Homo sapiens 243-251
9684745-16 1998 The results suggest that increasing cellular concentration of retinoic acids in in vitro differentiating keratinocytes is achieved by a combination of increased activity of the retinoic acid synthesis pathway and increased cellular content of CRABP-II. Tretinoin 62-75 cellular retinoic acid binding protein 2 Homo sapiens 243-251
10766166-6 2000 B94 induction by RA occurred within 1 h, did not require new protein synthesis, and was inhibited by actinomycin D, suggesting rapid transcriptional activation. Tretinoin 17-19 TNF alpha induced protein 2 Homo sapiens 0-3
10766166-7 2000 B94 was also induced by RA in NB4, UF1, and HL-60 cells, but not in other hematopoietic cell lines tested, suggesting that its up-regulation by RA may be specific to cells that express PML-RARalpha or are at the late myeloblast or promyelocyte stage of myeloid development. Tretinoin 24-26 TNF alpha induced protein 2 Homo sapiens 0-3
10766166-7 2000 B94 was also induced by RA in NB4, UF1, and HL-60 cells, but not in other hematopoietic cell lines tested, suggesting that its up-regulation by RA may be specific to cells that express PML-RARalpha or are at the late myeloblast or promyelocyte stage of myeloid development. Tretinoin 144-146 TNF alpha induced protein 2 Homo sapiens 0-3
10798446-7 2000 The expression of ZAN75 was transiently increased at both the mRNA and the protein levels when P19 cells were treated with retinoic acid to induce neuronal differentiation. Tretinoin 123-136 zinc finger protein 326 Mus musculus 18-23
11189515-1 1998 OBJECTIVE: To evaluate the clinical significance of expression of interleukin-(IL-8) and its type A receptor(IL-8RA) in acute promyelocytic leukemia(APL) patients under all trans-retinoic acid(ATRA) induction. Tretinoin 173-192 C-X-C motif chemokine receptor 1 Homo sapiens 109-115
11189515-1 1998 OBJECTIVE: To evaluate the clinical significance of expression of interleukin-(IL-8) and its type A receptor(IL-8RA) in acute promyelocytic leukemia(APL) patients under all trans-retinoic acid(ATRA) induction. Tretinoin 193-197 C-X-C motif chemokine receptor 1 Homo sapiens 109-115
10359529-5 1999 RA-treatment induced two peaks of p21 synthesis: early (from the 2nd to the 6th hour), dependent on PML/RAR alpha expression and associated with G1-S transition and high CDK activity; late (from 3rd to the 4th day), independent from PML/RAR alpha and associated with G1 block and low CDK activity. Tretinoin 0-2 PML nuclear body scaffold Homo sapiens 233-246
11189515-9 1998 CONCLUSION: ATRA inhibited IL-8 secretion of APL cells while increased the expression of IL-8RA. Tretinoin 12-16 C-X-C motif chemokine receptor 1 Homo sapiens 89-95
10723064-10 2000 However, RA was found to inhibit almost completely the expression of the myelin basic protein. Tretinoin 9-11 myelin basic protein Rattus norvegicus 73-93
10330422-4 1999 Reporter gene studies showed that C/EBPepsilon promoter/enhancer activity increased in a retinoid-dependent fashion via the retinoic acid response element (RARE) present in the promoter region of C/EBPepsilon. Tretinoin 124-137 CCAAT enhancer binding protein epsilon Homo sapiens 34-46
10203615-1 1999 We analyzed the efficacy of all-trans retinoic acid (ATRA) as an early treatment for four acute promyelocytic leukemia (APL) patients in remission who were PML/RARalpha-positive by reverse transcription-polymerase chain reaction or fluorescence in situ hybridization. Tretinoin 28-51 PML nuclear body scaffold Homo sapiens 156-159
10702251-7 2000 We have also determined that human recombinant UGT2B7 can glucuronidate atRA, 4-OH-RA, and 4-OH-RAc with activities similar to those found in human liver microsomes. Tretinoin 72-76 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 47-53
9635125-2 1998 We studied the interaction of T3, glucocorticoids, all-trans retinoic acid (RA), and 9-cis retinoic acid (9cRA) on the expression of the rat alpha 1-acid glycoprotein (AGP) gene in vitro. Tretinoin 51-74 orosomucoid 1 Rattus norvegicus 168-171
9635125-2 1998 We studied the interaction of T3, glucocorticoids, all-trans retinoic acid (RA), and 9-cis retinoic acid (9cRA) on the expression of the rat alpha 1-acid glycoprotein (AGP) gene in vitro. Tretinoin 76-78 orosomucoid 1 Rattus norvegicus 141-166
9570764-6 1998 We also identify three potential retinoic acid response elements in the Hoxa4 5" flanking region, one of which is identical to a well-characterized element flanking the Hoxd4 gene. Tretinoin 33-46 homeobox D4 Mus musculus 169-174
10692107-0 2000 Keratin 4 upregulation by retinoic acid in vivo: a sensitive marker for retinoid bioactivity in human epidermis. Tretinoin 26-39 keratin 4 Homo sapiens 0-9
10203615-1 1999 We analyzed the efficacy of all-trans retinoic acid (ATRA) as an early treatment for four acute promyelocytic leukemia (APL) patients in remission who were PML/RARalpha-positive by reverse transcription-polymerase chain reaction or fluorescence in situ hybridization. Tretinoin 28-51 retinoic acid receptor alpha Homo sapiens 160-168
9669677-6 1998 In addition, during ATRA-induced myeloid differentiation, gene expression of STAT1, STAT2, and p48 was upregulated. Tretinoin 20-24 signal transducer and activator of transcription 1 Homo sapiens 77-82
10203615-1 1999 We analyzed the efficacy of all-trans retinoic acid (ATRA) as an early treatment for four acute promyelocytic leukemia (APL) patients in remission who were PML/RARalpha-positive by reverse transcription-polymerase chain reaction or fluorescence in situ hybridization. Tretinoin 53-57 PML nuclear body scaffold Homo sapiens 156-159
9669677-6 1998 In addition, during ATRA-induced myeloid differentiation, gene expression of STAT1, STAT2, and p48 was upregulated. Tretinoin 20-24 signal transducer and activator of transcription 2 Homo sapiens 84-89
10739005-6 2000 After the induction of the granulocytic differentiation of HL-60 cells with all trans retinoic acid (ATRA) or dimethylsulfoxide (DMSO), the abl and bcr homologous genes were repositioned closer to the nuclear periphery and the average distances between homologous abl-abl and bcr-bcr genes as well as between heterologous abl-bcr genes were elongated as compared with untreated human leukemic promyelocytic HL-60 cells. Tretinoin 86-99 BCR activator of RhoGEF and GTPase Homo sapiens 148-151
10203615-1 1999 We analyzed the efficacy of all-trans retinoic acid (ATRA) as an early treatment for four acute promyelocytic leukemia (APL) patients in remission who were PML/RARalpha-positive by reverse transcription-polymerase chain reaction or fluorescence in situ hybridization. Tretinoin 53-57 retinoic acid receptor alpha Homo sapiens 160-168
9627120-1 1998 The PLZF gene was identified first by its fusion with the retinoic acid receptor alpha gene in the t(11;17) translocation associated with a retinoic acid resistant form of acute promyelocytic leukemia (APL). Tretinoin 58-71 zinc finger and BTB domain containing 16 Homo sapiens 4-8
10203615-7 1999 These findings suggest that early treatment of ATRA for PML/RARalpha-positive APL patients in remission may have a therapeutic benefit and prolong the duration of hematological remission without chemotherapy. Tretinoin 47-51 PML nuclear body scaffold Homo sapiens 56-59
10203615-7 1999 These findings suggest that early treatment of ATRA for PML/RARalpha-positive APL patients in remission may have a therapeutic benefit and prolong the duration of hematological remission without chemotherapy. Tretinoin 47-51 retinoic acid receptor alpha Homo sapiens 60-68
9579574-4 1998 Electrophoretic mobility shift and super-shift assays using a DR2 ("direct repeat" 2) RA response element demonstrated DNA-binding of RARalpha, RARgamma, RXRalpha and RXRbeta in nuclear extracts of FTC-133 and anaplastic HTh74 cells. Tretinoin 86-88 retinoid X receptor alpha Homo sapiens 154-162
10191271-12 1999 Thus our results indicate that Aldh1 can function in retinoic acid synthesis under physiological conditions, but that the closely related Aldh-pb does not share this property. Tretinoin 53-66 aldehyde dehydrogenase 1 family member A1 Homo sapiens 31-36
9477316-10 1998 Retinoic acid beads mimic the effect produced by the somites in repressing MafB/Kr in r5/6 and progressively inducing it more rostrally as its concentration increases. Tretinoin 0-13 MAF bZIP transcription factor B Gallus gallus 75-79
10660575-2 2000 In this study, we determined whether all-trans-retinoic acid (tRA) and follicle-stimulating hormone (FSH) modulate RARalpha receptor subcellular localization, leading to changes in its transcriptional activity and protein expression in mouse Sertoli cell lines. Tretinoin 37-60 retinoic acid receptor, alpha Mus musculus 115-123
10660575-2 2000 In this study, we determined whether all-trans-retinoic acid (tRA) and follicle-stimulating hormone (FSH) modulate RARalpha receptor subcellular localization, leading to changes in its transcriptional activity and protein expression in mouse Sertoli cell lines. Tretinoin 62-65 retinoic acid receptor, alpha Mus musculus 115-123
10194425-2 1999 Granulocyte colony-stimulating factor (G-CSF) has been considered to be potentially synergistic with ATRA in this regard. Tretinoin 101-105 colony stimulating factor 3 Homo sapiens 0-37
10897415-3 2000 cPLA2-deficient PLB-985 cells differentiate similarly to control PLB-985 cells in response to retinoic acid, DMSO or 1,25 dihydroxyvitamin D3 indicating that cPLA2 is not involved in the differentiation process. Tretinoin 94-107 phospholipase A2 group IVA Homo sapiens 0-5
10075839-11 1999 As retinoic acid response elements are present in the promoter regions of both tTG and stromelysin-3 genes, we propose that RA might increase the amount of cell death in the INZs through a direct modulation of tTG expression and that it also contributes to the process of tissue remodeling, which accompanies cell death, through an up-regulation of stromelysin-3 expression in the INZs. Tretinoin 3-16 matrix metallopeptidase 11 Mus musculus 87-100
10840075-6 2000 A similar marked increase in the soluble adhesion molecules ICAM-1, and to a lesser extent VCAM-1, released from the four-week bone marrow stroma was observed after RA treatment. Tretinoin 165-167 intercellular adhesion molecule 1 Homo sapiens 60-66
9490815-12 1998 When cells were grown in the presence of 10 microM retinoic acid in order to synchronize the cell line in the G1 phase of the cell cycle, h-eag current was reduced to less than 5 % of the control value, while the delayed rectifier channel was expressed more abundantly. Tretinoin 51-64 potassium voltage-gated channel subfamily H member 1 Homo sapiens 138-143
9490815-13 1998 Down-regulation of h-eag by long-term exposure to retinoic acid was paralleled by a right shift in the activation potential of HERG-like channels. Tretinoin 50-63 potassium voltage-gated channel subfamily H member 1 Homo sapiens 19-24
9490815-15 1998 Acute application of 10 microM retinoic acid blocked the delayed rectifier channel but enhanced the h-eag current. Tretinoin 31-44 potassium voltage-gated channel subfamily H member 1 Homo sapiens 100-105
10714240-2 2000 The biological action of retinoic acid and synthetic analogs, referred to as retinoids, is mediated by RAR alpha, RAR beta, or RAR gamma and/or by RXR alpha, RXR beta, or RXR gamma, all being nuclear receptors. Tretinoin 25-38 retinoid X receptor alpha Homo sapiens 147-156
10075839-11 1999 As retinoic acid response elements are present in the promoter regions of both tTG and stromelysin-3 genes, we propose that RA might increase the amount of cell death in the INZs through a direct modulation of tTG expression and that it also contributes to the process of tissue remodeling, which accompanies cell death, through an up-regulation of stromelysin-3 expression in the INZs. Tretinoin 3-16 matrix metallopeptidase 11 Mus musculus 349-362
9502786-0 1998 Retinoic acid inhibits induction of c-Jun protein by ultraviolet radiation that occurs subsequent to activation of mitogen-activated protein kinase pathways in human skin in vivo. Tretinoin 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41
10075839-11 1999 As retinoic acid response elements are present in the promoter regions of both tTG and stromelysin-3 genes, we propose that RA might increase the amount of cell death in the INZs through a direct modulation of tTG expression and that it also contributes to the process of tissue remodeling, which accompanies cell death, through an up-regulation of stromelysin-3 expression in the INZs. Tretinoin 124-126 transglutaminase 2, C polypeptide Mus musculus 79-82
10075839-11 1999 As retinoic acid response elements are present in the promoter regions of both tTG and stromelysin-3 genes, we propose that RA might increase the amount of cell death in the INZs through a direct modulation of tTG expression and that it also contributes to the process of tissue remodeling, which accompanies cell death, through an up-regulation of stromelysin-3 expression in the INZs. Tretinoin 124-126 matrix metallopeptidase 11 Mus musculus 87-100
9488655-5 1998 These results indicate that PML is a critical component of the RA pathway and that disruption of its activity by the PML-RARalpha fusion protein may be important in APL pathogenesis. Tretinoin 63-65 retinoic acid receptor, alpha Mus musculus 121-129
10588863-2 1999 Treating neurula-stage Xenopus embryos with retinoic acid (RA) causes a specific block in cardiomyocyte development that correlates with a progressive reduction in the region of the presumptive heart-forming region expressing Nkx2.5. Tretinoin 44-57 NK2 homeobox 5 S homeolog Xenopus laevis 226-232
10075839-11 1999 As retinoic acid response elements are present in the promoter regions of both tTG and stromelysin-3 genes, we propose that RA might increase the amount of cell death in the INZs through a direct modulation of tTG expression and that it also contributes to the process of tissue remodeling, which accompanies cell death, through an up-regulation of stromelysin-3 expression in the INZs. Tretinoin 124-126 transglutaminase 2, C polypeptide Mus musculus 210-213
10588863-2 1999 Treating neurula-stage Xenopus embryos with retinoic acid (RA) causes a specific block in cardiomyocyte development that correlates with a progressive reduction in the region of the presumptive heart-forming region expressing Nkx2.5. Tretinoin 59-61 NK2 homeobox 5 S homeolog Xenopus laevis 226-232
10588863-9 1999 Regulatory mechanisms altered by excess RA must function normally to limit GATA-4/5/6 expression levels, to define the region of Nkx2.5 expression and regulate myocardial differentiation. Tretinoin 40-42 NK2 homeobox 5 S homeolog Xenopus laevis 129-135
10588879-2 1999 RALDH-2 and CYP26, two key enzymes that carry out retinoic acid (RA) synthesis and degradation, respectively, were cloned from the chick and show significant homology with their orthologs in other vertebrates. Tretinoin 50-63 aldehyde dehydrogenase 1 family member A2 Gallus gallus 0-7
10588879-8 1999 RA-synthesizing and -degrading enzymatic activities were measured biochemically in regions expressing RALDH-2 or CYP26. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Gallus gallus 102-109
9562262-3 1998 The constitutive expression of high levels of IL-15 mRNA was observed in all the cell lines examined, including Y79 retinoblastoma, IMR-32 neuroblastoma, SK-N-SH neuroblastoma, U-373MG glioma, KG-1-C glioma, NTera2 teratocarcinoma and neurons derived from NTera2 cells following treatment with retinoic acid (RA). Tretinoin 294-307 interleukin 15 Homo sapiens 46-51
9562262-3 1998 The constitutive expression of high levels of IL-15 mRNA was observed in all the cell lines examined, including Y79 retinoblastoma, IMR-32 neuroblastoma, SK-N-SH neuroblastoma, U-373MG glioma, KG-1-C glioma, NTera2 teratocarcinoma and neurons derived from NTera2 cells following treatment with retinoic acid (RA). Tretinoin 309-311 interleukin 15 Homo sapiens 46-51
10094952-1 1999 We observed that all-trans-retinoic acid (RA) down-regulated insulin-like growth factor binding proteins (IGFBPs) in cultured human hepatoma cells (Hep 3B, PLC/PRF/5, and Hep G2); therefore, we characterized the role of this down-regulation in cell growth. Tretinoin 17-40 insulin like growth factor binding protein 1 Homo sapiens 106-112
9468588-7 1998 These data show that activation of intact retinoid signaling by RA can induce GRP, a growth factor that can act as a tumor promoter. Tretinoin 64-66 gastrin releasing peptide Homo sapiens 78-81
10597280-0 1999 The induction and activation of STAT1 by all-trans-retinoic acid are mediated by RAR beta signaling pathways in breast cancer cells. Tretinoin 41-64 signal transducer and activator of transcription 1 Homo sapiens 32-37
10597280-4 1999 First, by using different receptor-selective retinoids, we demonstrated that RAR beta induction in MCF-7 cells by all-trans-retinoic acid (atRA) was associated with the activation of STAT1 gene transcription. Tretinoin 114-137 signal transducer and activator of transcription 1 Homo sapiens 183-188
10597280-4 1999 First, by using different receptor-selective retinoids, we demonstrated that RAR beta induction in MCF-7 cells by all-trans-retinoic acid (atRA) was associated with the activation of STAT1 gene transcription. Tretinoin 139-143 signal transducer and activator of transcription 1 Homo sapiens 183-188
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 38-42 signal transducer and activator of transcription 1 Homo sapiens 51-56
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 38-42 signal transducer and activator of transcription 1 Homo sapiens 186-191
10094952-1 1999 We observed that all-trans-retinoic acid (RA) down-regulated insulin-like growth factor binding proteins (IGFBPs) in cultured human hepatoma cells (Hep 3B, PLC/PRF/5, and Hep G2); therefore, we characterized the role of this down-regulation in cell growth. Tretinoin 17-40 heparan sulfate proteoglycan 2 Homo sapiens 156-159
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 38-42 signal transducer and activator of transcription 1 Homo sapiens 186-191
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 signal transducer and activator of transcription 1 Homo sapiens 51-56
9436983-0 1998 p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells. Tretinoin 66-79 activating transcription factor 2 Homo sapiens 9-14
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 signal transducer and activator of transcription 1 Homo sapiens 186-191
9436983-0 1998 p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells. Tretinoin 66-79 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 119-124
10094952-1 1999 We observed that all-trans-retinoic acid (RA) down-regulated insulin-like growth factor binding proteins (IGFBPs) in cultured human hepatoma cells (Hep 3B, PLC/PRF/5, and Hep G2); therefore, we characterized the role of this down-regulation in cell growth. Tretinoin 42-44 insulin like growth factor binding protein 1 Homo sapiens 106-112
9436983-7 1998 The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. Tretinoin 157-170 activating transcription factor 2 Homo sapiens 61-66
9436983-7 1998 The phosphorylation of the serine residue at position 121 of ATF-2 appears to be induced by protein kinase C alpha (PKC alpha) after treatment of cells with retinoic acid (RA) or induction with E1A. Tretinoin 172-174 activating transcription factor 2 Homo sapiens 61-66
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 signal transducer and activator of transcription 1 Homo sapiens 186-191
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 signal transducer and activator of transcription 1 Homo sapiens 51-56
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 signal transducer and activator of transcription 1 Homo sapiens 186-191
10597280-5 1999 The direct involvement of RAR beta in atRA-induced STAT1 gene activation was further demonstrated by showing that transfection with an anti-sense RAR beta construct blocked atRA-induced STAT1 expression in MCF-7 cells whereas introduction of a sense-RAR beta construct resulted in STAT1 induction by atRA in MDA-MB 231 cells. Tretinoin 173-177 signal transducer and activator of transcription 1 Homo sapiens 186-191
10597280-6 1999 In addition, we showed that STAT1 was phosphorylated/activated under atRA treatment of MCF-7 cells; this process required the involvement of RAR beta and protein synthesis. Tretinoin 69-73 signal transducer and activator of transcription 1 Homo sapiens 28-33
9457077-3 1998 In F9 teratocarcinoma cell line, RA-induced differentiation is accompanied by increased expression of the RAR beta, RXR alpha, and alpha-fetoprotein (AFP) genes. Tretinoin 33-35 retinoid X receptor alpha Homo sapiens 116-125
9457077-6 1998 In this paper, we have examined the RA-mediated regulation of the RAR, RXR, peroxisome proliferator-activated receptor (PPAR), and AFP genes in Hep3B cells. Tretinoin 36-38 retinoid X receptor alpha Homo sapiens 71-74
10094952-1 1999 We observed that all-trans-retinoic acid (RA) down-regulated insulin-like growth factor binding proteins (IGFBPs) in cultured human hepatoma cells (Hep 3B, PLC/PRF/5, and Hep G2); therefore, we characterized the role of this down-regulation in cell growth. Tretinoin 42-44 heparan sulfate proteoglycan 2 Homo sapiens 156-159
10631814-0 1999 The vimentin promoter as a tool to analyze the early events of retinoic acid-induced differentiation of cultured embryonal carcinoma cells. Tretinoin 63-76 vimentin Mus musculus 4-12
10094952-2 1999 Treatment with 10 micromol/L RA revealed a rapid decrease in IGFBP-3 within 2 days, and continued treatment with RA for 6 days resulted in a time-dependent stimulation of Hep 3B cell growth. Tretinoin 29-31 insulin like growth factor binding protein 3 Homo sapiens 61-68
9536220-0 1998 Suprabasal expression of epidermal alpha 2 beta 1 and alpha 3 beta 1 integrins in skin treated with topical retinoic acid. Tretinoin 108-121 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 43-49
10094952-3 1999 However, RA treatment decreased IGFBP-1 in PLC/PRF/5 cells and in Hep G2 cells, and the growth-stimulatory activity of RA was transient and less prominent, and was finally obliterated in both cell lines. Tretinoin 9-11 insulin like growth factor binding protein 1 Homo sapiens 32-39
9536220-0 1998 Suprabasal expression of epidermal alpha 2 beta 1 and alpha 3 beta 1 integrins in skin treated with topical retinoic acid. Tretinoin 108-121 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 62-68
10537125-2 1999 However, little is known about the influence of RA on the expression of the prepro-TRH gene. Tretinoin 48-50 thyrotropin releasing hormone Mus musculus 83-86
10094952-3 1999 However, RA treatment decreased IGFBP-1 in PLC/PRF/5 cells and in Hep G2 cells, and the growth-stimulatory activity of RA was transient and less prominent, and was finally obliterated in both cell lines. Tretinoin 9-11 heparan sulfate proteoglycan 2 Homo sapiens 43-46
10094952-5 1999 The addition of IGFBP-3 (1,000 ng/mL) inhibited the growth of Hep 3B cells and counteracted the growth-stimulatory activity of RA, but not completely, suggesting that RA has direct growth-stimulatory activity and that this is enhanced by autocrine down-regulation of IGFBP-3. Tretinoin 127-129 insulin like growth factor binding protein 3 Homo sapiens 16-23
10525374-6 1999 The binding of SiHa cells to ECM proteins (fibronectin, vitronectin, laminin, collagen IV) was drastically reduced when cells were treated with ATRA at 10 microM for 96 h in culture. Tretinoin 144-148 vitronectin Homo sapiens 56-67
9641219-0 1998 Effects of retinoic acid on the expression of a tumor rejection antigen (heat shock protein gp96) in human cervical cancer. Tretinoin 11-24 SPT20 homolog, SAGA complex component Homo sapiens 48-71
10094952-5 1999 The addition of IGFBP-3 (1,000 ng/mL) inhibited the growth of Hep 3B cells and counteracted the growth-stimulatory activity of RA, but not completely, suggesting that RA has direct growth-stimulatory activity and that this is enhanced by autocrine down-regulation of IGFBP-3. Tretinoin 127-129 insulin like growth factor binding protein 3 Homo sapiens 267-274
9641219-0 1998 Effects of retinoic acid on the expression of a tumor rejection antigen (heat shock protein gp96) in human cervical cancer. Tretinoin 11-24 heat shock protein 90 beta family member 1 Homo sapiens 92-96
9641219-4 1998 A number of key elements in this pathway, including major histocompatibility complex (MHC) class I molecules as well as adhesion/co-stimulation molecules such as ICAM-1 have reported to be sensitive to retinoic acid up-regulation. Tretinoin 202-215 intercellular adhesion molecule 1 Homo sapiens 162-168
10525374-7 1999 Interestingly, when ATRA-treated (10 microM, 96 h) SiHa cells were allowed to grow for 15 days in ATRA-free complete medium the binding of SiHa cells to fibronectin and vitronectin was inhibited, even after 15 days of drug withdrawal, whereas cell adhesion to laminin and collagen IV returned to normal within 3-7 days. Tretinoin 20-24 vitronectin Homo sapiens 169-180
10525374-7 1999 Interestingly, when ATRA-treated (10 microM, 96 h) SiHa cells were allowed to grow for 15 days in ATRA-free complete medium the binding of SiHa cells to fibronectin and vitronectin was inhibited, even after 15 days of drug withdrawal, whereas cell adhesion to laminin and collagen IV returned to normal within 3-7 days. Tretinoin 98-102 vitronectin Homo sapiens 169-180
10525374-8 1999 The comparative immunoprecipitation of two cell surface integrin receptors (alpha5beta1 and alphavbeta3) shows the effect of ATRA on the expression of alpha5, alphav, and beta1 subunits. Tretinoin 125-129 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 151-176
9641219-5 1998 In this study we analyzed at the transcriptional (Northern blot) and post-transcriptional levels (Western blot) the effects of retinoic acid on the expression of the tumor rejection antigen (heat shock protein gp96) in three human cervical carcinoma cell lines. Tretinoin 127-140 SPT20 homolog, SAGA complex component Homo sapiens 166-189
10094952-5 1999 The addition of IGFBP-3 (1,000 ng/mL) inhibited the growth of Hep 3B cells and counteracted the growth-stimulatory activity of RA, but not completely, suggesting that RA has direct growth-stimulatory activity and that this is enhanced by autocrine down-regulation of IGFBP-3. Tretinoin 167-169 insulin like growth factor binding protein 3 Homo sapiens 16-23
9641219-5 1998 In this study we analyzed at the transcriptional (Northern blot) and post-transcriptional levels (Western blot) the effects of retinoic acid on the expression of the tumor rejection antigen (heat shock protein gp96) in three human cervical carcinoma cell lines. Tretinoin 127-140 heat shock protein 90 beta family member 1 Homo sapiens 210-214
9641219-6 1998 Exposure of therapeutic doses of retinoic acid (i.e. 1 microM) significantly and consistently increased the expression of heat shock protein gp96 (Western blot analysis) on CaSki, SiHa and HT-3 cervical cancer cell lines. Tretinoin 33-46 heat shock protein 90 beta family member 1 Homo sapiens 141-145
9641219-8 1998 Taken together, our results show that retinoic acid can significantly increase the expression of yet another immunologically important cell molecule, the tumor rejection antigen heat shock protein gp96 in human cervical cancer. Tretinoin 38-51 SPT20 homolog, SAGA complex component Homo sapiens 154-177
9641219-8 1998 Taken together, our results show that retinoic acid can significantly increase the expression of yet another immunologically important cell molecule, the tumor rejection antigen heat shock protein gp96 in human cervical cancer. Tretinoin 38-51 heat shock protein 90 beta family member 1 Homo sapiens 197-201
10502285-0 1999 Retinoic acid and 1,25-dihydroxyvitamin D3 inhibit tenascin-C expression in rat glioma C6 cells. Tretinoin 0-13 tenascin C Rattus norvegicus 51-61
10502285-4 1999 Here we demonstrate that Tn-C RNA expression in glioma C6 cells is inhibited in a dose-dependent manner by retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25-D3). Tretinoin 107-120 tenascin C Rattus norvegicus 25-29
10094952-5 1999 The addition of IGFBP-3 (1,000 ng/mL) inhibited the growth of Hep 3B cells and counteracted the growth-stimulatory activity of RA, but not completely, suggesting that RA has direct growth-stimulatory activity and that this is enhanced by autocrine down-regulation of IGFBP-3. Tretinoin 167-169 insulin like growth factor binding protein 3 Homo sapiens 267-274
10508860-8 1999 PS1 suppressed c-jun-associated apoptosis by retinoic acid in F9 embryonic carcinoma cells, whereas this suppression of apoptosis is attenuated by mutation in PS1. Tretinoin 45-58 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-20
9412494-8 1998 These genes-Rara, Thra, and Erbb2- encode receptors for retinoic acid, thyroxine, and neuregulin, respectively. Tretinoin 56-69 retinoic acid receptor, alpha Mus musculus 12-16
10094952-9 1999 From these observations, we propose that RA down-regulates IGFBPs, which in turn causes autocrine modulation of cell growth independent of IGF in hepatoma cells in vitro or in vivo. Tretinoin 41-43 insulin like growth factor binding protein 1 Homo sapiens 59-65
10355579-3 1999 To investigate the mechanism of this sensitisation, the hypothesis was tested that ATRA augments cellular ara-CTP levels in human-derived myelogenous leukemia HL-60 cells. Tretinoin 83-87 solute carrier family 25 member 1 Homo sapiens 110-113
9444955-0 1997 Functional interference between retinoic acid or steroid hormone receptors and the oncoprotein Fli-1. Tretinoin 32-45 Fli-1 proto-oncogene, ETS transcription factor Homo sapiens 95-100
9444955-3 1997 Overexpression of Fli-1 inhibits the retinoic acid-induced activation of genes carrying a functional retinoic acid response element (RARE). Tretinoin 37-50 Fli-1 proto-oncogene, ETS transcription factor Homo sapiens 18-23
9444955-3 1997 Overexpression of Fli-1 inhibits the retinoic acid-induced activation of genes carrying a functional retinoic acid response element (RARE). Tretinoin 101-114 Fli-1 proto-oncogene, ETS transcription factor Homo sapiens 18-23
10497330-4 1999 1]) describes the phenotype of a gene knockout for an enzyme, retinaldehyde dehydrogenase 2 (RALDH-2), that synthesizes retinoic acid (RA) in the early embryo. Tretinoin 120-133 aldehyde dehydrogenase 1 family member A2 Homo sapiens 62-91
10497330-4 1999 1]) describes the phenotype of a gene knockout for an enzyme, retinaldehyde dehydrogenase 2 (RALDH-2), that synthesizes retinoic acid (RA) in the early embryo. Tretinoin 120-133 aldehyde dehydrogenase 1 family member A2 Homo sapiens 93-100
10497330-4 1999 1]) describes the phenotype of a gene knockout for an enzyme, retinaldehyde dehydrogenase 2 (RALDH-2), that synthesizes retinoic acid (RA) in the early embryo. Tretinoin 93-95 aldehyde dehydrogenase 1 family member A2 Homo sapiens 62-91
10520028-10 1999 Thus, ATRA dramatically altered the adhesion phenotype on NB-4 cells: ATRA induced rolling largely attributable to E-selectin, abrogated alpha4 integrin dependent rolling, and promoted acquisition of beta2 integrin dependent firm adherence and transmigration. Tretinoin 6-10 immunoglobulin binding protein 1 Homo sapiens 137-143
10355579-4 1999 MATERIALS AND METHODS: The effect of ATRA and 13-cis-retinoic acid on ara-CTP accumulation and ara-C-induced apoptosis was studied. Tretinoin 37-41 solute carrier family 25 member 1 Homo sapiens 74-77
10355579-6 1999 RESULTS: Pretreatment of HL-60 cells with ATRA (0.01-1 microM) caused a significant decrease in intracellular ara-CTP levels; e.g., incubation for 72 hours with ATRA 1 microM prior to one hour ara-C 10 microM reduced ara-CTP levels to 41% +/- 4% of control. Tretinoin 42-46 solute carrier family 25 member 1 Homo sapiens 114-117
10355579-6 1999 RESULTS: Pretreatment of HL-60 cells with ATRA (0.01-1 microM) caused a significant decrease in intracellular ara-CTP levels; e.g., incubation for 72 hours with ATRA 1 microM prior to one hour ara-C 10 microM reduced ara-CTP levels to 41% +/- 4% of control. Tretinoin 42-46 solute carrier family 25 member 1 Homo sapiens 221-224
10519672-6 1999 Proliferating cell nuclear antigen labeling indices were reduced after treatment with all-trans retinoic acid and 13-cis retinoic acid at early time points post-injury. Tretinoin 96-109 proliferating cell nuclear antigen Rattus norvegicus 0-34
9398535-2 1997 A novel retinoic acid-inducible cDNA clone, designated RI58, was isolated from a cDNA library constructed from retinoic acid-treated NB4 cells by differential hybridization. Tretinoin 8-21 interferon induced protein with tetratricopeptide repeats 5 Homo sapiens 55-59
9398535-2 1997 A novel retinoic acid-inducible cDNA clone, designated RI58, was isolated from a cDNA library constructed from retinoic acid-treated NB4 cells by differential hybridization. Tretinoin 111-124 interferon induced protein with tetratricopeptide repeats 5 Homo sapiens 55-59
10355579-6 1999 RESULTS: Pretreatment of HL-60 cells with ATRA (0.01-1 microM) caused a significant decrease in intracellular ara-CTP levels; e.g., incubation for 72 hours with ATRA 1 microM prior to one hour ara-C 10 microM reduced ara-CTP levels to 41% +/- 4% of control. Tretinoin 161-165 solute carrier family 25 member 1 Homo sapiens 114-117
9398535-6 1997 Culture supernatant from retinoic acid-treated NB4 cells also induced RI58 expression similarly as rhIFN-alpha. Tretinoin 25-38 interferon induced protein with tetratricopeptide repeats 5 Homo sapiens 70-74
9398535-8 1997 These results indicate that RI58 is induced by retinoic acid stimulation through autocrinally secreted IFN-alpha from NB4 cells. Tretinoin 47-60 interferon induced protein with tetratricopeptide repeats 5 Homo sapiens 28-32
10355579-6 1999 RESULTS: Pretreatment of HL-60 cells with ATRA (0.01-1 microM) caused a significant decrease in intracellular ara-CTP levels; e.g., incubation for 72 hours with ATRA 1 microM prior to one hour ara-C 10 microM reduced ara-CTP levels to 41% +/- 4% of control. Tretinoin 161-165 solute carrier family 25 member 1 Homo sapiens 221-224
9398535-9 1997 In the retinoic acid-treated NB4 cells, the expression of RI58 was increased along the process of differentiation. Tretinoin 7-20 interferon induced protein with tetratricopeptide repeats 5 Homo sapiens 58-62
10501184-2 1999 RA treatment of SH-SY5Y cells induces the appearance of functional Trk B and Trk C receptors. Tretinoin 0-2 neurotrophic receptor tyrosine kinase 3 Homo sapiens 77-82
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 brain derived neurotrophic factor Homo sapiens 61-94
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 brain derived neurotrophic factor Homo sapiens 96-100
10501184-3 1999 Acute stimulation of RA-predifferentiated SH-SY5Y cells with brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), or neurotrophin 4/5 (NT-4/5), but not nerve growth factor (NGF), induces Trk autophosphorylation, followed by phosphorylation of Akt and the extracellular signal-regulated kinases (ERKs) 1 and 2. Tretinoin 21-23 neurotrophin 3 Homo sapiens 103-117
9361184-1 1997 The receptors for retinoic acid (RA) and for 1 alpha,25-dihydroxyvitamin D3 (VD), RAR, RXR, and VDR are ligand-inducible members of the nuclear receptor superfamily. Tretinoin 18-31 retinoid X receptor alpha Homo sapiens 87-90
10024510-1 1999 To investigate which retinoid receptors are critical in the regulation by all-trans-retinoic acid (RA) of the mucin genes MUC2, MUC5AC and MUC5B in cultured normal human tracheobronchial epithelial (NHTBE) cells, we used pan-RAR-, pan-RXR- and RAR- isotype (alpha, beta and gamma)-selective agonists and RARalpha- and RARgamma-selective antagonists (RAR is RA receptor and RXR is retinoid X receptor). Tretinoin 99-101 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 128-134
9361184-1 1997 The receptors for retinoic acid (RA) and for 1 alpha,25-dihydroxyvitamin D3 (VD), RAR, RXR, and VDR are ligand-inducible members of the nuclear receptor superfamily. Tretinoin 18-31 vitamin D receptor Homo sapiens 96-99
10369076-0 1999 IGF-I and retinoic acid regulate the distribution pattern of IGFBPs synthesized by the canine mammary tumor cell line CMT-U335. Tretinoin 10-23 insulin like growth factor binding protein 2 Canis lupus familiaris 61-67
9417874-0 1997 Reduction of both RAR and RXR levels is required to maximally alter sensitivity of CA-OV3 ovarian tumor cells to growth suppression by all-trans-retinoic acid. Tretinoin 135-158 retinoid X receptor alpha Homo sapiens 26-29
10459851-7 1999 Both ligand binding and Western blot analyses revealed that epidermal growth factor receptor (EGF-R) was stimulated by 20 nM T but was suppressed by 0.1 microM RA, which also attenuated the stimulating effects of T on EGF-R in NRP-152 and to a lesser extent in NRP-154 cells. Tretinoin 160-162 epidermal growth factor receptor Rattus norvegicus 60-92
10459851-7 1999 Both ligand binding and Western blot analyses revealed that epidermal growth factor receptor (EGF-R) was stimulated by 20 nM T but was suppressed by 0.1 microM RA, which also attenuated the stimulating effects of T on EGF-R in NRP-152 and to a lesser extent in NRP-154 cells. Tretinoin 160-162 epidermal growth factor receptor Rattus norvegicus 94-99
10459851-7 1999 Both ligand binding and Western blot analyses revealed that epidermal growth factor receptor (EGF-R) was stimulated by 20 nM T but was suppressed by 0.1 microM RA, which also attenuated the stimulating effects of T on EGF-R in NRP-152 and to a lesser extent in NRP-154 cells. Tretinoin 160-162 epidermal growth factor receptor Rattus norvegicus 218-223
9351827-0 1997 Phosphorylation of activation functions AF-1 and AF-2 of RAR alpha and RAR gamma is indispensable for differentiation of F9 cells upon retinoic acid and cAMP treatment. Tretinoin 135-148 interferon gamma receptor 2 Homo sapiens 40-53
10021349-3 1999 Since Meis2 has recently been shown to be upregulated by retinoic acid in P19 EC cells (Oulad-Abdelghani, M., Chazaud, C., Bouillet, P., Sapin, V., Chambon, P. and Dolle, P. (1997) Dev. Tretinoin 57-70 Meis homeobox 2 Homo sapiens 6-11
9371525-3 1997 In this study we have evaluated, by a cytofluorimetric method, the presence of HSP-70 in HL-60 cells during treatment with all-trans retinoic acid (ATRA), 9-cis retinoic acid (9-cis RA), and 13-cis retinoic acid (13-cis RA). Tretinoin 161-174 heat shock protein family A (Hsp70) member 4 Homo sapiens 79-85
9371525-8 1997 This reduced production of HSP-70 caused by ATRA and by 9-cis RA, though to a lesser extent, could render the cells more sensitive to cytotoxic agents and could provide the rationale for the efficacy of ATRA + chemotherapy combinations. Tretinoin 44-48 heat shock protein family A (Hsp70) member 4 Homo sapiens 27-33
10407146-1 1999 Some members of the human alcohol dehydrogenase (ADH) family possess retinol dehydrogenase activity and may thus function in production of the active nuclear receptor ligand retinoic acid. Tretinoin 174-187 alcohol dehydrogenase 1B (class I), beta polypeptide Homo sapiens 49-52
10408388-2 1999 This study analyses the ability of all-trans retinoic acid (RA) to alter both sICAM and mICAM-1 expression in C8161 and Hs294T human melanoma cell lines and investigates the involvement of ICAM-1 in the interaction between tumour and lymphokine-activated killer (LAK) cells using the Cr-51 release assay. Tretinoin 45-58 intercellular adhesion molecule 1 Homo sapiens 89-95
10408388-2 1999 This study analyses the ability of all-trans retinoic acid (RA) to alter both sICAM and mICAM-1 expression in C8161 and Hs294T human melanoma cell lines and investigates the involvement of ICAM-1 in the interaction between tumour and lymphokine-activated killer (LAK) cells using the Cr-51 release assay. Tretinoin 60-62 intercellular adhesion molecule 1 Homo sapiens 89-95
10408388-4 1999 Addition of blocking ICAM-1 antibody (10 microg ml(-1)) to the C8161 cells at an effector:tumour cell ratio of 40:1 caused a 2.3-fold reduction in lysis of tumour cells and a 3-fold reduction in lysis of RA-treated cells. Tretinoin 204-206 intercellular adhesion molecule 1 Homo sapiens 21-27
10022522-3 1999 Treatment with retinoic acid for periods of < or = 4 h resulted in dephosphorylation of nuclear U1 70K protein without affecting its abundance. Tretinoin 15-28 small nuclear ribonucleoprotein U1 subunit 70 Homo sapiens 99-105
10448709-8 1999 Furthermore, injection of either thyroid hormone receptor alpha 1 or v-erbA mRNA repressed a reporter gene that contained a retinoic acid response element, demonstrating the ability of the thyroid hormone receptor alpha 1 to repress retinoic acid signaling during gastrulation. Tretinoin 124-137 thyroid hormone receptor alpha a Danio rerio 33-65
10448709-8 1999 Furthermore, injection of either thyroid hormone receptor alpha 1 or v-erbA mRNA repressed a reporter gene that contained a retinoic acid response element, demonstrating the ability of the thyroid hormone receptor alpha 1 to repress retinoic acid signaling during gastrulation. Tretinoin 124-137 thyroid hormone receptor alpha a Danio rerio 189-221
10448709-8 1999 Furthermore, injection of either thyroid hormone receptor alpha 1 or v-erbA mRNA repressed a reporter gene that contained a retinoic acid response element, demonstrating the ability of the thyroid hormone receptor alpha 1 to repress retinoic acid signaling during gastrulation. Tretinoin 233-246 thyroid hormone receptor alpha a Danio rerio 33-65
10448709-8 1999 Furthermore, injection of either thyroid hormone receptor alpha 1 or v-erbA mRNA repressed a reporter gene that contained a retinoic acid response element, demonstrating the ability of the thyroid hormone receptor alpha 1 to repress retinoic acid signaling during gastrulation. Tretinoin 233-246 thyroid hormone receptor alpha a Danio rerio 189-221
10022522-6 1999 Tumor necrosis factor-alpha, which enhances the posttranscriptional action of retinoic acid, reduced U1 70K mRNA expression, while an inhibition of retinoic acid action by transforming growth factor-beta was associated with a marked increase in U1 70K mRNA levels. Tretinoin 78-91 small nuclear ribonucleoprotein U1 subunit 70 Homo sapiens 101-107
10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 intercellular adhesion molecule 1 Homo sapiens 98-104
10386957-4 1999 Upon differentiation of SHSY5Y cells with retinoic acid, we found that the phosphorylation of high molecular mass (NF-H) and medium molecular mass (NF-M) NFs increased, whereas the CDK-5 protein level and kinase activity were unaffected. Tretinoin 42-55 neurofilament medium chain Homo sapiens 148-152
10373566-2 1999 APLs with PML-RARalpha or PLZF-RARalpha fusion protein differ only in their response to retinoic acid (RA) treatment: the t(15;17) (PML-RARalpha-positive) APL blasts are sensitive to RA in vitro, and patients enter disease remission after RA treatment, while those with t(11;17) (PLZF-RARalpha-positive) APLs do not. Tretinoin 31-33 zinc finger and BTB domain containing 16 Homo sapiens 26-30
10022522-6 1999 Tumor necrosis factor-alpha, which enhances the posttranscriptional action of retinoic acid, reduced U1 70K mRNA expression, while an inhibition of retinoic acid action by transforming growth factor-beta was associated with a marked increase in U1 70K mRNA levels. Tretinoin 148-161 small nuclear ribonucleoprotein U1 subunit 70 Homo sapiens 245-251
10213518-2 1999 The present study was conducted to examine whether TGF-beta2 is involved in the inhibition of forelimb bud development caused by all-trans-retinoic acid (RA). Tretinoin 129-152 transforming growth factor, beta 2 Rattus norvegicus 51-60
10406468-0 1999 Identification of a retinoic acid-inducible element in the murine PTH/PTHrP (parathyroid hormone/parathyroid hormone-related peptide) receptor gene. Tretinoin 20-33 parathyroid hormone 1 receptor Mus musculus 77-142
10406468-2 1999 Retinoic Acid (RA) is a potent inducer of extraembryonic endoderm formation and PTH/PTHrP-receptor expression in embryonal carcinoma (EC) and embryonal stem (ES) cells. Tretinoin 0-13 parathyroid hormone 1 receptor Mus musculus 80-98
10406468-2 1999 Retinoic Acid (RA) is a potent inducer of extraembryonic endoderm formation and PTH/PTHrP-receptor expression in embryonal carcinoma (EC) and embryonal stem (ES) cells. Tretinoin 15-17 parathyroid hormone 1 receptor Mus musculus 80-98
10406468-3 1999 Using the P19 EC cell line, we have characterized promoter elements of the murine PTH/PTHrP-receptor gene that are involved in this RA-induced expression. Tretinoin 132-134 parathyroid hormone 1 receptor Mus musculus 82-100
10406468-10 1999 The presence of RXR (alpha, beta, or gamma) in the complexes binding to the R-DR1 suggests that RXR homodimers are involved in RA-induced expression of the PTH/PTHrP-receptor gene. Tretinoin 127-129 parathyroid hormone 1 receptor Mus musculus 156-174
10406468-11 1999 The importance of the R-DR1 for RA-induced expression of PTH/ PTHrP-receptor was shown by an inactivating mutation of the R-DR1, which severely impairs RA-induced expression of PTH/PTHrP-receptor promoter reporter constructs. Tretinoin 32-34 parathyroid hormone 1 receptor Mus musculus 57-76
10406468-11 1999 The importance of the R-DR1 for RA-induced expression of PTH/ PTHrP-receptor was shown by an inactivating mutation of the R-DR1, which severely impairs RA-induced expression of PTH/PTHrP-receptor promoter reporter constructs. Tretinoin 32-34 parathyroid hormone 1 receptor Mus musculus 177-195
10475063-1 1999 We have characterized an element (differentiation response element, DRE) in the promoter region of the c-jun gene that is both necessary and sufficient for retinoic acid (RA) and adenovirus early region (E1A) mediated up-regulation of c-jun gene expression during the differentiation of F9 cells. Tretinoin 156-169 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108
10475063-1 1999 We have characterized an element (differentiation response element, DRE) in the promoter region of the c-jun gene that is both necessary and sufficient for retinoic acid (RA) and adenovirus early region (E1A) mediated up-regulation of c-jun gene expression during the differentiation of F9 cells. Tretinoin 171-173 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108
10473117-8 1999 Wnt-3a, a gene that has been shown to be essential for tail bud formation, is specifically down-regulated in the tail bud of retinoic acid-treated embryos, as early as 2 h after retinoic acid treatment and Wnt-3a transcripts become undetectable by 10 h. In contrast, Wnt-5a and RAR-gamma are still detectable in the tail bud at that time. Tretinoin 125-138 wingless-type MMTV integration site family, member 5A Mus musculus 267-273
10473117-8 1999 Wnt-3a, a gene that has been shown to be essential for tail bud formation, is specifically down-regulated in the tail bud of retinoic acid-treated embryos, as early as 2 h after retinoic acid treatment and Wnt-3a transcripts become undetectable by 10 h. In contrast, Wnt-5a and RAR-gamma are still detectable in the tail bud at that time. Tretinoin 125-138 retinoic acid receptor, gamma Mus musculus 278-287
10339585-4 1999 In contrast to bone marrow cells from PLZF-RARalpha transgenic mice, those from NPM-RARalpha transgenic mice could be induced to differentiate by all-trans-retinoic acid (ATRA). Tretinoin 146-169 retinoic acid receptor, alpha Mus musculus 84-92
10339585-4 1999 In contrast to bone marrow cells from PLZF-RARalpha transgenic mice, those from NPM-RARalpha transgenic mice could be induced to differentiate by all-trans-retinoic acid (ATRA). Tretinoin 171-175 retinoic acid receptor, alpha Mus musculus 84-92
10330422-5 1999 The RA-induced expression of C/EBPepsilon markedly increased in U937 myelomonoblasts that were induced to express promyelocytic leukemia/RARalpha (PML/RARalpha), but not in those induced to express promyelocytic leukemia zinc finger/RARalpha (PLZF/RARalpha). Tretinoin 4-6 zinc finger and BTB domain containing 16 Homo sapiens 243-247
10367173-2 1999 PURPOSE: 9-cis retinoic acid (ALRT 1057; 9cRA) is a promising new retinoid that binds to all known retinoic acid receptors (RAR and RXR), potentially providing it with a broader spectrum of biologic activity than either 13-cis retinoic acid or all-trans retinoic acid. Tretinoin 15-28 myotubularin related protein 11 Homo sapiens 42-45
10367173-2 1999 PURPOSE: 9-cis retinoic acid (ALRT 1057; 9cRA) is a promising new retinoid that binds to all known retinoic acid receptors (RAR and RXR), potentially providing it with a broader spectrum of biologic activity than either 13-cis retinoic acid or all-trans retinoic acid. Tretinoin 15-28 retinoid X receptor alpha Homo sapiens 132-135
10094816-3 1999 This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern. Tretinoin 5-7 RB transcriptional corepressor like 2 Homo sapiens 181-184
10075839-0 1999 Essential roles of retinoic acid signaling in interdigital apoptosis and control of BMP-7 expression in mouse autopods. Tretinoin 19-32 bone morphogenetic protein 7 Mus musculus 84-89
10503735-0 1999 All-trans retinoic acid inhibits the growth of breast cancer cells by up-regulating ICAM-1 expression. Tretinoin 10-23 intercellular adhesion molecule 1 Homo sapiens 84-90
10503735-4 1999 Results indicate that breast cancer (BC) cell lines exposed to ATRA selectively up-modulate the surface expression of ICAM-1/CD54, a molecule regulating cell/cell contacts. Tretinoin 63-67 intercellular adhesion molecule 1 Homo sapiens 118-124
10503735-4 1999 Results indicate that breast cancer (BC) cell lines exposed to ATRA selectively up-modulate the surface expression of ICAM-1/CD54, a molecule regulating cell/cell contacts. Tretinoin 63-67 intercellular adhesion molecule 1 Homo sapiens 125-129
10202931-3 1999 Ultraviolet irradiation caused a near-total loss of retinoic acid induction of two RAR/RXR target genes, cellular retinoic acid binding protein-II and RA 4-hydroxylase, but did not affect 1,25-dihydroxyvitamin D3 induction of the vitamin D receptor/RXR-regulated gene vitamin D 24-hydroxylase. Tretinoin 52-65 retinoid X receptor alpha Homo sapiens 87-90
10202931-3 1999 Ultraviolet irradiation caused a near-total loss of retinoic acid induction of two RAR/RXR target genes, cellular retinoic acid binding protein-II and RA 4-hydroxylase, but did not affect 1,25-dihydroxyvitamin D3 induction of the vitamin D receptor/RXR-regulated gene vitamin D 24-hydroxylase. Tretinoin 52-65 cellular retinoic acid binding protein 2 Homo sapiens 105-146
10068679-14 1999 We conclude that retinoids or combination of retinoids with specificities for both RAR and RXR may markedly enhance the ability of ATRA to inhibit clonal growth and induce differentiation of HL-60 and NB4 leukemic cells. Tretinoin 131-135 retinoid X receptor alpha Homo sapiens 91-94
10070102-7 1999 The mutant retained DNA binding activity in the presence of retinoid X receptor-gamma to an RA response element in the hSP-B promoter. Tretinoin 92-94 retinoid X receptor gamma Homo sapiens 60-85
10066345-0 1999 The regulatory effects of all-trans-retinoic acid on isotype switching: retinoic acid induces IgA switch rearrangement in cooperation with IL-5 and inhibits IgG1 switching. Tretinoin 26-49 LOC105243590 Mus musculus 157-161
10066345-4 1999 RA has another effect on isotype switching; RA strongly inhibits IL-4-dependent IgG1 and IgE production. Tretinoin 0-2 LOC105243590 Mus musculus 80-84
10066345-4 1999 RA has another effect on isotype switching; RA strongly inhibits IL-4-dependent IgG1 and IgE production. Tretinoin 44-46 LOC105243590 Mus musculus 80-84
10066345-11 1999 These results indicated that RA can regulate isotype switching at the level of germline transcription and directs switching to IgA with the help of IL-5 and inhibits IgG1 switching. Tretinoin 29-31 LOC105243590 Mus musculus 166-170
10082656-0 1999 Retinoic acid potentiates TNF-alpha-induced ICAM-1 expression in normal human epidermal keratinocytes. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 44-50
10082656-5 1999 However, at high Ca2+ (1500 microM), ICAM-1 levels were augmented in response to RA-treatment. Tretinoin 81-83 intercellular adhesion molecule 1 Homo sapiens 37-43
10082656-7 1999 RA potentiated the TNF-alpha-induced ICAM-1 response in all Ca2+-concentrations. Tretinoin 0-2 intercellular adhesion molecule 1 Homo sapiens 37-43
10049581-7 1999 Retinoic acid is involved in vertebrate anteroposterior axis formation and cellular differentiation and has been shown to modulate gene expression controlling early embryonal development, suggesting a developmental role for RAI2. Tretinoin 0-13 retinoic acid induced 2 Homo sapiens 224-228
9973257-1 1999 In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Tretinoin 19-32 retinoid X receptor alpha Homo sapiens 96-115
9973257-1 1999 In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Tretinoin 19-32 retinoid X receptor alpha Homo sapiens 117-120
9973257-1 1999 In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Tretinoin 34-36 retinoid X receptor alpha Homo sapiens 96-115
9973257-1 1999 In the presence of retinoic acid (RA), the retinoid receptors, retinoic acid receptor (RAR) and retinoid X receptor (RXR), are able to up-regulate transcription directly by binding to RA-responsive elements on the promoters of responsive genes. Tretinoin 34-36 retinoid X receptor alpha Homo sapiens 117-120
9973257-5 1999 Using a mammalian two-hybrid system, we report here that human RARalpha (hRARalpha) can disrupt in a RA-dependent manner the homo- and heterodimerization properties of c-Jun and c-Fos. Tretinoin 63-65 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 168-173
9973257-5 1999 Using a mammalian two-hybrid system, we report here that human RARalpha (hRARalpha) can disrupt in a RA-dependent manner the homo- and heterodimerization properties of c-Jun and c-Fos. Tretinoin 63-65 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-183
9973257-6 1999 This inhibition of dimerization is cell specific, occurring only in those cells that exhibit RA-induced repression of AP-1 transcriptional activity. Tretinoin 93-95 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122
10023688-6 1999 RA treatment led to PLZF/RARalpha degradation. Tretinoin 0-2 zinc finger and BTB domain containing 16 Homo sapiens 20-24
9926928-0 1999 Retinoic acid inhibits transformation by preventing phosphatidylinositol 3-kinase dependent activation of the c-fos promoter. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115
9926928-2 1999 Inhibition of transformation results from a retinoic acid-dependent failure of cells to fully express the c-fos proto-oncogene. Tretinoin 44-57 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111
9926928-3 1999 Retinoic acid prevents transactivation of the c-fos promoter by disrupting signaling between tyrosine kinases at the plasma membrane and trans-acting factors at the c-fos promoter. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51
9926928-3 1999 Retinoic acid prevents transactivation of the c-fos promoter by disrupting signaling between tyrosine kinases at the plasma membrane and trans-acting factors at the c-fos promoter. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170
10027563-3 1999 Exposure to RA caused an immediate up-regulation of NeuroD, increased p21 expression, and concurrent exit from cell cycle. Tretinoin 12-14 KRAS proto-oncogene, GTPase Rattus norvegicus 70-73
10027563-5 1999 An accompanying effect of RA was to sustain or up-regulate trkA, trkB, trkC, and p75NGFR expression. Tretinoin 26-28 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 59-63
10780480-3 1999 In wild type F9 cells, induction of c-jun gene was observed at 18 h after treatment with RA. Tretinoin 89-91 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41
10780480-4 1999 Interestingly, RA-dependent expression of c-jun gene was not induced in cells expressing the p300-directed ribozyme. Tretinoin 15-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-47
9463728-0 1997 Changes in human serum alcohol dehydrogenase activity during retinoic acid treatment of cancer patients. Tretinoin 61-74 aldo-keto reductase family 1 member A1 Homo sapiens 23-44
9463728-12 1997 The data from this study also suggest that retinoic acid has a positive feedback effect on total ADH activity after 1 week of treatment. Tretinoin 43-56 aldo-keto reductase family 1 member A1 Homo sapiens 97-100
9345016-0 1997 Induction of apoptosis without differentiation by retinoic acid in PLB-985 cells requires the activation of both RAR and RXR. Tretinoin 50-63 retinoid X receptor alpha Homo sapiens 121-124
9365539-2 1997 APL is characterized by three distinct and unique features: i) the accumulation in the bone marrow of tumor cells with promyelocytic features; ii) the invariable association with specific translocations which always involve chromosome 17 and the Retinoic Acid Receptor alpha (RAR alpha) locus; iii) the exquisite sensitivity of APL blasts to the differentiating action of Retinoic Acid (RA). Tretinoin 276-278 retinoic acid receptor, alpha Mus musculus 246-274
9365540-0 1997 Retinoic acid downregulates growth, fibronectin and RAR alpha in 3T3 cells: Ha-ras blocks this response and RA metabolism. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 52-61
21235904-1 1997 Retinoic acid (RA) and the retinoids are potent hormones derived from the nutrient vitamin A; they bind members of the nuclear steroid receptor family (RAR, RXR), which are ligand-dependent trans-activators of target gene transcription. Tretinoin 0-13 Rab40B, member RAS oncogene family Mus musculus 152-155
21235904-1 1997 Retinoic acid (RA) and the retinoids are potent hormones derived from the nutrient vitamin A; they bind members of the nuclear steroid receptor family (RAR, RXR), which are ligand-dependent trans-activators of target gene transcription. Tretinoin 15-17 Rab40B, member RAS oncogene family Mus musculus 152-155
9404823-0 1997 Modulation of P-glycoprotein activity by glial factors and retinoic acid in an immortalized rat brain microvessel endothelial cell line. Tretinoin 59-72 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 14-28
9377582-4 1997 The c-jun-transfected MCF7 cells had increased basal AP-1 transactivation activity and increased expression of AP-1-regulated genes but were resistant to the antiproliferative effects of atRA. Tretinoin 187-191 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9
9377582-5 1997 However, MCF7 cells transfected with a deletion mutant of c-jun, TAM-67, which lacks most of the amino-terminal transactivation domain of cJun and is unable to activate AP-1-dependent gene expression, were sensitive to the growth-inhibitory effects of atRA. Tretinoin 252-256 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63
9377582-9 1997 However, retinoic acid responsive element DNA binding activity was intact in c-jun-transfected cells. Tretinoin 9-22 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82
9326603-5 1997 The transcriptional synergy by TSA and RA required the RA-responsive element and a functional retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimer, both obligatory for RA-dependent transcription. Tretinoin 39-41 retinoid X receptor alpha Homo sapiens 94-113
9326603-5 1997 The transcriptional synergy by TSA and RA required the RA-responsive element and a functional retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimer, both obligatory for RA-dependent transcription. Tretinoin 39-41 retinoid X receptor alpha Homo sapiens 115-118
9326603-8 1997 Finally, we show that TSA alone or in combination with RA increases in vivo endonuclease sensitivity within the RA-responsive promoter, suggesting that TSA treatment might alter a local chromatin environment to enhance RXR/RAR heterodimer action. Tretinoin 55-57 retinoid X receptor alpha Homo sapiens 219-222
9362447-9 1997 RA treatment dramatically induced a DR5-binding RXRalpha-RARbeta heterodimer. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 48-56
9387884-5 1997 When RA-treated aggregates of P19 cells were cultured under conditions permissive for neurite outgrowth, we observed a significant increase in the amount of detectable NF-L protein localized within morphologically distinct neurons. Tretinoin 5-7 neurofilament light chain Homo sapiens 168-172
9359633-4 1997 Results obtained suggest that chick embryo hepatocytes growth in an exclusive serum dependent way shows an early sensibility to EGF stimulation as regards to the proliferative activity and amino acid transport, responds to retinoic acid treatment and lack of contact inhibition. Tretinoin 223-236 epidermal growth factor Gallus gallus 128-131
10213518-2 1999 The present study was conducted to examine whether TGF-beta2 is involved in the inhibition of forelimb bud development caused by all-trans-retinoic acid (RA). Tretinoin 154-156 transforming growth factor, beta 2 Rattus norvegicus 51-60
10213518-5 1999 In the 100 mg/kg group, a dose at which RA caused reduction defects of forearm bones, TGF-beta2 expression was observed in the distal margin of forelimb buds, in which no expression was observed in the control and 50 mg/kg group. Tretinoin 40-42 transforming growth factor, beta 2 Rattus norvegicus 86-95
10213518-8 1999 The whole embryo culture system also showed that the expression of TGF-beta2 was induced at the concentration of 3 microg/mL in the same region as found in forelimb buds of embryos from dams administered a teratogenic dosage of RA in vivo. Tretinoin 228-230 transforming growth factor, beta 2 Rattus norvegicus 67-76
9331266-11 1997 Addition of 1 microM retinoic acid enhanced the cell density-induced downregulation of CD44 mRNA, but did not significantly affect the CD44 cell surface protein expression. Tretinoin 21-34 CD44 molecule (Indian blood group) Homo sapiens 87-91
10213518-9 1999 Local application of TGF-beta2 to the distal margin of the forelimb bud in Day 12 embryos reduced proximodistal growth and protein content in forelimb buds for 24 h in culture even without RA treatment. Tretinoin 189-191 transforming growth factor, beta 2 Rattus norvegicus 21-30
9272954-5 1997 Comparative analysis of the retinoid responses of Hoxd4, Hoxa4 and Hoxb4 reveals that, while they can be rapidly induced by RA, there is a window of competence for this response, which is different to that of more 3" Hox genes. Tretinoin 124-126 homeobox B4 Homo sapiens 67-72
10213518-11 1999 Neutralization of TGF-beta2 with its antibody in the distal margin of forelimb buds partially prevented the RA-induced inhibition of forelimb bud growth in the whole embryo culture system. Tretinoin 108-110 transforming growth factor, beta 2 Rattus norvegicus 18-27
10213518-12 1999 These results suggest that RA-induced TGF-beta2 in the distal margin of forelimb buds may be involved in RA-induced inhibition of forelimb bud growth via reduction of cell proliferation in the distal margin, and RA-induced TGF-beta2 in the prechondrogenic area may inhibit chondrogenesis in the future forearm bones, followed by reduction defects of the forearm bones. Tretinoin 27-29 transforming growth factor, beta 2 Rattus norvegicus 38-47
10213518-12 1999 These results suggest that RA-induced TGF-beta2 in the distal margin of forelimb buds may be involved in RA-induced inhibition of forelimb bud growth via reduction of cell proliferation in the distal margin, and RA-induced TGF-beta2 in the prechondrogenic area may inhibit chondrogenesis in the future forearm bones, followed by reduction defects of the forearm bones. Tretinoin 27-29 transforming growth factor, beta 2 Rattus norvegicus 223-232
9342843-11 1997 In ATRA-sensitive but not ATRA-resistant NB4 cells, ATRA down-regulated retinoid X receptor-alpha (RXR alpha) expression, a known marker of ATRA response in parental NB4 cells. Tretinoin 3-7 retinoid X receptor alpha Homo sapiens 72-97
10102471-8 1999 However, in HL-525 cells either pretreated by retinoic acid that reinduces PKCbeta gene expression or transfected with PKCbeta cDNA, PMA significantly activated PAI-1 synthesis and adhesion of cells. Tretinoin 46-59 serpin family E member 1 Homo sapiens 161-166
9342843-11 1997 In ATRA-sensitive but not ATRA-resistant NB4 cells, ATRA down-regulated retinoid X receptor-alpha (RXR alpha) expression, a known marker of ATRA response in parental NB4 cells. Tretinoin 3-7 retinoid X receptor alpha Homo sapiens 99-108
9342843-12 1997 Notably, engineered overexpression of RXR alpha in ATRA-sensitive NB4 cells did not block ATRA-mediated growth suppression. Tretinoin 51-55 retinoid X receptor alpha Homo sapiens 38-47
9277051-3 1997 CD15 and CD11b were expressed on the APL cells in vivo as neutrophil maturation markers, while growth activity of the cells was decreased during ATRA administration. Tretinoin 145-149 integrin subunit alpha M Homo sapiens 9-14
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 150-163 zinc finger and BTB domain containing 16 Homo sapiens 35-39
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 40-42 zinc finger and BTB domain containing 16 Homo sapiens 35-39
10219964-7 1999 Retinol, retinoic acid and cholecalciferol were strong inhibitors for xenobiotic oxidations catalysed by recombinant CYP1A1, 2C8 and 2C19. Tretinoin 9-22 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 117-123
9245716-1 1997 Following induction of cell differentiation in vitro, an increase in Syk activity was observed only in HL60 cells differentiation into granulocytes induced by all trans retinoic acid (RA) but not into macrophages induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) or monocytes induced by sodium butyrate. Tretinoin 169-182 spleen associated tyrosine kinase Homo sapiens 69-72
9245716-1 1997 Following induction of cell differentiation in vitro, an increase in Syk activity was observed only in HL60 cells differentiation into granulocytes induced by all trans retinoic acid (RA) but not into macrophages induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) or monocytes induced by sodium butyrate. Tretinoin 184-186 spleen associated tyrosine kinase Homo sapiens 69-72
9245716-3 1997 Anti-phosphotyrosine blot revealed that tyrosine phosphorylation of Syk was significantly increased as the function of induction time by RA, but not by TPA and sodium butyrate, suggesting that tyrosine phosphorylation might account for Syk activation. Tretinoin 137-139 spleen associated tyrosine kinase Homo sapiens 68-71
10199205-11 1999 Although ATRA was administered at a dose of 80 mg/day for more than 2 months, the number of myelocytes and promyelocytes increased Finally CAG (cytarabine, aclarubicin, G-CSF) therapy was initiated, but the patient died due to intracranial invasion and hemorrhage accompanied by disseminated intravascular coagulation. Tretinoin 9-13 colony stimulating factor 3 Homo sapiens 169-174
9245716-3 1997 Anti-phosphotyrosine blot revealed that tyrosine phosphorylation of Syk was significantly increased as the function of induction time by RA, but not by TPA and sodium butyrate, suggesting that tyrosine phosphorylation might account for Syk activation. Tretinoin 137-139 spleen associated tyrosine kinase Homo sapiens 236-239
9218601-4 1997 However, when IGF-I is added to RA-treated cells, the proportion of CD11b-positive cells increases to a level similar to that in RA-treated cells cultured in serum-containing medium. Tretinoin 32-34 integrin subunit alpha M Homo sapiens 68-73
9915823-6 1999 Although the expression level of ALT III was found to be much lower in most tissues and cells compared with that of PLCdelta4, it was significantly higher in some neural cells, such as NIE-115 cells and p19 cells differentiated to neural cells by retinoic acid. Tretinoin 247-260 glutamic pyruvic transaminase, soluble Mus musculus 33-36
9212063-13 1997 An intron fragment 3" of exon 1C conferred retinoic acid responsivity when fused to a reporter gene plasmid, suggesting a molecular mechanism for the previously observed ability of retinoic acid to induce the VDR. Tretinoin 43-56 vitamin D receptor Homo sapiens 209-212
9212063-13 1997 An intron fragment 3" of exon 1C conferred retinoic acid responsivity when fused to a reporter gene plasmid, suggesting a molecular mechanism for the previously observed ability of retinoic acid to induce the VDR. Tretinoin 181-194 vitamin D receptor Homo sapiens 209-212
9989277-13 1999 Consistent with increased substrate-driven retinoic acid synthesis in SCC, the expression of transglutaminase 1 was suppressed to a greater extent in the SCCs than in NHK, when cells were exposed to equivalent medium concentrations of retinol. Tretinoin 43-56 serpin family B member 3 Homo sapiens 70-73
9223607-5 1997 RA administration to old mice (24 h before sacrifice) was able to restore the amount of mRNA of nuclear receptors and of RC3. Tretinoin 0-2 neurogranin Mus musculus 121-124
9223607-6 1997 It is hypothesized that a decrease in the cellular action of RA and T3 could play a role, via a decrease in the expression of RC3, in the alteration of synaptic plasticity occurring in aged mice. Tretinoin 61-63 neurogranin Mus musculus 126-129
9888461-0 1999 Transcriptional repression of the human collagenase-1 (MMP-1) gene in MDA231 breast cancer cells by all-trans-retinoic acid requires distal regions of the promoter. Tretinoin 100-123 matrix metallopeptidase 1 Homo sapiens 55-60
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 175-188 signal transducer and activator of transcription 1 Homo sapiens 88-145
9891864-10 1999 The demonstration that PML-RAR alpha is degraded, perhaps via a ubiquitin-dependent pathway, in response to ATRA. Tretinoin 108-112 PML nuclear body scaffold Homo sapiens 23-26
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 190-194 signal transducer and activator of transcription 1 Homo sapiens 88-145
9186002-4 1997 Here we have studied the activation and induction of IFN-specific transcription factors signal transducer and activator of transcription (STAT) 1, STAT2, and p48 in all-trans-retinoic acid (ATRA)-differentiated myeloid leukemia cells using promyelocytic NB4, myeloblastic HL-60, and monoblastic U937 cells as model systems. Tretinoin 190-194 signal transducer and activator of transcription 2 Homo sapiens 147-152
9186002-7 1997 However, during ATRA-induced differentiation, steady-state STAT1, STAT2, and especially p48 mRNA and corresponding protein levels were elevated both in NB4 and U937 cells, apparently correlating to an enhanced responsiveness of these cells to IFNs. Tretinoin 16-20 signal transducer and activator of transcription 1 Homo sapiens 59-64
9186002-7 1997 However, during ATRA-induced differentiation, steady-state STAT1, STAT2, and especially p48 mRNA and corresponding protein levels were elevated both in NB4 and U937 cells, apparently correlating to an enhanced responsiveness of these cells to IFNs. Tretinoin 16-20 signal transducer and activator of transcription 2 Homo sapiens 66-71
9186002-8 1997 ATRA treatment of NB4 cells sensitized them to IFN action as seen by increased IFN-gamma activation site DNA-binding activity or by efficient formation of IFN-alpha-specific ISGF3 complex and subsequent oligoadenylate synthetase and MxB gene expression. Tretinoin 0-4 signal transducer and activator of transcription 1 Homo sapiens 174-179
9186002-8 1997 ATRA treatment of NB4 cells sensitized them to IFN action as seen by increased IFN-gamma activation site DNA-binding activity or by efficient formation of IFN-alpha-specific ISGF3 complex and subsequent oligoadenylate synthetase and MxB gene expression. Tretinoin 0-4 MX dynamin like GTPase 2 Homo sapiens 233-236
9192867-0 1997 Human TAF(II)135 potentiates transcriptional activation by the AF-2s of the retinoic acid, vitamin D3, and thyroid hormone receptors in mammalian cells. Tretinoin 76-89 TATA-box binding protein associated factor 4 Homo sapiens 6-16
9192867-3 1997 We show that expression of hTAF(II)135 in mammalian cells strongly and selectively potentiates transcriptional stimulation by the activation function-2 (AF-2) of the retinoic acid, thyroid hormone, and vitamin D3 receptors (RAR, TR, and VDR), but does not affect the AF-2s of the estrogen (ER) or retinoid X (RXR) receptors. Tretinoin 166-179 TATA-box binding protein associated factor 4 Homo sapiens 27-38
9891864-10 1999 The demonstration that PML-RAR alpha is degraded, perhaps via a ubiquitin-dependent pathway, in response to ATRA. Tretinoin 108-112 retinoic acid receptor alpha Homo sapiens 27-36
20426546-10 1999 Addition of ATRA or 9-cis-retinoic acid (9CRA) to cultures of fetal progenitors or HL-60 cells, resulted in a time- and dose-dependent increase in CD38 expression, ATRA being the more potent of the two retinoids. Tretinoin 12-16 CD38 molecule Homo sapiens 147-151
9148917-1 1997 A subset of nuclear receptors, including those for thyroid hormone (TR), retinoic acid, vitamin D3, and eicosanoids, can form heterodimers with the retinoid X receptor (RXR) on DNA regulatory elements in the absence of their cognate ligands. Tretinoin 73-86 retinoid X receptor alpha Homo sapiens 148-167
9148917-1 1997 A subset of nuclear receptors, including those for thyroid hormone (TR), retinoic acid, vitamin D3, and eicosanoids, can form heterodimers with the retinoid X receptor (RXR) on DNA regulatory elements in the absence of their cognate ligands. Tretinoin 73-86 retinoid X receptor alpha Homo sapiens 169-172
20426546-10 1999 Addition of ATRA or 9-cis-retinoic acid (9CRA) to cultures of fetal progenitors or HL-60 cells, resulted in a time- and dose-dependent increase in CD38 expression, ATRA being the more potent of the two retinoids. Tretinoin 164-168 CD38 molecule Homo sapiens 147-151
20426546-11 1999 However, ATRA inhibited colony formation, reduced the expansion of CFC and accelerated the loss of CD34 expression at doses required for the induction of CD38 expression. Tretinoin 9-13 CD38 molecule Homo sapiens 154-158
20426546-12 1999 DISCUSSION: ATRA-induced CD38 expression on cells to levels comparable to those found on progenitors in vivo. Tretinoin 12-16 CD38 molecule Homo sapiens 25-29
9135005-1 1997 The role of the cellular retinoic acid binding protein type II (CRABPII) in the retinoic acid (RA) signaling pathway is poorly understood. Tretinoin 25-38 cellular retinoic acid binding protein 2 Homo sapiens 64-71
9882496-9 1999 Interestingly, transcripts encoding mP450RAI, a cytochrome P450, the product of which is believed to catabolize retinoic acid, were abundant in the retinoid-poor region of the caudal embryo. Tretinoin 112-125 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 36-44
9135005-1 1997 The role of the cellular retinoic acid binding protein type II (CRABPII) in the retinoic acid (RA) signaling pathway is poorly understood. Tretinoin 65-67 cellular retinoic acid binding protein 2 Homo sapiens 16-62
9135005-3 1997 Ectopic CRABPII expression supported dose-dependent growth inhibition by RA in SC115-resistant but not MDA-MB-231-resistant cells, indicating that CRABPII is sufficient to rescue RA antiproliferation in a permissive background. Tretinoin 9-11 cellular retinoic acid binding protein 2 Homo sapiens 147-154
9135005-3 1997 Ectopic CRABPII expression supported dose-dependent growth inhibition by RA in SC115-resistant but not MDA-MB-231-resistant cells, indicating that CRABPII is sufficient to rescue RA antiproliferation in a permissive background. Tretinoin 73-75 cellular retinoic acid binding protein 2 Homo sapiens 8-15
9180290-9 1997 RT-PCR analysis of the colonies resulting from the action of the combination IFN alpha plus ATRA showed the presence of an increased number of BCR-ABL-negative colonies relatively to what was observed with IFN alpha alone. Tretinoin 92-96 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 143-150
9882496-10 1999 mP450RAI was rapidly induced by retinoic acid treatment in vivo, consistent with previous studies suggesting that it plays a critical role in retinoid signaling. Tretinoin 32-45 cytochrome P450, family 26, subfamily a, polypeptide 1 Mus musculus 0-8
9831819-6 1999 RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. Tretinoin 0-2 adenosylmethionine decarboxylase 1 Bos taurus 116-150
9200136-0 1997 Retinoic acid induces a tissue-specific deletion in the expression domain of Otx2. Tretinoin 0-13 orthodenticle homeobox 2 Homo sapiens 77-81
9831819-6 1999 RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. Tretinoin 0-2 adenosylmethionine decarboxylase 1 Bos taurus 152-157
9111003-4 1997 Physiological concentrations of retinoic acid were found to simultaneously induce stromelysin-3 and repress interstitial collagenase. Tretinoin 32-45 matrix metallopeptidase 11 Homo sapiens 82-95
9831819-7 1999 The putrescine content was significantly increased in RA-treated RPE cells up until 24 h, while spermidine, spermine and N1-acetylspermidine contents were significantly increased until 16 h. Our findings suggest that RA treatment increases the intracellular polyamine concentration of RPE cells via activation of ODC, SAMDC and SAT and that this results in the promotion of RPE cell growth until the cells reach full confluency. Tretinoin 217-219 adenosylmethionine decarboxylase 1 Bos taurus 318-323
9111003-6 1997 Furthermore, in transient transfection experiments, the activity of the stromelysin-3 promoter was induced by retinoic acid through endogenous receptors acting on a DR1 retinoic acid-responsive element. Tretinoin 110-123 matrix metallopeptidase 11 Homo sapiens 72-85
9894157-6 1998 In contrast, the FEN-1 mRNA level showed a sharp decrease in HL-60 cells differentiated by dimethyl-sulfoxide, all-trans retinoic acid or 12-O-tetradecanoylphorbol-13-acetate. Tretinoin 121-134 flap structure-specific endonuclease 1 Homo sapiens 17-22
9092506-1 1997 Induction of murine STAT1 gene expression by retinoic acid. Tretinoin 45-58 signal transducer and activator of transcription 1 Mus musculus 20-25
9092506-2 1997 We have previously demonstrated that up-regulation of STAT1 protein by all-trans-retinoic acid (RA) in interferon (IFN)-unresponsive cells permits growth inhibition by IFNs. Tretinoin 75-94 signal transducer and activator of transcription 1 Mus musculus 54-59
9092506-2 1997 We have previously demonstrated that up-regulation of STAT1 protein by all-trans-retinoic acid (RA) in interferon (IFN)-unresponsive cells permits growth inhibition by IFNs. Tretinoin 96-98 signal transducer and activator of transcription 1 Mus musculus 54-59
9869297-4 1998 This 3" enhancer contains three sequences that are highly conserved in similar RA-inducible enhancers identified in the murine and human Hoxa1 genes and in the chicken Hoxb1 gene. Tretinoin 79-81 homeobox B1 Gallus gallus 168-173
9092506-3 1997 Here, we show that the promoter of STAT1 directly responds to retinoic acid treatment. Tretinoin 62-75 signal transducer and activator of transcription 1 Mus musculus 35-40
9853959-0 1998 Ectopic expression of hoxb2 after retinoic acid treatment or mRNA injection: disruption of hindbrain and craniofacial morphogenesis in zebrafish embryos. Tretinoin 34-47 homeobox B2a Danio rerio 22-27
9224660-5 1997 Its transcription was also activated by retinoic acid receptor (RAR) which binds as a heterodimer with RXR to a retinoic acid responsive element (RARE) in the downstream region. Tretinoin 40-53 retinoic acid receptor, alpha Mus musculus 64-67
9122176-3 1997 In this report, we present evidence that RA down-regulates MGP gene expression in different rat and human cell lines via endogenous retinoid receptors [RA receptor (RAR) and retinoid X receptor (RXR)]. Tretinoin 41-43 matrix Gla protein Rattus norvegicus 59-62
9122176-3 1997 In this report, we present evidence that RA down-regulates MGP gene expression in different rat and human cell lines via endogenous retinoid receptors [RA receptor (RAR) and retinoid X receptor (RXR)]. Tretinoin 41-43 retinoid X receptor alpha Homo sapiens 174-193
9122176-3 1997 In this report, we present evidence that RA down-regulates MGP gene expression in different rat and human cell lines via endogenous retinoid receptors [RA receptor (RAR) and retinoid X receptor (RXR)]. Tretinoin 41-43 retinoid X receptor alpha Homo sapiens 195-198
9122176-7 1997 Furthermore, electrophoretic mobility-shift assays performed with proteins from RA-treated cells show that endogenous RAR/RXR binds to the NRE. Tretinoin 80-82 retinoid X receptor alpha Homo sapiens 122-125
9122176-9 1997 Our results indicate that RA-mediated repression of the hMGP gene is due to binding of liganded RAR/RXR to a novel negative RA response element. Tretinoin 26-28 retinoid X receptor alpha Homo sapiens 100-103
9122176-9 1997 Our results indicate that RA-mediated repression of the hMGP gene is due to binding of liganded RAR/RXR to a novel negative RA response element. Tretinoin 96-98 retinoid X receptor alpha Homo sapiens 100-103
9853959-7 1998 Treatments with retinoic acid produced a phenotype similar to that of ectopic hoxb2 expression, including ectopic krx20 (but not valentino) expression in the eye, and fusion of cartilages from pharyngeal arches 1 and 2. Tretinoin 16-29 early growth response 2b Danio rerio 114-119
9890601-7 1999 RA treatment caused an increase of CRBP I mRNA; conversely, treatment with DEX caused a decrease in CRBP I mRNA that was prevented by concomitant treatment with RA. Tretinoin 0-2 retinol binding protein 1 Rattus norvegicus 35-41
9828118-0 1998 Induction of lactoferrin expression in murine ES cells by retinoic acid and estrogen. Tretinoin 58-71 lactotransferrin Mus musculus 13-24
9890601-7 1999 RA treatment caused an increase of CRBP I mRNA; conversely, treatment with DEX caused a decrease in CRBP I mRNA that was prevented by concomitant treatment with RA. Tretinoin 161-163 retinol binding protein 1 Rattus norvegicus 100-106
9890601-8 1999 These data suggest CRBP I may play a role in RA-induced septation, in the inhibition of septation caused by DEX, and in the ability of RA to prevent DEX-blocked septation. Tretinoin 45-47 retinol binding protein 1 Rattus norvegicus 19-25
9890601-8 1999 These data suggest CRBP I may play a role in RA-induced septation, in the inhibition of septation caused by DEX, and in the ability of RA to prevent DEX-blocked septation. Tretinoin 135-137 retinol binding protein 1 Rattus norvegicus 19-25
9124579-6 1997 The mRNA level for cellular retinol binding protein I, a gene with RA responsive element (RARE), was also suppressed by 78% in BDL. Tretinoin 67-69 retinol binding protein 1 Rattus norvegicus 19-53
9121125-4 1997 Expression of HB5 and HF2 antigens was down-regulated during cellular differentiation of G3 cells by retinoic acid or N,N"-hexamethylene-bis-acetamide treatment, whereas that of HE11 antigen was up-regulated with cellular differentiation by retinoic acid. Tretinoin 101-114 complement factor H Homo sapiens 22-25
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 151-164 heat shock protein 90 beta family member 1 Homo sapiens 54-59
9828118-3 1998 Lactoferrin expression is controlled by different regulators, including retinoic acid and estrogen. Tretinoin 72-85 lactotransferrin Mus musculus 0-11
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 151-164 heat shock protein 90 beta family member 1 Homo sapiens 308-313
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 166-168 heat shock protein 90 beta family member 1 Homo sapiens 54-59
9883882-1 1998 We studied the regulation of the beta-galactoside alpha2,6-sialyltransferase (hST6Gal I) gene during HL-60 cell differentiation induced with dimethyl sulfoxide (DMSO), all transretinoic acid (ATRA), and phorbol myristate acetate (PMA). Tretinoin 172-190 ST6 beta-galactoside alpha-2,6-sialyltransferase 1 Homo sapiens 78-87
9883882-1 1998 We studied the regulation of the beta-galactoside alpha2,6-sialyltransferase (hST6Gal I) gene during HL-60 cell differentiation induced with dimethyl sulfoxide (DMSO), all transretinoic acid (ATRA), and phorbol myristate acetate (PMA). Tretinoin 192-196 ST6 beta-galactoside alpha-2,6-sialyltransferase 1 Homo sapiens 78-87
10743065-2 1997 METHODS: The relationship between molecular chaperone Grp94 and c-myc oncogene expression in the human colorectal carcinoma cell line CCL229, CX-1 and retinoic acid (RA) induced CCL229 by both of digoxin labelled c-myc cDNA probe spot by-bridization and RT-PCR with endoplasmic reticulum molecular chaperone Grp94 proximal 3" end oligonucletide primers was investigated. Tretinoin 166-168 heat shock protein 90 beta family member 1 Homo sapiens 308-313
9828118-6 1998 We show here that while no lactoferrin protein or mRNA was detected in untreated murine embryonic stem cells, retinoic acid and estrogen can induce high levels lactoferrin expression in these cells. Tretinoin 110-123 lactotransferrin Mus musculus 160-171
10743065-5 1997 CONCLUSION: The Grp94 normal expression (Grp94 alpha), which was undetectable in CCL229 cells increased after RA induction. Tretinoin 110-112 heat shock protein 90 beta family member 1 Homo sapiens 16-21
10743065-5 1997 CONCLUSION: The Grp94 normal expression (Grp94 alpha), which was undetectable in CCL229 cells increased after RA induction. Tretinoin 110-112 heat shock protein 90 beta family member 1 Homo sapiens 41-46
9806904-12 1998 Under the same reaction conditions, GSTP1-1 was much less effective in catalysing the steric conversion of 9-cis-retinoic acid to t-RA, indicating that the enzyme was stereospecific for the conversion of 13-cRA to t-RA. Tretinoin 214-218 glutathione S-transferase pi 1 Homo sapiens 36-43
9865735-1 1998 The up-regulation of cellular retinoic acid binding protein-II (CRABP-II) has been invoked as an important mechanism of clinically acquired resistance to all-trans retinoic acid (RA) therapy in acute promyelocytic leukemia (APL). Tretinoin 30-43 cellular retinoic acid binding protein 2 Homo sapiens 64-72
9865735-1 1998 The up-regulation of cellular retinoic acid binding protein-II (CRABP-II) has been invoked as an important mechanism of clinically acquired resistance to all-trans retinoic acid (RA) therapy in acute promyelocytic leukemia (APL). Tretinoin 65-67 cellular retinoic acid binding protein 2 Homo sapiens 21-62
9078282-1 1997 Transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK) is stimulated by cAMP, the thyroid hormone tri-iodothyronine (T3) and retinoic acid (RA). Tretinoin 157-159 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 65-70
9806904-13 1998 These observations suggest that enzymic catalysis was the primary mechanism for the GSTP1-1-dependent conversion of 13-cRA to t-RA. Tretinoin 126-130 glutathione S-transferase pi 1 Homo sapiens 84-91
9879990-11 1998 Our results show that the nuclear receptors and RXR-alpha play a critical role in mediating growth suppression by RA in ovarian cancer cells. Tretinoin 114-116 retinoid X receptor alpha Homo sapiens 48-57
9764578-0 1998 Establishment of a retinoic acid-resistant human acute promyelocytic leukaemia (APL) model in human granulocyte-macrophage colony-stimulating factor (hGM-CSF) transgenic severe combined immunodeficiency (SCID) mice. Tretinoin 19-32 colony stimulating factor 2 Homo sapiens 100-148
9858140-1 1998 Recognition that cellular retinoic acid binding protein (CRABP)-I and CRABP-II are found in different cell types has provided additional support for the presumably divergent roles of these two proteins in mediating retinoic acid (RA) effects in human skin. Tretinoin 215-228 cellular retinoic acid binding protein 2 Homo sapiens 70-78
9811861-2 1998 Here, we show that RA, after 2-3 h of incubation with cultured neonatal-rat cardiac fibroblasts, dramatically alters the intracellular distribution of M6P/IGF2R as well as that of cathepsin B (a lysosomal protease bearing M6P). Tretinoin 19-21 insulin-like growth factor 2 receptor Rattus norvegicus 151-160
9811861-5 1998 Furthermore, the RA-induced translocation of cathepsin B was not observed in M6P/IGF2R-deficient P388D1 cells but occurred in stably transfected P388D1 cells expressing the receptor, suggesting that the effect of RA might be the result of direct interaction with M6P/IGF2R, rather than the result of binding to the nuclear receptors. Tretinoin 17-19 cathepsin B Mus musculus 45-56
9811861-5 1998 Furthermore, the RA-induced translocation of cathepsin B was not observed in M6P/IGF2R-deficient P388D1 cells but occurred in stably transfected P388D1 cells expressing the receptor, suggesting that the effect of RA might be the result of direct interaction with M6P/IGF2R, rather than the result of binding to the nuclear receptors. Tretinoin 213-215 cathepsin B Mus musculus 45-56
9022057-5 1997 Throughout placentation, the expression patterns of the CRABP I and II genes partly overlap in the decidual tissue and the vacuolar zones of the decidua, suggesting a role for these binding proteins in sequestering free retinoic acid from maternal blood, thus regulating its availability to the embryo. Tretinoin 220-233 cellular retinoic acid binding protein I Mus musculus 56-63
9043087-6 1997 In addition, M33 null mutant mice show an aggravation of the skeletal malformations when treated to RA at embryonic day 7.5, leading to the hypothesis that, during development, the M33 gene might play a role in defining access to retinoic acid response elements localised in the regulatory regions of several Hox genes. Tretinoin 230-243 chromobox 2 Mus musculus 13-16
9043087-6 1997 In addition, M33 null mutant mice show an aggravation of the skeletal malformations when treated to RA at embryonic day 7.5, leading to the hypothesis that, during development, the M33 gene might play a role in defining access to retinoic acid response elements localised in the regulatory regions of several Hox genes. Tretinoin 230-243 chromobox 2 Mus musculus 181-184
9879709-0 1998 Expression of two even-skipped genes eve1 and evx2 during zebrafish fin morphogenesis and their regulation by retinoic acid. Tretinoin 110-123 even-skipped-like1 Danio rerio 37-41
9879709-6 1998 Exposure of the regenerates to retinoic acid (RA) modifies the boundaries of eve1 and evx2 expression: the signal is down-regulated in the ray region and up-regulated in the interray region. Tretinoin 31-44 even-skipped-like1 Danio rerio 77-81
9764578-0 1998 Establishment of a retinoic acid-resistant human acute promyelocytic leukaemia (APL) model in human granulocyte-macrophage colony-stimulating factor (hGM-CSF) transgenic severe combined immunodeficiency (SCID) mice. Tretinoin 19-32 colony stimulating factor 2 Homo sapiens 150-157
9879709-6 1998 Exposure of the regenerates to retinoic acid (RA) modifies the boundaries of eve1 and evx2 expression: the signal is down-regulated in the ray region and up-regulated in the interray region. Tretinoin 46-48 even-skipped-like1 Danio rerio 77-81
9147069-1 1997 Increasing evidence suggests that the retinoid-X receptors (RXR-alpha,-beta,-gamma) play a crucial role in regulating the transcriptional activity of several steroid hormone receptors, including the receptors for retinoic acid (RAR-alpha,-beta,-gamma), 1,25-dihydroxyvitamin D3 and thyroid hormone. Tretinoin 213-226 retinoid X receptor alpha Homo sapiens 60-69
9748586-11 1998 This suggests that retinoic acid may be an important inductive signal which regulates the developmental and tissue-specific expression of Ptx2. Tretinoin 19-32 paired-like homeodomain 2 Rattus norvegicus 138-142
21533369-4 1997 In this study, we explored the effects of estradiol and two differentiating agents, the progestin ORG2058 and retinoic acid, on BRCA1 mRNA expression in human estrogen and progesterone receptor positive MCF-7 cells. Tretinoin 110-123 BRCA1 DNA repair associated Homo sapiens 128-133
9795362-0 1998 Retinoic acid stimulates IGF binding protein (IGFBP)-6 and depresses IGFBP-2 and IGFBP-4 in SK-N-SH human neuroblastoma cells. Tretinoin 0-13 insulin like growth factor binding protein 6 Homo sapiens 25-54
9795362-0 1998 Retinoic acid stimulates IGF binding protein (IGFBP)-6 and depresses IGFBP-2 and IGFBP-4 in SK-N-SH human neuroblastoma cells. Tretinoin 0-13 insulin like growth factor binding protein 4 Homo sapiens 81-88
9795362-5 1998 Analysis of transcriptional activity of the IGFBP-2, -4 and -6 genes in isolated nuclei (run-on experiments) showed that RA increased the transcriptional activity of the IGFBP-6 gene, reduced that of the IGFBP-4 gene and had no effect on that of the IGFBP-2 gene. Tretinoin 121-123 insulin like growth factor binding protein 6 Homo sapiens 170-177
9795362-5 1998 Analysis of transcriptional activity of the IGFBP-2, -4 and -6 genes in isolated nuclei (run-on experiments) showed that RA increased the transcriptional activity of the IGFBP-6 gene, reduced that of the IGFBP-4 gene and had no effect on that of the IGFBP-2 gene. Tretinoin 121-123 insulin like growth factor binding protein 4 Homo sapiens 204-211
9795362-6 1998 Northern blot analysis following treatment with actinomycin D showed that RA increased the stability of IGFBP-6 mRNA by a factor of 2.6, decreased that of IGFBP-2 mRNA by a factor of 2.3 and failed to affect IGFBP-4 mRNA. Tretinoin 74-76 insulin like growth factor binding protein 6 Homo sapiens 104-111
9795362-6 1998 Northern blot analysis following treatment with actinomycin D showed that RA increased the stability of IGFBP-6 mRNA by a factor of 2.6, decreased that of IGFBP-2 mRNA by a factor of 2.3 and failed to affect IGFBP-4 mRNA. Tretinoin 74-76 insulin like growth factor binding protein 4 Homo sapiens 208-215
9795362-10 1998 With RA-induced differentiation, IGFBP-6 is strongly stimulated, whereas IGFBP-2 and IGFBP-4 are severely depressed, which would suggest that each IGFBP plays a specific role. Tretinoin 5-7 insulin like growth factor binding protein 6 Homo sapiens 33-40
9795362-10 1998 With RA-induced differentiation, IGFBP-6 is strongly stimulated, whereas IGFBP-2 and IGFBP-4 are severely depressed, which would suggest that each IGFBP plays a specific role. Tretinoin 5-7 insulin like growth factor binding protein 4 Homo sapiens 85-92
9015314-2 1997 There are three types of nuclear receptors for all-trans retinoic acid in mammals, RAR alpha, RAR beta, and RAR gamma, which transduce the retinoic acid signal by inducing or repressing the transcription of target genes (Leid, M., P. Kastner, and P. Chambon. Tretinoin 57-70 retinoic acid receptor, alpha Mus musculus 83-92
9015314-2 1997 There are three types of nuclear receptors for all-trans retinoic acid in mammals, RAR alpha, RAR beta, and RAR gamma, which transduce the retinoic acid signal by inducing or repressing the transcription of target genes (Leid, M., P. Kastner, and P. Chambon. Tretinoin 57-70 retinoic acid receptor, gamma Mus musculus 108-117
9773980-6 1998 In addition, the NCoR interaction domains interact much more strongly with the TR than those present in the silencing mediator of retinoic acid and TRs (SMRT). Tretinoin 130-143 nuclear receptor corepressor 1 Homo sapiens 17-21
9067636-3 1997 Treatment with retinoic acid (RA, 1 microM) or 1,250(OH)2-vitamin D3 (1,25-D3, 10 nM) increased the expression of the monocytic surface antigens CD11b plus CD11c, and CD11b, CD11c, CD14 plus CD18, respectively. Tretinoin 15-28 integrin subunit alpha M Homo sapiens 145-150
9067636-3 1997 Treatment with retinoic acid (RA, 1 microM) or 1,250(OH)2-vitamin D3 (1,25-D3, 10 nM) increased the expression of the monocytic surface antigens CD11b plus CD11c, and CD11b, CD11c, CD14 plus CD18, respectively. Tretinoin 15-28 integrin subunit alpha M Homo sapiens 167-172
9925375-7 1998 Finally, RA diminished the magnitude of the thyroid hormone (T3)-mediated increase in Na,K-ATPase beta1 subunit mRNA, while RA had no effect on the stimulation of alpha3 mRNA content by T3. Tretinoin 9-11 ATPase Na+/K+ transporting subunit beta 1 Rattus norvegicus 86-111
9763571-3 1998 During RA-induced differentiation of human leukemia HL-60 cells, levels of TOPO I remained unchanged, whereas the levels and phosphorylation of TOPO IIalpha and TOPO IIbeta proteins were increased twofold to fourfold and fourfold to eightfold, respectively. Tretinoin 7-9 DNA topoisomerase II beta Homo sapiens 161-172
9763571-5 1998 The increased level of TOPO IIbeta protein was also detected in differentiated cells subsequently cultured for 96 hours in RA-free medium. Tretinoin 123-125 DNA topoisomerase II beta Homo sapiens 23-34
9763571-6 1998 Pulse chase experiments in cells labeled with 35S-methionine showed that the rate of degradation of TOPO IIbeta protein in control cells was about twofold faster than that in the differentiated RA-treated cells. Tretinoin 194-196 DNA topoisomerase II beta Homo sapiens 100-111
9763571-11 1998 Results suggest that TOPO IIbeta protein levels are posttranscriptionally regulated and that degradation of TOPO IIbeta is decreased during RA-induced differentiation. Tretinoin 140-142 DNA topoisomerase II beta Homo sapiens 108-119
8989665-3 1997 Cells treated for 24 h with retinoic acid (10 microM) showed a threefold increase in 125I-CNTF binding sites and were up to five times more sensitive to CNTF than untreated cells in stimulating the tyrosine phosphorylation of the transcription factor STAT3. Tretinoin 28-41 ciliary neurotrophic factor Homo sapiens 90-94
9740074-2 1998 Because preclinical data showed that all-trans-retinoic acid (RA) inhibited SCLC growth, altered myc expression, and blocked transition to a treatment-resistant phenotype, a Phase II trial was designed to determine the effects of the combination of RA, cisplatin, and etoposide in patients with SCLC. Tretinoin 37-60 MYC proto-oncogene, bHLH transcription factor Homo sapiens 97-100
8989665-3 1997 Cells treated for 24 h with retinoic acid (10 microM) showed a threefold increase in 125I-CNTF binding sites and were up to five times more sensitive to CNTF than untreated cells in stimulating the tyrosine phosphorylation of the transcription factor STAT3. Tretinoin 28-41 ciliary neurotrophic factor Homo sapiens 153-157
8989665-6 1997 The retinoic acid-induced increase in 125I-CNTF binding could be prevented by administration of either cycloheximide or actinomycin D, whereas neither agent altered the TPA-induced decrease in 125I-CNTF binding. Tretinoin 4-17 ciliary neurotrophic factor Homo sapiens 43-47
8989665-7 1997 In addition, levels of mRNA for both the CNTF receptor alpha and gp130 subunits increased twofold as measured by RNase protection after treatment with retinoic acid for 30 h. The increase in CNTF receptor alpha subunit mRNA was not due to a decrease in its turnover rate, and therefore, was likely due to an increase in gene expression. Tretinoin 151-164 ciliary neurotrophic factor Homo sapiens 41-45
8989665-7 1997 In addition, levels of mRNA for both the CNTF receptor alpha and gp130 subunits increased twofold as measured by RNase protection after treatment with retinoic acid for 30 h. The increase in CNTF receptor alpha subunit mRNA was not due to a decrease in its turnover rate, and therefore, was likely due to an increase in gene expression. Tretinoin 151-164 ciliary neurotrophic factor Homo sapiens 191-195
8989665-8 1997 Thus, retinoic acid and TPA regulate CNTF receptors on neuroblastoma cells differently, and the results demonstrate the importance of transcriptional control of CNTF receptors and also implicate translational and post-translational mechanisms in the regulation of cytokine receptors and responses on neurons. Tretinoin 6-19 ciliary neurotrophic factor Homo sapiens 37-41
9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 33-52 myotubularin related protein 11 Homo sapiens 242-245
9290118-2 1997 In a number of human cell lines, trans-retinoic acid upregulates c-myc mRNA expression in colonic mucosa by reverse transcription polymerase chain reaction and correlated the results with serum concentrations of all-trans- (ATRA), 13-cis-(13-cRA), and total retinoic acid. Tretinoin 39-52 myotubularin related protein 11 Homo sapiens 242-245
9788609-1 1998 TCF17, the human homologue of the rat zinc finger gene Kid1, is highly expressed in neurons derived from the retinoic acid-treated human embryonal carcinoma (EC) cell line, NTERA-2. Tretinoin 109-122 zinc finger protein 354A Homo sapiens 0-5
9826179-4 1998 A technique that characterizes RA-binding proteins according to their isoelectric point showed both CRABP I and CRABP II to be present in the cerebellum and P19 cells, and only CRABP II to be present in the choroid plexus. Tretinoin 31-33 cellular retinoic acid binding protein I Mus musculus 100-107
9770359-3 1998 In order to begin to understand the tissue-specific roles of these interacting factors, we determined the expression pattern and activity of the pRB, E2F, cyclin, cdk, and CKI families of cell cycle regulatory proteins during retinoic acid-induced (neuronal pathway) and DMSO-induced (cardiac muscle pathway) differentiation of the pluripotent murine embryonal carcinoma cell line, P19. Tretinoin 226-239 RB transcriptional corepressor 1 Mus musculus 145-148
8940196-6 1996 In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene"s promoter which is required to confer RA induction through RAR.RXR heterodimers. Tretinoin 67-69 retinoid X receptor alpha Homo sapiens 220-223
9740074-2 1998 Because preclinical data showed that all-trans-retinoic acid (RA) inhibited SCLC growth, altered myc expression, and blocked transition to a treatment-resistant phenotype, a Phase II trial was designed to determine the effects of the combination of RA, cisplatin, and etoposide in patients with SCLC. Tretinoin 62-64 MYC proto-oncogene, bHLH transcription factor Homo sapiens 97-100
8940196-6 1996 In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene"s promoter which is required to confer RA induction through RAR.RXR heterodimers. Tretinoin 123-125 retinoid X receptor alpha Homo sapiens 220-223
9990415-7 1998 The two tretinoin formulations also resulted in similar significant increases in CRABP-II compared to the cream vehicle (P < 0.001). Tretinoin 8-17 cellular retinoic acid binding protein 2 Homo sapiens 81-89
9693115-3 1998 Although both proteins interact with retinoids, RBP exhibits a broad specificity, binding retinol, retinoic acid and retinaldehyde with roughly equal affinities, whereas ERABP is specific for all-trans- and 9-cis-retinoic acids. Tretinoin 99-112 retinol binding protein 4 Rattus norvegicus 48-51
9821019-0 1998 Effect of retinoid (vitamin A or retinoic acid) treatment (hormonal imprinting) through breastmilk on the glucocorticoid receptor and estrogen receptor binding capacity of the adult rat offspring. Tretinoin 33-46 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 106-129
8939936-2 1996 The cellular effects of RA are dependent upon the complement of nuclear receptors expressed (RARs and RXRs), which transduce retinoid signals into transcriptional regulation, the presence of cellular retinoid-binding proteins (CRABP and CRBP), which may be involved in RA metabolism, and the activity of RA metabolizing enzymes. Tretinoin 24-26 arginyl-tRNA synthetase 1 Danio rerio 93-97
8895748-7 1996 Introduction of a recombinant RARalpha expression vector into benign keratinocyte tumor cells reduced the S-phase population and inhibited [3H]thymidine incorporation in response to retinoic acid. Tretinoin 182-195 retinoic acid receptor, alpha Mus musculus 30-38
9693115-8 1998 Whereas the wild-type ERABP binds only retinoic acid, the double mutant is capable of binding retinol, retinoic acid and retinaldehyde with similar affinities. Tretinoin 39-52 lipocalin 5 Rattus norvegicus 22-27
9751115-7 1998 Id1 transcripts are present in P19 cells and are transiently decreased on day 2 of DMSO differentiation but remain elevated in DMSO-treated P19(RXR-alpha) and in P19 cells treated simultaneously with retinoic acid and DMSO. Tretinoin 200-213 inhibitor of DNA binding 1, HLH protein Mus musculus 0-3
9693115-8 1998 Whereas the wild-type ERABP binds only retinoic acid, the double mutant is capable of binding retinol, retinoic acid and retinaldehyde with similar affinities. Tretinoin 103-116 lipocalin 5 Rattus norvegicus 22-27
9699512-8 1998 The RAR alpha-specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXR alpha in mediating the biological effects of retinoids on JEG-3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. Tretinoin 4-6 retinoid X receptor alpha Homo sapiens 153-162
9693115-9 1998 These observations provide experimental support for the proposition that the charged residues near the open end of the binding pocket are responsible for restricting the specificity of ERABP for retinoic acid. Tretinoin 195-208 lipocalin 5 Rattus norvegicus 185-190
8931868-2 1996 Cellular RA-binding protein (CRABP) II has been found to be a marker of RA activity in human skin. Tretinoin 9-11 cellular retinoic acid binding protein 2 Homo sapiens 29-38
9720909-0 1998 The effect of retinoic acid on the activation of the human H19 promoter by a 3" downstream region. Tretinoin 14-27 H19 imprinted maternally expressed transcript Homo sapiens 59-62
8931868-10 1996 RA-induced skin erythema was not obvious until 24 to 48 h. We conclude, therefore, that induction of RIS-1 and CRABP II mRNA levels by topical RA in human skin are early, coordinated molecular events which precede the clinical cutaneous erythematous response to RA. Tretinoin 0-2 cellular retinoic acid binding protein 2 Homo sapiens 111-119
9737693-8 1998 YJ cells treated in vitro with 2 microM RA differentiated into metamyelocytes and band neutrophils, and increased the number of nitroblue tetrazolium (NBT)-positive cells and increased gp91phox mRNA expression. Tretinoin 40-42 cytochrome b-245 beta chain Homo sapiens 185-193
8863732-4 1996 RA appears to reduce the stability of ETnMG1 transcript. Tretinoin 0-2 early transposon element MG1 Mus musculus 38-44
9742685-0 1998 Retinol and retinoic acid bind to a surface cleft in bovine beta-lactoglobulin: a method of binding site determination using fluorescence resonance energy transfer. Tretinoin 12-25 beta-lactoglobulin Bos taurus 60-78
9720909-5 1998 Moreover, the activation of the H19 promoter by retinoic acid in cells derived from human testicular germ cell tumors is dependent upon the 3" downstream region. Tretinoin 48-61 H19 imprinted maternally expressed transcript Homo sapiens 32-35
9742685-1 1998 Two potential ligand binding sites in the lipocalin beta-lactoglobulin have been postulated for small hydrophobic molecules such as retinol or retinoic acid. Tretinoin 143-156 beta-lactoglobulin Bos taurus 52-70
9742685-3 1998 In order to discriminate between these two possibilities, we measured the efficiency of fluorescence resonance energy transfer between the two intrinsic Trp-residues of beta-lactoglobulin and the ligands retinol, retinoic acid and bis-ANS. Tretinoin 213-226 beta-lactoglobulin Bos taurus 169-187
9181055-0 1996 Ha-ras oncogene transformation abolishes retinoic acid-induced reduction of intracellular fibronectin. Tretinoin 41-54 Harvey rat sarcoma virus oncogene Mus musculus 0-6
9181055-6 1996 Transformation of NIH-3T3 cells with an activated Ha-ras oncogene downmodulated RAR expression and also abolished responsiveness to RA. Tretinoin 80-82 Harvey rat sarcoma virus oncogene Mus musculus 50-56
9181055-7 1996 A variety of approaches permitted the following conclusions: 1) RA-dependent FN downmodulation is mediated by RARs, 2) retinoid X receptors (RXRs) mediate the observed reduction of RAR alpha by RA, and 3) the blockade of RA responsiveness by Ha-ras-transfected cells cannot be overcome by overexpression of RAR alpha. Tretinoin 64-66 retinoic acid receptor, alpha Mus musculus 181-190
9181055-7 1996 A variety of approaches permitted the following conclusions: 1) RA-dependent FN downmodulation is mediated by RARs, 2) retinoid X receptors (RXRs) mediate the observed reduction of RAR alpha by RA, and 3) the blockade of RA responsiveness by Ha-ras-transfected cells cannot be overcome by overexpression of RAR alpha. Tretinoin 64-66 Harvey rat sarcoma virus oncogene Mus musculus 242-248
9716179-2 1998 The effects of RA are mediated by a family of ligand-dependent transcription factors, the RA receptors and the retinoid X receptors (RXR). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 111-131
9716179-2 1998 The effects of RA are mediated by a family of ligand-dependent transcription factors, the RA receptors and the retinoid X receptors (RXR). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 133-136
9181055-7 1996 A variety of approaches permitted the following conclusions: 1) RA-dependent FN downmodulation is mediated by RARs, 2) retinoid X receptors (RXRs) mediate the observed reduction of RAR alpha by RA, and 3) the blockade of RA responsiveness by Ha-ras-transfected cells cannot be overcome by overexpression of RAR alpha. Tretinoin 64-66 retinoic acid receptor, alpha Mus musculus 307-316
9716179-10 1998 RXR-gamma expression produced significant reduction in levels of RA-responsive genes including the cyclin-dependent kinase inhibitors p21Cip1/WAF1 and p27Kip1, resulting in increased cdc2 and cdk2 kinase activity and RB phosphorylation. Tretinoin 65-67 retinoid X receptor alpha Homo sapiens 0-3
9720909-6 1998 The possibility that the action of retinoic acid on the H19 promoter is an indirect one and involves a member of the AP2 transcription factor family is discussed. Tretinoin 35-48 H19 imprinted maternally expressed transcript Homo sapiens 56-59
9699718-1 1998 Embryonic mouse upper-lip skin explants treated with 16.7 microM all-trans retinoic acid (tRA) give rise to a glandular metaplasia of hair vibrissa follicles; however, at this concentration, tRA can activate not only the three retinoic acid receptors (RARalpha, beta, and gamma), but also the retinoid X receptors (RXRalpha, beta, and gamma) as a consequence of its isomerization to 9-cis retinoic acid. Tretinoin 75-88 retinoic acid receptor, alpha Mus musculus 252-260
9699718-1 1998 Embryonic mouse upper-lip skin explants treated with 16.7 microM all-trans retinoic acid (tRA) give rise to a glandular metaplasia of hair vibrissa follicles; however, at this concentration, tRA can activate not only the three retinoic acid receptors (RARalpha, beta, and gamma), but also the retinoid X receptors (RXRalpha, beta, and gamma) as a consequence of its isomerization to 9-cis retinoic acid. Tretinoin 90-93 retinoic acid receptor, alpha Mus musculus 252-260
9181055-8 1996 These studies have identified fibronectin and RAR alpha as RA targets in fibroblast cells and have shown that oncogenic transformation renders the cells resistant to RA action. Tretinoin 59-61 retinoic acid receptor, alpha Mus musculus 46-55
8877104-7 1996 Stimulation by RA resulted in increased RAR beta/RXR DNA binding, activated RARE-dependent transcription, and increased expression of RAR-beta. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 49-52
9651402-3 1998 Here we demonstrate that retinoic acid can induce the accumulation of alphaB-crystallin in N/N1003A lens cells and that retinoic acid receptor heterodimers (retinoic acid receptor/retinoid X receptor; RAR/RXR) can transactivate LSR1 and LSR2 in cotransfection experiments. Tretinoin 25-38 retinoic acid receptor, alpha Mus musculus 201-204
8877104-8 1996 Concomitant stimulation by VitD3 inhibited the RA-stimulated formation of RAR beta/RXR heterodimers, favoring VDR/RXR binding to the RARE. Tretinoin 47-49 retinoid X receptor alpha Homo sapiens 83-86
9657734-0 1998 Mutations in the E-domain of RAR portion of the PML/RAR chimeric gene may confer clinical resistance to all-trans retinoic acid in acute promyelocytic leukemia. Tretinoin 114-127 retinoic acid receptor alpha Homo sapiens 29-32
8877104-8 1996 Concomitant stimulation by VitD3 inhibited the RA-stimulated formation of RAR beta/RXR heterodimers, favoring VDR/RXR binding to the RARE. Tretinoin 47-49 vitamin D receptor Homo sapiens 110-113
8877104-8 1996 Concomitant stimulation by VitD3 inhibited the RA-stimulated formation of RAR beta/RXR heterodimers, favoring VDR/RXR binding to the RARE. Tretinoin 47-49 retinoid X receptor alpha Homo sapiens 114-117
8752109-0 1996 Retinoic acid increases hydroxyindole-O-methyltransferase activity and mRNA in human Y-79 retinoblastoma cells. Tretinoin 0-13 acetylserotonin O-methyltransferase Homo sapiens 24-57
9651402-4 1998 DNase I footprinting experiments demonstrated that purified RAR/RXR heterodimers will occupy sequences resembling retinoic acid response elements within LSR1 and LSR2. Tretinoin 114-127 deoxyribonuclease I Mus musculus 0-7
9651402-4 1998 DNase I footprinting experiments demonstrated that purified RAR/RXR heterodimers will occupy sequences resembling retinoic acid response elements within LSR1 and LSR2. Tretinoin 114-127 retinoic acid receptor, alpha Mus musculus 60-63
9657734-1 1998 The binding of all-trans retinoic acid (ATRA) to the ligand-binding region in the E-domain of retinoic acid receptor-alpha modifies the transcriptional activity of RARalpha protein. Tretinoin 15-38 retinoic acid receptor alpha Homo sapiens 94-122
9676192-7 1998 This dynamic pattern of RA response was a direct result of localized RALDH2, since hearts of cultured embryos were uniformly competent to respond to an exogenous RA challenge. Tretinoin 24-26 aldehyde dehydrogenase 1 family member A2 Homo sapiens 69-75
8752109-2 1996 Here we present the first evidence that retinoic acid (RA) stereoisomers are potent regulators of HIOMT in the human retinoblastoma-derived Y-79 cell line. Tretinoin 40-53 acetylserotonin O-methyltransferase Homo sapiens 98-103
9657734-1 1998 The binding of all-trans retinoic acid (ATRA) to the ligand-binding region in the E-domain of retinoic acid receptor-alpha modifies the transcriptional activity of RARalpha protein. Tretinoin 15-38 retinoic acid receptor alpha Homo sapiens 164-172
8752277-1 1996 Signalling by all-trans retinoic acid is mediated through RXR-RAR retinoid receptor heterodimers, in which RXR has been considered to act as a transcriptionally silent partner. Tretinoin 24-37 retinoid X receptor alpha Homo sapiens 58-61
9657734-1 1998 The binding of all-trans retinoic acid (ATRA) to the ligand-binding region in the E-domain of retinoic acid receptor-alpha modifies the transcriptional activity of RARalpha protein. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 94-122
8752277-1 1996 Signalling by all-trans retinoic acid is mediated through RXR-RAR retinoid receptor heterodimers, in which RXR has been considered to act as a transcriptionally silent partner. Tretinoin 24-37 retinoid X receptor alpha Homo sapiens 107-110
8752277-3 1996 6) human acute promyelocytic leukaemia cells treated with either an RAR-alpha-selective agonist alone, or certain RAR-alpha antagonists in combination with an RXR agonist, receptor-DNA binding is induced in vivo, resulting in expression of the target genes of retinoic acid as well as acute promyelocytic leukaemia protein (PML) relocation to nuclear bodies and differentiation before apoptosis. Tretinoin 260-273 retinoid X receptor alpha Homo sapiens 159-162
9657734-1 1998 The binding of all-trans retinoic acid (ATRA) to the ligand-binding region in the E-domain of retinoic acid receptor-alpha modifies the transcriptional activity of RARalpha protein. Tretinoin 40-44 retinoic acid receptor alpha Homo sapiens 164-172
9690135-6 1998 All-trans retinoic acid also promotes proliferation of both cell types and, most interestingly, replaces the requirement-for a physiological level of Ca2+ in the fibroblast cultures. Tretinoin 10-23 carbonic anhydrase 2 Homo sapiens 150-153
9657734-2 1998 ATRA probably induces differentiation of acute promyelocytic leukemia (APL) cells by binding to the E-domain of the RARalpha portion (RARalpha /E-domain) of PML/RARalpha chimeric protein. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 116-124
9657734-2 1998 ATRA probably induces differentiation of acute promyelocytic leukemia (APL) cells by binding to the E-domain of the RARalpha portion (RARalpha /E-domain) of PML/RARalpha chimeric protein. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 134-142
9657734-2 1998 ATRA probably induces differentiation of acute promyelocytic leukemia (APL) cells by binding to the E-domain of the RARalpha portion (RARalpha /E-domain) of PML/RARalpha chimeric protein. Tretinoin 0-4 PML nuclear body scaffold Homo sapiens 157-160
8869596-3 1996 The aim of this study was therefore to examine the effect of retinoic acid and growth on type I collagen on PTH/PTH-related protein (PTHrP) receptor mRNA expression in the osteosarcoma osteoblast-like cell line UMR 106-06. Tretinoin 61-74 parathyroid hormone-like hormone Rattus norvegicus 133-138
9657734-2 1998 ATRA probably induces differentiation of acute promyelocytic leukemia (APL) cells by binding to the E-domain of the RARalpha portion (RARalpha /E-domain) of PML/RARalpha chimeric protein. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 134-142
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 37-50 retinoid X receptor alpha Homo sapiens 152-171
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 152-171
8707417-2 1996 RAR-beta transcription is induced by retinoic acid (RA) through retinoid receptors which bind as heterodimers of a RA-activated RA receptor (RAR) and a retinoid X receptor to the RA-responsive element in the RAR-beta promoter region (beta RARE). Tretinoin 52-54 retinoid X receptor alpha Homo sapiens 152-171
9578604-2 1998 G-CSF enhanced O-2 generating ability of HL-60 cells whose differentiation had been initiated by dimethylsulfoxide (DMSO) or retinoic acid (RA). Tretinoin 140-142 immunoglobulin kappa variable 1D-39 Homo sapiens 15-18
9657734-3 1998 Therefore, molecular alteration in the RARalpha /E-domain of the chimeric gene is one mechanism by which patients with APL may acquire resistance to ATRA therapy. Tretinoin 149-153 retinoic acid receptor alpha Homo sapiens 39-47
9570750-11 1998 When treated with retinoic acid, rfp reassociates with the NBs in a pattern similar to non APL cells. Tretinoin 18-31 tripartite motif containing 27 Homo sapiens 33-36
9657734-10 1998 These findings suggest that mutations in the RARalpha /E-domain of the PML/RARalpha chimeric gene may confer clinical resistance to ATRA therapy in patients with APL. Tretinoin 132-136 retinoic acid receptor alpha Homo sapiens 45-53
9570757-8 1998 PCNA immunoreactivity significantly increased after 8 hours treatment of RA or TPA, suggesting a hyperproliferative growth response. Tretinoin 73-75 proliferating cell nuclear antigen Rattus norvegicus 0-4
8668198-4 1996 Deletion of the hormone-dependent transactivation function of the retinoid X receptor, the common subunit of heterodimeric nuclear receptors, significantly impairs hormone-dependent transcription by retinoic acid, thyroid hormone, and vitamin D receptors. Tretinoin 199-212 retinoid X receptor alpha Homo sapiens 66-85
9657734-10 1998 These findings suggest that mutations in the RARalpha /E-domain of the PML/RARalpha chimeric gene may confer clinical resistance to ATRA therapy in patients with APL. Tretinoin 132-136 PML nuclear body scaffold Homo sapiens 71-74
9579536-5 1998 In contrast, the construct containing the VDRE of the human 24-hydroxylase gene was induced several fold by 1,25(OH)2D3 in normal human keratinocytes and by both 1,25(OH)2D3 and all-trans retinoic acid in SCC4 and SCC12B2 cells. Tretinoin 188-201 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 60-74
8663043-3 1996 The CRABPI gene is regulated in an unusual fashion; CRABPI message and protein levels are induced at low concentrations of RA, but induction is diminished at higher concentrations. Tretinoin 5-7 cellular retinoic acid binding protein I Mus musculus 52-58
9657734-10 1998 These findings suggest that mutations in the RARalpha /E-domain of the PML/RARalpha chimeric gene may confer clinical resistance to ATRA therapy in patients with APL. Tretinoin 132-136 retinoic acid receptor alpha Homo sapiens 75-83
9531570-0 1998 Reduced retinoic acid-sensitivities of nuclear receptor corepressor binding to PML- and PLZF-RARalpha underlie molecular pathogenesis and treatment of acute promyelocytic leukemia. Tretinoin 8-21 zinc finger and BTB domain containing 16 Homo sapiens 88-92
9679985-8 1998 RA reduced the amount of unphosphorylated RAR-alpha, whose activation is necessary for RA-induced differentiation and arrest. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 42-51
9531570-6 1998 This ATRA-insensitive interaction between N-CoR and PLZF-RARalpha was mediated by the N-terminal PLZF moiety of the chimera. Tretinoin 5-9 zinc finger and BTB domain containing 16 Homo sapiens 97-101
9507016-8 1998 Furthermore, c-fos expression was inhibited by agonists of retinoic acid receptors (RARs) or retinoid X receptors (RXRs), and suppression of c-fos promoter activity by t-RA was abrogated by treatment with antagonists of RAR-alpha or of all the RXRs. Tretinoin 168-172 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18
8650192-0 1996 RIG-E, a human homolog of the murine Ly-6 family, is induced by retinoic acid during the differentiation of acute promyelocytic leukemia cell. Tretinoin 64-77 lymphocyte antigen 6 complex Mus musculus 37-41
8655603-9 1996 Retinoic acid was less effective in inhibiting thymidine incorporation when cells were stimulated with insulin, des(1-3) IGF-I, or Long(R3) IGF-I when compared to cells stimulated with native IGF-I or serum. Tretinoin 0-13 IGFI Bos taurus 121-126
8655603-9 1996 Retinoic acid was less effective in inhibiting thymidine incorporation when cells were stimulated with insulin, des(1-3) IGF-I, or Long(R3) IGF-I when compared to cells stimulated with native IGF-I or serum. Tretinoin 0-13 IGFI Bos taurus 140-145
8655603-9 1996 Retinoic acid was less effective in inhibiting thymidine incorporation when cells were stimulated with insulin, des(1-3) IGF-I, or Long(R3) IGF-I when compared to cells stimulated with native IGF-I or serum. Tretinoin 0-13 IGFI Bos taurus 140-145
8655603-13 1996 Thus, RA is a potent but transient inhibitor of bovine mammary epithelial cell proliferation, and this growth inhibition is correlated with increased IGFBP-2 accumulation and inhibition of IGF-I stimulated IGFBP-3 protein secretion. Tretinoin 6-8 IGFI Bos taurus 189-194
9507016-8 1998 Furthermore, c-fos expression was inhibited by agonists of retinoic acid receptors (RARs) or retinoid X receptors (RXRs), and suppression of c-fos promoter activity by t-RA was abrogated by treatment with antagonists of RAR-alpha or of all the RXRs. Tretinoin 168-172 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 141-146
9488655-4 1998 PML was needed for the RA-dependent transactivation of the p21WAF1/CIP1 gene, which regulates cell cycle progression and cellular differentiation. Tretinoin 23-25 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 67-71
9671939-2 1998 We have therefore investigated whether members of this family are also expressed during regeneration of the adult urodele limb and are regulated by retinoic acid (RA), since this derivative induces proximodistal duplications in regenerating limbs, and has been shown to regulate sonic hedgehog (shh) in the developing limbs of birds and mammals. Tretinoin 148-161 sonic hedgehog L homeolog Xenopus laevis 285-293
9468588-0 1998 Induction of gastrin releasing peptide by all-trans retinoic acid in small cell lung cancer cells. Tretinoin 52-65 gastrin releasing peptide Homo sapiens 13-38
8782080-1 1996 Studies were performed to determine whether ARP-1, which is an orphan receptor of the steroid receptor superfamily, inhibits basal activity of the human placental lactogen (hPL) promoter and the increase in hPL promoter activity in response to the receptors for thyroid hormone (TR) and retinoic acid (RAR). Tretinoin 287-300 actin related protein 1A Homo sapiens 44-49
8782080-4 1996 Mobility shift assays demonstrated that ARP-1 binds specifically to a composite steroid response element on the hPL promoter that confers retinoic acid and T3 responsiveness. Tretinoin 138-151 actin related protein 1A Homo sapiens 40-45
9505268-7 1998 In contrast, RA potentiated the increase of KGF and decrease of HGF transcripts induced by DEX. Tretinoin 13-15 fibroblast growth factor 7 Rattus norvegicus 44-47
9671939-2 1998 We have therefore investigated whether members of this family are also expressed during regeneration of the adult urodele limb and are regulated by retinoic acid (RA), since this derivative induces proximodistal duplications in regenerating limbs, and has been shown to regulate sonic hedgehog (shh) in the developing limbs of birds and mammals. Tretinoin 163-165 sonic hedgehog L homeolog Xenopus laevis 285-293
9505268-7 1998 In contrast, RA potentiated the increase of KGF and decrease of HGF transcripts induced by DEX. Tretinoin 13-15 hepatocyte growth factor Rattus norvegicus 64-67
9486654-5 1998 Consistent with these observations, inhibitors of histone deacetylase dramatically potentiate retinoid-induced differentiation of RA-sensitive, and restore retinoid responses of RA-resistant, APL cell lines. Tretinoin 130-132 histone deacetylase 9 Homo sapiens 50-69
9486654-5 1998 Consistent with these observations, inhibitors of histone deacetylase dramatically potentiate retinoid-induced differentiation of RA-sensitive, and restore retinoid responses of RA-resistant, APL cell lines. Tretinoin 178-180 histone deacetylase 9 Homo sapiens 50-69
9486655-7 1998 PLZF-RARalpha contains a second, RA-resistant binding site in the PLZF amino-terminal region. Tretinoin 5-7 zinc finger and BTB domain containing 16 Homo sapiens 0-4
8817450-0 1996 Retinoic acid and methylation cis-regulatory elements control the mouse tissue non-specific alkaline phosphatase gene expression. Tretinoin 0-13 alkaline phosphatase, liver/bone/kidney Mus musculus 72-112
9649586-5 1998 The percentages of cells expressing cell-surface pIgR after 24, 48 and 72 h of treatment with RA, IL-4 and IFN-gamma were 66 +/- 10, 90 +/- 5 and 92 +/- 1, respectively, significantly higher than the percentages seen without RA treatment, which were 32 +/- 2.3, 72 +/- 1.2 and 30 +/- 7, respectively. Tretinoin 225-227 polymeric immunoglobulin receptor Homo sapiens 49-53
8664346-10 1996 The 3 alpha-HSD-like protein was strikingly down-regulated by "priming" doses of ATRA. Tretinoin 81-85 aldo-keto reductase family 1 member C4 Homo sapiens 4-15
9486655-7 1998 PLZF-RARalpha contains a second, RA-resistant binding site in the PLZF amino-terminal region. Tretinoin 5-7 zinc finger and BTB domain containing 16 Homo sapiens 66-70
9486655-10 1998 Therefore, recruitment of histone deacetylase is crucial to the transforming potential of APL fusion proteins, and the different effects of RA on the stability of the PML-RARalpha and PLZF-RARalpha co-repressor complexes determines the differential response of APLs to RA. Tretinoin 140-142 zinc finger and BTB domain containing 16 Homo sapiens 184-188
9488621-3 1998 The translocation t(11;17)(q23;q21) leading to a PLZF/RARalpha rearrangement has been described in a very small number of cases and has been associated with a poor response to ATRA and an adverse prognosis. Tretinoin 176-180 zinc finger and BTB domain containing 16 Homo sapiens 49-53
9488639-8 1998 However, eosinophil-derived neurotoxin and eosinophil cationic protein were not detected or were only detected at a low level in the lysates of the HML cells treated with RA. Tretinoin 171-173 ribonuclease A family member 3 Homo sapiens 43-70
9649586-6 1998 In addition, the intensity of fluorescence of pIgR-positive cells was significantly higher in the RA-treated cultures than in the cultures without RA treatment. Tretinoin 98-100 polymeric immunoglobulin receptor Homo sapiens 46-50
9649586-6 1998 In addition, the intensity of fluorescence of pIgR-positive cells was significantly higher in the RA-treated cultures than in the cultures without RA treatment. Tretinoin 147-149 polymeric immunoglobulin receptor Homo sapiens 46-50
8702216-4 1996 Further, Mo7 and Mo7-P210 cells showed different responses concerning c-Rel after stimulation with cytokines and retinoic acid. Tretinoin 113-126 REL proto-oncogene, NF-kB subunit Homo sapiens 70-75
9443071-4 1998 We have studied the influence of calcitriol, dexamethasone, retinoic acid, and estradiol on the COL 1A1 gene expression by determining the secretion of the C-terminal propeptide (PICP) and the levels of alpha 1(I) procollagen mRNA in cultured human MG-63 and SaOs-2 osteoblast-like osteosarcoma cells. Tretinoin 60-73 collagen type I alpha 1 chain Homo sapiens 96-103
9649586-8 1998 These data indicate that RA strongly interacts with IL-4 and IFN-gamma to regulate pIgR expression in HT-29 cells, suggesting that vitamin A may be required for proper in vivo regulation of IgA transport in response to mucosal infections. Tretinoin 25-27 polymeric immunoglobulin receptor Homo sapiens 83-87
9443071-9 1998 Retinoic acid, in turn, decreased the levels of alpha 1(I) procollagen mRNA and secreted PICP by slowing down transcription of the COL1A1 gene without any effect on message stability. Tretinoin 0-13 collagen type I alpha 1 chain Homo sapiens 48-70
9649586-8 1998 These data indicate that RA strongly interacts with IL-4 and IFN-gamma to regulate pIgR expression in HT-29 cells, suggesting that vitamin A may be required for proper in vivo regulation of IgA transport in response to mucosal infections. Tretinoin 25-27 immunoglobulin heavy variable 4-38-2-like Homo sapiens 190-193
9443071-9 1998 Retinoic acid, in turn, decreased the levels of alpha 1(I) procollagen mRNA and secreted PICP by slowing down transcription of the COL1A1 gene without any effect on message stability. Tretinoin 0-13 collagen type I alpha 1 chain Homo sapiens 131-137
8639429-7 1996 Preincubation of ATRA-treated NB4 cells with MoAbs anti-VLA4 and anti-LFA1, the VCAM-1 and ICAM-1 counter-receptors respectively, resulted in a significant inhibition of adhesion. Tretinoin 17-21 intercellular adhesion molecule 1 Homo sapiens 91-97
9750235-9 1998 Phosphorylation of the retinoblastoma gene product in cells of embryonic mouse adenocarcinoma (line p19) changes in response to cloning or stimulation of differentiation by retinoic acid. Tretinoin 173-186 cyclin dependent kinase inhibitor 2D Mus musculus 100-103
8658506-5 1996 In the same model, AGN 193109 also decreased topical irritation induced by the natural RAR agonist, all-trans-retinoic acid. Tretinoin 100-123 retinoic acid receptor, alpha Mus musculus 87-90
9462740-5 1998 Histone deacetylase inhibitors such as Trichostatin A (TSA), in combination with RA, can overcome the transcriptional repressor activity of PML-RARalpha and PLZF-RARalpha as well as the unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA. Tretinoin 81-83 retinoic acid receptor, alpha Mus musculus 144-152
9462740-5 1998 Histone deacetylase inhibitors such as Trichostatin A (TSA), in combination with RA, can overcome the transcriptional repressor activity of PML-RARalpha and PLZF-RARalpha as well as the unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA. Tretinoin 81-83 retinoic acid receptor, alpha Mus musculus 162-170
9462740-5 1998 Histone deacetylase inhibitors such as Trichostatin A (TSA), in combination with RA, can overcome the transcriptional repressor activity of PML-RARalpha and PLZF-RARalpha as well as the unresponsiveness of PLZF-RARalpha-expressing leukaemic cells to RA. Tretinoin 81-83 retinoic acid receptor, alpha Mus musculus 162-170
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 141-154 retinoic acid receptor, gamma Mus musculus 46-55
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 141-154 retinoic acid receptor, alpha Mus musculus 57-66
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 178-191 retinoic acid receptor, gamma Mus musculus 46-55
9442090-6 1998 In wild-type F9 cells and derivatives lacking RAR gamma, RAR alpha, and/or RXR alpha, we observed a direct relationship between the level of retinoic acid metabolic activity and retinoic acid-induced P450RAI mRNA. Tretinoin 178-191 retinoic acid receptor, alpha Mus musculus 57-66
9442090-7 1998 These experiments, as well as others using synthetic receptor subtype-specific retinoids, suggest that the RAR gamma and RXR alpha receptors mediate the effects of retinoic acid on the expression of the P450RAI gene. Tretinoin 164-177 retinoic acid receptor, gamma Mus musculus 107-116
9462716-8 1998 Exposure to the combination of IFN-gamma plus retinoic acid significantly up-regulated (in an additive manner) HLA-Class-I and ICAM-1 molecules as compared with the levels obtainable after exposure to IFN-gamma alone. Tretinoin 46-59 intercellular adhesion molecule 1 Homo sapiens 127-133
9627685-4 1996 Recently, it was reported that VDR forms homodimers and heterodimers with the nuclear receptors for all-trans retinoic acid and thyroid hormone. Tretinoin 110-123 vitamin D receptor Homo sapiens 31-34
8626453-0 1996 Retinoic acid down-regulation of fibronectin and retinoic acid receptor alpha proteins in NIH-3T3 cells. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 49-77
8626453-2 1996 All-trans-retinoic acid (RA) markedly reduced the level of intracellular fibronectin (FN) in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 0-23 Harvey rat sarcoma virus oncogene Mus musculus 208-214
8626453-2 1996 All-trans-retinoic acid (RA) markedly reduced the level of intracellular fibronectin (FN) in a time- and concentration-dependent fashion in NIH-3T3 cells, but not in NIH-3T3 cells transformed by an activated Ha-ras oncogene. Tretinoin 25-27 Harvey rat sarcoma virus oncogene Mus musculus 208-214
8626453-7 1996 Transformation of NIH-3T3 cells with an activated Ha-ras oncogene down-modulated RAR expression and abolished responsiveness to RA. Tretinoin 81-83 Harvey rat sarcoma virus oncogene Mus musculus 50-56
8634447-10 1996 We conclude that the RAR/RXR pathway is more important than RXR/RXR pathway for differentiation and proliferation of acute myeloid leukemic cells, and certain retinoids or combination of retinoids with both RAR and RXR specificities may synergistically enhance the differentiation activity of ATRA, which may be relevant in several clinical situations. Tretinoin 293-297 retinoid X receptor alpha Homo sapiens 25-28
8631251-0 1996 Ectopic expression of Hoxa-1 in the zebrafish alters the fate of the mandibular arch neural crest and phenocopies a retinoic acid-induced phenotype. Tretinoin 116-129 homeobox B1b Danio rerio 22-28
9681834-0 1998 p27Kip1: a key mediator of retinoic acid induced growth arrest in the SMS-KCNR human neuroblastoma cell line. Tretinoin 27-40 cyclin dependent kinase inhibitor 1B Homo sapiens 0-7
8631251-2 1996 In this study, we show that the phenotype induced by exogenous retinoic acid in the zebrafish can also be generated by the overexpression of Hoxa-1 following injection of synthetic RNA into the fertilised egg. Tretinoin 63-76 homeobox B1b Danio rerio 141-147
8631251-4 1996 We show that exogenously applied retinoic acid causes the ectopic accumulation of Hoxa-1 message during gastrulation in the hypoblast in the head region. Tretinoin 33-46 homeobox B1b Danio rerio 82-88
8631251-6 1996 These results are discussed in terms of the role of Hoxa-1 in controlling anterior hindbrain patterning and the relationship between expression of Hoxa-1 and retinoic acid. Tretinoin 158-171 homeobox B1b Danio rerio 147-153
8603611-4 1996 The most dramatic effect of RA on IGFBPs++ in all cell types tested was to increase IGFBP-6 messenger RNA (mRNA) abundance more than 1000% of the control value. Tretinoin 28-30 insulin like growth factor binding protein 6 Homo sapiens 84-91
8603611-8 1996 Cycloheximide abolished the RA-stimulated increase in IGFBP-6 mRNA and reduced baseline IGFBP-5 mRNA levels, but did not affect RA-modulated mRNA levels of the other IGFBPs. Tretinoin 28-30 insulin like growth factor binding protein 6 Homo sapiens 54-61
9464546-5 1998 Furthermore, the RA-inducible expression of MyoD gene is lost in C2-dnRXR but not in C2-dnRAR cells, indicating that each family of retinoid receptors RAR and RXR may regulate distinct subsets of RA-responsive genes. Tretinoin 17-19 retinoid X receptor alpha Homo sapiens 70-73
9426695-6 1998 Using fluorescent microscopy and the terminal deoxyribonucleotidyl transferase (TdT) assay, we demonstrated that induction of apoptosis by trans-RA contributed to its growth-inhibitory effect in trans-RA-sensitive lung cancer cell lines. Tretinoin 139-147 DNA nucleotidylexotransferase Homo sapiens 37-78
9426695-6 1998 Using fluorescent microscopy and the terminal deoxyribonucleotidyl transferase (TdT) assay, we demonstrated that induction of apoptosis by trans-RA contributed to its growth-inhibitory effect in trans-RA-sensitive lung cancer cell lines. Tretinoin 139-147 DNA nucleotidylexotransferase Homo sapiens 80-83
8603611-9 1996 RA modestly increased the stabilities of all four IGFBP mRNAs, which could contribute to the observed increases in IGFBP-3 and IGFBP-4 mRNA levels; however, the 217% increase in the IGFBP-5 mRNA half- life in the presence of RA could not contribute to the reduction in mRNA levels. Tretinoin 0-2 insulin like growth factor binding protein 4 Homo sapiens 127-134
9681834-6 1998 RA induced an increase in the expression of p27Kip1 but not p21Cip1. Tretinoin 0-2 cyclin dependent kinase inhibitor 1B Homo sapiens 44-51
9183635-4 1996 Retinoic acid receptor (RAR) of HSG cells revealed a transcriptional activity in vivo, and the heterodimerization between RAR and 9-cis retinoic acid receptor (RXR) is requisite for the binding with a specific DNA element termed RA response element in vitro. Tretinoin 24-26 retinoid X receptor alpha Homo sapiens 160-163
9183635-5 1996 RXR alpha and RXR beta were cloned from HSG cells, and these RXRs, together with RAR, seemed to play a physiological role in RA signaling in vivo. Tretinoin 81-83 retinoid X receptor alpha Homo sapiens 0-9
9417101-4 1998 cPLA2-deficient PLB-985 cells differentiate similarly to control PLB-985 cells in response to retinoic acid or 1,25-dihydroxyvitamin D3, indicating that cPLA2 is not involved in the differentiation process. Tretinoin 94-107 phospholipase A2 group IVA Homo sapiens 0-5
9536220-5 1998 Topical application of RA (0.1%) for 2 weeks resulted in marked suprabasal expression of alpha 2, alpha 3 and beta 1 integrin subunits, whereas alpha 6 and beta 4 staining remained on basal keratinocytes. Tretinoin 23-25 integrin subunit beta 1 Homo sapiens 110-125
9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 8-44
9536220-7 1998 Treatment of HaCaT keratinocytes in culture with RA (1 mumol/L) enhanced alpha 2 and beta 1 mRNA abundance. Tretinoin 49-51 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 85-91
9536220-8 1998 Furthermore, RA slightly up-regulated the expression of alpha 2, alpha 3 and beta 1 integrin subunits on primary epidermal keratinocytes and HaCaT cells in culture with no effect on cell proliferation. Tretinoin 13-15 integrin subunit beta 1 Homo sapiens 77-92
9536220-9 1998 These results provide evidence that RA-elicited epidermal hyperplasia is associated with aberrant suprabasal expression of alpha 2 beta 1 and alpha 3 beta 1 integrins, and that this also involves direct stimulation of keratinocyte integrin expression by RA. Tretinoin 36-38 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 131-137
9536220-9 1998 These results provide evidence that RA-elicited epidermal hyperplasia is associated with aberrant suprabasal expression of alpha 2 beta 1 and alpha 3 beta 1 integrins, and that this also involves direct stimulation of keratinocyte integrin expression by RA. Tretinoin 36-38 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 150-156
9473674-7 1998 BMP2 treatment, on the other hand, promoted the effect of RA on the suppressions of trkA mRNA levels and the NGF-dependent survival of the SCG neurons. Tretinoin 58-60 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 84-88
8783199-6 1996 Here the effects of CNTF, which did not induce neural differentiation, were enhanced by differentiation with 12-O-tetradecanoylphorbol 13-acetate (10 nM) and prevented by retinoic acid (10 microM). Tretinoin 171-184 ciliary neurotrophic factor Homo sapiens 20-24
9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 46-51
8882725-1 1996 Rae-1 cDNA is one of the retinoic acid (RA) inducible cDNA clones in mouse embryonal carcinoma F9 cells. Tretinoin 25-38 ribonucleic acid export 1 Mus musculus 0-5
8882725-1 1996 Rae-1 cDNA is one of the retinoic acid (RA) inducible cDNA clones in mouse embryonal carcinoma F9 cells. Tretinoin 40-42 ribonucleic acid export 1 Mus musculus 0-5
9596679-5 1998 Thus, As2O3- or retinoic acid (RA)-induced PML/RARalpha degradation may be a prerequisite, but is not sufficient for the full differentiative/apoptotic response to these drugs. Tretinoin 31-33 PML nuclear body scaffold Homo sapiens 43-46
9517505-5 1998 The most significant effects were a decreased sensitivity of HL-60 to LAK lysis with RA (p < 0.001) and TPA (p < 0.001), and an increased susceptibility of U937 to LAK lysis with GM-CSF (p < 0.0001). Tretinoin 85-87 alpha kinase 1 Homo sapiens 70-73
9596679-5 1998 Thus, As2O3- or retinoic acid (RA)-induced PML/RARalpha degradation may be a prerequisite, but is not sufficient for the full differentiative/apoptotic response to these drugs. Tretinoin 31-33 retinoic acid receptor alpha Homo sapiens 47-55
9667638-6 1998 Treatment with cytotoxic drug (colchicine) or retinoic acid (RA) resulted in a slight increase in P-gp activity in the parental and RAR alpha-infected melanoma cells, whereas the increase in P-gp function in the infected hepatoma cells (both human and rat) was very prominent. Tretinoin 46-59 retinoic acid receptor alpha Homo sapiens 132-141
9585081-9 1998 Antigen expression was decreased after culture with ATRA for all beta1-integrins (except CD49b and CD49f) and pseudoimmunoglobulins (except CD54) tested. Tretinoin 52-56 integrin subunit beta 1 Homo sapiens 65-80
8637715-0 1996 Overexpression of both RAR and RXR restores AP-1 repression in ovarian adenocarcinoma cells resistant to retinoic acid-dependent growth inhibition. Tretinoin 105-118 retinoid X receptor alpha Homo sapiens 31-34
8547646-4 1996 An RAR alpha-selective ligand used with an RXR-selective ligand generated the same responses as did all-trans RA or 9-cis RA, which affect both families of receptors, suggesting an important role for RAR alpha among RAR subtypes in eliciting cellular response. Tretinoin 3-5 retinoid X receptor alpha Homo sapiens 43-46
9585081-11 1998 The modifications in the expression of the beta1-integrins and pseudo immunoglobulins were not specific to ATRA-induced differentiation, but commonly observed with differentiation. Tretinoin 107-111 integrin subunit beta 1 Homo sapiens 43-58
9667638-6 1998 Treatment with cytotoxic drug (colchicine) or retinoic acid (RA) resulted in a slight increase in P-gp activity in the parental and RAR alpha-infected melanoma cells, whereas the increase in P-gp function in the infected hepatoma cells (both human and rat) was very prominent. Tretinoin 61-63 retinoic acid receptor alpha Homo sapiens 132-141
9573222-2 1998 We show that a crucial viral control element, the major immediate-early enhancer, can be activated by retinoic acid (RA) via multiple RA-responsive elements (DR2) that bind retinoid X receptor-retinoic acid receptor (RAR) heterodimers with apparent dissociation constants ranging from 15 to 33 nM. Tretinoin 102-115 retinoic acid receptor alpha Homo sapiens 217-220
9383709-14 1997 Also, RA blocked the stimulation of PG synthesis induced by OP-1; whereas OP-1 decreased cell division engendered by RA. Tretinoin 6-8 bone morphogenetic protein 7 Homo sapiens 60-64
9383709-14 1997 Also, RA blocked the stimulation of PG synthesis induced by OP-1; whereas OP-1 decreased cell division engendered by RA. Tretinoin 117-119 bone morphogenetic protein 7 Homo sapiens 74-78
9439457-2 1997 Some of the genes reported to be involved in this disorder, such as those for lipoprotein lipase (LPL) and apolipoprotein (apo) C-III, are controlled by a peroxisome proliferator-activated receptor (PPAR)/retinoic acid receptor X (RXR) regulatory system, which is retinoic acid dependent. Tretinoin 205-218 retinoid X receptor alpha Homo sapiens 231-234
8537382-4 1995 Transient cellular transfections demonstrate that TGIF inhibits the 9-cis-retinoic acid-dependent RXR alpha transcription activation of the retinoic acid responsive element. Tretinoin 74-87 retinoid X receptor alpha Homo sapiens 98-107
8536680-2 1995 We have previously shown that transcription of the PEPCK gene was stimulated by isoprenaline and retinoic acid in 3T3-F442A adipocytes. Tretinoin 97-110 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 51-56
9573222-2 1998 We show that a crucial viral control element, the major immediate-early enhancer, can be activated by retinoic acid (RA) via multiple RA-responsive elements (DR2) that bind retinoid X receptor-retinoic acid receptor (RAR) heterodimers with apparent dissociation constants ranging from 15 to 33 nM. Tretinoin 117-119 retinoic acid receptor alpha Homo sapiens 217-220
9573222-2 1998 We show that a crucial viral control element, the major immediate-early enhancer, can be activated by retinoic acid (RA) via multiple RA-responsive elements (DR2) that bind retinoid X receptor-retinoic acid receptor (RAR) heterodimers with apparent dissociation constants ranging from 15 to 33 nM. Tretinoin 134-136 retinoic acid receptor alpha Homo sapiens 217-220
7576177-4 1995 Retinoic acid receptors (RARs) also bind as heterodimers with RXR to the DR-8, and this binding is enhanced in the presence of retinoic acid (RA) and/or 9-cis RA. Tretinoin 127-140 retinoid X receptor alpha Homo sapiens 62-65
7576177-4 1995 Retinoic acid receptors (RARs) also bind as heterodimers with RXR to the DR-8, and this binding is enhanced in the presence of retinoic acid (RA) and/or 9-cis RA. Tretinoin 25-27 retinoid X receptor alpha Homo sapiens 62-65
9447705-6 1997 In addition, our data suggest that TR alpha 1 can repress retinoic acid (RA)-signaling during early development. Tretinoin 58-71 thyroid hormone receptor alpha a Danio rerio 35-45
9664142-7 1998 The specific expression patterns of MMP-1 and TIMP-2 were detected and regulated by RA in almost all cell lines, whereas expression of MMP-2 and TIMP-1 was not influenced by RA treatment. Tretinoin 84-86 matrix metallopeptidase 1 Homo sapiens 36-41
9447705-6 1997 In addition, our data suggest that TR alpha 1 can repress retinoic acid (RA)-signaling during early development. Tretinoin 73-75 thyroid hormone receptor alpha a Danio rerio 35-45
9447831-7 1997 Addition of ATRA induced the progressive expression and accumulation of p22phox, p91phox, p47phox and p67phox. Tretinoin 12-16 cytochrome b-245 beta chain Homo sapiens 81-88
9447831-7 1997 Addition of ATRA induced the progressive expression and accumulation of p22phox, p91phox, p47phox and p67phox. Tretinoin 12-16 neutrophil cytosolic factor 1 Homo sapiens 90-97
7576177-4 1995 Retinoic acid receptors (RARs) also bind as heterodimers with RXR to the DR-8, and this binding is enhanced in the presence of retinoic acid (RA) and/or 9-cis RA. Tretinoin 142-144 retinoid X receptor alpha Homo sapiens 62-65
7592579-3 1995 The endogenous retinoid hormones, all-trans-retinoic acid and 9-cis-retinoic acid, and the synthetic retinoic acid receptor-selective compound, TTNPB, also stimulate 24-(OH)ase. Tretinoin 34-57 cytochrome P450, family 24, subfamily a, polypeptide 1 Mus musculus 166-176
9348290-2 1997 RXRalpha-/-/ RARalpha-/- cells were resistant to retinoic acid treatment for the induction of primitive and parietal endodermal differentiation, as well as for antiproliferative and apoptotic responses, whereas they could differentiate into visceral endodermlike cells, as previously observed for RXRalpha-/- cells. Tretinoin 49-62 retinoic acid receptor, alpha Mus musculus 13-21
7566126-2 1995 On response elements consisting of direct repeats spaced by five base pairs (DR + 5 elements), RAR/RXR heterodimers activate transcription in response to RAR-specific ligands, such as all-trans-retinoic acid (RA). Tretinoin 188-207 retinoid X receptor alpha Homo sapiens 99-102
9607768-7 1998 Similarly, retinoic-acid-induced transcriptional upregulation of the cell-cycle inhibitor p21Cip1 required normal levels of p300, but not CBP, whereas the reverse was true for p27Kip1. Tretinoin 11-24 cyclin dependent kinase inhibitor 1B Homo sapiens 176-183
7566126-2 1995 On response elements consisting of direct repeats spaced by five base pairs (DR + 5 elements), RAR/RXR heterodimers activate transcription in response to RAR-specific ligands, such as all-trans-retinoic acid (RA). Tretinoin 95-97 retinoid X receptor alpha Homo sapiens 99-102
9334271-3 1997 Accordingly, Hoxb-8 expression is rapidly induced by retinoic acid (RA) treatment in the anterior of the forelimb in a spatial and temporal manner that is consistent with the induction of Shh and formation of the ZPA. Tretinoin 53-66 zona pellucida glycoprotein 2 Gallus gallus 213-216
9334271-3 1997 Accordingly, Hoxb-8 expression is rapidly induced by retinoic acid (RA) treatment in the anterior of the forelimb in a spatial and temporal manner that is consistent with the induction of Shh and formation of the ZPA. Tretinoin 68-70 zona pellucida glycoprotein 2 Gallus gallus 213-216
9365540-1 1997 Retinoic acid (RA) reduced growth, fibronectin, and retinoic acid receptor (RAR alpha) in NIH 3T3 cells but not in cells transformed by the Ha-ras oncogene. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 76-85
9365540-1 1997 Retinoic acid (RA) reduced growth, fibronectin, and retinoic acid receptor (RAR alpha) in NIH 3T3 cells but not in cells transformed by the Ha-ras oncogene. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 76-85
9365540-3 1997 H-ras transformation downregulated RAR expression and abolished responsiveness to RA. Tretinoin 35-37 Harvey rat sarcoma virus oncogene Mus musculus 0-5
9605760-6 1998 Although GDNF alone induced a rather weak differentiation independent of the disease stages, the enhancement of neurite outgrowth induced by treatment with both GDNF and all-trans-retinoic acid was significantly correlated with younger age (less than 1 year; P = 0.0039), non-stage 4 diseases (P = 0.0023), a single copy of N-myc (P = 0.027), and high levels of TRK-A expression (P = 0.0062). Tretinoin 174-193 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 324-329
9365540-4 1997 Ha-ras-transformed cells were as active as normal NIH-3T3 cells in RA uptake but were unable to degrade it to medium oxidation product, so that, paradoxically, the resistant cells accumulated 20-30-fold as much RA as the sensitive cells. Tretinoin 67-69 Harvey rat sarcoma virus oncogene Mus musculus 0-6
9365540-4 1997 Ha-ras-transformed cells were as active as normal NIH-3T3 cells in RA uptake but were unable to degrade it to medium oxidation product, so that, paradoxically, the resistant cells accumulated 20-30-fold as much RA as the sensitive cells. Tretinoin 211-213 Harvey rat sarcoma virus oncogene Mus musculus 0-6
9343411-3 1997 RA markedly increased restriction site accessibility within the promoter, including a site near the RA responsive element (RARE) to which the nuclear receptor retinoid X receptor (RXR)-RAR heterodimer binds. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 123-126
7485518-3 1995 Previous studies of lipid-laden rat pulmonary interstitial fibroblasts (LIF) have shown that their elastin synthesis is increased in vitro by retinoic acid (RA). Tretinoin 142-155 LIF, interleukin 6 family cytokine Rattus norvegicus 72-75
7485518-3 1995 Previous studies of lipid-laden rat pulmonary interstitial fibroblasts (LIF) have shown that their elastin synthesis is increased in vitro by retinoic acid (RA). Tretinoin 142-155 elastin Rattus norvegicus 99-106
7485518-3 1995 Previous studies of lipid-laden rat pulmonary interstitial fibroblasts (LIF) have shown that their elastin synthesis is increased in vitro by retinoic acid (RA). Tretinoin 157-159 LIF, interleukin 6 family cytokine Rattus norvegicus 72-75
7485518-3 1995 Previous studies of lipid-laden rat pulmonary interstitial fibroblasts (LIF) have shown that their elastin synthesis is increased in vitro by retinoic acid (RA). Tretinoin 157-159 elastin Rattus norvegicus 99-106
7485518-4 1995 We hypothesized that temporal changes in the endogenous RA content of LIF may correlate with changes in elastin synthesis by these cells. Tretinoin 56-58 LIF, interleukin 6 family cytokine Rattus norvegicus 70-73
7485518-4 1995 We hypothesized that temporal changes in the endogenous RA content of LIF may correlate with changes in elastin synthesis by these cells. Tretinoin 56-58 elastin Rattus norvegicus 104-111
7485518-13 1995 These findings are consistent with the hypothesis that endogenous RA could contribute to the postnatal increase in elastin production by pulmonary fibroblasts. Tretinoin 66-68 elastin Rattus norvegicus 115-122
9343411-3 1997 RA markedly increased restriction site accessibility within the promoter, including a site near the RA responsive element (RARE) to which the nuclear receptor retinoid X receptor (RXR)-RAR heterodimer binds. Tretinoin 100-102 retinoic acid receptor, alpha Mus musculus 123-126
9343411-4 1997 These changes coincided with RA-induced alterations in the DNase I hypersensitivity pattern in and around the promoter. Tretinoin 29-31 deoxyribonuclease I Mus musculus 59-66
9366521-2 1997 RA causes cell cycle arrest at low cell density and significant morphological changes in U343 cells, reflected by reorganization of the intermediate filament, GFAP, and actin. Tretinoin 0-2 glial fibrillary acidic protein Homo sapiens 159-163
9576918-6 1998 Myb-Ets also antagonizes the biological response of erythrocytic progenitor cells to RA and thyroid hormone. Tretinoin 85-87 MYB proto-oncogene, transcription factor Homo sapiens 0-3
9344589-0 1997 Stable transfection of U937 cells with sense or antisense RXR-alpha cDNA suggests a role for RXR-alpha in the control of monoblastic differentiation induced by retinoic acid and vitamin D. Tretinoin 160-173 retinoid X receptor alpha Homo sapiens 58-67
9344589-0 1997 Stable transfection of U937 cells with sense or antisense RXR-alpha cDNA suggests a role for RXR-alpha in the control of monoblastic differentiation induced by retinoic acid and vitamin D. Tretinoin 160-173 retinoid X receptor alpha Homo sapiens 93-102
7563063-2 1995 CRABPI binds all-trans retinoic acid and some retinoic acid metabolites with nanomolar affinities. Tretinoin 23-36 cellular retinoic acid binding protein I Mus musculus 0-6
7563063-2 1995 CRABPI binds all-trans retinoic acid and some retinoic acid metabolites with nanomolar affinities. Tretinoin 46-59 cellular retinoic acid binding protein I Mus musculus 0-6
9576918-8 1998 Here, we demonstrate that RA inhibits the expression of the endogenous Myb target gene tom-1. Tretinoin 26-28 MYB proto-oncogene, transcription factor Homo sapiens 71-74
7500834-0 1995 Promoter activity of the gene encoding the beta-amyloid precursor protein is up-regulated by growth factors, phorbol ester, retinoic acid and interleukin-1. Tretinoin 124-137 amyloid beta precursor protein Rattus norvegicus 43-73
9370309-8 1997 RT-PCR analysis of human fibroblasts indicates constitutive low-level expression of cKrox which can be transiently elevated by treatment with retinoic acid. Tretinoin 142-155 zinc finger and BTB domain containing 7B Homo sapiens 84-89
9326447-9 1997 These data are consistent with the hypothesis that holo-CRBP serves as substrate for retinoic acid biosynthesis because they show that the substrate and the enzyme occur in the same cellular loci in vivo. Tretinoin 85-98 retinol binding protein 1 Rattus norvegicus 56-60
9576918-8 1998 Here, we demonstrate that RA inhibits the expression of the endogenous Myb target gene tom-1. Tretinoin 26-28 target of myb1 membrane trafficking protein Homo sapiens 87-92
9576918-9 1998 Conversely, Myb functions as a potent inhibitor of RA-induced biological responses. Tretinoin 51-53 MYB proto-oncogene, transcription factor Homo sapiens 12-15
7615086-0 1995 Transcriptional regulation of carbonic anhydrase II by retinoic acid in the human pancreatic tumor cell line DANG. Tretinoin 55-68 carbonic anhydrase 2 Homo sapiens 30-51
9619634-8 1998 Retinoic acid (RA)-induced differentiation and growth inhibition of neuroblastoma cells was associated with an increase in type 1 GAP120 and neurofibromin mRNA, and a decrease in p21ras-GTP. Tretinoin 15-17 HRas proto-oncogene, GTPase Homo sapiens 179-185
7615086-2 1995 We have developed the human pancreatic duct cell line DANG as a model to study the effects of all-trans-retinoic acid (ATRA) on CA II gene expression. Tretinoin 94-117 carbonic anhydrase 2 Homo sapiens 128-133
7615086-2 1995 We have developed the human pancreatic duct cell line DANG as a model to study the effects of all-trans-retinoic acid (ATRA) on CA II gene expression. Tretinoin 119-123 carbonic anhydrase 2 Homo sapiens 128-133
9390004-3 1997 In mid-gestation mouse embryos the expression of both the transgene and the endogenous protein was elevated under the condition of hypovitaminosis A, suggesting that depletion of retinoic acid (RA) induced CRABP-I expression in embryos. Tretinoin 179-192 cellular retinoic acid binding protein I Mus musculus 206-213
9390004-3 1997 In mid-gestation mouse embryos the expression of both the transgene and the endogenous protein was elevated under the condition of hypovitaminosis A, suggesting that depletion of retinoic acid (RA) induced CRABP-I expression in embryos. Tretinoin 194-196 cellular retinoic acid binding protein I Mus musculus 206-213
7615086-3 1995 ATRA treatment resulted in a time- and dose-dependent inhibition of CA II mRNA concentrations in DANG cells. Tretinoin 0-4 carbonic anhydrase 2 Homo sapiens 68-73
9578604-2 1998 G-CSF enhanced O-2 generating ability of HL-60 cells whose differentiation had been initiated by dimethylsulfoxide (DMSO) or retinoic acid (RA). Tretinoin 125-138 colony stimulating factor 3 Homo sapiens 0-5
9390004-8 1997 It was concluded that RA had a suppressive effect on CRABP-I gene expression in embryos and P19 cells and the effect could be mediated through RAR beta, RAR gamma or RXR alpha. Tretinoin 22-24 cellular retinoic acid binding protein I Mus musculus 53-60
9390004-8 1997 It was concluded that RA had a suppressive effect on CRABP-I gene expression in embryos and P19 cells and the effect could be mediated through RAR beta, RAR gamma or RXR alpha. Tretinoin 22-24 retinoic acid receptor, gamma Mus musculus 153-162
9617539-10 1998 All-trans retinoic acid induced RAR beta mRNA expression in corneal and conjunctival fibroblasts. Tretinoin 10-23 retinoic acid receptor beta Oryctolagus cuniculus 32-40
7631783-3 1995 Surprisingly, homozygous mutant mice were resistant to fourfold higher doses of retinoic acid than wild-type mice as well as to elevated doses of the synthetic retinoids, indicating that RAR gamma may have a major role in mediating retinoid toxicity, a finding that possibly has practical implications for reducing the toxicity of synthetic retinoids in clinical use. Tretinoin 80-93 retinoic acid receptor, gamma Mus musculus 187-196
9617539-15 1998 The data suggest a relationship between the induction of RAR beta mRNA expression and inhibition of cell proliferation by retinoic acid. Tretinoin 122-135 retinoic acid receptor beta Oryctolagus cuniculus 57-65
9392513-2 1997 The tissues that express CRABP-I, i.e. the central nervous system (CNS), neural crest, branchial arches, limb bud and frontonasal mass, coincide with those that are most sensitive to unphysiological retinoic acid (RA) concentrations. Tretinoin 199-212 cellular retinoic acid binding protein I Mus musculus 25-32
9392513-8 1997 One of these regulatory elements has the hallmarks of an RA response element, suggesting that CRABP-I expression in neural tissue can be directly modulated by RA via the RARs/RXRs. Tretinoin 57-59 cellular retinoic acid binding protein I Mus musculus 94-101
9679546-4 1998 Seven repeat retinoic acid response element (RARE) consensus half sites, A(G)GG(T)TC(G)A at +1521 to +1644 were identified in the cloned hGSTP1*C. Five of the RARE half-sites had the minimal spacer nucleotide requirement for functionality and DNA mobility shift analysis with different pairs of the RARE half-sites and supershift studies using antibodies against RAR-beta showed significant binding of nuclear protein complexes from RA-treated cells to these RAREs. Tretinoin 13-26 glutathione S-transferase pi 1 Homo sapiens 137-143
9276475-8 1997 De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis. Tretinoin 165-178 cytidine/uridine monophosphate kinase 1 Homo sapiens 128-131
9260895-1 1997 We have investigated the regulation of transcription factors HNF-3alpha and HNF-3beta during the retinoic acid-mediated differentiation of mouse P19 cells. Tretinoin 97-110 forkhead box A1 Mus musculus 61-71
7790895-7 1995 Using an antagonist selective for the retinoic acid receptor-alpha subtype, Ro 41-5253, we found that the effects of t-RA and 9c-RA on acetylcholine levels were abolished. Tretinoin 117-121 retinoic acid receptor, alpha Mus musculus 38-66
7786028-1 1995 Two families of nuclear retinoid receptors, retinoic acid receptor and retinoid X receptor (RAR and RXR respectively), and a family of cellular retinoic acid-binding proteins (CRABPI and II) participate in the retinoic acid (RA) signaling pathway. Tretinoin 44-57 retinoid X receptor alpha Homo sapiens 100-103
7786028-1 1995 Two families of nuclear retinoid receptors, retinoic acid receptor and retinoid X receptor (RAR and RXR respectively), and a family of cellular retinoic acid-binding proteins (CRABPI and II) participate in the retinoic acid (RA) signaling pathway. Tretinoin 92-94 retinoid X receptor alpha Homo sapiens 100-103
9531570-8 1998 As the above-noted results predict, histone deacetylase inhibitors antagonize oncogenic activities of the PML-RARalpha fusion protein and partially relieve transcriptional repression by PLZF as well as inhibitory effect of PLZF-RARalpha on ATRA response. Tretinoin 240-244 PML nuclear body scaffold Homo sapiens 106-110
7786028-6 1995 Furthermore, 9-cis RA, a ligand that binds to both the RAR and the RXR families, selectively activates the CRABPII gene. Tretinoin 19-21 retinoid X receptor alpha Homo sapiens 67-70
7786028-6 1995 Furthermore, 9-cis RA, a ligand that binds to both the RAR and the RXR families, selectively activates the CRABPII gene. Tretinoin 19-21 cellular retinoic acid binding protein 2 Homo sapiens 107-114
9303343-0 1997 Expression of the transcription factor slug correlates with growth of the limb bud and is regulated by FGF-4 and retinoic acid. Tretinoin 113-126 snail family transcriptional repressor 2 Gallus gallus 39-43
9303343-10 1997 The fact that slug expression pattern correlates with areas of growth in the limb, and is maintained by FGF-4 and down-regulated by retinoic acid, indicates that slug-expressing cells play a crucial role in growth and patterning of the chick limb. Tretinoin 132-145 snail family transcriptional repressor 2 Gallus gallus 14-18
9303343-10 1997 The fact that slug expression pattern correlates with areas of growth in the limb, and is maintained by FGF-4 and down-regulated by retinoic acid, indicates that slug-expressing cells play a crucial role in growth and patterning of the chick limb. Tretinoin 132-145 snail family transcriptional repressor 2 Gallus gallus 162-166
7626495-1 1995 The two cellular retinoic acid binding proteins, CRABP I and CRABP II, belong to a family of small cytosolic lipid binding proteins and are highly conserved during evolution. Tretinoin 17-30 cellular retinoic acid binding protein 2 Homo sapiens 61-69
9531596-0 1998 Retinoic acid selectively inhibits lipopolysaccharide induction of tissue factor gene expression in human monocytes. Tretinoin 0-13 coagulation factor III, tissue factor Homo sapiens 67-80
7556883-0 1995 Retinoic acid induction of mouse cellular retinoic acid-binding protein-I gene expression is enhanced by sphinganine. Tretinoin 0-13 cellular retinoic acid binding protein I Mus musculus 33-73
9219948-1 1997 Retinoic acid treatment of NT-era2/cl.D1 (NT2) cells, a human teratocarcinoma cell line, yields 95% pure cultures of terminally differentiated neuronal cells. Tretinoin 0-13 claudin 1 Homo sapiens 35-40
9531596-2 1998 Lipopolysaccharide (LPS)-induced monocyte TF expression is downregulated by the nuclear hormone all-trans retinoic acid (ATRA). Tretinoin 96-119 coagulation factor III, tissue factor Homo sapiens 42-44
7556883-1 1995 Cellular retinoic acid-binding protein-I (CRABP-I) gene expression is induced in mouse embryonal carcinoma P19 cells specifically by retinoic acid (RA) and the induction is enhanced by sphinganine. Tretinoin 9-22 cellular retinoic acid binding protein I Mus musculus 42-49
9531596-2 1998 Lipopolysaccharide (LPS)-induced monocyte TF expression is downregulated by the nuclear hormone all-trans retinoic acid (ATRA). Tretinoin 121-125 coagulation factor III, tissue factor Homo sapiens 42-44
7556883-1 1995 Cellular retinoic acid-binding protein-I (CRABP-I) gene expression is induced in mouse embryonal carcinoma P19 cells specifically by retinoic acid (RA) and the induction is enhanced by sphinganine. Tretinoin 43-45 cellular retinoic acid binding protein I Mus musculus 0-40
7556883-2 1995 The effects of retinoic acid and sphinganine on CRABP-I gene expression can be accounted for by a stimulation of its transcription rate. Tretinoin 15-28 cellular retinoic acid binding protein I Mus musculus 48-55
9352625-3 1997 Retinoic acid (RA-, 1 microM)-treatment and aggregation for 4 days induced and greatly increased MASH-1, neuroD and NSCL-2 mRNA in P19 cells. Tretinoin 0-13 achaete-scute family bHLH transcription factor 1 Mus musculus 97-103
9531596-3 1998 In this study, we examined the mechanism by which ATRA inhibits monocyte TF expression. Tretinoin 50-54 coagulation factor III, tissue factor Homo sapiens 73-75
7731708-2 1995 The effects of RA are mediated through multiple members of the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families of nuclear transcription factors. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 96-115
7731708-2 1995 The effects of RA are mediated through multiple members of the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families of nuclear transcription factors. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 117-120
9224784-4 1997 SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells. Tretinoin 109-113 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 38-44
9224784-4 1997 SDS-PAGE and Western blot analysis of UGT1.1-transfected HK293 membrane proteins photolabeled with [11,12-3H]atRA revealed a protein of approximately 56 kDa that was labeled by [3H]atRA, detected by anti-pNP UGT antibody and not present in membranes from nontransfected HK293 cells. Tretinoin 181-185 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 38-44
7731708-4 1995 Using NTera2/clone D1 (NT2/D1) human embryonal carcinoma cells as a model, we report that the RA induced terminal differentiation of these cells into a neuronal phenotype is characterized by an increase in expression of RAR alpha, RAR beta, RAR gamma, and a slight induction of RXR alpha. Tretinoin 94-96 retinoid X receptor alpha Homo sapiens 278-287
9531596-4 1998 We show that ATRA selectively inhibited LPS induction of TF expression in human monocytes and monocytic THP-1 cells without affecting LPS induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8). Tretinoin 13-17 coagulation factor III, tissue factor Homo sapiens 57-59
9531596-8 1998 Our results demonstrate that ATRA selectively inhibited LPS-induced TF gene transcription in human monocytic cells by a mechanism that does not involve repression of AP-1- or NF-kappaB-mediated transcription. Tretinoin 29-33 coagulation factor III, tissue factor Homo sapiens 68-70
9211989-4 1997 Upon RA treatment both Tn polypeptides were also found in extracellular matrix preparations of the differentiated cells. Tretinoin 5-7 tenascin C Homo sapiens 23-25
9546726-5 1998 CRABP(II), whose presence has been previously shown to correlate with retinoic acid synthesis in the uterine epithelium, was specifically localized to the luminal epithelium at Day 1, being stronger on the mesometrial side, and then fell to lower levels. Tretinoin 70-83 cellular retinoic acid binding protein 2 Rattus norvegicus 0-9
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 159-172 zinc finger and BTB domain containing 16 Homo sapiens 41-45
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 174-178 zinc finger and BTB domain containing 16 Homo sapiens 41-45
9217822-0 1997 Effect of topical tretinoin on non-sun-exposed human skin connective tissue: induction of tenascin but no major effect on collagen metabolism. Tretinoin 18-27 tenascin C Homo sapiens 90-98
7726832-2 1995 The inhibitory effect of okadaic acid on elastin mRNA levels was efficiently prevented by retinoic acid and cycloheximide and was further enhanced by phorbol ester treatment. Tretinoin 90-103 elastin Homo sapiens 41-48
7714081-0 1995 Retinoic acid induces intercellular adhesion molecule-1 hyperexpression in human thyroid carcinoma cell lines. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 22-55
7714081-4 1995 In the present study, we investigated, by flow cytometry, the effect of retinoic acid on the surface expression of ICAM-1 in human thyroid carcinoma cell lines. Tretinoin 72-85 intercellular adhesion molecule 1 Homo sapiens 115-121
9546726-11 1998 The presence of CRABP(II) suggests that local generation of retinoic acid is important in these processes. Tretinoin 60-73 cellular retinoic acid binding protein 2 Rattus norvegicus 16-25
7714081-6 1995 All of them produced constitutively ICAM-1; its surface expression and specific messenger ribonucleic acid (mRNA) levels were increased significantly by retinoic acid in all except the WRO cell line. Tretinoin 153-166 intercellular adhesion molecule 1 Homo sapiens 36-42
7714081-8 1995 Furthermore, cytokines, such as interferon-gamma and tumor necrosis factor-alpha, both individually and, to a greater extent, in combination with retinoic acid, increased ICAM-1 surface expression and its mRNA levels. Tretinoin 146-159 intercellular adhesion molecule 1 Homo sapiens 171-177
7714081-9 1995 In conclusion, retinoic acid is able to induce ICAM-1 up-regulation via mRNA accumulation in human thyroid carcinoma cell lines. Tretinoin 15-28 intercellular adhesion molecule 1 Homo sapiens 47-53
7720576-1 1995 A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Tretinoin 15-34 retinoic acid receptor, gamma Mus musculus 159-168
9186002-0 1997 Retinoic acid induces signal transducer and activator of transcription (STAT) 1, STAT2, and p48 expression in myeloid leukemia cells and enhances their responsiveness to interferons. Tretinoin 0-13 signal transducer and activator of transcription 1 Homo sapiens 22-79
9186002-0 1997 Retinoic acid induces signal transducer and activator of transcription (STAT) 1, STAT2, and p48 expression in myeloid leukemia cells and enhances their responsiveness to interferons. Tretinoin 0-13 signal transducer and activator of transcription 2 Homo sapiens 81-86
7720576-1 1995 A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Tretinoin 21-34 retinoic acid receptor, gamma Mus musculus 159-168
7720578-8 1995 In particular, retinoic acid treatment essentially abolishes Xotx2 expression in neuroectoderm. Tretinoin 15-28 orthodenticle homeobox 2 S homeolog Xenopus laevis 61-66
9138088-0 1997 Effects of TPA, bryostatin 1, and retinoic acid on PO-B, AP-1, and AP-2 DNA binding during HL-60 differentiation. Tretinoin 34-47 transcription factor AP-2 alpha Homo sapiens 67-71
9502726-6 1998 The in vitro differentiation with retinoic acid and cAMP led to a 5- to 10-fold induction of flk-1, von Willebrand Factor (vWF), TM, GATA-4 and GATA-6. Tretinoin 34-47 Von Willebrand factor Mus musculus 100-121
7533818-0 1995 Retinoic acid inhibits basal and interferon-gamma-induced expression of intercellular adhesion molecule 1 in monocytic cells. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 72-105
7533818-4 1995 Treatment with indomethacin prevented and prostaglandin E2 (PGE2), dibutyryl-cAMP, or forskolin mimicked reduction of basal ICAM-1 expression by RA, indicating that this effect of RA is mediated by PGE2 synthesis and subsequent cAMP elevation. Tretinoin 145-147 intercellular adhesion molecule 1 Homo sapiens 124-130
9502726-6 1998 The in vitro differentiation with retinoic acid and cAMP led to a 5- to 10-fold induction of flk-1, von Willebrand Factor (vWF), TM, GATA-4 and GATA-6. Tretinoin 34-47 Von Willebrand factor Mus musculus 123-126
7533818-4 1995 Treatment with indomethacin prevented and prostaglandin E2 (PGE2), dibutyryl-cAMP, or forskolin mimicked reduction of basal ICAM-1 expression by RA, indicating that this effect of RA is mediated by PGE2 synthesis and subsequent cAMP elevation. Tretinoin 180-182 intercellular adhesion molecule 1 Homo sapiens 124-130
7533818-5 1995 In contrast, suppression of IFN-gamma-induced ICAM-1 expression by RA was only partly reversible by indomethacin, suggesting that inhibition of IFN-gamma stimulation was not completely due to cyclooxygenase induction. Tretinoin 67-69 intercellular adhesion molecule 1 Homo sapiens 46-52
9502726-6 1998 The in vitro differentiation with retinoic acid and cAMP led to a 5- to 10-fold induction of flk-1, von Willebrand Factor (vWF), TM, GATA-4 and GATA-6. Tretinoin 34-47 thrombomodulin Mus musculus 129-131
7533818-8 1995 RA also blocked ICAM-1 induction by IFN-gamma in isolated human blood monocytes. Tretinoin 0-2 intercellular adhesion molecule 1 Homo sapiens 16-22
9672841-0 1998 Mesenchymal changes associated with retinoic acid induced cleft palate in CD-1 mice. Tretinoin 36-49 CD1 antigen complex Mus musculus 74-78
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 31-44 retinoid X receptor alpha Homo sapiens 68-71
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 31-44 retinoid X receptor alpha Homo sapiens 91-94
9177427-5 1997 The combination of MK5 plus all-trans retinoic acid (ATRA) resulted in enhanced induction of apoptosis in both freshly isolated APL cells and NB4 cells as compared to each reagent alone. Tretinoin 53-57 MAPK activated protein kinase 5 Homo sapiens 19-22
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-44 retinoic acid receptor, gamma Mus musculus 60-68
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-44 retinoic acid receptor, gamma Mus musculus 122-130
7530213-0 1995 The combination of Steel factor and GM-CSF blocks apoptosis induced by retinoic acid and upregulates AP-1 in a human growth factor-dependent cell line. Tretinoin 71-84 KIT ligand Homo sapiens 19-31
9544986-4 1998 Thus, the retinoic acid response mediated by RAR alpha is weak in these cells. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 45-54
7576948-8 1995 In addition, CD44 expression can be upmodulated parallel to differentiation or maturation as induced by retinoic acid, bromodeoxyuridine or phorbol ester. Tretinoin 104-117 CD44 molecule (Indian blood group) Homo sapiens 13-17
7536752-7 1995 Culture of HL-60 cells in medium containing dimethylsulfoxide, retinoic acid, and 1,25 dihydroxyvitamin D3, agents that stimulate the differentiation of HL-60 along myeloid pathways, also caused the induction of IFI 16 mRNA. Tretinoin 63-76 interferon gamma inducible protein 16 Homo sapiens 212-218
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-44 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-44 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-44 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-43 retinoic acid receptor, gamma Mus musculus 60-68
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-43 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-43 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-43 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 30-43 retinoic acid receptor, gamma Mus musculus 122-130
9187263-7 1997 The induction of apoptosis by retinoic acids is mediated by RARgamma because (a) the phenomenon can be reproduced only by RARgamma-selective retinoic acid analogs, (b) the cell death induced by either retinoic acids or RARgamma analogs can be inhibited by RARgamma-specific antagonists, and (c) CD4+CD8+ thymocytes express RARgamma. Tretinoin 201-215 retinoic acid receptor, gamma Mus musculus 60-68
7536752-10 1995 The nuclear localization of IFI 16 antigen was confirmed by immunohistochemical staining of HL-60 cells treated with IFN-gamma, dimethylsulfoxide, and retinoic acid. Tretinoin 151-164 interferon gamma inducible protein 16 Homo sapiens 28-34
18475624-5 1995 Co-incubation of RA inhibited PAF-induced PMN aggregation, the release of acid phosphatase from PMNs, and PMN chemotaxis to zymosan-activated serum and histamine while the expression of ICAM-1 and ELAM-1 did not change. Tretinoin 17-19 intercellular adhesion molecule 1 Homo sapiens 186-192
9579690-6 1998 These findings may raise the possibility that prostaglandin-D-synthase in CSF is involved in retinoic acid action on the brain. Tretinoin 93-106 prostaglandin D2 synthase Rattus norvegicus 46-70
7802648-7 1994 On the other hand, both 1,25(OH)2D3 and retinoic acid separately stabilized the VDR mRNA levels increasing the apparent half-life by 11 h and 6 h, respectively. Tretinoin 40-53 vitamin D receptor Homo sapiens 80-83
9130390-3 1997 Our results are noteworthy as SnPP is being used for the amelioration and management of hyperbilirubinemia, and they emphasize that the combined dosing of retinoic acid and SnPP attenuates the suppression of the activity of HMOX, thereby decreasing plasma bilirubin levels. Tretinoin 155-168 heme oxygenase 1 Rattus norvegicus 224-228
9611775-6 1998 G-Rh2 and G-Rh3 arrested the cell cycle at the G1/S phase, consistent with the ability to induce differentiation in a decreasing order of retinoic acid > G-Rh2 > G-Rh3. Tretinoin 138-151 Rh associated glycoprotein Homo sapiens 2-5
9153406-4 1997 Analyses of the distribution of limiting amounts of [3H]-all-trans-retinoic acid between cytoplasmic retinoic acid binding proteins, CRABP-I and CRABP-II, and the purified heterocomplexes indicate that all-trans-retinoic acid binds with comparable affinity to CRABP-I and the heterocomplexes, but with approximately 10-fold less affinity to CRABP-II. Tretinoin 61-80 cellular retinoic acid binding protein 2 Homo sapiens 341-349
9169003-3 1997 We investigated the expression of the co-repressor (SMRT) and co-activator (Trip 1) for retinoid and thyroid-hormone receptors in several neuroectodermal tumour cell lines, and its modulation by all-trans-retinoic acid, as well as by synthetic agonists, for RAR alpha, RAR beta, RAR gamma and RXR. Tretinoin 199-218 eukaryotic translation initiation factor 3 subunit I Homo sapiens 76-82
7988722-0 1994 Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression. Tretinoin 0-13 brain-derived neurotrophic factor Rattus norvegicus 22-26
7988722-0 1994 Retinoic acid induces BDNF responsiveness of sympathetic neurons by alteration of Trk neurotrophin receptor expression. Tretinoin 0-13 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 82-85
7988722-3 1994 Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of trkA mRNA and induced the expression of trkB mRNA. Tretinoin 122-135 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 198-202
9611775-6 1998 G-Rh2 and G-Rh3 arrested the cell cycle at the G1/S phase, consistent with the ability to induce differentiation in a decreasing order of retinoic acid > G-Rh2 > G-Rh3. Tretinoin 138-151 Rh associated glycoprotein Homo sapiens 159-162
7988722-3 1994 Here we show that the treatment of the cultured sympathetic neurons from newborn rat superior cervical ganglia (SCG) with retinoic acid (RA), a derivative of vitamin A, suppressed the expression of trkA mRNA and induced the expression of trkB mRNA. Tretinoin 137-139 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 198-202
9506453-2 1998 RAR directly bind and are activated by two naturally occurring isomers of retinoic acid (RA), all-trans retinoic acid (t-RA) and 9-cis retinoic acid (9c-RA). Tretinoin 89-91 retinoic acid receptor alpha Homo sapiens 0-3
9115293-0 1997 Identification and characterization of a retinoic acid-regulated human homologue of the unc-33-like phosphoprotein gene (hUlip) from neuroblastoma cells. Tretinoin 41-54 dihydropyrimidinase like 3 Homo sapiens 121-126
9506453-6 1998 [3H]All-trans retinol (t-ROL) added to suspensions of intact epidermal cells was metabolically converted to [3H]t-RA, which bound to RAR. Tretinoin 114-116 retinoic acid receptor alpha Homo sapiens 133-136
9506453-11 1998 Incubation of cells with [3H]9c-RA alone resulted in substantial (38%) binding of [3H]t-RA to RAR, in addition to binding of [3H]9c-RA, due to isomerization of [3H]9c-RA to [3H]t-RA. Tretinoin 32-34 retinoic acid receptor alpha Homo sapiens 94-97
7890140-1 1994 Regulation of expression of transforming growth factor-beta 3 (TGF-beta 3) and the cellular retinoic acid-binding proteins-I and II (CRABP-I, -II) by retinoic acid (RA) and TGF-beta was examined in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Tretinoin 92-105 cellular retinoic acid binding protein I Mus musculus 133-140
7890140-1 1994 Regulation of expression of transforming growth factor-beta 3 (TGF-beta 3) and the cellular retinoic acid-binding proteins-I and II (CRABP-I, -II) by retinoic acid (RA) and TGF-beta was examined in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Tretinoin 134-136 cellular retinoic acid binding protein I Mus musculus 83-131
9137089-0 1997 Vitronectin expression in differentiating neuroblastic tumors: integrin alpha v beta 5 mediates vitronectin-dependent adhesion of retinoic-acid-differentiated neuroblastoma cells. Tretinoin 130-143 vitronectin Homo sapiens 96-107
9137089-8 1997 These data suggest that the synthesis of vitronectin and the ability of integrin alpha v beta 5 to mediate vitronectin adhesion on retinoic-acid-differentiated neuroblastoma cells may promote differentiation of neuroblastoma cells in vivo. Tretinoin 131-144 vitronectin Homo sapiens 107-118
9506453-13 1998 Competition studies revealed that 9c-RA was 6-fold less effective than t-RA at displacing [3H]t-RA bound to RAR in nuclear extracts. Tretinoin 37-39 retinoic acid receptor alpha Homo sapiens 108-111
7695840-4 1994 Retinoic acid increased the effect of IL-6 on alpha-1-antichymotrypsin (ACT) and fibrinogen (FBG) on the level of both proteins and mRNAs. Tretinoin 0-13 serpin family A member 3 Homo sapiens 46-70
9142499-7 1997 Moreover, several of the vertebral defects inherent to the RAR gamma null phenotype were abolished by RA treatment specifically at 10.5 dpc, suggesting that RAR alpha and/or RAR beta isoforms may substitute for certain RAR gamma functions, and that RAR gamma may elicit its normal effects on vertebral morphogenesis at this developmental stage. Tretinoin 59-61 retinoic acid receptor, alpha Mus musculus 157-166
9506453-14 1998 At ratios of 9c-RA to t-RA of 4:1 or lower, RAR in nuclear extracts bound t-RA exclusively. Tretinoin 16-18 retinoic acid receptor alpha Homo sapiens 44-47
9142499-7 1997 Moreover, several of the vertebral defects inherent to the RAR gamma null phenotype were abolished by RA treatment specifically at 10.5 dpc, suggesting that RAR alpha and/or RAR beta isoforms may substitute for certain RAR gamma functions, and that RAR gamma may elicit its normal effects on vertebral morphogenesis at this developmental stage. Tretinoin 59-61 retinoic acid receptor, gamma Mus musculus 219-228
9485034-5 1998 After retinoic acid-induced differentiation, only the PSA-positive, neuron-like cell type gave clear signals for ST8SiaII and ST8SiaIV in in situ hybridization, whereas both signals were drastically reduced in the weakly PSA-positive substrate adherent phenotype. Tretinoin 6-19 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2 Homo sapiens 113-121
9142499-7 1997 Moreover, several of the vertebral defects inherent to the RAR gamma null phenotype were abolished by RA treatment specifically at 10.5 dpc, suggesting that RAR alpha and/or RAR beta isoforms may substitute for certain RAR gamma functions, and that RAR gamma may elicit its normal effects on vertebral morphogenesis at this developmental stage. Tretinoin 59-61 retinoic acid receptor, gamma Mus musculus 219-228
9174119-4 1997 DDRA, however, showed higher affinity than RA for RXR alpha. Tretinoin 2-4 retinoid X receptor alpha Homo sapiens 50-59
9096882-3 1997 The activity of retinoic acid can be inhibited in cells carrying dominant negative mutations of RAR alpha. Tretinoin 16-29 retinoic acid receptor, alpha Mus musculus 96-105
7931079-9 1994 OAP confers to Oct-2 responsivity to both TPA/Ca2+ and RA, since specific mutations of the AP-1/OAP-binding site significantly reduce the transactivation by Oct-2 in response to TPA and Ca2+ and abolish the inhibition by RA. Tretinoin 55-57 POU class 2 homeobox 2 Homo sapiens 15-20
7931079-9 1994 OAP confers to Oct-2 responsivity to both TPA/Ca2+ and RA, since specific mutations of the AP-1/OAP-binding site significantly reduce the transactivation by Oct-2 in response to TPA and Ca2+ and abolish the inhibition by RA. Tretinoin 55-57 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-95
7931079-9 1994 OAP confers to Oct-2 responsivity to both TPA/Ca2+ and RA, since specific mutations of the AP-1/OAP-binding site significantly reduce the transactivation by Oct-2 in response to TPA and Ca2+ and abolish the inhibition by RA. Tretinoin 55-57 POU class 2 homeobox 2 Homo sapiens 157-162
7931079-9 1994 OAP confers to Oct-2 responsivity to both TPA/Ca2+ and RA, since specific mutations of the AP-1/OAP-binding site significantly reduce the transactivation by Oct-2 in response to TPA and Ca2+ and abolish the inhibition by RA. Tretinoin 221-223 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-95
7931079-9 1994 OAP confers to Oct-2 responsivity to both TPA/Ca2+ and RA, since specific mutations of the AP-1/OAP-binding site significantly reduce the transactivation by Oct-2 in response to TPA and Ca2+ and abolish the inhibition by RA. Tretinoin 221-223 POU class 2 homeobox 2 Homo sapiens 157-162
8071372-8 1994 Mature (spliced) alkaline phosphatase mRNA accumulated in the non-matrix (DNase I/salt eluate, nuclear membrane) and cytoplasmic fractions of retinoic acid-treated cells at more than 100-fold greater levels than in control cells. Tretinoin 142-155 deoxyribonuclease 1 Rattus norvegicus 74-81
9460497-1 1998 A woman with t(15;17) and PML/RAR alpha positive acute promyelocytic leukemia (APL-M3v) achieved a complete remission (CR) with cytogenetic and molecular conversion, after one-month ATRA plus idarubicin treatment. Tretinoin 182-186 PML nuclear body scaffold Homo sapiens 26-39
8092987-5 1994 Squalene, cholesterol and retinoic acid isomers showed no affinity, suggesting that E-FABP displays high specificity for fatty acids. Tretinoin 26-39 fatty acid binding protein 5 Homo sapiens 84-90
9077482-4 1997 In contrast, SR11237 did not synergize with but antagonized an RAR-selective ligand activation of a retinoic acid-responsive element (DR5) via endogenous RAR-RXR. Tretinoin 100-113 retinoic acid receptor, alpha Mus musculus 63-66
9077482-4 1997 In contrast, SR11237 did not synergize with but antagonized an RAR-selective ligand activation of a retinoic acid-responsive element (DR5) via endogenous RAR-RXR. Tretinoin 100-113 retinoic acid receptor, alpha Mus musculus 154-157
9077483-10 1997 Addition of 9-c-RA or t-RA to 1,25(OH)2D3, however, caused a synergistic increase in 24-OHase mRNA. Tretinoin 22-26 cytochrome P450 family 24 subfamily A member 1 Homo sapiens 85-93
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen activator, urokinase receptor Homo sapiens 138-142
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 79-81 plasminogen activator, urokinase receptor Homo sapiens 247-251
9134503-7 1997 Induction of differentiation of mouse embryonal carcinoma F9 cells and human embryonal carcinoma NTERA-2 clone D1 (NT2/D1) cells by all-trans retinoic acid was accompanied by a down-regulation of GCNF/RTR. Tretinoin 142-155 nuclear receptor subfamily 6 group A member 1 Homo sapiens 196-200
9134503-7 1997 Induction of differentiation of mouse embryonal carcinoma F9 cells and human embryonal carcinoma NTERA-2 clone D1 (NT2/D1) cells by all-trans retinoic acid was accompanied by a down-regulation of GCNF/RTR. Tretinoin 142-155 nuclear receptor subfamily 6 group A member 1 Homo sapiens 201-204
9024695-8 1997 The levels of CHO1/MKLP1 increase in the presence of retinoic acid but decrease in the presence of cAMP, consistent with a role for the protein in dendritic differentiation. Tretinoin 53-66 kinesin family member 23 Homo sapiens 14-18
9024695-8 1997 The levels of CHO1/MKLP1 increase in the presence of retinoic acid but decrease in the presence of cAMP, consistent with a role for the protein in dendritic differentiation. Tretinoin 53-66 kinesin family member 23 Homo sapiens 19-24
7528580-1 1994 The mouse cellular retinoic acid binding protein-I (CRABP-I) gene is specifically up-regulated by retinoic acid (RA) in P19 mouse embryonal carcinoma cells, and its expression in animals is spatially and temporally restricted to RA-sensitive tissues during embryonic development. Tretinoin 19-32 cellular retinoic acid binding protein I Mus musculus 52-59
7528580-1 1994 The mouse cellular retinoic acid binding protein-I (CRABP-I) gene is specifically up-regulated by retinoic acid (RA) in P19 mouse embryonal carcinoma cells, and its expression in animals is spatially and temporally restricted to RA-sensitive tissues during embryonic development. Tretinoin 53-55 cellular retinoic acid binding protein I Mus musculus 10-50
7528580-1 1994 The mouse cellular retinoic acid binding protein-I (CRABP-I) gene is specifically up-regulated by retinoic acid (RA) in P19 mouse embryonal carcinoma cells, and its expression in animals is spatially and temporally restricted to RA-sensitive tissues during embryonic development. Tretinoin 113-115 cellular retinoic acid binding protein I Mus musculus 10-50
7528580-1 1994 The mouse cellular retinoic acid binding protein-I (CRABP-I) gene is specifically up-regulated by retinoic acid (RA) in P19 mouse embryonal carcinoma cells, and its expression in animals is spatially and temporally restricted to RA-sensitive tissues during embryonic development. Tretinoin 113-115 cellular retinoic acid binding protein I Mus musculus 52-59
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 192-194 plasminogen activator, urokinase receptor Homo sapiens 247-251
9519778-6 1998 Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs alpha and gamma potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. Tretinoin 192-194 plasminogen activator, urokinase receptor Homo sapiens 247-251
12174299-0 1998 Study on the Mechanism of Fibronectin Adhesion to NIH3T3 cell Stimulated by Retinoic Acid. Tretinoin 76-89 fibronectin 1 Mus musculus 26-37
7521841-1 1994 Induction of differentiation of F9 teratocarcinoma stem cells by retinoic acid and cAMP has been shown to involve the activation of the transcription factor AP-1 (a heterodimer of the proto-oncogene products c-Fos and c-Jun); moreover, stable expression of either Fos or Jun drives F9 cells into differentiation. Tretinoin 65-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-161
7521841-1 1994 Induction of differentiation of F9 teratocarcinoma stem cells by retinoic acid and cAMP has been shown to involve the activation of the transcription factor AP-1 (a heterodimer of the proto-oncogene products c-Fos and c-Jun); moreover, stable expression of either Fos or Jun drives F9 cells into differentiation. Tretinoin 65-78 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 208-213
7521841-1 1994 Induction of differentiation of F9 teratocarcinoma stem cells by retinoic acid and cAMP has been shown to involve the activation of the transcription factor AP-1 (a heterodimer of the proto-oncogene products c-Fos and c-Jun); moreover, stable expression of either Fos or Jun drives F9 cells into differentiation. Tretinoin 65-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 218-223
7521841-1 1994 Induction of differentiation of F9 teratocarcinoma stem cells by retinoic acid and cAMP has been shown to involve the activation of the transcription factor AP-1 (a heterodimer of the proto-oncogene products c-Fos and c-Jun); moreover, stable expression of either Fos or Jun drives F9 cells into differentiation. Tretinoin 65-78 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 210-213
9045990-0 1997 Alterations in Msx 1 and Msx 2 expression correlate with inhibition of outgrowth of chick facial primordia induced by retinoic acid. Tretinoin 118-131 msh homeobox 1 Gallus gallus 15-20
9028332-0 1997 Stat1 is induced and activated by all-trans retinoic acid in acute promyelocytic leukemia cells. Tretinoin 44-57 signal transducer and activator of transcription 1 Homo sapiens 0-5
9028332-1 1997 Treatment of freshly isolated acute promyelocytic leukemia (APL) cells and the myelogenous leukemia cell lines, NB4, HL-60, and U937, with all-trans retinoic acid (ATRA) results in a remarkable elevation in the amounts of Stat1 alpha and Stat2 proteins. Tretinoin 149-162 signal transducer and activator of transcription 1 Homo sapiens 222-227
9028332-1 1997 Treatment of freshly isolated acute promyelocytic leukemia (APL) cells and the myelogenous leukemia cell lines, NB4, HL-60, and U937, with all-trans retinoic acid (ATRA) results in a remarkable elevation in the amounts of Stat1 alpha and Stat2 proteins. Tretinoin 149-162 signal transducer and activator of transcription 2 Homo sapiens 238-243
9028332-1 1997 Treatment of freshly isolated acute promyelocytic leukemia (APL) cells and the myelogenous leukemia cell lines, NB4, HL-60, and U937, with all-trans retinoic acid (ATRA) results in a remarkable elevation in the amounts of Stat1 alpha and Stat2 proteins. Tretinoin 164-168 signal transducer and activator of transcription 1 Homo sapiens 222-227
12174299-4 1998 The cell adhesion to fibronectin was promoted by 20% with 32 &mgr;mol/L RA, but not to polylysine. Tretinoin 76-78 fibronectin 1 Mus musculus 21-32
9028332-1 1997 Treatment of freshly isolated acute promyelocytic leukemia (APL) cells and the myelogenous leukemia cell lines, NB4, HL-60, and U937, with all-trans retinoic acid (ATRA) results in a remarkable elevation in the amounts of Stat1 alpha and Stat2 proteins. Tretinoin 164-168 signal transducer and activator of transcription 2 Homo sapiens 238-243
9028332-4 1997 Transient transfection experiments show that ATRA enhances the transactivating properties of Stat1 alpha observed on an appropriate reporter gene, in the presence of the RAR alpha retinoic acid receptor, but not in the presence of the PML-RAR protein. Tretinoin 45-49 signal transducer and activator of transcription 1 Homo sapiens 93-98
9391084-6 1997 Here, we show that the M6P/IGF-II receptor also binds RA with high affinity at a site that is distinct from those for M6P and IGF-II, as identified by a photoaffinity labeling technique. Tretinoin 54-56 insulin like growth factor 2 Homo sapiens 27-33
9009083-7 1997 NB4 cells did not express EVI-1 under basal conditions, but expressed EVI-1 after ATRA-induced differentiation. Tretinoin 82-86 MDS1 and EVI1 complex locus Homo sapiens 70-75
9009083-8 1997 When NB4 cells were exposed to ATRA and transferred to cultures with N,N"-hexamethylene-bis-acetamide (HMBA), differentiation occurred but EVI-1 RNA was not detected, indicating that EVI-1 expression was not required for terminal, NB4 differentiation. Tretinoin 31-35 MDS1 and EVI1 complex locus Homo sapiens 183-188
9009083-13 1997 In conclusion, this study demonstrates the EVI-1 gene is consistently expressed in APL cells either constitutively or after ATRA treatment. Tretinoin 124-128 MDS1 and EVI1 complex locus Homo sapiens 43-48
9009083-14 1997 ATRA represents the first biologically active agent shown to specifically regulate EVI-1 expression in blood cells. Tretinoin 0-4 MDS1 and EVI1 complex locus Homo sapiens 83-88
7895580-5 1994 These results raise the possibility that the previously reported suppression by RA of PGCL3 invasion and metastasis may be related to suppression of cell adhesion and motility resulting from the decreased expression of the LN-R and AMF-R respectively. Tretinoin 80-82 autocrine motility factor receptor Homo sapiens 223-237
8074702-7 1994 Our data suggest that ARP subfamily member(s) may modulate RA mediated transcription in epidermis. Tretinoin 59-61 arginine-glutamic acid dipeptide repeats Homo sapiens 22-25
9009083-15 1997 In contrast to previous studies in AML and MDS, the pattern of EVI-1 expression suggests it may facilitate rather than inhibit myeloid differentiation during ATRA treatment. Tretinoin 158-162 MDS1 and EVI1 complex locus Homo sapiens 63-68
8074666-0 1994 Synergistic differentiation of U937 cells by all-trans retinoic acid and 1 alpha, 25-dihydroxyvitamin D3 is associated with the expression of retinoid X receptor alpha. Tretinoin 55-68 retinoid X receptor alpha Homo sapiens 142-167
9391084-7 1997 We also show that the binding of RA to the M6P/IGF-II receptor enhances the primary functions of this receptor. Tretinoin 33-35 insulin like growth factor 2 Homo sapiens 47-53
9391084-9 1997 These findings suggest that the M6P/IGF-II receptor mediates a RA response pathway that is important in cell growth regulation. Tretinoin 63-65 insulin like growth factor 2 Homo sapiens 36-42
9391084-10 1997 This discovery of the interaction of RA with the M6P/IGF-II receptor may have important implications for our understanding of the roles of RA and the M6P/IGF-II receptor in development, carcinogenesis, and lysosomal enzyme-related diseases. Tretinoin 37-39 insulin like growth factor 2 Homo sapiens 53-59
9015348-0 1997 Application of photoaffinity labeling with [11,12-3H]all-trans-retinoic acid to characterization of rat liver microsomal UDP-glucuronosyltransferase(s) with activity toward retinoic acid. Tretinoin 53-76 UDP glycosyltransferase 2 family, polypeptide B Rattus norvegicus 121-148
9391084-10 1997 This discovery of the interaction of RA with the M6P/IGF-II receptor may have important implications for our understanding of the roles of RA and the M6P/IGF-II receptor in development, carcinogenesis, and lysosomal enzyme-related diseases. Tretinoin 37-39 insulin like growth factor 2 Homo sapiens 154-160
9015348-0 1997 Application of photoaffinity labeling with [11,12-3H]all-trans-retinoic acid to characterization of rat liver microsomal UDP-glucuronosyltransferase(s) with activity toward retinoic acid. Tretinoin 63-76 UDP glycosyltransferase 2 family, polypeptide B Rattus norvegicus 121-148
7913411-9 1994 Using a novel CaM kinase II inhibitor, KN-62, we demonstrated that retinoic acid stimulated ICAM-1 expression in a CaM kinase II-dependent fashion. Tretinoin 67-80 intercellular adhesion molecule 1 Homo sapiens 92-98
9181129-2 1997 Members of the RAR family (types alpha, beta and gamma and their isoforms alpha 1, alpha 2, beta 1 to beta 4, and gamma 1 and gamma 2) are activated by most physiologically occurring retinoids (all-trans RA, 9-cis RA, 4oxo RA and 3,4 dihyroRA). Tretinoin 204-206 retinoic acid receptor, alpha Mus musculus 15-18
9391084-10 1997 This discovery of the interaction of RA with the M6P/IGF-II receptor may have important implications for our understanding of the roles of RA and the M6P/IGF-II receptor in development, carcinogenesis, and lysosomal enzyme-related diseases. Tretinoin 139-141 insulin like growth factor 2 Homo sapiens 53-59
8981241-7 1997 The DOR-LI pattern of distribution in NG108-15 cells differentiated with RA appeared to be consistent with the DOR-LI detected in the CNS. Tretinoin 73-75 opioid receptor, delta 1 Mus musculus 4-7
9426223-2 1997 RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines. Tretinoin 81-94 ret proto-oncogene Homo sapiens 0-3
8981241-7 1997 The DOR-LI pattern of distribution in NG108-15 cells differentiated with RA appeared to be consistent with the DOR-LI detected in the CNS. Tretinoin 73-75 opioid receptor, delta 1 Mus musculus 111-114
7965021-6 1994 Because TTR has high-affinity binding sites for both thyroxine and retinol binding protein, its potential role as a mediator of combined thyroid hormone and retinoic acid availability in brain is of further interest. Tretinoin 157-170 transthyretin Rattus norvegicus 8-11
9426223-2 1997 RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines. Tretinoin 81-94 ret proto-oncogene Homo sapiens 120-123
8022710-6 1994 Androgen-induced levels of both prostate-specific antigen (PSA) and human glandular kallikrein-1 (hKLK2) mRNAs were significantly repressed by RA in a dose- and time-dependent manner. Tretinoin 143-145 kallikrein related peptidase 2 Homo sapiens 98-103
8954945-3 1996 In retinoic acid-differentiated SH-SY5Y cells and primary cultures of rat cortical neurons, BDNF treatment similarly caused the association of SHP-2 with p85. Tretinoin 3-16 brain-derived neurotrophic factor Rattus norvegicus 92-96
9426223-2 1997 RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines. Tretinoin 96-98 ret proto-oncogene Homo sapiens 0-3
8959344-10 1996 Stimulation of AP1 activity by phorbol ester was suppressed by retinoic acid, and cotransfection with a c-jun expression vector reversed the retinoic acid response. Tretinoin 63-76 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-18
7914163-0 1994 Expression of the LIM class homeobox gene Xlim-1 in pronephros and CNS cell lineages of Xenopus embryos is affected by retinoic acid and exogastrulation. Tretinoin 119-132 LIM homeobox 1 L homeolog Xenopus laevis 42-48
9426223-2 1997 RET expression is enhanced in vitro by several differentiating agents, including retinoic acid (RA), which up-regulates RET expression in neuroblastoma cell lines. Tretinoin 96-98 ret proto-oncogene Homo sapiens 120-123
7914163-6 1994 Enhancement of Xlim-1 expression by retinoic acid (RA) was first detectable in the dorsal mesoderm at initial gastrula. Tretinoin 36-49 LIM homeobox 1 L homeolog Xenopus laevis 15-21
8959344-10 1996 Stimulation of AP1 activity by phorbol ester was suppressed by retinoic acid, and cotransfection with a c-jun expression vector reversed the retinoic acid response. Tretinoin 141-154 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-18
8959344-10 1996 Stimulation of AP1 activity by phorbol ester was suppressed by retinoic acid, and cotransfection with a c-jun expression vector reversed the retinoic acid response. Tretinoin 141-154 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-109
8959344-11 1996 Based on these data, we suggest that suppression of involucrin promoter activity by retinoic acid may be mediated through interaction with the AP1 transcriptional complex. Tretinoin 84-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 143-146
7914163-6 1994 Enhancement of Xlim-1 expression by retinoic acid (RA) was first detectable in the dorsal mesoderm at initial gastrula. Tretinoin 51-53 LIM homeobox 1 L homeolog Xenopus laevis 15-21
7914163-7 1994 During gastrulation and early neurulation, RA strongly enhanced Xlim-1 expression in all three lineages and also expanded its expressing domains; this overexpression correlated well with RA phenotypes such as enlarged pronephros and hindbrain-like structure. Tretinoin 43-45 LIM homeobox 1 L homeolog Xenopus laevis 64-70
9426223-5 1997 Finally, our functional analysis of a candidate RA response element present in the RET promoter provides new hints for the understanding of the interaction between nuclear receptors and their specific recognition sites. Tretinoin 48-50 ret proto-oncogene Homo sapiens 83-86
9394035-17 1997 Erythrocyte ALDH-1-effected oxidation of other aldehydes to their corresponding acids, e.g. retinaldehyde to retinoic acid, may also be of pharmacological and/or physiological significance since a wide variety of aldehydes are known to be substrates for ALDH-1. Tretinoin 109-122 aldehyde dehydrogenase 1 family member A1 Homo sapiens 12-18
8203489-6 1994 Although RA increased VDR levels, RA did not potentiate the effect of 1,25(OH)2D on ALP activity. Tretinoin 9-11 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 22-25
9394035-17 1997 Erythrocyte ALDH-1-effected oxidation of other aldehydes to their corresponding acids, e.g. retinaldehyde to retinoic acid, may also be of pharmacological and/or physiological significance since a wide variety of aldehydes are known to be substrates for ALDH-1. Tretinoin 109-122 aldehyde dehydrogenase 1 family member A1 Homo sapiens 254-260
9389530-4 1997 IGF-1 also decreased PRL and GH-mRNA response to T3, retinoic acid, and Fk in GH3 cells. Tretinoin 53-66 insulin-like growth factor 1 Rattus norvegicus 0-5
8163572-3 1994 Previous studies of the mechanism of action of retinoids in non-chondrogenic cells have concluded that retinoic acid is a negative regulator of AP-1 responsive metalloprotease genes. Tretinoin 103-116 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-148
8163572-4 1994 We show that inhibition of expression of the cartilage phenotype by retinoic acid in epiphyseal chondrocytes is associated with positive regulation of AP-1 responsive metalloprotease genes, as well as induction of gene expression for the two components of the transcription factor AP-1, c-fos and c-jun. Tretinoin 68-81 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 151-155
8163572-4 1994 We show that inhibition of expression of the cartilage phenotype by retinoic acid in epiphyseal chondrocytes is associated with positive regulation of AP-1 responsive metalloprotease genes, as well as induction of gene expression for the two components of the transcription factor AP-1, c-fos and c-jun. Tretinoin 68-81 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 281-285
8163572-4 1994 We show that inhibition of expression of the cartilage phenotype by retinoic acid in epiphyseal chondrocytes is associated with positive regulation of AP-1 responsive metalloprotease genes, as well as induction of gene expression for the two components of the transcription factor AP-1, c-fos and c-jun. Tretinoin 68-81 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 287-292
8163572-4 1994 We show that inhibition of expression of the cartilage phenotype by retinoic acid in epiphyseal chondrocytes is associated with positive regulation of AP-1 responsive metalloprotease genes, as well as induction of gene expression for the two components of the transcription factor AP-1, c-fos and c-jun. Tretinoin 68-81 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 297-302
9494568-0 1997 Effects of tamoxifen and retinoic acid on cell growth and c-myc gene expression in human breast and cervical cancer cells. Tretinoin 25-38 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63
8163572-6 1994 The present investigation demonstrates that regulation of AP-1 responsive genes by retinoic acid can be either positive or negative, depending on the target cell type, and illuminates new mechanisms by which retinoic acid and other retinoids may exert control during development and growth of the limb. Tretinoin 83-96 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-62
8163572-6 1994 The present investigation demonstrates that regulation of AP-1 responsive genes by retinoic acid can be either positive or negative, depending on the target cell type, and illuminates new mechanisms by which retinoic acid and other retinoids may exert control during development and growth of the limb. Tretinoin 208-221 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-62
8058068-6 1994 The glucocorticoid accessory activity of the AF1 element maps to the same 12-base pair sequence (TGACCTTTGGCC) involved in the response of the PEPCK gene to retinoic acid. Tretinoin 157-170 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 143-148
9326242-0 1997 Retinoic acid induces aggregation of the acute promyelocytic leukemia cell line NB-4 by utilization of LFA-1 and ICAM-2. Tretinoin 0-13 intercellular adhesion molecule 2 Homo sapiens 113-119
8149483-4 1994 TPA treatment resulted in an approximately 67% decrease in the specific binding of [3H]RA to RAR. Tretinoin 87-89 retinoic acid receptor, alpha Mus musculus 93-96
8149483-5 1994 In a more detailed time course, application of 20 nmol of TPA to mouse skin led to 20, 36, 92 and 0% decrease in the binding of [3H]RA to mouse epidermal RAR at 2, 4, 12 and 72 h after treatment respectively. Tretinoin 132-134 retinoic acid receptor, alpha Mus musculus 154-157
8149483-6 1994 Okadaic acid, an inhibitor of protein phosphatases 1 and 2A but a mouse skin tumor promoter, also inhibited the binding of RA to RAR. Tretinoin 123-125 retinoic acid receptor, alpha Mus musculus 129-132
9364928-3 1997 The neuroendocrine convertase PC2 and 7B2, its specific binding protein, are co-induced during neuronal differentiation of P19 cells with retinoic acid, whereas the other convertases are not or follow different patterns of temporal expression. Tretinoin 138-151 proprotein convertase subtilisin/kexin type 2 Homo sapiens 30-41
7512261-2 1994 Transcription of the oncodevelopmental protein, alpha-fetoprotein (AFP), is stimulated by retinoic acid (RA) in neoplastic cells. Tretinoin 90-103 alpha fetoprotein Gallus gallus 48-65
7512261-2 1994 Transcription of the oncodevelopmental protein, alpha-fetoprotein (AFP), is stimulated by retinoic acid (RA) in neoplastic cells. Tretinoin 90-103 alpha fetoprotein Gallus gallus 67-70
9414661-0 1997 All-trans-retinoic acid-dependent inhibition of E-cadherin-based cell adhesion with concomitant dephosphorylation of beta-catenin in metastatic human renal carcinoma cells. Tretinoin 0-23 catenin beta 1 Homo sapiens 117-129
7512261-2 1994 Transcription of the oncodevelopmental protein, alpha-fetoprotein (AFP), is stimulated by retinoic acid (RA) in neoplastic cells. Tretinoin 105-107 alpha fetoprotein Gallus gallus 48-65
7512261-2 1994 Transcription of the oncodevelopmental protein, alpha-fetoprotein (AFP), is stimulated by retinoic acid (RA) in neoplastic cells. Tretinoin 105-107 alpha fetoprotein Gallus gallus 67-70
7512261-6 1994 AFP-RXRE conferred a marked RA responsiveness in the cotransfection with retinoid X receptor (RXR), but not with retinoic acid receptors (RARs). Tretinoin 28-30 alpha fetoprotein Gallus gallus 0-3
9414661-6 1997 E-Cadherin and beta-catenin were each localized mainly at the cell-cell adherent junctions of colonizing cell populations that had been treated with ATRA. Tretinoin 149-153 catenin beta 1 Homo sapiens 15-27
9414661-9 1997 ATRA-induced clustering of MM-3 cells may be linked to the state of tyrosine phosphorylation of beta-catenin. Tretinoin 0-4 catenin beta 1 Homo sapiens 96-108
8297336-0 1994 Effect of retinoic acid on mucin gene expression in rat airways in vitro. Tretinoin 10-23 solute carrier family 13 member 2 Rattus norvegicus 27-32
8297336-6 1994 When retinoic acid was added at 96 h to the latter cultures, the mucin mRNA was prominent again after additional incubation for 24 and 48 h. Northern-blot analyses of tracheal RNA showed a diffuse band at approx. Tretinoin 5-18 solute carrier family 13 member 2 Rattus norvegicus 65-70
9535176-2 1997 The PML-RAR alpha fusion gene plays an important role in leukemogenesis through antagonizing retinoic acid signalling and the regulatory pathways mediated by PML. Tretinoin 93-106 PML nuclear body scaffold Homo sapiens 4-7
8280758-0 1994 Retinoic acid inhibition of thyroxine binding to human transthyretin. Tretinoin 0-13 transthyretin Homo sapiens 55-68
8280758-4 1994 In the present studies, retinoic acid was examined for its ability to displace thyroxine from binding sites on human transthyretin (TTR). Tretinoin 24-37 transthyretin Homo sapiens 117-130
8280758-4 1994 In the present studies, retinoic acid was examined for its ability to displace thyroxine from binding sites on human transthyretin (TTR). Tretinoin 24-37 transthyretin Homo sapiens 132-135
9535176-2 1997 The PML-RAR alpha fusion gene plays an important role in leukemogenesis through antagonizing retinoic acid signalling and the regulatory pathways mediated by PML. Tretinoin 93-106 retinoic acid receptor alpha Homo sapiens 8-11
9535176-4 1997 The therapeutic effect of ATRA in APL has been associated with the direct modulation of PML-RAR alpha, the restoration of the differentiation pathways regulated by wild-type RAR/retinoid X receptor heterodimer and PML. Tretinoin 26-30 PML nuclear body scaffold Homo sapiens 88-91
8032159-2 1994 However, mammalian ADH has also been shown to function in vitro as a retinol dehydrogenase in the conversion of retinol (vitamin A alcohol) to retinoic acid, a hormone which regulates gene expression at the transcriptional level. Tretinoin 143-156 aldo-keto reductase family 1 member A1 Homo sapiens 19-22
9535176-4 1997 The therapeutic effect of ATRA in APL has been associated with the direct modulation of PML-RAR alpha, the restoration of the differentiation pathways regulated by wild-type RAR/retinoid X receptor heterodimer and PML. Tretinoin 26-30 retinoic acid receptor alpha Homo sapiens 92-95
8032159-6 1994 Human ADH exists as a family of isozymes encoded by seven genes which are differentially expressed in adult and fetal mammalian tissues, being found preferentially in the epithelial cells which are known to synthesize and respond to retinoic acid. Tretinoin 233-246 aldo-keto reductase family 1 member A1 Homo sapiens 6-9
9535176-4 1997 The therapeutic effect of ATRA in APL has been associated with the direct modulation of PML-RAR alpha, the restoration of the differentiation pathways regulated by wild-type RAR/retinoid X receptor heterodimer and PML. Tretinoin 26-30 retinoic acid receptor alpha Homo sapiens 174-177
8269997-0 1994 The expression of retinoid X receptor genes is regulated by all-trans- and 9-cis-retinoic acid in F9 teratocarcinoma cells. Tretinoin 81-94 retinoid X receptor alpha Homo sapiens 18-37
9535176-4 1997 The therapeutic effect of ATRA in APL has been associated with the direct modulation of PML-RAR alpha, the restoration of the differentiation pathways regulated by wild-type RAR/retinoid X receptor heterodimer and PML. Tretinoin 26-30 PML nuclear body scaffold Homo sapiens 178-217
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 37-50 retinoid X receptor alpha Homo sapiens 111-130
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 37-50 retinoid X receptor alpha Homo sapiens 132-135
9295294-5 1997 mCAR1, like hCAR, binds as a heterodimer with the retinoid X receptor to the retinoic acid response element from the promoter of the retinoic acid receptor beta2 isoform. Tretinoin 77-90 carbonic anhydrase 1 Mus musculus 0-5
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 52-54 retinoid X receptor alpha Homo sapiens 111-130
8269997-1 1994 Two classes of nuclear receptors for retinoic acid (RA) have been identified--retinoic acid receptor (RAR) and retinoid x receptor (RXR). Tretinoin 52-54 retinoid X receptor alpha Homo sapiens 132-135
9281352-10 1997 Conversely, several combinations of RAR/RXR closely mimicked the differentiation effects observed with all-trans retinoic acid. Tretinoin 113-126 retinoic acid receptor alpha Homo sapiens 36-39
7529599-0 1994 Regulation of vitronectin receptor expression by retinoic acid on human melanoma cells. Tretinoin 49-62 vitronectin Homo sapiens 14-25
7529599-6 1994 Although the mechanism by which retinoic acid regulates the expression of vitronectin receptor in MeWo cells needs further examination, this system may represent a good model for understanding the role of this receptor in melanoma progression, as well the molecular basis for retinoic acid therapy in these tumors. Tretinoin 32-45 vitronectin Homo sapiens 74-85
7529599-6 1994 Although the mechanism by which retinoic acid regulates the expression of vitronectin receptor in MeWo cells needs further examination, this system may represent a good model for understanding the role of this receptor in melanoma progression, as well the molecular basis for retinoic acid therapy in these tumors. Tretinoin 276-289 vitronectin Homo sapiens 74-85
7808033-1 1994 Retinoic acids exert a wide range of biological activities following binding to the cognate nuclear receptors, which has several members (RAR-alpha, beta, gamma and RXR-alpha, beta, gamma). Tretinoin 0-14 retinoid X receptor alpha Homo sapiens 165-174
7815843-4 1994 In vitro treatment with ATRA consistently increased the expression of CD15, CD11b, and CD45R0 on leukemic promyelocytes; these changes were paralleled by a decrease of CD45RA display. Tretinoin 24-28 integrin subunit alpha M Homo sapiens 76-81
9242531-0 1997 Molecular remission in PML/RAR alpha-positive acute promyelocytic leukemia by combined all-trans retinoic acid and idarubicin (AIDA) therapy. Tretinoin 97-110 retinoic acid receptor alpha Homo sapiens 27-36
7815843-4 1994 In vitro treatment with ATRA consistently increased the expression of CD15, CD11b, and CD45R0 on leukemic promyelocytes; these changes were paralleled by a decrease of CD45RA display. Tretinoin 24-28 protein tyrosine phosphatase receptor type C Homo sapiens 87-91
9258346-0 1997 Retinoic acid regulates the expression of insulin-like growth factors I and II in osteoblasts. Tretinoin 0-13 insulin-like growth factor 1 Rattus norvegicus 42-78
8260698-2 1993 A stereoisomer of retinoic acid, 9-cis-retinoic acid, is a high-affinity ligand for RXR and binds efficiently to RAR. Tretinoin 18-31 retinoid X receptor alpha Homo sapiens 84-87
8260698-3 1993 In contrast, all-trans-retinoic acid interacts 40-fold less efficiently with RXR as compared with RAR. Tretinoin 13-36 retinoid X receptor alpha Homo sapiens 77-80
9258346-4 1997 Retinoic acid caused a transient increase in IGF I and IGF II mRNA levels after 6 h, but after 24 and 48 h of treatment a dose-dependent decrease was observed. Tretinoin 0-13 insulin-like growth factor 1 Rattus norvegicus 45-50
7503983-0 1993 Retinoic acid posttranscriptionally up-regulates proteolipid protein gene expression in C6 glioma cells. Tretinoin 0-13 proteolipid protein 1 Homo sapiens 49-68
9258346-6 1997 Retinoic acid treatment for 48 h decreased IGF I polypeptide levels in the culture medium. Tretinoin 0-13 insulin-like growth factor 1 Rattus norvegicus 43-48
7503983-3 1993 Retinoic acid (RA), but not dexamethasone, estradiol, insulin, growth hormone, or vitamin D3, had a drastic effect, increasing 10-20-fold the level of PLP mRNA. Tretinoin 0-13 proteolipid protein 1 Homo sapiens 151-154
7503983-3 1993 Retinoic acid (RA), but not dexamethasone, estradiol, insulin, growth hormone, or vitamin D3, had a drastic effect, increasing 10-20-fold the level of PLP mRNA. Tretinoin 15-17 proteolipid protein 1 Homo sapiens 151-154
7503983-7 1993 In contrast, we found that retinoic acid augmented PLP mRNA stability, causing a substantial increase in its half-life. Tretinoin 27-40 proteolipid protein 1 Homo sapiens 51-54
9258346-8 1997 The decay of IGF I and II mRNA in transcriptionally arrested Ob cells was similar in control and retinoic acid-treated cells. Tretinoin 97-110 insulin-like growth factor 1 Rattus norvegicus 13-25
9258346-9 1997 After 2 h, retinoic acid increased the rates of IGF I and II transcription, as determined by a nuclear run-on assay and heterogeneous nuclear RNA levels, but after 24 h retinoic acid was inhibitory. Tretinoin 11-24 insulin-like growth factor 1 Rattus norvegicus 48-53
9258346-11 1997 In conclusion, following a small transient increase, retinoic acid causes a pronounced decrease in IGF I and IGF II mRNA expression in Ob cells. Tretinoin 53-66 insulin-like growth factor 1 Rattus norvegicus 99-104
9258346-12 1997 However, treatment with retinoic acid causes a decrease in IGF I and an increase in IGF II polypeptide levels. Tretinoin 24-37 insulin-like growth factor 1 Rattus norvegicus 59-64
8226882-6 1993 Retinoic acid (RA) had an effect similar to T3 reducing basal CAT activity and the response to TPA and forskolin by 40-50% in cells co-transfected with the c-fos promoter and an expression vector for the RA receptor. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 156-161
8226882-6 1993 Retinoic acid (RA) had an effect similar to T3 reducing basal CAT activity and the response to TPA and forskolin by 40-50% in cells co-transfected with the c-fos promoter and an expression vector for the RA receptor. Tretinoin 15-17 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 156-161
9258350-3 1997 They were also potent and effective antagonists of retinoic acid (RA) induced gene transcription at RAR alpha. Tretinoin 51-64 retinoic acid receptor alpha Homo sapiens 100-109
9258350-3 1997 They were also potent and effective antagonists of retinoic acid (RA) induced gene transcription at RAR alpha. Tretinoin 66-68 retinoic acid receptor alpha Homo sapiens 100-109
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 40-42 PML nuclear body scaffold Homo sapiens 194-197
8238530-3 1993 Because pulmonary retinoid stores decline just before the fourth postnatal day, we also hypothesized that this decline could be accompanied by the utilization of retinoic acid, one of the most biologically active retinoids, in a regulatory process that increases elastin synthesis. Tretinoin 162-175 elastin Rattus norvegicus 263-270
8238530-4 1993 If these hypotheses are correct, then retinoic acid should increase elastin synthesis by pulmonary cells. Tretinoin 38-51 elastin Rattus norvegicus 68-75
9234742-4 1997 These data demonstrate that PML-RAR alpha and PLZF-RAR alpha have similar (inhibitory) effects on RA-independent differentiation and opposite (stimulatory or inhibitory) effects on RA-dependent differentiation and that they behave in vivo as RA-dependent enhancers or inhibitors of RA-responsive genes, respectively. Tretinoin 32-34 PML nuclear body scaffold Homo sapiens 28-31
8238530-6 1993 Retinoic acid produced a two- to threefold increase in the steady-state level of elastin mRNA, in soluble elastin, and in insoluble elastin. Tretinoin 0-13 elastin Rattus norvegicus 81-88
8238530-6 1993 Retinoic acid produced a two- to threefold increase in the steady-state level of elastin mRNA, in soluble elastin, and in insoluble elastin. Tretinoin 0-13 elastin Rattus norvegicus 106-113
9234742-5 1997 Their different activities on the RA signalling pathway might underlie the different responses of PML-RAR alpha and PLZF-RAR alpha APLs to RA treatment. Tretinoin 34-36 PML nuclear body scaffold Homo sapiens 98-101
8238530-6 1993 Retinoic acid produced a two- to threefold increase in the steady-state level of elastin mRNA, in soluble elastin, and in insoluble elastin. Tretinoin 0-13 elastin Rattus norvegicus 106-113
8238530-7 1993 The transcriptional initiation rate of the elastin gene was 1.8-fold higher in nuclei that were isolated from retinoic acid-treated cells than in nuclei that were isolated from control cells. Tretinoin 110-123 elastin Rattus norvegicus 43-50
9234742-5 1997 Their different activities on the RA signalling pathway might underlie the different responses of PML-RAR alpha and PLZF-RAR alpha APLs to RA treatment. Tretinoin 34-36 retinoic acid receptor alpha Homo sapiens 102-111
8238530-10 1993 These findings suggest that retinoic acid is a potential regulator of elastin synthesis in developing pulmonary alveoli. Tretinoin 28-41 elastin Rattus norvegicus 70-77
9234742-5 1997 Their different activities on the RA signalling pathway might underlie the different responses of PML-RAR alpha and PLZF-RAR alpha APLs to RA treatment. Tretinoin 34-36 retinoic acid receptor alpha Homo sapiens 121-130
8404668-4 1993 We report here that retinoic acid (RA) reduces the level of Myf5 message in both mouse C2 and rat L6 cell lines, probably at the transcriptional level, because Myf5 mRNA stability is not affected by RA. Tretinoin 20-33 myogenic factor 5 Mus musculus 60-64
9234742-5 1997 Their different activities on the RA signalling pathway might underlie the different responses of PML-RAR alpha and PLZF-RAR alpha APLs to RA treatment. Tretinoin 102-104 PML nuclear body scaffold Homo sapiens 98-101
8404668-4 1993 We report here that retinoic acid (RA) reduces the level of Myf5 message in both mouse C2 and rat L6 cell lines, probably at the transcriptional level, because Myf5 mRNA stability is not affected by RA. Tretinoin 35-37 myogenic factor 5 Mus musculus 60-64
9234742-7 1997 Deletion of the PLZF POZ domain partially abrogated the inhibitory effect of PLZF-RAR alpha on RA-induced differentiation and on RA-mediated type II TGase up-regulation, suggesting that POZ-mediated protein interactions might be responsible for the inhibitory transcriptional activities of PLZF-RAR alpha. Tretinoin 82-84 retinoic acid receptor alpha Homo sapiens 295-304
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 145-158 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289
15625843-1 1997 OBJECTIVE: To analyze the conversion of RARalpha/PML gene in acute promyelocytic leukemia (APL) patients before and after treatment with all-trans retinoic acid (ATRA) followed by intensive consolidation chemotherapy (ICC) and allogeneic bone marrow transplantation (allo-BMT). Tretinoin 137-160 retinoic acid receptor alpha Homo sapiens 40-48
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 175-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289
8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 198-200 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289
8415704-6 1993 In view of the association between AP-1 activity and hemopoietic differentiation, we suggest that these properties of PML-RAR alpha could contribute to the leukemic phenotype and its response to RA. Tretinoin 122-124 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-39
8287793-2 1993 Two classes of cellular proteins, which specifically bind all-trans retinoic acid, are thought to mediate its action: the nuclear retinoic acid receptors (RAR alpha, beta, gamma), and the cytoplasmic binding proteins known as cellular retinoic acid-binding proteins I and II (CRABP I and II). Tretinoin 68-81 retinoic acid receptor, alpha Mus musculus 155-164
8287793-2 1993 Two classes of cellular proteins, which specifically bind all-trans retinoic acid, are thought to mediate its action: the nuclear retinoic acid receptors (RAR alpha, beta, gamma), and the cytoplasmic binding proteins known as cellular retinoic acid-binding proteins I and II (CRABP I and II). Tretinoin 68-81 cellular retinoic acid binding protein I Mus musculus 276-290
8405666-0 1993 Midkine, a retinoic acid-inducible growth/differentiation factor: immunochemical evidence for the function and distribution. Tretinoin 11-24 midkine Rattus norvegicus 0-7
15625843-1 1997 OBJECTIVE: To analyze the conversion of RARalpha/PML gene in acute promyelocytic leukemia (APL) patients before and after treatment with all-trans retinoic acid (ATRA) followed by intensive consolidation chemotherapy (ICC) and allogeneic bone marrow transplantation (allo-BMT). Tretinoin 137-160 PML nuclear body scaffold Homo sapiens 49-52
15625843-1 1997 OBJECTIVE: To analyze the conversion of RARalpha/PML gene in acute promyelocytic leukemia (APL) patients before and after treatment with all-trans retinoic acid (ATRA) followed by intensive consolidation chemotherapy (ICC) and allogeneic bone marrow transplantation (allo-BMT). Tretinoin 162-166 retinoic acid receptor alpha Homo sapiens 40-48
15625843-1 1997 OBJECTIVE: To analyze the conversion of RARalpha/PML gene in acute promyelocytic leukemia (APL) patients before and after treatment with all-trans retinoic acid (ATRA) followed by intensive consolidation chemotherapy (ICC) and allogeneic bone marrow transplantation (allo-BMT). Tretinoin 162-166 PML nuclear body scaffold Homo sapiens 49-52
8179844-7 1993 In vitro, embryonic sympathetic neurons require exposure to environmental cues, such as basic FGF and retinoic acid to acquire neurotrophin-responsiveness; in contrast, embryonic sensory neurons acquire neurotrophin-responsiveness on schedule in the absence of these molecules. Tretinoin 102-115 brain derived neurotrophic factor Homo sapiens 127-139
15625843-3 1997 RESULTS: RARalpha/PML fusion gene was positive in 75% of the patients after achieving complete remission with ATRA, and turned negative in 83% of the patients after ICC. Tretinoin 110-114 retinoic acid receptor alpha Homo sapiens 9-17
15625843-3 1997 RESULTS: RARalpha/PML fusion gene was positive in 75% of the patients after achieving complete remission with ATRA, and turned negative in 83% of the patients after ICC. Tretinoin 110-114 PML nuclear body scaffold Homo sapiens 18-21
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, metabotropic 8 Mus musculus 308-314
8167569-6 1993 RXR homodimers recognize a subset of retinoic acid responsive elements (RARE). Tretinoin 37-50 retinoid X receptor alpha Homo sapiens 0-3
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, metabotropic 1 Mus musculus 353-359
9263586-1 1997 P19 embryonal carcinoma cells differentiate into neurons, astrocytes, and fibroblast-like cells following induction with retinoic acid. Tretinoin 121-134 interleukin 23 subunit alpha Homo sapiens 0-3
7915634-6 1993 RA is known to induce Xlim-1 in Xenopus embryos and to lead to anterior malformations. Tretinoin 0-2 LIM homeobox 1 L homeolog Xenopus laevis 22-28
8394351-8 1993 However, a VDR-RAR heterodimer binds to the osteocalcin response element and mediates activation by all-trans-retinoic acid. Tretinoin 100-123 vitamin D receptor Homo sapiens 11-14
9242425-4 1997 We demonstrate here that the expression of Indian hedgehog mRNA and protein is upregulated dramatically as F9 cells differentiate in response to retinoic acid, into either parietal endoderm or embryoid bodies, containing an outer visceral endoderm layer. Tretinoin 145-158 hedgehog Drosophila melanogaster 50-58
9224765-7 1997 Following retinoic acid-induced P19 differentiation predominantly to the smooth muscle cell lineage, high expression of alpha7 was detected along with partial dependence on alpha7 for binding to laminin. Tretinoin 10-23 integrin alpha 7 Mus musculus 120-126
8336949-5 1993 The increase in PMA-dependent c-fos expression required pretreatment of cells with RA for at least 2-4 h and was achieved at doses as low as 10(-10) M. Nuclear run-on experiments and transient transfection assays using a chimeric reporter gene construct with sequences from the c-fos promoter indicated that RA did not affect PMA-dependent c-fos transcription. Tretinoin 83-85 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35
8336949-5 1993 The increase in PMA-dependent c-fos expression required pretreatment of cells with RA for at least 2-4 h and was achieved at doses as low as 10(-10) M. Nuclear run-on experiments and transient transfection assays using a chimeric reporter gene construct with sequences from the c-fos promoter indicated that RA did not affect PMA-dependent c-fos transcription. Tretinoin 83-85 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 278-283
8336949-5 1993 The increase in PMA-dependent c-fos expression required pretreatment of cells with RA for at least 2-4 h and was achieved at doses as low as 10(-10) M. Nuclear run-on experiments and transient transfection assays using a chimeric reporter gene construct with sequences from the c-fos promoter indicated that RA did not affect PMA-dependent c-fos transcription. Tretinoin 83-85 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 278-283
8336949-5 1993 The increase in PMA-dependent c-fos expression required pretreatment of cells with RA for at least 2-4 h and was achieved at doses as low as 10(-10) M. Nuclear run-on experiments and transient transfection assays using a chimeric reporter gene construct with sequences from the c-fos promoter indicated that RA did not affect PMA-dependent c-fos transcription. Tretinoin 308-310 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35
9262057-10 1997 On exposure to retinoic acid, an immediate and prolonged upregulation of RAR-alpha mRNA expression, lasting for more than 12 hours, occurred in all sensitive cell lines, but only minimal or transient induction was seen in resistant cells. Tretinoin 15-28 retinoic acid receptor alpha Homo sapiens 73-82
7686749-0 1993 Retinoic acid and estrogen modulation of insulin-like growth factor binding protein-4 gene expression and the estrogen receptor status of human breast carcinoma cells. Tretinoin 0-13 insulin like growth factor binding protein 4 Homo sapiens 41-85
8251723-5 1993 6 cases (RAEB 4, RA 1, RAS 1) were treated with all-trans retinoic acid used as an inducer of differentiation, 2 of them were effective. Tretinoin 58-71 RA1 Homo sapiens 17-21
7684042-15 1993 RA enhanced IGFBP-6 gene expression by threefold in MDA-MB-231 cells, whereas IGF-1 had no effect on IGFBP-6 gene expression in either cell line. Tretinoin 0-2 insulin like growth factor binding protein 6 Homo sapiens 12-19
9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 40-53 retinoic acid receptor alpha Homo sapiens 146-155
9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 159-173 retinoic acid receptor alpha Homo sapiens 146-155
9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 279-293 retinoic acid receptor alpha Homo sapiens 146-155
8104776-13 1993 When we proximalized the positional memory of a distal blastema with retinoic acid, we find that the early expression level of Hox-4.5 is also proximalized. Tretinoin 69-82 homeobox D8 Homo sapiens 127-134
9223123-0 1997 P53 synthesis and phosphorylation in the aging diet-restricted rat following retinoic acid administration. Tretinoin 77-90 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 0-3
8097725-3 1993 We have investigated the role of retinoic acid receptor alpha (RAR alpha) in retinoic acid-dependent induction of HOX-2 gene expression in embryocarcinoma (EC) cells by using the P19 RAC65 EC cell line, which is retinoic acid-resistant due to the expression of a dominant negative RAR alpha. Tretinoin 33-46 retinoic acid receptor, alpha Mus musculus 63-72
8097725-3 1993 We have investigated the role of retinoic acid receptor alpha (RAR alpha) in retinoic acid-dependent induction of HOX-2 gene expression in embryocarcinoma (EC) cells by using the P19 RAC65 EC cell line, which is retinoic acid-resistant due to the expression of a dominant negative RAR alpha. Tretinoin 77-90 retinoic acid receptor, alpha Mus musculus 33-61
8097725-3 1993 We have investigated the role of retinoic acid receptor alpha (RAR alpha) in retinoic acid-dependent induction of HOX-2 gene expression in embryocarcinoma (EC) cells by using the P19 RAC65 EC cell line, which is retinoic acid-resistant due to the expression of a dominant negative RAR alpha. Tretinoin 77-90 retinoic acid receptor, alpha Mus musculus 63-72
8097725-5 1993 This shows that RAR alpha is involved in HOX gene induction by retinoic acid. Tretinoin 63-76 retinoic acid receptor, alpha Mus musculus 16-25
9223123-4 1997 After 36 h of RA dosing, the PAGE patterns of p53 synthesis and phosphorylation in Y/AL and O/DR rats were very similar. Tretinoin 14-16 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 46-49
9223123-10 1997 After RA dosing, cyclin protein inhibitors (p16, p21, p27) revealed robust labeling with their respective antibodies in Y/AL and O/DR rats as analyzed by Western blotting. Tretinoin 6-8 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 54-57
15624327-7 1997 The differences between PML-RARalpha and PLZF-RARalpha may in part explain the apparent resistance of APL with t(11;17) to differentiating effect of all-trans retinoic acid (ATRA). Tretinoin 174-178 retinoic acid receptor alpha Homo sapiens 28-36
9177240-7 1997 Retinoic acid treatment of HL60 promyelocytic leukemia cells for 24 hr induced C/EBPepsilon mRNA levels by 4-fold, while prolonged treatment gradually reduced mRNA expression to pretreatment levels. Tretinoin 0-13 CCAAT enhancer binding protein epsilon Homo sapiens 79-91
8384232-3 1993 We have previously demonstrated a rapid and pronounced increase in steady-state cellular RA-binding protein II (CRABP-II)mRNA levels after topical RA treatment. Tretinoin 89-91 cellular retinoic acid binding protein 2 Homo sapiens 112-120
8384232-5 1993 The induction of CRABP-II mRNA in response to 0.1% RA cream was maximal by 16 h (elevenfold relative to untreated skin), and persisted at near-maximal levels (eight-fold) for up to 4 d. RA was potent in eliciting this response, as approximately half-maximal stimulation was observed after 16 h of treatment with 0.001% RA. Tretinoin 51-53 cellular retinoic acid binding protein 2 Homo sapiens 17-25
8384232-5 1993 The induction of CRABP-II mRNA in response to 0.1% RA cream was maximal by 16 h (elevenfold relative to untreated skin), and persisted at near-maximal levels (eight-fold) for up to 4 d. RA was potent in eliciting this response, as approximately half-maximal stimulation was observed after 16 h of treatment with 0.001% RA. Tretinoin 51-53 cellular retinoic acid binding protein 2 Homo sapiens 17-25
8944070-7 1996 Treatment of rat mammary tumor cell lines with retinoic acid increased MK expression, decreased proliferation, and markedly reduced colony-forming efficiency in agar. Tretinoin 47-60 midkine Rattus norvegicus 71-73
9268491-6 1997 However, when these cells were induced by retinoic acid to differentiate, Ca2+-dependent PC-PLC and gamma-GT activities decreased significantly, together with alpha-fetoprotein expression. Tretinoin 42-55 gamma-glutamyltransferase 1 Rattus norvegicus 100-108
8810324-0 1996 Identification of a novel retinoic acid response element in the promoter region of the retinol-binding protein gene. Tretinoin 26-39 retinol binding protein 4 Homo sapiens 87-110
8810324-9 1996 Thus, the retinoic acid induction of the RBP gene is mediated by a novel and complex responsive unit formed by two distinct elements located in a specific sequence context and the interplay of the retinoid receptors with Sp1 is required for induction. Tretinoin 10-23 retinol binding protein 4 Homo sapiens 41-44
8449605-8 1993 In contrast, fos-specific mRNA and protein in aberrant crypt foci significantly increased when 150 mg/kg all-trans retinoic acid was added to the diet. Tretinoin 115-128 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-16
8449605-9 1993 The most important findings of this investigation are that intervention with all-trans retinoic acid in the pre-malignant stage of colon carcinogenesis is effective in decreasing the number and growth of aberrant crypt foci and altering the expression of the c-myc and c-fos genes. Tretinoin 87-100 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 269-274
9368678-0 1997 Insulin-like growth factor binding protein-3 and -5 are regulated by transforming growth factor-beta and retinoic acid in the human prostate adenocarcinoma cell line PC-3. Tretinoin 105-118 insulin like growth factor binding protein 3 Homo sapiens 0-51
8382210-0 1993 Retinoic acid induces adult muscle cell differentiation mediated by the retinoic acid receptor-alpha. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 72-100
8798739-7 1996 A probable in vivo ligand for BLBP is docosahexaenoic acid (DHA), since its binding affinity (Kd approximately 10 nM) is the highest yet reported for an FABP/ligand interaction, exceeding even the affinity of retinoic acid for its binding proteins. Tretinoin 209-222 fatty acid binding protein 7 Homo sapiens 30-34
8841418-4 1996 In fibroblasts, IGFBP-6 levels are regulated by retinoic acid, and we postulated that retinoic acid may regulate IGF II in bone by altering IGFBP-6 synthesis. Tretinoin 86-99 insulin-like growth factor 2 Rattus norvegicus 113-119
8823154-0 1996 Involvement of alcohol dehydrogenase, short-chain dehydrogenase/reductase, aldehyde dehydrogenase, and cytochrome P450 in the control of retinoid signaling by activation of retinoic acid synthesis. Tretinoin 173-186 aldo-keto reductase family 1 member A1 Homo sapiens 15-36
8823154-5 1996 Members of the alcohol dehydrogenase and short-chain dehydrogenase/reductase enzyme families catalyze the reversible interconversion of retinol and retinal, the rate-limiting step, whereas members of the aldehyde dehydrogenase and cytochrome P450 enzyme families catalyze the irreversible oxidation of retinal to retinoic acid. Tretinoin 313-326 aldo-keto reductase family 1 member A1 Homo sapiens 15-36
8439447-5 1993 13-CRA, like other retinoic acid compounds, was known to stimulate B-cell activities in vivo and in vitro but effects on dividing lupus T cells had not been studied. Tretinoin 19-32 myotubularin related protein 11 Homo sapiens 3-6
8381482-4 1993 Teratogenic doses of RA increase the level of RAR-beta 2 mRNA, RAR-alpha 2 mRNA, CRBP-I mRNA and CRABP-II mRNA in mouse conceptuses and embryos. Tretinoin 21-23 retinoic acid receptor, alpha Mus musculus 46-49
8381482-4 1993 Teratogenic doses of RA increase the level of RAR-beta 2 mRNA, RAR-alpha 2 mRNA, CRBP-I mRNA and CRABP-II mRNA in mouse conceptuses and embryos. Tretinoin 21-23 retinoic acid receptor, alpha Mus musculus 63-66
8823154-7 1996 Taking into account enzymatic properties and coenzyme preferences, a case can be made that class IV alcohol dehydrogenase catalyzes retinol oxidation to provide retinal for retinoic acid synthesis, whereas microsomal retinol dehydrogenase (a short-chain dehydrogenase/reductase) catalyzes the reduction of retinal to retinol to promote retinoid storage. Tretinoin 173-186 aldo-keto reductase family 1 member A1 Homo sapiens 100-121
9368678-6 1997 Cells treated with RA (0-1 microM) also showed a time- and dose-dependent increase in IGFBP-3 protein and mRNA levels. Tretinoin 19-21 insulin like growth factor binding protein 3 Homo sapiens 86-93
9175760-0 1997 Regulation by thyroid hormone and retinoic acid of the CCAAT/enhancer binding protein alpha and beta genes during liver development. Tretinoin 34-47 CCAAT/enhancer binding protein alpha Rattus norvegicus 55-91
8797830-2 1996 Here we show that the same enzyme is inducible by retinoic acid in P19 teratocarcinoma cells, and we report the cloning from P19 cells of a cDNA encoding a novel dehydrogenase, named retinaldehyde dehydrogenase-2 (RALDH-2). Tretinoin 50-63 aldehyde dehydrogenase 1 family member A2 Homo sapiens 183-212
8797830-2 1996 Here we show that the same enzyme is inducible by retinoic acid in P19 teratocarcinoma cells, and we report the cloning from P19 cells of a cDNA encoding a novel dehydrogenase, named retinaldehyde dehydrogenase-2 (RALDH-2). Tretinoin 50-63 aldehyde dehydrogenase 1 family member A2 Homo sapiens 214-221
8095151-1 1993 Here we describe experiments detailing the developmental expression, and the inducibility by all-trans retinoic acid (RA) of six members of the Xenopus Hox-2 complex of homeobox-containing genes. Tretinoin 118-120 homeobox B7 S homeolog Xenopus laevis 152-157
8093325-0 1993 Identification of a retinoic acid response element upstream of the murine Hox-4.2 gene. Tretinoin 20-33 homeobox D4 Mus musculus 74-81
8093325-4 1993 The expression of murine Hox-4.2 and its human homolog, HOX4B, is increased in embryonal carcinoma (EC) cell lines upon RA treatment (M. S. Featherstone, A. Baron, S. J. Gaunt, M.-G. Mattei, and D. Duboule, Proc. Tretinoin 120-122 homeobox D4 Mus musculus 25-32
8093325-11 1993 Using transient expression assays, we showed that luciferase reporter gene constructs carrying genomic sequences located upstream of Hox-4.2 responded to RA in murine P19 EC cells. Tretinoin 154-156 homeobox D4 Mus musculus 133-140
8093325-15 1993 In addition, the response to RA could be inhibited by expressing a dominant negative form of RAR alpha in transfected P19 EC cells. Tretinoin 29-31 retinoic acid receptor, alpha Mus musculus 93-102
8765051-1 1996 Retinoic acid (RA)-induced endodermal differentiation of F9 teratocarcinoma cells is accompanied by altered of many genes, including the retinoic acid receptor (RAR) alpha, beta, and gamma and retinoic x receptor (RXR) alpha and gamma genes. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 137-159
8765051-1 1996 Retinoic acid (RA)-induced endodermal differentiation of F9 teratocarcinoma cells is accompanied by altered of many genes, including the retinoic acid receptor (RAR) alpha, beta, and gamma and retinoic x receptor (RXR) alpha and gamma genes. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 161-164
9153223-0 1997 All-trans-retinoic acid increases transforming growth factor-beta2 and insulin-like growth factor binding protein-3 expression through a retinoic acid receptor-alpha-dependent signaling pathway. Tretinoin 0-23 insulin like growth factor binding protein 3 Homo sapiens 71-115
8765051-1 1996 Retinoic acid (RA)-induced endodermal differentiation of F9 teratocarcinoma cells is accompanied by altered of many genes, including the retinoic acid receptor (RAR) alpha, beta, and gamma and retinoic x receptor (RXR) alpha and gamma genes. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 137-159
8765051-1 1996 Retinoic acid (RA)-induced endodermal differentiation of F9 teratocarcinoma cells is accompanied by altered of many genes, including the retinoic acid receptor (RAR) alpha, beta, and gamma and retinoic x receptor (RXR) alpha and gamma genes. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 161-164
1282237-0 1992 Quantitation of human cellular retinoic acid-binding protein II (CRABP-II) RNA from cultured human skin fibroblast cells and human skin biopsies treated with retinoic acid. Tretinoin 31-44 cellular retinoic acid binding protein 2 Homo sapiens 65-73
1282237-1 1992 A polymerase chain reaction (PCR) method has been validated for the quantitation of retinoic acid (RA) induction of cellular retinoic acid-binding protein II (CRABP-II) RNA from cultured human skin fibroblasts and human skin biopsies. Tretinoin 84-97 cellular retinoic acid binding protein 2 Homo sapiens 116-157
1282237-1 1992 A polymerase chain reaction (PCR) method has been validated for the quantitation of retinoic acid (RA) induction of cellular retinoic acid-binding protein II (CRABP-II) RNA from cultured human skin fibroblasts and human skin biopsies. Tretinoin 84-97 cellular retinoic acid binding protein 2 Homo sapiens 159-167
8813719-8 1996 Using synthetic RA analogs, which selectively activate RARs and RXRs, the RAR partner within the heterodimeric complex appeared to be sufficient while the RXR partner was insufficient to independently activate transcription. Tretinoin 16-18 retinoid X receptor alpha Homo sapiens 64-67
9153223-0 1997 All-trans-retinoic acid increases transforming growth factor-beta2 and insulin-like growth factor binding protein-3 expression through a retinoic acid receptor-alpha-dependent signaling pathway. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 137-165
1282237-1 1992 A polymerase chain reaction (PCR) method has been validated for the quantitation of retinoic acid (RA) induction of cellular retinoic acid-binding protein II (CRABP-II) RNA from cultured human skin fibroblasts and human skin biopsies. Tretinoin 99-101 cellular retinoic acid binding protein 2 Homo sapiens 116-157
1282237-1 1992 A polymerase chain reaction (PCR) method has been validated for the quantitation of retinoic acid (RA) induction of cellular retinoic acid-binding protein II (CRABP-II) RNA from cultured human skin fibroblasts and human skin biopsies. Tretinoin 99-101 cellular retinoic acid binding protein 2 Homo sapiens 159-167
1333043-0 1992 Activation of the phosphoenolpyruvate carboxykinase gene retinoic acid response element is dependent on a retinoic acid receptor/coregulator complex. Tretinoin 57-70 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 18-51
8687453-0 1996 AP-2 gene expression and modulation by retinoic acid during keratinocyte differentiation. Tretinoin 39-52 transcription factor AP-2 alpha Homo sapiens 0-4
1333043-1 1992 The accessory factor 1 (AF1) element is an upstream transcriptional control region that plays a role in the response of the phosphoenolpyruvate carboxykinase (PEPCK) gene to both glucocorticoids and retinoic acid. Tretinoin 199-212 interferon gamma receptor 2 Homo sapiens 24-27
8687453-3 1996 Continuous treatment of the keratinocyte cell cultures with retinoic acid (RA) resulted in a premature downregulation of AP-2 mRNA levels, and the transcripts of K4 and AhR remained at basal levels. Tretinoin 60-73 transcription factor AP-2 alpha Homo sapiens 121-125
1333043-1 1992 The accessory factor 1 (AF1) element is an upstream transcriptional control region that plays a role in the response of the phosphoenolpyruvate carboxykinase (PEPCK) gene to both glucocorticoids and retinoic acid. Tretinoin 199-212 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 124-157
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 0-23 insulin like growth factor binding protein 3 Homo sapiens 69-76
1333043-1 1992 The accessory factor 1 (AF1) element is an upstream transcriptional control region that plays a role in the response of the phosphoenolpyruvate carboxykinase (PEPCK) gene to both glucocorticoids and retinoic acid. Tretinoin 199-212 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 159-164
1333043-2 1992 We demonstrate here that retinoic acid receptor alpha (RAR alpha) binds to a sequence within the AF1 element, TGACCT (site B), that is a consensus retinoic acid response element (RARE) half-site. Tretinoin 25-38 interferon gamma receptor 2 Homo sapiens 97-100
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 0-23 insulin like growth factor binding protein 3 Homo sapiens 111-118
1333043-5 1992 Mutational analysis of the AF1 element shows that the RAR alpha/CR complex is the trans-acting unit that mediates the retinoic acid response of the PEPCK gene. Tretinoin 118-131 interferon gamma receptor 2 Homo sapiens 27-30
8662962-7 1996 Gel shift analysis showed that purified calreticulin inhibited the binding of endogenous RAR to a beta-RA response element oligonucleotide, only if added prior to the addition of the oligonucleotide. Tretinoin 98-105 retinoic acid receptor, alpha Mus musculus 89-92
8662962-11 1996 Cyclic AMP may act to antagonize RA action by both decreasing RAR expression (Y. Xiao, D. Desai, T. Quick, and R. M. Niles, J. Tretinoin 33-35 retinoic acid receptor, alpha Mus musculus 62-65
1333043-5 1992 Mutational analysis of the AF1 element shows that the RAR alpha/CR complex is the trans-acting unit that mediates the retinoic acid response of the PEPCK gene. Tretinoin 118-131 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 148-153
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 25-29 insulin like growth factor binding protein 3 Homo sapiens 69-76
8660922-0 1996 AP-2.2: a novel AP-2-related transcription factor induced by retinoic acid during differentiation of P19 embryonal carcinoma cells. Tretinoin 61-74 transcription factor AP-2 alpha Homo sapiens 0-4
8660922-0 1996 AP-2.2: a novel AP-2-related transcription factor induced by retinoic acid during differentiation of P19 embryonal carcinoma cells. Tretinoin 61-74 transcription factor AP-2 alpha Homo sapiens 16-20
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 25-29 insulin like growth factor binding protein 3 Homo sapiens 111-118
8660922-1 1996 A 2.8-kb cDNA encoding a new transcription factor (AP-2.2) has been cloned from mouse P19 embryonal carcinoma cells, in which the corresponding mRNA begins to accumulate 30 min after retinoic acid (RA) addition. Tretinoin 183-196 transcription factor AP-2, gamma Mus musculus 51-57
9184230-1 1997 The vigorous retinoic acid (RA)-dependent activation of the retinoic acid receptor beta2 (RARbeta2) gene in embryonal carcinoma (EC) cells is mediated by retinoid receptor heterodimers (RXR-RAR) binding to RAREs that are closely positioned to the TATA box and an EC cell-specific co-factor activity termed E1A-LA. Tretinoin 13-26 retinoic acid receptor alpha Homo sapiens 90-93
8660922-1 1996 A 2.8-kb cDNA encoding a new transcription factor (AP-2.2) has been cloned from mouse P19 embryonal carcinoma cells, in which the corresponding mRNA begins to accumulate 30 min after retinoic acid (RA) addition. Tretinoin 198-200 transcription factor AP-2, gamma Mus musculus 51-57
8649786-0 1996 Differential changes of retinoid-X-receptor (RXR alpha) and its RAR alpha and PML-RAR alpha partners induced by retinoic acid and cAMP distinguish maturation sensitive and resistant t(15;17) promyelocytic leukemia NB4 cells. Tretinoin 112-125 retinoid X receptor alpha Homo sapiens 24-43
8649786-0 1996 Differential changes of retinoid-X-receptor (RXR alpha) and its RAR alpha and PML-RAR alpha partners induced by retinoic acid and cAMP distinguish maturation sensitive and resistant t(15;17) promyelocytic leukemia NB4 cells. Tretinoin 112-125 retinoid X receptor alpha Homo sapiens 45-54
1283474-10 1992 The increase in the thickness of the epidermal HYA meshwork after 6 months and the blister fluid HYA after 2 weeks may indicate that HYA is involved in the epidermal change induced by topical retinoic acid therapy. Tretinoin 192-205 lysine demethylase 5D Homo sapiens 47-50
1283474-10 1992 The increase in the thickness of the epidermal HYA meshwork after 6 months and the blister fluid HYA after 2 weeks may indicate that HYA is involved in the epidermal change induced by topical retinoic acid therapy. Tretinoin 192-205 lysine demethylase 5D Homo sapiens 97-100
1283474-10 1992 The increase in the thickness of the epidermal HYA meshwork after 6 months and the blister fluid HYA after 2 weeks may indicate that HYA is involved in the epidermal change induced by topical retinoic acid therapy. Tretinoin 192-205 lysine demethylase 5D Homo sapiens 97-100
1478921-1 1992 This paper shows that Me2SO, all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3), but not 12-O-tetradecanoyl phorbol-13-acetate (PMA) are potent inducers of MRP-8/14 protein complex in human leukemic cells. Tretinoin 54-56 ATP binding cassette subfamily C member 11 Homo sapiens 189-194
8780892-0 1996 Regulation by retinoic acid of insulin-degrading enzyme and of a related endoprotease in human neuroblastoma cell lines. Tretinoin 14-27 insulin degrading enzyme Homo sapiens 31-55
9184230-1 1997 The vigorous retinoic acid (RA)-dependent activation of the retinoic acid receptor beta2 (RARbeta2) gene in embryonal carcinoma (EC) cells is mediated by retinoid receptor heterodimers (RXR-RAR) binding to RAREs that are closely positioned to the TATA box and an EC cell-specific co-factor activity termed E1A-LA. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 90-93
8780892-5 1996 Since retinoic acid plays a relevant role in controlling the growth of these cells and affects the expression of IDE, we have also: (a) identified the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) expressed in these cell lines and (b) by means of synthetic retinoid analogues identified the RAR/RXR isoforms whose activation may be sufficient to induce the expression of the IDE gene. Tretinoin 6-19 insulin degrading enzyme Homo sapiens 113-116
8780892-5 1996 Since retinoic acid plays a relevant role in controlling the growth of these cells and affects the expression of IDE, we have also: (a) identified the retinoic acid receptors (RARs) and retinoid X receptors (RXRs) expressed in these cell lines and (b) by means of synthetic retinoid analogues identified the RAR/RXR isoforms whose activation may be sufficient to induce the expression of the IDE gene. Tretinoin 6-19 retinoid X receptor alpha Homo sapiens 208-211
1328196-4 1992 The retinoic acid-induced activation was 3-4-fold higher with RXR alpha than with either RAR alpha or RAR beta. Tretinoin 4-17 retinoid X receptor alpha Homo sapiens 62-71
1363087-1 1992 Exogenous retinoic acid (RA) has teratogenic effects on vertebrate embryos and alters Hox-C gene expression in vivo and in vitro. Tretinoin 25-27 homeobox C cluster Mus musculus 86-91
9139741-5 1997 RA treatment did not change the expression of Jun family members; however, it decreased the expression of c-Fos. Tretinoin 0-2 FBJ osteosarcoma oncogene Mus musculus 106-111
1363087-2 1992 We wish to examine whether RA has a role in the normal regulation of Hox-C genes, and whether altered Hox-C gene expression in response to RA leads to abnormal morphology. Tretinoin 139-141 homeobox C cluster Mus musculus 102-107
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 48-61 retinoid X receptor alpha Homo sapiens 194-213
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 48-61 retinoid X receptor alpha Homo sapiens 215-218
8964830-1 1996 When human breast cancer T47D cells were treated with all-trans-retinoic acid (RA), the RA 4- and 18-hydroxylase activities were induced in microsomes in a time-dependent manner, indicating that these cells readily metabolized RA into more polar compounds, such as all-trans-4-hydroxy-RA and all-trans-18-hydroxy-RA. Tretinoin 54-77 RA4 Homo sapiens 88-92
8964830-1 1996 When human breast cancer T47D cells were treated with all-trans-retinoic acid (RA), the RA 4- and 18-hydroxylase activities were induced in microsomes in a time-dependent manner, indicating that these cells readily metabolized RA into more polar compounds, such as all-trans-4-hydroxy-RA and all-trans-18-hydroxy-RA. Tretinoin 79-81 RA4 Homo sapiens 88-92
8810827-3 1996 Apo-CRBP and ethanol inhibit the cytosolic but not the microsomal retinol dehydrogenase, the latter being the primary enzyme in the rate-limiting step in retinoic acid synthesis. Tretinoin 154-167 retinol binding protein 1 Rattus norvegicus 4-8
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 63-65 retinoid X receptor alpha Homo sapiens 194-213
1326406-1 1992 Using several naturally occurring and synthetic retinoic acid (RA)-responsive reporter genes, we show that the patterns of transcriptional activation by various retinoic acid receptor (RAR) and retinoid X receptor (RXR) forms vary according to the nature of the RA response element and the context of the stimulated promoter. Tretinoin 63-65 retinoid X receptor alpha Homo sapiens 215-218
9165121-6 1997 Finally, Xotx1 and Xotx2 are activated by factors involved in head formation and repressed by a posteriorizing signal like retinoic acid. Tretinoin 123-136 orthodenticle homeobox 1 L homeolog Xenopus laevis 9-14
8639786-3 1996 We investigated how LFA-1/ICAM-1-mediated adhesion and aggregation are regulated in HL-60 cells induced to differentiate into neutrophils by retinoic acid (RA). Tretinoin 141-154 intercellular adhesion molecule 1 Homo sapiens 26-32
9203140-2 1997 A new retinoic acid-inducible gene, Stra6, has been identified in P19 embryonal carcinoma cells using a subtractive hybridization cDNA cloning technique. Tretinoin 6-19 signaling receptor and transporter of retinol STRA6 Homo sapiens 36-41
8639786-3 1996 We investigated how LFA-1/ICAM-1-mediated adhesion and aggregation are regulated in HL-60 cells induced to differentiate into neutrophils by retinoic acid (RA). Tretinoin 156-158 intercellular adhesion molecule 1 Homo sapiens 26-32
8639786-5 1996 When cultured with RA for 24 hours, HL-60 cells were able to adhere to ICAM-1 constitutively. Tretinoin 19-21 intercellular adhesion molecule 1 Homo sapiens 71-77
8639786-8 1996 Although ICAM-1 was intensely expressed on RA-induced HL-60 cells, these cells did not show any cellular aggregation. Tretinoin 43-45 intercellular adhesion molecule 1 Homo sapiens 9-15
8639786-9 1996 The HL-60 cells transfected with the active form of Ras (Val12) exhibited LFA-1/ICAM-1-dependent aggregation by RA stimulation without change in the avidity of LFA-1. Tretinoin 112-114 intercellular adhesion molecule 1 Homo sapiens 80-86
1355009-0 1992 Differential susceptibility of cultured human melanoma cell lines to enhancement by retinoic acid of intercellular adhesion molecule 1 expression. Tretinoin 84-97 intercellular adhesion molecule 1 Homo sapiens 101-134
1355009-2 1992 The present study has shown that the differentiating agent retinoic acid (RA) up-regulates ICAM-1 expression by melanoma cells in a dose- and time-dependent fashion. Tretinoin 59-72 intercellular adhesion molecule 1 Homo sapiens 91-97
1355009-2 1992 The present study has shown that the differentiating agent retinoic acid (RA) up-regulates ICAM-1 expression by melanoma cells in a dose- and time-dependent fashion. Tretinoin 74-76 intercellular adhesion molecule 1 Homo sapiens 91-97
1355009-6 1992 Nevertheless, RA-insensitive as well as RA-sensitive melanoma cell lines displayed a higher increase in ICAM-1 expression following incubation with RA and cytokines than following incubation with each of them. Tretinoin 14-16 intercellular adhesion molecule 1 Homo sapiens 104-110
1355009-6 1992 Nevertheless, RA-insensitive as well as RA-sensitive melanoma cell lines displayed a higher increase in ICAM-1 expression following incubation with RA and cytokines than following incubation with each of them. Tretinoin 40-42 intercellular adhesion molecule 1 Homo sapiens 104-110
1355009-6 1992 Nevertheless, RA-insensitive as well as RA-sensitive melanoma cell lines displayed a higher increase in ICAM-1 expression following incubation with RA and cytokines than following incubation with each of them. Tretinoin 40-42 intercellular adhesion molecule 1 Homo sapiens 104-110
1355009-7 1992 Analysis of the distribution in the melanoma cell lines of retinoic acid receptors (RARs) showed a relationship between susceptibility to a RA-mediated increase of ICAM-1 expression and RAR beta expression, suggesting that the latter receptor may play a role in the phenomenon. Tretinoin 84-86 intercellular adhesion molecule 1 Homo sapiens 164-170
1355009-8 1992 RAR alpha and RAR gamma were present in RA-sensitive and -insensitive melanoma cell lines, suggesting that they play a role in the enhancement by RA of cytokine-mediated up-regulation of ICAM-1 expression. Tretinoin 0-2 intercellular adhesion molecule 1 Homo sapiens 187-193
1324435-5 1992 6) form a heterodimer that activates acyl-CoA oxidase gene expression in response to either clofibric acid or the retinoid X receptor-alpha ligand, 9-cis retinoic acid, an all-trans retinoic acid metabolite; simultaneous exposure to both activators results in a synergistic induction of gene expression. Tretinoin 154-167 retinoid X receptor alpha Homo sapiens 114-139
8793849-5 1996 Reporters containing single copies of these elements conferred 9-cis retinoic acid responsiveness to cells cotransfected with an RXR alpha expressing plasmid. Tretinoin 69-82 retinoid X receptor alpha Homo sapiens 129-138
8631848-12 1996 Thus, RA augmentation of STAT1 may be an early step in the cooperative anti-tumor effects of IFN and RA. Tretinoin 6-8 signal transducer and activator of transcription 1 Homo sapiens 25-30
8622986-4 1996 PLZF-RARalpha and PML-RARalpha have essentially the same ligand-binding affinities and can bind in vitro to retinoic acid response elements (RAREs) as homodimers or heterodimers with RXRalpha. Tretinoin 108-121 zinc finger and BTB domain containing 16 Homo sapiens 0-4
1323347-0 1992 Stimulation of tissue plasminogen activator production by retinoic acid: synergistic effect on protein kinase C-mediated activation. Tretinoin 58-71 chromosome 20 open reading frame 181 Homo sapiens 15-43
8622986-8 1996 These different protein-protein interactions and the target gene specificities of PLZF-RARalpha and PML-RARalpha may underlie, at least in part, the apparent resistance of APL with t(11;17) to differentiation effects of all-trans-retinoic acid. Tretinoin 224-243 zinc finger and BTB domain containing 16 Homo sapiens 82-86
1323347-1 1992 Trans retinoic acid (t-RA) stimulated the production of tissue plasminogen activator (tPA) in HeLa-S3 and human umbilical vein endothelial cells (huvecs) in a dose-dependent manner with maximal release (four to five times control) at 40 nmol/L and 40 mumol/L, respectively. Tretinoin 0-19 chromosome 20 open reading frame 181 Homo sapiens 56-84
9194390-9 1997 ATRA was restarted along with granulocyte-colony stimulating factor (G-CSF). Tretinoin 0-4 colony stimulating factor 3 Homo sapiens 69-74
1323347-1 1992 Trans retinoic acid (t-RA) stimulated the production of tissue plasminogen activator (tPA) in HeLa-S3 and human umbilical vein endothelial cells (huvecs) in a dose-dependent manner with maximal release (four to five times control) at 40 nmol/L and 40 mumol/L, respectively. Tretinoin 0-19 chromosome 20 open reading frame 181 Homo sapiens 86-89
1323347-1 1992 Trans retinoic acid (t-RA) stimulated the production of tissue plasminogen activator (tPA) in HeLa-S3 and human umbilical vein endothelial cells (huvecs) in a dose-dependent manner with maximal release (four to five times control) at 40 nmol/L and 40 mumol/L, respectively. Tretinoin 21-25 chromosome 20 open reading frame 181 Homo sapiens 56-84
1323347-1 1992 Trans retinoic acid (t-RA) stimulated the production of tissue plasminogen activator (tPA) in HeLa-S3 and human umbilical vein endothelial cells (huvecs) in a dose-dependent manner with maximal release (four to five times control) at 40 nmol/L and 40 mumol/L, respectively. Tretinoin 21-25 chromosome 20 open reading frame 181 Homo sapiens 86-89
1323347-2 1992 In endothelial cells, the stimulation of tPA production by phorbol 12-myristate 13-acetate (PMA) was potentiated 1.9-fold by 10 mumol/L t-RA, or 1.8 times the additive effect. Tretinoin 136-140 chromosome 20 open reading frame 181 Homo sapiens 41-44
1323347-3 1992 In HeLa cells, total tPA secretion with 10 nmol/L PMA was increased from 43 ng/mL to 96 ng/mL by 40 nmol/L t-RA, which was two times the additive effect. Tretinoin 107-111 chromosome 20 open reading frame 181 Homo sapiens 21-24
1323347-4 1992 Higher concentrations of t-RA (400 nmol/L) depressed tPA secretion by itself and also suppressed PMA-induced tPA production by 50%. Tretinoin 25-29 chromosome 20 open reading frame 181 Homo sapiens 53-56
1323347-4 1992 Higher concentrations of t-RA (400 nmol/L) depressed tPA secretion by itself and also suppressed PMA-induced tPA production by 50%. Tretinoin 25-29 chromosome 20 open reading frame 181 Homo sapiens 109-112
8612676-1 1996 NCR-G3 cells were established from a testicular embryonal carcinoma and are highly multipotential, differentiating into trophectoderm cells upon exposure to retinoic acid. Tretinoin 157-170 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 0-3
1323347-6 1992 t-RA (40 nmol/L) and 10 micrograms/mL histamine or 10 U/mL thrombin combined to induce tPA production 3.4 and 1.3 times the additive effect in HeLa cells. Tretinoin 0-4 chromosome 20 open reading frame 181 Homo sapiens 87-90
9092831-6 1997 Retinoic acid production, analyzed by high-performance liquid chromatography, was observed for the epithelial cells from the uteri of prepubertal animals treated with PMSG, cells previously shown to express CRABP(II) and confirmed here to continue to express it in culture. Tretinoin 0-13 cellular retinoic acid binding protein 2 Rattus norvegicus 207-216
1323347-8 1992 Nor did 10 nmol/L PMA and 40 nmol/L t-RA together affect cAMP levels, suggesting that t-RA-mediated potentiation of PMA-induced tPA production occurred via a mechanism that was independent of cAMP levels. Tretinoin 86-90 chromosome 20 open reading frame 181 Homo sapiens 128-131
1323347-11 1992 These studies suggest that the mechanism mediating t-RA stimulation of tPA production interacts with the PKC pathway, resulting in synergism. Tretinoin 51-55 chromosome 20 open reading frame 181 Homo sapiens 71-74
8626539-7 1996 The binding of RXRalpha homodimers and RXRalpha/T3Rbeta heterodimers is associated with ligand-dependent activation by 9-cis-RA or repression by T3. Tretinoin 119-127 retinoid X receptor alpha Homo sapiens 15-23
8626539-7 1996 The binding of RXRalpha homodimers and RXRalpha/T3Rbeta heterodimers is associated with ligand-dependent activation by 9-cis-RA or repression by T3. Tretinoin 119-127 retinoid X receptor alpha Homo sapiens 39-47
9092831-10 1997 Thus, this system revealed an important difference in retinoid metabolism between cells expressing CRABP and CRABP(II) and suggests CRABP(II) may participate in retinoic acid production and/or secretion. Tretinoin 161-174 cellular retinoic acid binding protein 2 Rattus norvegicus 132-141
8610177-4 1996 Addition of RA to the culture medium at the time of antisense injection restored normal development implicating the role of RBP in embryonic RA synthesis. Tretinoin 12-14 retinol binding protein 4, plasma Mus musculus 124-127
1286212-4 1992 More specifically, retinoic acid cannot be either diffusing from a ZPA source or participate in an autocatalytic gradient formation. Tretinoin 19-32 zona pellucida glycoprotein 2 Gallus gallus 67-70
9097025-11 1997 These results suggest that upregulation of ADH-IV and ALDH-I gene expression in primitive streak mesoderm may lead to retinoic acid synthesis and initiation of retinoid signaling during mouse embryogenesis. Tretinoin 118-131 aldehyde dehydrogenase 2, mitochondrial Mus musculus 54-60
10743138-2 1997 The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased. Tretinoin 53-55 MYC proto-oncogene, bHLH transcription factor Homo sapiens 215-220
1321332-0 1992 Repression by ARP-1 sensitizes apolipoprotein AI gene responsiveness to RXR alpha and retinoic acid. Tretinoin 86-99 actin related protein 1A Homo sapiens 14-19
1321332-4 1992 In a more recent series of experiments, we found that site A is a retinoic acid (RA) response element that responds preferentially to the recently identified RA-responsive receptor RXR alpha over the previously characterized RA receptors RAR alpha and RAR beta. Tretinoin 66-79 retinoid X receptor alpha Homo sapiens 181-190
1321332-4 1992 In a more recent series of experiments, we found that site A is a retinoic acid (RA) response element that responds preferentially to the recently identified RA-responsive receptor RXR alpha over the previously characterized RA receptors RAR alpha and RAR beta. Tretinoin 81-83 retinoid X receptor alpha Homo sapiens 181-190
1321332-6 1992 Transient transfection assays showed that site A is necessary and sufficient for RXR alpha-mediated transactivation of the apoAI gene basal promoter in human hepatoma HepG2 cells in the presence of RA and that this transactivation is abolished by increasing amounts of cotransfected ARP-1. Tretinoin 198-200 retinoid X receptor alpha Homo sapiens 81-90
1321332-10 1992 However, while ARP-1 alone or ARP-1 and RXR alpha together dramatically repress expression in the absence of RA, the repression by ARP-1 and RXR alpha together, but not ARP-1 alone, is almost completely alleviated in the presence of RA. Tretinoin 233-235 retinoid X receptor alpha Homo sapiens 141-150
8728106-3 1996 The mRNA expression of CNTF and neurotrophins in BIM cells was differently regulated by the stimulation with cAMP, FGF and retinoic acid. Tretinoin 123-136 ciliary neurotrophic factor Homo sapiens 23-27
8626114-9 1996 Secretion of either TGF-beta 1 or TGF-beta 2 is significantly increased (P<0.05) in response to RA, both in RA-sensitive and in RA-resistant cells. Tretinoin 99-101 transforming growth factor beta 2 Homo sapiens 34-44
9068616-2 1997 Retinoic acid, a by-product of photoreceptor signaling and a potent modulator of hormonal transcription control, is one candidate for regulating the arrestin mRNA levels. Tretinoin 0-13 S-antigen, retina and pineal gland (arrestin) Mus musculus 149-157
8726400-3 1996 In vitro treatment with ATRA dramatically modifies the adhesion phenotype of APL blast cells, promoting a consistently striking up-regulation of CD11b, CD11c, CD15, CD65, CD54, and CD38. Tretinoin 24-28 integrin subunit alpha M Homo sapiens 145-150
1431336-5 1992 Treatment of LoVo/Dx with differentiating agents (dimethylformamide and retinoic acid) led to a decreased expression of the adhesion molecules, including NCA, accompanied by increased resistance to LAK-mediated lysis. Tretinoin 72-85 alpha kinase 1 Homo sapiens 198-201
9067579-3 1997 An HL-60 subline resistant to RA (HL-60 R) contains a point mutation which results in a truncation of 52 amino acids at the COOH end of RAR alpha. Tretinoin 30-32 retinoic acid receptor alpha Homo sapiens 136-145
1324421-6 1992 RXR alpha complexes with RAR alpha, RAR beta, and RAR gamma bound selectively to retinoic acid responsive elements from the human RAR beta 2 gene (hRAR beta 2), the gene of the rat cellular retinol binding protein I and the human apolipoprotein A1 gene. Tretinoin 81-94 retinoid X receptor alpha Homo sapiens 0-9
8726400-3 1996 In vitro treatment with ATRA dramatically modifies the adhesion phenotype of APL blast cells, promoting a consistently striking up-regulation of CD11b, CD11c, CD15, CD65, CD54, and CD38. Tretinoin 24-28 intercellular adhesion molecule 1 Homo sapiens 171-175
9085275-4 1997 In contrast, retinoic acid-induced differentiated cells expressed as high levels of Xist as female primary cells. Tretinoin 13-26 X inactive specific transcript Homo sapiens 84-88
8636104-5 1996 Greater binding is observed at these sites by electrophoretic mobility shift assay when cells are cultured with RA and cyclic AMP analogs versus RA alone, and no binding is seen in extracts from RA-treated F9 RAR gamma-/- cells which lack RAR gamma mRNA and protein. Tretinoin 112-114 retinoic acid receptor, gamma Mus musculus 239-248
8600986-1 1996 The complex of microsomal UDP-glucuronosyl transferases (UGT; EC 2.4.1.17) of rat liver catalyzes the formation of retinoyl beta-glucuronide (RAG) from retinoic acid (RA) and retinyl beta-glucuronide (ROG) from retinol (ROL) in the presence of UDP-glucuronic acid (UDPGA). Tretinoin 152-165 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 26-55
8600986-1 1996 The complex of microsomal UDP-glucuronosyl transferases (UGT; EC 2.4.1.17) of rat liver catalyzes the formation of retinoyl beta-glucuronide (RAG) from retinoic acid (RA) and retinyl beta-glucuronide (ROG) from retinol (ROL) in the presence of UDP-glucuronic acid (UDPGA). Tretinoin 152-165 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 57-60
8600986-1 1996 The complex of microsomal UDP-glucuronosyl transferases (UGT; EC 2.4.1.17) of rat liver catalyzes the formation of retinoyl beta-glucuronide (RAG) from retinoic acid (RA) and retinyl beta-glucuronide (ROG) from retinol (ROL) in the presence of UDP-glucuronic acid (UDPGA). Tretinoin 142-144 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 26-55
8600986-1 1996 The complex of microsomal UDP-glucuronosyl transferases (UGT; EC 2.4.1.17) of rat liver catalyzes the formation of retinoyl beta-glucuronide (RAG) from retinoic acid (RA) and retinyl beta-glucuronide (ROG) from retinol (ROL) in the presence of UDP-glucuronic acid (UDPGA). Tretinoin 142-144 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 57-60
1590797-0 1992 Activin synergistically increased c-jun mRNA in P19 embryonal carcinoma cells in the presence of retinoic acid. Tretinoin 97-110 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-39
1590797-3 1992 Activin (lng/ml) was sufficient to induce the synergistic increase of c-jun mRNA in P19 EC cells with all-trans-retinoic acid. Tretinoin 102-125 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-75
1567193-1 1992 Hepatic cytosol from normal deermice having cytosolic alcohol dehydrogenase (ADH+) also displays retinol dehydrogenase activity and converts retinol to retinoic acid, whereas cytosol from ADH- deermice lacks these enzyme activities and does not produce retinoic acid. Tretinoin 152-165 aldo-keto reductase family 1 member A1 Homo sapiens 54-75
1567193-1 1992 Hepatic cytosol from normal deermice having cytosolic alcohol dehydrogenase (ADH+) also displays retinol dehydrogenase activity and converts retinol to retinoic acid, whereas cytosol from ADH- deermice lacks these enzyme activities and does not produce retinoic acid. Tretinoin 152-165 aldo-keto reductase family 1 member A1 Homo sapiens 77-81
1567193-1 1992 Hepatic cytosol from normal deermice having cytosolic alcohol dehydrogenase (ADH+) also displays retinol dehydrogenase activity and converts retinol to retinoic acid, whereas cytosol from ADH- deermice lacks these enzyme activities and does not produce retinoic acid. Tretinoin 253-266 aldo-keto reductase family 1 member A1 Homo sapiens 77-81
1567193-5 1992 Microsomal retinol dehydrogenase also catalyzes the reduction of retinal to retinol, thereby explaining the decrease in retinoic acid production from retinol in liver cytosol of ADH+ deermice when microsomes are added. Tretinoin 120-133 aldo-keto reductase family 1 member A1 Homo sapiens 178-182
8600986-9 1996 Different UGT enzymes might well act on different geometric isomers of RA. Tretinoin 71-73 beta-1,3-glucuronyltransferase 2 Rattus norvegicus 10-13
9057134-0 1997 Retinoic acid induced neural differentiation in a neuroectodermal cell line immortalized by p53 deficiency. Tretinoin 0-13 transformation related protein 53, pseudogene Mus musculus 92-95
8648186-1 1996 Cellular retinoic acid binding protein II (CRABP II) mRNA is selectively induced by all-trans retinoic acid in human skin and dermal fibroblasts. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 43-51
1311241-4 1992 In this work, retinoic acid (RA) added to Ob 17 cells at growth arrest impaired morphological differentiation and the development of both late (malic enzyme and GPDH) and early (LPL) phenotypes regardless of whether T3 was added. Tretinoin 14-27 glycerol phosphate dehydrogenase 2, mitochondrial Mus musculus 161-165
1311241-4 1992 In this work, retinoic acid (RA) added to Ob 17 cells at growth arrest impaired morphological differentiation and the development of both late (malic enzyme and GPDH) and early (LPL) phenotypes regardless of whether T3 was added. Tretinoin 14-27 lipoprotein lipase Mus musculus 178-181
1311241-4 1992 In this work, retinoic acid (RA) added to Ob 17 cells at growth arrest impaired morphological differentiation and the development of both late (malic enzyme and GPDH) and early (LPL) phenotypes regardless of whether T3 was added. Tretinoin 29-31 glycerol phosphate dehydrogenase 2, mitochondrial Mus musculus 161-165
1311241-4 1992 In this work, retinoic acid (RA) added to Ob 17 cells at growth arrest impaired morphological differentiation and the development of both late (malic enzyme and GPDH) and early (LPL) phenotypes regardless of whether T3 was added. Tretinoin 29-31 lipoprotein lipase Mus musculus 178-181
8622645-6 1996 Although VDR can bind as a homodimer to the osteopontin gene vitamin D response element, we find that a RXR-VDR heterodimer must be the transactivating species from the element in vivo, since RXR enhances and 9-cis RA and other RXR-specific ligands attenuate this induction. Tretinoin 215-217 retinoid X receptor alpha Homo sapiens 104-107
9057134-2 1997 All-trans retinoic acid (RA) induced bulk formation of neurons both in several p53-deficient neuroepithelial cell lines and in wild-type neural cells derived from early embryonic (E9-E12) forebrain vesicles. Tretinoin 10-23 transformation related protein 53, pseudogene Mus musculus 79-82
8617282-4 1996 Known activators of peroxisome proliferator-activated receptor include polyunsaturated fatty acids and, for RXR, the 9-cis isomer of retinoic acid. Tretinoin 133-146 retinoid X receptor alpha Homo sapiens 108-111
1347750-8 1992 Explant experiments showed that Xlim-1 mRNA is induced by the mesoderm-inducer activin A and by retinoic acid, which is not a mesoderm inducer but affects patterning during Xenopus embryogenesis; application of activin A and retinoic acid together results in synergistic induction. Tretinoin 96-109 LIM homeobox 1 L homeolog Xenopus laevis 32-38
1347750-8 1992 Explant experiments showed that Xlim-1 mRNA is induced by the mesoderm-inducer activin A and by retinoic acid, which is not a mesoderm inducer but affects patterning during Xenopus embryogenesis; application of activin A and retinoic acid together results in synergistic induction. Tretinoin 225-238 LIM homeobox 1 L homeolog Xenopus laevis 32-38
8604295-1 1996 Several members of the nuclear receptor superfamily including RXR (retinoid X receptor) bind to a specific retinoic acid response element (site A) of the apoAI promoter. Tretinoin 107-120 retinoid X receptor alpha Homo sapiens 62-65
9057134-2 1997 All-trans retinoic acid (RA) induced bulk formation of neurons both in several p53-deficient neuroepithelial cell lines and in wild-type neural cells derived from early embryonic (E9-E12) forebrain vesicles. Tretinoin 25-27 transformation related protein 53, pseudogene Mus musculus 79-82
8604312-0 1996 A novel type of retinoic acid response element in the second intron of the mouse H2Kb gene is activated by the RAR/RXR heterodimer. Tretinoin 16-29 retinoic acid receptor, alpha Mus musculus 111-114
9057134-3 1997 Forty-eight-hour treatment with 10(-6) M RA was necessary and sufficient to initiate neuron formation by p53(-/-)-progenitors, but neuronal characteristics appeared with a delay of 3-4 days. Tretinoin 41-43 transformation related protein 53, pseudogene Mus musculus 105-108
1567788-5 1992 Moderate to high levels of hsp60 mRNA and protein could be induced in the THP-I monocytic leukemia cell line by heat shock, retinoic acid, interferon (IFN)-gamma or tumor necrosis factor (TNF)-alpha treatment, the highest levels obtained with a combination of IFN-gamma/TNF-alpha. Tretinoin 124-137 heat shock protein family D (Hsp60) member 1 Homo sapiens 27-32
9040935-3 1997 We describe here the changes in the expression and DNA binding activity of the WT1 gene product in P19 embryonal carcinoma cells and embryonic stem cells triggered to differentiate by either retinoic acid (RA) or DMSO. Tretinoin 191-204 WT1 transcription factor Mus musculus 79-82
1376612-4 1992 We show that the putative endoderm-specific markers are localized to the endoderm in mature EBs, and that AFP mRNA is localized to the apical edge of the VE in RA EBs. Tretinoin 160-162 alpha fetoprotein Mus musculus 106-109
8624608-0 1996 All-trans retinoic acid inhibits binding of 1,25-dihydroxy-vitamin D3 to the vitamin D receptor in cultured human keratinocytes. Tretinoin 10-23 vitamin D receptor Homo sapiens 77-95
8624608-6 1996 The purpose of the present study was to determine the effect of all-trans RA on the binding of 1,25-dihydroxy-vitamin D3 (1,25 (OH)2D3) to the vitamin D3 receptor (VDR) of cultured human KCs. Tretinoin 74-76 vitamin D receptor Homo sapiens 143-162
8624608-6 1996 The purpose of the present study was to determine the effect of all-trans RA on the binding of 1,25-dihydroxy-vitamin D3 (1,25 (OH)2D3) to the vitamin D3 receptor (VDR) of cultured human KCs. Tretinoin 74-76 vitamin D receptor Homo sapiens 164-167
1315216-6 1992 To examine further the possibility that the trophic actions of retinoic acid upon expression of the thymosin beta 10 gene involved retinoid receptors, neuroblastoma cells were transiently transfected with an expression vector encoding the nuclear retinoic acid receptor (alpha) protein. Tretinoin 63-76 thymosin, beta 10 Rattus norvegicus 100-116
8624608-15 1996 These results are in contrast to results with other cell types in which RA upregulates binding of 1,25 (OH)2D3 to the VDR. Tretinoin 72-74 vitamin D receptor Homo sapiens 118-121
9040935-3 1997 We describe here the changes in the expression and DNA binding activity of the WT1 gene product in P19 embryonal carcinoma cells and embryonic stem cells triggered to differentiate by either retinoic acid (RA) or DMSO. Tretinoin 206-208 WT1 transcription factor Mus musculus 79-82
9040935-5 1997 During RA-induced but not DMSO-induced differentiation of P19 EC cells, WT1 expression and DNA binding are strongly activated. Tretinoin 7-9 WT1 transcription factor Mus musculus 72-75
9040935-6 1997 Treatment of embryonic stem cells with RA resulted in a similar activation of WT1. Tretinoin 39-41 WT1 transcription factor Mus musculus 78-81
9040935-11 1997 Our results demonstrate that expression of WT1 is induced in specific cell types during RA-induced differentiation of P19 EC cells, reflecting the tissue-specific expression of WT1 in vivo. Tretinoin 88-90 WT1 transcription factor Mus musculus 43-46
8780165-5 1996 Clinically achievable doses of RA rapidly caused large- and small-vessel endothelial cells to become refractory to stimulation of migration either by tumor-conditioned media or purified angiogenic factors (a-fibroblast growth factor (aFGF), bFGF, vascular endothelial GF, platelet-derived GF, TGF beta-1, and IL-8). Tretinoin 31-33 fibroblast growth factor 1 Rattus norvegicus 206-232
8780165-5 1996 Clinically achievable doses of RA rapidly caused large- and small-vessel endothelial cells to become refractory to stimulation of migration either by tumor-conditioned media or purified angiogenic factors (a-fibroblast growth factor (aFGF), bFGF, vascular endothelial GF, platelet-derived GF, TGF beta-1, and IL-8). Tretinoin 31-33 fibroblast growth factor 1 Rattus norvegicus 234-238
1531473-6 1992 These results indicated that TGF-beta 1 could induce phosphatidylinositol-glycan-linked Fc gamma RIII (Fc gamma RIII-I) in THP-1 cells in the presence of RA. Tretinoin 154-156 Fc gamma receptor IIIa Homo sapiens 88-101
1531473-6 1992 These results indicated that TGF-beta 1 could induce phosphatidylinositol-glycan-linked Fc gamma RIII (Fc gamma RIII-I) in THP-1 cells in the presence of RA. Tretinoin 154-156 Fc gamma receptor IIIa Homo sapiens 103-116
1370674-7 1992 The result that RA induced expression of keratins K6, K16, and K17, as commonly expressed in hyperproliferative epidermis, is consistent with the notion that retinoids increase epidermal cell proliferation in the basal and/or lower spinous layers. Tretinoin 16-18 keratin 17 Homo sapiens 63-66
8570209-8 1996 Leukemogenesis in t(11;17) APL may be related to interference with ATRA-mediated differentiation due to sequestration of RXR by the PLZF-RAR alpha chimera. Tretinoin 67-71 retinoid X receptor alpha Homo sapiens 121-124
8570219-0 1996 RXR alpha is essential for mediating the all-trans retinoic acid-induced growth arrest of C2 myogenic cells. Tretinoin 51-64 retinoid X receptor alpha Homo sapiens 0-9
8570219-6 1996 Our results show that RXR alpha restores the response to RA in this subclone with respect to AP1 inhibition and growth arrest. Tretinoin 57-59 retinoid X receptor alpha Homo sapiens 22-31
8570219-7 1996 These observations indicate that RXR alpha plays a crucial role in mediating RA induced growth arrest of C2 myogenic cells. Tretinoin 77-79 retinoid X receptor alpha Homo sapiens 33-42
8993032-2 1997 In P19 EC cells RA treatment stimulates induction of the RAR beta gene, while it represses Oct3/4 gene expression. Tretinoin 16-18 POU class 5 homeobox 1 Homo sapiens 91-97
8536624-0 1996 Thyroid hormone and retinoic acid induce the synthesis of insulin-like growth factor-binding protein-4 in mouse osteoblastic cells. Tretinoin 20-33 insulin-like growth factor binding protein 4 Mus musculus 58-102
9016793-3 1997 We demonstrated previously that ELP1, the repressor type isoform of ELP, competes for binding with the retinoic acid receptor and represses retinoic acid-induced transactivation. Tretinoin 103-116 KDEL endoplasmic reticulum protein retention receptor 2 Homo sapiens 32-36
8536624-5 1996 We observed an up-regulation of the 2.6-kilobase IGFBP-4 mRNA transcript in the presence of T3 or retinoic acid. Tretinoin 98-111 insulin-like growth factor binding protein 4 Mus musculus 49-56
8536624-10 1996 Our data show that thyroid hormone and retinoic acid stimulate transcription of IGFBP-4 mRNA in osteoblasts, resulting in increased IGFBP-4 secretion into the medium. Tretinoin 39-52 insulin-like growth factor binding protein 4 Mus musculus 80-87
8536624-10 1996 Our data show that thyroid hormone and retinoic acid stimulate transcription of IGFBP-4 mRNA in osteoblasts, resulting in increased IGFBP-4 secretion into the medium. Tretinoin 39-52 insulin-like growth factor binding protein 4 Mus musculus 132-139
8536624-11 1996 IGFBP-4, a known inhibitor of cellular proliferation, might contribute to the antiproliferative effect of T3 and retinoic acid on osteoblasts. Tretinoin 113-126 insulin-like growth factor binding protein 4 Mus musculus 0-7
8727369-11 1996 Suppression of matrilysin expression by treated with all-trans retinoic acid (ATRA) or introduction of anti-sense matrilysin decreased the invasive ability in vitro. Tretinoin 53-76 matrix metallopeptidase 7 Mus musculus 15-25
9016793-3 1997 We demonstrated previously that ELP1, the repressor type isoform of ELP, competes for binding with the retinoic acid receptor and represses retinoic acid-induced transactivation. Tretinoin 103-116 nuclear receptor subfamily 5 group A member 1 Homo sapiens 32-35
8727369-11 1996 Suppression of matrilysin expression by treated with all-trans retinoic acid (ATRA) or introduction of anti-sense matrilysin decreased the invasive ability in vitro. Tretinoin 78-82 matrix metallopeptidase 7 Mus musculus 15-25
9016793-6 1997 Interestingly, the activator-type ELP isoforms were capable of repressing retinoic acid-induced transactivation through binding to the retinoic acid receptor binding element. Tretinoin 74-87 nuclear receptor subfamily 5 group A member 1 Homo sapiens 34-37
9607169-2 1997 The mechanisms involved in the regulation of gene expression by the retinoids is at least partially known and involves binding of the RAR and RXR to retinoic acid response elements. Tretinoin 149-162 retinoic acid receptor alpha Homo sapiens 134-137
8964570-2 1996 Retinol-binding protein (RBP) is the specific blood carrier transporting ROL, the precursor of the retinoic acid (RA) hormone, to target tissues. Tretinoin 99-112 retinol binding protein 4 Homo sapiens 0-23
8964570-2 1996 Retinol-binding protein (RBP) is the specific blood carrier transporting ROL, the precursor of the retinoic acid (RA) hormone, to target tissues. Tretinoin 99-112 retinol binding protein 4 Homo sapiens 25-28
8964570-2 1996 Retinol-binding protein (RBP) is the specific blood carrier transporting ROL, the precursor of the retinoic acid (RA) hormone, to target tissues. Tretinoin 114-116 retinol binding protein 4 Homo sapiens 0-23
8964570-2 1996 Retinol-binding protein (RBP) is the specific blood carrier transporting ROL, the precursor of the retinoic acid (RA) hormone, to target tissues. Tretinoin 114-116 retinol binding protein 4 Homo sapiens 25-28
9053327-2 1997 They mediate the effects of retinoic acid primarily as heterodimers of retinoic acid receptors (RARs) and retinoid X receptors (RXRs). Tretinoin 28-41 retinoid X receptor beta L homeolog Xenopus laevis 106-126
9053327-2 1997 They mediate the effects of retinoic acid primarily as heterodimers of retinoic acid receptors (RARs) and retinoid X receptors (RXRs). Tretinoin 28-41 retinoid X receptor beta L homeolog Xenopus laevis 128-132
9049836-5 1997 On the other hand, we confirm inhibition of the neuronal differentiation upon retinoic acid (RA) treatment of B-myb transfected cells. Tretinoin 78-91 MYB proto-oncogene like 2 Homo sapiens 110-115
21544324-10 1996 Treatment with retinoic acid increased RAR-alpha level in C4I, HT-3, and CaSki; RAR-beta in HT-3; and RAR-gamma in HT-3 and C4I cells. Tretinoin 15-28 retinoic acid receptor, alpha Mus musculus 39-48
21544324-10 1996 Treatment with retinoic acid increased RAR-alpha level in C4I, HT-3, and CaSki; RAR-beta in HT-3; and RAR-gamma in HT-3 and C4I cells. Tretinoin 15-28 retinoic acid receptor, gamma Mus musculus 102-111
8557772-0 1996 Induction of transforming growth factor-beta autocrine activity by all-trans-retinoic acid and 1 alpha,25-dihydroxyvitamin D3 in NRP-152 rat prostatic epithelial cells. Tretinoin 67-90 Nrp Rattus norvegicus 129-132
8557772-3 1996 In this study the role of the transforming growth factor-beta (TGF-beta) growth inhibitors, in promoting the biological activities of all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) was studied in NRP-152 cells, a nontumorigenic epithelial line derived from rat dorsal-lateral prostate. Tretinoin 134-157 Nrp Rattus norvegicus 228-231
8557772-3 1996 In this study the role of the transforming growth factor-beta (TGF-beta) growth inhibitors, in promoting the biological activities of all-trans-retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2D3) was studied in NRP-152 cells, a nontumorigenic epithelial line derived from rat dorsal-lateral prostate. Tretinoin 159-161 Nrp Rattus norvegicus 228-231
8557772-5 1996 A monoclonal antibody against TGF-beta and TGF-beta 1 latency associated peptide (LAP), both of which neutralize all three TGF-beta isoforms, each block the ability of RA to inhibit growth of NRP-152 cells by > 95%. Tretinoin 168-170 Nrp Rattus norvegicus 192-195
8954724-6 1996 CNOT gene expression from young nodes was maintained in vivo, but required in vitro the addition of retinoic acid. Tretinoin 100-113 notochord homeobox Gallus gallus 0-4
8557772-7 1996 The ability of RA to upregulate fibronectin and thrombospondin expression in NRP-152 cells was also blocked by the monoclonal antibody. Tretinoin 15-17 Nrp Rattus norvegicus 77-80
8557780-4 1996 Treatment of UMR 201 cells with all-trans-retinoic acid which induces them to acquire a more differentiated phenotype, also led to a time-dependent decrease in PTHrP mRNA levels as determined by RT-PCR, Northern blot analysis, and in situ hybridization. Tretinoin 32-55 parathyroid hormone-like hormone Rattus norvegicus 160-165
8530518-9 1995 Here, we show that conformationally restricted RXR-specific retinoids, at doses that are per se inactive, are able to potentiate by up to one order of magnitude the pro-differentiating effects of all-trans retinoic acid and an RAR alpha-selective synthetic retinoid. Tretinoin 206-219 retinoid X receptor alpha Homo sapiens 47-50
8977160-9 1996 Treatment with retinoic acid led to a disappearance of cx31 in the choriocarcinoma. Tretinoin 15-28 gap junction protein, beta 3 Rattus norvegicus 55-59
8749832-8 1995 Class I ADH catalyzes the rate-limiting step in oxidation of retinol (ROH) to RA, and ethanol (ETOH) to acetic acid, thus establishing competition for ADH between ROH and ETOH. Tretinoin 78-80 aldo-keto reductase family 1 member A1 Homo sapiens 8-11
8749832-8 1995 Class I ADH catalyzes the rate-limiting step in oxidation of retinol (ROH) to RA, and ethanol (ETOH) to acetic acid, thus establishing competition for ADH between ROH and ETOH. Tretinoin 78-80 aldo-keto reductase family 1 member A1 Homo sapiens 151-154
8749832-12 1995 ADH binds ingested ETOH, thus deregulating RA homeostasis leading to improper RA signal transduction. Tretinoin 43-45 aldo-keto reductase family 1 member A1 Homo sapiens 0-3
9222608-0 1996 Transient accumulation, phosphorylation and changes in the oligomerization of Hsp27 during retinoic acid-induced differentiation of HL-60 cells: possible role in the control of cellular growth and differentiation. Tretinoin 91-104 heat shock protein family B (small) member 1 Homo sapiens 78-83
8749832-12 1995 ADH binds ingested ETOH, thus deregulating RA homeostasis leading to improper RA signal transduction. Tretinoin 78-80 aldo-keto reductase family 1 member A1 Homo sapiens 0-3
7588278-5 1995 Moreover, using rats of various retinoid status, we investigated whether the expression of target genes for vitamin A (RAR beta and CRBP-I) is regulated by retinoic acid (RA) in the adult rat tibia. Tretinoin 156-169 retinol binding protein 1 Rattus norvegicus 132-138
9222608-3 1996 We have examined the fate of Hsp27 transiently expressed during the retinoic acid (tRA)-induced granulocytic differentiation of human leukemic HL-60 cells. Tretinoin 68-81 heat shock protein family B (small) member 1 Homo sapiens 29-34
8943395-5 1996 Although all-trans-retinoic acid also induced CD38 expression on stimulated B and T cells, it was less effective than 1,25(OH)2D3. Tretinoin 9-32 CD38 molecule Homo sapiens 46-50
7493637-7 1995 RA also increased PKC enzymatic activity in intact cells as determined by phosphorylation of the PKC-specific endogenous substrate MARCKS. Tretinoin 0-2 myristoylated alanine rich protein kinase C substrate Mus musculus 131-137
7493637-8 1995 However, while RA induced a five- to eightfold increase in total cellular PKC alpha protein levels, it only increased MARCKS phosphorylation by twofold. Tretinoin 15-17 myristoylated alanine rich protein kinase C substrate Mus musculus 118-124
8946934-3 1996 RA stimulates the IL-3-induced growth by additionally recruiting quiescent stem and progenitor cells out of the G0/G1-phase and by increasing the cell cycle traverse rate. Tretinoin 0-2 interleukin 3 Homo sapiens 18-22
8666585-5 1995 The induction of the wild-type MCP-1 promoter construct by shear stress was attenuated by pretreating the cells with 1 microM dexamethasone or 1 microM retinoic acid 12 h before the shear stress experiments. Tretinoin 152-165 C-C motif chemokine 2 Bos taurus 31-36
8916959-5 1996 Similarly, interferons could act on APL cells, alone or in combination with all-trans retinoic acid (RA), especially if the PML/RAR alpha fusion transcript that results from the t(15; 17) is induced by interferon. Tretinoin 86-99 PML nuclear body scaffold Homo sapiens 124-137
7492559-1 1995 Cellular retinoic acid binding protein-I (CRABP-I) and cellular retinoic acid binding protein-II (CRABP-II) are highly homologous, 15 kDa proteins which bind all-trans-retinoic acid. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 55-96
7492559-1 1995 Cellular retinoic acid binding protein-I (CRABP-I) and cellular retinoic acid binding protein-II (CRABP-II) are highly homologous, 15 kDa proteins which bind all-trans-retinoic acid. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 98-106
7492559-10 1995 The pattern of intermolecular NOESY cross-peaks between 13C-labeled protons in the ring portion of retinoic acid and protein protons were different between CRABP-I and CRABP-II. Tretinoin 99-112 cellular retinoic acid binding protein 2 Homo sapiens 168-176
8916959-5 1996 Similarly, interferons could act on APL cells, alone or in combination with all-trans retinoic acid (RA), especially if the PML/RAR alpha fusion transcript that results from the t(15; 17) is induced by interferon. Tretinoin 101-103 PML nuclear body scaffold Homo sapiens 124-137
8950195-0 1996 Retinoic acid affects the expression rate of the differentiation-related genes aryl hydrocarbon receptor, ARNT and keratin 4 in proliferative keratinocytes only. Tretinoin 0-13 aryl hydrocarbon receptor nuclear translocator Homo sapiens 106-110
8950195-6 1996 When keratinocytes were continuously treated with 1 microM retinoic acid (RA), the upregulation of AhR- and ARNT-mRNA levels was inhibited as was keratin 4-expression, a marker of HaCaT-keratinocyte differentiation. Tretinoin 59-72 aryl hydrocarbon receptor nuclear translocator Homo sapiens 108-112
8950195-6 1996 When keratinocytes were continuously treated with 1 microM retinoic acid (RA), the upregulation of AhR- and ARNT-mRNA levels was inhibited as was keratin 4-expression, a marker of HaCaT-keratinocyte differentiation. Tretinoin 74-76 aryl hydrocarbon receptor nuclear translocator Homo sapiens 108-112
7499345-10 1995 These data indicate that short-chain dehydrogenases/reductase isozymes expressed tissue-distinctively catalyze the first step of retinoic acid biogenesis from the physiologically most abundant substrate, CRBP. Tretinoin 129-142 retinol binding protein 1 Rattus norvegicus 204-208
8950195-9 1996 Our data suggest that the regulation of AhR-, ARNT- and keratin 4-expression by RA is indirect and mediated by a yet to be identified factor. Tretinoin 80-82 aryl hydrocarbon receptor nuclear translocator Homo sapiens 46-50
8981396-2 1996 One antibody, Alz14A, specifically detected a 53 kDa protein in retinoic acid-treated P19 cells and mouse brain protein extracts consistent with the predicted PS-1 molecular weight. Tretinoin 64-77 presenilin 1 Mus musculus 159-163
7585519-0 1995 The H-ras oncogene interferes with retinoic acid signaling and metabolism in NIH3T3 cells. Tretinoin 35-48 Harvey rat sarcoma virus oncogene Mus musculus 4-9
7585519-3 1995 HPLC analysis of the media and cell extracts demonstrated that H-ras-transformed cells metabolize RA to a much lesser extent than control cells, resulting in a higher concentration of RA in H-ras cells. Tretinoin 98-100 Harvey rat sarcoma virus oncogene Mus musculus 63-68
7585519-3 1995 HPLC analysis of the media and cell extracts demonstrated that H-ras-transformed cells metabolize RA to a much lesser extent than control cells, resulting in a higher concentration of RA in H-ras cells. Tretinoin 98-100 Harvey rat sarcoma virus oncogene Mus musculus 190-195
8982867-1 1996 Rae1 alpha, Rae1 beta, and Rae1 gamma cDNAs isolated from retinoic acid-treated mouse embryonal carcinoma F9 cells encode cell surface proteins sharing partial homology with MHC class I molecules, and mRNAs corresponding to these cDNAs were detected exclusively in early mouse embryos, especially in the head region. Tretinoin 58-71 retinoic acid early transcript 1, alpha Mus musculus 0-10
7585519-3 1995 HPLC analysis of the media and cell extracts demonstrated that H-ras-transformed cells metabolize RA to a much lesser extent than control cells, resulting in a higher concentration of RA in H-ras cells. Tretinoin 184-186 Harvey rat sarcoma virus oncogene Mus musculus 63-68
7585519-3 1995 HPLC analysis of the media and cell extracts demonstrated that H-ras-transformed cells metabolize RA to a much lesser extent than control cells, resulting in a higher concentration of RA in H-ras cells. Tretinoin 184-186 Harvey rat sarcoma virus oncogene Mus musculus 190-195
7585519-6 1995 These data demonstrate that, even though H-ras-transformed cells accumulate up to 20 fold the concentration of RA as NIH-3T3 cells, they fail to show transglutaminase induction, suggesting that H-ras interferes with signal transduction by RA. Tretinoin 111-113 Harvey rat sarcoma virus oncogene Mus musculus 41-46
7585519-6 1995 These data demonstrate that, even though H-ras-transformed cells accumulate up to 20 fold the concentration of RA as NIH-3T3 cells, they fail to show transglutaminase induction, suggesting that H-ras interferes with signal transduction by RA. Tretinoin 111-113 Harvey rat sarcoma virus oncogene Mus musculus 194-199
7585519-6 1995 These data demonstrate that, even though H-ras-transformed cells accumulate up to 20 fold the concentration of RA as NIH-3T3 cells, they fail to show transglutaminase induction, suggesting that H-ras interferes with signal transduction by RA. Tretinoin 239-241 Harvey rat sarcoma virus oncogene Mus musculus 41-46
7545101-2 1995 GH receptor binding is positively modulated by a number of factors, including retinoic acid and dexamethasone, whereas fetal calf serum strongly decreases the binding. Tretinoin 78-91 growth hormone receptor Rattus norvegicus 0-11
7559803-9 1995 Treatment with the IGF-I receptor blocking antibody, alpha IR-3, restores RA-induced growth inhibition of IGF-I-treated or IGF-II-overexpressing MCF-7 cells, indicating that the IGF-I receptor is mediating these effects. Tretinoin 74-76 insulin like growth factor 1 receptor Homo sapiens 19-33
8982867-1 1996 Rae1 alpha, Rae1 beta, and Rae1 gamma cDNAs isolated from retinoic acid-treated mouse embryonal carcinoma F9 cells encode cell surface proteins sharing partial homology with MHC class I molecules, and mRNAs corresponding to these cDNAs were detected exclusively in early mouse embryos, especially in the head region. Tretinoin 58-71 retinoic acid early transcript beta Mus musculus 12-21
8930166-2 1996 The following agents inhibited phorbol 12-myristate 13-acetate-stimulated O2- generation significantly in the all-trans retinoic acid-treated HL-60 cells (expressed as percentage of control, P < .05): 1) PKC inhibitors: staurosporine (100 nM, 3 +/- 1%); Ro 31-8220 (1 microM, 3 +/- 2%); sphingosine (100 microM, 15 +/- 7%); 2) PSP 1 and 2a inhibitors, okadaic acid (10 microM, 35 +/- 1%); calyculin A (10 microM, 73 +/- 1%); 3) MAPK inhibitor: SB-203580 (100 microM, 62 +/- 1%); 4) PTP inhibitors: phenylarsine oxide (1 microM, 12 +/- 9%); diamide (1 mM, 21 +/- 11%); and 5) secretory phospholipase A2 inhibitors: manoalide (1 microM, 24 +/- 10%); scalaradial (1 microM, 11 +/- 4%). Tretinoin 120-133 paraspeckle component 1 Homo sapiens 330-342
7664289-0 1995 Stromelysin-3 is overexpressed by stromal elements in primary non-small cell lung cancers and regulated by retinoic acid in pulmonary fibroblasts. Tretinoin 107-120 matrix metallopeptidase 11 Homo sapiens 0-13
1315012-0 1992 Retinoic acid, bound to its nuclear receptor, enhances the expression of the gene for phosphoenolpyruvate carboxykinase. Tretinoin 0-13 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 86-119
1315012-3 1992 Retinoic acid, bound to its nuclear receptor, stimulates transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme in gluconeogenesis, by binding to a short element of the promoter region of the PEPCK gene. Tretinoin 0-13 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 87-120
1315012-3 1992 Retinoic acid, bound to its nuclear receptor, stimulates transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme in gluconeogenesis, by binding to a short element of the promoter region of the PEPCK gene. Tretinoin 0-13 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 122-127
1315012-3 1992 Retinoic acid, bound to its nuclear receptor, stimulates transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme in gluconeogenesis, by binding to a short element of the promoter region of the PEPCK gene. Tretinoin 0-13 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 235-240
7654186-0 1995 Retinoid receptors cause distortion of the retinoic acid response element in the phosphoenolpyruvate carboxykinase gene promoter. Tretinoin 43-56 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 81-114
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 30-43 retinoid X receptor alpha Homo sapiens 78-81
8906421-0 1996 Erythropoietin in mouse avascular yolk sacs is increased by retinoic acid. Tretinoin 60-73 erythropoietin Mus musculus 0-14
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 30-43 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 111-144
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 30-43 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 146-151
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 74-76 retinoid X receptor alpha Homo sapiens 78-81
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 74-76 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 111-144
7654186-2 1995 We have previously shown that retinoic acid receptor/retinoid X receptor (RAR/RXR) binds a DR1 RARE within the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter and is the trans-acting complex that mediates the retinoic acid (RA) response. Tretinoin 74-76 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 146-151
7654186-8 1995 The results of a phasing analysis demonstrated that RAR/RXR heterodimers did not induce a static DNA bend, in either the presence or the absence of RA. Tretinoin 52-54 retinoid X receptor alpha Homo sapiens 56-59
1309942-5 1992 t-RA may be converted to a more proximate ligand that directly binds and activates RXR alpha, and we have developed a method of nuclear receptor-dependent ligand trapping to test this hypothesis. Tretinoin 0-4 retinoid X receptor alpha Homo sapiens 83-92
1309942-6 1992 Here we report the identification of a stereoisomer of retinoic acid, 9-cis retinoic acid, which directly binds and activates RXR alpha. Tretinoin 55-68 retinoid X receptor alpha Homo sapiens 126-135
7654186-9 1995 A cyclization kinetics assay was employed to show that RAR/RXR binding affected DNA ring closure in a phase-sensitive, RA-insensitive, manner. Tretinoin 55-57 retinoid X receptor alpha Homo sapiens 59-62
8906421-14 1996 EPO and EPR appear to be synthesized in the endodermal cells of the VYSs that are likely to respond to the circumstances induced by RA. Tretinoin 132-134 erythropoietin Mus musculus 0-3
8574944-1 1995 The effects of retinoic acid (RA), and calcitriol are mediated by specific nuclear receptors (RARs and VDR, respectively). Tretinoin 15-28 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 103-106
8574944-1 1995 The effects of retinoic acid (RA), and calcitriol are mediated by specific nuclear receptors (RARs and VDR, respectively). Tretinoin 30-32 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 103-106
8574944-5 1995 At threshold concentrations (1 nM) both 9-cis RA and at-RA markedly inhibited the resorption induced by calcitriol (1 pM). Tretinoin 46-48 retinol dehydrogenase 5 Mus musculus 40-45
1363722-0 1992 Xenopus Hox-2 genes are expressed sequentially after the onset of gastrulation and are differentially inducible by retinoic acid. Tretinoin 115-128 homeobox B7 S homeolog Xenopus laevis 8-13
1363722-1 1992 In this paper, we review experiments to characterise the developmental expression and the responses to all-trans retinoic acid (RA) of six members of the Hox-2 complex of homeobox-containing genes, during the early development of Xenopus laevis. Tretinoin 113-126 homeobox B7 S homeolog Xenopus laevis 154-159
1363722-1 1992 In this paper, we review experiments to characterise the developmental expression and the responses to all-trans retinoic acid (RA) of six members of the Hox-2 complex of homeobox-containing genes, during the early development of Xenopus laevis. Tretinoin 128-130 homeobox B7 S homeolog Xenopus laevis 154-159
7556191-7 1995 Exposure of HUVEC to 1 microM retinoic acid or the retinobenzoic acid, Ch55, led to the induction of the two RAR-beta mRNAs, RXR-alpha mRNA and CRBP-I mRNA, whereas the expression of the other receptor and CRABP-I transcripts did not change appreciably. Tretinoin 30-43 retinoid X receptor alpha Homo sapiens 125-134
8794365-4 1996 Although several chimeric proteins activated both RAR and RXR target genes, fusion of the NT16 transactivation domain to the N terminus of RAR permitted specific activation of reporter genes containing retinoic acid response elements. Tretinoin 202-215 retinoic acid receptor alpha Homo sapiens 139-142
7489817-0 1995 Differential regulation of AP1 activity by retinoic acid in hormone-dependent and -independent breast cancer cells. Tretinoin 43-56 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-30
7489817-5 1995 AP1 overexpression abrogated RA repression in MCF7 cells. Tretinoin 29-31 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-3
1371335-5 1992 Release of the differentiation block in the ras-transformed 32DC13(G) cells by co-treatment with retinoic acid and G-CSF partially restored the normal c-fos and c-jun mRNA induction pattern, suggesting that the proper activation of these genes may be important for myeloid differentiation. Tretinoin 97-110 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 151-156
1371335-5 1992 Release of the differentiation block in the ras-transformed 32DC13(G) cells by co-treatment with retinoic acid and G-CSF partially restored the normal c-fos and c-jun mRNA induction pattern, suggesting that the proper activation of these genes may be important for myeloid differentiation. Tretinoin 97-110 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-166
1764077-0 1991 Altered response to growth factors or retinoic acid in phenotypic transformation of normal rat kidney cells expressing human c-fos gene. Tretinoin 38-51 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 125-130
8794365-7 1996 These observations support the existence of two distinct retinoid signalling pathways predicted on the basis of biochemical and pharmacologic studies and provide direct evidence that the programs of differentiation elicited by retinoic acid in these cells are mediated by a specific subset of binding sites for RAR-RXR heterodimers. Tretinoin 227-240 retinoic acid receptor alpha Homo sapiens 311-314
1764077-8 1991 Expression of the human c-fos gene may compensate the signal to phenotypic transformation induced by TGF beta as well as retinoic acid or PDGF or bFGF. Tretinoin 121-134 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-29
8795626-0 1996 Retinoic acid stimulates alpha-CAMKII gene expression in PC12 cells at a distinct transcription initiation site. Tretinoin 0-13 calcium/calmodulin-dependent protein kinase II alpha Mus musculus 25-37
1662118-2 1991 A strategy of sequential screening of expression libraries with a retinoic acid response element and RAR identified a cDNA encoding a coregulator highly related to RXR alpha. Tretinoin 66-79 retinoid X receptor alpha Homo sapiens 164-173
1839359-2 1991 Here we show that treatment of two human neuroblastoma cell lines, SY5Y and IMR32, with RA resulted in a fivefold increase of the integrin alpha 1/beta 1 expression. Tretinoin 88-90 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 147-153
8541212-8 1995 Treatment of zebrafish embryos with retinoic acid affects the svp[40] step gradient and causes an elimination of a regional expression domain in the retina. Tretinoin 36-49 nuclear receptor subfamily 2, group F, member 2 Danio rerio 62-68
7501302-4 1995 Comparison of the partial nucleotide sequences of these clones with sequences in DNA databases indicated that one of these clones was identical to a region of the mouse Oct-3 gene, which has been shown to be dramatically repressed by RA. Tretinoin 234-236 POU domain, class 5, transcription factor 1 Mus musculus 169-174
8795626-4 1996 RA increased the level of endogenous alpha-CaMKII mRNA in untransfected PC12 cells by 4.4-fold. Tretinoin 0-2 calcium/calmodulin-dependent protein kinase II alpha Mus musculus 37-49
1839359-9 1991 These data show that RA, a naturally occurring morphogen implicated in embryonic development, can selectively regulate the expression of integrin complexes in neuronal cells and suggest an important role of the alpha 1/beta 1 laminin receptor in the morphological differentiation of nerve cells. Tretinoin 21-23 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 219-225
8948123-0 1996 Retinoic acid: identification of specific receptors through which it may mediate transcriptional regulation of fibronectin gene in bovine lens epithelial cells. Tretinoin 0-13 fibronectin 1 Bos taurus 111-122
1657967-0 1991 Identification of a retinoic acid response element in the human oxytocin promoter. Tretinoin 20-33 oxytocin/neurophysin I prepropeptide Homo sapiens 64-72
1657967-13 1991 Our studies constitute the first report of a RARE in a neuropeptide gene and define a mechanism by which OT gene expression can be modulated by retinoic acid. Tretinoin 144-157 oxytocin/neurophysin I prepropeptide Homo sapiens 105-107
7638203-2 1995 RA at physiological concentrations suppresses the increase in cell size and induction of a genetic marker for hypertrophy, the atrial natriuretic factor (ANF) gene. Tretinoin 0-2 natriuretic peptide A Rattus norvegicus 127-152
7638203-2 1995 RA at physiological concentrations suppresses the increase in cell size and induction of a genetic marker for hypertrophy, the atrial natriuretic factor (ANF) gene. Tretinoin 0-2 natriuretic peptide A Rattus norvegicus 154-157
8948123-1 1996 To elucidate in detail the regulatory mechanisms by which the fibronectin mRNA and protein are altered by all-trans retinoic acid (RA) in bovine lens epithelial (LE) cells, we have investigated the transcription mechanism and the occurrence of nuclear receptors for RA in the nuclei of cultured LE cells. Tretinoin 116-129 fibronectin 1 Bos taurus 62-73
1668276-2 1991 There are three known types of nuclear receptors for RA in mammals, RAR-alpha, RAR-beta and RAR-gamma, which transduce the RA signal by inducing or repressing the transcription of target genes. Tretinoin 53-55 retinoic acid receptor, alpha Mus musculus 68-77
1668276-2 1991 There are three known types of nuclear receptors for RA in mammals, RAR-alpha, RAR-beta and RAR-gamma, which transduce the RA signal by inducing or repressing the transcription of target genes. Tretinoin 53-55 retinoic acid receptor, gamma Mus musculus 92-101
7615548-2 1995 These processes correlate with expression of the retinoic acid receptor (RAR) beta gene, which is induced through a retinoic acid response element (beta RARE). Tretinoin 49-62 retinoic acid receptor, alpha Mus musculus 73-76
8948123-1 1996 To elucidate in detail the regulatory mechanisms by which the fibronectin mRNA and protein are altered by all-trans retinoic acid (RA) in bovine lens epithelial (LE) cells, we have investigated the transcription mechanism and the occurrence of nuclear receptors for RA in the nuclei of cultured LE cells. Tretinoin 131-133 fibronectin 1 Bos taurus 62-73
7628539-11 1995 In order to further define molecules important in regulating the response of senescent dermal fibroblasts to retinoids, we demonstrate here that retinoic acid induces CRABP-II messenger RNA in human dermal fibroblasts in a dose-dependent manner. Tretinoin 145-158 cellular retinoic acid binding protein 2 Homo sapiens 167-175
8875079-0 1996 Expression of the beta 4 integrin subunit in the mouse heart during embryonic development: retinoic acid advances beta 4 expression. Tretinoin 91-104 basic helix-loop-helix family, member e23 Mus musculus 18-24
7628539-16 1995 Taken together, these data suggest that retinoic acid plays a central role in the regulation of CRABP-II gene expression in the dermal fibroblast and that this molecule is the major mediator of the cytoplasmic effects of retinoids in dermal fibroblasts. Tretinoin 40-53 cellular retinoic acid binding protein 2 Homo sapiens 96-104
7790389-3 1995 Therefore, the mechanistic aspects of TIMP-1 regulation by retinoic acid in primary cultures of rat calvarial bone cell populations were studied and compared with those of TGF-beta 1 to determine if modulation of TIMP-1 would augment MMP expression. Tretinoin 59-72 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 38-44
1685987-0 1991 Chicken homeobox gene Msx-1: structure, expression in limb buds and effect of retinoic acid. Tretinoin 78-91 msh homeobox 1 Gallus gallus 22-27
1685987-11 1991 This indicates that retinoic acid alters the marginal presumptive non-cartilage forming mesenchyme cell lineage through suppression of Msx-1 expression. Tretinoin 20-33 msh homeobox 1 Gallus gallus 135-140
7790389-4 1995 Retinoic acid was found to reduce TIMP-1 mRNA levels after 24 and 72 hr of culture by up to 60% in a dose-dependent manner. Tretinoin 0-13 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 34-40
8875079-0 1996 Expression of the beta 4 integrin subunit in the mouse heart during embryonic development: retinoic acid advances beta 4 expression. Tretinoin 91-104 basic helix-loop-helix family, member e23 Mus musculus 114-120
7790389-6 1995 TIMP-1 mRNA had a half life of approximately 14 hr and this was unaltered by retinoic acid treatment, suggesting that retinoic acid exerts its effects on TIMP-1 transcriptionally. Tretinoin 118-131 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 0-6
7790389-6 1995 TIMP-1 mRNA had a half life of approximately 14 hr and this was unaltered by retinoic acid treatment, suggesting that retinoic acid exerts its effects on TIMP-1 transcriptionally. Tretinoin 118-131 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 154-160
1680399-0 1991 Regulation by retinoic acid of ICAM-1 expression on human tumor cell lines. Tretinoin 14-27 intercellular adhesion molecule 1 Homo sapiens 31-37
1680399-1 1991 In a group of four human tumor cell lines comprising one melanoma, one glioma, one teratocarcinoma and one neuroblastoma, the expression of the intercellular adhesion molecule-1 (ICAM-1) was found to be significantly increased following treatment with 10 microM of all-trans retinoic acid. Tretinoin 275-288 intercellular adhesion molecule 1 Homo sapiens 144-177
7790389-7 1995 When retinoic acid was added to cycloheximide-treated cultures TIMP-1 mRNA levels were reduced at 5 hr compared with controls. Tretinoin 5-18 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 63-69
8952164-2 1996 APL is characterized by three distinct and unique features: i) accumulation in the bone marrow of tumor cells with promyelocytic features; ii) invariable association with specific translocations which always involve chromosome 17 and the retinoic acid receptor alpha (RAR alpha) locus; iii) exquisite sensitivity of APL blasts to the differentiating action of retinoic acid (RA). Tretinoin 238-251 retinoic acid receptor alpha Homo sapiens 268-277
7790389-8 1995 This showed that ongoing protein synthesis was not required to mediate the retinoic acid repression of TIMP-1 mRNA levels and supports the evidence that retinoic acid acts at the transcriptional level to reduce TIMP-1 expression. Tretinoin 153-166 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 211-217
7790389-10 1995 Thus, these studies have revealed that TIMP-1 regulation by retinoic acid is different in osteoblasts from other cells and that retinoic acid has the property of generating resorptive and formative cell phenotypes in a tissue-specific manner. Tretinoin 60-73 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 39-45
7790389-10 1995 Thus, these studies have revealed that TIMP-1 regulation by retinoic acid is different in osteoblasts from other cells and that retinoic acid has the property of generating resorptive and formative cell phenotypes in a tissue-specific manner. Tretinoin 128-141 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 39-45
1680399-1 1991 In a group of four human tumor cell lines comprising one melanoma, one glioma, one teratocarcinoma and one neuroblastoma, the expression of the intercellular adhesion molecule-1 (ICAM-1) was found to be significantly increased following treatment with 10 microM of all-trans retinoic acid. Tretinoin 275-288 intercellular adhesion molecule 1 Homo sapiens 179-185
1680399-5 1991 Retinoic acid induced ICAM-1 expression in greater than 80% of the cells and increased the levels of expression by 2.5 to 3-fold. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 22-28
1680399-6 1991 Immunoprecipitation studies in biosynthetically labeled cells as well as RNase protection analysis confirmed that retinoic acid treatment increased the amount of ICAM-1 at both the protein and mRNA level. Tretinoin 114-127 intercellular adhesion molecule 1 Homo sapiens 162-168
7794283-6 1995 Retinoic acid and thyroid hormones increased AM production to 400% and 150% after 14 h incubation. Tretinoin 0-13 adrenomedullin Rattus norvegicus 45-47
8952164-2 1996 APL is characterized by three distinct and unique features: i) accumulation in the bone marrow of tumor cells with promyelocytic features; ii) invariable association with specific translocations which always involve chromosome 17 and the retinoic acid receptor alpha (RAR alpha) locus; iii) exquisite sensitivity of APL blasts to the differentiating action of retinoic acid (RA). Tretinoin 268-270 retinoic acid receptor alpha Homo sapiens 238-266
1682132-5 1991 Treatment with RA caused a concentration-dependent change in the pattern of expression of Xhox3 and serotonin and resulted in the ectopic appearance of immunoreactive neurons in anterior regions of the CNS, including the forebrain. Tretinoin 15-17 even-skipped homeobox 1 L homeolog Xenopus laevis 90-95
8882165-0 1996 Growth hormone binds to a single high affinity receptor site on mouse osteoblasts: modulation by retinoic acid and cell differentiation. Tretinoin 97-110 growth hormone Mus musculus 0-14
1649749-3 1991 Treatment with retinoic acid decreased GAG synthesis in cultured chondrocytes and the number of PTH receptors, measured by binding of [125I]-[Nle8,18,Tyr34]bovine PTH-(1-34) amide to the cells. Tretinoin 15-28 parathyroid hormone Bos taurus 96-99
1855468-0 1991 Opposing effects of retinoic acid and dexamethasone on cellular retinol-binding protein ribonucleic acid levels in the rat. Tretinoin 20-33 retinol binding protein 1 Rattus norvegicus 55-87
7769256-8 1995 Addition of 10(-7) M retinoic acid to cultured differentiating keratinocytes significantly down-regulated the expression of SPRR2 and SPRR3 transcripts and slightly decreased that of SPRR1. Tretinoin 21-34 small proline rich protein 3 Homo sapiens 134-139
7745731-2 1995 Physiological responses to retinoic acid involve two distinct subfamilies of nuclear receptors, the RA receptors (RARs) and retinoid X receptors (RXRs), which function by activating transcription as heterodimeric or RXR homodimeric complexes from cis-acting DNA response elements. Tretinoin 27-40 retinoid X receptor alpha Homo sapiens 146-149
1855468-5 1991 Retinoic acid administration increased the amount of lung CRBP mRNA only, whereas dexamethasone decreased both lung and liver CRBP mRNA abundance. Tretinoin 0-13 retinol binding protein 1 Rattus norvegicus 58-62
8827086-8 1996 Further comparative studies indicate that upregulation of PSA is common to various differentiation inducers, including all-trans-retinoic acid, 1,25-dihydroxyvitamin D3, and butyrate but is not induced by other antitumor agents of clinical interest such as suramin. Tretinoin 119-142 kallikrein related peptidase 3 Homo sapiens 58-61
1855468-6 1991 In animals treated with both retinoic acid and dexamethasone, CRBP mRNA abundance was also reduced. Tretinoin 29-42 retinol binding protein 1 Rattus norvegicus 62-66
1855468-7 1991 We conclude that CRBP gene expression can be modulated by both retinoic acid and dexamethasone in the vitamin A-sufficient animal. Tretinoin 63-76 retinol binding protein 1 Rattus norvegicus 17-21
7609647-5 1995 Indirect immunofluorescent staining showed that in RA-treated, morphologically differentiated P19 cells NF-66 was expressed in neuron-like cells characterized by phase bright cell bodies and long neuritic processes. Tretinoin 51-53 internexin neuronal intermediate filament protein alpha Homo sapiens 104-109
8753812-2 1996 G-CSF protein was neither produced during PMA-induced differentiation nor in response to retinoic acid (RA) alone. Tretinoin 89-102 colony stimulating factor 3 Homo sapiens 0-5
2059629-10 1991 The Vmax for retinal formation from holo-CRBP was 14-17 pmol min-1 (mg of protein)-1, a rate sufficiently high to generate adequate retinal to contribute significantly to retinoic acid synthesis. Tretinoin 171-184 retinol binding protein 1 Rattus norvegicus 41-45
8753812-2 1996 G-CSF protein was neither produced during PMA-induced differentiation nor in response to retinoic acid (RA) alone. Tretinoin 104-106 colony stimulating factor 3 Homo sapiens 0-5
8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 colony stimulating factor 3 Homo sapiens 50-55
7729586-0 1995 Anteriorization of CRABP-I expression by retinoic acid in the developing mouse central nervous system and its relationship to teratogenesis. Tretinoin 41-54 cellular retinoic acid binding protein I Mus musculus 19-26
7729586-2 1995 Since the central nervous system (CNS) represents a major site of the teratogenic action of retinoic acid (RA), we have also determined the effects of exposure of high levels of RA on CRABP-I expression within the CNS. Tretinoin 178-180 cellular retinoic acid binding protein I Mus musculus 184-191
8753812-4 1996 The synergistic interaction between PMA and RA on G-CSF production appeared to be mediated primarily through production of interleukin-1 beta (IL-1 beta) since neutralization of IL-1 beta activity inhibited about 80% of G-CSF production. Tretinoin 44-46 colony stimulating factor 3 Homo sapiens 220-225
8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 67-69 colony stimulating factor 3 Homo sapiens 83-88
2049087-6 1991 Neurotrophic activity of retinoic acid may be mediated by MK. Tretinoin 25-38 midkine Rattus norvegicus 58-60
8753812-5 1996 It has been previously reported that IL-1 potently synergizes with RA to stimulate G-CSF production by THP-1 cells pretreated with PMA Using synthetic ligands to RA receptors (RAR) and retinoid X receptors (RXR) that selectively bind and activate RAR-RXR and RXR-RXR dimers respectively, we showed that the ability of RA to synergize with IL-1 was signaled through RAR-RXR heterodimer pathway. Tretinoin 162-164 colony stimulating factor 3 Homo sapiens 83-88
7876220-1 1995 Cellular retinoic acid-binding protein type II (CRABP-II) is one of two small molecular weight, cytosolic proteins which specifically bind retinoic acid (RA). Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 48-56
8753812-6 1996 Finally, we demonstrated that RA can also enhance IL-1-induced G-CSF production in primary monocytes of human peripheral blood. Tretinoin 30-32 colony stimulating factor 3 Homo sapiens 63-68
7876220-1 1995 Cellular retinoic acid-binding protein type II (CRABP-II) is one of two small molecular weight, cytosolic proteins which specifically bind retinoic acid (RA). Tretinoin 49-51 cellular retinoic acid binding protein 2 Homo sapiens 0-46
8874749-0 1996 Topical tretinoin increases dermal mast cells, induces epidermal mast cell growth factor (c-kit ligand) and modulates its distribution in hairless mice. Tretinoin 8-17 kit ligand Mus musculus 65-88
7876220-7 1995 Taken together these data demonstrate that Arg132 is a critical amino acid residue for the binding of RA by CRABP-II. Tretinoin 102-104 cellular retinoic acid binding protein 2 Homo sapiens 108-116
7532580-5 1995 Treatment with retinoic acid (RA, 100 nM) increased medium concentrations of IGFBP-3 to 175 +/- 8% (mean +/- SE, n = 4), and IGFBP-6 to 217 +/- 20% of control values. Tretinoin 30-32 insulin like growth factor binding protein 6 Homo sapiens 125-132
7532580-8 1995 IGFBP-6 increased 12-fold with RA + forskolin and 20-fold with RA + dbcAMP. Tretinoin 31-33 insulin like growth factor binding protein 6 Homo sapiens 0-7
7532580-8 1995 IGFBP-6 increased 12-fold with RA + forskolin and 20-fold with RA + dbcAMP. Tretinoin 63-65 insulin like growth factor binding protein 6 Homo sapiens 0-7
1673925-5 1991 LFB3 expression starts before that of LFB1 during mouse and rat development, and is strongly increased upon retinoic acid induced differentiation of F9 embryonic carcinoma cells. Tretinoin 108-121 HNF1 homeobox B Mus musculus 0-4
1645738-5 1991 RA also caused a rapid increase in the expression of the early response gene, c-fos, but did not effect the expression of egr-1. Tretinoin 0-2 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 78-83
7532580-10 1995 The stimulatory effect of RA + forskolin on IGFBP-3 was partially reversed by estrogen, whereas RA + forskolin-stimulated IGFBP-6 levels were further increased by estrogen. Tretinoin 96-98 insulin like growth factor binding protein 6 Homo sapiens 122-129
8874749-0 1996 Topical tretinoin increases dermal mast cells, induces epidermal mast cell growth factor (c-kit ligand) and modulates its distribution in hairless mice. Tretinoin 8-17 kit ligand Mus musculus 90-102
7823950-4 1995 The absence of RAR alpha is associated with a reduction in the RA-induced expression of both the CRABP-II and Hoxb-1 (formerly 2.9) genes. Tretinoin 15-17 cellular retinoic acid binding protein 2 Homo sapiens 97-105
1680379-4 1991 Pem mRNA is induced 35-fold in ES cells differentiated in the absence of retinoic acid. Tretinoin 73-86 reproductive homeobox 5 Mus musculus 0-3
1673698-7 1991 Increased numbers of CD4+ T cells accompanied by prominence of dermal dendrocytes in the papillary dermis and focal keratinocyte expression of intercellular adhesion molecule-1 were observed in retinoic acid-treated biopsies. Tretinoin 194-207 intercellular adhesion molecule 1 Homo sapiens 143-176
8874749-13 1996 These findings show that topical tretinoin can induce epidermal MGF along with an associated mast cell hyperplasia. Tretinoin 33-42 kit ligand Mus musculus 64-67
7822324-9 1995 Plasma all-trans-retinoic acid levels for the TTR- mice were 2.3-fold higher than those of wild type (425 versus 190 ng/dl). Tretinoin 7-30 transthyretin Mus musculus 46-49
8816844-7 1996 RA treatment increased the levels of the three RAR mRNAs in most of the cell lines but had no effect on the RXR mRNAs. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 47-50
7645423-13 1995 Also, Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced TGF-beta 1 and TGF-beta 2 expression about 3- and 50-fold, respectively. Tretinoin 79-81 transforming growth factor beta 2 Homo sapiens 115-125
1826464-2 1991 TH1 clones are very sensitive to ATRA-mediated inhibition of DNA synthesis while TH2 clones are very resistant, but both TH1 and TH2 clones show significant down-modulation of surface transferrin receptors after ATRA exposure. Tretinoin 33-37 negative elongation factor complex member C/D Homo sapiens 0-3
1826464-2 1991 TH1 clones are very sensitive to ATRA-mediated inhibition of DNA synthesis while TH2 clones are very resistant, but both TH1 and TH2 clones show significant down-modulation of surface transferrin receptors after ATRA exposure. Tretinoin 212-216 negative elongation factor complex member C/D Homo sapiens 0-3
1826464-2 1991 TH1 clones are very sensitive to ATRA-mediated inhibition of DNA synthesis while TH2 clones are very resistant, but both TH1 and TH2 clones show significant down-modulation of surface transferrin receptors after ATRA exposure. Tretinoin 212-216 negative elongation factor complex member C/D Homo sapiens 121-124
8801163-2 1996 Recently this leukemia was further characterized by an exquisite sensitivity to all-trans retinoic acid"s differentiation effect and the production of a fusion gene altering the gene of RARalpha and a novel gene PML. Tretinoin 90-103 retinoic acid receptor alpha Homo sapiens 186-194
2030332-5 1991 However, RA increased the magnitude of PTH-rP-stimulated changes in Ca2+i without affecting the concentration required for a maximal response. Tretinoin 9-11 parathyroid hormone-like hormone Rattus norvegicus 39-45
8777434-5 1995 All trans-retinoic acid (RA) abolished the transformation of the 43C line and TPA-treated RELcJ1 cells, suggesting that RA could decrease AP1 activity in these cells despite c-fos or c-jun overexpression. Tretinoin 4-23 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 174-179
7851664-0 1995 Developmental regulation of Fos-protein during proliferative growth of the otic vesicle and its relation to differentiation induced by retinoic acid. Tretinoin 135-148 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-31
8774352-6 1996 In contrast to the stimulatory effect of GM-CSF, hydrocortisone, dexamethasone or all-trans-retinoic acid at 1 x 10(-7) to 1 x 10(-5) M inhibited the constitutive expression of activin A and greatly suppressed the GM-CSF-stimulated production. Tretinoin 82-105 colony stimulating factor 2 Homo sapiens 214-220
7851664-7 1995 Fos was readily induced by mitogens like serum and bombesin and this induction was inhibited by 25 nM retinoic acid, an inhibitor of cell proliferation in the otic vesicle.c-fos antisense oligonucleotides inhibited growth in the otic vesicle in parallel with a reduction in Fos expression. Tretinoin 102-115 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-3
7851664-7 1995 Fos was readily induced by mitogens like serum and bombesin and this induction was inhibited by 25 nM retinoic acid, an inhibitor of cell proliferation in the otic vesicle.c-fos antisense oligonucleotides inhibited growth in the otic vesicle in parallel with a reduction in Fos expression. Tretinoin 102-115 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177
7851664-7 1995 Fos was readily induced by mitogens like serum and bombesin and this induction was inhibited by 25 nM retinoic acid, an inhibitor of cell proliferation in the otic vesicle.c-fos antisense oligonucleotides inhibited growth in the otic vesicle in parallel with a reduction in Fos expression. Tretinoin 102-115 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 274-277
7706939-3 1995 Northern blot analysis revealed that retinoic acid is a potent inducer of CRBP mRNA, causing a 7.5-fold rise in mRNA levels in primary adipocytes and a 9.5-fold rise in BFC-1 beta adipocytes. Tretinoin 37-50 retinol binding protein 1 Rattus norvegicus 74-78
2002849-0 1991 Conversion by retinoic acid of anterior cells into ZPA cells in the chick wing bud. Tretinoin 14-27 zona pellucida glycoprotein 2 Gallus gallus 51-54
2002849-2 1991 When RA is applied to the anterior of the chick wing bud, a mirror-image duplication of the limb pattern develops that is identical to the pattern resulting from grafts of posterior tissue (zone of polarizing activity, or ZPA). Tretinoin 5-7 zona pellucida glycoprotein 2 Gallus gallus 222-225
2002849-4 1991 The ZPA-mimicking action of RA has led to the hypothesis that exogenously applied RA acts by providing graded spatial information across the anterior-posterior limb axis. Tretinoin 28-30 zona pellucida glycoprotein 2 Gallus gallus 4-7
2002849-4 1991 The ZPA-mimicking action of RA has led to the hypothesis that exogenously applied RA acts by providing graded spatial information across the anterior-posterior limb axis. Tretinoin 82-84 zona pellucida glycoprotein 2 Gallus gallus 4-7
2002849-6 1991 A hybrid interpretation has also been suggested whereby ZPA cells are formed in response to RA exposure and then begin to release retinoids that act as graded spatial cues. Tretinoin 92-94 zona pellucida glycoprotein 2 Gallus gallus 56-59
2002849-8 1991 The results of our studies indicate that the action of RA is to change anterior cells into ZPA cells. Tretinoin 55-57 zona pellucida glycoprotein 2 Gallus gallus 91-94
7706939-4 1995 This induction of CRBP mRNA was dose-dependent at retinoic acid concentrations ranging between 10(-8) and 10(-5) M. Retinoic acid induction of CRBP mRNA levels showed a short lag period (6 h) and reached a maximal level of induction by 12 h in BFC-1 beta adipocytes and by 48 h in primary epididymal adipocytes. Tretinoin 50-63 retinol binding protein 1 Rattus norvegicus 18-22
7706939-4 1995 This induction of CRBP mRNA was dose-dependent at retinoic acid concentrations ranging between 10(-8) and 10(-5) M. Retinoic acid induction of CRBP mRNA levels showed a short lag period (6 h) and reached a maximal level of induction by 12 h in BFC-1 beta adipocytes and by 48 h in primary epididymal adipocytes. Tretinoin 50-63 retinol binding protein 1 Rattus norvegicus 143-147
7706939-4 1995 This induction of CRBP mRNA was dose-dependent at retinoic acid concentrations ranging between 10(-8) and 10(-5) M. Retinoic acid induction of CRBP mRNA levels showed a short lag period (6 h) and reached a maximal level of induction by 12 h in BFC-1 beta adipocytes and by 48 h in primary epididymal adipocytes. Tretinoin 116-129 retinol binding protein 1 Rattus norvegicus 18-22
7706939-4 1995 This induction of CRBP mRNA was dose-dependent at retinoic acid concentrations ranging between 10(-8) and 10(-5) M. Retinoic acid induction of CRBP mRNA levels showed a short lag period (6 h) and reached a maximal level of induction by 12 h in BFC-1 beta adipocytes and by 48 h in primary epididymal adipocytes. Tretinoin 116-129 retinol binding protein 1 Rattus norvegicus 143-147
7706939-5 1995 Nuclear run-on transcription assays of retinoic acid-induced BFC-1 beta adipocytes indicated that the rate of CRBP gene transcription is enhanced 3.6- to 4.3-fold by retinoic acid. Tretinoin 39-52 retinol binding protein 1 Rattus norvegicus 110-114
7706939-5 1995 Nuclear run-on transcription assays of retinoic acid-induced BFC-1 beta adipocytes indicated that the rate of CRBP gene transcription is enhanced 3.6- to 4.3-fold by retinoic acid. Tretinoin 166-179 retinol binding protein 1 Rattus norvegicus 110-114
1650576-7 1991 These results clearly show that RAR alpha and RAR gamma 1 can transactivate the RAR beta gene; that RAR beta can stimulate its own expression and that resistance to RA in RAC65 cells is probably due to the altered RAR alpha transcript present in these cells. Tretinoin 32-34 retinoic acid receptor, alpha Mus musculus 214-223
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 235-248 aldo-keto reductase family 1 member A1 Homo sapiens 83-86
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 235-248 aldo-keto reductase family 1 member A1 Homo sapiens 172-175
1996113-8 1991 Since ADH catalyzes the conversion of retinol to retinal, which can be further converted to retinoic acid by aldehyde dehydrogenase, these results suggest that retinoic acid activation of ADH3 constitutes a positive feedback loop regulating retinoic acid synthesis. Tretinoin 92-105 aldo-keto reductase family 1 member A1 Homo sapiens 6-9
1996113-8 1991 Since ADH catalyzes the conversion of retinol to retinal, which can be further converted to retinoic acid by aldehyde dehydrogenase, these results suggest that retinoic acid activation of ADH3 constitutes a positive feedback loop regulating retinoic acid synthesis. Tretinoin 160-173 aldo-keto reductase family 1 member A1 Homo sapiens 6-9
7719237-7 1995 Finally, the relative resistance to ATRA of NB4.306 and NB4.007/6 was evaluated by comparing the phenotypic (CD11b) changes induced by ATRA in these two lines with those induced in the parental, ATRA-sensitive, NB4 cell line. Tretinoin 135-139 integrin subunit alpha M Homo sapiens 109-114
8684004-2 1996 Detection of the PML/RARalpha fusion gene in APL blasts is critical to start promptly the specific therapy with all-trans retinoic acid (ATRA). Tretinoin 112-135 PML nuclear body scaffold Homo sapiens 17-20
7746099-2 1995 The present study was performed to examine the effect of RA on osteoclast-like cell formation in the presence or absence of osteoblasts and to study whether RA would affect osteopontin mRNA expression in isolated rabbit osteoclasts. Tretinoin 157-159 osteopontin Oryctolagus cuniculus 173-184
7746099-4 1995 Also, RA caused a stimulation of osteoclast-like cell formation from hemopoietic blast cells supported by granulocyte macrophage-colony stimulating factor (GM-CSF) in mouse spleen cell cultures. Tretinoin 6-8 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 106-154
7746099-4 1995 Also, RA caused a stimulation of osteoclast-like cell formation from hemopoietic blast cells supported by granulocyte macrophage-colony stimulating factor (GM-CSF) in mouse spleen cell cultures. Tretinoin 6-8 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 156-162
7746099-5 1995 However, RA did not affect blast cell number in these cultures and significantly inhibited GM-CSF-stimulated proliferation of hemopoietic blast cells. Tretinoin 9-11 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 91-97
7746099-7 1995 Moreover, RA caused a stimulation of osteopontin mRNA expression in isolated rabbit osteoclasts. Tretinoin 10-12 osteopontin Oryctolagus cuniculus 37-48
7746099-8 1995 The present study demonstrated for the first time that RA stimulated osteoclast-like cell formation, presumably through directly acting on the hemopoietic blast cells, and that RA stimulated osteopontin mRNA expression in isolated rabbit osteoclasts. Tretinoin 177-179 osteopontin Oryctolagus cuniculus 191-202
1846397-0 1991 Retinoic acid regulates thymosin beta 10 levels in rat neuroblastoma cells. Tretinoin 0-13 thymosin, beta 10 Rattus norvegicus 24-40
1846397-6 1991 In several neuroblastomas, including the B103 and B104 lines, retinoic acid elicits a time- and dose-dependent increase in the content of thymosin beta 10, but not that of thymosin beta 4. Tretinoin 62-75 thymosin, beta 10 Rattus norvegicus 138-154
1846598-6 1991 Interestingly, the expression of mRAR-alpha 2, in contrast to that of the mRAR-alpha 1 isoform, was induced by retinoic acid (RA) in EC cells, thus suggesting the presence of two promoters in the 5" region of the mRAR-alpha gene, which differ in their response to RA. Tretinoin 111-124 retinoic acid receptor, alpha Mus musculus 33-43
8684004-2 1996 Detection of the PML/RARalpha fusion gene in APL blasts is critical to start promptly the specific therapy with all-trans retinoic acid (ATRA). Tretinoin 112-135 retinoic acid receptor alpha Homo sapiens 21-29
7748789-0 1995 c-otx2 is expressed in two different phases of gastrulation and is sensitive to retinoic acid treatment in chick embryo. Tretinoin 80-93 orthodenticle homeobox 2 Gallus gallus 2-6
8684004-2 1996 Detection of the PML/RARalpha fusion gene in APL blasts is critical to start promptly the specific therapy with all-trans retinoic acid (ATRA). Tretinoin 137-141 PML nuclear body scaffold Homo sapiens 17-20
7748789-14 1995 The second phase of c-otx2 expression is sensitive to an early treatment with retinoic acid. Tretinoin 78-91 orthodenticle homeobox 2 Gallus gallus 22-26
8684004-2 1996 Detection of the PML/RARalpha fusion gene in APL blasts is critical to start promptly the specific therapy with all-trans retinoic acid (ATRA). Tretinoin 137-141 retinoic acid receptor alpha Homo sapiens 21-29
8668150-6 1996 Unilateral deletions and site-directed mutagenesis identified the J site of the apo A-II promoter mediating the responsiveness to RA. Tretinoin 130-132 apolipoprotein A2 Homo sapiens 80-88
7541561-2 1995 AFP is not expressed in undifferentiated F9 cells but is induced when cells differentiate as cell aggregates in the presence of retinoic acid. Tretinoin 128-141 alpha fetoprotein Mus musculus 0-3
2059565-1 1991 A cloned thymosin beta-10 cDNA was used to study modulation of thymosin beta-10 mRNA levels in the rat B104 neuroblastoma cell line in response to retinoic acid. Tretinoin 147-160 thymosin, beta 10 Rattus norvegicus 9-25
2059565-1 1991 A cloned thymosin beta-10 cDNA was used to study modulation of thymosin beta-10 mRNA levels in the rat B104 neuroblastoma cell line in response to retinoic acid. Tretinoin 147-160 thymosin, beta 10 Rattus norvegicus 63-79
2059565-3 1991 Addition of retinoic acid to the culture medium induced a dose- and time-dependent increase in thymosin beta-10 mRNA abundance. Tretinoin 12-25 thymosin, beta 10 Rattus norvegicus 95-111
2059565-4 1991 Additional studies showed that although thymosin beta-4 and beta-10 are coexpressed in this cell line, the stimulatory action of retinoic acid is specific for the thymosin beta-10 gene. Tretinoin 129-142 thymosin, beta 10 Rattus norvegicus 163-179
9387319-2 1996 ELISA method was used in detecting levels of serum granulocyle colony-stimulating factor (G-CSF) in 47 cases of APL during treatment with ATRA. Tretinoin 138-142 colony stimulating factor 3 Homo sapiens 51-88
2265702-1 1990 Treatment of Cloudman S91 melanoma cells with retinoic acid (RA) inhibits MSH-induced tyrosinase activity and melanin formation [(1990) J. Tretinoin 46-59 msh homeobox 1 Mus musculus 74-77
2265702-1 1990 Treatment of Cloudman S91 melanoma cells with retinoic acid (RA) inhibits MSH-induced tyrosinase activity and melanin formation [(1990) J. Tretinoin 61-63 msh homeobox 1 Mus musculus 74-77
2265702-5 1990 We report here, however, that in spite of inhibiting MSH-induced pigmentation, RA treatment caused a marked increase in MSH binding capacity for both cell surface and internal MSH binding sites. Tretinoin 79-81 msh homeobox 1 Mus musculus 53-56
2265702-5 1990 We report here, however, that in spite of inhibiting MSH-induced pigmentation, RA treatment caused a marked increase in MSH binding capacity for both cell surface and internal MSH binding sites. Tretinoin 79-81 msh homeobox 1 Mus musculus 120-123
2265702-5 1990 We report here, however, that in spite of inhibiting MSH-induced pigmentation, RA treatment caused a marked increase in MSH binding capacity for both cell surface and internal MSH binding sites. Tretinoin 79-81 msh homeobox 1 Mus musculus 120-123
7897699-7 1994 RA is more effective than bFGF in inhibiting myelin basic protein mRNA expression in these cells, and like bFGF, it preserves their bipotential character. Tretinoin 0-2 myelin basic protein Rattus norvegicus 45-65
9387319-2 1996 ELISA method was used in detecting levels of serum granulocyle colony-stimulating factor (G-CSF) in 47 cases of APL during treatment with ATRA. Tretinoin 138-142 colony stimulating factor 3 Homo sapiens 90-95
9387319-4 1996 After ATRA treatment, both serum G-CSF level and WBC number increased in 68.1% of the cases. Tretinoin 6-10 colony stimulating factor 3 Homo sapiens 33-38
7843800-0 1994 Retinoic acid modulation of mucin mRNA in rat tracheal explants: response to actinomycin D, cycloheximide, signal transduction effectors and antisense oligodeoxynucleotide. Tretinoin 0-13 solute carrier family 13 member 2 Rattus norvegicus 28-33
7843800-3 1994 The usual precipitous drop in mucin mRNA in cultures lacking retinoic acid (RA-) was prevented by actinomycin D. Tretinoin 61-74 solute carrier family 13 member 2 Rattus norvegicus 30-35
2265702-10 1990 It appears that in suppressing MSH-induced melanogenesis, RA elicited a compensatory up-regulation of the MSH receptor system. Tretinoin 58-60 msh homeobox 1 Mus musculus 31-34
2265702-10 1990 It appears that in suppressing MSH-induced melanogenesis, RA elicited a compensatory up-regulation of the MSH receptor system. Tretinoin 58-60 msh homeobox 1 Mus musculus 106-109
8674128-3 1996 All trans retinoic acid (RA) enhanced the production of IgA at high concentrations (10-100 nM) in the presence of IL-5. Tretinoin 10-23 interleukin 5 Mus musculus 114-118
1700780-0 1990 Mapping of a retinoic acid-responsive element in the promoter region of the complement factor H gene. Tretinoin 13-26 complement factor H Homo sapiens 87-95
7969156-2 1994 This activation involves binding of the RAR/retinoid X receptor (RAR/RXR) heterodimer to the RA-responsive element (beta RARE). Tretinoin 40-42 retinoid X receptor alpha Homo sapiens 69-72
8674128-3 1996 All trans retinoic acid (RA) enhanced the production of IgA at high concentrations (10-100 nM) in the presence of IL-5. Tretinoin 25-27 interleukin 5 Mus musculus 114-118
8674128-7 1996 Addition of IL-5 to the system showed a synergistic effect which could be attenuated by addition of low concentrations of RA (about 1 nM). Tretinoin 122-124 interleukin 5 Mus musculus 12-16
7986828-5 1994 To try to understand these clinical findings, the complex formed between the VDRE and one or more proteins in the nuclear extracts of cultured skin fibroblasts treated with 1,25-dihydroxyvitamin D-3 (1,25(OH)2D3), retinoic acid (RA), and/or triiodothyronine (T3) was investigated since such complexes are likely to precede the transcription of the VDR gene. Tretinoin 214-227 vitamin D receptor Homo sapiens 77-80
8679712-3 1996 However, we noted that retinoic acid treatment without prior aggregation, is sufficient to induce expression of the neuronal markers GAP-43 and NF-165. Tretinoin 23-36 growth associated protein 43 Homo sapiens 133-139
7986828-5 1994 To try to understand these clinical findings, the complex formed between the VDRE and one or more proteins in the nuclear extracts of cultured skin fibroblasts treated with 1,25-dihydroxyvitamin D-3 (1,25(OH)2D3), retinoic acid (RA), and/or triiodothyronine (T3) was investigated since such complexes are likely to precede the transcription of the VDR gene. Tretinoin 229-231 vitamin D receptor Homo sapiens 77-80
7986828-6 1994 Complex formation in the control cells with an intact VDR was increased by treatment with either 0.1 nM, 1 nM, 10 nM 1,25(OH)2D3, 100 nM RA, or 100 nM T3; however, combinations of these compounds did not produce an additive effect. Tretinoin 137-139 vitamin D receptor Homo sapiens 54-57
2172246-1 1990 Differentiation of the murine embryonal carcinoma (EC) cell lines F-9 and PC-13, induced by beta-all transretinoic acid (RA) resulted in an increased level of two lysosomal-associated membrane glycoproteins (LAMP-1 and LAMP-2). Tretinoin 92-119 lysosomal-associated membrane protein 1 Mus musculus 208-214
1982997-4 1990 However, RA treatment concomitant with MDI addition inhibited triacylglycerol accumulation (I0.5 = 6 nM) and the accumulation of the differentiation-dependent mRNAs encoding the adipocyte lipid-binding protein (ALBP) and stearoyl-CoA desaturase 1 (SCD1). Tretinoin 9-11 stearoyl-Coenzyme A desaturase 1 Mus musculus 221-246
1982997-4 1990 However, RA treatment concomitant with MDI addition inhibited triacylglycerol accumulation (I0.5 = 6 nM) and the accumulation of the differentiation-dependent mRNAs encoding the adipocyte lipid-binding protein (ALBP) and stearoyl-CoA desaturase 1 (SCD1). Tretinoin 9-11 stearoyl-Coenzyme A desaturase 1 Mus musculus 248-252
7998926-2 1994 RAR-beta and CRABP II mRNA was induced by both all-trans and 9-cis retinoic acid in SH SY 5Y cells. Tretinoin 67-80 cellular retinoic acid binding protein 2 Homo sapiens 13-21
8679712-4 1996 In agreement, immunohistochemistry revealed the presence of GAP-43 positive cells in these embryonic stem cell monolayers after three days of retinoic acid (RA) treatment. Tretinoin 142-155 growth associated protein 43 Homo sapiens 60-66
7998926-7 1994 The induction of RAR-beta and CRABP II by all-trans retinoic acid was maintained in the subsequent absence of all-trans retinoic acid, whereas induction by 9-cis retinoic acid was dependent on its continued presence in the culture medium. Tretinoin 52-65 cellular retinoic acid binding protein 2 Homo sapiens 30-38
2172788-0 1990 Transcription factor Sp1 is important for retinoic acid-induced expression of the tissue plasminogen activator gene during F9 teratocarcinoma cell differentiation. Tretinoin 42-55 chromosome 20 open reading frame 181 Homo sapiens 82-110
8703836-0 1996 Inhibition of growth and induction of apoptosis by all-trans retinoic acid in lymphoid cell lines transfected with the PML/RAR alpha fusion gene. Tretinoin 51-74 retinoic acid receptor alpha Homo sapiens 119-132
2172788-1 1990 The induced differentiation of F9 cells by retinoic acid (RA) and cyclic AMP (cAMP) activated transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 43-56 chromosome 20 open reading frame 181 Homo sapiens 115-143
2172788-1 1990 The induced differentiation of F9 cells by retinoic acid (RA) and cyclic AMP (cAMP) activated transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 43-56 chromosome 20 open reading frame 181 Homo sapiens 145-149
2172788-1 1990 The induced differentiation of F9 cells by retinoic acid (RA) and cyclic AMP (cAMP) activated transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 58-60 chromosome 20 open reading frame 181 Homo sapiens 115-143
2172788-1 1990 The induced differentiation of F9 cells by retinoic acid (RA) and cyclic AMP (cAMP) activated transcription of the tissue plasminogen activator (t-PA) gene. Tretinoin 58-60 chromosome 20 open reading frame 181 Homo sapiens 145-149
7977784-8 1994 RA repressed serum-stimulated induction of the immediate early genes c-fos and c-jun, whose protein products dimerize to form AP-1. Tretinoin 0-2 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 69-74
7977784-8 1994 RA repressed serum-stimulated induction of the immediate early genes c-fos and c-jun, whose protein products dimerize to form AP-1. Tretinoin 0-2 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-84
7977784-10 1994 That repression of c-fos by RA might contribute to anti-AP-1 activity was suggested by experiments with an antisense c-fos expression vector, which demonstrated that c-fos induction was required for serum-stimulated AP-1 activity. Tretinoin 28-30 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 19-24
7977784-10 1994 That repression of c-fos by RA might contribute to anti-AP-1 activity was suggested by experiments with an antisense c-fos expression vector, which demonstrated that c-fos induction was required for serum-stimulated AP-1 activity. Tretinoin 28-30 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 117-122
7977784-10 1994 That repression of c-fos by RA might contribute to anti-AP-1 activity was suggested by experiments with an antisense c-fos expression vector, which demonstrated that c-fos induction was required for serum-stimulated AP-1 activity. Tretinoin 28-30 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 117-122
1700414-5 1990 We also found that the levels of CA II homologous RNA increase in the pancreatic adenocarcinoma cell lines following treatment with the differentiating agent, retinoic acid. Tretinoin 159-172 carbonic anhydrase 2 Homo sapiens 33-38
8703836-1 1996 The interaction of an exogenous PML/RAR alpha fusion gene associated with acute promyelocytic leukaemia, with all-trans retinoic acid (ATRA) was examined in two lymphoid cell lines. Tretinoin 110-133 PML nuclear body scaffold Homo sapiens 32-45
8703836-1 1996 The interaction of an exogenous PML/RAR alpha fusion gene associated with acute promyelocytic leukaemia, with all-trans retinoic acid (ATRA) was examined in two lymphoid cell lines. Tretinoin 135-139 PML nuclear body scaffold Homo sapiens 32-45
7886692-4 1994 wt PLA2 inhibitors such as p-bromophenacyl bromide, aristolochic acid, nordihydroguaiaretic acid, all trans-retinal and all trans-retinoic acid on the action of these enzymes. Tretinoin 124-143 phospholipase A2, group IB, pancreas Mus musculus 3-7
8703836-4 1996 ATRA also induced apoptosis, as assessed by fragmentation of genomic DNA, in L121OPML/RAR alpha and MOLT-4PML/RAR alpha cells but not in control cells. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 86-95
7919389-7 1994 This is the first report that the MCP-1 gene is RA-responsive in myeloid cell lines and is expressed in neutrophils. Tretinoin 48-50 chemokine (C-C motif) ligand 2 Mus musculus 34-39
8703836-4 1996 ATRA also induced apoptosis, as assessed by fragmentation of genomic DNA, in L121OPML/RAR alpha and MOLT-4PML/RAR alpha cells but not in control cells. Tretinoin 0-4 retinoic acid receptor alpha Homo sapiens 110-119
8703836-5 1996 The exogenous PML/RAR alpha fusion gene therefore probably mediates the effects of ATRA on cell growth and apoptosis in these cell lines. Tretinoin 83-87 PML nuclear body scaffold Homo sapiens 14-27
2272313-5 1990 These effects of retinoic acid were preceded by an increased expression of proto-oncogene raf and transient expression of proto-oncogene fos. Tretinoin 17-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 137-140
2272313-6 1990 The maximum level of fos expression was observed at 15 min and of raf at 12 hr after exposure to retinoic acid. Tretinoin 97-110 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 21-24
8655599-0 1996 Synergistic stimulation of gamma-glutamyl transpeptidase and alkaline phosphatase activities by retinoic acid and astroglial factors in immortalized rat brain microvessel endothelial cells. Tretinoin 96-109 gamma-glutamyltransferase 1 Rattus norvegicus 27-56
2163993-7 1990 Both gp175 and gp250 showed the greatest increase in fucosylation at 10(-5) M, which was also the dose at which RA induced laminin maximally, while the fucosylation of gp400 was greatest at 10(-8) M RA and declined at higher concentrations. Tretinoin 112-114 sortilin related receptor 1 Homo sapiens 15-20
2163993-7 1990 Both gp175 and gp250 showed the greatest increase in fucosylation at 10(-5) M, which was also the dose at which RA induced laminin maximally, while the fucosylation of gp400 was greatest at 10(-8) M RA and declined at higher concentrations. Tretinoin 199-201 sortilin related receptor 1 Homo sapiens 15-20
7741659-1 1994 The developing dentition is known to express the complete set of retinoic acid (RA) nuclear receptors and cytoplasmic RA-binding proteins (CRABPI and II), and RA is required for in vitro mouse molar morphogenesis, so the role of RA during in vitro mouse incisor development was investigated. Tretinoin 118-120 cellular retinoic acid binding protein I Mus musculus 139-152
7741659-1 1994 The developing dentition is known to express the complete set of retinoic acid (RA) nuclear receptors and cytoplasmic RA-binding proteins (CRABPI and II), and RA is required for in vitro mouse molar morphogenesis, so the role of RA during in vitro mouse incisor development was investigated. Tretinoin 118-120 cellular retinoic acid binding protein I Mus musculus 139-152
8655599-2 1996 The effects of bFGF, astroglial factors, and retinoic acid (a cell differentiation agent) on GTP and ALP activities were separately or simultaneously studied in order to define optimal culture conditions for induction of these two specific enzymes of the blood-brain barrier. Tretinoin 45-58 gamma-glutamyltransferase 1 Rattus norvegicus 93-96
8655599-5 1996 Addition of bFGF, astroglial factors, or retinoic acid induced the formation of these three-dimensional structures and in consequence an increase in GTP and ALP activities. Tretinoin 41-54 gamma-glutamyltransferase 1 Rattus norvegicus 149-152
8655599-6 1996 For retinoic acid and astroglial factors, this increase could also be explained by the stimulation of either GTP or ALP expression in the phenotypically distinct positive cells associated with aggregates. Tretinoin 4-17 gamma-glutamyltransferase 1 Rattus norvegicus 109-112
7803267-9 1994 In APL cases ATRA generated an asynchronous phenotype (CD15+, CDw65+, CD11b+, CD11a-), undetectable on normally maturing myeloid cells, but consistent with the concept that incomplete differentiation, in terms of surface molecule expression, can be sufficient to obtain therapeutic results. Tretinoin 13-17 integrin subunit alpha M Homo sapiens 70-75
2108933-0 1990 Enhanced expression of the proto-oncogenes fos and raf in the rhabdomyosarcoma cell line BA-HAN-1C after differentiation induction with retinoic acid and N-methylformamide. Tretinoin 136-149 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 43-46
2108933-6 1990 Furthermore, a transient expression of c-fos could be observed 15 and 30 min after exposure to RA. Tretinoin 95-97 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 39-44
8655599-7 1996 Simultaneous treatment with retinoic acid and astroglial factors had a synergistic effect on GTP and ALP expression and thus may allow these distinct cells to evolve toward a more differentiated state. Tretinoin 28-41 gamma-glutamyltransferase 1 Rattus norvegicus 93-96
8670228-1 1996 We previously reported that CD38 characterized as an ecto-enzyme of NAD+ glycohydrolase (NADase) was specifically induced by retinoic acid (RA) in human promyelocytic leukemia HL-60 cells and that anti-CD38 monoclonal antibody (mAb) induced tyrosine phosphorylation of cellular proteins in the RA-differentiated cells. Tretinoin 125-138 CD38 molecule Homo sapiens 28-32
1691021-2 1990 cDNAs corresponding to K8 and K18 mRNAs were cloned and used to study the change in the abundance of these mRNAs during differentiation of F9 cells into parietal endoderm-like cells by treatment with retinoic acid (RA) or with RA and dibutyryl cAMP (Bt2cAMP). Tretinoin 200-213 keratin 8 Homo sapiens 23-25
7607086-4 1994 We have also found that exogenous retinoic acid can mimic the effect of this negative signal and reduces the anterior domain of Otx2 expression. Tretinoin 34-47 orthodenticle homeobox 2 Mus musculus 128-132
8670228-1 1996 We previously reported that CD38 characterized as an ecto-enzyme of NAD+ glycohydrolase (NADase) was specifically induced by retinoic acid (RA) in human promyelocytic leukemia HL-60 cells and that anti-CD38 monoclonal antibody (mAb) induced tyrosine phosphorylation of cellular proteins in the RA-differentiated cells. Tretinoin 125-138 CD38 molecule Homo sapiens 202-206
8670228-1 1996 We previously reported that CD38 characterized as an ecto-enzyme of NAD+ glycohydrolase (NADase) was specifically induced by retinoic acid (RA) in human promyelocytic leukemia HL-60 cells and that anti-CD38 monoclonal antibody (mAb) induced tyrosine phosphorylation of cellular proteins in the RA-differentiated cells. Tretinoin 140-142 CD38 molecule Homo sapiens 28-32
7854354-4 1994 Using a RA-responsive element and reporter gene construct transfected into a T cell, we found: 1) T cell activation and PKC activators enhance transactivation by RA, 2) down-regulation of PKC protein has little effect on RA transactivation but abolishes superinduction by phorbol ester, which is restored by cotransfection of a PKC alpha-expression vector, and 3) cotransfection of dominant-negative c-jun does not prevent superinduction by phorbol ester. Tretinoin 8-10 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 400-405
2157210-5 1990 The conservation of the RAR-gamma isoforms from mouse to human together with their patterns of expression suggests that they perform specific functions, which may account for the pleiotropic effect of retinoic acid in embryogenesis and development. Tretinoin 201-214 retinoic acid receptor, gamma Mus musculus 24-33
8670228-1 1996 We previously reported that CD38 characterized as an ecto-enzyme of NAD+ glycohydrolase (NADase) was specifically induced by retinoic acid (RA) in human promyelocytic leukemia HL-60 cells and that anti-CD38 monoclonal antibody (mAb) induced tyrosine phosphorylation of cellular proteins in the RA-differentiated cells. Tretinoin 140-142 CD38 molecule Homo sapiens 202-206
8670228-2 1996 In the present study, we found that CD38/NADase was induced in human monocytic leukemia THP-1 cells not only by RA but also by dibutyryl cAMP, which had no effect on the induction of CD38 in HL-60 cells. Tretinoin 112-114 CD38 molecule Homo sapiens 36-40
7945224-2 1994 Retinoic acid (RA) caused a 5-fold induction of PEPCK mRNA within 6 h in these cells with a half-maximal effective concentration of approximately 75 microM. Tretinoin 0-13 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 48-53
8670228-3 1996 Similarly in the RA-differentiated HL-60 cells, tyrosine phosphorylation by anti-CD38 mAb was also observed in the CD38-expressing THP-1 cells, regardless of whether CD38 was induced by RA or dibutyryl cAMP. Tretinoin 17-19 CD38 molecule Homo sapiens 81-85
7945224-2 1994 Retinoic acid (RA) caused a 5-fold induction of PEPCK mRNA within 6 h in these cells with a half-maximal effective concentration of approximately 75 microM. Tretinoin 15-17 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 48-53
8670228-5 1996 Thus, the induction of CD38/NADase appeared to be not limited for RA-dependent differentiation and not always linked to protein-tyrosine phosphorylation in human leukemic cell lines. Tretinoin 66-68 CD38 molecule Homo sapiens 23-27
1967980-2 1990 Oct-3, which recognizes the typical octamer motif (ATTTGCAT) as well as the AT-rich sequence TTAAAATTCA, is present in P19 stem cells but disappears when the cells are induced to differentiate by retinoic acid (RA). Tretinoin 196-209 POU domain, class 5, transcription factor 1 Mus musculus 0-5
1967980-2 1990 Oct-3, which recognizes the typical octamer motif (ATTTGCAT) as well as the AT-rich sequence TTAAAATTCA, is present in P19 stem cells but disappears when the cells are induced to differentiate by retinoic acid (RA). Tretinoin 211-213 POU domain, class 5, transcription factor 1 Mus musculus 0-5
8967521-13 1996 However, the cPLA2 and PGHS-2 genes were expressed in squamous cultures only after 3 days of RA treatment coincident with redifferentiation of the culture to a mucociliary phenotype. Tretinoin 93-95 phospholipase A2 group IVA Rattus norvegicus 13-18
1967980-5 1990 mRNA of 1.5 kb coding for Oct-3 is abundant in P19 stem cells but is dramatically repressed during RA-induced differentiation. Tretinoin 99-101 POU domain, class 5, transcription factor 1 Mus musculus 26-31
2294153-6 1990 Retinoic acid (RA) exerted a time-dependent suppressive effect on LPL secretion by BMMs (46% within 16 hr and 83% within 6 d), had a relatively small effect on secretion from J774.1 cells (approximately 20% in 72 hr) and had no effect on LPL secretion by Tg-M phi. Tretinoin 0-13 lipoprotein lipase Mus musculus 66-69
2294153-6 1990 Retinoic acid (RA) exerted a time-dependent suppressive effect on LPL secretion by BMMs (46% within 16 hr and 83% within 6 d), had a relatively small effect on secretion from J774.1 cells (approximately 20% in 72 hr) and had no effect on LPL secretion by Tg-M phi. Tretinoin 0-13 lipoprotein lipase Mus musculus 238-241
8090764-1 1994 The cellular retinoic acid binding proteins I and II (CRABPI and CRABPII) bind retinoic acid with high affinity, exhibit distinct patterns of expression during embryonic development, and are thought to play important roles in the RA signaling pathway. Tretinoin 13-26 cellular retinoic acid binding protein I Mus musculus 54-60
8090764-1 1994 The cellular retinoic acid binding proteins I and II (CRABPI and CRABPII) bind retinoic acid with high affinity, exhibit distinct patterns of expression during embryonic development, and are thought to play important roles in the RA signaling pathway. Tretinoin 79-92 cellular retinoic acid binding protein I Mus musculus 54-60
8063765-0 1994 Retinoic acid suppression of c-fos gene inhibits expression of tumor necrosis factor-alpha-induced monocyte chemoattractant JE/MCP-1 in clonal osteoblastic MC3T3-E1 cells. Tretinoin 0-13 chemokine (C-C motif) ligand 2 Mus musculus 127-132
8063765-4 1994 In the present study, we examined the effect of retinoic acid (RA) on the cytokine-induced JE/MCP-1 expression in the cells. Tretinoin 48-61 chemokine (C-C motif) ligand 2 Mus musculus 94-99
8063765-4 1994 In the present study, we examined the effect of retinoic acid (RA) on the cytokine-induced JE/MCP-1 expression in the cells. Tretinoin 63-65 chemokine (C-C motif) ligand 2 Mus musculus 94-99
8063765-5 1994 RA significantly inhibited the JE/MCP-1 gene expression by at least 6 h of pretreatment, and the inhibition was pretreatment time-dependent and occurred at the transcriptional level of the JE/MCP-1 gene expression. Tretinoin 0-2 chemokine (C-C motif) ligand 2 Mus musculus 34-39
8063765-5 1994 RA significantly inhibited the JE/MCP-1 gene expression by at least 6 h of pretreatment, and the inhibition was pretreatment time-dependent and occurred at the transcriptional level of the JE/MCP-1 gene expression. Tretinoin 0-2 chemokine (C-C motif) ligand 2 Mus musculus 192-197
8792006-5 1996 RA-induced expression of thymosin beta-10, an apoptotic accelerant, was associated with increased nuclear DNA nicking as measured using TUNEL. Tretinoin 0-2 thymosin beta 10 Homo sapiens 25-41
8063765-6 1994 The RA-induced inhibition of the JE/MCP-1 gene product was also evidenced by both an assay involving immunoprecipitation with JE/MCP-1-specific antiserum and an assay for monocyte chemotaxis. Tretinoin 4-6 chemokine (C-C motif) ligand 2 Mus musculus 36-41
8063765-6 1994 The RA-induced inhibition of the JE/MCP-1 gene product was also evidenced by both an assay involving immunoprecipitation with JE/MCP-1-specific antiserum and an assay for monocyte chemotaxis. Tretinoin 4-6 chemokine (C-C motif) ligand 2 Mus musculus 129-134
7917989-6 1994 The biological importance of s-RBP expression in keratinocytes and fibroblasts is not known, but hypothetically this protein may be involved in the intracellular shuttling of retinol and retinoic acid, or in the retransportation of cellular retinoids into the extracellular space. Tretinoin 187-200 retinol binding protein 4 Homo sapiens 31-34
33801464-4 2021 Overexpression of SARS-CoV-2 N resulted in the attenuation of retinoic acid inducible gene-I (RIG-I)-like receptor-mediated interferon (IFN) production and IFN-induced gene expression. Tretinoin 62-75 DExD/H-box helicase 58 Homo sapiens 94-99
23624502-0 2013 Small GTPase Rab39A interacts with UACA and regulates the retinoic acid-induced neurite morphology of Neuro2A cells. Tretinoin 58-71 uveal autoantigen with coiled-coil domains and ankyrin repeats Mus musculus 35-39
23624502-3 2013 shRNA-mediated knockdown of endogenous Rab39A or UACA in mouse neuroblastoma Neuro2A cells resulted in a change in retinoic acid-induced neurite morphology from a multipolar morphology to a bipolar morphology. Tretinoin 115-128 uveal autoantigen with coiled-coil domains and ankyrin repeats Mus musculus 49-53
23624502-4 2013 Taken together, these findings indicate that UACA functions as a Rab39A effector in the retinoic acid-induced differentiation of Neuro2A cells. Tretinoin 88-101 uveal autoantigen with coiled-coil domains and ankyrin repeats Mus musculus 45-49
8620598-4 1996 Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. Tretinoin 37-39 galactosidase, beta 1 Mus musculus 87-105
7934625-0 1994 The prevention of adipose differentiation of 3T3-L1 cells caused by retinoic acid is elicited through retinoic acid receptor alpha. Tretinoin 68-81 retinoic acid receptor, alpha Mus musculus 102-130
7521445-11 1994 CONCLUSIONS: Our results suggest that pluripotent human EC cells differentiate in response to OP-1 and that this factor can modulate the differentiation induced by retinoic acid. Tretinoin 164-177 bone morphogenetic protein 7 Homo sapiens 94-98
8037774-2 1994 However, pEL98 expression remained at the low level during granulocytic differentiation of the cells by the treatment with all-trans retinoic acid. Tretinoin 133-146 S100 calcium binding protein A4 Homo sapiens 9-14
8620598-4 1996 Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. Tretinoin 37-39 galactosidase, beta 1 Mus musculus 87-95
34935440-1 2022 Recent studies demonstrated that the signaling activity of the cytosolic pathogen sensor retinoic acid-inducible gene-I (RIG-I) is modulated by a variety of post-translational modifications (PTMs) to fine-tune the antiviral type I interferon (IFN) response. Tretinoin 89-102 DExD/H-box helicase 58 Homo sapiens 121-126
8620598-4 1996 Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. Tretinoin 37-39 galactosidase, beta 1 Mus musculus 107-115
8620598-4 1996 Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. Tretinoin 143-145 galactosidase, beta 1 Mus musculus 87-105
7519968-7 1994 Retinoic acid enhanced the expression of secretory luminal cell-associated cytokeratins 8 and 18 in semi-confluent cultures. Tretinoin 0-13 keratin 8 Homo sapiens 75-96
8620598-4 1996 Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. Tretinoin 143-145 galactosidase, beta 1 Mus musculus 87-95
34850108-7 2021 Notably, the activity of retinoic acid receptor alpha (RARalpha) occupied regions can either increase or decrease upon the addition of its ligand, retinoic acid, with the direction of the change correlating with spacing and orientation of the RARalpha consensus motif and the co-occurrence of additional sequence motifs. Tretinoin 147-160 retinoic acid receptor, alpha Mus musculus 25-53
8620598-4 1996 Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. Tretinoin 143-145 galactosidase, beta 1 Mus musculus 107-115
34850108-7 2021 Notably, the activity of retinoic acid receptor alpha (RARalpha) occupied regions can either increase or decrease upon the addition of its ligand, retinoic acid, with the direction of the change correlating with spacing and orientation of the RARalpha consensus motif and the co-occurrence of additional sequence motifs. Tretinoin 147-160 retinoic acid receptor, alpha Mus musculus 55-63
8780054-4 1996 When treated with retinoic acid, these transformed lines differentiated into neurons and survived better than did nontransformed parental P19 cells. Tretinoin 18-31 interleukin 23 subunit alpha Homo sapiens 138-141
34850108-7 2021 Notably, the activity of retinoic acid receptor alpha (RARalpha) occupied regions can either increase or decrease upon the addition of its ligand, retinoic acid, with the direction of the change correlating with spacing and orientation of the RARalpha consensus motif and the co-occurrence of additional sequence motifs. Tretinoin 147-160 retinoic acid receptor, alpha Mus musculus 243-251
34288810-10 2021 These results demonstrate that ATRA suppresses chondrogenesis in rEHBMCs by inhibiting the expression of HoxD9 and its downstream protein targets, including Sox9 and Col2a1. Tretinoin 31-35 SRY-box transcription factor 9 Rattus norvegicus 157-161
8007990-11 1994 GATA-4 DNA binding activity was significantly up-regulated in triiodothyronine- or retinoic acid-treated cardiomyocytes. Tretinoin 83-96 GATA binding protein 4 Homo sapiens 0-6
8735598-0 1996 EGF increases retinoid X receptor-alpha expression in human trophoblastic cells in culture: relationship with retinoic acid induced human chorionic gonadotropin secretion. Tretinoin 110-123 epidermal growth factor Homo sapiens 0-3
8080909-1 1994 Retinols and retinoic acid (vitamin A) are essential for embryonic development; they are transported in circulation bound to retinol-binding protein (RBP). Tretinoin 13-26 retinol binding protein 4 Sus scrofa 150-153
8735598-2 1996 In these cells, RA potentiated the hCG secretion increase induced by EGF. Tretinoin 16-18 epidermal growth factor Homo sapiens 69-72
34811400-7 2021 Among them, a novel highly conserved RAR-induced enhancer was identified downstream of the HoxB locus and driving expression in the nervous system and in the gut in a RA-dependent manner. Tretinoin 167-169 retinoic acid receptor, alpha Mus musculus 37-40
34811400-8 2021 Finally, ATAC-seq data unveiled the role of the RAR-direct targets Hnf1ba and Gata6 in opening chromatin at many regulatory loci upon RA treatment. Tretinoin 134-136 retinoic acid receptor, alpha Mus musculus 48-51
7512975-0 1994 Retinoic acid enhances adhesiveness, laminin and integrin beta 1 synthesis, and retinoic acid receptor expression in F9 teratocarcinoma cells. Tretinoin 0-13 integrin subunit beta 1 Homo sapiens 49-64
7512975-8 1994 These studies demonstrate that RA increases cell to substrate interactions by increasing the biosynthesis of laminin and beta 1 integrin. Tretinoin 31-33 integrin subunit beta 1 Homo sapiens 121-136
8620495-2 1996 All-trans-retinoic acid exerts its effects by activation of retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 60-82
8163945-3 1994 Both RA isoforms inhibited in a reversible and dose-dependent fashion, the proliferation of multi- but not single-factor responsive Lin-Sca-1+ progenitor cells. Tretinoin 5-7 ataxin 1 Mus musculus 136-141
34775955-11 2021 Furthermore, our results revealed that CRBP-1 could increase the intracellular levels of retinoic acid, which induced the activation of RARs/RXRs leading to the transcriptional expression of WIF1, a secreted antagonist of the Wnt/beta-catenin signaling pathway, by physically interacting with the region on WIF1 promoter. Tretinoin 89-102 WNT inhibitory factor 1 Homo sapiens 191-195
34775955-11 2021 Furthermore, our results revealed that CRBP-1 could increase the intracellular levels of retinoic acid, which induced the activation of RARs/RXRs leading to the transcriptional expression of WIF1, a secreted antagonist of the Wnt/beta-catenin signaling pathway, by physically interacting with the region on WIF1 promoter. Tretinoin 89-102 WNT inhibitory factor 1 Homo sapiens 307-311
8176247-0 1994 A pleiotropic response is induced in F9 embryonal carcinoma cells and rhino mouse skin by All-trans-retinoic acid, a RAR agonist but not by SR11237, a RXR-selective agonist. Tretinoin 90-113 retinoic acid receptor, alpha Mus musculus 117-120
34830183-0 2021 Olfactory Receptor OR7A17 Expression Correlates with All-Trans Retinoic Acid (ATRA)-Induced Suppression of Proliferation in Human Keratinocyte Cells. Tretinoin 63-76 olfactory receptor family 7 subfamily A member 17 Homo sapiens 19-25
8620495-2 1996 All-trans-retinoic acid exerts its effects by activation of retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 0-23 retinoic acid receptor alpha Homo sapiens 84-87
34830183-0 2021 Olfactory Receptor OR7A17 Expression Correlates with All-Trans Retinoic Acid (ATRA)-Induced Suppression of Proliferation in Human Keratinocyte Cells. Tretinoin 78-82 olfactory receptor family 7 subfamily A member 17 Homo sapiens 19-25
34830183-6 2021 We demonstrated that OR7A17 is expressed in HaCaT keratinocytes, and its expression was downregulated by ATRA. Tretinoin 105-109 olfactory receptor family 7 subfamily A member 17 Homo sapiens 21-27
8790939-7 1996 On the other hand, in suspension culture with 1 microM retinoic acid (RA), the condition for neural differentiation of P19 cells, the CL6 cells developed into neurons with poor outgrowth. Tretinoin 55-68 interleukin 23 subunit alpha Homo sapiens 119-122
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 4-8 olfactory receptor family 7 subfamily A member 17 Homo sapiens 35-41
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 4-8 olfactory receptor family 7 subfamily A member 17 Homo sapiens 145-151
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 137-141 olfactory receptor family 7 subfamily A member 17 Homo sapiens 35-41
34830183-7 2021 The ATRA-induced downregulation of OR7A17 was attenuated via RAR alpha or RAR gamma antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Tretinoin 137-141 olfactory receptor family 7 subfamily A member 17 Homo sapiens 145-151
34830183-9 2021 Mechanistically, OR7A17 overexpression reversed the ATRA-induced attenuation of Ca2+ entry. Tretinoin 52-56 olfactory receptor family 7 subfamily A member 17 Homo sapiens 17-23
8179592-2 1994 In this study we have used reverse transcription (RT) and competitive polymerase chain reaction (cPCR) to investigate the effects of RA on CRABP-II expression levels in the human osteosarcoma cell line MG-63. Tretinoin 133-135 cellular retinoic acid binding protein 2 Homo sapiens 139-147
8179592-3 1994 Two different isomers of RA, all-trans (at) and 9-cis RA, were chosen since at-RA but not 9-cis RA binds to CRABP-II. Tretinoin 25-27 cellular retinoic acid binding protein 2 Homo sapiens 108-116
8179592-6 1994 Thus, although 9-cis RA does not bind to CRABP-II, it induces CRABP-II expression more efficiently than at-RA in human osteosarcoma cells. Tretinoin 21-23 cellular retinoic acid binding protein 2 Homo sapiens 62-70
7512566-7 1994 Retinoic acid increased IGFBP-6 by 3-fold in NHF and AG2804-conditioned media, maximal at approximately 100 nM retinoic acid. Tretinoin 0-13 insulin like growth factor binding protein 6 Homo sapiens 24-31
34830183-10 2021 Our findings indicated that ATRA suppresses cell proliferation through the downregulation of OR7A17 via RAR alpha- and gamma-mediated retinoid signaling. Tretinoin 28-32 olfactory receptor family 7 subfamily A member 17 Homo sapiens 93-99
34830183-11 2021 Taken together, OR7A17 is a potential therapeutic target for ameliorating the anti-proliferative effects of ATRA. Tretinoin 108-112 olfactory receptor family 7 subfamily A member 17 Homo sapiens 16-22
8790939-7 1996 On the other hand, in suspension culture with 1 microM retinoic acid (RA), the condition for neural differentiation of P19 cells, the CL6 cells developed into neurons with poor outgrowth. Tretinoin 55-68 insulin induced gene 1 Homo sapiens 134-137
8790939-7 1996 On the other hand, in suspension culture with 1 microM retinoic acid (RA), the condition for neural differentiation of P19 cells, the CL6 cells developed into neurons with poor outgrowth. Tretinoin 70-72 interleukin 23 subunit alpha Homo sapiens 119-122
34830120-7 2021 In AtT20, a pituitary gland adenoma cell line elevating or reducing Crabp1 level correspondingly increases or decreases FKBP5 expression, and its endogenous Crabp1 level is elevated by GR agonist dexamethasone or RA treatment. Tretinoin 213-215 cellular retinoic acid binding protein I Mus musculus 68-74
8157636-4 1994 The K70M beta-lactoglobulin exhibited a marked decrease in its binding of retinoic acid compared to the F136A, K141M, and wild-type proteins. Tretinoin 74-87 beta-lactoglobulin Bos taurus 9-27
8790939-7 1996 On the other hand, in suspension culture with 1 microM retinoic acid (RA), the condition for neural differentiation of P19 cells, the CL6 cells developed into neurons with poor outgrowth. Tretinoin 70-72 insulin induced gene 1 Homo sapiens 134-137
8149476-7 1994 The retinoic acid analogue RO-109359 which, unlike RA, does not have tumor promoting activity per se, inhibited the TPA-induced increase in epidermal GM-CSF mRNA levels. Tretinoin 4-17 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 150-156
34830120-7 2021 In AtT20, a pituitary gland adenoma cell line elevating or reducing Crabp1 level correspondingly increases or decreases FKBP5 expression, and its endogenous Crabp1 level is elevated by GR agonist dexamethasone or RA treatment. Tretinoin 213-215 cellular retinoic acid binding protein I Mus musculus 157-163
34830120-9 2021 Furthermore, RA and stress can increase Crabp1 level, which would up-regulate FKBP5 thereby de-sensitizing feedback inhibition of HPA axis (by decreasing GR signaling) and increasing the risk of stress-related disorders. Tretinoin 13-15 cellular retinoic acid binding protein I Mus musculus 40-46
34830120-9 2021 Furthermore, RA and stress can increase Crabp1 level, which would up-regulate FKBP5 thereby de-sensitizing feedback inhibition of HPA axis (by decreasing GR signaling) and increasing the risk of stress-related disorders. Tretinoin 13-15 FK506 binding protein 5 Mus musculus 78-83
8149483-1 1994 During studies to determine the mechanism of tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA), we found that TPA downregulates mouse epidermal retinoic acid nuclear receptors (RAR), a superfamily of nuclear steroid/thyroid receptors implicated in mediating effects of retinoic acid (RA). Tretinoin 156-169 retinoic acid receptor, alpha Mus musculus 189-192
8149483-1 1994 During studies to determine the mechanism of tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA), we found that TPA downregulates mouse epidermal retinoic acid nuclear receptors (RAR), a superfamily of nuclear steroid/thyroid receptors implicated in mediating effects of retinoic acid (RA). Tretinoin 189-191 retinoic acid receptor, alpha Mus musculus 156-187
8149483-2 1994 Application of TPA to mouse skin decreased the binding of [3H]RA to RAR from mouse epidermal nuclear extracts. Tretinoin 62-64 retinoic acid receptor, alpha Mus musculus 68-71
8149483-3 1994 In this experiment, 20 nmol of TPA was applied to mouse skin and 3.5 h later binding of [3H]RA to RAR was analyzed by chromatography on a size-exclusion column. Tretinoin 92-94 retinoic acid receptor, alpha Mus musculus 98-101
8790944-0 1996 Induction of mcl1/EAT, Bcl-2 related gene, by retinoic acid or heat shock in the human embryonal carcinoma cells, NCR-G3. Tretinoin 46-59 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 13-21
34523975-15 2021 The present study identified the interaction proteins of VP56 and found that VP56 and VP4 bind to the different domains of the viral RNA sensor retinoic acid-inducible gene I (RIG-I) in grass carp to block RIG-I sensing of viral RNA and induce RIG-I degradation by the proteasomal pathway to attenuate signaling transduction, thereby suppressing interferons (IFNs) and antiviral effectors, facilitating viral replication. Tretinoin 144-157 DExD/H-box helicase 58 Homo sapiens 176-181
34523975-15 2021 The present study identified the interaction proteins of VP56 and found that VP56 and VP4 bind to the different domains of the viral RNA sensor retinoic acid-inducible gene I (RIG-I) in grass carp to block RIG-I sensing of viral RNA and induce RIG-I degradation by the proteasomal pathway to attenuate signaling transduction, thereby suppressing interferons (IFNs) and antiviral effectors, facilitating viral replication. Tretinoin 144-157 DExD/H-box helicase 58 Homo sapiens 206-211
8790944-7 1996 The expression of mcl1/EAT, the Bcl-2 related gene, was increased at an early stage of the retinoic acid-induced differentiation and preceded the up-regulation of cytokeratin and hCG genes after ratinoic acid treatment. Tretinoin 91-104 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 18-26
34523975-15 2021 The present study identified the interaction proteins of VP56 and found that VP56 and VP4 bind to the different domains of the viral RNA sensor retinoic acid-inducible gene I (RIG-I) in grass carp to block RIG-I sensing of viral RNA and induce RIG-I degradation by the proteasomal pathway to attenuate signaling transduction, thereby suppressing interferons (IFNs) and antiviral effectors, facilitating viral replication. Tretinoin 144-157 DExD/H-box helicase 58 Homo sapiens 244-249
8056833-10 1994 RA inhibition of UVB-induced melanogenesis acts at the post-transcriptional level leading to a decreased tyrosinase and TRP-1 synthesis. Tretinoin 0-2 tyrosinase-related protein 1 Mus musculus 120-125
8618456-6 1996 These data, along with previous reports of rare variant translocations in APL, indicate that while dysregulation of RARA by gene fusion may be essential for the APL phenotype, the particular fusion partner may determine clinicopathological aspects, including presentation, response to treatment with all-trans retinoic acid (ATRA), and prognosis. Tretinoin 310-323 retinoic acid receptor alpha Homo sapiens 116-120
8152301-8 1994 Treatment of KHOS cells with retinoic acid and dexamethasone, which are known to suppress c-fos/c-jun and AP-1, suppressed the production of the MPs. Tretinoin 29-42 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-95
34680392-4 2021 Here, using a panel of human AML cell lines and primary AML patient specimens harboring IDH mutations, we showed that the production of an oncometabolite (R)-2-HG by IDH mutant enzymes induces vitamin D receptor-related transcriptional changes, priming these AML cells to differentiate with pharmacological doses of ATRA and/or VD. Tretinoin 316-320 vitamin D receptor Homo sapiens 193-211
8152301-8 1994 Treatment of KHOS cells with retinoic acid and dexamethasone, which are known to suppress c-fos/c-jun and AP-1, suppressed the production of the MPs. Tretinoin 29-42 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 96-101
8618456-6 1996 These data, along with previous reports of rare variant translocations in APL, indicate that while dysregulation of RARA by gene fusion may be essential for the APL phenotype, the particular fusion partner may determine clinicopathological aspects, including presentation, response to treatment with all-trans retinoic acid (ATRA), and prognosis. Tretinoin 325-329 retinoic acid receptor alpha Homo sapiens 116-120
8152301-8 1994 Treatment of KHOS cells with retinoic acid and dexamethasone, which are known to suppress c-fos/c-jun and AP-1, suppressed the production of the MPs. Tretinoin 29-42 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-110
34643182-5 2021 Tbx5 promotes posterior second heart field identity in a positive feedback loop with RA, antagonizing a Fgf8-Cyp regulatory module to restrict FGF activity to the anterior. Tretinoin 85-87 fibroblast growth factor 8 Mus musculus 104-108
34643182-5 2021 Tbx5 promotes posterior second heart field identity in a positive feedback loop with RA, antagonizing a Fgf8-Cyp regulatory module to restrict FGF activity to the anterior. Tretinoin 85-87 fibroblast growth factor 8 Mus musculus 143-146
8657131-8 1996 Thus, the unresponsiveness of 3T3-L1 preadipocytes to RA after the induction of differentiation is initially due to the reduction in cellular RAR concentration rather than to the induction of PPARgamma. Tretinoin 54-56 retinoic acid receptor alpha Homo sapiens 142-145
34448811-10 2021 CPI-455 treatment or KDM5A knockout could greatly sensitize NB4 cells to all-trans retinoic acid-induced differentiation. Tretinoin 83-96 lysine demethylase 5A Homo sapiens 21-26
8690916-7 1996 However, noninflammatory stimuli induced qualitatively similar changes in M phi and EC; all-trans retinoic acid and prostaglandin E up-regulated surface TM, and PMA decreased TM expression. Tretinoin 98-111 thrombomodulin Homo sapiens 153-155
34595229-3 2021 Retinoic acid-inducible gene-I (RIG-I)serves as an innate immune sensor and plays a key role in host antiviral defenses. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 32-37
8114692-2 1994 MB67 binds and transactivates the retinoic acid response elements that control expression of the retinoic acid receptor beta 2 and alcohol dehydrogenase 3 genes, both of which consist of a direct repeat hexamers related to the consensus AGGTCA, separated by 5 bp. Tretinoin 34-47 nuclear receptor subfamily 1 group I member 3 Homo sapiens 0-4
8114692-5 1994 The transactivation of retinoic acid response elements by MB67 is weaker than that conferred by the retinoic acid receptors but does not require the presence of all-trans retinoic acid, 9-cis-retinoic acid, or any exogenously added ligand. Tretinoin 23-36 nuclear receptor subfamily 1 group I member 3 Homo sapiens 58-62
8114692-5 1994 The transactivation of retinoic acid response elements by MB67 is weaker than that conferred by the retinoic acid receptors but does not require the presence of all-trans retinoic acid, 9-cis-retinoic acid, or any exogenously added ligand. Tretinoin 100-113 nuclear receptor subfamily 1 group I member 3 Homo sapiens 58-62
8114692-6 1994 We propose that MB67 plays an important role in the complex network of proteins that govern response to retinoic acid and its metabolites. Tretinoin 104-117 nuclear receptor subfamily 1 group I member 3 Homo sapiens 16-20
8302850-3 1994 In transient-expression assays, both the PLZF(A)-RAR alpha and PLZF(B)-RAR alpha fusion proteins like the PML-RAR alpha protein resulting from the well-known t(15;17) translocation in APL, antagonized endogenous and transfected wild-type RAR alpha in the presence of retinoic acid. Tretinoin 267-280 zinc finger and BTB domain containing 16 Homo sapiens 41-45
8302850-3 1994 In transient-expression assays, both the PLZF(A)-RAR alpha and PLZF(B)-RAR alpha fusion proteins like the PML-RAR alpha protein resulting from the well-known t(15;17) translocation in APL, antagonized endogenous and transfected wild-type RAR alpha in the presence of retinoic acid. Tretinoin 267-280 zinc finger and BTB domain containing 16 Homo sapiens 63-67
8302850-6 1994 These abnormal transactivation properties observed in retinoic acid-sensitive myeloid cells strongly implicate the PLZF-RAR alpha fusion proteins in the molecular pathogenesis of APL. Tretinoin 54-67 zinc finger and BTB domain containing 16 Homo sapiens 115-119
8288643-3 1994 The element RE3 which is the major retinoic acid (RA) response element also binds the transcription factors HNF-4 and ARP-1. Tretinoin 35-48 hepatic nuclear factor 4, alpha Mus musculus 108-113
8288643-3 1994 The element RE3 which is the major retinoic acid (RA) response element also binds the transcription factors HNF-4 and ARP-1. Tretinoin 50-52 hepatic nuclear factor 4, alpha Mus musculus 108-113
34410954-0 2021 Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model. Tretinoin 20-24 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 57-64
34410954-3 2021 MATERIALS AND METHODS: K562 cells were treated with IM and with the combined therapy of ATRA together with IM for 48 and 72 h. The expression of BCR-ABL gene and multidrug resistance gene ABCB1 were evaluated using RT-qPCR. Tretinoin 88-92 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 145-152
8838863-7 1996 In this study, we show that these cells also express retinoid X receptor (RXR)-alpha, RXR-beta, and RXR-gamma and that RA treatment down-regulates the expression of RXR-gamma. Tretinoin 119-121 retinoid X receptor beta Mus musculus 86-94
34419449-9 2021 RA levels in Rdh10+/- male GM decrease 38% relative to WT. Tretinoin 0-2 retinol dehydrogenase 10 Homo sapiens 13-18
34419449-13 2021 Comparatively, RA in Rdh10+/- female GM decreases by less than half the male decrease, from a more modest decrease in Rdh10 and an increase in the estrogen-induced retinol dehydrogenase Dhrs9. Tretinoin 15-17 retinol dehydrogenase 10 Homo sapiens 21-26
34419449-13 2021 Comparatively, RA in Rdh10+/- female GM decreases by less than half the male decrease, from a more modest decrease in Rdh10 and an increase in the estrogen-induced retinol dehydrogenase Dhrs9. Tretinoin 15-17 retinol dehydrogenase 10 Homo sapiens 118-123
34419449-13 2021 Comparatively, RA in Rdh10+/- female GM decreases by less than half the male decrease, from a more modest decrease in Rdh10 and an increase in the estrogen-induced retinol dehydrogenase Dhrs9. Tretinoin 15-17 dehydrogenase/reductase 9 Homo sapiens 186-191
8305467-14 1994 Experiments on retinoic acid formation under 18O2 or H2(18)O demonstrated that the oxygen of water was incorporated into retinoic acid by the retinal oxidase, but not molecular oxygen. Tretinoin 15-28 aldehyde oxidase 1 Oryctolagus cuniculus 142-157
8305467-14 1994 Experiments on retinoic acid formation under 18O2 or H2(18)O demonstrated that the oxygen of water was incorporated into retinoic acid by the retinal oxidase, but not molecular oxygen. Tretinoin 121-134 aldehyde oxidase 1 Oryctolagus cuniculus 142-157
8152429-2 1994 The retinoic acid receptor (RAR), as a heterodimer with the retinoid-x receptor (RXR), binds to DNA recognition sites, referred to as retinoic acid response elements (RAREs), that are generally composed of a direct repeat of the half-site core motif PuGGTCA spaced by 2 (DR-2) or 5 (DR-5) basepairs. Tretinoin 4-17 retinoid X receptor alpha Homo sapiens 60-79
8152429-2 1994 The retinoic acid receptor (RAR), as a heterodimer with the retinoid-x receptor (RXR), binds to DNA recognition sites, referred to as retinoic acid response elements (RAREs), that are generally composed of a direct repeat of the half-site core motif PuGGTCA spaced by 2 (DR-2) or 5 (DR-5) basepairs. Tretinoin 4-17 retinoid X receptor alpha Homo sapiens 81-84
8641674-0 1996 [Alterations of protein phosphatases, PP2A and PP1, during retinoic acid-induced differentiation of HL-60 cells]. Tretinoin 59-72 protein phosphatase 2 phosphatase activator Homo sapiens 38-42
34452533-6 2021 ATRA inhibited the replication of SARS-CoV-2 in VeroE6/TMPRSS2 and Calu-3 cells, with IC50 = 2.69 +- 0.09 microM in the former and 0.82 +- 0.01 microM in the latter. Tretinoin 0-4 transmembrane protease serine 2 Chlorocebus sabaeus 55-62
8641674-1 1996 Alterations of protein phosphatases, PP2A and PP1, during the retinoic acid-induced differentiation of HL-60 cells have been investigated. Tretinoin 62-75 protein phosphatase 2 phosphatase activator Homo sapiens 37-41
7991790-2 1994 Proteins in the 20-kDa range, conceptus-secreted retinol-binding protein (RBP), bound both [3H]retinol and [3H]RA specifically. Tretinoin 111-113 retinol binding protein 4 Sus scrofa 49-72
8641674-2 1996 The PP2A activity determined with myelin basic protein (MBP) as a substrate showed a sharp transient increase at 18 h of incubation of the cells with retinoic acid, whereas during incubation without retinoic acid, the activity remained at the initial level. Tretinoin 150-163 protein phosphatase 2 phosphatase activator Homo sapiens 4-8
7991790-2 1994 Proteins in the 20-kDa range, conceptus-secreted retinol-binding protein (RBP), bound both [3H]retinol and [3H]RA specifically. Tretinoin 111-113 retinol binding protein 4 Sus scrofa 74-77
8641674-2 1996 The PP2A activity determined with myelin basic protein (MBP) as a substrate showed a sharp transient increase at 18 h of incubation of the cells with retinoic acid, whereas during incubation without retinoic acid, the activity remained at the initial level. Tretinoin 199-212 protein phosphatase 2 phosphatase activator Homo sapiens 4-8
7991790-3 1994 Cross-competition experiments indicate that [3H]RA was completely displaced with excess cold retinol; however, excess cold RA did not completely displace [3H]retinol, suggesting that conceptus RBP has greater affinity for retinol than RA. Tretinoin 48-50 retinol binding protein 4 Sus scrofa 193-196
8641674-4 1996 The PP2A activity of the cells incubated for 18 h with retinoic acid was much more greatly activated by protamine compared with the activity of the cells incubated without retinoic acid. Tretinoin 55-68 protein phosphatase 2 phosphatase activator Homo sapiens 4-8
34253866-9 2021 To translate our results into a potential pharmacological therapeutic strategy, we tested the effect of systemic treatment with the global methyl donor S-adenosyl methionine (SAM), for supplementing DNA methylation, or retinoic acid, for activating RORA downstream pathways. Tretinoin 219-232 RAR related orphan receptor A Homo sapiens 249-253
7504177-15 1993 The previously characterized retinoic acid-responsive gene, Xhox.lab2, can be induced by thyroid hormone in embryos ectopically expressing thyroid hormone receptor and is less responsive to retinoic acid in such embryos. Tretinoin 29-42 homeobox A1 S homeolog Xenopus laevis 60-69
7504177-15 1993 The previously characterized retinoic acid-responsive gene, Xhox.lab2, can be induced by thyroid hormone in embryos ectopically expressing thyroid hormone receptor and is less responsive to retinoic acid in such embryos. Tretinoin 190-203 homeobox A1 S homeolog Xenopus laevis 60-69
8238530-0 1993 Retinoic acid increases elastin in neonatal rat lung fibroblast cultures. Tretinoin 0-13 elastin Rattus norvegicus 24-31
8641674-4 1996 The PP2A activity of the cells incubated for 18 h with retinoic acid was much more greatly activated by protamine compared with the activity of the cells incubated without retinoic acid. Tretinoin 172-185 protein phosphatase 2 phosphatase activator Homo sapiens 4-8
34372519-2 2021 Contrary to the Old World mammarenavirus group, these viruses are not able to completely suppress the innate immune response and trigger a robust interferon (IFN)-I response via retinoic acid-inducible gene I (RIG-I). Tretinoin 178-191 DExD/H-box helicase 58 Homo sapiens 210-215
8641674-5 1996 These results strongly suggest a conversion of PP2A holoenzyme from PP2A1 to PP2A0 during the initial process of the retinoic acid-induced differentiation. Tretinoin 117-130 protein phosphatase 2 phosphatase activator Homo sapiens 47-51
8600156-4 1996 Expression of the mcl-1 mRNA was found to increase rapidly in ML-1 cells exposed to inducers of monocyte/macrophage differentiation (phorbol esters or lymphocyte conditioned medium), but not cells exposed to an inducer of granulocyte differentiation (retinoic acid). Tretinoin 251-264 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 18-23
34136084-11 2021 The Numb fate determinant protein thus appears to regulate the retinoic acid embryonic morphogen using the Fgr Src-Family-Kinase. Tretinoin 63-76 NUMB endocytic adaptor protein Homo sapiens 4-8
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 CD8a molecule Homo sapiens 136-139
8105479-5 1993 In contrast, transcripts encoding Hoxb-1 (Hox-2.9) and cellular RA binding protein II (CRABPII) are activated by RA for a longer period of time in the RAR gamma-/- lines compared to the wild-type F9 line. Tretinoin 64-66 cellular retinoic acid binding protein 2 Homo sapiens 87-94
8400267-4 1993 CRABPII, an RA cytoplasmic binding protein linked to RA"s metabolization pathway, is induced by ATRA in different cell systems. Tretinoin 96-100 cellular retinoic acid binding protein 2 Homo sapiens 0-7
8400267-9 1993 High levels of CRABPII (median, 20 fmol/mg of protein) were detected in the cells of the 4 patients at relapse but were not detected before ATRA therapy. Tretinoin 140-144 cellular retinoic acid binding protein 2 Homo sapiens 15-22
34088744-4 2021 Mechanistically, intestinal cDC1-derived PD-L1, TGFbeta, and retinoic acid contributed to the generation of gut-tropic CCR9+CD103+FoxP3+CD8+ Tregs Last, CD103-deficient CD8+ T cells lacked tolerogenic activity in vivo, indicating a role for CD103 in FoxP3+CD8+ Treg function. Tretinoin 61-74 CD8a molecule Homo sapiens 256-259
8631988-8 1996 Both retinoic acid and a retinoid selective for the nuclear retinoic acid receptors were very potent suppressors of cornifin beta expression while an analog selective for the nuclear retinoid X receptors was much less effective, suggesting that a specific retinoid signaling pathway is involved in this suppression. Tretinoin 5-18 small proline rich protein 1B Homo sapiens 116-129
35594692-4 2022 In a 3D culture system, RA promoted capillary sprout development and promoted the subsequent adipogenesis of intramuscular SVF cells by activating VEGFA/VEGFR2 signaling. Tretinoin 24-26 kinase insert domain receptor Homo sapiens 153-159
8274452-8 1993 Although this difference in retinoid X receptor alpha expression could contribute to RA resistance, the mechanism involved in producing this resistance could not be fully elucidated in these studies. Tretinoin 85-87 retinoid X receptor alpha Homo sapiens 28-53
8274453-9 1993 Retinoic acid-treated, but not untreated, cells lost expression of vimentin and fibronectin, gained the ability to incorporate acetylated low density lipoprotein, and expressed Factor VIII-related antigen. Tretinoin 0-13 vimentin Mus musculus 67-75
8681349-9 1996 The fibronectin and type I collagen depositions in pre-migratory outflow tract cardiac jelly in retinoic acid-treated embryonic heart were reduced compared to those in the control. Tretinoin 96-109 fibronectin 1 Mus musculus 4-15
8162338-1 1993 Mammalian cell cytoplasm contains at least two proteins which bind retinoic acid (RA): CRABP I and CRABP II. Tretinoin 67-80 cellular retinoic acid binding protein 2 Homo sapiens 99-107
8162338-1 1993 Mammalian cell cytoplasm contains at least two proteins which bind retinoic acid (RA): CRABP I and CRABP II. Tretinoin 82-84 cellular retinoic acid binding protein 2 Homo sapiens 99-107
35565751-1 2022 Cellular retinoic acid binding proteins (CRABP1 and CRABP2) bind all-trans-retinoic acid (atRA), the active metabolite of vitamin A, with high affinity. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 52-58
35565751-1 2022 Cellular retinoic acid binding proteins (CRABP1 and CRABP2) bind all-trans-retinoic acid (atRA), the active metabolite of vitamin A, with high affinity. Tretinoin 65-88 cellular retinoic acid binding protein 2 Homo sapiens 52-58
35565751-1 2022 Cellular retinoic acid binding proteins (CRABP1 and CRABP2) bind all-trans-retinoic acid (atRA), the active metabolite of vitamin A, with high affinity. Tretinoin 90-94 cellular retinoic acid binding protein 2 Homo sapiens 52-58
35565751-2 2022 CRABP1 and CRABP2 have been shown to interact with the atRA-clearing cytochrome P450 enzymes CYP26B1 and CYP26C1 and with nuclear retinoic acid receptors (RARs). Tretinoin 130-143 cellular retinoic acid binding protein 2 Homo sapiens 11-17
35565751-3 2022 We hypothesized that CRABP1 and CRABP2 also alter atRA metabolism and clearance by CYP26A1, the third key atRA-metabolizing enzyme in the CYP26 family. Tretinoin 50-54 cellular retinoic acid binding protein 2 Homo sapiens 32-38
8375477-6 1993 Although c-jun expression was induced with RA, rapid and predominant induction of junB expression was specifically observed with NaB, which is regulated by both transcriptional and post-transcriptional mechanisms. Tretinoin 43-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-14
8598228-1 1996 B-myb and c-myb expression is high in neuroblastoma cells and declines during retinoic acid-induced differentiation. Tretinoin 78-91 MYB proto-oncogene like 2 Homo sapiens 0-5
8413217-0 1993 Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 186-205
8413217-6 1993 Region II binding activity was present in undifferentiated cells at low levels but was greatly augmented by RA treatment because of activation of a nuclear hormone receptor heterodimer composed of the retinoid X receptor (RXR beta) and the RA receptor (RAR beta). Tretinoin 108-110 retinoid X receptor alpha Homo sapiens 201-220
35493071-7 2022 Rbp7 deficient adipocytes had opposite effects of the overexpression, which were rescued by RA supplementation. Tretinoin 92-94 retinol binding protein 7, cellular Mus musculus 0-4
35493071-8 2022 Indirect assessment of relative nuclear RA levels using RAR response element (RARE)-Luc reporter assay demonstrated that Rbp7 overexpression significantly increased RARE-Luc reporter activity. Tretinoin 40-42 retinol binding protein 7, cellular Mus musculus 121-125
35493071-9 2022 Rbp7 overexpression significantly increased expression of Raldh1, responsible for RA production, and up-regulation of Lrat and Cyp26a1, involved in retinol storage and RA catabolism, respectively, in 3T3-L1 adipocytes. Tretinoin 82-84 retinol binding protein 7, cellular Mus musculus 0-4
8214087-10 1993 Retinoic acid further increased steady-state mRNA levels and MGP secretion at later culture intervals, an effect which was serum dependent. Tretinoin 0-13 matrix Gla protein Rattus norvegicus 61-64
8598228-1 1996 B-myb and c-myb expression is high in neuroblastoma cells and declines during retinoic acid-induced differentiation. Tretinoin 78-91 MYB proto-oncogene, transcription factor Homo sapiens 10-15
8708944-0 1996 Influence of retinoic acid on the expression of cytokeratins, vimentin and ICAM-1 in human gingival epithelia in vitro. Tretinoin 13-26 vimentin Homo sapiens 62-70
8359222-10 1993 Moreover, the interaction between GalTase and these glycoproteins exhibited characteristic changes during retinoic acid-induced F9 cell differentiation. Tretinoin 106-119 beta-4-galactosyltransferase 7 Drosophila melanogaster 34-41
35412614-4 2022 Here, we integrate RNA-seq, histone modification ChIP-seq, and ATAC-seq data to show that loss of PBRM1 results in de novo gains in H3K4me3 peaks throughout the epigenome including activation of a retinoic acid biosynthesis and signaling gene signature. Tretinoin 197-210 polybromo 1 Homo sapiens 98-103
35412614-5 2022 We show that one such target gene, ALDH1A1, which regulates a key step in retinoic acid biosynthesis, is consistently upregulated with PBRM1 loss in ccRCC cell lines and primary tumors, as well as non-malignant cells. Tretinoin 74-87 polybromo 1 Homo sapiens 135-140
35412614-9 2022 Implications: This study implicates the SWI/SNF subunit and tumor suppressor PBRM1 in the regulation of promoter histone modifications and retinoic acid biosynthesis and signaling pathways in ccRCC and functionally validates one such target gene, the aldehyde dehydrogenase ALDH1A1. Tretinoin 139-152 polybromo 1 Homo sapiens 77-82
8708944-8 1996 The results showed that RA had minor effects on the marker expression of JE but markedly enhanced expression of cytokeratins 8, 18, 19, vimentin and ICAM-1 in OGE. Tretinoin 24-26 vimentin Homo sapiens 136-144
8396608-7 1993 In contrast to these data, both CD271 and all-trans retinoic acid caused marked and significant (p < 0.05) elevation of cellular retinoic acid-binding protein-II (CRABP-II) messenger ribonucleic acid steady-state levels as judged by quantitative RNA blot analysis. Tretinoin 52-65 cellular retinoic acid binding protein 2 Homo sapiens 123-164
8652410-0 1996 Developmental expression and differential regulation by retinoic acid of Xenopus COUP-TF-A and COUP-TF-B. Tretinoin 56-69 nuclear receptor subfamily 2, group F, member 5 S homeolog Xenopus laevis 81-90
8396608-7 1993 In contrast to these data, both CD271 and all-trans retinoic acid caused marked and significant (p < 0.05) elevation of cellular retinoic acid-binding protein-II (CRABP-II) messenger ribonucleic acid steady-state levels as judged by quantitative RNA blot analysis. Tretinoin 52-65 cellular retinoic acid binding protein 2 Homo sapiens 166-174
8410463-6 1993 Individually, RA and calcitriol induced mRNA expression for ALP, matrix-gla protein (MGP), and osteopontin (OP). Tretinoin 14-16 matrix Gla protein Rattus norvegicus 65-83
8410463-6 1993 Individually, RA and calcitriol induced mRNA expression for ALP, matrix-gla protein (MGP), and osteopontin (OP). Tretinoin 14-16 matrix Gla protein Rattus norvegicus 85-88
8410463-8 1993 The combination of RA and calcitriol had a synergistic effect on ALP, OP, and especially MGP mRNA expression but significantly reduced the expression of pro-alpha 1(I) collagen mRNA. Tretinoin 19-21 matrix Gla protein Rattus norvegicus 89-92
8410463-9 1993 AA enhanced the effect of RA on the expression of pro-alpha 1(I) collagen, MGP, and ALP mRNAs as well as the effect of calcitriol on OP and MGP. Tretinoin 26-28 matrix Gla protein Rattus norvegicus 75-78
35402250-7 2022 The addition of tretinoin significantly improved the efficacy of anti-CTLA4/anti-PD-L1 combination therapy, and staggered scheduling was more efficacious than concomitant scheduling, in a dose-dependent manner. Tretinoin 16-25 cytotoxic T-lymphocyte-associated protein 4 Mus musculus 70-75
35402250-8 2022 The positive effects of tretinoin could be extended to ICT antibodies targeting OX40, GITR and CTLA4 monotherapy in multiple cancer models. Tretinoin 24-33 cytotoxic T-lymphocyte-associated protein 4 Mus musculus 95-100
8652410-13 1996 Retinoic acid (RA) treatment enhances xCOUP-TF-A expression in neurula stage embryos, whereas the expression of xCOUP-TF-B is inhibited during the same developmental period. Tretinoin 0-13 nuclear receptor subfamily 2, group F, member 5 S homeolog Xenopus laevis 38-48
35236271-4 2022 ADAM10 is the main alpha-secretase that cleaves APP, and it is regulated by the metabolic product of vitamin A (retinoic acid), which is being widely used recently in AD research as a target for treatment. Tretinoin 112-125 ADAM metallopeptidase domain 10 Rattus norvegicus 0-6
8652410-13 1996 Retinoic acid (RA) treatment enhances xCOUP-TF-A expression in neurula stage embryos, whereas the expression of xCOUP-TF-B is inhibited during the same developmental period. Tretinoin 15-17 nuclear receptor subfamily 2, group F, member 5 S homeolog Xenopus laevis 38-48
8361753-9 1993 Activity of the RB1 promoter was found to be stimulated in retinoic-acid induced differentiated P19 cells compared to undifferentiated P19; this stimulation required intact Sp1 and ATF sites but not the putative E2F/DRTF1 binding site. Tretinoin 59-72 RB transcriptional corepressor 1 Mus musculus 16-19
20650177-14 1996 Possibly a-tRAG acts by way of limited hydrolysis to retinoic acid. Tretinoin 53-66 WD repeat domain 7 Mus musculus 11-15
8363581-6 1993 Northern-blot analysis with the IL-8R1 cDNA as probe revealed abundant expression of transcripts of different size in human neutrophils and low-level expression of a single RNA species in HL-60 cells differentiated with dimethyl sulphoxide and retinoic acid. Tretinoin 244-257 C-X-C motif chemokine receptor 1 Homo sapiens 32-38
8336949-0 1993 Synergistic increase of phorbol ester-induced c-fos mRNA expression by retinoic acid through stabilization of the c-fos message. Tretinoin 71-84 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51
35225106-8 2022 Consistently, in the GPL rat model, we observed a similar disorder; however, ATRA supplementation significantly not only corrected the disorder by increasing Rdh10, Aldh1a1 and decreasing Cyp26b1, but also reduced claudin-18 (P < 0.05). Tretinoin 77-81 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 188-195
8336949-0 1993 Synergistic increase of phorbol ester-induced c-fos mRNA expression by retinoic acid through stabilization of the c-fos message. Tretinoin 71-84 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-119
8555488-1 1996 We have recently found that all-trans retinoic acid (ATRA) upregulates thrombomodulin (TM) and downregulates tissue factor (TF) expression in acute myelogenous leukemia (AML) M3 cells (NB4) and acute monoblastic leukemia cells (U937) (Koyama et al, Blood 84:3001, 1994). Tretinoin 38-51 coagulation factor III, tissue factor Homo sapiens 109-122
8336949-3 1993 We now report, that RA synergistically enhances the induction of c-fos, but not c-jun mRNA by PMA in cells whose growth was stimulated by RA alone. Tretinoin 20-22 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-70
8394014-2 1993 The action of RA is thought to be mediated in part by the three nuclear receptors (RAR alpha, -beta, and -gamma), each of which is expressed as multiple isoforms. Tretinoin 14-16 retinoic acid receptor, alpha Mus musculus 83-111
8389913-9 1993 RXR alpha also transactivates promoter expression via the GB element in vivo in response to retinoic acid but in a largely EF-C-independent manner. Tretinoin 92-105 retinoid X receptor alpha Homo sapiens 0-9
35237663-2 2022 Among the nucleic acid sensors, activation of the RNA sensor Retinoic Acid-inducible Gene (RIG-I) using small hairpin RNAs has been shown to elicit powerful innate and adaptive immune responses. Tretinoin 61-74 DExD/H-box helicase 58 Homo sapiens 91-96
35144761-4 2022 IL-17REhighCCR10+ Th17 expressed more retinoic acid-related orphan receptor gamma t but fewer T-box-expressed-in-T-cells than IL-17RElowCCR10- Th17. Tretinoin 38-51 interleukin 17A Mus musculus 0-16
8555488-1 1996 We have recently found that all-trans retinoic acid (ATRA) upregulates thrombomodulin (TM) and downregulates tissue factor (TF) expression in acute myelogenous leukemia (AML) M3 cells (NB4) and acute monoblastic leukemia cells (U937) (Koyama et al, Blood 84:3001, 1994). Tretinoin 38-51 coagulation factor III, tissue factor Homo sapiens 124-126
8321221-1 1993 AP-2 is a retinoic acid-inducible and developmentally regulated activator of transcription. Tretinoin 10-23 transcription factor AP-2 alpha Homo sapiens 0-4
8555488-1 1996 We have recently found that all-trans retinoic acid (ATRA) upregulates thrombomodulin (TM) and downregulates tissue factor (TF) expression in acute myelogenous leukemia (AML) M3 cells (NB4) and acute monoblastic leukemia cells (U937) (Koyama et al, Blood 84:3001, 1994). Tretinoin 53-57 coagulation factor III, tissue factor Homo sapiens 109-122
35203546-0 2022 Somatostatin-Mediated Regulation of Retinoic Acid-Induced Differentiation of SH-SY5Y Cells: Neurotransmitters Phenotype Characterization. Tretinoin 36-49 somatostatin Homo sapiens 0-12
35203546-4 2022 Our results indicate that SST potentiates RA-induced differentiation of SH-SY5Y cells and involves regulating the subcellular distribution and expression of neurotransmitter markers and synaptophysin translocation to neurites in a time-dependent manner, anticipating the therapeutic implication of SST in neurodegeneration. Tretinoin 42-44 somatostatin Homo sapiens 26-29
8555488-1 1996 We have recently found that all-trans retinoic acid (ATRA) upregulates thrombomodulin (TM) and downregulates tissue factor (TF) expression in acute myelogenous leukemia (AML) M3 cells (NB4) and acute monoblastic leukemia cells (U937) (Koyama et al, Blood 84:3001, 1994). Tretinoin 53-57 coagulation factor III, tissue factor Homo sapiens 124-126
35203546-4 2022 Our results indicate that SST potentiates RA-induced differentiation of SH-SY5Y cells and involves regulating the subcellular distribution and expression of neurotransmitter markers and synaptophysin translocation to neurites in a time-dependent manner, anticipating the therapeutic implication of SST in neurodegeneration. Tretinoin 42-44 synaptophysin Homo sapiens 186-199
8388815-4 1993 In this paper we demonstrate that met/HGF/SFR mRNA, protein, and its ligand are expressed at a low level in undifferentiated P19 cells and that their expression is increased as P19 cells are induced to differentiate into neuroectodermal derivatives following treatment with retinoic acid (RA) and into mesodermal derivatives following treatment with dimethyl sulfoxide (DMSO). Tretinoin 274-287 hepatocyte growth factor Mus musculus 38-41
8555488-12 1996 Anticoagulant effects of ATRA, ie, upregulation of TM expression and downregulation of TF expression, are applied not only to established cell lines of specific subtypes (M3 and M5) but also to more universal AML (most cases of M3 and M5 and a part of the other types of AML) cells freshly isolated from patients. Tretinoin 25-29 coagulation factor III, tissue factor Homo sapiens 87-89
8866697-3 1996 At 10 microM RA a 3-fold increase in DOR mRNA at 48 h, and later (144 h) alterations were observed in NMDAR1 mRNA levels. Tretinoin 13-15 glutamate receptor, ionotropic, NMDA1 (zeta 1) Mus musculus 102-108
7684485-0 1993 Altered levels and splicing of the amyloid precursor protein in the adult rat hippocampus after treatment with DMSO or retinoic acid. Tretinoin 119-132 amyloid beta precursor protein Rattus norvegicus 35-60
8387013-6 1993 When older cultures (P1 and P2) were treated with RA, the cells acquired a characteristic epithelioid shape and increased their APase activity. Tretinoin 50-52 perforin 1 Gallus gallus 21-30
8387121-8 1993 CRABP (II), expressed in the developmental stage of the fetus, is suggested to modulate the action of retinoic acid as a "morphogen". Tretinoin 102-115 cellular retinoic acid binding protein 2 Homo sapiens 0-10
35123596-5 2022 NK cell levels decreased significantly in the patients in DEC and DEC/ATRA group after treatment (P<0.05); After treatment, the levels of CD8+ and CD3+T cells in the patients treated by DEC /priming regimen significantly increased (P<0.05), while the levels of CD3-HLA-DR+ B cells significantly decreased (P<0.05). Tretinoin 70-74 CD8a molecule Homo sapiens 138-141
8869967-3 1996 The effects of trans-retinoic acid (RA) on proliferation and cytokine gene expression in the human lung carcinoma Lu-CSF-1 are reported. Tretinoin 15-34 colony stimulating factor 1 Homo sapiens 117-122
8455948-1 1993 The thyroid hormone receptor alpha (THRA or c-erbA-1) gene belongs to a family of genes that encode nuclear receptors for various hydrophobic ligands such as steroids, retinoic acid and thyroid hormones. Tretinoin 168-181 thyroid hormone receptor alpha Homo sapiens 4-34
8455948-1 1993 The thyroid hormone receptor alpha (THRA or c-erbA-1) gene belongs to a family of genes that encode nuclear receptors for various hydrophobic ligands such as steroids, retinoic acid and thyroid hormones. Tretinoin 168-181 thyroid hormone receptor alpha Homo sapiens 36-40
8869967-3 1996 The effects of trans-retinoic acid (RA) on proliferation and cytokine gene expression in the human lung carcinoma Lu-CSF-1 are reported. Tretinoin 36-38 colony stimulating factor 1 Homo sapiens 117-122
8455948-1 1993 The thyroid hormone receptor alpha (THRA or c-erbA-1) gene belongs to a family of genes that encode nuclear receptors for various hydrophobic ligands such as steroids, retinoic acid and thyroid hormones. Tretinoin 168-181 thyroid hormone receptor alpha Homo sapiens 44-52
7501971-4 1996 We have previously identified six HOX genes (HOXC6, HOXC8, HOXD1, HOXD4, HOXD8, and HOXD9), by a sensitive PCR-based approach, in a cDNA library prepared from the human LA-N-5 NB cell line induced to differentiate with RA. Tretinoin 219-221 homeobox C6 Homo sapiens 45-50
8460936-10 1993 The ability of liver to esterify retinol in vivo was correlated with the in vitro activity of LRAT after retinoic acid induction. Tretinoin 105-118 lecithin retinol acyltransferase Rattus norvegicus 94-98
8950833-7 1996 Pentoxifylline (40 mumol/L), retinoic acid (0.01 mmol/L) and cyclosporin A (0.08 mumol/L) inhibited TF expression when added concurrently with LPS or TNF, but not when added 4 h after stimulation. Tretinoin 29-42 tumor necrosis factor Bos taurus 150-153
8460936-11 1993 We conclude that retinoic acid, an important end product of retinol metabolism, regulates a key aspect of hepatic retinol metabolism through its regulatory activity on liver LRAT. Tretinoin 17-30 lecithin retinol acyltransferase Rattus norvegicus 174-178
8463554-1 1993 The effect of retinoic acid (RA) on thyroid peroxidase (TPO) and thyroglobulin (Tg) gene expression was investigated in cultured human thyrocytes. Tretinoin 29-31 thyroid peroxidase Homo sapiens 56-59
8463554-5 1993 Furthermore, RA inhibited forskolin and 8-Bromo-cyclic-AMP-induced TPO and Tg gene expression, suggesting a distal action site for these cAMP mediated gene expressions. Tretinoin 13-15 thyroid peroxidase Homo sapiens 67-70
8463554-7 1993 The increased de novo TPO was markedly inhibited by RA. Tretinoin 52-54 thyroid peroxidase Homo sapiens 22-25
8463554-11 1993 In conclusion, RA inhibits the synthesis of TPO and Tg via the suppression of thyroid-specific gene expression although the exact site of RA action on these genes in human thyroids remains to be further elucidated. Tretinoin 15-17 thyroid peroxidase Homo sapiens 44-47
8463554-12 1993 These results suggest that RA may play a regulatory role in Tg and TPO gene expression, subsequently resulting in the suppression of thyroid hormone synthesis. Tretinoin 27-29 thyroid peroxidase Homo sapiens 67-70
8950833-9 1996 In contrast, exposure to LPS or TNF for 6 h induced marked expression of TF mRNA, which was inhibited by treatment with pentoxifylline, retinoic acid and cyclosporin A. Tretinoin 136-149 tumor necrosis factor Bos taurus 32-35
8381905-8 1993 When the cells are induced to differentiate along the neuronal pathway with retinoic acid, the levels of transcripts for both GAD genes rise dramatically. Tretinoin 76-89 glutamate decarboxylase 1 Homo sapiens 126-129
8530418-0 1995 Multiple functions of the TR2-11 orphan receptor in modulating activation of two key cis-acting elements involved in the retinoic acid signal transduction system. Tretinoin 121-134 nuclear receptor subfamily 2 group C member 1 Homo sapiens 26-29
7497526-3 1995 RA induced the expression of IL-5 and TGF-beta 2 mRNAs in the LPS-stimulated cells. Tretinoin 0-2 interleukin 5 Mus musculus 29-33
8097171-6 1993 Furthermore, retinoic acid-coated bead implants, which diminish cell death in the anterior necrotic zone, elicit a local inhibition of GHox-7 expression in the proximal anterior peripheral mesoderm. Tretinoin 13-26 msh homeobox 1 Gallus gallus 135-141
8396187-6 1993 In addition, 1 microM RA significantly reduced basal and TSH-induced TPO mRNA levels in normal, goitrous and adenomatous cells, but did not alter TGB mRNA levels. Tretinoin 22-24 thyroid peroxidase Homo sapiens 69-72
7497526-10 1995 These findings suggest that RA induces IgA production by (IL-5 + LPS)-stimulated B-cells in TGF-beta-independent and TGF-beta-dependent manners. Tretinoin 28-30 interleukin 5 Mus musculus 58-62
8929647-3 1995 Culture of his marrow cells at diagnosis showed that granulocyte colony-stimulating factor (G-CSF) promoted cell proliferation, while all-trans retinoic acid (ATRA) inhibited the proliferative effect of G-CSF and induced differentiation. Tretinoin 144-157 colony stimulating factor 3 Homo sapiens 203-208
1334022-2 1992 We have constructed a mutant RAR alpha that both exhibits dominant-negative activity against the normal RAR alpha in transient expression assays in mouse fibroblasts and inhibits retinoic acid-induced neutrophilic differentiation of the HL-60 human promyelocytic leukemia cell line. Tretinoin 179-192 retinoic acid receptor, alpha Mus musculus 29-38
8929647-3 1995 Culture of his marrow cells at diagnosis showed that granulocyte colony-stimulating factor (G-CSF) promoted cell proliferation, while all-trans retinoic acid (ATRA) inhibited the proliferative effect of G-CSF and induced differentiation. Tretinoin 159-163 colony stimulating factor 3 Homo sapiens 203-208
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 174-187 retinoic acid receptor alpha Homo sapiens 65-68
1445851-7 1992 RBP containing retinoic acid did not bind to TTR even at the high salt concentration. Tretinoin 15-28 retinol binding protein 4 Homo sapiens 0-3
1445851-8 1992 The data suggest that the TTR binding site on RBP is in close proximity to the retinoid binding site and that the head group of retinoic acid, when bound to RBP, presents steric hindrance for the interactions with TTR. Tretinoin 128-141 transthyretin Homo sapiens 26-29
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 174-187 retinoic acid receptor alpha Homo sapiens 70-79
1445851-8 1992 The data suggest that the TTR binding site on RBP is in close proximity to the retinoid binding site and that the head group of retinoic acid, when bound to RBP, presents steric hindrance for the interactions with TTR. Tretinoin 128-141 retinol binding protein 4 Homo sapiens 46-49
1445851-8 1992 The data suggest that the TTR binding site on RBP is in close proximity to the retinoid binding site and that the head group of retinoic acid, when bound to RBP, presents steric hindrance for the interactions with TTR. Tretinoin 128-141 retinol binding protein 4 Homo sapiens 157-160
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 65-67 retinoic acid receptor alpha Homo sapiens 70-79
1445851-8 1992 The data suggest that the TTR binding site on RBP is in close proximity to the retinoid binding site and that the head group of retinoic acid, when bound to RBP, presents steric hindrance for the interactions with TTR. Tretinoin 128-141 transthyretin Homo sapiens 214-217
7565738-3 1995 The greatest RA-dependent transactivation, seen with DR15, was similar to that observed with the canonical DR5. Tretinoin 13-15 TNF receptor superfamily member 10b Homo sapiens 107-110
1385214-9 1992 In contrast, the beta 2 isoform is expressed only transiently after RA-induction despite the continuous presence of RA. Tretinoin 68-70 hemoglobin, beta adult minor chain Mus musculus 17-23
1385214-9 1992 In contrast, the beta 2 isoform is expressed only transiently after RA-induction despite the continuous presence of RA. Tretinoin 116-118 hemoglobin, beta adult minor chain Mus musculus 17-23
7565739-2 1995 For ligand-induced activation by the retinoic acid receptor-retinoid X receptor (RAR-RXR) heterodimer, the RAR beta 2 promoter is dependent on the presence of E1A or E1A-like activity, since this promoter is activated by retinoic acid only in cells expressing such proteins. Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 81-84
7565739-4 1995 We now show that direct interaction between RAR and E1A is a requirement for retinoic acid-induced RAR beta 2 activation. Tretinoin 77-90 retinoic acid receptor alpha Homo sapiens 44-47
1334013-1 1992 The regulatory effects of retinoic acid (RA) on retinoic acid receptor (RAR) alpha, beta and gamma mRNA were examined in the F9 mouse teratocarcinoma cells. Tretinoin 41-43 retinoic acid receptor, alpha Mus musculus 48-82
7548224-3 1995 Differentiation of the HL-60 cells by all-trans retinoic acid resulted in a reduced growth rate and a marked decrease in the intracellular concentration of eEF-2. Tretinoin 48-61 eukaryotic translation elongation factor 2 Homo sapiens 156-161
1334013-6 1992 Short term treatment (< or = 24 hours) of RA induced both 3.1 and 3.3 kb RAR gamma transcripts. Tretinoin 45-47 retinoic acid receptor, gamma Mus musculus 76-85
1329924-10 1992 Besides these 2 proteins, we saw proteins of M(r) 51,000 (p51) and 55,000 that were covalently labeled by E2 in MCF-7 cells and by RA in both MCF-7 and MCF-7/AdrR cells. Tretinoin 131-133 zinc finger protein 398 Homo sapiens 58-61
1327537-0 1992 All-trans and 9-cis retinoic acid induction of CRABPII transcription is mediated by RAR-RXR heterodimers bound to DR1 and DR2 repeated motifs. Tretinoin 20-33 cellular retinoic acid binding protein 2 Homo sapiens 47-54
1327537-0 1992 All-trans and 9-cis retinoic acid induction of CRABPII transcription is mediated by RAR-RXR heterodimers bound to DR1 and DR2 repeated motifs. Tretinoin 20-33 retinoid X receptor alpha Homo sapiens 88-91
1327537-1 1992 Two cooperating retinoic acid response elements (RAREs) in the cellular retinoic acid-binding protein II (CRABPII) gene mediate differential transcriptional transactivation by retinoic acid receptors (RARs) and retinoid X receptors (RXRs) in P19 embryonal carcinoma cells. Tretinoin 16-29 cellular retinoic acid binding protein 2 Homo sapiens 63-104
8519445-4 1995 Retinoic acid decreased N-myc and c-myc and induced neurite outgrowth (a differentiation marker). Tretinoin 0-13 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 24-29
1327537-1 1992 Two cooperating retinoic acid response elements (RAREs) in the cellular retinoic acid-binding protein II (CRABPII) gene mediate differential transcriptional transactivation by retinoic acid receptors (RARs) and retinoid X receptors (RXRs) in P19 embryonal carcinoma cells. Tretinoin 16-29 cellular retinoic acid binding protein 2 Homo sapiens 106-113
1328295-10 1992 These data suggest that there are sufficient amounts of retinoic acid in treated skin to activate gene transcription over both RARs and RXR-alpha. Tretinoin 56-69 retinoid X receptor alpha Homo sapiens 136-145
8519445-4 1995 Retinoic acid decreased N-myc and c-myc and induced neurite outgrowth (a differentiation marker). Tretinoin 0-13 MYC proto-oncogene, bHLH transcription factor Homo sapiens 34-39
8714690-1 1995 We have examined the accumulation of MAP1A in retinoic acid induced P19 embryonal carcinoma (EC) neurons. Tretinoin 46-59 microtubule associated protein 1A Homo sapiens 37-42
1331926-1 1992 Retinoic acid inhibits the enzyme collagenase by forming an inactive complex between the liganded nuclear retinoic acid receptors and c-Jun, a protein that is itself an activator of the collagenase gene. Tretinoin 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 134-139
1339275-0 1992 A retinoic acid response element from the rat CRBPI promoter is activated by an RAR/RXR heterodimer. Tretinoin 2-15 retinol binding protein 1 Rattus norvegicus 46-51
7657595-1 1995 We have recently identified a small region (amino acids 405-419) within the ligand binding domain of a truncated human retinoic acid receptor alpha (delta 419) that is required for binding of 9-cis-retinoic acid (RA), but not all-trans-retinoic acid (t-RA). Tretinoin 229-249 retinoic acid receptor alpha Homo sapiens 119-147
1385460-9 1992 In epithelial cell cultures induced by retinoic acid (RA) treatment, each of the desmosomal proteins is organized into punctate desmosome-like structures with the appearance of simple epithelial K8/K18 IFs. Tretinoin 39-52 keratin 8 Homo sapiens 195-205
7657595-8 1995 Data presented here suggest that high affinity 9-cis-RA binding to a hRAR alpha depends on an interaction with the two amino acids methionine 406 and isoleucine 410. Tretinoin 47-55 retinoic acid receptor alpha Homo sapiens 69-79
1360810-3 1992 RA treatment of F9 cells causes the appearance of a DNAse I hypersensitive site 3" of Hox-1.6, approximately 5 kb downstream of the Hox-1.6 promoter, and this site has been shown to reflect the presence of an RA-responsive enhancer 3" of the gene. Tretinoin 0-2 deoxyribonuclease I Mus musculus 52-59
7658715-0 1995 Isoforms of PML-retinoic acid receptor alpha fused transcripts affect neither clinical features of acute promyelocytic leukemia nor prognosis after treatment with all-trans retinoic acid. Tretinoin 16-29 PML nuclear body scaffold Homo sapiens 12-15
1323566-11 1992 RA alleviates the inhibition of myogenic differentiation, probably by activating MyoD protein and myogenin gene transcription. Tretinoin 0-2 myogenin Rattus norvegicus 98-106
8578951-3 1995 Our results showed that endothelial cells incubated in vitro with retinoic acid increased the release of tissue plasminogen activator to the supernatant without concomitant secretion of plasminogen activator inhibitor-1. Tretinoin 66-79 serpin family E member 1 Homo sapiens 186-219
1328967-2 1992 All-trans-retinoic acid (t-RA) has been known to be a high-affinity ligand for RAR but only a weak ligand for RXR, while the endogenous ligand for RXR was unknown. Tretinoin 0-23 retinoid X receptor alpha Homo sapiens 110-113
1328967-2 1992 All-trans-retinoic acid (t-RA) has been known to be a high-affinity ligand for RAR but only a weak ligand for RXR, while the endogenous ligand for RXR was unknown. Tretinoin 25-29 retinoid X receptor alpha Homo sapiens 110-113
1332208-1 1992 In these studies, we wished to determine the effect of teratogenic doses of retinoic acid on the expression of cellular retinoic acid binding protein I (CRABP-I) mRNA, cellular retinoic acid binding protein II (CRABP-II) mRNA, cellular retinol binding protein I (CRBP-I) mRNA, and cellular retinol binding protein II (CRBP-II) mRNA in mouse conceptuses. Tretinoin 76-89 cellular retinoic acid binding protein I Mus musculus 111-151
1332208-1 1992 In these studies, we wished to determine the effect of teratogenic doses of retinoic acid on the expression of cellular retinoic acid binding protein I (CRABP-I) mRNA, cellular retinoic acid binding protein II (CRABP-II) mRNA, cellular retinol binding protein I (CRBP-I) mRNA, and cellular retinol binding protein II (CRBP-II) mRNA in mouse conceptuses. Tretinoin 76-89 cellular retinoic acid binding protein I Mus musculus 153-160
7619051-2 1995 Pretreatment of keratinocytes with all-trans-retinoic retinoic acid inhibited the EGF induction of ODC activity. Tretinoin 54-67 epidermal growth factor Homo sapiens 82-85
1334737-1 1992 Many of the biological effects of retinoic acid are mediated by its nuclear receptors (RAR-alpha, RAR-beta, and RAR-gamma), and each of these three receptors exist in multiple isoforms. Tretinoin 34-47 retinoic acid receptor, alpha Mus musculus 87-96
1334737-1 1992 Many of the biological effects of retinoic acid are mediated by its nuclear receptors (RAR-alpha, RAR-beta, and RAR-gamma), and each of these three receptors exist in multiple isoforms. Tretinoin 34-47 retinoic acid receptor, gamma Mus musculus 112-121
1384809-0 1992 Effects of lithium chloride and retinoic acid on the expression of genes from the Xenopus laevis Hox 2 complex. Tretinoin 32-45 homeobox B7 S homeolog Xenopus laevis 97-102
7619051-4 1995 Treatment with all-trans-retinoic acid for 24 h resulted in a dose- and time-dependent decrease of up to 52% in EGF binding to EGF receptors and a 30-75% decrease in EGF-receptor quantity. Tretinoin 15-38 epidermal growth factor Homo sapiens 112-115
7619051-4 1995 Treatment with all-trans-retinoic acid for 24 h resulted in a dose- and time-dependent decrease of up to 52% in EGF binding to EGF receptors and a 30-75% decrease in EGF-receptor quantity. Tretinoin 15-38 epidermal growth factor Homo sapiens 127-130
7619051-4 1995 Treatment with all-trans-retinoic acid for 24 h resulted in a dose- and time-dependent decrease of up to 52% in EGF binding to EGF receptors and a 30-75% decrease in EGF-receptor quantity. Tretinoin 15-38 epidermal growth factor Homo sapiens 127-130
1314955-6 1992 We also find that retinoic acid-dependent transactivation by retinoic acid receptors is inhibited by the truncated ErbA proteins. Tretinoin 18-31 thyroid hormone receptor alpha Homo sapiens 115-119
7619051-5 1995 In addition, when cells were treated with both UV radiation and all-trans-retinoic acid, their effects were additive in causing a decrease in EGF binding. Tretinoin 68-87 epidermal growth factor Homo sapiens 142-145
7547504-9 1995 In contrast, the osteoinductive effect of matrix from retinoic acid-treated cells was blocked with both vgr-1 and TGF-beta 1 antibodies, suggesting that TGF-beta 1 may act prior to vgr-1 during osteoblastic differentiation. Tretinoin 54-67 bone morphogenetic protein 6 Mus musculus 104-109
1315627-5 1992 partially inhibited (61%) the induction of ODC by BSF at 5 h. In addition, retinoic acid (RA, 5 micrograms per mouse given 30 min before BSF) effectively inhibited BSF-induced ODC by 68%, while indomethacin (100 micrograms per mouse 2 h before BSF) had little or no effect. Tretinoin 75-88 ornithine decarboxylase, structural 1 Mus musculus 176-179
1315627-5 1992 partially inhibited (61%) the induction of ODC by BSF at 5 h. In addition, retinoic acid (RA, 5 micrograms per mouse given 30 min before BSF) effectively inhibited BSF-induced ODC by 68%, while indomethacin (100 micrograms per mouse 2 h before BSF) had little or no effect. Tretinoin 90-92 ornithine decarboxylase, structural 1 Mus musculus 43-46
1315627-5 1992 partially inhibited (61%) the induction of ODC by BSF at 5 h. In addition, retinoic acid (RA, 5 micrograms per mouse given 30 min before BSF) effectively inhibited BSF-induced ODC by 68%, while indomethacin (100 micrograms per mouse 2 h before BSF) had little or no effect. Tretinoin 90-92 ornithine decarboxylase, structural 1 Mus musculus 176-179
1315216-8 1992 Northern blot and slot-blot analyses revealed that neuronal cells overexpressing RAR alpha-mRNA exhibited an enhanced sensitivity to exogenous and endogenous retinoic acid in terms of thymosin beta 10 mRNA. Tretinoin 158-171 thymosin, beta 10 Rattus norvegicus 184-200
1531473-0 1992 Induction of phosphatidylinositol-glycan-linked Fc gamma RIII in human monocytic THP-1 cells by transforming growth factor-beta 1 and retinoic acid. Tretinoin 134-147 Fc gamma receptor IIIa Homo sapiens 48-61
7547504-9 1995 In contrast, the osteoinductive effect of matrix from retinoic acid-treated cells was blocked with both vgr-1 and TGF-beta 1 antibodies, suggesting that TGF-beta 1 may act prior to vgr-1 during osteoblastic differentiation. Tretinoin 54-67 bone morphogenetic protein 6 Mus musculus 181-186
1310350-4 1992 RXR alpha interacts both with TRs and with RARs, forming heterodimers in solution that strongly interact with a variety of T3/retinoic acid response elements. Tretinoin 126-139 retinoid X receptor alpha Homo sapiens 0-9
7615640-0 1995 Expression of Notch 1, 2 and 3 is regulated by epithelial-mesenchymal interactions and retinoic acid in the developing mouse tooth and associated with determination of ameloblast cell fate. Tretinoin 87-100 notch 1 Mus musculus 14-30
1310350-5 1992 Transfection experiments show that RXR alpha can greatly enhance the transcriptional activity of TR and RAR at low retinoic acid concentrations that do not significantly activate RXR alpha itself. Tretinoin 115-128 retinoid X receptor alpha Homo sapiens 35-44
1310351-0 1992 Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling. Tretinoin 56-69 retinoid X receptor alpha Homo sapiens 0-19
1310351-1 1992 Cellular responsiveness to retinoic acid and its metabolites is conferred through two structurally and pharmacologically distinct families of receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 27-40 retinoid X receptor alpha Homo sapiens 195-215
1310351-1 1992 Cellular responsiveness to retinoic acid and its metabolites is conferred through two structurally and pharmacologically distinct families of receptors: the retinoic acid receptors (RAR) and the retinoid X receptors (RXR). Tretinoin 27-40 retinoid X receptor alpha Homo sapiens 217-220
7615982-7 1995 Gel mobility shift analysis revealed that retinoid receptors in nuclear extracts from human skin formed a specific complex with a DNA probe containing the retinoic acid response element in the mouse CRBP gene. Tretinoin 155-168 retinol binding protein 1, cellular Mus musculus 199-203
1334741-5 1992 RBP-retinol circulation supplies target cells, which then activate retinol into retinoic acid (RA) if they possess the NAD-dependent enzymatic oxidation system. Tretinoin 80-93 retinol binding protein 4 Homo sapiens 0-3
7775578-2 1995 The application of RA on primary cultures of embryonic somites, limb buds, and neonatal limbs inhibited myogenic differentiation in a dose-dependent way as indicated by the repression of: (a) myotube formation, (b) myosin heavy chain protein accumulation, (c) myosin light chain (MLC) 1/3, alpha sk-actin and myogenic factor transcript expression. Tretinoin 19-21 myosin, light polypeptide 3 Mus musculus 260-288
1334741-5 1992 RBP-retinol circulation supplies target cells, which then activate retinol into retinoic acid (RA) if they possess the NAD-dependent enzymatic oxidation system. Tretinoin 95-97 retinol binding protein 4 Homo sapiens 0-3
1728634-5 1992 Similar changes in TGF-beta 1 and TGF-beta 2 immunoreactivity and mRNA levels, as observed in retinoic acid-treated skin, were observed in skin following topical application of the irritant sodium lauryl sulfate, indicating that the alterations induced by retinoic acid were not specific. Tretinoin 94-107 transforming growth factor beta 2 Homo sapiens 34-44
7540644-0 1995 Modulation of human G-CSF receptor mRNA and protein in normal and leukemic myeloid cells by G-CSF and retinoic acid. Tretinoin 102-115 colony stimulating factor 3 receptor Homo sapiens 20-34
1728634-5 1992 Similar changes in TGF-beta 1 and TGF-beta 2 immunoreactivity and mRNA levels, as observed in retinoic acid-treated skin, were observed in skin following topical application of the irritant sodium lauryl sulfate, indicating that the alterations induced by retinoic acid were not specific. Tretinoin 256-269 transforming growth factor beta 2 Homo sapiens 34-44
7540644-0 1995 Modulation of human G-CSF receptor mRNA and protein in normal and leukemic myeloid cells by G-CSF and retinoic acid. Tretinoin 102-115 colony stimulating factor 3 Homo sapiens 20-25
7540644-6 1995 Whereas G-CSF did not affect mRNA levels for its receptor in myeloid leukemic cell lines, exposure of the acute promyelocytic cell line, NB4, to all-trans retinoic acid induced a striking increase in G-CSF receptor mRNA expression and resulted in increased G-CSF receptor surface expression. Tretinoin 155-168 colony stimulating factor 3 receptor Homo sapiens 200-214
1299410-3 1992 Using a structural approach to identify domains of the glucocorticoid receptor responsible for interactions with affiliated transacting factors and DNA, we have identified a putative helix-turn-zipper motif that is conserved in all steroid, thyroid hormone, retinoic acid, and vitamin-D3 receptors. Tretinoin 258-271 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 55-78
7540644-6 1995 Whereas G-CSF did not affect mRNA levels for its receptor in myeloid leukemic cell lines, exposure of the acute promyelocytic cell line, NB4, to all-trans retinoic acid induced a striking increase in G-CSF receptor mRNA expression and resulted in increased G-CSF receptor surface expression. Tretinoin 155-168 colony stimulating factor 3 receptor Homo sapiens 257-271
1748717-0 1991 Dexamethasone and retinoic acid regulate the expression of epidermal growth factor receptor mRNA by distinct mechanisms. Tretinoin 18-31 epidermal growth factor receptor Rattus norvegicus 59-91
1748717-1 1991 Retinoic acid and dexamethasone have antagonistic effects on epidermal growth factor (EGF) receptor expression in fetal rat lung (FRL) cells: Receptor synthesis is enhanced by retinoic acid and reduced by dexamethasone. Tretinoin 0-13 epidermal growth factor receptor Rattus norvegicus 61-99
1748717-1 1991 Retinoic acid and dexamethasone have antagonistic effects on epidermal growth factor (EGF) receptor expression in fetal rat lung (FRL) cells: Receptor synthesis is enhanced by retinoic acid and reduced by dexamethasone. Tretinoin 176-189 epidermal growth factor receptor Rattus norvegicus 61-99
1961035-3 1991 Some blast cells were stimulated by RA in the presence of rGM-CSF and rIL-3 and inhibited when cultured with RA and rG-CSF. Tretinoin 36-38 colony stimulating factor 2 Rattus norvegicus 58-65
1961035-7 1991 Colony formation was stimulated by RA in the presence of rGM-CSF or rIL-3 but inhibited by RA with rG-CSF. Tretinoin 35-37 colony stimulating factor 2 Rattus norvegicus 57-64
7540644-7 1995 The effect of retinoic acid on G-CSF receptor mRNA on NB4 cells occurred early, before morphologic evidence of differentiation, and required protein synthesis. Tretinoin 14-27 colony stimulating factor 3 receptor Homo sapiens 31-45
7540644-8 1995 All-trans retinoic acid also upregulated G-CSF receptor mRNA in the myeloid leukemia cell line HL-60. Tretinoin 0-23 colony stimulating factor 3 receptor Homo sapiens 41-55
1795406-8 1991 In embryonal carcinoma cells, both the abundance of ezrin and the proportion of ezrin associated with the cytoskeletal fraction increase upon induction of neuronal differentiation with retinoic acid. Tretinoin 185-198 ezrin Rattus norvegicus 52-57
1795406-8 1991 In embryonal carcinoma cells, both the abundance of ezrin and the proportion of ezrin associated with the cytoskeletal fraction increase upon induction of neuronal differentiation with retinoic acid. Tretinoin 185-198 ezrin Rattus norvegicus 80-85
7540644-10 1995 Furthermore, the ability of retinoic acid to up-regulate G-CSF receptor may account for the synergistic effect of G-CSF and retinoic acid in differentiation induction of acute promyelocytic leukemia. Tretinoin 28-41 colony stimulating factor 3 receptor Homo sapiens 57-71
7540644-10 1995 Furthermore, the ability of retinoic acid to up-regulate G-CSF receptor may account for the synergistic effect of G-CSF and retinoic acid in differentiation induction of acute promyelocytic leukemia. Tretinoin 28-41 colony stimulating factor 3 Homo sapiens 57-62
1651173-1 1991 The vitamin A derivative retinoic acid exerts its effects on transcription through two distinct classes of nuclear receptors, the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). Tretinoin 25-38 retinoid X receptor alpha Homo sapiens 167-186
7540644-10 1995 Furthermore, the ability of retinoic acid to up-regulate G-CSF receptor may account for the synergistic effect of G-CSF and retinoic acid in differentiation induction of acute promyelocytic leukemia. Tretinoin 124-137 colony stimulating factor 3 receptor Homo sapiens 57-71
7540644-10 1995 Furthermore, the ability of retinoic acid to up-regulate G-CSF receptor may account for the synergistic effect of G-CSF and retinoic acid in differentiation induction of acute promyelocytic leukemia. Tretinoin 124-137 colony stimulating factor 3 Homo sapiens 57-62
1646397-6 1991 These results indicate that different RAREs may play a fundamental role in defining distinctive retinoic acid cellular response pathways and suggest that retinoic acid response pathways mediated by RXR alpha play an important role in cholesterol and retinoid transport and metabolism. Tretinoin 96-109 retinoid X receptor alpha Homo sapiens 198-207
7656409-0 1995 Reversal of alcohol"s effects on neurite extension and on neuronal GAP43/B50, N-myc, and c-myc protein levels by retinoic acid. Tretinoin 113-126 growth associated protein 43 Homo sapiens 67-76
1646397-6 1991 These results indicate that different RAREs may play a fundamental role in defining distinctive retinoic acid cellular response pathways and suggest that retinoic acid response pathways mediated by RXR alpha play an important role in cholesterol and retinoid transport and metabolism. Tretinoin 154-167 retinoid X receptor alpha Homo sapiens 198-207
7656409-0 1995 Reversal of alcohol"s effects on neurite extension and on neuronal GAP43/B50, N-myc, and c-myc protein levels by retinoic acid. Tretinoin 113-126 MYC proto-oncogene, bHLH transcription factor Homo sapiens 89-94
7656409-5 1995 Five nM retinoic acid alone induced differentiation and increased GAP43/B50 levels to 230% of control. Tretinoin 8-21 growth associated protein 43 Homo sapiens 66-71
1877746-0 1991 A hypothetical mechanism for fetal alcohol syndrome involving ethanol inhibition of retinoic acid synthesis at the alcohol dehydrogenase step. Tretinoin 84-97 aldo-keto reductase family 1 member A1 Homo sapiens 115-136
7656409-5 1995 Five nM retinoic acid alone induced differentiation and increased GAP43/B50 levels to 230% of control. Tretinoin 8-21 growth associated protein 43 Homo sapiens 72-75
7656409-6 1995 These retinoic acid-induced increases in GAP43/B50 and neurite outgrowth, and decreases in N-myc and c-myc, were reversed dose-dependently by alcohol (0-0.5%). Tretinoin 6-19 growth associated protein 43 Homo sapiens 41-50
7656409-6 1995 These retinoic acid-induced increases in GAP43/B50 and neurite outgrowth, and decreases in N-myc and c-myc, were reversed dose-dependently by alcohol (0-0.5%). Tretinoin 6-19 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 91-96
7656409-6 1995 These retinoic acid-induced increases in GAP43/B50 and neurite outgrowth, and decreases in N-myc and c-myc, were reversed dose-dependently by alcohol (0-0.5%). Tretinoin 6-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 101-106
1848696-2 1991 In this report we demonstrate that retinoic acid (RA) also regulates PEPCK expression by inducing a 3-fold increase in the rate of transcription of the PEPCK gene. Tretinoin 35-48 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 69-74
1848696-2 1991 In this report we demonstrate that retinoic acid (RA) also regulates PEPCK expression by inducing a 3-fold increase in the rate of transcription of the PEPCK gene. Tretinoin 35-48 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 152-157
7536661-0 1995 Insulin-like growth factor (IGF) I and retinoic acid induce the synthesis of IGF-binding protein 5 in rat osteoblastic cells. Tretinoin 39-52 insulin-like growth factor binding protein 5 Rattus norvegicus 77-98
1848696-2 1991 In this report we demonstrate that retinoic acid (RA) also regulates PEPCK expression by inducing a 3-fold increase in the rate of transcription of the PEPCK gene. Tretinoin 50-52 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 69-74
1848696-2 1991 In this report we demonstrate that retinoic acid (RA) also regulates PEPCK expression by inducing a 3-fold increase in the rate of transcription of the PEPCK gene. Tretinoin 50-52 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 152-157
1848696-3 1991 A RA response element located between -468 and -431 in the PEPCK promoter mediates a 7-fold increase in expression of a chimeric construct containing the basal PEPCK promoter ligated to the chloramphenicol acetyltransferase reporter gene. Tretinoin 2-4 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 59-64
1848696-3 1991 A RA response element located between -468 and -431 in the PEPCK promoter mediates a 7-fold increase in expression of a chimeric construct containing the basal PEPCK promoter ligated to the chloramphenicol acetyltransferase reporter gene. Tretinoin 2-4 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 160-165
7536661-5 1995 Treatment of Ob cells with either IGF-I or all-trans-retinoic acid (RA) caused a time- and dose-dependent increase in IGFBP-5 messenger RNA (mRNA) levels, as determined by Northern blot analysis. Tretinoin 53-66 insulin-like growth factor binding protein 5 Rattus norvegicus 118-125
7536661-5 1995 Treatment of Ob cells with either IGF-I or all-trans-retinoic acid (RA) caused a time- and dose-dependent increase in IGFBP-5 messenger RNA (mRNA) levels, as determined by Northern blot analysis. Tretinoin 68-70 insulin-like growth factor 1 Rattus norvegicus 34-39
7536661-5 1995 Treatment of Ob cells with either IGF-I or all-trans-retinoic acid (RA) caused a time- and dose-dependent increase in IGFBP-5 messenger RNA (mRNA) levels, as determined by Northern blot analysis. Tretinoin 68-70 insulin-like growth factor binding protein 5 Rattus norvegicus 118-125
1706723-0 1991 Effects of retinoic acid on NIH3T3 cell transformation by the H-ras oncogene. Tretinoin 11-24 Harvey rat sarcoma virus oncogene Mus musculus 62-67
1706723-1 1991 Exposure of NIH3T3 cells to retinoic acid resulted in a dose-dependent modulation of transformed focus formation after transfection with an activated H-ras oncogene. Tretinoin 28-41 Harvey rat sarcoma virus oncogene Mus musculus 150-155
1706723-6 1991 A transformed cell line containing H-ras underwent reversion of the transformed phenotype after 4 weeks of treatment with retinoic acid, as determined by alterations in cell morphology and anchorage-independent growth. Tretinoin 122-135 Harvey rat sarcoma virus oncogene Mus musculus 35-40
2059565-6 1991 Blockade of protein synthesis with cycloheximide abrogated the stimulatory action of retinoic acid upon thymosin beta-10 mRNA accumulation; this observation suggests that activation of the thymosin beta-10 gene in this cell line by retinoic acid is dependent upon the de novo synthesis of a labile protein. Tretinoin 85-98 thymosin, beta 10 Rattus norvegicus 104-120
7672716-3 1995 In four of the patients PCR was positive for the PML/RAR alpha transcript immediately after ATRA treatment and/or after the first consolidation chemotherapy course. Tretinoin 92-96 PML nuclear body scaffold Homo sapiens 49-62
2059565-6 1991 Blockade of protein synthesis with cycloheximide abrogated the stimulatory action of retinoic acid upon thymosin beta-10 mRNA accumulation; this observation suggests that activation of the thymosin beta-10 gene in this cell line by retinoic acid is dependent upon the de novo synthesis of a labile protein. Tretinoin 85-98 thymosin, beta 10 Rattus norvegicus 189-205
2059565-6 1991 Blockade of protein synthesis with cycloheximide abrogated the stimulatory action of retinoic acid upon thymosin beta-10 mRNA accumulation; this observation suggests that activation of the thymosin beta-10 gene in this cell line by retinoic acid is dependent upon the de novo synthesis of a labile protein. Tretinoin 232-245 thymosin, beta 10 Rattus norvegicus 189-205
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 41-54 retinol binding protein 4 Homo sapiens 241-244
1768424-2 1991 Tritiated analogues of retinol (ROL) and retinoic acid corresponding to substituted benzo[b]thiophene (CD-270) alcohol and carboxylic acid, respectively, were used for the binding studies of the cellular retinoic acid-(CRABP-) and retinol-(CRBP-) binding proteins in human epidermal cells and serum retinol-binding protein (RBP). Tretinoin 204-217 retinol binding protein 4 Homo sapiens 241-244
7727406-7 1995 In addition, hRAR alpha and the minimal hormone binding domain (amino acids 186-410) bound ATRA with a positive, cooperative mechanism. Tretinoin 91-95 retinoic acid receptor alpha Homo sapiens 13-23
2176887-5 1990 However, at 40 degrees C, PEPCK gene expression was stimulated by the combination of DEX plus retinoic acid; additionally, DEX and retinoic acid potentiated the Bt2cAMP-mediated PEPCK induction. Tretinoin 131-144 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 178-183
2176887-6 1990 In RALA255-10G cells, optimal PEPCK gene expression required the simultaneous presence of DEX, retinoic acid, and Bt2cAMP; DEX had to be present at all times. Tretinoin 95-108 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 30-35
7542037-2 1995 We report here that neurotrophin receptors are differentially expressed in distinct populations of retinoic acid-differentiated P19 cells. Tretinoin 99-112 interleukin 23 subunit alpha Homo sapiens 128-131
7733941-2 1995 Herein we report on the relative levels of Ah-receptor-mRNA and TCDD-induced cytochrome P450 1A1 (Cyp1A1)-mRNA and their modulation by retinoic acid in the human keratinocyte cell line HaCaT. Tretinoin 135-148 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 77-96
2257974-4 1990 After formation of parietal endoderm-like cells by addition of retinoic acid (RA) to BRL-CM, the 1.8-kb transcript of TGF beta 1 and PDGF-A expression were reduced, IGF II mRNA and a single TGF beta 3 transcript of 3.8 kb were induced while PDGF-B and TGF beta 4 remained virtually unchanged. Tretinoin 63-76 insulin-like growth factor 2 Rattus norvegicus 165-171
2257974-4 1990 After formation of parietal endoderm-like cells by addition of retinoic acid (RA) to BRL-CM, the 1.8-kb transcript of TGF beta 1 and PDGF-A expression were reduced, IGF II mRNA and a single TGF beta 3 transcript of 3.8 kb were induced while PDGF-B and TGF beta 4 remained virtually unchanged. Tretinoin 63-76 platelet derived growth factor subunit B Rattus norvegicus 241-247
2178220-5 1990 Treatment with 10(-7) and 10(-6) M beta-all-trans-retinoic acid (RA) for 24 h caused a 1.5- to 2-fold increase in RAR alpha and RAR gamma mRNA, whereas lower concentrations of RA were ineffective. Tretinoin 65-67 retinoic acid receptor, alpha Mus musculus 114-123
7733941-2 1995 Herein we report on the relative levels of Ah-receptor-mRNA and TCDD-induced cytochrome P450 1A1 (Cyp1A1)-mRNA and their modulation by retinoic acid in the human keratinocyte cell line HaCaT. Tretinoin 135-148 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 98-104
2178220-5 1990 Treatment with 10(-7) and 10(-6) M beta-all-trans-retinoic acid (RA) for 24 h caused a 1.5- to 2-fold increase in RAR alpha and RAR gamma mRNA, whereas lower concentrations of RA were ineffective. Tretinoin 65-67 retinoic acid receptor, gamma Mus musculus 128-137
2178220-11 1990 However, S91-C154, a RA-resistant mutant subclone derived from S91-C2 cells, showed mRNA levels of RAR alpha and RAR gamma and induction of RAR beta by RA similar to those detected in the sensitive S91-C2 cells. Tretinoin 21-23 retinoic acid receptor, alpha Mus musculus 99-108
7895645-7 1995 In addition, IGF-I and -II opposed the stimulatory effect of retinoic acid on collagenase transcripts. Tretinoin 61-74 insulin-like growth factor 1 Rattus norvegicus 13-26
2178220-11 1990 However, S91-C154, a RA-resistant mutant subclone derived from S91-C2 cells, showed mRNA levels of RAR alpha and RAR gamma and induction of RAR beta by RA similar to those detected in the sensitive S91-C2 cells. Tretinoin 21-23 retinoic acid receptor, gamma Mus musculus 113-122
7895645-8 1995 Immunoreactive collagenase levels were not detectable in control or IGF-treated cultures, but IGF-I and -II decreased the levels induced by retinoic acid by 70-90%. Tretinoin 140-153 insulin-like growth factor 1 Rattus norvegicus 94-107
7752674-0 1995 Upregulation of p21 RAS levels in HL-60 cells during differentiation induction with DMSO, all-trans-retinoic acid and TPA. Tretinoin 90-113 HRas proto-oncogene, GTPase Homo sapiens 16-23
2288880-0 1990 Characterization of epidermal growth factor receptor induction by retinoic acid in a chemically transformed rat liver cell line. Tretinoin 66-79 epidermal growth factor receptor Rattus norvegicus 20-52
2288880-10 1990 This indicates that RA induction of EGF receptor synthesis in GP6ac cells involves signaling pathways distinct from those utilized by phorbol esters. Tretinoin 20-22 epidermal growth factor receptor Rattus norvegicus 36-48
2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tretinoin 128-141 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-107
2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tretinoin 128-141 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 211-216
2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tretinoin 128-141 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-231
2178224-6 1990 These results suggest that RA inhibits collagenase transcription at least in part through inhibition of c-fos. Tretinoin 27-29 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-109
2164682-1 1990 A sequence that confers transcriptional responsiveness to retinoic acid was identified in the promoter of the mouse retinoic acid receptor (RAR) beta gene. Tretinoin 58-71 retinoic acid receptor, alpha Mus musculus 116-138
7891690-7 1995 DNA-binding analysis revealed that RAR gamma Bm382 is able to form a heterodimer with the retinoid X receptor and bind to the different types of retinoic acid response elements with almost the same efficiency as normal RAR. Tretinoin 145-158 retinoic acid receptor alpha Homo sapiens 35-38
2164682-1 1990 A sequence that confers transcriptional responsiveness to retinoic acid was identified in the promoter of the mouse retinoic acid receptor (RAR) beta gene. Tretinoin 58-71 retinoic acid receptor, alpha Mus musculus 140-143
2164682-4 1990 This element conferred retinoic acid responsiveness on heterologous promoters via all three subtypes of RAR yet failed to support transcriptional activation by the thyroid hormone, estrogen, glucocorticoid, or vitamin D receptors. Tretinoin 23-36 retinoic acid receptor, alpha Mus musculus 104-107
7706255-0 1995 Retinoic acid induction of human tissue-type plasminogen activator gene expression via a direct repeat element (DR5) located at -7 kilobases. Tretinoin 0-13 TNF receptor superfamily member 10b Homo sapiens 112-115
1698521-4 1990 ES cells exposed to RA in the presence of LIF/DIA largely resembled F9 EC + RA after 5 days, while ES cells deprived of LIF/DIA formed a culture with mixed phenotype resembling P19 EC + RA. Tretinoin 20-22 LIF, interleukin 6 family cytokine Rattus norvegicus 42-45
7706255-1 1995 All-trans-retinoic acid (RA) and retinoids induce synthesis of tissue-type plasminogen activator (t-PA) in endothelial and neuroblastoma cells in vitro and in rats in vivo. Tretinoin 0-23 plasminogen activator, tissue type Rattus norvegicus 63-96
7706255-1 1995 All-trans-retinoic acid (RA) and retinoids induce synthesis of tissue-type plasminogen activator (t-PA) in endothelial and neuroblastoma cells in vitro and in rats in vivo. Tretinoin 0-23 plasminogen activator, tissue type Rattus norvegicus 98-102
7706255-1 1995 All-trans-retinoic acid (RA) and retinoids induce synthesis of tissue-type plasminogen activator (t-PA) in endothelial and neuroblastoma cells in vitro and in rats in vivo. Tretinoin 25-27 plasminogen activator, tissue type Rattus norvegicus 63-96
7706255-1 1995 All-trans-retinoic acid (RA) and retinoids induce synthesis of tissue-type plasminogen activator (t-PA) in endothelial and neuroblastoma cells in vitro and in rats in vivo. Tretinoin 25-27 plasminogen activator, tissue type Rattus norvegicus 98-102
7706255-5 1995 A functional retinoic acid response element (RARE), consisting of a direct repeat of the GGGTCA motif spaced by 5 nucleotides (t-PA/DR5), was localized at -7.3 kilobases. Tretinoin 13-26 TNF receptor superfamily member 10b Homo sapiens 132-135
7706255-6 1995 The t-PA/DR5 element interacted with the heterodimer composed of retinoic acid receptor alpha and retinoid X receptor alpha in vitro, whereas its mutation abolished induction by RA in transient expression. Tretinoin 178-180 TNF receptor superfamily member 10b Homo sapiens 9-12
7532580-0 1995 Insulin-like growth factor-binding protein-3 production by MCF-7 breast cancer cells: stimulation by retinoic acid and cyclic adenosine monophosphate and differential effects of estradiol. Tretinoin 101-114 insulin like growth factor binding protein 3 Homo sapiens 0-44
7532580-5 1995 Treatment with retinoic acid (RA, 100 nM) increased medium concentrations of IGFBP-3 to 175 +/- 8% (mean +/- SE, n = 4), and IGFBP-6 to 217 +/- 20% of control values. Tretinoin 15-28 insulin like growth factor binding protein 3 Homo sapiens 77-84
7532580-5 1995 Treatment with retinoic acid (RA, 100 nM) increased medium concentrations of IGFBP-3 to 175 +/- 8% (mean +/- SE, n = 4), and IGFBP-6 to 217 +/- 20% of control values. Tretinoin 30-32 insulin like growth factor binding protein 3 Homo sapiens 77-84
7867602-1 1995 In this study, we have demonstrated that retinoic acid (RA) and thyroid hormone (T3) stimulate the synthesis and release of human placental lactogen (hPL), one of the major secretory products of syncytiotrophoblast cells. Tretinoin 41-54 galectin 1 Homo sapiens 150-153
7605750-4 1995 Using probes for zebrafish krx20 and pax2, it is demonstrated that retinoic acid affects the expression domains of these regulatory genes in a manner that is consistent with the neuroanatomical data. Tretinoin 67-80 early growth response 2b Danio rerio 27-32
2159384-5 1990 Unexpectedly, cotransfection of Jun and Fos expression vectors suppresses basal level transcription of the osteocalcin gene and suppresses induction by both retinoic acid and vitamin D3. Tretinoin 157-170 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-43
7852380-4 1995 In cultured keratinocytes, all-trans retinoic acid, 9-cis retinoic acid, and CD367 activated beta RARE but not RXRE via endogenous RAR.RXR (ED50 = 2.3, 3.8, and 0.3 nM, respectively) whereas SR11237 showed no significant effect. Tretinoin 37-50 retinoic acid receptor alpha Homo sapiens 98-101
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 230-239
7869768-0 1995 Effect of retinoic acid isomers on proliferation, differentiation and PML relocalization in the APL cell line NB4. Tretinoin 10-23 PML nuclear body scaffold Homo sapiens 70-73
2157970-5 1990 In addition, we show that both RAR gamma isoforms are expressed maximally at midgestation in structures known to be affected adversely by retinoic acid administration to pregnant mice. Tretinoin 138-151 retinoic acid receptor, gamma Mus musculus 31-40
1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 36-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88
7660322-0 1995 Maternal restraint stress-enhanced teratogenicity of all-trans-retinoic acid in CD-1 mice. Tretinoin 53-76 CD1 antigen complex Mus musculus 80-84
1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 36-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-119
1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 51-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88
1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 51-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-119
1963081-3 1990 This induction is an indirect response to RA and requires a functional AP1 binding site within the c-jun promoter. Tretinoin 42-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-74
1963081-3 1990 This induction is an indirect response to RA and requires a functional AP1 binding site within the c-jun promoter. Tretinoin 42-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-104
1963081-8 1990 By contrast, the induction of c-fos by phorbol esters or cAMP is greatly diminished after RA treatment. Tretinoin 90-92 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35
1963081-13 1990 Thus, the induction of c-jun transcription by RA, although indirect, can have an important role in the differentiation process. Tretinoin 46-48 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-28
7831296-0 1995 A retinoic acid-triggered cascade of HOXB1 gene activation. Tretinoin 2-15 homeobox B1 Homo sapiens 37-42
2124549-0 1990 Effect of retinol and retinoic acid supplemented diets on cytochrome P-450 content and UDP glucuronosyltransferase activities in vitamin A-deficient rat liver. Tretinoin 22-35 UDP glycosyltransferase 2 family, polypeptide B Rattus norvegicus 87-114
7831296-3 1995 We have identified an RA-responsive element in the promoter of HOXB1 gene composed of two functionally separable sites: (i) a DR-2 sequence, which is the direct target of the RA receptor retinoid X receptor heterodimer; and (ii) a motif for an RA-inducible and tissue-specific coactivator termed retinoid-inducible protein. Tretinoin 22-24 homeobox B1 Homo sapiens 63-68
7831296-3 1995 We have identified an RA-responsive element in the promoter of HOXB1 gene composed of two functionally separable sites: (i) a DR-2 sequence, which is the direct target of the RA receptor retinoid X receptor heterodimer; and (ii) a motif for an RA-inducible and tissue-specific coactivator termed retinoid-inducible protein. Tretinoin 175-177 homeobox B1 Homo sapiens 63-68
7831297-1 1995 We have recently identified a promoter proximal retinoic acid (RA)-responsive site in the 5" region of the HOXB1 gene. Tretinoin 48-61 homeobox B1 Homo sapiens 107-112
2084113-4 1990 We have shown that anti-estrogens induce the production of TGF-beta 1 in mammary carcinoma cells and fetal fibroblasts, whereas retinoic acid specifically induces TGF-beta 2 in primary epidermal keratinocytes. Tretinoin 128-141 transforming growth factor beta 2 Homo sapiens 163-173
7831297-1 1995 We have recently identified a promoter proximal retinoic acid (RA)-responsive site in the 5" region of the HOXB1 gene. Tretinoin 63-65 homeobox B1 Homo sapiens 107-112
7831297-2 1995 In this report, we have identified the second RA-responsive site in the 3" region of the HOXB1 gene. Tretinoin 46-48 homeobox B1 Homo sapiens 89-94
7851378-5 1995 However, when coincubated with activin A, retinoic acid specifically induced the synthesis of thromboxane-A-synthase-specific mRNA and induced an increase in enzyme activity with a synergistic effect on cyclooxygenase-1 protein and mRNA. Tretinoin 42-55 prostaglandin-endoperoxide synthase 1 Mus musculus 203-219
33819809-7 2021 Mechanistically, the retinoic acid-inducible gene I (RIG-I) pathway in MDMs was stimulated by EBV-encoded small RNA-1 (EBER-1) whereas the inhibition of these pathways by BX-795 almost abolished the production of these two cytokines and IDO induction. Tretinoin 21-34 DExD/H-box helicase 58 Homo sapiens 53-58
7756127-3 1995 This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA. Tretinoin 140-142 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 44-50
33807534-1 2021 The mitochondrial antiviral-signaling protein (MAVS, also known as VISA, IPS-1, or CARDIF) plays an essential role in the type I interferon (IFN) response and in retinoic acid-inducible gene I (RIG-I) mediated antiviral innate immunity in mammals. Tretinoin 162-175 DExD/H-box helicase 58 Homo sapiens 194-199
7756127-3 1995 This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA. Tretinoin 210-212 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 44-50
7756127-5 1995 Using the reverse transcriptase-polymerase chain reaction, we have demonstrated that the effects of 3-methylcholanthrene, dimethylbenz[a]anthracene and RA on CYP1A1 expression correlate with an increase of CYP1A1 mRNA level. Tretinoin 152-154 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 158-164
7756127-5 1995 Using the reverse transcriptase-polymerase chain reaction, we have demonstrated that the effects of 3-methylcholanthrene, dimethylbenz[a]anthracene and RA on CYP1A1 expression correlate with an increase of CYP1A1 mRNA level. Tretinoin 152-154 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 206-212
8589757-1 1995 The 5 Kd (MW), retinoic acid responsive thymosin beta-10 protein is expressed at relatively high levels in embryonic tissues, and its mRNA is abundant in a variety of tumors and tumor cell lines. Tretinoin 15-28 thymosin beta 10 Homo sapiens 40-56
33237598-4 2021 Our analysis revealed an over-representation of the newly identified upper wound fibroblasts in regenerative wound conditions, which express the retinoic acid binding protein Crabp1. Tretinoin 145-158 cellular retinoic acid binding protein I Mus musculus 175-181
30309678-5 2018 mRNA expression of Oct4 and Dazl were downregulated in embryonic stem cells by the retinoic acid group, whereas Mvh transcription was reduced by retinoic acid and estrogen group in these cells compared to the control group. Tretinoin 145-158 DEAD box helicase 4 Mus musculus 112-115
30309678-6 2018 But, retinoic acid with estrogen group-treated cells exhibited increased mRNA expression of Stra8, Fragilis, Sycp3, GDF9, and Stella compared to untreated controls. Tretinoin 5-18 developmental pluripotency-associated 3 Mus musculus 126-132
8773125-2 1995 The presence of PML/RAR-alpha fusion gene produced as a result of the unique chromosomal translocation in APML is a marker of the sensitivity to ATRA therapy. Tretinoin 145-149 PML nuclear body scaffold Homo sapiens 16-19
25360083-5 2014 We report that ATRA-BDNF induced significant increases in expression of key synaptic genes, brain-specific miRNA and miRNA biogenesis machinery, and in AChE activity, compared with ATRA alone. Tretinoin 15-19 brain derived neurotrophic factor Homo sapiens 20-24
8773125-2 1995 The presence of PML/RAR-alpha fusion gene produced as a result of the unique chromosomal translocation in APML is a marker of the sensitivity to ATRA therapy. Tretinoin 145-149 retinoic acid receptor alpha Homo sapiens 20-29
7775389-1 1995 Retinoic acid-induced differentiation of human leukemic HL-60 cells is accompanied with the early induction of an ecto-enzyme of NAD+ glycohydrolase (NADase), which has recently been identified as human leukocyte cell surface antigen CD38 [Kontani, K. et al. Tretinoin 0-13 CD38 molecule Homo sapiens 234-238
7988794-1 1994 The developmental expression of retinoic acid (RA) nuclear receptors RAR(alpha, beta, gamma) and RXR(alpha, beta, gamma) was analysed during mouse odontogenesis by in situ hybridization on frozen sections and compared with the expression patterns of the cellular retinoic acid binding proteins CRABPI and II. Tretinoin 32-45 retinoic acid receptor, alpha Mus musculus 69-119
7988794-1 1994 The developmental expression of retinoic acid (RA) nuclear receptors RAR(alpha, beta, gamma) and RXR(alpha, beta, gamma) was analysed during mouse odontogenesis by in situ hybridization on frozen sections and compared with the expression patterns of the cellular retinoic acid binding proteins CRABPI and II. Tretinoin 47-49 retinoic acid receptor, alpha Mus musculus 69-119
7775389-6 1995 The prior treatment was, however, not essential for the toxin-induced inhibition of the cell differentiation; the inhibition by the addition of pertussis toxin was still observed even after retinoic acid-induced expression of CD38 antigen. Tretinoin 190-203 CD38 molecule Homo sapiens 226-230
7775389-10 1995 Thus, the whole process of the retinoic acid-induced cell differentiation appeared to consist of two distinguishable periods in terms of sensitivity to pertussis toxin; the toxin-insensitive early period characterized by the induction of CD38 NADase activity and the toxin-sensitive late period in which the secretion of a differentiation-supporting factor might be involved. Tretinoin 31-44 CD38 molecule Homo sapiens 238-242
34936504-10 2022 Dual-luciferase reporter assay and electrophoretic mobility shift assay showed that NR1D1 inhibited Atg5 transcription by binding to two putative retinoic acid-related orphan receptor response elements within the promoter. Tretinoin 146-159 nuclear receptor subfamily 1, group D, member 1 Mus musculus 84-89
7719245-13 1995 The comparison of the biological activities mediated by PML-RAR alpha and PLZF-RAR alpha may give new insights into the pathogenesis as well as the mechanisms of ATRA-induced differentiation in APL. Tretinoin 162-166 PML nuclear body scaffold Homo sapiens 56-59
34288810-0 2021 All-trans-retinoic acid suppresses rat embryo hindlimb bud mesenchymal chondrogenesis by modulating HoxD9 expression. Tretinoin 0-23 homeo box D9 Rattus norvegicus 100-105
34288810-6 2021 Sox9 and Col2a1 in rEHBMCs were downregulated by ATRA in a dose-dependent manner at both mRNA and protein levels. Tretinoin 49-53 SRY-box transcription factor 9 Rattus norvegicus 0-4
34288810-7 2021 Similarly, HoxD9 was downregulated by ATRA in a dose-dependent manner, in parallel with the cartilage-specific molecules Sox9 and Col2a1. Tretinoin 38-42 homeo box D9 Rattus norvegicus 11-16
7719245-13 1995 The comparison of the biological activities mediated by PML-RAR alpha and PLZF-RAR alpha may give new insights into the pathogenesis as well as the mechanisms of ATRA-induced differentiation in APL. Tretinoin 162-166 retinoic acid receptor alpha Homo sapiens 60-69
34288810-7 2021 Similarly, HoxD9 was downregulated by ATRA in a dose-dependent manner, in parallel with the cartilage-specific molecules Sox9 and Col2a1. Tretinoin 38-42 SRY-box transcription factor 9 Rattus norvegicus 121-125
7719245-13 1995 The comparison of the biological activities mediated by PML-RAR alpha and PLZF-RAR alpha may give new insights into the pathogenesis as well as the mechanisms of ATRA-induced differentiation in APL. Tretinoin 162-166 retinoic acid receptor alpha Homo sapiens 79-88
34288810-9 2021 Overexpression of HoxD9 reversed the effects of ATRA. Tretinoin 48-52 homeo box D9 Rattus norvegicus 18-23
34288810-10 2021 These results demonstrate that ATRA suppresses chondrogenesis in rEHBMCs by inhibiting the expression of HoxD9 and its downstream protein targets, including Sox9 and Col2a1. Tretinoin 31-35 homeo box D9 Rattus norvegicus 105-110
7706222-7 1994 Furthermore, cellular ELP binding elements and the Moloney leukemia virus long terminal repeat were activated by retinoic acid. Tretinoin 113-126 nuclear receptor subfamily 5 group A member 1 Homo sapiens 22-25
7969156-1 1994 Retinoic acid (RA) activates transcription of the RA receptor beta 2 (RAR beta 2) gene in embryonal carcinoma (EC) cells. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 70-73
34537259-8 2021 The expression levels of retinoic acid inducible gene I (RIG-I), melanoma differentiation-associated gene-5(MDA5), Toll-like receptor3(TLR3) and interferon regulatory Factor 3(IRF3), as well as IFNalpha and IFNbeta, were increased in parallel with MxA upregulation. Tretinoin 25-38 DExD/H-box helicase 58 Homo sapiens 57-62
7969156-1 1994 Retinoic acid (RA) activates transcription of the RA receptor beta 2 (RAR beta 2) gene in embryonal carcinoma (EC) cells. Tretinoin 15-17 retinoic acid receptor alpha Homo sapiens 70-73
7969156-2 1994 This activation involves binding of the RAR/retinoid X receptor (RAR/RXR) heterodimer to the RA-responsive element (beta RARE). Tretinoin 40-42 retinoic acid receptor alpha Homo sapiens 65-68
7961949-1 1994 The three-dimensional structures of complexes between bovine plasma retinol-binding protein (RBP) and three retinol analogs with different end groups (fenretinide, all-trans retinoic acid, and axerophthene) have been determined to 1.8-1.9-A resolution. Tretinoin 168-187 retinol binding protein 4 Bos taurus 93-96
34766598-10 2021 In addition, deficiency in retinoic acid and thyroxine transport was exhibited by the dramatic increase of transthyretin (TTHY). Tretinoin 27-40 transthyretin Homo sapiens 107-120
34766598-10 2021 In addition, deficiency in retinoic acid and thyroxine transport was exhibited by the dramatic increase of transthyretin (TTHY). Tretinoin 27-40 transthyretin Homo sapiens 122-126
7999103-0 1994 GDP-ribosyl cyclase activity as a measure of CD38 induction by retinoic acid in HL-60 cells. Tretinoin 63-76 CD38 molecule Homo sapiens 45-49
34827649-0 2021 Similarities in DSG1 and KRT3 Downregulation through Retinoic Acid Treatment and PAX6 Knockdown Related Expression Profiles: Does PAX6 Affect RA Signaling in Limbal Epithelial Cells? Tretinoin 53-66 desmoglein 1 Homo sapiens 16-20
7999103-1 1994 Retinoic acid (RA) treatment of HL-60 cells induces surface expression of CD38. Tretinoin 0-13 CD38 molecule Homo sapiens 74-78
7999103-1 1994 Retinoic acid (RA) treatment of HL-60 cells induces surface expression of CD38. Tretinoin 15-17 CD38 molecule Homo sapiens 74-78
7961696-4 1994 When the cells were treated with retinoic acid either alone or in the presence of cAMP for 120 h, PKC alpha mRNA and protein levels increased, whereas those of PKC beta and PKC gamma became undetectable. Tretinoin 33-46 protein kinase C gamma Homo sapiens 173-182
34147602-6 2021 Via chip-qPCR and RT-qPCR, genes involved in lipid metabolism and cell proliferation were target genes of RARalpha/RXRalpha in small intestinal organoids treated with RA and lipid micelles. Tretinoin 167-169 retinoic acid receptor, alpha Mus musculus 106-114
7958440-0 1994 Reciprocal changes in Hox D13 and RAR-beta 2 expression in response to retinoic acid in chick limb buds. Tretinoin 71-84 homeobox D13 Gallus gallus 22-29
7958440-0 1994 Reciprocal changes in Hox D13 and RAR-beta 2 expression in response to retinoic acid in chick limb buds. Tretinoin 71-84 retinoic acid receptor beta Gallus gallus 34-42
7958440-6 1994 However, we find that the effect of RA on Hox D13 gene expression at the distal end of wing buds at stage 25/26 is downregulation of transcript expression. Tretinoin 36-38 homeobox D13 Gallus gallus 42-49
7958440-7 1994 Furthermore, we find that activation of ectopic Hox D13 expression in response to implantation of RA beads along the anterior margin at stage 20/21 is indirect. Tretinoin 98-100 homeobox D13 Gallus gallus 48-55
7958440-8 1994 Finally, the effects of RA exposure on Hox D13 expression appear to directly correlate with effects on the pattern of distal skeletal elements. Tretinoin 24-26 homeobox D13 Gallus gallus 39-46
7958454-8 1994 Similarly to the parental cell line, addition of RA to P19 cells overexpressing Wnt-1 induced the neuroectodermal pathway, but expression of cell type-specific markers such as MASH-1, HNK-1, and GAP-43 was diminished and the morphology of neuronal processes, stained with an antibody to neurofilament, was abnormal. Tretinoin 49-51 growth associated protein 43 Homo sapiens 195-201
21559674-1 1994 The expression of alpha, beta and gamma retinoic acid receptors (RAR) was analyzed by reverse transcription polymerase chain reaction (RT/PCR) in several neuroblastoma derived cell lines before and after exposure to 10 nM retinoic acid. Tretinoin 40-53 retinoic acid receptor alpha Homo sapiens 65-68
21559674-4 1994 These data suggest that each NB cell line follows a particular retinoic acid-dependent differentiation route, at least with regard to the expression of RAR alpha, beta and gamma receptors. Tretinoin 63-76 retinoic acid receptor alpha Homo sapiens 152-161
7868977-0 1994 Effect of vitamin A deficiency and retinoic acid repletion on intestinal and hepatic apolipoprotein A-I mRNA levels of adult rats. Tretinoin 35-48 apolipoprotein A1 Rattus norvegicus 85-103
7868977-6 1994 Treatment of vitamin A-deficient rats with a single dose of retinoic acid (20 micrograms, 20 h before tissues were collected) reduced the hepatic apoA-I mRNA/beta-actin ratio by about 40%, while further reduction (about 60-65%) was observed after two treatments with retinoic acid. Tretinoin 60-73 apolipoprotein A1 Rattus norvegicus 146-152
7967725-9 1994 These mutated RAR receptors exhibit a reduced affinity for retinoic acid while retaining the ability to bind to a retinoic acid response element on DNA. Tretinoin 59-72 retinoic acid receptor alpha Homo sapiens 14-17
7967725-9 1994 These mutated RAR receptors exhibit a reduced affinity for retinoic acid while retaining the ability to bind to a retinoic acid response element on DNA. Tretinoin 114-127 retinoic acid receptor alpha Homo sapiens 14-17
7853357-5 1994 The dissociation constants (Kd) for RA were 1.4 nM for GST-hRAR alpha, 1.4 nM for GST-hRAR beta, and 3.3 nM for GST-mRAR gamma, respectively. Tretinoin 36-38 retinoic acid receptor alpha Homo sapiens 59-69
7934155-4 1994 Its cellular distribution is completely reorganized when compared to that of PML: the hybrid is found in multiple small nuclear substructures and upon retinoic acid treatment, it goes back to the normal PML localization, that is in typical well organized nuclear bodies. Tretinoin 151-164 PML nuclear body scaffold Homo sapiens 77-80
7934155-4 1994 Its cellular distribution is completely reorganized when compared to that of PML: the hybrid is found in multiple small nuclear substructures and upon retinoic acid treatment, it goes back to the normal PML localization, that is in typical well organized nuclear bodies. Tretinoin 151-164 PML nuclear body scaffold Homo sapiens 203-206
7934155-6 1994 Expression of PML-RAR alpha in HL60 or U937 cell has been shown to block their maturation while it can force their differentiation at high doses of retinoic acid. Tretinoin 148-161 PML nuclear body scaffold Homo sapiens 14-17
7934155-6 1994 Expression of PML-RAR alpha in HL60 or U937 cell has been shown to block their maturation while it can force their differentiation at high doses of retinoic acid. Tretinoin 148-161 retinoic acid receptor alpha Homo sapiens 18-27
7934155-7 1994 Different mechanisms are proposed to explain how PML-RAR alpha blocks differentiation and how this may be reversed by retinoic acid. Tretinoin 118-131 PML nuclear body scaffold Homo sapiens 49-52
7934155-7 1994 Different mechanisms are proposed to explain how PML-RAR alpha blocks differentiation and how this may be reversed by retinoic acid. Tretinoin 118-131 retinoic acid receptor alpha Homo sapiens 53-62
7831584-4 1994 The presence of the PML/retinoic acid receptor-alpha (PML/RAR-alpha) fusion gene, produced as a result of the unique chromosomal translocation in APL, is a marker of sensitivity to ATRA. Tretinoin 181-185 PML nuclear body scaffold Homo sapiens 20-23
7831584-4 1994 The presence of the PML/retinoic acid receptor-alpha (PML/RAR-alpha) fusion gene, produced as a result of the unique chromosomal translocation in APL, is a marker of sensitivity to ATRA. Tretinoin 181-185 retinoic acid receptor alpha Homo sapiens 24-52
7831584-4 1994 The presence of the PML/retinoic acid receptor-alpha (PML/RAR-alpha) fusion gene, produced as a result of the unique chromosomal translocation in APL, is a marker of sensitivity to ATRA. Tretinoin 181-185 PML nuclear body scaffold Homo sapiens 54-67
7878635-6 1994 Since the TM antigen levels in the ATRA-treated cells also paralleled the TM mRNA levels, the data suggests that TM induction in the HL-60 cells cultured with ATRA reflected the levels of TM biosynthesis and was independent of HL-60 differentiation into neutrophilic cells. Tretinoin 35-39 thrombomodulin Homo sapiens 74-76
7878635-6 1994 Since the TM antigen levels in the ATRA-treated cells also paralleled the TM mRNA levels, the data suggests that TM induction in the HL-60 cells cultured with ATRA reflected the levels of TM biosynthesis and was independent of HL-60 differentiation into neutrophilic cells. Tretinoin 35-39 thrombomodulin Homo sapiens 74-76
7878635-6 1994 Since the TM antigen levels in the ATRA-treated cells also paralleled the TM mRNA levels, the data suggests that TM induction in the HL-60 cells cultured with ATRA reflected the levels of TM biosynthesis and was independent of HL-60 differentiation into neutrophilic cells. Tretinoin 35-39 thrombomodulin Homo sapiens 74-76
7878635-7 1994 It was postulated that the appearance of TM with cofactor activity in neutrophilic cells differentiated from leukemic cells may contribute to prevention of vascular thrombosis in differentiation therapy of patients with acute promyelocytic leukemia by ATRA. Tretinoin 252-256 thrombomodulin Homo sapiens 41-43
7945330-7 1994 When F9 EC cells are induced to differentiate by treatment with RA for 48 h, there is a complete loss of the DNA/protein complex containing Oct-3. Tretinoin 64-66 POU class 5 homeobox 1 Homo sapiens 140-145
8093047-1 1994 An ecto-enzyme of NAD glycohydrolase induced by retinoic acid in human leukemic HL-60 cells is attributed to the molecule of leukocyte cell surface antigen CD38 (Kontani, K., et al. Tretinoin 48-61 CD38 molecule Homo sapiens 156-160
8077233-2 1994 Transcriptional down-regulation of thrombomodulin occurs following exposure of cultured endothelial cells to cytokines, while up-regulation is induced by retinoic acid and dibutyryl cyclic AMP. Tretinoin 154-167 thrombomodulin Homo sapiens 35-49
7818095-9 1994 In the RA-treated fetuses, the expression of C-CAM was higher in the epithelium of the oral cavity than in that of the nasal cavity, with a distinct borderline between differentiating nasal and oral epithelium of the palatal shelves. Tretinoin 7-9 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 45-50
7519122-0 1994 PML/RAR alpha+ U937 mutant and NB4 cell lines: retinoic acid restores the monocytic differentiation response to vitamin D3. Tretinoin 47-60 PML nuclear body scaffold Homo sapiens 0-13
7949394-9 1994 Treatment of parallel 3-week-old cultures with RA (10-100 nM) rapidly increased expression of the APase, ON, and OP genes severalfold. Tretinoin 47-49 secreted protein acidic and cysteine rich Gallus gallus 105-107
7522191-2 1994 In this study we found that most of the vimentin of undifferentiated HL60 and cells induced to differentiate either along the monocytoid pathway by 12-O-tetradecanoylphorbol-13-acetate (TPA) or along the granulocytic pathway by retinoic acid was soluble in a buffer containing 1% Triton X-100/0.6 mol/l KCl in which the intermediate filament proteins usually are not soluble. Tretinoin 228-241 vimentin Homo sapiens 40-48
34392174-8 2021 All-trans retinoic acid (ATRA) is a potent inducer of CD38 and improves social behavior, but it is toxic and teratogenic. Tretinoin 0-23 CD38 antigen Mus musculus 54-58
34392174-8 2021 All-trans retinoic acid (ATRA) is a potent inducer of CD38 and improves social behavior, but it is toxic and teratogenic. Tretinoin 25-29 CD38 antigen Mus musculus 54-58
34696339-2 2021 NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). Tretinoin 110-123 influenza virus NS1A binding protein Homo sapiens 0-3
34696339-2 2021 NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). Tretinoin 110-123 DExD/H-box helicase 58 Homo sapiens 142-147
34417575-0 2021 All-trans retinoic acid impairs glucose-stimulated insulin secretion by activating the RXR/SREBP-1c/UCP2 pathway. Tretinoin 0-23 uncoupling protein 2 Rattus norvegicus 100-104
34417575-5 2021 Importantly, ATRA impaired glucose-stimulated insulin secretion (GSIS) and increased the expression of sterol regulatory element-binding protein 1c (SREBP-1c) and uncoupling protein 2 (UCP2) in the rat pancreas. Tretinoin 13-17 uncoupling protein 2 Rattus norvegicus 163-183
34417575-5 2021 Importantly, ATRA impaired glucose-stimulated insulin secretion (GSIS) and increased the expression of sterol regulatory element-binding protein 1c (SREBP-1c) and uncoupling protein 2 (UCP2) in the rat pancreas. Tretinoin 13-17 uncoupling protein 2 Rattus norvegicus 185-189
34193153-4 2021 METHODS: Cellular retinoic acid (RA) binding protein 1 (Crabp1) knockout (CKO) mice were used for in vivo studies. Tretinoin 33-35 cellular retinoic acid binding protein I Mus musculus 56-62
34205274-0 2021 FMRP Interacts with RARalpha in Synaptic Retinoic Acid Signaling and Homeostatic Synaptic Plasticity. Tretinoin 41-54 fragile X messenger ribonucleoprotein 1 Mus musculus 0-4
34205274-0 2021 FMRP Interacts with RARalpha in Synaptic Retinoic Acid Signaling and Homeostatic Synaptic Plasticity. Tretinoin 41-54 retinoic acid receptor, alpha Mus musculus 20-28
34205274-4 2021 Here, we show that RARalpha, the RA receptor critically involved in synaptic RA signaling, directly interacts with FMRP. Tretinoin 77-79 retinoic acid receptor, alpha Mus musculus 19-27
34205274-4 2021 Here, we show that RARalpha, the RA receptor critically involved in synaptic RA signaling, directly interacts with FMRP. Tretinoin 77-79 fragile X messenger ribonucleoprotein 1 Mus musculus 115-119
34205274-6 2021 Blocking the interaction between FMRP and RARalpha with a small peptide corresponding to the critical binding site in RARalpha abolishes RA-induced increases in excitatory synaptic transmission, recapitulating the phenotype seen in the Fmr1 knockout mouse. Tretinoin 137-139 fragile X messenger ribonucleoprotein 1 Mus musculus 33-37
34205274-6 2021 Blocking the interaction between FMRP and RARalpha with a small peptide corresponding to the critical binding site in RARalpha abolishes RA-induced increases in excitatory synaptic transmission, recapitulating the phenotype seen in the Fmr1 knockout mouse. Tretinoin 137-139 retinoic acid receptor, alpha Mus musculus 42-50
34205274-6 2021 Blocking the interaction between FMRP and RARalpha with a small peptide corresponding to the critical binding site in RARalpha abolishes RA-induced increases in excitatory synaptic transmission, recapitulating the phenotype seen in the Fmr1 knockout mouse. Tretinoin 137-139 retinoic acid receptor, alpha Mus musculus 118-126
34205274-7 2021 Taken together, these data suggest that not only are functional FMRP and RARalpha necessary for RA-dependent homeostatic synaptic plasticity, but that the interaction between these two proteins is essential for proper transcription-independent RA signaling. Tretinoin 96-98 fragile X messenger ribonucleoprotein 1 Mus musculus 64-68
34205274-7 2021 Taken together, these data suggest that not only are functional FMRP and RARalpha necessary for RA-dependent homeostatic synaptic plasticity, but that the interaction between these two proteins is essential for proper transcription-independent RA signaling. Tretinoin 96-98 retinoic acid receptor, alpha Mus musculus 73-81
34136084-0 2021 Role for Fgr and Numb in retinoic acid-induced differentiation and G0 arrest of non-APL AML cells. Tretinoin 25-38 NUMB endocytic adaptor protein Homo sapiens 17-21
34136084-8 2021 If RA-induced Fgr expression is ablated by a CRISPR-KO; then the RA-induced (p-tyr) phosphorylation of NUMB and enhanced NUMB-binding and (p-tyr)phosphorylation of select signalosome components are lost. Tretinoin 3-5 NUMB endocytic adaptor protein Homo sapiens 103-107
34136084-8 2021 If RA-induced Fgr expression is ablated by a CRISPR-KO; then the RA-induced (p-tyr) phosphorylation of NUMB and enhanced NUMB-binding and (p-tyr)phosphorylation of select signalosome components are lost. Tretinoin 3-5 NUMB endocytic adaptor protein Homo sapiens 121-125
34136084-8 2021 If RA-induced Fgr expression is ablated by a CRISPR-KO; then the RA-induced (p-tyr) phosphorylation of NUMB and enhanced NUMB-binding and (p-tyr)phosphorylation of select signalosome components are lost. Tretinoin 65-67 NUMB endocytic adaptor protein Homo sapiens 103-107
34136084-8 2021 If RA-induced Fgr expression is ablated by a CRISPR-KO; then the RA-induced (p-tyr) phosphorylation of NUMB and enhanced NUMB-binding and (p-tyr)phosphorylation of select signalosome components are lost. Tretinoin 65-67 NUMB endocytic adaptor protein Homo sapiens 121-125
34136084-10 2021 In sum we find that NUMB acts as a scaffold for a signaling machine that functions to propel RA-induced differentiation and G1/0 arrest, and that Fgr binding to NUMB turns the function on. Tretinoin 93-95 NUMB endocytic adaptor protein Homo sapiens 20-24
34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 128-131
34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 ETS variant transcription factor 4 Homo sapiens 139-143
34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 zinc finger E-box binding homeobox 1 Homo sapiens 155-159
34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 zinc finger E-box binding homeobox 1 Homo sapiens 160-165
35213790-8 2022 Formation velocity of atRA was approximately threefold higher (p = 0.0001) in omental AT (9.8 (7.6, 11.2)) pmol/min/mg) than subcutaneous AT (3.2 (2.1, 4.0) pmol/min/mg) and correlated with ALDH1A2 expression in omental AT (beta-coefficient = 3.07, p = 0.0007) and with ALDH1A1 expression in subcutaneous AT (beta-coefficient = 0.13, p = 0.003). Tretinoin 22-26 aldehyde dehydrogenase 1 family member A2 Homo sapiens 190-197
35213790-10 2022 Our findings suggest that ALDH1A2 is the primary mediator of atRA formation in omental AT, whereas ALDH1A1 is the principal atRA-synthesizing enzyme in subcutaneous AT. Tretinoin 61-65 aldehyde dehydrogenase 1 family member A2 Homo sapiens 26-33
35338668-6 2022 Semiquantitative RT-PCR showed that the transcription level of gp91-phox is significantly increased in ATRA and L-theanine-cotreated cells. Tretinoin 103-107 cytochrome b-245 beta chain Homo sapiens 63-72
35538058-6 2022 Instead, loss of HK3 but not HK2 led to increased sensitivity to ATRA-induced cell death in AML cell lines. Tretinoin 65-69 hexokinase 3 Homo sapiens 17-20
35538058-7 2022 We found that HK3 knockout (HK3-null) AML cells showed an accumulation of reactive oxygen species (ROS) as well as DNA damage during ATRA-induced differentiation. Tretinoin 133-137 hexokinase 3 Homo sapiens 14-17
35538058-7 2022 We found that HK3 knockout (HK3-null) AML cells showed an accumulation of reactive oxygen species (ROS) as well as DNA damage during ATRA-induced differentiation. Tretinoin 133-137 hexokinase 3 Homo sapiens 28-31
35538058-11 2022 Our findings provide evidence that HK3 is dispensable for glycolytic activity in AML cells while promoting cell survival, possibly through direct interaction with the BH3-only protein BIM during ATRA-induced neutrophil differentiation. Tretinoin 195-199 hexokinase 3 Homo sapiens 35-38
35565751-6 2022 In comparison, the apparent kcat value was about 30% lower (0.71 +- 0.07 min-1 for holo-CRABP1 and 0.75 +- 0.09 min-1 for holo-CRABP2) in the presence of CRABPs than with free atRA (1.07 +- 0.08 min-1). Tretinoin 176-180 cellular retinoic acid binding protein 2 Homo sapiens 127-133
35158158-8 2022 The frequency of the GA genotype of the single nucleotide polymorphism rs17204573 of the RORA (Retinoic Acid related orphan receptor alpha) gene was significantly lower among subjects (27.3%, N = 54) as compared to controls (42.9%, OR:0.5, CI: 0.26-0.96, p value 0.035). Tretinoin 95-108 RAR related orphan receptor A Homo sapiens 89-93
35217789-1 2022 Cellular retinoic acid-binding protein 1 (CRABP1) binds retinoic acid (RA) specifically in the cytoplasm with unclear functions. Tretinoin 56-69 cellular retinoic acid binding protein I Mus musculus 0-40
35217789-1 2022 Cellular retinoic acid-binding protein 1 (CRABP1) binds retinoic acid (RA) specifically in the cytoplasm with unclear functions. Tretinoin 56-69 cellular retinoic acid binding protein I Mus musculus 42-48
35217789-1 2022 Cellular retinoic acid-binding protein 1 (CRABP1) binds retinoic acid (RA) specifically in the cytoplasm with unclear functions. Tretinoin 71-73 cellular retinoic acid binding protein I Mus musculus 0-40
35217789-1 2022 Cellular retinoic acid-binding protein 1 (CRABP1) binds retinoic acid (RA) specifically in the cytoplasm with unclear functions. Tretinoin 71-73 cellular retinoic acid binding protein I Mus musculus 42-48
35149723-4 2022 Results suggested that elevated Pax6 expression was driven by the increased activity of the RA signaling pathway in the Rybp-/- neural cultures. Tretinoin 92-94 RING1 and YY1 binding protein Mus musculus 120-124
35149723-9 2022 Our results thus provide novel insights on the dynamic regulation of Pax6 and RA signaling by RYBP during mouse neural development. Tretinoin 78-80 RING1 and YY1 binding protein Mus musculus 94-98
34982407-5 2022 Two piRNAs, DQ582359 and DQ596268, were increasingly upregulated during the RA-induced differentiation and involved in regulating the expression of neuronal markers, MAP2 and TUBB3. Tretinoin 76-78 microtubule associated protein 2 Homo sapiens 166-170
35173714-10 2022 Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. Tretinoin 13-17 DExD/H-box helicase 58 Homo sapiens 109-114
34954769-7 2022 Furthermore, western blot and RT-qPCR also suggested that ginsenoside Rg1 could activate the protein expression of Nrf2 and heme oxygenase-1 (HO-1) after SCI, and the inhibition of ATRA on these improvements further verified the neuroprotective effect of Nrf2 and HO-1 in ginsenoside Rg1 on SCI. Tretinoin 181-185 heme oxygenase 1 Rattus norvegicus 264-268
7925013-7 1994 Since retinoic acid and at least one of the retinoic acid receptors (RAR alpha) have been localized to the developing neural retina, these results suggest that retinoic acid may play a role in the normal development of photoreceptor cells in vivo. Tretinoin 6-19 retinoic acid receptor, alpha Rattus norvegicus 69-78
7925013-7 1994 Since retinoic acid and at least one of the retinoic acid receptors (RAR alpha) have been localized to the developing neural retina, these results suggest that retinoic acid may play a role in the normal development of photoreceptor cells in vivo. Tretinoin 44-57 retinoic acid receptor, alpha Rattus norvegicus 69-78
7925028-0 1994 Exposure to retinoic acid before or after the onset of somitogenesis reveals separate effects on rhombomeric segmentation and 3" HoxB gene expression domains. Tretinoin 12-25 homeobox B cluster Mus musculus 129-133
7925028-3 1994 In contrast, exposure to RA at early somite stages results in near-normal rhombomeric segmentation; rhombomeric gene expression domains indicate that only rhombomere 2 has changed its genetic identity to that of rhombomere 4, the other preotic segments showing normal expression patterns for HoxB genes and Krox-20. Tretinoin 25-27 homeobox B cluster Mus musculus 292-296
7925028-3 1994 In contrast, exposure to RA at early somite stages results in near-normal rhombomeric segmentation; rhombomeric gene expression domains indicate that only rhombomere 2 has changed its genetic identity to that of rhombomere 4, the other preotic segments showing normal expression patterns for HoxB genes and Krox-20. Tretinoin 25-27 early growth response 2 Mus musculus 307-314
7925028-4 1994 The results indicate that RA has separable effects (1) on the genes mediating the process of rhombomeric segmentation per se, such as Krox-20, and (2) on the genes that influence the nature of the structures that subsequently develop from the individual rhombomeres, such as the Hox genes. Tretinoin 26-28 early growth response 2 Mus musculus 134-141
7520101-4 1994 In contrast, cells induced by G-CSF or GM-CSF alone showed increased DNA syntheses, the levels of which were not significantly affected by the combination of ATRA with CSFs. Tretinoin 158-162 colony stimulating factor 3 Homo sapiens 30-35
7520101-4 1994 In contrast, cells induced by G-CSF or GM-CSF alone showed increased DNA syntheses, the levels of which were not significantly affected by the combination of ATRA with CSFs. Tretinoin 158-162 colony stimulating factor 2 Homo sapiens 39-45
7520101-5 1994 Interestingly, G-CSF or GM-CSF potentiated the capability of ATRA-induced cells to reduce nitroblue tetrazolium (NBT), while G-CSF or GM-CSF alone induced no NBT reduction. Tretinoin 61-65 colony stimulating factor 3 Homo sapiens 15-20
7520101-5 1994 Interestingly, G-CSF or GM-CSF potentiated the capability of ATRA-induced cells to reduce nitroblue tetrazolium (NBT), while G-CSF or GM-CSF alone induced no NBT reduction. Tretinoin 61-65 colony stimulating factor 2 Homo sapiens 24-30
7520101-6 1994 Furthermore, in several patients examined, APL cells induced by ATRA with G-CSF showed an increased activity of chemotaxis and CD11a expression. Tretinoin 64-68 colony stimulating factor 3 Homo sapiens 74-79
7520101-7 1994 These findings suggest that G-CSF or GM-CSF can potentiate differentiation of ATRA-induced APL cells while stimulating their proliferating activity as well, and that G-CSF, rather than GM-CSF, may be a useful adjunct to promote ATRA-induced differentiation of APL. Tretinoin 78-82 colony stimulating factor 3 Homo sapiens 28-33
7520101-7 1994 These findings suggest that G-CSF or GM-CSF can potentiate differentiation of ATRA-induced APL cells while stimulating their proliferating activity as well, and that G-CSF, rather than GM-CSF, may be a useful adjunct to promote ATRA-induced differentiation of APL. Tretinoin 78-82 colony stimulating factor 2 Homo sapiens 37-43
7520101-7 1994 These findings suggest that G-CSF or GM-CSF can potentiate differentiation of ATRA-induced APL cells while stimulating their proliferating activity as well, and that G-CSF, rather than GM-CSF, may be a useful adjunct to promote ATRA-induced differentiation of APL. Tretinoin 228-232 colony stimulating factor 3 Homo sapiens 166-171
8018923-4 1994 In the present investigation, we showed using the APL-derived NB4 cell line that expression of the annexin VIII gene is regulated at the transcription level during induced differentiation by all-trans retinoic acid (ATRA). Tretinoin 201-214 annexin A8 like 1 Homo sapiens 99-111
8018923-4 1994 In the present investigation, we showed using the APL-derived NB4 cell line that expression of the annexin VIII gene is regulated at the transcription level during induced differentiation by all-trans retinoic acid (ATRA). Tretinoin 216-220 annexin A8 like 1 Homo sapiens 99-111
8018923-7 1994 After ATRA-induced differentiation of NB4 cells, the annexin VIII protein level reduced gradually, but a detectable level persisted even after 4 days of induction. Tretinoin 6-10 annexin A8 like 1 Homo sapiens 53-65
8018923-8 1994 Because annexin VIII mRNA becomes undetectable after 48 hours of ATRA induction, this result indicates that annexin VIII is a relatively stable protein. Tretinoin 65-69 annexin A8 like 1 Homo sapiens 108-120
17180006-3 1994 In studying the mechanism mediating RA-resistance, we noted that invariably RA-resistant NB cell lines constitutively express Insulin-like Growth Factor 2 (IGF2) (Gaetano, 1991b). Tretinoin 36-38 insulin like growth factor 2 Homo sapiens 126-154
17180006-3 1994 In studying the mechanism mediating RA-resistance, we noted that invariably RA-resistant NB cell lines constitutively express Insulin-like Growth Factor 2 (IGF2) (Gaetano, 1991b). Tretinoin 36-38 insulin like growth factor 2 Homo sapiens 156-160
17180006-5 1994 Coincidentally, RA induces IGF2 mRNA and protein secretion in 15N NB cells (Matsumoto, 1992). Tretinoin 16-18 insulin like growth factor 2 Homo sapiens 27-31
17180006-6 1994 In this study we isolated RA-resistant 15N cell lines and analyzed their growth properties and changes in cell cycle related (cdc2, cdk2, cyclins A, B, D and E) and early response (fos and jun) gene expression to evaluate the role IGF2 may play in mediating RA resistance. Tretinoin 26-28 cyclin dependent kinase 1 Homo sapiens 126-130
17180006-6 1994 In this study we isolated RA-resistant 15N cell lines and analyzed their growth properties and changes in cell cycle related (cdc2, cdk2, cyclins A, B, D and E) and early response (fos and jun) gene expression to evaluate the role IGF2 may play in mediating RA resistance. Tretinoin 26-28 insulin like growth factor 2 Homo sapiens 231-235
17180006-7 1994 We found that exogenous IGF2 stimulates growth in 15N and is capable of altering RA induced inhibition of NB cell growth. Tretinoin 81-83 insulin like growth factor 2 Homo sapiens 24-28
8014006-4 1994 Somatic differentiated derivatives (e.g., EC cells treated with retinoic acid) contained decreased levels of globo-series glycolipids and increased levels of lacto- and ganglio-series glycolipids, including GD3, GT3 and GD2. Tretinoin 64-77 GRDX Homo sapiens 207-210
7947321-7 1994 It is likely, that during normal X. laevis embryogenesis, concentrations of RA in RA-responsive cells are modulated by the xCRABP gene product. Tretinoin 76-78 cellular retinoic acid binding protein 2 L homeolog Xenopus laevis 123-129
8200066-0 1994 Retinoic acid and beta-carotene inhibit fibronectin synthesis and release by fibroblasts; antagonism to phorbol ester. Tretinoin 0-13 fibronectin 1 Mus musculus 40-51
8200066-2 1994 We have now studied the action of RA and carotenoids on FN synthesis and release. Tretinoin 34-36 fibronectin 1 Mus musculus 56-58
8200066-3 1994 Using mouse fibroblasts (C3H/10T1/2 cells), we found that RA inhibited release of FN into the medium in a time- and concentration-dependent manner (e.g. 90% inhibition in 48 h with 1 x 10(-6) M RA). Tretinoin 58-60 fibronectin 1 Mus musculus 82-84
8200066-4 1994 RA caused inhibition of synthesis, as well as a time- and concentration-dependent decrease in FN mRNA. Tretinoin 0-2 fibronectin 1 Mus musculus 94-96
8200066-5 1994 A second phenomenon we observed was the greatly increased binding of FN to the surface of the cells, both in dimeric and multimeric forms, caused by RA treatment. Tretinoin 149-151 fibronectin 1 Mus musculus 69-71
8200066-7 1994 We postulate that the combined action of RA in causing decreased FN synthesis and increased FN binding to the cell surface is the reason for the apparent antagonism of RA to the TPA-stimulated release of FN. Tretinoin 41-43 fibronectin 1 Mus musculus 65-67
8200066-7 1994 We postulate that the combined action of RA in causing decreased FN synthesis and increased FN binding to the cell surface is the reason for the apparent antagonism of RA to the TPA-stimulated release of FN. Tretinoin 41-43 fibronectin 1 Mus musculus 92-94
8200066-7 1994 We postulate that the combined action of RA in causing decreased FN synthesis and increased FN binding to the cell surface is the reason for the apparent antagonism of RA to the TPA-stimulated release of FN. Tretinoin 41-43 fibronectin 1 Mus musculus 92-94
8200066-7 1994 We postulate that the combined action of RA in causing decreased FN synthesis and increased FN binding to the cell surface is the reason for the apparent antagonism of RA to the TPA-stimulated release of FN. Tretinoin 168-170 fibronectin 1 Mus musculus 92-94
8200066-7 1994 We postulate that the combined action of RA in causing decreased FN synthesis and increased FN binding to the cell surface is the reason for the apparent antagonism of RA to the TPA-stimulated release of FN. Tretinoin 168-170 fibronectin 1 Mus musculus 92-94
8182938-10 1994 That RA promotes both neutrophil and monocyte differentiation has implications for the use of RA and D3 in treatment of leukemias and provides insight into mechanisms whereby RAR, VDR and RXR facilitate monocyte differentiation. Tretinoin 5-7 retinoic acid receptor alpha Homo sapiens 175-178
7511442-13 1994 In NB4 cells, ATRA induces G-CSF, alpha, and beta retinoic acid receptor transcripts, whereas G-CSF has minor effects on the expression of these mRNAs. Tretinoin 14-18 colony stimulating factor 3 Homo sapiens 27-32
7511050-0 1994 Retinoic acid-induced expression of CD38 antigen in myeloid cells is mediated through retinoic acid receptor-alpha. Tretinoin 0-13 CD38 molecule Homo sapiens 36-40
7511050-0 1994 Retinoic acid-induced expression of CD38 antigen in myeloid cells is mediated through retinoic acid receptor-alpha. Tretinoin 0-13 retinoic acid receptor alpha Homo sapiens 86-114
7511050-4 1994 Recently we reported that all-trans-retinoic acid (ATRA) is a potent and highly specific inducer of CD38 expression in human promyelocytic leukemia cells. Tretinoin 26-49 CD38 molecule Homo sapiens 100-104
7511050-4 1994 Recently we reported that all-trans-retinoic acid (ATRA) is a potent and highly specific inducer of CD38 expression in human promyelocytic leukemia cells. Tretinoin 51-55 CD38 molecule Homo sapiens 100-104
7511050-5 1994 Here we report that ATRA-induced expression of CD38 antigen in myeloid cells is mediated through retinoic acid-alpha receptor (RAR alpha). Tretinoin 20-24 CD38 molecule Homo sapiens 47-51
7511050-5 1994 Here we report that ATRA-induced expression of CD38 antigen in myeloid cells is mediated through retinoic acid-alpha receptor (RAR alpha). Tretinoin 20-24 retinoic acid receptor alpha Homo sapiens 127-136
7511050-7 1994 Retroviral vector-mediated transduction of RA receptor (RAR alpha) into this HL-60R subclone completely restored the sensitivity of these cells to ATRA in terms of their ability to express CD38. Tretinoin 147-151 retinoic acid receptor alpha Homo sapiens 56-65
7511050-7 1994 Retroviral vector-mediated transduction of RA receptor (RAR alpha) into this HL-60R subclone completely restored the sensitivity of these cells to ATRA in terms of their ability to express CD38. Tretinoin 147-151 CD38 molecule Homo sapiens 189-193
7511050-10 1994 Following culture with ATRA, increased CD38 protein levels were also observed in normal CD34+ bone marrow cells, but not on normal circulating granulocytes. Tretinoin 23-27 CD38 molecule Homo sapiens 39-43
21566987-4 1994 The stimulation of t-RA on LPS-mediated G-CSF secretion was dose-dependent and was observed at t-RA concentration of as low as 10(-10) M. Some other retinoids were also as effective as t-RA, whereas other steroids were either less or not effective or inhibitory on LPS-mediated G-CSF secretion. Tretinoin 19-23 colony stimulating factor 3 Homo sapiens 40-45
21566987-4 1994 The stimulation of t-RA on LPS-mediated G-CSF secretion was dose-dependent and was observed at t-RA concentration of as low as 10(-10) M. Some other retinoids were also as effective as t-RA, whereas other steroids were either less or not effective or inhibitory on LPS-mediated G-CSF secretion. Tretinoin 19-23 colony stimulating factor 3 Homo sapiens 278-283
21566987-4 1994 The stimulation of t-RA on LPS-mediated G-CSF secretion was dose-dependent and was observed at t-RA concentration of as low as 10(-10) M. Some other retinoids were also as effective as t-RA, whereas other steroids were either less or not effective or inhibitory on LPS-mediated G-CSF secretion. Tretinoin 95-99 colony stimulating factor 3 Homo sapiens 40-45
8139911-1 1994 The polymorphic nature of sequences which act as retinoic acid response elements (RAREs and RXREs) in transactivation assays in mammalian cells, suggests that elements consisting of a direct repetition of a half site motif, separated by 1 to 5 base pairs (DR1 to DR5), are targets for retinoic acid (RA) signalling. Tretinoin 82-84 TNF receptor superfamily member 10b Homo sapiens 263-266
8018561-5 1994 This fragment included the E2F binding site in the c-myc P2 promoter region, and a difference of shifted bands between RA-treated and untreated HL60 cells was due to complex formation of E2F and retinoblastoma protein. Tretinoin 119-121 MYC proto-oncogene, bHLH transcription factor Homo sapiens 51-56
8018561-6 1994 The present results suggest that E2F plays an important role in the process of cell differentiation by RA and that a change of the E2F binding pattern induced by RA contributes to the suppression of c-myc gene expression preceding granulocytic differentiation. Tretinoin 162-164 MYC proto-oncogene, bHLH transcription factor Homo sapiens 199-204
8125162-3 1994 Recently, three nuclear receptors specific for retinoic acid (RAR alpha, RAR beta, and RAR gamma) have been cloned and all are members of a large multigene family of ligand-inducible transcription enhancer factors. Tretinoin 47-60 retinoic acid receptor alpha Homo sapiens 62-71
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 38-40 basic helix-loop-helix family, member e23 Mus musculus 66-72
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 38-40 basic helix-loop-helix family, member e23 Mus musculus 202-208
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 55-57 basic helix-loop-helix family, member e23 Mus musculus 66-72
8011555-3 1994 It has been previously shown that the RA modulation of RAR beta 2/beta 4 transcripts is achieved at the level of transcriptional initiation via a RA response element (RARE) present in the P2 RAR beta 2/beta 4 promoter. Tretinoin 55-57 basic helix-loop-helix family, member e23 Mus musculus 202-208
7509793-14 1994 These results indicated that a large fraction of the RA was bound to vimentin by an ester bond. Tretinoin 53-55 vimentin Homo sapiens 69-77
7509793-17 1994 These results indicate that retinoylation is a new modification of vimentin that may be an early event in RA-induced differentiation of HL60 cells. Tretinoin 106-108 vimentin Homo sapiens 67-75
8119934-11 1994 Under these conditions, retinoic acid also caused a rapid increase in cardiac GLUT4 mRNA levels from hypothyroid neonates. Tretinoin 24-37 solute carrier family 2 member 4 Rattus norvegicus 78-83
7509208-6 1994 mRNA of NAP is known to be induced by in vitro treatment of the cells with granulocyte colony-stimulating factor (G-CSF), which is enhanced by a simultaneous addition of retinoic acid. Tretinoin 170-183 colony stimulating factor 3 Homo sapiens 75-112
7509208-6 1994 mRNA of NAP is known to be induced by in vitro treatment of the cells with granulocyte colony-stimulating factor (G-CSF), which is enhanced by a simultaneous addition of retinoic acid. Tretinoin 170-183 colony stimulating factor 3 Homo sapiens 114-119
8298127-5 1994 In FCS- liquid-suspension culture supplemented with saturating Ep level and low-dose IL-3/GM-CSF, adult HPC undergo unilineage erythropoietic differentiation: Here again, treatment with high-dose RA induces a shift from the erythroid to granulocytic differentiation pathway. Tretinoin 196-198 interleukin 3 Homo sapiens 85-89
8298127-5 1994 In FCS- liquid-suspension culture supplemented with saturating Ep level and low-dose IL-3/GM-CSF, adult HPC undergo unilineage erythropoietic differentiation: Here again, treatment with high-dose RA induces a shift from the erythroid to granulocytic differentiation pathway. Tretinoin 196-198 colony stimulating factor 2 Homo sapiens 90-96
7910023-7 1994 Significantly, the DNase I hypersensitive site pattern of this region of the Hox-1 cluster is not altered when F9 stem cells are differentiated with retinoic acid, suggesting that sequential activation of Hox genes by retinoic acid is not due to a sequential opening of the chromatin structure in the Hox gene region. Tretinoin 149-162 homeobox A5 Homo sapiens 77-82
7910023-7 1994 Significantly, the DNase I hypersensitive site pattern of this region of the Hox-1 cluster is not altered when F9 stem cells are differentiated with retinoic acid, suggesting that sequential activation of Hox genes by retinoic acid is not due to a sequential opening of the chromatin structure in the Hox gene region. Tretinoin 218-231 homeobox A5 Homo sapiens 77-82
8301142-0 1994 Retinoic acid inhibition of IL-1-induced IL-6 production by human lung fibroblasts. Tretinoin 0-13 interleukin 1 alpha Homo sapiens 28-32
8309256-0 1994 Poor response to all-trans retinoic acid therapy in a t(11;17) PLZF/RAR alpha patient. Tretinoin 27-40 retinoic acid receptor alpha Homo sapiens 68-77
8309256-11 1994 These results suggest that the t(11;17) (PLZF/RAR alpha) case of this study was less responsive to ATRA therapy than t(15;17) (PML/RAR alpha) cases and raises the question of the definition of this novel AML subtype. Tretinoin 99-103 retinoic acid receptor alpha Homo sapiens 46-55
8289783-14 1994 In accordance with the suggestion that suppression of Oct-3/4 expression is a crucial step during embryogenesis, the Oct-3/4 upstream region contains multiple targets for RA-induced repression, probably to ensure accurate and prompt repression of Oct-3/4 expression. Tretinoin 171-173 POU class 5 homeobox 1 Homo sapiens 117-124
8287974-4 1994 Because of its effects on cell growth and differentiation and its increasing clinical use as a differentiating agent, we examined the effect of retinoic acid (RA) on hsp28 during differentiation of the human leukemic HL-60 cell line. Tretinoin 144-157 heat shock protein family B (small) member 1 Homo sapiens 166-171
8287974-4 1994 Because of its effects on cell growth and differentiation and its increasing clinical use as a differentiating agent, we examined the effect of retinoic acid (RA) on hsp28 during differentiation of the human leukemic HL-60 cell line. Tretinoin 159-161 heat shock protein family B (small) member 1 Homo sapiens 166-171
8287974-6 1994 Furthermore, hsp28 phosphorylation transiently increased within one hour following treatment with RA. Tretinoin 98-100 heat shock protein family B (small) member 1 Homo sapiens 13-18
8287974-7 1994 Interestingly, in contrast to other differentiating agents the induction of hsp28 by RA was post-transcriptionally mediated with hsp28 protein and mRNA being discordantly regulated. Tretinoin 85-87 heat shock protein family B (small) member 1 Homo sapiens 76-81
8287974-7 1994 Interestingly, in contrast to other differentiating agents the induction of hsp28 by RA was post-transcriptionally mediated with hsp28 protein and mRNA being discordantly regulated. Tretinoin 85-87 heat shock protein family B (small) member 1 Homo sapiens 129-134
8287974-8 1994 These observations underscore the complex regulation of hsp28 by RA during granulocytic differentiation of human leukemic cells and indicate hsp28 as an intermediary in the pathway through which retinoids exert their growth and differentiative effects. Tretinoin 65-67 heat shock protein family B (small) member 1 Homo sapiens 56-61
7923565-3 1994 Because encapsulation of certain drugs in lipid vesicles (liposomes) has been shown to result in reduced toxic effects, we studied the in vitro interaction of liposome-encapsulated all-trans-retinoic acid (L-ATRA) with a SCC line (MDA 886Ln) and its multicellular tumor spheroid (MTS) model. Tretinoin 181-204 serpin family B member 3 Homo sapiens 221-224
8127013-3 1994 This paper describes the effects of RA on a human renal adenocarcinoma cell line (PAD) under different growth conditions, and its interactions with epidermal growth factor (EGF). Tretinoin 36-38 epidermal growth factor Homo sapiens 173-176
8127013-7 1994 RA by itself was unable to reverse contact inhibition of PAD cell growth (NS vs. control), but it synergistically enhanced the mitogenic effect of EGF on confluent monolayers (110 +/- 0.6% vs. EGF alone; P < 0.05). Tretinoin 0-2 epidermal growth factor Homo sapiens 147-150
8127013-10 1994 Thus, our data show that RA is directly mitogenic for serum starved human renal adenocarcinoma cells and that it exerts complex modulation of cell growth in the presence of EGF and serum components. Tretinoin 25-27 epidermal growth factor Homo sapiens 173-176
7972206-0 1994 Expression of nerve growth factor receptor mRNAs and clinical response to retinoic acid in neuroblastoma. Tretinoin 74-87 nerve growth factor receptor Homo sapiens 14-42
7972206-2 1994 Clinical response to retinoic acid was noted only in the two children with tumors coexpressing trk protooncogene mRNA, encoding an essential part of the nerve growth factor (NGF) high affinity receptor, and low affinity NGF receptor gene (LNGFR) mRNA. Tretinoin 21-34 nerve growth factor receptor Homo sapiens 220-232
7972206-5 1994 We hypothesize that part of the therapeutic effect of retinoic acid in neuroblastoma in vivo may be exerted via increased NGF receptor expression and NGF sensitivity. Tretinoin 54-67 nerve growth factor receptor Homo sapiens 122-134
8219191-3 1993 Interferon-gamma and retinoic acid downregulated PU.1 expression in marrow macrophages. Tretinoin 21-34 Spi-1 proto-oncogene Homo sapiens 49-53
8274453-9 1993 Retinoic acid-treated, but not untreated, cells lost expression of vimentin and fibronectin, gained the ability to incorporate acetylated low density lipoprotein, and expressed Factor VIII-related antigen. Tretinoin 0-13 fibronectin 1 Mus musculus 80-91
8395911-0 1993 Occurrence of resistance to retinoic acid in the acute promyelocytic leukemia cell line NB4 is associated with altered expression of the pml/RAR alpha protein. Tretinoin 28-41 retinoic acid receptor alpha Homo sapiens 141-150
8243888-2 1993 We report here that, compared to RA treatment alone, RA combined with the PKC stimulator 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced the regulated expression of the immunophenotypic differentiation markers SSEA-3, a globo-series carbohydrate, and the ganglio-series carbohydrate antigens GD2 and GD3. Tretinoin 53-55 GRDX Homo sapiens 304-307
8370963-0 1993 Expression of cornifin in squamous differentiating epithelial tissues, including psoriatic and retinoic acid-treated skin. Tretinoin 95-108 small proline rich protein 1B Homo sapiens 14-22
8370963-4 1993 This induction of cornifin expression is suppressed by retinoic acid and several of its analogs. Tretinoin 55-68 small proline rich protein 1B Homo sapiens 18-26
8370963-12 1993 Cornifin expression correlates generally with squamous differentiation in a variety of tissues and is abnormally regulated in psoriatic skin and in skin treated topically with retinoic acid. Tretinoin 176-189 small proline rich protein 1B Homo sapiens 0-8
8364891-0 1993 Retinoic acid induces insulin-like growth factor II expression in a neuroblastoma cell line. Tretinoin 0-13 insulin like growth factor 2 Homo sapiens 22-51
8364891-2 1993 We examined the relationship of IGF-II expression to the in vitro differentiation induced by retinoic acid (RA). Tretinoin 93-106 insulin like growth factor 2 Homo sapiens 32-38
8364891-2 1993 We examined the relationship of IGF-II expression to the in vitro differentiation induced by retinoic acid (RA). Tretinoin 108-110 insulin like growth factor 2 Homo sapiens 32-38
8364891-3 1993 We find that RA stimulates an increase in IGF-II messenger RNA (mRNA) in the SK-N-SH (SH) neuroblastoma cell line. Tretinoin 13-15 insulin like growth factor 2 Homo sapiens 42-48
8364891-5 1993 A RA dose response test indicates that an increase in IGF-II mRNA occurs within 2 days in SH cells treated with doses of RA from 1 x 10(-8) to 1 x 10(-5) M. We suggest that IGF-II expression may be regulated either directly or indirectly by RA in vitro and may lead to neuroblastoma differentiation. Tretinoin 2-4 insulin like growth factor 2 Homo sapiens 54-60
8364891-5 1993 A RA dose response test indicates that an increase in IGF-II mRNA occurs within 2 days in SH cells treated with doses of RA from 1 x 10(-8) to 1 x 10(-5) M. We suggest that IGF-II expression may be regulated either directly or indirectly by RA in vitro and may lead to neuroblastoma differentiation. Tretinoin 2-4 insulin like growth factor 2 Homo sapiens 173-179
8364891-5 1993 A RA dose response test indicates that an increase in IGF-II mRNA occurs within 2 days in SH cells treated with doses of RA from 1 x 10(-8) to 1 x 10(-5) M. We suggest that IGF-II expression may be regulated either directly or indirectly by RA in vitro and may lead to neuroblastoma differentiation. Tretinoin 121-123 insulin like growth factor 2 Homo sapiens 54-60
8364891-5 1993 A RA dose response test indicates that an increase in IGF-II mRNA occurs within 2 days in SH cells treated with doses of RA from 1 x 10(-8) to 1 x 10(-5) M. We suggest that IGF-II expression may be regulated either directly or indirectly by RA in vitro and may lead to neuroblastoma differentiation. Tretinoin 121-123 insulin like growth factor 2 Homo sapiens 173-179
8364891-5 1993 A RA dose response test indicates that an increase in IGF-II mRNA occurs within 2 days in SH cells treated with doses of RA from 1 x 10(-8) to 1 x 10(-5) M. We suggest that IGF-II expression may be regulated either directly or indirectly by RA in vitro and may lead to neuroblastoma differentiation. Tretinoin 121-123 insulin like growth factor 2 Homo sapiens 54-60
8364891-5 1993 A RA dose response test indicates that an increase in IGF-II mRNA occurs within 2 days in SH cells treated with doses of RA from 1 x 10(-8) to 1 x 10(-5) M. We suggest that IGF-II expression may be regulated either directly or indirectly by RA in vitro and may lead to neuroblastoma differentiation. Tretinoin 121-123 insulin like growth factor 2 Homo sapiens 173-179
8104620-6 1993 To date 6 Homeobox genes (HoxC6, HoxC8, HoxD1, HoxD4, HoxD8, and HoxD9) have been identified in the cDNA library prepared from LA-N-5 cells treated with retinoic acid. Tretinoin 153-166 homeobox C6 Homo sapiens 26-31
8104620-6 1993 To date 6 Homeobox genes (HoxC6, HoxC8, HoxD1, HoxD4, HoxD8, and HoxD9) have been identified in the cDNA library prepared from LA-N-5 cells treated with retinoic acid. Tretinoin 153-166 homeobox D4 Homo sapiens 47-52
8104620-6 1993 To date 6 Homeobox genes (HoxC6, HoxC8, HoxD1, HoxD4, HoxD8, and HoxD9) have been identified in the cDNA library prepared from LA-N-5 cells treated with retinoic acid. Tretinoin 153-166 homeobox D9 Homo sapiens 65-70
8103115-4 1993 Concomitantly, RA reduced the specific activities of two catecholamine synthetic enzymes, tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) and the level of norepinephrine (NE). Tretinoin 15-17 dopamine beta-hydroxylase Rattus norvegicus 120-145
8103115-4 1993 Concomitantly, RA reduced the specific activities of two catecholamine synthetic enzymes, tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) and the level of norepinephrine (NE). Tretinoin 15-17 dopamine beta-hydroxylase Rattus norvegicus 147-150
8103115-5 1993 After a 2 week treatment with 5 microM RA, ChAT was increased by 5-10 fold, whereas TH and DBH were decreased by 10-15 fold and 2-3 fold, respectively, as compared to sympathetic neurons grown in the absence of RA. Tretinoin 39-41 dopamine beta-hydroxylase Rattus norvegicus 91-94
8391258-2 1993 It is shown that the expression of human glutathione S-transferase P1-1 (GSTP1-1) is suppressed by retinoic acid (RA) as the result of decreased transcription from its gene, GSTP1. Tretinoin 114-116 glutathione S-transferase pi 1 Homo sapiens 73-78
8391258-3 1993 Chloramphenicol acetyltransferase (CAT) assays indicate that the effect of RA on the transcription of a GSTP1 promoter-CAT fusion gene is mediated by the region -99 to +72 of GSTP1. Tretinoin 75-77 glutathione S-transferase pi 1 Homo sapiens 104-109
8391258-3 1993 Chloramphenicol acetyltransferase (CAT) assays indicate that the effect of RA on the transcription of a GSTP1 promoter-CAT fusion gene is mediated by the region -99 to +72 of GSTP1. Tretinoin 75-77 glutathione S-transferase pi 1 Homo sapiens 175-180
8391258-4 1993 A consensus activator protein 1-binding site, located at nucleotide position -59 to -65 of GSTP1, is suggested to be responsible for RA repression. Tretinoin 133-135 glutathione S-transferase pi 1 Homo sapiens 91-96
8391258-5 1993 This effect of RA on GSTP1 expression is mediated by the human beta-type RA receptor, hRAR beta, but not the chicken retinoid X receptor, cRXR. Tretinoin 15-17 glutathione S-transferase pi 1 Homo sapiens 21-26
8105613-0 1993 Expression of stratum corneum chymotryptic enzyme in reconstructed human epidermis and its suppression by retinoic acid. Tretinoin 106-119 kallikrein related peptidase 7 Homo sapiens 14-49
8105613-3 1993 The SCCE-specific monoclonal antibody TE-9B showed positive immunofluorescence staining of high suprabasal keratinocytes, mainly in the stratum granulosum, in normal non-palmo-plantar human epidermis as well as in reconstructed epidermis in the absence of RA. Tretinoin 256-258 kallikrein related peptidase 7 Homo sapiens 4-8
8331499-7 1993 Treatment of GOTO with 10(-5) mol/L all-trans-retinoic acid (RA) for 72 hours markedly decreased both N-myc expression and invasiveness. Tretinoin 36-59 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 102-107
8331499-7 1993 Treatment of GOTO with 10(-5) mol/L all-trans-retinoic acid (RA) for 72 hours markedly decreased both N-myc expression and invasiveness. Tretinoin 61-63 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 102-107
8397079-10 1993 Similarly, expression of CRBP I in the choroid plexuses, which develop abnormally in conditions of vitamin A deficiency, is consistent with observations indicating that this binding protein mediates the synthesis of RA in tissues requiring high levels of RA for their normal developmental programme. Tretinoin 216-218 retinol binding protein 1, cellular Mus musculus 25-31
8397079-10 1993 Similarly, expression of CRBP I in the choroid plexuses, which develop abnormally in conditions of vitamin A deficiency, is consistent with observations indicating that this binding protein mediates the synthesis of RA in tissues requiring high levels of RA for their normal developmental programme. Tretinoin 255-257 retinol binding protein 1, cellular Mus musculus 25-31
8397079-11 1993 RAR-beta and CRABP II, which are both RA-inducible, were coexpressed with CRBP I in the choroid plexus and in many other sites, perhaps reflecting the fact that all three genes are RA-inducible. Tretinoin 14-16 retinol binding protein 1, cellular Mus musculus 74-80
7683344-13 1993 In additional studies, retinoic acid induced a dose-dependent increase in prostate specific antigen (PSA) secretion at concentrations of 0.1 to 1 microM. Tretinoin 23-36 kallikrein related peptidase 3 Homo sapiens 74-99
7683344-13 1993 In additional studies, retinoic acid induced a dose-dependent increase in prostate specific antigen (PSA) secretion at concentrations of 0.1 to 1 microM. Tretinoin 23-36 kallikrein related peptidase 3 Homo sapiens 101-104
7683344-15 1993 also enhanced the secretion of PSA by LNCaP cells, and this effect was potentiated in a dose-dependent fashion by the addition of retinoic acid at 0.1-10 microM. Tretinoin 130-143 kallikrein related peptidase 3 Homo sapiens 31-34
7683344-17 1993 Overall, retinoic acid had a biphasic effect on LNCaP proliferation and promoted the secretion of PSA. Tretinoin 9-22 kallikrein related peptidase 3 Homo sapiens 98-101
7683344-19 1993 In addition, the ability of retinoic acid to increase PSA secretion may complicate the interpretation of serum PSA levels used for diagnostic and prognostic purposes. Tretinoin 28-41 kallikrein related peptidase 3 Homo sapiens 54-57
7683344-19 1993 In addition, the ability of retinoic acid to increase PSA secretion may complicate the interpretation of serum PSA levels used for diagnostic and prognostic purposes. Tretinoin 28-41 kallikrein related peptidase 3 Homo sapiens 111-114
8387200-0 1993 Retinoic acid is a negative regulator of the Epstein-Barr virus protein (BZLF1) that mediates disruption of latent infection. Tretinoin 0-13 protein Zta Human gammaherpesvirus 4 73-78
8484778-3 1993 Induction of p53 mRNA expression was also observed in cells treated with 10(-8) M retinoic acid, after 18 h of incubation. Tretinoin 82-95 transformation related protein 53, pseudogene Mus musculus 13-16
8484778-5 1993 c-fos mRNA levels decreased rapidly and were barely detectable after 2 h of exposure to retinoic acid. Tretinoin 88-101 FBJ osteosarcoma oncogene Mus musculus 0-5
7683471-7 1993 Moreover, a retinoic acid-mediated K14 reduction was concomitant with a 4.0-fold increase in cisplatin resistance in PC10. Tretinoin 12-25 keratin 14 Homo sapiens 35-38
8490200-0 1993 Inhibition of c-myc in breast and ovarian carcinoma cells by 1,25-dihydroxyvitamin D3, retinoic acid and dexamethasone. Tretinoin 87-100 MYC proto-oncogene, bHLH transcription factor Homo sapiens 14-19
8490200-2 1993 The downregulation of the c-myc protooncogene by 1,25-dihydroxyvitamin D3 (calcitriol), retinoic acid (RA) and dexamethasone (Dex) is closely associated with growth inhibition in leukemic cells. Tretinoin 88-101 MYC proto-oncogene, bHLH transcription factor Homo sapiens 26-31
8395280-2 1993 The expressed recombinant RARs (rRARs: rRAR alpha/E, rRAR beta/E and rRAR gamma) showed nearly the same magnitude of binding affinity toward [3H]retinoic acid (RA) as hRARs extracted from human cells (Ka values: 6.0 x 10(9) M-1 for rRAR alpha/E and 2.7 x 10(10) M-1 for both rRAR beta/E and rRAR gamma). Tretinoin 145-158 retinoic acid receptor, alpha Rattus norvegicus 39-49
8455626-2 1993 We show that Oct-1, a ubiquitously expressed octamer-binding protein known to be regulated posttranslationally, can also be regulated at the levels of mRNA and protein synthesis by IL-6 and by retinoic acid (RA) in human embryonal carcinoma cells. Tretinoin 193-206 POU class 2 homeobox 1 Homo sapiens 13-18
8455626-2 1993 We show that Oct-1, a ubiquitously expressed octamer-binding protein known to be regulated posttranslationally, can also be regulated at the levels of mRNA and protein synthesis by IL-6 and by retinoic acid (RA) in human embryonal carcinoma cells. Tretinoin 208-210 POU class 2 homeobox 1 Homo sapiens 13-18
8466534-0 1993 Enhancement of perforin by retinoic acid is mediated by protein kinase C. We previously demonstrated that interleukin-2 induced murine lymphokine-activated killer cell activity is augmented by retinoic acid. Tretinoin 27-40 interleukin 2 Mus musculus 106-119
8466534-0 1993 Enhancement of perforin by retinoic acid is mediated by protein kinase C. We previously demonstrated that interleukin-2 induced murine lymphokine-activated killer cell activity is augmented by retinoic acid. Tretinoin 193-206 interleukin 2 Mus musculus 106-119
8461021-0 1993 Retinoic acid inhibits DNA and albumin synthesis stimulated by growth factor in adult rat hepatocytes in primary culture. Tretinoin 0-13 myotrophin Rattus norvegicus 63-76
8506078-0 1993 Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: retinoic acid may induce IGF-2. Tretinoin 95-108 insulin like growth factor 2 Homo sapiens 14-19
8506078-0 1993 Modulation of IGF-2 expression during growth and differentiation of human neuroblastoma cells: retinoic acid may induce IGF-2. Tretinoin 95-108 insulin like growth factor 2 Homo sapiens 120-125
8506078-3 1993 IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. Tretinoin 27-40 insulin like growth factor 2 Homo sapiens 0-5
8506078-3 1993 IGF-2 mRNA is increased by retinoic acid (RA) only in the clones. Tretinoin 42-44 insulin like growth factor 2 Homo sapiens 0-5
8506078-7 1993 The data suggest that IGF-2 expression is correlated with growth, and may counteract the growth retardation, neurite outgrowth and programmed cell death effects of retinoic acid. Tretinoin 164-177 insulin like growth factor 2 Homo sapiens 22-27
8506078-8 1993 Therefore the autocrine pattern of IGF-2 production by neuroblastoma cells may promote RA-resistance. Tretinoin 87-89 insulin like growth factor 2 Homo sapiens 35-40
7683888-7 1993 Retinoic acid preferentially increased synthesis of alpha-1-antichymotrypsin, ceruloplasmin and plasminogen activator inhibitor-1. Tretinoin 0-13 ceruloplasmin Homo sapiens 78-91
7683888-7 1993 Retinoic acid preferentially increased synthesis of alpha-1-antichymotrypsin, ceruloplasmin and plasminogen activator inhibitor-1. Tretinoin 0-13 serpin family E member 1 Homo sapiens 96-129
8384553-6 1993 Our results demonstrate for the first time the association of a variant chromosomal translocation involving the RAR alpha gene with APL, further implicating the RAR alpha in leukaemogenesis and also suggesting an important role for PLZF as well as retinoic acid and its receptors in myeloid maturation. Tretinoin 248-261 retinoic acid receptor alpha Homo sapiens 112-121
8387038-3 1993 Retinoic acid (RA), but not estradiol or dexamethasone, is also able to enhance MyoD gene expression (about threefold). Tretinoin 0-13 myogenic differentiation 1 Mus musculus 80-84
8387038-3 1993 Retinoic acid (RA), but not estradiol or dexamethasone, is also able to enhance MyoD gene expression (about threefold). Tretinoin 15-17 myogenic differentiation 1 Mus musculus 80-84
8387038-9 1993 This study provides clear evidence for an important role of RA on MyoD gene expression and myogenesis and suggests that T3 and RA could play overlapping, but distinct, roles on muscle development. Tretinoin 60-62 myogenic differentiation 1 Mus musculus 66-70
8382032-2 1993 We have identified transcripts and nuclear RA receptor (RAR) protein in a clonal line of human neuroblastoma cells that differentiate in response to RA. Tretinoin 43-45 retinoic acid receptor alpha Homo sapiens 56-59
8425196-10 1993 Retinoic acid, dexamethasone, or forskolin inhibits induction of anchorage independence by tumor necrosis factor alpha, interleukin 1 alpha, and transfected v-jun. Tretinoin 0-13 interleukin 1 alpha Mus musculus 120-139
8381395-6 1993 There was a pronounced redistribution of peripherin to neurites formed in response to dibutyryl cyclic adenosine monophosphate (dbcAMP) and all-trans-retinoic acid (RA). Tretinoin 140-163 peripherin Homo sapiens 41-51
8381395-6 1993 There was a pronounced redistribution of peripherin to neurites formed in response to dibutyryl cyclic adenosine monophosphate (dbcAMP) and all-trans-retinoic acid (RA). Tretinoin 165-167 peripherin Homo sapiens 41-51
8381395-8 1993 Both dbcAMP and RA induced a redistribution of peripherin to neurite extensions, but only treatment with RA increased the level of the protein as demonstrated with NUB-6A4 and NUB-6C4 subclones. Tretinoin 16-18 peripherin Homo sapiens 47-57
8419327-1 1993 beta-All-trans-retinoic acid (RA)-induced endodermal differentiation of mouse F9 teratocarcinoma cells is accompanied by changes in glycoprotein glycosylation, including expression of i antigen (i.e. polylactosamine) and leukophytohemagglutinin-reactive oligosaccharides (i.e. -GlcNAc beta 1-6Man alpha 1-6-branched N-linked). Tretinoin 30-32 hemoglobin, beta adult major chain Mus musculus 285-291
8388158-3 1993 A region in the promoter for the human ADH3 gene was previously shown to function as a retinoic acid response element (RARE), prompting an hypothesis for a positive feedback mechanism for controlling retinoic acid synthesis. Tretinoin 87-100 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 39-43
8388158-3 1993 A region in the promoter for the human ADH3 gene was previously shown to function as a retinoic acid response element (RARE), prompting an hypothesis for a positive feedback mechanism for controlling retinoic acid synthesis. Tretinoin 200-213 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 39-43
8350952-0 1993 Modulation of leukosialin (sialophorin, CD43 antigen) on the cell surface of human hematopoietic cell lines induced by cytokins, retinoic acid and 1,25(OH)2-vitamin D3. Tretinoin 129-142 LOC105369247 Homo sapiens 14-25
8350952-4 1993 Retinoic acid down-regulated leukosialin on both U-937 monocyte-like cells and the CALLA+ ALL cell line REH. Tretinoin 0-13 LOC105369247 Homo sapiens 29-40
8350952-5 1993 In contrast to these data, interferon-gamma, TNF-alpha, retinoic acid and 1,25(OH)2-vitamin D3 induced the up-regulation of leukosialin in a promyelocytic leukemia cell line HL-60. Tretinoin 56-69 LOC105369247 Homo sapiens 124-135
8489769-0 1993 Effects of retinoic acid on interleukin-1 alpha and -1 beta expression by normal human keratinocytes cultured in defined medium. Tretinoin 11-24 interleukin 1 alpha Homo sapiens 28-59
8489769-2 1993 We investigated the effects of retinoic acid (RA) treatments on IL-1 alpha and -beta protein and mRNA expression of normal human keratinocytes cultured in low-calcium defined medium with or without hydrocortisone. Tretinoin 46-48 interleukin 1 alpha Homo sapiens 64-84
8489769-5 1993 Release of both IL-1 alpha and -beta in culture supernatants was detectable only after RA treatment and in the absence of hydrocortisone. Tretinoin 87-89 interleukin 1 alpha Homo sapiens 16-26
1341059-0 1992 Retinoic acid prevents cytokine-induced suppression of thrombomodulin expression on surface of human umbilical vascular endothelial cells in vitro. Tretinoin 0-13 thrombomodulin Homo sapiens 55-69
1281867-0 1992 Identification of the retinoic acid and thyroid hormone receptor-responsive element in the human K14 keratin gene. Tretinoin 22-35 keratin 14 Homo sapiens 97-100
1281867-1 1992 The promoter of human K14 keratin gene, specific for the basal layer of stratified epithelia, is regulated by nuclear receptors for retinoic acid and thyroid hormone. Tretinoin 132-145 keratin 14 Homo sapiens 22-25
1281867-3 1992 To identify the retinoic acid-responsive site, we have devised a simple site-specific mutagenesis method and introduced mutations into the K14 keratin gene promoter. Tretinoin 16-29 keratin 14 Homo sapiens 139-142
1333043-9 1992 Taken together, our results show that the AF1 element contains an RARE that mediates a retinoic acid response by binding an RAR alpha/coregulator complex; this coregulator is presumably RXR alpha. Tretinoin 87-100 retinoic acid receptor alpha Homo sapiens 124-133
1331075-7 1992 Both pathways were shown to be dependent on catalytically active enzyme, to be potentiated by retinoic acid treatment, and to regulate uPA transcriptionally. Tretinoin 94-107 plasminogen activator, urokinase Mus musculus 135-138
1331079-4 1992 In this study, we showed that TR formed heterodimers with RAR and RXR on a retinoic acid (RA) response element and two TREs. Tretinoin 75-88 retinoic acid receptor alpha Homo sapiens 58-61
1328864-3 1992 When F9 cells are stably transfected with a truncated RAR alpha lacking the E/F domain necessary for ligand binding and RAR/RXR dimerization, action at retinoid response elements is suppressed and cells produce a retinoic acid-resistant phenotype; i.e., they are blocked in differentiation (A. S. Espeseth, S. P. Murphy, and E. Linney, Genes Dev. Tretinoin 213-226 retinoic acid receptor alpha Homo sapiens 54-57
1363087-0 1992 Exogenous retinoic acid rapidly induces anterior ectopic expression of murine Hox-2 genes in vivo. Tretinoin 10-23 homeobox B cluster Mus musculus 78-83
1382963-4 1992 RA alone resulted in increased IGFBP-4 levels and the appearance of IGFBP-3 in the CM. Tretinoin 0-2 insulin like growth factor binding protein 3 Homo sapiens 68-75
1382963-5 1992 The combination of RA and IGF-I, which resulted in decreased cellular proliferation, was associated with the appearance of IGFBP-3 in the CM at levels far exceeding those seen with RA alone. Tretinoin 19-21 insulin like growth factor binding protein 3 Homo sapiens 123-130
1357767-0 1992 Induction of tissue transglutaminase and apoptosis by retinoic acid in the limb bud. Tretinoin 54-67 transglutaminase 2, C polypeptide Mus musculus 13-36
1329717-6 1992 Moreover, we found that administration of retinol and retinoic acid to normal rats caused the overexpression of RAR beta transcripts (2-15-fold) when compared with the control levels of RAR beta mRNA, although the levels of RAR alpha and RAR gamma mRNAs were not affected. Tretinoin 54-67 retinoic acid receptor, alpha Rattus norvegicus 224-233
1390181-7 1992 It is well established that RA enters the nucleus where it binds to an RA receptor (RAR), and that the RA-RAR complex then binds to specific RA response elements in the DNA, modulating the expression of target genes. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 71-82
1390181-7 1992 It is well established that RA enters the nucleus where it binds to an RA receptor (RAR), and that the RA-RAR complex then binds to specific RA response elements in the DNA, modulating the expression of target genes. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 84-87
1390181-7 1992 It is well established that RA enters the nucleus where it binds to an RA receptor (RAR), and that the RA-RAR complex then binds to specific RA response elements in the DNA, modulating the expression of target genes. Tretinoin 28-30 retinoic acid receptor alpha Homo sapiens 106-109
1333403-6 1992 Interestingly, the expression of the three genes, RAR-beta, CRABP II and CRBP I, is induced by retinoic acid, which suggests a link between the synthesis of RA from retinol and the control of expression of subsets of RA-responsive genes. Tretinoin 95-108 retinol binding protein 1, cellular Mus musculus 73-79
1333403-6 1992 Interestingly, the expression of the three genes, RAR-beta, CRABP II and CRBP I, is induced by retinoic acid, which suggests a link between the synthesis of RA from retinol and the control of expression of subsets of RA-responsive genes. Tretinoin 50-52 retinol binding protein 1, cellular Mus musculus 73-79
1321136-0 1992 Retinoic acid activation and thyroid hormone repression of the human alcohol dehydrogenase gene ADH3. Tretinoin 0-13 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 96-100
1321136-3 1992 A region in the human ADH3 promoter from -328 to -272 base pairs was shown previously to function as a retinoic acid response element (RARE), prompting an hypothesis for a positive feedback mechanism controlling retinoic acid synthesis (Duester, G., Shean, M. L., McBride, M. S., and Stewart, M. J. Tretinoin 103-116 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 22-26
1627335-2 1992 In this study, we describe the induction of Hox 1.3 expression by retinoic acid (RA) in human bronchial fibroblasts (HBF) derived from explants of bronchial tissue. Tretinoin 66-79 homeobox A5 Homo sapiens 44-51
1627335-2 1992 In this study, we describe the induction of Hox 1.3 expression by retinoic acid (RA) in human bronchial fibroblasts (HBF) derived from explants of bronchial tissue. Tretinoin 81-83 homeobox A5 Homo sapiens 44-51
1627335-3 1992 Using Northern blot analysis, we show that RA induces Hox 1.3 mRNA 3- to 10-fold over steady-state levels within 2 h after addition of RA to HBF culture medium. Tretinoin 43-45 homeobox A5 Homo sapiens 54-61
1627335-3 1992 Using Northern blot analysis, we show that RA induces Hox 1.3 mRNA 3- to 10-fold over steady-state levels within 2 h after addition of RA to HBF culture medium. Tretinoin 135-137 homeobox A5 Homo sapiens 54-61
1627335-10 1992 Although downstream target genes for Hox 1.3 have not yet been identified, it is likely that the induction of Hox 1.3 by RA is an early step in a cascade of RA-induced changes in gene expression in bronchial fibroblasts. Tretinoin 121-123 homeobox A5 Homo sapiens 37-44
1627335-10 1992 Although downstream target genes for Hox 1.3 have not yet been identified, it is likely that the induction of Hox 1.3 by RA is an early step in a cascade of RA-induced changes in gene expression in bronchial fibroblasts. Tretinoin 121-123 homeobox A5 Homo sapiens 110-117
1627335-10 1992 Although downstream target genes for Hox 1.3 have not yet been identified, it is likely that the induction of Hox 1.3 by RA is an early step in a cascade of RA-induced changes in gene expression in bronchial fibroblasts. Tretinoin 157-159 homeobox A5 Homo sapiens 37-44
1627335-10 1992 Although downstream target genes for Hox 1.3 have not yet been identified, it is likely that the induction of Hox 1.3 by RA is an early step in a cascade of RA-induced changes in gene expression in bronchial fibroblasts. Tretinoin 157-159 homeobox A5 Homo sapiens 110-117
1427597-10 1992 Moreover, a retinoic acid-mediated K14 reduction was concomitant with a 4.0-fold transient increase in CDDP resistance in PC10. Tretinoin 12-25 keratin 14 Homo sapiens 35-38
1419902-4 1992 Although other examples of overlapping, opposite-strand eukaryotic genes exist, N-myc and N-cym are unique in that they appear to be coregulated in tumor cell lines under basal growth conditions and in response to the differentiating agent retinoic acid. Tretinoin 240-253 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 80-85
1534272-6 1992 In contrast, cells exposed to RA contained larger amounts of alpha-actinin, vinculin, talin, lipocortin I, and lipocortin II, as determined with their respective antibodies followed by flow cytometric analysis as described above. Tretinoin 30-32 annexin A2 Homo sapiens 111-124
1534272-8 1992 Treatment of HL-60/S4 with RA led to increases in vinculin, talin, lipocortin I, and lipocortin II. Tretinoin 27-29 annexin A2 Homo sapiens 85-98
1534272-9 1992 An RA-resistant clone, designated HL-60/R3, constitutively expressed larger amounts of alpha-actinin, vinculin, lipocortin I, and lipocortin II than parental HL-60 cells. Tretinoin 3-5 CD1d molecule Homo sapiens 34-42
1534272-9 1992 An RA-resistant clone, designated HL-60/R3, constitutively expressed larger amounts of alpha-actinin, vinculin, lipocortin I, and lipocortin II than parental HL-60 cells. Tretinoin 3-5 annexin A2 Homo sapiens 130-143
1534272-10 1992 Treatment of HL-60/R3 with RA resulted in decreases in the amounts of these actin-binding proteins. Tretinoin 27-29 CD1d molecule Homo sapiens 13-21
1622141-3 1992 The proliferative stimulus of IL-3 overrode and reversed the antiproliferative actions of both RA and vitamin D, the latter being more sensitive to the counter-acting effect of IL-3. Tretinoin 95-97 interleukin 3 Homo sapiens 30-34
1622141-4 1992 Whereas only high concentrations of IL-3: 1000 or more U/ml were able to oppose the antiproliferative effect of RA, all concentrations of IL-3 including the low concentration of 10 U/ml, significantly counteracted the anti-proliferative action of vitamin D. Tretinoin 112-114 interleukin 3 Homo sapiens 36-40
1622141-5 1992 RA restrained the proliferative stimulus of IL-3 partly at low physiological concentrations and almost completely at high pharmacological concentrations. Tretinoin 0-2 interleukin 3 Homo sapiens 44-48
1622141-7 1992 Whereas RA restrained the proliferative stimulus of IL-3, vitamin D failed to restrain it. Tretinoin 8-10 interleukin 3 Homo sapiens 52-56
1622141-9 1992 The present results suggest that the clinical use of the combination of low concentration of IL-3 with RA and not with vitamin D might restrain the progression of myeloid leukaemia incurred during the treatment with IL-3 in some preleukaemic patients. Tretinoin 103-105 interleukin 3 Homo sapiens 93-97
1622141-9 1992 The present results suggest that the clinical use of the combination of low concentration of IL-3 with RA and not with vitamin D might restrain the progression of myeloid leukaemia incurred during the treatment with IL-3 in some preleukaemic patients. Tretinoin 103-105 interleukin 3 Homo sapiens 216-220
1591333-0 1992 The 18-kDa mouse epididymal protein (MEP 10) binds retinoic acid. Tretinoin 51-64 lipocalin 5 Mus musculus 37-43
1591333-5 1992 Therefore, it was of interest to determine whether MEP 10 possessed the same ability to bind retinoic acid. Tretinoin 93-106 lipocalin 5 Mus musculus 51-57
1373689-0 1992 Retinoic acid acts to neutralize the inhibitory effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on alkaline phosphatase activity of neutrophils that is induced by granulocyte colony-stimulating factor (G-CSF). Tretinoin 0-13 colony stimulating factor 2 Homo sapiens 58-106
1373689-0 1992 Retinoic acid acts to neutralize the inhibitory effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on alkaline phosphatase activity of neutrophils that is induced by granulocyte colony-stimulating factor (G-CSF). Tretinoin 0-13 colony stimulating factor 2 Homo sapiens 108-114
1373689-0 1992 Retinoic acid acts to neutralize the inhibitory effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on alkaline phosphatase activity of neutrophils that is induced by granulocyte colony-stimulating factor (G-CSF). Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 183-220
1373689-0 1992 Retinoic acid acts to neutralize the inhibitory effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on alkaline phosphatase activity of neutrophils that is induced by granulocyte colony-stimulating factor (G-CSF). Tretinoin 0-13 colony stimulating factor 3 Homo sapiens 222-227
1373689-4 1992 Moreover, we found that the simultaneous addition of retinoic acid completely neutralized this inhibitory effect of GM-CSF. Tretinoin 53-66 colony stimulating factor 2 Homo sapiens 116-122
1373689-6 1992 These results indicate that retinoic acid neutralizes the inhibitory effect of GM-CSF on the induction of NAP activity through the change of the NAP mRNA level. Tretinoin 28-41 colony stimulating factor 2 Homo sapiens 79-85
1323569-3 1992 We have compared the patterns of RAR expression in human keratinocytes and dermal fibroblasts in vitro, and studied the effects of retinoic acid on RAR expression. Tretinoin 131-144 retinoic acid receptor alpha Homo sapiens 148-151
1610391-0 1992 Lipoprotein lipase enzyme expression in 3T3-L1 adipocytes is posttranscriptionally down-regulated by retinoic acid. Tretinoin 101-114 lipoprotein lipase Homo sapiens 0-18
1610391-1 1992 The effects of all-trans retinoic acid (RA) on the lipoprotein lipase (LPL) activity, synthesis and mRNA content in 3T3-L1 adipocytes were studied. Tretinoin 40-42 lipoprotein lipase Homo sapiens 51-69
1610391-1 1992 The effects of all-trans retinoic acid (RA) on the lipoprotein lipase (LPL) activity, synthesis and mRNA content in 3T3-L1 adipocytes were studied. Tretinoin 40-42 lipoprotein lipase Homo sapiens 71-74
1610391-2 1992 When fully differentiated 3T3-L1 adipocytes were exposed to RA, dose-dependent suppression of LPL activity was observed. Tretinoin 60-62 lipoprotein lipase Homo sapiens 94-97
1610391-6 1992 These results suggest that RA can specifically down-regulate LPL enzyme expression in adipocytes at the posttranscriptional level. Tretinoin 27-29 lipoprotein lipase Homo sapiens 61-64
1350056-8 1992 Instead, retinoic acid destabilized TAT mRNA. Tretinoin 9-22 tyrosine aminotransferase Rattus norvegicus 36-39
1350056-9 1992 The half-life values of TAT mRNA in DEX/Bt2cAMP- and DEX/Bt2cAMP/retinoic acid-treated cells were approximately 235-270 min and 90-100 min, respectively. Tretinoin 65-78 tyrosine aminotransferase Rattus norvegicus 24-27
1350056-10 1992 Our results indicate that inhibition of TAT expression by retinoic acid was regulated primarily at the posttranscriptional level. Tretinoin 58-71 tyrosine aminotransferase Rattus norvegicus 40-43
1581607-2 1992 We have tested the potential negative regulatory role of JunB during the retinoic acid induced differentiation of F9 murine embryonal carcinoma cells. Tretinoin 73-86 jun B proto-oncogene Mus musculus 57-61
1624219-3 1992 All-trans-retinoic acid (RA) at 10(-8) M potentiated the proliferative response by fivefold at saturating levels of IL-2. Tretinoin 0-23 interleukin 2 Mus musculus 116-120
1624219-3 1992 All-trans-retinoic acid (RA) at 10(-8) M potentiated the proliferative response by fivefold at saturating levels of IL-2. Tretinoin 25-27 interleukin 2 Mus musculus 116-120
1624219-9 1992 HT-2 proliferative responses to rIL-2 were potentiated as much as fourfold by 10(-10) M RA. Tretinoin 88-90 interleukin 2 Rattus norvegicus 32-37
1370608-0 1992 Retinoic acid stimulates expression of thrombomodulin, a cell surface anticoagulant glycoprotein, on human endothelial cells. Tretinoin 0-13 thrombomodulin Homo sapiens 39-53
1370608-1 1992 Differences between up-regulation of thrombomodulin by retinoic acid and cyclic AMP. Tretinoin 55-68 thrombomodulin Homo sapiens 37-51
1370608-3 1992 In this paper, we demonstrate that retinoic acid (RA) causes an increase in TM antigen on human umbilical vein endothelial cells (HUVECs) in vitro. Tretinoin 35-48 thrombomodulin Homo sapiens 76-78
1370608-3 1992 In this paper, we demonstrate that retinoic acid (RA) causes an increase in TM antigen on human umbilical vein endothelial cells (HUVECs) in vitro. Tretinoin 50-52 thrombomodulin Homo sapiens 76-78
1370608-4 1992 The effect of RA on the surface TM level of HUVECs was dose-dependent in the range from 0.01 to 10 microM-RA. Tretinoin 14-16 thrombomodulin Homo sapiens 32-34
1370608-4 1992 The effect of RA on the surface TM level of HUVECs was dose-dependent in the range from 0.01 to 10 microM-RA. Tretinoin 106-108 thrombomodulin Homo sapiens 32-34
1370608-7 1992 The effects of RA on cell surface TM activity and antigen levels were parallel in all experiments. Tretinoin 15-17 thrombomodulin Homo sapiens 34-36
1370608-12 1992 Northern blot analysis showed that treatment of HUVECs with 8-bromo cyclic AMP, RA or RA plus 8-bromo cyclic AMP increased TM mRNA levels by 2.2-, 4.5- and 5.5-fold respectively compared with the untreated control. Tretinoin 80-82 thrombomodulin Homo sapiens 123-125
1370608-12 1992 Northern blot analysis showed that treatment of HUVECs with 8-bromo cyclic AMP, RA or RA plus 8-bromo cyclic AMP increased TM mRNA levels by 2.2-, 4.5- and 5.5-fold respectively compared with the untreated control. Tretinoin 86-88 thrombomodulin Homo sapiens 123-125
1370608-14 1992 These results indicate that the expression of TM is not only controlled by the intracellular cyclic AMP level but is also affected by RA, and suggest that RA-induced up-regulation of TM on HUVECs is independent of cyclic AMP regulation. Tretinoin 134-136 thrombomodulin Homo sapiens 46-48
1370608-14 1992 These results indicate that the expression of TM is not only controlled by the intracellular cyclic AMP level but is also affected by RA, and suggest that RA-induced up-regulation of TM on HUVECs is independent of cyclic AMP regulation. Tretinoin 155-157 thrombomodulin Homo sapiens 46-48
1370608-14 1992 These results indicate that the expression of TM is not only controlled by the intracellular cyclic AMP level but is also affected by RA, and suggest that RA-induced up-regulation of TM on HUVECs is independent of cyclic AMP regulation. Tretinoin 155-157 thrombomodulin Homo sapiens 183-185
1320576-8 1992 In addition, in two RAC65 clones in which wild-type hRAR alpha was stably transfected RA-sensitivity was restored and in one RAR beta expression could be induced by RA. Tretinoin 20-22 retinoic acid receptor alpha Homo sapiens 52-62
1363667-3 1992 However, since exogenous retinoic acid induces expression of RAR beta, but not grafted ZPA, the ZPA is unlikely to produce retinoic acid. Tretinoin 25-38 retinoic acid receptor beta Gallus gallus 61-69
1661301-0 1991 All-trans retinoic acid modulates the retinoic acid receptor-alpha in promyelocytic cells. Tretinoin 10-23 retinoic acid receptor alpha Homo sapiens 38-66
1766678-0 1991 Expression of the ret proto-oncogene in human neuroblastoma cell lines and its increase during neuronal differentiation induced by retinoic acid. Tretinoin 131-144 ret proto-oncogene Homo sapiens 18-21
1766678-4 1991 Expression of proto-ret in the SH-4305 cells increased markedly after treatment with retinoic acid for 1 day, with concomitant morphological change, namely neurite outgrowth, and induction of neurofilament mRNA expression. Tretinoin 85-98 ret proto-oncogene Homo sapiens 20-23
1683482-2 1991 In this study, we have examined transcription of the Hox-2.1 gene during differentiation of F9 embryonal carcinoma cells induced by treatment with retinoic acid. Tretinoin 147-160 homeobox B5 Mus musculus 53-60
1939209-0 1991 Induction of expression of the alpha v beta 1 and alpha v beta 3 integrin heterodimers during retinoic acid-induced neuronal differentiation of murine embryonal carcinoma cells. Tretinoin 94-107 hemoglobin, beta adult major chain Mus musculus 39-45
1939209-11 1991 The retinoic acid-induced expression of beta 1 occurred at the level of mRNA expression which also paralleled neuronal differentiation, but peaked slightly ahead of the cell surface expression of beta 1. Tretinoin 4-17 hemoglobin, beta adult major chain Mus musculus 40-46
1939209-11 1991 The retinoic acid-induced expression of beta 1 occurred at the level of mRNA expression which also paralleled neuronal differentiation, but peaked slightly ahead of the cell surface expression of beta 1. Tretinoin 4-17 hemoglobin, beta adult major chain Mus musculus 196-202
1939209-13 1991 These data demonstrate that retinoic acid strongly induces the expression of the integrin heterodimer alpha v beta 1 and also, to a smaller extent, the expression of alpha v beta 3. Tretinoin 28-41 hemoglobin, beta adult major chain Mus musculus 110-116
1939209-14 1991 The retinoic acid-induced, high level surface expression of the alpha v beta 1 heterodimer is tightly correlated with the induction of neuronal differentiation by retinoic acid. Tretinoin 4-17 hemoglobin, beta adult major chain Mus musculus 72-78
1939209-14 1991 The retinoic acid-induced, high level surface expression of the alpha v beta 1 heterodimer is tightly correlated with the induction of neuronal differentiation by retinoic acid. Tretinoin 163-176 hemoglobin, beta adult major chain Mus musculus 72-78
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 4-23 interleukin 1 alpha Homo sapiens 189-217
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 4-23 interleukin 1 alpha Homo sapiens 219-229
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 25-29 interleukin 1 alpha Homo sapiens 189-217
1717193-1 1991 All trans-retinoic acid (ATRA) and related compounds, at concentrations ranging from 10(-8) to 10(-6) M, augmented the proliferation of human synovial fibroblasts (HSN) stimulated by human interleukin-1 alpha or -beta (IL-1 alpha, IL-beta) and both the acidic and basic forms of fibroblast growth factor (FGFa, FGFb). Tretinoin 25-29 interleukin 1 alpha Homo sapiens 219-229
1661245-10 1991 A point mutation has been identified in the RAR alpha gene of embryonal carcinoma cells resistant to retinoic acid. Tretinoin 101-114 retinoic acid receptor alpha Homo sapiens 44-53
1808207-10 1991 Conversely, when exposed to retinoic acid, an inducer of differentiation, lamin A-expressing P19 cells are able to differentiate normally. Tretinoin 28-41 lamin A/C Gallus gallus 74-81
1682879-0 1991 The expression of murine Hox-2 genes is dependent on the differentiation pathway and displays a collinear sensitivity to retinoic acid in F9 cells and Xenopus embryos. Tretinoin 121-134 homeobox B cluster Mus musculus 25-30
1682879-1 1991 In this paper we describe experiments that detail the response of murine Hox-2 genes to cellular differentiation and retinoic acid in cell culture. Tretinoin 117-130 homeobox B cluster Mus musculus 73-78
1682879-2 1991 Hox-2 genes are transiently activated in differentiating ES cells even in the absence of retinoic acid (RA), indicating that their induction is a normal aspect of differentiation. Tretinoin 89-102 homeobox B cluster Mus musculus 0-5
1682879-2 1991 Hox-2 genes are transiently activated in differentiating ES cells even in the absence of retinoic acid (RA), indicating that their induction is a normal aspect of differentiation. Tretinoin 104-106 homeobox B cluster Mus musculus 0-5
1682879-8 1991 Therefore RA exerts its effects on Hox-2 expression by upregulating or modulating genes which are already active, rather than by turning-on silent genes. Tretinoin 10-12 homeobox B cluster Mus musculus 35-40
1682879-11 1991 Together these findings suggest that the collinear response to RA is highly conserved in vertebrates and combined with the ability of RA to modify expression during cellular differentiation could be an important feature of the Hox-2 cluster itself used to generate the spatially-restricted patterns of gene expression in embryogenesis. Tretinoin 63-65 homeobox B cluster Mus musculus 227-232
1682879-11 1991 Together these findings suggest that the collinear response to RA is highly conserved in vertebrates and combined with the ability of RA to modify expression during cellular differentiation could be an important feature of the Hox-2 cluster itself used to generate the spatially-restricted patterns of gene expression in embryogenesis. Tretinoin 134-136 homeobox B cluster Mus musculus 227-232
1812132-7 1991 Our results suggest that in the medial epithelial cells of the palate, retinoic acid sustains the expression of the EGF receptor and the binding of EGF at a time when the expression in control medial cells has declined, and these control cells subsequently undergo programmed cell death. Tretinoin 71-84 epidermal growth factor Homo sapiens 116-119
1812132-7 1991 Our results suggest that in the medial epithelial cells of the palate, retinoic acid sustains the expression of the EGF receptor and the binding of EGF at a time when the expression in control medial cells has declined, and these control cells subsequently undergo programmed cell death. Tretinoin 71-84 epidermal growth factor Homo sapiens 148-151
1917145-5 1991 At week 18, quantitative histological analysis showed that prolonged administration of RA resulted in a significant reduction in the number, size and volume of GGT-positive and GST-P-positive hepatic lesions. Tretinoin 87-89 gamma-glutamyltransferase 1 Rattus norvegicus 160-163
1654565-9 1991 In contrast, liver, lung, and testes RAR-alpha transcripts remained either unchanged or showed only a slight increase in response to retinoic acid. Tretinoin 133-146 retinoic acid receptor, alpha Rattus norvegicus 37-46
1793734-7 1991 Inactivation of this repressor following retinoic acid treatment resulted in several peaks of activation of the Krox-24 gene, mediated by different mechanisms, some of which did not require de novo protein synthesis. Tretinoin 41-54 early growth response 1 Mus musculus 112-119
1721002-5 1991 The results suggest that RA not only inhibits the proliferative action of G-CSF, but also retains and enhances the action of G-CSF to induce differentiation. Tretinoin 25-27 colony stimulating factor 3 Homo sapiens 74-79
1721002-5 1991 The results suggest that RA not only inhibits the proliferative action of G-CSF, but also retains and enhances the action of G-CSF to induce differentiation. Tretinoin 25-27 colony stimulating factor 3 Homo sapiens 125-130
1648728-6 1991 These data suggest that the RAR alpha may form a nonproductive complex with c-Jun and provides a simple mechanisms by which retinoic acid may limit cell growth and possibly malignant progression. Tretinoin 124-137 retinoic acid receptor alpha Homo sapiens 28-37
1908849-8 1991 Our results suggest a close relationship between increase of tumor weight and stimulation of serum IGF-1 level by RA in tumor-bearing rats. Tretinoin 114-116 insulin-like growth factor 1 Rattus norvegicus 99-104
1827755-4 1991 Leukosialin from RA-resistant and 6-TG-resistant HL-60 sublines migrated much more slowly than those from wild-type HL-60 cells when applied to sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Tretinoin 17-19 LOC105369247 Homo sapiens 0-11
2015403-0 1991 Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF. Tretinoin 109-122 colony stimulating factor 2 Homo sapiens 140-165
2015403-0 1991 Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF. Tretinoin 109-122 colony stimulating factor 2 Homo sapiens 167-170
1848877-3 1991 Size exclusion FPLC of 0.6 M NaCl nuclear extracts prepared from keratome biopsies revealed two peaks of specific [3H] retinoic acid (RA) binding at Mr 45 and 18 kDa, in agreement with the expected sizes of RAR and cellular RA binding protein. Tretinoin 134-136 retinoic acid receptor alpha Homo sapiens 207-210
2025238-2 1991 We report a new retinoid-binding protein (Ret BP) with a molecular size of 4,000 that binds retinol, retinoic acid, and some of their derivatives. Tretinoin 101-114 ret proto-oncogene Gallus gallus 42-45
1996113-0 1991 Retinoic acid response element in the human alcohol dehydrogenase gene ADH3: implications for regulation of retinoic acid synthesis. Tretinoin 0-13 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 71-75
1996113-0 1991 Retinoic acid response element in the human alcohol dehydrogenase gene ADH3: implications for regulation of retinoic acid synthesis. Tretinoin 108-121 alcohol dehydrogenase 1C (class I), gamma polypeptide Homo sapiens 71-75
1670759-1 1991 Although mRNA for the retinoic acid receptor alpha (RAR-alpha) is expressed in many different myeloid leukemias, most of these leukemia cells exhibit little if any phenotypic response when exposed to retinoic acid (RA). Tretinoin 22-35 retinoic acid receptor alpha Homo sapiens 52-61
1670759-1 1991 Although mRNA for the retinoic acid receptor alpha (RAR-alpha) is expressed in many different myeloid leukemias, most of these leukemia cells exhibit little if any phenotypic response when exposed to retinoic acid (RA). Tretinoin 52-54 retinoic acid receptor alpha Homo sapiens 22-50
1987282-8 1991 The granulocytic differentiation of the cells treated with retinoic acid was accompanied by intense expression of fgr, but weak or no expression of lyn and fyn gene. Tretinoin 59-72 FYN proto-oncogene, Src family tyrosine kinase Homo sapiens 156-159
1822392-4 1991 As the antiestrogenic effect of retinoic acid was increased by cotransfecting acid receptor(s) RAR alpha, beta, gamma, we concluded that RAR(s) is(are) involved in the antiestrogenic effect of retinoic acid. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 95-104
1822392-4 1991 As the antiestrogenic effect of retinoic acid was increased by cotransfecting acid receptor(s) RAR alpha, beta, gamma, we concluded that RAR(s) is(are) involved in the antiestrogenic effect of retinoic acid. Tretinoin 32-45 retinoic acid receptor alpha Homo sapiens 95-98
1966045-3 1990 We report here the gene expression patterns, as revealed by in situ hybridisation, of the retinoic acid receptors alpha, beta and gamma (RAR-alpha, -beta and -gamma), and the cellular binding proteins for retinol and retinoic acid (CRBP, CRABP) in non-neural tissues of mouse embryos during the period of organogenesis. Tretinoin 90-103 retinol binding protein 1, cellular Mus musculus 232-236
2256914-4 1990 Second, activin inhibits the retinoic acid (RA) induced differentiation of P19 cells to neurons and glial cells. Tretinoin 29-42 inhibin subunit beta E Homo sapiens 8-15
2256914-4 1990 Second, activin inhibits the retinoic acid (RA) induced differentiation of P19 cells to neurons and glial cells. Tretinoin 44-46 inhibin subunit beta E Homo sapiens 8-15
2123747-0 1990 Different regulation of mid-size neurofilament and N-myc mRNA expression during neuroblastoma cell differentiation induced by retinoic acid. Tretinoin 126-139 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 51-56
2167156-6 1990 Interstitial collagenase mRNA expression was significantly decreased by treatment with either transforming growth factor-beta 1 or retinoic acid in A2058 melanoma cells. Tretinoin 131-144 matrix metallopeptidase 1 Homo sapiens 0-24
2201551-2 1990 In HL-R5 cells, resistant to the induction of differentiation by retinoic acid but not DMSO, the characteristic c-myc down-regulation which is associated with HL-60 differentiation, as well as increased levels of MRP8 and MRP14, is detectable only after DMSO treatment. Tretinoin 65-78 MYC proto-oncogene, bHLH transcription factor Homo sapiens 112-117
2164926-12 1990 Similarly, PTH also inhibited heterologous up-regulation of VDR and VDR mRNA induced by retinoic acid. Tretinoin 88-101 vitamin D receptor Rattus norvegicus 60-63
2164926-12 1990 Similarly, PTH also inhibited heterologous up-regulation of VDR and VDR mRNA induced by retinoic acid. Tretinoin 88-101 vitamin D receptor Rattus norvegicus 68-71
2163931-2 1990 Induction of c-fos transcripts was not observed at times early or late during retinoic acid-promoted differentiation, but a decrease in c-myc mRNA was noted as early as 1 h after retinoic acid dosing. Tretinoin 179-192 MYC proto-oncogene, bHLH transcription factor Homo sapiens 136-141
1970751-5 1990 Kinetic study revealed that retinoic acid augmented significantly LAK cell activity when incubated in IL-2-containing culture as short as for 6 h before cytotoxicity was measured. Tretinoin 28-41 interleukin 2 Mus musculus 102-106
1970751-7 1990 Retinoic acid was found to augment LAK cell activity in a wide range of IL-2 concentrations (750-12,000 IU/ml), even at 6,000 IU/ml where the maximal induction of LAK cell activity had been reached. Tretinoin 0-13 interleukin 2 Mus musculus 72-76
1970751-11 1990 Overall these results demonstrated that IL-2-induced LAK cell activity was enhanced by retinoic acid and that the augmentation may be mediated by means of enhanced expression of cellular serine protease activity. Tretinoin 87-100 interleukin 2 Mus musculus 40-44
2107263-3 1990 Trans retinoic acid (RA), at concentrations as low as 0.1 nM, inhibited the induction of tyrosinase, dopachrome conversion factor, and melanogenesis, but had no effect on the basal levels of either enzyme or of cellular melanin content. Tretinoin 0-19 tyrosinase Mus musculus 89-99
2107263-3 1990 Trans retinoic acid (RA), at concentrations as low as 0.1 nM, inhibited the induction of tyrosinase, dopachrome conversion factor, and melanogenesis, but had no effect on the basal levels of either enzyme or of cellular melanin content. Tretinoin 21-23 tyrosinase Mus musculus 89-99
2154975-4 1990 Further, the binding selectivity of the RAR products toward all-trans-retinoic acid (RA), Am80 and Ch55 was studied by filter binding assay. Tretinoin 64-83 retinoic acid receptor alpha Homo sapiens 40-43
2317454-8 1990 P47 was also found in HL-60 promyelocytes (especially after differentiation with retinoic acid), U937 histiocytes, HEL leukaemia cells, and Raji "B" lymphoblasts. Tretinoin 81-94 pleckstrin Homo sapiens 0-3
33972395-6 2021 Elevated retinoic acid catabolism due to increased levels of the cytochrome P450 superfamily member Cyp26b1 as a result of decreased Erf levels appears to be the underlying mechanism leading to defective differentiation. Tretinoin 9-22 Ets2 repressor factor Mus musculus 133-136
33972395-7 2021 Exogenous addition of retinoic acid can rescue the osteogenic differentiation defect suggesting that Erf affects cranial bone mineralization during skull development through retinoic acid gradient regulation. Tretinoin 22-35 Ets2 repressor factor Mus musculus 101-104
33972395-7 2021 Exogenous addition of retinoic acid can rescue the osteogenic differentiation defect suggesting that Erf affects cranial bone mineralization during skull development through retinoic acid gradient regulation. Tretinoin 174-187 Ets2 repressor factor Mus musculus 101-104
33824267-0 2021 MLL5 improves ATRA driven differentiation and promotes xenotransplant engraftment in acute promyelocytic leukemia model. Tretinoin 14-18 lysine methyltransferase 2E (inactive) Homo sapiens 0-4
33824267-3 2021 Additionally, MLL5 overexpression increased the responsiveness of APL leukemic cells to all-trans retinoic acid (ATRA)-induced differentiation, via regulation of the epigenetic modifiers SETD7 and LSD1. Tretinoin 98-111 lysine methyltransferase 2E (inactive) Homo sapiens 14-18
33824267-3 2021 Additionally, MLL5 overexpression increased the responsiveness of APL leukemic cells to all-trans retinoic acid (ATRA)-induced differentiation, via regulation of the epigenetic modifiers SETD7 and LSD1. Tretinoin 113-117 lysine methyltransferase 2E (inactive) Homo sapiens 14-18
33824267-3 2021 Additionally, MLL5 overexpression increased the responsiveness of APL leukemic cells to all-trans retinoic acid (ATRA)-induced differentiation, via regulation of the epigenetic modifiers SETD7 and LSD1. Tretinoin 113-117 SET domain containing 7, histone lysine methyltransferase Homo sapiens 187-192
33824267-4 2021 In silico analysis indicated that APL blasts with MLL5high transcript levels were associated with retinoic acid binding and downstream signaling, while MLL5low blasts displayed decreased expression of epigenetic modifiers (such as KMT2C, PHF8 and ARID4A). Tretinoin 98-111 lysine methyltransferase 2E (inactive) Homo sapiens 50-54
33824267-6 2021 Concordantly, evaluation of engrafted blasts revealed increased responsiveness of MLL5-expressing cells to ATRA-induced granulocytic differentiation. Tretinoin 107-111 lysine methyltransferase 2E (inactive) Homo sapiens 82-86
33801464-4 2021 Overexpression of SARS-CoV-2 N resulted in the attenuation of retinoic acid inducible gene-I (RIG-I)-like receptor-mediated interferon (IFN) production and IFN-induced gene expression. Tretinoin 62-75 nucleocapsid phosphoprotein Severe acute respiratory syndrome coronavirus 2 29-30
7568495-9 1995 Retinoic acid-induced fetal mouse forelimb syndactyly was observed in all the groups; 81 percent of E17 limbs, 75 percent of PN limbs, and 77 percent of E13+4 limbs had syndactyly. Tretinoin 0-13 skull morphology 19 Mus musculus 153-156
34309195-2 2022 In this study, we fabricated T1 contrast Mn-porphyrin (MnTPPS4 )/retinoic acid-chitosan ionic-complex nanoparticles (MRC NPs). Tretinoin 65-78 CD200 molecule Homo sapiens 117-120
34309195-6 2022 Hepatocytes uptake assay proved retinoic acid-specific targeting of MRC NPs. Tretinoin 32-45 CD200 molecule Homo sapiens 68-71
34599982-8 2022 While SF2 regulates myelogenous cell leukemia-1 (Mcl-1, anti-apoptotic factor), RA treatment reduced the level of Mcl-1L (full-length Mcl-1 long) and increased the level of Mcl-1S (Mcl-1 short; a short splicing variant of the Mcl-1). Tretinoin 80-82 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 114-120
34599982-8 2022 While SF2 regulates myelogenous cell leukemia-1 (Mcl-1, anti-apoptotic factor), RA treatment reduced the level of Mcl-1L (full-length Mcl-1 long) and increased the level of Mcl-1S (Mcl-1 short; a short splicing variant of the Mcl-1). Tretinoin 80-82 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 173-179
34599982-10 2022 In contrast, treatment with a Mcl-1L inhibitor enhanced RA-induced cell differentiation. Tretinoin 56-58 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 30-36
34599982-11 2022 These results indicate that RA activates PKA in the nucleus, increases phosphorylation of SF2, raises levels of Mcl-1S and lowers levels of Mcl-1L, resulting in the induction of differentiation. Tretinoin 28-30 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 112-118
34599982-11 2022 These results indicate that RA activates PKA in the nucleus, increases phosphorylation of SF2, raises levels of Mcl-1S and lowers levels of Mcl-1L, resulting in the induction of differentiation. Tretinoin 28-30 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 140-146
34348549-2 2022 The improvement of APL outcome is mainly due to two agents, which target the typical translocation t(15;17) and its fusion transcript PML-RARalpha responsible for initiating and maintaining the disease: all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 203-226 retinoic acid receptor alpha Homo sapiens 138-146
34348549-2 2022 The improvement of APL outcome is mainly due to two agents, which target the typical translocation t(15;17) and its fusion transcript PML-RARalpha responsible for initiating and maintaining the disease: all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). Tretinoin 228-232 retinoic acid receptor alpha Homo sapiens 138-146
34861212-0 2022 Topical retinoic acid induces corneal strengthening by upregulating transglutaminase 2 in murine cornea. Tretinoin 8-21 transglutaminase 2, C polypeptide Mus musculus 68-86
34546543-5 2022 Three samples in which CD11b increased in response to ATRA had an inversion of chromosome 16 as well as the CBFB-MYH11 fusion gene, and the fourth sample was from a patient with KMT2A-rearranged, therapy-related AML. Tretinoin 54-58 core-binding factor subunit beta Homo sapiens 108-112
34546543-6 2022 In conclusion, we identified a subgroup of non-APL AML patients with inv(16) and CBFB-MYH11 as the most sensitive to ATRA-mediated differentiation in vitro, and our results can help identify patients who may benefit from ATRA treatment. Tretinoin 117-121 core-binding factor subunit beta Homo sapiens 81-85
34934174-0 2021 A specific inhibitor of ALDH1A3 regulates retinoic acid biosynthesis in glioma stem cells. Tretinoin 42-55 aldehyde dehydrogenase 1 family member A3 Homo sapiens 24-31
34945773-1 2021 BACKGROUND: Recent reports indicate the potential role of the stimulated by retinoic acid 6 (STRA6) protein in developing insulin resistance. Tretinoin 76-89 signaling receptor and transporter of retinol STRA6 Homo sapiens 93-98
34784434-5 2021 Quantification of mRNA and protein expression revealed dysregulation in the first step of RA biosynthesis consistent with reduced RA including decreased protein expression of retinol dehydrogenase (RDH)-10 and increased protein expression of RDH11 and dehydrogenase/reductase (DHRS)-4 in asthmatic lung. Tretinoin 90-92 retinol dehydrogenase 11 Homo sapiens 242-247
34784434-7 2021 Further, basal RA levels and RA biosynthetic capabilities were decreased in asthmatic human ASM cells. Tretinoin 15-17 H19 imprinted maternally expressed transcript Homo sapiens 92-95
34784434-7 2021 Further, basal RA levels and RA biosynthetic capabilities were decreased in asthmatic human ASM cells. Tretinoin 29-31 H19 imprinted maternally expressed transcript Homo sapiens 92-95
34784434-8 2021 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin 44-46 H19 imprinted maternally expressed transcript Homo sapiens 19-22
34784434-8 2021 Treatment of human ASM cells with all-trans RA (ATRA) or the RARgamma-specific agonist (CD1530) resulted in the inhibition of mitogen-induced cell proliferation and AP-1-dependent transcription. Tretinoin 48-52 H19 imprinted maternally expressed transcript Homo sapiens 19-22
34569079-4 2021 It has been found that epidermal growth factor (EGF), taurine, and retinoic acid (RA) initially act in the instructive as well as lineage-restricted way in the progenitor lineage for producing neuroretinal cells or photoreceptor like cells from stem cell. Tretinoin 82-84 epidermal growth factor Homo sapiens 23-46
34943872-0 2021 Targeting CAMKK2 and SOC Channels as a Novel Therapeutic Approach for Sensitizing Acute Promyelocytic Leukemia Cells to All-Trans Retinoic Acid. Tretinoin 120-143 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 10-16
34943872-5 2021 Moreover, ATRA treatment of APL cells led to a significant activation of calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) and its downstream effector AMP-activated protein kinase (AMPK), linking Ca2+ signaling to autophagy. Tretinoin 10-14 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 73-125
34943872-5 2021 Moreover, ATRA treatment of APL cells led to a significant activation of calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) and its downstream effector AMP-activated protein kinase (AMPK), linking Ca2+ signaling to autophagy. Tretinoin 10-14 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 127-133
34943872-6 2021 Pharmacological inhibition of SOC channels and CAMKK2 enhanced ATRA-induced cell differentiation and death. Tretinoin 63-67 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 47-53
34943872-7 2021 Altogether, our results unravel an ATRA-elicited signaling pathway that involves SOC channels/CAMKK2 activation, induction of autophagy, inhibition of cellular differentiation and suppression of cell death. Tretinoin 35-39 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 94-100
34943872-8 2021 We suggest that SOC channels and CAMKK2 may constitute novel drug targets for potentiating the anti-cancer effect of ATRA in APL patients. Tretinoin 117-121 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 33-39
34899669-9 2021 Collectively, this study shows that HSP27 dampens EMCV infectivity by positively regulating EMCV-triggered retinoic acid-inducible gene (RIG)-I-like receptor (RLR)/melanoma differentiation-associated gene 5 (MDA5) signal pathway, while EMCV proteins 2Cpro and 3Apro interact with HSP27 and degrade HSP27 protein expression to allow EMCV proliferation. Tretinoin 107-120 heat shock protein family B (small) member 1 Homo sapiens 36-41
34899669-9 2021 Collectively, this study shows that HSP27 dampens EMCV infectivity by positively regulating EMCV-triggered retinoic acid-inducible gene (RIG)-I-like receptor (RLR)/melanoma differentiation-associated gene 5 (MDA5) signal pathway, while EMCV proteins 2Cpro and 3Apro interact with HSP27 and degrade HSP27 protein expression to allow EMCV proliferation. Tretinoin 107-120 interferon induced with helicase C domain 1 Homo sapiens 208-212
34817042-9 2021 Expression of OCT4 gene dropped after RA treatment, but it was recovered in NT2-RA-VH cells. Tretinoin 38-40 POU class 5 homeobox 1 Homo sapiens 14-18
34836244-6 2021 All-trans retinol also travels through the bloodstream bound to retinol binding protein 4 (RBP4), where it enters cells with the assistance of the transmembrane transporters, stimulated by retinoic acid 6 (STRA6) in peripheral tissues or retinol binding protein 4 receptor 2 (RBPR2) in systemic tissues (e.g., in the retina and the liver, respectively). Tretinoin 189-202 signaling receptor and transporter of retinol STRA6 Homo sapiens 206-211
34831243-5 2021 We show that primary liver cells sense RNA through retinoic acid-inducible gene I (RIG-I) like receptor (RLR) and Toll-like receptor 3 (TLR3) pathways. Tretinoin 51-64 DExH-box helicase 58 Homo sapiens 105-108
34390859-1 2021 OBJECTIVE: The nuclear receptor corepressor 1 (NCOR1) and the silencing mediator of retinoic acid and thyroid hormone (SMRT, also known as NCOR2) play critical and specific roles in nuclear receptor action. Tretinoin 84-97 nuclear receptor co-repressor 2 Mus musculus 119-123
34390859-1 2021 OBJECTIVE: The nuclear receptor corepressor 1 (NCOR1) and the silencing mediator of retinoic acid and thyroid hormone (SMRT, also known as NCOR2) play critical and specific roles in nuclear receptor action. Tretinoin 84-97 nuclear receptor co-repressor 2 Mus musculus 139-144
34087410-6 2021 While the recruitment of PU.1 was significantly impaired to the Il9 gene in the presence of calcitriol or retinoic acid in Th9 cells, addition of both vitamins together increased the recruitment of PU.1 to the Il9 gene. Tretinoin 106-119 Spi-1 proto-oncogene Homo sapiens 25-29
34535740-7 2021 Another Pin1 inhibitor, all-trans retinoic acid (ATRA)-a commercially available drug used to treat acute promyelocytic leukemia (APL) and which both activates the retinoic acid receptor and inhibits the activity of Pin1-similarly reduced the proliferation of SARS-CoV-2. Tretinoin 24-47 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 8-12
34535740-7 2021 Another Pin1 inhibitor, all-trans retinoic acid (ATRA)-a commercially available drug used to treat acute promyelocytic leukemia (APL) and which both activates the retinoic acid receptor and inhibits the activity of Pin1-similarly reduced the proliferation of SARS-CoV-2. Tretinoin 24-47 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 215-219
34535740-7 2021 Another Pin1 inhibitor, all-trans retinoic acid (ATRA)-a commercially available drug used to treat acute promyelocytic leukemia (APL) and which both activates the retinoic acid receptor and inhibits the activity of Pin1-similarly reduced the proliferation of SARS-CoV-2. Tretinoin 49-53 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 8-12
34535740-7 2021 Another Pin1 inhibitor, all-trans retinoic acid (ATRA)-a commercially available drug used to treat acute promyelocytic leukemia (APL) and which both activates the retinoic acid receptor and inhibits the activity of Pin1-similarly reduced the proliferation of SARS-CoV-2. Tretinoin 49-53 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 215-219
34417282-7 2021 We show that the major substrate for RA, retinol binding protein 4, is decreased in AU rats, and retinol cell surface receptor declines with chronological age. Tretinoin 37-39 retinol binding protein 4 Rattus norvegicus 41-66
34292881-7 2021 These data provide direct functional evidence that uterine RAR-mediated RA signaling is crucial for mammalian embryo implantation, and its disruption leads to failure of uterine receptivity and decidualization resulting in severely compromised fertility. Tretinoin 72-74 retinoic acid receptor alpha Homo sapiens 59-62
34288263-8 2021 Moreover, all-trans-retinoic acid, which enhances CD38 expression and induces cell differentiation in myeloma cells, reduced B-cell marker expression and the BCL2/BCL2L1 ratio in myeloma cell lines, leading to reduced efficacy of venetoclax. Tretinoin 10-33 CD38 molecule Homo sapiens 50-54
34573521-6 2021 The in vitro supplementation of CanL spleen leukocytes with ATRA, 1,25(OH)2VD3, and SZn, in addition to a soluble leishmania antigen (SLA) treatment, increased the NO and ROS levels, while the treatments with only ATRA and SZn increased the TNF-a levels. Tretinoin 214-218 tumor necrosis factor Canis lupus familiaris 241-246
34244292-6 2021 Upon RA treatment of Satb2 wt ESCs, SATB2 interacts with ZFP451 and the LSD1/CoREST complex and gains binding at differentiation genes, which is not observed in RA-treated Satb2 K R cells. Tretinoin 5-7 REST corepressor 1 Homo sapiens 77-83
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 88-92 sphingosine kinase 1 Homo sapiens 132-137
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 88-92 sphingosine kinase 1 Homo sapiens 166-170
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 275-279 sphingosine kinase 1 Homo sapiens 132-137
34122632-4 2021 The results of cell proliferation assay and reverse transcription-PCR demonstrated that ATRA may exert synergistic effects with the SphK1 inhibitor SKI 5C or the pan-SphK inhibitor SKI II to inhibit the proliferation of K562 cells and upregulate the expression levels of the ATRA-inducible enzyme cytochrome P450 26A1 (CYP26A1). Tretinoin 275-279 sphingosine kinase 1 Homo sapiens 166-170
34122632-5 2021 Knocking down the expression of SphK1 or SphK2 in K562 cells by small interfering RNA enhanced the inhibitory effects of ATRA and induced the expression of CYP26A1. Tretinoin 121-125 sphingosine kinase 1 Homo sapiens 32-37
34299349-3 2021 RA signaling is mediated by the following two nuclear retinoic receptor subtypes: the retinoic acid receptor (RAR) and the retinoic X receptor (RXR), and their isoforms. Tretinoin 0-2 retinoic acid receptor alpha Homo sapiens 110-113
34299349-5 2021 For example, chromosomal translocation involving RARA occurs in acute promyelocytic leukemia (APL), and all-trans retinoic acid (ATRA) is a highly effective and even curative therapeutic for APL patients. Tretinoin 104-127 retinoic acid receptor alpha Homo sapiens 49-53
34299349-5 2021 For example, chromosomal translocation involving RARA occurs in acute promyelocytic leukemia (APL), and all-trans retinoic acid (ATRA) is a highly effective and even curative therapeutic for APL patients. Tretinoin 129-133 retinoic acid receptor alpha Homo sapiens 49-53
34307338-12 2021 Altogether, we discovered that embryonic craniofacial muscle defects caused by excessive RA signaling were associated with the downregulation of Pitx2, Tbx1, MyoD1, and Dlx5/6, and reduced survival of cranial myogenic precursor cells. Tretinoin 89-91 T-box 1 Mus musculus 152-156
34307338-12 2021 Altogether, we discovered that embryonic craniofacial muscle defects caused by excessive RA signaling were associated with the downregulation of Pitx2, Tbx1, MyoD1, and Dlx5/6, and reduced survival of cranial myogenic precursor cells. Tretinoin 89-91 myogenic differentiation 1 Mus musculus 158-163
34244516-4 2021 scRNA-seq further identify retinoic acid signaling as a critical regulator of cell fate switch between TGFbeta-induced tendon and fibrocartilage lineages. Tretinoin 27-40 transforming growth factor alpha Mus musculus 103-110
34203012-4 2021 We show that CD38 expression can be modulated by adding all-trans retinoic acid (ATRA) or interferon-alpha to MM cells to further fine-tune these effects. Tretinoin 66-79 CD38 molecule Homo sapiens 13-17
34203012-4 2021 We show that CD38 expression can be modulated by adding all-trans retinoic acid (ATRA) or interferon-alpha to MM cells to further fine-tune these effects. Tretinoin 81-85 CD38 molecule Homo sapiens 13-17
34140003-9 2021 Resistance to all-trans retinoic acid (ATRA) was also overcomed by targeting AXL-RTK with R428 in APL (p < 0.05). Tretinoin 14-37 AXL receptor tyrosine kinase Homo sapiens 77-80
34140003-9 2021 Resistance to all-trans retinoic acid (ATRA) was also overcomed by targeting AXL-RTK with R428 in APL (p < 0.05). Tretinoin 39-43 AXL receptor tyrosine kinase Homo sapiens 77-80
34113673-10 2021 Treatment with RA for 14 days increased the expression of DAZL and FRAGILIS and maintained the mRNA levels of STRA8 in bovine fetal AT-MSCs transfected with bi-cistronic and tri-cistronic vectors. Tretinoin 15-17 deleted in azoospermia like Bos taurus 58-62
34068960-0 2021 All-Trans Retinoic Acid Increases DRP1 Levels and Promotes Mitochondrial Fission. Tretinoin 0-23 dynamin 1 like Homo sapiens 34-38
34068960-5 2021 Our results showed that ATRA increases DRP1 protein levels, increases the localization of DRP1 to mitochondria in isolated mitochondrial preparations. Tretinoin 24-28 dynamin 1 like Homo sapiens 39-43
34068960-5 2021 Our results showed that ATRA increases DRP1 protein levels, increases the localization of DRP1 to mitochondria in isolated mitochondrial preparations. Tretinoin 24-28 dynamin 1 like Homo sapiens 90-94
34068960-8 2021 In conclusion, ATRA results in a pharmacologically mediated increase in the DRP1 protein. Tretinoin 15-19 dynamin 1 like Homo sapiens 76-80
34120916-9 2021 We focus on the pivotal role of ALDH1A1, an enzyme expressed by dopaminergic neurons for the detoxification of these neurons, which is under the control of retinoic acid. Tretinoin 156-169 aldehyde dehydrogenase 1 family member A1 Homo sapiens 32-39
35001679-5 2022 More important, expanded Shh signaling in the ventral forebrain, as well as partial abrogation of midfacial defects in Rdh10 mutants via inhibition of Hh signaling, indicates that misregulation of Shh signaling underlies the pathogenesis of reduced RA signaling-associated midfacial defects. Tretinoin 249-251 sonic hedgehog signaling molecule Homo sapiens 197-200
35622143-1 2022 Acute promyelocytic leukemia (APL) is a hematological malignancy driven by the oncoprotein PML-RARalpha, which can be treated with arsenic trioxide (As2O3) or/and all-trans retinoic acid. Tretinoin 166-186 PML nuclear body scaffold Homo sapiens 91-94
35622143-1 2022 Acute promyelocytic leukemia (APL) is a hematological malignancy driven by the oncoprotein PML-RARalpha, which can be treated with arsenic trioxide (As2O3) or/and all-trans retinoic acid. Tretinoin 166-186 retinoic acid receptor alpha Homo sapiens 95-103
35594436-12 2022 Upon retinoic acid-induction, differentiated neurons with eEF1A2 knockdown exhibited shorter neurite length than untransfected cells, which was associated with the reduction of tyrosine hydroxylase and suppression of MAP2 at 10 days of differentiation. Tretinoin 5-18 eukaryotic translation elongation factor 1 alpha 2 Homo sapiens 58-64
35278669-5 2022 In addition, we observed that ATRA could induce KCs to produce IL-1beta through retinoic acid receptor (RAR) in vitro. Tretinoin 30-34 interleukin 1 alpha Homo sapiens 63-71
35574006-2 2022 The synthesis of retinoic acid from retinal in the seminiferous epithelium is a result of the action of aldehyde dehydrogenases termed ALDH1A1, ALDH1A2, and ALDH1A3. Tretinoin 17-30 aldehyde dehydrogenase 1 family member A1 Homo sapiens 135-142
35574006-2 2022 The synthesis of retinoic acid from retinal in the seminiferous epithelium is a result of the action of aldehyde dehydrogenases termed ALDH1A1, ALDH1A2, and ALDH1A3. Tretinoin 17-30 aldehyde dehydrogenase 1 family member A3 Homo sapiens 157-164
35467087-0 2022 Arsenic trioxide induces the differentiation of retinoic acid-resistant neuroblastoma cells via upregulation of HoxC9. Tretinoin 48-61 homeobox C9 Homo sapiens 112-117
35467087-3 2022 However, silencing HoxC9 promoter by EZH2-induced H3K27me3 hypermethylation can lead to RA resistance. Tretinoin 88-90 homeobox C9 Homo sapiens 19-24
35467087-5 2022 OBJECTIVES: In our study, we attempted to obtain some insight into the mechanisms of differentiation of RA-resistant NB cells by detecting the expressions of HoxC9 and EZH2 in NB cells treated with ATO, so as to provide a basis for the subsequent treatment of RA-resistant NB by ATO. Tretinoin 104-106 homeobox C9 Homo sapiens 158-163
35467087-5 2022 OBJECTIVES: In our study, we attempted to obtain some insight into the mechanisms of differentiation of RA-resistant NB cells by detecting the expressions of HoxC9 and EZH2 in NB cells treated with ATO, so as to provide a basis for the subsequent treatment of RA-resistant NB by ATO. Tretinoin 260-262 homeobox C9 Homo sapiens 158-163
35468223-4 2022 We find that ATRA treatment in combination with inhibition of PI3K (ZSTK474), mTOR (WYE132) or PI3K/mTOR (BEZ235, dactolisib) drastically reduces protein levels of the proto-oncogene MYC. Tretinoin 13-17 MYC proto-oncogene, bHLH transcription factor Homo sapiens 183-186
35456995-0 2022 Inhibition of RhoA and Cdc42 by miR-133a Modulates Retinoic Acid Signalling during Early Development of Posterior Cardiac Tube Segment. Tretinoin 51-64 cell division cycle 42 Gallus gallus 23-28
35456995-7 2022 Additionally, retinoic acid represses miR-133a, while it increases Raldh2, Tbx5 and AMHC1. Tretinoin 14-27 T-box 5 Gallus gallus 75-79
35456995-8 2022 Given that RhoA and Cdc42 are involved in Raldh2 expression and that they are modulated by miR-133a, which is influenced by retinoic acid signalling, our results suggest the presence of a negative feedback mechanism between miR-133a and retinoic acid during early development of the posterior cardiac tube segment. Tretinoin 124-137 cell division cycle 42 Gallus gallus 20-25
35456995-8 2022 Given that RhoA and Cdc42 are involved in Raldh2 expression and that they are modulated by miR-133a, which is influenced by retinoic acid signalling, our results suggest the presence of a negative feedback mechanism between miR-133a and retinoic acid during early development of the posterior cardiac tube segment. Tretinoin 237-250 cell division cycle 42 Gallus gallus 20-25
35397003-8 2022 To test the functional significance of these findings, we ectopically expressed wild-type alpha-synuclein in retinoic acid-differentiated dopaminergic SH-SY5Y cells which resulted in decreased levels of NMNAT3 protein plus a neurite pathology which could be rescued by FK866, an inhibitor of nicotinamide phosphoribosyltransferase that acts as a key enzyme in the regulation of NAD+ synthesis. Tretinoin 109-122 synuclein alpha Homo sapiens 90-105
35394423-0 2022 Completion of neural crest cell production and emigration is regulated by retinoic-acid-dependent inhibition of BMP signaling. Tretinoin 74-87 bone morphogenetic protein 1 Homo sapiens 112-115
35394423-4 2022 Inhibition of retinoic acid signaling in the neural tube prevents the normal upregulation of BMP inhibitors in the nascent roof plate and prolongs the period of BMP responsiveness which otherwise ceases close to roof plate establishment. Tretinoin 14-27 bone morphogenetic protein 1 Homo sapiens 93-96
35394423-4 2022 Inhibition of retinoic acid signaling in the neural tube prevents the normal upregulation of BMP inhibitors in the nascent roof plate and prolongs the period of BMP responsiveness which otherwise ceases close to roof plate establishment. Tretinoin 14-27 bone morphogenetic protein 1 Homo sapiens 161-164
35394423-9 2022 Collectively, our results demonstrate that neural tube-derived retinoic acid, via inhibition of BMP signaling, is an essential factor responsible for the end of neural crest generation and the proper segregation of dorsal neural lineages. Tretinoin 63-76 bone morphogenetic protein 1 Homo sapiens 96-99
35151642-0 2022 ATRA promotes PD-L1 expression to control gastric cancer immune surveillance. Tretinoin 0-4 CD274 molecule Homo sapiens 14-19
35151642-3 2022 We herein reported the mechanism underlying ATRA-induced PD-L1 expression in GC cells and the effects of ATRA on cancer-associated immunosuppression in vitro and in vivo. Tretinoin 44-48 CD274 molecule Homo sapiens 57-62
35151642-4 2022 ATRA enhanced PD-L1 expression through increasing its protein stability and protein synthesis, which was suppressed by JAK pan-inhibitor ruxolitinib (RUX), but was enhanced by the combination with IFN-gamma. Tretinoin 0-4 CD274 molecule Homo sapiens 14-19
35151642-5 2022 In T-cell-mediated killing assay, the upregulation of PD-L1-induced by ATRA rendered GC cells strongly resistant to activated T-cell killing, which was reversed by RUX. Tretinoin 71-75 CD274 molecule Homo sapiens 54-59
35151642-6 2022 In vivo, PD-L1 antibody restricted tumor growth, however, ATRA antagonized PD-L1 antibody efficacy. Tretinoin 58-62 CD274 molecule Homo sapiens 75-80
35151642-7 2022 Importantly, RUX not only inhibited the expression of PD-L1 induced by ATRA, but also re-sensitive GC cells to PD-L1 antibody. Tretinoin 71-75 CD274 molecule Homo sapiens 54-59
35151642-8 2022 In conclusion, our study illustrated that ATRA attenuated the effect of PD-L1 blockade through upregulating PD-L1 and blocking PD-L1 expression is an important role for the generation of effective anti-tumor immune response in the combination of immunotherapy and chemotherapy or targeted therapy. Tretinoin 42-46 CD274 molecule Homo sapiens 72-77
35151642-8 2022 In conclusion, our study illustrated that ATRA attenuated the effect of PD-L1 blockade through upregulating PD-L1 and blocking PD-L1 expression is an important role for the generation of effective anti-tumor immune response in the combination of immunotherapy and chemotherapy or targeted therapy. Tretinoin 42-46 CD274 molecule Homo sapiens 108-113
35151642-8 2022 In conclusion, our study illustrated that ATRA attenuated the effect of PD-L1 blockade through upregulating PD-L1 and blocking PD-L1 expression is an important role for the generation of effective anti-tumor immune response in the combination of immunotherapy and chemotherapy or targeted therapy. Tretinoin 42-46 CD274 molecule Homo sapiens 127-132
35078784-0 2022 Targeting S100A9-ALDH1A1-retinoic acid signaling to suppress brain relapse in EGFR-mutant lung cancer. Tretinoin 25-38 aldehyde dehydrogenase 1 family member A1 Homo sapiens 17-24
35182953-0 2022 The expression of Slit2 and Robo1 increased during retinoic acid syndrome in acute promyelocytic leukemia and impacted differentiated cell migration. Tretinoin 51-64 slit guidance ligand 2 Homo sapiens 18-23
35182953-0 2022 The expression of Slit2 and Robo1 increased during retinoic acid syndrome in acute promyelocytic leukemia and impacted differentiated cell migration. Tretinoin 51-64 roundabout guidance receptor 1 Homo sapiens 28-33
35304896-2 2022 TLR5 was expressed in embryoid body derived from mouse embryonic stem cells (mESCs) and betaIII-tubulin-positive cells under all-trans retinoic acid-treated condition. Tretinoin 135-148 toll-like receptor 5 Mus musculus 0-4
35327497-0 2022 hTERT DNA Methylation Analysis Identifies a Biomarker for Retinoic Acid-Induced hTERT Repression in Breast Cancer Cell Lines. Tretinoin 58-71 telomerase reverse transcriptase Homo sapiens 0-5
35327497-4 2022 Previous works showed that all-trans retinoic acid (ATRA) induces hTERT repression in acute promyelocytic leukemia cells, resulting in their death. Tretinoin 27-50 telomerase reverse transcriptase Homo sapiens 66-71
35327497-4 2022 Previous works showed that all-trans retinoic acid (ATRA) induces hTERT repression in acute promyelocytic leukemia cells, resulting in their death. Tretinoin 52-56 telomerase reverse transcriptase Homo sapiens 66-71
35327497-7 2022 We observed an inverse relationship between hTERT expression after ATRA treatment and the methylation level of a specific CpG at chr5: 1,300,438 in a region of hTERT gene at -5 kb of the transcription initiation site. Tretinoin 67-71 telomerase reverse transcriptase Homo sapiens 44-49
35327497-7 2022 We observed an inverse relationship between hTERT expression after ATRA treatment and the methylation level of a specific CpG at chr5: 1,300,438 in a region of hTERT gene at -5 kb of the transcription initiation site. Tretinoin 67-71 telomerase reverse transcriptase Homo sapiens 160-165
35327497-8 2022 This observation highlighted the significance of this region, whose methylation profile could represent a promising biomarker to predict the sensitivity to ATRA-induced hTERT repression in specific breast cancer subtypes. Tretinoin 156-160 telomerase reverse transcriptase Homo sapiens 169-174
35327497-9 2022 As hTERT repression promotes drug-induced cell death, checking the methylation status of this unique region and the specific CpG included can help in decision-making to include ATRA in combination therapy and contributes to a better clinical outcome. Tretinoin 177-181 telomerase reverse transcriptase Homo sapiens 3-8
35372365-7 2022 The first pulse of RA ensures the transition of undifferentiated type A spermatogonia to differentiated A1 spermatogonia and upregulates STRA8 expression in Gc. Tretinoin 19-21 stimulated by retinoic acid gene 8 Mus musculus 137-142
35204227-6 2022 However, ATRA treatment attenuated TGEV-induced IPEC-J2 cells damage by upregulating the mRNA expressions of ZO-1, Occludin, and Mucin-1. Tretinoin 9-13 zonula occludens 1 Sus scrofa 109-113
35204227-6 2022 However, ATRA treatment attenuated TGEV-induced IPEC-J2 cells damage by upregulating the mRNA expressions of ZO-1, Occludin, and Mucin-1. Tretinoin 9-13 occludin Sus scrofa 115-123
35204227-7 2022 ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Tretinoin 0-4 apoptosis regulator BAX Sus scrofa 210-213
35204227-7 2022 ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Tretinoin 0-4 apoptosis regulator Bcl-2 Sus scrofa 215-220
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 glutathione peroxidase 2 Homo sapiens 281-285
35197751-0 2022 Impact of preconditioning stem cells with all-trans retinoic acid signaling pathway on cisplatin-induced nephrotoxicity by down-regulation of TGFbeta1, IL-6, and caspase-3 and up-regulation of HIF1alpha and VEGF. Tretinoin 52-65 vascular endothelial growth factor A Rattus norvegicus 207-211
35154092-8 2022 Here we show that select novel rexinoids act as ATRA mimics, as they cause increased CCR9 and alpha4beta7 expression and enhanced migration to the CCR9 ligand, CCL25 in vitro, even in the absence of ATRA. Tretinoin 48-52 C-C motif chemokine ligand 25 Homo sapiens 160-165
35154092-9 2022 Conversely, other rexinoids act synergistically with ATRA, as culturing cells with suboptimal doses of both compounds resulted in CCR9 expression and migration to CCL25. Tretinoin 53-57 C-C motif chemokine ligand 25 Homo sapiens 163-168
34673934-6 2022 Mechanistically, we showed that NUP98-JADE2 could impair all-trans retinoic acid (ATRA)-mediated transcriptional control and myeloid differentiation. Tretinoin 82-86 jade family PHD finger 2 Homo sapiens 38-43
35013142-10 2022 The results indicate that ATRA causes a significant down-regulation of CRLS1 (Cardiolipin-synthase-1) and LPCAT1 (Lysophosphatidylcholine-Acyltransferase-1) mRNAs which code for two enzymes catalyzing the last steps of cardiolipin synthesis. Tretinoin 26-30 cardiolipin synthase 1 Homo sapiens 71-76
35013142-10 2022 The results indicate that ATRA causes a significant down-regulation of CRLS1 (Cardiolipin-synthase-1) and LPCAT1 (Lysophosphatidylcholine-Acyltransferase-1) mRNAs which code for two enzymes catalyzing the last steps of cardiolipin synthesis. Tretinoin 26-30 cardiolipin synthase 1 Homo sapiens 78-100
2628742-7 1989 One micromolar of retinoic acid alone led to a small increase in expression of osteonectin mRNA but prevented any further increase when Dex was added to retinoic acid-treated cells. Tretinoin 18-31 secreted protein acidic and cysteine rich Rattus norvegicus 79-90
2628742-9 1989 Dexamethasone increased the transcriptional activity of an osteonectin-chloramphenicol acetyltransferase construct; 100 nM Dex resulted in a 3-fold increase over control cells which was attenuated when 1 microM retinoic acid was added to the incubation, while retinoic acid alone resulted in a 2-fold increase in transcriptional activity. Tretinoin 211-224 secreted protein acidic and cysteine rich Rattus norvegicus 59-70
2628742-9 1989 Dexamethasone increased the transcriptional activity of an osteonectin-chloramphenicol acetyltransferase construct; 100 nM Dex resulted in a 3-fold increase over control cells which was attenuated when 1 microM retinoic acid was added to the incubation, while retinoic acid alone resulted in a 2-fold increase in transcriptional activity. Tretinoin 260-273 secreted protein acidic and cysteine rich Rattus norvegicus 59-70
2909388-2 1989 Using RA-treated NHIK 3025 cells as immunogen we prepared murine monoclonal antibodies (IgG1) which recognized an RA-induced cell-surface antigen which could not be detected in untreated NHIK 3025 cells. Tretinoin 6-8 CD53 molecule Homo sapiens 125-145
2747270-5 1989 The analysis of two variants, HL-R5 and HL-D4, selected by this procedure for resistance to retinoic acid and DMSO, respectively, suggests the existence of different pathways used by the two agents which converge before the onset of terminal differentiation. Tretinoin 92-105 heat shock protein family D (Hsp60) member 1 Homo sapiens 40-45
2645590-4 1989 Human skin extracts incubated with either [3H]retinol or [3H]retinoic acid and analyzed by PAGE is a novel technique for the study of cellular retinol-(CRBP) and retinoic acid-(CRABP) binding proteins; it allows one to more specifically analyse these binding proteins and differentiate them from RBP. Tretinoin 61-74 retinol binding protein 4 Homo sapiens 153-156
3063603-7 1988 Expression of endogenous AP-2 is repressed in a hepatoma cell line and stimulated following retinoic-acid-induced differentiation of a human teratocarcinoma cell line. Tretinoin 92-105 transcription factor AP-2 alpha Homo sapiens 25-29
3190677-0 1988 Retinoic acid rapidly induces lung cellular retinol-binding protein mRNA levels in retinol deficient rats. Tretinoin 0-13 retinol binding protein 1 Rattus norvegicus 35-67
3190677-2 1988 The level of lung CRBP mRNA increased 2.3-fold one hour after oral administration of retinoic acid to retinol deficient rats. Tretinoin 85-98 retinol binding protein 1 Rattus norvegicus 18-22
3190677-4 1988 Our data indicate that retinoic acid regulates CRBP mRNA level in the whole animal and this rapid effect suggests a role for CRBP in the mechanism of vitamin A action at genomic level. Tretinoin 23-36 retinol binding protein 1 Rattus norvegicus 47-51
3190677-4 1988 Our data indicate that retinoic acid regulates CRBP mRNA level in the whole animal and this rapid effect suggests a role for CRBP in the mechanism of vitamin A action at genomic level. Tretinoin 23-36 retinol binding protein 1 Rattus norvegicus 125-129
2842422-4 1988 RA, but not ROH, significantly enhanced ADA activity in a monocytic leukemia cell (THP-1) line. Tretinoin 0-2 adenosine deaminase Homo sapiens 40-43
2842422-5 1988 Addition of RA or the tumor promoter, phorbol 12-myristic 13-acetate (PMA), to HPBM or THP-1 cells resulted in significant increases in 5NT activity with opposite effects on ADA activity. Tretinoin 12-14 adenosine deaminase Homo sapiens 174-177
2455651-5 1988 In addition, retinoic acid counteracted the stimulating effect of insulin upon LPL activity, but affected neither the mitotic process nor the spontaneous emergence of LPL activity. Tretinoin 13-26 lipoprotein lipase Mus musculus 79-82
2898782-5 1988 Hox-5.1 transcripts were detected in mouse embryos, in adult mouse testis, kidney, heart, and intestine, and in mouse embryonal carcinoma cells treated with retinoic acid. Tretinoin 157-170 homeobox D4 Mus musculus 0-7
3349487-1 1988 Evidence is presented that inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ornithine decarboxylase (ODC; EC 4.1.1.17) by retinoic acid may involve inhibition of protein kinase C-mediated synthesis of ODC mRNA. Tretinoin 138-151 ornithine decarboxylase, structural 1 Mus musculus 92-115
3349487-1 1988 Evidence is presented that inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ornithine decarboxylase (ODC; EC 4.1.1.17) by retinoic acid may involve inhibition of protein kinase C-mediated synthesis of ODC mRNA. Tretinoin 138-151 ornithine decarboxylase, structural 1 Mus musculus 117-120
3349487-1 1988 Evidence is presented that inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ornithine decarboxylase (ODC; EC 4.1.1.17) by retinoic acid may involve inhibition of protein kinase C-mediated synthesis of ODC mRNA. Tretinoin 138-151 ornithine decarboxylase, structural 1 Mus musculus 217-220
3349487-4 1988 Application of 17 nmol of retinoic acid 1 h before application of TPA to mouse skin inhibited the induction of both ODC mRNA and ODC activity. Tretinoin 26-39 ornithine decarboxylase, structural 1 Mus musculus 116-119
3349487-4 1988 Application of 17 nmol of retinoic acid 1 h before application of TPA to mouse skin inhibited the induction of both ODC mRNA and ODC activity. Tretinoin 26-39 ornithine decarboxylase, structural 1 Mus musculus 129-132
3349487-7 1988 Exposure of primary cultures of newborn epidermal cells to retinoic acid, in conjunction with TPA, inhibited the synthesis of ODC mRNA and failed to alter the half-life of ODC mRNA. Tretinoin 59-72 ornithine decarboxylase, structural 1 Mus musculus 126-129
3349487-8 1988 These results implicate the role of transcription activation in TPA-induced ODC gene expression and indicate that retinoic acid may inhibit TPA-induced ODC gene transcription. Tretinoin 114-127 ornithine decarboxylase, structural 1 Mus musculus 152-155
3349487-9 1988 We also found that protein kinase C may play a role in the mechanism of inhibition by retinoic acid of ODC gene expression. Tretinoin 86-99 ornithine decarboxylase, structural 1 Mus musculus 103-106
3349487-10 1988 Supporting evidence is the finding that L-alpha-dioctanoylglycerol, an activator of protein kinase C, is a Stage II mouse skin tumor promoter and the application of retinoic acid 1 h before application of L-alpha-dioctanoylglycerol to mouse skin inhibited the induction of ODC activity and ODC mRNA as well as tumor promotion by L-alpha-dioctanoylglycerol. Tretinoin 165-178 ornithine decarboxylase, structural 1 Mus musculus 273-276
3349487-10 1988 Supporting evidence is the finding that L-alpha-dioctanoylglycerol, an activator of protein kinase C, is a Stage II mouse skin tumor promoter and the application of retinoic acid 1 h before application of L-alpha-dioctanoylglycerol to mouse skin inhibited the induction of ODC activity and ODC mRNA as well as tumor promotion by L-alpha-dioctanoylglycerol. Tretinoin 165-178 ornithine decarboxylase, structural 1 Mus musculus 290-293
3349487-11 1988 Taken together, one may conclude that the mechanism of inhibition of TPA-induced ODC by retinoic acid may involve the inhibition of protein kinase C-mediated accumulation of newly synthesized ODC mRNA. Tretinoin 88-101 ornithine decarboxylase, structural 1 Mus musculus 81-84
3349487-11 1988 Taken together, one may conclude that the mechanism of inhibition of TPA-induced ODC by retinoic acid may involve the inhibition of protein kinase C-mediated accumulation of newly synthesized ODC mRNA. Tretinoin 88-101 ornithine decarboxylase, structural 1 Mus musculus 192-195
3133373-2 1988 Like retinoic acid, 14 retinobenzoic acids inhibited the induction of ornithine decarboxylase (ODC) by teleocidin in mouse skin. Tretinoin 5-18 ornithine decarboxylase, structural 1 Mus musculus 70-93
3133373-2 1988 Like retinoic acid, 14 retinobenzoic acids inhibited the induction of ornithine decarboxylase (ODC) by teleocidin in mouse skin. Tretinoin 5-18 ornithine decarboxylase, structural 1 Mus musculus 95-98
3283748-0 1988 Inhibition of phorbol ester-induced ornithine decarboxylase gene transcription by retinoic acid: a possible mechanism of antitumor promoting activity of retinoids. Tretinoin 82-95 ornithine decarboxylase, structural 1 Mus musculus 36-59
3318709-5 1987 This technique allowed study of the binding of several natural and synthetic retinoids on the plasma carrier of natural vitamin A for the first time; it was found that only natural retinoids, including retinoic acid, bind to RBP in vitro; retinoic acid binding was found to induce major conformational changes in the protein. Tretinoin 202-215 retinol binding protein 4 Homo sapiens 225-228
3691668-5 1987 Before differentiation, induction and maintenance of elevated c-abl RNA levels depend on the presence of retinoic acid in the medium. Tretinoin 105-118 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 62-67
3691668-6 1987 After differentiation c-abl RNA levels decline only partially when retinoic acid is removed. Tretinoin 67-80 c-abl oncogene 1, non-receptor tyrosine kinase Mus musculus 22-27
3566730-0 1987 Retinol-binding protein in human serum: conformational changes induced by retinoic acid binding. Tretinoin 74-87 retinol binding protein 4 Homo sapiens 0-23
3566730-4 1987 All-trans-retinoic acid (RA) was found to bind to apo-RBP and to significantly modify the tertiary structure of the protein; this raises the question of RBP involvement in the transport of RA. Tretinoin 0-23 retinol binding protein 4 Homo sapiens 54-57
3566730-4 1987 All-trans-retinoic acid (RA) was found to bind to apo-RBP and to significantly modify the tertiary structure of the protein; this raises the question of RBP involvement in the transport of RA. Tretinoin 25-27 retinol binding protein 4 Homo sapiens 54-57
3566730-4 1987 All-trans-retinoic acid (RA) was found to bind to apo-RBP and to significantly modify the tertiary structure of the protein; this raises the question of RBP involvement in the transport of RA. Tretinoin 189-191 retinol binding protein 4 Homo sapiens 153-156
3566730-5 1987 reconstitution of holo-RBP using apo-RBP from delipidized serum was achieved only after its incubation with natural all-trans-retinoids such as retinol, 3-dehydroretinol and retinoic acid but not with synthetic analogs of retinoic acid (13-cis-retinoic acid, TMMP, 13-cis-TMMP, TTNPB). Tretinoin 174-187 retinol binding protein 4 Homo sapiens 23-26
3566730-5 1987 reconstitution of holo-RBP using apo-RBP from delipidized serum was achieved only after its incubation with natural all-trans-retinoids such as retinol, 3-dehydroretinol and retinoic acid but not with synthetic analogs of retinoic acid (13-cis-retinoic acid, TMMP, 13-cis-TMMP, TTNPB). Tretinoin 174-187 retinol binding protein 4 Homo sapiens 37-40
3566730-5 1987 reconstitution of holo-RBP using apo-RBP from delipidized serum was achieved only after its incubation with natural all-trans-retinoids such as retinol, 3-dehydroretinol and retinoic acid but not with synthetic analogs of retinoic acid (13-cis-retinoic acid, TMMP, 13-cis-TMMP, TTNPB). Tretinoin 222-235 retinol binding protein 4 Homo sapiens 23-26
3566730-5 1987 reconstitution of holo-RBP using apo-RBP from delipidized serum was achieved only after its incubation with natural all-trans-retinoids such as retinol, 3-dehydroretinol and retinoic acid but not with synthetic analogs of retinoic acid (13-cis-retinoic acid, TMMP, 13-cis-TMMP, TTNPB). Tretinoin 222-235 retinol binding protein 4 Homo sapiens 37-40
3008983-6 1986 Because retinoids do not directly affect TPA binding to PK-C, the data suggest that (i) the presence of retinoic acid results in the exposure of heretofore cryptic TPA-binding sites in the membrane, where this binding is most likely related to the alteration of membrane structure and (ii) de novo ODC induction is not required for retinoid-dependent inhibition of PK-C, although the TPA induction of PK-C appears to be necessary with regard to ODC induction. Tretinoin 104-117 ornithine decarboxylase, structural 1 Mus musculus 298-301
3008983-6 1986 Because retinoids do not directly affect TPA binding to PK-C, the data suggest that (i) the presence of retinoic acid results in the exposure of heretofore cryptic TPA-binding sites in the membrane, where this binding is most likely related to the alteration of membrane structure and (ii) de novo ODC induction is not required for retinoid-dependent inhibition of PK-C, although the TPA induction of PK-C appears to be necessary with regard to ODC induction. Tretinoin 104-117 ornithine decarboxylase, structural 1 Mus musculus 445-448
3940182-10 1986 Elimination of ODC induction by topical application of retinoic acid or injection of cycloheximide concurrent with the first application of TPA did not restore the ability of a second application of TPA to induce ODC. Tretinoin 55-68 ornithine decarboxylase, structural 1 Mus musculus 15-18
3732659-2 1986 When cultured with retinoic acid at a concentration of 10(-7) M, single NG2 cells irreversibly differentiated to parietal endoderm, as identified by morphological criteria and immunohistochemical staining. Tretinoin 19-32 chondroitin sulfate proteoglycan 4 Mus musculus 72-75
3732659-4 1986 However, when retinoic acid was added to monolayer groups of NG2 cells, not all of the cells were induced to differentiate. Tretinoin 14-27 chondroitin sulfate proteoglycan 4 Mus musculus 61-64
3872306-0 1985 Enhancement of colony-stimulating-factor--dependent clonal growth of murine macrophage progenitors and their phagocytic activity by retinoic acid. Tretinoin 132-145 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 15-40
3872306-1 1985 The effect of retinoic acid (RA) on the colony-stimulating-factor-dependent clonal growth of myeloid progenitors was assessed in semisolid agar cultures of mouse bone marrow cells using L-cell-conditioned medium that gave rise to macrophage colonies, granulocyte colonies, and mixed macrophage-granulocyte colonies and clusters. Tretinoin 14-27 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 40-65
3872306-1 1985 The effect of retinoic acid (RA) on the colony-stimulating-factor-dependent clonal growth of myeloid progenitors was assessed in semisolid agar cultures of mouse bone marrow cells using L-cell-conditioned medium that gave rise to macrophage colonies, granulocyte colonies, and mixed macrophage-granulocyte colonies and clusters. Tretinoin 29-31 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 40-65
3917400-0 1985 Inhibition of ornithine decarboxylase by retinoic acid and difluoromethylornithine in relation to their effects on differentiation and proliferation. Tretinoin 41-54 ornithine decarboxylase, structural 1 Mus musculus 14-37
3917400-4 1985 Both DFMO and RA reduce ornithine decarboxylase activity, polyamine levels and inhibit cell proliferation of F9 cells. Tretinoin 14-16 ornithine decarboxylase, structural 1 Mus musculus 24-47
3917400-6 1985 RA inhibits the induction of ODC by insulin, serum and to a lesser extent that of epidermal growth factor (EGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA). Tretinoin 0-2 ornithine decarboxylase, structural 1 Mus musculus 29-32
6322972-1 1984 We investigated the ability of retinoic acid (RA) to alter the binding of epidermal growth factor (EGF) to Rat-1 and Swiss mouse 3T3 cells, the EGF-related induction of ornithine decarboxylase (ODC) activity and DNA synthesis. Tretinoin 31-44 ornithine decarboxylase, structural 1 Mus musculus 169-192
6305950-0 1983 Synthesis of laminin and entactin by F9 cells induced with retinoic acid and dibutyryl cyclic AMP. Tretinoin 59-72 nidogen 1 Mus musculus 25-33
6573723-3 1983 On a molar basis, PGD2 was a better inhibitor than PGA2 or 16, 16-dimethyl-PGE2-methyl ester (di-M-PGE2) and in higher concentrations (10(-6)-10(-7)M), comparable to retinoic acid. Tretinoin 166-179 prostaglandin D2 synthase (brain) Mus musculus 18-22
6959135-3 1982 Retinoic acid, a derivative of vitamin A, inhibited in a dose-dependent manner both the increase in OrnDCase activity and the release of FN induced by TPA. Tretinoin 0-13 ornithine decarboxylase, structural 1 Mus musculus 100-108
7083472-7 1982 Hence, at four levels of retinoic acid (0.17, 1.70, 17.0 and 170 nmol), which all inhibited the TPA-induced ODC effectively, there was no change in the total number of basal cells that divided during 16-48 h after TPA-application. Tretinoin 25-38 ornithine decarboxylase, structural 1 Mus musculus 108-111
7448775-0 1981 Differential retinoic acid inhibition of ornithine decarboxylase induction by 12-O-tetradecanoylphorbol-13-acetate and by germicidal ultraviolet light. Tretinoin 13-26 ornithine decarboxylase, structural 1 Mus musculus 41-64
7448775-1 1981 Several retinoids including retinoic acid effectively inhibit phorbol ester-mediated tumor promotion and ornithine decarboxylase (ODC) induction in mouse epidermis. Tretinoin 28-41 ornithine decarboxylase, structural 1 Mus musculus 105-128
7448775-1 1981 Several retinoids including retinoic acid effectively inhibit phorbol ester-mediated tumor promotion and ornithine decarboxylase (ODC) induction in mouse epidermis. Tretinoin 28-41 ornithine decarboxylase, structural 1 Mus musculus 130-133
7448775-2 1981 To understand better the possible cellular site of action of retinoids, the inhibitory action of retinoic acid on the induction of ODC was compared for two distinctly different inducers, namely, 12-O-tetradecanoylphorbol-13-acetate (TPA) and germicidal ultraviolet light (UV), in primary mouse epidermal cell cultures. Tretinoin 97-110 ornithine decarboxylase, structural 1 Mus musculus 131-134
7448775-3 1981 It was found that the induction of ODC by TPA is almost completely prevented by 0.1 to 1 microM retinoic acid while the induction by UV is only moderately inhibited. Tretinoin 96-109 ornithine decarboxylase, structural 1 Mus musculus 35-38
7448775-5 1981 When added after the inducer, retinoic acid loses its effectiveness as an inhibitor more rapidly for TPA induction than for UV induction of ODC. Tretinoin 30-43 ornithine decarboxylase, structural 1 Mus musculus 140-143
7448775-9 1981 The preferential inhibition by retinoic acid of ODC induction by TPA is interpreted to result from specific interference at a unique and early site of interaction of TPA with the cell. Tretinoin 31-44 ornithine decarboxylase, structural 1 Mus musculus 48-51
679197-0 1978 Effects of retinoic acid and juvenile hormone on the induction of ornithine decarboxylase activity by 12-O-tetradecanoylphorbol-13-acetate. Tretinoin 11-24 ornithine decarboxylase, structural 1 Mus musculus 66-89
861945-0 1977 Vitamin A acid (retinoic acid), a potent inhibitor of 12-O-tetradecanoyl-phorbol-13-acetate-induced ornithine decarboxylase activity in mouse epidermis. Tretinoin 0-14 ornithine decarboxylase, structural 1 Mus musculus 100-123
861945-0 1977 Vitamin A acid (retinoic acid), a potent inhibitor of 12-O-tetradecanoyl-phorbol-13-acetate-induced ornithine decarboxylase activity in mouse epidermis. Tretinoin 16-29 ornithine decarboxylase, structural 1 Mus musculus 100-123
33757404-8 2021 RA shifted the polarization away from the M1 state by negative regulation of IKKalpha/beta, p65, and miR-21. Tretinoin 0-2 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 77-90
33757404-9 2021 RA hindered the phosphorylation of IKKalpha/beta, translocation of p65 into the nucleus, and the subsequent upregulation of miR-21. Tretinoin 0-2 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 35-48
34050114-0 2021 All-trans retinoic acid reduces mammalian target of rapamycin via a Sirtuin1-dependent mechanism in neurons. Tretinoin 0-23 sirtuin 1 Homo sapiens 68-76
34050114-7 2021 The results of this study demonstrated that atRA may protect LPS-induced neuronal inflammation through suppressing mTOR signaling. Tretinoin 44-48 mechanistic target of rapamycin kinase Rattus norvegicus 115-119
34031932-2 2021 Retinoic acid-inducible gene (RIG)-I-like receptors (RLR), including melanoma differentiation-associated protein 5 (MDA5) and RIG-I, recognize the double-strand (ds) virus RNA and induce the production of Type I interferon (Type I IFN) as well as pro-inflammatory cytokines like Interleukin (IL)-6. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 126-131
34023650-3 2021 Different from MX781, WA15 eliminates RARalpha antagonist activity but inhibits 9-cis-RA-induced RXRalpha transactivation activity in a dose-dependent manner. Tretinoin 80-88 retinoid X receptor alpha Homo sapiens 97-105
33947313-9 2021 As compared to the normal group, lung tissue from cell line induced cancer control group had less RAR-beta protein expression while the ATRA treated group showed enhanced RAR-beta protein expression. Tretinoin 136-140 retinoic acid receptor, alpha Mus musculus 171-179
33947313-10 2021 This indicates that the anti-metastasis effects of ATRA might have shown the induction of RAR-beta expression and subsequent molecular signaling pathways to regulate the homeostasis of biochemical changes. Tretinoin 51-55 retinoic acid receptor, alpha Mus musculus 90-98
33556379-4 2021 RA-differentiation induced an upregulation of ace2 and tmprss2 gene expression while inducing downregulation of ctsb and ctsl. Tretinoin 0-2 cathepsin B Homo sapiens 112-116
33907248-6 2021 In addition, EGCG increased expression of neutrophil differentiation markers such as CD11b, CD14, CD15 and CD66 in NB4 cells; and the combination of all-trans retinoic acid (ATRA) plus EGCG yield higher increase the expression of CD15 marker. Tretinoin 149-172 integrin subunit alpha M Homo sapiens 85-90
33997692-4 2021 We show that in NB4 (APL/AML-M3) cells, ATRA activates canonical myeloid lineage factors-including SPI1, CEBPE, and STAT1-to direct near-normal differentiation toward mature granulocytes. Tretinoin 40-44 signal transducer and activator of transcription 1 Homo sapiens 116-121
33328130-3 2021 In contrast, IL-33, together with retinoic acid, induces IL-10-producing immunosuppressive ILC2s. Tretinoin 34-47 interleukin 10 Homo sapiens 57-62
33495312-0 2021 Clinical responsiveness to All-trans Retinoic Acid is potentiated by LSD1 inhibition and associated with a quiescent transcriptome in myeloid malignancies. Tretinoin 37-50 lysine demethylase 1A Homo sapiens 69-73
33495312-11 2021 CONCLUSIONS: These data indicate that LSD1 inhibition sensitizes AML cells to ATRA and may restore ATRA responsiveness in subsets of MDS and AML patients. Tretinoin 78-82 lysine demethylase 1A Homo sapiens 38-42
33495312-11 2021 CONCLUSIONS: These data indicate that LSD1 inhibition sensitizes AML cells to ATRA and may restore ATRA responsiveness in subsets of MDS and AML patients. Tretinoin 99-103 lysine demethylase 1A Homo sapiens 38-42
33372298-5 2021 Initially identified for its role in promoting meiotic progression in oocytes through Grb2 and MAP kinase activity, AJUBA also maintains cytoskeletal tension permitting epidermal tissue development and responds to retinoic acid committing cells to initiate development of surface epidermal layer. Tretinoin 214-227 ajuba LIM protein Homo sapiens 116-121
33785613-1 2021 Retinoic acid-inducible gene I (RIG-I) is a sensor that recognizes cytosolic double-stranded RNA derived from microbes to induce host immune response. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 32-37
33531433-7 2021 We propose that Zic1 anteriorly establishes a program of RA containment and regulation through activation of Cyp26c1 and Pitx2c that cooperates to promote PPR specification in a spatially restricted domain. Tretinoin 57-59 paired like homeodomain 2 L homeolog Xenopus laevis 121-127
33570783-9 2021 Moreover, it led to a significant reduction of the all-trans retinoic acid target gene pitx2 in NCC-derived periocular mesenchyme. Tretinoin 51-74 paired like homeodomain 2 L homeolog Xenopus laevis 87-92
33659900-2 2021 In protocol 1, we use retinoic acid (RA) to induce pain, itch, and heat mediating dI4/dI6 interneurons, and in protocol 2, RA with bone morphogenetic protein 4 (RA+BMP4) is used to induce proprioceptive dI1s and mechanosensory dI3s in hPSC cultures. Tretinoin 37-39 beta Spectrin Drosophila melanogaster 86-89
33572750-7 2021 We reveal the critical relevance of retinoic X receptor (RXR) heterodimers in upstream retinoic acid metabolism and their relationship with thyroid hormone signaling. Tretinoin 87-100 retinoid X receptor alpha Homo sapiens 36-55
33572750-7 2021 We reveal the critical relevance of retinoic X receptor (RXR) heterodimers in upstream retinoic acid metabolism and their relationship with thyroid hormone signaling. Tretinoin 87-100 retinoid X receptor alpha Homo sapiens 57-60
33485967-2 2021 The bioactive derivative of vitamin A, retinoic acid (RA) was shown to regulate major metabolic genes including phosphoenolpyruvate carboxykinase, fatty acid synthase, carnitine palmitoyltransferase 1, and glucokinase among others. Tretinoin 39-52 fatty acid synthase Homo sapiens 147-166
33485967-2 2021 The bioactive derivative of vitamin A, retinoic acid (RA) was shown to regulate major metabolic genes including phosphoenolpyruvate carboxykinase, fatty acid synthase, carnitine palmitoyltransferase 1, and glucokinase among others. Tretinoin 39-52 glucokinase Homo sapiens 206-217
33490645-5 2021 Semiquantitative RT-PCR showed that transcription level of gp91-phox was certainly decreased (to ~70%) in ATRA plus ellagic acid-treated cells, while that of gp91-phox was significantly increased (to ~160%) in ATRA plus urolithin A-treated cells. Tretinoin 106-110 cytochrome b-245 beta chain Homo sapiens 59-68
33490645-5 2021 Semiquantitative RT-PCR showed that transcription level of gp91-phox was certainly decreased (to ~70%) in ATRA plus ellagic acid-treated cells, while that of gp91-phox was significantly increased (to ~160%) in ATRA plus urolithin A-treated cells. Tretinoin 210-214 cytochrome b-245 beta chain Homo sapiens 59-68
32518366-2 2021 A conventional model of RARalpha function relies upon retinoic acid (RA)-liganded RARalpha binding to specific DNA motifs to regulate gene expression in the nucleus. Tretinoin 54-67 retinoic acid receptor, alpha Mus musculus 24-32
32518366-2 2021 A conventional model of RARalpha function relies upon retinoic acid (RA)-liganded RARalpha binding to specific DNA motifs to regulate gene expression in the nucleus. Tretinoin 54-67 retinoic acid receptor, alpha Mus musculus 82-90
32518366-2 2021 A conventional model of RARalpha function relies upon retinoic acid (RA)-liganded RARalpha binding to specific DNA motifs to regulate gene expression in the nucleus. Tretinoin 24-26 retinoic acid receptor, alpha Mus musculus 82-90
33317048-3 2020 Hydroxylumisterols function as reverse agonists of the retinoic acid-related orphan receptors alpha and gamma (RORalpha/gamma) and can interact with the non-genomic binding site of the vitamin D receptor (VDR). Tretinoin 55-68 RAR related orphan receptor A Homo sapiens 94-125
32961175-3 2020 In chicks and humans, RALDH2 has been detected in a population of hitherto uncharacterized choroidal cells.Therefore, the aim of this study was to identify the RALDH2+ cell type(s) in the choroid and determine how these cells modulate atRA concentrations during periods of visually guided eye growth. Tretinoin 235-239 aldehyde dehydrogenase 1 family member A2 Homo sapiens 22-28
33077479-10 2020 CONCLUSION: The ATRA-induced differentiated cell lines could be used as alternatives to neutrophils to investigate the effects of HRG on neutrophils. Tretinoin 16-20 histidine rich glycoprotein Homo sapiens 130-133
33077479-12 2020 Significance Statement Human neutrophils exhibit varying responses to histidine-rich glycoprotein (HRG); however, all-trans retinoic acid-induced differentiated neutrophil-like cell (NLC) lines can be used as reliably proxies to investigate the effects of HRG on neutrophils. Tretinoin 124-137 histidine rich glycoprotein Homo sapiens 70-97
33077479-12 2020 Significance Statement Human neutrophils exhibit varying responses to histidine-rich glycoprotein (HRG); however, all-trans retinoic acid-induced differentiated neutrophil-like cell (NLC) lines can be used as reliably proxies to investigate the effects of HRG on neutrophils. Tretinoin 124-137 histidine rich glycoprotein Homo sapiens 256-259
33463083-18 2020 Although all-trans retinoic acid (ATRA) has been demonstrated to suppress differentiation of IL-17-producing conventional T-helper cells (Th17) in vitro, the therapeutic application of ATRA in vivo is limited by the compound"s potential side effects caused by its instability and lack of receptor specificity. Tretinoin 19-32 interleukin 17A Homo sapiens 93-98
33463083-18 2020 Although all-trans retinoic acid (ATRA) has been demonstrated to suppress differentiation of IL-17-producing conventional T-helper cells (Th17) in vitro, the therapeutic application of ATRA in vivo is limited by the compound"s potential side effects caused by its instability and lack of receptor specificity. Tretinoin 34-38 interleukin 17A Homo sapiens 93-98
33304850-3 2020 All-trans retinoic acid (ATRA) plus arsenic trioxide (ATO) without chemotherapy has become a first-line treatment for newly diagnosed APL and has been adopted in guidelines or expert recommendations from the NCCN and ELN and in China. Tretinoin 0-23 elastin Homo sapiens 217-220
33304850-3 2020 All-trans retinoic acid (ATRA) plus arsenic trioxide (ATO) without chemotherapy has become a first-line treatment for newly diagnosed APL and has been adopted in guidelines or expert recommendations from the NCCN and ELN and in China. Tretinoin 25-29 elastin Homo sapiens 217-220
33196459-7 2020 In retinoic acid-differentiated ATXN3/Q75-GFP SH-SY5Y cells inflamed with IFN-gamma-primed HMC3 conditioned medium, treatment with the tested compounds mitigated the increased caspase 1 activity and lactate dehydrogenase release, reduced polyQ aggregation and ROS and/or promoted neurite outgrowth. Tretinoin 3-16 ataxin 3 Homo sapiens 32-37
32865844-2 2020 In the present study, the in vivo effects of ATRA, calcitriol, and their combinations on the expression of murine CD4+ T cell cytokines and their specific transcription factors in experimental autoimmune encephalomyelitis (EAE)-induced mice were explored. Tretinoin 45-49 CD4 antigen Mus musculus 114-117
32372724-6 2020 By using an established cell model for studying neurogenesis, NTera2/D1 (NT2) cells, we found that a particular PIWI homolog, PIWIL4 was increasingly upregulated throughout the course of all-trans retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 197-210 piwi like RNA-mediated gene silencing 1 Homo sapiens 112-116
32372724-6 2020 By using an established cell model for studying neurogenesis, NTera2/D1 (NT2) cells, we found that a particular PIWI homolog, PIWIL4 was increasingly upregulated throughout the course of all-trans retinoic acid (RA)-mediated neuronal differentiation. Tretinoin 212-214 piwi like RNA-mediated gene silencing 1 Homo sapiens 112-116
33102941-5 2021 These effects are mainly ascribed to the stereoselective interaction between chiral helical nanofibers and retinol-binding protein 4 (RBP4, a key protein in the retinoic acid (RA) metabolic pathway). Tretinoin 161-174 retinol binding protein 4 Homo sapiens 107-132
33102941-5 2021 These effects are mainly ascribed to the stereoselective interaction between chiral helical nanofibers and retinol-binding protein 4 (RBP4, a key protein in the retinoic acid (RA) metabolic pathway). Tretinoin 161-174 retinol binding protein 4 Homo sapiens 134-138
33102941-5 2021 These effects are mainly ascribed to the stereoselective interaction between chiral helical nanofibers and retinol-binding protein 4 (RBP4, a key protein in the retinoic acid (RA) metabolic pathway). Tretinoin 176-178 retinol binding protein 4 Homo sapiens 107-132
33024217-5 2020 We sought to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the expression of FABP5 acts as a novel positive regulator of ST2 expression in alveolar ECs to generate retinoic acid (RA) and supports the synthesis of RA from type II alveolar ECs to suppress excessive activation of innate lymphoid cell (ILC) 2 during allergic lung inflammation. Tretinoin 200-213 interleukin 1 receptor-like 1 Mus musculus 157-160
32736174-5 2020 This could be reversed by knockdown of the deltex-1 gene, following the attenuation of retinoic acid-related orphan receptor gammat (RORgammat) and its DNA-binding activity in nuclei. Tretinoin 87-100 deltex E3 ubiquitin ligase 1 Homo sapiens 43-51
33003409-8 2020 Taken together, our results suggest that in the P19 cells, PRDM3 contributed to neurogenesis and its expression was stimulated by the synergism between GATA6 and the retinoic acid signaling pathway. Tretinoin 166-179 MDS1 and EVI1 complex locus Homo sapiens 59-64
32998330-0 2020 Evi1 Counteracts Anti-Leukemic and Stem Cell Inhibitory Effects of All-Trans Retinoic Acid on Flt3-ITD/Npm1c-Driven Acute Myeloid Leukemia Cells. Tretinoin 67-90 MDS1 and EVI1 complex locus Homo sapiens 0-4
32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 MDS1 and EVI1 complex locus Homo sapiens 51-55
32998330-3 2020 atRA promoted stemness of MLL-AF9-driven AML in an Evi1-dependent manner but had the opposite effect in Flt3-ITD/Nup98-Hoxd13-driven AML. Tretinoin 0-4 homeobox D13 Homo sapiens 119-125
32998330-7 2020 atRA inhibited leukemia cell viability and stem cell-related properties, and these effects were counteracted by overexpression of Evi1. Tretinoin 0-4 MDS1 and EVI1 complex locus Mus musculus 130-134
32932813-7 2020 In parallel, the addition of RA to either CD3/CD28 or phorbol myristate acetate (PMA)/ionomycin during QVOA and TILDA, respectively, was shown to augment reactivation of the replication-competent viral reservoir in anti-retroviral therapy (ART)-suppressed RMs as shown by a greater than 2.3-fold increase for QVOA and 1 to 2-fold increments for multi-spliced RNA per million CD4+ T cells. Tretinoin 29-31 CD4 molecule Macaca mulatta 375-378
32932813-8 2020 The use of RA can be a useful approach to enhance the efficiency of current protocols used for in vitro and potentially in vivo estimates of CD4+ T cell latent reservoirs. Tretinoin 11-13 CD4 molecule Macaca mulatta 141-144
32932813-9 2020 In addition, flow cytometry analysis revealed that RA improved estimates of various viral reservoir assays by eliciting broad CD4 T-cell activation as demonstrated by elevated CD25 and CD38 but reduced CD69 and PD-1 expressing cells. Tretinoin 51-53 CD4 molecule Sus scrofa 126-129
32905764-5 2020 We find that all-trans retinoic acid upregulates RBM20 expression and reverts the splicing, calcium handling, and contractility defects in iPSC-CMs with different causal RBM20 mutations. Tretinoin 23-36 RNA binding motif protein 20 Homo sapiens 49-54
32905764-5 2020 We find that all-trans retinoic acid upregulates RBM20 expression and reverts the splicing, calcium handling, and contractility defects in iPSC-CMs with different causal RBM20 mutations. Tretinoin 23-36 RNA binding motif protein 20 Homo sapiens 170-175
32504068-4 2020 Furthermore, we revealed that the anti-inflammatory effect of beta-sitosterol resulted from its inhibitory effect on retinoic acid-inducible gene I (RIG-I) signaling, led to decreased STAT1 signaling, thus affecting the transcriptional activity of ISGF3 (interferon-stimulated gene factor 3) complexes and resulting in abrogation of the IAV-induced proinflammatory amplification effect in IFN-sensitized cells. Tretinoin 117-130 DExD/H-box helicase 58 Homo sapiens 149-154
32504068-4 2020 Furthermore, we revealed that the anti-inflammatory effect of beta-sitosterol resulted from its inhibitory effect on retinoic acid-inducible gene I (RIG-I) signaling, led to decreased STAT1 signaling, thus affecting the transcriptional activity of ISGF3 (interferon-stimulated gene factor 3) complexes and resulting in abrogation of the IAV-induced proinflammatory amplification effect in IFN-sensitized cells. Tretinoin 117-130 signal transducer and activator of transcription 1 Homo sapiens 184-189
32504068-4 2020 Furthermore, we revealed that the anti-inflammatory effect of beta-sitosterol resulted from its inhibitory effect on retinoic acid-inducible gene I (RIG-I) signaling, led to decreased STAT1 signaling, thus affecting the transcriptional activity of ISGF3 (interferon-stimulated gene factor 3) complexes and resulting in abrogation of the IAV-induced proinflammatory amplification effect in IFN-sensitized cells. Tretinoin 117-130 signal transducer and activator of transcription 1 Homo sapiens 248-253
32520724-5 2020 Doses as low as 0.01microM reduced transcript levels of the retinoic acid response genes Stra8 and Rarbeta without affecting germ cell number. Tretinoin 60-73 retinoic acid receptor, alpha Mus musculus 99-106
32141090-0 2020 Retinoic acid-loading of the major birch pollen allergen Bet v 1 may improve specific allergen immunotherapy: in silico, in vitro and in vivo data in BALB/c mice. Tretinoin 0-13 delta/notch-like EGF repeat containing Mus musculus 57-60
32171039-8 2020 Interestingly, the data suggest that all-trans retinoic acid (ATRA)-induced ADAM17-mediated MerTK cleavage plays a critical role in regulating the levels of MerTK receptor on macrophages and that this pathway is impaired in NASH fibrosis. Tretinoin 62-66 ADAM metallopeptidase domain 17 Homo sapiens 76-82
31987884-1 2020 We analyzed the role of Wnt inhibitory factor 1 (Wif1) in normal and acanthotic epidermis of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans-retinoic acid (ATRA)-treated and basal cell carcinoma (BCC)-bearing mice. Tretinoin 139-162 Wnt inhibitory factor 1 Mus musculus 24-47
31987884-1 2020 We analyzed the role of Wnt inhibitory factor 1 (Wif1) in normal and acanthotic epidermis of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans-retinoic acid (ATRA)-treated and basal cell carcinoma (BCC)-bearing mice. Tretinoin 139-162 Wnt inhibitory factor 1 Mus musculus 49-53
31987884-3 2020 Within the hyperplastic epidermis of TPA- or ATRA-treated or BCC-bearing murine skin, Wif1 and K10 overlap in Ki67neg suprabasal layers, while basal epidermal layers expressing Ki67, and BCCs expressing Wif1 mRNA, are free of Wif1 protein. Tretinoin 45-49 Wnt inhibitory factor 1 Mus musculus 86-90
31987884-3 2020 Within the hyperplastic epidermis of TPA- or ATRA-treated or BCC-bearing murine skin, Wif1 and K10 overlap in Ki67neg suprabasal layers, while basal epidermal layers expressing Ki67, and BCCs expressing Wif1 mRNA, are free of Wif1 protein. Tretinoin 45-49 antigen identified by monoclonal antibody Ki 67 Mus musculus 110-114
31987884-3 2020 Within the hyperplastic epidermis of TPA- or ATRA-treated or BCC-bearing murine skin, Wif1 and K10 overlap in Ki67neg suprabasal layers, while basal epidermal layers expressing Ki67, and BCCs expressing Wif1 mRNA, are free of Wif1 protein. Tretinoin 45-49 Wnt inhibitory factor 1 Mus musculus 203-207
31987884-3 2020 Within the hyperplastic epidermis of TPA- or ATRA-treated or BCC-bearing murine skin, Wif1 and K10 overlap in Ki67neg suprabasal layers, while basal epidermal layers expressing Ki67, and BCCs expressing Wif1 mRNA, are free of Wif1 protein. Tretinoin 45-49 Wnt inhibitory factor 1 Mus musculus 203-207
32780252-3 2020 Retinoic acid via cellular retinoic acid binding protein 2 (CRABP2) is involved in cell cycle arrest, apoptosis and differentiation, while it via fatty acid binding protein 5 (FABP5) is involved in survival, cell proliferation and angiogenesis, which pathway gets activated depends on the CRABP2/FABP5 ratio. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 18-58
32780252-3 2020 Retinoic acid via cellular retinoic acid binding protein 2 (CRABP2) is involved in cell cycle arrest, apoptosis and differentiation, while it via fatty acid binding protein 5 (FABP5) is involved in survival, cell proliferation and angiogenesis, which pathway gets activated depends on the CRABP2/FABP5 ratio. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 60-66
32780252-3 2020 Retinoic acid via cellular retinoic acid binding protein 2 (CRABP2) is involved in cell cycle arrest, apoptosis and differentiation, while it via fatty acid binding protein 5 (FABP5) is involved in survival, cell proliferation and angiogenesis, which pathway gets activated depends on the CRABP2/FABP5 ratio. Tretinoin 0-13 fatty acid binding protein 5 Homo sapiens 146-174
32780252-3 2020 Retinoic acid via cellular retinoic acid binding protein 2 (CRABP2) is involved in cell cycle arrest, apoptosis and differentiation, while it via fatty acid binding protein 5 (FABP5) is involved in survival, cell proliferation and angiogenesis, which pathway gets activated depends on the CRABP2/FABP5 ratio. Tretinoin 0-13 fatty acid binding protein 5 Homo sapiens 176-181
32780252-3 2020 Retinoic acid via cellular retinoic acid binding protein 2 (CRABP2) is involved in cell cycle arrest, apoptosis and differentiation, while it via fatty acid binding protein 5 (FABP5) is involved in survival, cell proliferation and angiogenesis, which pathway gets activated depends on the CRABP2/FABP5 ratio. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 289-295
32780252-3 2020 Retinoic acid via cellular retinoic acid binding protein 2 (CRABP2) is involved in cell cycle arrest, apoptosis and differentiation, while it via fatty acid binding protein 5 (FABP5) is involved in survival, cell proliferation and angiogenesis, which pathway gets activated depends on the CRABP2/FABP5 ratio. Tretinoin 0-13 fatty acid binding protein 5 Homo sapiens 296-301
32774702-6 2020 Bioinformatics results indicated that retinoic acid (RA) was likely to be the signaling pathway that Baicalin targeted on, and this was confirmed by whole-mount RALDH2 in situ hybridization and quantitative PCR of HH10 chick embryos in the absence/presence of Baicalin. Tretinoin 38-51 aldehyde dehydrogenase 1 family member A2 Gallus gallus 161-167
32615991-9 2020 Western blot analysis indicated that protein levels of retinoic acid receptor alpha (RARalpha), MMP2, MMP9, and AT1 were dramatically affected by ATRA treatment. Tretinoin 146-150 retinoic acid receptor, alpha Mus musculus 55-83
32615991-9 2020 Western blot analysis indicated that protein levels of retinoic acid receptor alpha (RARalpha), MMP2, MMP9, and AT1 were dramatically affected by ATRA treatment. Tretinoin 146-150 retinoic acid receptor, alpha Mus musculus 85-93
32615991-9 2020 Western blot analysis indicated that protein levels of retinoic acid receptor alpha (RARalpha), MMP2, MMP9, and AT1 were dramatically affected by ATRA treatment. Tretinoin 146-150 matrix metallopeptidase 2 Mus musculus 96-100
32615991-10 2020 CONCLUSIONS: In conclusion, ATRA attenuates the progression of Ang II-induced AAAs, possibly by downregulating MMP2, MMP9, and AT-1 expression. Tretinoin 28-32 matrix metallopeptidase 2 Mus musculus 111-115
32032659-3 2020 Roscovitine co-treatment enhanced ATRA-induced expression of pS259- pS289/296/301- pS621-c-Raf, pS217/221-Mek, Src Family Kinases (SFKs) Lyn and Fgr and SFK Y416 phosphorylation, adaptor proteins c-Cbl and Slp-76, Vav, and acetylated 14-3-3 in the signalsome. Tretinoin 34-38 lymphocyte cytosolic protein 2 Homo sapiens 206-212
32032659-5 2020 Consistent with signalsome hyper-activation, roscovitine co-treatment enhanced ATRA-induced G1/0 arrest and expression of differentiation markers, CD11b, ROS and p47 Phox. Tretinoin 79-83 integrin subunit alpha M Homo sapiens 147-152
32032659-5 2020 Consistent with signalsome hyper-activation, roscovitine co-treatment enhanced ATRA-induced G1/0 arrest and expression of differentiation markers, CD11b, ROS and p47 Phox. Tretinoin 79-83 neutrophil cytosolic factor 1 Homo sapiens 162-170
32032659-7 2020 Lyn-knockdown enhanced ATRA-induced up-regulation of key signalsome molecules, c-Raf, pS259-c-Raf, pS289/296/301-c-Raf, Vav1, SLP-76, and Fgr, but with essentially total loss of pY416-SFK. Tretinoin 23-27 lymphocyte cytosolic protein 2 Homo sapiens 126-132
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 12-16 neutrophil cytosolic factor 1 Homo sapiens 68-76
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 12-16 integrin subunit alpha M Homo sapiens 78-83
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 134-138 neutrophil cytosolic factor 1 Homo sapiens 68-76
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 134-138 integrin subunit alpha M Homo sapiens 78-83
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 134-138 neutrophil cytosolic factor 1 Homo sapiens 68-76
32032659-8 2020 Compared to ATRA-treated wt-parental cells, differentiation markers p47 phox, CD11b, G1/G0 arrest and ROS production were enhanced in ATRA-treated Lyn-knockdown stable transfectants, and addition of roscovitine further enhanced these ATRA-inducible markers. Tretinoin 134-138 integrin subunit alpha M Homo sapiens 78-83
32902409-0 2020 CD44 and vimentin, markers involved with epithelial-mesenchymal transition: A proteomic analysis of sequential proteins extraction of triple-negative breast cancer cells after treatment with all-trans retinoic acid. Tretinoin 191-214 CD44 molecule (Indian blood group) Homo sapiens 0-4
32902409-7 2020 We have found that all-trans retinoic acid results in significantly reduced levels of vimentin and CD44 in both the cytoplasmic and membrane fractions. Tretinoin 29-42 CD44 molecule (Indian blood group) Homo sapiens 99-103
31949266-0 2020 Correction: The acetyltransferase GCN5 maintains ATRA-resistance in non-APL AML. Tretinoin 49-53 lysine acetyltransferase 2A Homo sapiens 34-38
32553152-4 2020 Hox5 induction is achieved by response to retinoic acid signaling, resulting in Jmjd3-dependent derepression of Polycomb chromatin and 3D conformational changes. Tretinoin 42-55 lysine demethylase 6B Homo sapiens 80-85
32124141-2 2020 The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA. Tretinoin 32-45 MDM2 proto-oncogene Homo sapiens 295-299
32119959-5 2020 Furthermore, the significantly reduced enrichment of CCCTC binding factor (CTCF) near the boundary where PTPN11 located, as well as the decreased H3K4me3 and increased H3K27me3 enrichment at PTPN11 upon ATRA treatment was observed. Tretinoin 203-207 CCCTC-binding factor Homo sapiens 53-73
32119959-5 2020 Furthermore, the significantly reduced enrichment of CCCTC binding factor (CTCF) near the boundary where PTPN11 located, as well as the decreased H3K4me3 and increased H3K27me3 enrichment at PTPN11 upon ATRA treatment was observed. Tretinoin 203-207 CCCTC-binding factor Homo sapiens 75-79
32119959-5 2020 Furthermore, the significantly reduced enrichment of CCCTC binding factor (CTCF) near the boundary where PTPN11 located, as well as the decreased H3K4me3 and increased H3K27me3 enrichment at PTPN11 upon ATRA treatment was observed. Tretinoin 203-207 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 105-111
32119959-5 2020 Furthermore, the significantly reduced enrichment of CCCTC binding factor (CTCF) near the boundary where PTPN11 located, as well as the decreased H3K4me3 and increased H3K27me3 enrichment at PTPN11 upon ATRA treatment was observed. Tretinoin 203-207 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 191-197
32366851-2 2020 Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). Tretinoin 34-47 mitochondrial antiviral signaling protein Mus musculus 105-146
32366851-2 2020 Upon sensing cytosolic viral RNA, retinoic acid-inducible gene-I-like receptors (RLRs) interact with the mitochondrial antiviral signaling protein (MAVS) and activate TANK-binding kinase 1 (TBK1) to induce type I interferon (IFN-I). Tretinoin 34-47 mitochondrial antiviral signaling protein Mus musculus 148-152
32006898-6 2020 Meanwhile, we found DAC and ATRA inhibited DNMT1, activated miR-34a via promoter hypomethylation, down-regulated its target MYCN and thus exerted a synergistic antineoplastic effect. Tretinoin 28-32 DNA methyltransferase 1 Homo sapiens 43-48
31659279-0 2020 Caspase-8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3 regulate retinoic acid-induced cell differentiation and necroptosis. Tretinoin 77-90 receptor-interacting serine-threonine kinase 3 Mus musculus 62-67
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 112-125 receptor-interacting serine-threonine kinase 3 Mus musculus 218-223
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 112-125 mixed lineage kinase domain-like Mus musculus 303-307
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 127-129 receptor-interacting serine-threonine kinase 3 Mus musculus 218-223
31659279-4 2020 Here, we show that knockdown of Caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripk1 and Ripk3; however, the enhancement of RA-induced cell differentiation is independent of Mlkl and necrosome formation. Tretinoin 127-129 mixed lineage kinase domain-like Mus musculus 303-307
31659279-5 2020 RA treatment obviously enhanced the expression of RA-specific target genes having the retinoic acid response element (RARE) in their promoter regions to induce cell differentiation, and induced marked expression of RIPK1, RIPK3, and MLKL to stimulate necroptosis. Tretinoin 0-2 receptor-interacting serine-threonine kinase 3 Mus musculus 222-227
31659279-5 2020 RA treatment obviously enhanced the expression of RA-specific target genes having the retinoic acid response element (RARE) in their promoter regions to induce cell differentiation, and induced marked expression of RIPK1, RIPK3, and MLKL to stimulate necroptosis. Tretinoin 0-2 mixed lineage kinase domain-like Mus musculus 233-237
31659279-7 2020 In Caspase-8-deficient as well as Caspase-8- and Mlkl-deficient mouse embryos, the expression of RA-specific target genes was obviously enhanced. Tretinoin 97-99 mixed lineage kinase domain-like Mus musculus 49-53
31659279-8 2020 Thus, Caspase-8, RIPK1, and RIPK3 regulate RA-induced cell differentiation and necroptosis both in vitro and in vivo. Tretinoin 43-45 receptor-interacting serine-threonine kinase 3 Mus musculus 28-33
32058275-2 2020 Retinoic acid receptor-related orphan receptor (ROR)-alpha has been shown to attenuate tumor invasiveness by inducing suppressive cell microenvironment, and its low expression was associated with a worse prognosis in HCC patients. Tretinoin 0-13 RAR related orphan receptor A Homo sapiens 14-58
32202429-6 2020 The spatiotemporal analysis of reactive oxygen species suggests a NOX2-dependent peak in cytoplasmic superoxide anions/hydrogen peroxide generation 2 h after retinoic acid stimulation. Tretinoin 158-171 cytochrome b-245 beta chain Homo sapiens 66-70
32290523-0 2020 All-trans Retinoic Acid-induced Abnormal Hippocampal Expression of Synaptic Genes SynDIG1 and DLG2 is Correlated with Anxiety or Depression-Like Behavior in Mice. Tretinoin 0-23 synapse differentiation inducing 1 Mus musculus 82-89
32290523-11 2020 To summarize, ATRA administration induced anxiety- and depression-like behavior accompanied by a decreased expression of DLG2 and an increased expression of SynDIG1. Tretinoin 14-18 synapse differentiation inducing 1 Mus musculus 157-164
32260461-10 2020 Quantitative PCR, Western blot, and immunofluorescent staining showed that retinoic acid receptor alpha (RARalpha) was upregulated by LPS or RA treatment, while the expression of DLX5 was downregulated. Tretinoin 105-107 retinoic acid receptor, alpha Mus musculus 75-103
32006103-1 2020 Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). Tretinoin 77-100 retinoic acid receptor, alpha Mus musculus 136-158
32006103-1 2020 Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). Tretinoin 77-100 retinoic acid receptor, alpha Mus musculus 160-163
32006103-1 2020 Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). Tretinoin 102-106 retinoic acid receptor, alpha Mus musculus 136-158
32006103-1 2020 Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). Tretinoin 102-106 retinoic acid receptor, alpha Mus musculus 160-163
32006103-10 2020 These atRA-induced changes were reverted by RAR inhibition. Tretinoin 6-10 retinoic acid receptor, alpha Mus musculus 44-47
31549280-1 2020 INTRODUCTION: Retinoic Acid Related Orphan Nuclear Receptor gamma T (RORgammaT) is a lineage specifying transcription factor for IL-17 expressing cells, which may contribute to the pathogenesis of Inflammatory Bowel Disease (IBD). Tretinoin 14-27 interleukin 17A Mus musculus 129-134
32319369-9 2020 The percentage of CD11b positive cells in ATRA+Tetrandrine group(43.62%+-1.38%) was significantly higher than that in Tetrandrine group(15.25%+-2.11%), ATRA group (28.84%+-7.53%) and control group(8.16%+-1.01%) (P<0.05). Tretinoin 42-46 integrin subunit alpha M Homo sapiens 18-23
32319369-9 2020 The percentage of CD11b positive cells in ATRA+Tetrandrine group(43.62%+-1.38%) was significantly higher than that in Tetrandrine group(15.25%+-2.11%), ATRA group (28.84%+-7.53%) and control group(8.16%+-1.01%) (P<0.05). Tretinoin 152-156 integrin subunit alpha M Homo sapiens 18-23
32209473-3 2020 Mechanistically, CD137 engagement activates TAK1 and subsequently stimulates the AMPK-PGC-1alpha axis to enhance expression of the Aldh1a2 gene encoding the retinoic acid (RA) metabolizing enzyme RALDH2. Tretinoin 157-170 TNF receptor superfamily member 9 Homo sapiens 17-22
32209473-3 2020 Mechanistically, CD137 engagement activates TAK1 and subsequently stimulates the AMPK-PGC-1alpha axis to enhance expression of the Aldh1a2 gene encoding the retinoic acid (RA) metabolizing enzyme RALDH2. Tretinoin 157-170 aldehyde dehydrogenase 1 family member A2 Homo sapiens 131-138
32209473-3 2020 Mechanistically, CD137 engagement activates TAK1 and subsequently stimulates the AMPK-PGC-1alpha axis to enhance expression of the Aldh1a2 gene encoding the retinoic acid (RA) metabolizing enzyme RALDH2. Tretinoin 157-170 aldehyde dehydrogenase 1 family member A2 Homo sapiens 196-202
32209473-3 2020 Mechanistically, CD137 engagement activates TAK1 and subsequently stimulates the AMPK-PGC-1alpha axis to enhance expression of the Aldh1a2 gene encoding the retinoic acid (RA) metabolizing enzyme RALDH2. Tretinoin 172-174 TNF receptor superfamily member 9 Homo sapiens 17-22
32209473-3 2020 Mechanistically, CD137 engagement activates TAK1 and subsequently stimulates the AMPK-PGC-1alpha axis to enhance expression of the Aldh1a2 gene encoding the retinoic acid (RA) metabolizing enzyme RALDH2. Tretinoin 172-174 aldehyde dehydrogenase 1 family member A2 Homo sapiens 131-138
32209473-3 2020 Mechanistically, CD137 engagement activates TAK1 and subsequently stimulates the AMPK-PGC-1alpha axis to enhance expression of the Aldh1a2 gene encoding the retinoic acid (RA) metabolizing enzyme RALDH2. Tretinoin 172-174 aldehyde dehydrogenase 1 family member A2 Homo sapiens 196-202
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 18-20 integrin subunit alpha M Homo sapiens 76-81
32209473-5 2020 Administration of RA in DC-specific CD137-/- mice represses IL-23-producing CD11b+CD103- DCs and TH17 cells, indicating that RA is a major inhibitory effector molecule against intestinal CD11b+CD103- DCs. Tretinoin 18-20 integrin subunit alpha M Homo sapiens 187-192
31812787-4 2020 This negative regulation requires co-incubation with the RXR agonist, retinoic acid. Tretinoin 70-83 retinoid X receptor alpha Homo sapiens 57-60
31924597-5 2020 Furthermore, we found Mel treatment increased the expression of G protein-coupled receptors MT2 and retinoic acid-related orphan receptors (RORs), eg. Tretinoin 100-113 RAR related orphan receptor A Homo sapiens 140-144
31656079-6 2020 Molecules such as Keap1/Nrf2, N-methyl-D-aspartate receptors (NMDRs), NF-kappaB, KRAS, kallistatin, gene associated with retinoic-interferon-induced mortality-19 and deregulated metabolic pathways are involved in ROS production in association with NADPH oxidase. Tretinoin 121-140 serpin family A member 4 Homo sapiens 87-98
32027669-0 2020 Cyp1b1 directs Srebp-mediated cholesterol and retinoid synthesis in perinatal liver; Association with retinoic acid activity during fetal development. Tretinoin 102-115 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 0-6
32027669-2 2020 Cyp1b1 is not expressed in perinatal liver but appears in the E9.5 embryo, close to sites of retinoic acid (RA) signaling. Tretinoin 93-106 cytochrome P450, family 1, subfamily b, polypeptide 1 Mus musculus 0-6
32062354-2 2020 Retinoic acid receptor-related orphan receptor A (RORA) is a member of the ROR subfamily of orphan receptors and plays an anti-tumor role in several cancers. Tretinoin 0-13 RAR related orphan receptor A Homo sapiens 14-48
32062354-2 2020 Retinoic acid receptor-related orphan receptor A (RORA) is a member of the ROR subfamily of orphan receptors and plays an anti-tumor role in several cancers. Tretinoin 0-13 RAR related orphan receptor A Homo sapiens 50-54
32062354-2 2020 Retinoic acid receptor-related orphan receptor A (RORA) is a member of the ROR subfamily of orphan receptors and plays an anti-tumor role in several cancers. Tretinoin 0-13 RAR related orphan receptor A Homo sapiens 50-53
31536749-8 2020 The increase in RA content was in line with the identified upregulation of retinoic acid anabolizing enzymes ALDH1A3 and DHRS3. Tretinoin 16-18 dehydrogenase/reductase 3 Homo sapiens 121-126
31536749-8 2020 The increase in RA content was in line with the identified upregulation of retinoic acid anabolizing enzymes ALDH1A3 and DHRS3. Tretinoin 75-88 dehydrogenase/reductase 3 Homo sapiens 121-126
31536749-10 2020 We then concluded that ALI/LLI dependent modulation of CLDN1 expression and TJ permeability is under the control of RA synthesis. Tretinoin 116-118 claudin 1 Homo sapiens 55-60
31173389-8 2020 TST1 is generated from an LTR12C promoter regulated by DNA methylation and retinoic-acid-related drugs. Tretinoin 75-88 TST1 Homo sapiens 0-4
32863302-8 2020 In the ATRA-experiment, ATRA suppressed the secretion of IL-6 and NO, downregulated the NF-kappaB P65 and Bcl-2, increased levels of autophagy marker protein LC3, but different doses of ATRA showed inconsistent regulatory effects on VEGF and MMP-9. Tretinoin 24-28 matrix metallopeptidase 9 Rattus norvegicus 242-247
32879257-4 2020 Here, we evaluated the binding affinity of several organotin compounds that are ligands of a receptor of retinoic acid, retinoid X receptor, by using radioligand binding assays. Tretinoin 105-118 retinoid X receptor alpha Homo sapiens 120-139
31740384-7 2020 Furthermore, the down-regulation of CDK2 sensitized AML cells to ATRA-induced engraftment prevention of leukemia cells in NOD-SCID mice and promotes the primary AML blasts differentiation when combined with ATRA. Tretinoin 65-69 cyclin-dependent kinase 2 Mus musculus 36-40
31740384-7 2020 Furthermore, the down-regulation of CDK2 sensitized AML cells to ATRA-induced engraftment prevention of leukemia cells in NOD-SCID mice and promotes the primary AML blasts differentiation when combined with ATRA. Tretinoin 207-211 cyclin-dependent kinase 2 Mus musculus 36-40
31950055-9 2019 Our results suggest that ATRA enhances flagellin-stimulated proinflammatory responses in human monocyte THP-1 cells by upregulating CD14 in a RAR/RXR-dependent manner. Tretinoin 25-29 retinoid X receptor alpha Homo sapiens 146-149
31766690-4 2019 However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. Tretinoin 218-221 vascular endothelial growth factor A Mus musculus 143-179
31766690-4 2019 However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. Tretinoin 218-221 vascular endothelial growth factor A Mus musculus 181-186
31766690-5 2019 When combined with ATM inhibitor KU-55933, tRA showed a greatly enhanced efficiency in inhibiting VEGFA expression and a much better protection of mouse skin from photo damage. Tretinoin 43-46 vascular endothelial growth factor A Mus musculus 98-103
31596288-11 2019 Specifically, through Smurf promotion of Smad5 ubiquitination, RA could inhibit the BMP4 signal transduction. Tretinoin 63-65 bone morphogenetic protein 4 Gallus gallus 84-88
31479736-11 2019 Simultaneously, RA significantly reduced the expression of the WNT genes cMyc, Lef1, Lrp5, Lrp6 and Wnt11 compared to the controls (p < 0.05). Tretinoin 16-18 low density lipoprotein receptor-related protein 6 Mus musculus 91-95
31479736-12 2019 In contrast, RA increased the expression of the WNT inhibitors Dkk1 at day 21 and Dkk2 at days 14 and 21 (p < 0.01). Tretinoin 13-15 dickkopf WNT signaling pathway inhibitor 2 Mus musculus 82-86
31576004-0 2019 The acetyltransferase GCN5 maintains ATRA-resistance in non-APL AML. Tretinoin 37-41 lysine acetyltransferase 2A Homo sapiens 22-26
31576004-3 2019 Here we demonstrate that the acetyltransferase GCN5 contributes to ATRA resistance in non-APL AML via aberrant acetylation of histone 3 lysine 9 (H3K9ac) residues maintaining the expression of stemness and leukemia associated genes. Tretinoin 67-71 lysine acetyltransferase 2A Homo sapiens 47-51
31576004-4 2019 We show that inhibition of GCN5 unlocks an ATRA-driven therapeutic response. Tretinoin 43-47 lysine acetyltransferase 2A Homo sapiens 27-31
31576004-8 2019 The high efficacy of the combined epigenetic treatment with GCN5 and LSD1 inhibitors may enable the use of ATRA for differentiation therapy of non-APL AML. Tretinoin 107-111 lysine acetyltransferase 2A Homo sapiens 60-64
31576004-8 2019 The high efficacy of the combined epigenetic treatment with GCN5 and LSD1 inhibitors may enable the use of ATRA for differentiation therapy of non-APL AML. Tretinoin 107-111 lysine demethylase 1A Homo sapiens 69-73
31645452-10 2019 Heat- and UV-inactivated rotavirus lost their oncolytic activity but kept their synergy with immune checkpoint-targeted antibodies through the up-regulation of the double-stranded RNA receptor retinoic acid-induced gene 1 (RIG-I). Tretinoin 193-206 DExD/H-box helicase 58 Homo sapiens 223-228
31566355-0 2019 Retinoic Acid Binding Leads to CRABP2 Rigidification and Dimerization. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 31-37
31566355-1 2019 Cellular retinoic acid-binding protein 2 (CRABP2) delivers all-trans retinoic acid (atRA) to retinoic acid receptors (RARs), allowing for the activation of specific gene transcription. Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 42-48
31566355-2 2019 The structural similarities between free and atRA-bound CRABP2 raise the questions of how atRA binding occurs and how the atRA:CRABP2 complex is recognized by downstream binding partners. Tretinoin 45-49 cellular retinoic acid binding protein 2 Homo sapiens 56-62
31566355-2 2019 The structural similarities between free and atRA-bound CRABP2 raise the questions of how atRA binding occurs and how the atRA:CRABP2 complex is recognized by downstream binding partners. Tretinoin 45-49 cellular retinoic acid binding protein 2 Homo sapiens 127-133
31566355-2 2019 The structural similarities between free and atRA-bound CRABP2 raise the questions of how atRA binding occurs and how the atRA:CRABP2 complex is recognized by downstream binding partners. Tretinoin 90-94 cellular retinoic acid binding protein 2 Homo sapiens 56-62
31566355-4 2019 The data showed that free CRABP2 displays widespread intermediate-time scale dynamics that is effectively suppressed upon atRA binding. Tretinoin 122-126 cellular retinoic acid binding protein 2 Homo sapiens 26-32
31566355-6 2019 Unexpectedly, CRABP2 rigidification in response to atRA binding leads to the stabilization of a homodimerization interface, which encompasses residues located on helix alpha2 and the betaC-betaD loop as well as residues on strands betaI-betaA and the betaH-betaI loop. Tretinoin 51-55 cellular retinoic acid binding protein 2 Homo sapiens 14-20
31566355-7 2019 Critically, this rigidification also affects CRABP2"s nuclear localization signal and RAR-binding motif, suggesting that the loss of conformational entropy upon atRA binding may be the key for the diverse cellular functions of CRABP2. Tretinoin 161-165 cellular retinoic acid binding protein 2 Homo sapiens 45-51
31566355-7 2019 Critically, this rigidification also affects CRABP2"s nuclear localization signal and RAR-binding motif, suggesting that the loss of conformational entropy upon atRA binding may be the key for the diverse cellular functions of CRABP2. Tretinoin 161-165 cellular retinoic acid binding protein 2 Homo sapiens 227-233
31591086-9 2019 More specifically, the expression of Shh and its downstream genes Ptch1 and Gli1 was spatiotemporally downregulated in the developing face of RA-treated embryos. Tretinoin 142-144 GLI family zinc finger 1 Homo sapiens 76-80
31485618-9 2019 These observations were accompanied by DNMT1 downregulation and CDKN1A upregulation, with a concomitant enhanced decrease in DNMT1 protein level, especially after ATRA treatment with CIF. Tretinoin 163-167 DNA methyltransferase 1 Homo sapiens 125-130
31370073-7 2019 ATRA inhibited platelet aggregation and adenosine triphosphate release induced by collagen (5 mug/mL) or thrombin (0.05 U/mL) in a dose-dependent manner without affecting P-selectin expression or surface levels of glycoprotein (GP) Ibalpha, GPVI, or alphaIIbbeta3. Tretinoin 0-4 glycoprotein Ib platelet subunit alpha Homo sapiens 214-239
31238067-0 2019 All-trans retinoic acid attenuates isoproterenol-induced cardiac dysfunction through Crabp1 to dampen CaMKII activation. Tretinoin 0-23 cellular retinoic acid binding protein I Mus musculus 85-91
31238067-3 2019 Here we examine whether the highly selective, endogenous ligand of Crabp1, all-trans retinoic acid (RA), can attenuate ISO-induced cardiac dysfunction. Tretinoin 75-98 cellular retinoic acid binding protein I Mus musculus 67-73
31238067-3 2019 Here we examine whether the highly selective, endogenous ligand of Crabp1, all-trans retinoic acid (RA), can attenuate ISO-induced cardiac dysfunction. Tretinoin 100-102 cellular retinoic acid binding protein I Mus musculus 67-73
31006867-0 2019 All-trans-retinoic acid activated mast cells via Mas-related G-protein-coupled receptor-X2 in retinoid dermatitis. Tretinoin 0-23 MAS-related GPR, member X2 Mus musculus 49-90
31006867-4 2019 A possible contribution of MRGPRX2 to contact dermatitis induced by RA has hitherto not been examined. Tretinoin 68-70 MAS-related GPR, member X2 Mus musculus 27-34
31006867-5 2019 OBJECTIVES: To investigate whether all-trans-RA (ATRA) activates mast cells via MRGPRX2/MrgprB2 (the mouse orthologue), contributing to the pathogenesis of retinoid-induced dermatitis. Tretinoin 35-47 MAS-related GPR, member X2 Mus musculus 80-87
31470289-5 2019 Cinnamic acid derivatives, such as artepillin C and caffeic acid phenethyl ester, present in the propolis extract suppressed the IL-17 production from cultured murine splenocytes through decreased retinoic acid-related orphan receptor gT expression. Tretinoin 197-210 interleukin 17A Mus musculus 129-134
31299488-5 2019 And overexpressing retinoic acid-inducible gene I (RIG-I) could significantly inhibit SVV propagation. Tretinoin 19-32 DExD/H-box helicase 58 Homo sapiens 51-56
31472680-0 2019 All trans-retinoic acid protects against acute ischemic stroke by modulating neutrophil functions through STAT1 signaling. Tretinoin 4-23 signal transducer and activator of transcription 1 Mus musculus 106-111
31472680-12 2019 The functions of neutrophil were indispensable in the protective effects of atRA and were associated with suppression to STAT1 signaling by atRA. Tretinoin 140-144 signal transducer and activator of transcription 1 Mus musculus 121-126
31434807-7 2019 We found that retinoic acid-related orphan receptor alpha (RORalpha) was increased by inflammatory mediators, such as IL-1beta, and bound to ANGPTL4 promoter in MSCs. Tretinoin 14-27 RAR related orphan receptor A Homo sapiens 59-67
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 119-142 cellular retinoic acid binding protein 2 Homo sapiens 0-40
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 119-142 cellular retinoic acid binding protein 2 Homo sapiens 42-48
31419991-2 2019 Cellular retinoic acid binding protein 2 (CRABP2) belongs to fatty acid binding protein (FABP) family which binds with all-trans retinoic acid (RA). Tretinoin 43-45 cellular retinoic acid binding protein 2 Homo sapiens 0-40
31406210-4 2019 Stimulation of myeloid blasts" maturation by all-trans retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (vitamin D) increased the CD11b+ fraction that expressed PD-1 ligands in response to IFN-gamma. Tretinoin 45-68 integrin subunit alpha M Homo sapiens 135-140
31406210-4 2019 Stimulation of myeloid blasts" maturation by all-trans retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (vitamin D) increased the CD11b+ fraction that expressed PD-1 ligands in response to IFN-gamma. Tretinoin 70-74 integrin subunit alpha M Homo sapiens 135-140
31125456-4 2019 Further, we demonstrate that the expression of CAII and CAIX in these cells is significantly up-regulated by the biologically active metabolites of vitamin A (all-trans retinoic acid) and vitamin D (1alpha,25-dihydroxyvitamin D3 ), respectively. Tretinoin 159-182 carbonic anhydrase 2 Homo sapiens 47-51
31280489-4 2019 Moderate hypoxia undermines iMF by enhancing NR2B-containing NMDA receptor signalling, which can be rescued by exogenous retinoic acid, a molecule necessary for iMF. Tretinoin 121-134 glutamate ionotropic receptor NMDA type subunit 2B Rattus norvegicus 45-49
31341279-6 2019 Loss of Hand2 also led to dysregulation of retinoic acid signalling and disruption of anterior-posterior patterning of cardiac progenitors. Tretinoin 43-56 heart and neural crest derivatives expressed 2 Homo sapiens 8-13
31418361-8 2019 The percentage of CD11b positive cells in ATRA+adenanthin group (43.62%+-1.38%) was higher than that in adenanthin group (28.15%+-1.78%), ATRA group (36.72%+-1.33%) and control group (7.99%+-1.78%) (P<0. Tretinoin 42-46 integrin subunit alpha M Homo sapiens 18-23
31418361-8 2019 The percentage of CD11b positive cells in ATRA+adenanthin group (43.62%+-1.38%) was higher than that in adenanthin group (28.15%+-1.78%), ATRA group (36.72%+-1.33%) and control group (7.99%+-1.78%) (P<0. Tretinoin 138-142 integrin subunit alpha M Homo sapiens 18-23
31418361-10 2019 The content of Prx III protein in adenanthin group was significantly higher than that in control group and ATRA group (P<0.05). Tretinoin 107-111 peroxiredoxin 3 Homo sapiens 15-22
31147716-4 2019 Enhancer deletion significantly inhibited expression of RA-induced Hoxa1 and endoderm master control genes such as Gata4 and Gata6. Tretinoin 56-58 GATA binding protein 4 Homo sapiens 115-120
31320612-6 2019 Moreover, RA treatment leads to suppression of BMP signaling by reducing the level of FBXO30 in mammalian cells and in mouse embryos with NTDs. Tretinoin 10-12 F-box protein 30 Homo sapiens 86-92
31053627-3 2019 We showed that dendritic cells (DCs), engineered to de novo produce high concentrations of both 1,25-dihydroxyvitamin D, the active vitamin D metabolite, and retinoic acid, an active vitamin A metabolite, augmented the induction of T cells that express both the regulatory molecule Foxp3 and the gut-homing receptor CCR9 in vitro and in vivo. Tretinoin 158-171 chemokine (C-C motif) receptor 9 Mus musculus 316-320
30576481-0 2019 Inhibition of protein phosphatase PPM1D enhances retinoic acid-induced differentiation in human embryonic carcinoma cell line. Tretinoin 49-62 protein phosphatase, Mg2+/Mn2+ dependent 1D Homo sapiens 34-39
30576481-5 2019 Here we report that PPM1D modulates retinoic acid (RA) signalling. Tretinoin 36-49 protein phosphatase, Mg2+/Mn2+ dependent 1D Homo sapiens 20-25
30576481-5 2019 Here we report that PPM1D modulates retinoic acid (RA) signalling. Tretinoin 51-53 protein phosphatase, Mg2+/Mn2+ dependent 1D Homo sapiens 20-25
30576481-8 2019 RA-induced cell differentiation was promoted by reducing PPM1D activity. Tretinoin 0-2 protein phosphatase, Mg2+/Mn2+ dependent 1D Homo sapiens 57-62
30576481-12 2019 Our study shows that PPM1D plays an important role in maintaining the undifferentiation state and a new function in RA-induced ERK regulation and cell differentiation. Tretinoin 116-118 protein phosphatase, Mg2+/Mn2+ dependent 1D Homo sapiens 21-26
28963040-3 2019 All-trans retinoic acid is a potent inducer of CD38 and can be used as a novel therapeutic strategy in autism. Tretinoin 0-23 CD38 antigen Mus musculus 47-51
31143119-6 2019 Our results also demonstrated that ATRA altered the expression of proliferation-related proteins, including CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 in VSMC. Tretinoin 35-39 cyclin D1 Mus musculus 108-116
31143119-6 2019 Our results also demonstrated that ATRA altered the expression of proliferation-related proteins, including CyclinD1, CyclinD3, CyclinA2, CDK2, CDK4, and CDK6 in VSMC. Tretinoin 35-39 cyclin-dependent kinase 2 Mus musculus 138-142
30746735-8 2019 Measurement of Vasa and Scp3 genes by RT-PCR confirmed the positive effects of retinoic acid on increasing of genes expression. Tretinoin 79-92 synaptonemal complex protein 3 Homo sapiens 24-28
31083206-14 2019 LESSONS: Both STAT5b-RARalpha-positive APL and PLZF-RARalpha-positive APL appear to be resistant to both ATRA and ATO, so combined chemotherapy and allo-HSCT should be considered. Tretinoin 105-109 zinc finger and BTB domain containing 16 Homo sapiens 47-51
30790712-6 2019 Furthermore, we found bivariate associations of Rargamma and Rxrgamma expressions with all-trans-retinoic acid concentrations and of Fgf21 expression with that of Rargamma. Tretinoin 91-110 retinoic acid receptor, gamma Mus musculus 48-56
30674471-10 2019 These unexpected results explain the less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nuclear bodies in APL eradication by the ATRA/arsenic combination. Tretinoin 175-179 FMS-like tyrosine kinase 3 Mus musculus 63-67
30894514-6 2019 We demonstrate that resveratrol interferes with the reprogramming of the retinoic acid signaling pathway in decidualizing HESCs by accelerating down-regulation of cellular retinoic acid-binding protein 2 (CRABP2) and retinoic acid receptor (RAR). Tretinoin 73-86 cellular retinoic acid binding protein 2 Homo sapiens 163-203
30894514-6 2019 We demonstrate that resveratrol interferes with the reprogramming of the retinoic acid signaling pathway in decidualizing HESCs by accelerating down-regulation of cellular retinoic acid-binding protein 2 (CRABP2) and retinoic acid receptor (RAR). Tretinoin 73-86 cellular retinoic acid binding protein 2 Homo sapiens 205-211
30601699-7 2019 In cultured mouse mesangial cells, treatment with ATRA or a retinoic acid receptor-alpha (RARalpha) agonist significantly decreased BMP4 and COL4 expression. Tretinoin 50-54 retinoic acid receptor, alpha Mus musculus 90-98
30601699-9 2019 Chromatin immunoprecipitation analysis and reporter assays indicated a putative RARE of the Bmp4 gene, located 11,488-11,501 bp upstream of exon 1A and bound to RARalpha and retinoid X receptor (RXR), which suppressed BMP4 expression after ATRA addition. Tretinoin 240-244 retinoic acid receptor, alpha Mus musculus 161-169
30601699-10 2019 ATRA suppressed BMP4 via binding of a RARalpha/RXR heterodimer to a unique RARE, alleviating glomerular matrix expansion in diabetic mice. Tretinoin 0-4 retinoic acid receptor, alpha Mus musculus 38-50
30529222-0 2019 Nuclear RXRalpha and RXRbeta receptors exert distinct and opposite effects on RA-mediated neuroblastoma differentiation. Tretinoin 78-80 retinoid X receptor alpha Homo sapiens 8-16
30529222-2 2019 The nuclear RXR receptors are one of the main mediators of RA cellular effects, classically by joining the direct receptors of RA, the nuclear RAR receptors, in RAR/RXR dimers which act as transcription factors. Tretinoin 59-61 retinoid X receptor alpha Homo sapiens 12-15
30529222-2 2019 The nuclear RXR receptors are one of the main mediators of RA cellular effects, classically by joining the direct receptors of RA, the nuclear RAR receptors, in RAR/RXR dimers which act as transcription factors. Tretinoin 59-61 retinoid X receptor alpha Homo sapiens 165-168
30529222-5 2019 In order to understand the roles of the expression of distinct RXR subtypes to RA signal transduction, we performed siRNA-mediated silencing of RXRalpha and RXRbeta during the first stages of SH-SY5Y differentiation. Tretinoin 79-81 retinoid X receptor alpha Homo sapiens 63-66
30529222-6 2019 Our results showed that RXRalpha is required for RA-induced neuronal differentiation of SH-SY5Y cells, since its silencing compromised cell cycle arrest and prevented the upregulation of neuronal markers and the adoption of neuronal morphology. Tretinoin 49-51 retinoid X receptor alpha Homo sapiens 24-32
30529222-9 2019 Our results indicate distinct functions for RXR subtypes during RA-dependent neuronal differentiation and reveal new perspectives for studying such receptors as clinical targets in therapies aiming at restoring neuronal function. Tretinoin 64-66 retinoid X receptor alpha Homo sapiens 44-47
30685069-5 2019 Exposure of P19 cells, in the presence of retinoic acid, BMP-2, or BMP-4 to Coco, at average sera level of MS patients failed to induce neuronal phenotype, in contrast to the average sera level of HC. Tretinoin 42-55 DAN domain BMP antagonist family member 5 Homo sapiens 76-80
30746761-4 2019 The docking studies indicated bexarotene as a lead compound that can activate various RXR receptor isoforms (alpha, beta, and gamma) and has a strong binding affinity to the receptor protein than retinoic acid, which is known as a natural endogenous RXR agonist. Tretinoin 196-209 retinoid X receptor alpha Homo sapiens 250-253
30906641-8 2019 In the present study, we succeeded in synergistically accelerating the ATRA-induced neuronal differentiation of MYCN-amplified neuroblastoma cells by combining a peptide derived from tenascin-C, termed TNIIIA2, which has a potent ability to activate beta1-integrins. Tretinoin 71-75 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 250-255
30658598-7 2019 U73122 (in the range of 5 to 40 muM) could suppress the secretion of TGF-beta2 induced by ATRA (p < 0.001), and 40 muM U73122 could completely inhibit the up-regulated effect of 10 muM ATRA. Tretinoin 188-192 transforming growth factor beta 2 Homo sapiens 69-78
30658598-9 2019 CONCLUSIONS: In RPE cells, ATRA stimulates the secretion of TGF-beta2 via the phospholipase C signaling pathway but not the adenylyl cyclase signaling pathway. Tretinoin 27-31 transforming growth factor beta 2 Homo sapiens 60-69
30442713-8 2019 We also found that retinoic acid-induced differentiation of mouse ES cells is accompanied by the enhanced degradation of the methylated SOX2 protein at both Lys-42 and Lys-117. Tretinoin 19-32 SRY (sex determining region Y)-box 2 Mus musculus 136-140
30671060-0 2018 Retinoic Acid Mediated Clearance of Citrobacter rodentium in Vitamin A Deficient Mice Requires CD11b+ and T Cells. Tretinoin 0-13 integrin subunit alpha M Homo sapiens 95-100
30392121-0 2019 PLGA-based control release of Noggin blocks the premature fusion of cranial sutures caused by retinoic acid. Tretinoin 94-107 noggin Mus musculus 30-36
30392121-7 2019 Recombinant mouse Noggin blocked the atRA-induced enhancement of osteogenesis of SMCs in vitro. Tretinoin 37-41 noggin Mus musculus 18-24
30392121-8 2019 In vivo, PLGA microsphere encapsulated with Noggin significantly prevented the atRA-induced suture fusion. Tretinoin 79-83 noggin Mus musculus 44-50
30392121-9 2019 Collectively, these data support the hypothesis that BMP signaling is involved in retinoic acid-induced premature fusion of cranial sutures, while PLGA microsphere-based control release of Noggin emerges as a promising strategy for prevention of atRA-induced suture fusion. Tretinoin 246-250 noggin Mus musculus 189-195
30446224-0 2018 Retinoic acid modulates iron metabolism imbalance in anemia of inflammation induced by LPS via reversely regulating hepcidin and ferroportin expression. Tretinoin 0-13 hepcidin antimicrobial peptide Mus musculus 116-124
30446224-7 2018 Furthermore, RA down-regulated the protein expression of hepcidin, toll-like receptor 4 (TLR4) and p-p65 in liver tissue, while up-regulated that of ferroportin. Tretinoin 13-15 hepcidin antimicrobial peptide Mus musculus 57-65
30446224-8 2018 RA modulates iron metabolism imbalance in AI induced by LPS via reversely regulating hepcidin and ferroportin expression, which might be mediated by TLT-4/NFkappaB signaling pathway. Tretinoin 0-2 hepcidin antimicrobial peptide Mus musculus 85-93
30184259-9 2018 In vitro experiments confirmed that CB1 receptor activation directly inhibits retinoic acid-induced nephrin expression in podocytes and IL-4-induced M2 polarization in macrophages. Tretinoin 78-91 nephrosis 1, nephrin Mus musculus 100-107
30276608-4 2018 CXCR5 is also expressed in HL-60 cells, a human acute myeloid leukemia line, following treatment with all-trans retinoic acid, which induces differentiation toward a neutrophil-like state. Tretinoin 112-125 C-X-C motif chemokine receptor 5 Homo sapiens 0-5
30276608-6 2018 Since CXCR5 has various membrane protein partners, we investigated whether CXCR5-driven all-trans retinoic acid-induced differentiation depends on its association with such partners. Tretinoin 98-111 C-X-C motif chemokine receptor 5 Homo sapiens 75-80
29569971-5 2018 We found that co-treatment with RA and bosutinib enhanced differentiation evidenced by increased CD11b expression, G1/G0 cell cycle arrest, and respiratory burst. Tretinoin 32-34 integrin subunit alpha M Homo sapiens 97-102
30497437-6 2018 We also found that the mechanisms triggered by ATRA in non-invasive breast tumor cells cultured under hypoxia is in part mediated by PLC-beta2, responsible to counteract the effects of low oxygen availability on CD133 levels. Tretinoin 47-51 phospholipase C beta 2 Homo sapiens 133-142
30209176-3 2018 During viral infection, LUBAC is reported to inhibit the induction of interferon (IFN) by the cytosolic RNA sensor retinoic acid-inducible gene I (RIG-I). Tretinoin 115-128 DExD/H-box helicase 58 Homo sapiens 147-152
29619864-7 2018 RESULTS: In the rat model of GS, the expressions of TRPC6 were significantly elevated compared with the normal rat group; however, the use of ATRA down-regulated the expression of TRPC6 in the glomeruli and attenuated glomerulosclerosis and proteinuria. Tretinoin 142-146 transient receptor potential cation channel, subfamily C, member 6 Rattus norvegicus 52-57
29619864-7 2018 RESULTS: In the rat model of GS, the expressions of TRPC6 were significantly elevated compared with the normal rat group; however, the use of ATRA down-regulated the expression of TRPC6 in the glomeruli and attenuated glomerulosclerosis and proteinuria. Tretinoin 142-146 transient receptor potential cation channel, subfamily C, member 6 Rattus norvegicus 180-185
30379862-8 2018 Retinaldehyde dehydrogenase 1 family, member A2 (ALDH1A2) and retinaldehyde dehydrogenase 1 family, member A3 (ALDH1A3), key enzymes for retinoic acid synthesis, were underexpressed in SS (-1.48 and -2.3-fold, respectively) and NASH (-1.47 and -2.6-fold, respectively) versus LD. Tretinoin 137-150 aldehyde dehydrogenase 1 family member A2 Homo sapiens 49-56
30379862-9 2018 In NASH, hepatic ALDH1A2 and ALDH1A3 were underexpressed and inversely correlated with plasma retinol levels, which may reduce retinoic acid in the liver. Tretinoin 127-140 aldehyde dehydrogenase 1 family member A2 Homo sapiens 17-24
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 40-53 retinoid X receptor alpha Homo sapiens 199-202
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 55-57 retinoid X receptor alpha Homo sapiens 178-197
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 55-57 retinoid X receptor alpha Homo sapiens 199-202
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 88-90 retinoid X receptor alpha Homo sapiens 178-197
30322383-1 2018 BACKGROUND: In the classical pathway of retinoic acid (RA) mediated gene transcription, RA binds to a nuclear hormone receptor dimer composed of retinoic acid receptor (RAR) and retinoid X receptor (RXR), to induce the expression of its downstream target genes. Tretinoin 88-90 retinoid X receptor alpha Homo sapiens 199-202
30322383-2 2018 In addition to nuclear receptors, there are other intracellular RA binding proteins such as cellular retinoic acid binding proteins (CRABP1 and CRABP2) and cytochrome P450 (CYP) enzymes, whose contributions to the RA signaling pathway have not been fully understood. Tretinoin 64-66 cellular retinoic acid binding protein 2 Homo sapiens 144-150
30104253-0 2018 E2F1 Mediates the Retinoic Acid-Induced Transcription of Tshz1 during Neuronal Differentiation in a Cell Division-Dependent Manner. Tretinoin 18-31 teashirt zinc finger homeobox 1 Homo sapiens 57-62
30104253-6 2018 We investigated the induction mechanisms of Tshz1, whose expression is induced by retinoic acid (RA) in a cell division-dependent manner. Tretinoin 82-95 teashirt zinc finger homeobox 1 Homo sapiens 44-49
30104253-6 2018 We investigated the induction mechanisms of Tshz1, whose expression is induced by retinoic acid (RA) in a cell division-dependent manner. Tretinoin 97-99 teashirt zinc finger homeobox 1 Homo sapiens 44-49
30104253-7 2018 Promoter analysis of Tshz1 revealed a specific region required for RA-dependent transcription. Tretinoin 67-69 teashirt zinc finger homeobox 1 Homo sapiens 21-26
30104253-8 2018 A series of experiments was used to identify E2F1 as the induction factor for the RA-dependent transcription of Tshz1 We propose that E2F1 mediates neuronal differentiation in a cell division-dependent manner. Tretinoin 82-84 teashirt zinc finger homeobox 1 Homo sapiens 112-117
29803924-9 2018 Furthermore, Rbp7 mRNA expression in 3T3-L1 cells was significantly up- and down-regulated by retinol and retinoic acid, respectively. Tretinoin 106-119 retinol binding protein 7, cellular Mus musculus 13-17
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 lecithin retinol acyltransferase Rattus norvegicus 82-86
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 retinoid isomerohydrolase RPE65 Rattus norvegicus 88-93
30030988-4 2018 Diabetes inhibited the expression of retinoic acid metabolism pathway genes- Lpl, Lrat, RPE65, Rdh5, Rdh10, Rdh12, Rlbp1 and Rbp1 and increased Crabp1. Tretinoin 37-50 retinol dehydrogenase 12 Rattus norvegicus 108-113
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 14-27 retinoid X receptor alpha Homo sapiens 112-116
29246089-1 2018 INTRODUCTION: Retinoic acid (RA) signaling through its receptors (RARA, RARB, RARG, and the retinoic X receptor RXRA) is essential for healthy placental and fetal development. Tretinoin 29-31 retinoid X receptor alpha Homo sapiens 112-116
30225259-10 2018 Our results suggest that ATRA enhances MMP-2 expression and secretion in human myeloid leukemia THP-1 cells in a calcium ion dependent manner through RAR/RXR signaling pathways, and this enhanced expression and secretion may be associated with the possible mechanisms of RAS. Tretinoin 25-29 retinoid X receptor alpha Homo sapiens 154-157
30139933-4 2018 Here, we construct a tumour microenvironment-responsive nanosystem, based on PEGylated polyethylenimine-coated gold nanoparticles, and utilise it to co-deliver all-trans retinoic acid (ATRA, an inducer of PSC quiescence) and siRNA targeting heat shock protein 47 (HSP47, a collagen-specific molecular chaperone) to re-educate PSCs. Tretinoin 170-183 serpin family H member 1 Homo sapiens 241-262
30139933-4 2018 Here, we construct a tumour microenvironment-responsive nanosystem, based on PEGylated polyethylenimine-coated gold nanoparticles, and utilise it to co-deliver all-trans retinoic acid (ATRA, an inducer of PSC quiescence) and siRNA targeting heat shock protein 47 (HSP47, a collagen-specific molecular chaperone) to re-educate PSCs. Tretinoin 170-183 serpin family H member 1 Homo sapiens 264-269
30134174-5 2018 Physiologically, we further show that the ZMYND8-P-TEFb complex-mediated transcriptional activation is required for all-trans retinoic acid (ATRA)-mediated differentiation of neuronal precursor cells. Tretinoin 126-139 zinc finger MYND-type containing 8 Homo sapiens 42-48
30134174-5 2018 Physiologically, we further show that the ZMYND8-P-TEFb complex-mediated transcriptional activation is required for all-trans retinoic acid (ATRA)-mediated differentiation of neuronal precursor cells. Tretinoin 141-145 zinc finger MYND-type containing 8 Homo sapiens 42-48
29945211-6 2018 Moreover, exposure to beta-CYP and 3-PBA at 100 muM inhibited all-trans retinoic acid (ATRA)-induced mRNA expressions of the granulocytic differentiation-related genes, CD11b and CSF-3R. Tretinoin 87-91 integrin subunit alpha M Homo sapiens 169-174
29706635-0 2018 Functional missense and splicing variants in the retinoic acid catabolizing enzyme CYP26C1 in idiopathic short stature. Tretinoin 49-62 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 83-90
29706635-3 2018 We have recently found that the retinoic acid degrading enzyme CYP26C1 modifies SHOX deficiency phenotypes toward more severe clinical manifestations. Tretinoin 32-45 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 63-70
29706635-3 2018 We have recently found that the retinoic acid degrading enzyme CYP26C1 modifies SHOX deficiency phenotypes toward more severe clinical manifestations. Tretinoin 32-45 short stature homeobox Homo sapiens 80-84
29868798-3 2018 Here, we show that ATRA up-regulates CD38 expression on AML blasts to sufficient levels that promote antibody-mediated fratricide following the addition of anti-CD38 daratumumab (DARA). Tretinoin 19-23 CD38 antigen Mus musculus 37-41
29868798-3 2018 Here, we show that ATRA up-regulates CD38 expression on AML blasts to sufficient levels that promote antibody-mediated fratricide following the addition of anti-CD38 daratumumab (DARA). Tretinoin 19-23 CD38 antigen Mus musculus 161-165
30073149-7 2018 To date, the most promising application of this therapeutic strategy appears to be combination therapy of LSD1 inhibitors with all-trans retinoic acid (ATRA) to reactivate myeloid differentiation in cells that are not spontaneously susceptible to ATRA treatment. Tretinoin 247-251 lysine demethylase 1A Homo sapiens 106-110
29921748-6 2018 In our study, retinoic acid (RA) was selected to downregulate the DSG1 expression, and lipopolysaccharide (LPS) was first used to identify the susceptibility of the DSG1-deficiency Hacat cells. Tretinoin 14-27 desmoglein 1 Homo sapiens 66-70
29674477-5 2018 ATRA increased the efficacy of anti-VEGFR2 antibodies alone and in combination with chemotherapy in preclinical breast cancer models. Tretinoin 0-4 kinase insert domain receptor Homo sapiens 36-42
29674477-6 2018 ATRA reverted the anti-VEGFR2-induced accumulation of intratumoral MDSC, alleviated hypoxia, and counteracted the disorganization of tumor microvessels. Tretinoin 0-4 kinase insert domain receptor Homo sapiens 23-29
29731343-3 2018 We show that switching occurs during normal development and is mediated by feedback between segment identity and the retinoic acid degrading enzymes, cyp26b1 and cyp26c1. Tretinoin 117-130 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 162-169
29621670-8 2018 Using the mammalian two retinoic acid response elements, the transcriptional activities by 2 agonists, 9cRA and PA024, were different among the RXR isoforms of each gastropod species. Tretinoin 24-37 retinoid X receptor alpha Homo sapiens 144-147
29748133-1 2018 Retinoic acid is the active metabolite of vitamin A and regulates several important cellular processes by activating retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 151-171
29748133-1 2018 Retinoic acid is the active metabolite of vitamin A and regulates several important cellular processes by activating retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 173-176
29748133-11 2018 These effects of retinoic acid are thought to be at least partially mediated by the retinoid receptors, as treatment of the neurons with synthetic RAR and RXR agonists produced a similar inhibition of ICa. Tretinoin 17-30 retinoid X receptor alpha Homo sapiens 155-158
29792731-2 2018 Apoptosis-related protein 3 (APR3) was recently discovered after treatment with all- trans retinoic acid, a pivotal molecule in RPE cells. Tretinoin 91-104 all-trans retinoic acid induced differentiation factor Homo sapiens 0-27
29792731-2 2018 Apoptosis-related protein 3 (APR3) was recently discovered after treatment with all- trans retinoic acid, a pivotal molecule in RPE cells. Tretinoin 91-104 all-trans retinoic acid induced differentiation factor Homo sapiens 29-33
29792731-6 2018 High doses of all- trans retinoic acid treatment were found to significantly induce APR3 expression, increase reactive oxygen species levels, and decrease ATP content, which were abolished by knockdown of APR3. Tretinoin 25-38 all-trans retinoic acid induced differentiation factor Homo sapiens 84-88
29792731-6 2018 High doses of all- trans retinoic acid treatment were found to significantly induce APR3 expression, increase reactive oxygen species levels, and decrease ATP content, which were abolished by knockdown of APR3. Tretinoin 25-38 all-trans retinoic acid induced differentiation factor Homo sapiens 205-209
29757260-6 2018 TFPI2 was vital in the ATRA-mediated suppression of HuH7 cell invasion. Tretinoin 23-27 MIR7-3 host gene Homo sapiens 52-56
29757260-8 2018 The knockdown of RARα or MAFB counteracted the ATRA-mediated suppression of HuH7 cell invasion while the knockdown of MAFF inhibited the invasion. Tretinoin 57-61 MIR7-3 host gene Homo sapiens 86-90
28993924-5 2018 In order to better understand the biological role of ACh in AD, we studied the effect of Abeta on the phosphorylation of the cytosolic phospholipase A2 (cPLA2) in the TB neuroectodermal cell line, which differentiates toward a neuronal phenotype when cultured in the presence of retinoic acid (RA). Tretinoin 294-296 phospholipase A2 group IVA Homo sapiens 153-158
28566049-2 2018 The ratio of FABP5 to CRABP-II in a cell may determine whether it undergoes natural apoptosis or unrestricted cell growth in the presence of retinoic acid. Tretinoin 141-154 fatty acid binding protein 5 Homo sapiens 13-18
28566049-2 2018 The ratio of FABP5 to CRABP-II in a cell may determine whether it undergoes natural apoptosis or unrestricted cell growth in the presence of retinoic acid. Tretinoin 141-154 cellular retinoic acid binding protein 2 Homo sapiens 22-30
29476041-7 2018 In support of this, CRABPs delivered 4-oxo-atRA and atRA for metabolism by CYP26C1. Tretinoin 43-47 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 75-82
29476041-8 2018 Despite the tight binding of 4-oxo-atRA and atRA with CRABPs, the apparent Michaelis-Menten constant in biological matrix (Km) value of these substrates with CYP26C1 was not increased when the substrates were bound with CRABPs, in contrast to what is predicted by free drug hypothesis. Tretinoin 35-39 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 158-165
29488605-2 2018 Gene associated with retinoid-interferon (IFN)-induced mortality-19 (Grim-19) is reported to be a cell death activator that may be used to define mechanisms involved in IFN-beta- and retinoic acid-induced cell death and apoptosis in a number of tumor cell lines. Tretinoin 183-196 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 69-76
29609731-3 2018 The level of VEGF in the RPE/choroid was significantly decreased in Aldh1a1-/- mice, and RA-dependent enhancement of VEGF was observed in primary RPE cells. Tretinoin 89-91 vascular endothelial growth factor A Mus musculus 117-121
29543331-5 2018 We show that in response to RA, TRIM24 serves as an adapter linking RARalpha to the proteasome for its degradation. Tretinoin 28-30 tripartite motif containing 24 Homo sapiens 32-38
29496480-0 2018 Coordinate regulation of retinoic acid synthesis by pbx genes and fibroblast growth factor signaling by hoxb1b is required for hindbrain patterning and development. Tretinoin 25-38 homeobox B1b Danio rerio 104-110
27996890-8 2018 The expression of ROR-gammat and IL-17 genes in the splenocytes of ATRA, calcitriol and combination- treated mice was significantly reduced compared to those of vehicle- treated mice (P < 0.05). Tretinoin 67-71 interleukin 17A Mus musculus 33-38
29480012-5 2018 We retrospectively validate our approach using mutagenesis data for retinoic acid binding to the Cellular Retinoic Acid Binding Protein II (CRABPII) system and then make prospective predictions that are borne out experimentally. Tretinoin 68-81 cellular retinoic acid binding protein 2 Homo sapiens 97-138
29480012-5 2018 We retrospectively validate our approach using mutagenesis data for retinoic acid binding to the Cellular Retinoic Acid Binding Protein II (CRABPII) system and then make prospective predictions that are borne out experimentally. Tretinoin 68-81 cellular retinoic acid binding protein 2 Homo sapiens 140-147
29480012-6 2018 The overall performance of our approach is supported by its success in identifying mutants that show high or even sub-nano-molar binding affinities of retinoic acid to the CRABPII system. Tretinoin 151-164 cellular retinoic acid binding protein 2 Homo sapiens 172-179
30460083-7 2018 Additionally, the proteolytic fragment of Mib was detected in differentiated P19 cells following treatment with RA. Tretinoin 112-114 MIB E3 ubiquitin protein ligase 1 Homo sapiens 42-45
29253589-5 2018 We report that differentiation of H9c2 cells with retinoic acid towards cardiomyocytes is accompanied by increased expression of mitochondrial proteins, oxygen consumption, and expression of the PA/PI binding protein, PITPNC1, and CDS1 immunoreactivity. Tretinoin 50-63 phosphatidylinositol transfer protein, cytoplasmic 1 Rattus norvegicus 218-225
29490681-8 2018 Furthermore, OLCs from the RA treated group, expressed significantly more of the meiosis regulatory gene Marf1 and the oocyte marker Oct4. Tretinoin 27-29 meiosis regulator and mRNA stability 1 Mus musculus 105-110
29490681-11 2018 RA treatment also improved the structural integrity of the OLCs produced by initiating the expression of all three zona pellucida transcripts (Zp1-3) and improving ZP3 expression levels and localization. Tretinoin 0-2 zona pellucida glycoprotein 1 Mus musculus 143-148
29490681-11 2018 RA treatment also improved the structural integrity of the OLCs produced by initiating the expression of all three zona pellucida transcripts (Zp1-3) and improving ZP3 expression levels and localization. Tretinoin 0-2 zona pellucida glycoprotein 3 Mus musculus 164-167
29467333-0 2018 CHD7 represses the retinoic acid synthesis enzyme ALDH1A3 during inner ear development. Tretinoin 19-32 chromodomain helicase DNA binding protein 7 Mus musculus 0-4
29467333-3 2018 Interestingly, upregulation or downregulation of retinoic acid (RA) signaling during embryogenesis also leads to developmental defects similar to those in CHARGE syndrome, suggesting that CHD7 and RA may have common target genes or signaling pathways. Tretinoin 49-62 chromodomain helicase DNA binding protein 7 Mus musculus 188-192
29467333-3 2018 Interestingly, upregulation or downregulation of retinoic acid (RA) signaling during embryogenesis also leads to developmental defects similar to those in CHARGE syndrome, suggesting that CHD7 and RA may have common target genes or signaling pathways. Tretinoin 64-66 chromodomain helicase DNA binding protein 7 Mus musculus 188-192
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 CD4 antigen Mus musculus 172-175
29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 CD4 antigen Mus musculus 239-242
29305158-0 2018 TBR2 antagonizes retinoic acid dependent neuronal differentiation by repressing Zfp423 during corticogenesis. Tretinoin 17-30 eomesodermin Homo sapiens 0-4
28960887-7 2018 Moreover, RAR/RXRalpha costimulation elevated VE-cadherin expression and improved barrier fidelity to levels that recapitulated the effects of RA. Tretinoin 10-12 retinoid X receptor alpha Homo sapiens 14-22
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 3-16 Wnt family member 5A Gallus gallus 68-71
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 3-16 Wnt family member 5A Gallus gallus 110-115
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 18-20 Wnt family member 5A Gallus gallus 68-71
28786525-3 2018 In retinoic acid (RA) induction experiments in vitro, we found that Wnt signaling expression was inhibited by Wnt5a-shRNA, resulting in decreased expression of corresponding marker genes in SSCs, C-kit, Cvh, integrin alpha6 and integrin beta1, but it was significantly promoted by RA treatment. Tretinoin 18-20 Wnt family member 5A Gallus gallus 110-115
29301505-9 2018 RESULTS: Treatment of IMR32 and BE2C cells in vitro with 10 muM ATRA resulted in a change in cell morphology, a 65% decrease in cell proliferation, upregulation of STMN4 and ROBO2 and downregulation of KLF4. Tretinoin 64-68 stathmin 4 Homo sapiens 164-169
29607925-8 2018 When RARalpha was blocked by LE540 in RAW264.7 macrophages, the inflammatory cytokines were enhancing, along with a decline of Akt phosphorylation but Forkhead box o (Foxo) 1, compared with the ATRA group. Tretinoin 194-198 retinoic acid receptor, alpha Mus musculus 5-13
29076503-3 2018 Here we report that the functionality of ALDH1A2, the rate-limiting enzyme of retinoic acid (RA) synthesis, is negatively regulated by UBE3A in a ubiquitylation-dependent manner. Tretinoin 78-91 aldehyde dehydrogenase 1 family member A2 Homo sapiens 41-48
29380316-4 2018 In the described method, the SH-SY5Y neuroblastoma cell line is differentiated to neuronal cell which expresses NSE, neuronal marker, and dopamine transporter (DAT) by treatment with all-trans-retinoic acid. Tretinoin 186-206 solute carrier family 6 member 3 Homo sapiens 138-158
29380316-4 2018 In the described method, the SH-SY5Y neuroblastoma cell line is differentiated to neuronal cell which expresses NSE, neuronal marker, and dopamine transporter (DAT) by treatment with all-trans-retinoic acid. Tretinoin 186-206 solute carrier family 6 member 3 Homo sapiens 160-163
29085977-0 2018 All-trans-retinoic acid ameliorates doxorubicin-induced cardiotoxicity: in vivo potential involvement of oxidative stress, inflammation, and apoptosis via caspase-3 and p53 down-expression. Tretinoin 0-23 tumor protein p53 Rattus norvegicus 169-172
29085977-9 2018 Pretreatment with ATRA maintained cardiac function biomarkers, and reduced proinflammatory cytokines, lipid peroxidation, and immunoexpression of caspase 3 and p53. Tretinoin 18-22 tumor protein p53 Rattus norvegicus 160-163
29155646-0 2018 Combination treatment of docosahexaenoic acid (DHA) and all-trans-retinoic acid (ATRA) inhibit IL-17 and RORgammat gene expression in PBMCs of patients with relapsing-remitting multiple sclerosis. Tretinoin 56-79 interleukin 17A Homo sapiens 95-100
29155646-0 2018 Combination treatment of docosahexaenoic acid (DHA) and all-trans-retinoic acid (ATRA) inhibit IL-17 and RORgammat gene expression in PBMCs of patients with relapsing-remitting multiple sclerosis. Tretinoin 81-85 interleukin 17A Homo sapiens 95-100
29155646-6 2018 RESULTS: The results showed that single treatment of ATRA (p = 0.05) could significantly decrease the expression of IL-17 gene and single treatment of ATRA (p = 0.04) and single treatment of DHA (p = 0.05) induced significant inhibition on the expression of RORgammat gene. Tretinoin 53-57 interleukin 17A Homo sapiens 116-121
29155646-7 2018 The suppressive effect of combined treatment with ATRA and DHA on IL-17 (p = 0.02) and RORgammat (p = 0.01) was also found significant showing that the combined treatments can have additive effects. Tretinoin 50-54 interleukin 17A Homo sapiens 66-71
29634397-7 2018 Results: RA-induced differentiation in the NT2/D1 cells significantly increased the expression of MAP2, NRG1, NRP1, NRP2, NEUROG1 and EN1 genes (genes linked to neural differentiation) compared with undifferentiated NT2/D1 cells. Tretinoin 9-11 engrailed homeobox 1 Homo sapiens 134-137
29212953-4 2017 Genes involved in catecholamine biosynthesis and cAMP signaling are upregulated in the adrenal glands of Siah1a-/- mice, while genes related to retinoic acid signaling and cholesterol biosynthesis are downregulated. Tretinoin 144-157 siah E3 ubiquitin protein ligase 1A Mus musculus 105-111
28851699-10 2017 ATRA-treated cGVHD B cells had elevated TLR9 and PAX5, but not BLIMP1 (a gene-expression pattern associated with mature follicular B cells) and also attained increased cytosine guanine dinucleotide responsiveness. Tretinoin 0-4 paired box 5 Homo sapiens 49-53
28849147-11 2017 These findings suggest that RA ameliorates photoaged skin through a RAR-mediated signaling pathway in mice. Tretinoin 28-30 retinoic acid receptor, alpha Mus musculus 68-71
29042924-9 2017 In addition, atRA was revealed to disrupt the cell cycle in the periderm by downregulating p21. Tretinoin 13-17 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 91-94
29018329-12 2017 Our findings indicate that IMR32 differentiation induced by CDDO in combination with ATRA enhances, differentiation followed by cell death via cAMP-response-element binding protein (CREB) independent and PPARgamma dependent signaling mechanisms. Tretinoin 85-89 cAMP responsive element binding protein 1 Homo sapiens 143-180
29018329-12 2017 Our findings indicate that IMR32 differentiation induced by CDDO in combination with ATRA enhances, differentiation followed by cell death via cAMP-response-element binding protein (CREB) independent and PPARgamma dependent signaling mechanisms. Tretinoin 85-89 cAMP responsive element binding protein 1 Homo sapiens 182-186
28566502-4 2017 The objective of the present study was to determine the physiological efficacy and impact of all-trans-retinoic acid (ATRA) and sodium butyrate (NaBu) in ameliorating the renal fibrosis, inflammation, and hypertension in Npr1 gene-disrupted haplotype (1-copy; +/-) mice (50% expression levels of NPRA). Tretinoin 93-116 natriuretic peptide receptor 1 Mus musculus 221-225
28566502-4 2017 The objective of the present study was to determine the physiological efficacy and impact of all-trans-retinoic acid (ATRA) and sodium butyrate (NaBu) in ameliorating the renal fibrosis, inflammation, and hypertension in Npr1 gene-disrupted haplotype (1-copy; +/-) mice (50% expression levels of NPRA). Tretinoin 93-116 natriuretic peptide receptor 1 Mus musculus 296-300
28566502-4 2017 The objective of the present study was to determine the physiological efficacy and impact of all-trans-retinoic acid (ATRA) and sodium butyrate (NaBu) in ameliorating the renal fibrosis, inflammation, and hypertension in Npr1 gene-disrupted haplotype (1-copy; +/-) mice (50% expression levels of NPRA). Tretinoin 118-122 natriuretic peptide receptor 1 Mus musculus 221-225
28566502-4 2017 The objective of the present study was to determine the physiological efficacy and impact of all-trans-retinoic acid (ATRA) and sodium butyrate (NaBu) in ameliorating the renal fibrosis, inflammation, and hypertension in Npr1 gene-disrupted haplotype (1-copy; +/-) mice (50% expression levels of NPRA). Tretinoin 118-122 natriuretic peptide receptor 1 Mus musculus 296-300
28566502-5 2017 Both ATRA and NaBu, either alone or in combination, decreased the elevated levels of renal proinflammatory and profibrotic cytokines and lowered blood pressure in Npr1+/- mice compared with untreated controls. Tretinoin 5-9 natriuretic peptide receptor 1 Mus musculus 163-167
28718066-9 2017 In the NTD model, the expression levels of Dvl, RhoA, and p-Jnk were significantly higher in the RA group than in the control group, whereas they were significantly reduced in the RA + taurine group. Tretinoin 97-99 dishevelled segment polarity protein 1 Mus musculus 43-46
28718066-9 2017 In the NTD model, the expression levels of Dvl, RhoA, and p-Jnk were significantly higher in the RA group than in the control group, whereas they were significantly reduced in the RA + taurine group. Tretinoin 97-99 mitogen-activated protein kinase 8 Mus musculus 60-63
28718066-9 2017 In the NTD model, the expression levels of Dvl, RhoA, and p-Jnk were significantly higher in the RA group than in the control group, whereas they were significantly reduced in the RA + taurine group. Tretinoin 180-182 dishevelled segment polarity protein 1 Mus musculus 43-46
28718066-9 2017 In the NTD model, the expression levels of Dvl, RhoA, and p-Jnk were significantly higher in the RA group than in the control group, whereas they were significantly reduced in the RA + taurine group. Tretinoin 180-182 mitogen-activated protein kinase 8 Mus musculus 60-63
28643469-3 2017 Silencing of cellular retinoic acid binding protein 2 (CRABP2) could impede the ATRA-induced upregulation of COL9A1, whereas overexpression of CRABP2 presented the opposite effect. Tretinoin 80-84 cellular retinoic acid binding protein 2 Homo sapiens 13-53
28643469-3 2017 Silencing of cellular retinoic acid binding protein 2 (CRABP2) could impede the ATRA-induced upregulation of COL9A1, whereas overexpression of CRABP2 presented the opposite effect. Tretinoin 80-84 cellular retinoic acid binding protein 2 Homo sapiens 55-61
28381549-7 2017 Notably, we also showed that treatment with retinoic acid enhanced NRIP1 binding to RARalpha RNA in situ hybridization confirmed Nrip1 expression in the developing urogenital system of the mouse. Tretinoin 44-57 retinoic acid receptor, alpha Mus musculus 84-92
28502478-4 2017 CRABP2 is a transcriptional co-activator of retinoic acid signaling. Tretinoin 44-57 cellular retinoic acid binding protein 2 Homo sapiens 0-6
28502478-12 2017 These data suggest a retinoic acid-independent, non-tumor suppressor role of CRABP2 for the survival of MPNST cells in vitro. Tretinoin 21-34 cellular retinoic acid binding protein 2 Homo sapiens 77-83
27862257-4 2017 In Retinoic acid (RA) induced in vitro differentiation assay, the expression of two germ cell marker genes, integrin alpha6, and integrin beta1, was observed to significantly increase, while it decreased dramatically when IHH was knocked down. Tretinoin 3-16 integrin subunit alpha 6 Gallus gallus 108-123
27862257-4 2017 In Retinoic acid (RA) induced in vitro differentiation assay, the expression of two germ cell marker genes, integrin alpha6, and integrin beta1, was observed to significantly increase, while it decreased dramatically when IHH was knocked down. Tretinoin 18-20 integrin subunit alpha 6 Gallus gallus 108-123
27862257-5 2017 Fluorescence activated cell sorting analysis showed that the proportion of integrin alpha6+ and integrin beta1+ cells in the RA group was significantly higher than that in the RA + siRNA- Indian Hedgehog (IHH) group. Tretinoin 125-127 integrin subunit alpha 6 Gallus gallus 75-90
28218902-0 2017 Retinoic acid directs breast cancer cell state changes through regulation of TET2-PKCzeta pathway. Tretinoin 0-13 protein kinase C zeta Homo sapiens 82-89
28218902-4 2017 Our data reveal that pharmacological concentration of ATRA effectively downregulates PKCzeta through activation of miR-200c, leading to a decrease of the stem cell-like populations from non-tumorigenic mammary epithelial cells and non-aggressive breast cancer cells. Tretinoin 54-58 protein kinase C zeta Homo sapiens 85-92
28396148-0 2017 DOK1/PPARgamma pathway mediates anti-tumor ability of all-trans retinoic acid in breast cancer MCF-7 cells. Tretinoin 64-77 docking protein 1 Homo sapiens 0-4
28396148-2 2017 This study experimentally revealed that ATRA treatment inhibited MCF-7 cell proliferation and promoted its apoptosis, along with an enhanced expression of docking protein 1 (DOK1). Tretinoin 40-44 docking protein 1 Homo sapiens 155-172
28396148-2 2017 This study experimentally revealed that ATRA treatment inhibited MCF-7 cell proliferation and promoted its apoptosis, along with an enhanced expression of docking protein 1 (DOK1). Tretinoin 40-44 docking protein 1 Homo sapiens 174-178
28396148-6 2017 Taken together, these results indicate that ATRA-enhanced expression of DOK1 activates PPARgamma leading to inhibition of cell proliferation and enhancement of cell apoptosis in MCF-7 cell. Tretinoin 44-48 docking protein 1 Homo sapiens 72-76
28492556-1 2017 Multiple lines of evidence have demonstrated that increased expression of phospholipid scramblase 1 (PLSCR1) is involved in the differentiation of acute myeloid leukemia (AML) cells by several differentiation-inducing agents including ATRA and phorbol 12-myristate 13-acetate. Tretinoin 235-239 phospholipid scramblase 1 Homo sapiens 74-99
28492556-1 2017 Multiple lines of evidence have demonstrated that increased expression of phospholipid scramblase 1 (PLSCR1) is involved in the differentiation of acute myeloid leukemia (AML) cells by several differentiation-inducing agents including ATRA and phorbol 12-myristate 13-acetate. Tretinoin 235-239 phospholipid scramblase 1 Homo sapiens 101-107
26886278-8 2017 ADH and ALDH can play also a crucial regulatory role in initiation and progression of malignant diseases by participation in retinoic acid synthesis and elimination of toxic acetaldehyde. Tretinoin 125-138 aldo-keto reductase family 1 member A1 Homo sapiens 0-3
28363907-3 2017 RA can promote gammadelta T cells to produce mTORC1-dependent IL-22 in the liver, but inhibits IFN-gamma and IL-17. Tretinoin 0-2 interleukin 17A Mus musculus 109-114
28209268-6 2017 We observed extension of neuritic processes and increased expression of neuronal markers (MAP2, tubulin-betaIII, and Tau) after RA stimulation, all these effects were decreased by the co-exposure to I-Hg. Tretinoin 128-130 microtubule associated protein 2 Homo sapiens 90-94
28207193-4 2017 The oxidation of vitamin A to retinal has recently been established as a critical nodal point in the synthesis of retinoic acid, and over the past decade, RDH10 and DHRS3 have emerged as the predominant enzymes that regulate this reversible reaction. Tretinoin 114-127 retinol dehydrogenase 10 Homo sapiens 155-160
28207193-4 2017 The oxidation of vitamin A to retinal has recently been established as a critical nodal point in the synthesis of retinoic acid, and over the past decade, RDH10 and DHRS3 have emerged as the predominant enzymes that regulate this reversible reaction. Tretinoin 114-127 dehydrogenase/reductase 3 Homo sapiens 165-170
28232491-9 2017 Importantly, disruption of the ROC-generated circuit by a knockdown of DHRS3 results in an increased flux through the RA biosynthesis pathway and elevated RA levels despite the decrease in RDH10 protein destabilized by the absence of DHRS3, hence demonstrating a loss of control. Tretinoin 118-120 dehydrogenase/reductase 3 Homo sapiens 71-76
28232491-9 2017 Importantly, disruption of the ROC-generated circuit by a knockdown of DHRS3 results in an increased flux through the RA biosynthesis pathway and elevated RA levels despite the decrease in RDH10 protein destabilized by the absence of DHRS3, hence demonstrating a loss of control. Tretinoin 155-157 dehydrogenase/reductase 3 Homo sapiens 71-76
28232491-10 2017 Thus, the bifunctional nature of ROC provides the RA-based signaling system with robustness by safeguarding appropriate RA concentration despite naturally occurring fluctuations in RDH10 and DHRS3. Tretinoin 50-52 retinol dehydrogenase 10 Homo sapiens 181-186
28232491-10 2017 Thus, the bifunctional nature of ROC provides the RA-based signaling system with robustness by safeguarding appropriate RA concentration despite naturally occurring fluctuations in RDH10 and DHRS3. Tretinoin 50-52 dehydrogenase/reductase 3 Homo sapiens 191-196
28232094-2 2017 Previously, we identified a dual histone reader ZMYND8 (zinc finger MYND (Myeloid, Nervy and DEAF-1)-type containing 8), to be a novel target of ATRA. Tretinoin 145-149 DEAF1, transcription factor Mus musculus 93-99
28189972-9 2017 By contrast, ATRA potently enhanced GM-CSF-dependent neutropoiesis in liquid culture from BALB/c or C57BL/6 bone-marrow. Tretinoin 13-17 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 36-42
28154153-5 2017 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Tretinoin 13-15 K(lysine) acetyltransferase 2A Mus musculus 25-29
28154153-5 2017 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Tretinoin 13-15 transforming, acidic coiled-coil containing protein 1 Mus musculus 54-59
28154153-5 2017 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Tretinoin 13-15 transforming, acidic coiled-coil containing protein 1 Mus musculus 94-99
28154153-5 2017 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Tretinoin 105-118 K(lysine) acetyltransferase 2A Mus musculus 25-29
28154153-5 2017 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Tretinoin 105-118 transforming, acidic coiled-coil containing protein 1 Mus musculus 54-59
28154153-5 2017 Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. Tretinoin 105-118 transforming, acidic coiled-coil containing protein 1 Mus musculus 94-99
28154153-6 2017 Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta. Tretinoin 14-16 K(lysine) acetyltransferase 2A Mus musculus 68-72
28154153-6 2017 Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta. Tretinoin 96-98 K(lysine) acetyltransferase 2A Mus musculus 68-72
28154153-7 2017 Last, we demonstrate that the diencephalic expansion and transcriptional defects seen in (Gcn5hat/hat ) mutants can be rescued with gestational RA supplementation, supporting a direct link between GCN5, TACC1, and RA signaling in the developing diencephalon. Tretinoin 144-146 K(lysine) acetyltransferase 2A Mus musculus 197-201
28154153-7 2017 Last, we demonstrate that the diencephalic expansion and transcriptional defects seen in (Gcn5hat/hat ) mutants can be rescued with gestational RA supplementation, supporting a direct link between GCN5, TACC1, and RA signaling in the developing diencephalon. Tretinoin 144-146 transforming, acidic coiled-coil containing protein 1 Mus musculus 203-208
28154153-8 2017 Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.SIGNIFICANCE STATEMENT Changes in diencephalic size and shape, as well as SNPs associated with retinoic acid (RA) signaling-associated genes, have been linked to neuropsychiatric disorders. Tretinoin 154-156 K(lysine) acetyltransferase 2A Mus musculus 65-69
28154153-8 2017 Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.SIGNIFICANCE STATEMENT Changes in diencephalic size and shape, as well as SNPs associated with retinoic acid (RA) signaling-associated genes, have been linked to neuropsychiatric disorders. Tretinoin 344-357 K(lysine) acetyltransferase 2A Mus musculus 65-69
28154153-8 2017 Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.SIGNIFICANCE STATEMENT Changes in diencephalic size and shape, as well as SNPs associated with retinoic acid (RA) signaling-associated genes, have been linked to neuropsychiatric disorders. Tretinoin 359-361 K(lysine) acetyltransferase 2A Mus musculus 65-69
28154153-10 2017 Here we demonstrate a novel role of the acetyltransferase GCN5 in a previously undescribed mechanism of RA signaling in the developing forebrain that is required to maintain the appropriate size of the diencephalon. Tretinoin 104-106 K(lysine) acetyltransferase 2A Mus musculus 58-62
28154153-11 2017 Together, our experiments identify a novel nonhistone substrate of GCN5, highlight an essential role for both GCN5 and RA signaling in early diencephalic development, and elucidate a novel molecular regulatory mechanism for RA signaling that is specific to the developing forebrain. Tretinoin 119-121 K(lysine) acetyltransferase 2A Mus musculus 67-71
28154153-11 2017 Together, our experiments identify a novel nonhistone substrate of GCN5, highlight an essential role for both GCN5 and RA signaling in early diencephalic development, and elucidate a novel molecular regulatory mechanism for RA signaling that is specific to the developing forebrain. Tretinoin 224-226 K(lysine) acetyltransferase 2A Mus musculus 67-71
28427488-1 2017 OBJECTIVE: This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 (Nr2e1) in retinoic acid (RA)-induced brain abnormality. Tretinoin 154-156 nuclear receptor subfamily 2, group E, member 1 Mus musculus 82-127
28427488-1 2017 OBJECTIVE: This study aimed to investigate the expression pattern and function of Nuclear receptor subfamily 2 group E member 1 (Nr2e1) in retinoic acid (RA)-induced brain abnormality. Tretinoin 154-156 nuclear receptor subfamily 2, group E, member 1 Mus musculus 129-134
28427488-6 2017 RESULTS: Nr2e1 expression was significantly downregulated in the brain and NSCs of RA-treated mouse embryos, and knockdown of Nr2e1 affected the proliferation of NSCs in vitro. Tretinoin 83-85 nuclear receptor subfamily 2, group E, member 1 Mus musculus 9-14
28427488-8 2017 CONCLUSION: Our study demonstrated that Nr2e1 could be regulated by RA, which would aid a better understanding of the mechanism underlying RA-induced brain abnormality. Tretinoin 68-70 nuclear receptor subfamily 2, group E, member 1 Mus musculus 40-45
28427488-8 2017 CONCLUSION: Our study demonstrated that Nr2e1 could be regulated by RA, which would aid a better understanding of the mechanism underlying RA-induced brain abnormality. Tretinoin 139-141 nuclear receptor subfamily 2, group E, member 1 Mus musculus 40-45
27677346-0 2017 Curcumin synergistically increases effects of beta-interferon and retinoic acid on breast cancer cells in vitro and in vivo by up-regulation of GRIM-19 through STAT3-dependent and STAT3-independent pathways. Tretinoin 66-79 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 144-151
27862498-8 2017 RESULTS: In ATRA-treated MSCs, expressions of COX-2, HIF-1, CXCR4, CCR2, VEGF, Ang-2 and Ang-4 increased compared to control groups. Tretinoin 12-16 C-X-C motif chemokine receptor 4 Rattus norvegicus 60-65
28153738-7 2017 This regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha/RXRalpha heterodimer. Tretinoin 19-32 retinoid X receptor alpha Homo sapiens 224-232
28153738-7 2017 This regulation by retinoic acid acts through the MYOC promoter which contains a critical cluster of four retinoic acid responsive elements (RAREs), with the RARE-DR2 presenting the strongest effect and binding the RARalpha/RXRalpha heterodimer. Tretinoin 106-119 retinoid X receptor alpha Homo sapiens 224-232
28529810-1 2017 Several variant RARA translocations have been reported in acute promyelocytic leukemia (APL) of which the t(11;17)(q23;q21), which results in a ZBTB16-RARA fusion, is the most widely identified and is largely resistant to therapy with all-trans retinoic acid (ATRA). Tretinoin 245-258 zinc finger and BTB domain containing 16 Homo sapiens 144-150
28529810-1 2017 Several variant RARA translocations have been reported in acute promyelocytic leukemia (APL) of which the t(11;17)(q23;q21), which results in a ZBTB16-RARA fusion, is the most widely identified and is largely resistant to therapy with all-trans retinoic acid (ATRA). Tretinoin 260-264 zinc finger and BTB domain containing 16 Homo sapiens 144-150
29911777-15 2017 From Verhoff van Gieson staining, the mean difference of elastin amount was 2.25+-3.30 units in tretinoin group and 5.40+-4.16 units in herbal extract group. Tretinoin 96-105 elastin Homo sapiens 57-64
27488085-0 2017 Retinoic Acid Improves Incidence and Severity of Necrotizing Enterocolitis by Lymphocyte Balance Restitution and Repopulation of LGR5+ Intestinal Stem Cells. Tretinoin 0-13 leucine rich repeat containing G protein coupled receptor 5 Mus musculus 129-133
27834666-8 2016 Immunocytochemistry/PCR results showed higher expression of Mvh, the PGC-specific marker, in 3 muM RA concentrations on the top of the STO feeder layer. Tretinoin 100-102 DEAD box helicase 4 Mus musculus 60-63
27793834-5 2016 The 25 nM RA dataset yielded a cohort of previously known caudal RA target genes including Fgf8 (repressed) and Sox2 (activated), plus novel early RA signaling targets with nearby conserved RA response elements. Tretinoin 10-12 SRY-box transcription factor 2 Homo sapiens 112-116
27779898-5 2016 The active form of VA, retinoic acid, may be related to the growth factor-beta and release of interleukin-10 (IL-10), thus involved with the resolution of the inflammation. Tretinoin 23-36 interleukin 10 Homo sapiens 94-108
27779898-5 2016 The active form of VA, retinoic acid, may be related to the growth factor-beta and release of interleukin-10 (IL-10), thus involved with the resolution of the inflammation. Tretinoin 23-36 interleukin 10 Homo sapiens 110-115
28003845-0 2016 All-trans retinoic acid and genistein induce cell apoptosis in OVCAR-3 cells by increasing the P14 tumor suppressor gene. Tretinoin 10-23 ribonuclease P/MRP subunit p14 Homo sapiens 95-98
28003845-1 2016 In this study, we evaluated the effects of all-trans retinoic acid (ATRA) alone or in combination with genistein (GEN) in p14 tumor suppressor gene and subsequent apoptosis of human ovarian carcinoma cells (OVCAR-3). Tretinoin 47-66 ribonuclease P/MRP subunit p14 Homo sapiens 122-125
28003845-1 2016 In this study, we evaluated the effects of all-trans retinoic acid (ATRA) alone or in combination with genistein (GEN) in p14 tumor suppressor gene and subsequent apoptosis of human ovarian carcinoma cells (OVCAR-3). Tretinoin 68-72 ribonuclease P/MRP subunit p14 Homo sapiens 122-125
28003845-6 2016 In conclusion, we confirm that GEN in combination with ATRA is an effective strategy to up regulate the p14 tumor suppressor gene and induce cell apoptosis in OVCAR-3 cell line. Tretinoin 55-59 ribonuclease P/MRP subunit p14 Homo sapiens 104-107
27861498-11 2016 Our analyses demonstrate that somite-derived RA functions to regulate components of the Notch and Cxcl12 chemokine signaling pathways during HSC formation. Tretinoin 45-47 chemokine (C-X-C motif) ligand 12a (stromal cell-derived factor 1) Danio rerio 98-104
27771497-6 2016 We demonstrated that exogenous RA had negative effects on incisor SCs and that this was accompanied by downregulation of Fgf10, a mesenchymally expressed SC survival factor in the mouse incisor. Tretinoin 31-33 fibroblast growth factor 10 Mus musculus 121-126
27771497-7 2016 Supplement of Fgf10 in incisor cultures completely blocked RA effects by antagonizing apoptosis and increasing proliferation in LaCL epithelial SCs. Tretinoin 59-61 fibroblast growth factor 10 Mus musculus 14-19
27771497-8 2016 In addition, Fgf10 obviously antagonized RA-induced downregulation of the SC marker Sox2 in incisor epithelial SCs. Tretinoin 41-43 fibroblast growth factor 10 Mus musculus 13-18
27771497-8 2016 In addition, Fgf10 obviously antagonized RA-induced downregulation of the SC marker Sox2 in incisor epithelial SCs. Tretinoin 41-43 SRY (sex determining region Y)-box 2 Mus musculus 84-88
27771497-9 2016 Our findings suggest that the negative effects of RA on incisor SCs result from inhibition of mesenchymal Fgf10. Tretinoin 50-52 fibroblast growth factor 10 Mus musculus 106-111
27157616-7 2016 More importantly, ATRA downregulated the expression of the CSC markers CD44 and ALDH as well as stemness genes such as Klf4 and Sox2 and induced differentiation of tumorspheres. Tretinoin 18-22 CD44 molecule (Indian blood group) Homo sapiens 71-75
27157616-7 2016 More importantly, ATRA downregulated the expression of the CSC markers CD44 and ALDH as well as stemness genes such as Klf4 and Sox2 and induced differentiation of tumorspheres. Tretinoin 18-22 Kruppel like factor 4 Homo sapiens 119-123
27157616-7 2016 More importantly, ATRA downregulated the expression of the CSC markers CD44 and ALDH as well as stemness genes such as Klf4 and Sox2 and induced differentiation of tumorspheres. Tretinoin 18-22 SRY-box transcription factor 2 Homo sapiens 128-132
27157616-8 2016 Finally, 2 weeks of daily ATRA treatment were sufficient to inhibit gastric tumor progression in vivo, which was associated with a decrease in CD44, ALDH1, Ki67 and PCNA expression in the remaining tumor cells. Tretinoin 26-30 CD44 molecule (Indian blood group) Homo sapiens 143-147
27565026-0 2016 Sox9b is a mediator of retinoic acid signaling restricting endocrine progenitor differentiation. Tretinoin 23-36 SRY-box transcription factor 9b Danio rerio 0-5
27166374-4 2016 This involves feed forward regulation of Raldh2, a rate-limiting enzyme for RA biosynthesis, and requires Med25 to coordinate RAR, STAT6 and chromatin remodeler, Brg1 to remodel the +1 nucleosome of Arg1 for transcription initiation. Tretinoin 76-78 aldehyde dehydrogenase 1 family member A2 Homo sapiens 41-47
27166374-4 2016 This involves feed forward regulation of Raldh2, a rate-limiting enzyme for RA biosynthesis, and requires Med25 to coordinate RAR, STAT6 and chromatin remodeler, Brg1 to remodel the +1 nucleosome of Arg1 for transcription initiation. Tretinoin 76-78 mediator complex subunit 25 Homo sapiens 106-111
27381866-0 2016 All-trans retinoic acid ameliorates glycemic control in diabetic mice via modulating pancreatic islet production of vascular endothelial growth factor-A. Tretinoin 10-23 vascular endothelial growth factor A Mus musculus 116-152
27381866-5 2016 The atRA-induced production of vascular endothelial growth factor-A from the pancreatic islets was possibly the key factor that mediated the restoration of islet vascularity and recovery of beta-cell mass. Tretinoin 4-8 vascular endothelial growth factor A Mus musculus 31-67
27322964-0 2016 IL-33 enhances retinoic acid signaling on CD4+ T cells. Tretinoin 15-28 interleukin 33 Mus musculus 0-5
27089940-0 2016 Retinoic acid suppresses IL-17 production and pathogenic activity of gammadelta T cells in CNS autoimmunity. Tretinoin 0-13 interleukin 17A Mus musculus 25-30
27089940-4 2016 We found that RA had a dramatic suppressive effect on IL-17A and IL-17F production by gammadelta T cells stimulated with IL-1beta and IL-23. Tretinoin 14-16 interleukin 17A Mus musculus 54-60
27654415-1 2016 Purpose: Increases in retinaldehyde dehydrogenase 2 (RALDH2) transcript in the chick choroid suggest that RALDH2 may be responsible for increases observed in all-trans-retinoic acid (atRA) synthesis during recovery from myopic defocus. Tretinoin 158-181 aldehyde dehydrogenase 1 family member A2 Gallus gallus 22-51
27654415-1 2016 Purpose: Increases in retinaldehyde dehydrogenase 2 (RALDH2) transcript in the chick choroid suggest that RALDH2 may be responsible for increases observed in all-trans-retinoic acid (atRA) synthesis during recovery from myopic defocus. Tretinoin 158-181 aldehyde dehydrogenase 1 family member A2 Gallus gallus 53-59
27654415-1 2016 Purpose: Increases in retinaldehyde dehydrogenase 2 (RALDH2) transcript in the chick choroid suggest that RALDH2 may be responsible for increases observed in all-trans-retinoic acid (atRA) synthesis during recovery from myopic defocus. Tretinoin 158-181 aldehyde dehydrogenase 1 family member A2 Gallus gallus 106-112
27654415-1 2016 Purpose: Increases in retinaldehyde dehydrogenase 2 (RALDH2) transcript in the chick choroid suggest that RALDH2 may be responsible for increases observed in all-trans-retinoic acid (atRA) synthesis during recovery from myopic defocus. Tretinoin 183-187 aldehyde dehydrogenase 1 family member A2 Gallus gallus 22-51
27654415-1 2016 Purpose: Increases in retinaldehyde dehydrogenase 2 (RALDH2) transcript in the chick choroid suggest that RALDH2 may be responsible for increases observed in all-trans-retinoic acid (atRA) synthesis during recovery from myopic defocus. Tretinoin 183-187 aldehyde dehydrogenase 1 family member A2 Gallus gallus 53-59
27654415-1 2016 Purpose: Increases in retinaldehyde dehydrogenase 2 (RALDH2) transcript in the chick choroid suggest that RALDH2 may be responsible for increases observed in all-trans-retinoic acid (atRA) synthesis during recovery from myopic defocus. Tretinoin 183-187 aldehyde dehydrogenase 1 family member A2 Gallus gallus 106-112
27343556-9 2016 Moreover, inhibition of Rbpj expression partially reversed atRA-induced MEE persistence and increased P21 expression. Tretinoin 59-63 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 102-105
27343556-10 2016 These findings demonstrate that atRA inhibits MEE degradation, which in turn induces a cleft palate, possibly through the Notch1/RBPjk/P21 signaling pathway. Tretinoin 32-36 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 135-138
27307294-9 2016 All-trans retinoic acid increased CD38 levels and decreased CD55 and CD59 expression on MM cells from patients who developed daratumumab resistance, to approximately pretreatment values. Tretinoin 10-23 CD55 molecule (Cromer blood group) Homo sapiens 60-64
27256846-0 2016 The BRPF2/BRD1-MOZ complex is involved in retinoic acid-induced differentiation of embryonic stem cells. Tretinoin 42-55 bromodomain and PHD finger containing, 1 Mus musculus 4-9
27256846-3 2016 BRPF2 depletion resulted in abnormal formation of embryoid bodies, downregulation of differentiation-associated genes, and persistent maintenance of alkaline phosphatase activity even after retinoic acid-induced differentiation, indicating impaired differentiation of BRPF2-depleted ESCs. Tretinoin 190-203 bromodomain and PHD finger containing, 1 Mus musculus 0-5
27445154-8 2016 Using both gain and loss of RA signaling approaches, we show that RA signaling in brain endothelial cells can inhibit WNT-beta-catenin transcriptional activity and that this is required to moderate the expression of WNT target Sox17. Tretinoin 28-30 catenin (cadherin associated protein), beta 1 Mus musculus 122-134
27445154-8 2016 Using both gain and loss of RA signaling approaches, we show that RA signaling in brain endothelial cells can inhibit WNT-beta-catenin transcriptional activity and that this is required to moderate the expression of WNT target Sox17. Tretinoin 66-68 catenin (cadherin associated protein), beta 1 Mus musculus 122-134
27199456-2 2016 We determined whether stimulation of Npr1 by all-trans retinoic acid (RA) and histone deacetylase (HDAC) inhibitor sodium butyric acid (SB) suppress the expression of cardiac disease markers. Tretinoin 45-68 natriuretic peptide receptor 1 Mus musculus 37-41
27199456-2 2016 We determined whether stimulation of Npr1 by all-trans retinoic acid (RA) and histone deacetylase (HDAC) inhibitor sodium butyric acid (SB) suppress the expression of cardiac disease markers. Tretinoin 70-72 natriuretic peptide receptor 1 Mus musculus 37-41
28591946-10 2016 Compared to CIA model group, the protein expressions of ADAMTS-4, MMP3, MMP1 were decreased in both ATRA groups ( P<0.05). Tretinoin 100-104 matrix metallopeptidase 3 Rattus norvegicus 66-70
27191344-10 2016 Treatment of breast cancer cells with probe 4 attenuates nuclear hormone receptor activity mediated by retinoic acid, an endogenous client lipid of CRABP2. Tretinoin 103-116 cellular retinoic acid binding protein 2 Homo sapiens 148-154
27103744-10 2016 However, cotreatment with ATRA reduces Bcl6 expression to baseline levels through suppression of interleukin-6 receptor signaling. Tretinoin 26-30 BCL6 transcription repressor Homo sapiens 39-43
26829212-3 2016 METHODS: Baseline and ATRA-induced expression of RIG-I in nine (3 wild type and 6 BRAF-mutant) melanoma cell lines was measured with Q-PCR and Western blot. Tretinoin 22-26 DExD/H-box helicase 58 Homo sapiens 49-54
26829212-8 2016 RESULTS: Short-term ATRA pre-treatment increases the expression of RIG-I in BRAF-mutant melanoma cells. Tretinoin 20-24 DExD/H-box helicase 58 Homo sapiens 67-72
26950191-5 2016 Western blot analyses revealed the rapid activation of Akt (Ser473) and p70S6K (Thr389) in ATRA-treated mASCs, and that levels of phosphorylated p70S6K were noticeably reduced in HtrA1-deficient mASCs. Tretinoin 91-95 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 72-78
26950191-5 2016 Western blot analyses revealed the rapid activation of Akt (Ser473) and p70S6K (Thr389) in ATRA-treated mASCs, and that levels of phosphorylated p70S6K were noticeably reduced in HtrA1-deficient mASCs. Tretinoin 91-95 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 145-151
26950191-6 2016 Further studies using mTOR inhibitor rapamycin and siRNA specific for the p70S6K gene Rps6kb1 confirmed ATRA-mediated mASC osteogenesis as being dependent on p70S6K activation. Tretinoin 104-108 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 74-80
26950191-6 2016 Further studies using mTOR inhibitor rapamycin and siRNA specific for the p70S6K gene Rps6kb1 confirmed ATRA-mediated mASC osteogenesis as being dependent on p70S6K activation. Tretinoin 104-108 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 86-93
26950191-6 2016 Further studies using mTOR inhibitor rapamycin and siRNA specific for the p70S6K gene Rps6kb1 confirmed ATRA-mediated mASC osteogenesis as being dependent on p70S6K activation. Tretinoin 104-108 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 158-164
27104669-0 2016 alpha-Mangostin, a Natural Agent, Enhances the Response of NRAS Mutant Melanoma to Retinoic Acid. Tretinoin 83-96 NRAS proto-oncogene, GTPase Homo sapiens 59-63
27074819-0 2016 The HER2 inhibitor TAK165 Sensitizes Human Acute Myeloid Leukemia Cells to Retinoic Acid-Induced Myeloid Differentiation by activating MEK/ERK mediated RARalpha/STAT1 axis. Tretinoin 75-88 signal transducer and activator of transcription 1 Homo sapiens 161-166
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 163-167 vascular endothelial growth factor D Homo sapiens 72-78
26818829-1 2016 The regulation of vascular endothelial growth factors C (VEGF-C) and D (VEGF-D), and their receptor VEGFR3 gene and protein expression by all-trans-retinoic acid (atRA) in A549 lung cancer cells, was investigated. Tretinoin 163-167 fms related receptor tyrosine kinase 4 Homo sapiens 100-106
26818829-2 2016 We showed that atRA treatment increased VEGF-C, VEGF-D, and VEGFR3 protein and mRNA contents in dose-dependent manner. Tretinoin 15-19 vascular endothelial growth factor D Homo sapiens 48-54
26818829-2 2016 We showed that atRA treatment increased VEGF-C, VEGF-D, and VEGFR3 protein and mRNA contents in dose-dependent manner. Tretinoin 15-19 fms related receptor tyrosine kinase 4 Homo sapiens 60-66
26818829-3 2016 atRA-mediated increase of both ligands and receptor expression correlated with the elevated level of retinoic acid receptor alpha (RARalpha) expression, while the level of another atRA receptor, peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta), was decreased. Tretinoin 0-4 peroxisome proliferator activated receptor delta Homo sapiens 250-258
26934949-3 2016 Apoptosis related protein 3 (Apr3) was originally cloned from HL-60 cells induced by all-trans retinoic acid (ATRA). Tretinoin 95-108 all-trans retinoic acid induced differentiation factor Homo sapiens 0-27
26934949-3 2016 Apoptosis related protein 3 (Apr3) was originally cloned from HL-60 cells induced by all-trans retinoic acid (ATRA). Tretinoin 95-108 all-trans retinoic acid induced differentiation factor Homo sapiens 29-33
26934949-3 2016 Apoptosis related protein 3 (Apr3) was originally cloned from HL-60 cells induced by all-trans retinoic acid (ATRA). Tretinoin 110-114 all-trans retinoic acid induced differentiation factor Homo sapiens 0-27
26934949-3 2016 Apoptosis related protein 3 (Apr3) was originally cloned from HL-60 cells induced by all-trans retinoic acid (ATRA). Tretinoin 110-114 all-trans retinoic acid induced differentiation factor Homo sapiens 29-33
26582233-6 2016 We also found that RA could significantly increase the expression of LC3-II and decrease the expression of p62 both in vivo and in vitro. Tretinoin 19-21 nucleoporin 62 Homo sapiens 107-110
26678800-3 2016 In this study, the expression of a common neuronal differentiation marker [neurofilament M (NF-M)] in human SK-N-SH neuroblastoma cells treated with 10muM all-trans retinoic acid (ATRA) showed significantly increased expression in accordance with reduced cell number. Tretinoin 165-178 neurofilament medium chain Homo sapiens 75-90
26678800-3 2016 In this study, the expression of a common neuronal differentiation marker [neurofilament M (NF-M)] in human SK-N-SH neuroblastoma cells treated with 10muM all-trans retinoic acid (ATRA) showed significantly increased expression in accordance with reduced cell number. Tretinoin 165-178 neurofilament medium chain Homo sapiens 92-96
26678800-3 2016 In this study, the expression of a common neuronal differentiation marker [neurofilament M (NF-M)] in human SK-N-SH neuroblastoma cells treated with 10muM all-trans retinoic acid (ATRA) showed significantly increased expression in accordance with reduced cell number. Tretinoin 180-184 neurofilament medium chain Homo sapiens 75-90
26678800-3 2016 In this study, the expression of a common neuronal differentiation marker [neurofilament M (NF-M)] in human SK-N-SH neuroblastoma cells treated with 10muM all-trans retinoic acid (ATRA) showed significantly increased expression in accordance with reduced cell number. Tretinoin 180-184 neurofilament medium chain Homo sapiens 92-96
26678800-6 2016 In addition, ATRA-induced stimulation of NF-M at 48 and 72h was enhanced by decreasing SOD activity using siRNA directed at MnSOD. Tretinoin 13-17 neurofilament medium chain Homo sapiens 41-45
26910576-8 2016 Their data demonstrated that PHOX2B acts as a prognostic marker in neuroblastoma and that retinoic acid-induced neuronal differentiation downregulates PHOX2B expression, thereby suppressing the self-renewal capacity of neuroblastoma cells and inhibiting tumorigenicity. Tretinoin 90-103 paired like homeobox 2B Homo sapiens 151-157
26329303-0 2016 Novel insights into a retinoic-acid-induced cleft palate based on Rac1 regulation of the fibronectin arrangement. Tretinoin 22-35 Rac family small GTPase 1 Homo sapiens 66-70
26329303-5 2016 Further analysis shows that RA treatment diminishes the region-distinctive expression of Rac1 within the palatal shelves, which reversely alters the fibrillar arrangement of FN. Tretinoin 28-30 Rac family small GTPase 1 Homo sapiens 89-93
26329303-6 2016 Furthermore, RA treatment disrupts the formation of lamellipodia, which are indicative structures of cell migration that are regulated by Rac1. Tretinoin 13-15 Rac family small GTPase 1 Homo sapiens 138-142
26527258-6 2016 That this may lead to an in vivo increase in RA is suggested by the later induction by TH of the RA-responsive gene Cyp26b1. Tretinoin 45-47 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 116-123
26527258-6 2016 That this may lead to an in vivo increase in RA is suggested by the later induction by TH of the RA-responsive gene Cyp26b1. Tretinoin 97-99 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 116-123
26566904-5 2016 We determined that RA is produced by pulmonary endothelial cells and regulates pulmonary angiogenesis and elastin synthesis by induction of VEGF-A and fibroblast growth factor (FGF)-18, respectively. Tretinoin 19-21 elastin Homo sapiens 106-113
26566904-5 2016 We determined that RA is produced by pulmonary endothelial cells and regulates pulmonary angiogenesis and elastin synthesis by induction of VEGF-A and fibroblast growth factor (FGF)-18, respectively. Tretinoin 19-21 fibroblast growth factor 18 Homo sapiens 151-184
26655721-0 2016 Selective Recognition of H3.1K36 Dimethylation/H4K16 Acetylation Facilitates the Regulation of All-trans-retinoic Acid (ATRA)-responsive Genes by Putative Chromatin Reader ZMYND8. Tretinoin 95-118 zinc finger MYND-type containing 8 Homo sapiens 172-178
26655721-0 2016 Selective Recognition of H3.1K36 Dimethylation/H4K16 Acetylation Facilitates the Regulation of All-trans-retinoic Acid (ATRA)-responsive Genes by Putative Chromatin Reader ZMYND8. Tretinoin 120-124 zinc finger MYND-type containing 8 Homo sapiens 172-178
26655721-6 2016 Interestingly, ZMYND8 was found to be recruited to several developmental genes, including the all-trans-retinoic acid (ATRA)-responsive ones, through its modified histone-binding ability. Tretinoin 98-117 zinc finger MYND-type containing 8 Homo sapiens 15-21
26655721-6 2016 Interestingly, ZMYND8 was found to be recruited to several developmental genes, including the all-trans-retinoic acid (ATRA)-responsive ones, through its modified histone-binding ability. Tretinoin 119-123 zinc finger MYND-type containing 8 Homo sapiens 15-21
26643910-7 2016 Using the human neuroblastoma SH-SY5Y cell line, we demonstrate that RA increases endogenous VGF expression (P<0.05) and VGF promoter activity (P<0.0001). Tretinoin 69-71 VGF nerve growth factor inducible Homo sapiens 93-96
26643910-7 2016 Using the human neuroblastoma SH-SY5Y cell line, we demonstrate that RA increases endogenous VGF expression (P<0.05) and VGF promoter activity (P<0.0001). Tretinoin 69-71 VGF nerve growth factor inducible Homo sapiens 124-127
26129652-3 2016 Here we show that RA acts cell intrinsically in developing gut-tropic pre-mucosal dendritic cell (pre-muDC) to effect the differentiation and drive the specialization of intestinal CD103(+)CD11b(-) (cDC1) and of CD103(+)CD11b(+) (cDC2). Tretinoin 18-20 integrin subunit alpha M Homo sapiens 189-194
26129652-3 2016 Here we show that RA acts cell intrinsically in developing gut-tropic pre-mucosal dendritic cell (pre-muDC) to effect the differentiation and drive the specialization of intestinal CD103(+)CD11b(-) (cDC1) and of CD103(+)CD11b(+) (cDC2). Tretinoin 18-20 integrin subunit alpha M Homo sapiens 220-225
27795714-10 2016 Moreover, pretreatment of cultured spermatogonia with the BMP4 antagonist Noggin could inhibit RA-induced expression of these two marker genes. Tretinoin 95-97 noggin Mus musculus 74-80
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 24-26 cellular retinoic acid binding protein 2 Homo sapiens 111-140
27830505-3 2016 Partitioning RA between RARs and PPARbeta/delta is governed by different intracellular lipid-binding proteins: cellular RA binding protein 2 (CRABP2) delivers RA to nuclear RARs and a fatty acid binding protein (FABP5) delivers the hormone from the cytosol to nuclear PPARbeta/delta. Tretinoin 24-26 cellular retinoic acid binding protein 2 Homo sapiens 142-148
27830505-4 2016 Consequently, RA signals through RARs in CRABP2-expressing cells, but activates PPARbeta/delta in cells that express a high level of FABP5. Tretinoin 14-16 cellular retinoic acid binding protein 2 Homo sapiens 41-47
27830505-4 2016 Consequently, RA signals through RARs in CRABP2-expressing cells, but activates PPARbeta/delta in cells that express a high level of FABP5. Tretinoin 14-16 peroxisome proliferator activated receptor delta Homo sapiens 80-88
27830505-4 2016 Consequently, RA signals through RARs in CRABP2-expressing cells, but activates PPARbeta/delta in cells that express a high level of FABP5. Tretinoin 14-16 fatty acid binding protein 5 Homo sapiens 133-138
27830505-5 2016 RA elicits different and sometimes opposing responses in cells that express different FABP5/CRABP2 ratios because PPARbeta/delta and RARs regulate the expression of distinct sets of genes. Tretinoin 0-2 fatty acid binding protein 5 Homo sapiens 86-91
27830505-5 2016 RA elicits different and sometimes opposing responses in cells that express different FABP5/CRABP2 ratios because PPARbeta/delta and RARs regulate the expression of distinct sets of genes. Tretinoin 0-2 cellular retinoic acid binding protein 2 Homo sapiens 92-98
27830505-5 2016 RA elicits different and sometimes opposing responses in cells that express different FABP5/CRABP2 ratios because PPARbeta/delta and RARs regulate the expression of distinct sets of genes. Tretinoin 0-2 peroxisome proliferator activated receptor delta Homo sapiens 114-122
26470995-3 2015 METHODS: Zebrafish embryos were exposed to ethanol in the absence or presence of aldh1a3 or Shh morpholino oligonucleotides (MOs), which disrupt retinoic acid (RA) or sonic hedgehog (Shh) function, respectively. Tretinoin 145-158 sonic hedgehog signaling molecule a Danio rerio 92-95
26618989-4 2015 We find that early embryonic rbp7a expression is negatively regulated by the Nodal/FoxH1-signaling pathway and we show that Nodal/FoxH1 activity has the opposite effect on aldh1a2, which encodes the major enzyme for early embryonic retinoic acid production. Tretinoin 232-245 forkhead box H1 Danio rerio 130-135
26609166-7 2015 Moreover, in neuromast, RA pathway regulates the transcription of p27(kip) and sox2 in supporting cells but not fgf3. Tretinoin 24-26 cyclin-dependent kinase inhibitor 1Bb Danio rerio 66-69
26609166-15 2015 RA pathway is activated very early upon hair cell loss, promotes cell proliferation of progenitor cells, and regulates two key genes, p27(kip) and sox2. Tretinoin 0-2 cyclin-dependent kinase inhibitor 1Bb Danio rerio 134-137
26165862-4 2015 The effect of the concentration of a strong sonic hedgehog (Shh) agonist (smoothened agonist [SAG]) and retinoic acid (RA) on expression of progenitor p3 and postmitotic V3 IN transcription factor markers (ie, Nkx2.2 and Sim1) was examined. Tretinoin 104-117 exosome component 10 Mus musculus 151-172
26556479-0 2015 Retinoic Acid Ameliorates Pancreatic Fibrosis and Inhibits the Activation of Pancreatic Stellate Cells in Mice with Experimental Chronic Pancreatitis via Suppressing the Wnt/beta-Catenin Signaling Pathway. Tretinoin 0-13 catenin (cadherin associated protein), beta 1 Mus musculus 174-186
26556479-6 2015 Suppression of pancreatic fibrosis upon administration of RA was confirmed based on reduction of histological damage, alpha-smooth muscle actin (alpha-SMA) expression and mRNA levels of beta-catenin, platelet-derived growth factor (PDGF)-Rbeta transforming growth factor (TGF)-betaRII and collagen 1alpha1 in vivo. Tretinoin 58-60 catenin (cadherin associated protein), beta 1 Mus musculus 186-198
26556479-8 2015 Nuclear translation of beta-catenin was significantly decreased following RA treatment, compared with cerulein-induced CP in mice and activated PSCs. Tretinoin 74-76 catenin (cadherin associated protein), beta 1 Mus musculus 23-35
26556479-10 2015 These results indicate a critical role of the Wnt/beta-catenin signaling pathway in RA-induced effects on CP and PSC regulation and support the potential of RA as a suppressor of pancreatic fibrosis in mice. Tretinoin 84-86 catenin (cadherin associated protein), beta 1 Mus musculus 50-62
26427713-8 2015 Induction of HWJMSCs with TCC in the presence of RA resulted in significant upregulation (P <= 0.05) of all germ cell-specific genes (c-Kit 2.6795 +- 0.75, DDX4 4.3188 +- 1.18, Piwil2 4.9962 +- 1.55, Dazl 6.1199 +- 0.78) compared to control and PCC + RA. Tretinoin 49-51 piwi like RNA-mediated gene silencing 2 Homo sapiens 180-186
26397153-10 2015 Further upregulating of CD11b expression and differential morphological changes were found in NB4-R1 cells with restored C/EBPalpha P42 after ATRA treatment. Tretinoin 142-146 integrin subunit alpha M Homo sapiens 24-29
26397460-8 2015 Knockdown of OTX2 expression by siRNA or pharmacologic inhibition by all-trans retinoic acid (ATRA) repressed OTX2 expression and cell proliferation and significantly decreased tumor growth in vivo. Tretinoin 79-92 orthodenticle homeobox 2 Homo sapiens 110-114
26397460-8 2015 Knockdown of OTX2 expression by siRNA or pharmacologic inhibition by all-trans retinoic acid (ATRA) repressed OTX2 expression and cell proliferation and significantly decreased tumor growth in vivo. Tretinoin 94-98 orthodenticle homeobox 2 Homo sapiens 13-17
26397460-8 2015 Knockdown of OTX2 expression by siRNA or pharmacologic inhibition by all-trans retinoic acid (ATRA) repressed OTX2 expression and cell proliferation and significantly decreased tumor growth in vivo. Tretinoin 94-98 orthodenticle homeobox 2 Homo sapiens 110-114
26775483-1 2015 OBJECTIVE: To observe the expression of phospholipid scramblase 1 (PLSCR1) in matrine (MAT) induced differentiation of all-trans retinoic acid (ATRA) resistant acute promyelocytic leukemia (APL) cells, and to explore its correlation to cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signal pathway. Tretinoin 119-142 phospholipid scramblase 1 Homo sapiens 40-65
26775483-1 2015 OBJECTIVE: To observe the expression of phospholipid scramblase 1 (PLSCR1) in matrine (MAT) induced differentiation of all-trans retinoic acid (ATRA) resistant acute promyelocytic leukemia (APL) cells, and to explore its correlation to cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signal pathway. Tretinoin 119-142 phospholipid scramblase 1 Homo sapiens 67-73
26775483-1 2015 OBJECTIVE: To observe the expression of phospholipid scramblase 1 (PLSCR1) in matrine (MAT) induced differentiation of all-trans retinoic acid (ATRA) resistant acute promyelocytic leukemia (APL) cells, and to explore its correlation to cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signal pathway. Tretinoin 144-148 phospholipid scramblase 1 Homo sapiens 40-65
26775483-1 2015 OBJECTIVE: To observe the expression of phospholipid scramblase 1 (PLSCR1) in matrine (MAT) induced differentiation of all-trans retinoic acid (ATRA) resistant acute promyelocytic leukemia (APL) cells, and to explore its correlation to cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signal pathway. Tretinoin 144-148 phospholipid scramblase 1 Homo sapiens 67-73
26775483-6 2015 RESULTS: MAT combined ATRA could significantly elevate positive rates of NBT and CD11 b in NB4-R1 cells, and significantly down-regulate the expression of PML/RARapha-fusion protein/gene (P < 0.05, P < 0.01). Tretinoin 22-26 integrin subunit alpha M Homo sapiens 81-87
26775483-13 2015 CONCLUSION: MAT combined ATRA could significantly induce the differentiation of NB4-R1 cells, and inhibit the expression of PML/RARalpha fusion gene/protein, which might be associated with up-regulating PLSCR1 expression. Tretinoin 25-29 phospholipid scramblase 1 Homo sapiens 203-209
26269506-8 2015 Cultured prepubertal rat peritubular cells also expressed SF-1 and PTCH1, but Cyp11a1 was expressed only after treatment with cAMP and retinoic acid. Tretinoin 135-148 cytochrome P450, family 11, subfamily a, polypeptide 1 Rattus norvegicus 78-85
26427057-4 2015 We also show that ATRA activates RAR and RXR bound to a conserved regulatory region to increase expression of the SALL4A transcription factor in spermatogonia. Tretinoin 18-22 retinoic acid receptor, alpha Mus musculus 33-36
26566473-6 2015 In promyelocytic NB4 cells, EGR1 levels were increased by D3, while Gfi-1 expression (which promotes the granulocytic lineage) was upregulated during D3-induced monocytic differentiation in HL60, and by RA treatment in monocytic U937 cells. Tretinoin 203-205 growth factor independent 1 transcriptional repressor Homo sapiens 68-73
26276871-1 2015 In the present study, we aimed at identifying the mechanisms whereby the vitamin A metabolite all-trans retinoic acid (RA) promotes the formation of plasma cells upon stimulation of B cells via the innate immunity receptors TLR9 and RP105. Tretinoin 104-117 CD180 molecule Homo sapiens 233-238
26276871-1 2015 In the present study, we aimed at identifying the mechanisms whereby the vitamin A metabolite all-trans retinoic acid (RA) promotes the formation of plasma cells upon stimulation of B cells via the innate immunity receptors TLR9 and RP105. Tretinoin 119-121 CD180 molecule Homo sapiens 233-238
26287738-2 2015 demonstrated that in the presence of IL-15, retinoic acid can act as an adjuvant and promote inflammation against dietary proteins. Tretinoin 44-57 interleukin 15 Homo sapiens 37-42
25931453-3 2015 Moreover, patients with APL carrying the PLZF-RARalpha fusion protein are partially resistant to ATRA treatment. Tretinoin 97-101 zinc finger and BTB domain containing 16 Homo sapiens 41-45
25931453-3 2015 Moreover, patients with APL carrying the PLZF-RARalpha fusion protein are partially resistant to ATRA treatment. Tretinoin 97-101 retinoic acid receptor, alpha Mus musculus 46-54
26035122-5 2015 RESULTS: Retinoic acid treatment reduces the expression of pancreatic stem cell markers CD24, CD44, CD133, and aldehyde dehydrogenase 1 but not c-Met. Tretinoin 9-22 CD44 molecule (Indian blood group) Homo sapiens 94-98
26225425-0 2015 All-Trans Retinoic Acid Induces TGF-beta2 in Intestinal Epithelial Cells via RhoA- and p38alpha MAPK-Mediated Activation of the Transcription Factor ATF2. Tretinoin 10-23 transforming growth factor beta 2 Homo sapiens 32-41
26225425-0 2015 All-Trans Retinoic Acid Induces TGF-beta2 in Intestinal Epithelial Cells via RhoA- and p38alpha MAPK-Mediated Activation of the Transcription Factor ATF2. Tretinoin 10-23 activating transcription factor 2 Homo sapiens 149-153
26225425-2 2015 The present study was designed to investigate all-trans retinoic acid (atRA) as an inducer of TGF-beta2 in intestinal epithelial cells (IECs) and to elucidate the involved signaling mechanisms. Tretinoin 46-69 transforming growth factor beta 2 Homo sapiens 94-103
26225425-2 2015 The present study was designed to investigate all-trans retinoic acid (atRA) as an inducer of TGF-beta2 in intestinal epithelial cells (IECs) and to elucidate the involved signaling mechanisms. Tretinoin 71-75 transforming growth factor beta 2 Homo sapiens 94-103
26225425-9 2015 CONCLUSIONS: AtRA induces TGF-beta2 expression in IECs via RhoA- and p38alpha MAPK-mediated activation of the transcription factor ATF2. Tretinoin 13-17 transforming growth factor beta 2 Homo sapiens 26-35
26186635-7 2015 The anti-apoptotic effects of ATRA were associated with partial inhibition of reactive oxygen species (ROS) production and significantly less phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, JNK, and ERK. Tretinoin 30-34 mitogen-activated protein kinase 8 Mus musculus 218-221
26023078-5 2015 The activity of RALDH2 in MMD ECFCs was assessed by in vitro tube formation assay and in vivo Matrigel plug assay in the presence of all-trans retinoic acid. Tretinoin 143-156 aldehyde dehydrogenase 1 family member A2 Homo sapiens 16-22
25738595-9 2015 The present study demonstrated that ATRA decreases the chondrogenesis of rEHBMCs by inhibiting cartilage-specific molecules, including aggrecan, Sox9 and Col2al, via regulating the expression of p53 and p21. Tretinoin 36-40 SRY-box transcription factor 9 Rattus norvegicus 145-149
25738595-9 2015 The present study demonstrated that ATRA decreases the chondrogenesis of rEHBMCs by inhibiting cartilage-specific molecules, including aggrecan, Sox9 and Col2al, via regulating the expression of p53 and p21. Tretinoin 36-40 KRAS proto-oncogene, GTPase Rattus norvegicus 203-206
25827071-4 2015 The potential of ATRA to stabilize p53 was almost completely abolished by knock-down of p14 in HepG2 cells and was not observed in p14-negative A549 cells. Tretinoin 17-21 ribonuclease P/MRP subunit p14 Homo sapiens 88-91
25827071-7 2015 Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis. Tretinoin 91-95 DNA methyltransferase 1 Homo sapiens 22-45
25827071-7 2015 Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis. Tretinoin 91-95 ribonuclease P/MRP subunit p14 Homo sapiens 112-115
25827071-7 2015 Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis. Tretinoin 91-95 MDM2 proto-oncogene Homo sapiens 116-120
25827071-8 2015 Therefore, we conclude that ATRA induces p14 promoter hypomethylation to trigger apoptosis. Tretinoin 28-32 ribonuclease P/MRP subunit p14 Homo sapiens 41-44
26065685-7 2015 However, CD11b expression induced by ATRA in HL60 cells was decreased by radotinib through upregulation of LYN. Tretinoin 37-41 integrin subunit alpha M Homo sapiens 9-14
26065685-9 2015 Radotinib also increased apoptosis of CD11b+ HL60 cells when they were differentiated by ATRA/dasatinib treatment. Tretinoin 89-93 integrin subunit alpha M Homo sapiens 38-43
26057209-6 2015 Concordantly, Trim71(-/-) mES show increased neural marker expression following treatment with retinoic acid. Tretinoin 95-108 tripartite motif-containing 71 Mus musculus 14-20
25753732-0 2015 The orphan GPCR, Gpr161, regulates the retinoic acid and canonical Wnt pathways during neurulation. Tretinoin 39-52 G protein-coupled bile acid receptor 1 Mus musculus 11-15
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein 1 Mus musculus 32-37
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein 12B Mus musculus 191-198
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock protein 14 Mus musculus 200-206
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 120-133 heat shock 105kDa/110kDa protein 1 Mus musculus 219-225
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein 1 Mus musculus 32-37
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein 12B Mus musculus 191-198
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock protein 14 Mus musculus 200-206
25352652-2 2015 Our previous studies found that Hsp25, HspB2, HspB3, HspB7, Hsp20, HspB9, HspB10, and Hsp40 may be related to all-trans retinoic acid (atRA)-induced phocomelic and other abnormalities, while HspA12B, HspA14, Trap1, and Hsp105 may be forelimb development-related genes; Grp78 may play an important role in forelimb development. Tretinoin 135-139 heat shock 105kDa/110kDa protein 1 Mus musculus 219-225
25929424-6 2015 All-trans retinoic acid, a derivative of vitamin A, reverses these effects, resulting in increased insulin sensitivity, suppression of the phosphoenolpyruvate carboxy kinase (PEPCK) gene, and the induction of the glucokinase gene. Tretinoin 0-23 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 139-173
25929424-6 2015 All-trans retinoic acid, a derivative of vitamin A, reverses these effects, resulting in increased insulin sensitivity, suppression of the phosphoenolpyruvate carboxy kinase (PEPCK) gene, and the induction of the glucokinase gene. Tretinoin 0-23 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 175-180
25929424-6 2015 All-trans retinoic acid, a derivative of vitamin A, reverses these effects, resulting in increased insulin sensitivity, suppression of the phosphoenolpyruvate carboxy kinase (PEPCK) gene, and the induction of the glucokinase gene. Tretinoin 0-23 glucokinase Homo sapiens 213-224
25515249-9 2015 RA significantly enhanced the expression of aquaporin 5 (AQP5). Tretinoin 0-2 aquaporin 5 Rattus norvegicus 44-55
25515249-9 2015 RA significantly enhanced the expression of aquaporin 5 (AQP5). Tretinoin 0-2 aquaporin 5 Rattus norvegicus 57-61
25727910-4 2015 RA induced neurite outgrowth of SH-SY5Y cells with an increase in DAergic neuron-like properties, including up-regulation of tyrosine hydroxylase, dopamine transporter, and vesicular monoamine transporter 2. Tretinoin 0-2 solute carrier family 6 member 3 Homo sapiens 147-167
25510432-4 2015 In contrast to other NUP98 fusions, cells transformed by the NUP98-RARG fusion were extremely sensitive to all-trans retinoic acid (ATRA) treatment. Tretinoin 132-136 retinoic acid receptor, gamma Mus musculus 67-71
25546009-7 2015 Remarkably, the reprogramming of epiblast stem cells into embryonic stem cell-like cells also requires low levels of RA, which can modulate Wnt signalling through physical interactions of RARs with beta-catenin. Tretinoin 117-119 catenin (cadherin associated protein), beta 1 Mus musculus 198-210
25737450-0 2015 Knockdown of SALL4 Protein Enhances All-trans Retinoic Acid-induced Cellular Differentiation in Acute Myeloid Leukemia Cells. Tretinoin 46-59 spalt like transcription factor 4 Homo sapiens 13-18
25737450-3 2015 Here we explored the effect of SALL4, a stem cell factor, on ATRA-induced AML differentiation in both ATRA-sensitive and ATRA-resistant AML cells. Tretinoin 61-65 spalt like transcription factor 4 Homo sapiens 31-36
24909169-4 2015 Retinoic acid-mediated differentiation of neuroblastoma restored CYLD expression and promoted SUMOylation of CYLD. Tretinoin 0-13 CYLD lysine 63 deubiquitinase Homo sapiens 65-69
24909169-4 2015 Retinoic acid-mediated differentiation of neuroblastoma restored CYLD expression and promoted SUMOylation of CYLD. Tretinoin 0-13 CYLD lysine 63 deubiquitinase Homo sapiens 109-113
24909169-6 2015 Overexpression of non-SUMOylatable mutant CYLD in neuroblastoma cells reduced retinoic acid-induced NF-kappaB activation and differentiation of cells, but instead promoted cell death. Tretinoin 78-91 CYLD lysine 63 deubiquitinase Homo sapiens 42-46
25724646-8 2015 Once the increased retinoic acid level in the foxc1a null embryos was reduced by knocking down aldh1a2, the reduced expression of myod1 was partially rescued by resuming expressions of fgf8a and deltaC in the somites of the mutant embryos. Tretinoin 19-32 forkhead box C1a Danio rerio 46-52
25724646-8 2015 Once the increased retinoic acid level in the foxc1a null embryos was reduced by knocking down aldh1a2, the reduced expression of myod1 was partially rescued by resuming expressions of fgf8a and deltaC in the somites of the mutant embryos. Tretinoin 19-32 myogenic differentiation 1 Danio rerio 130-135
25477000-7 2015 Furthermore, we have identified a novel pathway involving all-trans retinoic acid (ATRA) and its receptor (RARgamma) signaling that inhibits type I NKT cells and, consequently, ALD. Tretinoin 68-81 retinoic acid receptor, gamma Mus musculus 107-115
26064333-1 2015 OBJECTIVE: This study was to investigate the effects of all-trans retinoic acid (ATRA) in combination with Genistein on the proliferation, expression of apoptosis related proteins and adhesion molecules (MUC1 and ICAM-1) and invasiveness of A549 cells, aiming to investigate whether combined therapy of ATRA and Genistein is superior to monotherapy in suppressing metastasis of lung cancer cells. Tretinoin 81-85 intercellular adhesion molecule 1 Homo sapiens 213-219
26064333-5 2015 RESULTS: Combined treatment with ATRA and Genistein was able to reduce the expressions of Bcl-2, MUC1 and ICAM-1 and exerted synergistic effects to inhibit the invasion of A549 cells. Tretinoin 33-37 intercellular adhesion molecule 1 Homo sapiens 106-112
26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 intercellular adhesion molecule 1 Homo sapiens 68-74
25677622-0 2015 Retinoic acid inhibits histone methyltransferase Whsc1 during palatogenesis. Tretinoin 0-13 nuclear receptor binding SET domain protein 2 Mus musculus 49-54
25805962-7 2015 RESULTS: ATRA (100 nM) induced granulocytic differentiation (upregulation of CD11b and downregulation of CD34) and the effect was potentiated by addition of G-CSF, while G-CSF alone had no effect on HT93A cells. Tretinoin 9-13 integrin subunit alpha M Homo sapiens 77-82
25557119-10 2015 However, when the differentiation of NB cell lines was induced by the use of all-trans retinoic acid, there was a corresponding decrease in PES1 expression. Tretinoin 87-100 pescadillo ribosomal biogenesis factor 1 Mus musculus 140-144
25504116-3 2015 In ESCs, Snai1 does not respond to TGFbeta or BMP4 signaling but it is induced by retinoic acid treatment, which induces the binding, on the Snai1 promoter, of the retinoid receptors RARgamma and RXRalpha, the dissociation of the Polycomb repressor complex 2 which results in the decrease of H3K27me3, and the increase of histone H3K4me3. Tretinoin 82-95 retinoid X receptor alpha Homo sapiens 196-204
25568183-7 2015 Hence, beta-catenin/TCF4 signaling induces local regulatory DC and regulatory T-cell phenotypes via the RA pathway, identifying this pathway as an important target for anticancer immunotherapy. Tretinoin 104-106 catenin (cadherin associated protein), beta 1 Mus musculus 7-19
25658587-9 2015 Alcohol dehydrogenase 5 (ADH5) and aldehyde dehydrogenase 1 family member A1 (ALDH1A1) are involved in RA synthesis in the cell. Tretinoin 103-105 alcohol dehydrogenase 4 (class II), pi polypeptide Gallus gallus 0-23
25658587-9 2015 Alcohol dehydrogenase 5 (ADH5) and aldehyde dehydrogenase 1 family member A1 (ALDH1A1) are involved in RA synthesis in the cell. Tretinoin 103-105 alcohol dehydrogenase 4 (class II), pi polypeptide Gallus gallus 25-29
25502770-3 2015 While ALDH1A1, ALDH1A2, and ALDH1A3 all form RA, the expression pattern and relative contribution of these enzymes to RA formation in the testis is unknown. Tretinoin 45-47 aldehyde dehydrogenase 1 family member A2 Homo sapiens 15-22
25502770-7 2015 In the absence of cellular retinol binding protein (CRBP)1, ALDH1A1 was predicted to be the main contributor to intratesticular RA formation, but when CRBP1 was present, ALDH1A2 was predicted to be equally important in RA formation as ALDH1A1. Tretinoin 219-221 aldehyde dehydrogenase 1 family member A2 Homo sapiens 170-177
25973309-7 2015 HMGB1 regulated the interactions between ubiquitin-binding adaptor protein p62/SQSTM and PML-RARalpha so as to affect the degradation of PML-RARalpha during ATRA-induced autophagy. Tretinoin 157-161 sequestosome 1 Homo sapiens 75-78
25481858-3 2015 ATRA/RA induced expression of CD11b in the BMC of the APL patient and in NB4 cells, but not in normal BMC or PBMC. Tretinoin 0-4 integrin subunit alpha M Homo sapiens 30-35
25595247-0 2015 Retinoic acid enhances the levels of IL-10 in TLR-stimulated B cells from patients with relapsing-remitting multiple sclerosis. Tretinoin 0-13 interleukin 10 Homo sapiens 37-42
25595247-3 2015 Importantly, RA enhanced the secretion of IL-10 by MS-derived B cells without affecting the levels of the pro-inflammatory cytokine TNF-alpha. Tretinoin 13-15 interleukin 10 Homo sapiens 42-47
25427913-6 2015 RA is synthesized from retinaldehyde by the retinaldehyde dehydrogenases, specifically ALDH1A1, ALDH1A2, ALDH1A3, and ALDH8A1. Tretinoin 0-2 aldehyde dehydrogenase 1 family member A2 Homo sapiens 96-103
25427913-6 2015 RA is synthesized from retinaldehyde by the retinaldehyde dehydrogenases, specifically ALDH1A1, ALDH1A2, ALDH1A3, and ALDH8A1. Tretinoin 0-2 aldehyde dehydrogenase 8 family member A1 Homo sapiens 118-125
24768681-8 2015 Such a strategy revealed that RA-induced neuronal differentiation involves the RARgamma2 subtype and requires RARgamma2 phosphorylation. Tretinoin 30-32 retinoic acid receptor, gamma Mus musculus 79-88
24768681-8 2015 Such a strategy revealed that RA-induced neuronal differentiation involves the RARgamma2 subtype and requires RARgamma2 phosphorylation. Tretinoin 30-32 retinoic acid receptor, gamma Mus musculus 110-119
25380237-3 2015 Previously, we found that all-trans retinoic acid (RA) induced the expression of differentiation markers and a truncated form of platelet-derived growth factor receptor (PDGFR)beta in rat gonocytes, as well as in F9 mouse embryonal carcinoma cells, an embryonic stem cell-surrogate that expresses somatic lineage markers in response to RA. Tretinoin 36-49 platelet derived growth factor receptor beta Rattus norvegicus 170-180
25380237-3 2015 Previously, we found that all-trans retinoic acid (RA) induced the expression of differentiation markers and a truncated form of platelet-derived growth factor receptor (PDGFR)beta in rat gonocytes, as well as in F9 mouse embryonal carcinoma cells, an embryonic stem cell-surrogate that expresses somatic lineage markers in response to RA. Tretinoin 51-53 platelet derived growth factor receptor beta Rattus norvegicus 170-180
25380237-7 2015 Inhibiting PDGFR kinase activity reduced RA-induced Stra8 expression. Tretinoin 41-43 stimulated by retinoic acid 8 Rattus norvegicus 52-57
25380237-10 2015 RA receptor-alpha inhibition partially reduced RA effects on Stra8 in gonocytes, indicating that RA acts in part via RA receptor-alpha. Tretinoin 0-2 stimulated by retinoic acid 8 Rattus norvegicus 61-66
25380237-10 2015 RA receptor-alpha inhibition partially reduced RA effects on Stra8 in gonocytes, indicating that RA acts in part via RA receptor-alpha. Tretinoin 47-49 stimulated by retinoic acid 8 Rattus norvegicus 61-66
25380237-11 2015 RA-induced gonocyte differentiation was significantly reduced by inhibiting SRC (v-src avian sarcoma [Schmidt-Ruppin A-2] viral oncogene) and JAK2/STAT5 (Janus kinase 2/signal transducer and activator of transcription 5) activities, implying that these signaling molecules play a role in gonocyte differentiation. Tretinoin 0-2 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 76-79
25380237-11 2015 RA-induced gonocyte differentiation was significantly reduced by inhibiting SRC (v-src avian sarcoma [Schmidt-Ruppin A-2] viral oncogene) and JAK2/STAT5 (Janus kinase 2/signal transducer and activator of transcription 5) activities, implying that these signaling molecules play a role in gonocyte differentiation. Tretinoin 0-2 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 83-86
25380237-11 2015 RA-induced gonocyte differentiation was significantly reduced by inhibiting SRC (v-src avian sarcoma [Schmidt-Ruppin A-2] viral oncogene) and JAK2/STAT5 (Janus kinase 2/signal transducer and activator of transcription 5) activities, implying that these signaling molecules play a role in gonocyte differentiation. Tretinoin 0-2 Janus kinase 2 Rattus norvegicus 142-146
25864812-7 2015 A descending trend in nestin and an ascending trend in MAP2, GAD, and GABA expression were observed from the first day until the last day between different concentrations of retinoic acid. Tretinoin 174-187 microtubule associated protein 2 Homo sapiens 55-59
25864812-7 2015 A descending trend in nestin and an ascending trend in MAP2, GAD, and GABA expression were observed from the first day until the last day between different concentrations of retinoic acid. Tretinoin 174-187 glutamate decarboxylase 1 Homo sapiens 61-64
25721651-1 2015 BACKGROUND/AIM: Vitamin A (all- trans -retinol, ATRol) serves as a precursor for all- trans -retinoic acid (ATRA), a ligand for the retinoic acid receptor (RAR), representing a potent regulator for many physiological processes. Tretinoin 81-106 retinoic acid receptor, alpha Mus musculus 132-154
25721651-1 2015 BACKGROUND/AIM: Vitamin A (all- trans -retinol, ATRol) serves as a precursor for all- trans -retinoic acid (ATRA), a ligand for the retinoic acid receptor (RAR), representing a potent regulator for many physiological processes. Tretinoin 81-106 retinoic acid receptor, alpha Mus musculus 156-159
25721651-1 2015 BACKGROUND/AIM: Vitamin A (all- trans -retinol, ATRol) serves as a precursor for all- trans -retinoic acid (ATRA), a ligand for the retinoic acid receptor (RAR), representing a potent regulator for many physiological processes. Tretinoin 108-112 retinoic acid receptor, alpha Mus musculus 132-154
25721651-1 2015 BACKGROUND/AIM: Vitamin A (all- trans -retinol, ATRol) serves as a precursor for all- trans -retinoic acid (ATRA), a ligand for the retinoic acid receptor (RAR), representing a potent regulator for many physiological processes. Tretinoin 108-112 retinoic acid receptor, alpha Mus musculus 156-159
25034783-3 2014 Levels of p62/SQSTM1 mRNA and protein were both significantly increased during all-trans retinoic acid (ATRA)-induced differentiation of AML cells through a mechanism that depends on NF-kappaB activation. Tretinoin 89-102 sequestosome 1 Homo sapiens 10-13
25034783-3 2014 Levels of p62/SQSTM1 mRNA and protein were both significantly increased during all-trans retinoic acid (ATRA)-induced differentiation of AML cells through a mechanism that depends on NF-kappaB activation. Tretinoin 89-102 sequestosome 1 Homo sapiens 14-20
25034783-3 2014 Levels of p62/SQSTM1 mRNA and protein were both significantly increased during all-trans retinoic acid (ATRA)-induced differentiation of AML cells through a mechanism that depends on NF-kappaB activation. Tretinoin 104-108 sequestosome 1 Homo sapiens 10-13
25034783-3 2014 Levels of p62/SQSTM1 mRNA and protein were both significantly increased during all-trans retinoic acid (ATRA)-induced differentiation of AML cells through a mechanism that depends on NF-kappaB activation. Tretinoin 104-108 sequestosome 1 Homo sapiens 14-20
25034783-5 2014 Interestingly, ATRA-induced p62/SQSTM1 upregulation was impaired in maturation-resistant AML cells but was reactivated when differentiation was restored in these cells. Tretinoin 15-19 sequestosome 1 Homo sapiens 28-31
25034783-5 2014 Interestingly, ATRA-induced p62/SQSTM1 upregulation was impaired in maturation-resistant AML cells but was reactivated when differentiation was restored in these cells. Tretinoin 15-19 sequestosome 1 Homo sapiens 32-38
24846581-8 2014 Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-beta1 (all p < 0.05). Tretinoin 37-41 NPHS1 adhesion molecule, nephrin Homo sapiens 106-113
24292673-0 2014 ZRF1 controls the retinoic acid pathway and regulates leukemogenic potential in acute myeloid leukemia. Tretinoin 18-31 DnaJ heat shock protein family (Hsp40) member C2 Homo sapiens 0-4
24292673-4 2014 Treatment with retinoic acid (RA), a differentiating agent currently used to treat certain AMLs, leads to a functional switch of ZRF1 from a negative regulator to an activator of differentiation. Tretinoin 15-28 DnaJ heat shock protein family (Hsp40) member C2 Homo sapiens 129-133
24292673-4 2014 Treatment with retinoic acid (RA), a differentiating agent currently used to treat certain AMLs, leads to a functional switch of ZRF1 from a negative regulator to an activator of differentiation. Tretinoin 30-32 DnaJ heat shock protein family (Hsp40) member C2 Homo sapiens 129-133
24292673-8 2014 Finally, ZRF1 knockdown cooperates with RA treatment in leukemia suppression in vivo. Tretinoin 40-42 DnaJ heat shock protein family (Hsp40) member C2 Homo sapiens 9-13
25403085-9 2014 CONCLUSIONS: According to our modeling of metabolic and signalization pathways using differentially expressed genes we have identified a network with major nodes (including Sirt3, Il1b, Cpt1b and Pparg) likely to underlie the observed strain specific response to ATRA. Tretinoin 263-267 peroxisome proliferator-activated receptor gamma Rattus norvegicus 196-201
25389900-6 2014 Retinoic acid, the main biologically active form of vitamin A, influences the expression of collagens, laminins, entactin, fibronectin, elastin and proteoglycans, which are the major components of the extracellular matrix. Tretinoin 0-13 elastin Homo sapiens 136-143
25014134-0 2014 Retinoic acid regulates several genes in bile acid and lipid metabolism via upregulation of small heterodimer partner in hepatocytes. Tretinoin 0-13 nuclear receptor subfamily 0, group B, member 2 Mus musculus 92-117
25014134-3 2014 In our previous studies, we have demonstrated the involvement of small heterodimer partner (SHP) in RA-induced signaling in a non-transformed hepatic cell line AML 12. Tretinoin 100-102 nuclear receptor subfamily 0, group B, member 2 Mus musculus 65-90
25014134-3 2014 In our previous studies, we have demonstrated the involvement of small heterodimer partner (SHP) in RA-induced signaling in a non-transformed hepatic cell line AML 12. Tretinoin 100-102 nuclear receptor subfamily 0, group B, member 2 Mus musculus 92-95
25014134-4 2014 In the present study, we have identified several critical genes in lipid homeostasis (Apoa1, Apoa2 and ApoF) that are repressed by RA-treatment in a SHP dependent manner, in vitro and also in vivo with the use of the SHP null mice. Tretinoin 131-133 apolipoprotein A-I Mus musculus 86-91
25014134-4 2014 In the present study, we have identified several critical genes in lipid homeostasis (Apoa1, Apoa2 and ApoF) that are repressed by RA-treatment in a SHP dependent manner, in vitro and also in vivo with the use of the SHP null mice. Tretinoin 131-133 nuclear receptor subfamily 0, group B, member 2 Mus musculus 149-152
25014134-4 2014 In the present study, we have identified several critical genes in lipid homeostasis (Apoa1, Apoa2 and ApoF) that are repressed by RA-treatment in a SHP dependent manner, in vitro and also in vivo with the use of the SHP null mice. Tretinoin 131-133 nuclear receptor subfamily 0, group B, member 2 Mus musculus 217-220
25014134-5 2014 In a similar manner, RA also represses several critical genes involved in bile acid metabolism (Cyp7a1, Cyp8b1, Mdr2, Bsep, Baat and Ntcp) via upregulation of SHP. Tretinoin 21-23 nuclear receptor subfamily 0, group B, member 2 Mus musculus 159-162
25014134-6 2014 Collectively our data suggest that SHP plays a major role in RA-induced potential changes in pathophysiology of metabolic disorders in the liver. Tretinoin 61-63 nuclear receptor subfamily 0, group B, member 2 Mus musculus 35-38
24436055-6 2014 Furthermore, we demonstrated that the binding of the protein complex including RACK1 to the SCN1A promoter motif was decreased in neuron-like differentiation of the NT2 cells induced by retinoic acid and resulted in the upregulation of SCN1A transcription. Tretinoin 186-199 receptor for activated C kinase 1 Homo sapiens 79-84
24436055-7 2014 Taken together, this study reports a novel role of RACK1 in regulating SCN1A expression that participates in retinoic acid-induced neuronal differentiation of NT2 cells. Tretinoin 109-122 receptor for activated C kinase 1 Homo sapiens 51-56
25135475-5 2014 Here, we demonstrate that the HOXA locus is organized by CTCF into chromatin loops and that CTCF depletion causes significantly enhanced activation of HOXA3 to -A7, -A9 to -A11, and -A13 in response to retinoic acid, with the highest effect observed for HOXA9. Tretinoin 202-215 CCCTC-binding factor Homo sapiens 57-61
25135475-5 2014 Here, we demonstrate that the HOXA locus is organized by CTCF into chromatin loops and that CTCF depletion causes significantly enhanced activation of HOXA3 to -A7, -A9 to -A11, and -A13 in response to retinoic acid, with the highest effect observed for HOXA9. Tretinoin 202-215 CCCTC-binding factor Homo sapiens 92-96
25240927-4 2014 These cells display morphological characteristics and express markers of the epicardial lineage, including the transcription factors WT1 and TBX18 and the retinoic acid-producing enzyme ALDH1A2. Tretinoin 155-168 aldehyde dehydrogenase 1 family member A2 Homo sapiens 186-193
25245097-10 2014 Furthermore, significant NEAT1 upregulation was observed during all-trans retinoic acid (ATRA)-induced NB4 cell differentiation. Tretinoin 74-87 nuclear paraspeckle assembly transcript 1 Homo sapiens 25-30
25245097-10 2014 Furthermore, significant NEAT1 upregulation was observed during all-trans retinoic acid (ATRA)-induced NB4 cell differentiation. Tretinoin 89-93 nuclear paraspeckle assembly transcript 1 Homo sapiens 25-30
25245097-12 2014 We show that reduction of NEAT1 by small interfering RNA (siRNA) blocks ATRA-induced differentiation. Tretinoin 72-76 nuclear paraspeckle assembly transcript 1 Homo sapiens 26-31
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 cyclin-dependent kinase 2 Mus musculus 155-159
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 proliferating cell nuclear antigen Mus musculus 161-167
25087568-4 2014 DNA binding data revealed that RA receptors retinoic acid receptor beta (RARbeta) and retinoid x receptor alpha (RXRalpha) bound to cell cycle genes Cdk1, Cdk2, Cyclin B, Cyclin E, and Cdc25a in mice with and without RA treatment. Tretinoin 31-33 proliferating cell nuclear antigen Mus musculus 171-177
25087568-5 2014 In addition, RA treatment induced novel binding of RARbeta/RXRalpha to Cdk1, Cdk2, Cyclin D, and Cdk6 genes. Tretinoin 13-15 cyclin-dependent kinase 2 Mus musculus 77-81
25087568-5 2014 In addition, RA treatment induced novel binding of RARbeta/RXRalpha to Cdk1, Cdk2, Cyclin D, and Cdk6 genes. Tretinoin 13-15 proliferating cell nuclear antigen Mus musculus 83-89
25087568-8 2014 RA signaling was implicated in normal liver regeneration as the mRNA levels of RARbeta, Aldh1a2, Crabp1, and Crbp1 were all induced 1.5 days after PH during the active phase of hepatocyte proliferation. Tretinoin 0-2 cellular retinoic acid binding protein I Mus musculus 97-103
25087568-9 2014 RA treatment prior to PH resulted in early up-regulation of RARbeta, Aldh1a2, Crabp1, and Crbp1, which was accompanied by an early induction of cell cycle genes. Tretinoin 0-2 cellular retinoic acid binding protein I Mus musculus 78-84
25027282-7 2014 Differentiation of APL by ATRA treatment reduced XAB2 expression levels in vivo. Tretinoin 26-30 XPA binding protein 2 Homo sapiens 49-53
24008270-1 2014 All-trans retinoic acid (ATRA) inhibits matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fibroblasts, skin fibroblasts, bronchoalveolar lavage cells and cancer cells, but activates MMP-9 in neuroblast and leukemia cells. Tretinoin 0-23 matrix metallopeptidase 9 Homo sapiens 77-82
24008270-1 2014 All-trans retinoic acid (ATRA) inhibits matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fibroblasts, skin fibroblasts, bronchoalveolar lavage cells and cancer cells, but activates MMP-9 in neuroblast and leukemia cells. Tretinoin 0-23 matrix metallopeptidase 9 Homo sapiens 187-192
24008270-1 2014 All-trans retinoic acid (ATRA) inhibits matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fibroblasts, skin fibroblasts, bronchoalveolar lavage cells and cancer cells, but activates MMP-9 in neuroblast and leukemia cells. Tretinoin 25-29 matrix metallopeptidase 9 Homo sapiens 77-82
24008270-1 2014 All-trans retinoic acid (ATRA) inhibits matrix metalloproteinase (MMP)-2 and MMP-9 in synovial fibroblasts, skin fibroblasts, bronchoalveolar lavage cells and cancer cells, but activates MMP-9 in neuroblast and leukemia cells. Tretinoin 25-29 matrix metallopeptidase 9 Homo sapiens 187-192
25047539-6 2014 Unlike SCF and BMP4, retinoic acid co-treatment enhanced VASA, GDF9 and SCP3 expression. Tretinoin 21-34 growth differentiation factor 9 Homo sapiens 63-67
25047539-6 2014 Unlike SCF and BMP4, retinoic acid co-treatment enhanced VASA, GDF9 and SCP3 expression. Tretinoin 21-34 synaptonemal complex protein 3 Homo sapiens 72-76
25124193-0 2014 Implications of the Wnt5a/CaMKII pathway in retinoic acid-induced myogenic tongue abnormalities of developing mice. Tretinoin 44-57 wingless-type MMTV integration site family, member 5A Mus musculus 20-25
25053430-1 2014 Retinoic acid (RA) generated in the mesoderm of vertebrate embryos controls body axis extension by downregulating Fgf8 expression in cells exiting the caudal progenitor zone. Tretinoin 0-13 fibroblast growth factor 8 Mus musculus 114-118
25053430-1 2014 Retinoic acid (RA) generated in the mesoderm of vertebrate embryos controls body axis extension by downregulating Fgf8 expression in cells exiting the caudal progenitor zone. Tretinoin 15-17 fibroblast growth factor 8 Mus musculus 114-118
25053430-5 2014 Epigenetic analysis using chromatin immunoprecipitation of trunk tissues from E8.25 wild-type and Raldh2(-/-) embryos lacking RA synthesis revealed RA-dependent recruitment of the repressive histone marker H3K27me3 and polycomb repressive complex 2 (PRC2) near the Fgf8 RARE. Tretinoin 148-150 fibroblast growth factor 8 Mus musculus 265-269
25053430-6 2014 The co-regulator RERE, the loss of which results in ectopic Fgf8 expression and somite defects, was recruited near the RARb RARE by RA, but was released from the Fgf8 RARE by RA. Tretinoin 119-121 arginine glutamic acid dipeptide (RE) repeats Mus musculus 17-21
25053430-6 2014 The co-regulator RERE, the loss of which results in ectopic Fgf8 expression and somite defects, was recruited near the RARb RARE by RA, but was released from the Fgf8 RARE by RA. Tretinoin 124-126 arginine glutamic acid dipeptide (RE) repeats Mus musculus 17-21
25053430-6 2014 The co-regulator RERE, the loss of which results in ectopic Fgf8 expression and somite defects, was recruited near the RARb RARE by RA, but was released from the Fgf8 RARE by RA. Tretinoin 124-126 fibroblast growth factor 8 Mus musculus 60-64
25053430-7 2014 Our findings demonstrate that RA directly represses Fgf8 through a RARE-mediated mechanism that promotes repressive chromatin, thus providing valuable insight into the mechanism of RA-FGF antagonism during progenitor cell differentiation. Tretinoin 30-32 fibroblast growth factor 8 Mus musculus 52-56
24798977-0 2014 LOX/COX inhibitors enhance the antineoplastic effects of all-trans retinoic acid in osteosarcoma cell lines. Tretinoin 67-80 lysyl oxidase Homo sapiens 0-3
24821728-3 2014 We found that PLZF-RARalpha can repress transcription of the p21WAF/CDKN1A gene, which encodes the negative cell cycle regulator p21 by binding to its proximal promoter Sp1-binding GC-boxes 3, 4, 5/6, a retinoic acid response element (RARE), and distal p53-responsive elements (p53REs). Tretinoin 203-216 zinc finger and BTB domain containing 16 Homo sapiens 14-18
24793772-6 2014 We show that the major benzodiazepine subtype (2alpha1, 2beta2, 1gamma2) is constitutively expressed in both undifferentiated P19 cells and retinoic acid (RA) differentiated P19 neurons. Tretinoin 140-153 hemoglobin, beta adult minor chain Mus musculus 57-71
24911586-8 2014 This study investigated the miRNAs modulation in an RA- induced testicular environment following the administration of all-trans RA (2 microM) and CYP26B1- inhibitor (1 microM) compared to control. Tretinoin 52-54 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 147-154
26237391-3 2014 Retinoic acid, the active metabolite of vitamin A, is involved in a wide range of biological processes, through binding and activation of nuclear receptors: retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 191-211
26237391-3 2014 Retinoic acid, the active metabolite of vitamin A, is involved in a wide range of biological processes, through binding and activation of nuclear receptors: retinoic acid receptors (RAR) and retinoid X receptors (RXR). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 213-216
24677291-0 2014 Retinoic acid induces mouse bone marrow-derived CD15+, Oct4+ and CXCR4+ stem cells into male germ-like cells in a two-dimensional cell culture system. Tretinoin 0-13 chemokine (C-X-C motif) receptor 4 Mus musculus 65-70
24677291-1 2014 We have examined the effect of retinoic acid (RA) on differentiation of bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells. Tretinoin 31-44 chemokine (C-X-C motif) receptor 4 Mus musculus 114-119
24677291-1 2014 We have examined the effect of retinoic acid (RA) on differentiation of bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells. Tretinoin 46-48 chemokine (C-X-C motif) receptor 4 Mus musculus 114-119
24677291-11 2014 Thus RA can induce differentiation of mouse bone marrow-derived CD15(+) , Oct4(+) and CXCR4(+) cells into male germ cells in vitro. Tretinoin 5-7 chemokine (C-X-C motif) receptor 4 Mus musculus 86-91
24709110-1 2014 CRABP-II, a retinoic acid binding protein, shuffles retinoic acid from cytoplasm into nucleus and forms a complex with nuclear retinoic acid receptor to facilitate transcriptional activities of retinoic acid. Tretinoin 12-25 cellular retinoic acid binding protein 2 Homo sapiens 0-8
24714214-4 2014 ATRA and NaBu promoted global acetylation of histones H3-K9/14 and H4-K12, reduced methylation of H3-K9 and H3-K27, and enriched accumulation of active chromatin marks at the Npr1 promoter. Tretinoin 0-4 natriuretic peptide receptor 1 Mus musculus 175-179
24714214-7 2014 Treatment with ATRA and NaBu synergistically attenuated the expression of alpha-SMA and PCNA and reduced systolic blood pressure in Npr1(+/-) mice. Tretinoin 15-19 proliferating cell nuclear antigen Mus musculus 88-92
24714214-7 2014 Treatment with ATRA and NaBu synergistically attenuated the expression of alpha-SMA and PCNA and reduced systolic blood pressure in Npr1(+/-) mice. Tretinoin 15-19 natriuretic peptide receptor 1 Mus musculus 132-136
24714214-8 2014 Our findings demonstrate that epigenetic upregulation of Npr1 gene transcription by ATRA and NaBu leads to attenuation of renal fibrotic markers and systolic blood pressure in mice with reduced Npr1 gene copy number, which will have important implications in prevention and treatment of hypertension-related renal pathophysiological conditions. Tretinoin 84-88 natriuretic peptide receptor 1 Mus musculus 57-61
24484607-4 2014 Four-day ATRA treatment increases beta-secretase 1 (BACE1) level, Abeta1-42 production, and receptor for advanced glycation end-products (RAGE) expression. Tretinoin 9-13 advanced glycosylation end-product specific receptor Homo sapiens 92-136
24484607-4 2014 Four-day ATRA treatment increases beta-secretase 1 (BACE1) level, Abeta1-42 production, and receptor for advanced glycation end-products (RAGE) expression. Tretinoin 9-13 advanced glycosylation end-product specific receptor Homo sapiens 138-142
24484607-5 2014 RAGE is a well-recognized receptor for Abeta, and the block of both RAGE and Abeta1-42 with specific antibodies strongly impairs neurite formation in ATRA-treated cells. Tretinoin 150-154 advanced glycosylation end-product specific receptor Homo sapiens 0-4
24484607-5 2014 RAGE is a well-recognized receptor for Abeta, and the block of both RAGE and Abeta1-42 with specific antibodies strongly impairs neurite formation in ATRA-treated cells. Tretinoin 150-154 advanced glycosylation end-product specific receptor Homo sapiens 68-72
24484607-6 2014 The involvement of Abeta1-42 and RAGE in ATRA-induced morphologic changes has been confirmed treating undifferentiated cells with different molecular assemblies of peptide: 1 muM monomeric, but not oligomeric, Abeta1-42 increases RAGE expression and favors neurite elongation. Tretinoin 41-45 advanced glycosylation end-product specific receptor Homo sapiens 33-37
24484607-6 2014 The involvement of Abeta1-42 and RAGE in ATRA-induced morphologic changes has been confirmed treating undifferentiated cells with different molecular assemblies of peptide: 1 muM monomeric, but not oligomeric, Abeta1-42 increases RAGE expression and favors neurite elongation. Tretinoin 41-45 advanced glycosylation end-product specific receptor Homo sapiens 230-234
24410928-8 2014 Our results show that the upregulating effect of atRA on TGF-beta1 was mediated by RARalpha, and the enhancing effect of atRA on IL-10 expression was mediated via RARbeta. Tretinoin 49-53 retinoic acid receptor, alpha Mus musculus 83-91
24524833-9 2014 CONCLUSION(S): These findings suggest that ALDH1A2 is the enzyme involved in retinoic acid biosynthesis in human germ cells. Tretinoin 77-90 aldehyde dehydrogenase 1 family member A2 Homo sapiens 43-50
24467691-9 2014 Protein expression of DAZL and STRA8 was greater in RA- and CYP26B1-I-treated testis culture, whereas DMRT1 showed greater protein expression for RA treatment, but not for CYP26B1-I treatment compared to control. Tretinoin 33-35 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 60-67
24608339-4 2014 Immunohistochemistry was performed on the tissue microarray using monoclonal antibodies which we have developed to the retinoic acid metabolising enzymes CYP26A1, CYP26B1, CYP26C1 and lecithin retinol acyl transferase (LRAT) using a semi-quantitative scoring scheme to assess expression. Tretinoin 119-132 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 172-179
24552295-2 2014 These studies have revealed the critical role of the vitamin A-active form, retinoic acid (RA) in the regulation of several developmental genes, including the important growth regulatory factor, transforming growth factor-beta2 (TGFbeta2), involved in early events of heart morphogenesis. Tretinoin 76-89 transforming growth factor beta 2 Homo sapiens 229-237
24552295-2 2014 These studies have revealed the critical role of the vitamin A-active form, retinoic acid (RA) in the regulation of several developmental genes, including the important growth regulatory factor, transforming growth factor-beta2 (TGFbeta2), involved in early events of heart morphogenesis. Tretinoin 91-93 transforming growth factor beta 2 Homo sapiens 229-237
24318876-7 2014 Retinoic acid, an endogenous compound that induces SHP, exhibited decreased hepatic levels during pregnancy in Tg-CYP2D6 mice. Tretinoin 0-13 nuclear receptor subfamily 0, group B, member 2 Mus musculus 51-54
24265455-10 2014 Further studies elucidated that hormone-sensitive lipase plays an important role in atRA-mediated regulation of the steroidogenic response that involves liver X receptor signaling. Tretinoin 84-88 lipase, hormone sensitive Mus musculus 32-56
24330068-0 2014 Nuclear Raf-1 kinase regulates the CXCR5 promoter by associating with NFATc3 to drive retinoic acid-induced leukemic cell differentiation. Tretinoin 86-99 C-X-C motif chemokine receptor 5 Homo sapiens 35-40
24330068-6 2014 We find that nuclear pS621 Raf-1 associates with NFATc3 near its cognate binding site in the promoter of CXCR5, a gene that must be up-regulated to drive RA-induced differentiation. Tretinoin 154-156 C-X-C motif chemokine receptor 5 Homo sapiens 105-110
24330068-7 2014 NFATc3 becomes immunoprecipitable with anti-phosphoserine serum, and CXCR5 is transcriptionally up-regulated upon RA-induced differentiation. Tretinoin 114-116 C-X-C motif chemokine receptor 5 Homo sapiens 69-74
23760401-6 2014 Notably, all-trans retinoic acid (ATRA) downregulated total beta-catenin, cell-surface and total CD44, reduced adhesion of lenalidomide-resistant myeloma cells and enhanced the activity of lenalidomide in a lenalidomide-resistant in vivo murine xenograft model. Tretinoin 9-32 catenin (cadherin associated protein), beta 1 Mus musculus 60-72
23760401-6 2014 Notably, all-trans retinoic acid (ATRA) downregulated total beta-catenin, cell-surface and total CD44, reduced adhesion of lenalidomide-resistant myeloma cells and enhanced the activity of lenalidomide in a lenalidomide-resistant in vivo murine xenograft model. Tretinoin 9-32 CD44 antigen Mus musculus 97-101
23760401-6 2014 Notably, all-trans retinoic acid (ATRA) downregulated total beta-catenin, cell-surface and total CD44, reduced adhesion of lenalidomide-resistant myeloma cells and enhanced the activity of lenalidomide in a lenalidomide-resistant in vivo murine xenograft model. Tretinoin 34-38 catenin (cadherin associated protein), beta 1 Mus musculus 60-72
23760401-6 2014 Notably, all-trans retinoic acid (ATRA) downregulated total beta-catenin, cell-surface and total CD44, reduced adhesion of lenalidomide-resistant myeloma cells and enhanced the activity of lenalidomide in a lenalidomide-resistant in vivo murine xenograft model. Tretinoin 34-38 CD44 antigen Mus musculus 97-101
24264050-2 2014 To better understand the mechanism underlying OST gene regulation, the effects of retinoic acid (RA) on OSTalpha/beta gene expression were investigated. Tretinoin 97-99 solute carrier family 51 subunit alpha Homo sapiens 104-117
24284210-5 2014 The AP difference is attributable to spatiotemporal inhibition of the clock gene her1 via retinoic acid (RA) regulation of the transcriptional repressor ripply1. Tretinoin 90-103 hairy-related 1 Danio rerio 81-85
24284210-5 2014 The AP difference is attributable to spatiotemporal inhibition of the clock gene her1 via retinoic acid (RA) regulation of the transcriptional repressor ripply1. Tretinoin 90-103 ripply transcriptional repressor 1 Danio rerio 153-160
24284210-5 2014 The AP difference is attributable to spatiotemporal inhibition of the clock gene her1 via retinoic acid (RA) regulation of the transcriptional repressor ripply1. Tretinoin 105-107 hairy-related 1 Danio rerio 81-85
24284210-5 2014 The AP difference is attributable to spatiotemporal inhibition of the clock gene her1 via retinoic acid (RA) regulation of the transcriptional repressor ripply1. Tretinoin 105-107 ripply transcriptional repressor 1 Danio rerio 153-160
25118897-0 2014 Neuroprotective properties of ciliary neurotrophic factor on retinoic acid (RA)-predifferentiated SH-SY5Y neuroblastoma cells. Tretinoin 61-74 ciliary neurotrophic factor Homo sapiens 30-57
25118897-0 2014 Neuroprotective properties of ciliary neurotrophic factor on retinoic acid (RA)-predifferentiated SH-SY5Y neuroblastoma cells. Tretinoin 76-78 ciliary neurotrophic factor Homo sapiens 30-57
25118897-2 2014 In this study, the biological effects of CNTF on retinoic acid (RA)-predifferentiated SH-SY5Y neuroblastoma cells and the underlying molecular mechanism of this effect were investigated for the first time. Tretinoin 49-62 ciliary neurotrophic factor Homo sapiens 41-45
25118897-2 2014 In this study, the biological effects of CNTF on retinoic acid (RA)-predifferentiated SH-SY5Y neuroblastoma cells and the underlying molecular mechanism of this effect were investigated for the first time. Tretinoin 64-66 ciliary neurotrophic factor Homo sapiens 41-45
25118897-3 2014 The results showed that RA was able to increase cells susceptibility to CNTF via regulating the expression levels of CNTF receptors. Tretinoin 24-26 ciliary neurotrophic factor Homo sapiens 72-76
25118897-3 2014 The results showed that RA was able to increase cells susceptibility to CNTF via regulating the expression levels of CNTF receptors. Tretinoin 24-26 ciliary neurotrophic factor Homo sapiens 117-121
25118897-5 2014 These findings suggested that JAK2/STAT3, as well as PI3K/Akt, play important roles in mediating the survival and neurite growth response of RA-predifferentiated cells to CNTF. Tretinoin 141-143 ciliary neurotrophic factor Homo sapiens 171-175
24030392-8 2013 On the whole, our results suggest that N4L could be a downstream component of the PI3K/Akt signaling pathway required for RA-induced differentiation of neuroblastoma SK-N-BE cells. Tretinoin 122-124 hedgehog acyltransferase Homo sapiens 166-170
24042439-10 2013 ATRA also blocked BLM-induced activation of the TGF-beta1/Smad3 signaling pathway in lung tissues, including expression of TGF-beta1, Smad3, p-Smad3, zinc-finger E-box-binding homeobox 1 and 2 (ZEB1 and ZEB2), and the high-mobility group AT-hook 2 (HMGA2). Tretinoin 0-4 zinc finger E-box binding homeobox 1 Rattus norvegicus 194-198
24176856-0 2013 Retinoic acid alters the proliferation and survival of the epithelium and mesenchyme and suppresses Wnt/beta-catenin signaling in developing cleft palate. Tretinoin 0-13 catenin (cadherin associated protein), beta 1 Mus musculus 104-116
24176856-5 2013 Moreover, Wnt/beta-catenin signaling was completely inhibited by RA in the early developing palate via its binding and activation with RA receptor (RAR) and is responsible for RA-induced cleft palate. Tretinoin 65-67 catenin (cadherin associated protein), beta 1 Mus musculus 14-26
24176856-5 2013 Moreover, Wnt/beta-catenin signaling was completely inhibited by RA in the early developing palate via its binding and activation with RA receptor (RAR) and is responsible for RA-induced cleft palate. Tretinoin 135-137 catenin (cadherin associated protein), beta 1 Mus musculus 14-26
23975865-4 2013 Genes involved in RA biosynthesis and metabolism, such as Adh1 and Raldh2, as well as RA receptors and IL-10, were induced in dendritic cells (DCs) via TLR2-dependent ERK signaling. Tretinoin 18-20 aldehyde dehydrogenase 1 family member A2 Homo sapiens 67-73
23980207-1 2013 Retinoic acid (RA) enhances TGF-beta-dependent differentiation of Foxp3(+) inducible regulatory T cells (iTregs) and inhibits Th17 differentiation by binding to the RA receptor (RAR)/retinoid X receptor (RXR) heterodimer. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 165-176
23980207-1 2013 Retinoic acid (RA) enhances TGF-beta-dependent differentiation of Foxp3(+) inducible regulatory T cells (iTregs) and inhibits Th17 differentiation by binding to the RA receptor (RAR)/retinoid X receptor (RXR) heterodimer. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 178-181
23980207-1 2013 Retinoic acid (RA) enhances TGF-beta-dependent differentiation of Foxp3(+) inducible regulatory T cells (iTregs) and inhibits Th17 differentiation by binding to the RA receptor (RAR)/retinoid X receptor (RXR) heterodimer. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 165-176
23980207-1 2013 Retinoic acid (RA) enhances TGF-beta-dependent differentiation of Foxp3(+) inducible regulatory T cells (iTregs) and inhibits Th17 differentiation by binding to the RA receptor (RAR)/retinoid X receptor (RXR) heterodimer. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 178-181
23980207-2 2013 The major physiologic RA, all-trans-RA, binds to RAR but not to RXR at physiological concentrations. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 49-52
23980207-2 2013 The major physiologic RA, all-trans-RA, binds to RAR but not to RXR at physiological concentrations. Tretinoin 36-38 retinoic acid receptor, alpha Mus musculus 49-52
24098526-1 2013 Peroxisome proliferator activator receptors (PPAR) ligands such as 15-Delta12,13-prostaglandin L(2) [PJ] and all trans retinoic acid (ATRA) have been shown to inhibit the development of liver fibrosis. Tretinoin 119-132 peroxisome proliferator-activated receptor gamma Rattus norvegicus 45-49
24098526-1 2013 Peroxisome proliferator activator receptors (PPAR) ligands such as 15-Delta12,13-prostaglandin L(2) [PJ] and all trans retinoic acid (ATRA) have been shown to inhibit the development of liver fibrosis. Tretinoin 134-138 peroxisome proliferator-activated receptor gamma Rattus norvegicus 45-49
23999499-3 2013 Here, we report that retinoic acid (RA), a vitamin A derivative, controls the homeostasis of pre-DC (precursor of DC)-derived splenic CD11b(+)CD8alpha(-)Esam(high) DCs and the developmentally related CD11b(+)CD103(+) subset within the gut. Tretinoin 36-38 CD8a molecule Homo sapiens 142-150
23999499-3 2013 Here, we report that retinoic acid (RA), a vitamin A derivative, controls the homeostasis of pre-DC (precursor of DC)-derived splenic CD11b(+)CD8alpha(-)Esam(high) DCs and the developmentally related CD11b(+)CD103(+) subset within the gut. Tretinoin 36-38 integrin subunit alpha M Homo sapiens 200-205
23999499-5 2013 In fate-tracking experiments, transfer of pre-DCs into RA-supplemented hosts resulted in near complete conversion of these cells into the CD11b(+)CD8alpha(-) subset, whereas transfer into vitamin A-deficient (VAD) hosts caused diversion to the CD11b(-)CD8alpha(+) lineage. Tretinoin 55-57 integrin subunit alpha M Homo sapiens 138-143
23999499-5 2013 In fate-tracking experiments, transfer of pre-DCs into RA-supplemented hosts resulted in near complete conversion of these cells into the CD11b(+)CD8alpha(-) subset, whereas transfer into vitamin A-deficient (VAD) hosts caused diversion to the CD11b(-)CD8alpha(+) lineage. Tretinoin 55-57 CD8a molecule Homo sapiens 146-154
23999499-5 2013 In fate-tracking experiments, transfer of pre-DCs into RA-supplemented hosts resulted in near complete conversion of these cells into the CD11b(+)CD8alpha(-) subset, whereas transfer into vitamin A-deficient (VAD) hosts caused diversion to the CD11b(-)CD8alpha(+) lineage. Tretinoin 55-57 integrin subunit alpha M Homo sapiens 244-249
23999499-5 2013 In fate-tracking experiments, transfer of pre-DCs into RA-supplemented hosts resulted in near complete conversion of these cells into the CD11b(+)CD8alpha(-) subset, whereas transfer into vitamin A-deficient (VAD) hosts caused diversion to the CD11b(-)CD8alpha(+) lineage. Tretinoin 55-57 CD8a molecule Homo sapiens 252-260
24099613-0 2013 All-transretinoic acid regulates Th1/Th2 balance in CD4+ T cells when GATA-3 is deficient. Tretinoin 4-22 negative elongation factor complex member C/D Homo sapiens 33-36
24099613-0 2013 All-transretinoic acid regulates Th1/Th2 balance in CD4+ T cells when GATA-3 is deficient. Tretinoin 4-22 GATA binding protein 3 Homo sapiens 70-76
24099613-3 2013 Therefore, the purpose of our study was to examine the effect of vitamin A metabolite all-trans retinoic acid (ATRA) on Th1-Th2 differentiation in CD4+ T cells under GATA-3 deficiency, which can induce Th1-polarizing condition. Tretinoin 96-109 negative elongation factor complex member C/D Homo sapiens 120-123
24099613-3 2013 Therefore, the purpose of our study was to examine the effect of vitamin A metabolite all-trans retinoic acid (ATRA) on Th1-Th2 differentiation in CD4+ T cells under GATA-3 deficiency, which can induce Th1-polarizing condition. Tretinoin 96-109 GATA binding protein 3 Homo sapiens 166-172
24099613-3 2013 Therefore, the purpose of our study was to examine the effect of vitamin A metabolite all-trans retinoic acid (ATRA) on Th1-Th2 differentiation in CD4+ T cells under GATA-3 deficiency, which can induce Th1-polarizing condition. Tretinoin 96-109 negative elongation factor complex member C/D Homo sapiens 202-205
24099613-3 2013 Therefore, the purpose of our study was to examine the effect of vitamin A metabolite all-trans retinoic acid (ATRA) on Th1-Th2 differentiation in CD4+ T cells under GATA-3 deficiency, which can induce Th1-polarizing condition. Tretinoin 111-115 negative elongation factor complex member C/D Homo sapiens 120-123
24099613-3 2013 Therefore, the purpose of our study was to examine the effect of vitamin A metabolite all-trans retinoic acid (ATRA) on Th1-Th2 differentiation in CD4+ T cells under GATA-3 deficiency, which can induce Th1-polarizing condition. Tretinoin 111-115 GATA binding protein 3 Homo sapiens 166-172
24099613-3 2013 Therefore, the purpose of our study was to examine the effect of vitamin A metabolite all-trans retinoic acid (ATRA) on Th1-Th2 differentiation in CD4+ T cells under GATA-3 deficiency, which can induce Th1-polarizing condition. Tretinoin 111-115 negative elongation factor complex member C/D Homo sapiens 202-205
24099613-5 2013 GATA-3 deficiency CD4+ T cells and normal CD4+ T were treated for 48 h with or without ATRA. Tretinoin 87-91 GATA binding protein 3 Homo sapiens 0-6
23906757-4 2013 Treatment with all-trans retinoic acid that is known to inhibit DNMT expression, also induced similar effects. Tretinoin 15-38 DNA methyltransferase 1 Homo sapiens 64-68
23803888-9 2013 RESULTS: Retinoic acid decreased the migration, invasion, and expression of MMP28 mRNA. Tretinoin 9-22 matrix metallopeptidase 28 Homo sapiens 76-81
23998581-2 2013 The results showed that ATRA had no influence on NB4-R1 cell proliferation, but enhanced the inhibitory effect of curcumin on NB4-R1 cell growth; the curcumin or ATRA alone did not affect NB4-R1 differentiation; curcumin combined with ATRA could obviously induce CD11b expression; the cell morphology showed obvious differentiation characteristics. Tretinoin 24-28 integrin subunit alpha M Homo sapiens 263-268
25206495-6 2013 Retinoic acid ment caused differential expression of three cell cycle-related genes p57kip2, Cdk5 and Spin, the expression levels of which were downregulated by retinoic acid and upregulated during normal neural tube formation. Tretinoin 0-13 spindlin 1 Rattus norvegicus 102-106
25206495-6 2013 Retinoic acid ment caused differential expression of three cell cycle-related genes p57kip2, Cdk5 and Spin, the expression levels of which were downregulated by retinoic acid and upregulated during normal neural tube formation. Tretinoin 161-174 spindlin 1 Rattus norvegicus 102-106
23541806-5 2013 Of note, myocardin-related transcription factor-A (MRTF-A), a major co-activator of serum response factor (SRF), was significantly activated and its nuclear localization was observed during RA-induced neural-like differentiation. Tretinoin 190-192 serum response factor Homo sapiens 84-105
23829413-0 2013 The cysteinyl leukotriene 2 receptor contributes to all-trans retinoic acid-induced differentiation of colon cancer cells. Tretinoin 62-75 cysteinyl leukotriene receptor 2 Homo sapiens 4-36
23829413-5 2013 In this study, we examined whether the balance between CysLT(1)R and CysLT(2)R could be restored by treatment with the cancer chemopreventive agent all-trans retinoic acid (ATRA). Tretinoin 158-171 cysteinyl leukotriene receptor 2 Homo sapiens 69-78
23829413-5 2013 In this study, we examined whether the balance between CysLT(1)R and CysLT(2)R could be restored by treatment with the cancer chemopreventive agent all-trans retinoic acid (ATRA). Tretinoin 173-177 cysteinyl leukotriene receptor 2 Homo sapiens 69-78
23829413-6 2013 METHODS: To determine the effect of ATRA on CysLT(2)R promoter activation, mRNA level, and protein level, we performed luciferase gene reporter assays, real-time polymerase chain reactions, and Western blots in colon cancer cell lines under various conditions. Tretinoin 36-40 cysteinyl leukotriene receptor 2 Homo sapiens 44-53
23829413-7 2013 RESULTS: ATRA treatment induces CysLT(2)R mRNA and protein expression without affecting CysLT(1)R levels. Tretinoin 9-13 cysteinyl leukotriene receptor 2 Homo sapiens 32-41
23742077-3 2013 As a prior gene microarray study revealed up-regulation of CCR3 in eosinophils stimulated with retinoic acids (RAs), the expression of functional CCR3 was examined. Tretinoin 95-109 C-C motif chemokine receptor 3 Homo sapiens 59-63
23742077-4 2013 We found that 9-cis RA and all-trans RA (ATRA) significantly induced surface CCR3 expression regardless of the presence of IL-3 or IL-5. Tretinoin 20-22 C-C motif chemokine receptor 3 Homo sapiens 77-81
23742077-4 2013 We found that 9-cis RA and all-trans RA (ATRA) significantly induced surface CCR3 expression regardless of the presence of IL-3 or IL-5. Tretinoin 37-39 C-C motif chemokine receptor 3 Homo sapiens 77-81
23742077-4 2013 We found that 9-cis RA and all-trans RA (ATRA) significantly induced surface CCR3 expression regardless of the presence of IL-3 or IL-5. Tretinoin 41-45 C-C motif chemokine receptor 3 Homo sapiens 77-81
23440512-2 2013 The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (atRA), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, RXRs, and PPARbeta/delta), polymorphic retinoic acid (RA) response elements, and multiple coregulators. Tretinoin 92-105 peroxisome proliferator activated receptor delta Homo sapiens 237-245
23440512-2 2013 The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (atRA), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, RXRs, and PPARbeta/delta), polymorphic retinoic acid (RA) response elements, and multiple coregulators. Tretinoin 107-111 peroxisome proliferator activated receptor delta Homo sapiens 237-245
23440512-2 2013 The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (atRA), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, RXRs, and PPARbeta/delta), polymorphic retinoic acid (RA) response elements, and multiple coregulators. Tretinoin 109-111 peroxisome proliferator activated receptor delta Homo sapiens 237-245
23472658-0 2013 IL-23/IL-17A axis correlates with the nitric oxide pathway in inflammatory bowel disease: immunomodulatory effect of retinoic acid. Tretinoin 117-130 interleukin 17A Homo sapiens 6-12
23524428-0 2013 All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions in vitro. Tretinoin 10-23 gap junction protein beta 1 Homo sapiens 123-127
23524428-8 2013 Moreover, ATRA induced upregulation of Cx32 and Cx43 at both the mRNA and protein levels in OSCC cells. Tretinoin 10-14 gap junction protein beta 1 Homo sapiens 39-43
23840757-7 2013 ATRA upregulated TRPC3, TRPC4 and TRPC6 expression and enhanced Ca(2+) influx in A549 cells, however, ATRA showed no direct effect on TRPC channels. Tretinoin 0-4 transient receptor potential cation channel subfamily C member 4 Homo sapiens 24-29
23864846-12 2013 Intercellular adhesion molecule-1 expression showed a significant increase in cells treated with PP2 in combination with ATRA, whereas cathepsin D expression showed a significant increase in cells treated with PP2 in combination with ATO. Tretinoin 121-125 intercellular adhesion molecule 1 Homo sapiens 0-33
23588680-0 2013 All-trans retinoic acid upregulates the expression of p53 via Axin and inhibits the proliferation of glioma cells. Tretinoin 10-23 axin 1 Homo sapiens 62-66
23588680-2 2013 In the present study, we demonstrated that ATRA activated the expression of p53 via Axin and induced cell cycle arrest at the G1/S phase and apoptosis of glioma cells. Tretinoin 43-47 axin 1 Homo sapiens 84-88
23588680-6 2013 Furthermore, loss-of-function of Axin in glioma cells by RNAi blocked ATRA-induced cell cycle phase arrest and apoptosis via downregulation of p53. Tretinoin 70-74 axin 1 Homo sapiens 33-37
23741453-0 2013 Retinoic acid-activated Ndrg1a represses Wnt/beta-catenin signaling to allow Xenopus pancreas, oesophagus, stomach, and duodenum specification. Tretinoin 0-13 N-myc downstream regulated 1 Xenopus tropicalis 24-30
23741453-0 2013 Retinoic acid-activated Ndrg1a represses Wnt/beta-catenin signaling to allow Xenopus pancreas, oesophagus, stomach, and duodenum specification. Tretinoin 0-13 catenin beta 1 Xenopus tropicalis 45-57
23741453-5 2013 Immunofluorescence data suggest that RA-activated Ndrg1a suppresses Wnt/beta-catenin signaling in Xenopus archenteron roof endoderm cells. Tretinoin 37-39 N-myc downstream regulated 1 Xenopus tropicalis 50-56
23741453-5 2013 Immunofluorescence data suggest that RA-activated Ndrg1a suppresses Wnt/beta-catenin signaling in Xenopus archenteron roof endoderm cells. Tretinoin 37-39 catenin beta 1 Xenopus tropicalis 72-84
23741453-7 2013 Furthermore, overexpression of the putative Wnt/beta-catenin target gene Atf3 phenocopied knockdown of Ndrg1a or inhibition of RA signaling, while Atf3 knockdown can rescue Ndrg1a knockdown phenotype. Tretinoin 127-129 catenin beta 1 Xenopus tropicalis 48-60
23734084-10 2013 RA was shown to interact with the UV-cone opsin, demonstrated by its ability to effect ligand-dependent activation of transducin by UV-cone opsin. Tretinoin 0-2 guanine nucleotide binding protein, alpha transducing 1 Mus musculus 118-128
23613978-5 2013 Retinoic acid receptor (RAR)-specific agonists were used in expression analysis to identify the RAR subtype involved upregulation of Csn3; a RARalpha-specific agonist mimicked the effects of ATRA on induction of Csn3 expression. Tretinoin 191-195 retinoic acid receptor, alpha Mus musculus 0-22
23613978-5 2013 Retinoic acid receptor (RAR)-specific agonists were used in expression analysis to identify the RAR subtype involved upregulation of Csn3; a RARalpha-specific agonist mimicked the effects of ATRA on induction of Csn3 expression. Tretinoin 191-195 retinoic acid receptor, alpha Mus musculus 24-27
23613978-5 2013 Retinoic acid receptor (RAR)-specific agonists were used in expression analysis to identify the RAR subtype involved upregulation of Csn3; a RARalpha-specific agonist mimicked the effects of ATRA on induction of Csn3 expression. Tretinoin 191-195 retinoic acid receptor, alpha Mus musculus 96-99
23613978-5 2013 Retinoic acid receptor (RAR)-specific agonists were used in expression analysis to identify the RAR subtype involved upregulation of Csn3; a RARalpha-specific agonist mimicked the effects of ATRA on induction of Csn3 expression. Tretinoin 191-195 retinoic acid receptor, alpha Mus musculus 141-149
23613978-6 2013 Therefore, RARalpha may be the RAR subtype mediating the effects of ATRA on the induction of Csn3 gene transcription in this differentiation-promoting process of P19 cells. Tretinoin 68-72 retinoic acid receptor, alpha Mus musculus 11-19
23613978-6 2013 Therefore, RARalpha may be the RAR subtype mediating the effects of ATRA on the induction of Csn3 gene transcription in this differentiation-promoting process of P19 cells. Tretinoin 68-72 retinoic acid receptor, alpha Mus musculus 11-14
23430257-1 2013 Activation of retinoic acid receptor (RAR) with all-trans-retinoic acid (RA) ameliorates glucose intolerance and insulin resistance in obese mice. Tretinoin 48-71 retinoic acid receptor, alpha Mus musculus 14-36
23430257-1 2013 Activation of retinoic acid receptor (RAR) with all-trans-retinoic acid (RA) ameliorates glucose intolerance and insulin resistance in obese mice. Tretinoin 48-71 retinoic acid receptor, alpha Mus musculus 38-41
23430257-1 2013 Activation of retinoic acid receptor (RAR) with all-trans-retinoic acid (RA) ameliorates glucose intolerance and insulin resistance in obese mice. Tretinoin 38-40 retinoic acid receptor, alpha Mus musculus 14-36
23396089-3 2013 Fenretinide and ATRA-induced gene expressions and DNA bindings were profiled using microarray and chromatin immunoprecipitation with anti-RXRalpha antibody. Tretinoin 16-20 retinoid X receptor alpha Homo sapiens 138-146
21626648-9 2013 The process of EB formation (mimicking the early postimplantation embryo development) is regulated by RA-induced apoptosis through the activation of caspase and P38 MAPK/JNK pathway. Tretinoin 102-104 mitogen-activated protein kinase 8 Mus musculus 170-173
23428742-7 2013 Microarray and q PCR analysis showed RA treatment did inhibit the motility of human RPE cells by inhibition of metalloproteinases (MMP) 1, 2, 9, fibronectin-1, transforming growth factor beta, thrombospondin-1, tenascin C, most collagen, integrin, laminin molecules and along enhancing E-cadherin and MMP3 genes expression. Tretinoin 37-39 tenascin C Homo sapiens 211-221
23318218-5 2013 mRNA and protein levels of the neural-markers Nestin, NSE, MAP-2, Tau and Tuj1 were stronger in neural-like cells derived from all-trans retinoic acid-pretreated mesenchymal stem cells than in those not pre-induction. Tretinoin 137-150 microtubule associated protein 2 Homo sapiens 59-64
23042455-4 2013 Using primary human endometrial stromal cells (ESCs) and a stable high telomerase-expressing ESC transfectant (T-HESC), we found that retinoic acid (RA) altered the phosphorylation status of Cx43 protein such that there was a decrease in the phosphorylated (P1 and P2) species accompanied by an increase in the non-phosphorylated (P0) form. Tretinoin 134-147 crystallin gamma F, pseudogene Homo sapiens 258-267
23042455-4 2013 Using primary human endometrial stromal cells (ESCs) and a stable high telomerase-expressing ESC transfectant (T-HESC), we found that retinoic acid (RA) altered the phosphorylation status of Cx43 protein such that there was a decrease in the phosphorylated (P1 and P2) species accompanied by an increase in the non-phosphorylated (P0) form. Tretinoin 149-151 crystallin gamma F, pseudogene Homo sapiens 258-267
23393141-5 2013 Moreover, upon induction by the beta-carotene derivative retinoic acid, this ISX binding decreased expression of a luciferase reporter gene in human colonic CaCo-2 cells indicating that ISX acts as a transcriptional repressor of BCMO1 expression. Tretinoin 57-70 beta-carotene oxygenase 1 Homo sapiens 229-234
23401586-5 2013 Conversely, mature naive CD4 cells have a lower sensitivity to retinoic acid, resulting in increased IFN-gamma production and subsequent IFN-gamma-mediated silencing of Foxp3 expression. Tretinoin 63-76 CD4 antigen Mus musculus 25-28
23486062-7 2013 Chemical inhibition of retinoic acid signalling partially suppresses precocious Oct4 downregulation and Stra8 activation in Rnf2-deficient female PGCs. Tretinoin 23-36 POU domain, class 5, transcription factor 1 Mus musculus 80-84
23460729-0 2013 BATF is required for normal expression of gut-homing receptors by T helper cells in response to retinoic acid. Tretinoin 96-109 basic leucine zipper transcription factor, ATF-like Mus musculus 0-4
23460729-1 2013 CCR9 and alpha4beta7 are the major trafficking receptors for lymphocyte migration to the gut, and their expression is induced during lymphocyte activation under the influence of retinoic acid (RA). Tretinoin 178-191 chemokine (C-C motif) receptor 9 Mus musculus 0-4
23460729-1 2013 CCR9 and alpha4beta7 are the major trafficking receptors for lymphocyte migration to the gut, and their expression is induced during lymphocyte activation under the influence of retinoic acid (RA). Tretinoin 193-195 chemokine (C-C motif) receptor 9 Mus musculus 0-4
23069989-8 2013 Both Noggin and retinoic acid (RA) support neuronal differentiation of ESCs, but they show different effects on their positional identity: whereas RA supports the typical gene expression profile of hindbrain neurons, Noggin induces a profile characteristic of dorsal telencephalic neurons. Tretinoin 31-33 noggin Mus musculus 217-223
23069989-8 2013 Both Noggin and retinoic acid (RA) support neuronal differentiation of ESCs, but they show different effects on their positional identity: whereas RA supports the typical gene expression profile of hindbrain neurons, Noggin induces a profile characteristic of dorsal telencephalic neurons. Tretinoin 147-149 noggin Mus musculus 5-11
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 136-165
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 9-22 cellular retinoic acid binding protein 2 Homo sapiens 167-173
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 9-22 fatty acid binding protein 5 Homo sapiens 204-232
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 9-22 fatty acid binding protein 5 Homo sapiens 234-239
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 24-26 cellular retinoic acid binding protein 2 Homo sapiens 136-165
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 24-26 cellular retinoic acid binding protein 2 Homo sapiens 167-173
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 24-26 fatty acid binding protein 5 Homo sapiens 204-232
23337719-1 2013 CONTEXT: Retinoic acid (RA) may promote survival or apoptosis of cells, depending on the levels of binding proteins: apoptosis-inducing cellular RA binding protein 2 (CRABP2), and cell survival-promoting fatty acid binding protein 5 (FABP5). Tretinoin 24-26 fatty acid binding protein 5 Homo sapiens 234-239
23337719-2 2013 Increased cellular uptake of retinol and altered actions of RA related to reduced expression of CRABP2 may contribute to the development of endometriosis. Tretinoin 60-62 cellular retinoic acid binding protein 2 Homo sapiens 96-102
23382200-0 2013 8-CPT-cAMP/all-trans retinoic acid targets t(11;17) acute promyelocytic leukemia through enhanced cell differentiation and PLZF/RARalpha degradation. Tretinoin 11-34 retinoic acid receptor, alpha Mus musculus 128-136
23382200-3 2013 Mechanistically, in combination with ATRA, 8-CPT-cAMP activates PKA, causing phosphorylation of PLZF/RARalpha at Ser765 and resulting in increased dissociation of the silencing mediator for retinoic acid and thyroid hormone receptors/nuclear receptor corepressor from PLZF/RARalpha. Tretinoin 37-41 retinoic acid receptor, alpha Mus musculus 101-109
23382200-3 2013 Mechanistically, in combination with ATRA, 8-CPT-cAMP activates PKA, causing phosphorylation of PLZF/RARalpha at Ser765 and resulting in increased dissociation of the silencing mediator for retinoic acid and thyroid hormone receptors/nuclear receptor corepressor from PLZF/RARalpha. Tretinoin 37-41 retinoic acid receptor, alpha Mus musculus 273-281
23382200-3 2013 Mechanistically, in combination with ATRA, 8-CPT-cAMP activates PKA, causing phosphorylation of PLZF/RARalpha at Ser765 and resulting in increased dissociation of the silencing mediator for retinoic acid and thyroid hormone receptors/nuclear receptor corepressor from PLZF/RARalpha. Tretinoin 190-203 retinoic acid receptor, alpha Mus musculus 101-109
23382200-5 2013 Meanwhile, 8-CPT-cAMP also potentiated ATRA-induced degradation of PLZF/RARalpha through its Ser765 phosphorylation. Tretinoin 39-43 retinoic acid receptor, alpha Mus musculus 72-80
23264745-7 2013 Mapping of the epigenetic signature of Meis1 revealed that RA induces a rapid increase in the H3K9/K14ac epigenetic mark at the proximal promoter and at two sites downstream of the transcription start site in WT, but not in RARgamma(-/-) cells. Tretinoin 59-61 Meis homeobox 1 Homo sapiens 39-44
23264745-8 2013 Thus, RA-associated increases in H3K9/K14ac epigenetic marks require RARgamma and are associated with increased Meis1 transcript levels, whereas H3K4me3 is present at the Meis1 proximal promoter even in the absence of RARgamma. Tretinoin 6-8 Meis homeobox 1 Homo sapiens 112-117
23264745-8 2013 Thus, RA-associated increases in H3K9/K14ac epigenetic marks require RARgamma and are associated with increased Meis1 transcript levels, whereas H3K4me3 is present at the Meis1 proximal promoter even in the absence of RARgamma. Tretinoin 6-8 Meis homeobox 1 Homo sapiens 171-176
23243270-7 2013 Multiplexing mAbs against CD11b and CD11c provided surrogate imaging biomarkers of differentiation therapy in an acute promyelocytic leukemia model treated with all-trans retinoic acid combined with the histone-deacetylase inhibitor valproic acid. Tretinoin 171-184 integrin subunit alpha M Homo sapiens 26-31
23484687-1 2013 To verify the differential expression of non-metastasis cell 3 (NME3) protein in HL-60 cells when they were induced to differentiate into monocyte and granulocyte like cells, and study its value in diagnosis of acute myeloid leukemia, all-trans retinoic acid (ATRA) and a new steroidal drug NSC67657 were employed to induce acute myeloid leukemia HL-60 cells into monocyte and granulocyte like cells. Tretinoin 245-258 carboxyl ester lipase pseudogene Homo sapiens 56-62
23484687-1 2013 To verify the differential expression of non-metastasis cell 3 (NME3) protein in HL-60 cells when they were induced to differentiate into monocyte and granulocyte like cells, and study its value in diagnosis of acute myeloid leukemia, all-trans retinoic acid (ATRA) and a new steroidal drug NSC67657 were employed to induce acute myeloid leukemia HL-60 cells into monocyte and granulocyte like cells. Tretinoin 260-264 carboxyl ester lipase pseudogene Homo sapiens 56-62
23714660-11 2013 ATRA also promoted the CD44(+)CD24(-) subpopulation to differentiate. Tretinoin 0-4 CD44 molecule (Indian blood group) Homo sapiens 23-27
23392891-0 2013 Differential regulation of TauT by calcitriol and retinoic acid via VDR/RXR in LLC-PK1 and MCF-7 cells. Tretinoin 50-63 retinoid X receptor alpha Homo sapiens 72-75
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 98-111 vitamin D receptor Homo sapiens 139-157
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 98-111 vitamin D receptor Homo sapiens 159-162
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 98-111 retinoid X receptor alpha Homo sapiens 192-195
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 113-115 vitamin D receptor Homo sapiens 139-157
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 113-115 vitamin D receptor Homo sapiens 159-162
23392891-3 2013 In this study, we test the hypothesis that the TauT gene is regulated by vitamin D(3) (VD(3)) and retinoic acid (RA) via activation of the vitamin D receptor (VDR) and retinoic acid receptor (RXR). Tretinoin 113-115 retinoid X receptor alpha Homo sapiens 192-195
23392891-6 2013 Expression of TauT was significantly increased by RA, which was synergized by the addition of VD(3) after RXR activation in LLC-PK1 cells. Tretinoin 50-52 retinoid X receptor alpha Homo sapiens 106-109
22878527-9 2013 We speculate that in suture mesenchymal cells, endogenous RBP4 receives retinol from STRA6 and the RBP4-retinol complex is stored in vesicles until needed for conversion to retinoic acid in the process of osteogenesis. Tretinoin 173-186 retinol binding protein 4 Homo sapiens 58-62
23982413-6 2013 K-ras mutant breast cancer cell line enriched for CSCs was resistant to ATRA, which was reversed by MAP kinase inhibitors. Tretinoin 72-76 KRAS proto-oncogene, GTPase Homo sapiens 0-5
23982413-7 2013 Thus, ATRA alone or in combination can be tested for efficacy using SOX2, CDX2, and K-ras mutation/MAPK activation status as biomarkers of response. Tretinoin 6-10 caudal type homeobox 2 Homo sapiens 74-78
23102850-3 2013 The objective was to elucidate the effects of exogenous RA and a RARalpha antagonist on gene expression of ALDH1, CYP26b1, RARalpha, cellular RA-binding protein II, and STRA8 in an in vitro organ culture model of canine testis. Tretinoin 56-58 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 114-121
23102850-8 2013 In conclusion, exogenous RA decreased mRNA abundance of ALDH1 and increased mRNA abundance of RA signaling molecules and its downstream effectors (CYP26b1, CRABII, and STRA8), whereas treatment with a RARalpha antagonist effectively decreased RARalpha and RA metabolism molecules and its downstream effectors in canine testis. Tretinoin 25-27 cytochrome P450 family 26 subfamily B member 1 Canis lupus familiaris 147-154
23718072-13 2013 As far as ADSCs, RA in combination with 5-azacytidine caused the elevation of expression of MAP2, but reduced the secretion of BDNF. Tretinoin 17-19 microtubule associated protein 2 Homo sapiens 92-96
23718072-13 2013 As far as ADSCs, RA in combination with 5-azacytidine caused the elevation of expression of MAP2, but reduced the secretion of BDNF. Tretinoin 17-19 brain derived neurotrophic factor Homo sapiens 127-131
23327868-1 2013 BACKGROUND: The cellular retinoic acid-binding protein II (CRABPII) and epidermal fatty acid-binding protein (E-FABP) both serving as the transport protein of retinoic acid (RA), through RA signal transduction pathway, commit the cell to opposite fate, apoptosis or survival. Tretinoin 174-176 cellular retinoic acid binding protein 2 Homo sapiens 16-57
23327868-1 2013 BACKGROUND: The cellular retinoic acid-binding protein II (CRABPII) and epidermal fatty acid-binding protein (E-FABP) both serving as the transport protein of retinoic acid (RA), through RA signal transduction pathway, commit the cell to opposite fate, apoptosis or survival. Tretinoin 174-176 cellular retinoic acid binding protein 2 Homo sapiens 59-66
23327868-1 2013 BACKGROUND: The cellular retinoic acid-binding protein II (CRABPII) and epidermal fatty acid-binding protein (E-FABP) both serving as the transport protein of retinoic acid (RA), through RA signal transduction pathway, commit the cell to opposite fate, apoptosis or survival. Tretinoin 174-176 fatty acid binding protein 5 Homo sapiens 72-108
23327868-1 2013 BACKGROUND: The cellular retinoic acid-binding protein II (CRABPII) and epidermal fatty acid-binding protein (E-FABP) both serving as the transport protein of retinoic acid (RA), through RA signal transduction pathway, commit the cell to opposite fate, apoptosis or survival. Tretinoin 174-176 fatty acid binding protein 5 Homo sapiens 110-116
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 84-106
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 108-111
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 84-106
23105114-1 2012 Retinoic acid (RA) regulates gene transcription by activating the nuclear receptors retinoic acid receptor (RAR) and peroxisome proliferator-activated receptor (PPAR) beta/delta and their respective cognate lipid-binding proteins CRABP-II and FABP5. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 108-111
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 retinoic acid receptor, alpha Mus musculus 115-118
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 retinoic acid receptor, alpha Mus musculus 212-215
23105114-3 2012 Here, we show that the RA-induced commitment of P19 stem cells to neuronal progenitors is mediated by the CRABP-II/RAR path and that the FABP5/PPARbeta/delta path can inhibit the process through induction of the RAR repressors SIRT1 and Ajuba. Tretinoin 23-25 ajuba LIM protein Mus musculus 237-242
23105114-5 2012 Hence, RA-induced neuronal differentiation is mediated through RAR in the early stages and through PPARbeta/delta in the late stages of the process. Tretinoin 7-9 retinoic acid receptor, alpha Mus musculus 63-66
22942074-3 2012 We found that exposure of embryos to exogenous RA induces a dramatic anterior expansion of the number of pharyngeal teeth that later form and shifts anteriorly the expression patterns of genes normally expressed in the posterior tooth-forming region, such as pitx2 and dlx2b. Tretinoin 47-49 distal-less homeobox 2b Danio rerio 269-274
22640830-7 2012 ATRA suppressed the expression of the stem cell markers Oct4, Sox2, Nestin and CD44 in HNSC CSCs and inhibited the proliferation of HNSC CSCs in vitro and in vivo. Tretinoin 0-4 SRY-box transcription factor 2 Homo sapiens 62-66
22640830-7 2012 ATRA suppressed the expression of the stem cell markers Oct4, Sox2, Nestin and CD44 in HNSC CSCs and inhibited the proliferation of HNSC CSCs in vitro and in vivo. Tretinoin 0-4 CD44 molecule (Indian blood group) Homo sapiens 79-83
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 25-38 retinoid X receptor alpha Homo sapiens 216-235
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 25-38 retinoid X receptor alpha Homo sapiens 237-240
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 40-42 retinoid X receptor alpha Homo sapiens 216-235
22871568-1 2012 The vitamin A derivative retinoic acid (RA) is an important regulator of mammalian adiposity and lipid metabolism, primarily acting at the gene expression level through nuclear receptors of the RA receptor (RAR) and retinoid X receptor (RXR) subfamilies. Tretinoin 40-42 retinoid X receptor alpha Homo sapiens 237-240
22871568-6 2012 We conclude that ATRA treatment enhances fatty acid catabolism in hepatocytes through RXR-mediated mechanisms that likely involve the transactivation of the PPARalpha:RXR heterodimer. Tretinoin 17-21 retinoid X receptor alpha Homo sapiens 86-89
22871568-6 2012 We conclude that ATRA treatment enhances fatty acid catabolism in hepatocytes through RXR-mediated mechanisms that likely involve the transactivation of the PPARalpha:RXR heterodimer. Tretinoin 17-21 retinoid X receptor alpha Homo sapiens 167-170
22789609-8 2012 ATRA-induced VDR protein in cytosol of KG-1 cells can be further activated by 1,25D to induce monocytic differentiation of these cells. Tretinoin 0-4 vitamin D receptor Homo sapiens 13-16
22949521-4 2012 Here, we provide evidence that the inhibitory effect of 9-cis-RA on cell proliferation depends on 9-cis-RA-dependent interaction of retinoid X receptor alpha (RXRalpha) with replication factor C3 (RFC3), which is a subunit of the RFC heteropentamer that opens and closes the circular proliferating cell nuclear antigen (PCNA) clamp on DNA. Tretinoin 61-64 retinoid X receptor alpha Homo sapiens 159-167
22949521-4 2012 Here, we provide evidence that the inhibitory effect of 9-cis-RA on cell proliferation depends on 9-cis-RA-dependent interaction of retinoid X receptor alpha (RXRalpha) with replication factor C3 (RFC3), which is a subunit of the RFC heteropentamer that opens and closes the circular proliferating cell nuclear antigen (PCNA) clamp on DNA. Tretinoin 61-64 replication factor C subunit 3 Homo sapiens 197-201
23064179-3 2012 Using an integrative approach based on several bioinformatics resources together with experimental validations, we indeed found that retinoic acid positively regulates miR-210 and miR-23a/24-2 expressions and is counteracted by estrogen. Tretinoin 133-146 microRNA 23a Homo sapiens 180-187
22681667-4 2012 In this study, we show that functionally suppressive, alloantigen-specific CD8(+) Foxp3(+) T cells can be induced and significantly expanded by stimulating naive CD8(+) T cells with donor dendritic cells in the presence of IL-2, TGF-beta1 and retinoic acid. Tretinoin 243-256 CD8a molecule Homo sapiens 75-78
23159076-8 2012 The VEGF mRNA level was further more decreased after RGZ + ATRA treatment. Tretinoin 59-63 vascular endothelial growth factor A Mus musculus 4-8
23158431-0 2012 [Effects of all trans retinoic acid on the expression alterations of beta-protein 1 in human breast cancer cell lines of MDA-MB-468 and MCF-7]. Tretinoin 22-35 distal-less homeobox 4 Homo sapiens 69-83
23158431-1 2012 OBJECTIVE: To explore the effects of all trans retinoic acid (ATRA) on the cell proliferation and expression alterations of beta-protein 1 (BP1) in human breast cancer cells lines of MDA-MB-468 and MCF-7. Tretinoin 47-60 distal-less homeobox 4 Homo sapiens 124-138
23158431-1 2012 OBJECTIVE: To explore the effects of all trans retinoic acid (ATRA) on the cell proliferation and expression alterations of beta-protein 1 (BP1) in human breast cancer cells lines of MDA-MB-468 and MCF-7. Tretinoin 47-60 distal-less homeobox 4 Homo sapiens 140-143
23158431-1 2012 OBJECTIVE: To explore the effects of all trans retinoic acid (ATRA) on the cell proliferation and expression alterations of beta-protein 1 (BP1) in human breast cancer cells lines of MDA-MB-468 and MCF-7. Tretinoin 62-66 distal-less homeobox 4 Homo sapiens 124-138
23158431-1 2012 OBJECTIVE: To explore the effects of all trans retinoic acid (ATRA) on the cell proliferation and expression alterations of beta-protein 1 (BP1) in human breast cancer cells lines of MDA-MB-468 and MCF-7. Tretinoin 62-66 distal-less homeobox 4 Homo sapiens 140-143
23158431-4 2012 RESULTS: After the treatment of ATRA, the proliferation of cells and the expression of BP1 decreased. Tretinoin 32-36 distal-less homeobox 4 Homo sapiens 87-90
23158431-7 2012 CONCLUSION: ATRA can inhibit the proliferation and the expression of BP1 in breast cancer cells. Tretinoin 12-16 distal-less homeobox 4 Homo sapiens 69-72
22270475-3 2012 Our results show that the expression of mouse liver, bone, and kidney ALP (mL/B/K-ALP) induced by ATRA in C3H10T 1/2 cells was related to the retinoic acid nuclear receptors, RARalpha and RARbeta, which are not involved in the MAPK pathway. Tretinoin 98-102 retinoic acid receptor, alpha Mus musculus 175-183
22808996-6 2012 The absence of retinoic acid-inducible gene I (RIG-I), a cytosolic RNA sensor, determined sensitivity to NDV. Tretinoin 15-28 DExD/H-box helicase 58 Homo sapiens 47-52
22806070-2 2012 Retinoic acid (RA), which is the biologically active form of vitamin A, acts through the nuclear hormone receptor RAR (RA receptor) to induce either gene activation or repression. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 114-117
22806070-2 2012 Retinoic acid (RA), which is the biologically active form of vitamin A, acts through the nuclear hormone receptor RAR (RA receptor) to induce either gene activation or repression. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 119-130
22806070-2 2012 Retinoic acid (RA), which is the biologically active form of vitamin A, acts through the nuclear hormone receptor RAR (RA receptor) to induce either gene activation or repression. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 114-117
22806070-2 2012 Retinoic acid (RA), which is the biologically active form of vitamin A, acts through the nuclear hormone receptor RAR (RA receptor) to induce either gene activation or repression. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 119-130
22204820-4 2012 We furthermore studied the expression of PTGES after treatment with ATRA in human monocyte-derived macrophages (MDMs) and bronchoalveolar lavage (BAL) cells. Tretinoin 68-72 prostaglandin E synthase Homo sapiens 41-46
22204820-8 2012 IL-13 suppressed the ATRA induced PTGES expression at both mRNA and protein level in MDM and BAL cells. Tretinoin 21-25 prostaglandin E synthase Homo sapiens 34-39
22204820-12 2012 These data indicate that ATRA is a potent inducer of PTGES expression in human macrophages but not in alternatively activated macrophages and suggest that the eicosanoid pathway is important for ATRA action in macrophages. Tretinoin 25-29 prostaglandin E synthase Homo sapiens 53-58
22493483-9 2012 Also, KLF15 binding to the promoter regions of nephrin and podocin was increased in RA-treated podocytes. Tretinoin 84-86 nephrosis 1, nephrin Mus musculus 47-54
22493483-9 2012 Also, KLF15 binding to the promoter regions of nephrin and podocin was increased in RA-treated podocytes. Tretinoin 84-86 nephrosis 2, podocin Mus musculus 59-66
21492869-4 2012 This suggests that the retinoic acid (RA) signaling pathway interacts with the Fgf10-Fgfr2IIIb signaling pathway during duodenal development. Tretinoin 23-36 fibroblast growth factor 10 Mus musculus 79-84
21492869-4 2012 This suggests that the retinoic acid (RA) signaling pathway interacts with the Fgf10-Fgfr2IIIb signaling pathway during duodenal development. Tretinoin 38-40 fibroblast growth factor 10 Mus musculus 79-84
22405964-6 2012 To further understand how retinoic acid regulates upper lip and palate morphogenesis we searched for genes downregulated in response to RARgamma inhibition in orofacial tissue, and uncovered homeobox genes lhx8 and msx2. Tretinoin 26-39 LIM homeobox 8 L homeolog Xenopus laevis 206-210
22405964-9 2012 These results suggest a model whereby retinoic acid signaling regulates Lhx8 and Msx2, which together direct the tissue growth and differentiation necessary for the upper lip and primary palate morphogenesis. Tretinoin 38-51 LIM homeobox 8 L homeolog Xenopus laevis 72-76
22162152-0 2012 Morphological defects in a novel Rdh10 mutant that has reduced retinoic acid biosynthesis and signaling. Tretinoin 63-76 retinol dehydrogenase 10 Homo sapiens 33-38
22162152-5 2012 Rdh10(m366Asp) mutant embryos have unique phenotypes, such as edema, a massive midline facial cleft, and neurogenesis defects in the forebrain, that will allow the identification of novel RA functions. Tretinoin 188-190 retinol dehydrogenase 10 Homo sapiens 0-5
22387108-0 2012 c-Jun N-terminal kinase controls a negative loop in the regulation of glial fibrillary acidic protein expression by retinoic acid. Tretinoin 116-129 glial fibrillary acidic protein Homo sapiens 70-101
22387108-2 2012 We and others have shown previously that retinoic acid and specific cytokines induce the expression of GFAP in neural precursor cells by activating the phosphatidylinositol-4,5-bisphosphate-3-kinase (PI3K) phosphorylation pathway. Tretinoin 41-54 glial fibrillary acidic protein Homo sapiens 103-107
22387108-3 2012 Here, we extend our previous work and show that retinoic acid also activates specifically the c-Jun N-terminal kinase (JNK) phosphorylation pathway, which in turn inhibits GFAP expression. Tretinoin 48-61 glial fibrillary acidic protein Homo sapiens 172-176
22374841-0 2012 Disease-stabilizing treatment with all-trans retinoic acid and valproic acid in acute myeloid leukemia: serum hsp70 and hsp90 levels and serum cytokine profiles are determined by the disease, patient age, and anti-leukemic treatment. Tretinoin 45-58 heat shock protein family A (Hsp70) member 4 Homo sapiens 110-115
22374841-6 2012 Furthermore, disease-stabilizing therapy altered the serum-cytokine profile, but the correlations between HSP70/HSP90/IL-1ra/HGF were maintained only when ATRA + valproic acid were combined with theophyllin but not when combined with cytarabine. Tretinoin 155-159 heat shock protein family A (Hsp70) member 4 Homo sapiens 106-111
21678401-10 2012 Finally, we found evidence for a feedback loop in which PBX reduces SF-1 mRNA levels while continued SF-1 expression blocks the RA-dependent increase in PBX levels. Tretinoin 128-130 splicing factor 1 Homo sapiens 101-105
22337869-1 2012 The transcription factor Kruppel-like factor 4 (KLF4) plays a critical role in vascular smooth muscle cell (VSMC) differentiation induced by all-trans-retinoic acid (ATRA). Tretinoin 141-164 Kruppel like factor 4 Homo sapiens 25-46
22337869-1 2012 The transcription factor Kruppel-like factor 4 (KLF4) plays a critical role in vascular smooth muscle cell (VSMC) differentiation induced by all-trans-retinoic acid (ATRA). Tretinoin 141-164 Kruppel like factor 4 Homo sapiens 48-52
22337869-1 2012 The transcription factor Kruppel-like factor 4 (KLF4) plays a critical role in vascular smooth muscle cell (VSMC) differentiation induced by all-trans-retinoic acid (ATRA). Tretinoin 166-170 Kruppel like factor 4 Homo sapiens 25-46
22337869-1 2012 The transcription factor Kruppel-like factor 4 (KLF4) plays a critical role in vascular smooth muscle cell (VSMC) differentiation induced by all-trans-retinoic acid (ATRA). Tretinoin 166-170 Kruppel like factor 4 Homo sapiens 48-52
22337869-2 2012 Although it has been demonstrated that ATRA stimulation augments both KLF4 protein and mRNA levels in VSMCs, the molecular mechanisms by which ATRA regulates Klf4 transcription are unknown. Tretinoin 39-43 Kruppel like factor 4 Homo sapiens 70-74
22337869-8 2012 These results suggest that RARalpha serves as an essential co-activator for ATRA signaling and that the recruitment of RARalpha to the KLF4-Sp1-YB1 complex, which leads to Klf4 expression in VSMCs, is independent of a retinoic acid response element. Tretinoin 218-231 Kruppel like factor 4 Homo sapiens 135-139
22291023-2 2012 Here, we report that a novel member of the short chain dehydrogenase/reductase superfamily, frog sdr16c5, acts as a highly active retinol dehydrogenase (rdhe2) that promotes retinoic acid biosynthesis when expressed in mammalian cells. Tretinoin 174-187 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 97-104
22291023-2 2012 Here, we report that a novel member of the short chain dehydrogenase/reductase superfamily, frog sdr16c5, acts as a highly active retinol dehydrogenase (rdhe2) that promotes retinoic acid biosynthesis when expressed in mammalian cells. Tretinoin 174-187 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 153-158
22291023-3 2012 In vivo assays of rdhe2 function show that overexpression of rdhe2 in frog embryos leads to posteriorization and induction of defects resembling those caused by retinoic acid toxicity. Tretinoin 161-174 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 61-66
22291023-6 2012 Analyses of retinoic acid levels using either endogenous retinoic acid-sensitive gene hoxd4 or retinoic acid reporter cell line both show that the levels of retinoic acid are significantly decreased in rdhe2 morphants. Tretinoin 12-25 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 202-207
22291023-6 2012 Analyses of retinoic acid levels using either endogenous retinoic acid-sensitive gene hoxd4 or retinoic acid reporter cell line both show that the levels of retinoic acid are significantly decreased in rdhe2 morphants. Tretinoin 57-70 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 202-207
22291023-6 2012 Analyses of retinoic acid levels using either endogenous retinoic acid-sensitive gene hoxd4 or retinoic acid reporter cell line both show that the levels of retinoic acid are significantly decreased in rdhe2 morphants. Tretinoin 57-70 short chain dehydrogenase/reductase family 16C member 5 Homo sapiens 202-207
22154861-9 2012 In particular, scaffold-based controlled delivery of RA enhanced MAP2 and RIP expression compared with bolus delivery despite lower amounts of drug (>8 times lower). Tretinoin 53-55 microtubule associated protein 2 Homo sapiens 65-69
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 alpha fetoprotein Mus musculus 108-111
21497500-7 2012 Under AL, ATRA reduced the average daily messenger RNA (mRNA) levels of some disease markers, such as liver Afp and jejunum Afp, Alt and Gadd45beta and aspartate transaminase (AST) protein in the serum, but increased the expression level of liver Crp mRNA. Tretinoin 10-14 alpha fetoprotein Mus musculus 124-127
22039172-8 2012 All-trans retinoic acid (atRA) induced CYPS1 mRNA expression more potently than 9-cis RA or 13-cis RA. Tretinoin 4-23 peptidylprolyl isomerase B Homo sapiens 39-44
22039172-8 2012 All-trans retinoic acid (atRA) induced CYPS1 mRNA expression more potently than 9-cis RA or 13-cis RA. Tretinoin 25-29 peptidylprolyl isomerase B Homo sapiens 39-44
22157753-9 2012 Overexpression of p38beta or Rac1 significantly enhanced (1.9- and 3.9-fold, respectively), the tRA-stimulated NIS expression in MCF-7 cells. Tretinoin 96-99 Rac family small GTPase 1 Homo sapiens 29-33
22490698-7 2012 RESULTS: The level of phosphorylated-STAT2 was obviously up-regulated in NB4 cells treated with ATRA for 72 hours, as well as the concentration of IFN-alpha in culture supernatants. Tretinoin 96-100 signal transducer and activator of transcription 2 Homo sapiens 37-42
23383387-5 2012 In sporadic ALS, the cytoplasmic binding protein that facilitates nuclear translocation of retinoic acid, cellular retinoic acid binding protein-II (CRABP-II), was localized to the nucleus and retinoic acid receptor beta (RARbeta) was significantly increased in motor neuron nuclei when compared to either familial ALS patients or non-neurologic disease controls. Tretinoin 91-104 cellular retinoic acid binding protein 2 Homo sapiens 106-147
23383387-5 2012 In sporadic ALS, the cytoplasmic binding protein that facilitates nuclear translocation of retinoic acid, cellular retinoic acid binding protein-II (CRABP-II), was localized to the nucleus and retinoic acid receptor beta (RARbeta) was significantly increased in motor neuron nuclei when compared to either familial ALS patients or non-neurologic disease controls. Tretinoin 91-104 cellular retinoic acid binding protein 2 Homo sapiens 149-157
22973984-5 2012 P27KIP1 was up-regulated during the differentiation process of both P19/ADAM23KD cells without RA induction, and P19 cells with RA induction. Tretinoin 95-97 cyclin-dependent kinase inhibitor 1B Mus musculus 0-7
22973984-5 2012 P27KIP1 was up-regulated during the differentiation process of both P19/ADAM23KD cells without RA induction, and P19 cells with RA induction. Tretinoin 128-130 cyclin-dependent kinase inhibitor 1B Mus musculus 0-7
22973984-7 2012 The findings indicate that ADAM23 suppresses neuronal differentiation through its disintegrin domain, and Adam23 KD up-regulates P27KIP1 in P19/ADAM23KD cells, one reason that P19/ADAM23KD cells can differentiate into neurons without RA induction. Tretinoin 234-236 cyclin-dependent kinase inhibitor 1B Mus musculus 129-136
21954838-10 2012 The addition of the growth factors ActA and BMP-7 enhanced the inductive effect of ATRA, as shown by the de novo expression of ZO-1 in addition to CK18 expression. Tretinoin 83-87 bone morphogenetic protein 7 Homo sapiens 44-49
22082219-0 2012 CRABP-II- and FABP5-independent all-trans retinoic acid resistance in COLO 16 human cutaneous squamous cancer cells. Tretinoin 42-55 fatty acid binding protein 5 Homo sapiens 14-19
22037423-6 2012 Moreover, there is concurrent induction of TRIAD1 and UBCH8 upon combinatorial treatment of acute promyelocytic leukemia cells with the pro-apoptotic epigenetic modulator valproic acid and the differentiation inducing agent all-trans retinoic acid. Tretinoin 234-247 ubiquitin conjugating enzyme E2 L6 Homo sapiens 54-59
22072756-4 2012 In this context, retinoic acid-inducible gene I (RIG-I) is the main cytosolic pattern recognition receptor known for detecting influenza A virus infection in mammalian cells. Tretinoin 17-30 antiviral innate immune response receptor RIG-I Anas platyrhynchos 49-54
23259068-0 2012 PKCdelta Regulates Translation Initiation through PKR and eIF2alpha in Response to Retinoic Acid in Acute Myeloid Leukemia Cells. Tretinoin 83-96 eukaryotic translation initiation factor 2A Homo sapiens 58-67
23259068-2 2012 Here, we investigated the regulation and role of eIF2alpha in acute promyelocytic (APL) and acute myeloid leukemia (AML) cells in response to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), the front-line therapies in APL. Tretinoin 152-165 eukaryotic translation initiation factor 2A Homo sapiens 49-58
23259068-2 2012 Here, we investigated the regulation and role of eIF2alpha in acute promyelocytic (APL) and acute myeloid leukemia (AML) cells in response to all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), the front-line therapies in APL. Tretinoin 167-171 eukaryotic translation initiation factor 2A Homo sapiens 49-58
23259068-3 2012 ATRA and ATO induce Ser-51 phosphorylation (inactivation) of eIF2alpha, through the induction of protein kinase C delta (PKCdelta) and PKR, but not other eIF2alpha kinases, such as GCN2 and PERK in APL (NB4) and AML cells (HL60, U937, and THP-1). Tretinoin 0-4 eukaryotic translation initiation factor 2A Homo sapiens 61-70
23259068-3 2012 ATRA and ATO induce Ser-51 phosphorylation (inactivation) of eIF2alpha, through the induction of protein kinase C delta (PKCdelta) and PKR, but not other eIF2alpha kinases, such as GCN2 and PERK in APL (NB4) and AML cells (HL60, U937, and THP-1). Tretinoin 0-4 eukaryotic translation initiation factor 2 alpha kinase 4 Homo sapiens 181-185
23285066-8 2012 Overexpression of transcription factor Nanog was possibly achieved through a RA-induced non-genomic c-Src/Stat3/Nanog signaling pathway mediated by the subcellular c-Src mRNA localization for the maintenance of pluripotency in tNSCs. Tretinoin 77-79 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 100-105
23285066-8 2012 Overexpression of transcription factor Nanog was possibly achieved through a RA-induced non-genomic c-Src/Stat3/Nanog signaling pathway mediated by the subcellular c-Src mRNA localization for the maintenance of pluripotency in tNSCs. Tretinoin 77-79 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 164-169
22962636-3 2012 Here we showed that retinoic acid and transforming growth factor-beta1 promoted the differentiation of CD8alphaalpha T cells from CD4 T cells in a Runx3-dependent manner. Tretinoin 20-33 CD4 antigen Mus musculus 130-133
22962636-3 2012 Here we showed that retinoic acid and transforming growth factor-beta1 promoted the differentiation of CD8alphaalpha T cells from CD4 T cells in a Runx3-dependent manner. Tretinoin 20-33 runt related transcription factor 3 Mus musculus 147-152
22147914-4 2011 Here, by using an RNAi E3-ubiquitin ligase entry screen, we identified CUL-3 and RBX1 as components of the E3 ubiquitin ligase involved in the RA-induced ubiquitination and subsequent degradation of SRC-3. Tretinoin 143-145 ring-box 1 Homo sapiens 81-85
22071108-3 2011 Upon meiosis initiation, Msx1 and Msx2 genes are strongly expressed in the foetal ovary, possibly stimulated by soluble factors found there: bone morphogenetic proteins Bmp2 and Bmp4, and retinoic acid. Tretinoin 188-201 msh homeobox 1 Homo sapiens 25-29
21725974-7 2011 SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Tretinoin 35-39 growth differentiation factor 15 Homo sapiens 93-98
21725974-7 2011 SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Tretinoin 35-39 intercellular adhesion molecule 1 Homo sapiens 100-105
21725974-7 2011 SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Tretinoin 35-39 C-X-C motif chemokine ligand 10 Homo sapiens 159-165
21720768-6 2011 By means of FITC-labeled tomato lectin affinity staining and flow-cytometry, it was found that the product of beta3GnT-2 and -8, polyLacNAc was also increased on the cell surface of HL-60 and NB4 treated with ATRA or DMSO, but unchanged when treated with PMA. Tretinoin 209-213 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 110-120
21989909-7 2011 By combining manipulation of gene function, cell transplantation approaches and transgenic reporter analysis we establish that Mnx1 functions downstream of RA within the endoderm to control cell fate decisions in the endocrine pancreas progenitor lineage. Tretinoin 156-158 motor neuron and pancreas homeobox 1 Danio rerio 127-131
21839859-0 2011 CD4+ Foxp3+ regulatory T cells induced by TGF-beta, IL-2 and all-trans retinoic acid attenuate obliterative bronchiolitis in rat trachea transplantation. Tretinoin 71-84 Cd4 molecule Rattus norvegicus 0-3
21839859-4 2011 We show that the combination of TGF-beta, Interleukin (IL)-2, and all-trans retinoic acid (atRA) could induce naive rat CD4(+)CD25(-) T cells to differentiate into CD4(+)CD25(+)Foxp3(+) T cells in vitro, and they acquired suppressive function. Tretinoin 76-89 Cd4 molecule Rattus norvegicus 120-123
21839859-4 2011 We show that the combination of TGF-beta, Interleukin (IL)-2, and all-trans retinoic acid (atRA) could induce naive rat CD4(+)CD25(-) T cells to differentiate into CD4(+)CD25(+)Foxp3(+) T cells in vitro, and they acquired suppressive function. Tretinoin 76-89 Cd4 molecule Rattus norvegicus 164-167
21839859-4 2011 We show that the combination of TGF-beta, Interleukin (IL)-2, and all-trans retinoic acid (atRA) could induce naive rat CD4(+)CD25(-) T cells to differentiate into CD4(+)CD25(+)Foxp3(+) T cells in vitro, and they acquired suppressive function. Tretinoin 91-95 Cd4 molecule Rattus norvegicus 120-123
21839859-4 2011 We show that the combination of TGF-beta, Interleukin (IL)-2, and all-trans retinoic acid (atRA) could induce naive rat CD4(+)CD25(-) T cells to differentiate into CD4(+)CD25(+)Foxp3(+) T cells in vitro, and they acquired suppressive function. Tretinoin 91-95 Cd4 molecule Rattus norvegicus 164-167
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 50-63 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 124-131
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 65-67 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 124-131
21906690-1 2011 INTRODUCTION: The cytochrome P450 CYP26 family of retinoic acid (RA) metabolizing enzymes, comprising CYP26A1, CYP26B1, and CYP26C1 is critical for establishing patterns of RA distribution during embryonic development and retinoid homeostasis in the adult. Tretinoin 173-175 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 124-131
21906690-3 2011 CYP26C1 has also been shown to efficiently metabolize the 9-cis isomer of RA. Tretinoin 74-76 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 0-7
21988834-1 2011 Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors (TFs) comprising retinoic acid receptor (RARalpha, beta, gamma) and retinoid X receptor (RXRalpha, beta, gamma). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 143-189
21988834-1 2011 Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors (TFs) comprising retinoic acid receptor (RARalpha, beta, gamma) and retinoid X receptor (RXRalpha, beta, gamma). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 191-199
21988834-1 2011 Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors (TFs) comprising retinoic acid receptor (RARalpha, beta, gamma) and retinoid X receptor (RXRalpha, beta, gamma). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 143-189
21988834-1 2011 Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors (TFs) comprising retinoic acid receptor (RARalpha, beta, gamma) and retinoid X receptor (RXRalpha, beta, gamma). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 191-199
21988834-3 2011 Using an RA-inducible differentiation model, we defined the temporal changes in the genome-wide binding patterns of RARgamma and RXRalpha and correlated them with transcription regulation. Tretinoin 9-11 retinoid X receptor alpha Homo sapiens 129-137
21691148-6 2011 These results provide evidence that the upregulation of Beclin 1 by ATRA constitutes an anti-apoptotic signal for maintaining the viability of mature APL cells, but has no crucial effect on the granulocytic differentiation. Tretinoin 68-72 beclin 1 Homo sapiens 56-64
21768647-6 2011 Moreover, together with Rara, Trim24 bound to the retinoic acid-responsive element of the Stat1 promoter and repressed its retinoic acid-induced transcription. Tretinoin 50-63 signal transducer and activator of transcription 1 Mus musculus 90-95
21733845-1 2011 The retinoic acid-related orphan nuclear receptor gammat (RORgammat)/RORgamma2 is well known as a master regulator of interleukin 17 (IL-17)-producing helper T (Th17) cell development. Tretinoin 4-17 interleukin 17A Mus musculus 118-132
21733845-1 2011 The retinoic acid-related orphan nuclear receptor gammat (RORgammat)/RORgamma2 is well known as a master regulator of interleukin 17 (IL-17)-producing helper T (Th17) cell development. Tretinoin 4-17 interleukin 17A Mus musculus 134-139
21519922-6 2011 Retinol, retinal, and retinoic acid (RA) induced Pck1 expression dose-dependently in primary hepatocytes. Tretinoin 22-35 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 49-53
21673049-4 2011 In this study, on the basis of immunocytochemical analysis, western blots, and quantitative real-time reverse transcription PCR, we could demonstrate a reduced expression of RXRalpha in choriocarcinoma cell lines and in human VTs after stimulation with the retinoids 9-cis-retinoic acid and all-trans-retinoic acid and the prostaglandin 15-deoxy-Delta(12,14)-prostaglandin J(2). Tretinoin 272-286 retinoid X receptor alpha Homo sapiens 174-182
21383690-5 2011 Immunofluorescence and western blot analysis indicated that RA induced the expression of lineage-specific differentiation markers Tuj1 and GFAP and reduced the expression of neural stem cell markers such as CD133, Msi-1, nestin and Sox-2. Tretinoin 60-62 glial fibrillary acidic protein Homo sapiens 139-143
21383690-5 2011 Immunofluorescence and western blot analysis indicated that RA induced the expression of lineage-specific differentiation markers Tuj1 and GFAP and reduced the expression of neural stem cell markers such as CD133, Msi-1, nestin and Sox-2. Tretinoin 60-62 SRY-box transcription factor 2 Homo sapiens 232-237
21608077-4 2011 When compared with wild-type ESCs and gastrulating embryos, Oct4 repression is lost and its proximal promoter is significantly hypomethylated in retinoic acid (RA)-differentiated GCNF(-/-) ESCs and GCNF(-/-) embryos. Tretinoin 145-158 nuclear receptor subfamily 6 group A member 1 Homo sapiens 179-183
21608077-4 2011 When compared with wild-type ESCs and gastrulating embryos, Oct4 repression is lost and its proximal promoter is significantly hypomethylated in retinoic acid (RA)-differentiated GCNF(-/-) ESCs and GCNF(-/-) embryos. Tretinoin 160-162 nuclear receptor subfamily 6 group A member 1 Homo sapiens 179-183
21608077-4 2011 When compared with wild-type ESCs and gastrulating embryos, Oct4 repression is lost and its proximal promoter is significantly hypomethylated in retinoic acid (RA)-differentiated GCNF(-/-) ESCs and GCNF(-/-) embryos. Tretinoin 160-162 nuclear receptor subfamily 6 group A member 1 Homo sapiens 198-202
21594970-3 2011 The expression of some genes (Shh, Ptch-1, Gsc, and Msx2) controlled by retinoic acid is downregulated in rat embryos exposed at the phylotypic stage to the triazole triadimefon (FON). Tretinoin 72-85 sonic hedgehog signaling molecule Rattus norvegicus 30-33
21594970-3 2011 The expression of some genes (Shh, Ptch-1, Gsc, and Msx2) controlled by retinoic acid is downregulated in rat embryos exposed at the phylotypic stage to the triazole triadimefon (FON). Tretinoin 72-85 goosecoid homeobox Rattus norvegicus 43-46
20887097-6 2011 Subsequent treatment of the DE cells by retinoic acid induced the formation of gut tube endoderm cells that expressed the specific marker Hnf1b. Tretinoin 40-53 HNF1 homeobox B Mus musculus 138-143
21514413-6 2011 Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. Tretinoin 21-23 fatty acid binding protein 5 Homo sapiens 254-259
21235714-1 2011 13-cis Retinoic acid (13cRA), a stereoisomeric form of retinoic acid, is naturally generated in the body and is also used clinically to treat acute promyelocytic leukemia, some skin diseases and cancer. Tretinoin 55-68 myotubularin related protein 11 Homo sapiens 24-27
21307853-5 2011 Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. Tretinoin 124-137 interleukin 15 Mus musculus 46-51
20717697-6 2011 Furthermore, E-cadherin and beta-catenin protein expression levels were increased by RA treatment. Tretinoin 85-87 catenin beta 1 Gallus gallus 28-40
20717697-9 2011 The proliferating effect of RA on PGCs was further confirmed by increased mRNA expression of cyclins, CCND1 and CCNE1, and cyclin-dependent kinases 6 and 2, which are critical for G1-S progression in cell cycle. Tretinoin 28-30 cyclin E1 Gallus gallus 112-117
21403633-9 2011 Moreover, recent work has determined that the vitamin A metabolite all-trans retinoic acid (RA) is the main molecular mechanism responsible for inducing gut-specific adhesion receptors (integrin a4b7and chemokine receptor CCR9) on lymphocytes. Tretinoin 77-90 chemokine (C-C motif) receptor 9 Mus musculus 222-226
21118818-0 2011 MicroRNAs-10a and -10b contribute to retinoic acid-induced differentiation of neuroblastoma cells and target the alternative splicing regulatory factor SFRS1 (SF2/ASF). Tretinoin 37-50 serine and arginine rich splicing factor 1 Homo sapiens 159-162
21118818-0 2011 MicroRNAs-10a and -10b contribute to retinoic acid-induced differentiation of neuroblastoma cells and target the alternative splicing regulatory factor SFRS1 (SF2/ASF). Tretinoin 37-50 serine and arginine rich splicing factor 1 Homo sapiens 163-166
21228001-9 2011 We show that RA downregulates the Hh signaling components ptc1 and smo in endodermal explants, indicating a possible molecular mechanism for blocking axial mesoderm-derived Hh ligands from the prepancreatic endoderm during the specification stage. Tretinoin 13-15 smoothened, frizzled class receptor Danio rerio 67-70
21427903-5 2011 RESULTS: (1) Gene-chip analysis showed that in RA-induced cleft palate group wnt8a and fgf9 were down-regulated, wnt3 and fgf10 were up-regulated in conversely. Tretinoin 47-49 fibroblast growth factor 10 Mus musculus 122-127
20974122-7 2011 Its expression was found to be strongly inhibited by DN-RARalpha, an inhibition relieved by pharmacological doses of all-trans retinoic acid (atRA) in culture and in vivo. Tretinoin 127-140 retinoic acid receptor, alpha Mus musculus 56-64
20974122-7 2011 Its expression was found to be strongly inhibited by DN-RARalpha, an inhibition relieved by pharmacological doses of all-trans retinoic acid (atRA) in culture and in vivo. Tretinoin 142-146 retinoic acid receptor, alpha Mus musculus 56-64
20888882-8 2011 The differentiated ADP induced by retinoic acid was characterized by immunostaining with anti-GFAP or anti-Tuj1 antibody. Tretinoin 34-47 glial fibrillary acidic protein Rattus norvegicus 94-98
21249211-9 2011 Overexpression of Cyp26b1 significantly suppressed the RA effect to induce expression of the gut-homing receptor CCR9 on T cells. Tretinoin 55-57 chemokine (C-C motif) receptor 9 Mus musculus 113-117
21148184-4 2011 In particular, we detected an expansion of the expression domains of the RA-catabolizing enzymes Cyp26a1 and Cyp26c1, and a downregulation of the RA-synthesizing enzyme Raldh3. Tretinoin 73-75 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 109-116
20857298-12 2011 CONCLUSIONS: Upregulation of PTHrP and PTHrP-R genes after prenatal treatment with RA in the nitrofen-induced HL suggests that RA may have a therapeutic potential in reverting lung hypoplasia in CDH, by stimulating surfactant production and alveolar maturation. Tretinoin 127-129 parathyroid hormone-like hormone Rattus norvegicus 29-34
20857298-12 2011 CONCLUSIONS: Upregulation of PTHrP and PTHrP-R genes after prenatal treatment with RA in the nitrofen-induced HL suggests that RA may have a therapeutic potential in reverting lung hypoplasia in CDH, by stimulating surfactant production and alveolar maturation. Tretinoin 127-129 parathyroid hormone-like hormone Rattus norvegicus 39-44
22110742-10 2011 Mechanistically, RA sensitization by MLN4924 was mediated via enhanced apoptosis, likely through accumulation of pro-apoptotic proteins NOXA and c-JUN, two well-known substrates of SAG-SCF E3 ligase. Tretinoin 17-19 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-150
22110742-10 2011 Mechanistically, RA sensitization by MLN4924 was mediated via enhanced apoptosis, likely through accumulation of pro-apoptotic proteins NOXA and c-JUN, two well-known substrates of SAG-SCF E3 ligase. Tretinoin 17-19 KIT ligand Homo sapiens 185-188
21575456-0 2011 [Effects of As2O3 and all-trans retinoic acid on the growth of HeLa cell line and their relation with gene NDRG1]. Tretinoin 22-45 N-myc downstream regulated 1 Homo sapiens 107-112
21575456-6 2011 Western blot and RT-PCR techniques showed that As2O3 and ATRA down-regulated the expressions of NDRG-1 protein and mRNA (P < 0.05). Tretinoin 57-61 N-myc downstream regulated 1 Homo sapiens 96-102
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 45-58 interleukin 12b Mus musculus 180-188
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 45-58 interleukin 12b Mus musculus 185-188
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 60-62 interleukin 12b Mus musculus 180-188
20826012-4 2010 Treatment with the transcriptional activator retinoic acid (RA) suppressed mRNA expression and protein release of several important cytokines (IL-1beta 4%, IL-6 21%, TNFalpha 30%, IL-12p40 42%, and IL-12p35/p40 27%; p<0.01). Tretinoin 60-62 interleukin 12b Mus musculus 185-188
20702419-1 2010 Transcription factor Foxm1 plays a critical role during embryonic development and its expression is repressed during retinoic acid (RA)-induced differentiation of pluripotent P19 embryonal carcinoma cells at the early stage, correlated with downregulation of expression of pluripotency markers. Tretinoin 117-130 forkhead box M1 Homo sapiens 21-26
20702419-1 2010 Transcription factor Foxm1 plays a critical role during embryonic development and its expression is repressed during retinoic acid (RA)-induced differentiation of pluripotent P19 embryonal carcinoma cells at the early stage, correlated with downregulation of expression of pluripotency markers. Tretinoin 132-134 forkhead box M1 Homo sapiens 21-26
20576349-4 2010 Downregulation of ALK protein by ATRA was accompanied by apoptosis in neuroblastoma cells with gene amplification or gain-of-function mutation of ALK but not in neuroblastoma cells without these genetic alterations. Tretinoin 33-37 ALK receptor tyrosine kinase Homo sapiens 18-21
20576349-4 2010 Downregulation of ALK protein by ATRA was accompanied by apoptosis in neuroblastoma cells with gene amplification or gain-of-function mutation of ALK but not in neuroblastoma cells without these genetic alterations. Tretinoin 33-37 ALK receptor tyrosine kinase Homo sapiens 146-149
20815781-7 2010 Vicinal dithiol-reactive phenylarsine oxide (50 nM) also increased CD11b expression induced by DMSO or ATRA. Tretinoin 103-107 integrin subunit alpha M Homo sapiens 67-72
20702525-4 2010 Partitioning of RA between the nuclear receptors RA receptor alpha and peroxisome-proliferator-activated receptor beta/delta is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. Tretinoin 16-18 peroxisome proliferator activated receptor delta Homo sapiens 71-118
20702525-4 2010 Partitioning of RA between the nuclear receptors RA receptor alpha and peroxisome-proliferator-activated receptor beta/delta is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. Tretinoin 16-18 cellular retinoic acid binding protein 2 Homo sapiens 179-208
20702525-4 2010 Partitioning of RA between the nuclear receptors RA receptor alpha and peroxisome-proliferator-activated receptor beta/delta is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. Tretinoin 16-18 cellular retinoic acid binding protein 2 Homo sapiens 210-216
20702525-4 2010 Partitioning of RA between the nuclear receptors RA receptor alpha and peroxisome-proliferator-activated receptor beta/delta is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. Tretinoin 16-18 fatty acid binding protein 5 Homo sapiens 222-250
20702525-4 2010 Partitioning of RA between the nuclear receptors RA receptor alpha and peroxisome-proliferator-activated receptor beta/delta is regulated by cytosol-to-nuclear shuttling proteins cellular RA binding protein 2 (CRABP2) and fatty acid binding protein 5 (FABP5), which induce apoptosis or enhance survival, respectively. Tretinoin 16-18 fatty acid binding protein 5 Homo sapiens 252-257
20709030-7 2010 After induced neurodifferentiation with all-trans retinoic acid, we observed significant neurodegeneration in SH-SY5Y cells stably transfected with miR-106b. Tretinoin 40-63 microRNA 106b Homo sapiens 148-156
20709030-10 2010 Our in vitro results suggested that Abeta42 oligomer-induced miR-106b leads to impairment in TGF-beta signaling through TbetaR II, concomitant with retinoic acid-induced neurodegeneration in SH-SY5Y cells. Tretinoin 148-161 microRNA 106b Homo sapiens 61-69
20951351-2 2010 In mammals, meiotic initiation requires retinoic acid (RA), which activates meiotic inducers, including Stra8, but how the switch to meiosis is controlled in male germ cells (spermatogonia) remains poorly understood. Tretinoin 40-53 stimulated by retinoic acid 8 Homo sapiens 104-109
20951351-2 2010 In mammals, meiotic initiation requires retinoic acid (RA), which activates meiotic inducers, including Stra8, but how the switch to meiosis is controlled in male germ cells (spermatogonia) remains poorly understood. Tretinoin 55-57 stimulated by retinoic acid 8 Homo sapiens 104-109
21313915-5 2010 In vitro administration of All-Trans Retinoic Acid (ATRA) increased dendritic growth and synaptophysin puncta intensity and increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin. Tretinoin 27-50 synaptophysin Homo sapiens 89-102
21313915-5 2010 In vitro administration of All-Trans Retinoic Acid (ATRA) increased dendritic growth and synaptophysin puncta intensity and increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin. Tretinoin 27-50 synaptophysin Homo sapiens 191-204
21313915-5 2010 In vitro administration of All-Trans Retinoic Acid (ATRA) increased dendritic growth and synaptophysin puncta intensity and increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin. Tretinoin 52-56 synaptophysin Homo sapiens 89-102
21313915-5 2010 In vitro administration of All-Trans Retinoic Acid (ATRA) increased dendritic growth and synaptophysin puncta intensity and increased expressions of neuronal nuclei, neuron specific enolase, synaptophysin. Tretinoin 52-56 synaptophysin Homo sapiens 191-204
20350780-4 2010 Treatment with retinoic acid (RA), a ligand for CRABP-II, induced HCC cell apoptosis more effectively in hypoxia than in normoxia, whereas hypoxia-induced CRABP-II expression attenuated RA-induced apoptosis. Tretinoin 15-28 cellular retinoic acid binding protein 2 Homo sapiens 48-56
20350780-4 2010 Treatment with retinoic acid (RA), a ligand for CRABP-II, induced HCC cell apoptosis more effectively in hypoxia than in normoxia, whereas hypoxia-induced CRABP-II expression attenuated RA-induced apoptosis. Tretinoin 15-28 cellular retinoic acid binding protein 2 Homo sapiens 155-163
20350780-4 2010 Treatment with retinoic acid (RA), a ligand for CRABP-II, induced HCC cell apoptosis more effectively in hypoxia than in normoxia, whereas hypoxia-induced CRABP-II expression attenuated RA-induced apoptosis. Tretinoin 30-32 cellular retinoic acid binding protein 2 Homo sapiens 48-56
20350780-4 2010 Treatment with retinoic acid (RA), a ligand for CRABP-II, induced HCC cell apoptosis more effectively in hypoxia than in normoxia, whereas hypoxia-induced CRABP-II expression attenuated RA-induced apoptosis. Tretinoin 30-32 cellular retinoic acid binding protein 2 Homo sapiens 155-163
20350780-5 2010 Inhibition of CRABP-II enhanced RA-induced apoptosis and sensitized RA-resistant HCC cells to RA cytotoxicity by attenuating p42/44 MAPK and Akt activation. Tretinoin 32-34 cellular retinoic acid binding protein 2 Homo sapiens 14-22
20870174-2 2010 RA augmentation involved the binding of retinoic acid receptor (RAR) and retinoid X receptor (RXR) to a dominant site in enhancer I and a subordinate site in the promoter. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 73-92
20870174-2 2010 RA augmentation involved the binding of retinoic acid receptor (RAR) and retinoid X receptor (RXR) to a dominant site in enhancer I and a subordinate site in the promoter. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 94-97
20690178-3 2010 Retinoic acid (RA) was used to induce the gut-specific homing receptor alpha(4)beta(7) efficiently and, to some extent, the chemokine receptor CCR9 on in vitro expanded Treg. Tretinoin 0-13 chemokine (C-C motif) receptor 9 Mus musculus 143-147
20690178-3 2010 Retinoic acid (RA) was used to induce the gut-specific homing receptor alpha(4)beta(7) efficiently and, to some extent, the chemokine receptor CCR9 on in vitro expanded Treg. Tretinoin 15-17 chemokine (C-C motif) receptor 9 Mus musculus 143-147
20648638-4 2010 RA acts through its binding to RA receptors (RAR) and retinoid X receptors (RXR), two members of the superfamily of nuclear receptors that act as ligand-dependent transcription factors. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 54-74
20648638-4 2010 RA acts through its binding to RA receptors (RAR) and retinoid X receptors (RXR), two members of the superfamily of nuclear receptors that act as ligand-dependent transcription factors. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 76-79
20615082-4 2010 ATO augmented ATRA-induced RAF/MEK/ERK axis signaling, expression of CD11b and p47(PHOX), and inducible oxidative metabolism. Tretinoin 14-18 integrin subunit alpha M Homo sapiens 69-74
20735826-15 2010 This RA signaling is essential for Nolz1-induced neurogenesis, which is impaired in a RA-free environment or in the presence of a RAR inverse agonist. Tretinoin 5-7 retinoic acid receptor, alpha Mus musculus 130-133
20727130-6 2010 Concerning PMN, retinoic acid induced an increase in both spontaneous migration and cell surface expression of CD11b in the two different age populations, whereas bactericidal activity and phagocytosis remained unchanged. Tretinoin 16-29 integrin subunit alpha M Homo sapiens 111-116
20716331-10 2010 In serum-containing medium, the expression percentages of CD133 and GFAP in the differentiated BTSCs were (2.29% +/- 0.27%) and (75.60% +/- 4.03%) respectively in the ATRA group, and (7.05% +/- 0.49%) and (12.51% +/- 0.77%) respectively in the control group. Tretinoin 167-171 glial fibrillary acidic protein Homo sapiens 68-72
20562004-7 2010 Thus, atRA was shown to induce BCRP gene expression probably via the RAR/RXR signalling pathway, resulting in effective removal of B[a]P metabolites from intestinal cells. Tretinoin 6-10 retinoid X receptor alpha Homo sapiens 73-76
20338915-0 2010 Retinoic acid represses CYP7A1 expression in human hepatocytes and HepG2 cells by FXR/RXR-dependent and independent mechanisms. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 86-89
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 retinoid X receptor alpha Homo sapiens 286-305
20338915-4 2010 Our present study revealed that CYP7A1 mRNA expression is greatly repressed by RA in both human hepatocytes and HepG2 cells where increased fibroblast growth factor 19 (FGF19) and small heterodimer partner (SHP) expressions were also observed, suggesting farnesoid X receptor (FXR) and retinoid X receptor (RXR) were activated. Tretinoin 79-81 retinoid X receptor alpha Homo sapiens 307-310
20338915-7 2010 Knocking down of FXR or RXRalpha by small interference RNA (siRNA) in human hepatocytes increased CYP7A1 basal expression, but the repressive effect of atRA persisted, suggesting there are also FXR/RXR-independent mechanisms mediating atRA repression of CYP7A1 expression. Tretinoin 152-156 retinoid X receptor alpha Homo sapiens 24-32
20338915-7 2010 Knocking down of FXR or RXRalpha by small interference RNA (siRNA) in human hepatocytes increased CYP7A1 basal expression, but the repressive effect of atRA persisted, suggesting there are also FXR/RXR-independent mechanisms mediating atRA repression of CYP7A1 expression. Tretinoin 152-156 retinoid X receptor alpha Homo sapiens 24-27
20689834-9 2010 BMP9-induced osteogenic differentiation and mineralization is synergistically enhanced by 9CRA and ATRA in vitro. Tretinoin 99-103 growth differentiation factor 2 Mus musculus 0-4
20211151-4 2010 The expression levels of CAR mRNA in human primary hepatocytes and HepG2 cells were increased by all-trans retinoic acid. Tretinoin 107-120 nuclear receptor subfamily 1 group I member 3 Homo sapiens 25-28
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 0-23 tumor necrosis factor receptor superfamily, member 1a Mus musculus 111-143
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 0-23 tumor necrosis factor receptor superfamily, member 1a Mus musculus 145-150
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 0-23 tumor necrosis factor receptor superfamily, member 1a Mus musculus 177-182
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 25-29 tumor necrosis factor receptor superfamily, member 1a Mus musculus 111-143
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 25-29 tumor necrosis factor receptor superfamily, member 1a Mus musculus 145-150
20414324-2 2010 All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-alpha-induced apoptosis in cancer cells. Tretinoin 25-29 tumor necrosis factor receptor superfamily, member 1a Mus musculus 177-182
20375987-0 2010 A human ALDH1A2 gene variant is associated with increased newborn kidney size and serum retinoic acid. Tretinoin 88-101 aldehyde dehydrogenase 1 family member A2 Homo sapiens 8-15
20375987-8 2010 As maternal vitamin A deficiency is widespread in developing countries and may compromise availability of retinol for fetal RA synthesis, our study suggests that the ALDH1A2 rs7169289(G) variant might be protective for such individuals. Tretinoin 124-126 aldehyde dehydrogenase 1 family member A2 Homo sapiens 166-173
20551924-2 2010 present evidence that fetal genetic variation in the 3" end of ALDH1A2 may influence nephrogenesis and blood retinoic acid levels. Tretinoin 109-122 aldehyde dehydrogenase 1 family member A2 Homo sapiens 63-70
20410309-0 2010 Transcriptional regulation of cannabinoid receptor-1 expression in the liver by retinoic acid acting via retinoic acid receptor-gamma. Tretinoin 80-93 retinoic acid receptor, gamma Mus musculus 105-133
20483764-2 2010 In the current study, we demonstrate that naive CD4+CD25-Foxp3- T cells specific for the myelin proteolipid protein (PLP)139-151 peptide can be converted into CD25+Foxp3+ induced Treg cells (iTregs) when stimulated in the presence of TGF-beta, retinoic acid, and IL-2. Tretinoin 244-257 interleukin 2 receptor, alpha chain Mus musculus 52-56
20598227-0 2010 Role of acetylated p53 in regulating the expression of map2 in retinoic acid-induced P19 cells. Tretinoin 63-76 microtubule associated protein 2 Homo sapiens 55-59
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 193-206 microtubule associated protein 2 Homo sapiens 91-123
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 193-206 microtubule associated protein 2 Homo sapiens 125-129
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 208-210 microtubule associated protein 2 Homo sapiens 91-123
20598227-1 2010 OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA). Tretinoin 208-210 microtubule associated protein 2 Homo sapiens 125-129
19651460-5 2010 In vitro co-culture experiments showed that RA treated THP-1 cells were more stimulatory for CD4(+) than for CD8(+) T cells, as determined by CFSE loss, in comparison to untreated THP-1 cells. Tretinoin 44-46 CD8a molecule Homo sapiens 109-112
20484817-4 2010 Here, we present evidence that endogenous RA acts as a major regulatory signal integrating Wnt and Tgfbeta pathways in the control of Fgf10 expression during induction of the mouse primordial lung. Tretinoin 42-44 fibroblast growth factor 10 Mus musculus 134-139
20187766-2 2010 Recently, all-trans retinoic acid has been shown that can lead T-cell response by suppressing Th17 development via retinoic acid receptor (RAR), but it is still unknown whether all-trans retinoic acid can modulate Th1 response of inflammatory bowel disease. Tretinoin 10-33 retinoic acid receptor, alpha Mus musculus 139-142
20187766-7 2010 All-trans retinoic acid treatment inhibited inflammatory responses as shown by lower histological inflammatory scores and MPO activity, compared with LE135 and medium groups. Tretinoin 10-23 myeloperoxidase Mus musculus 122-125
19937743-9 2010 Thus, the specific defects in spermiogenesis in RARalpha-deficient testes may correlate with a disrupted cyclic expression of RA-responsive structural components, including vimentin, a downregulation of connexin-40 in spermatogenic cells, and delayed assembly of ZO-1 into Sertoli cell tight junctions. Tretinoin 48-50 vimentin Mus musculus 173-181
20308937-7 2010 ALDH1A2 encodes retinaldehyde dehydrogenase (RALDH) 2, which synthesizes RA in fetal tissues. Tretinoin 45-47 aldehyde dehydrogenase 1 family member A2 Homo sapiens 0-7
20308937-8 2010 We also found that homozygosity for the (A) allele of the rs12724719 SNP in the CRABP2 gene (CRABP2rs12724719(A/A)) was associated with 4.4-fold increase in umbilical cord serum RA. Tretinoin 81-83 cellular retinoic acid binding protein 2 Homo sapiens 93-99
20620545-7 2010 The CsA+ATRA group showed a marked reduction in PCNA- and CD68-positive cells: namely, 33.96 +/- 8.65% versus 60.17 +/- 17.74% (P < .01) and 17.63 +/- 4.24% versus 32.13 +/- 9.26 (P < .01), respectively. Tretinoin 8-12 proliferating cell nuclear antigen Rattus norvegicus 48-52
20228061-1 2010 In preadipocytes, retinoic acid (RA) regulates gene expression by activating the nuclear RA receptor (RAR) and its cognate intracellular lipid-binding protein CRABP-II. Tretinoin 18-31 cellular retinoic acid binding protein 2 Homo sapiens 159-167
20228061-1 2010 In preadipocytes, retinoic acid (RA) regulates gene expression by activating the nuclear RA receptor (RAR) and its cognate intracellular lipid-binding protein CRABP-II. Tretinoin 33-35 cellular retinoic acid binding protein 2 Homo sapiens 159-167
20228061-3 2010 The data presented here indicate that the diminished ability of RA to activate RAR following induction of differentiation stems from down-regulation of CRABP-II. Tretinoin 64-66 cellular retinoic acid binding protein 2 Homo sapiens 152-160
20231276-1 2010 Retinoic acid (RA), a vitamin A metabolite, regulates transcription by binding to RA receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 82-93
20231276-1 2010 Retinoic acid (RA), a vitamin A metabolite, regulates transcription by binding to RA receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 95-98
20231276-1 2010 Retinoic acid (RA), a vitamin A metabolite, regulates transcription by binding to RA receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 82-93
20231276-1 2010 Retinoic acid (RA), a vitamin A metabolite, regulates transcription by binding to RA receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 95-98
20106871-6 2010 Wnt-4 may control meiosis via these proteins since the Cyp26b1 enzyme is known to degrade retinoic acid (RA) and inhibit meiosis in the male embryo, and Stra8 induces meiosis in the female through RA. Tretinoin 90-103 Wnt family member 4 Homo sapiens 0-5
20106871-6 2010 Wnt-4 may control meiosis via these proteins since the Cyp26b1 enzyme is known to degrade retinoic acid (RA) and inhibit meiosis in the male embryo, and Stra8 induces meiosis in the female through RA. Tretinoin 105-107 Wnt family member 4 Homo sapiens 0-5
20122913-0 2010 Retinoic acid signaling in perioptic mesenchyme represses Wnt signaling via induction of Pitx2 and Dkk2. Tretinoin 0-13 wingless-type MMTV integration site family, member 5A Mus musculus 58-61
20122913-0 2010 Retinoic acid signaling in perioptic mesenchyme represses Wnt signaling via induction of Pitx2 and Dkk2. Tretinoin 0-13 dickkopf WNT signaling pathway inhibitor 2 Mus musculus 99-103
19778331-0 2010 Changes in cell characteristics due to retinoic acid; specifically, a decrease in the expression of claudin-1 and increase in claudin-4 within tight junctions in stratified oral keratinocytes. Tretinoin 39-52 claudin 1 Homo sapiens 100-122
19778331-6 2010 The RT-PCR showed that retinoic acid significantly reduced the expression of claudin-1 mRNA, whereas it dramatically enhanced expression of claudin-4 mRNA. Tretinoin 23-36 claudin 1 Homo sapiens 77-86
19778331-8 2010 In the culture with retinoic acid, the flattened uppermost cells were absent and there claudin-1 was less present, but claudin-4 was prominently present in all layers. Tretinoin 20-33 claudin 1 Homo sapiens 87-96
19778331-10 2010 Along with the change of claudin species, the expressions of keratin 7, keratin 8 and keratin 18, as markers for the simple epithelium, were clearly stimulated by retinoic acid. Tretinoin 163-176 keratin 8 Homo sapiens 72-81
19778331-11 2010 CONCLUSION: Retinoic acid changed the expression of tight junction constituent molecules, such as claudin-1 and claudin-4, in oral keratinocytes. Tretinoin 12-25 claudin 1 Homo sapiens 98-107
20089289-4 2010 Experiments using cell cycle arrest reagents (all-trans retinoic acid (RA) and colchicine) confirmed that L1 proteins expressed from PV Nat L1 genes were facilitated in G2/M-like KCs upon differentiation. Tretinoin 56-69 bromodomain containing 2 Homo sapiens 136-139
20159962-0 2010 Opposing effects of retinoic acid and FGF9 on Nanos2 expression and meiotic entry of mouse germ cells. Tretinoin 20-33 nanos C2HC-type zinc finger 2 Mus musculus 46-52
20159962-5 2010 We observed that the promeiotic factor AtRA, an analog of retinoic acid (RA), downregulates NANOS2 levels, in both fetal and postnatal gonocytes, while promoting meiosis. Tretinoin 39-43 nanos C2HC-type zinc finger 2 Mus musculus 92-98
20159962-5 2010 We observed that the promeiotic factor AtRA, an analog of retinoic acid (RA), downregulates NANOS2 levels, in both fetal and postnatal gonocytes, while promoting meiosis. Tretinoin 58-71 nanos C2HC-type zinc finger 2 Mus musculus 92-98
20159962-5 2010 We observed that the promeiotic factor AtRA, an analog of retinoic acid (RA), downregulates NANOS2 levels, in both fetal and postnatal gonocytes, while promoting meiosis. Tretinoin 41-43 nanos C2HC-type zinc finger 2 Mus musculus 92-98
19448158-4 2010 This includes monitoring of retinoic acid (RA) response element (RARE) activation with RARE-lacZ mice, RA supplementation studies, systematic analyses of the expression profile of key elements in the RA signaling pathway within the developing diaphragm, and the in utero delivery of a RA receptor (RAR) antagonist. Tretinoin 43-45 retinoic acid receptor, alpha Mus musculus 65-68
20072156-3 2010 Here, we provide the first demonstration that onzin expression is significantly downregulated during differentiation induction of acute myeloid leukemic (AML) cell lines and primary cells by all-trans retinoic acid (ATRA) and especially by phorbol 12-myristate 13-acetate (PMA). Tretinoin 201-214 placenta associated 8 Homo sapiens 46-51
20072156-3 2010 Here, we provide the first demonstration that onzin expression is significantly downregulated during differentiation induction of acute myeloid leukemic (AML) cell lines and primary cells by all-trans retinoic acid (ATRA) and especially by phorbol 12-myristate 13-acetate (PMA). Tretinoin 216-220 placenta associated 8 Homo sapiens 46-51
20133701-6 2010 P19 cells depleted of Ajuba are highly sensitized to all-trans retinoic acid (atRA)-induced transcription and differentiation. Tretinoin 63-76 ajuba LIM protein Homo sapiens 22-27
20133701-6 2010 P19 cells depleted of Ajuba are highly sensitized to all-trans retinoic acid (atRA)-induced transcription and differentiation. Tretinoin 78-82 ajuba LIM protein Homo sapiens 22-27
20133701-8 2010 Stimulation of cells with atRA results in the dissociation of Ajuba from these regions. Tretinoin 26-30 ajuba LIM protein Homo sapiens 62-67
20035057-10 2010 Activation of RXRalpha by retinoic acids increased the cyclin E1 promoter activity indicating retinoic acid-mediated signaling positively controls cyclin E1 gene expression. Tretinoin 26-40 cyclin E1 Mus musculus 55-64
20035057-10 2010 Activation of RXRalpha by retinoic acids increased the cyclin E1 promoter activity indicating retinoic acid-mediated signaling positively controls cyclin E1 gene expression. Tretinoin 26-39 cyclin E1 Mus musculus 55-64
20081195-4 2010 Consistent with expression of raldh2 in the dorsal interneurons of tetrapods, we also found that raldh2 is expressed in dorsal interneurons throughout the agnathan spinal cord, suggesting ancestral roles for RA signaling in the ontogenesis of intraspinal proprioception. Tretinoin 208-210 aldehyde dehydrogenase 1 family member A2 Gallus gallus 97-103
20110328-2 2010 We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinol-binding-protein-deficient (Rbp4(-/-)) mice. Tretinoin 24-37 retinol binding protein 4, plasma Mus musculus 249-253
20110328-2 2010 We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinol-binding-protein-deficient (Rbp4(-/-)) mice. Tretinoin 39-41 retinol binding protein 4, plasma Mus musculus 249-253
20043138-0 2010 Influence of LOX/COX inhibitors on cell differentiation induced by all-trans retinoic acid in neuroblastoma cell lines. Tretinoin 77-90 lysyl oxidase Homo sapiens 13-16
20043138-1 2010 We investigated the possible modulation by LOX/ COX inhibitors of all-trans retinoic acid (ATRA)-induced cell differentiation in two established neuroblastoma cell lines, SH-SY5Y and SK-N-BE(2). Tretinoin 76-89 lysyl oxidase Homo sapiens 43-46
20043138-1 2010 We investigated the possible modulation by LOX/ COX inhibitors of all-trans retinoic acid (ATRA)-induced cell differentiation in two established neuroblastoma cell lines, SH-SY5Y and SK-N-BE(2). Tretinoin 91-95 lysyl oxidase Homo sapiens 43-46
20155467-10 2010 After treatment with 10 mumol/L ATRA for 48 h, the Caspase3 and Caspase8 were significantly activated as compared with the control group (P<0.05). Tretinoin 32-36 caspase 8 Rattus norvegicus 64-72
20032483-0 2010 All-trans retinoic acid lowers serum retinol-binding protein 4 concentrations and increases insulin sensitivity in diabetic mice. Tretinoin 10-23 retinol binding protein 4, plasma Mus musculus 37-62
20032483-3 2010 In this study, we sought to determine whether retinoic acid (RA) administration decreases serum RBP4 and suppresses insulin resistance in diabetic ob/ob mice. Tretinoin 46-59 retinol binding protein 4, plasma Mus musculus 96-100
20032483-3 2010 In this study, we sought to determine whether retinoic acid (RA) administration decreases serum RBP4 and suppresses insulin resistance in diabetic ob/ob mice. Tretinoin 61-63 retinol binding protein 4, plasma Mus musculus 96-100
20032483-7 2010 RA treatment reduced body weight (P < 0.05), basal serum glucose (P < 0.001), serum retinol (P < 0.01), and RBP4 (P < 0.05). Tretinoin 0-2 retinol binding protein 4, plasma Mus musculus 117-121
20236590-8 2010 After treatment by ATRA, level of integrin beta1 mRNA in A431 cells significantly decreased compared with untreated control (P < 0.05), and the ratios between the intensity values of integrin beta1 to beta-actin were 0.071 +/- 0.025 and 0.029 +/- 0.018 at 24 h and 48 h, respectively, whereas in controls were 0.148 +/- 0.027 and 0.136 +/- 0.011 (P < 0.05). Tretinoin 19-23 integrin subunit beta 1 Homo sapiens 34-48
20236590-8 2010 After treatment by ATRA, level of integrin beta1 mRNA in A431 cells significantly decreased compared with untreated control (P < 0.05), and the ratios between the intensity values of integrin beta1 to beta-actin were 0.071 +/- 0.025 and 0.029 +/- 0.018 at 24 h and 48 h, respectively, whereas in controls were 0.148 +/- 0.027 and 0.136 +/- 0.011 (P < 0.05). Tretinoin 19-23 integrin subunit beta 1 Homo sapiens 186-200
20460768-0 2010 All-trans retinoic acid alleviates hepatic ischemia/reperfusion injury by enhancing manganese superoxide dismutase in rats. Tretinoin 10-23 superoxide dismutase 2 Rattus norvegicus 84-114
20460768-8 2010 The results demonstrate that atRA pretreatment attenuates liver I/R injury by inhibiting the release of malondialdehyde (MDA) and by enhancing the activity of superoxide dismutase (SOD). Tretinoin 29-33 superoxide dismutase 2 Rattus norvegicus 181-184
20460768-9 2010 To gain insight into the mechanism of the SOD up-regulation by atRA, the activity of p38 mitogenactivated protein kinase (p38MAKP) and Akt was measured. Tretinoin 63-67 superoxide dismutase 2 Rattus norvegicus 42-45
19747912-1 2010 Vav1 plays an important role in the all-trans retinoic acid (ATRA)-induced completion of the differentiation program of acute promyelocytic leukemia (APL)-derived cells, in which it strengthens the drug effects and is involved in the regulation of maturation-related proteins, such as the CD11b surface antigen. Tretinoin 46-59 integrin subunit alpha M Homo sapiens 289-294
19747912-1 2010 Vav1 plays an important role in the all-trans retinoic acid (ATRA)-induced completion of the differentiation program of acute promyelocytic leukemia (APL)-derived cells, in which it strengthens the drug effects and is involved in the regulation of maturation-related proteins, such as the CD11b surface antigen. Tretinoin 61-65 integrin subunit alpha M Homo sapiens 289-294
19747912-6 2010 The reported data suggest that the ATRA-induced increase of Vav1 expression and tyrosine phosphorylation may be involved in recruiting PU.1 to its consensus sequence on the CD11b promoter and, ultimately, in regulating CD11b expression during the late stages of neutrophil differentiation of APL-derived promyelocytes. Tretinoin 35-39 integrin subunit alpha M Homo sapiens 173-178
19747912-6 2010 The reported data suggest that the ATRA-induced increase of Vav1 expression and tyrosine phosphorylation may be involved in recruiting PU.1 to its consensus sequence on the CD11b promoter and, ultimately, in regulating CD11b expression during the late stages of neutrophil differentiation of APL-derived promyelocytes. Tretinoin 35-39 integrin subunit alpha M Homo sapiens 219-224
19897601-3 2010 We also explored mechanisms underlying the ability of retinoic acid, dexamethasone, and the protein kinase A activator forskolin to induce VDR up-regulation as well. Tretinoin 54-67 vitamin D receptor Homo sapiens 139-142
19934264-0 2010 Reciprocal roles of SIRT1 and SKIP in the regulation of RAR activity: implication in the retinoic acid-induced neuronal differentiation of P19 cells. Tretinoin 89-102 sirtuin 1 Homo sapiens 20-25
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 135-146
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 148-151
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 135-146
20042001-1 2010 Retinoic acid (RA) was found to be a ligand for peroxisome proliferation-activated receptor delta (PPARdelta) as well as the classical RA receptor (RAR). Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 148-151
20042001-2 2010 Carrier proteins that move the RA from the cytosol into the nucleus are the fatty acid-binding protein 5 (FABP5), activating PPARdelta, and the cellular retinoic acid-binding protein II (CRABPII), activating RAR. Tretinoin 31-33 retinoic acid receptor, alpha Mus musculus 208-211
19861119-0 2009 NR4A orphan nuclear receptors influence retinoic acid and docosahexaenoic acid signaling via up-regulation of fatty acid binding protein 5. Tretinoin 40-53 fatty acid binding protein 5 Homo sapiens 110-138
19861119-2 2009 In silico analysis of human promoters identified fatty acid binding protein 5 (FABP5), a protein shown to enhance retinoic acid-mediated PPARbeta/delta signaling, as a potential Nurr1 target gene. Tretinoin 114-127 fatty acid binding protein 5 Homo sapiens 49-77
19861119-2 2009 In silico analysis of human promoters identified fatty acid binding protein 5 (FABP5), a protein shown to enhance retinoic acid-mediated PPARbeta/delta signaling, as a potential Nurr1 target gene. Tretinoin 114-127 fatty acid binding protein 5 Homo sapiens 79-84
19861119-2 2009 In silico analysis of human promoters identified fatty acid binding protein 5 (FABP5), a protein shown to enhance retinoic acid-mediated PPARbeta/delta signaling, as a potential Nurr1 target gene. Tretinoin 114-127 peroxisome proliferator activated receptor delta Homo sapiens 137-145
19861119-2 2009 In silico analysis of human promoters identified fatty acid binding protein 5 (FABP5), a protein shown to enhance retinoic acid-mediated PPARbeta/delta signaling, as a potential Nurr1 target gene. Tretinoin 114-127 nuclear receptor subfamily 4 group A member 2 Homo sapiens 178-183
19799567-4 2009 PBX1 is present in the protein complex formed at this site with nuclear proteins from uninduced cells, whereas both PBX1 and MEIS1 proteins were detected in the complex created with extract from RA (retinoic acid)-induced NT2/D1 cells. Tretinoin 195-197 Meis homeobox 1 Homo sapiens 125-130
19799567-4 2009 PBX1 is present in the protein complex formed at this site with nuclear proteins from uninduced cells, whereas both PBX1 and MEIS1 proteins were detected in the complex created with extract from RA (retinoic acid)-induced NT2/D1 cells. Tretinoin 199-212 Meis homeobox 1 Homo sapiens 125-130
19799567-5 2009 By functional analysis we also showed that mutations of the PBX1/MEIS1-binding sites resulted in profound reduction of SOX3 promoter responsiveness to RA. Tretinoin 151-153 Meis homeobox 1 Homo sapiens 65-70
19799861-3 2009 Systematic yeast two-hybrid assays showed that in the presence of RA, TGR interacts with RAR via the LxxLL motif (NR box) located between the Grx and TrxR domains of TGR. Tretinoin 66-68 retinoic acid receptor, alpha Mus musculus 89-92
19850744-3 2009 Previously, all-trans retinoic acid (ATRA) was shown to increase the nuclear localization and transcriptional activity of RARA in Sertoli cells. Tretinoin 12-35 retinoic acid receptor, alpha Mus musculus 122-126
19850744-3 2009 Previously, all-trans retinoic acid (ATRA) was shown to increase the nuclear localization and transcriptional activity of RARA in Sertoli cells. Tretinoin 37-41 retinoic acid receptor, alpha Mus musculus 122-126
19850744-6 2009 In the presence of ATRA, lysine 166 (K166) and K171 of RARA were modified at a physiological concentration of SUMO-2, whereas in the absence of ATRA, K399 was the only site that was modified, but at a higher SUMO-2 concentration. Tretinoin 19-23 retinoic acid receptor, alpha Mus musculus 55-59
19211146-7 2009 However, administration of ATRA to NOD mice in which the proportion and function of CD4(+)Foxp3(+) Treg cells was abrogated by cyclophosphamide (CY), failed to permit progression to T1D. Tretinoin 27-31 CD4 antigen Mus musculus 84-87
19614676-7 2009 Conversely, treatment with retinoic acid, an inducer of TG2, significantly decreased EGF-induced EGFR dimerization and its phosphorylation with a significant increase in TG2 expression and its catalysed products, isopeptide bonds, in both subpopulations. Tretinoin 27-40 epidermal growth factor receptor Rattus norvegicus 97-101
19486889-0 2009 All-trans retinoic acid increases KLF4 acetylation by inducing HDAC2 phosphorylation and its dissociation from KLF4 in vascular smooth muscle cells. Tretinoin 0-23 Kruppel like factor 4 Homo sapiens 34-38
19486889-0 2009 All-trans retinoic acid increases KLF4 acetylation by inducing HDAC2 phosphorylation and its dissociation from KLF4 in vascular smooth muscle cells. Tretinoin 0-23 Kruppel like factor 4 Homo sapiens 111-115
19486889-1 2009 The zinc finger transcription factor Kruppel-like factor 4 (KLF4) has been implicated in vascular smooth muscle cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 154-167 Kruppel like factor 4 Homo sapiens 37-58
19486889-1 2009 The zinc finger transcription factor Kruppel-like factor 4 (KLF4) has been implicated in vascular smooth muscle cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 154-167 Kruppel like factor 4 Homo sapiens 60-64
19486889-1 2009 The zinc finger transcription factor Kruppel-like factor 4 (KLF4) has been implicated in vascular smooth muscle cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 169-173 Kruppel like factor 4 Homo sapiens 37-58
19486889-1 2009 The zinc finger transcription factor Kruppel-like factor 4 (KLF4) has been implicated in vascular smooth muscle cell differentiation induced by all-trans retinoic acid (ATRA). Tretinoin 169-173 Kruppel like factor 4 Homo sapiens 60-64
19486889-3 2009 Here, we show that ATRA-induced histone deacetylase 2 (HDAC2) phosphorylation at Ser424 in VSMCs and inhibited the interaction of HDAC2 with KLF4. Tretinoin 19-23 Kruppel like factor 4 Homo sapiens 141-145
19450544-3 2009 We have recently found that all-trans retinoic acid (ATRA) stimulates EAAC1 expression and anionic amino acid transport in C6 rat glioma cells. Tretinoin 28-51 solute carrier family 1 member 1 Rattus norvegicus 70-75
19450544-3 2009 We have recently found that all-trans retinoic acid (ATRA) stimulates EAAC1 expression and anionic amino acid transport in C6 rat glioma cells. Tretinoin 53-57 solute carrier family 1 member 1 Rattus norvegicus 70-75
19700620-7 2009 By contrast, a ;fusion-resistant" gene, Raldh3 (also known as Aldh1a3), that encodes a retinoic acid-synthesizing enzyme is ectopically expressed in the upper lip primordia of Lrp6-deficient embryos, indicating a region-specific role of the Wnt/beta-catenin signaling pathway in repressing retinoic acid signaling. Tretinoin 87-100 catenin (cadherin associated protein), beta 1 Mus musculus 245-257
19764225-5 2009 The bioassay-derived activity, expressed as all-trans-retinoic acid (all-transRA) equivalents (ATRA-EQ) were 10.9 +/- 2.2 and 1.7 +/- 1.0 ng/L in the STP influents and effluents, respectively, while the ATRA-EQs were as high as 7.1 and 8.3 ng/L in the two rivers receiving STP effluents. Tretinoin 44-67 thyroid hormone receptor interactor 10 Homo sapiens 150-153
19467017-14 2009 CONCLUSION: Concomitant RXRalpha activation by ATRA enhanced the inhibitory effects of RGZ on myeloma cell proliferation, cell cycle, apoptosis and differentiation. Tretinoin 47-51 retinoid X receptor alpha Homo sapiens 24-32
19539783-0 2009 Effect of retinoic acid signaling on Wnt/beta-catenin and FGF signaling during body axis extension. Tretinoin 10-23 catenin (cadherin associated protein), beta 1 Mus musculus 41-53
19539783-5 2009 Following loss of RA signaling, the caudal expression domains of Fgf8, Wnt8a, and Wnt3a expand anteriorly into the trunk, but no change is observed in caudal expression of Fgf4 or Fgf17 plus caudal expression of Fgf18 and Cdx1 is reduced. Tretinoin 18-20 fibroblast growth factor 8 Mus musculus 65-69
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 14-27 signal transducer and activator of transcription 1 Homo sapiens 141-191
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 14-27 signal transducer and activator of transcription 1 Homo sapiens 193-198
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 14-27 signal transducer and activator of transcription 1 Homo sapiens 291-296
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 245-258 signal transducer and activator of transcription 1 Homo sapiens 141-191
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 245-258 signal transducer and activator of transcription 1 Homo sapiens 193-198
18926686-7 2009 The effect of retinoic acid was dependent on new protein synthesis, was obstructed by a deacetylase inhibitor and was partly eliminated by a signal transducer and activator of transcription-1 (STAT1)/methyltransferase inhibitor, indicating that retinoic acid induces a new protein, possibly STAT1, that is involved in inhibiting NF-kappaB. Tretinoin 245-258 signal transducer and activator of transcription 1 Homo sapiens 291-296
19527685-0 2009 All-trans retinoic acid-induced ADAM28 degrades proteoglycans in human chondrocytes. Tretinoin 10-23 ADAM metallopeptidase domain 28 Homo sapiens 32-38
19698107-0 2009 The angiogenic factor midkine is regulated by dexamethasone and retinoic acid during alveolarization and in alveolar epithelial cells. Tretinoin 64-77 midkine Rattus norvegicus 22-29
19698107-10 2009 DEX treatment of rat pups decreased, and RA treatment increased lung MK expression, whereas concurrent DEX+RA treatment prevented the DEX-induced decrease in MK expression. Tretinoin 41-43 midkine Rattus norvegicus 69-71
19698107-10 2009 DEX treatment of rat pups decreased, and RA treatment increased lung MK expression, whereas concurrent DEX+RA treatment prevented the DEX-induced decrease in MK expression. Tretinoin 107-109 midkine Rattus norvegicus 158-160
19723072-1 2009 Acute promyelocytic leukemia KG1 cells with t(11;17) PLZF-RARalpha respond poorly to the differentiation inducer all-trans retinoic acid (RA), and the reason for the RA resistance is the recruitment of histone deacetylase by PLZF-RARalpha. Tretinoin 123-136 zinc finger and BTB domain containing 16 Homo sapiens 53-57
19723072-1 2009 Acute promyelocytic leukemia KG1 cells with t(11;17) PLZF-RARalpha respond poorly to the differentiation inducer all-trans retinoic acid (RA), and the reason for the RA resistance is the recruitment of histone deacetylase by PLZF-RARalpha. Tretinoin 58-60 zinc finger and BTB domain containing 16 Homo sapiens 53-57
19767821-8 2009 Together, results indicate that the coordinate signaling by two independent pathways, one involving canonical Wnt-beta-catenin activation of target genes and the other with Galpha13 signaling to ERM proteins to modulate cytoarchitectural changes, is required during the retinoic acid induced differentiation of F9 cells to primitive endoderm. Tretinoin 270-283 wingless-type MMTV integration site family, member 6 Mus musculus 110-113
19767821-8 2009 Together, results indicate that the coordinate signaling by two independent pathways, one involving canonical Wnt-beta-catenin activation of target genes and the other with Galpha13 signaling to ERM proteins to modulate cytoarchitectural changes, is required during the retinoic acid induced differentiation of F9 cells to primitive endoderm. Tretinoin 270-283 catenin (cadherin associated protein), beta 1 Mus musculus 114-126
19046768-0 2009 NDRG1 contributes to retinoic acid-induced differentiation of leukemic cells. Tretinoin 21-34 N-myc downstream regulated 1 Homo sapiens 0-5
19046768-1 2009 N-Myc downstream-regulated gene 1 (NDRG1) protein has been shown to be up-regulated during leukemic cell differentiation induced by some differentiation-inducing agents such as all-trans retinoic acid (ATRA). Tretinoin 187-200 N-myc downstream regulated 1 Homo sapiens 0-33
19046768-1 2009 N-Myc downstream-regulated gene 1 (NDRG1) protein has been shown to be up-regulated during leukemic cell differentiation induced by some differentiation-inducing agents such as all-trans retinoic acid (ATRA). Tretinoin 187-200 N-myc downstream regulated 1 Homo sapiens 35-40
19046768-1 2009 N-Myc downstream-regulated gene 1 (NDRG1) protein has been shown to be up-regulated during leukemic cell differentiation induced by some differentiation-inducing agents such as all-trans retinoic acid (ATRA). Tretinoin 202-206 N-myc downstream regulated 1 Homo sapiens 0-33
19046768-1 2009 N-Myc downstream-regulated gene 1 (NDRG1) protein has been shown to be up-regulated during leukemic cell differentiation induced by some differentiation-inducing agents such as all-trans retinoic acid (ATRA). Tretinoin 202-206 N-myc downstream regulated 1 Homo sapiens 35-40
19046768-3 2009 In this work, we show that inducible NDRG1 expression can drive leukemic U937 cells to undergo differentiation, while the knock-down of NDRG1 expression by specific small interfering RNA significantly antagonizes ATRA-induced differentiation of leukemic cells, proposing the role of NDRG1 in leukemic cell differentiation. Tretinoin 213-217 N-myc downstream regulated 1 Homo sapiens 136-141
19046768-3 2009 In this work, we show that inducible NDRG1 expression can drive leukemic U937 cells to undergo differentiation, while the knock-down of NDRG1 expression by specific small interfering RNA significantly antagonizes ATRA-induced differentiation of leukemic cells, proposing the role of NDRG1 in leukemic cell differentiation. Tretinoin 213-217 N-myc downstream regulated 1 Homo sapiens 136-141
19477923-1 2009 We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. Tretinoin 53-66 PBX/knotted 1 homeobox 1 Homo sapiens 140-145
19477923-1 2009 We have analyzed the role of actin polymerization in retinoic acid (RA)-induced HoxB transcription, which is mediated by the HoxB regulator Prep1. Tretinoin 68-70 PBX/knotted 1 homeobox 1 Homo sapiens 140-145
19477923-4 2009 RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. Tretinoin 0-2 homeobox B2 Homo sapiens 44-49
19477923-4 2009 RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. Tretinoin 0-2 PBX/knotted 1 homeobox 1 Homo sapiens 110-115
19477923-4 2009 RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. Tretinoin 0-2 POTE ankyrin domain family member F Homo sapiens 117-127
19477923-4 2009 RA treatment induces the recruitment to the HoxB2 gene enhancer of a complex composed of "elongating" RNAPII, Prep1, beta-actin, and N-WASP as well as the accessory splicing components p54Nrb and PSF. Tretinoin 0-2 WASP like actin nucleation promoting factor Homo sapiens 133-139
19578722-0 2009 Regulation of CD11b transcription by decreasing PRC2 and increased acH4 level during ATRA-induced HL-60 differentiation. Tretinoin 85-89 integrin subunit alpha M Homo sapiens 14-19
19358898-5 2009 All-trans retinoic acid (atRA) is a specific substrate for CYP2C39 and not catalyzed by CYP2C38. Tretinoin 0-23 cytochrome P450, family 2, subfamily c, polypeptide 39 Mus musculus 59-66
19358898-5 2009 All-trans retinoic acid (atRA) is a specific substrate for CYP2C39 and not catalyzed by CYP2C38. Tretinoin 25-29 cytochrome P450, family 2, subfamily c, polypeptide 39 Mus musculus 59-66
19233184-0 2009 Gut homing receptors on CD8 T cells are retinoic acid dependent and not maintained by liver dendritic or stellate cells. Tretinoin 40-53 CD8a molecule Homo sapiens 24-27
19233184-2 2009 In mice, imprinting of CCR9 and alpha4beta7 is dependent on retinoic acid during T-cell activation. Tretinoin 60-73 chemokine (C-C motif) receptor 9 Mus musculus 23-27
19233184-10 2009 CONCLUSIONS: Imprinting and plasticity of gut-homing human CD8 T cells requires primary activation or reactivation by gut DCs and is retinoic acid dependent. Tretinoin 133-146 CD8a molecule Homo sapiens 59-62
19715998-3 2009 The aim of this study was to establish if RA synergizing with TGF-beta induced antigen specific CD4(+) CD25(high) Foxp3(+) Treg portraying gut homing receptors. Tretinoin 42-44 CD4 antigen Mus musculus 96-99
19472184-11 2009 Results suggest that ATRA activates the p38 MAPK signal pathway with resultant degradation of SRC-3, and that p38 MAPK is involved in the regulation of RARalpha-mediated signaling in developing neurons. Tretinoin 21-25 nuclear receptor coactivator 3 Mus musculus 94-99
19364826-4 2009 RA treatment of obese mice induced expression of PPARbeta/delta and RAR target genes involved in regulation of lipid homeostasis, leading to weight loss and improved insulin responsiveness. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 68-71
19451220-4 2009 Here we show that, like PML/RARA, PLZF/RARA expression leads to recruitment of the Polycomb-repressive complex 2 (PRC2) Polycomb group (PcG) complex to RA response elements. Tretinoin 28-30 zinc finger and BTB domain containing 16 Homo sapiens 34-38
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 zinc finger and BTB domain containing 16 Homo sapiens 76-80
19451220-6 2009 Upon treatment with ATRA, ectopic recruitment of PRC2 by either PML/RARA or PLZF/RARA is lost, whereas PRC1 recruited by PLZF/RARA remains, resulting in persistent RA-insensitive gene repression. Tretinoin 20-24 zinc finger and BTB domain containing 16 Homo sapiens 121-125
19380778-9 2009 Collectively, we have shown that Th17 cells express a functional IL-13R and that IL-13 negatively regulates IL-17A and IL-21 production by decreasing retinoic acid-related-gammaT expression and while increasing phosphorylation of STAT6 and GATA3 expression. Tretinoin 150-163 interleukin 17A Mus musculus 108-114
19380778-9 2009 Collectively, we have shown that Th17 cells express a functional IL-13R and that IL-13 negatively regulates IL-17A and IL-21 production by decreasing retinoic acid-related-gammaT expression and while increasing phosphorylation of STAT6 and GATA3 expression. Tretinoin 150-163 interleukin 21 Mus musculus 119-124
19190084-0 2009 GM-CSF and IL-4 synergistically trigger dendritic cells to acquire retinoic acid-producing capacity. Tretinoin 67-80 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 0-6
19190084-13 2009 The results suggest that GM-CSF and RA itself are pivotal among multiple microenvironment factors that enable intestinal DCs to produce RA. Tretinoin 136-138 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 25-31
19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 383-388
18720064-3 2009 ATRA is a potent inhibitor of activator protein 1, a transcription factor of the JNK pathway. Tretinoin 0-4 mitogen-activated protein kinase 8 Mus musculus 81-84
19385038-9 2009 After induction by retinoic acid for 7 days, some isolated cells differentiated to spermatogonial stem-like cells, expressing Mvh, Stra-8, Hsp90-a, integrinb1 and a6. Tretinoin 19-32 DEAD box helicase 4 Mus musculus 126-129
19162023-3 2009 Combined treatment of retinoic acid, sonic hedgehog, and noggin in the presence of VN allows hESCs to differentiate into O4-positive oligodendrocytes. Tretinoin 22-35 vitronectin Homo sapiens 83-85
19250215-2 2009 In a previous study we indicated that xanthine dehydrogenase (XDH) is able to oxidize actively both all-trans-retinol (t-ROL) bound to the CRBP (holo-CRBP) and all-trans-retinaldehyde (t-RAL) to all-trans-retinoic acid (t-RA) in human mammary epithelial cells (HMEC). Tretinoin 195-218 RAS like proto-oncogene A Homo sapiens 187-190
19015161-3 2009 L-PGDS bound all three ligands with high affinity, while betaLG and RBP could bind only RA. Tretinoin 88-90 retinol binding protein 4 Homo sapiens 68-71
19015161-5 2009 Alternatively, the radius of gyration of betaLG and RBP was 20.3 and 26.2 A, respectively, and was almost the same before and after RA binding. Tretinoin 132-134 retinol binding protein 4 Homo sapiens 52-55
18957410-2 2009 In this study, we identified a classical retinoic acid-responsive element in the first intron in the IGFBP-6 gene adjacent to a consensus AP-1 binding site, both elements essential for rexinoid-induced expression of IGFBP-6. Tretinoin 41-54 insulin like growth factor binding protein 6 Homo sapiens 101-108
18957410-2 2009 In this study, we identified a classical retinoic acid-responsive element in the first intron in the IGFBP-6 gene adjacent to a consensus AP-1 binding site, both elements essential for rexinoid-induced expression of IGFBP-6. Tretinoin 41-54 insulin like growth factor binding protein 6 Homo sapiens 216-223
18984738-7 2009 Depletion of CD4(+)CD25(+) Treg cells impaired the inhibitory effect of ATRA on islet-infiltrating T-cells and blocked its protective effect on diabetes. Tretinoin 72-76 CD4 antigen Mus musculus 13-16
18984738-8 2009 Therefore, ATRA treatment induced Treg cell-dependent immune tolerance by suppressing both CD4(+) and CD8(+) Teff cells while promoting Treg cell expansion. Tretinoin 11-15 CD4 antigen Mus musculus 91-94
18633436-0 2009 Matrix metalloproteinase-21 expression is associated with keratinocyte differentiation and upregulated by retinoic acid in HaCaT cells. Tretinoin 106-119 matrix metallopeptidase 21 Homo sapiens 0-27
18633436-6 2009 Of various agents tested in HaCaT cell cultures, only retinoic acid (10(-6) M) and staurosporine (2.5 x 10(-8) M) upregulated MMP-21 mRNA and protein expression, whereas tumor promoters, hormones, or dexamethasone were without effect. Tretinoin 54-67 matrix metallopeptidase 21 Homo sapiens 126-132
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 61-63 integrin subunit alpha M Homo sapiens 114-119
19127080-4 2009 Our study demonstrates that nicotinamide in combination with RA or D3 affected induced expression levels of CD38, CD11b and CD14, suggesting a cooperative function of nicotinamide and RA or D3. Tretinoin 184-186 integrin subunit alpha M Homo sapiens 114-119
19288751-5 2009 The position of retinoic acid production and CYP26b1 expression that metabolizes RA to an inactive form regulates Stra8 expression. Tretinoin 16-29 stimulated by retinoic acid 8 Homo sapiens 114-119
18845239-4 2008 Using in vitro cell and in vivo mouse models, we report that RA, specifically all-trans-RA (atRA) at concentrations implicated in toxicity, can activate NRF2 and induce NRF2 target genes, particularly the subunits of the rate-limiting enzyme of glutathione biosynthesis, glutamate cysteine ligase (GCLM/GCLC). Tretinoin 92-96 glutamate-cysteine ligase, catalytic subunit Mus musculus 303-307
18845239-5 2008 RNA interference-mediated silencing of NRF2, but not of retinoid X receptor-alpha and -beta, reduced basal and atRA-induced GCLM/GCLC gene expression. Tretinoin 111-115 glutamate-cysteine ligase, catalytic subunit Mus musculus 129-133
18922886-1 2008 The retinoic acids all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9C-RA) and the retinoic acid receptors RAR and RXR significantly induce transcriptional activity from a 200-bp PKD1 proximal promoter in transfected mammalian cells. Tretinoin 4-18 retinoid X receptor alpha Homo sapiens 123-126
18922886-1 2008 The retinoic acids all-trans retinoic acid (AT-RA) and 9-cis retinoic acid (9C-RA) and the retinoic acid receptors RAR and RXR significantly induce transcriptional activity from a 200-bp PKD1 proximal promoter in transfected mammalian cells. Tretinoin 4-17 retinoid X receptor alpha Homo sapiens 123-126
19029830-2 2008 RA exerts its biological functions primarily through binding to and activating nuclear RA receptors (RARs, which include the RAR alpha, beta and gamma isotypes RARA, RARB and RARC). Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 160-164
19029830-7 2008 This result, along with the observation that in response to pharmacological inhibition of the RA signaling, hepatocytes lacking Trim24 loose their ability to proliferate, strongly implicates Rara as a proto-oncogene in hepatocytes and demonstrates that overactivated RA signaling is deleterious to liver homeostasis. Tretinoin 94-96 retinoic acid receptor, alpha Mus musculus 191-195
19029830-7 2008 This result, along with the observation that in response to pharmacological inhibition of the RA signaling, hepatocytes lacking Trim24 loose their ability to proliferate, strongly implicates Rara as a proto-oncogene in hepatocytes and demonstrates that overactivated RA signaling is deleterious to liver homeostasis. Tretinoin 267-269 retinoic acid receptor, alpha Mus musculus 191-195
18669599-5 2008 Light-triggered alterations in circulatory ATRA levels regulated ecto-5"-nucleotidase gene expression by retinoic acid receptor retinoic acid receptor-alpha and modulated 5"-AMP levels in blood and were associated with mPlrp2 and mClps expression in the livers. Tretinoin 43-47 retinoic acid receptor, alpha Mus musculus 128-156
18669599-5 2008 Light-triggered alterations in circulatory ATRA levels regulated ecto-5"-nucleotidase gene expression by retinoic acid receptor retinoic acid receptor-alpha and modulated 5"-AMP levels in blood and were associated with mPlrp2 and mClps expression in the livers. Tretinoin 43-47 pancreatic lipase-related protein 2 Mus musculus 219-225
18767146-7 2008 Differential expression of the retinoic acid target genes, RARB, CRABP1, and CRABP2, indicated that deletion of TBL1XR1 compromised the function of SMRT/N-CoR in the appropriate control of gene expression. Tretinoin 31-44 cellular retinoic acid binding protein 2 Homo sapiens 77-83
18786169-5 2008 It is capable of independently mediating the RA effect in a heterologous promoter context and its disruption caused significant reduction of RA/RXR transactivation of the SOX3 promoter. Tretinoin 45-47 retinoid X receptor alpha Homo sapiens 144-147
18786169-6 2008 Furthermore, by using synthetic antagonists of retinoid receptors, we have shown for the first time, that RA-induced SOX3 gene expression could be significantly down-regulated by the synthetic antagonist of RXR. Tretinoin 106-108 retinoid X receptor alpha Homo sapiens 207-210
18987198-5 2008 The activity of cyclin-dependent kinase 5, a major kinase involved in both APP and tau phosphorylation, was markedly downregulated by ATRA treatment. Tretinoin 134-138 cyclin-dependent kinase 5 Mus musculus 16-41
18687807-2 2008 For example, it was suggested recently that retinoic acid (RA) is a ligand for PPARbeta/delta and potentiates cell proliferation by activating PPARbeta/delta. Tretinoin 44-57 peroxisome proliferator activated receptor delta Homo sapiens 79-87
18687807-2 2008 For example, it was suggested recently that retinoic acid (RA) is a ligand for PPARbeta/delta and potentiates cell proliferation by activating PPARbeta/delta. Tretinoin 44-57 peroxisome proliferator activated receptor delta Homo sapiens 143-151
18687807-2 2008 For example, it was suggested recently that retinoic acid (RA) is a ligand for PPARbeta/delta and potentiates cell proliferation by activating PPARbeta/delta. Tretinoin 59-61 peroxisome proliferator activated receptor delta Homo sapiens 79-87
18687807-2 2008 For example, it was suggested recently that retinoic acid (RA) is a ligand for PPARbeta/delta and potentiates cell proliferation by activating PPARbeta/delta. Tretinoin 59-61 peroxisome proliferator activated receptor delta Homo sapiens 143-151
18687807-11 2008 In contrast, the observed inhibition of cell proliferation in mouse and human keratinocytes by RA is mediated by PPARbeta/delta-independent mechanisms and is inconsistent with the notion that RA potentiates cell proliferation by activating PPARbeta/delta. Tretinoin 95-97 peroxisome proliferator activated receptor delta Homo sapiens 113-121
18719224-6 2008 In addition to developing a method to test specific gene function in GS cells, we demonstrate that retinoic acid (RA) triggers GS cells to shift to a differentiated, premeiotic state lacking OCT4 and PLZF expression and colonization activity. Tretinoin 99-112 zinc finger and BTB domain containing 16 Homo sapiens 200-204
18719224-6 2008 In addition to developing a method to test specific gene function in GS cells, we demonstrate that retinoic acid (RA) triggers GS cells to shift to a differentiated, premeiotic state lacking OCT4 and PLZF expression and colonization activity. Tretinoin 114-116 zinc finger and BTB domain containing 16 Homo sapiens 200-204
18959816-4 2008 Protein levels of NF-kappaB p65 and relB were clearly enhanced during retinoic acid-induced differentiation. Tretinoin 70-83 avian reticuloendotheliosis viral (v-rel) oncogene related B Mus musculus 36-40
18847503-15 2008 Pathway analysis suggests that CDC2, CHEK1, CDC45L and MCM6 are key players in mediating the biological activity of RA in B16 melanoma cells. Tretinoin 116-118 checkpoint kinase 1 Mus musculus 37-42
18838813-4 2008 ATRA inhibited the expression of tyrosinase and TRP-1, and retinol inhibited the expression of tyrosinase, in a dose-dependent manner. Tretinoin 0-4 tyrosinase-related protein 1 Mus musculus 48-53
18632758-7 2008 DHRS9 is involved in the synthesis of ATRA from vitamin A. Tretinoin 38-42 dehydrogenase/reductase 9 Homo sapiens 0-5
18446820-0 2008 Characterization of alterations of Rb2/p130 tumor suppressor in all-trans-retinoic acid resistant SK-OV3 ovarian carcinoma cells. Tretinoin 74-87 RB transcriptional corepressor like 2 Homo sapiens 35-38
18446820-0 2008 Characterization of alterations of Rb2/p130 tumor suppressor in all-trans-retinoic acid resistant SK-OV3 ovarian carcinoma cells. Tretinoin 74-87 RB transcriptional corepressor like 2 Homo sapiens 39-43
18446820-12 2008 It is possible that this hyperphosphorylated form can be responsible for the decreased Rb2/p130 functional activity observed in SK-OV3 cells and may contribute to the resistance of these cells to ATRA mediated growth suppression. Tretinoin 196-200 RB transcriptional corepressor like 2 Homo sapiens 87-90
18446820-12 2008 It is possible that this hyperphosphorylated form can be responsible for the decreased Rb2/p130 functional activity observed in SK-OV3 cells and may contribute to the resistance of these cells to ATRA mediated growth suppression. Tretinoin 196-200 RB transcriptional corepressor like 2 Homo sapiens 91-95
18987612-7 2008 The RA-induced neuronal differentiation was determined based on changes in the expression of protein markers characteristic for undifferentiated (Oct-4) and neuron-like cell differentiated cells (N-cadherin and III-beta tubulin). Tretinoin 4-6 cadherin 2 Mus musculus 196-206
18839023-0 2008 Inhibition of all-trans retinoic acid on MDM2 gene expression in astrocytoma cell line SHG-44. Tretinoin 24-37 MDM2 proto-oncogene Homo sapiens 41-45
18839023-1 2008 OBJECTIVE: To investigate the impact of all-trans retinoic acid (ATRA) on MDM2 gene expression in astrocytoma cell line SHG-44, and to provide basic data for further research on the progression mechanism and gene therapy of human astrocytoma. Tretinoin 40-63 MDM2 proto-oncogene Homo sapiens 74-78
18839023-1 2008 OBJECTIVE: To investigate the impact of all-trans retinoic acid (ATRA) on MDM2 gene expression in astrocytoma cell line SHG-44, and to provide basic data for further research on the progression mechanism and gene therapy of human astrocytoma. Tretinoin 65-69 MDM2 proto-oncogene Homo sapiens 74-78
18839023-2 2008 METHODS: The differential expressions of MDM2 gene and protein in SHG-44 cells were detected by cDNA microarray and Western blot, respectively, before and after treatment of ATRA. Tretinoin 174-178 MDM2 proto-oncogene Homo sapiens 41-45
18839023-5 2008 RESULTS: The intensity ratio of ATRA-treated to untreated SHG-44 cell was 0.37 in the cDNA microarray, suggesting that the expression of MDM2 gene was down-regulated in SHG-44 cells after treatment with ATRA. Tretinoin 32-36 MDM2 proto-oncogene Homo sapiens 137-141
18839023-5 2008 RESULTS: The intensity ratio of ATRA-treated to untreated SHG-44 cell was 0.37 in the cDNA microarray, suggesting that the expression of MDM2 gene was down-regulated in SHG-44 cells after treatment with ATRA. Tretinoin 203-207 MDM2 proto-oncogene Homo sapiens 137-141
18839023-7 2008 Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells. Tretinoin 83-87 MDM2 proto-oncogene Homo sapiens 61-65
18839023-7 2008 Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells. Tretinoin 83-87 POTE ankyrin domain family member F Homo sapiens 69-79
18839023-7 2008 Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells. Tretinoin 83-87 MDM2 proto-oncogene Homo sapiens 225-229
18839023-7 2008 Western blot demonstrated that the optical density ratios of MDM2 to beta-actin in ATRA-treated and untreated SHG-44 were 14.02+/-0.35 and 21.40+/-0.58 (t = 24.728, P = 0.000), respectively, suggesting that the expression of MDM2 protein was inhibited in ATRA-treated SHG-44 cells. Tretinoin 255-259 MDM2 proto-oncogene Homo sapiens 61-65
18839023-9 2008 CONCLUSION: ATRA can inhibit MDM2 gene expression in SHG-44 cells, and MDM2 is related to astrocytoma progression. Tretinoin 12-16 MDM2 proto-oncogene Homo sapiens 29-33
18425745-3 2008 Previous studies show that excessive atRA led to growth inhibition and p21 accumulation in mouse embryonic palatal mesenchymal (MEPM) cells. Tretinoin 37-41 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 71-74
18425745-4 2008 We reported here the identification of p21 as a required mediator during atRA-induced growth inhibition. Tretinoin 73-77 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 39-42
18425745-7 2008 Western blot analysis revealed that atRA treatment led to an increase in p21 level and a decrease in cyclin D1 protein and Rb phosphorylation. Tretinoin 36-40 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 73-76
18425745-7 2008 Western blot analysis revealed that atRA treatment led to an increase in p21 level and a decrease in cyclin D1 protein and Rb phosphorylation. Tretinoin 36-40 cyclin D1 Mus musculus 101-110
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 84-88 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 55-58
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 196-200 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 55-58
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 196-200 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 153-156
18425745-8 2008 Using luciferase assay with reporter gene regulated by p21 promoter, we showed that atRA increased the reporter activity in a dose-dependent manner; and p21 siRNA blocked the growth inhibition by atRA, suggesting that p21 is required for atRA-mediated growth inhibition. Tretinoin 196-200 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 153-156
18408763-2 2008 RARalpha heterodimerizes with the retinoid X receptor-alpha (RXRalpha) and transcriptionally regulates myeloid differentiation in response to ATRA (all-trans retinoic acid). Tretinoin 142-146 retinoic acid receptor, alpha Mus musculus 0-8
18408763-2 2008 RARalpha heterodimerizes with the retinoid X receptor-alpha (RXRalpha) and transcriptionally regulates myeloid differentiation in response to ATRA (all-trans retinoic acid). Tretinoin 148-171 retinoic acid receptor, alpha Mus musculus 0-8
18571505-5 2008 Adding AG1296 with RA increased secretion of TNF-alpha, IL-8, and MMP-9 expression. Tretinoin 19-21 matrix metallopeptidase 9 Homo sapiens 66-71
18639684-17 2008 Both NGF and BDNF had only a modest synergistic effect when given after ATRA treatment. Tretinoin 72-76 brain derived neurotrophic factor Homo sapiens 13-17
18512782-9 2008 IL-17 production was completely abrogated by anti-IL-1 or IL-1 receptor antagonist and partially inhibited by anti-IL-6, anti-IL-2, or exogenous retinoic acid, but not by anti-tumor necrosis factor alpha. Tretinoin 145-158 interleukin 17A Homo sapiens 0-5
18512787-11 2008 CONCLUSION: An aggrecanase other than ADAMTS-4 and ADAMTS-5 is expressed in mouse cartilage and is up-regulated by retinoic acid but not IL-1alpha. Tretinoin 115-128 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2) Mus musculus 51-59
18462200-7 2008 NPM3 proteins were localized in the nucleoli and nuclei of the cells and expression was decreased during RA-induced differentiation. Tretinoin 105-107 nucleoplasmin 3 Mus musculus 0-4
18280705-0 2008 Histidase expression in human epidermal keratinocytes: regulation by differentiation status and all-trans retinoic acid. Tretinoin 106-119 histidine ammonia-lyase Homo sapiens 0-9
18082883-0 2008 Retinoid X receptor alpha is highly phosphorylated in retinoic acid-resistant HL-60R cells and the combination of 9-cis retinoic acid plus MEK inhibitor induces apoptosis in the cells. Tretinoin 54-67 retinoid X receptor alpha Homo sapiens 0-25
18082883-1 2008 We examined the effects of 9-cis retinoic acid (RA) on the expression levels of retinoid X receptor alpha (RXR alpha) and its phosphorylated form (p-RXR alpha) in HL-60 and HL-60R cells. Tretinoin 48-50 retinoid X receptor alpha Homo sapiens 80-105
18082883-1 2008 We examined the effects of 9-cis retinoic acid (RA) on the expression levels of retinoid X receptor alpha (RXR alpha) and its phosphorylated form (p-RXR alpha) in HL-60 and HL-60R cells. Tretinoin 48-50 retinoid X receptor alpha Homo sapiens 107-116
18082883-1 2008 We examined the effects of 9-cis retinoic acid (RA) on the expression levels of retinoid X receptor alpha (RXR alpha) and its phosphorylated form (p-RXR alpha) in HL-60 and HL-60R cells. Tretinoin 48-50 retinoid X receptor alpha Homo sapiens 149-158
18082883-2 2008 9-cis RA reduced both RXR alpha and p-RXR alpha in HL-60 cells, but did neither in HL-60R cells. Tretinoin 6-8 retinoid X receptor alpha Homo sapiens 22-31
18082883-2 2008 9-cis RA reduced both RXR alpha and p-RXR alpha in HL-60 cells, but did neither in HL-60R cells. Tretinoin 6-8 retinoid X receptor alpha Homo sapiens 38-47
18082883-3 2008 However, when the HL-60R cells were treated with the combination of 9-cis RA plus PD98059, MEK inhibitor, the p-RXR alpha and RXR alpha proteins all markedly decreased. Tretinoin 74-76 retinoid X receptor alpha Homo sapiens 112-121
18082883-3 2008 However, when the HL-60R cells were treated with the combination of 9-cis RA plus PD98059, MEK inhibitor, the p-RXR alpha and RXR alpha proteins all markedly decreased. Tretinoin 74-76 retinoid X receptor alpha Homo sapiens 126-135
18082883-5 2008 Phosphorylation of RXR alpha might be associated with RA-resistance in HL-60R cells. Tretinoin 54-56 retinoid X receptor alpha Homo sapiens 19-28
18497940-0 2008 ERAP140/Nbla10993 is a novel favorable prognostic indicator for neuroblastoma induced in response to retinoic acid. Tretinoin 101-114 nuclear receptor coactivator 7 Homo sapiens 0-7
18497940-0 2008 ERAP140/Nbla10993 is a novel favorable prognostic indicator for neuroblastoma induced in response to retinoic acid. Tretinoin 101-114 nuclear receptor coactivator 7 Homo sapiens 8-17
18497940-4 2008 During the all-trans-retinoic acid (ATRA)-mediated neuronal differentiation in neuroblastoma-derived RTBM1 cells, the expression levels of ERAP140/Nbla10993 increased at the mRNA level. Tretinoin 11-34 nuclear receptor coactivator 7 Homo sapiens 139-146
18497940-4 2008 During the all-trans-retinoic acid (ATRA)-mediated neuronal differentiation in neuroblastoma-derived RTBM1 cells, the expression levels of ERAP140/Nbla10993 increased at the mRNA level. Tretinoin 11-34 nuclear receptor coactivator 7 Homo sapiens 147-156
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 38-40 cellular retinoic acid binding protein 2 Homo sapiens 124-132
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 38-40 fatty acid binding protein 5 Homo sapiens 163-168
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 38-40 peroxisome proliferator activated receptor delta Homo sapiens 191-199
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 38-40 peroxisome proliferator activated receptor delta Homo sapiens 324-332
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 peroxisome proliferator activated receptor delta Homo sapiens 191-199
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 peroxisome proliferator activated receptor delta Homo sapiens 324-332
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 peroxisome proliferator activated receptor delta Homo sapiens 191-199
18495924-5 2008 The observations that partitioning of RA between its two receptors is regulated by two intracellular lipid-binding proteins-CRABP-II, which targets RA to RAR, and FABP5, which delivers it to PPARbeta/delta-further suggest that RA resistance may stem from the deregulation of the binding proteins, resulting in activation of PPARbeta/delta rather than RAR. Tretinoin 125-127 peroxisome proliferator activated receptor delta Homo sapiens 324-332
18495924-6 2008 Here, we show that, in the RA-resistant mouse model of breast cancer MMTV-neu, RA indeed activates the nonclassical RA receptor PPARbeta/delta. Tretinoin 27-29 peroxisome proliferator activated receptor delta Homo sapiens 128-136
18495924-6 2008 Here, we show that, in the RA-resistant mouse model of breast cancer MMTV-neu, RA indeed activates the nonclassical RA receptor PPARbeta/delta. Tretinoin 79-81 peroxisome proliferator activated receptor delta Homo sapiens 128-136
18354155-2 2008 TCI induced Ag-specific IgA Ab-secreting cells expressing CCR9 and CCR10 in the small intestine in a retinoic acid-dependent manner. Tretinoin 101-114 chemokine (C-C motif) receptor 9 Mus musculus 58-62
18241852-6 2008 Microarray analyses revealed that RA-treated CYP26A1(-/-) ES cells exhibited lower mRNA levels than Wt ES cells for genes involved in differentiation, particularly in neural (Epha4, Pmp22, Nrp1, Gap43, Ndn) and smooth muscle differentiation (Madh3, Nrp1, Tagln Calponin, Caldesmon1). Tretinoin 34-36 EPH receptor A4 Homo sapiens 175-180
18164278-0 2008 Gene expression profiling elucidates a specific role for RARgamma in the retinoic acid-induced differentiation of F9 teratocarcinoma stem cells. Tretinoin 73-86 retinoic acid receptor, gamma Mus musculus 57-65
18164278-1 2008 The biological effects of all-trans-retinoic acid (RA), a major active metabolite of retinol, are mainly mediated through its interactions with retinoic acid receptor (RARs alpha, beta, gamma) and retinoid X receptor (RXRs alpha, beta, gamma) heterodimers. Tretinoin 26-49 retinoic acid receptor, alpha Mus musculus 168-216
18164278-1 2008 The biological effects of all-trans-retinoic acid (RA), a major active metabolite of retinol, are mainly mediated through its interactions with retinoic acid receptor (RARs alpha, beta, gamma) and retinoid X receptor (RXRs alpha, beta, gamma) heterodimers. Tretinoin 51-53 retinoic acid receptor, alpha Mus musculus 168-216
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 114-127 retinoid x receptor, beta a Danio rerio 200-205
18158153-2 2008 Using RT-PCR, it was shown that the ovaries and testes express enzymes that synthesize and metabolize the hormone retinoic acid (RA) (raldh2 and cyp26a, respectively), and RA receptors (raraa, rarga, rxrba, rxrbb, rxrga but not rxrab). Tretinoin 129-131 retinoid x receptor, beta a Danio rerio 200-205
17937658-3 2008 However, little is known about the role of RA in the physiological regulation of CREB expression in the early mucous differentiation of NHTBE cells. Tretinoin 43-45 cAMP responsive element binding protein 1 Homo sapiens 81-85
17937658-9 2008 We conclude that RA up-regulates CREB gene expression during the early stage of NHTBE cell differentiation and that RA-inducible Sp1 plays a major role in up-regulating human CREB gene expression. Tretinoin 17-19 cAMP responsive element binding protein 1 Homo sapiens 33-37
17937658-9 2008 We conclude that RA up-regulates CREB gene expression during the early stage of NHTBE cell differentiation and that RA-inducible Sp1 plays a major role in up-regulating human CREB gene expression. Tretinoin 116-118 cAMP responsive element binding protein 1 Homo sapiens 175-179
18006504-0 2008 A MAPK-positive feedback mechanism for BLR1 signaling propels retinoic acid-triggered differentiation and cell cycle arrest. Tretinoin 62-75 C-X-C motif chemokine receptor 5 Homo sapiens 39-43
18006504-4 2008 Unlike wild-type parental cells, RA-treated BLR1 knock-out cells failed to show RAF and consequential MEK and ERK phosphorylation, failed to accumulate CDK inhibitors that control G(1)/S transition, and failed to differentiate and arrest in response to RA, whereas ectopically overexpressing BLR1 enhanced MAPK signaling and caused accelerated RA-induced differentiation and arrest. Tretinoin 33-35 C-X-C motif chemokine receptor 5 Homo sapiens 44-48
18156191-7 2008 RA restored the ratio of Bcl-2 to Bax, inhibited cleavage of caspase-3 and -9, and prevented the decreases in the levels of SOD-1 and SOD-2. Tretinoin 0-2 superoxide dismutase 2 Rattus norvegicus 134-139
18327422-6 2008 RESULTS: TACO gene down-regulation observed with vitamin D(3)/RA treatment occurred through modulation of this gene via the VDR/RXR response sequence present in the promoter region of TACO gene. Tretinoin 62-64 vitamin D receptor Homo sapiens 124-127
18327422-6 2008 RESULTS: TACO gene down-regulation observed with vitamin D(3)/RA treatment occurred through modulation of this gene via the VDR/RXR response sequence present in the promoter region of TACO gene. Tretinoin 62-64 retinoid X receptor alpha Homo sapiens 128-131
17561254-3 2008 For HL60 cells, ATRA induced major increases in descending order of CD38, CD11b, CD45RO, CD11c, CD54 and CD36 with repression of CD117 and CD44. Tretinoin 16-20 integrin subunit alpha M Homo sapiens 74-79
17561254-3 2008 For HL60 cells, ATRA induced major increases in descending order of CD38, CD11b, CD45RO, CD11c, CD54 and CD36 with repression of CD117 and CD44. Tretinoin 16-20 intercellular adhesion molecule 1 Homo sapiens 96-100
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 intercellular adhesion molecule 1 Homo sapiens 74-78
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 integrin subunit alpha M Homo sapiens 87-92
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 CD53 molecule Homo sapiens 94-98
17561254-4 2008 For NB4 cells, ATRA induced major increases in descending order of CD11c, CD54, CD11a, CD11b, CD53, CD65, CD138, CD66c and T-cell receptor alpha/beta (TCRalpha/beta), with repression of CD38 and CD9. Tretinoin 15-19 CD9 molecule Homo sapiens 195-198
17561254-6 2008 Approximately half of the antigens up-regulated by ATRA on NB4 cells were adhesion molecules, including CD11a, CD11b, CD11c, CD54, CD66c and CD138, consistent with the increased adhesiveness of leukaemia cells observed for APL patients treated with ATRA. Tretinoin 51-55 integrin subunit alpha M Homo sapiens 111-116
17561254-6 2008 Approximately half of the antigens up-regulated by ATRA on NB4 cells were adhesion molecules, including CD11a, CD11b, CD11c, CD54, CD66c and CD138, consistent with the increased adhesiveness of leukaemia cells observed for APL patients treated with ATRA. Tretinoin 51-55 intercellular adhesion molecule 1 Homo sapiens 125-129
17561254-8 2008 For NB4 cells, ATRA induced some remarkable increases in CD antigens not seen for HL60: CD14 (16.6-fold), CD32 (27.8), CD53 (20.5), CD65 (139), CD66c (79.7), CD126 (15.1), and CD138 (57.6). Tretinoin 15-19 CD53 molecule Homo sapiens 119-123
17920233-0 2008 Combined treatment of P-gp-positive L1210/VCR cells by verapamil and all-trans retinoic acid induces down-regulation of P-glycoprotein expression and transport activity. Tretinoin 79-92 phosphoglycolate phosphatase Mus musculus 22-26
17920233-0 2008 Combined treatment of P-gp-positive L1210/VCR cells by verapamil and all-trans retinoic acid induces down-regulation of P-glycoprotein expression and transport activity. Tretinoin 79-92 phosphoglycolate phosphatase Mus musculus 120-134
17825242-0 2008 The effect of retinoic acid on a zinc finger transcription factor, AJ18, during differentiation of a rat clonal preosteoblastic cell line, ROB-C20, into osteoblasts. Tretinoin 14-27 zinc finger protein 354C Rattus norvegicus 67-71
17825242-13 2008 CONCLUSIONS: This study supports the hypothesis that RA may restrict to the differentiation of C20 cells into mature osteoblasts via inductive AJ18 expression with activation of multiple signal pathways. Tretinoin 53-55 zinc finger protein 354C Rattus norvegicus 143-147
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 238-242 CCAAT/enhancer binding protein beta Rattus norvegicus 83-102
19068145-11 2008 The suppressive effect of ATRA on the activation of activator protein-1 (AP-1) and nuclear factor-IL-6 (NF-IL-6) was reproduced by the MEK1 (mitogen-activated protein extracellularly regulated kinase kinase 1) inhibitor PD-98059, whereas ATRA and PD-98059 had no effect on NF-kappaB activation. Tretinoin 238-242 CCAAT/enhancer binding protein beta Rattus norvegicus 104-111
19068145-12 2008 CONCLUSIONS: Among RAR and RXR agonists, only ATRA inhibited IL-1-induced IL-6 expression in rat synovial fibroblasts by inhibiting ERK1/2 pathway and subsequent activation of AP-1 and NF-IL-6 independently of RAR. Tretinoin 46-50 CCAAT/enhancer binding protein beta Rattus norvegicus 185-192
17727842-0 2008 Overexpression of CRABPI in suprabasal keratinocytes enhances the proliferation of epidermal basal keratinocytes in mouse skin topically treated with all-trans retinoic acid. Tretinoin 160-173 cellular retinoic acid binding protein I Mus musculus 18-24
17727842-1 2008 We investigated whether ectopic expression of CRABPI, a cellular retinoic acid binding protein, influenced the actions of all-trans retinoic acid (ATRA) in transgenic (TG) mice. Tretinoin 65-78 cellular retinoic acid binding protein I Mus musculus 46-52
17727842-1 2008 We investigated whether ectopic expression of CRABPI, a cellular retinoic acid binding protein, influenced the actions of all-trans retinoic acid (ATRA) in transgenic (TG) mice. Tretinoin 147-151 cellular retinoic acid binding protein I Mus musculus 46-52
17727842-5 2008 Ectopically overexpressed CRABPI in suprabasal keratinocytes, but not in basal keratinocytes, enhanced the thickening of the epidermis induced by topical ATRA treatments (10 microM, 400 microl for 4 days) by 1.59+/-0.2-fold (p<0.05). Tretinoin 154-158 cellular retinoic acid binding protein I Mus musculus 26-32
17712061-0 2008 All-trans-retinoic acid stimulates translation and induces spine formation in hippocampal neurons through a membrane-associated RARalpha. Tretinoin 0-23 retinoic acid receptor, alpha Mus musculus 128-136
17712061-9 2008 Prolonged atRA stimulation reduced surface/total RARalpha by 43%, suggesting internalization, whereas brain-derived nerve growth factor or bicuculline increased the ratio by approximately 1.8-fold. Tretinoin 10-14 retinoic acid receptor, alpha Mus musculus 49-57
19012162-0 2008 Effects of retinoic acid on the expressions of Vangl1 and vangl2 in mouse fetuses. Tretinoin 11-24 VANGL planar cell polarity 2 Mus musculus 58-64
19012162-1 2008 This study reports the effects of retinoic acid on the spatiotemporal expressions of Vangl1 and Vangl2 in mouse fetuses. Tretinoin 34-47 VANGL planar cell polarity 2 Mus musculus 96-102
19012162-8 2008 In conclusion, Vangl1 and Vangl2 transcript downregulation might be implicated in the occurrence of mouse NTDs induced by retinoic acid. Tretinoin 122-135 VANGL planar cell polarity 2 Mus musculus 26-32
17928352-9 2008 The interaction between U95 and GRIM-19 is thus functionally and metabolically significant in HHV-6B-infected cells and may be a means through which HHV-6B modulates cell death signals by interferon and retinoic acid. Tretinoin 203-216 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 32-39
19079159-1 2008 Recent studies have highlighted a central role for intestinal dendritic cells (DCs) and vitamin A metabolite retinoic acid (RA) in the generation of alpha4beta7(+) CCR9(+)"gut tropic" effector T cells. Tretinoin 109-122 chemokine (C-C motif) receptor 9 Mus musculus 164-168
19079159-1 2008 Recent studies have highlighted a central role for intestinal dendritic cells (DCs) and vitamin A metabolite retinoic acid (RA) in the generation of alpha4beta7(+) CCR9(+)"gut tropic" effector T cells. Tretinoin 124-126 chemokine (C-C motif) receptor 9 Mus musculus 164-168
18254885-2 2008 Retinoic acid can also bind to the orphan nuclear receptor peroxisome proliferator-activated receptor beta/delta (PPAR beta/delta), resulting in stimulation of cell growth and inhibition of apoptosis. Tretinoin 0-13 peroxisome proliferator activated receptor delta Homo sapiens 114-123
18254885-3 2008 To bind to RAR, retinoic acid is carried into the nucleus by the cytosolic cellular retinoic acid-binding protein-II; to bind to PPAR beta/delta, it is transported into the nucleus by the cytosolic fatty acid-binding protein 5. Tretinoin 16-29 cellular retinoic acid binding protein 2 Homo sapiens 75-116
18254885-3 2008 To bind to RAR, retinoic acid is carried into the nucleus by the cytosolic cellular retinoic acid-binding protein-II; to bind to PPAR beta/delta, it is transported into the nucleus by the cytosolic fatty acid-binding protein 5. Tretinoin 16-29 peroxisome proliferator activated receptor delta Homo sapiens 129-138
18254885-3 2008 To bind to RAR, retinoic acid is carried into the nucleus by the cytosolic cellular retinoic acid-binding protein-II; to bind to PPAR beta/delta, it is transported into the nucleus by the cytosolic fatty acid-binding protein 5. Tretinoin 16-29 fatty acid binding protein 5 Homo sapiens 198-226
17223720-11 2008 RA treatment of normoxic and mild hyperoxic groups increased mRNA VEGF-A expression by about 50%. Tretinoin 0-2 vascular endothelial growth factor A Mus musculus 66-72
17223720-13 2008 Higher VEGF-A mRNA expression in the 80% hyperoxic group treated with RA was not significant compared to the 80% hyperoxic group. Tretinoin 70-72 vascular endothelial growth factor A Mus musculus 7-13
17944879-5 2007 Upon neuronal differentiation of P19 cells with retinoic acid, Bsx gene expression increased, whereas that of the REST gene decreased. Tretinoin 48-61 brain specific homeobox Mus musculus 63-66
18000064-2 2007 We show that CRABPI (encoding cellular retinoic acid binding protein I) is a target of PLZF, which is fused to RARalpha by the t(11;17)(q23;q21) translocation associated with retinoic acid (RA)-resistant acute promyelocytic leukemia (APL). Tretinoin 39-52 cellular retinoic acid binding protein I Mus musculus 13-19
18000064-2 2007 We show that CRABPI (encoding cellular retinoic acid binding protein I) is a target of PLZF, which is fused to RARalpha by the t(11;17)(q23;q21) translocation associated with retinoic acid (RA)-resistant acute promyelocytic leukemia (APL). Tretinoin 39-52 retinoic acid receptor, alpha Mus musculus 111-119
17971411-8 2007 Retinoic-acid-induced differentiation resulted in more consistent patterns of replication and upregulation of Polg, Polg2 and Tfam, whereas siRNA knockdown demonstrated that steady-state expression of POLG is essential for maintaining pluripotency. Tretinoin 0-13 polymerase (DNA directed), gamma Mus musculus 110-114
17971411-8 2007 Retinoic-acid-induced differentiation resulted in more consistent patterns of replication and upregulation of Polg, Polg2 and Tfam, whereas siRNA knockdown demonstrated that steady-state expression of POLG is essential for maintaining pluripotency. Tretinoin 0-13 polymerase (DNA directed), gamma Mus musculus 201-205
17486602-1 2007 Cellular retinoic acid binding protein (CRABP) is a member of intracellular lipid-binding protein (iLBP), and closely associated with retinoic acid (RA) activity. Tretinoin 9-22 cellular retinoic acid binding protein Bombyx mori 40-45
17486602-1 2007 Cellular retinoic acid binding protein (CRABP) is a member of intracellular lipid-binding protein (iLBP), and closely associated with retinoic acid (RA) activity. Tretinoin 41-43 cellular retinoic acid binding protein Bombyx mori 0-38
17486602-2 2007 We have cloned the CRABP gene from silkworm pupae and studied the interaction between Bombyx mori CRABP (BmCRABP) and all-trans retinoic acid (atRA). Tretinoin 128-141 cellular retinoic acid binding protein Bombyx mori 19-24
17486602-2 2007 We have cloned the CRABP gene from silkworm pupae and studied the interaction between Bombyx mori CRABP (BmCRABP) and all-trans retinoic acid (atRA). Tretinoin 128-141 cellular retinoic acid binding protein Bombyx mori 105-112
17486602-2 2007 We have cloned the CRABP gene from silkworm pupae and studied the interaction between Bombyx mori CRABP (BmCRABP) and all-trans retinoic acid (atRA). Tretinoin 143-147 cellular retinoic acid binding protein Bombyx mori 19-24
17486602-3 2007 The MTT assay data indicated that when BmCRABP is overexpressed in Bm5 cells, the cells dramatically resisted to atRA-induced growth inhibition. Tretinoin 113-117 cellular retinoic acid binding protein Bombyx mori 39-46
17486602-4 2007 Conversely, the cells were sensitive to atRA treatment upon knocking down the BmCRABP expression. Tretinoin 40-44 cellular retinoic acid binding protein Bombyx mori 78-85
17486602-5 2007 Subcellular localization revealed that BmCRABP is a cytoplasm protein, even when treated with atRA, the CRABP still remained in the cytoplasm. Tretinoin 94-98 cellular retinoic acid binding protein Bombyx mori 39-46
17486602-5 2007 Subcellular localization revealed that BmCRABP is a cytoplasm protein, even when treated with atRA, the CRABP still remained in the cytoplasm. Tretinoin 94-98 cellular retinoic acid binding protein Bombyx mori 41-46
17849154-5 2007 Half of the dams in the LPD group were injected intraperitoneally with retinoic acid (20 mg/kg) during gestation at embryonic day 11.5. Tretinoin 71-84 acyl-CoA synthetase bubblegum family member 1 Rattus norvegicus 24-27
17823279-4 2007 Previous studies from our laboratory identified a novel gene product, gene associated with retinoid-interferon-induced mortality (GRIM)-19, as an IFN/all-trans retinoic acid-induced growth suppressor. Tretinoin 160-173 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 91-138
17917245-7 2007 Introduction of siRNA against GATA-1 markedly reduced the ATRA-induced differentiation markers including CD11b and CCR3, as well as reduced eotaxin-2/CCL24 production. Tretinoin 58-62 integrin subunit alpha M Homo sapiens 105-110
17917245-7 2007 Introduction of siRNA against GATA-1 markedly reduced the ATRA-induced differentiation markers including CD11b and CCR3, as well as reduced eotaxin-2/CCL24 production. Tretinoin 58-62 C-C motif chemokine receptor 3 Homo sapiens 115-119
18179744-3 2007 A study on the effect of all-trans retinoic acid (RA) on cell growth, expression of GRIM-19 and content and activity of complex I of the mitochondrial respiratory chain in normal human keratinocytes (NHEK) and mouth carcinoma cells with low (HN) and high (KB) transformation grade was carried out. Tretinoin 50-52 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 84-91
18179744-4 2007 In NHEK cells, RA treatment resulted in growth suppression, significant overexpression of GRIM-19 protein, enhanced content of complex I but depressed activity of NADH-UQ oxidoreductase activity of the complex. Tretinoin 15-17 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 90-97
17538076-7 2007 Together, these data indicate that regulation of HSD17B2 mRNA levels and enzymatic activity by RA in the placenta is mediated by RARA and RXRA. Tretinoin 95-97 retinoid X receptor alpha Homo sapiens 138-142
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 interleukin 17A Homo sapiens 252-257
17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 interleukin 17A Homo sapiens 252-257
17525233-4 2007 The global levels of the histone K27 methyltransferase EZH2 also decreased with RA treatment. Tretinoin 80-82 enhancer of zeste 2 polycomb repressive complex 2 subunit Mus musculus 55-59
17525233-6 2007 In contrast, direct RA-responsive genes that are rapidly induced, such as Hoxa1, showed a loss of EZH2 binding and K27me3 after only a few hours of RA treatment. Tretinoin 20-22 enhancer of zeste 2 polycomb repressive complex 2 subunit Mus musculus 98-102
17525233-6 2007 In contrast, direct RA-responsive genes that are rapidly induced, such as Hoxa1, showed a loss of EZH2 binding and K27me3 after only a few hours of RA treatment. Tretinoin 148-150 enhancer of zeste 2 polycomb repressive complex 2 subunit Mus musculus 98-102
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 40-53 integrin subunit alpha M Homo sapiens 80-85
17697320-6 2007 Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response. Tretinoin 55-57 integrin subunit alpha M Homo sapiens 80-85
17634193-9 2007 Our data support a novel mechanism of RA-Tgfbeta-Fgf10 interactions in the developing foregut, in which endogenous RA controls Tgfbeta activity in the prospective lung field to allow local expression of Fgf10 and induction of lung buds. Tretinoin 38-40 fibroblast growth factor 10 Mus musculus 49-54
17634193-9 2007 Our data support a novel mechanism of RA-Tgfbeta-Fgf10 interactions in the developing foregut, in which endogenous RA controls Tgfbeta activity in the prospective lung field to allow local expression of Fgf10 and induction of lung buds. Tretinoin 38-40 fibroblast growth factor 10 Mus musculus 203-208
17226773-4 2007 We found that Oct4 and SF-1 were co-expressed in undifferentiated human embryonal carcinoma NCCIT cells and downregulated during retinoic acid-mediated differentiation. Tretinoin 129-142 splicing factor 1 Homo sapiens 23-27
17297443-3 2007 GRIM-19 physically interacts with HtrA2 and augments cell death in an IFN/all-trans retinoic acid (RA)-dependent manner. Tretinoin 99-101 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 0-7
17921113-11 2007 These results suggest that N-cadherin may be essential for RA-induced cardiomyogenesis in mouse ES cells in vitro. Tretinoin 59-61 cadherin 2 Mus musculus 27-37
17679169-9 2007 ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both the cell lines. Tretinoin 0-4 thyroid stimulating hormone receptor Homo sapiens 19-24
17679169-9 2007 ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both the cell lines. Tretinoin 0-4 thyroid peroxidase Homo sapiens 87-90
17451432-8 2007 Treatment of cells with the RARalpha/RXRalpha ligands, all-trans retinoic acid and 9-cis-retinoic acid, reduced and increased GnRH II gene expression in TE671 and JEG-3 cells, respectively. Tretinoin 65-78 retinoid X receptor alpha Homo sapiens 37-45
17451684-8 2007 Following RA induction, quantitative RT-PCR analysis demonstrated downregulation of nestin, PAX-6, thy1.1, and PKCalpha, and upregulation of rhodopsin, glial fibrillary acidic protein (GFAP), and CrX. Tretinoin 10-12 protein kinase C, alpha Rattus norvegicus 111-119
17451684-8 2007 Following RA induction, quantitative RT-PCR analysis demonstrated downregulation of nestin, PAX-6, thy1.1, and PKCalpha, and upregulation of rhodopsin, glial fibrillary acidic protein (GFAP), and CrX. Tretinoin 10-12 glial fibrillary acidic protein Rattus norvegicus 185-189
17426037-0 2007 Activation of the kinase activity of ATM by retinoic acid is required for CREB-dependent differentiation of neuroblastoma cells. Tretinoin 44-57 cAMP responsive element binding protein 1 Homo sapiens 74-78
17426037-4 2007 RA rapidly activates the activity of ATM kinase, leading to the ATM-dependent phosphorylation of the CREB protein, extrusion of neuritic processes, and differentiation of SH-SY5Y cells into neuronal-like cells. Tretinoin 0-2 cAMP responsive element binding protein 1 Homo sapiens 101-105
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 91-95 CD68 molecule Homo sapiens 283-287
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 91-95 integrin subunit alpha M Homo sapiens 289-294
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 91-95 matrix metallopeptidase 9 Homo sapiens 300-326
17369494-4 2007 Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid (ATRA) to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9). Tretinoin 91-95 matrix metallopeptidase 9 Homo sapiens 328-332
17325034-5 2007 The conversion of GDP-RAC1 to GTP-RAC1 parallels the activation of c-SRC as early as 15 min following all-trans-retinoic acid treatment in LA-N-5 cells. Tretinoin 106-125 Rac family small GTPase 1 Homo sapiens 18-26
17325034-5 2007 The conversion of GDP-RAC1 to GTP-RAC1 parallels the activation of c-SRC as early as 15 min following all-trans-retinoic acid treatment in LA-N-5 cells. Tretinoin 106-125 Rac family small GTPase 1 Homo sapiens 22-26
17185629-0 2007 Lipopolysaccharide opposes the induction of CYP26A1 and CYP26B1 gene expression by retinoic acid in the rat liver in vivo. Tretinoin 83-96 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 56-63
17185629-5 2007 We investigated the regulation of CYP26A1 and CYP26B1 mRNA levels by RA and LPS in the rat liver, as the liver is centrally involved in retinoid metabolism and the acute-phase response to LPS. Tretinoin 69-71 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 46-53
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 0-2 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 41-48
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 0-2 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 208-215
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 157-159 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 41-48
17185629-7 2007 RA-induced responses of both CYP26A1 and CYP26B1 were significantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. Tretinoin 157-159 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 41-48
17600477-9 2007 ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both cell lines. Tretinoin 0-4 thyroid stimulating hormone receptor Homo sapiens 19-24
17600477-9 2007 ATRA repressed the TSH-R mRNA levels in the normal thyroid cell line and increased the TPO and Tg mRNA levels slightly in both cell lines. Tretinoin 0-4 thyroid peroxidase Homo sapiens 87-90
17255106-3 2007 Retinoic acid was more effective than interleukin-1alpha (IL) in promoting cleavage at these sites in ADAMTS-5-deficient cartilage. Tretinoin 0-13 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2) Mus musculus 102-110
17255106-9 2007 ADAMTS-5, but not ADAMTS-1, -4, or -9, was up-regulated 8-fold by retinoic acid and 17-fold by IL-1alpha treatment. Tretinoin 66-79 a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 5 (aggrecanase-2) Mus musculus 0-8
16713227-0 2007 Nuclear receptor binding to the retinoic acid response elements of the phosphoenolpyruvate carboxykinase gene in vivo: effects of vitamin A deficiency. Tretinoin 32-45 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 71-104
16713227-3 2007 We have identified nuclear receptors that bind to retinoic acid response elements (RAREs) in the PEPCK promoter by electrophoretic mobility shift assay and have verified these in vivo using chromatin immunoprecipitation (ChIP) in mouse liver. Tretinoin 50-63 phosphoenolpyruvate carboxykinase 1, cytosolic Mus musculus 97-102
17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 87-100 transcription factor AP-2 alpha Homo sapiens 16-19
17187826-1 2007 BACKGROUND: The AP2 transcription factor family is a set of developmentally regulated, retinoic acid (RA) inducible genes, which regulate expression of estrogen receptor-alpha (ERalpha) in breast carcinoma. Tretinoin 102-104 transcription factor AP-2 alpha Homo sapiens 16-19
17187826-14 2007 Because CRABPII mediates growth suppressive effects of RA in breast cancer, the data suggest that AP2 factors have the ability to mediate RA responsiveness through the regulation of CRABP II expression. Tretinoin 55-57 transcription factor AP-2 alpha Homo sapiens 98-101
17170071-8 2007 These results suggest that switching of the ubiquitin/proteasome-dependent degradation of RXRalpha by phosphorylation in leiomyomas may be responsible for the accumulation of the receptor and the consequent dysregulation of retinoic acid target genes. Tretinoin 224-237 retinoid X receptor alpha Homo sapiens 90-98
17314664-2 2007 Choline acetyltransferase, the enzyme promoting acetylcholine synthesis, and the vesicular acetylcholine transporter are modulated by retinoic acid treatment. Tretinoin 134-147 choline O-acetyltransferase Rattus norvegicus 0-25
17314664-2 2007 Choline acetyltransferase, the enzyme promoting acetylcholine synthesis, and the vesicular acetylcholine transporter are modulated by retinoic acid treatment. Tretinoin 134-147 solute carrier family 18 member A3 Rattus norvegicus 81-116
17283134-0 2007 Knockdown of XAB2 enhances all-trans retinoic acid-induced cellular differentiation in all-trans retinoic acid-sensitive and -resistant cancer cells. Tretinoin 37-50 XPA binding protein 2 Homo sapiens 13-17
17283134-0 2007 Knockdown of XAB2 enhances all-trans retinoic acid-induced cellular differentiation in all-trans retinoic acid-sensitive and -resistant cancer cells. Tretinoin 97-110 XPA binding protein 2 Homo sapiens 13-17
17283134-4 2007 We therefore focused on defining the effect of XAB2 on cellular differentiation in the presence of ATRA treatment. Tretinoin 99-103 XPA binding protein 2 Homo sapiens 47-51
17283134-5 2007 In the present study, we showed that overexpression of XAB2 inhibited ATRA-induced cellular differentiation in human rhabdomyosarcoma cell line, and that knockdown of XAB2 by small interfering RNA (siRNA) increased ATRA-sensitive cellular differentiation in the human promyelocytic leukemia cell line HL60 at both physiologic (10(-9)-10(-8) mol/L) and therapeutic (10(-7) mol/L) concentrations of ATRA. Tretinoin 70-74 XPA binding protein 2 Homo sapiens 55-59
17070795-5 2007 Analysis of the expression of Raldh2 and local treatments with retinoic acid indicate that this signaling pathway mediates apoptosis in myogenic cells, appearing also involved in tendon maturation. Tretinoin 63-76 aldehyde dehydrogenase 1 family member A2 Homo sapiens 30-36
17241391-6 2007 Nonetheless, a stronger association between beta1 integrin and intracytoplasmatic proteins of focal contacts was observed in coimmunoprecipitation experiments after RA treatment, suggesting improved connection with the actin cytoskeleton. Tretinoin 165-167 integrin subunit beta 1 Homo sapiens 44-58
17113230-3 2007 We generated WldS or Nmnat1-overexpressing Neuro2A cell lines, in which neuronal differentiation including neurite elongation can be induced by retinoic acid. Tretinoin 144-157 nicotinamide nucleotide adenylyltransferase 1 Mus musculus 21-27
17204142-15 2007 Pre-incubation of SH-SY5Y human neuroblastoma cells with either RAR-pan-antagonist LE540 or MAP kinase kinase 1 (MEK-1) inhibitor PD98059 resulted in the abolition of ATRA-induced COX-2 promoter activity, COX-2 protein expression and PGE2 production whereas the retinoid X receptor pan-antagonist HX531, the p38 MAPK inhibitor SB203580 or the c-Jun kinase inhibitor SP600125 did not have any effect. Tretinoin 167-171 retinoid X receptor alpha Homo sapiens 262-281
17244022-7 2007 We also demonstrate that addition of fibroblast growth factor (FGF)-10 is able to partially prevent apoptosis and rescue exocrine differentiation and branching morphogenesis in atRA-treated cultures but not in mice lacking the FGF receptor 2-IIIb, suggesting the effects of FGF-10 are mediated through this receptor. Tretinoin 177-181 fibroblast growth factor 10 Mus musculus 37-70
17244022-7 2007 We also demonstrate that addition of fibroblast growth factor (FGF)-10 is able to partially prevent apoptosis and rescue exocrine differentiation and branching morphogenesis in atRA-treated cultures but not in mice lacking the FGF receptor 2-IIIb, suggesting the effects of FGF-10 are mediated through this receptor. Tretinoin 177-181 fibroblast growth factor 10 Mus musculus 274-280
17064353-2 2007 A 4-day treatment with retinoic acid (RA), which promoted neural differentiation of EBs, substantially increased the expression of the Wnt antagonist Dkk-1, and induced the synthesis of the Wnt/Dkk-1 co-receptor LRP6. Tretinoin 23-36 low density lipoprotein receptor-related protein 6 Mus musculus 212-216
17064353-2 2007 A 4-day treatment with retinoic acid (RA), which promoted neural differentiation of EBs, substantially increased the expression of the Wnt antagonist Dkk-1, and induced the synthesis of the Wnt/Dkk-1 co-receptor LRP6. Tretinoin 38-40 low density lipoprotein receptor-related protein 6 Mus musculus 212-216
17064353-3 2007 Recombinant Dkk-1 applied to EBs behaved like RA in inducing the expression of the neural markers nestin and distal-less homeobox gene (Dlx-2). Tretinoin 46-48 distal-less homeobox 2 Mus musculus 136-141
18274629-3 2007 Using these criteria, it was recently demonstrated that all-trans-retinoic acid (RA), the activator of the classical retinoic acid receptor RAR, also serves as a ligand for PPARbeta/delta. Tretinoin 56-79 peroxisome proliferator activated receptor delta Homo sapiens 173-181
18274629-3 2007 Using these criteria, it was recently demonstrated that all-trans-retinoic acid (RA), the activator of the classical retinoic acid receptor RAR, also serves as a ligand for PPARbeta/delta. Tretinoin 81-83 peroxisome proliferator activated receptor delta Homo sapiens 173-181
18274629-4 2007 Partitioning of RA between its two receptors was found to be regulated by FABP5, which delivers it to PPARbeta/delta, and cellular RA binding protein II (CRABP-II), which targets it to RAR. Tretinoin 16-18 fatty acid binding protein 5 Homo sapiens 74-79
18274629-4 2007 Partitioning of RA between its two receptors was found to be regulated by FABP5, which delivers it to PPARbeta/delta, and cellular RA binding protein II (CRABP-II), which targets it to RAR. Tretinoin 16-18 peroxisome proliferator activated receptor delta Homo sapiens 102-110
18274629-4 2007 Partitioning of RA between its two receptors was found to be regulated by FABP5, which delivers it to PPARbeta/delta, and cellular RA binding protein II (CRABP-II), which targets it to RAR. Tretinoin 16-18 cellular retinoic acid binding protein 2 Homo sapiens 122-152
18274629-4 2007 Partitioning of RA between its two receptors was found to be regulated by FABP5, which delivers it to PPARbeta/delta, and cellular RA binding protein II (CRABP-II), which targets it to RAR. Tretinoin 16-18 cellular retinoic acid binding protein 2 Homo sapiens 154-162
18274629-5 2007 Consequently, RA activates PPARbeta/delta in cells that display a high FABP5/CRABP-II expression ratio. Tretinoin 14-16 peroxisome proliferator activated receptor delta Homo sapiens 27-35
18274629-5 2007 Consequently, RA activates PPARbeta/delta in cells that display a high FABP5/CRABP-II expression ratio. Tretinoin 14-16 fatty acid binding protein 5 Homo sapiens 71-76
18274629-5 2007 Consequently, RA activates PPARbeta/delta in cells that display a high FABP5/CRABP-II expression ratio. Tretinoin 14-16 cellular retinoic acid binding protein 2 Homo sapiens 77-85
17097063-0 2006 All-trans retinoic acid increases expression of aquaporin-5 and plasma membrane water permeability via transactivation of Sp1 in mouse lung epithelial cells. Tretinoin 10-23 aquaporin 5 Mus musculus 48-59
17097063-3 2006 We report here that all-trans retinoic acid (atRA) increases plasma membrane water permeability, AQP5 mRNA and protein expression, and AQP5 promoter activity in MLE-12 cells. Tretinoin 20-43 aquaporin 5 Mus musculus 97-101
17097063-3 2006 We report here that all-trans retinoic acid (atRA) increases plasma membrane water permeability, AQP5 mRNA and protein expression, and AQP5 promoter activity in MLE-12 cells. Tretinoin 20-43 aquaporin 5 Mus musculus 135-139
17097063-3 2006 We report here that all-trans retinoic acid (atRA) increases plasma membrane water permeability, AQP5 mRNA and protein expression, and AQP5 promoter activity in MLE-12 cells. Tretinoin 45-49 aquaporin 5 Mus musculus 97-101
17097063-3 2006 We report here that all-trans retinoic acid (atRA) increases plasma membrane water permeability, AQP5 mRNA and protein expression, and AQP5 promoter activity in MLE-12 cells. Tretinoin 45-49 aquaporin 5 Mus musculus 135-139
16817226-0 2006 Transcriptional regulation of the homeobox gene NKX3.1 by all-trans retinoic acid in prostate cancer cells. Tretinoin 68-81 NK3 homeobox 1 Homo sapiens 48-54
16817226-3 2006 In this study, we have characterized regulation of NKX3.1 expression by all-trans retinoic acid (tRA), a naturally occurring vitamin A metabolite that is accumulated at high levels in the prostate. Tretinoin 82-95 NK3 homeobox 1 Homo sapiens 51-57
16817226-3 2006 In this study, we have characterized regulation of NKX3.1 expression by all-trans retinoic acid (tRA), a naturally occurring vitamin A metabolite that is accumulated at high levels in the prostate. Tretinoin 97-100 NK3 homeobox 1 Homo sapiens 51-57
17001693-11 2006 Fenretinide, a novel synthetic retinoic acid (RA) analog lowers RBP4 in glucose intolerant obese mice. Tretinoin 31-44 retinol binding protein 4, plasma Mus musculus 64-68
17132853-3 2006 The physiological effects of retinoic acids (RAs) are mediated by members of two families of nuclear receptors, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs), which are encoded by three distinct human genes, RXRalpha, RXRbeta, and RXRgamma. Tretinoin 29-43 retinoid X receptor alpha Homo sapiens 233-241
16732315-1 2006 Gene associated with retinoid interferon-induced mortality (GRIM)-19, an inhibitor of transcription factor STAT3, was originally identified as a critical regulatory protein in a genetic screen that was designed to identify the gene products necessary for Interferon (IFN)-beta- and retinoic acid-induced cell death. Tretinoin 282-295 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 30-68
16954206-8 2006 Overexpression of GCNF in NT2 cells resulted in repression of CRIPTO-1 transcription, whereas expression of the transcription-activating fusion construct GCNF-VP16 led to an induction of the CRIPTO-1 gene and prevented its retinoic acid-induced down-regulation. Tretinoin 223-236 nuclear receptor subfamily 6 group A member 1 Homo sapiens 154-158
16954206-8 2006 Overexpression of GCNF in NT2 cells resulted in repression of CRIPTO-1 transcription, whereas expression of the transcription-activating fusion construct GCNF-VP16 led to an induction of the CRIPTO-1 gene and prevented its retinoic acid-induced down-regulation. Tretinoin 223-236 host cell factor C1 Homo sapiens 159-163
16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 174-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-83
16979656-1 2006 CRABPII is a small, cytosolic protein that solubilizes and transfers retinoic acid (RA) to the nucleus while also enhancing its transcriptional activity. Tretinoin 69-82 cellular retinoic acid binding protein 2 Homo sapiens 0-7
16979656-6 2006 Comparison of our apo-WT with a mutant apo-CRABPII structure shows that mutation of Arg111, a conserved residue of CRABPII and a key residue in RA binding, causes structural changes in the molecule. Tretinoin 44-46 cellular retinoic acid binding protein 2 Homo sapiens 115-122
16956736-0 2006 PDGF-C participates in branchial arch morphogenesis and is down-regulated by retinoic acid. Tretinoin 77-90 platelet-derived growth factor, C polypeptide Mus musculus 0-6
16956736-5 2006 We examined the effects of RA on PDGF-C and its receptor PDGFR-alpha expressions. Tretinoin 27-29 platelet-derived growth factor, C polypeptide Mus musculus 33-39
16956736-6 2006 We demonstrated that administration of RA to mouse embryos resulted in dramatic losses of PDGF-C and its receptor PDGFR-alpha. Tretinoin 39-41 platelet-derived growth factor, C polypeptide Mus musculus 90-96
16671099-5 2006 All-trans retinoic acid also induced LCN2 protein, particularly in T47D cells. Tretinoin 10-23 lipocalin 2 Homo sapiens 37-41
16619265-8 2006 Further studies revealed that pretreatment with 10 microM BQ-123, a selective endothelin-1 receptor (ETAR) antagonist, for 2 h can significantly counteract the inhibition of 5 microM atRA treatment for 2 h of dHAND mRNA and protein expression. Tretinoin 183-187 hand Drosophila melanogaster 209-214
16932348-0 2006 Downregulation of topoisomerase IIbeta in myeloid leukemia cell lines leads to activation of apoptosis following all-trans retinoic acid-induced differentiation/growth arrest. Tretinoin 123-136 DNA topoisomerase II beta Homo sapiens 18-38
16728697-1 2006 In an acute promyelocytic leukemia (APL)-transplantable mouse model, we previously reported the presence of antibodies recognizing PML-RARalpha and RARalpha in the sera of ATRA-treated mice. Tretinoin 172-176 retinoic acid receptor, alpha Mus musculus 148-156
16806149-9 2006 Explant culture of RALDH2-deficient foreguts show a capacity to undergo lung budding and early branching in the presence of RA or FGF10. Tretinoin 19-21 fibroblast growth factor 10 Mus musculus 130-135
16724877-5 2006 Topical retinol and retinoic acid also increased the basal levels of epidermal CD44 and hyaluronate, although their preventive effect on UV-induced decrease of these molecules was less pronounced as compared to topical retinaldehyde. Tretinoin 20-33 CD44 antigen Mus musculus 79-83
16936753-0 2006 Rb2/p130 and protein phosphatase 2A: key mediators of ovarian carcinoma cell growth suppression by all-trans retinoic acid. Tretinoin 109-122 RB transcriptional corepressor like 2 Homo sapiens 0-3
16936753-0 2006 Rb2/p130 and protein phosphatase 2A: key mediators of ovarian carcinoma cell growth suppression by all-trans retinoic acid. Tretinoin 109-122 RB transcriptional corepressor like 2 Homo sapiens 4-8
16936753-3 2006 All-trans-retinoic acid (ATRA) has been shown to arrest the growth of ovarian carcinoma cells in G0/G1 and to significantly elevate levels of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 0-23 RB transcriptional corepressor like 2 Homo sapiens 142-145
16936753-3 2006 All-trans-retinoic acid (ATRA) has been shown to arrest the growth of ovarian carcinoma cells in G0/G1 and to significantly elevate levels of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 0-23 RB transcriptional corepressor like 2 Homo sapiens 146-150
16936753-3 2006 All-trans-retinoic acid (ATRA) has been shown to arrest the growth of ovarian carcinoma cells in G0/G1 and to significantly elevate levels of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 25-29 RB transcriptional corepressor like 2 Homo sapiens 142-145
16936753-3 2006 All-trans-retinoic acid (ATRA) has been shown to arrest the growth of ovarian carcinoma cells in G0/G1 and to significantly elevate levels of Rb2/p130 protein, a member of the retinoblastoma family of tumor suppressors. Tretinoin 25-29 RB transcriptional corepressor like 2 Homo sapiens 146-150
16936753-4 2006 As ATRA treatment leads to a significant increase in the amount of Rb2/p130 protein but not mRNA, the elevated levels of Rb2/p130 protein is likely the result of increased stability. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 67-70
16936753-4 2006 As ATRA treatment leads to a significant increase in the amount of Rb2/p130 protein but not mRNA, the elevated levels of Rb2/p130 protein is likely the result of increased stability. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 71-75
16936753-4 2006 As ATRA treatment leads to a significant increase in the amount of Rb2/p130 protein but not mRNA, the elevated levels of Rb2/p130 protein is likely the result of increased stability. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 121-124
16936753-4 2006 As ATRA treatment leads to a significant increase in the amount of Rb2/p130 protein but not mRNA, the elevated levels of Rb2/p130 protein is likely the result of increased stability. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 125-129
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 55-58
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 59-63
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 96-99
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 100-104
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 96-99
16936753-11 2006 In ATRA-treated ovarian carcinoma cells, PP2A binds to Rb2/p130 and dephosphorylates the NLS of Rb2/p130 leading to the interaction of importin alpha with Rb2/p130. Tretinoin 3-7 RB transcriptional corepressor like 2 Homo sapiens 100-104
16712891-5 2006 atRA-induced apoptosis was associated with upregulation of bcl-2, translocation of bax protein to the mitochondria from the cytosol, activation of caspase-3 and cytochrome c release into cytosol. Tretinoin 0-4 BCL2-associated X protein Mus musculus 83-86
16712891-5 2006 atRA-induced apoptosis was associated with upregulation of bcl-2, translocation of bax protein to the mitochondria from the cytosol, activation of caspase-3 and cytochrome c release into cytosol. Tretinoin 0-4 caspase 3 Mus musculus 147-156
16712891-6 2006 atRA-induced apoptosis was abrogated by z-DEVD-fmk, a caspase-3 specific inhibitor, and z-VAD-fmk, a general caspase inhibitor, suggesting that the atRA-induced cell death of MEPM cells occurs through the cytochrome c- and caspase-3-dependent pathways. Tretinoin 0-4 caspase 3 Mus musculus 54-63
16712891-6 2006 atRA-induced apoptosis was abrogated by z-DEVD-fmk, a caspase-3 specific inhibitor, and z-VAD-fmk, a general caspase inhibitor, suggesting that the atRA-induced cell death of MEPM cells occurs through the cytochrome c- and caspase-3-dependent pathways. Tretinoin 0-4 caspase 3 Mus musculus 223-232
16712891-6 2006 atRA-induced apoptosis was abrogated by z-DEVD-fmk, a caspase-3 specific inhibitor, and z-VAD-fmk, a general caspase inhibitor, suggesting that the atRA-induced cell death of MEPM cells occurs through the cytochrome c- and caspase-3-dependent pathways. Tretinoin 148-152 caspase 3 Mus musculus 54-63
16712891-6 2006 atRA-induced apoptosis was abrogated by z-DEVD-fmk, a caspase-3 specific inhibitor, and z-VAD-fmk, a general caspase inhibitor, suggesting that the atRA-induced cell death of MEPM cells occurs through the cytochrome c- and caspase-3-dependent pathways. Tretinoin 148-152 caspase 3 Mus musculus 223-232
16712891-7 2006 In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase (p38), as well as an early but transient activation of extracellular signal-regulated kinase (ERK). Tretinoin 13-17 mitogen-activated protein kinase 8 Mus musculus 72-95
16712891-7 2006 In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase (p38), as well as an early but transient activation of extracellular signal-regulated kinase (ERK). Tretinoin 13-17 mitogen-activated protein kinase 8 Mus musculus 97-100
16823827-5 2006 The data in this report show that both the DOK1 and the DOK2 adaptor proteins are constitutively expressed in the myelomonoblastic leukemia cell line, HL-60, and that expression of both proteins is induced by the chemotherapeutic differentiation causing agents, all-trans retinoic acid (atRA) and 1,25-dihydroxyvitamin D3 (VD3). Tretinoin 272-285 docking protein 1 Homo sapiens 43-47
16823827-5 2006 The data in this report show that both the DOK1 and the DOK2 adaptor proteins are constitutively expressed in the myelomonoblastic leukemia cell line, HL-60, and that expression of both proteins is induced by the chemotherapeutic differentiation causing agents, all-trans retinoic acid (atRA) and 1,25-dihydroxyvitamin D3 (VD3). Tretinoin 287-291 docking protein 1 Homo sapiens 43-47
16885356-3 2006 Recent studies have implicated APC in controlling retinoic acid biosynthesis during normal intestinal development through a WNT-independent mechanism. Tretinoin 50-63 APC regulator of WNT signaling pathway Danio rerio 31-34
16885356-4 2006 Paradoxically, however, previous studies found that dietary supplementation of Apc(MIN) mice with retinoic acid failed to abrogate adenoma formation. Tretinoin 98-111 APC regulator of WNT signaling pathway Danio rerio 79-82
16699180-7 2006 APC mutant zebrafish express higher levels of C/EBP-beta than wild-type animals, and retinoic acid supplementation reduces C/EBP-beta expression to basal levels. Tretinoin 85-98 CCAAT enhancer binding protein beta Danio rerio 123-133
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 37-50 neurotrophin 3 Homo sapiens 129-148
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 37-50 neurotrophin 3 Homo sapiens 218-237
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 52-54 neurotrophin 3 Homo sapiens 129-148
16849523-1 2006 In several neuroblastoma cell lines, retinoic acid (RA)-induced differentiation is coupled to increased expression of functional neurotrophic factor receptors, including Trk family receptors and the glial cell-derived neurotrophic factor receptor, Ret. Tretinoin 52-54 neurotrophin 3 Homo sapiens 218-237
16849523-5 2006 Using a 2"-fluoro-RNA aptamer and a truncated Ret protein as specific inhibitors of Ret, we show that RA-induced differentiation is mediated by a positive autocrine loop that sustains Ret downstream signaling and depends on glial cell-derived neurotrophic factor expression and release. Tretinoin 102-104 neurotrophin 3 Homo sapiens 243-262
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 85-98 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 47-54
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 100-102 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 47-54
16933217-1 2006 BACKGROUND: CYP26A1, together with CYP26B1 and CYP26C1, are key enzymes of all-trans retinoic acid (RA) inactivation and their specific and restricted expression in developing embryos participate in the fine tuning RA levels. Tretinoin 215-217 cytochrome P450 family 26 subfamily C member 1 Homo sapiens 47-54
16617325-5 2006 The down-modulation of the expression of Akt protein in HL-60 cells using siRNA reduces the CD11b expression in ATRA-treated cells. Tretinoin 112-116 integrin subunit alpha M Homo sapiens 92-97
16617325-8 2006 In contrast, the presence of Akt inhibitors reduced the expression of CD11b in ATRA-treated NB4 cells. Tretinoin 79-83 integrin subunit alpha M Homo sapiens 70-75
16574167-7 2006 Decreases in CyclinB2 and BIRC5 mRNA induced by FK506 or retinoic acid, both of which exert potentiation of NGF-induced neurite outgrowth effects but with different mechanisms, also correlated with their neurite outgrowth activities. Tretinoin 57-70 baculoviral IAP repeat containing 5 Homo sapiens 26-31
16800923-8 2006 10 nmol/L ATRA plus 100 microg/ml bestatin for 72 hours prominently elevated CD11b expression in NB4 cells as compared with ATRA alone treated NB4 cells (P < 0.01). Tretinoin 10-14 integrin subunit alpha M Homo sapiens 77-82
16764683-0 2006 Correlation of Hsp110 expression with caspase-3 and -9 during apoptosis induced by in vivo embryonic exposition to retinoic acid or irradiation in early mouse craniofacial development. Tretinoin 115-128 heat shock 105kDa/110kDa protein 1 Mus musculus 15-21
16764683-0 2006 Correlation of Hsp110 expression with caspase-3 and -9 during apoptosis induced by in vivo embryonic exposition to retinoic acid or irradiation in early mouse craniofacial development. Tretinoin 115-128 caspase 3 Mus musculus 38-54
16875555-13 2006 CONCLUSION: The VEGF-C via VEGFR-3 signaling pathway could promote the proliferation of leukemic cells by autocrine pathway and inhibit the cell differentiation mediated by ATRA and chemotherapy-induced apoptosis. Tretinoin 173-177 fms related receptor tyrosine kinase 4 Homo sapiens 27-34
16430862-3 2006 JWA (AF070523) is a novel all-trans retinoic acid (ATRA) responsible gene that initially isolated from ATRA-treated primary human tracheal bronchial epithelial cells. Tretinoin 51-55 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 0-3
16430862-5 2006 Our results showed that JWA was not only regulated by ATRA but also by several other differentiation inducers such as phorbol-12-myristate-13-acetate (TPA), arabinoside (Ara-C), and hemin, involved in the mechanisms of differentiation along different lineages of myeloid leukemia cells arrested at different stages of development. Tretinoin 54-58 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 24-27
16430862-8 2006 However, in NB4 cells treated with ATRA, dissimilar with others, the expression of JWA was down-regulated, and the induced cellular differentiation could be enhanced by silencing of JWA. Tretinoin 35-39 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 83-86
16430862-8 2006 However, in NB4 cells treated with ATRA, dissimilar with others, the expression of JWA was down-regulated, and the induced cellular differentiation could be enhanced by silencing of JWA. Tretinoin 35-39 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 182-185
16261163-4 2006 We found that both RARbeta2 and Cyp26a1 genes are epigenetically silenced in the absence of DNA methylation in RAC65, a P19 embryocarcinoma cell line derivative carrying a dominant-negative RARalpha mutant and resistant to the growth-inhibitory and differentiation effects of RA. Tretinoin 19-21 retinoic acid receptor, alpha Mus musculus 190-198
20483243-2 2006 To elucidate the common role of RA on vertebrate embryos, we first sought to clone a homologous gene to human raldh2 from fugu, Takifugu rubripes. Tretinoin 32-34 aldehyde dehydrogenase 1 family member A2 Homo sapiens 110-116
16223781-6 2006 This effect was significantly enhanced by ATRA/FK228 administered in combination, due in part to increased H4 and H3-Lys9 acetylation of the MDR1 promoter and recruitment of the nuclear transcription factor Y alpha (NFYA) transcription activator to the CCAAT box. Tretinoin 42-46 nuclear transcription factor Y subunit alpha Homo sapiens 178-214
16223781-6 2006 This effect was significantly enhanced by ATRA/FK228 administered in combination, due in part to increased H4 and H3-Lys9 acetylation of the MDR1 promoter and recruitment of the nuclear transcription factor Y alpha (NFYA) transcription activator to the CCAAT box. Tretinoin 42-46 nuclear transcription factor Y subunit alpha Homo sapiens 216-220
16439309-0 2006 Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Tretinoin 0-13 lymphocyte cytosolic protein 2 Homo sapiens 36-42
16291826-4 2006 A broad caspase inhibitor (z-VAD-fmk), caspase-9 inhibitor z-LEHD-fmk and caspase-3 inhibitor (z-DEVD-fmk) blocked atRA-induced DNA fragmentation and sub-G1 fraction, but not caspase-8 inhibitor z-IETD-fmk. Tretinoin 115-119 caspase 3 Mus musculus 74-83
16291826-6 2006 A weaker increase in RAR-alpha mRNA was seen only at the highest concentration of atRA (5 muM). Tretinoin 82-86 retinoic acid receptor, alpha Mus musculus 21-30
16291826-7 2006 The pan RAR antagonist, BMS493, completely abrogated atRA-induced DNA fragmentation, Sub-G1 fraction, and caspase-3 activation. Tretinoin 53-57 retinoic acid receptor, alpha Mus musculus 8-11
16291826-7 2006 The pan RAR antagonist, BMS493, completely abrogated atRA-induced DNA fragmentation, Sub-G1 fraction, and caspase-3 activation. Tretinoin 53-57 caspase 3 Mus musculus 106-115
16291826-8 2006 Taken together, these findings show that caspase-mediated induction of apoptosis by atRA is an RAR-dependent signaling pathway. Tretinoin 84-88 retinoic acid receptor, alpha Mus musculus 95-98
16273324-7 2006 The effects of RA were associated with improved differentiation of the cardiac myocytes, as assessed from the expression of atrial natriuretic factor and the morphology of the contractile apparatus. Tretinoin 15-17 natriuretic peptide A Rattus norvegicus 124-149
16323176-0 2006 The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia. Tretinoin 93-116 histone deacetylase 9 Homo sapiens 4-23
16323176-0 2006 The histone deacetylase (HDAC) inhibitor valproic acid as monotherapy or in combination with all-trans retinoic acid in patients with acute myeloid leukemia. Tretinoin 93-116 histone deacetylase 9 Homo sapiens 25-29
16612131-9 2006 Induction of kappa-opioid receptor gene by retinoic acid resulted in increased binding of Sp1 transcription factor to the promoter of the kappa-opioid receptor. Tretinoin 43-56 opioid receptor kappa 1 Homo sapiens 13-34
16612131-9 2006 Induction of kappa-opioid receptor gene by retinoic acid resulted in increased binding of Sp1 transcription factor to the promoter of the kappa-opioid receptor. Tretinoin 43-56 opioid receptor kappa 1 Homo sapiens 138-159
16125842-2 2005 However, we report here that GDNF and neurturin blocked the growth inhibitory and neuritogenic effects of all-trans-retinoic acid in neuroblastoma cells in vitro. Tretinoin 106-129 neurturin Homo sapiens 38-47
16251210-6 2005 RA signaling was found to play a role in regulating the expression of EphB2, EphB3 and ephrin B2, three molecules whose graded expression in the retina along the DV axis is important for establishing the correct retinotectal map. Tretinoin 0-2 ephrin B2 Gallus gallus 87-96
16393152-10 2005 By using pharmacologic modulators of signalling pathways implicated in TSC, we showed that the impairment in Kir channel function was not affected by rapamycin inhibition of the mTOR/S6K pathway, but was reversed by decreasing CDK2 activity with roscovitine or retinoic acid. Tretinoin 261-274 cyclin-dependent kinase 2 Mus musculus 227-231
16324150-5 2005 Furthermore, flow cytometric analyses showed that HL-60 cells, human promyelocytic leukemia cell line, wherein TRAP220 was down-regulated, did not differentiate efficiently into monocytes and granulocytes by stimulation with 1,25-dihydroxyvitamin D(3) and all-trans retinoic acid, correspondingly. Tretinoin 266-279 mediator complex subunit 1 Homo sapiens 111-118
16275619-4 2005 RA enhanced the immunoglobulin synthesis by tonsillar B cells in anti-CD40 plus IL-10-mediated culture system. Tretinoin 0-2 interleukin 10 Homo sapiens 80-85
16403252-7 2005 HDAC inhibitors such as trichostatin A, in combination with ATRA, induce differentiation of the blast/promyelocytic cells from PLZF-RARa/RARa-PLZF double TM, but not ATRA alone. Tretinoin 60-64 retinoic acid receptor, alpha Mus musculus 132-136
16403252-7 2005 HDAC inhibitors such as trichostatin A, in combination with ATRA, induce differentiation of the blast/promyelocytic cells from PLZF-RARa/RARa-PLZF double TM, but not ATRA alone. Tretinoin 60-64 retinoic acid receptor, alpha Mus musculus 137-141
16279945-7 2005 To elucidate a possible regulatory mechanism of APLP2 shedding in the neuronal context, we examined retinoic acid-induced differentiation of neuroblastoma cells. Tretinoin 100-113 amyloid beta (A4) precursor-like protein 2 Mus musculus 48-53
16279945-8 2005 Retinoic acid treatment of two neuroblastoma cell lines upregulated the expression of both APLP2 and ADAM10, thus leading to an increased release of soluble APLP2. Tretinoin 0-13 amyloid beta (A4) precursor-like protein 2 Mus musculus 91-96
16279945-8 2005 Retinoic acid treatment of two neuroblastoma cell lines upregulated the expression of both APLP2 and ADAM10, thus leading to an increased release of soluble APLP2. Tretinoin 0-13 amyloid beta (A4) precursor-like protein 2 Mus musculus 157-162
16249480-12 2005 sPLA(2) upregulation by RA was confirmed by Western blot analysis. Tretinoin 24-26 phospholipase A2 group IIA Homo sapiens 0-6
16040168-5 2005 The IgG2a/IgG1 ratio was lower in mice treated with ATRA. Tretinoin 52-56 LOC105243590 Mus musculus 10-14
16093312-0 2005 Vitamin A and immune function: retinoic acid modulates population dynamics in antigen receptor and CD38-stimulated splenic B cells. Tretinoin 31-44 CD38 antigen Mus musculus 99-103
16096367-4 2005 TrxR1 was also recently identified as one key enzyme involved in cell death induced by interferon-beta (IFN-beta)/all-trans retinoic acid (ATRA) anti-cancer treatment. Tretinoin 124-137 thioredoxin reductase 1 Homo sapiens 0-5
16096367-4 2005 TrxR1 was also recently identified as one key enzyme involved in cell death induced by interferon-beta (IFN-beta)/all-trans retinoic acid (ATRA) anti-cancer treatment. Tretinoin 139-143 thioredoxin reductase 1 Homo sapiens 0-5
16204045-2 2005 However, elevating the levels of cyclic AMP (cAMP) confers onto retinoid X receptor (RXR)-selective agonists ("rexinoids") the ability to induce terminal granulocyte differentiation and apoptosis of all-trans retinoic acid-resistant and insensitive AML cells and patients" blasts. Tretinoin 209-222 retinoid X receptor alpha Homo sapiens 64-83
16204045-2 2005 However, elevating the levels of cyclic AMP (cAMP) confers onto retinoid X receptor (RXR)-selective agonists ("rexinoids") the ability to induce terminal granulocyte differentiation and apoptosis of all-trans retinoic acid-resistant and insensitive AML cells and patients" blasts. Tretinoin 209-222 retinoid X receptor alpha Homo sapiens 85-88
16166633-6 2005 Loss of repression of ES cell marker genes Oct4, Nanog, Sox2, FGF4, and Stella was observed upon treatment of GCNF-/- ES cells with retinoic acid. Tretinoin 132-145 SRY (sex determining region Y)-box 2 Mus musculus 56-60
16277846-0 2005 [JWA gene in regulating committed differentiation of HL-60 cells induced by ATRA, Ara-C and TPA]. Tretinoin 76-80 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 1-4
16277846-2 2005 By using FCM, the changes of CD13, CD14, CD15, CD11b and cell cycles were detected in HL-60 cells treated with ATRA (10(-6) mol/L), Ara-C (10 ng/ml) and TPA (10(-8) mol/L) respectively. Tretinoin 111-115 integrin subunit alpha M Homo sapiens 47-52
16007204-6 2005 Interestingly, while the upregulation of STAT-1 by IFNgamma is partially inhibited by RA, IFNgamma is shown to repress RA-driven TGFbeta-2 induction, pointing to the involvement of alternative mechanism(s) in IFNgamma-RA synergism. Tretinoin 86-88 signal transducer and activator of transcription 1 Homo sapiens 41-47
16052510-5 2005 The decrease in N-terminal phosphorylation of c-Jun does not appear to be modulated by JNK or ERK, since their protein expression patterns and kinase activity do not correlate with the repression of AP-1 activity following treatment with atRA. Tretinoin 238-242 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51
16026781-12 2005 Maternal supplementation of RA rescues early dorsal pancreas development and restores endodermal Pdx 1 and mesenchymal Isl 1 expression as well as endocrine cell differentiation. Tretinoin 28-30 ISL1 transcription factor, LIM/homeodomain Mus musculus 119-124
15927671-6 2005 Furthermore, serum levels of IL-8, MIP-1beta and RANTES were increased during the course of ATRA treatment in both APL patients who developed APL differentiation syndrome. Tretinoin 92-96 C-C motif chemokine ligand 5 Homo sapiens 49-55
15989786-0 2005 [The effect of retinoic acid on C3 and factor B secretion of human alveolar type II epithelial cells induced with cytokines]. Tretinoin 15-28 complement C3 Homo sapiens 32-47
15989786-1 2005 AIM: To explore the effect of retinoic acid (RA)on C3 and factor B (Bf) secretion by human alveolar type II epithelial cell line A549 induced with cytokines. Tretinoin 30-43 complement C3 Homo sapiens 51-66
15949696-1 2005 The effects of fatty acids and retinoic acid (carotene) on brown adipose tissue differentiation are mediated by activation of the transcription factors PPARgamma and PPARalpha in combination with RXR. Tretinoin 31-44 retinoid X receptor alpha Homo sapiens 196-199
15841082-2 2005 A recently discovered gene, GRIM-19 has been found to fulfil two roles within the cell: as a member of the interferon-beta and retinoic acid-induced pathway of cell death, and as part of the mitochondrial Complex I assembly. Tretinoin 127-140 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 28-35
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 30-32 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 84-89
15907483-5 2005 Interestingly, retinoic acid (RA) signaling induced the recruitment of HIF-1 on the PEPCK promoter, resulting from the functional interaction of HIF-1 and ATF-2 with coactivator CBP. Tretinoin 30-32 activating transcription factor 2 Homo sapiens 155-160
15836616-0 2005 Activation of Rac1 by phosphatidylinositol 3-kinase in vivo: role in activation of mitogen-activated protein kinase (MAPK) pathways and retinoic acid-induced neuronal differentiation of SH-SY5Y cells. Tretinoin 136-149 Rac family small GTPase 1 Homo sapiens 14-18
15836616-4 2005 Here, we demonstrate that RA promotes activation of Rac1 in SH-SY5Y cells in a transamidation-independent manner. Tretinoin 26-28 Rac family small GTPase 1 Homo sapiens 52-56
15744343-0 2005 ID1 and ID2 are retinoic acid responsive genes and induce a G0/G1 accumulation in acute promyelocytic leukemia cells. Tretinoin 16-29 inhibitor of DNA binding 2 Homo sapiens 8-11
15744343-4 2005 ATRA induced a rapid increase in ID1 and ID2, both in the APL cell line NB4 as well as in primary patient cells. Tretinoin 0-4 inhibitor of DNA binding 2 Homo sapiens 41-44
15744343-7 2005 The simultaneous upregulation of ID1 and ID2, and the downregulation of E2A suggest a role for bHLH proteins in the induction of differentiation of APL cells following ATRA treatment. Tretinoin 168-172 inhibitor of DNA binding 2 Homo sapiens 41-44
15744343-10 2005 These results indicate that ID1 and ID2 are important retinoic acid responsive genes in APL, and suggest that the inhibition of specific bHLH transcription factor complexes may play a role in the therapeutic effect of ATRA in APL. Tretinoin 218-222 inhibitor of DNA binding 2 Homo sapiens 36-39
15734730-6 2005 These results are confirmed in the F9 teratocarcinoma cell line, a model for retinoic acid-induced visceral endoderm differentiation in which we demonstrate that ablation of retinoic acid-induced Dab2 expression levels, by stable siRNA silencing of Dab2, blocks visceral endoderm differentiation. Tretinoin 174-187 disabled 2, mitogen-responsive phosphoprotein Mus musculus 196-200
15734730-6 2005 These results are confirmed in the F9 teratocarcinoma cell line, a model for retinoic acid-induced visceral endoderm differentiation in which we demonstrate that ablation of retinoic acid-induced Dab2 expression levels, by stable siRNA silencing of Dab2, blocks visceral endoderm differentiation. Tretinoin 174-187 disabled 2, mitogen-responsive phosphoprotein Mus musculus 249-253
15777796-2 2005 Retinoic acid (RA) stimulates these events, including upregulation of expression and activity of alkaline phosphatase (APase), expression of annexins II, V, and VI proteins, which bind to membranes and form Ca(2+) channels, expression of osteocalcin and runx2, another mineralization-related protein and terminal differentiation-related transcription factor, and ultimately mineralization. Tretinoin 0-13 bone gamma-carboxyglutamate protein Gallus gallus 238-249
15721283-5 2005 Both RA isoforms also reduced IFN-gamma-induced activation of signal transducers and activators of transcription (STAT)1, STAT3, Janus kinase (JAK)1, and JAK2. Tretinoin 5-7 Janus kinase 2 Rattus norvegicus 154-158
15721283-8 2005 Suppressors of cytokine signaling (SOCS), which are negative regulators of the JAK/STAT pathway, may be candidate mediators of the anti-inflammatory function of RA. Tretinoin 161-163 cytokine inducible SH2-containing protein Rattus norvegicus 35-39
15816857-0 2005 Retinoic acid activates human secretin gene expression by Sp proteins and nuclear factor I in neuronal SH-SY5Y cells. Tretinoin 0-13 secretin Homo sapiens 30-38
15733075-0 2005 Retinoic acid increases tissue and plasma contents of nerve growth factor and prevents neuropathy in diabetic mice. Tretinoin 0-13 nerve growth factor Mus musculus 54-73
15733075-2 2005 Retinoic acid (RA) promotes the endogenous expression of nerve growth factor and its receptor. Tretinoin 0-13 nerve growth factor Mus musculus 57-76
15733075-2 2005 Retinoic acid (RA) promotes the endogenous expression of nerve growth factor and its receptor. Tretinoin 15-17 nerve growth factor Mus musculus 57-76
15733075-10 2005 RESULTS: Contents of NGF in healthy untreated mice were 1490 +/- 190 pg mg(-1) in nerve and 113 +/- 67 pg mg(-1) in serum; in diabetic untreated mice the values were 697 +/- 219 pg mL(-1) in nerve and 55 +/- 41 pg mL(-1) in serum; and in diabetic mice treated with RA the values were 2432 +/- 80 pg mL(-1) in nerve and 235 +/- 133 pg mg(-1) in serum (P < 0.002). Tretinoin 265-267 nerve growth factor Mus musculus 21-24
15664402-5 2005 However, in atRA-treated SHR, a significant upregulation of APJ and apelin expression was observed in both heart and aorta (p<0.05), accompanied by a reduction of AT(1) expression, an elevation of serum nitric oxide levels and a subsequent decrease of blood pressure. Tretinoin 12-16 apelin receptor Rattus norvegicus 60-63
15537748-9 2005 Furthermore, atRA treatment reduced phosphorylated Rb and decreased cdk2 and cdk4 kinase activity. Tretinoin 13-17 cyclin-dependent kinase 2 Mus musculus 68-72
15606616-11 2005 ATRA also suppressed the expression of inducible nitric oxide synthetase (iNOS) and monocyte chemoattractant protein-1 (MCP-1) in the kidney. Tretinoin 0-4 chemokine (C-C motif) ligand 2 Mus musculus 84-118
15606616-11 2005 ATRA also suppressed the expression of inducible nitric oxide synthetase (iNOS) and monocyte chemoattractant protein-1 (MCP-1) in the kidney. Tretinoin 0-4 chemokine (C-C motif) ligand 2 Mus musculus 120-125
15601824-5 2004 We identified potential target genes for BAF180 in heart development, such as S100A13 as well as retinoic acid (RA)-induced targets RARbeta2 and CRABPII. Tretinoin 97-110 cellular retinoic acid binding protein 2 Homo sapiens 145-152
15601824-5 2004 We identified potential target genes for BAF180 in heart development, such as S100A13 as well as retinoic acid (RA)-induced targets RARbeta2 and CRABPII. Tretinoin 112-114 polybromo 1 Homo sapiens 41-47
15601824-5 2004 We identified potential target genes for BAF180 in heart development, such as S100A13 as well as retinoic acid (RA)-induced targets RARbeta2 and CRABPII. Tretinoin 112-114 cellular retinoic acid binding protein 2 Homo sapiens 145-152
15516979-4 2004 Protein half-life analyses showed that PML-RARalpha enhanced MNK1 protein stability in U937 cells and ATRA exposure decreased MNK1 half-life in NB4 cells. Tretinoin 102-106 MAPK interacting serine/threonine kinase 1 Homo sapiens 126-130
15358764-3 2004 These data suggest a model wherein APC controls enterocyte differentiation by controlling retinoic acid production. Tretinoin 90-103 APC regulator of WNT signaling pathway Danio rerio 35-38
15358764-5 2004 To examine the relationship between APC and retinoic acid biosynthesis in normal enterocytes, we have identified two novel zebrafish retinol dehydrogenases, termed zRDHA and zRDHB, that show strong expression within the gut of developing zebrafish embryos. Tretinoin 44-57 APC regulator of WNT signaling pathway Danio rerio 36-39
15358764-6 2004 Morpholino knockdown of either APC or zRDHB in zebrafish embryos resulted in defects in structures known to require retinoic acid. Tretinoin 116-129 APC regulator of WNT signaling pathway Danio rerio 31-34
15531370-0 2004 CYP26A1 and CYP26C1 cooperate in degrading retinoic acid within the equatorial retina during later eye development. Tretinoin 43-56 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 12-19
15531370-6 2004 As explanation, we found that CYP26C1, another RA-degrading enzyme, had emerged centrally in a narrower domain within the RA-poor stripe. Tretinoin 47-49 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 30-37
15531370-6 2004 As explanation, we found that CYP26C1, another RA-degrading enzyme, had emerged centrally in a narrower domain within the RA-poor stripe. Tretinoin 122-124 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 30-37
15531370-7 2004 While RA applications increased retinal Cyp26a1 expression, they slightly reduced Cyp26c1. Tretinoin 6-8 cytochrome P450, family 26, subfamily c, polypeptide 1 Mus musculus 82-89
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 0-23 brain derived neurotrophic factor Homo sapiens 50-54
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 0-23 glial fibrillary acidic protein Homo sapiens 194-225
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 0-23 glial fibrillary acidic protein Homo sapiens 227-231
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 25-27 brain derived neurotrophic factor Homo sapiens 50-54
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 25-27 glial fibrillary acidic protein Homo sapiens 194-225
15530878-4 2004 All-trans-retinoic acid (RA) induction caused the BDNF-MSCs to differentiate into neural cells with significantly increased expressions of such neural-specific proteins as nestin, NeuN, O4, and glial fibrillary acidic protein (GFAP). Tretinoin 25-27 glial fibrillary acidic protein Homo sapiens 227-231
15477383-0 2004 Upregulation of angiotensin-converting enzyme 2 by all-trans retinoic acid in spontaneously hypertensive rats. Tretinoin 61-74 angiotensin I converting enzyme 2 Rattus norvegicus 16-47
15477383-2 2004 To further validate effects of atRA on the RAS and to assess the possibility that atRA affects the activity of angiotensin-converting enzyme 2 (ACE2), gene, and protein expression of ACE2 have been examined by real-time polymerase chain reaction and Western blot methods in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Tretinoin 82-86 angiotensin I converting enzyme 2 Rattus norvegicus 111-142
15477383-2 2004 To further validate effects of atRA on the RAS and to assess the possibility that atRA affects the activity of angiotensin-converting enzyme 2 (ACE2), gene, and protein expression of ACE2 have been examined by real-time polymerase chain reaction and Western blot methods in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Tretinoin 82-86 angiotensin I converting enzyme 2 Rattus norvegicus 144-148
15477383-2 2004 To further validate effects of atRA on the RAS and to assess the possibility that atRA affects the activity of angiotensin-converting enzyme 2 (ACE2), gene, and protein expression of ACE2 have been examined by real-time polymerase chain reaction and Western blot methods in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Tretinoin 82-86 angiotensin I converting enzyme 2 Rattus norvegicus 183-187
15477383-5 2004 However, in atRA-treated SHR, a significant upregulation of ACE2 expression was observed in heart and kidney. Tretinoin 12-16 angiotensin I converting enzyme 2 Rattus norvegicus 60-64
15550114-6 2004 We investigated the effects of all-trans retinoic acid on the production of MCP-1 under high glucose conditions in cultured mouse podocytes. Tretinoin 41-54 chemokine (C-C motif) ligand 2 Mus musculus 76-81
15371543-5 2004 RA-mediated phosphorylation of CREB leads to a direct stimulation of CREB-dependent transcriptional activity and to activation of the expression of genes such as c-fos, which do not contain RAREs but contain cAMP response elements (CREs) in their promoters. Tretinoin 0-2 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 162-167
15382060-9 2004 In an RTBM1 neuroblastoma cell line, hTTL was increased after treating the cells with bone morphogenetic protein 2 (BMP2) or all-trans retinoic acid (RA), which induced neuronal differentiation. Tretinoin 135-148 tubulin tyrosine ligase Homo sapiens 37-41
15382060-9 2004 In an RTBM1 neuroblastoma cell line, hTTL was increased after treating the cells with bone morphogenetic protein 2 (BMP2) or all-trans retinoic acid (RA), which induced neuronal differentiation. Tretinoin 150-152 tubulin tyrosine ligase Homo sapiens 37-41
15376324-4 2004 Exposure of rat embryos to excess atRA at times ranging from E9.25 to E12 leads to altered NEDD9 expression in the developing hindbrain within 6 hr. Tretinoin 34-38 neural precursor cell expressed, developmentally down-regulated 9 Rattus norvegicus 91-96
15376324-6 2004 A putative retinoic acid response element in the 5" region of the NEDD9 promoter binds specifically to a RXR/RAR heterodimer and forms a higher molecular weight complex upon addition of a retinoic acid receptor-specific antibody. Tretinoin 11-24 retinoid X receptor alpha Homo sapiens 105-108
15646024-0 2004 Retinoic acid administration and vitamin A status modulate retinoid X receptor alpha and retinoic acid receptor alpha levels in mouse brown adipose tissue. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 89-117
15646024-2 2004 RA was previously shown to down-regulate the steady state levels of retinoic acid receptor alpha (RARalpha) and retinoid X receptor alpha (RXRalpha) in primary brown adipocytes differentiated in culture. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 68-96
15646024-2 2004 RA was previously shown to down-regulate the steady state levels of retinoic acid receptor alpha (RARalpha) and retinoid X receptor alpha (RXRalpha) in primary brown adipocytes differentiated in culture. Tretinoin 0-2 retinoic acid receptor, alpha Mus musculus 98-106
15449376-7 2004 Overexpression of BTG1 mRNA was also observed in the CR state of all-trans-retinoic acid (ATRA)-treated AML-M3 patients and ATRA-treated HL-60 cells. Tretinoin 65-88 BTG anti-proliferation factor 1 Homo sapiens 18-22
15449376-7 2004 Overexpression of BTG1 mRNA was also observed in the CR state of all-trans-retinoic acid (ATRA)-treated AML-M3 patients and ATRA-treated HL-60 cells. Tretinoin 90-94 BTG anti-proliferation factor 1 Homo sapiens 18-22
15449376-7 2004 Overexpression of BTG1 mRNA was also observed in the CR state of all-trans-retinoic acid (ATRA)-treated AML-M3 patients and ATRA-treated HL-60 cells. Tretinoin 124-128 BTG anti-proliferation factor 1 Homo sapiens 18-22
15573757-5 2004 RESULTS: Above 10(-6) mol/L retinoic acid enhanced the growth suppression (suppression ratio > or = 69.2%, P<0.01), apoptosis (Apoptosis ratio > or = 23.8%, P<0.05) and down-regulation of the expression of cyclin D1 (expression ratio < or = 14.2%, P<0.05) induced by above 10(-7) mol/L docetaxol in PC-3 cells. Tretinoin 28-41 cyclin D1 Mus musculus 218-227
15634573-5 2004 When ATRA + SQ22536 group compared with ATRA group, the positivity of CD11b decreased from (95.9 +/- 2.5)% to (60.3 +/- 7.1)%, while the A(540) in NBT reduction assay decreased from 0.585 +/- 0.092 to 0.170 +/- 0.028 (P < 0.05). Tretinoin 5-9 integrin subunit alpha M Homo sapiens 70-75
15634573-5 2004 When ATRA + SQ22536 group compared with ATRA group, the positivity of CD11b decreased from (95.9 +/- 2.5)% to (60.3 +/- 7.1)%, while the A(540) in NBT reduction assay decreased from 0.585 +/- 0.092 to 0.170 +/- 0.028 (P < 0.05). Tretinoin 40-44 integrin subunit alpha M Homo sapiens 70-75
15634573-7 2004 When ATRA + forskolin group compared with ATRA group, the positivity of CD11b increased from (34.3 +/- 5.3)% to (94.6 +/- 2.4)%, while the A(540) in NBT reduction assay increased from 0.110 +/- 0.028 to 0.395 +/- 0.049 (P < 0.05). Tretinoin 5-9 integrin subunit alpha M Homo sapiens 72-77
15325130-3 2004 Further increases in PrPres accumulation were observed in ScN2a cells treated with retinoic acid, a compound that is associated with neuronal differentiation. Tretinoin 83-96 sodium voltage-gated channel alpha subunit 2 Homo sapiens 58-63
15325130-7 2004 The survival of retinoic acid-treated ScN2a cells co-cultured with microglia was significantly reduced when compared to untreated ScN2a cells and an inverse correlation was demonstrated between the PrPres content of cells and their survival when co-cultured with microglia. Tretinoin 16-29 sodium voltage-gated channel alpha subunit 2 Homo sapiens 38-43
15325130-7 2004 The survival of retinoic acid-treated ScN2a cells co-cultured with microglia was significantly reduced when compared to untreated ScN2a cells and an inverse correlation was demonstrated between the PrPres content of cells and their survival when co-cultured with microglia. Tretinoin 16-29 sodium voltage-gated channel alpha subunit 2 Homo sapiens 130-135
15325130-8 2004 The production of interleukin-6 by microglia cultured with retinoic acid-treated ScN2a cells was significantly higher than that of microglia cultured with untreated ScN2a cells. Tretinoin 59-72 sodium voltage-gated channel alpha subunit 2 Homo sapiens 81-86
15328022-5 2004 Furthermore, we show that RA activity is essential in the lung field to maintain lung cell identity in the endoderm; RAR antagonism disrupts expression of thyroid transcription factor 1 (Ttf1), an early marker of the respiratory region in the endoderm, and surfactant protein C (Sp-C) mRNAs. Tretinoin 26-28 transcription termination factor 1 Rattus norvegicus 187-191
15302581-8 2004 A bovine ZNF470 cDNA clone was used to examine expression of ZNF470 in bovine articular chondrocytes treated with retinoic acid to stimulate dedifferentiation. Tretinoin 114-127 zinc finger protein 470 Bos taurus 9-15
15302581-8 2004 A bovine ZNF470 cDNA clone was used to examine expression of ZNF470 in bovine articular chondrocytes treated with retinoic acid to stimulate dedifferentiation. Tretinoin 114-127 zinc finger protein 470 Bos taurus 61-67
15302581-9 2004 Bovine ZNF470 expression was undetectable in freshly isolated bovine articular chondrocytes, but was dramatically upregulated in dedifferentiated retinoic acid-treated chondrocytes. Tretinoin 146-159 zinc finger protein 470 Bos taurus 7-13
15313187-6 2004 Thus, the RANKL/OPG ratio was markedly increased, suggesting a potential mechanism of ATRA-induced bone resorption. Tretinoin 86-90 TNF superfamily member 11 Homo sapiens 10-15
15342476-4 2004 Recent work has demonstrated that the expression of val itself depends on three factors: retinoic acid (RA) signals from the paraxial mesoderm; fibroblast growth factor (Fgf) signals from r4; and variant hepatocyte nuclear factor 1 (vhnf1, also known as tcf2), a homeodomain transcription factor expressed posterior to the r4-5 boundary. Tretinoin 89-102 v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog Ba Danio rerio 52-55
15342476-4 2004 Recent work has demonstrated that the expression of val itself depends on three factors: retinoic acid (RA) signals from the paraxial mesoderm; fibroblast growth factor (Fgf) signals from r4; and variant hepatocyte nuclear factor 1 (vhnf1, also known as tcf2), a homeodomain transcription factor expressed posterior to the r4-5 boundary. Tretinoin 104-106 v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog Ba Danio rerio 52-55
15342476-6 2004 We show that RA induces val expression via activation of vhnf1 expression in the hindbrain. Tretinoin 13-15 v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog Ba Danio rerio 24-27
15640094-4 2004 The ligands of the retinoic acid acceptor RXR cannot induce teratogenesis, but they can enhance the teratogenesis of the RAR stimulus. Tretinoin 19-32 retinoid X receptor alpha Homo sapiens 42-45
15218018-2 2004 We have previously reported that the activation of c-Jun amino-terminal kinase (JNK) is required for the retinoic acid-induced neural differentiation of P19 cells. Tretinoin 105-118 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-56
15166231-0 2004 The synergistic effect of dexamethasone and all-trans-retinoic acid on hepatic phosphoenolpyruvate carboxykinase gene expression involves the coactivator p300. Tretinoin 44-67 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 79-112
15166231-1 2004 Activation of phosphoenolpyruvate carboxykinase (PEPCK) gene transcription in response to all-trans-retinoic acid (RA) or a glucocorticoid such as dexamethasone (Dex) requires a distinct arrangement of DNA-response elements and their cognate transcription activators on the gene promoter. Tretinoin 93-113 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 14-47
15166231-1 2004 Activation of phosphoenolpyruvate carboxykinase (PEPCK) gene transcription in response to all-trans-retinoic acid (RA) or a glucocorticoid such as dexamethasone (Dex) requires a distinct arrangement of DNA-response elements and their cognate transcription activators on the gene promoter. Tretinoin 93-113 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 49-54
15207915-3 2004 In the present study, we examined the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid (RA)-differentiated human SH-SY5Y neuroblastoma cells. Tretinoin 106-119 brain derived neurotrophic factor Homo sapiens 62-95
15207915-3 2004 In the present study, we examined the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid (RA)-differentiated human SH-SY5Y neuroblastoma cells. Tretinoin 106-119 brain derived neurotrophic factor Homo sapiens 97-101
15207915-3 2004 In the present study, we examined the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid (RA)-differentiated human SH-SY5Y neuroblastoma cells. Tretinoin 121-123 brain derived neurotrophic factor Homo sapiens 62-95
15207915-3 2004 In the present study, we examined the regulation of FOXO3a by brain-derived neurotrophic factor (BDNF) in retinoic acid (RA)-differentiated human SH-SY5Y neuroblastoma cells. Tretinoin 121-123 brain derived neurotrophic factor Homo sapiens 97-101
15215172-11 2004 In the presence of RA, active forms of both MMP-1 and MMP-9 were reduced. Tretinoin 19-21 matrix metallopeptidase 9 Homo sapiens 54-59
15016629-7 2004 Pretreatment with all-trans-retinoic acid enhanced the contractions and the release of histamine induced by LTB(4), without affecting either the contractions induced by histamine or the histamine release evoked by calcium ionophore A23187. Tretinoin 18-41 prostaglandin reductase 1 Cavia porcellus 108-114
15188435-5 2004 We suggest that a gradient of RA within the mesoderm generated by Raldh2 and catabolized by Cyp26C1 could be responsible for patterning the hindbrain. Tretinoin 30-32 aldehyde dehydrogenase 1 family member A2 Gallus gallus 66-72
15157739-1 2004 In the present study, we analyzed the influence of retinoic acids on the expression of alpha-1 acid glycoprotein (AGP). Tretinoin 51-65 orosomucoid 1 Rattus norvegicus 114-117
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 196-204
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 239-247
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 196-204
15126328-5 2004 Retinoic acid (RA)-induced neuroblastoma cell proliferation/differentiation transition is associated with decreased CAK activity, as evidenced by a switch from CAK hyperphosphorylation of pRb and RXRalpha to hypophosphorylation of pRb and RXRalpha. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 239-247
15126328-6 2004 Manipulation of MAT1 abundance shows that MAT1 reduction mimics RA-induced hypophosphorylation of pRb/RXRalpha, proliferation inhibition, and neurite outgrowth, whereas MAT1 overexpression resists these RA actions. Tretinoin 64-66 retinoid X receptor alpha Homo sapiens 102-110
15189689-10 2004 IL-12, IFN-gamma, IL-4 and IL-10 were detected at mRNA levels by RT-PCR to understand the roles of DC treated with RA in regulation of Th1/Th2 balance. Tretinoin 115-117 negative elongation factor complex member C/D Homo sapiens 135-138
15020229-3 2004 Retinoic acid (RA)-induced differentiation increased PLD1 and PLD2 mRNA levels and PLD activity that was responsive to phorbol myristate acetate. Tretinoin 0-13 phospholipase D2 Homo sapiens 62-66
15020229-3 2004 Retinoic acid (RA)-induced differentiation increased PLD1 and PLD2 mRNA levels and PLD activity that was responsive to phorbol myristate acetate. Tretinoin 15-17 phospholipase D2 Homo sapiens 62-66
15109540-0 2004 Combination of all-trans retinoic acid and lithium chloride surmounts a retinoid differentiation block induced by expression of Scl and Rbtn2 transcription factors in myeloid leukemia cells. Tretinoin 25-38 LIM domain only 2 Homo sapiens 136-141
15109540-3 2004 Addition of LiCl to ATRA treatment restored the capacity of both Scl- and Rbtn2-expressing cells to respond to the retinoid in a synergistic manner. Tretinoin 20-24 LIM domain only 2 Homo sapiens 74-79
15109540-5 2004 These findings suggest that if Scl and/or Rbtn2 are involved in the non-responsiveness of AML patients to ATRA-induced differentiation, addition of LiCl may reverse insensitivity. Tretinoin 106-110 LIM domain only 2 Homo sapiens 42-47
14993281-2 2004 RA is known to induce expression of the Burkitt"s lymphoma receptor 1 (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA. Tretinoin 0-2 C-X-C motif chemokine receptor 5 Homo sapiens 40-69
14993281-2 2004 RA is known to induce expression of the Burkitt"s lymphoma receptor 1 (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA. Tretinoin 0-2 C-X-C motif chemokine receptor 5 Homo sapiens 71-75
14993281-2 2004 RA is known to induce expression of the Burkitt"s lymphoma receptor 1 (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA. Tretinoin 0-2 C-X-C motif chemokine receptor 5 Homo sapiens 254-258
14993281-14 2004 In sum the results of the present study indicate that RA-induced expression of blr1 expression depends on a novel RA response element. Tretinoin 54-56 C-X-C motif chemokine receptor 5 Homo sapiens 79-83
14993281-14 2004 In sum the results of the present study indicate that RA-induced expression of blr1 expression depends on a novel RA response element. Tretinoin 114-116 C-X-C motif chemokine receptor 5 Homo sapiens 79-83
14743441-7 2004 In addition, RA-treated CD133+ cells expressed cell type-specific markers for oligodendrocytes including myelin basic protein (MBP) as shown by RT-PCR, proteolipid protein (PLP) by Western blot analysis, and cyclic nucleotide phosphodiesterase (CNPase) by immunostaining. Tretinoin 13-15 proteolipid protein 1 Homo sapiens 173-176
14743441-7 2004 In addition, RA-treated CD133+ cells expressed cell type-specific markers for oligodendrocytes including myelin basic protein (MBP) as shown by RT-PCR, proteolipid protein (PLP) by Western blot analysis, and cyclic nucleotide phosphodiesterase (CNPase) by immunostaining. Tretinoin 13-15 phosphodiesterase 3B Homo sapiens 208-243
14743441-7 2004 In addition, RA-treated CD133+ cells expressed cell type-specific markers for oligodendrocytes including myelin basic protein (MBP) as shown by RT-PCR, proteolipid protein (PLP) by Western blot analysis, and cyclic nucleotide phosphodiesterase (CNPase) by immunostaining. Tretinoin 13-15 phosphodiesterase 3B Homo sapiens 245-251
14960230-3 2004 METHODS: After treated with all-trans-retinoic acid(RA) and telomerase antisense oligodeoxynucleotide (ASODN) respectively, the expression of CXCR4 mRNA and CXCR4 protein in NPC CNE1 and CNE2Z cells were determined by in situ hybridization and immunohistochemistry, respectively; the distribution of cell cycle was examined with flow cytometry and the proliferation of cells was identified by MTT method. Tretinoin 28-51 C-X-C motif chemokine receptor 4 Homo sapiens 142-147
14960230-3 2004 METHODS: After treated with all-trans-retinoic acid(RA) and telomerase antisense oligodeoxynucleotide (ASODN) respectively, the expression of CXCR4 mRNA and CXCR4 protein in NPC CNE1 and CNE2Z cells were determined by in situ hybridization and immunohistochemistry, respectively; the distribution of cell cycle was examined with flow cytometry and the proliferation of cells was identified by MTT method. Tretinoin 28-51 C-X-C motif chemokine receptor 4 Homo sapiens 157-162
12832282-5 2004 Serum-free, exogenous ATRA-free medium conditioned by LICs rich in retinol storage granules caused a 10-fold greater increase of CRBP-I mRNA in PMVCs than media conditioned by LICs with few retinol storage granules. Tretinoin 22-26 retinol binding protein 1 Rattus norvegicus 129-135
14960275-4 2004 RA activates Thylacine1 expression in rostral PSM directly. Tretinoin 0-2 mesoderm posterior homolog A L homeolog Xenopus laevis 13-23
14960275-5 2004 RA also activates Thylacine1 expression in the caudal PSM indirectly by inducing the expression of MKP3, an inhibitor of the FGF signaling pathway. Tretinoin 0-2 mesoderm posterior homolog A L homeolog Xenopus laevis 18-28
14715249-7 2004 In investigating possible mechanisms for IGFBP-3 regulation of atRA-sensitivity, we found that IGFBP-3 blocked the formation of RAR:RXR heterodimers and disrupted the ligand-inducible receptor complex. Tretinoin 63-67 retinoid X receptor alpha Homo sapiens 132-135
14741354-4 2004 TRF2 was up-regulated in P19 embryonal carcinoma cells at the early stage of induced neural differentiation with retinoic acid treatment. Tretinoin 113-126 telomeric repeat binding factor 2 Homo sapiens 0-4
14592536-4 2004 In the present study, we found that formation of TR3/RXRalpha heterodimers in the nucleus and their subsequent translocation into the cytoplasm, in association with regulation of apoptosis-related proteins Bcl-2, Bcl-xl and Bax, was critical for apoptosis induction by ATRA in breast cancer cells MCF-7. Tretinoin 269-273 retinoid X receptor alpha Homo sapiens 53-61
14592536-6 2004 However, in ATRA-induced gastric cancer cells MGC80-3, RXRalpha heterodimerised with RARalpha but not with TR3, and remained in the nucleus exerting its effect on cell cycle regulation. Tretinoin 12-16 retinoid X receptor alpha Homo sapiens 55-63
14592536-8 2004 Furthermore, we demonstrated that the effects of ATRA depend on the relative levels of TR3, RARalpha and RXRalpha expression in cancer cells. Tretinoin 49-53 retinoid X receptor alpha Homo sapiens 105-113
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoid X receptor alpha Homo sapiens 79-87
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoid X receptor alpha Homo sapiens 109-117
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoid X receptor alpha Homo sapiens 109-117
14592536-9 2004 In ATRA-induced MCF-7 cells, highly expressed TR3 favours the formation of TR3/RXRalpha and promotes the TR3/RXRalpha signalling pathway causing apoptosis; while in ATRA-induced MGC80-3 cells, high expression of RARalpha favours the formation of RARalpha/RXRalpha and promotes the RXRalpha/RARalpha signalling pathway in mediating cell cycle regulation. Tretinoin 3-7 retinoid X receptor alpha Homo sapiens 109-117
15111235-3 2004 RA/TPA treated cells exhibited the highest levels of tyrosine hydroxylase and DAT but lower levels of vesicular monoamine transporter. Tretinoin 0-2 solute carrier family 6 member 3 Homo sapiens 78-81
15111235-5 2004 RA/TPA differentiated cells evidenced high sensitivity to the neurotoxic effects of MPP+ (0.03 to 3.0 mM), and the neurotoxic effects of MPP+ were blocked with the DAT inhibitor 1-(2-[bis(4-fluorophenyl)methoxy]ethyl)-4-(3-phenylpropyl)piperazine (GBR 12909). Tretinoin 0-2 solute carrier family 6 member 3 Homo sapiens 164-167
14659877-10 2003 GATA-4 and -6 were detected in nuclear extracts prepared from retinoic acid treated HepG2 cells using Western blot assays. Tretinoin 62-75 GATA binding protein 4 Homo sapiens 0-13
14609562-0 2003 Interactions of testosterone and all-trans retinoic acid in regulation of androgen receptor expression in rat lacrimal gland. Tretinoin 43-56 androgen receptor Rattus norvegicus 74-91
14609562-1 2003 All-trans retinoic acid down-regulates androgen receptor (AR) expression in lacrimal gland acinar cells in culture. Tretinoin 10-23 androgen receptor Rattus norvegicus 39-56
14609562-1 2003 All-trans retinoic acid down-regulates androgen receptor (AR) expression in lacrimal gland acinar cells in culture. Tretinoin 10-23 androgen receptor Rattus norvegicus 58-60
14609562-2 2003 The goal of this study was to determine if retinoic acid inhibits androgen-stimulated up-regulation of AR protein and AR mRNA expression in lacrimal glands of orchiectomized rats in vivo. Tretinoin 43-56 androgen receptor Rattus norvegicus 103-105
14609562-2 2003 The goal of this study was to determine if retinoic acid inhibits androgen-stimulated up-regulation of AR protein and AR mRNA expression in lacrimal glands of orchiectomized rats in vivo. Tretinoin 43-56 androgen receptor Rattus norvegicus 118-120
14609562-12 2003 Delivery of retinoic acid at 20 or 50 mg kg(-1) day(-1) simultaneously with a 2.5 mg kg(-1) testosterone injection prevented restoration of lacrimal gland AR expression and significantly reduced AR mRNA expression. Tretinoin 12-25 androgen receptor Rattus norvegicus 155-157
14609562-12 2003 Delivery of retinoic acid at 20 or 50 mg kg(-1) day(-1) simultaneously with a 2.5 mg kg(-1) testosterone injection prevented restoration of lacrimal gland AR expression and significantly reduced AR mRNA expression. Tretinoin 12-25 androgen receptor Rattus norvegicus 195-197
14609562-13 2003 A pharmacologic dose of retinoic acid inhibits AR expression in lacrimal gland acinar cells in vivo, as well as in vitro. Tretinoin 24-37 androgen receptor Rattus norvegicus 47-49
14585314-2 2003 In its active form, retinoic acid, it controls the regular differentiation as a ligand for retinoic acid receptors (RAR, RXR) and is involved in the integration (gap junction formation) of cell formations [Nature 37 (1994) 528; International Review of Cytology. Tretinoin 20-33 retinoid X receptor alpha Homo sapiens 121-124
14597230-5 2003 We observed that retinoic acid (RA)-induced neuronal differentiation of human SH-SY5Y cells resulted in increased expression of APP, APLP1 and APLP2. Tretinoin 17-30 amyloid beta precursor like protein 1 Homo sapiens 133-138
14597230-5 2003 We observed that retinoic acid (RA)-induced neuronal differentiation of human SH-SY5Y cells resulted in increased expression of APP, APLP1 and APLP2. Tretinoin 32-34 amyloid beta precursor like protein 1 Homo sapiens 133-138
13129847-8 2003 At this phase, cardiac AP patterning by RA is consistent with localized action of RA by regulated activation of the Raldh2 gene within an embryonic domain. Tretinoin 82-84 aldehyde dehydrogenase 1 family member A2 Homo sapiens 116-122
14560020-2 2003 Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. Tretinoin 41-64 retinoic acid receptor, alpha Mus musculus 24-27
14560020-2 2003 Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. Tretinoin 41-64 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 106-140
14560020-2 2003 Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. Tretinoin 41-64 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 142-147
14560020-2 2003 Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. Tretinoin 66-70 retinoic acid receptor, alpha Mus musculus 24-27
14560020-2 2003 Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. Tretinoin 66-70 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 106-140
14560020-2 2003 Retinoic acid receptor (RAR) activators (all-trans-retinoic acid [ATRA] and TTNPB) were found to increase ATP-binding cassette transporter 1 (ABCA1) mRNA and protein in macrophages. Tretinoin 66-70 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 142-147
14597990-9 2003 These data indicate that TF expression in APL cells is exacerbated by the presence of the PML/RARalpha fusion protein, and implicates the loss of Fos/Jun binding to the TF promoter in ATRA-induced suppression of TF. Tretinoin 184-188 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-149
12915404-10 2003 Our data suggest that ATRA mediates growth inhibition by stabilizing Rb2/p130 via a mechanism that involves induction of PP2A, an enzyme that can potentially dephosphorylate Rb2/p130, thereby protecting it from degradation by the proteasome. Tretinoin 22-26 RB transcriptional corepressor like 2 Homo sapiens 69-72
12915404-10 2003 Our data suggest that ATRA mediates growth inhibition by stabilizing Rb2/p130 via a mechanism that involves induction of PP2A, an enzyme that can potentially dephosphorylate Rb2/p130, thereby protecting it from degradation by the proteasome. Tretinoin 22-26 RB transcriptional corepressor like 2 Homo sapiens 73-77
12915404-10 2003 Our data suggest that ATRA mediates growth inhibition by stabilizing Rb2/p130 via a mechanism that involves induction of PP2A, an enzyme that can potentially dephosphorylate Rb2/p130, thereby protecting it from degradation by the proteasome. Tretinoin 22-26 RB transcriptional corepressor like 2 Homo sapiens 174-177
12915404-10 2003 Our data suggest that ATRA mediates growth inhibition by stabilizing Rb2/p130 via a mechanism that involves induction of PP2A, an enzyme that can potentially dephosphorylate Rb2/p130, thereby protecting it from degradation by the proteasome. Tretinoin 22-26 RB transcriptional corepressor like 2 Homo sapiens 178-182
14581379-10 2003 All-trans-retinoic acid, a prototypic AP-1 antagonist, blocked bryostatin-mediated induction of COX-2. Tretinoin 0-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-42
12964005-12 2003 For example, either PC-SPES (0.5 micro l/ml) or ATRA (10(-8) mol/l) induced 23 and 18% of HL-60 cells, respectively to express CD11b on day 2 of culture; and when both were combined, 60% of HL-60 cells were stimulated to express CD11b antigen. Tretinoin 48-52 integrin subunit alpha M Homo sapiens 127-132
12964005-12 2003 For example, either PC-SPES (0.5 micro l/ml) or ATRA (10(-8) mol/l) induced 23 and 18% of HL-60 cells, respectively to express CD11b on day 2 of culture; and when both were combined, 60% of HL-60 cells were stimulated to express CD11b antigen. Tretinoin 48-52 integrin subunit alpha M Homo sapiens 229-234
12958591-0 2003 All-trans retinoic acid is a ligand for the orphan nuclear receptor ROR beta. Tretinoin 0-23 RAR related orphan receptor B Homo sapiens 68-76
12958591-3 2003 Using nondenaturing mass spectrometry and scintillation proximity assays we found that all-trans retinoic acid (ATRA) and several retinoids bind to the ROR beta ligand-binding domain (LBD). Tretinoin 97-110 RAR related orphan receptor B Homo sapiens 152-160
12958591-3 2003 Using nondenaturing mass spectrometry and scintillation proximity assays we found that all-trans retinoic acid (ATRA) and several retinoids bind to the ROR beta ligand-binding domain (LBD). Tretinoin 112-116 RAR related orphan receptor B Homo sapiens 152-160
12958591-5 2003 ATRA and related retinoids inhibit ROR beta but not ROR alpha transcriptional activity suggesting that high-affinity, subtype-specific ligands could be designed for the identification of ROR beta target genes. Tretinoin 0-4 RAR related orphan receptor B Homo sapiens 35-43
12958591-5 2003 ATRA and related retinoids inhibit ROR beta but not ROR alpha transcriptional activity suggesting that high-affinity, subtype-specific ligands could be designed for the identification of ROR beta target genes. Tretinoin 0-4 RAR related orphan receptor B Homo sapiens 187-195
14500356-10 2003 Furthermore, affected transgenic epidermis had reduced levels of retinoic acid receptoralpha (RARalpha) and retinoic X receptor (RXRalpha), and supplementation with exogenous retinoic acid prevented the skin phenotype. Tretinoin 65-78 retinoic acid receptor, alpha Mus musculus 94-102
12941622-2 2003 RA is produced by the mesenchyme at all sites, and subsets of mesenchymal cells express the RA synthetic enzyme RALDH2, independent of M/E interactions. Tretinoin 92-94 aldehyde dehydrogenase 1 family member A2 Homo sapiens 112-118
12941622-4 2003 At all sites, expression of additional RA signaling molecules (RARalpha, RARbeta, RXR, CRABP1) depends on M/E interactions. Tretinoin 39-41 retinoid X receptor alpha Homo sapiens 82-85
12956703-2 2003 We suggest that the transcriptional activator retinoic acid (RA), takes part in gene regulation after peripheral nerve injury and that RA signalling is activated via the cellular retinoic acid binding protein (CRABP)-II and cellular retinol binding protein (CRBP)-I. Tretinoin 46-59 cellular retinoic acid binding protein 2 Homo sapiens 210-219
12956703-2 2003 We suggest that the transcriptional activator retinoic acid (RA), takes part in gene regulation after peripheral nerve injury and that RA signalling is activated via the cellular retinoic acid binding protein (CRABP)-II and cellular retinol binding protein (CRBP)-I. Tretinoin 61-63 cellular retinoic acid binding protein 2 Homo sapiens 210-219
12956703-2 2003 We suggest that the transcriptional activator retinoic acid (RA), takes part in gene regulation after peripheral nerve injury and that RA signalling is activated via the cellular retinoic acid binding protein (CRABP)-II and cellular retinol binding protein (CRBP)-I. Tretinoin 135-137 cellular retinoic acid binding protein 2 Homo sapiens 210-219
12842345-3 2003 In this work, we compared the chemical stability of tretinoin (TRA) in methanol and in vesicular suspensions exposed both to UV and artificial daylight conditions with the aim of evaluating the potential of niosomes as topical carriers capable of improving the stability of photosensitive drugs. Tretinoin 52-61 T cell receptor alpha locus Homo sapiens 63-66
12842345-10 2003 Tretinoin incorporated in P90 or Span vesicles presented a half-life shorter or very close to that of the free drug. Tretinoin 0-9 cellular inhibitor of PP2A Homo sapiens 26-29
12801520-12 2003 The combination of PD98059 and SB203580 almost completely suppressed the enhancement by retinoic acid of VEGF synthesis induced by TGF-beta. Tretinoin 88-101 vascular endothelial growth factor A Mus musculus 105-109
12801520-13 2003 Taken together, our results strongly suggest that both p44/p42 MAP kinase and p38 MAP kinase take part in TGF-beta-stimulated VEGF synthesis in osteoblasts, and that retinoic acid upregulates the VEGF synthesis. Tretinoin 166-179 vascular endothelial growth factor A Mus musculus 126-130
12801520-13 2003 Taken together, our results strongly suggest that both p44/p42 MAP kinase and p38 MAP kinase take part in TGF-beta-stimulated VEGF synthesis in osteoblasts, and that retinoic acid upregulates the VEGF synthesis. Tretinoin 166-179 vascular endothelial growth factor A Mus musculus 196-200
12839938-4 2003 Gel shift analysis indicated that PPAR gamma, in the presence of RXR, formed a strong complex with a retinoic acid response element (beta retinoic acid response element) in the RAR beta promoter. Tretinoin 101-114 retinoid X receptor alpha Homo sapiens 65-68
12839938-4 2003 Gel shift analysis indicated that PPAR gamma, in the presence of RXR, formed a strong complex with a retinoic acid response element (beta retinoic acid response element) in the RAR beta promoter. Tretinoin 133-151 retinoid X receptor alpha Homo sapiens 65-68
12767051-0 2003 Induction of leukotriene C4 synthase after the differentiation of rat basophilic leukemia cells with retinoic acid and a low dose of actinomycin D and its suppression with methylprednisolone. Tretinoin 101-114 leukotriene C4 synthase Rattus norvegicus 13-36
12782018-7 2003 RA treatment also resulted in decreased nuclear p21 and decreased expression of cytosolic as well as nuclear p27 at 72 h in the fetuses. Tretinoin 0-2 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 48-51
12841584-6 2003 In this study it is shown for the first time that the retinoic acid-induced neuronal differentiation of NTERA2 cells is accompanied by down-regulation of SOX2 and up-regulation of SOX3 gene during early phases of induction. Tretinoin 54-67 SRY-box transcription factor 2 Homo sapiens 154-158
12841584-7 2003 These data suggest that the effects of retinoic acid on neural differentiation of NTERA2 EC cells might be mediated by modulation of SOX2 and SOX3 gene expression. Tretinoin 39-52 SRY-box transcription factor 2 Homo sapiens 133-137
12776186-3 2003 We investigated the effects of RA on the regulation of the IGF-IR and its key signaling elements: IRS-1, IRS-2, and SHC. Tretinoin 31-33 insulin like growth factor 1 receptor Homo sapiens 59-65
14509846-0 2003 Expression of Sec61 alpha in F9 and P19 teratocarcinoma cells after retinoic acid treatment. Tretinoin 68-81 Sec61 alpha 1 subunit (S. cerevisiae) Mus musculus 14-25
14509846-10 2003 It was also demonstrated that Sec61 alpha expression is stimulated in F9 cells after retinoic acid treatment for 72 hours. Tretinoin 85-98 Sec61 alpha 1 subunit (S. cerevisiae) Mus musculus 30-41
14509846-12 2003 These data indicate that the expression of Sec61 alpha is enhanced with retinoic acid induced differentiation of F9 teratocarcinoma cells. Tretinoin 72-85 Sec61 alpha 1 subunit (S. cerevisiae) Mus musculus 43-54
12873158-4 2003 Flow cytometric analysis of CD11b antigen expression, as a marker of differentiation, indicated that all-trans-retinoic acid (ATRA) gave improved differentiation (>80% of cells differentiated at 96 h) when compared with dimethylformamide (DMF) (<60% of cells differentiated at 96 h). Tretinoin 101-124 integrin subunit alpha M Homo sapiens 28-33
12873158-4 2003 Flow cytometric analysis of CD11b antigen expression, as a marker of differentiation, indicated that all-trans-retinoic acid (ATRA) gave improved differentiation (>80% of cells differentiated at 96 h) when compared with dimethylformamide (DMF) (<60% of cells differentiated at 96 h). Tretinoin 126-130 integrin subunit alpha M Homo sapiens 28-33
12755330-10 2003 The effects of the growth factors activin A, retinoic acid (RA) and basic fibroblast growth factor (bFGF) on the regulation of Xlmx1b were also studied. Tretinoin 45-58 LIM homeobox transcription factor 1, beta, gene 1 S homeolog Xenopus laevis 127-133
12588859-0 2003 Developing with lethal RA levels: genetic ablation of Rarg can restore the viability of mice lacking Cyp26a1. Tretinoin 23-25 retinoic acid receptor, gamma Mus musculus 54-58
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 25-27 retinoic acid receptor, gamma Mus musculus 35-39
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 25-27 fibroblast growth factor 8 Mus musculus 212-216
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 172-174 retinoic acid receptor, gamma Mus musculus 25-33
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 172-174 retinoic acid receptor, gamma Mus musculus 35-39
12588859-4 2003 Ablation of the gene for RARgamma (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm. Tretinoin 172-174 fibroblast growth factor 8 Mus musculus 212-216
12594186-6 2003 Furthermore, we found that administration of 10(-7) M retinoic acid (RA) to embryoid bodies increased the percentage of MLC2v(-)ANP(+) cells; this also increased the expression of atrial-specific genes in the Nkx2.5/GFP(+) fraction, in a time- and dose-dependent fashion. Tretinoin 54-67 myosin, light polypeptide 2, regulatory, cardiac, slow Mus musculus 120-125
12632092-2 2003 We have investigated the effects of all-trans retinoic acid (atRA) on the mRNA and protein levels of ABCA1 in THP-1 cells. Tretinoin 46-59 ATP binding cassette subfamily A member 1 Homo sapiens 101-106
12632092-2 2003 We have investigated the effects of all-trans retinoic acid (atRA) on the mRNA and protein levels of ABCA1 in THP-1 cells. Tretinoin 61-65 ATP binding cassette subfamily A member 1 Homo sapiens 101-106
12632092-3 2003 Our results show that both mRNA and protein levels of ABCA1 were significantly increased upon treatment with atRA. Tretinoin 109-113 ATP binding cassette subfamily A member 1 Homo sapiens 54-59
12632092-4 2003 Since ABCA1 is highly regulated by liver X receptor (LXR) we also analysed the mRNA and protein expressions of LXR-alpha and LXR-beta in the THP-1 cells after treatment with atRA. Tretinoin 174-178 ATP binding cassette subfamily A member 1 Homo sapiens 6-11
12632092-6 2003 In conclusion, our results show that LXR-alpha and ABCA1 are simultaneously induced by atRA. Tretinoin 87-91 ATP binding cassette subfamily A member 1 Homo sapiens 51-56
12646620-3 2003 Previous studies in our laboratory have demonstrated that retinoic acids, physiological ligands for the nuclear retinoid receptors, selectively inhibit TCR-mediated death under in vitro conditions, and the inhibition is mediated via the retinoic acid receptor (RAR) alpha. Tretinoin 58-72 retinoic acid receptor, alpha Mus musculus 261-264
12676320-1 2003 The germ cell nuclear factor (GCNF, NR6A1) is a nuclear orphan receptor that functions as a transcriptional repressor and is transiently expressed in mammalian carcinoma cells during retinoic acid (RA) induced neuronal differentiation. Tretinoin 183-196 nuclear receptor subfamily 6 group A member 1 Homo sapiens 4-28
12676320-1 2003 The germ cell nuclear factor (GCNF, NR6A1) is a nuclear orphan receptor that functions as a transcriptional repressor and is transiently expressed in mammalian carcinoma cells during retinoic acid (RA) induced neuronal differentiation. Tretinoin 183-196 nuclear receptor subfamily 6 group A member 1 Homo sapiens 30-34
12676320-1 2003 The germ cell nuclear factor (GCNF, NR6A1) is a nuclear orphan receptor that functions as a transcriptional repressor and is transiently expressed in mammalian carcinoma cells during retinoic acid (RA) induced neuronal differentiation. Tretinoin 183-196 nuclear receptor subfamily 6 group A member 1 Homo sapiens 36-41
12676320-1 2003 The germ cell nuclear factor (GCNF, NR6A1) is a nuclear orphan receptor that functions as a transcriptional repressor and is transiently expressed in mammalian carcinoma cells during retinoic acid (RA) induced neuronal differentiation. Tretinoin 198-200 nuclear receptor subfamily 6 group A member 1 Homo sapiens 4-28
12676320-1 2003 The germ cell nuclear factor (GCNF, NR6A1) is a nuclear orphan receptor that functions as a transcriptional repressor and is transiently expressed in mammalian carcinoma cells during retinoic acid (RA) induced neuronal differentiation. Tretinoin 198-200 nuclear receptor subfamily 6 group A member 1 Homo sapiens 30-34
12676320-1 2003 The germ cell nuclear factor (GCNF, NR6A1) is a nuclear orphan receptor that functions as a transcriptional repressor and is transiently expressed in mammalian carcinoma cells during retinoic acid (RA) induced neuronal differentiation. Tretinoin 198-200 nuclear receptor subfamily 6 group A member 1 Homo sapiens 36-41
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 73-86 sphingosine-1-phosphate receptor 3 Homo sapiens 143-149
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 73-86 sphingosine-1-phosphate receptor 3 Homo sapiens 151-156
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 88-90 sphingosine-1-phosphate receptor 3 Homo sapiens 143-149
12577307-3 2003 The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. Tretinoin 88-90 sphingosine-1-phosphate receptor 3 Homo sapiens 151-156
12577307-4 2003 S1P-evoked increases in [Ca(2+)](i) in S1P(3) R-predominant BCCs were suppressed by concentrations of VD3 and RA which decreased expression of S1P(3) Rs, despite RA-induced increases in S1P(2) Rs. Tretinoin 110-112 sphingosine-1-phosphate receptor 3 Homo sapiens 39-45
12577307-4 2003 S1P-evoked increases in [Ca(2+)](i) in S1P(3) R-predominant BCCs were suppressed by concentrations of VD3 and RA which decreased expression of S1P(3) Rs, despite RA-induced increases in S1P(2) Rs. Tretinoin 110-112 sphingosine-1-phosphate receptor 3 Homo sapiens 143-149
12591602-0 2003 The role of a retinoic acid response element in establishing the anterior neural expression border of Hoxd4 transgenes. Tretinoin 14-27 homeobox D4 Mus musculus 102-107
12591602-2 2003 The sequence of regulatory elements, including a DR5 type retinoic acid response element (RARE) required for Hoxd4 neural enhancer activity, are highly conserved. Tretinoin 58-71 homeobox D4 Mus musculus 109-114
12606762-6 2003 In contrast to carcinoma cells, NAG-1 expression is effectively induced by retinoic acid and the RAR-selective pan-agonist in normal HTBE cells and accompanies the inhibition of squamous differentiation and the initiation of normal differentiation. Tretinoin 75-88 growth differentiation factor 15 Homo sapiens 32-37
12482873-2 2003 We have previously demonstrated that the small 15-kDa cellular RA-binding protein II (CRABPII) is a coactivator present in the RA-dependent nuclear complex. Tretinoin 63-65 cellular retinoic acid binding protein 2 Homo sapiens 86-93
12562531-3 2003 Previous studies suggest that retinoic acid (RA) decreases Na+-dependent glutamate uptake and increases GTRAP3-18 protein expression. Tretinoin 30-43 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 104-113
12562531-3 2003 Previous studies suggest that retinoic acid (RA) decreases Na+-dependent glutamate uptake and increases GTRAP3-18 protein expression. Tretinoin 45-47 ADP ribosylation factor like GTPase 6 interacting protein 5 Homo sapiens 104-113
12573541-10 2003 RT-PCR analysis revealed that the mVGAT gene was expressed at a high level in retinoic acid-treated P19 embryonal carcinoma cells, at a very low level in non-treated P19 cells, and not detectably expressed in Neuro-2a neuroblastoma cells. Tretinoin 78-91 solute carrier family 32 (GABA vesicular transporter), member 1 Mus musculus 34-39
12409287-2 2003 Using cDNA microarray, we identified a clone, DD4, that contains the cDNA of a novel gene, spurt (secretory protein in upper respiratory tracts) that was significantly induced by all-trans-retinoic acid in primary cultured human tracheobroncheal epithelia. Tretinoin 179-202 aldo-keto reductase family 1 member C4 Homo sapiens 46-49
14571131-3 2003 Induction of CNTN4 mRNA expression in human neuroblastoma tumor cells treated with retinoic acid correlated with a block in retinoid-induced neuritogenesis. Tretinoin 83-96 contactin 4 Homo sapiens 13-18
12771467-7 2003 The combination of all-trans-retinoic acid (tretinoin, TRA) with hydroquinone or 4-hydroxyanisole is also known to produce synergetic skin depigmentation. Tretinoin 19-42 T cell receptor alpha locus Homo sapiens 55-58
12492469-2 2003 Synaptophysin and synapsin I, another synaptic vesicle protein, are also expressed by retinoic acid-induced neuronally differentiated P19 teratocarcinoma cells. Tretinoin 86-99 synaptophysin Homo sapiens 0-13
12492469-2 2003 Synaptophysin and synapsin I, another synaptic vesicle protein, are also expressed by retinoic acid-induced neuronally differentiated P19 teratocarcinoma cells. Tretinoin 86-99 synapsin I Homo sapiens 18-28
12518169-3 2003 The hepatocellular carcinoma cell line HuH-7 was treated with 10(-7) mol/L all-trans RA (ATRA) and 9-cis RA (9-CRA). Tretinoin 85-87 MIR7-3 host gene Homo sapiens 39-44
12518169-3 2003 The hepatocellular carcinoma cell line HuH-7 was treated with 10(-7) mol/L all-trans RA (ATRA) and 9-cis RA (9-CRA). Tretinoin 89-93 MIR7-3 host gene Homo sapiens 39-44
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 21-23 brain derived neurotrophic factor Homo sapiens 124-128
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 21-23 brain derived neurotrophic factor Homo sapiens 185-189
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 163-176 brain derived neurotrophic factor Homo sapiens 89-122
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 163-176 brain derived neurotrophic factor Homo sapiens 124-128
12927207-6 2003 Also in these cells, RA induces the expression of TrkB, the tyrosine kinase receptor for brain-derived neurotrophic factor (BDNF), and 4 days of pretreatment with retinoic acid confers BDNF responsiveness to the APP promoter. Tretinoin 163-176 brain derived neurotrophic factor Homo sapiens 185-189
12453908-11 2002 Levels of latent and active MMP-9 and MMP-13 were elevated 4- and 10-fold, respectively, in STZ-D skin and reduced by 50-75% (P < 0.05) by RA. Tretinoin 142-144 matrix metallopeptidase 9 Rattus norvegicus 28-33
12453908-11 2002 Levels of latent and active MMP-9 and MMP-13 were elevated 4- and 10-fold, respectively, in STZ-D skin and reduced by 50-75% (P < 0.05) by RA. Tretinoin 142-144 matrix metallopeptidase 13 Rattus norvegicus 38-44
12492429-10 2002 These data suggest that SK-N-SH cells differentiated by brief treatment with RA may represent an unlimited source of neuron-like cells suitable for studying molecular events associated with activation of human NR1/NR2B receptors. Tretinoin 77-79 hedgehog acyltransferase Homo sapiens 24-28
12468597-0 2002 Feedback regulation of beta,beta-carotene 15,15"-monooxygenase by retinoic acid in rats and chickens. Tretinoin 66-79 beta-carotene oxygenase 1 Rattus norvegicus 23-62
12468597-3 2002 We found dose-dependent decreases in intestinal beta,beta-carotene monooxygenase activity after oral administration to rats of retinyl acetate (up to -79%), beta-carotene (up to -79%), apo-8"-carotenal (up to -56%), all-trans retinoic acid (up to -88%), and 9-cis retinoic acid (up to -67%). Tretinoin 216-239 beta-carotene oxygenase 1 Rattus norvegicus 48-52
12468597-7 2002 In a transcriptional study in chickens, treatment with retinoic acid resulted in low expression of the intestinal betaCMOOX. Tretinoin 55-68 beta-carotene oxygenase 1 Rattus norvegicus 114-123
12553043-3 2002 ATRA significantly and dose-dependently inhibited matrigel membrane invasion of the cells by 53%, inhibited MMP-2 activity by 71%, MMP-9(80%), alpha-(59%) and beta-(65%) catenin expression at 10 microM (p < 0.01). Tretinoin 0-4 matrix metallopeptidase 9 Rattus norvegicus 131-136
12445492-0 2002 cDNA cloning and expression of rat leukotriene C(4) synthase: elevated expression in rat basophilic leukemia-1 cells after treatment with retinoic acid. Tretinoin 138-151 leukotriene C4 synthase Rattus norvegicus 35-60
12445492-6 2002 While RBL-1 cells after the culture for 48 h in the presence of 0.1 microg/ml all trans -retinoic acid (RA) exhibited 27 times higher LTC(4) S activity than control cells, Northern-blot analysis of RA-treated cells showed upregulation of LTC(4) S mRNA. Tretinoin 82-102 leukotriene C4 synthase Rattus norvegicus 134-142
12445492-6 2002 While RBL-1 cells after the culture for 48 h in the presence of 0.1 microg/ml all trans -retinoic acid (RA) exhibited 27 times higher LTC(4) S activity than control cells, Northern-blot analysis of RA-treated cells showed upregulation of LTC(4) S mRNA. Tretinoin 82-102 leukotriene C4 synthase Rattus norvegicus 238-246
12445492-6 2002 While RBL-1 cells after the culture for 48 h in the presence of 0.1 microg/ml all trans -retinoic acid (RA) exhibited 27 times higher LTC(4) S activity than control cells, Northern-blot analysis of RA-treated cells showed upregulation of LTC(4) S mRNA. Tretinoin 104-106 leukotriene C4 synthase Rattus norvegicus 134-142
12445492-6 2002 While RBL-1 cells after the culture for 48 h in the presence of 0.1 microg/ml all trans -retinoic acid (RA) exhibited 27 times higher LTC(4) S activity than control cells, Northern-blot analysis of RA-treated cells showed upregulation of LTC(4) S mRNA. Tretinoin 104-106 leukotriene C4 synthase Rattus norvegicus 238-246
12171913-0 2002 Induction of the mouse kappa-opioid receptor gene by retinoic acid in P19 cells. Tretinoin 53-66 opioid receptor, kappa 1 Mus musculus 23-44
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 110-123 opioid receptor, kappa 1 Mus musculus 10-31
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 110-123 opioid receptor, kappa 1 Mus musculus 33-36
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 125-127 opioid receptor, kappa 1 Mus musculus 10-31
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 125-127 opioid receptor, kappa 1 Mus musculus 33-36
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 145-147 opioid receptor, kappa 1 Mus musculus 10-31
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 145-147 opioid receptor, kappa 1 Mus musculus 33-36
12171913-1 2002 The mouse kappa-opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. Tretinoin 145-147 opioid receptor, kappa 1 Mus musculus 217-220
12171913-6 2002 Collectively, enhanced binding of Sp1 to promoter I of the KOR gene as a result of inhibiting the ERK pathway contributes to RA induction of this gene in P19. Tretinoin 125-127 opioid receptor, kappa 1 Mus musculus 59-62
12237846-0 2002 p16(ink4a) and retinoic acid modulate rhoA and GFAP expression during induction of a stellate phenotype in U343 MG-A astrocytoma cells. Tretinoin 15-28 glial fibrillary acidic protein Homo sapiens 47-51
12237846-4 2002 We showed that p16 expression and RA treatment led to an increase in the expression of GFAP, as well as its reorganization but that it did not significantly affect actin or vimentin expression. Tretinoin 34-36 glial fibrillary acidic protein Homo sapiens 87-91
12163600-0 2002 Viral interferon regulatory factor 1 of Kaposi"s sarcoma-associated herpesvirus interacts with a cell death regulator, GRIM19, and inhibits interferon/retinoic acid-induced cell death. Tretinoin 151-164 NADH:ubiquinone oxidoreductase subunit A13 Homo sapiens 119-125
12063257-0 2002 Activation of the beta-catenin/Lef-Tcf pathway is obligate for formation of primitive endoderm by mouse F9 totipotent teratocarcinoma cells in response to retinoic acid. Tretinoin 155-168 catenin (cadherin associated protein), beta 1 Mus musculus 18-30
12063257-2 2002 We investigated whether the beta-catenin/Lef-Tcf-sensitive transcriptional pathway activated by Frizzled-1 plays a role in the retinoic acid-induced pathway to primitive endoderm formation. Tretinoin 127-140 catenin (cadherin associated protein), beta 1 Mus musculus 28-40
12063257-7 2002 These data reveal the obligate role of the beta-catenin/Lef-Tcf transcriptional pathway in the action of the morphogen retinoic acid. Tretinoin 119-132 catenin (cadherin associated protein), beta 1 Mus musculus 43-55
12186855-3 2002 Consistent with a role in neural promotion, REN overexpression induced neuronal differentiation as well as growth arrest and p27Kip1 expression in CNS and PNS neural progenitor cell lines, and its inhibition impaired retinoic acid induction of neurogenin-1 and NeuroD expression. Tretinoin 217-230 neurogenin 1 Mus musculus 244-256
12165850-5 2002 Differentiation induced by retinoic acid results in the gain of ERK-dependent control of cyclin D1 expression and of S phase progression. Tretinoin 27-40 cyclin D1 Mus musculus 89-98
12139725-0 2002 Simultaneous induction of matrix metalloproteinase-9 and interleukin 8 by all-trans retinoic acid in human PL-21 and NB4 myeloid leukaemia cells. Tretinoin 84-97 matrix metallopeptidase 9 Homo sapiens 26-52
12139725-3 2002 We investigated effects of ATRA on MMP expression in two human myeloid leukaemia cell lines, PL-21 and NB4. Tretinoin 27-31 matrix metallopeptidase 9 Homo sapiens 35-38
12139725-6 2002 Stimulation with ATRA significantly increased MMP-9 levels approximately three- to fivefold in both PL-21 and NB4-conditioned media. Tretinoin 17-21 matrix metallopeptidase 9 Homo sapiens 46-51
12139725-7 2002 MMP-9 mRNA levels increased in ATRA-treated cells and was almost in parallel with the increase in MMP-9 activity, suggesting that ATRA induced MMP-9 by activating its gene expression. Tretinoin 31-35 matrix metallopeptidase 9 Homo sapiens 0-5
12139725-7 2002 MMP-9 mRNA levels increased in ATRA-treated cells and was almost in parallel with the increase in MMP-9 activity, suggesting that ATRA induced MMP-9 by activating its gene expression. Tretinoin 31-35 matrix metallopeptidase 9 Homo sapiens 98-103
12139725-7 2002 MMP-9 mRNA levels increased in ATRA-treated cells and was almost in parallel with the increase in MMP-9 activity, suggesting that ATRA induced MMP-9 by activating its gene expression. Tretinoin 31-35 matrix metallopeptidase 9 Homo sapiens 98-103
12139725-7 2002 MMP-9 mRNA levels increased in ATRA-treated cells and was almost in parallel with the increase in MMP-9 activity, suggesting that ATRA induced MMP-9 by activating its gene expression. Tretinoin 130-134 matrix metallopeptidase 9 Homo sapiens 0-5
12139725-7 2002 MMP-9 mRNA levels increased in ATRA-treated cells and was almost in parallel with the increase in MMP-9 activity, suggesting that ATRA induced MMP-9 by activating its gene expression. Tretinoin 130-134 matrix metallopeptidase 9 Homo sapiens 98-103
12139725-7 2002 MMP-9 mRNA levels increased in ATRA-treated cells and was almost in parallel with the increase in MMP-9 activity, suggesting that ATRA induced MMP-9 by activating its gene expression. Tretinoin 130-134 matrix metallopeptidase 9 Homo sapiens 98-103
12139725-9 2002 IL-8, chemokine for neutrophils and a potent inducer of MMP-9, was also induced by ATRA in PL-21 cells. Tretinoin 83-87 matrix metallopeptidase 9 Homo sapiens 56-61
12139725-12 2002 These observations suggest that ATRA can induce both MMP-9 and IL-8, but IL-8 is not involved in ATRA-induced MMP-9 expression. Tretinoin 32-36 matrix metallopeptidase 9 Homo sapiens 53-58
12139725-13 2002 As MMP-9 can truncate and activate IL-8, simultaneous induction of MMP-9 and IL-8 by ATRA could activate leucocytes excessively, causing the hyper-inflammatory events in retinoic acid syndrome. Tretinoin 85-89 matrix metallopeptidase 9 Homo sapiens 67-72
12441652-0 2002 Foxa (HNF3) up-regulates vitronectin expression during retinoic acid-induced differentiation in mouse neuroblastoma Neuro2a cells. Tretinoin 55-68 vitronectin Mus musculus 25-36
12441652-1 2002 Accumulation of vitronectin protein increased in the conditioned medium of mouse neuroblastoma Neuro2a cells during retinoic acid-induced differentiation. Tretinoin 116-129 vitronectin Mus musculus 16-27
12441652-2 2002 To study the regulatory mechanism of the increase in vitronectin expression during the differentiation, the activity of the -527/+95 vitronectin promoter was observed in Neuro2a cells with or without retinoic acid treatment. Tretinoin 200-213 vitronectin Mus musculus 133-144
12441652-10 2002 These results demonstrate that Foxa up-regulates the vitronectin expression during the retinoic acid-induced differentiation in Neuro2a cells. Tretinoin 87-100 vitronectin Mus musculus 53-64
11997393-1 2002 Molecular genetic studies have indicated that alcohol dehydrogenase may be involved in the synthesis of retinoic acid, a hormonal molecule regulating diverse cellular functions at the transcriptional level. Tretinoin 104-117 aldo-keto reductase family 1 member A1 Homo sapiens 46-67
12052888-1 2002 Up-regulation of the c-jun gene is a critical event in the retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 59-72 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26
12052888-1 2002 Up-regulation of the c-jun gene is a critical event in the retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 74-76 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26
12074569-4 2002 Western blot analysis showed that treatment with ATRA increased C/EBPalpha and beta expression, but decreased that of C/EBPdelta. Tretinoin 49-53 CCAAT enhancer binding protein delta Homo sapiens 118-128
12056806-6 2002 Real-time quantitative PCR analysis confirmed an increase in ARHGAP10 expression during differentiation of HL-60 cells with all-trans-retinoic acid and hematopoietic stem cells with erythropoietin, suggesting that this gene could play a role in normal hematopoiesis. Tretinoin 134-147 Rho GTPase activating protein 10 Homo sapiens 61-69
12225397-9 2002 We speculate that the remarkable induction of gp91phox and p47phox protein is associated with an increase in superoxide-generating activity due to the synergistic effect of ATRA plus GM-CSF. Tretinoin 173-177 cytochrome b-245 beta chain Homo sapiens 46-54
11983289-3 2002 We report a significant transcriptional upregulation of all three synapsins (synapsin I, 2.1-fold; synapsin II, 2.6-fold; and synapsin III, 5.5-fold) by retinoic acid-induced differentiation of NTera-2cl.D1 cells, a human paradigm for neuronal differentiation. Tretinoin 153-166 synapsin I Homo sapiens 77-87
12223961-1 2002 The active metabolite of vitamin A (retinoic acid, RA) acts through the nuclear receptors RARalpha, beta and gamma and RXRalpha, beta and gamma. Tretinoin 36-49 retinoic acid receptor, alpha Mus musculus 90-98
11969262-6 2002 Endogenous RA is a relevant regulator of the secondary palate PCD since this was reduced by a retinol dehydrogenase inhibitor and an RAR specific antagonist. Tretinoin 11-13 Rab40B, member RAS oncogene family Mus musculus 133-136
12031648-5 2002 RESULTS: Expression of the MmTRA1b gene was markedly induced during granulocytic differentiation of promyelocytic leukemia NB4 and HT93 cells induced by all-trans retinoic acid (ATRA). Tretinoin 157-176 phospholipid scramblase 1 Homo sapiens 27-34
12061140-12 2002 HGF production in cultured cells is induced by PKC-activating agents, cAMP-elevating agents, PKA-activating agents, growth factors, and inflammatory cytokines; and it is inhibited by TGF-beta, glucocorticoids, 1,25-dihydroxyvitamin D3, and retinoic acid. Tretinoin 240-253 hepatocyte growth factor Rattus norvegicus 0-3
11964368-0 2002 all-trans-Retinoic acid increases nitric oxide synthesis by endothelial cells: a role for the induction of dimethylarginine dimethylaminohydrolase. Tretinoin 0-23 dimethylarginine dimethylaminohydrolase 2 Mus musculus 107-146
11964368-10 2002 The DDAH inhibitor 4124W significantly reduced the induction of NO synthesis by atRA. Tretinoin 80-84 dimethylarginine dimethylaminohydrolase 2 Mus musculus 4-8
11964368-13 2002 Our data suggests that the induction of NO synthesis by atRA may be facilitated by DDAH II. Tretinoin 56-60 dimethylarginine dimethylaminohydrolase 2 Mus musculus 83-87
11896294-4 2002 In the present study the influence of phytol and phytanic acid (a RXR-selective ligand) on the teratogenicity of retinol and the RAR-selective ligand all-trans-retinoic acid was investigated by coadministration experiments on day 8.25 of gestation in NMRI mice. Tretinoin 154-173 Rab40B, member RAS oncogene family Mus musculus 129-132
12004806-9 2002 This combination of Mlt and 9cRA could be a potentially useful clinical treatment regimen for breast cancer since it allows the use of lower doses of retinoic acid, thus, avoiding the toxic side effects associated with the use of high dose retinoids. Tretinoin 150-163 myotubularin related protein 11 Homo sapiens 29-32
11945128-0 2002 Discovery and design of retinoic acid receptor and retinoid X receptor class- and subtype-selective synthetic analogs of all-trans-retinoic acid and 9-cis-retinoic acid. Tretinoin 121-144 retinoid X receptor alpha Homo sapiens 51-70
11739380-0 2002 Receptor for advanced glycation end products plays a more important role in cellular survival than in neurite outgrowth during retinoic acid-induced differentiation of neuroblastoma cells. Tretinoin 127-140 advanced glycosylation end-product specific receptor Homo sapiens 0-44
11739380-4 2002 In this study we have investigated a possible role of RAGE and amphoterin in the retinoic acid-induced differentiation of neuroblastoma cells. Tretinoin 81-94 advanced glycosylation end-product specific receptor Homo sapiens 54-58
11739380-7 2002 Interestingly, the survival of the neuroblastoma cells treated with retinoic acid was partly dependent on the expression of RAGE, and inhibition of RAGE function partially blocked the increase in anti-apoptotic protein Bcl-2 following retinoic acid treatment. Tretinoin 68-81 advanced glycosylation end-product specific receptor Homo sapiens 124-128
11739380-7 2002 Interestingly, the survival of the neuroblastoma cells treated with retinoic acid was partly dependent on the expression of RAGE, and inhibition of RAGE function partially blocked the increase in anti-apoptotic protein Bcl-2 following retinoic acid treatment. Tretinoin 235-248 advanced glycosylation end-product specific receptor Homo sapiens 148-152
11792692-6 2002 Thus, the increased heterodimerization of RXR with RAR by retinoic acid treatment seemed to reduce the RXR available for CAR heterodimerization, resulting in the repression of CAR activity. Tretinoin 58-71 retinoid X receptor alpha Homo sapiens 42-45
11792692-6 2002 Thus, the increased heterodimerization of RXR with RAR by retinoic acid treatment seemed to reduce the RXR available for CAR heterodimerization, resulting in the repression of CAR activity. Tretinoin 58-71 retinoid X receptor alpha Homo sapiens 103-106
11807825-13 2002 In conclusion, RA and PGE(2) upregulate BMP-7 protein expression both in vitro and in vivo. Tretinoin 15-17 bone morphogenetic protein 7 Homo sapiens 40-45
11804787-4 2002 We further show that retinoic acid induced interdigital apoptosis is also correlated with a downregulation of BAG-1 expression. Tretinoin 21-34 BCL2-associated athanogene 1 Mus musculus 110-115
11777343-5 2002 All-trans-retinoic acid (ATRA) treatment of HPV-immortalized HEN-16-2 cells and transformed/MDR HEN-16-2/CDDP cells inhibited telomerase activity and downregulated expression of hTERT mRNAs containing full-length functional and a defective RT motif, but there were no changes in hTR and TP1 expression. Tretinoin 0-23 telomerase associated protein 1 Homo sapiens 287-290
11777343-5 2002 All-trans-retinoic acid (ATRA) treatment of HPV-immortalized HEN-16-2 cells and transformed/MDR HEN-16-2/CDDP cells inhibited telomerase activity and downregulated expression of hTERT mRNAs containing full-length functional and a defective RT motif, but there were no changes in hTR and TP1 expression. Tretinoin 25-29 telomerase associated protein 1 Homo sapiens 287-290
11821953-1 2002 Since retinoic acid receptor (RAR)-beta mRNA is frequently lost during esophageal carcinogenesis and esophageal cancer cells that do not express RAR-beta are resistant to retinoic acid (RA), we stably transfected RAR-beta expression vector into an esophageal cancer cell line TE-8 and an antisense RAR-beta into TE-3 cells. Tretinoin 6-19 retinoic acid receptor, alpha Mus musculus 30-33
11841795-11 2002 Similarly, incubation with ATRA resulted in a greater induction of CRABP II in these cells. Tretinoin 27-31 cellular retinoic acid binding protein 2 Homo sapiens 67-75
12053118-6 2002 RA dramatically inhibits this process via suppression of c-fos/c-jun expression and inhibition of the c-Jun N-terminal kinase activation. Tretinoin 0-2 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62
12053118-6 2002 RA dramatically inhibits this process via suppression of c-fos/c-jun expression and inhibition of the c-Jun N-terminal kinase activation. Tretinoin 0-2 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-68
12053118-6 2002 RA dramatically inhibits this process via suppression of c-fos/c-jun expression and inhibition of the c-Jun N-terminal kinase activation. Tretinoin 0-2 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-107
11825567-1 2002 Induced by retinoic acid and implicated in playing a role in development, rodent RAE-1 proteins are ligands for the activating immunoreceptor NKG2D, widely expressed on natural killer cells, T cells, and macrophages. Tretinoin 11-24 ribonucleic acid export 1 Homo sapiens 81-86
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 39-58
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 60-63
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 39-58
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 60-63
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 65-78 retinoid X receptor alpha Homo sapiens 39-58
11812818-1 2001 Retinoic acid (RA) binds and activates retinoid X receptor (RXR)/retinoic acid receptor (RAR) heterodimers, which regulate the transcription of genes that have retinoic acid response elements (RARE). Tretinoin 65-78 retinoid X receptor alpha Homo sapiens 60-63
11751425-10 2001 Chromatin condensation and PARP cleavage are observed in both RARalpha- and RARgamma-transduced cells indicating an RA-induced apoptosis that may be caspase dependent. Tretinoin 62-64 poly (ADP-ribose) polymerase family, member 1 Mus musculus 27-31
11733135-8 2001 Most notably, AhR, HNF-3 and N-Oct3 have already been shown to respond to RA treatment of EC cells, while E47, HNF-3, MAZ, N-Oct3 and Pit-1a have been implicated in embryonic, muscle or neural development. Tretinoin 74-76 forkhead box M1 Homo sapiens 19-24
11555654-4 2001 LiCl alone, or in combination with all-trans-retinoic acid, increased cellular levels of ubiquitinated retinoic acid receptor alpha and markedly reduced chymotryptic-like activity of WEHI-3B D(+) 20 S and 26 S proteasome enzymes. Tretinoin 35-58 retinoic acid receptor, alpha Mus musculus 103-131
11555654-7 2001 This effect has significant consequences in stabilizing the retinoic acid receptor alpha protein levels that are necessary to promote continued differentiation of leukemia cells in response to all-trans-retinoic acid. Tretinoin 196-216 retinoic acid receptor, alpha Mus musculus 60-88
11690641-8 2001 This study indicates that food compounds such as phytanic acid and DHA that are RXR-agonists and have an impact on intestinal CYP26 gene expression and metabolism of all-trans-RA in intestinal cells. Tretinoin 176-178 retinoid X receptor alpha Homo sapiens 80-83
11676881-6 2001 In addition, retinoic acid increased the protein level of p16 (218.75%, P <0.05) and induced p21 protein expression; meanwhile, p27 was undetectable by immunocytochemistry in both control and retinoic acid-treated hepatic stellate cells. Tretinoin 13-26 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 58-61
11676881-6 2001 In addition, retinoic acid increased the protein level of p16 (218.75%, P <0.05) and induced p21 protein expression; meanwhile, p27 was undetectable by immunocytochemistry in both control and retinoic acid-treated hepatic stellate cells. Tretinoin 13-26 KRAS proto-oncogene, GTPase Rattus norvegicus 96-99
11676881-8 2001 CONCLUSIONS: Up-regulation of p16 and p21 on post-transcriptional level may contribute, in part, to retinoic acid inhibition of transforming growth factor beta 1-initiated rat hepatic stellate cells activation in vitro. Tretinoin 100-113 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 30-33
11676881-8 2001 CONCLUSIONS: Up-regulation of p16 and p21 on post-transcriptional level may contribute, in part, to retinoic acid inhibition of transforming growth factor beta 1-initiated rat hepatic stellate cells activation in vitro. Tretinoin 100-113 KRAS proto-oncogene, GTPase Rattus norvegicus 38-41
11526443-1 2001 Retinoic acid (RA) induces differentiation of S91 melanoma cells through activation of RA receptor (RAR)gamma without affecting cell viability. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 100-103
11526443-1 2001 Retinoic acid (RA) induces differentiation of S91 melanoma cells through activation of RA receptor (RAR)gamma without affecting cell viability. Tretinoin 15-17 retinoic acid receptor, alpha Mus musculus 100-103
11513861-2 2001 Concomitant with this RA-induced neural differentiation, we observed an activation of the c-Jun amino-terminal kinase (JNK). Tretinoin 22-24 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-95
15018820-1 2001 Cellular retinoic acid binding protein I (CRABP-I) plays a role in retinoic acid (RA) metabolism or transport. Tretinoin 9-22 cellular retinoic acid binding protein I Mus musculus 42-49
15018820-1 2001 Cellular retinoic acid binding protein I (CRABP-I) plays a role in retinoic acid (RA) metabolism or transport. Tretinoin 43-45 cellular retinoic acid binding protein I Mus musculus 0-40
11591116-5 2001 Second, we showed that lym-Spo11 is strongly induced (above eightfold) in the IgA CSR system of LPS-stimulated mu(+)B cells in the presence of all-trans retinoic acid and IL-4. Tretinoin 153-166 SPO11 initiator of meiotic double stranded breaks Mus musculus 27-32
11399774-9 2001 Additional experiments showed that all-trans-retinoic acid causes large induction of the transcription factor STAT1, while IFN-gamma causes activation of STAT1 such that it binds to the GAS/Sp1 site in the ACAT-1 P1 promoter. Tretinoin 35-58 signal transducer and activator of transcription 1 Homo sapiens 110-115
11331070-6 2001 Retinoid X receptor alpha (RXRalpha) was also decreased, albeit to a lesser extent, in RA-treated cells. Tretinoin 87-89 retinoid X receptor alpha Homo sapiens 0-25
11331070-6 2001 Retinoid X receptor alpha (RXRalpha) was also decreased, albeit to a lesser extent, in RA-treated cells. Tretinoin 87-89 retinoid X receptor alpha Homo sapiens 27-35
11331070-8 2001 An electrophoretic mobility shift assay, using nuclear extracts from RA-treated cells, showed that a reduction in complex formation with hormone response elements correlated with the reduction of RAR and RXR protein. Tretinoin 69-71 retinoid X receptor alpha Homo sapiens 204-207
11434680-8 2001 In cells induced to differentiate by ATRA, CD11b expression seems more closely related to inositol uptake than to PKC activity while the expression of TF and TM show the opposite pattern, which suggests cellular events regulated at a different level within a common signal transduction pathway. Tretinoin 37-41 integrin subunit alpha M Homo sapiens 43-48
11401397-0 2001 Retinoic acid inhibits cardiac neural crest migration by blocking c-Jun N-terminal kinase activation. Tretinoin 0-13 mitogen-activated protein kinase 8 Mus musculus 66-89
11401397-3 2001 The present study examines the relationship between RA and mitogen-activated protein kinase signaling in neural crest cells and demonstrates that c-Jun N-terminal kinase (JNK) activation is severely repressed by RA. Tretinoin 52-54 mitogen-activated protein kinase 8 Mus musculus 146-169
11401397-3 2001 The present study examines the relationship between RA and mitogen-activated protein kinase signaling in neural crest cells and demonstrates that c-Jun N-terminal kinase (JNK) activation is severely repressed by RA. Tretinoin 52-54 mitogen-activated protein kinase 8 Mus musculus 171-174
11401397-3 2001 The present study examines the relationship between RA and mitogen-activated protein kinase signaling in neural crest cells and demonstrates that c-Jun N-terminal kinase (JNK) activation is severely repressed by RA. Tretinoin 212-214 mitogen-activated protein kinase 8 Mus musculus 146-169
11401397-3 2001 The present study examines the relationship between RA and mitogen-activated protein kinase signaling in neural crest cells and demonstrates that c-Jun N-terminal kinase (JNK) activation is severely repressed by RA. Tretinoin 212-214 mitogen-activated protein kinase 8 Mus musculus 171-174
11401397-9 2001 These data demonstrate that the JNK signaling pathway and c-Jun activation are critical for cardiac neural crest outgrowth and are potential targets for the action of RA. Tretinoin 167-169 mitogen-activated protein kinase 8 Mus musculus 32-35
11599126-9 2001 Heat treatment after the initiation of differentiation by cAMP or RA accelerated the expression of GFAP or PLP mRNAs. Tretinoin 66-68 glial fibrillary acidic protein Rattus norvegicus 99-103
11306173-6 2001 A marked reduction of VEGF-C mRNA expression was also found when HB2 cells were treated with agonists of peroxisome proliferator-activated receptor gamma (PPARgamma, troglitazone), retinoic acid receptor (RAR, all-trans retinoic acid) and retinoid X receptor (RXR, 9-cis retinoic acid). Tretinoin 181-194 retinoic acid receptor, alpha Mus musculus 205-208
11274759-3 2001 Cell differentiation and apoptosis following ATRA treatment were investigated using flow cytometry and caspase-3 assay. Tretinoin 45-49 caspase 3 Mus musculus 103-112
11060298-0 2001 Activation of Rac1 and the p38 mitogen-activated protein kinase pathway in response to all-trans-retinoic acid. Tretinoin 87-110 Rac family small GTPase 1 Homo sapiens 14-18
11060298-6 2001 To obtain information on the functional role of the Rac1/p38/MAPKAPK-2 pathway in RA signaling, the effects of pharmacological inhibition of p38 on RA-induced gene transcription and cell differentiation were determined. Tretinoin 82-84 Rac family small GTPase 1 Homo sapiens 52-56
11780200-3 2001 RESULTS: Significant upregulation of IGF-I, IGF-IR and IGF-IIR mRNA was found at 6-24 hours in CBL incubated with physiologic concentrations of RA as compared to those without RA. Tretinoin 144-146 insulin like growth factor 1 receptor Homo sapiens 44-50
11332745-0 2001 Nongenomic vitamin D3 analogs activating ERK2 in HL-60 cells show that retinoic acid-induced differentiation and cell cycle arrest require early concurrent MAPK and RAR and RXR activation. Tretinoin 71-84 retinoid X receptor alpha Homo sapiens 173-176
11036068-7 2001 Upon treatment of the cells with RA, time-dependent increases in the ratio of RARbeta to RXRalpha and the phosphorylated form of Sp1 were observed. Tretinoin 33-35 retinoid X receptor alpha Homo sapiens 89-97
11163789-8 2001 These results strongly support that RA induces only a transient expression of the mFuc-TIV gene in cell aggregates but a more persistent expression of the mFuc-TIX gene at the transcription level throughout neural cell differentiation. Tretinoin 36-38 fucosyltransferase 9 Mus musculus 155-163
11285139-0 2001 Coordinate regulation of RARgamma2, TBP, and TAFII135 by targeted proteolysis during retinoic acid-induced differentiation of F9 embryonal carcinoma cells. Tretinoin 85-98 retinoic acid receptor, gamma Mus musculus 25-34
11245337-9 2001 In T-47D breast cancer cells, which express RARalpha, RXRalpha and ER, 17beta-HSD reductive activity increased 1.76-fold (p < 0.001), five days following treatment with 10 nM retinoic acid. Tretinoin 178-191 retinoid X receptor alpha Homo sapiens 54-62
11196162-1 2001 Histone deacetylase (HDAC)-dependent transcriptional repression of the retinoic acid (RA)-signaling pathway underlies the differentiation block of acute promyelocytic leukemia. Tretinoin 71-84 histone deacetylase 9 Homo sapiens 0-19
11196162-1 2001 Histone deacetylase (HDAC)-dependent transcriptional repression of the retinoic acid (RA)-signaling pathway underlies the differentiation block of acute promyelocytic leukemia. Tretinoin 71-84 histone deacetylase 9 Homo sapiens 21-25
11196162-1 2001 Histone deacetylase (HDAC)-dependent transcriptional repression of the retinoic acid (RA)-signaling pathway underlies the differentiation block of acute promyelocytic leukemia. Tretinoin 86-88 histone deacetylase 9 Homo sapiens 0-19
11196162-1 2001 Histone deacetylase (HDAC)-dependent transcriptional repression of the retinoic acid (RA)-signaling pathway underlies the differentiation block of acute promyelocytic leukemia. Tretinoin 86-88 histone deacetylase 9 Homo sapiens 21-25
11196162-5 2001 Accordingly, we show that AML1/ETO, the commonest AML-associated fusion protein, is an HDAC-dependent repressor of RA signaling. Tretinoin 115-117 histone deacetylase 9 Homo sapiens 87-91
11211936-0 2001 Retinoic acid-induced blr1 expression requires RARalpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation. Tretinoin 0-13 C-X-C motif chemokine receptor 5 Homo sapiens 22-26
11211936-0 2001 Retinoic acid-induced blr1 expression requires RARalpha, RXR, and MAPK activation and uses ERK2 but not JNK/SAPK to accelerate cell differentiation. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 57-60
11211936-1 2001 Upstream signaling requirements of retinoic acid (RA)-induced blr1 expression and downstream signaling consequences of blr1 over-expression in a human myeloid leukemia cell line demonstrate that mitogen-activated protein kinase (MAPK) signaling complexes are involved in both avenues. Tretinoin 35-48 C-X-C motif chemokine receptor 5 Homo sapiens 62-66
11211936-1 2001 Upstream signaling requirements of retinoic acid (RA)-induced blr1 expression and downstream signaling consequences of blr1 over-expression in a human myeloid leukemia cell line demonstrate that mitogen-activated protein kinase (MAPK) signaling complexes are involved in both avenues. Tretinoin 50-52 C-X-C motif chemokine receptor 5 Homo sapiens 62-66
11211936-2 2001 RA-induced myeloid differentiation and G1/G0 growth arrest of HL-60 cells is known to require the activation of the RARalpha and RXR retinoid receptors, as well as activation of the MAPK, ERK2. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 129-132
11920244-10 2001 Moreover, all-trans retinoic acid may be effective in modulating in vivo the TF transcription induced by endotoxin. Tretinoin 10-33 tissue factor Oryctolagus cuniculus 77-79
11149424-0 2001 Retinoic acid (RA) receptor transcriptional activation correlates with inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced ornithine decarboxylase (ODC) activity by retinoids: a potential role for trans-RA-induced ZBP-89 in ODC inhibition. Tretinoin 204-212 ornithine decarboxylase, structural 1 Mus musculus 155-158
11374031-3 2001 We found that MGP transcription is downregulated by retinoic acid and transforming growth factor beta (TGF beta) whereas it is upregulated by vitamin D3 and cyclic AMP. Tretinoin 52-65 matrix Gla protein Rattus norvegicus 14-17
11121017-7 2000 Additionally, the composition of mRNAs detected in HuB-mRNP complexes changed dramatically after induction of neuronal differentiation with retinoic acid. Tretinoin 140-153 ELAV like RNA binding protein 2 Homo sapiens 51-54
10995752-5 2000 Retinoic acid receptor alpha (RARalpha) transactivates the ALDH1 gene promoter through a complex with an RA response-like element (RARE) located at -91/-75 bp, which bound to the RARalpha/retinoid X receptor beta heterodimer. Tretinoin 30-32 retinoic acid receptor, alpha Mus musculus 0-28
10995752-5 2000 Retinoic acid receptor alpha (RARalpha) transactivates the ALDH1 gene promoter through a complex with an RA response-like element (RARE) located at -91/-75 bp, which bound to the RARalpha/retinoid X receptor beta heterodimer. Tretinoin 30-32 retinoic acid receptor, alpha Mus musculus 179-187
11058790-0 2000 Effect of retinoic acid and ethanol on retinoic acid receptor beta and glial fibrillary acidic protein mRNA expression in human astrocytoma cells. Tretinoin 10-23 glial fibrillary acidic protein Homo sapiens 71-102
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 31-44 glial fibrillary acidic protein Homo sapiens 80-111
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 31-44 glial fibrillary acidic protein Homo sapiens 113-117
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 46-48 glial fibrillary acidic protein Homo sapiens 80-111
11058790-2 2000 The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. Tretinoin 46-48 glial fibrillary acidic protein Homo sapiens 113-117
11058790-6 2000 RA prevented the ethanol-induced increase in GFAP mRNA. Tretinoin 0-2 glial fibrillary acidic protein Homo sapiens 45-49
11071654-4 2000 Consistent with the hypothesis, the HIV-1 protease inhibitors enhanced the ability of ATRA to inhibit growth and induce differentiation of HL-60 and NB4 myeloid leukemia cells, as measured by expression of CD11b and CD66b cell surface antigens, as well as reduction of nitroblue tetrazolium. Tretinoin 86-90 integrin subunit alpha M Homo sapiens 206-211
11776129-0 2000 Mechanism of inhibition on activator protein-1 activity by all-trans retinoic acid in gastric cancer cells. Tretinoin 69-82 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-46
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-49
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-55
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 69-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-49
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 69-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-55
11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 69-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150
11776129-5 2000 ATRA can also inhibit the expression of cJun and cFos. Tretinoin 0-4 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-44
11776129-5 2000 ATRA can also inhibit the expression of cJun and cFos. Tretinoin 0-4 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-53
11776129-6 2000 One of the mechanisms for ATRA to inhibit the growth of gastric cancer cells may be through its inhibitory effect on the AP-1 activity and its influence on up-regulation of RAR alpha expression. Tretinoin 26-30 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 121-125
11776129-8 2000 CONCLUSIONS: ATRA inhibits the growth of gastric cancer cells through the regulation of AP-1 activity. Tretinoin 13-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 88-92
11024001-0 2000 The human uncoupling protein-3 gene promoter requires MyoD and is induced by retinoic acid in muscle cells. Tretinoin 77-90 uncoupling protein 3 Homo sapiens 10-30
11024001-2 2000 UCP-3 mRNA is expressed in cultured muscle cells (C2C12 or L6E9) only when differentiated, at which stage UCP-3 is highly induced by all-trans retinoic acid (RA). Tretinoin 143-156 uncoupling protein 3 Homo sapiens 0-5
11024001-2 2000 UCP-3 mRNA is expressed in cultured muscle cells (C2C12 or L6E9) only when differentiated, at which stage UCP-3 is highly induced by all-trans retinoic acid (RA). Tretinoin 143-156 uncoupling protein 3 Homo sapiens 106-111
11024001-2 2000 UCP-3 mRNA is expressed in cultured muscle cells (C2C12 or L6E9) only when differentiated, at which stage UCP-3 is highly induced by all-trans retinoic acid (RA). Tretinoin 158-160 uncoupling protein 3 Homo sapiens 0-5
11024001-2 2000 UCP-3 mRNA is expressed in cultured muscle cells (C2C12 or L6E9) only when differentiated, at which stage UCP-3 is highly induced by all-trans retinoic acid (RA). Tretinoin 158-160 uncoupling protein 3 Homo sapiens 106-111
11024001-5 2000 We have characterized the RA response element that controls the induction by RA in the 5" noncoding region of the UCP-3 gene. Tretinoin 26-28 uncoupling protein 3 Homo sapiens 114-119
11024001-5 2000 We have characterized the RA response element that controls the induction by RA in the 5" noncoding region of the UCP-3 gene. Tretinoin 77-79 uncoupling protein 3 Homo sapiens 114-119
11024001-6 2000 Deletion and point-mutation analysis of the hUCP-3 promoter led us to identify a direct-repeat element with one base-pair spacing (DR1) at position -71/-59 responsible for the induction by RA of the activity of the promoter. Tretinoin 189-191 uncoupling protein 3 Homo sapiens 44-50
10913132-2 2000 Glucocorticoids, retinoic acid, and glucagon (via its second messenger, cAMP) stimulate PEPCK gene transcription, whereas insulin, phorbol esters, cytokines, and oxidative stress have an opposing effect. Tretinoin 17-30 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 88-93
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 127-140 retinoid X receptor alpha Homo sapiens 205-230
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 127-140 retinoid X receptor alpha Homo sapiens 232-240
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 142-144 retinoid X receptor alpha Homo sapiens 205-230
11027556-2 2000 This study demonstrates that HNF1alpha as well as HNF4alpha genes contain a direct repeat with a space of one nucleotide (DR1)-retinoic acid (RA) response element that can be bound and regulated by RA and retinoid x receptor alpha (RXRalpha) complex. Tretinoin 142-144 retinoid X receptor alpha Homo sapiens 232-240
11027556-8 2000 These data suggest that the differentiation effect of RA on hepatocyte may be due to direct interaction of RXRalpha with the RA-responsive elements on the HNF1alpha and HNF4alpha genes. Tretinoin 54-56 retinoid X receptor alpha Homo sapiens 107-115
11027556-8 2000 These data suggest that the differentiation effect of RA on hepatocyte may be due to direct interaction of RXRalpha with the RA-responsive elements on the HNF1alpha and HNF4alpha genes. Tretinoin 125-127 retinoid X receptor alpha Homo sapiens 107-115
11354514-0 2000 Correlation of HSP110 expression with all-trans retinoic acid-induced apoptosis. Tretinoin 48-61 heat shock 105kDa/110kDa protein 1 Mus musculus 15-21
11354514-2 2000 In the present study, we describe the strong expression of the same HSP110 in mesectodermal cells undergoing apoptosis after all-trans retinoic acid (RA) administration. Tretinoin 135-148 heat shock 105kDa/110kDa protein 1 Mus musculus 68-74
11354514-2 2000 In the present study, we describe the strong expression of the same HSP110 in mesectodermal cells undergoing apoptosis after all-trans retinoic acid (RA) administration. Tretinoin 150-152 heat shock 105kDa/110kDa protein 1 Mus musculus 68-74
11354514-8 2000 Twelve hours after RA administration, the increase in the number of HSP110-positive cells is greater than the increase in the number of TUNEL-positive cells. Tretinoin 19-21 heat shock 105kDa/110kDa protein 1 Mus musculus 68-74
11354514-10 2000 We suggest that HSP110 expression could represent a biochemical event of apoptotic cell death induced by RA, associated with early stages of the apoptotic process. Tretinoin 105-107 heat shock 105kDa/110kDa protein 1 Mus musculus 16-22
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 66-69
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 143-146
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 66-69
10979971-1 2000 Retinoic acid (RA) signaling is mediated by its nuclear receptors RXR and RAR, which bind to their cognate response elements as a heterodimer, RXR/RAR, and act in concert with coregulatory factors to regulate gene transcription on ligand binding. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 143-146
10970819-0 2000 Insulin-like growth factor binding protein-6 inhibits the growth of human bronchial epithelial cells and increases in abundance with all-trans-retinoic acid treatment. Tretinoin 143-156 insulin like growth factor binding protein 6 Homo sapiens 0-44
10970819-5 2000 IGFBP-6 was detected by immunohistochemical staining in the basal epithelial layer of human bronchial organ cultures, and all-trans-retinoic acid (t-RA) treatment increased the intensity of IGFBP-6 immunostaining. Tretinoin 122-145 insulin like growth factor binding protein 6 Homo sapiens 190-197
10970819-5 2000 IGFBP-6 was detected by immunohistochemical staining in the basal epithelial layer of human bronchial organ cultures, and all-trans-retinoic acid (t-RA) treatment increased the intensity of IGFBP-6 immunostaining. Tretinoin 147-151 insulin like growth factor binding protein 6 Homo sapiens 190-197
10999756-11 2000 Pharmacological dietary RA stimulated RARalpha, RARbeta, and RARgamma as early as day 1 by 2-, 4-, and 2.1-fold, respectively, without effect on lung RARs. Tretinoin 24-26 retinoic acid receptor, gamma Mus musculus 61-69
10976918-6 2000 We also show that the RARalpha AF-1 and AF-2 activation functions, but not their phosphorylation sites, are involved in the induction of RA-responsive genes in a differential promoter context-dependent manner. Tretinoin 22-24 interferon gamma receptor 2 Homo sapiens 31-44
10919981-2 2000 Before this time, the rat lung contains a relatively large supply of endogenous retinyl ester that, together with its metabolite retinoic acid, has been shown to increase elastin gene expression and the number of alveoli. Tretinoin 129-142 elastin Rattus norvegicus 171-178
10833461-3 2000 Among the UGT2B subfamily, UGT2B7, a UGT enzyme present in the liver and several steroid target tissues, is an important member since it conjugates a large variety of compounds including estrogens, androgens, morphine, AZT, and retinoic acid. Tretinoin 228-241 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 27-33
10835357-1 2000 The pleiotropic effects of active retinoids are transduced by their cognate nuclear receptors, retinoid X receptors (RXRs) and retinoic acid receptors (RARs), which act as transcriptional regulators activated by two stereoisomers of retinoic acid (RA): 9-cis RA (9-cRA) and all-trans RA (a-tRA). Tretinoin 127-140 myotubularin related protein 11 Homo sapiens 265-268
10835357-1 2000 The pleiotropic effects of active retinoids are transduced by their cognate nuclear receptors, retinoid X receptors (RXRs) and retinoic acid receptors (RARs), which act as transcriptional regulators activated by two stereoisomers of retinoic acid (RA): 9-cis RA (9-cRA) and all-trans RA (a-tRA). Tretinoin 127-140 T cell receptor alpha locus Homo sapiens 290-293
10835357-1 2000 The pleiotropic effects of active retinoids are transduced by their cognate nuclear receptors, retinoid X receptors (RXRs) and retinoic acid receptors (RARs), which act as transcriptional regulators activated by two stereoisomers of retinoic acid (RA): 9-cis RA (9-cRA) and all-trans RA (a-tRA). Tretinoin 152-154 myotubularin related protein 11 Homo sapiens 265-268
10835357-1 2000 The pleiotropic effects of active retinoids are transduced by their cognate nuclear receptors, retinoid X receptors (RXRs) and retinoic acid receptors (RARs), which act as transcriptional regulators activated by two stereoisomers of retinoic acid (RA): 9-cis RA (9-cRA) and all-trans RA (a-tRA). Tretinoin 152-154 T cell receptor alpha locus Homo sapiens 290-293
10828080-10 2000 Addition of retinol (10(-8)-10(-5) m) or all-trans-retinoic acid (10(-10)-10(-6) m) rapidly up-regulates CRBP expression. Tretinoin 41-64 retinol binding protein 1 Rattus norvegicus 105-109
10883402-1 2000 Individual and combined effects of several isomers of retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on interferon-gamma (IFN-gamma) secretion by blood mononuclear leukocytes (MNL) from nulliparous and postparturient Holstein cattle were evaluated in vitro. Tretinoin 54-67 interferon gamma Bos taurus 120-136
10883402-1 2000 Individual and combined effects of several isomers of retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on interferon-gamma (IFN-gamma) secretion by blood mononuclear leukocytes (MNL) from nulliparous and postparturient Holstein cattle were evaluated in vitro. Tretinoin 54-67 interferon gamma Bos taurus 138-147
10883402-1 2000 Individual and combined effects of several isomers of retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on interferon-gamma (IFN-gamma) secretion by blood mononuclear leukocytes (MNL) from nulliparous and postparturient Holstein cattle were evaluated in vitro. Tretinoin 69-71 interferon gamma Bos taurus 120-136
10883402-1 2000 Individual and combined effects of several isomers of retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on interferon-gamma (IFN-gamma) secretion by blood mononuclear leukocytes (MNL) from nulliparous and postparturient Holstein cattle were evaluated in vitro. Tretinoin 69-71 interferon gamma Bos taurus 138-147
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 32-45 cellular retinoic acid binding protein 2 Homo sapiens 0-7
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 32-45 retinoid X receptor alpha Homo sapiens 125-128
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 1-3 retinoid X receptor alpha Homo sapiens 125-128
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 47-49 cellular retinoic acid binding protein 2 Homo sapiens 0-7
10860396-2 2000 CRABPII, when combined with its retinoic acid (RA) ligand, interacts specifically with the liganded RA receptor complex (RAR.RXR), which is bound to the RA response elements of particular genes in order to greatly activate their expression. Tretinoin 47-49 retinoid X receptor alpha Homo sapiens 125-128
10777532-0 2000 Silencing mediator of retinoic acid and thyroid hormone receptors, as a novel transcriptional corepressor molecule of activating protein-1, nuclear factor-kappaB, and serum response factor. Tretinoin 22-35 serum response factor Homo sapiens 167-188
10786691-3 2000 The actions of retinoic acid in skin keratinocytes are mediated primarily by nuclear retinoic acid receptor gamma (RARgamma) and retinoid X receptor alpha (RXRalpha). Tretinoin 15-28 retinoid X receptor alpha Homo sapiens 129-154
10786691-3 2000 The actions of retinoic acid in skin keratinocytes are mediated primarily by nuclear retinoic acid receptor gamma (RARgamma) and retinoid X receptor alpha (RXRalpha). Tretinoin 15-28 retinoid X receptor alpha Homo sapiens 156-164
10771516-1 2000 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, beta, and gamma) and retinoid X receptors (RXR alpha, beta, and gamma). Tretinoin 26-39 retinoic acid receptor, alpha Mus musculus 86-94
10771516-1 2000 The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, beta, and gamma) and retinoid X receptors (RXR alpha, beta, and gamma). Tretinoin 41-43 retinoic acid receptor, alpha Mus musculus 86-94
10692469-2 2000 For the first time, we have shown that SF1 and Oct-3/4 are co-expressed in embryonal carcinoma (EC) P19 cells, and their expression is down-regulated with very similar kinetics following retinoic acid (RA) induced differentiation of these cells, suggesting a functional relationship between the two. Tretinoin 187-200 splicing factor 1 Homo sapiens 39-42
10692469-2 2000 For the first time, we have shown that SF1 and Oct-3/4 are co-expressed in embryonal carcinoma (EC) P19 cells, and their expression is down-regulated with very similar kinetics following retinoic acid (RA) induced differentiation of these cells, suggesting a functional relationship between the two. Tretinoin 202-204 splicing factor 1 Homo sapiens 39-42
10692469-3 2000 Previously, we have shown that the Oct-3/4 promoter harbors an RA-responsive element, RAREoct, which functions in EC cells as a binding site for positive regulators of transcription, such as RAR and RXR. Tretinoin 63-65 retinoid X receptor alpha Homo sapiens 199-202
10792271-0 2000 Histone deacetylase inhibitor but not arsenic trioxide differentiates acute promyelocytic leukaemia cells with t(11;17) in combination with all-trans retinoic acid. Tretinoin 150-163 histone deacetylase 9 Homo sapiens 0-19
10792271-8 2000 These results indicate that APL cells with t(11;17) need a higher concentration of ATRA than those with t(15;17) to differentiate and suggest that HDAC inhibitor is a promising differentiation enhancer in APL with t(11;17). Tretinoin 83-87 histone deacetylase 9 Homo sapiens 147-151
10677260-1 2000 Endogenous patterns of retinoic acid (RA) signaling in avian cardiac morphogenesis were characterized by localized expression of a key RA-synthetic enzyme, RALDH2, which displayed a biphasic pattern during heart development. Tretinoin 23-36 aldehyde dehydrogenase 1 family member A2 Homo sapiens 156-162
10677260-1 2000 Endogenous patterns of retinoic acid (RA) signaling in avian cardiac morphogenesis were characterized by localized expression of a key RA-synthetic enzyme, RALDH2, which displayed a biphasic pattern during heart development. Tretinoin 38-40 aldehyde dehydrogenase 1 family member A2 Homo sapiens 156-162
10677260-1 2000 Endogenous patterns of retinoic acid (RA) signaling in avian cardiac morphogenesis were characterized by localized expression of a key RA-synthetic enzyme, RALDH2, which displayed a biphasic pattern during heart development. Tretinoin 135-137 aldehyde dehydrogenase 1 family member A2 Homo sapiens 156-162
10698945-0 2000 Structure of the RXR-RAR DNA-binding complex on the retinoic acid response element DR1. Tretinoin 52-65 retinoid X receptor alpha Homo sapiens 17-20
10698945-2 2000 We describe the 1.70 A resolution structure of the ternary complex of RXR and RAR DNA-binding regions in complex with the retinoic acid response element DR1. Tretinoin 122-135 retinoid X receptor alpha Homo sapiens 70-73
10653609-8 2000 Retinoic acid treatment further increased the RIIbeta level and further inhibited the growth of RIIbeta-overexpressing cells, showing strong correlation between the level of RIIbeta and growth inhibition. Tretinoin 0-13 protein kinase cAMP-dependent type II regulatory subunit beta Homo sapiens 46-53
10653609-8 2000 Retinoic acid treatment further increased the RIIbeta level and further inhibited the growth of RIIbeta-overexpressing cells, showing strong correlation between the level of RIIbeta and growth inhibition. Tretinoin 0-13 protein kinase cAMP-dependent type II regulatory subunit beta Homo sapiens 96-103
10653609-8 2000 Retinoic acid treatment further increased the RIIbeta level and further inhibited the growth of RIIbeta-overexpressing cells, showing strong correlation between the level of RIIbeta and growth inhibition. Tretinoin 0-13 protein kinase cAMP-dependent type II regulatory subunit beta Homo sapiens 96-103
10653609-9 2000 However, RIIbeta-overexpressing cells did not show any sign of neuronal differentiation and responded to retinoic acid in the same way as parental cells. Tretinoin 105-118 protein kinase cAMP-dependent type II regulatory subunit beta Homo sapiens 9-16
10653609-10 2000 These data suggest that protein kinase A participates in the retinoic acid-induced growth inhibition through the up-regulation of RIIbeta/type II protein kinase A. Tretinoin 61-74 protein kinase cAMP-dependent type II regulatory subunit beta Homo sapiens 130-137
10694373-0 2000 Modulation of uncoupling protein 2 and uncoupling protein 3: regulation by denervation, leptin and retinoic acid treatment. Tretinoin 99-112 uncoupling protein 2 Rattus norvegicus 14-59
10694373-7 2000 RA (7.5 mg/kg) increased UCP1 mRNA but decreased UCP2 and UCP3 mRNA by 50%, whereas methylprednisolone (65 mg/kg, two doses 24 h apart) suppressed all three uncoupling proteins by greater than 60%. Tretinoin 0-2 uncoupling protein 2 Rattus norvegicus 49-53
10714763-2 2000 In F9 cells, the level of the cellular retinoic acid binding protein I (CRABP I) mRNA is greatly reduced after exposure of the cultured cells to exogenous RA. Tretinoin 73-75 cellular retinoic acid binding protein I Mus musculus 30-70
10640427-4 2000 Northern blot analysis demonstrates that blr1 mRNA expression increases within 9 h of retinoic acid treatment, well before functional differentiation or G(1)/G(0) growth arrest at 48 h or onset of morphological changes, suggesting a possible regulatory function. Tretinoin 86-99 C-X-C motif chemokine receptor 5 Homo sapiens 41-45
10640427-7 2000 Induction of blr1 mRNA by retinoic acid is not blocked by the protein synthesis inhibitor cycloheximide. Tretinoin 26-39 C-X-C motif chemokine receptor 5 Homo sapiens 13-17
10640427-8 2000 In HL-60 cells stably transfected with blr1 cDNA, ectopic expression of blr1 causes an increase in ERK2 MAPK activation and promotes retinoic acid-induced G(1)/G(0) growth arrest and cell differentiation. Tretinoin 133-146 C-X-C motif chemokine receptor 5 Homo sapiens 39-43
10640427-8 2000 In HL-60 cells stably transfected with blr1 cDNA, ectopic expression of blr1 causes an increase in ERK2 MAPK activation and promotes retinoic acid-induced G(1)/G(0) growth arrest and cell differentiation. Tretinoin 133-146 C-X-C motif chemokine receptor 5 Homo sapiens 72-76
10640427-9 2000 The early expression of blr1 mRNA during differentiation, its ability to increase ERK2 activation, and its enhancement of retinoic acid-induced differentiation suggest that blr1 expression may be involved in retinoic acid-induced HL-60 differentiation. Tretinoin 122-135 C-X-C motif chemokine receptor 5 Homo sapiens 24-28
10640427-9 2000 The early expression of blr1 mRNA during differentiation, its ability to increase ERK2 activation, and its enhancement of retinoic acid-induced differentiation suggest that blr1 expression may be involved in retinoic acid-induced HL-60 differentiation. Tretinoin 122-135 C-X-C motif chemokine receptor 5 Homo sapiens 173-177
10640427-9 2000 The early expression of blr1 mRNA during differentiation, its ability to increase ERK2 activation, and its enhancement of retinoic acid-induced differentiation suggest that blr1 expression may be involved in retinoic acid-induced HL-60 differentiation. Tretinoin 208-221 C-X-C motif chemokine receptor 5 Homo sapiens 24-28
10640427-9 2000 The early expression of blr1 mRNA during differentiation, its ability to increase ERK2 activation, and its enhancement of retinoic acid-induced differentiation suggest that blr1 expression may be involved in retinoic acid-induced HL-60 differentiation. Tretinoin 208-221 C-X-C motif chemokine receptor 5 Homo sapiens 173-177
10646501-7 2000 In contrast, MMP-9 was inducible by RA, TNFalpha, or PMA. Tretinoin 36-38 matrix metallopeptidase 9 Homo sapiens 13-18
10646501-8 2000 MMP-9 was progressively enhanced by RA as a function of time exposure until day 14. Tretinoin 36-38 matrix metallopeptidase 9 Homo sapiens 0-5
10646501-9 2000 The addition of TNFalpha or PMA potentiated RA-induced MMP-9 expression with a synergic maximal effect at day 14 of RA exposure. Tretinoin 44-46 matrix metallopeptidase 9 Homo sapiens 55-60
10646501-10 2000 Immunoreactive MMP-9 was located early in outgrowing neurites, but only at day 14 of RA exposure in extensive neuritic networks. Tretinoin 85-87 matrix metallopeptidase 9 Homo sapiens 15-20
10674634-2 2000 Differentiation and the inhibition of proliferation by 9-cis RA, but not all-trans RA, were inhibited by the RXR-homodimer antagonist LG745. Tretinoin 61-63 retinoid X receptor alpha Homo sapiens 109-112
10674634-4 2000 These data suggest that the effects of 9-cis RA are mediated via both RXR-homodimers and heterodimers. Tretinoin 45-47 retinoid X receptor alpha Homo sapiens 70-73
10627451-1 2000 The retinoic acid receptor (RAR) agonist, all-trans retinoic acid (ATRA), is a potent inducer of terminal differentiation of malignant promyelocytes, but its effects on more primitive hematopoietic progenitors and stem cells are less clear. Tretinoin 42-65 retinoic acid receptor, alpha Mus musculus 4-26
10627451-1 2000 The retinoic acid receptor (RAR) agonist, all-trans retinoic acid (ATRA), is a potent inducer of terminal differentiation of malignant promyelocytes, but its effects on more primitive hematopoietic progenitors and stem cells are less clear. Tretinoin 42-65 retinoic acid receptor, alpha Mus musculus 28-31
10627451-1 2000 The retinoic acid receptor (RAR) agonist, all-trans retinoic acid (ATRA), is a potent inducer of terminal differentiation of malignant promyelocytes, but its effects on more primitive hematopoietic progenitors and stem cells are less clear. Tretinoin 67-71 retinoic acid receptor, alpha Mus musculus 4-26
10627451-1 2000 The retinoic acid receptor (RAR) agonist, all-trans retinoic acid (ATRA), is a potent inducer of terminal differentiation of malignant promyelocytes, but its effects on more primitive hematopoietic progenitors and stem cells are less clear. Tretinoin 67-71 retinoic acid receptor, alpha Mus musculus 28-31
10627451-2 2000 We previously reported that pharmacologic levels (1 micromol) of ATRA enhanced the generation of colony-forming cell (CFC) and colony-forming unit-spleen (CFU-S) in liquid suspension cultures of lin- c-kit+ Sca-1+ murine hematopoietic precursors. Tretinoin 65-69 ataxin 1 Mus musculus 207-212
10627451-4 2000 ATRA enhanced the ex vivo maintenance and production of competitive repopulating STRCs and LTRCs from lin- c-kit+ Sca-1+ cells cultured in liquid suspension for 14 days. Tretinoin 0-4 ataxin 1 Mus musculus 114-119
10627451-7 2000 The data suggest that the RAR agonist ATRA enhances the maintenance and self-renewal of short- and long-term repopulating stem cells. Tretinoin 38-42 retinoic acid receptor, alpha Mus musculus 26-29
10721822-1 2000 Retinoic acid, vitamin D3 and triiodothyronine regulate keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors for retinoic acid (RAR-alpha,-gamma), vitamin D3 (VDR), thyroid hormone (TR-alpha,-beta) plus the common heterodimer partners, the 9-cis-retinoic acid receptors (RXR-alpha,-beta). Tretinoin 0-13 T cell receptor alpha locus Homo sapiens 258-266
10721822-1 2000 Retinoic acid, vitamin D3 and triiodothyronine regulate keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors for retinoic acid (RAR-alpha,-gamma), vitamin D3 (VDR), thyroid hormone (TR-alpha,-beta) plus the common heterodimer partners, the 9-cis-retinoic acid receptors (RXR-alpha,-beta). Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 347-356
10721822-1 2000 Retinoic acid, vitamin D3 and triiodothyronine regulate keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors for retinoic acid (RAR-alpha,-gamma), vitamin D3 (VDR), thyroid hormone (TR-alpha,-beta) plus the common heterodimer partners, the 9-cis-retinoic acid receptors (RXR-alpha,-beta). Tretinoin 189-202 T cell receptor alpha locus Homo sapiens 258-266
10721822-1 2000 Retinoic acid, vitamin D3 and triiodothyronine regulate keratinocyte proliferation and differentiation--processes that are disturbed in psoriatic skin--via binding to nuclear receptors for retinoic acid (RAR-alpha,-gamma), vitamin D3 (VDR), thyroid hormone (TR-alpha,-beta) plus the common heterodimer partners, the 9-cis-retinoic acid receptors (RXR-alpha,-beta). Tretinoin 189-202 retinoid X receptor alpha Homo sapiens 347-356
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 41-54 retinoic acid receptor, alpha Mus musculus 152-155
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 41-54 retinoic acid receptor, alpha Mus musculus 281-289
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 41-54 retinoic acid receptor, gamma Mus musculus 291-299
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 56-58 retinoic acid receptor, alpha Mus musculus 152-155
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 56-58 retinoic acid receptor, alpha Mus musculus 281-289
11237167-3 2000 The effects of active form of vitamin A, retinoic acid (RA), are believed to be mediated by specific nuclear receptor proteins [retinoic acid receptor (RAR)] which are members of the steroid and thyroid/retinoid receptor superfamily of ligand dependent transcriptional regulators, RARalpha, RARgamma, RXRalpha, and RXRbeta mRNA were abundant in adipose tissue and 3T3-L1 adipose cells. Tretinoin 56-58 retinoic acid receptor, gamma Mus musculus 291-299
10711420-8 2000 Conversely, retinoic acid abrogated the cadmium-provoked stimulation of AP-1 binding and transactivation capacity, and greatly inhibited the stimulation of binding caused by camptothecin and X-rays. Tretinoin 12-25 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-76
10634639-6 2000 Adenosine deaminase-resistant analogs such as fludarabine (FLU) and cladribine (CdA) also induced the differentiation of human myelomonocytic leukemia cells, and these analogs synergistically enhanced the differentiation induced by all-trans retinoic acid (ATRA) or VD3. Tretinoin 236-255 adenosine deaminase Homo sapiens 0-19
10634639-6 2000 Adenosine deaminase-resistant analogs such as fludarabine (FLU) and cladribine (CdA) also induced the differentiation of human myelomonocytic leukemia cells, and these analogs synergistically enhanced the differentiation induced by all-trans retinoic acid (ATRA) or VD3. Tretinoin 257-261 adenosine deaminase Homo sapiens 0-19
10608897-1 1999 Retinoic acid (RA) regulation of cellular proliferation and differentiation is mediated, at least in part, through two related nuclear receptors, RAR and RXR. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 154-157
10608897-1 1999 Retinoic acid (RA) regulation of cellular proliferation and differentiation is mediated, at least in part, through two related nuclear receptors, RAR and RXR. Tretinoin 15-17 retinoid X receptor alpha Homo sapiens 154-157
10585260-7 1999 As seen in cells induced to differentiate by the RAR agonist all-trans-retinoic acid, RXR activation led to an increase in the number of cells in G1 phase. Tretinoin 61-84 retinoid X receptor alpha Homo sapiens 86-89
10518498-4 1999 We also demonstrate that Shh is required for the activation of posterior HoxD genes by retinoic acid. Tretinoin 87-100 sonic hedgehog signaling molecule a Danio rerio 25-28
10529422-12 1999 These data, which indicate that retinoic acid signaling through RARalpha and/or RARbeta is essential for the specification of rhombomere identities and for the control of caudal hindbrain segmentation by restricting the expression domains of kreisler and of Krox-20, also strongly suggest that this signaling plays a crucial role in the posteriorization of the hindbrain neurectoderm. Tretinoin 32-45 retinoic acid receptor, alpha Mus musculus 64-72
10560916-8 1999 In contrast, CaMKI transcript and protein is expressed in uninduced cells and is induced by all-trans retinoic acid. Tretinoin 102-115 calcium/calmodulin dependent protein kinase I Homo sapiens 13-18
10610177-2 1999 Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). Tretinoin 121-134 tripartite motif containing 24 Homo sapiens 23-32
10610177-2 1999 Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). Tretinoin 121-134 retinoid X receptor alpha Homo sapiens 37-45
10610177-2 1999 Here we show that PML, Tif1alpha and RXRalpha/RARalpha function together in a transcription complex that is dependent on retinoic acid (RA). Tretinoin 46-48 retinoid X receptor alpha Homo sapiens 37-45
10525337-9 1999 We also present data showing that both treatment with retinoic acid and the overexpression of a constitutively active form of a retinoic acid receptor caused the suppression of Xepsin mRNA transcription, suggesting that anterior-posterior patterning in the central nervous system and in the epidermis may share common endogenous factors, i.e. , retinoids, in the Xenopus embryo. Tretinoin 54-67 epidermis specific serine protease L homeolog Xenopus laevis 177-183
10573135-5 1999 These results suggest that hypophosphorylation of pRB and repression of cyclin D3 and cdc25A are induced synergistically by treatment with ATRA plus GM-CSF in ML-1 cells. Tretinoin 139-143 cell division cycle 25A Homo sapiens 86-92
10524192-6 1999 Treatment of NT2/D1 cells with all-trans retinoic acid (atRA) is accompanied first by an up-regulation followed later by a down-regulation of hGCNF and its mRNA. Tretinoin 41-54 nuclear receptor subfamily 6 group A member 1 Homo sapiens 142-147
10524192-6 1999 Treatment of NT2/D1 cells with all-trans retinoic acid (atRA) is accompanied first by an up-regulation followed later by a down-regulation of hGCNF and its mRNA. Tretinoin 56-60 nuclear receptor subfamily 6 group A member 1 Homo sapiens 142-147
10524192-7 1999 Temporary up-regulation in NT2/D1 cells after treatment with atRA suggests that hGCNF is important for human neural determination and differentiation. Tretinoin 61-65 nuclear receptor subfamily 6 group A member 1 Homo sapiens 80-85
10479651-3 1999 In the current study, we show 9-cis retinoic acid (RA), a ligand for the nuclear hormone receptor retinoid X receptor (RXR) and retinoic acid receptor (RAR), markedly induces the expression of MCP-1. Tretinoin 51-53 retinoid X receptor alpha Homo sapiens 119-122
10479651-6 1999 Expression of PPARgamma, a heterodimer partner of RXR, is also markedly induced by RA in THP-1 cells. Tretinoin 83-85 retinoid X receptor alpha Homo sapiens 50-53
10427141-6 1999 These findings suggest that AH136B cells in the sub-G1 phase can not recover tumorigenicity, and that the administration of a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, such as 25-OH, and ATRA may be effective in treating patients with hepatoma. Tretinoin 197-201 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 126-166
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 27-40 cellular retinoic acid binding protein 2 Homo sapiens 197-205
10446126-1 1999 The pleiotropic effects of retinoic acid (RA) in mammalian cells are mediated by two classes of proteins: the retinoic acid receptors (RAR) and cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 42-44 cellular retinoic acid binding protein 2 Homo sapiens 197-205
10446126-3 1999 The equilibrium dissociation constants of complexes of CRABP-I or CRABP-II with RA were found to differ by 2-fold. Tretinoin 56-58 cellular retinoic acid binding protein 2 Homo sapiens 66-74
10446126-6 1999 The rate constant for movement of RA from CRABP-II, but not from CRABP-I, to RAR strongly depended on the concentration of the acceptor. Tretinoin 34-36 cellular retinoic acid binding protein 2 Homo sapiens 42-50
10446318-4 1999 The phosphorylation at the Tau-1 (Ser-195/Ser-198/Ser-199/Ser-202) and PHF-1 (Ser-396/Ser-404) sites was increased, mostly in the retinoic acid treated cells, whereas phosphorylation of tau at the 12E8 (Ser-262/Ser-356) epitope was decreased in both groups by approximately 60%. Tretinoin 130-143 PHD finger protein 1 Homo sapiens 71-76
10470859-13 1999 These effects of RA were neither blocked by a potent RA nuclear receptor (RAR) antagonist (AGN193109), nor mimicked by a selective RAR agonist (TTNPB), suggesting that the observed effects of RA are independent of RARs. Tretinoin 17-19 retinoic acid receptor, alpha Mus musculus 74-77
10413451-4 1999 This effect evidently reflected on HERG currents: In fact, RA produced an increase in HERG current density which was strongly potentiated by BDNF. Tretinoin 59-61 brain derived neurotrophic factor Homo sapiens 141-145
10400643-12 1999 The anti-apoptotic action of t-RA was ascribed, at least in part, to dual suppression of the cell death pathway mediated by JNK and AP-1. Tretinoin 29-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-136
10397716-0 1999 All-trans retinoic acid delays the differentiation of primitive hematopoietic precursors (lin-c-kit+Sca-1(+)) while enhancing the terminal maturation of committed granulocyte/monocyte progenitors. Tretinoin 10-23 ataxin 1 Mus musculus 100-105
10397716-4 1999 At 7 and 14 days of culture, a substantially greater percentage of cells cultured with ATRA did not express lineage-associated antigens (55.4% at day 7 and 68.6% at day 14) and retained expression of Sca-1 (44.7% at day 7 and 79.9% at day 14) compared with cells grown in its absence (lin- cells: 31.5% at day 7 and 4% at day 14; Sca-1(+): 10.4% at day 7 and 0.7% at day 14). Tretinoin 87-91 ataxin 1 Mus musculus 200-205
10397716-4 1999 At 7 and 14 days of culture, a substantially greater percentage of cells cultured with ATRA did not express lineage-associated antigens (55.4% at day 7 and 68.6% at day 14) and retained expression of Sca-1 (44.7% at day 7 and 79.9% at day 14) compared with cells grown in its absence (lin- cells: 31.5% at day 7 and 4% at day 14; Sca-1(+): 10.4% at day 7 and 0.7% at day 14). Tretinoin 87-91 ataxin 1 Mus musculus 330-335
10407146-10 1999 These findings suggest that ADH1B has a limited capacity to metabolize retinols, but that ADH4 is well suited to function in the metabolism of many diverse retinols and is predicted to participate in the synthesis of the active ligands all-trans-retinoic acid, 9-cis-retinoic acid, 3, 4-didehydroretinoic acid, 4-oxo-retinoic acid, and 4-hydroxy-retinoic acid. Tretinoin 240-259 alcohol dehydrogenase 1B (class I), beta polypeptide Homo sapiens 28-33
10395942-0 1999 Retinoic acid repressed the expression of c-fos and c-jun and induced apoptosis in regenerating rat liver after partial hepatectomy. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 42-47
10395942-4 1999 Northern blot analysis revealed that RA repressed the expression of c-fos and c-jun at 15 and 30 min with the up-regulation of retinoic acid receptor gamma (RARgamma) and RARbeta at 2 h after PH. Tretinoin 37-39 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 68-73
10395942-4 1999 Northern blot analysis revealed that RA repressed the expression of c-fos and c-jun at 15 and 30 min with the up-regulation of retinoic acid receptor gamma (RARgamma) and RARbeta at 2 h after PH. Tretinoin 37-39 retinoic acid receptor, gamma Rattus norvegicus 127-155
10395942-4 1999 Northern blot analysis revealed that RA repressed the expression of c-fos and c-jun at 15 and 30 min with the up-regulation of retinoic acid receptor gamma (RARgamma) and RARbeta at 2 h after PH. Tretinoin 37-39 retinoic acid receptor, gamma Rattus norvegicus 157-165
10395942-8 1999 These results suggest that RA exerts the antiproliferative activity only on the early stage of liver regeneration accompanied by the repression of c-fos and c-jun expression and induction of apoptosis. Tretinoin 27-29 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 147-152
10357892-0 1999 Differential distribution of retinoic acid synthesis in the chicken embryo as determined by immunolocalization of the retinoic acid synthetic enzyme, RALDH-2. Tretinoin 118-131 aldehyde dehydrogenase 1 family member A2 Gallus gallus 150-157
10357892-1 1999 Retinaldehyde dehydrogenase type 2 (RALDH-2) is a major retinoic acid generating enzyme in the early embryo. Tretinoin 56-69 aldehyde dehydrogenase 1 family member A2 Gallus gallus 0-34
10357892-1 1999 Retinaldehyde dehydrogenase type 2 (RALDH-2) is a major retinoic acid generating enzyme in the early embryo. Tretinoin 56-69 aldehyde dehydrogenase 1 family member A2 Gallus gallus 36-43
10357892-2 1999 Here we report the immunolocalization of this enzyme (RALDH-2-IR) in stage 6-29 chicken embryos; we also show that tissues that exhibit strong RALDH-2-IR in the embryo contain RALDH-2 and synthesize retinoic acid. Tretinoin 199-212 aldehyde dehydrogenase 1 family member A2 Gallus gallus 54-61
10336890-0 1999 The vitamin D receptor binds in a transcriptionally inactive form and without a defined polarity on a retinoic acid response element. Tretinoin 102-115 vitamin D receptor Homo sapiens 4-22
10336890-1 1999 Heterodimers of the vitamin D receptor (VDR) with the retinoid X receptor (RXR) bind in a transcriptionally unproductive manner to the retinoic acid response element present in the retinoic acid receptor-beta2 promoter. Tretinoin 135-148 vitamin D receptor Homo sapiens 20-38
10336890-1 1999 Heterodimers of the vitamin D receptor (VDR) with the retinoid X receptor (RXR) bind in a transcriptionally unproductive manner to the retinoic acid response element present in the retinoic acid receptor-beta2 promoter. Tretinoin 135-148 vitamin D receptor Homo sapiens 40-43
10336890-1 1999 Heterodimers of the vitamin D receptor (VDR) with the retinoid X receptor (RXR) bind in a transcriptionally unproductive manner to the retinoic acid response element present in the retinoic acid receptor-beta2 promoter. Tretinoin 135-148 retinoid X receptor alpha Homo sapiens 54-73
10336890-1 1999 Heterodimers of the vitamin D receptor (VDR) with the retinoid X receptor (RXR) bind in a transcriptionally unproductive manner to the retinoic acid response element present in the retinoic acid receptor-beta2 promoter. Tretinoin 135-148 retinoid X receptor alpha Homo sapiens 75-78
10320326-2 1999 Retinal dehydrogenase type II (RalDH2) catalyzes this last step in the production of retinoic acid in the early embryo, possibly producing this putative morphogen to initiate pattern formation. Tretinoin 85-98 aldehyde dehydrogenase 1 family member A2 Homo sapiens 31-37
10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 2 Homo sapiens 103-111
10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 2 Homo sapiens 169-177
10222145-10 1999 As in wild-type HL-60, retinoic acid induced the early down-regulation of RXRalpha in mutant transfectants similar to wild-type middle T transfectants, consistent with no loss or gain of relevant functions due to the mutations. Tretinoin 23-36 retinoid X receptor alpha Homo sapiens 74-82
10207061-1 1999 The multiple biologic activities of retinoic acid (RA) are mediated through RAR and retinoid X receptor (RXR) nuclear receptors that interact with specific DNA target sequences as heterodimers (RXR-RAR) or homodimers (RXR-RXR). Tretinoin 36-49 retinoic acid receptor, alpha Mus musculus 76-79
10207061-1 1999 The multiple biologic activities of retinoic acid (RA) are mediated through RAR and retinoid X receptor (RXR) nuclear receptors that interact with specific DNA target sequences as heterodimers (RXR-RAR) or homodimers (RXR-RXR). Tretinoin 36-49 retinoic acid receptor, alpha Mus musculus 198-201
10207061-1 1999 The multiple biologic activities of retinoic acid (RA) are mediated through RAR and retinoid X receptor (RXR) nuclear receptors that interact with specific DNA target sequences as heterodimers (RXR-RAR) or homodimers (RXR-RXR). Tretinoin 51-53 retinoic acid receptor, alpha Mus musculus 76-79
10207061-1 1999 The multiple biologic activities of retinoic acid (RA) are mediated through RAR and retinoid X receptor (RXR) nuclear receptors that interact with specific DNA target sequences as heterodimers (RXR-RAR) or homodimers (RXR-RXR). Tretinoin 51-53 retinoic acid receptor, alpha Mus musculus 198-201
10340464-8 1999 These results suggest that MMP-2-like and MMP-9-like gelatinases play a role in ECM remodeling during regeneration, and that gelatinases are involved in the excessive dedifferentiation after RA treatment. Tretinoin 191-193 matrix metallopeptidase 9 Homo sapiens 42-47
10340473-4 1999 Upon induction of endodermal differentiation with 10(-7) M RA, the gene expression of mDab2 was increased gradually during the first 96 h. Neither undifferentiated F9 cells, nor the undifferentiated aggregate cells without RA expressed mDab2. Tretinoin 59-61 disabled 2, mitogen-responsive phosphoprotein Mus musculus 86-91
10340473-4 1999 Upon induction of endodermal differentiation with 10(-7) M RA, the gene expression of mDab2 was increased gradually during the first 96 h. Neither undifferentiated F9 cells, nor the undifferentiated aggregate cells without RA expressed mDab2. Tretinoin 59-61 disabled 2, mitogen-responsive phosphoprotein Mus musculus 236-241
10340473-5 1999 Whole-mount in situ hybridization and quantitative RT-PCR also showed that the temporal expression pattern of the mDab2 gene coincides with the initiation pattern of RA synthesis that occurs during mouse embryogenesis. Tretinoin 166-168 disabled 2, mitogen-responsive phosphoprotein Mus musculus 114-119
10340473-7 1999 All the data indicate that mDab2 may play an important role in RA-induced signal transduction during mouse development. Tretinoin 63-65 disabled 2, mitogen-responsive phosphoprotein Mus musculus 27-32
10190983-1 1999 Retinal oxidase (EC 1.2.3.11) is a molybdenum-containing flavoenzyme with high enzymatic activity as to retinoic acid synthesis. Tretinoin 104-117 aldehyde oxidase 4 Mus musculus 0-15
10190983-10 1999 The purified recombinant retinal oxidase from Escherichia coli showed a typical spectrum of aldehyde oxidases and a lower Km (3.8 microM) for retinal and a higher Vmax (807 nmol/min/mg protein) for retinoic acid synthesis than those of rabbit retinal oxidase (8 microM and 496 nmol/min/mg protein). Tretinoin 198-211 aldehyde oxidase 1 Oryctolagus cuniculus 25-40
10191271-11 1999 Injection of ALDH1, but not ALDH-PB, mRNA stimulated retinoic acid synthesis in Xenopus embryos at the blastula stage. Tretinoin 53-66 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 13-18
10075839-16 1999 Therefore, RA may exert some of its effects on anteroposterior autopod patterning through controlling BMP-7 expression. Tretinoin 11-13 bone morphogenetic protein 7 Mus musculus 102-107
10085078-0 1999 Xenopus cytosolic thyroid hormone-binding protein (xCTBP) is aldehyde dehydrogenase catalyzing the formation of retinoic acid. Tretinoin 112-125 C-terminal binding protein 2 like S homeolog Xenopus laevis 0-49
10085078-0 1999 Xenopus cytosolic thyroid hormone-binding protein (xCTBP) is aldehyde dehydrogenase catalyzing the formation of retinoic acid. Tretinoin 112-125 C-terminal binding protein 2 like S homeolog Xenopus laevis 51-56
10085078-10 1999 Our results demonstrate that xCTBP is identical to ALDH1 and suggest that this protein might modulate RA synthesis and intracellular level of free T3. Tretinoin 102-104 C-terminal binding protein 2 like S homeolog Xenopus laevis 29-34
10085078-10 1999 Our results demonstrate that xCTBP is identical to ALDH1 and suggest that this protein might modulate RA synthesis and intracellular level of free T3. Tretinoin 102-104 aldehyde dehydrogenase 1 family member A1 L homeolog Xenopus laevis 51-56
10026278-1 1999 The all-trans retinoic acid and 9-cis retinoic acid receptors (RAR and RXR, respectively) belong to a family of ligand inducible transcription factors, which exert their effect via binding to hormone response elements. Tretinoin 14-27 retinoid X receptor alpha Homo sapiens 71-74
10026291-1 1999 Microsomal enzymes that catalyze the first step in the biosynthesis of retinoic acid from retinal, retinol dehydrogenases (RDHs), access retinol bound to cellular retinol-binding protein (CRBP). Tretinoin 71-84 short chain dehydrogenase/reductase family 9C member 7 Homo sapiens 99-121
10026291-1 1999 Microsomal enzymes that catalyze the first step in the biosynthesis of retinoic acid from retinal, retinol dehydrogenases (RDHs), access retinol bound to cellular retinol-binding protein (CRBP). Tretinoin 71-84 short chain dehydrogenase/reductase family 9C member 7 Homo sapiens 123-127
10082656-9 1999 In summary, our results establish retinoic acid as an enhancer of TNF-alpha-induced ICAM-1 levels in NHK. Tretinoin 34-47 intercellular adhesion molecule 1 Homo sapiens 84-90
10070861-5 1999 RA at both doses significantly decreased the labelling index and TGF-alpha immunoreactivity of gastric cancers, which were enhanced by administration of sodium chloride, and significantly increased the apoptotic index of cancers, which was lowered by administration of sodium chloride. Tretinoin 0-2 transforming growth factor alpha Rattus norvegicus 65-74
10070861-6 1999 These findings suggest that RA attenuates gastric carcinogenesis, enhanced by sodium chloride, by increasing apoptosis, decreasing DNA synthesis, and reducing TGF-alpha expression in gastric cancers. Tretinoin 28-30 transforming growth factor alpha Rattus norvegicus 159-168
9880524-4 1999 We show that the RA-induced differentiation toward PrE is accompanied by a sustained increase in Ras activity and that ectopic expression of oncogenic Ha-Ras is sufficient to induce PrE differentiation. Tretinoin 17-19 Harvey rat sarcoma virus oncogene Mus musculus 151-157
9923548-10 1999 all-trans-Retinoic acid (ATRA) concentrations were about 5% of the 13-CRA concentrations detected in plasma, 68% of those found in liver, and 20% of those found in tumor. Tretinoin 0-23 LUC7 like 3 pre-mRNA splicing factor Homo sapiens 70-73
9923548-10 1999 all-trans-Retinoic acid (ATRA) concentrations were about 5% of the 13-CRA concentrations detected in plasma, 68% of those found in liver, and 20% of those found in tumor. Tretinoin 25-29 LUC7 like 3 pre-mRNA splicing factor Homo sapiens 70-73
9882496-4 1999 Retinoic acid receptor gamma (RARgamma) mediates these effects on the caudal neural tube at 8.5 days postcoitum, as RARgamma-/- mice are completely resistant to spina bifida induced by retinoic acid at this stage. Tretinoin 185-198 retinoic acid receptor, gamma Mus musculus 0-28
9882496-4 1999 Retinoic acid receptor gamma (RARgamma) mediates these effects on the caudal neural tube at 8.5 days postcoitum, as RARgamma-/- mice are completely resistant to spina bifida induced by retinoic acid at this stage. Tretinoin 185-198 retinoic acid receptor, gamma Mus musculus 30-38
9882496-4 1999 Retinoic acid receptor gamma (RARgamma) mediates these effects on the caudal neural tube at 8.5 days postcoitum, as RARgamma-/- mice are completely resistant to spina bifida induced by retinoic acid at this stage. Tretinoin 185-198 retinoic acid receptor, gamma Mus musculus 116-124
10052016-6 1999 Furthermore, our results emphasize that the combined dosing of RA with tin-metalloporphyrins leads to a substantial decline in bilirubin levels due to a profound inhibition of HMOX in the probed tissues. Tretinoin 63-65 heme oxygenase 1 Rattus norvegicus 176-180
9988880-9 1999 As several of these genes are transcriptionally regulated by retinoic-acid-responsive elements in their promoter regions, phenytoin-induced alterations in expression of the RAR isoforms may have severe downstream consequences in the regulation of events necessary for normal craniofacial development. Tretinoin 61-74 retinoic acid receptor, alpha Mus musculus 173-176
9869297-10 1998 A single Hoxb1 CE1 binding complex is also detected by gel shift assays in nuclear extracts prepared from both stem and RA-treated F9 cells. Tretinoin 120-122 catalase activity, liver Mus musculus 15-18
11367680-5 1998 However, immunostaining data showed that beta-catenin was translocalized into nuclei after retinoic acid induced P19 cell aggregates were trypsinized and cultured in serum free N2 medium for 2 and 4 d. In this period, transcription of En-2, a downstream target gene of Wnt signal, increased evidently. Tretinoin 91-104 catenin (cadherin associated protein), beta 1 Mus musculus 41-53
12016958-7 1998 From the view of morphology, cell cycle, growth inhibition, cytokeratin 4 expression, dye transfer and tumorigenecity, the results demonstrated that DMSO as well as ATRA could induce differentiation of human esophageal cancer cells. Tretinoin 165-169 keratin 4 Homo sapiens 60-73
9806904-13 1998 These observations suggest that enzymic catalysis was the primary mechanism for the GSTP1-1-dependent conversion of 13-cRA to t-RA. Tretinoin 126-130 myotubularin related protein 11 Homo sapiens 119-122
9824353-0 1998 Stromelysin 3 is overexpressed in human pancreatic carcinoma and regulated by retinoic acid in pancreatic carcinoma cell lines. Tretinoin 78-91 matrix metallopeptidase 11 Homo sapiens 0-13
9870533-4 1998 Furthermore, we propose a role for Msx-1 in retinoic acid-induced cleft palate, since retinoic acid inhibits Msx-1 mRNA expression in palate mesenchymal cells. Tretinoin 44-57 msh homeobox 1 Mus musculus 35-40
9870533-4 1998 Furthermore, we propose a role for Msx-1 in retinoic acid-induced cleft palate, since retinoic acid inhibits Msx-1 mRNA expression in palate mesenchymal cells. Tretinoin 44-57 msh homeobox 1 Mus musculus 109-114
9870533-4 1998 Furthermore, we propose a role for Msx-1 in retinoic acid-induced cleft palate, since retinoic acid inhibits Msx-1 mRNA expression in palate mesenchymal cells. Tretinoin 86-99 msh homeobox 1 Mus musculus 109-114
9870533-6 1998 These data suggest a mechanistic interaction between retinoic acid, transforming growth factor beta, and Msx-1 in the etiology of retinoic acid-induced cleft palate. Tretinoin 130-143 msh homeobox 1 Mus musculus 105-110
9790391-0 1998 Retinoic acid up-regulates the expression of major histocompatibility complex molecules and adhesion/costimulation molecules (specifically, intercellular adhesion molecule ICAM-1) in human cervical cancer. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 172-178
9790391-2 1998 To investigate whether enhanced immunogenicity might be responsible for such efficacy, we evaluated the effects of retinoic acid on the expression of major histocompatibility complex class I and class II and intercellular adhesion molecule ICAM-1 in human cervical carcinoma cell lines. Tretinoin 115-128 intercellular adhesion molecule 1 Homo sapiens 240-246
9790391-6 1998 Exposure to therapeutic doses of retinoic acid were able to significantly increase the expression of major histocompatibility complex class I and ICAM-1 antigens in all the cell lines when compared with untreated tumor cells but were not able to induce the expression of class II surface human leukocyte antigens. Tretinoin 33-46 intercellular adhesion molecule 1 Homo sapiens 146-152
9773973-0 1998 Structural requirements of the glucocorticoid and retinoic acid response units in the phosphoenolpyruvate carboxykinase gene promoter. Tretinoin 50-63 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 86-119
9773973-3 1998 The PEPCK promoter also contains a retinoic acid response unit (RARU) that consists of two retinoic acid response elements (RARE1 and RARE2) that bind retinoic acid receptor/9-cis-retinoic acid receptor heterodimers. Tretinoin 35-48 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 4-9
9773973-3 1998 The PEPCK promoter also contains a retinoic acid response unit (RARU) that consists of two retinoic acid response elements (RARE1 and RARE2) that bind retinoic acid receptor/9-cis-retinoic acid receptor heterodimers. Tretinoin 91-104 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 4-9
9773973-6 1998 We reasoned that each response might require a unique structural assembly and therefore tested how various arrangements of the PEPCK promoter affect the actions of either glucocorticoids or retinoic acid. Tretinoin 190-203 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 127-132
9737849-13 1998 Thus, the widening of the ligand entrance required for entry of retinoic acid appears to be a property of monomeric apo-CRABPII. Tretinoin 64-77 cellular retinoic acid binding protein 2 Homo sapiens 120-127
9727829-4 1998 We also showed that retinoic acid mediated activation of the HNF-3alpha gene required -4 kb of the HNF-3alpha promoter region in F9 teratocarcinoma transfections. Tretinoin 20-33 forkhead box A1 Mus musculus 61-71
9727829-4 1998 We also showed that retinoic acid mediated activation of the HNF-3alpha gene required -4 kb of the HNF-3alpha promoter region in F9 teratocarcinoma transfections. Tretinoin 20-33 forkhead box A1 Mus musculus 99-109
9846167-6 1998 In contrast, RA abolished the collagen-induced increase in ALP mRNA and PTH/PTHrP receptor mRNA. Tretinoin 13-15 parathyroid hormone-like hormone Rattus norvegicus 76-81
10921031-3 1998 Bone marrow MNC IL-8RA was measured by flow cytometry after cultured with ATRA (10(-6) mmol/L). Tretinoin 74-78 C-X-C motif chemokine receptor 1 Homo sapiens 16-22
9738944-2 1998 Using rat muscle PAD cDNA as a probe, we obtained two novel cDNAs, PAD-R11 and PAD-R4, from immortalized rat keratinocytes treated with all-trans retinoic acid. Tretinoin 146-159 peptidyl arginine deiminase 1 Rattus norvegicus 67-74
9738944-2 1998 Using rat muscle PAD cDNA as a probe, we obtained two novel cDNAs, PAD-R11 and PAD-R4, from immortalized rat keratinocytes treated with all-trans retinoic acid. Tretinoin 146-159 peptidyl arginine deiminase 4 Rattus norvegicus 79-85
9740690-0 1998 Effects of retinoic acid combined with irradiation on the expression of major histocompatibility complex molecules and adhesion/costimulation molecules ICAM-1 in human cervical cancer. Tretinoin 11-24 intercellular adhesion molecule 1 Homo sapiens 152-158
9740690-8 1998 In a similar fashion, retinoic acid was also able to significantly increase the expression of MHC Class I and ICAM-1 antigens when compared to untreated tumor cells but was not able to induce the expression of HLA Class II surface antigens. Tretinoin 22-35 intercellular adhesion molecule 1 Homo sapiens 110-116
9740690-9 1998 Exposure to the combination of radiation plus retinoic acid significantly upregulated HLA Class I and ICAM-1 molecules in an additive manner when compared to the levels obtainable with the exposure to radiation or retinoic acid alone. Tretinoin 46-59 intercellular adhesion molecule 1 Homo sapiens 102-108
9740690-9 1998 Exposure to the combination of radiation plus retinoic acid significantly upregulated HLA Class I and ICAM-1 molecules in an additive manner when compared to the levels obtainable with the exposure to radiation or retinoic acid alone. Tretinoin 214-227 intercellular adhesion molecule 1 Homo sapiens 102-108
9732061-10 1998 All-trans retinoic acid acts to inhibit induction of c-Jun protein by ultraviolet irradiation, thereby preventing increased matrix metalloproteinases and ensuing dermal damage. Tretinoin 10-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-58
9744516-0 1998 Expression of vitamin D receptor (VDR) in HL-60 cells is differentially regulated during the process of differentiation induced by phorbol ester, retinoic acid or interferon-gamma. Tretinoin 146-159 vitamin D receptor Homo sapiens 14-32
9744516-0 1998 Expression of vitamin D receptor (VDR) in HL-60 cells is differentially regulated during the process of differentiation induced by phorbol ester, retinoic acid or interferon-gamma. Tretinoin 146-159 vitamin D receptor Homo sapiens 34-37
9744516-1 1998 The effects of three inducers of differentiation, phorbol myristate acetate (PMA), retinoic acid (RA) and interferon-gamma (IFN-gamma), on the temporal regulation of vitamin D receptor (VDR) expression in HL-60 cells were analyzed by Northern blotting and immunofluorescence assays. Tretinoin 83-96 vitamin D receptor Homo sapiens 166-184
9744516-1 1998 The effects of three inducers of differentiation, phorbol myristate acetate (PMA), retinoic acid (RA) and interferon-gamma (IFN-gamma), on the temporal regulation of vitamin D receptor (VDR) expression in HL-60 cells were analyzed by Northern blotting and immunofluorescence assays. Tretinoin 83-96 vitamin D receptor Homo sapiens 186-189
9704013-6 1998 Adherence, which is important for MO differentiation, induced CRABP II expression, but the addition of 10(-7) M retinoic acid inhibited the upregulation of CRABP II expression during MO/MAC differentiation. Tretinoin 112-125 cellular retinoic acid binding protein 2 Homo sapiens 156-164
9639524-6 1998 IL-7 and IL-15 also supported the growth of SeAx cells in the presence of the apoptosis inducing agents dexamethasone and retinoic acid. Tretinoin 122-135 interleukin 15 Homo sapiens 9-14
9697046-0 1998 All-trans-retinoic acid down-regulates elastin promoter activity elevated by ultraviolet B irradiation in cultured skin fibroblasts. Tretinoin 0-23 elastin Homo sapiens 39-46
9697046-4 1998 Consequently, we examined the effects of all-trans-retinoic acid (t-RA) and UVB on elastin gene expression in cultured human skin fibroblasts in vitro. Tretinoin 41-64 elastin Homo sapiens 83-90
9697046-7 1998 Also t-RA inhibited the increase in elastin mRNA level following a single exposure to UVB by approximately 16%, and the increase in promotor activity by about 65%. Tretinoin 5-9 elastin Homo sapiens 36-43
9697046-8 1998 The inhibitory effect of t-RA on elastin induced by UVB was also demonstrated by indirect immunofluorescence studies. Tretinoin 25-29 elastin Homo sapiens 33-40
9697850-4 1998 Characterization of a prerhombomeric enhancer from Hoxb4 reveals that a retinoic acid (RA) response element is an essential component of the early neural response to somite (s) signaling and can interpret positional information for setting the anterior boundary of expression. Tretinoin 72-85 homeobox B4 Homo sapiens 51-56
9697850-4 1998 Characterization of a prerhombomeric enhancer from Hoxb4 reveals that a retinoic acid (RA) response element is an essential component of the early neural response to somite (s) signaling and can interpret positional information for setting the anterior boundary of expression. Tretinoin 87-89 homeobox B4 Homo sapiens 51-56
9649304-4 1998 Point mutations that reduced transactivation by atRA also reduced atRA-induced transrepression of AP1 transcription, correlating ligand-induced activation and repression. Tretinoin 48-52 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-101
9649304-4 1998 Point mutations that reduced transactivation by atRA also reduced atRA-induced transrepression of AP1 transcription, correlating ligand-induced activation and repression. Tretinoin 66-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-101
9662427-4 1998 Incubation with RA did not alter NGFI-A mRNA levels, but significantly reduced the NGFI-B and c-fos response to NGF and serum. Tretinoin 16-18 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 94-99
9662427-6 1998 Sequences contained within the 5" flanking region of the c-fos gene confer responsiveness to NGF and mediate the inhibitory effect of RA. Tretinoin 134-136 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 57-62
9641974-8 1998 Finally, retinoic acid proximalizes both the level of Emx-2 expression and the positional memory of the blastema suggesting Emx-2 may participate in pattern formation by specifying positional information. Tretinoin 9-22 empty spiracles homeobox 2 Homo sapiens 54-59
9641974-8 1998 Finally, retinoic acid proximalizes both the level of Emx-2 expression and the positional memory of the blastema suggesting Emx-2 may participate in pattern formation by specifying positional information. Tretinoin 9-22 empty spiracles homeobox 2 Homo sapiens 124-129
9635125-0 1998 Thyroid hormone, all-trans retinoic acid, and 9-cis retinoic acid functioned as negative modulators of the effect of glucocorticoid on induction of alpha 1-acid glycoprotein mRNA in RLN-10 cells. Tretinoin 17-40 orosomucoid 1 Rattus norvegicus 148-173
9635125-2 1998 We studied the interaction of T3, glucocorticoids, all-trans retinoic acid (RA), and 9-cis retinoic acid (9cRA) on the expression of the rat alpha 1-acid glycoprotein (AGP) gene in vitro. Tretinoin 51-74 orosomucoid 1 Rattus norvegicus 141-166
9664142-7 1998 The specific expression patterns of MMP-1 and TIMP-2 were detected and regulated by RA in almost all cell lines, whereas expression of MMP-2 and TIMP-1 was not influenced by RA treatment. Tretinoin 84-86 TIMP metallopeptidase inhibitor 2 Homo sapiens 46-52
9575180-3 1998 Ligand dependent activation or repression of retinoid-regulated genes is dependent on the binding of retinoic acid receptor (RAR)/9-cis-retinoic acid receptor (RXR) heterodimers to retinoic acid response element (RARE). Tretinoin 101-114 retinoid X receptor alpha Homo sapiens 160-163
9605760-0 1998 Glial cell line-derived neurotrophic factor/neurturin-induced differentiation and its enhancement by retinoic acid in primary human neuroblastomas expressing c-Ret, GFR alpha-1, and GFR alpha-2. Tretinoin 101-114 neurturin Homo sapiens 44-53
9600845-10 1998 A three-step mechanism of RA entry has been proposed, addressing the opening of the RA entrance, the electrostatic potential that directs entry of RA into the binding pocket, and the intramolecular interactions that stabilize the RA.CRABPII complex via locking the three flexible structural elements when RA is bound. Tretinoin 26-28 cellular retinoic acid binding protein 2 Homo sapiens 233-240
9600845-10 1998 A three-step mechanism of RA entry has been proposed, addressing the opening of the RA entrance, the electrostatic potential that directs entry of RA into the binding pocket, and the intramolecular interactions that stabilize the RA.CRABPII complex via locking the three flexible structural elements when RA is bound. Tretinoin 84-86 cellular retinoic acid binding protein 2 Homo sapiens 233-240
9600845-10 1998 A three-step mechanism of RA entry has been proposed, addressing the opening of the RA entrance, the electrostatic potential that directs entry of RA into the binding pocket, and the intramolecular interactions that stabilize the RA.CRABPII complex via locking the three flexible structural elements when RA is bound. Tretinoin 84-86 cellular retinoic acid binding protein 2 Homo sapiens 233-240
9600845-10 1998 A three-step mechanism of RA entry has been proposed, addressing the opening of the RA entrance, the electrostatic potential that directs entry of RA into the binding pocket, and the intramolecular interactions that stabilize the RA.CRABPII complex via locking the three flexible structural elements when RA is bound. Tretinoin 84-86 cellular retinoic acid binding protein 2 Homo sapiens 233-240
9600845-10 1998 A three-step mechanism of RA entry has been proposed, addressing the opening of the RA entrance, the electrostatic potential that directs entry of RA into the binding pocket, and the intramolecular interactions that stabilize the RA.CRABPII complex via locking the three flexible structural elements when RA is bound. Tretinoin 84-86 cellular retinoic acid binding protein 2 Homo sapiens 233-240
9578604-2 1998 G-CSF enhanced O-2 generating ability of HL-60 cells whose differentiation had been initiated by dimethylsulfoxide (DMSO) or retinoic acid (RA). Tretinoin 125-138 immunoglobulin kappa variable 1D-39 Homo sapiens 15-18
9550729-4 1998 Misexpression of SOX1 can substitute for the requirement of retinoic acid to impart neural fate to competent ectodermal P19 cells. Tretinoin 60-73 SRY-box transcription factor 1 Homo sapiens 17-21
9617548-1 1998 PURPOSE: We investigated the effect of retinoic acid (RA) on basic fibroblast growth factor (bFGF)-stimulated proliferation of cultured human retinal pigment epithelial (hRPE) cells and of 125I-bFGF-binding to the bFGF plasma membrane receptors of hRPE. Tretinoin 54-56 ribulose-5-phosphate-3-epimerase Homo sapiens 170-174
9547504-7 1998 The effect of ATRA on Sgp-2 expression may be direct, since the promoter of Sgp-2 contains a putative ATRA-responsive element (RARE). Tretinoin 14-18 clusterin Rattus norvegicus 22-27
9547504-7 1998 The effect of ATRA on Sgp-2 expression may be direct, since the promoter of Sgp-2 contains a putative ATRA-responsive element (RARE). Tretinoin 14-18 clusterin Rattus norvegicus 76-81
9547504-7 1998 The effect of ATRA on Sgp-2 expression may be direct, since the promoter of Sgp-2 contains a putative ATRA-responsive element (RARE). Tretinoin 102-106 clusterin Rattus norvegicus 22-27
9547504-7 1998 The effect of ATRA on Sgp-2 expression may be direct, since the promoter of Sgp-2 contains a putative ATRA-responsive element (RARE). Tretinoin 102-106 clusterin Rattus norvegicus 76-81
9531570-8 1998 As the above-noted results predict, histone deacetylase inhibitors antagonize oncogenic activities of the PML-RARalpha fusion protein and partially relieve transcriptional repression by PLZF as well as inhibitory effect of PLZF-RARalpha on ATRA response. Tretinoin 240-244 zinc finger and BTB domain containing 16 Homo sapiens 223-227
9573364-4 1998 Cross-competition experiments showed that BDNF is the preferred ligand and cross-linking of [125I]BDNF resulted in a doublet at 160 kd that was increased in RPE cells incubated in all-trans retinoic acid. Tretinoin 190-203 brain derived neurotrophic factor Homo sapiens 42-46
9573364-4 1998 Cross-competition experiments showed that BDNF is the preferred ligand and cross-linking of [125I]BDNF resulted in a doublet at 160 kd that was increased in RPE cells incubated in all-trans retinoic acid. Tretinoin 190-203 brain derived neurotrophic factor Homo sapiens 98-102
17168502-1 1998 It has been demonstrated that glial fibrillary acidic protein (GFAP)-positive astrocyte precursors will differentiate in response to application of retinoic acid (RA), whereas GFAP/oligodendrocyte type 2-astrocyte progenitors will be inhibited from differentiating and continue to be mitotically active in the presence of RA. Tretinoin 148-161 glial fibrillary acidic protein Homo sapiens 30-61
17168502-1 1998 It has been demonstrated that glial fibrillary acidic protein (GFAP)-positive astrocyte precursors will differentiate in response to application of retinoic acid (RA), whereas GFAP/oligodendrocyte type 2-astrocyte progenitors will be inhibited from differentiating and continue to be mitotically active in the presence of RA. Tretinoin 148-161 glial fibrillary acidic protein Homo sapiens 63-67
17168502-1 1998 It has been demonstrated that glial fibrillary acidic protein (GFAP)-positive astrocyte precursors will differentiate in response to application of retinoic acid (RA), whereas GFAP/oligodendrocyte type 2-astrocyte progenitors will be inhibited from differentiating and continue to be mitotically active in the presence of RA. Tretinoin 163-165 glial fibrillary acidic protein Homo sapiens 30-61
17168502-1 1998 It has been demonstrated that glial fibrillary acidic protein (GFAP)-positive astrocyte precursors will differentiate in response to application of retinoic acid (RA), whereas GFAP/oligodendrocyte type 2-astrocyte progenitors will be inhibited from differentiating and continue to be mitotically active in the presence of RA. Tretinoin 163-165 glial fibrillary acidic protein Homo sapiens 63-67
17168502-1 1998 It has been demonstrated that glial fibrillary acidic protein (GFAP)-positive astrocyte precursors will differentiate in response to application of retinoic acid (RA), whereas GFAP/oligodendrocyte type 2-astrocyte progenitors will be inhibited from differentiating and continue to be mitotically active in the presence of RA. Tretinoin 322-324 glial fibrillary acidic protein Homo sapiens 63-67
17168502-2 1998 The authors sought to determine if cells taken from glial tumors that were GFAP positive retained the ability to differentiate following application of RA in vitro, as their normal astrocytic counterparts do. Tretinoin 152-154 glial fibrillary acidic protein Homo sapiens 75-79
9494123-5 1998 Indole-3-carbinol, tamoxifen, 4"-hydroxytamoxifen, and 9-cis,retinoic acid decreased the ratio; the effects of all trans-retinoic acid and 2,3,7,8-tetrachlorodibenzo-p-dioxin were concentration dependent; the antiestrogen ICI 182,780 increased the 16alpha-/2-OHE1 metabolite ratio. Tretinoin 61-74 ATPase H+ transporting accessory protein 1 Homo sapiens 248-255
9749798-7 1998 The number of calretinin-expressing neurons increased further when cultures were treated with a combination of bFGF and retinoic acid. Tretinoin 120-133 calbindin 2 Rattus norvegicus 14-24
9544984-3 1998 The activity of this enzyme is controlled by several hormones, including glucocorticoids, glucagon, retinoic acid, and insulin, that principally affect the rate of transcription of the PEPCK gene. Tretinoin 100-113 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 185-190
9579690-6 1998 These findings may raise the possibility that prostaglandin-D-synthase in CSF is involved in retinoic acid action on the brain. Tretinoin 93-106 colony stimulating factor 2 Rattus norvegicus 74-77
9504637-0 1998 Accumulation of catalytically active PKC-zeta into the nucleus of HL-60 cell line plays a key role in the induction of granulocytic differentiation mediated by all-trans retinoic acid. Tretinoin 170-183 protein kinase C zeta Homo sapiens 37-45
9504637-1 1998 The effect of differentiating doses of all-trans retinoic acid (ATRA, 10(-6) M) and vitamin D3 (10(-7) M) was investigated on the nuclear levels of endogenous ceramide and protein kinase C-zeta (PKC-zeta) catalytic activity in HL-60 myeloid cells. Tretinoin 49-62 protein kinase C zeta Homo sapiens 172-193
9504637-1 1998 The effect of differentiating doses of all-trans retinoic acid (ATRA, 10(-6) M) and vitamin D3 (10(-7) M) was investigated on the nuclear levels of endogenous ceramide and protein kinase C-zeta (PKC-zeta) catalytic activity in HL-60 myeloid cells. Tretinoin 64-68 protein kinase C zeta Homo sapiens 172-193
9504637-2 1998 ATRA induced a parallel increase of ceramide and catalytically active PKC-zeta into the nuclear compartment of HL-60 cells (peak at 72 h). Tretinoin 0-4 protein kinase C zeta Homo sapiens 70-78
9504637-4 1998 Pretreatment of HL-60 cells with high pharmacological concentrations of exogenously-added C2-ceramide (10(-6) M) completely blocked the ATRA-mediated activation of nuclear PKC-zeta. Tretinoin 136-140 protein kinase C zeta Homo sapiens 172-180
9608736-2 1998 The intracellular retinoic acid binding protein CRABP-I has a high affinity for RA, and is thought to be involved in the mechanism of RA signalling. Tretinoin 80-82 cellular retinoic acid binding protein I Mus musculus 48-55
9478951-2 1998 In chondrocytes, CD-RAP is down-regulated by retinoic acid. Tretinoin 45-58 MIA SH3 domain containing Mus musculus 17-23
9478951-7 1998 In contrast, increased concentration of AP-2, stimulated by retinoic acid, led to decreased transcription of the CD-RAP promoter, an effect that was abolished by mutation of the AP-2 binding site. Tretinoin 60-73 MIA SH3 domain containing Mus musculus 113-119
9425271-9 1997 These results show that RA but not DMSO induces the expression of GM3, GD3, GT1b and GQ1b synthases, and particularly GD3 synthase mRNA, in the ganglioside biosynthetic pathway during the neural differentiation of embryonic carcinoma P19 cells. Tretinoin 24-26 granulocyte macrophage antigen 3 Mus musculus 66-69
9360992-0 1997 Characterization and retinoic acid responsiveness of the murine Hoxd4 transcription unit. Tretinoin 21-34 homeobox D4 Mus musculus 64-69
9371525-3 1997 In this study we have evaluated, by a cytofluorimetric method, the presence of HSP-70 in HL-60 cells during treatment with all-trans retinoic acid (ATRA), 9-cis retinoic acid (9-cis RA), and 13-cis retinoic acid (13-cis RA). Tretinoin 133-146 heat shock protein family A (Hsp70) member 4 Homo sapiens 79-85
9371525-3 1997 In this study we have evaluated, by a cytofluorimetric method, the presence of HSP-70 in HL-60 cells during treatment with all-trans retinoic acid (ATRA), 9-cis retinoic acid (9-cis RA), and 13-cis retinoic acid (13-cis RA). Tretinoin 148-152 heat shock protein family A (Hsp70) member 4 Homo sapiens 79-85
9371525-3 1997 In this study we have evaluated, by a cytofluorimetric method, the presence of HSP-70 in HL-60 cells during treatment with all-trans retinoic acid (ATRA), 9-cis retinoic acid (9-cis RA), and 13-cis retinoic acid (13-cis RA). Tretinoin 161-174 heat shock protein family A (Hsp70) member 4 Homo sapiens 79-85
9409303-9 1997 Incubation of brain capillaries with retinoic acid (10 mumol/L) and dibutyryl cAMP (3 mmol/L) resulted in a 4-fold increase in TM mRNA at 4 and 8 hours, respectively, followed by an increase in protein C activation. Tretinoin 37-50 thrombomodulin Bos taurus 127-129
9337137-0 1997 Meis2, a novel mouse Pbx-related homeobox gene induced by retinoic acid during differentiation of P19 embryonal carcinoma cells. Tretinoin 58-71 Meis homeobox 2 Mus musculus 0-5
9295294-5 1997 mCAR1, like hCAR, binds as a heterodimer with the retinoid X receptor to the retinoic acid response element from the promoter of the retinoic acid receptor beta2 isoform. Tretinoin 77-90 CXADR Ig-like cell adhesion molecule Homo sapiens 12-16
9295294-5 1997 mCAR1, like hCAR, binds as a heterodimer with the retinoid X receptor to the retinoic acid response element from the promoter of the retinoic acid receptor beta2 isoform. Tretinoin 77-90 retinoid X receptor alpha Homo sapiens 50-69
9284950-4 1997 Retinoic acid arrested T-47D proliferation, induced PKC alpha expression and concomitantly repressed PKC zeta expression. Tretinoin 0-13 protein kinase C zeta Homo sapiens 101-109
9284950-5 1997 The changes in PKC alpha and PKC zeta reflect retinoic acid-induced changes in mRNA. Tretinoin 46-59 protein kinase C zeta Homo sapiens 29-37
9281352-10 1997 Conversely, several combinations of RAR/RXR closely mimicked the differentiation effects observed with all-trans retinoic acid. Tretinoin 113-126 retinoid X receptor alpha Homo sapiens 40-43
9295165-0 1997 Post-transcriptional regulation of LTC4 synthase activity by retinoic acid in rat basophilic leukemia cells. Tretinoin 61-74 leukotriene C4 synthase Rattus norvegicus 35-48
9295165-6 1997 These results indicate that RA-induced enhancement of LTC4 production and its inhibition by DEX and CSA was determined by post-transcriptional regulation of LTC4 synthase. Tretinoin 28-30 leukotriene C4 synthase Rattus norvegicus 157-170
9277454-3 1997 Previous investigations demonstrated that exogenous retinoic acid increases elastin production in cultured neonatal lung fibroblasts and increases the number of alveoli when it is administered to neonatal rats. Tretinoin 52-65 elastin Rattus norvegicus 76-83
9258346-4 1997 Retinoic acid caused a transient increase in IGF I and IGF II mRNA levels after 6 h, but after 24 and 48 h of treatment a dose-dependent decrease was observed. Tretinoin 0-13 insulin-like growth factor 2 Rattus norvegicus 55-61
9258346-7 1997 In contrast, 48 h exposure to retinoic acid increased IGF II polypeptide levels, possible due to increased levels of IGF binding protein-6. Tretinoin 30-43 insulin-like growth factor 2 Rattus norvegicus 54-60
9258346-11 1997 In conclusion, following a small transient increase, retinoic acid causes a pronounced decrease in IGF I and IGF II mRNA expression in Ob cells. Tretinoin 53-66 insulin-like growth factor 2 Rattus norvegicus 109-115
9258346-12 1997 However, treatment with retinoic acid causes a decrease in IGF I and an increase in IGF II polypeptide levels. Tretinoin 24-37 insulin-like growth factor 2 Rattus norvegicus 84-90
9262312-1 1997 Retinoid induction of epidermal hyperplasia was investigated in hairless mice with synthetic ligands for the retinoic acid (RAR) and retinoid X (RXR) nuclear receptors. Tretinoin 109-122 Rab40B, member RAS oncogene family Mus musculus 124-127
9234742-2 1997 APLs with the PML-RAR alpha or the PLZF-RAR alpha fusion protein are phenotypically indistinguishable except that they differ in their sensitivity to retinoic acid (RA)-induced differentiation: PML-RAR alpha blasts are sensitive to RA and patients enter disease remission after RA treatment, while patients with PLZF-RAR alpha do not. Tretinoin 40-42 zinc finger and BTB domain containing 16 Homo sapiens 35-39
9234742-4 1997 These data demonstrate that PML-RAR alpha and PLZF-RAR alpha have similar (inhibitory) effects on RA-independent differentiation and opposite (stimulatory or inhibitory) effects on RA-dependent differentiation and that they behave in vivo as RA-dependent enhancers or inhibitors of RA-responsive genes, respectively. Tretinoin 51-53 zinc finger and BTB domain containing 16 Homo sapiens 46-50
9234742-4 1997 These data demonstrate that PML-RAR alpha and PLZF-RAR alpha have similar (inhibitory) effects on RA-independent differentiation and opposite (stimulatory or inhibitory) effects on RA-dependent differentiation and that they behave in vivo as RA-dependent enhancers or inhibitors of RA-responsive genes, respectively. Tretinoin 51-53 zinc finger and BTB domain containing 16 Homo sapiens 46-50
9234742-5 1997 Their different activities on the RA signalling pathway might underlie the different responses of PML-RAR alpha and PLZF-RAR alpha APLs to RA treatment. Tretinoin 34-36 zinc finger and BTB domain containing 16 Homo sapiens 116-120
9234742-7 1997 Deletion of the PLZF POZ domain partially abrogated the inhibitory effect of PLZF-RAR alpha on RA-induced differentiation and on RA-mediated type II TGase up-regulation, suggesting that POZ-mediated protein interactions might be responsible for the inhibitory transcriptional activities of PLZF-RAR alpha. Tretinoin 82-84 zinc finger and BTB domain containing 16 Homo sapiens 16-20
9234742-7 1997 Deletion of the PLZF POZ domain partially abrogated the inhibitory effect of PLZF-RAR alpha on RA-induced differentiation and on RA-mediated type II TGase up-regulation, suggesting that POZ-mediated protein interactions might be responsible for the inhibitory transcriptional activities of PLZF-RAR alpha. Tretinoin 82-84 zinc finger and BTB domain containing 16 Homo sapiens 77-81
9234742-7 1997 Deletion of the PLZF POZ domain partially abrogated the inhibitory effect of PLZF-RAR alpha on RA-induced differentiation and on RA-mediated type II TGase up-regulation, suggesting that POZ-mediated protein interactions might be responsible for the inhibitory transcriptional activities of PLZF-RAR alpha. Tretinoin 82-84 zinc finger and BTB domain containing 16 Homo sapiens 77-81
9263583-2 1997 In the mouse embryocarcinoma cell line P19, one of the best established systems to study neurogenesis in vitro, it was shown by RT-PCR and in situ hybridization that the neuronal differentiation process, induced by retinoic acid, is characterized by an early increase in the expression of mGluR3, mGluR7 and mGluR8 and a late rise in the mRNA levels of mGluR1 and mGluR5, whereas mGluR2 and mGluR4 seem to be constitutively expressed. Tretinoin 215-228 glutamate receptor, ionotropic, AMPA3 (alpha 3) Mus musculus 289-295
9233805-7 1997 We furthermore identified a retinoic acid response element (RARE) in the sonic hedgehog upstream region which can be bound by retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers in vitro and confers retinoic acid inducibility to the sonic hedgehog promoter in the HeLa cell system. Tretinoin 28-41 retinoid X receptor alpha Homo sapiens 159-178
9233805-7 1997 We furthermore identified a retinoic acid response element (RARE) in the sonic hedgehog upstream region which can be bound by retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers in vitro and confers retinoic acid inducibility to the sonic hedgehog promoter in the HeLa cell system. Tretinoin 28-41 retinoid X receptor alpha Homo sapiens 180-183
9233805-7 1997 We furthermore identified a retinoic acid response element (RARE) in the sonic hedgehog upstream region which can be bound by retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers in vitro and confers retinoic acid inducibility to the sonic hedgehog promoter in the HeLa cell system. Tretinoin 126-139 retinoid X receptor alpha Homo sapiens 180-183
9223123-10 1997 After RA dosing, cyclin protein inhibitors (p16, p21, p27) revealed robust labeling with their respective antibodies in Y/AL and O/DR rats as analyzed by Western blotting. Tretinoin 6-8 proliferating cell nuclear antigen Rattus norvegicus 17-23
9223123-10 1997 After RA dosing, cyclin protein inhibitors (p16, p21, p27) revealed robust labeling with their respective antibodies in Y/AL and O/DR rats as analyzed by Western blotting. Tretinoin 6-8 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 44-47
9223123-10 1997 After RA dosing, cyclin protein inhibitors (p16, p21, p27) revealed robust labeling with their respective antibodies in Y/AL and O/DR rats as analyzed by Western blotting. Tretinoin 6-8 KRAS proto-oncogene, GTPase Rattus norvegicus 49-52
9223123-11 1997 The O/AL animals showed marginally detectable antibody recognition of the cyclin inhibitors after RA dosing. Tretinoin 98-100 proliferating cell nuclear antigen Rattus norvegicus 74-80
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 0-23 transforming growth factor beta 2 Homo sapiens 55-64
9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 25-29 transforming growth factor beta 2 Homo sapiens 55-64
9184230-1 1997 The vigorous retinoic acid (RA)-dependent activation of the retinoic acid receptor beta2 (RARbeta2) gene in embryonal carcinoma (EC) cells is mediated by retinoid receptor heterodimers (RXR-RAR) binding to RAREs that are closely positioned to the TATA box and an EC cell-specific co-factor activity termed E1A-LA. Tretinoin 13-26 retinoid X receptor alpha Homo sapiens 186-189
9184230-1 1997 The vigorous retinoic acid (RA)-dependent activation of the retinoic acid receptor beta2 (RARbeta2) gene in embryonal carcinoma (EC) cells is mediated by retinoid receptor heterodimers (RXR-RAR) binding to RAREs that are closely positioned to the TATA box and an EC cell-specific co-factor activity termed E1A-LA. Tretinoin 28-30 retinoid X receptor alpha Homo sapiens 186-189
9097972-2 1997 Retinoids that activated RXR alpha inhibited cell growth in the range as all-trans-retinoic acid and 9-cis-retinoic acid. Tretinoin 73-96 retinoid X receptor alpha Homo sapiens 25-34
9165121-6 1997 Finally, Xotx1 and Xotx2 are activated by factors involved in head formation and repressed by a posteriorizing signal like retinoic acid. Tretinoin 123-136 orthodenticle homeobox 2 S homeolog Xenopus laevis 19-24
9097025-2 1997 Retinoid signaling involves a two-step metabolic event in which retinol is first converted to retinal, and then retinal is converted to the active ligand retinoic acid, which modulates the transcriptional activity of a nuclear retinoic acid receptor (RAR). Tretinoin 154-167 retinoic acid receptor, alpha Mus musculus 251-254
9097025-10 1997 On the other hand, RAR alpha and RAR gamma expression is widespread and present at E6.5 prior to retinoic acid detection. Tretinoin 97-110 retinoic acid receptor, alpha Mus musculus 19-28
9097025-10 1997 On the other hand, RAR alpha and RAR gamma expression is widespread and present at E6.5 prior to retinoic acid detection. Tretinoin 97-110 retinoic acid receptor, gamma Mus musculus 33-42
9209396-1 1997 We have constructed dominant-negative retinoic acid receptors (RARs) by substituting single amino acid which has been found in a dominant-negative thyroid hormone receptor, and have expressed the dominant-negative RAR in the epidermis, a potential target organ of retinoic acid (RA). Tretinoin 38-51 retinoic acid receptor, alpha Mus musculus 63-66
9050783-7 1997 However, in Pax6(Sey-Neu)/ Pax6(Sey-Neu) embryos, retinoic acid (RA) is not produced by the frontonasal mesenchyme, which normally provides local retinoid signals to the placode and forebrain. Tretinoin 50-63 neuralized E3 ubiquitin protein ligase 1 Homo sapiens 36-39
9078282-1 1997 Transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK) is stimulated by cAMP, the thyroid hormone tri-iodothyronine (T3) and retinoic acid (RA). Tretinoin 142-155 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 30-63
9078282-1 1997 Transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK) is stimulated by cAMP, the thyroid hormone tri-iodothyronine (T3) and retinoic acid (RA). Tretinoin 142-155 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 65-70
9078282-1 1997 Transcription of the gene for phosphoenolpyruvate carboxykinase (PEPCK) is stimulated by cAMP, the thyroid hormone tri-iodothyronine (T3) and retinoic acid (RA). Tretinoin 157-159 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 30-63
8999826-2 1997 It has been suggested that electrostatic interactions are critical for binding of retinoic acid by cellular retinoic acid-binding proteins (CRABP-I and CRABP-II). Tretinoin 82-95 cellular retinoic acid binding protein 2 Homo sapiens 152-160
8999826-3 1997 However, the roles of two conserved arginine residues (Arg-111 and Arg-131 in CRABP-I; Arg-111 and Arg-132 in CRABP-II) that interact with the carboxyl group of retinoic acid have not been evaluated. Tretinoin 161-174 cellular retinoic acid binding protein 2 Homo sapiens 110-118
9121703-0 1997 Increased gene expression of beta-amyloid precursor protein and its homologues APLP1 and APLP2 in human neuroblastoma cells in response to retinoic acid. Tretinoin 139-152 amyloid beta precursor like protein 1 Homo sapiens 79-84
9121703-3 1997 In this paper we show that APLP1 and APLP2 mRNA expression is upregulated during RA-induced differentiation of human SH-SY5Y neuroblastoma cells. Tretinoin 81-83 amyloid beta precursor like protein 1 Homo sapiens 27-32
9049046-0 1997 Retinoic acids and dexamethasone alter cell-surface density of beta 2-integrins and ICAM-1 on human leukemic (HMC-1) mast cells. Tretinoin 0-14 intercellular adhesion molecule 1 Homo sapiens 84-90
9607169-2 1997 The mechanisms involved in the regulation of gene expression by the retinoids is at least partially known and involves binding of the RAR and RXR to retinoic acid response elements. Tretinoin 149-162 retinoid X receptor alpha Homo sapiens 142-145
8971075-2 1997 Glucagon (via the second messenger cAMP), retinoic acid, and glucocorticoids stimulate transcription of the PEPCK gene, whereas insulin and phorbol esters have a dominant inhibitory effect. Tretinoin 42-55 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 108-113
8954975-2 1996 The level of MK mRNA increased in a time-dependent manner in the presence of FSH or retinoic acid (RA). Tretinoin 84-97 midkine Rattus norvegicus 13-15
8954975-2 1996 The level of MK mRNA increased in a time-dependent manner in the presence of FSH or retinoic acid (RA). Tretinoin 99-101 midkine Rattus norvegicus 13-15
8922411-5 1996 Sequence analysis of the apoE promoter indicated the presence of several AP-2 consensus sequences that could mediate the stimulatory effect of cAMP and retinoic acid. Tretinoin 152-165 transcription factor AP-2 alpha Homo sapiens 73-77
8950195-0 1996 Retinoic acid affects the expression rate of the differentiation-related genes aryl hydrocarbon receptor, ARNT and keratin 4 in proliferative keratinocytes only. Tretinoin 0-13 keratin 4 Homo sapiens 115-124
8950195-6 1996 When keratinocytes were continuously treated with 1 microM retinoic acid (RA), the upregulation of AhR- and ARNT-mRNA levels was inhibited as was keratin 4-expression, a marker of HaCaT-keratinocyte differentiation. Tretinoin 59-72 keratin 4 Homo sapiens 146-155
8950195-6 1996 When keratinocytes were continuously treated with 1 microM retinoic acid (RA), the upregulation of AhR- and ARNT-mRNA levels was inhibited as was keratin 4-expression, a marker of HaCaT-keratinocyte differentiation. Tretinoin 74-76 keratin 4 Homo sapiens 146-155
8950195-9 1996 Our data suggest that the regulation of AhR-, ARNT- and keratin 4-expression by RA is indirect and mediated by a yet to be identified factor. Tretinoin 80-82 keratin 4 Homo sapiens 56-65
8977666-3 1996 Five weeks of topical RA led to thickening of the spinous and granular compartments, induction of keratins K6, K16 and K17, and suppression of filaggrin expression. Tretinoin 22-24 keratin 17 Mus musculus 119-122
8982867-1 1996 Rae1 alpha, Rae1 beta, and Rae1 gamma cDNAs isolated from retinoic acid-treated mouse embryonal carcinoma F9 cells encode cell surface proteins sharing partial homology with MHC class I molecules, and mRNAs corresponding to these cDNAs were detected exclusively in early mouse embryos, especially in the head region. Tretinoin 58-71 retinoic acid early transcript gamma Mus musculus 27-37
8794365-7 1996 These observations support the existence of two distinct retinoid signalling pathways predicted on the basis of biochemical and pharmacologic studies and provide direct evidence that the programs of differentiation elicited by retinoic acid in these cells are mediated by a specific subset of binding sites for RAR-RXR heterodimers. Tretinoin 227-240 retinoid X receptor alpha Homo sapiens 315-318
8891892-0 1996 Retinoic acid stimulates expression of the functional osteoclast integrin alpha v beta 3: transcriptional activation of the beta 3 but not the alpha v gene. Tretinoin 0-13 integrin subunit alpha V Homo sapiens 65-88
8876671-0 1996 Protection against malignant conversion in SENCAR mouse skin by all trans retinoic acid: inhibition of the ras p21-processing enzyme farnesyltransferase and Ha-ras p21 membrane localization. Tretinoin 74-87 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 111-114
8876671-0 1996 Protection against malignant conversion in SENCAR mouse skin by all trans retinoic acid: inhibition of the ras p21-processing enzyme farnesyltransferase and Ha-ras p21 membrane localization. Tretinoin 74-87 Harvey rat sarcoma virus oncogene Mus musculus 157-163
8876671-0 1996 Protection against malignant conversion in SENCAR mouse skin by all trans retinoic acid: inhibition of the ras p21-processing enzyme farnesyltransferase and Ha-ras p21 membrane localization. Tretinoin 74-87 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 164-167
8876671-5 1996 In this study, we assessed whether the protective effect of RA against malignant conversion involves the inhibition of ras p21 processing in those tumors that contain the activated ras oncogene. Tretinoin 60-62 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 123-126
8876671-8 1996 Furthermore, the tissue samples from RA-treated groups in different protocols also showed significantly diminished membrane localization of Ha-ras p21, with a concomitant increase in cytosolic Ha-ras p21 levels. Tretinoin 37-39 Harvey rat sarcoma virus oncogene Mus musculus 140-146
8876671-8 1996 Furthermore, the tissue samples from RA-treated groups in different protocols also showed significantly diminished membrane localization of Ha-ras p21, with a concomitant increase in cytosolic Ha-ras p21 levels. Tretinoin 37-39 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 147-150
8876671-8 1996 Furthermore, the tissue samples from RA-treated groups in different protocols also showed significantly diminished membrane localization of Ha-ras p21, with a concomitant increase in cytosolic Ha-ras p21 levels. Tretinoin 37-39 Harvey rat sarcoma virus oncogene Mus musculus 193-199
8876671-8 1996 Furthermore, the tissue samples from RA-treated groups in different protocols also showed significantly diminished membrane localization of Ha-ras p21, with a concomitant increase in cytosolic Ha-ras p21 levels. Tretinoin 37-39 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 200-203
8876671-10 1996 Taken together, these results indicate a strong correlation between the inhibition of ras p21 farnesylation because of a decrease in FTase activity by RA and its protective effect against malignant conversion of papillomas to carcinomas. Tretinoin 151-153 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 90-93
8931111-5 1996 These results strongly suggest that RA suppresses the phospholipase D activated by PGF2 alpha in osteoblast-like cells and that the effect of RA is exerted at the point between PGF2 alpha receptor and G-protein. Tretinoin 142-144 prostaglandin F receptor Mus musculus 177-196
8784454-0 1996 Synthesis and structure-activity relationships of retinoid X receptor selective diaryl sulfide analogs of retinoic acid. Tretinoin 106-119 retinoid X receptor alpha Homo sapiens 50-69
8754738-17 1996 RA alone reduced TBG secretion to 76% of the control value. Tretinoin 0-2 serpin family A member 7 Homo sapiens 17-20
8709642-2 1996 All-trans retinoic acid (ATRA) and 1 alpha, 25 dihydroxyvitamin D3 (VD3) induce differentiation of HL60 cells into CD11b+ mature granulocytes and monocytes, respectively. Tretinoin 0-23 integrin subunit alpha M Homo sapiens 115-120
8709642-2 1996 All-trans retinoic acid (ATRA) and 1 alpha, 25 dihydroxyvitamin D3 (VD3) induce differentiation of HL60 cells into CD11b+ mature granulocytes and monocytes, respectively. Tretinoin 25-29 integrin subunit alpha M Homo sapiens 115-120
8709642-5 1996 In contrast, the VD3-treated CD11b- HL60 cells, which failed to undergo differentiation and human erythroleukemic cell line K562, exposed to ATRA retained high levels of telomerase activity. Tretinoin 141-145 integrin subunit alpha M Homo sapiens 29-34
8913320-4 1996 9-cis RA, a high-affinity ligand for RXR, greatly enhanced D3-induced CD14 expression in U937 cells, while RA alone did not induce CD14 expression. Tretinoin 6-8 retinoid X receptor alpha Homo sapiens 37-40
8755574-3 1996 Clinical remissions induced with all-trans retinoic acid (RA) treatment in acute promyelocytic leukemia are linked to PML/RARalpha expression in leukemic cells. Tretinoin 43-56 retinoic acid receptor, alpha Mus musculus 122-130
8755574-15 1996 Retinoic acid treatment of irradiated PML/RARalpha mice enhanced granulocyte recovery. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 42-50
8974789-9 1996 The resistance of malignant cells to apoptosis, in Chronic Myeloid Leukemia, due to bcr-abl oncogene, has been partially explained by conformational changes in p53 expression and is reversed by retinoic acid. Tretinoin 194-207 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 84-91
8687453-3 1996 Continuous treatment of the keratinocyte cell cultures with retinoic acid (RA) resulted in a premature downregulation of AP-2 mRNA levels, and the transcripts of K4 and AhR remained at basal levels. Tretinoin 75-77 transcription factor AP-2 alpha Homo sapiens 121-125
8687453-5 1996 The data suggest a role for AP-2 as an intermediate factor in the pathway of RA action in keratinocyte differentiation, explaining both the downregulation of K4 and AhR transcript levels in proliferative keratinocytes and the loss of RA effects in already differentiated cells. Tretinoin 77-79 transcription factor AP-2 alpha Homo sapiens 28-32
8687453-5 1996 The data suggest a role for AP-2 as an intermediate factor in the pathway of RA action in keratinocyte differentiation, explaining both the downregulation of K4 and AhR transcript levels in proliferative keratinocytes and the loss of RA effects in already differentiated cells. Tretinoin 77-79 keratin 4 Homo sapiens 158-160
8687453-5 1996 The data suggest a role for AP-2 as an intermediate factor in the pathway of RA action in keratinocyte differentiation, explaining both the downregulation of K4 and AhR transcript levels in proliferative keratinocytes and the loss of RA effects in already differentiated cells. Tretinoin 234-236 transcription factor AP-2 alpha Homo sapiens 28-32
8687458-6 1996 mRNAs encoding the neural genes Wnt-1, MASH1, the light and medium isoforms of neurofilaments, and the neurotransmitter-synthesizing enzyme glutamic acid decarboxylase are all strongly upregulated by retinoic acid treatment; expression of these genes occurs in a temporal pattern resembling that in the developing brain. Tretinoin 200-213 achaete-scute family bHLH transcription factor 1 Mus musculus 39-44
8674128-3 1996 All trans retinoic acid (RA) enhanced the production of IgA at high concentrations (10-100 nM) in the presence of IL-5. Tretinoin 10-23 immunoglobulin heavy constant alpha Mus musculus 56-59
8674128-3 1996 All trans retinoic acid (RA) enhanced the production of IgA at high concentrations (10-100 nM) in the presence of IL-5. Tretinoin 25-27 immunoglobulin heavy constant alpha Mus musculus 56-59
8655595-1 1996 Retinoic acid receptor (RAR) alpha and gamma mRNAs were constitutively expressed in B16 melanoma cells with or without retinoic acid (RA) treatment. Tretinoin 119-132 retinoic acid receptor, alpha Mus musculus 0-22
8655595-1 1996 Retinoic acid receptor (RAR) alpha and gamma mRNAs were constitutively expressed in B16 melanoma cells with or without retinoic acid (RA) treatment. Tretinoin 119-132 retinoic acid receptor, alpha Mus musculus 24-27
8655595-1 1996 Retinoic acid receptor (RAR) alpha and gamma mRNAs were constitutively expressed in B16 melanoma cells with or without retinoic acid (RA) treatment. Tretinoin 24-26 retinoic acid receptor, alpha Mus musculus 0-22
8738758-3 1996 In this study we use Northern blot analysis, double-label immunocytochemistry, and single cell RNA analysis using polymerase chain reaction to show that RA-treated P19 cells with neuronal-like morphology also express neuronal nicotinic acetylcholine receptor (nAChR) subunits alpha 3, alpha 4, and beta 2. Tretinoin 153-155 immunoglobulin binding protein 1 Homo sapiens 285-292
8738758-4 1996 Greater than 80% of RA-treated P19 cells with a neuronal-like phenotype express nAChR alpha 4 subunit transcripts and both alpha 4 and beta 2 protein. Tretinoin 20-22 immunoglobulin binding protein 1 Homo sapiens 86-93
8738758-4 1996 Greater than 80% of RA-treated P19 cells with a neuronal-like phenotype express nAChR alpha 4 subunit transcripts and both alpha 4 and beta 2 protein. Tretinoin 20-22 immunoglobulin binding protein 1 Homo sapiens 123-141
9019245-8 1996 RA-treated embryos were subsequently analyzed for appropriate cardiac myocyte differentiation using antibody staining and ELISA analysis to detect sarcomeric myosin heavy chain, tropomyosin, titin, and alpha-actinin protein expression. Tretinoin 0-2 titin Gallus gallus 191-196
8735598-5 1996 In parallel, we demonstrated that the choriocarcinoma cells JEG 3, which respond to RA by an increase in hCG secretion, express constitutively high levels of RXR alpha protein. Tretinoin 84-86 retinoid X receptor alpha Homo sapiens 158-167
8735598-6 1996 Furthermore, RXR alpha-transfected trophoblastic cells also become RA responsive for hCG secretion. Tretinoin 67-69 retinoid X receptor alpha Homo sapiens 13-22
8735598-7 1996 All these data suggest that RXR alpha expression is modulated by EGF, and may be involved in the effect of RA on hCG secretion. Tretinoin 107-109 retinoid X receptor alpha Homo sapiens 28-37
8605358-7 1996 Furthermore, A-NB4 cells were capable of differentiating when treated with all-trans retinoic acid (ATRA), as manifested by enhanced NBT reduction and CD11b expression. Tretinoin 85-98 integrin subunit alpha M Homo sapiens 151-156
8605358-7 1996 Furthermore, A-NB4 cells were capable of differentiating when treated with all-trans retinoic acid (ATRA), as manifested by enhanced NBT reduction and CD11b expression. Tretinoin 100-104 integrin subunit alpha M Homo sapiens 151-156
8620495-2 1996 All-trans-retinoic acid exerts its effects by activation of retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 0-23 retinoid X receptor alpha Homo sapiens 93-112
8620495-2 1996 All-trans-retinoic acid exerts its effects by activation of retinoic acid receptor (RAR) and retinoid X receptor (RXR) heterodimers. Tretinoin 0-23 retinoid X receptor alpha Homo sapiens 114-117
8790944-0 1996 Induction of mcl1/EAT, Bcl-2 related gene, by retinoic acid or heat shock in the human embryonal carcinoma cells, NCR-G3. Tretinoin 46-59 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 114-117
8790944-1 1996 NCR-G3 cells were established from a testicular embryonal carcinoma and were differentiated into multi-lineages including trophectoderm cells by exposure to retinoic acid. Tretinoin 157-170 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 0-3
8790944-3 1996 As we assumed that genes responsible for differentiation were differentially expressed at the early stage of retinoic acid-induced differentiation, we prepared a cDNA library from retinoic acid-treated NCR-G3 cells. Tretinoin 180-193 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 202-205
8626419-0 1996 Identification and charaterization of the second retinoic acid response element in the phosphoenolpyruvate carboxykinase gene promoter. Tretinoin 49-62 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 87-120
8626419-1 1996 A previously characterized retinoic acid response element (RARE1) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter confers approximately 50% of the response of this gene to retinoic acid (RA). Tretinoin 27-40 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 73-106
8626419-1 1996 A previously characterized retinoic acid response element (RARE1) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter confers approximately 50% of the response of this gene to retinoic acid (RA). Tretinoin 27-40 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 108-113
8626419-1 1996 A previously characterized retinoic acid response element (RARE1) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter confers approximately 50% of the response of this gene to retinoic acid (RA). Tretinoin 187-200 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 73-106
8626419-1 1996 A previously characterized retinoic acid response element (RARE1) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter confers approximately 50% of the response of this gene to retinoic acid (RA). Tretinoin 187-200 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 108-113
8626419-1 1996 A previously characterized retinoic acid response element (RARE1) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter confers approximately 50% of the response of this gene to retinoic acid (RA). Tretinoin 59-61 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 73-106
8626419-1 1996 A previously characterized retinoic acid response element (RARE1) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter confers approximately 50% of the response of this gene to retinoic acid (RA). Tretinoin 59-61 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 108-113
8882470-1 1996 Elastin expression in cultured vascular smooth muscle cell (VSMC) was found to be enhanced by potent inhibitors of VSMC proliferation including minoxidil, heparin and retinoic acid. Tretinoin 167-180 elastin Homo sapiens 0-7
8622645-7 1996 Conversely, when VDR is overexpressed, vitamin D3 attenuates 9-cis RA induction from an RXR-responsive element. Tretinoin 67-69 vitamin D receptor Homo sapiens 17-20
8622645-7 1996 Conversely, when VDR is overexpressed, vitamin D3 attenuates 9-cis RA induction from an RXR-responsive element. Tretinoin 67-69 retinoid X receptor alpha Homo sapiens 88-91
8630264-16 1996 Interestingly, RA enhanced mucin secretion by SPOC1 cells during the early plateau stage of culture but there were no differences due to RA late in the culture period. Tretinoin 15-17 solute carrier family 13 member 2 Rattus norvegicus 27-32
8708944-0 1996 Influence of retinoic acid on the expression of cytokeratins, vimentin and ICAM-1 in human gingival epithelia in vitro. Tretinoin 13-26 intercellular adhesion molecule 1 Homo sapiens 75-81
8708944-8 1996 The results showed that RA had minor effects on the marker expression of JE but markedly enhanced expression of cytokeratins 8, 18, 19, vimentin and ICAM-1 in OGE. Tretinoin 24-26 intercellular adhesion molecule 1 Homo sapiens 149-155
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 79-92 cellular retinoic acid binding protein 2 Homo sapiens 244-252
8615638-2 1996 Recently we reported that interferon-gamma (IFN-gamma) modulates the action of retinoic acid (RA): IFN-gamma increased expression of retinoic acid receptor-gamma (RAR-gamma) and suppressed the increase of retinoic acid binding protein type II (CRABP-II) expression. Tretinoin 94-96 cellular retinoic acid binding protein 2 Homo sapiens 244-252
8615638-7 1996 In contrast with SKBR-3 and BT-20 cells a combination of ATRA with IFN-alpha markedly reduced ATRA mediated CRABP II induction. Tretinoin 57-61 cellular retinoic acid binding protein 2 Homo sapiens 108-116
8615638-7 1996 In contrast with SKBR-3 and BT-20 cells a combination of ATRA with IFN-alpha markedly reduced ATRA mediated CRABP II induction. Tretinoin 94-98 cellular retinoic acid binding protein 2 Homo sapiens 108-116
8615638-8 1996 These results suggest that two factors may be responsible for synergistic action of RA and IFN-alpha: the inhibition of the CRABP II expression and an IFN-alpha/RA mediated upregulation of RAR-gamma. Tretinoin 84-86 cellular retinoic acid binding protein 2 Homo sapiens 124-132
8931954-7 1996 Following 4 days of maturation with ATRA, the cells would increase F-actin content in response to interleukin-8, ingest latex beads, migrate in a chemotaxis chamber, reduce NBT, and express CD11b. Tretinoin 36-40 integrin subunit alpha M Homo sapiens 190-195
8866697-1 1996 We determined the effects of all-trans retinoic acid (RA) on the levels of delta opioid receptor (DOR) mRNA and N-Methyl-D-Aspartate receptor (NMDAR1) mRNA in neuroblastoma x glioma hybrid cells (NG108-15) by use of quantitative solution hybridization assays. Tretinoin 39-52 opioid receptor, delta 1 Mus musculus 75-96
8866697-1 1996 We determined the effects of all-trans retinoic acid (RA) on the levels of delta opioid receptor (DOR) mRNA and N-Methyl-D-Aspartate receptor (NMDAR1) mRNA in neuroblastoma x glioma hybrid cells (NG108-15) by use of quantitative solution hybridization assays. Tretinoin 54-56 opioid receptor, delta 1 Mus musculus 75-96
8866697-1 1996 We determined the effects of all-trans retinoic acid (RA) on the levels of delta opioid receptor (DOR) mRNA and N-Methyl-D-Aspartate receptor (NMDAR1) mRNA in neuroblastoma x glioma hybrid cells (NG108-15) by use of quantitative solution hybridization assays. Tretinoin 54-56 opioid receptor, delta 1 Mus musculus 98-101
8866697-3 1996 At 10 microM RA a 3-fold increase in DOR mRNA at 48 h, and later (144 h) alterations were observed in NMDAR1 mRNA levels. Tretinoin 13-15 opioid receptor, delta 1 Mus musculus 37-40
8723391-4 1996 Human thyroid hormone, retinoic acid, vitamin D, and several orphan receptors prefer to work as heterodimers with retinoic X receptor (RXR). Tretinoin 23-36 retinoid X receptor alpha Homo sapiens 135-138
8808408-1 1996 Using a differential subtractive hybridization cloning procedure we have recently identified the AP-2.2 gene as a novel early retinoic acid-induced gene in murine P19 embryonal carcinoma cells. Tretinoin 126-139 transcription factor AP-2, gamma Mus musculus 97-103
8524212-5 1995 In contrast, at the same concentrations, various combinations of RAR (RAR alpha, RAR beta, or RAR gamma) and RXR selective retinoids resulted in synergistic induction of all retinoic acid (RA) target genes examined, as well as in cell differentiation. Tretinoin 174-187 retinoid X receptor alpha Homo sapiens 109-112
8582598-10 1995 The uptake of labeled RA correlated well with RAR or RAR alpha concentration in the corresponding tissues. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 46-49
8582598-10 1995 The uptake of labeled RA correlated well with RAR or RAR alpha concentration in the corresponding tissues. Tretinoin 22-24 retinoic acid receptor, alpha Mus musculus 53-62
7565739-2 1995 For ligand-induced activation by the retinoic acid receptor-retinoid X receptor (RAR-RXR) heterodimer, the RAR beta 2 promoter is dependent on the presence of E1A or E1A-like activity, since this promoter is activated by retinoic acid only in cells expressing such proteins. Tretinoin 37-50 retinoid X receptor alpha Homo sapiens 85-88
7488024-1 1995 In this study, we analyzed the role of the TATA box in the regulation of the phosphoenolpyruvate carboxykinase (PEPCK) gene expression by dexamethasone (DEX), retinoic acid (RA), glucagon (via cAMP) and insulin (INS). Tretinoin 159-172 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 77-110
7488024-1 1995 In this study, we analyzed the role of the TATA box in the regulation of the phosphoenolpyruvate carboxykinase (PEPCK) gene expression by dexamethasone (DEX), retinoic acid (RA), glucagon (via cAMP) and insulin (INS). Tretinoin 159-172 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 112-117
7657606-6 1995 However, a specific cis-acting retinoic acid responsive element of the DR1 type was identified in the proximal region (-385) of the ST3 gene promoter. Tretinoin 31-44 matrix metallopeptidase 11 Homo sapiens 132-135
8690727-0 1995 Loss of immunostaining of the RBP-J kappa transcription factor upon F9 cell differentiation induced by retinoic acid. Tretinoin 103-116 retinol binding protein 4 Homo sapiens 30-33
7656983-1 1995 We have found that the gene expression of the ninth member of the fibroblast growth factor (FGF) family, FGF9 was induced during retinoic acid(RA)-induced neuronal differentiation of murine embryonal carcinoma P19 cells. Tretinoin 129-142 fibroblast growth factor 9 Homo sapiens 92-95
7662588-7 1995 All-trans-retinoic acid, the progesterone analog R-5020, and prednisone were found to induce heterologous up-regulation of the VDR. Tretinoin 0-23 vitamin D receptor Homo sapiens 127-130
7631783-0 1995 Marked resistance of RAR gamma-deficient mice to the toxic effects of retinoic acid. Tretinoin 70-83 retinoic acid receptor, gamma Mus musculus 21-30
7631783-2 1995 To test the role of the nuclear retinoic acid receptor (RAR gamma) in this process we produced mice with a targeted disruption of the RAR gamma gene and examined toxic effects of repeated doses of retinoic acid and two other synthetic retinoids, Ro 15-1570 and Ro 40-6055. Tretinoin 32-45 retinoic acid receptor, gamma Mus musculus 56-65
7601313-2 1995 To better understand the early steps of development of paired fin buds in fish, we have analyzed the regulation of the zebrafish Sonic hedgehog gene (shh/vhh-1) in response to retinoic acid. Tretinoin 176-189 sonic hedgehog signaling molecule a Danio rerio 150-153
7601313-2 1995 To better understand the early steps of development of paired fin buds in fish, we have analyzed the regulation of the zebrafish Sonic hedgehog gene (shh/vhh-1) in response to retinoic acid. Tretinoin 176-189 sonic hedgehog signaling molecule a Danio rerio 154-159
7601313-3 1995 Systemic administration of retinoic acid (RA) to zebrafish embryos during the initial stages of pectoral fin bud development resulted in the induction of ectopic expression of shh/vhh-1 on the anterior margin of the bud under the apical ectodermal ridge and in abnormal pectoral fin bud morphology. Tretinoin 27-40 sonic hedgehog signaling molecule a Danio rerio 176-179
7601313-3 1995 Systemic administration of retinoic acid (RA) to zebrafish embryos during the initial stages of pectoral fin bud development resulted in the induction of ectopic expression of shh/vhh-1 on the anterior margin of the bud under the apical ectodermal ridge and in abnormal pectoral fin bud morphology. Tretinoin 27-40 sonic hedgehog signaling molecule a Danio rerio 180-185
7476969-8 1995 In contrast, the S369A mutation slightly decreased both DNA binding and the efficiency of PKA to enhance RA-induced transactivation by RAR alpha 1. Tretinoin 105-107 retinoic acid receptor, alpha Mus musculus 135-146
7794283-0 1995 Adrenocortical steroids, thyroid hormones and retinoic acid augment the production of adrenomedullin in vascular smooth muscle cells. Tretinoin 46-59 adrenomedullin Rattus norvegicus 86-100
7775578-3 1995 Expression of retinoic acid receptors (RAR) was also affected by RA treatment, specifically RAR gamma transcripts were induced. Tretinoin 39-41 retinoic acid receptor, gamma Mus musculus 92-101
7737364-0 1995 Transcriptional modulation of the human intercellular adhesion molecule gene I (ICAM-1) by retinoic acid in melanoma cells. Tretinoin 91-104 intercellular adhesion molecule 1 Homo sapiens 80-86
7738355-8 1995 These data suggest that RAR-gamma is an important regulator of retinoic acid efficacy in skin and further, that the irritation associated with the use of retinoids is most likely a receptor-mediated process. Tretinoin 63-76 retinoic acid receptor, gamma Mus musculus 24-33
7669688-10 1995 Retinoic acid treatment during epiboly alters the hindbrain domains of pou-2, suggesting that the entire anterior hindbrain acquires r4-like properties. Tretinoin 0-13 POU domain, class 5, transcription factor 3 Danio rerio 71-76
7712490-5 1995 We find that the addition of BDNF to SY5Y cells induced to express p145TrkB by retinoic acid treatment does not significantly affect cell proliferation yet will support cell survival. Tretinoin 79-92 brain derived neurotrophic factor Homo sapiens 29-33
7713893-2 1995 Although the basis for the oncogenic action of v-ErbA is unknown, expression of this protein is known to inhibit thyroid hormone and retinoic acid induction of target genes. Tretinoin 133-146 thyroid hormone receptor alpha Homo sapiens 49-53
7705655-4 1995 In this respect they are similar to heterodimers formed between RXR and the receptor for all-trans retinoic acid, RAR. Tretinoin 99-112 retinoid X receptor alpha Homo sapiens 64-67
7532580-5 1995 Treatment with retinoic acid (RA, 100 nM) increased medium concentrations of IGFBP-3 to 175 +/- 8% (mean +/- SE, n = 4), and IGFBP-6 to 217 +/- 20% of control values. Tretinoin 15-28 insulin like growth factor binding protein 6 Homo sapiens 125-132
7605750-4 1995 Using probes for zebrafish krx20 and pax2, it is demonstrated that retinoic acid affects the expression domains of these regulatory genes in a manner that is consistent with the neuroanatomical data. Tretinoin 67-80 paired box 2a Danio rerio 37-41
7862171-6 1995 GAL4-RXR activates transcription from GAL4 response elements in the presence of 9-cis RA. Tretinoin 86-88 galectin 4 Homo sapiens 0-4
7862171-6 1995 GAL4-RXR activates transcription from GAL4 response elements in the presence of 9-cis RA. Tretinoin 86-88 retinoid X receptor alpha Homo sapiens 5-8
7862171-6 1995 GAL4-RXR activates transcription from GAL4 response elements in the presence of 9-cis RA. Tretinoin 86-88 galectin 4 Homo sapiens 38-42
28306119-8 1995 In situ hybridization experiments showed that RXR-alpha transcripts were present throughout the epithelium and mesenchyme of the chick wing bud at stages when retinoic acid can affect a-p patterning. Tretinoin 159-172 retinoid X receptor alpha Gallus gallus 46-55
28306119-10 1995 These data suggest that RXR-alpha, but not RXR-gamma, could mediate the effects of locally applied retinoic acid on a-p patterning in the chick wing bud. Tretinoin 99-112 retinoid X receptor alpha Gallus gallus 24-33
7852380-4 1995 In cultured keratinocytes, all-trans retinoic acid, 9-cis retinoic acid, and CD367 activated beta RARE but not RXRE via endogenous RAR.RXR (ED50 = 2.3, 3.8, and 0.3 nM, respectively) whereas SR11237 showed no significant effect. Tretinoin 37-50 retinoid X receptor alpha Homo sapiens 111-114
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 10-23 retinoid X receptor alpha Homo sapiens 68-71
7852380-5 1995 All-trans retinoic acid, 9-cis retinoic acid, and SR11237 activated RXRE via overexpressed RXR.RXR (ED50 = 110, 120, and 11 nM, respectively), indicating interconversion between retinoic acid isomers, whereas co-overexpression of RAR alpha or RAR gamma suppressed this activation. Tretinoin 10-23 retinoid X receptor alpha Homo sapiens 91-94
21153145-5 1995 The all-trans and 9-cis retinoic acids alone each caused increased ALPA of IEC-6 cells without altering steady-state levels of ALP mRNA, suggesting that retinoic acids may regulate ALPA of IEC-6 cells at a posttranscriptional level. Tretinoin 24-38 PDZ and LIM domain 3 Rattus norvegicus 67-70
7826398-1 1995 We have identified and sequenced a new gene from human cells that is responsive to DNA damage and retinoic acid treatment, and it is highly expressed in brain and reproductive organs (BRE). Tretinoin 98-111 BRISC and BRCA1 A complex member 2 Homo sapiens 184-187
8001276-11 1995 Retinoic acid induced an increase in PKC-alpha expression together with a more differentiated phenotype. Tretinoin 0-13 protein kinase C, alpha Rattus norvegicus 37-46
7586754-5 1995 Exogenous retinoic acid, a teratogen that is known to affect the formation of the midbrain-hindbrain boundary, has a profound affect on both wnt1 and pax2 expression at gastrulation. Tretinoin 10-23 paired box 2a Danio rerio 150-154
7706939-7 1995 Treatment of both primary and BFC-1 beta adipocytes with triiodothyronine alone had no effect on CRBP mRNA levels; however, when adipocytes were treated with a mixture of triiodothyronine and retinoic acid, the induction of CRBP mRNA levels by retinoic acid was reduced. Tretinoin 192-205 retinol binding protein 1 Rattus norvegicus 224-228
7706939-8 1995 In summary, these studies indicate that CRBP gene expression is regulated by retinoic acid, dexamethasone, and triiodothyronine; thus suggesting that retinol uptake, intracellular transport, and metabolism are dynamically regulated in adipocytes. Tretinoin 77-90 retinol binding protein 1 Rattus norvegicus 40-44
7719245-13 1995 The comparison of the biological activities mediated by PML-RAR alpha and PLZF-RAR alpha may give new insights into the pathogenesis as well as the mechanisms of ATRA-induced differentiation in APL. Tretinoin 162-166 zinc finger and BTB domain containing 16 Homo sapiens 74-78
8688195-1 1995 The three retinoic acid receptors (RAR alpha, RAR beta and RAR gamma) are known to modulate the transcription of target genes through interaction of the individual receptors with their naturally occurring ligand, retinoic acid (RA). Tretinoin 10-23 retinoic acid receptor, alpha Mus musculus 35-44
8688195-1 1995 The three retinoic acid receptors (RAR alpha, RAR beta and RAR gamma) are known to modulate the transcription of target genes through interaction of the individual receptors with their naturally occurring ligand, retinoic acid (RA). Tretinoin 10-23 retinoic acid receptor, gamma Mus musculus 59-68
8688195-1 1995 The three retinoic acid receptors (RAR alpha, RAR beta and RAR gamma) are known to modulate the transcription of target genes through interaction of the individual receptors with their naturally occurring ligand, retinoic acid (RA). Tretinoin 35-37 retinoic acid receptor, gamma Mus musculus 59-68
7982932-3 1994 After binding to a direct repeat of this hexamer with a one-base pair spacer, retinoid X receptor homodimers are able to activate transcription in the presence of the ligand 9-cis-retinoic acid. Tretinoin 179-193 retinoid X receptor alpha Homo sapiens 78-97
7697779-0 1994 Synthesis of 9E- and 9Z-locked retinoic acid analogs as ligands for RAR and RXR. Tretinoin 31-44 retinoid X receptor alpha Homo sapiens 76-79
7798613-2 1994 Biologic activity was shown by the induction of cellular retinoic acid-binding protein type 2 (CRABP 2) mRNA and protein; the rank order for CRABP-2 increase was retinoic acid > retinaldehyde > 9 cis retinoic acid > retinol > beta carotene. Tretinoin 57-70 cellular retinoic acid binding protein 2 Homo sapiens 95-102
7970716-0 1994 Retinoic acid suppresses polyoma virus transformation by inhibiting transcription of the c-fos proto-oncogene. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 89-94
7970716-3 1994 In this report we present the results of experiments that demonstrate that retinoic acid does indeed inhibit transcriptional transactivation of the c-fos promoter by polyoma virus, as well as by calf serum and purified serum growth factors. Tretinoin 75-88 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 148-153
7970716-5 1994 Restoration of c-fos expression, even in the presence of retinoic acid, restored transformation, indicating that retinoic acid inhibition of c-fos expression is sufficient to explain the retinoid suppression of transformation. Tretinoin 113-126 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 15-20
7970716-5 1994 Restoration of c-fos expression, even in the presence of retinoic acid, restored transformation, indicating that retinoic acid inhibition of c-fos expression is sufficient to explain the retinoid suppression of transformation. Tretinoin 113-126 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 141-146
7970716-6 1994 These results identify the c-fos proto-oncogene as a key nuclear target for mT-dependent transformation and show that the anticarcinogenic properties of retinoic acid can be brought about by inhibiting c-fos expression. Tretinoin 153-166 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 27-32
7970716-6 1994 These results identify the c-fos proto-oncogene as a key nuclear target for mT-dependent transformation and show that the anticarcinogenic properties of retinoic acid can be brought about by inhibiting c-fos expression. Tretinoin 153-166 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 202-207
7999013-1 1994 Basal and stimulated activity of the c-fos promoter is reduced by triiodothyronine (T3) and retinoic acid (RA) in GH1 cells. Tretinoin 92-105 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 37-42
7999013-1 1994 Basal and stimulated activity of the c-fos promoter is reduced by triiodothyronine (T3) and retinoic acid (RA) in GH1 cells. Tretinoin 107-109 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 37-42
7947970-4 1994 The binding properties of mouse CRABP-I and -II purified from Escherichia coli were examined to further understand their role in intracellular retinoic acid processing. Tretinoin 143-156 cellular retinoic acid binding protein I Mus musculus 32-47
7980440-2 1994 In H4IIE rat hepatoma cells, glucocorticoids, retinoic acid and cyclic AMP (cAMP) increase PEPCK gene transcription whereas insulin and phorbol esters have the opposite effect. Tretinoin 46-59 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 91-96
7525098-4 1994 We have found that the promoter of the K13 gene contains a sequence element GGTTCA(N)5TGTTCT, in the following referred to as K13-RARE, that is highly related to the natural retinoic acid responsive element (RARE) of the retinoic acid receptor beta 2 gene. Tretinoin 174-187 hemoglobin, beta adult minor chain Mus musculus 244-250
7967734-4 1994 In vitro treatment with ATRA consistently increased the expression of CD15, CD11b, and CD45R0 on leukemic promyelocytes; these changes were paralleled by a decrease of CD45RA display. Tretinoin 24-28 integrin subunit alpha M Homo sapiens 76-81
7967734-4 1994 In vitro treatment with ATRA consistently increased the expression of CD15, CD11b, and CD45R0 on leukemic promyelocytes; these changes were paralleled by a decrease of CD45RA display. Tretinoin 24-28 protein tyrosine phosphatase receptor type C Homo sapiens 87-91
7877619-2 1994 In this study we demonstrate that the RA-dependent transcriptional increase in zif268 gene expression is mediated by the interaction of RA receptors (RARs) with a 17 base pair sequence in the zif268 promoter containing a single half-site motif (GTTCA), identical to each of the direct repeats seen in the RAR beta 2 gene. Tretinoin 38-40 retinoic acid receptor, alpha Mus musculus 150-153
7881766-0 1994 Retinoic acid induces expression of PA-FABP (psoriasis-associated fatty acid-binding protein) gene in human skin in vivo but not in cultured skin cells. Tretinoin 0-13 fatty acid binding protein 5 Homo sapiens 36-43
7881766-0 1994 Retinoic acid induces expression of PA-FABP (psoriasis-associated fatty acid-binding protein) gene in human skin in vivo but not in cultured skin cells. Tretinoin 0-13 fatty acid binding protein 5 Homo sapiens 45-92
7881766-2 1994 In this study we demonstrate that PA-FABP transcripts are expressed in human skin in vivo and that topical application of 0.05% retinoic acid (RA) cream results in a rapid induction of PA-FABP transcripts following treatment for 16 hours and persists at increasing levels after 48 and 96 h of RA treatment. Tretinoin 128-141 fatty acid binding protein 5 Homo sapiens 34-41
7881766-2 1994 In this study we demonstrate that PA-FABP transcripts are expressed in human skin in vivo and that topical application of 0.05% retinoic acid (RA) cream results in a rapid induction of PA-FABP transcripts following treatment for 16 hours and persists at increasing levels after 48 and 96 h of RA treatment. Tretinoin 128-141 fatty acid binding protein 5 Homo sapiens 185-192
7881766-2 1994 In this study we demonstrate that PA-FABP transcripts are expressed in human skin in vivo and that topical application of 0.05% retinoic acid (RA) cream results in a rapid induction of PA-FABP transcripts following treatment for 16 hours and persists at increasing levels after 48 and 96 h of RA treatment. Tretinoin 143-145 fatty acid binding protein 5 Homo sapiens 34-41
7881766-2 1994 In this study we demonstrate that PA-FABP transcripts are expressed in human skin in vivo and that topical application of 0.05% retinoic acid (RA) cream results in a rapid induction of PA-FABP transcripts following treatment for 16 hours and persists at increasing levels after 48 and 96 h of RA treatment. Tretinoin 143-145 fatty acid binding protein 5 Homo sapiens 185-192
7881766-2 1994 In this study we demonstrate that PA-FABP transcripts are expressed in human skin in vivo and that topical application of 0.05% retinoic acid (RA) cream results in a rapid induction of PA-FABP transcripts following treatment for 16 hours and persists at increasing levels after 48 and 96 h of RA treatment. Tretinoin 293-295 fatty acid binding protein 5 Homo sapiens 34-41
7881766-2 1994 In this study we demonstrate that PA-FABP transcripts are expressed in human skin in vivo and that topical application of 0.05% retinoic acid (RA) cream results in a rapid induction of PA-FABP transcripts following treatment for 16 hours and persists at increasing levels after 48 and 96 h of RA treatment. Tretinoin 293-295 fatty acid binding protein 5 Homo sapiens 185-192
7881766-3 1994 The PA-FABP mRNA response to RA was reduced by approximately 50% when patients concurrently were treated with RA and 0.025% clobetasol propionate (CLO) for 48 and 96 h, whereas treatment with CLO alone resulted in PA-FABP transcript levels not significantly different from vehicle-treated skin. Tretinoin 29-31 fatty acid binding protein 5 Homo sapiens 4-11
7881766-3 1994 The PA-FABP mRNA response to RA was reduced by approximately 50% when patients concurrently were treated with RA and 0.025% clobetasol propionate (CLO) for 48 and 96 h, whereas treatment with CLO alone resulted in PA-FABP transcript levels not significantly different from vehicle-treated skin. Tretinoin 29-31 fatty acid binding protein 5 Homo sapiens 214-221
7881766-3 1994 The PA-FABP mRNA response to RA was reduced by approximately 50% when patients concurrently were treated with RA and 0.025% clobetasol propionate (CLO) for 48 and 96 h, whereas treatment with CLO alone resulted in PA-FABP transcript levels not significantly different from vehicle-treated skin. Tretinoin 110-112 fatty acid binding protein 5 Homo sapiens 4-11
7881766-3 1994 The PA-FABP mRNA response to RA was reduced by approximately 50% when patients concurrently were treated with RA and 0.025% clobetasol propionate (CLO) for 48 and 96 h, whereas treatment with CLO alone resulted in PA-FABP transcript levels not significantly different from vehicle-treated skin. Tretinoin 110-112 fatty acid binding protein 5 Homo sapiens 214-221
7881766-4 1994 When comparing the effects of a well-known irritant, sodium lauryl sulfate (SLS), to those of RA and its vehicle, 0.05% RA cream but not 2% SLS in RA vehicle caused PA-FABP mRNA induction after 16 h. SLS treatment of human skin for 96 h caused a slight increase in PA-FABP transcripts, but markedly less than that observed in response to RA treatment. Tretinoin 120-122 fatty acid binding protein 5 Homo sapiens 165-172
7881766-4 1994 When comparing the effects of a well-known irritant, sodium lauryl sulfate (SLS), to those of RA and its vehicle, 0.05% RA cream but not 2% SLS in RA vehicle caused PA-FABP mRNA induction after 16 h. SLS treatment of human skin for 96 h caused a slight increase in PA-FABP transcripts, but markedly less than that observed in response to RA treatment. Tretinoin 120-122 fatty acid binding protein 5 Homo sapiens 265-272
7881766-4 1994 When comparing the effects of a well-known irritant, sodium lauryl sulfate (SLS), to those of RA and its vehicle, 0.05% RA cream but not 2% SLS in RA vehicle caused PA-FABP mRNA induction after 16 h. SLS treatment of human skin for 96 h caused a slight increase in PA-FABP transcripts, but markedly less than that observed in response to RA treatment. Tretinoin 120-122 fatty acid binding protein 5 Homo sapiens 165-172
7881766-4 1994 When comparing the effects of a well-known irritant, sodium lauryl sulfate (SLS), to those of RA and its vehicle, 0.05% RA cream but not 2% SLS in RA vehicle caused PA-FABP mRNA induction after 16 h. SLS treatment of human skin for 96 h caused a slight increase in PA-FABP transcripts, but markedly less than that observed in response to RA treatment. Tretinoin 120-122 fatty acid binding protein 5 Homo sapiens 265-272
7881766-4 1994 When comparing the effects of a well-known irritant, sodium lauryl sulfate (SLS), to those of RA and its vehicle, 0.05% RA cream but not 2% SLS in RA vehicle caused PA-FABP mRNA induction after 16 h. SLS treatment of human skin for 96 h caused a slight increase in PA-FABP transcripts, but markedly less than that observed in response to RA treatment. Tretinoin 120-122 fatty acid binding protein 5 Homo sapiens 165-172
7881766-4 1994 When comparing the effects of a well-known irritant, sodium lauryl sulfate (SLS), to those of RA and its vehicle, 0.05% RA cream but not 2% SLS in RA vehicle caused PA-FABP mRNA induction after 16 h. SLS treatment of human skin for 96 h caused a slight increase in PA-FABP transcripts, but markedly less than that observed in response to RA treatment. Tretinoin 120-122 fatty acid binding protein 5 Homo sapiens 265-272
7853357-5 1994 The dissociation constants (Kd) for RA were 1.4 nM for GST-hRAR alpha, 1.4 nM for GST-hRAR beta, and 3.3 nM for GST-mRAR gamma, respectively. Tretinoin 36-38 retinoic acid receptor, gamma Mus musculus 116-126
7931079-4 1994 This Oct-2-dependent transactivation is inhibited by RA. Tretinoin 53-55 POU class 2 homeobox 2 Homo sapiens 5-10
7931079-5 1994 The presence of an intact COOH-terminal domain of Oct-2 contributes to both TPA/Ca2+-induced transactivation and the RA-mediated repression. Tretinoin 117-119 POU class 2 homeobox 2 Homo sapiens 50-55
8093047-1 1994 An ecto-enzyme of NAD glycohydrolase induced by retinoic acid in human leukemic HL-60 cells is attributed to the molecule of leukocyte cell surface antigen CD38 (Kontani, K., et al. Tretinoin 48-61 CD53 molecule Homo sapiens 135-155
8071361-0 1994 Retinoic acid induction of human cellular retinoic acid-binding protein-II gene transcription is mediated by retinoic acid receptor-retinoid X receptor heterodimers bound to one far upstream retinoic acid-responsive element with 5-base pair spacing. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 33-74
8071361-1 1994 We previously cloned the human cellular retinoic acid-binding protein-II (CRABPII) gene and demonstrated a rapid and transient increase in retinoic acid (RA)-dependent transcription in cultured human skin fibroblasts. Tretinoin 40-53 cellular retinoic acid binding protein 2 Homo sapiens 74-81
8071361-1 1994 We previously cloned the human cellular retinoic acid-binding protein-II (CRABPII) gene and demonstrated a rapid and transient increase in retinoic acid (RA)-dependent transcription in cultured human skin fibroblasts. Tretinoin 75-77 cellular retinoic acid binding protein 2 Homo sapiens 31-72
8071361-4 1994 By deletion analysis, a region essential for RA induction located approximately -5.6 kilobases upstream from the human CRABPII gene start site was identified. Tretinoin 45-47 cellular retinoic acid binding protein 2 Homo sapiens 119-126
8071361-5 1994 Sequencing and mutational analysis identified a direct repeat (GGGTCAttggaAGGACA) with 5-base pair spacing (DR-5) that is critical for RA-mediated induction of human CRABPII gene transcription. Tretinoin 135-137 cellular retinoic acid binding protein 2 Homo sapiens 166-173
7913411-0 1994 Retinoic acid-stimulated intercellular adhesion molecule-1 expression on SK-N-SH cells: calcium/calmodulin-dependent pathway. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 25-58
8018338-5 1994 RA-induced LTC4 synthase activity, which was determined by enzyme assay, was also inhibited by DEX by 65% in a cell-free system. Tretinoin 0-2 leukotriene C4 synthase Rattus norvegicus 11-24
8018338-8 1994 The induction of new LTC4 synthase activity by RA and inhibition of the RA-induced activity by DEX are important regulatory mechanisms of LTC4 synthesis. Tretinoin 47-49 leukotriene C4 synthase Rattus norvegicus 21-34
7981626-0 1994 Glucocorticoids antagonize retinoic acid stimulation of PEPCK gene transcription in 3T3-F442A adipocytes. Tretinoin 27-40 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 56-61
7981626-2 1994 The regulation of PEPCK gene expression by retinoic acid (RA) and dexamethasone (DEX) was studied in 3T3-F442A adipocytes maintained in a serum-free medium. Tretinoin 43-56 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 18-23
7981626-2 1994 The regulation of PEPCK gene expression by retinoic acid (RA) and dexamethasone (DEX) was studied in 3T3-F442A adipocytes maintained in a serum-free medium. Tretinoin 58-60 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 18-23
7981626-10 1994 Thus, in adipocytes, the PEPCK gene regulatory region between -2100 and +69 bp mediates both stimulation by RA and repression by DEX of RA action. Tretinoin 108-110 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 25-30
7981626-10 1994 Thus, in adipocytes, the PEPCK gene regulatory region between -2100 and +69 bp mediates both stimulation by RA and repression by DEX of RA action. Tretinoin 136-138 phosphoenolpyruvate carboxykinase 2, mitochondrial Homo sapiens 25-30
17180006-0 1994 Signals transduced via insulin-like growth factor I receptor (IGF(R)) mediate resistance to retinoic acid-induced cell growth arrest in a human neuroblastoma cell line. Tretinoin 92-105 insulin like growth factor 1 receptor Homo sapiens 23-60
17180006-0 1994 Signals transduced via insulin-like growth factor I receptor (IGF(R)) mediate resistance to retinoic acid-induced cell growth arrest in a human neuroblastoma cell line. Tretinoin 92-105 insulin like growth factor 1 receptor Homo sapiens 62-68
17180006-8 1994 Finally we show that by blocking the Insulin-like Growth Factor Receptor (IGF1(R)) with a monoclonal antibody (alpha-IR3) in the presence of RA the growth of RAR cell lines could be completely blocked. Tretinoin 141-143 insulin like growth factor 1 receptor Homo sapiens 74-81
7524626-5 1994 XLFB3 is not expressed in the rostral part of all three germ layers, with coincident anterior borders that are shifted anteriorly by treatment of developing embryos with retinoic acid. Tretinoin 170-183 HNF1 homeobox B S homeolog Xenopus laevis 0-5
7524626-6 1994 XLFB3 is a useful marker of early endoderm differentiation and its expression pattern along the antero-posterior axis, as well as the response to retinoic acid treatment, suggests a role in early morphogenesis. Tretinoin 146-159 HNF1 homeobox B S homeolog Xenopus laevis 0-5
7947324-5 1994 Undifferentiated P19 cells were found to express EAR2 mRNA and the expression level was only slightly elevated by RA-treatment. Tretinoin 114-116 eosinophil-associated, ribonuclease A family, member 2 Mus musculus 49-53
7974255-2 1994 Retinoic acid (RA) is known to inhibit the chondrogenic differentiation of C 5.18 cells and this may parallel the teratogenic effects of retinoids in vivo; however, the question as to which of the 3 retinoic acid receptors (RAR alpha, beta, gamma) or the 3 retinoid X receptors (RXR alpha, beta, gamma) mediate this RA-induced inhibition remains unanswered. Tretinoin 0-13 retinoid X receptor alpha Homo sapiens 279-288
7974255-9 1994 9-cis RA, which binds to the 3 RARs with affinities similar to RA and also binds to the 3 RXRs, was less active (IC50 8 x 10(-9) M), suggesting that RXR binding interferes with the inhibitory effect of ligand-activated RARs. Tretinoin 6-8 retinoid X receptor alpha Homo sapiens 90-93
8206989-3 1994 Curiously, 9-cis-RA competes for [3H]t-RA binding to mouse RAR alpha, beta, and gamma with IC50 values of 31, 8, and 60 nM, respectively, while t-RA itself does not exhibit such differential competition (IC50 values for RARs, 5 nM). Tretinoin 11-19 retinoic acid receptor, alpha Mus musculus 59-68
8029022-0 1994 Retinoic acid-mediated activation of HNF-3 alpha during EC stem cell differentiation. Tretinoin 0-13 forkhead box A1 Mus musculus 37-48
8029022-1 1994 We present evidence demonstrating that the liver-enriched transcription factor HNF-3 alpha is activated upon retinoic acid-induced differentiation of mouse F9 embryonal carcinoma cells. Tretinoin 109-122 forkhead box A1 Mus musculus 79-90
8175747-4 1994 Moreover, repression by ARP-1 is overcome by the retinoid X receptor RXR alpha in the presence of retinoic acid. Tretinoin 98-111 actin related protein 1A Homo sapiens 24-29
8175780-10 1994 The MMPI synthesized by retinol-treated EC was immunologically related to tissue inhibitor of metalloproteinases, type 1 (TIMP-1), and the MMPI produced by retinoic acid-treated cells was related to TIMP-2, as indicated by biosynthetic labeling and immunoprecipitation studies as well as Western blot analysis. Tretinoin 156-169 TIMP metallopeptidase inhibitor 2 Homo sapiens 199-205
7916330-5 1994 However, the residual ICAM-1 inducing activity (up to 30% of ICAM-1 induction) could not be associated with any known ICAM-1 inducers (IFN gamma, TNF alpha, TNF beta, IL-1 alpha, IL-1 beta, IL-4, retinoic acid, LPS). Tretinoin 196-209 intercellular adhesion molecule 1 Homo sapiens 22-28
8182938-10 1994 That RA promotes both neutrophil and monocyte differentiation has implications for the use of RA and D3 in treatment of leukemias and provides insight into mechanisms whereby RAR, VDR and RXR facilitate monocyte differentiation. Tretinoin 5-7 vitamin D receptor Homo sapiens 180-183
8182938-10 1994 That RA promotes both neutrophil and monocyte differentiation has implications for the use of RA and D3 in treatment of leukemias and provides insight into mechanisms whereby RAR, VDR and RXR facilitate monocyte differentiation. Tretinoin 5-7 retinoid X receptor alpha Homo sapiens 188-191
7512566-7 1994 Retinoic acid increased IGFBP-6 by 3-fold in NHF and AG2804-conditioned media, maximal at approximately 100 nM retinoic acid. Tretinoin 111-124 insulin like growth factor binding protein 6 Homo sapiens 24-31
7909996-8 1994 RA treatment of E17 rat lung explants in culture resulted in a significant dose- and time-dependent increase in Hox A5, B5, and B6 mRNA levels. Tretinoin 0-2 homeo box A5 Rattus norvegicus 112-118
8120040-2 1994 Thus ADH participates in the conversion of retinol (vitamin A alcohol) to retinoic acid, a regulatory ligand for the retinoic acid receptor class of transcription factors. Tretinoin 74-87 aldo-keto reductase family 1 member A1 Homo sapiens 5-8
8120040-4 1994 However, human ADH expression patterns have not been analyzed in early embryonic tissues, which are known to synthesize and respond to retinoic acid such as the neural tube and limb buds. Tretinoin 135-148 aldo-keto reductase family 1 member A1 Homo sapiens 15-18
8120040-9 1994 These findings indicate that at least one human ADH isozyme may exist in the correct tissues to act as an embryonic retinol dehydrogenase catalyzing the synthesis of retinoic acid. Tretinoin 166-179 aldo-keto reductase family 1 member A1 Homo sapiens 48-51
8018561-4 1994 Mobility shift assays with respect to the P2 promoter region revealed that the 15-base pair fragment located between P1 and P2 promoters was responsive to the RA treatment. Tretinoin 159-161 crystallin gamma F, pseudogene Homo sapiens 117-126
8125161-0 1994 Retinoic acid inhibition of insulin-like growth factor I stimulation of c-fos mRNA levels in a breast carcinoma cell line. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-77
8125161-5 1994 Pretreatment of MCF-7 cells with 1 microM RA blocked IGF-I-mediated enhancement of c-fos mRNA levels by approximately 70%. Tretinoin 42-44 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88
8125161-6 1994 The maximal RA effect (80% inhibition) on IGF-I stimulation of c-fos mRNA levels was noted within 2 h of exposure to RA. Tretinoin 12-14 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-68
8125161-6 1994 The maximal RA effect (80% inhibition) on IGF-I stimulation of c-fos mRNA levels was noted within 2 h of exposure to RA. Tretinoin 117-119 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-68
8125161-8 1994 Preexposure of cells to RA results in a significant decrease (P < 0.05) in c-fos mRNA stability. Tretinoin 24-26 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-83
8125161-10 1994 We conclude that RA-mediated inhibition of IGF-I stimulation of c-fos mRNA may represent a potential mechanism by which RA inhibits IGF-I stimulation of growth. Tretinoin 17-19 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-69
8125161-10 1994 We conclude that RA-mediated inhibition of IGF-I stimulation of c-fos mRNA may represent a potential mechanism by which RA inhibits IGF-I stimulation of growth. Tretinoin 120-122 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-69
8016390-6 1994 In parallel, RA induced the expression of the monocytic surface antigen CD11b, but not CD14. Tretinoin 13-15 integrin subunit alpha M Homo sapiens 72-77
8061932-2 1994 Because CRABP II protein is strongly induced by topical retinoic acid, the respective roles of the two proteins in the pharmacological activity and toxicity of topical retinoids deserve particular attention. Tretinoin 56-69 cellular retinoic acid binding protein 2 Homo sapiens 8-16
8061932-5 1994 We found that CRABP II protein and mRNA were strongly increased upon retinoic acid application: this induction was significantly inhibited by concomitant application of triamcinolone acetonide; a more potent steroid, difluocortolone valerate, was also found to diminish normal endogenous expression of CRABP II. Tretinoin 69-82 cellular retinoic acid binding protein 2 Homo sapiens 14-22
8061932-5 1994 We found that CRABP II protein and mRNA were strongly increased upon retinoic acid application: this induction was significantly inhibited by concomitant application of triamcinolone acetonide; a more potent steroid, difluocortolone valerate, was also found to diminish normal endogenous expression of CRABP II. Tretinoin 69-82 cellular retinoic acid binding protein 2 Homo sapiens 302-310
8113407-0 1994 Retinoic acid suppresses parathyroid hormone (PTH) secretion and PreproPTH mRNA levels in bovine parathyroid cell culture. Tretinoin 0-13 parathyroid hormone Bos taurus 25-44
8113407-0 1994 Retinoic acid suppresses parathyroid hormone (PTH) secretion and PreproPTH mRNA levels in bovine parathyroid cell culture. Tretinoin 0-13 parathyroid hormone Bos taurus 46-49
8113407-8 1994 Combined treatment with 10(-6) M retinoic acid and 10(-8) M 1,25(OH)2D3 more effectively decreased PTH secretion and preproPTH mRNA than did either compound alone. Tretinoin 33-46 parathyroid hormone Bos taurus 99-102
8113407-9 1994 These data indicate that retinoic acid: (a) elicits a bioresponse in bovine parathyroid cells; (b) attenuates PTH expression at the protein and mRNA levels, and (c) acts independently of 1,25(OH)2D3 in the control of PTH expression. Tretinoin 25-38 parathyroid hormone Bos taurus 110-113
8113407-9 1994 These data indicate that retinoic acid: (a) elicits a bioresponse in bovine parathyroid cells; (b) attenuates PTH expression at the protein and mRNA levels, and (c) acts independently of 1,25(OH)2D3 in the control of PTH expression. Tretinoin 25-38 parathyroid hormone Bos taurus 217-220
8309256-0 1994 Poor response to all-trans retinoic acid therapy in a t(11;17) PLZF/RAR alpha patient. Tretinoin 27-40 zinc finger and BTB domain containing 16 Homo sapiens 63-67
8309256-11 1994 These results suggest that the t(11;17) (PLZF/RAR alpha) case of this study was less responsive to ATRA therapy than t(15;17) (PML/RAR alpha) cases and raises the question of the definition of this novel AML subtype. Tretinoin 99-103 zinc finger and BTB domain containing 16 Homo sapiens 41-45
8276858-7 1994 This suggests that the J6 gene is likely to be transactivated by the GATA-2, GATA-3, or related transcription factor, which is activated by retinoic acid during F9 cell differentiation. Tretinoin 140-153 GATA binding protein 3 Homo sapiens 77-83
7866431-0 1994 Characterization of the human MSX-1 promoter and an enhancer responsible for retinoic acid induction. Tretinoin 77-90 msh homeobox 1 Homo sapiens 30-35
7866431-3 1994 We have examined the effects of RA on the human MSX-1 (formerly named HOX-7) gene expression in cultured EC cells (NT2/D1). Tretinoin 32-34 msh homeobox 1 Homo sapiens 48-53
8111244-0 1994 Specific induction of LTC4 synthase by retinoic acid in rat basophilic leukemia-1 cells. Tretinoin 39-52 leukotriene C4 synthase Rattus norvegicus 22-35
8111244-1 1994 Overnight (10-16 h) incubation of retinoic acid (RA), a derivative of vitamin A, specifically induced LTC4 synthase activity (5 to 10-fold), but not LTA4 hydrolase activity in the lysate of rat basophilic leukemia-1 (RBL-1) cells. Tretinoin 34-47 leukotriene C4 synthase Rattus norvegicus 102-115
8111244-1 1994 Overnight (10-16 h) incubation of retinoic acid (RA), a derivative of vitamin A, specifically induced LTC4 synthase activity (5 to 10-fold), but not LTA4 hydrolase activity in the lysate of rat basophilic leukemia-1 (RBL-1) cells. Tretinoin 49-51 leukotriene C4 synthase Rattus norvegicus 102-115
8111244-2 1994 A time course study revealed that the increase of LTC4 synthase activity was time dependent and that the peak value was obtained after a 24-hour incubation with RA. Tretinoin 161-163 leukotriene C4 synthase Rattus norvegicus 50-63
7516169-0 1994 Induction of intercellular adhesion molecule 1 expression on normal human keratinocytes by retinoic acid: comparison of cultured keratinocytes and skin explants. Tretinoin 91-104 intercellular adhesion molecule 1 Homo sapiens 13-46
7516169-5 1994 These findings indicate that RA, in a therapeutical range of concentrations can induce or stimulate ICAM-1 expression in normal human keratinocytes. Tretinoin 29-31 intercellular adhesion molecule 1 Homo sapiens 100-106
7516425-3 1993 Though vitamin A status is known to positively regulate the gene expression of CRBP I in the extrahepatic tissues, in the present study we observed that the amount of the CRBP I transcript in liver was neither reduced by vitamin A-deficiency, nor affected by replenishment with an excess dose of all-trans retinoic acid. Tretinoin 306-319 retinol binding protein 1 Rattus norvegicus 171-177
8242764-0 1993 Retinoic acid promotes proliferation and induces expression of retinoic acid receptor-alpha gene in murine T lymphocytes. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 63-91
8242764-4 1993 Expression of RAR-alpha mRNA in antigen-stimulated T lymphocyte cultures was upregulated by retinoic acid in a dose-dependent manner; maximal expression occurred within 6 hr of culture and in response to 10(-9)-10(-7) mol/liter retinoic acid. Tretinoin 92-105 retinoic acid receptor, alpha Mus musculus 14-23
8242764-4 1993 Expression of RAR-alpha mRNA in antigen-stimulated T lymphocyte cultures was upregulated by retinoic acid in a dose-dependent manner; maximal expression occurred within 6 hr of culture and in response to 10(-9)-10(-7) mol/liter retinoic acid. Tretinoin 228-241 retinoic acid receptor, alpha Mus musculus 14-23
8408080-9 1993 Retinol, as well as retinoic acid, stabilized both compact I and II RBP intermediates to DTT-induced unfolding, suggesting that RBP assumes different conformations in the ER in the presence and absence of a ligand. Tretinoin 20-33 retinol binding protein 4 Homo sapiens 68-71
8408080-9 1993 Retinol, as well as retinoic acid, stabilized both compact I and II RBP intermediates to DTT-induced unfolding, suggesting that RBP assumes different conformations in the ER in the presence and absence of a ligand. Tretinoin 20-33 retinol binding protein 4 Homo sapiens 128-131
8413615-0 1993 Residues in the TATA-binding protein required to mediate a transcriptional response to retinoic acid in EC cells. Tretinoin 87-100 TATA-box binding protein Homo sapiens 16-36
8413615-5 1993 TBP is thus a target for retinoic acid-dependent transactivation in EC cells by providing a surface for interaction with the EC cell-specific E1A-like activity. Tretinoin 25-38 TATA-box binding protein Homo sapiens 0-3
8253072-0 1993 Chimeric retinoic acid/thyroid hormone receptors implicate RAR-alpha 1 as mediating growth inhibition by retinoic acid. Tretinoin 9-22 RAB40B, member RAS oncogene family L homeolog Xenopus laevis 59-62
8394693-6 1993 Treatment of 3T3-L1 cells with 1 microM RA led to a 4-5-fold increase in the RAR gamma mRNA level, but only a trace amount of RAR beta mRNA was detected. Tretinoin 40-42 retinoic acid receptor, gamma Mus musculus 77-86
8394722-0 1993 Induction of TrkB by retinoic acid mediates biologic responsiveness to BDNF and differentiation of human neuroblastoma cells. Tretinoin 21-34 brain derived neurotrophic factor Homo sapiens 71-75
8394722-3 1993 In this study, we show that RA treatment of neuroblastoma cells induces the expression of TrkB, the receptor for the neurotrophins BDNF, NT-3, and NT-4/5. Tretinoin 28-30 brain derived neurotrophic factor Homo sapiens 131-135
8394722-4 1993 BDNF addition to RA-treated SH-SY5Y neuroblastoma cells stimulated the tyrosine phosphorylation of TrkB and neuronal differentiation. Tretinoin 17-19 brain derived neurotrophic factor Homo sapiens 0-4
8394722-5 1993 RA treatment of KCNR neuroblastoma cells, which constitutively express BDNF mRNA, resulted in the expression of TrkB and differentiation in the absence of added BDNF. Tretinoin 0-2 brain derived neurotrophic factor Homo sapiens 71-75
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 152-165 retinoid X receptor alpha Homo sapiens 51-70
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 152-165 retinoid X receptor alpha Homo sapiens 26-29
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 167-169 retinoid X receptor alpha Homo sapiens 51-70
8257090-1 1993 Retinoid X Receptor beta (RXRB) is a member of the retinoid X receptor (RXR) family of nuclear receptors which are involved in mediating the effects of retinoic acid (RA). Tretinoin 167-169 retinoid X receptor alpha Homo sapiens 26-29
8104620-6 1993 To date 6 Homeobox genes (HoxC6, HoxC8, HoxD1, HoxD4, HoxD8, and HoxD9) have been identified in the cDNA library prepared from LA-N-5 cells treated with retinoic acid. Tretinoin 153-166 homeobox D1 Homo sapiens 40-45
8104620-6 1993 To date 6 Homeobox genes (HoxC6, HoxC8, HoxD1, HoxD4, HoxD8, and HoxD9) have been identified in the cDNA library prepared from LA-N-5 cells treated with retinoic acid. Tretinoin 153-166 homeobox D8 Homo sapiens 54-59
8100485-13 1993 Retinoic acid has recently been reported to induce ICAM-1 expression on human tumour cells. Tretinoin 0-13 intercellular adhesion molecule 1 Homo sapiens 51-57
8100485-15 1993 In contrast to IFN gamma-induced ICAM-1 expression, retinoic-acid-induced ICAM-1 expression was inhibited by TGF beta on two of the three responsive lines. Tretinoin 52-65 intercellular adhesion molecule 1 Homo sapiens 74-80
8100575-3 1993 The binding of the glucocorticoid receptor was higher in vitamin A--deficient rats than in controls and restored by retinoic acid supplementation, but did not differ from controls in the vitamin A--overloaded rats. Tretinoin 116-129 nuclear receptor subfamily 3, group C, member 1 Rattus norvegicus 19-42
8496619-0 1993 Differential regulation of tyrosinase activity in skin of white and black individuals in vivo by topical retinoic acid. Tretinoin 105-118 tyrosinase Homo sapiens 27-37
8496619-2 1993 Because retinoic acid regulates tyrosinase activity in melanoma cells, we analyzed modulation of pigmentation in vivo by retinoic acid. Tretinoin 8-21 tyrosinase Homo sapiens 32-42
8496619-6 1993 In contrast, retinoic acid treatment significantly induced (2.7 times, n = 8) tyrosinase activity, compared to vehicle treatment, in white skin. Tretinoin 13-26 tyrosinase Homo sapiens 78-88
8496619-7 1993 Melanin content, however, remained unchanged at 4 d. In separate experiments, tyrosinase activity in white subjects (n = 25) was increased 16% (p = 0.01) in sodium lauryl sulfate-treated skin, and 77% (p = 0.0005) in retinoic acid-treated skin, compared to vehicle-treated skin. Tretinoin 217-230 tyrosinase Homo sapiens 78-88
8496619-8 1993 The effect of retinoic acid on tyrosinase activity could be differentiated from non-specific irritation, because tyrosinase activity in retinoic acid-treated skin was significantly greater (52%, p = 0.004) than sodium lauryl sulfate-treated skin. Tretinoin 14-27 tyrosinase Homo sapiens 31-41
8496619-8 1993 The effect of retinoic acid on tyrosinase activity could be differentiated from non-specific irritation, because tyrosinase activity in retinoic acid-treated skin was significantly greater (52%, p = 0.004) than sodium lauryl sulfate-treated skin. Tretinoin 136-149 tyrosinase Homo sapiens 31-41
8496619-8 1993 The effect of retinoic acid on tyrosinase activity could be differentiated from non-specific irritation, because tyrosinase activity in retinoic acid-treated skin was significantly greater (52%, p = 0.004) than sodium lauryl sulfate-treated skin. Tretinoin 136-149 tyrosinase Homo sapiens 113-123
8496619-11 1993 Western analysis revealed that induction of tyrosinase activity by retinoic acid also was not associated with increased tyrosinase protein content (n = 9), indicating that regulation of tyrosinase activity by retinoic acid occurs through a post-translational mechanism. Tretinoin 67-80 tyrosinase Homo sapiens 44-54
8496619-12 1993 These data demonstrate that low tyrosinase activity in white skin in vivo is retinoic acid inducible and high tyrosinase activity in black skin in vivo is neither further induced nor reduced by retinoic acid. Tretinoin 77-90 tyrosinase Homo sapiens 32-42
8251184-1 1993 Nuclear retinoic acid receptors RAR alpha, RAR beta and RAR gamma are transcription factors that bind all-trans retinoic acid as their ligand and mediate its action by activating particular set of genes that contain retinoic acid responsive elements in their promoter-enhancers. Tretinoin 8-21 retinoic acid receptor, alpha Mus musculus 32-41
8251184-1 1993 Nuclear retinoic acid receptors RAR alpha, RAR beta and RAR gamma are transcription factors that bind all-trans retinoic acid as their ligand and mediate its action by activating particular set of genes that contain retinoic acid responsive elements in their promoter-enhancers. Tretinoin 8-21 retinoic acid receptor, gamma Mus musculus 56-65
8251184-1 1993 Nuclear retinoic acid receptors RAR alpha, RAR beta and RAR gamma are transcription factors that bind all-trans retinoic acid as their ligand and mediate its action by activating particular set of genes that contain retinoic acid responsive elements in their promoter-enhancers. Tretinoin 112-125 retinoic acid receptor, alpha Mus musculus 32-41
8251184-1 1993 Nuclear retinoic acid receptors RAR alpha, RAR beta and RAR gamma are transcription factors that bind all-trans retinoic acid as their ligand and mediate its action by activating particular set of genes that contain retinoic acid responsive elements in their promoter-enhancers. Tretinoin 112-125 retinoic acid receptor, gamma Mus musculus 56-65
8397079-9 1993 For instance, expression of CRABP I in the migrating cells that give rise to the olivary and pontine nuclei, which develop abnormally in conditions of retinoid excess, is consistent with observations from a variety of other systems indicating that CRABP I limits the access of RA to the nuclear receptors in normal physiological conditions. Tretinoin 29-31 cellular retinoic acid binding protein I Mus musculus 248-255
8474450-2 1993 Expression of Rex-1 is reduced at the transcriptional level when F9 cells are induced by the addition of retinoic acid (RA) to differentiate. Tretinoin 105-118 zinc finger protein 42 Mus musculus 14-19
8385674-2 1993 This study compared the effects of TGF-beta 1 and BMP 4 on the gene expression of a retinoic acid (RA) responsive rat clonal preosteoblast cell line, UMR 201, as well as the way in which these proteins interact with RA in these cells. Tretinoin 84-97 bone morphogenetic protein 4 Rattus norvegicus 50-55
8385674-2 1993 This study compared the effects of TGF-beta 1 and BMP 4 on the gene expression of a retinoic acid (RA) responsive rat clonal preosteoblast cell line, UMR 201, as well as the way in which these proteins interact with RA in these cells. Tretinoin 99-101 bone morphogenetic protein 4 Rattus norvegicus 50-55
8460936-0 1993 Regulation of hepatic lecithin: retinol acyltransferase activity by retinoic acid. Tretinoin 68-81 lecithin retinol acyltransferase Rattus norvegicus 22-55
8460936-4 1993 The present studies were designed to determine whether liver LRAT activity is regulated in vivo by retinoic acid, a principal active metabolite of retinol. Tretinoin 99-112 lecithin retinol acyltransferase Rattus norvegicus 61-65
8460936-6 1993 Following treatment with a single 2-micrograms dose of retinoic acid, LRAT activity increased significantly while, following treatment with a single 20-micrograms dose, liver LRAT activity equalled that of vitamin A-sufficient adult rats. Tretinoin 55-68 lecithin retinol acyltransferase Rattus norvegicus 70-74
8460936-6 1993 Following treatment with a single 2-micrograms dose of retinoic acid, LRAT activity increased significantly while, following treatment with a single 20-micrograms dose, liver LRAT activity equalled that of vitamin A-sufficient adult rats. Tretinoin 55-68 lecithin retinol acyltransferase Rattus norvegicus 175-179
8460936-7 1993 Retinoic acid was more effective than an equimolar quantity of retinol in restoring LRAT activity in the vitamin A-deficient rat liver. Tretinoin 0-13 lecithin retinol acyltransferase Rattus norvegicus 84-88
8460936-8 1993 The increase in hepatic LRAT activity after administration of retinoic acid occurred rapidly, reaching a maximum within 12-16 h but declining again after 48-72 h. Studies were conducted in vivo to gain insight into the level of regulation of LRAT by retinoic acid. Tretinoin 62-75 lecithin retinol acyltransferase Rattus norvegicus 24-28
8460936-8 1993 The increase in hepatic LRAT activity after administration of retinoic acid occurred rapidly, reaching a maximum within 12-16 h but declining again after 48-72 h. Studies were conducted in vivo to gain insight into the level of regulation of LRAT by retinoic acid. Tretinoin 62-75 lecithin retinol acyltransferase Rattus norvegicus 242-246
8460936-8 1993 The increase in hepatic LRAT activity after administration of retinoic acid occurred rapidly, reaching a maximum within 12-16 h but declining again after 48-72 h. Studies were conducted in vivo to gain insight into the level of regulation of LRAT by retinoic acid. Tretinoin 250-263 lecithin retinol acyltransferase Rattus norvegicus 24-28
8460936-8 1993 The increase in hepatic LRAT activity after administration of retinoic acid occurred rapidly, reaching a maximum within 12-16 h but declining again after 48-72 h. Studies were conducted in vivo to gain insight into the level of regulation of LRAT by retinoic acid. Tretinoin 250-263 lecithin retinol acyltransferase Rattus norvegicus 242-246
8460936-9 1993 The increase in LRAT activity by retinoic acid in the vitamin A-deficient rat was blocked completely by both actinomycin D and cycloheximide. Tretinoin 33-46 lecithin retinol acyltransferase Rattus norvegicus 16-20
7683888-0 1993 Regulation of synthesis of some proteinase inhibitors in human hepatoma cells HepG2 by cytokines, hepatocyte growth factor and retinoic acid. Tretinoin 127-140 endogenous retrovirus group K member 9 Homo sapiens 32-42
7683888-7 1993 Retinoic acid preferentially increased synthesis of alpha-1-antichymotrypsin, ceruloplasmin and plasminogen activator inhibitor-1. Tretinoin 0-13 serpin family A member 3 Homo sapiens 52-76
8384553-5 1993 In addition, the PLZF mRNA levels were down-regulated in NB-4 and HL-60 promyelocytic cell lines in response to retinoic acid-induced granulocytic differentiation and were very low in mature granulocytes. Tretinoin 112-125 zinc finger and BTB domain containing 16 Homo sapiens 17-21
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 17-30 retinoic acid receptor, alpha Mus musculus 48-51
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 17-30 retinoic acid receptor, alpha Mus musculus 125-128
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 48-50 retinoic acid receptor, alpha Mus musculus 125-128
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 83-85 retinoic acid receptor, alpha Mus musculus 48-51
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 83-85 retinoic acid receptor, alpha Mus musculus 125-128
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 83-85 retinoic acid receptor, alpha Mus musculus 48-51
8388240-1 1993 Induction of the retinoic acid receptor beta 2 (RAR beta 2) gene by retinoic acid (RA) is mediated by a RA response element (RARE), which represents a high affinity binding site for RAR/RXR heterodimers acting at this site as RA-inducible transcription activators. Tretinoin 83-85 retinoic acid receptor, alpha Mus musculus 125-128
8382035-4 1993 In binding studies the equilibrium dissociation constant, Kd, of retinoic acid (RA) for E. coli-derived CRABP-I and CRABP-II was 6.8 and 39 nM, respectively. Tretinoin 65-78 cellular retinoic acid binding protein 2 Homo sapiens 116-124
8382035-4 1993 In binding studies the equilibrium dissociation constant, Kd, of retinoic acid (RA) for E. coli-derived CRABP-I and CRABP-II was 6.8 and 39 nM, respectively. Tretinoin 80-82 cellular retinoic acid binding protein 2 Homo sapiens 116-124
8382035-6 1993 RA competed with the binding of CD 367 to CRABP-I and CRABP-II with IC50 values of 20.0 and 90.0 nM, respectively. Tretinoin 0-2 cellular retinoic acid binding protein 2 Homo sapiens 54-62
8382035-9 1993 These data demonstrate that E. coli-derived CRABP-I has a higher affinity for RA than CRABP-II and that retinoic acid metabolites have a lower affinity for these proteins. Tretinoin 45-47 cellular retinoic acid binding protein 2 Homo sapiens 86-94
8382035-10 1993 The observed difference in affinity for RA supports the idea that CRABP-I, which is constitutively expressed, and CRABP-II, which is induced by RA, have different functions in the cell. Tretinoin 40-42 cellular retinoic acid binding protein 2 Homo sapiens 114-122
8424959-4 1993 However, differentiation of P19 embryonal carcinoma cells into neuronal cell types by exposure to retinoic acid resulted in the induction of MASH1 RNA expression. Tretinoin 98-111 achaete-scute family bHLH transcription factor 1 Mus musculus 141-146
8388158-1 1993 Vertebrate alcohol dehydrogenase (ADH) plays a role in many alcohol/aldehyde interconversions including the oxidation of retinol to retinaldehyde, the rate-limiting step in the synthesis of retinoic acid. Tretinoin 190-203 aldo-keto reductase family 1 member A1 Homo sapiens 11-32
8388158-1 1993 Vertebrate alcohol dehydrogenase (ADH) plays a role in many alcohol/aldehyde interconversions including the oxidation of retinol to retinaldehyde, the rate-limiting step in the synthesis of retinoic acid. Tretinoin 190-203 aldo-keto reductase family 1 member A1 Homo sapiens 34-37
8388158-2 1993 Recent molecular genetic studies on human ADH genes has lent support to a physiological role for ADH in retinoic acid synthesis. Tretinoin 104-117 aldo-keto reductase family 1 member A1 Homo sapiens 42-45
8388158-2 1993 Recent molecular genetic studies on human ADH genes has lent support to a physiological role for ADH in retinoic acid synthesis. Tretinoin 104-117 aldo-keto reductase family 1 member A1 Homo sapiens 97-100
8388158-8 1993 Regulation of ADH gene expression by retinoid and thyroid hormones suggests that ADH plays an important role in retinoic acid synthesis. Tretinoin 112-125 aldo-keto reductase family 1 member A1 Homo sapiens 14-17
8388158-8 1993 Regulation of ADH gene expression by retinoid and thyroid hormones suggests that ADH plays an important role in retinoic acid synthesis. Tretinoin 112-125 aldo-keto reductase family 1 member A1 Homo sapiens 81-84
8382933-6 1993 In contrast to the effects of RA on osteoblast-related gene regulation, RA was found to increase the quantity of estrogen receptor as well as of 1,25-dihydroxy vitamin D3 receptor (VDR) in BFO cells. Tretinoin 72-74 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 160-179
8382933-6 1993 In contrast to the effects of RA on osteoblast-related gene regulation, RA was found to increase the quantity of estrogen receptor as well as of 1,25-dihydroxy vitamin D3 receptor (VDR) in BFO cells. Tretinoin 72-74 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 181-184
8382933-8 1993 These RA effects on ER and VDR seem to be specific, since glucocorticoid receptor quantities were not affected by RA treatment. Tretinoin 6-8 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 27-30
8095151-1 1993 Here we describe experiments detailing the developmental expression, and the inducibility by all-trans retinoic acid (RA) of six members of the Xenopus Hox-2 complex of homeobox-containing genes. Tretinoin 103-116 homeobox B7 S homeolog Xenopus laevis 152-157
7691069-0 1993 Retinoic acid receptor and retinoid X receptor expression in retinoic acid-resistant human tumor cell lines. Tretinoin 61-74 retinoid X receptor alpha Homo sapiens 27-46
8093812-6 1993 In addition, v-erbA-RXR-alpha heterodimers specifically bind natural thyroid hormone-responsive elements (TREs) but not retinoic acid-responsive elements (RAREs). Tretinoin 120-133 retinoid X receptor alpha Homo sapiens 20-29
1334086-7 1992 The CRABP-II mRNA was rapidly induced within 2-6 h in cultured human skin fibroblasts by retinoic acid, reaching a plateau after 6 h of treatment. Tretinoin 89-102 cellular retinoic acid binding protein 2 Homo sapiens 4-12
1333043-9 1992 Taken together, our results show that the AF1 element contains an RARE that mediates a retinoic acid response by binding an RAR alpha/coregulator complex; this coregulator is presumably RXR alpha. Tretinoin 87-100 interferon gamma receptor 2 Homo sapiens 42-45
1333043-9 1992 Taken together, our results show that the AF1 element contains an RARE that mediates a retinoic acid response by binding an RAR alpha/coregulator complex; this coregulator is presumably RXR alpha. Tretinoin 87-100 retinoid X receptor alpha Homo sapiens 186-195
1331079-4 1992 In this study, we showed that TR formed heterodimers with RAR and RXR on a retinoic acid (RA) response element and two TREs. Tretinoin 75-88 retinoid X receptor alpha Homo sapiens 66-69
1383035-5 1992 The combined data suggest that the defect in RAC65 RAR alpha results in reduced expression of the CRABP gene after RA treatment and, therefore, increased flow of RA into the nucleus. Tretinoin 45-47 retinoic acid receptor, alpha Mus musculus 51-60
1417866-1 1992 S14 gene transcription is induced by retinoic acid (RA) in cultured adipocytes, but not preadipocytes. Tretinoin 37-50 thyroid hormone responsive Mus musculus 0-3
1417866-1 1992 S14 gene transcription is induced by retinoic acid (RA) in cultured adipocytes, but not preadipocytes. Tretinoin 52-54 thyroid hormone responsive Mus musculus 0-3
1332671-17 1992 The sharp increases in CRABP-II levels are associated with an alteration in the differentiation programme, as well as with cell response to retinoic acid overload, whereas CRABP-I might be a marker for terminal differentiation. Tretinoin 140-153 cellular retinoic acid binding protein 2 Homo sapiens 23-31
1363087-1 1992 Exogenous retinoic acid (RA) has teratogenic effects on vertebrate embryos and alters Hox-C gene expression in vivo and in vitro. Tretinoin 10-23 homeobox C cluster Mus musculus 86-91
1382963-4 1992 RA alone resulted in increased IGFBP-4 levels and the appearance of IGFBP-3 in the CM. Tretinoin 0-2 insulin like growth factor binding protein 4 Homo sapiens 31-38
1328857-11 1992 Our data suggest that the COUP receptors are a novel class of RAR and RXR regulators that can restrict RA signaling to certain elements. Tretinoin 62-64 retinoid X receptor alpha Homo sapiens 70-73
1339275-1 1992 The expression of the rat cellular retinol binding protein I (rCRBPI) can be upregulated in vivo by retinoic acid (RA). Tretinoin 100-113 retinol binding protein 1 Rattus norvegicus 26-60
1339275-1 1992 The expression of the rat cellular retinol binding protein I (rCRBPI) can be upregulated in vivo by retinoic acid (RA). Tretinoin 100-113 retinol binding protein 1 Rattus norvegicus 62-68
1527087-11 1992 The rates of retinoic acid synthesis from CRBP-retinal, with a series of increasing apoCRBP concentrations, exceeded the rates that would be supported by the free retinal present. Tretinoin 13-26 retinol binding protein 1 Rattus norvegicus 42-46
1527087-14 1992 These results also suggest a novel role for CRBP in retinoid metabolism, facilitating the conversion of retinal into retinoic acid. Tretinoin 117-130 retinol binding protein 1 Rattus norvegicus 44-48
1451960-2 1992 In the embryonal carcinoma cell line F9 considerable constitutive levels of hsp25 were observed which could be slightly increased by treatment with retinoic acid. Tretinoin 148-161 heat shock protein 1 Mus musculus 76-81
1451960-5 1992 Induction of differentiation caused by prolonged cell culture, retinoic acid treatment, or embryoid body formation, however, resulted in an increase of the level of hsp25. Tretinoin 63-76 heat shock protein 1 Mus musculus 165-170
1333403-7 1992 The transcript distribution of CRABP I and II is discussed in relation to the teratogenic effects of RA, and compared to the RA-sensitive pattern of expression of other important developmental genes. Tretinoin 101-103 cellular retinoic acid binding protein I Mus musculus 31-38
1323566-0 1992 Retinoic acid induces myogenin synthesis and myogenic differentiation in the rat rhabdomyosarcoma cell line BA-Han-1C. Tretinoin 0-13 myogenin Rattus norvegicus 22-30
1323566-3 1992 Upon induction with RA, BA-Han-1C cells expressed also myogenin, in contrast to BA-Han-1B cells which never activated any of the genes encoding muscle bHLH factors. Tretinoin 20-22 myogenin Rattus norvegicus 55-63
1378478-1 1992 We have previously shown that cellular retinoic acid-binding protein II (CRABP-II), but not cellular retinoic acid-binding protein I (CRABP-I), mRNA expression is markedly induced in human skin by topical retinoic acid. Tretinoin 39-52 cellular retinoic acid binding protein 2 Homo sapiens 73-81
1321136-0 1992 Retinoic acid activation and thyroid hormone repression of the human alcohol dehydrogenase gene ADH3. Tretinoin 0-13 aldo-keto reductase family 1 member A1 Homo sapiens 69-90
1321136-1 1992 Mammalian alcohol dehydrogenase (ADH) catalyzes the oxidation of retinol to retinaldehyde, the rate-limiting step in the synthesis of retinoic acid. Tretinoin 134-147 aldo-keto reductase family 1 member A1 Homo sapiens 10-31
1321136-1 1992 Mammalian alcohol dehydrogenase (ADH) catalyzes the oxidation of retinol to retinaldehyde, the rate-limiting step in the synthesis of retinoic acid. Tretinoin 134-147 aldo-keto reductase family 1 member A1 Homo sapiens 33-36
1321136-2 1992 There exists a family of ADH isozymes encoded by unique genes, and it is unclear which isozymes are most important for regulation of retinoic acid synthesis during differentiation or development. Tretinoin 133-146 aldo-keto reductase family 1 member A1 Homo sapiens 25-28
1321791-1 1992 Two highly conserved forms of cellular retinoic acid binding protein (CRABP-I and CRABP-II) have been described, and one, CRABP-II, is highly expressed in human skin. Tretinoin 39-52 cellular retinoic acid binding protein 2 Homo sapiens 82-90
1321791-1 1992 Two highly conserved forms of cellular retinoic acid binding protein (CRABP-I and CRABP-II) have been described, and one, CRABP-II, is highly expressed in human skin. Tretinoin 39-52 cellular retinoic acid binding protein 2 Homo sapiens 122-130
1568207-0 1992 Retinoic acid inhibition of serum-induced c-fos transcription in a fibrosarcoma cell line. Tretinoin 0-13 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 42-47
1568207-2 1992 Northern analysis revealed that both chronic (7 days) and acute (6 h) retinoic acid treatment of serum-stimulated SSV-NRK cells caused a 6-fold decrease in c-fos mRNA levels. Tretinoin 70-83 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 156-161
1568207-6 1992 Because it has been shown that c-fos expression plays a pivotal role in mitogenesis of quiescent fibroblasts, we conclude that the retinoic acid-mediated down-regulation of c-fos expression is a mechanism for growth inhibition in SSV-NRK cells. Tretinoin 131-144 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 31-36
1568207-6 1992 Because it has been shown that c-fos expression plays a pivotal role in mitogenesis of quiescent fibroblasts, we conclude that the retinoic acid-mediated down-regulation of c-fos expression is a mechanism for growth inhibition in SSV-NRK cells. Tretinoin 131-144 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 173-178
1315627-5 1992 partially inhibited (61%) the induction of ODC by BSF at 5 h. In addition, retinoic acid (RA, 5 micrograms per mouse given 30 min before BSF) effectively inhibited BSF-induced ODC by 68%, while indomethacin (100 micrograms per mouse 2 h before BSF) had little or no effect. Tretinoin 75-88 ornithine decarboxylase, structural 1 Mus musculus 43-46
1312497-4 1992 Recently, we demonstrated that all-trans retinoic acid (RA) serves as a "pro-hormone" to the isomer 9-cis RA, which is a high-affinity ligand for the human RXR alpha. Tretinoin 41-54 retinoid X receptor alpha Homo sapiens 156-165
1312497-4 1992 Recently, we demonstrated that all-trans retinoic acid (RA) serves as a "pro-hormone" to the isomer 9-cis RA, which is a high-affinity ligand for the human RXR alpha. Tretinoin 56-58 retinoid X receptor alpha Homo sapiens 156-165
1312497-4 1992 Recently, we demonstrated that all-trans retinoic acid (RA) serves as a "pro-hormone" to the isomer 9-cis RA, which is a high-affinity ligand for the human RXR alpha. Tretinoin 106-108 retinoid X receptor alpha Homo sapiens 156-165
1547944-10 1992 Interestingly, the amount of PEA3 mRNA is down-regulated during retinoic acid-induced differentiation of mouse embryonic cell lines. Tretinoin 64-77 ets variant 4 Mus musculus 29-33
1311101-0 1992 Retinoid X receptor-COUP-TF interactions modulate retinoic acid signaling. Tretinoin 50-63 retinoid X receptor alpha Homo sapiens 0-19
1741406-10 1992 Id-2 expression is modulated in association with retinoic acid-induced ganglionic differentiation of the neuroblastoma cell line SMS-KCNR. Tretinoin 49-62 inhibitor of DNA binding 2 Homo sapiens 0-4
1545783-0 1992 Histone H1(0) mRNA and protein accumulate early during retinoic acid induced differentiation of synchronized embryonal carcinoma cells. Tretinoin 55-68 H1.0 linker histone Homo sapiens 0-13
1545783-4 1992 During retinoic acid induced differentiation of mitotically synchronized PC13 EC cells, accumulation of H1(0) mRNA starts in the first cell cycle. Tretinoin 7-20 H1.0 linker histone Homo sapiens 104-109
1538719-5 1992 Phenobarbital-inducible P-450 2B4 also had high activity in the 4-hydroxylation reaction of retinoids, and cytochrome b5 was found to increase the activity of P-450 2B4 with each substrate but to increase the activity of P-450 1A2 only with retinoic acid. Tretinoin 241-254 cytochrome b5 Oryctolagus cuniculus 107-120
1310260-1 1992 All-trans retinoic acid (RA) has previously been shown to modulate the transcriptional properties of the retinoic acid receptor (RAR) and retinoid X receptor (RXR). Tretinoin 10-23 retinoid X receptor alpha Homo sapiens 138-157
1310260-1 1992 All-trans retinoic acid (RA) has previously been shown to modulate the transcriptional properties of the retinoic acid receptor (RAR) and retinoid X receptor (RXR). Tretinoin 10-23 retinoid X receptor alpha Homo sapiens 159-162
1310260-1 1992 All-trans retinoic acid (RA) has previously been shown to modulate the transcriptional properties of the retinoic acid receptor (RAR) and retinoid X receptor (RXR). Tretinoin 25-27 retinoid X receptor alpha Homo sapiens 138-157
1310260-1 1992 All-trans retinoic acid (RA) has previously been shown to modulate the transcriptional properties of the retinoic acid receptor (RAR) and retinoid X receptor (RXR). Tretinoin 25-27 retinoid X receptor alpha Homo sapiens 159-162
1310260-3 1992 We report here an experimental approach that has identified 9-cis RA as an RXR ligand. Tretinoin 66-68 retinoid X receptor alpha Homo sapiens 75-78
1370436-1 1992 Incubation of the human glioma cell line HS 683 in the presence of IFN-gamma or retinoic acid strongly stimulates the cell-surface expression of the intercellular adhesion molecule ICAM-1. Tretinoin 80-93 intercellular adhesion molecule 1 Homo sapiens 181-187
1370436-12 1992 However, the inhibition of retinoic-acid-induced ICAM-1 expression cannot be explained by the same mechanisms. Tretinoin 27-40 intercellular adhesion molecule 1 Homo sapiens 49-55
1733233-6 1992 Other differentiating agents, dimethyl sulfoxide, retinoic acid, and dexamethasone, also increased levels of MRP-8 and MRP-14 mRNA. Tretinoin 50-63 S100 calcium binding protein A9 Homo sapiens 119-125
1576967-3 1992 MASH1 and MASH2 display complementary patterns of expression during the retinoic-acid-induced neuronal differentiation of P19 cells. Tretinoin 72-85 achaete-scute family bHLH transcription factor 2 Homo sapiens 10-15
1576967-5 1992 In contrast, MASH2 mRNA is expressed in undifferentiated P19 cells and is repressed by retinoic acid treatment. Tretinoin 87-100 achaete-scute family bHLH transcription factor 2 Homo sapiens 13-18
1320576-0 1992 Retinoic acid resistance of the variant embryonal carcinoma cell line RAC65 is caused by expression of a truncated RAR alpha. Tretinoin 0-13 retinoic acid receptor, alpha Mus musculus 115-124
1363667-2 1992 Retinoic acid has been considered to be a putative morphogen released from the ZPA. Tretinoin 0-13 zona pellucida glycoprotein 2 Gallus gallus 79-82
1363667-4 1992 From the result that retinoic acid-treated cells induce digit duplication, retinoic acid converts anterior cells into ZPA cells. Tretinoin 21-34 zona pellucida glycoprotein 2 Gallus gallus 118-121
1363667-4 1992 From the result that retinoic acid-treated cells induce digit duplication, retinoic acid converts anterior cells into ZPA cells. Tretinoin 75-88 zona pellucida glycoprotein 2 Gallus gallus 118-121
1341049-7 1992 Administration of retinoic acid to BA-Han-1C cells leads to the accumulation of myogenin mRNA approximately 48 h after the addition of RA. Tretinoin 18-31 myogenin Rattus norvegicus 80-88
1660713-7 1991 Preincubation for 3 days with either tumour necrosis factor alpha (TNF alpha) or retinoic acid (RA) both decreased the specific binding of 125I-PTHrP-(1-84) to about 40% of control levels. Tretinoin 81-94 parathyroid hormone-like hormone Rattus norvegicus 144-149
1660713-7 1991 Preincubation for 3 days with either tumour necrosis factor alpha (TNF alpha) or retinoic acid (RA) both decreased the specific binding of 125I-PTHrP-(1-84) to about 40% of control levels. Tretinoin 96-98 parathyroid hormone-like hormone Rattus norvegicus 144-149
1939209-3 1991 An examination of the expression of the extracellular matrix receptors, integrins, during this retinoic acid-induced differentiation period, demonstrated a specific and strong induction of expression of two polypeptides (130 and 115 kDa) immunoprecipitated with an anti-human vitronectin receptor antiserum. Tretinoin 95-108 vitronectin Mus musculus 276-287
1682879-10 1991 In Xenopus embryos treated with RA, homologues of the Hox-2 genes also displayed a temporal and dose response collinearity with gene organisation. Tretinoin 32-34 homeobox B7 S homeolog Xenopus laevis 54-59
1656224-0 1991 Specificity of a retinoic acid response element in the phosphoenolpyruvate carboxykinase gene promoter: consequences of both retinoic acid and thyroid hormone receptor binding. Tretinoin 17-30 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 55-88
1656224-0 1991 Specificity of a retinoic acid response element in the phosphoenolpyruvate carboxykinase gene promoter: consequences of both retinoic acid and thyroid hormone receptor binding. Tretinoin 125-138 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 55-88
1656224-1 1991 The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Tretinoin 17-30 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 67-100
1656224-1 1991 The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Tretinoin 17-30 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 102-107
1656224-1 1991 The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Tretinoin 32-34 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 67-100
1656224-1 1991 The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Tretinoin 32-34 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 102-107
1656224-1 1991 The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Tretinoin 54-56 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 67-100
1656224-1 1991 The ability of a retinoic acid (RA) response element (RARE) in the phosphoenolpyruvate carboxykinase (PEPCK) gene promoter to mediate effects of either RA or thyroid hormone (T3) on gene expression was studied. Tretinoin 54-56 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 102-107
1656224-5 1991 In contrast, the PEPCK RARE mediated six- to eightfold induction of CAT expression by RA. Tretinoin 23-25 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 17-22
1655528-1 1991 Treatment of mouse embryonal carcinoma (F9) cells with retinoic acid, an inducer of F9 cell differentiation, greatly increased the level of mRNA specific to one of the heat-shock proteins (HSP86). Tretinoin 55-68 heat shock protein 90, alpha (cytosolic), class A member 1 Mus musculus 189-194
1654334-1 1991 Retinoic acid-induced expression of CRABP-II but not CRABP-I in adult human skin in vivo and in skin fibroblasts in vitro. Tretinoin 0-13 cellular retinoic acid binding protein 2 Homo sapiens 36-44
1654334-6 1991 External application of 0.1% retinoic acid cream in vivo for 16 h resulted in a 16-fold induction of CRABP-II transcripts, while CRABP-I mRNA remained undetectable. Tretinoin 29-42 cellular retinoic acid binding protein 2 Homo sapiens 101-109
1654334-7 1991 Expression of CRABP-II, but not CRABP-I mRNA, was also markedly increased (greater than 15-fold) by retinoic acid treatment of fibroblasts cultured from human skin, whereas no significant induction of CRABP-II mRNA was observed in human lung fibroblasts. Tretinoin 100-113 cellular retinoic acid binding protein 2 Homo sapiens 14-22
1654334-9 1991 The marked inducibility of the CRABP-II gene is compatible with the idea that this isoform is important in retinoic acid-mediated regulation of human skin growth and differentiation. Tretinoin 107-120 cellular retinoic acid binding protein 2 Homo sapiens 31-39
1651942-7 1991 Cx37 transcripts were also found to increase two to threefold in response to retinoic acid treatment of cultured embryonic carcinoma F9 cells. Tretinoin 77-90 gap junction protein, alpha 4 Mus musculus 0-4
1651173-1 1991 The vitamin A derivative retinoic acid exerts its effects on transcription through two distinct classes of nuclear receptors, the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). Tretinoin 25-38 retinoid X receptor alpha Homo sapiens 188-191
1651173-2 1991 We provide evidence that expression of the gene for cellular retinol-binding protein type II (CRBPII), a key protein in the intestinal absorption of vitamin A, is dramatically up-regulated by retinoic acid in the presence of RXR but not RAR. Tretinoin 192-205 retinoid X receptor alpha Homo sapiens 225-228
1648728-1 1991 We present evidence that retinoic acid can down-regulate transcriptional activation by the nuclear protooncogene c-jun. Tretinoin 25-38 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-118
1648728-6 1991 These data suggest that the RAR alpha may form a nonproductive complex with c-Jun and provides a simple mechanisms by which retinoic acid may limit cell growth and possibly malignant progression. Tretinoin 124-137 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 76-81
1657566-5 1991 RA was found to also induce the biologically active, high-affinity NGF receptor: high-affinity receptors were undetectable on dissociated E7 sympathetic neurons and were observed in vitro only in RA-treated neurons. Tretinoin 0-2 nerve growth factor receptor Gallus gallus 67-79
1657566-5 1991 RA was found to also induce the biologically active, high-affinity NGF receptor: high-affinity receptors were undetectable on dissociated E7 sympathetic neurons and were observed in vitro only in RA-treated neurons. Tretinoin 196-198 nerve growth factor receptor Gallus gallus 67-79
2010091-1 1991 The mammalian transcription factor AP-2 is a sequence-specific DNA-binding protein expressed in neural crest lineages and regulated by retinoic acid. Tretinoin 135-148 transcription factor AP-2 alpha Homo sapiens 35-39
1706327-6 1991 Treatment of LoVo sublines with differentiating agents (dimethylformamide and retinoic acid) led to a decreased expression of all adhesion molecules studied, accompanied by increased resistance to LAK-mediated lysis. Tretinoin 78-91 alpha kinase 1 Homo sapiens 197-200
1850510-1 1991 The thyroid hormone receptor alpha (THRA or c-erbA-1) gene belongs to a family of genes which encode nuclear receptors for various hydrophobic ligands such as steroids, vitamin D, retinoic acid and thyroid hormones. Tretinoin 180-193 thyroid hormone receptor alpha Homo sapiens 4-34
1850510-1 1991 The thyroid hormone receptor alpha (THRA or c-erbA-1) gene belongs to a family of genes which encode nuclear receptors for various hydrophobic ligands such as steroids, vitamin D, retinoic acid and thyroid hormones. Tretinoin 180-193 thyroid hormone receptor alpha Homo sapiens 36-40
1850510-1 1991 The thyroid hormone receptor alpha (THRA or c-erbA-1) gene belongs to a family of genes which encode nuclear receptors for various hydrophobic ligands such as steroids, vitamin D, retinoic acid and thyroid hormones. Tretinoin 180-193 thyroid hormone receptor alpha Homo sapiens 44-52
1996113-0 1991 Retinoic acid response element in the human alcohol dehydrogenase gene ADH3: implications for regulation of retinoic acid synthesis. Tretinoin 0-13 aldo-keto reductase family 1 member A1 Homo sapiens 44-65
1996113-0 1991 Retinoic acid response element in the human alcohol dehydrogenase gene ADH3: implications for regulation of retinoic acid synthesis. Tretinoin 108-121 aldo-keto reductase family 1 member A1 Homo sapiens 44-65
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 0-13 aldo-keto reductase family 1 member A1 Homo sapiens 60-81
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 0-13 aldo-keto reductase family 1 member A1 Homo sapiens 83-86
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 0-13 aldo-keto reductase family 1 member A1 Homo sapiens 172-175
1996113-1 1991 Retinoic acid regulation of one member of the human class I alcohol dehydrogenase (ADH) gene family was demonstrated, suggesting that the retinol dehydrogenase function of ADH may play a regulatory role in the biosynthetic pathway for retinoic acid. Tretinoin 235-248 aldo-keto reductase family 1 member A1 Homo sapiens 60-81
1705423-3 1991 Increased expression of RAR alpha increased the induction of tissue TG by retinoic acid. Tretinoin 74-87 retinoic acid receptor, alpha Mus musculus 24-27
1705423-4 1991 In contrast, decreased RAR alpha expression, using an antisense RAR alpha expression vector, diminished the normal level of tissue TG induction caused by retinoic acid. Tretinoin 154-167 retinoic acid receptor, alpha Mus musculus 23-26
1705423-4 1991 In contrast, decreased RAR alpha expression, using an antisense RAR alpha expression vector, diminished the normal level of tissue TG induction caused by retinoic acid. Tretinoin 154-167 retinoic acid receptor, alpha Mus musculus 64-67
1705423-5 1991 Transfectants overexpressing RAR beta were also more responsive to retinoic acid for the induction of tissue TG, although the magnitude of TG induction was not as great as resulted from RAR alpha overexpression. Tretinoin 67-80 retinoic acid receptor, alpha Mus musculus 29-32
1705423-6 1991 These results indicate that the levels of the RAR alpha and RAR beta dictate the magnitude of tissue TG induction by retinoic acid. Tretinoin 117-130 retinoic acid receptor, alpha Mus musculus 46-49
1705423-6 1991 These results indicate that the levels of the RAR alpha and RAR beta dictate the magnitude of tissue TG induction by retinoic acid. Tretinoin 117-130 retinoic acid receptor, alpha Mus musculus 60-63
1997209-3 1991 We show here that the mRNA and protein for the microtubule component MAP2 is also induced by retinoic acid. Tretinoin 93-106 microtubule associated protein 2 Homo sapiens 69-73
1657330-2 1991 In addition, exposure of the cells for 24h to dexamethasone, estradiol, retinoic acid, or triiodothyronine resulted in a dose-dependent accumulation of hVDR mRNA. Tretinoin 72-85 vitamin D receptor Homo sapiens 152-156
2176887-0 1990 Induction of phosphoenolpyruvate carboxykinase gene expression by retinoic acid in an adult rat hepatocyte line. Tretinoin 66-79 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 13-46
2176887-3 1990 We have shown previously that RALA255-10G cells express only low levels of liver-specific genes such as albumin and tyrosine aminotransferase at 33 degrees C. In the present study, we demonstrated that at 33 degrees C, PEPCK synthesis and mRNA expression could be detected only in the simultaneous presence of dexamethasone (DEX), retinoic acid, and dibutyryl-cAMP (Bt2cAMP). Tretinoin 331-344 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 219-224
2176887-5 1990 However, at 40 degrees C, PEPCK gene expression was stimulated by the combination of DEX plus retinoic acid; additionally, DEX and retinoic acid potentiated the Bt2cAMP-mediated PEPCK induction. Tretinoin 94-107 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 26-31
1701721-3 1990 Only retinoic acid, however, was effective at inhibiting the activation of dopachrome isomerase, another regulatory enzyme in melanogenesis. Tretinoin 5-18 dopachrome tautomerase Mus musculus 75-95
1698671-3 1990 Retinoic acid induced primitive endoderm differentiation of F9 cells and simultaneously activated tissue plasminogen activator synthesis. Tretinoin 0-13 chromosome 20 open reading frame 181 Homo sapiens 98-126
2119291-0 1990 Leukemia inhibitory factor binds with high affinity to preosteoblastic RCT-1 cells and potentiates the retinoic acid induction of alkaline phosphatase. Tretinoin 103-116 LIF, interleukin 6 family cytokine Rattus norvegicus 0-26
2119291-1 1990 This study examines the effect of leukemia inhibitory factor (LIF) on preosteoblastic rat calvaria (RCT-1) cells, which acquire osteoblastic properties when treated with retinoic acid (RA). Tretinoin 170-183 LIF, interleukin 6 family cytokine Rattus norvegicus 34-60
2119291-1 1990 This study examines the effect of leukemia inhibitory factor (LIF) on preosteoblastic rat calvaria (RCT-1) cells, which acquire osteoblastic properties when treated with retinoic acid (RA). Tretinoin 170-183 LIF, interleukin 6 family cytokine Rattus norvegicus 62-65
2119291-1 1990 This study examines the effect of leukemia inhibitory factor (LIF) on preosteoblastic rat calvaria (RCT-1) cells, which acquire osteoblastic properties when treated with retinoic acid (RA). Tretinoin 185-187 LIF, interleukin 6 family cytokine Rattus norvegicus 34-60
2119291-1 1990 This study examines the effect of leukemia inhibitory factor (LIF) on preosteoblastic rat calvaria (RCT-1) cells, which acquire osteoblastic properties when treated with retinoic acid (RA). Tretinoin 185-187 LIF, interleukin 6 family cytokine Rattus norvegicus 62-65
2119291-2 1990 LIF potentiated the increase in alkaline phosphatase (AP) activity produced by RA. Tretinoin 79-81 LIF, interleukin 6 family cytokine Rattus norvegicus 0-3
2170427-6 1990 LIF treatment of the preosteoblast cell line, UMR 201, enhanced the alkaline phosphatase response of these cells to retinoic acid. Tretinoin 116-129 LIF, interleukin 6 family cytokine Rattus norvegicus 0-3
2371287-8 1990 The presence of retinoic acid was required for maximal PUFA-dependent growth inhibition of A549 or B16 cells by TGF-beta 1 under some, but not all, conditions. Tretinoin 16-29 pumilio RNA binding family member 3 Homo sapiens 55-59
2159896-5 1990 These results suggest that crucial roles of endogenous RA in facial development depend on differential functions of the RAR subtypes. Tretinoin 55-57 retinoic acid receptor, alpha Mus musculus 120-123
2153560-1 1990 The human embryonal carcinoma (EC) cell line Tera 2 clone 13 (T2/13) can be induced to differentiate in vitro into neuroectodermal cell types with retinoic acid. Tretinoin 147-160 solute carrier family 25 member 5 Homo sapiens 62-67
2176907-1 1990 The development of cytochrome b558 (Cyt b) as determined spectrophotometrically, was investigated in human polymorphonuclear neutrophils (PMN), monocytes (MN) and during differentiation of HL-60 and U 937 cells induced by retinoic acid (RA) alone or in combination with IFN gamma. Tretinoin 222-235 mitochondrially encoded cytochrome b Homo sapiens 19-31
2176907-1 1990 The development of cytochrome b558 (Cyt b) as determined spectrophotometrically, was investigated in human polymorphonuclear neutrophils (PMN), monocytes (MN) and during differentiation of HL-60 and U 937 cells induced by retinoic acid (RA) alone or in combination with IFN gamma. Tretinoin 222-235 mitochondrially encoded cytochrome b Homo sapiens 36-41
2176907-1 1990 The development of cytochrome b558 (Cyt b) as determined spectrophotometrically, was investigated in human polymorphonuclear neutrophils (PMN), monocytes (MN) and during differentiation of HL-60 and U 937 cells induced by retinoic acid (RA) alone or in combination with IFN gamma. Tretinoin 237-239 mitochondrially encoded cytochrome b Homo sapiens 19-31
2176907-1 1990 The development of cytochrome b558 (Cyt b) as determined spectrophotometrically, was investigated in human polymorphonuclear neutrophils (PMN), monocytes (MN) and during differentiation of HL-60 and U 937 cells induced by retinoic acid (RA) alone or in combination with IFN gamma. Tretinoin 237-239 mitochondrially encoded cytochrome b Homo sapiens 36-41
2176907-5 1990 In differentiated HL-60 and U 937 cells, the oxidative metabolism increases in parallel with Cyt b specific contents, both being enhanced by the addition of IFN gamma to the RA treatment. Tretinoin 174-176 mitochondrially encoded cytochrome b Homo sapiens 93-98
33824267-3 2021 Additionally, MLL5 overexpression increased the responsiveness of APL leukemic cells to all-trans retinoic acid (ATRA)-induced differentiation, via regulation of the epigenetic modifiers SETD7 and LSD1. Tretinoin 98-111 lysine demethylase 1A Homo sapiens 197-201
33824267-3 2021 Additionally, MLL5 overexpression increased the responsiveness of APL leukemic cells to all-trans retinoic acid (ATRA)-induced differentiation, via regulation of the epigenetic modifiers SETD7 and LSD1. Tretinoin 113-117 lysine demethylase 1A Homo sapiens 197-201
7568495-9 1995 Retinoic acid-induced fetal mouse forelimb syndactyly was observed in all the groups; 81 percent of E17 limbs, 75 percent of PN limbs, and 77 percent of E13+4 limbs had syndactyly. Tretinoin 0-13 skull development traits QTL 10 Mus musculus 100-103
8070357-8 1994 All-trans-retinoic acid and 9-cis-retinoic acid increased CG secretion and CG alpha and CG beta mRNAs, but clofibric acid blunted these stimulatory effects. Tretinoin 0-23 chorionic gonadotropin subunit beta 3 Homo sapiens 88-95
34365653-4 2022 RA signaling in DCs is required for the production of food allergen-specific IgE and IgG1. Tretinoin 0-2 LOC105243590 Mus musculus 85-89
34599982-7 2022 We found that RA treatment increased the level of PKA-phosphorylated SF2 but decreased the level of SF2. Tretinoin 14-16 serine and arginine rich splicing factor 1 Homo sapiens 69-72
34599982-7 2022 We found that RA treatment increased the level of PKA-phosphorylated SF2 but decreased the level of SF2. Tretinoin 14-16 serine and arginine rich splicing factor 1 Homo sapiens 100-103
34599982-11 2022 These results indicate that RA activates PKA in the nucleus, increases phosphorylation of SF2, raises levels of Mcl-1S and lowers levels of Mcl-1L, resulting in the induction of differentiation. Tretinoin 28-30 serine and arginine rich splicing factor 1 Homo sapiens 90-93
34546543-5 2022 Three samples in which CD11b increased in response to ATRA had an inversion of chromosome 16 as well as the CBFB-MYH11 fusion gene, and the fourth sample was from a patient with KMT2A-rearranged, therapy-related AML. Tretinoin 54-58 integrin subunit alpha M Homo sapiens 23-28
34836491-6 2021 Nor was RA-induced upregulation of p-tyr phosphorylation of p47phox, a member of the NADPH complex that produces ROS, a putative phosphorylation dependent signaling regulator. Tretinoin 8-10 neutrophil cytosolic factor 1 Homo sapiens 60-67
34784434-5 2021 Quantification of mRNA and protein expression revealed dysregulation in the first step of RA biosynthesis consistent with reduced RA including decreased protein expression of retinol dehydrogenase (RDH)-10 and increased protein expression of RDH11 and dehydrogenase/reductase (DHRS)-4 in asthmatic lung. Tretinoin 90-92 retinol dehydrogenase 10 Homo sapiens 175-205
34943872-5 2021 Moreover, ATRA treatment of APL cells led to a significant activation of calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) and its downstream effector AMP-activated protein kinase (AMPK), linking Ca2+ signaling to autophagy. Tretinoin 10-14 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 163-191
34943872-5 2021 Moreover, ATRA treatment of APL cells led to a significant activation of calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) and its downstream effector AMP-activated protein kinase (AMPK), linking Ca2+ signaling to autophagy. Tretinoin 10-14 protein kinase AMP-activated non-catalytic subunit beta 1 Homo sapiens 193-197
34836244-6 2021 All-trans retinol also travels through the bloodstream bound to retinol binding protein 4 (RBP4), where it enters cells with the assistance of the transmembrane transporters, stimulated by retinoic acid 6 (STRA6) in peripheral tissues or retinol binding protein 4 receptor 2 (RBPR2) in systemic tissues (e.g., in the retina and the liver, respectively). Tretinoin 189-202 retinol binding protein 4 Homo sapiens 64-89
34836244-6 2021 All-trans retinol also travels through the bloodstream bound to retinol binding protein 4 (RBP4), where it enters cells with the assistance of the transmembrane transporters, stimulated by retinoic acid 6 (STRA6) in peripheral tissues or retinol binding protein 4 receptor 2 (RBPR2) in systemic tissues (e.g., in the retina and the liver, respectively). Tretinoin 189-202 retinol binding protein 4 Homo sapiens 91-95
34472453-3 2021 Here, we discuss RA metabolism in the testis as well as the roles of stimulated by retinoic acid gene 8 (STRA8) and MEIOSIN, which are responsive to RA and are critical for meiosis. Tretinoin 149-151 stimulated by retinoic acid 8 Homo sapiens 69-103
34472453-3 2021 Here, we discuss RA metabolism in the testis as well as the roles of stimulated by retinoic acid gene 8 (STRA8) and MEIOSIN, which are responsive to RA and are critical for meiosis. Tretinoin 149-151 stimulated by retinoic acid 8 Homo sapiens 105-110
34528674-4 2021 Using in vitro cultures of embryonic mouse stromal cells, we show that retinoic acid mediated signaling is important for the differentiation of precursors towards the Cxcl13pos follicular dendritic cell (FDC) lineage, while blocking lymphotoxin mediated Ccl19pos fibroblastic reticular cell (FRC) lineage differentiation. Tretinoin 71-84 chemokine (C-X-C motif) ligand 13 Mus musculus 167-173
34166654-5 2021 Embryos lacking dermal Ezh2 have elevated epidermal proliferation and differentiation that can be rescued by small molecule inhibition of retinoic acid (RA) signaling. Tretinoin 138-151 enhancer of zeste 2 polycomb repressive complex 2 subunit Mus musculus 23-27
34166654-5 2021 Embryos lacking dermal Ezh2 have elevated epidermal proliferation and differentiation that can be rescued by small molecule inhibition of retinoic acid (RA) signaling. Tretinoin 153-155 enhancer of zeste 2 polycomb repressive complex 2 subunit Mus musculus 23-27
34480899-10 2021 These results suggest that P450 27C1 directly accepts all-trans retinol and retinaldehyde from CRBP-1 and all-trans retinoic acid from CRABP-2, but not from CRABP-1. Tretinoin 116-129 cellular retinoic acid binding protein 2 Homo sapiens 135-142
34087410-3 2021 Calcitriol (1,25-dihydroxyvitamin D3) and retinoic acid possess hormone-like properties and are the bioactive metabolites of vitamin D and A, respectively, that signal through heterodimers containing the common retinoid X receptor. Tretinoin 42-55 retinoid X receptor alpha Homo sapiens 211-230
34087410-8 2021 Importantly, retinoic acid negated the effect of calcitriol and impaired the binding of VDR on the Il9 gene by dampened VDR-RXR formation. Tretinoin 13-26 vitamin D receptor Homo sapiens 88-91
34087410-8 2021 Importantly, retinoic acid negated the effect of calcitriol and impaired the binding of VDR on the Il9 gene by dampened VDR-RXR formation. Tretinoin 13-26 vitamin D receptor Homo sapiens 120-123
34087410-8 2021 Importantly, retinoic acid negated the effect of calcitriol and impaired the binding of VDR on the Il9 gene by dampened VDR-RXR formation. Tretinoin 13-26 retinoid X receptor alpha Homo sapiens 124-127
34572134-9 2021 We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Tretinoin 55-68 aldehyde dehydrogenase 1 family member A2 Homo sapiens 46-53
34572134-9 2021 We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Tretinoin 55-68 matrix metallopeptidase 9 Homo sapiens 126-131
34572134-9 2021 We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Tretinoin 70-72 aldehyde dehydrogenase 1 family member A2 Homo sapiens 46-53
34572134-9 2021 We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Tretinoin 70-72 matrix metallopeptidase 9 Homo sapiens 126-131
34417282-8 2021 Other affected components of RA signaling include selective increases in AI animals in hippocampal synthesis (RALDH1) and catabolism of RA (CYP26B1), RA receptor alpha, the RA regulated ionotropic glutamate receptor (GluR1), as well as fragile X mental retardation protein. Tretinoin 29-31 cytochrome P450, family 26, subfamily b, polypeptide 1 Rattus norvegicus 140-147
34410954-7 2021 CONCLUSION: Combined ATRA and IM therapy was shown to be effective in decreasing BCR-ABL and ABCB1 genes, possibly through the differentiation of blast cells, demonstrating that the therapy could be potentially effective in the blast crisis of the disease and for those patients who develop resistance to available CML treatments. Tretinoin 21-25 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 85-88
34417575-7 2021 Srebp-1c or Ucp2 silencing attenuated GSIS impairment by reversing the ATRA-induced increase in UCP2 expression and decrease in ATP content. Tretinoin 71-75 uncoupling protein 2 Rattus norvegicus 12-16
34417575-7 2021 Srebp-1c or Ucp2 silencing attenuated GSIS impairment by reversing the ATRA-induced increase in UCP2 expression and decrease in ATP content. Tretinoin 71-75 uncoupling protein 2 Rattus norvegicus 96-100
34417575-10 2021 In conclusion, ATRA impaired GSIS partly by activating the RXR/SREBP-1c/UCP2 pathway, thus worsening diabetic symptoms. Tretinoin 15-19 uncoupling protein 2 Rattus norvegicus 72-76
34458260-5 2021 We suggest RA signaling-mediated regulation of VIPR1 and KRT7 as the underlying mechanism for lumen formation, rather than apoptosis in the organoid culture system. Tretinoin 11-13 keratin 7 Mus musculus 57-61
34447379-2 2021 Murine studies have also demonstrated that RXR agonists have anti-inflammatory effects by enhancing the ability of all-trans-retinoic acid (atRA) to promote T-regulatory cell (Treg) induction and reduce Th17 differentiation in vitro. Tretinoin 115-138 retinoid X receptor alpha Homo sapiens 43-46
34447379-2 2021 Murine studies have also demonstrated that RXR agonists have anti-inflammatory effects by enhancing the ability of all-trans-retinoic acid (atRA) to promote T-regulatory cell (Treg) induction and reduce Th17 differentiation in vitro. Tretinoin 140-144 retinoid X receptor alpha Homo sapiens 43-46
34430707-5 2021 By microArray analysis, lncRNA HAGLR was observed to be significantly upregulated during the RA-induced SH-SY5Y differentiation. Tretinoin 93-95 HOXD antisense growth-associated long non-coding RNA Homo sapiens 31-36
34430707-11 2021 The rescue experiments verified that recovery of miR-130a-3p in HAGLR-overexpressing SH-SY5Y cells could successfully overcome the RA-induced SH-SY5Y differentiation by targeting MeCP2. Tretinoin 131-133 HOXD antisense growth-associated long non-coding RNA Homo sapiens 64-69
34244292-6 2021 Upon RA treatment of Satb2 wt ESCs, SATB2 interacts with ZFP451 and the LSD1/CoREST complex and gains binding at differentiation genes, which is not observed in RA-treated Satb2 K R cells. Tretinoin 5-7 lysine demethylase 1A Homo sapiens 72-76
34381879-0 2021 Knock-in of the duck retinoic acid-inducible gene I (RIG-I) into the Mx gene in DF-1 cells enables both stable and immune response-dependent RIG-I expression. Tretinoin 21-34 antiviral innate immune response receptor RIG-I Anas platyrhynchos 53-58
34381879-0 2021 Knock-in of the duck retinoic acid-inducible gene I (RIG-I) into the Mx gene in DF-1 cells enables both stable and immune response-dependent RIG-I expression. Tretinoin 21-34 antiviral innate immune response receptor RIG-I Anas platyrhynchos 141-146
34381879-3 2021 It is suggested that differences in the pathogenicity of AIV infection between waterfowls and chickens are related to the expression of retinoic acid-inducible gene I (RIG-I), a pattern recognition receptor that chickens evolutionally lack. Tretinoin 136-149 antiviral innate immune response receptor RIG-I Anas platyrhynchos 168-173
34299349-3 2021 RA signaling is mediated by the following two nuclear retinoic receptor subtypes: the retinoic acid receptor (RAR) and the retinoic X receptor (RXR), and their isoforms. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 123-142
34299349-3 2021 RA signaling is mediated by the following two nuclear retinoic receptor subtypes: the retinoic acid receptor (RAR) and the retinoic X receptor (RXR), and their isoforms. Tretinoin 0-2 retinoid X receptor alpha Homo sapiens 144-147
34207434-7 2021 ICAM-1 universally present throughout U87MG was enhanced by ATRA, of interest for chemotherapy targeting studies. Tretinoin 60-64 intercellular adhesion molecule 1 Homo sapiens 0-6
34211477-0 2021 Retinoic Acid: A New Old Friend of IL-17A in the Immune Pathogeny of Liver Fibrosis. Tretinoin 0-13 interleukin 17A Homo sapiens 35-41
34211477-4 2021 Retinoic acid (active metabolite of vitamin A) is able to regulate the differentiation of IL-17A+/IL-22-producing cells as well as the expression of profibrotic markers. Tretinoin 0-13 interleukin 17A Homo sapiens 90-96
34211477-4 2021 Retinoic acid (active metabolite of vitamin A) is able to regulate the differentiation of IL-17A+/IL-22-producing cells as well as the expression of profibrotic markers. Tretinoin 0-13 interleukin 22 Homo sapiens 98-103
34199197-6 2021 Co-treatment with gap junction enhancers such as all-trans retinoic acid (ATRA) and quinoline showed potentiating effects with FSK on cell survival via activation of cAMP/PKA/CREB. Tretinoin 49-72 cAMP responsive element binding protein 1 Homo sapiens 175-179
34199197-6 2021 Co-treatment with gap junction enhancers such as all-trans retinoic acid (ATRA) and quinoline showed potentiating effects with FSK on cell survival via activation of cAMP/PKA/CREB. Tretinoin 74-78 cAMP responsive element binding protein 1 Homo sapiens 175-179
35001679-3 2022 In the present study, we show that Rdh10 loss of function leads to a substantial reduction in retinoic acid (RA) signaling in the developing frontonasal process during early embryogenesis, which results in a variety of craniofacial anomalies, including midfacial cleft and ectopic chondrogenic nodules. Tretinoin 94-107 retinol dehydrogenase 10 Homo sapiens 35-40
35001679-3 2022 In the present study, we show that Rdh10 loss of function leads to a substantial reduction in retinoic acid (RA) signaling in the developing frontonasal process during early embryogenesis, which results in a variety of craniofacial anomalies, including midfacial cleft and ectopic chondrogenic nodules. Tretinoin 109-111 retinol dehydrogenase 10 Homo sapiens 35-40
35594436-12 2022 Upon retinoic acid-induction, differentiated neurons with eEF1A2 knockdown exhibited shorter neurite length than untransfected cells, which was associated with the reduction of tyrosine hydroxylase and suppression of MAP2 at 10 days of differentiation. Tretinoin 5-18 microtubule associated protein 2 Homo sapiens 217-221
35147911-4 2022 To this end, we examined the effects of intrathecal injection of all-trans retinoic acid (ATRA)-preconditioned bone marrow mesenchymal stem cells (BM-MSCs) (ATRA-MSCs) on autophagy activity and the HMGB1/NF-kappaB/NLRP3 inflammatory pathway in an SCI rat model. Tretinoin 157-161 high mobility group box 1 Rattus norvegicus 198-203
35574006-2 2022 The synthesis of retinoic acid from retinal in the seminiferous epithelium is a result of the action of aldehyde dehydrogenases termed ALDH1A1, ALDH1A2, and ALDH1A3. Tretinoin 17-30 aldehyde dehydrogenase 1 family member A2 Homo sapiens 144-151
35574006-5 2022 The cell specific elimination of Aldh1a2 gene showed that retinoic acid synthesis by Sertoli cells is required for the initial round of spermatogonial differentiation but that there is no requirement for retinoic acid synthesis by germ cells. Tretinoin 58-71 aldehyde dehydrogenase 1 family member A2 Homo sapiens 33-40
35456995-0 2022 Inhibition of RhoA and Cdc42 by miR-133a Modulates Retinoic Acid Signalling during Early Development of Posterior Cardiac Tube Segment. Tretinoin 51-64 ras homolog family member A Gallus gallus 14-18
35456995-7 2022 Additionally, retinoic acid represses miR-133a, while it increases Raldh2, Tbx5 and AMHC1. Tretinoin 14-27 aldehyde dehydrogenase 1 family member A2 Gallus gallus 67-73
35456995-8 2022 Given that RhoA and Cdc42 are involved in Raldh2 expression and that they are modulated by miR-133a, which is influenced by retinoic acid signalling, our results suggest the presence of a negative feedback mechanism between miR-133a and retinoic acid during early development of the posterior cardiac tube segment. Tretinoin 124-137 ras homolog family member A Gallus gallus 11-15
35456995-8 2022 Given that RhoA and Cdc42 are involved in Raldh2 expression and that they are modulated by miR-133a, which is influenced by retinoic acid signalling, our results suggest the presence of a negative feedback mechanism between miR-133a and retinoic acid during early development of the posterior cardiac tube segment. Tretinoin 237-250 ras homolog family member A Gallus gallus 11-15
35456995-8 2022 Given that RhoA and Cdc42 are involved in Raldh2 expression and that they are modulated by miR-133a, which is influenced by retinoic acid signalling, our results suggest the presence of a negative feedback mechanism between miR-133a and retinoic acid during early development of the posterior cardiac tube segment. Tretinoin 237-250 aldehyde dehydrogenase 1 family member A2 Gallus gallus 42-48
35078784-0 2022 Targeting S100A9-ALDH1A1-retinoic acid signaling to suppress brain relapse in EGFR-mutant lung cancer. Tretinoin 25-38 S100 calcium binding protein A9 Homo sapiens 10-16
35078784-5 2022 Mechanistically, S100A9 upregulates ALDH1A1 expression and activates the retinoic acid (RA) signaling pathway in osimertinib-refractory cancer cells. Tretinoin 73-86 S100 calcium binding protein A9 Homo sapiens 17-23
35078784-5 2022 Mechanistically, S100A9 upregulates ALDH1A1 expression and activates the retinoic acid (RA) signaling pathway in osimertinib-refractory cancer cells. Tretinoin 88-90 S100 calcium binding protein A9 Homo sapiens 17-23
35304896-2 2022 TLR5 was expressed in embryoid body derived from mouse embryonic stem cells (mESCs) and betaIII-tubulin-positive cells under all-trans retinoic acid-treated condition. Tretinoin 135-148 tubulin, beta 3 class III Mus musculus 88-103
35318262-0 2022 All-trans retinoic acid changes muscle fiber type via increasing GADD34 dependent on MAPK signal. Tretinoin 10-23 protein phosphatase 1, regulatory subunit 15A Mus musculus 65-71
35318262-3 2022 However, the role of growth arrest and DNA damage-inducible protein 34 (GADD34), one of the downstream factors of PERK, and the effects of ATRA on GADD34 expression in muscle remain unclear. Tretinoin 139-143 protein phosphatase 1, regulatory subunit 15A Mus musculus 147-153
35318262-6 2022 ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on GADD34 mRNA via p-38 MAPK, resulting in the instability of GADD34 mRNA. Tretinoin 0-4 protein phosphatase 1, regulatory subunit 15A Mus musculus 100-106
35318262-6 2022 ATRA also inhibited the interaction of TTP, which induces mRNA degradation, with AU-rich element on GADD34 mRNA via p-38 MAPK, resulting in the instability of GADD34 mRNA. Tretinoin 0-4 protein phosphatase 1, regulatory subunit 15A Mus musculus 159-165
35303942-1 2022 Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are cytosolic pattern recognition receptors that initiate innate antiviral immunity. Tretinoin 0-13 DExD/H-box helicase 58 Homo sapiens 32-37
35066375-0 2022 All-trans retinoic acid inhibits HCV replication by downregulating core levels via E6AP-mediated proteasomal degradation. Tretinoin 10-23 ubiquitin protein ligase E3A Homo sapiens 83-87
35066375-1 2022 Here, we found that all-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, strengthens the anti-viral defense mechanism of E6-associated protein (E6AP) that downregulates hepatitis C virus (HCV) Core levels via ubiquitin-dependent proteasomal degradation. Tretinoin 23-43 ubiquitin protein ligase E3A Homo sapiens 177-181
35066375-1 2022 Here, we found that all-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, strengthens the anti-viral defense mechanism of E6-associated protein (E6AP) that downregulates hepatitis C virus (HCV) Core levels via ubiquitin-dependent proteasomal degradation. Tretinoin 45-49 ubiquitin protein ligase E3A Homo sapiens 177-181
35066375-2 2022 For this effect, ATRA downregulated both protein and enzyme activity levels of DNA methyltransferase 1 and 3b and activated E6AP expression via promoter hypomethylation in HepG2 cells but not in Hep3B cells, in which p53 was absent. Tretinoin 17-21 DNA methyltransferase 1 Homo sapiens 79-109
35066375-2 2022 For this effect, ATRA downregulated both protein and enzyme activity levels of DNA methyltransferase 1 and 3b and activated E6AP expression via promoter hypomethylation in HepG2 cells but not in Hep3B cells, in which p53 was absent. Tretinoin 17-21 ubiquitin protein ligase E3A Homo sapiens 124-128
35066375-3 2022 Ectopic p53 expression but not E6AP overexpression restored the ability of ATRA to downregulate HCV Core levels in Hep3B cells, suggesting a direct role of p53 in the E6AP-mediated ubiquitination of HCV Core. Tretinoin 75-79 ubiquitin protein ligase E3A Homo sapiens 167-171
35237315-9 2022 RA also enhanced the expression of BARD1 and of the 90 kDa BRCA1 isoform. Tretinoin 0-2 breast cancer 1, early onset Mus musculus 59-64
35171653-7 2022 Treatment of wild-type mice with retinoic acid (RA) suppressed the capacity of C. acnes to form acne-like lesions, inhibited adipogenesis, and enhanced cathelicidin expression in preadipocytes, but lesions were unresponsive in Camp-/- mice, despite the anti-adipogenic action of RA. Tretinoin 33-46 cathelicidin antimicrobial peptide Mus musculus 227-231
35164690-1 2022 BACKGROUND: Retinoic acid-related orphan receptor alpha (RORA) has been reported to be suppressed in autistic patients and is associated with autism spectrum disorders (ASD), although the potential role and mechanism of RORA on gastrointestinal (GI) symptoms in ASD patients is still not reported. Tretinoin 12-25 RAR related orphan receptor A Homo sapiens 57-61
35164690-1 2022 BACKGROUND: Retinoic acid-related orphan receptor alpha (RORA) has been reported to be suppressed in autistic patients and is associated with autism spectrum disorders (ASD), although the potential role and mechanism of RORA on gastrointestinal (GI) symptoms in ASD patients is still not reported. Tretinoin 12-25 RAR related orphan receptor A Homo sapiens 220-224
35204227-7 2022 ATRA treatment also attenuated TGEV-induced apoptosis in IPEC-J2 cells by downregulating the expression of Caspase-3, which is related to the inhibition of death receptor (Fas and Caspase-8) and mitochondrial (Bax, Bcl-2, and Caspase-9) pathways. Tretinoin 0-4 Fas cell surface death receptor Sus scrofa 172-175
35204227-8 2022 Moreover, ATRA treatment prevented TGEV-induced ROS and MDA production and the upregulation of P38MAPK phosphorylation level, which is related to the increase in the activities of antioxidant enzymes (SOD, CAT, and T-AOC) and the mRNA abundance of antioxidant-related genes (GPX1, GPX2, SOD1, CAT, GCLC, and GCLM). Tretinoin 10-14 glutathione peroxidase 1 Homo sapiens 275-279
35197751-0 2022 Impact of preconditioning stem cells with all-trans retinoic acid signaling pathway on cisplatin-induced nephrotoxicity by down-regulation of TGFbeta1, IL-6, and caspase-3 and up-regulation of HIF1alpha and VEGF. Tretinoin 52-65 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 193-202
35159132-7 2022 Binding of RA to RARs regulates recruitment of transcriptional coregulators such as nuclear receptor coactivator (NCOA) or nuclear receptor corepressor (NCOR), which in turn control binding of the generic coactivator p300 or the generic corepressor PRC2. Tretinoin 11-13 E1A binding protein p300 Mus musculus 217-221
35111166-5 2021 ANKRD55 expression levels are further enhanced by retinoic acid agonist AM580 but downregulated following maturation with interferon (IFN)-gamma and lipopolysaccharide (LPS). Tretinoin 50-63 ankyrin repeat domain 55 Homo sapiens 0-7
35013142-10 2022 The results indicate that ATRA causes a significant down-regulation of CRLS1 (Cardiolipin-synthase-1) and LPCAT1 (Lysophosphatidylcholine-Acyltransferase-1) mRNAs which code for two enzymes catalyzing the last steps of cardiolipin synthesis. Tretinoin 26-30 lysophosphatidylcholine acyltransferase 1 Homo sapiens 106-112
35013142-10 2022 The results indicate that ATRA causes a significant down-regulation of CRLS1 (Cardiolipin-synthase-1) and LPCAT1 (Lysophosphatidylcholine-Acyltransferase-1) mRNAs which code for two enzymes catalyzing the last steps of cardiolipin synthesis. Tretinoin 26-30 lysophosphatidylcholine acyltransferase 1 Homo sapiens 114-155